ICU Opinion: I have worked in ICUs long enough to have been through plenty of The Joint Commission (TJC, formerly JCAHO) survey weeks. And I have to admit, the longer I do this, the more skeptical I become about how much of the bureaucracy around hospital accreditation actually makes patients safer. I am not against standards. Hospitals need outside scrutiny and TJC has done important work. Medication safety, infection prevention, handoffs and procedural safeguards matter. Outside pressure has helped change practices that needed to change. My problem is when patient safety turns into compliance theater. If you've worked in a hospital during survey week, you know the ritual. Suddenly everyone is worried about where your coffee is sitting. Tape disappears from walls. Doors, ceiling tiles, refrigerators and labels become urgent concerns. At least my beloved ultrasound machine is finally back where it belongs and plugged into the wall! Then administrators who rarely set foot on the unit, and probably haven't visited us since the ribbon-cutting ceremony, show up to remind us about rules that somehow become much more important when the surveyors are in the building. Meanwhile, the ICU is still the ICU. A nurse is titrating three vasopressors, managing CRRT and trying to stop a delirious patient from pulling out his femoral arterial line. Someone is intubating. Another patient is spitting at us and demanding to leave AMA. But please, let's talk about that covered cup. The coffee is actually a good example of the larger problem. Even the famous “TJC says you can't drink at the nursing station” rule isn't that simple. Hospitals can designate safe areas for food and drink based on exposure risk. But by the time a rule works its way through hospital committees, policies and layers of administration, the nuance is often gone. Rules beget rules. Hospitals write policies around standards. Consultants prepare hospitals for surveys. Staff are prepared for the consultants who are preparing everyone for the survey. My work mailbox gets an email every other day warning me about the visit. Eventually, nobody remembers whether a requirement came from CMS, OSHA, TJC, the hospital—or something somebody heard years ago that somehow became hospital law. All of this takes time. So what are we getting in return? A BMJ study of more than 4.2 million Medicare admissions found no significant 30-day mortality associated with accreditation, or for TJC-accredited hospitals compared with other independent accreditors. That doesn't settle whether accreditation works. Mortality is only one outcome. But it should make us question the assumption that more compliance automatically means better care. There is also a part of this system worth being transparent about. Hospitals pay accrediting organizations to evaluate them. TJC has a controlled affiliate, Joint Commission Resources, that provides education and consulting services related to accreditation and quality. That relationship does not by itself mean anything improper is happening. Formal safeguards separate the accreditation and consulting functions to address potential or perceived conflicts of interest. Still, I think it's reasonable to ask how that relationship works and how those safeguards are maintained. To be clear: I don't want to abolish accreditation or leave hospitals to police themselves. My point is simpler: if we're going to ask a nurse or physician to do something in the name of patient safety, we should be able to show that it actually makes patients safer. Every requirement costs something: money, another click in the EHR, another mandatory module or a few more minutes spent on compliance instead of with a patient. We ask for evidence before we do things to our patients. I don't think it's unreasonable to ask for evidence before we make clinicians do things in the name of protecting them. The ICU does not become safer because TJC survey week started. And yes, let the night-shift ICU nurse drink her coffee.

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Here @Turningthe_Tide, we discuss Bozeat et al's paper on whether crystalloid still belongs in the first hours of trauma haemorrhage - When fluid has a job - When it does not - How permissive hypotension and vasopressors fit - Why “the bag is already up” is not an indication. #FOAMed #FOAMcc fluids.info/members/articles…

ICU Controversies #001 - The answer: 799 votes. 39% chose C: Ophthalmology. The Infectious Diseases Society of America agrees. The American Academy of Ophthalmology does NOT. Same patient. Same candidemia. Two major societies. Different recommendations. Here’s why 👇 —— REPLY 1 —— IDSA: Dilated ophthalmologic examination for all non-neutropenic patients with candidemia within the first week. AAO: Do NOT routinely screen asymptomatic patients; examine patients with signs or symptoms suggesting ocular infection. Why the disagreement? Candida can seed the eye but clinically important endophthalmitis is uncommon, and the evidence supporting universal screening is limited. —— REPLY 2 —— Here’s the key distinction: Finding an abnormality ≠ proving that screening improves outcomes. Fundoscopy can detect asymptomatic ocular disease and can change antifungal choice and duration. What remains uncertain is whether routinely screening every asymptomatic patient actually prevents vision loss or improves other patient-centered outcomes. That uncertainty helps explain why major guidelines have reached different conclusions. Traditional board answer: C. Real-world answer: still controversial.

ICU Controversies #001 - The answer: Interesting results. 39.0% chose C: Eye exam. Nearly 1/3 chose TEE. So… who is right? Well, it depends on whom you ask. 👇 Infectious Diseases Society of America (IDSA): C American Academy of Ophthalmology (AAO): Not necessary to perform an eye exam And THAT is the controversy. Let's unpack it… Candida can hematogenously seed the eye → chorioretinitis/endophthalmitis. Finding ocular disease matters because it may change the antifungal agent, duration of therapy, and occasionally require intravitreal therapy or vitrectomy. But true Candida endophthalmitis is uncommon, diagnostic definitions have varied considerably, and we lack convincing evidence that screening every asymptomatic patient improves clinical outcomes. And here is the twist in THIS patient: He has two features associated with higher risk of ocular involvement: → Candida albicans → Total parenteral nutrition A 2023 meta-analysis of 8,599 screened patients found: • Ocular candidiasis: 10.7% • Concordant Candida endophthalmitis: 1.8% More recent studies continue to find asymptomatic ocular disease and management changes after fundoscopy. So what is the answer? For a traditional board-style question: C. For actual ICU practice in 2026? There is no universal consensus. #FOAMed #FOAMcc #MedEd #medtwitter #idtwitter

