ADAM nasal CPAP circuit adaptation: a case report.

ADAM (Airway Delivery And Management) circuitry for nasal continuous positive airway pressure (CPAP) (administration/delivery) was not successful in the delivery of nasal CPAP to a patient. Adaptations to the circuitry were necessary to obtain a more comfortable fit.

Determinants of outcome after pulmonary contusion.

During the past 5 1/2 years, 86 patients were treated for pulmonary contusion resulting from blunt trauma. Injury mechanism was motor vehicle in 65 patients (76%), farming in nine (10%), fall in eight (9%), and miscellaneous in four (5%). There were 68 males (79%) and 18 females. Ages ranged from 4 to 75 years (mean, 32 years). Twenty-two patients (26%) presented in hypovolemic shock. Injury Severity Score (ISS) averaged 26 (range, 9-57). Intubation was performed in the Emergency Department in 21 patients (24%), 19 of whom were severely hypoxic with pO2/FIO2 ratio less than 300. Thirty-four patients were ultimately treated with mechanical ventilation for 1 to 103 days (mean, 9.1 days). The average hospital stay was 22 days. Eleven patients (13%) died. Mortality was significantly greater (p less than 0.05) in patients with ISS greater than or equal to 25, initial Glasgow Coma Scale less than or equal to 7, transfusion of greater than three units of blood, and pO2/FIO2 less than 300. Mortality was not correlated with either presence of shock or amount of intravenous fluid administration. Eighteen patients with concomitant flail chest demonstrated no increase in mortality but were likely to require mechanical ventilation (p less than 0.05). The extent of contusion assessed on admission chest roentgenogram was not predictive of mortality or need for intubation. We recommend aggressive treatment of associated injuries, craniocerebral trauma, and selective mechanical ventilation based upon degree of intrapulmonary shunt.

Chondrosarcoma: a case report with left atrial involvement and systemic embolization.

A 26-year-old white man underwent amputation of the right lower extremity for a chondrosarcoma of the distal femur. Eleven years later, after a long symptom-free interval, he was hospitalized for rapidly progressive dyspnea, pleuritic chest pain, and hemoptysis resulting from a large pulmonary metastasis that had extended directly to the left atrium via the pulmonary vein. Within 24 hours of hospitalization, obstruction of the left commom iliac artery by tumor embolus necessitated embolectomy. This represents the second report of a metastatic chondrosarcoma involving the left atrium. The case presented clinically as an atrial myxoma and disseminated via the systemic circulation with a rapidly downhill course therafter.

Spontaneous fibrinolysis in pulmonary embolism.

This study correlated levels of activated fibrinolysis with the presence, extent, and rate of resolution of angiographically documented pulmonary emboli. Pulmonary emboli demonstrable by angiography were associated with detectable fibrin split products in the serum of 24 of 25 patients. In the absence of increased fibrin split products, pulmonary emboli large enough to be demonstrated by angiography were found in only 2 of 25 positive pulmonary angiograms. Spontaneous resolution of pulmonary emboli could not be correlated with the the concentration or persistence of fibrin split products but did correlate well with the presence of a reversible precipitating cause. Thrombophlebitis in the absence of clinical evidence of pulmonary embolism was not associated with increased concentrations of fibrin split products in eight of nine patients. The one patient with increased fibrin split product concentration had evidence on lung scan of silent pulmonary embolism.

Hypoxemia in pulmonary embolism, a clinical study.

The cause of hypoxemia was studied in 21 patients with no previous heart or lung disease shortly after an episode of acute pulmonary embolism. The diagnosis was based on pulmonary angiography demonstrating distinct vascular filling defects or "cutoffs." It was found that virtually all of the hypoxemia in patients with previously normal heart and lungs could be accounted for on the basis of shunt-like effect. The magnitude of the shunting did not correlate with the percent of the pulmonary vascular bed occluded nor with the mean pulmonary artery pressure. The shunts tended to gradually recede over about a month after embolism. Patients without pulmonary infarction were able to inspire 80-111% of their predicted inspiratory capacities, and this maneuver temporarily diminished the observed shunt. Patients with pulmonary infarcts were able to inhale only to 60-69% of predicted inspiratory capacity, and this did not reverse shunting. These data suggest that the cause of right-to-left shunting in patients with pulmonary emboli is predominantly atelectasis. When the elevation of mean pulmonary artery pressure was compared to cardiac index per unit of unoccluded lung, it fell within the range of pulmonary hypertension predicted from published data obtained in patients with exercise in all except one case. This observation suggests that pulmonary vasoconstriction following embolism is not important in humans, although these data are applicable only during the time interval in which our patients were studied and in patients receiving heparin.