Chapter 1 1.

0 Introduction Compartment syndrome is a painful condition that occurs when pressure within the muscles builds to dangerous levels. It occurs when there is increased pressure within a confined space in the body. It usually occurs in areas of the body known as fascial compartments. Fascial compartments are found around muscles. The fascial compartment is a special tissue that forms a membrane layer around the muscle. Fascia do not expand. So, any swelling in a compartment will lead to increased pressure in that area, which will press on the muscles, blood vessels, and nerves. If this pressure is high enough, blood flow to the compartment will be blocked. This can lead to permanent injury to the muscle and nerves. If the pressure lasts long enough, the muscles may die and the limb may need to be amputated. The increased pressure decreases blood flow, which prevents nourishment and oxygen from reaching nerve and muscle cells. Compartment syndrome can be either acute or chronic. Acute compartment syndrome is a medical emergency. It is usually caused by a severe injury including fractures, contusions, bleeding disorders, burns, trauma, postischemic swelling, and gunshot wounds.Chronic compartment syndrome, also known as exertional compartment syndrome, is usually not a medical emergency. It is most often caused by athletic exertion. In acute compartment syndrome, unless the pressure is relieved quickly, permanent disability and tissue death may result. This does not usually happen in chronic (exertional) compartment syndrome. Compartment syndrome most often occurs in the anterior (front) compartment of the lower leg (calf). It can also occur in other compartments in the leg, as well as in the arms, hands, feet, and buttocks.

Chapter 2 Literature Review 2.1 Acute Compartment Syndrome

Acute compartment syndrome is a potentially devastating condition in which the pressure within an osseofascial compartment rises to a level that decreases the perfusion gradient across tissue capillary beds, leading to cellular anoxia, muscle ischemia, and eventually death. It typically occurs subsequent to a traumatic event, most commonly a fracture. However it can be initiated by a variety of injuries including burns and medical conditions such as bleeding disorders. The incidence of compartment syndrome is 7.3 per 100,000 in men (average age, 30 years) and 0.7 per 100,000 in women (average age, 44 years). The most common cause of acute compartment syndrome are fractures (69%); fracture of the tibial diaphysis was most frequent (36%), followed by distal radius fractures (9.8%). Soft-tissue injury without fracture was the second most common cause (23.2%), with 10% of these occurring in patients taking anticoagulants or with a bleeding disorder. Diagnosis is primarily clinical, supplemented by compartment pressure measurements. Certain anesthetic techniques, such as nerve blocks and other forms of regional and epidural anesthesia, reportedly contribute to a delay in diagnosis. Basic science data suggest that the ischemic threshold of normal muscle is reached when pressure within the compartment is elevated to 20 mm Hg below the diastolic pressure or 30 mm Hg below the mean arterial blood pressure. Definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release), with subsequent fracture reduction or stabilization and vascular repair, if needed. The goal of decompression is restoration of muscle perfusion within 6 hours. Long surgical cuts are made through the fascia to relieve the pressure. The wounds can be left open (covered with a sterile dressing) and closed during a second surgery, usually 48 - 72 hours later. Skin grafts may be needed to close the wound.

