Wernicke encephalopathy
Unfortunately, Wernicke’s encephalopathy is often undiagnosed – presumably because it is relatively uncommon and has a variable clinical presentation - Sara Kohnke
image by: Mothposs Studio
HWN Suggests
Don’t seek, don’t find: The diagnostic challenge of Wernicke’s encephalopathy
WE is a serious and underdiagnosed disease. Historically thought to be a disease of alcohol misuse, it is now well recognized that many conditions can cause WE. WE after bariatric surgery is increasingly common and clinical biochemists have a unique opportunity to make sure the diagnosis is considered when a patient presents with unexplained neurological features. The diagnosis of WE is difficult and requires integration of clinical signs,
MRI appearance and biochemistry results, and is complicated by the urgent need to start treatment before confirming the diagnosis. Thiamine is a safe and effective treatment and should be given prophylactically to high-risk groups. The prognosis…
Resources
Management
Signs and symptoms are generally unreliable in the diagnosis. The classic triad of encephalopathy, ophthalmoplegia, and ataxia is present in only ~15% of cases. Among non-alcoholic patients with Wernicke encephalopathy, the triad is even less common. There is no well-defined dosing regimen, nor high-quality evidence. Articles often recommend the following: i) 500 mg IV TID for 2-3 days, followed by ii) 200-500 mg IV daily for ~5 days or until clinical improvement ceases, followed by iii) oral thiamine (e.g., 100-500 mg PO TID)
Take Home Points
Wernicke encephalopathy is characterized by ataxia, altered mental status and ophthalmoplegia but patients are unlikely to have all these components. Suspect Wernicke encephalopathy in any patient that is at risk of malnutrition or malabsorption and has any one of the classic symptoms. Prophylactic administration of thiamine 100 mg IV/IM to at risk patients can prevent development of the disease. Once Wernicke encephalopathy has developed, it must be treated with high-dose, IV thiamine.
Thiamine
... thiamine 500 mg IV infusion over 30 minutes, 3 times daily for 3 days. then thiamine 250 mg IV or IM, daily for 3 to 5 days or until clinical improvement ceases
Wernicke encephalopathy: a medical emergency
There is insufficient evidence from randomized controlled trials to dictate optimal treatment for Wernicke encephalopathy caused by alcohol misuse. Although European guidelines recommend acute treatment with at least 200 mg thiamine intravenously or intramuscularly three times daily for two to three days, the efficacy of higher doses requires further study. Dramatic resolution of neurologic signs signals adequate treatment and confirms the clinical diagnosis of Wernicke encephalopathy.
Wernicke Encephalopathy—Clinical Pearls
Wernicke encephalopathy (WE) was first described by Carl Wernicke in 1881. WE is caused by thiamine deficiency. Alcoholism is the most common etiologic factor associated with WE in the United States, but it can occur in any patient with a nutritional deficiency state such as hyperemesis gravidarum, intestinal obstruction, and malignancy. WE is a clinical diagnosis.
Wernicke’s Encephalopathy Diagnosis and Treatment
Although thiamine replacement therapy is the recommended treatment for Wernicke’s encephalopathy, randomized control trials have not provided sufficient evidence to suggest an optimal dose, frequency, route or duration of treatment.
Wernicke’s encephalopathy — from basic science to clinical practice. Part 1: Understanding the role of thiamine
Wernicke’s encephalopathy (WE) is an acute neuropsychiatric state. Untreated, WE can lead to coma or death, or progress to Korsakoff syndrome (KS). KS is a dementia characterized by irreversible loss of anterograde memory.1,2 Thiamine (vitamin B1) deficiency lies at the heart of this condition. Hence, understanding thiamine is essential for understanding the etiology of WE, its prophylaxis and treatment.
Wernicke’s Encephalopathy: Increasing Clinician Awareness of This Serious, Enigmatic, Yet Treatable Disease
Wernicke’s encephalopathy is a clinical diagnosis made on a syndromic level. At present, there are no biomarkers that can be used to formulate or confirm the diagnosis. If Wernicke’s encephalopathy is suspected, it is critical to initiate immediate treatment with intravenous thiamine,
Non–Alcohol-Related Wernicke’s Encephalopathy: Diagnosis and Treatment
Have you ever wondered whether, and why, Wernicke’s encephalopathy (WE) can develop in someone who does not have an alcohol use disorder? Have you been uncertain about how best to treat WE? If you have, the following case vignette and discussion should prove useful.
