Infective endocarditis refers to inflammation of the endocardium of the heart valves or ventricular wall due to direct infection by bacteria, fungi and other microorganisms such as viruses, rickettsia, chlamydia, spirochetes, etc. It is distinct from non-infective endocarditis due to rheumatic fever, rheumatoid fever, systemic lupus erythematosus, etc. In the past, the disease was referred to as bacterial endocarditis, but this is no longer used because it is not comprehensive enough. The typical clinical manifestations of infective endocarditis include fever, murmur, anemia, embolism, skin lesions, splenomegaly and positive blood cultures. Kailun Zhang, Department of Cardiac Surgery, Wuhan Union Medical College Hospital
【Clinical manifestations
(A) Acute infective endocarditis Often occurs in normal hearts, and endocarditis in the right side of the heart occurring in addicts of intravenous narcotics also tends to be acute. The pathogenic organisms are usually highly virulent bacteria, such as Staphylococcus aureus or fungi. The onset is often sudden, with high fever, chills, and marked signs of systemic toxemia, often as part of a serious systemic infection. The course is often rapid and aggressive, easily masking the clinical signs of acute infective endocarditis, with a high-pitched murmur or rapid change in the nature of the original murmur occurring within a short period of time due to acute damage to the heart valves and tendons. It can often progress rapidly to acute congestive heart failure leading to death.
On the involved endocardium, especially in mycotic infections, large, brittle redundancies may adhere, and the dislodged bacterial-bearing emboli may cause multiple emboli and metastatic abscesses, including myocardial abscesses, brain abscesses, and septic meningitis. If the emboli originate from an infected right-sided heart cavity, pneumonia, pulmonary embolism, and single or multiple lung abscesses may develop. The skin may have polymorphous petechiae and purpura-like hemorrhagic damage. Splenomegaly may be present in a small number of patients.
(b) Subacute infective endocarditis Most patients have a slow onset with only nonspecific insidious symptoms, such as general malaise, fatigue, hypothermia, and weight loss. A few start in the form of complications of the disease, such as embolism, unexplained stroke, progressive exacerbation of heart valve disease, intractable heart failure, glomerulonephritis, and the development of heart valve murmurs after surgery.
Fever is the most common, with variable fever patterns, most often irregular, intermittent or tachyphylaxis, with chills and sweating. The fever may be intermittent or tachypnoea, accompanied by chills and sweating, or low fever only. The body temperature is mostly between 37.5 and 39°C, but can be as high as 40°C or more. Approximately 3% to 15% of patients have normal or below normal body temperature, mostly in elderly patients and in patients with cerebral hemorrhage or subarachnoid hemorrhage due to embolism or ruptured fungal aneurysm, as well as in severe heart failure and uremia. In addition, those who have applied antibiotics, antipyretics, and hormones before the diagnosis of the disease may also be temporarily unfebrile.
Progressive anemia is present in 70% to 90% of patients, sometimes to a severe degree, and is even the most prominent symptom. Anemia causes general weakness, weakness and shortness of breath. Patients with longer disease duration often have generalized pain, which may be due to toxemia or embolism in various parts of the body. Arthralgia, low back pain and myalgia are more common at the onset of the disease, mainly involving the gastrocnemius and femoral muscles, ankle and wrist joints, and may also show multiple joint involvement. If there is severe bone pain during the course of the disease, it should be considered that it may be caused by osteochondritis, subperiosteal hemorrhage or embolism, embolic aneurysm compressing the bone or osteo-vascular aneurysm.
The clinical presentation is more variable in older patients, and fever is often misdiagnosed as a respiratory or other infection. Heart murmurs are also often mistaken for degenerative valve disease in the elderly and ignored. Some patients may have no fever or heart murmur, but may present with neurological or psychiatric changes, heart failure or hypotension. There is a tendency to have neurological complications and renal insufficiency.
Signs are mainly the murmur of the original heart disease or the murmur of the previously normal heart. Changes in the nature of the murmur during the course of the disease are often due to anemia, tachycardia, or other hemodynamic changes. About 15% of patients start without a heart murmur and develop a murmur during treatment. A few patients do not develop a murmur until 2 to 3 months after treatment, and occasionally no murmur occurs for years after cure. In subacute infective endocarditis, right-sided valve damage is uncommon. 2/3 of right-sided hearts with endocarditis, especially those invading the tricuspid valve, may also be murmur-free when the superfluous organisms proliferate on the endocardium of the ventricular wall and on aortic atherosclerotic plaques, but the latter is rare.
The incidence of skin and mucosal lesions such as petechiae, linear hemorrhages under the nail bed, Osler’s nodes, and Janeway damage has decreased significantly in the last 30 years. Petechiae are caused by toxins acting on capillaries to increase their fragility and rupture or by embolism, and can occur in clusters or individually. The incidence is the highest, but has decreased from 85% before the application of antibiotics to 19% to 40%. It is mostly seen in the conjunctival membranes of the eyelids, oral mucosa, chest and dorsal skin of the hands and feet, lasts for several days and reappears after disappearing, its center may be whitish, but subocular conjunctival hemorrhage can also occur in lipid microembolism caused by extracorporeal cardiac surgery, thus it is thought that petechiae with a grayish center are more important than yellow ones. Systemic purpura may occasionally occur. The incidence of Osler’s nodes has decreased from 50% to 10%-20%, and they are purple or red, slightly above the skin surface, smuggling about 1-2 mm, and up to 5-15 mm, mostly on the palmar surface of the end of the fingers or toes, with pressure pain between the size of the fissure or the bottom of the foot, often lasting 4-5 days to subside. Osler’s nodes are not unique to this disease, but can also be found in SLE, typhoid, and lymphoma. Small painless hemorrhagic or erythematous lesions 1-4 mm in diameter on the palms and soles of the feet are called Janeway lesions. Pestle-like fingers (toes) are now rare. Retinal lesions are most often hemorrhagic, fan-shaped or round, and may have white centers, sometimes with only round white spots called Roth spots on the fundus.
The spleen is often mildly to moderately enlarged and may be tender with tenderness. The incidence of splenomegaly has decreased significantly from the previous incidence.