Right Here, Right Now! A Situational Awareness Framework for Invasive Procedures in Prehospital Care

10 Sep

It is 02:40. You arrive on the scene of a car accident. Your patient is trapped, hypotensive, and combative. You carry the drugs, the airway kit, the blood, and the scalpel. You are trained in all of it. The receiving trauma centre is 40 minutes away by road.

The question is not can you. The question is should you, here, now.

That question is answered badly more often than we admit, and it is almost never answered badly because of a knowledge gap. It is answered badly because of a situational awareness failure. The clinician knows the procedure. What they lose is the picture around it.

Situational awareness is not “being alert”

Endsley’s classic model gives us three levels, and they map onto procedural decisions almost perfectly:

  1. Perception — what is in front of me? Physiology, scene, team, kit, clock, transport time, weather, hazards.
  2. Comprehension — what does it mean? What trajectory is this patient actually on?
  3. Projection — what happens next? What does this patient look like in ten minutes with the procedure, and what do they look like without it?

Level 3 is where invasive procedures are decided. It is also the level that collapses first under stress, task load, and noise. Under pressure we drop back to Level 1, we see the monitor, we see the wound, we reach for the kit, and the projection never happens.

The framework below exists for one reason: to force Level 3 thinking at the moment we are least likely to do it naturally.

Three filters, applied in order

Filter 1 — Indication: does the physiology demand this before definitive care?

Note the wording. The question is not “is this procedure indicated for this condition.” It is “is it indicated in this phase of care.”

Sort your indications into two buckets:

  • Time-critical — the patient deteriorates or dies before arrival without it. Tension pneumothorax. Obstructed or unprotectable airway. Catastrophic external haemorrhage. A pulseless, grossly deformed limb.
  • Deferrable — the receiving team will do it faster, cleaner, and with imaging, lighting, and backup. Central access. Definitive fracture management. Most diagnostics.

Only time-critical indications survive this filter. Everything else stops here, no matter how comfortable you are performing it.

Filter 2 — Opportunity: is there a window where this displaces nothing more important?

This is the most under-used axis in prehospital decision making, and the one where good services differentiate themselves.

Transport time is the master variable. A six-minute run to a trauma centre removes the indication for nearly every on-scene procedure. A sixty-minute rural, mountain, or offshore evacuation restores it. The same patient, the same physiology, two entirely different correct answers. If your protocol doesn’t bend to transport time, your protocol is not a decision aid, it’s a habit.

Forced time is free time. Entrapment, prolonged extrication, waiting on the aircraft, these create windows that would otherwise be wasted. This is when you do the thing you would never stop for.

Default phase rule: on scene, do only what cannot be done moving. Push everything else into the transport phase.

But watch for reverse-window environments. In the back of a small aircraft, a cramped ambulance, or a winch operation, some procedures become impossible once you are moving. There, the opportunity is before departure, not en route. This inverts the default rule, and the inversion has to be recognised out loud — it is a classic source of “we’ll do it on the way” decisions that quietly become “we never did it.”

Filter 3 — Feasibility: can this be done well, here, by this team?

Estimate first-pass success in these conditions, not in the resus room where you last did it.

The honest inputs:

  • Operator currency, not certification. When did you last actually do this?
  • Number of trained hands available.
  • Physical access to the head, chest, or limb.
  • Light, noise, space, temperature, weather, contamination.
  • And the one people skip: can this team manage the complication this procedure creates?

A procedure performed badly is usually worse than a procedure not performed at all. That sentence is worth putting on a wall.

The fourth filter nobody writes down

You can satisfy indication, opportunity, and feasibility and still be wrong, if failure is unrecoverable.

A failed intraosseous costs you thirty seconds and a needle. A failed RSI in a patient who was, until that moment, ventilating adequately can cost you the patient.

Weight your feasibility threshold against the downside, not the upside. High-consequence-of-failure procedures need a much higher bar than their success rates alone would suggest.

And one more thing that is always true: opportunity cost is never zero. Time spent is transport delayed, monitoring degraded, and the team leader’s attention consumed. Every procedure must buy back more time-critical physiology than it costs.

