How should I rapidly evaluate and manage metabolic acidosis in a critically ill child in the ICU?

Rapid Evaluation and Management of Metabolic Acidosis in Critically Ill Children

Establish effective ventilation immediately, obtain venous blood gas with electrolytes, calculate the anion gap, and begin targeted resuscitation based on the underlying cause while monitoring glucose and ionized calcium.

Initial Assessment and Stabilization

Airway and breathing take absolute priority because up to 40% of cardiac output is consumed by work of breathing in critically ill children, and intubation with mechanical ventilation can reverse shock by reducing this metabolic demand. 1

Immediate Airway Management

• Assess for increased work of breathing, hypoventilation, or altered mental status—these clinical findings mandate intubation without waiting for confirmatory laboratory tests. 1
• As sepsis progresses, children develop metabolic acidosis and risk respiratory acidosis from parenchymal lung disease or inadequate respiratory effort due to altered mental status. 1
• Use ketamine with atropine pretreatment as the sedative/induction regimen of choice to maintain cardiovascular integrity during intubation. 1
• Avoid etomidate, as it suppresses the endogenous stress hormone response. 1
• Volume load and provide peripheral or central inotropic/vasoactive support before and during intubation due to relative or absolute hypovolemia and cardiac dysfunction. 1

Essential Monitoring Parameters

• Continuous pulse oximetry, electrocardiography, blood pressure with attention to pulse pressure (wide pulse pressure suggests low SVR; narrow pulse pressure suggests high SVR). 1
• Temperature, urine output (target >1 mL/kg/h), glucose, and ionized calcium. 1
• Mental status assessment—therapeutic endpoints include normal mental status, capillary refill ≤2 seconds, warm extremities, and normal blood pressure for age. 1

Diagnostic Evaluation

Obtain Venous Blood Gas and Electrolytes

• Venous pH is typically ~0.03 units lower than arterial pH and can be used for ongoing monitoring after the diagnosis is confirmed, eliminating the need for repeat arterial blood gases in most cases. 2
• Measure serum bicarbonate from the basic metabolic panel—the "CO2" on a BMP reflects total serum CO2 (predominantly bicarbonate), not arterial PCO2. 2
• Metabolic acidosis is characterized by primary reduction in serum bicarbonate (<22 mmol/L) associated with blood pH <7.35. 2

Calculate the Anion Gap

• Anion gap = Na⁺ − (HCO₃⁻ + Cl⁻), with normal values of 10–12 mEq/L. 2
• An anion gap >12 mEq/L signifies accumulation of unmeasured anions such as lactate, ketoacids, uremic toxins, or ingested toxins. 2
• Determining the presence or absence of an anion gap is the first step in ascertaining the etiology of metabolic acidosis. 3

Additional Diagnostic Studies

• Measure plasma glucose, serum/urine ketones, lactate, creatinine, and urea at initial presentation. 2
• Calculate effective serum osmolality: 2[Na measured (mEq/L)] + glucose (mg/dL)/18 to assess for osmolal gap in suspected toxic ingestions. 2
• Evaluate urine pH and serum potassium levels, which may be useful in certain settings. 3

Circulation and Fluid Resuscitation

Vascular Access and Initial Resuscitation

• Rapidly attain vascular access—establish intraosseous access if reliable venous access cannot be obtained within minutes. 1
• Commence fluid resuscitation immediately unless hepatomegaly or rales are present (though rales may be heard in pneumonia-related sepsis and do not always imply fluid overload). 1
• Administer isotonic saline (0.9% NaCl) at 15–20 mL/kg/h during the first hour to restore intravascular volume and renal perfusion. 2

Inotropic Support for Fluid-Refractory Shock

• Begin a peripheral inotrope (low-dose dopamine or epinephrine) if a second peripheral IV/intraosseous catheter is in place while establishing central venous access. 1
• When administered peripherally, infuse the inotrope as a dilute solution or with a carrier solution to ensure timely delivery to the heart. 1
• Reduce dosage if evidence of peripheral infiltration or ischemia occurs, as alpha-adrenergic effects occur at higher concentrations. 1
• Central dopamine, epinephrine, or norepinephrine can be administered as first-line drugs based on hemodynamic state once central access is established. 1

Sodium Bicarbonate Therapy

Indications and Dosing

• Routine initial use of sodium bicarbonate to treat cardiac arrest is not recommended. 1
• Sodium bicarbonate may be used in patients with documented metabolic acidosis after effective ventilation has been established (effective ventilation is needed to allow elimination of excess CO2 produced by bicarbonate). 1
• Dosing: 1–2 mEq/kg IV/IO given slowly; do not give by endotracheal route. 1
• Only the 0.5 mEq/mL concentration should be used for newborn infants; dilution of available stock solutions may be necessary. 1
• Do not mix sodium bicarbonate with vasoactive amines or calcium. 1

