The reduction in mortality in acute appendicitis during the past 40 years constitutes a remarkable achievement. Unfortunately, there remains a comparatively high death rate in this disease in small infants.Evidence exists that this is due, in part, to a lack of progress in the early diagnosis of this disorder. It appears that the great advances in technical and therapeutic procedures have obscured the importance of early diagnosis. For this reason it seems worth while to review the factors responsible for delay in diagnosis and to discuss some of the associated problems.This study concerns itself with (a) a report of acute appendicitis with perforation in a 15-day-old infant with survival; (b) an analysis of acute appendicitis in infants 36 months of age or younger, from 1942 to 1952, at the Los Angeles County Hospital, and (c) a survey of the literature. Acute Appendicitis in aFifteen-Day-Old Boy A full-term boy was born on Jan. 27, 1950. During the week preceding his normal delivery, the infant's mother and sister had been ill with moderately severe viral infections. At the age of 15 days, the infant was seen in the office of one of us (M. J. N.) with a history of episodes of restlessness and crying of two days' duration. During the first 36 hours the discomfort was apparently mild and occurred mainly at the time of feedings. At the end of this time, he became increasingly irritable, slept poorly, refused feed¬ ings, and for the first time appeared ill. No vomiting had occurred, and the infant had not appeared to be feverish.Initial examination revealed an acutely ill in¬ fant with slightly sunken eyes and a depressed anterior fontanel. The abdomen was markedly distended and generally rigid and tender. No masses were palpable. Peristalsis was diminished.The rectal temperature was 101.8 F. ; the white blood count was 7400, with 58% polymorphonu¬ clear cells (30% nonsegmented cells). The infant was admitted to Cedars of Lebanon Hospital the same afternoon. The repeat white blood count was 6100, with 65% polymorphonuclear cells (42% nonsegmented cells), red blood count 5,620,000, and hemoglobin 17 gm. The urine showed no abnormalities. A preoperative diagnosis of peri¬ tonitis probably secondary to a perforated ap¬ pendix was made. Eight hours were required for preoperative preparation, i. e., correction of fluid and electrolyte imbalance, antibiotic therapy, nasogastric suction, and additional consultation.At surgery (approximately 60 hours after onset), the peritoneal cavity contained a grayishyellow, cloudy fluid. There was a thick fibrinopurulent exúdate in the ileocecal area. The appendix lay free in the right iliac fossa, was acutely inflamed and showed a 2-ram. perforation near its midpoint. An appendectomy was per¬ formed and the wound closed without drainage. Culture of the peritoneal exúdate grew Escherichia coli and nonhemolytic streptococci. Penicillin was administered for seven days and streptomycin for three days. The infant made an uneventful recovery and was discharged on the eighth post¬ operati...

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Twenty-one cases of pneumothorax of the newly-born have been recorded in medical literature. A recent review by Glaser and Landau' emphasi7ed the rarity of the condition, the high mortality, the greater incidence in the male sex, the predominance of left-sided involvement and the difficulties that arise in an attempt to explain satisfactorily the origin of this interesting and unusual complication. Willi recognized three groups of cases, classified according to their etiology, as mechanical, infectious, or congenital.The first group includes such causative agents as forcible artificial respiration, the use of the Drinker respirator, obstruction of the air passages by aspirated amniotic material, enlargement of the thymus and collapse of the epiglottis. The exact significance of obstruction to the ingress of air in the production of a pneumothorax is by no means as obvious as certain writers suggest. Many cases of obstruction accomipanied by the most laboured inspiratory efforts have been observed in cases of congenital laryngeal stridor, subglottic stenosis and other malformations of the: upper respiratory passages without the escape of air into the pleural cavity. A recentlv observed case of obstruction due to aspirated amniotic material showed at autopsy a few marginal emphysematous bullae but not a pneumothorax notwithstanding very strenuous inspiratory efforts for several hours before death. It appears as a possibility at least, that histological studies of serial sections may disclose congenital defects in the lung tissue as the primary cause and mechanical obstruction to the entrance of air as a necessary but secondary factor in the development of this type of pneumothorax.Three cases have been placed by Wilkinson2 in the infectious group. He demonstrated coilclusively in his own case that the formation of a pulmonary abscess which ruptured into the pleural cavity was caused by multiple septic pulmonary emboli and was not secondary to a low grade inhalation pneumonia starting at birth, a mechanism suggested by other investigators. The emboli were attributable to a septicaemia originating in all likelihood from an omphalitis or a circumcision wound. Unfortunately knowledge of neonatal septicaemias is still imperfect. Their occurrence. has been noted in on 7 June 2019 by guest. Protected by copyright.

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