Compartmental Syndromes.

Diagnosis

How are compartmental syndromes diagnosed?

Most compartmental syndromes may be diagnosed on the basis of clinical symptoms and signs alone. These include:

1. pain out of proportion to what is anticipated from the clinical situation,
2. weakness of the muscles in the compartment,
3. pain on passive stretch of the muscles of the compartment,
4. hypesthesia in the distribution of the nerves coursing through the compartment, and
5. tenseness of the compartmental envelope.

In certain instances adjunctive diagnostic techniques such as tissue pressure measurement and direct nerve stimulation may be useful in the diagnosis of compartmental syndromes.

The period of risk for compartmental syndromes appears to extend at least to three, and possibly to six, days after the initial cause of compartmental swelling.

Arterial occlusion and primary nerve injury may produce a clinical picture similar to that of a compartmental syndrome; yet the differential diagnosis can usually be made by careful clinical examination with occasional recourse to ancillary diagnostic techniques.

Movies

• Anterior compartment of the leg (0.33 MB)
• Deep posterior compartment of the leg (0.28 MB)
• Tissue pressure measurement (1.63 MB)
• Diagnosis of a compartmental syndrome (somewhat lengthy) (1.30 MB)

Clinical diagnosis

The essential elements in diagnosing a compartmental syndrome are revealed in its definition: a compartmental syndrome is a condition in which increased pressure within a limited space compromises the circulation and function of the contents of that space. Thus, to make a rigorous diagnosis of this condition, the physician should have evidence for increased tissue pressure, inadequate tissue perfusion, and loss of tissue function.. When all of these are present, the diagnosis of a compartmental syndrome may be made with assurance; when one or more of these factors is absent, the diagnosis is less secure.

Evidence for increased tissue pressure may include the patient's complaints of tightness or pressure in the involved area. The physician may perceive tenseness of the compartmental envelope by palpation. Or he may detect significantly increased tissue pressure by direct pressure measurement.

Evidence for inadequate perfusion of local tissue may include the symptom of pain out of proportion to what would be anticipated from the clinical situation. For example, one would not anticipate a progressive increase in pain from a properly splinted fracture. Requests by the patient for more analgesic medication are often discounted by nurses and physicians, but may actually provide a vital clue to the onset of locally insufficient blood flow. Pain on stretch of the intracompartmental muscles is a useful indication of inadequate local perfusion, particularly if these muscles have not been otherwise injured.

Although muscle blood flow may be quantitated in the laboratory with various measurement techniques these techniques are as yet difficult to apply to the clinical situation. Even if such quantification were practical, the results would only be useful if the circulatory requirements of the tissue in question were known.

Peripheral pulses are frequently normal in compartmental syndromes because intracompartmental pressures are usually insufficient to affect arterial flow. Thus, whereas diminished pulses suggest reduced arterial flow from some cause or other, the presence of distal pulses provides no information about the adequacy of compartmental perfusion. A similar statement may be made about the presence of Doppler signals distal to the compartments In our investigations of a model compartmental syndrome in humans, we found that an excellent Doppler signal could be detected in the presence of severely compromised compartmental function.

One may reasonably ask whether compromised tissue perfusion may be determined from tissue pressure measurements alone. Whereas intramuscular pressures in excess of 20 mm Hg are abnormal and have been shown to reduce tissue blood flow and oxygenation, 5, 6 they do not necessarily indicate inadequate tissue perfusion. The local circulatory effect of a given tissue pressure depends upon the pressure tolerance of the tissue (see Chapter 4). However, a rough guideline may be derived from our past experience with clinical tissue pressure monitoring: significantly compromised tissue perfusion is likely when tissue pressure exceeds 45 mm Hg.

Evidence for abnormal tissue function includes weakness of the intracompartmental muscles and hypesthesia in the distribution of nerves coursing through the involved compartment. Because both nerve and muscle function may be altered by direct injury, evidence of progressive functional losses after an initial injury is a particularly important sign of a compartmental syndrome. Detection of this progression is obviously dependent upon good neuromuscular examinations repeated frequently and documented adequately.

