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Remember to Take Your Vitamins…
EM:RAP COMMENTARY
Remember to Take Your Vitamins. Andrew Grock, MD; Jeff Lapoint, DO; Paul Jhun, MD; Mel Herbert, MD 0196-0644/$-see front matter Copyright © 2016 by the American College of Emergency Physicians. http://dx.doi.org/10.1016/j.annemergmed.2016.07.029
SEE RELATED ARTICLE, P. e65. [Ann Emerg Med. 2016;68:389-391.] Editor’s note: Annals has partnered with Hippo Education and EM:RAP, enabling our readers without subscriptions to Hippo EM Board Review or EM:RAP to enjoy their commentary on Annals publications. This article did not undergo peer review and may not reflect the view and opinions of the editorial board of Annals of Emergency Medicine. There are no financial relationships or other consideration between Annals and Hippo Education, EM:RAP or its authors.
ANNALS CASE A 45-year-old man with a medical history of schizophrenia presented to the emergency department (ED) with vague complaints, weakness, and fatigue, as well as bleeding gums. His symptoms had developed gradually ever since he had difficulty with mobility from a fall 5 weeks ago. He denied illicit drugs or prescription medications. On examination, he was mildly tachycardic, appeared dehydrated and cachectic, and had bleeding gums, as well as multiple perifollicular hyperkeratotic papules with surrounding hemorrhage. Diagnosis? Scurvy.1 VITAMINS: WE TAKE THEM FOR GRANTED Okay, once you stop saying, “Yarr, matey,” let go of your finger hook, and open that one eye, let’s dust off some cobwebs in your mind to talk about vitamin deficiencies. Now, although popular culture would lead you to believe that scurvy, or vitamin C deficiency, is a disease unique to pirates who sail the 7 seas or to those from developing countries, malnutrition and vitamin deficiencies in chronically alcohol-dependent patients are surprisingly more common than you think. For example, one necropsy study on deceased chronically alcohol-dependent patients found pathologic findings of Wernicke’s encephalopathy in 59% of patients.2 Even more concerning, one study showed that in 80% to 90% of these patients, the diagnosis was missed!3 This month, we’d love to show you what you may have been missing every time Johnny Walker comes through those revolving doors.M&M (morbidity and mortality) style. M&Ms do come in a variety of flavors! Volume 68, no. 3 : September 2016
CASE 1 An elderly, daily chronic drinker presents to your ED after a fall, with unknown loss of consciousness or head trauma. He reports tripping over something, but is unsure what. After getting a snarky call back from your radiologist for your patient’s 20th negative head computed tomography (CT) result, the patient finally metabolizes to freedom and is stable for discharge. Out of sight, out of mind.until he arrives later that night because of another fall over another unknown object. A more thorough history reveals decreased night vision. Diagnosis? Vitamin A deficiency. Keep in mind that the liver contains 90% of the body’s vitamin A reserves and secretes it into the body when needed. In chronic alcoholism, decreased nutritional intake and ethanol uptake induce and accelerate vitamin A breakdown, leading to low vitamin A levels and decreased night vision, even blindness!4 Talk about adding insult to injury for cirrhotic, alcohol-dependent patients! They’re already at increased risk of falls, as well as increased risk of subdural hematomas from those falls. Tack on some vitamin A deficiency so they can’t see at night! Other adverse effects of low vitamin A in chronically alcohol-dependent patients include increased risk of lung and gastrointestinal cancers and pulmonary infections.4,5 Sure, kick ’em while they’re down, right? Now, you would think that treatment would be fairly straightforward. If only it were so simple. In a cruel catch22 that would make Joseph Heller proud, giving too much vitamin A to a patient who actively abuses alcohol can lead to vitamin A–induced liver toxicity.4 Geez, these patients just can’t seem to get a break. So if you clinically suspect vitamin A deficiency and are second-guessing the safety of your unreliable patient, admission is reasonable while you wait for those send-out laboratory results to come back. Once vitamin A deficiency is confirmed, published dosing guidelines recommend vitamin A 100,000 units intramuscularly once daily for 3 days, followed by 50,000 units intramuscularly once daily for 14 days, and oral supplementation of 10,000 to 20,000 units by mouth once daily for 2 months (best of luck on that compliance).6 Annals of Emergency Medicine 389
