Beriberi: Difference between revisions
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==Background== | ==Background== | ||
*Dry Beriberi: neuro | *Dry Beriberi: neuro symptoms caused by thiamine deficiency | ||
*Wet Beriberi: cardiac | *Wet Beriberi: cardiac symptoms caused by thiamine deficiency | ||
*Infantile Beriberi: neuro/cardiac | *Infantile Beriberi: neuro/cardiac symptoms caused by thiamine deficiency in <1 year old infant | ||
===Causes=== | ===Causes=== | ||
*Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement | *Anything that causes [[thiamine deficiency|thiamine (vitamin B1) deficiency]]: poor dietary intake, malabsorption, increased metabolic requirement | ||
**Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis | **Chronic [[alcoholism]], dieting/fasting/starvation, [[anorexia nervosa|anorexia]], [[vomiting]]/[[diarrhea]], unbalanced TPN, GI surgery, malignancy, [[dialysis complications|dialysis]], [[AIDS]], [[IBD]], [[pancreatitis]], liver disease, [[thyrotoxicosis]] | ||
===Pathophysiology=== | ===Pathophysiology=== | ||
*Thiamine is a cofactor for enzymes required in: | *Thiamine is a cofactor for enzymes required in: | ||
** | **Krebs cycle | ||
**Pentose phosphate pathway | **Pentose phosphate pathway | ||
**Alpha-ketoglutarate dehydrogenase | **Alpha-ketoglutarate dehydrogenase | ||
** | **Pyruvate dehydrogenase. | ||
*Because thiamine is an important cofactor in critical pathways for energy production, deficiency results in lactic acidosis and alteration of brain metabolism. | *Because thiamine is an important cofactor in critical pathways for energy production, deficiency results in lactic acidosis and alteration of brain metabolism. | ||
*Thiamine is also important for lipid metabolism and may affect myelin sheath formation. This may explain peripheral neuropathy symptoms in dry beriberi. | *Thiamine is also important for lipid metabolism and may affect myelin sheath formation. This may explain peripheral neuropathy symptoms in dry beriberi. | ||
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==Clinical Features== | ==Clinical Features== | ||
===Dry Beriberi=== | ===Dry Beriberi=== | ||
*Symmetrical peripheral neuropathy (motor and sensory) mostly distal extremities | *Symmetrical peripheral neuropathy ([[weakness|motor]] and [[numbness|sensory]]) mostly distal extremities | ||
===Wet Beriberi=== | ===Wet Beriberi=== | ||
*CHF, high output heart failure, cardiomegaly, peripheral edema, tachycardia, DOE/PND/orthopnea | *[[CHF]], [[high output heart failure]], cardiomegaly, peripheral edema, [[tachycardia]], [[SOB|DOE/PND/orthopnea]] | ||
*Can include neuropathy seen in Dry Beriberi | *Can include neuropathy seen in Dry Beriberi | ||
===Infantile Beriberi=== | ===Infantile Beriberi=== | ||
*CHF, cardiomegaly, tachycardia, cyanosis, dyspnea, weight loss, marasmus, vomiting, loud cry, nystagmus, seizure | *[[CHF]], cardiomegaly, [[tachycardia]], [[hypoxia|cyanosis]], [[shortness of breath (peds)|dyspnea]], [[failure to thrive (peds)|weight loss]], marasmus, [[nausea and vomiting (peds)|vomiting]], loud cry, [[nystagmus]], [[seizure (peds)|seizure]] | ||
===Bariatric Beriberi=== | ===Bariatric Beriberi=== | ||
*Occurs 1-3 months post- | *Occurs 1-3 months post-[[weight loss surgery complications|bariatric surgery]] | ||
*Causes are multifactorial, including low nutritional intake, poor baseline nutrition, persistent vomiting, malabsorption | *Causes are multifactorial, including low nutritional intake, poor baseline [[malnutrition|nutrition]], persistent [[vomiting]], malabsorption | ||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
{{ | {{Vitamin deficiencies DDX}} | ||
== | ==Evaluation== | ||
*Clinical diagnosis | *Clinical diagnosis | ||
== | ==Management== | ||
''If you suspect Beriberi then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high'' | ''If you suspect Beriberi then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high'' | ||
#Thiamine 50- | #[[Thiamine]] 50-100mg IV/IM q day x 7-14 days, then 10mg PO q day until complete recovery | ||
#Magnesium; hypomagnesemic state may be resistant to thiamine administration | #[[Magnesium]]; hypomagnesemic state may be resistant to thiamine administration | ||
#Multivitamin (at risk for other vitamin deficiencies) | #Multivitamin (at risk for other vitamin deficiencies) | ||