The framework applied

ProcedureVerdictWhy
Finger thoracostomyUsually yesImmediate indication, seconds to perform, low feasibility bar
Tourniquet / pelvic binderUsually yesFast, high yield, very hard to do badly
Blood or plasmaYes, but en routeIndication is now; opportunity is the transport phase. Don’t stop for it
Prehospital RSICase by caseIndication must be strong, feasibility bar high, failure unrecoverable
Front of neck access (FONA)Yes. the moment CICO is declaredAll three filters resolve instantly: indication is absolute, opportunity is zero-later, feasibility is adequate anywhere. The only real failure mode is delay
Resuscitative thoracotomyNarrow, but nowTight indication and high feasibility bar — yet there is zero later opportunity
Central access, definitive splintingUsually noFails the indication filter — deferrable to hospital

Note how differently the same three filters weight each row. Thoracostomy passes on speed. Thoracotomy passes on the total absence of a later window. RSI is genuinely contested because the fourth filter, consequence of failure, dominates it.

FONA is the instructive outlier. It is the one row where every filter aligns and the framework has almost nothing to weigh, indication is absolute, there is no later window, and the technical bar is low enough to be met on a roadside with a scalpel and a bougie. And yet it is the procedure most often performed too late. That tells you something important: the framework’s job is not only to stop unnecessary procedures, but to remove hesitation from necessary ones. In a can’t-intubate-can’t-oxygenate situation, the decision has already been made by the physiology; the clinician’s only remaining task is to notice that, say it out loud, and cut. Services that drill the declaration — “this is a CICO, I am doing a FONA” — consistently do it faster than services that drill only the technique.

The cognitive traps, and what to do about them

The failure modes are predictable, which means they are defensible:

  • Procedural momentum — “I’ve started, so I’ll finish.”
  • Task fixation — the operator’s world shrinks to a 10cm square, and whole-scene awareness goes with it.
  • Capability bias — “we carry it, so we should use it.” Kit generates its own indications if you let it.
  • Skill-decay overconfidence — the gap between what you are credentialed to do and what you are currently good at.

Countermeasures that actually work in the field

A verbalised stop moment. Before any invasive procedure, say out loud: the indication, the window, and who is doing it. Thirty seconds. Its purpose is not permission — it is a shared mental model, and it gives the quietest person on the team a legitimate moment to say “wait.”

Pre-committed limits. Two attempts, then plan B. Decided before you start, never during. Limits set mid-procedure are not limits; they are negotiations you will lose.

A declared exit strategy before the first attempt. If this fails, we do this. Named, agreed, understood by everyone.

Time called aloud by someone not performing the procedure. “Eight minutes on scene.” Neutral, non-accusatory, relentless.

The team leader keeps their hands free during high-risk procedures. Someone must retain the global picture, and it cannot be the person with a laryngoscope in their hand.

The principle underneath all of it

On scene, you are not treating the disease You are buying the patient safe passage to somewhere the disease can be treated.

Every invasive procedure has to justify itself against that sentence. If it doesn’t buy passage, it costs it.

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When “no difference” isn’t the same as “doesn’t work”: reading REBOARREST trial carefully

12 Jul Paramedics performing CPR and medical treatment on a patient on the pavement with ambulance nearby
Paramedics performing CPR and medical treatment on a patient on the pavement with ambulance nearby

A critical review of the first randomised trial of prehospital REBOA in non-traumatic out-of-hospital cardiac arrest.

Mario Rugna

A technique JUST for TRAUMA

REBOA was not designed for cardiac arrest. It grew out of trauma care, as a way to buy time in patients bleeding to death from injuries no tourniquet can reach non-compressible torso haemorrhage. The idea is mechanical and direct: thread a balloon catheter up the femoral artery, inflate it in the aorta, and physically dam the flow above the bleeding source. Occlude in Zone 1 (the descending thoracic aorta) or Zone 3 (below the renal arteries) depending on where the haemorrhage sits, and you both slow the exsanguination and prop up the pressure reaching the heart and brain.

That is the world REBOA has lived in for most of its history. The case series, the registries, the device approvals all sit within traumatic haemorrhage and traumatic cardiac arrest. In that setting the balloon does two jobs at once: it controls bleeding and augments proximal perfusion pressure.

REBOARREST is different! That’s WHY

Non-traumatic cardiac arrest is a fundamentally different problem, and that is what makes REBOARREST unusual. The patient isn’t bleeding; the heart has simply stopped. Occluding the thoracic aorta during chest compressions redistributes the little flow that CPR generates toward the coronary and cerebral circulations, raising coronary perfusion pressure in the way adrenaline is meant to. It is REBOA repurposed as “mechanical adrenaline,” stripped of the haemorrhage-control rationale that justified it everywhere else.

