- Email: [email protected]
Wernicke’s Encephalopathy After Gastric Bypass that Masqueraded as Acute Psychosis: A Case Report
CASE REPORTS
Wernicke’s Encephalopathy After Gastric Bypass that Masqueraded as Acute Psychosis: A Case Report Robert W. Worden, MEd, and Henry M. Allen, DO College of Osteopathic Medicine, Oklahoma State University, Tulsa, Oklahoma Wernicke’s encephalopathy was originally described more than a decade ago. It has been reported after many causes of malnutrition. This case presents a patient with thiamine deficiency after gastric bypass, although unusual in itself, further complicating the case was the initial diagnosis of acute psychosis that was scheduled for electroconvulsive therapy. After recognition and intervention, the patient was successfully treated with thiamine replacement and parenteral nutrition. (Curr Surg 63: 114-116. © 2006 by the Association of Program Directors in Surgery.) KEY WORDS: thiamine, gastric bypass, polyneuropathy, wer-
nicke encephalopathy, beriberi
INTRODUCTION Wernicke’s encephalopathy (WE) is classically associated with chronic alcoholism. However, there have been an increased number of reports of WE in association with severe reduction in dietary intake.1 This syndrome is the result of a deficiency of vitamin B1 or thiamine (an essential coenzyme in intermediate carbohydrate metabolism). It classically presents with the neurological triad of ophthalmoplegia, ataxia, and mental changes. The authors report a case of a woman that developed both WE and “dry” beriberi after undergoing roux-en-y gastric bypass (RYGBP) for morbid obesity, but her condition was initially diagnosed as acute psychosis.
CASE REPORT This case is unusual in that the condition of the patient was initially diagnosed as acute psychosis and she was admitted to the psychiatric unit where she was being considered for electroconvulsive therapy. The patient was a 32-year-old black woman who underwent laparoscopic RYGBP. Preoperatively, her weight was 282 lbs.
Correspondence: Inquiries to Robert W. Worden, MEd, P.O. Box 542, Crescent, OK 73028; fax: (815) 333-4821; e-mail: [email protected]
114
with a body mass index (BMI) of 44. She was neurologically intact, with no focal deficits, and with the exception of hypertension, hypercholesteremia, and obstructive sleep apnea, she was in good health. The operative procedure created a 20-ml gastric pouch with an 80-cm efferent limb. Postoperatively, the patient reported almost continual vomiting. She was instructed on an appropriate diet and was placed on an oral multivitamin. At 1 month, the patient had lost 54 pounds. At 15 weeks after surgery, the patient returned to the surgeons office unable to walk. She was lethargic and tachycardic. At that point she was admitted for intravenous hydration and evaluation. She was subsequently transferred to a psychiatric facility for what was thought to be a conversion disorder. She was scheduled for electroconvulsive therapy. Because of her profound medical illnesses, she was transferred to an acute care facility for evaluation. At the time of admission, 17 weeks postoperative, the patient was confused, disoriented, tachycardic, and was found to have iron-deficient anemia. From the physical examination, a lumbar puncture was performed. The spinal fluid protein was elevated at 159 mg/dl (normal 12 to 60). It was thought that the patient might have a viral encephalopathy. Vitamin studies, to include B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin), were ordered, as well as thyroid studies. Before obtaining the specimen for testing, the patient was given 100 mg of intramuscular thiamine; therefore, the thiamine result of 1256 pg/ml (normal 211 to 911) was not diagnostic. After the administration of 3 doses of thiamine 100 mg intramuscularly, the patient did regain some muscle strength; however, she still had some retrograde and anterograde amnesia. She was then transferred to a skilled nursing facility. The patient subsequently deteriorated and returned to the acute care facility at 21 weeks postoperative. At this time, she had peripheral neuropathy in a stocking distribution to the level of the tibial tuberosity bilaterally. She complained of an extreme burning sensation. Her deep tendon reflexes were decreased, as was her muscle strength in all extremities. She was also noted to have a lateral nystagmus. Throughout the previous 6 weeks, the patient continued to
CURRENT SURGERY • © 2006 by the Association of Program Directors in Surgery Published by Elsevier Inc.
