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Anaphylaxis

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Republic of Iraq
Ministry of Higher Education
University of Baghdad
College of Medicine

Anaphylaxis
Supervised By
Professor Dr. Aida R. Al-Derzi

Done By
Ahmed Hussein Mahmood
‫احمد حسين محمود كاظم‬
Third Grade
Group
A1
 Contents
1.1 Introduction………………………………………………….……3
1.2 Mechanisms and Causes…………………….…………….………3
1.3 Clinical features……………………………………….……….….4
1.4 Differential diagnosis…….……….……………………………….6
1.5 Treatment…………………….……………………………………6
1.6 Prevention…………………………………………………………7
1.7 Summary ……………….…………………………………………7
1.8 References…………………………………………………………8

List of abbreviation
IgE Immunoglobulin E (Epsilon)

2
 1.1 Introduction

Anaphylaxis is a life-threatening type I hypersensitivity reaction, triggered by

exposure to a wide range of antigens and involving multiple organ systems. It's
immediate reaction like urticaria and angioedema. The reaction may be mild &
localized one, e.g. allergic conjunctivitis or it may be severe generalized reaction,
e.g. anaphylactic shock. Anaphylaxis is not common, but prevalence and incidence
figures in general population are unavailable because it is not a reportable disease.
The diagnosis must be made on the basis of clinical findings and treatment initiated
with the greatest urgency because the mortality rate approaches 10% in anaphylactic
shock. Allergic reactions under anesthesia occur once in every 5,000-25,000
anesthetics with a 3.4% mortality which is significantly lower than that in general
medical practice [1].

Fig (1): Anaphylactic urticaria and angioedema. *

1.2 Mechanism and Causes

The interaction of allergen and immunoglobulin E (IgE) antibody triggers

mediator release, resulting in the reaction affecting multiple target organs. The
release of mediators such as histamine and many others, from the mast cells and
basophils is responsible for the immediate clinical manifestations of anaphylaxis. It
includes 2 phases, initial phase which includes releasing of already stored materials
like histamine and eosinophils chemotactic factor of anaphylaxis and a late phase
response caused by the recruitment of other inflammatory cells, including slow
reacting material, bradykinin, prostaglandin and platelet chemotactic factor, late
3
phase occurs hours after the initial reaction. Anaphylaxis is usually thought of as an
IgE-mediated allergic reaction to such things common triggers included foods (e.g.,
peanuts, fish, nuts, eggs), drugs (NSAIDs, aspirin, penicillin, cephalosporins,
insulin, sulfonamides, blood products, vaccines in atopic persons who have genetic
predisposition to have more expression of IL-4 which makes class switching of IgE
and make person allergic [2]. The mast cell, however, can be induced to react by other
non-immunologic means, including direct activation by exercise, opiates, and
possibly radiocontrast agents, disturbances of arachidonic acid metabolism by cyclo-
oxygenase inhibitors such as aspirin and nonsteroidal anti-inflammatory drugs
(NSAIDs). This is the mechanism for anaphylactoid reactions where the term
‘anaphylactoid’ is used to designate reactions that are indistinguishable from
anaphylaxis but lack a demonstrable IgE allergic mechanism. In other cases, the
reaction is triggered by a physical activity such as exercise, and a few patients have
recurrent idiopathic “anaphylaxis”. Some patients have repeated anaphylactic
episodes without the cause being determined. In a recent study of 266 patients
referred for evaluation when obvious causes (e.g., insect stings, immunotherapy) had
been eliminated, 37% were determined to have idiopathic disease [3].

