Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the bodys acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. Metabolic acidosis can lead to acidemia, which is defined as arterial blood pH that is lower than 7.35. Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low to high. Acute metabolic acidosis, lasting from minutes to several days, often occurs during serious illnesses or hospitalizations, and is generally caused when the body produces an excess amount of organic acids (ketoacids in ketoacidosis, or lactic acid in lactic acidosis). A state of chronic metabolic acidosis, lasting several weeks to years, can be the result of impaired kidney function (chronic kidney disease) and/or bicarbonate wasting. The adverse effects of acute versus chronic metabolic acidosis also differ, with acute metabolic acidosis impacting the cardiovascular system in hospital settings, and chronic metabolic acidosis affecting muscles, bones, kidney and cardiovascular health. Signs and symptoms
Acute metabolic acidosis
Symptoms are not specific, and diagnosis can be difficult unless patients present with clear indications for arterial blood gas sampling. Symptoms may include palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain.
It is often associated with poor prognosis, with a mortality rate as high as 57% if the pH remains untreated at 7.20. At lower pH levels, acute metabolic acidosis can lead to impaired circulation and end organ function. Chronic Metabolic Acidosis
Chronic metabolic acidosis commonly occurs in people with Chronic Kidney Disease with an eGFR of less than 45 ml/min/1.73m2, most often with mild to moderate severity; however, metabolic acidosis can manifest earlier on in the course of Chronic Kidney Disease. Multiple animal and human studies have shown that metabolic acidosis in Chronic Kidney Disease, given its chronic nature, has a profound adverse impact on cellular function, overall contributing to high morbidities in patients. The most adverse consequences of chronic metabolic acidosis in people with Chronic Kidney Disease and in particular, for those who have end-stage renal disease (ESRD), are detrimental changes to the bones and muscles. Acid buffering leads to loss of bone density, resulting in an increased risk of bone fractures, renal osteodystrophy, and bone disease; as well, increased protein catabolism leads to muscle wasting. Furthermore, metabolic acidosis in Chronic Kidney Disease is also associated with a reduction in eGFR; it is both a complication of Chronic Kidney Disease, as well as an underlying cause of Chronic Kidney Disease progression. Treatment
Treatment of metabolic acidosis depends on the underlying cause, and should target reversing the main process. When considering course of treatment, it is important to distinguish between acute versus chronic forms.