ORTHOPAEDIC ESSAYS

Faculty of Medical Sciences

Mona Campus

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 Table of Contents

Classification of Fractures

Management of an Open Fracture

Physeal fractures

Slipped Upper Femoral Epiphysis

Compartment Syndrome

Acute Osteomyelitis

Acute Management of Spinal Injuries

Management of the Paraplegic

Fractures around the Elbow in Children

Rheumatoid Arthritis

The Pathological and Radiological Changes In Osteoarthritis

Pathological and radiological changes in Tuberculosis Arthritis

Management of Hip Fractures in the Elderly

Management of Shaft of Femur Fractures in Adults

Management of Fractures of the shaft of the femur in Children

Management of Colle’s Fracture

Hand Infections

Carpal Tunnel Syndrome

De Quervain’s Tenosynovitis

Trigger finger (Digital Tenovaginitis Stenosans)

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Ganglion

Causes and Treatment of Scoliosis

Investigation of Bone Tumors

Lower Back Pain

Special Features of Individual Lesions:

Acute Paronychiae

Felon/Whitlow:

Bacterial Flexor Tenosynovitis(Tendon Sheath Infections)

Palmar Space Infections

Subcutaneous infection:

Web Space Infections

Dorsal Subaponeurotic Space Infection

Cellulitis

Radial and Ulnar Bursal Infections

Bite Wounds to the Hands

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Classification of Fractures

The classic definition of a fracture is a structural break in the continuity of a bone, epiphyseal
plate or a cartilaginous joint surface resulting from forces exerted exceeding that which the
structural component can withstand.

Fractures may be classified according to a number of criteria. According to its:

- Aetiology: Stress
Pathological
Traumatic
- Pattern
- Site
- Complete / Incomplete
- Relationship of the fracture fragments to each other : Displaced / Angulated etc
- Relationship of the fracture to the external environment : Open /Closed
- Presence or absence of complications.
- Mechanism of Injury.

According to Aetiology

Stress Fractures:
Also called fatigue fractures usually are thought to result due to overuse of the region causing
repeated stress or pressure e.g. repeated running, dancing, marching or prolonged walking .It
occurs when muscles become fatigued and unable to absorb added shock .As a result most stress
fractures, approximately 50%, are usually found in the weight bearing bones of lower limb
particularly the metatarsal, fibula and tibia bones.
There is no single specific causative injury as in traumatic fractures.

Clinical Presentation
Patients usually complain of gradual onset pain within the affected region which is affected by
continued activity and relieved by rest. Swelling may eventually present.
Palpation of the bone may reveal local tenderness.

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Radiological Evidence
Nothing may be visualized at first until some two to four weeks after. The fracture may only be
revealed as a hairline crack with a zone of callus surrounding it this being the most striking
feature. This zone may eventually form a dense fusiform mass around the site of fracture. It is
usually transverse in nature rarely with any displacement.

Pathological Fractures
This is a fracture caused by trivial injury to a bone already weakened by disease. May also occur
spontaneously .The causative pathology may be very obvious as in the case of advanced primary
malignancy but sometimes the pathological fracture may be the first sign of an occult primary.

Clinical Presentation
The patient may admit to having previous local pain or discomfort to the region.

Radiological Evidence
The fracture line is usually transverse and clean cut otherwise is dependent upon the underlying
pathology e.g. Multiple Myeloma – Multiple lytic lesions.

Causative Pathology
Generalised Disorders

Children Adults Elderly

Osteogenesis Imperfecta Osteomalacia Generalised Osteoporosis
Rickets Osteosclerosis Paget’s disease of Bone
Parathyroid Osteodystrophy Diffuse metastatic disease
Diffuse Metastatic Multiple Myelomatosis
Carcinoma

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Localised Pathology

Infections Benign Malignant

Pyogenic Osteomyelitis Solitary Bone Cyst Secondary Deposit from
primary lesion in e.g.
Breast, Prostate , Kidney,
Thyroid
Syphilitic Infection Endochondroma Primary Malignant Tumour
e.g. Ewing’s Tumour
Osteoclastoma Metastatic carcinoma

Traumatic Fractures
The most common category of fractures occurring in bone that was previously disease free.
May occur as a result of direct violence or indirect violence.
Direct Force: applied directly to the site of fracture, e.g. MVA, wt. dropped on the foot
Indirect Force: transmitted along the bone to cause the fracture, e.g. falling on an outstretched
hand and fracturing the humerus.

Pattern of Fracture
Transverse – Cuts across bone at right angles. Most likely due to a perpendicular
force and is relatively stable.

Spiral: Due to twisting force. Is likely to become re-displaced unless internally fixed

Oblique: Slant and unstable therefore are likely to become re-displaced after closed
manipulation.

Comminuted: Splintered or crushed or fractures that involve more than two fragments.
They usually occur as a result of high energy force and are often
associated with soft tissue or neurovascular damage.
Unstable and require open reduction internal fixation.

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Greenstick – More common in children especially before the age of ten. Is of an
incomplete nature due to the resilience of the bone.

Impacted – Ends of bone jammed together.

Compression fractures – The spongy bone substance is crushed such that the original
trabecula cannot be restored.

Greenstick

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Site

A fracture may be described based on the location along the bone. Long bone fractures may
occur in the:
- epiphysis
- physis
- metaphysis
- diaphysis
Fractures may also occur in the joint or not:
- intra articular
- extra articular

Physeal fractures are further classified based on radiological classification: Salter Harris
Classification:

 . Grade 1 – separation of the epiphysis from the metaphysis

 Grade 2– separation with the fracture extending through the metaphysis (MOST
COMMON)

 Grade 3– separation with the fracture extending through the epiphysis (intra-articular)

 Grade 4 – separation with the fracture extending through both epiphysis and metaphysis
and is also intra-articular

 Grade 5 – crush injury to the growth plate

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 Salter Harris Classification

Grade I and II have a better prognosis and can be managed by closed reduction.
Grades III and IV have a worse prognosis and must be managed by open reduction.

Extent
A fracture may be – incomplete e.g. Greenstick fractures in children
Hairline or Crack Fractures
Buckle Fractures
Incomplete fractures are more stable and can be managed by non surgical means. The patient
may also start weight bearing earlier.

Complete
A total break in the bone from one cortical region to the opposing. If undisplaced is relatively
stable and will heal if immobilized. If displaced requires reduction.

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Relationship of the Fracture Fragments to Each Other
- Displaced / Un-displaced
- Angulated / Not Angulated

Displaced – Fragments are offset from each other

-The position of the distal fragment is described in comparison to the proximal
fragment.

Angulated – Describes the relation of the fracture to the midline of the body .There is loss
of the normal longitudinal axis of the bone.

Mechanism of Fracture
Tension – Sudden forceful pull of the bone. Usually leads to a transverse fracture due
to direct force e.g. being struck.
Compression – Squeezing type force compressing the bone from both the top and the
bottom.
Shearing – Forces applied from opposite directions. Usually produces a combination
of oblique and transverse fractures.
Rotation/Torsion – the top and bottom of the bone turn either in opposite directions or
in the same direction at different speeds. Usually results in spiral
fractures.

Relationship of Fracture to the Exterior Environment

Open fractures are those in which a compromised skin wound exposes the ends of the fracture,
such that there is a direct communication between the outer body surface and the fracture. Closed
fractures are those fractures with no communication between the skin and fractured bone ends.
A closed fracture is less likely to become infected by microbes, unlike open fractures where
antibiotic treatment must be initiated.

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Gustillo & Anderson in 1984 classified open fractures in the following way:
Grade I bone sticking out (size, soft tissue damage, comminuted/ simple, contamination)
wound < 1cm
little soft tissue damage
simple fracture pattern
Minimal Contamination
Rate of Infection 0-2%

Grade II
wound > 1cm
moderate soft tissue damage
modest fracture comminution
Moderate Contamination
Rate of Infection 2-7%

Grade IIIA
extensive soft tissue injury
adequate soft tissue available to cover the fractured bone
high energy trauma
Severe Contamination
Rate of Infection 7-10%

Grade IIIB
extensive soft tissue injury
significant periosteal stripping
exposure of bone, will require flap coverage
Mass contamination
Rate of Infection 10-25%

Grade IIIC
any open fracture that is associated with an arterial injury that must be repaired for the
limb survival regardless of soft or hard tissue injury.
Rate of Infection 25-80%
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Complicated or Uncomplicated
A complicated fracture results in local or systemic problems which arise from either the fracture
itself or intervention.

Immediate
Soft Tissue Injury: Nerves, vessels, tendons, muscle.
Haemorrhage

Early
Compartment Syndrome
Fat Embolism (fat from bone into circulation)
Deep Vein Thrombosis

Late
Infection
Delayed / Mal / Non Union
Osteopaenia
Muscle atrophy
Post Traumatic Arthritis /Disuse Atrophy
Reflex Sympathetic Dystrophy
Joint Stiffness

Fracture Healing

Healing of fractures begins as soon as the bone is broken, provided the conditions are favourable.
Healing proceeds through several stages until the bone is consolidated. Following impact energy
is absorbed and this leads to mechanical and structural failure, and disruption of blood supply.
For healing to occur certain things are required:

1. Adequate blood supply

2. Relative immobility of the bone ends
3. Absence of infection or tumour
4. Apposition of the bone ends without other tissue in between

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The repair of cortical bone shows striking differences from the repair of cancellous bone, and the
pattern of healing in a given bone is probably influenced by such factors as rigidity of fixation of
the fragments and the closeness of the coaptation (the adaptation or adjustment of parts to each other:)

Healing of cortical bone is divided into five stages:

A. Stage of haematoma (inflammatory phase)
B. Stage of subperiosteal and endosteal cellular proliferation (Granulation tissue formation)
C. Stage of callus formation
D. Stage of consolidation (Lamellar bone deposition)
E. Stage of remodeling

Stage of haematoma (0-4 days)

The most important stage in fracture healing is the inflammatory phase and subsequent
hematoma formation. It is during this stage that the cellular signaling mechanisms work via
chemotaxis and an inflammatory mechanism to attract the cells necessary to initiate the healing
response. Following fracture, blood entravasates into the spaces between the bone fragments into
the surrounding soft tissue and bone marrow, and the haversion canals. As in the repair of all
wounds, healing begins with the clotting of the entravasated blood. Organization of the
haematoma begins within 24 hours. Blood clot is invaded by granulation tissue, which consists
of a loose meshwork of capillaries and young fibroblast. Deprived of blood supply, the
osteocytes near the surfaces die.

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Stage of subperiosteal and endosteal cellular proliferation (4-14 days)

The most prominent feature in the early stages of repair is the proliferation of cells from the
surface of the periosteum close to the fracture. These cells are precursors of osteoblasts, which
later lay down the intercellular substance. The cells form active tissue that surround each
fragment and grow towards the other fragment. Cellular tissue is not formed by organization of
the clotted fracture haematoma. Blood clot plays little or no role; it is pushed aside by
proliferating tissue and eventually reabsorbed. Simultaneously with the subperiosteal
proliferation there is cellular activity within the medullary canal, where the proliferating cells
appear to be derived from the endosteal and from marrow tissue of each fragment. This tissue
also grows forward to meet and blend with similar tissue growing from the other fragment.
Islands of cartilage may be present.

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Stage of callus (14 days onwards)

A callus is an unorganized meshwork of woven bone developed on the pattern of the original
fibrin clot, which is formed following the fracture of a bone and normally ultimately replaced by
hard adult bone. During callus formation, cell proliferation and differentiation begin to produce
osteoblasts and chondroblasts in the granulation tissue. The osteoblasts and chondroblasts
synthesize the extracellular organic matrices of woven bone and cartilage respectively, and then
the newly formed bone is mineralized. This stage requires 4-16 weeks. This is called “woven”
bone and gives rigidity to the fracture. Woven bone is visible on radiographs and gives the first
radiological indication that fracture is uniting.

Stage of consolidation

This is where there is the conversion of the woven bone that forms the primary callus to a more
mature bone with a typical lamellar structure. This stage involves the combined activity of
osteoclasts and osteoblasts.

Stage of remodeling

Completion of union of the newly formed bone often forms a bulbous collar, which surrounds
the bone and obliterates the medullary canal. Months following union, the bone is gradually
strengthened along the lines of stress at the expense of surplus bone outside the lines of stress
which are slowly removed. The process of remodeling is constantly going on in every bone
throughout life and becomes obvious after a fracture. The final 2 stages require 1-4 years.

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Figure: Stages of trabecular bone healing

Difference in Repair of Cancellous Bone

- Bone is of a uniform spongy texture with no medullary canal .There is a relatively
Broader area of contact between the fragments and the open meshwork of trabeculae
allows easier penetration by bone forming tissue.
- Union can occur directly between bone surfaces and does not have to occur via an
External callus and endosteal callus.
- The first stage of healing is the formation of the haematoma into which new blood
vessels and proliferating osteogenic from the fracture surfaces penetrate until they meet
and fuse with similar tissue growing out from the opposing fragment. Osteoblasts then
lay down the intercellular matrix which becomes calcified to form woven bone.

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Speed of Healing and Perfection of Fracture Repair
This is influenced by local and systemic factors . These include :

Local Factors Systemic Factors

Immobilisation Metabolic & nutritional deficiencies
Poor Blood Supply Sepsis
Poor Reduction Radiotherapy
Infection Chemotherapy
Allergic Reactions Sickle Cell Disease
Age Collagen Vascular Disease
Drugs eg Antiepileptics ,NSAIDS Vascular Insufficiency
Hormones Type of Bone Fractured
Synovial Fluid Fracture in a Joint

Complications of Fracture Healing

 Delayed Union
 Mal Union
 Non Union
 Fibrous Union
 Arthritis
 Pseudo arthritis

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Management of an Open Fracture

An open fracture or compound fracture is one in which the fracture or associated

haematoma is in direct communication with a body cavity or the external environment by way of
a breach in the soft tissues and skin. Open fractures are at risk of becoming infected, as the
communication with the outside surface serves as a portal of entry for pathogenic organisms.
Complications of an infected open fracture include osteomyelitis (the most dreaded complication
as it is difficult to treat), delayed union and non-union.
The goals of treating an open fracture are:
1. to prevent infection
2. to allow fracture healing
3. to restore function

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Open fractures have been classified by Gustillo and Anderson . This classification gives an
indication of the risk of infection and aids in the determination of the most suitable treatment of
the fracture.

Gustillo-Anderson Classification of Open Fractures

Type I Wound less than 1cm long

Moderately clean puncture where spike of bone has pierced the skin
Little soft tissue damage
No crushing
Fracture usually simple, transverse or oblique with little comminution
(Infection rate: 0-2%)
Type II Laceration more than 1 cm long
No extensive tissue damage, flap or contusion
Slight to moderate crushing injury
Moderate comminution
Moderate contamination
(Infection rate: 2-7%)
Type III Extensive damage to soft tissues,
High degree of contamination
Fractures caused by high velocity trauma
III A Includes any segmental or severely comminuted closed or open fractures,
Soft tissue coverage of the bone is adequate
(Infection rate: 7%)
III B Extensive injury to or loss of soft tissue, with periosteal stripping and exposure
of bone
Massive contamination
Severe comminution of fracture
After debriment a segment of bone is exposed and a local or free flap is
required to cover it.
(Infection rate: 10-25%)

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 III C Any fracture with an arterial injury, which requires repair, regardless of the
degree of soft tissue injury.
(Infection rate: 25-80%)
(Amputation rate: 50%)

Immediate management
1. Resuscitation
2. Pulses
3. Neurological assessment
4. Application of sterile moist dressing
5. Immunization
6. Intravenous antibiotics
7. Analgesics
8. Investigations
9. Splinting

The initial evaluation of a patient with an open fracture involves performing a thorough
initial evaluation to identify any life and limb threatening conditions. Approximately 30% of
patients with open fractures have other life threatening problems. The evaluation entails
stabilising the airway and cervical spine, ensuring that the airway is patent, assessing if the
patient is breathing and assessing the circulatory status. Intravenous access should be set up and
blood taken off for complete blood count and group and cross match.
Initially, the circulation to the extremity and its neurologic function are assessed. Check
for:
a) Distal pulses
b) Check the temperature of the area also look for pallor
c) Distal neurodeficiency- motor and sensory
d) Range of motion
Palpate for the posterior tibial artery. If there are no pulses palpated distally, one needs to ensure
that this is not due to swelling in the area. In that event do Doppler ultrasound studies which will
show if there is patency of the vasculature. However if the swelling is not sufficient to prevent
palpation of the pulses, and yet no pulses are evident on palpation, try to manipulate/realign the
limb as the absence of pulsations may be due to kinking of the vessel. If after reducing the
fracture, no pulses are evident, perform Doppler ultrasound or the more invasive arteriogram. If
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the arteriogram is not available or there is not enough time i.e. 4 to 6 hours have elapsed since
the accident (time is of the essence), an explorative operation is indicated. It is of note that if the
patient is already hypotensive, hypovolemic, elderly, the acceptable ischaemic time is reduced to
< 4 hours.
For the neurological examination of the affected limb there must be adequate knowledge
of the dermatomes and myotomes. The goal of the neurological assessment is to determine if the
limb is insensate or not.
Once the patient is assessed as being stable, a history should be taken to determine the
mechanism of injury, if there was loss of consciousness, presence of pain in other sites (which
points to other injuries), past medical history and mental status of the patient .
Physical examination is divided into 2 parts. There is an initial survey to determine the
presence and extent of other injuries, followed by a more in depth second surveillence. Once the
patient is haemodynamically stable, more attention is paid to the fracture site.
The skin around the wounds is examined. The entire circumference of the wound is
examined. The “ One look technique” should be implemented The wound should not be
subjected to repeated examination, but should be photographed then kept covered with moist
sterile dressing, until it can be visualized under optimum conditions in the operating room. The
moist sterile dressing help prevents infection and desiccation (to dry up) of the wound.
Prophylaxis for tetanus should be administered. Wounds that are prone to tetanus
infection are those that are seen by the doctor 8-24 hours after injury, barnyard contamination
and those with devitalised tissues. If the patient was fully immunised in the past but has not
received a booster in over 10 years, then 0.5ml of tetanus toxoid is given subcutaneously. In
patients who have not received a full course of immunization, passive immunization with 250-
500 units of human tetanus immune globulin (tetanus immunoglobulin) intramuscularly
should be administered in addition to the tetanus toxoid. Penadur 1.2 MU intramuscularly is
also administered to destroy any tetanus spores.
Intravenous antibiotics should be given in the emergency room and continued for only 2
to 3 days. Prolonged antibiotics for more than 3 days do not further prevent infection. Restricting
the antibiotics should minimize the emergence of resistant bacteria. The antibiotic of choice is a
cephalosporin such as cefuroxime 1.5g stat. If it is a Type II or III fracture add an
aminoglycoside such as gentamycin to cover both gram positive and gram negative bacteria.
Analgesics should be given such as , 75mg IM Voltaren (diclofenac sodium) stat. Initial
use of pethidine should be avoided in the head injury patient as it may be difficult to determine if

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the onset of drowsiness is due to the narcotic or circulatory failure. Nota Bene, narcotics should
not be administered prior to obtaining informed consent for surgery.
During the resuscitative interventions blood is taken off for complete blood count (Hb,
WBC, Platelets) and group and crossmatching. The limb is splinted . This provides some element
of pain relief and helps to prevent further soft tissue damage. Thereafter, the patient should be
sent to the radiological department to take the relevant X-rays. AP and lateral X-rays should be
taken of the joint above and the joint below the open fracture site. Air in the soft tissue spaces
will indicate the presence of an open fracture.

Intra-operative Management
The intra-operative and post-operative management of the open fracture primarily entails:
a) Prevention of infection
b) Wound closure
c) Healing of the fracture

Operative debridement and copious irrigation of the open fracture should be conducted
under sterile conditions. The goal is to avoid infection; this is the most important principle. The
wound should be cleaned with alcohol, iodophors or chlorohexidine. A tourniquet should not be
used for it is important to be able to distinguish between living and dead tissue. Small wounds
should be extended and excised to allow adequate exposure and until a healthy bleeding edge to
the incision is obtained. There should be sufficient debridement, irrigation and preservation of
the periosteum. Working systemically from superficial to deep layers the wound should be
explored and damaged tissue excised cleanly with curved scissors. All devascularised bone and
soft tissues should be debrided. A bone fragment that is wholly denuded of all soft tissue should
be removed carefully, but no bone with adherent soft tissue should be excised, no matter how
flimsy the attachment or precarious the blood supply. Irrigation can remove enough wound
bacteria to cross the threshold to non-infected states, but only if irrigant is delivered with
sufficiently high pressure to mechanically disrupt bacterial adherence to the wound surface. Type
II and III fractures should be irrigated with 5 to 10 litres of saline.
Non-viable muscle can be identified by the 4 “C’s” namely:
1. Colour
2. Consistency
3. Contraction
4. Circulation
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Thus, non-viable muscle is identified by its dark or dusky, non-pink colour, its mushy
consistency, the absence of contraction when pinced with forceps or cut with cautery and, the
absence of bleeding from a cut surface. The best indicator of viability is bleeding during
debridement. Unattached bone should be discarded. The fascia should be incised parallel to the
muscle fibres in both directions, the underlying muscle surrounding the tract should be opened in
the direction of its fibres to the degree necessary to achieve exposure adequate to inspect the
tract, remove foreign bodies and excise non-viable muscle. IV fluorescein dye may be used to
aid identification of dead tissue. Staged surgical debridement may be necessary at 48 hour
intervals. Note that wounds contaminated by dirt (eg. grease, asphalt etc.), need aggressive
repeated debridement in order to avoid infections and subsequent osteomyelitis. Second-look
debridement can performed at 24 to 48 hours depending on the extent of the damage.
It is then essential to stabilize the fracture. Stabilization of the fracture reduces the rate of
infection, promotes soft tissue healing, facilitates wound care, and allows mobilization of the
limb. This is particularly important in multiple trauma patients. It is preferably performed at the
time of initial debridement. No one method is optimum for stabilization of all open wounds. Use
of external fixators is versatile; it provides easy access to wounds during healing and ease of
application with minimum operative trauma. However it is not devoid of associated risks namely
pin site infection. Other options include intramedullary nailing, plate and screws (useful in
displaced intra-articular fracture fixation), splints casts and traction (can be used in stable type I
fractures, beware compartment syndrome). A wound culture should be done at the end of the
procedure. The patient should be placed on prophylactic antibiotics for 3 days.
A broad-spectrum antibiotic, for example a cephalosporin or an aminoglycoside may be
employed.
Soft tissue coverage of the wound should be done as early as possible to avoid infection
and to optimize the milieu for bone healing. Options in coverage and closure of the wound
include primary delayed closure, suturing the skin directly, splint skin grafts and flaps. The
placement of bone grafts in open fractures is a controversial technique. Posteromedial or
posterolateral bone grafting can be done without disrupting non-unions if alignment is
satisfactory. The choice depends on the age and needs of the patient, location size and condition
of the defect, the likelihood that further reconstruction will be needed, the associated zone of
surrounding soft tissue injury and the tissues available for the flap. The types of flap include
fasciocutaneous, transposed muscle pedicle or free microvascular muscle flap.

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 In most cases, a delayed primary closure is performed for open wounds, but surgical
incisions made during the case can be closed primarily, antibiotic bead pouch is a useful method
of covering the wound.
Patients treated for open fractures must be closely monitored for signs of infection. The
temperature chart should always be referred to and any large sustained increases in temperature
taken as an indication to inspect the wound. However if by one week the temperature values are
normal and the wound is not draining , the plastic surgeon may be contacted for wound coverage.
Thereafter the progress of the fracture is monitored. The fracture is allowed to heal. One
should look for any bone defects, if any are present then within 6 weeks a bone graft should be
done.
Compartment syndrome can occur in open fractures. Absolute indications for amputation
include a Type III C injury accompanied by damage to the posterior tibial nerve or a Type III C
injury with massive loss of bone i.e. a macerated, insensate limb.
As a result of the risks and complications of infection, open fractures should be treated
carefully and as quickly as possible to avoid any such complications, especially the extreme
complication of amputation of the affected limb.

Physeal fractures

Physeal fractures are fractures through a growth plate or physis; therefore, they are unique to
paediatric patients. Cartilage cells in the joint receive their blood supply from metaphyseal and
epiphysial blood vessels, and grow from the epiphysis towards the metaphysis. Damage to either
epiphyseal or metaphyseal vascular supply disrupts bone growth, but damage to the cartilage
may not be significant if the surfaces are reapposed. Typically, physis closure occurs during the
teenage years, when the two vascular beds touch, and no further bone growth is possible. The
Salter-Harris classification of the injury categorizes these fractures anatomically and by virtue of
the regions damaged provides a guide to the treatment of the patient and clues to possible long-
term complications. The basic types of injuries include the following:

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Type I Salter-Harris fracture type I

This is a transverse fracture through the

hypertrophic zone of the physis. In this injury, the width
of the physis is increased. The growing zone of the physis
usually is not injured, and growth disturbance is
uncommon. On examination, the child has point
tenderness at the epiphyseal plate.

Salter-Harris fracture
Type II
type II
This is a fracture through the physis and metaphysis, but the
epiphysis is not involved. These fractures may cause
minimal shortening but rarely result in functional
limitations. Type II is the most common Salter-Harris
fracture.

Type III

This is a fracture through the physis and the epiphysis. This

fracture passes through the hypertrophic layer of the physis
and extends to split the epiphysis, inevitably damaging the
reproductive layer of the physis. This type of fracture is
prone to chronic disability because, by crossing the physis, it
extends into the articular surface of the bone. However, it
rarely results in significant deformity and therefore has a
Salter-Harris fracture type
relatively favourable prognosis. The treatment for this
III
fracture is often surgical.

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Type IV

A Type IV fracture passes through the epiphysis, physis, Salter-Harris fracture type IV
and metaphysis. Similar to a type III fracture, a type IV
fracture is also intra-articular and it can therefore result in
chronic disability. By interfering with the growing layer of
cartilage cells, these fractures can cause premature focal
fusion of the involved bone and cause deformity of the
joint.

Type V

A compression or crush injury of the epiphyseal

Salter-Harris fracture type V
plate with no associated epiphyseal or metaphyseal
fracture. This fracture is associated with growth
disturbances at the physis. Initially, diagnosis may be
difficult, and is often made retrospectively after
premature closure of the physis is observed. In the older
teenagers, the diagnosis is particularly difficult. The
clinical history is paramount in the diagnosis of this
fracture, typically involving an axial load injury. These
injuries have a poor functional prognosis.

When all types of Salter-Harris fractures are considered, the rate of growth disturbance is
approximately 30%. However, only 2% of Salter-Harris fractures result in a significant
functional disturbance.

Rare types of Salter-Harris fractures include type VI: injury to the perichondral structures, type
VII: isolated injury to the epiphyseal plate, type VIII: isolated injury to the metaphysis, with a
potential injury related to endochondral ossification, and type IX: injury to the periosteum that
may interfere with membranous growth.

Diagnosis of physeal fractures is based upon historical information, physical examination as well
as radiographic procedures.
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History
May present with
- History of trauma. If there is severe compression, think type V
- Pain at the site
- Loss of function

Examination
May see
- Deformities
- Tenderness at site
- Pain on movement and abnormal movement

Investigation

Plain film radiography always is the preferred examination in a suspected fracture. CT with
multiplanar reconstruction and MRI may help to determine appropriate management and assist in
surgical planning. X-ray findings vary according to the type of Salter-Harris fracture. With type
I fractures, initial radiographs may suggest separation of the physis, but this separation may not
be apparent. However, soft tissue swelling is present, and its centre typically overlies the physis.
Follow-up radiographs obtained 7-10 days after injury help in establishing the diagnosis. New
bone growth (adjacent sclerosis and periosteal reaction) along the epiphyseal plate confirms the
diagnosis. In type V injuries, initial plain radiographs may not show a fracture line, similar to
images of type I fractures. However, soft tissue swelling at the physis is present.

Management

With negative radiographs and point tenderness over a physis, it is prudent to treat patients as if
they have Salter-Harris type I injury. It is equally prudent to counsel the parents and patients
regarding the potential for future growth abnormalities, even with minor injuries. Parents
should be counselled that treatment is being given for the “worst case” scenario, and it may
well turn out that their child does not have a fracture, but that this can only be determined with
serial radiographs.