The function of muscles at risk is graded on a zero to five scale (where zero indicates no function and five indicates normal function). Toe extension must be specifically examined because a patient without any anterior compartment function can "wiggle his toes" quite well by using his toe flexors and then allowing his toes to spring back to the neutral position. Sensation is a bit more difficult to quantitate, but most observers could agree on definitions of normal, slightly diminished, significantly diminished, and absent.

It is important to record the time and results of these examinations so that changes in the patient's condition may be easily determined. A shorthand notation is useful.

In most cases, the diagnosis of a compartmental syndrome can be made from the clinical evaluation alone. The symptoms and signs usually associated with a compartmental syndrome may be summarized as follows:

1. Pain out of proportion to what is anticipated from the clinical situation.
2. Weakness of the muscles in the compartment.
3. Pain on passive stretch of the muscles in the compartment.
4. Hypesthesia in the distribution of the nerves coursing through the compartment.
5. Tenseness of the compartmental envelope.

Adjunctive diagnostic techniques

Although the clinical examination is the cornerstone of the diagnosis of compartmental syndromes, it has two distinct disadvantages: (a) it is partially subjective, and (b) it requires cooperation from the patient. Furthermore, in certain situations the clinical evaluation may be insufficient to allow the examiner to distinguish among several possible causes of neuromuscular deficit. In these instances, quantitative, objective techniques such as tissue pressure measurement and direct nerve stimulation may be useful adjuncts.

Tissue Pressure Measurement

Tissue pressure measurement may be of great value in the diagnosis of compartmental syndromes because it quantitates the physical factor responsible for the syndrome. A tissue pressure in excess of 45 mm Hg is usually associated with a compartmental syndrome, and a tissue pressure of 60 mm Hg or higher consistently gives rise to this condition. Because the tolerance of tissue for increased pressure may be reduced by such factors as shock, arterial occlusion, and limb elevation, compartmental syndromes may occur at significantly lower tissue pressures (see Chapter 4).

Tissue pressure measurement is most often useful where the diagnosis of a compartmental syndrome cannot be established or excluded on the basis of symptoms and signs alone. The clinical presentation is likely to be ambiguous in a patient who has more proximal neurologic lesions involving peripheral nerves or the central nervous system, a patient with other causes of compartmental ischemia, or a patient with such anxiety that the usual tests for compartmental function are unreliable. (Even in these situations, however, the clever clinician is sometimes able to make use of withdrawal reflexes or Babinski signs to evaluate compartmental function.)

Another application of pressure monitoring is in the early detection of compartmental syndromes in patients at risk for this condition. The pressure is continuously monitored in the compartment judged to be at highest risk (the one that is clinically tightest, the one that has received the most direct trauma, or the one known to be most predisposed to the development of compartmental syndromes). Pressure monitoring is continued until the question of a compartmental syndrome is resolved-a period that usually does not extend beyond three days. The infusion technique is of particular value in this application because it allows continuous pressure monitoring for extended periods.

A typical example of the usefulness of continuous pressure monitoring is the case of a 22-year-old man whose leg had been pinned for five hours beneath a heavy sign. Continuous monitoring of the pressure within the anterior compartment indicated a rise in tissue pressure from 20 to 50 mm Hg in the first two hours after the patient's admission to the hospital. This rapid pressure increase heralded the onset of a compartmental syndrome, which was successfully treated by prompt surgical decompression.

