Metabolic acidosis

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Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body’s 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 an arterial blood pH lower than 7.37, which itself is a result of acidosis - the process in the body that causes a low pH in blood and tissues.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, normal, to high.

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. People with acute metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur.

Chronic metabolic acidosis: Chronic metabolic acidosis has non-specific clinical symptoms but can be readily diagnosed by testing serum bicarbonate levels in patients with Chronic Kidney Disease as part of a comprehensive metabolic panel. Patients with CKD Stages G3-G5 should be routinely screened for metabolic acidosis.

Pathophysiology Compensatory mechanisms: Metabolic acidosis is characterized by a low concentration of bicarbonate (HCO−3), which can happen with increased generation of acids (such as ketoacids or lactic acid), excess loss of HCO−3 by the kidneys or gastrointestinal tract, or an inability to generate sufficient HCO−3. Thus demonstrating the importance of maintaining balance between acids and bases in the body for maintaining optimal functioning of organs, tissues and cells. The body regulates the acidity of the blood by four buffering mechanisms.

• Bicarbonate buffering system

• Intracellular buffering by absorption of hydrogen atoms by various molecules, including proteins, phosphates and carbonate in bone.

• Respiratory compensation. Hyperventilation will cause more carbon dioxide to be removed from the body and thereby increase pH. • Kidney compensation

Treatment Acute Metabolic Acidosis: Bicarbonate therapy is generally administered In patients with severe acute acidemia (pH < 7.11), or with less severe acidemia (pH 7.1-7.2) who have severe acute kidney injury. Bicarbonate therapy is not recommended for people with less severe acidosis (pH ≥ 7.1), unless severe acute kidney injury is present. In the BICAR-ICU trial, bicarbonate therapy for maintaining a pH >7.3 had no overall effect on the composite outcome of all-cause mortality and the presence of at least one organ failure at day 7. However, amongst the sub-group of patients with severe acute kidney injury, bicarbonate therapy significantly decreased the primary composite outcome, and 28-day mortality, along with the need for dialysis.

Chronic Metabolic Acidosis: For people with Chronic Kidney Disease, treating metabolic acidosis slows the progression of chronic kidney disease.Dietary interventions for treatment of chronic metabolic acidosis include base-inducing fruits and vegetables that assist with reducing the urine net acid excretion, and increase TCO2. Recent research has also suggested that dietary protein restriction, through ketoanalogue-supplemented vegetarian very low protein diets are also a nutritionally safe option for correction of metabolic acidosis in people with Chronic Kidney Disease.

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Endocrinology and Metabolism: Open Access
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