Metabolic acidosis.
Acta Med Indones
;
2007 Jul-Sep; 39(3): 145-50
Artigo
em Inglês
| IMSEAR
| ID: sea-47014
ABSTRACT
Acute metabolic acidosis is frequently encountered in critically ill patients. Metabolic acidosis can occur as a result of either the accumulation of endogenous acids that consumes bicarbonate (high anion gap metabolic acidosis) or loss of bicarbonate from the gastrointestinal tract or the kidney (hyperchloremic or normal anion gap metabolic acidosis). The cause of high anion gap metabolic acidosis includes lactic acidosis, ketoacidosis, renal failure and intoxication with ethylene glycol, methanol, salicylate and less commonly with pyroglutamic acid (5-oxoproline), propylene glycole or djenkol bean (gjenkolism). The most common causes of hyperchloremic metabolic acidosis are gastrointestinal bicarbonate loss, renal tubular acidosis, drugs-induced hyperkalemia, early renal failure and administration of acids. The appropriate treatment of acute metabolic acidosis, in particular organic form of acidosis such as lactic acidosis, has been very controversial. The only effective treatment for organic acidosis is cessation of acid production via improvement of tissue oxygenation. Treatment of acute organic acidosis with sodium bicarbonate failed to reduce the morbidity and mortality despite improvement in acid-base parameters. Further studies are required to determine the optimal treatment strategies for acute metabolic acidosis.
Texto completo:
DisponíveL
Índice:
IMSEAR (Sudeste Asiático)
Assunto principal:
Acidose
/
Acidose Tubular Renal
/
Bicarbonatos
/
Acidose Láctica
/
Humanos
/
Doença Aguda
/
Fatores de Risco
/
Cetoacidose Diabética
/
Bicarbonato de Sódio
Tipo de estudo:
Estudo de etiologia
/
Fatores de risco
Idioma:
Inglês
Revista:
Acta Med Indones
Ano de publicação:
2007
Tipo de documento:
Artigo
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