Cocaine Induced Hypertensive Intraparenchymal Hemorrhage

Clinical history: A 37-year-old female presented to the emergency room after awakening at 4 a.m. with right sided weakness. Neurological exam confirmed loss of strength on the right side, loss of sensation in the right upper extremity, and a positive right sided Babinski sign. A CT of the head demonstrated the following:

Large intraparenchymal hemorrhage of the left parietal lobe with surrounding edema

Erosion of the nasal septum with history of cocaine use

Diagnosis: Cocaine induced hypertensive intraparenchymal hemorrhage

Discussion: Differential considerations for a spontaneous intracerebral hemorrhage in a relatively young patient include underlying vascular lesions, such as an arteriovenous malformation, cavernoma, middle cerebral artery aneurysm or pseudoaneurysm, underlying neoplasm, venous infarction, vasculitis, coagulopathy, Moya Moya disease, and drug-induced hypertension. In our patient (a cocaine abuser) the associated nasal septum erosion with the acute intracranial hematoma are highly indicative of cocaine-induced hypertensive hemorrhage.

Patients with hypertensive cardiovascular disease are more predisposed to cocaine induced intracerebral hemorrhage. The mechanism of action is thought to result from cocaine induced alteration of cerebral autoregulation in the context of increased cerebral flow secondary to cocaine induced hypertension, though further studies are needed to confirm this hypothesis.

Patients with spontaneous intracerebral hemorrhage (ICH) secondary to cocaine have a poor prognosis compared to patients with cocaine-negative spontaneous ICH. Cocaine users usually are more likely to have intraventricular extension, which our patient demonstrated on follow-up MRI, and have a more severe clinical presentation. Cocaine users with spontaneous ICH also have worse functional outcome at discharge and a higher rate of death compared to their cocaine-negative counterparts. One study demonstrated cocaine users are three times more likely to die during their acute hospitalization from a spontaneous ICH.

Inhaled cocaine abuse can cause inflammation and ulceration of the nasal mucosa with perforation of the septum. The mechanism of nasal inflammation and necrosis by cocaine is multifactorial; local ischemic vasoconstrictor effect, local trauma, irritation of the mucosa secondary to mixed substances, deficit in mucociliary transport and, rarely, secondary bacterial infection. Frequent and prolonged inhalation can cause osteocartilaginous necrosis, which can extend to the paranasal sinuses. In rare circumstances, the hard palate can become necrotic and perforate.

After the clinical team stabilized our patient, she was discharged to a rehabilitation center, with focal deficits as described in her presentation.

References:

Kibayashi, Mastri A, Hirsch C. Cocaine induced intracerebral hemorrhage: Analysis of predisposing factors and mechanisms causing hemorrhagic strokes. Hum Pathol. 1995 Jun;26(6):659-63.

Levine SR, Brust JC, Futrell N, et al. Cerebrovascular complications of the use of the "crack" form of alkaloidal cocaine. N Engl J Med. 1990 Sep 13;323(11):699-704.

Martin-Schild S, Albright K, Hallevi H, et al. Intracerebral hemorrhage in cocaine users. Stroke. 2010; 41: 680-684.

Rachapalli SM, Kiely PD. Cocaine-induced midline destructive lesions mimicking ENT-limited Wegener's granulomatosis. Scand J Rheumatol 2008;37(6):477-80.

Seyer BA, Grist W, Muller S. Aggressive destructive midfacial lesion from cocaine abuse. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;94(4):465-70.
 

Alan Alexander, MD, and Erini Makariou, MD, Georgetown University Hospital, Department of Radiology