Acute Compartment Syndrome

 

Divya Shaji Cherian

Nurse Educator, MGM Medical College and Hospital, Kamothe

 

ABSTRACT:

Compartment syndrome is ‘an elevation of the interstitial pressure in a closed osseofascial compartment that results in micro vascular compromise’. Compartment syndrome may be acute or chronic, depending on the cause of the increased pressure and how long the symptoms last. Compartment syndrome may affect any compartment, including the hand, forearm, upper arm, abdomen, buttock, and entire lower extremity. Acute compartment syndrome (ACS) most often develops after significant trauma, especially long bone fractures. However, ACS may also occur following minor trauma or from non-traumatic causes. Symptoms of ACS are pain out of proportion to apparent injury, Persistent deep ache or burning pain, Paresthesias (onset within approximately 30 minutes to two hours of ACS; suggests ischemic nerve dysfunction) Acute compartment syndrome (ACS) is diagnosed on the basis of clinical findings. Immediate surgical consultation should be obtained if ACS is suspected. Hyperbaric oxygen has been described as adjunct treatment for ACS.

 

 

 

INTRODUCTION:

Compartment syndrome is ‘An elevation of the interstitial pressure in a closed osseofascial compartment that results in micro vascular compromise’. Compartment syndrome may be acute or chronic, depending on the cause of the increased pressure and how long the symptoms last.⁽¹⁾

 

Acute compartment syndrome occurs when the tissue pressure within a closed muscle compartment exceeds the perfusion pressure and results in muscle and nerve ischemia. It typically occurs subsequent to a traumatic event, most commonly a fracture.⁽²⁾

 

Chronic compartment syndrome (CCS) is a recurrent syndrome during exercise or work. CCS is characterized by pain and disability that subside when the precipitating activity is stopped but that return when the activity is resumed. Although CSS is more common in the anterior compartment of the lower leg, it has been described in the forearm of motocross racers and other athletes.⁽³⁾

 

STATISTICS:

The incidence of compartment syndrome depends on the patient population studied and the etiology of the syndrome. In a study by Qvarfordt and colleagues, 14% of patients with leg pain were noted to have anterior compartment syndrome⁽⁴⁾, compartment syndrome was seen in 1-9% of leg fractures. Compartment syndrome may affect any compartment, including the hand, forearm, upper arm, abdomen, buttock,⁽⁵⁾ and entire lower extremity.

 

The true prevalence of chronic exertional compartment syndrome (CECS) in the general population is unknown ^(6). Observational studies provide some sense of the prevalence of CECS among certain populations: A retrospective study of active Unites States military personnel reported 4100 cases of CECS between 2006 and 2011, for an incidence rate of 0.49 cases per 1000 person-years. Age was the most significant risk factor with the adjusted incidence rate ratio for personnel over 40 years almost nine times that of personnel under 20 years (IRR 8.77; 95% CI 7.31-10.52)⁽⁷⁾.

 

ETIOLOGY:

Acute compartment syndrome (ACS) most often develops soon after significant trauma, particularly involving long bone fractures. However, ACS may also occur following minor trauma or from nontraumatic causes. In brief, any condition that decreases the capacity of a compartment or increases the volume of fluid within a compartment raises intracompartmental pressure and places the patient at risk for developing compartment syndrome. Common sites include the leg and forearm ^{(8, 9)}.

 

ACS can also occur in the foot, thigh, and gluteal region. ACS is seen more often in patients under 35 years of age.⁽¹⁰⁾ Young men appear to have the highest incidence, particularly after fractures of the tibial diaphysis and distal radius. This may be explained by the relatively larger muscle mass of men contained within fascial compartments that do not change in size once growth is complete. In one case series of 164 patients with ACS, fracture was the cause in 69 percent of cases. Fractures of the tibial diaphysis (36 percent) and the distal radius (9.8 percent) accounted for the largest share. According to this case series, approximately 20 percent of tibial diaphyseal fractures that lead to ACS are sustained during sports. Soft tissue injury without a fracture was the cause in 23 percent of patients.⁽¹¹⁾

 

Long bone fracture—Fractures account for approximately 75 percent of cases of ACS⁽¹²⁾. Risk increases with comminuted fractures⁽¹³⁾. The tibia is involved most often⁽¹⁴⁾, with ACS developing in approximately 1 to 10 percent of such fractures.^(15-17).

