consultant in ICM&anaesth.; POCUS: FAMUS+FUSIC supervisor, FUSIC heart, CACTUS lung mentor; regional anaesth.; airway lead; retired ATLS/ETC/ALS/GIC instructor

Redhill, England
Joined November 2018
some says #POCUS answers (to the basic #FICE #CUSIC #FAMUS questions) are binary: yes/no. but imo there must be 3: - yes - no - i don’t know 3rd is not cool, but absolutely valid and most importantly: safe
We need to teach how doubt is not to be feared but welcomed. It's OK to say, "I don't know."
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🚆 Heading to DAS Wales 2026? Save with special Great Western Railway fares to Newport! Join us at ICC Wales, 11–13 November, to shape the future of airway management. Register now and secure your place! Plan your journey: das2026.co.uk/travel #DAS2026
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Mátyás Andorka retweeted
The programmes for the 23rd ACCS and 16th Ultrasound in Acute Care for April next year is done and sent to the faculties for approval. There may be some conflicts and will be addressed as soon as it is known. It took more than 8 days to do the programme. It looks good. The programme covers two keynote addresses by Prof Joana Berger-Estilita and Prof Sadie Diamon-Fox (Workplace Environment, Culture, and Well-being in Healthcare and Language Models and AI in healthcare and research) We have five pro-con debates done by the experts and two mini meetings with in this meeting - Mini IFAD and Mini IWin. The programme covers the entire ICU topics including rehabilitation, end of life care, research for the young and many more. What are you waiting for? come and join us. Programmes and online registration will be available by the end of the week at critcaresymposium.co.uk
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Mátyás Andorka retweeted
#Urosepsis - complicated UTI: 10 high-yield ICU pearls #004 Some colleagues hate the term “urosepsis.” I’m not going to die on that hill. I think we have more important things to worry about, like what to do when a crashing-and-burning patient arrives in our ICU from the ED, or returns from the OR, with urosepsis. Oops, I did it again! The antibiotics are running, the fluids are in, the MAP looks better... but the infected kidney may still be obstructed. We may have improved the numbers without fixing the problem. Here are my 10 high-yield pearls. At least I hope they’re worth remembering: 1. An infected, obstructed kidney is an emergency Think of it as an abscess that cannot drain. We give antibiotics, fluids, vasopressors. The blood pressure improves and we feel better. But the kidney is still infected and obstructed. Infected obstruction means urgent decompression. 2. No hydronephrosis doesn’t mean no obstruction Hydronephrosis may be minimal or even absent, particularly early in the course or in a severely dehydrated patient. Ultrasound can miss ureteral stones; noncontrast CT gives us a better look at their size, location, and associated obstruction. And don’t dismiss a stone because it’s tiny. Even a 1-2 mm stone in the ureter can obstruct an infected kidney and cause major trouble. It’s not the size of the stone. It’s where it is and what it’s obstructing. 3. A clean urinalysis doesn’t exclude an infected kidney Uncommon, but if you’ve been in the game as long as I have, you’ll probably see it. With complete ureteral obstruction, infected urine may be trapped above the stone while the bladder urine looks surprisingly clean! The opposite trap exists too: bacteriuria plus a stone doesn’t prove the urinary tract is the source. Keep looking for another one. Treat the patient, not the urine dipstick. 4. Source control cannot wait until morning A patient with sepsis from an infected, obstructed kidney needs drainage urgently. If they arrive in the middle of the night, this may mean calling urology or IR at 3:00 am. Nobody loves those calls, but sometimes they simply cannot wait. Even a relatively stable patient with suspected infected obstruction needs urgent assessment and a drainage plan. The clock matters. Unfortunately, it doesn’t care what time it is. 5. Stent or nephrostomy? The best one is the one that drains A ureteral stent drains internally from the renal pelvis to the bladder; a percutaneous nephrostomy drains the collecting system through the flank. Which is better? It depends: anatomy, bleeding risk, anesthesia, technical feasibility, local expertise, and availability. At 3:00 am, that last one suddenly matters a lot! Either approach can be difficult or fail. An impacted stone may be impossible to cross, and distorted anatomy can hide the ureteral orifice. Nephrostomy can be tricky with minimal dilation, difficult access, body habitus, or bleeding risk. Don’t debate the perfect technique. Have a rescue plan. 6. Nephrostomy often means prone. Plan the airway first Before sending a critically ill patient to IR, ask: Can they tolerate the position? Can IR do it supine-oblique in this patient? What happens if they deteriorate? Would securing the airway beforehand be safer? You don’t want to code your patient in the IR suite. Trust me on this one! Decide on the airway before the patient is face-down. 7. Antibiotics: look back before you look forward Get blood and urine cultures early, preferably before antibiotics, but never at the expense of delaying treatment in septic shock. In patients with recurrent UTIs, prior instrumentation, stents, or multiple admissions, I always want to know what grew last time, and the time before that. And to my anesthesiology friends: please don’t automatically give cefazolin (Ancef) to the patient coming for a stent exchange who has already had five admissions with MDR Acinetobacter and Pseudomonas. Check the old cultures. Yesterday’s microbiology may guide today’s antibiotics. 