2.3 Etiology of Acute Compartment Syndrome

A variety of injuries and medical conditions may initiate acute compartment syndrome. Fractures, contusions, bleeding disorders, burns, trauma, postischemic swelling, tight casts, dressings, or external wrappings and gunshot wounds are some of the most frequent causes. The cause of an increased ICP can either be due to an increase in compartmental content or a decrease in compartment size. Increased content can be divided into oedema due to prolonged limb compression or post-trauma, haemorrhage due to vessel laceration or a combination of both, fractures. A decrease in compartment size can occur with constrictive casts, circular dressings and extensive burns. Anatomic structures, including epimysium, fascia, and skin, may limit the potential size of a compartment. Therefore, closure of incisions or defects in these structures should not be done acutely when the patient is at risk for compartment syndrome. Thermal injuries, especially circumferential third-degree burns, can cause an acute compartment syndrome by forming inelastic constrictions, eschars, and massive edema which, in combination, result in ischemia to neurovascular and muscular structures. Circumferential wraps, such as casting material or cast padding, can lead to restriction of compartment expansion and increased compartmental pressure. Releasing all circumferential dressings, splitting casts, and cutting casting material results in a marked decrease in intracompartmental pressure. As mentioned above this syndrome is most often caused by fractures 69%, followed by soft-tissue injuries without fractures 23%, with 10% of these occurring in patients taking anticoagulants or with a bleeding disorder. Traction, ankle joint position, and limb positioning have been shown to affect compartment volume and pressure and to contribute to the formation of compartment syndromes. Traction causes the fascia to tighten and constrict the limb, decreasing the compartment volume. After cast application, the pressure in both the anterior and deep posterior compartments increases three- to seven-fold, depending on the position of the ankle.Ankle plantar flexion of 0 to 37 is the most protective position for minimizing the combined risks of anterior and posterior compartment syndromes.
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2.4 Pathophysiology The pathophysiologic mechanism that causes compartment syndromes is increased tissue pressure and the resulting development of ischemia, which leads to irreversible muscle damage. Cellular anoxia is the final common pathway of all of the varieties of compartment syndrome. However, the interaction between increased compartment pressure, blood pressure, and blood flow are incompletely understood. It was originally suggested that there was a threshold compartment pressure above which irreversible changes would occur. More recent evidence indicates that the absolute difference between compartment pressure and blood pressure is the critical variable. To avoid collapsing of the veins, the pressure inside the veins cannot be less than that of the surrounding tissue. An increase in compartment pressure results in an increase in venous pressure, leading to a decrease in the arteriovenous gradient. Change in the local vascular resistance can accommodate for some of the reduction in the arteriovenous gradient; however, this change becomes ineffective with increasing tissue pressure. Compartment syndrome occurs when the local arteriovenous gradient does not allow sufficient blood flow to meet the metabolic demands of the tissue. Vascular tone, blood pressure, duration of pressure elevation, and metabolic demands of the tissue are important in determining whether a compartment syndrome will occur. Muscle ischemia can lead to release of myoglobin from damaged muscle cells. During reperfusion, myoglobin is released into the circulation with other inflammatory and toxic metabolites. Myoglobinuria, metabolic acidosis, and hyperkalemia can lead to renal failure, shock, hypothermia, and cardiac arrhythmias and/or failure. The development and extent of these systemic effects depends on the severity and duration of compromised tissue perfusion and the size and number of muscle compartments involved. There are three main mechanisms that are hypothesized to cause compartment syndrome. One idea is the increase in arterial pressure (due to increased blood flow due to trauma or excessive exercise) causes the arteries to spasm and this causes the pressures in the muscle to increase even further. Second, obstruction of the microcirculatory system is hypothesized. Finally, there is the idea of arterial or venous collapse due to transmural pressure.

It is concluded that the ischemic threshold of skeletal muscle, beyond which irreversible tissue damage occurs after 8 hours, is directly related to the difference between the compartment and mean arterial or diastolic pressures. The critical tissue pressure differentials were 30 mm Hg from mean arterial pressure and 20 mm Hg from diastolic blood pressure. A similar study performed showed threshold for muscle necrosis was 20 mm Hg less than the diastolic pressure. These findings support the hypothesis that tissue damage is directly related to absolute difference between compartment pressure and blood pressure and that this difference is a variable that affects not only microvascular perfusion but also the onset of tissue damage.

2.4 Diagnosis History and physical examination Critical to recognizing compartment syndrome is having and maintaining a high index of suspicion and performing serial examinations in patients at risk to document changes over time .Patient history is important for determining the mechanism of injury and whether there are associated risk factors for developing compartment syndrome.The classic clinical diagnosis encompasses the six Ps: pain, pressure, pulselessness, paralysis, paresthesia, and pallor. Pain is often reported early and almost universally. The description is usually of severe, deep, constant, and poorly localized pain, sometimes described as out of proportion with the injury. The pain is aggravated by stretching the muscle group within the compartment and is not relieved by analgesia up to and including morphine. However, pain may be an unreliable indicator and may be absent in an established compartment syndrome.3 Pain perception may be diminished or absent in the obtunded patient, thus requiring additional diagnostic methods.7 The absence of pain in a compartment syndrome is often caused by a superimposed central or peripheral neural deficit. A recent study shows that pain-based assessment criteria cannot be absolutely relied upon especially when the presentation is atypical.

