Endocarditis is an inflammation of the inner lining of the heart, usually affecting the heart valves. It is commonly caused by bacterial infections entering the bloodstream through procedures like dental work or via IV drug use. Common symptoms include fever, weakness, and murmurs heard on exam. Diagnosis involves blood cultures, echocardiograms, and other tests. Treatment requires long-term intravenous antibiotics for up to 6 weeks along with surgery to repair or replace damaged valves if needed. Preventive measures include maintaining good oral hygiene, treating infections promptly, and living a healthy lifestyle.
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 valves’
lining and sometimes heart
chambers’ 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
Vegetation:
• Primary lesion of IE, consist of fibrin,
leukocytes, platelets, and microbes
that adhere to the valve surface or
endocardium.
Embolization
• The loss of portions of these friable
vegetations into the circulation results
in embolization
Systemic embolization:
• left heart vegetation, progressing to
various organ and to the extremities
causing limb infarction
• Right-side heart lesions embolize to
the lungs
Local 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
• Osler’s nodes------painful, tender, red or blue , pea-size nodes
• Janeway's lesion --- pain less erythematous, flat, small red spots on
palm and sole
• Ruth’s spots -------- retinal hemorrhage reveals on fundoscopy
Late Manifestations: secondary to IE
• Splenomegaly
• Flanks pain, abdominal rigidity, pulmonary edema
• Hemiplegia, change in consciousness, gangrene
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
Drug therapy
Antibiotics
• IV antibiotic therapy takes up
to six weeks.
Steroids:
• To treat inflammation
• To reduce autoimmune response
• To prevent permanent heart
damage
NSAIDs:
• To relieve pain
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. Surgery
• 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 – there are some specific
diets you can follow that have been proven to reduce the risk of
heart disease.
• Drink less alcohol.
• Manage stress