ABSTRACT
A case of extrinsic nonvalvular mitral obstruction due to a large epicardial hematoma in a patient with rheumatoid constrictive pericarditis is described. The patient had longstanding rheumatoid arthritis and a mitral diastolic murmur developed. Mitral obstruction was confirmed by a hemodynamic study. Coronary angiography and left ventricular angiography showed severely diseased coronary arteries and a distorted left ventricular cavity. Autopsy demonstrated rheumatoid arthritis, a normal mitral valve, thickened pericardium, and epicardial hematoma surrounding both ventricles at the atrioventricular junctional level.
Subject(s)
Hematoma/complications , Mitral Valve/pathology , Pericardial Effusion/complications , Pericarditis, Constrictive/complications , Arthritis, Rheumatoid/complications , Heart Valve Diseases/etiology , Humans , Male , Middle AgedABSTRACT
The purpose of this project was the development of a small animal model and the use of external gamma imaging for the study of acute post-inhalation permeability changes. New Zealand white rabbits were anesthetized with ketamine and acepromazine IM, intubated, and a catheter placed in an ear artery. Smoke was produced by burning absorbent cotton in a combustion chamber supplied with 10 liters/min of air. Smoke was delivered to a holding chamber, allowed to cool to room temperature, and immediately delivered to the animals via endotracheal tube. Animals were allowed to inhale smoke for 3 sessions of 2 to 3 minutes. Blood samples were collected for the measurement of PO2, PCO2, and COHb. Lungs were removed at 3 to 4 days postinjury and subjected to microscopic histologic analysis. The results of six animal experiments showed a significant inhalation injury. The mean COHb level was 48% (range, 36%-58%). The change in the pre- and post-injury PO2 and PCO2 values were not significant (mean PO2, 66 mm Hg; mean PCO2, 32 mm Hg). Histologic evaluation of the lungs of three animals at 24 hrs postinjury revealed extensive loss of tracheal epithelium extended to many terminal bronchi. Inflammation of surrounding tissue, including edema and increased migration of polymorphonuclear cells, was also present. Analysis of tissue obtained at 10 to 14 days showed reparative reepithelialization of trachea and major bronchi but acute inflammation and loss of intralobar bronchi. Inflammatory exudate extended to adjacent alveoli. In conjunction with the above model we have developed a method for the noninvasive measurement of lung permeability changes.(ABSTRACT TRUNCATED AT 250 WORDS)
