Search

FATAL HEMORRHAGE as a delayed complication of tracheotomy has rarely been reported. In 1924 Schlaepfer discussed this event in relation to patients who had undergone tracheotomy for laryngeal diphtheria.1 The bleeding in those instances developed several days to months after the surgical procedure. It was apparently unrelated to the presence or absence of the tracheal cannula and presumably resulted from rupture of an aneurysm that formed as a consequence of an operative injury to, and subsequent development of necrotizing inflammation within, the wall of a large artery or vein. Not until 32 years later did Davis and Southwick 2 call attention to another mechanism of delayed fatal hemorrhage after tracheotomy, namely, pressure-induced erosion of the cannula through the tracheal wall into the innominate artery. Death of their two patients occurred within two and five weeks of operation, respectively. The type of complication described by these authors deserves wider

During en-ntered four cases of fatal pulmonary thromboembolism in which symptoms and signs referable to the nervous system were sufficiently prominent to mask the true nature of the underlying disease. An analysis of these cases revealed certain clues that might have led to the correct premortem diagnosis. The purpose of this report is to emphasize those clues and to review the neurological manifestations of pulmonary thromboembolism. REPORT OF CASES CASE —This 61-year-old man was well until he fainted while carrying a beer cooler to his car. Upon regaining consciousness, he noticed weakness in his right arm, frontal headache, and pain in the right side of the chest, all of which subsided within a few hours. He remained asymptomatic until three days later when he fainted while eating breakfast. His private physician found him to have "low blood pressure" and mental confusion and referred him for further evaluation and therapy.On

Salmonella enteritidis14C-endotoxin was recovered predominantly from the nuclear and mitochondrial subcellular fractions of livers and spleens of mice and rats, 3.5 hr and 3 days after intravenous administration. Of the recovered radioactivity, 10 to 20% was present in the liver mitochondrial fraction as high-molecular-weight, biologically active material, suggesting the presence of intact endotoxin. Autoradiographic studies demonstrated nuclear and cytoplasmic labeling in the liver and at least nuclear label in spleen cells. The resistance of rats, as compared to mice, to the induction of amyloidosis does not appear to be based on a difference in subcellular localization of endotoxin within the reticuloendothelial system.

A patient had primary systemic amyloidosis with severe cardiac involvement and IgG paraproteinemia. Numerous intramural coronary arteries were occluded by amyloid deposits, but arteriosclerosis of the extramural arteries was absent. The amyloid coronary artery disease was associated with angina pectoris, a myocardial infarct, and mural thrombi which resulted in cerebral, renal, pulmonic, and coronary arterial emboli.

Over 1,000 cases of polyarteritis nodosa have been reported in the medical literature. It is, therefore, rather surprising that so little documentation of the radiographic features of this disease is available. Recently, a few reports of cases with arteriographically demonstrable intrarenal aneurysms have appeared (Bron, Strott and Shapiro, 1965; Fleming and Stern, 1965; Horner, Hunt, Kincaid and De-Weed, 1966; Chudacek, 1966; 1967; Lang, 1967), and it appears that the demonstration of bilateral multiple intrarenal aneurysms, particularly involving the arcuate and interlobar vessels, is diagnostic of polyarteritis (Bron et al., 1965).The nephrotomographic appearance of polyarteritis in the kidneys has not previously been mentioned in the literature.In this communication we record the sixth case of polyarteritis nodosa with angiographic demonstration of renal artery aneurysms and also show an interesting sequence of changing nephrotomograms which probably is specifically diagnostic of perirenal haematomas in this disease.This 37-year-old white male first presented with polyarthritis in 1959, and a diagnosis of rheumatoid arthritis was made by his local physician. In 1967, he was found to have hypertension. L.E. preparations were reported as positive at that time and a diagnosis of systemic lupus erythematosus was made.On his first admission to the National Institutes of Health in October, 1967 he had a blood pressure of 160/130, joint deformities suggestive of rheumatoid arthritis, iatrogenic Cushing's disease, microscopic haematuria, BFT positive in a dilution of 1 to 2,048 and negative L.E. preps.