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.
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
Osteogenesis Imperfecta
Rickets

Adults
Osteomalacia
Osteosclerosis
Parathyroid Osteodystrophy
Diffuse Metastatic

Elderly
Generalised Osteoporosis
Pagets disease of Bone
Diffuse metastatic disease
Multiple Myelomatosis

Carcinoma
Localised Pathology
Infections
Pyogenic Osteomyelitis

Benign
Solitary Bone Cyst

Malignant
Secondary Deposit from
primary lesion in e.g.
Breast, Prostate , Kidney,

Syphilitic Infection

Endochondroma

Thyroid
Primary Malignant Tumour

Osteoclastoma

e.g. Ewings Tumour

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.
2

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.
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

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 metaphysi

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

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.
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.
5

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.
Gustillo & Anderson in 1984 classified open fractures in the following way:

Grade I
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.
6

Rate of Infection 25-80%

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
Deep Vein Thrombosis
Late
Delayed / Mal / Non Union
Infection
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
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

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.

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.
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.

10

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.

Speed of Healing and Perfection of Fracture Repair

This is influenced by local and systemic factors . These include :
Local Factors
Immobilisation
Poor Blood Supply
Poor Reduction
Infection
Allergic Reactions

Systemic Factors
Metabolic & nutritional deficiencies
Sepsis
Radiotherapy
Chemotherapy
Sickle Cell Disease
11

Age
Drugs eg Antiepileptics ,NSAIDS
Hormones
Synovial Fluid

Collagen Vascular Disease

Vascular Insufficiency
Type of Bone Fractured
Fracture in a Joint

Complications of Fracture Healing

Delayed Union

Mal Union

Non Union

Fibrous Union

Arthritis

Pseudo arthritis

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

12

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

Type II

(Infection rate: 0-2%)

Laceration more than 1 cm long
No extensive tissue damage, flap or contusion
Slight to moderate crushing injury
Moderate comminution
Moderate contamination

Type III

(Infection rate: 2-7%)

Extensive damage to soft tissues,
High degree of contamination

III A

Fractures caused by high velocity trauma

Includes any segmental or severely comminuted closed or open fractures,
Soft tissue coverage of the bone is adequate

III B

(Infection rate: 7%)

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.

III C

(Infection rate: 10-25%)

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
13

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 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 .

14

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 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 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
15

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 Cs namely:
1. Colour
2. Consistency
3. Contraction
4. Circulation
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
16

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 nonunions 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.
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

17

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 longterm complications. The basic types of injuries include the following:

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 I

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

18

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 relatively favourable prognosis.
The treatment for this fracture is often surgical.

Salter-Harris fracture type IV

Salter-Harris fracture type

III

Type IV
A Type IV fracture passes through the epiphysis, physis, 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.

Salter-Harris fracture type V

Type V
A compression or crush injury of the epiphyseal

19

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.
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

20

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.
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.
21

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.
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 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.

22

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.
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

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.
23

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)

Restricting Splints, Improperly placed casts, tight dressings

Circumferential Burns

Malfunctioning sequential compression devices (SCDs)

Tight boots

Internal increase in compartment volume

o

Fractures ( most common )

Hemorrhage (trauma, coumadin, tissue plasminogen activator [TPA])

Hemophilia

Gun shot wound to thigh

Massive intravenous fluid infusion

Compartment fluid injection

Crush injuries

Rhabdomyolysis

Gastrocnemius or peroneus muscle tear

Androgen abuse/muscle hypertrophy

Tumours

Ruptured bakers cyst

Snake envenomation

Infection : Clostridium Perfringens

Drug /Alcohol Abuse or Coma : Lying on limb for hours

24

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.
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.
Clinical Presentation (6 Ps)
1) Pain: Most common and consistent sign. Its 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 1 st dorsal
cleft of the foot (deep peroneal distribution) is the area effected.))
NB: Dont use pinprick to test nerve distribution because the pain fibers are the smallest and the last to
be compromised, use two-point discrimination.

25

3) Pallor this occurs as the muscles and other soft tissues are no longer perfused with 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), highenergy 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.
Diagnosis
Intra-compartmental pressures can be measured and the limb assessed. The Whitesides 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.

