
🇮🇹 Internist working in IMCU. Innate passion for learning 👨🏻💻. ❤️ #POCUS, #CriticalCare and anything with caffeine☕. Supporting #FOAMed ☄️.
Piacenza, Emilia Romagna
Joined May 2011
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...🧵This is a thread about 8.4% sodium bicarbonate (aka bicarb amp) in critical care.
This the first part in a series of three about sodium bicarbonate 🧂in critical care:
🧐I will get in deep to complexities, benefits, risks and clinical implications of this (overused) drug.
😱 Can you believe these serum sodium and osmolarity levels are real? 😅 🧂
Which is your personal record? 🇮🇹
@IM_Crit_ @icmteaching @kidney_boy @iceman_ex @ross_prager @ThinkingCC @cliffreid @drshahrul80 @eddyjoemd @FH_Verbrugge @intensivaev @nickmmark @NephroP @lzavorszky
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Helmet NIV - the 🇮🇹 experience.
Highly recommended lecture by @DomGrieco at @ISICEM 2026.
youtu.be/ENhGUtzRUAA?is=A8RP… – at Piacenza, Emilia Romagna
@IM_Crit_ @iceman_ex @icmteaching @emcrit @CriticalCareNow @PulmCrit @giovannilandoni @nickmmark @ross_prager @ThinkingCC – at Piacenza, Emilia Romagna
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You can guess potassium level by looking at EKG 😅 🦈.
> loss of P waves
> STEMI - like pattern V1-V3 (shark fin)
@smithECGBlog @IM_Crit_ @PulmCrit @iceman_ex @ThinkingCC @EM_RESUS – at Piacenza, Emilia Romagna
🚨Alarm bells always go off when I see “cellulitis with septic shock”. It’s either nec fasc with septic shock or toxic shock syndrome.
#criticalcare – at Piacenza, Emilia Romagna
🦠 Recently I faced a refractory septic shock in cellulitis due to suspected TSS.
My key points (@emcrit) ✍️:
🔑 shock out of proportion to the infectious focus. Most patients with cellulitis don't develop septic shock – so this is unusual and suggests toxic shock syndrome.
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📜 The monitor often tells only a part of the story...📜
💡AF in acute care is rarely “just an arrhythmia.” It is a window into the patient’s underlying physiology.
👁️In acute critical care every episode of AF deserves a search for the trigger before a search for the right drug.
🔥The challenge is determining whether the arrhythmia is the culprit—or merely a witness to a much larger physiological crisis.
👇🏻
open.substack.com/pub/drarih… – at Piacenza, Emilia Romagna
any critical care pearl? @IM_Crit_ @iceman_ex @msiuba @Wilkinsonjonny @PulmCrit @icmteaching @nickmmark @ross_prager @ThinkingCC – at Piacenza, Emilia Romagna
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📜 A critical care tale📜
💬 "It's not always sepsis fault."
👉🏻 unclear clinical picture consisting of overwhelmimg AKI and thrombocytopenia should prompt you considering TMAs (aHUS, STEC-HUS, TTP).
journal.chestnet.org/article… – at Piacenza, Emilia Romagna
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"The first physician to see the patient often makes the decision that matters the most." #criticalcare – at Piacenza, Emilia Romagna
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💥2026 IDSA UPDATE on the Treatment of AntimicrobialResistant Gram-Negative Infections.💥
My take-home messages:
👉🏻Any gram-negative organism has the potential to carry ESBL genes; however, they are most prevalent in Escherichia coli, Klebsiella pneumoniae, and Klebsiella oxytoca. Routine ESBL testing is not performed by most clinical microbiology laboratories and is not considered compulsory by the CLSI[21]. Rather, E. coli, K. pneumoniae, or K. oxytoca isolates resistant to ceftriaxone (i.e., ceftriaxone minimum inhibitory concentrations [MICs] ≥4 µg/mL) is a threshold commonly acknowledged as a surrogate for ESBL-production.
