Infective endocarditis and stroke: pearls

.  The classic triad of infective endocarditis and stroke of fever, murmur and acute neurologic deficit is uncommon, occurring in less than half of patients, with murmur occurring in less than one third (due to decline of valvular disease as a cause) ; fever, embolism and high sed rate may also be seen in NBTE, arteritis with PAN, other rheumatologic disease, or atrial myxoma. 


2.  Organisms are more diverse than previously with Streptococcus representing only 60 percent, including resistant Group D Strep viridans (enterococcus faecalis) and Strep bovis  (associated with GI neoplasia).  Staph aureus is seen in up to 30 % especially those with i-v drug abuse, recent surgery, and no preexisting valve lesion. Patients with prosthetic valves may get S aureus and S epidermidis.  Others, including immunocompromised may get HACEK bacteria and fungi ( hemophilus, actinobacillus, cardiobacterium, Eikinella, Kinzella).  Among pretreated groups, culture negative disease has increased to 5.5 %.


3. Early onset (at presentation of first 48 hours) of neurologic symptoms is more common with Staph aureus than with streptococcal infections, that can occur late (54 v 19 %).  Late embolism is especially common among patients with prosthetic valves (14/15 late strokes in one series had prosthetic valves).  In native valve endocarditis, anticoagulation is of no benefit , certainly for at least 48 hours or until infection is controlled.


4. Cardiac vegetations initially larger than 10 mm are high risk, and are best seen with TEE rather than TTE.  Embolic rate is much higher in presence of visible lesions, and vice versa, visible lesions are much more common among patients with detectable emboli.  The 10 mm size may "open the debate" about the need for valve replacement.


5.  The discovery of endocarditis without emboli does not dictate the cessation of otherwise needed anticoagulant therapy. 


6.  If cardiac surgery is needed, timing is dictated by common sense.  One such protocol is to wait at least five days (until the edema of the stroke has settled) before considering operation, if possible.


7.  Use heparin fairly early on (certainly within 48 hours) of stroke with prosthetic valves with endocarditis, especially if subclinical INR was found on presentation.  Discontinue anticoagulation if possible in most cases of fungal endocarditis.


8.  Intracranial hemorrhage (3-6 % of patients) occurs with aneurysm rupture, septic arteritis, conversion of a bland infarct, and late effects of immune deposition.  Septic bacterial aneurysms may occur at distal branch points, but mycotic aneurysms, large ones, may occur proximally.  However, one study suggested the vast majority of patients with aneurysms had abnormal CT scan.  Present blood on CT or (if headache is present) pleocytosis on CSF examination weighs towards four vessel angiogram. 


9.  Serial angiography is indicated for mycotic aneurysms which may heal  with antibiotics.


10.  Special concern exists among patients with line induced sepsis and bland infarction that could result in late S Aureus superinfection of an initially bland infarct.  Full infective endocarditis treatment regimen may be warranted in these patients and TEE may alternatively show evidence of vegetations. 


Unknown angles
1.  Role of MRA/ CTA
2.  When surgery is required

Percentage of patients with stroke with prior TIA

Hackam DG, Kapral  MK, Wang JT et al.  Most stroke patients do not get a warning: a population based cohort study.  Neurology 73: 1074-1075, 2008.

cites data suggesting 17 % of CVA patients have prior TIA.  Authors review 16, 409 charts.  Timing of TIA is not addressed. 12.4  % had prior TIA, but 20% of those with large arter TIA's, much lower with hemorrhagic stroke (5%), somewhat higher with ischemic stroke (15 %).  Risk factors to have prior TIA: older, DM, HTN, AF, CHF,angina, PAD. Patients without TIA were more likely to die in  hospital, arrest, or not be discharged to home.