Acute Compartment Syndrome
Treatment
Prompt surgical consultation for decompressive fasciotomy is paramount to the management of acute compartment syndrome in the ED. When acute compartment syndrome is suspected, elevation of the affected extremity is suggested in an attempt to decrease swelling.27 The optimum height of elevation remains controversial; to prevent a decrease in arterial blood flow, it has been suggested not to raise the affected extremity above the level of the heart.8
A low systemic BP should be corrected to hopefully increase the compartment perfusion, and any applied external compressive forces (eg, casts, splints, dressings, eschars) should be removed.8 Removal of a cast can reduce the intracompartment pressure by 85%.5 Finally, applying cool compresses to the affected region can help reduce edema as a temporizing measure. Direct application of ice to the skin should be avoided to prevent cold-induced injury to the skin.
Appropriate medical resuscitation is imperative to good outcomes. Identifying and intervening when hypotension is present is necessary to improve tissue perfusion. Cellular derangement and death that can lead to hypocalcaemia, hyperkalemia, metabolic acidosis, and renal failure, require prompt recognition and correction.
At-Risk Populations
Pediatric Patients
Diagnosis of acute compartment syndrome in the general pediatric population is very difficult and therefore unfortunately associated with delays in diagnosis. The average time from injury to diagnosis can vary from 18.2to 31.1 hours.28,29 In children younger than age 3 years, 60% of acute compartment syndrome cases are due to trauma; 27% are due to invasive infections; and 13% develop from intravenous (IV) infiltration.30 Supracondylar humerus fractures are associated with increased risk of compartment syndrome. The volar compartment of the forearm is at risk after reduction of the fracture and when the elbow is flexed beyond 90°.31
Intubated and Obtunded Patients
Intubated and obtunded patients require special attention to prevent and/or identify the presence of acute compartment syndrome. Since clinical examination for compartment syndrome in these patients is unreliable, serial or continuous compartment pressure measurements are required to monitor for acute compartment syndrome.
Laboratory analysis, including monitoring of CPK levels, can also help identify developing compartment syndrome in intubated, sedated, or neurologically compromised patients.32 Onset of unexplained myoglobinuria or acute renal failure in an intubated patient should lead to consideration of compartment syndrome. In addition to laboratory studies, examination of atypical locations, such as the back or gluteal compartments, can also assist in identifying compartment syndrome in impaired patients.
Complications
The complications of compartment syndrome can be severe, and are typically organized as early and late stages of the disease.
Early Clinical Complications
Even with prompt diagnosis, acute compartment syndrome can lead to significant metabolic derangements. Patients with compartment syndrome are at significant risk for rhabdomyolysis and resultant renal failure from acute tubal necrosis. Likewise, both myocyte damage and death can cause extracellular electrolyte shifts, and hyperkalemia, metabolic acidosis, and hypocalcemia are frequently encountered under these circumstances.
Late Clinical Complications
Necrotic muscle is a significant risk factor for bacterial superinfection.33 Necrotic muscle may quickly be seeded by bacteria, and lead to sepsis. Necrotic muscle may therefore require repeated debridement and even possible extremity amputation for infection control. Likewise, muscle necrosis can lead to muscle contractures and loss of function of the affected extremity.3
Medicolegal Complications
Delay in the diagnosis of acute compartment syndrome has become an increasing source of medicolegal liability. In a 2004 review by Bhattacharyya and Vrahas34 of 23 years of claims from a medical malpractice insurer, only 19 claims were made for compartment syndrome. In this series, the following four risk factors were associated with an unsuccessful defense: (1) a linear association between the number of documented cardinal signs of compartment syndrome and an indemnity payment; (2) delays in fasciotomy; (3) poor communication with the patient and nursing staff; (4) and failure to intervene after documentation of an abnormal physical finding. All of the above were associated with a negative legal outcome.
Case Conclusion
The patient had a firm anterior compartment, CPK of 9,100 IU/L, normal renal function, compartment pressure of 60 mm Hg, and diastolic pressure of 80 mm Hg at the time of the procedure. Because the patient had a delta pressure of 20 mm Hg, orthopedic services were consulted, and the patient was taken to the operating room, where he underwent a bicompartment fasciotomy of the right lateral calf. The compartments were tense when opened and there was no evidence of myonecrosis. The patient was given continuous IV fluids and observed in the hospital for 2 days as his CPKs trended downward without subsequent renal injury.
Conclusion
Compartment syndrome requires high clinical suspicion for early diagnosis and treatment to prevent major disability. Early recognition of this condition is paramount, as the classical presentation of the five “Ps”—pain, pallor, pulselessness, paresthesias, and paralysis—are all late findings associated with irreversible consequences.
