It is far more common in men than women, with a reported annual incidence of 7.3 per 100,000 and 0.7 per 100,000 respectively.
To understand the pathogenesis of compartment syndrome in the leg, one needs to appreciate that the deep fascia and long bones divide the leg into four distinct compartments - anterior, lateral, superficial posterior and deep posterior.
Under normal circumstances, the pressure inside each compartment is quite low (typically between 0 to 8 mmHg). This is well below the capillary closing pressure.
Unfortunately, the deep fascia is relatively inelastic, i.e. the volume of each compartment is fixed. Thus, even minor derangements in tissue homeostasis may result in rapid increases in compartmental pressure.
In this regard, elevation of tissue pressures may occur either because of increased compartmental contents (i.e. bleeding following trauma, edema secondary to nephrotic syndrome, or tissue destruction following snakebite); because of diminished compartment volume (i.e. after burns, or due to tight plaster casts); and very rarely, because of injuries to the microvasculature (i.e. in diabetes).
In practice, the commonest cause is a fracture of the tibial diaphysis, followed by blunt soft-tissue injury.
If the compartmental pressure rises above the capillary closing pressure, circulation shuts down, resulting in intra-compartmental ischemia and progressive necrosis of the muscles.
In turn, the skeletal muscles respond to the ischemia by releasing histamine-like substances which increase vascular permeability. Plasma leaks out of the capillaries, aggravating the tissue edema and worsening the ischemia.
Compartment syndrome of the leg is a clinical diagnosis, with the classical features being:
- Severe pain, typically increasing over time and often resistant to analgesics. In patients with a history of trauma, the pain is usually out of proportion to the apparent injury.
- Worsening of the pain when passively stretching the muscles within the affected compartment.
- A palpably tense compartment.
- Weakness and paresthesia of the areas supplied by nerves traversing the compartment. Note that these are late features and indicate the severe compromise.
It is uncommon for the compartment pressure to rise above the arterial pressure - thus pedal pulses and distal capillary filling are often normal. Pulselessness and diminished capillary filling are more likely due to arterial injury, or compression by a hematoma.
Note that non-classical presentations are common. In particular, pain is a highly unreliable symptom as it is subjective, difficult to elicit in patients with altered mentation, and sometimes absence in established compartment syndrome.
Where the clinical picture is equivocal, compartment pressure measurement may aid the decision-making process. Most authorities agree that an absolute resting pressure of over 30 to 45 mmHg, or within 30 mmHg of the diastolic blood pressure is suggestive of compartment syndrome.
Once the diagnosis is made, the most important step of the management is prompt decompression of the compartment via a fasciotomy.
All four compartments are usually decompressed, in order to avoid missing an affected compartment. This may be performed via a single incision or a double incision, which should extend across the entire length of the muscle and involve all layers of the skin to the deep fascia (as these may otherwise restrict expansion).
Following surgery, the wounds should be left open to allow the compartmental swelling to subside. In certain patients, repeated debridement to remove necrotic soft tissue may be necessary.
Wound closure may be achieved via several techniques. Split-thickness skin grafting is often employed. Delayed primary closure is an alternative, but may require an extended delay (to allow approximation with minimal or no skin tension). Vacuum-assisted wound closure is another option gaining popularity.
In the long term, these patients should receive physical therapy to regain function and facilitate rehabilitation.
During the acute stage, close observation for rhabdomyolysis, acute renal failure and sepsis is important.
The morbidity of acute compartment syndrome is directly related to the timing of decompression. When performed within 12 hours of onset, normal limb function is regained in 68% of patients. If delayed beyond this point, this declines to 8%.
Key long-term complications include residual numbness, peroneal nerve palsy, and limited motor function of the involved muscles.
Complications of fasciotomy include wound infections, decreased sensibility within the wound area, tethered tendons, and recurrent ulcerations within the wound closure area.
The main causes of mortality are sepsis and multiorgan failure.
Watch this video for more illustration.
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