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Paeds Topicsnephrology-urology-fluids-and-electrolytes

Paeds · nephrology-urology-fluids-and-electrolytes

Acid-base disorders in children

Also known as Acid-base disorders in children · Acid-base disturbances · Metabolic acidosis · Metabolic alkalosis · Respiratory acidosis · Respiratory alkalosis · Anion gap · Winters formula · Mixed acid-base disorder · Delta gap

Fellowship guide to acid-base disorders in children: a systematic six-step approach to any blood gas, the anion gap and its albumin correction, Winters formula for the expected pCO2 in metabolic acidosis, the delta gap for mixed disorders, and the compensation rules for each of the four primary disorders, anchored in diabetic ketoacidosis as the commonest high anion gap metabolic acidosis, diarrhoea and renal tubular acidosis as the normal anion gap acidoses, chloride-responsive metabolic alkalosis, and the respiratory acidoses and alkaloses of bronchiolitis, asthma and hyperventilation.

high17 referencesUpdated 15 July 202631 min readSource-verified · Sept 2026

Checked against its sources on 3 Sept 2026

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RACP DWERACP DCEMRCPCH Theory

Red flags

  • A pH below 7.1 with haemodynamic instability is an emergency — secure the airway and breathing, treat shock, and reserve intravenous sodium bicarbonate for pH below 6.9 in DKA or for hyperkalaemia, because routine bicarbonate worsens cerebral oedema and lactate
  • A metabolic acidosis with a measured pCO2 higher than the Winters expected value (1.5 times bicarbonate plus 8) means a coexisting respiratory acidosis — the patient is failing to compensate and the airway or ventilation needs attention
  • A high anion gap metabolic acidosis in a child is diabetic ketoacidosis until proven otherwise, but a normal anion gap acidosis with diarrhoea or a positive urine anion gap points to bicarbonate loss and changes the pathway entirely
  • Over-rapid correction of chronic respiratory acidosis with mechanical ventilation causes post-hypercapnic alkalosis, a fall in ionised calcium, seizures and arrhythmia — lower the pCO2 slowly

Life stages

neonateinfanttoddlerpreschoolschool-ageadolescentyoung-adult-transition

Care settings

ed-acutewardpicunicuoutpatient

Clinical exam formats

written-only

Board mappings

  • The six-step systematic approach to any paediatric blood gas
  • The anion gap and Winters formula for compensation
  • The four primary acid-base disorders and their causes
  • High versus normal anion gap metabolic acidosis and the delta gap for mixed disorders
  • Winters expected pCO2 and detecting a coexisting respiratory disorder
  • Chloride-responsive versus chloride-resistant metabolic alkalosis
  • Interpreting a venous or arterial blood gas in a sick child
  • Recognising diabetic ketoacidosis as the commonest high anion gap acidosis
  • When bicarbonate is and is not indicated in severe acidosis
  • Short case: a child in DKA with a high anion gap metabolic acidosis
  • Long case: chronic respiratory acidosis in neuromuscular disease
  • Communication station explaining the blood gas result to the team
  • Nephrology and fluids: acid-base disorders and the anion gap in children
  • Respiratory: respiratory acidosis and alkalosis in the sick child
  • Endocrine: diabetic ketoacidosis and its characteristic gas
  • Acid-base physiology: buffers, the Henderson-Hasselbalch equation and compensation
  • Calculation of the anion gap and the expected pCO2 (Winters formula)
  • The four primary disorders and their paediatric causes
  • Bedside interpretation of a paediatric blood gas with a systematic approach
  • Communication: explaining an abnormal blood gas result to the family
  • Acid-base disorders: the four primary disorders and their causes in children
  • The anion gap and the distinction of high from normal gap acidosis
  • Respiratory compensation and the Winters formula
  • Patient Care: systematic blood gas interpretation in the sick child
  • Medical Knowledge: acid-base physiology, compensation and the anion gap
  • Systems-Based Practice: recognising iatrogenic acid-base disorders and preventing harm
  • Nephrology: acid-base disorders and the anion gap in children
  • The Winters formula and the delta gap for mixed disorders
  • Diabetic ketoacidosis as the archetypal high anion gap metabolic acidosis
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Practise this topic

  • Short-answer question1
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Target exams

