Rohit Patnaik

D.M. Critical Care, Intensivist, Avid Reader, Cricket buff #zentensivist #ultrascoundrel #pocusmaniac #clinicalproblemsolver

[Internal Medicine @pgMedicine]

ALL, AML, CML and CLL

[Philippe Rola @ThinkingCC]

No. Check for tolerance first. Responsiveness does not equal need, nor benefit. Maximizing output was shown decades ago to not be a viable strategy. Optimize tissue perfusion. Learners, please reconsider a forward-flow-centric approach. Focus on tissue perfusion, and the two do NOT have a linear relationship. Understand hemodynamic interfaces. Ping @icmteaching @khaycock2 @EMNerd_ @edu_kattan @ross_prager

[Rafael Sirera @ProfSirera]

Urine Albumin-to-Creatinine Ratio (UACR) has largely replaced traditional microalbuminuria measurement in modern practice because it is simpler, reliable, and more practical for population screening, especially in patients with diabetes or hypertension. Microalbuminuria remains relevant as a historical concept or when 24-hour urine collections are specifically required.

[Rohit @ai_rohitt]

INSTEAD OF WATCHING AN HOUR OF NETFLIX TONIGHT.

This 1 hour Stanford lecture by Joel Peterson will teach you more about negotiation and getting what you want than most people learn in years.

Bookmark it and give it an hour, no matter what.

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🧠 Hypertonic Saline or Mannitol for Cerebral Edema?

Cerebral edema and intracranial hypertension remain among the most common life-threatening problems in neurocritical care. The Neurocritical Care Society guideline provides several practical bedside recommendations.

🔹 Hypertonic saline (HTS) is generally preferred over mannitol for acute ICP control in TBI and intracerebral hemorrhage due to more reliable and sustained ICP reduction.

🔹 Both HTS and mannitol effectively reduce ICP, but neither has consistently demonstrated improved long-term neurological outcomes.

🔹 In subarachnoid hemorrhage, symptom-triggered HTS boluses are favored over targeting a specific serum sodium concentration.

🔹 In acute ischemic stroke, either HTS or mannitol may be used, but routine prophylactic mannitol administration is discouraged.

🔹 Corticosteroids should not be used for intracerebral hemorrhage, as evidence suggests no benefit and potential harm.

🔹 The major exception is bacterial meningitis, where dexamethasone reduces neurological sequelae and should be administered before or with the first antibiotic dose.

⚠️ Safety matters. Severe hypernatremia (>155–160 mEq/L) and hyperchloremia (>110–115 mEq/L) are associated with increased risk of acute kidney injury and require close monitoring.

Take-home message: Hyperosmolar therapy remains a cornerstone of cerebral edema management, but treatment should be individualized according to the underlying neurological pathology rather than pursuing arbitrary sodium targets.

#NeurocriticalCare #ICU #CriticalCare #TBI #Stroke #SAH #ICH #CerebralEdema #HypertonicSaline #Mannitol #NeuroICU

Reference 📚

Cook AM, Jones GM, Hawryluk GWJ, et al. Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients. Neurocrit Care. 2020;32:647-666. DOI: 10.1007/s12028-020-00959-7.

[IMCrit @IM_Crit_]

Our reaction to any new study is either “I don’t believe it” or “I knew it”...
A NEJM trial in ICU pts w acute resp failure found that mucolytics (carbocisteine & hypertonic saline) don’t help. My ICU rounds line “mucolytics are useless” may need an update: “and possibly harmful”

[CardiovascularCorner @TrackYourHeart]

Echocardiographic evaluation of LV diastolic function made simple by ASE😍

[Dr. Chacón-Lozsán F .'. @franciscojlk]

🫀 The Most Dangerous Moment in the ICU May Last Less Than 60 Seconds

We often think of tracheal intubation as an airway procedure. Physiologically, it is a profound cardiovascular intervention.

Why Do ICU Patients Crash During Intubation?

The problem begins before the laryngoscope enters the mouth.

