Chấn thương cơ xương potx

Acute Compartment Syndrome in Lower Extremity Musculoskeletal Trauma Abstract 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 death. A variety of injuries and medical conditions may initiate acute compartment syndrome, including fractures, contusions, bleeding disorders, burns, trauma, postischemic swelling, and gunshot wounds. 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. On diagnosis of impending or true compartment syndrome, immediate measures must be taken. Complete fasciotomy of all compartments involved is required to reliably normalize compartment pressures and restore perfusion to the affected tissues. Recognizing compartment syndromes requires having and maintaining a high index of suspicion, performing serial examinations in patients at risk, and carefully documenting changes over time. T he importance of timely diagno- sis and management of compart- ment syndrome was recently empha- sized in a review of the medical-legal aspects of this condition. 1 McQueen et al 2 studied 164 patients (149 men, 15 women) with acute traumatic compartment syndrome. The inci- dence of compartment syndrome was 7.3 per 100,000 in men (average age, 30 years) and 0.7 per 100,000 in women (average age, 44 years). 2 The most common cause of acute com- partment syndrome in this series was fracture (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 com- mon cause (23.2%), with 10% of these occurring in patients taking an- ticoagulants or with a bleeding disor- der. The incidence of compartment syndrome associated with high- and Steven A. Olson, MD, and Robert R. Glasgow, MD Dr. Olson is Associate Professor, Division of Orthopaedic Surgery, Duke University, Durham, NC. Dr. Glasgow is Orthopaedic Surgeon, Division of Orthopaedic Surgery, Royal Alexander Hospital, Edmonton, AB, Canada. None of the following authors or the departments with which they are affiliated has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Olson and Dr. Glasgow. Reprint requests: Dr. Olson, Duke University, Box 3389, Durham, NC 27710. J Am Acad Orthop Surg 2005;13:436- 444 Copyright 2005 by the American Academy of Orthopaedic Surgeons. 436 Journal of the American Academy of Orthopaedic Surgeons low-energy injuries is nearly equal. The presence of open wounds does not mean that compartments are de- compressed; compartment syndrome is seen after open fractures. 2-4 Etiology A variety of injuries and medical conditions may initiate acute com- partment syndrome (Table 1). Frac- tures; contusions; bleeding disor- ders; burns; trauma; postischemic swelling; tight casts, dressings, or external wrappings; and gunshot wounds are some of the most fre- quent causes. 2-12 Anatomic struc- tures, 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. Ther- mal injuries, especially circumferen- tial third-degree burns, can cause an acute compartment syndrome by forming inelastic constrictions, es- chars, and massive edema which, in combination, result in ischemia to neurovascular and muscular struc- tures. 2,5,7,13 Circumferential wraps, such as casting material or cast pad- ding, can lead to restriction of com- partment expansion and increased compartmental pressure. 8,13,14 Re- leasing all circumferential dressings, splitting casts, and cutting casting material results in a marked decrease in intracompartmental pressure. Pneumatic antishock garments have been associated with lower ex- tremity compartment syndromes. Templeman et al 9 reported on a pa- tient who developed bilateral com- partment syndromes in uninjured extremities after wearing a pneu- matic antishock garment. However, inflation pressures <50 mm Hg in these garments have been used for long periods of time (eg, 48 hours for pelvic fractures) without adverse se- quelae. 9 Traction, ankle joint position, and limb positioning have been shown to affect compar tment volume and pressure and to contribute to the formation of compartment syn- dromes. 3,8,10,11,13,15,16 Traction causes the fascia to tighten and constrict the limb, decreasing the compart- ment volume. Shakespeare and Henderson 15 described compartmen- tal pressure changes during calca- neal traction for tibial fractures. Pressure in the anterior and deep posterior compartments rose linear- ly with increasing traction, up to 9.1 kg (Figure 1). The pressure did not fall during the time the traction was applied. For each increase of 1 kg in longitudinal traction, the compart- ment pressure within the deep pos- terior compartment increased by more than 5%; pressure in the ante- rior compartment increased by <2%. Intramuscular pressure is lowest in the anterior compartment with the ankle in the neutral to dorsiflexed position; it is lowest in the deep pos- terior compartment when the ankle is in the plantarflexed position. 13 Longitudinal calcaneal traction tends to dorsiflex the ankle and in- crease the pressure in the deep pos- terior compartment more than in the anterior compartment. After cast application, the pressure in both the anterior and deep posterior compart- ments increases three- to seven-fold, depending on the position of the an- kle. 13 Ankle plantar flexion of 0° to 37° is the most protective position for minimizing the combined risks of anterior and posterior compart- ment syndromes. 