Something we use on a daily basis as physicians but so much goes behind the scenes!
Here is the inside story on how @UpToDate does what it does.
From my experience as an author/section editor for UpToDate for 20 years, here is how it works. It’s amazing!
Every day a team of people @UpToDate scour the top medical journals (and major meeting abstracts) for articles of importance. In my case they pertain to myeloma and related disorders. Any article that is felt to be important is sent to a expert MD medical editor at UpToDate who reviews the paper. If the information is felt to be important, the relevant chapter is updated with this content, summarized in a few sentences in Word track and then sent to the author of the chapter who is a top expert in the field.
As an author I have to review the update in detail and then make a decision whether to include the new information, and whether the way it has been incorporated is correct or needs to be edited.
Once I make a decision, it is then reviewed by an expert section editor. For 15 years for me, the section editor was Dr. Robert Kyle! (Currently I’m the section editor and we have about 6 experts serve as authors on over 40 chapters pertaining to myeloma and related disorders). The section editor independently decides whether the author made the right call and either approves or we have a back and forth till we agree.
The updated chapter is then reviewed again by the expert MD editor at UpToDate and then posted.
For important phase III trials or FDA approvals we usually make the update within a week. Sometimes by the next day! With so many important papers, every week there are 2-3 updates pertaining to my chapters that go through the above process! It’s hard work but it keeps me ridiculously current. And more importantly it keeps the content accurate and current. This is not random addition of new information. It’s vetted information that’s added.
Every UpToDate chapter is also peer reviewed annually. Each chapter also undergoes an annual author and editor review to make sure that the overall content and flow is good and to delete content that may be no longer important or accurate. The extraordinary process and rigor involved is why it’s such an invaluable irreplaceable resource. It is AMAZING and hard to replicate.
UpToDate is easy to navigate. But the newly launched UpToDate Expert AI takes it to the next level! It makes the entire content available to query just like you query a top ranked LLM. But it’s not searching the random internet or a stack of published articles. It’s primarily trained and derives vetted and adjudicated UpToDate content. It will not randomly hallucinate. It will not list 10 options for treatment newly diagnosed myeloma but will give you what experts currently feel is the best option based on the latest evidence. All answers are referenced and pointing to specific content sections in UpToDate (which also has links to source material). So you can immediately get all the background information if you need more detail.
Working with UpToDate has helped my career immensely. For the last 20 years it has been impossible for me to not know about every important study related to myeloma and related disorders as they get published! For 20 years, I have received a precise summary of every important article published in my field. More importantly I am forced to read them, review the source material, and make a judgment call. As a result I remember this stuff. A gift indeed!
Himanshu Rawal MD retweeted
❓ Can we assess alveolar recruitability in severe #ARDS? 🫁
de Fonseca Reis & colleagues evaluate 4️⃣ methods….
chestcc.org/article/S2949-78…
#OpenAccess in #journal_CHESTCritCare
Himanshu Rawal MD retweeted
What is the dyssynchrony in the waveforms below? Mode is Pressure Support. Poll and explanations below!
Himanshu Rawal MD retweeted
ICU waveforms quiz: what’s wrong in this picture and what should you do to fix it?
Himanshu Rawal MD retweeted
The central theorem of RV failure 😁
In LV failure, excessive afterload reduction can cause systemic hypotension (MAP << 60mm), vasodilatory shock, systemic malperfusion, and death.
In RV failure, excessive afterload reduction doesn't really exist. Low pulmonary artery pressures are well tolerated (the lung remains well perfused by *dual* pulmonary & bronchial artery circulations).
This essential difference opens a unique avenue for treating RV failure with much more aggressive afterload reduction (as compared to LV failure).
The RV is different from the LV and requires unique management strategies (not just copy/pasting a generic LV failure strategy).
#ThePeoplesVentricle
Himanshu Rawal MD retweeted
SEARCH algorithm: Chronic Thromboembolism Phenotypes after Acute Pulmonary Embolism.
⚡️🫁❤️🩹🩻🩺😱😨
@ERSpublications @EuroRespSoc @ALATorax
@pneumosbpt @separrespira
doi.org/10.1183/13993003.015…
Every time I see a continuous renal replacement (CRRT) order for an ultrafiltration rate of 25 mL/hour, a small part of me dies
If we're afraid that the patient will crash from removing 0.4 mL/min, perhaps we should also stop sending blood cultures and morning labs...
