From the Guidelines
Wernicke syndrome is a serious neurological disorder caused by thiamine (vitamin B1) deficiency that requires immediate treatment with thiamine supplementation, typically starting with oral thiamine 200–300 mg d−1 and vitamin B compound strong 1 or 2 tablets three times a day, or full dose daily intravenous vitamin B preparation, if necessary, as stated in the British Obesity and Metabolic Surgery Society guidelines 1.
Key Points
- Wernicke syndrome presents with a classic triad of symptoms: confusion, abnormal eye movements (nystagmus and ophthalmoplegia), and difficulty with coordination and walking (ataxia) 1.
- Thiamine deficiency is the primary cause of Wernicke syndrome, and it can occur after bariatric surgery or in other conditions with malnutrition 1.
- Treatment must be initiated before giving glucose to prevent worsening of symptoms, as oral or intravenous glucose can precipitate Wernicke–Korsakoff syndrome 1.
- Early recognition and prompt treatment are crucial for preventing irreversible brain damage and reducing morbidity and mortality associated with Wernicke syndrome.
Management
- The British Obesity and Metabolic Surgery Society guidelines recommend giving additional thiamine and vitamin B compound strong immediately to people at risk of thiamine deficiency or with clinical suspicion of acute deficiency 1.
- Vitamin B12, copper, and vitamin E levels should be assessed and any deficiencies corrected, and people with neurological symptoms should be referred to a neurologist 1.
- The guidelines also emphasize the importance of awareness among healthcare professionals, including emergency department staff, about this preventable complication and its management 1.
From the Research
Definition and Causes of Wernicke Syndrome
- Wernicke syndrome, also known as Wernicke's encephalopathy (WE), is a neurologic emergency caused by thiamine (vitamin B1) deficiency 2, 3, 4, 5, 6.
- The primary culprit of thiamine deficiency is alcohol abuse, but non-alcoholic WE can also occur due to other factors such as malnutrition, hyperemesis gravidarum, intestinal obstruction, and malignancy 3, 4, 6.
Clinical Symptoms and Diagnosis
- The classic triad of clinical symptoms includes confusion, ophthalmoplegia, and gait ataxia, but these symptoms are only present in 10-33% of cases 3, 4, 6.
- Mental status changes, ocular dysfunction, and gait apraxia are common findings, but the diagnosis of WE remains primarily clinical 4.
- Neuroimaging plays an important role in the diagnosis of non-alcoholic WE, especially in cases with atypical clinical presentations 3.
Treatment and Prognosis
- Timely administration of thiamine is critical for treatment, and the route and dosage remain controversial 4.
- High-dose intravenous thiamine and simultaneous treatment of magnesium deficiency are recommended 5.
- Failure to treat WE promptly can lead to permanent neurological morbidity, mortality, or the development of Korsakoff syndrome, characterized by memory impairment and confabulation 2, 4, 5.