27
If displacement has occurred it should be corrected as soon as possible after the injury because
even the delay of a day or two may render the reduction considerably more difficult.
Types I& II: - These fractures are generally treated by closed reduction & immobilized in
POP casts.The period of immobilization after a type II epiphysial displacement can be shorter
than for a fracture, for it has been shown that the epiphysis unites in about half the time required
for an equivalent fracture in the same group.

Types III & IV: - these fractures are intra-articular and as a result need to be treated by open
reduction and internal fixation. This is to prevent:
1) secondary osteoarthritis &
2) growth disturbances resulting from callus bridge formation.

Type V fractures: In type V fractures the cartilage cells of the physis are crushed and,
regardless of the form of treatment, growth disturbance may still occur

All these fractures are relatively unstable and union must be firm before movement of the
joint is allowed. This is usually present by about six weeks.

Complications
There are two main concerns with physeal fractures:
1. growth disturbances and
2. secondary osteoarthritis.

Growth disturbances
Growth disturbances can take the form of a limb length discrepancy, or an angulation
deformity. If the growth plate is damaged in such a way that a bony bridge develops between
the epiphyses and metaphyses, this can lead to premature fusion of the growth plate resulting
in a growth disturbance.

If the whole plate is affected, there will be a resultant shortening of the entire bone length, thus
leading to a limb length discrepancy. This is of particular concern in the lower limbs as this can
lead to problems in gait & back problems including scoliosis (secondary). The more skeletally
immature the patient, the greater the degree of shortening will be.

28
If only a part of the plate is affected, the one side of the bone will grow faster than the other,
resulting in an angular deformity. Angulation deformity will also occur if there is premature
arrest in one bone of a pair (as in the forearm & leg) e.g. valgus deformity in the ankle region
will occur if growth is arrested in the lower epiphyses of the fibula but continues in the tibia.

Children can also get hyperemia (excess of blood in a body part) of the physes causing increased growth of
that limb.

Other complications
The other complications seen here are the same as for any fracture: -
- Osteoarthritis (intra-articular fractures)
- Non-Union
- Mal-Union

Slipped Upper Femoral Epiphysis

This is a condition of early childhood in which the upper femoral epiphysis is displaced from its
normal position upon the femoral neck. The displacement occurs at the growth plate. The cause
is unknown but the condition is often associated with overweight from endocrine dysfunction,
but in other cases the patient is of normal build.

In this condition the underlying pathology is associated with loosening of the junction between
the capital epiphysis and the femoral neck. With the downward pressure of weight bearing and
the upward pull of the muscles on the femur the epiphysis is displaced. Displacement is always
backwards and downwards, so that the epiphysis comes to lie at the back of the femoral neck.

The displacement is usually gradual but it may occur suddenly due to an injury such as a fall.
When left undisturbed the epiphysis fuses to the femoral neck in the abnormal position. The
consequent deformity of the articular surface then predisposes to the later development of
osteoarthritis.

29
Regarding the clinical features, the patient is usually between the ages of 10 and 20 years. In
less than half of the cases both hips are affected, though seldom at the same time. Typically there
is a gradual onset of pain in the hip with a limp. Sometimes the pain is felt mainly in the knee.
On examination there is restriction of flexion, abduction and medial rotation. Lateral rotation and
adduction are usually increased and, the limb tends to lie in lateral rotation. Forcing movement in
the restricted range exacerbates the pain.

Radiographs, in particular lateral radiographs, are essential in the management of the patient.
Slight displacement is easily overlooked if antero-posterior films alone are examined. In the
lateral film the epiphysis is seen to be tilted over towards the back of the femoral neck, the
posterior ‘horn’ being lower than the anterior, whereas in the normal hip they are level.

X-ray of Left Slipped Upper Femoral Epiphysis

30
Compartment Syndrome

Compartment Syndrome (CS) is a limb threatening and life threatening condition in which
perfusion pressure falls below tissue pressure within a closed fascial space with subsequent
compromise of circulation and function of tissues. The most commonly affected fascial
compartments are of the leg and forearm however any compartment may be affected including
the abdomen.
Two types of compartment syndrome have been described: Chronic and Acute.

Acute Compartment Syndrome – Occurs subsequent to trauma commonly fractures.

Progressive worsening of symptoms,
Irreversible nerve and muscle injury occur in hours.

Chronic Compartment Syndrome – Recurrent syndrome that occurs with exercise.

Occurs bilaterally
Symptoms subside in ~ 1 hour post exercise.

Aetiology

 External restriction of compartment

o Military antishock trousers (MAST)

o Restricting Splints, Improperly placed casts, tight dressings
o Circumferential Burns
o Malfunctioning sequential compression devices (SCDs)
o Tight boots

 Internal increase in compartment volume

o Fractures ( most common )

o Hemorrhage (trauma, coumadin, tissue plasminogen activator [TPA])
o Hemophilia (prone to spontaeneous haemorrhage)
o Gun shot wound to thigh
o Massive intravenous fluid infusion
o Compartment fluid injection
31
 o Crush injuries
o Rhabdomyolysis
o Gastrocnemius or peroneus muscle tear
o Androgen abuse/muscle hypertrophy
o Tumours
o Ruptured bakers cyst
o Snake envenomation
o Infection : Clostridium Perfringens (gas gangrene)
o Drug /Alcohol Abuse or Coma : Lying on limb for hours

Pathophysiology

Different theories have been put forward to explain this syndrome. The most recent popular
proposal is based on the fact that various osseofascial compartments have a relatively fixed
volume; introduction of excess fluid or extraneous constriction increases pressure and decreases
tissue perfusion, until no oxygen is available for cellular metabolism.

Tissue perfusion is determined by measuring capillary perfusion pressure (CPP) minus the
interstitial fluid pressure. TP=CPP-IFP

Normally cellular metabolism requires 5-7 mm Hg oxygen tension; this is easily maintained with
the CPP averaging 25 mm Hg and interstitial pressure 4-6 mm Hg. However, rising interstitial
pressure overwhelms perfusion pressure.

With this blood flow through the capillaries stops and with it oxygen delivery ceases. Hypoxic
injury causes cells to release vasoactive substances (e.g., histamine, serotonin), which increase
endothelial permeability. Capillaries therefore allow continued fluid loss, which increases tissue
pressure and advances injury. Nerve conduction slows, tissue pH falls due to anaerobic
metabolism, surrounding tissue suffers further damage, and muscle tissue suffers necrosis,
releasing myoglobin. The end result is loss of the extremity and, possibly, the loss of life.

32
Clinical Presentation (6 P’s)

1) Pain: Most common and consistent sign. It’s described as pain out of proportion to the
normal clinical course i.e. greater than that expected for the type of injury sustained. It is
a diffuse, intense pain that is exacerbated by movement, touch, pressure, stretch, and
elevation or placing in a dependent position. Results mainly from muscle ischaemia.

2) Paresthesia: As nerves become ischemic they produce paresthesia in the cutaneous

distribution of the nerves in the affected compartments (i.e. on and anterior compartment
syndrome of the leg the 1st dorsal cleft of the foot (deep peroneal distribution) is the area
effected.))
NB: Don’t use pinprick to test nerve distribution because the pain fibers are the smallest
and the last to be compromised, use two-point discrimination. Significantly 2 pt
discrimination is the 1st
thing to go.
3) Pallor – this occurs as the muscles and other soft tissues are no longer perfused with
limb
oxygenated blood. The digits of the distal portion of the limit start to change colour, and
become bluish-gray, this is more apparent in Caucasians.

4) Perishing cold – also due to decreased tissue perfusion, preventing warming.

5) Pulselessness – this is a late sign of CS

6) Paralysis – occurs secondary to the patient experiencing severe pain with movement of
the limb.

There is also marked muscle tenderness and weakness.

History should reveal the mechanism of injury because CS is likely to occur with fractures (long
bone), high-energy trauma, penetrating injuries (gun shot/stab wound), venous injuries, or crush
injuries. Also, rule out other causes of diminished sensation and weakness e.g. spinal cord
injury.

33
Diagnosis
Intra-compartmental pressures can be measured and the limb assessed. The Whiteside’s
method of measuring is considered one of the better methods. A simple pressure-measuring
device consisting of a needle and plastic tubing filled with saline solution and air attached to a
mercury manometer is used.

It is to be noted that normally the pressure within the fascial compartment is 0-5
mmHg. However, blood flow through the microcirculation of capillaries is impaired when
intra-compartment pressures rise to 30 mmHg or more. Inadequate tissue perfusion and
relative ischaemia commences when the pressure within the closed compartment lies
between 30mm`Hg of the patient’s diastolic pressure. Thus, when the pressure equals
or exceeds the patient’s diastolic pressure effective tissue perfusion ceases.
Muscles tolerate 3-4 hours of ischemia well (critical ischemic time of a limb), but by 5-6
hours the damage is irreversible.

Absence of the above equipment has lead clinicians to use two clinical tests in the diagnosis:
- Pain on passive extension of fingers/toes
- Loss of active flexion of distal IP joints of 1st & 2nd finger

34
Differential Diagnosis
o Cellulitis
o DVT & thrombophlebitis
o Gas gangrene
o Peripheral vascular injuries
o Necrotizing fascitis
o Rhabdomyolysis
o Jellyfish envenomations

Investigations

1) Compartment Pressure Measurement: Tonometers – confirm the diagnosis > 30 mmHg.

2) Doppler studies – used to detect distal pulsations
3) CBC: r/o cellulitis- WBC, Hb, Plt (hemostasis)
4) CPK and Serum Mb: released due to the breakdown of muscles.
5) Urinalysis: initially may be positive for blood but negative for RBC’s on microscopic
analysis, which may indicate Mb in the urine
6) PT, PTT: blood-clotting screen
7) X-rays- 2 planes
8) U/S: may help to evaluate arterial flow or visualize any DVT

Cpk - In tissues and cells that consume ATP rapidly, especially skeletal muscle, but
also brain,photoreceptor cells of the retina, hair cells of the inner ear, spermatozoa and smooth muscle,
phosphocreatine serves as an energy reservoir for the rapid buffering and regeneration of ATP in situ, as
well as for intracellular energy transport by the phosphocreatine shuttle or circuit. Thus creatine kinase is
an important enzyme in such tissues.

Clinically, creatine kinase is assayed in blood tests as a marker of myocardial infarction (heart
attack), rhabdomyolysis (severe muscle breakdown), muscular dystrophy, and in acute renal failure.

35
Treatment

If trauma is the cause, since most cases of CS is due to trauma, resuscitation: stabilize the
patient by ABC management.
 Give oxygen to increase pO2
 IV hydration as indicated
 Refer to general surgery or orthopedic where necessary
 Take measures that would reduce the likelihood of CS which include:
- Elevation of the affected limb above the level of the heart.
- Dressings should be removed if a CS is suspected clinically. One
reason is for proper evaluation; the other is to reduce the intra-
compartment pressure, which can be surprisingly elevated with
tight dressings.
- Remove cast if present.

 Reduce fractures or dislocations, which may have damaged or kinked a

blood vessel.
- Casts should be bi-valved in high-risk situations. A tight cast in
the face of continued swelling can lead to the development of CS.
After a cast is in place, the neuromuscular exam should be
performed frequently.
 In the case of Volkmann’s ischemic contracture, apply hot water bags on
the other limbs to promote vasodilatation.
 Surgical Intervention includes fasciotomy.
The fascia is divided along the length of the compartment to release pressure within. The
skin is also left open for several days to weeks because some post-ischemic swelling occurs
after surgical decompression.

36
NB: Consider bicarbonate or acetazolamide to alkalinize the urine to help prevent
myoglobinuria. This occurs after reperfusion of the damaged tissue, where the myoglobin in the
muscle is released and precipitates in the renal tubules, primarily in acidic urine, leading towards
renal failure.

Fasciotomy has been the treatment of choice in this condition. Even the sequelae from prophylactic
fasciotomy is less then the damage acquired from delay in treatment of Compartment Syndrome. It
carries the disadvantage of presenting an open wound, which is subject to infection, as well as prolonging
the hospital stay of the patient.

Mannitol infusions, to try and osmotically lure the intracompartmental fluid back into the blood stream in
order to lessen the intracompartmental pressure is receiving some recent recognition of success.
Hyperbaric Oxygenation has, also, been recognized as a fairly successful remedy for this condition.

Complications

 Tissue Damage- irreversible tissue death can occur in 4-12 hours depending on the tissue
type and the compartmental pressure. Permanent disabilities result from undiagnosed CS
 Amputation- sometimes tissue is beyond repair and the only measure to prevent
gangrene and possibly death is this.
 Renal Failure- this primarily occurs after reperfusion of the damaged tissue following
fasciotomy, where the Myoglobin in the muscle is released and precipitates in the renal
tubules, primarily in acidic urine, resulting in myoglobinuria and possibly leading to renal
failure. Evidenced by multi-coloured urine. Prevention includes generous fluids and
alkalization of the urine.

 Cosmetic deformity from fasciotomy

 Volkmann Ischemic Contractures- After prolonged ischemia; the muscles are
eventually replaced by fibrous tissue, which threatens to produce a disabling
contracture—seen most often in the flexor muscles of the forearm or leg.

37
 Cycle of Volkmann’s Ischaemia

Arterial
Painful
damage Ischaemia
Reduced Pale
blood Pulseless
flow Paraesthetic
Paralysed
Oedema
Direct
injury

Increased
compartment
pressure

 Death- can occur through an infectious etiology or through hyperkalemia secondary to

tissue death, causing cardiac arrhythmias.

Chronic Compartment Syndrome

Chronic compartment syndrome is a not a medical emergency and affects athletes. It results from
the vascular engorgement of muscles during exercise superimposed on muscle hypertrophied by
prolonged training. It is characterized by exercise-induced pain and swelling that is relieved by
rest. It usually occurs in the lower leg and is occasionally accompanied by numbness or difficulty
in plantar flexion. Symptoms dissipate quickly when activity stops, but compartment pressures
may remain elevated for some time afterwards.

38
Diagnosis

Chronic compartment syndrome must be differentiated from other

pains in the lower leg, such as stress fractures of the shinbone
(tibia) and tendonitis. To diagnose chronic compartment syndrome,
the physician measures the intramuscular pressure before exercise,
one minute after exercise and at five minutes intervals after
exercise, until pressure returns to resting pressure, or 20min have
elapsed. Post exercise pressures in excess of 15 mmHg persisting
for longer than 15 minutes is indicative of chronic compartment
syndrome.

Treatment

Conservative treatment is the mainstay of therapy. It entails:

 Refraining from the offending activity, applying ice and elevating the limb slightly.
 Do not wrap the leg because this will increase the pressure and aggravate the condition.
 Take aspirin or ibuprofen to reduce inflammation.
 Cross-training with low-impact activities may be permitted as long as symptoms do not
return.

Surgical release may be needed if conservative treatment is ineffective.

39
Acute Osteomyelitis
-Pathogenesis, diagnosis and treatment

Osteomyelitis is infection of bone and the surrounding soft tissue by pyogenic organisms leading
to inflammatory destruction of bone, bone necrosis and new bone formation. It can be acute,
chronic or subacute.The exact incidence is not known but approximately 50% of cases in the
United States occur in children occurring in 1 in every 5000. There tends to be a male
preponderance in all age groups and this is thought to be due to their increased chance of trauma
from risk taking behaviour or involvement in physical activity that predispose to bone injury
.Exact ratio is 2: 1 male : female .

The aetiology of acute osteomyelitis can be placed into 2 categories:

- Haematogenous Spread from a distant soft tissue focus
- Direct/Contiguous Spread from an adjacent soft tissue lesion

Haematogenous Spread
This includes bacterial seeding via blood from for example: a boil, infected skin abrasion,
pharyngitis. This tends to occur mostly in children at the metaphyseal sinusoids due to the
apparent slowing of blood flow within this region predisposing to thrombosis and avascular
necrosis. Osteomyelitis from route is usually of a slow development and insidious onset.
Common Organisms according to age:
o Newborns (<4months): Staph. aureus, Enterobacter species, group A and B
Streptococcus species
o Children (aged 4 mths. to 4yrs): Staph. aureus, group A Streptococcus species,
Haemophilus influenzae, and Enterobacter species
o Children, adolescents (aged 4 to adult): Staph. aureus (80%), group A
Streptococcus species, H influenzae, and Enterobacter species
o Adult: Staph. aureus and occasionally Enterobacter or Streptococcus species.
Staphylococcus Aureus accounts for 90 % of cases overall.

40
Direct/Contiguous Spread

Direct inoculation of bone from an adjacent site such as: an open fracture, puncture wound of the
foot (diabetic foot). Clinical manifestations are more localized in this type of spread and tend to
involve multiple organisms.
Common organisms: Staphylococcus Aureus (80%), Escherichia Coli, Pseudomonas
Aeruginosa and anaerobes.

Disease states known to predispose patients to osteomyelitis include diabetes mellitus, sickle cell
disease, acquired immune deficiency syndrome (AIDS), IV drug abuse, alcoholism, chronic
steroid use, immunosuppression, and chronic joint disease. In addition the presence of a
prosthetic orthopedic device is an independent risk factor as is any recent orthopedic surgery or
open fracture.

Sickle Cell Disease: Salmonella sp. and Staph. Aureus

IV drug users: Candida Albicans, Pseudomonas.

Metaphysis involved in children, in infants and adults can be diaphyseal, metaphyseal or

epiphyseal.

Pathogenesis

Stage 1 - The infecting organism reaches the bone from a distant or local focus of infection. The
initiating bacteremia in the case of haemategenous spread, may have followed an insignificant
event such as injury to the gastro-intestinal mucosa during defaecation, or minor skin infections
such as a boil or a sore throat. In rare cases infection may pass through the spinal venous plexus
from an infected intra-pelvic lesion.
Normally, the infection develops in the metaphysis or epiphysis of a long bone. The metaphysis
is the most commonly affected area because its arterial supply comes from arcades coursing
upwards from the shaft which curve to enter the metaphysis. They form end-arteries which are
narrow resulting in, sluggish blood flow. This compounded by the low oxygen tension of the
metaphyseal blood, provides the perfect milieu for bacterial growth. Bacteria will proliferate and
incite an acute inflammatory reaction. The swelling associated with inflammation is however
impeded by the rigid structure of the bone. There is a resulting rise in the intra-osseous pressure,
leading to vascular compromise and so the bone becomes hypoxic. The formation of pus also
41
occurs and in an effort to alleviate this pressure, some of the pus tracks through the Haversion
and Volksman canals in the bony cortex to the periosteum.

Stage 2 - The bone is progressively weakened, and pus eventually leaks out via the path of least
resistance into the sub-periosteal space forming a sub-periosteal abscess. . Lifting of the
periosteum further impairs the blood supply to the affected region, leading to ischaemia.

Stage 3 - The pressure in this area also rises until it bursts through the periosteum and tracks up
to the skin forming a sinus.

As the disease progresses septic thrombosis of the blood vessels usually ensue, causing
ischaemia and necrosis of the bone. This avascular dead bone, or sequestrum, separates the
underlying living bone while new bone formation occurs, just below the periosteum. This new
bone is called the involucrum. Other factors contributing to bone death include, decease pH, low
oxygen tension, toxin and destructive enzyme release.
Usually, the epiphyseal plate acts as a barrier to the spread of infection, but in children less than
two years old, the epiphyses, epiphyseal plate and metaphyses all have a common blood supply.
Hence the infection can be spread to involve the epiphyses and cause joint involvement. There
are certain joints however which the metaphyses in within the joint cavity (gleno-humeral joint,
elbow joint, hip and knee joint) and there can be joint involvement via direct spread. Even
though the joint may not be infected, an effusion of clear fluid into the joint called a sympathetic
effusion may occur.

Clinical features

History
Haematogenous Spread Acute osteomyelitis has an insidious onset. Direct spread Osteomyelitis
is more localized with prominent symptoms.
The patient will complain of:

o Abrupt onset of high fever (fever is present in only 50% of neonates with
osteomyelitis)
o Irritability

42
 o Malaise
o Restriction of movement (pseudoparalysis of limb in neonates)
o Local swelling, redness and tenderness
o Fatigue

NB. If haemategenous spread is suspected inquire about:

o Recent infection?
o Chronic Illness e.g. Sickle cell, Diabetes?
o Recent trauma?

Special care must be taken with neonates. They may present with a history of stopped feeding,
irritable, vomiting, high or low temperatures as well as pseudo-paralysis.

Physical examination

 Fever (present in only 50% of neonates)

 Edema
 Warmth
 Fluctuance
 Tenderness to palpation
 Reduction in the use of the extremity (eg, reluctance to ambulate, if the lower extremity
is involved or pseudoparalysis of limb in neonates)
 Sinus tract drainage (usually a late finding or one that occurs with chronic infection)
 Distant focus or local soft tissue focus may be evident

Sites Involved: Femur (30%), Tibia (30%), Humerus (10%), Fibula (5%), Calcaneal infections
are usually associated with puncture wounds especially in diabetics .Vertebral Disease
uncommon in adults and rare in children. Intravenous drug users usually have unusual foci such
as ribs, clavicle and pubis.

Differential Diagnosis
i. Rheumatic fever
ii. Septic arthritis- decreased joint movement and joint pain
43
iii. Scurvy
iv. Syphilitic metaphysitis
v. Bone tumour- differential diagnosis for Brodie’s abscess

Investigations

1. Complete Blood Count: White blood cells usually elevated but frequently are normal. A
leftward shift may be observed with increased polymorph nuclear cells.
2. C Reactive Protein : usually elevated and more specific, more useful than ESR
3. Erythrocyte Sedimentation Rate: Elevated in 90% but non specific.
4. Culture/Aspirate findings may be negative in 25% of cases.
5. Blood Cultures Positive in 50 – 75 % of cases.
6. WBC and WBC differential
There is a decrease in packed cell volume and haemoglobin in acute osteomyelitis. White
cell count and differential reveal a marked leucocytosis, and neutrophilia (bacterial infection).
Both the ESR and CRP levels will be elevated. C-reactive protein is however a better index of
infection as it is more sensitive than the ESR. CRP falls more quickly and is therefore a better
prognostic marker and, is useful for assessing response to treatment. The ESR however remains
elevated for longer periods despite adequate treatment. Blood cultures may help to isolate and
identify the causative microorganism. A bone marrow or subperiosteal aspirate should also be
performed and the sample sent for gram stain, culture and sensitivity.

Imaging

X ray:

Suggested initially by soft tissue damage 3-5 days after infection. Bony changes are not evident
until 14 – 21 days after initial infection and are usually evidenced by periosteal reaction followed
by cortical or medullary lucencies. By 28 days approximately 90% of patients show some
change. The plain X-ray also helps to rule out Ewing’s sarcoma as a differential diagnosis.

44
 Plain X-ray and Bone scan of patient with Osteomyelitis

Ultrasonography

Can show some evidence 2-5 days after infection. Features evident include: soft tissue swelling,
fluid collection and periosteal reaction. It can also be used to guide aspiration. It does not allow
for evaluation of the bony cortex.

CT scan

Useful in evaluation of spinal vertebrae lesions. It may also be superior in areas of complex
anatomy such as the pelvis.

MRI

Effective in early detection of osteomyelitis. Found to be more superior to X rays or CT scan but
is expensive.

45
Diagnosis requires 2 of the 4 following criteria:

o Purulent material on aspiration of affected bone

o Positive findings on bone tissue or blood culture
o Localized classic physical findings of bony tenderness, with overlying soft-tissue
erythema or edema, fever
o Positive radiological imaging study

Treatment
o Intravenous Antibiotics should be selected to cover gram-positive and gram-negative
organisms until results are available.
o Treatment is required parenterally: 4 to 6 weeks
o The following are recommendations for the initiation of empiric antibiotic treatment
based on the age of the patient and mechanism of infection:
 With hematogenous osteomyelitis (newborn to adult): the infection agents
include Staph. aureus, Enterobacter species, group A and B Streptococcus
species, and H influenzae.
 Primary treatment includes a combination of penicillinase-resistant
synthetic penicillin and a 3rd generation cephalosporin.
 Alternate therapy- vancomycin or clindamycin and a 3rd generation
cephalosporin
 For adults, in addition to those mentioned above, ciprofloxacillin
and rifampin may be an appropriate combination therapy.
 If there is evidence of infection with gram-negative bacilli, include
a 3rd generation cephalosporin
 In patients with sickle cell anemia and OM, the primary bacterial causes are
Staph. aureus and Salmonellae species.
 Primary choice for Tx- fluoroquinolone (ototoxic)(not in children).
 Alternative choice- 3rd generation cephalosporin, e.g. ceftriaxone
 When a nail puncture occurs through an athletic shoe, the infecting agents
may include Staph. aureus and Pseudomonas aeruginosa.
 Primary antibiotics- ceftazidime or cefepime
 Alternative Tx- ciprofloxacin
46
  For patients with OM due to trauma, the infecting agents include Staph.
aureus, coliform bacilli, and Pseudomonas aeruginosa.
 Primary Tx- naficillin and ciprofloxacin
 Alternative- vancomycin and 3rd generation cephalosporin with
antipseudomonal activity.

Surgical Intervention
If response is sub optimal or if large areas of bone destruction exist, surgical debridement of
necrotic tissue is needed.
Surgery might be needed to drain a paravertebral or epidural abscess or to stabilize the spine to
prevent injury.
Surgical debridement of necrotic tissue plus antibiotics with broad coverage is required.
Skin or pedicle grafts may be needed to close large surgical defects, and antibiotic Treatment
should be continued for >3wk after debridement.

Complications
1. Chronic osteomyelitis- this is the number one complication. Secondary delay in diagnosis
attenuated antibiotic treatment and inadequate surgical debridement increase the risk for
the complication.
2. Septic arthritis
3. Brodie’s abscess- small intraosseous abscess that frequently involves cortex and is walled
off by reactive bone. Develops when antibiotics impair bacterial growth but don’t
eradicate them so, immune system walls off theses organisms by creating circumscribed
sclerosed area.
4. Sclerosing osteomyelitis of Gatre- rare, typically in jaw
5. Pathological fractures
6. Soft tissue infection
7. Disseminated infection – sepsis
8. Damage to growth plate
9. Loss of limb
10. Subacute osteomyelitis- bacteria escape from walled off abscess causing reinfection

47
Acute Management of Spinal Injuries

Spinal injuries may be the result of a motor vehicle accident, gunshot wound, domestic
and industrial accidents or sporting incidents. Acute spinal cord injury (SCI) is due to a traumatic
injury that either results in a bruise (also called a contusion), a partial tear, or a complete tear
(called a transection) in the spinal cord. All multi-trauma patients should be assumed to have
sustained spinal injuries until it can be proven otherwise. The essentials of securing the airway,
allowing for proper ventilation and ensuring proper haemodynamic stability is to be done with
little or no unnecessary movements of patients spine. Once these parameters have been
established the attention must be made to immobilization of the entire spinal column at the
accident site until a major axial injury has been ruled out. As far as possible, multiple evaluations
should be performed by the same examiner, so that any evolving neurologic deficits can be
detected in a timely fashion.

Acute Management
Acute management of the spinal injury begins with general management of trauma dictated by
the ATLS protocol.
1. Primary Survey
i. Airway
ii. Breathing
iii. Circulation and cervical spine
iv. Disability
v. Exposure

Ensure the patient has a patent airway. Assess breathing by looking, listening and feeling
for breath sounds. Ensure the patient has adequate perfusion of tissues by assessing peripheral
pluses for example the carotid and radial pluses.

A cervical collar should be placed to immobilize the neck , especially in conscious

patients with a history of trauma to the head, neck, or back who report any neurological
symptoms, even if transient. Complete head and neck immobilization on a spine board should
also be performed until appropriate evaluation can be conducted. This is done to prevent
48
movement and exacerbation of the spinal injury. The trunk should be straightened and any
rotation corrected. During lifting and turning the whole spine should be maintained in the neutral
position. This is achieved by log rolling the patient and may require more than one person.
Transfer to the hospital should be done as soon as possible. Special care needs to be taken during
transport to the hospital, to ensure that the patient does not move.