EM:RAP Commentary
CASE 2 A 56-year-old lifetime, daily, heavy drinker presents with altered mental status. On examination, he is ataxic and confused, which seems related to his presumed intoxication. Curiously, though, his physical examination reveals bilateral lateral rectus palsies. His 21st head CT result is unremarkable and, despite hours in the ED, his mental status is not improving. Diagnosis? Ah, yes, I think we all know this one. The classic bizz-buzz vitamin deficiency in chronically alcoholdependent patients: thiamine, or vitamin B1, deficiency presenting as Wernicke’s encephalopathy. The mnemonic WACO (pronounced “wacko”), or “Wernicke’s Ataxia Confusion Ophthalmoplegia,” can be used, although this triad is present in only one third of cases.7 Buyer beware, especially because the ophthalmoplegia doesn’t always scream obvious! with gaze palsies, but can be subtle with nystagmus or ptosis (sigh). The classic scenario is when you’re ready to street someone who should be sober, when you notice a wide-based gait and on testing see that the patient can’t even come close on tandem gait testing. If this improves after 500 mg of thiamine intravenously and some glucose, you nailed the diagnosis. Have skeptical hospitalists? Video the before-and-after gait change, drop the mic, and walk away. Sadly, even with treatment, half of patients recover incompletely and are left with ataxia and other gait disturbances.6 Don’t forget that Wernicke’s partner in crime, Korsakoff syndrome, presents with memory loss and confabulation.8 Last, it’s important to know that there isn’t a definitive laboratory or imaging test you can order to diagnose Wernicke’s encephalopathy.... We can actually be clinicians on this one and this is all you.9 Treatment for our patient above is mildly complicated because oral thiamine absorption is variable in the presence of ethanol and the literature provides multiple recommendations for dosing.9 Now, if you suspect Wernicke’s encephalopathy, remember that your typical banana bag with a prophylactic dose of 100 mg of thiamine intravenously doesn’t cut it. Wernicke’s encephalopathy requires thiamine 500 mg intravenously up front, before any glucose load (in the form of dextrose or food). The Royal College of Physicians guideline recommends thiamine 500 mg intravenously every 8 hours for at least 3 days, followed by oral supplementation.10 It’s also important to know that improvement in signs and symptoms isn’t always fast and dramatic, so don’t be discouraged if it doesn’t work instant miracles like your favorite commercial thrombolytic for strokes (oh, snap! yes we just went there). Oh, and while we’re on the topic of banana bags, routine use of this medical Jamba Juice is not indicated. Let’s be honest with ourselves: most of our 390 Annals of Emergency Medicine
Grock et al
chronically alcohol-dependent patients are not severely vitamin deficient. Banana bags are an expensive way to make expensive urine. Reserve the magic juice for those you clinically suspect have a nutritional deficiency.11 CASE 3 A 43-year-old woman, well known to your ED for chronic alcohol use, presents after a Good Samaritan called 911 for “abnormal behavior.” History is difficult because she is making grandiose claims, pacing up and down the hallway and threatening staff members. On examination, she has an erythematous, scaly rash to her face and other sun-exposed areas. Diagnosis? Yes, we’re baiting you to go for alcohol abuse with a sunburn. Unfortunately, you should have listened to your inner Admiral Ackbar: “It’s a trap!” Although classic