The spectrum of pediatric injuries after a bomb blast.

The spectrum of pediatric injuries seen after a bomb blast is poorly documented. The pathophysiology of blast injuries differ significantly from other forms of trauma and typically result in large numbers of distinctly patterned injuries. On April 19, 1995, a truck bomb was detonated directly adjacent to the Alfred P. Murrah Federal Building in Oklahoma City, Oklahoma. A total of 816 adults and children were injured or killed as a direct result of the blast. Twenty infants and children were seated by the window of the second floor day care center at the time of the explosion. The injuries incurred by all children involved in the blast were studied. Nineteen children, 16 of whom were in the day care center, died as a direct result of the blast. The injury patterns among the 19 dead children included a 90% (17 of 19) incidence of skull fractures, 15 of those with cerebral evisceration (skull capping); 37% with abdominal or thoracic injuries; 31% amputations; 47% arm fractures, 26% leg fractures; 21% burns; and 100% with extensive cutaneous contusions, avulsions, and lacerations. Forty-seven children sustained nonfatal injuries with only seven children requiring hospitalization. The injuries sustained by the seven hospitalized children included two open, depressed skull fractures, with partially extruded brain, two closed head injuries, three arm fractures, one leg fracture, one arterial injury, one splenic injury, five tympanic membrane perforations, three corneal abrasions, and four burn cases (1 > 40% body surface area [BSA]). After a bomb blast, pediatric patients sustain a high incidence of cranial injuries. Fractures and traumatic amputations are common. Intraabdominal and thoracic injuries occur frequently in the deceased but infrequently in survivors.

Polymorphonuclear leukocyte function in HIV-1-infected chimpanzees.

The chemiluminescent characteristics of enriched populations of neutrophils from control and HIV-infected chimpanzees were assessed. Neutrophils from HIV-infected chimpanzees were suppressed in their ability to generate a normal response to particulate and soluble stimuli when compared to normal and hepatitis non-A, non B-infected controls. Particulate (latex beads) stimulation of neutrophils resulted in an aberrant response when contrasted with controls. Normal control responses were characteristically biphasic while the response from hepatitis NANB HIV-infected chimpanzees was not biphasic. Neutrophils challenged with a soluble (phorbol ester) stimulant also demonstrated a suppressed response. These data suggest that HIV infection has an additive suppressive effect on neutrophil function in chimpanzees previously infected with hepatitis NANB. The suppression of chimpanzee neutrophil function following HIV infection is similar to that seen in other non-primate viral and retroviral infections.