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An event is serious (based on the ICH definition) when the patient outcome is:
* death
* life-threatening
* hospitalisation
* disability
* congenital anomaly
* other medically important event
A 9-year-old boy developed sinus bradycardia during treatment with hydrocortisone for adrenal insufficiency, septic shock and adrenal crisis.
The boy, who had a history of panhypopituitarism secondary to pituitary hypoplasia presented to the emergency department with a one day history of fever, vomiting and diarrhoea. Five days before this presentation, he presented with coughing and received 5 day course of clarithromycin. At the time of current presentation, his family took him to the hospital as he was unable to tolerate the clarithromycin and appeared confused and sleepy while at home. He had a history of well controlled hypothyroidism, adrenal insufficiency and growth hormone deficiency. He had been receiving levothyroxine sodium [levothyroxine], hydrocortisone 12 mg/m2/day [initial route not stated] and growth hormone therapy at bedtime for 4 yrears. Physical examinations were observed as follow: BP 95/50 mmHg, HR 115 beats per minute (BPM), temperature 380C, oxygen saturation 99% on room air, height 110cm (25th percentile) and weight 23kg (50th percentile). Subsequently, he was observed to be moderately dehydrated and lethargic with coarse rales over the lungs and increased bowel sounds. The work-up study showed elevated levels of C-reactive protein and procalcitonin. A chest radiograph revealed pulmonary infiltrates. Initially, he took an isotonic sodium chloride and IV bolus hydrocortisone 50 mg/m2. Subsequently, 30 minutes after admission, he developed respiratory arrest with hypotension and hypoglycaemia. Subsequently, he received a second hydrocortisone bolus and isotonic sodium chloride, as parenteral glucose supplementation, by considering the diagnosis of acute adrenal crisis and septic shock. Also decided to give mechanical ventilator support. Further, he also received midazolam and fentanyl for sedation. He exhibited a lack of response to hydrocortisone as part of treatment for refractory shock; hence, its dose was increased to 300 mg/m2/day as a continuous IV infusion. Subsequently, his dopamine administration was initiated and thereafter, he was transferred to the intensive care unit. His treatment was also initiated with ceftriaxone and metronidazole. Subsequently, his BP was improved on the stress dose of hydrocortisone and hydration. But within 24h after treatment, he developed bradycardia with HR of 45 BPM. Subsequently, the diagnosis of sinus bradycardia was confirmed [duration of treatment to reaction onset not stated].
Later, the boy's levothyroxine sodium and unspecified growth hormone therapies were started. On day 2, vancomycin was added to his therapy. He was on intubation until day 3, followed by remarkable recovery was occurred. Thereafter, dopamine was stopped. In spite of discontinuation of midazolam and fentanyl on day 3, his HR was observed between 35 and 75 BPM. Although he was asymptomatic, received atropine once. On day 6, while taking hydrocortisone 100 mg/m2/day, when his lowest HR was 35 BPM. Following atropine administration, his HR fluctuated between 50 and 75 BPM. Subsequently, hydrocortisone infusion was slowly tapered to 25 mg/m2/day. Subsequently, on day 10, he was transitioned to oral hydrocortisone. On day 15, the bradycardia finally resolved after the dose was tapered to 12 mg/m2 /day. His medications were examined for negative chronotropy and hydrocortisone and vancomycin were suspected to have the potential for bradycardia. As vancomycin treatment was started following the documentation of bradycardia; hence, hydrocortisone-induced bradycardia was confirmed. During his hospital stay, his HR remained within the normal limit. Subsequently, on day 17, he was discharged. After discharge, since 1 year, he remained in good health with no problems detected on follow-ups at the endocrinology and cardiology units.