Many critically ill patients survive on a fragile compensatory state characterized by:
🔹 Endogenous catecholamine surge
🔹 Tachycardia
🔹 Vasoconstriction
🔹 Increased myocardial oxygen demand

What appears to be "stable" hemodynamics may actually represent physiological exhaustion.

The moment induction drugs are administered, this compensatory sympathetic drive disappears.

The result? A sudden reduction in:
• Systemic vascular resistance
• Cardiac output
• Coronary perfusion pressure
• Organ blood flow

This phenomenon has been termed adrenergic collapse.

Intubation Is a Hemodynamic Timeline

The authors propose viewing intubation as a sequence of cumulative threats rather than a single procedure:
1️⃣ Pre-induction adrenergic dependence
2️⃣ Sympatholysis after induction
3️⃣ Apnea, hypoxemia, hypercapnia, and acidosis
4️⃣ Transition to positive-pressure ventilation
5️⃣ Post-intubation ventilator and sedation effects

Each phase adds physiological stress.

Together, they can culminate in cardiovascular collapse.

The Propofol Question

One of the most clinically relevant findings is the growing evidence regarding induction agent selection.

In the INTUBE cohort, propofol was associated with a higher risk of cardiovascular collapse and was the only modifiable risk factor consistently identified.

The review therefore suggests:
✅ Ketamine
✅ Etomidate
as preferred induction agents in patients at risk of hemodynamic instability, while propofol should be used cautiously in shock states.

Positive Pressure Ventilation: The Forgotten Hemodynamic Challenge

Once the tube is secured, many clinicians relax.

The physiology is only beginning.

Positive-pressure ventilation:
🔹 Reduces venous return
🔹 Increases intrathoracic pressure
🔹 Raises right ventricular afterload
🔹 May precipitate right ventricular failure

This is particularly relevant in ARDS, pulmonary hypertension, pulmonary embolism, and severe hypoxemic respiratory failure.

Reference 📚

Kotani Y, Koroki T, Hayashi Y, Russotto V. The hemodynamics of tracheal intubation in critically ill patients: a narrative review. Journal of Intensive Care. 2026;14:42. DOI: 10.1186/s40560-026-00877-4.

[Critical Care Reviews @CritCareReviews]

Today's Paper of the Day is:

Lung fuction impairment following cerebral ischemic stroke: Pathophysiology, mechanisms, and clinical challenges

https://t.co/JKgcYjlUQ5

Join us to read 1 paper per day and stay up-to-date as we cover the spectrum of critical care across 2026

[NephroPOCUS @NephroP]

How to do SVC #POCUS 📹 + an illustration of abnormal SVC Doppler patterns.
#VExUS #eVExUS #Nephpearls
From 🔗J Am Soc Echocardiogr. 2023;36(5):447-463. doi: 10.1016/j.echo.2023.01.017

[Critical Care Reviews @CritCareReviews]

#CCR26 #VICTORYtrial published now in @JAMA_current, with @seymoc (Associate Editor for Critical Care, JAMA) chairing this session in Belfast!

https://t.co/iVwisFFlwP

[𝘈𝘯𝘢𝘦𝘴𝘵𝘩𝘦𝘴𝘪𝘢 @Anaes_Journal]

Is it time for an objective classification for difficult facemask ventilation?

Introducing the MASCAN score!

#anaesthesia #MedTwitter

https://t.co/gac3kdGSdp

[NephroPOCUS @NephroP]

Pleased to have had the opportunity to write this CJASN editorial @asnpublications on the USE-the-FORCE-for-Acute Kidney Injury trial by our Canadian colleagues.
🔗https://t.co/3ouwPLv2wZ
I'm especially glad to see mainstream #nephrology journals taking interest in multi-organ #POCUS. Even better, I managed to sneak my proprietary hemodynamic circuit illustration into the article!!

