Enjoy!

Casey Parker | BroomeDocs | April 2026

The modern management of proper pulmonary embolism (not the common little ones) has been evolving rapidly in the last decade. The range of acronym-based trials can seem a little dizzying. We now have PERT teams with a quiver of expensive catheters to shoot into our patients pulmonary vessels. However, we need to know what the data tells us. Not about catheters, but about our patients.

We’ve had four major PE trials drop in the last six months. Two of them were published in the New England Journal and Circulation, presented at ACC and TCT to standing rooms of interventionalists with catheters in their pockets. The internet lit up. Guidelines will be rewritten. Hospitals will buy expensive devices.

And if you work in a regional or rural hospital — which is most of the planet — almost none of it changes what you do on a Tuesday night when a sick patient rolls through your door.

Here’s what the evidence actually says, and here’s what to do with it.

A Quick Reckoning with the Evidence Base

Before we talk strategies, let’s be honest about the trials. The vast majority of recent PE intervention trials share two features that should make us cautious:

1. Surrogate endpoints. The RV/LV ratio on CT is not a patient outcome. It is a number on a scan. It has never been validated as a surrogate for death, function, or quality of life. Trial after trial has shown you can improve this number dramatically while patients go on to live identical lives — or die from your intervention’s bleeding complications.

2. Industry funding. HI-PEITHO (Boston Scientific), PEERLESS (Inari Medical), FLAME (Inari), FLASH registry (Inari), STORM-PE (device manufacturer). Every major trial producing a “positive” result in the catheter and device space was designed, run, and in many cases analysed by the companies selling the product being tested. The independently-funded trials — PEITHO, STRATIFY — consistently produce more sobering findings.

This doesn’t mean the data are fabricated. It means we should read them the way we’d read a pharmaceutical company’s drug trial: carefully, with both eyes on the patient-oriented outcomes and a hand ready to cover the surrogate endpoints.

With that said — here’s where we actually are.

First, a Note on Terminology

If you’ve been following along, you’ll know I wrote a separate post covering the new 2026 AHA/ACC PE Classification System when it dropped in February. The short version: the old “low risk / submassive / massive” language is being retired in favour of a five-category A–E system that incorporates clinical severity scores, biomarkers, RV imaging, haemodynamic parameters, and a respiratory modifier. It’s a more granular and physiologically honest framework, and it’s worth familiarising yourself with if you haven’t already.

For this post I’ll use the new categories where relevant, but I’ll keep the old terms alongside them — because most of us still think in “massive and submassive” and the trial literature uses that language throughout. The rough mapping is: New AHA/ACC Category Old terminology What it means clinically A Low risk Asymptomatic, low severity score — can go home B Low risk Symptomatic, low severity score — early discharge reasonable C1–C3 Submassive / intermediate Elevated severity score ± biomarkers ± RV dysfunction, haemodynamically stable D1–D2 Submassive trending to high Incipient cardiopulmonary failure, haemodynamics still compensating but precarious E Massive / high risk Cardiopulmonary failure, persistent hypotension, shock, arrest

Add the “R” modifier (e.g., C3R, D2R) when there’s significant respiratory compromise on top of haemodynamic findings. It’s genuinely useful shorthand when you’re on the phone to retrieval at midnight trying to convey exactly how sick your patient is and where on the spectrum they sit.

The key clinical insight from the new system: the old “submassive” bucket was always too wide. A C1 patient with mildly elevated PESI and no biomarkers is a fundamentally different clinical problem to a D2 patient with RV dilation, elevated troponin, and a lactate trending up. The new categories force more precision — and that precision matters when you’re deciding whether to give thrombolytics, call for retrieval, or watch and wait.

What Fifteen Trials Tell Us (The Short Version)

Heparin alone is not as bad as you think

The long-term follow-up of PEITHO — the largest and most rigorous dataset in this field — followed over 700 submassive PE patients for nearly three years. At that point, the patients who received heparin alone were alive in the same proportions, breathing equally well, walking equally far, and had equivalent right heart function compared to those who got full-dose thrombolysis. Identical rates of chronic thromboembolic pulmonary hypertension too.

Let that sink in. The heparin patients caught up completely.

Thrombolysis for submassive PE: real benefit is narrow, real harm is common

Full-dose systemic thrombolysis in submassive PE reduces haemodynamic deterioration events. It does not reduce mortality. It causes a 10-fold increase in intracranial haemorrhage (2% vs 0.2%). And the long-term outcomes are identical.

