Unusual complications of heroin abuse: Transverse myelitis, rhabdomyolysis, compartment syndrome, and ARF

Abstract

Introduction. Heroin overdose can cause various rare neurological complications like spongiform leukoencephalopathy, seizures, stroke, toxic amblyopia, transverse myelopathy, mononeuropathy, plexopathy, acute inflammatory demyelinating polyradiculoneuropathy, rhabdomyolysis, compartment syndrome, fibrosing myopathy, and acute bacterial myopathy. We report here the simultaneous presentation of multiple complications of heroin toxicity. Case report. A young heroin addict was found unarousable lying in the lotus posture. Examination showed quadriplegia and left leg gangrene. He subsequently developed heroin-induced transverse myelitis, rhabdomyolysis, left leg compartment syndrome, and myoglobin-induced acute renal failure. Discussion. This case leads us to consider a common linked or systemic mechanism of injury rather than a local mechanism when multiple simultaneous organ failure occurs complicating heroin abuse.

Keywords: :

• Heroin
• Transverse myelitis
• Rhabdomyolysis
• Compartment syndrome

Introduction

Heroin is amongst the most widely used drugs of abuse (1). Commonly administered intravenously, it is also sometimes used through intramuscular, subcutaneous, or intranasal routes. Most fatal heroin overdoses occur when the drug is administered intravenously (2). A small number of heroin-related deaths have been associated with intranasal administration (3,4).

Heroin is known to cause various medical and neurological problems (5). Some of the rare reported complications of heroin overdose are noncardiogenic pulmonary edema (7,8), endocarditis (6), wound botulism (6), and neurological complications (9), like spongiform leukoencephalopathy, stroke, toxic amblyopia, transverse myelopathy, mononeuropathy, acute inflammatory demyelinating polyradiculoneuropathy, rhabdomyolysis, compartment syndrome, fibrosing myopathy, and acute bacterial myopathy.

We report here a highly unusual manifestation of heroin overdose in a young addict who presented with transverse myelitis and rhabdomyolysis leading to compartment syndrome and renal failure within a few hours of intranasal administration.

Case report

A 30-year-old man, a known substance abuser, was found unconscious, lying in the abnormal lotus posture, leaning forwards with legs crossed, the neck flexed and head resting against the wall, 10 hours after taking heroin by intranasal route. He was brought to the emergency room where after intravenous Naloxone he regained full consciousness. However, he complained of inability to move his extremities, swelling of the left leg below the knee, and urinary retention. He was also unable to feel any sensation below his neck. There were no seizures, tremors, fever, excessive sweating, lacrimation, hallucinations, or any other features of drug withdrawal. No history of neck trauma, use of any medication, or abuse of any other drug including alcohol in the recent past was found. The family and past medical histories were non-contributory.

Physical examination revealed loss of strength and absent reflexes in all extremities. Bilateral extensor plantar response could be elicited. Sensations were absent below the spinal level of C3. There was fullness of the urinary bladder. The higher mental functions including orientation, attention span, speech and comprehension were normal, and cranial nerves were intact. There was marked tense swelling of the left leg below the knee. The overlying skin was cold and bluish purple in color suggestive of pregangrene. The pulses could not be palpated distal to the femoral pulse in the left lower limb. Laboratory investigations showed normal blood counts, ESR, and liver function tests. Blood urea was 234 mg/dl, creatinine- 6.2 mg/dl, K+− 6.0 mmol/L. Urine was cola colored with specific gravity of 1.018, 2+ protein, 4+ for blood with few RBCs and many pigmented casts, suggestive of myoglobinuria. Sodium, calcium, phosphorus, uric acid levels, coagulation profile, chest x-ray, and ECG were normal. Creatinine phosphokinase was 38905 U/L, LDH - 620 U/L, myoglobin level − 200,000 μg/L. HIV and antinuclear antibodies were negative. CT scan of cervical spine did not reveal any spinal injury. MR imaging (Fig. 1) of spine revealed an expanded cervical cord with patchy increased intramedullary signal intensity extending from C2 to D1 level with effacement of ventral and dorsal subarachnoid spaces suggestive of transverse myelitis. Spinal fluid analysis was normal. Color doppler study of arterial system showed absent filling of the infrapopliteal arterial system of left leg with compartmental swelling. The poisoning was confirmed by demonstration of heroin metabolites O-monoacetylmorphine and morphine in the urine. Results of tests for cocaine, benzodiazepine, barbiturate, cannabinoids, amphetamine and LSD metabolites were negative. There was no trace of alcohol in the blood.

