Patient management following extremity fasciotomy

INTRODUCTION — Extremity fasciotomy is the only recognized treatment for acute compartment syndrome and may be limb saving. Reperfusion following fasciotomy causes local and systemic effects that can be life-threatening and can complicate wound management.

The management of the patient following extremity fasciotomy, including management of reperfusion, wound care, and methods and timing of fasciotomy wound closure, will be reviewed here. Preoperative management and the indications, diagnosis, and techniques used to perform fasciotomy are discussed elsewhere. (See "Acute compartment syndrome of the extremities" and "Lower extremity fasciotomy techniques".)

ISCHEMIA-REPERFUSION — Local and systemic consequences of ischemia-reperfusion occur after fasciotomy. Increased blood flow in the muscle following restoration of normal tissue pressure usually causes muscle edema. The extent of extremity swelling depends upon the duration and severity of ischemia, the predominant muscle cell type within a muscle, the location and mass of ischemic muscle, and the status of the venous circulation.

Animal studies show that cellular damage starts approximately three hours after a complete ischemic insult and is nearly complete by six hours [1]. In humans, the level of tolerance to an ischemic insult varies, and not all ischemic insults are complete. Patients with underlying peripheral artery disease may exhibit less than expected swelling due to the protective effects of preexisting arterial collaterals that lessen the severity of ischemia [2]. There is also evidence from animal studies that ischemic preconditioning in skeletal muscle may mitigate the severity of muscle injury, remote organ injury, and mortality after major ischemic events [3,4].

Swelling may be limited if there is incomplete reperfusion due to microvascular thrombosis. With prolonged ischemia, a "no reflow phenomenon" occurs that is characterized by capillary occlusion from endothelial swelling, plugging of capillaries with red and white blood cells, and increased interstitial pressure [5,6]. Reperfusion may occur at the macrovascular level, but there is no tissue perfusion. Clinically, this manifests as myonecrosis with minimal extremity swelling.

Successful reperfusion liberates the byproducts of muscle ischemia and cell necrosis (rhabdomyolysis) into the circulation, including potassium, phosphate, organic acids, myoglobin, creatine kinase, and thromboplastin. The systemic effects of these byproducts may include hyperkalemia, hyperphosphatemia, metabolic acidosis, and myoglobinuria, which can cause acute kidney injury, elevation of serum creatine kinase levels, and disseminated intravascular coagulation. (See 'Management of reperfusion' below.)

Muscles differ in their susceptibility to ischemic injury based upon the predominant muscle fiber type that is present [7]. Type I fibers rely primarily on oxidative metabolism of triglycerides, making these fibers vulnerable to ischemia. In comparison, type II fibers use anaerobic metabolism of glycogen, and, as a result, these fibers tolerate ischemia to a greater degree. Differences in muscle fiber distribution may explain, in part, the higher incidence of compartment syndrome in the anterior compartment of the leg, compared with the superficial posterior compartment (figure 1). The tibialis anterior muscle is comprised primarily of type I fibers, whereas the gastrocnemius muscle has primarily type II fibers.

Although fasciotomy leading to reperfusion is generally limb saving, crush injuries involving large muscle groups (eg, buttock, thigh) may be prone to life-threatening complications from reperfusion [8,9]. The magnitude of the reperfusion insult may be so severe that sudden cardiac arrest can occur as a consequence of hyperkalemia with or without severe metabolic acidosis. (See "Lower extremity fasciotomy techniques", section on 'Contraindications' and 'Management of reperfusion' below.)

Interruption of venous outflow due to venous obstruction or surgical ligation after trauma may aggravate swelling. In the injured extremity, venous repair of major veins of the leg, such as the femoral or popliteal vein, is performed whenever feasible to prevent increased venous pressure that can lead to prolonged muscle swelling and compartment syndrome. When the venous injury cannot be repaired, prophylactic fasciotomy is frequently performed. (See "Severe upper extremity injury in the adult patient" and "Lower extremity fasciotomy techniques", section on 'Prevention'.)

MANAGEMENT OF REPERFUSION — The initial management of reperfusion injury is focused on restoration of intravascular volume, followed by prevention and treatment of associated metabolic abnormalities. The most serious abnormalities include hyperkalemia, metabolic acidosis, and acute kidney injury due to myoglobinuria.