[Critical Care Reviews @CritCareReviews]

Extracorporeal Membrane Oxygenation in Refractory Cardiac Arrest: Current Evidence, Clinical Pathways and Future Directions  

CCR Journal Watch
https://t.co/Sp06oA6IDG

[MedicoNotes @MedicoNotes]

🧠 Stroke Localization Made Simple

⸻

1️⃣ MCA Stroke (Middle Cerebral Artery)

➊ Face & arm weakness > leg weakness
➋ Contralateral sensory loss
➌ Dominant side → Aphasia
➍ Non-dominant side → Neglect

💡 Remember:
MCA = “M” for Mouth & aRM involvement

⸻

2️⃣ ACA Stroke (Anterior Cerebral Artery)

➊ Leg weakness > arm weakness
➋ Personality changes
➌ Abulia (loss of motivation)
➍ Urinary incontinence

💡 Think:
ACA affects the medial brain → lower limb area

⸻

3️⃣ PCA Stroke (Posterior Cerebral Artery)

➊ Contralateral homonymous hemianopia
➋ Visual symptoms
➌ Alexia without agraphia
➍ Macular sparing

💡 Classic clue:
“I can write… but I can’t read”

⸻

4️⃣ Lateral Medullary Syndrome (PICA)

➊ Dysphagia & hoarseness
➋ Vertigo, nystagmus, ataxia
➌ Ipsilateral facial sensory loss
➍ Contralateral body pain/temperature loss
➎ Horner syndrome

💡 Crossed findings = brainstem lesion

⸻

5️⃣ Medial Medullary Syndrome (ASA)

Remember the “3 M’s”:

➊ Medial lemniscus → ↓ vibration/proprioception
➋ Motor pathway → contralateral weakness
➌ Medulla CN XII → tongue deviation

⸻

🎯 Stroke localization becomes easy when you recognize the pattern!

📚 Master neurology with our high-yield Neurology Book 🧠
Available now at:

🌐 https://t.co/2UQyCbb6in

#Neurology #Stroke #MedEd #USMLE #Medical

[Critical Care Reviews @CritCareReviews]

When Mechanical Power Remains High Despite Conventional Lung-Protective Settings: A Physiology-Driven Bedside Framework  

CCR Journal Watch
https://t.co/Sp06oA6IDG

[Critical Care Reviews @CritCareReviews]

Today's Paper of the Day is:

Advances in achieving lung and diaphragm-protective ventilation

https://t.co/JKgcYjlUQ5

Join us to read 1 paper per day and stay up-to-date as we cover the spectrum of critical care across 2026

[NephroPOCUS @NephroP]

#POCUS #echofirst #Nephpearls
RVOT pulse-wave Doppler can provide useful clues about pulmonary vascular resistance.
In normal individuals (A), the waveform has a smooth, dome-shaped appearance, with peak velocity occurring in mid-systole, reflecting a compliant, low-resistance pulmonary circulation.
As RV afterload increases, the waveform gradually becomes more triangular. The RVOT acceleration time shortens, and the peak velocity shifts earlier into systole (B).
With further increases in pulmonary vascular impedance and reduced arterial compliance, a characteristic mid-systolic notch may appear (C), creating the classic "W sign."
In advanced pulmonary hypertension with RV failure, the Doppler envelope becomes smaller and more abbreviated, with a very short and steep AccT (D). This reflects rapid equilibration of RVOT and proximal pulmonary artery pressures due to severe afterload elevation.
Like most POCUS findings, RVOT Doppler should be interpreted in the context of the overall echocardiographic picture rather than in isolation.

[Ross Prager @ross_prager]

https://t.co/5inbAYKy2C

[NephroPOCUS @NephroP]

The 60/60 sign is a cardiac #POCUS finding used to support the bedside diagnosis of acute pulmonary embolism. It refers to the simultaneous presence of two measurements, both involving the number 60.

RV outflow tract (RVOT) acceleration time ≤60 ms - This is the time from the onset of blood flow through the pulmonary valve to its peak velocity. In acute PE, the sudden obstruction causes blood to accelerate and decelerate abnormally fast, producing a "truncated" or shortened flow profile.

Pulmonary artery systolic pressure (PASP) ≤60 mmHg (but >30 mmHg) - estimated via the tricuspid regurgitation jet.

In acute PE, the thin-walled right ventricle cannot generate very high pressures because it has not had time to adapt. A PASP above 60 mmHg suggests a chronic process (e.g., chronic pulmonary hypertension) where the RV has hypertrophied over time