Primary Management

in General, Vascular
and Thoracic Surgery

A Practical Approach
Daniele Bissacco
Alberto M. Settembrini
Andrea Mazzari
Editors

123
Primary Management in General, Vascular
and Thoracic Surgery
Daniele Bissacco  •  Alberto M. Settembrini 
Andrea Mazzari
Editors

Primary Management in
General, Vascular and
Thoracic Surgery
A Practical Approach
Editors
Daniele Bissacco Alberto M. Settembrini
Vascular Surgery Unit Vascular Surgery Unit
Fondazione IRCCS Ca’ Granda Ospedale Fondazione IRCCS Ca’ Granda Ospedale
Maggiore Policlinico Maggiore Policlinico
Milan, Italy Milan, Italy

Andrea Mazzari
Mini-invasive and General Surgery Unit
Ospedale Cristo Re
Rome, Italy

ISBN 978-3-031-12562-1    ISBN 978-3-031-12563-8 (eBook)

https://doi.org/10.1007/978-3-031-12563-8

© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether
the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of
illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and
transmission or information storage and retrieval, electronic adaptation, computer software, or by similar
or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication
does not imply, even in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
The publisher, the authors, and the editors are safe to assume that the advice and information in this book
are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the
editors give a warranty, expressed or implied, with respect to the material contained herein or for any
errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional
claims in published maps and institutional affiliations.

This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Preface

A specialist doctor is a man who knows more and more about less and less.
Dr. William J. Mayo
Fudit equum magno tellus percussa tridenti.
Virgilio, Georgiche 1 1-42
These are two phrases that strike us to the heart.
Mayo is the founder of one of the most important hospitals in the world, and his
phrase is a motto for all doctors who have married their work following the deep
meaning of the word “doctor” by taking care of all patients.
Virgil’s phrase must be translated into medical words considering that the teacher
must prepare young surgeons to learn and make their own the lessons received from
the experience of the elders.
Medicine is a field where changes are inevitable, but changes are not always
evolutions. To be good doctors, it is imperative to know the biology and processes
of the body’s biological behavior and, from there, try to identify changes and evolu-
tions in therapies and treatments.
Indeed, in surgery it is essential to know the difference between the basics and
the evolution of techniques.
The basics of surgery are the cornerstones of surgical growth for surgeons, but all
good doctors and surgeons must keep in mind that the first approach to the patient
is the correct diagnosis and management.
Why? The question can be answered by tracing its historical development over
the centuries to identify the fundamental steps that depend closely on the evolution
of thought. Why? The basis of surgery is not the hands but the head.
The decision-making process is the first and sometimes the most important con-
dition to be addressed before treatment.
Our book is intended to be a concise but comprehensive guide for quick consul-
tation by our younger colleagues on various clinical situations.
This book is for young surgeons by young surgeons. SPIGC (Italian
Polyspecialistic Society of Young Surgeons) has endorsed this publication because
who can be a better advisor to a young surgeon than another young surgeon who is
more experienced, more skilled, and knowledgeable in a specific field.
Practical advice is given for all stages of management, and all chapters are rich
in references and illustrations to provide additional reading to those who want more
in-depth coverage.

v
vi Preface

This is the reason why the authors have written very practical and up-to-date
chapters on different but frequent pathologies of the most critical surgical fields:
general, thoracic, and vascular surgery.

Milan, Italy Daniele Bissacco

Milan, Italy  Alberto M. Settembrini
Rome, Italy  Andrea Mazzari
Contents

1 Historical Overview ����������������������������������������������������������������������������������   1

E. Botteri, F. Bongiovanni, R. L. Meniconi, and E. Grespi

Part I Surgical Instruments and Materials

2 
Surgical Instruments and Materials in General Surgery����������������������   7
Andrea Mazzari, Pasquina M. C. Tomaiuolo,
and Roberto Luca Meniconi
3 
Surgical Instruments and Materials in Thoracic Surgery ��������������������  15
Valeria Musso and Francesco Damarco
4 
Surgical Instruments and Materials in Vascular Surgery����������������������  21
Ilenia D’Alessio and Matteo Marone

Part II Neck
5 Supra-aortic Trunks Emergency Conditions������������������������������������������  33
Enza Lucia Castronovo, Daniele Bissacco, D’Oria Mario,
Alberto M. Settembrini, and Sirignano Pasqualino
6 
Upper Airways Tract in Emergency Settings������������������������������������������  49
Diotti Cristina and Francesco Damarco
7 
Multidisciplinary Surgical Consensus on Neck Emergencies����������������  63
Emanuela Fuccillo and Marco Giovenzana

Part III Chest
8 Chest: Surgical Anatomy and General Consideration
in Emergency Settings ������������������������������������������������������������������������������  73
Valeria Musso and Francesco Damarco
9 Acute Aortic Syndromes and Thoracic Aortic Aneurysms:
From Diagnosis to Treatment��������������������������������������������������������������������  81
Andrea Xodo, Andrea Gallo, Paolo Magagna, and Mario D’Oria

vii
viii Contents

10 Pulmonary and Thoracic Emergencies����������������������������������������������������  97

Francesco Damarco
11 Upper Gastrointestinal Tract Acute Conditions�������������������������������������� 119
Marco Giovenzana, Beatrice Giuliani, and Nicolò Maria Mariani
12 Multidisciplinary
 Surgical Consensus on Chest Emergencies�������������� 129
Francesco Damarco, Marco Giovenzana, Diotti Cristina,
and Valeria Musso

Part IV Abdomen
13 Abdomen:
 Surgical Anatomy and General Consideration
in Emergency Settings ������������������������������������������������������������������������������ 137
Sarah Molfino, Giampaolo Bertoloni, and Gian Luca Baiocchi
14 Acute Abdominal Aorta and Visceral Vessel Disease������������������������������ 145
Davide Esposito and Elena Giacomelli
15 A
 cute Abdomen and Acute Abdominal Conditions�������������������������������� 153
Emanuele Botteri, Gianmaria Casoni Pattacini, Alessio Giordano,
and Francesca Ratti
16 Abdominal
 Emergencies Requiring a Multidisciplinary Approach������ 175
Andrea Mazzari, Pasquina M. C. Tomaiuolo, Alessio Giordano,
Roberto Luca Meniconi, and Alberto M. Settembrini
Part V Upper and Lower Limbs
17 Upper
 and Lower Limbs: Surgical Anatomy and General
Consideration in Emergency Settings������������������������������������������������������ 191
Matteo Marone and Ilenia D’Alessio
18 Acute
 and Chronic Limb Ischemia���������������������������������������������������������� 199
Giuseppe Galzerano, Edoardo Pasqui, Gianluca Chierchini,
Alberto M. Settembrini, and Pasqualino Sirignano
19 Popliteal
 Artery Aneurysm and Non-­atherosclerotic Limb Disease������ 207
Alberto M. Settembrini and Pasqualino Sirignano

Part VI Specific Clinical Pictures: Surgeon Perspectives

20 The
 Infected and Septic Patient���������������������������������������������������������������� 221
Emanuele Botteri, Nicoletta Lazzeri, Silvia Mazzoleni,
and Frank A. Rasulo
21 Hemorrhagic Patient �������������������������������������������������������������������������������� 233
Samuele Colombo and Daniele Bissacco
22 The Polytrauma Patient���������������������������������������������������������������������������� 239
Matteo Marone and Ilenia D’Alessio
Historical Overview
1
E. Botteri, F. Bongiovanni, R. L. Meniconi, and E. Grespi

1.1 New Science

Understanding the origins of ‘new’ scientific knowledge, understanding what and

who took the first steps towards breaking free from superstition, supernatural,
rigid and immutable beliefs, is a considerable cultural step and one which brings
full enjoyment of what science can offer us both as individuals and as members of
the scientific community. Above all, intellectual effort calls for a critical mind, in
order not to simply accept what is transmitted to us. Thinking can and should be
remodelled by everyone, according to well-accepted methods to make it ever
more detailed and in keeping with the reality we wish to convey. It requires intel-
lectual honesty, as well as specialised training, and once conclusions have been
reached about any piece of work, the results should be conveyed to everyone
involved. While ‘our’ centuries-old science has managed to overcome supersti-
tion, an anti-scientific attitude has remained on the side-lines of human thought,
threatening its very foundations whenever an immediate explanation to a phenom-
enon cannot be provided. Science takes time and requires patience, a sound mind
and method.
Let us not forget that many of the western world’s values and perceptions are
inspired by the scientific method and the resulting technical progress. The ‘Scientific

E. Botteri (*)
General Surgery Unit, ASST Spedali Civili di Brescia, Brescia, Italy
F. Bongiovanni · E. Grespi
Department of Anesthesiology and Intensive Care Medicine II, Spedali Civili, University of
Brescia, Brescia, Italy
R. L. Meniconi
Department of General Surgery and Organ Transplantation, Azienda Ospedaliera San
Camillo-Forlanini, Rome, Italy

© The Author(s), under exclusive license to Springer Nature 1

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_1
2 E. Botteri et al.

Method’, its concepts and its dissemination underpinned the veritable knowledge
revolution of the seventeenth century. The Scientific Method represents ‘the rules of
the game’ and covers three elements in its scope:

1. LOGIC and its inductive methods (the effects are observed to confirm the causes,
according to a process of subsequent reasoning) and deductive methods (from
the cause, the effects are hypothesised, according to a process of prior reasoning).
2. Systematic application of OBSERVATION, not for mere description purposes,
but rather in order to inspire EXPERIMENTATION. Every hypothesis must go
hand in hand with repetition and reproducible tests in order for it to be affirmed.
3. Speaking the same language: the language of MATHEMATICS. Galileo Galilei
claimed that ‘the universe is written in the language of mathematics’. Used in
Plato’s era as the language of nature, especially in geometry, to avoid being mis-
led by pure sensory experiences.

The main advocates of this development were three scientists closely linked to
one another by the knowledge that ‘we have been too inefficient thus far’, Galileo
Galilei, Renè Descartes and Francis Bacon.
Nevertheless, New Science figured little, at least to begin with, in the world in
which it emerged. Inevitably, new institutions were needed; composed of people
involved with specific scientific fields, supported by patrons or corporations with
the aim of facilitating communication and debate in the scientific community—the
SCIENTIFIC SOCIETIES were born.
1606 saw the launch of Rome’s Lincean Academy, quickly followed by the
Accademia del Cimento (1657), Paris’ Academy of Sciences (1666) and the Royal
Society (1660). In the latter, the influence of the new cultural climate was so strong
that the fine arts, rhetoric, metaphysics and theology were excluded from the Articles
of Association (without, however, undermining their prominence). The importance
of communicating ideas was supported by their own dissemination means and jour-
nals such as the Philosophical Transaction, Acta Eruditorum and the Journal de
Savants.
At all levels, scientific research products should therefore be made accessible,
employing the correct language for the target audience.

1.2 Young People in Science

When we speak about young people in science, particularly about the contribution,
young people have made, make and will make, is not only a matter of age. Being
young implies a new mental approach and boundless physical endurance. One could
wonder who was the first ‘young surgeon’ to have both a young mind and a youthful
age. There is no doubt as to the answer: Giovanni Battista Morgagni (Forlì 1682-­
Padua 1771). He studied under Valsalva in Bologna before moving to the Republic
of Venice and finally settling down in Padua in 1711, when he was called to the
second chair of theoretical medicine.
1  Historical Overview 3

One of his many accomplishments was the sacrilegious method of ‘looking into
a body’ according to a new perspective that began to weaken the old assumption that
diseases were linked to an imbalance of humours (humourism), opening the door to
the idea of diseased organs and of symptoms being the ‘cry of the suffering organs’.
From Morgagni we can draw inspiration for the times in which we are about to
move away from clinical practice, touching upon research and experimentation:
curiosity, critical analysis, accepting findings which are in contradiction with previ-
ous hypotheses (indestructible unless proved otherwise) and dissemination capac-
ity. Morgagni’s work marked the beginning of pathology as we know it today: the
result of systematic observation and experimentation.
When Morgagni was aged only 22, he was named president of the Accademia
degli Inquieti, which managed to make reforms, drawing on the experience of the
Accademia del Cimento, by bringing to the fore investigative enquiries and consul-
tations, and relegating theoretical debates to a marginal role. The turning point came
in 1705 when he gave a reading of the first volume of his publication, Adversaria
Anatomica. The publication of all of these papers when Morgagni was only 24, gave
him instant international recognition as an anatomist.
Another positively larger-than-life young man, and probably for this reason,
highly creative and steadfast, was Thomas Fogarty (1934). We all know his name
thanks to his famous catheter for embolectomy which we use in our operating the-
atres, but probably only a few people are aware that the commercialisation and
widespread use of this instrument began when Fogarty was only 29  years old.
During the years spent at the Good Samaritan Hospital (where he worked as a medi-
cal instrument maintenance technician) he met Dr. Jack Cranley—his main men-
tor—and the man who inspired him to study medicine. The fact of being present
during a number of surgical procedures, meant that he witnessed the death and
suffering of a several patients suffering from acute artery ischemia. After resolving
various technical difficulties, he managed to develop his instrument in 1960, but no
one acknowledged the significance of the idea. Only a few years later, as he was
finishing his specialisation at Oregon University, did he successfully put forward his
idea to the cardiac surgeon, Al Star, who helped him to obtain the final patent in
1969. From this instrument came the idea in 1965 for the design of the first angio-
plasty balloon.
Of course, Gianbattista and Thomas are only two well-known examples of what
a young person driven by interest and passion can achieve. Unquestionably, the his-
tory of surgery is brimming with contributions by young, motivated men and women
to whom we should express our gratitude each day and from whom we should draw
inspiration.
 Part I
Surgical Instruments and Materials
Surgical Instruments and Materials
in General Surgery 2
Andrea Mazzari, Pasquina M. C. Tomaiuolo,
and Roberto Luca Meniconi

2.1 Cut and Dissect Instruments

Dissection of tissues can be done with scalpel, scissors, (Fig. 2.1) or through the use
of energy such as ultrasonic devices, laser, and radiofrequency. Conventionally,
scalpels have been used to make surgical incisions by manually cutting through tis-
sue using a sharp blade. Scalpel consists of a blade and handle and is usually used
for initial incision. Different blades are marked with a number.
Scissors are used for cutting tissue, suture, or for dissection. Scissors can be
straight or curved, and may be used for cutting heavy or fine structures.
Since its introduction in the early part of the twentieth century, electrosurgery
has been used as an alternative tool for creating incisions [1, 2]. Two different surgi-
cal effects can be achieved with electrosurgery, namely cutting and coagulating. In
the cutting mode, a continuous current rapidly produces extreme heat causing intra-
cellular water to boil and cells to explode into steam. As a result, the heat produced
in the cells dries up the tissue but is not intense enough to evaporate intracellular
water. The coagulating mode results in a greater degree of thermal damage and
necrosis of adjacent tissues.
Electrosurgery can be performed using either monopolar or bipolar energy in
conjunction with a specialized instrument.

A. Mazzari (*) · P. M. C. Tomaiuolo

General Surgery Unit, Ospedale Cristo Re, Rome, Italy
R. L. Meniconi
Department of General Surgery and Organ Transplantation, Azienda Ospedaliera San
Camillo-Forlanini, Rome, Italy

© The Author(s), under exclusive license to Springer Nature 7

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_2
8 A. Mazzari et al.

Scalpels Scissors Forceps

Clamp instruments Intestinal clamp Needle holders

Fig. 2.1  Open surgery—surgical instruments

2.1.1 Monopolar Electrosurgery

Monopolar electrosurgery can be used for several modalities including cut, blend,
desiccation, and fulguration. Using a pencil instrument, the active electrode is
placed in the entry site and can be used to cut tissue and coagulate bleeding. The
return electrode pad is attached to the patient, so the electrical current flows from
the generator to the electrode through the target tissue, to the patient return pad and
back to the generator. Monopolar electrosurgery is the most commonly used because
of its versatility and effectiveness.

2.1.2 Bipolar Electrosurgery

Bipolar electrosurgery uses lower voltages so less energy is required. But, because
it has limited ability to cut and coagulate large bleeding areas, it is more ideally used
for those procedures where tissues can be easily grabbed on both sides by the for-
ceps electrode. Electrosurgical current in the patient is restricted to just the tissue
between the arms of the forceps electrode. With bipolar electrosurgery, the risk of
patient burns is reduced significantly. In the most common techniques, the surgeon
uses forceps that are connected to the electrosurgical generator. The current moves
2  Surgical Instruments and Materials in General Surgery 9

through the tissue that is held between the forceps. Because the path of the electrical
current is confined to the tissue between the two electrodes, it can be used in patients
with electrical implanted devices, to prevent a short-circuit or misfire.

2.1.3 Ultrasonic Energy

Ultrasonic dissection technology works by generating a high-frequency ultrasound

producing three main effects:

1. Cavitation/tissue fragmentation (and dissection) caused by cellular destruction

secondary to intracellular fluid evaporation.
2. Cooptation/coagulation: caused by conversion of ultrasonic energy into a local-
ized heat, this has been reported to reach from 60 °C to 100 °C. Denaturation of
collagen in the walls of hollow structures can result in the occlusion or sealing of
the lumen.
3. Cutting which is achieved by the “sharp” blade mode.

It has been reported that with ultrasonic energy, there is a minimal lateral spread
of vibration current in the surrounding tissues minimizing the risk of injury com-
pared with monopolar electrocautery.

2.1.4 Radiofrequency Energy

The main functionality of radiofrequency energy is to seal and coagulate. Hemostasis

is obtained by melting the collagen and elastin in the vessel walls; in clinical prac-
tice this technology can seal blood vessels up to 7 mm in diameter.

2.2 Grasp and Hold Instruments

Forceps are the grasping instruments that allow the surgeon to manipulate tissue, to
facilitate dissection or suturing by holding the edges of tissue (Fig. 2.1). They have
multiple uses other than holding skin when suturing: extracting needles, passing
ligatures to other instruments around vessels, grasping vessels to apply diathermy.
They could have various forms and designs and are probably the most commonly
used instrument. Forceps can be toothed (serrated) or non-toothed at the tip. Tissue
forceps are non-toothed and used for fine handling; DeBakey forceps are used for
atraumatic dissection of soft tissues and vessels; Adson forceps are toothed at the tip
and are used for skin closure; Bonney forceps are used for holding thick tissue, like
during fascial closure.
It is strongly recommended to use intestinal forceps when manipulating the
bowel to avoid incidental enterotomies especially in emergency setting, when the
intestinal wall could be frailty for edema due to peritonitis.
10 A. Mazzari et al.

2.3 Clamp Instruments

Clamping instruments are used to constrict tissue, structures, and vessels. They
could be curved on flat, on the side or straight. There are specifically designed
clamps for delicate tissue especially in vascular and in gastrointestinal surgery. The
jaws of these instruments are designed to prevent tissue damage: the intestinal
clamps have flexible and long jaws that allow a proper occlusion of the bowel but
prevent any damage (Fig. 2.1).
Hemostatic clamps are used to occlude vessels prior to ligating or to provide
hemostasis.

2.4 Suture Instruments

Needle holder (Fig. 2.1) and forceps are used for handsewn suture with absorbable
or not absorbable suture materials. Needles come in many shapes and cutting edges
for various applications. Sutures are available in sizes between 5 and 11/0. Higher
numbers indicate larger suture diameter (e.g., 2 is larger than 1), and more zeros
indicate smaller suture diameter (e.g., 4/0 is smaller than 3/0, or 0). There are two
main types of suture: braided and non-braided (or monofilament); the second one
can be absorbable and non-absorbable. Additionally, suture can be made with natu-
ral or synthetic materials.

2.5 Suction Instruments

Suction devices are attached to a vacuum source via suction tubing and are used to
remove blood and body fluid; they have various designs and “tips” attached to a
form of handle to allow suctioning of everything from small wounds to large
abdominal wounds.

2.6 Surgical Staplers and Clips

Surgical stapling devices have changed gastrointestinal surgery; the first one was
built in 1908 by Humer Hultl. Nowadays they are used both for open and laparo-
scopic surgery. Surgical staplers can seal tissue through metal clips that allows the
correct vascularization of the tissues. They are used to perform intestinal anastomo-
ses making theme quicker and easier, and for vascular ligations. Linear staplers with
a double or triple layer allows a safe closure of the tissue, but they do not have a
cutting system. Linear cutter creates a linear cut and immediately staples both free
2  Surgical Instruments and Materials in General Surgery 11

edges. Circular staplers are cylindrical in shape with a cone at the tip that can be
removable: they are used to perform end-to-end or side-to-end anastomosis in
colorectal and esophageal surgery.
Construction of intestinal anastomosis is a hallmark of surgical training; surgical
staplers facilitate the surgeon but there is no evidence that demonstrate any superi-
ority of the stapled over handsewn anastomosis [3].
Clips used in the ligation of vessels may be in metal, polymeric or absorbable
material.

2.7 Retractors

Retractors are the instruments designed to expose tissue and organs during the sur-
gical procedure, they could be hand-held or self-retained, and have a large variety of
sizes. An optimal view is mandatory for a safe procedure. The hand retractors could
be single or double ended and usually have a comfortable design. The self-retaining
retractors have multiple blades for different tissues and depth, in most cases can be
attached directly to the table to guarantee more stability in open large abdominal
surgery. Disposable self-retractors are useful to prevent surgical site infection, espe-
cially in emergency setting when the surgical field is often contaminated [4]
(Fig. 2.2).

Hand-held retractor Disposable self-retractor

Fig. 2.2 Retractors
12 A. Mazzari et al.

2.8 Laparoscopic Surgery

Laparoscopic surgery has emerged over the past two decades as the surgical
approach of choice in the treatment of many digestive disorders. Laparoscopy has
its role in the management of abdominal surgical emergencies since it provides the
same benefits: less postoperative pain and shorter length of hospital stay when com-
pared to laparotomy [5, 6]. In emergency surgery, the laparoscopic approach pro-
vides a better view of the abdominal cavity, giving the opportunity for a precise
diagnosis and, at the same time, a definitive treatment. However, its role in the
management of acute abdomen is strongly influenced by the laparoscopic skills of
the surgeon.
Most of the instruments are similar to those used in open surgery, adapted to fit
through ports placed through the skin. The camera, connected to light source
through a fiber-optic cable, magnifies the image and is connected to a monitor that
can be viewed by the surgical team. Camera vision can provide different angle of
vision, the most used are 0° and 30°. The instruments are inserted into the abdomen
between trocar and ports with different diameter (3  mm, 5  mm, 10–12  mm) and
length. Trocars can be bladed or not bladed; all the trocars have a seal which main-
tain pneumoperitoneum during the surgical procedure. Laparoscopic instruments
are similar to open and are 30–33 cm long (Fig. 2.3). Their main parts are handles
with or without ratchet device, rotator that allow a full rotation device and the opera-
tive inner that can be easily assembled. The working part as in open surgery is used
to dissect, aspirate, grasp, retract, cut, suture, and cauterize tissue.

Veress needle Trocars Laparoscopic

instruments

Fig. 2.3  Laparoscopic surgery—surgical instruments

2  Surgical Instruments and Materials in General Surgery 13

References
1. Anderson TL, Thomassee MS. Principles of electrosurgery and laser energy applied to gyne-
cologic surgery. In: Jones III HW, Rock JA, editors. Te Linde’s operative gynecology. 11th ed.
Philadelphia: Wolters Kluwer; 2015. p. 249–64.
2. Charoenkwan K, Iheozor-Ejiofor Z, Rerkasem K, Matovinovic E. Scalpel versus electrosur-
gery for major abdominal incisions. Cochrane Database Syst Rev. 2017;6(6):CD005987.
3. Neutzling CB, Lustosa SA, Proenca IM, da Silva EM, Matos D.  Stapled versus handsewn
methods for colorectal anastomosis surgery. Cochrane Database Syst Rev. 2012;(2):CD003144.
https://doi.org/10.1002/14651858.CD003144.pub2.
4. Cheng KP, Roslani AC, Sehha N, Kueh JH, Law CW, Chong HY, Arumugam K.  ALEXIS
O-Ring wound retractor vs conventional wound protection for the prevention of surgical site
infections in colorectal resections1. Colorectal Dis. 2012;14:e346–51.
5. Agresta F, Arezzo A, Allaix ME, Arolfo S, Anania G. Current status of laparoscopic colorectal
surgery in the emergency setting. Updat Surg. 2016 Mar;68(1):47–52.
6. Ahmed SE, Anshu J, Sarah N, Madan J, Dharmendra G. Role and outcome of laparoscopic/
minimally invasive surgery for variety of colorectal emergencies. Surg Laparosc Endosc
Percutan Tech. 2020;30(5):451–3.
Surgical Instruments and Materials
in Thoracic Surgery 3
Valeria Musso and Francesco Damarco

This chapter briefly describes the most used surgical instruments and devices in
thoracic surgery, in an emergency setting. In addition we focused on the most com-
mon procedures performed in emergency.

3.1 Thoracentesis

Thoracentesis is often used in the Emergency Room as a both diagnostic and thera-
peutic procedure in patients presenting with pleural effusion. There are several com-
mercial pre-packaged kits available, containing the necessary items to perform a
thoracentesis (Fig. 3.1). In general, standard set consists of:
• Protective equipment: sterile gloves, eye protection, face mask.
• Field preparation: sterile drapes, skin sterilizing fluid (chlorhexidine or povidone-­
iodine solution).
• Ultrasonography (optional): Convex or linear probe with a sterile sheath cover.
The use of ultrasonography to identify the appropriate location for the procedure
or for direct guidance improves the safety of thoracentesis.
• Local anesthetic agent (1–2% lidocaine), 21 or 22-gauge needle, and a syringe
for injection.
• Thoracentesis needle: the most commonly used is an 8-Charriere (1 Ch = 1/3 mm)
over-the-needle catheter; otherwise Seldinger technique can be employed

V. Musso
University of Milan, Milan, Italy
e-mail: [email protected]
F. Damarco (*)
Thoracic Surgery and Lung Transplant Unit, Fondazione IRCCS Ca’ Granda Ospedale
Maggiore Policlinico, University of Milan, Milan, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 15

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_3
16 V. Musso and F. Damarco

Fig. 3.1  Pre-packaged set

for thoracentesis, including
needles, three-way
stopcock, and a
drainage bag

Fig. 3.2  Detail of a Veress

needle

(requiring a wire, dilator, and a 6–14 Ch catheter); some kits contain a Veress
needle (Fig. 3.2).
• Three-way stopcock, a 30–50 ml syringe, drainage bag.
• Sterile containers for pleural fluid collection.
3  Surgical Instruments and Materials in Thoracic Surgery 17

3.2 Tube Thoracostomy

The insertion of a chest tube is a simple procedure, and yet, severe complications
may arise if not performed properly. Different characteristics of chest tube are sum-
marized in Table 3.1.
The indications and technique will be discussed further in the text (Chap. 7
“Chest: surgical anatomy and general consideration in emergency settings”; Chap.
9 “Pulmonary and thoracic emergencies”).

Box 3.1 Preparation for chest tube insertion

• Obtain informed consent (unless it is an emergency)
• Monitor vital parameters
• Large-bore intravenous line
• Exams (if possible): ECG, blood tests, chest X-rays, CT scan in case of
trauma, ultrasound for guidance.
• Adequate analgesia, consider mild sedation

In case of small-bore chest tubes, the drainage can be inserted with the Seldinger
technique or using the pre-packaged kit.
The instruments required to insert a chest tube are listed below:
• Protective equipment: sterile gloves, eye protection, face mask.
• Field preparation: sterile drapes, skin sterilizing fluid (chlorhexidine or povidone-­
iodine solution).
• Ultrasonography (optional): Convex or linear probe with a sterile sheath cover.
The use of ultrasonography to identify the appropriate location for the procedure
or for direct guidance improves the efficacy of chest tube placing, especially in
case of pleural effusion.
• Local anesthetic agent (1–2% lidocaine), 21- or 22-gauge needle and a syringe
for injection.
• Scalpel with a n°10 or 11 blade.
• Gauze sponges.
• Straight- and curved-blade Mayo scissors.
• Chest tube: the diameter ranges from 8 to 36 Ch.
• Clamp.
• Closed system drain (including water) and tubing.
• Needle holder.
• Non-adsorbable 0 or 1-0 suture.

Table 3.1  Chest tube characteristics

Chest tube characteristic
Material Silicone; polyvinyl chloride
Caliber From 8Ch to 36Ch
Shape Straight; angled; Pigtail
Other With internal, external, or no mandril
18 V. Musso and F. Damarco

Box 3.2 Type of drainage systems

• Unidirectional flutter valves (Heimlich): The distal portion can be con-
nected to a bag or a suction device, or left open. It is useful in an outpatient
setting.
• Traditional water seal and drainage bottle (Bulau): A one-bottle system
allows for fluid and air drainage; a two- or three-bottle system is required
for suction.
• Disposable drainage systems: There are many types of devices available,
working as one-, two-, or three-bottle systems; they can be used with por-
table suction units.
• Digital drainage systems: These devices constantly record the presence of
air-leaks and fluid output; they integrate suction units.

3.3 Thoracotomy

Thoracic trauma, related to both blunt and penetrating mechanism of injury, can
determine devastating damages with an elevated morbidity and mortality. The initial
evaluation in case of trauma of the thoracic cavity should always be based on an
Advanced Trauma Life Support (ATLS) program. In selected patients and clinical
circumstances, resuscitative thoracotomy (or emergency department thoracotomy
in general) can be performed to pursue damage control such as to temporize hemor-
rhage or decompress cardiac tamponade.

Box 3.3 Initial assessment for severe thoracic trauma

• Monitor vital parameters
• At least one large-bore intravenous access
• Endotracheal tube
• Nasogastric tube

A sterile tray with the equipment to perform thoracotomy should be available

at all times in the trauma room. Together with sterile drapes, sterilizing fluid,
gloves, and other protective equipment, the set should include the following
instruments:

• Scalpel holder and blades; electrocautery.

• Gauze sponges and a suction unit.
• Tissue forceps: Quénu forceps, long DeBakey tissue forceps; grasping forceps:
Duval, Lovelace lung grasping forceps.
• Allison lung retractor.
• Scissors: long curved Mayo scissors, long curved Metzenbaum scissors.
3  Surgical Instruments and Materials in Thoracic Surgery 19

• Rib spreader: Burford-Finochietto, Tuffier; sternal retractor; Farabeuf retractors.

• Giertz-Shoemaker rib shears.
• Sternal saw (e.g., Gigli, oscillating); Lebsche sternal chisel.
• Mallet.
• Aortic clamps, angled and curved: Fogarty aortic cross-clamp, DeBakey aorta
clamp; hemostatic clamps: Satinsky clamp. A Foley catheter may also be of aid
to control the hemorrhage.
• Bailey rib contractor.
• Needle holder: DeBakey, Ryder.
• Sutures.

3.4 Video-assisted Thoracic Surgery (VATS)

As VATS surgery becomes increasingly employed, even in the emergency set-

ting, surgeons are required to know the basic instrumentation to perform thora-
coscopic procedures. In general, the instruments are thinner than those used for
open surgery, their fulcrum is located at the distal end, and they have a
curved shape.
Instead of a rib spreader, trocars or wound retractors are used to improve expo-
sure, causing less pain and reducing the incidence of rib fractures.
A thoracoscope is used for visualization: 0° and 30° scopes are the most fre-
quently used.
The VATS surgery set (Fig. 3.3) usually consists of non-traumatic graspers, dis-
secting forceps, and a dissecting suction tube. For dissection an electrocautery
hook, an ultrasonic dissector-coagulator, or bipolar electrocautery devices can be

Fig. 3.3 Video-assisted
thoracic surgery set
20 V. Musso and F. Damarco

used. Endoscopic stapling devices are fundamental to safely divide lung paren-
chyma, vessels, and bronchi, providing adequate hemostasis and aerostasis.

Further Reading
Rutherford CJ. Differentiating surgical instruments. Philadelphia: F.A. Davis Company; 2012.
Surgical Instruments and Materials
in Vascular Surgery 4
Ilenia D’Alessio and Matteo Marone

4.1 Introduction

In the vascular emergency setting, the main objective is to stop the bleeding and/or
re-establish blood flow to a specific anatomic district.
To achieve this, the emergency physician and/or vascular surgeon has access to
multiple kinds of surgical and endovascular materials, which can be used according
to patient characteristics and prompt availability.
To facilitate the lecture of this chapter, we have decided to divide surgical instru-
ments and materials in a vascular and an endovascular section, even if they are often
used together during hybrid procedures.

4.1.1 Open Surgery

The basic techniques and exposure of single vessels will be discussed in the follow-
ing chapters. Here below we will describe the general principles of vascular surgery.

1. The basic concept is to approach and expose the vessel using the most direct and
easier route possible, avoiding iatrogenic damages. Anatomic landmarks, loca-
tion of pulses, and/or both are typically used to guide the initial skin incision.

I. D’Alessio (*)
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
Department of Vascular Surgery, Fondazione “A. De Gasperis” ASST Grande Ospedale
Metropolitano Niguarda, Milan, Italy
e-mail: [email protected]
M. Marone
Department of Surgery, Tygerberg Hospital, Cape Town, South Africa

© The Author(s), under exclusive license to Springer Nature 21

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_4
22 I. D’Alessio and M. Marone

2. Once the sheath is reached, it is incised and the vessel’s adventitia is held and
retracted in one direction.
3. The exposure of the vessel is carried out close to the edge of the blood ves-
sel wall.
4. Once the vessel is isolated, it can be circumferentially dissected and encircled
using vessel loops.
5. Blood vessel control can be achieved in different ways: using vascular clamps,
balloon occlusion, vessel loops, tourniquets, internal occluders or also, espe-
cially during emergency procedures, using direct finger compression.
6. Before interrupting blood flow (approximately 3–5  min), the patient must be
adequately anti-coagulated (unfractionated heparin at a dose of 75–100 Ui/kg
intravenously). The Activated Clotting Time (ACT) can be measured 180 s after
the heparin administrations and it should reach values of more than 250 s. It is
useful to monitor the ACT values during the procedure [1, 2].

To perform these basic steps, the surgeon needs the following instruments:

• Clamps (Fig. 4.1)
They are surgical instruments used to occlude a vessel from outside, without
damaging it, they are considered atraumatic for vessels’ wall. Clamps allow the
surgeon to open the vessel (perform an arteriotomy) and work inside the ves-
sel itself.

Fig. 4.1  Examples of

vascular clamp (first image
represents a DeBakey
clamp, the second image
represents a Dietrich camp)
4  Surgical Instruments and Materials in Vascular Surgery 23

It is important to clamp the artery opposing the healthy wall to the plaque (if
present) to avoid the plaque rupture.
Clamps are usually divided according to vessels’ size: large, medium, and
small vessels or into totally occluding and partially occluding [2].
Below you can find the most common vascular clamps:
–– DeBakey aortic clamp (supraceliac, infrarenal aorta)
–– Fogarty aortic clamp (infrarenal aorta, aortic grafts, calcified aorta)
–– DeBakey peripheral vascular clamp (iliac arteries and common carotid
arteries)
–– Satinsky clamp (aorta; vena cava)
–– Cooley Derra Clamp (graft limbs)
–– Dietrich bulldog (small vessels)
• Needle Holders, Forceps, and Scissors
Needle holders are devices created to handle needles in a precise way, reduc-
ing the risk of injury for the operator itself. The choice of needle holder is dic-
tated by the size of the needle and by the surgeon preferences. The Mayo-Hegar
needle holder is used with large needles, while Castroviejo needle holders are
typically used with fine vascular needles.
The forceps used during vascular procedures typically have fine, non-crush-
ing jaws, exemplified by the DeBakey forceps. They are useful because it allows
the surgeon to touch the vessels without provoking important injuries to the arte-
rial or venous wall.
Metzenbaum and Church scissors are used for the dissection of blood vessels.
Special Potts scissors with various angulations are used to enlarge and shape
arteriotomies and venotomies (Fig. 4.2) [1].
• Suture
They are traditionally divided in absorbable/non-absorbable and mono/multi-
filament. In vascular surgery the favorite suture materials are non-absorbable
monofilament sutures due to their non-traumatic action on the vessel itself.
Non-absorbable monofilament sutures are used for vascular anastomoses and
repairs. Vascular sutures are usually double-armed with a needle on each end to
allow continuous suturing in both directions.

Fig. 4.2  Potts scissors

24 I. D’Alessio and M. Marone

Table 4.1  Fogarty catheter classification based on color code, French size, and balloon diameter
Balloon
Color French diameter
code size (Fr) (mm) Target vessel
Violet 2 4 Foot and hand vessels
Green 3 5 Leg and forearm vessels
Red 4 9 Popliteal artery, superficial and common femoral
artery, external iliac artery, brachial artery, subclavian
artery
White 5 11 Popliteal artery, superficial and common femoral
artery, external and common iliac artery, brachial
artery, subclavian artery
Blue 6 13 External and common iliac artery, aorta
Yellow 7 14 External and common iliac artery, aorta

Commonly used monofilament sutures include: polypropylene, polybutester,

and polytetrafluoroethylene (PTFE).
PTFE sutures are quite recent and they were developed to minimize the nee-
dle hole bleeding that is often seen when polypropylene sutures are used with
PTFE grafts or patches. They are designed so that there is minimal difference in
the diameters of the needle and the suture [2].
In an emergency setting, it is useful to know the existence of the:
• Fogarty catheter®, it is a hollow tube with an inflatable balloon attached to its tip.
The catheter is inserted into the blood vessel through a clot. The balloon is then
inflated to extract the clot from the vessel. It is available in different lengths and
sizes, and is often color coded by size (Table 4.1). They can be also used to clamp
the target vessel from the inside (inflating the balloon) and this is useful espe-
cially if the wall of the vessel is extremely damaged.
• Aortic Balloons occlusion (see endovascular section)

4.1.2 Endovascular Surgery

The goal of this section is to provide a “step-by-step” guide to obtain a safe vascular
access in an emergency setting.
Basic endovascular skills are integral part of vascular and trauma patient care and
often offer rapid solutions to complex clinical problems (i.e., clamp a broken aorta
using aortic balloons occlusion). Moreover, nowadays, endovascular procedures are
the mainstream of treatment during the non-operative management of many trau-
matic injuries like: splenic injuries, hepatic injuries, and pelvic injuries [3].
In the previous section (see open surgery) we have analyzed the basic techniques
to obtain the surgical exposure of a vessel, now we’ll list the principles of percuta-
neous access:

1. Choose the more appropriate puncture site according to the planned procedure.
2. Pick an access site that is far enough from the lesion so the sheath may be placed
without encountering the lesion itself.
4  Surgical Instruments and Materials in Vascular Surgery 25

3. Feel the artery intended for puncture and palpate anatomic landmarks.
4. Use ultrasound guidance to visualize the artery and its relationship to anatomic
landmarks.
5. If you encounter a problem, hold pressure for a few minutes and start again. It’s
rare to have any significant damage to the access artery from the needle alone [3].

Usually to obtain a percutaneous access you’ll need to: a sterile swab, a scalpel,
a hemostat, a percutaneous entry needle, a syringe with local anesthetic, and a
guidewire. These instruments are required to perform the Seldinger technique, also
known as Seldinger wire technique, a surgical procedure to obtain safe access to
blood vessels. Using ultrasounds to locate the vessel and to choose the ideal punc-
ture side will help you avoiding failure and access-related complications
(Fig. 4.3) [4].
The main steps of the procedures are the following:

1. Inject the anesthetic into the subcutaneous tissue that surrounds the area desig-
nated for the puncture, remember to inject the solution also close to the artery in
order to avoid pain stimulations during the procedures.
2. The entry needle approaches the artery at a 45° angle (Fig. 4.3a).
3. A pulsate backbleeding indicates that the needle tip is in the artery (Fig. 4.3a).
4. While the non-dominant hand holds the needle, the dominant hand retrieves the
guidewire, straightens its tip, and inserts it into the needle hub (Fig. 4.3b).
5. When the guidewire is parked far in the target artery, the needle is retrieved and
a coaxial dilator system is advanced over the guidewire (Fig. 4.3c, d).
6. The starter guide and the inner trocar are removed, and, at this point it is possible
introduce the desired wire for the case (Fig. 4.3e) [3].

In some cases it is mandatory a surgical exposure of the vessel, especially in case

of diffuse atheromasia, in this case we talk about hybrid approach.
To perform these basic steps the surgeon needs:

• Entry needle:
It is a sharp hollow needle (usually 18 gauge) usually between 2 and 3.5
inches in length whose beveled tip is placed into the anterior wall of the artery.
These kinds of needles can accommodate a 0.035 inch guidewire. However, fine
needles (21 gauge) can be used to access to small vessel like the radial and pedid-
ial artery.
• Guidewire:
The guidewire you introduce initially must be stiff enough to serve as an ini-
tial rail for sheath, its tip must be atraumatic, so that if plaque is encountered, it
is not disrupted. The initial guidewire must be inserted into the vessel for a suf-
ficient length to not have unintentional displacement. Usually access is per-
formed with 0.035-inch diameter guidewires using, e.g., Starter Guidewire.
There are many types of guidewires and they are classified according to their
length, the shape of the tip, their material and their diameters. The main diame-
ters used are 0.035 inch, 0.018 inch, and 0.014 inch.
26 I. D’Alessio and M. Marone

Fig. 4.3 Seldinger
technique

e
4  Surgical Instruments and Materials in Vascular Surgery 27

• Sheath: The sheath placement permits a safe and hemostatic access. The main
role of the sheath is to provide protection of the access site from the irregular
edges of endovascular devices, because it reduces the friction encountered at the
access site when manipulating a selective catheter into a branch. An access
sheath has one way hemostatic valve, a dilator to stiffen it during placement, and
a side arm port that is used for the administration of medication or contrast. The
sheath is advanced always with its dilator to avoid damages by the hollow sheath
tip. Sheaths are sized according to the largest diameter catheter the sheath will
accept [3, 4].
The physician has available a wide variety of guides, sheets, and catheters. A
deeper treatise is beyond the purpose of this chapter, if the reader is interested we
suggest to look at an endovascular handbook.
Once gained the access to the vessel, there are several diagnostic and thera-
peutic options.
The physician may need to perform an angiography to detect the source of a
bleeding, and he/she can use a variety of coils, plugs, glues, and hemostatic
devices to embolize a vessel or even put stents (covered or uncovered) to com-
plete the procedure.
More detailed:
• Coils and Plugs:
The coils and plugs are vascular embolization devices that occlude vessels’
lumen. Usually they are used in an emergency setting to control hemorrhage. For
instance, in a blunt splenic injury with a grading less than III instead of a sple-
nectomy the surgeon can perform an endovascular ligation of the splenic artery
occluding it with coil and plug. As a result, the spleen is partially excluded from
the arterial system and the bleeding stops.
• Stents: The stents are metallic scaffolding used to dilate an occluded vessel. They
are specially designed mesh metal tubes that are inserted into the body in a col-
lapsed state on a catheter. They can be divided into balloon expandable and self-­
expandable. Balloon expandable stents have a high radial force and they can be
used to dilate thigh strictures that are not really flexible. In contrast, self-­
expandable stents have a good flexibility and they can navigate really well in a
vessel but their radial force is weak.
• Angioplasty balloon: The angioplasty balloon is a small balloon inserted into an
atherosclerotic vessel and inflated to crush and disrupt the atherosclerotic plaque
and re-establish the patency of the lumen. They come in different size: there are
big balloon used for the aorta and little balloon used for the coronary arteries. In
emergency setting they can be used to internally clamp a vessel or to treat a dis-
section flap [3, 5, 6].
• Stent graft: The stent graft is self- or balloon expandable stent, covered with a
polytetrafluoroethylene or woven Dacron layer that makes them impermeable to
blood. They are useful to exclude vascular aneurysm from the blood flow, in dif-
ferent parts of the body and they come in different size and shape according to
their purposes. Ruptured vessels can be treated in an endovascular fashion using
a stent graft to cover the vascular injury and stop the bleeding. However, espe-
28 I. D’Alessio and M. Marone

cially if we speak about penetrating trauma, these kinds of procedures have a

great risk of postoperative device infection [3, 5].
• REBOA™:
It is the acronyms for Resuscitative Endovascular Balloon Occlusion of the
Aorta. They are balloon designed to be inserted (percutaneously or with a ­femoral
artery cut-down) without guidewires in the body of in-extremis patients in order
to occlude the aorta from inside. As a consequence these balloons can stop the
bleeding and at the same time they help centralizing the blood flow to noble
organs such as the brain, the heart, and the lungs. The REBOA™ can be used not
only in a hospital setting but also in a prehospital and street setting. The scenario
where it is mostly used is blunt trauma with non-compressible hemorrhages like:
pelvic fractures, solid organ injuries, mesenteric injuries. The main drawback of
the device is that it is often inserted in a chaotic environment with no guidewire
and without fluoroscopy and this can result in a wrong positioning of the device
and in vascular injuries. In addition, once the balloon is inflated it creates a state
of total vascular occlusion downstream and this can create severe ischemic dam-
age especially to kidney, bowel, liver, and biliary tract [7, 8].

4.1.3 Hybrid Surgery

Nowadays, it has become far more common the use of hybrid theater especially in
tertiary hospitals. A hybrid suite is an operating theater integrated with diagnostic
devices like mobile C arms. These rooms allow the surgeon the possibility to per-
form open procedures and to complete them using endovascular technique. A clear
example of the utility of these places can be seen thinking of peripheral bypass. The
vascular surgeon can perform the bypass in a comfortable setting and at the end of
the procedure can perform double subtraction angiography (DSA) and percutane-
ous balloon angioplasty as in a normal angio-suit.
In first world countries hybrid room is used also as shock room in big trauma
centers. For trauma purpose this setting offer important advantage like the possibil-
ity to perform an active resuscitation while the vascular surgeon performs an angi-
ography using a vascular access. This allows to minimize the time between the
arrival of the patient in the emergency room and the diagnostic and treatment phase.
These rooms can allow the vascular and trauma surgeon to perform also computed
tomography scan on the resuscitation table, giving important advantages especially
in patients with traumatic brain injuries.
The drawbacks of this kind of setting are that these rooms are expensive, they
need specifically trained professionals to function, and they cannot be set up in
every hospital.
4  Surgical Instruments and Materials in Vascular Surgery 29

Key Messages
• Knowledge of materials and techniques allows the best and safest vascular
approach for the injured vessel.
• Before going to the operating room and start a procedure check which
materials are available and if you are familiar with them.
• Ask for help to a senior consultant if you are not familiar with a particu-
lar device.
• Consider every time the possibility of endovascular procedures.
• Hybrid procedures are becoming the mainstream of treatment of trauma
and vascular patients.
• Infections can occur after endovascular procedures for trauma and a close
follow-up is needed.
• Be ready with a backup plan because endovascular devices can fail.
• Be open to any technological advancement.

Acknowledgments  The authors of this chapter would like to acknowledge Monika D’Alessio for
the original drawings.

References
1. Rutherford RB.  Atlas of vascular surgery: basic techniques and exposures. Philadelphia:
W.B. Saunders Company; 1993. p. 267.
2. Sidawy AN, Perler BA.  Rutherford’s vascular surgery and endovascular therapy. 9th ed.
Amsterdam: Elsevier; 2018.
3. Schneider PA. Endovascular Skills Guidewire and catheter skills for endovascular surgery. 4th
ed. Boca Raton, FL: CRC Press; 2019.
4. Chaikof EL, Cambria RP.  Atlas of vascular surgery and endovascular therapy. 1st ed.
Philadelphia: Saunders; 2014.
5. Mao H, Wang F, Bao J, Chen Z.  Conventional endovascular devices. Endovasc Surg Dev.
2018:9–28. https://doi.org/10.1007/978-­981-­10-­8270-­2_2.
6. Jing Z, Mao H, Weihui D. Endovascular surgery and devices. Endovasc Surg Dev. 2018; https://
doi.org/10.1007/978-­981-­10-­8270-­2.
7. Kpodonu J. Manual of thoracic endoaortic surgery. Cham: Springer; 2010.
8. Kpodonu J, Haulon S. Atlas of advanced endoaortic surgery. Cham: Springer; 2013.
Part II
Neck
Supra-aortic Trunks Emergency
Conditions 5
Enza Lucia Castronovo, Daniele Bissacco, D’Oria Mario,
Alberto M. Settembrini, and Sirignano Pasqualino

5.1 Introduction

Emergency supra-aortic trunks (SATs) disease includes a group of urgent onset

­conditions involving the origin of the common carotid arteries, subclavian arteries,
internal carotid arteries (ICAs), and vertebral arteries. These pathologies represent
one of the main causes of death and disability in the occidental population and
require prevention and rapid management when symptomatic. Among SATs patholo-
gies, ICA and/or vertebral stenosis or occlusion due to atherosclerosis or other fac-
tors are the most frequent and fearsome conditions, being responsible for the majority
of SATs’ urgencies. In particular, ICA plaque is considered one of the main causes of
ischemic stroke, one of the most cause of death in the USA and Europe. Subclavian
arteries rarely lead to urgent conditions, although their acute occlusion may provoke
vertebral insufficiency and/or ischemic complications of the upper limbs.
The aim of this chapter is to provide clinical and instrumental information to bet-
ter recognize and diagnose SATs emergent/urgent conditions, to describe the best
first management and treatment choice for each scenario, particularly in case of
cerebrovascular complications related to ICA stenosis or occlusion.

E. L. Castronovo · D. Bissacco (*) · A. M. Settembrini

Vascular Surgery Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico,
Milan, Italy
D. Mario
Division of Vascular and Endovascular Surgery, Cardiovascular Department, University
Hospital of Trieste ASUGI, Trieste, Italy
S. Pasqualino
Department of Surgery “Paride Stefanini”, “Sapienza” University of Rome – Vascular and
Endovascular Surgery Unit, Ospedale Sant’Andrea, Rome, Italy

© The Author(s), under exclusive license to Springer Nature 33

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_5
34 E. L. Castronovo et al.

5.2 Anatomy of Supra-aortic Trunks

The term “supra-aortic trunks” (SAT) includes the vessels (brachiocephalic trunk
[BCT], left common carotid artery [LCCA], and left subclavian artery [LSA]) aris-
ing from the aortic arch (Fig. 5.1). BCT also called anonymous artery is 5–7 cm
long and arises from the aortic arch and goes up the upper mediastinum to the right
sternoclavicular joint, where it divides into its final branches: the right subclavian
artery and the right common carotid artery. ACL arises from the aortic arch near
BTC. It originates on the left side of the trachea. Its mediastinal course is more or
less vertical, so it travels like the RCCA in the lateral sulcus of the neck. The origin
of LSA is usually approximately 1 cm distant from that of LCCA. Its mediastinal
course is vertical and leads it to the base of the left supraclavicular cavity. The com-
mon carotids have a vertical course in the lateral margin of the neck up to the man-
dibular angle where the ICA and the external carotid artery (ECA) originate at the
level of C4. They run inside the vascular fascia with the jugular vein and the vagus
nerve along the neck. Then, the ICA enters the skull through the external opening of
the carotid canal and divides into seven segments depending on the areas crossed.
Along its course, the ICA divides into its two terminals called the anterior and
middle cerebral arteries.
The ICA supplies the brain including the eyes, while the external carotid the
face, scalp, skull, and meninges.

a b c d

Fig. 5.1  Anatomy of supra-aortic trunks. (a) Normal anatomy. (b) Bovine arch. (c) Lusoria sub-
clavian artery. (d) Anatomy of common, internal and external carotid arteries. (e) Intra-operative
carotid anatomy. From: Rutherford's Vascular Surgery and Endovascular Therapy, E-Book.
Elsevier Health Sciences (2018)
5  Supra-aortic Trunks Emergency Conditions 35

5.3 Stroke

Stroke causes 1.1 million deaths annually in Europe and 5.5 million in the USA
making it the second commonest cause of death. Furthermore, more than half of
stroke survivors experience complex disability for one or more aspects in everyday
activities [1, 2]. The World Health Organization (WHO) has defined stroke as focal,
occasionally global, loss of neurological function lasting >24 h (or leading to death)
and that it has a vascular etiology. The Stroke Council of the American Heart
Association/American Stroke Association defined transient ischemic attack (TIA):
“A transient episode of neurological dysfunction caused by focal cerebral, spinal
cord or retinal ischemia, without acute infarction” [3, 4]. Silent infarction is defined
as “imaging or neuropathological evidence of cerebral/retinal infarction without a
history of acute neurological dysfunction attributable to the lesion” [5]. TIA can be
further classified in other subgroups: crescendo TIAs and “stroke-in-evolution.”
Crescendo TIAs are multiple TIAs within a short time period, with full recovery in
between. The exact number and/or frequency has never been defined, but at least
three events in 7 days would seem reasonable. “Stroke-in-evolution” is a fluctuating
deficit (never fully back to normal) or a progressively worsening neurological
deficit.
Stroke can be also classified as hemorrhagic (8–18%) or ischemic (72–87%),
depending on its main cause [4, 6].
The main causes of ischemic stroke are thromboembolism from the internal
carotid artery (ICA) or middle cerebral artery (MCA) territory (25%), small vessel
intracranial disease (25%), cardiac embolism (20%), other specified rarer causes
(5%), and unknown causes despite investigation (25%) [1, 7].

5.4 Internal Carotid Artery Stenosis

Stenosis of ICA is defined as the presence of a plaque—lipidic, fibrotic, calcific, or

mixed—that narrow the ICA lumen. Carotid artery atherosclerosis represents the
major clinical risk factors for ischemic stroke. Overall, about 10–15% of all strokes
follow thromboembolism from a previously asymptomatic ICA stenosis >50% [1].

5.4.1 Etiology

The main risk factors for developing carotid stenosis are the same as for atheroscle-
rotic and other arterial disease. Selective screening for asymptomatic carotid steno-
ses may be considered in patients with multiple vascular risk factors [1].

5.4.2 Asymptomatic and Symptomatic Patients

Patients with carotid stenosis have an overall increased risk of cardiovascular events.
Extracranial carotid stenosis usually occurs without symptoms until the stroke begins.
36 E. L. Castronovo et al.

Asymptomatic (>6 months symptoms of stroke/TIA) carotid disease

Imaging of carotid
artery disease
(DUS, CTA/MRA)

Carotis stenosis Carotid occlusion

<60% or near occlusion Carotid stenosis 60-99%

Life expectancy > 5

BMT NO years?
Radiological
features
suggesting higher
stroke risk?

YES

CEA + BMT (Should be)/

CAS+BMT (may be)

Fig. 5.2  Management of asymptomatic carotid stenosis

The presence of “significant” (degree of stenosis 60–99%) carotid bifurcation

disease is a target for surgery. They are not an emergent/urgent condition and can be
managed by their medical doctor. Figure 5.2 shows the management of asymptom-
atic patients. In patients with neurological symptoms (symptomatic patients) the
presence of carotid bifurcation disease should be detected, while its absence should
lead to a search for another source of symptoms. Symptomatic patients always rep-
resent an emergent/urgent condition and must be promptly managed in the emer-
gency room. Figure  5.3 shows the flowchart to management of symptomatic
patients.
5  Supra-aortic Trunks Emergency Conditions 37

Symptomatic (<6 months symptoms of stroke/TIA) carotid disease

Imaging of carotid
artery disease (DUS,
CTA/MRA)

Carotid
Carotid occlusion Carotid stenosis Carotid stenosis
stenosis
or near occlusion 50-69% 70-99%
< 50%

CEA +BMT is
CEA + BMT (Should recommended/
CEA/CAS may be be)/
considered in case BMT:
CAS+BMT (may be) CAS + BMT (should
of recurrent - antiplatelet
therapy be considered in
symptoms despite
-lipid-lower patients with high
BMT
therapy risk for CEA)
-antihypertensive
drugs
-antidiabetic drugs

Fig. 5.3  Management of symptomatic carotid stenosis

5.4.3 Clinical Presentation

Symptoms related to stroke or TIA conditions depend on the extent and area affected
by the ischemia. For this reason, there are symptoms related to the carotid territory
(brain hemisphere, parietal area, temporal or frontal area) and symptoms related to
the vertebro-basilar territory (see paragraph 7) (occipital area, brain stem, cerebel-
lum). Carotid territory symptoms include:

• Hemi-sensory impairment, as numbness, paresthesia of face, arm, leg or all

the soma.
• Hemimotor deficits (weakness of face/arm/leg, or limb clumsiness).
• Higher cortical dysfunction (dysphasia/aphasia, visuospatial problems).
• Amaurosis Fugax (transient monocular blindness): transient impairment or loss
of vision in one eye.
• Retinal infarction (analogous to stroke): permanent visual loss.
38 E. L. Castronovo et al.

• Ocular ischemia syndrome is nearly always associated with severe extracranial

ICA stenotic/occlusive disease, although if collateralization via the circle of
Willis is extremely poor, it can occur in patients with 50% stenoses [1].

5.4.4 Diagnosis

Color Duplex ultrasound (CDUS) scan is recommended as a first-line method for

identifying and assessing the extent and severity of extracranial carotid stenosis [1].
When diagnosis is uncertain or when considering treatment, the estimate of Duplex
ultrasound stenosis should be confirmed by computed tomographic angiography
(CTA) or magnetic resonance angiography (MRA). Catheter angiography is now
rarely required unless there are discrepancies on non-invasive imaging [1].

5.4.5 Treatment

In patients with asymptomatic carotid stenosis, secondary prevention with control

of risk factors and the best medical therapy (BMT) (antiplatelet therapy, lipid-­
lowering therapy, antihypertensive treatment, and strict glycemic control in diabetic
patients) are mandatory. In addition to BMT, the treatment options for treating
carotid stenosis are carotid endarterectomy (CEA) and carotid stent (CAS).
European guidelines suggest CEA should be considered in patients with asymptom-
atic 60–99% stenosis and imaging characteristics that may be associated with an
increased risk, provided documented perioperative stroke/death rates are <3% of
late ipsilateral stroke and the patient’s life expectancy exceeds 5  years. Carotid
stenting may be considered in selected asymptomatic patients who have been
deemed by the multidisciplinary team to be “high risk for surgery”: clinically sig-
nificant cardiac disease (congestive heart failure, abnormal stress test, or need for
open-heart surgery); severe pulmonary disease; contralateral carotid occlusion; con-
tralateral laryngeal nerve palsy; previous radical neck surgery, cervical radiation
therapy; recurrent stenosis after CEA and age >80 years [1]. The American Heart
Association has repeatedly advised that only “highly selected” asymptomatic
patients should undergo CEA but never defined what “highly selected” means [1].
In patients with symptomatic carotid disease, the goal of treatment is tertiary
prevention to reduce the risk of recurrent TIA or stroke. Following an ischemic
stroke, the risk for a recurrent ischemic stroke is 2% at 7 days, 4% at 30 days, 12%
at 1 year, and 29% at 5 years. The risk of death after an initial ischemic stroke is 7%
at 7 days, 14% at 30 days, 27% at 1 year, and 53% at 5 years [2].
Figure 5.3 shows the algorithm detailing the management of symptomatic carotid
stenosis.
The risk of recurrent stroke is highest in the first few days/weeks after symptom
onset. It’s important to start mono or dual antiplatelet therapy (DAPT) early [1].
5  Supra-aortic Trunks Emergency Conditions 39

In patients with carotid stenosis 50–99% CEA or CAS are recommended. At the
2-year follow-up, there was a highly significant reduction in ipsilateral stroke inci-
dence (9% vs. 26%) in patients who underwent CEA [2].
According to European guidelines in patients with recent (<6 months) symptom-
atic 70–99% carotid stenosis CEA is recommended, while it should be performed in
patients who have 50–69% carotid stenoses and who are aged >70 years [1]. CAS
may be considered in patients who have 50–69% carotid symptomatic stenoses,
according to American Heart Association and Society of Vascular Surgery [2].
In the scientific community, there is still an active controversy about the ideal
timing of intervention.
There is increasing evidence that CEA confers maximum benefit if performed
<14 days, after 48 h had elapsed, each of the national audits showed that CEA could
be performed within 3–7 days and 14 days with low procedural risks [1]. Performing
CAS in the early time period after symptom onset is controversial and the literature
contains conflicting data [1, 2]. When revascularization is not recommended?
Revascularization should be deferred in patients with 50–99% stenoses who suffer
a disabling stroke (modified Rankin score ≥ 3), whose area of infarction exceeds
one-third of the ipsilateral middle cerebral artery territory, or who have altered con-
sciousness/drowsiness, to minimize the risks of postoperative parenchymal hemor-
rhage. Patients with 50–99% stenoses who present with stroke-in-evolution or
crescendo transient ischemic attacks should be considered for urgent carotid endar-
terectomy, preferably <24 h [1].
What to do when patients underwent intravenous thrombolysis? Early carotid
endarterectomy (within 14 days) should be considered after intravenous thromboly-
sis in symptomatic patients if they make a rapid neurological recovery (Rankin
0–2), the area of infarction is less than one-third of the ipsilateral middle cerebral
artery territory, a previously occluded middle cerebral artery mainstem has recana-
lized, there is a 50–99% carotid stenosis and no evidence of parenchymal hemor-
rhage or significant brain edema [1].

