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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT  
Year : 2011  |  Volume : 22  |  Issue : 6  |  Page : 1223-1225
Rhabdomyolysis, acute kidney injury and transverse myelitis due to naive heroin exposure


Department of Nephrology, All India Institute of Medical Sciences, New Delhi, India

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Date of Web Publication8-Nov-2011
 

   Abstract 

Heroin exposure can cause various complications like seizures, stroke, spongiform encephalopathy, transverse myelopathy, plexopathy, compartment syndrome, rhabdomyolysis and renal failure due to various mechanisms. We report here a young male who smoked heroin for the first time and developed transverse myelitis, rhabdomyolysis and acute kidney injury requiring dialysis. His renal recovery was complete by four weeks, while neurological improvement occurred 8 to 12 weeks later. This case suggests a common pathogenic mechanism of heroin intoxication involving multiple systems of the body.

How to cite this article:
Gupta A, Khaira A, Lata S, Agarwal SK, Tiwari SC. Rhabdomyolysis, acute kidney injury and transverse myelitis due to naive heroin exposure. Saudi J Kidney Dis Transpl 2011;22:1223-5

How to cite this URL:
Gupta A, Khaira A, Lata S, Agarwal SK, Tiwari SC. Rhabdomyolysis, acute kidney injury and transverse myelitis due to naive heroin exposure. Saudi J Kidney Dis Transpl [serial online] 2011 [cited 2019 Nov 12];22:1223-5. Available from: http://www.sjkdt.org/text.asp?2011/22/6/1223/87239

   Introduction Top


The common modes of heroin abuse include inhalation and intravenous use. Rhabdomyolysis and acute kidney injury have been reported as a complication of heroin addiction and over-dose. [1],[2],[3],[4] However, it is rare in addicts who abstained from heroin for quite some time before resorting to it again. We encountered a young male who developed transverse myelitis, rhabdomyolysis and acute kidney injury after smoking heroin for the first time ever. The first inhaled exposure of heroin presenting with a combination of the above features has never been reported earlier.


   Case Report Top


A 30-year-old-male presented with inability to move the lower limbs, handgrip weakness and inability to pass urine for 24 hours. He had been found unconscious in the field and was taken to a nearby health center where he was catheterized and one liter of urine was drained. The patient was referred to our institute the next day. At admission, he was fully conscious and denied use of any intravenous drugs, alcohol abuse or self-medication. He gave no history of prior neurological symptoms, recent trauma, back pain, fever or bleeding diathesis. He, however, admitted that he smoked heroin for the first time, with a friend.

On examination, he had a pulse rate of 74/min, respiratory rate of 20/min and blood pressure of 134/82 mmHg in the right arm in supine position, and all peripheral pulses were palpable.

There were no signs of external injury. Chest, cardiovascular system and abdominal examination were normal. Neurological examination showed normal higher mental functions and cranial nerves. He had partial handgrip weakness in both hands and flaccid paraplegia, with a power of 0/5. Deep tendon reflexes were preserved in upper limbs and absent in lower limbs. Plantars were not elicitable on both sides. Touch and pinprick sensation were diminished below the T9 level. There were no signs of meningeal irritation or spinal tenderness. Fundus examination was normal.

Investigations on admission showed hemoglobin of 11.2 g/dL, total leukocyte count of 14200/mm³ with a normal differential count, blood urea of 145 mg/dL, serum creatinine of 6.0 mg/ dL, sodium of 136 meq/L, potassium of 5.0 meq/L, calcium of 6.4 mg/dL and phosphate of 10 mg/dL. He had elevated serum uric acid of 8.8 mg/dL, serum aspartate aminotransferase (SGOT) of 570 U/L and alanine aminotransferase (SGPT) of 394 U/L. The serum creatine kinase (CPK) was 3200 U/L, lactate dehydrogenase (LDH) was 254 U/L and serum myoglobin was 16,590 μg/mL, indicating that all parameters were significantly elevated. Blood gas analysis showed pH of 7.26, bicarbonate of 14.4 meq/L, PCO 2 of 26 mmHg and oxygen saturation of 98% on room air. Urine examination however could not be done due to anuria. Based on clinical examination and laboratory investigations, a provisional diagnosis of acute kidney injury with transverse myelitis with spinal shock was made and he was started on hemodialysis (HD) via temporary femoral catheter. The magnetic resonance imaging (MRI) showed long segment of central spinal cord hypo-intensity lesion on T1 images. On T2-weighted images, there were hyper-intense lesions in the cervical and upper thoracic cord regions, extending from C2 to T2, with tapering ends. MRI findings were consistent with the diagnosis of transverse myelitis [Figure 1].
Figure 1: T2-weighted sagittal images showing expansion of cervical spinal cord, with central hyperintense signal suggestive of transverse myelitis.

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The patient was pulsed with intravenous methyl prednisolone 750 mg daily for three days. Further investigations showed normal prothrombin and activated partial thromboplastin time. Antinuclear antibodies and antiphospholipid antibodies were negative and C3 and C4 complement levels were normal. Serology for human immunodeficiency virus (HIV), hepatitis B surface antigen and anti-hepatitis C virus were negative. Doppler study of aorta and renal vessels was normal. A diagnosis of acute kidney injury, atraumatic rhabdomyolysis and transverse myelitis, probably related to toxin, was made and the patient was put on thrice-a-week hemodialysis (HD) through double-lumen jugular catheter. He required eight sessions of HD over the next 20 days, when his renal functions started improving and the patient went into diuretic phase. Renal biopsy was deferred in view of recovering renal functions. By three weeks, his CPK, LDH and SGOT became normal [Table 1]. His lower limb power recovered by eight weeks and he regained bladder sensation by the end of twelve weeks.
Table 1: Trend of laboratory parameters with time.

