Infective Endocarditis Flashcards
What will characterize the acute course of presentation of infective endocarditis?
Rapid onset, with large vegetations involving previously NORMAL valves
- > high fever, acute pulmonary edema due to regurgitation
- > high rate of embolic complications infarcting tissues
What will characterize the subacute course of presentation of infective endocarditis?
Long illness, lasting weeks to months, with small vegetations involving previously DISEASED or ABNORMAL valves
- > low grade fever, may be intermittent
- > constitutional symptoms will be associated: fatigue, anorexia, wasting, night sweats, myalgias
- > Immune complex deposition likely - causing arthritis / hematuria
What are the common classifications of IE by host substrate?
Native valve endocarditis (NVE)
Prosthetic valve endocarditis (PVE)
Endocarditis in the setting of IV drug use
What are some miscellaneous classifications of IE by substrate?
- Endarteritis of coarctation - in the aorta
2. Endocarditis of prosthetic material -> i.e. kids operated on for congenital heart disease
Most common causes of native valve endocarditis?
Staphylococcus aureus and Streptococcus spp.
Most common cause of prosthetic valve endocarditis?
Staphylococcus epidermidis
Why does having foreign material in the circulation (i.e. pacemakers, IV lines) predispose you to endocarditis?
It has no endothelium -> cannot stop the clotting cascade. Perfect nidus for thrombus -> endocarditis transition
What does it mean when you begin to see first or second degree AV block in a patient with IE?
Poor prognosis -> probable formation of abscess in the conducting system of the heart
Why types of endocarditis can lead to septic pulmonary embolism?
Triscuspid or pulmonary valve endocarditis
What are some common metastatic infections which can occur as a result of septic emboli in the left heart?
Septic joints, and vertebral osteomyelitis (will manifest as back pain)
What are the “vascular phenomena” resulting from septic
emboli?
- Infarct of a tissue - i.e. renal artery or splenic artery
- Mycotic aneurysms - due to embolization to vasa vasorum of arteries -> localized aneurysm formation in many vessels, especially cerebral
What are the complications of IE caused by immune complex deposition?
- Glomerulonephritis -> acute renal failure
- Polyserositis -> arthritis
- Vasculitis -> rashes
What age group gets most IE and why?
> 60 years old, because greater than 50% of cases are due to predilection from calcific aortic stenosis
What are the clinical symptoms exhibited by most patients in endocarditis?
Fever, new or changing heart murmur
Constitutional symptoms if subacute
How an IE cause neurologic symptoms, flank pain, chest pain, gangrene, and blindness?
All of these are embolic complications
Neurologic: embolic stroke Flank pain: Renal artery Chest pain: pulmonary embolism Gangrene: deposition in extremities Blindness: Central retinal artery
What are Janeway lesions and what organism is usually associated with them?
Small, PAINLESS, hemorrhagic macular lesions of PALMS and SOLES
->S. aureus is associated
What are Roth spots? how do they look?
Emboli to retina causing hemorrhage with a clear center which is coagulated fibrin
-> can be seen in other diseases as well (diabetes, leukemia, pernicious anemia)
Where else on the face can hemorrhages occur on IE?
Most frequently conjunctival and subconjunctival hemorrhaging
What are splinter hemorrhages? Why do they happen?
Linear, red / brown lines seen in MID (not traumatic) nail beds of fingers / toes
Happen due to vasculitis or hemorrhage in distal capillaries from microemboli
What can be seen in IE due to immune complex deposition in small vessels, and will cover entire feet sometimes?
Petechiae -> small hemorrhages of skin or mucous membranes
What are Osler’s nodes? How do you remember their different from Janeway lesions?
PAINFUL, RAISED lumps sometimes with clear centers, usually on pads of fingers and toes, due to immune complex deposition with acute inflammation
- > acute inflammation / edema is what makes them raised up and painful
- > Janeway lesions are just infarct / bleeding not associated with inflammation
Is IE associated with anemia? What does this do to ESR?
Yes -> especially in chronic, subacute infection
Tends to elevate ESR -> fewer RBCs to block droppage -> rate of droppage / sedimentation is faster
What is the most sensitive test for IE and why is this not typically done?
Transesophageal echocardiography (TEE) -> 90% detection of vegetations >1mm in size
Not typically done because it’s expensive and invasive -> transthoracic echo is much cheaper and 65% sensitive for >3 mm in size
What are the major duke criteria for infective endocarditis?
Major:
- Typical organisms identified from two separate blood cultures @ different locations
- Single positive blood culture with Coxiella burnetti
- New valvular regurgitation or positive TEE
What are the minor duke criteria for IE?
- Predisposition factors for IE
- Fever
- Vascular phenomena - i.e. infarcts, mycotic aneurysms
- Immunologic phenomena - i.e. arthritis, GN
- One positive blood culture
How many major / minor criteria do you need for a DEFINITIVE IE diagnosis?
Two major or One major and three minor or Five minor
When is surgery for IE indicated?
Persistent infection or recurrent emboli despite 7-10 days of adequate antibiotics (often two)
Annular or aortic abscess
Congestive heart failure
What procedures warrant prophylaxis with antibiotics for the transient bacteremia they will incur?
- Dental procedures
2. Cystoscopy if infection is present -> high risk of enterococcal endocarditis
What patients are at high risk with transient bacteremia and should thus receive prophylaxis during these procedures?
- Prior history of endocarditis
- Prosthetic valves
- Cardiac transplant recipients
- Congenital heart diseases -> unrepaired cyanotic, prosthetic material within 6 months of repair surgery, or residual defect adjacent to prosthetic material from repair surgery
