A DROWSY TODDLER
History
Jonathan is a 21-month-old boy referred to the paediatric day unit by his GP. He was seen in the surgery the previous day with diarrhoea and vomiting and seemed to have tummy ache. The vomit contained a small amount of fresh blood, but as he was otherwise well and cardiovascularly stable, admission had been deferred because his mother is 36 weeks into her fourth pregnancy. Instead, later that day, the GP rang to check how he was and was reassured to hear that he seemed to have recovered and was tolerating drinks and some food. However, this morning he seems lethargic and a finger-prick blood glucose test performed by his GP was only 3.1 mmol/L. Jonathan is the youngest of three children, the older two being 6 and 3 years old. His father is in the navy and is currently at sea.
Examination
He looks unwell. His airway is patent, his respiratory rate is 26 breaths/min and his pulse rate is 180 beats/min with a capillary refill time of 5 s. His blood pressure is 60/35 mmHg. He is jaundiced. Both heart sounds are present and normal. Examination of the respiratory and abdominal systems is normal. He is drowsy but knows his mother and responds to her voice. He resists examination and withdraws to pain. There is no meningism and there are no focal neurological signs.
NVESTIGATIONS
Normal
Haemoglobin 12.3g/dL 11.5–15.5 g/dL
White cell count 8.4 109/L 6.0 –17.5 109/L
Platelets 140 109/L 150–400 109/L
Prothrombin time 19 s 11–15 s
Partial thromboplastin time 32 s 25–35 s
Sodium 138 mmol/L 138–146 mmol/L
Potassium 3.6 mmol/L 3.5–5.0 mmol/L
Urea 8.2 mmol/L 1.8–6.4 mmol/L
Creatinine 33 µmol/L 27–62 µmol/L
Glucose 2.9 mmol/L 3.3–5.5 mmol/L
Bilirubin 85 mmol/L 2–26 mmol/L
Alanine aminotransferase (ALT) 1875 IU/L 5–45 IU/L
Alkaline phosphatase 2624 IU/L 145–420 IU/L
Albumin 32 g/L 39–50 g/L
C-reactive protein 6 mg/L 6 mg/L
Lactate 3.2 0.8–1.5 mmol/L
Venous blood gas on 15 L/min of oxygen
pH 7.28 7.35–7.45
PCO2 3.8 kPa 4.5–6.0 kPa
Bicarbonate 17 mmol/L 22–29 mmol/L
Questions • What pathological processes are evident from his clinical signs and investigations? • What is the most likely unifying cause? • How is this condition managed?
Medicine
Firstly, this boy has acute liver dysfunction. He has a prolonged prothrombin time, hypoglycaemia and low albumin – these are markers of the manufacturing processes of the liver. There is liver inflammation with an elevated ALT and bilirubin. Secondly, he has clinical and biochemical evidence of tissue underperfusion and increased anaerobic metabolism. He has a tachycardia, borderline hypotension and a prolonged capillary refill time with a metabolic acidosis and a high lactate. There is a compensatory reduction in the PCO2 (see Case 86, p. 253). Thirdly, there are clinical symptoms and signs suggestive of mild encephalopathy, although his drowsiness could be due to the hypoglycaemia. Finally, note the high urea. This could be due to dehydration but his diarrhoea and vomiting were resolving and the creatinine is normal. It is more likely to be due to the digestion of blood following upper gastrointestinal tract bleeding. Ask about melaena stools. The most likely unifying cause is some form of poisoning. This history is classical for iron toxicity. Iron is corrosive to the gastrointestinal mucosa, causing abdominal pain, nausea, vomiting and diarrhoea within a few hours of ingestion with haematemesis and bloody diarrhoea in more severe toxicity. Thereafter, there is an interlude with an apparent recovery from about 8–16 hours. This boy has entered the third stage (16–24 hours) with progressive systemic involvement due to the vasodilator effects of iron and mitochondrial poisoning. Toxicity is related to the amount of ferrous iron ingested, which varies according to the particular iron salt. All preparations carry this information, e.g. a ferrous fumarate tablet 210 mg contains 65 mg of ferrous iron. Toxicity is unlikely if 20 mg/kg is ingested but the risk increases steadily thereafter. Not many tablets are needed to cause significant poisoning.
Management of iron poisoning
• Give oxygen and intravenous fluids to manage poor perfusion
• Treat hypoglycaemia
• Send the family home to check for missing drugs and to bring in any remaining drugs for identification
• Whole iron tablets are radio-opaque – an abdominal X-ray to confirm ingestion may help
• Try to remove the poison. If taken within 1 hour of presentation or tablets visible in stomach on X-ray, consider gastric lavage with a wide-bore tube
• Measure serum iron urgently, but remember that it may be spuriously low if taken 8 hours post-ingestion
• Try to estimate the quantity of iron ingested and the risk of toxicity
• Discuss with National Poisons Information Service (24 hour service) who will advise about treatment with desferrioxamine, a specific chelator of iron
• Discuss with a specialist liver unit
This child’s mother was receiving iron treatment during her pregnancy and found the pack in his bedroom. Iron is one of the most common causes of childhood accidental poisoning because iron-containing preparations are widely available and often resemble sweets. Some units ask a health visitor to undertake a home visit after any case of accidental poisoning to assess overall home safety and to remind parents about keeping all drugs out of reach of children.
KEY POINTS
• Advice should be sought from the National Poisons Information Service if there is any doubt about the management of a case of poisoning.
• Iron is one of the most common causes of childhood poisoning.
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