Compartmental Syndromes.

Pressure tolerance

Tolerance of tissue for increased pressure

Increased tissue pressure compromises nerve and muscle function.

The time required to produce functional abnormalities is related to the severity of the pressure-induced circulatory compromise.

Nerve and muscle have a significant potential for recovery and reconstruction following ischemic injury.

Individuals differ with regard to the amount of pressure their limbs can tolerate before neuromuscular deficits are produced.

Hypotension, hemorrhage, arterial occlusion, and limb elevation all appear to reduce the tolerance of limbs for increased tissue pressure.

In Chapter 3 we saw that increased pressure compromises tissue blood flow, tissue oxygenation, and tissue function.. In dealing with clinical compartmental syndromes, the physician is concerned with the pressure tolerance of the tissue, i.e., how much pressure tissue can tolerate before its function becomes abnormal. Abnormal tissue function ensues when local blood flow is reduced to the point where it no longer meets the tissue's metabolic demands.

The pressure tolerance of tissue depends on several factors:

1. The specific effect of increased tissue pressure on local blood flow in the tissue under consideration.
2. The metabolic demands of the tissue.
3. The duration of increased tissue pressure.

Each of these factors may vary from one clinical situation to another. The specific relationship of tissue pressure and tissue blood flow is affected by the presence of hypotension, shock, arterial occlusion, and limb elevation. The metabolic demands of tissue are related to the presence and severity of local tissue injury. Finally, the duration of increased pressure depends on the rate of onset of the compartmental syndrome and the promptness with which it is treated. Thus, the tolerance of tissue for increased tissue pressure will vary considerably among patients. Because of this variability, one specific value for tissue pressure tolerance cannot be applied to the general population. With this perspective, let us review some of the specific data available on the tolerance of nerve and muscle for increased tissue pressure in animal and human model systems.

Tolerance of nerve for increased tissue pressure

Several recent studies have investigated the effects of different tissue pressures on nerve function. Sheridan et all inflated a latex balloon within the anterior compartment of rabbits to investigate the effects of different pressures on the response of nerve and muscle to direct electrical stimulation. Only one of the four rabbits receiving a pressure of 40 mm Hg for six hours demonstrated a loss of response to the electrical stimulus. An applied pressure of 60 mm Hg for six hours produced more consistent functional losses. Each rabbit receiving a pressure of 100 mm Hg for 8 or 12 hours lost all discernible response to nerve or muscle stimulation.

In a different rabbit model system in which external pneumatic pressure was applied, we investigated the effects of different pressures on the conduction velocity of the tibial nerves. Each pressure tested was applied for a period of five hours. Conduction ceased completely in nine animals: seven of the eight that received 80 mm Hg, one that received 70 mm Hg, and one that received 60 mm Hg. An average of 2.2+1.6 hours intervened between the application of pressure and the cessation of conduction in these nine animals (range: eight minutes to four hours).

Rorabeck and Clarke 3 investigated the effect of a pressure-controlled infusion of autologous blood into the anterior compartments of dogs. They found that a pressure of 40 mm Hg reduced peroneal nerve conduction velocity from 40 to 30 m/sec over 2.5 hours. A pressure of 80 mm Hg arrested peroneal nerve conduction after four hours.

Hargens et al 4 investigated a model compartmental syndrome in which tissue pressure was elevated by the pressure-controlled infusion of autologous plasma. They found no changes in peroneal nerve conduction velocity when 10 mm Hg was applied for eight hours. Although there was some slowing of nerve conduction when a pressure of 30 mm Hg was applied for 8 hours and when 40 mm Hg was applied for 14 hours, neither of these conditions was sufficient to arrest nerve conduction. A pressure of 50 mm Hg exerted for 330 minutes did arrest conduction. Less time was required to arrest nerve conduction at higher tissue pressures: nerve conduction ceased after only 50 minutes when a pressure of 120 mm Hg was applied.

