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Hyperchloraemic acidosis consistent with ammonium chloride administration
  1. A Bajpai,
  2. A Tikaria,
  3. S K Kabra,
  4. L S Arya
  1. All India Institute of Medical Sciences, New Delhi, India;

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    We report an infant with recurrent self limiting hyperchloraemic acidosis. This 1 month old girl was admitted with vomiting, decreased feeding, and rapid breathing. On examination she was lethargic and tachypnoeic with normal blood pressure and peripheral perfusion. Investigations revealed uncompensated metabolic acidosis and uraemia (table 1). She was managed with antibiotics and sodium bicarbonate and showed rapid improvement in acidosis and uraemia in 48 hours. Following discharge she was brought to the outpatient department on multiple occasions with vomiting, failure to thrive, and tachypnoea. She was readmitted at the age of 4 months with lethargy, tachypnoea, uncompensated hyperchloraemic acidosis, and uraemia. She was managed with antibiotics and sodium bicarbonate; the biochemical parameters normalised over 52 hours.

    Negative urinary anion gap, normal urinary to blood CO2 difference, and fractional excretion of bicarbonate excluded distal and proximal renal tubular acidosis in this child.1 Acidic urine in the presence of systemic acidosis and extremely high levels of serum and urinary chloride pointed to a chloride load overwhelming renal excretory capabilities.2 Negative anion gap of −17.6 mmol/l indicated an excess of unmeasured cation to the level of 30 mmol/l. This, combined with transient increase of urea with normal levels of creatinine and renal ultrasound indicated the possibility of ammonium (NH4+) load, and the clinicolaboratory picture of the child was explained on the basis of ammonium chloride load. Chloride levels of the milk and water given to the child as well as blood gas and serum chloride levels in the parents were normal.

    Ammonium chloride is used in the metallurgy industry in our city and is readily available. The possibility of Munchausen by proxy syndrome was therefore considered once investigations for environmental overload were non-contributory; this however could not be proved as the mother repeatedly denied administration of ammonium chloride. The child was discharged on normal feeding without any treatment. At three months follow up the child was growing normally, and did not have tachypnoea, vomiting, or acidosis. The findings of this case are suggestive of exogenous ammonium chloride administration, a possibility that should be considered in unexplained hyperchloraemic metabolic acidosis with negative urinary anion gap and high urinary chloride levels.

    Table 1

    Laboratory findings in the child