Neurologic Complications of Gastric Partitioning

AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS, THE OBESITY SOCIETY, AND AMERICAN SOCIETY FOR METABOLIC & BARIATRIC SURGERY MEDICAL GUIDELINES FOR CLINICAL PRACTICE FOR THE PERIOPERATIVE NUTRITIONAL, METABOLIC, AND NONSURGICAL SUPPORT OF THE BARIATRIC SURGERY PATIENT

“…Although thiamine deficiency has multiple manifestations, neurologic symptoms are predominant in this patient population ( 464 (EL 3), 594 (EL 4), 597 (EL 3), 606 (EL 3), 607 (EL 4), 609 (EL 4)) . Acute neurologic deficits as a result of thiamine deficiency have been reported as soon as 1–3 months after bariatric surgery ( 610 , 611 , 612 , 613 , 614 , 615 , 616 , 617 , 618 , 619 (EL 3–4)) . Early recognition is paramount to initiate appropriate supplementation and avoid potential complications resulting from the administration of dextrose‐containing solutions ( 606 (EL 3)) .…”

The Neurological Complications of Bariatric Surgery

“…While vitamin B 1 deficiency was considered in the differential diagnosis, the authors believed that this disorder was likely the consequence of rapid metabolism of fat in obesity. 60 Other investigators have proposed that some of the neurological complications that follow bariatric surgery, such as peripheral neuropathy or psychosis, arise from multifactorial causes. 61 Recurrent spells of encephalopathy characterized by confusion, behavioral abnormalities, weakness, lethargy, ataxia, and dysarthria occurring with lactic acidosis may occur after jejunoileostomy for morbid obesity.…”

The neurologic complications of bariatric surgery

“…Similarly, Paulson and colleagues reported six patients with a clinical picture characterized by confusion, abnormal behavior, profound leg weakness, diminished or absent muscle stretch reflexes, and in three, ophthalmoplegia, or nystagmus (Paulson et al, 1985). While thiamine deficiency was considered in the differential diagnosis, the authors believed that this disorder was likely the consequence of rapid metabolism of fat in obesity (Paulson et al, 1985). Other investigators have proposed that some of the neurologic complications which follow bariatric surgery, such as the peripheral neuropathy or psychosis, arise from multifactorial causes (Seehra et al, 1996;Thaisetthawatkul et al, 2004).…”

“…The authors suggested that a toxin from rapid fat catabolism or loss of carnitine were responsible rather than thiamine or another vitamin deficiency (Feit et al, 1982). Similarly, Paulson and colleagues reported six patients with a clinical picture characterized by confusion, abnormal behavior, profound leg weakness, diminished or absent muscle stretch reflexes, and in three, ophthalmoplegia, or nystagmus (Paulson et al, 1985). While thiamine deficiency was considered in the differential diagnosis, the authors believed that this disorder was likely the consequence of rapid metabolism of fat in obesity (Paulson et al, 1985).…”