Fig (2): Allergic triggers. *

1.3 Clinical Features

Anaphylactic shock is caused by vasodilation and vascular leakage resulting

from enhanced permeability of the postcapillary venules in the vascular beds of
visceral organs, skin, and mucous membranes. Bronchial and gastrointestinal muscle
spasms produce acute airway obstruction and colicky abdominal pain. Increased
4
vascular permeability in the skin results in pruritus, urticaria, and angioedema. The
clinical manifestations of anaphylaxis can occur within seconds of antigen exposure.
With fatal reactions, the respiratory and cardiovascular systems are often affected
initially. Respiratory manifestations include stridor, difficulty in breathing, cyanosis
and even pulmonary edema. Severe upper airway obstruction by angioedema can
lead to asphyxia while lower airway obstruction with wheezing and chest tightness
is caused by bronchospasm. Laryngeal edema may be experienced as lump in throat.
The commonest cardiovascular manifestation is severe hypotension, usually caused
by a massive shift of fluid from the intravascular to the extravascular space.
Arrhythmias are not uncommon. Profound losses of intravascular volume can occur
quickly as a result of increased vascular permeability. Patients compensate through
maximal vasoconstriction initiated by the release of catecholamines and angiotensin.
Gastrointestinal symptoms include nausea, vomiting, diarrhea, and abdominal pain.
Flushing, diaphoresis, urticaria, pruritus and angioedema are cutaneous signs.
Patients may experience a feeling of impending doom and light headedness and
sometimes sense a metallic taste in the mouth. In most cases, the slower the onset of
symptoms, the less severe is the reaction. Some patients experience recurrence of
symptoms hours after apparent remission of the initial reaction (late-phase
anaphylaxis). In patients taking beta-blockers, anaphylaxis is often severe and may
be refractory to conventional management [4].

Fig (3): Signs and symptoms of anaphylaxis. *

5
 1.4 Differential Diagnosis

When a patient presents with sudden symptoms of dizziness, syncope, or

flushing, rapid assessment is essential so that an appropriate course of management
can be determined. Many conditions need to be considered. The vasovagal reaction
is the one most commonly confused with anaphylaxis. It usually follows a painful
intervention such as an injection and is manifested by pallor, light-headedness,
nausea, profuse diaphoresis and syncope. Symptoms improve promptly with
recumbency and disappear altogether without treatment in 20 to 30 minutes. The
lack of pruritus in the presence of a slow pulse rate and normal blood pressure
distinguishes a vasovagal attack from anaphylaxis. Ingestion of spoiled fish from the
tuna family may result in urticaria, pruritus, flushing, gastrointestinal upset, and
headache. The cause of this reaction is, a histamine like substance (saurine) produced
through bacterial contamination. Other factors, such as the presence of a carcinoid
tumor or a reaction between alcohol and chlorpropamide, can cause flushing-type
reactions [5].

1.5 Treatment

Treatment of anaphylaxis consists of both short- and long-term management.

The immediate goal is to maintain an adequate airway and support the blood
pressure. Patients having severe reactions should be given oxygen. Epinephrine
should be administered as soon as the diagnosis is made. Conventionally it is given
subcutaneously every 10 to 20 minutes until the patient’s condition is stable.
However, in life-threatening reactions with shock, intravenous administration may
be necessary, this route, however, poses risks of ventricular arrhythmias and
myocardial ischemia. For this reason, intravenous epinephrine is given slowly in low
doses. Commonly available ampoule of adrenaline when diluted in a 10 ml syringe
will have a concentration equivalent to 1:10000 solution. It should be given over at
least a 10-minute period, but the dose is usually limited to 3 mL for an average sized
(70 kg) adult [6]. Antihistamines are useful as second line therapy when a prolonged
course is suspected. Diphenhydramine hydrochloride can be given orally,
intramuscularly, or intravenously. The combined use of H1 and H2 histamine
6
antagonists is controversial, but cimetidine has been used. Corticosteroids may not
be helpful in immediate management of anaphylaxis but can be useful in treating
prolonged urticaria or a late phase response. Methylprednisolone sodium succinate
is usually given in large doses every 6 hours. Bronchospasm should be treated with
inhaled beta2 agonists, with the option of using intravenous aminophylline in
resistant cases [7].

