Continuing Education Activity

Thiamine (vitamin B1) is the first vitamin identified and a critical cofactor in cellular energy metabolism, nerve conduction, and myelin maintenance. Vitamin B1 deficiency is a common, underrecognized cause of multisystem illness that spans cardiovascular, neurologic, and metabolic complications across inpatient and outpatient settings, including dry and wet beriberi and the potentially life-threatening neurologic manifestations of Wernicke encephalopathy and Wernicke–Korsakoff syndrome. This activity reviews the dietary sources of thiamine, mechanisms of deficiency, and populations at highest risk, including individuals with chronic alcohol use disorder, malnutrition, bariatric surgery, diuretic use, and increased metabolic demand. 

This course also explores the recognition of early and advanced clinical features of thiamine deficiency, relevant laboratory and imaging findings, and evidence-based treatment strategies. Participants will also gain an understanding of empiric parenteral thiamine in at-risk patients, appropriate dosing regimens, and prevention during refeeding or alcohol withdrawal. This activity for healthcare professionals is designed to enhance the learner's competence in identifying vitamin B1 deficiency, performing the recommended evaluation, and implementing an appropriate interprofessional approach to manage this condition to reduce morbidity and mortality and improve neurologic and cardiovascular outcomes through informed, patient-centered care.

Objectives:

• Identify patients at high risk for vitamin B1 deficiency who warrant empiric parenteral treatment.
• Assess clinical manifestations of thiamine deficiency affecting the neurologic and cardiovascular systems.
• Determine when empiric parenteral thiamine therapy is indicated in high-risk patients.
• Coordinate management strategies with interprofessional team members to improve care and outcomes in patients with vitamin B1 deficiency.

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Introduction

Thiamine, identified many years ago as the first vitamin and designated vitamin B1, functions as a critical catalyst in energy generation through the decarboxylation of branched-chain amino acids and alpha-ketoacids. This vitamin also acts as a coenzyme for transketolase reactions in the form of thiamine pyrophosphate. An additional, not fully defined role involves the propagation of nerve impulses and the maintenance of the myelin sheath.[1] This water-soluble vitamin occurs naturally in meat, beef, pork, legumes, whole grains, and nuts. In contrast, milled rice and processed grains contain minimal thiamine because manufacturing processes remove much of the vitamin. Certain foods, including tea, coffee, raw fish, and shellfish, contain thiaminases, which function as enzymes that degrade thiamine.

Thiamine deficiency affects the cardiovascular, nervous, and immune systems and commonly manifests as wet beriberi, dry beriberi, or Wernicke-Korsakoff syndrome. Worldwide prevalence remains highest in populations relying on polished rice or milled cereals as staple foods and among individuals with chronic alcohol use disorder. Dry beriberi presents with symmetrical peripheral neuropathy, whereas wet beriberi presents with high-output heart failure. Wernicke-Korsakoff syndrome may involve central nervous system manifestations such as gait abnormalities, altered mental status, and ocular findings.[2] Wernicke encephalopathy represents the most severe acute neurologic manifestation of thiamine deficiency and may progress to Korsakoff syndrome without timely thiamine replacement. Detailed discussion of diagnosis and management appears in the dedicated StatPearls article on Wernicke encephalopathy and Wernicke–Korsakoff syndrome.[3]

Etiology

Thiamine deficiency can result from any of the following:

• Poor intake

  • Diets primarily high in polished rice/processed grains
  • Chronic alcoholism
  • Parenteral nutrition without adequate thiamine supplementation
  • Gastric bypass surgery
• Poor absorption

  • Malnutrition
  • Gastric bypass surgery [4]
  • Malabsorption syndrome
• Increased loss 

  • Diarrhea
  • Hyperemesis gravidarum
  • Diuretic use
  • Renal replacement therapy
• Increased thiamine utilization

  • Pregnancy
  • Lactation
  • Hyperthyroidism
  • Refeeding syndrome
• Drugs leading to thiamine deficiency
• Diuretics [5]

