Metabolic Acidosis Nursing Management and Interventions

Metabolic acidosis is an acid-base imbalance from excessive absorption or retention of acid, or excessive excretion of bicarbonate, driven by an underlying disorder. It never stands alone, so treat the cause while you support the patient. The symptoms come from the body trying to compensate through the lungs, kidneys, and cells.

Metabolic acidosis presents with a normal or high anion gap. Direct loss of bicarbonate, gain of chloride, or decreased ammonia production keeps the anion gap within normal limits; accumulation of organic anions such as ketones or lactic acid produces high anion gap acidosis. Compensation includes increased respirations to blow off excess CO2, increased ammonia formation, and acid (H+) excretion by the kidneys with retention of bicarbonate and sodium.

High anion gap acidosis occurs in diabetic ketoacidosis; severe malnutrition or starvation; alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets or lipid administration; poisoning such as salicylate intoxication (after the initial stage) and paraldehyde intoxication; and drug therapy such as acetazolamide (Diamox) and NH4Cl. Normal anion gap acidosis goes with loss of bicarbonate, as in renal tubular acidosis, hyperalimentation, vomiting or diarrhea, small-bowel or pancreatic fistulas, and ileostomy, and with IV sodium chloride in preexisting kidney dysfunction or acidifying drugs such as ammonium chloride.

Care Setting

Metabolic acidosis is a complication of a broader problem and may require inpatient care in a medical-surgical or subacute unit.

Related Concerns

Plans of care specific to predisposing factors, fluid and electrolyte imbalances, renal dialysis, respiratory acidosis (primary carbonic acid excess), and respiratory alkalosis (primary carbonic acid deficit).

Causes

Anaerobic carbohydrate metabolism, renal insufficiency and failure, diarrhea and intestinal malabsorption, ketoacidosis, lactic acidosis, prolonged fasting, salicylate poisoning, oliguric renal disease, and abnormal bicarbonate losses (loss of fluid from the lower GI tract from surgery, drains, or severe diarrhea).

Complications

Coma, arrhythmias, and cardiac arrest.

Signs and Symptoms

Headache, drowsiness and confusion, weakness, increased respiratory rate and depth, and nausea and vomiting. Diminished cardiac output with a pH below 7 produces hypotension, cold clammy skin, and cardiac arrhythmias.

Assessment

Activity and rest: lethargy, fatigue, muscle weakness. Circulation: hypotension, wide pulse pressure, a weak or irregular pulse (dysrhythmias), and jaundiced sclera, skin, or mucous membranes with liver failure. Elimination: diarrhea, dark or concentrated urine. Food and fluid: anorexia, nausea and vomiting, poor skin turgor, dry mucous membranes. Neurosensory: headache, drowsiness, decreased mental function, changes in sensorium (stupor, confusion, lethargy, depression, delirium, coma), decreased deep-tendon reflexes, and muscle weakness. Respiration: dyspnea on exertion, hyperventilation, and Kussmaul's respirations (deep, rapid breathing). Safety: fever and signs of sepsis, with a history of blood product transfusion or hepatitis exposure. Teaching and learning: history of alcohol abuse and use of carbonic anhydrase inhibitors or anion-exchange resins such as cholestyramine (Questran).

Diagnostic Studies

Arterial pH below 7.35 confirms metabolic acidosis. In severe states pH may fall to 7.10, the partial pressure of arterial carbon dioxide (PaCO2) may be normal or below 34 mmHg, and bicarbonate may fall below 22 mEq/L. PaCO2 runs less than 35 mm Hg and base excess is negative. Anion gap is higher than 14 mEq/L (high anion gap) or in the range of 10 to 14 mEq/L (normal anion gap). Serum potassium is increased, above 5.5 mEq/L from chemical buffering (except in diarrhea and renal tubular acidosis), and serum chloride is increased. Serum glucose may be decreased or increased depending on etiology and runs above 150 mg/dl in diabetics. Serum ketones are increased in diabetes, starvation, and alcohol intoxication, and plasma lactic acid is elevated in lactic acidosis. Urine pH is decreased, below 4.5 in the absence of renal disease. ECG shows cardiac dysrhythmias (bradycardia) and changes associated with hyperkalemia, such as a tall T wave.

Nursing Priorities

Achieve homeostasis, prevent or minimize complications, and provide information about the condition, prognosis, and treatment needs.

Discharge Goals

Physiological balance restored, free of complications, condition and treatment needs understood, and a plan in place to meet needs after discharge.

Treatment

Give sodium bicarbonate IV for severe cases, evaluate and correct electrolyte imbalances, and ultimately correct and manage the underlying cause.

Nursing Interventions and Considerations

Keep sodium bicarbonate ampules handy for emergency administration. Monitor vital signs, laboratory results, and level of consciousness frequently, and watch for a decreasing level of consciousness. Record intake and output accurately to monitor renal function. Position the patient to prevent aspiration, since vomiting is common. Prepare for possible seizures and take precautions. Provide good oral hygiene after vomiting, using sodium bicarbonate washes to neutralize acid in the patient's mouth.