4  Acid-Base Disorders

Author

Prof. Sampson Antwi

4.1 Introduction

Acid-base balance is vital for normal cellular metabolism and physiological function. In children, acid-base disturbances can arise from a variety of causes and often signal serious underlying pathology. The developing physiology of infants and children also makes them particularly vulnerable to imbalances.

This guide aims to provide medical students, particularly in Ghana, with a comprehensive understanding of acid-base disorders, their causes, clinical manifestations, diagnosis, and management, with a focus on conditions commonly encountered in paediatric practice in resource-limited settings.

4.2 Physiology of Acid-Base Balance

4.2.1 Normal pH and Buffer

  • Normal arterial blood pH: 7.35 – 7.45
  • Key buffer systems:
    • Bicarbonate buffer (HCO₃⁻ / H₂CO₃)
    • Phosphate buffer
    • Protein buffer (e.g., haemoglobin)

4.2.2 Regulation Mechanisms

  1. Lungs: Excrete CO₂ (volatile acid)
  2. Kidneys: Reabsorb bicarbonate and excrete H⁺ (non-volatile acids)
  3. Buffers: Immediate but temporary pH regulation

4.3 Classification of Acid-Base Disorders

Acid-base disorders are classified as:

  1. Metabolic Acidosis
  2. Metabolic Alkalosis
  3. Respiratory Acidosis
  4. Respiratory Alkalosis

Each has compensatory mechanisms that attempt to restore pH toward normal.

4.4 Metabolic Acidosis

4.4.1 Definition

Characterized by decreased pH and bicarbonate (< 22 mmol/L)

4.4.2 Causes

In Ghana and other resource-limited settings, common causes include:

High Anion Gap Normal Anion Gap (Hyperchloremic)
Diabetic ketoacidosis (DKA) Diarrhea (bicarbonate loss)
Lactic acidosis (sepsis, hypoxia, severe anaemia) Renal tubular acidosis (RTA)
Inborn errors of metabolism Early renal failure
Uraemia Use of carbonic anhydrase inhibitors

Anion Gap (AG) = Na⁺ – (Cl⁻ + HCO₃⁻)
Normal AG: 8 – 12 mmol/L

4.4.3 Clinical Features

  • Kussmaul breathing (deep, rapid)
  • Lethargy, confusion
  • Hypotension
  • Signs of dehydration

4.4.4 Diagnosis

  • Arterial blood gas (ABG): ↓pH, ↓HCO₃⁻
  • Serum electrolytes
  • Urine analysis (in RTA)
  • Blood glucose and ketones (in DKA)

4.4.5 Management

  • Treat the underlying cause
  • Rehydration (e.g., with normal saline)
  • DKA: Insulin therapy, fluids, potassium replacement
  • Severe acidosis (pH < 7.1): Consider sodium bicarbonate cautiously
  • Monitor electrolytes, especially K⁺

4.5 Metabolic Alkalosis

4.5.1 Definition

Elevated pH and bicarbonate (> 28 mmol/L)

4.5.2 Causes

Chloride-Responsive Chloride-Resistant
Vomiting or nasogastric suction Primary hyperaldosteronism
Diuretic therapy Congenital adrenal hyperplasia
Volume depletion Severe hypokalemia

4.5.3 Clinical Features

  • Muscle cramps, weakness
  • Tetany (due to hypocalcemia)
  • Hypoventilation (compensatory)
  • Confusion, seizures (severe)

4.5.4 Diagnosis

  • ABG: ↑pH, ↑HCO₃⁻
  • Serum electrolytes: Look for hypokalemia, hypochloremia
  • Urine chloride

4.5.5 Management

  • Volume replacement with normal saline
  • Potassium supplementation
  • Correct underlying cause
  • If resistant to saline: consider aldosterone antagonists (e.g., spironolactone)

4.6 Respiratory Acidosis

4.6.1 Definition

↓pH and ↑pCO₂ (> 45 mmHg)

4.6.2 Causes

Due to hypoventilation:

  • CNS depression (head injury, infections)
  • Neuromuscular disorders (e.g., Guillain-Barré syndrome)
  • Chest wall deformities
  • Airway obstruction (e.g., asthma, foreign body)
  • Respiratory muscle fatigue

