Search PubMed⌕ Search

Biomedical subjects

A A Fowler

Publications and source records attributed to A A Fowler.

80 records · Page 5Linked to original sources
PubMed1983

Adult respiratory distress syndrome: risk with common predispositions.

A 1-year survey of patients in three hospitals identified 936 patients who had one predisposition and 57 who had several predispositions to the adult respiratory distress syndrome. From the total predisposed population of 993 patients, 68 subsequently developed the syndrome. An additional 20 patients developed the syndrome from causes other than eight identified predispositions, to bring the total of patients studied to 88. A highly significant difference (p less than 0.0001) was found in the incidence rates of the syndrome between patients with one and several predispositions (5.8 versus 24.6 per 100 patients). Within 72 hours of onset of predisposition, 89.5% of patients who developed the syndrome had been intubated and placed on mechanical ventilation. Fifty-seven of the 88 patients (64.8%) with the syndrome died. By the 14th day 90% of deaths had occurred. There were no age- or sex-specific differences in either incidence or mortality rates. Case fatality rates of the syndrome were high in all predisposed groups.

Adult↗
PubMed1982

Thrombolytic therapy. For pulmonary embolism and deep venous thrombosis.

Thrombolytic agents are effective in acute pulmonary embolism and thrombosis in the popliteal and proximal deep veins. Patients with recent thromboemboli, as manifested by onset of symptoms within the previous five days, respond best. Bleeding complications can be greatly reduced by proper patient selection and by avoidance of invasive procedures. Thrombolytic agents are easily administered, and laboratory monitoring has been simplified. Anticoagulants must be given when thrombolytic therapy is completed, since the thrombotic tendency probably still exists.

Blood Coagulation Tests↗
PubMed1982

Superior vena cava syndrome as a cause of pleural effusion.

The development in the postoperative period of the superior vena cava syndrome resulted in a persistent right-sided, transudative pleural effusion. It appears that the increased systemic venous pressure from left innominate thrombosis leading to superior vena cava obstruction in association with chest tube drainage connected to suction (increased intrapleural negative pressure) produced hydrostatic imbalances that resulted in increased pleural fluid formation and collection.

Coronary Artery Bypass↗
PubMed1982

Another look at ARDS.

ARDA is a common clinical problem resulting in acute respiratory failure in many and death in the majority of patients with a wide variety of direct and indirect pulmonary insults. ARDS is widely recognized and appropriately treated by empiric supportive care. Pharmacologic approaches to support the circulation are established. The use of corticosteroids remains controversial. The future depends upon unraveling the biologic mysteries which lead to the cascade of events which result in ARDA. This will establish a basis for further improvements in management.

Adrenal Cortex Hormones↗
PubMed1981

Focal pulmonary edema after massive pulmonary embolism.

We report here the occurrence of focal pulmonary edema within 4 h after massive acute pulmonary embolism. The edema appeared to develop only in areas with intact pulmonary arterial blood flow and occurred in the apparent absence of left ventricular dysfunction. This pattern of pulmonary edema after precapillary obstruction is similar to that seen in animal models of permeability pulmonary edema induced by acute nonuniform pulmonary arterial obstruction.

Adolescent↗
PubMed1978

Positive end-expiratory pressure in the management of lobar atelectasis.

Positive end-expiratory pressure (PEEP) has been extensively utilized in the treatment of severe hypoxemia from noncardiogenic pulmonary edema. The usefulness of therapy with PEEP in the management of lobar atelectasis has not been previously stressed. Recently, we observed four patients with lobar atelectasis who failed to respond to the usual conservative measures of endotracheal suctioning and thoracic physiotherapy. Atelectasis was confirmed by physical examination and chest x-ray films, and three of the four patients subsequently underwent fiberoptic bronchoscopic examination. Endobronchial obstruction was not found, and despite extensive irrigation and suctioning, the atelectasis failed to resolve. Therapy with PEEP was then added, with pressures of 5 to 15 cm H2O. Serial chest x-ray films disclosed resolution of the atelectasis within 4 1/2 hours in two patients, within 14 hours in one patient, and within 24 hours in the remaining patient.

Adolescent↗
PubMedDate not supplied

Hemodynamic effects of bradykinin antagonism in porcine gram-negative sepsis.

Activation of the kallikrein-kinin system in sepsis has long been recognized, but its role, beneficial or pathologic, has not been defined. Recently, however, specific bradykinin (BK) antagonists have become available and this study investigated the effects of a BK antagonist, NPC17731 (Scios-Nova) on systemic and pulmonary hemodynamics in a model of gram-negative sepsis. Anesthetized swine were studied for 5 h receiving a 1-h infusion of saline (controls, group 1, N = 8) or live Pseudomonas aeruginosa (septic, group 2, N = 8). Group 3 (treatment, N = 6) received NPC17731 (5 mg/kg initial bolus followed by 1 mg/kg hourly) just prior to the onset of sepsis. Group 2 animals showed a rapid decrease in systemic arterial pressure (SAP) from 30 min onward, and sustained significant hypotension from 2 h onward. In group 3, SAP fell similarly until 2 h then progressively rose, returning to baseline levels by 5 h. In contrast, cardiac index fell progressively from 3 h onward in groups 2 and 3. Systemic vascular resistance index (SVRI) fell significantly by 2 h in group 2 animals, recovering to baseline by 5 h. Group 3 showed a similar initial fall followed by a rebound increase in SVRI, which, at 5 h was significantly raised above the other groups. Group 2 developed significant, persistent pulmonary artery hypertension which was not reduced by NPC17731. The data imply a significant role for bradykinin in the pathogenesis of hypotension in septic shock in this model. Septic shock was reversed by a BK antagonist which increased peripheral resistance without affecting cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