Log rolling

2. Secondary Survey – A.M.P.L.E History

i. Associated illness
ii. Mechanism of injury
iii. Past Medical History
iv. Last Meal
v. Events Surrounding Injury

A detailed history including the mechanism of injury, localization of any neck or back
pain, numbness, tingling, weakness, ability to pass urine, should be elicited. Spinal injury should
be strongly suspected in any major accident, fall from an appreciable height, facial or head
injury. For the unconscious patient, the clinician should have a high index of suspicion of spinal
49
cord injury and their spines must be adequately immobilized, following the steps mentioned
above. The conscious patient should be placed supine while the unconscious patient should be
placed in the lateral position.

Advanced Trauma Life Support (ATLS) is a training program for doctors and Advanced
Practice/Critical Care Paramedics in the management of acute trauma cases, developed by
the American College of Surgeonss
Primary Survey

The first and key part of the assessment of patients presenting with trauma is called the primary survey.
During this time, life-threatening injuries are identified and simultaneously resuscitation is begun. A simple
mnemonic, ABCDE, is used as a memory aid for the order in which problems should be addressed.

A Airway

B Breathing

C Circulation

D Disabilities

E Expose/Environment

A - Airway Maintenance with Cervical Spine Protection

The first stage of the primary survey is to assess the airway. If the patient is able to talk, the airway is
likely to be clear. If the patient is unconscious, he/she may not be able to maintain his/her own airway.
The airway can be opened using a chin lift or jaw thrust. Airway adjuncts may be required. If the airway is
blocked (e.g, by blood or vomit), the fluid must be cleaned out of the patient's mouth by the help of
sucking instruments. in case of obstruction pass endotrachial tube.
B - Breathing and Ventilation

The chest must be examined by inspection, palpation, percussion and auscultation. Subcutaneous
emphysema and tracheal deviation must be identified if present. Life-threatening chest injuries,
including tension pneumothorax, open pneumothorax, flail chest and massive haemothorax must be
identified and rapidly treated. Flail chest, penetrating injuries and bruising can be recognised by
inspection.
C - Circulation with Hemorrhage Control

Hemorrhage is the predominant cause of preventable post-injury deaths. Hypovolemic shock is caused
by significant blood loss. Two large-bore intravenous lines are established and crystalloid solution given.
If the patient does not respond to this, type-specific blood, or O-negative if this is not available, should be

50
given. External bleeding is controlled by direct pressure. Occult blood loss may be into the chest,
abdomen, pelvis or from the long bones.
D - Disability (Neurologic Evaluation)

During the primary survey a basic neurological assessment is made, known by the mnenomic AVPU
(alert, verbal stimuli response, painful stimuli response, or unresponsive). A more detailed and rapid
neurological evaluation is performed at the end of the primary survey. This establishes the patient's level
of consciousness, pupil size and reaction, lateralizing signs, and spinal cord injury level.

The Glasgow Coma Scale is a quick method to determine the level of consciousness, and is predictive of
patient outcome. If not done in the primary survey, it should be performed as part of the more detailed
neurologic examination in the secondary survey. An altered level of consciousness indicates the need for
immediate reevaluation of the patient's oxygenation, ventilation, and perfusion status. Hypoglycemia and
drugs, including alcohol, may influence the level of consciousness. If these are excluded, changes in the
level of consciousness should be considered to be due to traumatic brain injury until proven otherwise.
E - Exposure / Environmental control

The patient should be completely undressed, usually by cutting off the garments. It is imperative to cover
the patient with warm blankets to prevent hypothermia in the emergency department. Intravenous fluids
should be warmed and a warm environment maintained. Patient privacy should be maintained.
Secondary Survey

When the primary survey is completed, resuscitation efforts are well established, and the vital signs are
normalizing, the secondary survey can begin.

The secondary survey is a head-to-toe evaluation of the trauma patient, including a complete history and
physical examination, including the reassessment of all vital signs. Each region of the body must be fully
examined. X-rays indicated by examination are obtained.

If at any time during the secondary survey the patient deteriorates, another primary survey is carried out
as a potential life threat may be present.

The person should be removed from the hard spine board and placed on a firm mattress as soon as
reasonably feasible as the spine board can rapidly cause skin breakdown and pain while a firm mattress
provides equivalent stability for potential spinal fractures.[

Examination
Log roll, looking for bruising on the back, palpate for a step, note any tenderness. A
thorough neurological examination should be performed as soon as possible. Examination
should include a complete assessment of motor, sensory, and reflex functions for both the
upper and lower extremities. Thereafter, thorough overall examination of cardiovascular,
respiratory, abdominal and musculoskeletal systems should be performed.
51
 Neurological assessment

Aims of neurological assessment include:

1. To determine the level of the lesion- counted as the lowest level at which neurological
function is intact bilaterally
2. To determine whether damage is complete or incomplete
3. To determine prognosis

It may be difficult until period of spinal shock (flaccidity, areflexia) is over (24-48 hrs after
injury).

Parameters to be assessed include:

 Tone
 Power
 Reflexes
 Sensation
 Cranial nerve function

Power

 Power of muscle groups (corticospinal tract)

C3-4-5
Diaphragm

Shrugging shoulders C4
Flex elbows C5,6
Extend elbows C7
Abduct fingers C8
Active chest expansion T1-T12
Hip flexion L2
Knee extension L3-4
Ankle dorsiflexion L5-S1
Ankle plantar flexion S1-S2
Eversion of foot L5
Inversion of foot L4

52
 MRC Power Grading
0 No active contraction

1 Visible contraction without movement

2 Movement with gravity eliminated

3 Movement against gravity
4 Movement against resistance but weak

5 Normal power

Reflexes

C5-6
Biceps

Triceps C6-7

Supinator C5-6

Knee jerk L3-4

Ankle jerk L5-S1

Plantar response If upgoing = UMN lesion

Babinski sign
Abdominal - If lost = UMN lesion
cutaneous reflexes
Digital rectal S 2, 3, 4
examination
Bulbo cavernosis Pull penis, causes anal sphincter
reflex tightening
If returned, period of spinal shock is
over

53
Sensation

 Sensation to pinprick (spinothalamic tracts)

 Sensation to fine touch, position and vibration (posterior column)
Neurological examination should be repeated to determine to progression or resolution of any
neurological deficits if present.

Radiological investigations

 X-rays- Cervical spine: AP, Lateral including C7/T1, open mouth view of odontoid.
Swimmers view or pull arms down. AP and lateral view of other tender areas of spine
 CT scan - shows bony injury
 MRI scan - shows soft tissue involvement

Definitive Management
The aims of definitive management are to preserve neurological function, relieve reversible
nerve or cord compression, stabilize the spine and rehabilitate the patient.

In the absence of neurological deficit:

 If stable spinal injury- pain relief, collar or brace.

 If unstable injury- reduce and hold secure until bone heals with Open Reduction internal
fixation or traction in tongs, halo vest

With complete sensory and motor loss:

 Usually an unstable injury

 Only consider conservative management for high thoracic injuries
 Early operative stabilization- to help with nursing, prevent spinal deformity and pain.
Speeds up rehabilitation

With Incomplete neurological loss:

 Stable injury- conservative bed rest, brace.

 Unstable injury- early reduction and stabilization.

54
Special features of Spinal Injuries
Incomplete injuries may show selective involvement of part of the cord.
Central cord syndrome: usually follows hyperextension injury in an elderly patient. Damage, to
the middle of the cord, results in paralysis. This predominantly affects the arms and hands.
Anterior cord syndrome: the front of the cord is damaged with paralysis and loss of pain
sensation but there is preservation of touch and joint position sense throughout the posterior
column of the spinal cord. The lesion results due to ischaemia of the cord due to loss of blood
supply from the anterior spinal artery.
Brown-Sequard Syndrome: comprises injury predominantly to one side of the spinal cord
causing motor loss on that side and pain and temperature loss on the opposite side.
Neurogenic Shock: the term generally used to describe the hypotension and bradycardia
associated with cervical or high thoracic spinal cord injury resulting in impairment of the
descending pathways.
Treatment: Elevate the patient’s legs to improve blood pressure. Atropine may be used to
counteract bradycardia. Atropine increases firing of the sinoatrial node (SA) and conduction through the atrioventricular
node (AV) of the heart, opposes the actions of the vagus nerve, blocks acetylcholine receptor sites, and
decreases bronchial secretions.

Autonomic Hyper reflexia: a medical emergency occurs as a result of a reflex action of the
autonomic nervous system due to stimulus, such as a distended bladder, faecal impaction,
precipitating a hypertensive episode that requires immediate treatment

Spinal Shock:
In any case of spinal cord injury, the risk of spinal shock is high. Spinal shock is a
phenomenon affecting the injured spinal cord where there is complete temporary loss of all
spinal activity distal to the level of cord injury, with a concomitant loss of bowel and bladder
function. At this time it is not possible to decide whether the spinal cord injury is a total
transection of the cord or a partial spinal injury. The hallmark of spinal shock is the absence of
the spinal reflexes, the bulbocavernosus reflex, which involves reflex tightening of the internal
anal sphincter around an inserted gloved finger in response to a squeeze of the glans penis,
clitoris or tug on a Foley catheter if the patient is catherterised. Also the anal reflex – where
pinprick in the perianal region elicits contraction of the external anal sphincter. Spinal shock
rarely last longer than 24-48 hrs, and it ends with the return of the bulbocavernosus reflex and
the anal reflex. If there is no resolution of sensory or motor function below the level of the lesion

55
in the presence of these reflexes, the patient will be diagnosed as having a complete transection
of the spinal cord. The longer the duration of spinal shock the worse the prognosis for recovery.

Initial Management
 Analgesic
 Oxygen therapy
 Nasogastric tube – due to a paralytic ileus in trauma patients
 Foley Catheter
 Nil Per oral
 Intravenous H2 antagonist – to prevent stress ulcers (Cushing’s ulcers)
 I.V. Fluids – especially in the case of hemorrhage. Low blood pressure in the setting of
acute spinal cord injury may represent internal hemorrhage or spinal shock. Spinal shock
results from loss of sympathetic control over the vasculature. This is identified as low
blood pressure without tachycardia. Whereas internal hemorrhage results in low blood
pressure with tachycardia
 Reduction of the Spine – done in an attempt to stabilize the spine and prevent
redisplacement. It is best done by skull traction under radiographic supervision,
where traction is applied through the use of skull calipers, the tips of which lies in
small holes placed through the outer table of the skull, where it is engaged in a pulley
system to which weights are added. It is important to monitor the patient’s
neurological function while in traction. An alternative form of reduction, once there is
no paraplegia, is the halo-thoracic support.
 Steroids – this is controversial. Methylprednisone has been shown to be of little
benefit. It reduces oedema and inflammation, and prevents cell degeneration. It is not
indicated when the patient’s spinal cord injuries are due to gunshot injuries.

56
Glasgow Coma Scale
Elements of the scale

Glasgow Coma Scale

1 2 3 4 5 6

Does not Opens eyes in response to Opens eyes in response Opens eyes
Eyes N/A N/A
open eyes painful stimuli to voice spontaneously

Oriented,
Makes no Utters inappropriate Confused,
Verbal Incomprehensible sounds converses N/A
sounds words disoriented
normally

Abnormal flexion to
Makes no Extension to painful stimuli Flexion / Withdrawal Localizes Obeys
Motor painful stimuli
movements (decerebrate response) to painful stimuli painful stimuli commands
(decorticate response)

The scale comprises three tests: eye, verbal and motor responses. The three values separately as well as their sum are considered.

The lowest possible GCS (the sum) is 3 (deep coma or death), while the highest is 15 (fully awake person).
Best eye response (E)

There are 4 grades starting with the most severe:

1. No eye opening

2. Eye opening in response to pain. (Patient responds to pressure on the patient’s fingernail bed; if this does not elicit a

response,supraorbital and sternal pressure or rub may be used.)

3. Eye opening to speech. (Not to be confused with an awaking of a sleeping person; such patients receive a score of 4, not

3.)

4. Eyes opening spontaneously

Best verbal response (V)

There are 5 grades starting with the most severe:

1. No verbal response

2. Incomprehensible sounds. (Moaning but no words.)

3. Inappropriate words. (Random or exclamatory articulated speech, but no conversational exchange)

4. Confused. (The patient responds to questions coherently but there is some disorientation and confusion.)

5. Oriented. (Patient responds coherently and appropriately to questions such as the patient’s name and age, where they

are and why, the year, month, etc.)

Best motor response (M)

There are 6 grades starting with the most severe:

57
 1. No motor response

2. Extension to pain (abduction of arm, internal rotation of shoulder, pronation of forearm, extension of wrist, decerebrate

response)

3. Abnormal flexion to pain (adduction of arm, internal rotation of shoulder, pronation of forearm, flexion of wrist, decorticate

response)

4. Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when supra-orbital pressure applied ;

pulls part of body away when nailbed pinched)

5. Localizes to pain. (Purposeful movements towards painful stimuli; e.g., hand crosses mid-line and gets

above clavicle when supra-orbital pressure applied.)

6. Obeys commands. (The patient does simple things as asked.)

Interpretation

Individual elements as well as the sum of the score are important. Hence, the score is expressed in the form "GCS 9 = E2 V4 M3 at

07:35".

Generally, brain injury is classified as:

 Severe, with GCS ≤ 8

 Moderate, GCS 9 - 12

 Minor, GCS ≥ 13.

Management of the Paraplegic

Paraplegia is defined as a loss or impairment of motor, sensory or both functions of the

lower part of the body including the legs due to a lesion in the neuromuscular system. It occurs
in patients with any spinal cord transection, tumour compression. High cervical transections may
also involve the upper limbs causing quadriplegia. Paraplegic patients are unable to move their
legs. They have no higher control (cerebral) over anything below the transection.
The spinal cord has no power of recovery after complete transection. Incomplete cord
lesions have a remarkable degree of recovery despite initial paralysis. Recovery may continue
for several months, but the earlier and more rapidly it begins, the better the prognosis. The cauda
equina, unlike the rest of the spinal cord, behaves like peripheral nerves in that they are able to
recover or regenerate provided their sheaths remain intact and in continuity. Damage to the
spinal cord or cauda equine complicates between 10 and 20% of all spinal injuries. Most of the
injuries occur in a younger 16-30 year age group, with an increasing incidence due to motor

58
vehicle accidents. An increasing number result from sporting accidents, particularly affecting
the cervical spine, which is now affected as frequently as injuries to the thoraco-lumbar region.
The immediate consequence of division of the cord is total suppression of function in the
segments below the lesion (spinal shock). The initial paralysis is flaccid, there is complete
sensory loss and the visceral reflexes are suppressed. This stage of spinal shock rarely lasts for
more than 48 hours. As it gradually passes off, the paralysis becomes spastic instead of flaccid,
and there is a return of exaggerated tendon and visceral reflexes unmodified by higher control.
The end of this stage of spinal shock is signaled by the return of the bulbocavernosus reflex
(which involves the S1, S2 and S3 nerve roots) is easily assessed and has important prognostic
significance. The return of this reflex activity, without recovery of sensibility or voluntary motor
power below the lesion, is diagnostic of complete transection of the spinal cord. Incomplete
spinal cord lesions are indicated by the preservation of sacral sensation or reflexes in the S4 and
S5 segments.
The only certain sign of continuity of axons in the spinal cord is the preservation or early
return of voluntary motor power and sensibility below the level of the lesion (incomplete
transection of the cord). In severe cauda equina injury the paralysis remains flaccid throughout.
The tendon and visceral reflexes are abolished below the lesion and do not return unless the
nerve fibres recover their function.
The exact diagnosis of paraplegia will become obvious any time between three days to three
weeks. The aim of the early treatment is to prevent bedsores and urinary sepsis as they are
the commonest cause of death. The next step is the rehabilitation of the paraplegic to enable
him or her to lead an independent life.

Complications of immobility
CNS – depression, dementia in the elderly
RS – atelectasis, URTI
GI – stress ulcers (cushings ulcers), constipation
CVS – DVT , PE, thrombophlebitis
GU – stones, UTI
Musculoskeletal – disuse atrophy, disuse osteopaenia, joint stiffness
Skin - decubitous ulcers, dry skin

59
The management of the paraplegic should therefore include the following. :

1. General care
2. Prevention of DVTs
3. Skin care
4. Management of Autonomic dysreflexia
5. Bladder care
6. Bowel care
7. Psychological care
8. Physiotherapy
9. Rehabilitation
10. Occupational therapy

General care
The general treatment is important as these patients in the early stages of their illness are
not capable of taking care of themselves. Nutrition support is important so as to prevent a
negative nitrogen balance and anaemia. A high protein diet and nutritional supplements to
prevent anaemia will increase the patient's resistance.

Prevention of Deep Vein Thrombosis

Paraplegics are prone to formation of DVT’s because they are bed ridden for prolonged
periods and this is further complicated by an accompanying hypercoagulable state. DVT
formation is a very important consideration when dealing with the management of the
paraplegic. DVT formation can be prevented by administering prophylactic treatment, in the
form of heparin, 5000 units SC bid. It can also be prevented, by passive movement during
physiotherapy, use of compression stockings and treatment of any hypercoagulable state and
adequate hydration.

Skin care
Normally pressure necrosis in hospitalized patients initiates after 2 hours. Due to loss of
sensation the skin is particularly prone to developing decubitus ulcers. Interventions aimed at
preventing these include:

60
 - Routinely turning the patient every 1 – 2 hours
- Padding regions prone to pressure sores: heel, sacrum, scapula, elbows, occiput.
- Massage to increase blood circulation and ensuring that the patient is dried, i.e. not lying
in urine or feces for too long
- Ripple Mattresses
- Daily search for signs of ischaemia. The patient must be taught self examination with
mirrors
- Escharectomy and debridement for existing wounds
- Making sure patient not lying in potentially harmful bodily waste

Musculoskeletal
At risk for muscle atrophy and joint stiffness due to disuse .Mainstay of overcoming this:
- Mainly physiotherapy with gentle passive joint exercises
- Spasticity may not improve with physiotherapy so pharmacological therapy may be
necessary eg Presynaptic Neurotransmitter Inhibitor.

Bladder Care
Stage of Spinal Shock
During the stage of spinal shock, there is retention of urine and as the paralyzed bladder
distends, there is overflow of urine from the distended bladder. The bladder acts as a denervated
organ and is unable to empty. The reflex centre for the bladder is at S2-S3 level in the cord and
this is controlled by the inhibiting influence of the higher centers in the cerebral cortex.

Automatic Neurogenic Bladder - (Upper Motor Neuron Bladder)

This is the type of neurogenic bladder occurring after complete transection of the cord
above S2 level. The reflex centers takes over the control of the bladder.
The reflex arc runs from the bladder to the sacral cord, synapses and runs back to the
bladder. The bladder becomes an organ controlled by a simple reflex. When the bladder is
distended with urine the patient involuntarily empties the bladder by the reflex activity. The
stimulus is either intrinsic from the bladder wall or extrinsic stimuli that provokes mass
movement. The patients have no real sensation of vesicle filling but the increasing size of the
bladder as the urine accumulates, produces sensation in the abdomen that they may interpret as

61
fullness of the bladder. Urination occurs without warning as soon as the reflex is closed by
summation of afferent stimuli. There will be minimal residual urine. This is called cord or
automatic bladder. This may take 2-6 weeks to develop.

Lower Motor Neuron Bladder

This occurs in injuries at the S2 level or below i.e. at the conus and cauda equina. This
destroys the reflex centre with the afferents and efferents in the nerve roots. This isolates the
bladder, which then depends on the intrinsic plexus in the musculature of the bladder wall i.e.
detrusor ganglia. This bladder which resumes some function is called autonomous bladder or
atonic bladder. The emptying can be assisted by manual pressure or by trained contraction of the
abdominal musculature. Due to spasm of the internal sphincter, the residual urine is large (300-
400 cc).

Treatment
The aims of bladder management include:
1. Avoidance of bladder over distension
2. Prevention of urinary infection
3. Restoration of continence, by bladder training
During the first 24 hours of retention, there is no urgency to interfere. When the patient
complains of discomfort, avoiding over distension is essential. This is accomplished by
intermittent urethral catheterization or indwelling catheter passed under strict aseptic conditions.
When drainage is established, the following other measures are undertaken to prevent
ascending urinary infection and avoid calculi formation:
a) A liberal fluid intake of 2-3 litres a day
b) Prophylactic antibiotics
c) Daily bladder wash
Yearly renal scans are also encouraged, as renal problems are responsible for the largest
morbidity and mortality rates. The stasis of urine in the bladder may lead to an ascending
urinary tract infection, which is still a source of mortality amongst the paraplegics.

62
 Retraining the Bladder
The recovery of bladder function may take some 2-6 weeks. When there are signs of motor
and sensory recovery, retraining of the bladder must be undertaken. This is done by clamping the
catheter and encouraging reflex emptying of the bladder. When automatic bladder with reflex
emptying is established the catheter is removed.
In cases of autonomous bladder the patient is taught methods like surprapubic compression
and increasing abdominal pressure. (If there is evidence of bladder neck contracture surgical
measures like bladder neck resection may be necessary.)

Bowel Care
The patient is kept NPO in the early stages after injury. This is because during spinal shock they
develop an ileus. Feeding is started after the patient has passed flatus or stool. Due to immobility
calcium is mobilized from bone slowing gastrointestinal mobility. Complication is constipation
so patient will require:
- Laxatives
- Proper nutrition : green leafy vegetables
- Fleet enemas
Also prone to stress ulcers so require prophylaxis against these: proton pump inhibitors.
Care also includes fecal softening achieved by the use of suppositories. If faecal impaction
occurs, it may be evacuated manually (digital evacuation).

Psychological Care
The emotional shock and depression following the realization that he or she will not walk
again is a most important factor in the total clinical evaluation of the patient. The patient has to
be counseled and given hope. Without such an emotional stabilization, it is impossible to obtain
the patient's motivation and cooperation in the treatment measures adopted.

Physiotherapy
Is aimed at maximizing the function the patient has and gaining of independence. This is
done through muscle strengthening exercises (of upper body) maximizing any movement and

63
function of lower limbs. Physiotherapy also helps to prevent contractures and DVT through self-
massage exercises. Physiotherapy is also important in patients who have paralysis of accessory
respiratory muscles. Chest physiotherapy is important in prevention of atelectasis and
subsequent hypostatic pneumonia. Chest physiotherapy encourages deep breathing, proper
coughing where capable and the use of vibrators to clear secretions.

Rehabilitation
The rehabilitation of paraplegic patients is one of the greatest achievements of medical
science. These patients need physical, psychological and economic independence and social
integration. Medical rehabilitation should start right from the earliest stage of treatment.
As mentioned before, regulated system of exercises is adopted to develop the unparalysed
muscles of the body. By using the muscles of the shoulder girdle and upper extremities, the
patient is trained to shift himself from the bed to the wheel chair and back. The trunk muscles
can be used to swing the paralyzed legs. With long calipers for the legs and a pair of crutches the
patient can be taught to ambulate by what is called the 'Tripod' gait. Other devices which aid
mobilization include the wheelchair and special shoes.

Occupational Therapy
A resettlement of these patients in useful occupations will go a long way in the
psychological readjustment, and make them economically independent and socially acceptable.
This is done through vocational and occupational therapy. It is geared towards improving the
skills of the patient so that they might be able to form a part of the workforce.

64
Fractures around the Elbow in Children

When discussing fractures in children, in general, it must be remembered that fractures behave
differently in children and in adults. The most obvious difference between the bones of children
and those of adults is the presence in childhood of cartilaginous growth plates. Pediatric elbow
fractures are different from many other pediatric injuries. They are associated with a relatively
high rate of complications, and the results of non operative management are not always good.
The child's elbow is well vascularized, and therefore fracture healing takes place very quickly.
Such a narrow window of opportunity makes it imperative that the fracture be properly managed
very quickly.

Besides the presence of growth plates there are also other factors which increase the risk of
fractures around the elbow and other regions in the paediatric age group.
1. Increased resilience of bone accounting for the occurrence of greenstick fractures in
children
2. The periosteum is only attached loosely to the diaphysis and is easily stripped off
3. Common fracture sites in adults are not always so common in children and vice versa.
4. Healing of childhood fractures is generally faster than in adults
5. Similarly remodeling is very active and complete in early childhood
6. Of importance in the talking about elbow region fractures the presence of
ossification centres that decrease the structural strength.

Anatomy Overview
The elbow is a complex hinged joint consisting of three bony articulations involving the distal
humerus and the proximal ulna and radius .Of these bones there are six ossification centres/sites.

Ossification Sites and Dates

There are also ligamentous structures within the elbow which aid in maintaining stability.
Muscles and tendons also traverse the joint.

65
As a result of the presence of these ossification centres fractures around the elbow account for 10
% of all fractures in children.

Clinical features
History
Typically the child falls on an outstretched arm. There is acute pain and swelling.

Examination
Swelling (may be severe or mild) and tenderness is present over the fracture site. The condition
is often associated with a limited range of motion at the adjacent joints.

Careful evaluation of the distal neurovascular structures must be done, as it is for all fractures. A
compartment syndrome must also be ruled out.

Commonest sites, in order of decreasing frequency, includes:

1. Supracondyle- seldom seen in adults; risk of brachial arterial injury

2. Lateral condyle- capitulum
3. Medial epicondyle
4. Radial head
5. Olecranon (ulna)
6. Trochlear
7. Lateral epicondyle

Site of Ossification Ossification Date

Capitular centre 8months to 1year
Radial centre 4years
Medial epicondyle centre 6years
Trochlear centre 6years
Lateral epicondyle centre 9 to 11 years
Olecranon 9 to 11 years

66
Supracondylar Fractures
These are the most common fractures around the elbow region in children accounting for
approximately 60 – 80 % of them. This fracture occurs as the child falls on the outstretched arm,
with the elbow slightly flexed. The olecranon snaps into the olecranon fossa and the impact is
enough to fracture the growing area above the condyles.
It is seldom seen in adults.

Pathology
50% are greenstick fractures. The fracture line dissects the distal metaphysis of the humerus.
Displacement, when it occurs, is characteristic: the lower fragment is displaced backwards and
angulated backwards.

Treatment
Undisplaced fractures: plaster is applied for no more than 3 weeks.

Displaced fractures: manipulative reduction under anaesthesia is required. Anaesthesia is

provided using a Bier’s block and sedation/analgesia with diazepam and pethidine. The lower
fragment is brought back into position by longitudinal traction on the limb and direct pressure
behind the olecranon with the elbow flexed 90o or more. Perfect anatomical reposition is not
essential provided any lateral tilting of the lower fragment is corrected, because remodeling can
gradually efface a moderate displacement as the bone grows. After reduction the limb is
immobilized with a back slab with elbow flexed more acutely than 90 o.

Unstable fractures: internal fixation is recommended with 2 Kirshner wires pinned

percutaneously. The first wire is placed through the lateral condyle obliquely upward and
medially to engage the medial humeral cortex. The next wire is placed medial and passed
obliquely upwards and laterally via the medial epicondyle. The 2 wires cross just above the
olecranon fossa.
Monitor the condition of the circulation ensuring that it is being maintained in the limb and cut a
window in the plaster over the radial artery so that radial pulse can be palpated.
Radiographs are taken at 48hrs and after 1week to check that reduction has been maintained.
Unity should occur within about 3-4 weeks. If satisfactory reduction cannot be maintained then
skin traction can be applied or the fracture can be reduced with internal fixation.
67
Complications

 Brachial artery injury

 Injury to median nerve
 Deformity from mal-union e.g. cubitus varus
 Joint stiffness
 Compartment syndrome
 Myositis ossificans

Lateral Condyle Fractures

Fractures of the lateral condyle represent 15--17% of pediatric elbow fractures occurring more
commonly than the medial condyle. Most fractures occur in patients with a peak age 5-7 years
.The most common mechanism of injury occurs when a varus force is applied to the elbow in
falling on the outstretched hand , causing the extensor muscles and lateral collateral ligaments to
avulse the lateral condyle. Appropriate management requires an understanding of the mechanism
of injury, as well as an awareness of operative indications and treatment methods to avoid
complications.

Clinical Presentation
Radiological Imaging
The fracture usually extends obliquely upwards and laterally from the capitular surface.
Displacement is rarely severe, but even moderate displacement is important because the fracture
involves the joint surface and cartilage is not seen on radiographs.
Radiological findings may appear smaller than actual in young children with most of the
detached fragment being cartilaginous.

