You are in: eMedicine Specialties > Orthopedic Surgery > TRAUMA Compartment Syndrome, Lower ExtremityArticle Last Updated: Nov 14, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Stephen Wallace, MD, Staff, Department of Emergency Medicine, Eastern Idaho Regional Medical Center Stephen Wallace is a member of the following medical societies: American Academy of Emergency Medicine Coauthor(s): Stuart Goodman, MD, PhD, FRCSC, FACS, Associate Chairman, Professor, Department of Functional Restoration, Division of Orthopedic Surgery, Stanford University; Head, Division of Orthopedic Surgery, Stanford University Medical Center; Douglas G Smith, MD, Associate Professor, Department of Orthopedic Surgery, University of Washington, Harborview Medical Center Editors: Steven I Rabin, MD, Clinical Associate Professor, Loyola University Medical Center; Chair, Department of Orthopedic Surgery, Dreyer Medical Clinic; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Samuel Agnew, MD, FACS, Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of Orthopedic Trauma, University of Florida at Jacksonville; Consulting Surgeon, Department of Orthopedic Surgery, McLeod Regional Medical Center; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Jason H Calhoun, MD, FAAOS, Chairman, J Vernon Luck Distinguished Professor, Department of Orthopedic Surgery, University of Missouri Author and Editor Disclosure Synonyms and related keywords: CS, chronic CS, chronic exertional CS, exertional CS, recurrent CS, subacute CS, Volkmann ischemia, chronic exertional compartment syndrome, exertional rhabdomyolysis, recurrent compartment syndrome, subacute compartment syndrome, fasciotomy, compartment release INTRODUCTIONSection 2 of 12
  Compartment syndrome (CS) is a condition in which the perfusion pressure falls below the tissue pressure in a closed anatomic space, with subsequent compromise of tissue circulation and function. Each muscle or muscle group is enclosed in a compartment bound by relatively rigid walls of bone and fascia. The compartments of the lower leg and the volar forearm are particularly prone to developing elevated compartment pressures. As many as 45% of all cases of CS are caused by tibial fractures. Other causes include any long-bone fracture, vascular injury, compression in the setting of a crush injury, drug overdose, and a tight cast or dressing. Late manifestations of CS include the absence of a distal pulse, extremity paresis, and hypoesthesia. If CS is strongly suspected in the clinical examination, operative decompression is the mainstay of therapy. Compartment-pressure measurements are usually reserved for diagnosing chronic CS, for evaluating comatose patients, or for other conditions in which the clinical examination findings are equivocal. Although rhabdomyolysis and subsequent renal failure are among the most severe life-threatening complications, Volkmann contractures are the more commonly observed limb deformities. This article discusses the current understanding of CS of the lower extremity. History of the ProcedureThe original description of CS was by Richard von Volkmann in 1872.1 von Volkmann described contractures of the forearm muscles following tight bandaging for a closed reduction of an elbow fracture. The contractures resulted from ischemic muscle necrosis, which was later termed CS. In 1926, Paul Jepson published his classic paper in which he described prompt surgical decompression for the prevention of paralysis and contracture.2 In 1941, Bywaters and Beall published research on the occurrence of CS following significant crush injuries during World War II.3 In the early 1900s, capsule and balloon measuring devices were implanted surgically and used to make the diagnosis of CS. In 1968, the wick-catheter technique was introduced; its application for compartment-pressure measurements was popularized by Mubarak et al in 1976.4 Almost concurrently in 1976, Matsen et al5 documented the high incidence of CS and recommended an infusion technique for continuous compartment-pressure measurements. More recently, portable surgical-tissue-pressure monitoring devices that are convenient and easy to use have become available from commercial sources. Chronic CS was not described until 1956 and was thought to be a form of shin splints (anterior tibial enthesitis).6 However, with the advent of the fitness boom and the increased popularity of endurance sports, additional research on exercise-induced leg pain has demonstrated that chronic CS is a well-defined clinical entity. ProblemCS occurs whenever increased tissue pressure in a