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Fasciotomy

Despite the fact that Richard von Volkmanns description of the sequelae of an untreated compartment syndrome of an extremity was published in 1881, it is interesting to note how much controversy and confusion persist regarding this topic more than 125 years later.1 On general/trauma and vascular surgery services, there are weekly discussions about this diagnosis such as the value of palpation of a compartment, the most accurate method of measuring compartment pressures, and the absolute numerical value that should prompt a fasciotomy. The value of nonoperative management including the best position for the involved extremity or the role of hyperbaric oxygen (HBO) is discussed as well. In addition, many experienced surgeons overlook the variability in patients responses to elevated compartment pressures in injured or ischemic extremities. Trainees continue to be unsure about the technical aspects of standard fasciotomies, including the skin incision used to decompress the volar compartments of the forearm or the location of the deep posterior muscle compartment of the leg. Finally, few general/trauma or vascular surgeons are aware of the numerous options for closure of fasciotomy sites or the long-term sequelae after extensive fasciotomies have been performed in injured or ischemic extremities. This article describes the history and current body of knowledge of compartment syndromes and fasciotomies in the extremities. Both welldocumented and preliminary studies are reviewed, and options for diagnosis, nonoperative management, operative management and closure are discussed. This article should be a road map for the surgical trainee or young surgeon and a continuing source of references and discussion for the established surgeon with extensive experience in managing patients who needed fasciotomies to treat compartment syndromes.

Denition of Compartment Syndrome and Fasciotomy


In the classic book entitled Compartmental Syndromes by Frederick A. Matsen III, MD, in 1980, a large number of synonyms for what surgeons now call compartment syndrome are listed.2 Included among these are Volkmanns ischemia, impending ischemic contracture, rhabdomyolysis, and calf
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hypertension.3 The terms compartment and compartmental syndrome are now widely accepted and used interchangeably in the surgical literature. Matsens denition that a compartmental syndrome is a condition in which increased pressure within a limited space compromises the circulation and function of the tissues within that space is still used by many authors.3 Matsens denition describes the 4 essential components of a compartment syndrome: limiting envelope, increased tissue pressure, reduced tissue circulation, and abnormalities in neuromuscular function. Of interest, increases in intracranial pressure, intrapericardial pressure, intra-abdominal pressure, and intracapsular organ pressure, all much discussed in the modern trauma center, cause a similar pathophysiology in their end organs.4 Although there are several potential limiting envelopes around the muscle compartments of an injured or ischemic extremity, the investing fascia is the one that most frequently contributes to a compartment syndrome. Fasciotomy refers to a surgical incision or splitting of the fascia to relieve a compartment syndrome.

History
In a paper by O. Hildebrand in 1906, there is a list of patients previously noted to have ischemic paralyzes and contractions, presumably from failure to treat compartment syndromes.5 In the 1st Group a 9-year old patient of a (Dr.) Frank Hamilton from 1855 is described. Nine months after suffering a fracture above the kondylen of the humerus, it was noted that the forearm and hand are nearly totally paralyzed and sometimes very painful.5 Garn states that this is the rst report of a patient with a presumed ischemic contracture from an untreated compartment syndrome.6 Most authors attribute the original description of the sequelae of an untreated compartment syndrome to the classic paper by F. Konig (in Gottingen), E. Richter (in Breslau), and R. Volkmann (in Halle) in 18811 (Fig 1). Richard von Volkmann was born in Leipzig, Germany, on August 17, 1830, graduated from medical school in 1854, and became Professor of Surgery and Director of the Surgical Clinic at Halle (near Leipzig) in 1867. He is credited with descriptions of cancers induced by exposure to tars and parafns (1875), rst excision for cancer of the rectum (1878), and the aforementioned manuscript on sequelae of untreated compartment syndromes.7 He eventually became President of the University of Halle and was a widely published poet under the pseudonym Richard Leander.6,7 In an earlier publication and in Die ischemischen Muskellanhmungen und -Kontrakturen or The Ischemic Paralysis of Muscles and Contraction, von Volkmann and his coauthors emphasized 4 features.1,8
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FIG 1. Richard von Volkmann (1830-1889) was Professor of Surgery, Director of the Surgical Clinic,
and, later, President of the University of Halle, Germany (near Leipzig). The adjacent picture is of the rst page of the classic article describing sequelae of an untreated compartment syndrome and coauthored by von Volkmann. (Reprinted with permission from Konig et al.1)

1. Tissure ischemia from loss of arterial inow for more than 6 hours. Kraske pointed out clearly in his impressive work, that even the muscles of animals can not stand a total cutting of the arterial ow of blood for more than six hours. 2. Cause of loss of arterial inow. Paralysis and contraction caused by bandages that are too tight, [especially at the forearm and the hand, more seldom at the lower limbs] have to be called ischemic. This is caused by continuous cutting off of the blood from artery. 3. Pathophysiology of untreated ischemia/compartment syndrome. The paralysis is based on the fact that the primitive bundles of muscles die away when they dont get oxygen. The contractile substance coagulates, decays in clods and is reabsorbed later (Heidelberg, Kraske). 4. Long-term prognosis. The prognosis of the ischemic paralysis of muscles and the contraction depends therefore on the amount of the collapsed and decayed bers. The worst cases on hands and ngers have to be considered as incurable. Garn has emphasized that von Volkmanns comments on tight bandages and occlusion of arterial inow as causes of the compartment syndrome rather than increased pressure within the muscle compartment (understood 90 to 100 years later) limit the value of this manuscript. He gives particular credit to E. Lesser, who subsequently described the increased connective tissue pattern and loss of intracellular nuclei seen microscopically in the muscles after untreated compartment syndromes.6,9
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FIG 2. Picture of rst page of the classic article by John B. Murphy (1857-1916) of Chicago in which fasciotomy was suggested if cyanosis of the whole forearm and hand developed after a fracture in the upper extremity. (Reprinted with permission from Murphy JB,11 Copyright 1914 American Medical Association. All rights reserved.)

In the aforementioned comprehensive review by O. Hildebrand in 1906, the pathophysiology of the compartment syndrome as currently understood is well described.5 Hildebrand states that muscle necrosis is because the bandages on the limb are too tight, or the small arteries can not extend due to the pressure of the tissue that lies around, or there is a congestion in the veins and capillary congestion. Similar comments were made in 1906 by L. Brandenheurer, who was the rst to describe the long-term sequelae of untreated compartment syndrome as Volkmanns ischemic contracture.10 John B. Murphy (1857-1916) of Chicago, well known for his description of the Murphy button for intestinal anastomosis and the end-to-end repair of an injured femoral artery, is credited with several seminal contributions to the knowledge of compartment syndromes. He described the bleeding and transudation of edema uid after fractures and stated that the tension in the subfascial zone in the forearm can be so great as to cause cyanosis of the whole forearm and hand.11 Remarkably, he then suggested that if the cyanosis still continues with the forearm extended and elevated, the fascia on the antero-ulnar side of the forearm should be split for a distance of 3 to 6 inches subcutaneously11 (Fig 2).
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Barney Brooks (1884-1952), rst Chief of Surgery at Vanderbilt University School of Medicine, hypothesized that venous obstruction was the cause of a later Volkmanns contracture based on his own laboratory studies in 1922. He stated that the etiologic factor is either an acute venous obstruction or a temporary pressure anemia followed by reestablishment of circulation to the damaged tissue.12 Paul N. Jepson, a fellow in orthopedic surgery at the Mayo Clinic at the time, subsequently performed a series of elegant experiments involving the etiology of ischemic contracture.13 Much as Brooks, he stated that the lesion of ischemic paralysis as seen in man was reproduced in animals by bandaging one extremity and by preventing the return of the venous blood. He noted that the intrinsic pressure causes local myositis and then a pressure on the nerves (usually the median and ulnar). He further stated that if the intrinsic pressure is relieved within a short time after the formation of the hematoma, the patient will usually recover.13 Therefore, both Murphy in 1914 and Jepson in 1926 suggested the benets of a fasciotomy in preventing a later ischemic contracture but not the immediate benet of relieving an acute compartment syndrome. Grifths classic article in 1940 was one of the rst to suggest that ischemic contractures were due to arterial injury and to the accompanying spasm of the collateral circulation.14 Also, he rst described the 4 Ps to aid in the diagnosis of a compartment syndrome. These included pain in the forearm with passive stretch, painless onset, pallor, and pulselessness. This list has, of course, been modied and extended and is used to describe signs of arterial occlusion and/or compartment syndrome in current textbooks. In similar fashion Foisies review of Volkmanns ischemic contracture in 1942 suggested that spasm of the main artery and the collateral circulation leading to nearly complete ischemia was the cause of posttraumatic contractures.15 He further stated that arterectomy gives the best results in stubborn cases.15 Garn states that the extensive dissection necessary to complete arterectomies by military surgeons in the 1940s undoubtedly included fasciotomies with subsequent resolution of the acute compartment syndrome.6 During the German blitzkrieg of London in World War II, patients with the related syndrome of crush injury, rhabdomyolysis, and secondary renal failure were well described by Bywaters and Beall.16 The difference between an acute compartment syndrome from venous obstruction due to increased tissue pressure versus an increased size of a crushed compartment due to direct muscle damage was not recognized at the time.
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FIG 3. Potential limiting envelopes around musculofascial compartments of extremities. (Reprinted with permission from Matsen FA III,2 www.orthop.washington.edu.)

H.J. Seddons review of Volkmanns Ischemia in the Lower Limb in 1966 was one of the rst to emphasize the problem of untreated compartment syndromes in the lower extremities.17 He described the connection between acute occlusion of a major named artery from orthopedic trauma or operation, secondary ischemia and swelling of muscle, and the importance of prompt incision of the overlying deep fascia.17 In Seddons well-documented cases the particular sensitivity of the exor hallucis longus muscle in the deep posterior muscle compartment of the leg to ischemia/edema after arterial occlusion in the thigh or knee was noted. Several studies in the 1970s documented that the application of external pressure to the extremities of both animal models and human subjects reduced local blood ow, muscle pO2, and velocity of nerve conduction.18-25 According to Matsen26 a set of theories to explain these phenomena was proposed,15,20,27,28 but it was the arteriovenous gradient theory (to be discussed) that is still accepted to this day.29-31 The relationship between ischemic, reperfusion, or traumatic edema, elevated pressures in myofascial compartments of the extremities, venous
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TABLE 1. Causes of increased content of a musculofascial compartment Edema of contents IschemiaIncreased capillary permeability Arterial occlusion Low ow state Near exsanguination/secondary extremity compartment syndrome Ischemia-reperfusion syndrome Septic shock Systemic inammatory response syndrome Thermal/electrical burn Intra-arterial injection of drug Venous outow obstruction Compressed extremity secondary to overdose of illicit drug Obstruction of venous outow (phlegmasia cerulea dolens) Improper positioning in operating room Nonischemic edema Edema of proximal extremity Orthopedic procedure (open reduction-internal xation/tibial osteotomy) Inltration/injection Inltration of venous infusion Injection of foreign material Medical causes (hypothyroidism, diabetes mellitus, leukemic inltrates, nephrotic syndrome, tetany, etc.) Hemorrhage into compartment Anticoagulation/bleeding disorder/coagulopathy Fracture of long bone Arterial injury Venous injury Increased size of contents Increased muscle mass from androgens/exercise Adapted with permission from Matsen FA III,2 www.orthop.washington.edu.

narrowing or occlusion, reduction in arteriovenous (AV) gradients, and the importance of early fasciotomy to relieve the increased pressure was subsequently described by numerous authors in the 1970s and 1980s.2,19,32-37

Etiology
Each muscle in a musculofascial compartment of an extremity is covered by a brous epimysium, and all muscles in the compartment are covered on some surface by investing brous fascia. The skin and any dressings, splints, or casts applied by physicians are the remaining 2 potential limiting envelopes38 (Fig 3). Therefore, compartment syndromes are caused by increased content or decreased volume of the compartment. The extensive list of causes of increased content (edema of contents, hemorrhage into compartment, increased size of contents; Table 1)
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TABLE 2. Causes of decreased volume of a musculofascial compartment Air splint Elastic wraps Excessive traction Pneumatic antishock garment Premature closure of fasciotomy site Tight splint or cast

is in marked contrast to the limited list of physician/treatment related causes of decreased volume4 (Table 2).

Pathophysiology
Many of the causes of edema of the contents of a compartment, the most common etiology of a compartment syndrome, are related to ischemia (Table 1). Ischemia leads to inefcient anaerobic metabolism at the cellular level, changes in cellular membrane function, and the presence of pores or gaps between endothelial cells.39 The break in integrity of the endothelium of a capillary results in increased capillary permeability, movement of intravascular uid into the interstitial space, and secondary edema. Therefore, it is not surprising that acute arterial occlusions from trauma or emboli or low ow states are so often followed by a compartment syndrome. In addition, there has long been evidence that the endothelial enzyme xanthine oxidase (catalyzes the oxidation of hypoxanthine to xanthine and of xanthine to uric acid) derived from xanthine dehydrogenase during ischemia is responsible for the subsequent production of superoxide radicals during reperfusion.40 The transformation of superoxide radicals to hydroxyl, carbon, and nitrogen free radicals leads to further injury to endothelial cells, calcium entry, activation of neutophils, and further edema in a myofascial compartment.41 Finally, the dying cells that are caused by ischemia-reperfusion release breakdown products that are procoagulants. Blaisdell has stated that activation of the intrinsic clotting system by these procoagulants is responsible for extension of venular thrombosis and vascular spasm in the arteriolar collateral.42 Both of these sequelae will, of course, further exacerbate edema in a myofascial compartment. The end result of an increase in the content or a decrease in the volume of a musculofascial compartment is a change in the aforementioned AV gradient as described by Matsen and others.2,19,32-37 Local blood ow is a function of arterial pressure, venous pressure, and vascular resistance as illustrated in the following equation26,43:
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FIG 4. The effect of increased tissue pressure on the local arteriovenous (AV) gradient. The AV gradient is indicated diagrammatically by the height of the capillary loops. Because local venous pressure (LVP) cannot be less than local tissue pressure (shaded block), increased local tissue pressure reduces the local AV gradient. (Reprinted with permission from Matsen FA III,2 www. orthop.washington.edu.)

LBF

PA

PV/R

where LBF is local blood ow, PA is local arterial pressure, PV is local venous pressure (LVP), and R is local vascular resistance. Matsen has stated that PV cannot be less than local tissue pressure.26 When tissue edema or hemorrhage is present in a musculofascial compartment or the compartment is being compressed externally, the increase in tissue pressure increases PV and decreases the local AV gradient (Figs 4 and 5). A further reduction in AV gradient will occur if PA is decreased.26 The process of vascular autoregulation (ie, a decrease in R in the formula above) can ameliorate the decrease in AV gradient and maintain local blood ow. When the decrease in AV gradient exceeds the compensation provided by autoregulation, capillary ow to O2-sensitive tissues such as muscles and nerves in a musculofascial compartment is inadequate. Based on numerous studies and clinical observations,44-52 Whitesides and Heckman have described the sequelae of ischemia in muscle or nerve from arterial occlusion (decreased PA) or compartment syndrome over time.48 First, in injuries that produce complete ischemia, skeletal muscles remained electrically responsive for up to 3 hours and survived for as long as 4 hours without irreversible damage. Second, total ischemia of 8 hours duration (in muscle) produced completely irreversible changes; variable results occurred after 6 hours of total ischemia. Third, peripheral nerves conducted impulses for 1 hour after the onset of total
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FIG 5. Effect of externally applied pressure (abscissa) on local AV gradient (ordinate). Arterial
pressure (PA) and venous pressure (PV) were measured in a human subject by direct cannulation of the dorsalis pedis artery and a dorsal foot vein, respectively. Higher applied pressures produced a lower AV gradient. (Reprinted with permission from Matsen FA III,2 www.orthop.washington.edu.)

ischemia and could survive for 4 hours with only neurapraxic damage. And, last, after 8 hours of total ischemia, axonotmesis was usual and irreversible changes in the nerve commonly occurred. Based on this pathophysiology, the extent of adverse sequelae once a compartment syndrome develops will depend upon: blood pressure, compartment pressure, time that elevated compartment pressure has been present, metabolic demands of muscles and nerves in the affected compartment, and individual susceptibility.