5.4.5.1 Complication Following Carotid Intervention

Complication after carotid surgery can be classified as local or systemic, early or
late. Figure  5.4 shows the management of complication following carotid
intervention.

• Stroke: emergency extracranial and intracranial CTA should be performed in

patients who experience early stroke.
• Renal dysfunction: CAS can cause contrast-induced nephropathy. Adequate fluid
resuscitation is recommended to avoiding acute kidney injury.
• Neck hematoma: If complicated by stridor or tracheal deviation, immediate
evacuation is mandatory [1].
• Cranial nerve injury: It is the most common neurologic complication of CEA. The
cranial nerve injuries can be managed expectantly.
• Prosthetic patch infection.
40 E. L. Castronovo et al.

CCA or ICA
INTRAOPERATIVE thrombosis/acute stent RE-EXPLORATION
thrombosis/vasospam

<6 SURGEON
hours FOR RE-
EXPLORATI-
EMERGENC ON
STROKE Y

>6 EMERGENCY
NIALAND Neurosurgeon
hours INTRACRAN
EXTRACRANIAL AND
POSTOPERATIVE
IAL CTA
INTRACRANIAL CTA

Blood
pressure
control

intravenous crystalloids
and volume expanders +
Blood vasopressors in pressure is
Haemodynamic <90mmHg.
pressure
instability SURGEON FOR RE-
control
EXPLORATION/thrombecto-
my or thrombolysis

antihypertensive medication

Neck
haematoma SURGEON for
immediate
COMPLICAT- evacuation
ION
FOLLOWING
CAROTID Prosthetic
DUS + CTA
INTERVENTI- Infection patch SURGEON
ON infection

medical therapy and serial

surveillance
<70%

Asymptomatic
medical therapy and serial surveillance or
70-99% redo CEA/CAS

Restenosis
<50% medical therapy and serial surveillance
Sympto
matic
Redo
50 -99%
CEA/CAS

Intravenous
fluid
Renal dysfunction resuscitation

Fig. 5.4  Management of complication following carotid interventions. CCA common carotid
artery, ICA internal carotid artery, ICH intracerebral haemorrhage, DUS doppler ultrasound, CTA
computed tomography angiography, CEA carotid endarterectomy, CAS carotid artery stenting

• Restenosis can occur asymptomatically or symptomatically. For asymptomatic

restenosis >70% serial surveillance and medical therapy is recommended; CEA
or CAS may be considered for 70–99% stenosis following MDT review. For
symptomatic restenosis 50–99% redo CEA/CAS should be considered, while
symptomatic <50% restenosis should be treated medically [1].
5  Supra-aortic Trunks Emergency Conditions 41

5.5 Carotid Artery Dissection

Carotid artery dissection is a relatively uncommon pathology that can be manifest

spontaneously without a clear etiology. Cervical carotid artery dissections are
responsible for only 2% of all ischemic strokes but account for 10–20% of strokes
in young and middle-aged patients [2].

5.5.1 Etiology

The etiology is unclear. It is documented that atherosclerosis and other known risk
factors for vascular disease are usually absent in patients with spontaneous carotid
artery dissection. Fibromuscular dysplasia, Ehlers–Danlos syndrome, cystic medial
necrosis, Marfan syndrome, autosomal dominant polycystic kidney disease, and
osteogenesis imperfecta type I have been implicated [2, 8]. Spontaneous carotid
artery dissection may manifest as an extension of the aortic type A dissection.

5.5.2 Clinical Presentation

The most common initial symptom in patients with spontaneous dissection of the
carotid artery is headache, partial unilateral Horner syndrome without facial anhi-
drosis and hemispheric symptoms. Patients with cervical carotid artery dissection
also suffer from neck pain, amaurosis fugax, anisocoria, pulsatile tinnitus, and cra-
nial nerve palsy (cranial nerves IX and XII). The prognosis after stroke caused by
dissection is worse than the prognosis after stroke caused by atherosclerosis [2].

5.5.3 Diagnosis

DUS is the first-line diagnostic methods but CTA and angiography are the gold
standards.

5.5.4 Treatment

Medical therapy is focalized on antithrombotic therapy to reduce stroke recurrence

and clinical worsening. Indications for surgical or endovascular treatment of acute
carotid artery dissection are fluctuating or deteriorating clinical neurologic symp-
toms despite medical treatment. Indications for surgery after 6 months of medical
treatment are persistent high-grade stenosis and a new or persistent aneurysm
greater than twice the diameter of the normal internal carotid segment [2]. The treat-
ment available are surgical or endovascular approach. There are no randomized tri-
als comparing open and endovascular treatment of patients with acute or late
sequelae of carotid dissection, and no clear indications regarding when either
approach might be preferred [2].
Figure 5.5 shows the management of patient with recent stroke.
42 E. L. Castronovo et al.

Patient with stroke

DUS excludes internal DUS detects internal

carotid stenosis carotid stenosis

SEE FIGURE 2
right emispheric,
vertebrobasilar and/or
left emispheric and vertebrobasilar and
left upperarm
left retinal symptoms right upperarm
symptoms
symptoms

emergency emergency emergency

extracranial and extracranial and extracranial and
thoraxCTA todetect thorax CTA to detect thoraxCTA to detect
left CCA left subclavian innominateartery
stenosis/occlusion stenosis/occlusion stenosis/occlusion

CALLVASCULAR
SURGEON FOR
REVASCULARIZATION

Fig. 5.5  Management of patients with stroke symptoms

5.6 Vertebral Artery Disease

Vertebrobasilar ischemia is less common than ischemic episodes related to internal

carotid artery disease, approximately 25% of all ischemic strokes do occur in the
distribution of the posterior brain circulation [2].

5.6.1 Etiology

The causes of vertebrobasilar stroke/TIA include low-flow hemodynamic ischemia,

cardioembolism, large artery thromboembolism, small artery disease and dissec-
tion; atherosclerosis of the vertebral or basilar arteries accounts for 20–25% of
strokes [1, 2].
The surgical anatomy of the paired vertebral arteries has traditionally been
divided into four segments: segment V1 includes the origin of the vertebral artery as
it arises from the subclavian artery to the point at which it enters the C6 transverse
5  Supra-aortic Trunks Emergency Conditions 43

process. This is the most common site of stenosis due to atherosclerotic lesions.
Segment V2 includes the segment of the artery buried deep within the inter-­
transversarium muscle and the cervical transverse processes of C6 to C2. This site
is unfrequently involved by atherosclerotic lesions but it is a frequent site for the
development of traumatic or spontaneous arteriovenous fistulas and pseudoaneu-
rysms secondary to trauma or dissection. Segment V3 includes the segment of the
vertebral artery that extends from the top of the transverse process of C2 to the
atlanto-occipital membrane at the base of the skull. The most common problems at
the V3 level are related to trauma and arterial dissection. Segment V4 includes the
intracranial, intradural portion of the vertebral artery beginning at the atlanto-­
occipital membrane and terminating as the two paired vertebral arteries that con-
verge to form the basilar artery. It is infrequently affected by atherosclerosis but is
prone to arteriovenous fistula formation and aneurysmal degeneration [2].

5.6.2 Clinical Presentation

Vertebrobasilar symptoms include vertigo, ataxia, eye movement disorders, bilat-

eral limb weakness, complete visual loss (cortical blindness), hemianopia, unilat-
eral weakness or numbness, dizziness, dysarthria, headache, and nausea/
vomiting [1].

5.6.3 Diagnosis

DUS is the first-line imaging method. DUS must be followed by contrast enhanced
magnetic resonance angiography (CEMRA) or CTA [1].

5.6.4 Treatment

Asymptomatic vertebral artery atherosclerotic lesions should not be treated by open

or endovascular interventions. BMT is recommended.
When vertebrobasilar symptoms occur, BMT plus vertebral artery revasculariza-
tion is recommended early after symptoms appear for 50–99% extracranial verte-
bral artery stenosis. In fact, stenoses of the vertebral arteries are associated with
high early recurrence stroke rates. Surgical approaches to lesions at the vertebral
artery origin include transposition to the ipsilateral CCA, vertebral artery reimplan-
tation, and vein bypass grafting from the subclavian artery. Few data are available
for endovascular treatment [9]. Figure  5.6 shows management of vertebrobasilar
symptoms onset.
44 E. L. Castronovo et al.

Vertebrobasilar
symptoms

DUS: extracranial
vertebral artery
stenosis/occlusion

SI NO

CEMRA/CTA INTRACRANIAL CTA

<50% stenosis 50-99% stenosis

BMT + Open BMT + Endovascular

BMT revascularization angioplasty/stenting

Fig. 5.6  Management of patient with vertebro-basilar symptoms

5.7 Vascular Injuries to the Cervical Vessels

Traumatic injuries to the cervical vessels are relatively uncommon and constitute
only about 5–10% of all vascular injuries. The patients are mostly young, and
despite the low incidence, mortality and morbidity are between 5% and 40%, and
persistent neurological consequences are reported in up to 80% of patients [10].
5  Supra-aortic Trunks Emergency Conditions 45

5.7.1 Etiology

The most common mechanism is penetrating injuries. Blunt is thought to be less

than 0.5% of all blunt traumas to the body, but recent reports indicate that many
blunt vascular injuries go undetected [2].
The common carotid is the most frequently injured major artery. The internal
carotid artery is involved in more than 90% of blunt injuries, most commonly its
distal parts. Injuries to the vertebral artery are less common because they are
well protected by osseous structures with an incidence of 0.20–0.77% of all
trauma admissions [2, 10]. Injuries to the thoracic outlet are extremely lethal.
Prehospital mortality is 50–80%, and of those who survive transport, 15% die
during treatment [2].

5.7.2 Clinical Presentation

In case of penetrating trauma, bleeding is the most frequent sign. In a penetrating

trauma there are “hard signs” and “soft signs” of vascular injury. Hard signs include
shock, refractory hypotension, pulsatile bleeding, bruit, enlarging hematoma, and
loss of pulse. Soft signs include history of bleeding at the scene of injury, stable
hematoma, nerve injury, proximity of injury track, and unequal upper extremity
blood pressure measurements [2]. In blunt carotid injuries, headache and/or cervical
pain are the most common symptoms, followed by symptoms indicating cerebral or
retinal ischemia due to embolization or thrombotic occlusion. A frequent type of
symptom is a typical transient ischemic attack but complete stroke or amaurosis
fugax also occurs. Horner’s syndrome may be present if superficial cervical gan-
glion lesions coexist. In cases of vertebral artery blunt injuries vertebrobasilar isch-
emia may be manifested with dizziness, vertigo, nausea, tinnitus, dysarthria,
dysphagia, ataxia, visual deficits, and hoarseness.
Secondary damage to the aerodigestive tract with dyspnea or stridor (for exam-
ple, compression of the airways by a large expanding hematoma) may be associ-
ated [10].
Difficulty swallowing, vocal cord paresis, hoarseness, inability to shrug, and
weakness may be present in case of cranial nerve injuries.

5.7.3 Diagnosis

The diagnosis of penetrating neck injury is usually obvious because bleeding is

present. However, it is important to note the extent of the trauma. In fact, mild exter-
nal signs of trauma can be associated with severe vascular injury or expanding
hematomas. The location of penetrating cervical injuries are generally divided into
three different zones. Zone I extends inferiorly from 1 cm above the manubrium to
include the thoracic outlet; zone II extends from the upper limit of zone I to the
46 E. L. Castronovo et al.

angle of the mandible; and zone III is between the angle of the mandible and the
base of the skull. Zone II is the most commonly injured (47%), followed by zone III
(19%) and zone I (18%) [2]. In zone II traumas if patients are stable and asymptom-
atic angiography, duplex ultrasound, and CT may be useful to rule out vascular
injuries. Exploration and the possibility of obtaining control are much easier in zone
II injuries. Injuries not penetrating the platysma need no further vascular evaluation.
In stable patients with zones I and III trauma CTA or DSA is always indicated. All
patients with neck trauma should have plain radiographs of the chest to rule out
occult hemothoraces, pneumothoraces, or aortic arch injury [10].
In patients admitted to ER for blunt neck trauma, it is important to perform a
careful neurological examination to obtain a baseline for later comparisons. In fact
half of the patients develop neurological symptoms within 24 h [10].
DUS can be considered as a screening method but in case of a negative study
CTA or digital subtraction angiography (DSA) is recommended. However, DSA has
several limitations such as invasiveness that carries a risk of stroke (<1.0%) and
cost [2].

5.7.4 Treatment

In the emergency scenario, the airway and breathing have priority, followed by the
control of bleeding in case of penetrating trauma. Patients with shock, active brisk
bleeding, rapidly expanding hematoma and those with neurological deficit or severe
airway obstruction should be transported to the operating room for immediate
exploration and treatment. Repair is recommended in all patients with penetrating
carotid injuries and the patient has no major neurological symptoms. For minor
injuries to the carotid artery, including those with small but adherent intimal flaps,
defects, or pseudoaneurysms <5 mm in size, repair is recommended in symptomatic
patients. If the patient is asymptomatic and there is no ongoing active bleeding, a
conservative approach with antithrombotic therapy and early follow-up imaging has
proven to be a safe alternative [2, 10].
In blunt trauma for asymptomatic injuries, including dissection, antithrombotic
therapy is usually the only treatment needed and is indicated to prevent thrombosis
of the injured segment and/or embolization from it.
Endovascular therapy has primarily been reserved for evolving dissections that
are surgically inaccessible, pseudoaneurysms that persist or enlarge after antithrom-
botic treatment, or patients with worsening neurologic symptoms on medical ther-
apy [2]. Based on the location of these injuries, endovascular therapy offers several
advantages over open repair. However injuries that appear to be easily accessible
during surgery and are symptomatic should be considered for repair while injuries
located at the base of the skull, the only option for treatment may be endovascular
exclusion [2, 10].
5  Supra-aortic Trunks Emergency Conditions 47

References
1. Naylor AR, Ricco JB, de Borst GJ, Debus S, de Haro J, Halliday A, Hamilton G, Kakisis J,
Kakkos S, Lepidi S, Markus HS, McCabe DJ, Roy J, Sillesen H, van den Berg JC, Vermassen
F, Esvs Guidelines Committee, Kolh P, Chakfe N, Hinchliffe RJ, Koncar I, Lindholt JS,
Vega de Ceniga M, Verzini F, Esvs Guideline Reviewers, Archie J, Bellmunt S, Chaudhuri
A, Koelemay M, Lindahl AK, Padberg F, Venermo M.  Editor’s Choice  - Management of
Atherosclerotic Carotid and Vertebral Artery Disease: 2017 Clinical Practice Guidelines of the
European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg. 2018;55(1):3–81.
https://doi.org/10.1016/j.ejvs.2017.06.021. Epub 2017 Aug 26.
2. Sidawy AN, Perler BA.  Rutherford’s vascular surgery and endovascular therapy, E-Book.
Amsterdam: Elsevier Health Sciences; 2018.
3. Albers GW, Caplan LR, Easton JD, Fayad PB, Mohr JP, Saver JL.  Sherman DG; TIA
Working Group. Transient ischemic attack  - proposal for a new definition. N Engl J Med.
2002;347(21):1713–6. https://doi.org/10.1056/NEJMsb020987.
4. AbuRahma AF, Avgerinos EM, Chang RW, Darling RC 3rd, Duncan AA, Forbes TL, Malas
MB, Perler BA, Powell RJ, Rockman CB, Zhou W. The Society for Vascular Surgery imple-
mentation document for management of extracranial cerebrovascular disease. J Vasc Surg.
2022;75(1S):26S–98S.
5. Sacco RL, Kasner SE, Broderick JP, Caplan LR, Connors JJ, Culebras A, Elkind MS, George
MG, Hamdan AD, Higashida RT, Hoh BL, Janis LS, Kase CS, Kleindorfer DO, Lee JM,
Moseley ME, Peterson ED, Turan TN, Valderrama AL, Vinters HV; American Heart Association
Stroke Council, Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular
Radiology and Intervention; Council on Cardiovascular and Stroke Nursing; Council on
Epidemiology and Prevention; Council on Peripheral Vascular Disease; Council on Nutrition,
Physical Activity and Metabolism. An updated definition of stroke for the 21st century: a
statement for healthcare professionals from the American Heart Association/American Stroke
Association. Stroke. 2013;44(7):2064–89. https://doi.org/10.1161/STR.0b013e318296aeca.
Epub 2013 May 7. Erratum in: Stroke. 2019 Aug;50(8):e239.
6. Shiber JR, Fontane E, Adewale A.  Stroke registry: hemorrhagic vs ischemic strokes. Am J
Emerg Med. 2010;28(3):331–3. https://doi.org/10.1016/j.ajem.2008.10.026.
7. Ay H, Arsava EM, Andsberg G, Benner T, Brown RD Jr, Chapman SN, Cole JW, Delavaran H,
Dichgans M, Engström G, Giralt-Steinhauer E, Grewal RP, Gwinn K, Jern C, Jimenez-Conde
J, Jood K, Katsnelson M, Kissela B, Kittner SJ, Kleindorfer DO, Labovitz DL, Lanfranconi S,
Lee JM, Lehm M, Lemmens R, Levi C, Li L, Lindgren A, Markus HS, McArdle PF, Melander
O, Norrving B, Peddareddygari LR, Pedersén A, Pera J, Rannikmäe K, Rexrode KM, Rhodes
D, Rich SS, Roquer J, Rosand J, Rothwell PM, Rundek T, Sacco RL, Schmidt R, Schürks
M, Seiler S, Sharma P, Slowik A, Sudlow C, Thijs V, Woodfield R, Worrall BB, Meschia
JF.  Pathogenic ischemic stroke phenotypes in the NINDS-stroke genetics network. Stroke.
2014;45(12):3589–96. https://doi.org/10.1161/STROKEAHA.114.007362. Epub 2014 Nov 6.
Erratum in: Stroke. 2015 Jan;46(1):e17.
8. Howard VJ, Meschia JF, Lal BK, Turan TN, Roubin GS, Brown RD Jr, Voeks JH, Barrett KM,
Demaerschalk BM, Huston J 3rd, Lazar RM, Moore WS, Wadley VG, Chaturvedi S, Moy CS,
Chimowitz M, Howard G, Brott TG. CREST-2 study investigators. Carotid revascularization
and medical management for asymptomatic carotid stenosis: Protocol of the CREST-2 clinical
trials. Int J Stroke. 2017;12(7):770–8. https://doi.org/10.1177/1747493017706238.
9. Featherstone RL, Brown MM.  The second european carotid surgery trial. Endovascular
Today. 2012;10:75–7. In: Naylor AR, Ricco JB, de Borst GJ, Debus S, de Haro J, Halliday
A, Hamilton G, Kakisis J, Kakkos S, Lepidi S, Markus HS, McCabe DJ, Roy J, Sillesen H,
van den Berg JC, Vermassen F, Esvs Guidelines Committee, Kolh P, Chakfe N, Hinchliffe
RJ, Koncar I, Lindholt JS, Vega de Ceniga M, Verzini F, Esvs Guideline Reviewers, Archie J,
48 E. L. Castronovo et al.

Bellmunt S, Chaudhuri A, Koelemay M, Lindahl AK, Padberg F, Venermo M. Editor's Choice -

Management of Atherosclerotic Carotid and Vertebral Artery Disease: 2017 Clinical Practice
Guidelines of the European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg.
2018;55(1):3–81. https://doi.org/10.1016/j.ejvs.2017.06.021. Epub 2017 Aug 26.
10. Wahlberg E, Olofsson P, Goldstone J. Vascular injuries to the neck. In: Emergency vascular
surgery: a practical guide. Cham: Springer; 2007. p. 3–14.
Upper Airways Tract in Emergency
Settings 6
Diotti Cristina and Francesco Damarco

6.1 Hemoptysis

Hemoptysis is defined as the expectoration of blood from the airways; it should be

distinguished from hemoptoe, defined as coughing of sputum with blood.
Its annual incidence is around 0.1% in out-patients, representing 0.2% of causes
of hospitalization; 10% of all episodes of hemoptysis occurs in patients with chronic
lung diseases [1]. It generally affects adults aged around 60–70, although in rare
cases it can occur in children.
Hemoptysis can be classified as mild (<20 mL in 24 h), moderate (20–600 mL in
24 h), and massive (>600 mL in 24 h) depending on the amount of blood.
More than 90% of episodes are self-limiting, but hemoptysis can be a life-­
threatening condition requiring an immediate intervention due to gas exchange
impairment and asphyxia.
Blood in the airways can cause respiratory failure due to impaired gas exchange:
since tracheobronchial dead space volume is around 150–200 mL, a bleeding vol-
ume >100 mL can lead to severe airway obstruction and cause asphyxia [2].
However, life-threatening conditions may occur even with a smaller amount of
blood, in case of reduced coughing reflex or previous impaired lung function.

D. Cristina
University of Milan, Milan, Italy
e-mail: [email protected]
F. Damarco (*)
Thoracic Surgery and Lung Transplant Unit,
Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, University of Milan,
Milan, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 49

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_6
50 D. Cristina and F. Damarco

6.1.1 Etiology

Bronchial arteries originate from the systemic circulation, generally from the
descending thoracic aorta more commonly between T5 and T6, but aberrant bron-
chial vessels may arise from other systemic arteries (e.g., aortic arch, subclavian
artery, internal mammary artery).
Some conditions (Table 6.1), such as chronic inflammation, neoplastic diseases,
or hypoxic vasoconstriction, lead to the release of angiogenetic factors that promote
vascular proliferation: in these cases bronchial arteries become thin and fragile and
may rupture under systemic pressure, causing airway bleeding. In more than 90% of
cases, bleeding arises from bronchial circulation; in only 5% of cases it originates
from pulmonary vessels [1, 3, 4].
Tuberculosis is the most common cause of hemoptysis worldwide [5], but in
about 40% of cases, the underlying cause of hemoptysis cannot be identified and
remains unknown.

6.1.2 Clinical Presentation

In patients presenting with blood expectoration, an accurate medical history should

be taken to define the amount of expectorated blood, the duration of symptoms,
previous episodes, smoking history, active medications, and underlying diseases
(lung, cardiac, malignancies, etc.). Hemoptysis should be distinguished from other
causes of bleeding from the gastroenteric tract (hematemesis) or the upper respira-
tory tract (mouth, gums, nose, and pharynx).
A quick initial clinical evaluation based on patient’s vital parameters and oxy-
genation is aimed at detecting any life-threatening situation, in particular an
impaired gas exchange, associated with cyanosis, dyspnea/tachypnea, and potential
loss of consciousness. In these cases, an immediate intervention is mandatory to
restore gas exchange, clear the blood form the airways, and avoid death.
Considering the different causes of hemoptysis, the physical examination can
show signs of pulmonary (e.g., altered breath murmurs, wheezes, crackles, pleural
friction) or cardiovascular disease (e.g., heart murmur in case of mitral stenosis,
hepatomegaly, and superior vena cava syndrome).

Table 6.1  Main causes of hemoptysis

Airway or lung infections (mainly tuberculosis and aspergillosis, that may be also associated
with vascular erosion causing massive bleeding)
Inflammatory airway or lung diseases (e.g., COPD)
Bronchial primitive malignancies or metastatic diseases
Bronchiectasis, cystic fibrosis
Increased pulmonary venous pressure (e.g., pulmonary edema, mitral stenosis)
Pulmonary artery embolism
Iatrogenic causes (e.g., anticoagulation therapies, transbronchial biopsies, foreign bodies,
surgical lung resections)
Other causes (e.g., vasculitis, vascular malformations, pulmonary hypertension, hemosiderosis,
NSCLC treatment with bevacizumab)
6  Upper Airways Tract in Emergency Settings 51

6.1.3 Diagnosis

Once defined the grade of hemoptysis and managed possible life-threatening situa-
tions, diagnostic procedures include:

• Blood tests with complete blood count (CBC), coagulation tests, biochemistry
and inflammation parameters.
• Chest X-ray: can show lung or airway lesions/masses, atelectasis, air broncho-
grams, pleural effusion, cardiomegaly.
• Multislice contrast-enhanced CT scan with CT angiography is useful in case of
doubt, massive or recurrent hemoptysis. This procedure can localize the site and
cause of hemoptysis, reveal active spots of bleeding and help plan a possible
embolization. Bronchial systemic arteries are considered pathological if >2 mm
in diameter and have a tortuous pathway.
• Bronchoscopy: useful in case of active bleeding, it can be performed with flexi-
ble or rigid instruments with both diagnostic (microbiological/cytological/histo-
logical samplings) and therapeutic purposes. Flexible bronchoscopy can be
performed at bedside, it is easier to handle and enables an accurate inspection of
the tracheobronchial tree; rigid bronchoscopy should be performed by highly
trained specialists in the operating room under general anesthesia and does not
allow the exploration of segmental bronchi.

6.1.4 Treatment

In case of mild or moderate self-limiting hemoptysis, conservative treatment and

management of the underlying disease is the treatment of choice. Tranexamic acid
(1–1.5 g bid or tid) can be administered orally [6] and further investigations on the
etiology may be performed in outpatient setting.
In case of active bleeding with stable vital parameters, hospitalization is recom-
mended and general indications for treatment include:

• Lateral decubitus with bleeding site down, if known, to protect airways and avoid
aspiration into the non-affected lung.
• Monitor vital signs and get an IV access.
• Antifibrinolytics agents may reduce duration and volume of bleeding, with a low
short-term risk of thromboembolism [6].
• Empiric broad-spectrum antibiotic therapy can be administered if an infective
cause is suspected.
• Bronchoscopy may be able to remove the blood, to identify the site, and to stop
the source of bleeding. Endobronchial instillation of vasoconstrictive agents,
cold saline solution, laser photocoagulation, or argon plasma electrocoagulation
are also useful. Temporary occlusion of the segmental bronchus with a balloon
catheter is suitable in case of peripheral bleeding.
• Angiographic bronchial artery embolization (BAE) can be performed to stop the
bleeding using metallic spirals or liquid agents. It is a safe non-surgical proce-
52 D. Cristina and F. Damarco

dure with high success rates. The main side effects of BAE are chest pain end
transient dysphagia; serious complications include spinal cord ischemia and
transverse myelitis if arteries supplying the spine are accidentally involved in the
embolization.
• Surgery is indicated in case of necrotizing tumors, cavernous tuberculosis or
aspergillomas, unsuccessful BAE or in rare cases of traumatic/iatrogenic events
of bleeding. The procedure should be performed as an elective surgery, after
stopping the bleeding and planning the extent and the feasibility of the lung
resection.
• Emergency surgical treatment is reserved to extreme cases of uncontrolled
hemoptysis and is associated with a high mortality rate (up to 50%) due to the
patient’s critical conditions related to hemodynamic and respiratory instability.

Algorithm 6.1  Algorithm for diagnosis and treatment of hemoptysis.

Box 6.1 Massive hemoptysis [3]

Life-threatening hemoptysis may be defined as any hemoptysis with:

• >100 mL in 24 h
• Abnormal gas exchange/airway obstruction
• Hemodynamic instability [4]

If the patient cannot eliminate the blood from the airways, is unconscious
and in severe respiratory failure:

• immediate orotracheal intubation with a large diameter tube (8–9 mm) to

protect the airways and ventilate the patient. Selective bronchial intubation
of the non-affected side can be performed with endotracheal tube, bron-
chial blockers, or Fogarty catheters.
• Patient should be monitored in the ICU.
• Blood and volume supply can be administered in case of hypovolemia.
• Flexible bronchoscopy through the tube or rigid bronchoscopy in combi-
nation with flexible bronchoscopy should be performed to maintain venti-
lation, remove blood and clots, identify the bleeding source, and obtain
hemostasis.
• Investigate the causes and treat the underlying disease.
• Once stabilized the patient, in case of persistent bleeding, BAE or surgical
resection may be considered as alternative therapeutic options.
6  Upper Airways Tract in Emergency Settings 53

6.2 Airway Obstruction

Airway obstruction is a potential life-threatening obstacle to the airflow and to ven-

tilation due to narrowing or occlusion of the airways.
It may be classified as acute or chronic, and be partial or complete, depending on
how much caliber of the airway is obstructed. Acute obstruction can be fatal in a few
minutes, compromising ventilation and causing asphyxia, and requires an immedi-
ate intervention.

6.2.1 Etiology

Common causes of airway obstruction are foreign bodies, benign or malignant

endotracheal lesions, tracheal stenosis occurring after prolonged intubation or tra-
cheostomy, edema, infections and abscesses, blunt or penetrating traumas and air-
way compression from extraluminal lesions (ab-extrinseco compression). Some
anatomic variants can contribute to the obstruction.

6.2.2 Clinical Presentation

Clinical presentation varies according to the site and the degree of obstruction.
Chronic or partial airway obstruction is a non-deferrable urgency, presenting with
dyspnea, accessory respiratory muscle use, laryngeal stridor, abnormal breath
sounds, and cough.
Acute airway obstruction is an emergency setting, associated with breathless-
ness, acute respiratory distress, cyanosis, altered consciousness, and agitation.
Often, the history of the event cannot be told by the patient and it may be reported
by bystanders or family members. A rapid clinical evaluation should include vital
parameters detection and exploration of the upper airways (nose, throat, pharynx,
head, and neck) and should be focused on identification of the possible causes of
obstruction.
Resuscitation and airway protection must be promptly carried out: the equipment
should include devices for nasotracheal or endotracheal intubation and surgical air-
way supplies.

6.2.3 Diagnosis

The exploration of the upper airways can be performed using nasal speculum, a
laryngoscope or via direct visualization. Other diagnostic tools (imaging tech-
niques, endoscopic procedures) should not delay the intervention in case of acute
distress and may be helpful to identify the etiology once the patient is stable.
54 D. Cristina and F. Damarco

Imaging techniques include head-neck and chest X-ray, CT scan, and MRI: in par-
ticular, CT scan is rapid, widely available and safe and provides information on
airway structure and diameter and possible causes of obstruction.
Examination should identify the type and size of the obstruction, in order to plan
the most effective intervention.

6.2.4 Treatment

In case of acute obstruction, airways need to be secured by the members of the

emergency staff involved. High-flow oxygen supply can temporarily increase air-
way patency with positive pressure and improve oxygenation during airway
intervention.
Procedure to secure the airways in acute life-threatening situations includes:

• Awake fiberoptic intubation (AFOI) allows airways intubation maintaining spon-

taneous breathing and avoiding the obstructing. This technique is useful in case
of supraglottic or glottic obstructions. Temporary complete obstruction of the
airways caused by the scope should be considered.
• Awake videolaryngoscopy is useful in case of laryngeal obstruction, is more
familiar with most anesthetists and it has same advantages of AFOI.
• Awake tracheostomy via percutaneous or surgical technique is the gold standard
management in acute upper airways obstruction but it can be difficult to perform
without sedation in critical situations.

6.2.5 Main Causes of Airway Obstruction

6.2.5.1 Foreign Bodies’ Inhalation

Foreign body (FB) inhalation is a common event in children, but many cases in
adults and elderly age are reported, mainly associated to dementia, alcohol con-
sumption, or poor dentition. In the USA, the mortality rate in kids <4 years old is
about 7%. Most frequently inhaled objects are food (peak incidence 1–2 years of
age), coins, small toys, seeds, nuts, and balloons, but in adults also medical instru-
ments, dental prostheses, and bones are common.
Especially in children, the patient is unable to explain what is happening, the
event of inhalation may be not immediately recognized, and the aspirated object can
escape detection of adults.
The aspirated object can cause various degrees of airway obstruction depending
on location and shape: partial occlusion can cause chronic symptoms, while com-
plete occlusion of the airway leads to sudden death. In case of complete obstruction,
the FB lying in the larynx or trachea causes acute choking and asphyxia: in this
scenario, an immediate intervention at the scene with the Heimlich maneuver, back
blows, chest or abdominal thrusts can be life-saving.
6  Upper Airways Tract in Emergency Settings 55

If the FB obstruct the vocal cords and prevents endotracheal intubation, an emer-
gency surgical or percutaneous airway is necessary: tracheostomy or needle crico-
thyroidotomy is preferred in children (the latter is avoided in children <8 years old).
If the FB is peripheral to the carina, the location in the bronchial tree depends on
the size of the object and the endobronchial structure: in children <15 years, left and
right mainstem bronchi have similar angulation and FB are found almost equally in
the two sides. Growing up, the right mainstem bronchus becomes linear and FB are
more frequently located on this side [7].
When the object lies in a lobar or sublobar bronchus, it causes inflammation,
edema, and granulation reaction that can make the identification and removal of the
FB harder. In particular, vegetables may swell in hours or days, thus worsening the
obstruction: some organic materials, such as peanuts, release acid particles that can
induce inflammation, edema, and erosion. The procedure of removal may be com-
plicated by bleeding and mediastinitis or bronchial fistulae may occur.
Typical signs and symptoms in the acute phase include cough and air trapping
and local emphysema distal to the obstruction due to a mechanism that prevents air
outflow. In the chronic phase recurrent infections (post-obstructive pneumonia, lung
abscesses) atelectasis, bronchiectasis, and hypoxic vasoconstriction are the most
common clinical signs. Rates of serious complications arise up to 2.5 times if the
diagnosis is >24  h after the inhalation. In case of non-specific symptoms, the
obstruction can be misdiagnosed and interpreted as asthma or chronic bronchitis.

Diagnostic tools include:

• Chest X-ray: Less than 20% of FB are radio-opaque, but some indirect signs of
FB inhalation, such as air trapping, monolateral hyperinflation, obstructive
emphysema, mediastinal shift, lobar atelectasis, or pneumomediastinum may be
recognized.
• CT scan allows the identification of the obstruction in the tracheobronchial tree
and localized areas of air trapping or atelectasis.
• Rigid bronchoscopy is the gold standard for the airway protection, diagnosis and
treatment of FB inhalation. Flexible bronchoscopy alone should not be per-
formed because of the high risk of dislocation of the FB during the procedure [8].

A clinical observation of 24–48 h is recommended after the extraction in order to

manage possible complications, such as re-expansion pulmonary edema, inflamma-
tion, hemoptysis, fever, up to ventilatory failure requiring ICU monitoring. In some
cases, repeated endoscopic procedures may be necessary.

6.2.5.2 Tracheal Stenosis

Tracheal stenosis often presents as a circumferential lesion caused by tissue reaction
after prolonged intubation, injuries, or radiation therapy. In rare cases it may be
congenital, when abnormal cartilages alter tracheal structure.
Clinical presentation includes characteristic inspiratory laryngeal stridor, in
addition to typical symptoms of airway occlusion.
56 D. Cristina and F. Damarco

Diagnostic evaluation should comprehend:

• Imaging tests (chest X-ray, CT scan with 3D reconstructions, MRI) provide
information about the location and the extension of the stenosis and allow an
adequate planning for invasive procedures.
• Flexible bronchoscopy is the gold standard procedure for the diagnosis of tra-
cheal stenosis. It allows to evaluate the caliber of residual lumen and to plan the
proper treatment [9].

Treatment options include:

• Observation in case of mild stenosis without relevant symptoms. Especially in
children, mild stenosis tends to improve with growing.
• Non-severe stenosis can be treated endoscopically using a balloon dilation pro-
cedure, with or without laser radial cutting of the scar tissue. Recurrence of scar
tissue can be avoided with topical instillation of steroids during the procedure [9].
• In cases of severe or recurrent stenosis, tracheal surgery is the treatment of
choice. If few tracheal rings are involved, the resection of the stenotic tract and
reconstruction by direct termino-terminal anastomosis can be performed; in case
of long-segment tracheal stenosis, a slide tracheoplasty is required [10].

6.2.5.3 Malignant Airway Obstruction

Airway obstruction can be a manifestation of advanced lung/tracheobronchial can-
cer or a metastatic disease that causes a mechanical obstruction to the airflow. Its
clinical presentation is usually late in the course of the disease and can be a cause
of death.
Malignant airway obstruction can result from a direct invasion of the tracheo-
bronchial lumen (intrinsic obstruction) or a compression from an extraluminal
growing disease (ab-extrinseco compression). In some advanced cases, both condi-
tions may contribute to the obstruction.
The most common causes of malignant airway obstruction are bronchogenic car-
cinomas (usually squamous cell lung cancer), or adjacent malignancies invading the
airways (esophageal, laryngeal thyroid). Primitive tracheal tumors are rare (about
0.6% of all respiratory tract malignancies) and mainly represented by squamous
cell, adenoid cystic and mucoepidermoid carcinoma [11].
Endoluminal lesion from metastatic diseases are uncommon and can occur
mainly in case of breast, renal colorectal cancer and melanoma.
About 20–30% of lung cancer patients may develop symptoms related to central
airway obstruction and invasion of tracheobronchial lumen (dyspnea, atelectasis,
localized wheezing, post-obstructive pneumonia, and hemoptysis) that can be dif-
ficult to manage in advanced oncological patients.
In case of suspected malignant airway obstruction, the past medical and onco-
logical history should be carefully investigated. Generally, airway obstruction
occurs in patients with a known, late-stage oncological disease, but sometimes air-
way obstruction is the first manifestation of the disease. After the acute management
of airway obstruction, an adequate diagnostic workup should be assessed.
6  Upper Airways Tract in Emergency Settings 57

If chest X-ray is not diagnostic, chest CT scan has a higher sensitivity (up to
98%) in detecting the type, the length, and the diameter of the obstruction and the
characteristics of the distal airways in order to plan the proper treatment.
Both flexible and rigid bronchoscopies are the procedure of choice for the
diagnosis and treatment of malignant obstruction: the lesion and the distal airways
can be directly visualized and tissue specimens can be collected for histological
analysis.
Flexible bronchoscopy should be performed carefully in order to avoid bleeding
or other serious complications leading to complete obstruction of the airways.
In urgent situation with severe respiratory distress, the priority is to secure the
airways: in these patients, an immediate endotracheal intubation is required and, if
possible, a rigid bronchoscopy performed by a skilled interventional pulmonology
team. If the equipment is not available, the patient should be transferred as soon as
possible to a specialized center.
Once stabilized the patient and defined the type of the obstruction, the treatment
depends on the extent and the stage of the malignancy and patient’s life expectancy.
Unfortunately, radical surgical treatment is often not viable in advanced malig-
nant diseases and the management is focused on palliation of symptoms and quality
of life improvement.
In these cases, interventional bronchoscopy is the treatment of choice [12] and
includes:

• Mechanical debulking in case of intrinsic obstruction, using rigid bronchoscope

to core the lesion, or endoscopic forceps to remove obstructive tissue, or
microdebriders.
• Balloon dilation or bronchoplasty involving the use of increasingly larger bal-
loons endoluminally can be performed both for intrinsic and extrinsic
obstructions.
• Thermal ablation using YAG laser, argon-plasma, electrocautery, cryotherapy.
• Airway stent placement (silicone and/or metallic), more efficient in extrinsic
compressions.
• Brachytherapy allowing endobronchial delivery of radiations via the placement
of radioactive substances using a flexible bronchoscope.

These interventional procedures are usually performed via rigid bronchoscopy,

that provides a better airway control in case of complications and allows ventilation
during the procedure.

6.3 Tracheobronchial Injuries

Tracheobronchial injuries (TBI) are an uncommon but potentially life-threatening

condition. They can be caused by penetrating or blunt traumas, or may be iatro-
genic injuries occurring during endotracheal intubation, endoscopic and surgical
procedures.
58 D. Cristina and F. Damarco

6.3.1 Etiology

Traumatic injuries may be caused by penetrating objects or by gunshots; knives usu-

ally cause lesions to the cervical trachea, though gunshot injuries can occur any-
where in the tracheobronchial tree.
Blunt traumas are often related to high-impact events on the chest that cause
forces of traction on the tracheobronchial tree or to direct hits on the neck. Most
blunt injuries involve the distal trachea and the right main bronchus [13].
Morbidity and mortality associated with traumatic tracheobronchial injures are
elevated, also due to serious concomitant traumas on other injured organs (facial
and head traumas, pulmonary contusions, intra-abdominal injuries, orthopedic frac-
tures): patients with multiple traumas should be managed in a high-volume
trauma center.
Iatrogenic injuries may be a complication of endotracheal intubation (especially
with double lumen tubes), tracheostomy, intrathoracic, esophageal, laryngeal and
neck surgery, or of endoscopic procedures (rigid bronchoscopy, EBUS, EUS). Some
anatomical variants including congenital abnormalities (tracheal diverticula,
Mounier-Kuhn syndrome) or distortions caused by neoplasms may be a risk factor
for iatrogenic damages.

6.3.2 Clinical Presentation

TBI should be early treated due to the potentially severe complications related to a
delayed diagnosis. Hoarseness, dysphonia, dysphagia, and stridor are often associ-
ated with a cervical trauma.
Subcutaneous emphysema, hemoptysis, pneumothorax, pneumomediastinum,
and air leakage from a chest penetrating trauma are related to a deeper TBI.
Tracheobronchial traumatic injuries are often associated with other major trau-
mas: in these cases some symptoms can be hidden and TBI can be misdiagnosed. If
TBI is not promptly recognized, granulation tissue and healing processes can mask
the lesion and late manifestations may occur: typical late findings are pneumonia,
bronchiectasis, atelectasis, and abscesses due to tracheobronchial stenosis.

6.3.3 Diagnosis

Chest X-ray is a useful diagnostic tool and can show pneumothorax, pneumomedi-
astinum, pneumopericardium, subcutaneous emphysema, mediastinal shift, tracheal
deviation, and deep cervical emphysema. Complete separation of the mainstem
bronchus may be associated with atelectasis and “fallen lung sign of Kumpe”
(appearance of collapsed lung away from the mediastinum when the bronchus is
completely detached while the vascular structures are intact) [14].
High resolution CT scan helps identifying the site and the extent of the lesion, as
well as other major injuries to intrathoracic structures. However, CT scan is
6  Upper Airways Tract in Emergency Settings 59

contraindicated in hemodynamically unstable patients which require an immediate

intervention.
Bronchoscopy is the gold standard procedure to directly identify the injury and
provides information about the site and the extent of the lesion. In case of suspected
esophageal involvement, esophagus should be investigated using EGDS or oral con-
trast imaging.

6.3.4 Management

Securing the airways is the first step in managing TBI, especially if associated with
other major traumas: patients in acute respiratory distress should be immediately
intubated under flexible bronchoscopy, if available. In case of open cervical traumas
or craniofacial traumas in which orotracheal intubation is difficult, tracheostomy
may be necessary to protect the airways. If the upper trachea is completely tran-
sected, intubation is challenging and the distal portion of the trachea should be
palpated into the mediastinum and directly intubated from the cervical wound.
Intubation is preferably performed with single lumen tube; in some cases a long
single lumen tube can be used in a mainstem bronchus to ensure single lung ventila-
tion. Once secured the airways and stabilized the patient, the treatment is planned
on extent, position, and type of TBI.
For superficial injuries, in clinically stable patients in spontaneous breathing
without O2 support conservative treatment with endoscopic regular follow-up is the
preferable choice: injuries up to 4 cm can be treated conservatively [15].
In case of lesions of the tracheobronchial mucosa with mediastinal emphysema,
antibiotic prophylactic therapy is still debated and the treatment of choice should be
individualized according to clinical presentation and to the extent of the injury.
For complete tracheobronchial injuries involving mediastinum, esophagus, and
soft tissues, a multidisciplinary evaluation is needed to determine the best therapeu-
tic approach: both surgical and endoscopic treatments should be evaluated.
Emergency surgical intervention is required in patients with progressive deterio-
ration of general conditions, air leak and failure in lung re-expansion despite chest
drainage, increasing subcutaneous emphysema and pneumomediastinum, esopha-
geal prolapse into the tracheal lumen and ineffective mechanical ventilation.
Primary surgical repair is also indicated in iatrogenic injuries.
Surgical approach should be planned according to the position of the injury and
the presence of other organs damaged [16]:

• If the lesion is in the proximal trachea (one/two cranial thirds), surgical repair
can be performed via cervicotomy with or without incision of the manubrium.
• For distal tracheal lesions (up to 2 cm above the carina) or for bronchial lesions,
right or left thoracotomy is the preferred surgical approach.
• Simple lacerations can be repaired using interrupted absorbable sutures.
• In case of more complex lesions, tracheobronchial resection and reconstruction
with end-to-end anastomosis is preferable.
60 D. Cristina and F. Damarco

An alternative to surgical treatment is endoscopic placement of self-expandable

stents, that mechanically cover the injury and promote healing processes and can be
removed after 4–6 weeks.
A regular bronchoscopic follow-up should be planned after surgical repair of
TBI, since one of the most common complications is tracheal stenosis.

6.4 Pneumomediastinum

Pneumomediastinum is a clinical condition associated with the presence of air in

the mediastinum. It is a rare situation and can be related to an underlying cause (e.g.,
blunt or penetrating chest trauma, infections, iatrogenic injuries) or can occur spon-
taneously without triggering factors.

6.4.1 Etiology

Pneumomediastinum can occur as a complication of surgical or endoscopic proce-

dures, after an intense Valsalva maneuver, vomiting or other causes of esophageal
rupture (Boerhaave syndrome, caustic ingestion), increase in intra-abdominal pres-
sure (pneumomediastinum during childbirth is known as Hamman’s syndrome),
and rapid ascend in scuba diving. It also may occur after a penetrating or blunt chest
trauma causing airways injury. Asthma, COPD and other chronic lung diseases,
tobacco and recreational drugs use are described as inducing factors. When a cause
cannot be identified, pneumomediastinum is defined as spontaneous.
Possible explanations for pneumomediastinum are:

• Increase in alveolar pressure that can cause ruptures in alveolar structures and
subsequent air leakage that reaches the mediastinum.
• Increase in mediastinal pressure that cause air passage in the mediastinal tissues,
subjected to a negative intrathoracic pressure.

Although it is rare, it is more common in young, tall, and thin men and patients
suffering from asthma or COPD [17].

6.4.2 Clinical Presentation

The main reported symptom is acute and sudden retrosternal chest pain referring to
the neck or the back, often misdiagnosed as spontaneous pneumothorax or heart
diseases.
Sometimes it arises following a causative factor such as cough, vomiting, and
Valsalva maneuver.
Other common symptoms are coughing, dyspnea, neck pain, hoarseness, dys-
phagia, rhinolalia, and subcutaneous emphysema involving chest, neck, and face.
Tachypnea and tachycardia may also occur.
6  Upper Airways Tract in Emergency Settings 61

Even if not frequent, Hamman’s sign is a specific sound audible on the

precordium.
In some cases, pneumomediastinum can be asymptomatic and the diagnosis is
only radiological.

6.4.3 Diagnosis

Imaging diagnostic tools include:

• Chest X-ray shows air in the mediastinal borders making the mediastinal pleura
visible. It can reveal an associated pneumothorax or pneumopericardium. Typical
radiological findings are “thymic sail” (superelevated triangular-shaped inferior
thymic margin due to air, common in children), “ring sign” (due to the air around
pulmonary artery), double bronchial wall, and air near the diaphragm or the
spine [17].
• High resolution CT scan provides information about the extent of the pneumo-
mediastinum and about the possible causes.
• Endoscopic procedures (bronchoscopy, EGD) are not routinely required in case
of spontaneous pneumomediastinum and should be performed only if an under-
lying cause related to esophageal or tracheobronchial injury is suspected.

6.4.4 Management

In most cases, spontaneous pneumomediastinum is a self-limiting condition and

does not require specific treatment: 24 h in-hospital observation and a symptomatic
therapy with analgesics and antitussives are recommended following diagnosis.
Once excluded possible underlying diseases and if the clinical conditions are stable,
the patient can be discharged with indication of bed rest. Air in the mediastinal
space is slowly reabsorbed by surrounding tissues and conservative treatment is
usually effective.
In case of associated pneumothorax, chest tube placement can be needed to avoid
air accumulation in the pleural and mediastinal space.
In rare cases, air leakage can continue causing cardiac tamponade and mediasti-
nal shift: in these cases, an emergent intervention for decompression via VATS or
thoracotomy is required.
Recurrences of pneumomediastinum are extremely rare and long-term follow-
up is usually unnecessary; in case of recurrence, more detailed investigation
should be assessed in order to define and treat a possible misdiagnosed underly-
ing cause.

Algorithm 6.2  Algorithm for diagnosis and treatment of pneumomediastinum.

62 D. Cristina and F. Damarco

References
1. Ittrich H, Bockhom M, Klose H, Simon M. The diagnosis and treatment of hemoptysis. Dtsch
Arztebl Int. 2017;114:371–81. https://doi.org/10.3238/arztebl.2017.0371.
2. Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med.
2000;28(5):1642–7. https://doi.org/10.1097/00003246-­200005000-­00066.
3. Lordan JL, Gascoigne A, Corris PA. The pulmonary physician in critical care Illustrative case
7: assessment and management of massive haemoptysis. Thorax. 2003;58:814–9. https://doi.
org/10.1136/thorax.58.9.814.
4. Blasi F, Tarsia P. Pathophysiology and causes of haemoptysis. In: Webb A, Fifner S, Gattinoni
L, Singer M, editors. Oxford Textbook of Critical Care. 2nd ed. Oxford University Press:
Oxford; 2016.
5. Yoon W, Kim JK, Kim YH, Chung TW, Kang HK.  Bronchial and nonbronchial systemic
artery embolization for life-threatening hemoptysis: comprehensive review. Radiographics.
2002;22(6):1395–409. https://doi.org/10.1148/rg.226015180.
6. Prutsky G, Domecq JP, Salazar CA, Accinelli R.  Antifibrinolytic therapy to reduce hae-
moptysis from any cause. Cochrane Database Syst Rev. 2016;(11):CD008711. https://doi.
org/10.1002/14651858.CD008711.pub3.
7. Warshawsky ME, Mosenifar Z Foreign Body Aspiration Updated: Oct 20, 2020. https://emedi-
cine.medscape.com/article/298940-­overview.
8. Faro A, Wood RE, Schechter MS, for the American Thoracic Society Ad Hoc Committee
on Flexible Airway Endoscopy in Children, et  al. Official American Thoracic Society
technical standards: flexible airway endoscopy in children. Am J Respir Crit Care Med.
2015;191(9):1066–80.
9. Bacon JL, Patterson CM, Madden BP.  Indications and interventional options for non-
resectable tracheal stenosis. J Thorac Dis. 2014;6(3):258–70. https://doi.org/10.3978/j.
issn.2072-­1439.2013.11.08.
10. Ulusan A, Sanli M.  FA Isik Surgical treatment of postintubationtracheal stenosis: a retro-
spective 22-patient series from a single center. Asian J Surg. 2018;41(4):356–62. https://doi.
org/10.1016/j.asjsur.2017.03.001.
11. Stevic R, Milenkovic B. Tracheobronchial tumors. J Thorac Dis. 2016;8(11):3401–13. https://
doi.org/10.21037/jtd.2016.11.24.
12. Simoff MJ, Lally B, Slade MG, Goldberg WG, Lee P, Michaud GC, Wahidi MM, Chawla
M. Symptom management in patients with lung cancer: Diagnosis and management of lung
cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guide-
lines. Chest. 2013;143(5 Suppl):e455S–97S. https://doi.org/10.1378/chest.12-­2366.
13. Karmy-Jones R, Wood DE. Traumatic injury to the trachea and bronchus. Thorac Surg Clin.
2007;17(1):35–46. https://doi.org/10.1016/j.thorsurg.2007.03.005.
14. Moser JB, Stefanidis K, Vlahos I.  Imaging evaluation of tracheobronchial injuries.
Radiographics. 2020;40(2):515–28. https://doi.org/10.1148/rg.2020190171. Epub 2020 Jan 24.
15. Altinok T, Can A.  Management of tracheobronchial injuries. Eurasian J Med.
2014;46(3):209–15. https://doi.org/10.5152/eajm.2014.42. Epub 2014 Aug 26
16. Grewal HS, Dangayach NS, Ahmad U, Ghosh S, Gildea T, Mehta AC.  Treatment of tra-
cheobronchial injuries: a contemporary review. Chest. 2019;155(3):595–604. https://doi.
org/10.1016/j.chest.2018.07.018. Epub 2018 Jul 27.
17. Kouritas VK, Papagiannopoulos K, Lazaridis G, Baka S, Mpoukovinas I, Karavasilis
V, Lampaki S, Kioumis I, Pitsiou G, Papaiwannou A, Karavergou A, Kipourou M,
Lada M, Organtzis J, Katsikogiannis N, Tsakiridis K, Zarogoulidis K, Zarogoulidis
P.  Pneumomediastinum. J Thorac Dis. 2015;7(Suppl 1):S44–9. https://doi.org/10.3978/j.
issn.2072-­1439.2015.01.11.
Multidisciplinary Surgical Consensus
on Neck Emergencies 7
Emanuela Fuccillo and Marco Giovenzana

7.1 General Approach to Neck Emergencies

1. Firstly, evaluate:
(a) airway patency assessment and breathing adequacy
(b) possible vascular complications
(c) possible involvement of other anatomical regions (e.g., expansion of an
infective process, involvement of the spine due to neck trauma...)
2. Secondly, define if the patient can be considered “stable” or “unstable.”

→ If the patient is unstable, the anesthetist-resuscitator and the ENT specialist

should be alerted immediately to achieve an early protection of the airways.
Below we present some of the signs and symptoms in the context of neck pathol-
ogies that can guide the clinical path in defining the patient’s condition (Table 7.1):

E. Fuccillo (*)
Otorhinolaryngology Unit, Head and Neck Department, ASST Santi Paolo e Carlo Hospital,
University of Milan, Milan, Italy
M. Giovenzana (*)
Unit of Hepatobiliary, Pancreatic, and Digestive Surgery, Department of Surgery, S. Paolo
Hospital, University of Milan, Milan, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 63

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_7
64 E. Fuccillo and M. Giovenzana

Table 7.1  Main clinical signs and symptoms of relevance to determine the degree of impairment

Suggestive of severe impairment Suggestive of mild Suggestive of initial/ suspected

impairment (possibility of impairment
changing the framework in
a shon time)

- Absence of vital signs - Tirage / comage / - Anamnesis of

stridor clysphagia, dysphonia,
respiratory distress
- Loss of consciousness - Dyspnea without compromisation
of vital functions
- Unrecognizable respiratory
- Bradypnea
movements
- Signs and symptoms of
- Asphyxia - Confusion ENT interest in
association with ongoing
infectious / inflammatory
- Peripheral vasoconstriction - Sweating signs / recent trauma/
new onset swelling / neck
- Massive bleeding - Tachycardia and or tracheal pain /
known head and neck
malignancy
- Abnormal chest
GCS score ↓
movements

- Bruising

- Subcutaneous
emphysema

- Cervical swelling

7.1.1 Airway Patency Assessment

The evaluation of airway patency and respiratory exchanges can take place through
indirect signs, which every doctor is required to know (refer to the dedicated chapter
of this book) or through a direct evaluation, which may include fiberoptic laryngos-
copy [1], bronchoscopy and completed by a radiological study (in emergency
department we refer in almost all cases to a neck and/or chest CT with and without
contrast) (Fig. 7.1).
In all cases of airway compromise, an anesthetist-resuscitator must be alerted for
prompt airway intubation: airway safety must precede any other type of examina-
tion. In all cases in which there is the suspected or confirmed difficulty of intubation
(e.g., expansive mass which compresses the glottis), the ENT team is required for
an emergency tracheotomy. If the patient is stable and if the ENT specialist is avail-
able, the execution of a flexible fiberoptic laryngoscopy [1] represents an indispens-
able tool for diagnostic completion. If the ENT specialist is not available, the
execution of an urgent CT without and with contrast material represents the first and
most complete and useful radiological evaluation during neck emergency [2].
7  Multidisciplinary Surgical Consensus on Neck Emergencies 65

REMEMBER: In adults, tumors represent the main cause of laryngeal dyspnea; in a smaller
number of cases, it is instead related to functional, neurological, infectious-inflammatory,
traumatic causes or by inhalation of foreign bodies. During the emergency practice, on the
contrary, inhalation of foreign bodies, tumors and infections represent the main causes of access to
an emergency department.

Evaluation of laryngeal patency

I. Clinical appearance of the patient (skin color, signs of agitation, presence of tirage /
cornage / stridor / sweating / loss of consciousness, and the observation of chest
excursion)

II. General hemodynamic evaluation (Heart rate, Respiratory rate, Pulse detection,
Blood pressure, Saturation, Cardiac and pulmonary auscultation)

Compromission of vital signs Initial signs of respiratory distress

Stable vital signs

Loss of consciousness Initial Hemodynamic compromission

Absence of signs of
respiratory distress
Respiratory distress Patient still conscious

Call Resuscitator anesthetist Urgent neck and chest CT Fibroscopic evaluation by an

for a prompt intubation ENT
Fibroscopic evaluation by an
Radiological evaluation
ENT specialist (tracheotomy) ENT

Fig. 7.1  Evaluation of laryngeal patency—Flowchart

7.1.2 Evaluation of Bleeding

When possible, the anamnestic evaluation is essential to raise a better diagnostic

suspicion.

• The first action required is to evaluate if the patient is “stable” or “unstable.”

