Infectious Diseases in Critical Care Medicine

are clinically ill with fevers of 1028 F accompanied by rigors. Blood culture positivity is

usually of high grade, i.e., 3/4–4/4. The diagnosis of septic thrombophlebitis may be suspected

on CT/MRI of the vein/removal of the CVC with pus emanating from the catheter wound. A

palpable cord is also often present. Therapy for septic thrombophlebitis is venotomy. After

venotomy if ABE is not present, anti–MSSA/MRSA therapy should be continued for two to

four weeks (1,7–13).

S. aureusABE

S. aureus(MSSA/MRSA) is the commonest cause of ABE. During a prolonged high-grade

MSSA/MRSA bacteremia,S. aureuscan attack normal or native heart valves. In contrast

subacute bacterial endocarditis (SBE) due avirulent pathogens, e.g., viridans streptococci

require preexisting valvular damage to cause SBE. The key factors that predispose to MSSA/

MRSA ABE are prolonged/high-grade MSSA/MRSA bacteremia from a distant focus,

e.g., abscess, CVC, pacemaker lead, or an invasive cardiac procedure such as radio frequency

ablation (RFA). ABE is not a complication of peripheral IV-line infections (11,13,35,36,39).

The clinical diagnosis ofS. aureusABE requires two key diagnostic components. Firstly,

the patient must have a continuous/prolonged high grade MSSA/MRSA bacteremia, i.e., 3/4

or 4/4 repeatedly. Secondly, demonstration of a vegetation by TTE/TEE is necessary.S. aureus

bacteremia that is not high grade/prolonged indicates a transient staphylococcal bacteremia

and is not indicative of endocarditis per se. In S. aureus endocarditis, the bacteremia

characteristically is of high grade and prolonged. Prolonged, high-grade S. aureus

bacteremia without vegetation on TTE/TEE should suggest intravascular or an extracardiac

Table 3 Diagnosis of CVC Infection

I. Epidemiologic diagnosis

lPatients with CVC who develop bacteremias (due to CVC pathogens)

lNo other site of infection with same organisms as in BCs

II. Clinical diagnosis of CVC infection

lCVC obviously infected CVC (only site erythematous/warmpurulent).

lIf present, culture purulent discharge.

lRemove CVC and culture tip.

III. Suspected CVC infection

lObtain BCs (4) from peripheral vein.

Do not obtain blood for BCs viatheCVC.

(Only draw BCs though CVC if no other venous access available)

lremove CVC and end culture tip for SQ catheter tip culture.

lif venous access still required, replace removed CVC over guidewire while BCs and removed CV tip

cultures pending.

.If CVC tip culture isnegative, continue to use replaced CVC.

.If CVC tip culture ispositive(>15 colonies) andisolate same as BC isolate taken from peripheral

vein, remove replaced CVC and insert new CVC at another site.

IV. Therapy of non-CVC infections
lDo not treat non-CVC infections
Positive BCs with negative culture of CVC tip.
Positive CVC tip culture with negative BCs.
Positive BCs with separate CVC catheter tip culture of<15 colonies.
lEmpiric therapy of CVC
Before BC results are known, direct antibiotic therapy against MSSA, aerobic GNBs, and VSE.
In institutions whereMSSA more prevalent than MRSA, begin therapy with meropenem.
In institutions whereMRSA are more prevalent than MSSA, begin therapy with tigacycline or
ceftriaxone plus linezolid. If no ABE, treat for 2 wk after CVC removal.
.If CVC infection due to MSSA, MRSA, or VRE, obtain baseline TTE and at 2 wk to r/o ABE.
When BC and CVC tip cultures are known.
Continue empiric therapy with meropenemif isolate is meropenem susceptible.
If isolate is meropenem-resistant, change therapy to tigecycline or ceftriaxone plus linezolid.

Abbreviations: CVC, central venous catheter; BCs, blood cultures; ABE, acute bacterial endocarditis; GNB, gram-

negative bacilli; IJ, internal jugular; SC, subclavian; TTE, transthoracic echocardiogram; VSE, vancomycin

sensitive enterococci.

210 Cunha