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.