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Responding Promptly to Acute Compartment Syndromes
Recognition of acute compartment syndromes depends on a high index of clinical suspicion. The authors review the causes, anatomic considerations, diagnosis, and management of these surgical emergencies.
By Saba Rizvi, MD, and Michael H. Catenacci, MD
An acute compartment syndrome occurs when increased interstitial pressure within an osteofascial compartment compromises its vascular supply. Emergency department clinicians must be alert for the signs and symptoms of this syndrome and initiate timely treatment. Delayed diagnosis and intervention can be devastating, leading to permanent impairment or loss of an affected extremity, rhabdomyolysis, renal failure, or even death.
Compartment syndrome was first recognized by the 19th-century German surgeon Richard von Volkmann in his study of traumatic limb injuries. Von Volkmann described sequelae of ischemia resulting from swelling and overly tight bandaging following elbow fracture. He proposed that prolonged hypoperfusion eventually leads to permanent neurovascular damage of the affected limb. The post-traumatic muscle contracture that occurs after this process bears his name (Volkmann’s ischemic contracture).
UNIQUE BLOOD AND NERVE SUPPLY
The muscle groups of the human limbs are divided into sections or compartments formed by strong and relatively unyielding fascial membranes. Each of these compartments has its own unique blood and nerve supply. In an acute compartment syndrome, perfusion pressure falls below tissue pressure in a closed anatomic space. Increased tissue pressure may occur through increased compartment contents or decreased compartment volume (see box below).
Compartment syndrome occurs most often after high-impact, long-bone fractures, particularly those involving the tibial diaphysis. The reported rate of compartment syndrome associated with tibial fracture is between 1% and 10%. Concomitant vascular injury increases the likelihood of developing compartment syndrome. The incidence is highest in the young, especially men, probably due to increased risk-taking behavior as well as participation in contact sports associated with high-energy injuries.
Compartment syndrome may also arise from processes as diverse as circumferential burns, arterial injuries, snake envenomations, intrauterine strangulation of a fetal limb by the umbilical cord, spider bites, revascularization procedures, prolonged immobilization, or even excessive exercise. A common misconception is that the syndrome is only seen with trauma; in fact, the current literature is replete with descriptions of compartment syndrome occurring without significant trauma.
ELEVATED INTRACOMPARTMENTAL PRESSURES
In a typical case of acute traumatic compartment syndrome, elevated intracompartmental pressures are generated from the force of contact, which may cause a fracture, soft-tissue crush injury, or disruption of the vascular supply with hematoma formation. The incidence of acute compartment syndrome has been shown to be directly proportional to the degree of soft-tissue and bone injury. For example, comminuted open tibial fractures have a higher incidence of compartment syndrome than closed fractures, probably due to the higher degree of force involved in the more severe open injury.
When elevated intracompartmental pressure exceeds tissue perfusion pressure, venous and capillary blood flow is impaired. As ischemia develops, tissue ox-ygenation decreases and energy stores are depleted. Intracellular calcium levels rise as adenosine triphosphate-dependent cell mem- brane transport pumps fail to maintain normal ion gradients. Relative intracellular hypercalcemia activates intracellular proteases, which degrade the metabolic machinery of the cell. With cell membrane breakdown, intracellular osmotically active compounds are extruded into the interstitium. These compounds include myoglobin, lactic dehydrogenase, creatine kinase, potassium, and phosphorus.
Local adverse effects occur when these compounds draw even more intravascular fluid into the interstitial space, creating a vicious circle of further increases in pressure and compartment tamponade. Distant effects include precipitation of myoglobin in the tubules of the kidney, leading to acute tubular necrosis and acute renal failure. Finally, persistent and prolonged ischemia can cause irreversible muscle necrosis and permanent nerve damage, leading to deformities and chronic contractures.