●Hyperkalemia – Hyperkalemia is treated to prevent life-threatening arrhythmias or cardiac arrest. Treatment is initiated based upon the presence of peaked T waves on the electrocardiogram (waveform 1). (See "Clinical manifestations of hyperkalemia in adults", section on 'Cardiac manifestations'.)

Peaked T waves in this setting are an indication for urgent therapy of hyperkalemia, since ongoing release of potassium from ischemic or necrotic muscle cells can lead to progressive and life-threatening hyperkalemia. Treatment of hyperkalemia in this setting may include multiple modalities, with intravenous calcium having the most rapid onset. In the absence of electrocardiographic changes, hyperkalemia can initially be managed by ensuring adequate urinary output, but careful monitoring of the serum potassium is warranted. The manifestations and treatment of hyperkalemia are discussed in detail elsewhere. (See "Treatment and prevention of hyperkalemia in adults".)

●Metabolic acidosis – Metabolic acidosis, usually lactic acidosis during reperfusion, may exacerbate hyperkalemia and induce hypotension. The initial management of lactic acidosis is focused on volume resuscitation to restore tissue perfusion, with a goal of achieving a urine output of 1 mL/kg per hour. Severe acidosis with an arterial pH below 7.10 to 7.15 may be treated with intravenous sodium bicarbonate. Issues related to the treatment of lactic acidosis are discussed in detail elsewhere. (See "Bicarbonate therapy in lactic acidosis" and "Approach to the adult with metabolic acidosis", section on 'Overview of therapy'.)

●Rhabdomyolysis and myoglobinuria – Rhabdomyolysis presents with elevated serum muscle enzymes (including creatine kinase), red to brown urine due to myoglobinuria if there is persistent renal function, and electrolyte abnormalities. Peak serum creatine kinase levels depend upon the volume of muscle breakdown and the muscle mass of the patient. Creatinine kinase values should be measured twice daily until decreasing levels are observed. (See "Rhabdomyolysis: Clinical manifestations and diagnosis".)

Aggressive saline hydration is the primary initial therapy of myoglobinuria, lowering the risk of induction of acute kidney injury. Other treatments may include bicarbonate or mannitol. The prevention and treatment of heme pigment-induced acute kidney injury is discussed in detail elsewhere. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)

Role of anticoagulation — A late consequence of muscle ischemia is capillary occlusion. Some authors have recommended high-dose systemic anticoagulation (typically using unfractionated heparin) as a means of limiting progressive small vessel occlusion. Because many inflammatory mediators are generated by the activation of clotting, anticoagulation may serve a dual purpose by limiting coagulation and the associated inflammation and swelling [10].

However, the risk of anticoagulation after fasciotomy may outweigh the theoretical benefits for many patients, and there are no convincing data to support its routine use in this setting. Anticoagulation is warranted for acute ischemia and compartment syndrome due to thromboembolism.

WOUND MANAGEMENT — Although fasciotomy is mandated by the diagnosis of an acute compartment syndrome, the wounds created from the fasciotomy procedure are associated with significant morbidity. The goals of wound management include identifying and debriding nonviable muscle and avoiding further muscle injury from wound desiccation. The optimal technique for managing fasciotomy wounds and timing of closure is unclear because of limited data. 

We suggest leaving fasciotomy wounds open rather than closure or graft coverage of the skin in the immediate postoperative period to facilitate assessment of tissue viability. Premature wound closure before adequate resolution of swelling can lead to recurrent compartment syndrome. Nonviable tissue within the wound can also lead to other wound complications such as infection. (See 'Wound complications' below.)

In the first 24 to 48 hours after fasciotomy, we prefer sterile saline gauze dressings that allow frequent wound assessment. Thereafter, we use a combination of active skin reapproximation and negative pressure wound therapy (NPWT) to aid with primary wound closure. Each approach has its benefits. In a meta-analysis of fasciotomy closure techniques, active skin reapproximation, using either skin approximation systems or gradual suture reapproximation, had the highest wound closure rates compared with NPWT (92 versus 78 percent) but at the expense of a higher complication rate (14.8 to 18.4 percent versus 2.49 percent) [11].