Specific Clinical Scenarios

Diabetic Ketoacidosis:

• Bicarbonate therapy is generally NOT indicated in DKA unless pH falls below 6.9–7.0. 2
• The cornerstone of DKA therapy is intravenous insulin combined with fluid resuscitation. 2
• Start continuous IV regular insulin at 0.1 U/kg/h after confirming serum potassium >3.3 mEq/L. 2
• When plasma glucose reaches ~250 mg/dL, reduce insulin to 0.05–0.1 U/kg/h and add 5–10% dextrose to IV fluids. 2
• Resolution criteria: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, and venous pH ≥7.3. 2

Septic Shock:

• Sodium bicarbonate should not be used to treat metabolic acidosis arising from tissue hypoperfusion in sepsis—instead focus treatment on restoring tissue perfusion with fluid resuscitation and vasopressors. 2

Cardiac Arrest:

• In cardiac arrest, a rapid IV dose of one to two 50 mL vials (44.6 to 100 mEq) may be given initially and continued at 50 mL every 5–10 minutes if necessary (as indicated by arterial pH and blood gas monitoring). 4

Hyperkalemia, Hypermagnesemia, or Calcium Channel Blocker Toxicity:

• Administer calcium chloride 20 mg/kg (0.2 mL/kg for 10% CaCl2) by slow push for cardiac arrest or infuse over 30–60 minutes for other indications. 1
• Calcium chloride administration results in more rapid increase in ionized calcium than calcium gluconate and is preferred for the critically ill child. 1

Sodium Channel Blocker Overdose:

• Titrate bicarbonate to maintain serum pH of 7.45–7.55, followed by infusion of 150 mEq NaHCO3/L solution to maintain alkalosis. 1

Monitoring During Treatment

Serial Laboratory Assessment

• Check venous pH and anion gap every 2–4 hours to assess resolution of acidosis. 2
• Monitor serum potassium every 2–4 hours because alkalinization drives potassium intracellularly and can precipitate life-threatening hypokalemia. 2
• Measure serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻) every 2–4 hours during active treatment. 2
• Once renal perfusion is restored and urine output established, add 20–30 mEq/L potassium (2/3 KCl and 1/3 KPO4) to maintenance fluids. 2

Clinical Response Indicators

• Improved mental status, capillary refill ≤2 seconds, warm extremities, and urine output >1 mL/kg/h. 1
• Normal blood pressure for age (noninvasive blood pressure only reliable when pulses palpable). 1
• Normal glucose and ionized calcium concentrations. 1

Common Pitfalls and Caveats

Ventilation Before Bicarbonate

• Never administer bicarbonate without first establishing effective ventilation, as bicarbonate generates CO2 that must be eliminated to prevent worsening acidosis. 1
• The body attempts to compensate for metabolic acidosis by increasing ventilation to eliminate CO2—intubation may be required to achieve adequate compensation. 2

Avoid Excessive Bicarbonate

• In less urgent forms of metabolic acidosis, it is unwise to attempt full correction of low total CO2 content during the first 24 hours, as this may be accompanied by unrecognized alkalosis due to delayed readjustment of ventilation. 4
• Achieving total CO2 content of about 20 mEq/L at the end of the first day will usually be associated with normal blood pH. 4
• Values brought to normal or above normal within the first day are very likely associated with grossly alkaline blood pH and undesired side effects. 4

Iatrogenic Hyperchloremic Acidosis

• Large-volume 0.9% saline infusion can produce dilutional hyperchloremic metabolic acidosis by increasing serum chloride and decreasing the strong ion difference. 2
• After initial resuscitation, consider switching to balanced crystalloids (Lactated Ringer's or Plasma-Lyte) to avoid additional chloride loading. 2

Hypokalemia Risk

• Insulin therapy, alkalinization, and correction of acidosis all drive potassium intracellularly, creating risk of severe hypokalemia. 2
• Do not start insulin in DKA if serum potassium is <3.3 mEq/L—replete potassium first. 2

Infants at Higher Risk

• Infants have lower erythrocyte CYB5R activity (50–60% of adult values) and higher levels of HbF, making them more susceptible to methemoglobinemia. 1
• Infants with marked metabolic acidosis from sepsis or diarrhea may improve with aggressive hydration and bicarbonate to correct acidosis alone if methemoglobin level is <20%. 1

Multiple Underlying Mechanisms

• Most ICU patients with metabolic acidosis have multiple underlying mechanisms present simultaneously (unmeasured anions in 98%, hyperchloremia in 80%, elevated lactate in 62%). 5
• Calculation of the albumin-corrected and lactate-corrected anion gap reliably determines these mechanisms. 5