vitamin B3 (niacin) deficiency (also known as pellagra) presents with the “3 D’s” (diarrhea, dermatitis, and dementia), there is an alcohol version of pellagra. Chronically alcohol-dependent patients can get pellagra as a result of nutritional deficiency, but their version of pellagra can include altered mental status. Alcoholic pellagra encephalopathy is characterized by pigmented rash of sunexposed areas, bright red tongue, diarrhea, memory loss, and disorientation. What’s more is that this presentation can also be mistaken for psychiatric pathology or alcohol withdrawal.12 A 1981 study found 20 of 74 (27%) of chronic alcohol dependent patients who died in a hospital had neuropathologic features of pellagra.13,14 To make matters worse, vitamin replacement with B1, B6, and B12 may aggravate or precipitate alcoholic pellagra encephalopathy. Wow! Now that’s a bad M&M. Treatment consists of 100 mg of oral niacinamide every 6 hours until resolution of the major signs and symptoms (often several days), followed by 50 mg every 8 to 12 hours until skin lesions heal.11,15 WAIT. BEER DOESN’T HAVE VITAMIN C? To be fair, there are quite a few other important vitamin deficiencies (vitamin B6 and magnesium, to name a few) that you may see in your chronically alcohol-dependent patients, but we’re running out of paper space. So let’s come full circle and finish this by saying a few words on scurvy. Chronically alcohol-dependent patients are at increased risk for vitamin C deficiency as a result of (you guessed it) limited nutritional intake. Patients typically present with generalized fatigue, poor wound healing, and increased bleeding, which can range from petechiae and ecchymoses to perifollicular hemorrhages, bleeding gums, or even hemarthrosis.5 Treatment is (surprise, surprise) vitamin C supplementation. Unfortunately, the body has decreasing Volume 68, no. 3 : September 2016
Grock et al
ability to absorb vitamin C at higher doses, with less than 50% absorbed at doses greater than 1 g. The standard dose varies from 200 to 1,000 mg daily by mouth, intravenously, intramuscularly, and subcutaneously until body stores are replenished, although patients have apparently made complete recoveries on doses as low as 6.5 mg per day, which you can easily get by eating an orange (or if you’re a British sailor wannabe, a lime).7,16 REMEMBER YOUR ABCs Pulling these 3 cases together, here’s a mnemonic to help you remember some key points: “You can’t get an A if you can’t see.” (Ask about night blindness, found in vitamin A deficiency.) “Don’t “Be 1” WACO.” (Think vitamin B1 deficiency and Wernicke’s¼Ataxia, Confusion, and Ophthalmoplegia.) “Three days of “sunburn” in a patient who thinks he’s 3 people?” (Remember the 3 D’s of vitamin B3 deficiency: diarrhea, dermatitis, and dementia.) “If you “C” bleeding, such as petechial, ecchymosis, bleeding gums, or perifollicular hemorrhage, think vitamin C.” BACK TO THE CASE The patient’s vitamin C level was undetectable! He received 500 mg vitamin C intravenously for 2 days and then 500 mg by mouth daily for 1 week, with significant improvement in symptoms and physical examination results. Now if only there were vitamin-enhanced beers. Oh, wait, there are.... Google it. Author affiliations: From the Department of Emergency Medicine, Keck School of Medicine of the University of Southern California and the Los Angeles County þ USC Medical Center, Los Angeles, California (Grock, Herbert); the Department of Emergency Medicine, Kaiser Permanente San Diego, San Diego, California (Lapoint); and the Department of Emergency Medicine, University of California San Francisco, San Francisco, California (Jhun). Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article as per ICMJE conflict
Volume 68, no. 3 : September 2016
EM:RAP Commentary of interest guidelines (see www.icmje.org). The authors have stated that no such relationships exist and provided the following details: Dr. Jhun reports other from Hippo Education, Inc., outside of the submitted work. Dr. Herbert reports other from EM:RAP and Hippo Education, Inc., outside of the submitted work.