RACP DWERACP DCEMRCPCH Theory

Red flags

  • A pH below 7.1 with haemodynamic instability is an emergency — secure the airway and breathing, treat shock, and reserve intravenous sodium bicarbonate for pH below 6.9 in DKA or for hyperkalaemia, because routine bicarbonate worsens cerebral oedema and lactate
  • A metabolic acidosis with a measured pCO2 higher than the Winters expected value (1.5 times bicarbonate plus 8) means a coexisting respiratory acidosis — the patient is failing to compensate and the airway or ventilation needs attention
  • A high anion gap metabolic acidosis in a child is diabetic ketoacidosis until proven otherwise, but a normal anion gap acidosis with diarrhoea or a positive urine anion gap points to bicarbonate loss and changes the pathway entirely
  • Over-rapid correction of chronic respiratory acidosis with mechanical ventilation causes post-hypercapnic alkalosis, a fall in ionised calcium, seizures and arrhythmia — lower the pCO2 slowly

Life stages

neonateinfanttoddlerpreschoolschool-ageadolescentyoung-adult-transition

Care settings

ed-acutewardpicunicuoutpatient

Clinical exam formats

written-only

Board mappings

  • The six-step systematic approach to any paediatric blood gas
  • The anion gap and Winters formula for compensation
  • The four primary acid-base disorders and their causes
  • High versus normal anion gap metabolic acidosis and the delta gap for mixed disorders
  • Winters expected pCO2 and detecting a coexisting respiratory disorder
  • Chloride-responsive versus chloride-resistant metabolic alkalosis
  • Interpreting a venous or arterial blood gas in a sick child
  • Recognising diabetic ketoacidosis as the commonest high anion gap acidosis
  • When bicarbonate is and is not indicated in severe acidosis
  • Short case: a child in DKA with a high anion gap metabolic acidosis
  • Long case: chronic respiratory acidosis in neuromuscular disease
  • Communication station explaining the blood gas result to the team
  • Nephrology and fluids: acid-base disorders and the anion gap in children
  • Respiratory: respiratory acidosis and alkalosis in the sick child
  • Endocrine: diabetic ketoacidosis and its characteristic gas
  • Acid-base physiology: buffers, the Henderson-Hasselbalch equation and compensation
  • Calculation of the anion gap and the expected pCO2 (Winters formula)
  • The four primary disorders and their paediatric causes
  • Bedside interpretation of a paediatric blood gas with a systematic approach
  • Communication: explaining an abnormal blood gas result to the family
  • Acid-base disorders: the four primary disorders and their causes in children
  • The anion gap and the distinction of high from normal gap acidosis
  • Respiratory compensation and the Winters formula
  • Patient Care: systematic blood gas interpretation in the sick child
  • Medical Knowledge: acid-base physiology, compensation and the anion gap
  • Systems-Based Practice: recognising iatrogenic acid-base disorders and preventing harm
  • Nephrology: acid-base disorders and the anion gap in children
  • The Winters formula and the delta gap for mixed disorders
  • Diabetic ketoacidosis as the archetypal high anion gap metabolic acidosis
Key answer

An acid-base disorder is a disturbance of the blood pH driven by a change in either the metabolic component (bicarbonate) or the respiratory component (carbon dioxide tension). [1] [2] The disciplined way to read any paediatric gas is a six-step systematic approach: name the pH, identify the primary process, calculate the anion gap, assess compensation with Winters formula, use the delta gap to unmask mixed disorders, and tie the numbers to the child at the bedside. [1] [3] Diabetic ketoacidosis is the commonest high anion gap metabolic acidosis in children, diarrhoea and renal tubular acidosis are the normal anion gap acidoses, and the respiratory acidoses and alkaloses track the work of breathing and the drive to ventilate. [2] [5]

Every blood gas is a story about two variables working in opposition. The Henderson-Hasselbalch equation sets the pH from the ratio of bicarbonate to dissolved carbon dioxide, and the body defends that ratio with two organs: the kidney controls bicarbonate over hours to days, and the lung controls carbon dioxide over seconds to minutes. When one variable moves abnormally, the other shifts in the same direction to pull the pH back toward normal, and that is called compensation. A disorder is "simple" when the compensation is appropriate and "mixed" when a second process is also at work, and the whole skill of acid-base interpretation is telling those two apart with a small set of calculations rather than guesswork. [1] [11]

In children, three things make the gas harder to read than in adults. Normal values shift with age, so a neonate runs a lower bicarbonate and carbon dioxide tension than a teenager. The common disorders differ, with diabetic ketoacidosis, bronchiolitis, asthma and inherited metabolic disease dominating rather than the chronic renal and respiratory disease of adults. And the child decompensates faster, because the smaller body buffers less acid and the airway gives way more quickly, so the gas is both a diagnostic and an emergency tool. This page builds the model around the systematic approach, then applies it to the four primary disorders and their paediatric causes. [2] [7]

