ICU Infectious Disease Pearls and Pet Peeves – Part2: These are some additional points and random thoughts regarding commonly used antimicrobial agents and frequently encountered ID clinical scenarios in the ICU. Comments from my ID and Pharm friends are welcome. Here it goes:
1. Candida pneumonia is essentially a non-existent entity (except in the presence of SEVERE immunodeficiency). Candida in the sputum is almost always a colonizer. You can use it as a marker of systemic candidiasis in order to justify antifungal coverage but the studies...
...are not supportive of significant clinical benefit
2. If u suspect Candida in a septic pt, echinocandin (not an azole) is the preferred empirical tx. Most people in US start w 100 mg of micafungin but u can easily give 150 or even 200 (if your pharmacist doesn't freak out...)
2. If u suspect Candida in a septic pt, echinocandin (not an azole) is the preferred empirical tx. Most people in US start w 100 mg of micafungin but u can easily give 150 or even 200 (if your pharmacist doesn't freak out...)
3. Almost everybody allergic to penicillin that presents to a US hospital with sepsis will receive cefepime (and vanco). So a few things about this antibiotic need to be kept in mind. The first is its neurotoxicity; nothing more needs to be said as this side effect has very good
“marketing” and almost everybody seems to be aware of it. What is less known is that cefepime provides no anaerobic coverage; therefore, if the patient has a perforated colon, cefepime alone will not be enough. Metronidazole has to be added
4. Despite the findings of 50 observational studies, the association of vancomycin+pip/tazo with creatinine-defined AKI may represent pseudo-toxicity as no changes in alternative biomarkers (cystatin-C, BUN), or hard clinical outcomes (dialysis or mortality) are usually seen
5. Vancomycin’s loading dose in an adult septic pt is not the “universal” 1 g, it is 20-30 mg/kg. Also, u may need ≥2g q8h when creat clearance is ≥ 80 mL/min/1.73m2 to achieve optimal therapeutic exposure. I am not -in general- a big fan of vanco but this is a huge discussion
6. We don’t have great evidence but I use linezolid vs vanco when treating MRSA pneumonia. Meta-analyses have shown that there is no mortality benefit but clinical cure & microbiological eradication rates are significantly ⬆️ in pts treated with linezolid. Interestingly enough,
there was no difference in nephrotoxicity and thrombocytopenia rates. What?
7. Linezolid belongs to the class of oxazolidinones, originally developed as monoamine oxidase inhibitors for tx of depression…
8. L provides anaerobic coverage; not perfect but good! It's better for Gram+ (vs Gram-) anaerobes; I would not trust it to treat Bacteroides fragilis
8. L provides anaerobic coverage; not perfect but good! It's better for Gram+ (vs Gram-) anaerobes; I would not trust it to treat Bacteroides fragilis
9. Linezolid has anti-mycobacterial action. What?
10. Linezolid belongs to time-dependent antibiotics. It is frequently under-dosed in critically ill pts, especially septic ones w augmented renal clearance. It is likely that ...
10. Linezolid belongs to time-dependent antibiotics. It is frequently under-dosed in critically ill pts, especially septic ones w augmented renal clearance. It is likely that ...
...continuous infusion will be proven a better way to administer it. In the meantime, I have low threshold of giving it at a dose of 600 mg iv q8h at least in the first few days
11. When you treat MSSA bacteremia, vancomycin is worse - NOT better - choice than cefazolin or nafcillin
12. The benefit of adding an aminoglycoside is controversial, but -in general- when I have strong suspicion for Gram-negative rod bacteremia (for example, a pt with hx of UTIs) the sicker the pt looks, the higher the chances I will give a dose of aminoglycoside. But...
...I give a real dose, not a homeopathic one. For example, gentamicin should be at least 7 mg/kg (PLoS One 2019; 14(1): e0210012) and not the “standard” 80 mg q8h
13. Please remember that in vitro testing correlates with in vivo phenomena but the correlation is not perfect. I have treated patients bacteremic w pan-drug resistant (yes, R to all antibiotics) Gram(-) bacteria and they survived. Some combinations of antibiotics may...
... sometimes show a synergistic effect even if the bacterium is resistant to the individual antibiotics plus the patient’s immune system plays an important role plus there are so may things we don’t know! Don't give up...
14. Vancomycin has synergistic effect with other antibiotics when used against some Gram-NEGATIVE bugs, for example with colistin on the treatment of carbapenem-resistant Acinetobacter. Yes, this is true...
15. Enterococci have intrinsic resistance to cephalosporins. Remember the cefepime story? Cefepime will not cover enterococcus…
16. Stenotrophomonas maltophilia is a weird bug; it is a Pseudomonas w kind of strict nutritional needs (steno = narrow and trophi= food/nutrition, in Greek). More importantly, it is not covered –as you might expect –from carbapenems. You need minocycline/quinolones/ TMP/SMX
17. Enterobacter cloacae is characterized by chromosomally encoded AmpC β-lactamase and has the ability to develop resistance to lactams DURING treatment. If the patient has Enterobacter bacteremia, I use a carbapenem
18. The specifics of a wound culture may be less important than the patient’s health status. That’s why revascularization or pressure relief may help with an ulcer healing more than a truckload of antibiotics
19. The absence of soft-tissue air does not exclude the diagnosis of necrotizing fasciitis. I will repeat it: the absence of soft-tissue air does not exclude the diagnosis of necrotizing fasciitis...
20. The best time to draw blood cultures (if not already done) in a newly admitted septic pt is when you place central lines. If you don’t do it yourself, nobody will do it faster than you. Also, you will have to start ABs ASAP, so what’s a better time to draw blood cultures?
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