ICU stories (a boring one…): If you work in a general ICU of a community hospital in United States, one of the common admissions you will get is the unfortunate resident of a nursing home or rehabilitation center that lives there for several decades & at some point becomes
febrile/“altered” & is sent to the ED for “evaluation”. The course is so predictable that we usually consider these admissions “boring”. This is the case of a middle-aged pt w cerebral palsy/mental retardation/seizures (on valproic)/PEG-chronic Foley in place who was sent to
the ED for fever+hypotension+tachycadia. Labs: WBC 15k, lactate 4.0. UA -as usually- suggestive of UTI (WBC>50, +bacteria, +nitrite, +esterase). CXR “clear” & pt w sat 99% on room air. Received ivf, Abx (pip/tazo + vanco) but due to persistent ⬇️BP, norepinephrine gtt was ordered
You check the pt's chart while calling back to "accept" the admission and you see this:
👆This is a common scenario where pts remain hypotensive for h in the ED/ICU waiting for fluids to "work" or even for pressors to "kick in". Especially after pressors are started, the nurses need to be trained to start "high" instead of following this extremely annoying protocol
While talkng to the ED attending, you had the luxury of time to check microbiology data from previous admissions. In the most recent one, the urine culture grew:
👆This is another common scenario where pts receive pip/tazo + vanco regardless of their history. The ED is a hectic place but it is inexcusable for the ICU to leave old records unchecked & not modify the antibiotics accordingly. The pt was ready to be transferred to the ICU
Would you ask anything else from the ED before transfer? What about a CT?
CT was ordered while patient was still in the ED. CT chest showed bilateral pulmonary emboli. This is from the L lung:
CT A/P showed:
What would you do?
The balloon of the Foley catheter was inflated in the penile urethra. Let's see:
Patient arrived in the ICU. Foley was advanced. Pip/tazo was changed to meropenem & heparin drip was added for PE. A lower extremities venous US was performed (I skip the heart POCUS). This is what you saw when you placed the linear probe in the L groin:
What do you think this 👆 is?
Oops, I hear you, I did not include compression. Here it is:
It was actually one of the DVT mimics. If you fan up and down, you see that it is a round structure (?lymph node) not a tubular one (like a vein should be). In addition, a CFV should be next to the CFA. Let's check again:
Patient was doing very well, fever had resolved, pressors had been stopped and while looking good, suffered a grand mal seizure and had to be intubated for airway protection. What happened? This 👇 happened:
Valproic acid levels ⬇️ significantly triggering a grand mal seizure. This is a well known interaction of carbapenems with valproic acid (VPA). Carbapenems inhibit the activity of the acylpeptide hydrolase enzyme that converts VPA-glucuronide to VPA, resulting in
greater elimination, a shortened half-life, and sub-therapeutic plasma concentrations of VPA (and occasionally breakthrough seizures...). journals.sagepub.com/doi/abs/10.117…
Actually our patient never had a seizure since the interaction was quickly recognized, the meropenem was changed to a different antibiotic and levetiracetam was used for a day
Take-home messages: 1. We should be careful when we manage "boring" cases 2. Pts, especially the ones that come to the ICU, can have more than 2 life-threatening diagnoses at the same time 3. Old microbiological date should be thoroughly reviewed in order
to choose the most appropriate antibiotics 4. We should be aware of DVT mimics 5. We should be aware of drug interactions that can make our treatment less effective or even harmful
It's December, already. The time of the year when I am trying to spend every last cent of the annual allowance given to us for continuing medical education (CME) by our employer. In essence, this is money that we have worked for and, since it won't carry over to next year, I hate
leaving it on the table. The problem is that if you buy a conference or a study course now, you have to watch everything - and submit proof of attendance/completion - before the end of the year. So, it's a very busy month dedicated to studying/reviewing educational material!
For example, I just finished watching the last one of the 93 lectures from The Hospitalist & Resuscitationist 2022 conference #HR2022. If you are an intensivist/internist/family medicine/EM physician, I have no doubt that u will find several pearls to bring back to your practice
Alcohol withdrawal syndrome: I don’t know if u have a similar experience in other countries (or other places in the States) but I've recently seen a big spike in alcohol abuse-related disorders, especially alcohol withdrawal syndrome (AWS). I'm obviously referring to severe AWS
that eventually will need to come to the ICU (if we have a bed available!). There are many fantastic, well-searched reviews on this topic but it may be hopefully interesting for some if I put “my way” out there & also for me to learn from your experience. Even though the focus
will be on the neuropsychiatric component, I believe it is quite important to highlight other parts of AWS management. To this end, I will use the assessment/plan “per organ” approach which is commonly used when we write progress notes here in US. Here it goes:
ICU stories: You get a call from outside 🏥 to accept a middle-aged pt w DM2/HTN/HLD/some type of solid Ca on chemo/obesity who presented to their ED w weakness/anxiety/"feeling cold". Vitals: BP 80-100, HR 130s (sinus tach), afebrile, Sat 100% on room air. Labs: WBC 13K, ...
... Lactate 5.2, creat 1.3. UA w some WBCs/bacteria. CXR clear. Norepi drip ordered but cancelled after BP improved to mid-90s, HR fell to 120s, & lactate ⬇️ to 2.5. What's your next step?
The discussion went like this:
Me: I will be happy to accept but I have no idea what we are treating. If it is sepsis, the source is unclear. And what about PE? Can you pls get a CT before sending?
ED: Sure, will do it. Thanks.
You go home & next am you learn that the CT showed:
ICU stories (from the trenches): It's been a bit more than 2 hrs in your night shift & you are checking some labs signed out to you to be followed on. A rapid response is called for "agitation" in Rm 666; in less than a minute the operator calls for a "Code Blue" in the same room
When u arrive @ the code, u see a very young pt white as a sheet w CPR in progress. Presented to ED 12 h earlier c/o non-bloody emesis & abd pain x 1 wk. Uses daily NSAIDs for chronic pain. Vitals in ED: 125/77, HR 125, Hb 7.9 g/dl. Guaiac(+) stools. Vitals improved w hydration
and EGD was performed that showed "normal esophagus, large amount of food in the stomach, 6 mm non-bleeding antral ulcer & a large non-bleeding duodenal bulb ulcer". Evaluation was thought to be "limited" & plan was to repeat EGD next am. Back to the code, which is a PEA arrest
ICU Infectious Disease Pearls and Pet Peeves-Part3: These are some extra points & random thoughts regarding commonly used antimicrobials & frequently encountered ID scenarios in the ICU. Comments from ID & Pharm friends are welcome as what I post comes from memory. Here it goes:
1. Especially in immunosuppressed patients with severe septic shock, don’t be in a hurry to de-escalate the antibiotics when the Microbiology lab calls you to report a positive blood culture result. In a number of patients, likely close to 5%, the bacteremias can be polymicrobial
2. The role of anaerobes in aspiration pneumonia is probably over-rated. Not much else to say here since the topic is extensively discussed recently. The message is that anaerobic coverage is frequently redundant. In addition, there is a huge debate about...
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...)