Colecalciferol/dexamethasone

Abstract

Various toxicities: case report An approximately 7-week-old boy [exact age at the time of reaction onset not stated] developed nephrocalcinosis, motor disorder syndrome, anxiety, regurgitation, cheek skin hyperaemia, peeling of the skin on the cheeks, constipation, decreased appetite, pale skin, cheek dryness, cyanosis of the nasolabial triangle, reduced tissue turgor, increased alkaline phosphatase level, decreased phosphorus level, increased parathyroid hormone level, increased total T3 level and colecalciferol intoxication following colecalciferol overdose due to erroneous administration of higher than the prescribed dose. Additionally, he developed hypertrophic cardiomyopathy following treatment with dexamethasone for colecalciferol intoxication [not all dosages and time to reaction onsets stated]. The boy had been born prematurely at 33 weeks of gestation with emergency surgical delivery due to the worsening of the fetal status. At birth, his condition was severe with diagnosis of respiratory failure and nervous system depression syndrome. He experienced various other morbidities including normochromic, mixed anaemia and hypertension and hydrocephalic syndrome. He was transferred to the ICU and was treated with various medications. His condition stabilised on day 4 of life allowing transfer to preterm care department. He was discharged on 27 November 2019 at postnatal age of 6 weeks in satisfactory condition. At discharge, the boy was prescribed oral colecalcaiferol [cholecalciferol; Aquadetrim] 1000 IU/day (2 drops/day) as prophylaxis for rickets. The mother was provided with recommendations on breastfeeding, feeding with Nutrilon Pre formula and administration of medications. Following discharge, his condition was satisfactory. However, the mother erroneously administered colecalciferol at a dose of 1.0 mL/day for 14 days, corresponding to 15,000 IU/day of colecalciferol instead of 1,000 IU/day (medication error). On the 7th day of this erroneous colecalciferol regimen, the restlessness (anxiety) of the child was observed with regurgitation of 10-15mL and peeling of the skin on the cheeks. On day 11 of erroneous regimen of colecalciferol, he experienced constipation, decreased appetite, increased regurgitation volume and increased regurgitation rate. He also exhibited increased cheek skin hyperaemia, nystagmus, pale skin, along with head and extremities tremor. During a paediatric examination at home, a local pediatrician evaluated his condition and clarified the nature of the implementation of medication administration. After detection of erroneous regimen of colecalciferol, the child was immediately hospitalised on 10 December 2019 at the age of 8 weeks. Upon admission, his condition was of moderate severity due to colecalciferol intoxication and neurological symptoms. Consciousness was lucid. He had a constant horizontal nystagmus and small-component tremor of head and extremities. Muscle tone was increased and reflexes are alive. When in traction, the boy was grouped as a block , the support on the feet was weak. The skin was pale along with cheek dryness and hyperaemia, cyanosis of the nasolabial triangle and reduced tissue turgor. On percussion, the sound with a box tint was determined over the lungs. On auscultation, the breathing was puerile with no wheezing. The pulse on the radial artery was rhythmic and of satisfactory quality. The heart region was visually unchanged with rhythmic and clear heart sounds. Urination was free and painless. Urine was light yellow with no dysuria. Urinalysis showed moderate haematuria, proteinuria and oxaluria. Blood biochemistry revealed increased alkaline phosphatase level. The boy was treated with sorbent therapy with sufficient water-drinking regimen. Colecalciferol was discontinued. Nutrilon Pre was replaced by Nutrilon-1. Blood concentration of 25 (OH)D was found to be 210 ng/mL, which was 2 times higher than the upper limit of the reference interval. A one-time urine sample revealed a decrease in phosphorus level. On 11 December 2019, he started receiving dexamethasone infusion with various other medications. On 14 December 2019, his condition improved, his appetite recovered, regurgitation appeared much less frequently and only after feeding. Stool was independent, once a day, semi-formed and without pathological impurities. No neurological symptoms (nystagmus, head and extremities tremor) were noted. Only significant restlessness was observed. The skin syndrome completely resolved. He began to gain weight. The follow-up blood test on 22 December 2019 revealed a decrease in the blood concentration of 25 (OH)D and a decrease in alkaline phosphatase level. However, laboratory investigation also revealed an hypercalcaemia. Phosphorus level in one-time urine continued to decrease. Ultrasound examination of the renal sinuses and parenchyma of both kidneys revealed echo pattern of single, small (1-2 mm) hyperechoic inclusions without acoustic shadow. Softening of the skull bones, compliance of the margins of the large genus, opening of the small genus, and open sagittal suture were noted. After 4 weeks from the time of admission (6 January 2020), positive weight gains was noted along with improvement in neurological status (no nystagmus or tremor, started to walk, glance fixed, monitors objects, the patient is grouped by hands, holds his head, reflexes are alive, muscular dystonia persists). He took up the prescribed amount of food and the regurgitations had stopped. The skull bones became dense, the small motley and sagittal suture closed, the large motley did not bulge, the edges were dense. Laboratory investigation revealed decrease in blood 25 (OH)D and alkaline phosphatase level. The levels of ionized calcium in the serum and total calcium also normalised. The spot urine phosphorus returned to the age normal. Ultrasound examination of the kidneys demonstrated positive dynamics in the form of a decrease in the number and value of hyperechoic inclusions without acoustic shadow. He was discharged on 27 January 2020 with normal levels of 25 (OH)D. Ultrasound of the kidneys showed a decrease in the number and echodensity of hyperechoic inclusions. ECG demonstrated an increase in the electrical activity of the left ventricle. Moderate left ventricular hypertrophy was detected. He was diagnosed with hypertrophic cardiomyopathy which was suspected to be due to long-term treatment with dexamethasone and concurrent hypercalcaemia. Assessment of thyroid status showed increased levels of parathyroid hormone and total T3 along with normal levels of thyroid-stimulating hormone and total T4. He was discharged in satisfactory condition at the age of 15 weeks with a final diagnosis of moderate overdose of colecalciferol with nephrocalcinosis, motor disorder syndrome and other associated toxicities. Rehospitalisation after 3-4 weeks was planned for monitoring of laboratory values and to decide alternative regimen for colecalciferol administration in the hospital setting.