Correspondence
Correction
Case 20-2008: Abdominal Pain and Weakness after Gastric Bypass Surgery
N Engl J Med 2008; 359:1850-1852October 23, 2008
- Article
To the Editor:
In the discussion of the Case Record by Bonkovsky et al. (June 26 issue)1 about a patient with porphyria who became symptomatic after gastric bypass surgery, there was no mention of the patient's nutritional care, which may have played a major contributory role. The persistent ketonuria before hospitalization indicates a daily carbohydrate intake of less than 100 g, whereas the very low serum creatinine level on admission indicates limited meat intake and a marked reduction in skeletal muscle, reflecting severe protein-calorie malnutrition.2 These findings are consistent with limited energy and protein intake postoperatively, which was at least 18 days before a subsequent hospital admission that was more than 5 weeks in duration. If the patient remained in a semistarved state in terms of protein and energy for that entire period, this would contribute substantially to the extreme motor weakness that increased with time and perhaps contributed to the continued activity of the porphyria. An additional factor is the possible contribution of deficiencies of thiamine and other micronutrients; these deficiencies have been observed previously after gastric bypass and are associated with polyneuropathy and encephalopathy.3-5
5 ReferencesBruce R. Bistrian, M.D., Ph.D.
Beth Israel Deaconess Medical Center, Boston, MA 022151
Case Records of the Massachusetts General Hospital (Case 20-2008). N Engl J Med 2008;358:2813-2825
Full Text | Web of Science | Medline2
Bistrian BR ,Blackburn GL ,Sherman M ,Scrimshaw NS . Therapeutic index of nutritional depletion in hospitalized patients. Surg Gynecol Obstet 1975;141:512-516
Web of Science | Medline3
Carrodeguas L ,Kaidar-Person O ,Szomstein S ,Antozzi P ,Rosenthal R . Preoperative thiamine deficiency in obese population undergoing laparoscopic bariatric surgery. Surg Obes Relat Dis 2005;1:517-522
CrossRef | Medline4
Juhasz-Pocsine K ,Rudnicki SA ,Archer RL ,Harik SI . Neurologic complications of gastric bypass surgery for morbid obesity. Neurology 2007;68:1843-1850
CrossRef | Web of Science | Medline5
Koffman BM ,Greenfield LJ ,Ali II ,Pirzada NA . Neurologic complications after surgery for obesity. Muscle Nerve 2006;33:166-176
CrossRef | Web of Science | Medline
To the Editor:
Bonkovsky et al. report an interesting case of a 57-year-old woman with abdominal pain and weakness 1 month after gastric bypass surgery for morbid obesity. The cause of the symptoms could have been a primary disease or a consequence of the bariatric surgery. Abdominal pain is a frequent symptom after surgery for obesity and is caused by a variety of postoperative complications (shown in Table 2 of the article). Neurologic complications (Table 1Table 1
Progressive Weakness after Bariatric Surgery.) are not uncommon after bariatric surgery and have been reported in 5 to 10% of patients.1 Any part of the nervous system may be involved, with a broad variety of symptoms. The majority of neurologic complications after bariatric surgery are caused by nutritional deficiencies, particularly deficiencies of iron, folate, vitamin B1, and vitamin B12, and they are mostly recognized as late complications.2 Vitamin B1 deficiency is a rare but important cause of early acute polyneuropathy after bariatric surgery.3 Furthermore, neurologic disorders may be the result of accelerated fat metabolism. Some authors suggest that a toxin from the fast metabolism of fat, a loss of carnitine, or lactate acidosis is responsible.1,2 3 ReferencesSammy A. Baierlein, M.D.
Anja Wistop, M.D.
Thomas Peters, M.D.