Until now, that idea rested almost entirely on physiological reasoning, animal data, case reports and small uncontrolled series. REBOARREST is the first randomised controlled trial to test it the first time REBOA has been asked, under proper experimental conditions, to prove itself outside of bleeding. That context is worth holding onto while reading what follows: a technique borrowed from one domain and applied to another carries its assumptions with it, and not all of them travel.

So WHAT!

The headline from REBOARREST is easy to summarise and easy to misread. Among 179 patients with non-traumatic out-of-hospital cardiac arrest (OHCA), adding resuscitative endovascular balloon occlusion of the aorta (REBOA) to advanced life support did not improve sustained ROSC: 28% in the intervention arm versus 26% in controls, an adjusted risk difference of 1.8% (95% CI −11 to 15, p=0.78). The graphical abstract states it plainly the strategy “did not significantly improve rates of sustained ROSC.”

A busy clinician skimming the abstract will file REBOA-for-OHCA under “tried, didn’t work.” The trial itself doesn’t support that conclusion, and the gap between what was found and what it means is the most interesting thing about this paper.

This is, first and foremost, a genuine achievement. It is the first RCT of REBOA in non-traumatic OHCA, run pragmatically across 12 sites in three countries, with concealed allocation, a blinded statistician, a prespecified analysis plan, an active data monitoring committee, and independent review of ALS quality. Those are not small things in prehospital research, where trials of this kind barely exist. But it’s worth being clear about what it can and cannot tell us.

The trial was built to detect an effect almost no intervention produces (not only in cardiac arrest)

REBOARREST was powered to detect a doubling of sustained ROSC from a baseline of 18% to 36%. The authors, to their credit, call this goal “optimistic.” It is more than that: powering a trial for a doubling means designing it to be blind to anything smaller. And in cardiac arrest, an absolute increase of even 5–10% in ROSC would be clinically meaningful and worth chasing.

This is the difference between absence of evidence and evidence of absence, and it matters. A non-significant p-value in an underpowered trial tells you the study couldn’t see an effect, not that no effect exists. REBOARREST cannot distinguish “REBOA doesn’t help” from “REBOA helps by a real but sub-doubling amount that this trial was never equipped to detect.”

Most of the intervention arm patients never got the intervention

The second structural issue compounds the first. Of 88 patients randomised to REBOA, only 51 (58%) actually underwent aortic occlusion. The rest didn’t: 19% achieved ROSC before the balloon could be inflated, 16% had an unsuccessful procedure, and 7% were aborted.

The primary intention-to-treat (ITT) analysis therefore compares a group in which four out of ten patients never received the treatment against a control group. This is a defensible and honest way to answer a strategy question “should an EMS system deploy REBOA in OHCA?” but it is not a clean test of whether aortic occlusion works physiologically. Dilution of this magnitude pushes the result mechanically toward the null before biology gets a say.

That’s why the as-treated (AT) signal deserves a mention, with heavy caveats. When patients who actually received occlusion were compared with controls, the first AT sensitivity analysis showed a significant benefit: a 16% absolute increase in sustained ROSC (95% CI 2 to 29, p=0.02). Read alone, that looks like the intervention doing exactly what it was supposed to. But this analysis conditions on a post randomisation event (whether the balloon went in and trims controls who died or achieved ROSC early) wide open to selection and time bias. It cannot confirm efficacy. What it can do is tell us ITT analysis is that the null result is hiding a signal worth taking seriously, not closing the book.

By the time the balloon inflated, the physiology may already have been lost

The rationale for REBOA in arrest is time critical: occlude the aorta, raise proximal and coronary perfusion pressure, mimic the haemodynamic effect of adrenaline, and buy a shot at ROSC. That logic depends entirely on getting there early.

In REBOARREST, the median interval from arrest to occlusion was 47 minutes. The authors name this “the major limitation,” and they’re right. By three-quarters of an hour, most of these patients were in prolonged, poor prognosis arrest, and the window in which augmented perfusion pressure might have mattered had largely closed. The trial reflects a mixed urban rural, largely helicopter dispatched system where reaching the patient takes time so what it really tested was late prehospital REBOA. Whether early occlusion (a metropolitan short-transport service, or an in-hospital arrest) would behave differently is a question this trial leaves wide open.

