Neurological and systemic effects of cocaine toxicity: A case report and review of the literature

Abstract

While historically utilized as a topical anesthetic and active ingredient in a variety of tonics, beverages and cure-alls, cocaine is a commonly abused illicit substance. Cocaine use is associated with a variety of neurological and systemic complications. The present study describes the case of a 23-year-old female patient presenting with profound neurological and systemic complications of cocaine, including coma, leukoencephaloapthy, neurogenic stunned myocardium, transaminitis, acute kidney injury, rhabdomyolysis and mononeuropathy. The supportive management and subsequent outcomes of the patients are discussed in detail. The approach to coma is also discussed, including stabilization and supportive care, diagnostic considerations and management. Key considerations relating prognosticating disorders of consciousness are also highlighted.

Keywords: cocaine; coma; leukoencephalopathy; overdose; toxicity.

Figure 1

Computed tomography: (A and B) Day 1, and (C and D) day 13. (A) Loss of gray and white matter differentiation in the cerebellar hemispheres, with mass effect on the fourth ventricle (white arrowhead) are observed. (B) Bilateral hypodensities in the globus pallidus (white arrows) are observed. (C) The resolution of gray and white matter changes in the cerebellar hemispheres can be seen. No mass effect on fourth ventricle (white arrowhead) can be observed. (D) Decreased attenuation of bilateral hypodensities in the globus pallidus can be seen (white arrows).

Figure 2

Magnetic resonance imaging of the patient on days 1 and 3. Day 1 magnetic resonance brain diffusion-weighted images, apparent diffusion coefficient sequences illustrating restricted diffusion involving the (A) bilateral cerebellar hemispheres, (B) hippocampi, and (C) globus pallidus and occipital lobes, (D) splenium of the corpus callosum and periventricular areas, (E) centrum semiovale, and (F) perirolandic regions. (G) Susceptibility weighted imaging sequences with petechial hemorrhage in occipital lobes and globus pallidus. (A-F, bottom row) Day 3 magnetic resonance brain fluid-attenuated inversion recovery (FLAIR) sequences illustrating the regression of restricted diffusion, increasing FLAIR hyperintensities and subtle enhancement in previously affected regions.

Figure 3

Clinical approach to the comatose patient: Stabilization, diagnosis (history, examination, investigations) and targeted management. Other considerations pertaining to the approach to an altered level of consciousness have been previously reported (3,4). ACTH, adrenocorticotropic hormone; AF, atrial fibrillation; AG, anion gap; ASM, anti-seizure medication; BB, beta blocker; BP, blood pressure; BUN, blood urea nitrogen; CNS, central nervous system; COPD, chronic obstructive pulmonary disease; CSF, cerebrospinal fluid; CT, computed tomography; CTS, contusion; DAI, diffuse axonal injury; DKA, diabetic ketoacidosis; d/o, diagnosis; DVST, dural venous sinus thrombosis; DVT, deep vein thrombosis; ECG, electrocardiography; EEG, electroencephalography; EDH, epidural hematoma; EtOH, ethanol; EV, endovascular thrombectomy; H/A, headache; HIBI, hypoxic ischemic brain injury; HIE, hepatic ischemic encephalopathy; HNK, hyperosmolar hyperglycemic non-ketotic coma; h/o, history of; HTN, hypertension; iCa, ionized calcium; infx, infectious; IPH, intraparenchymal hemorrhage; IPPV, intermittent positive-pressure ventilation; IST, immunosuppressive therapy; IVF, intravenous fluids; IVH, intraventricular hemorrhage; IVIG, intravenous immunoglobulin; LOC, level of consciousness; LV, left ventricle; MRb, MR brain; NCCTh, non-enhanced CT head; NPPV, non-invasive positive pressure ventilation; NSx, neurosurgical; N/V, nausea/vomiting; OG, osmolar gap; OM, otitis media; PLEX, plasma exchange; PNA, pneumonia; PRES, posterior reversible encephalopathic syndrome; PTU, propylthiouracil; RCVS, reversible cerebral vasoconstriction syndrome; RRT, renal placement therapy; Rx, treatment; SAH, subarachnoid hemorrhage; SDH, subdural hematoma; SIADH, syndrome of inappropriate antiduretic hormone secretion; SIRS, systemic inflammatory response syndrome; Sx, symptoms; Sz, seizure; tSAH, traumatic subarachnoid hemorrhage; T3, triiodothyronine; T4, thyroxine; TBI, traumatic brain injury; TPO, thyroid peroxidase; TSH, thyroid stimulating hormone; v/a, visual acuity; VTE, venous thromboembolism; WBC, white blood cells.