Treatment
Undisplaced fractures: immobilization in a plaster for a few weeks, followed by physiotherapy-
elbow exercises.

Displaced fractures: serious because they have the potential to cause permanent disability.
68
 o Closed reduction by manipulation is attempted under anaesthesia; if successful, then
immobilization in plaster with elbow at 90o until union occurs.
o Failure of closed reduction will result in ORIF- the fracture is exposed surgically and
reduced, and the condylar fragment is fixed in position by small screw (a Herbert dual-
pitch scaphoid screw may be used) driven from the lateral aspect of the detached
fragment obliquely into the expanded lower end of the humerus.

Complications

 Non-union: requires internal fixation

 Deformity: secondary to mal-union or physeal damage which retard growth.
o If the lateral condyle is affected the deformity will be that of cubitus valgus;
medial condyle affected cause cubitus varus.
Treatment if it is marked involves supracondylar osteotomy of the humerus.
 Frictional neuritis of the ulnar nerve: occurs in cubitus valgus in which the nerve is
angled behind the medial epicondyle resulting in ulnar paralysis.
Treatment involves transposition of the nerve from its post-epicondylar groove to in front
of the elbow.
 Osteoarthritis: occurs when a condylar fracture leaves permanent deformity or
irregularity of the articular surface.

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Epicondyle Fractures
Whereas most condylar fractures affect the lateral side, epicondylar fractures usually affect the
medial.

 More often in children than in adults.

 Caused by direct violence or avulsion injury (more common) in which the
epicondyle is pulled off by the attached flexor muscles during a fall and is
usually associated with dislocation or momentary subluxation of the
elbow.

70
Treatment

Uncomplicated fractures: only symptomatic treatment is required.

Slight displacement: immobilize in plaster for 3 weeks to relieve pain then restore joint
movement by active exercises.

Severe displacement: with medial instability of the elbow joint Open Reduction Internal
Fixation is required.

Complications

1) Inclusion of the medial epicondylar fragment in the elbow joint.

Occurs when the separated fragment of the medial epicondyle is ‘sucked’ into the joint
cavity and may become jammed between the joint surfaces. It is not completely loose
and free within the joint; it retains its attachment to the forearm flexor muscles.

Treatment: The fragment must be removed from the joint. Under anaesthesia the wrist
and fingers are extended fully to put the flexor muscles on the stretch, while the joint is
widened at the medial side by abduction of the forearm and the negative pressure within
the joint released by the insertion of a hollow needle.
If this manoeuvre fails, surgery is required.

2) Injury to the ulnar nerve: may occur immediately with displaced fractures or later
because of friction upon a roughened groove.

Treatment: transpose ulnar nerve from its groove behind the medial epicondyle to a new
bed in the soft tissues at the front of the elbow.

Monteggia Fractures
Monteggia fractures in children are easily manageable if recognized and treated soon after injury.
Only about 1% of all forearm fractures in children are classified as Monteggia fractures.

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Consists of a combination of fracture of the upper half of the ulna and radial head dislocation.
The displacement is anteriorly.

Treatment
Manipulation and Reduction with full supination of the forearm. Immobilise in plaster for ~ 12
weeks.
Surgically: If reduction fails or there is redisplacement reduction and internal fixation of the ulna
along with replacement of radius.

Proximal Radius Fracture

Proximal radius fractures in children, unlike those in adults, generally involve the metaphysis or
the physis, and not the radial head. These injuries occur most commonly between ages 8 and 12
and result from a fall onto an outstretched hand with a valgus moment directed through the
radius.

Treatment

The goal of treatment is to restore the ability to supinate and pronate, usually about 60° in either
direction.

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Olecranon Fractures
Fracture of the olecranon process is not a very common fracture, and usually comes about by a
fall unto a point on the elbow. It usually occurs in adults. The treatment depends on the type of
fracture:
 Crack fracture: The only treatment necessary is to immobilize the elbow with a light
plaster splint for 2-3 weeks.
 Clean fracture with separation: Operation is advised due to difficulty in gaining perfect
reduction by closed methods because the action of triceps will angulate and distract the
fragments. Rigid fixation is attained by a long coarse-threaded cancellous screw passed
down the bone from the upper surface of the olecranon, or by short stiff parallel wires
driven vertically across the fracture, combined with a tense figure-of -eight loop of wire.
73
  Comminuted fracture: Perfect fixation of the fragments is usually impractical, though it is
sometimes possible to achieve acceptable fixation by the use of a contoured plate and
screws. More ferquently, the olecranon fragments are excised by dissecting them out
from the aponeurosis that forms the insertion of the triceps and sewing the triceps to the
stump of the ulna by strong sutures passed through small drill holes in the bone.

Complications
 Non-union
 Mal-union
 Osteoarthritis

Rheumatoid Arthritis

Pathological & Radiological Changes

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of undetermined etiology

involving primarily the synovial membranes and articular structures of multiple joints. The
disease is often progressive and results in pain, stiffness, and swelling of joints. In late stages
deformity and ankylosis develop. It is often associated with mild constitutional symptoms and
nearly always affects several joints at the same time (polyarthritis).

Incidence

 approx. 1% of the population worldwide

 female:male 4:1
 Any age, peak time of presentation: 35-45 years
 Associated with genetic factors- HLA-DR4 or HLA-DR1: class II MHC genes

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Aetiology

 Cause unknown
 2 possible theories
1) Infective: possible by virus or mycoplasma or diphtheroid organisms- results
in release of antigen type II collagen factors from the patient’s on articular
cartilage initiating an autoimmune response.
2) Autoimmune: no doubt that it plays a major role in the progression but not
clear to whether it is the initial cause.
The classic rheumatoid factor is IgM antiglobulin- divided the disease into
seropositive and seronegative.

Pathological Changes

In the normal joints, the synovium is a thin delicate lining which is a source of nutrients for the
avascular cartilage. The synovial cells synthesizes lubricants e.g. hyaluronic acid and collagens
and fibronectin that form the framework of the synovial interstitium.

The earliest changes are swelling and congestion of the synovial membrane and the underlying
connective tissues, followed by hyperplasia, and then pannus (a sheet of inflammatory granulation tissue that

spreads from the synovial membrane and invades the joint in rheumatoid arthritis ultimately leading to fibrous ankylosis) formation. This is
then responsible for the cartilage, bone, ligament, and tendon destrution.
The synovial membrane becomes infiltrated with lymphocytes (esp. CD4 T-cells), plasma cells,
and macophages. This arises by activation of helper T cells responding to some arthritogenic
agent, possibly a microbe. Activated CD4+ cells produce a number of cytokines that have 2
principal effects: 1) activation of macrophages and other cells in the joint space, which release
tissue-destructive enzymes and other factors that perpetuate inflammation; and 2) activation of B
cells, proliferating and some differentiate into antibody-secreting cells, which some are directed
against self-constituents. The resultant autoimmune reactions damage the joints and are believed
to play an important role in disease progression.
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Cytokines such as IL-1, IL-6, CSF-1 and TNF alpha are released by macrophages and
fibroblasts. These cause proliferation of the cells of the synovium, increase prostaglandin
production, increase matrix degrading protease activity and are responsible for fever and bone
resorption.

Due to cellular proliferation and increased surface area of the synovium, inflammatory exudates
lead to the formation of a synovial effusion. This takes place during the active phases of the
disease. Initially, it contains predominantly lymphocytes, but after about 6 weeks, the cells are
mainly polymorphs with some rheumatoid arthritis cells (rhagocytes). These are leucocytes
containing cytoplasmic inclusions, which can be shown to contain IgM rheumatoid factor.

The synovium becomes thickened not only due to the cellular infiltration, but also due to tissue
hypertrophy. At the synovial cartilage junction, the proliferative synovium penetrates deep to the
cartilage, as well as spreading over the cartilage to form a pannus. The first lesion is the
characteristic angular erosion that results. The destruction is due to action of collagenase. The
early stages of angular erosions are not seen radiologically and so the pathological changes are
more advanced than the radiological ones.

The pathological changes are not confined to joints only; tendon and bone can be affected as
well. The synovitis can affect tendon sheath lining and this can result in impaired movement of
tendons due to mechanical impedance of following fibrosis and adhesions (and thus cause a
synovitis). This enlargement of synovial sheaths forms the characteristic dorsal sheath effusion
of RA. Also, infiltration of tendons can lead to rupture. Early inflammatory changes can also
affect bone by causing periarticular osteopenia and periosteal hyperaemia. Bone resorption,
however, depends on osteoclastic activity to remove calcium before collagenase can degrade the
collagen matrix, and both prostaglandins and cytokines released from T cells and macrophages
can stimulate osteoclastic activity.

After months or years of activity the disease process tends to become less active, usually leaving
a number of joints permanently damaged.

Other changes include: vasculitic, ophthalmic, pulmonary and cardiac lesions; skin - formation
of subcutaneous nodules, which are firm and non-tender and round to oval. They represent areas
76
of necrosis surrounded by numerous fibroblasts, lymphocytes, and plasma cells at pressure points
such as the elbow.

Key changes:
 Inflammation (acute and chronic) and hyperplasia of synovium
 Destruction of articular cartilage
 ‘Pannus’ of granulation tissue covering and destroying articular cartilage (caused by
cytokines derived from macrophages)
 Bony erosions (activation of osteoclasts)
 Fibrosis leading to fusion of joints (fibrous ankylosis)

Normal joint

Clinical Features

 Usually middle-aged female

 Onset - insidious
 Joint pain, stiffness, and symmetrical swelling of a number of peripheral joints e.g. hand,
wrists, feet, knees and elbows higher incidence than lumbar/thoracic spine, shoulders,
and hips.
 Pain and stiffness worse when activity is resumed after rest, e.g. when getting out of bed
in the mornings
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  Symptoms of anaemia, malaise, lethargy, may have a fever
 Progression features -
 Swam neck deformity of fingers
 Boutonniere deformity (fixed flexion of the proximal interphalangeal joint and
extension of the terminal interphalangeal joint)
 Z deformity of the thumb
 Rheumatoid nodules
 Wasting- muscle of the hands

Joints commonly affected in RA Clinical features of Rheumatoid arthritis

Examination

 Swollen joints
 Warmth
 Decrease range of movements and stiffness
 Movement causes pain

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NB: Do x-ray of C-spine - may have destruction of bone and ligaments despite minor
symptoms; may lead to subluxation hence the spinal cord is in jeopardy.

Radiological Features

Important in judging the course of RA and efficacy of treatment

Stages: I- Periarticular osteoporosis, periositis & soft tissue swelling

II- Uniform loss of articular cartilage (joint space)
III- Marginal erosions (“rat bite” erosions)
IV- Joint deformity including: subluxation, dislocation, articular bony destruction,
Bony ankylosis and complete destruction of the joint space.

At first there is no alteration from normal. Later there is diffuse rarefraction in areas of the joint.
Eventually destruction of joint cartilage may lead to narrowing of the cartilage space and in
severe cases to localized erosion of the bone ends. Radiologically revealed joint damage is a sign
of the irreversible results of chronic inflammation
The earliest radiographic changes more commonly occur in the hands and feet. In the hands the
earliest changes are seen at the MCP joints and PIP joints where marginal erosions can be
detected. Deformities such as ulnar deviation, boutonniere, swan neck and spindle digit are also
more closely examined on X-ray.

The earliest changes in the feet include osteoporosis of the MTP joints and erosive changes of
the metatarsals heads. The DIP joints are usually spared. Other radiologic features of the
rheumatoid foot include the lanois deformity, which involves the dorsal subluxation of the MIP
joints with fibular deviation of the digit, and hallux valgus.

Aside from plain X-ray, radioisotope bone scans, may be used to indicate increased uptake
around an inflamed joint due to increase blood flow. It doesn’t offer any great advantage over
plain X-ray in making a diagnosis and assessment of RA. CT scan and MRI can further delineate
what was described above; also MRI may be necessary to indicate any cord compression.

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NB: the rheumatoid process causes permanent damage to articular cartilage so secondary
osteoarthritic changes are superimposed at later stages.

Decrease joint space, rat bitten bone edges, peri-articular osteopaenia and some soft tissue swelling (inconsistent)

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 Radiograph of hands of patient with Rheumatoid arthritis

Important other investigations

 ESR, CRP- increase during active phase

 Latex fixation or Rose-Waaler test for rheumatoid factor
o Positive in about 80% of cases, negative in 20%

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Criteria for Diagnosis

 Morning stiffness (>1hr)

 Arthritis of three or more joint areas
 Arthritis of hand joints
 Symmetrical arthritis
 Rheumatoid nodules
 Rheumatoid factor
 Radiological change

NB: Diagnosis made on the presence of four or more criteria.

Other medical conditions that may give joint changes similar to RA and should be ruled
out, these include:

o Psoriasis
o Reiter’s syndrome (urethritis, arthritis, conjunctivitis and hyperkeratotic eruptions on the
skin)
o SLE
o Scleroderma - a chronic autoimmune disease characterized by fibrosis (or hardening), vascular alterations, and autoantibodies

These conditions are all seronegative for RF and may be associated with ankylosing
spondylitis (from Greek ankylos, bent; spondylos, vertebrae)

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Treatment

Unsatisfactory; no specific cure.

o Rest: evidence that continued use of joints activity with RA can lead to increased
pain, inflammation, muscle wasting and spasm, as well as increasing the severity of
constitutional symptoms; therefore, rest can be very beneficial in the active stage
o Drugs: two main aims-

 to alleviate the pain and swelling of joints, which is done by 1st line
drugs (analgesics) e.g. NSAIDs
 to modify the course of the disease with 2nd line drugs- e.g. Gold,
Penicillamine, anti-malarial drugs, Sulphasalazine,
immunosuppressive drugs e.g. Methotrexate and Azanthioprine
 3rd line drugs- steroids (oral corticosteroids) rarely used

o Intra-articular injections- corticosteroids useful in relieving the symptoms of pain and

swelling of joints involved in active phase.

o Physiotherapy: aim to maintain a range of motion in the joints, to minimize disuse

atrophy of muscle, deformity and excessive articular trauma and to provide local rest

Surgical management

 Synovectomy: a prophylactic and therapeutic measure- can reduce pain and improve
tendon function and prevent tendon rupture
 Osteotomy to correct deformity
 Arthroplasty- replacement of joint
 Arthrodesis- fusion of joint

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Rheumatoid Arthritis - Staging Scheme

Useful because it allows the pathological features to be correlated to the radiographic changes
and this allows a rational approach to treatment.

Stage 1: correlates with presentation of an antigen to T-cells and is an asymptomatic stage

Stage 2: there is T and B cell proliferation with anginogenesis in the synovial membrane. This is
associated with mild systemic symptoms and swelling of joints

Stage 3: associated with synovial cell proliferation and neutrophil accumulation with no cartilage
involvement. The symptoms are as for stage 2, but more severe and there may be rheumatoid
nodules. There are x-ray changes of soft tissue swelling.

Stage 4: characterized by polarization of synovitis into an invasive pannus, activation of

chondrocytes and enzyme degradation of the cartilage. This is characterized by x-ray evidence
of periarticular osteopenia.

Stage 5: there are erosions of subchondral bone with invasion of cartilage by pannus,
chondrocyte proliferation and stretched ligaments around the joints. This results in loss of
function and deformity and instability of joints, together with extra-articular manifestation. X-
rays show early erosions and narrowing of joint spaces.

NB: It is at stage 4 that there is irreversible cartilage damage and so treatment of RA should start
early to hopefully prevents this form from occurring.

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The Pathological and Radiological Changes In Osteoarthritis

Osteoarthritis (OA) is a degenerative disorder involving the articular surface of joints

accompanied by new growth of cartilage and bone at the joint margins (osteophytes) and
capsular fibrosis.It is by far the most common type of arthritis and is found more commonly in
middle aged women and elderly people 80- 90 % > 65 years affecting particularly the weight
bearing joints. Other characteristic features of osteoarthritis are softening and disintegration of
articular cartilage, with reactive phenomena such as vascular congestion and osteoblastic activity
in the subarticular bone. Osteoarthritis differs from simple wear and tear of joints in several
ways:
 It is not necessarily age related.
 It is asymmetrically distributed and often localized to only one part of the joint.
 It is more clearly related to impact loading than to frictional wear.
 It progresses steadily, often resulting in pain and dysfunction of the joint.
Osteoarthritis is not accompanied by any systemic illness, and although there are sometimes
signs of inflammation, it is not primarily an inflammatory disorder.

Historically, osteoarthritis has been divided into primary and secondary forms, although this
division is somewhat artificial.
In the broadest sense of the term, primary osteoarthritis is an idiopathic phenomenon, occurring
in previously intact joints, with no apparent initiating factor. Primary osteoarthritis is related to
the aging process and typically occurs in older individuals. Some clinicians limit primary
osteoarthritis to the joints of the hands (specifically the distal interphalangeal joints, proximal
interphalangeal joints, and joints at the base of the thumb), whereas others include the knees,
hips, spine (apophyseal articulations), and hands as potential sites of involvement. The term
primary or idiopathic osteoarthritis may become obsolete as underlying causes of osteoarthritis
are discovered. For instance, many investigators believe that most cases of primary osteoarthritis
of the hip may, in fact, be due to subtle or even unrecognizable congenital or developmental
defects.
Secondary osteoarthritis refers to degenerative disease of the synovial joints that results from
some predisposing condition, usually trauma that has adversely altered the articular cartilage and
or subchondral bone of the affected joints. Secondary osteoarthritis often occurs in relatively
young individuals.

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Some of the causes of secondary osteoarthritis are:

Causes of Secondary Osteoarthritis

Developmental Inflammatory
 Perthe's disease - The disease is characterized  Rheumatoid arthritis
by idiopathic avascular osteonecrosis of the capital
femoral epiphysis of the femoral head leading to an interruption of
 Septic arthritis
the blood supply of the head of the femur close to the hip joint. The
 Haemophilia
disease is typically found in young children, and it can lead to
osteoarthritis in adults
 Gout - It is caused by elevated levels of uric acid in
 Slipped upper femoral epiphysis the blood which crystallize and are deposited in joints, tendons,
and surrounding tissues. The metatarsal-phalangeal joint at the
 Developmental dysplasia of the hip base of the big toe is the most common affected, in around half of
all cases.

Traumatic Aseptic necrosis

 Intra-articular fracture  Corticosteroids
 Meniscectomy- rupturing of one or more of the  Sickle-cell disease
fibrocartilage strips in the knee called menisci
 SLE

Metabolic Neuropathic
 Haemochromatosis - iron overload  Diabetes mellitus
 Wilson's disease - copper accumulates in tissues  Peripheral nerve lesions
Endocrine Miscellaneous
 Acromegaly  Paget's disease
 Gaucher's disease

Pathophysiology
Normal articular cartilage is composed of:

1. Water 65 – 80 % wet weight responsible for nutrition and lubrication

2. Type II Collagen 90 % responsible for tensile strength
3. Proteoglycans 10 – 15 % responsible for compressive strength
4. Chondroitin Sulphate 4 & 6
5. Keratin sulphate

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With age there are changes in the composition of articular cartilage. There is an decrease in the
water content , collagen becomes disorderly and there is accompanying breakdown of the matrix
.In osteoarthritis as opposed to aging there is an increase in water content, collagen also becomes
disorderly with breakdown of the matrix .In the initial phase chondrocytes attempt to compensate
for the imbalance between breakdown and production .This may lead to an initial thickening of
the articular cartilage and enable the joint to maintain normal function for years.Eventually, the
arrangement and size of collagen fibers are altered and the proteoglycans begin to break down
faster than they can be synthesized. The decreased proteoglycan content and altered collagen
structure of the matrix result in a deterioration of the cartilage's normal physiologic properties.
As the cartilage softens, secondary damage to chondrocytes causes release of cell enzymes and
further matrix breakdown. Cartilage deformation may also add to the stress on the collagen
network, thus amplifying the changes in a cycle that leads to tissue breakdown.
As articular cartilage is responsible for absorbing, dissipating and distributing force, when
damaged, constant wear and tear causes some of this stress to be placed on the subchondral bone.
As the cartilage becomes eroded, fragments may break loose and float within the joint capsule.
These loose pieces of cartilage can damage the synovial lining of the joint and interfere with
proper joint function.
Progressive damage to the cartilage results in narrowing of the space between the two bones
(joint space) because areas of bone become denuded of cartilage. The underlying subchondral
bone may form a new articulating surface in the joint and become smooth and polished, like
marble. This is called eburnation.

With this there is formation of focal trabecular degeneration, subchondral cyst ( fluid-filled sac that extrudes from
the joint, consisting of thickened joint material) formation and reactive sclerosis in the area of most stress.

Remaining cartilage is capable of regenerating , repair and remodeling .Cartilage at the edge of
the joint revert to a more youthful form of growth and endochondral ossification giving rise to
osteophytes otherwise known as ‘spurs’.
Although osteoarthritis is thought of as being non inflammatory there is some element of
inflammation involved in the synovial fluid of the affected joint. The fragments of broken
cartilage released into the synovial fluid are phagocytosed by macrophages resulting in a chronic
low grade inflammation. This results in inflammation of the synovial membrane causing
thickening. This may be absent in early disease.

87
The synovium then acts as a source of cartilage degradation enzymes and cytokines such as IL 1,
IL 6 and TNF alpha. This also stimulates the chondrocytes to release more degrading enzymes.
The inflammation seen in osteoarthritis is however a mild form unlike in rheumatoid arthritis.

The pathological features are therefore:

 Thinning and loss of the articular cartilage due to progressive cartilage destruction.
 Loss of smooth surface of the articular cartilage
 Development of a smooth and polished surface of the exposed bone
(Eburnation).
 Bony thickening
 Formation of cystic spaces in the subchondral bone
 Ossification of outgrowths of cartilage – osteophytes or bony spurs
 Subchondral sclerosis (hardening ) of the underlying bone
 Capsular fibrosis

Pattern of Involvement
Knee – Assymetric
Hip – Superolateral
Hand – Distal Interphalangeal Joint more common.

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Clinical Features
Usually middle aged patient more commonly female complaining of:
Joint Pain aggravated by exertion and relieved by rest .With time relief by rest becomes less. At
a late stage pain felt while lying in bed.
Insidious onset and increases slowly over months to years
Stiffness in joint after periods of inactivity
Intermittent swelling suggesting an effusion or Continuous swelling suggestive of large
osteophytes.
Deformity
Decrease function : A limp , difficulty climbing stairs using the toilet or dressing .
Sleep Disturbance due to pain .

On Examination
Wasting of muscles surrounding the affected joint
Decreasing range of movement
Crepitus of joints
Increased warmth over the joint
Effusion in joint
Antalgic gait if lower limb involved

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Radiological Changes
X Ray
Uneven narrowing of the joint space (may cause a varus or valgus deformity)
Subchondral sclerosis
+/- Subchondral cyst
Marginating osteophytes
Joint deformity may be demonstrated in some cases
In the late stage, displacement of the joint is common and bone destruction may be severe.

This modality gives such reliable evidence that other radiological forms are not usually used.

Radionuclide scanning
Technetium-99 shows increased activity during the bone phase in the subchondral region of
affected joint; due to increased vascularity and new bone formation

Angiography
This can be used for demonstration of increase intra-osseous pressure due to marked vascularity
and venous congestion of the subchondral bone

Arthoscopy
This shows cartilage damage long before x-ray changes appear .

Treatment
90
Conservative
Weight Loss
Pain Relief : NSAIDS
Physical Therapy : Range of movement exercises
Intra articular steroid injection
Supportive Measures eg. External brace
Visco Supplementation
Chondroprotective Supplements : Chondroitin Sulphat and Glucosamine

Surgical
Indicated if conservative treatment is unsuccessful
Wash out of Synovial Fluid especially used in knee
Osteotomy
Arthrodesis – joint fusion
Arthroplasty – joint replacement
Orthoscopic debridement

Complications

Capsular herniation: OA of the knee is sometimes associated with a marked effusion and
herniation of the posterior capsule (Baker’s cyst)
Loose bodies: cartilage and bone fragments may give rise to loose bodies, resulting in episodes
of locking
Rotator cuff dysfunction: OA of the acromioclavicular joint may cause rotator cuff
impingement, tenditis, or cuff rupture
Spinal stenosis: long-standing hypertrophic OA of the lumbar apophyseal joints may give rise to
acquired spinal stenosis
Spondylolisthesis: in patients over 60 years of age, destructive OA of the apophyseal joints may
result in severe segmental instability and spondylolisthesis (degenerative spondyl. which almost
always occurs at L4, 5)

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Pathological and radiological changes in

Tuberculosis Arthritis
Tuberculosis arthritis is a joint infection with the tubercle bacillus (usually human type & rarely
bovine).

Aetiology and Pathogenesis

The infection is usually acquired form another patient with open pulmonary tuberculosis (i.e.
tuberculosis of the lung with cavitations). There may also be haematogenous spread of the
bacillus from a distant site to the joint. The infection may spread from an adjacent site via direct
extension.

Tuberculosis of bone is a relatively rare disease. Tuberculous arthritis in recent times is most
often seen in association with chronic immunosuppression (AIDS, organ transplantation) or in
chronic debilitation (weakening) (narcotic addicts, alcoholism).

The joints most frequently affected are the vertebral joints of the thoracic or lumbar spine,
followed next in frequency by the hip and knee. However, no joint is immune to Tuberculosis
infection.

Whatever the mechanism, the presence of the bacillus induces an inflammatory reaction on the
synovial membrane. There is a subsequent infiltration with macrophages, giant cells & other
inflammatory cells, and as a result if becomes thickened. The affected synovium grows as a
pannus (similar the rheumatoid arthritis) over the articular cartilage and subchondral bone,
destroying it, and eroding the bone along the joint margins. There is also slow formation of an
abscess (‘cold’ or chronic abscess) as opposed to florid abscess formation in pyogenic arthritis.
This abscess may spread to the skin surface forming a chronic tuberculous sinus.

 If the disease is arrested before the articular cartilage and bone have been damaged, then
function of the joint can be restored. Otherwise, permanent joint impairment ensues.

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Clinical features

Symptoms
- History of contact with TB infection
- Pain in the joint
- Swelling on the joint
- Decrease function of the joints

Signs
- Increased temperature around affected joint
- Restricted movements in all directions
- Sharp protective muscle spasm with forced movement
- Muscle wasting (disuse)
- Abscess or sinus over joint
- TB lesion elsewhere in the body

Investigations

Radiology
1. Plain X-Ray/MRI/CT Scan
- The earliest radiological feature is diffuse rarefraction ( become less dense) of the
bone and adjacent joint
- Joint narrowing
- Erosion of articular cartilage
- Must do Chest X-Ray

As the disease resolves, the bones harden again & the rarefraction becomes gradually less
apparent.

2. Bone Scan
- Shows increased uptake in affected areas

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Other investigations
1. ESR – usually elevated. Can be used to monitor treatment
2. Mantoux Test – positive
3. Joint aspirate culture

Treatment
 Bed rest or immobilize joint (eg splinting )
 Analgesics or hot /cold compresses for pain relief
 Drug (antibacterial):rifampicin, isoniazid, pyrazinamide, ethambutol, and
streptomycin for 6 – 9 mths with DOTS .
 Surgery to drain spinal abscesses or stabilize spine .

Complications
 Sinus Formation
 Secondary Infection via a sinus track
 Spread of disease
 Vertebral collapse resulting in kyphosis
 Spinal cord compression
 Joint Destruction

Management of Hip Fractures in the Elderly

Hip fractures involve fracture of any aspect of proximal femur, from the head to the first 4-5 cm
of the sub-trochanteric area. Fracture of the hip can have devastating consequences. This is
particularly true in older persons, who often suffer this calamity. Aside from considerable risks
of morbidity and death, hip fracture causes loss of mobility and can significantly reduce the
patient's quality of life.

The head and neck of the femur is structured in such a way that allows for the transmission of
body weight efficiently, with minimum bone mass, by appropriate distribution of the bony
trabeculae in the neck. This allows for an efficient system to withstand load bearing and torsion
under normal stresses of locomotion and weight bearing. All of this is lost in a fractured hip.
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Incidence and Mechanism

Fractures of the neck of femur are common in the elderly. It does occur occasionally in young
adults and even in children. . In young persons, trauma associated with significant kinetic energy
is required to cause a hip fracture. For example, 75% of all femoral head fractures, more
common among young patients, occur as a result of motor vehicle accidents. In older persons,
more than 90% of these fractures result from trauma or torsion associated with a minor fall. They
also can occur in the absence of an obvious traumatic event. Fractures of the neck of the femur
are common in persons over the age of 60 years, and especially in women in whom there is a
tendency for the bone to become increasingly fragile as a consequence of post-menopausal
osteoporosis. Women lose approximately 58% of their bone density by the time they reach their
eighties as compared to males (38% bone density lost), especially around the neck of the femur. .
It is also more common in whites than non-whites due to  incidence of osteoporosis in whites.