The one number that would explain the result was never recorded

Here is the quiet problem at the centre of the paper. The entire hypothesis rests on REBOA raising aortic and coronary perfusion pressure, and blood pressure was never measured. The Prytime catheter used in Italy lacked the equipment; the Reboa Medical catheter used elsewhere couldn’t measure pressure without exceeding its CE approval. Intra-aortic pressure data simply don’t exist.

So when the primary outcome comes back null, we can’t tell which of three very different stories is true: the balloon failed to raise coronary perfusion pressure, or it raised pressure but too late, or it raised pressure and ROSC still didn’t follow. EtCO₂ did rise significantly after occlusion but that was measured only within the occlusion subgroup, with no contemporaneous control comparison, so it’s a within group observation consistent with the mechanism rather than between group proof of it.

The endpoint that moved isn’t the endpoint that matters

Sustained ROSC ≥20 minutes is a surrogate. What patients and families care about is survival with an intact brain, and on those measures the arms were flat and consistent: 30-day survival was 7% in both groups, and good neurological outcome (mRS 0–3) was 6% versus 3%, not significant.

Even if the ROSC trend had been real, it didn’t carry through to survival or neurology. But the mirror image is also true: a trial powered on ROSC is hopelessly underpowered for these harder outcomes, so it can’t rule a survival difference in or out either.

So what does REBOARREST actually tell us?

On feasibility and safety, the trial is convincing. A two-person prehospital team can perform this procedure with a short procedure time (median 14 minutes from randomisation to occlusion), acceptable cannulation success, and no excess of adverse events. That’s a real, well-supported result, and it opens the door to other endovascular interventions in the field.

On efficacy, the honest verdict is: unproven, not disproven. What REBOARREST demonstrates is that a strategy of late prehospital REBOA, in a mixed urbanrural, expert-staffed, ECPR adjacent system, did not improve a surrogate outcome in a trial that could only ever have detected a very large effect, that never delivered the intervention to 42% of the treatment arm, and that never measured the pressure it was built around.

That is not “REBOA doesn’t work in cardiac arrest.” It’s “we still don’t know, and here’s exactly why we don’t.” The right response to this trial isn’t to abandon the question. It’s to design the study REBOARREST couldn’t be: earlier occlusion, invasive pressure monitoring, a realistic effect size, and enough events to see it. The as treated signal is reason enough to build it.

Reference: Brede et al. Prehospital resuscitative endovascular balloon occlusion of the aorta in non-traumatic out-of-hospital cardiac arrest (REBOARREST): an international, multicentre, open label, pragmatic, randomised, controlled trial. Critical Care 2026;30:324.

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Defibrillation Strategies: Why AHA’s position on VC and DSED is Controversial

1 Feb

New 2025 Guidelines on Cardiopulmonary Resuscitation stated that alternative strategy for defibrillation of persistent VF/pVT are not yet ready for prime line based on the actual available evidences.

Previously ILCOR stated about the same topic: We suggest that a double sequential defibrillation strategy (weak recommendation, low certainty of evidence) or a vector change defibrillation strategy (weak recommendation, very low certainty of evidence) may be considered for adults with cardiac arrest who remain in ventricular fibrillation or pulseless ventricular tachycardia after 3 or more consecutive shocks.

So AHA degraded the ILCOR “may be considered to a “non useful” despite the same level of grade and evidences. Let’s see why and why THIS IS WRONG

AHA: It found significant improvement in survival at hospital discharge with VC and DSED compared to standard defibrillation by intention-to-treat, but notably not when trial findings were analyzed by the treatment strategy patients actually received

In summary, AHA highlighted one point for not suggesting VC or DSED over standard defibrillation. The reason is that the DOSE VF trial did not show any statistically relevant advantage in “per protocol analysis”!

I’m not a methodologist but I think that any of them can suffer of an heart attack hearing this statement! Intention to treat analysis is the core of randomization!

To summarize this concept here is a head to head compare between Intention to treat analysis VS per protocol analysis 

ApproachStatistically Strong?Less Bias?More Power?
Intention-to-treat✅ Yes (most robust)✅ Low bias❌ Less power
Treatment / Per-protocol❌ No (can be biased)❌ Higher bias✅ More power

In randomized control trials, analyzing patients “per protocol” removes the advantages of randomization. This choice degrades the study results to an observational level. So AHA statement is incorrect and the trial results are highly relevant

AHA: Furthermore, in a secondary exploratory analysis a significant survival benefit from DSD was only observed in the 17% of study patients in whom VF was incessant, and not in the vast majority (83%) of patients in whom VF recurred after a successful shock.