ICU Controversies #001: A 68-year-old man with short bowel syndrome requiring chronic TPN is admitted to the ICU with septic shock. His central line is removed and antibiotic/antifungal therapy is started. Blood cultures grow Candida albicans. TTE shows preserved LV function, mild TR, and NO vegetations. He has no visual symptoms. Which consultation is most appropriate next? A. Cardiology for transesophageal echo B. Interventional radiology for tunneled central venous catheter C. Ophthalmology for dilated retinal examination D. Nothing else is needed What’s your answer? 👇 #FOAMed #FOAMcc #MedEd #medtwitter #idtwitter

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#ICU Visuals #001: Why does #thiamine deficiency cause lactate to rise? The entire physiology in one figure 👇

#Thiamine in the ICU: 10 high-yield pearls 1. Unexplained lactate? Think thiamine. Thiamine is required for pyruvate dehydrogenase. Deficiency blocks conversion of pyruvate to acetyl-CoA, shunting pyruvate toward lactate and impairing mitochondrial aerobic metabolism. Thus, thiamine deficiency belongs in the differential diagnosis for otherwise unexplained lactic acidosis. 2. Thiamine deficiency in the ICU is not rare. ~30-70% of critically ill patients are thiamine-deficient. Many arrive deficient; others develop deficiency during critical illness because of increased metabolic demand, inadequate intake, or losses. 3. The bedside phenotype is more important than waiting for a thiamine level. High-risk situations include malnutrition, alcohol-related liver disease, bariatric surgery, renal replacement therapy, polyuria/DKA, chronic diuretic therapy, unexplained encephalopathy, unexplained lactate elevation, and sepsis. 4. Starting nutrition can unmask the deficiency. Glucose administration increases carbohydrate metabolism and thiamine utilization. A malnourished patient may therefore develop rising lactate after initiation of enteral/parenteral nutrition. Refeeding syndrome is not simply a phosphorus/potassium problem; thiamine deficiency can be central to its pathophysiology. 5. Dialysis and polyuria are major clues. Thiamine can be lost during continuous RRT, hemodialysis, and peritoneal dialysis. Renal losses also rise with polyuria, including the diuretic phase of AKI, post-transplant polyuria, DKA, and chronic diuretic therapy in heart failure. 6. Do not wait for the classic Wernicke's triad. Altered mental status, ocular abnormalities, and gait ataxia are rarely all present together. I think I have seen it only a few times. In an at-risk ICU patient with otherwise unexplained encephalopathy, absence of the complete triad should not reassure you. 7. A plasma thiamine concentration is not a great “rule-out” test. Testing is often unavailable and expensive, and blood concentration does not necessarily reflect tissue thiamine status. I don't even remember when I last ordered the test (if ever...). Erythrocyte transketolase activity is physiologically more informative, but its cutoffs are poorly defined. Just recognize the risk population and consider a therapeutic trial rather than wait for laboratory confirmation. 8. The sepsis data are more nuanced than “thiamine works” or “thiamine doesn't work.” Thiamine is not expected to improve hard outcomes in the overall septic-shock population. Some subgroup analyses and meta-analyses suggest signals for improved lactate clearance and organ function, particularly renal outcomes. I don't consider it a magic drug... 9. Thiamine alone ≠ HAT (hydrocortisone + ascorbic acid +thiamine) therapy. Do not interpret negative trials of HAT as proof that correcting thiamine deficiency is useless. Large HAT RCTs failed to demonstrate the dramatic clinical benefit initially claimed, and a VICTAS secondary analysis raised concerns about longer-term outcomes. That is a different question from replacing thiamine in a patient likely to be deficient. 10. The kidney may be an important target organ. Renal tubular cells are highly energy dependent. Across secondary analyses, observational data, and meta-analytic evidence, thiamine supplementation -particularly in deficient patients- shows a signal toward less AKI progression, better renal recovery, and less need for RRT, although individual RCTs have not consistently demonstrated significant benefit in unselected populations. Rule of thumb: “⬆️ lactate + risk factor + no good explanation" → think B1 deficiency” Especially think about it when you see malnutrition/refeeding, alcoholism/cirrhosis, dialysis, polyuria/DKA, chronic diuretics, unexplained encephalopathy, sepsis, or otherwise unexplained persistent hyperlactatemia. I usually include it in the admission orders for most of my ICU patients along with DVT and GI prophylaxis...! Thiamine deficiency behaves less like an obscure vitamin deficiency and more like a potentially reversible form of mitochondrial energy failure. Or that's how I like to think about it. #foamed #foamcc #meded

There are now two #RSIs that worry me. One can rapidly take away a patient's ability to breathe. The other could give an #AI system the ability to recursively improve beyond humanity's ability to reliably control it. Rapid Sequence Intubation. Recursive Self-Improvement. Both present an alignment problem. For one, we have an algorithm. For the other, we have a research problem. Be safe.

Answer: B. Cerebral arterial vasospasm, producing delayed cerebral ischemia (DCI). Neurologic deterioration occurs on day 6, the classic window for DCI after aneurysmal subarachnoid hemorrhage; it typically develops about 3–14 days after the bleed. New aphasia, gaze preference, facial weakness, and leg weakness indicate a focal ischemic deficit. Repeat CT shows no rebleeding, intraparenchymal hemorrhage, or hydrocephalus, making those alternative causes less likely. Nimodipine lowers the risk of DCI but does not eliminate it and does not reliably prevent angiographic vasospasm. Strictly, the clinical diagnosis is delayed cerebral ischemia due to symptomatic vasospasm; among the answer choices, cerebral arterial vasospasm is the best response.

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