The only people who unambiguously benefit from systemic tPA are those whose PE is killing them right now — the haemodynamically unstable, the peri-arrest, the ones going down in front of you.

The catheter does nothing the drug can’t do through a drip

STRATIFY (2026) is the trial that should have changed everything but probably won’t, because it wasn’t funded by anyone trying to sell a catheter. It randomised intermediate-risk PE patients to three arms: heparin alone, 20mg alteplase via the EKOS pulmonary artery catheter, or 20mg alteplase through a peripheral IV over 6 hours.

The catheter and the drip were identical on every outcome including the disease-oriented thrombus burden score. Identical efficacy. Identical bleeding rates. The only difference was that the catheter costs around $5,000 more per patient and requires an operator and a procedure suite.

And the heparin arm? Zero deaths at 3 months. Both thrombolysis arms: 4.3% mortality, with the majority of deaths being bleeding-related (GI bleeds and intracranial haemorrhages).

The new devices are impressive, but the evidence is thin

PEERLESS showed that large-bore mechanical thrombectomy (FlowTriever) is roughly equivalent to catheter-directed thrombolysis in intermediate-risk PE — less ICU time, similar mortality, similar bleeding. HI-PEITHO showed that USAT catheter thrombolysis reduces haemodynamic deterioration compared to heparin alone, with a number-needed-to-treat of 16 and no mortality benefit.

Both trials are industry-funded, open-label, and use composite endpoints that dissolve when you look at the hard outcomes alone. Neither has demonstrated that the intervention saves lives or improves long-term function compared to anticoagulation.

PEERLESS II — comparing thrombectomy to heparin alone — is the trial we actually need. It’s enrolling now.

What This Means If You Work Where the Buck Stops

Here’s the thing: the entire catheter-directed thrombolysis vs mechanical thrombectomy debate is essentially irrelevant to most of the hospitals in Australia, and most hospitals on the planet. There is no FlowTriever at Fitzroy Crossing Hospital. There is no interventional radiologist in Cloncurry at midnight. In most of regional and rural Australia, the choice isn’t which device — it’s what drug, at what dose, and when.

That’s actually a liberating framing. Because the evidence supports a perfectly rational approach that requires nothing more than heparin and alteplase, both of which you almost certainly have in your pharmacy cupboard right now!

The Framework: Three Patients, Three Paths

Patient 1: Category E — Massive PE (haemodynamically unstable)

AHA/ACC Category E: Hypotension, shock, cardiac arrest, or obvious haemodynamic deterioration from PE

This is not an ambiguous situation. Act.

The mortality of untreated massive PE is horrifying — upwards of 30–50%. The mortality benefit of thrombolysis in this group is biologically plausible and supported by observational data, even without an RCT (none will ever exist for obvious ethical reasons). The calculus here is simple: untreated, they will likely die; thrombolysed, some will survive and some will bleed. Bleeding is recoverable from. Death is not.

Give systemic alteplase. Standard dosing: 100mg IV over 2 hours. If in cardiac arrest or imminent arrest: 50mg IV bolus. Stop heparin during the infusion; restart without a loading dose 2–3 hours after the alteplase completes.

If thrombolysis is absolutely contraindicated (recent neurosurgery, active intracranial pathology, recent major haemorrhage) — this is a retrieval call. Get help. Get the patient moving.

Key point: Don’t let the absence of CT confirmation delay treatment in a dying patient with a convincing clinical picture. Bedside echo showing RV dilation and McConnell’s sign, plus the clinical context, is enough to act on.

Patient 2: Categories C3 and D — Submassive PE (haemodynamically stable, but worried)

AHA/ACC Categories C3/D1–D2: Normal BP. RV strain on imaging or echo. Elevated troponin or BNP. Perhaps mildly tachycardic, mildly hypoxic, but not crashing. The D categories in particular represent patients on the edge of compensation — incipient cardiopulmonary failure.

This is where most of the controversy lives — and where the evidence most clearly supports a conservative default.

The question isn’t “should I thrombolyse?” The question is: “Is this patient genuinely trending towards haemodynamic collapse, or are they stable with risk markers that happen to look scary?”

The PEITHO data show that in unselected intermediate-risk patients, thrombolysis doesn’t save lives and produces identical long-term function — but does cause intracranial haemorrhages. STRATIFY shows that even low-dose thrombolysis in this group may produce more deaths than heparin alone, and no functional gain.