Diagnosis
There is much information on the differences in symptoms and signs in extremities in which there is an arterial injury or occlusion, a neurapraxia, crush injury, or a compartment syndrome53,54 (Table 3). Yet, criteria for the diagnosis of a compartment syndrome vary considerably among general, trauma, and vascular surgeons. Depending on the patients
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TABLE 3. Differences between an extremity with arterial occlusion, neurapraxia, crush injury or a
compartment syndrome

Arterial occlusion Tense compartment Pain with stretch Paresthesia or anesthesia Paresis or paralysis Pulses intact

Neurapraxia

Crush injury / * ?

Compartment syndrome

Adapted with permission from Mubarak and Carroll.53 *Edema develops over time.

clinical problem, the time available to perform a comprehensive history and physical examination, operative ndings, treatment, and the surgeons belief in measurements of compartment pressure, there are several diagnostic pathways that may be chosen.

History and Physical Examination Are Limited or Were Not Performed


There are injured patients, particularly those with a traumatic brain injury, injury to the spinal cord, alcohol intoxication, or use of illicit drugs, in whom a history and physical examination of an extremity are limited. The issue of limited communication is present, also, in very young patients or in older patients with acute peripheral arterial occlusions in the presence of sequelae of a prior cerebrovascular accident. The same would be true in other injured patients with active bleeding from multiple injuries or a solitary injury to an extremity that mandates an emergency operation. With any of these scenarios, some surgeons will perform a fasciotomy at the rst operation without measuring compartment pressures when they believe a high risk situation or patient is present. Examples of patients thought to be at high risk to develop a posttraumatic or postoperative compartment syndrome are listed in Table 4.32,55,56 This aggressive approach in high risk patients in the absence of a conrmatory history and physical examination or documentation of elevated compartment pressures undoubtedly results in a certain number of unnecessary fasciotomies. On the other hand, it eliminates the need for serial physical examinations or serial/continuous measurements of compartment pressure. Most importantly, it avoids delays in diagnosis that accounted for some of the nearly 20% return to the operating room for delayed fasciotomies in one older series.57
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TABLE 4. Patients at high risk to develop a compartment syndrome in an extremity32,60 History Hypotension in the eld Delay in treatment, especially if no arterial inow for 4 to 6 hours Disproportionate pain Limited physical examination Patient with ongoing hypotension during resuscitation or operation Evidence of crush injury Extremity is swollen with or without local injury Operative ndings and treatment Combined arterial and venous injuries, especially to the popliteal artery and vein Need for arterial or venous ligation or early thrombosis of repair

History and Physical Examination Can Be Performed


The most important elements of the patients history of the present illness as related to the development of a compartment syndrome are hypotension in the eld in the presence of an obvious injury to an extremity, a delay in revascularization, or the presence of disproportionate pain. Both hypotension from bleeding and loss of arterial inow are causes of the previously described ischemic edema in the compartments of extremities. Ischemic edema is progressive over time and, therefore, aggravated by a delay in revascularization. Pain or tightness disproportionate to the magnitude of injury, particularly after revascularization, relocation of a dislocated joint, or realignment of a displaced fracture, is often present in the patient with an undiagnosed compartment syndrome.55,58-60 One current textbook chapter describes the pain as unrelenting and seems to be unrelated to the position of the extremity or to immobilization.61 This element of the history of the present illness is obviously subjective and affected by the patients level of consciousness, response to pain, and effects of analgesics and sedatives. It is interesting, however, that senior surgeons who have missed the diagnosis of a compartment syndrome in the past often recall the disproportionate pain described by the patient (Fig 6). The 5 components of a physical examination pertinent to an extremity in which a compartment syndrome may or may not be present are inspection, palpation and passive stretch of muscles in the compartments, evaluation of sensory function, evaluation of motor function, and evaluation of perfusion.4,37,59-63 Swelling of an injured or uninjured extremity in the patient with a secondary extremity compartment syndrome (SECS) (to be discussed) is present on inspection in many patients with compartment syndromes.
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FIG 6. Loss of right anterior compartment muscles in patient with missed compartment syndrome after repair of injury to popliteal artery at outside hospital. Patient was transferred for nancial reasons and because of disproportionate pain after successful revascularization.

This is a nonspecic nding since most patients with fractures, dislocations, contusions, crush injuries, or gunshot wounds have swelling of the injured extremity without a compartment syndrome being present. Also, it may not be possible to visualize swelling in the anterior and deep posterior compartments of the leg or the deep volar compartment of the forearm. The presence of an open fracture on inspection of the injured extremity is one nding that, in the minds of some trainees, precludes the presence of a compartment syndrome. This is an incorrect assumption since 6% to 9% of open fractures in the lower extremities have been associated with compartment syndromes in the past.64,65 The same caution holds true with palpation of the supercial compartments of an extremity to elicit tenderness. Although tenderness is usually present when a compartment syndrome exists, it may, of course, be related to the original injury. A more helpful maneuver is to see if pain is described by passive stretching of the muscles in the musculofascial compartment through movement of ngers or toes.58,59,61 For example, forced plantar exion of the toes and ankle would stretch the muscles in the anterior compartment of the leg and cause pain if a compartment
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FIG 7. Crush injury to right forearm resulting in compartment syndrome with tapering of major arteries and temporary occlusion of collateral arteries. (Reprinted with permission from Feliciano DV.4)

syndrome is present. This would depend, of course, on the magnitude of the original injury in the anterior compartment. Because nerves in a compartment are so sensitive to diminished oxygen delivery, a change in sensation in the distal distribution of a nerve over time is a late sign that is strongly suggestive that a compartment syndrome is present. In the patient with an anterior compartment syndrome of the leg, dysfunction of the deep peroneal (anterior tibial) nerve may manifest as anesthesia, hypesthesia, or parethesias in the dorsal web space between toes 1 and 2 of the foot.59-63 In similar fashion, there would be a decrease in 2-point discrimination in the same sensory area.59 Weakness of muscles within the affected compartment is another late sign, as is weakness in muscles distally that are innervated by a nerve that passes through the compartment.59,62 In the patient with an anterior compartment syndrome of the leg, weakness of dorsiexion of the ankle and toes would be present. Paralysis of the muscles in the involved compartment would suggest that the diagnosis of a compartment syn792 Curr Probl Surg, October 2009

FIG 8. Same patient as in Fig 7 after supercial and deep exor compartments of right forearm
opened with a fasciotomy. Note restoration of ow through major and collateral arteries. (Reprinted with permission from Feliciano DV.4)

drome has been delayed signicantly, that a proximal injury to the involved nerve is present, or that a crush injury has occurred. The signs of a compartment syndrome described above occur at compartment pressures signicantly lower than arterial systolic and diastolic pressures. Therefore, the presence of palpable pulses at the ankle or wrist in the injured extremity does not rule out the presence of a more proximal compartment syndrome. In one of Matsens experiments, excellent Doppler signals were noted to be present in human volunteers despite the presence of severely compromised compartmental function.25 On rare occasions, compartment pressures will be high enough to cause tapering of major arteries and temporary occlusion of collateral arteries on intraoperative arteriograms4 (Figs 7 and 8). Expanding on Grifths previously mentioned list of symptoms and signs related to the presence of a compartment syndrome, Table 5 describes the 6 Ps and a T.14,60 These symptoms and signs described above as related to some of the most common individual compartment
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TABLE 5. Symptoms and signs of a compartment syndrome using the 6 Ps and a T14,60 Pain with late onset and disproportionate to injury Pain on passive stretch of muscles Paresthesias in distal nerve distribution Paralysis of muscles Pulses present Progression and Tense compartment

FIG 9. Symptoms and signs of anterior compartment syndrome of the leg. DPN, deep peroneal nerve;
EDL, extensor digitorum longus muscle; EHL, extensor hallucis muscle; TA, tibialis anterior muscle. (Reprinted with permission from Matsen FA III,2 www.orthop.washington.edu.)

syndromes are summarized in Figs 9, 10, and 11 from Matsens textbook.62

Compartment Pressures
Measurement of the compartment pressure in an extremity is appropriate in the following circumstances: (1) when a comprehensive history and physical examination cannot be performed in the preoperative or postoperative period; (2) when there are no or few high risk criteria in a patient with a moderately severe injury to an extremity; and (3) when there is concern about performing an unnecessary fasciotomy (ie, conversion of closed to open fracture). Of interest, another indication that was suggested in one orthopedic trauma center in the past is all patients with tibial
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FIG 10. Symptoms and signs of deep posterior compartment syndrome of the leg. FDL, exor digitorum longus muscle; FHL, exor hallucis longus muscle; PTN, posterior tibial nerve; TP, tibialis posterior muscle. (Reprinted with permission from Matsen FA III,2 www.orthop.washington.edu.)

FIG 11. Symptoms and signs of volar compartment syndrome of the forearm. FCR, exor carpi radialis
muscle; FCU, exor carpi ulnaris muscle; FDP, exor digitorum profundus muscle; FDS, exor digitorum supercialis muscle; FPL, exor pollicis longus muscle; MN, median nerve; PL, palmaris longus muscle; UN, ulnar nerve. (Reprinted with permission from Matsen FA III,2 www.orthop. washington.edu.)

fractures.66 Unfortunately, the controversies described in the introduction to this article have not been resolved at this time. Available Techniques for Measurement. Following the rst measurement of compartment pressure by saline injection by French and Prince in 1962, several other techniques and devices for measurement have been developed.67 These include the needle injection technique (regular or side-port needle), the wick catheter, the slit catheter, use of needle with
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FIG 12. Regular needle injection technique to measure compartment pressure. (Reprinted with
permission from Whitesides et al.33)

arterial line and standard monitor, and the Stryker Intra-Compartmental Pressure Monitor System (Stryker Instruments, Kalamazoo, MI). In all of these techniques, compartment pressure should be measured within several centimeters of a fracture site if one is present.47 Several of these techniques are used rarely in the modern era, and the interested reader is referred to the gures describing them in the 1981 monograph by S.J. Mubarak and A.R. Hargens68 and to a chapter in a current orthopedics textbook.61 The regular needle injection technique described by Whitesides and colleagues33 in 1975 involves the use of a mercury manometer, a 20-mL syringe, intravenous extension tubing, and an 18-gauge needle. It is illustrated in Fig 12 for comparison to some of the simpler techniques used currently. Movement of the air-saline column after injection of a small amount of saline into the tissue is the point at which the compartment pressure is read on the manometer.33 The continuous infusion technique, a modication of the regular needle technique, was subsequently developed by Matsen and Krugmire.36 Because of changes in tissue compliance at higher compartment pressures, this technique has been reported to yield higher pressures than actually exist.69 The wick catheter has a piece of absorbable suture (polyglycolic acid) placed inside polyethylene 60 (PE 60) tubing.70,71 Other components include a 3-way stopcock, pressure transducer, and pressure recorder. After calibration with saline in the tubing, the wick catheter is inserted into the compartment through a large needle or trocar (which is then
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FIG 13. Stryker Intra-Compartmental Pressure Monitor System. (Photograph courtesy of Stryker Instruments, Kalamazoo, MI.) (Color version of gure is available online.)

withdrawn). The compartment pressure is read on the attached pressure monitor. The major advantage of this technique is that it allows for continuous measurement of compartment pressure without a continuous saline infusion.4 An obvious concern over time is hydrolysis of the polyglycolic acid suture, as is a blood clot around the tip.61,68 The slit catheter is created by placing ve 3-mm longitudinal slits at the end of the PE 60 tubing.69 After the saline ush and calibration, the catheter is inserted into the compartment at an oblique angle through a 16-gauge needle, which is then withdrawn. The compartment pressure is then read on an attached digital recorder.61,69 In the original study on the use of the slit catheter, the results were comparable to use of the wick catheter.69 Use of a 16-gauge needle attached to arterial tubing that is then connected to a standard transducer/monitor available in any operating room or intensive care unit is the technique preferred by the authors.72 After ushing the tubing and needle with saline, the needle is held just above the compartment, and a 0 reading is obtained on the monitor. The needle is then placed into the compartment, a small amount of saline is ushed, and a direct reading is soon available on the monitor. When the pressure measurement is inconsistent with the clinical situation, a repeat measurement or more at another site is appropriate. The Stryker Intra-Compartmental Pressure Monitor System (Stryker Instruments, Kalamazoo, MI) includes a measuring instrument, disposable syringe preloaded with saline and a side-ported, noncoring 18-gauge disposable needle73 (Fig 13). After ushing, the hand-held monitor is placed at the level of the compartment to be measured for a 0 reading. The compartment pressure is read off the monitor after allowing for a decrease in the original value over 15 to 20 seconds. Numerous studies have compared the results of measurements of
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TABLE 6. Accuracy in the measurement of compartment pressures: a comparison of three commonly


used devices

Slope Setup* SSP SS SSL ALSP ALS ALSL WSSP WSS WSSL Mean and standard error 0.98 1.06 1.05 0.97 0.99 0.99 0.98 1.26 1.24 0.01 0.03 0.01 0.00 0.01 0.00 0.02 0.03 0.02 P value 0.008 0.014 0.001 0.001 0.538 0.001 0.440 0.001 0.001 0.43 10.30 3.34 1.25 21.85 0.56 2.43 1.66 3.02

Intercept (mm Hg [kPa]) Mean and standard error 0.39 (0.06 1.22 (1.37 0.26 ( 0.45 0.13 ( 0.17 0.65 (2.91 0.19 (0.07 0.94 (0.32 1.29 ( 0.22 1.14 (0.40 0.05) 0.16) 0.03) 0.02) 0.09) 0.03) 0.13) 0.17) 0.15) P value 0.264 0.001 0.001 0.001 0.001 0.004 0.010 0.199 0.009 R2 value 0.9816 0.9358 0.9953 0.9977 0.9749 0.9978 0.9115 0.9502 0.9219

Reprinted with permission from The Journal of Bone and Joint Surgery, Inc. from Boody and Wongworawat.79 *SSP, Stryker device with side-port needle; SS, Stryker device with straight needle; SSL, Stryker device with slit catheter; ALSP, arterial line manometer with side-port needle; ALS, arterial line manometer with straight needle; ALSL, arterial line manometer with slit catheter; WSSP, Whitesides apparatus with side-port needle; WSS, Whitesides apparatus with straight needle; WSSL, Whitesides apparatus with slit cathether.