The assessment of the “volume status,” or the potential entity of the bleeding, can
also be made considering the parameters reported in Table 7.2.
66 E. Fuccillo and M. Giovenzana

Table 7.2  Evaluation parameters of potential blood and water losses

Degree of severity Estimated blood loss Clinical appearance

Mild 0 – 20% Pallor
Cold
Moderate 20 – 40% Oliguria
Anuria
Strict > 40% Agitation
Anxiety
Restlessness
loss of consciousness
Coma

If the patient is “stable,” we can proceed with radiological evaluation through an

angio-CT and/or a neck and chest CT with and without contrast material (depending
on the suspicion). If the patient is hemodynamically unstable, the first necessity is
to stop the bleeding through exploration and surgical hemostasis, which requires
securing the airway through oro-tracheal intubation, or a surgical tracheotomy in
cases where it is not possible to intubate the patient (e.g., a patient with a fracture
that does not allow hyperextension of the neck or with expansive masses that do not
allow the correct visualization of the glottic plane), it is essential to contact the ENT
team to perform an urgent tracheotomy. Secondly, evaluate an adequate restore of
volumes.

7.1.3 Evaluation of a Possible Involvement

of the Surrounding Tissues

1. Anamnesis (e.g., spinal injury, tooth infection).

2. In case of suspicion of involvement of surrounding tissues and if the patient is
stable, imaging should always be planned. The CT scan with and without con-
trast material represents the best examination to evaluate the possible progres-
sion of inflammatory/infective/neoplastic pathologies or to localize possible
trauma/presence of foreign bodies. In selected cases, the CT scan will be com-
pleted with an MRI that—however—is usually difficult to be performed in the
emergency regime. If a traumatic vascular lesion is suspected → an angiographic
assessment should be performed to evaluate the need for an immediate therapeu-
tic intervention

7.2 Etiologies of Neck Emergencies

7.2.1 Traumatic Neck Emergencies

When possible, collect an accurate anamnesis to understand the mechanism of

trauma (Table 7.3) [3].
7  Multidisciplinary Surgical Consensus on Neck Emergencies 67

Table 7.3  Main possible mechanisms of neck trauma distinguishing between extrinsic and intrin-
sic forces

“EXTRINSIC” FORCES “INTRINSIC” FORCES

Blunt traumas Iatrogenic procedures

(sports or motor vehicle accidents)

Penetrating traumas Ingestion/Inhalation of foreign bodies

(gunshot wounds, stab wounds)

Hanging and strangulation traumas Caustics

7.2.2 Remember

7.2.2.1 Extrinsic Forces

1. When the platysma is overcome, there is a greater risk of involvement of vital

structures [4].
2. The sternocleidomastoid muscle separates the neck into two different triangles;
the anterior triangle contains larynx, trachea, pharynx, esophagus, and major
vascular structures, while the posterior triangle contains muscles, the spinal
accessory nerve, and the spinal column.
3. In case of strangulation and/or hanging, we must consider also possible hypoxic
suffering of the brain and/or head tissues.
4. Vascular injuries should be always suspected and investigated with radiologi-
cal images.
5. Avoid any type of stress and/or traction in case of suspicion of infringement of
the spine.

7.2.2.2 Intrinsic Forces

Foreign Bodies
In case of ingestion of foreign bodies, patients may present with choking abscesses,
most of which occur from the casual inhalation of food fragments. If the foreign
body obstructs the laryngeal lumen in its entirety and/or oropharyngeal space, the
patient can also die quickly from asphyxiation; if it is not possible to carry out quick
ejection maneuvers, the urgent execution of an endoscopy is essential, with instru-
ments equipped with an operating channel or with available surgical instruments for
the extraction of foreign bodies, possibly by “4 hands” procedure (one operator
guarantees the vision while the second operator proceeds with the extraction).
68 E. Fuccillo and M. Giovenzana

7.2.2.3 Caustics
Find out about the type of caustic and the amount ingested.
Endoscopy should often be repeated within 24 h.

7.2.2.4 Non-traumatic Neck Emergencies

Non-traumatic emergencies of the neck can occur in healthy patients and/or as a
possible complication of already known malignant conditions. Among the possible
non-traumatic etiopathogenesis, the main ones are therefore represented by infec-
tive and/or inflammatory, congenital, hemorrhagic, malignant diseases, and compli-
cations during systemic pathology [5].

7.2.3 Infections

The presence of a previous malignant pathology and/or of any condition of immuno-­

compromission (e.g., diabetes, HIV, chronic steroid intake) indicates that the patient
requires closer surveillance. Along with systemic symptoms, characterized by fever,
fatigue, and alteration of blood tests, patients often report pain at the site of infec-
tion. In most cases, neck infections are due to spreading at the level of the neck
spaces [6, 7].

7.2.4 Malignant

A neck mass or adenopathy should always be investigated in subjects with a history

of malignant disease. If possible, it is necessary to request clinical documentation or
collect thorough anamnestic information. When there is a suspected or proven air-
way or vascular compromise, the first step to do is to ensure patient stability. In
these cases, a laryngoscopic evaluation is often indispensable and is possibly fol-
lowed by dedicated imaging.

7.2.5 Emergencies Occurring in Patients

with Tracheostomy Tube

Knowledge of the main components of the tracheostomy tube represents the essen-
tial condition to deal with possible emergencies in patients with tracheal cannula.
We recommend you turn to the in-depth texts before being caught unprepared!
→ firstly: Why was a tracheostomy performed on the patient?? Was the proce-
dure surgical or percutaneous?

• The surgical timing is important because stomal infections and bleeding are the
most common complications during the first days, while percutaneous approach
could be complicated by posterior tracheal wall lesion (more often if compared
7  Multidisciplinary Surgical Consensus on Neck Emergencies 69

to surgical tracheostomy). Moreover, percutaneous approach is less complicated

by surgical site infections and postsurgical bleeding [8].
• Secondly, distinguish between the type of emergency.

Below we present some of the main possible emergencies occurring in patients

with tracheostomy tube.

7.2.5.1 Obstruction
Often due to mucus or clotted blood.
First to do → remove the inner cannula and check the patency of the tracheal
cannula through a suction tube. If the obstruction persists an urgent endoscopic
examination should be performed to role out the presence of plugs/other obstructions.

7.2.5.2 Bleeding
If the cannula has a cuff → inflate the cuff to protect the airway.
If the bleeding is massive (early postoperative or in case of patients with relaps-
ing malignant disease/presence of metastases with involvement of vessels) → surgi-
cal inspection and hemostasis (alert an anesthetist-resuscitator for performing
control of bleeding in the operating room).
If the bleeding is superficial/mild and the parameters are stable try to manage it
with local measures such as packing and alert ENT to perform an endoscopic
examination.

7.2.5.3 Infection
• Severe tracheal infections are rare and often require a surgical debridement [8],
other minor infections normally do not appear in an emergency regime and they
are usually managed by using antibiotics and realizing chronic wound
medications.

7.2.5.4 Dislodgment
First days after tracheostomy it could be due to a “false tract” (cannula is not prop-
erly lodged), which should be revealed by an endoscopic evaluation. If possible, an
attempt and adequate accommodation through the use of a guide (for example, a
tube changer) or surgical instruments that can keep in maintaining the tracheostomy
lumen open (e.g., nasal speculum, Laborde Tracheal Dilator).
If replacement is not possible, consider an urgent oro-tracheal intubation in order
to stabilize patient and wait for the ENT to perform a surgical inspection.

7.2.5.5 Tracheal stenosis

It often occurs in patients with a long-term tracheostomy tube.
→ Flexible bronchoscopy:

1. If the patient is stable → evaluate the tracheal stenosis by considering different

possible therapeutic approach based on the dimension of the stenosis (e.g., surgi-
cal/endoscopical).
2. If the patient is unstable → urgent surgical treatment.
70 E. Fuccillo and M. Giovenzana

References
1. Lewis SR, Butler AR, Parker J, Cook TM, Smith AF.  Videolaryngoscopy versus direct
laryngoscopy for adult patients requiring tracheal intubation. Cochrane Database Syst Rev.
2016;11(11):CD011136.
2. Cunqueiro A, Gomes WA, Lee P, Dym RJ, Scheinfeld MH. CT of the neck: image analysis and
reporting in the emergency setting. Radiographics. 2019;39(6):1760–81.
3. Alao T, Waseem M. Neck trauma. 2021 Feb 10.
4. Jain RK, Chakraborty P, Joshi P, Pradhan S, Kumari R. Penetrating neck injuries: from ER to
OR. Indian J Otolaryngol Head Neck Surg. 2019;71(Suppl 1):352–7.
5. Kamalian et al. Nontraumatic head and neck emergencies; 2019.
6. Boscolo Rizzo P, Stellin M, et al. Deep Neck Space Infections: a study of 365 cases highlight-
ing recommendations for management and treatment. Eur Arch Otolaryngol. 2012; https://doi.
org/10.1007/s00405-­011-­1761-­1.
7. Bakir S, et  al. Deep neck space infections: a retrospective review of 173 cases. Am J
Otolaryngol. 2012; https://doi.org/10.1016/j.amjoto.2011.01.003.
8. Fernandez-Bussy S, Mahajan B, Folch E, Caviedes I, Guerrero J, Majid A, et  al.
Tracheostomy tube placement: early and late complications. J Bronchology Interv Pulmonol.
2015;22(4):357–64.
Part III
Chest
Chest: Surgical Anatomy and General
Consideration in Emergency Settings 8
Valeria Musso and Francesco Damarco

In order to manage and perform interventional and surgical procedures in the emer-
gency settings, it is mandatory to know the anatomy of the chest wall. This chapter
briefly reviews the anatomy of the thorax, focusing on the most important aspects to
be considered when performing an invasive procedure in the emergency setting.

8.1 Chest Wall Surface Landmarks

There are several surface landmarks which should be taken in consideration when
placing a thoracic incision, especially in an urgent context. Depending on the clini-
cal situation, the thoracic incision must provide access to pulmonary hilum, trachea,
and great thoracic vessels. Knowing the level of the diaphragm is also necessary to
perform a tube thoracostomy or a thoracentesis.
The skeletal structures (sternum, costae, scapula, and vertebral column) of the
chest provide readily palpable surgical landmarks. The upper margins of the thorax
are bounded by the suprasternal notch above the sternum, the 1st ribs, and T1 pos-
teriorly. The inferior limits of the thoracic cavity, separating it from the abdominal
cavity, are formed by the sternal xiphoid process, the 7th to 10th costal cartilages,
the 11th ribs, the arch of the 12th rib, and T12. The following vertical lines (Figs. 8.1
and 8.2) are commonly used to establish the correct site for incisions:

V. Musso
University of Milan, Milan, Italy
e-mail: [email protected]
F. Damarco (*)
Thoracic Surgery and Lung Transplant Unit, Fondazione IRCCS Ca’ Granda Ospedale
Maggiore Policlinico, University of Milan, Milan, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 73

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_8
74 V. Musso and F. Damarco

Fig. 8.1  Anterior chest

wall lines: (a) midsternal
line; (b) parasternal line;
(c) midclavicular line

a b c

Fig. 8.2  Axillary lines: (a)

posterior axillary line; (b)
midaxillary line; (c)
anterior axillary line

a b c
8  Chest: Surgical Anatomy and General Consideration in Emergency Settings 75

Table 8.1  Surface landmarks of the chest wall

Surface landmark Underlying structure
Sternal manubrium Aortic arch, left brachiocephalic vein
Angle of Louis/T4 Tracheal bifurcation; azygos arch to SVC junction
(right); right to left lymphatic duct crossing; left
recurrent laryngeal nerve
Sternal body, III-VI costal Heart
cartilages
T4/T5 posteriorly, 4th rib laterally, Right pulmonary horizontal fissure
III intercostal space anteriorly
T4/T5 posteriorly, V right Right pulmonary oblique fissure
intercostal space laterally, 6th rib
anteriorly
T4 posteriorly, 5th rib and V left Left pulmonary oblique fissure
intercostal space laterally, 6th rib
anteriorly
Tip of the scapula Seventh intercostal space

• midsternal line, running down the middle of the sternum

• parasternal line, running along the lateral margins of the sternum
• midclavicular line, passing through the middle of the clavicles
• anterior axillary, midaxillary, and posterior axillary line, passing through the
anterior axillary fold, the apex of the axilla and the posterior limit of the axilla,
respectively

A transverse prominence called the angle of Louis (or sternal angle) can be
appreciated at the T4 vertebral level, marking the manubriosternal junction and the
second pair of costal cartilages. Table 8.1 reports the most important surface land-
marks and the underlying structures. The nipple usually marks the 4th intercostal
space in men, lateral to the midclavicular line, while in women its position varies
depending on the size and shape of mammary glands. The xiphoid process lies at the
T9 vertebral level. Posteriorly, the tip of the scapula lies on the 7th intercostal space,
but when the patients lies in lateral position with the shoulder in about 100° of flex-
ion, the tip of the scapula marks the 5th intercostal space.

8.2 Muscles of the Chest Wall

Understanding the anatomy of the chest wall musculature is essential in order to

perform any surgical procedure, especially in an emergency setting. The anterior
portion of the chest wall musculature is formed by the pectoralis major muscles,
which originate from the sternum, the clavicle, and the costal cartilages (2nd to 6th);
its insertion is located on the bicipital groove of the humerus, and its lower margins
form the anterior form of the axilla. The pectoralis minor muscles lie deeper to the
pectoralis major: they arise from the anterior surfaces of the ribs (2nd to 5th), form-
ing a tendon which inserts onto the coracoid process of the scapula. These two
muscles are both inspiratory muscles. The antero-inferior portion of the chest wall
is also covered by fibers of the rectus abdominis muscle and the abdominal external
oblique muscle: they are both expiratory muscles.
76 V. Musso and F. Damarco

The latero-posterior aspect of the thorax is more complex, as it is formed by

three different muscle layers: we will only discuss the most important ones. The
superficial back muscles originate from the vertebral column and insert to the shoul-
der, thus being responsible for movements of the upper limb. From external to deep,
these are the trapezius, the latissimus dorsi, the rhomboids, and the serratus anterior:

• Trapezius: It originates from the occipital bone and the spinous process of the C7
and all the thoracic vertebrae. Its insertion is located on the lateral portion of the
clavicle, the acromion process, and the spine of the scapula.
• Latissimus dorsi: It is the largest muscle of the thorax. Its aponeurosis originates
from the spinous process of T6-T12, the lumbodorsal fascia, the iliac crest and
the external surface of the lower 3–4 ribs. This insertion lies in the intertubercu-
lar sulcus of the humerus, also forming the posterior fold of the axilla.
• Rhomboids: The rhomboid minor arises from the spinous processes of C7-T1
and attaches medially on the spine of the scapula; the rhomboid major arises
immediately caudally originating from T2-T5 and attaching to the medial border
of the scapula. In some cases, the two rhomboids can be fused.
• Serratus anterior muscle: It originates from the surface of the first 8 ribs on the
lateral side of the chest and inserts along the anterior aspect and the medial bor-
der of the scapula.

A thinning of the chest wall muscles in the posterior chest wall at the level of the
6th and 7th rib is described as the triangle of auscultation: Its borders are formed by
the horizontal fibers of the latissimus dorsi inferiorly, the vertebral border of the
scapula laterally and superiorly, and the lateral margin of the trapezius medially and
superiorly. This triangle allows for a better auscultation and is also used as a surface
marker for surgical approaches and regional nerve blockade for pain relief.

Box 8.1 Surgical access: Thoracotomy

In case of emergency, the anterolateral approach with the patients lying supine
is usually the preferred one. If necessary, the access to the mediastinum can be
improved by extending the incision across the sternum, as the so-called “hemi-
clamshell.” In such case, the internal mammary vessels should be ligated.

• The incision is usually made throughout the 4th or 5th intercostal space,
curving along the submammary crease (and retracting the mammary gland
cranially in female patients) from the parasternal line to the posterior axil-
lary line. The subcutaneous tissue is divided deep to the pectoralis fascia.
• The pectoralis major is divided at the 4th intercostal space; laterally, the
serratus muscle is divided.
• The intercostal muscles are divided and the pleural space is entered bluntly
from the lateral portion of the incision, right along the upper margin of the
rib below, in order to avoid damaging the neurovascular intercostal bundle.
This must be done with caution so as not to injure the lung, especially in
case of adhesions.
• The remaining intercostal space is cut open using electrocautery.
• A Finochietto retractor is used to held the thoracotomy open at right angles.
8  Chest: Surgical Anatomy and General Consideration in Emergency Settings 77

Box 8.2 Surgical access: Median sternotomy

The patient is supine and his arms are tucked.

• The skin incision begins at the suprasternal notch and runs across the mid-
sternal line right beyond the xiphoid process. The subcutaneous tissue is
incised until reaching the pectoral fascia.
• The cranial portion of the manubrium is exposed by retracting the cranial
portion of the incision, and the crossing jugular tributary veins are identi-
fied. The interclavicular ligament is divided.
• The retrosternal space is opened bluntly cranially and caudally.
• Cautery can be used to further mark the midsternal line; palpation of the
intercostal spaces bilaterally can also be of aid in order to identify the
midline.
• Lungs are deflated by disconnecting the ventilator before dividing the ster-
num using a reciprocating saw. Bleeding from the bone and the periosteum
is immediately controlled using cautery, gauze packing, and bone wax (or
biodissolvable bone hemostats).
• A sternal spreader is placed to obtain appropriate exposure.

8.3 Anatomy of the Intercostal Space

Proceeding from superficially to the deeper layer, the intercostal space is covered by
3 intercostal muscles (external, inner, and innermost); the fibers of the external and
inner intercostal muscles run in opposed directions. The innermost intercostal mus-
cles’ fibers run vertically along the intercostal space.
On the lower margin of each rib, between the innermost fascia and the inner
intercostal muscles, lies the neurovascular bundle, which is formed, from upper to
lower, by the intercostal vein, artery, and nerve.
Notably, intercostal muscles can be used as a muscle flap for the protection of
tracheal, bronchial, or esophageal anastomosis.

Box 8.3 Chest tube placement

The indications for thoracostomy tube placement are several, and they will be
partially discussed in Chap. 11 “Pulmonary and thoracic emergencies.” It is
also important to select the appropriate diameter and type of tube (≥16 Ch) or
catheter (≤14 Ch) depending on the patient and the condition requiring pleural
drainage. The instruments required for chest tube placing are listed in Chap. 2
“Surgical instruments and materials in thoracic surgery.” The patient can be
positioned supine, in a semi-recumbent position (semi-Fowler or Fowler) or in
a lateral recumbent position, depending on the patient’s clinical condition and
the operator’s preference. Imaging guided (CT, US) thoracostomy improves
the safety and efficacy of the procedure.
78 V. Musso and F. Damarco

• Chest tubes are usually placed in the so-called “triangle of safety,” which
is defined anteriorly by the lateral edge of the pectoralis major, superiorly
by the base of the axilla, posteriorly by the anterior margin of the latissi-
mus dorsi, and inferiorly by a horizontal line at the level of the nipple.
In urgent setting, some authors prefer to insert chest tube in the second
intercostal space on the anterior midclavicular line in case of pneumotho-
rax, and on the 4th to 6th intercostal space laterally for pleural fluid
drainage.
• After preparing the sterile field, inject with local anesthetic at the level of
the skin incision at the upper margin of the lower rib in order to avoid the
neurovascular bundle. The needle should be kept perpendicular to the chest
wall, aspirating at each advance of the needle so as to avoid intravascular
injection, until air or fluid is aspirated, thus confirming the correct site for
chest tube placement.
• After incising the skin, the previously anesthetized subcutaneous tissue
and the muscular layers are bluntly dissecting using curved Mayo scissors
or a Kelly clamp.
• The Mayo scissors are then pushed through the parietal pleura and then
opened in order to widen the defect as required, depending on the diameter
of the tube.
• The tube is then inserted following the same path: the tip of the catheter is
usually directed to the pulmonary apex in case of pneumothorax, and to the
pulmonary bases in case of pleural effusion.
• Once in the correct position, the tube is secured using a non-­
absorbable suture.

8.4 Anatomy of the Pleura

The pleura is a serous membrane covering the lungs (visceral pleura) and the inner
part of the chest wall (parietal pleura), excluding the pulmonary hilum. Inferiorly,
the continuation of the visceral and parietal pleurae forms the pulmonary ligament.
The parietal pleura covers the internal aspects of the thoracic wall, thus separating
the pleural cavity from the mediastinum. The parietal pleura is usually divided in
the following portions: the dome of the pleura, the costal, the mediastinal, and the
diaphragmatic part. The pleural space between the two pleurae is normally col-
lapsed and contains about 10 ml of pleural fluid, which helps the sliding between the
two pleural surfaces during respiration.

8.5 Anatomy of the Lungs

The lungs are located in the pleural space in the chest. The right lung is composed
of three lobes: upper, medium, and lower lobe. The left lung only has two lobes, the
upper and the lower. The lower lobe is separated from the upper and middle one by
8  Chest: Surgical Anatomy and General Consideration in Emergency Settings 79

the oblique (major) fissure, which is also found on the left lung. The horizontal fis-
sure separates the upper and middle lobe. Every lobe can be divided into broncho-
pulmonary segments, which are supplied by their own bronchus and vascular
structures.
The pulmonary hilum is composed of the bronchus, the pulmonary artery, and
the superior and inferior pulmonary vein; these structures however are located in
different positions in the left and right hilum. On both sides, the phrenic nerve and
the vagus nerve, together with their vascular bundles, run on the anterior and poste-
rior border of the hilum, respectively.
On the right side, the hilum is encircled by the azygos vein, the superior and the
inferior vena cava. On the left side, the aortic arch passes above the superior aspect
of the hilum, while the descending aorta lies behind the hilum and the vagus nerve.
The esophagus runs vertically in the mediastinum behind the right and left hila.
The bronchial arteries originate mostly from the anterolateral portion of the aorta
or its branches, or from the intercostal arteries (usually on the right side). They run
along the posterior wall of the bronchi.

8.6 Anatomy of the Mediastinum

The mediastinum is the central region of the thoracic cavity located/situated between
the two lungs. Conventionally it is divided into superior, anterior, middle, and pos-
terior compartments. The superior compartment contains the upper portion of sev-
eral thoracic structures: esophagus, great vessels, trachea, thymus. The anterior
compartment’s margins are formed by the posterior portion of the sternum anteri-
orly and the pericardium posteriorly: the rest of the thymus is located in this com-
partment. The middle portion of the mediastinum contains the pericardium, the
intrapericardiac vessels, the heart, and the main carina. The esophagus, the thoracic
duct, and the descending aorta form the posterior compartment.

Further Reading
Nomori H, Okada M. Illustrated anatomical segmentectomy for lung cancer. Japan: Springer; 2012.
Testut L, Jacob O. Trattato di anatomia topografica. 2a edizione. Edra Edizione; 2015.
Acute Aortic Syndromes and Thoracic
Aortic Aneurysms: From Diagnosis 9
to Treatment

Andrea Xodo, Andrea Gallo, Paolo Magagna,

and Mario D’Oria

9.1 Introduction

Acute aortic dissection (AD), the most common form of acute aortic syndrome
(AAS), is a relatively rare but highly lethal disease: population-based studies sug-
gest that the incidence of acute AD ranges from 3.5 to 6.0 cases per 100,000 person-­
years [1]. Risk factors for the development of AAS mainly reflect conditions
associated with increased wall shear stress (hypertension and physical trauma), with
chronic or acute exposure of the aorta to elevated intraluminal pressures, and/or
abnormalities of the aortic media (syndromic and non-syndromic genetic diseases,
including Marfan and Ehlers-Danlos syndromes, annuloaortic ectasia, and bicuspid
aortic valve) [2]. In the classical definition, AD requires a tear in the intimal aortic
wall, that is commonly preceded by medial wall degeneration or medial cystic
necrosis. The blood passes through the tear that separates the intima from the media
or from the adventitia, creating a dual channel that comprises a “false lumen” (FL)
and a “true lumen” (TL). In addition to AD, two other distinct conditions require
further description. Intramural hematoma (IMH), in contrast to AD, lacks an

A. Xodo
Division of Vascular and Endovascular Surgery, Department of Cardiac, Thoracic, Vascular
Sciences and Public Health, Padova University School of Medicine, Padova, Italy
A. Gallo
Internal Medicine Unit, Department of Medicine, “Sant’Anna” Hospital, Como, Italy
P. Magagna
Operative Unit of Cardiac Surgery, Department of Cardiac and Vascular Surgery, ULSS 8
Berica, “San Bortolo” Hospital, Vicenza, Italy
M. D’Oria (*)
Division of Vascular and Endovascular Surgery, Cardiovascular Department, University
Hospital of Trieste ASUGI, Trieste, Italy
e-mail: mario.d’[email protected]

© The Author(s), under exclusive license to Springer Nature 81

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_9
82 A. Xodo et al.

identifiable communication between the two lumens: different mechanisms for eti-
ology have been proposed for this disease, including microscopic tears in the intima
and rupture of the vasa vasorum. Penetrating atherosclerotic ulcer (PAU) is instead
defined as an atherosclerotic lesion that penetrates the internal lamina of the aortic
wall, also known with the term of “ulcer-like projections.”
All these mechanisms that weaken the medial layers of the aorta, may lead to
increased tension on the aortic wall, which can induce aortic dilation with conse-
quent aneurysm formation, frank acute AD from IMH or PAU, or aortic rupture.
Furthermore, AD can present with complications in the acute phase that requires
expedite treatment.
Descending thoracic aortic aneurysms (TAAs), similar to other aortic aneurys-
mal disease, rarely manifest with symptoms and about 95% of the patients are
asymptomatic at time of diagnosis [3]. Nevertheless, TAAs can lead to catastrophic
complications, mainly rupture with hemorrhagic shock, why they are termed “silent
killers.” Blunt thoracic aortic injury (BTAI) is also sometimes included in the spec-
trum of AAS, but will not be discussed in this chapter.
Indications for the elective treatment of these pathologic entities when asymp-
tomatic (usually within the context of incidental findings during imaging examina-
tions performed for other medical or surgical reasons) are largely dependent on their
size, etiology, and morphology. They will not be discussed further in this chapter,
which will focus on the presentation, diagnosis, and management of AAS/TAA in
the urgent/emergent setting. This chapter will focus on those AAS and TAA that
require immediate attention from the clinician and prompt referral to cardiovascular
specialists. The need for immediate treatment is usually dictated by the presence of
symptoms and severity of presentation but may be also prompted or exacerbated
when large aortic diameters, rapid size growth, or other alarming radiologic signs
are encountered.

9.2 Anatomical Classification

The majority of TAAs are degenerative (i.e., atherosclerotic) in nature, while other
causes include traumatic, mycotic, or related to vascular genetic disorders; aneurys-
mal evolution is indeed included among late aortic events of patients with AD.
Historically, classification of AAS was based on the anatomic location of the
intimal entry tear that results in a separation of the aortic layers, and also on the
longitudinal extension of the dissection flap. There are two main schemes that have
been classically used to classify AD; the first one, the original “DeBakey classifica-
tion” was described in 1965 and is based upon the site of origin of the dissection and
its distal extension:

• Type 1 originates in the ascending aorta and to at least the aortic arch.
• Type 2 originates in and is limited to the ascending aorta.
• Type 3 begins in the descending aorta and extends distally above (type 3A) or
below (type 3B) the diaphragm.
9  Acute Aortic Syndromes and Thoracic Aortic Aneurysms: From Diagnosis… 83

a b

1 2
0 3

Type A (Stanford)
Non A non B
Type B (Stanford)

Fig. 9.1 (a) Ishimaru Classification. (b) Stanford Classification

The more widely adopted “Stanford system” instead classifies dissections into
two types, based on whether the ascending or descending part of the aorta is involved
(Fig. 9.1):

• Type A aortic dissection (TAAD) involves the ascending aorta, regardless of the
site of the primary intimal tear.
• Type B aortic dissection (TBAD) originates distal to the left subclavian artery
(LSA) and only involves the descending aorta [4].

A new classification has recently been proposed, with the aim of describing more
precisely the involvement of the aortic arch. In this classification, the distinction
between type A and type B is given by the entry tear zone (according to the classi-
fication of Ishimaru), and type A is represented only by an entrance door in zone
0 [5, 6].
TAAs are localized dilatations in the descending thoracic aorta, secondary to
weakening and subsequent expansion of the aortic wall. When all aneurysms of the
thoracic aorta are considered, those of the ascending aorta are the most common
(40%), while aneurysms of the descending thoracic aorta account for 35% of TAAs,
and aortic arch aneurysms (15%) or thoraco-abdominal aortic aneurysms (10%)
84 A. Xodo et al.

account for smaller percentages [7]. The descending thoracic aorta can be divided
into three sections:

–– Extent A: distal of the LSA to the 6th thoracic intercostal space.

–– Extent B: 6th to the 12th intercostal space.
–– Extent C: the entire descending aorta from LSA to the 12th intercostal space.

9.3 Temporal Classification

The temporal classification of the AD originates from the studies of Hirst and col-
leagues, who observed a markedly higher mortality, for both type A and type B
dissections, in the first 14 days after the onset of the disease [8]. Based on these
observations, the authors defined the AD as acute in the first 14 days from the symp-
tom onset and as chronic as >14 days from symptom onset.
However, Hirst’s observations date back to the 1950s, and since then huge
improvements have emerged in diagnostic imaging, medical treatment, and surgical
therapy, mainly owing to the endovascular innovation over the past 25  years.
Thoracic endovascular aortic repair (TEVAR), in particular, has revolutionized the
management and treatment of AD; due to this reason, more recent documents clas-
sify patients with AD into hyperacute (<24  h), acute (1–14  days), sub-acute
(15–90 days), and chronic (>90 days), relating to the time of onset of complications
requiring intervention [5, 9, 10].

9.4 Clinical Presentation

The pivotal symptom in the whole spectrum of AAS is acute thoracic pain, usually
localized between the scapula and described as stabbing, ripping, or fluctuating; it
is present in the majority of patients, with a severe initial intensity.
Pain usually reflects the entry tear site and may migrate in relation to the extent
of the AD: its radiation to the neck, throat, teeth, or jaw may indicate an ascending
aorta involvement; conversely, back pain or abdominal pain may herald a descend-
ing aorta localization.
Coronary malperfusion associated with TAAD is rare but when it occurs it may
be fatal to the patient, as a result of AMI or fatal arrhythmia; in these cases, the onset
symptomatology may include chest pain or cardiac arrest. In a large series of 464
patients, the majority of patients complained of chest pain (72.7%): anterior chest
pain was typical in patients with TAAD, whereas patients with TBAD more often
experienced pain in the back and abdomen [11].
A thorough clinical examination has a crucial role in patient with suspected
AAS: assessment of arterial pulses should involve radial, brachial, femoral, and
distal pulses, in addition to abdominal aorta palpation. The absence of a peripheral
pulse, associated with clinical signs of ischemia, could suggest a malperfusion, that
occurs in up to 40% of complicated TBAD [12].
9  Acute Aortic Syndromes and Thoracic Aortic Aneurysms: From Diagnosis… 85

Signs attributable to connective tissue diseases (e.g., Marfan syndrome) will be

sought during the medical examination. Aortic regurgitation should be suspected in
case of diastolic murmur; if dissection causes bleeding into the pericardium, distant
heart sounds secondary to pericardial effusion may be noted, with signs and symp-
toms of cardiac tamponade (Beck’s triad).
Neurologic deficits might be identified on presentation, as partial or complete
loss of sensory or motor function; they can be caused by persistent or transient isch-
emic stroke, spinal cord ischemia, and branch vessel malperfusion.
The initial clinical presentation of AAS has major implication for both patient
management and outcomes: this spectrum of conditions, in particular acute AD,
may be classified as “uncomplicated,” “high risk,” and “complicated.” Uncomplicated
acute AD is defined for those patients without evidence of rupture or end-organ
malperfusion, while complicated TBAD refers to malperfusion syndrome involving
visceral, renal or extremity ischemia, rupture or impending rupture. The “high-risk”
category includes clinical and radiological signs which were devised to identify
those patients at increased risk of worse prognosis into a complicated AAS.
TAAs are usually asymptomatic and their diagnosis is often incidental. By con-
trast, when symptomatic, they usually cause severe pain or a feeling of fullness in
the chest. Rupture of TAAs is a life-threatening condition that usually presents with
massive hemothorax accompanied by dyspnea, syncope, and hemorrhagic shock. In
much rare instances, the symptoms may include signs of distal embolism related to
a mural thrombus or signs of compression of adjacent structures (trachea, bronchus,
esophagus), causing dyspnea, bronchospasm, cough, hemoptysis, dysphagia, or
hematemesis in case of aorto-esophageal/bronchial fistula [13].

9.5 Diagnosis

The urgent approach to the AAS/TAA (Fig. 9.2) requires optimization of resources

within a short timeframe. The role of a quick yet exhaustive physical examination
in patients with suspected AAS/TAA has been emphasized in the previous para-
graphs. Obviously, acquiring a focused medical history in these patients helps to
guide the diagnostic process: details that are particularly helpful to assess will
include past medical history (hypertension, heart disease), family history (sudden
death or aortic diseases), and chronic medications, which should all be assessed
upon admission of the patient(s).
Patients presenting to the emergency department with typical chest pain should
undergo an electrocardiogram (ECG) and serum troponin determination, to rule out
acute myocardial infarction (AMI). It is important to note, however, that the ECG
can be abnormal in up to 70% of patients with ascending aortic dissection. If the
diagnosis of myocardial infarction is doubtful, other diagnostic studies should be
performed promptly to rule out aortic dissection. A chest X-ray might be helpful to
rule out alternative diagnoses provided it does not delay prompt referral of patients,
and may show an enlargement of the upper mediastinal shadow or a pleural effu-
sion. However, it should be borne in mind that up to 10–15% of patients with acute
 86

DECISION MAKING FOR PATIENTS WITH SUSPECTED ACUTE AORTIC

SYNDROME OR THRORACIC AORTIC ANEURYSM
UNCOMPLICATED TBAD: no rupture or
malperfusion, no high risk features
Patient admitted with chest or
back pain
HIGH RISK TBAD: patients with:
• refractory pain or hypertension
• bloody pleural effusion
Clinical examination, blood
• aortic diameter > 40 mm
biomarkers, ECG, fast TEE
• radiographic malperfusion only
• entry tear in the lesser curve
• false lumen > 22 mm, readmission
PULMUNARY EMBOLYSM URGENT CTA
ACUTE MYOCARDIAL INFARCTION
COMPLICATED TBAD: rupture or malperfusion

AAS
THORACIC AORTIC ANEURYSM

TYPE A AORTIC TYPE B AORTIC THORACIC AORTIC

DISSECTION DISSECTION ANEURYSM

Open surgical repair after UNCOMPLICATED or COMPLICATED Signs of rupture,

initial risk assessment HIGH RISK TBAD TBAD Symptomatic TAA

Medical treatment as Surgical treatment Surgical treatment

first line, surgical (endovascular as (endovascular as
treatment (endovascular first line) first line)
as first line) if necessary

Fig. 9.2  Flowchart for decision-making and initial management of acute aortic syndromes
A. Xodo et al.
9  Acute Aortic Syndromes and Thoracic Aortic Aneurysms: From Diagnosis… 87

AD will have normal findings on chest radiography [14]. Therefore, while abnor-
mality noted on ECG and chest X-ray might guide the initial assessment, they lack
enough sensitivity or specificity to either exclude or confirm the diagnosis of AAS
in patients presenting with typical symptoms, and a high index of clinical suspicion
remains paramount.
D-dimer is probably the most widely available diagnostic biomarker for pulmo-
nary embolism; several investigators have demonstrated that a cut-off level of
500 ng/mL is highly sensitive to rule out classical acute AD within the first 6 h of
symptom onset and highest in the first hour [15, 16]. Nevertheless, it should be
noted that low D-dimer levels may be found in patients with IMH, PAU, and/or AD
with thrombosis of the false lumen (FL); at the same time, it may be elevated in
many other disorders, including AMI complicated by mural thrombus and acute
pulmonary embolism. In summary, high D-dimer level largely decreases the possi-
bility of acute AD (although it cannot be used as a stand-alone indicator for its
diagnosis), while low D-dimer rates moderately increase the possibility of acute
AD [16].
Transthoracic echocardiography (TTE) is widely used in thoracic emergencies: a
TTE focusing on the aortic valve complex, the ascending aorta, and the function of
the left and right heart can provide useful information for time-sensitive clinical
decision-making. However, although TTE is an excellent tool for quickly detecting
life-threatening complications of acute AD, such as aortic regurgitation, pericardial
effusion or cardiac tamponade, and wall movement abnormalities, its accuracy for
AD remains relatively low (sensitivity range from 77 to 80%, specificity from 93 to
96%) [17]; therefore, a negative TTE does not rule out acute AD [18]; however, TTE
is strongly recommended as an initial imaging investigation.
Transesophageal echocardiography has a limited role in urgency; however, it is
an easy and useful tool in the operating theatre to guide the correct placement of the
stent graft in case of TBAD.
Current diagnostic techniques for both AAS and TAAs focus on the use of com-
puted tomography angiography (CTA). CTA is the most widely used modality
worldwide, due to its cost and easy accessibility, providing meaningful anatomical
information about the aorta and surrounding structures. It also allows surgeons to
collect details necessary to plan and carry out interventions when needed. Ideally,
the CTA should include the entire aorta, from the supra-aortic trunks to the femoral
vessels. Using CTA, the morphologic characteristics of the entire aorta can be stud-
ied, in particular its diameters, the presence of intraluminal thrombus, the presence
of IMH/PAU or calcifications, the state of peripheral vessels and of the main
branches (including signs of malperfusion), as well as secondary evidence of end-­
organ damage or impending aortic rupture. Nevertheless, CTA may have several
limitations, in particular for patients with history of allergic reactions to iodinated
contrast media or for those with end-stage renal disease, for whom iodinated con-
trast loading could cause contrast-induced nephropathy. Despite these issues, CTA
is an established imaging technique for diagnosing AAS in urgency and emergency
settings, and last-generation multidetector CT scanners have improved the sensitiv-
ity and specificity of diagnosis for aortic disease, enabling rapid acquisition of
88 A. Xodo et al.

images with minimal contrast load. The electrocardiographic gated technique has
virtually eliminated the pulsation artifacts in the ascending aorta, allowing a sub-
stantially better assessment of subtle aortic abnormalities, previously underesti-
mated by uncontrolled CTA.  While CTA remains the cornerstone for the initial
diagnosis of patients with AAS, magnetic resonance imaging (MRI) may play a role
during follow-up for identification of complications following a previous AAS, in
order to reduce the overall burden of radiation exposure and iodinated contrast [19].

9.6 Primary Management

The concept of primary management of AAS should encompass those conditions

where there is a high risk of imminent aortic rupture or frank complications have
already arisen, allowing early identification of patients at such risk, rapid institution
of medical treatment, prompt execution of CTA from the neck to the groin, strategic
centralization to high-volume centers, and urgent/emergent aortic repair when indi-
cated with post-procedure care in dedicated intensive care units.

9.6.1 Initial Management in Case of Stable

and Uncomplicated Patients

In all patients with acute AD, PAU, and IMH, blood pressure (BP) and heart rate
control are recommended in order to decrease the aortic wall stress and to limit the
extension of the dissection, thereby reducing the risk of end-organ damage and aor-
tic rupture.
Since uncontrolled hypertension associated with acute AD is considered a hyper-
tensive emergency, systolic blood pressure should be immediately kept within 120
and 100 mmHg, with heart rate <60 bpm. In this scenario, intra-venous drugs with
short half-life are preferred: International guidelines recommend the association of
a beta-blocker, as esmolol, and a vasodilator such as sodium nitroprusside or nitro-
glycerine or nicardipine. Alternatives are beta-blockers as labetalol or metoprolol
but with the downside of a longer half-life compared with esmolol (Table 9.1) [20].
Medical therapy is almost important for prevention: all hypertensive patients with
aortic dilatation, whether associated with Marfan syndrome, bicuspid aortic valve
disease, or not, should have their BP controlled.
Analgesia is important to obtain adequate control of pain, with use of opiates
when indicated and continuous monitoring in intensive care or coronary care units.
Initial management of AAS could involve high-intensity serial imaging in the
acute phase of TBAD, IMH, and PAU, to identify complicated cases for early inter-
vention and selection of patients at high risk of disease progression.
Table 9.1  Drugs indicated for blood pressure and heart rate control in acute AD
Onset of Duration Most relevant side
Group of medications Drug action of action Dose Contraindications effects
Beta-blockers Esmolol 1–2 min 10– 0.5–1 mg/kg as i.v. bolus; 2nd–3rd degree AV Bradycardia,
30 min 50–300 lg/kg/min as i.v. block, systolic heart Bronchoconstriction
infusion failure, asthma,
Metoprolol 1–2 min 5–8 h 2.5–5 mg i.v. bolus over bradycardia
2 min—may be repeated
every 5 min to a max. dose
of 15 mg
Labetalol 5–10 min 3–6 h 0.25–0.5 mg/kg i.v. bolus;
2–4 mg/min infusion until
goal is reached, thereafter
5–20 mg/h
Nitrovasodilators Sodium Immediate 1–2 min 0.3–10 lg/kg/min i.v. Liver/kidney failure, Headache, reflex
nitroprusside infusion, increase by 0.5 lg/ severe aortic stenosis Tachycardia, cyanide
kg/min every 5 min until intoxication for
target BP values nitroprusside
Nitroglycerine 1–5 min 3–5 min 5–200 lg/min i.v. infusion, 5
lg/min increase every 5 min
Dihydropyridine class Nicardipine 5–15 min 30– 5–15 mg/h i.v. infusion,
of calcium channel 40 min starting dose 5 mg/h,
blockers (vasodilators) increase every 15–30 min
9  Acute Aortic Syndromes and Thoracic Aortic Aneurysms: From Diagnosis…

with 2.5 mg until goal BP,

thereafter decrease to
3 mg/h
89
90 A. Xodo et al.

9.6.2 Initial Management in Case of Unstable

and Complicated Patients

Patients presenting with circulatory shock should be immediately taken to the oper-
ating room after a diagnostic CTA scan. The management of hemorrhagic shock is
crucial for the patient’s outcome, with the aim to restore organ perfusion and sys-
tolic blood pressure range through aggressive fluid replacement. However, infusing
large volumes of cold fluid causes dilutional and hypothermic coagulopathy; these
factors, added with acidosis, may lead to increased bleeding [21].
In case of aortic rupture, an alternative to the “normotensive resuscitation” is
represented by the “permissive” hypotension resuscitation: the aim of this strategy
is to obtain a target systolic blood pressure of 50 mmHg to 100 mmHg, preventing
blood loss and reducing the clot disruption caused by the rapid increase in systolic
blood pressure. The use of this technique also avoids the dilution of coagulation
factors, platelets, and fibrinogen, thereby reducing the decrease in temperature
which may inhibit the enzymatic activity involved in the function of platelets and
coagulation factor [22].
Along with replacing blood volume, massive-transfusion protocols with a mini-
malized imbalance in plasma, platelet, and red-cell units improve survival through
the optimization of hemostasis. Moreover, for patients taking any anticoagulant
medications is important to administer pharmacologic adjuncts to reverse antico-
agulation [23].
The presence of cardiac tamponade should prompt urgent aortic repair; this con-
dition is the most common cause of death in patients with TAAD and tamponade-­
induced hypotension, associated with aortic rupture, has been identified as a major
risk factor for peri-operative mortality in these patients. Pre-operative pericardial
drainage may be an effective temporizing strategy in selected patients with TAAD
complicated by cardiac tamponade.

9.7 Principles of Surgical Treatment

9.7.1 Type A Aortic Dissection

The goal of surgery in the case of a TAAD is to avoid rupture of the ascending aorta,
cardiac tamponade, insufficiency of the aortic valve, or coronary artery dissection
resulting in AMI. The treatment of TAAD is therefore usually of cardiac surgery
relevance, with the replacement of the ascending aorta; nevertheless, the aortic arch
and the supra-aortic branches are often involved and a hemiarch or an entire aortic
arch may require a more extensive approach, also combining the principles of open
arch surgery and endovascular descending thoracic aorta repair by “elephant trunk”
or “frozen elephant trunk” technique, although aortic arch surgery under emergency
conditions carries much higher rates of peri-operative morbidity and mortality,
based on the extent and location of the intimal tear and on the age of the patient. The
aortic valve can also be replaced in case of insufficiency, using either a composite
9  Acute Aortic Syndromes and Thoracic Aortic Aneurysms: From Diagnosis… 91

valvulated graft (with a mechanical or a biologic valve); this procedure has been
described by Dr. Bentall and Dr. De Bono. There are two widely used techniques for
valve-sparing root replacement: aortic root reimplantation (David procedure) and
aortic root remodeling (Yacoub procedure) [24]. The presence of IMH at the AsAO
level is considered, due to its possible evolution, such as a TAAD and so treated
immediately.

9.7.2 Type B Aortic Dissection

The main aims of acute repair when treating a type B aortic dissection are to cover
the primary entry tear, to decrease the blood pressure in the FL while re-establishing
adequate pressures in the TL, to prevent the extension of the dissection and to pro-
mote the FL thrombosis, inducing a positive aortic remodeling and resolve end-­
organ malperfusion (Fig. 9.3) when clinically relevant.
Thoracic endovascular aortic repair (TEVAR) is the currently accepted method
of treatment in complicated or high-risk TBAD, with open repair considered only in
case of particular contraindications to TEVAR [25]. Despite the vulnerability and
fragility of the aorta during the hyperacute phase, associated with high mortality
and morbidity rates, several studies have suggested that more favorable remodeling
may be observed in case of early interventions.
Although coverage of the descending thoracic aorta with stent grafts is usually
limited to the least extent possible in the acute phase, to reduce the risk of post-­
procedural spinal cord ischemia (SCI), peri-operative adjuncts (e.g., cerebrospinal
fluid drainage) may be considered to decrease this risk, although their use may be
troublesome in critical patients. Also, TEVAR often requires deployment of the

a b

Fig. 9.3 (a) Superior mesenteric artery dissection, associated with a narrow compression of the
true lumen, with a “radiological sign” of malperfusion. (b) Autopsy detail of a visceral vessel dis-
section, with a clear distinction between the two lumens
92 A. Xodo et al.

endograft across or proximally to the origin of the LSA to obtain an adequate proxi-
mal seal; intentional coverage of the LSA appears feasible in the urgent scenario,
carrying a low risk of stroke, SCI, or left arm ischemia. However, LSA preservation
is recommended for long aortic coverage (>200 mm) in order to decrease the risk of
SCI, and in other selected circumstances (e.g., dominant left vertebral artery, patent
bypass from the LIMA, or functional hemodialysis access). Different techniques
and approaches are in use to ensure LSA revascularization, including open surgical
procedures (bypass or transposition) or endovascular tools (chimney grafts, in situ
fenestration or dedicated custom-made or off-the-shelf endografts) [26, 27]. Late
complications of TEVAR in case of TBAD may include poor remodeling of the
aortic wall, which may lead to aneurysmal degeneration over a number of years, and
development of stent-graft induced new entry tears (SINE), which are usually
caused by excessive stent-graft oversizing (a common technical issues with TEVAR
for dissection as opposed to TEVAR for aneurysms) and can be a significant source
for secondary interventions during follow-up.

9.7.3 Penetrating Aortic Ulcer and Intramural Hematoma

Patients presenting with uncomplicated IMH (Fig.  9.4) and PAU are primarily
treated by medical therapy alone, with intensive care monitoring as appropriate, in
similar fashion to those presenting with TBAD. However, patients with a PAU that
initially measures >20 mm in diameter or >10 mm in depth might have a higher risk
of disease progression and could be considered candidates for early endovascular
repair. The role of endovascular treatment of IMH is still debated; however, the

a b

Fig. 9.4 (a, b) Acute IMH appear as shown by the orange arrow as focal, crescentic, high-­
attenuating regions of eccentrically thickened aortic wall on non-contrast CT
9  Acute Aortic Syndromes and Thoracic Aortic Aneurysms: From Diagnosis… 93

treatment is recommended in case of expansion of the hematoma, progression to

frank AD, associated PAU, or intimal tear disruption [28, 29].

9.7.4 Thoracic Aortic Aneurysm

Prior to the endovascular era, open repair was the gold standard also for descending
thoracic aortic aneurysms, requiring thoracotomy, aortic cross-clamping, aneurysm
resection, and aortic replacement with a prosthetic graft. Owing to the advance-
ments of endovascular techniques and technologies over the last two decades,
TEVAR currently allows a minimally invasive procedure yet highly effective proce-
dure compared with open surgical repair, decreasing operative time and blood loss.
An initial diameter of 60 mm carries an annual risk of rupture of 10%, while inter-
vention in TAAs below 55 mm may not afford a survival benefit. Indications for
elective treatment exist for patients with TAAs >56–59 mm, reserving open surgical
repair (OSR) treatment for fit patients considered unsuitable for TEVAR. Rupture of
TAAs (Fig. 9.5) is an emergent condition regardless of the hemodynamic stability
of the patient, with high associated mortality rates. TEVAR has showed favorable
outcomes as compared to open repair. For the procedure to be successful and dura-
ble, adequate proximal and distal sealing zones are required to avoid development
of type 1A or 1B endoleaks, thereby obtaining a complete exclusion of the aneu-
rysm. Chest drainage may also be required to relieve respiratory function.

a b

Fig. 9.5 (a) Large PAU in the inner curve of the aortic arch (orange arrow). (b) Large rup-
tured TAA
94 A. Xodo et al.

9.8 Conclusions

AAS are fatal cardiovascular emergencies that require complex treatment by several
specialists referred in high-volume centers. In this chapter these pathologies, includ-
ing TAAs, have been examined, from diagnosis to their initial treatment. Due to
their peculiarity, blunt traumatic injuries of the descending thoracic aorta (which are
mainly located at the aortic isthmus) and pseudoaneurysms have not been taken into
consideration, although they share many similar aspects in terms of presentation,
diagnosis, and management with the pathological entities discussed in this chapter.

References
1. Mussa FF, Horton JD, Moridzadeh R, et al. Acute aortic dissection and intramural hematoma:
a systematic review. JAMA. 2016;316:754–63.
2. Bossone E, LaBounty TM, Eagle KA. Acute aortic syndromes: diagnosis and management, an
update. Eur Heart J. 2018;39:739–749d.
3. Ziganshin BA, Elefteriades JA. Treatment of thoracic aortic aneurysm: role of earlier interven-
tion. Semin Thorac Cardiovasc Surg. 2015;27:135–43.
4. Levy D, Goyal A, Grigorova Y, et al. Aortic dissection. In: StatPearls. Treasure Island, FL:
StatPearls Publishing; 2021. http://www.ncbi.nlm.nih.gov/books/NBK441963/ (Accessed 1
May 2021).
5. Lombardi JV, Hughes GC, Appoo JJ, et al. Society for Vascular Surgery (SVS) and Society
of Thoracic Surgeons (STS) reporting standards for type B aortic dissections. J Vasc Surg.
2020;71:723–47.
6. Ishimaru S. Endografting of the aortic arch. J Endovasc Ther. 2004;11(Suppl 2):II62–71.
7. Bickerstaff LK, Pairolero PC, Hollier LH, et al. Thoracic aortic aneurysms: a population-based
study. Surgery. 1982;92:1103–8.
8. Hirst AE, Johns VJ, Kime SW.  Dissecting aneurysm of the aorta: a review of 505 cases.
Medicine (Baltimore). 1958;37:217–79.
9. Lombardi JV, Cambria RP, Nienaber CA, et al. Prospective multicenter clinical trial (STABLE)
on the endovascular treatment of complicated type B aortic dissection using a composite
device design. J Vasc Surg. 2012;55:629–640.e2.
10. White RA, Miller DC, Criado FJ, et  al. Report on the results of thoracic endovascular
aortic repair for acute, complicated, type B aortic dissection at 30 days and 1 year from a
­multidisciplinary subcommittee of the Society for Vascular Surgery Outcomes Committee. J
Vasc Surg. 2011;53:1082–90.
11. Hagan PG, Nienaber CA, Isselbacher EM, et al. The international registry of acute aortic dis-
section (IRAD): new insights into an old disease. JAMA. 2000;283:897.
12. Gargiulo M, Massoni CB, Gallitto E, et al. Lower limb malperfusion in type B aortic dissec-
tion: a systematic review. Ann Cardiothorac Surg. 2014;3:35167–367.
13. Ciccone MM, Dentamaro I, Masi F, et al. Advances in the diagnosis of acute aortic syndromes:
Role of imaging techniques. Vasc Med. 2016;21:239–50.
14. Nienaber CA, Fattori R, Mehta RH, et al. Gender-related differences in acute aortic dissection.
Circulation. 2004;109:3014–21.
15. Suzuki T, Bossone E, Sawaki D, et  al. Biomarkers of aortic diseases. Am Heart
J. 2013;165:15–25.
16. Watanabe H, Horita N, Shibata Y, et al. Diagnostic test accuracy of D-dimer for acute aortic
syndrome: systematic review and meta-analysis of 22 studies with 5000 subjects. Sci Rep.
2016;6:26893.
9  Acute Aortic Syndromes and Thoracic Aortic Aneurysms: From Diagnosis… 95

17. Khandheria BK, Tajik AJ, Taylor CL, et  al. Aortic dissection: review of value and limita-
tions of two-dimensional echocardiography in a six-year experience. J Am Soc Echocardiogr.
1989;2:17–24.
18. Goldstein SA, Evangelista A, Abbara S, et  al. Multimodality imaging of diseases of the
thoracic aorta in adults: from the American Society of Echocardiography and the European
Association of Cardiovascular Imaging: endorsed by the Society of Cardiovascular Computed
Tomography and Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr.
2015;28:119–82.
19. Grist TM, Rubin GD. Imaging of acute aortic syndromes. In: Hodler J, Kubik-Huch RA, von
Schulthess GK, editors. Diseases of the chest, breast, heart and vessels 2019–2022: diagnos-
tic and interventional imaging. Cham: Springer; 2019. http://www.ncbi.nlm.nih.gov/books/
NBK553865/ (Accessed 25 June 2021).
20. Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH Guidelines for the management of
arterial hypertension. Eur Heart J. 2018;39:3021–104.
21. Winstedt D, Thomas OD, Nilsson F, et al. Correction of hypothermic and dilutional coagulopa-
thy with concentrates of fibrinogen and factor XIII: an in vitro study with ROTEM. Scand J
Trauma Resusc Emerg Med. 2014;22:73.
22. Moreno DH, Cacione DG, Baptista-Silva JC.  Controlled hypotension versus normotensive
resuscitation strategy for people with ruptured abdominal aortic aneurysm. Cochrane Database
Syst Rev. 2018;6:CD011664.
23. Hemorrhagic Shock | NEJM, https://www.nejm.org/doi/full/10.1056/nejmra1705649
(Accessed 4 July 2021).
24. Hussain ST, Svensson LG. Surgical techniques in type A dissection. Ann Cardiothorac Surg.
2016;5:233–5.
25. Nienaber CA, Kische S, Rousseau H, et al. Endovascular repair of type B aortic dissection:
long-term results of the randomized investigation of stent grafts in aortic dissection trial. Circ
Cardiovasc Interv. 2013;6:407–16.
26. D’Oria M, Kärkkäinen JM, Tenorio ER, et al. Perioperative Outcomes of Carotid-Subclavian
Bypass or Transposition versus Endovascular Techniques for Left Subclavian Artery
Revascularization during Nontraumatic Zone 2 Thoracic Endovascular Aortic Repair in the
Vascular Quality Initiative. Ann Vasc Surg. 2020;69:17–26.
27. Piffaretti G, Pratesi G, Gelpi G, et  al. Comparison of two different techniques for isolated
left subclavian artery revascularization during thoracic endovascular aortic repair in zone 2. J
Endovasc Ther. 2018;25:740–9.
28. Evangelista A, Czerny M, Nienaber C, et al. Interdisciplinary expert consensus on manage-
ment of type B intramural haematoma and penetrating aortic ulcer. Eur J Cardiothorac Surg.
2015;47:209–17.
29. Editor’s Choice - Management of Descending Thoracic Aorta Diseases | Elsevier Enhanced
Reader. https://doi.org/10.1016/j.ejvs.2016.06.005.
Pulmonary and Thoracic Emergencies
10
Francesco Damarco

Thoracic disorders are one of the most common reasons for presentation to the
emergency department. It is due to various conditions that involve several organs,
ranging from benign to life threatening.
Pulmonary diseases can present with pain, dyspnea, and respiratory failure but
these symptoms are not always specific for a certain clinical situation
(Algorithm 10.1).
Differential diagnoses in chest pain are:

• Cardiac (angina, acute myocardial infarction, pericarditis).

• Vascular (aortic dissection, pulmonary embolism).
• Thoracic (pneumothorax, pleural effusion, hemothorax, empyema, chylothorax,
trauma with rib/sternal fractures, flail chest, pneumonia/pleuritis, superior vena
cava syndrome).

Box 10.1 Key investigationMonitoring of vital parameters

• History: characteristics of the patient’s pain (site, type, quality, onset, dura-
tion, precipitating factors), risk factors, medical history
• Physical evaluation: chest pain, dyspnea, respiratory failure, sweating,
breathlessness, cough, hemoptysis, nausea and vomiting, fever, trauma
• Exams: ECG, blood test with biomarkers, ABG, chest X-rays, CT scan in
case of trauma, ultrasound

F. Damarco (*)
Thoracic Surgery and Lung Transplant Unit, Fondazione IRCCS Ca’ Granda Ospedale
Maggiore Policlinico, University of Milan, Milan, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 97

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_10
98 F. Damarco

Algorithm 10.1  Simplified flowchart for patients with chest pain.

CHEST PAIN, DYSPNEA

Clinical Evaluation

Diagnostic tests

Blood Tests ECG Chest X-ray

Non Suggestive Suggestive/Diagnostic Suggestive/Diagnostic Non Suggestive Non Suggestive Suggestive/Diagnostic

Pneumothorax
ST elevation ST depression
Other causes Other causes Other causes Pleural Effusion
Hemothorax
Empyema
Pericarditis STEMI NSTEMI Unstable Angina
Fractures

Pneumonia
Pleuritis

Pulmonary edema

10.1 Pneumothorax

Pneumothorax is defined as the presence of air in the pleural space resulting in lung
collapse (Fig. 10.1).
Depending on etiology it can be classified in spontaneous, primary (PSP) or
secondary to underlying lung disease (SSP), and non-spontaneous [1, 2].

10.1.1 Etiology

10.1.1.1 Primary Spontaneous Pneumothorax (PSP)

PSP occurs in apparently normal lung in absence of external circumstances. It
seems to be due to small subpleural blebs or bullae disruption, but the underlying
pathogenic mechanism is not fully understood. It is more common in young and tall
men between the ages of 10 and 30. The incidence ranges from 7.4 to 37 per 100,000
population per year [3, 4]. Smoking is a significant risk factor. PSP typically occurs
at rest and it can be associated with chest pain, and dyspnea [5].
Small and asymptomatic first episode requires observation only followed by dis-
charge. In case of first large and symptomatic episode, the patient should be treated
air evacuation using aspiration or by placing a chest tube. A definite surgical treat-
ment is normally proposed after a second episode, or in case of professional risks
(e.g., airline personnel). Recurrence rate is estimated to be approximately 32%, with
most occurring within the first year [6]. This finding increases exponentially with
following pneumothorax episodes.