Default strategy: Anticoagulate well. Heparin infusion. Observe closely. Set a clear trigger threshold.

Triggers for escalation to systemic thrombolysis:

• Sustained hypotension (SBP 15 minutes, not explained by another cause)
• Clinical deterioration — increasing oxygen requirements, worsening tachycardia, altered mental state, rising lactate
• Bedside echo showing worsening RV function or new right heart dilatation
• You are genuinely worried this patient is going down

Do not thrombolyse purely because the CT showed a large clot burden, or the troponin is elevated, or the RV/LV ratio is >1.0. These are risk stratification markers, not treatment indications in themselves. The control arms of multiple trials demonstrate that most patients satisfying these criteria do fine with heparin.

If you decide to give low-dose thrombolysis: 50mg alteplase IV over 2 hours (consider as low as 0.5mg/kg in smaller patients or those at higher bleeding risk). This is not validated against full-dose in powered RCTs but is widely used and produces lower bleeding rates. Stop heparin during infusion.

If there is a contraindication to thrombolysis and the patient is deteriorating: This is your retrieval call. The conversation with the receiving centre now involves whether mechanical thrombectomy is available and appropriate. Give that history clearly: haemodynamic status, echo findings, reason for contraindication, current anticoagulation.

Patient 3: Categories B–C2 — Submassive PE (stable, incidental RV strain, doing OK)

AHA/ACC Categories B, C1, C2: Normal BP, saturating well, mildly tachycardic, troponin mildly elevated, RV/LV >1 on CT, but sitting comfortably asking for a cup of tea.

Anticoagulate. Watch. Resist the urge to do more.

The evidence is remarkably consistent here: these patients have excellent outcomes with heparin alone. The long-term PEITHO data, STRATIFY, and STORM-PE all tell the same story — zero to near-zero mortality in haemodynamically stable intermediate-risk patients managed with anticoagulation. You are not withholding life-saving treatment. You are applying the most evidence-supported therapy available.

Consider admission, telemetry monitoring, and a low threshold for reassessment. If they deteriorate, you escalate. That’s the evidence-based approach.

The Rural Dilemma: Give tPA Now vs. Wait 12 Hours for a Catheter?

This is the question that doesn’t appear in any of the trial papers, because none of them were run in hospitals where the nearest interventional suite is a RFDS flight away. But it’s the question that actually matters if you work in regional and remote medicine.

The scenario: you have a submassive PE patient who is borderline — not crashing yet, but worrying you. You’re considering whether to give peripheral alteplase now, or transfer them to a tertiary centre for catheter-directed therapy. The retrieval will take 12 hours minimum. What do you do?

STRATIFY has effectively answered this question, even though it wasn’t designed to. It showed that 20mg alteplase delivered peripherally through an IV produces identical outcomes to the same dose delivered through a $5,000 pulmonary artery catheter by an interventional specialist. If the drug is the treatment — and the evidence strongly suggests it is — then the catheter is just an expensive delivery mechanism for something you can give through a cannula right now.

So reframe the decision. It’s not “peripheral tPA now vs catheter-directed tPA later.” It’s really two separate questions:

Question 1: Does this patient need thrombolysis at all?

Question 2: If yes, why would I wait 12 hours to give it?

The Decision Framework

Work through it like this:

If the patient is haemodynamically unstable or deteriorating rapidly:

Don’t retrieve. Treat. Give alteplase peripherally now. Notify retrieval so they’re aware and can assist with post-lysis management or escalation if it fails — but the treatment decision is made here, because the treatment window is now. A patient in haemodynamic collapse cannot wait twelve hours for a catheter. And when they arrive at the tertiary centre twelve hours later having received peripheral alteplase, the interventional cardiologist will not be disappointed — because that’s what they would have done too, just through a longer tube.

If the patient is stable but deteriorating slowly — tachycardia climbing, O2 requirements creeping up, echo getting worse:

This is the hardest call. Two reasonable paths:

Option A — Treat and transfer: Give peripheral alteplase now (50mg over 2 hours, or consider 0.5mg/kg if smaller or higher bleeding risk). Notify retrieval. Transfer once stable post-lysis. The patient arrives at the tertiary centre having already received the most effective reperfusion available. The interventional team can reassess and manage residual clot burden or any complications.