compartment pressure in both laboratory and clinical settings over the past 40 years.68,69,74-79 One of the most comprehensive and current used a graduated cylinder to generate a known pressure.79 This cylinder was used to compare pressure measurements with the Whitesides apparatus, the Stryker device, and an arterial line manometer (straight needle, side-port needle, slit catheter for each) (Table 6).79 The Whitesides system overestimated pressure and had the highest standard error based on repeated measurements. The Stryker device and the arterial line manometer with straight needles tended to overestimate pressure. Using regression data, the most accurate systems/devices were the arterial line with slit catheter, arterial line with side-port needle, and Stryker device with slit catheter. The least accurate systems/devices (worst rst) were the Whitesides system with side-port needle, Whitesides system with slit catheter, and the Stryker device with straight needle. In addition to the well-known techniques and devices described above, the recent orthopedic literature has included reports on several new devices.80 Agudelo and colleagues81 described a commercial device that measures intramuscular pressure in addition to removing uid from the muscle compartment. In a preliminary study of 14 patients with tibial plateau or shaft fractures, intramuscular pressures in the anterior and posterior compartments of the leg were lower when the device was used. The differences, however, were not statistically signicant. Wiemann and
798 Curr Probl Surg, October 2009

colleagues82 described use of noninvasive pulsed phase-locked loop ultrasound for detecting intramuscular pressures in the leg of normal human volunteers and 6 patients. There was a linear correlation between the results obtained with pulsed phase-locked loop ultrasound and standard measurements obtained with a slit catheter. Numerical Values that Should Prompt Fasciotomy. Many general, trauma, and vascular surgeons use an absolute numerical value to prompt a fasciotomy. This is especially true in the previously described patients in whom a preoperative history and physical examination are limited or cannot be performed and when the patient is not at high risk for developing a compartment syndrome (Table 4). In part, the rationale has been that a compartment pressure (normal 4-7 mm Hg with the wick method and 9-11 mm Hg with continuous method) that exceeds capillary pressure (20-30 mm Hg) will occlude all ow into local tissues.28,75 Matsen rejected this microvascular occlusion theory in his textbook. He stated that a rise in tissue (compartment) pressure will increase venous pressure based on older studies and, therefore, capillary pressure must also rise.75 In contrast, Mubarak and Hargens recommend decompressive fasciotomy when compartment pressures rise above 30 mm Hg and when there are clinical ndings of a compartment syndrome.68,71,83 Other authors have suggested 40 mm Hg74 or 45 mm Hg37 pressure as an indication for fasciotomy, but often adding the caveat that choosing a single value is not appropriate for all patients. A numerical gure of 30 to 35 mm Hg is still used in many centers in the groups of patients mentioned above, even when clinical ndings of a compartment syndrome (other than swelling) cannot be assessed. And, the American College of Surgeons Committee on Trauma poster (2002) entitled Management of Peripheral Vascular Trauma states that fasciotomy for compartment pressure 30 to 35 mm Hg is appropriate.84 The advantages of this simplistic approach include the following: (1) avoid the need for continuous or repeated measurements of compartment pressure; (2) avoid missed compartment syndromes in unresponsive patients; and (3) avoid delayed secondary emergency operations to perform fasciotomy in critically ill patients. The disadvantages include the following: (1) conversion of closed to open fractures; (2) addition of large incisions and open wounds in injured patients; (3) need for prolonged wound care in some patients; (4) long-term residual muscle weakness noted in some patients (to be discussed); and (5) extensive scars on the extremity. It has long been recognized that there is a range of tolerance in muscles and nerves to external pressures applied to the limbs of laboratory animals.21 Matsen and others have documented the same in human
Curr Probl Surg, October 2009 799

subjects and patients.25,85 In one often quoted study, 42 patients at risk for compartment syndromes were frequently examined.85 No patient whose peak pressure was 45 mm Hg or less developed a compartment syndrome. Five of the seven with pressure between 45 and 60 mm Hg developed compartment syndromes, and all of those with peak pressure of 60 mm Hg or more developed compartment syndromes. Matsens conclusion, in contrast to that of Mubarak and Hargens described above, is that there is no critical pressure that can serve as a general criterion for diagnosis and treatment of a compartment syndrome. Thomas E. Whitesides, Jr, and colleagues from the Department of Orthopaedics at Emory University rst suggested use of the p as a prompter to perform fasciotomy for a compartment syndrome in 1975.33,86 p or differential pressure is dened as the difference in millimeters of mercury (mm Hg) between the patients diastolic blood pressure and compartment pressure.33,48 The differential pressure is different from the concept of compartment perfusion pressure (CPP) used in some experimental studies (ie, CPP mean arterial pressure minus compartment pressure). The critical value is based on studies documenting that healthy muscle becomes ischemic when compartment pressure is within 10 mm Hg of the diastolic blood pressure.45-47,49-52 In injured and edematous tissue, perfusion is decreased and ischemia will increase as well. Updating the original range described in the 1975 publication, Whitesides and Heckman48 recommended that fasciotomy be performed as the compartment pressure approaches 20 mm below diastolic blood pressure in 1996. This was indicated in any patient who has a worsening clinical condition, a documented rising pressure, signicant tissue injury, or a history of 6 hours of total ischemia of an extremity.48 Using a p of 30 mm Hg, McQueen, Christie, and Court-Brown66 prospectively studied 116 patients with tibial diaphyseal fractures. Only 3 patients required a below knee fasciotomy based on the differential pressure. The authors stated that use of a compartment pressure measurement of 30 mm Hg alone would have led to 50 fasciotomies instead of the 3 that were performed. In similar fashion, use of a compartment pressure measurement of 40 mm Hg alone would have led to 27 fasciotomies in the series. Based on 6-month follow-up data, the authors concluded that a differential pressure of 30 mm Hg led to no missed cases of acute compartment syndrome.66 The same group prospectively studied 101 patients with tibial fractures whose compartment pressures could be monitored. The outcomes in patients with below knee compartment pressures greater or less than 30 mm Hg was similar as long as the differential pressure was less than 30 mm Hg. Therefore, the major advantages of using differential
800 Curr Probl Surg, October 2009

pressure are: (1) it accounts for changes in the patients blood pressure (whereas use of absolute measurements only does not), and (2) it has been evaluated clinically in patients with tibial fractures and has been found to avoid unnecessary fasciotomies. The major disadvantage is that it requires serial or continuous measurement of compartment pressures in the extremity in question.

Near-Infrared Spectroscopy
Near-infrared spectroscopy (NIR) using a commercially available oximeter (Biospectrometer-NB Oximeter; Hutchinson Technology, Hutchinson, MN) to diagnose compartment syndrome has been undergoing evaluation for approximately 10 years.87-90 The technique has been used in trauma centers to evaluate the effectiveness of resuscitation as well. The NIR probe has a 25-W tungsten halogen bulb, a shield to keep out ambient light, and emitting and receiving bers. It emits photons that pass through tissue (or blood vessels in other applications) at a certain depth and are reected back to the receiving bers. Basically, the detector is a beroptic-coupled spectrometer. Filters are present in the system to eliminate light wavelengths that are not pertinent to the tissue being studied. The device measures wavelengths of hemoglobin and oxyhemoglobin, but not carboxyhemoglobin or myogloblin, and calculates an StO2 or saturation of tissue oxygenation.87-90 In the laboratory study by Arbabi and colleagues,87 a decrease in skeletal muscle StO2 was noted in the limb of a pig with a compartment syndrome. The authors stated that the StO2 values were easily distinguishable from the values associated with severe, combined hypotension and hypoxia in their model. The authors concluded that NIR might be particularly useful in critically injured and unstable patients. A similar study in which loss of dorsiexion despite stimulation of the peroneal nerve in the presence of a compartment syndrome documented that StO2 was a more constant predictor of twitch loss than perfusion pressure.88 A clinical study by Giannotti and colleagues89 evaluated the use of NIR in 9 patients with compartment syndromes (pressure 64 17 mm Hg) and 33 surgical patients without a compartment syndrome. There was a signicant increase in StO2 in the leg compartment with the highest compartment pressure after fasciotomy was performed (56 27% to 82 16%; P 0.017). The latter value approximated the 87 7% in matched control patients with trauma to the same extremity without a compartment syndrome.89 Gentilello and colleagues90 compared NIR to differential pressure in 25
Curr Probl Surg, October 2009 801

volunteers who were subjected to serial calf compressions to reduce StO2. Outcome variables were conduction by the deep peroneal nerve, cutaneous sensitivity in the distribution of the deep peroneal nerve, and pain. Both sensitivity and specicity were signicantly greater with the NIR than with differential pressure. All of these reports document that tissue oxygen saturation can be used for early detection of ischemia and/or neuromuscular dysfunction in patients with a compartment syndrome in an extremity. The NIR device is easy to use, sensitive, and would be of benet in assessing the musculofascial compartments of patients in whom a history and comprehensive physical examination cannot be obtained. Whether it has more clinical benet than serial differential pressure measurements is unclear at this time.

Secondary Extremity Compartment Syndrome (SECS)


SECS is a rare complication that is presumably part of the postresuscitation systemic inammatory response syndrome (SIRS). SIRS was dened by the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference in 1992.91 SECS was originally described as a capillary leak syndrome in individual case reports in the 1980s and 1990s. The clinical presentation was described in detail in 10 patients and named by members of the authors group at Grady Memorial Hospital/Emory University in 2002.92 The clinical presentation of SECS is signicant edema and associated compartment syndromes in 2 to 4 injured or noninjured extremities after massive resuscitation. The incidence among all trauma admissions in the original series over nearly 6 years was only 0.08%. All of the patients had been injured (mean Injury Severity Score 29 17), the mean initial base decit was 12.8 8.8 mEq/L (range, 1.3 to 30.8) and the mean number of transfusions of packed red blood cells over the rst 24 hours after injury was 23.0 16.3 (range, 7-57 units).92 The total volume of crystalloid solutions and packed red blood cells infused until multiple compartment syndromes developed was 11 to 74 liters. Of interest, 10 of the 11 upper extremities and 12 of the 20 lower extremities that developed compartment syndromes did not have any obvious injuries. Also, the mean number of extremities per patient that developed a compartment syndrome was 3.1. Reecting the systemic insult that characterizes all patients with SECS, the mortality rate in the series was 70%. Causes of death were multiple organ failure in 5 patients, brain death in 1, and a presumed pulmonary embolus in 1.
802 Curr Probl Surg, October 2009

A reasonably similar group of patients with acute lower extremity compartment syndrome was reported by Kosir and colleagues93 in 2007. The 9 patients described had a mean Injury Severity Score of 32.0 12.5, a mean base decit of 12.9 5.9 mEq/L, and a mortality rate of 67%. The authors described an aggressive screening protocol to rule out compartment syndromes using differential pressures measured every 4 hours for 48 hours (later changed to 24 hours). A second series of 17 patients from Grady Memorial Hospital/Emory University was reported in 2007 also.94 The incidence among 11,468 trauma admissions was 0.148%. As in the previous series, the patients were severely injured with a mean Injury Severity Score of 36.3 16.6, a mean base decit of 13.3 mEq/L, and an average time from admission to diagnosis of SECS of 32.6 hours. Before the development of SECS, patients received a mean 20.9 11.0 units of blood and 24.6 14 liters of crystalloid solutions. The most disheartening aspect of the report was the need for 7 amputations in 46 affected extremities. The mortality rate remained high at 35.3% and increased to 75% in patients requiring hemodialysis. SECS should be suspected in any injured patient who presents with profound hypotension, an Injury Severity Score 25, and need for transfusion of at least 10 units of packed red blood cells as part of acute, intraoperative, or postoperative resuscitation. The appearance of total body edema during resuscitation should prompt measurements of compartment pressures in all involved extremities. When elevated compartment pressures or decreased differential pressures indicate the need for multiple fasciotomies in more than 1 extremity, 2 surgical teams should be available in the operating room to avoid delays.

Nonsurgical Therapy
The standard of care for treatment of the compartment syndrome is operative decompression. Various other treatment modalities have, however, been described. It should be understood that any deviation from the standard of care should be approached with some degree of trepidation. If nonsurgical therapy is to be pursued in the asymptomatic patient with elevated compartment pressures, the patient should have extremely close clinical monitoring with serial measurements of serum creatine phosphokinase (CPK) and urine myoglobin at a minimum. A worsening clinical examination, increasing compartment pressures, persistence of elevated CPK levels, or the presence of myogloblin in the urine (toxic to glomeruli) mandate operative decompression of the affected compartments.95,96
Curr Probl Surg, October 2009 803

Position of the Extremity/Compression Bandage


With edema present in the extremity in which a compartment syndrome may occur or already exist, it would be logical for the surgical team to elevate the extremity. Unfortunately, this is an error in management of the patient. Elevation of the extremity decreases local arterial pressure, decreases the local AV gradient, and exaggerates the circulatory effect of any given tissue pressure increase.23,26,34 Compression with elastic bandages will, of course, cause an increase in LVP and an associated decrease in the AV gradient also.

Observation
Robinson and colleagues97 reported on 6 patients under the age of 30 who had developed an anterior thigh compartment syndrome with pressures greater than 30 mm Hg in the absence of a fracture of the femur. All were managed successfully without operation and, at 6 months after injury, all had good function in the affected limb. Robinson suggested that this clinical scenario should be considered for nonoperative management.97 Nonoperative management in this scenario has been employed successfully even with extremely high compartment pressures. Riede and colleagues98 described a 16-year-old boy who sustained a high energy blow to the anterior thigh during a soccer match. The patient presented 24 hours after the injury with a pressure of 80 to 100 mm Hg in the anterior (quadriceps) compartment. Rather than fasciotomy, the patient was placed on bed rest for 48 hours with the limb immobilized (knee extended) and with local cooling applied. The pressure in the anterior compartment of the thigh 50 hours after admission was 40 mm Hg. The patient was started on physical therapy with passive range-of-motion exercises 48 hours after admission, and these exercises were gradually advanced. After 14 weeks, the patient began jogging and returned to full, unrestricted activity at 6 months.98 Although nonoperative management may be considered in these extremely rare clinical situations, it is not applicable in the vast majority of symptomatic patients with elevated compartment pressures.

Hyperbaric Oxygen (HBO)99


The use of HBO therapy in the treatment of compartment syndromes is controversial. Theoretically, treatment with HBO increases the amount of oxygen dissolved in plasma and tissue uids. It also causes vasoconstriction through the action of increased oxygen partial pressure on the blood vessel,
804 Curr Probl Surg, October 2009

and the diminished blood ow is compensated for by the hyperoxygenation.100 The overall effect is maintenance of oxygenation, decreased capillary blood pressure, and decreased edema. Strauss and colleagues100 investigated the use of HBO therapy as a primary treatment for elevated intracompartmental pressures in a canine model. In their small study, they found that HBO-treated animals had decreased edema and greatly reduced muscle necrosis compared with the untreated animals. The results of the study led the authors to conclude that HBO therapy may be indicated in patients with elevated compartment pressures that are borderline with regard to needing surgical decompression to prevent progression, in patients in whom fasciotomy must be delayed, and as an adjunct postoperatively.100 The same group subsequently found HBO to be similarly useful in the scenario of compartment syndromes associated with hemorrhagic hypotension.101 In human studies, Strauss and Hart102 subsequently averted fasciotomy and had good functional outcomes in 10 patients with compartment syndromes using HBO treatment. Similarly, Gold and colleagues103 reported on the use of HBO in conjunction with mannitol and antivenin to avoid the need for fasciotomy in a patient following rattlesnake envenomation on the hand. A compartment pressure of 55 mm Hg was documented in the patients thenar eminence, and signs and symptoms consistent with a compartment syndrome were noted in the forearm, although pressures were not documented. The patient was offered fasciotomy, but refused, and nonoperative management was necessary. Following treatment with antivenin, mannitol, and HBO at 2.4 atm, the compartment pressure in the hand was reassessed and found to be 30 to 32 mm Hg. The patient recovered without sequelae.103 Although it would be inappropriate to recommend HBO as an alternative to the operative management of compartment syndrome, it is not likely to be harmful99 when used as adjunctive therapy as suggested in various case reports.101,104,105 Additional clinical studies will be needed to conrm the efcacy of HBO as the primary or sole treatment of a compartment syndrome.