10.1.1.2 Secondary Spontaneous Pneumothorax (SSP)

SSP is secondary to underlying disease. It presents male preponderance with a peak
of incidence after 55  years. Any lung disease can lead to pneumothorax, but the
10  Pulmonary and Thoracic Emergencies 99

Fig. 10.1  Right- and left-sided spontaneous pneumothorax. The arrow indicates the edge of the
collapsed lung

most commonly related are: COPD/emphysema (50–70%), cystic fibrosis (3–4%),

cancer (16%), necrotizing lung infections (e.g. Pneumocystis jirovecii; Bacterial
pneumoniae; Tuberculosis), HIV, thoracic endometriosis, genetic disorders (e.g.,
Marfan syndrome; Ehlers-Danlos syndrome; homocystinuria; Birt–Hogg–Dubé
syndrome), cystic disorders (e.g., lymphangioleiomyomatosis; Langerhans cell his-
tiocytosis) [2].
In SSP, dyspnea is usually more severe and requires treatment procedures.

Box 10.2 Catamenial pneumothorax

Catamenial pneumothorax defines a recurrent lung collapse in women of
reproductive age in conjunction with . Pneumothorax usually occurs right-
sided, within 72 h before or after the start of menstruation with combination
of chest pain, dyspnea, and hemoptysis. The etiology is not fully understood
but it seems to be due to the presence of ectopic endometrial tissue into the
thoracic cavity. can be presumed by recurrence rates of pneumothorax in a
woman of reproductive age with endometriosis. Thoracic surgical procedures
are used for confirmation. Surgical treatment with potential diaphragmatic
plication, pleurodesis, or pleurectomy is the treatment of choice. Hormonal
treatment helps to prevent recurrences of catamenial and/or endometriosis-
related pneumothorax [7].

10.1.1.3 Non-spontaneous Pneumothorax

Non-iatrogenic traumatic pneumothorax should be suspected in all patients under-
going significant trauma and it is due to blunt or more commonly penetrating tho-
racic trauma.
With non-penetrating injury, air enters the pleural space if the visceral pleura is
lacerated secondary to a rib fracture or dislocation. In addition, abrupt chest com-
pression increases the alveolar pressure, causing alveolar rupture.
100 F. Damarco

With penetrating trauma (e.g., impalement on a foreign body, stab wounds, gun-
shot wounds) air can access the pleural space directly through the chest wall or from
the tracheobronchial tree if the visceral pleura is torn.
Iatrogenic pneumothorax is a traumatic pneumothorax that develops as a compli-
cation of an invasive procedure. Mechanical ventilation (7%), pacemaker insertion,
subclavian vein catheterization (22%), thoracentesis (20%), thoracic needle aspira-
tion/biopsy (24%), and transbronchial lung biopsy are the most common causes of
iatrogenic pneumothorax [8].

10.1.2 Signs and Symptoms

Pneumothorax is typically characterized by sudden onset, chest pain radiated to the

scapula, dyspnea, and breathlessness. Especially in PSP, symptoms may be minimal
or absent.
Clinical examination includes hyper-resonant percussion and reduced/absent
breath sounds on the affected side. Hypoxia, acute respiratory distress, tachypnea,
and hypotension are usually present in tension pneumothorax.
The imaging size of pneumothorax does not always correspond to the severity of
the symptoms.

10.1.3 Diagnosis

Erect chest X-ray is the gold standard for the detection of pneumothorax. In some
cases, expiratory film can help to identify pneumothorax. CT scan is not a primary
diagnostic imaging, but it is generally used in trauma setting or for complex or
uncertain cases. Bedside ultrasound can be useful in trauma setting and critically ill
patients.
Pneumothorax is classified in “small” or “large” sized depending on whether the
distance between the lung margin and the chest wall is <2  cm or ≥2  cm: ACCP
guidelines measure the distance from the lung apex to the cupola, while BTS guide-
lines estimate the intrapleural distance at the level of the hilum.

10.1.4 Management and Treatment [9, 10]

Invasive approach is highly variable depending on the different institutions, but all
patients with pneumothorax must receive care with attention to respiratory stabili-
zation. In the following evaluation, you will need to decide if the air should be
removed from the pleural space and what method to use (Algorithm 10.2).
In non-tension pneumothorax patients are clinically stable and a conservative
management is often appropriate. Instead, tension pneumothorax is a medical
10  Pulmonary and Thoracic Emergencies 101

Fig. 10.2  A massive

left-­sided tension
pneumothorax. The arrow
indicates the edge of the
collapsed lung.

emergency requiring urgent measures with prompt decompression: it occurs when

the air enters into the pleural space but is not able to fully exit due to a one-way
valve mechanism (Fig. 10.2). It leads to a gradual increase of intrapleural pressure,
displace of mediastinal structures, and a compromised cardiopulmonary function.
Tension pneumothorax does not require radiological confirmation [11, 12].

Box 10.3 Oxygen tips

Supplemental administration of oxygen in pneumothorax accelerates the rate
of pleural air absorption in clinical and experimental situations. Use high con-
centration oxygen in all patients if not contraindicated by the underlying dis-
ease [13].

For PSP [9, 10]:

• Clinically stable patients with detected small volume pneumothorax should be
observed and discharged in case of stability at the following chest X-ray.
Indication to return in the event of worsening breathlessness.
• Selected asymptomatic patients with a large pneumothorax may be managed by
observation alone.
• Breathless patients associated with any size of pneumothorax should undergo
invasive approach.
–– BTS guidelines propose needle aspiration (14–16G) as first choice option. If
aspiration is unsuccessful, insertion of a small-bore (<14Ch) chest drain is
recommended.
102 F. Damarco

–– ACCP guidelines suggest insertion of a small-bore (<14Ch) catheter or

moderate-­sized (16–22Ch) chest tube.
–– Moderate/large (16–28Ch) chest drain is required in unstable patients with
large pneumothorax.

For SPP [9, 10]:

• Guidelines recommend hospitalization for secondary spontaneous

pneumothorax.
• Use small-bore (<14Ch) chest drain for stable patients with small/large
pneumothorax.
• For unstable patients guidelines suggest moderate/large (16-28Ch) chest drain.
• Referral to a thoracic surgeon for recurrence prevention.

For Traumatic pneumothorax:

• Traumatic non-iatrogenic pneumothorax is usually managed with the insertion

of a large bore chest tube (28–32Ch) because chest trauma is often associated
with hemothorax or could require mechanical ventilation.
• Observation and following discharge in clinically stable patients with detected
small volume iatrogenic pneumothorax.
• In breathlessness patients or large iatrogenic pneumothorax, needle aspiration or
insertion of a small-bore chest drain may be required.

For Tension pneumothorax:

• Immediate decompression by placing a large bore (14–16G) needle in the second

intercostal space at the midclavicular line or in the fifth intercostal space at the
anterior axillary line.
• Insert a chest drain following needle decompression.

For any patient [9, 10]:

• In case of air leak (>48 h) or incomplete re-expansion, suction may be appropriate.

• In case of prolonged air leaks (>5 days) or failure of lung re-expansion, referral
to a thoracic surgeon for definitive treatment (bleb/bullectomy combined with
pleural abrasion/pleurectomy/chemical pleurodesis).
Algorithm 10.2  Flowchart for management of pneumothorax.

PNEUMOTHORAX

SPONTANEOUS NON SPONTANEOUS

PRIMARY PNEUMOTHORAX (PSP) SECONDARY PNEUMOTHORAX (SSP) TRAUMATIC PNEUMOTHORAX IATROGENIC PNEUMOTHORAX

Size<2cm Size>2cm
Size<2cm Size>2cm Size>2cm Size<2cm
- ADMIT and/or and/or
and/or and/or and/or and/or
- Consider ATB Asymptomatic Breathless
Asymptomatic Breathless Breathless Asymptomatic

- OBSERVATION NEEDLE ASPIRATION

Size<2cm Unstable
- OXYGEN (14-16 G)
and/or and/or
- OBSERVATION NEEDLE ASPIRATION - OBSERVATION FOR 24h Stable Ventilation
- OXYGEN (14-16 G) - OXYGEN

CXR stable after 6h Success Deterioration

or or or
CXR stable after 6h Success Deterioration Resolution Resolution Failure
Deterioration Deterioration Success - CHEST DRAIN (8-14Ch) - CHEST DRAIN (<28Ch)
or or or or or
10  Pulmonary and Thoracic Emergencies

Resolution Resolution Failure Failure Resolution

DISCHARGE - ADMIT
Clinical review in 48-72h - CHEST DRAIN (8-14Ch)
DISCHARGE - ADMIT DISCHARGE
Clinical review in 48-72h - CHEST DRAIN (8-14Ch) Clinical review in 48-72h
Success No Re-expansion
or and/or
Resolution Ait leaks >48 h
Success No Re-expansion SURGERY
or and/or for recurrence
Resolution Ait leaks >48 h
- Remove Chest Drain
- DISCHARGE
SUCTION (-20cmH2O)
- Remove Chest Drain
SUCTION (-20cmH2O)
- DISCHARGE

Success Deterioration
Success Deterioration or or
or or Resolution Failure
Resolution Failure

- Remove Chest Drain

- DISCHARGE SURGERY
- Remove Chest Drain
SURGERY
- DISCHARGE
103
104 F. Damarco

10.2 Pleural Effusion

Pleural effusion is defined as an abnormal deposition of fluid in the pleural space. It

occurs, unilaterally or bilaterally, in several disease processes.

10.2.1 Etiology

Various pathogenic mechanisms lead to fluid accumulation by increasing the rate of

pleural fluid formation or by reducing the fluid absorption (Table 10.1). Around 1.5
million people each year in the United States develop pleural effusion, with an
approximate 1.1 to 1.3 million resulting from nonmalignant causes (NMPE) [8].
Malignant pleural effusion (MPE) accounts for 15–35% of all pleural effusions,
and the most involved tumors are lung, breast cancers and lymphomas.
It is important to distinguish if the patient has a transudative (typically caused by
increased hydrostatic pressures, decreased oncotic pressure, increased negative
intrapleural pressure, or fluid migration through the diaphragm) or exudative (due to
increased capillary permeability, inflammatory processes or obstruction of pleural
lymphatic drainage) pleural effusion according to their protein content.

10.2.2 Signs and Symptoms

Pleural effusion is typically characterized by dyspnea, chest pain, cough, malaise,

and fever.
Chest pain is frequently worsened by deep inspiration or movements.
Cough is usually dry and non-productive.
Dyspnea is not always proportional to the amount of the pleural effusion. Small
amounts of effusion can be asymptomatic, even though patients with MPE more
frequently present with dyspnea.
Clinical examination includes attenuated/absent tactile fremitus, dull or flat per-
cussion, and reduced/absent breath sounds on the affected side.

Table 10.1  Main differential diagnoses of pleural effusion

Main differential diagnoses of pleural effusion
Transudative pleural effusion Exudative pleural effusion
Congestive heart failure Neoplastic diseases
Cirrhosis Infectious diseases
Nephrotic syndrome Iatrogenic or trauma (hemothorax;
chylothorax)
Hypoalbuminemia Chylothorax
Superior vena cava obstruction Pulmonary embolization
Peritoneal dialysis Collagen vascular diseases
Atelectasis Lymphatic abnormalities
10  Pulmonary and Thoracic Emergencies 105

Bilateral effusion is typically present in heart failure. The loculation of pleural

space occurs more frequently in intense pleural inflammation such as parapneu-
monic effusion, empyema, and hemothorax.

10.2.3 Diagnosis

Erect chest X-ray is the first test in the detection of pleural effusion (Fig. 10.3). The
posteroanterior view shows blunting of the lateral costophrenic angle when effusion
exceeds 200 mL, while in the lateral view the posterior costophrenic angle is oblit-
erated when fluid is over 50 mL.
Thoracic ultrasound is highly sensitive for pleural effusion and detects small
amount of fluid (<50 mL). It provides an accurate characterization of effusion, the
identification of potential loculation, the evaluation of pleural thickening and it
allows to define the appropriate site for thoracentesis/chest tube placement [14].
The use of ultrasound for guidance reduces the risks of complication during inva-
sive procedures (4% vs 9.5%) [15, 16].
CT scan yields excellent identification of pleural thickening, pleural or lung
masses, and detection of loculated fluid amount.
FDG-PET is useful for differentiating benign and malignant effusion.
Thoracentesis plays a diagnostic and therapeutic role at the same time: it helps to
relieve the dyspnea in symptomatic patients and allows to collect pleural fluid for
further tests. The first step in the diagnosis of pleural effusion is the distinction
between transudative and exudative analyzing the levels of protein and lactate

Fig. 10.3  A large

left-sided pleural effusion
on chest X-ray
106 F. Damarco

dehydrogenase in the pleural fluid and serum according to Light’s criteria [17]. A
pleural effusion is likely exudative if at least one of the following exists:

• The ratio of pleural fluid protein to serum protein is greater than 0.5.
• The ratio of pleural fluid LDH and serum LDH is greater than 0.6.
• Pleural fluid LDH is greater than 0.6 or 2/3 times the normal upper limit for
serum. Different laboratories have different values for the upper limit of serum
LDH, but examples include 200 and 300 IU/L.

It is also possible to perform biochemical, cytological, and microbiological anal-

ysis of pleural fluid as shown in Table 10.2.
Furthermore, appearance and smell of pleural effusion provide additional infor-
mation. Turbid pleural fluid can indicate increased cellular or lipid contents (empy-
ema, chylothorax). For example, reddish effusion suggests blood presence in pleural
fluid (malignant disease, trauma, hemothorax), while a brownish color denotes a
long-standing process.

Table 10.2  Routine pleural fluid tests for pleural effusion [14]
Routine pleural fluid tests for pleural effusion
Value Suggested diagnosis
Adenosine >40 U/L TBC (>90%); empyema (60%);
deaminase complicated parapneumonic effusion
(30%)
Amylase >upper limit of normal Malignancy; esophageal rupture
Culture ± Infection
Cytology ± Malignancy
Flow cytometry ± Lymphoma
Glucose <60 mg/dL Empyema; TBC (20%); malignancy
Hematocrit fluid/ ≥0.5 Hemothorax
blood ratio
LDH 2 Any exudative effusion

> 3 upper limits of normal

for serum LDH
Lymphocytes >50% Malignancy; TBC; Pulmonary embolism
Neutrophils >50% Parapneumonic effusion
NT-pro-BNP >1500 pg/mL Heart failure
pH <7.20 Complicated parapneumonic effusion;
empyema; malignancy; esophageal
rupture
Protein >3 g/dL Any exudative effusion
RBC count >100,000/mm3 Trauma; malignancy; parapneumonic
effusion; pulmonary embolism
Triglycerides >110 mg/dL Chylothorax
WBC count >10,000/mm3 Empyema
10  Pulmonary and Thoracic Emergencies 107

10.2.4 Management and Treatment

• Asymptomatic patients with transudative effusion do not routinely require inva-

sive pleural procedures.
• Symptomatic NMPE are normally responsive to drainage and treatment depend-
ing on the etiology of the primary disorder. A drainage technique involves US-­
guided needle thoracentesis or chest tube placement. BTS guidelines suggest to
drain less than 1500 mL in one sitting with thoracentesis to reduce the risk of
re-expansion pulmonary edema [18]. In case of chest tube placement, ERS/
EACTS prefer large bore chest tubes (20–24 Ch) while other authors suggest
similar outcomes with smaller diameter [19]. A significant percentage of patients
present recurrence of pleural effusion: in these situations it is mandatory to repeat
thoracentesis, maximize primary therapy, and re-evaluate the patients to exclude
pleural infections, non-expendable lung, malignancy, or other diagnoses.
Symptomatic patients with recurrence of nonmalignant pleural effusion despite
of maximized medical therapy and repeated thoracentesis or chest placement are
candidates for indwelling pleural catheter (IPC) and/or pleurodesis using a
chemical sclerosant or manual abrasion.
• MPE usually represents advanced disease and average survival is around
3–12  months, therefore invasive treatments are intended to relieve symptoms
[20]. The risk of recurrence should be considered so, after initial drainage, a
definitive intervention with indwelling pleural catheter and/or talc pleurodesis is
mandatory [16]. Talc is the most effective agent for chemical pleurodesis: talc
poudrage is associated with a lower recurrence rate than talc slurry, but surgical
procedures are more invasive and present more potential complications. IPC is
also a valid option in the management of malignant trapped lung, where patients
would not benefit from chemical pleurodesis.
Algorithm 10.3  Simplified flowchart for diagnosis and management of pleural effusion.
108

PLEURAL EFFUSION

FLUID ASPIRATION

FLUID TESTS: see box

Protein < 3 g/dL Borderlines values Protein > 3 g/dL

Apply Light's Criteria

- PF/serum protein ratio
- PF/serum LDH ratio
- PF LDH

Transudate Exudate

- Congestive heart failure

- Cirrhosis Malignancy Infection/Pneumonia Empyema Hemothorax Chylothorax Others
- Nephrotic syndrome
- Hypoalbuminemia Symptomatic Symptomatic ATB Stabilization
Diet?
- Superior vena caval obstruction
TREAT - REPEATED THORACENTHESIS TREAT - REPEATED THORACENTHESIS - CHEST DRAIN CHEST DRAIN - Somatostatin
- Peritoneal dialysis UNDERLYING UNDERLYING Resolution - Octreotide
- INDWELLING CATHETER - INDWELLING CATHETER - Fibrinolytic (28-32 Ch)
- Atelectasis DISEASE - PLEURODESIS DISEASE - PLEURODESIS - Thoracentesis
Pleural Toilette SURGERY Resolution - Chest drain
Resolution
VATS Pleurodesis

Thoracic duct ligation

Decortication
Asymptomatic Symptomatic Resolution
Thoracotomy Thoracic duct embolization

TREAT
- THORACENTHESIS
UNDERLYING
- CHEST DRAIN (14-24 Ch)
DISEASE
F. Damarco
10  Pulmonary and Thoracic Emergencies 109

10.2.5 Hemothorax

Hemothorax is defined as the collection of blood in the pleural space (Fig. 10.4);

approximately 300,000 cases are estimated every year in the United States.
Bleeding may arise from lung parenchyma, chest wall, pleura, mediastinum,
great vessels, diaphragm, and abdomen. It is classified into three major groups,
depending on the etiology.
Traumatic hemothorax is the most common, due to blunt or penetrating injuries
to the chest. Blunt thoracic trauma occurs more frequently with an overall mortality
of 9.4%, which is significantly increased in case of penetrating chest injuries [21].
Hemothorax may also be the result of spontaneous causes (spontaneous pneu-
mothorax, infectious processes, coagulopathies, and malignancies) or iatrogenic
causes (most commonly during thoracentesis, central venous catheterization, tube
thoracostomy, and thoracotomy).
Hemothorax has respiratory and hemodynamic implication with potential devel-
opment of hypoventilation, hypovolemia, and decreased cardiac output: rapid eval-
uation and intervention are crucial.
Clinical findings of hemothorax are broad and may often mimic other conditions.
Signs and symptoms are dyspnea, tachypnea, hypoxia, hypotension, reduced/absent
tactile fremitus, dull or flat percussion, and reduced/absent breath sounds on the
affected side. Always check for signs of chest contusion, injury, ecchymosis, tender-
ness, paradoxical chest wall movements, and “seat belt sign.”
Chest X-ray is still the initial diagnostic approach, but ultrasound is fast and
more portable. It allows to determine quality and quantity of effusion and it has
higher sensitivity especially in FAST protocols. After this assessment, CT can be
performed to evaluate further chest detail.
All patients with hemothorax must receive care with particular attention to car-
diorespiratory stabilization. Minimal blood collection (<300–400 mL) in the pleural
space usually requires only conservative management with observation and

Fig. 10.4  CT scan shows

a massive right-sided
hemothorax
110 F. Damarco

frequent imaging. Moderate and massive hemothoraces should be evacuated with a

large bore chest tube (28–32 Ch): always check for the fluid output.
Consult a cardiothoracic specialist if: >1500  mL of blood drainage in 24  h;
500 mL/h for 2–4 consecutive hours after tube placement; cardiac tamponade; chest
wall or great vessel injury.
Antibiotic treatment reduces the rate of infectious complications.
Retained hemothorax after evacuation is associated with significant risks for
developing late complications such as empyema and fibrothorax, so in this situation
all patients should undergo pleural toilette, debridement, and decortication via
video-assisted thoracic surgery (VATS) or thoracotomy [22].

10.2.6 Empyema

Empyema is defined as pus in the pleural space. In the United States, the incidence
is approximately 32,000 cases per year. It is mainly caused by pulmonary infection
as community- and hospital-acquired pneumonia (CAP and HAP, 55–75%), but it
can also occur as a result of thoracic-esophageal surgery (12–21%), thoracic trauma
(3–6%), pneumothorax, hemothorax, and lung abscess (9–15%).
Risk factors for the development of empyema are diabetes mellitus, malignancy,
and immunodeficiency; morbidity and mortality of pleural empyema remain high
especially in these already vulnerable patients.
Aerobic gram-positive and gram-negative bacteria are predominant in
community-­acquired empyema (Streptococcus species, E. coli, K. pneumoniae),
MRSA and gram-negative (Pseudomonas, Enterobacteriaceae) are more frequently
related to hospital-acquired infection, while S. aureus is commonly seen in trau-
matic and surgical settings.
Microorganisms reach the pleural space through the damaged endothelium and
inflammatory mediators: pathogenic material promotes fibrin depositions and
suprainfection. These events led to septation with loculated effusion and progres-
sion to entrapped lung [23].
Patients with empyema typically present chest pain, fever, sputum production,
and cough often associated with fatigue. On physical examination crackles, dull or
flat percussion, and reduced/absent breath sounds on the affected side may be pres-
ent. Laboratory tests reveal elevated infection parameters but the confirmation of
certain infection on the effusion is low.
Chest X-ray is probably the first imaging test, but ultrasound allows to determine
quality and quantity of effusion, to estimate potential fluid septations or loculations
and to guide chest tube placement or thoracentesis. Contrast-enhanced chest CT is
the gold standard (Fig. 10.5): thickening of visceral and parietal pleura with separa-
tion by a pleural fluid is pathognomonic for empyema (“split pleural sign”).
Thoracentesis is a useful diagnostic tool and it allows for fluid evaluation. A
turbid-purulent fluid, a pH <7.2, polymorphonucleocyte predominance, low glu-
cose, and LDH >1000 UI/L effusion support the diagnosis of empyema and require
surgical drainage.
10  Pulmonary and Thoracic Emergencies 111

Fig. 10.5  A massive

left-­sided empyema. The
arrow indicates the “split
pleural sign”

The American Thoracic Society classified empyema in three stages as a sequence

of events, characterized by different therapeutic indications:

• The exudative phase with fluid accumulation (2–5  days from the onset of
pneumonia).
• The fibrinopurulent phase with the fluid colonization and the progression of
infection leading to loculations (5–10 days after onset).
• The organized phase in which infection progression leads to fibrosis and
entrapped lung.

At the onset of empyema, antimicrobial therapy is the gold standard treatment. The
recommended treatments for CAP are third- or fourth-generation cephalosporin plus
metronidazole or ampicillin with a beta-lactamase inhibitor. In case of HAP or trau-
matic and surgical empyema, coverage of MRSA and Pseudomonas is essential by
adding vancomycin, cefepime, and metronidazole or piperacillin-tazobactam.
If disease progresses, medium-large bore chest tube insertion (16–28 Ch) with
evacuation of effusion is required and usually sufficient in 75% of the cases. The
adjunctive instillation of fibrinolytic agents helps to debride septation facilitating
the exit of the pleural fluid.
When sepsis persists and the lung is not properly unfolded in the pleural cavity,
surgical intervention is mandatory. Minimally invasive approach can be proposed
for the fibrinopurulent phase to perform pleural toilette, while pleural decortication
usually requires thoracotomy [24].

10.2.7 Chylothorax

Chylothorax is the accumulation of chyle in the pleural cavity due to rupture or

obstruction of the thoracic duct or its branches. It can be classified as traumatic 50%
(complication of surgery, blunt or penetrating injury), non-traumatic 44% (malig-
nancy, infection, congenital disorder, and other conditions), and idiopathic 6%.
112 F. Damarco

The effusion is typically turbid and milky, and the amount varies widely up to
>1000 mL per 24 h.
Clinical features depend on the rate of chyle loss as well as the etiology.
Symptoms can follow pleural effusion expression: dyspnea, cough, and eventually
chest pain.
The loss of protein, fats, vitamins, and ions can result in malnutrition, weight
loss, muscle wasting, and electrolyte disorder, especially in chronic conditions.
On physical examination dull or flat percussion and reduced/absent breath
sounds may be present on the affected side.
Investigation of chylothorax begins with the confirmation of the diagnosis by
fluid analysis and ends with the discovery of the etiology. The pleural fluid is very
rich in large chain fatty acids and lymphocytes.
Definitive management of chylothorax depends on the cause and it can include
dietary therapy, use of somatostatin/octreotide, thoracentesis or chest tube insertion,
pleurodesis, thoracic duct ligation or embolization [25].

10.3 Trauma: Rib Fractures, Sternal Fractures,

Diaphragm Injury

Traumas are one of the main causes of mortality worldwide. Specifically, thoracic
traumas represent the leading cause of mortality along with vertebral and cranial
traumas.
The outcome is determined by the severity of the trauma: the first assessment
should evaluate circulation and airways considering respiratory and hemodynamics
parameters. Major life-threatening conditions to consider after thoracic traumas are
massive hemothorax, tension and open pneumothorax, flail chest, respiratory
obstruction, air embolism, and cardiac tamponade. Nevertheless, emergency ster-
notomies and thoracotomies are required in 1–2% of cases [26].
Frequent thoracic site injured by a trauma is the chest wall, followed by pleura
and lung parenchyma.

10.3.1 Rib Fractures

Rib fractures are the most common type of injury (35–40%), mainly located along
4th–9th ribs along the mid-axillary line (Fig. 10.6). Due to the support of the scap-
ula, shoulders, and clavicle, fractures of the first and second rib are rare and imply
high-energy trauma.
The majority of rib fractures are associated with blunt trauma (e.g., motor vehi-
cle crashes, falls), but they can also result from penetrating injury, severe coughing,
bone metastasis, or athletic activities.
Typical symptoms are point tenderness and pain, exacerbated by coughing, deep
breathing, and movement.
10  Pulmonary and Thoracic Emergencies 113

Fig. 10.6  Multiple rib fractures as indicated by the arrows

Ecchymosis and bone crepitus may be present on physical examination.

Several complications are related with rib fractures such as hemothorax, pleural
effusion, pneumothorax, pneumonia, ARDS, and organ injury (e.g., pleural, lung,
cardiac, bronchial, liver, spleen damage): therefore, it is important to identify poten-
tial associated problems.
Fractures of ribs 1st–3rd may be associated with mediastinal and great vessels
injury; fractures from 9th to 12th can result in intra-abdominal lesions. Displaced
rib fractures increase the risk of injury to the intercostal blood vessels and to the
lung parenchyma.
Chest X-ray is the first diagnostic tool but it can be falsely negative. Chest CT is
more specific and it allows to identify even small alterations in cortical bone and
quantify possible organ damages.
Optimal treatment depends on type and extension of rib fracture. A conservative
management based on pain control and pulmonary rehabilitation is the standard of
care for non-displaced fractures with a good prognostic outcome. Adequate pain
alleviation using nonsteroidal anti-inflammatory drugs, opioids, or intercostal nerve
blocks is essential to avoid complications as well as incentive spirometry to prevent
atelectasis. The pain can persist for several days after the injury, but most rib frac-
tures fix within 6–12 weeks.
Patients are able to return to work within a few days, but for heavy labor or sport
at least 3 weeks off are recommended.
Indication to surgical fixation aims to prevent potential complications, but there
is no consensus. Stabilization is typically proposed in selected patients when rib
stumps are severely displaced or in case of flail chest: bicortical screws, Kirschner’s
wires, Judet’s struts, titanium bar, and intramedullary rods or splints are the most
used devices.
Flail Chest is the paradoxical movement of the chest wall that occurs during
breathing when three or more consecutive ribs are fractured in two places. This
floating segment of rib sections and soft tissues moves independently from chest
wall, outward during expiration and inward during inspiration, and it is usually
114 F. Damarco

associated with underlying pneumothorax, pulmonary contusion, and/or

hemothorax.
Pain, low chest wall expansion, increase in respiratory work, and the paradoxical
movement with mediastinal shift can result in respiratory and hemodynamic
impairment.
Diagnosis is most often clinical with confirmation of the paradoxical motion dur-
ing breathing. Crepitus of the flail segment on palpation and chest X-ray can help
confirm the clinical situation.
The treatment of flail chest is based on supportive care, strong respiratory phys-
iotherapy, and analgesic pain medications. Mechanical ventilation may be neces-
sary in unstable patients with severe pulmonary dysfunction. As mentioned above,
corrective surgery can be proposed to reduce risk of pneumonia, morbidity and
mortality or in non-ventilable patient.

10.3.2 Sternal Fractures

Sternal fractures usually result from blunt anterior chest-wall trauma, deceleration
injuries, athletic injuries, and falls (incidence 3–6.8%). They can occur in isolated
or associated injuries, but the prognosis is mostly excellent. Fractures are more
prevalent in older patients and females.
The most common site of the fractures is located in the body and in the sternal
manubrium, oblique or transverse.
Typical signs and symptoms are acute sternal pain and point tenderness, exacer-
bated by coughing, deep breathing, and movement. Ecchymosis, bone crepitus, and
eventual step deformity may be present on physical examination.
Chest X-ray is the gold standard investigation: lateral projection usually allows
to diagnose displacement or dislocation, while antero-posterior view helps to detect
eventual further injuries (Fig. 10.7).
Chest CT is suitable to determine secondary trauma.
Patients with sternal fractures should be assessed according to ATLS guidelines,
as well as all chest trauma.
ECG and cardiac enzymes generally suffice for stable patients with isolated ster-
nal fractures.
Echocardiography, continuous monitoring, and ICU admission for unstable
patients with intrathoracic injuries, especially if myocardial contusion is
suspected.
Routine hospital admission is warranted in high-impact trauma, major co-­
morbidities, inadequate pain control, or severely displaced fractures [27].
Pain control and pulmonary rehabilitation are the treatment of choice for isolated
sternal fractures. They will recover spontaneously in around 10–12 weeks.
Complications can involve painful pseudoarthrosis and overlap deformities.
Therefore, surgical fixation is requested in selected cases of non-union or chronic
sternal pain. Transverse and oblique fractures of the sternal body generally require
10  Pulmonary and Thoracic Emergencies 115

a b

Fig. 10.7 (a) The arrow indicates the sternal fracture; (b) Example of metal bar placement for
sternal fracture

longitudinal fixation with metallic prosthesis. Longitudinal, sternocostal split or

oblique fractures of sternal manubrium are stabilized using transversal plate or bar
from rib to rib [28].

10.3.3 Diaphragm Injuries

Diaphragm injuries are a rare complication following blunt and penetrating trauma
(0.8–15%).
Two-thirds of all diaphragm injuries are associated with blunt traumas because
of a sudden increase in intra-abdominal pressure. On the right side diaphragm is
well protected by the liver, therefore injuries occur most commonly on the left side.
As a consequence of the muscular defect, abdominal organs may herniate into
the chest leading to inappropriate ventilation, obstruction, or rupture of the abdomi-
nal viscera.
Signs can be either thoracic or abdominal and they include flat lung percussion,
reduced/absent breath sounds, and auscultation of bowel sounds in the chest.
Dyspnea, respiratory distress, chest/abdominal pain, nausea and vomiting due to
obstruction of the viscera may arise depending on timing and severity of the clinical
situation.
In an acute setting, diaphragm injury is hard to diagnose. Most of the time chest
X-ray can show diaphragm elevation, atelectasis, blunting of the costophrenic sinus,
and visceral herniation with diffuse gas bubbles.
116 F. Damarco

Focal constriction of the abdominal organs through the diaphragm defect, called
“collar sign,” is another suggestive sign.
When in doubt, abnormal positioning of nasogastric tube can support the diagno-
sis but CT scanning allows to confirm not only diaphragm damages but also other
potential concomitant injures.
In the acute phase, the main treatments are based on ATLS guidelines. In case of
prompt diagnosis, reduction of visceral herniation and repairing of diaphragm
defects under laparotomy or laparoscopy is the gold standard for hemodynamically
stable patients. In case of delayed confirmation, video-assisted thoracoscopic sur-
gery and thoracotomy are usually required to help lysis and visceral reduction
[29, 30].

References
1. Baumann MH, Noppen M.  Pneumothorax. Respirology. 2004;9(2):157–64. https://doi.
org/10.1111/j.1440-­1843.2004.00577.x.
2. Sahn SA, Heffner JE.  Spontaneous pneumothorax. N Engl J Med. 2000;342(12):868–74.
https://doi.org/10.1056/NEJM200003233421207.
3. Gupta D, Hansell A, Nichols T, Duong T, Ayres JG, Strachan D. Epidemiology of pneumotho-
rax in England. Thorax. 2000;55(8):666–71. https://doi.org/10.1136/thorax.55.8.666.
4. Noppen M, De Keukeleire T.  Pneumothorax. Respiration. 2008;76(2):121–7. https://doi.
org/10.1159/000135932. Epub 2008 Jun 26.
5. Tschopp JM, Bintcliffe O, Astoul P, Canalis E, Driesen P, Janssen J, Krasnik M, Maskell N,
Van Schil P, Tonia T, Waller DA, Marquette CH, Cardillo G. ERS task force statement: diag-
nosis and treatment of primary spontaneous pneumothorax. Eur Respir J. 2015;46(2):321–35.
https://doi.org/10.1183/09031936.00219214. Epub 2015 Jun 25.
6. Walker SP, Bibby AC, Halford P, Stadon L, White P, Maskell NA. Recurrence rates in pri-
mary spontaneous pneumothorax: a systematic review and meta-analysis. Eur Respir
J. 2018;52(3):1800864. https://doi.org/10.1183/13993003.00864-­2018.
7. Visouli AN, Zarogoulidis K, Kougioumtzi I, Huang H, Li Q, Dryllis G, Kioumis I, Pitsiou G,
Machairiotis N, Katsikogiannis N, Papaiwannou A, Lampaki S, Zaric B, Branislav P, Porpodis
K, Zarogoulidis P. Catamenial pneumothorax. J Thorac Dis. 2014;6(Suppl 4):S448–60. https://
doi.org/10.3978/j.issn.2072-­1439.2014.08.49.
8. Light RW. Pleural diseases. 6th ed. Philadelphia: Lippincott Williams & Wilkins (LWW); 2013.
9. Baumann MH, Strange C, Heffner JE, Light R, Kirby TJ, Klein J, Luketich JD, Panacek
EA.  Sahn SA; AACP Pneumothorax Consensus Group. Management of spontaneous pneu-
mothorax: an American College of Chest Physicians Delphi consensus statement. Chest.
2001;119(2):590–602. https://doi.org/10.1378/chest.119.2.590.
10. MacDuff A, Arnold A, Harvey J, BTS Pleural Disease Guideline Group. Management of spon-
taneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010. Thorax.
2010;65 Suppl 2:ii18–31. https://doi.org/10.1136/thx.2010.136986.
11. Hallifax R, Janssen JP.  Pneumothorax-Time for New Guidelines? Semin Respir Crit Care
Med. 2019;40:314–22.
12. Choi WI.  Pneumothorax. Tuberc Respir Dis (Seoul). 2014;76(3):99–104. https://doi.
org/10.4046/trd.2014.76.3.99. Epub 2014 Mar 29.
13. Chadha TS, Cohn MA.  Noninvasive treatment of pneumothorax with oxygen inhalation.
Respiration. 1983;44(2):147–52. https://doi.org/10.1159/000194541.
14. Na MJ. Diagnostic tools of pleural effusion. Tuberc Respir Dis (Seoul). 2014;76(5):199–210.
https://doi.org/10.4046/trd.2014.76.5.199. Epub 2014 May 29. PMID: 24920946; PMCID:
PMC4050067
10  Pulmonary and Thoracic Emergencies 117

15. Gordon CE, Feller-Kopman D, Balk EM, Smetana GW. Pneumothorax following thoracente-
sis: a systematic review and meta-analysis. Arch Intern Med. 2010;170(4):332–9. https://doi.
org/10.1001/archinternmed.2009.548.
16. Feller-Kopman DJ, Reddy CB, DeCamp MM, Diekemper RL, Gould MK, Henry T, Iyer
NP, Lee YCG, Lewis SZ, Maskell NA, Rahman NM, Sterman DH, Wahidi MM, Balekian
AA. Management of malignant pleural effusions. An Official ATS/STS/STR Clinical Practice
Guideline. Am J Respir Crit Care Med. 2018;198(7):839–49. https://doi.org/10.1164/
rccm.201807-­1415ST.9.
17. Light RW, Macgregor MI, Luchsinger PC, Ball WC Jr. Pleural effusions: the diagnostic sepa-
ration of transudates and exudates. Ann Intern Med. 1972;77(4):507–13. https://doi.org/10.732
6/0003-­4819-­77-­4-­507.
18. Havelock T, Teoh R, Laws D, Gleeson F, BTS Pleural Disease Guideline Group. Pleural pro-
cedures and thoracic ultrasound: British Thoracic Society Pleural Disease Guideline 2010.
Thorax. 2010;65 Suppl 2:ii61–76. https://doi.org/10.1136/thx.2010.137026.
19. Thethi I, Ramirez S, Shen W, Zhang D, Mohamad M, Kaphle U, Kheir F.  Effect of chest
tube size on pleurodesis efficacy in malignant pleural effusion: a meta-analysis of randomized
controlled trials. J Thorac Dis. 2018;10(1):355–62. https://doi.org/10.21037/jtd.2017.11.134.
20. Bibby AC, Dorn P, Psallidas I, Porcel JM, Janssen J, Froudarakis M, Subotic D, Astoul P, Licht
P, Schmid R, Scherpereel A, Rahman NM, Cardillo G, Maskell NA. ERS/EACTS statement on
the management of malignant pleural effusions. Eur Respir J. 2018;52(1):1800349. https://doi.
org/10.1183/13993003.00349-­2018.
21. Broderick SR.  Hemothorax: Etiology, diagnosis, and management. Thorac Surg Clin.
2013;23(1):89–96. https://doi.org/10.1016/j.thorsurg.2012.10.003. vi–vii. Epub 2012 Nov 3.
22. Zeiler J, Idell S, Norwood S, Cook A. Hemothorax: a review of the literature. Clin Pulm Med.
2020;27(1):1–12. https://doi.org/10.1097/CPM.0000000000000343. Epub 2020 Jan 10.
23. Hecker A, Padberg W, Browder T, Spain DA. Empyema and effusions. In: Galante JM, Coimbra
R, editors. Thoracic surgery for the acute care surgeon. Cham: Springer; 2021. p. 69–82.
24. Garvia V, Paul M.  Empyema. [Updated 2021 Aug 11]. In: StatPearls [Internet]. Treasure
Island, FL: StatPearls Publishing; 2021 Jan.
25. McGrath EE, Blades Z, Anderson PB.  Chylothorax: aetiology, diagnosis and therapeutic
options. Respir Med. 2010;104(1):1–8. https://doi.org/10.1016/j.rmed.2009.08.010. Epub
2009 Sep 18.
26. Dogrul BN, Kiliccalan I, Asci ES, Peker SC.  Blunt trauma related chest wall and pulmo-
nary injuries: an overview. Chin J Traumatol. 2020;23(3):125–38. https://doi.org/10.1016/j.
cjtee.2020.04.003. Epub 2020 Apr 20.
27. Khoriati AA, Rajakulasingam R, Shah R. Sternal fractures and their management. J Emerg
Trauma Shock. 2013;6(2):113–6. https://doi.org/10.4103/0974-­2700.110763.
28. Bentley TP, Ponnarasu S, Journey JD. Sternal fracture. 2020 Nov 18. In: StatPearls [Internet].
Treasure Island, FL: StatPearls Publishing; 2021 Jan.
29. Bosanquet D, Farboud A, Luckraz H.  A review diaphragmatic injury. Respir Med
CME. 2009;2(1):1–6. https://doi.org/10.1016/j.rmedc.2009.01.002. ISSN 1755-0017
30. Lee K, Kashyap S, Atherton NS.  Diaphragm Injury. 2021 Aug 1. In: StatPearls [Internet].
Treasure Island, FL: StatPearls Publishing; 2021 Jan.
Upper Gastrointestinal Tract Acute
Conditions 11
Marco Giovenzana, Beatrice Giuliani,
and Nicolò Maria Mariani

11.1 General Approach to Upper Gastrointestinal Bleeding

Firstly, assess the patient’s hemodynamic stability, and proceed with resuscitation if
necessary. Secondly, diagnostic studies, usually endoscopy, follow with the aim of
diagnosis, and treatment of the specific disorder, when possible [1, 2].

11.1.1 Assessment of Hemodynamic Stability

The initial evaluation consists of a history of symptoms, physical examination, and

laboratory tests. The aim is to evaluate the severity of the bleed and identify poten-
tial sources of the bleed.

• Patients with acute upper gastrointestinal (GI) bleeding commonly present with
hematemesis and/or melena, if there have been warnings in the previous days.
Symptoms that suggest a severe bleeding are orthostatic dizziness, confusion,
angina, tachycardia, and cold extremities.
• The physical examination is a fundamental part of the evaluation of hemody-
namic stability. The first assessment is to determine whether there are any signs
of bleeding in the stool (proctorragy or melena).
–– If the patient is undergoing martial therapy and reports black, tarry stool, the
presence of melena cannot be defined with certainty. In this case perform
hydrogen peroxide test: H2O2 generates foam in the presence of blood.

M. Giovenzana (*) · B. Giuliani · N. M. Mariani

Unit of Hepatobiliary, Pancreatic, and Digestive Surgery, Department of Surgery,
S. Paolo Hospital, University of Milan, Milan, Italy
e-mail: [email protected]; [email protected];
[email protected]

© The Author(s), under exclusive license to Springer Nature 119

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_11
120 M. Giovenzana et al.

If the patient is unstable, it is essential to immediately stabilize the patient

according to the common accepted guidelines: placement of at least two periph-
eral venous accesses of large caliber, administration of O2 therapy, placement of
a bladder catheter, and especially volemic adjustment while waiting for blood
tests, on the basis of which, in case of anemia, you can possibly set up a transfu-
sion therapy with blood derivatives. In order to know more quickly the state of
anemia of the patient, the execution of an arterial blood gases can be useful, as
its result is almost immediate.
The placement of a nasogastric tube is still debated, between those who are in
favor of its placement, in order to quantify the blood loss and to avoid possible
pneumonia ab ingestis, and those who are against, not considering the maneuver
of any obvious benefit, as well as possible source of recurrence or new bleeding.
In our experience, it is a usual practice because it allows immediate evaluation
of the bleeding characteristic. If ongoing bleeding, we perform a gastric lavage,
better with cold water and ice, with the goal of vasoconstricting, reducing the
bleeding, and flush the stomach of clots so as to facilitate subsequent interven-
tion by the endoscopist. In any case, remember that blood spillage can cause
anemia and melena with falsely negative nasogastric stagnation.
To facilitate endoscopy and decrease the risk of aspiration in patient with cur-
rent hematemesis or altered metal status/respiratory, elective endotracheal intu-
bation can be taken into consideration.
–– Always monitor ABCDE parameters: clinical status, vital signs, cardiac
rhythm, urine output, nasogastric output.
• Laboratory tests should include a complete blood count, liver and coagulation
studies, and serum chemistries. Moreover, serial electrocardiograms and cardiac
enzymes are suggested in patients who are at increased risk for a myocardial
infarction.
False positive:
The initial hemoglobin value may be falsely normal, because the patient is
losing whole blood.
False negative:
Typically, after 24 h or more, the hemoglobin level will decline because the
fluid administration during volemic resuscitation dilutes the blood.
–– Importance of vital parameters, i.e., hypotension, anuria, tachycardia, unless
the patient is on beta-blocker therapy.
• Administration of proton pump inhibitor (PPI), prokinetics, and vasoactive drugs
is indicated, while there is no evidence for tranexamic acid in the treatment of
upper GI bleeding.

11.1.2 Diagnostic Studies

Upper endoscopy is the diagnostic and therapeutic gold standard procedure for
acute upper GI bleeding.
Early endoscopy (within 12–24 h) is recommended for most patients with acute
upper GI bleeding, while in the case of a stable patient, the endoscopic procedure
11  Upper Gastrointestinal Tract Acute Conditions 121

can be performed in deferred urgency; however, if the patient remains unstable,

early endoscopic examination can significantly improve survival [3].
In emergency, in acute esophageal variceal hemorrhages as bridging therapy
while waiting for the endoscopic procedure, the positioning of a Sengstaken-­
Blakemore probe represents a save-life procedure [4]. It consists of two Foley bal-
loons at its caudal end: a more distal one, useful for anchoring beyond the cardia,
and an oblong one, more proximal, to ensure a progressive pressure at the distal
esophageal level, offering a control of bleeding by compression of the varices. If it
is used, remember to proceed to a progressive and not too rapid increase in the infla-
tion pressure of the esophageal balloon, in order to limit any episodes of emesis and
to cause iatrogenic injury of the distal esophagus.
Other diagnostic tests for acute upper GI bleeding may include CT angiography
(CTA) and angiography, which can report active bleeding. In patients with melena
and a negative upper endoscopy, a colonoscopy can be performed unless an alterna-
tive source of the bleeding has been identified.

11.2 Etiologies of Upper Gastrointestinal Bleeding

and Therapeutic Approach

It’s important to investigate whether there have been previous episodes of upper GI
bleeding, since almost 60% of patients whith a history of an upper GI hemorrhage,
bleed from the same lesion. Moreover, analyze any important comorbid conditions
in the patient’s past medical history that may lead to upper GI bleeding or may influ-
ence the clinical management.

11.2.1 Esophagus

Esophageal varices represent the leading cause of esophageal bleeding, followed by

bleeding from Mallory-Weiss lesions secondary to reflux disease.
Endoscopic hemostasis is the therapy of choice, in particular in an urgent/emer-
gency context, as it allows to perform an injection and/or mechanical hemostasis
through the positioning of clips.
Surgical treatment, challenging both for the urgency and for the difficulty in
reaching and controlling the distal esophagus, is not advisable as a treatment of first
choice and would in any case require a resective approach, not easy to perform from
a technical point of view.

11.2.2 Stomach

Gastric bleeding is usually secondary to chronic erosive gastric disease or an ulcer.

In most cases it is a slow and constant bleeding, which is the reason why the patient
presents to the general practitioner or to the emergency room complaining of
melena; in rare cases in which the bleeding is massive, you can also see episodes of
hematemesis.
122 M. Giovenzana et al.

The therapy consists of endoscopic hemostasis by injection of adrenaline or

placement of metal clips, or radiological embolization. The surgical approach rep-
resents the last choice and consists of gastric resection or ulcer suturing.

• False negative: Dieulafoy’s lesion, a vascular anomaly with a tortuous artery in

the thickness of the submucosal tonaca that can be the cause of even massive
gastrointestinal bleeding, is difficult to diagnose endoscopically because of the
massive presence of blood, the size of the lesion, and the intermittent nature of
the bleeding.

11.2.3 Duodenum

Bleeding secondary to duodenal ulcer. Unlike gastric bleeding, which, if massive,

may give hematemesis, bleeding from a duodenal ulcer is more often an intermittent
or tassel-like bleed and therefore the patient’s primary presenting symptom in the
emergency department will be melena, lipothymia, and fatigue, rather than pain.

11.3 General Approach to Upper

Gastrointestinal Perforation

Clinical manifestations of upper gastrointestinal perforation depend on the nature of

the substances released (gas, succus entericus, bile, blood), as well as the ability of
the surrounding tissues to contain those contents.
Full-thickness injury and subsequent perforation of the upper gastrointestinal
tract can be caused by different etiologies, including:

• Instrumentation (e.g., endoscopy, instillation of contrast, cautery application

during surgery)
• Trauma (blunt or penetrating)
• Medications, other ingestions, foreign body
• Vomiting
• Neoplasms

11.3.1 Assessment of Hemodynamic Stability

A detailed history is important in evaluating patients with neck, chest, and abdomi-
nal pain. Physical examination should include vital signs, a complete examination
of the abdomen, chest, and neck. Vital signs may initially be normal or reveal mild
tachycardia or hypothermia. As the inflammatory response progresses, fever and
other signs of sepsis may develop.
Palpation of the neck and chest should search for signs of subcutaneous emphy-
sema and auscultation and percussion of the chest for signs of effusion. Abdominal
11  Upper Gastrointestinal Tract Acute Conditions 123

examination may initially be relatively normal or reveal only mild focal tenderness,
as with tamponade or retroperitoneal perforations.

11.3.2 Diagnostic Studies

The presence of air outside the gastrointestinal tract in the abdomen (i.e., pneumo-
peritoneum) or mediastinum (i.e., pneumomediastinum), or complications associ-
ated with perforation leads to the diagnosis.
The diagnostic evaluation in mild symptomatic patients often begins with upright
radiographs of the chest and abdomen, while the first diagnostic approach in severe
acute conditions is computed tomography (CT).

• In our experience, when there is a suspicion of perforation, we perform a CT

scan with oral administration of Gastrografin, as it confirms the original hypoth-
esis and allows us to see the site of the perforation and its extent (tamponade or
diffuse perforation). This information is critical to the decision of subsequent
management.

11.4 Etiologies of Upper Gastrointestinal Perforation

and Therapeutic Approach

The past medical history should include questioning about prior attacks of abdomi-
nal or chest pain, recent upper-GI procedures (placement of nasogastric tube, endos-
copy, surgery), malignancy, abdominal trauma, ingested foreign bodies (e.g., fish or
chicken bone ingestion), and medical conditions (e.g., peptic disease), with particu-
lar attention to medication that predispose to gastrointestinal perforation (e.g.,
NSAIDs).

11.4.1 Esophagus

Perforation of the esophagus is more often iatrogenic (endoscopy, surgery) followed

by non-iatrogenic penetrating or blunt traumatism. Other causes may include
tumors, foreign body or caustic ingestion, pneumatic injury, vomiting or, more
rarely, it is spontaneous (Boerhaave’s syndrome).
From the therapeutic point of view, it is necessary to keep the patient fasting,
setting an adequate infusion therapy, a correct analgesic therapy and administering
proton pump inhibitors intravenously; a broad-spectrum antibiotic therapy is advis-
able in order to limit possible septic complications (mediastinitis, pleurisy). An
infectiological consultation could help in the choice of the most appropriate drug.
In case of esophageal perforation, given its particularity and the difficulty of its
management, it is mandatory to alert the surgical team immediately for the possible
intervention [5].
124 M. Giovenzana et al.

11.4.2 Stomach

Gastric perforation is mainly caused by a peptic ulcer which, whether or not it has
previously bled, causes full-thickness damage to the gastric wall, creating a continu-
ous solution between the intragastric acid environment and the abdominal cavity.
The presenting symptom is stabbing pain in the epigastrium and radiating to the left
hypochondrium, sometimes to the back. Among the prodromes, melena may be
present if there has been continuous bleeding in the days preceding the actual per-
foration. A history of non-specific pain and subsequent continued NSAID therapy
may also be a warning sign of perforation.

• Remember that in case of a tamponade ulcer, the abdomen may not be peritonitic.

Other causes include iatrogenic (endoscopy, surgery) or non-iatrogenic trauma,

ingested foreign bodies, and neoplasm (particularly during chemotherapy).
The perforated tamponated gastric ulcer can be managed conservatively: the set-
ting of an adequate infusion therapy and with proton pump inhibitors, together with
a broad-spectrum antibiotic therapy is essential. In case of open perforation in the
abdomen, peritonism, hemodynamic instability, or sepsis, it is essential to alert the
surgical team for exploratory treatment in an emergency. The best surgical approach,
if anesthesiologically permissive, is laparoscopic.

11.4.3 Duodenum

Perforation is less frequent and is more often related to endoscopic or surgical pro-
cedures than to the ulcer itself or to the perforation of a duodenal diverticulum,
usually located between the second and third portion of the viscera.

• If the patient is hemodynamically stable, given the largely retroperitoneal posi-

tion of the duodenum, these types of perforations are often managed
conservatively.
• In general, in case of upper-GI perforation, the hemodynamic stability of the
patient, the septic status, and the extent of the perforation itself guide the thera-
peutic choice:
–– Diffuse perforation (e.g., peritonitis) and instability/septicemia: surgical
intervention.
–– Localized, tamponade perforation and hemodynamic stability: multimodal or
step-by-step approach (endoscopist-interventional radiology and surgeon).

11.5 General Approach to Upper Gastrointestinal Ingestion

of Foreign Bodies and Food Impactions

Foreign body ingestion and food impactions are not uncommon event that occur
accidentally in adults.
11  Upper Gastrointestinal Tract Acute Conditions 125

11.5.1 Assessment of Hemodynamic Stability

The symptomatology is characterized by acute onset of dysphagia, foreign body

sensation, mostly retrosternal, refusal to eat, wheezing, hypersalivation, and pain.
It’s always essential to investigate the type of foreign body, the time of ingestion,
and the presence and type of ongoing symptoms. In fact, foreign bodies represent a
rather dangerous event, both for their nature and for their shape and size: there are
objects of spheroidal shape and therefore not dangerous, but with a possible harmful
content, such as a battery, or objects of non-toxic material, such as a toothpick, but
with a sharp shape and therefore potentially harmful to the hollow viscera of the
gastro-enteric tract.
Physical examination should also include an inspection of the oro- and hypo-
pharynx, neck, chest, and abdomen to identify patients with esophageal obstruction
(drooling and inability to swallow liquids), or perforation.

11.5.2 Diagnostic Studies

From a diagnostic point of view, radiographic localization and identification of for-

eign bodies is valuable in guiding management.
Chest-abdomen X-ray can confirm the size, shape, number, and location of a
radio-opaque foreign body while food bolus, thin metal objects, wood, plastic,
glass, and bones are not readily seen. CT is therefore a second-level diagnostic
study, indicated but not mandatory for all cases of foreign body ingestion.

11.5.2.1 Esophagus
In an emergency context the only examination that may have a value is the CT scan,
initially even without contrast medium: it can document the distension of the esoph-
agus upstream of the foreign body/bolus, the size, the possible presence of mineral-
ized material and free periesophageal air in case of perforation; the use of contrast
could possibly facilitate the recognition of structures, such as the esophageal wall,
with respect to foreign material.

11.5.2.2 Stomach
In asymptomatic patients, the priority is to establish the characteristics of the object
by performing a chest-abdomen X-ray in order to document the position of the
same; If the examination is not diriment for the location of the foreign body or
shows possible complications (e.g., intra-abdominal free air), an abdominal CT
scan with contrast medium is mandatory.

11.6 Etiologies and Therapeutic Approach

The approach to management is guided by the initial evaluation.

126 M. Giovenzana et al.

11.6.1 Esophagus

If the patient is compliant and the bolus consists of material of soft consistency
(rice, pasta, bread, meat, fruit, vegetables), the “push” method can be used, which
allows, through the positioning of a nasogastric tube, the progression of the bolus
into the stomach by mechanical push. This maneuver, we reiterate, must be per-
formed only when there is adequate certainty of the nature of the bolus and without
forcing the push if the probe should not progress beyond the obstacle, in order to
avoid any esophageal injury. Some authors also suggest the use of coke [6] in an
attempt to mobilize the bolus, although this technique is certainly less effective and
has a high failure rate. In case the bolus is made of material potentially harmful to
the bowel, such as a bone, the endoscopist’s intervention is essential for its removal
[7]; the urgency of the procedure is related in particular to the symptoms and to the
possible detection of complications on imaging, if performed.

• Emergent endoscopy (2–6 h) is indicated in patients with any of the following:

–– Complete esophageal obstruction as evidenced by drooling and an inability to
handle oral secretions
–– Disk batteries in the esophagus
–– Sharp-pointed objects in the esophagus
• Urgent endoscopy (within 24  h): Any other foreign body should be retrieved
within the 24 h following the ingestion, because the risk of complications dra-
matically increases with time.

11.6.2 Stomach and Proximal Duodenum

A foreign body potentially harmful, by shape and/or nature, which is located in the
stomach or proximal duodenum, should be removed as soon as possible, in order to
limit the early progression of the same along the intestinal tract, an event that would
make surgery the only possible treatment of removal.
Foreign bodies that should be removed are definitely sharp metal objects (e.g.,
sewing needles), old batteries, and razor blades; all other foreign bodies should be
considered potentially harmful and each case should be discussed with the reference
endoscopist specialist. This evidence lies in the fact that potentially non-injurious
objects (medium-sized coin, new generation batteries, dental prostheses) may not
lead to a perforation of the digestive tract but could still be obstructive at any level
of the jejunum-ileum but especially at the ileo-cecal valve; in this case it may be
necessary to perform a colonoscopy or, if ineffective, surgery (enterotomy and
removal of the foreign object).

• Food and objects: Therapeutic management is endoscopic, except on rare occa-

sions, such as:
–– Bolus without bones or liches
–– Perforation (see above)
–– Object no longer detectable or removable endoscopically
• Remember that therapeutic choice is also time-related.
11  Upper Gastrointestinal Tract Acute Conditions 127

11.7 Ingestion of Caustics

The ingestion of caustics is usually due to a voluntary gesture performed for the
purpose of self-harm even if, in some cases, the event may occur involuntarily [8].
The first thing to verify is the nature of the product and the likely amount ingested.
These data, together with the objective examination, are fundamental to be able to
identify the therapy and the eventual necessary investigations. Caustic substances
can be divided into three groups: strong acids (e.g., hydrochloric, sulfuric, nitric,
phosphoric, hydrofluoric acids), strong alkalis (e.g., ammonia, sodium carbonate,
sodium hydroxide, potassium hydroxide), and oxidizing agents (e.g., peroxides,
potassium permanganate). The most frequent and severe lesions for the esophagus
are due to basic caustic substances (bleach) and for the stomach to acids (button
batteries). The greatest injuries are localized to the antrum due to pyloric spasm.
Once the patient has been evaluated, it is essential to contact the Poison Centre,
active 7/24, and communicate all the data collected. It is then the specialist who
recommends the optimal therapy to be administered and the timing for the endo-
scopic examination. On the other hand, it is always useful to perform a CT scan of
the neck, chest, and abdomen with contrast medium to evaluate the integrity of the
potentially damaged viscera, the detection of extraluminal air, collections, or addi-
tional alterations.

• Do not place a nasogastric tube by yourself! Some combinations of caustics can

damage the mucosa which, with the placement of nasogastric tube, would risk
perforation. Always follow the instructions of the Poison Centre.