Epidemiology

Worldwide, vitamin B1 deficiency is primarily due to inadequate dietary intake, particularly in diets that are mainly polished rice and grains. In Western countries, vitamin B1 deficiency most commonly presents in patients suffering from alcoholism or chronic illness. Special populations of individuals also at risk for vitamin B1 deficiency include pregnant women, those requiring parental feeding, individuals who have undergone bariatric surgery, those with overall poor nutritional status, and patients on chronic diuretic therapy, as it increases urinary losses.[6] The deficiency of this vitamin in women can cause infantile beriberi, which this article will not specifically address.[7]

Pathophysiology

Depletion of thiamine stores typically occurs within about 4 weeks after cessation of intake, after which clinical symptoms begin to emerge.

Dry Beriberi

Dry beriberi develops with central nervous system involvement and most often results from inadequate nutritional intake. Neurologic manifestations include impaired reflexes and symmetrical motor and sensory deficits affecting the extremities. Pathologic changes include loss of myelin without evidence of acute inflammation.

Wernicke-Korsakoff Syndrome

Wernicke encephalopathy represents another form of dry beriberi and manifests as an acute thiamine-deficiency–related encephalopathy. Impaired activity of thiamine pyrophosphate–dependent enzymes, including pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and transketolase, leads to selective injury in regions with high metabolic demand, eg, the mammillary bodies, medial thalami, periaqueductal gray, tectal plate, and cerebellar vermis.[8]

Clinical progression follows a characteristic sequence beginning with nausea and vomiting, followed by horizontal nystagmus, ocular nerve palsy, fever, ataxia, and worsening mental impairment that may culminate in Korsakoff syndrome. Meaningful improvement remains possible only before the development of Korsakoff syndrome, and fewer than 50% of affected patients experience substantial recovery despite treatment.

Wet Beriberi

Wet beriberi involves the cardiovascular system and results in impaired cardiac function with subsequent edema and fluid retention. Myocardial dysfunction arises from an overuse injury. Wet beriberi constitutes a medical emergency and may lead to death within days without prompt treatment. Thiamine supplementation supports gradual recovery, although most patients require aggressive supportive care in an ICU setting.

History and Physical

Clinical History

Evaluation for vitamin B1 deficiency commonly involves a history of poor nutritional intake, excessive alcohol consumption, or membership in high-risk populations, including pregnant women, individuals who have undergone bariatric surgery, patients receiving prolonged diuretic therapy, and those with overall poor nutritional status.

Early manifestations of vitamin B1 deficiency include anorexia, irritability, and difficulty with short-term memory. Progressive thiamine deficiency may lead to sensory loss in the extremities and symptoms of heart failure, including swelling of the hands or feet and chest pain related to demand ischemia. Additional complaints may include vertigo, diplopia, and worsening memory impairment. Family members or close contacts often report confusion or behaviors consistent with confabulation.

Physical Exam

Dry beriberi demonstrates findings consistent with symmetric peripheral neuropathy, including both motor and sensory deficits, along with diminished reflexes. Wet beriberi reflects cardiovascular compromise caused by impaired myocardial energy metabolism and dysautonomia, with physical findings, eg, dilated cardiomyopathy, tachycardia, high-output congestive heart failure, and peripheral edema. Overlapping clinical features frequently occur between wet and dry beriberi, and paresthesias may serve as an initial presenting symptom in either condition.

Wernicke encephalopathy classically presents with a triad of ocular abnormalities, including nystagmus and ophthalmoplegia, altered mental status, and gait disturbances (eg, ataxia). The complete triad appears infrequently, and clinicians should presume Wernicke encephalopathy in at-risk patients with compatible findings. Prompt initiation of empiric parenteral thiamine remains recommended once suspicion arises and should not await laboratory or imaging confirmation.[9] Wernicke encephalopathy, accompanied by memory impairment and psychosis with confabulation, aligns with the diagnosis of Wernicke–Korsakoff syndrome.[1][10] Please see StatPearls' companion resource, "Wernicke-Korsakoff Syndrome," for further information.  