13 Table 1 Causes of Compartment Syndrome Fracture Soft-tissue trauma without fracture Intracompartmental bleeding Tight casts, dressings, or external wrappings Thermal injury, burn eschar Extravasation of intravenous infusion Venous obstruction Reperfusion injury following prolonged ischemia Penetrating trauma Figure 1 Change in compartment pressure (percent) with increasing calcaneal pin traction (kg) in patients with tibial shaft fractures. (Adapted with permission from Shakespeare DT, Henderson NJ: Compartmental pressure changes during calcaneal traction in tibial fractures. J Bone Joint Surg Br 1982;64:498-499.) Steven A. Olson, MD, and Robert R. Glasgow, MD Volume 13, Number 7, November 2005 437 Compartment syndromes have been described with prolonged use of the Lloyd-Davies (lithotomy) po- sition with flexion, elevation, and abduction of the well leg during in- tramedullary nailing of femoral frac- tures. 11,13 The combined effects of direct compression on the leg, com- pressive circumferential bindings or stockings, sequential inflatable de- vices, and relative elevation of the limb contribute to increased com- partment pressure, decreased com- partment volume, and decreased blood flow, leading to the formation of compartment syndromes. 11 Many authors have discussed ele- vated compartment pressures asso- ciated with intramedullary nailing of tibial fractures. 4,16-20 The etiology of acute compartment syndrome as- sociated with intramedullary fixa- tion is multifactorial: tissue damage secondary to the injury causes swell- ing, traction decreases the volume of the compartments, reaming forces blood and marrow into the compart- ments, and limb supports may cause outflow constriction. 16 Moed and Strom, 18 using a canine model, found that pressure changes during ream- ing were transient, returning to base- line or lower after the reamer was removed from the intramedullary canal. After nail insertion, the pres- sure remained elevated in the an- terolateral compartment and was transiently elevated in the posterior compartment. Mawhinney et al 20 showed that peak pressures were reached after the first two reaming cycles. Several authors have recom- mended using an unreamed nail in tibial fractures with associated compartment syndrome, or in pa- tients without compartment syn- drome who have elevated compart- ment pressures, in order to minimize pressure elevation during the pro- cedure. 16-19 Tornetta and French 16 reported on anterior compartment pressures during unreamed tibial nailing without traction. Eight of 20 patients had transient compartment pressure elevation ≥40 mm Hg (max- imum, 58 mm Hg); all pressures returned to below 20 mm Hg by the end of the procedure. The authors concluded that patients with a tibial fracture who demonstrate signs and symptoms of an acute compartment syndrome on presentation should undergo a four-compartment fasci- otomy before intramedullary nail- ing, and that pressure elevations during nailing should be minimized by avoiding prolonged traction. McQueen and Court-Brown 4 used continuous compartment pressure monitoring during tibial nailing in a prospective study of 116 patients. Use of reamed versus unreamed nail- ing had no effect on the incidence of compartment syndrome. Tibial nail- ing with or without prior canal ream- ing is a safe method of managing tibial shaft fractures at risk for com- partment syndrome. Prolonged fixed traction should be avoided to the ex- tent possible. Pathophysiology of Ischemia The pathophysiologic mechanism that causes compartment syn- dromes is increased tissue pressure and the resulting development of is- chemia, which leads to irreversible muscle damage. Cellular anoxia is the final common pathway of all of the varieties of compartment syn- drome. However, the interaction be- tween increased compartment pres- sure, 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. 21 More recent evidence indicates that the absolute differ- ence between compartment pressure and blood pressure is the critical variable. 21-26 To avoid collapsing of the veins, the pressure inside the veins cannot be less than that of the surrounding tissue. 7,27 An increase i n compartment pressure results in an increase in venous pressure, leading to a decrease in the arteriovenous gradient. 7 Change in the local vascu- lar resistance can accommodate for some of the reduction in the arterio- venous gradient; however, this change becomes ineffective with in- creasing tissue pressure. Compart- ment syndrome occurs when the lo- cal arteriovenous gradient does not allow sufficient blood flow to meet the metabolic demands of the tis- sue. 7 Vascular tone, blood pressure, duration of pressure elevation, and metabolic demands of the tissue are important in determining whether a compartment syndrome will oc- cur. 7 Muscle ischemia can lead to re- lease of myoglobin from damaged muscle cells. During reperfusion, myoglobin is released into the cir- culation with other inflammatory and toxic metabolites. Myoglobin- uria, metabolic acidosis, and hyper- kalemia can lead to renal failure, shock, hypother mia, and cardiac arrhythmias and/or failure. The de- velopment and extent of these sys- temic effects depends on the sever- ity and duration of compromised tissue perfusion and the size and number of muscle compartments involved. 