26

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 10-30mmHg of the
patients diastolic pressure. Thus, when the pressure equals or exceeds the patients 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

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 RBCs 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

27

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 Volkmanns 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.
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.
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.
28

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. 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 contractureseen most often in the flexor muscles
of the forearm or leg.

Cycle of Volkmanns Ischaemia

Arterial
damage

Ischaemia

Reduced
blood flow

Painful
Pale Pulseless
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.
29

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.

Acute Osteomyelitis
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

30

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.
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.

31

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 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
32

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)

Irritability

Malaise

Restriction of movement (pseudoparalysis of limb in neonates)

Local swelling, redness and tenderness

Fatigue

NB. If haemategenous spread is suspected inquire about:

o

Recent infection?

Chronic Illness e.g. Sickle cell, Diabetes?

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
33

i.

Rheumatic fever

ii.

Septic arthritis- decreased joint movement and joint pain

iii.

Scurvy

iv.

Syphilitic metaphysitis

v.

Bone tumour- differential diagnosis for Brodies 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. Both the ESR and CRP levels will be elevated. Creactive 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
Ewings sarcoma as a differential diagnosis.

34

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.

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:
35

 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 (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

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.

36

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. Brodies abscess- small intraosseous abscess that frequently involves cortex and is walled off by reactive
bone. Develops when antibiotics impair bacterial growth but dont 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

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 multitrauma 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
37

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 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.
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 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.

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.
38

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 of muscle groups (corticospinal tract

Diaphragm
Shrugging shoulders

C3-4-5
C4

Flex elbows
Extend elbows

C5,6
C7

Abduct fingers

C8

Active chest expansion

T1-T12

Hip flexion
Knee extension
Ankle dorsiflexion

L2
L3-4
L5-S1

Ankle plantar flexion

S1-S2

Eversion of foot
Inversion of foot

L5
L4

39

MRC Power Grading

0

No active contraction

Visible contraction without movement

Movement with gravity eliminated

3
4

Movement against gravity

Movement against resistance but weak

Normal power

Reflexes

Biceps
Triceps

C5-6
C6-7

Supinator

C5-6

Knee jerk

L3-4

Ankle jerk

L5-S1

Plantar response

If upgoing = UMN lesion

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

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.

40

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.

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.
41

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 patients legs to improve blood pressure. Atropine may be used to counteract
bradycardia.
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 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

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
42

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
patients 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 patients
spinal cord injuries are due to gunshot injuries.

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 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
43

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.
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 DVTs 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.
44

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:
-

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 fullness of the bladder. Urination occurs without warning as soon as the reflex is closed by

45

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.

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.

46

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 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
47

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.

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

48

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

are

the

most

common fractures around

Site of Ossification

Ossification Date

Capitular centre

8months to 1year

Radial centre

4years

children accounting for

Medial epicondyle centre

6years

approximately 60 80 %

Trochlear centre

6years

of them. This fracture

Lateral epicondyle centre

9 to 11 years

occurs as the child falls

the

elbow

region

in

on the outstretched arm,

Olecranon
9 to 11 years
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.
49

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
Biers 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 90 o
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.
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
50

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.
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.

51

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.

Treatment
Uncomplicated fractures: only symptomatic treatment is required.

52

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.
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.
53

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

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 23 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.

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.

54

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

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 patients 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.
55

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 formation. This is then responsible for the cartilage, bone,
ligament, and tendon destruction.
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 antibodysecreting 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.
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
56

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 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

57

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

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

Examination

Swollen joints

Warmth

Decrease range of movements and stiffness

Movement causes pain

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
58

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

59

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%

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 Reiters syndrome (urethritis, arthritis, conjunctivitis and hyperkeratotic eruptions on the skin)
o SLE
o Scleroderma
60

These conditions are all seronegative for RF and may be associated with ankylosing spondylitis
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 2 nd line drugs- e.g. Gold, Penicillamine, antimalarial 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

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
61

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.

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
62

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.

Causes of Secondary Osteoarthritis

Developmental

Inflammatory

Perthe's disease

Rheumatoid arthritis

Slipped upper femoral epiphysis

Septic arthritis

Developmental dysplasia of the hip

Haemophilia

Traumatic

Gout
Aseptic necrosis

Intra-articular fracture

Corticosteroids

Meniscectomy

Sickle-cell disease

Metabolic

SLE
Neuropathic

Haemochromatosis

Diabetes mellitus

Wilson's disease

Peripheral nerve lesions

Endocrine

Miscellaneous

Paget's disease

Gaucher's disease

Acromegaly

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

63

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 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.
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.

