Biomedical subjects
Publications and source records attributed to D C Tyler.
Chronic stool retention with soiling is a common and distressing condition in children. Diagnosis and treatment generally involve both medical and psychological aspects. This case addresses a potentially life-threatening complication of shock occurring during treatment of chronic stool retention with castor oil, and also explores the psychosocial factors felt to be contributory.
A 7-yr-old boy undergoing treatment for respiratory failure after near-drowning developed a pneumomediastinum. Intracranial hypertension refractory to previously successful therapy led to placement of a mediastinal tube, after which intracranial pressure decreased and was easier to control. A pneumomediastinum may cause intracranial hypertension by interfering with venous drainage from the cranium.
In a 1980 Washington State Supreme Court decision, brain death was recognized as a means of determining death, but the court declined to specify a procedural mechanism to be followed. According to a survey of hospitals in Washington, the decision has had little impact in the state, apparently due to the medical profession's unfamiliarity with it. As a result of the survey, we have identified problems of procedure and interaction with the legal system. A consensus of those contacted was that no formal, hospital-mandated definition of brain death is needed.
Airway obstruction caused by the epiglottis was seen in a 4-month-old boy. Biopsy showed multiple dilated lymphatic vessels, and spontaneous resolution occurred over a period of one year. The possible causes for lymphangiectasis of the epiglottis are discussed.
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We investigated the effects of meconium on the lungs of an adult rabbit model to distinguish between mechanical obstruction of airways and chemical pneumonitis. After the rabbits were anesthetized and intubated, 20% human meconium in saline was instilled into the trachea. Arterial and mixed venous blood gases, functional residual capacity, cardiac output vascular pressures, calculated venous admixture, and pulmonary vascular resistance were measured. Sections of affected lung tissue were examined microscopically. The results were consistent with an early mechanical obstruction of airways with gradual development of chemical pneumonitis over 48 hours.
We investigated the effects of varying inspired oxygen concentrations on the resolution of oleic acid-induced lung injury in rabbits. Rabbits were injected intravenously with oleic acid and maintained in room air, or exposed to 60, 70, or 80% oxygen for periods of 7 or 10 days. Oleic acid caused hemorrhagic pulmonary edema with hypoxemia. Hypoxemia was more profound in the oxygen-treated animals, a difference that was significant after 7 days' exposure to 60 and 70% oxygen, and after 4 days to 80% oxygen. Mortality was increased in the animals maintained in 80% oxygen. The data suggest that environmental oxygen concentrations greater than 60% interfere with the return to normal lung function following oleic acid injury in rabbits. The hypoxemia may be due to either mismatching of ventilation and perfusion or to a diffusion block resulting from the increased septal width. There was no evidence of massive pulmonary edema as a cause of the hypoxemia. It was not possible to distinguish between injury primarily caused by oxygen and its interference with the healing process.
We investigated the effects of an inspiratory positive pressure plateau produced by a high (4/1) inspiratory-expiratory (I/E) ratio in rabbits with pulmonary edema induced with oleic acid. With an inspiratory pressure plateau, intrapulmonary shunt was significantly reduced compared to a standard 1/2 I/E ratio. Reduction in shunt was also obtained when positive end-expiratory pressure (PEEP) was added to the 1/2 I/E ratio ventilatory pattern. Since the improvement in shunt could have been caused by either recruitment of alveoli or by maintenance of lung volume at end exhalation we measured tidal volume and thoracic gas volume to distinguish between the two. With both patterns, improvement in shunt was associated with an increase in thoracic gas volume. The increase in thoracic gas volume was greater with PEEP than with 4/1 for an equivalent increase in mean airway pressure. The results suggest that an inspiratory pressure plateau improves gas exchange in pulmonary edema, but that this improvement occurs because of an increase in end-expiratory lung volume. Positive end-expiratory pressure is a preferable method of increasing end expiratory lung volume because a greater increase occurs for the same change in airway pressure.