myofascial compartment compromises blood flow to the muscles and nerves within that compartment, resulting in tissue and nerve damage. Two types of CS have been identified, acute and chronic. Acute CS typically occurs subsequent to a traumatic event, most commonly fractures. Symptoms worsen acutely, and irreversible nerve injury and muscle necrosis occur within hours. Chronic CS (also known as chronic exertional CS, exertional CS, recurrent CS, or subacute CS) is a recurrent syndrome that occurs with exercise or work. Originally described in 1956, chronic exertional CS was previously thought to be an atypical form of shin splints.6 This syndrome is usually observed in competitive or collegiate athletes. Often, it occurs bilaterally, and similar to claudication, the pain it causes may be reproducible at a specific exercise distance or time interval. For example, most long-distance runners reproducibly experience the onset of pain within 15 minutes of initiating their run. Athletes may not be able to play through the severe pain. However, runners may be able to continue running with a modified flatfoot strike. Symptoms tend to subside within 1 hour of terminating the activity and are minimal during normal daily activities but return when activity is resumed. In 1990, Pedowitz et al proposed criteria for the diagnosis of chronic CS.7 One or more of the following is required:
FrequencyThe incidence of acute CS varies depending on the inciting event. In 1981, DeLee and Stiehl found that 6% of patients with open tibia fractures developed CS, compared with only 1.2% of patients with closed tibia fractures.8 The reported incidence of CS may underestimate the true incidence because the syndrome may go undetected in severely traumatized patients. The prevalence of CS is much higher in patients who have an associated vascular injury. In 1988, Feliciano et al reported that 19% of patients with vascular injury required fasciotomy,9 but other patients have an estimated 30% incidence. The true incidence of CS that is associated with vascular trauma may not be known because many vascular surgeons perform a prophylactic fasciotomy at the time of the vascular repair in high-risk patients. The incidence of chronic CS in athletes has not been determined. EtiologyCS may be the result of either externally applied compressive forces or internally expanding forces. Fractures, vascular injuries, deep venous thrombosis (DVT), overexertion, fluid sequestration, or prolonged compression (as from a cast or other cause) may lead to CS. As many as 45% of all CS cases are caused by tibial fractures. DVT rarely leads to CS, except in the most severe form of DVT, phlegmasia cerulea dolens. Acute CS has also been reported to follow minor trauma, such as twisting the calf while running, skiing on moguls, and weightlifting. In a 2000 article, Verdolin et al reported a case of bilateral lower extremity CS following prolonged surgery in the lithotomy position with the use of compression stocking devices.10 Chronic CS is usually observed in long-distance runners, basketball players, skiers, and soccer players. This condition is usually the result of minor trauma or repetitive microtrauma (overexertion). The etiology of CS is as follows:
PathophysiologyCS develops after elevated compartment pressure causes muscle and nerve ischemia. Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure. This is also stated by the following formula: LBF = (PA - PV)/R Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can be readily obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg.11 When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur. With myocyte necrosis, myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood. One milliosmole (mOsm) is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure. When tissue blood flow is further diminished, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues to propagate. Some reduction in the local AV gradient can be compensated for by changes in local vascular resistance (autoregulation). However, compartment tamponade occurs as arterial blood flow is occluded. In 1995, Shrier and Magder questioned this traditional hypothesis for the pathophysiology of CS and postulated that within muscle compartments, a critical closing pressure exists (similar to West zone II in lung physiology).12 The authors showed that the increase in this critical closing pressure, which they called Pcrit, rather than an increase in arterial resistance, results in decreased blood flow. The transmural pressure at which blood flow ceases depends on adrenergic tone