Ileus and Intra-Abdominal Hypertension due to Phosphate- Containing Enema.

The most well known complications of fleet enema solution are cardiac insufficiency, renal failure, water-electrolyte imbalance, and ileus. A 7-y-old girl with phenylketonuria and long-term constipation was admitted to the emergency department with symptoms of seizure, vomiting and abdominal distention. Laboratory results revealed hypocalcemia and hyperphosphatemia. ECG findings showed normal sinus rhythm and prolonged QT interval. At the follow-up, the patient's abdominal distention was markedly increased. She was evaluated for a surgical pathology and, this was considered unlikely. Intra-abdominal pressure (IAP) was 19.5 mmHg. Gastric and colonic decompression, intravenous 10 % calcium gluconate were applied. After 2 d of treatment, the patient's condition became stable, and serum calcium and phosporus normalized to 8.8 mg/dl and 4.0 mg/dl, respectively. Abdominal distention regressed and the last IAP measurement was 3.5 mmHg. Thus, IAP measurements are a useful adjunct in clinical follow-up of patients with progressive abdominal distention due to phosphate enema use.

The comparison of thyroxine versus thyroxine plus oral iodine in the treatment of congenital hypothyroidism due to iodine deficiency.

AIM: Iodine deficiency is one of the most important causes of congenital hypothyroidism. In addition to thyroid hormone replacement, iodine supplementation is also given to newborns with congenital hypothyroidism due to iodine deficiency. We aimed to determine whether it is beneficial to administer iodine supplementation in addition to the L-thyroxine (L-T4) treatment of newborns with congenital hypothyroidism due to iodine deficiency. MATERIALS AND METHODS: Of 51 newborns, 26 who were diagnosed with congenital hypothyroidism due to iodine deficiency were treated with L-T4. The remaining 25 cases were given L-T4 plus 100 µg/day of oral iodine. Free triiodothyronine (fT3), free thyroxine (fT4), thyroid-stimulating hormone (TSH), thyroglobulin (TG), thyroid volume, urine iodine and breast milk iodine levels were measured in the first and third months of treatment, and the data were compared between the two groups. RESULTS: First- and third-month values of fT3, fT4, TSH, TG and thyroid volume for both groups were statistically similar. There was no significant difference between the two groups in respect to falling levels of fT3 and TSH, the rate of increase of fT4 levels or the shrinkage rate of thyroid volume. CONCLUSION: In this study, the addition of oral iodine to L-T4 treatment provided no benefit compared to treatment with L-T4 alone.

Iodine deficiency: a probable cause of neural tube defect.

INTRODUCTION: Iodine deficiency is the most devastating event in developing brain in the fetus and neonate. Iodine is absolutely necessary on the myelination, neuronal differentiation, and formation of neural processes, synaptogenesis, and neuronal migration by thyroidal hormones throughout pregnancy and shortly after birth. Neural tube defects (NTD) form after third and fourth gestational weeks and their etiologies are multifactorial. CASE REPORT: We herein present a male newborn with iodine deficiency and thoracic neuroenteric cyst bound to a myelomeningocele via a pedinculi. We hypothesize that iodine deficiency may be a cause of NTD, and iodine supplementation in preconception and pregnancy may prevent NTD.