In a human model systems we investigated the effect of different externally applied pressures on the nerve conduction velocity and clinical neurological examinations of three normal subjects. Pressures were applied for a maximum of 80 minutes. Each subject demonstrated a different tolerance for increased tissue pressure. Subject 1 maintained essentially normal function until the tissue pressure (as measured by the continuous infusion technique) exceed 65 mm Hg. Subject 2 tolerated pressures up to 75 mm Hg, and subject 3 tolerated pressures only as high as 55 mm Hg. This variability in pressure tolerance could not be attributed to differences in systemic blood pressure. When the pressure tolerance for each subject was exceeded, clinical and electrophysiologic changes occurred in a reproducible sequence.

Tolerance of muscle for increased tissue pressure

It is more difficult to quantify the effect of increased tissue pressure on muscle function than on nerve function. For example, we have been unable to develop a good model for the measurement of the strength of muscle contraction in a limb with increased tissue pressure. The only studies of muscle function found in the literature are those of Sheridan et all in which the response of muscle to direct electrical stimulation was observed.

Other investigators have correlated the amount and duration of pressure application with evidence of muscle damage. In their model compartmental syndrome, Rorabeck and Clarke 3 found increased femoral vein creatinine phosphokinase activity when a pressure of 40 mm Hg was applied to the anterior compartments of dogs. However, the absolute value of this enzyme could not be correlated with the amount of pressure applied. Similar findings were noted for lactic dehydrogenase. Hargens et al 7 investigated the effects of increased pressure in their model system using technetium-99m stannous pyrophosphate. They found that in the dog, intracompartmental pressures in excess of 20 mm Hg produced a significant uptake of the label when maintained for eight hours. From this point the amount of uptake increased dramatically as higher pressures were applied.

Recovery of nerve and muscle

Both nerve and muscle have the capacity for recovery after a significant ischemic insult. Rorabeck and Clarke 3 studied the recovery of canine nerve function for six hours after surgical treatment of model compartmental syndromes. In these short-term studies they found that if surgical decompression was performed within four hours after the initiation of a compartmental syndrome, nerve conduction velocity always returned to normal regardless of the amount or duration of pressure application. If surgical decompression was performed 12 hours after a pressure of 40 mm Hg or more was introduced, the nerve conduction velocity did not return to normal within the six-hour period of observation. In his studies of tourniquet palsy in rabbits, Lundborg 3 demonstrated that the extent and rapidity of nerve recovery depend on the duration of the ischemic insult. All 10 animals with two hours of nerve ischemia recovered after two weeks. Out of 12 animals with six hours of nerve ischemia, only 5 had recovered six weeks later.

Sanderson et al 9 and Vracko and Bendittl indicated that as long as the basal lamina remained intact, muscle had a significant potential for reconstruction after an ischemic insult.

Because nerve and muscle have the potential to recover after an ischemic insult, caution should be used in applying the term "irreversible" to ischemic damage. For the same reason, debridement of potentially viable muscle and nerve at the time of surgical decompression should be kept at an absolute minimum.

Clinical data on pressure tolerance

To help elucidate pressure tolerance in the clinical situation, we investigated 42 patients at risk for compartmental syndromes. These patients were frequently examined for clinical evidence of a compartmental syndrome. Tissue pressure in the compartment at greatest risk was continuously monitored with the infusion technique. No patient whose peak pressure was 45 mm Hg or less developed a clinical compartmental syndrome, whereas all of those with peak pressures of 60 mm Hg or more did develop a clinical compartmental syndrome. Five of the seven with pressures between 45 and 60 mm Hg developed compartmental syndromes, while two did not. Thus, these patients varied significantly with regard to their pressure tolerance.

The variability in pressure tolerance among individuals is of particular interest for two reasons:

1. It indicates that there is no "critical pressure" that can serve as a general criterion for diagnosis and treatment of a compartmental syndrome.
2. It prompts us to investigate the factors responsible for this variability in pressure tolerance to gain a better understanding of the compartmental syndrome.