0149-7944/06/$30.00 doi:10.1016/j.cursur.2005.06.004
have nausea and vomiting. She continued to be unable to walk, and the amnesia persisted. A barium swallow study with a small bowel follow-through was obtained and was reported as normal. After an interdisciplinary discussion with the gastric surgeon, the nutritionist, and the internist, it was felt that the patient was malnourished and vitamin deficient. The patient was started on intramuscular thiamine and total parenteral nutrition with a multivitamin and trace elements. After several days of thiamine, the patient’s neurological symptoms began to resolve slowly. She regained some muscle strength, the nystagmus resolved, but the peripheral neuropathy continued. The patient was started on venlafaxine and gabapentin for the peripheral neuropathy symptoms. She was also transferred to a rehabilitation facility for continued therapy.
DISCUSSION A BMI of 25 or greater is considered overweight. A BMI of 30 or higher is considered obese, and morbid obesity is present with a BMI of 40 or higher. The prevalence of obesity has increased from 1962 to 2000. According to the 2000 Census, it was estimated that 10 million people had a BMI of 35 to 40, and an additional 5 to 6 million have a BMI of greater than 40. It equates to approximately 1 in 4 adults.2 Because of the ever increasing number of obese persons, the number of surgeries performed for obesity increased from 16,000 to 103,000 during a 13-year period ending in 2003.3 The basis of bariatric surgery is either malabsorptive or restrictive or a combination of both.2 The RYGBP is primarily a restrictive operation; however, it also has a malabsorptive component. This procedure has been considered the “gold standard” of obesity operations. The restrictive portion of this procedure consists of creating a small gastric pouch to limit the amount of food that can be eaten. To augment the weight loss, a malabsorptive component is created by bypassing the distal stomach, duodenum, and the first part of the jejunum. The gastric pouch is usually 30 ml or less. It is commonly known that the RYGBP causes irondeficiency anemia and vitamin B12 malabsorption.2 Iron deficiency is primarily caused by decreased absorption, whereas vitamin B12 deficiency is caused by multiple mechanisms. Iron absorption occurs primarily in the duodenum, and because of the malabsorptive component of the RYGBP, iron deficiency is relatively common. Menstruating women are particularly prone to iron-deficient anemia.4 Vitamin B12 absorption requires an intrinsic factor derived from pariental cells in the gastric mucosa. It also requires an acidic pH and finally ultimate absorption in the ileum. All 3 of these mechanisms are deficient after RYGBP.5 All RYGBP patients have the need for permanent vitamin and mineral supplementation. Another common side effect of the RYGBP is vomiting. It occurs after most restrictive procedures. Although uncommon, intractable vomiting has been reported after restrictive procedures.4 Thiamine (Vitamin B1) was the first B complex vitamin identified. Thiamine absorption occurs via carrier mediated acCURRENT SURGERY • Volume 63/Number 2 • March/April 2006
tive transport6 throughout the intestines, with the highest portion in the duodenum,7,8 which is bypassed as part of the RYGBP procedure. The physiologically active form, thiamine pyrophosphate, functions as an intermediary in many essential reactions. The decarboxylation of alpha-keto acids and the utilization of pentose in the hexose monophosphate shunt are dependent on thiamine. The 3 primary enzymes with thiamine are alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase (PDH), and transketolase.9 The main function of these enzymes is in the generation of adenosine triphosphate (ATP). Decreased enzyme activity can result in decreased ATP production, which can result in ultimate cell death. Additionally, acetylcholine and myelin synthesis are dependent on PDH.10 Wernicke’s encephalopathy was first reported in 1881 by Carl Wernicke. First called “polioencephalitis hemorrhagica superioris,” it was a fatal syndrome characterized by ophthalmoplegia, ataxia, and confusion. The first reported patients were 2 alcoholics and a woman with persistent vomiting after ingestion of sulfuric acid.11 Although confusion is the most common initial presentation of WE, other disturbances in consciousness and mentation can occur. Patients can be