Discover and read the best of Twitter Threads about #EMBound
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ICU stories (common): Middle-aged pt w hx of COPD was brought to the ED by EMS after SOB x 2 days. No fever or chest pain. Very quickly after ED arrival, he was intubated. CXR showed hyperinflated, “COPD” lungs. Here depicted in two images: 
Post-intubation ABGs showed:
BP dropped post-intubation to 55/40; propofol was started & then discontinued due to hypotension. iv fluids (2L Lactate Ringer's) were started & patient was brought to the ICU w SBP in upper 80s. Re-institution of propofol led again to hypotension. What would be the next step?
ICU pictorials: A patient was admitted for "weakness". Unimpressive vitals / phys exam / labs. A few days later because of temp 101 F, a fever w/u was initiated. Due to "SOB", a CT chest angio was done:
👆Massive saddle PE extending in both sides w evidence of R heart strain
Echo findings:
I was checking again today about DKA/HHS in a very modern & easy to read textbook and I saw this about the Na correction:
The Katz correction factor is 1.6 mEq/L for every 100 mg/dL that the serum Glu exceeds 100 mg/dL & the Hillier correction factor is 2.4 mEq/L
amjmed.com/article/S0002-…
amjmed.com/article/S0002-…
It seems that the textbook 👆 uses a sodium correction factor of < 1.0 mEq/L for every 100 mg/dL of Glu above 100 or applies the correction starting from a higher Glu level (probably 200 mg/dL?)
ICU stories: Pt w "severe COPD" (ex-smoker; FEV1 30%) / chronic hypoxic-hypercapnic resp failure on 2-4 l/m O2 @ home / diastolic HF / HTN / HLD was brought to the ED due to "altered mental status" & "shortness of breath". S/he left the hospital 3-4 months ago after an episode
of "COPD exacerbation" (the 4th during the last 12 months). In the ED: sat in low 80s & after a brief non-rebreather mask trial, pt was placed on NIV. ABGs: PCO2>100 (above detection limit), pH 7.14, HCO3 undetectable. Pt suffered 2 grand mal seizures, & after receiving
lorazepam & 2l NS, s/he was intubated (roc+keta) & rushed to the ICU. Per ED: ECG w sinus tach & CXR "COPD lungs" & R basilar infiltrate. Labs: WBC 14K, creat 2.0 (baseline 1.4). You examine the pt quickly: sedated-?paralyzed/decr BS & wheezing bil/trace ext edema/skin not cold
Now that the #Match2023 dust has settled, we have celebrated our newly matched M4s, and as @CORD_EM's #CORDAA23 gets started, I wanted to put together some thoughts on the #EM #Match2023, highlight some facts, and answer some questions. Buckle in folks, and let’s get started! 🧵
We know the drop in applicants is multifactorial, EM is about problem-solving, we're working to make the ED a better place for ourselves/our patients, & at the end of the day the majority of EM docs will still tell you how much pride we take in our work & being badass #EMdocs. 🧵
First, those who were shocked by the # of unfilled positions in the EM #Match2023 were not following the preliminary applicant data we have had since @ERASinfo released data in Oct. showing 3,023 students had applied to EM at that time (down from 3,632 in the #Match2022). 🧵
ICU stories (a brief one): 60 yo male w lung cancer / CAD / HTN / HLD / status post chemotherapy a month ago presented to the ED w SOB/cough/weakness after failing outpatient tx w azithromycin. CT chest: no PE but positive for bilateral consolidations:
Patient came to the ICU intubated, sedated, on pressors & antibiotics for PNA. Next step: POCUS. PLAX looked "weird", so Doppler and "zoomed" views were recorded:
PSAX & subcostal views:
ICU stories (from the trenches): 70 yo pt w hx of A-fib/CAD/ICM w EF 25%/VT ablation s/p BiV ICD/CKD/HTN/HLD/peripheral vasc dz/COPD etc presented to outside 🏥 w SOB/weakness/falls. Labs: wbc 15k/creat 3.5 (baseline 2.0)/INR: 8.5/AST/ALT/Tbil: 180/250/3.0, lactate 3.5
RUQ US was obtained to work-up elevated LFTs:
Diagnosed w bilateral PNA/AKI/liver dysfunction. Treated for sepsis w ivf boluses, broad-spectrum antibiotics, steroids, bicarb. Continue to get worse; due to ⬆️O2 needs, transferred to our 🏥. I saw her the next am: in resp distress while on BiPAP 15/10-100%, abg 7.26/50/70/19.