Overview & Definition

Acid-base homeostasis keeps the arterial pH between 7.35 and 7.45 by balancing acid generation against excretion. The body produces acid constantly from protein metabolism and carbon dioxide load, and it disposes of it through the lung (as carbon dioxide) and the kidney (as titratable acid and ammonium). A disorder arises when generation overwhelms excretion, or when excretion fails, and the result is a pH that drifts outside the normal range. The venous or arterial blood gas measures the three numbers that define the disturbance: pH, the carbon dioxide tension, and the bicarbonate concentration. [1] [11]

The first decision on any gas is the pH itself. Acidemia is a pH below 7.35 and alkalemia is a pH above 7.45; a pH within the normal range with abnormal carbon dioxide and bicarbonate means a mixed disorder or a fully compensated single disorder. The pH names the dominant process and sets the direction of the analysis, because the body never over-compensates. If the pH is acidemic, the primary process is an acidosis; if it is alkalemic, the primary process is an alkalosis, and only then do the carbon dioxide and bicarbonate reveal whether that process is metabolic or respiratory. [1] [2]

Four primary disorders cover almost everything a clinician meets. Metabolic acidosis is a fall in bicarbonate from acid gain or bicarbonate loss. Metabolic alkalosis is a rise in bicarbonate from acid loss or bicarbonate gain. Respiratory acidosis is a rise in carbon dioxide tension from hypoventilation. Respiratory alkalosis is a fall in carbon dioxide tension from hyperventilation. Each has a characteristic compensation, and the task of the systematic approach is to confirm that the compensation is appropriate, because an inappropriate compensation unmasks a second disorder. [1] [3]

The body never over-compensates

The direction of the pH names the primary process. If the pH is acidemic the primary process is an acidosis; if alkalemic it is an alkalosis. A normal pH with abnormal carbon dioxide and bicarbonate means two opposing disorders are present, because appropriate compensation pulls the pH toward but never beyond 7.40. [1] [2]

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References17ShowHide
  1. [1]Berend K; de Vries AP; Gans RO Physiological approach to assessment of acid-base disturbances. N Engl J Med, 2014.PMID 25295502
  2. [2]Carmody JB; Norwood VF A clinical approach to paediatric acid-base disorders. Postgrad Med J, 2012.PMID 22267531
  3. [3]Kraut JA; Madias NE Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol, 2010.PMID 20308999
  4. [4]Rastegar M; Nagami GT Non-Anion-Gap Metabolic Acidosis: A Clinical Approach to Evaluation. Am J Kidney Dis, 2017.PMID 28029394
  5. [5]Dhatariya KK; Glaser NS; Codner E; Umpierrez GE Diabetic ketoacidosis. Nat Rev Dis Primers, 2020.PMID 32409703
  6. [6]Calimag APP; Chlebek S; Lerma EV Diabetic Ketoacidosis. Disease-a-Month, 2023.PMID 35577617
  7. [7]Zieg J; Ghose S; Raina R Electrolyte disorders related emergencies in children. BMC Nephrol, 2024.PMID 39215244
  8. [8]Batlle D; Ba Aqeel SH; Marquez A The Urine Anion Gap in Context. Clin J Am Soc Nephrol, 2018.PMID 29311217
  9. [9]Giglio S; Montini G; Trepiccione F; Gambaro G Distal renal tubular acidosis: a systematic approach from diagnosis to treatment. J Nephrol, 2021.PMID 33770395
  10. [10]Wilson RF; Spencer AR; Tyburski JG; Dolman H Bicarbonate therapy in severely acidotic trauma patients increases mortality. J Trauma Acute Care Surg, 2013.PMID 23271076
  11. [11]Berend K; Duits AJ The role of the clinical laboratory in diagnosing acid-base disorders. Crit Rev Clin Lab Sci, 2019.PMID 30917291
  12. [12]Luke RG; Galla JH Does chloride play an independent role in the pathogenesis of metabolic alkalosis? Semin Nephrol, 1989.PMID 2772432
  13. [13]Lopez-Garcia SC, Emma F, Walsh SB, et al. Treatment and long-term outcome in primary distal renal tubular acidosis Nephrol Dial Transplant, 2019.PMID 30773598
  14. [14]Rosenbloom AL The management of diabetic ketoacidosis in children Diabetes Ther, 2010.PMID 22127748
  15. [15]Jaber S, Paugam C, Futier E, et al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial Lancet, 2018.PMID 29910040
  16. [16]Wrenn K The delta (delta) gap: an approach to mixed acid-base disorders Ann Emerg Med, 1990.PMID 2240729
  17. [17]Figge J, Jabor A, Kazda A, et al. Anion gap and hypoalbuminemia Crit Care Med, 1998.PMID 9824071

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