apathetic, inattentive, and indifferent to their surroundings5 or agitated.9 It is now known that the cerebellar vermis is sensitive to thiamine deficiency, in particular the purkinje cells. The purkinje cells have widespread connections to the cerebral hemispheres and the extrapyramidal connections. The damage to the purkinje cells can result in motor problems, including ataxia, but also impairment of executive functions, learning, and memory.10 The ataxia associated with WE is classically of stance and gait and in the acute stages may present with the inability to stand or walk without assistance.9,12 Wernicke’s encephalopathy can also alter sympathetic outflow. It can result in postural hypotension, syncope, and mild hypothermia.12 The currently accepted diagnosis of WE has been reported after various gastric surgeries,1,6,11,13-17 after prolonged total parenteral nutrition,18 and after prolonged intravenous therapy,8 in a person who was on a hunger strike19 and after hyperemesis gravidarum.20,21 Beriberi was described in the late 19th century as a degenerative disorder of peripheral nerves.12 Dry beriberi is manifested by polyneuritis, weakness, pain, and convulsions.22 Lower limbs are effected earlier and with more severity than upper extremities. The cerebrospinal fluid in patients with beriberi can show only a modest elevation of protein. Although axonal degeneration occurs with destruction of both the axon and the myelin sheath, regeneration may occur over the period of several months with correction of the vitamin deficiency.12 Peripheral neuropathy after surgery for obesity has been termed bariatric beriberi. It has been reported as early as 6 weeks postoperatively and as late as 3 years after surgery.5 Unless treated early in the course of the disease, the peripheral neuropathy is often persistent. Patients need to be followed closely after RYGBP to monitor the rate of weight loss. A loss of greater than 7 kg per month is considered excessive. Additionally, patients with persistent 115
vomiting should be carefully evaluated,15 because both WE and peripheral neuropathy can occur despite oral supplementation in patients with persistent vomiting.5
CONCLUSION Gastric bypass surgery is increasingly employed for the treatment of morbid obesity, and this case emphasizes the importance of vitamin replacement postoperatively. Without question, this case could have easily resulted in devastating consequences for the patient had the diagnosis of WE been missed. Furthermore, this case also emphasizes the importance of a potentially serious complication of this surgery and the need for early vitamin supplementation, particularly thiamine.
REFERENCES 1. Oczkowski WJ, Kertesz A. Wernicke’s encephalopathy
after gastroplasty for morbid obesity. Neurology. 1985;35: 99-101. 2. Buchwald H. Overview of bariatric surgery. J Am Coll
Surg. 2002;194:367-375. 3. Steinbrook R. Surgery for severe obesity. N Engl J Med.
2004;350:1075-1079. 4. Gorecki P, Wise L. Complications of combined gastric
restrictive and malabsorptive procedures: part 1. Curr Surg. 2003;60:138-142. 5. Berger JR. The neurological complications of bariatric
surgery. Arch Neurol. 2004;61:1185-1188. 6. Marcus R, Coulston AM. Water soluable vitamins: The
vitamin B complex and ascorbic acid. In: Hardman JG, Limbird LE, Gilman AG, editors. Goodman and Gilman’s the Pharmacological Basis of Therapeutics. 10th ed. New York: McGraw-Hill; 2001:1753-1771. 7. Koike H, Misu K, Hattori N, et al. Postgastrectomy poly-
neuropathy with thiamine deficiency. J Neurol Neurosurg Psych. 2001;71:357-362.
at: http://www.niaaa.nih.gov/publications/arh27-2/134142.htm. Accessed September 29, 2004. 11. Cirignotta F, Manconi M, Mondini S, Buzzi G, Ambro-
setto P. Wernicke-Korsakoff encephalopathy and polyneuropathy after gastroplasty for morbid obesity. Arch Neurol. 2000;57:1356-1359. 12. Victor M, Rooper A. Diseases of the nervous system due
to nutritional deficiency. In: Wonsiewicz MJ, Medine MP, Navrozou M, editors. Adams and Victor’s Principles of Neurology. New York: McGraw-Hill; 2001:12051232. 13. Haid RW, Gutmann L, Crosby TW. Wernicke-Korsakoff
encephalopathy after gastric plication. JAMA. 1982;247: 2566-2567. 14. Albina JE, Stone W, Bates M, Felder M. Catastrophic
weight loss after vertical banded gastroplasty:malnutrition and neurologic alterations. J Parenter Enteral Nutr. 1988; 12:619-620. 15. Salas-Salvado J, Garcia-Lorda P, Cuatrecasas G, et. al.
