Postgastroplasty Polyneuropathy

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Some patients undergoing bariatric, or weight reduction, surgery develop a syndrome of acute or subacute sensory loss, weakness, and areflexia in the limbs, usually following a period of dramatic weight loss and repeated bouts of protracted vomiting. y A few patients have also developed a type of encephalopathy that is clinically and pathologically identical to WKS, with or without an associated polyneuropathy. y Indeed, Wernicke and Korsakoff each described young women with intractable vomiting in their original reports: One woman had attempted suicide by drinking sulfuric acid, whereas the other had hyperemesis gravidarum. [8]

Of 37 cases of postgastroplasty polyneuropathy reviewed, 26 developed neuropathy alone, 2 had encephalopathy, and 9 had features of both. y , y , y y y y y One patient developed blindness and optic neuropathy. Intractable vomiting is a constant feature. The syndrome may present suddenly several months after surgical procedures that include gastrojejunostomy, gastric stapling, vertical banding gastroplasty, and gastrectomy with Roux-en-Y anastomosis. y Following a period of recurrent vomiting and precipitous weight loss, patients develop numbness and tingling in the soles of the feet, calves, and thighs. Distal or proximal weakness may develop, and the patient may have difficulty arising form a chair or climbing stairs. Pain is not a dominant feature, unlike nutritional neuropathy, in which the calves are often exquisitely tender. Examination shows symmetrical sensory loss in the legs more than the arms, muscle weakness, and areflexia. Patients may develop quadriparesis and prolonged or permanent disability. When the condition is accompanied by encephalopathy, patients may demonstrate confusion, memory loss, and affective disturbances. Many patients have been mistakenly diagnosed early in their course as having a conversion disorder.

In this setting, Guillain-Barre syndrome, cobalamin myeloneuropathy, critical illness polyneuropathy, compressive radiculopathy, WKS, beriberi, Strachan's syndrome, hypocalcemia, and hypomagnesemia should be considered in the differential diagnosis.

Nerve conduction studies show severe reduction of sensory and motor action potentials, variable slowing, and absent or prolonged late responses in this disorder. Needle examination shows diffuse denervation with fibrillations, consistent with an axonal and demyelinating sensorimotor polyneuropathy. The polyneuropathy is axonal and demyelinating in type, acute in onset, and slow to resolve. Pathological studies have shown lipid-laden neurons and Schwann cells surrounding demyelinating and degenerating axons. y

Although thiamine deficiency has been suggested as the cause, reports documenting low thiamine activity are lacking. Furthermore, the pathology of the peripheral nerve is unlike any known nutritional neuropathy, and some patients have developed the neuropathy despite adequate nutritional supplementation. y The pathophysiology of this disorder is unknown, but may be related to the rapid mobilization of lipid in the surgically starved. Controversy exists whether vitamin and nutritional supplementation alone or reversal of the surgical procedure is most helpful in resolving the neuropathy. All patients following bariatric surgery should adhere to a strict dietary regimen with additional vitamins. If vomiting develops, patients should receive parenteral nutrition, vitamins, and thiamine. Most patients recover fully, but some have residual weakness and sensory loss. The degree of disability appears to depend on the duration and severity of symptoms before diagnosis and treatment.


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