Infective Endocarditis as a Complication of Heroin Use

Neufeld, Gwynne K.; Branson, C G; Marshall, Lila; Banks, Tazewell; Ali, Nayab

doi:10.1097/00007611-197609000-00014

Cited by 18 publications

(1 citation statement)

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“…However, their frequency and the causal relationship between cocaine abuse and cerebral vasculitis is still subject to debate (Kaye and Fainstat, 1987; Krendel et al ., 1990; Fredericks et al ., 1991; Martin et al ., 1995; Aggarwal et al ., 1996). Other possible mechanisms of the increased stroke risk include emboli from drug impurities (Delaney and Estes, 1980), paradoxical fat embolism (Bitar and Gomez, 1993), infectious emboli from the heart (Neufeld et al ., 1976; Kaku and Lowenstein, 1990), acute severe increase in blood pressure (Green et al ., 1990; Perez et al ., 1999), cerebral arterial vasospasm (Wang et al ., 1990; Nolte et al ., 1996), cardiomyopathy‐induced emboli (Sauer, 1991), hypoxia during a drug overdose (Jensen et al ., 1990; Zuckerman et al ., 1996) and allergic reactions to the drug or its additives (Delaney and Estes, 1980). Amphetamines and cocaines rapidly increase the heart rate and blood pressure (Gold and Miller, 1997; King and Ellinwood, 1997).…”

Section: Strokesmentioning

confidence: 99%

Neurological complications of drug abuse: pathophysiological mechanisms

Neiman

Haapaniemi

Hillbom

2000

Euro J of Neurology

158

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Drug abuse is associated with a variety of neurological complications. The use of certain recreational drugs shows a marked temporal association with the onset of both haemorrhagic and ischaemic strokes, the majority of which develop within minutes to 1 h after the administration of the index drug. Delayed onset of stroke has also been observed. Acute, severe elevation of blood pressure, cardiac dysrhythmias, cerebral vasospasm, vasculitis, embolization due to infective endocarditis or dilated cardiomyopathy, embolization due to foreign material injected with the diluents under non-sterile conditions and 'street drug' contaminants with cardiovascular effects have been suggested as possible underlying mechanisms. Rupture of aneurysms and arteriovenous malformations have been detected in up to half of the patients with haemorrhagic stroke due to cocaine abuse. The less common findings reported have included a mycotic cerebrovascular aneurysm in a patient with infective endocarditis and haemorrhagic stroke. In addition to stroke, cocaine seems to provoke vascular headache. Seizures precipitated by recreational drug abuse are usually caused by acute intoxication in contrast to the withdrawal seizures encountered in subjects with alcohol abuse. Movement disorders and cerebral atrophy correlating with the duration of abuse have been described. Snorting of organic solvents may cause encephalopathy. Cases of spongiform leukoencephalopathy in heroin addicts have also been reported. Peripheral neuropathy is occasionally precipitated by drug poisoning after intravenous administration. Impurities of the drug, risky administration techniques, and the use of mixtures of various drugs, frequently with simultaneous alcohol drinking, should be taken into account when assessing the background of the adverse event as well as the overall lifestyle of the addicted subjects.

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