I am just saying...
Himanshu Rawal MD retweeted
We cut our AI bill by 30%.
Cheaper Inference sells access to most models cheaper than the list price.
Same models. Same API format. Smaller bill.
You can use OpenAI, Anthropic, and Google models through one OpenAI-compatible API.
Just switch your endpoint
Himanshu Rawal MD retweeted
Fresh Blog: Why I think hyperangulated videolarygnoscopy should be the mainstay of ICU intubations:
📹 People actually use the tool correctly
📹 Master one technique for easy & hard airways
📹 Compatible with steep bed angulation
📹 The fresh COVALENT RCT 😁
(#1/2)
Himanshu Rawal MD retweeted
🫁🎥 August 2026 Airway of the Month is live: “Paralysis Pending!” 👇
🔗 Current Airway of the month
airwayofthemonth.com/aotm-cu…
The cords are visible. The tube is ready. So why wait? ⏳
🪤A good glottic view does not automatically mean ideal intubating conditions.
The airway begins with heavy secretions and difficult tongue control. 👅💦
With a Mac-style VL blade, enter on the right and sweep the tongue left; with a hyperangulated blade, enter midline and scoop. Then suction early to optimize the view. 🧹👀
But seeing the glottis does not mean the airway is ready for the tube.
‼️The vocal cords are still moving‼️
Paralysis is not only for laryngoscopy—it also facilitates smoother, less traumatic ET Tube passage.
🚫💪 Instead of forcing the tube through, 🚁stage the ETT just above the glottis. If oxygenation and hemodynamics remain acceptable, pause ⏸️, maintain the view, let the paralytic work, and then advance. ➡️🫁
Verbalize the plan to the room: 🗣️
“Great view. Tube ready. Cords not relaxed. We’re waiting.”
✅ Optimize the blade path
✅ Suction early
✅ Stage—don’t ram
✅ Treat resistance as feedback
✅ Remember: a controlled pause is still control
A controlled pause is not loss of control. A good view should reduce urgency, not create it. 🎯
Keep pushing airway education forward—just don’t keep pushing the ETT. 😉
🔗Current Airway of the month
airwayofthemonth.com/aotm-cu…
🔗Airway of the month series
airwayofthemonth.com/airway-…
#AirwayOfTheMonth #AirwayManagement #FOAMed #EmergencyMedicine #VideoLaryngoscopy #aotm #ParalysisPending
Himanshu Rawal MD retweeted
For the love of god please stop withholding ceftriaxone in patients with anaphylaxis to penicillin
Himanshu Rawal MD retweeted
ARISE-FLUIDS has arrived and it's awesome 🥳
For over a decade, the Surviving Sepsis Guidelines recommended that septic patients get at least 30 cc/kg fluid. In the United States, these guidelines were weaponized into performance metrics, pressuring clinicians to prescribe arbitrary volumes to every patient.
Evidence-based clinicians have LONG known that this guideline lacked evidentiary support. For example, I've attached a picture of a blog I wrote about this back in 2017. Despite the lack of evidentiary support and some evidence of harm, the Surviving Sepsis Guidelines INSISTED on perpetually recommending 30 cc/kg fluid resuscitation.
We finally have a prospective RCT demonstrating that mandating early administration of 30 cc/kg fluid (as compared to early vasopressors) doesn't help and may actually cause harm.
It's important to note that all of the hard endpoints in this trial were neutral (e.g., mortality, days free of organ support).
I still think that 30 cc/kg fluid is a pretty reasonable volume of fluid for *most* patients. But the study does suggest that giving too much fluid may promote edema - so we should be *thoughtful* about this intervention rather than mandating it for every septic patient.
Based on the subgroup analysis, the fluid-conservative strategy may have helped the subgroup of pneumonia patients the most. This is statistically nonsignificant but aligns with my expectation. ARDSy patients often don't respond well to fluid. (In contrast, I really doubt that a liter of fluids in either direction matters for most urosepsis patients.)
