Gluteal compartment syndrome following prolonged immobilization in the setting of polysubstance use: A two-patient case series

Abstract

Introduction

Gluteal compartment syndrome (GCS) is a rare, often overlooked emergency caused by rising compartment pressures leading to muscle and nerve ischemia, frequently after substance-related immobilization. Nonspecific symptoms such as diffuse pain and reduced mobility contribute to delayed diagnosis, increasing risk of irreversible neuromuscular injury and death.

Case summary

Two cases of GCS following polysubstance overdose are presented.

• •Case 1: A 44-year-old male developed right-sided GCS with extensive gluteal muscle necrosis following delayed diagnosis, initially misattributed to cellulitis. Despite decompressive fasciotomy, he suffered irreversible muscle loss.
• •Case 2: A 35-year-old male presented with multisite compartment syndrome of the left gluteal, forearm, and lower leg compartments. Prompt recognition and surgical decompression preserved overall tissue viability.

Discussion

Diagnosis of GCS relies on a combination of laboratory findings such as markedly elevated creatinine kinase, and focused physical examination particularly tense gluteal swelling, pain disproportionate to the clinical scenario, and progressive neurological deficits, including sciatic nerve dysfunction or foot drop. Imaging is often nonspecific, and clinical outcomes are dependent highly on early fasciotomy. These cases highlight the variable clinical course of GCS and the diagnostic challenges in patients found immobile after overdose.

Conclusion

Clinicians should remain vigilant of the possibility of GCS in patients immobilized after drug overdose. Early recognition is critical to reducing morbidity and mortality within these patients. Prompt surgical consultation and early fasciotomy are essential to prevent irreversible neuromuscular damage and poor functional recovery.

Introduction

Gluteal compartment syndrome (GCS) is a rare but potentially life-threatening condition. The deep anatomical location of the gluteal compartment and nonspecific early symptoms often delay diagnosis, allowing the intercompartmental pressure to rise and compromises perfusion. This results in ischemia and necrosis of the gluteal muscles and adjacent neurovascular structures [1], [2], [3]. Delayed diagnosis of GCS can lead to irreversible muscle necrosis, sciatic nerve palsy, and even fatal systemic complications such as rhabdomyolysis-induced cardiac arrest. Reported etiologies of GCS include prolonged surgical positioning, traumatic injury, and immobilization secondary to intoxication or loss of consciousness [19]. In a systematic review of 139 cases, substance-related immobilization accounted for over one-third, making it one of the leading risk factors [4], [6].

Patients presenting prolonged immobilization secondary to polysubstance-induced loss of consciousness are predisposed to sustained recumbency and external compression, promoting ischemia and concurrent necrosis of the gluteal and upper extremity muscles [5]. With rising rates of substance abuse, the pathophysiologic mechanism is being increasingly recognized cause of GCS [17]. Despite this, the condition remains underdiagnosed compared to limb compartment syndromes [18].

Diagnostic evaluation is complicated by limited history, unreliable examination findings, and comorbidities such as rhabdomyolysis and acute kidney injury. Systemic complications—including volume depletion, myoglobin-induced nephrotoxicity, and severe hyperkalemia—can precipitate life-threatening arrhythmias or cardiac arrest if not promptly recognized and treated [7]. Beyond the typical elevation in creatine kinase (CK), gluteal compartment syndrome may also cause elevations in AST and ALT. Although these markers may be mistaken for hepatic dysfunction, their elevation in the context of rhabdomyolysis can support the diagnosis when interpreted appropriately [8].

Despite an increasing number of reported cases, the clinical course and functional outcomes of GCS related to polysubstance use remain poorly defined. The diagnosis primary relies on a high index of clinical suspicion, characterized by severe gluteal pain out of proportion to the injury, occasionally accompanied by tense buttock swelling, and in later stages, sciatic nerve dysfunction manifesting as paresthesia or weakness of the posterior thigh [1], [9], [10]. Surgical fasciotomy and debridement are the only definitive treatments, and residual neurologic deficits, particularly sciatic nerve palsy and foot drop, are common even with intervention [11]. We present two cases of GCS associated with polysubstance overdose and prolonged immobilization, highlighting the diagnostic challenges, surgical management, and variable clinical outcomes [12]. These cases emphasize the need to maintain a high index of suspicion for GCS in any patient found immobilized after substance use, even in the absence of trauma or in those transferred from outside facilities after several days of treatment.

Case 1

Late recognition of gluteal compartment syndrome with complete muscle necrosis.

