CASE REPORT


https://doi.org/10.5005/jp-journals-10082-03200
SBV Journal of Basic, Clinical and Applied Health Science
Volume 6 | Issue 4 | Year 2023

Wernicke’s Encephalopathy Not So Uncommon: A Case Report


Ankush Balasaheb Kolhehttps://orcid.org/0000-0002-8698-2548

Department of Medicine, Medicover Hospitals, Aurangabad, Maharashtra, India

Corresponding Author: Ankush Balasaheb Kolhe, Department of Medicine, Medicover Hospitals, Aurangabad, Maharashtra, India, Phone: +91 9975636094, e-mail: ankushkolhe59@gmail.com

How to cite this article: Kolhe AB. Wernicke’s Encephalopathy Not So Uncommon: A Case Report. J Basic Clin Appl Health Sci 2023;6(4):79–82.

Source of support: Nil

Conflict of interest: None

Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.

Received on: 26 June 2023; Accepted on: 08 August 2023; Published on: 30 September 2023

ABSTRACT

Chronic alcoholic patients present with multiple disorders. Central nervous system involvement is common in patients with chronic alcoholism. Most of them present with hepatic encephalopathy. Patients with alcohol use also have a thiamine deficiency because of chronic malnutrition. A potential life-threatening complication of thiamine deficiency is Wernicke’s encephalopathy. Wernicke’s encephalopathy is characterized by a triad of symptoms: ophthalmoplegia (eye signs), cerebellar dysfunction, ataxia, and altered mental state (confusion). Most patients with Wernicke’s encephalopathy are alcoholics. We presented a case of Wernicke’s encephalopathy, who presented with seizures followed by unconsciousness and coma. Magnetic resonance imaging of the brain is suggestive of cytotoxic injury with diffuse cerebellar edema.

Keywords: Alcoholism, Case report, Coma, Seizure, Wernicke’s encephalopathy.

INTRODUCTION

Chronic alcoholic patients present with multiple disorders. Central nervous system involvement is common in patients with chronic alcohol use.1 Most of them present with hepatic encephalopathy. Patients with alcohol use also have a thiamine deficiency because of chronic malnutrition. A potential life-threatening complication of thiamine deficiency is Wernicke’s encephalopathy.2 Wernicke encephalopathy is characterized by a triad of symptoms: ophthalmoplegia (eye signs), cerebellar dysfunction, ataxia, and altered mental state (confusion).3 Most patients with Wernicke’s encephalopathy are alcoholics.

CASE PRESENTATION

A 34-year-old male was admitted to the hospital with a history of an episode of generalized clonic–tonic convulsion followed by unresponsive and unconscious with downward gaze. His Glasgow coma scale (GCS) was 3/15. He was suspected to have encephalopathy and was evaluated further. He was hemodynamically stable without any inotropic support. He was electively intubated for airway protection in view of his low GCS. All his blood tests were performed, suspecting hepatic encephalopathy, but it was absolutely normal. A cerebrospinal fluid study was done, which was also a normal limit. Magnetic resonance imaging of the brain is suggestive of cytotoxic injury with diffuse cerebellar edema (Fig. 1). Echocardiography was within limits. All the other laboratory parameters were within normal limits (Table 1). We ruled out all other causes of acute encephalopathy. We started him on intravenous thiamine, suspecting vitamin deficiency causing encephalopathy. He responded very well to intravenous thiamine and recovered within 4 days of hospitalization.

Table 1: Pathology reports
Profile Routine profile
Parameter Value Reference range Parameter Value Reference range
Troponin I 0.1 <10 Random sugar 138 70–140 mg/dL
NT pro-BNP 200 <400 Sodium 143 135–155 mmol/L
Total bilirubin 0.32 0.1–1.2 mg/dL Potassium 3.81 3.5–4.5 mmol/L
Direct bilirubin 0.15 0.0–0.4 mg/dL Urea 32.9 17–45 mg/dL
Indirect bilirubin 0.17 0.9–1.0 mg/dL Creatinine 0.90 0.7–1.3 mg/dL
Serum procalcitonin 0.160 <0.5 ng/mL White blood cells 12,700 4000–10,000 cells/cumm
Alkaline phosphatase 158.7 40–130 U/L Hemoglobin 14.9 11.5–15.5 gm/dL
HIV-I and -II Non-reactive Mean corpuscular volume (MCV) 95.0 83–11
HBsAg Non-reactive Platelet count 195,000 150,000–410,000/cumm
Anti-HCV Non-reactive Neutrophils 83 40–80%
APTT 27 25–40 seconds Lymphocytes 11 20–40%
PT 11 10–16 seconds INR 0.9 0.8–1.5
APTT, activated partial thromboplastin time; HBsAg, hepatitis B surface antigen; HIV, human immunodeficiency virus; HCV, hepatitis C virus; INR, international normalized ratio; NT Pro BNP, N-terminal pro-B-type natriuretic peptide; PT, prothrombin time

Figs 1A and B: Magnetic resonance imaging scan

DISCUSSION

Chronic alcoholic patients present with multiple neurological disorders. Cerebrospinal fluid involvement is common in patients with chronic alcohol use.1 Most of them present with hepatic encephalopathy. Patients with alcohol use also have a thiamine deficiency because of chronic malnutrition.1 A potential life-threatening complication of thiamine deficiency is Wernicke’s encephalopathy. Wernicke encephalopathy is characterized by a triad of symptoms: ophthalmoplegia (eye signs), cerebellar dysfunction, ataxia, and altered mental state (confusion).2 Most patients with Wernicke’s encephalopathy are alcoholics. Our patient responded very well to intravenous thiamine and we also ruled out hepatic and viral causes of encephalopathy in this patient.

CONCLUSION

Chronic alcoholic patients can present with multiple neurological illnesses. Most of them have hepatic involvement, and the cause of their encephalopathy is due to hepatic etiology. But vitamin deficiency is also a very important cause of encephalopathy, particularly in alcoholic patients due to nutritional deficiency. We must consider thiamine deficiency as a cause of encephalopathy while treating encephalopathy patients, especially those who are alcoholics, because thiamine deficiency is one of the common causes of encephalopathy.

ORCID

Ankush Balasaheb Kolhe https://orcid.org/0000-0002-8698-2548

REFERENCES

1. Harper C. Thiamine (vitamin B1) deficiency and associated brain damage is still common throughout the world and prevention is simple and safe! Eur J Neurol 2006;13(10):1078–1082. DOI: 10.1111/j.1468-1331.2006.01530.x.

2. Naidoo DP, Bramdev A, Cooper K. Wernicke’s encephalopathy and alcohol-related disease. Postgrad Med J 1991;67(793):978–981. DOI: 10.1136/pgmj.67.793.978.

3. Chung SP, Kim SW, Yoo IS, et al. Magnetic resonance imaging as a diagnostic adjunct to Wernicke encephalopathy in the ED. Am J Emerg Med 2003;21(6):497–502. DOI: 10.1016/s0735-6757(03)00094-9.

________________________
© The Author(s). 2023 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and non-commercial reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.