8. Decompression doesn’t always mean immediate improvement The patient goes for drainage and we expect things to turn around. Instead, they come back looking considerably worse. Sometimes this is progression of severe sepsis; bacteremia and manipulation of an infected collecting system may also contribute. Excessive irrigation or contrast injection can raise intrarenal pressure, another reason to be cautious. Source control is essential, but don’t be surprised if the patient gets worse before getting better. 9. Still septic after a stent? Question the drainage The antibiotics are in. The stent was placed. Yet the fever persists, pressor requirements are climbing, or organ dysfunction is worsening. Before blaming “sepsis,” ask: Is the stent where it should be? Has it migrated? Is the kidney actually draining? A KUB can check stent position; ultrasound or CT can look for persistent obstruction or another source. Sometimes it’s not that treatment needs more time. It’s that source control was never achieved. A stent in the procedure note doesn’t guarantee a drained kidney. 10. Drain the infection first. Deal with the stone later. The emergency procedure is about drainage, not winning the battle against the stone. Drain the kidney, treat the infection, stabilize the patient, then deal with the stone. And stents and nephrostomy tubes need a plan too: follow-up, exchange, or removal. We may be done with the ICU part of the story, but the patient isn’t necessarily done with the problem. Sometimes the most important thing in the ICU is recognizing when antibiotics are not enough. #foamed #foamcc
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🧠 Registration now open for the FUSIC® & CACTUS® Neuro Beginners Courses, November 2026 📅 Monday 9 and Tuesday 10 November (one-day course, run on each date) 📍 UCLH Education Centre, 250 Euston Road, London 👥 20 places per course Learn the fundamentals of NeuroPOCUS for critical care with an expert faculty of adult and paediatric NeuroPOCUS specialists from across the UK. ✅ More hands-on scanning time to refine your technique, using Philips Healthcare machines ✅ Dedicated adult and paediatric stations ✅ Registration (£350) includes ongoing monthly webinars and remote mentoring via the Presuna platform, supporting you through to accreditation Course Directors: Dr Manni Waraich & Dr Bogdana Zoica Open to clinicians from all backgrounds: ICM, anaesthesia, emergency medicine, acute medicine, prehospital care, stroke, hepatology, cardiology, neuroradiology and neurosurgery 🧠 To register, email [email protected] with your current clinical grade and level of ultrasound experience, and we will send you the payment link. #NeuroPOCUS #FUSIC #CACTUS
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Mátyás Andorka retweeted
Is it a surprise that there are so many concerns with LAST with continuous SPIP blockade? Fig 1. Blue dot: ribs Large white dot: major arterial perforators Fig 2. Black dot = ITA perforators Fig 3. Coronal section Br J Plast Surg. 1986; 39: 287-99
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Mátyás Andorka retweeted
Heading home from @EBPOM Dingle. Outstanding quote of the conference
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🫀Diastolic pressure in septic shock: MAP tells us how low the pressure is. DAP may help explain why. The 2026 Surviving Sepsis Campaign recommends an initial MAP target of 65 mmHg and norepinephrine as first line vasopressor therapy. But Sanchez Escalante and Teboul highlight an important physiological gap: the guidelines do not specify how arterial pressure should help us decide when norepinephrine is actually needed. Septic hypotension is not a single phenotype. A MAP of 55 mmHg may result predominantly from vasoplegia, low cardiac output, or both. Treating these situations identically makes little physiological sense. This is where diastolic arterial pressure (DAP) becomes useful. DAP is strongly influenced by arterial tone, but also by heart rate and arterial compliance. In a hypotensive patient with hypoperfusion, a very low DAP, for example <50 mmHg, can therefore support the hypothesis that loss of vascular tone is an important component of shock. The authors also discuss the diastolic shock index, HR/DAP, as another way of integrating vascular tone with heart rate. The therapeutic implication is compelling: MAP <65 + DAP <50 + hypoperfusion: vasoplegia is likely important → consider early norepinephrine. MAP <65 + DAP >50 + hypoperfusion: low cardiac output may contribute more → assess fluid responsiveness and cardiac function rather than reflexively escalating norepinephrine. Recent observational data strengthen this hypothesis. Norepinephrine started within 25 minutes was associated with more favorable outcomes when DAP was <50 mmHg, while the same association was not observed with higher DAP. Importantly, this does not establish causality or validate 50 mmHg as a universal threshold. And DAP should not replace MAP. MAP remains the principal perfusion pressure target. DAP instead provides phenotypic information that may help determine what is producing the hypotension. Its interpretation must consider heart rate, age, arterial stiffness and aortic regurgitation. MAP can remain our first target while DAP, capillary refill time, pulse pressure, fluid responsiveness and echocardiography help us identify the mechanism and choose the treatment. That is the transition from protocol driven resuscitation toward physiology guided hemodynamic phenotyping. Reference 📚 Sanchez Escalante C, Teboul JL. 2026. Am J Respir Crit Care Med. doi.org/10.1093/ajrccm/aamag… #CriticalCare #Sepsis #SepticShock #Hemodynamics #Vasopressors #Norepinephrine #PrecisionMedicine