Pressure or firmness in the compartment, a direct manifestation of increased intracompartmental pressure, is the earliest and may be the only objective finding of early compartment syndrome. Peripheral pulses are palpable and, unless a major arterial injury is present, capillary refill is routinely present. Only rarely is the compartment pressure elevated sufficiently to occlude arterial pressure. Paresis is difficult to interpret and may be caused by muscle ischemia, nerve ischemia, guarding secondary to pain, or a combination of all three. True paralysis is a late finding that is caused by prolonged nerve compression or irreversible muscle damage. Paresthesia is an early sign of compartment syndrome that, without treatment, progresses to hypesthesia and anesthesia. Sensory symptoms and signs are often the first indication of nerve ischemia. The duration and degree of pressure elevation leading to irreversible nerve injury secondary to compression is uncertain.Typically, abnormal neurologic findings are associated with nerves that course through affected compartments. The isolated finding of paresthesia is frequently resolved with the release of constricting wraps or bandages alone. Although frequently listed as one of the Ps, pallor is uncommon. It occurs in the rare circumstance in which arterial inflow is severely diminished.

Compartment Pressure Measurement The majority of compartment syndromes can be diagnosed from the clinical assessment of the patient. However there are methods of measuring the ICP, which is often done to confirm the diagnosis. It is of particular value in three groups of patients. 1. uncooperative or unreliable patients (e.g. children, intoxicated adults) 2. unresponsive patients (e.g. unconscious) 3. patients with a nerve deficit due to another cause To measure the ICP, a catheter is placed into the compartment at a level close to that of the fracture (approximately 1.5 cm). One must ideally measure the ICP in all compartments of the limb, not just those that are most affected.

This often is not practical, particularly in the leg, so in a conscious patient measurement needs to be performed in the compartment that appears more swollen. In case of fractures the measurement is best done at a distance of about 2 cm from the fracture site. There are several different methods of measuring the ICP, such as a wick catheter or simple needle manometry, so become familiar with the one available in your hospital. Most departments have dedicated compartmental monitoring devices that can give continuous readings. There has been much debate over the level of ICP that necessitates a fasciotomy. The normal resting ICP is 0-8 mmHg, with pain and paraesthesia appearing at pressures between 20 and 30 mmHg. Some authors use an ICP of more than 30 mmHg as the cut-off point for doing a fasciotomy . A prospective study by McQueen et al used a differential pressure (difference between the diastolic blood pressure and the ICP) of less than 30 mmHg as an indication for fasciotomy in compartment syndrome; this led to no compartment syndromes being missed and appears to be a more reliable method compared to the use of an absolute value of ICP alone. Indeed, if an ICP of more than 30 mmHg was used as the critical ICP, 50 patients (43%) would have had unnecessary fasciotomies. Much of the variability in reported pressure thresholds may be due to differences in perfusion state of the limbs. It is thought that a patient with a diastolic pressure of 80 mmHg is likely to tolerate a tissue pressure of 30 mmHg without ischaemia, but a hypotensive patient with a diastolic pressure of similar to the tissue pressure is not. The ideal pressure threshold for performing fasciotomy is still unknown and the literature recommends treating each patient on the basis of their clinical presentation and the progression of their signs and symptoms. In recent times, a differential pressure of 30 mmHg or less is seen as the limit to consider an urgent fasciotomy. It is important to note that in the presence of a clinical suspicion of compartment syndrome, a negative ICP measurement should not exclude the diagnosis, but close observation of symptom progression and serial measurements should be performed. Is important to understand whether the trend of ICP variation and clinical symptoms evolve towards improvement or deterioration. Laboratory Tests
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Serum creatine phosphokinase, which reflects muscle necrosis, has been used as an indicator of compartment syndrome. Decompression should result in a downward trend of creatine phosphokinase levels. Persistently high levels or progression indicates inadequate decompression and ongoing muscle necrosis. Myoglobin, a breakdown product of muscle cell lysis, is evidenced by myoglobinuria. It can be misinterpreted as hematuria; a definitive diagnosis is indicated by a positive urine benzidine test for occult blood in the absence of red blood cells. Myoglobin is toxic to glomeruli of the kidney and leads to renal failure when the compartment syndrome is not adequately treated.