 

Another case series reported on 113 patients with ACS over an eight year period⁽¹⁸⁾. The authors found that cases of ACS without a fracture were at significantly greater risk for delayed diagnosis and treatment (i.e., fasciotomy). At fasciotomy, 20 percent of patients without a fracture had muscle necrosis requiring debridement, compared with 8 percent of patients with a fracture.⁽¹⁸⁾

 

Both closed and open fracture treatment can increase compartment pressure and the risk for ACS⁽⁹⁾. Treatment of fractures should be performed as soon as possible, but clinicians should monitor patients for signs of ACS following these procedures. Closed fracture reduction decreases the volume and alters the configuration of tissue compartments increasing compartment pressures. According to one prospective observational study involving distal radius fractures, pressures peak immediately after reduction and before a cast is split.⁽¹⁹⁾ After splitting, pressures drop precipitously. A second pressure peak is seen approximately four hours after reduction and dissipates more gradually over several hours. Overly constrictive casts placed at any time during fracture management can lead to ACS. In addition, even non-constricting casts can contribute to ACS if there is significant swelling after the reduction. ⁽¹⁹⁾

 

Open fracture reduction and fixation also lead to increases in compartment pressures. Pressures during intramedullary nailing of the tibia appear to peak during the procedure and decrease over the following 36 hours. ⁽²⁰⁾ Compartment pressures following volar plating of distal radius fractures appear to diminish substantially during the 24 hour period following surgery.⁽²¹⁾

 

Trauma without fracture—other forms of trauma not involving a fracture can predispose a patient to ACS. Possible causes include forceful direct trauma to a tissue compartment (e.g, crush injury), severe thermal burns, overly constrictive bandages (usually circumferential), penetrating trauma, injury to vascular structures in the extremities, and in some cases, even minor injuries. Patients with a bleeding diathesis and those who continue to use an injured limb are at increased risk.⁽²²⁾ Thermal injuries, particularly full-thickness burns, can cause ACS secondary to tissue constriction, eschar, & edema.⁽²³⁾

 

Unconscious or obtunded patients with prolonged limb compression, either during surgery or due to recreational drug abuse, can develop ACS secondary to soft tissue injury and swelling.⁽²⁴⁾ Victims of penetrating extremity trauma are also susceptible to developing ACS.⁽²⁵⁾

 

Vascular, particularly arterial, injury is an important cause of ACs.⁽²⁶⁾ Arterial bleeding increases compartment pressures and muscle deprived of arterial blood flow becomes ischemic and prone to reperfusion injury, which in turn causes swelling and a further increase in compartment pressures. In addition, muscle that has sustained a previous ischemic insult is less tolerant of increased tissue pressure.⁽²⁷⁾ Venous injury (eg, traumatic deep vein harvest, direct vein trauma) is also associated with an increased risk of ACS.^(28-29)

 

Reports of minor trauma leading to ACS include cases involving the peroneal compartment following a minor ankle inversion injury⁽³⁰⁾, compartments of the foot after an inversion injury⁽³¹⁾, and the upper extremity after it was struck by a baseball⁽³²⁾. Intramuscular hemorrhage following minor trauma in patients taking anticoagulants also increases the risk for developing ACS. Some researchers believe that relatively larger muscle volumes may be a risk factor for ACS, which explains why men are generally more susceptible.⁽³³⁾

 

Nontraumatic causes—ACS from nontraumatic causes occurs less frequently. It may be related to ischemia-reperfusion injury, thrombosis, bleeding disorders, vascular disease, nephrotic syndrome (or other conditions that decrease serum osmolarity), certain animal envenomations and bites, extravasations of IV fluids, injection of recreational drugs, and prolonged limb compression.^(33-36)

 

Revascularization procedures and treatments, such as extremity bypass surgery, embolectomy, and thrombolysis, increase the risk for ACS.⁽³⁶⁾ This phenomenon is known as post ischemic compartment syndrome and is due to tissue swelling from reperfusion. The syndrome can occur from a few hours following the procedure up to several days later.⁽³⁷⁾ Residual effects from anesthesia and postoperative sedation can make early detection of ACS more difficult immediately after surgery.

 

Anticoagulation following surgery, such as prophylaxis against deep vein thrombosis, may contribute to ACS. ⁽³⁸⁾Symptoms can mimic postoperative pain making the diagnosis difficult. Iatrogenic injury of arteries or veins in anti-coagulated patients is another potential cause.⁽³⁹⁾ The use of intraaortic balloon pumps has been associated with ACS.⁽⁴⁰⁾

 

Drug abusers can develop ACS following intravenous or inadvertent intraarterial injection of drugs.^{(41, 42)} Group A streptococcus infections of muscle can be complicated by ACS.⁽⁴³⁾

 

Four cases of ACS associated with thrombolytic agents have been reported.⁽⁴⁴⁾ Intramuscular hemorrhage in patients treated chronically with anticoagulants can progress to ACS.^{(45, 46)}

 

A number of surgical procedures involving the leg (eg, saphenous vein harvest) have been associated with ACS in case reports.^{(48, 49)}

 

PATHOPHYSIOLOGY:

ACS is defined as ‘a critical pressure increase within a confined compartmental space causing a decline in the perfusion pressure to the tissue within that compartment’.^(50,) It can occur with any elevation in interstitial pressure within an Osseo-fascial compartment. Tissue perfusion is proportional to the difference between capillary perfusion pressure (CPP) and the interstitial fluid pressure.