This is a great example of the over-reach of guidelines and protocoled medicine. People get all upset about practice variation, so sometimes they try to stomp it out using guidelines and protocols. But these guidelines are highly fallible, so what may occur is that you standardize care in a way that harms everyone equally. 🤦♂️
Himanshu Rawal MD retweeted
New in @CritCareMed: our meta-analysis of 16 RCTs (1,620 adults) suggests nebulized heparin in acute respiratory failure may lower mortality (RR 0.79, 95% CI 0.66–0.95) and increase ventilation-free days, with no safety signal. pubmed.ncbi.nlm.nih.gov/4214…
Himanshu Rawal MD retweeted
🫁 Chest tubes are far more than “just a drain.”
This review is an excellent reminder that successful pleural management depends on understanding physiology, imaging, drainage mechanics, and complications.
Several practical concepts stand out:
📡 Image guidance matters.
Ultrasound is now the standard for pleural drainage, improving success and reducing complications compared with blind insertion. CT guidance becomes essential for loculated, fissural, or complex collections.
📏 Bigger is not always better.
Small bore pigtail catheters are increasingly supported for many pleural effusions and pneumothoraces, often causing less pain and fewer complications. Large bore tubes still retain value in:
• hemothorax
• empyema
• persistent air leak
• mechanically ventilated pneumothorax
⚠️ One of the most misunderstood areas remains chest drainage systems.
The paper clearly explains: • tidaling
• bubbling interpretation
• water seal physiology
• suction management
• digital drainage systems
Importantly, continuous bubbling is not automatically “normal.” It may indicate a persistent air leak, tube malfunction, or incomplete pleural sealing.
Another excellent point: 🧠 excessive suction may sometimes prolong alveolar or bronchopleural fistula healing.
Finally, the review highlights serious complications clinicians must actively anticipate: • tube malposition
• arterial injury
• persistent air leak
• reexpansion pulmonary edema
Chest tube management is not a nursing afterthought. It is dynamic pleural physiology at the bedside.
📖 Ukeh I et al. Seminars in Interventional Radiology. 2022;39:234–247. doi.org/10.1055/s-0042-17512…
Himanshu Rawal MD retweeted
🍽️ ICU nutrition: we’ve been doing it wrong for years?
More calories
More protein
Earlier feeding
Sounds logical
But physiology disagrees
⚠️ The key update
High-quality RCTs now show:
❌ Early full-dose nutrition
→ NO benefit
→ Potential harm
Especially in:
• Shock
• Multiorgan failure
• High metabolic stress
👉 This is not neutral
👉 This is dangerous practice
🧠 Critical illness is not static
It evolves through metabolic phases:
1. Acute catabolic phase
2. Stabilization phase
3. Recovery phase
👉 Feeding must follow physiology
Not protocols
🔥 Phase 1: Acute catabolic
• High inflammation
• Insulin resistance
• Endogenous substrate mobilization
👉 The body is NOT ready for full nutrition
💡 Strategy:
✔️ Permissive underfeeding
✔️ Low protein
Why?
Because early overload leads to:
• Hyperglycemia
• Hepatic dysfunction
• Renal stress
• Impaired autophagy
👉 You are feeding dysfunction, not recovery
⚖️ Phase 2: Stabilization
• Inflammation decreasing
• Organ function improving
👉 Now metabolism starts to tolerate nutrition
💡 Strategy:
✔️ Slow escalation
✔️ Daily reassessment
⚠️ Red flags:
• Hypophosphatemia
• Hyperglycemia
→ Patient is NOT ready
💪 Phase 3: Recovery
• Anabolism returns
• Mobility improves
👉 NOW nutrition matters most
💡 Strategy:
✔️ Higher calories
✔️ Higher protein
✔️ Combine with rehab
👉 This is where you rebuild muscle and function
📊 The real takeaway
Nutrition is NOT:
❌ A fixed prescription
❌ A calorie target
It is:
✔️ A dynamic therapy
✔️ A metabolic intervention
🎯 The new principle
“Start low
Advance judiciously
Individualize throughout”
👉 Precision ICU nutrition
⚠️ Final thought
Overfeeding early harms
Underfeeding late harms
👉 Timing is everything
📚 Stoppe C et al. Curr Opin Clin Nutr Metab Care 2026
DOI: 10.1097/MCO.0000000000001186
Himanshu Rawal MD retweeted
🧠 CO₂ is not just a number...It is a powerful brain modulator.
🚨 In acute brain injury (ABI), PaCO₂ = cerebral blood flow control
Every intensivist knows it…
But we still underestimate it.
