Essential Notes for MRCS - Book 2(B)

Microbiology of tetanus
Tetanus is caused by Clostridium tetani:
Gram-positive rods
Obligate anaerobes

Two toxins are produced:
Tetanospasmin (carried to the CNS; affects motor neurones) • Tetanolysin (haemolytic)

Risk factors for tetanus
Wounds that occurred more than 6 hours ago • Blunt, crush or missile injuries • Contaminated wounds
Presence of devitalised or infected tissue

Prophylaxis for tetanus
Wound management: this involves debridement of the wound, decontamination, lavage (the solution to
pollution is dilution) and consider delayed secondary closure.

Immunological prophylaxis: if patient has had three or more previous doses of tetanus toxoid (ie
previous full course):
>10 years since last dose – repeat in all cases • >5 years since last dose – repeat for tetanusprone wounds

If patient has had less than three previous doses of tetanus toxoid:
Give tetanus toxoid dose
Give tetanus immunoglobulin for tetanusprone wounds

Treatment of tetanus
Muscle relaxants
Respiratory support
Surgical debridement
Antitoxin
Antibiotics (penicillin)

Necrotising fasciitis



In a nutshell ...

Necrotising fasciitis is an infection of the dermis and subcutaneous tissues with tissue necrosis. It
causes skin blisters and crepitus, with rapid advancement. Fever, septic shock and organ failure can
occur. Necrotising fasciitis commonly affects the limbs or male genitalia (Fournier’s gangrene).

Microbiology of necrotising fasciitis

Commonly a synergistic infection with anaerobic and aerobic organisms • Can occur with S. pyogenes
infection

Risk factors for necrotising fasciitis

Diabetes
Peripheral vascular disease
Alcoholism
Perineal injury

Treatment of necrotising fasciitis

Blood culture
Monitor and support organ function • Aggressive debridement beyond the visible zone of infection •
Broad-spectrum antibiotics

Fractures and soft-tissue problems

Open fractures with soft-tissue injury or loss require soft-tissue cover. The infection rate is inversely
related to the time to definitive cover (ie any delay increases the risk of infection). Soft-tissue cover may
be achieved by primary closure, split-skin graft, local flaps or free microvascular flaps. If there is an
associated bony defect an acute shortening procedure may be appropriate. Best results are obtained by
early involvement of the plastic surgical team.

Swelling complicates all injuries – severe swelling around the fracture site may result in fracture blisters.
Moderate to severe swelling will result in an increased rate of wound problems and infection. Open
reduction and internal fixation should be deferred until the soft tissues permit. Ankle and calcaneal
fractures are particularly prone to swelling. An unstable ankle fracture may be temporarily held in a cast
or with an external fixator until the soft tissues settle.

4.3 L ate local complications of fractures Fractures and avascular necrosis

Joints with extensive, convex articular surfaces are at risk of avascular necrosis (AVN). The blood supply
to subchondral bone enters the bone at a site distant from the articular surface. Fractures across this bone,
carrying the blood supply, will result in AVN. Increased displacement and associated soft-tissue stripping

increase the risk of AVN. Early and anatomical reduction and fixation may reduce the incidence of AVN.

Typical sites for AVN
Femoral head from intracapsular fracture of the proximal femur • Proximal scaphoid from a fracture of the
waist of the scaphoid • Humeral head from proximal humeral fracture (typically three- or four-part
fracture where articular and tuberosity fragments are separate)
Body of talus from a neck of talus fracture

Features of AVN
Pain
Chondrolysis and chondral flaps (seen on MRI) • Articular collapse (seen on plain films)

Management of AVN
Avoid weight bearing across the joint – may revascularise given time (revascularisation demonstrated by
MRI or bone scan, or by evidence of bone resorption on plain films)
Revascularisation procedures such as vascularised fibula grafts in the femoral head or core decompression
• Arthrodesis or arthroplasty

Fractures and myositis ossificans

Myositis ossificans can occur after a fracture or muscle injury. It is calcification within muscle.

Typical sites for myositis ossificans
Quadriceps
Gluteals
Biceps
Intrinsic muscles of the hand

Treatment of myositis ossificans
Differentiate from other calcifying lesions (eg osteosarcoma) • Symptomatic treatment in the acute phase
(3–6 months) • May be excised if still symptomatic when calcification is mature (12–18 months) •
NSAIDs and radiotherapy have been used to reduce incidence but no definite benefit has been proved

Fractures and complex regional pain syndrome (CRPS)

CRPS type I

Also known as:
Reflex sympathetic dystrophy (RSD) • Sudeck’s atrophy
Algodystrophy
Shoulder–hand syndrome

This is a poorly understood condition. It may be an exaggeration of the normal sympathetic response to
injury. CRPS type I occurs in the upper and lower limbs. It is seen in up to 30% of cases after distal
radial fracture. It may occur after any minor or major injury.

Primary clinical features of CRPS type I
Pain (out of proportion to the injury) • Swelling
Stiffness
Colour change (usually redness, but the limb may take on pale or blue coloration)

Other signs
Temperature change
Sudomotor changes (initially hyperhidrosis; later dry skin) • Trophic skin changes and osteoporosis •
Palmar fibromatosis

Three stages of CRPS type I
Stage I: pain and tenderness, with warm, dry and swollen erythematous limb • Stage II: cool, sweaty and
swollen cyanotic limb • Stage III: stiffness, atrophy and osteoporosis

Aetiology of CRPS type I
Many theories have been proposed for the aetiology of CRPS I:
Injury alters afferent neurones: This results in altered sympathetic activity, through interaction either
locally or in the cord • Altered sympathetic activity (vasomotor and sudomotor) results in swelling,
stiffness and colour change • Reduced venous drainage perpetuates condition (this may be due to
vasomotor changes, dependent limb or subclavian vein stenosis)

Treatment of CRPS type I
Usually this is a self-limiting condition in minor cases, but it may result in permanent decreased function
if swelling and stiffness are allowed to persist. The cycle of pain–swelling–stiffness– pain must be
broken.
Intensive physiotherapy (and splintage if required) • Optimised analgesia
Sympathetic blockade (or surgical sympathectomy)

CRPS type II

This is also known as causalgia. It has the same features as CRPS type I, with a demonstrable nerve
lesion. Medications such as amitriptyline and pregabalin may be helpful.

Surgical decompression and neurolysis may be of benefit in resistant cases that do not respond to non-
surgical treatment.