MOST COMMON SITES
Being familiar with the anatomy and contents of each compartment allows clinicians to better detect neurovascular deficits and also recognize which compartments are more at risk than others. Accurately monitoring invasive pressure also requires strict attention to compartmental boundaries and avoidance of neurovascular structures.
A compartment syndrome can occur anywhere in the human body where there is a defined compartment. Upper extremity, lower extremity, hand, foot, eye, and abdominal compartment syndromes have all been described. The following sites for compartment syndrome are the most commonly seen:
Arm compartments. The proximal arm has two compartments, anterior and posterior. The anterior compartment contains the flexors of the arm and the ulnar, median, and radial nerves. The posterior compartment contains the triceps muscles, which perform arm extension. The upper arm compartments can tolerate greater volumes, so they are better able to withstand greater increases in pressure.
The forearm is separated into four compartments: the superficial and deep volar compartments, the dorsal compartment, and the lateral compartment containing the mobile wad of Henry (see image below). The volar and dorsal compartments are separated by a firm interosseous membrane. A connective tissue septum separates the lateral compartment from the antebrachial fascia. The volar compartment contains the digital flexors, and the dorsal compartment contains the extensors.
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Diagram shows a cross section of the upper third of the forearm.
FCU = flexor carpi ulnaris; FDS = flexor digitorum superficialis; FCR = flexor carpi radialis; PT = pronator teres;?FDP = flexor digitorum profundus; FPL = flexor pollicus longus;?ECU = extensor carpi ulnarus; EDQ = extensor digiti quinti; EDC = extensor digitorum communis; ECRB = extensor carpi radialis brevis; ECRL = extensor carpi radialis longus; BR = brachioradialis?
Source: Rowland SA (see Suggested Reading). |
In the upper extremity, the volar forearm compartments are at the highest risk of developing compartment syndrome from traumatic injury. The most frequent injuries associated with compartment syndrome here are supracondylar humerus fractures in pediatric patients and distal radius fractures in adults.
Hand compartments. The hand has 10 small compartments named for the muscle groups contained therein: the hypothenar, the thenar, the adductor pollicis, four dorsal interossei, and three volar interossei. Compartment syndrome of the hand is rare. In one case series, 11 of 19 patients developed the disorder as a result of intravenous injections, with the remainder due to gunshot wounds, crush injuries, prolonged pressure on an immobilized hand, and complications related to an arterial line or arthrodesis of the wrist.
Gluteal region compartments. The gluteal region is divided into three compartments by fasciae continuous with the fascia lata muscle of the thigh. The fasciae splits to encase muscle groups that form three separate compartments: the gluteus maximus, the gluteus medius and minimus, and the tensor fascia lata. Although case reports of gluteal compartment syndrome are rare, they have been described in the literature secondary to falls from a height.
Proximal lower extremity compartment. This region has anterior, posterior, and medial compartments. The incidence of compartment syndrome in this area is less than in the lower leg due to the large size of the muscle groups and greater interconnectivity between the compartments.
Lower leg compartments. The lower leg has anterior, lateral, superficial posterior, and deep posterior compartments (see image below). The anterior compartment of the lower extremity is the most common site of compartment syndrome described in the literature. This compartment contains the four extensors of the foot, the anterior tibial artery, and the deep peroneal nerve. Early signs of compartment syndrome affecting this site are loss of sensation between the first and second toes and weakness of foot dorsiflexion. Late sequelae include foot drop, claw foot (contracture of foot flexors), and neuropathy in the distribution of the peroneal nerve.
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Diagram shows a transverse section through the middle portion of the left leg.
Source: Mubarak SJ, Owen CA (see Suggested Reading). |
The lateral compartment houses muscles that aid in foot eversion and plantar flexion. The superficial peroneal nerve travels through this compartment to supply sensation to the lower leg and foot. The superficial posterior compartment contains the muscles of plantar flexion. No neurovascular structures traverse this compartment. The deep posterior compartment contains muscles that aid in foot plantar flexion, as well as the tibial nerve, posterior tibial artery, and peroneal artery. Increased compartment pressure here may lead to plantar hypoesthesia, weakness of toe flexion, tenseness in the distal medial part of the leg, and pain on passive toe extension.