Time to Act on the Inadequate Management of Wernicke's Encephalopathy in the UK
Chronic alcohol misusers may present acutely to hospital in a state of intoxication/withdrawal, which can mask the confusion and ataxia of an underlying WE episode. These patients may also be abusive to staff, which can result in failure to offer the attention and treatment needed. A number of conditions may coexist with alcohol misuse disorders, and these co-morbidities can increase the risk of developing WE.
Myths and Misconceptions of Wernicke’s Encephalopathy: What Every Emergency Physician Should Know
First described in 1881, Wernicke’s encephalopathy continues to be an unrecognized and often misunderstood disease. The cause of Wernicke’s encephalopathy is thiamine deficiency as a result of any nutritionally deficient state, though many physicians erroneously consider this disease to be confined only to alcoholics. Unfortunately, the syndrome is most often recognized only on autopsy, especially among nonalcoholics. Despite advances in magnetic resonance imaging, Wernicke’s encephalopathy remains primarily a clinical diagnosis. The common clinical findings include mental status changes, ocular dysfunction, and gait ataxia.
Her Legs Would Barely Follow Her Brain. Then She Saw Double.
Wernicke’s encephalitis was named after a German physician, Carl Wernicke, who first described the wide gait, eye-muscle deficiencies and confusion that characterize this vitamin deficiency. Thiamine’s job in the body is to break down and use carbohydrates and fats. Without it, the body runs out of gas, and nothing can get done. Vitamin B1 doesn’t last long in the body, so it’s important to replace what is lost regularly.
Put Thiamine in Liquor
The disease can begin over a period of weeks. Ocular muscles become weak or paralyzed. The sense of balance is affected, sometimes so badly that it is impossible to walk. Amnesia and general confusion take over. Finally, the victim may lapse into a coma and die.
Research Check: can even moderate drinking cause brain damage?
And it’s well established heavy drinking over ten years or more can cause significant cognitive difficulties. These include disorders such as Korsakoff’s Syndrome and Wernicke’s Encephalopathy, where memory and other essential thinking functions, as well as motor co-ordination, are severely and permanently damaged. But what about those of us who have two to three drinks a night?
The Effects of Chronic Heavy Drinking on Brain Function Are Underdiagnosed
Experts say alcohol-related brain damage is underdiagnosed and often confused with Alzheimer’s disease, other forms of dementia or just getting older.
Think Like a Doctor: Dazed and Confused Solved
Though alcoholism is the most common condition linked to Wernicke’s, it is not the only one. Diseases that cause extended periods of fasting or persistent vomiting have also been linked to the disorder. Newest among these are patients who have a history of gastric surgery – particularly weight loss surgery. Several recent studies suggest that the disorder is often unrecognized.
Don’t seek, don’t find: The diagnostic challenge of Wernicke’s encephalopathy
In the past, Wernicke’s encephalopathy was described almost exclusively in the alcohol-dependent population. However, in current times, Wernicke’s encephalopathy is also well recognized in many other patient groups, including patients following bariatric surgery, gastrointestinal surgery, cancer and pancreatitis.
Alcohol.org
Discover why drinking too much is usually credited as a direct cause of Wernicke-Korsakoff syndrome and how alcohol abuse increases your chances.
MedlinePlus
Wernicke encephalopathy and Korsakoff syndrome are different conditions that often occur together. Both are due to brain damage caused by a lack of vitamin B1.
NINDS
Wernicke's encephalopathy is a degenerative brain disorder caused by the lack of thiamine (vitamin B1). It may result from alcohol abuse, dietary deficiencies, prolonged vomiting, eating disorders, or the effects of chemotherapy. B1 deficiency causes damage to the brain's thalamus and hypothalamus.
StatPearls
Wernicke encephalopathy (WE) is an acute neurological condition characterized by a clinical triad of ophthalmoparesis with nystagmus, ataxia, and confusion. This is a life-threatening illness caused by thiamine deficiency, which primarily affects the peripheral and central nervous systems. This disorder should be differentiated from Korsakoff syndrome which is preventable and is usually suspected as a consequence of at least one episode of Wernicke’s encephalopathy.
Introducing Stitches!
Your Path to Meaningful Connections in the World of Health and Medicine
Connect, Collaborate, and Engage!
Coming Soon - Stitches, the innovative chat app from the creators of HWN. Join meaningful conversations on health and medical topics. Share text, images, and videos seamlessly. Connect directly within HWN's topic pages and articles.