as well as the interstitial pressure; the pressure at which this occurs is still under debate. However, in general, compartmental pressures higher than 30 mm Hg require surgical intervention. Untreated, within 6-10 hours, the final result of such high compartmental pressures is muscle infarction, tissue necrosis, and nerve injury. For unclear reasons, CS that is associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively.13 Pressure-induced functional deficits are likely due to decreased tissue perfusion rather than a direct mechanical effect. Therefore, the amount of pressure a limb can tolerate depends on limb elevation, blood pressure, hemorrhage, and arterial occlusion. In addition to local morbidity caused by muscle necrosis and tissue ischemia, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation. This circulating myoglobin results in renal injury. Advanced CS may result in rhabdomyolysis, and conversely, rhabdomyolysis may result in CS. Patient mortality is usually due to renal failure or sepsis from difficult wound management. The mechanism of CS following vascular trauma may differ slightly from the above scenario because most cases occur with reperfusion. This reperfusion syndrome is likely related to the ischemic depletion of high-energy phosphate forms and ischemic muscle injury. The pathogenesis of chronic CS was described by Reneman in 1975.14 Muscle bulk increases 20% during exercise and contributes to the transient increase in intracompartmental pressure. Repetitive muscle contraction alone can increase intramuscular pressure to levels that may cause transient ischemia. Chronic CS occurs when the pressure between successive contractions remains high and impedes blood flow. As the pressure rises, arterial flow during muscle relaxation decreases, and the patient experiences muscle cramping. The anterior and lateral compartments of the lower leg are commonly affected; the deep and posterior compartments are less commonly involved. ClinicalThe traditional 5 P's of acute ischemia in a limb (ie, pain, paresthesia, pallor, pulselessness, poikilothermia) are not clinically reliable and manifest only in the late stages of CS. Symptomatically, the patient with CS may experience crescendo pain that is out of proportion to the original injury. The pain is also deep and aching in nature and is worsened by passive stretching of the involved muscles. The patient may describe a tense feeling in the extremity. Pain, however, should not be a sine qua non of CS. Paresthesia, or numbness, is an unreliable early symptom. On physical examination, evidence of trauma and gross deformity should alert the physician to the possibility of a developing CS. Comparison of the affected limb to the unaffected limb is useful. Excessively vigorous examination of a tibial fracture should be avoided because this may exacerbate irritation of the deep posterior compartment. In the clinical scenario in which there is evidence of trauma and gross deformity, a claw-toe deformity might occur; therefore, the patient should be evaluated for such a condition. Sensory nerves tend to be affected before the motor nerves, and selected nerves may be more susceptible than others in the same compartment. For example, in acute anterior lower leg CS, the first sign to present may be numbness between the first 2 toes (superficial peroneal nerve). Decreased 2-point discrimination is the most consistent early finding, and correlation has also been reported between diminished vibration sense (256 cycles/s) and increasing compartment pressure. On deep palpation, a firm wooden feeling is a specific sign when present. Bullae may also be observed. If objective evidence of a major sensory deficit or loss of peripheral pulse is found, the syndrome is far advanced. Laboratory testing that reveals a creatine kinase (CK) measurement that is greater than or equal to 1000-5000 U/mL or demonstrates the presence of myoglobinuria may alert the physician to the occurrence of CS. Patients with chronic CS typically have pain, a tight sensation, and weakness of the muscles of the involved compartment. In anterior CS, a runner may develop foot slap on heel-strike due to weakness of the tibialis anterior. INDICATIONSSection 3 of 12