👉🏻 If piperacillin-tazobactam is initiated as empiric therapy for an uUTI caused by an organism subsequently identified as an ESBL-E and the patient demonstrates clinical improvement, neither a change in therapy nor an extension of treatment duration is necessary. The panel suggests piperacillin-tazobactam as an alternative treatment option for
cUTI caused by ESBL-E in patients who are not critically ill and who do not have concomitant bacteremia. In contrast, piperacillin-tazobactam is not suggested for the treatment of ESBL-E
infections at sites outside of the urinary tract, even when in vitro susceptibility to piperacillin tazobactam is demonstrated.
👉🏻 Cefepime is suggested for the treatment of infections caused by organisms at moderate risk of significant AmpC production (i.e., E. cloacae complex, K. aerogenes, C. freundii, H. alvei), if cefepime MICs are in the susceptible or susceptible dose-dependent range (i.e., ≤8 µg/mL) and provided an ESBL gene has not been identified.
👉🏻 Ceftriaxone (or cefotaxime or ceftazidime) is not suggested for the treatment of invasive infections caused by organisms at moderate risk of clinically significant AmpC production (i.e., E. cloacae complex, K. aerogenes, C. freundii, H. alvei). In cases of non-severe infection in which ceftriaxone was initiated empirically, and the patient demonstrates clinical improvement with adequate source control, continuation of ceftriaxone to complete the treatment course may be reasonable.
👉🏻 Piperacillin-tazobactam is not suggested for the treatment of invasive infections caused by Enterobacterales at moderate risk of clinically significant inducible AmpC production. In light of the limited ability of tazobactam to protect piperacillin from AmpC hydrolysis in vitro and at least a few observational studies suggesting poorer clinical outcomes with the use of piperacillin-tazobactam compared to cefepime/carbapenems, the panel suggests caution with
prescribing piperacillin-tazobactam for serious infections caused by AmpC-E.
👉🏻 For patients who are critically ill and/or have hypoalbuminemia, imipenem or meropenem are preferred over ertapenem. In contrast to imipenem and meropenem, ertapenem is highly protein bound, resulting in a prolonged serum half-life[83]. In patients with hypoalbuminemia, the unbound fraction of ertapenem increases, leading to enhanced clearance and a shortened serum half-life.
🔥Meropenem 🔥
> uUTI: 1 grams IV every 8 hours, infused over 30 minutes
> All other infections: 1-2 gram IV every 8 hours, infused over 3 hours (if feasible);
👉🏻 2 g preferred for obesity, central nervous system infections, and extracorporeal membrane oxygenation or CrCL ≥130 mL/min . – at Piacenza, Emilia Romagna
🔥🔥IDSA AMR Guidance 2026🔥🔥
🔺Notable Updates from the 2024 IDSA AMR Guidance Document
IDSA 2026 Guidance on the Treatment of Antimicrobial-Resistant Gram-Negative Infections
🔺ESBL, AmpC Enterobacterales
🔺CRE
🔺DTR P. aeruginosa
🔺CRAB
🔺Stenotrophomonas maltophilia
Including updates in antimicrobial selection, dosing strategies, and management approaches.
🔺Meropenem dosing update: individualized dosing approach (1–2 g IV q8h) with higher doses considered in selected clinical scenarios.
Info inspired / credit to @RabeaAgeeli , #IDXposts
idsociety.org/practice-guide…
Can shock be normotensive?
Shock is perhaps one of the most overused word in acute care.
However, shock and systemic hypotension are not interchangeable concepts.
Firstly, not all shocks are the same: if the phenotype is non-distributive, compensatory endogenous sympathetic hyperactivation may increase SVR, preserving MAP and so masking hypotension.
💡Consider cardiogenic, hemorrhagic and obstructive shock (eg. PE): we may be faced (at least in the hyperacute phase) with normotensive shock.
This concept is important because these patients do not require vasopressors (at least in the hyperacute phase), but rather inotropes, blood transfusions, and thrombolysis, respectively, in order to restore perfusion.
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The dangerous truth:
Some of the sickest patients look deceptively stable early.
#criticalcare
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👉🏻 Let's start talking about "perfusion responsiveness” or “flow-responsiveness” as CRT response to hemodynamic manipulation.