Nice paper on cardiorenal syndrome (CJASN; 2023. doi: doi.org/10.2215/CJN.00…)
Proposed pathophysiological pathways leading to the cardiorenal syndrome and its complications
Proposed pathophysiological pathways leading to the cardiorenal syndrome and its complications
"The inciting event is usually an acute decompensation of heart failure. This may lead to either arterial underfilling or venous congestion as mediators that promote neurohormonal activity, inflammation, & endothelial dysfunction. In combination, these pathways lead to ⬇️ in GFR.
Complications include Na avidity and fluid retention, reduced kidney clearance, and endocrine function, all of which further perpetuate the pathophysiology".
ICU stories (a brief one): One hour before the end of the am shift, u walk around in the ICU to make sure thinks look OK before u type your sign-out note. You spot the resp therapist & the nurse bagging the pt in Rm 306. From the hallway, u see the monitor: HR 160, RR/45, Sat 70%
This is a 30 yo pt w hx of a catastrophic brain bleed, s/p trach & PEG, admitted 2 wks ago w MDR Klebsiella UTI. Doing well, on trach mask 28%, until the episode of acute/unexpected desaturation
When u examine the pt, s/he is in extremis (accessory muscle use-tachycardic-tachypneic-diaphoretic). BP: 105/55. You grab the stethoscope that the resp therapist wears around his neck & you hear breath sounds in both sides (pt is skinny...)
I just read this 👇 in the Comprehensive Critical Care: Adult, 3rd Edition; 2022 (@SCCM book). Are we still targeting CVP > 8?
Judging from yesterday's post, many friends are interested in how to get the most out of these books 👇 and ace the exams, so a few more tips are on their way:
1. Tylenol use can lead to high anion gap metabolic acidosis. Don’t ask me about the mechanism!
2. Every patient who manages to fly eastbound with Southwest Airlines & subsequently develops pneumonia not responding to common antibiotics has actually blastomycosis
2. Every patient who manages to fly eastbound with Southwest Airlines & subsequently develops pneumonia not responding to common antibiotics has actually blastomycosis
3. Every oncology patient who receives chemo is destined to develop tumor lysis syndrome. Please learn about hydration/allopurinol/rasburicase
4. Along these lines, every oncology patient on immunotherapy will develop pneumonitis. Remember the steroids from yesterday’s post?
4. Along these lines, every oncology patient on immunotherapy will develop pneumonitis. Remember the steroids from yesterday’s post?
ICU stories: 65 yo pt, fairly healthy besides HTN & an episode of diverticulitis 3 y ago, is brought to the ED due to 2 wks' hx of abd pain & 1 d hx of N/V ("coffee-ground"). Looked "bad". SBP in 60s - improved to 80s w ivf. Intubated. Had CT A/P 👇:
While you review the CT images, you get the lab results: Lactate 10, WBC 3K, INR 2.0, BUN/Creat 100/3.0, CRP 500 mg/l, Procalcitonin 300. The ED is calling you for the admission. What consult(s) do you ask?
The CT A/P showed a large amount of free intra-peritoneal air; stomach & SB were mildly distended & partially fluid-filled. There was colonic diverticulosis without diverticulitis & mild wall thickening involving the descending colon & the sigmoid colon
ICU stories: 70 yo pt without medical hx but tobacco use (2 ppd x 40 y) was admitted w shortness of breath a wk ago. CXR/chest CT without PE/infiltrate. Was in afib/RVR on admission; placed on heparin & dilt/b-blocker (w some hypotension). Remained dyspneic, at times restless,
“requiring” multiple sedatives, & eventually was brought to the ICU. Intubated for "resp distress" & mental status changes. "Formal" echo, the day of ICU transfer, showed “LVEF 20% w global LV dysfunction”. On the vent 50% - peep 10. BP 110-130/60-70. Lactate < 2.0
Cards follow for "well compensated heart failure". A look w POCUS upon ICU admission:
How do you examine the lower extremity venous system when you look for deep vein thrombosis? What points do you check with the probe? Do you use Doppler? What are the recommended protocols? The Society of Radiologists in Ultrasound recommends a complete duplex ultrasound:
👆 The black rectangles represent the extent of the compression US. The gray rectangles are the sites of Doppler.
