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I completed my medical school and background EM training from India (Christian Medical College, Vellore and Apollo Hospitals, Hyderabad) where I worked for 4 years. Following this, I devoted (with all my heart) about 1.5 years to do US Medical Licensing Exams. My stint towards an EM Residency in States did not work but it took me to places and it has been quite a journey. I then relocated to London, England to work as a Registrar (Non-Trainee) in A&E. This gave me an opportunity to better understand NHS, EM training pathways and more importantly the EM Mindsets in the United Kingdom. 

Currently, I am pursuing Higher Specialist Training in Emergency Medicine at South East Scotland Deanery where I have the honour and privilege of training under some of the most innovative brains in the field of Emergency Medicine. Over the past few years, I have realised that LEARNING and UNLEARNING (which can be challenging!) is equally important to deliver cutting edge care to our patients.And through this blog, I aspire to disseminate knowledge, assist trainees with exams and stay up to date with contemporary EM literature. I have always been an avid FOAMed supporter because FOAMed has always played an indispensable role during my training. 


Lakshay Chanana
ST4 EM Trainee 
Edinburgh, Scotland
drlakshayem@gmail.com

Monday, June 12, 2017

Wernicke's Encephalopathy

Wernicke’s encephalopathy (WE) is a neuropsychiatric disorder which arises as a result of thiamine deficiencyIn 80% of cases, the diagnosis is not made clinically prior to autopsy and inadequate treatment can leave the patient with permanent neurological sequelae and can possibly lead to Korsakoff syndrome. Therefore over-dignosis is preferred over under-diagnosis. Just like several other disease entities, Wernicke’s encephalopathy can be precipitated by other clinical diseases such as sepsis. 


Many physicians consider this only restricted to alcoholics which is not the case. Especially among non-alcoholics, the diagnosis is missed. 

WE is a result of thiamine deficiency, which can occur in ANY nutritionally deficient state. 


Classic Triad

The classic clinical triad of Wernicke’s encephalopathy consists of mental status changes, ophthalmoplegia, and gait ataxia. Complete triad is present only in about 10% cases. Other signs of disease such as hypothermia, vestibular dysfunction, and other ocular abnormalities can be presentOut of the eye signs, nystagmus is the most common ocular abnormality, not complete ophthalmoplegia. 

Reliance on the presence of the clinical triad as the sole criterion for disease is often inadequate and may lead to under diagnosis.



Risk Factors for WE:
  • Alcohol Abuse (inadequate dietary intake, reduced GI absorption, and decreased hepatic storage)
  • AIDS
  • Malignancy
  • Hyperemesis Gravidarum
  • Post Surgical Patients
  • Post Gastric Bypass



Thiamine Deficiency Syndromes





Why thiamine is so important?
Thiamine is a cofactor for several essential enzymes. Because thiamine-dependent enzymes play an important role in cerebral energy use, deficiency may initiate tissue injury by inhibiting metabolism in brain regions with high metabolic requirements. A decrease in their activity may lead to increased buildup of toxic intermediates. Lactate accumulation occurs both in the brain and serum because pyruvate cannot enter the Krebs cycle. 


Malnutrition + elevated lactate - Think thiamine deficiency


CNS lesions

The lesions of Wernicke’s encephalopathy occur in a symmetrical distribution in structures surrounding the third ventricle, aqueduct, and fourth ventricle. MRI is the imaging of choice. The mammillary bodies are involved in up to 80% of cases; atrophy of these structures is specific for Wernicke’s encephalopathy. However, empiric treatment is a norm in ED. 


Korsakoff Syndrome
Korsakoff syndrome refers to a persistent state of mental dysfunction characterized by memory impairment associated with confabulation. 


Differential Diagnosis
  • Intracranial Hemmorhage
  • Stroke
  • Cerebral Venous Thrombosis
  • Delirium Tremens
  • Hepatic Encephalopathy
  • Intracranial Space Occupying Lesions
  • Cerebellar Disease
  • Meningitis
  • Marchiafava-Bignami disease (demyelination of the corpus callous due to nutritional deficiencies)

Treatment

Low suspicion of disease - a minimum of 100 mg IV
Highly suspected disease - 500 mg IV

Administration of thiamine improves disease to some degree in almost all cases; however, persistent neurologic dysfunction is common. 


All patients presumed to have Wernicke’s Encephalopathy or at risk of developing Wernicke’s Encephalopathy should receive two pairs* of vials of Pabrinex in 100 ml of crystalloid i.v. over 30 minutes initially in A&E.


*(1 pair = ampoule 1 + ampoule 2). Pabrinex is available as 5ml or 10ml pairs of ampoules. 


IV thrice daily dosing is generally continued for 3-5 days for an established diagnosis and then oral Thiamine 100mg OD is continued for a month. On extremely rare occasions, Thiamine may cause allergic reactions and anaphylaxis. 


Glucose before thiamine Myth!

Iatrogenic exacerbation of Wernicke’s encephalopathy can occur with prolonged glucose or carbohydrate loading in the absence of adequate thiamine. A single acute administration of glucose does not appear to cause this effect. Urgent administration of glucose should not be withheld pending thiamine administration. 


IV Fluids to sober them up?
There is no evidence that intravenous fluids expedite sobriety in patients with acute alcohol intoxication. Read more on REBELEM and St.Emlyn's


References:
  1. Reuler JB, Girard DE, Cooney TG. Current concepts. Wernicke’s encephalopathy. N Engl J Med. 1985;312:1035-1039.
  2. Watson AJ, Walker JF, Tomkin GH, et al. Acute Wernicke’s encephalopathy precipitated by glucose loading. Ir J Med Sci. 1981;150:301-303.
  3. Zimitat C, Nixon PF. Glucose loading precipitates acute encephalopathy in thiamin-deficient rats. Metab Brain Dis. 1999; 14:1-20.
  4. Zimitat C, Nixon PF. Glucose induced IEG expression in the thiamin-deficient rat brain. Brain Res. 2001;892:218-227. 59. Hack JB, Hoffman RS. Thiamine before glucose to prevent Wernicke encephalopathy: examining the conventional wisdom. JAMA. 1998;279:583-584. 
  5. https://www.medicines.org.uk/emc/medicine/6571
  6. Donnino MW, Vega J, Miller J, Walsh M. Myths and misconceptions of Wernicke’s encephalopathy: what every emergency physician should know. Annals of emergency medicine. 2007 Dec 31;50(6):715-21.


Posted by:

              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic

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