Tips and pitfalls about testing CRT in daily clinical practice?🤔
@ThinkingCC @icmteaching @IM_Crit_ @khaycock2 @katiewiskar @msiuba @nickmmark @ross_prager @NephroP @iceman_ex
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👉 Hemodynamic incoherence =
Persistent microcirculatory failure despite restored systemic hemodynamics
🧠 Shock is not a blood pressure problem...It is a coherence problem.
🚨 New paradigm: Hemodynamic incoherence
👉 You normalize MAP
👉 You fix cardiac output
❌ But the patient is still in shock
💥 Why?
Because macrocirculation ≠ microcirculation
⚡ Definition that changes everything
👉 Hemodynamic incoherence =
Persistent microcirculatory failure despite restored systemic hemodynamics
🧬 The real battlefield is the microcirculation
▪️ Capillaries
▪️ Endothelium
▪️ Glycocalyx
▪️ Cellular oxygen use
👉 Not just MAP and CO
🔥 5 key mechanisms
Shock disrupts microcirculation through:
▪️ Venous congestion
▪️ Vasoconstriction (overdrive)
▪️ Vasoplegia (failure to constrict)
▪️ Endothelial dysfunction
▪️ Microthrombosis
🧩 Game changer: SLOOP phenotypes
🅢 Stasis → congestion, high CVP
🅛 Leakage → capillary leak, edema
🅞 Occlusion → vasoconstriction
🅞 Obstruction → microthrombi
🅟 Paralysis → vasoplegia
👉 Same shock ≠ same physiology
⚠️ Clinical mistake we all make
Treat shock as ONE disease
👉 It is not
🚀 Implication
👉 You can normalize BP and still kill the patient
Because:
👉 Oxygen delivery ≠ oxygen utilization
🛠️ Real bedside approach
👉 Multimodal monitoring:
▪️ Macro (MAP, CO)
▪️ Micro (CRT, PI, HVM)
▪️ Ultrasound (VExUS, cardiac)
▪️ Labs (lactate, endothelial markers)
👉 Integration is mandatory
🔥 Take-home
Shock resuscitation should be:
✔️ Phenotype-driven
✔️ Microcirculation-aware
✔️ Personalized
🚨 Final message
👉 We don’t treat pressure
👉 We don’t treat numbers
We treat perfusion coherence
📚 Huang et al. Shock 2025
doi.org/10.1097/SHK.00000000…
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Increasing systemic blood flow does not reverse tissue hypoperfusion in some patients with septic shock (often in late stages), due to loss of hemodynamic coherence aka macro-to-microcirculatory uncoupling.
Assessing microcirculatory dysfunction is the future of care.
Creatinine is:
▪️ Late
▪️ Diluted by fluids
▪️ Affected by muscle mass
▪️ Misleading in ICU
🧠 AKI is not just creatinine.
And KDIGO 2026 makes that very clear.
🚨 Big shift in thinking
Acute Kidney Injury (AKI):
👉 Is no longer defined only by creatinine rise
Now includes:
✔️ Serum creatinine
✔️ Urine output
✔️ Biomarkers of kidney damage/stress
👉 Even structural injury alone can define AKI
⚠️ The clinical reality
Creatinine is:
▪️ Late
▪️ Diluted by fluids
▪️ Affected by muscle mass
▪️ Misleading in ICU
👉 Meaning:
We diagnose AKI too late
🧬 New paradigm: function + damage
KDIGO 2026 introduces a 3-axis model:
🟠 Functional decline (SCr, urine output)
🔵 Structural injury (biomarkers)
🟣 Time (AKI → AKD → CKD continuum)
👉 This is a major conceptual upgrade
📊 New AKI definition
AKI is present if ANY of the following:
✔️ ↑ SCr ≥0.3 mg/dL in 48h
✔️ ↑ SCr ≥1.5x baseline in 7 days
✔️ ↓ urine output <0.5 ml/kg/h ≥6h
✔️ Positive kidney damage biomarker
🧠 Staging is now multidimensional
Not just creatinine anymore:
▪️ C → Creatinine
▪️ U → Urine output
▪️ B → Biomarkers
👉 A patient can be:
➡️ C0 U0 B1 = subclinical AKI
🔥 Why this matters in ICU
This explains what we see daily:
✔️ “Normal creatinine”
✔️ But worsening outcomes
✔️ Especially in sepsis, surgery, shock
👉 Because injury precedes dysfunction
⚡ Key clinical implications
1. Earlier diagnosis → before irreversible damage
2. Better risk stratification → biomarkers + clinical models
3. Targeted prevention → not one-size-fits-all
4. Dynamic monitoring → AKI is a trajectory, not a moment
🫀 Hemodynamic connection
KDIGO reinforces:
👉 Kidney = perfusion-dependent organ
✔️ MAP ≥65 mmHg as baseline target but Individualized for chronic HTN patients
✔️ Avoid dopamine (finally dead for renal protection) 🙏🏼
👉 Cardio-renal integration is central
💧 Fluid strategy update
✔️ Prefer crystalloids over colloids
✔️ Prefer buffered solutions over saline
✔️ Avoid both overload AND hypovolemia
👉 “More fluids” ≠ better kidneys
🚀 Future direction
KDIGO 2026 is clearly moving toward:
▪️ Biomarker-guided care
▪️ Early phenotyping
▪️ Personalized kidney protection strategies
▪️ Continuum thinking (AKI → AKD → CKD)
🎯 Take-home
AKI is not a number.