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   Discussion Top


Heroin abuse can lead to rhabdomyolysis as a consequence of immunologic/hypersensitivity reaction, or possibly a direct myotoxic effect. Other mechanisms include presence of hypothermia, hypoxia, acidosis and mental obtundation/coma as a consequence of heroin itself or a contaminant, resulting in prolonged immobility, compression and muscle injury. [2] It is often difficult to comment which mechanism causes rhabdomyolysis in a particular case. Our patient presented with acidosis and gave a history of prolonged immobility. However, we cannot exclude the contribution of other mechanisms. Rhabdomyolysis may mimic transverse myelitis for which a careful differential diagnosis is warranted. [5]

Monoparesis, quadriparesis, transverse myelitis and rhabdomyolysis, along with lumbosacral plexopathy, have been described previously as various neurological complications of heroin abuse. [6],[7] However, the combination of rhabdomyolysis, acute kidney injury and transverse myelitis occurring together in a patient has been uncommonly described. [8],[9]

Our case is unique in some aspects. Firstly, it occurred in a naïve heroin user, which has not been reported. The previous reports of association of heroin abuse and transverse myelitis have been in cases who had abstained from its use for some period before starting its abuse again. [10],[11] Although first-use reactions with drugs are known to occur, but, as with many drug allergies, sensitization must occur first. Upon re-exposure to the drug, a hypersensitivity reaction ensues via haptenation of the drug with an in vivo protein. [12] In the background of the available facts, it is impossible to rule out hypersensitivity as a mechanism that is responsible for his presentation. Secondly, the vehicle of heroin delivery was cigarette smoking in our case. Cases reported earlier had used intravenous injections or intranasal insufflations as a vehicle for heroin abuse. With the HIV infection on the increase, smoking or insufflation would be the preferred route among heroin abusers, and this sort of atypical presentation has to be considered in the differential diagnosis. In conclusion, heroin exposure can present as a variety of neurological and renal complications that should be looked into and sought early. Even the first use of heroin can prove fatal. The physicians should be sensitized enough to recognize such a variable presentation of heroin toxicity.

 
   References Top

1.Vitris M, Saissy JM, Gohard R, Raux O, Diatta B, Kemps J. Heroin-induced acute rhabdomyolysis. Dakar Med 1991;36:15-8.  Back to cited text no. 1
    
2.Wan SH, Szeto ML. Rhabdomyolysis and heroin addiction. Hong Kong Med J 1995;1:266-8.  Back to cited text no. 2
    
3.Kathrein H, Kirchmair W, Konig P, von Dittrich P. Rhabdomyolysis with acute kidney failure after heroin poisoning. Dtsch Med Wochenschr 1983;108: 464-7.  Back to cited text no. 3
    
4.Rice EK, Isbel NM, Becker GJ, Atkins RC, McMahon LP. Heroin overdose and myoglobinuric acute renal failure. Clin Nephrol 2000;54:449-54.  Back to cited text no. 4
    
5.Yang CC, Yang GY, Ger J, Tsai WJ, Deng JF. Severe rhabdomyolysis mimicking transverse myelitis in a heroin addict. J Toxicol Clin Toxicol 1995;33:591-5.  Back to cited text no. 5
    
6.Diaz Guzman J, Pastor Valverde C, Gil Grande R, Alonso Ortiz A, Trueba Gutierrez JL. Rhabdomyolysis and lumbosacral plexopathy in intravenous drug addict: report of a case. Ann Med Interna 1996; 13:84-6.  Back to cited text no. 6
    
7.Challenor YB, Richter RW, Bruun B, Pearson J. Nontraumatic plexitis and heroin addiction. JAMA 1973;225:958-61.  Back to cited text no. 7
    
8.Kumar R, West DM, Jingree M, Laurence AS. Unusual consequences of heroin overdose: rhabdomyolysis, acute renal failure, paraplegia and hypercalcaemia. Br J Anaesth 1999;83:496-8.  Back to cited text no. 8
    
9.Sahni V, Garg D, Garg S, Agarwal SK, Singh NP. Unusual complications of heroin abuse: Transverse myelitis, rhabdomyolysis, compartment syndrome, and ARF. Clin Toxicol 2008;46:153-5.  Back to cited text no. 9
    
10.Ell JJ, Uttley D, Silver JR. Acute myelopathy in association with heroin addiction. J Neurol Neurosurg Psychiatry 1981;44:448-50.  Back to cited text no. 10
    
11.Grassa C, Montanari E, Scaglioni A, Passeri S, Saginario M. Acute heroin myelopathy-case report. Ital J Neurol Sci 1984;5:63-6.  Back to cited text no. 11
    
12.McCreary M, Emerman C, Hanna J, Simon J. Acute myelopathy following intranasal insufflation of heroin: a case report. Neurology 2000;55:316-7.  Back to cited text no. 12
    

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Correspondence Address:
Ankur Gupta
Department of Nephrology, All India Institute of Medical Sciences, New Delhi
India
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PMID: 22089788

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