A 44-year-old man with polysubstance use disorder (fentanyl, cocaine, phencyclidine, and marijuana) and a history of bilateral total hip arthroplasties for femoral neck fractures sustained in a motor vehicle collision was found unresponsive at home after suspected fentanyl use with unknown down time. Upon arrival to the emergency department (ED) at an outside facility, he was hypoxic, tachycardic, and unable to provide a reliable history. Initial laboratory studies, Table 1, revealed a creatine kinase level of 7800 U/L, creatinine 2.65 mg/dL, lactic acid 4.57 mmol/L, and markedly elevated transaminases (AST 1413 U/L and ALT 343 U/L). Urine toxicology was positive for cocaine, phencyclidine, and tetrahydrocannabinol.

Table 1.

Patient 1 initial laboratory results. Reference ranges obtained from the institutional clinical laboratory (2025).

Laboratory test	Patient initial lab values	Reference Range	Interpretation
Creatine kinase, U/L	7800	46–171	Markedly elevated; consistent with rhabdomyolysis
Creatinine, mg/dL	2.65	0.5–1.3	Elevated; acute kidney injury
Lactic acid, mmol/L	4.57	0.5–2.0	Elevated; lactic acidosis
Aspartate aminotransferase (AST), U/L	1413	10–45	Markedly elevated; hepatocellular injury or muscle breakdown
Alanine aminotransferase (ALT), U/L	343	12–78	Elevated; hepatocellular injury or muscle breakdown

Computed tomography (CT) of the abdomen and pelvis demonstrated mild right gluteal stranding without fluid collection and was interpreted as cellulitis, therefore; intravenous ceftriaxone and vancomycin were initiated. The patient was transferred to our institution for further medical management.

He reported diffuse numbness and an inability to move the right leg when he became more alert and oriented. His pain localized to the right gluteal region and creatine kinase rose to >39,000 U/L, consistent with severe muscle injury. Despite aggressive therapy directed at rhabdomyolysis and a presumptive soft-tissue infection, the gluteal pain intensified with a decline in motor function over the next several days. Orthopedic surgery was consulted at this time. Examination revealed a tense, indurated gluteal compartment with marked pain on passive hip motion, absent ankle dorsiflexion and plantarflexion, paralysis of the extensor hallucis longus, and diffuse sensory loss. Distal pulses remained palpable. The constellation of findings was most consistent with gluteal compartment syndrome, and after informed discussion, the patient consented to urgent operative decompression.

He underwent emergent right gluteal fasciotomy with the application of negative pressure wound therapy (NPWT). Intraoperative exploration revealed pan-necrosis of the gluteus maximus, medius, and minimums; the musculature was bloodless, discolored, noncontractile, and clearly nonviable. Debridement was advanced to healthy margins and carried down to bone, which was preserved. The sciatic nerve appeared dusky but remained in continuity. He subsequently returned to the operating room for irrigation and debridement with reapplication of NPWT. The muscle was noted to be healthy at that time, without signs of infection. He remained hemodynamically stable in the immediate postoperative period without complications. Plastic surgery was engaged for reconstructive planning, and multidisciplinary care with nephrology and physical therapy was instituted. With substantial loss of the gluteal muscle mass, rehabilitation began with the expectation of a prolonged convalescence and guarded functional recovery. The patient was subsequently lost to follow-up, presumed deceased.

Case 2

Early multisite decompression preserving tissue viability.

A previously healthy 35-year-old man was found unresponsive at home beside a deceased partner after an unknown duration of immobilization. In the ED, he was anxious but oriented, complained of severe left leg pain with numbness, endorsed intense thirst, and was unable to recall preceding events. He acknowledged marijuana use; urine toxicology returned positive for cocaine and cannabinoids.

On examination, he was tachycardic, the left calf was tense and exquisitely tender to palpation, and the left foot was cyanotic, cool, with absent dorsalis pedis and posterior tibial pulses by Doppler. The left buttock was firm and tender compared to the contralateral side. The left forearm compartments demonstrated similar tense fullness. In contrast, the right upper and lower extremities were neurovascularly intact with nontender compartments. Neurologic assessment revealed a dense distal deficit in the lower left limb, with complete paralysis and loss of sensation to the foot. Partial sensory preservation was seen proximally toward the knee.

Initial laboratory studies, Table 2, demonstrated severe hyperkalemia (potassium 9.0 mmol/L) with corresponding ECG T-wave changes, rhabdomyolysis (creatine kinase >100,000 U/L), acute kidney injury (creatinine 3.5 mg/dL), lactic acidosis (lactate 3.9 mmol/L), leukocytosis (27 × 10 [3]/μL), elevated transaminases, and hyponatremia.

Table 2.

Patient 2 initial laboratory results. Reference ranges obtained from the institutional clinical laboratory (2025).

