MCQ: Vomiting in a neonate | ABGs interpretation

Correct Answer: A. Metabolic alkalosis with appropriate respiratory compensation

Explanation: Hypertrophic Pyloric Stenosis and Acid–Base Imbalance

This infant’s clinical presentation is characteristic of hypertrophic pyloric stenosis (HPS), a condition caused by hypertrophy and hyperplasia of the pyloric muscle, resulting in gastric outlet obstruction.

Typical clinical features include:

• Age usually 2–8 weeks.

• Progressive projectile, non-bilious vomiting.

• Persistent hunger after vomiting.

• Poor weight gain or weight loss.

• Dehydration.

• A palpable olive-shaped mass in the upper abdomen in some infants.

The key examination concept is the acid–base disturbance caused by repeated loss of gastric hydrochloric acid.

Step 1: Identify the primary acid–base disorder

The arterial blood gas shows:

• pH: 7.52

• HCO₃⁻: 38 mmol/L

• PaCO₂: 48 mmHg

A pH above 7.45 indicates alkalemia. The elevated bicarbonate concentration identifies a primary metabolic process.

Therefore, the primary disorder is metabolic alkalosis.

Step 2: Assess respiratory compensation

Respiratory compensation for metabolic alkalosis occurs through hypoventilation, which increases PaCO₂ and partially counteracts the rise in pH.

One commonly used formula is:

Expected PaCO₂ = 40 + 0.6 × (HCO₃⁻ − 24)

Increase in bicarbonate:

38 − 24 = 14 mmol/L

Expected PaCO₂:

40 + (0.6 × 14) = 48.4 mmHg

The measured PaCO₂ is 48 mmHg, which closely matches the expected value.

Thus, the final interpretation is:

Metabolic alkalosis with appropriate respiratory compensation.

The measured PaCO₂ does not suggest an additional primary respiratory disorder.

Mechanism of metabolic alkalosis in pyloric stenosis

1. Gastric acid loss

Repeated vomiting causes loss of hydrochloric acid (HCl).

Loss of hydrogen ions (H⁺) leads to metabolic alkalosis, while chloride loss contributes to hypochloremia.

2. Volume depletion

Vomiting causes extracellular fluid depletion, activating the renin–angiotensin–aldosterone system. The kidneys retain sodium and water while increasing potassium and hydrogen ion excretion.

3. Maintenance of alkalosis

Volume depletion, chloride depletion, and potassium depletion impair renal bicarbonate excretion and maintain the metabolic alkalosis.

The characteristic biochemical pattern is hypochloremic, hypokalemic metabolic alkalosis, although the degree of potassium depletion may vary.

Why the other options are incorrect

B. Metabolic alkalosis with additional respiratory acidosis

Incorrect. Although PaCO₂ is elevated relative to the normal value, it is appropriate for the degree of metabolic alkalosis. An additional respiratory acidosis would be suspected if PaCO₂ were substantially higher than the expected compensatory value.

C. Respiratory alkalosis with metabolic compensation

Incorrect. Primary respiratory alkalosis is associated with a reduced PaCO₂. In this case, PaCO₂ is elevated and bicarbonate is markedly increased, supporting primary metabolic alkalosis.

D. Normal anion gap metabolic acidosis with respiratory compensation

Incorrect. Metabolic acidosis is characterized by a reduced bicarbonate concentration. The elevated bicarbonate and alkalemic pH are inconsistent with this diagnosis.

E. Mixed metabolic alkalosis and metabolic acidosis

Incorrect. The provided blood gas values are adequately explained by metabolic alkalosis with appropriate respiratory compensation. No additional metabolic acidosis is demonstrated by these values alone.

Postgraduate Examination Pearls

• Hypertrophic pyloric stenosis classically causes hypochloremic, hypokalemic metabolic alkalosis.

• Vomiting causes loss of gastric hydrogen and chloride ions.

• Volume depletion and secondary aldosterone activation contribute to potassium loss and maintenance of alkalosis.

• Always assess respiratory compensation before diagnosing a mixed acid–base disorder.

• Dehydration and electrolyte abnormalities must be corrected before pyloromyotomy.

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External Resources

1. Royal Children’s Hospital Melbourne: Pyloric stenosis clinical practice guideline — clinical presentation, investigations, fluid management, and preoperative correction.

2. Emmett M. Metabolic Alkalosis: A Brief Pathophysiologic Review — mechanisms underlying the generation and maintenance of metabolic alkalosis.

3. Pathophysiology, Evaluation, and Management of Metabolic Alkalosis — detailed discussion of respiratory compensation, chloride depletion, and clinical management.

4. Interpretation of arterial blood gas — a practical review of acid–base analysis and recognition of mixed disorders.

References

1. Royal Children’s Hospital Melbourne. Pyloric stenosis: clinical practice guideline [Internet]. Melbourne: Royal Children’s Hospital Melbourne. Available from: https://www.rch.org.au/clinicalguide/guideline_index/Pyloric_Stenosis/

2. Emmett M. Metabolic alkalosis: a brief pathophysiologic review. Clin J Am Soc Nephrol. 2020;15(12):1848-1856. doi:10.2215/CJN.16041219.

3. Do C, Vasquez PC, Soleimani M. Pathophysiology, evaluation, and management of metabolic alkalosis. Am J Kidney Dis. 2021;77(3):404-414. doi:10.1053/j.ajkd.2020.09.014.

4. Berend K, de Vries APJ, Gans ROB. Physiological approach to assessment of acid–base disturbances. N Engl J Med. 2014;371(15):1434-1445. doi:10.1056/NEJMra1003327.