REFERENCES 1. Berrevoets M, Bleeker-Rovers C. Man with bleeding gums and skin rash. Ann Emerg Med. 2016;68:e65-e66. 2. Naidoo DP, Bramdev A, Cooper K. Autopsy prevalence of Wernicke’s encephalopathy in alcohol-related disease. S Afr Med J. 1996;86: 1110-1112. 3. Thomson AD. Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. Alcohol Alcohol Suppl. 2000;35:2-7. 4. Leo MA, Lieber CS. Alcohol, vitamin A, and beta-carotene: adverse interactions, including hepatotoxicity and carcinogenicity. Am J Clin Nutr. 1999;69:1071-1085. 5. Ginsburg BY. Goldfrank’s Toxicologic Emergencies, 10th Edition. New York, NY: McGraw-Hill; 2015:Chapter 47. 6. Lexicomp® Online. Hudson, OH: Lexi-Comp Inc; 2016. Accessed July 15, 2016. 7. Hemphill J III, Smith WS, Gress DR. Neurologic critical care, including hypoxic-ischemic encephalopathy, and subarachnoid hemorrhage. In: Kasper D, Fauci A, Hauser S, et al, eds. Harrison’s Principles of Internal Medicine, 19th Edition. New York, NY: McGraw-Hill; 2015. 8. Russell RM, Suter PM. Vitamin and trace mineral deficiency and excess. In: Kasper D, Fauci A, Hauser S, et al, eds. Harrison’s Principles of Internal Medicine, 19th Edition. New York, NY: McGraw-Hill; 2015. 9. Thomson AD, Marshall EJ, Bell D. Time to act on the inadequate management of Wernicke’s encephalopathy in the UK. Alcohol Alcohol. 2013;48:4-8. 10. Thomson AD, Cook CCH, Touquet R, et al. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and emergency department. Alcohol Alcohol. 2002;37:513-521. 11. Li SF, Jacob J, Feng J, et al. Vitamin deficiencies in acutely intoxicated patients in the ED. Am J Emerg Med. 2008;26:792-795. 12. Lopez M, Olivares JM, Berrios GE. Pellagra encephalopathy in the context of alcoholism: review and case report. Alcohol Alcohol. 2014;49:38-41. 13. Cook CC, Hallwood PM, Thomson AD. B vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol Alcohol. 1998;33:317-336. 14. Ishii N, Nishihara Y. Pellagra among chronic alcoholics: clinical and pathological study of 20 necropsy cases. J Neurol Neurosurg Psychiatry. 1981;44:209-215. 15. Hegyi J, Schwartz RA, Hegyi V. Pellagra: dermatitis, dementia, and diarrhea. Int J Dermatol. 2004;43:1-5. 16. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol. 1999;41:895-906; quiz 907-910.
Annals of Emergency Medicine 391
Remember to Take Your Vitamins. Andrew Grock, MD; Jeff Lapoint, DO; Paul Jhun, MD; Mel Herbert, MD 0196-0644/$-see front matter Copyright © 2016 by the American College of Emergency Physicians. http://dx.doi.org/10.1016/j.annemergmed.2016.07.029
SEE RELATED ARTICLE, P. e65. [Ann Emerg Med. 2016;68:389-391.] Editor’s note: Annals has partnered with Hippo Education and EM:RAP, enabling our readers without subscriptions to Hippo EM Board Review or EM:RAP to enjoy their commentary on Annals publications. This article did not undergo peer review and may not reflect the view and opinions of the editorial board of Annals of Emergency Medicine. There are no financial relationships or other consideration between Annals and Hippo Education, EM:RAP or its authors.