7 By using objective, noninvasive techniques, experimental and clini- cal investigators have determined the changes in muscle blood flow that occur during compartment syn- drome. 24 Induced compartment syn- dromes in dogs revealed three histo- logic regions of muscle injury. 24 In skeletal muscle, the central portion of the muscle becomes ischemic first. The surrounding zone of mus- cle tissue then shows evidence of partial ischemic injury with in- creased tissue edema and swelling. The peripheral layers of muscle are the last to be affected, often remain- ing normal in incomplete compart- ment syndromes. Microangiograms showed an abundance of epimysial vessels with occlusion of central penetrating branches in specimens from severe cases. 24 Acute Compartment Syndrome in Lower Extremity Musculoskeletal Trauma 438 Journal of the American Academy of Orthopaedic Surgeons Using autologous plasma infusion in a canine compartment syndrome model, Heckman et al 21 studied the ischemic threshold of muscle by in- ducing elevated pressures for 8 hours. Irreversible histologic chang- es, including focal muscle infarction and fibrosis, were documented in all compartments subjected to tissue pressures within 10 mm Hg of dia- stolic pressure. None of the animals with a difference in perfusion pres- sure >30 mm Hg from mean arterial and >20 mm Hg from diastolic pres- sure demonstrated any evidence of irreversible changes, although occa- sional cells underwent myofibrillar degeneration. Mean compartment pressures of 59 mm Hg with ade- quate perfusion pressure were toler- ated for 8 hours without evidence of infarction. The authors concluded that the ischemic threshold of skel- etal muscle, beyond which irrevers- ible tissue damage occurs after 8 hours, is directly related to the dif- ference between the compartment and mean arterial or diastolic pres- sures. The critical tissue pressure differentials were ≤30 mm Hg from mean arterial pressure and ≤20 mm Hg from diastolic blood pressure. 21 Matava et al 22 performed a similar study in canines and also found that the threshold for muscle necrosis was 20 mm Hg less than the diastol- ic pressure. These findings support the hypothesis that tissue damage is directly related to absolute differ- ence between compartment pressure and blood pressure and that this dif- ference is a variable that affects not only microvascular perfusion but also the onset of tissue damage. Bernot et al 25 observed that mus- cle subjected to ischemia before compartment pressurization had a lower threshold for metabolic deteri- oration than did nontraumatized muscle. Hypoxic metabolic changes occurred in the postischemic limbs in all compartments with a perfu- sion pressure (∆P) <40 mm Hg. The metabolic deterioration observed was more rapid and severe as the ∆P value diminished toward a value of 10 mm Hg. Normal limbs did not become metabolically compromised until the ∆P value declined to <30 mm Hg. Postischemic muscle is more easily and much more rapidly compromised metabolically by in- creased interstitial pressure than is normal muscle. 25 Vollmar et al 26 used a skinfold chamber to examine vessel response to increased pressure in hamsters. Venules exhibited early reduction in size proportional to external pres- sure. No similar change was observed in arterioles. This study suggests that impaired venous drainage with cap- illary stasis but without arteriolar constriction is a significant patho- physiologic component in the devel- opment of compartment syndrome. Diagnosis History and Physical Examination Critical to recognizing compart- ment syndrome is having and main- taining a high index of suspicion and performing serial examinations in patients at risk to document chang- es over time. 2,5-7,12 Patient history is important for determining the me- chanism of injury and whether there are associated risk factors for devel- oping compartment syndrome. 6 The classic clinical diagnosis encompass- es the six Ps: pain, pressure, pulse- lessness, paralysis, paresthesia, and pallor. 12 Pain out of proportion to the in- jury, aggravated by passive stretching of muscle groups in the correspond- ing compartment, is one of the earli- est and most sensitive clinical signs of compartment syndrome. However , pain may be an unreliable indicator and may be absent in an established compartment syndrome. 3 Pain per- ception may be diminished or absent in the obtunded patient, thus requir- ing additional diagnostic methods. 7 The absence of pain in a compart- ment syndrome is often caused by a superimposed central or peripheral neural deficit. However, McQueen and Court-Brown 4 reported a patient in whom a compartment syndrome was diagnosed by increased compart- ment pressures before the onset of signs or symptoms. Pressure or firmness in the com- partment, a direct manifestation of increased intracompartmental pres- sure, is the earliest and may be the only objective finding of early com- partment syndrome. Peripheral puls- es are palpable and, unless a major arterial injury is present, capillary refill is routinely present. Only rare- ly is the compartment pressure ele- vated sufficiently to occlude arterial pressure. 