Wernicke’s syndrome after bariatric surgery. Clin Nutr. 2000;19:371-373. 16. Towbin A, Inge T, Garcia V, et. al. Beriberi after gastric
bypass surgery in adolescence. J Pediatr. 2004;145:263267. 17. Feit H, Glasberg M, Ireton C, Rosenberg R, Thal E. Pe-
ripheral neuropathy and starvation after gastric partitioning for morbid obesity. Ann Int Med. 1982;96:453-455. 18. Hahn J, Berquist W, Alcorn D, Chamberlain L, Bass D.
Wernicke encephalopathy and beriberi during total parenteral nutrition attributable to multivitamin infusion shortage. Pediatrics [serial online] .1998;101(1) . Available at: http://www.pediatrics.org/cgi/content/full/101/ 1/e10. Accessed September 29, 2004. 19. Pentland B, Mawdsley C. Wernicke’s encephalopathy fol-
8. Nadel AM, Burger PC. Wernicke encephalopathy follow-
lowing “hunger strike.” Postgrad Med J. 1982;58: 427-428.
ing prolonged intravenous therapy. JAMA. 1976;235: 2403-2405.
20. Nightingale S, Bates D, Heath P, Barron S. Wernicke’s
9. Kinsella LJ, Riley DE. Nutritional deficiencies and syn-
dromes associated with alcoholism. In: Goetz CG, editor. Textbook of Clinical Neurology. 2nd ed. Philadelphia, PA: Elsevier; 2003:873-894. 10. Martin PR, Singleton CK, Hiller-Strumhofel S. The role
of thiamine deficiency in alcoholic brain disease. National Institute on Alcohol Abuse and Alcoholism. Available
116
encephalopathy in hyperemesis gravidarum. Postgrad Med J. 1982;58:558-559. 21. Spruill SC, Kuller JA. Hyperemesis gravidarum compli-
cated by wernicke’s encephalopathy. Obstet Gynecol. 2002;99:875-877. 22. Gollobin C, Marcus WY. Bariatric beriberi. Obes Surg.
2002;12:309-311.
CURRENT SURGERY • Volume 63/Number 2 • March/April 2006
Wernicke’s Encephalopathy After Gastric Bypass that Masqueraded as Acute Psychosis: A Case Report Robert W. Worden, MEd, and Henry M. Allen, DO College of Osteopathic Medicine, Oklahoma State University, Tulsa, Oklahoma Wernicke’s encephalopathy was originally described more than a decade ago. It has been reported after many causes of malnutrition. This case presents a patient with thiamine deficiency after gastric bypass, although unusual in itself, further complicating the case was the initial diagnosis of acute psychosis that was scheduled for electroconvulsive therapy. After recognition and intervention, the patient was successfully treated with thiamine replacement and parenteral nutrition. (Curr Surg 63: 114-116. © 2006 by the Association of Program Directors in Surgery.) KEY WORDS: thiamine, gastric bypass, polyneuropathy, wer-
nicke encephalopathy, beriberi
INTRODUCTION Wernicke’s encephalopathy (WE) is classically associated with chronic alcoholism. However, there have been an increased number of reports of WE in association with severe reduction in dietary intake.1 This syndrome is the result of a deficiency of vitamin B1 or thiamine (an essential coenzyme in intermediate carbohydrate metabolism). It classically presents with the neurological triad of ophthalmoplegia, ataxia, and mental changes. The authors report a case of a woman that developed both WE and “dry” beriberi after undergoing roux-en-y gastric bypass (RYGBP) for morbid obesity, but her condition was initially diagnosed as acute psychosis.
CASE REPORT This case is unusual in that the condition of the patient was initially diagnosed as acute psychosis and she was admitted to the psychiatric unit where she was being considered for electroconvulsive therapy. The patient was a 32-year-old black woman who underwent laparoscopic RYGBP. Preoperatively, her weight was 282 lbs.