Free Radical Scavengers


Mannitol is one of the cornerstones of the medical management of rhabdomyolysis for its properties as a free radical scavenger, volume expander, and osmotic diuretic.106-108 It has also been evaluated for use in the treatment of an acute compartment syndrome in animal models. Better and colleagues109 used the injection of autologous plasma to induce an acute compartment syndrome with a pressure of 100 mm Hg in 12 hind limbs of 7 consecutive canines. The study group received 20% mannitol intravenously at a rate of 0.15 mL/min/kg, while the control
Curr Probl Surg, October 2009 805

group received a similar volume of saline. Compartment pressures were monitored continuously, and no surgical intervention was performed. The authors found that the reduction in pressure over time was signicantly greater in the treated animals compared with the controls. They concluded that mannitol may have future potential as an adjunct in the management of acute compartment syndrome in man. Additionally, they suggested that it may buy time when immediate fasciotomy cannot be performed.109 Other authors using a similar model have not found mannitol to be benecial in preserving function and advocate fasciotomies.110 The use of mannitol in the treatment of acute compartment syndrome has not been studied extensively in humans, and its role should be limited to the management of rhabdomyolysis at this time.

Recombinant Factor VIIA


The use of recombinant factor VIIa (rFVIIa) has been described in an isolated case report as a primary treatment for a compartment syndrome of the forearm in an infant with end-stage liver disease (ESLD). Alioglu and colleagues111 reported on a 9-month-old with a severe coagulopathy due to ESLD who developed an expanding hematoma of the forearm following catheterization of the brachial artery. Despite a documented pressure of 74 mm Hg in the exor compartment of the left forearm, the authors felt that the patient was not a candidate for fasciotomy due to a persistent coagulopathy. The child received 2 bolus infusions of rFVIIa dosed at 90 g/kg with cessation of bleeding into the forearm. The compartment syndrome resolved within 4 hours of the second bolus of rFVIIa, and the hematoma of the forearm resolved over the ensuing several days without sequelae. Unfortunately, the patient died of ESLD 1 month later and, therefore, no long-term follow-up on the forearm was possible.111 rFVIIa has also been reported to be successful in the treatment of bleeding following fasciotomy in a patient with hemophilia A.112 As in other surgical or injured patients, rFVIIa should be an adjunct in the management of bleeding after fasciotomy in patients with a refractory coagulopathy.

Elastic Tourniquet
Shah and colleagues113 described a 52-year-old man who developed a compartment syndrome of the right forearm as a result of the inadvertent infusion of uid under pressure during elective cardiac surgery. The arm was not monitored during the infusion since it was under drapes and not accessible. The patient was noted to have a cold, tense, pulseless right
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upper extremity at the conclusion of the cardiac surgical procedure. Compartment pressures were measured at 43 mm Hg in the supercial exor compartment and 57 mm Hg in the deep exor compartment of the patients forearm. The affected upper extremity was elevated and wrapped tightly from the ngers to the axilla with an Esmarch bandage. This was followed by manual compression distally to proximally and removal of the Esmarch wrapping. The sequence was repeated a total of 15 times. Following this intervention, the hand was noted to be warm with good capillary rell, tension in the forearm was diminished, and both radial and ulnar arterial pulses returned. Compartment pressures in both the supercial exor and deep exor compartments had decreased to 28 mm Hg. At 1-week follow-up, the patient had normal 2-point discrimination in all ngers as well as full strength and range of motion.113

Leeches
The use of leeches to treat a compartment syndrome that developed in the forearm following cardiac catheterization via a radial artery approach has been described. Leeches were applied to the volar surface of the patients arm, and they removed approximately 145 mL of blood with marked improvement in symptoms. No further therapy was required and, at 3 months follow-up, the patient had a normal neurologic examination.114 As noted in a subsequent letter to the editor, this case report must be viewed with caution. The authors of the case report do not document the measurement of compartment pressures in the affected limb, which makes the original diagnosis uncertain.115 Therefore, the application of leeches as a denitive therapy for a compartment syndrome cannot be recommended at this time.

Operative Techniques
Operative decompression is indicated in virtually all symptomatic patients with elevated pressures in the musculofascial compartment of an extremity. In addition to the traditional open techniques, both subcutaneous116,117 and endoscopic-assisted118-120 fasciotomies have been described. Subcutaneous fasciotomies are not anatomically precise, may injure the supercial peroneal nerve in the distal leg, do not ensure adequate decompression in the acute setting, and should be avoided.121 Endoscopic techniques are best limited to the treatment of chronic exertional compartment syndromes. Although the endoscopic technique does reduce elevated compartment pressures in an in vitro model, open fasciotomy provides signicantly greater decompression.120 The open
Curr Probl Surg, October 2009 807

technique is, therefore, the most appropriate technique in the acute setting. The most important elements of an open fasciotomy are timely and adequate incisions of both the skin and the fascia.122 In Matsens textbook, the concept of a rebound compartment syndrome is discussed.123 This is dened as postischemic swelling after decompression of one limiting envelope causing a sufcient pressure increase within another envelope to produce a rebound compartmental syndrome.123 Therefore, postischemic swelling after release of a tight cast or dressing might result in the fascia becoming the limiting envelope (ie, the classic compartment syndrome). And, performing a fasciotomy through a limited skin incision as practiced in the past might result in the skin becoming the limiting envelope as postischemic swelling occurs in the released compartment.123 This has been documented clinically.124,125 Delay in decompression of a musculofascial compartment in the symptomatic patient must be avoided. Once the diagnosis is made, the patient should be brought emergently to the operating room since any delay in decompression increases the likelihood of permanent neurovascular compromise or loss of the limb. In one review of fasciotomies in the extremities following trauma, 75% of amputations of the lower extremities were related to either a delay in fasciotomy or performing an inadequate fasciotomy.57 More recent studies support the need for early, adequate fasciotomies as well. A retrospective review of combat casualties noted that patients undergoing a delayed fasciotomy had twice the rate of amputation as well as a 3-fold higher mortality. Patients who required revision of the fasciotomies, most commonly extension of the fascial incision or opening of additional compartments, had a 4-fold increase in mortality.126 Patients undergoing fasciotomy following trauma, particularly those who have developed the SECS, may be critically ill. If multiple extremities require operative intervention, it is advisable to have 2 operative teams involved to facilitate the prompt decompression of the affected compartments and minimize time in the operating room. In patients who are deemed too unstable to transport to the operating room, the procedure can be successfully accomplished at the bedside in the intensive care unit.

Open Fasciotomy in the Lower Extremity4,32,35,57,61,80,123,127-142


Thigh.61,127 The 3 anatomic compartments of the thigh are the anterior (extensor), posterior (exor or hamstring), and medial (adductor). The
808 Curr Probl Surg, October 2009

boundaries of the anterior compartment are the medial intermuscular septum (between vastus medialis, an extensor, and the adductors) and the lateral intermuscular septum (between extensors and exors) of the thigh. It contains the quadriceps muscle group including the rectus femoris (hip exion, knee extension), vastus medialis, vastus intermedius, and vastus lateralis muscles (knee extensors), the sartorius muscle (hip and knee exion) and the femoral nerve. The boundaries of the posterior compartment are the lateral intermuscular septum and medially by the poorly developed posterior intermuscular septum of the thigh (between exors and adductors). It contains the biceps femoris, semitendinosus and semimembranosus muscles (hip exion, knee exion), and the sciatic nerve. The boundaries of the medial compartment are the medial and posterior intermuscular septa. It contains the adductor muscle group including the adductor longus, adductor brevis and adductor magnus, the pectineus muscle (oor of medial femoral triangle), the gracilis muscle (weak knee exion), and the obturator nerve. To decompress the musculofascial compartments of the thigh, the entire lower extremity is prepared and draped from the iliac crest to the toenails (in case the musculofascial compartments of the leg need decompression as well). A 2-skin incision, 3-compartment fasciotomy is performed, if needed. Fasciotomy of the Anterior Compartment of the Thigh. First, a 30-cm anterolateral skin incision is made starting at the intertrochanteric line laterally and extending to the lateral condyle of the femur. Next, the iliotibial tract (thickened fascia lata overlying vastus lateralis muscle) is identied and opened for the length of the skin incision. Manual elevation of the fascial envelope anteriorly will ensure decompression of the rectus femoris and remaining vastus muscles. Fasciotomy of the Posterior Compartment of the Thigh. The exposed vastus lateralis muscle is mobilized superiorly and medially. In large and muscular men, this can be difcult and the use of 2 Richardson retractors for lifting is helpful. Next, the exposed lateral intermuscular septum, a very thick structure, is then incised for the length of the skin incision to decompress the posterior compartment. Fasciotomy of the Medial Compartment of the Thigh. Pressures in the medial compartment of the thigh often return to the normal range following decompression of the anterior and posterior compartments. Therefore, the pressure in the medial compartment is reassessed at this time to avoid an unnecessary skin incision and fasciotomy. A 30-cm long medial thigh skin incision is made over the course of the greater saphenous vein, which is preserved, and extending to the medial condyle of the femur. The sartorius muscle (anterior compartment) is then identied
Curr Probl Surg, October 2009 809

and rotated anterolaterally. Last, the medial compartment is opened with a longitudinal fascial incision for the length of the skin incision. Leg. The 4 anatomic compartments of the leg are the anterior (ankle/toe extension), lateral (foot eversion, plantar exion), supercial posterior (knee exion, ankle exion), and deep posterior (foot inversion, toe exion). The boundaries of the anterior compartment are the tibia medially, the anterior intermuscular septum laterally, and the interosseous membrane posteriorly. It contains the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius muscles, the deep peroneal (anterior tibial) nerve, and the anterior tibial artery with its venae comitantes. The boundaries of the lateral compartment of the leg are the anterior and posterior intermuscular septae. It contains the peroneus longus and peroneus brevis muscles and the supercial peroneal (musculocutaneous) nerve. The boundaries of the supercial posterior compartment are the posterior intermuscular septum posterolaterally, the transverse intermuscular septum anteriorly, and the deep fascia of the leg posteriorly. It contains the triceps surae muscles (gastrocnemius and soleus muscles) and the plantaris tendon (descends between the gastrocnemius and soleus muscles). The boundaries of the deep posterior compartment are the tibia, interosseous membrane, and bula anteriorly and the transverse intermuscular septum posteriorly. It contains the exor hallucis longus, and exor digitorum (FDS) longus, tibialis posterior muscles, tibial nerve, the posterior tibial artery and its venae comitantes, and the peroneal artery and its venae comitantes. Historically, the 2-skin incision, 4-compartment fasciotomy has been the most widely used method of decompressing the compartments of the leg and was employed routinely in World War II.128 Numerous singleincision techniques have been described since this time as well. In 1967, Kelly and Whitesides129 described a single-incision procedure involving resection of the bula. Patman and Thompson32 also advocated this technique. The advantages of the 2-incision procedure are that it involves no resection of bone, can be performed under local anesthesia if necessary, and is faster and relatively safer since deep dissection is minimized.35 The technique of bulectomy is now of historic interest only, but other single-incision techniques are still employed.61 Various techniques have been described for a single-incision, 4-compartment fasciotomy of the leg without bulectomy. Nghiem and Boland130 reported on 3 patients who underwent 4-compartment fasciotomy with incision of the interosseous membrane and the posterior intermuscular septum through an anterolateral skin incision. Rollins and colleagues131 described a technique that involves a lateral skin incision leading directly to the lateral compartment. Flaps are mobilized to allow
810 Curr Probl Surg, October 2009

access to both the anterior and supercial posterior compartments. The deep posterior compartment is then decompressed by detaching the soleus muscle from the bula to access the transverse intermuscular septum. Incision of this septum releases the deep posterior compartment. Cooper has described decompression of the leg through a single lateral incision along the bula.132 In Coopers technique, the lateral compartment is opened directly. The anterior compartment is decompressed by retracting the peroneal muscles to expose the anterior intermuscular septum which is incised. The edge of the bula is then identied by retracting the peroneal muscles anteriorly. The deep posterior compartment is opened by incising the transverse intermuscular septum just posterior to the bula, while the supercial is released by division of the posterior intermuscular septum. Although the techniques of single-incision fasciotomy provide adequate decompression, they can be best applied when the soft tissue is not distorted since they all involve a degree of intricate dissection. Since this is often not the case after trauma, the 2-skin incision technique is probably safer and should be used in most instances to decompress a compartment syndrome in the leg.35 The technique most commonly used for a decompression of the leg is the 2-skin incision fasciotomy as described by Mubarak and Owen.35 To decompress the leg, the entire lower extremity is prepared and draped from the inguinal ligament to the toes (in case the musculofascial compartments of the thigh need decompression as well). Fasciotomy of the Anterior and Lateral Compartments of the Leg (Fig 14). First, a 25- to 30-cm anterolateral incision is made 2-cm anterior to the shaft of the bula. This incision is approximately halfway between the anterior border of the tibia and the shaft of the bula in the average-sized patient. Next, using rake retractors and the electrocautery device, skin and subcutaneous tissue aps are raised anteriorly and laterally to provide complete exposure of the anterior and lateral compartments under their investing fascia. A small transverse incision is made exposing the anterior intermuscular septum if this cannot be clearly seen as it is the boundary between the anterior and lateral compartments as mentioned above. The fascia over the anterior compartment is then opened midway between the anterior border of the tibia and the anterior intermuscular septum for the length of the skin incision. The fascia over the lateral compartment is then opened midway between the anterior intermuscular septum and the shaft of the bula for the length of the skin incision. Extra caution must be taken in dividing the fascia over the distal one third of the lateral compartment since the supercial peroneal (musculocutaneous) nerve
Curr Probl Surg, October 2009 811

FIG 14. Two-skin incision four-compartment fasciotomy for decompression of compartments of the leg.
(Copyright 1988 Baylor College of Medicine.)

comes through the fascia at this point and continues in a subcutaneous course. Some authors recommend aiming the scissors (that are used to open the lateral compartment distally) at the lateral malleolus. The 2 longitudinal fasciotomy incisions performed through the same anterolateral skin incision are approximately 5 to 6 cm apart. Fasciotomy of the Supercial Posterior Compartment of the Leg. A 25- to 30-cm medial skin incision is made 2 cm posterior to the posteromedial edge of the tibia from the level of the tibial tubercle to 2 cm proximal to the medial malleolus. Every effort should be made to preserve the greater saphenous vein and associated saphenous nerve in the subcutaneous tissue after this skin incision is made. Next, the fascia over the supercial posterior compartment is then opened 2 cm posterior to the posteromedial edge of the tibia for the length of the skin incision. Fasciotomy of the Deep Posterior Compartment of the Leg.133 The deep posterior compartment of the leg immediately beneath the tibia is covered by the triceps surae muscles in the proximal one third of the leg. Therefore, the soleal bridge is detached from the tibia with the electrocautery until the FDS longus and tibialis posterior muscles can be decompressed for the length of the skin incision.80 Foot. Foot compartment syndrome (FCS) is estimated to develop in approximately 10% of calcaneal fractures with a wide range reported in the literature.134 Myerson,135 for example, reported an incidence of FCS of 17% for calcaneal fractures and 41% for crush injuries of the foot.
812 Curr Probl Surg, October 2009