References
1. Fingerhut A, et al., editors. Emergency Surgery Course (ESC®) Manual: the official ESTES/
AAST Guide. Cham: Springer; 2016.
2. Boffard K.  Manual of definitive surgical trauma care. 5th ed. Boca Raton, FL: CRC Press
Taylor & Francis Group; 2019.
3. Fujishiro M, Iguchi M, Kakushima N, Kato M, Sakata Y, Hoteya S, Kataoka M, Shimaoka S,
Yahagi N, Fujimoto K. Guidelines for endoscopic management of non-variceal upper gastro-
intestinal bleeding. Dig Endosc. 2016;28(4):363–78. https://doi.org/10.1111/den.12639. Epub
2016 Apr 5.
4. Powell M, Journey JD.  Sengstaken-Blakemore Tube. 2020 Jun 4. In: StatPearls [Internet].
Treasure Island, FL: StatPearls Publishing; 2021 Jan.
5. Aiolfi A, Micheletto G, Guerrazzi G, Bonitta G, Campanelli G, Bona D. Minimally invasive
surgical management of Boerhaave’s syndrome: a narrative literature review. J Thorac Dis.
2020;12(8):4411–7. https://doi.org/10.21037/jtd-­20-­1020.
6. Baerends EP, Boeije T, Van Capelle A, Mullaart-Jansen NE, Burg MD, Bredenoord AJ. Cola
therapy for oesophageal food bolus impactions a case series. Afr J Emerg Med. 2019;9(1):41–4.
https://doi.org/10.1016/j.afjem.2018.09.005. Epub 2018 Oct 13.
128 M. Giovenzana et al.

7. Birk M, Bauerfeind P, Deprez PH, Häfner M, Hartmann D, Hassan C, Hucl T, Lesur G,

Aabakken L, Meining A. Removal of foreign bodies in the upper gastrointestinal tract in adults:
European Society of Gastrointestinal Endoscopy (ESGE) Clinical Guideline. Endoscopy.
2016;48(5):489–96. https://doi.org/10.1055/s-­0042-­100456. Epub 2016 Feb 10.
8. Hoffman RS, Burns MM, Gosselin S.  Ingestion of Caustic Substances. N Engl J Med.
2020;382(18):1739–48. https://doi.org/10.1056/NEJMra1810769.
Multidisciplinary Surgical Consensus
on Chest Emergencies 12
Francesco Damarco , Marco Giovenzana,
Diotti Cristina , and Valeria Musso

Clinical case: A 58-year-old male patient, with an history of alcohol abuse, current
smoker under antipsychotic therapy, appeared in emergency department for chest
pain after vomiting. Cardiological emergencies were immediately excluded (EKG
and blood tests were negative). The CT scan with oral contrast showed pneumome-
diastinum and extravasation of contrast from distal esophagus: a collection of fluid
with air-fluid levels was described in the posterior mediastinum, at the level of the
right inferior pulmonary vein. At the abdominal scan, there was evidence of pneu-
moperitoneum at the esophageal-gastric passage and at the small gastric curvature,
with extravasation of free contrast.
Considering the clinical deterioration and the radiological findings, the patient
was taken to the operating room: a right posterolateral thoracotomy was performed
through the sixth space access. Samples of pleural fluid were collected for culture
examination. After opening the mediastinal pleura, the esophagus was isolated
below the inferior pulmonary vein. Using the endoscope, a 4 cm long laceration was
identified immediately above the cardia, and the breach was sutured directly.
Indocyanine green test was performed, with evidence of good visceral esophageal
vascularization. An intercostal muscle flap was used to buttress the suture and a

F. Damarco (*)
Thoracic Surgery and Lung Transplant Unit, Fondazione IRCCS Ca’ Granda Ospedale
Maggiore Policlinico, University of Milan, Milan, Italy
e-mail: [email protected]
M. Giovenzana
Unit of Hepatobiliary, Pancreatic, and Digestive Surgery, Department of Surgery,
S. Paolo Hospital, University of Milan, Milan, Italy
e-mail: [email protected]
D. Cristina · V. Musso
University of Milan, Milan, Italy
e-mail: [email protected]; [email protected]

© The Author(s), under exclusive license to Springer Nature 129

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_12
130 F. Damarco et al.

drainage tube was placed in the mediastinum. Methylene blue was administered
through the nasogastric tube to check for leakage, and an abdominal drainage tube
was placed in the supramesocolic lodge after washing it thoroughly; the last step
was the packing of the jejunostomy.
On the seventh postoperative day, due to the evidence on the CT scan of two
fistulas in the distal third of the esophagus, a prosthesis was placed endoscopically.
The postoperative course was characterized by the onset of infectious, respiratory,
and renal complications; enteral nutrition was reintroduced 1 month after surgery,
with no complications.

12.1 Spontaneous Esophageal Injuries

Esophageal injuries (EI) are an uncommon but potentially lethal event. A multidis-
ciplinary approach involving all the relevant actors (thoracic and general surgeons,
endoscopists, anesthesiologists, and radiologists) has proven to reach better
outcomes.
EI are characterized by transmural disruptions of the esophageal wall. The leak-
age of esophageal contents into the surrounding structures leads to local and sys-
temic inflammation, and increases the risk of sepsis [1].
Overall incidence is unclear but esophageal perforation presents high mortality
rate ranging from 4% to 40%. The outcome depends on several factors, but essen-
tially on early diagnosis and proper treatment.
Esophageal injuries are mainly iatrogenic (e.g., naso-enteric tube placement,
endoscopic exams, surgical procedures), traumatic (e.g., blunt or penetrating
trauma), or spontaneous (e.g., Boerhaave syndrome) [2].
Spontaneous rupture, or Boerhaave syndrome from the name of the doctor who
first described it in 1729, represents 15% of all injuries, estimated in 3.1 cases per
1,000,000 per year [3].
It most commonly occurs in connection with vomiting, as a consequence of an
increase in intraluminal esophageal pressure, and less frequently with childbirth, or
seizure [4].
It appears usually among patients aged 50–70  years and chronic alcohol con-
sumption is a risk factor.
Although injuries can occur along the entire esophagus, the perforation is most
commonly observed in the left posterior aspect of the distal esophagus [5].
Esophageal rupture may be followed by serious complications such as mediasti-
nitis, abscess formation, and multiple organ dysfunction. It is therefore important to
obtain a proper picture of the clinical condition.
EI can be misdiagnosed as cardio-pericardial (e.g., myocardial infarction, peri-
carditis, acute aortic syndrome, pulmonary embolism), respiratory (e.g., spontane-
ous pneumothorax, pneumonia), or abdominal pathological conditions (e.g.,
perforated peptic ulcer).
It is a rare life-threatening condition and requires urgent diagnosis and treatment:
patient outcomes are directly related to the timing.
12  Multidisciplinary Surgical Consensus on Chest Emergencies 131

12.1.1 Signs and Symptoms

Retrosternal chest pain is the main symptom (70%) and it may radiate to the left
shoulder or to the back depending on the injury’s location. Dyspnea and vomiting
are very frequent (25%) [5].
Mackler’s triad, including vomiting, subcutaneous emphysema, and thoracic
pain, is pathognomonic for esophageal perforation but unfortunately is
uncommon [6].
Atypical symptoms such as tachypnea, tachycardia, odynophagia, hypotension,
restlessness, and cyanosis may also be present.
Pneumomediastinum can be a significant associated clinical finding with the
characteristic Hamman’s sign, a clicking or crunching sound synchronous with the
heartbeat, which can be heard over the precordium.

• Cervical perforation: neck pain, dysphagia, or dysphonia.

• Intrathoracic perforation: sepsis may rapidly develop.
• Intra-abdominal perforation: epigastric pain with eventual irradiation to the
shoulder, back pain, and an inability to lie supine or possible eventual acute (sur-
gical) abdomen.

12.1.2 Diagnosis

Laboratory findings may be not specific, and Boerhaave syndrome is often diag-
nosed incidentally during the evaluation of a chest pain [6].
Chest X-ray usually shows signs of pneumothorax, pneumomediastinum, or
pleural effusion.
Esophagogram with water-soluble contrast (e.g., Gastrografin®) can help to con-
firm the diagnosis and to locate the perforation.
CT scan is extremely effective in detecting perforations. Typical findings include
esophageal wall edema and thickening, periesophageal fluid with or without gas
bubbles, mediastinal widening, and air and fluid in the pleural spaces or retroperito-
neum. The ingestion of Gastrografin® allows to estimate the esophageal perfora-
tions, their extension, and to guide any subsequent therapeutic interventions [5]
(Fig. 12.1).
EGDS is not early recommended for diagnosis, since it may aggravate the rup-
ture increasing the air and the esophageal contents in the mediastinum and pleu-
ral space.

12.1.3 Thoracic Treatments

The management of Boerhaave syndrome is still an unsolved problem, and the dif-
ferent therapeutic approaches depend on the esophageal injuries and the patient’s
conditions at the time of presentation [7] (Table 12.1).
132 F. Damarco et al.

Fig. 12.1  Left distal esophageal rupture associated with pleural effusion, periesophageal fluid,
and pneumomediastinum. Gastrografin® helps to locate the perforation

Table 12.1  Esophageal rupture management

Medical management:
Avoidance of all oral intake
Nutritional support, typically parenteral
Intravenous broad-spectrum antibiotics
Intravenous proton pump inhibitor
Drainage of fluid collections/debridement of infected and necrotic tissue, if present
Surgery:
Patients who are not candidates for or who fail conservative management require surgical
approach

Surgery is the most widely used approach and should be performed within 24 h
from the onset of symptoms: beyond this timing, mortality exceeds 56% and
increases with the passing of the hours [8].
Proper management in esophageal injuries includes fluid replacement, nutri-
tional support, control of sepsis with antibiotics, drainage, and primary repair of the
perforation.
Conservative treatments should be applied only in selected patients because in
esophageal perforations it is difficult to treat the infection.
Surgical procedures and primary repair remain the gold standard therapy: they
range from simple drainage, to debridement, repair of the perforation, or esophagec-
tomy. The specific procedure depends on etiology and site of perforation, time from
diagnosis, and surgeon’s experience.
Chest or mediastinal drainage helps to control the sepsis (the positioning tech-
nique of a chest tube has already been discussed in Chap. 8 “Chest: surgical anat-
omy and general consideration in emergency settings”), but it is often not enough.
12  Multidisciplinary Surgical Consensus on Chest Emergencies 133

Early diagnosis and primary repair play a key role in patient survival: it was tra-
ditionally performed using open thoracotomy, but the use of minimally invasive
approach is progressively increasing [7].
Irrigation of pleural space, drainage and debridement, direct suture of the esoph-
ageal mucous membrane with the muscularis propria and adventitia are the most
common procedures.
Soft tissue coverage with intercostal muscle flap or omental patch increases the
tightness of the sutures.
In some cases, esophagectomy is required [9].
The general principles for the management of an intra-abdominal esophageal
perforation include a careful dissection to isolate the esophagus without damaging
vital structures, removal of debris and devitalized tissues, and debridement of the
area of perforation. Laparotomy is usually the preferred approach.
Following primary suture repair, the hiatus is closed posteriorly with interrupted
silk sutures. A Dor or a Nissen (fundoplication) is used to buttress the site of repair
depending on the site of perforation and patients’ preoperative history of swallow-
ing dysfunction. Finally, drainages are placed near the site of repair, and a feeding
jejunostomy tube can be placed for postoperative alimentation.
In the postoperative period, attention must be paid to nutritional support and
decompression of the first intestinal tract. The most common postoperative compli-
cation is the leakage from the suture, which occurs in up to 40% of the operated
patients: to decrease that chance it is necessary to cover the site of perforation
through appropriate vascularized tissue. Moreover, the use of indocyanine green
appears to be an option to verify the vascularization of the flaps.
Endoscopic treatments should be considered in patients with extensive underly-
ing comorbidities who are unlikely to tolerate surgery. They include esophageal
stent placement or endoscopic vacuum-assisted closure (EVAC) in order to stimu-
late granulation tissue and healing by second intent.

12.2 Conclusion

Boerhaave syndrome is rare, and there is limited evidence to guide management.

For this reason, a multidisciplinary approach among general surgeon, thoracic
surgeon, and endoscopist is essential to ensure the best treatment for the patient.

References
1. Mubang RN, Sigmon DF, Stawicki SP.  Esophageal Trauma. StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2021. [cited 2021 Sep 21]. Available from: http://www.ncbi.
nlm.nih.gov/books/NBK470161/
2. Kassem MM, Wallen JM.  Esophageal Perforation And Tears [Internet]. StatPearls Internet.
StatPearls Publishing; 2021. [cited 2021 Sep 21]. Available from: https://www.ncbi.nlm.nih.
gov/books/NBK532298/
3. Brinster CJ, Singhal S, Lee L, Marshall MB, Kaiser LR, Kucharczuk JC.  Evolving options
in the management of esophageal perforation. Ann Thorac Surg. 2004;77:1475–83. Elsevier
134 F. Damarco et al.

4. Triadafilopoulos G, Lamont JT, Grover S.  Boerhaave syndrome: effort rupture

of the esophagus [Internet]. Available from: https://www.uptodate.com/contents/
boerhaave-­syndrome-­effort-­rupture-­of-­the-­esophagus
5. Garas G, Zarogoulidis P, Efthymiou A, Athanasiou T, Tsakiridis K, Mpaka S, et al. Spontaneous
esophageal rupture as the underlying cause of pneumothorax: early recognition is crucial. J
Thorac Dis [Internet]. AME Publishing Company; 2014 [cited 2021 Sep 21];6. Available from:
https://jtd.amegroups.com/article/view/3546
6. Dinic BR, Ilic G, Rajkovic ST, Stoimenov TJ. Boerhaave syndrome - case report. Sao Paulo
Med J. 2016;135:71–5. Associação Paulista de Medicina - APM
7. Eroglu A, Aydin Y, Yilmaz O. Thoracic perforations—surgical techniques. Ann Transl Med.
2018;6:40.
8. Kiladze AM, Imnadze T, Benidze S, Kepuladze O. Successful primary repair in a late presen-
tation of Boerhaave’s syndrome. Case report. Ann Ital Chir. 2021;10:S2239253X21035623.
9. Minnich DJ, Yu P, Bryant AS, Jarrar D, Cerfolio RJ. Management of thoracic esophageal per-
forations. Eur J Cardiothorac Surg. 2011;40(4):931–7. S1010794011000194.
 Part IV
Abdomen
Abdomen: Surgical Anatomy
and General Consideration 13
in Emergency Settings

Sarah Molfino, Giampaolo Bertoloni,
and Gian Luca Baiocchi

13.1 Basic Surgical Abdominal Anatomy

The abdominal cavity has a complex and intricate anatomy. A physician must know
in which area of the abdomen every major structure is located to understand the
clinical presentation of abdominal pathologies and/or in trauma situations to esti-
mate which organs are most likely injured. The general surgeon, especially in emer-
gency situations, uses this knowledge to execute the most advantageous surgical
approach for a particular situation [1].

13.1.1 Surface Anatomy of the Abdomen and Abdominal Wall

13.1.1.1 Boundaries
Superior:
• Xiphoid process
• Costal cartilages of the 7th–10th ribs

S. Molfino (*) · G. Bertoloni

Department of Clinical and Experimental Sciences, Surgical Clinic, University of Brescia,
Brescia, Italy
Third Division of General Surgery, ASST Brescia Civili Hospital, Brescia, Italy
G. L. Baiocchi
Department of Clinical and Experimental Sciences, Surgical Clinic, University of Brescia,
Brescia, Italy
General Surgery, ASST Cremona, Cremona, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 137

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_13
138 S. Molfino et al.

Inferior:
• Pubic bone and pubic symphysis
• Inguinal ligaments
Lateral:
• Superior: inferior aspect of the 10th rib
• Inferior: iliac crest
Landmarks
1 Umbilicus
2 Linea alba: fibrous junction of the right and left rectus muscles that runs down the
midline of the abdomen
3 Semilunar lines: lateral borders of the rectus abdominis muscles.
4 Anterior superior iliac spine
5 Pubic symphysis
6 Inguinal grooves

13.1.1.2 Lines and Planes

• Right and left midclavicular lines
• Subcostal plane
• Transtubercular, or intertubercular, plane

13.1.1.3 Regions of the Abdomen

• Right and left hypochondria
• Epigastrium
• Right and left lateral abdominal regions or flanks
• Umbilical
• Right and left inguinal regions or iliac fossae
• Hypogastrium

13.1.1.4 Abdominal Wall

Layers:
• Skin
• Superficial fascia (subcutaneous tissue): Superficial fatty layer (Camper’s fascia)
and deeper membranous layer (Scarpa’s fascia)
• Anterior fascial layer: Anterior rectus sheath (medial) and external abdominal
oblique fascia (lateral)
• Abdominal muscles: Rectus abdominis–External abdominal oblique–Internal
abdominal oblique–Transversus abdominis
• Posterior fascial layer: Posterior rectus sheath (medial; ends at the arcuate line
midway between umbilicus and pubic symphysis) and transversalis fascia
(lateral)
• Peritoneum
13  Abdomen: Surgical Anatomy and General Consideration in Emergency Settings 139

13.1.1.5 Inguinal Canals

Boundaries:
• Superior: inferior edge of the internal oblique and transverse abdominal muscles
• Inferior: inguinal ligament (continuation of the external abdominal oblique
aponeurosis)
• Anterior: aponeurosis of the abdominal external oblique muscle
• Posterior: transversalis fascia and interfoveolar ligament
Course:
• The inguinal canal is approximately 4  cm long, situated in the lower anterior
abdominal wall, connecting its outer and inner layers above the inguinal liga-
ment (superior anterior iliac spine to pubic tubercle).
• Runs from an upper lateral to an inferior medial direction.
• Inner orifice/deep inguinal ring: evagination of the transversalis fascia (sur-
rounding the spermatic cord as the internal spermatic fascia).
• External orifice/superficial inguinal ring: fissure in the aponeurosis of the
abdominal external oblique muscle.

13.2 Initial Assessment of the Patient with Abdominal Pain

Abdominal pain is the most common reason for a visit to the emergency department
(ED) and is the presenting issue in a high percentage of medicolegal actions against
both general and pediatric physicians. The modern physician should be humbled by
the fact that, despite diagnostic and therapeutic advances (computed tomography
[CT], ultrasonography, and laparoscopy), the misdiagnosis rate of the most com-
mon surgical emergency, acute appendicitis, has changed little over time.

13.2.1 Assessment of the Patient’s Pain [2]

The classic PQRST mnemonic for a complete pain history is as follows:

• P3—Positional, palliating, and provoking factors
• Q—Quality
• R3—Region, radiation, referral
• S—Severity
• T3—Temporal factors (time and mode of onset, progression, previous episodes)
This mnemonic will help to ensure a thorough history, but rigidly following the
above sequence does not allow for a smooth patient interview, so the authors prefer
to ask the patient where they feel the pain (location), what kind of pain it is (charac-
ter), when and how it began (onset), how bad it is (intensity), and where else they
feel it, what makes it worse or better, how it has changed over time, and whether
they have ever had it before.
140 S. Molfino et al.

Embryology determines where a patient will “feel” visceral pain, which is gener-
ally perceived in the midline because afferent impulses from visceral organs are
poorly localized.
Clinicians should seek to distinguish between the dull, poorly localized, aching, or
gnawing pain generated by viscerally innervated organs, compared with the character-
istically “sharp,” more defined and localized somatic pain caused by irritation of the
parietal peritoneum or other somatically innervated structures. Somatic pain is trans-
mitted via the spinal nerves from the parietal peritoneum or mesodermal structures of
the abdominal wall. Noxious stimuli to the parietal peritoneum may be inflammatory
or chemical in nature (e.g., blood, infected peritoneal fluid, and gastric contents).
Acute-onset pain, especially if severe, should prompt immediate concern about a
potential intra-abdominal catastrophe. The foremost consideration would be a vas-
cular emergency such as a ruptured abdominal aortic aneurysm (AAA) or aortic
dissection. Other considerations for pain of acute onset include a perforated ulcer,
volvulus, mesenteric ischemia, and torsion; however, these conditions may also
occur without an acute onset.
The neural pathways give rise to predictable patterns of referred pain and radia-
tion. Kehr’s sign is a classic example where diaphragmatic irritation, usually from
free intraperitoneal blood, causes shoulder pain.
Persistent worsening pain is worrisome, while pain that is improving is typically
favorable. Serious causes of abdominal pain generally present early in their course;
however, delays in presentation can occur, especially in the elderly. Certain patterns
of progression can be diagnostic, such as the migration of pain in appendicitis where
the initial distention of the appendix causes a periumbilical visceral pain that shifts
to the right lower quadrant once the inflammatory process is detected by the somatic
sensors of the parietal peritoneum. Although labeled “colic,” gallbladder pain is
generally not paroxysmal, and it almost never lasts less than 1 h, with an average of
5–16  h duration, and ranging up to 24  h. Small bowel obstruction typically pro-
gresses from an intermittent (“colicky”) pain to more constant pain when distention
occurs. One would only expect somatic pain (arising from transmural ischemia or
perforation contiguous to the parietal peritoneum) late in the course of a bowel
obstruction.
Gastrointestinal and urinary symptoms are the primary focus; however, it is
important to ask about fever and cardiopulmonary symptoms. Associated symptoms
should be placed in the clinical context, including the patient’s age and the current
point in the course of the illness.
With appendicitis, most physicians expect the patient to report anorexia.
However, pooling of the literature indicates that, while this is a discriminatory
symptom, it is only present in 68% of patients with appendicitis. The report of this
symptom decreases to 20–44% in elderly patients with appendicitis.
Vomiting may occur in almost any abdominal disease.
While diarrhea is a frequent accompaniment of more benign abdominal condi-
tions, its presence alone should never rule out serious disease. For example, diarrhea
is common with mesenteric ischemia and is frequently reported in conditions such
as appendicitis.
13  Abdomen: Surgical Anatomy and General Consideration in Emergency Settings 141

Many genitourinary tract diseases can present with abdominal pain. Conversely,
any inflammatory process contiguous to the genitourinary tract (including appendi-
citis, cholecystitis, pancreatitis, or any inflammatory process involving bowel) may
result in both pyuria and dysuria.

13.2.2 Physical Examination

The general appearance of the patient is noted first. An “ill-appearing” patient with
abdominal pain is always of great concern given the variety of potentially lethal
underlying causes. On the other hand, especially in the elderly, the clinician must
not be misled by the well appearing patient who may still have serious underlying
disease. The clinician should take note of the patient’s position, spontaneous move-
ments, respiratory pattern, and facial expression.
Take care of:
• Vital signs
• Abdominal examination (inspection, auscultation, percussion, and palpation)
• Test for peritoneal irritation
Determining the presence or absence of peritonitis is a primary objective of the
abdominal examination; unfortunately, the methods for detecting it are often inac-
curate. Traditional rebound testing is performed by gentle depression of the abdom-
inal wall for approximately 15–30  s with sudden release. The patient is asked
whether the pain was greater with downward pressure or with release. Despite limi-
tations, the test was one of the most useful in a meta-analysis of articles investigat-
ing the diagnosis of appendicitis in children.

13.2.3 Approach to the Unstable Patient [3]

On occasion, a patient with acute abdominal pain will present in extremis. The ill-­
appearing patient with abdominal pain requires immediate attention. This is particu-
larly so in the elderly, as the overall mortality rate for all older patients with acute
abdominal pain ranges from 11% to 14%, and those presenting in an unstable fash-
ion have an even poorer prognosis.
The usual sequence of resuscitation is applied to the unstable abdominal pain
patient with airway control achieved as necessary. Hypotension requires the parallel
process of treatment and an early assessment for life-threatening conditions requir-
ing emergent surgical intervention. Hypotension from blood and fluid loss from the
gastrointestinal tract is usually apparent from the history coupled with a digital
rectal examination. If this evidence is lacking in the patient with abdominal pain,
there needs to be early consideration of third spacing, which can cause enormous
fluid shifts into the bowel lumen or peritoneal space in bowel obstruction or other
intestinal catastrophes. Bedside ultrasonography is an extremely useful diagnostic
adjunct in such patients. In the older patient, hypotension should prompt an
142 S. Molfino et al.

immediate search for an abdominal aortic aneurysm, immediately followed by

sonographic evaluation of the inferior vena cava for intravascular volume status, and
sonography of the heart, pleural, and peritoneal spaces to exclude massive effusions
or evidence of massive pulmonary embolus. Bedside echocardiography will also
identify severe global myocardial depression as a cardiogenic cause of shock. In the
younger patient, a large amount of free fluid detected by ultrasound in an unstable
patient is most commonly due to rupture of an ectopic pregnancy, spleen, or hemor-
rhagic ovarian cyst. An immediate urine pregnancy test will be the first step in dis-
tinguishing these.
The proper place for the unstable patient with an acute abdominal aortic aneu-
rysm is the operating room or, in some centers, the interventional suite for emer-
gency aortic stent placement. Attempts to obtain CT imaging may cause fatal delays
in definitive treatment. With a high clinical index of suspicion (if possible, sup-
ported by emergency bedside ultrasonography), most patients sent directly to sur-
gery will be found to have an acute AAA, and nearly all others will have an
alternative diagnosis that still needs operative intervention.

13.2.4 Diagnostic Studies

Appropriate diagnostic testing is covered in the respective chapters for specific enti-
ties; however, it must be emphasized that there are significant limitations of imaging
and laboratory studies in the evaluation of acute abdominal pain and all diagnostic
tests have a false-negative rate. If the history and physical examination leads to a
high pre-test probability of a disease, a negative test cannot exclude the diagnosis.
For example, the total leukocyte count can be normal in the face of serious infection
such as appendicitis or cholecystitis. CT is frequently used in evaluation of the
patient with abdominal pain. Clinicians are enamored with the recent advances in
the technology that have allowed for improved image resolution and shorter acquisi-
tion times along with coronal and three-dimensional reconstruction. However, it
remains an imperfect test for conditions such as appendicitis and may add little to
the clinical assessment.
Plain abdominal radiographs are of limited utility in the evaluation of acute
abdominal pain. Although they may be helpful (free intraperitoneal air, calcified
aortic aneurysm, air fluid levels in obstruction), other diagnostic studies are almost
always indicated or perform better as the initial testing. If plain radiographs are
utilized, the limitations must be appreciated. For example, a standard upright film
will not demonstrate free air in up to 40% of patients with a perforated ulcer.
The oft repeated axiom of “treat the patient, not the test” certainly applies in the
patient with acute abdominal pain. An unexpected negative test result should prompt
a reassessment of the patient and consideration for observation and repeat examina-
tion for disease progression. Whenever the diagnosis is in question, serial examina-
tion as an inpatient in an observation unit or in the ED is a sound strategy. When a
patient is discharged home after an evaluation for abdominal pain, the authors rec-
ommend instructions to return if the pain worsens, new vomiting or fever occurs, or
13  Abdomen: Surgical Anatomy and General Consideration in Emergency Settings 143

if the pain persists beyond 8–12 h. Such instructions are targeted at ensuring the
return of a patient who has progressed from an early appendicitis or small bowel
obstruction, the two most common surgical entities erroneously discharged
from an ED.

13.3 Some Useful Considerations in Emergency Setting

13.3.1 Timing of Surgery

Emergency surgery is required for many patients suffering from trauma, acute (sur-
gical) disease process, or surgical complications. However, not all emergencies are
equal. Some need surgery as soon as possible, for example, patients with major
intra-abdominal hemorrhage or vascular compromise associated with bowel isch-
emia. Patients with generalized peritonitis might benefit from a short period for
stabilizing the physiology as long as antimicrobial treatment is promptly started,
and the delay does not exceed a couple of hours. The acceptable delay for patients
where prolonged delay might lead to generalized peritonitis and poorer outcome
(acute appendicitis) or more invasive surgical treatment and prolonged hospital stay
(acute cholecystitis), respectively, is more controversial, and the trends seem to go
in opposing directions. Nonoperative management with antibiotic treatment for
acute uncomplicated appendicitis is gaining more favor, whereas early (laparo-
scopic) cholecystectomy for acute cholecystitis or even symptomatic cholelithiasis
is supported by several recent studies. Most surgeons would agree that patients with
non-strangulated small bowel obstructions or infected pancreatic necrosis (unless in
septic shock) do not need to be operated on in the middle of the night, and the same
is true for many other abdominal emergencies. Finally, there are many nonelective
procedures that are performed by emergency surgery teams that are not true emer-
gencies such as changing dressings in open abdomen patients or performing trache-
ostomies for patients from intensive care or acute neurology units. Prioritizing
emergency operations by urgency and using some form of categorization into differ-
ent groups is becoming more common. The so-called traffic light color coding sys-
tem has been used at the Helsinki University hospital for a decade. It consists of
three categories coded red (surgery as soon as possible), orange (surgery within
24 h), and yellow (surgery within 48 h). Only patients with red code are operated on
at nighttime. The majority of emergency surgery is performed during the daytime
(three designated operation tables for emergency surgery) or during the evening
shift ending at 22.00 h. Several studies show that in most patients with a surgical
emergency, an operation performed as soon as possible is beneficial from a medical
point of view, as it reduces complications and length of hospital stay. It saves hospi-
tal resources (every day spent waiting in a surgical ward for an emergency operation
is a wasted day), and patients appreciate not having to wait for surgery longer than
necessary. However, nighttime surgery is expensive and might not be as safe as
surgery performed during regular hours. The solution to the dilemma could include
the following components at least. Emergency surgery should be seen as an equal to
144 S. Molfino et al.

elective surgery, thereby guaranteeing sufficient daytime operating room capacity,

and should probably be separated to an independent “production line” not affected
by unexpected delays in elective procedures requiring substitute personnel from the
emergency surgery teams. Accumulation of patients waiting for emergency surgery
should be minimized by a flexible system that permits adjustments to the inevitable
day-to-day variation in patient numbers [4].

13.3.2 Role of Laparoscopy in Emergency Setting

Abdominal emergencies can also be operated on through the laparoscopic approach:

the approach can be diagnostic laparoscopy, surgery assisted by laparoscopy or
laparotomy directed according to the findings of the laparoscopy. The general con-
traindications refer above all to the state of haemodynamic instability of the patient
and to seriously ill patients (ASA IV). In the absence of any specific counter-­
indications for the specific laparoscopic procedure to be carried out, many abdomi-
nal diseases requiring emergency surgery can be performed with the laparoscopic
approach. The most frequent indications are appendicitis, acute cholecystitis, gas-
troduodenal perforation, occlusion of the small intestine, and some abdominal trau-
mas. With a correct selection of patients and the appropriate experience of the
surgeon, the results are excellent and better than open surgery (less infection of the
wound, complications, hospital stay, and postoperative pain). A detailed explana-
tion is given of the basic aspects of the surgical technique in the most frequent
procedures of emergency laparoscopy [5].

13.3.3 Final Consideration

Patients undergoing emergency abdominal surgery managed by high volume sur-

geons have better survival outcomes. These findings contribute to the ongoing dis-
cussion regarding configuration of emergency surgery services and emphasize the
need for effective clinical governance regarding observed variation in outcomes
within and between institutions [6].

References
1. Henry Gray’s Anatomy of the Human Body. ISBN:8821431320.
2. Abbott J. Pelvic pain: lessons from anatomy and physiology. J Emerg Med. 1990;8:441–7.
3. Silen W. Cope’s early diagnosis of the acute abdomen. In: Principles of diagnosis in acute
abdominal disease. New York: Oxford; 2010. p. 3–17.
4. Leppäniemi A.  What is acceptable delay in emergency abdominal surgery? Scand J Surg.
2013;102:54.
5. The role of laparoscopy in emergency abdominal surgery. ISBN 978-88-470-2326-0 e-ISBN
978-88-470-2327-7. https://doi.org/10.1007/978-­88-­470-­2327-­7. New York: Springer.
6. Nally DM, Sørensen J, Valentelyte G, et al. Volume and in-hospital mortality after emergency
abdominal surgery: a national populationbased study. BMJ Open. 2019;9:e032183. https://doi.
org/10.1136/bmjopen-­2019-­032183.
Acute Abdominal Aorta and Visceral
Vessel Disease 14
Davide Esposito and Elena Giacomelli

14.1 Introduction

Data from the National Hospital Ambulatory Medical Care Survey of 2006
(NHAMCS) reports that abdominal pain is the most common specific principal rea-
son given by adult patients for visiting the Emergency Department after chest
pain [1].
The evaluation of a patient presenting at the emergency department with acute
abdominal aorta or visceral vessel disease is very often difficult since the clinical
diagnosis is made elusive by the non-specificity of the symptoms, such as abdomi-
nal pain, back pain, or hypo/hypertension.

14.2 Acute Abdominal Aorta

Acute disorders of the abdominal aorta include a range of conditions which could
be potentially lethal and require prompt recognition and management. In this sce-
nario, imaging plays a crucial role in rendering it possible to make a precise diagno-
sis. Computed tomography (CT) represents the first-line imaging approach, with
magnetic resonance imaging (MRI) as an alternative method for stable patients who
have a contraindication to iodinated contrast [2].
Acute abdominal aortic syndrome comprises unstable or ruptured aneurysm,
penetrating atherosclerotic ulcer, intramural hematoma (IMH) and dissection, but
also more unusual conditions such as inflammation, infection, traumatic injury,

D. Esposito · E. Giacomelli (*)

Department of Vascular and Endovascular Surgery, Careggi University Hospital of Florence,
Florence, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 145

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_14
146 D. Esposito and E. Giacomelli

fistulization, and occlusion of the abdominal aorta, all of which could likely be cata-
strophic if misdiagnosed.

14.2.1 Abdominal Aortic Aneurysm

An aneurysm is defined as a dilation, more or less circumscribed, of the caliber of

an artery [3]. The current definition of abdominal aortic aneurysm (AAA) is based
on the measurement of the diameter of the abdominal aorta: an aneurysm is consid-
ered a diameter greater than or equal to 3 cm [4]. The prevalence of AAA increases
with age and is most common in men [5]. The segment of aorta most commonly
involved is the infrarenal.
The most threatening complication of an AAA is rupture, with mortality rates
ranging from 70% to 94% [6]. The risk of aneurysm rupture increases with AAA
diameter, aneurysm expansion rate, smoking, and uncontrolled hypertension [7].
Rupture usually presents with a classic clinical manifestation consisting of pain
(abdominal, back or flank), hypotension, and a pulsatile mass.
The suspicion of an aneurysm rupture must be investigated using CT imaging.
The primary imaging findings of AAA rupture include a retroperitoneal hematoma
extending directly from the aneurysm and active extravasation of contrast material
(Fig. 14.1a). In case of impending or contained rupture, the findings may be much
more subtle, including perianeurysmal soft tissue stranding.

a b

c d

Fig. 14.1  CT images of ruptured abdominal aortic aneurysm (a), penetrating atherosclerotic ulcer
(b), intramural hematoma (c), aortic dissection (d)
14  Acute Abdominal Aorta and Visceral Vessel Disease 147

Treatment of an acute or impending rupture can be both endovascular aneurysm

repair (EVAR) and open surgery.
BOX Signs of acute or impending rupture of aneurysms of the abdominal aorta:

Clinical: pain (abdominal, back or flank), hypotension, pulsatile mass.

Diagnostic: retroperitoneal hematoma, active contrast extravasation, perianeu-
rysmal stranding.

14.2.2 Penetrating Atherosclerotic Ulcer

The term penetrating atherosclerotic ulcer (PAU) describes an ulcerating atheroscle-

rotic lesion that penetrates the intima and progresses through the internal elastic
lamina into the media [8]. It is most common in older patients and results from
preexisting atherosclerotic disease most frequently in the middle and distal thirds of
the thoracic aorta. Typically, patients present with acute intense chest pain, often
described as tearing, ripping, migrating, or pulsating [9].
PAU may resolve spontaneously, but can progress to an enlarging IMH, dissec-
tion, subadventitial pseudoaneurysm, or rupture.
On imaging, PAU presents as a focal outpouching of the aortic lumen with asso-
ciated hematoma in the aortic media (Fig. 14.1b).
If the pathology involves the ascending aorta, early/urgent or emergent surgical
intervention is recommended [10]; when it involves the descending aorta, if asymp-
tomatic, aggressive (antihypertensive) medical therapy in combination with close
clinical and radiographic follow-up is recommended [11], if symptomatic or with
signs of progression, endovascular stent-grafting (TEVAR) should be the treatment
of choice [10].
BOX Signs of penetrating atherosclerotic ulcer:

Clinical: acute intense chest pain, described as tearing, ripping, migrating, or

pulsating.
Diagnostic: focal outpouching of the aortic lumen with associated hematoma in
the aortic media.

14.2.3 Intramural Hematoma

IMH is caused by spontaneous rupture of the vasa vasorum into the aortic media
with resultant weakening of the aortic wall. Other theories describing the pathogen-
esis include thrombosis of a dissection lumen, microscopic intimal tears, progres-
sion from a PAU, and traumatic medial injury [8]. Clinical features of IMH are chest
pain radiating to the back and hypertension.
On CT and MR imaging, IMH appears as an eccentric, crescent-shaped collec-
tion of blood in the aortic wall (Fig. 14.1c).
148 D. Esposito and E. Giacomelli

If an IMH involves the ascending aorta, surgical treatment is offered to prevent

rupture and progression to classic aortic dissection. Conservative management is
indicated for an IMH of the descending aorta.
BOX Signs of intramural hematoma:

Clinical: chest pain radiating to the back and hypertension.

Diagnostic: eccentric, crescent-shaped collection of blood in the aortic wall.

14.2.4 Aortic Dissection

Aortic dissection occurs when blood enters the medial layer of the aortic wall
through a tear or penetrating ulcer in the intima and tracks longitudinally along with
the media, forming a second blood-filled channel (false lumen) within the ves-
sel wall.
The most common risk factor for aortic dissection is uncontrolled hypertension,
even if there are other characteristic conditions associated with its development
such as Marfan syndrome, bicuspid aortopathy, vasculitis, cocaine use, and preg-
nancy [12].
Clinical manifestations depend on the location of the dissection: when occurring
proximally in the abdominal aorta, it may involve the mesenteric and/or renal arter-
ies, leading in some cases to end-organ ischemia and causing affected patients to
present with abdominal and/or flank pain; when distally, it may occlude the iliac
and/or femoral arteries, leading to lower extremity ischemia; patients could also
present with paraplegia if the artery of Adamkiewicz is involved.
Abdominal aortic dissection appears on imaging studies as an intimal flap divid-
ing the aorta into true and false lumens. The true lumen typically is smaller than the
false lumen, is surrounded by calcifications when present, and enhances more rap-
idly than the false lumen (Fig. 14.1d).
Treatment options include aggressive blood pressure control with beta-blockers
as they reduce both blood pressure and also heart rate, or immediate surgical repair
depending on the extension of the pathology.
BOX Signs of aortic dissection:

Clinical: if mesenteric and/or renal arteries involved, patients could present with
abdominal and/or flank pain; if iliac and/or femoral arteries involved, lower
extremity ischemia.
Diagnostic: intimal flap dividing the aorta into true and false lumens.

14.3 Abdominal Visceral Vessel Disease

Abdominal visceral vessel diseases are time-sensitive conditions which put perfu-
sion of critical organs at risk, leading to the potential for ischemia, infarction, and
translocation of enteric microbes, bacteremia, and sepsis.
14  Acute Abdominal Aorta and Visceral Vessel Disease 149

In visceral artery conditions, blood flow through these arteries becomes reduced
or blocked. Most often, the narrowing or blockage is caused by thrombosis; more
rarely, visceral artery disease involves aneurysms formation or is secondary to
abdominal traumas.

14.3.1 Mesenteric Ischemia

Mesenteric ischemia refers to vascular compromise of the bowel and its mesentery
that in the acute setting has a very high mortality if not treated promptly.
It presents clinically as a severe abdominal pain that is disproportionate to exam-
ination findings and that responds poorly to analgesia.
Mesenteric ischemia can be classified into acute (most common) or chronic
and specifically, in the acute setting, it could be determined by either arterial
thrombosis/embolism, venous thrombosis, or non-occlusive mesenteric isch-
emia (NOMI).
CT is now the investigation of choice for patients with suspected intestinal isch-
emia, by virtue of its capacity to volumetrically assess the whole abdomen in mul-
tiple vascular phases and to diagnose alternative causes of acute abdominal pain.
Common CT imaging features result from the bowel wall necrosis and perforation
and include: pneumatosis intestinalis (gas in intestinal wall), pneumatosis portalis
(gas in the portal vein or in mesenteric vein), pneumoperitoneum (perforation of the
bowel), submucosal hemorrhage and free fluid in the abdomen [13].
In general, treatment is surgical and depends on the severity and extension of the
ischemia, with the need of bowel viability assessment and eventual necrotic tissue
resection, along with endovascular thrombolysis/thrombectomy when needed.
BOX Signs of mesenteric ischemia:

Clinical: severe abdominal pain that is disproportionate to examination findings

and that responds poorly to analgesia.
Diagnostic: pneumatosis intestinalis, pneumatosis portalis, pneumoperitoneum,
submucosal hemorrhage and free fluid in the abdomen.

14.3.2 Visceral Artery Aneurysms

Visceral artery aneurysms, which include renal and splanchnic lesions, are quite
rare and usually asymptomatic. According to a large case series, 95% of the
visceral artery aneurysms are detected during routine investigation into unre-
lated abdominal symptoms, with splenic and hepatic representing the most com-
mon types; aneurysms that rupture are typically greater than 2  cm, so this is
often considered the threshold for repair in patients with asymptomatic dis-
ease [14].
Most of the times these aneurysms go asymptomatic until the time of rupture,
which is a rare occurrence commonly presenting with abdominal pain.
150 D. Esposito and E. Giacomelli

SVS Clinical Practice Guidelines on the Management of Visceral Aneurysms

Gastric and Gastroepiploic Arteries

Hepatic Artery Repair all aneurysms regardless of size Splenic Artery
• Symptomatic • All pseudoaneurysms
• Size >2cm • Size >3cm
• Growth >0.5cm/year • All sizes in women of
childbearing age
Pancreaticoduodenal and
Gastroduodenal Arteries Celiac Artery
Repair all aneurysms regardless of size • All pseudoaneurysms
• Size >2cm
Renal Artery
Superior Mesenteric Artery • Symptomatic
Repair all aneurysms regardless • Size >3cm
• All sized
of size
- in women of childbearing age
Colic Artery - in patients with refractory
Jejunal and Ileal Arteries hypertension and renal artery
• Symptomatic Repair all aneurysms
regardless of size stenosis
• Size >2cm

Fig. 14.2  Schematic representation of SVS Clinical Practice Guidelines on the Management of
Visceral Aneurysms [15]

Focusing on splenic artery aneurysms, there is an increased prevalence of this

disease in women, particularly those who are multiparous, so a high index of suspi-
cion must be taken in such scenarios.
Hepatic artery aneurysms instead are more common in men and are typically
associated to vascular diseases such as fibromuscular dysplasia and polyarteritis
nodosa; unruptured hepatic artery aneurysms could cause symptoms secondary to
compression on the biliary tree.
Renal artery aneurysms are not infrequently bilateral and mostly of saccular type
occurring prevalently at the bifurcation of the main renal artery or first-order branch.
Visceral vessel aneurysms appear on CT imaging as contrast-filled outpouching
in the course of the artery.
Treatment recommendations vary according to the different types of visceral
artery involved and are schematically reassumed in Fig. 14.2 [15].
BOX Signs of visceral artery aneurysms:

Clinical: most of the times asymptomatic, unless nearby compression or rupture.

Diagnostic: contrast-filled outpouching in the course of the artery.

References
1. Pitts SR, Niska RW, Xu J, Burt CW. National Hospital Ambulatory Medical Care Survey: 2006
emergency department summary. Natl Health Stat Rep. 2008;7:1–38.
2. Mellnick VM, Heiken JP. The acute abdominal aorta. Radiol Clin N Am. 2015;53(6):1209–24.
3. Johnston KW, Rutherford RB, Tilson MD, Shah DM, Hollier L, Stanley JC. Suggested stan-
dards for reporting on arterial aneurysms. Subcommittee on Reporting Standards for Arterial
Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and
14  Acute Abdominal Aorta and Visceral Vessel Disease 151

North American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg.
1991;13(3):452–8.
4. Wanhainen A, Themudo R, Ahlström H, Lind L, Johansson L. Thoracic and abdominal aortic
dimension in 70-year-old men and women - a population-based whole-body magnetic reso-
nance imaging (MRI) study. J Vasc Surg. 2008;47(3):504–12.
5. Bengtsson H, Bergqvist D, Sternby NH. Increasing prevalence of abdominal aortic aneurysms.
A necropsy study. Eur J Surg. 1992;158(1):19–23.
6. Assar AN, Zarins CK. Ruptured abdominal aortic aneurysm: a surgical emergency with many
clinical presentations. Postgrad Med J. 2009;85(1003):268–73.
7. Aggarwal S, Qamar A, Sharma V, Sharma A. Abdominal aortic aneurysm: a comprehensive
review. Exp Clin Cardiol. 2011;16(1):11–5.
8. Ko JP, Goldstein JM, Latson LA, Azour L, Gozansky EK, Moore W, Patel S, Hutchinson
B.  Chest CT angiography for acute aortic pathologic conditions: pearls and pitfalls.
Radiographics. 2021;41(2):399–424.
9. Lansman SL, Saunders PC, Malekan R, Spielvogel D.  Acute aortic syndrome. J Thorac
Cardiovasc Surg. 2010;140(6 Suppl):S92–7. discussion S142–S146.
10. Baikoussis NG, Apostolakis EE. Penetrating atherosclerotic ulcer of the thoracic aorta: diag-
nosis and treatment. Hell J Cardiol. 2010;51(2):153–7.
11. Khosa F, Krinsky G, Macari M, Yucel EK, Berland LL.  Managing incidental findings on
abdominal and pelvic CT and MRI, Part 2: white paper of the ACR Incidental Findings
Committee II on vascular findings. J Am Coll Radiol. 2013;10(10):789–94.
12. Bhalla S, Menias CO, Heiken JP. CT of acute abdominal aortic disorders. Radiol Clin N Am.
2003;41(6):1153–69.
13. Furukawa A, Kanasaki S, Kono N, Wakamiya M, Tanaka T, Takahashi M, Murata K.  CT
diagnosis of acute mesenteric ischemia from various causes. AJR Am J Roentgenol.
2009;192(2):408–16.
14. Pulli R, Dorigo W, Troisi N, Pratesi G, Innocenti AA, Pratesi C. Surgical treatment of visceral
artery aneurysms: A 25-year experience. J Vasc Surg. 2008;48(2):334–42.
15. Chaer RA, Abularrage CJ, Coleman DM, Eslami MH, Kashyap VS, Rockman C, Murad
MH. The Society for Vascular Surgery clinical practice guidelines on the management of vis-
ceral aneurysms. J Vasc Surg. 2020;72(1S):3S–39S.
Acute Abdomen and Acute Abdominal
Conditions 15
Emanuele Botteri, Gianmaria Casoni Pattacini,
Alessio Giordano, and Francesca Ratti

15.1 Acute Calculus Cholecystitis

15.1.1 Introduction

The estimated overall prevalence of gallstones is 10–15% in the general population,

with some differences across countries. Between 20 and 40% of patients with gall-
stones will develop gallstone-related complications, with an incidence of 1–3%
annually; acute calculus cholecystitis (ACC) is the first clinical presentation in
10–15% of the cases [1, 2]. In 95% of cases ACC is caused by gallstones, while in
the remaining 5% of cases it can be associated with cardiovascular disorders, fol-
lowing trauma or severe burns, following abdominal or cardiac surgery, in pro-
longed fasting typical of critically ill patients, in severe immunodeficiencies, in
elderly and diabetic patients [3].

E. Botteri (*)
General Surgery Unit, ASST Spedali Civili di Brescia, Brescia, Italy
G. C. Pattacini
General Surgery, Emergency Surgery and New Technologies, Baggiovara’s Hospital,
Modena, Italy
A. Giordano
General Surgery Unit, Azienda ASL Toscana Centro, Nuovo Ospedale “S. Stefano”,
Prato, Italy
F. Ratti
Hepatobiliary Surgery Unit, Ospedale San Raffaele, Milan, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 153

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_15
154 E. Botteri et al.

15.1.2 Diagnostic Criteria for ACC

The useful features for the diagnosis of ACC are:

• History and clinical examination: fever, right upper quadrant pain or tenderness,
vomiting or food intolerance; Murphy’s sign
• Laboratory tests: elevated C-reactive protein, elevated white blood cell count
• Imaging: signs suggestive of gallbladder inflammation

The Tokyo Guidelines 2013 and 2018 (TG13/TG18) [4, 5] defined an algorithm
that allows to better define a suspected or certain diagnosis of acute cholecystitis
following 3 diagnostic criteria (Table 15.1).

15.1.3 Which Initial Imaging Technique Should Be Used in Case

of a Suspected Diagnosis of ACC?

The generally accepted imaging findings of acute cholecystitis are thickening of the
gallbladder wall (≥4 mm), enlargement of the gallbladder (long axis ≥8 cm, short
axis ≥4 cm), gallstones or retained debris, fluid accumulation around the gallblad-
der, and linear shadows in the fatty tissue around the gallbladder [6]. Abdominal US
should be the first method of diagnostic imaging used for acute cholecystitis.
However, as a causative stone in the gallbladder or bile duct may not always be
clearly identifiable on abdominal US and the diagnosis of gangrenous cholecystitis
may be difficult [7], it is also recommended that contrast-enhanced CT or MRI be
performed if required [8].

15.1.4 Stratification of the Risk and Severity of ACC

The TG13 confirmed by TG18 made it possible to classify ACC according to 3

degrees of severity (mild, moderate, and severe) taking into consideration specific
biohumoral and clinical parameters (Table 15.2).

Table 15.1  TG18/TG13 diagnostic criteria for acute cholecystitis [4, 5]

A. Local signs of inflammation, etc.

(1) Murphy’s sign, (2) RUQ mass/pain/tenderness
B. Systemic signs of inflammation, etc.
(1) Fever, (2) elevated CRP, (3) elevated WBC count
C. Imaging findings
Imaging findings characteristic of acute cholecystitis
Suspected diagnosis: one item in A + one item in B
Definite diagnosis: one item in A + one item in B + C
15  Acute Abdomen and Acute Abdominal Conditions 155

Table 15.2  TG ACC severity grading [9]

Grade I Grade II Grade III
Mild Moderate Severe
Patient with no signs of Associated with one of the Associated with dysfunction
organ dysfunction and with following conditions: of one of the following
mild inflammation of the 1. WBC >18,000/mm3 bodies:
gallbladder 2. Palpable gallbladder in 1. Cardiovascular
right hypochondrium dysfunction:
3. Duration of symptoms >72 h hypotension that requires
4. Marked local inflammation dopamine ≥5 μg/kg/min or
(gangrenous cholecystitis, liver other vasoactive amines
abscess, biliary peritonitis, 2. Neurological
cholecystitis emphysematous) dysfunction: decrease in
the level of consciousness
3. Respiratory dysfunction:
PaO2/FiO2<300
4. Renal dysfunction:
Oliguria, Creatinine
>2.0 mg / dl
5. Hepatic dysfunction:
PT-INR >1.5
6. Blood dysfunctions: PLT
<100,000/mm3

15.1.5 When ACC Was Associated Common Bile Duct Stones:

Which Tools to Use for Suspicion and Diagnosis
at Presentation?

Choledocholithiasis, i.e., the presence of common bile duct stones (CBDS), is

reported to occur in 10% to 20% of gallstone cases, with lower incidence, rang-
ing from 5 to 15%, in case of ACC [10]. In order to assess the risk for CBDS,
WSES guidelines [11] suggest to perform liver function tests (LFTs), including
ALT, AST, bilirubin, ALP, GGT, and abdominal US in all patients with ACC. The
visualization of a stone in the common bile duct at transabdominal US was a
predictor of CBDS in patients with ACC while an increased diameter of com-
mon bile duct was an indirect sign of stone presence but was not sufficient to
identify ACC patients with CBDS.  The American Society of Gastrointestinal
Endoscopy and the Society of American of Gastrointestinal Endoscopic
Surgeons combined the published validated clinical scores and proposed a risk
stratification of CBDS in three different classes, defined as follows: low risk
(<10%), moderate risk (10–50%), and high risk (> 50%) of CBDS [12] (Tables
15.3 and 15.4). This proposed classification has clear clinical implications:
patients with a low risk of CBDS should be operated without further investiga-
tion; patients with moderate risk should be evaluated with a second-­level exami-
nation, either preoperatively with endoscopic US (EUS) or magnetic resonance
cholangiopancreatography (MRCP) or intraoperatively with laparoscopic US
156 E. Botteri et al.

Table 15.3  Predictive CBDS factors [12]

Very strong factors Strong factors Moderate factors
Evidence of stones in CBDS during • Common bile duct • Abnormal liver
ultrasound of the abdomen diameter> 6 mm tests
• Total bilirubin >4 mg/dl • Age >55 years
• Direct bilirubin • Clinical
>1.8–4 mg/dl pancreatitis

Table 15.4  Risk classes for CBDS [12]

High risk Moderate risk Low risk
Very strong factors presence Strong and moderate factors presence No predictive factors

(LUS) or intraoperative cholangiography (IOC), in order to select patients who

need stone removal; finally, according to local expertise, laparoscopic transcys-
tic CBD exploration is a valuable option. Patients with high risk of CBDS
should undergo pre- or intra- or postoperative endoscopic retrograde cholangio-­
pancreatography (ERCP) depending on local expertise and availability.
CBDS could be removed with several techniques and a variation of timing: pre-
operative ERCP with sphincterotomy, intraoperative ERCP with sphincterotomy,
laparoscopic or open common bile duct exploration, postoperative ERCP with
sphincterotomy. A systematic review assessed the differences between these tech-
niques [13]. No differences in terms of morbidity, mortality, and success rate were
reported. Therefore, these techniques can be considered suitable options, depending
on local expertise and availability.

15.1.6 Surgical Treatment of ACC

The laparoscopic cholecystectomy was recommended as the first-line treatment for

patients with ACC [6, 7]. The laparoscopic approach should always be attempted
except in cases of absolute anesthetic contraindications or severe hemodynamic
instability.
Laparoscopic cholecystectomy in acute cholecystitis was associated with a
reduction in mortality rates, infectious complications of the surgical site and
pneumonia and a clear reduction in the average postoperative hospital stay,
when compared to the traditional open approach [14–16]. The subtotal chole-
cystectomy is an option when the critical view of safety cannot be obtained. It
is preferable to perform a cholecystectomy as soon as possible, after patient
admission, preferably within 72 h of the onset of symptoms [4, 5] or in any case
within 7  days from hospital admission and within 10  days from the onset of
symptoms.
15  Acute Abdomen and Acute Abdominal Conditions 157

15.1.7 Alternative Treatment for Patients with ACC: Observation

and Techniques for Gallbladder Drainage

A RCT with long-term follow-up of 14 years showed that about 30% of patients
treated conservatively developed recurrent gallstone-related complications and 60%
of patients had undergone cholecystectomy subsequently [17]. TG13 on ACC [6, 7]
considered percutaneous transhepatic gallbladder drainage (PTGBD) as mandatory
for patients with severe-grade ACC and also suggested its use in the moderate grade
if conservative treatment fails. The revised TG18, based on recent studies, proposed
that severe-grade cholecystitis, under certain strict criteria, may be treated with
laparoscopic cholecystectomy [5, 18]. Gallbladder drainage decompresses the
infected bile or pus in the gallbladder, removing the infected collection without
removing the gallbladder. Gallbladder drainage may be an option in patients who
failed conservative management after a variable time of 24–48 h and who present
with strict contraindications for surgery.

15.1.8 Antibiotic Therapy

Biliary penetration of different antibiotics (indicated as the ratio of bile-to-serum

concentrations) are listed in Table  15.5 [19], suggested by 2020 WSES update
guidelines.

Table 15.5  Antibiotics biliary penetration

Good penetration efficiency antibiotics Bile/ Low penetration efficiency antibiotics Bile/
Serum (≥5) Serum (<5)
Piperacillin/Tazobactam Cefotaxime
Tigecycline Meropenem
Ciprofloxacin Ceftazidime
Ampicillin/Sulbactam Vancomycin
Ceftriaxone Amikacin
Levofloxacin Gentamicin
Penicillin G Cefepime
Amoxicillin/Clavulanate Imipenem
158 E. Botteri et al.

15.2 Acute Colonic Diverticulitis

15.2.1 Introduction

Acute left-sided colonic diverticulosis is common in Western countries with its

prevalence increasing throughout the world, which is likely due to changes in life-
style [20]. Although left-sided colonic diverticulosis remains more common among
elderly patients, a dramatic rise of its incidence has been seen in younger age groups
in recent years [21]. Recent evidence suggests that lifetime risk of developing acute
left-sided colonic diverticulitis (ALCD) is about 4% among patients with diverticu-
losis [22].

15.2.2 Which Classification Should Be Used in Patients

with ALCD?

A proposal for a CT-guided classification of ALCD was published in 2015 by the

WSES acute diverticulitis working group [23] and confirmed by recent update of
this guideline [24]. It may guide clinicians in the management of acute diverticulitis
and may be universally accepted for day-to-day practice (Table 15.6).

15.2.3 The Diagnosis of ALCD

In patients with suspected ALCD, a complete assessment of the patients using clini-
cal history, signs, laboratorial inflammation markers, and radiological findings was
performed. Clinical findings of patients having ALCD include acute pain or tender-
ness in the left lower quadrant that may be associated with increased inflammatory
markers, including C-reactive protein (CRP) and white blood cell count (WBC).
CRP has been identified as a useful biomarker of inflammation, and it may be useful
in the prediction of the clinical severity of acute diverticulitis as demonstrated by
several recent studies [25]. CT is the gold standard for both the diagnosis and the
staging of patients with ALCD due to its excellent sensitivity and specificity [26].

Table 15.6  WSES acute diverticulitis classification [24]

Uncomplicated acute diverticulitis Complicated acute diverticulitis
Stage 0: Diverticula, thickening of • Stage 1a: Pericolic air bubbles or small amount of
the wall, increased density of the pericolic fluid without abscess (within 5 cm from
pericolic fat inflammed bowel segment)
• Stage 1b: Abscess ≤4 cm
• Stage 2a: Abscess >4 cm
• Stage 2b: Distant gas (>5 cm from inflammed bowel
segment)
Stage 3: Diffuse fluid without distant free gas
Stage 4: Diffuse fluid with distant free gas
15  Acute Abdomen and Acute Abdominal Conditions 159

CT scan can also rule out other diagnoses such as ovarian pathology, or leaking
aortic or iliac aneurysm. CT findings in patients with ALCD may include diverticu-
losis with associated colon wall thickening, fat stranding, phlegmon, extraluminal
gas, abscess formation, or intra-abdominal free fluid CT criteria may also be used to
determine the grade of severity and may drive treatment planning of patients [27].
US is a real-time dynamic examination with wide availability and easy accessibility
[28]. Its limitations include operator dependency, poor assessment in obese patients,
and difficulty in the detection of free gas and deeply located abscesses [29].