4.6.3 Clinical Features

  • Altered mental status
  • Headache
  • Tachycardia
  • Cyanosis
  • Papilledema (chronic)

4.6.4 Diagnosis

  • ABG: ↓pH, ↑pCO₂

  • Evaluate oxygenation (PaO₂)

  • Chest X-ray, pulmonary function tests (if available)

4.6.5 Management

  • Support ventilation (e.g., oxygen, non-invasive or mechanical ventilation)
  • Treat the underlying cause (e.g., bronchodilators for asthma)
  • Caution: Over-oxygenation can suppress respiratory drive in chronic cases

4.7 Respiratory Alkalosis

4.7.1 Definition

  • ↑pH and ↓pCO₂ (< 35 mmHg)

4.7.2 Causes

  • Anxiety, pain (hyperventilation)
  • Fever
  • Sepsis
  • Salicylate poisoning (early)
  • Central causes (e.g., meningitis)
  • High altitude (rare in Ghana)

4.7.3 Clinical Features

  • Light-headedness, dizziness
  • Perioral numbness
  • Muscle cramps
  • Tachypnoea

4.7.4 Diagnosis

  • ABG: ↑pH, ↓pCO₂
  • Serum calcium and phosphate (often decreased)

4.7.5 Management

  • Address the underlying cause
  • Calm the child (rebreathing bag if appropriate)
  • Treat fever or infections
  • Sedation may be necessary in extreme anxiety

4.8 Mixed Acid-Base Disorders

Children can present with more than one disorder simultaneously, especially in critical illness.

Examples:

  • DKA with vomiting → Metabolic acidosis + metabolic alkalosis
  • Sepsis with respiratory failure → Metabolic acidosis + respiratory acidosis

Clues to Mixed Disorders:

  • pH is normal, but CO₂ and HCO₃⁻ are abnormal
  • Compensation appears inadequate or excessive

Use Winter’s formula to assess expected respiratory compensation in metabolic acidosis:

Expected pCO₂ = (1.5 × HCO₃⁻) + 8 ± 2

4.9 Pediatric Considerations

  • Neonates have immature kidneys → limited ability to excrete acid
  • Dehydration is a common cause of acid-base disturbances
  • Malaria, severe diarrhoea, and pneumonia are leading paediatric conditions in Ghana that may present with acid-base imbalance

4.10 Laboratory Evaluation

Key investigations:

  1. ABG Analysis
  2. Serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻)
  3. Anion gap calculation
  4. Urine pH and electrolytes (in RTA)
  5. Lactate, ketones, glucose

4.11 Approach to a Child with Suspected Acid-Base Disorder

  1. Assess airway, breathing, and circulation (ABC)
  2. Clinical history
    • Diarrhoea, vomiting, fever, polyuria
    • Diabetes, drug use
  3. Examination
    • Level of consciousness
    • Respiratory pattern (Kussmaul, hypoventilation)
    • Signs of dehydration or oedema
  4. ABG + Electrolytes
  5. Determine primary disorder and compensation
  6. Treat the cause and monitor

4.12 Resource-Limited Considerations (Ghana Context)

  • ABGs may not be widely available — rely on clinical signs, serum bicarbonate, venous blood gases
  • In emergencies, treat based on likely diagnosis (e.g., give fluids for suspected DKA even before lab confirmation)
  • Point-of-care testing (glucometers, lactate meters) can aid rapid decision-making

4.13 Summary Table

Disorder pH HCO₃⁻ pCO₂ Compensation
Metabolic Acidosis ↓ ↓ ↓ (respiratory) Hyperventilation
Metabolic Alkalosis ↑ ↑ ↑ Hypoventilation
Respiratory Acidosis ↓ ↑ (renal) ↑ Renal HCO₃⁻ retention
Respiratory Alkalosis ↑ ↓ (renal) ↓ Renal HCO₃⁻ loss

4.14 Conclusion

Understanding acid-base disorders in children is crucial for early recognition and effective treatment, particularly in acute settings like emergency departments and paediatric wards. In Ghana, common contributors include dehydration from diarrhoea, infections, and diabetic ketoacidosis (DKA). A systematic clinical and laboratory approach allows timely diagnosis and management, even in resource-constrained environments.