Release of the compartments of the foot has also been suggested as an adjunct to fasciotomy of the leg in select patients undergoing limb revascularization after trauma.136 The anatomy of the foot has been extensively and variously described. Authors have spoken about spaces,137,138 layers,139 and compartments,140-142 leading to some confusion. The modern concept of the anatomy of the foot was described by Manoli and Weber141 following a series of anatomic studies including both dissection and injection on 17 specimens of adult lower limbs. They demonstrated 9 compartments of the foot including 5 conned to the forefoot, 3 passing through the entire length of the foot, and 1 conned to the hindfoot.141 The medial, supercial, and lateral compartments pass through the entire length of the foot. The boundaries of the medial compartment are the fascia of the abductor hallucis muscle medially and the medial intermuscular septum. It contains the abductor hallucis and exor hallucis brevis muscles. The boundaries of the supercial compartment are the plantar fascia and the medial and lateral intermuscular septi. It contains the FDS brevis muscle, the distal tendon of the FDS muscle, and the 4 lumbrical muscles. The boundaries of the lateral compartment are the fascia overlying the abductor digiti minimi muscle laterally and by the lateral intermuscular septum medially. It contains the abductor digiti minimi and exor digiti minimi muscles.141 The adductor compartment is conned to the forefoot and includes the adductor hallucis muscle. The 4 separate interosseous compartments are conned to the forefoot, as well, and the boundaries are the deep fascial membrane of the adductor compartment or supercial compartment inferiorly, the metatarsal bones medially and laterally, and by the dorsal interosseous muscular fascia superiorly.141 The sole compartment of the hindfoot is the calcaneal compartment, and the boundaries are a fascial plane extending between the intermuscular septi supercially, by the intermuscular septi, medially and laterally, and by the calcaneus and tarsal bones on its deep aspect. It contains the quadratus plantae muscle. Consultation with a foot surgeon is appropriate if one is available since the anatomy is complex. Myerson142 described a dorsal, 2-incision technique to alleviate a compartment syndrome of the foot; however, this approach does not directly decompress the calcaneal compartment. He suggested adding a hindfoot fasciotomy through a third incision in select cases. A single medial incision has been suggested by others, but this approach is limited by the need for extensive dissection, making it difcult in the severely traumatized foot, and a lack of decompression of
Curr Probl Surg, October 2009 813

the calcaneal compartment.140 Following their extensive anatomic study, Manoli and Weber141 recommended a 3-incision technique to decompress the 9 compartments of the foot. Fasciotomy of the Foot. A skin incision is made medially over the heel, parallel to and 3 cm supercial to the plantar surface. The incision is carried down to the fascia of the medial compartment, which is opened longitudinally with an incision 1 cm superior to its inferior border. The remaining 1-cm fascial strip can be followed laterally as a marker for the deeper incisions. The abductor hallucis muscle is retracted superiorly, and the attachment to the lateral fascial wall of the medial compartment is opened. The fascia superior to the fascial strip is incised while avoiding the lateral plantar nerve and artery just deep to it. This incision is extended to decompress the calcaneal compartment. A second deep incision is made inferiorly to the fascial strip for the length of the incision providing access to the lateral compartment, which is released with an incision on the inferomedial aspect of its fascia.141 The forefoot is decompressed with 2 incisions made on the dorsum of the foot over the second and fourth metatarsal shafts. The subcutaneous tissue is elevated medially and laterally through each dorsal incision to expose each of the 4 interosseous compartments, and these compartments are opened longitudinally. The dorsal and plantar interossei between the rst and second metatarsals are stripped from the second metatarsal and retracted medially to access the adductor compartment. This maneuver exposes the fascia of the adductor compartment, which is incised longitudinally to complete the fasciotomy of the foot.141

Open Fasciotomy in the Upper Extremity143


Compartment syndrome of the upper extremity is an uncommon clinical entity. In one review, only 18.4% of all fasciotomies performed were in the upper extremity and the vast majority of these were in the forearm.143 As an isolated compartment syndrome of the arm is so rare, the presence of a documented compartment syndrome in the arm mandates assessment of the forearm. Arm.144 The 2 anatomic compartments of the arm are the anterior (exor) and posterior (extensor). The 2 compartments are separated by the medial and lateral intermuscular septi. The anterior compartment contains the biceps brachii (long and short heads; shoulder and elbow exion, forearm supination) and brachialis muscles, the musculocutaneous, median and ulnar nerves, and the brachial artery and its venae comitantes. The posterior compartment contains the triceps brachii muscle (long, lateral, and medial heads; shoulder and elbow extension, arm adduction), the radial nerve, and the radial collateral and middle collateral arteries.
814 Curr Probl Surg, October 2009

To decompress the musculofascial compartments of the arm, the entire upper extremity is prepared and draped from the mid-clavicular area to the ngernails (in case the musculofascial compartments of the forearm need decompression as well). Fasciotomy of the Anterior and Posterior Compartments of the Arm Using 1 Skin Incision. A 15-cm skin incision is made over the medial intermuscular septum, carefully avoiding the underlying neurovascular bundle. Using rake retractors and the electrocautery device, skin and subcutaneous tissue aps are raised anteriorly and posteriorly. The fascia over the anterior compartment is then opened midway between the anterior border of the biceps muscle and the medial intermuscular septum for the length of the skin incision. The fascia over the posterior compartment is then opened midway between the posterior border of the triceps muscle and the medial intermuscular septum for the length of the skin incision. Fasciotomy of the Anterior and Posterior Compartments of the Arm Using 2 Skin Incisions. A 15-cm skin incision starting medial to the bicipital sulcus is extended up the anteromedial arm to the acromion and through the fascia to decompress the anterior compartment. A 15-cm skin incision starting at the tip of the olecranon is extended up the posterolateral arm and through the fascia to decompress the posterior compartment. Forearm.144-151 The 3 anatomic compartments of the forearm are the volar (exor), dorsal (extensor), and lateral (mobile wad). The volar compartment lies anterior to the lateral intermuscular septum, radius, interosseous membrane, ulna, and medial intermuscular septum and is separated from the lateral compartment by the supercial radial nerve and radial artery and vein. It contains a supercial group of muscles including the exor carpi radialis, palmaris longus, exor carpi ulnaris (FCU), FDS supercialis and pronator teres as well as a deep group of muscles including the FDS profundus, exor pollicis longus, and pronator quadratus (some authors consider this to be a separate compartment).149,150 Other contents depending on the level include the median and ulnar nerves, the deep branch of the radial nerve, the radial artery and vein, the ulnar artery and vein, and the anterior interosseous nerve, artery, and vein. The dorsal compartment lies posterior to the lateral intermuscular septum, radius, interosseous membrane, ulna, and medial intermuscular septum. It contains a supercial group of muscles including the extensor digitorum communis, extensor carpi ulnaris, and extensor digiti minimi as well as a deep group of muscles including the abductor pollicis longus, extensor pollicis brevis and longus, extensor indicis, and the supinator. Other contents include the posterior interosseous nerve, artery, and vein. The lateral compartment lies superior to the lateral intermuscular septum and
Curr Probl Surg, October 2009 815

FIG 15. Proximal aspect of skin incision used in volar-ulnar approach to decompress the volar and lateral compartments of the forearm.

is separated from the volar compartment by the supercial radial nerve and radial artery and vein. It contains the brachioradialis and extensor carpi radialis longus and brevis muscles, but no other major nerves or blood vessels. To decompress the musculofascial compartments of the forearm, the entire upper extremity is prepared and draped from the mid-clavicular area to the ngernails (in case the musculofascial compartments of the arm need decompression as well). Because of the difculty surgeons have in remembering the direction of the skin incision in the Henry approach to decompression of the volar compartment of the forearm, the senior author uses and teaches the volar-ulnar approach in his academic surgical practice (Fig 15). Fasciotomy of the Volar and Lateral Compartments of the Forearm (Volar-Ulnar Approach). A transverse incision starting distal to the antecubital crease on the radial side of the forearm is extended to the ulnar side of the forearm and then turned 90. The longitudinal component of the incision is extended down the ulnar side of the forearm until it reaches the wrist, where it curves medially to the mid-aspect of the volar
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FIG 16. Access to the deep exor compartment of the forearm by retraction of the exor carpi ulnaris
(FCU) and exor digitorum (FDS) muscles. (Reprinted with permission from Twaddle and Amendola.61)

wrist. The incision is now extended and curved into the thenar crease of the palm. By dividing the underlying fascia at the transverse origin of the incision distal to the antecubital crease, the muscles of the lateral (mobile wad) compartment are decompressed. The fascia underlying the longitudinal and wrist components of the skin incision is opened, thereby decompressing the supercial exor muscles of the forearm and the carpal tunnel.151 The space between the FCU and FDS muscles (exing the ngers will help differentiate these muscles) is separated with retractors, and the ulnar nerve and artery are visualized lying on the deep exor compartment (Fig 16). The deep exor compartment is opened longitudinally after retracting the ulnar artery and nerve laterally and ligating any small arterial branches in the area where the fasciotomy is to be performed. Ideally, the fascia over each deep volar muscle should be incised.149 If there is continued tightness at the level of the wrist, the tunnels of the median and ulnar nerves should be divided. Fasciotomy of the Dorsal Compartment of the Forearm. Pressures in the dorsal compartment of the forearm often return to the normal range following decompression of the volar and lateral compartments. Therefore, the pressure in the dorsal compartment is reassessed at this time to
Curr Probl Surg, October 2009 817

avoid an unnecessary skin incision and fasciotomy. After the forearm is pronated, a longitudinal skin incision from 2 cm lateral to and 2 cm distal to the lateral epicondyle of the humerus to the mid-aspect of the posterior wrist is made. A longitudinal fasciotomy to decompress the supercial muscles of the dorsal compartment is made between the extensor carpi radialis brevis and extensor digitorum communis muscles (extending the ngers will help differentiate these muscles). Wrist and Hand.151-155 The carpal tunnel on the exor aspect of the wrist is the only compartment in this location, and a carpal tunnel release is usually performed as part of the fasciotomy of the volar compartment of the forearm as described previously.151,152,155 A delay in reestablishing arterial inow into the forearm and hand, ligation of the major veins of the arm or forearm, marked traumatic disruption of the soft tissues of the arm (traumatic near-amputation), a crush injury, or a compression syndrome may result in a compartment syndrome of the hand on rare occasions. Consultation with a hand surgeon is appropriate if one is available. The hand has thenar, hypothenar, adductor, and 4 interossei compartments. An injection study published in 1980 demonstrated that the traditional 4 interossei compartments were actually divided into 3 palmar and 4 dorsal compartments, bringing the total number of compartments in the hand to 10.153 Other anatomic studies have demonstrated a signicant amount of variation in these 10 fascial compartments.154 Fortunately, despite the described variations, the compartments of the hand can be adequately decompressed with the traditional 4-incision fasciotomy.155 Fasciotomy of the Hand. Two 4-cm longitudinal incisions are made on the dorsum of the hand over the metacarpal bones of the index and ring ngers. Fascial incisions are then made along both sides of these metacarpals, thereby releasing the 4 dorsal interosseous muscles. The rst palmar interosseous and adductor compartments are opened by blunt dissection along the ulnar aspect of the index metacarpal bone. The second and third palmar interosseous compartments are released by dissection along the radial aspect of the ring and small metacarpal bones. A longitudinal incision is then made along the radial side of the rst metacarpal bone to release the thenar compartment. A longitudinal incision is made along the ulnar aspect of the fth metacarpal bone to release the hypothenar compartment.

Techniques of Closure
The performance of an adequate and timely fasciotomy, as previously described in this manuscript, will allow for salvage of many threatened
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extremities. Once the acute insult and resultant tissue edema begin to resolve, attention should be focused on care of the open wound in preparation for delayed primary closure or coverage with a partial thickness skin graft. More complex closure techniques, including the use of rotational and free aps, are rarely utilized.57 In one of the rst modern series, Sheridan and Matsen156 treated 49 patients who had undergone a fasciotomy in the leg or forearm and reported only a 23% rate of delayed primary closure while the remaining patients required split thickness skin grafts. In another large series published several years later, Feliciano and colleagues57 reported a delayed closure rate approaching 50% in 122 patients undergoing a fasciotomy in the leg or forearm after trauma. In that report, they noted that delayed closure with vertical mattress sutures tied over several days was used with success in many patients in the later stages of their series. This option was the precursor for many of the current techniques that have decreased the need for coverage of fasciotomy wounds with skin grafts.

Viscoelastic Properties of Skin


Before discussing modern closure techniques, a discussion of several important properties of skin is warranted. The structural components of the skin include collagen, elastic bers, and ground substance. Collagen bers are made of bundles of collagen brils, which, in turn, are composed of bundles of collagen laments. In the relaxed state, collagen bers are in a convoluted array, but when skin is stretched, the bers quickly realign to parallel rows.157 Elastic bers are much ner than collagen bers and are composed of elastin and microbrillar proteins. They serve to return the collagen bers to their relaxed posture, but can be fragmented with excess stretch leading to a loss of skin recoil.158 Ground substance is composed mostly of proteoglycans and serves to ll the interstices between the collagen and elastic bers as a supporting structure and lubricant. As skin ages, there is a decrease in type I collagen as well as ground substance, which leads to a loss of approximately 6% of dermal thickness per decade of adult life.159 Because of its complex structure, skin has both viscous and elastic properties and is, therefore, considered a viscoelastic substance. A purely elastic material will recover dimension and shape after deformation without energy cost.160 A purely viscous substance will yield continuously under a load and will not recover spontaneously, since energy is required to return the substance to its prior state.160 Skin has both viscous and elastic properties and will have incomplete recovery of shape after stretch. Therefore, skin is inherently extensible. This extensibility is
Curr Probl Surg, October 2009 819

mostly related to the reorganization of collagen bers from a convoluted matrix to parallel rows as mentioned previously. This is inherently intuitive to most surgeons, who have noted that approximating the skin over a large wound or incision is easier at the end of the closure than at the beginning as the skin loosens up. Other concepts that are important to understand are mechanical and biologic creep. The term creep refers to the stretching of a material under a constant load over time.157 As skin is stretched beyond its normal extensibility, elastic bers will fracture and water will be displaced from the ground substance. This is termed mechanical creep, and it allows for further elongation of the skin over the course of several minutes and partially explains why placing several wide-spaced stay sutures is helpful when attempting to close a wide wound.161,162 Biologic creep occurs over the course of several days and is the result of generation of new skin tissue after application of persistent stretching forces.163 Described nicely by Johnson and colleagues,164 biologic creep is the principle behind conventional tissue expanders and skin growth during pregnancy, with morbid obesity, and over large benign tumors. An understanding of the viscoelastic properties of skin, as well as an understanding of mechanical and biologic creep, allows for a basis to discuss the following techniques of closure.