15.2.4 The Nonoperative Treatment

15.2.4.1 Stage 0: Uncomplicated Acute Diverticulitis

Uncomplicated acute diverticulitis is defined as localized diverticular inflammation
without any abscess or perforation. In recent years, several studies demonstrated
that antimicrobial treatment was not superior to withholding antibiotic therapy, in
terms of clinical resolution, in patients with mild unperforated diverticulitis [30].
The current consensus is that uncomplicated acute diverticulitis may be a self-­
limiting condition in which local host defenses can manage the inflammation with-
out antibiotics in immunocompetent patients. In this context, antibiotics are not
necessary in the treatment of uncomplicated disease [24]. If antibiotic therapy is
necessary, oral administration of antibiotics may be equally as effective as intrave-
nous administration. An expeditious switch from intravenous to oral may allow a
rapid patient discharge [31]. Patients with uncomplicated acute diverticulitis symp-
toms without significant comorbidities, who are able to take fluids orally and man-
age themselves at home, can be treated as outpatients. They should be re-evaluated
within 7  days from the time of the diagnosis. However, if the clinical condition
deteriorates, re-evaluation should be carried out earlier. Patients with significant
comorbidities and unable to take fluids orally should be treated in hospital with
intravenous fluids.

15.2.4.2 Stage 1 and 2: Locally Complicated Acute Diverticulitis

Approximately 15–20% of patients admitted with acute diverticulitis have an
abscess on CT scan [32]. In presence of pericolic air bubbles, small amount of peri-
colic fluid without abscess (within 5 cm from inflammed bowel segment) (Stage 1a)
and in presence of abscess (Stage 1b or 2a) the treatment required was always anti-
biotic therapy. If the abscess is limited in size (Stage 1b), systemic antibiotic ther-
apy alone is considered safe and effective in removing the abscess and solving acute
inflammation with a pooled failure rate of 20% and a mortality rate of 0.6% [33].
The size of 4–5 cm may be a reasonable limit between antibiotic treatment alone,
versus percutaneous drainage combined with antibiotic treatment in the manage-
ment of diverticular abscesses [34]. A high suspicion for surgical control of the
septic source should be maintained and a surgical treatment should be performed if
the patient shows a worsening of inflammatory signs or the abscess does not reduce
with medical therapy.
160 E. Botteri et al.

15.2.4.3 Stage 2b: The Role of Nonoperative Treatment

Although most patients hospitalized for acute diverticulitis can be managed by non-
operative treatment, up to 25% may require urgent operative intervention [35].
Highly selected group of patients at this stage may be treated by conservative treat-
ment. However, it may be associated with a significant failure rate (57–60%) and a
careful clinical and CT monitoring is mandatory [36]. Moreover, nearly 60%
patients with distant intraperitoneal gas were primarily treated by surgery.

15.2.5 Operative Treatment

15.2.5.1 Stage 3 and 4

The recent update WSES guidelines [24] recommend Hartmann’s Procedure (HP)
for managing diffuse peritonitis in critically ill patients and in selected patients with
multiple comorbidities. Whereas in clinically stable patients with no comorbidities
suggest primary resection with anastomosis with or without a diverting stoma. The
same authors suggest to perform an emergency laparoscopic sigmoidectomy only if
technical skills and equipment are available. In fact, laparoscopic sigmoidectomy
for diverticulitis had initially been confined to the elective setting. A damage control
surgical strategy may be useful for patients in physiological extremis from abdomi-
nal sepsis [37]. The initial surgery focuses on control of the sepsis, and a subsequent
operation deals with the anatomical restoration of the gastrointestinal tract, after a
period of physiological resuscitation. Laparoscopic lavage and drainage can poten-
tially avoid a stoma in patients with diffuse peritonitis. It consists of the laparo-
scopic aspiration of pus followed by abdominal lavage and the placement of
abdominal drains, which remain for many days after the procedure. However, it
cannot be considered the first-line treatment in patients with diverticular peritonitis,
as confirmed by the last WSES guidelines [24].

15.2.6 The Planning Elective Resection in Cases of Acute

Diverticulitis Treated Nonoperatively

Currently, the decision to perform an elective resection after one or more episodes of
AD should be undertaken on a case-by-case basis, considering risk factors, complica-
tions, age, and severity of episodes as well as the patient’s personal circumstances and
comorbidities (e.g., immunosuppressed patients). In particular the WSES suggest
planning of an elective sigmoid resection after a single episode of ALCD treated con-
servatively in high-risk patients, such as immunocompromised patients [24].

15.2.7 Antibiotic Therapy

The most common organisms that cause diverticulitis are E. coli, K. pneumoniae,
and B. fragilis; thus, empiric therapy should at a minimum cover these organisms.
Empiric therapy should also be guided by the severity of illness of the patient and
15  Acute Abdomen and Acute Abdominal Conditions 161

the extent of disease. Antibiotic therapy plays an important role in the management
of complicated acute diverticulitis. Typically, it is an empiric antibiotic treatment.
The regimen should depend on the severity of infection, the pathogens presumed to
be involved, and the risk factors indicative of major resistance patterns. Patients
who have signs of sepsis beyond 5 to 7 days of adequate antibiotic treatment warrant
aggressive diagnostic investigation in search of a reservoir of infection. For patients
with complicated diverticulitis with an abscess, fistula, obstruction, or perforation,
four therapy with cefazolin, cefuroxime, or ceftriaxone, all plus metronidazole or
ampicillin/sulbactam alone or ertapenem can be used. For patients with complicated
diverticulitis associated with sepsis, consider broader coverage for Enterobacteriaceae
and Pseudomonas with piperacillin/tazobactam or cefepime plus metronidazole.
For patients with severe penicillin allergies, consider fluoroquinolone or aztreonam-­
based regimens, making sure to include anaerobic coverage unless moxifloxacin is
used. Moxifloxacin has anaerobic activity; thus, addition of metronidazole is not
needed when using this agent. Vancomycin should be added to ciprofloxacin and
aztreonam in patients presenting with sepsis as these agents do not have Gram-­
positive activity to cover streptococci or enterococci.

15.3 Sigmoid Volvulus

15.3.1 Introduction

The term “volvulus” identifies the torsion of a segment of the gastrointestinal tract
(from Latin “volvēre,” meaning “to roll or twist”). The incidence of SV varies
worldwide. High incidence has been reported in regions such as Latin America,
Africa, Eastern Europe, Scandinavia, Russia, Middle East, Pakistan, and India,
where this condition has been defined as endemic [38]. In these regions, sigmoid
volvulus accounts for 20 to 54% of intestinal obstructions as opposed to low-­
incidence areas such as North America, Western Europe, and Australia, where SV
accounts for 3–5% of intestinal obstructions [39].

15.3.2 Diagnosis

Common investigations include abdominal X-ray, contrast enema, or a CT scan,

while endoscopy serves as a diagnostic and therapeutic technique and will be dis-
cussed in detail later in this chapter. Diagnostic accuracy of abdominal X-ray ranges
from 57 to 90% [40]. Classic radiological findings include a markedly distended
ahaustral sigmoid loop, that appears as a “coffee bean” (also known as “bent inner
tube sign”) with its apex projected under the left hemidiaphragm, which has a high
specificity, although it is not always present [41]. Other highly specific radiological
signs are the convergence of three radiopaque lines to the left inferior quadrant
(Frimann-Dahl sign), and the identification of the sigmoid colon above the trans-
verse colon. CT scan, albeit seldom required for diagnosis, has a high accuracy in
detecting SV [42], with a sensitivity of 100% and a specificity >90%, showing a
162 E. Botteri et al.

whirled sigmoid pedicle, and is currently the preferred diagnostic study modality
due to its rapidity and availability. Moreover, it can detect intestinal pneumatosis
that appears as air bubbles within the bowel wall as a sign of sigmoid ischemia [43].
Endoscopic findings include a mucosal twisting with obstruction at the rectosig-
moid junction.

15.3.3 Management

15.3.3.1 Nonoperative Treatment

Recently, the American Society for Gastrointestinal Endoscopy (ASGE) pro-
duced practice guidelines on the role of endoscopy in the management of colonic
volvulus [44].
Patients with signs of complicated SV (peritonitis or perforation), recurrent vol-
vulus, or unsuccessful nonoperative management are not eligible for endoscopic
decompression and should be immediately referred for surgical management [45].
For patients who are eligible for nonoperative management, endoscopic deten-
tion represents the procedure of choice for SV decompression [46].
Endoscopic reduction is successful in 40–90% of cases [47, 48]. After successful
detorsion of SV, elective surgical treatment should be strongly considered during
the index admission if the patient can tolerate it after adequate preparation, since
recurrence rates as high as 86% have been reported [48] and emergency surgery is
associated with a considerable mortality risk.

15.3.4 Operative Treatment

15.3.4.1 Urgent Setting

Two possible scenarios represent an absolute indication for urgent surgical manage-
ment: endoscopic management failure or the impossibility to perform it; suspicion
or evidence of colonic ischemia, perforation or clinical findings suggestive of peri-
tonitis and septic shock [46].
Surgical resection of the involved colonic segment is generally recommended,
since simple detorsion carries a high mortality and recurrence risk [46].
The decision to perform a Hartmann’s procedure, or a primary colorectal anasto-
mosis with or without proximal diversion, is currently controversial.
Currently available data does not support the use of one technique over the other,
and the decision on which approach to adopt highly depends on the surgeon’s judge-
ment. Nonetheless, several factors should be taken into account when deciding to
perform an anastomosis, including patient’s hemodynamic status, septic status,
comorbidities, medications, functional status, intraoperative findings, and tissues
viability.
15  Acute Abdomen and Acute Abdominal Conditions 163

15.3.4.2 Elective Setting

If nonoperative management is successful and the patient’s surgical risk is reason-
able, current consensus is that surgical intervention should be performed within
2 days of SV reduction or within the index admission [46].
Among the number of procedures that have been proposed in this setting (includ-
ing Hartmann’s resection, resection and anastomosis, detorsion alone, detorsion and
colopexy and percutaneous colostomy), resection of the redundant sigmoid colon
with primary anastomosis seems to have the best results in terms of preventing
recurrence [45, 46].

15.4 Acute Appendicitis

15.4.1 Introduction

In young people, acute appendicitis (AA) is one of the most common cause of surgi-
cal acute abdomen. Lifetime risk of AA is 8.6% for male and 6.9% for women [49].
The peak of incidence is between 10 and 20 years old. Every year about 50,000 of
appendectomies are performed in the UK and 300,000 in the USA. In our country
the annual incidence of AA is 0.2%. The mortality for AA is 0.3% for uncompli-
cated conditions, but this percentage rises up to 1.7% in the complicated forms. AA
can hide the presence of malignancies and often the onset symptoms are in 50% of
appendiceal neoplasms, in 40% of cecum colon cancers and in 15% of whole colon
cancers AA represents the onset condition [50].

15.4.2 Classification

There are several classifications for AA, but the most recent is proposed by Gomes
et al. [51] and it is based on intraoperative findings:

• Non-complicated Acute Appendicitis:

–– Grade 0: Normal Looking Appendix (Endoappendicitis – Periappendicitis)
–– Grade 1: Inflamed Appendix (Hyperemia, edema with or without fibrin, with-
out or little pericolic fluid)
• Complicated Acute Appendicitis:
–– Grade 2: Necrosis A Segmental (without or little pericolic fluid)
B Base Necrosis (without or little pericolic fluid)
–– Grade 3: Inflammatory tumor A Phlegmon
B Abscess <5 cm
C Abscess >5 cm without peritoneal free air
–– Grade 4: Perforated diffuse peritonitis with or without peritoneal free air
164 E. Botteri et al.

15.4.3 Diagnosis and Indication

Symptoms and Sign [52]:

• Right Iliac Fossa (RIF) pain 91.2% (looking for: Rovsing’s sign, Psoas’ sign,
Obturator sign)
• RIF tenderness or RIF rebound tenderness 69.9%
• Diffuse rebound tenderness or muscular defense 11.7%
• Vomiting 42%
• Fever 24.7%
• White Blood Cell (WBC) count >10,000 GB 24.7%
• CRP >10 mg/l 46.1%

15.4.4 Diagnostic Scores (Tables 15.7 and 15.8)

15.4.5 Therapy

The “gold standard” for the treatment of AA is appendectomy. If experienced team

and equipment are present, laparoscopic appendectomy (LA) should represent the
first choice since it offers advantages in terms of less pain, reduced LOS, lower occur-
rence of surgical site infection (SSI), earlier return to work, and overall costs. LA
shows clear benefit in the treatment of obese or elderly patients and those with comor-
bidities. Several data from literature found LA more beneficial and cost-­effective than
open surgery also for complicated AA [52]. Nonoperative management with antibi-
otic therapy can be successful in selected patients in order to avoid surgery. This
approach must be proposed only to patients with low risk of complicated AA, often at
first admission for RIF pain. The patients should receive initial intravenous antibiotics
with subsequent conversion to oral treatment. The clinical monitoring should continue
until the symptoms disappear. The risk of recurrence is up to 38%.

Table 15.7 Alvarado Alvarado score

Score [53] Feature Score
Migration of pain 1
Anorexia 1
Nausea 1
Tenderness in right lower quadrant 2
Rebound pain 1
Elevated temperature 1
Leukocytosis 2
Shift of white blood cell count to the left 1
Total 10
<5 Sensibility, exclusion of AA 99% (IC 95%, 97–99%)
15  Acute Abdomen and Acute Abdominal Conditions 165

Table 15.8  Appendicitis Inflammatory Response (AIR) [54]

Variables Score
Vomiting 1
Right iliac fossa pain 1
White blood cell count
• 10.000–14.000 /dl 1
• ≥15.000/dl 2
CRP
• 10–49 g/L 1
• ≥50 g/L 2
Polymorphonuclear leukocytes
• 70–84% 1
• ≥85% 2
Pyrexal (>38.5 °C) 1
Rebound tenderness or guarding
• Light 1
• Medium 2
• Strong 3
<4 Sensibility, exclusion of AA 96% >8 specificity, diagnosis of AA 99%

15.4.6 Tips and Tricks for Laparoscopic Appendectomy

15.4.6.1 Patients Position

Supine, general anesthesia.
First operator on the left side.

15.4.6.2 Trocars Position

• Hasson’s trocar umbilical
• 5 mm Left iliac fossa
• 5 mm–10 mm suprapubic

15.4.6.3 Diagnostic Laparoscopy

• Abdominal fluid (ascites, purulent, fecaloid)
• Gallbladder disease
• Gynecological disease
• Meckel diverticulum
• Other?

15.4.6.4 Mesoappendix Dissection

Monopolar electrocoagulation and bipolar energy are the most cost-effective
techniques.
High energy devices can be used without clear advantages.
166 E. Botteri et al.

15.4.6.5 Stapler vs Endoloop for Stump Closure

The choice should be individualized on the basis of cecum and appendicular stump
condition. If it were possible to use both, endoloops might be preferred for lowering
the costs but operative time maybe longer.

15.4.6.6 Vesical Catheter

It should be placed after general anesthesia and remove before the awakening. Its
role is to protect the bladder during the insertion of suprapubic trocar.

15.4.6.7 Drainage
The choice should be individualized based on intraoperative findings.

15.4.6.8 SILA (Single Incision Laparoscopic Appendectomy)

Only for cosmetic intent in center with adequate experience.

Inclusion criteria for SILA:

• Normal weight female
• Uncomplicated appendicitis
• Without risk factor for incisional hernia (diabetes, smoke, umbilical hernia, mid-
line diastasis)

15.5 Acute Presentation of Abdominal Wall Disease

15.5.1 Epidemiology and Clinical Presentation

The wall abdominal diseases are traditionally divided into three categories:
• Primitive: arising from a weakness of abdominal wall
• Recurrent: occurring after surgery for a primitive hernia
• Incisional hernia: occurring along the course of a surgical scar

Lifetime risk of groin hernia occurrence is 27–43% for male and 3–6% for
female [55]. The reasons that lead a patient to emergency ward are:

• Swelling and pain localized in the hernia area

• Irreducibility
• Irreducibility with pain (suspicion of incarceration)
• Occlusion

15.5.2 Diagnosis

15.5.2.1 Blood Exam

• Complete blood count: leukocytosis
• Lactate and CRP: high level
15  Acute Abdomen and Acute Abdominal Conditions 167

• Hepatic function
• Kidney function
• Coagulation

15.5.2.2 Radiological Exams

• US in the hernia area and abdominal
• Abdominal and chest RX
• Enhanced CT scan with contrast

If surgeon is involved in urgent consultation for abdominal wall disease, there

will be three ways he can take:
• Complete resolution of the problem and refer the patient to elective surgery. The
reduction maneuverers are successful. The pain is restored and the laboratory test
or radiological finding is normal.
• Resolution of the problem and refer the patient to deferred urgency. The reduc-
tion maneuverers are successful but the pain is still present. Probably the
patients have had other similar episodes in their life. The laboratory test or
radiological finding is not normal and may show inflammation pattern or
abdominal effusion.
• Failure of conservative approach and emergency surgery. The reduction maneu-
verers are not successful. This approach must be chosen in the presence of a high
suspect of bowl ischemia or confirmed by CT scan.

15.5.3 Surgery for Hernias

The steps during emergency surgery for hernia are:

• Isolation of the hernia content
• Check of the viability of the hernia content with possible resection (bowel or
omentum)
• Reduction of the hernia content
• Defect closure (with or without mesh repair)

15.5.4 Surgery for Urgent Groin Hernia

In surgical ward, the first attempt worth making is manual reduction.

This procedure could cause excruciating pain then the aid of a mild sedation can
increase the success rate. In the absence of intestinal ischemic suffering, the treat-
ment of choice is anterior approach with mesh repair. The viability of the content
can be evaluated intraoperatively through a small incision in the peritoneal sac. This
maneuver allows the collection of peritoneal fluid or the resection of a necrotic tract
of omentum. If the effusion is purulent or fecal and if there is high suspect of bowel
involvement, the abdominal cavity must be controlled by laparoscopy or laparot-
omy. The main contraindications to diagnostic laparoscopy are related to the
168 E. Botteri et al.

patient’s hemodynamic status, the bowel distension, and the low laparoscopic expe-
rience of the surgical team. In case of clear fecal contamination, the mesh repair
must be avoided.

15.5.5 Incisional and Other Midline Hernias

The urgent treatment of midline hernias including umbilical ones rely on the same
advices of groin hernias. The isolation of hernia content evaluating the viability, its
liberation from the crawler followed by the reduction in abdominal cavity and the
defect repair are the main phases of the surgery. The incision can be used for the
diagnostic laparotomy with the possibility of intestinal resection or other required
procedure.
Incisional hernia can be challenge due to the scar of previous surgery. The fascial
weakness almost always requires prosthetic repair. Incisional hernia often has a
visceral involvement and, in urgent setting, the risk of visceral damage is high.
Moreover, at the end of the reduction of the content it is impossible to proceed with
a direct closure of the defect. In these cases, it is indicated the use of a biologic mesh
to restore the abdominal wall.

15.6 Anorectal Emergencies

15.6.1 Introduction

The term “anorectal emergencies” refers to anorectal disorders presenting with

some alarming symptoms such as acute anal pain and bleeding that might require an
immediate management. They are represented by: thrombosed external hemor-
rhoids, thrombosed or strangulated internal hemorrhoids, anorectal abscess, rectal
prolapse, anal fissure, rectal bleeding. Diagnosis of any of anorectal emergencies
must include a physical examination that should include inspection of perianal tis-
sues, anorectal digital examination, and anoscopy when available based on the
patient’s symptoms and pain [56].

15.6.2 Acute Thrombosed External Hemorrhoids

Classic symptoms of presentation are acute anal pain with a newly enlarged or ten-
der blush lump at the anal verge. Some patients can describe a recent history of
constipation or prolonged straining.
The management of this acute condition can be conservative or surgical depend-
ing on patient’s symptoms.
The conservative treatment includes anti-inflammatory analgesics, phlebotonics,
warm size bath and drugs avoiding constipation. The excision of thrombosed exter-
nal hemorrhoid with surgical removal of the clot is reserved in patients with severe
pain within 48–72 h from the onset of symptoms [57].
15  Acute Abdomen and Acute Abdominal Conditions 169

15.6.3 Thrombosed Internal Hemorrhoids

Internal hemorrhoid may become strangulated and thrombosed when prolapsed part
is left protruded until vascular compromise. The management consists in manual
reduction of the masses to relieve patient’s pain then an urgent hemorrhoidec-
tomy [58].

15.6.4 Rectal Bleeding

Rectal bleeding is a symptom that can represent different types of pathology of

gastrointestinal tract like hemorrhoids, anal fissure, IBD, and rectal neoplasm. The
patient history and the physical examination are necessary to differentiate the pos-
sible reason of the bleeding. The blood may be spotted on the toilet paper or could
be on the toilette. Usually it is characterized by a painless passage of bright-red
blood during bowel movements. In patients with rectal bleeding, an anoscopy and
colonoscopy are mandatory to rule out the pathology that cause the bleeding [59].

15.6.5 Anal Fissure

Painful defecation with or without passage of red blood is a typical symptom of this
condition. The patient can describe that the pain may last from minutes to hours
after defecation. Patients are basically pain-free between bowel movement. During
the anoscopy is visible a small linear laceration of the anoderm (acute anal fissure).
For those who experience a long history of painful defecation a chronic linear lac-
eration of the anoderm is visible, with hypertrophic anal papilla and enlarged peri-
anal skin tag (chronic anal fissure). For acute anal fissure a conservative management
is the treatment of choice that includes adequate pain control, stool softeners, topi-
cal nitrate and topical calcium channel blocker. For patient with chronic anal fissure,
a botulin injection or a lateral anal sphincterotomy remains the treatment of
choice [60].

15.6.6 Anorectal Abscess

The anorectal abscess is one of the most frequent anorectal emergencies in the
ED. They usually originate from an infected anal gland located in the anal mucosa.
The abscess can reach the inter-sphincteric area, supra-elevator space, perianal
region, deep post-anal space, and ischiorectal fossa. Most of the abscess can be
diagnosed with a careful history and physical examination that must include anorec-
tal digital examination. Patient usually refer anal pain, fever, and the presence of a
tender mass. The fluctuation of the abscess can’t be evident. An endoanal ultraso-
nography, a CT scan, or MRI of the pelvis may add some additional information on
the extension and exact location of the abscess and help to make the correct decision
170 E. Botteri et al.

on the management. The gold standard treatment is an adequate drainage of the

abscess that can be done in ED with some sedation or in operating room, depending
on the exact location of the abscess and surgeon’s experience. An expert surgeon on
colorectal disease may provide a definitive treatment of anal fistula but this type of
approach is still in debate [61].

15.6.7 Rectal Prolapse

Classical signs of rectal prolapse are protruding full-thickness rectal wall with con-
centric rings of mucosa. It is important to differentiate between rectal prolapse or
prolapsed internal hemorrhoid because of the different types of management needed.
Clinical and physical examination of anal region are mandatory. An irreducible
rectal prolapse is quite rare but can happen.
For strangulated irreducible rectal prolapse an emergent surgery with rectosig-
moidectomy is the treatment of choice. For all those rectal prolapse that can de
reduce a conservative treatment and elective surgery can be scheduled [62].

15.6.8 Bowel Obstruction

15.6.8.1 Introduction
A complete history, laboratory tests, and physical examination must be done for all
patients attending to the emergency department with abdominal pain. It is very
important to know about when the abdominal pain has begun, the type of pain and
when was the last pass of gas/defecation. A history of previous abdominal surgery
or episode of obstruction or presence of diverticula or rectal bleeding are important
news to know in order to think about the possibility of a bowel obstruction. The
main cause of bowel obstruction can be differentiated between small bowel obstruc-
tion and large bowel obstruction. For small bowel obstruction the main causes are
adhesions and hernias, the remaining are malignancies, carcinomatosis, endome-
triosis, IBD, foreign bodies, and bezoars. For large bowel obstruction, the main
causes are malignancies, diverticular stenosis, and volvulus (Fig. 15.1).

15.6.9 Diagnosis

The initial radiological examination on the guide of the clinical presentation is rep-
resented by standard abdominal X-ray and ultrasound. On the basis of this exam, a
CT scan can be performed to better understand the level of the obstruction.
Supportive treatment with hydration, anti-emetics, and bowel rest must be done. A
nasogastric suction is useful for initial diagnosis and treatment. A CV must be
insert. Low arterial blood pH and high lactic acid level may be useful in the diagno-
sis of intestinal ischemia. In case of small bowel obstruction for adhesions, a water-­
soluble contrast administration can be performed. It is a feasible NOM with low
15  Acute Abdomen and Acute Abdominal Conditions 171

OBSTRUCTION?

History taking, phisical examination, laboratory testing US, X-ray

Yes
ABDOMINAL WALL HERNIA? MANUAL REDUCTION? Yes

CT scan No
level and casue of obstruction? Ischemia? Perforation?

SMALL BOWEL LARGE BOWEL

Ischemia? – Perforation?
Endoscopy
Adhesions Neoplasm
No
Internal hernia
No
Neoplasm – volvolus – Diverticular stenos
Yes

EFFECTIVE CONSERVATIVE TREATMENT? EFFECTIVE CONSERVATIVE TREATMENT?

No
Yes No
EMERGENCY SURGERY Yes ELECTIVE SURGERY
DISCHARGE (same admission)

Fig. 15.1  Management strategy of bowel obstruction (for about 90% of causes)

morbidity and mortality. Colonoscopy is limited to the large bowel obstruction. To

minimize the burden of ionizing radiation in children and pregnant women, mag-
netic resonance imaging is a valid alternative examination to computed tomography
scan for bowel obstruction [63].

15.6.10 Therapy

15.6.10.1 Conservative Treatment

NOM is safe and useful for all small bowel obstruction caused by adhesions. Water
soluble administration is useful. Evidence are lacking but for many authors 72 h of
duration is safe and appropriate. In case of hernia a manual reduction has to be
attempted. In case of unsuccessful reduction emergency surgery is needed.
Diverticular obstruction can be solved with NOM. Sigmoid volvulus may benefit of
endoscopic detorsion. In case of colonic necrosis, immediate surgery is needed. In
case of left colon cancer obstruction, a self-expanding stent as bridge to surgery in
centers with adequate expertise must be preferred to a diverting stoma [64].

15.6.10.2 Surgery
For abdominal wall complicated hernia, surgery is the treatment of choice. A pros-
thetic repair is mandatory. Diagnostic laparoscopy is useful to assess the bowel
viability after reduction. Adhesiolysis for small bowel obstruction can be performed
laparoscopically or by open surgery. In case of small bowel tumors, resection and
anastomosis following oncological principles must be done. For large bowel
obstruction, caused by a sigmoid volvulus, surgery is necessary in case of multiple
episodes or ischemia and perforation. For large bowel tumors, surgery is needed
when a “bridge to surgery” is not possible [60, 61].
172 E. Botteri et al.

References
1. Shaffer EA. Epidemiology and risk factors for gallstone disease: has the paradigm changed in
the 21st century? Curr Gastroenterol Rep. 2005;7(2):132–40. Return to ref 1 in article
2. Kratzer W, Mason RA, Kächele V. Prevalence of gallstones in sonographic surveys worldwide.
J Clin Ultrasound. 1999;27(1):1–7.
3. Friedman GD.  Natural history of asymptomatic and symptomatic gallstones. Am J Surg.
1993;165(4):399–404.
4. Yokoe M, Takada T, Strasberg SM, et al. TG13 diagnostic criteria and severity grading of acute
cholecystitis (with videos). J Hepatobiliary Pancreat Sci. 2013;20(1):35–46.
5. Okamoto K, Suzuki K, Takada T, Strasberg SM, Asbun HJ, Endo I.  Tokyo Guidelines
2018: flowchart for the management of acute cholecystitis. J Hepatobiliary Pancreat Sci.
2018;25(1):55–72.
6. Kaoutzanis C, Davies E, Leichtle SW, Welch KB, Winter S, Lampman RM, et al. Abdominal
ultrasound versus hepato-imino diacetic acid scan in diagnosing acute cholecystitis–what is
the real benefit? J Surg Res. 2014;1:44–52.
7. Fuks D, Mouly C, Robert B, Hajji H, Yzet T, Regimbeau J-M. Acute cholecystitis: preopera-
tive CT can help the surgeon consider conversion from laparoscopic to open cholecystectomy.
Radiology. 2012;263:128–38.
8. Kiewiet JJ, Leeuwenburgh MM, Bipat S, Bossuyt PM, Stoker J, Boermeester MA. A system-
atic review and meta-analysis of diagnostic performance of imaging in acute cholecystitis.
Radiology. 2012;264:708–20.
9. Yokoe M, Takada T, Strasberg SM, et al. New diagnostic criteria and severity assessment of acute
cholecystitis in revised Tokyo guidelines. J Hepatobiliary Pancreat Sci. 2012;19(5):578–85.
10. Khalfallah M, Dougaz W, Bedoui R, et al. Validation of the Lacaine-Huguier predictive score
for choledocholithiasis: prospective study of 380 patients. J Visc Surg. 2012;149(1):66–72.
11. Pisano M, Allievi N, Gurusamy K, et al. 2020 World Society of Emergency Surgery updated
guidelines for the diagnosis and treatment of acute calculus cholecystitis. World J Emerg Surg.
2020;15(1):61. https://doi.org/10.1186/s13017-­020-­00336-­x.
12. Maple JT, Ben-Menachem T, Anderson MA, et al. The role of endoscopy in the evaluation of
suspected choledocholithiasis. Gastrointest Endosc. 2010;71(1):1–9.
13. Dasari BVM, Tan CJ, Gurusamy KS, et al. Surgical versus endoscopic treatment of bile duct
stones. Cochrane Database Syst Rev. 2013;(9):CD003327. https://doi.org/10.1002/14651858.
CD003327.pub4.
14. Sartelli M, Catena F, Ansaloni L, et al. Complicated intra-abdominal infections worldwide: the
definitive data of the CIAOW Study. World J Emerg Surg. 2014;9:37.
15. Coccolini F, Catena F, Pisano M, et al. Open versus laparoscopic cholecystectomy in acute
cholecystitis. Systematic review and meta-analysis. Int J Surg. 2015;18:196–204.
16. Gurusamy KS, Davidson C, Gluud C, Davidson BR.  Early versus delayed laparoscopic
cholecystectomy for people with acute cholecystitis. Cochrane Database Syst Rev.
2013;2013(6):CD005440.
17. Schmidt M, Sondenaa KVM, et al. Long-term follow-up of a randomized controlled trial of
observation versus surgery for acute cholecystitis: non-operative management is an option in
some patients. Scand J Gastroenterol. 2011;46:1257–62.
18. Mori Y, Itoi T, Baron TH, et al. Tokyo Guidelines 2018: management strategies for gallblad-
der drainage in patients with acute cholecystitis (with videos). J Hepatobiliary Pancreat Sci.
2018;25(1):87–95.
19. Schau H-P. Antibiotics in laboratory medicine, 2nd ed. In: Lorian V, editors. 1259 S, 371 Abb,
323 Tab Balt Angeles-Sydney Williams Wilkins J Basic Microbiol. 1986.
20. Weizman AV, Nguyen GC.  Diverticular disease: epidemiology and management. Can J
Gastroenterol. 2011;25:385–9.
21. Schoetz DJ.  Diverticular disease of the colon: a century-old problem. Dis Colon Rectum.
1999;42:703–9.
15  Acute Abdomen and Acute Abdominal Conditions 173

22. Shahedi K, Fuller G, Bolus R, Cohen E, Vu M, Shah R, et al. Long-term risk of acute diverticuli-
tis among patients with incidental diverticulosis found during colonoscopy. Clin Gastroenterol
Hepatol. 2013;11:1609–13.
23. Sartelli M, Catena F, Ansaloni L, Coccolini F, Griffiths EA, Abu-Zidan FM, et  al. WSES
guidelines for the management of acute left sided colonic diverticulitis in the emergency set-
ting. World J Emerg Surg. 2016;11:37.
24. Sartelli M, Weber DG, Kluger Y, et al. 2020 update of the WSES guidelines for the management
of acute colonic diverticulitis in the emergency setting. World J Emerg Surg. 2020;15(1):32.
https://doi.org/10.1186/s13017-­020-­00313-­4.
25. Kechagias A, Rautio T, Kechagias G, Mäkelä J. The role of C-reactive protein in the prediction
of the clinical severity of acute diverticulitis. Am Surg. 2014;80:391–5.
26. Laméris W, van Randen A, Bipat S, Bossuyt PM, Boermeester MA, Stoker J. Graded compres-
sion ultrasonography and computed tomography in acute colonic diverticulitis: meta- analysis
of test accuracy. Eur Radiol. 2008;18:2498–511.
27. Sartelli M, Moore FA, Ansaloni L, Di Saverio S, Coccolini F, Griffiths EA, et al. A proposal
for a CT driven classification of left colon acute diverticulitis. World J Emerg Surg. 2015;10:3.
28. Mazzei MA, Cioffi Squitieri N, Guerrini S, Stabile Ianora AA, Cagini L, Macarini L, et al.
Sigmoid diverticulitis: US findings. Crit Ultrasound J. 2013;5(Suppl. 1):S1–5.
29. Puylaert JB. Ultrasound of colon diverticulitis. Dig Dis. 2012;30:56–9.
30. Shabanzadeh DM, Wille-Jørgensen P. Antibiotics for uncomplicated diverticulitis. Cochrane
Database Syst Rev. 2012;11:CD009092.
31. Fozard JB, Armitage NC, Schofield JB, Jones OM. Association of Coloproctology of Great
Britain and Ireland. ACPGBI position statement on elective resection for diverticulitis. Color
Dis. 2011;13:1–11.
32. Vennix S, Musters GD, Mulder IM, Swank HA, Consten EC, Belgers EH, et al. Laparoscopic
peritoneal lavage or sigmoidectomy for perforated diverticulitis with purulent peritonitis: a
multicentre, parallel-group, randomised, open-label trial. Lancet. 2015;386(10000):1269–77.
33. Gregersen R, Mortensen LQ, Burcharth J, Pommergaard HC, Rosenberg J.  Treatment of
patients with acute colonic diverticulitis complicated by abscess formation: a systematic
review. Int J Surg. 2016;35:201–8.
34. Penna M, Markar SR, Mackenzie H, Hompes R, Cunningham C.  Laparoscopic lavage ver-
sus primary resection for acute perforated diverticulitis: review and meta-analysis. Ann Surg.
2018;267:252–8.
35. Feingold D, Steele SR, Lee S, Kaiser A, Boushey R, Buie WD, et al. Practice parameters for
the treatment of sigmoid diverticulitis. Dis Colon Rectum. 2014;57:284–94.
36. Dharmarajan S, Hunt SR, Birnbaum EH, Fleshman JW, Mutch MG. The efficacy of nonop-
erative management of acute complicated diverticulitis. Dis Colon Rectum. 2011;54:663–71.
37. Weber DG, Bendinelli C, Balogh ZJ. Damage control surgery for abdominal emergencies. Br
J Surg. 2014;101:e109–18.
38. Heis HA, Bani-Hani KE, Rabadi DK, Elheis MA, Bani-Hani BK, Mazahreh TS, Bataineh
ZA, Al-Zoubi NA, Obeidallah MS.  Sigmoid volvulus in the Middle East. World J Surg.
2008;32:459–64.
39. Lal SK, Morgenstern R, Vinjirayer EP, Matin A.  Sigmoid volvulus an update. Gastrointest
Endosc Clin N Am. 2006;16:175–87.
40. Tiah L, Goh SH.  Sigmoid volvulus: diagnostic twists and turns. Eur J Emerg Med.
2006;13:84–7.
41. Raveenthiran V. Observations on the pattern of vomiting and morbidity in patients with acute
sigmoid volvulus. J Postgrad Med. 2004;50:27–9.
42. Burrell HC, Baker DM, Wardrop P, Evans AJ. Significant plain film findings in sigmoid volvu-
lus. Clin Radiol. 1994;49:317–9.
43. Feldman D. The coffee bean sign. Radiology. 2000;216:178–9.
44. Atamanalp SS. Treatment of sigmoid volvulus: a single-center experience of 952 patients over
46.5 years. Tech Coloproctol. 2013;17:561–9.
174 E. Botteri et al.

45. Perrot L, Fohlen A, Alves A, Lubrano J. Management of the colonic volvulus in. J Visc Surg.
2016;153:183–92.
46. Levsky JM, Den EI, DuBrow RA, Wolf EL, Rozenblit AM. CT findings of sigmoid volvulus.
AJR Am J Roentgenol. 2010;194:136–43.
47. Naveed M, Jamil LH, Fujii-Lau LL, et al. American Society for Gastrointestinal Endoscopy
guideline on the role of endoscopy in the management of acute colonic pseudo-obstruction and
colonic volvulus. Gastrointest Endosc. 2020;91:228–35.
48. Bruzzi M, Lefèvre JH, Desaint B, Nion-Larmurier I, Bennis M, Chafai N, Tiret E, Parc
Y.  Management of acute sigmoid volvulus: short- and long-term results. Colorectal Dis.
2015;17:922–8.
49. Baird DLH, Simillis C, Kontovounisios C, Rasheed S, Tekkis PP.  Acute appendicitis.
BMJ. 2017;357:j1703. https://doi.org/10.1136/bmj.j1703.
50. Dionigi R, Chirurgia, Basi teoriche e chirurgia generale, quinta edizione.
51. Gomes CA, Sartelli M, Di Saverio S, Ansaloni L, Catena F, Coccolini F, Inaba K, Demetriades
D, Gomes FC, Gomes CC. Acute appendicitis: proposal of a new comprehensive grading sys-
tem based on clinical, imaging and laparoscopic findings. World J Emerg Surg. 2015;10:60.
https://doi.org/10.1186/s13017-­015-­0053-­2. eCollection 2015. Review
52. Saverio D, et al. WSES Jerusalem guidelines for diagnosis and treatment of acute appendici-
tis. World J Emerg Surg. 2016;11:34. https://doi.org/10.1186/s13017-­016-­0090-­5. eCollection
2016. Review.
53. Ohle R, et al. The Alvarado score for predicting acute appendicitis: a systematic review. BMC
Med. 2011;9:139.
54. Andersson M, Andersson RE.  The appendicitis inflammatory response score: a tool for
the diagnosis of acute appendicitis that outperforms the Alvarado score. World J Surg.
2008;32(8):1843–9.
55. Kingsnorth A, LeBlanc K. Hernias: inguinal and incisional. Lancet. 2003;362:1561–71.
56. Sammarco G, Trompetto M, Gallo G.  Thrombosed external haemorrhoids: a clinician’s
dilemma. Rev Recent Clin Trials. 2019;14:232–4.
57. G.  Gallo,J.  Martellucci, A.  Sturiale, G.  Clerico, G.  Milito, F.  Marino,· G.  Cocorullo,
P.  Giordano, M.  Mistrangelo, M.  Trompetto Consensus statement of the Italian society of
colorectal surgery (SICCR): management and treatment of hemorrhoidal disease. Tech
Coloproctol. 2020;24:145–164. https://doi.org/10.1007/s10151-­020-­02149-­1.
58. Fargo MV, Latimer KM. Evaluation and management of common anorectal conditions. Am
Fam Physician. 2012;85:624–30.
59. Rex DK, Boland CR, Dominitz JA, et  al. Colorectal cancer screening: recommendations
for physicians and patients from the US multi-society task force on colorectal cancer. Am J
Gastroenterol. 2017;112:1016–30.
60. Perry WB, Dykes SL, Buie WD, Rafferty JF.  Practice parameters for the management of
anal fissures (3rd revision). Dis Colon Rectum. 2010;53:1110–5. https://doi.org/10.1007/
DCR.0b013e3181e23dfe.
61. Lohsiriwat V, Yodying H, Lohsiriwat D.  I. Incidence and factors influencing the develop-
ment of fistula-in-ano after incision and drainage of perianal abscesses. J Med Assoc Thail.
2010;93:61–5.
62. Tou S, Brown SR, Nelson RL.  Surgery for complete (full-thickness) rectal prolapse in
adults. Cochrane Database Syst Rev. 2015;11:CD001758. https://doi.org/10.1002/14651858.
CD001758.
63. Di Saverio S, Coccolini F, Galati M, et al. Bologna guidelines for diagnosis and management
of adhesive small bowel obstruction (ASBO): 2013 update of the evidence-based guidelines
from the world society of emergency surgery ASBO working group. World J Emerg Surg.
2013; https://doi.org/10.1186/1749.
64. Frago R, Ramirez E, Millan M, Kreisler E, del Valle E. Biondo. Current management of acute
malignant large bowel obstruction: a systematic review. S. Am J Surg. 2014;207(1):127–38.
Abdominal Emergencies Requiring
a Multidisciplinary Approach 16
Andrea Mazzari, Pasquina M. C. Tomaiuolo,
Alessio Giordano, Roberto Luca Meniconi,
and Alberto M. Settembrini

16.1 Aortoenteric Fistula Clinical Case

A 77-year-old Caucasian man consulted his general practitioner concerning a

2-week history of worsening weakness and was referred to the emergency depart-
ment to detect an abdominal bruit. At arrival, the patient was pale, apyretic, eupneic,
conscious, and oriented. Physical examination confirmed a mesogastric bruit asso-
ciated with an abdominal pulsatile mass. Melanic stool was found on rectal exami-
nation. No history of previous surgery. At the blood tests, leukocytosis, mild anemia,
and alteration of the renal function were revealed. An urgent esophagogastroduode-
noscopy (EGD) was arranged, but after a sudden drop in the patient’s blood pres-
sure, and enhanced abdominal CT was obtained first. The examination revealed a
63  mm thick-walled infrarenal aortic aneurysm associated with distension of the
small bowel loops by fluid content.
The patient was immediately transferred to the operating theatre, and a signifi-
cant amount of fresh blood (400 mL) was aspirated through the nasogastric tube
during anesthetic preparation. The laparotomy disclosed an aneurysm of inflamma-
tory appearance, adherent to the fourth portion of the duodenum and surrounded by

A. Mazzari (*) · P. M. C. Tomaiuolo

General Surgery Unit, Ospedale Cristo Re, Rome, Italy
A. Giordano
General Surgery Unit, Azienda ASL Toscana Centro, Nuovo Ospedale “S. Stefano”,
Prato, Italy
R. L. Meniconi
Department of General Surgery and Organ Transplantation, Azienda Ospedaliera San
Camillo-Forlanini, Rome, Italy
A. M. Settembrini
Vascular Surgery Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico,
Milan, Italy

© The Author(s), under exclusive license to Springer Nature 175

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_16
176 A. Mazzari et al.

a small retroperitoneal hematoma. Following aortic and iliac cross-clamping, dis-

section of the aneurysmatic aortic wall from the duodenum was performed and a
1 cm aorto-duodenal fistula was found upon removal of a fresh clot. The peritoneal
cavity was irrigated with rifampicin, the duodenal wall was sutured, and the aorta
was repaired by silver-impregnated prosthetic interposition. The aneurysmatic wall
was closed above the prosthesis and a pedicle of omentum was interposed between
the aortic wall and the duodenum.
Blood cultures were negative for bacterial or fungal infection; therefore, a wide-­
spectrum antibiotic therapy with imipenem was administered for 30 days. On post-
operative day 15, the patient was transferred to a rehabilitation center and discharged
2 weeks later.

16.1.1 Introduction

Aortoenteric fistula (AEF) is encountered in urgent diseases; it is a communication

between the aorta and the bowel, initially described by Sir Astley Cooper in 1829
[1], caused by erosion between aortic and gastrointestinal wall. AEF can be primary
or secondary.
Primary aortoenteric fistula (PAEF) is a rare condition that develops between the
native aorta and gastrointestinal tract, usually in the presence of an abdominal aortic
aneurysm (AAA).
Secondary aortoenteric fistula (SAEF) occurs if a previous aortic reconstruction
has been performed, usually at the level of the anastomosis where the friction is
high. The prevalence of PAEF is estimated to be between 0.04% and 0.07% based
on autopsy studies [2, 3].
More frequent location of fistulas is the third portion of the duodenum, which is
involved in more than 50% of cases [4].
Even though the diagnosis is challenging, prompt management is mandatory to
avoid the patient’s death: insidious episodes of gastrointestinal (GI) bleeding are
frequently under-diagnosed until the occurrence of a massive hemorrhage. If left
untreated, the overall mortality rate is almost 100% [4].

16.1.2 Pathogenesis

A PAEF occurs without prior aortic surgery, and aortic aneurysms are the most
common etiology; however, other causes can be gastrointestinal malignancies, sep-
tic aortitis, tuberculosis, and radiation therapy.
SAEF is correlated in the most part with a graft infection, and its incidence is
lower following endovascular aortic aneurysm repair (EVAR) but much higher after
emergent open repair of ruptured AAA due to the increased likelihood of bacterial
contamination of the graft and bowel trauma during hurried surgical dissection.
After open repair the infection can be the beginning of the contamination of the
graft into the bowel or the mechanical erosion can cause the detachment of the
proximal anastomosis with the development of a pseudoaneurysm or the direct
16  Abdominal Emergencies Requiring a Multidisciplinary Approach 177

involvement of the third or fourth portion of the duodenum (which is extraperito-

neal!): this explains why after a surgical AAA repair it is mandatory to cover with
the residual AAA sac or greater omentum the graft and the anastomosis.
After EVAR, an AEF can be related to mechanical failure of the stent-graft: rup-
ture or migration of the device in the aneurysmatic sac and constant pressuriza-
tion of it.
The median interval from the original operation to the development of AEF is
around 2–4 years [5].

16.1.3 Clinical Presentation

The classic triad of symptoms of AEF as GI bleeding, sepsis, and abdominal pain is
rarely found. The clinical presentation has a broad spectrum of symptoms varying
from malaise to sudden hematemesis or melena or chronic anemia associated with
fever. GI bleeding is the most common initial symptom and occurs in nearly 70% of
patients; other symptoms reported are back pain and fever; sometimes a minor
bleeding, usually self-limiting (Herald sign), can precede a massive gastrointestinal
bleeding [6].

16.1.3.1 Diagnosis
In the Emergency Room, a patient, after collection of medical history (if possible to
know previous aortic surgery), should be subjected to angio-CT that can reveal
communication between the intestine and aorta or air bubbles around the aorta
peculiar impregnation of the bowel (Fig. 16.1).
Extravasation of contrast in intestinal lumen is rare but pathognomonic of aorto-
enteric fistula. Other not specific signs include effacement of periaortic fat, thicken-
ing of bowel wall close to the aorta.

Fig. 16.1  CT axial (blue arrow) and sagittal (red arrow) view of air bubbles into aortic endograft
after endovascular aneurysm repair. It is a CT sign of contamination between GI tract and aortic
aneurysm
178 A. Mazzari et al.

However, signs of suspected graft infection can be signs of AEF: perigraft gas
collections, increase in perigraft soft tissue or fluid, pseudoaneurysm, disappear-
ance of the continuous calcific aneurysm wrapping around the graft [7].
A second step test, if the patient is stable, is the esophagogastroduodenoscopy
(EGD) that has low diagnostic accuracy: it could provide a more detailed look of
duodenum (a trick is to use a longer endoscope) and visualize an AEF, sometimes
with the underlying aortic graft material, and may also show active bleeding, as well
as an adherent clot within the bowel. Only 25–50% of AEF are discovered by endos-
copy due to the difficulty of visualizing the duodenum [8].

16.1.4 Decision-Making

The appropriate management of patients with massive bleeding due to aortoenteric

fistula is still a significant challenge in the surgical setting. Timely recognition of
hemorrhagic shock and subsequent treatment by evidence-based recommendations
are crucial to patient outcome.
Treatment modalities include:

• Patient airway control, maintaining adequate ventilation and oxygenation, secure

venous access with two large-bore cannulas.
• Avoid or correct hypothermia, acidosis, hypocalcemia (maintain Ca2+
>1.1 mmol/L).
• Crystalloid infusions (<3 L in the first 6 h).
• Systolic blood pressure of 80–90 mmHg achieved.
• Start massive infusion protocol as soon as possible.
• Obtain laboratory measures: full blood count, PT, fibrinogen, calcium, lac-
tate, BE, pH.
• Tranexamic acid administrated and prothrombin complex in patients pre-treated
with warfarin or NAO.
• Fibrinogen maintained at 1.5–2 g/dl.
• Platelets maintained at >100 × 109/L.
• Target Hb level 7–9 g/dl achieved.

In unstable patients, decision-making must be rapid. Emergency surgical explo-

ration in a patient with GI hemorrhage is the correct approach. The goal is to main-
tain the patient’s life, so laparotomy should be the first approach, and then the
surgeon has to take into account limb preservation.
Appropriate preparation of the patient provides to start broad-spectrum gram-­
positive and gram-negative antibiotic therapy.
16  Abdominal Emergencies Requiring a Multidisciplinary Approach 179

16.1.5 Vascular Management

When a surgeon faces an AEF, he should keep in mind the hazards of going into
infected fields, choosing the right abdominal approach, removing the graft, and
revascularizing the limbs through two techniques: in situ or extra-anatomic
revascularization.
When the surgical approach is decided, the surgeon should consider facing a
hostile abdomen with a conglomerate of bowel loops that adheres to the retroperito-
neum. The abdominal approach can be through a midline incision or a retroperito-
neal incision.
For the in situ revascularization, autologous grafts (such as the saphenous vein,
the superficial femoral vein, the endarterectomized superficial femoral artery) and
biological conduits of arterial allografts or bovine pericardium grafts can be safely
used in the infected fields; silver-impregnated or other impregnated grafts can be
alternatively used but with higher re-infection risk (Fig. 16.2).

Fig. 16.2  In situ

revascularization with
biological graft in bovine
pericardium after AEF
removal
180 A. Mazzari et al.

For extra-anatomic revascularization, prosthetic materials can be considered out

of the infected field: in our opinion, silver-impregnated or antibiotics (rifampin or
tobramycin) bonded grafts reduce the risk of graft infection. After aortic stump
closure, extra-anatomic revascularization provides an axillo-femoral or bifemoral
bypass or other less frequent revascularization techniques from the thoracic aorta to
the limbs.
In case of hemodynamic instability, a staged approach with endovascular treat-
ment of the bleeding by deploying an endograft in the aorta can be chosen. This is a
bridge procedure before the total removal of infected grafts. A trick could be to use
an infrarenal fixation endograft to reduce the challenge of suprarenal cross-­clamping
during its removal.

16.1.6 Bowel Reconstruction

The management of bowel defects depends on the site and the size of the fistula.
Laparotomy is required with a midline or subcostal incision in aorto-duodenal fis-
tula when bowel defect is less than 3–4 cm and the intestinal wall is not involved in
massive inflammatory process, a duodenorraphy can be performed (Fig. 16.3). The
reconstruction should be seromuscular in transverse direction with absorbable
suture; it is mandatory to avoid tension above the suture line to prevent leakage. A
small, half-circle needle is placed through the edge of the defect, approximately 0.5
to 1.0 cm from the edge of the perforation. Three or four sutures are placed and are
then tied to close the duodenal defect; the omental patch is placed on the tied sutures.
When the bowel defect is more extensive than 3–4 cm a duodenal resection with
duodenojejunal anastomosis is the preferred option. A right-sided visceral mobili-
zation and intestinal derotation maneuver (Cattell-Braasch-Valdoni maneuver) will
completely expose the duodenal-jejunal junction and its mesentery. The proximal
jejunum was transected approximately 5–10 cm distal to the ligament of Treitz, and

Fig. 16.3  From left to right, evidence of duodenal lesion of the AEF and duodenorraphy
16  Abdominal Emergencies Requiring a Multidisciplinary Approach 181

the mesentery was sequentially ligated and divided. Dissection continued proxi-
mally to involve the fourth and third portions of the duodenum; an end-to-end duo-
denojejunal anastomosis is performed. To avoid injury of the ampulla of Vater, a
cholecystectomy is systematically performed and a Fogarty catheter is placed in the
duodenum through the cystic duct. A feeding jejunostomy can be helpful for nutri-
tional support in the postoperative period.
The volume of gastric and pancreatic-biliary secretions can be decreased from
the duodenal suture lines by routinely using an anterograde drainage including a
nasogastric tube located in the second portion of the duodenum and a transcystic
biliary drain. Other techniques can be used to divert the digestive enzymes from
repairs. A triple-tube decompression, including a nasogastric tube or gastrostomy
and two jejunostomies, one retrograde for duodenal decompression and one antero-
grade for enteral nutrition is provided.
When AEF occurs in jejunum ileum, sigmoid colon, ascending/descending
colon, a midline incision is the preferred option; a bowel resection should be con-
sidered in case of large defect with thickened intestinal wall due to edema or inflam-
mation. A primary anastomosis should be performed, there is no difference between
handsewn or stapled anastomosis, it depends on surgeon preferences and experience.
Omentoplasty is useful to exclude the digestive suture or anastomosis from the
graft to reduce septic complications.

16.1.7 Postoperative Time and Long-Term Follow-up

Postoperatively, these patients are frequently debilitated and have at least an ele-
ment of systemic sepsis. Multisystem support in the intensive care setting is
required, and a multidisciplinary team approach that includes specialists in inten-
sive care, infectious disease, and nutrition offers the best chance of survival.
Even if antibiotics are continued, late infections can occur; therefore, these
patients should be periodically reevaluated.

16.1.8 Take-home Messages (Fig. 16.4)

1. Endovascular is only as a bridge procedure in acute bleeding.

2. Graft removal and flow restoration is the treatment of choice.
3. In situ reconstruction only with biologic grafts or extra-anatomical revascular-
ization is better.
4. Omentoplasty or myoplasty is mandatory to protect the aortic stump.
5. Single stitches reinforced by autologous pledgets to close the aorta.
6. Size and site of bowel defect is crucial for bowel reconstruction.
7. Suture closure of intestinal wall when defect is smaller than 3–4 cm.
182 A. Mazzari et al.

Suspected AEF

Unstable Herald bleed, stable

Emergency exploration EGDS and CT

Positive for GI source Bothnegative
+
+
No AEF AEF Appropriate GI Aortogram Tagged WBC scan
management
− −

Clamp or balloon control EAB rebleed stable

2-3 days explore observe

Graft excision Graft excision

Viable extremities Non viable extremities

In situ if minimal Close if unstable,

Close and observe EAB if stable contamination interval amputation

Fig. 16.4  Therapeutic algorithm in AEF

8. Intestinal resection when bowel defect larger is than 3–4 cm or malacic intesti-
nal wall.
9. Decompression of the bowel by a second nasogastric tube over the Treitz or by
jejunostomy.

16.2 Acute and Chronic Mesenteric Ischemia Clinical Case

An 81-year-old female was referred to the emergency department due to abdominal

pain, nausea, and vomiting with a history of atrial fibrillation. Physical examination
confirmed abdominal bruit associated with diffuse peritonitis. ECG demonstrated
an acute atrial fibrillation, and blood tests showed leukocytosis with mild anemia.
An abdominal CT scan revealed thrombotic occlusion of the superior mesenteric
artery associated to small bowel and right colon abnormal distension, with intrapa-
rietal air in the intestinal wall. The patient was immediately transferred to operative
theatre for an urgent laparotomy. At laparotomy all the small bowel, the right and
transverse colon were dilatated, intestinal wall appeared thickened with associated
edema and clinical sign of ischemia. A retrograde access to SMA was performed
that confirmed thrombotic occlusion of the artery, revascularization was obtained by
a Fogarty catheter. A damage control surgery with closure of the abdomen with
negative pressure was preferred by the general surgeon to perform a second look to
avoid an intestinal resection and anastomosis in critical condition. On Postoperative
Day (POD) 2, the patient was again referred to the operative theatre, all the colon
showed a good vascularization, a resection of 80 cm of small bowel was performed
due to segmental ischemia. An intestinal anastomosis with double stapling tech-
nique was done and the abdomen was definitively closed. The postoperative course
was uneventful except for a pulmonary complication treated by antibiotic therapy.
The patient was discharged in 22 POD.
16  Abdominal Emergencies Requiring a Multidisciplinary Approach 183

16.2.1 Introduction

Acute and chronic mesenteric ischemia (AMI and CMI) is a syndrome caused by
inadequate blood flow through the mesenteric vessels with the high risk of gangrene
development of bowel wall.
AMI is when symptoms occur in the first hours up to 24–48 h and duration is less
than 2 weeks; subacute when a new symptomatic condition over chronic symptoms
between 2 to 4 weeks.
CMI happens when mesenteric circulation fails to provide the postprandial
response that is required to supply oxygen for the metabolic processes.
The overall prevalence of AMI is 0.1% of all hospital admissions; venous throm-
bosis is found in approximately 0.001% of patients who undergo exploratory lapa-
rotomy. CMI accounts <2% of all admissions for gastrointestinal conditions and
median age of 65 years old (40 to 90 years) and female to male ratio is 3–4:1 [9, 10].

16.2.2 Mesenteric Collateral Patterns

To know the collateral pattern of mesenteric arterial and venous circulation is essen-
tial to understand the pathogenesis and to have a correct approach to the pathology.
The gastroduodenal and pancreaticoduodenal arteries provide collateralization
between the CT and SMA; the marginal artery of Drummond and the arc of Riolan
connect the left colic artery (inferior mesenteric artery) to the middle colic artery
(SMA); the term central anastomotic artery describes marked enlargement that
occurs in the arc of Riolan in patients with high-grade stenosis or occlusion of the
SMA and collateralization via a patent inferior mesenteric artery (IMA). This artery
lies in the mesentery in close proximity to the inferior mesenteric vein: inadvertent
ligation, division or thrombosis of this important collateral artery during aortic expo-
sure or other operative procedures may result in acute ischemia or bowel gangrene.
The internal iliac arteries provide a collateral pathway via the hemorrhoidal branches.
The venous network provides the superior mesenteric vein (SMV) formed by the
jejunal, ileal, ileocolic, right colic, and middle colic veins, which drain the small
intestine cecum, ascending colon, and transverse colon. The right gastroepiploic
vein drains the stomach to the SMV, whereas the inferior pancreaticoduodenal vein
drains the pancreas and duodenum. The inferior mesenteric vein (IMV) drains the
descending colon, the sigmoid colon, and the rectum through the left colic vein, the
sigmoid branches, and the superior rectal vein, respectively. The IMV usually joins
the splenic vein, which then joins the SMV to form the portal vein.

16.2.3 Pathogenesis

The diagnosis of AMI can be quite challenging: symptoms are initially nonspecific,
before evidence of peritonitis and often diagnosis and treatment are delayed when
pathology is advanced.
184 A. Mazzari et al.

About risk factors: for AMI include atherosclerosis, arrhythmias, hypovolemia,

congestive heart failure (CHF), recent myocardial infarction (MI), valvular disease,
advanced age, and intra-abdominal malignancy [9, 10]; for CMI the most important
cause is atherosclerosis associated with plaques in aorta and renal arteries. A non-
atherosclerotic disease can also affect CMI such as vasculitis (giant cell arteritis,
Takayasu’s disease, and polyarteritis nodosa), systemic lupus, Buerger’s disease,
spontaneous dissections, fibromuscular dysplasia, neurofibromatosis, radiation
arteritis, mesenteric venous stenosis, or occlusion [11].
AMI can be caused by an arterial disease or mechanical obstruction of the intes-
tine (e.g., internal hernia with strangulation, volvulus, or intussusception). In the
first case it may be subdivided into non-occlusive mesenteric ischemia (NOMI—20%)
and occlusive mesenteric arterial ischemia (OMAI—embolic in 50% and throm-
botic in 25%): the latter can be due to arterial embolism (AMAE) and acute mesen-
teric arterial thrombosis (AMAT) or dissection. It can also be caused by mesenteric
venous thrombosis (MVT in less than 10%) [12].
Mesenteric vein thrombosis primarily occurs in the absence of any identifiable
factor or secondary as after surgical ligation (splenic vein for splenectomy or portal
vein or the superior mesenteric vein (SMV) as part of damage control surgery). The
bowel becomes edematous and the intestinal outflow decreases, worsening progres-
sively until it impedes the inflow of arterial blood, leading to bowel ischemia. The
colon is usually spared because of better collateral circulation and the ischemia has
a patchy distribution.
Once bowel wall infarction has occurred, mortality may be as high as 90%. Even
with good treatment, as many as 50–80% of patients die [12].