*Give thiamine BEFORE glucose in patients requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly | *Give thiamine BEFORE glucose in patients requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly | ||
==Disposition== | |||
==Prevention== | |||
{{Vitamin prophylaxis for ETOH}} | |||
==Disposition== | ==Disposition== | ||
==See Also== | ==See Also== | ||
*[[Thiamine]] | |||
*[[Thiamine deficiency]] | *[[Thiamine deficiency]] | ||
==References== | ==References== | ||
# Donnino, Michael, et al. “Myths and misconceptions of wernicke’s encephalopathy: what every emergency physician should know.” Annals of emergency medicine. 2007. Vol 50, no 6. Pages 715-721. | #Donnino, Michael, et al. “Myths and misconceptions of wernicke’s encephalopathy: what every emergency physician should know.” Annals of emergency medicine. 2007. Vol 50, no 6. Pages 715-721. | ||
# Sechi, GianPietro; Serra, Alessandro. “Wernicke’s encephalopathy: new clnical settings and recent advances in diagnosis and management.” Neurology. Vol 6, May 2007. Pages 442-455 | #Sechi, GianPietro; Serra, Alessandro. “Wernicke’s encephalopathy: new clnical settings and recent advances in diagnosis and management.” Neurology. Vol 6, May 2007. Pages 442-455 | ||
[[Category: | <references/> | ||
[[Category: | [[Category:Neurology]] | ||
[[Category:Cardiology]] |
Revision as of 16:51, 16 October 2019
Background
- Dry Beriberi: neuro symptoms caused by thiamine deficiency
- Wet Beriberi: cardiac symptoms caused by thiamine deficiency
- Infantile Beriberi: neuro/cardiac symptoms caused by thiamine deficiency in <1 year old infant
Causes
- Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement
- Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis
Pathophysiology
- Thiamine is a cofactor for enzymes required in:
- Krebs cycle
- Pentose phosphate pathway
- Alpha-ketoglutarate dehydrogenase
- Pyruvate dehydrogenase.
- Because thiamine is an important cofactor in critical pathways for energy production, deficiency results in lactic acidosis and alteration of brain metabolism.
- Thiamine is also important for lipid metabolism and may affect myelin sheath formation. This may explain peripheral neuropathy symptoms in dry beriberi.
Clinical Features
Dry Beriberi
Wet Beriberi
- CHF, high output heart failure, cardiomegaly, peripheral edema, tachycardia, DOE/PND/orthopnea
- Can include neuropathy seen in Dry Beriberi
Infantile Beriberi
- CHF, cardiomegaly, tachycardia, cyanosis, dyspnea, weight loss, marasmus, vomiting, loud cry, nystagmus, seizure
Bariatric Beriberi
- Occurs 1-3 months post-bariatric surgery
- Causes are multifactorial, including low nutritional intake, poor baseline nutrition, persistent vomiting, malabsorption
Differential Diagnosis
Vitamin deficiencies
- Vitamin A deficiency
- Vitamin B deficiencies
- Vitamin B1 deficiency (Thiamine)
- Vitamin B3 deficiency (Pellagra)
- Vitamin B9 deficiency (Folate)
- Vitamin B7 deficiency (Biotin)
- Vitamin B12 deficiency
- Vitamin C deficiency (Scurvy)
- Vitamin D deficiency (Rickets)
- Vitamin E deficiency
- Vitamin K deficiency
- Zinc deficiency
Evaluation
- Clinical diagnosis
Management
If you suspect Beriberi then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high
- Thiamine 50-100mg IV/IM q day x 7-14 days, then 10mg PO q day until complete recovery
- Magnesium; hypomagnesemic state may be resistant to thiamine administration
- Multivitamin (at risk for other vitamin deficiencies)
- Give thiamine BEFORE glucose in patients requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly
Disposition
Prevention
Vitamin Prophylaxis for Chronic alcoholics
- At risk for thiamine deficiency, but no symptoms: thiamine 100mg PO q day
- Give multivitamin PO; patient at risk for other vitamin deficiencies
Banana bag
The majority of chronic alcoholics do NOT require a banana bag[1][2]
- Thiamine 100mg IV
- Folate 1mg IV (cheaper PO)
- Multivitamin 1 tab IV (cheaper PO)
- Magnesium sulfate 2mg IV
- Normal saline as needed for hydration
Disposition
See Also
References
- Donnino, Michael, et al. “Myths and misconceptions of wernicke’s encephalopathy: what every emergency physician should know.” Annals of emergency medicine. 2007. Vol 50, no 6. Pages 715-721.
- Sechi, GianPietro; Serra, Alessandro. “Wernicke’s encephalopathy: new clnical settings and recent advances in diagnosis and management.” Neurology. Vol 6, May 2007. Pages 442-455