ENDOCARDITIS.pptx
- 1. ENDOCARDITIS Prepared by Nursing Instructor Mrs. Safoora Qureshi CON, PIMS
- 2. Endocardium ⢠Inner/deepest layer of the heart ⢠Consist of flattened epithelial cells ⢠Lines the heart chambers and valves ⢠Prevent friction ⢠Promote smooth flow of the blood
- 3. Endocarditis ⢠Is the inflammation of endocardium, the inner most layer of the heart ⢠Infective endocarditis (IE) is an infection of the inner surface of the heart, usually the valves ⢠IE is a potentially fatal inflammation of heart valvesâ lining and sometimes heart chambersâ lining. ⢠IE is typically a bacterial infection and less commonly a fungal infection
- 4. Etiology Bacteria: ⢠Staphylococcus aureus is the most virulent organism causing IE ⢠Streptococcus viridian, ⢠Enterocolli ⢠Gram-positive and Gram- negative bacilli Fungus: ⢠Candida albicans Viruses: ⢠Coxsackie B virus
- 5. Risk Factors ⢠Older age. ⢠Artificial heart valves. ⢠Germs are more likely to attach to an artificial (prosthetic) valves ⢠Damaged heart valves. ⢠such as rheumatic fever or infection ⢠Congenital heart defects. ⢠such as an irregular heart or abnormal heart valves ⢠Implanted heart device. ⢠such as a pacemaker, causing an infection of the heart's lining. ⢠A history of endocarditis ⢠Poor dental health ⢠Long-term catheter use (indwelling caths or PD cath)
- 6. Classification Sub-Acute Endocarditis: Develops gradually over a period of weeks to several months ⢠Most frequently seen in patients with ⢠Damage heart. ⢠Preexisting valvular disease Acute Infective Endocarditis: ⢠Develops suddenly and may become life threatening with days ⢠Primarily affect people with ⢠Normal heart. ⢠Healthy valves and ⢠Present as a rapidly progressive illness
- 7. Pathophysiology Predisposing factors contribute to development of IE 1. A damage endocardial surface ⢠Provide an environment conducive to bacterial growth such as valvular disease, RHD, CHD 2. Portal of entry: ⢠Endocardial defects, a dental procedure or oral lesion may offered bacteria access to bloodstream Mechanism ďVegetation: ⢠Primary lesion of IE, consist of fibrin, leukocytes, platelets, and microbes that adhere to the valve surface or endocardium. ďEmbolization ⢠The loss of portions of these friable vegetations into the circulation results in embolization ďSystemic embolization: ⢠left heart vegetation, progressing to various organ and to the extremities causing limb infarction ⢠Right-side heart lesions embolize to the lungs ďLocal infection: ⢠cause damage to the valves or their supporting structure, result in dysrhythmias, valvular incompetency, HF
- 8. Damage to endothelial surface from anatomic or traumatic changes Primary focus of infection from causative agents Vegetation: consist of fibrin, leukocytes, microbes on valve surface & endocardium Local valve damage Management antibiotics not Bacteria, virus, fungus Right-side heart embolization Lung Infiltration of supportive structure Left-side heart embolization Brain liver spleen kidney limb Recovery Sepsis, HF, Heart block Pulmonary embolism Infective Endocarditis Pathophysiology
- 10. Clinical manifestation ⢠Non- specific or Systemic illness: ⢠Low grade fever, chill ⢠Weakness, malaise, fatigue ⢠Arthralgia, myalgia, back pain ⢠Abdominal discomfort ⢠Weight loss, ⢠Headache ⢠Feet legs swollen ⢠Clubbing of fingers
- 11. Vascular Manifestation ⢠Murmurs ⢠Slinter hemorrhage ------ black longitudinal streaks in nail beds ⢠Petechiae ⢠Oslerâs nodes------painful, tender, red or blue , pea-size nodes ⢠Janeway's lesion --- pain less erythematous, flat, small red spots on palm and sole ⢠Ruthâs spots -------- retinal hemorrhage reveals on fundoscopy Late Manifestations: secondary to IE ⢠Splenomegaly ⢠Flanks pain, abdominal rigidity, pulmonary edema ⢠Hemiplegia, change in consciousness, gangrene
- 12. Oslerâs nodes Janeway's lesion Slinter streaks Ruthâs spots
- 14. Diagnosis History and Physical Assessment: ⢠Blood test ⢠blood culture test: ⢠Transthoracic Echocardiogram ⢠Transesophageal echocardiogram/Ultrasound ⢠Electrocardiogram / (ECG or EKG) ⢠Chest X-ray ⢠to find lug problems such as lung collapse and pulmonary edema
- 15. Treatment ⢠Antibiotics ⢠Infective Endocarditis will be treated with intravenous antibiotic therapy. Antibiotic therapy typically takes up to six weeks. ⢠Steroids: as a immunosuppressant ⢠To treat inflammation ⢠To reduce autoimmune response and prevent permanent heart damage ⢠NSAIDs: ⢠To relieve pain
- 16. Collaborative Care ďDrug therapy ď§ Antibiotics ⢠IV antibiotic therapy takes up to six weeks. ď§ Steroids: ⢠To treat inflammation ⢠To reduce autoimmune response ⢠To prevent permanent heart damage ď§ NSAIDs: ⢠To relieve pain ď Nursing Management ⢠Strict bed rest ⢠Restrict visitors ⢠Keep in prop upped position ⢠Monitor ⢠vital signs, oxygen saturation ⢠intake output ⢠Meet nutritional requirement ⢠Psychological support
- 17. ďSurgery ⢠Indications ⢠Prolonged infective endocarditis ⢠damaged heart valves caused by endocarditis ⢠Purpose; ⢠To remove dead tissue, scar tissue, fluid buildup, or debris from infected tissue. ⢠To repair or remove damaged heart valve ⢠To replace it with either man-made material or animal tissue.
- 19. Prevention Healthy Life Style: ⢠Be smoke-free. ⢠Be more active. ⢠Aim for a healthy weight. ⢠Eat a healthy balanced diet â there are some specific diets you can follow that have been proven to reduce the risk of heart disease. ⢠Drink less alcohol. ⢠Manage stress