Laboratory test	Patient's result	Reference range	Interpretation
Creatine kinase, U/L	>100,000 U/L	46–171 U/L	Severely elevated; consistent with rhabdomyolysis
Creatinine, mg/dL	5.2 mg/dL	0.5–1.3 mg/dL	Elevated; consistent with acute kidney injury
Lactic acid, mmol/L	5.8 mmol/L	0.5–2.2 mmol/L	Elevated; consistent with lactic acidosis
Aspartate aminotransferase (AST), U/L	2300 U/L	10–45 U/L	Markedly elevated; consistent with muscle injury
Alanine aminotransferase (ALT), U/L	420 U/L	12–78 U/L	Elevated; consistent with muscle and hepatic injury
Blood urea nitrogen (BUN), mg/dL	86 mg/dL	6–22 mg/dL	Severely elevated; consistent with renal failure
Potassium, mmol/L	7.3 mmol/L	3.6–5.2 mmol/L	Severely elevated; consistent with hyperkalemia
Urine myoglobin	Positive	Negative	Positive; consistent with rhabdomyolysis

Non-contrast CT of the head revealed no acute abnormalities. He was treated with intravenous calcium, insulin with dextrose, bicarbonate, along with aggressive crystalloid resuscitation. A temporary dialysis catheter was placed, and hemodialysis was initiated. Empiric ceftriaxone was administered; sequential compression devices were applied. Emergent consultations were obtained from orthopedic and vascular surgery for suspected multisite compartment syndromes.

The patient was urgently taken to the operating room, where orthopedic surgeons performed a left gluteal fasciotomy through a Kocher–Langenbeck approach, decompressing the gluteus maximus, medius, and minimus with limited debridement of nonviable muscle. A fascial release of the vastus lateralis was added to complete lateral compartmental decompression of the hip. The left forearm underwent combined volar and dorsal releases with extension to the carpal tunnel and thenar spaces; all incisions were left open and dressed to allow for edema egress and planned reassessment. Vascular surgeons subsequently performed four-compartment fasciotomies of the left leg. The superficial posterior compartment appeared viable, while the deep posterior and anterolateral compartments were dusky with muscle demonstrating poor contractility to electrical stimulation. Following decompression, distal perfusion improved with a palpable popliteal pulse and restoration of distal Doppler signals.

In the immediate postoperative period, the patient was successfully extubated and underwent hemodialysis. That afternoon, he experienced a generalized seizure accompanied by apnea, necessitating re-intubation and initiation of levetiracetam therapy. A repeat CT scan of the head demonstrated no acute intracranial abnormalities. On postoperative day 3, the patient returned to the operating room for staged wound management. Orthopedic surgery irrigated and closed the left gluteal and forearm incisions with debridement of nonviable tissue. Vascular surgery debrided necrotic anterior and lateral leg musculature down to bone, closed the lateral incision with a biologic dressing, and applied NPWT to the medial incision.

Over the following two weeks, the patient underwent serial debridement with NPWT. The vascular surgery team performed excisional debridement of nonviable anterior and lateral compartment musculature with subsequent wound VAC placement.

Over the following two weeks, the Vascular and burn surgery was consulted for anticipated grafting and excisional debridement of nonviable skin and subcutaneous tissue was performed, followed by application of large NPWT. After approximately 14 days of wound VAC therapy, there was a healthy granulating bed observed, and management was transitioned to wet-to-dry dressings in preparation for future grafting.

While in the intensive care unit, CT angiography identified a left popliteal thrombus, which was treated with therapeutic apixaban. Rhabdomyolysis-associated acute kidney injury progressed to dialysis dependence, requiring thrice-weekly hemodialysis via tunneled catheter, adjunctive erythropoiesis-stimulating therapy, and intravenous iron for anemia of chronic kidney disease. He was discharged to inpatient rehabilitation in a dialysis-dependent state, with a negative-pressure wound device remaining on the lateral leg, while the gluteal, forearm, and medial leg incisions were closed and stable. At discharge, a left foot drop persisted. On subsequent outpatient review, the foot drop remained unchanged, though the patient reported gradual overall functional improvement.

Discussion

Gluteal and multisite compartment syndromes are rare entities that pose substantial diagnostic challenges [12]. In our series of substance-related immobilization, patients consistently presented after an unknown period of down time with severe rhabdomyolysis and neurologic compromise. Diagnosis is often hindered by the deep location of the gluteal compartments beneath extensive soft tissue, unreliable histories, altered mentation, and overlapping deficits from rhabdomyolysis and hypoperfusion [6]. Our cases demonstrate that careful gluteal examination and distal neurovascular assessment, interpreted alongside rising creatine kinase and worsening pain, can prompt timely fasciotomy even when imaging is nonspecific.