You can find the cited secondary analysis here: The impact of alternate defibrillation strategies on shock-refractory and recurrent ventricular fibrillation: A secondary analysis of the DOSE VF cluster randomized controlled trial. And the following are the results:

Shock-Refractory VF (n. 60)

Shock-Recurrent VF (n. 285)

In both cases, recurrent or persistent, even if not always statistically significant, DSD and VC performed much better than standard defibrillation WITH RESULTS ABSOLUTELY CLINICALLY RELEVANT ON ALL MAJOR OUTCOMES

AHA: The interval between each sequential “double” shock required for successfully terminating VF has also been shown experimentally (animal studies 10-100 Mses) and demonstrated in DOSE-VF itself (mean interval 650 Mses. ) to require a level of precision (separated by milliseconds) unlikely to be consistently achievable by manual activation of two defibrillators. 

Th is totally wrong. The small ( 10- 100 Mses) cited from the guidelines refers to experimental animal study . DOSE-VF trial demonstrates statistically significant superiority to standard defibrillation. This superiority is observed with intervals >500 Msec that is absolutely replicable in clinical practice. The investigators also demonstrated the increase of advantages for shorter intervals. But, this increase is not seen at 10 Mses, which is only referred to in animal studies.

        • DSED and VC are superior to standard defibrillation on every clinical relevant clinical outcome
        • DSED and VC uphold clinical advantages on both persistent and recurrent VF/pVT
        • When you chose DSED the interval between the 2 shocks is easily reproducible in clinical practice

        In case of VF/pVT. First approach:

        If recurrent or refractory VF/pVT

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        Safer Ventilation Strategies

        28 Jul

        Is This The End?

        28 Jun

        Do not move! Spinal immobilization or spinal motor restriction: the long-lasting debate from the Napoleonic Wars to 2024 SIMEU policy statement

        Chest compressions in Traumatic CIRCULATORY Arrest

        16 Jun
        References

        Time to trash proximal tibia and 15 mm IO needle in adult & paediatric cardiac arrest!

        14 May

        References:

        Kwong S, Kothary S, Poncinelli LL. Skeletal development of the proximal humerus in the pediatric population: MRI features. AJR Am J Roentgenol. 2014 Feb;202(2):418-25. doi: 10.2214/AJR.13.10711. PMID: 24450686.

        Reid C, Fogg T, Healy G. Deformation of a humeral intraosseous catheter due to positioning for thoracostomy. Clin Exp Emerg Med. 2018 Sep;5(3):208-209. doi: 10.15441/ceem.17.243. Epub 2018 Sep 30. PMID: 30269457; PMCID: PMC6166044.

        Hamam MS, Klausner HA, France J, Tang A, Swor RA, Paxton JH, O’Neil BJ, Brent C, Neumar RW, Dunne RB, Reddi S, Miller JB. Prehospital Tibial Intraosseous Drug Administration is Associated with Reduced Survival Following Out of Hospital Cardiac Arrest: A study for the CARES Surveillance Group. Resuscitation. 2021 Oct;167:261-266. doi: 10.1016/j.resuscitation.2021.06.016. Epub 2021 Jul 5. PMID: 34237357.

        Rayas EG, Winckler C, Bolleter S, Stringfellow M, Miramontes D, Shumaker J, Lewis A, Wampler D. Distal femur versus humeral or tibial IO, access in adult out of hospital cardiac resuscitation. Resuscitation. 2022 Jan;170:11-16. doi: 10.1016/j.resuscitation.2021.10.041. Epub 2021 Nov 5. PMID: 34748766.

        Wang D, Deng L, Zhang R, Zhou Y, Zeng J, Jiang H. Efficacy of intraosseous access for trauma resuscitation: a systematic review and meta-analysis. World J Emerg Surg. 2023 Mar 14;18(1):17. doi: 10.1186/s13017-023-00487-7. PMID: 36918947; PMCID: PMC10012735.

        Maxien D, Wirth S, Peschel O, Sterzik A, Kirchhoff S, Kreimeier U, Reiser MF, Mück FG. Intraosseous needles in pediatric cadavers: Rate of malposition. Resuscitation. 2019 Dec;145:1-7. doi: 10.1016/j.resuscitation.2019.09.028. Epub 2019 Oct 1. PMID: 31585187.

        Confirming Tracheal Intubation: stop wasting your time!

