Abstract
A male patient in his fifties presented to his local hospital with numbness and weakness of the right leg which left him unable to mobilise. He reported injecting heroin the previous morning. Following an initial diagnosis of acute limb ischaemia the patient was transferred to a tertiary centre where Computed Tomography Angiography was reported as normal. Detailed neurological examination revealed weakness in hip flexion and extension (1/5 on the Medical Research Council scale) with complete paralysis of muscle groups distal to this. Sensation to pinprick and light touch was globally reduced. Blood tests revealed acute kidney injury with raised creatinine kinase and the patient was treated for rhabdomyolysis. Orthopaedic referral was made the following day and a diagnosis of gluteal compartment syndrome (GCS) was made. Emergency fasciotomy was performed 56 hours after the onset of symptoms. There was immediate neurological improvement following decompression and the patient was rehabilitated with complete nerve recovery and function at eight-week follow-up. This is the first documented case of full functional recovery following a delayed presentation of GCS with sciatic nerve palsy. We discuss the arguments for and against fasciotomy in cases of compartment syndrome with significant delay in presentation or diagnosis.
Highlights
Compartment syndrome occurs due to increased pressure within a fascial compartment
Sciatic nerve dysfunction is commonly associated with Gluteal compartment syndrome (GCS), despite the nerve being enclosed within a separate compartment
We present a case of GCS presenting with profound sciatic nerve dysfunction and rhabdomyolysis with a long delay in diagnosis and treatment
Summary
Compartment syndrome occurs due to increased pressure within a fascial compartment. Due to the fixed volume of these compartments, any increase in fluid within the interstitium will reduce the arteriovenous pressure gradient, resulting in reduced tissue perfusion and cell death [1]. Sciatic nerve dysfunction is commonly associated with GCS, despite the nerve being enclosed within a separate compartment. This is thought to be due to external compression on the arterial supply to the sciatic nerve, which most commonly arises from the medial circumflex femoral and inferior gluteal arteries [10,11,12,13]. We present a case of GCS presenting with profound sciatic nerve dysfunction and rhabdomyolysis with a long delay in diagnosis and treatment (over 56 hours). Despite this delay and systemic complications, the patient underwent emergency fasciotomy and made a strong postoperative recovery with a full return of function at eight weeks after discharge
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