CLINICAL AND BIOCHEMICAL ASPECTS OF THIAMINE TREATMENT FOR METABOLIC-ACIDOSIS DURING TOTAL PARENTERAL-NUTRITION

Citation
H. Nakasaki et al., CLINICAL AND BIOCHEMICAL ASPECTS OF THIAMINE TREATMENT FOR METABOLIC-ACIDOSIS DURING TOTAL PARENTERAL-NUTRITION, Nutrition, 13(2), 1997, pp. 110-117
Citations number
21
Categorie Soggetti
Nutrition & Dietetics
Journal title
Nutrition
ISSN journal
08999007 → ACNP
Volume
13
Issue
2
Year of publication
1997
Pages
110 - 117
Database
ISI
SICI code
0899-9007(1997)13:2<110:CABAOT>2.0.ZU;2-3
Abstract
We encountered six cases of total parenteral nutrition (TPN) -associat ed lactic acidosis during the 6-y period of 1988-1993. The patients we re characterized by severe disease of the digestive organs, minimal fo od intake before surgery, and postoperative TPN with no food intake an d with no vitamin supplements. Within 4 wk of TPN, they developed hypo tension (80/60 mmHg), Kussmaul's respiration, and clouding of consciou sness, as well as abdominal pain not directly related to the underlyin g disease. Routine laboratory examinations revealed no acute aggravati on in hepatic, renal, or pancreatic functions. Arterial blood gas anal ysis showed pH less than or equal to 7.134 and base excess less than o r equal to -17.5 mmol/L. Additional laboratory examinations revealed s erum lactate greater than or equal to 10.9 mmol/L, serum pyruvate grea ter than or equal to 159 mu mol/L, and lactate/pyruvate ratio greater than or equal to 0.029. None of the patients responded to sodium bicar bonate or other conventional emergency treatments for shock and lactic acidosis. After the first case, we suspected that thiamine deficiency might be responsible for this pathologic condition. Serum thiamine wa s proved to be less than or equal to 196 nmol/L in 5 patients. Thiamin e replenishment at intravenous doses of 100 mg every 12 h resolved lac tic acidosis and improved the clinical condition in 3 patients. This a rticle includes a review of 11 relevant reports published from 1982-19 92 and a discussion of the biochemical mechanism of onset of thiamine deficiency-associated lactic acidosis. We emphasize the needs (1) to s upplement TPN with thiamine-containing vitamins for the patients whose food intake does not meet nutritional requirements; (2) to monitor th e patients routinely measuring serum thiamine concentration and erythr ocyte transketolase activity during TPN; and (3) to intravenously repl enish using high-dose thiamine simultaneously with the manifestation o f signs and symptoms of lactic acidosis. (C) Elsevier Science Inc.