NPWT can be used until muscle swelling has regressed but by itself may not promote primary wound closure. If primary closure cannot be achieved within two weeks, we proceed with skin grafting. Some have suggested the use of synthetic skin replacement in the interim (See 'Active skin reapproximation' below and 'Negative pressure wound therapy' below and 'Synthetic skin replacement' below and 'Skin closure' below.)

Active skin reapproximation — A variety of methods can be used to limit skin retraction and promote apposition of the dermal edges in conjunction with NPWT, or for patients who are not candidates for NPWT while awaiting skin closure or grafting. If silastic bands are used in conjunction with NPWT, the sponge for the NPWT system should be placed superficial to the silastic bands.

Among the simpler, less costly approaches are placement at the time of the fasciotomy of cutaneous sutures, or silastic vessel loops anchored to staples on the skin edges (figure 2) [12,13]. Commercially available devices for this purpose are available (eg, Sure-Close suturing system, Marburger Skin Approximation System, Wisebands device, Canica device) [14-18]. A small trial compared NPWT with wound approximation using the shoelace technique [19]. The time to wound closure was significantly longer in the NPWT group (19.1 versus 15.1 days), with 6 of 42 patients requiring skin grafts compared with 0 of 40 in the shoelace group. NPWT was also more costly. In a later trial, patients were randomly assigned to wound closure under tension (ie, shoelace closure) or NPWT [20]. Among patients who were not able to be closed at the initial return to the operating room, more patients experienced wound closure with the shoelace technique compared with NPWT (100 percent [5 of 5] versus 11 percent [1 of 9]). The trial was stopped early by the Institutional Review Board because of the large difference in treatment outcome.

Negative pressure wound therapy — NPWT, also called vacuum-assisted wound closure, refers to wound dressing systems that intermittently or continuously apply subatmospheric pressure to the surface of a wound. NPWT decreases tissue edema, enhances local blood flow, promotes granulation tissue, and decreases bacterial colonization. The general mechanism of action of NPWT and the placement and management of the NPWT device are discussed separately. (See "Negative pressure wound therapy".)

Although there are no randomized trials comparing NPWT with standard gauze dressings for fasciotomy closure, retrospective studies show a decrease in the time to skin closure or grafting [21,22]. The larger of these studies compared 458 wounds treated with NPWT with 270 treated with standard gauze dressings. The skin closure rate was significantly higher for NPWT compared with gauze dressings (83 versus 56 percent), and the time to skin closure was significantly lower (5.2 versus 6.5 days) [21].

Synthetic skin replacement — Temporary synthetic skin replacement (SSR) has been proposed as an alternative to NPWT, especially in children. A single-center retrospective study found that children treated with a temporary, bilaminate SSR was associated with fewer procedures, fewer days to definitive wound closure, and a shorter length of stay compared with NPWT [23]. This approach has not been validated in other studies, however.

Hyperbaric oxygen — Animal studies and case reports describe hyperbaric oxygen as adjunct treatment for the management of wounds following fasciotomy [24-32]. Further research is needed to determine the appropriate role of hyperbaric oxygen therapy. (See "Hyperbaric oxygen therapy".)

Skin closure — Once the viability of the muscle is confirmed and muscle swelling has regressed, skin closure becomes the primary focus. Skin closure is usually achieved by bringing the edges together primarily, skin grafting, or, less commonly, a myocutaneous flap. In an occasional patient, the wounds may be left to heal by secondary intention. Appropriate timing of the closure is important to avoid recurrent compartment syndrome that can occur by closing the skin prematurely.

Delayed skin closure is appealing because it offers definitive closure soon after fasciotomy. However, delayed skin closure is often not feasible due to residual swelling. One study found that delayed skin closure less than five days postoperatively produced an undesirable increase in intracompartment pressures (>30 mmHg) in 7 of 12 patients [33]. The authors suggest that measuring intracompartment pressures during delayed skin closure might avoid this complication. Skin closure between 8 and 14 days postoperatively may decrease the incidence of wound complications and decrease the length of stay compared with later closure [34,35].