Factors affecting the pressure tolerance of tissue

The arteriovenous gradient theory for the pathogenesis of a compartmental syndrome (see Chapter 3) enables us to predict that any cause of lowered local arterial pressure will diminish the pressure tolerance of tissue. We have investigated the effects on pressure tolerance of four clinically common causes of reduced local arterial pressure: anesthetic-induced hypotension, hemorrhagic shock, arterial occlusion, and limb elevation. In a rabbit model system we investigated the effect of hypotension induced by halothane anesthetic on muscle blood flow and muscle PO2. 2 A pressure of 60 mm Hg was applied to a hindlimb in two groups of animals: one in which the halothane anesthetic used for preparation was discontinued immediately after preparation, and a second in which the halothane anesthetic was continued throughout the entire five-hour period of pressure application. The circulatory effect of 60 mm Hg was much more profound in the hypotensive animals.

In a second study we investigated the effect of hemorrhagic shock in a rabbit model systems This condition is particularly important clinically because individuals sustaining compartmental syndromes from trauma may also sustain hemorrhagic shock. We investigated the effects on the pressure tolerance of rabbit hindlimbs of an acute 20% hemorrhage produced by the removal of 12 cc of whole blood per kilogram. This 20% hemorrhage reduced mean arterial blood pressure from a mean value of 88_12 to 75_1 1 mm Hg. An applied pressure of 40 mm Hg led to significantly greater reductions in muscle nitrogen washout, muscle oxygenation, and muscle action potential amplitude in the hemorrhage group as compared with the nonhemorrhage group. 11

Zweifach et al 12 investigated the effect of hemorrhage on the uptake of technetium-99m after the application of different intracompartmental pressures in dogs. In this study some animals were bled until mean arterial pressure reached 65 mm Hg. An applied pressure of 25 mm Hg produced the same effect in the hypotensive animal that a pressure of 40 to 50 mm Hg produced in a normotensive animal.

We carried out a study of the effect of superficial femoral arterial ligation on the response of rabbit muscle to an applied pressure of 40 mm Hg l3. Although arterial ligation alone produced significant decrements in muscle nitrogen washout, PO2, and action potential amplitude, all of these parameters fell to zero when the external pressure of 40 mm Hg was applied.

We also manipulated the pressure tolerance of normal human limbs. Instead of inducing systemic hypotension by hemorrhage or anesthetic, we induced local arterial hypotension by elevating the limbs above the level of the heart. Limb elevation reduced local arterial pressure by an amount equal to the pressure produced by the column of blood from the limb to the heart. This hydrostatic column pressure may be calculated by dividing the amount of limb elevation above the heart in centimeters by 1.3 cm of whole blood per millimeter of mercury l3-14.

Elevation of a limb from the dependent position may lower local venous pressure; however, elevation cannot lower local venous pressure below the level of local tissue pressure. Thus, for any given tissue pressure, elevation of a limb above the supine position reduces the local arteriovenous gradient. The diminished pressure tolerance of elevated limbs was apparent in our series of experiments in which anterior compartment muscle PO2 was measured in normal subjects l5. A pressure of 20 mm Hg applied to a limb elevated 54 cm above the heart reduced muscle PO2 by the same amount as a pressure of 60 mm Hg applied to the limb level with the heart.

We demonstrated the functional significance of this lowering of pressure tolerance by limb elevation in another series of experiments. 5 Here, nerve conduction velocity was measured in level and elevated limbs receiving different applied pressures. Once more the tolerance of the limbs for increased tissue pressure was diminished by an amount equal to the hydrostatic column pressure produced by the limb elevation.

These investigations of elevated limbs are clinically important in that they suggest that limbs with compartments showing signs of inadequate blood flow should not be elevated. In this situation, elevation will lower local arterial pressure but will not affect local venous pressure. Thus, the arteriovenous gradient will be further diminished when blood flow is already inadequate. These findings have proved clinically useful: on several occasions the symptoms and signs of compartmental syndromes have resolved upon lowering the affected limbs from an elevated position. Unnecessary surgical decompression has thereby been avoided.

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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