In the setting of classic CS presentation and physical examination findings, no further diagnostic workup is needed. No consensus exists regarding the pressure for which fasciotomy should be performed. In 1975, Whitesides et al noted that fasciotomy should be performed when compartment pressure rises to within 10-30 mm Hg of the patient's diastolic blood pressure (this value has been coined the delta-P).6 In 1996, McQueen and Court-Brown,15 studying CS in dogs, affirmed the difference of 30 mm Hg between the compartment pressure and the diastolic blood pressure as a more reliable measure than absolute pressure measurements. Many surgeons now use a measured compartment pressure of 30 mm Hg as a cutoff for fasciotomy. Multiple pressure readings are often obtained, and the clinician must decide how to incorporate these readings with the clinical picture in the decision-making process. In addition to direct pressure measurements, other less invasive compartment blood flow–measurement techniques have been studied. These include laser Doppler, methoxy isobutyl isonitrile–enhanced magnetic resonance imaging (MIBI MRI), phosphate nuclear MRI (P-NMR), thallium-201 (201Tl) and technetium-99m (99mTC) sestamibi, and xenon (Xe) scanning. In the setting of a vascular injury, a fasciotomy should be performed on high-risk patients before arterial exploration. High-risk patients include those with prolonged ischemia time, significant preoperative hypotension, associated crush injury, combined arterial and venous injury, or the need for a major venous ligation in the popliteal or femoral area. RELEVANT ANATOMYSection 4 of 12
CONTRAINDICATIONSSection 5 of 12
If CS is diagnosed late, fasciotomy is of little benefit. In fact, fasciotomy is probably contraindicated after the third or fourth day following the onset of CS, and when performed late, severe infection usually develops in the necrotic muscle. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
Other Tests
Diagnostic Procedures
Histologic FindingsHistology is usually not helpful. If necrotizing fasciitis is in the differential diagnosis, intraoperative cultures and a Gram stain may be of benefit. TREATMENTSection 7 of 12
Medical therapy
Surgical therapyThe definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release) with subsequent orthopedic reduction or fracture stabilization and vascular repair, if needed. The goal of decompression is restoration of muscle perfusion within 6 hours. Although several surgical techniques have been described, the double-incision fasciotomy of the lower leg is the most common approach. To minimize soft-tissue injury, especially in the setting of fracture/CS, some surgeons prefer a single-incision approach. Regardless of the approach used, adequate exposure of the entire anterior compartment and, in particular, the peroneal nerve is paramount. Preoperative detailsPartial vascular occlusion may cause a pseudo-CS. Preoperative angiography may be needed to exclude adductor canal compression syndrome and popliteal artery entrapment. In cases of suspected CS, immobilize tibial fractures with the ankle in slight plantar flexion, which decreases the deep posterior compartment pressure and does not lead to an increase in the anterior compartment pressure. (Note: Postoperatively, the ankle is held at 90° to prevent equinus deformity.) Plaster casts should be bivalved, and Webril padding should be split. Intraoperative detailsFasciotomy for acute CS of the thigh Have the anesthesiologist administer an anti-staphylococcal antibiotic (eg, cefazolin or a broad-spectrum cephalosporin). Prepare and drape the thigh in standard surgical fashion. Make a lateral incision beginning just distal to the intertrochanteric line and extending to the lateral epicondyle. Use subcutaneous dissection to expose the iliotibial band, and then make a straight incision through the iliotibial band in line with its fibers. Carefully reflect the vastus lateralis off the lateral intermuscular septum, making sure to coagulate all perforating vessels as they are encountered. Make a 1- to 2-cm incision in the lateral intermuscular septum, and using Metzenbaum scissors, extend the septum proximally and distally along the length of the incision. After the anterior and posterior compartments have been released, measure the pressure of the medial compartment. If the pressure is elevated, make a separate medial incision to release the adductor compartment. Before closing, ensure that meticulous hemostasis has been obtained. Pack the wound open and apply a large, bulky dressing. In 1-3 days, the patient is returned to the operating suite, at which time any additional necrotic muscle is debrided. This process may be required several times. If possible, the skin is loosely approximated during the final operation. Fasciotomy for CS of the lower leg Single- and double-incision techniques have been described. The double-incision technique is safer and more effective and should be used in general. Double-incision fasciotomy (see Images 1-2)