7 Paresis is difficult to interpret and may be caused by muscle ischemia, nerve ischemia, guarding secondary to pain, o r a combination of all three. True paralysis is a late finding that is caused by prolonged nerve compres- sion or irreversible muscle damage. Paresthesia is an early sign of com- partment syndrome that, without treatment, progresses to hypesthesia and anesthesia. Sensory symptoms and signs are often the first indica- tion of nerve ischemia. 3 Matava et al 22 have shown that peripheral nerve tissue is actually more sensi- tive to an ischemic event than mus- cle, with nerve function ceasing af- ter 75 minutes of total ischemia. The duration and degree of pressure elevation leading to irreversible nerve injury secondary to compres- sion is uncertain. 22 Typically , abnor- mal neurologic findings are associat- ed with nerves that course through affected compartments. The isolated finding of paresthesia is frequently resolved with the release of con- stricting wraps or bandages alone. Although frequently listed as one of the “P’s,” pallor is uncommon. It oc- curs in the rare circumstance in which arterial inflow is severely di- minished. McQueen et al 3 reported a mean of 7 hours from fracture manipula- tion and fixation to the development of a compartment syndrome in 13 Steven A. Olson, MD, and Robert R. Glasgow, MD Volume 13, Number 7, November 2005 439 fracture patients undergoing com- partment pressure monitoring. Four patients had delayed onset of com- partment syndrome at 14 to 24 hours after fracture manipulation and fixation. 3 However, compart- ment syndrome occasionally occurs 2 to 4 days after the precipitating event; therefore, late onset must be considered. 27 Associated conditions can affect susceptibility to compartment syn- drome or contribute to missed diag- nosis. The perfusion gradient may be inadequate in the presence of systemic hypotension, even with compartments that are supple to physical examination. Anesthetic techniques have been reported to contribute to a delay in diagnosis. Compartment syndromes after sur- gery done to manage fractures have been associated with the use of local nerve blocks, epidural anesthesia, and other forms of regional ane- sthesia. 28-32 Patients receiving epi- dural anesthesia have been reported to be four times as likely to have a neurologic complication than those receiving systemic narcotics. 32 Epi- dural anesthesia increases local blood flow secondary to sympa- thetic blockade, thereby potentially exacerbating swelling of an injured extremity. 32 The use of local anes- thetics combined with narcotics during epidural anesthesia has been shown to increase the likelihood of missed compartment syndromes and is not recommended in the at- risk patient. 31,33 Compartment Pressure Measurement Sometimes the clinical picture may be borderline or the patient ex- amination may be equivocal, unreli- able, or unobtainable. In such in- stances, measuring compartment pressures is recommended to aid the decision-making process. McQueen and Court-Brown 4 reported a pro- spective clinical series using con- tinuous compartment monitoring. When a difference between compart- ment pressure and diastolic blood pressure ≥30 mm Hg was main- tained and compartments were not released, patients had normal mus- cle function at the time of follow-up. Data from preclinical research stud- ies suggest that the ischemic thresh- old of muscle is a perfusion pressure of at least 20 mm Hg between the compartment pressure and the dia- stolic pressure. 21 In a fracture at risk, measuring compartment pressures early in the course of treatment can provide a reference point to detect a trend if later compartment pressure measurements are needed. Various methods of measuring compartment pressures have been described. 34-39 The two most com- mon techniques are a slit catheter and the side port needle. The slit catheter is a low-volume infusion technique. 34 The measurement cath- eter may be left in situ within the compartment for repeated or contin- uous compartment pressure mea- surements over a period of hours. Side port needles, which were de- veloped to measure multiple com- partments, have gained widespread popularity. Moed and Thorderson 35 reported that no statistically signif- icant difference was found between the measurements obtained with the slit catheter and the side port needle. However, measurements with a standard 18-gauge needle were high- er than both the slit catheter and side port needle by nearly 20 mm Hg. Therefore, a standard 18-gauge needle is less accurate and cannot be recommended. Several commercial- ly available pressure measurement devices are available for determining intracompartmental pressures. The location in the compartment from which the measurement is taken is important for accuracy. Seiler et al 37 determined that unin- jured compartments exhibited clin- ically significant intracompartmen- tal pressure measurement variability in the forearm. In their study of 25 patients with closed tibial fracture, Heckman et al 23 reported a relation- ship between compartmental tissue pressure and the distance from the site of the fracture (Figure 2). Pres- Figure 2 The mean compartment tissue pressure measurement in a series of tibial shaft fractures. The pressures are presented by location relative to the tibial fracture site. Data suggest that the highest pressures occur within 5 cm of the fracture. (Adapted with permission from Heckman MM, Whitesides TE Jr, Grewe SR, Rooks