ANNALS CASE A 45-year-old man with a medical history of schizophrenia presented to the emergency department (ED) with vague complaints, weakness, and fatigue, as well as bleeding gums. His symptoms had developed gradually ever since he had difficulty with mobility from a fall 5 weeks ago. He denied illicit drugs or prescription medications. On examination, he was mildly tachycardic, appeared dehydrated and cachectic, and had bleeding gums, as well as multiple perifollicular hyperkeratotic papules with surrounding hemorrhage. Diagnosis? Scurvy.1 VITAMINS: WE TAKE THEM FOR GRANTED Okay, once you stop saying, “Yarr, matey,” let go of your finger hook, and open that one eye, let’s dust off some cobwebs in your mind to talk about vitamin deficiencies. Now, although popular culture would lead you to believe that scurvy, or vitamin C deficiency, is a disease unique to pirates who sail the 7 seas or to those from developing countries, malnutrition and vitamin deficiencies in chronically alcohol-dependent patients are surprisingly more common than you think. For example, one necropsy study on deceased chronically alcohol-dependent patients found pathologic findings of Wernicke’s encephalopathy in 59% of patients.2 Even more concerning, one study showed that in 80% to 90% of these patients, the diagnosis was missed!3 This month, we’d love to show you what you may have been missing every time Johnny Walker comes through those revolving doors.M&M (morbidity and mortality) style. M&Ms do come in a variety of flavors! Volume 68, no. 3 : September 2016
CASE 1 An elderly, daily chronic drinker presents to your ED after a fall, with unknown loss of consciousness or head trauma. He reports tripping over something, but is unsure what. After getting a snarky call back from your radiologist for your patient’s 20th negative head computed tomography (CT) result, the patient finally metabolizes to freedom and is stable for discharge. Out of sight, out of mind.until he arrives later that night because of another fall over another unknown object. A more thorough history reveals decreased night vision. Diagnosis? Vitamin A deficiency. Keep in mind that the liver contains 90% of the body’s vitamin A reserves and secretes it into the body when needed. In chronic alcoholism, decreased nutritional intake and ethanol uptake induce and accelerate vitamin A breakdown, leading to low vitamin A levels and decreased night vision, even blindness!4 Talk about adding insult to injury for cirrhotic, alcohol-dependent patients! They’re already at increased risk of falls, as well as increased risk of subdural hematomas from those falls. Tack on some vitamin A deficiency so they can’t see at night! Other adverse effects of low vitamin A in chronically alcohol-dependent patients include increased risk of lung and gastrointestinal cancers and pulmonary infections.4,5 Sure, kick ’em while they’re down, right? Now, you would think that treatment would be fairly straightforward. If only it were so simple. In a cruel catch22 that would make Joseph Heller proud, giving too much vitamin A to a patient who actively abuses alcohol can lead to vitamin A–induced liver toxicity.4 Geez, these patients just can’t seem to get a break. So if you clinically suspect vitamin A deficiency and are second-guessing the safety of your unreliable patient, admission is reasonable while you wait for those send-out laboratory results to come back. Once vitamin A deficiency is confirmed, published dosing guidelines recommend vitamin A 100,000 units intramuscularly once daily for 3 days, followed by 50,000 units intramuscularly once daily for 14 days, and oral supplementation of 10,000 to 20,000 units by mouth once daily for 2 months (best of luck on that compliance).6 Annals of Emergency Medicine 389
EM:RAP Commentary
CASE 2 A 56-year-old lifetime, daily, heavy drinker presents with altered mental status. On examination, he is ataxic and confused, which seems related to his presumed intoxication. Curiously, though, his physical examination reveals bilateral lateral rectus palsies. His 21st head CT result is unremarkable and, despite hours in the ED, his mental status is not improving. Diagnosis? Ah, yes, I think we all know this one. The classic bizz-buzz vitamin deficiency in chronically alcoholdependent patients: thiamine, or vitamin B1, deficiency presenting as Wernicke’s encephalopathy. The mnemonic WACO (pronounced “wacko”), or “Wernicke’s Ataxia Confusion Ophthalmoplegia,” can be used, although this triad is present in only one third of cases.7 Buyer beware, especially because the ophthalmoplegia