Closure Techniques
Delayed Primary Closure. Delayed primary closure is the simplest closure technique and should be used whenever feasible. Efforts to minimize edema, such as elevation of the leg or forearm and compression with elastic bandages, should be used once a fasciotomy is performed. Delayed primary closure may be attempted as soon as the edema begins to resolve and may require a staged approach, with partial closure being accomplished at the rst reoperation and further closure on subsequent days. The tension techniques described below are useful adjuncts to this staged approach. Several groups have recommended specic suturing techniques when dealing with large wounds (Fig 17). Disaia and colleagues165 successfully used a running near-near-far-far stitch in a series of large open wounds. Specically, a number 2 nylon suture is used with the near stitch being placed 5 to 10 mm from the wound edge and the far stitch 3 to 6 cm from the wound edge with the suture advanced on the far-far limb. This is not a skin everting suture and must be reinforced with intermittent mattress sutures in areas where the skin tends to roll in. This technique has been used by several authors with success, although the authors of this review have no experience with it.165-168 In our
820 Curr Probl Surg, October 2009

FIG 17. Delayed skin closure over fasciotomy site using vertical mattress sutures.

experience, staged closure with vertical mattress sutures in combination with one or more of the techniques described below will allow for closure of many of these wounds. If wound closure is near complete or if the closure is felt to be too tight, the skin may be pie crusted to relieve some of the tension (Fig 18). This, in essence, creates a meshed full thickness skin graft over the open wound. The pie crust incisions generally heal with minimal scarring. This technique may assist with wound closure in cases where a few extra centimeters are needed to achieve full closure. Shoelace Technique. The shoelace is a relatively simple and inexpensive technique designed to improve closure rates after a fasciotomy. Based on the concept of biologic creep, it is designed to facilitate closure
Curr Probl Surg, October 2009 821

FIG 18. Pie crust incisions to allow for delayed skin closure over fasciotomy site.

of wounds over the course of several days. Credit for the initial description goes to Cohn and colleagues169 in a report from 1986. In this report, the authors describe 2 patients with a forearm compartment syndrome treated with volar fasciotomy. At the initial operation, vessel loops were threaded in a crisscross fashion and secured to the skin with skin staples. They were then tied to create light tension on the wound. At 48 hours, each patient had their vessel loops tightened, and both patients achieved skin closure on the fth postoperative day. Neither had a complication, and both had normal function of the extremity postoperatively. Since this initial report, multiple authors have described the successful use of this technique in small series of patients with closure rates up to 100% over the course of 5 days to 3 weeks.170-175 In our experience, the shoelace technique is simple and effective since it does not require specialized equipment. The vessel loops may be placed at the rst operation or at a subsequent washout at 48 to 72 hours (Fig 19). The surgeon may tighten these at the bedside or the patient may be returned to the operating room for formal closure when appropriate. Multiple authors have described modications of the shoelace technique using alternate materials. Taylor and colleagues176 described the use of specially designed skin anchors, duoderm, and silicon elastomeres in 6 fasciotomy wounds with an 100% closure rate and no complications. Mbubaegbu and Stallard177 described a similar technique using a series of
822 Curr Probl Surg, October 2009

FIG 19. Shoelace technique for gradual delayed skin closure over fasciotomy site.

plaster strips that were applied serially over the course of weeks on an outpatient basis. Harrah and colleagues178 reported success with a similar technique using simple steri-strips. Although the noninvasive nature of these latter techniques may allow for outpatient care in remote areas or in patients with isolated injuries, they offer little advantage over the standard and more durable technique using vessel loops as shoelaces in most centers. Mechanical Devices. A variety of mechanical devices, which have been designed to help improve closure of large wounds, have been applied to fasciotomy incisions. Many of these devices utilize the same concept of biologic creep that the shoelace technique is based on. In addition, many have been used intraoperatively to facilitate mechanical creep and stretch wounds for immediate closure. There are a number of devices on the market and, although experience with many of these devices is institution specic, several are worthy of discussion. One of the earlier devices was designed by Hirshowitz and colleagues179 in 1993 and utilizes 2 long pins threaded through the dermis that are attached to 2 U-shaped arms that are equipped with hooks to engage the pins. Finally, a threaded screw is passed between the centers of the arms and is tightened using a tension knob. The rst case series reported the successful closure of 5 large wounds in 1 operative session over 30 to 60 minutes. The wounds
Curr Probl Surg, October 2009 823

were related to excision of skin cancer in 1 patient, a fasciotomy in 1 patient, and traumatic wounds in 3 patients. The largest wound dimension was in the patient with a fasciotomy, who had a 27 15-cm open wound on the calf.179 Other groups have published similar results.180-183 The second generation of this device was utilized by Narayanan and colleagues in 1995.184 Termed the Sure-Closure (Life Medical Sciences, Princeton, NJ) device, the design is similar to Hirshowitzs device, with 2 pins placed through the dermis and 2 U-shaped arms with a tension bar. This device was utilized in 24 patients with a variety of wounds and led to a 100% closure rate in this series. Intraoperatively, the practice of loadcycling was used to enhance the skins mechanical creep. The device would be tightened and the wound partially closed. The device was then loosened for short periods of relaxation, followed by another cycle of tightening, closure, and loosening. In 21 of 24 patients, closure was accomplished in 1 operation over a maximum of 100 minutes. Three other patients required a second operation for full wound closure at 3 days. Of note, 11 (46%) patients underwent delayed revision of their wounds. These results were compared with a similar group of 16 patients treated with conventional wound care, of whom 8 were able to undergo primary closure and 4 (50%) required delayed revision of their wounds.184 The authors felt that this device was a simple and effective way to achieve wound closure in patients with large wounds. Several other groups have reported similar results.185-187 The STAR (Suture Tension Adjustment Reel; WoundTEK Inc., Newport, RI) is a simpler device designed with a similar objective. In a series from the University of Miami, this device was placed at the completion of the fasciotomy or on the following day at the bedside.188 The device consists of 2 shells, 1 anchoring shell, and 1 winding shell, which are connected by heavy nylon suture. The winder shell was tightened at the bedside using a wrench, and the wounds were reapproximated and closed over several days under local anesthesia without a return trip to the operating room. In this series, 13 patients had successful closure of their wounds (average initial width 7.6 cm) with only 1 minor infectious complication.188 The devices were removed at the bedside on nal wound closure. The main advantage of this device over the Sure-Closure device is its compact size. One of the most recent devices to be studied in the civilian trauma population is the Wisebands device (Wisebands Ltd., Ofakim, Israel). The Wisebands is another mechanical device that utilizes a suture needle, elastic band, and rotating knob with a tension feedback control device.
824 Curr Probl Surg, October 2009

FIG 20. Dynamic wound closure device used for gradual delayed skin closure over fasciotomy site (DWC; Canica, Almonte, ON, Canada). (Reprinted with permission from Singh et al.190)

Tension is set at 1 kg/cm2, and the skin is allowed to stretch over time. Further tightening is then performed as the wound is gradually closed. In one series, 14 of 18 fasciotomy wounds were able to be closed without complication over an average of 6 days.189 Recent military experience in Iraq has led to the development of the Dynamic Wound Closure Device (DWC; Canica, Almonte, ON, Canada). This device employs Silastic elastomeres to assist with wound closure (Fig 20). In the initial series, 10 of 11 (91%) patients underwent successful closure of their fasciotomy incisions with this device. The one failure was related to a thrombotic complication due to heparin-induced thrombocytopenia with subsequent amputation. The mean wound diameter was 8.1 cm, and the average time to closure was 2.6 days.190 In summary, many mechanical devices have been described to assist in closure of fasciotomy wounds. Most reports in the literature are case reports or case series, and the use of these devices is extremely institution specic. Although many seem to allow for up to 100% rates of wound closure, it is unclear if they offer substantial advantages over the simpler and cheaper delayed vertical mattress suture closure or shoelace techCurr Probl Surg, October 2009 825

nique described previously for fasciotomy sites with modest to moderate swelling of the underlying muscles. Negative Pressure Techniques.191 Negative pressure techniques have become popular to assist in closing the abdominal midline aponeurosis after damage control laparotomy. Indeed, Vacuum Assisted Fascial Closure, utilizing the KCI (San Antonio, TX) Wound V.A.C. system, has led to closure rates of the midline aponeurosis of up to 88% in this extremely sick patient population.192-194 Based on this success, it would seem that negative pressure techniques would also be helpful in closing large subcutaneous wounds. Unfortunately, there are currently few meaningful data supporting the use of this technique to improve wound closure rates in fasciotomy incisions. In 2006, Yang and colleagues195 published one of the few experiences with the Wound V.A.C. in this group of patients. In this study, they compared 34 patients who were treated with V.A.C. therapy versus a similar number of historic controls. V.A.C. patients had the dressing applied at the rst operation and had a dressing change every 48 hours. They then had delayed primary closure or skin grafting when it was deemed appropriate. The historic controls had wound care with standard gauze dressing followed by closure or skin grafting as appropriate. Of note, there was a need for a skin graft for closure in 27% in the V.A.C. group versus 36% in the control group (P 0.43); however, the wounds were able to be closed or grafted faster in the V.A.C. group (6 days vs 16 days in controls, P 0.0001). It is unclear whether the V.A.C. or some other factor was responsible for this ability to close or cover a wound earlier.195 No data are available comparing V.A.C. therapy to the shoelace or other skin-stretching techniques. Therefore, although negative pressure techniques have proven useful in aponeurotic closure over the open abdomen, their role in dealing with fasciotomy wounds is unclear at this time.

Recommendations
Fasciotomy, although often a necessary and limb-saving procedure, leads to signicant acute and long-term morbidity. Once a patient has stabilized and wound edema has begun to resolve, aggressive efforts to close fasciotomy wounds should be made. Multiple techniques to assist in wound closure are available and should be given consideration. Although mechanical devices and negative pressure dressings are becoming more and more commonplace, there is little convincing evidence that they offer much benet over the simple closure techniques described. Moreover, these techniques have the advantage of being cheap, simple, and utilizing materials that are available in most operating rooms.
826 Curr Probl Surg, October 2009

TABLE 7. Long-term sequelae of fasciotomy Chronic limb pain Limited to fasciotomy Altered sensation Limited to fasciotomy (primary closure) Limited to fasciotomy (skin graft) Dry skin Pruritus Discoloration of skin Edema Venous ulceration Contracture Muscle herniation Reprinted with permission from Fitzgerald et al.196 54% 10% 95% 100% 40% 40% 20% 30% 15% 13% 26% 13%

Long-Term Sequelae
Although there is an abundance of data regarding the acute management and in-hospital complications of fasciotomy, the topic of long-term sequelae after this procedure has been poorly studied. As is typical of a trauma population, patients undergoing fasciotomy are young, mobile, and healthy and many are lost to follow-up. Further complicating matters is the difculty in determining which disabilities are the result of the fasciotomy and which are related to the injury that prompted the procedure. With these limitations in mind, several recent studies are worthy of discussion. In 2000, Fitzgerald and colleagues196 published their experience with the care of 60 patients who had undergone 45 leg and 15 forearm fasciotomies. Most of these patients were male (90%), and the average patient age was 28 years. Associated extremity fractures were present in 81% of the patients, and coverage of the wound was accomplished with primary closure in 25 patients and skin grafting in the remaining 35 patients. On follow-up evaluation at an average of 59 months (range, 25-117 months), 54% of patients complained of chronic pain in the extremity, with 10% of patients localizing it to the fasciotomy site. Almost all patients had some alteration in local sensation, and in 84% of the patients, this was limited to the fasciotomy site. This alteration in sensation was more common after skin grafting (100%) than after primary closure (40%). There were a variety of other complaints (Table 7). In addition, patients were often unhappy with the cosmesis of their wounds. This led to a change in occupation in 12% and a change in hobbies in 28%. Finally, 23% reported that they always kept their wounds covered with clothing.196
Curr Probl Surg, October 2009 827

Another report of long-term morbidity described 18 patients who had follow-up at an average of 62 months after a fasciotomy in the thigh. All patients had some form of chronic pain or difculty with ambulation. Eight patients underwent strength and endurance testing in the quadriceps and hamstring muscle groups. Compared with the patients healthy extremities, quadriceps strength and endurance were decreased 52% and 23%, respectively. In addition, hamstring strength and endurance were reduced 64% and 19%, respectively.197 This was more pronounced with a higher Injury Severity Score and if the patient had had myonecrosis, which, as mentioned previously, is an example of the difculty in determining the contribution of the fasciotomy itself to a patients long-term disability. Finally, a recent study documented a 2.4-year follow-up on 24 patients who underwent a fasciotomy in the leg after blunt trauma.198 All patients underwent delayed primary closure of the fasciotomy site during the initial hospital stay. Despite this fact, circumference of the injured leg was asymmetric with the patients healthy leg in 67% of patients. Approximately one half had an increase in circumference in their injured leg and one half had a decrease in circumference compared with the healthy leg. Moreover, more that one half of the patients had limitations in plantar exion of the injured leg and nearly 70% had reduced dorsal extension of the ankle. Muscle strength for dorsal extension was reduced 27%, and strength of plantar exion was reduced 23%. Finally, 15% of patients had chronic pain at rest and an additional 26% had pain with exertion. More than one half the patients reported a sensory decit despite no patient requiring a skin graft.198 As with the prior study, this report makes little mention of the extent of the patients original injuries, so it is hard to ascertain the true effect of the fasciotomy itself on chronic symptoms.

Summary
Fasciotomy is a common and often limb-saving procedure that is performed as part of both elective and emergent operative procedures in the extremities. This review describes the history, denes the disease, and describes the options for diagnosing a compartment syndrome. The technical aspects of both decompressing affected compartments and covering the fasciotomy wound are described as well. Finally, the sparse data on long-term sequelae are reviewed. With a working knowledge of the techniques of diagnosis and management in this article, limbs of many critically ill patients may be salvaged.
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REFERENCES
1. Konig F, Richter E, Volkmann R. Die ischaemischen Muskellahmungen undKontrakturen. Centralblatt fur Chirurgie 1881;51:801-3. 2. Matsen FA III. Compartmental Syndromes. New York: Grune & Stratton; 1980. 3. Masten FA III. Denition of the compartmental syndrome. In: Matsen FA III, ed. Compartmental Syndromes. New York: Grune & Stratton; 1980:3-6. 4. Feliciano DV. The management of extremity compartment syndrome. In: Cameron JL, ed. Current Surgical Therapy. 9th ed. Philadelphia: Mosby Elsevier; 2008: 1032-7. 5. Hildebrand O. Die Lehre von den ischamische Muskellahmungen und Kontrakturen. Samml Klin Vortrage 1906;122:559-84. 6. Garn SR. Historical review. In: Mubarak SJ, Hargens AR, eds. Compartment Syndromes and Volkmanns Contracture (Saunders Monographs in Clinical Orthopaedics, Volume III). Philadelphia: WB Saunders; 1981:6-16. 7. Rutkow IM. The nineteenth century. In: Rutkow IM, ed. Surgery. An illustrated history. St. Louis: Mosby; 1993:321-503. 8. Volkmann R von. Krakenheiten der Bewegungsorgane. In: Handbuch der Chirurgie(Pitha-Billroth). Erlangen 1869;2:846. (Cited by Garn SR, ref. #6). 9. Lesser E. Untersuchungen uber ischamische Muskellahmungen und Muskelkontrakturen. Samml Klin Vortrage 1884;249. (Cited by Garn SR, ref. #6). 10. Bardenheuer L. Die ischamische Kontraktur und Gangran als Folge der Arterienverletzung. Leutholds Gedenkschr 1906;2:87-131. 11. Murphy JB. Myositis. Ischemic myositis: inltration myositis: cicatricial muscular or tendon xation in forearm: internal, external and combined compression myositis, with subsequent musculotendinous shortening. JAMA 1914;69:1249-55. 12. Brooks B. Pathologic changes in muscle as a result of disturbances of circulation. Arch Surg 1922;5:188-216. 13. Jepson PN. Ischaemic contracture. Ann Surg 1926;89:785-95. 14. Grifths D. Volkmanns ischaemic contracture. Br J Surg 1940;28:239-60. 15. Foisie PS. Volkmanns ischemic contracture. An analysis of its proximate mechanism. N Engl J Med 1942;226:671-9. 16. Bywaters EGL, Beall D. Crush injuries with impairment of renal function. BMJ 1941;1:427-32. 17. Seddon HJ. Volkmanns ischaemia in the lower limb. J Bone Joint Surg Br 1966;48:627-36. 18. Rorabeck CH, Clarke KM. The pathophysiology of the anterior tibial compartment syndrome: an experimental investigation. J Trauma 1978;18:299-304. 19. Rorabeck CH, MacNab I. The pathophysiology of the anterior tibial compartmental syndrome. Clin Orthop Relat Res 1975;113:52-7. 20. Dahn I, Lassen NA, Westling H. Blood ow in human muscles during external pressure or venous stasis. Clin Sci 1967;32:467-73. 21. Sheridan GW, Matsen FA, Krugmire RB. Further investigations on the pathophysiology of the compartment syndrome. Clin Orthop Relat Res 1977;123:266-70. 22. Matsen FA, King RV, Krugmire RB, Mowery CA, Roche T. Physiological effects of increased tissue pressure. Int Orthop (SICOT) 1979;3:237-44. 23. Matsen FA, Krugmire RB, King RV. Increased tissue pressure and its effects on
Curr Probl Surg, October 2009 829

24.

25.

26. 27. 28.

29. 30. 31.

32. 33.

34. 35. 36. 37. 38. 39.

40. 41.

