Endocarditis

The interval between the initiating bacteraemia and the onset of symptoms of endocarditis is estimated to be less than two weeks. The condition begins with complaints of fever, body ache, malaise, night sweats and chilly sensation. Occassionally embolic episode or heart failure maybe the first manifestation. Weight loss and anemia are seen later [7].

The patients are often elderly. They may complain of myalgia and arthalgia. A patient with fever and heart murmur should always be suspected of endocarditis.

The cardinal features on examination are pyrexia, pallor, petechia, splenomegaly and clubbing of digits. Cardiac examination reveals murmur related to underlying heart disease and one may find change in character of murmurs due to development of endocarditis. Signs of heart failure may develop. The spleen is soft and non tender. Apart from the skin, petechia may be seen in the oral cavity, conjunctivae and even on the retina of the eye (Roth spots). Small flat erythematous non tender macules are seen mainly on the thenar and hypothenar eminences (Janeway lesions); these blanch with pressure. Splinter hemorrhages may develop. Embolic lesions such as hard painful, tender, subcutaneous swellings occur in the fingers, toes, palms and soles (Osler's nodes) occur. Hematuria is common. Arthritis of major joints is frequently seen.

Anemia is almost universal and is normochromic normocytic due to bone marrow depression. Leucocyte count is mildly elevated. High ESR is always present. Urine examination reveals albuminuria and microscopic hematuria. Liver biochemistry is often disturbed mainly an increased alkaline phosphate. Serum immunoglobulins are increased but total complement and C3 complement are decreased owing to immune complex formation. Blood culture is positive in almost two third of the cases.

Transesophageal approach is used in echocardiography to visualize vegetations but smaller sized ones can be missed. This is the greatest sensitivity for detection of vegetations. Vegetation may persist despite treatment. Chest X-ray to demonstrate heart failure or emboli in the right sided endocarditis.

Any underlying infection should be treated [8]. The endocarditis is treated with antibiotics chosen on the results of the blood culture. The treatment should continue for 4 to 6 weeks. The microbes in the vegetation being deep seated and surrounded by a fibrin mesh in the relatively poorly vascularised vegetation masses. Hence antibiotics should be administered in large doses. In addition to drug therapy patient should be given complete bed rest, properly regulated fluids, electrolytes and diet and other medications as dictated by an individual case like digoxin, diuretics and ACE inhibitors for heart failure. Most cases show good response to treatment and four weeks of treatment suffice even for virulent organisms [9].

Surgery is required if the following conditions occur:

• Extensive damage of a valve
• Early infection of prosthetic material
• Worsening renal failure
• Embolization
• Progressive cardiac failure

This generally depends on the complications which develop, if left untreated endocarditis can be fatal. Heart failure is the single most important complication responsible for high morbidity and mortality.

Mortality rates for treated endocarditis range from 16 to 27%. Factors associated with mortality include age above 65 years of age [6], additional underlying debilitating medical disorders, and development of congestive heart failure and major embolic complications mainly of the central nervous system. Mortality rates also depend upon infecting organisms being much lower with Streptococcus and quite high with Staphylococcus.

Relapse maybe seen within the first two months of cessation of therapy and blood cultures commonly involve same organisms, indicating that the vegetation was not adequately sterilized during previous drug therapy.

Endocarditis can be classified into infective and non-infective endocarditis. Infective endocarditis is caused by many organisms which can be bacterial, viral or fungal. Presently, the main causative agents are bacteria the three most common being:

• Streptococcus viridians: These organisms are part of bacterial flora of the pharynx and upper respiratory tract and infection may follow a dental extraction, cleaning, tonsillectomy or bronchoscope.
• Enterococcus faecalis: Is found in perianal and faecal bacterial flora. Common in the elderly with infections related to the genitourinary area.
• Staphylococcus aureus: This organism is responsible for 50% of acute cases. Patients with central venous catheters used for parenteral feeding or temporary pacemaker electrode catheters are prone to this infection. Cellulitis and skin abscesses are often originating found in drug addicts who mainline.

Other organisms such as fungal agents like Aspergillus species and Candida albicans [3] are common in intravenous drug addicts, alcoholics and patients with prosthetic heart valves. Prosthetic valve endocarditis risk is greatest during initial 6 months of surgery.

Another type of endocarditis known as native valve endocarditis (NVP) also occurs post surgery [4]. Mitral valve prolapse has emerged as a prominent predisposing structural cardiac abnormality largely confined to patients with both prolapse and mitral regurgitation murmur. In patients with RHD, endocarditis occurs more commonly on the mitral valve, the next common site being the aortic valve. Amongst adults, the most common predisposing congenital conditions are patent ductus arteriosus, ventricular septal defect and bicuspid aortic valve.