doesn’t always scream obvious! with gaze palsies, but can be subtle with nystagmus or ptosis (sigh). The classic scenario is when you’re ready to street someone who should be sober, when you notice a wide-based gait and on testing see that the patient can’t even come close on tandem gait testing. If this improves after 500 mg of thiamine intravenously and some glucose, you nailed the diagnosis. Have skeptical hospitalists? Video the before-and-after gait change, drop the mic, and walk away. Sadly, even with treatment, half of patients recover incompletely and are left with ataxia and other gait disturbances.6 Don’t forget that Wernicke’s partner in crime, Korsakoff syndrome, presents with memory loss and confabulation.8 Last, it’s important to know that there isn’t a definitive laboratory or imaging test you can order to diagnose Wernicke’s encephalopathy.... We can actually be clinicians on this one and this is all you.9 Treatment for our patient above is mildly complicated because oral thiamine absorption is variable in the presence of ethanol and the literature provides multiple recommendations for dosing.9 Now, if you suspect Wernicke’s encephalopathy, remember that your typical banana bag with a prophylactic dose of 100 mg of thiamine intravenously doesn’t cut it. Wernicke’s encephalopathy requires thiamine 500 mg intravenously up front, before any glucose load (in the form of dextrose or food). The Royal College of Physicians guideline recommends thiamine 500 mg intravenously every 8 hours for at least 3 days, followed by oral supplementation.10 It’s also important to know that improvement in signs and symptoms isn’t always fast and dramatic, so don’t be discouraged if it doesn’t work instant miracles like your favorite commercial thrombolytic for strokes (oh, snap! yes we just went there). Oh, and while we’re on the topic of banana bags, routine use of this medical Jamba Juice is not indicated. Let’s be honest with ourselves: most of our 390 Annals of Emergency Medicine
Grock et al
chronically alcohol-dependent patients are not severely vitamin deficient. Banana bags are an expensive way to make expensive urine. Reserve the magic juice for those you clinically suspect have a nutritional deficiency.11 CASE 3 A 43-year-old woman, well known to your ED for chronic alcohol use, presents after a Good Samaritan called 911 for “abnormal behavior.” History is difficult because she is making grandiose claims, pacing up and down the hallway and threatening staff members. On examination, she has an erythematous, scaly rash to her face and other sun-exposed areas. Diagnosis? Yes, we’re baiting you to go for alcohol abuse with a sunburn. Unfortunately, you should have listened to your inner Admiral Ackbar: “It’s a trap!” Although classic vitamin B3 (niacin) deficiency (also known as pellagra) presents with the “3 D’s” (diarrhea, dermatitis, and dementia), there is an alcohol version of pellagra. Chronically alcohol-dependent patients can get pellagra as a result of nutritional deficiency, but their version of pellagra can include altered mental status. Alcoholic pellagra encephalopathy is characterized by pigmented rash of sunexposed areas, bright red tongue, diarrhea, memory loss, and disorientation. What’s more is that this presentation can also be mistaken for psychiatric pathology or alcohol withdrawal.12 A 1981 study found 20 of 74 (27%) of chronic alcohol dependent patients who died in a hospital had neuropathologic features of pellagra.13,14 To make matters worse, vitamin replacement with B1, B6, and B12 may aggravate or precipitate alcoholic pellagra encephalopathy. Wow! Now that’s a bad M&M. Treatment consists of 100 mg of oral niacinamide every 6 hours until resolution of the major signs and symptoms (often several days), followed by 50 mg every 8 to 12 hours until skin lesions heal.11,15 WAIT. BEER DOESN’T HAVE VITAMIN C? To be fair, there are quite a few other important vitamin deficiencies (vitamin B6 and magnesium, to name a few) that you may see in your chronically alcohol-dependent patients, but we’re running out of paper space. So let’s come full circle and finish this by saying a few words on scurvy. Chronically alcohol-dependent patients are at increased risk for vitamin C deficiency as a result of (you guessed it) limited nutritional intake. Patients typically present with generalized fatigue, poor wound healing, and increased bleeding, which can range from petechiae and ecchymoses to perifollicular hemorrhages, bleeding gums, or even hemarthrosis.5 Treatment is (surprise, surprise) vitamin C supplementation. Unfortunately, the body has decreasing Volume 68, no. 3 : September 2016
