Dose-dependent relapse of hiatus hernia after administration of intrathecal baclofen treatment--a rare complication.

INTRODUCTION: Intrathecal baclofen treatment (ITB) is widely used in children with cerebral palsy. Although this treatment effectively reduces spasticity, diverse side effects are reported. CASE REPORT: We report about a boy with severe asphyxia-induced encephalopathy with bilateral cerebral palsy. After starting the intrathecal baclofen treatment, he episodically showed symptoms of severe gastroesophageal reflux with pale skin color, vomiting, massive drooling, acid regurgitation, and reduced well-being. An open ventral semifundoplication was done some years ago to treat a gastroesophageal reflux. These symptomatic episodes occurred strongly dose-dependent and were not observed during the short test procedure. CONCLUSION: For the first time, a strong dose-dependent treatment with ITB was documented as a cause for the above episodes and relapsing re-herniations.

[A new possible phenotype of carbimazole embryopathy: A case report]. / Un nouveau phénotype possible d'embryopathie au carbimazole : à propos d'une observation.

Many disorders have been described in infants exposed to carbimazole during the first weeks of pregnancy. The most common of them are congenital aplasia cutis, choanal atresia and esophageal atresia. Rather unspecific dysmorphic features and developmental delay have also been reported. This set of congenital malformations suggests the existence of a phenotype of carbimazole embryopathy. To date, about 30 cases have been reported. We report on a new case of pregnancy accidentally conducted under carbimazole which gave birth to a newborn presenting with a hypertrophic pyloric stenosis associated with hiatus hernia and tracheomalacia. These anomalies have been associated with other malformations already identified in children exposed in utero to carbimazole such as scalp defects, retrognathia and gothic palate. As no relation between propylthiouracil and congenital malformations has yet been described, this drug seems highly preferable for pregnant women presenting with hyperthyroidism during the 1st trimester of their pregnancy.

Oxygen-induced vasodilation is blunted in pulmonary arterioles from fetal rats with nitrofen-induced congenital diaphragmatic hernia.

BACKGROUND/PURPOSE: Persistent pulmonary hypertension contributes to the high mortality rate associated with congenital diaphragmatic hernia (CDH). Oxygen is an important stimulus for pulmonary vasodilation in the perinatal period. The authors have investigated the responses of isolated pulmonary arterioles from fetal rats with and without CDH to an increase in oxygen tension. METHODS: CDHs were induced in fetal rats by feeding nitrofen to timed-pregnant rats at midgestation. A third-generation pulmonary arteriole was isolated from the right lung at term. Isolated arterioles were pressurized at their "optimal distending pressure." Diameter changes in response to an increase in oxygen tension from 25 to 40 mm Hg ("hypoxic" conditions) to 90 to 150 mm Hg ("normoxic" conditions) were recorded for K(+) preconstricted arterioles from control rats, from rats with nitrofen-induced CDH, and from rats that were nitrofen exposed but did not have a CDH. RESULTS: "Normoxic" exposure reversed the K(+) preconstriction in control arterioles by 124 +/- 26%. In contrast, arterioles from rats with nitrofen-induced CDH dilated significantly less than controls (20 +/- 15% of the K(+) preconstriction). The responses of arterioles from rats that were nitrofen exposed but did not get a CDH were not different (P >.05) from controls. CONCLUSIONS: Oxygen-induced vasodilation is blunted in pulmonary arterioles from rats with nitrofen-induced CDH. Blunted oxygen-induced vasodilation may contribute to persistent pulmonary hypertension in CDH. J Pediatr Surg 36:593-597.

Congenital anomalies in two infants born after gestational gamma-globulin prophylaxis.

The offspring of two women given prophylactic gamma-globulin 50 and 54 days after their last menstrual periods had congenital duodenal stenosis and a paraoesophageal hiatus hernia, respectively. The possibility that gamma-globulin may have contributed to these malformations is discussed.

Association of aspirin ingestion with symptomatic esophageal hiatus hernia.

The observed association of aspirin ingestion and symptomatic esophageal hiatus hernia is ascribed by me to injury of the esophageal mucosa during delayed passage of ingested aspirin from mouth to stomach. Physiologic alterations attributable to esophageal hiatus hernia act to prolong contact between swallowed material and the esophageal mucosa. This prolongation of contact between swallowed aspirin and the esophageal mucosa predisposes patients with esophageal hiatus hernia, and who are aspirin-users, to develop symptomatic esophagitis. Clinical data obtained from human subjects are presented which show that swallowed material may become trapped for extended periods in the esophagi of patients with esophageal hiatus hernia. Also, the capability of aspirin to injure alkaline mucosa by direct contact, in the absence of acid, is demonstrated.

[Hiatal hernia during a course of indirect anticoagulant treatment]. / Ernia jatale rivelata casualmente in corso di terapia con anticoagulanti indiretti

A personal case of haematemesis in a patient subjected to indirect management with anticoagulants is reported. The prothrombin values were not within the danger limits. Some concise notes on the points raised by this finding are presented and essential features of the diagnosis and treatment are discussed.

The relationship between hiatus hernia and tricyclic antidepressants: a report of five cases.

Of five patients who were receiving tricyclic antidepressants, two experienced an aggravation of preexisting hiatus hernia, and three with previously normal gastrointestinal X rays developed hiatal herination. The author suggests that this group of drugs may exert an anticholinergic effect on the esophageal sphincter and reduce the tone of the esophagogastric sphincter, thus aggravating existing hiatus hernia or causing its development.