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Acid-base disorders in liver disease – a review article
Summarized from Scheiner B, Lindner G, Reiberger T et al. Acid-base disorders in liver disease. Journal of Hepatology 2017 epub 27th June (ahead of print publication)
Discussion of acid-base physiology usually focuses mainly on the role of lungs and kidneys, and it is a disease that affects the function of these two organs that are usually invoked when considering, in general terms, acid-base disorders. As the authors of this review article make clear, the liver also plays an important role in acid-base regulation, and liver disease (particularly cirrhosis and acute liver failure) can be associated with a range of acid-base disorders, the most commonly quoted being respiratory alkalosis.
The article begins by considering four aspects of liver function that impact normal acid-base regulation. The first highlights the significant role of the liver in lactate metabolism/elimination. The capacity of the liver to convert lactate to glucose (hepatic gluconeogenesis) is vital to avoiding accumulation of lactate and associated acidosis.
The second highlights the role of the liver in albumin synthesis; at physiological pH albumin behaves as a weak acid. The third highlights the role of the liver in keto-acid production; and the fourth highlights the role of liver in urea production, during which the principal buffer base, bicarbonate is consumed.
As a preamble to substantive discussion of acid-base disorders in liver disease, the authors provide some background information on application of the alternative model of acid-base analysis developed by Stewart in the 1980s known as the physical-chemical acid-base model.
They briefly discuss how this differs from the traditional model of analysis based on pH, pCO2, bicarbonate and standard base excess, and introduce the concept (derived from Stewart’s work) of base excess subsets that take individual account of the effect of excess-free water, chloride, albumin and lactate concentrations on acid-base status.
Equations for calculation of each of these base excess subsets are provided. The authors explain and demonstrate throughout this paper that the traditional model of acid-base analysis supplemented by this alternative model can provide a more complete account of acid-base status of patients with liver disease than the traditional method alone.
Under the heading “alkalinizing factors in patients with cirrhosis” the authors discuss the mechanisms that give rise to hyperventilation and consequent respiratory alkalosis, the most often quoted acid-base disorder to affect cirrhotic patients. There is also discussion of the potential for metabolic alkalosis that results from reduced albumin in cirrhosis (a reminder that albumin acts as a weak acid).
Under the heading “acidifying factors in patients with cirrhosis” the pathogenesis of dilution hyponatremia in cirrhosis is discussed and the reason that dilution hyponatremia has an acidifying effect is explained. Hyperchloremic acidosis represents another acidifying disorder that is frequently observed in cirrhosis patients. Mechanisms for development of hyperchloremic acidosis discussed include: compensation for chronic respiratory alkalosis, use of lactulose to treat hepatic encephalopathy, and renal tubular acidosis.
The authors observe that these acidifying and alkalinizing metabolic factors frequently cancel each other out in patients with stable (compensated) cirrhosis, giving the false impression of normal acid-base status if pH and standard base excess are used alone to assess cirrhotic patients.
Other topics considered in this article include: acid-base status of critically ill patients with cirrhosis (i.e. severe decompensated cirrhosis); and acid-base disorders in acute liver failure.
The article ends with seven case presentations (six cirrhosis, one acute liver failure). For each of these, results of blood gas analysis and other laboratory tests (electrolytes, albumin, lactate, etc.) are used to make a detailed interpretation of acid-base status.
In all cases the authors demonstrate how acid-base interpretation is enhanced by calculation of base excess subsets in accordance with the Stewart approach to acid-base analysis. For each of the case studies the authors also describe in outline the clinical significance of the acid-base disturbance found and the implication for treatment and further testing/investigation.
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