Cocaine-induced rhabdomyolysis and compartment syndrome

Background

Cocaine can be used via intravenous injection, nasal insufflation and its freebase form (‘crack’) can be smoked. According to a survey in 2011, nearly 40% of 1.3 million emergency department (ED) visits for drug abuse or misuse could be attributed to cocaine.1

Cocaine is a potent stimulator of sympathetic nervous system and its use can result in ischaemic complications through vasoconstriction of cerebral, coronary and peripheral vasculature.2 Although there are several case reports of cocaine abuse resulting in rhabdomyolysis,3 likely due to vasoconstriction of peripheral vasculature, compartment syndrome in the absence of trauma or prolonged immobilisation is a rare phenomenon.

We present a unique case of bilateral lower extremity rhabdomyolysis and compartment syndrome attributed to cocaine use.

Case presentation

A male patient in his 30s, without significant medical or surgical history, presented to the ED with a 12-hour history of severe pain and weakness in bilateral lower extremities. He reported that the pain started suddenly, burning in characteristic, constant and got worse with leg movement. He denied any recent trauma, falls, prolonged immobilisation, loss of consciousness, fever, chills, sick contacts, shortness of breath, chest pain, abdominal pain, saddle anaesthesia or urinary incontinence. He endorsed nasal insufflation of cocaine and heroin but denied intravenous drug use. He reported chronic cocaine use through nasal insufflation and using it 1 day prior to onset of symptoms. His family history was only significant for hypertension in his father. He did not take any long-term medications and denied any allergies.

In the ED, vital signs were significant for tachycardia with a maximum heart rate of 110 beats per minute and the rest of his vitals were within normal limits. On physical examination, the patient appeared to be in significant distress due to pain. Bilateral lower extremities were cool to touch and there were exquisite tenderness and stiffness noted on palpation of calf muscles. There was delayed capillary refill in both feet. No obvious signs of external injury on either of his lower extremities were present. Dorsalis pedis and posterior tibial pulses were neither palpable bilaterally nor audible on Doppler. A neurological examination of the lower extremity was limited due to severe pain and the patient’s reluctance to move his legs, but plantar reflexes were absent bilaterally and sensory deficits were noted in the left foot.

Investigations

In the ED, basic metabolic panel and complete blood counts were obtained. There were significant abnormalities noted which included sodium of 131 mmol/L (normal 136–145 mmol/L), potassium of 5.4 mmol/L (normal 3.4–5.3 mmol/L), calcium of 5.7 mg/dL (normal 8.7–10.5 mg/dL), phosphorus of 7.3 mg/dL (normal 2.7–4.5 ng/dL), blood urea nitrogen of 45 mg/dL (normal 8–21 mg/dL), creatinine of 3.7 mg/dL (normal 0.5–1.3 mg/dL), bicarbonate of 15 mmol/L (normal 22–33 mmol/L) and white cell count of 29.4x10⁹/L (normal 4.0–11.0x10⁹/L) with 88.9% neutrophils. Other laboratory abnormalities included a lactic acid level of 4.9 mmol/L (normal 0.5–1.9 mmol/L), creatine kinase of >40 000 U/L (normal 24–204 U/L), serum myoglobin >30 000 ng/mL (normal 28–72 ng/dL), aspartate aminotransferase (AST) 3398 U/L (normal 10–25 U/L) and alanine aminotransferase (ALT) 979 U/L (normal 10–55 U/L). Alkaline phosphatase and total bilirubin were within normal limits. Urinalysis was significant for redcell count of 12/high power field (normal 0–4/high power field) and urinary drug screen was positive for cocaine and negative for opiates. An electrocardiogram was obtained to evaluate for any changes due to hyperkalaemia, however, it was only significant for sinus tachycardia. Due to concern for compartment syndrome, a CT angiogram (CTA) of the chest/abdomen/pelvis with runoff was obtained. Results were significant for suboptimal opacification of arteries below the knee bilaterally, without any obvious vascular occlusion along with oedematous changes in proximal soleus musculature and perimuscular oedema bilaterally (figure 1).

Differential diagnosis

On initial presentation, the patient’s symptoms appeared to be consistent with a pathology involving the lumbar spinal cord given the severe pain in bilateral lower extremities. Epidural abscess, lumbar disc herniation and anterior spinal artery stenosis were initially considered; however, these could not explain the physical examination findings or laboratory abnormalities that were consistent with rhabdomyolysis. The patient vehemently denied intravenous drug use, and did not have any fever or focal tenderness over his lumbar spine. He also deniedhistory of trauma and did not have a personal or family history of coagulopathy. Additionally, his rectal tone was intact, denied saddle anaesthesia, and did not have urinary retention or incontinence, which was less suggestive of a pathology involving the spinal cord or cauda equina.

Due to the absence of dorsalis pedis pulses in bilateral lower extremities, compartment syndrome, thromboembolic phenomenon or vasculitis was considered. CTA of the chest, abdomen, and pelvis with runoff did not show any focal occlusion or vascular abnormalities. Since thromboembolic phenomenon was considered, COVID-19 antigen with nucleic acid amplification technique was also checked and was negative. Since ALT and AST were also elevated, toxic or infectious hepatitis was also considered; however, the serology was negative for hepatitis A, B and C, and his serum acetaminophen level was normal as well. Serum ammonia and coagulation profile were within normal limits. Elevated AST and ALT were determined to be secondary to rhabdomyolysis. The patient did not provide any history of trauma and there was no evidence of external injuries on physical examination. He denied loss of consciousness that could lead to prolonged immobilisation, resulting in rhabdomyolysis and compartment syndrome. In light of these findings, rhabdomyolysis was attributed to cocaine use, which may have resulted in vasospasm, as noted on CTA, and lead to ischaemic injury to the muscle and, subsequently, compartment syndrome due to significant muscular oedema. His acute kidney injury and electrolyte abnormalities could all be attributed to rhabdomyolysis.

Treatment

The patient was started on continuous heparin infusion due to a concern for vascular occlusion but was discontinued once vascular occlusion was ruled out on CTA with runoff. Given the concern for compartment syndrome, the patient was taken emergently to the operating room for fasciotomies of bilateral lower extremities (figures 2–5). During surgery, superficial and deep compartments in bilateral lower extremities were noted to be bulging but the muscles were viable without any evidence of necrosis. A wound vacuum was applied to bilateral lower extremities and the patient was transferred to the intensive care unit. Since the patient was oliguric with significant acute kidney injury, intravenous bicarbonate infusion and diuresis with furosemide was attempted. Due to persistent renal failure and poor urinary output, the decision was made to start haemodialysis through a temporary dialysis catheter placed in the left internal jugular vein on the second day of admission. With the ongoing dialysis requirements, a tunnelled dialysis catheter was eventually placed on the ninth day of admission.

Outcome and follow-up

Following his surgery, the creatine kinase levels trended downwards and eventually decreased to a normal level of 82 U/L within 2 weeks. He was evaluated by plastic surgery and the plan was to close the lower extremity incisions with split thickness skin graft. While it was considered on the 10th day of admission, the procedure was delayed until the 20th day of admission due to excessive drainage (figures 6 and 7).

His kidney functions also recovered by the third week of hospitalisation. The tunnelled dialysis catheter was removed on the 29th day of admission and he was, subsequently, discharged on the same day to inpatient rehabilitation facility.