Acid-base disorders in children — viva

Opening (must-hit)

"This child has a severe high anion gap metabolic acidosis from diabetic ketoacidosis, and he is compensating appropriately with his breathing. I work through the gas systematically: the pH of 7.12 is acidemia; the bicarbonate of 6 is low and the pCO2 is low, so the primary process is a metabolic acidosis; the anion gap of 28 is high, confirming acid gain; the Winters expected pCO2 is 1.5 times 6 plus 8, equal to 17, with a range of 15 to 19, and his measured 18 falls within that range, so the respiratory compensation is appropriate and there is no coexisting respiratory disorder. The picture with hyperglycaemia and ketones is DKA. My immediate management is structured fluid resuscitation, then a fixed-rate insulin infusion once I know the potassium, careful potassium replacement, and monitoring for cerebral oedema. I would not give bicarbonate here." [1][5]

Examiner: "Why do you calculate the anion gap, and would you correct it for albumin?"

"The anion gap separates acid gain from bicarbonate loss. It is sodium minus chloride plus bicarbonate, normal 8 to 12, and a high gap means an unmeasured acid has accumulated, as with the ketones here. A normal gap would mean bicarbonate has been lost, as in diarrhoea or renal tubular acidosis, and the whole pathway would change. Yes, I correct for albumin in the sick child, because albumin carries much of the unmeasured negative charge and a low albumin narrows the gap, hiding a high gap acidosis. The correction is to add 2.5 mmol per litre to the gap for every 10 g per litre the albumin falls below 40. In this child, unless the albumin were very low, the gap of 28 would remain clearly high after correction." [3][4]

Examiner: "What does the delta gap add, and when would you use it?"

"The delta gap unmixes disorders when the anion gap is high. The delta ratio is the change in the anion gap over the change in the bicarbonate, which is the measured gap minus 12 over 24 minus the bicarbonate. A ratio of 1 to 2 means a pure high gap acidosis, because each excess unmeasured anion consumes roughly one bicarbonate. A ratio below 1 means an additional normal gap metabolic acidosis is present, as if this child also had severe diarrhoea, and a ratio above 2 means an additional metabolic alkalosis, as if he had been vomiting. For this child the ratio is about 16 over 18, around 0.9, so near-pure. I use it whenever the gap is high, because a single headline read can hide a layered disorder." [3][4]

Examiner: "Suppose the pCO2 were 30 instead of 18. What would that tell you?"

"A measured pCO2 of 30, against a Winters expected of about 17, is far higher than the compensation predicts, and it means a coexisting respiratory acidosis. The child would not be compensating adequately for the metabolic acidosis, his breathing would be failing, and I would need to reassess the airway and breathing immediately, with a low threshold for respiratory support. This is the value of Winters formula: it turns a guess about whether the child is tiring into a calculation, and a higher-than-expected pCO2 is the red flag that the airway or ventilation needs attention. Oxygen saturation can be normal while the carbon dioxide climbs, so the gas is essential in any tiring child." [1][3]

Examiner: "Would you give bicarbonate, and what is the evidence?"

"No, not in this child, because his pH is above 6.9 and the modern evidence argues against routine bicarbonate. The trials in severe metabolic acidosis have not shown a mortality benefit, and bicarbonate therapy in severely acidotic patients has been associated with increased mortality through worsened hypernatraemia, fluid overload and paradoxical intracellular acidosis. I reserve bicarbonate for the narrow exceptions: a pH below 6.9 with haemodynamic instability unresponsive to fluids, life-threatening hyperkalaemia, or specific toxin removal such as tricyclic or salicylate overdose. Even then it is given by the specialist team. The principle is to treat the cause, and here the cause is ketogenesis, which the insulin switches off." [10][5]

Examiner: "Now flip it — an infant with projectile vomiting and an alkalosis. How do you think?"

"This is the other end of the acid-base spectrum, a metabolic alkalosis, and in a 6-week-old with projectile non-bilious vomiting it is pyloric stenosis. The gas shows a high pH and high bicarbonate, and the electrolytes show the characteristic hypokalaemic hypochloraemic alkalosis with a low urine chloride. The mechanism is gastric loss of hydrogen and chloride, maintained by volume and chloride depletion that drives distal hydrogen and potassium secretion. It is chloride-responsive, so it corrects with normal saline and potassium chloride, which I give to correct the deficit and the anaesthetic risk before any surgery. The definitive treatment is a pyloromyotomy, and the alkalosis resolves as feeding resumes. The urine chloride, low here, distinguishes it from the chloride-resistant alkaloses of mineralocorticoid excess, which do not correct with saline." [12][4]

Closing summary

"In summary: every paediatric gas gets the six-step systematic approach — pH, primary process, anion gap with albumin correction, Winters compensation, delta gap, and clinical correlation. Diabetic ketoacidosis is the commonest high anion gap acidosis in children, managed with fluids and insulin and not bicarbonate. A normal gap points to diarrhoea or renal tubular acidosis. Metabolic alkalosis splits by the urine chloride into chloride-responsive (vomiting, pyloric stenosis) and chloride-resistant (mineralocorticoid excess). And the principle throughout is to treat the cause, because correcting the pH without addressing the cause does not help and often harms." [1][3]