Metabolic Acidosis in Children

Introduction to Metabolic Acidosis in Children

Metabolic acidosis is an acid-base disorder characterized by a primary decrease in serum bicarbonate (HCO3-) concentration, resulting in a decrease in blood pH. It occurs when there is either an excess production of acids, increased loss of bicarbonate, or a failure to excrete sufficient amounts of acid.

In pediatric patients, metabolic acidosis is a common and potentially serious condition that can arise from various underlying disorders. It requires prompt recognition and management to prevent complications and improve outcomes. Understanding its pathophysiology, causes, and appropriate interventions is crucial for healthcare providers caring for children.

Pathophysiology of Metabolic Acidosis

The development of metabolic acidosis involves several key mechanisms:

  1. Bicarbonate Loss or Consumption:
    • Gastrointestinal losses (e.g., diarrhea)
    • Renal losses (e.g., renal tubular acidosis)
    • Consumption in buffering excess acids
  2. Acid Generation or Retention:
    • Increased endogenous acid production (e.g., lactic acidosis, ketoacidosis)
    • Ingestion of acid-producing substances
    • Impaired renal acid excretion
  3. Compensatory Mechanisms:
    • Respiratory: Hyperventilation to decrease PaCO2
    • Renal: Increased acid excretion and bicarbonate reabsorption
    • Buffer Systems: Utilization of extracellular and intracellular buffers

In children, these mechanisms may be more pronounced or limited depending on age, developmental stage, and underlying conditions. Infants and young children are particularly susceptible to metabolic acidosis due to their higher metabolic rates and limited renal compensatory capacity.

Etiology of Metabolic Acidosis in Children

Metabolic acidosis in pediatric patients can result from various causes, broadly categorized as:

1. Increased Anion Gap Metabolic Acidosis

  • Lactic acidosis:
    • Tissue hypoxia (shock, severe anemia)
    • Inborn errors of metabolism
  • Ketoacidosis:
    • Diabetic ketoacidosis
    • Starvation ketosis
  • Renal failure
  • Toxins and ingestions:
    • Salicylates
    • Methanol
    • Ethylene glycol
  • Inborn errors of metabolism:
    • Organic acidemias
    • Fatty acid oxidation defects

2. Normal Anion Gap Metabolic Acidosis

  • Gastrointestinal bicarbonate loss:
    • Diarrhea
    • Intestinal or pancreatic fistulas
  • Renal tubular acidosis:
    • Distal (Type 1) RTA
    • Proximal (Type 2) RTA
    • Hyporeninemic hypoaldosteronism (Type 4 RTA)
  • Ureterosigmoidostomy
  • Carbonic anhydrase inhibitors (e.g., acetazolamide)
  • Early renal failure

Clinical Presentation of Metabolic Acidosis in Children

The clinical manifestations of metabolic acidosis can vary depending on the severity, rate of onset, and underlying cause. Common signs and symptoms include:

  • Respiratory:
    • Tachypnea (Kussmaul breathing in severe acidosis)
    • Respiratory distress
  • Neurological:
    • Altered mental status, ranging from lethargy to coma
    • Headache
    • Confusion
  • Cardiovascular:
    • Tachycardia
    • Hypotension (in severe cases)
    • Decreased cardiac contractility
  • Gastrointestinal:
    • Nausea and vomiting
    • Abdominal pain
  • Musculoskeletal:
    • Muscle weakness
    • Bone demineralization (in chronic acidosis)

In infants and young children, nonspecific symptoms such as poor feeding, irritability, and failure to thrive may be present. The clinical picture is often dominated by the underlying condition causing the metabolic acidosis, such as dehydration in diarrhea or specific symptoms related to inborn errors of metabolism.

Diagnosis of Metabolic Acidosis in Children

Diagnosing metabolic acidosis involves a combination of clinical assessment, laboratory tests, and evaluation of the underlying cause:

1. Laboratory Findings

  • Arterial Blood Gas (ABG) or Venous Blood Gas (VBG):
    • Decreased pH (< 7.35)
    • Decreased HCO3- (< 22 mEq/L)
    • Compensatory decrease in PaCO2
  • Serum Electrolytes:
    • Calculation of anion gap: AG = [Na+] - ([Cl-] + [HCO3-])
    • Normal anion gap: 8-12 mEq/L (may be lower in children)
  • Additional Tests Based on Suspected Etiology:
    • Serum lactate
    • Serum ketones
    • Renal function tests
    • Toxicology screens

2. Diagnostic Approach

  1. Confirm the presence of metabolic acidosis
  2. Determine if it's an increased anion gap or normal anion gap acidosis
  3. Evaluate for common causes based on clinical presentation and patient history
  4. Consider rare causes if common etiologies are ruled out

3. Additional Investigations

  • Urinalysis and urine pH
  • Plasma amino acids and urine organic acids (for suspected inborn errors of metabolism)
  • Imaging studies as indicated by clinical presentation

It's crucial to consider the patient's age, clinical context, and the presence of mixed acid-base disorders when interpreting results and formulating a diagnosis.

