Aurelia Bihari PhD1Christopher Del Balso MBBS MSc FRCSC1 and Abdel‐Rahman Lawend MD PhD FRCSC1 Division of Orthopaedic Surgery, Department of Surgery, University Hospital, London Health Sciences Centre, Western University, London, ON, Canada Acute CS is caused by elevated pressure within a closed osteofascial compartment. CS can develop in response to a multitude of traumatic injuries and medical comorbidities: fractures, burns, exercise, crush injuries, and ischemia‐reperfusion injury;1 less common causes may include bleeding disorders,2 diabetes, administration of statins,3,4 infection,5 hypothyroidism,6 lithotomy position,7 snake bites,8 arterial rupture,9 and blast injuries.10 A high index of suspicion for CS is required for all fractures, in particular those within the forearm and leg, regardless of whether the fracture(s) are closed or open. Serial examination is the key to diagnosis and avoidance of a missed CS. McQueen, Gaston et al. (level I evidence) evaluated the occurrence of acute CS; they reported that CS can occur in every muscle compartment of the upper extremity, lower extremity, and trunk; leg (80% of all cases) and forearm are most frequently involved.1 Age and sex play a role in the likelihood of CS development: male patients under 35 years of age are prone to developing CS more often.1 CS is most commonly due to closed long‐bone fractures (75% of cases),11,12 in which the fascia is maintained. Comminuted fractures increase the risk further.12 In adults, the most common cause of CS is tibial fracture (approximately 1–10%),11,13 followed by the fractures of forearm bones (distal radius). In children, supracondylar humerus fractures are the most common cause.14 Open fractures can result in CS development if a sufficient portion of the deep fascia or skin remains intact (level III evidence).15 In both volar plating of distal radius fractures and intramedullary nailing of tibial fractures, ICP has been found to peak during the procedure, followed by a decrease postoperatively over 24 hours,16 and 36 hours,17 respectively. Trauma patients without fracture may be at significantly greater risk of delayed CS diagnosis and fasciotomy (level I evidence)2: 20% of patients without fracture had muscle necrosis that required debridement, versus debridement being necessary in 8% of patients with fractures. CS appears to be less frequent in nontraumatic cases. It may be caused by ischemia‐reperfusion injury, thrombosis, and bleeding disorders, among a variety of other conditions. Sustained external pressure on an extremity can precipitate CS.18,19 This can occur in an unconscious patient (i.e. drug overdose, poor surgical position technique). CS is less frequent in nontraumatic cases, and is usually caused by a sustained external pressure on an extremity.18,19 Diagnosis of acute CS is challenging, as there is no true diagnostic test; instead, the surgeon must rely on the clinical examination and observation of CS signs and symptoms.20 Although the timing of the appearance of specific signs and symptoms varies, they all tend to appear in stepwise fashion. Clues indicating a developing CS include the rapid progression of symptoms over a few hours, as well as the presence of multiple findings that are consistent with impending CS. Thus, all patients at risk of CS should be serially evaluated; special attention must be paid to any tense and painful muscle compartment. If acute CS is suspected on the basis of risk factors and clinical findings, ICP measurements should be obtained without delay.21 ICP measurements are of particular use in intubated, sedated, and/or obtunded patients. CS remains a clinical diagnosis; history and repeated physical exams are critical to timely diagnosis. A low threshold for fasciotomy should be maintained when clinical signs are present. Obtaining ICP measurements should not delay a patient being brought to the operating room. Level II evidence indicates that the first symptoms of acute CS are disproportionate pain relative to the injury and pain on passive muscle stretch (PPS),22,23 often coupled with a progressive increase in analgesia requirements.24 Both pain out of proportion to what is expected of the injury (based on the physical examination) and PPS are the most sensitive clinical findings (19%) and are often the only observation that precedes ischemic dysfunction in the nerves and muscles of the affected compartment.22,23 While the specificity of both pain measures is high (97%), the sensitivity is very poor (19%); thus, absence of pain may be a useful measure in ruling out acute CS.22 Approximately one hour after the onset of ischemia, the patient may experience the first sensory changes (level II evidence).23 As a clinical measure of acute CS, paranesthesia has a sensitivity of 13% and a specificity of 98%.22 Unfortunately, paresis and/or paralysis of the muscles of the involved compartment are considered signs of a late acute CS; at this stage, the patient is less likely to respond to fasciotomy.22,25 The lack of a pulse rarely occurs in CS patients; alternatively, the presence of a pulse does not exclude CS.26
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Acute Compartment Syndrome
Clinical scenario
Top three questions
Question 1: In patients with CS, do open fractures pose greater risk of missed diagnosis and delayed fasciotomy compared to closed fractures?
Rationale
Clinical comment
Available literature and quality of the evidence
Findings
Resolution of clinical scenario
Question 2: In patients with CS, are patients who undergo compartment pressure monitoring diagnosed faster than patients undergoing clinical assessment?
Rationale
Clinical comment
Available literature and quality of the evidence
Findings
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