Anemia That Presented with Desaturation: A Focus on Core Con
A 3-year old boy presented to the emergency department with an acute history of 4-5 episodes of hematuria over the past 6 hours and a history of parents' noticing pallor since a day before. He was apparently well and healthy the previous day. The child was irritable on presentation, with tachycardia and tachypnoea. On primary assessment, he had warm extremities, a palpable liver, minimal crepts, and a gallop rhythm. The blood pressure was maintained. The presiding doctor noticed that the child's saturation on the pulse oximeter is 68–72%, and the child was immediately put on non-rebreathable mask at 10liters/minute. The saturation rose to 74–80%. There was no visible cyanosis over fair skin, and the sensorium was normal with a Glasgow Coma Scale (GCS) of 15/15.

The complete blood count revealed a hemoglobin of 3.8g/dL, with a hematocrit of 13.1% and a normal bleeding profile. Total bilirubin was 3.7mg% with an indirect component of 2.7mg%. While the pulse oximeter continued to show a poor saturation (80%), the blood gas reports painted an entirely different picture: pH, 7.5; pCO2, 24.9mmHg; pO2, 215.3mmHg; HCO3, 19.2mmol/L; lactates, 3.5mmol/L; and saturation (SaO2), 99.8%. With a wide saturation gap, abnormal forms of hemoglobin were suspected, and a co-oximetry on arterial blood was requested—which came positive for methemoglobinemia (MetHb: 10.4%), with an O2Hb (oxygenated Hb) of 87.4% and an HHb (deoxygenated Hb) of 0.3%. The peripheral smear was suggestive of acute hemolysis (with iron deficiency anemia): severe anisocytosis, polychromasia, spherocytes, severe hypochromia, and nucleated red blood cells (RBC).

Glucose-6 phosphate dehydrogenase (G6PD) was normal. In view of cardiac failure, injection furosemide at a dose of 1mg/kg was administered. The child was transfused packed red blood cells at 5cc/kg, and ascorbic acid at a dose of 10mg was started. We did not administer methylene blue, as the threshold percentage of methemoglobin (MetHb) was not high enough to warrant, and any risk of hemolysis due to an oxidizing agent would further jeopardize the child.

The child improved over the course of the next 2 days, requiring two more blood transfusions, and was discharged on the 4th day after admission. The author could not find any concrete source of methemoglobinemia poisoning for the child: as the child came from an urban slum neighborhood, we suspected contamination of their water source and tested the water samples for nitrates and nitrites, which were NIL.

A history of mothball use in the household was elicited. With a mild presentation and no history of vomiting, diarrhoea, and seizure, we suspected paradichlorobenzene (PDB) mothball poisoning over naphthalene and camphor. We performed a point-of-care test to differentiate between the three. As per work by Moss et al, camphor, PDB, and naphthalene can be differentiated based on their density using a combination of water and 50% dextrose. Since the mothball sank in water but floated in the D50 solution, it was concluded as consisting of naphthalene.