64

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 of the underlying bone
Capsular fibrosis
Pattern of Involvement
Knee Assymetric
Hip Superolateral
Hand Distal Interphalangeal Joint more common.

65

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
Radiological Changes
X Ray
Uneven narrowing of the joint space
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.

66

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
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

67

Complications
Capsular herniation: OA of the knee is sometimes associated with a marked effusion and herniation of the
posterior capsule (Bakers 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)

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 (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.

68

Clinical features
Symptoms
-

History of contact with TB infection

Pain in the joint

Swelling on the joint

Decrease function of the joints

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

Signs

Investigations
Radiology
1. Plain X-Ray/MRI/CT Scan
-

The earliest radiological feature is diffuse rarefraction 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

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

69

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 subtrochanteric 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.

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.
70

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.

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

71

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
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 Shentons 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.
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
Blood supply to the head and neck of femur

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

72

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 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.

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).

73

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. Extra-capsular fractures do not have this
problem & are hence easier to treat.

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
Young/active patient
1)compression screws
develop AVN then

Inactive- Austin

Moore prosthesis

(hemiarthroplasty

Older patient

flap

if

1) quadratus femoris
Active- total hip

2) free graft

replacement

3) THR

(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.
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).

74

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.
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:
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.
75

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:
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

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

Management of Shaft of Femur Fractures in Adults

76

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

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 ABCs 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

77

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

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

78

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 Poveys splint

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 Poveys 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 patients 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

79

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.

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
80

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
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 Bryants traction. The fracture unites in 2 weeks time with
profuse callus formation.
Treatment in Young Children
81

Gallows or Bryants 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 childs 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 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
ischaemiaa 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.
Complications (in both adults and children)

Simultaneous dislocation of hip

Injury to major artery

82

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 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 1 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.
83

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.
Management of Colles Fracture
A Colles 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 Colles 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.

84

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 Smiths fracture.
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 Colles 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.
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

85

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
Management
Involves: 1) disimpaction; 2) reduction; 3) immobilization
The first step is anaesthesia: general or locala regional block (Biers 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 patients 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
examiners 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.

86

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 Biers 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.
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 fractureplaster 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 malunion.

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.

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.
87

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. (Darrochs 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.
Sudecks Post Traumatic Osteodystrophy: A Colles fracture is the commonest cause of Sudecks
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.

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
88

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 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

89

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

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

90

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 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.

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.

91

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

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
92

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

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.
93

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. 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.

94

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 Kanavels 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

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
95

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.
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

96

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.

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
97

Tenderness

Swelling

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

A sinus with purulent drainage may be present.

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.

* Barbers 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.

98

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.

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
99

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:

Tetanus booster (0.5 cc Tetox)

Broad spectrum antibiotics (Penadur)

Extensive irrigation

Leave wound open

100

Diagram Showing Incision for the Various Infections

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

101

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 and palmar digital
branches which supply the radial three and a half digits as well as the nail beds and distal dorsal skin .

102

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

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 motion

Connective tissue disease

especially in patients whose jobs require

Gout or pseudogout

repeated forceful finger and wrist flexion

Nonspecific flexor tenosynovitis*

and extension

Rheumatoid arthritis
Labourers using vibrating machinery as
are office workers especially typists and
data entry clerks

103

*--Most common cause of carpal tunnel syndrome.

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
This occurs over the radial 3 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.
Tinels 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 digits.
Positive in Carpal Tunnel Syndrome.
Phalens 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
104

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. Raynauds 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.

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.

105

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

De Quervains Tenosynovitis
De Quervains 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.
Tendon affected by De Quervain's tenosynovitis:

106

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 Quervains Tenosynovitis

Carpal Tunnel Syndrome

Rheumatoid Arthritis

Cervical Radiculopathy

Diagnosis of the condition is based on history and clinical examination. With DeQuervains 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 Finkelsteins 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 patients 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
DeQuervains Tenosynovitis.

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
107

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

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 tendon 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.