Correspondence: Inquiries to Robert W. Worden, MEd, P.O. Box 542, Crescent, OK 73028; fax: (815) 333-4821; e-mail: [email protected]
114
with a body mass index (BMI) of 44. She was neurologically intact, with no focal deficits, and with the exception of hypertension, hypercholesteremia, and obstructive sleep apnea, she was in good health. The operative procedure created a 20-ml gastric pouch with an 80-cm efferent limb. Postoperatively, the patient reported almost continual vomiting. She was instructed on an appropriate diet and was placed on an oral multivitamin. At 1 month, the patient had lost 54 pounds. At 15 weeks after surgery, the patient returned to the surgeons office unable to walk. She was lethargic and tachycardic. At that point she was admitted for intravenous hydration and evaluation. She was subsequently transferred to a psychiatric facility for what was thought to be a conversion disorder. She was scheduled for electroconvulsive therapy. Because of her profound medical illnesses, she was transferred to an acute care facility for evaluation. At the time of admission, 17 weeks postoperative, the patient was confused, disoriented, tachycardic, and was found to have iron-deficient anemia. From the physical examination, a lumbar puncture was performed. The spinal fluid protein was elevated at 159 mg/dl (normal 12 to 60). It was thought that the patient might have a viral encephalopathy. Vitamin studies, to include B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin), were ordered, as well as thyroid studies. Before obtaining the specimen for testing, the patient was given 100 mg of intramuscular thiamine; therefore, the thiamine result of 1256 pg/ml (normal 211 to 911) was not diagnostic. After the administration of 3 doses of thiamine 100 mg intramuscularly, the patient did regain some muscle strength; however, she still had some retrograde and anterograde amnesia. She was then transferred to a skilled nursing facility. The patient subsequently deteriorated and returned to the acute care facility at 21 weeks postoperative. At this time, she had peripheral neuropathy in a stocking distribution to the level of the tibial tuberosity bilaterally. She complained of an extreme burning sensation. Her deep tendon reflexes were decreased, as was her muscle strength in all extremities. She was also noted to have a lateral nystagmus. Throughout the previous 6 weeks, the patient continued to
CURRENT SURGERY • © 2006 by the Association of Program Directors in Surgery Published by Elsevier Inc.
0149-7944/06/$30.00 doi:10.1016/j.cursur.2005.06.004
have nausea and vomiting. She continued to be unable to walk, and the amnesia persisted. A barium swallow study with a small bowel follow-through was obtained and was reported as normal. After an interdisciplinary discussion with the gastric surgeon, the nutritionist, and the internist, it was felt that the patient was malnourished and vitamin deficient. The patient was started on intramuscular thiamine and total parenteral nutrition with a multivitamin and trace elements. After several days of thiamine, the patient’s neurological symptoms began to resolve slowly. She regained some muscle strength, the nystagmus resolved, but the peripheral neuropathy continued. The patient was started on venlafaxine and gabapentin for the peripheral neuropathy symptoms. She was also transferred to a rehabilitation facility for continued therapy.
DISCUSSION A BMI of 25 or greater is considered overweight. A BMI of 30 or higher is considered obese, and morbid obesity is present with a BMI of 40 or higher. The prevalence of obesity has increased from 1962 to 2000. According to the 2000 Census, it was estimated that 10 million people had a BMI of 35 to 40, and an additional 5 to 6 million have a BMI of greater than 40. It equates to approximately 1 in 4 adults.2 Because of the ever increasing number of obese persons, the number of surgeries performed for obesity increased from 16,000 to 103,000 during a 13-year period ending in 2003.3 The basis of bariatric surgery is either malabsorptive or restrictive or a combination of both.2 The RYGBP is primarily a restrictive operation; however, it also has a malabsorptive component. This procedure has been considered the “gold standard” of obesity operations. The restrictive portion of this procedure consists of creating a small gastric pouch to limit the amount of food that can be eaten. To augment the weight loss, a malabsorptive component is created by bypassing the distal stomach, duodenum, and the first part of the jejunum. The gastric pouch is usually 30 ml or less. It is commonly known that the RYGBP causes irondeficiency anemia and vitamin B12 malabsorption.2 Iron deficiency is primarily caused by decreased absorption, whereas vitamin B12 deficiency is caused by multiple mechanisms. Iron absorption occurs primarily in the duodenum, and because of the malabsorptive component of the RYGBP, iron deficiency is