FIG. 1. MRI of the cervical spine showing expanded cervical cord with patchy increased intramedullary signal intensity (see arrows) extending from C2 to D1 level with effacement of ventral and dorsal subarachnoid spaces suggestive of transverse myelitis.

Acute compartment syndrome due to rhabdomyolysis was suspected and a fasciotomy was performed the next day. The leg vessels were exposed and found to be normal. Following the procedure the pulses returned but extensive damage to the soft tissues was done already. Over the next few days the patient remained oliguric and there was a serial rise in blood urea and creatinine levels. A diagnosis of myoglobin induced acute renal failure was made and the patient started on continuous veno-venous hemofiltration (CVVH) following which the blood levels of urea, creatinine and myoglobin decreased. Due to respiratory distress he was put on mechanical ventilation. Despite this supportive therapy, he succumbed to worsening renal failure and ventilator associated pneumonia after 13 days. The relatives did not give consent, so an autopsy could not be performed.

Discussion

Various neurological and neuromuscular complications (9) of heroin abuse have been described. Rhabdomyolysis has been associated with the use of opioids, alcohol and other drugs (10–13). Rhabdomyolysis can lead to acute renal failure due to direct toxicity of metabolites like ferrihemate (13,14), tubular obstruction due to protein, uric acid crystals, and myoglobin casts, or by reduction in renal blood flow as a result of renal vasoconstriction. Compartment syndrome is described as a consequence of rhabdomyolysis due to muscle swelling. Heroin-induced compartment syndrome though described, is a rare entity (15). The pathophysiology of rhabdomyolysis in heroin overdose remains unexplained. A multifactorial pathogenesis including acidosis, hypoxia, muscle compression, direct toxic, or immunological effects of the drug or its contaminant (12) has been suggested.

Acute transverse myelitis as a complication of heroin overdose was first described in 1968 (16). Since then some other cases have been reported mostly with intravenous (17,18) use and one case with intranasal (19) insufflation of heroin. In most of the reports except one (18) the patients developed myelitis on a single use of heroin after a variable period of abstinence leading credence to a possible hypersensitivity mechanism. Most of the addicts developed myelitis in the thoracic ‘watershed’ area of the cord. Suggested mechanisms (19) of heroin-induced myelopathy include embolism, hypotension, direct toxicity, vasculitis, and hypersensitivity (16–18) reactions.

In the present case; the clinical presentation, the presence of heroin metabolites in urine, high myoglobin and CK levels, myoglobinuria, azotemia, arterial ultrasonographic study, and cervical spine MRI; support the diagnosis of heroin associated rhabdomyolysis, ARF, compartment syndrome, and acute transverse myelitis. A unique feature of this case is the simultaneous onset of both rhabdomyolysis and transverse myelitis in a single patient following heroin abuse. Myelitis following intranasal insufflation of heroin has been reported only once (19) previously. In the present case involvement of the cervical spine rather than the “watershed” thoracic spine (16) is not consistent with the proposed ischemic mechanism of myelitis. This patient also developed acute compartment syndrome leading to muscle necrosis – a complication rarely reported with heroin (15).

In many ways our case is similar to an earlier reported case (20) in which severe rhabdomyolysis, ARF, hypercalcemia, disseminated intravascular coagulopathy, and paraplegia below T12 were seen following intravenous heroin overdose. The probable cause of paraplegia in that case was lumbosacral plexopathy and the patient eventually recovered. The simultaneous occurrence of multiple complications involving diverse organ systems suggests a linked or systemic mechanism of injury. A previously described case of heroin induced cardiac rhabdomyolysis (21) also pointed towards a systemic rather than a local mechanism. The idea that opioids modulate (22) the immune system is not new. Both (23) decreased as well as increased immunological reactions are described after heroin use. Direct toxic or immune mediated damage due to heroin or its contaminants, posture related mechanical factors causing compressive or ischemic damage are possibilities that would explain the pathogenesis of complications experienced by the patient in this case.