MD: Compartment pressure in association with closed tibial fractures: The relationship between tissue pressure, compartment, and the distance from the site of the fracture. J Bone Joint Surg Am 1994;76:1285-1292.) Acute Compartment Syndrome in Lower Extremity Musculoskeletal Trauma 440 Journal of the American Academy of Orthopaedic Surgeons sure was measured at the fracture site and in 5-cm increments distal and proximal. The highest pressure recorded was in the deep posterior or anterior compartment, or both. Eighty-nine percent of compart- ments had the highest pressure mea- surement at the fracture site: 5% at 5 cm distal and 2% at 5 cm proxi- mal. The mean difference in pressure 5 cm from the highest level recorded was 10 mm Hg. These data indicate that pressure measurements should be performed within all compart- ments and at multiple sites, particu- larly within 5 cm of the level of in- jury. 23 Compartment pressure measure- ment is indicated whenever the diag- nosis is uncertain in a patient at risk. Several clinical scenarios fall into this category (Table 2). One of the most beneficial uses of compart- ment pressure measurement is for distinguishing an undermedicated patient from one who is developing compartment syndrome. This di- lemma can occur when a long-acting anesthetic block wears off without appropriate systemic pain medica- tion. In this scenario, the pain can be severely increased with passive range of motion, and residual pares- thesias can remain from a nerve block. It is often helpful to obtain a baseline set of pressure measure- ments in at-risk compartments in a patient who cannot be examined for an extended period. When subse- quent physical examination findings are of concern (eg, increased swell- ing, firmness in the limb), a second set of compar tment pressures can provide evidence of a trend, in addi- tion to the actual ∆P value at the time of pressure measurement. Ob- tunded patients with an increasing trend in pressure should be moni- tored closely. At our institution, a ∆P value of 20 mm Hg from measured compart- ment pressure to diastolic blood pressure is an absolute indicator for fasciotomy. This approach was adopted for three reasons. (1) Basic science data suggest that a ∆P value of 20 mm Hg is safe. (2) In the inves- tigations of McQueen and Court- Brown, 4 fasciotomies were per- formed for a ∆P value of 30 mm Hg and did not identify an absolute min- imal ∆P threshold. (3) In our experi- ence, many patients in the operating room have vasodilatory effects of an- esthesia, leading to transiently low diastolic blood pressure with normo- tensive systolic pressures. In the lat- ter situation, a patient with com- partment pressures in the mid 20s with a supple limb may have a ∆P value <30 mm Hg with the diastolic blood pressure. Laboratory Tests Serum creatine phosphokinase, which reflects muscle necrosis, has been used as an indicator of compart- ment syndrome. 12 Decompression should result in a downward trend of creatine phosphokinase levels. Per- sistently high levels or progression indicates inadequate decompression and ongoing muscle necrosis. Myo- globin, a breakdown product of mus- cle cell lysis, is evidenced by myo- globinuria. It can be misinterpreted as hematuria; a definitive diagnosis is indicated by a positive urine ben- zidine test for occult blood in the ab- sence of red blood cells. Myoglobin is toxic to glomeruli of the kidney and leads to renal failure when the com- partment syndrome is not ade- quately treated. 12 Treatment Following the diagnosis of impend- ing or true compartment syndrome, immediate measures are necessary to ensure that the deleterious se- quelae of compartment syndrome do not occur. First, casts or occlu- sive dressings should be split com- pletely. Cast padding or circumfer- ential dressings should be released around their entire circumference. The affected limb should not be elevated higher than the patient’s heart in order to maximize perfu- sion while minimizing swelling. 7 When, despite these steps, the clin- ical diagnosis of compartment syn- drome remains clear, emergent and complete fasciotomy of all compart- ments with elevated pressures is necessary to reliablynormalize com- partment pressures and restore per- fusion 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 au- thors favor limited incisions, claim- ing low morbidity, while others recommend long incisions, em- phasizing that these are required to decompress affected compar tments adequately. 40-42 Several instances have been reported in which the skin continued to cause compres- sion after fasciotomy through short incisions. 