ABSTRACT
A retrospective review of 36 patients with infective endocarditis by strict case definition was performed from 1972 through April of 1984. Male to female ratio was 1:1.25, with mean age of 19.1. Thirty of the 36 patients(83.3%) had the history of predisposing heart diseases: congenital heart disease was most frequent one below the age of 20, rheumatic heart disease between the age of 20-39 and degenerative heart disease above the age of 40. The commonest presenting symptoms were fever, dyspnea, and malaise, and the commonest signs were fever, murmur, and hepatomegaly. Average hemoglobinand hematocrit were 10.1g/dl and 30.8% respectively, showing moderate degree of anemia. White cell count was 11,600+/-5400/mm3 and erythrocyte sedimentation rate was 46+/-18mm/hr. Over four fifths of the patients demonstrated proteinuria and elevated C-reactive protein. Two thirds of the patients showed microscopic hematuria and one third showed positive rheumatoid factor. Eight patients(22.2%) showed arrhythmia and 4(11.1%) showed conduction abnormalities on electrocardiography. The commonest etiologic microorganisms were alpha-hemolytic streptococcus(30.6%) and staphylococcus aureus(22.2%). Abacteremic cases were found in 38.9% of the patients. To compared with alpha-hemolytic streptoccus endocarditis the cases caused by staphylococcus aureus showed the shorter duration of symptoms before admission, the less frequent complication, the higher fever, and the more elevated white cell counts. To penicillin, alpha-hemolytic streptococcus was sensitive in most cultures and staphylococcus arueus was resistant in half of them, and to aminoglycosides vice versa. To cefazolin, both microorganisms were sensitive in most cultures. In 18 of 24(75%) patients vegetation was visualized by echocardiography. The most frequent site of involvement was the mitral valve. And in vegetation detected group complication rate by embolism was found to be higher. The common complications were congestive heart gailure in 24(66.75%), embolism in 8(22.2%), and metastatic infection in 6(16.7%). The mortality rate of infective endocarditis was 25%, and the causes of death were cerebral embolism in 3(8.3%), septic septic shock in 3(8.3%), congestive heart failure in 2(5.6%), and mycotic aneurysmal rupture in 1(2.8%). Conclusively in infective endocarditis the author observed the increasing prevalence of degenerative heart disease as a prdisposing heart disease and increasing incidence of staphylococcus aureus as a causative microorganism. Adn the differences of clinical characteristics between staphylococcus ureus and alpha-hemolytic streptococcus endocarditis would be helpful in diagnosis and treatment of infective endocarditis as well as recognition of prognosis.
Subject(s)
Female , Humans , Male , Aminoglycosides , Anemia , Aneurysm, Infected , Arrhythmias, Cardiac , Blood Sedimentation , C-Reactive Protein , Cause of Death , Cefazolin , Cell Count , Diagnosis , Dyspnea , Echocardiography , Electrocardiography , Embolism , Endocarditis , Estrogens, Conjugated (USP) , Fever , Heart , Heart Defects, Congenital , Heart Diseases , Heart Failure , Hematocrit , Hematuria , Hepatomegaly , Incidence , Intracranial Embolism , Mitral Valve , Mortality , Penicillins , Prevalence , Prognosis , Proteinuria , Retrospective Studies , Rheumatic Heart Disease , Rheumatoid Factor , Rupture , Shock, Septic , Staphylococcus , Staphylococcus aureus , StreptococcusABSTRACT
The authors reported here a 23 years-old female patient with acute renal failure and anaphylaxis induced by rifampicin, who was suffered from exudative pericarditis. The diagnosis was made by its reproducibility with rifampicin. The pathogenesis of acute renal failure and anaphylaxis in this case was thought to be immunologic mechanism, because of elevated IgE and depressed complements. Relevant literature was also reviewed.
Subject(s)
Female , Humans , Young Adult , Acute Kidney Injury , Anaphylaxis , Complement System Proteins , Diagnosis , Immunoglobulin E , Pericarditis , RifampinABSTRACT
Heart failure is a recognized, although uncommon, cause of massive liver cell necrosis, the clinical consequence of which are intermingled with those of cardiac insufficiency in most case. But, hepatic coma is rerely caused by hepatic congestion only. We report the three cases with heart failure resulted in massive liver cell necrosis and fulminant hepatic failure. The manifestations of fulminant hepatic failure were hepatic encephalopathy, jaundice, marked increase of prothrombin time and serum transaminase and there were no evidences of viral hepatitis and toxic hepatitis as a cause of liver failure.