Option B — Expedite transfer, treat en route or on arrival: Anticoagulate fully, arrange urgent retrieval, have alteplase drawn up and ready. Treat if they deteriorate during transfer or in the first few hours of transit. This is reasonable only if the trajectory is slow and transfer is genuinely fast — within 3–4 hours. For a 12-hour transfer window, this option is clinically risky.

The key point: if you think this patient is going to need thrombolysis at any point in the next 12 hours, give it now. Peripheral alteplase is not a lesser treatment you offer because you can’t do the real thing. It is the real thing.

If the patient is stable and improving on heparin:

Then they don’t need thrombolysis — peripherally or via catheter. Transfer for monitoring and definitive care is appropriate, but this is not a thrombolysis decision at all. The catheter lab at the tertiary centre is irrelevant.

If thrombolysis is contraindicated:

This is the one genuine indication for urgent transfer to access catheter-based or mechanical therapy. Recent neurosurgery, active intracranial pathology, significant recent haemorrhage — these patients cannot receive peripheral tPA, and if they deteriorate, the only option is mechanical clot removal. Flag this early. Transfer early. Don’t wait until they’re crashing.

The Conversation with the Receiving Team

When you call retrieval or the receiving unit, the new category system earns its keep here — it’s a much more precise handover tool than “submassive.” Use it:

“I have a Category D2R PE — RV/LV ratio 1.1 on CT, echo shows big RV with TAPSE of 10mm, troponin positive, on 6L O2, haemodynamically stable but trending. Thrombolysis is [indicated / not yet indicated / contraindicated because _]. Transfer time is approximately 12 hours. My question is: if this patient needs thrombolysis in the next 12 hours, should I give it peripherally now, or is there a specific reason to wait for catheter-based delivery?”

In almost every case, the honest answer from a well-read tertiary clinician will be: give it peripherally now if they need it. STRATIFY tells you the catheter adds nothing. HI-PEITHO’s benefit was in early treatment — the intervention was delivered within 2 hours of randomisation. A 12-hour delay to catheter delivery almost certainly forfeits whatever advantage catheter timing might theoretically offer.

The One Exception Worth Knowing

PEERLESS showed that large-bore mechanical thrombectomy reduces clinical deterioration compared to CDT, and produces faster early haemodynamic recovery. For the rare patient with massive PE where thrombolysis has failed — ongoing haemodynamic instability 60–90 minutes after alteplase — mechanical thrombectomy is a genuine escalation option that peripheral drugs cannot replicate. This is the patient worth urgent transfer for, and worth a direct conversation with interventional cardiology at the receiving centre while you’re still managing them.

But note: this is the post-lysis failure scenario, not the pre-treatment decision. And it applies to massive PE, not to the stable submassive patient for whom the evidence base consistently shows anticoagulation alone is adequate.

The Bottom Line on the Rural Dilemma

The catheter is not a reason to delay treatment in a deteriorating patient. If the patient needs thrombolysis, peripheral alteplase is the right treatment — not a compromise while you wait for the real thing to become available 700km away. Give it, transfer the patient, and let the receiving team manage what comes next.

The only patients who genuinely need urgent transfer before treatment are those where thrombolysis is contraindicated and mechanical options are the only path. Everyone else either needs treatment now (give it) or doesn’t need more than heparin (transfer routinely and safely).

Practical Anticoagulation Notes

Unfractionated heparin (UFH): Preferred in patients where you might need to reverse anticoagulation rapidly (potential thrombolysis candidate, haemodynamically borderline). Target aPTT 60–100 seconds.

LMWH or DOAC: Perfectly acceptable in stable patients where you are confident thrombolysis is off the table. Rivaroxaban or apixaban have the convenience advantage in hospitals with limited nursing resources.

During and after thrombolysis: Hold heparin during alteplase. Restart heparin (no loading bolus) 2–3 hours after alteplase completion once aPTT <80. Do not combine therapeutic LMWH with alteplase — PEITHO’s catastrophic ICH rate was partly driven by simultaneous full-dose tenecteplase plus full-dose heparin bolus.

The Catheter Question for Rural Clinicians: What to Tell Your Retrieval Service

You don’t have a catheter lab. That’s fine — the evidence says you don’t need one for the majority of PE patients.

