THU0526 Acute paraspinal muscle necrosis with crack cocaine and heroin; a case report. (12th June 2018)

• Record Type: Journal Article
• Authors: Masood, A.; Attipoe, L.; D'Cruz, D.; Al-Saraj, S.; Williams, S.; Sabzevari, K.
• Is Part Of: Annals of the rheumatic diseases. Volume 77(2018)Supplement 2
• Page Start: 468
• Page End: 468
• Publication Date: 2018-06-12
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2018-eular.2294
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Cocaine can cause serious muscle injury ranging from asymptomatic creatine phosphokinase (CK) elevation to massive rhabdomyolysis with acute renal failure. Muscle injury is more common after intravenous use or after smoking the alkaloid freebase (crack cocaine) because of the more rapid effect and higher blood levels of the drug achieved via those routes. The onset of symptoms is acute and can even happen with one time drug use. Objectives: to broaden the knowledge about severe focal myositis as a consequence of crack cocaine abuse Methods: We report a case of Acute Paraspinal myositis and Rhabdomyolysis in a previously healthy African gentleman after smoking crack cocaine and heroin. Results: 35 years old gentleman, previously well, presented to the emergency with 12 hour history of severe lower back pain and stiffness in the absence of any trauma or systemic symptoms. On admission he was conscious and alert with tenderness and stiffness of paraspinal muscles, urinary retention requiring catheterization but no muscle weakness. Serum Creatinine was elevated at 597 µmol/L and Creatine Kinase was 66000 U/L. Urinalysis showed haematoproteinuria (3+blood, 4+protein). Patient reported smoking crack cocaine and snorting heroin, as well as drinking alcohol 12 hours before the onset of symptoms. Drug screen was positive for cocaine and benzodiazipines while autoimmune serology was negative for ANA, muscle specific antibodies anti-GBM and ANCA-antibody. Infection screen was negative and Urine and blood cultures were sterile. STIR images on MR scan revealed ill-defined areas in the paraspinal muscles consistent with Myositis. The muscle biopsy showed necrosis and focal intense infiltration by sheets of macrophages associated with proliferation of myoblast forming multinucleated giant cells but no evidence of granuloma formation the overall appearances being consistent with focal myositis. Serum Creatinine and CK improved progressively. He was treated with a tapering dose of steroids for 8 weeks while clinical and biochemical markers continued to improve. Conclusions: Drug induced Rhabdomyolysis can occur with cocaine, heroin and alcohol but it is the first reported case of focal myopathy affecting Paraspinal Muscles alone. There is one case report in the literature suggesting isolated myopathy with cocaine in the absence of central nervous system manifestations. One of the main differentials in such a scenario is Pyomyositis which requires early identification and prompt treatment to prevent systemic complications. References: [1] Zuckner J. Drug-related myopathies. Rheum Dis Clin North Am1994;20(4):1017–1032. [2] Pogue VA, Nurse HM. Cocaine-associated acute myoglobinuric renal failure. Am J Med1989;86(2):183–186. [3] Brazeau GA, McArdle A, Jackson MJ. Effects of cocaine on leakage of creatine kinase from skeletal muscle: in vitro and in vivo studies in mice. Life Sci1995;57(17):1569–1578. [4] Brody SL, Wrenn KD, Wilber MM, et al. Predicting the severity of cocaine-associated rhabdomyolysis. Ann Emerg Med1990;19(10):1137–1143. [5] Grob D. Rhabdomyolysis and drug-related myopathies. Curr Opin Rheumatol1990;2(6):908–915. [6] Roth D, Alarcón FJ, Fernandez JA, et al. Acute rhabdomyolysis associated with cocaine intoxication. N Engl J Med1988;319(11):673–677. Disclosure of Interest: None declared