Paediatrics: Other acid-base problems

Other acid-base problems

Since respiratory derangements in acid–base have already been discussed, we will restrict this section to metabolic acidosis. An aci-dotic pH (<7.30), with low bicarbonate (<20mmol/L), suggests a primary metabolic acidosis. In an emergency, an alkalotic pH (>7.50) with raised bicarbonate (>30mmol/L) is most usually seen when supportive ventila-tion has been started in a patient with chronic hypercapnia.

Differential diagnosis of metabolic acidosis

Calculate the anion gap (AG)

AG = [Na] – ([HCO₃] + [Cl])

Normal AG = 10–12mmol/L

Increased anion gap metabolic acidosis

This is due to the production of exogenous acid. As an aide-mémoire, think of ‘a mudpile’

·  Alcohol or aspirin

·  Methanol

·  Uraemia

·  DKA

·  Paraldehyde

·  Ingestion or inborn error

·  Lactate

·  Ethylene glycol

Normal anion gap metabolic acidosis

This is commonly due to loss of bicarbonate from the gut or kidney, or impaired acid secretion by the kidney

·  Diarrhoea

·  Type I (distal) renal tubular acidosis (RTA): inability to excrete hydrogen ion; urine pH always high (>6.5); caused by a variety of medications or inherited; often associated with hypokalaemia and hypercalciuria

·  Type (proximal) II RTA: impaired reabsorption of bicarbonate from proximal tubule: usually associated with other proximal tubular dysfunction such as phosphaturia or glycosuria (Fanconi syndrome)

·  Type IV (hyperkalaemic) RTA—inadequate aldosterone production or inability to respond to it: seen in acute pyelonephritis or obstructive uropathy

Clinical assessment

History

A thorough history is important. You will need to identify any symptoms of fever, flank pain, and vomiting (pyelonephritis), lethargy, or altered mental state (metabolic disease or poisoning). Then ask specific questions about the gastrointestinal and renal tracts, and growth. Last there may be a significant family history of renal disease, kidney stones, or early infant death.

Examination

A full examination is needed. Assess:

·Hydration.

·Growth.

·Respiratory state (compensation for metabolic acidosis).

·Abdomen.

·CNS.

Investigations

Until you know the diagnosis, the key tests are as follows.

·Blood. FBC with differential, serum electrolytes with urea and creatinine, glucose, LFTs (transaminases), arterial or capillary blood gas, lactate, pyruvate, ketone, plasma amino acids, ammonia, carnitine, and drug screen.

·Urine: urinalysis, ketones, reducing substances, organic and amino acids, and drug screen.

·Imaging: renal US scan looking for nephrocalcinosis (type I RTA).

Monitoring

Ensure the ABCs. Then, the form and type of monitoring will be dictated by the patient’s condition. Start with continuous pulse oximetry and ECG monitoring, and intermittent BP monitoring. Follow hourly output.

Therapy

If the patient is dehydrated then this problem should be treated with oral or IV replacement. This alone may improve serum bicarbonate. However, for the specific metabolic disorders:

·Increased AG: identify cause and treat;

·Distal or proximal RTA: bicarbonate supplementation;

·Hyperkalaemic RTA: correct serum bicarbonate and increase fluids to improve sodium delivery to the distal tubule (this will enhance potassium secretion).

Bicarbonate treatment

If you are using bicarbonate then:

·Estimate the deficit = (20 – [HCO₃]) x weight (kg) x 0.5mmol;

·  Replace over 24–48hr with oral supplements.