What is the difference between Wernicke (Wernicke's) encephalopathy and beriberi in terms of clinical presentation and treatment?

From the Guidelines

Wernicke encephalopathy and beriberi are distinct clinical entities caused by thiamine deficiency, differing in their presentation and treatment, with Wernicke encephalopathy requiring immediate high-dose parenteral thiamine replacement. The clinical presentation of Wernicke encephalopathy primarily affects the central nervous system, characterized by the classic triad of confusion, ataxia, and ophthalmoplegia, although all three symptoms appear together in only about 10-20% of cases 1. In contrast, beriberi affects the peripheral nervous system and cardiovascular system, manifesting in two main forms: dry beriberi (peripheral neuropathy with numbness, pain, and weakness in extremities) and wet beriberi (cardiovascular symptoms including edema, tachycardia, high-output heart failure, and in severe cases, cardiovascular collapse) 1.

Some key differences between the two conditions include:

• Clinical presentation: Wernicke encephalopathy presents with central nervous system symptoms, while beriberi presents with peripheral nervous system and cardiovascular symptoms
• Treatment approach: Wernicke encephalopathy requires high-dose parenteral thiamine replacement, while beriberi typically responds to lower doses of thiamine
• Risk factors: Both conditions are most common in alcoholics, malnourished individuals, and those with malabsorption disorders

The treatment for both conditions requires immediate thiamine replacement, but dosing differs. Wernicke encephalopathy requires high-dose parenteral thiamine, typically 500 mg IV three times daily for 2-3 days, followed by 250 mg daily until symptoms improve, then oral maintenance therapy 1. Beriberi typically responds to lower doses, often 50-100 mg IV or IM daily until symptoms improve, followed by oral thiamine 10-25 mg daily 1. Early recognition and treatment are essential to prevent permanent neurological damage or death. It is also crucial to note that oral or intravenous glucose must not be given to people at risk of or with suspected thiamine deficiency as it can precipitate Wernicke–Korsakoff syndrome 1.

From the FDA Drug Label

Indications and Usage Thiamine hydrochloride injection is effective for the treatment of thiamine deficiency or beriberi whether of the dry (major symptoms related to the nervous system) or wet (major symptoms related to the cardiovascular system) variety Thiamine hydrochloride injection should be used where rapid restoration of thiamine is necessary, as in Wernicke’s encephalopathy, infantile beriberi with acute collapse, cardiovascular disease due to thiamine deficiency, or neuritis of pregnancy if vomiting is severe.

The main difference between Wernicke's encephalopathy and beriberi is the clinical presentation:

• Wernicke's encephalopathy requires rapid restoration of thiamine, indicating a more acute and severe condition.
• Beriberi can be dry (major symptoms related to the nervous system) or wet (major symptoms related to the cardiovascular system). In terms of treatment, both conditions are treated with thiamine hydrochloride injection when rapid restoration of thiamine is necessary, such as in Wernicke's encephalopathy or severe cases of beriberi 2.

From the Research

Clinical Presentation

• Wernicke encephalopathy (WE) is an acute neurologic disorder characterized by a triad of ophthalmoplegia, ataxia, and mental confusion, attributable to thiamine (vitamin B1) deficiency 3.
• Beriberi is the systemic counterpart of thiamine deficiency and often manifests in cardiovascular collapse, with two clinical presentations: dry beriberi presenting with neuropathy, and wet beriberi presenting with heart failure, with or without neuropathy 4.
• Dry beriberi can mimic the most common form of Guillain-Barre syndrome (GBS), an acute inflammatory demyelinating polyradiculoneuropathy (AIDP) 4.
• Severe thiamine deficiency results in Wernicke's encephalopathy, which can progress to Korsakoff's syndrome if undiagnosed or inadequately treated 5.

Treatment

• Early diagnosis of WE is important, as treatment with thiamine in the acute stages can reverse neurologic and cardiovascular abnormalities 3.
• Thiamine repletion leads to rapid clinical improvement and can prevent irreversible neurologic sequelae, including Korsakoff syndrome 4.
• Patients with malabsorption due to gastrointestinal disorders have an increased risk of thiamine deficiency, and folate deficiency can worsen this vitamin malabsorption 6.
• Administration of prophylactic multivitamin supplements is recommended in patients at risk as routine clinical practice 6.
• The best treatment for Korsakoff's syndrome is timely recognition of Wernicke's encephalopathy and appropriate intervention and prevention 5.

Key Differences

• WE is usually associated with alcoholism and malnutrition, while beriberi is often related to dietary deficiency alone 3.
• WE can result from dietary deficiency alone, while thiamine deficiency associated with alcohol misuse/dependence may require higher doses of thiamine for successful treatment 5.
• The damage caused by the combination of thiamine deficiency and alcohol metabolism probably interferes with adequate thiamine transport at a number of sites in the body, including the blood-brain barrier 5.