Evaluation

Detection of vitamin B1 deficiency depends on careful integration of clinical history and physical examination findings, followed by laboratory evaluation for diagnostic confirmation.[11]

Laboratory Studies

Laboratory assessment may include a functional enzymatic assay of transketolase activity, with measurements obtained before and after the addition of thiamine pyrophosphate. A stimulation response greater than 25% indicates abnormal enzyme activity. Quantification of thiamine or its phosphorylated esters in serum or blood may be performed using high-performance liquid chromatography. Measurement of whole-blood thiamine diphosphate by this method reflects tissue stores more accurately than serum thiamine levels.[11]

Urine testing remains available but lacks reliability for assessing total-body thiamine status. Vitamin B1 deficiency may also lead to metabolic acidosis secondary to lactate accumulation. Serum vitamin B1 levels provide limited reliability as indicators of overall stores and fail to exclude deficiency in patients with suspected Wernicke encephalopathy.

Additional Diagnostic Studies

Additional diagnostic studies may be warranted based on clinical presentation and comorbidities, eg, transthoracic echocardiography or thyroid-stimulating hormone measurement in cases of new-onset heart failure.

Radiographic evaluation with brain MRI may provide supportive evidence for Wernicke encephalopathy, most often demonstrating bilateral T2 or FLAIR hyperintensity involving the medial thalami, mammillary bodies, periaqueductal region, and tectal plate. Normal findings on early MRI do not exclude the diagnosis, and imaging should not delay empiric thiamine administration in patients with suspected Wernicke encephalopathy.[12][13] Please see StatPearls' companion resource, "Wernicke-Korsakoff Syndrome," for further information on evaluation.  

Treatment / Management

Acute Thiamine D eficiency

Immediate intervention remains critical in patients with acute vitamin B1 deficiency with clinical features of cardiovascular or neurologic conditions. Administer parenteral thiamine before or concurrently with any glucose or nutritional support in at-risk patients, without awaiting laboratory or imaging confirmation.[14][7] A guideline-supported regimen involves 200 mg of thiamine administered intravenously (IV) or orally 3 times daily until clinical symptoms resolve or improvement plateaus. Following this initial phase, the patient should transition to 10 mg/day of oral thiamine until full recovery is expected.[9][7][9]

An alternative high-dose regimen commonly used in clinical practice includes 500 mg IV, infused over 30 minutes, 2 to 3 times daily for 2 days, followed by 250 mg IV or intramuscularly (IM) daily for 3 to 5 days, and subsequent continuation with high-dose oral thiamine.[15] The selection of a dosing strategy should consider illness severity, timing of nutrition or glucose administration, and local institutional protocols. Please see StatPearls' companion resource, "Wernicke-Korsakoff Syndrome," for further information on diagnostic criteria, imaging patterns, treatment, and follow-up.

Refeeding and Alcohol Withdrawal Prophylaxis

For refeeding or alcohol withdrawal prophylaxis, administer thiamine before or concurrently with glucose or nutritional support in malnourished, alcohol-dependent, or other high-risk patients to prevent Wernicke encephalopathy. Several professional societies recommend 100 to 200 mg/day (approximately 2 mg/kg, maximum 100–200 mg/day) around the time of nutrition initiation.[16]

Differential Diagnosis

The differential diagnosis for vitamin B1 deficiency is broad, given the nonspecific symptoms that may occur in the initial stages and the extensive range of cardiac and nervous system dysfunction associated with thiamine deficiency, including:

• Delirium
• Depression
• Folic acid deficiency
• Hyperthyroidism
• Cardiomyopathy secondary to other causes, eg, alcoholic or diabetic heart disease
• Delusional disorder
• Nerve entrapment syndromes
• Other psychiatric disorders
• Diabetic ketoacidosis

Prognosis

The overall prognosis for patients with vitamin B1 deficiency is good, as this condition is easily treatable and most signs and symptoms resolve with thiamine supplementation. Cardiac dysfunction seen in wet beriberi can be expected to improve within 24 hours of initiation of treatment. Symptoms of dry beriberi may improve or resolve. Ocular signs and encephalopathy often improve with prompt therapy, but established Korsakoff syndrome is frequently only partially reversible despite adequate repletion.[17] Other symptoms of thiamine deficiency, eg, anorexia and irritability, are expected to improve gradually.

