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Severe anaemia and altered mental status in the young paediatric patient

A 2-year-old previously healthy male presented to the paediatric emergency department (ED) with vomiting and decreased energy. The patient began vomiting 2 days prior, with two episodes of non-bloody non-bilious emesis per day, and reduced intake and urination. On the day of presentation, he developed significantly reduced activity and was difficult to keep awake. There was no fever, diarrhoea, rash or localised swelling. The medical history was significant for pica, and vaccines were up to date. The family denied any trauma, diet abnormalities or sick contacts. On arrival in the ED, he had a temperature of 37.1 C, blood pressure 94/61, heart rate 100, respiratory rate 30 and oxygen saturation 100%. The patient was asleep on the gurney and waking only to painful stimuli. Airway was patent, cardiopulmonary exam was unremarkable and peripheral pulses were intact, in the setting of prolonged capillary refill at 4 seconds. His pupils were equal, round and reactive to light. Patient was negative for nuchal rigidity, patellar reflexes were 2+ bilaterally and tone was normal. He opened his eyes and actively moved all extremities in response to painful stimuli. Abdominal exam revealed no tenderness, distension, hepatosplenomegaly or masses. Skin exam had no evidence of ecchymoses, petechiae, rashes or oedema. There were no musculoskeletal abnormalities. The initial differential diagnoses included hypoglycaemia, dehydration, toxic ingestion, intussusception and trauma. Glucose level was unremarkable at 7.66 mmol/L (range 3.33–5.55). Studies were significant for mild leukocytosis 14.4 × 10/L (range 4.5–12.7) with neutrophilic predominance 86%, thrombocytosis 654 × 10/L (130–450) and severe microcytic anaemia. Anaemia was demonstrated by haemoglobin 64 g/L (110–142), haematocrit 0.256% (0.332–0.425), low mean corpuscular volume 54.7 fL (72–90), low mean corpuscular haemoglobin concentration (MCHC) 25% (31.8–36.8) and elevated red cell distribution width 27% (11.7–14.9). Urinalysis was notable for 2+ ketones and elevated specific gravity 1.031 (1.005–1.030). Comprehensive metabolic panel, lipase, lead level, and serum and urine drug screens were unremarkable, and blood and urine cultures were obtained. Preliminary interpretation of head computed tomography (CT) was within normal limits (Fig. 1). Focused Assessment with Sonography for Trauma was negative. Abdominal X-ray, diagnostic abdominal ultrasound and electrocardiogramwere unremarkable. The patient’s responsiveness on serial neurologic exams improved during this observation period; he woke and responded to non-painful tactile stimuli during re-evaluations, and made appropriate eye contact. Given the patient’s significant anaemia and altered mental status, haematology and critical care were consulted and further laboratory testing was obtained. Iron studies were significant for severely low iron <10 μg/dL (50–212), low ferritin 3.6 ng/mL (23.9–336.2), elevated transferrin 365 mg/dL (203–362) and elevated unsaturated iron-binding capacity 428 μg/dL (155–355). Direct Coombs, G6PD, uric acid, lactate dehydrogenase, prothrombin time, partial thromboplastin time and faecal occult blood testing were unremarkable. Packed red blood cell transfusion was ordered and the patient was admitted to the paediatric intensive care unit. On arrival to the paediatric intensive care unit, the patient was tachypnoeic and hypertensive with a blood pressure of 158/72. Magnetic resonance imaging (MRI), magnetic resonance angiography (MRA) and magnetic resonance venography (MRV) were ordered due to ongoing altered mental status. Prior to imaging, Key Points 1 Cerebral venous sinus thrombosis can rarely occur in association with iron deficiency anaemia. This can occur in patients without underlying hypercoagulable conditions. 2 The greatest sensitivity for the diagnosis of cerebral venous sinus thrombosis is by magnetic resonance imaging with magnetic resonance venography or computed tomography with venography. 3 Acute treatment of anaemic patients with cerebral venous sinus thrombosis requires both anticoagulation and anaemia management.