More extensive fasciotomy wounds, particularly open wounds associated with massive post-fasciotomy muscle swelling, could require several weeks to achieve closure. These wounds are candidates for closure with a skin graft [34-37]. Myocutaneous flap coverage is a rare adjunct that may be needed if neurovascular structures or vascular grafts are exposed. (See "Surgical reconstruction of the lower extremity".)

COMPLICATIONS — The complications related to fasciotomy are multifactorial. Most complications are related to the underlying condition or injury that indicated the need for compartment decompression. The acute compartment syndrome may cause further injury, and the lack of timely diagnosis and treatment of acute compartment syndrome can be catastrophic. The fasciotomy can be an additional source of morbidity.

Technical complications related to fasciotomy technique are largely preventable. Persistent or recurrent compartment syndrome can occur if fascial incisions are not adequate to permit complete decompression of the compartment or if selective fasciotomy has been performed [36]. (See "Lower extremity fasciotomy techniques", section on 'Technical complications'.)

Persistent neurologic deficits — Persistent neurologic deficits are the most common complication of the treatment of extremity compartment syndrome [38]. Following lower extremity fasciotomy, impaired neurologic function of some type is evident in 7 to 36 percent of limbs [39-41]. Nerve injury is due to soft tissue trauma, nerve ischemia during the interval of increased compartment pressure, or as a consequence of the fasciotomy incisions or dissection. Nerve injury as a technical complication during fasciotomy is discussed in detail elsewhere. (See "Lower extremity fasciotomy techniques", section on 'Neurovascular injury'.)

The most common neuropathic symptom is altered sensation at the margins of the incision, which was documented in 77 percent of patients in a retrospective review of 60 patients [42]. Chronic pain syndromes developed in 10 of these patients (17 percent) at a mean follow-up of 59 months. (See "Complex regional pain syndrome in adults: Pathogenesis, clinical manifestations, and diagnosis".)

Pain management is a critical issue in many patients with persistent neurologic deficits. Appropriate referral to a pain specialist should be made if pain persists after all visible wounds have healed. (See "Complex regional pain syndrome in adults: Treatment, prognosis, and prevention" and "Evaluation of chronic non-cancer pain in adults" and "Approach to the management of chronic non-cancer pain in adults".)

Wound complications — Wound complications after fasciotomy may occur immediately in the postoperative period or be delayed for months to years. Early wound complications occur in up to 40 percent of patients following lower extremity fasciotomy [34,39,43]. Risk factors for wound complications include the presence of vascular injury, greater than an eight-hour time interval between the injury and fasciotomy, a lower extremity site, and prophylactic fasciotomy [43]. Issues related to prophylactic fasciotomy are discussed elsewhere. (See "Lower extremity fasciotomy techniques", section on 'Prevention'.)

Wound infection occurs in 4 to 7 percent of extremity fasciotomies [34,39]. Prophylactic antibiotics should be given at the time of the fasciotomy procedure and discontinued within 24 hours. Wound infection is treated as indicated by positive wound cultures with antibiotics based upon sensitivity testing. (See "Lower extremity fasciotomy techniques", section on 'Preparation'.)

During fasciotomy, muscle devascularization may result from soft tissue debridement or during the fasciotomy procedure. In one study, repeat debridement for muscle necrosis or invasive sepsis was required in 16 percent of patients [34].

Many authors have hypothesized that early closure with a skin graft decreases the risk of complications, but data to support this notion are limited. In one series, a significantly lower rate of wound complications was found for wounds closed with a split-thickness skin graft compared with skin closure (5 versus 51 percent) [34].

Late wound complications are reported in 4 to 38 percent of limbs [34,39,42,43]. In a retrospective study of 60 patients, 26 percent had tethered scars, 13 percent had recurrent ulceration, 13 percent had muscle herniation, and 7 percent had tethered tendons [42]. Poor wound healing and late wound ulceration are more likely to occur in the presence of extremity ischemia.

Venous insufficiency — Lower extremity fasciotomy may predispose the patient to the late development of chronic venous disease. The diagnosis and management of lower extremity chronic venous disease is discussed elsewhere. (See "Overview of lower extremity chronic venous disease".)