Management of Metabolic Acidosis in Children

The management of metabolic acidosis in pediatric patients focuses on addressing the underlying cause, correcting severe acidemia, and preventing complications:

1. Treat the Underlying Cause

  • Fluid resuscitation for dehydration
  • Insulin and fluids for diabetic ketoacidosis
  • Antibiotics for sepsis
  • Dialysis for severe renal failure
  • Specific treatments for inborn errors of metabolism

2. Supportive Care

  • Ensure adequate oxygenation and ventilation
  • Maintain circulation with fluid management and inotropes if necessary
  • Correct electrolyte imbalances (particularly potassium)

3. Bicarbonate Therapy

Use with caution and only in specific situations:

  • Severe acidemia (pH < 7.1) with hemodynamic instability
  • Some cases of renal tubular acidosis
  • Certain toxicities (e.g., salicylate poisoning)

Calculate bicarbonate deficit: 0.5 × weight (kg) × (desired - current HCO3-)

4. Renal Replacement Therapy

  • Consider in severe, refractory acidosis
  • Necessary in some cases of acute kidney injury or inborn errors of metabolism

5. Specific Therapies

  • Thiamine for suspected pyruvate dehydrogenase deficiency
  • Carnitine for certain organic acidemias
  • Citrate supplements for renal tubular acidosis

6. Monitoring and Follow-up

  • Serial blood gas measurements and electrolyte monitoring
  • Continuous cardiorespiratory monitoring
  • Neurological assessments

The approach should be tailored to the individual patient, considering age, severity of acidosis, and underlying condition. Rapid correction of chronic acidosis should be avoided to prevent complications such as cerebral edema.



Metabolic Acidosis in Children
  1. What is the definition of metabolic acidosis?
    Metabolic acidosis is defined as a decrease in blood pH (<7.35) due to a primary decrease in serum bicarbonate concentration (<22 mEq/L).
  2. What are the common causes of metabolic acidosis in children?
    Common causes include diarrhea, diabetic ketoacidosis, renal tubular acidosis, inborn errors of metabolism, and certain toxins or medications.
  3. How does the respiratory system compensate for metabolic acidosis?
    The respiratory system compensates by increasing minute ventilation, leading to a decrease in PaCO2.
  4. What is the anion gap, and how is it used in evaluating metabolic acidosis?
    The anion gap is the difference between measured cations and anions. It helps differentiate between high anion gap and normal anion gap metabolic acidosis.
  5. What are the clinical manifestations of severe metabolic acidosis?
    Symptoms may include deep, rapid breathing (Kussmaul respirations), fatigue, nausea, vomiting, and in severe cases, altered mental status and cardiovascular collapse.
  6. How does chronic metabolic acidosis affect bone health in children?
    Chronic metabolic acidosis can lead to increased bone resorption and decreased bone formation, potentially impacting growth and bone density.
  7. What is the role of sodium bicarbonate in treating metabolic acidosis?
    Sodium bicarbonate may be used in severe metabolic acidosis, but its use is controversial and generally reserved for cases with pH <7.1 or bicarbonate <8 mEq/L.
  8. How does diabetic ketoacidosis (DKA) cause metabolic acidosis?
    In DKA, insulin deficiency leads to increased lipolysis and ketone body production, resulting in a high anion gap metabolic acidosis.
  9. What is the significance of calculating the delta gap in mixed acid-base disorders?
    The delta gap helps identify the presence of a concurrent metabolic alkalosis or acidosis in patients with high anion gap metabolic acidosis.
  10. How does lactic acidosis contribute to metabolic acidosis in critically ill children?
    Lactic acidosis occurs in conditions of tissue hypoperfusion or hypoxia, leading to anaerobic metabolism and lactic acid production.
  11. What is the impact of metabolic acidosis on potassium balance?
    Metabolic acidosis can cause a shift of potassium out of cells, potentially leading to hyperkalemia.
  12. How does renal tubular acidosis (RTA) differ from other causes of metabolic acidosis?
    RTA is characterized by a normal anion gap metabolic acidosis due to impaired renal acid excretion or bicarbonate reabsorption.
  13. What is the role of tromethamine (THAM) in managing metabolic acidosis?
    THAM is an alternative buffer to sodium bicarbonate, particularly useful in situations where sodium or volume overload is a concern.
  14. How does salicylate poisoning cause a mixed acid-base disorder?
    Salicylate poisoning typically causes a mixed high anion gap metabolic acidosis and respiratory alkalosis.
  15. What is the significance of the Winter's formula in assessing respiratory compensation for metabolic acidosis?
    Winter's formula (Expected PaCO2 = 1.5 x [HCO3-] + 8 ± 2) helps determine if respiratory compensation is appropriate for the degree of metabolic acidosis.


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