The diagnosis of gluteal compartment syndrome relies primarily on hallmark clinical findings, including tense swelling, pain out of proportion to examination, and progressive neurologic deficits such as foot drop [10]. Imaging findings are often nonspecific and should not delay intervention, while compartment pressure measurements may support the diagnosis but are unnecessary in the presence of clear clinical evidence [1], [9], [10]. Physical examination therefore remains the most reliable diagnostic tool, and urgent surgical fasciotomy is the definitive therapy [13]. Prompt diagnosis remains the cornerstone of effective management, as functional recovery is time dependent — ischemic injury progresses to irreversible myonecrosis as duration of hypoperfusion lengthens [14]. In our patients, early recognition of tense compartments with evolving neurovascular compromise prompted immediate consultation and expedited fasciotomy, which improved the outcome despite multisite, severe disease [3], [8]. Nevertheless, outcomes remain closely linked to time to decompression; recovery diminishes as delays accrue, and even with rapid intervention, the postoperative course can vary, as case 2 illustrates.

When clinical trajectories diverge from the expected course, a structured re-evaluation of the physical examination becomes critical. Studies in trauma populations suggest that approximately 35% of patients have previously undiagnosed injuries identified during follow-up examinations, and nearly half of these findings require a change in management [20]. Insufficient initial assessment can therefore result in missed injuries or delayed diagnosis. Additionally, unrecognized abnormalities on prior imaging may go unnoticed, underscoring the importance of a comprehensive head-to-toe reassessment as symptoms evolve. A repeat comprehensive physical examination combined with chart and imaging review after stabilization has been reported to identify a Type I missed-injury rate of approximately 4.3% and a Type II rate of 1.5%, demonstrating that tertiary surveys improve the detection of clinically significant injuries initially overlooked [21]. In the context of GCS, where evolving neurological deficits, rising creatine kinase levels, or worsening pain may represent the earliest warning signs, this careful re-evaluation may prompt repeat diagnostic assessment and help prevent further delays in decompression.

Substance use is a well-established precipitant of compartment syndrome [4]. Patients discovered unresponsive after drug exposure therefore face a heightened risk of atypical compartment involvement, including the gluteal region [15]. This observation aligns with prior systematic reviews identifying immobilization after intoxication or loss of consciousness as the second most common etiology following perioperative positioning [6]. In such cases, polysubstance exposure can amplify the extent of myonecrosis and exacerbate systemic derangements such as hyperkalemia and acute kidney injury [7].

The management of these patients is inherently multidisciplinary. Orthopedic, vascular, and burn surgeons coordinate staged fasciotomies, perform serial debridement, and oversee advanced wound management. Nephrology provides renal replacement therapy and managed anemia with targeted strategies. Critical care teams stabilized perfusion and oxygenation, titrate ventilatory support, managed nutrition, and transitioned analgesia to multimodal regimens. This coordinated approach is essential—it can be decisive for survival and supports a safe transition to rehabilitation.

Despite timely diagnosis and aggressive management, prognosis in multisite compartment syndromes remains guarded. Dialysis dependence, thromboembolic events, and permanent neurologic deficits are frequent sequelae [16]. In our series, persistent left foot drop in one patient represents a concrete marker of durable functional loss despite early decompression and comprehensive rehabilitation. These outcomes underscore the high morbidity associated with gluteal and multisite compartment syndromes, even with optimal treatment.

Conclusion

Multisite compartment syndromes, particularly those involving the gluteal region, remain rare and diagnostically challenging, especially in patients with polysubstance intoxication. These cases highlight the importance of prompt recognition guided by physical examination and laboratory evaluation rather than reliance on imaging findings. Successful management requires coordinated, multidisciplinary care. There remains a high potential for long-term morbidity, including dialysis dependence and persistent neurologic deficits, despite early recognition and intervention. These cases contribute to the limited body of literature on multisite compartment syndromes and underscore the need for heightened clinical suspicion in intoxicated or immobilized patients.

CRediT authorship contribution statement

Mark Gamadia: Data curation, Writing – original draft. Robert Garner: Conceptualization, Data curation, Project administration, Writing – original draft, Writing – review & editing. Daulton Sauce: Writing – review & editing. Molly Black: Supervision.

Ethical statement

Written informed consent for the case reports was provided by the patient. IRB approval obtained by our academic institution.

Disclaimer

None of the authors listed have any financial ties with any biotechnology companies. This case report was not incentivized by industry financial or material support. This research was supported (in whole or in part) by HCA Healthcare and/or an HCA Healthcare affiliated entity. The views expressed in this publication represent those of the author(s) and do not necessarily represent the official views of HCA Healthcare or any of its affiliated entities.

Funding statement

No funding was received for this case review.

Declaration of competing interest

The authors declare no competing interests.