        2 Jul

        Intro

        The methods to confirm tracheal intubation (and exclude accidental oesophageal intubation) are classically divided in Techniques not requiring manual ventilation and Techniques requiring manual ventilation::

        1. Techniques not requiring manual ventilation
          • Inspection of the vocal cords: there should be visual confirm- ation that the tube lies surrounded by the glottic structures
          • Palpation of the trachea: an assistant palpating the external trachea may feel vibrations, corresponding to the tube passing the tracheal rings
          • Oesophageal detector device: Tracheal placement results in free aspiration of gas from the lungs; in oesophageal intubation, the walls of the oesophagus collapse around the tube lumen preventing gas flow
        2. Techniques requiring manual ventilation:
          • Sounds
          • Compliance: A ‘normal’ compliance during manual ventilation
          • Inspection of the chest: Good expansion of the chest on manual ventilation
          • Auscultation of the epigastrium
          • Auscultation of the chest
          • CO2 detection
            • Capnography – a normal capnogram for at least six breaths suggests tracheal intubation
            • Capnometry – a change in indicator to denote CO2 suggests tracheal intubation

        Despite nowadays is evident that CO2 detection is the gold standard in terms of sensibility and specificity, our daily practice in managing airways still and strongly rely on clinical methods to confirm when the tube is correctly posed in the trachea and not in the oesophagus.

        The article

        Hansel, J., Law, J.A., Chrimes, N., Higgs, A. and Cook, T.M. (2023),

        Clinical tests for confirming tracheal intubation or excluding oesophageal intubation: a diagnostic test accuracy systematic review and meta-analysis. Anaesthesia. https://doi.org/10.1111/anae.16059

        In this meta-analysis the authors investigated the literature about the reliability of different methods to confirm tracheal intubation and exclude oesophageal intubation.

        This is a clinically relevant point cause the unrecognised oesophageal intubation leads to catastrophic consequences on patients health.

        Which Clinical test they evaluated:

        How they presented the data

        The false positive rate (FPR)

        The FPR indicates how often any sign that is considered suggestive of successful tracheal intubation (for example chest rising or hearing breath sounds),might occur despite the tube is not in the trachea but in the oesophageal. Usually an acceptable number of FPR can be 0,1 (or the 10% (10 out of 100) of the total positive results) but you can understand how in this case, considered the high clinical relevance of the topic we have to reach for lower FPR the 1 out of 10.

        The Likelihood Ratio (LR): positive (LR+) or negative (LR-)

        The positive LR (LR+) indicates how many times is more probable that the tube is the trachea than in the oesophagus the investigated sign is present

        A test with a LR+=10 (cut off value for reliability) means that there is 10 times more probability that the tube is really in the trachea than in the oesophagus

        The negative LR (LR-) indicates how many times is more probable that the tube is the oesophagus han in the trachea if the investigated sign is present

        A test with a LR- of 0.1 (cut off value for reliability) means that there is 1/10 times more probability that the tube is in the oesophagus than in the trachea.

        What they found

        Conclusion

        The available data strongly suggest that clinical signs lack the discriminatory power to exclude oesophageal intubation to a sufficient degree to ensure patient safety when capnography is not available or doubted. The oesophageal detector device performs better than clinical examination, and in resource-limited environments with no access to capnography, may be sufficiently sensitive and specific to help guide decision-making.

        Clinical Practice Take Home Message

        Based on the result of this study when available use waveform capnography to confirm tracheal intubation and exclude oesophageal intubation. Clinical tests can be dangerously misleading and potentially a waste of precious time in difficult environments as emergency prehospital setting.

        In poor resources systems if any form of ETCO2 is not available, the most reliable test to confirm tracheal intubation is the Oesophageal detector device.

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        God save the King!

        27 Jun

        Matthew E. Prekker, M.D., M.P.H.,  Brian E. Driver, Video versus Direct Laryngoscopy for Tracheal Intubation of Critically Ill Adults

        The DirEct versus VIdeo LaryngosCopE (DEVICE) trial is a prospective, multicentre, non-blinded, randomised trial being conducted in 7 EDs and 10 ICUs in the USA

        Critically ill adults undergoing tracheal intubation randomly assigned to the video-laryngoscope group or the direct-laryngoscope group

        The primary outcome was successful intubation on the first attempt.

        The secondary outcome was the occurrence of severe complications during intubation: severe hypoxemia, severe hypotension, new or increased vasopressor use, cardiac arrest, or death.

        The trial was stopped for efficacy at the time of the single preplanned interim analysis.