relatively common. Menstruating women are particularly prone to iron-deficient anemia.4 Vitamin B12 absorption requires an intrinsic factor derived from pariental cells in the gastric mucosa. It also requires an acidic pH and finally ultimate absorption in the ileum. All 3 of these mechanisms are deficient after RYGBP.5 All RYGBP patients have the need for permanent vitamin and mineral supplementation. Another common side effect of the RYGBP is vomiting. It occurs after most restrictive procedures. Although uncommon, intractable vomiting has been reported after restrictive procedures.4 Thiamine (Vitamin B1) was the first B complex vitamin identified. Thiamine absorption occurs via carrier mediated acCURRENT SURGERY • Volume 63/Number 2 • March/April 2006
tive transport6 throughout the intestines, with the highest portion in the duodenum,7,8 which is bypassed as part of the RYGBP procedure. The physiologically active form, thiamine pyrophosphate, functions as an intermediary in many essential reactions. The decarboxylation of alpha-keto acids and the utilization of pentose in the hexose monophosphate shunt are dependent on thiamine. The 3 primary enzymes with thiamine are alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase (PDH), and transketolase.9 The main function of these enzymes is in the generation of adenosine triphosphate (ATP). Decreased enzyme activity can result in decreased ATP production, which can result in ultimate cell death. Additionally, acetylcholine and myelin synthesis are dependent on PDH.10 Wernicke’s encephalopathy was first reported in 1881 by Carl Wernicke. First called “polioencephalitis hemorrhagica superioris,” it was a fatal syndrome characterized by ophthalmoplegia, ataxia, and confusion. The first reported patients were 2 alcoholics and a woman with persistent vomiting after ingestion of sulfuric acid.11 Although confusion is the most common initial presentation of WE, other disturbances in consciousness and mentation can occur. Patients can be apathetic, inattentive, and indifferent to their surroundings5 or agitated.9 It is now known that the cerebellar vermis is sensitive to thiamine deficiency, in particular the purkinje cells. The purkinje cells have widespread connections to the cerebral hemispheres and the extrapyramidal connections. The damage to the purkinje cells can result in motor problems, including ataxia, but also impairment of executive functions, learning, and memory.10 The ataxia associated with WE is classically of stance and gait and in the acute stages may present with the inability to stand or walk without assistance.9,12 Wernicke’s encephalopathy can also alter sympathetic outflow. It can result in postural hypotension, syncope, and mild hypothermia.12 The currently accepted diagnosis of WE has been reported after various gastric surgeries,1,6,11,13-17 after prolonged total parenteral nutrition,18 and after prolonged intravenous therapy,8 in a person who was on a hunger strike19 and after hyperemesis gravidarum.20,21 Beriberi was described in the late 19th century as a degenerative disorder of peripheral nerves.12 Dry beriberi is manifested by polyneuritis, weakness, pain, and convulsions.22 Lower limbs are effected earlier and with more severity than upper extremities. The cerebrospinal fluid in patients with beriberi can show only a modest elevation of protein. Although axonal degeneration occurs with destruction of both the axon and the myelin sheath, regeneration may occur over the period of several months with correction of the vitamin deficiency.12 Peripheral neuropathy after surgery for obesity has been termed bariatric beriberi. It has been reported as early as 6 weeks postoperatively and as late as 3 years after surgery.5 Unless treated early in the course of the disease, the peripheral neuropathy is often persistent. Patients need to be followed closely after RYGBP to monitor the rate of weight loss. A loss of greater than 7 kg per month is considered excessive. Additionally, patients with persistent 115
vomiting should be carefully evaluated,15 because both WE and peripheral neuropathy can occur despite oral supplementation in patients with persistent vomiting.5
CONCLUSION Gastric bypass surgery is increasingly employed for the treatment of morbid obesity, and this case emphasizes the importance of vitamin replacement postoperatively. Without question, this case could have easily resulted in devastating consequences for the patient had the diagnosis of WE been missed. Furthermore, this case also emphasizes the importance of a potentially serious complication of this surgery and the need for early vitamin supplementation, particularly thiamine.
REFERENCES 1. Oczkowski WJ, Kertesz A. Wernicke’s encephalopathy
after gastroplasty for morbid obesity. Neurology. 1985;35: 99-101. 2. Buchwald H. Overview of bariatric surgery. J Am Coll
Surg. 2002;194:367-375. 3. Steinbrook R. Surgery for severe obesity. N Engl J Med.
