Search PubMed⌕ Search

Biomedical subjects

M J Knapp

Publications and source records attributed to M J Knapp.

31 records · Page 2Linked to original sources

Nontraumatic prehospital sudden death in young adults.

The clinical and/or autopsy records of 83 consecutive adults presenting with nontraumatic prehospital sudden death (NPSD) in a single county were reviewed. Coronary artery disease (CAD) was the primary cause of death in individuals 36 to 45 years old. Non-CAD cardiac disease was the second most common cause of NPSD in this age group. Between the ages of 18 and 35 years, non-CAD cardiac disease was the primary cause and toxic ingestions were the second most common. Patients with rhythms other than ventricular fibrillation/tachycardia, asystole, or electromechanical dissociation on presentation to the emergency room (ER) were more likely to survive. Patients with asystole in the ER were more likely to die in the ER than were patients with other rhythms. Patients with toxic ingestions tended to have a better prognosis for successful resuscitation and for ultimate survival. Age, sex, bystander cardiopulmonary resuscitation, and time in the field were not significant prognostic variables. Patients with abdominal hemorrhage (eight of 83) as the cause of NPSD may represent a subgroup for whom a special approach is warranted. None of these patients survived. Early detection by culdocentesis or paracentesis in female patients of reproductive age and nasogastric lavage or stool occult blood testing could lead to more vigorous fluid resuscitation and early surgical intervention in abdominal hemorrhage.

Adolescent↗

Pleural amyloidosis.

Pleural amyloidosis has been reported rarely, and the diagnosis of this disease by Cope needle biopsy has, to our knowledge, been reported only once previously. We report two patients in whom the diagnosis of pleural amyloidosis was made by biopsy specimens obtained in the examination of large, unilateral pleural effusions. In one patient, the diagnosis was made by Cope needle biopsy. The clinical and diagnostic significance of these cases are discussed.

Aged↗

Hypoxia enhances unilateral lung injury by increasing blood flow to the injured lung.

We hypothesized that in unilateral lung injury, bilateral hypoxic ventilation would induce vasoconstriction in the normal lung, redirect blood flow to the injured lung, and cause enhanced edema formation. Unilateral left lung injury was induced by intrabronchial instillation of 1.5 ml/kg of 0.1 N HCl. After HCl injury, blood flow to the injured left lung decreased progressively from 0.70 +/- 0.04 to 0.37 +/- 0.05 l/min and percent of flow to the injured left lung (QL/QT) decreased from 37.7 +/- 2.2 to 23.6 +/- 2.2% at 240 min. Exposure to hypoxia (12% O2) for three 10-min episodes did not affect QL/QT in normal animals, but after unilateral HCl injury, it caused blood flow to the injured left lung to increase significantly. A concomitant decrease in blood flow occurred to the noninjured right lung, resulting in a significant increase in QL/QT. The enhanced blood flow to the injured lung was associated with a significant increase in the wet-to-dry lung weight ratio in the dependent regions of the injured lung. These findings demonstrate that in unilateral HCl-induced lung injury, transient hypoxia can enhance blood flow to the areas of injury and increase lung edema formation.

Animals↗