Acid-base disorders in children — formative SAQs

SAQ 1 (10)

A 9-year-old girl presents to the emergency department with a two-day history of polyuria, polydipsia, vomiting and abdominal pain. She is drowsy and dehydrated, with deep sighing respirations at 36 per minute. A venous gas shows pH 7.10, pCO2 16 mmHg, bicarbonate 5 mmol per litre, sodium 132, chloride 98, glucose 28 mmol per litre, and ketones are positive. [5][1]

1. Apply the six-step systematic approach to this blood gas and state the primary disorder and its severity. (3) [1][3]
2. Calculate the anion gap and interpret it, and calculate the expected pCO2 using Winters formula and comment on whether the respiratory compensation is appropriate. (4) [1][3]
3. Outline the immediate management and explain why intravenous sodium bicarbonate is not indicated. (3) [5][10]

Model answer

Six-step approach and primary disorder. Step 1, the pH of 7.10 is acidemia. Step 2, the bicarbonate of 5 mmol per litre is low and the pCO2 is low, so the primary process is a metabolic acidosis with respiratory compensation. The severity is profound. Steps 3 to 6 follow. The picture is diabetic ketoacidosis, given the hyperglycaemia, ketosis, dehydration and Kussmaul respirations, and the deep sighing breathing is the body attempting to blow off carbon dioxide to compensate for the metabolic acidosis. [1][5]

Anion gap, Winters formula and compensation. Step 3, the anion gap is sodium minus chloride plus bicarbonate, which is 132 minus 98 plus 5, equal to 29 mmol per litre, well above the normal 8 to 12, confirming a high anion gap metabolic acidosis from ketoacid accumulation. Step 4, the Winters expected pCO2 is 1.5 times the bicarbonate plus 8, which is 1.5 times 5 plus 8, equal to 15.5, with a range of about 13 to 18 mmHg. The measured pCO2 of 16 falls within that range, so the respiratory compensation is appropriate and there is no coexisting respiratory disorder. The delta ratio, as a check, is the gap change over the bicarbonate change, which is 29 minus 12 over 24 minus 5, equal to 17 over 19 or about 0.9, suggesting a near-pure high gap acidosis with a hint of volume contraction. [1][3]

Management and the bicarbonate question. Immediate management follows the DKA protocol: structured intravenous fluid resuscitation to restore the circulating volume and correct the deficit, a fixed-rate intravenous insulin infusion at 0.1 units per kilogram per hour started once the potassium is known and replacement potassium begun, and close monitoring for the cerebral oedema that is the feared complication. Intravenous sodium bicarbonate is not indicated here: the pH is above 6.9, and bicarbonate has not shown a mortality benefit in DKA and is associated with harm through carbon dioxide generation that worsens intracellular acidosis, hypernatraemia and fluid overload, and a shift of potassium into cells. The acidosis corrects as fluids and insulin switch off ketogenesis. [5][10]

SAQ 2 (10)

A 6-week-old infant presents with projectile non-bilious vomiting for three days and is clinically dehydrated. A venous gas shows pH 7.50, pCO2 50 mmHg, bicarbonate 38 mmol per litre, sodium 135, chloride 88, potassium 2.9. [12][1]

1. Apply the six-step approach and name the primary disorder. (3) [1][12]
2. Explain the mechanism of the metabolic alkalosis in this infant, and why the potassium and chloride are low. (4) [12][4]
3. Outline the immediate fluid and electrolyte management and the definitive treatment. (3) [12][5]

Model answer

Six-step approach and primary disorder. Step 1, the pH of 7.50 is alkalemia. Step 2, the bicarbonate of 38 mmol per litre is high and the pCO2 is mildly elevated at 50, so the primary process is a metabolic alkalosis with modest respiratory compensation. The picture, in a 6-week-old with projectile non-bilious vomiting and a hypokalaemic hypochloraemic alkalosis, is pyloric stenosis. [1][12]

Mechanism of the alkalosis and the electrolytes. Persistent vomiting of gastric acid removes hydrogen and chloride, generating a hypochloraemic metabolic alkalosis. The volume and chloride depletion maintain it: as the kidney reabsorbs sodium in the distal nephron without chloride, it exchanges it for hydrogen and potassium, worsening the alkalosis and producing the hypokalaemia. The urine chloride is low (the kidney is chloride-hungry), which is the hallmark of a chloride-responsive metabolic alkalosis. The respiratory compensation raises the pCO2 to blunt the alkalemia, but it is limited. [12][4]

Fluid and electrolyte management and definitive treatment. Immediate management is resuscitation with intravenous normal saline and potassium chloride to correct the volume, chloride and potassium deficit, because the alkalosis and hypokalaemia are anaesthetic risks and must be corrected before any surgery. The definitive treatment is surgical pyloromyotomy after stabilisation, and the alkalosis resolves as feeding resumes. The chloride-responsive alkalosis corrects with saline and potassium, not with acid, and the principle is to restore chloride and volume so the kidney can excrete the excess bicarbonate. [12][5]