A single-incision fasciotomy is presented in Image 3. Postoperative detailsMonitor the patient's hemodynamic status and maintain adequate blood pressure and volume status. If rhabdomyolysis occurs, continue hydration, monitor urine output and kidney function, and watch potassium status closely. Daily redress wounds that are left open, and undertake subsequent operative debridements as needed. Prophylactic antibiotics may be of benefit. Follow-up
COMPLICATIONSSection 8 of 12
Postoperative motor deficits resulting from CS are initially treated with appropriate orthotic devices (eg, a footdrop brace when the anterior compartment of the leg is affected). If function does not return in about 1 year, tendon transfer and other forms of reconstructive surgery may be considered. Volkmann contracture is the residual limb deformity that continues over weeks to months following untreated acute CS or ischemia from persistent arterial insufficiency. Approximately 1-10% of all cases of CS develop Volkmann contracture.16 Infection is a serious complication of CS. In a retrospective review by Matsen et al,23 11 of 24 extremities that had late surgical decompression developed infections. Five (almost one half) of these infections led to an amputation. Hypesthesia and painful dysesthesia can also result from CS. These may resolve slowly with time. Diphenylhydantoin or phenytoin (Dilantin; Pfizer Inc, New York, NY), gabapentin (Neurontin; Pfizer Inc), and carbamazepine (Tegretol; Novartis, East Hanover, NJ) may be of some value in making the patient more comfortable. Recurrent CS has occurred in athletes and is thought to be related to severe scarring and the subsequent closing of the initial compartment release. Systemic complications include acute renal failure, sepsis, and acute respiratory distress syndrome (ARDS). Most fatalities are due to prolonged intensive care admissions with sepsis and multisystem organ failure. OUTCOME AND PROGNOSISSection 9 of 12
Acute CS may have disastrous outcomes. Muscles tolerate 4 hours of ischemia well, but by 8 hours, the damage is often irreversible. If fasciotomy is performed within 25-30 hours following onset of acute CS, the prognosis is good. Little or no return of muscle function can be expected when the diagnosis and treatment are delayed. Despite early and aggressive fasciotomy, nearly 20% of patients may have persistent sensory or motor deficits at 1-year follow-up.16 Tendon transfers and foot stabilization may be indicated as late treatment for CS, but in most patients, enough scarring and contracture eventually develop in the anterior musculature to prevent footdrop. However, a footdrop brace is indicated for the first few months following onset of CS until fibrosis occurs. Most athletes experience persistent gastrocnemius and soleus muscle weakness; this is thought to be due to the loss of the supporting compartment fascia. In a 1998 study by Awbrey, 44 of 46 patients undergoing compartment release for lower leg chronic CS had excellent pain relief with unimpaired running at 1- and 9-year follow-up.24 FUTURE AND CONTROVERSIESSection 10 of 12
In cases of fasciotomy for anterior exertional CS, lateral compartment fasciotomy may not be necessary. A 1999 study by Schepsis et al demonstrated similar outcomes in athletes with chronic CS who were treated either by single-compartment or dual-compartment release.25 Compartment syndrome in women Kaper et al have suggested that women may be more susceptible to chronic lower leg CS than men are.26 Compartment syndrome following arthroscopy Studies by Nillius and Rooser in 1983,27 Peek and Haynes in 1984,28 and Fruensgaard and Holm in 198829 document the incidence of CS following knee arthroscopy and evaluate fasciotomies as treatment. However, Kaper et al have suggested that emergency fasciotomies are not absolutely indicated.26 Rather, observation of the patient in the recovery room, with serial examinations and repeat compartment-pressure measurements, may be considered. Pressure measurements of the contralateral extremity may be useful as a control to verify the accuracy of the readings. If persistently elevated pressures are recorded or the development of clinical findings consistent with CS are noted, the patient can still be returned to the operating room within the 6 hours prior to development of irreversible myonecrosis. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Compartment Syndrome, Lower Extremity excerpt Article Last Updated: Nov 14, 2007 | ||||||||||||||||||||||||||
