Parenteral nutrition thiamin

Cases of Wernicke s encephalopathy caused by thiamine deficiency during parenteral nutrition are reported (21). 

A young man developed marked deterioration in his vision and oscillating vision, despite normal optic fundi, during parenteral nutrition he went on to develop a characteristic Wernicke s encephalopathy, confirmed by characteristic findings on MRI brain scan (42). The serum vitamin Bi concentration was 110 pg/ml (reference range 200-500). He responded fuUy to thiamine 300 mg/day in addition to betamethasone for 4 weeks. 

Parenteral nutrition was used to support a patient requiring autologous blood stem-cell transplantation, but vitamins were excluded (the reason was not identified). After about 28 days, the patient suddenly developed severe metabolic acidosis, heart failure, and deep coma. Thiamine was immediately infused, with rapid improvement. 

A further consequence of thiamine depletion during parenteral nutrition can be severe lactic acidosis (44). Six cases have been described from Japan with associated hypotension, Kussmaul s respiration, and clouding of consciousness, as well as abdominal pain not directly related to the underlying disease. During parenteral nutrition administration there was blockade of oxidative decarboxylation of alpha-keto acids such as pyruvate and alpha-ketoglutarate, resulting in pjruvate accumulation and massive lactate production. None of the patients responded to sodium bicarbonate or other conventional emergency treatments for shock and lactic acidosis. Thiamine replenishment with intravenous doses of 100 mg every 12 hours resolved the lactic acidosis and improved the clinical condition of three patients. 

These various reports stress the need to supplement parenteral nutrition with thiamine-containing vitamins unless there is adequate dietary intake, and to monitor serum thiamine and erythrocyte transketolase activity so that supplementary thiamine can be given in good time, if necessary intravenously (45). Giving thiamine will not rectify the various disorders if hepatic function is severely disturbed, because then thiamine is not phosphorylated and hence remains physiologically inactive. 

Lactic acidosis can occur through thiamine deficiency during parenteral nutrition (73). 

A 13-year-old boy underwent bone marrow transplantation and received parenteral nutrition without vitamins. After 15 days he had acute life-threatening lactic acidosis refractory to bicarbonate and Tris. Intravenous thiamine 100 mg produced satisfactory clinical and biochemical responses. 

The authors suggested that in any patient receiving parenteral nutrition without added vitamins who develops lactic acidosis, thiamine deficiency should be suspected. 

Nakasaki H, Ohta M, Soeda J, Makuuchi H, Tsuda M, Tajima T, Mitomi T, Fujii K. Clinical and biochemical aspects of thiamine treatment for metabohc acidosis dnring total parenteral nutrition. Nutrition 1997 13(2) 110-17. 

Schiano TD, Klang MG, Quesada E, Scott F, Tao Y, Shike M. Thiamine status in patients receiving long-term home parenteral nutrition. Am J Gastroenterol 1996 91(12) 2555-9. 

Centers for Disease Control and Prevention. Lactic acidosis traced to thiamin deficiency related to nationwide shortage of multivitamins fortotal parenteral nutrition—United States, 1997. JAMA 1997 278 109-111. 

Classic beri-beri, rarely seen in the United States and Europe, except in alcoholism (P4), is endemic in the Far East because of the prevalent diet of decorticated rice (F6). It occurs in two forms wet beri-beri, characterized by edema and cardiovascular symptoms (G6), and dry beri-beri with peripheral neuritis, paralysis, and atrophy of the muscles. Conditions which may predispose to deficiency by increasing thiamine requirements are pregnancy (see section 2.4), and lactation, hyperthyroidism, malignant disease, febrile conditions, increased muscular activity, high carbohydrate diets, and parenteral administration of glucose solutions. A constant supply of thiamine is required for optimal nutrition because storage in the liver and elsewhere is limited. Thiamine is synthesized by bacteria in the intestinal tract of various animals, but this is not a dependable source for man. 

Wernicke s encephalopathy is an acute, potentially reversible nemological disorder caused by severe thiamine deficiency, commonly occurring with chronic alcoholism, poor nutrition, long-term parenteral feeding, hyperemesis gravidarum or bariatric surgery. 

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