40 Cohen et al 40 deter- mined the effect of the length of the skin incision in posttraumatic compartment syndromes of the lower extremity treated with fascial decompression using a two-incis- ion technique. The affected com- partments initially were released through 8-cm incisions and the pres- Table 2 Indications for Compartment Pressure Measurement One or more symptoms of compartment syndrome with confounding factors (eg, neurologic injury, regional anesthesia, undermedication) No symptoms other than increased firmness or swelling in the limb in an awake, alert patient receiving regional anesthesia for postoperative pain control Unreliable or unobtainable examination with firmness or swelling in the injured extremity Prolonged hypotension and a swollen extremity with equivocal firmness Spontaneous increase in pain in the limb after receiving adequate pain control Steven A. Olson, MD, and Robert R. Glasgow, MD Volume 13, Number 7, November 2005 441 sures recorded. The skin incisions were enlarged by 2-cm increments until readings showed no further de- crease. The final length of the ex- tended incisions averaged 16 cm ± 4 cm. Mean final pressure in the com- partments, which required exten- sion of the incisions, was 13 mm Hg, notably less than pre-extension re- cordings. Long incisions add little to morbidity and influence neither the complication rate nor the late func- tional result. Long incisions also eliminate the risk of the skin acting as an unrecognized compartment envelope, which is especially impor- tant during the hyperemic period following decompression of an is- chemic compartment. 40,42 Compartment syndromes can oc- cur in a variety of locations in the lower extremity, such as the gluteal musculature, thigh, lower leg, and foot. Regardless of location, the key in treatment is to adequately decom- press the muscles involved. In the gluteal region, a posterior incision that provides access to the gluteus maximus and the abductor muscula- ture is adequate. In the thigh, a long single lateral incision can adequate- ly decompress the anterior and pos- terior compartments. Occasionally, a medial adductor incision is re- quired, as well. A one- or two- incision approach can be used in the lower leg. Generally, a long single lateral incision is sufficient for a four-compartment fasciotomy. The one-incision procedure should be performed through a long incision based over the anterolateral calf. The extended incision is made from within 5 cm of either end of the fibula. The basic technique involves identifying the septum between the anterior and lateral compartments, then performing a fasciotomy on each of these compartments. Care should be taken to avoid injury to the superficial peroneal nerve distal- ly. Lateral compartment muscula- ture is then elevated off the posteri- or intramuscular septum. Incision of this intramuscular septum provides access to the lateral portion of the superficial posterior compartment. The superficial compartment is mo- bilized posteriorly to give access to the deep posterior compartment in order to perform the fasciotomy. In the two-incision technique, the location of the medial skin incision is important. The bulk of the mus- culature in the superficial posterior compartment is proximal and re- quires a proximal extent to the inci- sion to adequately decompress the region. However, the bulk of the deep posterior musculature is locat- ed in the distal half of the limb. Ad- equate decompression requires de- taching the soleus origin from the medial aspect of the tibial shaft. Therefore, to adequately decompress all four compartments through two incisions, long medial and lateral in- cisions are required. Foot compart- ment syndrome is typically treated with two longitudinal incisions in the dorsum of the foot, one centered over the fourth metatarsal and one over the space between the first and second metatarsals. Adequate de- compression requires release of the fascia of the intrinsic foot muscles attaching to the metatarsals. In their study of secondary clo- sure of the skin following fascioto- my for acute compartment syn- drome, Wiger et al 43 noted that tight closures may increase intramuscular pressure to dangerous levels. To pre- vent this, limb swelling must be re- duced before secondary closure. Pa- tients were encouraged to perform concentric muscular activity and weight-bearing exercises to assist in reducing elevated intramuscular pressures of the swollen extremities. Active contraction of muscle en- hances lymph flow, and the normal increase of hydrostatic pressure is a powerful edema-reducing mecha- nism. At follow-up, there were no signs of ischemic muscular contrac- ture when intramuscular pressure did not exceed 30 mm Hg during sec- ondary closure in a normotensive patient. 43 At our institution, the fasciotomy site is typically dressed with a wound vac sponge. The patient is re- turned to the operating room 3 to 5 days later to attempt closure. When muscle necrosis is a possibility, the patient must return to surgery after 24 to 48 hours for débridement. Wound closure should not be at- tempted until all necrotic tissue is débrided. Direct closure can be at- tempted when the wound approxi- mates without excess tension. When the wound edges will not oppose easily, split-thickness skin graft is indicated. Outcomes and Complications Sheridan and Matsen 44 reported the clinical outcome of 44 patients who underwent decompressive fasciot- omy. Twenty-two patients were treated with fasciotomy before 12 hours and 22 after 12 hours. In the first group, 68% of patients had nor- mal lower extremity function at the time of final follow-up, compared with only 8% in the delayed- treatment group. 