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Submitted by: Steven Guptha
The prototypic lesion of infective endo carditis, the vegetation is a mass of platelets, fibrin, micro colonies of microorganisms, and scant inflammatory cells.
Infection most commonly involves heart valves (either native or prosthetic) but may also occur on the low-pressure side of the ventricular septum at the site of a defect, on the mural endocardium where it is damaged by aberrant jets of blood or foreign bodies, or on intracardiac devices themselves.
The analogous process involving arteriovenous shunts, arterioarterial shunts (patent ductus arteriosus), or a coarctation of the aorta is called infective endarteritis.
Endocarditis may be classified according to the temporal evolution of disease, the site of infection, the cause of infection, or a predisposing risk factor such as injection drug use.
While rates of congenital heart diseases remain constant, other predisposing conditions in developed countries have shifted from chronic rheumatic heart disease to illicit IV drug use, degenerative valve disease, intracardiac devices, and health careassociated infection. The incidence of endocarditis is notably increased among the elderly.
Although many species of bacteria and fungi cause sporadic episodes of endocarditis, only a few bacterial species cause the majority of cases.
The pathogens vary somewhat with the clinical types of endocarditis, in part because of different portals of entry.
The oral cavity, skin, and upper respiratory tract are the respective primary portals for the viridans streptococci, staphylococci, and Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella causing community-acquired native valve endocarditis.
Streptococcus bovis originates from the gastrointestinal tract, where it is associated with polyps and colonic tumors, and enterococci enter the bloodstream from the genitourinary tract.
Prosthetic valve endocarditis arising within 2 months of valve surgery is generally the result of intraoperative contamination of the prosthesis or a bacteremic postoperative complication.
The nosocomial nature of these infections is reflected in their primary microbial causes: coagulase-negative staphylococci ,S. aureus, facultative gram-negative bacilli, diphtheroids, and fungi.
Transvenous pacemaker lead and/or implanted defibrillatorassociated endocarditis is usually nosocomial.
Endocarditis occurring among injection drug users, especially when infection involves the tricuspid valve, is commonly caused by S. aureus strains.
Number of these cases are caused by Pseudomonas aeruginosa and Candida species, and sporadic cases are due to unusual organisms such as Bacillus, Lactobacillus, and Corynebacterium species.
Tropheryma whipplei causes an indolent, culture-negative, afebrile form of endocarditis.
Organisms that cause endocarditis generally enter the bloodstream from mucosal surfaces, the skin, or sites of focal infection. Except for more virulent bacteria e.g., S. aureus that can adhere directly to intact endothelium or exposed subendothelial tissue, microorganisms in the blood adhere to sites at NBTE. If resistant to the bactericidal activity of serum and the microbicidal peptides released locally by platelets, the organisms proliferate and induce a procoagulant state at the site by eliciting tissue factor from adherent monocytes or, in the case of S. aureus, from monocytes and from intact endothelium. Fibrin deposition combines with platelet aggregation, stimulated by tissue factor and independently by proliferating microorganisms, to generate an infected vegetation.
The pathophysiologic consequences and clinical manifestations of endocarditisother than constitutional symptoms, which probably result from cytokine productionarise from damage to intracardiac structures; embolization of vegetation fragments, leading to infection or infarction of remote tissues; hematogenous infection of sites during bacteremia.
The clinical syndrome of infective endocarditis is highly variable and spans a continuum between acute and subacute presentations. Native valve endocarditis (whether acquired in the community or in association with health care), prosthetic valve endocarditis, and endocarditis due to injection drug use share clinical and laboratory manifestations.
2. Chills and sweats
3. Anorexia, weight loss, malaise
4. Myalgias, arthralgias
5. Heart murmur
6. New/worsened regurgitant murmur
9. Peripheral manifestations (Osler’s nodes, subungual hemorrhages, Janeway lesions, Roth’s spots)
Elevated erythrocyte sedimentation rate
Elevated C-reactive protein level
It suits to slow pulse but primarily strong
There is great weakness of cardiac tissue and secondarily pulse becomes weak
Extra exertion increases its rapidity but diminishes its force
This makes the pulse irregular and intermittent
Heart feels as if stood still
There is weakness and numbness of the left arm and often blueness of the surface of the body
The patient fears that heart would stop beating if he does not make a move
The characteristic symptom in this remedy is sensation as if heart is grasped with an iron band.
There is soreness and constriction of the chest and it has pains shooting to the left arm.
There is edema and quick throbbing intense and hard pulse which may be intermittent.
There is great irritation of cardiac nerves.
Useful in intense palpitations and fluterring of heart.
Difficult breathing, suffocation, fainting, violent palpitations and inability to lie down are the symptoms.
It is the remedy for painful affections of the heart.
There are sharp shooting pains from the heart to the back and radiating from the heart down the arm ,over the chest and down the spine.
There is palpitation worse from any movement of the arm or body.
There is a purring sensation left in the cardiac region.
The pulse is intermittent and the slightest motion of the arm and hands makes the patient worse.
Irregular and tumultuous action of the heart is also met in this remedy.
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