What you do need to know is how to communicate the rare patient who might benefit from escalation:

Refer for consideration of catheter-directed therapy or mechanical thrombectomy when:

• Massive PE where systemic thrombolysis has failed or is absolutely contraindicated
• Submassive PE with clinical deterioration despite optimal anticoagulation, where thrombolysis is contraindicated (recent surgery, active intracranial pathology, recent stroke)
• Large clot burden, significant haemodynamic compromise, and the patient is heading in the wrong direction.

Don’t refer for catheter-directed therapy because: The CT showed a big clot. The troponin is elevated. The RV/LV ratio is >1.0. The patient is stable and improving on heparin. These are not indications for invasive intervention.

The Bottom Line (Written for the 2am Brain)

The fancy catheter trials are interesting. The device company registries are beautifully produced. The win ratios and composite endpoints are statistically elegant.

But when you strip them back to what matters — does this patient live, does this patient bleed, can this patient walk up the stairs in six months — the evidence keeps saying the same thing: heparin is remarkably effective, thrombolysis saves lives in the truly unstable, and everything else is yet to prove its worth.

For most submassive PE patients in most hospitals, the evidence-based management plan is:

1. Anticoagulate promptly and well
2. Watch closely
3. Have a clear escalation trigger
4. Know how to give alteplase safely when that trigger is met
5. Know who to call when it’s not enough

That’s it. No catheter required.

Further Reading (The Good Stuff)

• PEITHO trial + long-term follow-up — Konstantinides et al, NEJM 2014 & JACC 2017. The foundational data on full-dose tPA in submassive PE.
• STRATIFY — Kjaergaard et al, Cardiovasc Res 2026. The trial that proves peripheral tPA = catheter tPA, and questions low-dose thrombolysis in stable patients.
• HI-PEITHO — Rosenfield, Konstantinides et al, NEJM March 2026. The EKOS trial. Important but industry-funded and open-label.
• PEERLESS — Jaber et al, Circulation 2024. FlowTriever vs CDT — thrombectomy wins on a composite driven by ICU utilisation, not hard outcomes.
• STORM-PE — Lookstein et al, Circulation 2026. Industry-run thrombectomy vs heparin — 2 deaths vs 0, no patient benefit.
• First10EM — STRATIFY & STORM-PE — Morgenstern, April 2026. Excellent independent critical appraisal. first10em.com
• PulmCrit — CDT vs peripheral tPA — Farkas. Consistently sceptical, consistently correct. emcrit.org/pulmcrit

The views in this post represent my own reading of the evidence and are not institutional guidelines. Clinical decisions should always account for individual patient factors. If in doubt — call for help.

Casey Parker is a Rural Generalist who happens to work in a large quaternary ED with all the bells n whistles. He is not funded by Boston Scientific, Inari Medical, or anyone making a catheter.

This talk contains a lot of pearls and some big picture strategies for the young EM doc.

This month we tackle bleeding brains, clotting eyes, doing less for pneumothoraces (or is it pneumothoraci? Oh, well its defintitley pl(e)ural!! hehehehe!!). We chat about intra-cardiac arrest echo and Macgyvering urine collection devices for a female patients… quite a mix eh?

As always the PDFs are clickable on the titales below, so read, critique and decide for yourself.

The YouTube version is below or over at Justin’s Youtube channel if you need more middle-aged, hirsute men on your algorithm!

Eyeball Strokes are not that dissimilar to other strokes… a total evidentiary mess!

Préterre C, Gaultier A, Obadia M, Vignal C, Mourand I, Plat J, Sablot D, Gaudron M, Rodier G, Godeneche G, Urbanczyk C, Marc G, Massardier E, Adam S, Boulanger M, Marcel S, Mechtouff L, Ronzière T, Calvière L, Godard-Ducceschi S, Barbin L, Lebranchu P, Guillon B; THEIA collaborators.Intravenous alteplase versus oral aspirin for acute central retinal artery occlusion within 4·5 h of severe vision loss (THEIA): a multicentre, double-dummy, patient-blinded and assessor-blinded, randomised, controlled, phase 3 trial. Lancet Neurol. 2025 Nov;24(11):909-919. doi: 10.1016/S1474-4422(25)00308-4. PMID: 41109232

Traumatic pneumothorax: Less is more; more or less…

Harrison M. Non-Invasive Management of Blunt Traumatic Pneumothorax-a Meta-Analysis. Emerg Med Australas. 2025 Dec;37(6):e70164. doi: 10.1111/1742-6723.70164. PMID: 41163445

Bottom line: Conservative management is a good option even for patients with blunt trauma, as long as you are being selective about the patient you chose, and consider factors like length of transfer to a trauma center, positive pressure use, and ease of chest tube placement in whatever setting the patient might be monitored. 