1.6 Prevention

The most important component of anaphylaxis management is prevention.

Identification and subsequent avoidance of the offending allergen or other
nonimmunologic causes seems an obvious first step. If there is definite history of
past anaphylactic reaction, it is advisable to select another agent or procedure. Since
stinging insects cannot be consistently avoided, venom immunotherapy, when
possible, offers an effective means of preventing life-threatening reactions. Patients,
who are sensitive to radiocontrast material, have a history of venom-sensitivity or
are receiving immunotherapy injections, should be advised to discontinue beta
blocker therapy beforehand. An effective pre-treatment schedule consisting of
corticosteroids, antihistamines, and ephedrine sulfate has been described for patients
with a history of reactions to radiocontrast materials who are undergoing repeated
studies [8]. Long term oral corticosteroid therapy every other morning has been
advocated for patients with life-threatening idiopathic anaphylaxis [9].

1.7 Summary

Anaphylaxis is a potentially fatal condition, type 1 hypersensitivity. Causes

range from bee stings to drugs, foods, and exercise. Onset is usually sudden, and a
delayed reaction may occur hours after the initial reaction. Treatment consists of
airway maintenance and support of the blood pressure with fluid expanders,
epinephrine and oxygen. Additional agents, such as corticosteroids, antihistamines,
7
 vasopressors, glucagon, atropine sulfate, and isoproterenol hydrochloride, can be
useful. Prevention is the most important part of anaphylaxis management, in patients
with known allergies, self-administration of epinephrine plays a key role in reducing
mortality.

1.8 References

1 Fisher MMD, More DG. The epidemiology and clinical features of anaphylactic reactions
in anaesthesia. Anaesth Intensive Care 2012; 9:226-34.
2. Marquardt DL, Wasserman SI. Anaphylaxis In: Middleton E Jr, Reed CE, Ellis EF, editors.
Allergy: Principles and practice 4th ed. St Louis: Mosby, 2007;1525-36.
3. Kemp SF, Lockey RF, Wolf BL et al. Anaphylaxis: a review of 266 cases. Arch Intern Med
2009;155(16):1749-54.
4. Davidson S, Ralston S, Penman I, Britton R, Strachan M, Hobson R, Davidson's principles
and practice of medicine.P.75-76 23rd ed. 2018.
5. Lieberman P. Distinguishing anaphylaxis from other serious disorders. J Respir Dis
2006;16(4)411-20.
6. Brown AF. Anaphylactic shock: mechanisms and treatment. J Accid Emerg Med 2012;
12:89-100.
7. Lawlor GJ Jr, Rosenblatt HM. Anaphylaxis. In: Lawlor GJ, Fischer TJ, Adelman DC,
editors. Manual of allergy and immunology. 3rd ed. Boston: Little, Brown,2008;244-52.
8. Greenberger PA, Patterson R, Radin RC. Two pretreatment regimens for high risk patients
receiving radiographic contrast media. J Allergy Clin Immunol 2007;74(4 Pt 1):540-3.
9. Patterson R, Clayton DE, Booth BH, et al. Fatal and near fatal idiopathic anaphylaxis.
Allergy Proc 2003;16(3):103-8.

Figures:
*Fig 1: Sampson HA, Muñoz-Furlong A, Campbell RL, et al. (February 2006). "Second
symposium on the definition and management of anaphylaxis: summary report—Second
National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis
Network symposium". The Journal of Allergy and Clinical Immunology. 117 (2): 391–7.
*Fig 2: "Anaphylaxis". National Institute of Allergy and Infectious Diseases. April 23,
2015. Archived from the original on 4 May 2015. Retrieved 4 February 2016.
*Fig 3: Davidson S, Ralston S, Penman I, Britton R, Strachan M, Hobson R, Davidson's
principles and practice of medicine.P.75 23rd ed. 2018.

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