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Severe Wernicke's Encephalopathy Associated with Cortical Ribboning and Intracranial Hemorrhage.

ABSTRACT: Wernicke's encephalopathy (WE) is a neurological emergency that results from thiamine deficiency. It is most commonly associated with chronic alcohol consumption but can result from any cause of impaired thiamine absorption or dietary intake. The classic triad of ophthalmoparesis, ataxia, and altered sensorium is rarely seen in toto, and while certain radiographic findings strongly correlate with the disease, one should have a low threshold to suspect (and promptly treat) patients in order to mitigate the risk of morbidity and mortality. However, atypical presentations can result in delayed or missed diagnoses. In this report, we describe a case of severe non-alcoholic WE associated with atypical brain Magnetic resonance imaging (MRI) manifestations of both cortical diffusion restriction and intracranial hemorrhage, which have previously been associated with poor outcomes. Early treatment with high-dose parenteral thiamine resulted in rapid improvement in ocular motility and reversal of MRI abnormalities, and on long-term follow up, the patient had made a marked functional improvement. This case highlights the importance of recognizing these unusual imaging features of WE in a patient with a compatible clinical syndrome in order to make a timely diagnosis and initiate treatment, as there is potential for a good clinical outcome despite these imaging findings.

SUBMITTER: DePolo D

PROVIDER: S-EPMC9485700 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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Severe Wernicke's Encephalopathy Associated with Cortical Ribboning and Intracranial Hemorrhage.

DePolo Daniel D Gillen Stefan S Marden Kyle K Rajagopalan Swarna S Thon Olga R OR Siegler James E JE Thon Jesse M JM

The Neurohospitalist 20220705 4

Wernicke's encephalopathy (WE) is a neurological emergency that results from thiamine deficiency. It is most commonly associated with chronic alcohol consumption but can result from any cause of impaired thiamine absorption or dietary intake. The classic triad of ophthalmoparesis, ataxia, and altered sensorium is rarely seen in toto, and while certain radiographic findings strongly correlate with the disease, one should have a low threshold to suspect (and promptly treat) patients in order to mi ...[more]

PMID: 36147752

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Project description:ObjectivesElevated intracranial pressure is one of the proposed mechanisms leading to poor outcomes in patients with intraventricular hemorrhage. We sought to characterize the occurrence and significance of intracranial hypertension in severe intraventricular hemorrhage requiring extraventricular drainage.DesignProspective analysis from two randomized, multicenter, clinical trials.SettingIntensive care units of 23 academic hospitals.PatientsOne hundred patients with obstructive intraventricular hemorrhage and intracerebral hemorrhage volume <30 mL requiring emergency extraventricular drainage from two randomized multicenter studies comparing intraventricular recombinant tissue plasminogen activator (n=78) to placebo (n=22).InterventionsIntracranial pressure was recorded every 4 hrs in all patients and before and after a 1-hr extraventricular drainage closure period after injection. Intracranial pressure readings were analyzed at predefined thresholds and compared between treatment groups, before and after injection of study agent, and before and after opening of third and fourth ventricles on computed tomography. Impact on 30-day outcomes was assessed.Measurements and main resultsInitial intracranial pressure ranged from -2 to 60 mm Hg (median; interquartile range, 11;10). Of 2576 intracranial pressure readings, 91.5% (2359) were ≤20 mm Hg, 1.6% were >30, 0.5% were >40, and 0.2% were >50 mm Hg. In a multivariate analysis, threshold events>20 mm Hg and >30 mm Hg were more frequent in placebo vs. recombinant tissue plasminogen activator-treated groups (p=.03 and p=.08, respectively). Intracranial pressure elevation>20 mm Hg occurred during a required 1-hr extraventricular drainage closure interval in 207 of 868 (23.8%) injections of study agent, although early reopening of the extraventricular drainage only occurred in 7.9%. After radiographic opening of the lower ventricular system, intracranial pressure events>20 mm Hg remained significantly associated with initial intraventricular hemorrhage volume (p=.002) and extraventricular drainage placement ipsilateral to the largest intraventricular hemorrhage volume (p=.001), but not with thrombolytic treatment (p=.05) or intracerebral hemorrhage volume (p=.14). Ventriculoperitoneal shunts were required in 13.6% of placebo and 6.4% of recombinant tissue plasminogen activator-treated patients (p=.37). Percentage of intracranial pressure readings per patient>30 mm Hg and initial intracerebral hemorrhage and intraventricular hemorrhage volumes were independent predictors of 30-day mortality after adjustment for other outcome predictors (p=.003, p=.03, and p<.001, respectively). Independent predictors of poor modified Rankin Scale score at 30 days were percent of intracranial pressure events>30 mm Hg per patient (p=.01; but not >20 mm Hg), both intracerebral hemorrhage and intraventricular hemorrhage volume, and pulse pressure.ConclusionsIntracranial pressure is not frequently elevated during monitoring and drainage with an extraventricular drainage in patients with severe intraventricular hemorrhage, although intracranial pressure >30 mm Hg predicts higher short-term mortality. Thrombolytic therapy may reduce the frequency of high intracranial pressure events. Intracranial pressure elevation appears to be significantly correlated with extraventricular drainage placement in the ventricle with greatest clot volume.

Dataset Information

Severe Wernicke's Encephalopathy Associated with Cortical Ribboning and Intracranial Hemorrhage.

Publications

Severe Wernicke's Encephalopathy Associated with Cortical Ribboning and Intracranial Hemorrhage.

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