That perforated gastric ulcers are of unusual occurrence in infants and children is well established. In a review of 248 cases of ulceration of the stomach in children, Theile (1, 2) found only 5 instances of perforation. Pendergrass and Booth (3) have also stressed the absolute and relative rarity of this complication in childhood as compared to its incidence in later life. The etiology of ulceration in children, with or without subsequent perforation, is obscure. Adler (4) attributed it to autodigestion occurring as a result of small hemorrhages during parturition. Other causative agents which have been suggested are direct trauma, infection, local disturbance of circulation from congestion, embolism, thrombosis, and vascular disease. The brilliant work of Cushing (5), following that of German investigators (7, 8), established a neurogenic origin for many gastric ulcers. Animal experiments and his observation of multiple ulcers of the stomach, frequently with perforation, following brain surgery, more especially operations in the region of the cerebellum, led him to the conclusion that injury or stimulation in this latter region may lead to the development of peptic ulcer. The establishment of the diagnosis of peptic ulcer in an infant is difficult. The only clinical sign is hemorrhage. According to Hurst and Stewart (9), 50 per cent of cases of melena in infancy are due to peptic ulcer. Roentgen examination should therefore be made, and if necessary repeated at frequent intervals, in any infant with bleeding from the gastro-intestinal tract, in order that an early diagnosis may be made. The following case is believed to be of interest because of the rarity of perforation of gastric ulcer in the newborn, for the association of the condition with intracranial injury, and as illustrating the importance of early roentgen diagnosis. Case Report The patient was a full-term male infant weighing 6 lb. 14 oz., the second child of a Puerto Rican mother. The prenatal course had been normal, and the mother's Mazzini test was negative. Labor pains began at noon, Oct. 9, 1948; the membranes ruptured at 2:30 p.m., and spontaneous delivery occurred at 10:20 p.m. of the same day. The infant was in a vertex presentation, left occiput anterior position. At no time were forceps used, nor was there any undue trauma associated with the birth. The child appeared well until the second day, when he passed two dark red stools and vomited dark brown fluid once. On physical examination he was described as a well nourished, normally developed baby. The skin was pale and free from petechiae. Examination of the head was negative. The chest was clear and the abdomen was soft. Bleeding and clotting times were within normal limits. The white cell count was 5,600, with 86 per cent polymorphonuclears, 10 per cent lymphocytes, and 4 per cent myelocytes; red cell count, 3,320,000; hemoglobin, 11.5 gm.; hematocrit reading, 40. There was no evidence of a blood dyscrasia.
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