The use of tissue pressure measurement in the diagnosis of compartmental syndromes assumes that the measured pressure accurately reflects the pressure within the compartment. There is always a danger, particularly in inexperienced hands, that the pressure reading is erroneous, due to such factors as an occluded catheter, a leaky connector, bubbles in the system, an inaccurately zeroed or calibrated transducer, incorrect catheter or needle placement, or misreading of the transducer monitor. Bleeding from the catheter insertion may falsely elevate local tissue pressure, particularly if a heparinized saline solution is used to flush the catheter. Finally, it must be remembered that tissue pressure cannot be measured in all parts of all compartments at risk. Thus, a sampling problem may exist: the maximum tissue pressure may be at some point other than where the tissue pressure is being measured. These potential sources of measurement error, along with the observation that pressure tolerance varies among individuals, indicate that the diagnosis of a compartmental syndrome cannot be based on pressure measurements alone.

Direct Nerve Stimulation

Time at risk

In considering patients at risk for a compartmental syndrome, one may appropriately ask, How long must the vigil be maintained? In our review of patients having surgical decompression for compartmental syndromes the interval between the etiological event (e.g., contusion or fracture) and the onset of the compartmental syndromes (that is, the earliest evidence of functional deficits related to the compartmental syndrome) averaged 15 hours. In our series of patients with deep posterior compartmental syndromes of the leg, l2 this interval ranged from two hours to six days, with mean and median values of approximately 1% days. In the latter series, the most rapid onset of a compartmental syndrome occurred in a 20-year-old male who sustained a severe contusion of his leg that was followed two hours later by deep and superficial posterior compartmental syndromes. The longest interval between the etiological event and the onset of a compartmental syndrome was six days. This occurred when anterior and deep posterior compartmental syndromes resulted from a compound fracture of the distal tibia and fibula.

In an unpublished study, Veith l3 prospectively monitored the anterior compartmental pressures in eight patients with displaced closed fractures of the tibial shaft. In each case he found that maximum pressure occurred 21 to 36 hours after the tibial fracture. None of these patients developed compartmental syndromes.

Because the time at risk for a compartmental syndrome extends to three, and possibly six, days after a significant extremity injury, the physician cannot relax his watch until the intracompartmental swelling has shown definite signs of resolution.

Differential diagnosis

Acute arterial occlusion, whether from arterial embolization or thrombosis, may mimic a compartmental syndrome by producing signs of compartmental ischemia and loss of neuromuscular function. In the case of isolated arterial occlusion, local tissue and venous pressures are normal. If increased tissue pressure additionally compromises compartmental blood flow, the patient has a superimposed compartmental syndrome. In this case the patient will benefit from surgical decompression. This procedure will improve the local arteriovenous gradient by lowering tissue pressure and local venous pressure.

When faced with a compartmental syndrome and a possible coexistent arterial injury, it is usually prudent to perform a surgical decompression immediately. Then if a significant arterial injury cannot be excluded, an arteriogram can be performed while the patient is still on the operating table so that prompt vascular repair may be carried out if needed. Arteriography performed before the patient is taken to the operating room may excessively delay surgical decompression.

Primary nerve injury may also present a problem in differential diagnosis. Nerve injury is expected to produce deficits in neuromuscular function, but these should not be progressive after the initial injury. Furthermore, signs and symptoms of ischemia and increased tissue pressure should be absent. Direct nerve stimulation as described above and standard nerve conduction velocity measurements may be useful diagnostic adjuncts. Electromyography is not likely to be helpful because several weeks are required before signs of denervation manifest themselves.

Other differential diagnostic possibilities include osteomyelitis, synovitis, tenosynovitis, and deep vein thrombosis, each of which may produce significant local swelling. A compartmental syndrome may be excluded if neuromuscular function is normal. However, it must be remembered that any condition that produces significant intracompartmental swelling may produce a compartmental syndrome.

The most challenging differential diagnostic problems occur when several potential causes of functional loss exist. An example is the loss of anterior compartmental function after an osteotomy of the tibial shaft to correct a valgus deformity. This functional loss could result from (a) a compartmental syndrome, (b) a traction injury to the peroneal nerve, or (c) a traction injury to the anterior tibial artery. l4.

10 surgery questions for your surgeon before having surgery

Surgery for Compartmental Syndromes at the University of Washington, Department of Orthopaedics and Sports Medicine, Seattle, Washington

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