16.2.4 Clinical Presentation

In normal conditions, approximately 20% of the cardiac output goes through the
mesenteric arteries and the flow increases after the ingestion of a meal, approaching
100–150% above normal (2000 mL/min) over the next 3–6 h.
In case of AMI, the patient develops continuous pain, unrelated to food intake,
because the mesenteric flow at rest is not guaranteed. This causes tissue hypoxia,
leading to initial bowel wall spasm and gut emptying by vomiting or diarrhea.
Symptoms of CMI include abdominal pain, weight loss, and “food fear.” The
abdominal pain is often postprandial and begins within a few minutes to 30 min
after meals, persisting for as long as 5–6 h.

16.2.5 Diagnosis

After clinical evaluation, the first step is a duplex study to evaluate the patency and
stenosis of celiac trunk (CT), superior mesenteric artery (SMA), and inferior mes-
enteric artery (IMA).
16  Abdominal Emergencies Requiring a Multidisciplinary Approach 185

Fig. 16.5  CT that shows AMI due to SMA thrombosis (blue arrow), left axial, right sagittal view

Diagnostic criteria include ≥70% stenosis with peak systolic velocities >275 cm/s
for the SMA and >200 cm/s for the celiac axis [13].
As second step CT or MRI should be performed. CT shows the quality of plaque
and length of stenosis and possible presence of post stenotic dilatation, conditions
that the surgeon should consider in the planning phase.
CT scan is considered the gold standard for diagnosing acute mesenteric isch-
emia (Fig.  16.5); in case of delayed recognition or non-exhaustive exams, many
patients undergo an exploratory laparotomy. With the advent of minimally invasive
surgery, diagnostic laparoscopy (DL) has taken a leading role as a less invasive
alternative to laparotomy for the early diagnosis of acute mesenteric ischemia, espe-
cially if we also consider the possibility to perform it at the bedside in the most criti-
cally ill patients. Bedside DL in the Intensive Care Unit (ICU) has been described
previously by several authors with a substantial confirmation of the above-­mentioned
advantages and the possibility to prevent unnecessary laparotomies. Moreover, a
negative or non-therapeutic laparotomy can be associated with a morbidity rate as
high as 5–22% and in some cases higher. Despite diagnostic laparoscopy is an
invaluable tool and can be conducted at the bedside in ICU patients, it has a reduced
sensitivity in the early stages of intestinal ischemia unfortunately because the
mucosa can be extensively ischemic while the bowel might still appear normal at
external inspection. This drawback can be overcome by using fluorescein-assisted
laparoscopy with indocyanine green (ICG), with which even early stages of isch-
emia can be identified.

16.2.6 Treatment

AMI should be immediately treated once recognized; meanwhile CMI can be

treated if pharmacological therapy is not sufficient and if the patient develops symp-
toms such as malabsorption, postprandial pain, vomiting, and diarrhea.
186 A. Mazzari et al.

The treatment algorithm should consider if exploratory laparotomy is indicated

and if etiology is established (arterial or venous and embolism or thrombosis).
Exploratory laparotomy is not always indicated as the first approach, but in some
cases highly suggested. If AMI is due to cardiac embolism, endovascular treatment
is not the ideal option because a thrombolysis can cause additional emboli to smaller
arteries; so an open vascular approach should be chosen; in case of thrombosis, an
endovascular approach can be the right choice for the recanalization.
If MVT is diagnosed, anti-coagulation is suggested unless there is direct evi-
dence of bowel gangrene. If a patient has peritoneal signs or evidence of bowel
gangrene, abdominal exploration is indicated regardless of the etiology.
About etiology, atherosclerotic lesions within the SMA and celiac axis represent
the group with a higher dilemma in terms of therapeutic options: open, endovascu-
lar, or hybrid. If no evidence of bowel gangrene and no definitive indication for
laparotomy, an endovascular approach alone, with or without a laparoscopic evalu-
ation could be evaluated.
A vascular approach can be made in open or endovascular surgery and usually
SMA is the main target.
Open surgery provides two approaches. One is endarterectomy or embolectomy
with angioplasty with patch closure of the artery; the other is performing a bypass
with autologous vein if there is frank necrosis or perforation or in the absence of
contamination using a polyester or rifampin-soaked graft. If a prosthetic conduit is
chosen, the graft should be covered by omentum.
Endovascular surgery has different approaches. Standard antegrade approach
through femoral or brachial access or with a retrograde open mesenteric stenting. In
the latter, a surgical exposure of SMA is performed by cranial retraction of the
transverse mesocolon and exposure of the root of the mesentery to the right side of
the abdomen. The mesentery is opened longitudinally on top of the SMA up to the
inferior edge of the pancreas, allowing for dissection and control of the SMA and
multiple jejunal branches. The segment of stenosis or occlusion is treated by pri-
mary stenting using a balloon-expandable stent [14].
After revascularization, the bowel is reassessed and additional bowel resection or
anastomosis is performed. Second-look laparotomy is indicated in patients with
severe ischemic changes or questionable bowel changes.

16.2.7 Damage Control Surgery

Many patients presenting with clinical signs of intestinal ischemia come to our
observation with septic shock and multiorgan failure.
The damage control surgery (DCS) is part of a multidisciplinary strategy known
as damage control management (DCM) with the resuscitation phase that will take
place in ICU.
The goal of the DMS is the resection of ischemic intestinal tract following open
abdomen (OA).
16  Abdominal Emergencies Requiring a Multidisciplinary Approach 187

The use of OA after perfusion restoration in a patient with acute mesenteric isch-
emia as in occlusive proximal or distal superior mesenteric artery emboli and non-­
occlusive mesenteric ischemia (e.g., post-arrest or resuscitation from shock/arrest)
should be considered in case of deranged physiology and bowel edema and neces-
sity to perform a second look or delayed anastomosis. Mesenteric venous thrombo-
sis requiring laparotomy does not routinely mandate OA as often as mesenteric
ischemia; however, the risk of abdominal hypertension imposes attention to intra-­
abdominal pressure.
Negative pressure wound therapy with continuous fascial traction should be sug-
gested as the preferred technique for temporary abdominal closure. Temporary
abdominal closure without negative pressure (e.g., Bogota bag) can be applied in
low resource settings.
Recent data from the International Register of Open Abdomen (IROA study)
showed that different techniques of OA resulted in different results according to the
treated disease (trauma and severe peritonitis) and if treated with or without nega-
tive pressure in terms of abdominal closure and mortality rate. The results favored
the nonnegative pressure systems in trauma and negative pressure temporary clo-
sure in severe peritonitis patients.
Open abdomen re-exploration should be conducted no later than 24–48  h
(Fig. 16.6). The abdomen should be maintained open if requirements for ongoing
resuscitation and/or the source of contamination persists, if a deferred intestinal
anastomosis is needed, if there is the necessity for a planned second look for the
ischemic intestine and, lastly, if there are concerns about abdominal compartment
syndrome development.

Fig. 16.6 Intestinal
resection after damage
control surgery
188 A. Mazzari et al.

16.2.8 Postoperative Management

Patients are allowed to resume a regular diet within 6–8 h. Anti-platelet therapy is
typically started prior to the vascular intervention with acetylsalicylic acid and con-
tinued indefinitely. Clopidogrel is started the day of the intervention with a loading
dose and continued for 6–8 weeks as a dual anti-platelet agent, after which patients
are kept on acetylsalicylic acid alone.
Follow-up includes clinical examination and duplex ultrasound every 6 months
during the first year and annually thereafter.

References
1. Cooper A. Lectures on principles and practice of surgery with additional notes and cases by
F. Tyrrell. 5th ed. Philadelphia, PA: Haswell, Barrington, & Haswell; 1839.
2. Hallett JW Jr, Marshall DM, Petterson TM, Gray DT, Bower TC, Cherry KJ Jr, Gloviczki P,
Pairolero PC. Graft-related complications after abdominal aortic aneurysm repair: reassurance
from a 36-year population-based experience. J Vasc Surg. 1997;25(2):277–84.; discussion
285–6. https://doi.org/10.1016/s0741-­5214(97)70349-­5.
3. O'Hara PJ, Hertzer NR, Beven EG, Krajewski LP. Surgical management of infected abdominal
aortic grafts: review of a 25-year experience. J Vasc Surg. 1986;3(5):725–31.
4. Lemos DW, Raffetto JD, Moore TC, Menzoian JO.  Primary aortoduodenal fistula: a case
report and review of the liter- ature. J Vasc Surg. 2003;37:686–9.
5. Bergqvist D, Björck M. Secondary arterioenteric fistulation - a systematic literature analysis.
Eur J Vasc Endovasc Surg. 2009;37:31–42.
6. Bunt TJ. Synthetic vascular grafts infections. II: graft enteric erosion and graft enteric fistulas.
Surgery. 1983;94:1.
7. Raman SP, Kamaya A, Federle M, et al. Aortoenteric fistulas: spectrum of CT findings. Abdom
Imaging. 2013;38:367–75.
8. Chung J. Management of aortoenteric fistula. Adv Surg. 2018;52(1):155–77.
9. Vokurka J, Olejnik J, Jedlicka V, et al. Acute mesenteric ischemia. Hepato-Gastroenterology.
2008;55:1349–52.
10. Tallarita T, Oderich GS, Macedo TA, et  al. Reinterventions for stent restenosis in patients
treated for atherosclerotic mesenteric artery disease. J Vasc Surg. 2011;54:1422–9.e1.
11. Poole JW, Sammartano RJ, Boley SJ. Hemodynamic basis of the pain of chronic mesenteric
ischemia. Am J Surg. 1987;153:171–6.
12. Schoots IG, Koffeman GI, Legemate DA, et al. Systematic review of survival after acute mes-
enteric ischaemia according to disease etiology. Br J Surg. 2004;91:17–27.
13. Moneta GL, Lee RW, Yeager RA, et al. Mesenteric duplex scanning: a blinded prospective
study. J Vasc Surg. 1993;17:79–84. discussion 5–6.
14. Tallarita T, Oderich G. Acute mesenteric vascular disease. In: Settembrini P, Minerva Medica,
editors. Vascular surgery: how when why Ed; 2017.
 Part V
Upper and Lower Limbs
Upper and Lower Limbs: Surgical
Anatomy and General Consideration 17
in Emergency Settings

Matteo Marone and Ilenia D’Alessio

17.1 Introduction

It is extremely important, for every emergency physician, the knowledge of the

surgical anatomy of the limbs since vascular injury is one of the most frequent
causes of limb loss in trauma and non-trauma situations.
Considering the upper limb, its vascular tree originates in different ways: on the
right side the subclavian artery originates from the brachiocephalic trunk and on the
left it originates from the aortic arch. The subclavian artery runs in the chest and
exits from it at the back of the clavicle, entering in the prescalenic area. At this level
the right laryngeal recurrent nerve is strictly attached to the subclavian artery. To
get vascular control at this level the best option is to proceed with a sternotomy and
entering the chest.
At the level of the interscalenic space, the subclavian artery runs between the
anterior and the mid scalene muscles and is surrounded by the brachial plexus. At
this level, during the dissection, care must be taken to avoid nerve injuries. The
favourite way to access this artery is by a supraclavicular incision.
At the level of postscalenic space the subclavian artery becomes axillary artery.
The latter runs below the pectoral major and it is divided by the pectoral minor in 3
segments. The best way to expose this artery is performing a subclavicular incision
and dividing the major and minor pectoralis muscles. The axillary vein usually is
encountered first and great care is needed in order to avoid venous and nerve injuries.

M. Marone
Department of Surgery, Tygerberg Hospital, Cape Town, South Africa
I. D’Alessio (*)
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
Department of Vascular Surgery, Fondazione “A. De Gasperis” ASST Grande Ospedale
Metropolitano Niguarda, Milan, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 191

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_17
192 M. Marone and I. D’Alessio

After the axillary artery, the vascular bundle enters in the arm and the artery is
named brachial artery. The brachial artery lies close to the brachial vein and the
median nerve, between the triceps and the biceps on the medial aspect of the arm.
At the level of the elbow the artery divides into the radial, ulnar and interosseous
artery. The access to the brachial artery at this level is through a straight incision
between triceps and biceps. The artery lies immediately below the fascia and it is
important in this case to identify and preserve the median nerve in order to avoid
injuries. If the artery needs to be isolated close to its bifurcation, then a lazy S inci-
sion needs to be performed and part of the biceps tendon is usually isolated.
Below the elbow radial and ulnar arteries lie deep, below the flexor muscles. The
best way to access these arteries is to isolate the bifurcation and follow them into the
arm. It is also possible to expose them at the level of the wrist but in this case great
care needs to be taken in order to avoid injuries to the median and ulnar nerve [1, 2].
Considering the lower limbs, the femoral artery originates from the external iliac
artery at the level of the inguinal ligament. The common femoral artery is located in
the inguinal triangle. The border of the inguinal triangle are the inguinal ligament,
the Sartorius muscle and the great abductor. At this level the common femoral artery
splits in the superficial femoral artery that runs in the medial aspect of the thigh and
the profunda femoral artery that lies deep close to the femur. To expose the common
femoral artery and its bifurcation the best option is to perform an arcuate incision at
the mid third of the groin. The artery is located lateral to the vein just below the
fascia. During the dissection it is important to move the fat pad lateral to medial in
order to avoid lymphatic leak.
The superficial femoral artery runs then in the Hunter channel. This channel is
delimited medially by the great adductor and superiorly by the Sartorius. At the end
of the channel the artery passes from medial to posterior perforating the adductor
channel. To expose the first part of the superficial femoral artery a medial thigh inci-
sion needs to be performed and the Sartorius muscle needs to be moved from medial
to lateral. To expose the distal part of the superficial femoral artery and the proximal
popliteal artery a medial thigh incision needs to be performed and the Sartorius
muscle needs to be moved from lateral to medial.
The superficial femoral artery continues into the popliteal artery. The latter runs
posterior to the knee and is divided into three portions: supra-articular, infra-­
articular and subarticular. The exposure of the popliteal artery below the knee is
performed through a medial incision in the upper leg. When the fascia is opened, the
gastrocnemius muscle is retracted laterally and the fat pad is exposed. Surgeons
usually encounter first the popliteal vein that can be mobilized and, below it, is pos-
sible to identify the artery itself.
The popliteal artery then gives the anterior tibial artery that runs in the anterior
compartment to the leg and the tibioperoneal trunk that divides in peroneal artery
and posterior tibial artery. The anterior and posterior tibial artery can be easily
exposed at the level of the talocalcaneal joint because they run not too deep and
close to the fascia [2, 3].
17  Upper and Lower Limbs: Surgical Anatomy and General Consideration… 193

17.2 Emergency Settings

In emergency settings, there are two types of clinical scenarios that we can face to:

• Ischaemic limb
• Haemorrhagic limb

In the ischaemic limb scenario patients present complaining of intense pain of

the affected limb, without irradiation, associated, in the early presentation, with loss
of sensation and, in the delayed presentation, with complete loss of sensation and
muscular function [4].
Causes of ischaemic limb in emergency situations can be numerous and can be
divided into trauma related, non-trauma related and iatrogenic injuries

• Trauma related causes include blunt and penetrating trauma. In blunt trauma
there is no open wound on the skin and the vessels can be injured due to forces
that compress the artery causing: rupture with thrombosis of the vessels or dis-
section (more common). Bones fractures can also kink the vascular bundle of the
limb, creating a total arterial and venous occlusion. In penetrating trauma, a for-
eign body penetrates the skin and can injure vascular structures causing: throm-
bosis or dissection [5, 6].
• Non-trauma related causes of limb ischaemia are acute ischaemia due to throm-
bosis of pre-existing plaque or distal embolization and dissection.
• Iatrogenic injuries can be caused by access site complications in endovascular
procedures.

In the haemorrhagic limb scenario patients present with a vascular lesion

actively bleeding, usually associated with tachycardia and low blood pressure. The
ABG (arterial blood gas) will show high lactate and base excess. Causes of haemor-
rhagic limb are penetrating traumas, due mainly from stab and gunshot wounds, but
also by iatrogenic procedure (e.g. bleeding from percutaneous access site). However,
also bone fractures can be associated with haemorrhage if the sharp edge of the
bone injuries the vascular bundle of the limb.

17.2.1 Signs of Vascular Lesions in Trauma Patients

Vascular lesions can present with hard signs or soft signs [7].
Hard signs are:

• Expanding haematoma
• Absent pulses
• Bruit or palpable thrill
• Active haemorrhage
194 M. Marone and I. D’Alessio

• Distal ischaemia-Ischaemic limb can be easily identified clinically looking at the

patient and looking for the “6P” of Pratt:
–– Pulseless
–– Pain
–– Paresthesia
–– Poikilothermia
–– Paralysis
–– Pallor

Soft signs are:

• Non-expanding haematoma
• Bleeding on the scene no more active
• Nerve injuries
• Proximity of the wound to the vessel
• ABI (Ankle Brachial Index) <0.9

17.2.2 Signs of Vascular Lesions in Non-trauma Patients

Patients with non-traumatic lesions usually present at E.D. (Emergency Department)

with signs of acute ischaemia that are easily recognizable remembering “6P” of
Pratt (see above). The most used classification to describe an ischaemic limb is
presented in the table below and is known as Rutherford classification, adopted by
SVS and ESVS (respectively Society of Vascular Surgery and European Society of
Vascular Surgery) [8, 9] (Table 17.1):
It’s important to know the existence of other two situations: blue toe syndrome
and chronic ischaemia. The former is a digital ischaemia with intact large vessel
circulation and is a variation of acute limb ischaemia, except that the size of the
embolic material is small enough to travel into the end arteries. The latter is a
chronic situation, in contrast to acute limb ischaemia, where repeated emboli to the

Table 17.1  Rutherford classification for acute ischaemia

Sensory Motor Arterial Venous
Category impairment impairment Doppler signal Doppler signal
Class I No No Audible Audible
Viable—no
immediate threat
Class IIa Minimal in the toes No Often inaudible Audible
Marginally or none
threatened
Class IIb Involves forefoot Mild to Usually Audible
immediately ±rest pain moderate inaudible
threatened
Class III Anaesthetic Paralytic/ Inaudible Inaudible
Irreversible rigour
17  Upper and Lower Limbs: Surgical Anatomy and General Consideration… 195

extremities can manifest with a stepwise deterioration of distal arterial flow from
individual embolic events that have either no or mild symptoms.

17.3 Diagnosis

It is important to recognize all types of vascular injuries, in order to avoid delay of

treatments, which can lead to serious long-term complications and eventually limb
loss. Once the clinical picture is defined, it is important to immediately call the
vascular physician on call, to proceed with the appropriate diagnostic and therapeu-
tic pathway.

17.3.1 Ischaemic Limb

In most cases, in trauma and non-trauma patients, DUS (Duplex Ultra Sound) is
promptly performed due to its non-invasiveness, furthermore it is a diagnostic
method radiation free and relatively cheap. DUS can show the presence of clot in
the artery. Recent clot is viewed as ipo-anechogenic material in the lumen of the
artery, while old clot is viewed as hyperechogenic material. In some centres, DUS
is used as the sole diagnostic method before taking the definitive management deci-
sion. Other surgeons prefer to perform a CTA (computed tomography angiography)
to all the patients presenting with ischaemic limbs. CTA allows a proper visualiza-
tion of the problem and is important to identify other injuries in case of trauma.
Nevertheless, this type of exam is expensive and its risks include radiation exposure
and contrast material nephropathy. There is no utility in performing a CT scan with-
out contrast material in the suspect of a vascular injury. DSA (digital subtraction
angiography) is the gold standard in the identification of vascular problems and it
can be performed in angiographic theatre, especially if below the knee problems are
suspected. In traumatized patient, it may be helpful to perform X-ray in order to
detect the presence of bone injuries [8, 10].

17.3.2 Haemorrhagic Limb

In this setting the physician usually faces an active bleeding coming from a skin
wound or an expanding haematoma in the limb. The diagnostic instruments used in
haemorrhagic patients are same used in the ischaemic patients: DUS, CTA, DSA
and, if appropriate, X-ray.
196 M. Marone and I. D’Alessio

17.4 Decision-making and Initial Management

In case of suspected vascular lesions, it is important to inform the trauma surgeon

on call immediately, because in limb injuries time is life. After 6 h of total ischaemia
the muscular structure of the limbs is completely dead and the only possible inter-
vention is the amputation. If the accepting hospital has no vascular surgery service,
it is mandatory to inform the trauma surgeon or general surgeon on call, which task
is to stabilize the patient to transport it to a tertiary facility.

17.4.1 Ischaemic Limb

For those who present with acute limb ischaemia, anticoagulation with a heparin
and intravenous fluid therapy should be promptly initiated prior to making plans for
intervention. These can be started while awaiting evaluation by a specialist trained
to treat the embolic event. Options for managing lower extremity embolism include
open embolectomy, thrombolysis and transcatheter thrombectomy. Factors such as
anatomy, degree of limb threat, runoff, aetiology and patient factors will guide the
choice of one over the other. (See Acute and Chronic limb ischaemia, cap 19.)
Usually, in case of embolic disease a simple unblocking with a Fogarty catheter can
be attempted performing a femoral artery cut down. The majority of the emboli stop
at the femoral bifurcation or at the level of the popliteal artery. Sometimes a popli-
teal cut down needs to be performed to re-vascularize the 3 leg vessels (anterior
tibial artery, posterior tibial artery, peroneal artery). In case of thrombotic disease
over a previous atherosclerotic plaque an embolectomy procedure can be attempted
but usually it fails. The best option is probably performing a DSA on table in order
to find an appropriate runoff vessel and proceed with a bypass using synthetic graft
or autologous vein. Vein is the favourite conduit if the target vessel is below the knee
while, for above the knee vessels, Dracon or PTFE (polytetrafluoroethylene) can
be chosen.

17.4.2 Haemorrhagic Limb

First of all, if patients arrive with a bleeding penetrating wound it is important to ask
one of the members of the team to stop the bleeding, while the leader of the team
performs the ABCDE primary survey (see Chap. 24). Haemostasis can be achieved
using direct compression with gauze at the beginning. If the injury is located in a
position where it can be compressed, a tourniquet can be applied at the base of the
limb that can remain in situ for a maximum of 6 h [11]. If the injury is located in a
non-compressible area like the subclavicular space, haemostasis can be achieved
using Foley’s catheter. Once the vascular control is achieved, the surgeon must eval-
uate the damage. It is mandatory to perform a debridement of the edge of the artery
in order to reduce the risk of contamination and the risk of anastomotic failure. If,
after the debridement, the edges of the artery are quite close, a primary repair can be
17  Upper and Lower Limbs: Surgical Anatomy and General Consideration… 197

attempted. This is the best options because it is a quick procedure and it does not use
any kind of graft. If the edges of the artery are distant, the situation is more complex.
In these cases, a bypass needs to be performed. The preferred conduit is in any case
the contralateral great saphenous vein. It is never an option to use the homolateral
saphenous vein because it can be injured or, if the deep veins are injured, it is impor-
tant to preserve it to allow an adequate venous outflow to the limb. Using a pros-
thetic graft is an option only if no other veins are available due to the high risk of
infection of this kind of conduit.
In case of hard signs, the patient must be referred immediately to the vascular
surgeon on call and he needs to go immediately to theatre in order to sort the prob-
lem out. Hard signs means that the patient is actively bleeding and it is almost cer-
tain to have vascular injuries at the site of the penetrating trauma. For this reason,
there is no need for further investigations. It is mandatory to order blood and blood
products for these types of patients because the risk of bleeding in theatre is really
high [7].
In case of soft signs, the treating physician needs to rule out the presence of a
vascular injury at the site of trauma. In order to do so the preferred techniques are
DUS and CTA. However, DSA remains the gold standard in the diagnosis of vascu-
lar injuries, especially if foreign bodies can create artefact in the CTA and DUS
images. In these kinds of patients there is time to diagnose the presence of an injury
and there is no rush to take the patient to theatre (if he/she is stable). Nerve injuries
are considered soft signs of vascular injuries because nerves run close to arteries and
veins. If there is a nerve fallout probably not only the nerve but also the vascular
bundle is damaged. In case of tract close to the anatomical location of the vascular
bundle, it is important to check the vascular structure for injuries, because gunshot
can create vascular dissection and damage to the surrounding tissue due to cavita-
tion mechanism and, if we speak about stab wound, the physician cannot have the
certainty of the direction of the penetration in the body [7].

Key messages
• The knowledge of upper and lower extremities surgical anatomy is manda-
tory to obtain a prompt and conscious approach to patients with ischaemic
and/or haemorrhagic signs.
• In emergency setting there are two possible scenarios: ischaemic limb and
haemorrhagic limb.
• To recognize an ischaemic limb remember the 6P of Pratt.
• The clinical diagnosis should precede the instrumental diagnosis that could
be made using: Doppler UltraSound, Computed Tomography Angiography
or Digital Subtraction Angiography.
• All ischaemic patients should be revascularized in 6 h (remember Time is
life) and treated, initially, with heparin and fluids.
• All instable haemorrhagic patients need to be treated as soon as possible.
198 M. Marone and I. D’Alessio

References
1. Swenson RS, Snow NJ, Catlin B. Vascular anatomy of the upper limbs. In: Crit Limb isch-
emia. Cham: Springer; 2017. p. 45–56. https://doi.org/10.1007/978-­3-­319-­31991-­9_7.
2. Anatomy, descriptive and surgical - Digital Collections - National Library of Medicine; n.d..
https://collections.nlm.nih.gov/catalog/nlm:nlmuid-­06220300R-­bk. (Accessed July 6, 2021).
3. Swenson RS, Snow NJ, Catlin B. Vascular anatomy of the lower limbs. In: Crit Limb Ischemia.
Cham: Springer; 2017. p. 57–70. https://doi.org/10.1007/978-­3-­319-­31991-­9_8.
4. Santistevan JR.  Acute limb ischemia: an emergency medicine approach. Emerg Med Clin
North Am. 2017;35:889–909. https://doi.org/10.1016/j.emc.2017.07.006.
5. D’Alessio I, Domanin M, Bissacco D, Romagnoli S, Rimoldi P, Sammartano F, et al. Operative
treatment and clinical outcomes in peripheral vascular trauma: the combined experience of
two centers in the endovascular era. Ann Vasc Surg. 2020;62:342–8. https://doi.org/10.1016/j.
avsg.2019.06.037.
6. Huber GH, Manna B. Vascular extremity trauma. Tamba, FL: StatPearls Publishing; 2021.
7. Romagnoli AN, Dubose J, Dua A, Betzold R, Bee T, Fabian T, et al. Hard signs gone soft:
A critical evaluation of presenting signs of extremity vascular injury. J Trauma Acute Care
Surg. 2021;90:1–10. https://doi.org/10.1097/TA.0000000000002958. Lippincott Williams
and Wilkins
8. Björck M, Earnshaw JJ, Acosta S, Bastos Gonçalves F, Cochennec F, Debus ES, et al. Editor’s
Choice – European Society for Vascular Surgery (ESVS) 2020 Clinical Practice Guidelines
on the Management of Acute Limb Ischaemia. Eur J Vasc Endovasc Surg. 2020;59:173–218.
https://doi.org/10.1016/j.ejvs.2019.09.006.
9. Hardman RL, Jazaeri O, Yi J, Smith M, Gupta R.  Overview of classification sys-
tems in peripheral artery disease. Semin Intervent Radiol. 2014;31:378–88. https://doi.
org/10.1055/s-­0034-­1393976.
10. McNally MM, Univers J.  Acute limb ischemia. Surg Clin North Am. 2018;98:1081–96.
https://doi.org/10.1016/j.suc.2018.05.002.
11. Kauvar DS, Dubick MA, Walters TJ, Kragh JF. Systematic review of prehospital tourniquet use
in civilian limb trauma. J Trauma Acute Care Surg. 2018;84:819–25. https://doi.org/10.1097/
TA.0000000000001826.
Acute and Chronic Limb Ischemia
18
Giuseppe Galzerano, Edoardo Pasqui, Gianluca Chierchini,
Alberto M. Settembrini, and Pasqualino Sirignano

18.1 Introduction

Limb ischemia is a common clinical condition that causes considerable morbidity

and mortality and represents a major drain on healthcare resources. Critical acute
(ALI) and chronic limb ischemia (CLI) represent a vascular emergency and are both
a life and limb threatening disease.
Best care is required to reduce mortality and morbidity.
Both conditions occur due to the cessation of arterial perfusion to an extremity.
If ALI is a vascular surgical emergency, also patients presenting with CLI need for
emergent treatment, including medical, surgical, and ischemic lesions management.
The management of ALI and CLI remain particularly challenging because ampu-
tation rates are variable and despite therapy and mortality rates range from 10 to
40% of all patients due to increase in cardiovascular risk for this cohort of patients.
Moreover, distinction between ALI and CLI patients should be difficult, and
patients admitted for ALI suffered chronic arterial disease. At last but not at least,
oftentimes, patients presenting with ALI and CLI are the sickest patient cohort that
vascular specialists treat.

G. Galzerano (*) · E. Pasqui · G. Chierchini

Department of Vascular Surgery, University Hospital of Siena, Siena, Italy
A. M. Settembrini
Department of Vascular Surgery, University Hospital of Siena, Siena, Italy
Vascular Surgery Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico,
Milan, Italy
P. Sirignano
Department of Vascular Surgery, University Hospital of Siena, Siena, Italy
Vascular Surgery Unit, Department of Surgery, “Paride Stefanini”, Sant’Andrea Hospital,
“Sapienza” University of Rome, Rome, Italy

© The Author(s), under exclusive license to Springer Nature 199

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_18
200 G. Galzerano et al.

Surgical management has improved according to technological innovation and

even if open surgical revascularization has been the mainstay of therapy, over the
last several years, many percutaneous technologies have emerged that have pro-
vided alternative modalities of restoring perfusion. In addition, pharmacological
development has provided new drugs, quickly become mandatory in emergent and
long-life treatment of these patients.

18.2 Multimodal Approach to ALI and CLI

Patients suffering ALI and CLI need a multidisciplinary approach.

Emergent management of these patients aims to prevent major cardiovascular
events, to treat ischemic pain and at last to guarantee distal perfusion.
Even if vascular surgeon could play a role of team leader, several specialists have
to be involved in ALI and CLI emergent management and moreover during follow-
­up. Particularly cardiological evaluation is mandatory, all ALI and CLI patients
should be considered at high risk for further cardiovascular complication and phar-
macological control of major CV risk factors as hypertension, diabetes, and LDL
level has to be started as soon as possible.
Anesthesiologists should be involved in management of ALI and CLI patients,
although surgical procedures require only local anesthesia.

Emergent treatment of ALI and CLI

• Drugs: ALI/CLI anticoagulation/antiaggregation
• Pain control: anesthesiological evaluation
• Cardiac status: cardiac evaluation and specific therapy (heart rate control, statins,
hypertension)
• Lesions control (CLI): foot drainage

18.3 Diagnostic Imaging

Imaging in ALI and CLI aim to identify anatomic localization of arterial occlusion.
Decision-making is crucial to reduce time to reperfusion and to minimize iodine
contrast acute kidney injuries.
Bed-side ultrasound evaluation should follow clinical evaluation. Patients sus-
pected for ALI and CLI have to be referred in centers that could guarantee complete
diagnostic and therapeutic management.
In terms of diagnostic accuracy, digital subtraction angiography (DSA) is still
considered the standard investigation for ALI and CLI. In patients with severe renal
insufficiency, carbon dioxide angiography may be considered. Isolated DSA should
be avoided, and it represents the first therapeutic line and should be performed in the
operating theater where we intend to revascularize the patient.
Duplex-Ultrasound evaluation (DUS) is able to obtain the necessary information
in 90% of cases where revascularization is considered, and is an accurate modality
with which to detect complete or incomplete obstruction in the common femoral,
superficial femoral, and popliteal arteries, and in bypass grafts. The diagnostic
18  Acute and Chronic Limb Ischemia 201

accuracy is lower for detection of stenosis or occlusions in the aorto-iliac and tibial
arteries. Computed tomography angiography (CTA) is considered more useful than
DSA because it can combine evaluation of the possible primary cause of ALI, with
high resolution evaluation of the outflow tract and provide a roadmap to guide treat-
ment in both conditions. However, as mentioned for DSA, there is an association
between the use of iodinated contrast and acute kidney injury and some papers
evidenced as patients treated based on DUS as the sole preoperative modality, pre-
sented similar outcomes to those who had preoperative computed tomography
angiography.

Imaging modality
CTA Ultrasound
Aortic +++ +
Iliac +++ +
Femoral +++ +++
Popliteal +++ ++
Tibial ++ +++ (hemodynamic evaluation)
Foot arteries − (completion DSA required) −

18.4 Surgical Approach to ALI and CLI

As mentioned current guidelines consider percutaneous approach as first-line treat-

ment for majority of patients suffering ALI and CLI.
However, patients suffering ALI and CLI have to be treated in centers that could
offer both techniques.
Operating theaters should be equipped for endovascular and open surgical treat-
ment at the same time.
Although the number of patients treated purely with the endovascular procedure has
grown, there is a significant number of patients that requires a combined (hybrid)
approach using both techniques, preferably in one session in both acute patients and on
chronic conditions. Moreover in an emergency setting or in some special conditions
(patient’s compliance, renal failure…) a comprehensive preoperative evaluation could
be disregarded. This results in uncertain operating strategy in most of the patients.
The majority of patients presents significant comorbidities and requires complex
multilevel arterial repair.
We could identify three different settings to perform both techniques:

• the interventional radiology suite, which is fully equipped for endovascular pro-
cedures, including excellent imaging tools and a broad portfolio of materials.
However, it is not ideal for open surgery.
• The operating room (OR) is ideal for open revascularization but is usually
equipped with only a mobile X-ray C-arm and a basic CAT laboratory. These
shortcomings can be reduced due to recent technological developments. The
modern C-arm already possesses the capability for digital subtract angiography
with high resolution, which allows for road mapping, data backup, etc. The ste-
202 G. Galzerano et al.

rility, illumination, and handling of the operating table are the advantages of an
OR. It may be equipped with an X-ray-transparent operating table and an auto-
matic injector for contrast agents. Although the image quality will never be the
same as it is in the intervention suite, it is still preferable to perform ALI cases
and CLI patients with undefined strategy.
• The third and ideal solution is a special hybrid operating theater that combines
the advantages of the two previous options, but at a greater cost.

In all settings an ultrasound machine and the possibility to employ DUS scan in
a sterile field became more and more mandatory. DUS allow access evaluation and
a noninvasive control of distal perfusion in all patients.
Even the next sentence might seem obvious, it is important to stress that physi-
cian who intend to treat ALI and CLI patients should have skillfulness, experience,
and competence in all diagnostic imaging evaluation and both operating techniques.
This goal could be achieved in a multidisciplinary team that could provide an
emergent and simultaneous procedure for all patients.

18.5 Operating Theater Requirements

• SPACE: One of the most necessary aspects that is often the least considered is the
need for adequate and proximate storage space for a stock of implantable materi-
als and disposable items that is easily and quickly retrievable. These will include
an inventory system to track and replace many readily used items, such as cathe-
ters, sheaths, wires, percutaneous transluminal angioplasty balloons, and stents.
In addition to space for storage, there is a need for increased working space within
the operating room. Meeting this increasing need for space may not necessarily be
obtained by expanding the total square footage of the room but by eliminating
unnecessary elements that obstruct the working space. Although a conventional
operating room requires some basics, such as an instrument table, operating table,
and anesthesia area, there is increased need in an endovascular suite to accom-
modate a movable table, the imaging equipment, and additional technologic sup-
plements, such as intravascular ultrasound, mechanical thrombolytic machinery,
and accessory tables to hold the percutaneous equipment. Furthermore, added
space is necessary to allow for flexibility when approaching patients with percu-
taneous access. It may be necessary to access a patient via either the brachial or
femoral artery, and the room must be convertible enough to accommodate this
capability. Steric constraints can be modeled using computer-­aided design appli-
cations to help the entire surgical team understand and optimize procedural flow.
• IMAGING ACQUISITION AND STORAGE: Pros and Cons using a portable
C-arm rather than fixed equipment could be resumed in: increasing imaging
quality reduce room flexibility. Data acquisition upgrades are not limited to the
addition of a C-arm. In addition, surgeons should consider the construction of a
control room. The control room houses the computer equipment necessary for
postprocessing of the images and provides for an ample workspace to accom-
plish this. This is not easy to obtain in the majority of old hospital.
18  Acute and Chronic Limb Ischemia 203

• DATA VISUALIZATION: capability to visualize preoperative data, and defini-

tion of intraoperative DSA improve results in ALI and CLI treatment.
• RADIATION PROTECTION: This point represents an issue for both patients
and physicians. The increased endovascular workload leads to considerably
extended exposure times for vascular surgeons comparable to those otherwise
only encountered in interventional radiology and cardiology. Therefore, it is
important that the vascular specialist is not only aware of all measures of radia-
tion protection for the patient and also for the operating room personnel but is
also fully informed on the topic of radiation protection at the administrative and
legal levels.
• FULL SURGICAL EQUIPMENT: Open surgical procedures could be less
invasive and more effective in CLI and ALI patients.

Surgical Vascular Access in Acute and Chronic Limb Ischemia Treatment

• Axillary artery: It could be dissected in the first and third part (minor
pectoralis muscle division)—axillo-femoral bypass, necklace bypass,
good access for endovascular procedure for aorto-iliac pathologies.
• Brachial artery: The whole artery could be isolated, distal part is com-
pressible so could be eligible as puncture site for percutaneous proce-
dures—Fogarty embolectomy of upper limbs, omeral access in
percutaneous or hybrid procedure-.
• Forearm arteries: Surgical exposure should be useful in posttraumatic
ischemic injuries; moreover, distal radial artery including snuff box seg-
ment represents a common percutaneous access.
• Descending thoracic aorta: It is uncommon cutdown in ischemic patients;
however, there are some reports in complete infrarenal aortic occlusion
treatment—thoracic aorta-femoral bypass.
• Infrarenal Aorta: Access to infrarenal aorta is necessary during aortic
endarterectomy or aorto-bifemoral bypass.
• Common and External Iliac arteries: iliac endarterectomy, cross over
bypass, iliac-femoral bypass.
• Common Femoral artery: This is the most common access in ischemic
patient treatment for surgical or endovascular procedures (fit for large per-
cutaneous access >8 Fr) (Fig. 18.1).
• Superficial Femoral artery: It represents an easy access during surgical
procedures in the medial and distal part; however, it is not eligible for non-­
US-­guided percutaneous access (Fig. 18.2).
• Popliteal artery: It represents the most common outflow vessel of infrain-
guinal bypass (Fig. 18.3).
• Below the knee and below the ankle vessels: They represent distal anas-
tomosis site of ultradistal bypass and they have an increasing role (as all
infrainguinal vessels) as puncture site for endovascular retrograde
recanalization.
204 G. Galzerano et al.

Fig. 18.1 Common
femoral artery surgical
access

Fig. 18.2 Distal
superficial femoral artery
surgical access
18  Acute and Chronic Limb Ischemia 205

Fig. 18.3  Distal popliteal

artery surgical access

18.6 Glossary of Most Common Procedure Using in Acute

and Chronic Limb Treatment

18.6.1 Thrombus Management

• “Fogarty Embolectomy” since 1963 represents the mainstay in thrombus removal

procedure for acute limb ischemia, more recently the original catheter was
improved with over the wire technology.
• Catheter directed thrombolysis (CDT): In catheter directed thrombolysis, throm-
bolytic medication (tissue plasminogen activator, t-PA) is infused over time that
spans hours to days, in the region of thrombus using a multi side-hole catheter.
• Pharmacomechanical thrombectomy and percutaneous aspiration thrombectomy:
• Pharmacomechanical thrombectomy (PMT) devices are utilized stand alone or
more commonly in adjunct with CDT with the goal of endovascular thrombus
maceration and removal. PMT devices in general can be categorized as rheolytic,
rotational, or ultrasound enhanced. Along with the introduction of aspiration,
PMT devices enhance the surgeon’s ability to remove thrombus quickly, result-
ing in lower doses of thrombolytic drugs and reducing the time to reperfusion.
Vacuum-assisted percutaneous aspiration thrombectomy (PAT) with the
Penumbra Indigo Mechanical Thrombectomy System (Penumbra, Alameda, CA,
USA) is emerging as an effective tool to remove thrombi and emboli from arter-
ies and veins.

18.6.2 Atherosclerotic Lesions Management

• Endarterectomy: It consists in surgical removal of the plaque. Moreover, using a

hybrid technique (Moll ring catheter), endarterectomy could be extended to arte-
rial segment far from surgical cutdown. Procedure could be completed with
patch angioplasty to improve long-term patency.
206 G. Galzerano et al.

• Bypass: It is probably the gold standard treatment in chronic ischemia treatment,

especially employed autologous conduit. However, improvement in e­ ndovascular
techniques is still reducing number of these procedures in the majority of vascu-
lar centers.
• Balloon angioplasty: It is the most used endovascular procedure and after
“Dotterization” the former one. Drug coated surfaces is one of the most common
improvement of this technique as scoring device or intravascular lithotripsy.
• Stenting: A peripheral artery stent is a metal mesh tube that expands inside an
artery. Use of stent as both primary treatment of bail-out is controversial.
Innovation development, including drug eluting technology, is still reviving
stenting in peripheral artery disease.
• Endovascular bypass: This technique involves cover stents deployment after
intraluminal recanalization.
• Endovascular Atherectomy: It represents a sort of endovascular endarterectomy.
It is an evolving technology with more and more devices available with promis-
ing results.

Further Reading
European Society for Vascular Surgery (ESVS). 2020 Clinical Practice Guidelines on the
Management of Acute Limb Ischaemia. Eur J Vasc Endovasc Surg. 2020;59:173e218.
Conte MS, Bradbury AW, Kolh P, White JV, Dick F, Fitridge R, Mills JL, Ricco JB, Suresh
KR, Murad MH, Aboyans V, Aksoy M, Alexandrescu VA, Armstrong D, Azuma N, Belch J,
Bergoeing M, Bjorck M, Chakfé N, Cheng S, Dawson J, Debus ES, Dueck A, Duval S, Eckstein
HH, Ferraresi R, Gambhir R, Gargiulo M, Geraghty P, Goode S, Gray B, Guo W, Gupta PC,
Hinchliffe R, Jetty P, Komori K, Lavery L, Liang W, Lookstein R, Menard M, Misra S, Miyata
T, Moneta G, Munoa Prado JA, Munoz A, Paolini JE, Patel M, Pomposelli F, Powell R, Robless
P, Rogers L, Schanzer A, Schneider P, Taylor S, De Ceniga MV, Veller M, Vermassen F, Wang
J, Wang S, GVG Writing Group for the Joint Guidelines of the Society for Vascular Surgery
(SVS), European Society for Vascular Surgery (ESVS), and World Federation of Vascular
Societies (WFVS). Global vascular guidelines on the management of chronic limb-threatening
ischemia. Eur J Vasc Endovasc Surg. 2019;58:S1eS109.
Vascular and endovascular surgical techniques: an Atlas. 4th Edition.
Dieter RS, Dieter RA Jr, Dieter RA III, Nanjundappa A. Critical limb ischemia, acute and chronic.
Cham: Springer; 2016.
2021 ESC Guidelines on cardiovascular disease prevention in clinical practice ESC Clinical
Practice Guidelines. https://doi.org/10.1093/eurheartj/ehab484
Patologia ostruttiva cronica aorto-iliaca e delle arterie degli arti inferiori. https://www.sicve.it/wp-­
content/uploads/2021/03/3-­lgsicve-­patologia-­ostruttiva-­cronica-­arti-­inferiori.pdf
Traumi vascolari periferici e ischemie acute degli arti https://www.sicve.it/wp-­content/
uploads/2021/03/7-­lgsicve-­traumi-­vascolari-­e-­ischemie-­acute.pdf
Popliteal Artery Aneurysm and
Non-­atherosclerotic Limb Disease 19
Alberto M. Settembrini and Pasqualino Sirignano

19.1 Thoracic Outlet Syndrome (TOS)

Thoracic outlet syndrome (TOS) describes one or more patterns of symptoms as a

result of compression of the neurovascular bundle at the thoracic outlet.
Neurogenic TOS (NTOS) is present when the brachial plexus is compressed at
the scalene triangle or by the pectoralis minor muscle as it inserts on the coracoid
process. Venous TOS (VTOS) is present when the vein is compressed by the ante-
rior junction of the clavicle and first rib, or, less commonly, by the pectoralis minor
muscle. It can manifest as acute thrombosis or by intermittent positional obstruction
despite an open vein. Arterial TOS (ATOS) is thought to be present when true arte-
rial damage occurs (thrombosis, distal embolization, and/or aneurysm formation),
but may also be described as present when occlusion of the artery causes true isch-
emic symptoms.
The incidence of TOS is from 3 to 80 per 1000 people, and between 2500 and
3000 first rib resections (FRR) are performed yearly in the United States.
To understand the pathophysiology, it is essential to know the anatomy of the
scalene triangle because its compression causes TOS. The triangle is formed by the
anterior scalene muscle, the middle scalene muscle, and, inferiorly, the upper border
of the first rib. This area has space just for its contents as subclavian artery, and
anything that narrows the triangle (posttraumatic fibrosis and scarring of the ante-
rior scalene muscle, a cervical rib or band) can cause its compression (Fig. 19.1).

A. M. Settembrini (*)
Vascular Surgery Unit, Fondazione IRCCS Ospedale Maggiore Policlinico, Milan, Italy
P. Sirignano
Vascular Surgery Unit, Department of Surgery, “Paride Stefanini”, Sant’Andrea Hospital,
“Sapienza” University of Rome, Rome, Italy

© The Author(s), under exclusive license to Springer Nature 207

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_19
208 A. M. Settembrini and P. Sirignano

Fig. 19.1  Right thoracic outlet. Nerve (yellow) compression can occur at the scalene triangle
(upper dotted line) or pectoralis minor space (lower dotted line), whereas venous compression
most often occurs at the costoclavicular space (medium dotted line). Arterial injury is most often
due to bone trauma at the scalene triangle. (from Reporting standards of the Society for Vascular
Surgery for thoracic outlet syndrome. Illig KA, Donahue D, Duncan A, Freischlag J, Gelabert H,
Johansen K et al. J Vasc Surg. 2016 Sep;64(3):e23–35)

In NTOS, local pain and tenderness are the symptoms of this compression and
they can be worsened by all the movements that narrow the triangle (arms overhead)
or stretch the brachial plexus.
19  Popliteal Artery Aneurysm and Non-atherosclerotic Limb Disease 209

In VTOS, the compression of the vein anteriorly at the junction of the first rib and
clavicle is the cause. Such compression can narrow the vein (intermittent positional
obstruction) or, much more commonly, cause no symptoms until actual vein injury
and thrombosis are present (effort thrombosis). Subclavius muscle, tendon, and cos-
toclavicular ligament are essential, but ultimately, the anterior portion of the rib (or
clavicle) must be addressed to treat this entity [1].
True ATOS (defined as actual damage to the artery with or without distal
sequelae) is almost always caused by a bony abnormality (cervical rib, abnormal
first rib, long C7 transverse process). It should be noted that cervical ribs are rela-
tively common (2.8% in women and 1.4% in men) [2].

19.1.1 Clinical Evaluation and Decision-Making

Patients with NTOS have symptoms caused by compression of the brachial plexus
at the scalene triangle. Patients usually have two different symptomatology. Firstly
pain and/or inflammation at the area of compression at anterior chest wall, axillary,
shoulder, trapezius, and neck pain, and typically have headaches as well. Secondly,
distal symptoms consistent with nerve compression: forearm and hand numbness,
pain, paresthesia, and, in advanced cases, weakness and/or atrophy. Maneuvers that
narrow the thoracic outlet (arms overhead or extended; elevated arm stress test) or
stretch the brachial plexus (dangling, driving, vacuuming, running, and upper limb
tension test).
VTOS is easier to diagnose. Patients always present acute thrombotic occlusion
of the subclavian vein, causing suddenly swollen arms, often with cyanosis and
dilated upper arm or chest wall collateral veins. In the history vigorous activity,
often with the arms overhead, will be present (hence the term “effort thrombosis”).
The acute thrombus is located very focally at the costoclavicular junction and later
after clot propagation duplex becomes positive. Diagnosis by a skilled vascular
ultrasonographer should be straightforward, although if suspicion is high and duplex
is negative, diagnostic venography should be performed.
ATOS can be diagnosed because it presents with distal ischemia and/or a palpa-
ble supra- or infraclavicular mass suggesting an aneurysm. Things that suggest
ATOS include young age, a bony abnormality, or absence of systemic atherosclero-
sis or inflammatory arteriopathies.
Decision-making in patients with a TOS depends on recognizing that the prob-
lem is due to the thoracic outlet. First, the original bony problem must be addressed,
usually by excision. Secondly, any arterial damage should be repaired, and, thirdly,
any distal issues should be addressed. Diagnosis is usually made by arteriography
and ultrasound, and a plain chest X-ray is mandatory.

19.1.2 Treatment

As mentioned above, the treatment depends on the cause of the TOS. The different
reasons provide different surgical approaches. There is the transaxillary approach,
210 A. M. Settembrini and P. Sirignano

especially in the case of the first rib removal in case of NTOS or ATOS, for VTOS
the supra- or para-clavicular access to remove the muscular conflict.

19.2 Adventitial Cystic Lesion of Popliteal Artery

Cystic adventitial disease (CAD) is an uncommon condition in which mucoid cysts

form within the adventitial layer of the arterial or venous wall. It is a rare cause of
intermittent claudication that was first described in 1947 by Atkins and Key.
The cystic lesion can affect arteries and veins, but venous involvement is spo-
radic. The popliteal artery is affected in about 85% of cases. The cysts may be uni-
locular or multilocular. Gelatinous material characteristically builds up within the
adventitial wall of the affected vessel resulting in narrowing of the lumen, compro-
mising distal blood flow.
The cause is still uncertain. One possibility can be repetitive trauma especially in
childhood; another reason could be a disorder of connective tissue or developmental
inclusion of mucin-secreting cells within the adventitia of the artery could allow a
cyst to develop within its adventitia or ganglion theory [3].

19.2.1 Clinical Evaluation and Decision-Making

Clinical evidence of this disease is usually in men (ratio to female 4:1) in the third
or fourth decade because there is an onset of claudication or symptoms referred to
as alteration of popliteal artery. Some degree of stenosis may be associated with the
cyst for an extended period with preservation of luminal patency in the popliteal
artery until the intracystic pressure exceeds that of the artery, causing compression
and occlusion or stenosis causing significant associated symptoms.
Patients can be evaluated with standard vascular evaluation in an outpatient
clinic, especially those without risk factors for peripheral vascular disease.
After the initial sudden onset of cramping pain in the calf, the patient may
experience some relief followed by typical intermittent claudication as good
collateral circulation develops as shown in peripheral atherosclerotic disease.
The Ishikawa sign is the loss of pedal pulses upon passive flexion of the knee
due to compression on the popliteal pulses by cysts and can be helpful in the
presence of large cysts.
At duplex the affected limb will show a flattening of the pulse wave below the
cystic lesion. Because of the excellent collateral circulation that usually develops in
young men, the total absence of pulse waves over the distal tibial arteries is rare.
Magnetic resonance and CTA can show the “scimitar sign” a smooth occluding
contour of the popliteal artery.
19  Popliteal Artery Aneurysm and Non-atherosclerotic Limb Disease 211

19.2.2 Treatment

Treatment of adventitial cystic disease of the popliteal artery can be conservative

through the aspiration, under duplex localization and percutaneous approach, of the
cyst eradicating it and resultant arterial stenosis or occlusion in some patients.
Because the cystic content is quite viscous and gelatinous, aspiration must be done
with a relatively large-bore needle.
A surgical intervention provides effective treatment. These can be the evacuation
of the cyst or enucleation in case of no occlusion of the artery approaching the pop-
liteal artery as the same for popliteal aneurysm through the posterior way with
S-shaped incision or medial incision.
If occlusion of the popliteal artery has occurred, a total resection and reconstruc-
tion with prosthesis or autogenous saphenous vein is the choice with better results
with a vein graft.
The recurrence rate of popliteal artery CAD after revascularization surgery is
very low (0% to 10%) compared with the rate after cyst excision alone (10–34%) [4].

19.3 Popliteal Entrapment

Popliteal entrapment syndrome is a rare, potentially limb-threatening, vascular dis-

order causing intermittent claudication in young adults without a previous history of
cardiovascular disorders. Similar to cystic lesions, this disease can be revealed in
young patients without any cardiovascular risk factor.
It was first described in 1879 by a medical student in Edinburgh, Scotland.
T. P. Anderson Stuart was dissecting the amputated leg of a 64-year-old man, and he
described the anatomic abnormality associated with the abnormal course of the pop-
liteal artery. Love and Whelan first used the term popliteal artery entrapment syn-
drome in reporting two cases in 1965.
Over the last decades, the incidence has increased to 0.17–3.5% [5]. Furthermore,
85% of patients affected with this condition are males, with almost 60% of cases
occurring in young athletes during the third decade of life [6] (Fig. 19.2). Moreover,
in about 30% of the cases, the disease has a bilaterally symptomatic presentation.

19.3.1 Clinical Evaluation and Decision-Making

The pathophysiology of this disease is understood considering the embryologic

development of structures of popliteal fossa: the in utero development of the gas-
trocnemius muscle is a dynamic process with the potential for the occurrence of
several anatomic abnormalities. The medial head of gastrocnemius muscle (MHGM)
is one of the most important causes of entrapment syndrome classified into six dif-
ferent types (Fig. 19.3).
212 A. M. Settembrini and P. Sirignano

Fig. 19.2  Lower limb

angiography that shows
thrombosis of popliteal
artery at the knee due to
entrapment of MHGM

Type I: MHGM is the typical position, but the popliteal artery has an aberrant
medial course under the muscle; Type II: MHGM insertion has a more lateral
way on the posterior face of the femur causing a medial and inferior course of the
popliteal artery.
Type III: Abnormal fibrous band or accessory muscle arising from the medial or
lateral condyle forcing the popliteal artery.
Type IV: Popliteal artery lying in its primitive deep or axial position within the
fossa, becoming compromised by the popliteus muscle or fibrous bands.
Type V: The entrapment of both the popliteal artery and vein due to any of the
causes mentioned above.
Type VI: The muscular hypertrophy, resulting in a functional compression of both
the popliteal artery and vein.
19  Popliteal Artery Aneurysm and Non-atherosclerotic Limb Disease 213

Popliteal vein Popliteal vein

Popliteal vein
Popliteal Tibial nerve Popliteal Tibial nerve Popliteal
artery artery Tibial nerve
artery
Lateral head Lateral head
of gastrocnemius of gastrocnemius Lateral head
of gastrocnemius
Medial Medial
Medial head of head of
head of gastrocnemius TYPE 1 gastrocnemius TYPE 2
gastrocnemius NORMAL COURSE

Popliteal vein Popliteal vein

Popliteal Popliteal Popliteal vein
Tibial nerve Tibial nerve Popliteal
artery artery Tibial nerve
Accessory slip Popliteus artery
of gastrocnemus Medial muscle,
head of Lateral head
fibrous band Lateral head
gastrocnemius of gastrocnemius
of nerve of gastrocnemius
Medial head branch
Medial
of gastrocnemius Medial
head of
head of
TYPE 3 TYPE 4 gastrocnemius TYPE 5
gastrocnemius

Fig. 19.3  Different types of popliteal entrapment. Two are the crucial points: medial head of the
gastrocnemius and the popliteal artery. (A. L. Rochier, B. E. Sumpio. variant popliteal entrapment
syndrome involving the lateral head of the gastrocnemius muscle: a case report, Ann Vasc Surg
2009;23:535.e5–535.e9)

Clinical evaluation should start with the history collecting. Usually the patients
are young and report symptoms similar to peripheral arterial disease with leg and
foot claudication, associated with lower extremity numbness, paresthesia, discolor-
ation, pallor, and coolness. Physical examination may reveal hypertrophy of the calf
muscles. A regular foot pulse disappearing during active plantar flexion and passive
dorsiflexion is a characteristic phenomenon. Usually the differential diagnosis is
with orthopedic syndromes [7].
The diagnosis can be confirmed with duplex ultrasound using provocative
maneuvers (leg/foot positioned first in a neutral position and then in resisted plantar
flexion) that provides a quick, inexpensive, and non-invasive initial screening test.
CTA or angio-MRI is mandatory to obtain a precise and definitive diagnosis.
The management is tailored to the patient based on the presence and absence of
the symptoms. Incidental findings can be conservatively treated, but if muscle inser-
tion abnormalities are the cause even in an asymptomatic patient, surgical correc-
tion is the preferred method of treatment.
In cases of extensive popliteal artery wall damage, occlusion, or aneurysm devel-
opment, interposition of a bypass graft using an autogenous vein has been proposed.
214 A. M. Settembrini and P. Sirignano

19.4 Popliteal Artery Aneurysm

Popliteal artery aneurysms (PA) are the most frequent peripheral aneurysm with
7/100,000 in men and 1/100,000 in women incidence.
The popliteal artery in normal anatomy has a mean diameter of 7 mm in men and
6 mm in women so the threshold for defining a popliteal artery aneurysm is more or
less an artery greater than 1 cm. Dilatation often is bilateral (Fig. 19.4, up to 60%)
and associated to other aneurysms mainly in abdominal district: 5% of people pre-
senting with an AAA have a popliteal aneurysm, while about 20% of people diag-
nosed with a popliteal aneurysm have a concomitant AAA [8, 9].

19.4.1 Clinical Evaluation and Decision-Making

Clinical presentation is a palpable mass in the popliteal fossa behind the knee, and
the chance to detect it is directly correlated with the dimension of the sac. Most
popliteal aneurysms are asymptomatic and can be discovered during routine physi-
cal examination or diagnostic imaging.
Most popliteal aneurysms are asymptomatic, like other aneurysms, but symp-
toms can be with claudication to critical limb ischemia in case of popliteal aneu-
rysm thrombosis. Popliteal aneurysms have a laminar thrombus inside the sac and
mechanical stress produced by the movements of the knee on the artery squeezes
out particles of the thrombus which embolizes the runoff vessels causing claudica-
tion or acute peripheral ischemia or blue toe syndrome.
Usually duplex studies can reveal in popliteal fossa the dilatation of the popliteal
artery; as second-level exams, a CT angio or MRI can be performed to plan for the
intervention, considering that CT angio is more helpful in case of endovascular treatment.