        Conclusions: Among critically ill adults undergoing tracheal intubation in an emergency department or ICU, the use of a videolaryngoscope resulted in a higher incidence of successful intubation on the first attempt than the use of a direct laryngoscope.

        Comment: This a long journey hopefully coming to an end. From 2022 we have clear evidences on the superiority of Video versus Direct laryngoscopy Hansel J, Rogers AM, Lewis SR, Cook TM, Smith AF. Videolaryngoscopy versus direct laryngoscopy for adults undergoing tracheal intubation. Cochrane Database Syst Rev. 2022 Apr 4;4(4):CD011136. doi: 10.1002/14651858.CD011136.pub3. PMID: 35373840; PMCID: PMC8978307.. Main airway management societies (Difficult Airway Society; Society for Airway Management; European Airway Management Society; All India Difficult Airway Society; Canadian Airway Focus Group; Safe Airway Society; and International Airway Management Society) recently updated their statements on preventing the accidental oesophageal intubation in that sense. Preventing unrecognised oesophageal intubation: a consensus guideline from the Project for Universal Management of Airways and international airway societies. The DEVICE trial is another brick in the wall of consciousness about superiority of VL vs DL despite some findings are not replicable ( ex. DL FPS 70,8%) in systems where airway management and expertise in DL is a longstanding tradition. But as said we didn’t need this trial to arrive at the conclusion of the journey.

        Use the videolaryngoscope (VL) as first choice in emergent tracheal intubation to improve first passage success and prevent accidental oesophageal intubation.

        Use direct laryngoscope (DL) just as rescue device in case of technical failure of the videolrayngoscope

        All medical systems involved in airway management need to be aware of this. A videolaryngoscope is no longer an option but a standard equipment. The best choice is to have both, standard and hyperangulated geometry blades, in adult and paediatric sizes.

        The first approach with a standard geometry blade permits to shift from VL to DL without changing device. The hyparangulated blade can be useful in selected cases even as first option..

        We also consequently need to shift paradigm from classical way of teaching airway management, to a VL first approach as default method and simulating any tech failure during the practical training forcing the trainee to use the DL as rescue plan.

        To let me know what is your opinion fill the survey at the link below:

        VL first approach

        Also read:

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        Don’t live me Breathless

        28 Jan

        Case presentation

        You arrive on the scene of a motorbike accident. The driver, a 50 years old male, at your arrival is in “Pain” state with eyes closed and you can hear just a “snoring” sound coming from his mouth. His vitals are: NIMBP 80 over 50, HR 110, A quick primary survey reveal a low level of consciousness (eyes closed no finalised arms movement) with restored airway patency that after basic airway manoeuvres and O2 therapy (SaO2 goes to 95%) no signs of tension pneumo. A quick look to the pelvis and legs reveal a suspected “open book” lesion and a bilateral femoral fracture. No PMH is available at the moment.

        Physiological response to shock

        From the primary survey and vitals you can understand the patient is compensating a state of profound (hypovolemic) shock and consequent organ low perfusion with a sympathetic activation. Endogenous adrenergic mediators are trying to restore organ perfusion by vasoconstriction and increase in cardiac output.

        First do not harm

        Can we kill a patient destroying the physiologic response to shock?

        The answer is YES! The need to protect airway performing a rapid pharmacological assisted airway management (RSI), can lead to bad consequences, destroying the physiological response to a state of profound shock.

        All sedative, analgesic and anaesthetic drugs in fact antagonise and depress the sympathetic adrenergic response physiologically targeted to restore perfusion to vital organs.

        First do not harm and choose minimal emodynamic impact type and dose of drugs to perform sedation. As we know (till now) the better choice are Ketamine and Etomidate with no clear evidences on which one is preferable. We for sure know that Ketamine can be dangerous in cathecolamine depleted patients and that this effect is dose dependent. So consider using a lower dose to reach dissociative threshold being conscious that can lead to a non ideal intubation condition.

        Reanimate first intubate later (aka DSI)

        https://m.facebook.com/photo.php/?fbid=1975674385934581

        After a dissociative dose of Ketamine, our next clinical target is to reanimate the patient form an oxygenation and/or an organ perfusion point of view.

        So we shift from a concept of Rapid Sequence Intubation to a more comprehensive plan of Delayed Sequence Airway Management. Delayed (Ketamine/Etomidate induced) to get time and reanimate, Airway Management intended as any plan (tracheal intubation, supraglottic airway) we can apply in that specific patient in the middle of the road or in other prehospital scenarios.