To Shock, or not to shock, that is the question… but weird data here makes it an odd answer

Gaspari R, Lindsay R, She T, Acuna J, Balk A, Bartnik J, Baxter J, Clare D, Caplan RJ, DeAngelis J, Filler L, Graham P, Hill M, Hipskind J, Joseph R, Kapoor M, Kummer T, Lewis M, Midgley S, Nalbandian A, Narveas-Guerra O, Nomura J, Sanjeevan I, Scheatzle M, Schnittke N, Secko M, Soucy Z, Stowell JR, Theophanous RG, Tozer J, Yates T, Gleeson T. Incidence and Clinical Relevance of Echocardiographic Visualization of Occult Ventricular Fibrillation: A Multicenter Prospective Study of Patients Presenting to the Emergency Department After Out-of-Hospital Cardiac Arrest. Ann Emerg Med. 2025 Oct;86(4):328-336. doi: 10.1016/j.annemergmed.2025.04.014. Epub 2025 Jun 30. PMID: 40590825

Don’t feel pressure to fix the pressure… your patient may benefit?

Shi AC, Taylor T, Huang CC, Singhal AB, Goldstein JN, Bevers MB, Hou PC. Early Intensive Blood Pressure Reduction After Intracerebral Hemorrhage Is Associated With Worse Functional Outcome: The Risk of Overshooting Blood Pressure Goals. Ann Emerg Med. 2025 Dec 9:S0196-0644(25)01303-4. doi: 10.1016/j.annemergmed.2025.10.009. Epub ahead of print. PMID: 41369631

Clinical decision rules vs commonsense…

Kerr G, Chown A, Mercuri M, Clayton N, Mercier É, Morris J, Jeanmonod R, Eagles D, Varner C, Barbic D, Parpia S, Buchanan IM, Ali M, Kagoma YK, Shoamanesh A, Engels P, Sharma S, Worster A, McLeod S, Émond M, Stiell I, Papaioannou A, de Wit K. Applying the Canadian Head CT Criteria to Older Adults Seen in the Emergency Department After a Fall. J Am Geriatr Soc. 2026 Feb;74(2):509-515. doi: 10.1111/jgs.70191. Epub 2025 Oct 31. PMID: 41170758

Adding insult to injury – food in the ED ‘aint great

Barrington V, Carter V, Tagg A, Hitch D. Food as a Component of Patient-Centred Care in Emergency Departments: Preliminary Findings. Emerg Med Australas. 2025 Oct;37(5):e70126. doi: 10.1111/1742-6723.70126. PMID: 40890898

Justin makes some rash decisions about golfers legs…

Cook K. Rash following a round of golf. Emerg Med J. 2026 Feb 24;43(3):150-166. doi: 10.1136/emermed-2025-215366. PMID: 41735021

Madame’s MacGyver Urinal. A problem that needed solving 100 years ago

Booth S, Ellis P, Lyttle MD, Lochab S, Pegrum J, Thomas S. Disposable female urinal bottle (the UniWee) improves patient experience for immobile women with lower limb fractures. Emerg Med J. 2025 Apr 22;42(5):326-333. doi: 10.1136/emermed-2024-214181. PMID: 40081970

The Paper

Pericardiocentesis, drainage and instilled tranexamic acid: definitive management in a 25-case series of penetrating cardiac tamponade.  Qandil, Mohammed et al.   Injury, Volume 0, Issue 0, 113106 

A prospective case series from Nasser Medical Complex, Khan Younis, Gaza — a 700-bed tertiary trauma centre managing an average of 200 war casualties per day. Twenty-five patients with penetrating cardiac tamponade. One cardiac surgeon covering the entire region. Some patients arriving by horse and cart.

What They Did

Standard teaching says penetrating cardiac tamponade = get to the OR. Thoracotomy. Cardiac surgeon. Job done.

That wasn’t an option in Gaza.