👉 PaCO₂ directly regulates cerebral blood flow (CBF)
✔️ ↑ PaCO₂ → vasodilation → ↑ CBF → ↑ ICP
✔️ ↓ PaCO₂ → vasoconstriction → ↓ CBF → ↓ ICP
📊 The physiology is almost linear
🧠 For every 1 mmHg ↑ PaCO₂
➡️ CBF increases ~3–6%
🧠 For every 1 mmHg ↓ PaCO₂
➡️ CBF decreases ~1-3%
⚠️ This is where we get it wrong
Hyperventilation = double-edged sword
✔️ Good → ↓ ICP
❌ Dangerous → ↓ CBF → ischemia
👉 Especially early after injury
🔥 Critical threshold
🚫 PaCO₂ ~25 mmHg
➡️ ↑ glutamate, lactate
➡️ ↓ cerebral perfusion
➡️ ↑ secondary brain injury
👉 Not theoretical. Clinically proven
📉 Outcome data
PaCO₂ follows a U-shaped mortality curve:
⬇️ <32 mmHg → ↑ mortality
⬆️ >45 mmHg → ↑ mortality
🎯 Sweet spot = 35-45 mmHg
🧠 Practical ICU targets
👉 No ICP crisis:
➡️ Aim normocapnia (35-45 mmHg)
👉 Elevated ICP:
➡️ Mild hypocapnia (32-35 mmHg)
➡️ Short-term only
👉 Refractory ICP / herniation:
➡️ Temporary aggressive hyperventilation
⚡ Key mistake to avoid
❌ Prolonged hyperventilation
👉 Leads to:
▪️ Cerebral ischemia
▪️ Worse long-term outcomes
▪️ Hidden hypoxia
🧬 Advanced insight
CO₂ works through:
✔️ CSF pH changes
✔️ Blood-brain barrier diffusion
✔️ Direct vascular tone modulation
👉 Faster and stronger than systemic pH effects
🫀 Clinical reality
Two patients. Same ICP.
But:
▪️ Different compliance
▪️ Different CO₂ reactivity
▪️ Different outcomes
👉 CO₂ must be individualized
🚀 Future direction
▪️ Brain oxygen-guided ventilation
▪️ Multimodal neuromonitoring
▪️ Personalized PaCO₂ targets
🎯 Take-home
CO₂ is not ventilation.
CO₂ is brain perfusion control.
👉 Treat it like a drug
👉 Dose it carefully
👉 Monitor the effect
📚 Taran et al. Intensive Care Med (2025) 51:1256–1259 doi.org/10.1007/s00134-025-0…
Himanshu Rawal MD retweeted
PAD reduzida no choque hemodinâmico é sempre sinônimo de vasoplegia? Nem sempre!
Entenda situações em que a PAD perde acurácia nessa associação.
Segue o fio 🧶
Himanshu Rawal MD retweeted
[1] #Hemodynamics Tweetorial #2
Heart failure pt in ICU is -3.5L after 2d of aggressive diuresis. On day 3, urine output is ⬇️and BUN/Cr is ⬆️
You personally wedge #PAC at bedside and obtain a mean wedge 17 mmHg (a normal mean wedge is 6-10 mmHg). Admission wedge was 24
Himanshu Rawal MD retweeted
🩻Contrast-induced AKI:
one of the biggest myths still shaping clinical decisions
For decades we were taught:
👉 “Contrast damages the kidneys”
👉 “Avoid CT with contrast in CKD”
👉 “Hydrate, protect, delay imaging if needed”
But what if… most of this is wrong?🤔
->The uncomfortable reality
Modern evidence shows:
👉 Low-osmolar contrast rarely causes true nephrotoxicity
👉 Even in CKD, AKI, and ICU patients
👉 The risk is often overestimated—or nonexistent
So where did the fear come from?
📍 1950s high-osmolar contrast (actually toxic)
📍 Poorly controlled observational studies
📍 “Creatinine rise = contrast injury” assumption
👉 Correlation became causation
👉 And the dogma stayed
⚠️What recent data tells us
✔ No difference in AKI rates with vs without contrast
✔ No benefit from bicarbonate, NAC, or aggressive hydration
✔ Even ICU and AKI patients show no worsening outcomes
->Translation to real life
👉 The patient was going to develop AKI anyway...Not because of contrast!!