42.
830

muscle oxygenation in level and elevated human limbs. Clin Orthop Relat Res 1979;144:311-20. Hargens AR, Romine JS, Sipe JC, Evans KL, Mubarak SJ, Akeson WH. Peripheral nerve-conduction block by high muscle compartment pressure. J Bone Joint Surg Am 1979;192-200. Matsen FA, Mayo KA, Krugmire RB, Sheridan GW, Kraft GH. A model compartmental syndrome in man with particular reference to the quantication of nerve function. J Bone Joint Surg Am 1977;59:648-53. Matsen FA III. Pathophysiology of increased tissue pressure. In: Matsen FA III, ed. Compartmental Syndromes. New York: Grune & Stratton; 1980:29-43. Burton AC. Relation of structure to function of the tissues of the wall of blood vessels. Physiol Rev 1954;34:619-42. Hargens AR, Mubarak SJ, Owen CA, Garetto LP, Akeson WH. Interstitial uid pressure in muscle and compartment syndrome in man. Microvasc Res 1977; 14:1-10. Kjellmer I. An indirect method for estimating tissue pressure with special reference to tissue pressure in muscle during exercise. Acta Physiol Scand 1964;62:31-40. Reneman RS. The posterior and lateral compartmental syndrome of the leg due to intensive use of muscles. Clin Orthop Relat Res 1975;113:69-80. Matsen FA, Wyss CR, Krugmire RB, Simmons CW, King RV. The effects of limb elevation and dependency on local arteriovenous gradients in normal human limbs with particular reference to limbs with increased tissue pressure. Clin Orthop Relat Res 1980;150:187-95. Patman RD, Thompson JE. Fasciotomy in peripheral vascular surgery. Report of 164 patients. Arch Surg 1970;101:663-72. Whitesides TE Jr, Haney TC, Morimoto K, Harada H. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop Relat Res 1975;113:43-51. Matsen FA. Compartmental syndrome. A unied concept. Clin Orthop Relat Res 1975;113:8-14. Mubarak SJ, Owen CA. Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg Am 1977;59:184-7. Matsen FA III, Krugmire RB Jr. Compartmental syndromes. Surg Gynecol Obstet 1978;147:943-9. Matsen FA III, Winquist RA, Krugmire RB Jr. Diagnosis and management of compartment syndromes. J Bone Joint Surg Am 1980;62:286-91. Matsen FA III. Etiologies of compartment syndromes. In: Matsen FA III, ed. Compartmental Syndromes. New York: Grune & Stratton; 1980:65-78. Mullins RJ. Shock, electrolytes, and uid. In: Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. Philadelphia: Elsevier Saunders; 2004:67-112. McCord JM. Oxygen-devised free radicals in postischemic tissue injury. N Engl J Med 1985;312:159-63. Abd-Elfattah AS, Higgins RSD, Lati R, Merrell RC. Targeting post-ischemic reperfusion injury: scientic dream and clinical reality. New Surgery 2001;1:41-51. Blaisdell FW. The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome. Cardiovasc Surg 2002;10:620-30.
Curr Probl Surg, October 2009

43. Feigl EO. Physics of the cardiovascular system. In: Rich TC, Ratton HD, eds. Physiology and Biophysics. Circulation, Respiration and Fluid Balance. Vol. 2. Philadelphia: Saunders; 1974:15. 44. Miller HH, Welch CS. Quantitative studies on the time factor in arterial injuries. Ann Surg 1949;130:428-38. 45. Whitesides TE Jr, Harada H, Morimoto K. Compartment syndromes and the role of fasciotomy, its parameters and techniques. Instr Course Lect 1977;26:179-96. 46. Heckmann MM, Whitesides TE Jr, Grewe SR, Rooks MD. Compartment pressure in association with closed tibial fractures: the relationship between tissue pressure, compartment, and distance from the site of the fracture. J Bone Joint Surg Am 1994;76:1285-92. 47. Heckmann MM, Whitesides TE Jr, Grewe SR, Judd RL, Miller M, Lawrence JH III. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma 1993;7:199-210. 48. Whitesides TE Jr, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg 1996;4:209-18. 49. Matava MJ, Whitesides TE Jr, Seiler JG III, Hewan-Lowe K, Hutton WC. Determination of the compartment pressure threshold of muscle ischemia in a canine model. J Trauma 1994;37:50-8. 50. Heppenstall RB, Scott R, Sapega A, Park YS, Chance B. A comparative study of the tolerance of skeletal muscle to ischemia. Tourniquet application compared with acute compartment syndrome. J Bone Joint Surg Am 1986;68:820-8. 51. Heppenstall RB, Sapega A, Alexander A, Scott R, Shenton D, Park YS, et al. The compartment syndrome: an experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop 1988;226:138-55. 52. Heppenstall RB, Sapega AA, Izant T, Fallon R, Shenton D, Park YS, et al. Compartment syndrome: a quantitative study of high-energy phosphorus compounds using 31P-magnetic resonance spectroscopy. J Trauma 1989;29:113-9. 53. Mubarak S, Carroll N. Volkmanns contracture in children: aetiology and prevention. J Bone Joint Surg Br 1979;61:285-93. 54. Kulber DA, Tompkins GS, Hiatt JR. Compartment syndrome. In: Hobson RW II, Wilson SE, Veith FJ, eds. Vascular Surgery. Principles and Practice. 3rd ed, revised and expanded. New York: Marcel Dekker Inc; 2004:1133-44. 55. Lagerstrom CF, Reed RLR II, Rowlands BJ, Fischer RP. Early fasciotomy for acute clinically evident posttraumatic compartment syndrome. Am J Surg 1989;158:36-9. 56. Thomas DD, Wilson RF, Wiencek RG. Vascular injury about the knee: improved outcome. Am Surg 1989;55:370-7. 57. Feliciano DV, Cruse PA, Spjut-Patrinely V, Burch JM, Mattox KL. Fasciotomy after trauma to the extremities. Am J Surg 1988;156:533-6. 58. Rorabeck C. The treatment of compartment syndromes of the leg. J Bone Joint Surg Br 1984;66:93-7. 59. White TO, Howell GED, Will EM, Court-Brown CM, McQueen MM. Elevated intramuscular compartment pressures do not inuence outcome after tibial fracture. J Trauma 2003;55:1133-8. 60. Kostler W, Strohm PC, Sudkamp NP. Acute compartment syndrome of the limb. Injury 2004;35:1221-7. 61. Twaddle BC, Amendola A. Compartment syndromes. In: Browner BP, Jupiter JB,
Curr Probl Surg, October 2009 831

62. 63.

64. 65. 66. 67. 68.

69.

70. 71.

72.

73. 74. 75. 76. 77.

78.

79.

Levine AM, Trafton PG, Krettek C, eds. Skeletal Trauma. Basic Science, Management, and Reconstruction. 4th ed. Philadelphia: Saunders Elsevier; 2009: 341-66. Matsen FA III. Diagnosis of compartmental syndromes. In: Matsen FA III, ed. Compartmental Syndromes. New York: Grune & Stratton; 1980:85-100. Owen CA. Clinical diagnosis of acute compartment syndromes. In: Mubarak SJ, Hargens AR, eds. Compartment Syndromes and Volkmanns Contracture (Saunders Monographs in Clinical Orthopaedics Volume III). Philadelphia: WB Saunders; 1981:98-105. DeLee JC, Stiehl JB. Open tibial fractures with compartment syndrome. Clin Orthop 1981;160:175-84. Blick SS, Brumback RJ, Poka A, Burgess AR, Ebraheim NA. Compartment syndrome in open tibial fractures. J Bone Joint Surg Am 1986;68:1348-53. McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg Br 1996;78:95-8. French EB, Price WH. Anterior tibial pain. BMJ 1962;II:1291-6. Hargens AR, Mubarak SJ. Laboratory diagnosis of acute compartment syndromes. In: Mubarak SJ, Hargens AR, eds. Compartment Syndromes and Volkmanns Contracture (Saunders Monographs in Clinical Orthopaedics, Volume III). Philadelphia: WB Saunders; 1981:106-22. Rorabeck CH, Castle GSP, Hardie R, Logan J. Compartment pressure measurements: an experimental investigation using the slit catheter. J Trauma 1981;21:446-9. Scholander PF, Hargens AR, Miller SL. Negative pressure in the interstitial uid of animals. Science 1968;161:321-8. Mubarak SJ, Hargens AR, Owen CA, Akeson WH, Garetto LP. The wick catheter technique for measurement of intramuscular pressure. A new research and clinical tool. J Bone Joint Surg Am 1976;58:1016-20. Wilson SC, Vrahas MS, Berson L, Paul EM. A simple method to measure compartment pressures using an intravenous catheter. Orthopaedics 1997;20:403-6. Stryker Instruments. The Stryker Intra-compartmental Pressure Monitor System. October 2007. Matsen FA, Mayo KA, Sheridan GW, Krugmire RB. Monitoring of intramuscular pressure. Surgery 1976;79:702-9. Matsen FA III. Tissue pressure and its measurement. In: Matsen FA III, ed. Compartmental Syndromes. New York: Grune & Stratton; 1980:7-28. McQueen M, Christie J, Court-Brown C. Compartment pressure after intramedullary nailing of the tibia. J Bone Joint Surg Br 1990;72:395-7. Moed B, Thorderson P. Measurement of intracompartmental pressure: a comparison of the slit catheter, sideported needle, simple needle. J Bone Joint Surg Am 1993;75:231-5. Uliasz A, Ishida J, Fleming J, Yamamoto L. Comparing the methods of measuring compartment pressures in acute compartment syndrome. Am J Emerg Med 2003;21:143-5. Boody AR, Wongworawat MD. Accuracy in the measurement of compartment pressures: a comparison of three commonly used devices. J Bone Joint Surg Am 2005;87:2415-22.
Curr Probl Surg, October 2009

832

80. Konstantakos EK, Dahlstrom DJ, Nelles ME, Laughlin RT, Prayson MJ. Diagnosis and management of extremity compartment syndromes: an orthopaedic perspective. Am Surg 2007;73:1199-209. 81. Agudelo JF, Morgan SJ, Schmidt A, Smith W, Odland R, Parekh A, et al. Management of acute compartment syndrome: randomized clinical trial evaluating a novel compartment syndrome catheter. Poster presented at the Orthopaedic Trauma Association Annual Meeting, Ottawa, Ontario, 2005. 82. Wiemann JM, Ueno T, Leek BT, Yost WT, Schwartz AK, Hargens AR. Noninvasive measurements of intramuscular pressure used pulsed phase-locked loop ultrasound for detecting compartment syndrome. A preliminary report. J Orthop Trauma 2006;20:458-63. 83. Mubarak SJ, Owen CA, Hargens AR, Garetto LP, Akeson WH. Acute compartment syndromes: diagnosis and treatment with the aid of a wick catheter. J Bone Joint Surg Am 1978;60:1091-5. 84. Feliciano DV. Management of Peripheral Vascular Trauma. Chicago: Subcommittee on Publications, American College of Surgeons Committee on Trauma; 2002. 85. Matsen FA III. Tolerance of tissue for increased pressure. In: Matsen FA III, ed. Compartmental Syndromes. New York: Grune & Stratton; 1980:45-64. 86. Whitesides TE Jr, Haney TC, Hirada H, Holmes HE, Morimoto K. A simple method for tissue pressure determination. Arch Surg 1975;110:1311-3. 87. Arbabi S, Brundage SI, Gentilello LM. Near-infrared spectroscopy: a potential method of continuous, transcutaneous monitoring for compartment syndrome in critically injured patients. J Trauma 1999;47:829-33. 88. Garr JL, Gentilello LM, Cole PA, Mock CN, Matsen FA 3rd. Monitoring for compartmental syndrome using near infrared spectroscopy: a noninvasive, continuous, transcutaneous monitoring technique. J Trauma 1999;46:613-8. 89. Giannotti G, Cohn SM, Brown M, Varela JE, McKenney MG, Wiseberg JA. Utility of near-infrared spectroscopy in the diagnosis of lower extremity compartment syndrome. J Trauma 2000;48:396-401. 90. Gentilello LM, Sanzone A, Wang L, Liv PY, Robinson L. Near-infrared spectroscopy versus compartment pressure for the diagnosis of lower extremity compartmental syndrome using electromyography-determined measurements of neuromuscular function. J Trauma 2001;51:1-9. 91. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. Denitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992;20:864-74. 92. Tremblay LN, Feliciano DV, Rozycki GS. Secondary extremity compartment syndrome. J Trauma 2002;53:833-7. 93. Kosir R, Moore FA, Selby JH, Cocanour CS, Kozar RA, Gonzalez EA, et al. Acute lower extremity compartment syndrome (ALECS) screening protocol in critically ill trauma patients. J Trauma 2007;63:268-75. 94. Goaley TJ Jr, Wyrzykowski AD, MacLeod JBA, Wise KB, Dente CJ, Salomone JP, et al. Can secondary compartment syndrome be diagnosed earlier? Am J Surg 2007;24:724-7. 95. Vitale GC, Richardson ND, George SM Jr, Miller FB. Fasciotomy for severe blunt and penetrating trauma of the extremity. Surg Gynecol Obstet 1988;166:397-401. 96. William AB, Luchette FA, Papaconstantinou HT, Lim E, Hurst JM, Johannigman
Curr Probl Surg, October 2009 833

97. 98. 99.

100.

101.

102. 103.

104.

105. 106. 107.

108. 109.

110.

111.

112.

113. 114.
834

JA, et al. The effect of early vs. late fasciotomy in the management of extremity trauma. Surgery 1997;122:861-6. Robinson D, On E, Halperin N. Anterior compartment syndrome of the thigh in athletes-indications for conservative treatment. J Trauma 1992;32:183-6. Riede U, Schmid MR, Romero J. Conservative treatment of an acute compartment syndrome of the thigh. Arch Orthop Trauma Surg 2007;127:269-75. Garcia-Covarrubias L, McSwain NE, Van Meter K, Bell RM. Adjuvant hyperbaric oxygen therapy in the management of crush injury and traumatic ischemia: an evidence based approach. Am Surg 2005;71:144-50. Strauss MB, Hargens AR, Gershuni DH, Greenberg DA, Crenshaw AG, Hart GB, et al. Reduction of skeletal muscle necrosis using intermittent hyperbaric oxygen in a model compartment syndrome. J Bone Joint Surg Am 1983;65:656-62. Skyhar MJ, Hargens AR, Strauss MB, Gershuni DH, Hart GB, Akeson WH. Hyperbaric oxygen reduces edema and necrosis of skeletal muscle in compartment syndromes associated with hemorrhagic hypotension. J Bone Joint Surg Am 1986;68:1218-24. Strauss MB, Hart GB. Hyperbaric oxygen therapy and the skeletal-muscle compartment syndrome. Contemp Orthop 1989;18:167-74. Gold BS, Barish RA, Dart RC, Silverman RP, Bochicchio GV. Resolution of compartment syndrome after rattlesnake envenomation utilizing non-invasive measures. J Emerg Med 2003;24:285-8. Abdullah MS, AL-Waili NS, Butler G, Baban NW. Hyperbaric oxygen as an adjunctive therapy for bilateral compartment syndrome, rhabdomyolysis and acute renal failure after heroin intake. Arch Med Res 2006;37:559-62. Fitzpatrick DT, Bryce M, Murphy PT. Adjunctive treatment of compartment syndrome with hyperbaric oxygen. Mil Med 1998;163:577-9. Slater MS, Mullins RJ. Rhabdomyolysis and myoglobinuric renal failure in trauma and surgical patients: a review. J Am Coll Surg 1998;186:693-716. Brown CV, Rhee P, Chan L, Evans K, Demetriades D, Velmahos GC. Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? J Trauma 2004;56:1191-6. Sharp LS, Rozycki GS, Feliciano DV. Rhabdomyolysis and secondary renal failure in critically ill surgical patients. Am J Surg 2004;188:801-6. Better OS, Zinman C, Reis ND, Har-Shai Y, Rubinstein I, Abassi Z. Hypertonic mannitol ameliorates intracompartmental tamponade in model compartment syndrome in the dog. Nephron 1991;58:344-6. Ricci MA, Graham AM, Corbisiero R, Baffour R, Mohamed F, Symes JF. Are free radical scavengers benecial in the treatment of compartment syndrome after acute arterial ischemia? J Vasc Surg 1989;9:244-50. Alioglu B, Avci Z, Baskin E, Ozcay F, Tuncay IC, Ozbek N. Successful use of recombinant factor VIIa (Novoseven) in children with compartment syndromes. J Pediatr Orthop 2006;26:815-7. Watts RG. Successful use of recombinant factor VIIa for emergency fasciotomy in a patient with hemophilia A and high-titer inhibitor unresponsive to factor viii inhibitor bypassing activity. Am J Hematol 2005;79:58-60. Shah JS, Anagnos DM, Noreet EA. Elastic tourniquet technique for decompression of extremity compartment syndrome. J Clin Anesth 2002;14:524-8. Heckmann JG, Dutsch M, Neundorfer B. Leech therapy in the treatment of median
Curr Probl Surg, October 2009

115.