44 Finkelstein et al 45 reported on five patients who underwent fasciotomy later than 35 hours after the estab- lished diagnosis of lower extremity compartment syndrome. In this ret- rospective review, one patient died of multisystem organ failure direct- ly related to complications from the fasciotomy. The remaining four pa- tients required amputation. Fitzgerald et al 41 reported on long-term sequelae of fasciotomy wounds in 60 patients and demon- strated that the patients frequently had complaints at the fasciotomy site. Seventy-seven percent reported decreased sensibility, 7% had teth- ered tendons, and 13% had recur- rent ulcerations within the wound closure area. 41 Although a fasciot- omy incision does result in some morbidity to the patient, the mor- bidity of an incompletely released compartment, delayed diagnosis, Acute Compartment Syndrome in Lower Extremity Musculoskeletal Trauma 442 Journal of the American Academy of Orthopaedic Surgeons or unrecognized compartment syn- drome is substantially worse. It is not possible to determine the precise time a compartment syn- drome begins. Therefore, it is not possible to know how long a com- partment syndrome has been estab- lished. Anecdotal reports suggest that performing a fasciotomy in the setting of a delayed diagnosis can be harmful to the patient and often re- sults in amputation. The dilemma is determining how late a presentation is too late for a fasciotomy. In general, clinical as- sessment of the limb helps with decision-making. The patient with clinical evidence of compartment syndrome who has the ability to vol- untarily contract muscles within the compartment has some viable mus- cle; therefore, fasciotomy is indicat- ed regardless of the delay. Fascioto- my is not performed when a patient has clinical evidence of compart- ment syndrome with a suspected du- ration ≥8 hours, has neither a nerve injury nor a nerve block that could potentially alter the clinical exami- nation, and has no demonstrable muscle function in any segment of the involved limb. Instead, the limb is aggressively splinted to maintain a functional position as the muscle develops fibrosis and contracture. Supportive care should be given for the potential risk of myoglobinuria, which may occur in this scenario. Summary Acute compar tment syndrome is a potentially devastating condition associated with musculoskeletal trauma. The final common path- way is cellular ischemia resulting from increased tissue pressure within an osseofascial compart- ment. Compartment syndrome can occur as a result of many different causes, such as fractures, contu- sions, bleeding disorders, burns, trauma, postischemic swelling, and gunshot wounds. Prompt diagnosis and treatment are key in limiting patient morbidity. The diagnosis of compartment syndrome is usually made based on clinical factors, such as pain, pressure, paresthesia, paral- ysis, and pulselessness. Adjunctive use of compartment pressure mea- surements is warranted in the ma- jority of patients. References Evidence-based Medicine: Moed and Thorderson (reference 35) report a comparison study of measurements of intracompartmental pressures (level II study), and Shakespeare et al (reference 34) compared the slit catheter with the wick catheter (level II study). Younger et al (refer- ence 14) compared prospectively plaster backslabs and plaster cast in a prospective cohort study (level II study). 1. Bhattacharyya T, Vrahas MS: The medical-legal aspects of compart- ment syndrome. J Bone Joint Surg Am 2004;86:864-868. 2. McQueen MM, Gaston P, Court- Brown CM: Acute compartment syn- drome: Who is at risk? JBoneJoint Surg Br 2000;82:200-203. 3. McQueen MM, Christie J, Court- Brown CM: Acute compartment syn- drome in tibial diaphyseal fractures. J Bone Joint Surg Br 1996;78:95-98. 4. McQueen MM, Court-Brown CM: Compartment monitoring in tibial fractures: The pressure threshold for decompression. J Bone Joint Surg Br 1996;78:99-104. 5. Mubarak SJ: Technique of diagnosis and treatment of the lower extremity compartment syndromes in children. Operative Techniques in Ortho- paedics 1995;5:178-189. 6. Gulli B, Templeman D: Compart- ment syndrome of the lower extrem- ity. Orthop Clin North Am 1994;25: 677-684. 7. Ouellette EA: Compartment syn- dromes in obtunded patients. Hand Clin 1998;14:431-450. 8. Janzing H, Broos P, Rommens P: Com- partment syndrome as a complication of skin traction in children with fem- oral fractures. J Trauma 1996;41:156- 158. 9. Templeman D, Lange R, Harms B: Lower-extremity compartment syn- dromes associated with use of pneu- matic antishock garments. J Trauma 1987;27:79-81. 10. Slater RR Jr, Weiner TM, Koruda MJ: Bilateral leg compartment syndrome complicating prolonged lithotomy position. Orthopedics 1994;17:954- 959. 11. Goldsmith AL, McCallum MI: Com- partment syndrome as a complication of the prolonged use of the Lloyd- Davies position. Anaesthesia 1996; 51:1048-1052. 12. Velmahos GC, Toutouzas KG: Vascu- lar trauma and compartment syn- dromes. Surg Clin North Am 2002;82: 125-141. 13. Weiner G, Styf J, Nakhostine M, Ger- shuni DH: Effect of ankle position and a plaster cast on intramuscular pres- sure in the human leg. J Bone Joint Surg Am 1994;76:1476-1481. 14. Younger AS, Curran P, McQueen MM: Backslabs and plaster casts: Which will best accommodate in- creasing intracompartmental pres- sures? Injury 1990;21:179-181. 15. Shakespeare DT, Henderson NJ: Compartmental pressure changes during calcaneal traction in tibial fractures. J Bone Joint Surg Br 1982; 64:498-499. 16. Tornetta P III, French BG: Compart- ment pressuresduring nonreamed tib- ial nailing without traction. J Orthop Trauma 1997;11:24-27. 