->The real problem: “Renalism”
👉 Avoiding necessary imaging
👉 Delaying diagnosis
👉 Choosing inferior tests
And that leads to:
❌ Missed PE
❌ Delayed sepsis source control
❌ Worse outcomes
->Clinical mindset shift
Instead of asking:
👉 “Will contrast harm the kidneys?”
We should ask:
👉 “Will NOT doing the scan harm the patient?”
->Who still deserves caution?
✔ eGFR <30
✔ Severe hemodynamic instability
✔ Multiple nephrotoxins
Even then:
👉 Optimize volume
👉 Minimize dose
👉 Don’t delay critical imaging
🤓Bottom line
✔ Contrast nephrotoxicity exists… but is rare
✔ The fear is bigger than the risk
✔ The harm of NOT imaging is often greater
In critical care
👉 We don’t treat creatinine
👉 We treat patients
And sometimes…
👉 The most dangerous thing is NOT the contrast
👉 It’s hesitation.
📃Reference
Florens N, Demiselle J.
Kidney360 7: 445–449, 2026. doi: doi.org/10.34067/KID.0000001…
Himanshu Rawal MD retweeted
🫀The failing right ventricle:
the most misunderstood chamber in critical care
For years, we focused on the left ventricle.
But in the ICU, the real killer is often the right ventricle.
->What is acute RV failure?
👉 Not just “weak contraction”
It’s a hemodynamic collapse syndrome:
RV dilation
↓ LV preload
↓ cardiac output
↑ venous congestion
➡️ → multi-organ failure
->The key pathophysiology (the vicious cycle)
1. ↑ Afterload (PE, ARDS, PH)
2. → RV dilation
3. → Septal shift → LV underfilling
4. → ↓ CO → hypotension
5. → ↓ RCA perfusion
6. → RV ischemia
👉 And the cycle accelerates
->The most important concept
👉 The RV does NOT tolerate pressure
Handles preload very well
Fails rapidly with afterload
➡️ Even small ↑ PVR → collapse
->Main causes you MUST think first
🔴 Pulmonary embolism
🔴 RV myocardial infarction
🔴 ARDS / mechanical ventilation
🔴 Decompensated pulmonary hypertension
🔴 Post-cardiac surgery
->Diagnosis is NOT obvious
There is no single sign.
👉 It requires suspicion + integration:
Clinical: congestion + hypoperfusion
ECG + biomarkers
POCUS (your best friend 🤓)
Hemodynamics
->Echo mindset (fast ICU approach)
👉 Don’t overcomplicate
Look for:
✔ RV dilation
✔ Septal shift (D-sign)
✔ TAPSE ↓
✔ Venous congestion
The real ICU mistake
❌ Treating RV failure like LV failure
->Management principles
👉 Think in 4 pillars:
1. Preload — “not too much, not too little”
Hypovolemic → small fluid
Congested → REMOVE fluid
👉 CVP is not a target, it’s a warning
2. Afterload, THE key target
✔ Treat PE
✔ Optimize ventilation
✔ Reduce PVR
👉 If afterload stays high → RV will fail
3. Contractility
Dobutamine
Milrinone
Levosimendan
👉 Choose based on context
4. Perfusion pressure
👉 Norepinephrine is your anchor
✔ Maintains coronary perfusion
✔ Supports RV function
->Ventilation: the silent killer
⚠️ Positive pressure = ↑ PVR
👉 Over-ventilate → worsen RV failure
->When nothing works
👉 Think early:
VA-ECMO
RV assist devices
🤓Key insight
This is NOT just a cardiac problem.
👉 It is a ventriculo–arterial coupling failure
When:
Ees / Ea ↓ → RV collapses
🤓Bottom line
✔ RV failure is preload dependent BUT afterload sensitive
✔ Small mistakes → rapid collapse
✔ Early recognition + physiology-based treatment saves lives
->Clinical mindset
👉 Don’t ask:
“Is the RV failing?”
👉 Ask:
“Why is the RV failing and, what is driving the afterload?”
📃Reference
Giannakoulas G. et al. European Heart Journal (2025) 00, 1–16 doi.org/10.1093/eurheartj/eh…





