2.5 Treatment Following the diagnosis of impending or true compartment syndrome, immediate measures are necessary to ensure that the deleterious sequelae of compartment syndrome do not occur. Acute compartment syndrome is a surgical emergency. There is no effective nonsurgical treatment. First, casts or occlusive dressings should be split completely. Cast padding or circumferential dressings should be released around their entire circumference. The affected limb should not be elevated higher than the patients heart in order to maximize perfusion while minimizing swelling. When, despite these steps, the clinical diagnosis of compartment syndrome remains clear, emergent and complete fasciotomy of all compartments with elevated pressures is necessary to reliably normalize compartment pressures and restore perfusion to the affected tissues. The length of skin incision has an effect on fascial decompression in the leg associated with an acute compartment syndrome. Some authors favor limited incisions, claiming low morbidity, while others recommend long incisions, emphasizing that these are required to decompress affected compartments adequately. Despite the problems associated with long skin incisions,open fasciotomy by incision of the skin and fascia is the most reliable method for adequate compartment decompression. But performing fasciotomies on a tense, swollen limb can be a daunting and difficult undertaking. Some recommend a technique using two incisions

Management of the fasciotomy wounds remains controversial. Wound complications were recorded in 51% of patients who had primary or delayed primary closure compared with 5% who had split skin grafts.10 If all devitalised tissue has been confidently excised we favour immediate coverage with meshed, split skin grafts secured with a foam vacuum suction dressing. Cosmetic appearance may be improved by subsequent scar revision. Fasciotomies are not benign procedures, and some evidence implies that they may lead to chronic venous insufficiency due to impairment of the calf muscle pump. The role of fasciotomy in cases of compartment syndrome that have been diagnosed at a late stage (after 8 hours) is questionable. Established myoneural deficits seldom recover after fasciotomy. Furthermore, fasciotomies performed after 35 hours from injury were invariably associated with severe infection and even death. Compartment syndrome remains a challenging condition, but significant morbidity can be avoided by prompt diagnosis and decompression using a careful two incision fasciotomy technique.

Chapter 3 3.1 Summary

Acute compartment syndrome with its risk of irreversible muscle and nerve necrosis can be both life- and limb-threatening. It has been described in association with trauma, crush injury, ischemia, and reperfusion episodes. Non-traumatic ACS occurs most commonly in the lower leg, but has also been reported in the forearm following muscle overuse, undue exertion, and bleeding diathesis. It requires urgent diagnosis and treatment. ompartment syndromes are characterized by increased tissue pressure within the confined space of the fascial sheaths. The lower extremities are affected more commonly than the upper extremities. Loss of integrity of the microcirculation with fluid exudation into the interstitial space results in edema formation, muscle swelling, and raised intracompartmental pressure, eventually leading to compression of blood vessels and nerves Acute compartment syndrome is of particular concern because the diagnosis must be made essentially on clinical grounds and must be acted upon promptly if serious and potentially irreversible injury to the relevant compartment is to be avoided. It is progressive and irreversible unless surgical decompression is performed. It has been reported that a tissue pressure 30 mm of Hg less than patients diastolic pressure is diagnostic. The perfusion of the compartment depends on the difference between the diastolic blood pressure and the intracompartmental pressure. They recommend fasciotomy when this pressure difference, known as the Delta p, is less than 30 mm Hg. Access to a precise, reliable, and noninvasive method for early diagnosis of acute compartment syndrome would be a landmark achievement in orthopaedic and emergency medicine.

References

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ALI MOGHTADERI, ROYA ALAVI-NAINI, HADI AZIMI COMPARTMENT SYNDROME: AN UNUSUAL COURSE FOR A RARE DISEASE, American Journal of Tropical Medicine and Hygiene August 2005 1. Steven A.Olson, R.R. Glaogow Acute Compartment Syndrome In Lower Extremity Musculoskeletal Trauma, American Academy of Orthopaedic Surgeons 2005 2. Micheal F Pearse, Lorraine H, Jagdeep N Acute Compartment Syndrome of the leg, British Medical 2002 3. Jonathan W, Dylan E G, Harold C N, Acute Compartment Syndrome with an atypical presentation, JRSM journal 2011

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