Foot compartments. The foot has nine complex compartments: the medial, central, and lateral compartments, as well as four compartments that contain the intrinsic muscles of the foot between the first and fifth metatarsals.
STEPWISE PROGRESSION OF SYMPTOMS
Signs and symptoms in compartment syndrome appear in a stepwise fashion. Initially, the most common symptom is pain out of proportion to the apparent injury. Patients usually describe a persistent deep ache, unrelieved by immobilization. Because most cases of acute compartment syndrome occur after traumatic injury, a high index of suspicion is crucial in patients presenting with fractures, as these patients will always present with a certain degree of pain.
As tissue pressure rises and compartments become tense, ischemic nerve dysfunction produces sensory loss and pain aggravated by passive range of motion. A tense compartment with a firm, “wood-like” feeling is the most important diagnostic finding on physical examination. If ischemia continues unchecked, paralysis and pallor from vascular insufficiency are seen. Of note, most patients will retain pulses indefinitely, because compartment pressures almost always remain lower than systolic blood pressure.
Symptoms of acute arterial injury delineated by the classic five P’s (pain, paresthesias, pallor, paralysis, and pulselessness) are often mistakenly applied to acute compartment syndrome. Pallor, paralysis, and diminished pulses are all late findings that suggest vascular disruption and significant damage that has already occurred. Making the diagnosis well before any of these signs appear is critical.
MEASURING COMPARTMENTAL PRESSURES
Maintaining a high index of clinical suspicion is the most important aspect of diagnosing acute compartment syndrome. In clear-cut cases, signs and symptoms are generally enough to prompt surgical intervention. However, diagnosis may prove difficult in the presence of altered mental status, multiple distracting injuries, or equivocal examination findings. In these cases, direct assessment of compartmental pressures is recommended.
There are three objective methods for measuring intracompartmental pressures: the handheld intracompartmental pressure monitor, the needle manometer, and the wick catheter. The pressure monitor is used most often because it is self-contained, convenient to use, and reliable. The device injects a small quantity of sterile saline into the compartment, then gives a reading of compartment pressure on a liquid-crystal display screen.
Erroneous values are the most frequent complication with these devices. The greatest risk to the patient occurs when a falsely low pressure reading is obtained, which can delay or even prevent emergency fasciotomy. To prevent inaccurate readings, take several readings over time, close to the injury site.
TRUE SURGICAL EMERGENCY
With all patients suspected of having compartment syndrome, basic resuscitative measures need to be undertaken, including ensuring an adequate airway, performing oxygenation and ventilation, and starting circulatory support. Associated life-threatening injuries should be identified and treated aggressively.
Acute compartment syndrome is a true surgical emergency. Early recognition is essential for limb salvage and can prevent considerable morbidity and mortality. Delaying diagnosis, relying on nonoperative management, and postponing fasciotomy may result in permanent neurovascular injury, chronic contractures, and deformities.
Affected limbs should be relieved immediately of any external pressure from dressings or casts. In obvious cases of compartment syndrome, decompressive fasciotomy should be performed without delay. Studies have shown that good outcomes are related to speed of decompression, since muscle necrosis can occur within six hours. The goal of fasciotomy is to decompress and open all tight fascial planes, thus restoring blood flow and decreasing elevated compartmental pressures. In settings where no surgeon is available, priority should be given to limb salvage by making a generous incision along the length of the compartment and leaving the wound open.
While the patient is being prepared for surgery, do not elevate the limb, because decreased arterial inflow can exacerbate ischemia. In an experimental model, with the leg elevated and venous stasis induced, Styf and colleagues showed a decrease in leg perfusion pressure with no change in intramuscular pressure. Both mannitol and hyperbaric oxygen therapy have been described as adjuncts in the management of patients with compartment syndrome. Further study of these agents is needed.