2-CUS (2-points compression US) includes compression of the femoral veins 1-2 cm above & below the saphenofemoral junction & the popliteal veins
up to the calf veins
2-CUS (2-points compression US) includes compression of the femoral veins 1-2 cm above & below the saphenofemoral junction & the popliteal veins
up to the calf veins
ECUS (extended compression US), includes compression US from the common femoral vein through the popliteal vein up to the calf veins confluence
CCUS (complete compression US), includes compression US from the common femoral vein to the ankle
CCUS (complete compression US), includes compression US from the common femoral vein to the ankle
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
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:
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:
This is the first year I have not applied for #Match2023
It’s the first time I’m not worrying if I did “enough” to finally get in.
And I have to say, I haven’t felt HAPPIER or more fulfilled in years.
1/
It’s the first time I’m not worrying if I did “enough” to finally get in.
And I have to say, I haven’t felt HAPPIER or more fulfilled in years.
1/
I had been running the #Match marathon for 4 years, kept pushing through, amping my experience, rewriting my PS, getting new LORs, working during a pandemic.
Kept ending up #unmatched, sometimes more heartbroken than the previous year, with no time to process what happened.
2/
Kept ending up #unmatched, sometimes more heartbroken than the previous year, with no time to process what happened.
2/
I had made every sacrifice to get into residency because that was the only way I saw my future as a physician
But that’s where I was wrong - I was stuck with tunnel vision of what it meant to succeed as a doctor
After #Match2022 I decided I was ending the toxic cycle
3/
But that’s where I was wrong - I was stuck with tunnel vision of what it meant to succeed as a doctor
After #Match2022 I decided I was ending the toxic cycle
3/
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: I love ID (or at least I did until COVID-19 came into our lives…) and for quite some time I wanted to write a relevant thread. These are some of the simple things that I always try to keep in mind and discuss/apply during rounds:
1. It’s a shame to treat an intubated pt for “pneumonia” without ever sending a tracheal aspirate culture. It’s the equivalent of treating “urosepsis” without being bothered to send a urine culture
2. There is potential for “source control” in (some) pts with pneumonia. It is...
2. There is potential for “source control” in (some) pts with pneumonia. It is...
...called “thoracentecis” and whatever may follow it can be a game-changer!
3. Many blood cultures grow contaminants. But if you decide to ignore a blood culture (+) for Gram-negative rods or S. aureus or fungi, you play with fire
4. If your pt has (severe) diarrhea +/- ...
3. Many blood cultures grow contaminants. But if you decide to ignore a blood culture (+) for Gram-negative rods or S. aureus or fungi, you play with fire
4. If your pt has (severe) diarrhea +/- ...
ICU (evolving) stories: A young patient was admitted with "aspiration pneumonia" a few days ago. On mechanical ventilation. Afebrile. Negative cultures. CXR when you first see him (ET tube a bit deep, by the way):
You take a look at the ventilator screen. Patient on assist/volume control, 25 breaths, Vt 300 cc, FiO2 80%, PEEP 5.
U are a strong believer of guideline-directed medical therapies (GDMT). U know that following the PEEP table - as used in the ARDSnet study (NEJM 2004; 351(4): 327-36.
doi: 10.1056/NEJMoa032193) - is a well-tested way to set PEEP. For FiO2 of 80%, the recommended PEEP is:
doi: 10.1056/NEJMoa032193) - is a well-tested way to set PEEP. For FiO2 of 80%, the recommended PEEP is:
ICU POCUS snippets: A bit of context: An elderly patient with hx of DM2 / HTN / HLD / peripheral vascular disease / ureteral stent & recurrent UTIs is admitted to the hospitalists’ service w diffuse abdominal pain, nausea & vomiting. Treated for a few days w antibiotics...
...but never really felt any better (weak/abd pain). Eventually, became hypotensive & was transferred to the ICU for “initiation of vasopressors”. Phys exam: diffuse abd tenderness. Formal echo earlier that day: "Normal LV/RV in size and systolic function". ICU POCUS was done...
...to gain more information regarding the cause of the abd pain and the hemodynamic picture. Some of the clips are shown here:
ICU POCUS snippets: Much has been said about how useful lung POCUS is for procedural guidance. First of all, it accurately reveals large effusions when the radiology report characterizes them as “small”. This is from a recent case of a pt intubated w community-acquired pneumonia
and what proved to be bilateral parapneumonic effusions:
Secondly, while the dogma (which, btw, I don’t recommend completely ignoring!) in thoracentesis is to insert the needle at the “triangle of safety”, bordered by the anterior border of the latissimus dorsi, the lateral border of the pectoralis major, the horizontal line at the...
