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Dragon, Caught: Acute-Onset Toxic Leukoencephalopathy After Inhaled Heroin Overdose
Description
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A6900 - Dragon, Caught: Acute-Onset Toxic Leukoencephalopathy After Inhaled Heroin Overdose
Author Block: N. Achamallah, Y. Matusov, J. C. Fried; Santa Barbara Cottage Hospital, Santa Barbara, CA, United States.
INTRODUCTION
Progressive toxic leukoencephalopathy (TLE) associated with heroin inhalation, or “chasing the dragon,” has been extensively described in the literature.1-6 This syndrome is characterized by motor symptoms and dysautonomia that develop over weeks to months.6,7 We present the first reported case of abrupt-onset inhaled heroin-associated TLE, one of three recently identified in our facility. These likely represent a previously unrecognized subset of “found down” patients with acute neurologic changes not attributable to hypoxemic encephalopathy.
CASE DESCRIPTION
A 20-year-old male was found unresponsive after being seen normal the evening prior. Toxicology was positive for opiates; friends confirmed inhaled heroin use. Initial concern was for hypoxic injury but MRI brain demonstrated changes consistent with TLE.
Over his first week of hospitalization the patient was tremulous with extensor posturing to stimulation. He sustained periods of dysautonomia with agitation, rigidity, hyperthermia, and tachycardia. On day seven he exhibited spontaneous eye opening, and at day nine he appeared to track. He continued to display small progressive improvements and at day 17 began physical and occupational therapy. At discharge to long-term care facility on day 34 he was speaking short sentences and tolerating dysphagia diet.
DISCUSSION
Since the year 2000 overdose-related deaths involving opioids have doubled.8 This is reflected as increased ICU admissions due to opioid overdose over the same period.9 Trends in usage patterns have also shifted over the last two decades; inhaled heroin use has nearly tripled.10
Identification of acute-onset TLE after heroin inhalation has distinct implications for neuro-prognostication. TLE classically progresses through three stages over weeks to months. The first, primarily cerebellar, includes motor restlessness and ataxia with pseudobulbar speech. This is followed by myoclonic jerks, choreoathetoid movements, and spastic paresis. Finally, approximately 25% of patients progress to akinetic mutism, extensor posturing, central pyrexia, and eventual death.3,11 Our patient presents acutely in stage three after having been previously asymptomatic.
MRI findings in this case are pathognomic for TLE. These include symmetrically increased T2-FLAIR signal intensity of cerebellar and posterior cerebral white
matter.7,12 Gray matter, which is extremely susceptible to hypoxic injury, is spared.12
Prolonged unresponsiveness in patients “found down” after heroin overdose is often attributed to hypoxic brain injury. Brain MRI is not generally included as part of routine workup. It should, however, be considered in patients with suspected inhaled heroin use due to the relatively favorable prognosis of TLE.13 The result may have significant impact on decisions about continuation of care.
Author Block: N. Achamallah, Y. Matusov, J. C. Fried; Santa Barbara Cottage Hospital, Santa Barbara, CA, United States.
INTRODUCTION
Progressive toxic leukoencephalopathy (TLE) associated with heroin inhalation, or “chasing the dragon,” has been extensively described in the literature.1-6 This syndrome is characterized by motor symptoms and dysautonomia that develop over weeks to months.6,7 We present the first reported case of abrupt-onset inhaled heroin-associated TLE, one of three recently identified in our facility. These likely represent a previously unrecognized subset of “found down” patients with acute neurologic changes not attributable to hypoxemic encephalopathy.
CASE DESCRIPTION
A 20-year-old male was found unresponsive after being seen normal the evening prior. Toxicology was positive for opiates; friends confirmed inhaled heroin use. Initial concern was for hypoxic injury but MRI brain demonstrated changes consistent with TLE.
Over his first week of hospitalization the patient was tremulous with extensor posturing to stimulation. He sustained periods of dysautonomia with agitation, rigidity, hyperthermia, and tachycardia. On day seven he exhibited spontaneous eye opening, and at day nine he appeared to track. He continued to display small progressive improvements and at day 17 began physical and occupational therapy. At discharge to long-term care facility on day 34 he was speaking short sentences and tolerating dysphagia diet.
DISCUSSION
Since the year 2000 overdose-related deaths involving opioids have doubled.8 This is reflected as increased ICU admissions due to opioid overdose over the same period.9 Trends in usage patterns have also shifted over the last two decades; inhaled heroin use has nearly tripled.10
Identification of acute-onset TLE after heroin inhalation has distinct implications for neuro-prognostication. TLE classically progresses through three stages over weeks to months. The first, primarily cerebellar, includes motor restlessness and ataxia with pseudobulbar speech. This is followed by myoclonic jerks, choreoathetoid movements, and spastic paresis. Finally, approximately 25% of patients progress to akinetic mutism, extensor posturing, central pyrexia, and eventual death.3,11 Our patient presents acutely in stage three after having been previously asymptomatic.
MRI findings in this case are pathognomic for TLE. These include symmetrically increased T2-FLAIR signal intensity of cerebellar and posterior cerebral white
matter.7,12 Gray matter, which is extremely susceptible to hypoxic injury, is spared.12
Prolonged unresponsiveness in patients “found down” after heroin overdose is often attributed to hypoxic brain injury. Brain MRI is not generally included as part of routine workup. It should, however, be considered in patients with suspected inhaled heroin use due to the relatively favorable prognosis of TLE.13 The result may have significant impact on decisions about continuation of care.
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