95% of cases involve marked displacement fractures with the shaft/distal fragments being
rotated laterally and displaced upwards. The remaining 5% involve impacted abduction
where the two fragments are firmly impacted together with slight abduction of the distal
fragment on the proximal.

The fracture may result either from rotation violence at the hip due to tripping and falling or
from direct violence over the lateral aspect of the hip by a fall on the side.
Causes

More than 90% of hip fractures in the elderly result from minor trauma or torsion associated with
a fall. They can even occur in the absence of any traumatic event. Risk factors for these fractures
include:
- Osteoporosis
- Cigarette smoking
- Institutional living
- Previous hip fracture
- Sedentary lifestyle
- Impaired vision
- Drugs that  bone mass e.g. furosemide, corticosteroids, thyroid
hormones, and phenytoin.

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Clinical Features

For displaced fractures:

History
 The patient is usually an elderly person, more often female, with a history of a fall and
inability to walk and weight bear on the affected limb.
 Level of activity before the accident
 PMH, PSH, Drugs
 Social history- important to know who takes care of the patient

Examination
 Marked external rotation of the limb often as much as 90o so that the patella and the foot
point laterally
 Limb is shortened by about 2 - 3cm
 All movements of the hip are extremely painful and limited
 Tenderness over fracture site

Impacted Abduction fractures

The history and signs are different. The patient may have been able to pick herself up and even
walk a few steps afterwards with assistance. Therefore, the patient may not seek medical
attention until days later. On examination, there is no detectable shortening; no detectable
rotational deformity; patient can move the hip through a moderate range without severe pain.

Investigations

1. Complete Blood Count : Hb - to detect anemia, required for surgery; PCV- if increased,
detect blood loss occurring within the hip joint; plt count- to assess haemostasis
2. Urea & Electrolytes- kidney function necessary for surgery
96
 3. Group & Cross Match- elderly patient are likely candidates for surgery, so important
4. Random Blood Glucose- screen for Diabetes Mellitus since it is a common chronic
illness
5. Electrocardiogram and Chest X Ray- to identify signs of heart or pulmonary problems
and to assess eligibility for surgery. This is indicated in all patients over 40 years.
Radiographic imaging – Anteroposterior & lateral views of both hip joints. In displaced
fractures, there is a break in Shenton’s line, which is an imaginary smooth line drawn from the
inferomedial aspect of the femoral neck to the inferior aspect of the superior pubic ramus.
External rotation is indicated by the prominence of the lesser trochanter. There may also be
evidence of osteoporosis. Undisplaced impacted fractures may be missed radiologically.

Shenton’s line

Classification

Two broad groups of fractures are recognized in the neck of femur

1) Intracapsular fractures

 Subcapital
 Transcervical
 Basal (basicervical)

2) Extracapsular fractures

 Intertrochanteric (Most common)

 Subtrochanteric

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Blood supply to the head and neck of femur

 The posterior capsule of the hip (retinacular vessels) – major supply

 Nutrient vessels from the femoral shaft
 Vessels in ligament of femoral head- foveolar artery via ligamentum teres

The profunda femoris artery arising from the femoral artery gives off the medial circumflex
femoral artery. This gives off lateral epiphyseal and superior and inferior metaphyseal arteries.
The lateral epiphyseal arteries are important and supply the lateral 2/3 of the femoral head. The
superior metaphyseal artery supplies the superior aspect of the femoral neck. The inferior
metaphyseal artery supplies the inferior part of the neck and the adjacent part of the head derived
from the metaphysis.

The medial epiphyseal artery supplies a circumfoveal sector of the head. It is a continuation of
the artery of the ligamentum teres, which arises from the acetabular branch of the obturator
artery.

In intracapsular fractures, the proximal fragment often loss part of its blood supply as a result of
a tear in the capsule, and hence, the treatment of this fracture is difficult.
Extracapsular fractures do not interfere with the posterior capsule, therefore management is
different.
The arteries traveling with the capsule are the major contributor to the blood supply of the head.
Hence extracapsular fractures do not cause avascular necrosis of the head of the femur which is
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one of the main complications of this type of fracture. Intracapsular fractures of the neck,
especially displaced fractures, often lead to avascular necrosis of the femoral head from
disruption of interosseous vascular channels and intracapsular vessels, which lie against the
periosteum of the femoral neck.

Classification (Garden).
This classification relies only upon the appearance of the hip on the AP radiograph. It is used to
determine the appropriate treatment.

Stage I : incomplete fracture of the neck (so-called abducted or impacted)

Stage II : complete without displacement

Stage III: complete with partial displacement: fragments are still connected by posterior
retinacular attachment; there is malalignment of the femoral trabeculae

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Stage IV : this is a complete femoral neck fracture with full displacement: the proximal fragment
is free and lies correctly in the acetabulum so that the trabeculae appear normally aligned.

Management

The aim of treatment in elderly patients is to get them up and about to their previous level of
activity as soon as possible. Hence long hospital stays with conservative treatment is
recommended.

Treatment is based upon

1. The location of the fracture

2. Physiological age of the patient

3. Degree of displacement

The first thing one needs to know is the location of the fracture i.e. whether it is intra-capsular
(subcapital/below head, transcervical & basicervical) or extra-capsular (intertrochanteric,
trochanteric & subtrochanteric). Basicervical fractures are treated as an extra-capsular fracture at
UHWI.
If the fracture is intra-capsular, there is likely to be compromise of the capsule & the capsular
arteries, which may lead to avascular necrosis of the head of the femur (33.3%) also 50% risk of
non-union since there are no muscles attached to give blood supply, the fracture site is bathe by
synovial fluid that washes the haematoma away and also has constituents that does not facilitate
haematoma fomation. Extra-capsular fractures do not have this problem & are hence easier to
treat.

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Protocol for Management of Hip Fractures

Extracapsular dynamic hip screw (DHS)

Fracture of the Neck of Femur
Intracapsular Undisplaced compression screws
(in all ages, i.e. rigid internal fixation)

Displaced

Older patient Young/active patient

Inactive- Austin Moore prosthesis (hemiarthroplasty) 1) compression screws
Active- total hip replacement (THR ) 2) if develop AVN then-
a) quadratus femoris flap
b) free graft
3) (THR)
4) arthrodesis

Management of Extracapsular Fractures

The principle of treatment is reduction of the fracture and maintenance of the fragments in good
position until union occurs.
Age is no consideration in these fractures.

Conservative Treatment:

This is only offered when surgery in unavailable or contraindications

This consists of the application of continuous skeletal traction. For cases with marked coxa vara,
continuous skeletal traction through the upper tibia is applied and the leg is immobilized in the
Bohler Braun splint and the foot of the bed is raised. Traction with 12-15lbs is sufficient. The
coxa vara gets corrected and the fracture unites in about 12 weeks. When the coxa vara is not
marked, skin traction in Thomas’ splint will be sufficient. .

The normal neck shaft angle is about 115 degrees. When the angle is reduced to nearer 90
degrees, the deformity is called Coxa Vara.

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Surgical Treatment:
This consists of manipulative reduction and internal fixation using a DHS (dynamic hip screw).
It enables earlier mobilization of the hip and weight bearing (within 1st 1-2 weeks).

The DHS will collapse by a few millimeters to allow compression of the fracture site, hence
healing, when the patient applies weight to the leg by standing. A rigid screw would keep the
fragments apart and may cause non-union.

Intracapsular Fractures: -

Management here depends upon if displaced or not, and also on the patients level of activity.

1. In non-displaced fractures, the capsule can be assumed to be intact, and

as a result, the major blood supply to the head is intact. Hence
compression screws can be used to secure the fracture.

2. If displaced, then the level of activity needs to be taken into consideration.

For patients who live a sedentary lifestyle, then hemi-arthroplasty with an
Austin-Moore prosthesis is the treatment of choice. With this they can
return to normal living in 2-3 days. It cannot be used for more active
patient because of the risk of osteoarthritis (prosthesis is stainless steel &
wears our acetabulum quickly). It will last for about 5 years. For more
active patients, total hip replacement would be warranted. This would last
about 10-20 years.

Hemiarthroplasty – This is usually the treatment of choice in older patient who are not very
active where the head of the femur is removed and replaced with a metallic prosthesis – Austin
Moore Prosthesis in which the stem is cemented into the medullary canal of the femoral shaft.
The patient may sit up the next day and ambulate within the next 48 hours.
The advantage of using Austin Moore prosthesis to treat intracapsular fractures of the neck of the
femur in the elderly are:
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 1. The patient is almost immediately mobile ( the next day )
2. It decreases the length of hospital stay
3. Since the displaced head of the femur was removed, there is no chance of avascular
necrosis. This negates the need to do repeat surgical procedures that are required should
avascular necrosis have occured, especially since elderly patients do not tolerate multiple
surgical procedures well.
4. The patient is elderly and not too active. Consequently, the Austin Moore prosthesis
should not wear out too quickly.

Disadvantages
1. The Austin Moore Prosthesis is easily worn by everyday use. Placement of the prosthesis
is therefore dependent on the activity level of the patient. As elderly people do minimal
activity this should not be a problem.
2. The prosthesis is made from stainless steel so heavy walking will wear the acetabulum
causing severe osteoarthritis. In such cases an excision arthroplasty or total hip
replacement is necessary.
Otherwise the prosthesis should last at least 5 years without problem.

Total Hip Replacement

If the patient was active in the premorbid state then a total hip replacement should be performed
which involves a metallic head rubbing against a plastic acteabulum.This placement can last for
10 – 20 years.

Complications of total hip operations

o Infection
o Dislocation
o Development of DVT and PE.

Other Aspects of Management

Hospitalization Prior to Surgery included:

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 1) pain relief- by use of analgesics and skin traction
2) hydration- IVFs
3) Prevention of complications of immobilization- DVT, bedsores, respiratory problems,
GU system, depression or disorientation.
Give chlorpromazine if patient becomes boisterous to sedate them

Post-op Management

 monitor fluid balance

 vitals
 analgesics
 ambulation ASAP
 Continue management if necessary until patient is fully walking, then plan for home
 Rehabilitation - depends on clinical scenario and premorbid presentation
 Remind patient not to cross legs as prosthesis may become dislocated
 Patient cannot do extremely strenuous activity like running a marathon

Prevention

 Get rid of loose rugs

 Rails in bathtubs
 Toilets not too low
 Adequate bathroom facilities
 Prevention osteoporosis via exercise and proper diet (from age 35)
Osteoporosis defined as bone density <25 from mean
Frequent bone density assessment in post-menopausal
Tx: bisphosphonates, vitamin D, calcium supplements, exercise against gravity

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Complications of immobility

RS – atelectasis, LRTI such as pneumonia

CVS – DVT, PE, venous stasis
GI – weight loss, malnutrition, constipation
GU – UTI, stone formation
CNS – depression
MS – osteopenia(Bone demineralization), joint stiffness, muscle atrophy, muscle contractures
Skin – decubitus ulcers
Atelectasis is defined as the lack of gas exchange within alveoli, due to alveolar collapse or fluid consolidation. It may affect part or all of one lung. It is a condition
where the alveoli are deflated, as distinct from pulmonary consolidation.

105
Management of Shaft of Femur Fractures in Adults

Being the strongest weight bearing bone in the body, fractures of the femur usually result from
high energy trauma such as high energy vehicular injury, fall from heights or bullet wounds.
Low energy trauma may also cause such fractures as the femur is a common site for pathological
lesions e.g. secondary neoplastic lesions. In such a case the fracture is usually in the upper part of
the bone .Traumatic fractures may occur at any point along the shaft and is equally common
along the entire shaft.
The pattern of the fracture is variable, and may be- transverse, oblique, spiral, comminuted or (in
children) greenstick type.

Review of Anatomy
The femur has the following powerful groups of muscles inserted into it:
1) Iliopsoas - a powerful flexor that inserts into the lesser trochanter
2) Gluteus medius and minimus, which powerfully abduct the hip, and are inserted into
the greater trochanter
3) The adductors longus, brevis, and magnus are inserted along the medial aspect of the
shaft
4) The gastrocnemius muscle origins are attached to the posterior aspect of the lower
end of the shaft.
These muscle attachments, cause the typical displacements of the fragments (angulation and
overlap) in the fractures at the proximal, middle, and distal thirds of the shaft of the femur, and
therefore, creating problems in maintaining the fragments in position after reduction.

Classification
 Subtrochanteric
 Mid Shaft
 Distal third including supracondylar fracture

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Management
Management of Femur Shaft Fractures begins with initially assessing the patient and taking a
history and examination.
Most femur fractures are usually associated with multiple injuries due to high energy and so
initial management will include:
Following ABC’s guideline and stopping excessive haemorrhage before assessing the fracture.
Once stable, attempt to get a history.

History
 Mechanism and time of Injury: Usually a Motor Vehicle Accident, Fall etc.
 Pain , Swelling , Deformity
 Inability to weight bear post injury
 Level of activity before the incident e.g. was the patient able to ambulate
 Presence of other injuries
 Past Medical History, mental status, occupation
Physical Examination
 General Examination for other life threatening injuries: Primary Survey
 Assess traumatized limb: Viabilty of limb distal to fracture (neurovascular)
 Range of movement
 Shortening of the limb

Investigations
 Complete Blood Count : Haemoglobin- to determine oxygen carrying capacity for surgery if
deemed necessary; PCV- increased in severe bleeding; Plts- decreased values indicate
problems with haemostasis
 Group and Cross Match : blood transfusion may be necessary
 Urea & Electrolytes, Random Blood Glucose
 Radiographic Imaging

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Radiological features
Imaging should include the joint above (hip) and the joint below (knee). X-rays including the
hip joint is mandatory as an associated dislocated hip could be missed in the clinical
examination.

`Treatment methods for fracture of femoral shaft include:

1. Closed reduction and spica cast immobilization

2. Skeletal traction (Steinmann Pin)
3. Femoral cast brace
4. External fixation
5. Internal fixation

 Medullary nail (closed or open technique)

 Interlocking medullary nail (distal 1/3 of femur unstable)

 Plate fixation

Femoral shaft in an adult rarely can be reduced and held in a plaster. The femur is surrounded by
large powerful muscles that exert angulatory forces on the fragments and in contrast to its base in
a small child, plaster immobilization early after a fracture of the shaft of femur in the adult
usually leads to displacement, angulation and unacceptable position. Intramedullary nailing with
interlocking screws as the method of choice has replaced the well-tried method of conservative
treatment sustained weight traction with limb support in a Thomas type splint. Nevertheless, it
must be remembered that by no means must every fracture of the femoral shaft lend itself to
intramedullary nailing. Many comminuted fractures close to the upper or lower end are
unsuitable.

Conservative treatment by sustained fraction

The principles of this method are:

 To reduce the fracture (if necessary) by traction and manipulation

 To support the limb in a Thomas or Povey’s splint

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  To maintain continuous traction by means of weight in order to correct length
Rehabilitation by exercises is begun at an early stage

Reduction: The use of anaesthetics is not always required. Traction is applied by either adhesive
skin strapping or Steinmann pin through the upper end of the tibia. By a combination of traction
and manipulation under radiographic or image intensifier control, an attempt is made to bring the
fragment into correct apposition and alignment.

Splintage: A Thomas’ splint with Pearson knee flexion attachment or a similar splint such as a
Povey’s splint is attached to limb and suspended from an overhead beam by a balance weight
technique. A suitable weight (4-6 kg, 10-15 lbs, according to patient’s build) is attached to the
traction cord. The knee is flexed 15 or 200 to permit control of rotation. Repeat X-rays are done
in the first two weeks and adjustments to sling and weight are made as required. The duration of
splinting varies; usually about 12-16 weeks. Therefore, while in bed, active exercises of the
lower leg and foot are important in preserving muscle tone and in preventing deformity. These
should be done immediately. Following the settling of initial pain of the fracture (about one
week), active quadriceps and knee exercises are begun. When the splint is removed (at stage of
union) the patient is allowed to exercise in bed before walking is begun. Thereafter,
rehabilitation is continued in the gym.

Cast and functional bracing

These are used for fractures of the lower half of the femur and especially in transverse or short
oblique type fractures, to reduce the time spent in bed with traction on the limb. Once the
fracture has become sticky at about 6-8 weeks post injury a plaster spica or a plaster splint with
longed knee section may substitute the traction apparatus.

Caution: Keep close check on alignment of fragments to avoid angulation at the fracture which
may lead to mal-union. Limited weight bearing on injured leg should be advised and the use of
crutches should be encouraged.

Conservative treatment with sustained traction is now considered an impractical method because
of the length of confinement to bed with its potential for complications and the economic
consideration of several weeks or months in hospital.

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Internal fixation

Internal fixation by intramedullary nailing now allows patients with femoral fracture to leave
hospital soon after treatment for the injury. Intramedullary nailing wherever possible should be
done by closed technique, i.e. without exposing the fracture itself thereby reducing the risk of
infection. Interlocking intramedullary nailing is more suitable for proximal and distal third
fractures. The intramedullary nailing is locked in place at the upper and lower ends by insertion
of cross screws through holes provided at the end of the nail. The locking screws prevent rotation
and thus increase stability.

Plate fixation

Comminuted fractures are less suitable for intramedullary nailing. The most accurate reduction
of comminuted fractures of the femoral shaft can be obtained with inter- fragmentary
compression and plate and screw fixation. This treatment allows early motion and good function.
There is a risk of infection and failure of fixation. Better results are had with indirect reduction of
intermediate fragments, preservation of soft tissue attachment (esp. medially) and final
compression with plating.

External fixation

This method is applicable mainly to open fractures with contamination where internal fixation
may be hazardous. Following reduction, stout pins transfix each fragment and the ends
protruding through the skin are anchored to an external steel bar by clamps or cement. External
fixators offer the advantage that any wound is easily accessible for treatment.

Complications
Immediate
Neurovascular Damage
Late
Ring Sequestrum
Cellulitis
Abscess
Osteomyelitis
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Management of Fractures of the shaft of the femur in
Children

Most fractures of the shaft of the femur in children are closed injuries and can and should be
treated by closed methods. Besides the usual mechanism of injury, femoral fractures can occur at
birth, can be caused by child abuse or can be pathologic. Quite often other severe injuries that
require treatment are also present. Fractures occur most commonly in the middle third.
The ideal treatment of fractures of the femur in children as one that:

o Controls alignment and length

o Does not compress or elevate the extremity excessively

o Comfortable for the child and convenient for the family

o Causes the least negative psychologic impact possible

Treatment options include cast bracing, immediate spica application, longitudinal skin traction
and 90 -90 skeletal traction. Ideal treatment depends on the age of the child, location and type of
fracture and family enviromnent.

Birth fracture
In newborn infants with birth fracture of the femur, the leg is suspended vertically from a frame
with skin traction to the leg. This is referred to as Gallows’ or Bryant’s traction. The fracture
unites in 2 weeks time with profuse callus formation.

Treatment in Young Children

Gallows or Bryant’s traction is convenient and satisfactory for children up to age 3 years.
Adhesive skin strapping is applied directly to the skin of the legs and the child’s lower limbs are
suspended from overhead beam. The cords are tightened so as to just raise the buttocks clear of
the mattress. The weight of the pelvis and lower trunk is sufficient to maintain full length of the
fracture. When stability, length and alignment are achieved, a spica cast is applied. Usually
adequate union of fracture is achieved by 3-4 weeks following skin traction. Note that the knees

111
of the child should be held in slight flexion with simple back splints held in position with crepe
bandages.
NB. Neglect of this precaution has led, very rarely, to spasm of the major artery of the limb and
consequent ischaemia—a disastrous complication. Also it is important that the strips of adhesive
strapping used to support the limbs be applied direct to the skin, and not over encircling
bandages: otherwise the limb may be constricted, with serious detriment to the circulation. As
after all injuries to the limbs, the state of the circulation should be watched carefully, especially
during the first 3 days.

Treatment in children age 2-10 years

At this age most femoral fractures occur. Skeletal traction is usually appropriate with the
application of a spica cast after approximately 3 weeks of traction. Immediate spica casting has
been recommended but best results with this method seem to be obtained in infants and young
children.

Treatment in children older than 10 years

Treatment of femoral shaft fractures in adolescents is somewhat controversial. Historically, these

fractures have been treated by non-operative methods. However, adolescents tolerate prolonged
immobilization less well than younger children and there have been reports of higher incidence
of knee pain, angulation of fracture and difficulty in maintaining length when 90 — 90 traction
(skeletal) treatment was used in these older children. Closed intramedullary nailing for almost all
femoral shaft fractures in patients older than 10 years is now preferred. If medullary nailing is
performed, however, the proximal and distal epiphyseal plates should be avoided. As in adults,
the fracture should be reduced before closed nailing.

External fixation

When an extensive soft tissue defect is present, an external fixator can be used as primary
treatment as in adults.

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Complications (in both adults and children)

 Simultaneous dislocation of hip

 Injury to major artery
 Injury to nerve
 Infection
 Delayed union
 Mal-union
 Non-union
 Stiffness of the knee
 Fat embolism syndrome
 Pulmonary embolism

Simultaneous dislocation of hip

Hip dislocation is sometimes not discovered because of inadequate x-ray exposures, i.e. does not
include the joint above the fracture site.

Injury to a major artery

Rarely, a sharp edge of the fractured bone may penetrate the soft tissues and damage the femoral
artery. The vessel may be severed or it may be severely contused and occluded. In either case
the outlook for the viability of the limb is grave unless continuity of the vessel can be restored by
immediate operation.

Injury to a nerve
A sharp fragment of bone at the time of the initial injury may strike a nerve trunk. The severity
of the damage can vary from transient neuropraxia to complete severance of the nerve
(neurotmesis). The sciatic nerve is obviously the most significant in this type of injury. As the

113
nerve is broad and divides into tibial and common peroneal components high up in the thigh, one
or other of these subdivisions may be injured while the other escapes.

Mal-union
The commonest complication of fracture of the femur is mal-union due to improper correction of
the lateral angulation. If the correction is overriding, the mal-union occurs with marked
shortening. If the shortening is more than 1½” it will need surgery by osteotomy and internal
fixation.

Non-union
Usually due to the interposition of soft tissues between the fragments. This will need operative
reduction and internal fixation with intra medullary nailing, supplemented with bone grafts.

Knee stiffness
Occurs due to prolonged immobilization, particularly in older patients. Every effort must be
made to prevent stiffness by regular physiotherapy. The causes are:
a) Adhesions inside the joint,
b) Adhesion of patella to the femur, and
c) Adhesion of quadriceps muscle to the fracture site more particularly in cases treated by open
operation.

114
Management of Colle’s Fracture

A Colle’s Fracture was first described in 1814 by Abraham Colles as a low energy extra articular
fracture of the distal radius occurring in people greater than 40 years particularly women. It is
used today to describe an extraarticular fracture of the distal 2 – 3 cm of the radius which may or
may not have an accompanying fracture of the ulna styloid without involvement of the
radiocarpal joint. It is noted to be the most common fracture of the wrist region usually
secondary to a fall on the outstretched hand in an attempt to break a fall but may occur secondary
to any forceful dorsiflexion of the wrist.

There are usually certain characteristics of the fracture. It is usually:

 Dorsally displaced
 Dorsally angulated
 Radially displaced
 Radially angulated
 Impacted

All these features result in a deformity classically described as the “Dinner Fork Deformity”
which characterizes a Colle’s Fracture. The result is dorsal depression in the lowest third of the
forearm (proximal to the fracture site). Immediately distal to this is a marked prominence caused
by the distal fragment being displaced backwards carrying with it the entire carpus and hand.
Anteriorly there is fullness where soft tissues are stretched over the forward projecting upper
fragment.

115
In a small proportion of cases, the deformity is the reverse, i.e. the lower fragment is displaced
forwards and rotated forward. This variation is known as a Smith’s fractured.

Incidence

It is the most common fracture seen in clinics. However, it is now the most common fracture at
all ages.
It occurs seldom in young adults but the true Colle’s fracture is more common in people >40
years, especially women. This is thought to be associated with the development of osteoporosis
in post-menopausal women.

Mechanism of Injury

Usually due to a fall on the outstretched hand. The elderly are also more prone to falling, another
contribution to epidemiology.

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Clinical Features

The typical displacement is reflected in a characteristic clinical appearance termed “Dinner Fork
Deformity” where there is dorsal depression in the lowest third of the forearm (proximal to the
fracture site). Immediately distal to this is a marked prominence caused by the distal fragment
being displaced backwards carrying with it the entire carpus and hand. Anteriorly there is
fullness where soft tissues are stretched over the forward projecting upper fragment.

History

 Fall on outstretched hand

 Pain, swelling
 Elderly women

Physical Examination

 Dinner Fork Deformity

 Tenderness
 Swelling
 Occasionally the fracture may be a simple one without displacement, recognized only by
pain and tenderness in the area.

Investigations

Often confirmed by radiography - AP and lateral of the wrist, forearm, and elbow

117
Management

 Involves: 1) disimpaction; 2) reduction; 3) immobilization

 The first step is anaesthesia: general or local—a regional block (Bier’s block) is most
commonly used and preferred because of the decreased risk of complications. It is used to
relax the muscles of the forearm.
 Disimpaction: the examiner grasps the patient’s hands as if shaking it. The fragments are
disimpacted by firm longitudinal traction against counter-traction provided by an assistant
who grasps the arm above the flexed elbow. NB: to check if disimpaction has been achieved,
grasp the distal fragment between the finger and thumb of one hand and proximal fragment
with the other hand.
 Reduction: using the thenar grip in which the examiner places the thenar eminence of one
of his hand over the distal fragment and applies firm dorsal pressure against the volar counter
pressure of the hand (thenar eminence) upon the shaft of the radius just proximal to the
fracture site. NB: in a left-handed fracture the examiner’s right hand is used to control the
distal fragment and the left hand to control the proximal fragment. In right-handed fracture,
the opposite is applied.
 Immobilization: plaster is applied with the wrist in a slight palmar flexion and ulnar
deviation. A dorsal (back) slab is initially put on to accommodate swelling in the acute phase
of the fracture. It is changed to a complete below the elbow cast 1 week later when the
swelling has subsided. While applying the plaster, a repeat thenar grip is done to mould the
plaster snugly to the fracture area, in order to prevent redisplacement. The patient should be
encouraged to elevate the hand above the elbow and exercise the fingers.

Immediately after reduction and application of the dorsal slab, the position of the fragments
should be checked via x-rays — AP and lateral. It should be repeated one week later, i.e., at the
time when the complete cast is to be put on because there is a risk of re-displacement as the soft
tissue swelling is decreased despite immobilization in plaster. If the check radiographs shows re-
displacement, further manipulative reduction under IV regional Bier’s block is advised. Usually
it is impossible to correct a re-displacement by manipulation if it has been allowed to persist for
>2 weeks. It is important to detect re-displacement early.
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For displaced fractures — plaster should be retained for 5-6 weeks, even then, the union is far
from consolidated but it is firm enough to prevent further displacement.

For undisplaced fracture—plaster can be removed in 3-4 weeks.

After POP is removed, a course of mobilizing and strengthening exercises for the fingers, wrists
and shoulders should be encouraged, so, full functioning of the joints can be restored.

External Fixation: an alternative in younger patients with severe comminuted or unstable

displaced fractures whose bones are not diseased or osteoporotic.
In these patients it is difficult to maintain full reduction by immobilization in POP.
Procedure: The proximal pins are placed in the proximal fragment. Distal pins are placed either
in the distal radial fragments or into the proximal ends of the index and middle metacarpals.
This technique may also be used for maintaining position of the fragments after corrective
osteotomy for mal-union.

Complications

Early

Median Nerve Compression: Persistent backward displacement of the lower fragment of the
radius may cause the lower end of the proximal fragment to impinge against the median nerve.
Treatment: if there are signs and symptoms of marked median nerve compression of the flexor
retinaculum, which can be divided surgically.