So the emergency physicians developed a protocol:

1. eFAST first — confirm tamponade (effusion >2.5cm with haematoma), confirm preserved cardiac activity
2. Pericardiocentesis — subxiphoid approach, ultrasound-guided, using a 16G dialysis catheter (importantly, NOT a standard pericardiocentesis kit — more on that below)
3. Aggressive manual aspiration — 50ml syringe, drain until haemodynamic improvement
4. Intrapericardial TXA — 1 gram (10ml) instilled directly into the pericardial space
5. Drain left in situ for 48 hours with daily echos

That’s it. No thoracotomy. Done in the ED.  Patients were followed and there is good granular data about each case in the text.

Inclusion / Exclusion

This is critical and I’ll return to it in the appraisal section.

Included: penetrating chest trauma + clinical obstructive shock + echo-confirmed tamponade, presenting within ~3 hours, with preserved cardiac activity.

Excluded: cardiac arrest, absent myocardial contractility on echo, unsurvivable injuries.

The Results

Most of the patients in this series were young ( many were children aged 4 – 18 years and young adults.)

96% survival to discharge (most stayed 5-7 days) — the one death was from severe brain injury, not cardiac
– 0% thoracotomy rate  — definitive treatment in every surviving patient
– 8% recurrence — two patients needing repeat drainage (still no thoracotomy)
– No immediate procedural complications
– Some pulmonary complications (pneumonia, atelectasis) — related to associated thoracic injuries, not the procedure

Compare that to their historical thoracotomy-first approach: ~50% mortality

These numbers are striking. Remarkable, even. Barely believable.

Critical Appraisal — The Good Stuff First

This is a prospective consecutive series with a standardised protocol. In the context of an active war zone with constrained resources and overwhelming patient volumes, that’s genuinely impressive methodological rigour. They weren’t just retrospectively pulling charts — they designed a protocol, stuck to it, and reported honestly.

The clinical outcomes speak for themselves. 96% survival in penetrating cardiac tamponade is extraordinary by any benchmark.

And the physiology actually makes sense. For a patient with preserved cardiac activity, the authors argue the injury likely represents a self-sealing wound, predominantly in a low-pressure chamber. The pericardium itself then acts as a natural tamponade once the blood is drained — and the hypothesis is that intrapericardial TXA stabilises the clot at the wound site, effectively plugging it.

The large-bore catheter point is worth highlighting for practical purposes. They specifically use a 16G dialysis catheter rather than a standard pericardiocentesis kit. Their argument: standard kits are too small-bore to adequately evacuate blood (as opposed to serous fluid). Clinically logical, and an important technical detail if anyone is considering replicating this.

Selection Bias — The Goldilocks Zone Problem

This is the thorniest issue (common in trauma papers) , and the authors deserve credit for acknowledging it openly — but it’s worth unpacking further.

The 25 patients in this series existed in a very specific physiological sweet spot. Too sick to ignore, not sick enough to be unsalvageable. Preserved cardiac activity, haemodynamically compromised but not arrested, penetrating wound that was almost certainly to a low-pressure chamber, and survived long enough to reach hospital. Goldilocks patients, essentially — and the protocol worked beautifully on them.

But here’s the survivorship bias problem baked into that selection: the patients who didn’t make it into this series either died before arrival (likely high-pressure chamber injuries that bled out), were in cardiac arrest on arrival (straight to emergency thoracotomy or palliation), or had unsurvivable associated injuries. We never see those patients in the data. The 96% survival figure applies only to the cohort that was already, by definition, selected to do reasonably well.

And here’s the uncomfortable flipside for those of us in better-resourced settings: in a major trauma centre with early surgical access, you’d never find out who the Goldilocks patients are.  The moment you have penetrating cardiac tamponade and a cardiothoracic team in the building, those patients are going to the OR. You never get to observe which ones might have sealed spontaneously with a drain and some TXA, because you never leave them alone long enough to find out.

Gaza’s resource constraints (there was only 1 cardiothoracic surgeon in the whole region) created the conditions for a natural experiment that no ethics committee in a well-resourced setting would ever approve.

But that sobering reality is also, paradoxically, this paper’s greatest contribution. Because what Gaza’s resource constraints have inadvertently created is a natural experiment.  Natural experiments, for all their methodological messiness, are extraordinarily valuable when they generate findings that challenge existing dogma.

We now have 25 consecutive cases with a standardised protocol and a 96% survival rate suggesting that a carefully selected subgroup of penetrating cardiac tamponade patients may not need a thoracotomy at all.   This is exactly what you need to justify a prospective multicentre trial — the kind that could be run in high-resource settings, randomising haemodynamically stable penetrating tamponade patients between the surgical standard of care and the pericardiocentesis-drain-TXA protocol, with full ethics oversight and a proper control arm.