In one study of 17 patients with a history of lower extremity fasciotomy for trauma, 8 had signs or symptoms of venous insufficiency [44]. Comparisons were made between the injured and uninjured extremities in these patients. Indicators of calf muscle pump dysfunction, including significantly decreased mean ejection fraction (32 versus 61 percent) and significantly increased mean residual volume fraction (59 versus 22 percent), were found in the injured limbs.

Limb loss — Acute lower extremity compartment syndrome is associated with a significant risk for limb loss [38]. Five to 21 percent of limbs treated with fasciotomy of the lower leg will require major amputation [34,39,40,43,45]. In multiple trauma patients, combined orthopedic and vascular injury, other severe injuries, or systemic factors may contribute to the need for amputation. The highest amputation rates occur in patients with vascular repairs that have occluded [34].

Regardless of the mechanism causing the compartment syndrome, limb loss is generally related to persistent ischemia such as incomplete fasciotomy or severe arterial disease, underlying systemic disease, or other injuries and not usually from a fasciotomy procedure-related issue [39]. (See "Lower extremity fasciotomy techniques", section on 'Technical complications'.)

Amputation after upper extremity compartment syndrome is rare. Two of the larger series reported no upper extremity amputations in a total of 233 patients [43,46].

MORTALITY — Reported mortality rates for patients requiring emergent lower extremity fasciotomy range from 11 to 25 percent [36,39,40,45]. Mortality is most often due to massive trauma, cardiopulmonary failure, or multisystem organ failure and usually not directly attributable to the fasciotomy procedure. In a series of 36 patients undergoing lower extremity fasciotomy for a variety of indications, multivariate analysis identified age >50 years as a significant predictor of poor outcome (death, amputation, or extremity dysfunction) following fasciotomy [40]. Older patients were more likely to have undergone fasciotomy as a result of a vascular procedure. Trauma patients were younger and had better overall outcomes [40,47].

The mortality rate following upper extremity fasciotomy appears to be lower at approximately 3 percent [46]. In a retrospective review of 139 patients with traumatic brachial artery injury, there was no difference in mortality rate for patients who required fasciotomy compared with those who did not (3.4 versus 2.7 percent) [46].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Extremity compartment syndrome".)

SUMMARY AND RECOMMENDATIONS

●Muscle reperfusion following extremity fasciotomy can lead to potentially life-threatening systemic complications and profound tissue swelling that complicates wound management. (See 'Ischemia-reperfusion' above.)

●The initial management of the systemic complications of reperfusion injury is focused on restoration of intravascular volume, followed by prevention and treatment of associated metabolic abnormalities including hyperkalemia, metabolic acidosis and myoglobinuria, which may lead to acute kidney injury. (See 'Management of reperfusion' above.)

●We suggest not closing the skin wounds until the fifth day following fasciotomy to permit assessment of the severity of swelling and viability of the muscle (Grade 2C). Premature closure before adequate resolution of swelling can lead to recurrent compartment syndrome. Nonviable tissue within the wound can also lead to other wound complications such as infection. (See 'Skin closure' above.)

●We use saline gauze dressings in the immediate postoperative period to allow frequent wound evaluation and interval debridement of necrotic tissue, as needed. Once the fasciotomy wounds are stable, we use active tension (eg, shoelace technique) with negative pressure wound therapy (NPWT) to facilitate fasciotomy closure. (See 'Wound management' above.)

●For wounds that cannot be closed within two weeks, we proceed with skin grafting, or sometimes myocutaneous flap coverage, but this is rarely necessary. In an occasional patient, the wounds may be left to heal by secondary intention. (See 'Skin closure' above.)

●Persistent neurologic deficits following fasciotomy for acute compartment syndrome are common. Nerve injury can be due to soft tissue injury from the inciting traumatic event; nerve ischemia during the interval of decreased compartment perfusion; or as a consequence of the fasciotomy incisions, dissection, or muscle debridement. (See 'Persistent neurologic deficits' above.)

●Wound complications are common, occurring in up to 40 percent of patients following lower extremity fasciotomy. Risk factors for wound complications include the presence of vascular injury, a greater than eight-hour time interval between the injury and fasciotomy, a lower extremity site, prophylactic fasciotomy, and premature fasciotomy wound closure. (See 'Wound complications' above.)