Loss of Reduction: This is most likely to occur within the first week. This can result in mal union
of the fragments i.e., with dorsal displacement and backward tilting of the distal fragment if not
detected early.

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Late

Mal Union: As a result of deformity their will be impaired wrist function.

Treatment: If the disability is severe, this may justify operation, where the bone is divided with
an osteotome and the lower segment is realigned in normal position and fixed with a screw.

Subluxation of the distal radioulnar joint: Caused by persistent upward displacement of the
distal fragment of the radius, which is thus slightly shortened while the ulnar remains of normal
length? Clinically, there is pain in the joint, especially during active movement of the wrist with
a need for forearm rotation. Wrist movements are impaired especially adduction and rotation.
Treatment: If the disability is troublesome, operation should be advised. A simple and reliable
method is to excise the lower end of the ulna, including its head and about 3 cm of the shaft.
(Darroch’s Operation).

Rupture of the Extensor Pollicis Longus Tendon: Tendon is liable to tear due to the sharp
bend made laterally as the tendon leaves the groove on the back of the lower end of the radius
.Rupture is preceded by fraying of the tendon over a length of 1-2 cm. The fracture does not have
to be severe. The interval between fracture and rupture of the tendon is four to eight weeks so
symptoms may develop while still in cast or just after removal. The patient may feel something
‘give way’ at the back of the wrist, or simply notice difficulty in using the thumb.
Treatment: Operation is advised, which most often entails transfer of the tendon of extensor
indices to activate the distal stump of extensor pollicis longus.

Stiffness of fingers or shoulder: Can be avoided by encouraging patient to exercise the fingers
and shoulders while in plaster. If not there is increased risk of stiffness especially in the elderly.

Sudeck’s Post Traumatic Osteodystrophy: A Colle’s fracture is the commonest cause of

Sudeck’s Osteodystrophy marked by increased swelling and pain with severe stiffness. Incidence
is very small.
Treatment: Conservative by elevation and intensive active exercises .Full recovery may take
several months.

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Hand Infections

Due to its inherent role and function in the human body, the hand is always at risk for
infections. Infections can turn a highly useful hand and upper extremity into a stiff and painful
appendage. Early diagnosis and prompt treatment, including antibiotic therapy and often surgical
debridement, are the cornerstones to successful treatment and restoration of hand function. The
fascial spaces of the hand are closed anatomic compartments, which when infected allow abscess
formation. Infections enter these spaces by direct puncture or by extension from an adjacent
closed-space infection. When abscesses form in these closed compartments, treatment with
systemic antibiotics alone is ineffective and surgical drainage is required.

The hand is prone to infections because of the following reasons:

1) Anatomical factors
a. The skin of the palm has a thin layer and is thus easily breached.
b. The presence of closed spaces with poor blood supply that may serve as a nidus for
infection
c. The proximity of the tendons and tendon sheaths to the palmar space allows spread of
infection
2) Local Factors
a. Virulence of the organism
b. The amount of wound contamination
c. The extent of soft tissue damage
3) Systemic factors
a. Malnutrition resulting in a decreased ability to fight infections
b. Diabetes mellitus
c. Other immunosuppressive states e.g. HIV, steroid therapy and other drugs

Aetiology
All types are caused by infection with pyogenic bacteria. Minor injury such as a prick,
abrasion or blister usually provides the route by which micro organisms can enter. Animal or
human bites may are also causes of hand infections. Haematogenous spread is rare. The usual

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 causative agent is staphylococcus aureus, which accounts for 50 – 80% of cases. Other
causative agents include –

 Streptococcus
 Gram negative bacteria – e.g. E. coli, klebsiella, Pseudomonas & Proteus (common in
immunocompromised states e.g. Diabetes mellitus)

Special conditions:
 Thorns - Sporothrix schenkii and asteroides
 Animal bites- Pasturella multocida
 Human bites - Einkenella corrodes
 Multiple organisms may be involved in Diabetes Mellitus

Overview of Anatomy of the Hand

Classification
Infections can occur in one of six spaces in the hand and therefore there are six types of
infections to be considered
 Paronychia – nail fold infection
 Pulp space (whitlow, felon)
 Deep Palmar Subfascial Space Infections- thenar, midpalmar and hypothenar spaces
 Other subcutaneous infections

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  Tendon sheath infection
 Radial and Ulnar Bursal Infections

Paronychiae and pulp space infections are the most common and flexor tendon sheath infections
the least common, but they all may cause important complications. Knowledge of the anatomy
of the hand is essential to the treatment of the infection in each space.

Clinical Features

The patient often gives a history of a recent boil on the finger or hand or of minor or major injury
such as a prick while gardening or a stick by an industrial sewing machine. There are symptoms
of local pain, often throbbing in nature, swelling and loss of function. On examination there is
hyperemia and there may be constitutional symptoms including pyrexia. When the mid-palmar
space is infected the swelling may appear more dorsally due to restriction by the palmar fascia.
Care must be taken not to mistake this for a problem in the dorsum of the hand because draining
the pus by a dorsal incision would be more difficult (having to go through more ligaments) and
may spread the infection. In flexor tendon sheath infection it is the thin synovial membrane
around the flexor sheath that is infected and the patient is in excruciating pain. The pain is
worsened by passive extension of the fingers as the tendon sheaths are stretched.

Investigations

General:
 Haemoglobin
 White blood cell and differential
 Erythrocyte sedimentation rate

Specific:
 Anaerobic and aerobic cultures
 Tissue for histology

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Principles of treatment

The aim of treatment is to stop the infection, provide pain relief where indicated and avoid the
need for surgery. This can be done by splinting or resting the hand, elevating the limb above the
level of the heart to reduce the oedema, analgesics and antibiotic drugs.

If suppuration (process of discharging puss) has already occurred as evidenced by severe throbbing pain,
intense local tenderness, pyrexia and loss of function then incision and drainage is required.
Physiotherapy utilizing whirlpads and saline soaks may also be useful.

Empirical antibiotics are directed against Staphylococcus aureus and other gram positive
organisms

Antibiotics that may be useful include:

 Cloxacillin
 Augmentin
 Cephalosporin

Special Features of Individual Lesions:

Acute Paronychiae
This is an infection of the area of the lateral nail fold which is typically due to superficial trauma.
It is primarily seen in domestic workers who hand wash, industrial chemical workers and nail
biters. Paronychia in children often is the result of finger sucking. Although typically starting as
a cellulitis, progression to abscess formation is not uncommon. Infection that spreads to the
proximal nail edge is termed an eponychia.

Treatment

 Early: Warm saline soaks, splinting, and antibiotics: oral Cloxacillin, Flucloxacillin with
rest and analgesia.

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  Late: incision and drainage of the area; irrigated with warm saline, and the option of
packing with Vaseline gauze for two days. Dry dressings are applied with finger exercise.
If mild, raise the cuticle or create a vertical incision through the cuticle on one or both side. If
the pus extends beneath the nail, the proximal 1/3 of the nail bed should be removed. This
can be distinguished by eliciting pain when pressure is applied to the centre of the nail.

Complications

It left untreated, paronychiae may lead to the development of osteomyelitis, shortening of the
phalanx as well as nail abnormalities.

Chronic Paronychia
A rare consequence of inadequate treatment of the acute form .Affects people who are constantly
exposed to water containing irritants e.g. housemaids, barmaids, swimmers and
immunosuppressed patients. In 85% of cases Candida Albicans is the causative organism.

Clinical Features

 Repeated episodes of inflammation, pain, swelling

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  Accumulation of cheesy material between the nail plate and the eponychium.
 Nail plate thickened, grooved and discoloured.

Treatment

Conservative

Use of gloves, frequent drying

Use of antifungals

Surgical

Eponychial marsupialization where the eponychia is lifted and removed by curettage

Felon/Whitlow:
This is an abscess of the terminal phalanx pulp and is the second most common hand infection.
Infection of the pulp of the distal phalanx is an orthopaedic emergency, as this is actually a
localized compartment syndrome. The most common cause is a puncture wound however an
inadequately treated paronychia or subungual abscess can be the causative factor. The index
finger and the thumb are most commonly affected.

Organism: Staphylococcus Aureus most commonly

Mixed and Opportunistic organisms in the immunocompromised.

The General findings are:

History:

 Classically severely painful and throbbing finger worsened when hand is placed in the
dependent position
 Tenderness
 Fever
 Loss of function
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Physical examination:

 Oedema
 Hyperaemia
 Tenderness
 Glistening stretched skin

The infection does not spread proximally (due to fascial barrier) past the distal interphalangeal
joint (DIPJ) unless there is associated infection of the flexor sheath, cellulitis or septic arthritis.

If left untreated complications may develop:

 Draining sinus
 Osteomyelitis of the distal phalanx (The distal phalanx is connected to thick skin
via numerous septae that transverse subcutaneous tissue. Pus between septae enters bone
as the path of least resistance. This infection may result in total bone destruction within
three days)
 Obliteration of the digital vessels with subsequent sloughing
 Flexor tenosynovitis
 Pyogenic Arthritis of the distal interphalangeal joint.

Treatment

Early: Antibiotics and elevation of limb with warm saline soaks. This is rarely successful and so
a surgical approach is usually undertaken

Surgery: A. The preferred method is a high lateral incision beginning just distal to the distal
digital crease. The incision is extended parallel and palmar to the lateral nail plate, dorsally
avoiding the neurovascular bundle. Unlike other previously advocated methods, this maintains
the volar finger pad as a unit and prevents instability of the distal fingertip.

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B. Another acceptable technique is to make a longitudinal, midline incision at the palmar aspect
of the distal pad which may offer greater access

Following incision one should irrigate and loosely pack the wound, and then immobilize the
finger. Treatment with cloxacillin is preferred and a follow-up appointment in 1 to 2 days for re-
evaluation should also be arranged

Herpetic Whitlow

Herpetic whitlow classically presents as grouped vesicles with an erythematous base on the
fingertip. It is caused by herpes simplex virus type I or II and is usually found in healthcare
workers, children with herpetic gingivostomatitis, or adults with genital herpes. As with other
recurrent herpetic infections, it resides in the dorsal root ganglion and sporadically reactivates
throughout the patient's lifetime. There may be an initial prodrome of pruritis, burning, and
paraesthesiae before the vesicles appear. The pain at this point is out of proportion to the clinical
findings. The lesions initially contain clear fluid but later can become purulent as they rupture
and form an exudative crust. At this stage, herpetic whitlow can be distinguished from a felon by
the absence of a tense distal finger pad in the former.
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Diagnosis is clinical; it can be confirmed by viral cultures or Tzanck smear preparations if a
pyogenic aetiology is being entertained. Treatment is supportive, with oral acyclovir reserved for
frequently recurring bouts or for immunocompromised patients. If the vesicles involve the nail
bed, unroofing them to relieve pressure and decrease pain has been advocated. This is solely a
symptomatic treatment and does not decrease healing time. A dry gauze dressing should be
placed, primarily to avoid infection transmission.

Complications of herpetic whitlow are: a) oral inoculation or transmission of virus

b) Inappropriate treatment (e.g., misdiagnosed as a felon) with incision and drainage, allowing
viral spread into healthy tissue and c) viremia occurrence.

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Bacterial Flexor Tenosynovitis (Tendon Sheath Infections)

Although a rare condition this is a true orthopaedic emergency and prompt treatment has to be
instituted if the functions of the fingers are to be preserved. It is often the result of puncture
wounds, animal bites or lacerations (i.e. penetrating injuries) and the infection is caused by
inoculation of bacteria into the flexor tendon sheath by way of the penetrating injury. The
infective organism is most frequently S. aureus followed by streptococci and pseudomonas. The
bacterial infection results in the development of a compartment syndrome that destroys the blood
supply to the tendon. Elevated pressure within the tendon sheath due to infection may impair
nutrient flow to the tendon. Resultant tendon necrosis and/or impaired function are disastrous
sequelae if elevated tendon sheath pressures not treated promptly and effectively. Bacterial
flexor tenosynovitis usually affects the central digits, as the thumb and little finger are able to
decompress into bursae.

Clinical features

Diagnosis is based on four cardinal features referred to as Kanavel’s Sign:

1) Circumferential fusiform finger swelling (boiled sausage) that ends distal to the distal

palmar crease

2) Tenderness over the entire tendon sheath

3) The finger is kept semi-flexed

4) Extension is extremely painful.

Complications:
 Necrosis of the tendons and adhesions between tendon sheath causing permanent
stiffness of the finger in semi-flexion
 Spread of infection to radial bursa (via the flexor sheath of thumb) and to the ulnar bursa
(from the sheath of the little finger)
 Suppurative arthritis and paralysis of the median nerve

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Treatment
 If diagnosis made < 24 hrs: IV administration of high dose Cephalosporins,
immobilization and elevation. (Culture Specimen should be taken).
 If >24 hrs or if conservative management fails surgery is indicated via incision and
drainage at the proximal and distal flexor sheath with placement of a catheter for
irrigation over 1-2 days.

Differential Diagnosis
 Herpetic whitlow
 Septic arthritis
 Gout.

Palmar Space Infections

These arise in the potential spaces within the palm. The may occur after direct penetrating injury,
but are commonly spread haematogenously from a foci of infection or as a result of injuries
involving the digits.

There are three palmar spaces: thenar, hypothenar and midpalmar.

Thenar space infections

This space lies deeply under the radial half of the hollow of the palm. It is the interval
between the adductor pollicis muscle behind and the flexor tendon of the index finger and the
first and second lumbrical muscles in front. Medially it is separated from the midpalmar space by
a fibrous septum that extends deeply from the fascia on the deep surface of the flexor tendons to
the fascia covering the interossei and the adductor pollicis muscle. It sometimes communicates
with the lumbrical canal; however it is rare for infections to spread along this route.

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Midpalmar space infections

This lies under the ulnar half of the palm between the interossei and the metacarpal bones
posteriorly and the flexor tendons of the middle, ring and little fingers anteriorly. Laterally the
space separated from the thenar space by a fibrous septum. Despite the communication between
a web space and the midpalmar space along the lumbrical canals, infection rarely spreads
through it.

Hypothenar space infections

This space lies medial to the midpalmer space. Infections of this space are extremely
uncommon. It manifests as swelling and tenderness in the hypothenar eminence.

Presentation

The thumb drains into the thenar space, the little finger drains into the hypothenar space, and the
other fingers drain into the midpalmar space. Therefore infections of the spaces that are as a
result of extension from digit infection will affect the respective deep palmar space.

The patient presents with dorsal swelling because of the tight palmar fascia on the volar aspect of
the palm. There is pain on finger movements. Clawed hand may be present because of the
accumulation of pus resulting in a rise in the pressure in the hand and the patient cannot extend
the fingers without pain.

Management:

Management of these types of infection is primarily via incision and drainage complemented by
the use of the relevant antibiotic. In palmar space surgery, care should be taken to avoid the
recurrent branch of the laryngeal nerve. In addition it should be noted that thenar and hypothenar
infections can drain into the space of Parona via the carpal tunnel resulting in the involvement of
the forearm. In order to avoid this occurrence, the incision should be extended and the carpal
tunnel decompressed at the time of surgery.

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Subcutaneous infection:
This is a spreading diffuse inflammation of the subcutaneous tissue usually caused by
beta hemolytic streptococcus. The infection may arise in any part of the hand or fingers.
Common sites are the middle or proximal segment of a finger, and the web spaces. There is
localized swelling with redness and tenderness. On many cases the infection has spread through
the skin from a subcuticular infection or blister. Care must be taken not to confuse subcutaneous
infections with the deep space infections. These infections can be complicated by sloughing of
the skin over the lesion and spread to the deep space or to the flexor tendon sheath.
The patient should be admitted and treated with intravenous antibiotics, along with
surgical drainage.

Web Space Infections

A web space abscess is usually caused by

- A fissure or puncture in the skin between the fingers

- infected distal palmar callus

- Septic subcutaneous lesion in the proximal finger

It is otherwise referred to as a ‘collar button’ abscess due to it hour glass appearance

On Examination

Over the dorsal and volar aspects of the region

 Tenderness
 Swelling

 Adjacent fingers in an abducted position as pus increases the intermetacarpal distance.

A sinus with purulent drainage may be present.

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Treatment

Incision (longitudinal) and drainage through both dorsal and volar incisions. Incising only one
side can lead to recurrent infections. Care should also be taken to avoid
cutting into the web itself as this may lead to severe bleeding and a prolonged healing. Incision
across the web space can lead to contracture formation. Both incisions should be irrigated,
packed open or drained and empiric antibiotics started .Culture specimen should be obtained
.Active range of motion exercise should also be started.

* Barber’s hand is an unusual type of web space infection

Dorsal Subaponeurotic Space Infection

The dorsal subaponeurotic space lies dorsal to the extensor tendons of the hand and infection of
this space is rare. It usually occurs in neglected injuries and is often the result of extravasations
of intravenous fluids, especially chemotherapeutic agents.

Swelling and erythema of the dorsum of the hand is the characteristic finding. There is marked

tenderness, local warmth and fluctuance. Incision (usually two parallel incisions on the dorsum
of the hand) and drainage are adequate treatment options. Antibiotic therapy is similar to that of
other hand infections, except in cases of chemotherapy where gram negative organisms are the
culprit of the infection. Improperly managed infections may have disastrous consequences.

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Cellulitis
This is a diffuse spreading inflammation along the subcutaneous tissue often caused by beta
hemolytic Streptococcus. It is characterized by hyperaemia, WBC infiltration, and oedema.

Early, superficial cases can be treated in the outpatient setting with a first-generation
cephalosporin or an antistaphylococcal penicillin. Rest and elevation are also recommended.
More severe or deep-seated cellulitis should be admitted for intravenous antibiotics. Diabetics'
infections are more often polymicrobial in origin, with gram-negative organisms cultured in
about one third of wounds. These patients require admission and treatment with IV antibiotics to
cover aerobic and anaerobic bacteria.

Drug abusers presenting with a hand cellulitis (usually from infected needle wounds) will often
have mixed anaerobic and aerobic organisms as the cause. Intravenous Antibiotic coverage is
also necessary in these cases, to include vancomycin if methicillin-resistant S. aureus is isolated
in wound cultures. In cases of hand cellulitis, the clinicians should be wary of an underlying
osteomyelitis, retained foreign body, abscess formation, or septic arthritis in the appropriate
clinical setting. Purulent discharge from a hand wound should be cultured in general, except for
healthy persons with superficial infections such as a paronychia.

Radial and Ulnar Bursal Infections

Infection occurs through extension of a tendon sheath infection.

Clinical Presentation

 Swelling
 Erythema
 Tenderness
Over the anatomic boundaries of the affected bursa.

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 Treatment

Incision and drainage with antibiotics. Wound is left open .tendon sheath infections are
treated .Range of movement exercises recommended. Wound allowed healing by secondary
intention.

Bite Wounds to the Hands

Human or animal bites to the hand pose a significant threat of infections due to the high bacterial
count of the oral flora. Although infections due to S. aureus and Streptococcus still predominate,
certain anaerobes are commonly isolated in bite wounds. Eikenella corrodens, an anaerobic
gram-negative rod, is found in about one third of human bite wounds. Pasteurella multocida, a
facultative anaerobe, is present in the flora of most cats and dogs and is often the cause of early
presentations of animal bite infections. Immunocompromised patients are at risk for fulminant
sepsis triggered by fastidious gram-negative bacilli found in dog or cat bite wound infections. A
frequent problem for the emergency physician is the evaluation of clenched fist injuries to the
metacarpophalangeal joints by human teeth, or "fight bites." After adequate exploration for
tendon or joint involvement and radiographic exclusion of foreign bodies, conservative
management is warranted. The wound should be copiously irrigated and, as with all bite or
contaminated wounds to the hand, left open to heal by secondary intention. Delayed primary
closure may be used for significant wounds in about 4 days if the wound has not become
infected. Patients with wounds involving joint, tendons, or deep spaces should be admitted for
intravenous antibiotics and irrigation in the operating room.

Prophylactic antibiotics for bite wounds should be initiated in all but very superficial wounds.
Either amoxicillin with clavulanic acid, a combination of penicillin plus dicloxicillin, or a
combination of penicillin and a first-generation cephalosporin should be adequate prophylaxis
for bite wounds of the hand. The patient should return at 24 hours for wound re-evaluation of
the wound. Established infections require consultation for admission and intravenous antibiotics.
Infections of the hand can spread to deep hand spaces or precipitate an osteomyelitis of the
underlying bone.

Therefore in summary treatment entails:

136
  Tetanus booster (0.5 cc Tetox)
 Broad spectrum antibiotics (Penadur)
 Extensive irrigation
 Leave wound open

Diagram Showing Incision for the Various Infections

137
Carpal Tunnel Syndrome

This is the most common entrapment neuropathy. It is characterized by compression of the

median nerve within the carpal tunnel which lies between the carpal bones and the flexor
retinaculum leading to impaired sensory and motor function of the hand over the distribution of
the median nerve. It occurs most often in patients 30 – 60 years old and is 5 times more common
in women than men. Older, overweight and physically inactive people are more likely to develop
Carpal Tunnel Syndrome.

Anatomy
The carpal tunnel is a open ended fibro osseous rigid compartment.
BORDERS
Floor : Bony Carpals
Walls : Bony Carpals
Roof: Transverse Carpal Ligament / Flexor Retinaculum

CONTENTS
1. Median nerve and its blood supply
2. Long flexor tendon of
 Flexor digitorium superficialis
 Flexor digitorium profundus
 Flexor pollicis longus
3. Lymphatics & Fat

The median nerve runs within the forearm beneath the flexor digitorum superficialis . It emerges
on the radial side of the tendons lying deep to the palmaris longus tendon . It then passes through
the carpal tunnel but before doing so gives off a palmar cutaneous branch.
In the tunnel it lies just beneath the flexor retinaculum and comes in contact with it on bending
the wrist or fingers .In the hand it gives off a muscular recurrent branch that supplies the thenar
muscles (flexor pollicis brevis, opponens pollicis, abductor pollicis brevis) and palmar digital branches which supply the
radial three and a half digits as well as the nail beds and distal dorsal skin.

138
T he car/Jal tunnel and the rout.e
o the medinn n erve

- carpal tunnel

Cross secUon orlhe wrls l

139
Aetiology
Due to the rigidity of this canal any factor decreasing the space will cause pressure against the
structures within. Particularly vulnerable to this is the median nerve.
Known aetiological factors include any:
- Increase in Volume of Contents e.g. pregnancy
- Decrease in size of the tunnel e.g. Trauma scarring & fibrosis
- Susceptibility e.g. Inflammatory conditions

Causes and Contributing Factors in Carpal Tunnel Syndrome

Aberrant anatomy Metabolic conditions

Anomalous flexor tendons Acromegaly
Congenitally small carpal canal Amyloidosis
Ganglionic cysts Diabetes
Lipoma Hypothyroidism or hyperthyroidism
Proximal lumbrical muscle insertion z
Thrombosed artery Increased canal volume
Congestive heart failure
Infections Edema
Lyme disease Obesity
Mycobacterial infection Pregnancy
Septic arthritis
Trauma
Inflammatory conditions Trauma caused by repetitive hand
Connective tissue disease motion especially in patients whose jobs
Gout or pseudogout require repeated forceful finger and wrist
Nonspecific flexor tenosynovitis* flexion and extension
Rheumatoid arthritis
Labourers using vibrating machinery as
are office workers especially typists and
data entry clerks

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*--Most common cause of carpal tunnel syndrome.

T- trauma
I- CVD, gout, flexor tendon tenosynovitis, Speptic arthritis, Lyme disease, mycoplasma
infection,
N- ganglion, lypoma
M – Acromegaly, thyroid dystrophy, diabetes, amyloidosis
↑contents/↓space- odema, pregnancy, obesity, congestive heart failure, abnormal attachment of
lumbricals

Pathology
As mentioned before, this condition occurs as a result of an increase in the pressure within the
carpal tunnel. The resultant pain experienced is thought to be due to ischaemia to the median
nerve rather than direct nerve damage.

Clinical Features
History
- Pain, numbness, tingling in the distribution of the nerve i.e. radial three and a half digits.
- Symptoms worse at nights with accompanying sleep disturbance due to pain ( nocturnal
parenthesis)
- Shaking, massaging, or elevating the hands can sometimes gain relief.
- Pain may radiate up the forearm to the elbow.
- Decreased grip strength with loss of dexterity. Dropping objects and less capable of
performing fine motor movements such as gripping or pinching.
- Symptoms are more common when a flexed wrist posture is assumed.

Physical Examination
Initially no findings
Atrophy of thenar muscles depending on severity
Blunting of sensation over median nerve

Blunting of Sensation

141
This occurs over the radial 3½ digits but not over the thenar eminence which is supplied by the
palmar branch of the median nerve that comes off above the flexor retinaculum and passes
superficial to it.
This fact can be used to differentiate CTS from median nerve damage at a higher level.

Tinel’s Test
Percussing / Tapping the volar wrist over the median nerve. A positive sign if there is resulting
shooting or shocking pain into hand over radial 3 ½ digits.
Positive in Carpal Tunnel Syndrome.

Phalen’s Test
Holding wrist in flexion for 60 seconds .A positive if there is resulting tingling / paresthesia in
the radial three and a half fingers.
Positive in Carpal Tunnel Syndrome.

Loss of two point discrimination.

Differential Diagnosis
These must be considered and ruled out due to the broad spectrum of symptoms associated with
Carpal Tunnel Syndrome.
1. Cervical Radiculopathy
2. Collagen Vascular Disorders
3. Thoracic Outlet Syndrome
4. Raynaud’s Phenomenon
5. Peripheral Neuropathies
6. Other Peripheral Entrapment Syndromes eg. Pronator syndrome

Investigations
- Nerve Conduction Studies : investigation of choice for site and severity of compression
- Electromyography
- Computed Tomography Scanning: displays bony structure but not soft tissue.
- Ultra Sound: does not show soft tissue planes adequately.
- Magnetic Resonance Imaging: Good soft tissue and bony imaging.
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Treatment
Based on the degree of severity, treatment is conservative or surgical. Aimed at relieving pain,
restoring normal sensation and preventing the problem from becoming worse.

Conservative
 Treat underlying condition
 Rest or Splint to restrict movement of wrist. Depending of the severity of the condition,
the splint may be worn during the day and/or night.
 (The length of time the splint is needed varies; usually a splint is worn until symptoms
subsided, which may be about 4-6weeks).
 NSAIDS to relieve pain.
 Steroid injections may produce temporary symptomatic relief.
Hydrocortisone/methylprednisone may be injected into the carpal tunnel to
decrease swelling.
Approximately 80 percent of patients with carpal tunnel syndrome initially respond to
conservative treatment; however, symptoms recur in 80 percent of these patients after one
year.

Surgical

More severe symptoms require surgical intervention via division of the flexor retinaculum to
decompress the median nerve. This may be performed endoscopically.

NB. Physiotherapy may be needed in severe cases in order to regain proper hand function.

Procedure - In carpal tunnel release surgery, the goal is to divide the transverse carpal ligament in two. This is a wide ligament that runs across the hand, from the

scaphoid bone to the hamate bone and pisiform. It forms the roof of the carpal tunnel, and when the surgeon cuts across it (i.e., in a line with the ring finger) it no

longer presses down on the nerve inside, relieving the pressure.

There are several carpal tunnel release surgery variations: each surgeon has differences of preference based on their personal beliefs and experience. All

techniques have several things in common, involving brief out patient procedures; palm or wrist incision(s); and cutting of the transverse carpal ligament.

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De Quervain’s Tenosynovitis

De Quervain’s disease is a stenosing tenosynovitis of the extensor pollicis brevis and abductor
pollicis longus in the first dorsal extensor compartment of the hand causing pain over the radial
styloid on movement.

The condition is a very common presentation occurring more often in middle aged women in an
8: 1 ratio of women to men.

The cause is unknown, however, it is thought that repetitive forceful ulnar deviation of the wrist
with the thumb adducted and flexed as during lifting of objects is a common inciting factor. As a
result it is found to be more common in mothers of infants , women who wash or those with jobs
that require recurrent activity of the hands e.g. Cooks in lifting a frying pan, causing limited
activity. The condition may also be seen in pregnancy, congestive cardiac failure and chronic
renal failure due to peripheral edema.