        A properly performed pre-oxygenation with the adjunct of apneic oxygenation can restore O2 levels giving us also a good reserve for following apnea times.

        Cautelative fluid administration (avoid fluids in trauma, use BLOOD) and, push dose (Epinephrine, Phenilephrine) or continuous infusion (Norepinephrine) vasopressors, can restore perfusion to abdominal and extra abdominal organs by increasing circulating volume and cardiac performance (Alfa and Beta agonist ).

        Delayed paralytic administration give us the time to perform a proper reanimation reanimation and to check the effects of our interventions.

        If everything goes well and the patient’s oxygenation and emodynamic state is compensated, we can administer paralytic, and go straight to perform tracheal intubation.

        But if the patient remains uncompensated despite all our efforts to correct the potentially lethal cause, our last weapon can be to preserve spontaneous breathing.

        Don’t live me breathless

        WHY? During inspiratory phase of respiratory cycle the negative intrathoracic pressure favourites venous return and increase the telediastolic volume of the left ventricle. The augmented left ventricle end diastolic pressure (LVEDP) according to Frank-Starling law improves myocardial performance increasing stroke volume and consequently cardiac output.

        The refractory shocked patient is heavily preload dependent and suppressing the inspiratory drive risk to worsen the already dramatic emodynamic state taking him on the irreversible part of the shock curve.

        We’ve got a plan

        We need to have a plan for high difficult physiological airways. This is just a small residual percentage of the airways we manage in our clinical practice, but can be dramatically catastrophic when we deal with those patients without a precise plan.

        We’ve got a backup plan

        But when intubation fails we need to have a backup plan!

        Case conclusion

        You understand the need to protect patient’s airways but also the extreme physiologic difficulty of this airway.

        After administering a dissociative dose of Ketamine, due to the failure of any try to restore perfusion, you decide to perform a DISSOCIATIVE INTUBATION using a videolaryngoscope with a hyperangulated blade and a bougie, AVOIDING PARALYSIS.

        Then you put the patient on ACV mechanical ventilation targeting a TV of 6 ml/kg and considering a “zero PEEP” strategy.

        Special Thanks to Scott Weingart and Jim DuCanto for the kindness and fundamental mentorship on inspiring and peer reviewing the algorithm

        References

        Brian E. Driver, Matthew E. Prekker, Robert F. Reardon, Benjamin J. Sandefur, Michael D. April, Ron M. Walls, Calvin A. Brown,
        Success and Complications of the Ketamine-Only Intubation Method in the Emergency Department,
        The Journal of Emergency Medicine

        Weingart SD, Trueger NS, Wong N, Scofi J, Singh N, Rudolph SS. Delayed sequence intubation: a prospective observational study. Ann Emerg Med. 2015 Apr;65(4):349-55. doi: 10.1016/j.annemergmed.2014.09.025. Epub 2014 Oct 23. PMID: 25447559.

        Merelman AH, Perlmutter MC, Strayer RJ. Alternatives to Rapid Sequence Intubation: Contemporary Airway Management with Ketamine. West J Emerg Med. 2019 May;20(3):466-471. doi: 10.5811/westjem.2019.4.42753. Epub 2019 Apr 26. PMID: 31123547; PMCID: PMC6526883.

        Ko BS, Ahn R, Ryoo SM, et al. Prevalence and outcomes of endotracheal intubation–related cardiac arrest in the ED. Am J Emerg Med. 2015;33(11):1642-5.

        Mort TC. Complications of emergency tracheal intubation: hemodynamic alterations – part I. J Intensive Care Med. 2007;22(3):157-65.

        Jarvis JL, Gonzales J, Johns D, et al. Implementation of a clinical bundle to reduce out-of-pospital peri-intubation hypoxia. Ann Emerg Med.2018;72(3):272-279.e1.

        Roantree RAG, Goldstein S. (2018). EMS, Facilitated Intubation Without 36.Paralytics. Treasure Island, Florida: StatPearls Publishing.

        Braude D, Palomo O, Beamsley A. Sedation only intubation. EM:RAP. 39.2013.

        Miller M, Kruit N, Heldreich C, et al. Hemodynamic response afterrapid sequence induction with ketamine in out-of-hospital patients 50. at risk of shock as defined by the shock index. Ann Emerg Med. 2016;68(2):181-8.e2.

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