116. 117.

118. 119.

120.

121. 122. 123. 124. 125. 126.

127.

128. 129. 130. 131. 132. 133.

nerve compression due to forearm hematoma. J Neurol Neurosurg Psychiatry 2005;76:1465-8. Schenker M, Murray A, Kay SPJ. Leech therapy in the treatment of median nerve compression due to forearm hematoma. J Neurol Neurosurg Psychiatry 2006; 77:799-800. Due J Jr, Norstrand K. A simple technique for subcutaneous fasciotomy. Acta Chir Scand 1987;153:521-2. Wood ML, Almekinders LC. Minimally invasive subcutaneous fasciotomy for chronic exertional compartment syndrome of the lower extremity. Am J Orthop 2004;33:42-4. Hallock GG. An endoscopic technique for decompressive fasciotomy. Ann Plast Surg 1999;43:668-70. Havig MT, Leversedge FJ, Seiler JG. Forearm compartment pressure: an in vitro analysis of open and endoscopic assisted fasciotomy. J Hand Surg 1999;24A: 1289-97. Leversedge FJ, Casey PJ, Seiler JH, Xerogeanes JW. Endoscopically assisted fasciotomy. Description of technique and in vitro assessment of lower-leg compartment decompression. Am J Sports Med 2002;30:272-8. Jensen SL, Sandermann J. Compartment syndrome and fasciotomy in vascular surgery. A review of 57 cases. Eur J Vasc Endovasc Surg 1997;13:48-53. Velmahos GC, Toutouzas KG. Vascular trauma and compartment syndromes. Surg Clin North Am 2002;82:125-41. Matsen FA III. Treatment of compartmental syndromes. In: Matsten FA III. Compartmental Syndromes. New York: Grune & Stratton; 1980:101-15. Gaspard DJ, Cohen JL, Gaspar MR. Decompression dermotomy. A limb salvage adjunct. JAMA 1972;220:831-3. Gaspard DJ, Kohl RD Jr. Compartmental syndromes in which the skin is the limiting boundary. Clin Orthop Relat Res 1975;113:65-8. Ritenour AE, Dorlac WC, Fang R, Woods T, Jenkins DH, Flaherty SF, et al. Complications after fasciotomy revision and delayed compartment release in combat patients. J Trauma 2008;64:S153-62. Mubarak SJ. Lower extremity compartment syndromes: Treatment. In: Mubarak SJ, Hargens AR, eds. Compartment Syndromes and Volkmanns Contracture (Saunders Monographs in Clinical Orthopaedics Volume III). Philadelphia: WB Saunders; 1981:147-65. DeBakey ME, Simeone FA. Battle injuries of the arteries in World War II. An analysis of 2,471 cases. Ann Surg 1946;123:534-79. Kelly RP, Whitesides TE. Transbular route for fasciotomy of the leg. J Bone Joint Surg Am 1967;49:1022-3. Nghiem DD, Boland JP. Four-compartment fasciotomy of the lower extremity without bulectomy: a new approach. Am Surg 1980;46:414-7. Rollins DL, Bernhard VM, Towne JB. Fasciotomy. An appraisal of controversial issues. Arch Surg 1981;116:1474-81. Cooper GG. A method of single-incision, four compartment fasciotomy of the leg. Eur J Vasc Surg 1992;6:659-61. Cheney RA, Melaragno PG, Prayson MJ, Bennett GL, Njus GL. Anatomic investigation of the deep posterior compartment of the leg. Foot Ankle Int 1998;19:98-101.
835

Curr Probl Surg, October 2009

134. Perry MD, Manoli A II. Foot compartment syndrome. Orthop Clin North Am 2001;32:103-11. 135. Myerson MS. Management of compartment syndromes of the foot. Clin Orthop 1991;271:239-47. 136. Ascer E, Strauch B, Calligaro KD, Gupta SK, Veith FJ. Ankle and foot fasciotomy and adjunctive technique to optimize limb salvage after revascularization for acute ischemia. J Vasc Surg 1989;9:594-7. 137. Grodinsky M. A study of the fascial spaces of the foot and their bearing on infections. Surg Gynecol Obstet 1929;49:737-51. 138. Loefer RD, Ballard A. Plantar fascial spaces of the foot and a proposed surgical approach. Foot Ankle 1980;1:11-4. 139. Henry AK. Extensile Exposure. 2nd ed. New York: Churchill Livingstone; 1982. 140. Bonutti PM, Bell GR. Compartment syndrome of the foot. J Bone Joint Surg Am 1986;68:1449-51. 141. Manoli A, Weber TG. Fasciotomy of the foot. An anatomical study with special reference to release of the calcaneal compartment. Foot Ankle 1990;10:267-75. 142. Myerson MS. Experimental decompression of the fascial compartments of the foot-the basis for fasciotomy in acute compartment syndromes. Foot Ankle 1988;8:308-14. 143. Dente CJ, Feliciano DV, Rozycki GS, Cava RA, Ingram WL, Salomone JP, et al. A review of upper extremity fasciotomies in a level I trauma center. Am Surg 2004;70:1088-93. 144. Gellman H, Buch K. Acute compartment syndrome of the arm. Hand Clin 1998;14:385-9. 145. Boles CA, Kannam S, Cardwell AB. The forearm: anatomy of muscle compartments and nerves. AJR Am J Roentgenol 2000;174:151-9. 146. Chan PSH, Steinberg DR, Pepe MD, Beredjiklian PB. The signicance of the three volar spaces in the forearm compartment syndrome: a clinical and cadaveric correlation. J Hand Surg 1998;23A:1077-81. 147. Ronel DN, Mtui E, Nolan WB. Forearm compartment syndrome: anatomical analysis of surgical approaches to the deep space. Plast Reconstr Surg 2004; 114:697-705. 148. Friedrich JB, Shin AY. Management of forearm compartment syndrome. Hand Clin 2007;23:245-54. 149. Allen MJ, Steingold RF, Kotecha M, Barnes M. The importance of the deep volar compartment in crush injuries of the forearm. Injury 1985;16:273-5. 150. Gelberman RH, Garn SR, Hergenroeder PT, Mubarak SJ, Menon J. Compartment syndromes of the forearm: diagnosis and treatment. Clin Orthop Relat Res 1981;161:252-61. 151. Oritz JA, Berger RA. Compartment syndrome of the wrist and hand. Hand Clin 1998;14:405-18. 152. Lampe EW. Surgical anatomy of the hand. Clin Symp (CIBA) 1969;21:65-109. 153. Halpern AH, Mochizuki RM. Compartment syndrome of the interosseous muscle of the hand. Orthop Rev 1980;3:121-7. 154. DiFelice A, Seiler JG, Whitesides TE. The compartments of the hand: an anatomic study. J Hand Surg 1998;23A:682-6. 155. Gulgonen A. Compartment syndrome. In Green DP, Hotchkiss RN, Pederson WC,
836 Curr Probl Surg, October 2009

156. 157. 158. 159. 160. 161. 162. 163. 164. 165.

166. 167. 168. 169.

170. 171. 172. 173.

174.

175. 176.

Wolfe SW, eds. Greens Operative Hand Surgery. 5th ed. Philadelphia: Elsevier Churchill Livingstone; 2005:1985-2006. Sheridan GW, Matsen FA. Fasciotomy in the treatment of the acute compartment syndrome. J Bone Joint Surg Am 1976;58:112-5. Gibson T. Physical properties of skin. In: McCarthy J, ed. Plastic Surgery. Philadelphia: WB Saunders; 1990:209-11. Gibson T, Kanadi R. Biochemical properties of tissue. Surg Clin North Am 1967;47:279-94. Branchet MC, Boisnic S, Frances C, Robert AM. Skin thickness changes in normal aging skin. Gerontology 1990;36:28-35. Brody G. The biochemical properties of tissue. In: Rudolph R, ed. Problems in Aesthetic Surgery. St. Louis: CV Mosby; 1986:49-56. Marquet BC. Rapid intraoperative distension using isotonic saline solution. Plast Reconstr Surg 1995;96:158-65. Baker SR. Fundamentals of expanded tissue. Head Neck 1991;13:158-65. Wilhelmi BJ, Blackwell SJ, Mancoll JS, Phillips LG. Creep vs. stretch: a review of the viscoelastic properties of skin. Ann Plast Surg 1998;41:215-9. Johnson T, Lowe L, Brown MD, Sullivan MJ, Nelson BR. Histology and physiology of tissue expansion. J Dermatol Surg Oncol 1993;19:1074-8. Disaia PJ, Creasman WT, Eddy G, Montz J. Experience with a mass closure technique using continuous looped polyglyconate absorbable suture. J Am Coll Surg 1994;178:177-80. Larsen JS, Ulin AW. Tensile strength advantage of the far-and-near suture technique. Surg Gynecol Obstet 1970;131:123-4. Bentley PG, Owen WJ, Girolami PL, Dawson JL. Wound closure with Dexon (polyglycolic acid) mass suture. Ann R Coll Surg Engl 1978;60:125-7. Shukla VK, Gupta A, Singh H, Pandey M, Gautam A. Cardiff repair of incisional hernia: a university hospital experience. Eur J Surg 1998;164:271-4. Cohn BT, Shall J, Berkowitz M. Forearm fasciotomy for acute compartment syndrome: a new technique for delayed primary closure. Orthopedics 1986;9: 1234-6. Chiverton N, Redden JF. A new technique for delayed primary closure of fasciotomy wounds. Injury 2000;31:21-4. Asgari MM, Spinelli HM. The vessel loop shoelace technique for closure of fasciotomy wounds. Ann Plast Surg 2000;44:225-9. Harris I. Gradual closure of fasciotomy wounds using a vessel loop shoelace. Injury 1993;24:565-72. Berman SS, Schilling JD, McIntyre KE, Hunter GC, Bernhard VM. Shoelace technique for delayed primary closure of fasciotomies. Am J Surg 1994;167:435-6. Galois L, Pauchot J, Pfeffer F, Kermarrec I, Traversari R, Mainard D, et al. Modied shoelace technique for delayed primary closure of the thigh after acute compartment syndrome. Acta Orthop Belg 2002;68:63-7. Zorilla P, Marin A, Gomez LA, Salido JA. Shoelace technique for gradual closure of fasciotomy wounds. J Trauma 2005;59:1515-7. Taylor RC, Reitsma BJ, Sarazin S, Bell MG. Early results using a dynamic method for delayed primary closure of fasciotomy wounds. J Am Coll Surg 2003; 197:872-8.
837

Curr Probl Surg, October 2009

177. Mbubaegbu CE, Stallard MC. A method of fasciotomy wound closure. Injury 1996;27:613-5. 178. Harrah J, Gates R, Carl J, Harrah JD. A simpler, less expensive technique for delayed primary closure of fasciotomies. Am J Surg 2000;180:55-7. 179. Hirshowitz B, Lindenbaum E, Har-Shai Y. A skin-stretching device for the harnessing of the viscoelastic properties of skin. Plast Reconstr Surg 1993;92: 260-70. 180. Ersek RA, Vazquez-Salisbury A. Wound closure using a skin-stretching device. Contemp Orthop 1994;28:495-500. 181. Boden BP, Buinewicz BR. Management of traumatic cutaneous defects by using a skin-stretching device. Am J Orthop 1995;11(suppl):27-30. 182. Foley AL. A new technique for closing wounds after surgery for breast melanoma. Plast Reconstr Surg 1995;95:418-9. 183. Parthington MT. Alternative approach to the problematic wound. Contemp Surg 1995;47:221-2. 184. Narayanan K, Futrell JW, Bentz M, Hurwitz D. Comparative clinical study of the Sure-Closure device with conventional wound closure techniques. Ann Plast Surg 1995;35:485-91. 185. Caruso DM, King TJ, Tsujimura RB, Weiland DE, Schiller WR. Primary closure of fasciotomy incisions with a skin-stretching device in patients with burn and trauma. J Burn Care Rehabil 1997;18:125-32. 186. Armstrong DG, Sorensen JC, Bushman TR. Exploiting the viscoelastic properties of pedal skin with the Sure-Closure skin stretching device. J Foot Ankle Surg 1995;34:247-53. 187. Narayanan K, Latenser BA, Jones LM, Stofman G. Simultaneous primary closure of four fasciotomy wounds in a single setting using the Sure-Closure device. Injury 1996;27:449-51. 188. McKenney MG, Nir I, Fee T, Martin L, Lentz K. A simple device for closure of fasciotomy wounds. Am J Surg 1996;172:275-7. 189. Barnea Y, Gur E, Amir A, Leshem D, Zaretski A, Miller E, et al. Delayed primary closure of fasciotomy wounds with Wisebands, a skin- and soft tissue-stretch device. Injury 2006;37:561-6. 190. Singh N, Bluman E, Starnes B, Andersen C. Dynamic wound closure for decompressive leg fasciotomy wounds. Am Surg 2008;74:217-20. 191. Weiland DE. Fasciotomy closure using simultaneous vacuum-assisted closure and hyperbaric oxygen. Am Surg 2007;73:261-6. 192. Miller PR, Meredith JW, Johnson JC, Chang MC. Prospective evaluation of vacuum-assisted fascial closure after open abdomen: planned ventral hernia rate is substantially reduced. Ann Surg 2004;239:604-16. 193. Suliburk JW, Ware DN, Balogh Z, McKinley BA, Cocanour CS, Kozar RA, et al. Vacuum-assisted wound closure achieves early fascial closure of open abdomens after severe trauma. J Trauma 2003;55:1155-61. 194. Stone PA, Hass SM, Flaherty SK, DeLuca JA, Lucente FC, Kusminsky RE. Vacuum-assisted fascial closure for patients with abdominal trauma. J Trauma 2004;57:1082-6. 195. Yang CC, Chang DS, Webb LX. Vacuum-assisted closure for fasciotomy wounds following compartment syndrome of the leg. J Surg Orthop Adv 2006;15:19-23.
838 Curr Probl Surg, October 2009

196. Fitzgerald AM, Gaston P, Wilson Y, Quaba A, McQueen MM. Long-term sequelae of fasciotomy wounds. Br J Plast Surg 2000;53:690-3. 197. Mithoefer K, Lhowe DW, Vrahas MS, Altman DT, Erens V, Altman GT. Functional outcome after acute compartment syndrome of the thigh. J Bone Joint Surg Am 2006;88:729-37. 198. Frink M, Klaus AK, Kuther G, Probst C, Gosling T, Kobbe P, et al. Long term results of compartment syndrome of the lower limb in polytraumatised patients. Injury 2006;38:607-13.

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