Complications

Thiamine deficiency can result in severe and potentially life-threatening complications affecting the nervous, cardiovascular, and immune systems. Neurologic manifestations include dry beriberi, characterized by symmetrical peripheral neuropathy and loss of myelin, and Wernicke encephalopathy, which can progress to Wernicke–Korsakoff syndrome if untreated, causing confusion, ataxia, ocular abnormalities, and long-term cognitive impairment. Cardiovascular involvement, as seen in wet beriberi, can lead to high-output heart failure, edema, and dilated cardiomyopathy, often requiring intensive supportive care. Early recognition and prompt thiamine supplementation prevent these complications, and no known toxicities occur with repletion, although rare cases of anaphylaxis or bronchospasm have been reported with high-dose intravenous administration.

Deterrence and Patient Education

Population-level data highlight preventable thiamine deficiencies in high-risk groups, emphasizing the importance of systematic screening and supplementation strategies.[18] Patient education for individuals with alcohol use disorder should include information on Korsakoff syndrome, given that excessive alcohol intake constitutes a significant cause of thiamine deficiency. Education should occur within the context of a structured substance use treatment program and integrate a comprehensive, interprofessional team approach to maximize the patient’s likelihood of success. Patients need to be educated about eating a healthy diet, cease tobacco, and abstaining from alcohol. The dietitian should educate the patient on foods that are rich in thiamine. Only through an interprofessional team approach can the morbidity of thiamine deficiency be reduced.

Management of other causes of beriberi requires addressing the underlying etiology. Once the primary condition has been corrected, patients should adopt a nutritionally appropriate diet that provides therapeutic thiamine levels to support recovery.[19] High-risk patients, including those with alcohol use disorder, malnutrition, postbariatric surgery, or undergoing dialysis, should receive education on the importance of early thiamine supplementation and the dangers of administering glucose without concurrent thiamine. Such interventions can prevent the development of Wernicke encephalopathy and reduce the risk of long-term cognitive impairment.

Enhancing Healthcare Team Outcomes

Thiamine (vitamin B1) plays a critical role in energy metabolism, nerve conduction, and myelin maintenance. Deficiency most commonly arises in populations with poor nutritional intake, chronic alcohol use, post-bariatric surgery, malnutrition, or dialysis dependence. Clinical manifestations range from dry beriberi, with peripheral neuropathy, to wet beriberi, causing high-output heart failure, and Wernicke encephalopathy, which can progress to Wernicke–Korsakoff syndrome, resulting in irreversible cognitive impairment if untreated. Early recognition and prompt administration of parenteral thiamine, especially before or with glucose or nutritional support, prevent serious neurologic and cardiovascular complications. Laboratory testing and imaging may support diagnosis, but empiric treatment should not be delayed, and education on thiamine supplementation remains vital for at-risk populations.

Optimal care requires coordinated efforts across the interprofessional team. Physicians, advanced practitioners, and general practitioners play a key role in diagnosing deficiency, initiating empiric thiamine therapy, and managing underlying conditions. Nurses monitor patient response, provide education, and ensure the timely administration of supplements. Pharmacists advise on dosing, route, and potential interactions, while dietitians guide therapeutic nutrition. Effective communication among team members enhances patient-centered care, improves safety by preventing delayed treatment, and supports team performance through coordinated management strategies tailored to individual patient risk factors.

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Disclosure: Kimberly Wiley declares no relevant financial relationships with ineligible companies.

Disclosure: Jagkirat Singh declares no relevant financial relationships with ineligible companies.