 

When fluid enters a fixed volume compartment, for example from bleeding, both the tissue and venous pressure increase. When this exceeds the CPP, capillary collapse with ensuing muscle and nerve ischemia occur. A similar reduction occurs in the CPP when the compartment size decreases (e.g. external compression) due to an increase in intracompartmental pressure, as well as a reduction in the arteriolar pressure.⁽⁵¹⁾

 

CLINICAL FEATURES:

Compartment syndrome is, for the most part, a clinical diagnosis. It is a diagnosis that is made over time as the evolution of signs and symptoms are assessed, rather than a diagnosis made in isolation at a

 

single time point. Serial examinations should always be performed, preferably by the same, experienced examiner.

 

The classic “P’s” described in compartment syndrome are pain, paresthesia, paralysis/paresis, pulselessness, and pallor.⁽⁵²⁾ Although all have a role in the diagnosis of compartment syndrome, the constellation of signs and symptoms and overall clinical picture are more important than the presence or absence of any particular finding.

 

Pain in ACS is described as out of proportion to the clinical examination or injury. Pain with passive stretch and rest pain are both usually present; however, pain can be absent in established or late-stage compartment syndrome. In addition, pain can be absent in the setting of central or peripheral nerve deficit or regional anesthesia.⁽⁵³⁾

 

Paresthesias are often the first indication of nerve ischemia. Altered sensation in the first dorsal web space of the foot could be the first indication of increased pressure in the anterior compartment related to ischemia of the deep peroneal nerve. If ischemia continues, paresthesia progresses to hypoesthesia and finally anesthesia.

 

Paresis or paralysis is often present in ACS but can be misleading as it could be the result of muscle ischemia, nerve ischemia, guarding secondary to pain, or a combination. True paralysis is a late finding indicative of prolonged nerve compression or irreversible muscle damage.

 

The loss of distal pulses with compartment syndrome is a late finding. It is rare for compartment pressure to be high enough to occlude arterial inflow and the absence of pulses could indicate an arterial injury. In addition, capillary refill is routinely present even in established ACS. Pallor is only present if arterial inflow is severely compromised or a vascular injury is present.

 

Increased firmness of compartment may be the only objective finding in developing compartment syndrome; however, Shuler et al revealed that manual detection of compartment pressure associated with critical elevations in ICP is poor, even by senior or experienced surgeons. ⁽⁵⁴⁾

 

DIAGNOSTIC EVALUATION:-

Diagnosing ACS is difficult in clinical practice, and even among expert surgeons there is great variability in the criteria for ACS. A recent study showed that the incidence of fasciotomy varied from 2 to 24%, highlighting the variability of surgical indications and the inconsistency in the clinical diagnosis.⁽⁵⁵⁾ Currently, the diagnosis is made on the basis of physical examination and repeated ICP measures, while a method for the accurate and reproducible diagnosis of ACS, especially in the polytraumatized and comatose patients, has yet to be developed.⁽⁵⁶⁾

 

Mubarak in 1976 showed that high ICP sustained for 6–8 hours results in irreversible soft tissue damage.⁽⁵⁷⁾ Many authors currently agree that ICP should be compared with systemic diastolic pressures.⁽⁵⁸⁾ Even if threshold of Δp at which surgical intervention is warranted is quoted to be between 30 mmHg and 45 mmHg according different authors, hypotensive patients with ICPs higher than 20 mmHg have an high risk of ACS. Non-invasive imaging techniques for determining ICP have been also proposed.These include near-infrared spectroscopy (NIRS) ultrasonic devices and laser Doppler flowmetry. ⁽⁵⁶⁾

MANAGEMENT:

Initial management involves removing any casts or dressings overlying the limb. An animal study showed that just cutting the cast reduced ICP by a mean of 65% with an additional 10–20% reduction after the padding was cut.⁽⁵⁹⁾  The standard treatment for ACS is emergent surgical fasciotomy. Fasciotomites can vary in surgical technique. Currently, both single and double incision techniques are used by surgeons.⁽⁶⁰⁾

 

Non operative management:

Whenever safe and possible, simple treatment measure in ACS include loosening ace wraps, compression dressings, splints and uni- or bivalving casts. Elevation of extremity no higher than the level of the heart facilitates venous drainage, reduces edema and maximize tissue perfusion.Further, avoidance of knee flexion and foot dorsiflexion will facilitate uncompromised circulation throughout a limb and limit increases in ICP in the deep posterior compartment respectively.⁽⁶¹⁾

CONCLUSION:

Acute compartment syndrome is a rare complication but serious orthopedic surgical emergency. ACS creates a myriad of symptoms that signal increased pressure in an affected muscle compartment resulting to compromised tissue perfusion. Clinical diagnosis of ACS can be difficult and is based largely on a thorough neurovascular assessment (the six P's) and a high clinical suspicion. ICP monitoring, used accurately, is an objective and valid test to confirm ACS diagnosis particularly in patients in whom subjective clinical assessment is unclear. Early consultation and collaboration with an orthopedic, vascular or general surgery team is critical for limb salvage. Timely surgical intervention with a fasciotomy is the primary treatment for ACS preventing potentially devastating and permanent downstream complications such as contractures, paralysis, amputation, multi-organ failure, and even death.

 

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Received on 15.01.2018        Modified on 30.03.2018

Accepted on 30.05.2018       ©A&V Publications All right reserved