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Mátyás Andorka retweeted
We do use it a LOT for rib fractures, but it’s also got loads of other indications. What’s your best use case for serratus plane block? Where are you getting the most success? If you haven’t used it all that much, here’s a new video that goes over the anatomy and how-to in detail: #Blocktober26 youtu.be/xoGnhgz_j4U?si=TVtw…
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So if you choose to do a more distal brachial plexus approach, especially with reduced volumes, it’s super easy to quickly add in a separate cervical plexus block. You’re RIGHT THERE anyway. And it’s slick and easy. Just slip the needle into the space between the sternocleidomastoid and the pre vertebral fascia covering the scalene muscles. That’s where the cervical plexus lives. And you can see here just how close it is to the interscalene nerve roots. #Blocktober26
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Mátyás Andorka retweeted
So while the muscle, fascia, and periosteum of the shoulder were likely well-covered by the brachial plexus block, the skin clearly wasn’t, which is why the patient jumped. But wait, we’ve done awake shoulder surgery before with brachial plexus block and everything was fine…what happened here?! It probably has to do with volume and location. With a true interscalene block, you’re sufficiently high up in the neck that any decent volume of local anesthetic is likely to cover not just C5 and C6, but spread up to C4 and C3, thereby blocking the cervical plexus. Not always the case with a more distal brachial plexus approach... #Blocktober26
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Daily reminder that fluid responsiveness is a normal physiologic state. Fluid unresponsiveness is someone tipping (or already in) to heart failure
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11 new Lung US accredited Physios in the UK & ROI n = 319 9 new Lung US Physio trainers/mentors n = 102 @ICS_updates @POCUS_CACTUS @ESICM @FAMUSultrasound @TheACPRC @WINFOCUS
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Mátyás Andorka retweeted
POCUS was drowning in the main feed. It has a home now. 🦇 Posters. Infographics, clip libraries. The blogs. Pop them in your Gel bag! 👇👇 icuwaveform.grok.me/pocus Open the site. Hit Follow the Waveform. That’s the sign-up. ⏺️ #FOAMed #FOAMcc #CriticalCare
🤖 Made with AI
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Mátyás Andorka retweeted
ICU literature never sleeps. You do. 😴 Waveform sifts the papers, the FOAMed and what’s actually buzzing, live, so you stop trawling at 23:00! 👍 Free..from Critical Care Northampton. Follow it....👇 icuwaveform.grok.me #POCUS #FOAMcc #FOAMed
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❤️Echocardiography in shock: stop asking only “What is the EF?” In undifferentiated shock, echocardiography is most useful when it answers physiological questions, not when it simply describes cardiac anatomy. Colebourn and Fisher propose a pragmatic 5 question framework for approaching the shocked patient: 1. What are the stroke volume and cardiac output? Start with flow. Importantly, cardiac index is not a binary marker of shock. A patient may maintain cardiac output through tachycardia despite a low stroke volume, while another may have low output because bradycardia prevents compensation. SVI, CI, heart rate and rhythm therefore need to be interpreted together. 2. If output is abnormal, why? LV failure? RV failure? Low preload? Valve disease? Mechanical complication? Obstruction? And do not forget dynamic LVOTO. Critical illness can combine low LV volume with hypercontractility, and escalating vasoactive support without recognising LVOTO may paradoxically worsen shock. This is also where LVEF can mislead us. A “normal” EF does not guarantee adequate forward flow. EF depends on LV volume and afterload and does not distinguish forward from regurgitant stroke volume. Vasoplegia may even make LV systolic function appear reassuring until vascular tone is restored. 3. Is left atrial pressure elevated? E/e′ >14 may support elevated LAP in general ICU populations, but performs less reliably in cardiogenic shock and should not be interpreted alone. A normal LA size does not exclude an acute rise in LAP. 4. Are pulmonary pressure and PVR elevated? Now the assessment moves to the RV pulmonary circulation interaction, where pressure, afterload and RV adaptation matter. 5. How is the situation evolving? Perhaps the most important question. The echo we see is not the patient's fixed cardiovascular phenotype. It is the heart under the current preload, afterload, vasoactive therapy and ventilatory conditions. Noradrenaline can increase BP while decreasing SV in one patient, yet increase both BP and SV in another. This is why critical care echocardiography should increasingly be thought of as: Flow → Mechanism → Filling pressures → RV pulmonary circulation → Response over time Not a photograph. A dynamic physiological assessment. This paper represents pragmatic expert guidance rather than a validated diagnostic algorithm. Reference📚 Colebourn C, Fisher R. A structured 5-question approach for echocardiographic evaluation of undifferentiated shock. Echo Res Pract. 2026;13:30. doi.org/10.1186/s44156-026-0… #CriticalCare #Echocardiography #POCUS #Shock #Hemodynamics #Cardiology #IntensiveCare
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