This combination of damaged valves, bacterial growth, and lack of a strong immune response results in infective endocarditis.Damage to the valves and endocardium can be caused by:
Altered, turbulent blood flow. The areas that fibrose, clot, or roughen as a result of this altered flow are known as jet lesions. Altered blood flow is more likely in high pressure areas, so ventricular septal defects or patent ductus arteriosus can create more susceptibility than atrial septal defects. Catheters, electrodes, and other intracardiac prosthetic devices. Solid particles from repeated intravenous injections. Chronic inflammation. Examples include auto-immune mechanisms and degenerative valvular lesions.The risk factors for infective endocarditis provide a more extensive list of conditions that can damage the heart. Diagnosis
In general, the Duke criteria should be fulfilled in order to establish the diagnosis of endocarditis. Although the Duke criteria are widely used, they have significant limitations. For example, the sensitivity of the Duke criteria for detecting infective endocarditis decreases when prosthetic heart valves are present.As the Duke criteria rely heavily on the results of echocardiography, research has addressed when to order an echocardiogram by using signs and symptoms to predict occult endocarditis among people who inject drugs and among non drug-abusing patients. However, this research is over twenty years old and it is possible that changes in the epidemiology of endocarditis and bacteria such as staphylococci make the following estimates incorrect. The blood tests C reactive protein (CRP) and procalcitonin have not been found to be particularly useful in helping make or rule out the diagnosis.
Has 82% incidence in diagnosis cases)However, in actuality, only a small percentage of patients experience all three symptoms, and the full triad occurs more frequently among those who have overused alcohol. Also a much more diverse range of symptoms has been found in patients with this condition, including:

pupillary changes, retinal hemorrhage, papilledema, impaired vision and hearing, vision loss
hearing loss,
fatigability, apathy, irritability, drowsiness, psycho and/or motor slowing
dysphagia, blush, sleep apnea, epilepsy and stupor
lactic acidosis
memory impairment, amnesia, depression, psychosis
hypothermia, polyneuropathy, hyperhidrosis.Although hypothermia is usually diagnosed with a body temperature of 35 °C / 95° Fahrenheit, or less, incipient cooling caused by deregulation in the central nervous system (CNS) needs to be monitored because it can promote the development of an infection. The patient may report feeling cold, followed by mild chills, cold skin, moderate pallor, tachycardia, hypertension, tremor or piloerection. External warming techniques are advised to prevent hypothermia.Among the frequently altered functions are the cardio circulatory. There may be tachycardia, dyspnea, chest pain, orthostatic hypotension, changes in heart rate and blood pressure. The lack of thiamine sometimes affects other major energy consumers, the myocardium, and also patients may have developed cardiomegaly. Heart failure with lactic acidosis syndrome has been observed. Cardiac abnormalities are an aspect of the WE, which was not included in the traditional approach, and are not classified as a separate disease. Infections have been pointed out as one of the most frequent triggers of death in WE.