Fig. 19.4  Axial images of bilateral popliteal aneurysm

19  Popliteal Artery Aneurysm and Non-atherosclerotic Limb Disease 215

19.4.2 Treatment

Considering that the popliteal aneurysm thrombosis can be a catastrophic condition

with high-grade acute limb ischemia due to the poor collateral network, it is crucial
to know when it is indicated the treatment of a popliteal aneurysm.
Some studies suggested a possible growth rate for asymptomatic popliteal aneu-
rysms: when <2 cm the annual expansion rate is about 1.5 mm/year, it increases at
3 mm/year when the diameter is between 2 cm and 3 cm and jumps at 3.7 mm/year
if it exceeds 3 cm [10].
In our experience, aneurysms smaller than 2 cm can cause acute limb ischemia,
which requires prompt intervention to reduce the risk of leg amputation.
In emergency in case of PA thrombosis thrombolysis is considered in most cases
the choice through the use of Urokinase and rt-PA. The advantage of the latter is the
shortened procedure, as its infusion usually takes considerably less time [11].
In any case, physicians should judge if the limb can sustain the obvious delay
associated with this technique: a motor deficit or sensory loss indicates the need for
immediate treatment.

19.4.3 BOX Indication for PA Treatment

Symptomatic aneurysms

• TREAT REGARDLESS OF SIZE (UNLESS UNFIT)

Asymptomatic aneurysm

• <2 cm: monitor
• 2–2.5 cm: consider treatment, but keep in mind
–– life expectancy (age and comorbidities)
–– operative risk
–– factors associated with possible evolution (thrombus, distortion)
• ≥2.5 cm: treat (unless unfit)

The approach to PA can be in open or endovascular surgery. The open treatment

provides two different surgical approaches: medial or posterior that have no signifi-
cant difference in terms of nerve lesions, but the posterior has shorter in-hospital
stay [12]. With the onset of stent-graft endovascular treatment of popliteal aneu-
rysm is preferred in many centers because it reduces the invasivity through the fem-
oral access and length of stay, but there is the risk of endoleak, the sac is not
removed, and the graft can slide down. So it is not indicated in giant aneurysms
because the involvement of the fossa risks remain important maintaining compres-
sive symptoms.
216 A. M. Settembrini and P. Sirignano

Through a medial approach, the operator can easily reach any arterial segment
proximal to the dilatation. Through an opening of the origin of the soleus muscle,
access to the lower popliteal artery, to the origin of the anterior tibial and the tibio-­
peroneal trunk, is obtained as well.
The advantages are the possibility to go up to superficial femoral artery or com-
mon femoral artery in case of highly calcified arteries and the saphenous vein har-
vesting; the disadvantages are complete removal of the aneurysmatic sac or complete
exclusion through ligation of every single collateral vessel is problematic.
The posterior approach can be used if the extension of the dilatation is limited to
the popliteal fossa (usually aneurysms behind the knee joint), this route has the
enviable advantage of allowing for a complete and easier aneurysmectomy and a
very short interposition graft and shorter hospital stay and quicker recovery [13].
The exposure, in prone patients, proceeds through veins (popliteal, small saphe-
nous, gastrocnemius veins) and nerves (sciatic nerve, tibial nerve, and common
fibular nerve). On the contrary, the harvesting of great saphenous vein is more com-
plex considering that a small saphenous vein is often too small to be the suitable
conduit.

19.4.4 BOX indications for type of PA treatment

19.4.4.1 Endovascular IF
• Adequate proximal and distal neck
• Possibly, diameter at proximal neck not very different from diameter at distal neck
• At least 1 (better if 2) runoff vessels
• Older patients
• Increased surgical risk

19.4.4.2 Open Surgery

Posterior approach
• Only for aneurysm limited to the popliteal fossa.
• Only if minimum probability of tibial arteries being involved in surgery.
• Plan vein harvesting in advance (proximal thigh vs. knee level vs. short
saphenous).
• Very short aneurysms can be substituted with prosthetic grafts (PTFE).

Medial approach
• The most versatile approach: allows for treating all kinds of aneurysms in all
situations: use whenever in doubt for any reason.
19  Popliteal Artery Aneurysm and Non-atherosclerotic Limb Disease 217

References
1. Illig KA, Doyle A.  A comprehensive review of Paget-Schroetter syndrome. J Vasc Surg.
2010;51:1538–47.
2. Viertel VG, Intrapiromkula J, Malufa F, et al. Cervical ribs: a common variant overlooked in
CT imaging. Am J Neuroradiol. 2012;33:2191–4.
3. Levien LJ, Benn CA.  Adventitial cystic disease: a unifying hypothesis. J Vasc Surg.
1998;28(2):193–205.
4. Bergan JJ, Yao JST, Flinn WR. Surgical management of young claudicants: adventitial cyst. In:
Bergan JJ, Yao JST, editors. Evaluation and treatment of upper and lower extremity circulatory
disorders. Orlando, FL: Grune & Stratton; 1984.
5. Wady H, Badar Z, Farooq Z, Shaw P, Kobayashi K. Avoiding the trap of misdiagnosis: valu-
able teaching points derived from a case of longstanding popliteal artery entrapment syn-
drome. Case Rep Med. 2018;2018:3214561.
6. Shahi N, Arosemena M, Kwon J, Abai B, Salvatore D, DiMuzio P.  Functional popliteal
artery entrapment syndrome: a review of diagnosis and management. Ann Vasc Surg. 2019
Aug;59:259–67.
7. Altintas U, Helgstrand UV, Hansen MA, Stentzer KF, Schroeder TV, Eiberg JP. Popliteal artery
entrapment syndrome: ultrasound imaging, intraoperative findings, and clinical outcome. Vasc
Endovasc Surg. 2013;47(7):513–8.
8. Lawrence PF, Lorenzo-Rivero S, Lyon JL. The incidence of iliac, femoral, and popliteal artery
aneurysms in hospitalized patients. J Vasc Surg. 1995;22(4):409–15. discussion 415–6.
9. Huang Y, Gloviczki P, Noel AA, et al. Early complications and long-term outcome after open
surgical treatment of popliteal artery aneurysms: is exclusion with saphenous vein bypass still
the gold standard? J Vasc Surg. 2007;45:706–13.
10. Pittathankal AA, Dattani R, Magee TR, et al. Expansion rates of asymptomatic popliteal artery
aneurysms. Eur J Vasc Endovasc Surg. 2004;27:382–4.
11. Thompson JF, Beard J, Scott DJ, et  al. Intraoperative thrombolysis in the management of
thrombosed popliteal aneurysms. Br J Surg. 1993;80:858–9.
12. Mazzaccaro D, Carmo M, Dallatana R, Settembrini AM, Barbetta I, Tassinari L, Roveri S,
Settembrini PG.  Comparison of posterior and medial approaches for popliteal artery aneu-
rysms. J Vasc Surg. 2015;62(6):1512–1520. https://doi.org/10.1016/j.jvs.2015.06.227. Epub
2015 Sep 12.
13. Best BD, Moore WS. The posterior approach for repair of popliteal artery aneurysms. J Vasc
Surg. 2006;43:940–4.
 Part VI
Specific Clinical Pictures: Surgeon Perspectives
The Infected and Septic Patient
20
Emanuele Botteri, Nicoletta Lazzeri, Silvia Mazzoleni,
and Frank A. Rasulo

20.1 Infection and Sepsis

20.1.1 Definitions

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated

host response to infection. Infection is defined as the invasion of normally sterile
tissue by organisms resulting in infectious pathology.
Bacteremia is the presence of viable bacteria in the blood.
Infections and/or bacteremia can lead, if not diagnosed or treated properly, to
sepsis or even to septic shock; therefore, care must be taken in identifying the sub-
jects at risk [1].

20.2 Epidemiology

20.2.1 Incidence

Since 1970s rates of sepsis have increased. A retrospective analysis of an interna-

tional database reported a global incidence of 437 per 100,000 person-years for
sepsis between the years 1995 and 2015, although this rate was not reflective of
contributions from low- and middle-income countries [2]. The Global Burden of
Disease Study reported that in 2017, an estimated 48.9 million incident cases of

E. Botteri (*)
Department of General Surgery Unit, ASST Spedali Civili di Brescia, Brescia, Italy
N. Lazzeri · S. Mazzoleni · F. A. Rasulo
Department of Anesthesiology and Intensive Care Medicine II, Spedali Civili, University of
Brescia, Brescia, Italy

© The Author(s), under exclusive license to Springer Nature 221

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_20
222 E. Botteri et al.

sepsis were reported [3]. Approximately 11 million deaths were reported, represent-
ing 19.7% of all global deaths. While incidence and mortality varied across regions,
the overall mortality decreased by almost 53% between 1990 and 2017. Moreover,
this study highlights the need for greater prevention and treatment of sepsis, particu-
larly in areas of the world with the lowest socio-demographic index.
Reasons for a possible increased rate of sepsis include advancing age, immuno-
suppression, and multidrug-resistant infection [4–6].
The incidence is also greatest during the winter, probably due to the increased
prevalence of respiratory infections [7].

20.2.2 Pathogens

The contribution of various infectious organisms to the burden of sepsis has changed
over time. Gram positive bacteria are the pathogens that are most commonly iso-
lated from patients with sepsis. The incidence of fungal sepsis has increased over
the past decade, but remains lower than bacterial sepsis [5]. In approximately half
of cases of sepsis, an organism is not identified (culture negative sepsis) [8].

20.3 Pathophysiology

When a pathogen enters a sterile site in the body, it is detected by the immune
system, which starts a host response. Innate immune cells, specifically macro-
phages, can recognize and bind non-self components on the surface of the patho-
gen, leading to phagocytosis of both invading bacteria and of debris from injured
tissue. Moreover, macrophages start releasing proinflammatory cytokines, with
consequent recruitment of additional inflammatory cells, namely leukocytes. If
the bacterial load is limited, a local host response is sufficient in clearing the
pathogen [9].
Sepsis occurs when activation of immune system exceeds the burden of the
local environment, leading to a generalized and sometimes dysregulated host
response involving multiple tissues, with consequent cellular injury and organ
dysfunction.
Some of the mechanisms proposed to explain this process of injury include:
tissue ischemia (insufficient oxygen relative to oxygen need), cytopathic injury
(direct cell injury by proinflammatory mediators and/or other products of inflam-
mation), and an altered rate of apoptosis (programmed cell death). No organ sys-
tem is protected from the consequences of sepsis. Those that are most commonly
involved include the circulation, lung, gastrointestinal tract, kidney, and nervous
system [10].
20  The Infected and Septic Patient 223

20.4 Disease Severity

Sepsis exists on a continuum of severity ranging from infection and bacteremia to

sepsis and septic shock, which can lead to multiple organ dysfunction syndrome
(MODS) and death.
According to the Society of Critical Care Medicine (SCCM) and the European
Society of Intensive Care Medicine (ESICM) we can define:
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host
response to infection.
Early sepsis—no formal definition of early sepsis has been validated until now.
Nevertheless, it is important to monitor patients at risk of developing more serious
infections or those that can progress to septic shock and MODS. The qSOFA (quick
Sequential Organ Failure Assessment score) is a simple and validated score that can
be used by non-intensivists to identify the subjects at risk of increased morbidity
and mortality. The three components of the scale are readily identifiable at the bed-
side and are allocated one point each:

• Respiratory rate ≥22/min

• Altered mentation
• Systolic blood pressure ≤100 mmHg

A score >2 indicates an increased risk of progression to septic shock and MODS.
The qSOFA score was originally validated in 2016 as most useful in patients
suspected as having sepsis outside of the intensive care unit (ICU) [11].
Septic shock—a state of severe hypotension that doesn’t respond to adequate
fluid resuscitation, that requires vasopressors to maintain a mean arterial pressure
(MAP) ≥65 mmHg and have lactate >2 mmol/L (>18 mg/dL).
Septic shock is a type of vasodilatory or distributive shock.
Multiple organ dysfunction syndrome—progressive organ failure requiring
immediate life support. MODS represents a final common stage of both infectious
and non-infectious insults.
Common parameters to be monitored in septic patients to diagnose MODS are
[12, 13]:

• Respiratory—Partial pressure of arterial oxygen (PaO2)/fraction of inspired oxy-

gen (FiO2) ratio
• Hematology—Platelet count
• Liver—Serum bilirubin
• Renal—Serum creatinine (or urine output)
• Brain—Glasgow coma score
• Cardiovascular—Hypotension and vasopressor requirement
224 E. Botteri et al.

In general, the greater the number of failing organs the higher the mortality, with
the greatest risk being associated with respiratory failure requiring mechanical
ventilation.
The most common manifestations of severe organ dysfunction are acute respira-
tory distress syndrome, acute renal failure, and disseminated intravascular coagula-
tion [14].

20.5 Risk Factors

Risk factors for sepsis include the following [15]:

• Intensive care unit admission.

• Bacteremia.
• Advanced age (≥65 years).
• Immunosuppression.
• Type 2 diabetes and obesity.
• Cancer.
• Community acquired pneumonia.
• Previous hospitalization.

20.6 Clinical Presentation and Diagnosis

Importantly, the presentation is nonspecific such that many other conditions (e.g.,
pancreatitis, acute respiratory distress syndrome) may present similarly.

20.6.1 Symptoms and Signs

• Specific to an infectious source (e.g., pain and purulent exudate in a surgical

wound may suggest an underlying abscess).
• Arterial hypotension (e.g., systolic blood pressure <90  mmHg, mean arterial
pressure <70 mmHg).
• Temperature >38.3 or <36 °C.
• Heart rate >90 beats/min.
• Tachypnea, respiratory rate >20 breaths/min.
• Altered mental status, obtundation, or restlessness.
• Oliguria urine (output <0.5 mL/kg/h for at least 2 h despite adequate fluid resus-
citation) or anuria.

These findings may be modified by preexisting disease or medications. As exam-

ples, older patients, diabetic patients, and patients who take beta-blockers may not
exhibit an appropriate tachycardia as blood pressure falls.
20  The Infected and Septic Patient 225

20.6.2 Laboratory Signs

• Leukocytosis (WBC > 12,000/μL) or leukopenia (WBC count < 4000/μL).

• Hyperglycemia (plasma glucose > 140 mg/dL) in the absence of diabetes.
• PCR.
• Arterial hypoxemia.
• Creatinine increase.
• Coagulation abnormalities (INR > 1.5 or aPTT > 60 s).
• Thrombocytopenia (platelet count < 100,000/μL).
• Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL).
• Hyponatremia, hyperkalemia.
• Hyperlactatemia: an elevated serum lactate (e.g., >2 mmol/L) can be a manifes-
tation of organ hypoperfusion [16].
• PCT elevated.

20.6.3 Imaging

To identify the focus of infection, multiple radiologic exams can be performed (RX,
TC, echography).

20.6.4 Microbiology

The identification of an organism in culture is highly supportive of the diagnosis of

sepsis. A key point in the appropriate management of septic shock is to obtain cul-
tures, including blood cultures, as soon as possible, always before starting any anti-
microbial treatment.

20.6.5 Diagnosis

A constellation of clinical, laboratory, radiologic, physiologic, and microbiologic

data is typically required for the diagnosis of sepsis and septic shock. The diagnosis
is often made empirically at the bedside upon presentation, or retrospectively when
follow-up data returns (e.g., positive blood cultures in a patient with endocarditis)
or a response to antibiotics is evident.

20.6.6 Initial Evaluation of Common Sources of Sepsis:

Symptoms/Signs

respiratory tract: pharyngeal inflammation, exudate, swelling and lymphadenopa-

thy, productive cough, pleuritic chest pain, consolidative auscultatory findings
226 E. Botteri et al.

central nervous system: altered mental status, signs of meningeal irritation, focal
signs, irritation at insertion site of peridural catheter
urinary tract: urgency, dysuria, loin, or back pain
vascular catheters: redness or drainage at insertion site
pleural catheter: redness or drainage at insertion site
gastrointestinal: abdominal pain, distension, diarrhea, and vomiting

20.6.7 Initial Microbiologic Evaluation

respiratory tract: throat swab for aerobic culture, sputum of good quality, rapid
influenza testing, urinary antigen testing (e.g., pneumococcus, legionella), quantita-
tive culture of protected brush or bronchoalveolar lavage
central nervous system: CSF analysis and culture
urinary tract: urine culture
vascular catheters: culture of blood (from the catheter and a peripheral site),
culture catheter tip (if removed)
pleural catheter: culture of pleural fluid (through catheter)
gastrointestinal: stool culture for Salmonella, Shigella, or Campylobacter; detec-
tion of Clostridium difficile toxin
intra-abdominal: aerobic and anaerobic culture of percutaneously or surgically
drained abdominal fluid collections [17]

20.7 Prognosis

Sepsis has a high mortality rate, estimated in a range from 10 to 52% [4, 5, 18–20].
Mortality rates increase linearly according to the disease severity [21].
Most deaths occur within the first 6  months, but the risk remains elevated at
2 years. Patients who survive sepsis are more likely to be admitted to long-term care
facilities in the first year after the initial hospitalization, and also appear to have a
persistent decrement in their quality of life [20, 22–24].
Clinical characteristics that impact the severity of sepsis and, therefore, the out-
come include the host’s response to infection, the site and type of infection, and the
timing and type of antimicrobial therapy.

20.8 Management of Sepsis and Septic Shock

The key point in managing sepsis and septic shock is to act fast, within the first
hours of onset of symptoms, to avoid increased morbidity and mortality. When
MODS ensues, the patient must be transferred to an ICU ward. The
20  The Infected and Septic Patient 227

recommendations cited in this chapter are taken from the “International Guidelines
for Management of Sepsis and Septic Shock: 2016” [25].

20.8.1 Initial Resuscitation

• Treatment and resuscitation should begin immediately at least 30 ml/kg of IV

crystalloid should be given within the first 3 h.
• Crystalloids are the fluids of choice for both initial resuscitation and subsequent
volume replacement. Both balanced crystalloid solutions and saline solutions
can be used; ringer lactate should be preferred as initial fluid.
• Albumin can be used for volume replacement in selected case; it is always
advised to contact the intensivist to implement fluid therapy as needed if the
target MAP of 65 mmHg is not reached with crystalloids.
• Following initial resuscitation, additional fluids should be given according to the
hemodynamic status, which must be reassessed frequently. Reassessment should
include a thorough clinical examination and evaluation of available physiologic
variables (heart rate, blood pressure, arterial oxygen saturation, respiratory rate,
temperature, urine output, and others, as available) as well as other noninvasive
or invasive monitoring, such as echocardiography. An initial reasonable target of
MAP is > 65  mmHg. Lactate levels can be used as markers of tissue
hypoperfusion.

20.8.2 Specimen Analysis

Appropriate culture specimen (including blood) should be obtained before starting

antimicrobial treatment in patients with suspicion of sepsis or septic shock. The col-
lection of these materials must not delay the onset of antimicrobial therapy.

20.8.3 Antimicrobial Therapy

• Antimicrobials must be started as soon as possible, ideally within 1 h from the
diagnosis of sepsis/septic shock.
• Starting with broad-spectrum antimicrobial therapy is a good strategy to cover
all likely pathogens (including fungi) while waiting for the results of culture
specimen. Consultation with an infectious disease specialist may be useful to
choose the appropriate treatment regimen.
• Antibiotic de-escalation can be started once pathogen identification, together
with its level of resistance, has occurred. It is advised to discuss every change in
antimicrobial therapy with an infectious disease specialist.
228 E. Botteri et al.

• A proper antimicrobial therapy should last around 7–10  days; longer courses
may be appropriate in patients with a slow clinical response, with undrainable
foci of infection, with bacteremia from S. aureus and from some fungal/viral
infections, and in immunocompromised patients. As usual, discussion with an
infectious disease specialist is essential to evaluate eventual continuation of
therapy.
• Procalcitonin can be measured throughout the septic state to evaluate the pro-
gression of the patient and can be viewed as a marker, together with other inflam-
mation markers, for eventual discontinuation of antimicrobial therapy.

20.8.4 Vasoactive Medications and Corticosteroids

• If MAP cannot be maintained >65 mmHg after appropriate fluid replacement, it

is recommended to contact the intensivist to evaluate the admission to ICU.
• Once admitted to the ICU, vasopressors can be started to.
• Norepinephrine must be the first vasopressor to be used in septic shock.
• If adequate pressure values cannot be maintained with noradrenaline alone,
either adrenaline, dobutamine, or vasopressin can be added.
• Hydrocortisone can be used in septic shock, at a dose of 200 mg/day.

20.8.5 Venous Thromboembolism Prophylaxis and Stress

Ulcer Prophylaxis

• LMWH can be used, in the absence of contraindications, in patients with septic

shock, to prevent TVP/PE.
• Gastroprotection is to be started as soon as possible once a day; if hydrocortisone
is added to therapy, the dose must be doubled.

The key points in the diagnosis and management of septic shock are summarized
in the flowchart below (Fig. 20.1).
20  The Infected and Septic Patient 229

Fig. 20.1 Flowchart—
identification and
management of sepsis Suspected sepsis

qSOFA >2

Evaluate signs and

symptoms of infection +
laboratory findings

Confirm Sepsis

1. Fluid resuscitation
2. Collect culture samples
3. Start empiric antibiotics

MAP < 65 mmHg despite

fluid resuscitation

SEPTIC SHOCK

ICU
230 E. Botteri et al.

References
1. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et  al.
The third international consensus definitions for sepsis and septic shock (Sepsis-3).
JAMA. 2016;315(8):801–10.
2. Fleischmann C, Scherag A, Adhikari NKJ, Hartog CS, Tsaganos T, Schlattmann P, et  al.
Assessment of global incidence and mortality of hospital-treated sepsis. Current estimates and
limitations. Am J Respir Crit Care Med. 2016;193(3):259–72.
3. Rudd KE, Johnson SC, Agesa KM, Shackelford KA, Tsoi D, Kievlan DR, et  al. Global,
regional, and national sepsis incidence and mortality, 1990–2017: analysis for the Global
Burden of Disease Study. Lancet Lond Engl. 2020;395(10219):200–11.
4. Martin GS, Mannino DM, Eaton S, Moss M. The epidemiology of sepsis in the United States
from 1979 through 2000. N Engl J Med. 2003;348(16):1546–54.
5. Kaukonen K-M, Bailey M, Suzuki S, Pilcher D, Bellomo R. Mortality related to severe sep-
sis and septic shock among critically ill patients in Australia and New Zealand, 2000–2012.
JAMA. 2014;311(13):1308–16.
6. Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology
of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of
care. Crit Care Med. 2001;29(7):1303–10.
7. Danai PA, Sinha S, Moss M, Haber MJ, Martin GS. Seasonal variation in the epidemiology of
sepsis. Crit Care Med. 2007;35(2):410–5.
8. Gupta S, Sakhuja A, Kumar G, McGrath E, Nanchal RS, Kashani KB. Culture-negative severe
sepsis: nationwide trends and outcomes. Chest. 2016;150(6):1251–9.
9. Chen GY, Nuñez G. Sterile inflammation: sensing and reacting to damage. Nat Rev Immunol.
2010;10(12):826–37.
10. Pinsky MR, Matuschak GM.  Multiple systems organ failure: failure of host defense
­homeostasis. Crit Care Clin. 1989;5(2):199–220.
11. Seymour CW, Liu VX, Iwashyna TJ, Brunkhorst FM, Rea TD, Scherag A, et al. Assessment of
clinical criteria for sepsis: for the third international consensus definitions for sepsis and septic
shock (Sepsis-3). JAMA. 2016;315(8):762–74.
12. Marshall JC, Cook DJ, Christou NV, Bernard GR, Sprung CL, Sibbald WJ. Multiple organ
dysfunction score: a reliable descriptor of a complex clinical outcome. Crit Care Med.
1995;23(10):1638–52.
13. Le Gall JR, Klar J, Lemeshow S, Saulnier F, Alberti C, Artigas A, et al. The Logistic Organ
Dysfunction system. A new way to assess organ dysfunction in the intensive care unit. ICU
Scoring Group. JAMA. 1996;276(10):802–10.
14. Rangel-Frausto MS, Pittet D, Costigan M, Hwang T, Davis CS, Wenzel RP.  The natu-
ral history of the systemic inflammatory response syndrome (SIRS). A prospective study.
JAMA. 1995;273(2):117–23.
15. Sands KE, Bates DW, Lanken PN, Graman PS, Hibberd PL, Kahn KL, et al. Epidemiology of
sepsis syndrome in 8 academic medical centers. JAMA. 1997;278(3):234–40.
16. Casserly B, Phillips GS, Schorr C, Dellinger RP, Townsend SR, Osborn TM, et  al. Lactate
measurements in sepsis-induced tissue hypoperfusion: results from the Surviving Sepsis
Campaign database. Crit Care Med. 2015;43(3):567–73.
17. Lynn WA, Cohen J. Microbiological requirements for studies of sepsis. In: Vincent J-L, Sibbald
WJ, curatori. Clinical trials for the treatment of sepsis [Internet]. Berlin: Springer; 1995 [citato
23 aprile 2021]. pp. 71–85. (Update in Intensive Care and Emergency Medicine). Disponibile
su. https://doi.org/10.1007/978-­3-­642-­79224-­3_5.
18. Vincent J-L, Sakr Y, Sprung CL, Ranieri VM, Reinhart K, Gerlach H, et al. Sepsis in European
intensive care units: results of the SOAP study. Crit Care Med. 2006;34(2):344–53.
19. Haas SA, Lange T, Saugel B, Petzoldt M, Fuhrmann V, Metschke M, et al. Severe hyperlacta-
temia, lactate clearance and mortality in unselected critically ill patients. Intensive Care Med.
2016;42(2):202–10.
20  The Infected and Septic Patient 231

20. Winters BD, Eberlein M, Leung J, Needham DM, Pronovost PJ, Sevransky JE.  Long-term
mortality and quality of life in sepsis: a systematic review. Crit Care Med. 2010;38(5):1276–83.
21. Kaukonen K-M, Bailey M, Pilcher D, Cooper DJ, Bellomo R. Systemic inflammatory response
syndrome criteria in defining severe sepsis. N Engl J Med. 2015;372(17):1629–38.
22. Meyer N, Harhay MO, Small DS, Prescott HC, Bowles KH, Gaieski DF, et al. Temporal trends
in incidence, sepsis-related mortality, and hospital-based acute care after sepsis. Crit Care
Med. 2018;46(3):354–60.
23. Wang T, Derhovanessian A, De Cruz S, Belperio JA, Deng JC, Hoo GS. Subsequent infections
in survivors of sepsis: epidemiology and outcomes. J Intensive Care Med. 2014;29(2):87–95.
24. Prescott HC, Osterholzer JJ, Langa KM, Angus DC, Iwashyna TJ. Late mortality after sepsis:
propensity matched cohort study. BMJ. 2016;353:i2375.
25. Briegel J, Möhnle P. [International guidelines from the Surviving Sepsis Campaign: 2016
update]. Anaesthesist. 2017;66(7):530–8.
Hemorrhagic Patient
21
Samuele Colombo and Daniele Bissacco

21.1 Diagnosis and Management

It is of vital importance to early recognize and treat a hemorrhagic shock, in fact,

death can occur within few hours of the onset of symptoms. The treatment consists
in identifying the source of the bleeding as quickly as possible, stopping it with
simple and effective maneuvers like direct manual compression or by means rapid
surgical maneuvers (Damage Control Surgery, DCS) and restoring a correct volume
of circulating blood. Hemorrhagic shock, especially when caused by occult sources
of bleeding, is difficult to diagnose based on signs and symptoms. In fact, in most
patients, hypotension is a late symptom that appears when there has been a loss of
about 30% of the circulating volume. This occurs due to compensatory mechanisms
such as peripheral vasoconstriction present mainly in young patients or pregnant
women. Other signs and symptoms such as tachycardia, tachypnea, paleness, and
altered consciousness (decrease in Glasgow GCS score) are also signs of late and
impending shock. It is important to remember that tachycardia may not be present,
even in the presence of significant blood loss, in patients taking beta blocker ther-
apy. Table 21.1 shows the four shock classes based on vital parameters, very useful
for quickly classifying the patient based on the severity of his condition.
In the initial evaluation of a patient who has a possible source of bleeding, as
mentioned above, it is very important to identify the source of hemorrhage as
quickly as possible. The most common sources of bleeding are the gastrointestinal

S. Colombo
Digestive Surgery Unit, European Institute of Oncology (Istituto Europeo di Oncologia, IEO),
Milan, Italy
e-mail: [email protected]
D. Bissacco (*)
Department of Vascular Surgery Unit, IRCCS Ca’ Granda Ospedale Maggiore Policlinico,
Milan, Italy

© The Author(s), under exclusive license to Springer Nature 233

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_21
234 S. Colombo and D. Bissacco

Table 21.1  The American College of Surgeons Advanced Trauma Life Support (ATLS) hemor-
rhagic shock classification
Blood loss Class I Class II Class III Class IV
HR beats/min <100 100–120 120–140 >140
Blood press Normal Normal Decrease (<90) Decrease
(mmHg)
Pulse press Normal Narrowed Narrowed Narrowed
Resp rate 14–20 20–30 30–40 >35
GCS Normal Normal Decrease Decrease
Base deficit 0 to −2 −2 to −6 −6 to −10 <−10
Blood loss ml (%) <750 (15) 750–1500 (15–30) 1500–2000 (30–40) >2000 (>40)

tract manifesting as hematemesis, melaena, proctorrhagia, or vaginal bleeding. In

these cases, the hemorrhage can clinically manifest itself with external bleeding
after a few hours from the onset, consequently causing a significant loss of circulat-
ing volume before reaching the identification of the hemorrhagic source. Other
areas of the body where the signs and symptoms of bleeding may be overlooked in
the initial stages of clinical evaluation are cavities such as chest, abdomen, or pelvis
and even more subtle is the retroperitoneum. In fact, large quantities of blood can be
collected in these spaces, causing severe hemorrhagic shocks. In other cases, how-
ever, such as bleeding from the upper airways (epistaxis or hemoptoe) or the lesion
of superficial vessels such as in the case of trauma, the source of bleeding is quickly
detectable, favoring a more timely intervention.

21.2 Imaging

As previously mentioned, the chest, abdomen, and pelvis are common sources of
bleeding in trauma patients. For this reason, these districts must be rapidly evaluated
with first level examinations such as chest and pelvic radiograph and a targeted
evaluation with ultrasound (Extended Focused Assessment with Sonography for
Trauma, EFAST) [1]. Furthermore, ultrasound is very useful in identifying occult
sources of bleeding even in non-traumatic patients. A diagnostic tool of extreme
usefulness is the CT scan with contrast enhancement which, however, should be
performed only as a second level examination in case the source of the bleeding
remains unrecognized at the first evaluation and if the patient has normal hemody-
namics or responsive to the fluid resuscitation. In case of massive hemorrhage,
before performing second level diagnostic examinations, it’s mandatory to obtain
the stabilization of the hemodynamic parameters by resuscitations maneuvers, such
as massive transfusion and surgical procedures (DCS) [2].

21.3 Lab Tests

The fastest laboratory test to evaluate the biochemical changes caused by bleeding
is the blood gas analysis. The base deficit and lactate values are, in fact, indirect
signs of peripheral oxygenation. Other laboratory tests useful for predicting the
21  Hemorrhagic Patient 235

need for a massive transfusion are hemoglobin (even if its decrease occurs later) and
INR. Platelets counts and fibrinogen levels should also be evaluated and normal-
ized. It is essential to detect coagulopathy and measure the rate of clot formation
using tests such as the thromboelastogram to guide ongoing resuscitation of blood
products by transfusion of coagulation factors. Electrolytes must also be measured
both in the initial stages and during resuscitation with blood products so that they
can be corrected early avoiding the onset of malignant arrhythmias [3, 4].

21.4 Treatment

Restoration of intravascular volume and rapid control of hemorrhage are the priori-
ties for the management of bleeding. Protocols of intravascular volume restoration
have evolved during the past several decades, finally getting back to a resuscitation
approach that supports the use of plasma, platelets, and red blood cells [5]. Massive-­
transfusion protocols is required to treat patients presenting with shock class III or
IV and any delay in their activation is associated with an increase in mortality.
Recent evidences indicate that a ratio of plasma to platelets to red cells close to
1-1-1 is safe and reduces short-term mortality from hemorrhage due to trauma. For
patients with hemorrhage from different causes than trauma, a ratio of platelets to
red cells of more than 1:2 reduced mortality in the first 48 h [6]. The anticoagulant
citrate is a usual component of all these blood products; it is rapidly metabolized by
the liver in healthy people, while in patients with hemorrhagic shock receiving a
large volume of blood product it can become toxic and cause life-threatening hypo-
calcemia and progressive coagulopathy [4]. For this reason it’s very important an
empirical calcium dosing and its correction during large-volume transfusions (e.g.,
1 G of intravenous calcium chloride after transfusion of the first 4 units of any blood
product). Despite a frequent use of isotonic crystalloid resuscitation in the early
management of bleeding, these solutions have no effective therapeutic benefit other
than a transient intravascular volume expansion. When isotonic crystalloid is over-
dosed, the risk of complications such as respiratory failure, compartment syn-
dromes, and coagulopathy increases. So it is safer to limit crystalloid infusions to
3 L in the first 6 h after arrival in Emergency Department (ED) [7]. As in prehospital
resuscitation, colloids or hypertonic saline have not proved of any benefit for the
management of severe bleeding [8]. Procoagulant hemostatic products, such as acti-
vated recombinant factor VII, prothrombin complex concentrate, tranexamic acid,
and fibrinogen, can be added to promote clot formation in patients with severe
bleeding [9], especially in patients taking oral anticoagulants affected by hemo-
philia. For these classes of patients, the use of these agents is accepted despite it is
considered off-label in healthy patients. However, the use of these drugs presents
some non-­negligible risks such as thrombotic complications, paradoxical hemor-
rhage, and multiorgan failure. For this reason it is important to refer to the protocols
and guidelines in force in your department. Norepinephrine and other vasoactive
drugs can be used to counteract hypotension in the early stages of shock.
Patients with acute hemorrhage caused by a traumatic event should be held less
than 15–20 min in the ED for initial diagnosis and resuscitation so as to decrease the
risk of death. Patients with hemorrhage in an extremity should be carried
236 S. Colombo and D. Bissacco

immediately to the OR for vascular exploration using a tourniquet to limit blood

loss in case of wounds far from joint areas such as armpits and groins. Avoid blind
exploration of the wound in the emergency room, especially with surgical instru-
ments like forceps or clamps due to reduction of the risk of iatrogenic vascular
injuries. In patients with torso injuries, EFAST is of vital importance to identify the
site of major bleeding so as to concentrate firstly DCS maneuvers (thoracostomy or
Extraperitoneal Pelvic Packing) in that district. Patients with exclusive abdominal
or pelvic bleeding from any source may benefit from a new technique called REBOA
(Resuscitative Endovascular Balloon Occlusion of the Aorta) [10]. REBOA is used
as a temporary bridge-system for performing second level diagnostic investigations
and for transporting the patient to the operating or angiography room for definitive
care by a temporary reduction of bleeding and normalization of vital parameters.

21.5 Conclusions

Patients with severe bleeding need adequate and on time hemostasis in order to
increase their survival chances. A prolonged time to hemostasis has been linked to
increased blood-transfusion requirements and increased mortality. The DCS maneu-
vers, described above, can be performed by trained personnel with experience in
trauma, but those who are not specialist in surgery can also be fundamental in sav-
ing patient’s life by implementing a few but precise precautions:

1. Recognize the signs and symptoms of bleeding early.

2. Stop bleeding immediately by manual pressure, direct soft tissue suturing, and
tourniquet placement.
3. Start infusion of liquids early, preferring the use of blood components.
4. In case of noncompressible torso hemorrhage, call early a specialist capable of
performing DCS maneuvers.
5. Once hemodynamic stability is achieved, transfer the patient as soon as possible
to a first level trauma center if it is not possible to guarantee all the necessary
care in your department.
6. Participate in training courses on bleeding management (such as the Stop the
Bleeding campaign) or in more intensive courses such as Advanced Trauma Life
Support (ATLS).

References
1. Davis JP, et al. Diagnostic accuracy of eFAST in the trauma patient: a systematic review and
me-ta-analysis. CJEM. 2019;21(6):727–38.
2. Chiara O, Cimbanassi S.  Protocolli per la gestione intraospedaliera del trauma maggiore.
Paris: Elsevier-Masson; 2008.
3. Sihler KC, et al. Complications of massive transfusion. Chest. 2010;137:209–20.
21  Hemorrhagic Patient 237

4. MacKay EJ, et al. Abnormal calcium levels during trauma resuscitation are associated with
increased mortality, increased blood product use, and greater hospital resource consumption: a
pilot investigation. Anesth Analg. 2017;125:895–901.
5. Spinella PC, et al. Whole blood: back to the future. Curr Opin Hematol. 2016;23:536–42.
6. Etchill EW, et al. Should all massively transfused patients be treated equally? An analysis of
massive transfusion ratios in the nontrauma setting. Crit Care Med. 2017;45:1311–6.
7. Shafi S, et  al. Bundles of care for resuscitation from hemorrhagic shock and severe brain
injury in trauma patients — translating knowledge into practice. J Trauma Acute Care Surg.
2016;81:780–94.
8. Lewis SR, et al. Colloids or crystalloids fluid replacement in critically people. Cochrane.
2018;8(8):CD000567.
9. Schöchl H, et al. Trauma bleeding management: the concept of goal-directed primary care.
Anesth Analg. 2014;119:1064–73.
10. Brenner M, et  al. Joint statement from the American College of Surgeons Committee on
Trauma (ACS COT) and the American College of Emergency Physicians (ACEP) regard-
ing the clinical use of Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA).
Trauma Surg Acute Care Open. 2018;3:1–3.
The Polytrauma Patient
22
Matteo Marone and Ilenia D’Alessio

22.1 Introduction

A polytrauma patient is a person who experiences injuries to multiple body parts

and organ systems as a result of an external physical force applied to that person [1].
There are two main types of trauma:

1. Blunt
2. Penetrating

In blunt trauma, also known as non-penetrating trauma, there is no perforation of

the skin by foreign body. Classical examples of non-penetrating trauma are motor
vehicle accidents. In contrast, in penetrating trauma there is a perforation of the skin
and foreign objects can penetrate the patient’s body. These objects can either enter
and exit the body or they can be retained by the body itself. Classical examples of
penetrating trauma are stab-wounds and gunshot-wounds [2, 3].
Polytrauma patients often experience a mixture of these two types of trauma, it
is common to see patients after a car accident (blunt trauma) with penetrating inju-
ries due to glasses or pieces of metal. Other types of injury include:

M. Marone
Department of Surgery, Tygerberg Hospital, Cape Town, South Africa
I. D’Alessio (*)
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
Department of Vascular Surgery, Fondazione “A. De Gasperis” ASST Grande Ospedale
Metropolitano Niguarda, Milan, Italy
e-mail: [email protected]

© The Author(s), under exclusive license to Springer Nature 239

Switzerland AG 2022
D. Bissacco et al. (eds.), Primary Management in General, Vascular and
Thoracic Surgery, https://doi.org/10.1007/978-3-031-12563-8_22
240 M. Marone and I. D’Alessio

• Thermal injuries
• Chemical injuries
• Blast injuries

Polytrauma patients are the patients whose management is the most difficult and
time consuming for emergency physicians. It can and it may involve a multidisci-
plinary trauma team with many figures as: emergency medical doctors, paramedics,
specialist doctors (surgeons, anaesthetists), nurses and residents in training. Usually
are needed many instruments (e.g. CT scan, Doppler Ultrasound, Chest XR).
Every member of the team needs to be specifically trained to accomplish particu-
lar tasks like: intubation, IV line insertion, ICD (Intercostal drain) positioning and
so on. It is mandatory that every member of the team communicate and refer his or
her action to the figure that guides the team: the Trauma Leader. The trauma leader
is a fundamental element of the team because it guides the resuscitation and takes
decisions about the diagnostic and therapeutic steps to perform. He or she gives
tasks to the other members of the team and his duties involve teaching and helping
other members of the team if they are unable to carry out the task assigned to them.
Patients treatment is not limited to one centre but it can involve many structures
and doctors and it is divided into three different phases:

1. Pre-hospital care
2. Acute care
3. Hospital care

When treating polytrauma patients it is important for every professional involved

to remember that trauma patients have a tri-modal distribution of death, that means
that mortality from trauma occurs mainly in the three peaks of Fig. 22.1 [4].
During the first peak death occurs within seconds or minutes from trauma and it
is usually from non-treatable injuries like: aortic complete transection, cardiac rup-
ture, high spine injuries, TBI (Traumatic Brain Injuries). There is no way to reduce
these peak but primary preventive measures.
Death within the second peak occurs between minutes to hours from trauma and
it can be prevented by the application of standard Advanced Trauma Life Support
(ATLS®) [5] principles in order to diagnose and treat causes like: injuries of spleen
and liver, haemopneumothorax, fractures, active bleeding and so on.
Death within the third peak occurs days to months after trauma and they can be
prevented by the appropriate management of the patient in every stage of the pre-­
hospital and hospital stay. Examples of problems that lead to death during this peak
are sepsis and organ failure.
As can be clearly seen, doctors cannot do anything to reduce the high of the first
peak but they have a fundamental role in reducing the mortality in the second and
third. This is possible having a good knowledge and applying ATLS principle to all
patients that arrive in the emergency department with a polytrauma.
22  The Polytrauma Patient 241

Aortic complete transection,

cardiac rupture, high spine
injuries, TBI (Traumatic
Brain Injuries)
DEATHS

Injuries of spleen
sepsis and organ
and liver,
failure
emopneumothorax,
fractures, active
bleeding

1 HOUR 3 HOURS 2-4 WEEKS

Fig. 22.1  Tri-modal distribution of causes of death in polytrauma patients

22.2 Signs and Symptoms

The main sign in polytrauma patients is shock, that is universally defined as the
inadequate delivery of oxygen and nutrients and the inadequate removal of toxic
metabolites to and from tissues that leads to the loss of cells’ function and causes
cell damage [6, 7].
During the initial phase of shock, cellular damages are reversible, however with
the persistence of the shock status these damages can become irreversible.
There are different types of shock:

• Haemorrhagic
• Non-haemorrhagic

Haemorrhagic shock is the most frequent cause of shock in polytrauma patients.

Until it is not proven differently doctors have to consider any polytrauma patients in
haemorrhagic shock. Patients can bleed from different sites and an easy way to not
miss any site is remembering the following phrase: “blood on the floor and four
more”. This simple expression identifies the potential bleeding site of a polytrauma
patient: “Blood on the floor” refers to the blood lost on the scene and during trans-
port from penetrating and open wounds. “Four more” represents the body spaces
where blood can collect in a closed trauma: chest, abdomen, pelvis and long bones
fractures [6].
242 M. Marone and I. D’Alessio

Non-haemorrhagic shock can be classified into:

• Cardiogenic
• Neurogenic—spinal
• Septic

It is extremely rare to have a septic shock in a recently traumatized patient, how-

ever, cardiogenic and spinal shock are not so rare. These types of shock have to be
ruled out in particular conditions. If patients have signs of high velocity chest impact
ECG and troponin level need to be checked. If patients have neurological problems
with high suspicion of spinal cord injuries, a CT scan to check for medulla injuries
needs to be performed [6].
Not every patient with shock is similar to one other. Depending on the gravity of
shock, patients can experience different signs and symptoms.
It is important, however, to remember that the heart rate is the first parameter to
change in response to blood loss and it’s the first parameter to change when doctors
infuse fluids in shock patients. Other parameters that can change are the urine out-
put and the mental status. The last parameter that varies is the blood pressure.
As shown in the table below (Table  22.1), there are four different classes of
shock depending on the percentage of blood loss.
It is important to recognize the appropriate class of shock in order to provide the
optimal fluid therapy for the patient. In fact, in class I or II crystalloids (e.g. lac-
tated Ringer’s/Hartman’s solution, acetate buffered solution, acetate and lactate
buffered solution, acetate and gluconate buffered solution, 0.45% NaCl (hypotonic
solution), 3% NaCl (hypertonic solution), 5% Dextrose in water) are a good option;
however, in class III and IV blood and blood products are probably the best choice.
In any case it is important in high volume trauma centres to use rotational throm-
boelastometry (ROTEM) in order to guide the infusion of blood and blood prod-
ucts [8].
Polytrauma patients always experience pain. Pain leads to tachycardia and dis-
comfort. It is important to provide every patient with appropriate analgesia.
Morphine IM (intramuscular) is often a good option because it is easily adminis-
tered and absorbed.

Table 22.1  Classes of shock

Class I Class II Class III Class IV
% of blood loss 0–15 15–30 30–40 >40
Heart rate bpm <100 100–120 120–140 >140
Blood pressure Normal Normal Reduced Reduced
Urine output >30 20–30 5–15 None
(ml)
Mental function Anxious Moderately anxious Confused Confused and lethargic
22  The Polytrauma Patient 243

22.3 Diagnosis

The diagnosis of polytrauma patients is represented by the primary and second-

ary survey.
During the primary survey it is mandatory to remove the clothes from the patients
in order to not miss any injuries. Every emergency physician should know ABCDE
ATLS principles [5, 9].

22.3.1 Briefly

A—Airways: In this phase it is important to check for signs of airways obstruction

like stridor, change in the voice level and so on. Immediate intubation is mandatory
in case of airways obstruction and neck haematoma, as well as if signs of fume
inhalation are present (burn nostril, carbon particle in the mouth). Succinylcholine
and ketamine are the drugs of choice for intubation. If the arterial blood gases show
high potassium, use Rocuronium and not Succinilcolina to avoid cardiac toxicity.
During this phase it is useful to check for neck injuries and jugular distention that
can be early signs of tension pneumothorax if monolateral or cardiac tamponade if
bilateral.
B—Breathing: During this phase it is fundamental to check for chest movement
and air entry on both sides of the thorax. If there is an open wound in the chest, it is
mandatory to suture it or close it with a three-sided adhesive dressing and insert an
ICD. In any case of reduced air entry in an hemithorax, it is mandatory to insert an
ICD and this needs to be done before the X-ray confirmation of the problem. If the
patient is in shock with reduced air entry on one side and with distended jugular
veins, a tension pneumothorax is suspected and a chest decompression with a 18G
needle in the second intercostal space needs to be performed immediately.
C—Circulation: During this phase, the physician has to monitor the patient with
12 lead ECG, a pressure cuff and an oximeter. The second step is to insert two large
IV lines (16–18G) and start infusing warm fluid. Before infusing, blood samples
need to be drawn for haematologic tests and blood chemistries (complete blood
count [CBC] and differential, platelet count, electrolytes, serum creatinine, liver
function tests, uric acid), in addition to toxicology and X-Match. If the patient is
unstable, it is advisable to activate immediately the local massive transfusion proto-
col. Check for possible open wounds and apply compression or tourniquet by Foley
catheter. During this phase the referring physician can apply pelvic binder and do
Focused Assessment with Sonography for Trauma (eco-FAST) to check for fluid in
the abdomen.
D—Disability: During this phase it is important to evaluate the Glasgow Coma
Scale and the gross body movements in order to detect possible nerve injuries. The
physician needs to evaluate the pupils and their light reactivity and reflexes. Careful
attention needs to be put in looking for signs of paraparesis or quadriplegia.
244 M. Marone and I. D’Alessio

E—Exposure: During this phase it is important to log-roll the patient protecting

the spine in order to check for other possible injuries and expose all the body.
The secondary survey follows the primary survey and it is performed on a stabi-
lized patient. It represents a head to toe examination comprehensive of full neuro-
logical examination, chest and abdominal examination and limb examination. The
only two XR needed during the primary survey are a chest XR and a pelvic XR. The
pelvic imaging is performed because it is really difficult to rule out pelvic fracture
clinically and the chest imaging is performed to check the appropriate position of all
the lines and tubes that the physician inserted during the resuscitation.

22.4 Therapy

Polytrauma patients, as we said, are shocked. In order to improve this status, it is

mandatory that every trauma patient is treated with 100% 02 facemask. This mea-
sure will increase the peripheral tissue oxygenation.
It is important and mandatory to keep the patient warm in order to avoid the
development of the lethal triad: hypothermia, hypercoagulability, acidosis. This can
be achieved using thermal blanket, heater devices and devices that allow the infu-
sion of warm fluid into the body.
In all the polytrauma patient it is mandatory to consider the C spine injured, if
not proven otherwise. In order to do so, the best way to clear it is using a CT scan,
that is more sensitive and specific than a plane XR. Until the CT scan is done, it is
important to maintain the neck immobilized with a C collar in situ.
In polytrauma patients with signs of shock, it is important to stop the bleeding to
stabilize the patient.
As previously stated, blood can come from five different sources:

• Open wound
• Bone fractures
• Pelvic fractures
• Chest
• Abdomen

In case of bone fracture with misalignment of the limb it is important to put the
limb on tractions and to reduce the fracture. Reducing the fracture will recreate a
sort of continuity in the bone reducing in this way the space where the blood can
collect. Traction is also important because it avoids the fracture to lose its alignment.
In case of pelvic fracture, it is important to close the pelvic ring in order to reduce
the space where the patient can bleed. There are different and effective ways to do
so. Special devices are called T-pods or pelvic binders. These devices are placed
around the hip of the trauma patient and allow the closure of the pelvic ring. The
same principle can be applied in rural setting using a towel to close the pelvis. There
22  The Polytrauma Patient 245

are two major currents of thought about pelvic fractures: some surgeons prefer to
apply pelvic binder to all trauma patients and then clear the pelvis with a pelvic XR;
others prefer to perform a manual examination of the pelvis and apply the binder
only in case of pelvic instability [10, 11].
If the pelvic bleeding persists, despite binder, probably the cause is arterial, in
this case interventional radiology can be involved to perform an embolization. The
use of Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) in
zone III (below renal arteries) can be a good option in these patients.
Considering the open wound their problem is that blood can come out from
them, especially if there is a vascular structure injuries underneath. Manual com-
pression is the most efficient way to stop the bleeding. However, this prevents one
member of the team from performing other tasks. If the open wound is on a limb,
the bleeding can be stopped using a tourniquet. This device can be used to exclude
the specific limb from the systemic circulation stopping arterial and venous flow.
Tourniquets need to be put in areas of the limb with only one bone underneath like
arm and tight in order to achieve a complete vascular occlusion. It is mandatory,
after the tourniquet is placed, to write on the patient the time of application. In fact,
one of the main tourniquet drawbacks is that they create a complete ischaemia of the
limb whom they are applied to. This means that the tourniquet needs to be removed
within 6 h from his application. If we consider wounds in non-compressible areas of
the body like the neck or the supraclavicular area, haemostasis can be achieved by
inflating Foley catheter in the wound. The balloon of the catheter will compress the
artery and the vein and will allow a temporary stop of the haemorrhage. More than
one Foley catheter can be placed in the same spot to stop the bleeding, if neces-
sary [12].
Considering the abdomen, its management is the priority of the trauma surgeon
on call. Emergency room laparotomies are not advisable for the lack of proper
instrumentation and illumination. If surgical control of the bleeding needs to be
achieved immediately the best way to do so is performing a resuscitative thoracot-
omy and cross clamp the aorta. Nowadays, with endovascular technique, an aortic
balloon occlusion can be performed using a technique called REBOA. In this situa-
tion a balloon is inflated in the aorta (usually zone I, above visceral arteries) in order
to exclude the abdomen from the aortic arterial blood flow to stabilize the patient [13].
Considering the chest, haemothorax and suspected haemothorax need to be
treated using ICD. The ICD output guides the physician in the following step. An
output of more than 1200 ml of blood is associated with haemodynamic instability
and indicates the necessity of performing a resuscitative thoracotomy. With this
procedure the chest is open passing through the fourth intercostal space in the emer-
gency department. This procedure allows the surgeon to control the bleeding directly
and to cross clamp the aorta in case of necessity. In responder patient a blood loss
of more than 200 ml every hours or more than 1200 ml indicates the necessity of a
thoracotomy in OR (operating room) [14].
246 M. Marone and I. D’Alessio

22.5 Diagnostic Algorithm (Fig. 22.2)

Dealing with a trauma patient after the initial resuscitation can be challenging.
Initial resuscitation helps identify the main problems that can lead a patient to
death. However, once the initial assessment is over the doctor in charge has to decide
what to do. The decision depends on the haemodynamic status of the patients. After
administering the first litre of fluid (crystalloid) to the patient, the trauma leader has
to assess the patient’s status.
There are three possible scenarios that he can face (see Table 22.2):

• Responder patient
• Transient responder patient
• Non-responder patient

To identify in which class the patient is, the physician has to evaluate the clinical
parameter, especially the heart rate (HR), the patient general condition (from pale to
pink) and most importantly the change in arterial blood gases (ABG) parameters of
lactates and base excess (BE).
If after the initial resuscitation the patient HR returns to normal values, the lac-
tates and the BE on ABG improve, probably this patient is a responder. In this case
eventually the bleeding stopped by itself. In this scenario the patient needs to be
referred to the trauma surgeon in order to be admitted in a trauma ward and continue
with clinical observation and further management.

Class II-IV
-BP systolic < 100mmHG
-HR>100
-Tachypnea
-Alterated mental status
-BE< 5
-Lactates > 4 mmol/1

Begin resuscitation
10-15min

-Multiple lerge IV lines

-Crystalloids
-Blood FEP administration (class
III-IV)

-Additional work-up
Rapid search for blood loss Response to resucitation -Continual assessment for OR
or IR intervention
-Physical examination
-eFAST
-Major blood loss or need for
-Chest XR
emergent intervention -Operating room (OR)
-Pelvic XR
-Minimal or no response to -Interventional radiology (IR)
resuscitation

Fig. 22.2  Diagnostic algorithm

22  The Polytrauma Patient 247

Table 22.2  Responses to initial fluid resuscitation

Responder Transient responder Non-responder
Vital signs Return Improve and then deteriorate after Do not improve
normal infusion
Blood loss Minimal Moderate Severe
Type of fluid for Crystalloid Blood X matched Blood massive
resus transfusion
Need for Not likely Interventional radiology Urgent OR
intervention

If after the initial resuscitation the patient HR, lactates and the BE on ABG
improve only for a short time during the fluid administration and after stopping the
infusion they deteriorate, probably this patient is a transient responder. In this case
the bleeding is not massive but it is still ongoing. In this scenario the best option is
to refer the patient to the trauma surgeon for further management and it is also use-
ful to involve the interventional radiologist on call for possible embolization or
angiosuit procedures.
If after the initial resuscitation the patient HR, lactates and BE do not improve,
this patient is a non-responder. In this case the bleeding is massive and still ongoing.
Urgent referral to trauma surgeon is mandatory in order to make a definitive plan to
stop the bleeding.

Key Messages
• Follow ABCDE and ATLS principle every time.
• Consider physiology, anatomy and mechanism of injuries.
• Check for signs of shock and consider every trauma patient in shock if not
proved otherwise.
• Assess the patient continuously, prevent the complications and sort the
problems out as they present to you.
• Trauma patients need fluids and blood, do not be afraid of infusing the
patient.
• Blood on the floor and 4 more.
• Stabilize the patients, intubate, ICD, pelvic binding, limb traction.
• Follow diagnostic algorithm, in trauma there is no space for inventions or
new techniques it is a matter of life or death.
248 M. Marone and I. D’Alessio

References
1. Trauma  - Ernest E.  Moore, David V.  Feliciano, Kenneth L.  Mattox | Consegna Gratis n.d.
https://www.libreriacortinamilano.it/scheda-­libro/ernest-­e-­moore-­david-­v-­feliciano-­kenneth-­
l-­m attox/trauma-­9 781259860676-­1 95349.html?utm_source=google_shopping&utm_
medium=cpc&utm_content=9781259860676&gclid=CjwKCAjwrPCGBhALEiwAUl9X0z
Dh95rugKSfthzQfbrgtQ-­t3h-­Oh9gJf1Hm0a2-­zUcBiGbrIKfj4hoCitcQAvD_BwE. Accessed
30 June 2021.
2. Störmann P, Wutzler S, Sommer K, Marzi I, Walcher F, Lustenberger T.  Gunshot and stab
wounds: diagnosis and treatment in the emergency department. Notfall Und Rettungsmedizin.
2016; https://doi.org/10.1007/s10049-­016-­0162-­9.
3. Tapia NM, Suliburk J, Mattox KL. The initial trauma center fluid management of penetrating
injury: A systematic review trauma. Clin Orthop Relat Res. 2013;471:3961–73. https://doi.
org/10.1007/s11999-­013-­3122-­4. Springer New York LLC
4. Hussmann B, Lendemans S. Pre-hospital and early in-hospital management of severe injuries:
changes and trends. Injury. 2014; https://doi.org/10.1016/j.injury.2014.08.016.
5. Galvagno SM, Nahmias JT, Young DA.  Advanced Trauma Life Support® Update 2019:
Management and Applications for Adults and Special Populations. Anesthesiol Clin.
2019;37:13–32. https://doi.org/10.1016/j.anclin.2018.09.009.
6. Choi NJ, Hong SK. Management of shock. Prim Manag Polytrauma. 2019:11–8. https://doi.
org/10.1007/978-­981-­10-­5529-­4_2. Springer: Singapore
7. Maegele M, Fröhlich M, Caspers M, Kaske S. Volume replacement during trauma resuscita-
tion: a brief synopsis of current guidelines and recommendations. Eur J Trauma Emerg Surg.
2017; https://doi.org/10.1007/s00068-­017-­0771-­0.
8. Wurster LA, Thakkar RK, Haley KJ, Wheeler KK, Larson J, Stoner M, et al. Standardizing
the initial resuscitation of the trauma patient with the Primary Assessment Completion Tool
using video review. J Trauma Acute Care Surg. 2017;82:1002–6. https://doi.org/10.1097/
TA.0000000000001417.
9. Laue F, Ramadanov N, Matthes G. Emergency room management for severely injured patients.
Notfall Und Rettungsmedizin. 2019; https://doi.org/10.1007/s10049-­018-­0552-­2.
10. Coccolini F, Stahel PF, Montori G, Biffl W, Horer TM, Catena F, et  al. Pelvic trauma:
WSES classification and guidelines. World J Emerg Surg. 2017; https://doi.org/10.1186/
s13017-­017-­0117-­6.
11. Miller PR, Moore PS, Mansell E, Meredith JW, Chang MC. External fixation or arteriogram in
bleeding pelvic fracture: Initial therapy guided by markers of arterial hemorrhage. J Trauma.
2003;54:437–43. https://doi.org/10.1097/01.TA.0000053397.33827.DD.
12. Kauvar DS, Dubick MA, Walters TJ, Kragh JF. Systematic review of prehospital tourniquet use
in civilian limb trauma. J Trauma Acute Care Surg. 2018;84:819–25. https://doi.org/10.1097/
TA.0000000000001826.
13. Leenen LP.  Abdominal trauma: from operative to nonoperative management. Injury.
2009;40:S62–8. https://doi.org/10.1016/j.injury.2009.10.038.
14. Ohrt-Nissen S, Colville-Ebeling B, Kandler K, Hornbech K, Steinmetz J, Ravn J, et  al.
Indication for resuscitative thoracotomy in thoracic injuries – adherence to the ATLS guide-
lines. A forensic autopsy based evaluation. Injury. 2016;47:1019–24. https://doi.org/10.1016/j.
injury.2015.10.034.