17. Hak DJ, Johnson EE: The use of the unreamed nail in tibial fractures with concomitant preoperative or intraop- erative elevated compartment pres- sure or compartment syndrome. JOr- thop Trauma 1994;8:203-211. 18. Moed BR, Strom DE: Compartment syndrome after closed intramedullary nailing of the tibia: A canine model and report of two cases. J Orthop Trau- ma 1991;5:71-77. 19. Georgiadis GM: Tibial shaft fractures complicated by compartment syn- drome: Treatment with immediate fasciotomy and locked unreamed nailing. J Trauma 1995;38:448-452. 20. Mawhinney IN, Maginn P, McCoy GF: Tibial compartment syndromes after tibial nailing. J Orthop Trauma 1994;8:212-214. 21. Heckman MM, Whitesides TE Jr, Grewe SR, Judd RL, Miller M, Lawrence JH III: Histologic determi- nation of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma 1993;7:199-210. 22. Matava MJ, Whitesides TE Jr, Seiler JG III, Hewan-Lowe K, Hutton WC: Determination of the compartment Steven A. Olson, MD, and Robert R. Glasgow, MD Volume 13, Number 7, November 2005 443 pressure threshold of muscle is- chemia in a canine model. J Trauma 1994;37:50-58. 23. Heckman MM, Whitesides TE Jr, Grewe SR, Rooks MD: Compartment pressure in association with closed tibial fractures: The relationship be- tween tissue pressure, compartment, and the distance from the site of the fracture. J Bone Joint Surg Am 1994; 76:1285-1292. 24. Har-Shai Y, Silbermann M, Reis ND, et al: Muscle microcirculatory im- pairment following acute compart- ment syndrome in the dog. Plast Re- constr Surg 1992;89:283-289. 25. Bernot M,Gupta R, Dobrasz J, Chance B, Heppenstall RB, Sapega A: The ef- fect of antecedent ischemia on the tol- erance of skeletal muscle to increased interstitial pressure. J Orthop Trauma 1996;10:555-559. 26. Vollmar B, Westermann S, Menger MD: Microvascular response to com- partment syndrome-like external pressure elevation: An in vivo fluores- cence microscopic study in the ham- ster striated muscle. J Trauma 1999; 46:91-96. 27. Matsen FA III, Winquist RA, Krug- mire RB Jr: Diagnosis and manage- ment of compartmental syndromes. J Bone Joint Surg Am 1980;62:286- 291. 28. Hyder N, Kessler S, Jennings AG, De Boer PG: Compartment syndrome in tibial shaft fracture missed because of a local nerve block. J Bone Joint Surg Br 1996;78:499-500. 29. Ananthanarayan C, Castro C, McKee N, Sakotic G: Compartment syn- drome following intravenous regional anesthesia. Can J Anesth 2000;47: 1094-1098. 30. Strecker WB, Wood MB, Bieber EJ: Compartment syndrome masked by epidural anesthesia for postoperative pain. J Bone Joint Surg Am 1986;68: 1447-1448. 31. Dunwoody JM, Reichert CC, Brown KL: Compartment syndrome associ- ated with bupivacaine and fentanyl epidural analgesia in pediatric ortho- paedics. J Pediatr Orthop 1997;17: 285-288. 32. Iaquinto JM, Pienkowski D, Thorns- berry R, Grant S, Stevens DB: In- creased neurologic complications as- sociated with postoperative epidural analgesia after tibial fracture fixation. Am J Orthop 1997;26:604-608. 33. Mubarak SJ, Wilton NC: Compart- ment syndromes and epidural analge- sia. J Pediatr Orthop 1997;17:282-284. 34. Shakespeare DT, Henderson NJ, Clough G: The slit catheter: A com- parison with the wick catheter in the measurement of compartment pres- sure. Injury 1982;13:404-408. 35. Moed BR, Thorderson PK: Measure- ment of intracompartmental pres- sure: A comparison of the slit cathe- ter, side-ported needle, and simple needle. J Bone Joint Surg Am 1993;75: 231-235. 36. Uppal GS, Smith RC, Sherk HH, Mooar P: Accurate compartment pressure measurement using the In- tervenous Alarm Control (IVAC) Pump: Report of a technique. J Orthop Trauma 1992;6:87-89. 37. Seiler JG III, Womack S, De L’Aune WR, Whitesides TE, Hutton WC: In- tracompartmental pressure measure- ments in the normal forearm. JOr- thop Trauma 1993;7:414-416. 38. Abraham P, Leftheriotis G, Saumet JL: Laser Doppler flowmetry in the di- agnosis of chronic compartment syn- drome. J Bone Joint Surg Br 1998;80: 365-369. 39. Willy C, Gerngross H, Sterk J: Mea- surement of intracompartmental pressure with use of a new electronic transducer-tipped catheter system. J Bone Joint Surg Am 1999;81:158- 168. 40. Cohen MS, Garfin SR, Hargens AR, Mubarak SJ: Acute compartment syn- drome: Effect of dermotomy on fascial decompression in the leg. J Bone Joint Surg Br 1991;73:287-290. 41. Fitzgerald AM, Gaston P, Wilson Y, Quaba A, McQueen MM: Long-term sequelae of fasciotomy wounds. Br J Plast Surg 2000;53:690-693. 42. Rush DS, Frame SB, Bell RM, Berg EE, Kerstein MD, Haynes JL: Does open fasciotomy contribute to morbidity and mortality after acute lower ex- tremity ischemia and revasculariza- tion? J Vasc Surg 1989;10:343-350. 43. Wiger P, Tkaczuk P, Styf J: Secondary wound closure following fasciotomy for acute compartment syndrome in- creases intramuscular pressure. JOr- thop Trauma 1998;12:117-121. 44. Sheridan GW, Matsen FA III: Fasciot- omy in the treatment of the acute compartment syndrome. J Bone Joint Surg Am 1976;58:112-115. 45. Finkelstein JA, Hunter GA, Hu RW: Lower limb compartment syndrome: Course after delayed fasciotomy. J Trauma 1996;40:342-344. Acute Compartment Syndrome in Lower Extremity Musculoskeletal Trauma 444 Journal of the American Academy of Orthopaedic Surgeons