108

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.

109

There are two classes of tenovaginitis:

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 Type

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

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
110

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.
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.

Greens 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
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)
111

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:

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
112

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.

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
113

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 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)

114

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.

115

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 in convex posteriorly (kyphosis) and the lumbar spine is convex
anteriorly (lordosis). Normally there should be no lateral curvature of the spine.

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.

116

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.

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

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
117

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 ribvertebral 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
118

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.

Adamssign
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.
Rissers 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.

Rissers Sign

119

Rissers 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 Cobbs angle, the degree of curvature is measured by drawing lines on the Xray 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 Cobbs angle. If Cobb's angle is 10 degrees or more the diagnosis of scoliosis is
confirmed.

120

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 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.
121

Milwaukee brace

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 is 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.

122

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 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
123

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.
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

124

Classification of Bone Tumours

Cell Type

Benign

Bone

Osteoid Osteoma

Malignant
Osteogenic Sarcoma

Osteoblastoma
Cartilage

Chondroma

Chondrosarcoma

Osteochondroma
Fibrous Tissue

Fibroma

Fibrosarcoma

Marrow

Eosinophilic Granuloma

Ewings 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

125

Most common malignancies producing skeletal metastases:

More than 75% of skeletal metastases originate from carcinomas of the
Adults

prostate, breast, kidney, and lung. Also 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.
Clinical Picture
History
Age of the patient: Certain tumours occur more commonly in certain age groups.
Age group

0 - 10

10 - 20

Most common benign

lesions
simple bone cyst
eosinophilic granuloma

Most common malignant tumors

Ewing's sarcoma
leukemic involvement
metastatic neuroblastoma

non-ossifying fibroma

osteosarcoma,

fibrous dysplasia

Ewing's sarcoma,
126

simple bone cyst

aneurysmal bone cyst
osteochondroma (exostosis)
osteoid osteoma
osteoblastoma
chondroblastoma
chondromyxoid fibroma
20 - 40

enchondroma
giant cell tumor

chondrosarcoma
metastatic tumors
myeloma

40 & above

osteoma

leukemic involvement
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:

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
Ewing's sarcoma
Multiple myeloma
Leukemia/lymphoma
Metastatic cancers

Most common skeletal sites

Hematopoietic marrow sites in the axial skeleton
(vertebrae, ribs, sternum, pelvis, cranium) and proximal
long bones (femur, humerus)
Metadiaphyseal regions of the tibia and distal femur

Non-ossifying fibroma

(80%) Does not occur in the flat bones, craniofacial

bones, the spine, or the small bones of the hands/feet.
127

Simple bone cyst

The vast majority of SBCs is found in the proximal

humerus (55%) and proximal femur (20%).

Adamantinoma

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

Chondroblastoma

Long bones (knee area, proximal humerus)-70%

Giant cell tumor

Knee area, distal radius (65%)

Enchondroma
Chondrosarcoma (primary,
and to the less extent
secondary)

Small bones of the hands and feet (60%). This is in fact

the commonest tumor at these sites.
Tends to develop in the axial skeleton with 25% to 30%
occurring in the pelvic bones

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

Chondromyxoid fibroma

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

128

Thorough physical examination of breast, prostate, thyroid, etc. if history suggestive of pathology in any of
the organ systems

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 (LFTs)
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
129

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.

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 Ennekings 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.
130

Parameter
Rate of Growth

Benign
Slow therefore body has

Malignant
Rapid Growth with ill

sufficient time to wall off

defined borders

tumor. Well defined area of

Bone Destruction

sclerosis
Thin the cortex making

Bony destruction with soft

Skip Lesions
Periosteal Reaction

bone prone to fracture

None
None

tissue extension
Present
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.
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 chestmost 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
131

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 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
132

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 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.
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 bye classified according to
aetiology. There are five major causes of back pain:
1) Spondylogenic: (The commonest causes)

133

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 (Potts 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.

4) Psychogenic: This must be considered whenever there may be some secondary gain obtained from the
declaration of back pain, such as in workmens 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, Scheurmanns kyphosis
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.

134

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
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
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
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
135

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

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
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, scheurmanns 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
136

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 tes

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

137

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

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
persistent sciatica. This separates nerve roots from protruding disc.
138

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.

139