👉 It is a dynamic, multidimensional syndrome
And if you wait for creatinine:
👉 You are already late
📚 Reference
Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2026 Jan;109(1S):S1-S99. doi: 10.1016/j.kint.2025.06.006.
❤️🩹☠️ Abiotrophia defectiva subacute endocarditis of bicuspid aortic valve causing severe regurgitation and immuno-mediated phenomena: complement-mediated leukocytoclastic vasculitis and AKI due to glomerulonephritis.
#criticalcare
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👉🏻emdocs.net/emdocs-podcast-ep… – at Piacenza, Emilia Romagna
Refractory septic shock is persistent hypoperfusion in a fluid-unresponsive patient requiring high-dose vasopressors (> 0.5 gamma/kg/min basal norepi equivalent) after appropriate resuscitation and after excluding other causes of shock. – at Assago, Lombardia
🤔When does septic shock become “refractory”?
We have used the term for years.
But until now, we never truly agreed on what it means.
A new joint Delphi consensus from SCCM and ESICM finally brings structure to one of the most critical, and most ambiguous concepts in intensive care
And the message is powerful:
Refractory septic shock is not defined by blood pressure.
It is defined by failed physiology.
Three key takeaways stand out.
->First, tissue perfusion is at the center of the definition.
Not MAP. Not urine output.
But persistent hypoperfusion:
Elevated lactate
Prolonged capillary refill time
Even after adequate resuscitation.
This is a major conceptual shift:
we are moving from pressure-based resuscitation → perfusion-based resuscitation.
->Second, dose matters more than the number of drugs.
The consensus highlights a threshold:
norepinephrine equivalents > 0.5 µg/kg/min
Not how many vasopressors you use,
but how much support is required to maintain circulation.
This reframes severity in a much more physiologically meaningful way.
->Third, and perhaps most important:
Refractory shock requires proof that you did everything right first.
Before labeling a patient as refractory, you must demonstrate:
1.Adequate fluid resuscitation
2.Lack of fluid responsiveness
3.Exclusion of other shock types using critical care ultrasound
->Only then, failure becomes “refractory.”
There is also what the consensus rejects, and this is equally important:
No fixed lactate cutoff
No ScvO₂
No urine output
No strict MAP threshold
Because reality is more complex than a number.
🤓Final definition:
Refractory septic shock is persistent hypoperfusion
in a fluid-unresponsive patient
requiring high-dose vasopressors
after appropriate resuscitation
and after excluding other causes of shock.
Why this matters?
This is not just semantics.
A clear definition means:
Better patient stratification
More meaningful clinical trials
Earlier recognition of the sickest patients
And ultimately, more targeted therapies
Because not all septic shock is the same.
And the sickest patients deserve a name, and a strategy.
📃Reference
Leone M Intensive Care Medicine. 2026.
doi.org/10.1007/s00134-026-0…
Deep dive into central lines management in critically ill patients.🇮🇹 #criticalcare – at Piacenza, Emilia Romagna
