Since the widespread availability of antibiotics, the disease pattern has drastically changed [5]. The mean age of patients has raised from 30 years to 50 years. Male to female ratio has increased. Incidence of infection due to Staphylococcus aureus and fungi has increased especially amongst drug abusers. The incidence of infective endocarditis has rasied amongst operated cardiac cases probably due to increased longevity of patients. The incidence of concomitant HIV infection and endocarditis has also increased. The middle aged and elderly are more prone to infective endocarditis (IE). In contrast, the disease is uncommon in children less than 2 years of age. It is more common in males with the ratio being 4:1, mainly because of increasing incidence of IV drug abuse.

The most marked diagnostic pathological feature of endocarditis is the development of vegetation which is either sessile or a polypoidal mass which is mobile and situated on the heart leaflets or defects.

Infection generally occurs along the edges of the heart valves, more commonly on the left side. The bacteria enter into the circulation by way of untreated or partially treated septic focus or by diagnostic or therapeutic instrumentation or along with indwelling canola or intravenous catheters used for long time. The lesion of infective endocarditis is a mass of fibrin, platelets and infecting organism known as vegetation. The chance of an organism sticking to a vegetation is increased because of clumping together of bacteria caused by agglutinating antibodies. They can develop because of repeated infection with the bacterium over a period of time. The vegetation may embolise to central nervous system leading to hemiplegic, meningitis, intracerebral haemorrhage, and encephalopathy and at a later date rupture of my mycotic aneurysms leading to haemorrhage.

The extracardiac manifestations result either from embolization or from deposition of immune complexes. The latter thought to be responsible for arthalgia, Roth spots, focal glomerulonephritis and acute vasculitis.

Those at risk of developing infective endocarditis should receive antibiotic therapy before undergoing a procedure likely to result in bacteraemia [10]. Since it is a condition associated with high morbidly and mortality it is worthwhile giving antibiotic prophylaxis to patients undergoing dental or invasive diagnostic or therapeutic procedures since they all are associated with transient bacteraemia. The form of prevention depends upon on the procedure and on the likelihood of endocarditis. High risk patients are those with prosthetic heart valve or a previous history of endocarditis.

Endocarditis is an inflammation of the endocardium or vascular endothelium of the heart. This condition may occur sometimes as a fulminating or acute infection but runs an insidious course and is generally known as subacute bacterial endocarditis (SBE) [1]. Endocarditis occurs most commonly on rheumatic (RHD) or congenitally abnormal valves as well as mitral valve prolapse and calcified aortic valve disease. It can occur in congenital conditions such as ventricular septal defect or persistent ductus arteriosus. Prosthetic valves or prosthetic vascular material may similarly be infected and thus, there is a rising incidence of this condition in developing countries.

It is classified into infective and non-infective endocarditis depending upon the etiological agent. Virulent organisms may infect healthy valves especially when the victim is debilitated or immunologically incompetent. The characteristic lesion is a variable sized amorphous mass of platelets and fibrin in which many microorganisms and scanty inflammatory cells are enmeshed [2].

The symptoms range from fever, weakness, tiredness and dyspnoea or maybe nonspecific. The treatment consists of a course of antibiotics mainly given intravenously and over a period of 4 to 6 weeks. Surgery may be required in case of damage to heart valves. The intensity and period of disease depends upon the type of organism involved.

Endocarditis is inflammation of the innermost lining of the heart which is mainly caused due to an infectious agent. The human heart consists of heart chambers and valves which can get inflamed and infected. It can affect any part of the heart from the muscles of the heart, the valves which prevent backward flow of blood or the inner lining of the heart. It occurs more in people who have a hereditary or a problem in the heart since birth, damaged heart valves or some heart valve surgery or a previous history of endocarditis. Commonest organisms which cause endocarditis are bacterial other being fungus. These microbes can enter the body through the blood stream either by an unclean injection use, some dental procedures or any other operations related to the airways, urinary tract and skin.

The clinical presentation mainly is a slow and gradual onset with fever, chills and night sweats. Tiredness, weakness and body pain may also be present. Small areas of sudden bleeding under the nails, red spots on the palms and soles and difficulty in breathing may also occur. Immediate medical attention should be given as if left untreated it can be fatal.

A thorough examination will reveal a murmur or a change in the heart murmur which will help your physician to conclude the diagnosis. Other tests required would be a blood culture, a complete blood count and a transesophageal echocardiogram. Immediate antibiotic therapy with hospitalization will be required. At least 4 to 6 weeks of drug therapy will be required. Surgery maybe required if the heart valves are damaged, cardiac failure setting in or there is severe spread to other vital organs. Prompt treatment reduces the morbidly and prevents more grave complications such as cardiac failure, brain involvement and stroke. To prevent these conditions certain high risk patients should take antibiotic therapy prior to any surgeries especially individuals with birth heart defects, heart valve problems or past history of this condition.

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8. Thuny F, Grisoli D, Collart F, Habib G, Raoult D. Management of infective endocarditis: challenges and perspectives. Lancet. Mar 10 2012;379(9819):965-75.
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10. Dajani AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAMA. Jun 11 1997;277(22):1794-801.

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