2004;350:1075-1079. 4. Gorecki P, Wise L. Complications of combined gastric
restrictive and malabsorptive procedures: part 1. Curr Surg. 2003;60:138-142. 5. Berger JR. The neurological complications of bariatric
surgery. Arch Neurol. 2004;61:1185-1188. 6. Marcus R, Coulston AM. Water soluable vitamins: The
vitamin B complex and ascorbic acid. In: Hardman JG, Limbird LE, Gilman AG, editors. Goodman and Gilman’s the Pharmacological Basis of Therapeutics. 10th ed. New York: McGraw-Hill; 2001:1753-1771. 7. Koike H, Misu K, Hattori N, et al. Postgastrectomy poly-
neuropathy with thiamine deficiency. J Neurol Neurosurg Psych. 2001;71:357-362.
at: http://www.niaaa.nih.gov/publications/arh27-2/134142.htm. Accessed September 29, 2004. 11. Cirignotta F, Manconi M, Mondini S, Buzzi G, Ambro-
setto P. Wernicke-Korsakoff encephalopathy and polyneuropathy after gastroplasty for morbid obesity. Arch Neurol. 2000;57:1356-1359. 12. Victor M, Rooper A. Diseases of the nervous system due
to nutritional deficiency. In: Wonsiewicz MJ, Medine MP, Navrozou M, editors. Adams and Victor’s Principles of Neurology. New York: McGraw-Hill; 2001:12051232. 13. Haid RW, Gutmann L, Crosby TW. Wernicke-Korsakoff
encephalopathy after gastric plication. JAMA. 1982;247: 2566-2567. 14. Albina JE, Stone W, Bates M, Felder M. Catastrophic
weight loss after vertical banded gastroplasty:malnutrition and neurologic alterations. J Parenter Enteral Nutr. 1988; 12:619-620. 15. Salas-Salvado J, Garcia-Lorda P, Cuatrecasas G, et. al.
Wernicke’s syndrome after bariatric surgery. Clin Nutr. 2000;19:371-373. 16. Towbin A, Inge T, Garcia V, et. al. Beriberi after gastric
bypass surgery in adolescence. J Pediatr. 2004;145:263267. 17. Feit H, Glasberg M, Ireton C, Rosenberg R, Thal E. Pe-
ripheral neuropathy and starvation after gastric partitioning for morbid obesity. Ann Int Med. 1982;96:453-455. 18. Hahn J, Berquist W, Alcorn D, Chamberlain L, Bass D.
Wernicke encephalopathy and beriberi during total parenteral nutrition attributable to multivitamin infusion shortage. Pediatrics [serial online] .1998;101(1) . Available at: http://www.pediatrics.org/cgi/content/full/101/ 1/e10. Accessed September 29, 2004. 19. Pentland B, Mawdsley C. Wernicke’s encephalopathy fol-
8. Nadel AM, Burger PC. Wernicke encephalopathy follow-
lowing “hunger strike.” Postgrad Med J. 1982;58: 427-428.
ing prolonged intravenous therapy. JAMA. 1976;235: 2403-2405.
20. Nightingale S, Bates D, Heath P, Barron S. Wernicke’s
9. Kinsella LJ, Riley DE. Nutritional deficiencies and syn-
dromes associated with alcoholism. In: Goetz CG, editor. Textbook of Clinical Neurology. 2nd ed. Philadelphia, PA: Elsevier; 2003:873-894. 10. Martin PR, Singleton CK, Hiller-Strumhofel S. The role
of thiamine deficiency in alcoholic brain disease. National Institute on Alcohol Abuse and Alcoholism. Available
116
encephalopathy in hyperemesis gravidarum. Postgrad Med J. 1982;58:558-559. 21. Spruill SC, Kuller JA. Hyperemesis gravidarum compli-
cated by wernicke’s encephalopathy. Obstet Gynecol. 2002;99:875-877. 22. Gollobin C, Marcus WY. Bariatric beriberi. Obes Surg.
2002;12:309-311.
CURRENT SURGERY • Volume 63/Number 2 • March/April 2006