My guest is Suraj Rajasimhan PharmD – Suraj is our brilliant EM Clinical Pharmacist and is an indispensable part of the ED. Follow him @Sraj726
Today we talk about the “Banana Bag”
You can enjoy the podcast here:
The Banana Bag – what is it? It usually contains dextrose, thiamine, folate, multivitamins, +/_ magnesium. Why? Acute alcohol intoxication is often accompanied by acute and chronic nutritional deficiencies
Alcoholic ketoacidosis should be suspected in patients with binge drinking and poor nutrition (acutely – ie no meals recently). Do not need to be an alcoholic to get it. Alcohol binge in a healthy patient with few meals can leade to AKA. Symptoms include nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension. Urine ketones may be falsely negative or only trace positive in alcoholic ketoacidosis. Alcohol metabolism depletes NAD, leaves excess NADH (so called reducing metabolic state). This skews ketoacids / beta-hydroxybutyrate and alpha-ketoglutarate toward beta-hydroxybutyrate. Although
AKA patients have depleted glycogen stores, serum glucose level can be often within the normal range. Lactic acidosis forms from a combination of dehydration and the impaired lactate dehydrogenase thus unable to convert lactate to pyruvate, thus impairing gluconeogenesis.
What is WE and Korsakoff Psychosis?
Wernicke’s encephalopathy and Korsakoff syndrome are linked disease states that are often under recognized in the critically ill and acutely intoxicated. Typically referred to as “Dry Beriberi” because of their lack of cardiovascular symptoms. Wet beriberi is presents with congestive heart failure from dilated cardiomyopathy.
Thiamine B1 is a cofactor for several essential enzymes in the Krebs cycle and the pentose phosphate pathway – alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase, and transketolase. alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase. The result is increases lactic acid production and impaired glucose metabolism especially in the CNS
Autopsy studies suggest that 12% of alcoholics have a Wernicke’s encephalopathy. Alcohol affects thiamine uptake and utilization. Also found in prolonged starvation, hyperemesis gravidarum, bariatric surgery (bariatric beriberi), and (HIV)/ (AIDS).
The most typical clinical manifestation was an altered mental status in patients with identified Wernicke’s encephalopathy at autopsy. Only 20% of these patients have received a clinical diagnosis of WE. Only 10% had a complete triad of symptoms of altered mental status, ophthalmoplegia, and ataxia.
Making the diagnosis
Thiamine levels are difficult to turn around and there is not a thiamine level that will result in WE in all patients. Thiamine levels are reduced in up to 80% of alcohol users.
Thus clinical recognition and prophylactic treatment are necessary.
According to the European Federation of Neurologic Societies the criteria for Wernicke’s encephalopathy he and Korsakoff syndrome should have 2 of the following 4 features
1) a nutritional deficiency is present (they look malnourished),
2) ocular abnormalities,
3) ataxia (i.e. cerebellar dysfunction), or
4) mental status changes or memory impairment
Unfortunately alter mental status occurs in virtually all patients who are acutely intoxicated or admitted to intensive care
The condition is not always 100% reversible, although ataxia and ophthalmoplegia usually resolve within hours after receiving thiamine if given early. Confusion improves but memory and learning difficulties often persist. Progression to Korsakoff psychosis usually results in permanent neurologic dysfunction.
|Supplement||Evidence level for routine use in critically ill patients||Signs and symptoms in alcohol withdrawal (you can apply to acute alcohol intoxication)||Dose|
|Dextrose||Adequate||nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension||D5 ½ NS run at maintenance (do not delay for thiamine)|
|Thiamine||Adequate||Altered MS, WE, KP, metabolic dysfunction||200 – 500 mg IV every 8 hrs|
|Folic Acid||Reasonable but weak||Megaloblastic anemia, confusion, depression, psychosis, seizures, sleep disturbance||0.4 to 1 mg day|
|Magnesium||Reasonable but weak||QT prolongation, altered MS, seizures, tremors, hyper-reflexia||64/ mg/kg on day 1, followed by 32 mg/kg on days 2 to 4|
What do we recommend?
First of all – Keep the Dextrose.
All the rest is patient specific – but start with clinical evaluation and a high index of suspicion.
Wernicke’s Triad = mental status changes, ophthalmoplegia, and ataxia
Other sx: hypothermia, vestibular dysfunction, nystagmus
These are vague and can be difficult to differentiate or use for diagnosis amongst alcoholic cerebellar degeneration and other comorbidities
Patients with chronic alcohol use are at risk for thiamine deficiency due to:
Decreased dietary intake
Decreased conversion to active form
Poor Absorption of Oral Thiamine
In HEALTHY adults, the MAX absorbed from a 30 mg dose was 4.5 mg
Thiamine absorption in alcoholics is reduced to 30-98% below the lower limit of normal
In alcoholics, 5 mg of a 100 mg TID PO regimen is estimated to be absorbed in 24 hours
How Much Thiamine?
100 MG IV dose in banana bags was chosen arbitrarily
Landmark study in patients with confirmed WE receiving 50-100 mg IV thiamine/day
84% developed Korsakoff Syndrome and long-term impairments
Minimum dose recommended to prevent/treat WE:
Royal College of Physicians: >500 mg IV QD or BID
European Federation of Neurological Societies: 200 mg IV TID
One study suggested that at least 200 mg IM thiamine daily may be required to improve symptoms
Thiamine is transported into the brain by both an active, saturable mechanism AND a passive mechanism
Goal would be to achieve a steep concentration gradient between serum and CNS
This is the justification for high IV doses
Single 50 mg IV dose has plasma ½ life of 1.5 hours and returns to initial levels within 6-12 hours
Optimal dosing interval = 8-12 hours
200 mg dose only costs $3
Take the thiamine out of the routine banana bag! If you are concerned about the possibility of WE – treat with the full dose of 200 mg at least.
200-500 mg IV Q8h for at least 72 hours or until WE is ruled out
Folic acid (folate)
Folate 400 -1000 mcg IV for several days
“Conversion to oral therapy is reasonable if no concomitant alcohol consumption will occur”
Magnesium 1 mEq/kg on the first day (in divided doses) and 0.5 mEq/kg/day over the next 3 days
Deficiency is common since EtOH use increases magnesium elimination
No substantial treatment effect
Better to target specific deficiencies
Cost $10 per vial
Flannery AH, Adkins DA, Cook AM. Unpeeling the evidence for the banana bag: evidence based recommendations for the management of alcohol-associated vitamin and electrolyte deficiencies in the ICU. Critical Care Medicine 2016:44;1545-1552
Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patietns with alcohol use disorders. Internal Medicine Journal 2014:44;911-915.
Glavin R, Brathen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. European Journal of Neurology 2010:17;1408-1418.
Thomson AD; Cook CC; Touquet R; Henry JA; The Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and Emergency Department. Alcohol Alcohol. 2002; 37(6):513-21 (ISSN: 0735-0414)