The eosinophilic leukocyte and the pathology of fatal bronchial asthma: evidence for pathologic heterogeneity.

Classically, bronchial asthma is associated with peripheral blood eosinophilia and striking eosinophilia of bronchial tissues and sputum. Evidence exists that eosinophil degranulation commonly occurs during bronchial asthma and eosinophil granule proteins are discharged onto damaged bronchial epithelium. Analyses of 10 patients with fatal asthma showed striking eosinophil participation in eight, whereas two patients showed marked epithelial desquamation in the virtual absence of eosinophils. These results point to the possibility that a pathologic heterogeneity exists in fatal bronchial asthma, with most, but not all, patients showing evidence of eosinophil participation.

An analysis of fifteen childhood asthma fatalities.

There is evidence from pediatric tertiary care centers in the United States that childhood deaths from asthma in hospitalized patients are becoming increasingly rare, while asthma mortality outside the hospital appears to be on the rise. When a young outpatient with asthma dies, the event is apt to be sudden and unanticipated and the victim is likely to be a preadolescent or adolescent who has suffered from asthma most of his or her life and who, despite ongoing bronchodilator therapy, requires hospitalizations for treatment of status asthmaticus. Patients in this age cohort have a strong tendency to underuse, overuse, or neglect to use prescribed medications, possibly as a gesture of emerging independence or because of the depression engendered by a chronic illness. In some instances serious psychosocial pathology accounts for noncompliance. For a patient with chronic asthma with a high-risk profile, any departure from an ongoing treatment regimen may result in respiratory failure. Pathologic complications of asthma may also act to upset the precarious physiologic equilibrium these patients have established. Unsuspected chronic pneumonia may lead to further increases in a chronically high degree of oxygen desaturation. Hypoxic seizures during an asthma attack may precipitate pulmonary edema. Tension pneumothorax has an even greater fatality potential for high-risk patients with asthma than it has for other patients with asthma, and pulmonary hypertension with cor pulmonale may develop because of chronic hypoxia. Some sudden deaths in children with chronic, severe asthma are unassociated with any of the above, making it necessary to entertain still other hypotheses.(ABSTRACT TRUNCATED AT 250 WORDS)

Asthma mortality in children: a 16-years experience at Children's Hospital of Philadelphia.

Over the 16-year period from August 1969 to August 1985, 15 children aged 9 to 19 years, well-known to physicians in the Allergy Section of the Children's Hospital of Philadelphia died unexpectedly of asthma outside the hospital. There were no deaths in hospitalized asthmatics during this time. Over half the deaths occurred since 1979, the same period in which significant increases in asthma deaths and hospitalizations were noted nationwide. The 15 children all had certain features in common and then subdivided into three subgroups. From analysis of the data five maxims for management of high-risk, chronic asthmatics were developed.

Unexpected death in childhood asthma. A review of 13 deaths in ambulatory patients.

Between January 1969 and January 1984, there were 13 deaths in ambulatory chronic asthmatics aged 9 to 19 years who had been followed up by physicians of the Allergy Section, Children's Hospital of Philadelphia. During this period, 5,686 children had been admitted to this institution for treatment of acute asthma and all had survived. Three possible causes for these deaths are suggested from a detailed review of each case. One cause may be medication-related, as exemplified by patient abuse of inhaled adrenergic drugs with concomitant erratic use of theophylline and corticosteroid drugs, or by physician failure to appreciate the need for corticosteroids. Serious behavioral disturbances account for some cases of medication misuse. A second cause of death may be an unsuspected pulmonary pathologic lesion, as revealed at autopsy, and a third cause may be sudden, intense airway narrowing, as has been reported in near deaths in hospitalized asthmatics.

Eosinophilic gastroenteritis in the pediatric patient.

Eosinophilic gastroenteritis is a diagnosis to be entertained whenever a patient had abdominal complaints accompanied by striking peripheral eosinophilia. A definitive diagnosis is of greater importance in this illness, since undiagnosed cases often undergo needless exploratory surgery. An infant seen at 2 years, 10 months of age with abdominal pain, nausea, and vomiting was found to have a white blood cell count of 50,000/cu mm with 54% eosinophils and eosinophilic ascites. An antral tissue biopsy yielded a diagnosis of eosinophilic gastroenteritis after many studies had been made to exclude other diagnoses. Treatment with intermittent courses of prednisone kept the patient relatively asymptomatic over the period of 20 years during which she remained under our care. Immunologic studies shed no light on the etiology of this patient's disorder. The literature dealing with diffuse, infiltrative eosinophilic gastroenteritis is reviewed.

Immunologic mechanisms responsible for adverse reactions to routine immunizations in children.

The principal licensed biologicals for human use in the United States have been listed with special emphasis given to antiviral vaccines. Possible adverse reactions of an immunologic nature which may be encountered in the use of these agents in routine immunization programs are described, while at the same time, their relative rarity is emphasized. The special problems one may encounter in immunizing the atopic child, the immunodeficient child, the child with active tuberculosis and the pregnant woman are considered separately, as are the undesirable consequences of hyperimmunization are mentioned.