Nobody would have designed that trial before this paper existed. They might now.

The TXA Question — Don’t Get Carried Away

The intrapericardial TXA is the most novel and attention-grabbing component of this protocol, and it will inevitably generate excitement in FOAMed circles. Pump the brakes a little.

The authors’ hypothesis is elegant — instilled TXA stabilises the clot at the myocardial wound site, forming a natural plug contained by the pericardium. Mechanistically plausible. But this paper proves absolutely nothing about TXA’s specific contribution, and it’s important to say that clearly.

Here’s the problem: there is no control group. Every patient received TXA, large-bore drainage, 48-hour drain monitoring and serial echos. You cannot unpick which element drove the outcome. And in this highly selected Goldilocks cohort — preserved contractility, low-pressure chamber injuries, self-limiting haemorrhage — there’s a very real possibility that most of these patients would have done just as well with aggressive drainage alone.

Add to that the likelihood that many of these patients also received systemic TXA as part of routine major trauma management — which is already standard of care in most conflict and resource-limited settings. If systemic TXA is already on board doing its job, what exactly is the intrapericardial dose adding? We simply don’t know.

The TXA instillation hypothesis is interesting enough to warrant formal investigation. But until someone runs a trial with a control arm, we’re essentially pattern-matching on 25 cases and telling a compelling story. Compelling stories are not the same as evidence.

File it under: interesting, biologically plausible, hypothesis-generating, not proven.

My Bayesian senses tell me the TXA is probably window dressing here — a biologically plausible but ultimately redundant addition to a protocol whose heavy lifting is being done by timely decompression and a drain big enough to actually do the job. I could be wrong. But I’d want a control arm before I start instilling TXA into pericardial spaces on the strength of 25 uncontrolled cases.

Clinical application

Most of us aren’t working in Khan Younis. But the question this paper raises is relevant everywhere outside a major cardiothoracic centre:

In a patient with penetrating cardiac tamponade and preserved cardiac activity, is pericardiocentesis + drain a viable primary strategy rather than just a bridge to surgery?

For those of us in rural and remote emergency medicine, let’s be honest about the trauma we actually see. In Broome, we’re dealing with blunt trauma — predominantly MVAs — and the occasional knife injury. Bullets and bombs in the bush are vanishingly rare. So the direct clinical translation from a Gaza war zone to the Kimberley is limited, and it would be a stretch to pretend otherwise.

But here’s the thing that does translate: time.

In Gaza, the authors estimate most patients arrived within 1-3 hours of injury. In rural WA, 3-6 hours from injury to definitive care is not the exception — it’s the norm. The RFDS is coming, the retrieval is happening, but it takes time. And that time gap is actually the key variable in this whole story.

So ask yourself: what does the surviving cohort of significant chest trauma look like at the 3-6 hour mark in a rural Australian ED? By definition, they’ve already declared themselves — they’re not the immediate exsanguinators, not the tension pneumos that killed someone on scene. They’re the ones whose physiology has found some kind of equilibrium, however fragile.

Sound familiar? That’s the Goldilocks zone again.

Whether we’ll ever see the specific tamponade pattern described in this paper in our rural survivors is uncertain — the injury mechanisms are different, and blunt cardiac injury behaves differently from a shrapnel wound to the right ventricle. But the underlying principle — that a haemodynamically tenuous patient at the far end of a long retrieval window might respond to aggressive pericardial decompression as a bridge or even definitive treatment — is worth holding onto.

It’s not a protocol change. Not yet. But it’s worth knowing, and worth having the kit and the skills ready.

Bottom Line

This is a case series, not an RCT. It’s small, uncontrolled, and conducted in an environment most of us will never work in. You can’t transplant 96% survival figures into a teaching hospital context and assume equivalence.

But the findings are hypothesis-generating in the best possible way. The protocol is logical, the technical components are reproducible, and the outcomes are remarkable. This paper deserves serious attention from trauma guidelines committees — particularly the large-bore drainage component, which is the element most likely to be driving these results and which warrants formal prospective evaluation.

And beyond the clinical content: the fact that this protocol was born out of necessity, refined under extraordinary pressure, and rigorously documented by clinicians working in a war zone — that alone demands our respect and attention.

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