In cases with equivocal findings, debate exists over what intracompartmental pressure mandates fasciotomy. Normal healthy muscle compartment pressure is up to 10 mm Hg. Capillary blood flow within a compartment may become compromised with pressures greater than 20 mm Hg. Myoneural tissue is at risk for ischemia and necrosis when pressures reach 30 to 40 mm Hg.
Some authors have based recommendations for fasciotomy on absolute compartment pressures, while others take into account the patient’s mean arterial or diastolic blood pressure. Studies examining absolute compartment pressure readings advocate 30 to 40 mm Hg as an indication for decompression. However, other authors dispute the utility of absolute pressure readings and recognize variability among patients and their tolerance to increased intracompartmental pressures. Variability may depend on the position of a limb relative to the heart, the mechanism of injury, and premorbid hypertension or peripheral vascular disease.
Whitesides and colleagues observed a major decline in muscle perfusion only when muscle compartment pressures were within 10 to 30 mm Hg of the diastolic blood pressure. They termed this pressure difference the “delta-P,” which equals the patient’s diastolic blood pressure minus the absolute compartment pressure. When this threshold was used to guide operative intervention, fewer patients required fasciotomy and no adverse sequelae occurred.
Whether an absolute reading of 30 to 40 mm Hg or an absolute pressure within 10 to 30 mm Hg of diastolic pressure is used, values should be discussed promptly with an orthopedic consultant. Be aware that hypotensive trauma patients, as well as those with premorbid peripheral vascular disease, may develop ischemia with lower absolute compartment pressure values.
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Choong PF: Acute compartment syndrome: ‘to cut or not to cut’. That is the question. ANZ J Surg 77(9):712, 2007.
David V, et al.: Bilateral gluteal compartment syndrome. A case report. J Bone Joint Surg Am 87(11):2541, 2005.
Frink, M, et al.: Long term results of compartment syndrome of the lower limb in polytraumatised patients. Injury 38(5):607, 2007.
Matsen FA III and Clawson DK??: The deep posterior compartmental syndrome of the leg. J Bone Joint Surg Am 57(1):34, 1975.
McQueen MM, et al.: Acute compartment syndrome. Who is at risk? J Bone Joint Surg Br 82(2):200, 2000.
Mubarak SJ and Owen CA: Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg Am 59(2):184, 1977.
Myerson MS: Management of compartment syndromes of the foot. Clin Orthop Relat Res Oct;271:239, 1991.
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Ouellette EA and Kelly R: Compartment syndromes of the hand. J Bone Joint Surg Am 78(10):1515, 1996.
Riede U, et al.: Conservative treatment of an acute compartment syndrome of the thigh. Arch Orthop Trauma Surg 127(4):269, 2007.
Rowland SA??: Fasciotomy: the treatment of compartment syndrome. In Green DP (ed): Operative Hand Surgery, 3rd ed, Churchill Livingstone, 1993.
Sheridan GW and Matsen FA 3rd: Fasciotomy in the treatment of acute compartment syndrome. J Bone Joint Surg Am 58(1):112, 1977.
Styf J and Wiger P: Abnormally increased intramuscular pressure in human legs: comparison of two experimental models. J Trauma 45(1):133, 1998.
Suzuki T, et al.: Arterial injury associated with acute compartment syndrome of the thigh following blunt trauma. Injury 36(1):151, 2005.
Tintinalli JE, et al. (eds): Emergency Medicine: A Comprehensive Study Guide, 6th ed, McGraw-Hill Professional, 2003, pp. 1746-1749.
Tiwari A, et al.: Acute compartment syndromes. Br J Surg 89(4):397, 2002.
Wattel F, et al.: Acute peripheral ischaemia and compartment syndromes: a role for hyperbaric oxygenation. Anaesthesia 53 (Suppl 2):63, 1998.
Whitesides TE, et al.: Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop Relat Res Nov-Dec(113):43, 1975.
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