Pediatric Metabolic Acidosis Treatment & Management

Inability to recognize the etiology of metabolic acidosis can lead to failure to treat the basic disease process. For example, a child who ingests windshield-wiper fluid containing ethylene glycol may present with severe metabolic acidosis, hypoglycemia, and coma. Failure to be adequately suspicious regarding this symptom complex would prevent the physician from obtaining immediate treatment (hemodialysis) for this patient.

Insulin administration is necessary in cases of diabetic ketoacidosis, and restoration of adequate perfusion with crystalloid administration is necessary in cases of dehydration. ^{[8, 9]} The same holds true for other diseases, such as renal failure and shock, that lead to metabolic acidosis.

In a retrospective chart review study, Cohen et al found evidence that subcutaneous regular insulin administered every 4 hours is a safe and effective alternative for the insulin treatment of pediatric diabetic ketoacidosis (DKA) with pH > 7.0. In the 76 DKA episodes in 52 patients included in the study, the investigators’ protocol resulted in recovery from DKA with a median time to DKA resolution of 10.3 (5.5, 14.2) hours. No incidents of cerebral edema, cardiac arrhythmias, or mortality occurred. ^[10]

Further inpatient management, including critical care, depends on the underlying etiology. Children with inherited metabolic abnormalities, poisoning, or renal failure may require hemodialysis. Children with lactic acidosis caused by circulatory failure, thiamine deficiency, or septic shock require appropriate supportive care that first addresses the ABCs and potentially includes fluid resuscitation, inotropic support, and antibiotics. Children with diabetic ketoacidosis must be treated with appropriate fluid and electrolyte therapy and insulin.

The underlying disease state (eg, diabetes, renal failure) may require diet modification.

A 2009 study concluded that albumin was not more effective than normal saline in initial hydration of dehydrated term infants with metabolic acidosis due to acute diarrhea. ^[11]

Go to Metabolic Acidosis in Emergency Medicine and Metabolic Acidosis for complete information on these topics.

Consultations depend on the underlying etiology of metabolic acidosis and include the following:

• Critical care specialist: in cases of metabolic acidosis with shock

• Nephrologist: in cases of children with renal failure, who may or may not require dialysis

• Geneticist: in cases of inborn errors of metabolism

• Surgeon: in cases where the underlying cause of metabolic acidosis is surgical in nature (necrotizing enterocolitis, malrotation, volvulus, ruptured appendicitis)

• Endocrinologist: in cases of children whose metabolic acidosis is caused by diabetic ketoacidosis

In instances in which the serum bicarbonate level is only mildly to moderately depressed (>10-12 mEq/L), bicarbonate replacement may not be necessary. If the underlying disease is treated appropriately, the kidneys are able to replenish bicarbonate stores within 3-4 days, unless significant renal dysfunction is present.

In some disease states, the use of bicarbonate therapy is clearly indicated. For patients with chronic renal failure or renal tubular acidosis (RTA), bicarbonate replacement is necessary because of known, ongoing bicarbonate losses. In salicylate intoxication, short-term therapy with bicarbonate to create an alkalemic environment enhances toxin elimination.

Emergent bicarbonate therapy may be warranted in decompensated shock states in patients with a pH of less than 7.15. Studies of human lactic acidosis have generally failed to demonstrate a hemodynamic benefit to bicarbonate therapy. ^[12] Patients with lactic acidosis from severe asthma exacerbations, however, may benefit from bicarbonate therapy. ^[13] A survey of pediatric acute care physicians published in 2013 showed that there is a range of opinions regarding the use of emergency bicarbonate therapy in shock and cardiac arrest. ^[14]

Calculating the amount of bicarbonate replacement necessary must take into account the effect of nonbicarbonate buffers on exogenously administered bicarbonate. Multiply the desired increase in plasma bicarbonate concentration by the apparent volume of distribution and weight. The bicarbonate deficit can be calculated as follows:

(Desired Bicarbonate - Measured Bicarbonate) x Weight (kg) x 0.6

The general recommendation is to replace only half of the total bicarbonate deficit during the first few hours of therapy.

Do not overestimate or overcorrect the bicarbonate deficit. Rapid infusion of bicarbonate for chronic conditions and overcorrection of the metabolic acidosis can lead to complications such as tetany, seizures, and hypokalemia by worsening the preexisting hypocalcemia and hypokalemia.

Doses of bicarbonate exceeding 1 mEq/kg per dose may lead to an alkaline overshoot. For each 0.1 increase in pH, oxygen availability may decrease by 10% because of the shift of the oxygen-hemoglobin dissociation curve to the left.

Parenteral forms of sodium bicarbonate are available as 4% (half strength) or 8% solutions. The sodium load can be significant when multiple bolus doses are administered.

If hypernatremia is a concern, consider continuous infusion of sodium bicarbonate as part of the maintenance intravenous solution. For example, 34 mEq/L of sodium bicarbonate can be added to a 0.22% sodium chloride solution to make up a 0.45% salt solution for maintenance intravenous therapy.

The use of sodium bicarbonate therapy in cases of diabetic ketoacidosis is controversial. A report by Glaser et al stated that patients with diabetic ketoacidosis who were treated with sodium bicarbonate were at increased risk for cerebral edema. ^[3]

In newborns, frequent administration of hypertonic solutions, such as sodium bicarbonate, have led to intracranial hemorrhage resulting from hyperosmolality and resultant fluid shifts from the intracellular space.

Rapid infusion of sodium bicarbonate to correct metabolic acidosis has led to paradoxical CNS acidosis in animal studies. The cause is believed to be sodium bicarbonate dissociating into carbon dioxide and water; carbon dioxide rapidly crosses the blood-brain barrier, but bicarbonate does not, leading to CNS acidosis.

Thiamine deficiency is a very rare cause of severe lactic acidosis and shock, which is often resistant to inotropic agents and volume resuscitation. Thiamine deficiency should be considered for patients with lactic acidosis and shock on long-term total parenteral nutrition without multivitamins for 2 or more weeks. Thiamine administration rapidly corrects the clinical symptomatology.

Tromethamine (also called THAM or tris [hydroxymethyl]-aminomethane) is a buffer that can be used to treat acidosis when concerns exist regarding carbon dioxide accumulation from the metabolism of administered sodium bicarbonate. THAM increases serum bicarbonate predictably:

• THAM + H₂ CO₃ → THAM-H + HCO₃

• H₂ CO₃ → CO₂ + H₂ O

• Dose: 1 mEq/kg

Hemodialysis

Hemodialysis is an option for correcting a severe metabolic acidosis associated with renal failure or intoxication with methanol or ethylene glycol. ^[15]

Surgical care

Surgical care may be indicated based on the etiology of metabolic acidosis. Tissue ischemia or necrosis from bowel obstruction or necrotizing enterocolitis, with or without peritonitis, may lead to metabolic acidosis.

Especially in newborns with necrotizing enterocolitis, metabolic acidosis may be the first laboratory abnormality associated with a surgical abdomen.