St. Claraspital Basel, 4016 Basel, Switzerland
sammybaierlein@web.de 1
Berger JR . The neurological complications of bariatric surgery. Arch Neurol 2004;61:1185-1189
CrossRef | Web of Science | Medline2
Paulson GW ,Martin EW ,Mojzisik C ,Carey LC . Neurologic complications of gastric partitioning. Arch Neurol 1985;42:675-677
CrossRef | Web of Science | Medline3
Halverson JD . Metabolic risk of obesity surgery and long-term follow-up. Am J Clin Nutr 1992;55:Suppl:602S-605S
Web of Science | Medline
To the Editor:
The reduction in food intake, frequent vomiting, and the loss of absorptive surface puts patients at risk of vitamin deficiency after bariatric surgery. In the case described, the patient's anorexia and severe peripheral neuropathy, which developed a few weeks after surgery, are consistent with thiamine deficiency. One of the most serious consequences of this deficiency is Wernicke's encephalopathy. The well-known triad of confusion, ophthalmoplegia, and ataxia plus typical laboratory or radiologic findings is not always present.1,2 The diagnosis of Wernicke's encephalopathy is usually missed clinically.3 Intravenous administration of dextrose or carbohydrate loading may worsen the course of this deficiency syndrome.1 Parenteral thiamine prevents or treats thiamine deficiency in poorly nourished patients.1,2
Perhaps thiamine deficiency played some part in the confusing and serious clinical course of this patient. It would be interesting to know whether she received parenteral vitamins at any point in her complicated course after bariatric surgery.
3 ReferencesFrances R. Frankenburg, M.D.
Edith Nourse Rogers Memorial Veterans Hospital, Bedford, MA 01730
frances.frankenburg@med. va. gov 1
Reuler JB ,Girard DE ,Cooney TG . Wernicke's encephalopathy. N Engl J Med 1985;312:1035-1039
Full Text | Web of Science | Medline2
Singh S ,Kumar A . Wernicke encephalopathy after obesity surgery: a systematic review. Neurology 2007;68:807-811
CrossRef | Web of Science | Medline3
Harper C . The incidence of Wernicke's encephalopathy in Australia -- a neuropathological study of 131 cases. J Neurol Neurosurg Psychiatry 1983;46:593-598
CrossRef | Web of Science | Medline
To the Editor:
Genetic testing may have established the diagnosis of variegate porphyria in this patient, but the apparent fact that there was no history of skin lesions before she received parenteral iron-containing hematin suggests newly unmasked porphyria cutanea tarda superimposed on variegate porphyria. (The occurrence of variegate and cutanea tarda porphyria in the same family has been described in persons with mixed Dutch and Bantu ancestry.1) Further genetic testing for mutations in the HFE hemochromatosis gene would help corroborate that porphyria cutanea tarda also was present in this patient.
In addition, there are two errors in Table 4 of the article. The deficient enzyme for protoporphyria (ferrochelatase) is missing from the table. “Hepatocarboxylporphyrin” should be heptacarboxylporphyrin (shown correctly in Table 5).
1 ReferencesJames Kalivas, M.D.
University of Arizona College of Medicine, Tucson, AZ 85724Author/Editor Response
Bistrian, Baierlein et al., and Frankenburg point out the most common causes of neurologic disorders after gastric bypass surgery. Thiamine deficiency is an important consideration, especially in patients with recurrent vomiting; however, vomiting was not a feature of this patient's presentation. During the first 6 weeks after surgery, she was consuming the recommended liquid nutritional drinks, eating soft food without difficulty, and taking multivitamins regularly.
When weakness suddenly developed, thiamine was administered intravenously and vitamin B12 was administered intramuscularly. The serum thiamine level obtained before thiamine administration was 72 nmol per liter (normal range, 87 to 286); the levels of vitamins A, B2, B6, B12, and folate were normal. Within 24 hours after intubation, a nasojejeunal tube was placed; 10 days later, laparoscopic exploration was performed that showed normal anatomy after gastric bypass, and a gastrostomy tube was placed in the bypassed gastric remnant. Thus, we believed her nutrition was adequate.
In response to the comment of Kalivas: subsequent testing for mutations in the gene for familial hemochromatosis (HFE) showed no mutations. However, the serum ferritin levels were persistently high after discontinuation of hematin infusions, and regular phlebotomy was recently begun for a presumptive diagnosis of acquired porphyria cutanea tarda. Kalivas also correctly points out in Table 4 the omission of ferrochelatase (the gene and enzyme that are defective in erythropoietic protoporphyria) and the misspelling of heptacarboxylporphyrin.
Janey S.A. Pratt, M.D.
Massachusetts General Hospital Weight Center, Boston, MA 02114Herbert L. Bonkovsky, M.D.
Carolinas Medical Center, Charlotte, NC 28232
