Carta Acesso aberto Revisado por pares

Neurologic Complications of Bariatric Surgery

2005; Elsevier BV; Volume: 80; Issue: 1 Linguagem: Inglês

10.1016/s0025-6196(11)62974-1

ISSN

1942-5546

Autores

Sonal Singh, Amit Nautiyal,

Tópico(s)

Alcoholism and Thiamine Deficiency

Resumo

To the Editor: In an otherwise comprehensive review of bariatric surgery, Presutti and colleagues1Presutti RJ Gorman RS Swain JM Primary care perspective on bariatric surgery.Mayo Clin Proc. 2004; 79: 1158-1166PubMed Google Scholar failed to address the neurologic complications after bariatric surgery, including Wernicke encephalopathy due to thiamine deficiency, which has become increasingly common. Neurologic complications have been reported to occur in 5% to 10% of patients after bariatric surgery.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar In a retrospective review of 556 patients who underwent bariatric surgery at the Mayo Clinic in Rochester, Minn, from 1980 through 2003, Thaisetthawatkul3Thaisetthawatkul P. Peripheral neuropathy following gastric bypass surgery. Paper presented at: 55th Annual Meeting of the American Academy of Neurology; Honolulu, Hawaii; March 29-April 5, 2003.Google Scholar identified 48 patients (8.6%) with complications affecting the peripheral nervous system. Any part of the neuraxis may be involved, resulting in encephalopathy, behavioral abnormalities, peripheral neuropathy, burning feet, meralgia paresthetica, myotonic syndrome, posterolateral myelopathy, and Wernicke encephalopathy.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar These complications usually manifest 3 to 20 months after surgery, and affected patients experience protracted vomiting, a symptom that may occur in up to one third of all patients who have undergone gastric bypass procedures.4Halverson JD Metabolic risk of obesity surgery and long-term follow-up.Am J Clin Nutr. 1992; 55: 602S-605SPubMed Google Scholar Most of these neurologic complications are the consequence of micronutrient deficiency. Wernicke encephalopathy occurs as a result of vitamin B1 deficiency. It is characterized by peripheral neuropathy, ophthalmoplegia, nystagmus, ataxia, and encephalopathy and may lead to permanent impairment of recent memory. Although most commonly described in the setting of alcohol abuse, several cases occurring after bariatric surgery have been reported in the world literature.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar The diagnosis of Wernicke encephalopathy requires 2 of the following 4 features: (1) dietary deficiency, (2) oculomotor abnormality, (3) cerebellar dysfunction, and (4) confusion or mild memory impairment.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar It may be seen relatively soon after surgery, usually within 8 to 15 weeks but occasionally as early as 6 weeks postoperatively.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar Peripheral neuropathy, which is more common than encephalopathy, may occur from 6 weeks to several years after bariatric surgery. When attributable to vitamin B1 deficiency after bariatric surgery, it has been referred to as bariatric beriberi.5Gollobin C Marcus WY Bariatric beriberi [editorial].Obes Surg. 2002; 12: 309-311Crossref PubMed Scopus (46) Google Scholar The neuropathy predominantly affects the lower limbs and is both sensory and motor, with variable involvement of each system.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar Bariatric surgery–induced vitamin B1 deficiency is invariably due to inadequate vitamin repletion and persistent, intractable vomiting. It may occur despite oral supplementation with thiamine because emesis precludes effective absorption. The clinical constellation of symptoms coupled with the response to administration of parenteral thiamine, especially in patients with features of encephalopathy, may be sufficient for diagnosis. Vitamin B1 deficiency can be confirmed by assessing the vitamin B1 pyrophosphate effect in erythrocyte transketolase studies.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar Magnetic resonance imaging of the brain may show hyperintense signal abnormalities on T2-weighted images in the dorsomedial thalamic nuclei, periaqueductal gray matter, and mammillary bodies.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar Recovery typically occurs within 3 to 6 months of initiation of therapy; however, neurologic recovery may be incomplete if the condition is not recognized and treated promptly.2Berger JR The neurological complications of bariatric surgery.Arch Neurol. 2004; 61: 1185-1189Crossref PubMed Scopus (87) Google Scholar Physicians caring for patients who have undergone bariatric surgery should be familiar with the constellation of neurologic disorders that may occur after such surgery and need to be particularly alert for Wernicke encephalopathy because it is a medical emergency that demands rapid diagnosis and intervention. Plastic Surgery After Bariatric Surgery and Massive Weight Loss: In ResponseMayo Clinic ProceedingsVol. 80Issue 1PreviewMy colleagues and I appreciate Drs Singh and Nautiyal's comments concerning the rare development of Wernicke encephalopathy in patients who have undergone obesity surgery. Our concise review was purposefully of limited scope and was not meant to be a complete review of all possible complications and sequelae of bariatric procedures. Being observant for the numerous potential nutritional deficiencies that may occur with this form of treatment is certainly a key role for primary care physicians. For those interested in a review of neurologic problems associated with obesity surgery, the article by Berger1 is an excellent resource. Full-Text PDF

Referência(s)