Acute Painful Neuropathy in a Heroin Body Packer

A broad range of peripheral neurological complications have been recognized in heroin addicts. Peripheral Nervous System (PNS) involvement, usually secondary to trauma during loss of consciousness, commonly manifests as compressive neuropathy or rhabdomyolysis. Other, rare, non traumatic PNS lesions include poliradiculopathy, plexopathy, Guillan-Barrè syndrome and mononeuropathy. Acute heroin related non compressive neuropathy is rare, and the aetiology is still unclear. In heroin abusers painful acute neuropathy has rarely been described. We report the case of a 33-year-old male with a history of heroin abuse. He was found in his home in coma, maintaining the same sitting position for several hours. He was admitted to the intensive care unit, where rhabdomyolysis complicated by acute renal failure was diagnosed, requiring treatment with haemodialysis. A Computed Tomography (CT) scan of the abdomen revealed the presence of several foreign bodies in sigma and the urinary exams showed high concentration of opiates, revealing that the patient was a body packer. Further laboratory exams showed Hepatitis C Virus (HCV) infection with normal liver function. Upon awakening, five days after admission, the patient complained of severe burning pain, mechanical allodynia, itch, tingling and pinprick sensation in both feet and legs. The Douleur Neuropathique en 4 Questions (DN4) scale was 8/10, Numeric Rating Scale (NRS) scale score was 9/10 and Neuropathic Pain Symptom Inventory (NPSI) score was 37. Neurologic examination showed reduced sensitivity to temperature and pinprick in both legs and feet. Neurophysiological evaluation, performed 4 weeks after admission, showed normal nerve conduction studies. Thermal Quantitative Sensory Testing (t-QST) showed a patchy distribution of cold and warm hypoesthesia in the lower limbs. The patient also described positive symptoms (hyperalgesia and aftersensation following hot stimuli, mechanical static and dynamic allodynia) in the same areas. Sympathetic Skin Response (SSR) performed in both arms and feet was normal. Laser Doppler Flowmetry showed reduced local vasodilation after heat stimulus (C-mediated local axonal reflex) and normal vasoconstriction reflex (mediated by adrenergic sympathetic fibres) distally in the legs. The patient declined undergoing a skin biopsy for diagnostic purposes. The clinical and neurophysiological findings indicate the presence of small fibre neuropathy, with main involvement of C fibres, following a length-dependent distribution. To relieve the severe painful symptoms the patient was treated with gabapentin, fentanyl, duloxetina and pregabalin, with a gradual resolution of pain. The follow up examination, performed after 12 months, showed an improvement of the small fibre related symptoms with resolution of spontaneous pain and attenuation of itch, tingling and pinprick sensation, confirmed by the t-QST evaluation. A broad range of peripheral neurological complications have been recognized in heroin abusers. Peripheral nerve lesions in drug addicts may be caused by injection of substances in the vicinity of a nerve, local infection or nerve compression during coma. Combined nerve or plexus lesions and rhabdomyolysis have been reported in relation to possible trauma but they may occur also without apparent trauma to muscles or nerves. In these latter cases toxic or allergic reaction to heroin or adulterants are probably more important causes of rhabdomyolysis and nerve lesions than limb compression. Reports on acute heroin-related non compressive neuropathy are scarce. Dabby et al. described six patients who developed acute PNS injury following intravenous or intranasal heroin self administration with no evidence of compression injury or inflammation. Four patients had plexopathy and two had symmetric distal axonal sensorimotor neuropathy; five had concomitant rhabdomyolysis. They proposed that a toxic mechanism could be responsible for acute neuropathy following heroin abuse. In heroin abusers painful complications have been reported, but the pain was related to myelopathy, plexopathy, sciatic neuropathy and rhabdomyolysis4; none of these cases had length-dependent symptoms or clinical signs of small fibre damage. Numerous studies in humans and animals report that opioids can elicit abnormal pain, like thermal hyperalgesia and/or mechanical allodynia, following both acute and chronic administration of morphine, heroin, methadone, fentanyl and remifentanil. The mechanism responsible for the tactile and thermal hypersensitivity observed following opioid exposure is still unclear. Many hypotheses have been put forward, including sensitization of peripheral nerve endings or second-order neurons, enhanced descending facilitation of nociceptive pathways, increased production, release and decreased re-uptake of neurotransmitters involved in nociception, activation of glial cells and opioid associated epigenetic changes in Deoxyribonucleic Acid (DNA) methylation. Prolonged exposure to opioids results in long-lasting neuroadaptive changes that promote a state of hypersensitivity to normal non-noxious tactile and to noxious thermal stimulation that may promote activation of the nociceptive system. The aetiology of acute PNS complication in heroin addicts can be related to different mechanisms. The impurities and additives present in illicit drugs may cause allergies and have their own toxic effects; mechanical trauma is a potential mechanism of focal nerve injury and rhabdomyolysis. Evidence of an immunologic cause has been found in three patients who developed acute brachial plexopathy and rhabdomyolysis after heroin administration and in one heroin addict who developed a lumbosacral plexus neuropathy and responded to steroid therapy. We describe the case of a body packer who developed acute painful neuropathy with involvement of small nerve fibre with concomitant rhabdomyolysis and acute renal failure. The patient was HCV positive; all the other causes of Small Fibre Neuropathy (SFN) were excluded. In our patient there was no evidence of an inflammatory or immunologic process and mechanical factors probably didn’t play a major role in the pathogenesis. The patient had a history of prolonged lying before arriving to the emergency room but the neuropathy was symmetric and distal, being inconsistent with focal trauma or compression. Acute renal failure and haemodialysis can be possible causes of SFN but in our patient there was not a correlation of the symptoms with the haemodialytic sessions and there was not an improvement of symptoms after achieving normal renal function. HCV infection can play a role in SFN, but the acute presentation of the symptoms in temporal relation with heroin intoxication and their gradual improvement suggest that a toxic effect of heroin or added substances can be responsible for neural and muscle toxicity in our patient. In conclusion a careful neurophysiological evaluation should be considered in heroin abusers presenting with acute pain to rule out SFN.