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This chapter discusses the diagnosis, evaluation and management of renal emergencies including metabolic acidosis, metabolic alkalosis, respiratory acidosis and respiratory alkalosis. The symptoms depend on the severity and etiology of the underlying acidosis, and are often nonspecific. Altered mental status, weakness, nausea, and abdominal pain are common. Hyperkalemia is often present due to transcellular shift of K-plus out of cells and H-plus into cells. Kussmaul respirations are classically associated with diabetic ketoacidosis (DKA), and refer to rapid, deep breathing. The critical presentation includes extreme acidemia that leads to neurological dysfunction (severe obtundation, coma, and seizures) as well as cardiovascular complications (arrhythmias, decreased cardiac contractility, arteriolar vasodilation, and decreased responsiveness to catecholamines). Profound hypotension and shock can result, which can complicate management since hypotension and shock are often the cause of the acidosis. If acidosis is due to DKA, treatment requires insulin and IV fluid resuscitation.
Capnography can provide important clues concerning the acid-base status of patients. Arterial blood gas analysis is essential to properly evaluate the acid-base status, and diagnose and treat underlying disorders. Acids and bases are constantly formed in the body as by-products of metabolism, and are carefully regulated. Buffering mechanisms include intracellular and extracellular chemical buffers, regulation of CO2 by the respiratory and central nervous systems (CNS), and control of bicarbonate by the kidney. Capillary blood samples can be used, particularly in children, to measure arterial blood gases (ABGs). Loop and thiazide diuretics can incite a metabolic alkalosis, while carbonic anhydrase inhibitors can cause a metabolic acidosis. Overdoses of drugs can produce mixed acid-base disorders, such as the combined metabolic acidosis and respiratory alkalosis from a salicylate overdose. Simple acid-base disorders involve a primary abnormality in either metabolism or respiration that produces a secondary change, or compensatory response, in the other component.
Stewart’s and Fencl’s methods have recently been proposed to interpret acid–base disorders where traditional theory has proven inadequate. Our objectives were to evaluate: (1) the occurrence of acid–base disturbances in critically ill patients and their trend over the first 3 intensive care unit days, (2) whether Stewart’s theory offers advantages over the traditional theory in the diagnosis of acid–base metabolic disturbances and (3) whether variables derived from Stewart’s and Fencl’s methods offer advantages over the traditional method to predict patient mortality.
Methods
A prospective cohort study in a general intensive care unit. Blood samples were analysed for arterial blood gases, electrolytes and proteins. PaCO2, pH, bicarbonate, base excess, standard base-excess, sodium, potassium, chloride, phosphorous, calcium, magnesium and lactate were measured. Anion gap, Stewart’s and Fencl’s variables were calculated.
Results
When using Stewart’s method, metabolic acidosis and metabolic alkalosis were found in 92.9% and 93.4% of samples, respectively. Corresponding figures obtained with the traditional method were 15% and 18.7%. In 245 (64.5%) samples, Stewart’s method revealed that metabolic acidosis and alkalosis were simultaneously present, whereas the traditional method revealed a normal acid–base status. Strong ion gap increased significantly over the first 3 intensive care unit days. Strong ion gap and lactate were independent predictors of 28-day mortality.
Conclusions
Metabolic acidosis by unmeasured anions is a clinically relevant phenomenon, which is correlated with mortality. Progressive metabolic acidosis may be ongoing in the early phase of critical illness despite the absence of acidaemia.
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