Grock et al
ability to absorb vitamin C at higher doses, with less than 50% absorbed at doses greater than 1 g. The standard dose varies from 200 to 1,000 mg daily by mouth, intravenously, intramuscularly, and subcutaneously until body stores are replenished, although patients have apparently made complete recoveries on doses as low as 6.5 mg per day, which you can easily get by eating an orange (or if you’re a British sailor wannabe, a lime).7,16 REMEMBER YOUR ABCs Pulling these 3 cases together, here’s a mnemonic to help you remember some key points: “You can’t get an A if you can’t see.” (Ask about night blindness, found in vitamin A deficiency.) “Don’t “Be 1” WACO.” (Think vitamin B1 deficiency and Wernicke’s¼Ataxia, Confusion, and Ophthalmoplegia.) “Three days of “sunburn” in a patient who thinks he’s 3 people?” (Remember the 3 D’s of vitamin B3 deficiency: diarrhea, dermatitis, and dementia.) “If you “C” bleeding, such as petechial, ecchymosis, bleeding gums, or perifollicular hemorrhage, think vitamin C.” BACK TO THE CASE The patient’s vitamin C level was undetectable! He received 500 mg vitamin C intravenously for 2 days and then 500 mg by mouth daily for 1 week, with significant improvement in symptoms and physical examination results. Now if only there were vitamin-enhanced beers. Oh, wait, there are.... Google it. Author affiliations: From the Department of Emergency Medicine, Keck School of Medicine of the University of Southern California and the Los Angeles County þ USC Medical Center, Los Angeles, California (Grock, Herbert); the Department of Emergency Medicine, Kaiser Permanente San Diego, San Diego, California (Lapoint); and the Department of Emergency Medicine, University of California San Francisco, San Francisco, California (Jhun). Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article as per ICMJE conflict
Volume 68, no. 3 : September 2016
EM:RAP Commentary of interest guidelines (see www.icmje.org). The authors have stated that no such relationships exist and provided the following details: Dr. Jhun reports other from Hippo Education, Inc., outside of the submitted work. Dr. Herbert reports other from EM:RAP and Hippo Education, Inc., outside of the submitted work.
REFERENCES 1. Berrevoets M, Bleeker-Rovers C. Man with bleeding gums and skin rash. Ann Emerg Med. 2016;68:e65-e66. 2. Naidoo DP, Bramdev A, Cooper K. Autopsy prevalence of Wernicke’s encephalopathy in alcohol-related disease. S Afr Med J. 1996;86: 1110-1112. 3. Thomson AD. Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. Alcohol Alcohol Suppl. 2000;35:2-7. 4. Leo MA, Lieber CS. Alcohol, vitamin A, and beta-carotene: adverse interactions, including hepatotoxicity and carcinogenicity. Am J Clin Nutr. 1999;69:1071-1085. 5. Ginsburg BY. Goldfrank’s Toxicologic Emergencies, 10th Edition. New York, NY: McGraw-Hill; 2015:Chapter 47. 6. Lexicomp® Online. Hudson, OH: Lexi-Comp Inc; 2016. Accessed July 15, 2016. 7. Hemphill J III, Smith WS, Gress DR. Neurologic critical care, including hypoxic-ischemic encephalopathy, and subarachnoid hemorrhage. In: Kasper D, Fauci A, Hauser S, et al, eds. Harrison’s Principles of Internal Medicine, 19th Edition. New York, NY: McGraw-Hill; 2015. 8. Russell RM, Suter PM. Vitamin and trace mineral deficiency and excess. In: Kasper D, Fauci A, Hauser S, et al, eds. Harrison’s Principles of Internal Medicine, 19th Edition. New York, NY: McGraw-Hill; 2015. 9. Thomson AD, Marshall EJ, Bell D. Time to act on the inadequate management of Wernicke’s encephalopathy in the UK. Alcohol Alcohol. 2013;48:4-8. 10. Thomson AD, Cook CCH, Touquet R, et al. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and emergency department. Alcohol Alcohol. 2002;37:513-521. 11. Li SF, Jacob J, Feng J, et al. Vitamin deficiencies in acutely intoxicated patients in the ED. Am J Emerg Med. 2008;26:792-795. 12. Lopez M, Olivares JM, Berrios GE. Pellagra encephalopathy in the context of alcoholism: review and case report. Alcohol Alcohol. 2014;49:38-41. 13. Cook CC, Hallwood PM, Thomson AD. B vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol Alcohol. 1998;33:317-336. 14. Ishii N, Nishihara Y. Pellagra among chronic alcoholics: clinical and pathological study of 20 necropsy cases. J Neurol Neurosurg Psychiatry. 1981;44:209-215. 15. Hegyi J, Schwartz RA, Hegyi V. Pellagra: dermatitis, dementia, and diarrhea. Int J Dermatol. 2004;43:1-5. 16. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol. 1999;41:895-906; quiz 907-910.
Annals of Emergency Medicine 391