Record C O, Iles R A, Cohen R D, Williams R
Gut. 1975 Feb;16(2):144-9. doi: 10.1136/gut.16.2.144.
In 28 patients with fulminant hepatic failure alkalaemia was present in 49 of a total of 65 observations. Alkalaemia was due primarlily to a low Pa, C02 in 30 instances and to raised plasma bicarbonate in 16 instances. Blood lactate, pyruvate, and acetoacetate were significantly raised, and in individual cases, blood citrate, succinate, and fumarate were elevated. Blood citrate rose progressively as the clinical condition worsened. Metabolic acidosis was only present in four patients. In three of these patients, all of whom had taken an overdose of paracetamol, the acidosis was severe, present before the onset of clinical heparic failure, and associated with hypoglycaemiaand mild hypotension. In two of these patients the acidosis was shown to be due to accumulation of lactic acid. Plasma free fatty acid concentrations were elevated out of proportion to the degree of ketosis.
在28例暴发性肝衰竭患者中,65次观察中有49次出现碱血症。碱血症主要是由于30例患者的动脉血二氧化碳分压(Pa, C02)降低,以及16例患者的血浆碳酸氢盐升高。血乳酸、丙酮酸和乙酰乙酸显著升高,个别病例中,血柠檬酸、琥珀酸和富马酸也升高。随着临床病情恶化,血柠檬酸逐渐升高。仅4例患者出现代谢性酸中毒。其中3例患者均过量服用了对乙酰氨基酚,酸中毒严重,在临床肝衰竭发作前就已出现,并伴有低血糖和轻度低血压。其中2例患者的酸中毒被证明是由于乳酸积累所致。血浆游离脂肪酸浓度升高的程度与酮症程度不相称。