Pathophysiology
The abductor pollicis longus and extensor pollicis brevis tendons belong to the first extensor
compartment. The stenosis occurs at a point where the direction of the tendons changes, that is,
where they cross the tip of the radial styloid process. Excessive friction from over-use causes a
reaction leading to inflammation of the tendons within their fibrous sheath beneath the extensor
retinaculum. As result there is associated swelling within a confined space which may lead to
entrapment of the superficial branch of the radial nerve also. This resultant pain and swelling
may further accentuate the obstruction to movement.
The tenosynovitis preceding the stenosis may result from a subclinical collagen disease or
recurrent mild trauma.

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Tendon affected by De Quervain's tenosynovitis:

The most common presentation is that of a middle aged female complaining of pain over the
dorsolateral aspect of the wrist provoked by lifting activities or movement of the wrist and thumb
.The following differentials may however be entertained :

- De Quervain’s Tenosynovitis
- Carpal Tunnel Syndrome
- Rheumatoid Arthritis
- Cervical Radiculopathy

Diagnosis of the condition is based on history and clinical examination. With DeQuervain’s there
is usually complaint of tenderness on palpation over the radial styloid. The overlying inflamed
tendon sheath may be thickened forming a visible and bone hard mass presenting as a firm
nodule on palpation. The best test for aiding in diagnosis is the Finkelstein’s Test where the
patient is asked to place the thumb in the palm and close the fingers over it. The physician then
gently moves the patient’s wrist into ulnar deviation. This maneuver causes maximal distal
excursion of the tendons and incites sharp pain at the radial styloid as a positive sign for
DeQuervain’s Tenosynovitis.

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Treatment
Management of the disease is initially conservative if the pain persists however; surgery is then
the treatment of choice.

Conservative

 Analgesia with physiotherapy and occupational modification

 Rest the thumb and wrist by wearing a wrist and thumb spica splint
 Steroid injections with methylprednisone to help decrease the inflammation and
swelling. The use of corticosteroid therapy in treating the disease is most
successful within the first six weeks after onset of the pain. Ten to twenty
milligrams of a prednisone suspension mixed with four to five milliliters of the
local anaesthetic 1% lidocaine are injected adjacent and parallel to the tendon
sheath at the area of maximal tenderness, just distal to the radial styloid. This
peritendinous infiltration may be repeated one or two times at one to two week
intervals, if necessary

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Surgical
 Indicated if the symptoms are long-standing or unresponsive to conservative
management
 Almost always curative and performed on an outpatient basis
 Involves a longitudinal incision of the tendon sheaths under local anaesthetic ( de-
roofing). Take care to avoid the sensory branch of the radial nerve – this is one of
the common and most important complications. This allows for unrestrained
tendon gliding.

After surgery, failure to obtain complete relief may be the result of

1) neuroma formation due to severing the branch of the radial nerve

2) volar subluxation of tendona because too much of the sheath is
removed
3) failure to find and release a separate aberrant tendon within a
separate compartment
4) hypertrophy of scar due to the longitudinal skin incision
.

As a result this procedure should be carried out with caution.

Trigger Finger

Trigger finger (Digital Tenovaginitis Stenosans) is a common condition where there is

thickening and constriction of the mouth of a fibrous digital sheath which interferes with the free
gliding of any digit in the hand. This condition is four times more common in women than in
men. The peak incidence occurs in individuals age fifty to sixty years, but it also occurs in
infants and young children. It occurs in the fingers (more so third and fourth) of middle aged
(adult type) and in the thumb of young children (infantile type). However, it can involve any
digit of the hand.

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Aetiology

In most cases the aetiology of trigger finger is unknown. However, systemic causes of the
condition include collagen vascular diseases, rheumatoid arthritis, diabetes mellitus, psoriatic
arthritis, amyloidosis, hypothyroidism and sarcoidosis. It may also occur secondary to infections
such as tuberculosis.
Trigger finger may be caused by highly repetitive or forceful use of the finger and thumb.
Prolonged, strenuous grasping, such as with power tools, may also aggravate the condition.
Congenital cases of trigger thumb generally are due to a nodule of the flexor pollicis longus
tendon. Farmers, industrial workers and musicians who rely on their fingers or thumbs for
multiple repetitive movements, frequently are affected by trigger finger.

Pathology

The underlying pathology of this condition involves a mismatch between the size of the flexor
tendon and its fibrous flexor sheath. The proximal part of the fibrous flexor sheath at the base of
a digit becomes thickened thereby constricting the mouth of the sheath. This leads to a
disproportionate width of the tendon, in that there is a decrease in the width opposite to the
constriction and swelling proximal to it. The nodular or swollen segment enters the narrowed
opening of the sheath with difficulty when an attempt is made to extend the finger, and this is
associated with a snapping sound.

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There are two classes of tenovaginitis (inflammation of a tendon sheath):
1) Adult Type
 Occurs in the fingers of middle-aged females mostly
 In patient with associated collagen diseases, several fingers may be involved

2) Infantile Type7C
 Occurs in the thumb of infants and young children
Adult Type

Presentation
 Tenderness at the base of affected finger
 Locking of finger in full flexion

 Locking may be overcome by either forceful effort or passive extension of the

fingers with the other hand
 Extension results in a click or snap

Examination
 Palpable nodule (usually slightly tender) at the base and will move with the
tendon

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 Infantile Tenovaginitis

Infantile Type

Presentation
 Presents with thumb locked in flexion
 May or may not be able to passively extend the thumb, therefore, sometimes
mistaken for a dislocation thumb or congenital anomaly

Examination
 Palpable nodule at base of the thumb

Diagnosis is usually based on history and clinical examination although the snap feature may be
difficult to reproduce on active movement.

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General Clinical Presentation:

Patients will usually present with a history of painful snapping of a digit during flexion and
extension. The digit may become stiff and locked down in a particular position, usually flexion
and requiring gentle passive manipulation to achieve full extension. Pain may be radiated over
the distal palm and along the digit. A nodule is usually palpable at the base of the finger and
there is tenderness over the affected digit. This nodule correlates with the swollen segment of the
tendon. In longstanding cases, the patient may be completely unable to straighten the locked
trigger finger. Infants and young children present with a fixed locked digit, usually the thumb,
which cannot be extended. Signs of underlying systemic conditions such as rheumatoid arthritis
may also be evident in them. It should be noted that because the deformity is often resistant to
correction, this condition in infants is often mistaken for a dislocated thumb or for a congenital
deformity.
Trigger finger is a clinical diagnosis. The nodule in the tendon may be easily palpated
and an audible snap appreciated when the triggering is released by forced extension of the digit.
Radiological studies are of little value.

Green’s classification

This is used only for clinical grading and documentation.

Grade 1 – Pretriggering – Pain; history of catching that is not demonstrable on clinical

examination; tenderness over the A1 pulley

Grade 2 – Active – Demonstrable catching but the patient can actively extend the digit

Grade 3 – Passive – Demonstrable locking requiring passive extension (grade 3A) or inability to
actively flex (grade 3B)

Grade 4 – Contracture- Demonstrable catching with fixed flexion contracture of the

proximal interphalangeal joint

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Differential Diagnoses:

Other causes that may simulate locking include:

 Collateral ligaments of the metacarpophalangeal joint catch on a bony prominence on the
side of the metacarpal head (osteophyte)
 Localized swelling on the Flexor digitorium profundus tendon trapped at the decussation
of the Flexor digitorium superficiales tendon
 Partially lacerated flexor tendon catches against the A1 pulley or Flexor digitorium
superficiales tendon decussation
 A nodule in the Flexor digitorium superficiales tendon catches against A3 pulley
 Locking is simulated by abnormal sesamoids
 Loose body present in the metacarpophalangeal joint
 Snapping or subluxating Extensor digitorium communis tendon

Management:

Treatment for trigger finger varies depending on the severity and duration. For mild infrequent
cases the following steps may be taken:-
Conservative Management
- Rest
To prevent the overuse of the fingers change or curtail daily activities that requires repeated
gripping action.
- Splinting
The metacarpophalangeal joint is splinted in approximately fifteen degrees of flexion.
Keeping the affected finger in a splint in the extended position for several weeks will aid in
resting the joint. It also prevents curling of the fingers during sleep which may exacerbate
the condition on waking.
- Gentle Finger Exercises & massage
This helps in maintaining the mobility of the fingers .Massage will help to reduce the pain.
- Soaking in warm water
May help to reduce the catching sensation.

For severe cases:

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Conservative Management
- Use of non steroidal anti inflammatory drugs.
This helps in reducing the inflammation and swelling of the tendon sheath
- Injection of steroids into the tendon sheath may help reduce inflammation. Typically, such
injection is performed using a 25-gauge needle to inject a mixture of 0.5-1.0 mL of 40
mg/mL corticosteroid (eg, methylprednisolone) and 0.5 mL of 1% lidocaine (without
epinephrine). A second corticosteroid injection may be performed 3-4 weeks later. The cure
rate for this conservative type of management is > 95%. It is thought however that if two
injections have not solved the triggering it is unlikely that further injections will and
additional injections risk weakening the tendons with subsequent tendon rupture.
Surgical Intervention
Indications
- Failure of splint / injections
- Irreducibly locked finger
- Trigger thumb in infants (without release via surgery these infants are likely to develop a
fixed flexion deformity of the interphalangeal joint.)

If the above measures fail then last resort is to surgically incise the fibro osseous canal to
allow the thickened tendon to glide without restraint. This may be done under local
anaesthesia on an outpatient basis and gives the added benefit of noting the disappearance of
the pathology by asking the patient to flex and extend the affected digit. The opening of the
sheath is deemed sufficient when triggering is no longer noted. Post surgery the patient
should be advised to begin moving the finger to prevent tissue adhesion at the surgical site.
Non-steroidal anti-inflammatory drugs and elevation are advised for a period of two to three
days afterwards.
A simpler procedure involves releasing the friction by percutaneously tearing the sheath
with the use of a wide bore needle.

Complications of both surgical interventions include:

- Neurovascular damage. (The thumb is particularly more vulnerable as the bundle lies closer
to the anterior midline of the digit and is in closer proximity to the constricting tendon
sheath)
- Infection
- Stiffness and scarring.
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Ganglion

A ganglion is a non cancerous fluid filled sac that is most commonly found on the dorsum of the
wrist, less frequently the palmar aspect of the hand, on a finger commonly the thumb or on the
lateral aspect of the knee or ankle .Ganglion may however occur anywhere on the body .It is the
commonest cystic swelling in the hand affecting adults more commonly 70% occurring in people
between the ages 20 – 40 years.

The aetiology of this lesion is not known .Many theories have been put forward these include:-
- products of a degenerative process
- benign tumours of tendon sheath or joint capsule

Pathophysiology
As said before the aetiology is unknown. Ganglion cysts are thought to occur adjacent to a joint
capsule or tendon sheath. Many theories have been put forward:
-It is thought that where there is a tear in the ligaments overlying the lining of tendons or
joints this causes the lining to herniate out of the ligamentous defect causing swelling
under the skin . As inflammation is often associated with this, the inflamed tissue
produces a clear viscous fluid which fills the protruding sac .Whether the initial tear is due to
injury , degeneration or underlying pathology is not sure .
-It is believed that they may result from a trauma or degenerative process or are actually
benign tumors of tendon sheath or joint capsule.

The firmness of the swelling is dependent on the amount of fluid within the sac.

Clinical Features

Usually there are no symptoms as they are often painless.

-Site:
The most frequent site of origin is the dorsum of the carpal bones just radial to the tendons of
the extensor digitorum communis, that is, at the back of the wrist. Ganglia on the dorsum of

154
 the wrist are usually firm, smooth, fluctuant and round. They become more prominent when
the wrist is flexed forward. The second most frequent site is on the distal volar -radial aspect
of the wrist between the tendons of flexor carpi radialis and abductor pollicis longus. Other
less common sites include the base of the fingers in the palm, at the fingertips, the outer
aspect of the knee and ankle and on the dorsum of the foot. They are often painless, but the
patient may complain of aching or of a feeling of weakness as well as mild discomfort.

-Size & Shape: Small Cyst (0.5 – 1.0 cm) tend to be tense and spherical
Large Cyst tend to be flattened and soft

Other Features:

- Not adherent to skin but adherent to deep structures.

- Fluctuant
- Transilluminable
- Multilocular/Unilocular
- Reducibility : may slip between underlying structures e.g. neighbouring
Bones when pressure is applied.
May rupture into the subcutaneous tissue and so seem to
Disappear suddenly (usually refill in a few months)

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Treatment
A ganglion is harmless so if it is not causing pain or limiting motion the physician may opt to
observe the swelling for any changes after reassuring the patient that it is harmless. If painful or
causing mechanical problems or if patient finds it unsightly the treatment options available are as
follows:

- Aspiration
Involves removal of the contents by inserting a wide bore needle into the cyst under
local anaesthesia .This is followed by injection of an anti inflammatory agent e.g.
steroids into the cyst to reduce the inflammation and decrease subsequent refilling.
recently it has been found that injecting hyaluronidase along with steroids after
aspiration has increased the cure rate from 56 % with just steroids to 89% with
a combination .

- Surgical Excision
If aspiration fails, then surgical removal may be considered as an outpatient procedure.
this involves identifying the entire cyst and removing it along with a portion of the
underlying tendon or joint capsule to which it is attached . The hand is then
splinted for 7 – 10 days. The procedure can become complicated depending on if the
cyst is located to vital structures such as nerves or vessels.
Normal activity may be resumed after two weeks for ganglia of the fingers and four to
Six weeks for those of the wrist.
Ganglia may reoccur after a successful surgery.

Complications
If ganglia arise deep in the wrist or palm they may cause motor or sensory impairment if they
interfere with ulnar or median nerves or their branches. If this is the case it demands immediate
operative excision.

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Causes and Treatment of Scoliosis

Scoliosis is a term used to describe an abnormal lateral curvature and rotation of the vertebral
column .It is usually accompanied by an abnormal kyphosis and lordosis which is secondary to
rotation of the vertebral body towards the convexity of the curve and rotation of the spinous
process away from the convexity.

Incidence
In the United States it is reported to be a relatively common condition with the incidence
dependent on the degree of curvature being described. Scoliosis of greater than 25 degrees has
been reported in about 1.5/1000 persons in the United States.

Anatomy Overview

The vertebral column is made up of 31 vertebral bodies: cervical, thoracic, lumbar, sacral and
coccyx.

The normal thoracolumbar spine is relatively straight in the sagittal plane and has a double curve
in the coronal plane. As shown below, the thoracic spine is convex posteriorly (kyphosis) and the
lumbar spine is convex anteriorly (lordosis). Normally there should be no lateral curvature of the
spine.

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Pathology
Any part of the thoraco-lumbar spine may be affected. There is a primary curve with secondary
compensatory curves above or below. The recognized types are lumbar, thoraco-lumbar, and
thoracic scoliosis. Lumbar curves being less deformed than thoracic curves.
As the disease progresses, the vertebrae and spinous processes in the area of the major curve
rotate toward the concavity of the curve. On the concave side of the curve, the ribs are close
together. On the convex side, they are widely separated.
As the vertebral bodies rotate, the spinous processes deviate more and more to the concave side
and the ribs follow the rotation of the vertebrae. The posterior ribs on the convex side are pushed
posteriorly, causing the characteristic rib hump seen in thoracic scoliosis. The anterior ribs on the
concave side are pushed anteriorly.

158
Typical distortion of vertebra and ribs in thoracic scoliosis as seen from below
Scoliosis also causes pathologic changes in the vertebral bodies and intervertebral discs, as
shown below.

Vertebrae and intervertebral discs are decreased in height on the concave side

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Classification

Scoliosis may be classified into two main forms namely, structural and non-structural. These
may be further subdivided as follows:

 Structural scoliosis
1. Infantile
2. Idiopathic
3. Secondary

 Non-structural scoliosis
1. Compensatory
2. Sciatic

There is an intrinsic abnormality of the spine present in structural scoliosis. Non-structural

scoliosis, on the other hand, is a temporary condition in which the spine is relatively normal. It
usually occurs as a result of another problem such as a limb length discrepancy.

Structural Scoliosis

Infantile scoliosis
Infantile scoiliosis is a structural form of scoliosis, which occurs in children younger than
age 3 years. It is seen more often in boys than girls and primarily affects the thoracic spine. The
curve is convex to the left. This form of scoliosis has no known cause and so is also referred to
as infantile idiopathic scoliosis. It is believed that the position in which an infant is laid down
may be a causative factor.
This form of scoliosis may be progressive, usually increasing rapidly or it may resolve
spontaneously. A method of differentiating resolving curves from progressive ones has been
devised and is based on the development of the rib-vertebral angle (RVA). This angle is
measured by drawing one line perpendicular to the apical vertebral endplate and another from the
midline of the neck to the middle of the head of the corresponding rib. The angle is formed by
the intersection of these lines. The difference in the rib-vertebral angles on the concave and
convex sides of the curve is known as the rib-vertebral angle difference. It was found that the rib-
vertebral angle difference is consistently greater in progressive curves. In addition an initial rib-
160
vertebral angle difference of 20 degrees or more is considered to be progressive until proven
otherwise.

The management of infantile scoliosis will

therefore depend on the type of curve. Resolving curves require follow-up observation only with
radiographic examinations every 4 to 6 months until the curve resolves. If the curve is considered
to be progressive a thoracic-lumbar-sacral brace or cervical-thoracic-lumbar-sacral back brace
will be necessary. The brace should be fitted properly in order to prevent further progression and
significant improvement can be obtained during the early period of skeletal growth.
However in cases of severe curvature or if the curve increases in spite of the use of a back
brace combined anterior and posterior artrhodesis of the spine may be necessary. The spine may
still need to be controlled by a brace even after surgery until growth is complete.

Idiopathic scoliosis
Idiopathic scoliosis is the most common and most important form of structural scoliosis. It
occurs in healthy, neurologically normal children, but its exact cause is unknown. The incidence
is higher in girls than in boys, and the scoliosis is more likely to progress in girls and so requires
treatment. Idiopathic scoliosis can be divided into three groups on the basis of age at onset:
infantile (birth-3 years); juvenile (4-9 years); and adolescent (over 10 years). Adolescent
idiopathic scoliosis is much more common than juvenile-onset scoliosis; and infantile idiopathic
scoliosis is very rare.
The curvature of the spine is usually first observed at school or following a regular visit
to the family doctor. It typically involves the thoracic or thoraco-lumbar spine. Right thoracic
curves are the commonest type of idiopathic structural scoliosis. Left thoracic curves in
adolescents with idiopathic scoliosis are rare and require further investigation via MRI. Lumbar
curves are usually to the left.
A thorough history and physical examination is usually the first step in the evaluation of patients
with suspected idiopathic scoliosis. Asymmetry of the posterior chest wall on bending forwards,
known as the Adams test, is the most striking and consistent feature in patients with idiopathic
scoliosis. There may be other associated findings such as asymmetry in shoulder height, apparent
leg length discrepancy, flank asymmetry, and asymmetry of the anterior chest wall. In lateral
curvature of the thoracic spine there may also be dorsal angulation of the ribs producing a rib
hump.
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 Adams’sign

It should be noted that the overall visible deformity tends to be worse with thoracic scoliosis than
with lumbar scoliosis. In addition the lateral curvature of the spine tends to increase until the end
of spinal growth and so the earlier the age of onset is the worse the prognosis.
Risser’s sign refers to the degree of ossification of the iliac apophyses. An apophysis is a growth
plate outside of a joint. Examples of apophyses include the calcaneal, tibial and iliac apophyses.
Once the iliac crests are completely ossified further progression of scoliosis is minimal as full
skeletal maturity has been attained. Ossification begins shortly after puberty.

Risser’s Sign

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Risser’s Scale
1- 0-25% ossification of iliac apophysis
2- up to 50%
3- Up to 75%
4- Up to 100%
5- Fusion

Radiographic evaluation of the spine is important in order to assess the location and degree of the
curvature. Anterior-posterior and lateral radiographs of the spine, including the iliac crest distally
and most of the cervical spine proximally, should be obtained with the patient standing. Right
and left bending films are usually obtained only when the patient is being evaluated for surgery
or bracing. On X-ray a primary curve is evident with other curves above and below the primary
curve known as compensatory curves.The compensatory curve develops as a result of nature's
attempt to keep the shoulders levels or maintain the level of the pelvis so that the legs remain
parallel respectively.
It is important to determine the degree of curvature from the radiograph. This involves
the measurement of Cobb's angle. In determining Cobb’s angle, the degree of curvature is
measured by drawing lines on the X-ray at the upper border of the uppermost vertebra of the
curve and the lower border of the lowermost vertebra of the curve. Upper and lower ends of the
curve are identified as the levels at which vertebral symmetry is regained. The vertebrae towards
the apex of the curve are asymmetrical. The angle subtended by these lines is the angle of
curvature or Cobb’s angle. If Cobb's angle is 10 degrees or more the diagnosis of scoliosis is
confirmed.

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 Cobb method for measurement of scoliosis

Treatment of idiopathic scoliosis is based on the degree of curvature, the likelihood of significant
progression and on the presence of any pain. In adolescent idiopathic structural scoliosis most
curves < 20 degrees resolve spontaneously or remain unchanged. Certain factors have been
found to be related to curve progression and these include gender, stage, and Risser's sign.
Progression is more likely in girls than in boys, especially premenarchal females. Curve
progression in adolescent idiopathic scoliosis is generally during the rapid adolescent growth
spurt before the onset of menses. The incidence of progression decreases as the child gets older.
Risser's sign is the degree of ossification of the iliac apophysis as seen on a radiograph. It is used
as a measure of skeletal maturity. If the iliac apophyses are not ossified it is referred to as a
Risser sign of 0. It has been found that children with a Risser sign of 0 tend to have curves,
which progress, by 10 degrees or more.

The Cobb's angle is the primary indicator in determining the form of treatment; whether it is
conservative or operative. If Cobb's angle is less the 40 degrees non-operative treatment is
primarily indicated. Conservative management of idiopathic scoliosis may include observation or
the use of back braces. In general children with a mild degree of curvature less than 25 to 30
degrees require no treatment and are simply observed and reviewed every four to six months. If
the angle of the curve lies between 30 to 40 degrees a back brace is recommended as the

164
preferred form of treatment; as progression of the curve is more likely. It is of note that the brace
only prevents at most, further progression of the scoiliosis, they do not correct the abnormal
curvature.

Many different designs of spinal back braces are used for idiopathic scoliosis. They can be
classified into two categories: cervical-thoracic-lumbar-sacral braces and thoracic-lumbar-sacral
braces. An example of the former is the Milwaukee brace, while the Boston brace and
Wilmington plastic jacket are examples of the latter type of back brace. The basic principle of
both types of back braces is to control lumbar lordosis by producing a forward pelvic tilt of the
pelvic girdle. The Milwaukee brace is used to correct high thoracic curves with an apex above
the seventh thoracic vertebra. If the apex of the thoracic curve is at the seventh thoracic vertebra
or below, the Boston brace is then more suitable for such lower curvatures.

With the Milwaukee brace, the lateral lumbar curve is controlled by direct pressure from a
molded lumbar pad that is built directly into the pelvic portion of the brace. Adjustable metal
uprights are attached to the neck ring. The throat mold of the neck ring maintains head position
over the occipital pads. As the patient levers against the occipital pads, extension of the spine is
obtained. The Milwaukee brace has to be worn throughout the entire day to be effective.
However the Boston brace is usually more acceptable to patients. It is designed to control lateral
curvature by flattening excessive lumbar lordosis. Patient and family compliance with brace
treatment is important if results are to be seen.

Milwaukee brace

165
Operative treatment is however necessary in certain situations. These are an increasing curve in
the growing child, a Cobb's angle greater than 40 degrees, severe deformity (>50 degrees angle
of curvature) with asymmetry of the trunk, associated pain, thoracic lordosis and if the curvature
is not controlled by nonoperative management. Thoracic lordosis is a particularly significant
indication for surgery as it has a detrimental effect on pulmonary function, and bracing only
worsens thoracic lordosis. Significant cosmetic deformity is associated with 40-to 50-degree
angle curves. The child is usually very unhappy with his or her appearance and so this is an
indication for surgery in order to prevent possible psychological problems.

Surgical correction of idiopathic scoliosis usually involves fusion of the joints of the vertebrae in
order to correct the curve. Harrington distraction rods or other internal corrective implants are
commonly used. The Harrington rod is inserted into the concavity of the curve between two
hooks, placed under the laminae of the top and bottom vertebrae, and then forcibly elongated to
produce straightening. Post operatively the correction of the spine must be protected while fusion
occurs and so the patient is placed in a plaster jacket. This method of surgery tends not to address
the associated rotational deformity of the spine and so additional segmental sublaminar wiring
beneath and around the Harrington rod at each vertebral level is recommended. This technique
will also provide more rigid fixation of the spine.

There are other methods of spinal instrumentation, which may be employed, for the correction of
more severe curvatures. Anterior correction and fixation using the Zielke instrumentation may be
used. The Luque technique is another alternative method, which involves fixation with metal
rods secured to the vertebrae posteriorly by multiple-level sublaminar wiring. Posterior
correction with devices that can be attached securely to the vertebrae by means of long pedicle
screws are used in Cotrel-Dubousset instrumentation. External correction by distraction between
a screwed-on metal skull band above and a pelvic band below may also be used. However it is to
be noted that neurological injury is a major risk with all of these various techniques.

Secondary scoliosis

Secondary scoliosis is another form of structural scoliosis but in this case the cause is
known. The abnormal lateral curvature of the spine is secondary to an underlying condition,
which may be neuropathic, myopathic or osteopathic. Neuropathic conditions include
poliomyelitis, cerebral palsy and neurofibromatosis. In these conditions the scoliosis is due to the
residual weakness of the nerves and muscles which support the spine, and so may be referred to

166
as neuromuscular or paralytic scoliosis. Muscular dystrophy is a myopathic condition, which
may cause a secondary scoliosis. Osteopathic problems such as congenital abnormalities of the
vertebrae, for example hemivertebrae or fused vertebrae (there is dedifferentiation of the
veretebrae resulting in vertebral fusion), are also common causes of secondary scoliosis.

The three most common causes of secondary scoliosis are congenital hemivertebrae,
polio and neurofibromatosis. In the patients with poliomyelitis the scoliosis is primarily due to
the unequal pull of muscles on both sides of the spine. The mechanism of scoliosis in
neurofiromatosis is still unclear.

The goal of treatment for secondary scoliosis is to restore spinal alignment, stabilize respiratory
function, and prevent progressive loss of independence. Thus the basic treatment modalities are
similar to those for idiopathic scoliosis: that is observation, use of back braces, and surgery.
Many cases of secondary scoliosis will however require operative intervention. Overall the aim
of treatment of structural scoliosis is to minimize progression or to correct the deformity to an
acceptable level at skeletal maturity.

Non-Structural Scoliosis

Compensatory

In non-structural scoliosis there is no underlying abnormality of the spine and the scoliosis is
therefore temporary. This form of scoliosis mainly involves compensatory scoliosis and sciatic
scoliosis. Compensatory scoliosis is usually a lumbar scoliosis, which develops in situations of
limb length discrepancy. The pelvis in such patients tilts toward the short side, producing a
postural curve in the opposite direction. It may also occur in patients with a fixed abduction or
adduction deformity at one of the hip joints. In both situations the lumbar spine is curved through
an angle equal to the pelvic tilt in order to maintain a vertical trunk. Treatment is therefore
unnecessary, as the scoliosis will resolve spontaneously once the pelvic tilt or limb length
discrepancy is corrected. However it the underlying problem remains untreated for a prolonged
period of time the lumbar scoliosis may become fixed by adaptive shortening of the tissues on
the concave side.

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Sciatic

Sciatic scoliosis is another temporary deformity produced by the protective action of muscles in
certain painful conditions of the spine. The underlying cause is usually a prolapsed disc, which
impinges on a lumbar or sacral nerve root of the sciatic nerve. An abnormal posture is
involuntarily assumed in order to reduce the pressure on the affected nerve and this causes the
development of a lumbar scoliosis. There is no associated rotation of the vertebrae. Patients will
present with a history of sudden onset of severe back pain, exacerbated by movement of the
spine. Management of this type of scoliosis mainly involves providing pain relief and addressing
the underlying problem.

