[Tracheoesophageal fistula secondary to ingestion of a button battery]. / Fístula traqueoesofágica secundaria a ingestión de pila de botón.

An eleven month old girl was admitted to a county hospital because of persistent low grade fever, cough, vomitus and food and oral fluids rejection. A small radiopaque, button sized, round object was seen impacted in the upper esophageal third on X ray examination and later extracted by endoscopy, corresponding to an electric cell, from a father's handwatch, which had been ingested by the baby without knowledge of parents about 30 h before. After 12 h fasting, oral feedings were resumed being apparently well tolerated, but in the following day fever and respiratory distress reappeared, together with drooling, cianosis, abdominal distention and pale skin. Patient was transferred to a regional hospital where extensive bilateral pneumonia and anemia were documented. Gastric drainage via nasogastric tube, antibiotic treatment, blood transfusion and oxygen therapy were given from admission, but she died within a few hours. At necropsy a 3 per 2.5 cm diameter orifice of sharp borders was seen in the upper third of the esophagus, communicating to tracheal lumen through its upper six cartilages. Extensive, severe, bilateral pneumonia was confirmed. When this kind of electric cells become impacted into the esophagus, wall necrosis may occur within 4 h and perforation within 8 to 12 h and can be prevented by immediate endoscopic extraction. Otherwise fistulae should be suspected and patients managed accordingly. Emergency room medical staff must always be aware of this potentially lethal condition and its proper management. Infants should not be permitted to play with such apparently innocent objects as battery operated handwatches.

[Neuronal intestinal dysplasia. Critical 10-years' analysis of clinical and biopsy diagnosis]. / Neuronale intestinale Dysplasie. Eine kritische 10-Jahres-Analyse klinischer und bioptischer Diagnostik.

61 cases of neuronal intestinal dysplasia are compared in a follow-up study. Two clinically and bioptically different types of intestinal dysplasia can be distinguished. One type with involvement of the sympathetic nerves and the clinical signs of intestinal spasticity, ulcerative colitis with haemorrhagic stools. Histotopochemically, this disease pattern shows aplasia or hypoplasia of the sympathetic nerves with enhanced parasympathetic activity (elevated acetylcholinesterase activity in the lamina propria mucosae and orbicular musculature). One type with involvement of the plexus submucosus clinically accompanied by adynamia of the colon with megacolon formation. This type becomes manifest usually around the 6th month of life. Bioptically there are large groups of ganglion cells and Schwann's cells, but there is also acetylcholinesterase activity as in the other type. This 2nd form is seen more frequently. A third form is a combination of both diseases. The incidence rate of neuronal intestinal dysplasia is equal to that of Hirschsprung's disease.