Investigation of Bone Tumors

Tumors of the bone are named after the primary type of tissue matrix formed by the
tumor itself. They can be divided into benign and malignant, with the malignant tumours being
further classified as primary or secondary. Secondary malignant tumours of bone are malignant
tumours that arise in another tissue in the body and metastasize to bone.
Bone tumours may be classified as:
 Benign
 Malignant
Primary
Secondary
- due to metastases from other malignant primaries
- extension into the bone from adjacent soft tissue malignancies
- malignant change of a previously benign lesion

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Classification of Bone Tumours
Cell Type Benign Malignant
Bone Osteoid Osteoma Osteogenic Sarcoma
Osteoblastoma

Cartilage Chondroma Chondrosarcoma

Osteochondroma

Fibrous Tissue Fibroma Fibrosarcoma

Marrow Eosinophilic Granuloma Ewing’s sarcoma

Multiple Myeloma

Vascular Haemangioma Angiosarcoma

Uncertain Giant Cell Tumor Malignant Giant Cell

( Osteoclastoma) Tumour
Cysts

Secondary Bone Tumours are commonly metastases of malignancies of the paired organs:
- Thyroid/Parathyroid
- Breast (most common 35%)
- Lung
- Adrenals
- Kidneys
- Prostate ( 30 % )

Tumours spread to bone by

 Direct invasion
 Haematogenous spread
 Lymphatic spread
 Spread by paravertebral venous plexus

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 Most common malignancies producing skeletal metastases:

More than 75% of skeletal metastases originate from

carcinomas of the prostate, breast, kidney, and lung. Also
Adults
common are metastases from thyroid and colon cancers. And
do not forget melanoma.

Children Neuroblastoma, rhabdomyosarcoma, and retinoblastoma

Radiographic appearance of the metastatic tumors can be

-Purely lytic (kidney, lung, colon, and melanoma)
-Purely blastic (prostate and breast carcinoma)
-Mixed lytic and blastic (most common appearance)

The diagnosis of a true tumour of the bone is very important both in therapeutic and
prognostic considerations. It is based on
1. Clinical features - A thorough clinical assessment eliciting the history and physical signs
is the first essential step
2. Laboratory investigations
3. Imaging technology- including both plain radiography and the modern imaging
technologies
4. Biopsy

If the clinical examination and/or plain radiographs suggest an aggressive or malignant

tumour, staging should be performed before biopsy. All radiographic studies are influenced by
surgical manipulation of the lesion, making interpretation more difficult. Bone scintigraphy,
computed tomography (CT) or MRI, and angiography are required to delineate local tumour
extent, vascular displacement, and compartmental localization.

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Clinical Picture

History
Age of the patient: Certain tumours occur more commonly in certain age groups.

Most common benign Most common malignant

Age group
lesions tumors

Ewing's sarcoma
simple bone cyst
0 - 10 leukemic involvement
eosinophilic granuloma
metastatic neuroblastoma

non-ossifying fibroma
fibrous dysplasia
simple bone cyst
aneurysmal bone cyst osteosarcoma,
10 - 20 osteochondroma (exostosis) Ewing's sarcoma,
osteoid osteoma
osteoblastoma
chondroblastoma
chondromyxoid fibroma

enchondroma
20 - 40 chondrosarcoma
giant cell tumor

metastatic tumors
myeloma
leukemic involvement
40 & above osteoma
chondrosarcoma
osteosarcoma (Paget's
associated)

Pain: Although a no specific symptom it aids in the differential diagnosis. It may

However be as a result of:

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  Growing lesions. This category includes locally aggressive lesions (e.g., aggressive
osteoblastoma ), and malignant tumors
 Pathologic fracture complicating either benign or malignant tumor
 Significant local tissue reaction to the tumor.

Osteoid Osteoma – Commonly presents with intensive night pain.

Location of the Problem Region: Many lesions favor certain bones

Lesions Most common skeletal sites

Ewing's sarcoma Hematopoietic marrow sites in the axial

Multiple myeloma skeleton (vertebrae, ribs, sternum, pelvis,
Leukemia/lymphoma cranium) and proximal long bones (femur,
Metastatic cancers humerus)

Metadiaphyseal regions of the tibia and distal

femur (80%) Does not occur in the flat
Non-ossifying fibroma
bones, craniofacial bones, the spine, or the
small bones of the hands/feet.

The vast majority of SBCs is found in the

Simple bone cyst proximal humerus (55%) and proximal
femur (20%).

Adamantinoma Mid-shaft of tibia (90%), jaw bones

Long bones (knee area, proximal humerus)-

Chondroblastoma
70%

Giant cell tumor Knee area, distal radius (65%)

Small bones of the hands and feet (60%).

Enchondroma This is in fact the commonest tumor at these
sites.

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 Chondrosarcoma (primary,
Tends to develop in the axial skeleton with
and to the less extent
25% to 30% occurring in the pelvic bones
secondary)

Fibrous dysplasia Femur, tibia, skull and ribs

Osteochondroma Knee area, proximal humerus, pelvis

Osteoblastoma Spine (30%), mandible, long bones

Osteogenic Sarcoma Proximal Tibia , Distal femur

Aneurysmal bone cyst Any bone; common in the spine

Knee area (30%), pelvis, small bones of the

Chondromyxoid fibroma
feet

Hemangioma Spine, craniofacial bones

Constitutional Symptoms: Weight loss, night sweats, fever, decreased appetite

NB Another important feature of bone tumour is the high risk of developing pathological
fractures especially in the infiltrated area of bone. This is more prevalent in patients with
metastatic bone disease, where approx. 10% of patients with metastatic bone tumours will suffer
from pathological fractures. The commonest sites of spread include the lumbar vertebrae, pelvis,
ribs, and long bones. In the case of spread to the vertebrae there can be spinal cord compression
leading to neurological signs.

Examination
 Swelling, local tenderness, deformity
 General, wasting, anorexia in case of malignant tumors
 May reveal primary focus of a metastatic lesion
 Symptoms associated with metastatic spread to other areas
 Deformity often associated with osteochondroma
 Thorough physical examination of breast, prostate, thyroid, etc. if history suggestive of
pathology in any of the organ systems
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 Pathological fracture is the other common presentation
In adults, a pathological fracture is likely to be secondary to metastasis whereas in
children it is likely to be secondary to a benign lesion such as a simple bone cyst.

Investigations
1) Complete Blood Count : Haemoglobin, Platelets and White Blood Cell Count
May give evidence of anaemia, thrombocytosis suggestive of multiple myeloma or
metastatic disease. Anaemia of malignancy usually a normochromic normocytic one.
2) C Reactive Protein : More sensitive than ESR
3) ESR : > 100 — bone tumour or multiple myeloma are of two differential diagnoses
Elevated ESR in infection, malignancy, collagen vascular disease.
4) Urine & Electrolytes to check renal function
Calcium, phosphate, proteins- albumin and globulin: multiple myeloma
Hypercalcemia may sometimes occur when there is excessive bone resorption
from widespread bone mets.
Serum globulin increased (multiple myeloma), ratio albumin-globulin 2:1 is
reversed.
5) Liver function tests (LFT’s)
6) Uric acid levels & urine examination (e.g., Bence-Jones protein in Multiple Myeloma.)
gives an idea about turnover of the disease
7) ALP
increased in bone forming tumours
8) PSA (acid phosphatase increased)
if metastatic prostate Ca is suspected, especially in elderly males
9) Thyroid function tests
if metastatic thyroid Ca is suspected
10) Lactate Dehydrogenase
prognostic factor in osteogenic sarcoma
increased levels suggest poor prognosis
11) Blood film
leukaemia , Rouleaux Formation – Multiple Myeloma
12) Protein Electrophoresis : M protein : Multiple Myeloma

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13) Radiological assessment

Radiological Findings
Plain radiography still has big role to play in arriving at an accurate diagnosis. Five
parameters are used:

1. The anatomical location of the lesion.

The tumour can be grouped according to the anatomical location as follows:
Diaphyseal : e.g. Ewing's Sarcoma
Diaphysio Metaphyseal : e.g. Chondrosarcoma
Metaphyseal : e.g. Osteosarcoma
Metaphysio Epiphyseal : e.g. Giant Cell tumour
Epiphyseal : e.g. Chondroblastoma

2. The borders of the tumour.

 Well defined border, a narrow transitional area and a reactive sclerosis means a
benign lesion
 Poorly defined margins indicate a malignant lesion.

3. Pattern of bone destruction

i. geographic pattern (slow growth)
ii. moth eaten pattern (moderate growth)
iii. permeative pattern (rapid growth)

4. Matrix formation: New bone formation is another parameter to be observed and may vary
from woolly masses to dense sclerosis.

5. Periosteal reaction is seen as a non-continuous and often laminated appearance. E.g. Sunray
appearance, Onion peel appearance.

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X-rays
Plain radiographs taken in perpendicular planes – antero-posterior (AP) and lateral –
remain essential to the characterization and diagnosis of lesions involving the skeleton. Selection
and interpretation of other imaging technique is often guided by the radiographic properties of
the lesion. Proper interpretation of a lesion seen on a radiograph can be summarized by
answering Enneking’s “four questions”:
 What is the anatomic location and extent of the lesion?
 What is the lesion doing to the bone?
 What is the bone doing to the lesion?
 Are there any radiographic peculiarities of the lesion that give a hint as to its tissue type?
Distinction between benign, aggressive, and frankly malignant lesions can be based upon this analysis.

There are differences in the appearance of benign and malignant tumors evident on plain x ray.

Parameter Benign Malignant

Rate of Growth Slow therefore body has Rapid Growth with ill
sufficient time to wall off defined borders
tumor. Well defined area of
sclerosis
Bone Destruction Thin the cortex making Bony destruction with soft
bone prone to fracture tissue extension
Skip Lesions None Present
Periosteal Reaction None Present

Computed Tomography scan

CT scans can identify the bony components of the tumour wall.It can assess bone formation or
calcified lesions and evaluate the integrity of the cortex. It is the best study to localize the nidus
of an osteoid osteoma. Computed tomography scanning allows accurate determination of intra-
and extraosseous extension of skeletal neoplasm. It accurately depicts the transverse anatomic
relationship of a tumour to the surrounding structures. By varying window settings, one can
study cortical bone, intramedullary space, adjacent muscles, and extraosseous soft tissue
extension. The anatomic compartmental involvement by soft tissue sarcomas is easily
determined.

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 Core needle biopsies guided by CT have proved to be effective in obtaining tissue for
diagnosis from difficult to reach or clinically occult sites.

CT of chest—most effective way of detecting pulmonary mets.

CT of Abdomen – can reveal abdominal malignancies.

Magnetic Resonance Imaging

MRI is now accepted as an accurate and valuable imaging technique and can provide high
contrast images in multiple planes. Excellent visualization of anatomic compartments,
neurovascular bundles, and areas of reactive tissue allows for detailed preoperative planning of
resection margins. Skip metastasis can be strikingly apparent and readily identifiable on sagittal
images. However, distinction between benign and low-grade malignant lesions (such as lipomas
versus well differentiated liposarcomas) cannot be reliably made based upon the MRI images
alone.

Nuclear Bone Scan

This is the best technique for detecting occult metastatic deposits in bone. It has a higher
sensitivity than x-rays and may identify other asymptomatic lesions. Nuclear bone scans also
picks up osteoblastic activity. Bone scintigraphy is useful for evaluating both bony and soft
tissue tumours. It assists in detecting metastatic disease, polyostitic involvement, intraosseous
extension of tumour, and the state of the bone underlying a primary soft tissue sarcoma.
Malignant tumours may present with skeletal metastasis (1.6%). The initial flow phase
corresponds to the vascularity of the tumour. Also histological tumour response to chemotherapy
can be predicted based upon comparison of pre- and post-treatment studies.

Angiography
A minimum of two views (biplane) is necessary to determine the relation of the major
blood vessels to the tumour. Extraosseous extension is easily demonstrated by angiography. As
experience with limb-sparing procedures has increased, surgeons have become aware of the need
to determine individual vascular patterns prior to resection. This is especially crucial for tumours
of the proximal tibia, where vascular anomalies are common. The increasing use of preoperative
intra-arterial chemotherapy has also increased the need for accurate angiography. Reduction of

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vascularity following chemotherapy can be correlated to the overall histologic response of the
tumour.

Other Investigations
The gross appearances of a tumour may be of diagnostic assistance however the microscopic
appearances are diagnostic, particularly when they are compatible with all other features, and no
diagnosis is acceptable in the absence of histological confirmation, which is obtained by biopsy.

Biopsy
A biopsy should be performed after the staging studies are obtained. If a resection is to be
performed, it is crucial that the location of the biopsy be in line with the anticipated incision for
the definitive procedure. Extreme care should be taken before biopsy not to contaminate
potential tissue planes or flaps, thus compromising the management of the lesion. Improper
biopsy technique often eliminates the opportunity for limb salvage technique. Thus the
Musculoskeletal Tumour Society has adopted the policy that only the surgeon who will
ultimately perform the final tumour resection should perform biopsies.

Biopsy is the most crucial procedure in the diagnosis of musculo-skeletal lesions. The
appropriate treatment cannot be initiated until the correct tissue diagnosis is available. Prior to
the biopsy, all specialists who may ultimately become involved in the patient's care should be
consulted as to the status of work up and pre-biopsy differential diagnosis.

Open Biopsy
Open biopsy has been the conventional method. It requires an incision under operating
room conditions. The least differentiated or least mineralized portion of the neoplasm is selected,
since this is usually the most representative portion of a malignant lesion. The periphery of any
malignant tumour is the most viable and diagnostic portion of the tumour, whereas the central
region is often necrotic

Closed Biopsy
A closed biopsy implies that no incision is required and that the tissue specimen is
obtained through skin puncture by a needle or trephine. It can be done under local anaesthesia

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and minimizes tissue contamination. Nowadays trocar biopsy is used widely. It cannot be done in
osteosclerotic bone tumours.

CT Assisted Needle Biopsy

Accurate localization of the tumour in sites like the spine and pelvis by CT enable closed
biopsy of these lesions. This avoids major surgical procedures for biopsy purposes. This can also
be done with image intensifiers.

To minimize contamination and reduce patient morbidity, needle biopsy of soft tissue masses
or extraosseous components should be attempted prior to an incisional biopsy whenever
possible. Needle or core biopsy of bone tumours often provides an adequate specimen for
diagnosis. Cooperation between the radiologist and the pathologist is vital to ensure that
adequate tissue is obtained. Radiographs should be obtained to show the position of the
trocar. Core biopsy is preferred if a limb sparing option exist, since it involves less
contamination. Also core biopsy has been shown to be as accurate as open biopsies and more
cost-effective. It is especially helpful in areas like the spine, pelvis and hips. If a core biopsy
proves to be inadequate a small incisional biopsy is performed

Lower Back Pain

Lower back pain is the second most common symptom-related reason for seeing a physician.
Surveys suggest that the lifetime incidence of lower back pain ranges from 60-90% with a 5%
annual incidence The medical literature has provided conflicting support for most proposed risk
factors which include involvement in occupations that require repetitive lifting, especially in
forward bending and twisting positions, exposure to vibration caused by motor vehicles or
industrial machinery, cigarette smoking, and morbid obesity. Lower back pain has also been
shown to be influenced heavily by job dissatisfaction, work conditions, legal and social factors,
financial stressors, and emotional circumstances.

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Causes:
Lower back pain may originate from structures of the lumbo-sacral spine (local) or referred from
structures away from the lumbo-sacral spine (referred pain). Lower back pain may therefore be
classified according to aetiology. There are five major causes of back pain:

1) Spondylogenic: (The commonest causes)

The commonest causes of lower back pain, with or without sciatica, are disorders of the lumbo-
sacral spine. These can be further divided into congenital and acquired causes. Acquired causes
include the following:
a) Trauma: Muscle strains, residual effects of fractures and dislocations, tendon sprains,
sacroiliac strain.
b) Infection: These include non-specific conditions such as osteomyelitis, as well as
more specific conditions like tuberculosis (Pott’s disease)
c) Inflammatory: Seronegatve arthropathies e.g. Ankylosing spondylitis
d) Degenerative: intervertebral disc prolapse, lumbar spondylosis and
osteoarthrosis of facet joints
e) Metabolic bone diseases: Osteoporosis and osteomalacia
f) Bony deformities: sondylolysis and spondylolisthesis
g) Neoplasm: benign neoplasms such as osteomas and hemangiomas, malignant
primaries such as multiple myelome, malignant secondaries such as those arising from
the thyroid, lung, breast, kidney and prostate

2) Viscerogenic: Lesions of the genito-urinary tract, pelvic organs as well as lesions of intra-
peritoneal or retro peritoneal organs that irritate the posterior peritoneum may cause lower back
pain.

3) Vasculogenic: Abnormalities of the descending aorta and iliac arteries, such as vascular
occlusions or dissecting aneurysms, may cause pain that is referred to the back.

4) Neurogenic: Infections and neoplasms that involve either the spinal cord or the cauda equina
may mimic disc herniation. These include conditions such as transverse myelitis, radiculitis and
neurofibromatosis.

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5) Psychogenic: This must be considered whenever there may be some secondary gain obtained
from the declaration of back pain, such as in workmen’s compensation. Although lower back
pain is sometimes a manifestation of psychosomatic illness, an underlying organic cause of the
pain must always be sought.

In children and adolescents, back pain usually has some recognizable cause such as:
-spondylosis, spondylolisthesis, infections, tumours, disc herniations, Scheurmann’s kyphosis

Spondylosis is a term referring to degenerative osteoarthritis of the joints between the centra of the spinal vertebrae and/or neural foraminae. In this condition
the interfacetal joints are not involved. If severe, it may cause pressure on nerve roots with subsequent sensory and/or motordisturbances, such
as pain, paresthesia, or muscle weakness in the limbs. When the space between two adjacent vertebrae narrows, compression of a nerve root emerging from
the spinal cord may result in radiculopathy (sensory and motor disturbances, such as severe pain in the neck, shoulder, arm, back, and/or leg, accompanied by
muscle weakness).

Spondylolisthesis describes the anterior displacement of a vertebra or the vertebral column in relation to the vertebrae below. A hangman's fracture is a specific
type of spondylolisthesis where the C1 vertebra is displaced anteriorly relative to the C2 vertebra due to fractures of the C2 vertebra's pedicles.

Spondylolysis is a defect of a vertebra. The great majority of cases occur in the lowest of thelumbar vertebrae (L5), but spondylolysis may also occur in the other
lumbar vertebrae, as well as in the thoracic vertebrae. it is typically caused by stress fracture of the bone, and is especially common in adolescents who overtrain
in activities such as tennis, diving, martial arts and gymnastics. The portion of the vertebra that is demeneralized in spondylolysis is a bone segment called the
pars interarticularis (which is part of a plate which is located, in technical terms, between the superior and inferior articular processes of a lumbar vertebra). In
spondylolysis, there is separation of the pars interarticularis. Spondylolysis can be a cause of abnormal movement of the spine (calledspondylolisthesis) and lead
to localized back pain.The defect is seen in this oblique lumbar radiograph: Image of Pars Defect. An oblique x-ray of the lumbar spine shows what appears to be
a "scotty dog" first described by Lachapelle:

Radicular pain, or radiculitis, is pain "radiated" along the dermatome (sensory distribution) of a nerve due to inflammation or other irritation of the nerve
root (radiculopathy) at its connection to the spinal column. A common form of radiculitis is sciatica – radicular pain that radiates along the sciatic nerve from the
lower spine to the lower back, gluteal muscles, back of the upper thigh, calf, and foot as often secondary to nerve root irritation from a spinal disc herniation or
from osteophytes in the lumbar region of the spine.

Transverse myelitis (in latin nomenclature: myelitis transversa) is a neurological disorder caused by an inflammatory process of the spinal cord, and can
cause axonal demyelination. The name is derived from Greek myelós referring to the "spinal cord", and the suffix -itis, which denotes inflammation.[1] Transverse
implies that the inflammation is across the thickness of the spinal cord.

Neurofibromatosis (commonly abbreviated NF) is a genetically-inherited disorder in which the nerve tissue grows tumors (i.e., neurofibromas) that may be
harmless or may cause serious damage by compressing nerves and other tissues. The disorder affects all neural crest cells (Schwann cells, melanocytes,
endoneurial fibroblasts).

Clinical features
The clinical presntation of the patient may give clues as to the cause of the pain. There are three
main categories of presentation: 1) Myelopathic, 2) Radiculopathic, 3) Localized.

Myelopathic presentation
o Signs of upper motor neuron lesion, that is, spasticity, hyperreflexia, upgoing
plantars, and weakness in the myotomes below the level.
o may have decreased sensation below the level
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 o bowel and bladder dysfunction
o these signs occur bilaterally

Causes include conditions affecting the spinal cord such as tumours, infections, lumbosaccral
stenosis and central disc herniation, trauma and scoliosis

Radiculopathic presentation
 signs of lower motor neuron lesion, including hypotonia and hyperreflexia
 there is also weakness in the myotomes and pain in the dermatomes affected
 these signs are usually unilateral

Causes include
-conditions affecting nerve root plexus
-prolapsed intervertebral disc
-osteophytes at the facet joints
-spinal stenosis

Spinal stenosis is a medical condition in which the spinal canal narrows and compresses the spinal cord and nerves. This is usually due to the common

occurrence of spinal degeneration that occurs with aging. It can also sometimes be caused by spinal disc herniation, osteoporosis or a tumor. In the cervical (neck)

and lumbar (low back) region it can be a congenital condition to varying degrees.

Spinal stenosis may affect the cervical, thoracic or lumbar spine. In some cases, it may be present in all three places in the same patient. Lumbar spinal stenosis

results in low back pain as well as pain or abnormal sensations in the legs, thighs, feet or buttocks, or loss of bladder and bowel control.

Localized presentation
There is no associated parasthesia of the skin, or weakness of the muscles below the level
of the lesion.
Causes include:
-conditions affecting vertebra and intervertebral disc
-arthyitides
-neoplasms
-infections, such as tuberculosis, osteomyelitis
-truama
-ligament strain
-spondylosis, spondylolisthesis
-congenital deformities
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Management
The first step to diagnosing the cause of lower back pain is taking a detailed history. It is
important to ascertain the following information:
1. Age of patient
2. Site of the pain- the patient should point to the site of the pain
3. Characteristics of the pain
- was the onset sudden or gradual
- is the pain intermittent or constant
- any relieving or aggravating factors (if no relief can be determined the a tumour
should be suspected)
- progression
- radicular symptoms, including radiation to the hip, knee and ankle
- relation to posture, eg, pain on lying down-infection, pain on sitting-
degenerative disease, pain on standing or walking- spinal

Remember it by SOCA PRO – site, onset, constant/not, aggravating/relieving

factors, progression, radiating/radicular pain and others

4. Constitutional symptoms- malignancy, tuberculosis

5. abdominal pain- viscerogenic
6. Joint pains- sign of systemic disease
7. Urinary tract symptoms- rule out renal disease
8. Erectile, bowel or bladder dysfunction- spinal chord compression
9. Personal history
 Job description
 Family unit
 school difficulties
 any emotional problems
10. History of cancer
11. History of infections
12. History of trauma

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Examination
All systems should be examined thoroughly to find an extrinsic cause of the back pain as well as
evidence of malignancy. With respect to the musculoskeletal system, certain things should be
noted:
1. Inspection
a. wasting, pallor
b. general facies
c. gait (wide based –myelopathy; leaning forward-stenosis; antalgic-painful)
d. posture and deformities of the spine (scoliosis, scheurmann’s kyphosis)
e. hemangiomas, hair patches and other midline defects (sign of underlying
spinal deformity)
2. Palpation
a. skin temperature and tenderness
b. bony contours- can feel step off in spondylolisthesis
c. all movements of the spine (flexion extension)- note any pain on movement
d. Flexibility of spine- stiff in ankylosing spondylitis

3. Other tests
 Straight leg raising (SLR) test – flexion of the hip to 90 degrees; numbness or pain
when the leg is lifted to 40 degrees may indicate nerve root compression
 Lasegue test – bring flexed limb down to the level where the patient just stops feeling
pain, and dorsiflex the foot (a nerve tension test, where it is positive for nerve
irritation as in the case of a herniated disc).
 Bowstring test – flexion of the knee and hip to 90 degrees while pressing into the
popliteal fossa to compress the tibial nerve. If the nerve is irritable then the patient
will feel pain radiating down the back of the thigh.
 Faber test-This is performed for evidence of sacroilitis. The patient is told to lie on
their abdomen and there is palpation over the midline and just left or right of the
midline.
 Motor, sensory and reflexes test

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Differences between mechanical and inflammatory low back pain:
Mechanical Inflammatory
Onset Acute Gradual
Age 15-60 < 40
Morning stiffness Absent Present
Effect of rest Improved Worsen
Effect of exercises Worsen Improved
Involvement of other systems Absent Eyes (Iritis), Joints
(Arthritis)
Neurological symptoms Radicular may reach Dull ache pain in the back,
the feet buttocks.

Investigations
The relevant investigations are dictated by history and the physical examination. A complete list
of the investigations is given below:

Haematology
The complete blood count is determined. This is abnormal in acute and chronic infection, and
haematological malignancies.

Chemical Pathology
- Erythrocyte sedimentation rate
- urea and electrolytes- Ca2+, PO42-
- proteins-albumin
- protein electrophoresis- myeloma
- alkaline phosphate- osteoblastome conditions
- Prostate Specific Antigen/ Acid Phosphatase- metastatic prostatic cancer
- Uric acid- increased cell turnover as in the case of tumours
- Collagen vascular screen- rheumatoid arthritis

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Radiology
- Plain x-ray of lumbar spine are done for: patients older than 50 years, trauma patients,
patients with pain at rest, unexplained weight loss, a history of cancer, neurological
defects or fever. The x-ray may show narrowed disc space and osteophytes, which are
in fact normal findings in patients over 60 years old. Flexion and extension views of
the spine will show how the vertebrae move over each other, and may identify
instability of the column. Oblique views if spondylolysis suspected may show the
‘scotty dog sign’ with colour.
- Magnetic Resonance Imaging or CT scan, these modalities are extremely sensitive
may show a prolapsed disc, spinal tumours, or spinal canal blockage.
- Bone scan (with Technecium 99m or Gallium). This can pick up infections, and areas
of osteoclastic activity as may occur in multiple myeloma.
- Discogram. This is performed if disc pain is suspected as in disc herniation. Normal
saline is injected into the disc space and check to see if it simulates pain.

Treatment
With lower back pain, the cause is directed at the cause. However, the exact cause of back pain is
found in only 15% of cases. Hence if no cause is found, the patients should be treated
symptomatically.

Initial treatment is directed at conservative management of the patient in order to relieve the
symptoms. The following general principles may be applied:

a. Complete bedrest for 1-2 weeks in acute cases.

b. Hard bed with low pillow.
c. Instruction in correct posture and back discipline (bending, carrying ...etc.).
d. Change to more suitable work (not involving bending, lifting or climbing).
e. Reduction of weight in obese patients.

Medical management of the patient may include the following:

a. Analgesics and muscle relaxants for pain and spasm.
b. Caudal epidural injection (50 ml of 0.5% procaine or lignocaine in normal saline) for

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 persistent sciatica. This separates nerve roots from protruding disc.
c. Chemonucleolysis (intradiscal injection of chymopapain, a proteolytic enzyme to break
chondromucoprotein-which may cause scarring)

Physical Therapy is a useful adjunct in the management of these patients:

a. Strengthing exercises (back extension and/or flexion exercises) preceded by local heat or ice.
b. Lumbosacral support: corset or brace.
c. Intermittent lumbar traction: 30-60 kg for 30-60 minutes at a time for persistent sciatica.
Continuous lumbar traction may be applied in hospital for acute cases.

If conservative management fails surgery may be considered. The indications for surgery are:
 Failure of conservative treatment.
 Evidence of nerve root or cauda equina compression
 Progressive muscle weakness due to root pressure
 Sphincteric disturbances
 Urinary Retention
 Congenital defect with severe disc lesion such as spinal cord stenosis and spondylolysis
 For diagnosis, eg tissure culture

The usual operation is a lamenectomy. Postoperatively, patient stays one week in

hospital, then one month of intensive rehabilitation before allowed to return to their normal
lifestyle.

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