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We discuss the diagnosis and management of SCAPE in the ED.

Hosts:

Download Leave a Comment Tags: Acute Pulmonary Edema, Critical Care

Course Highlights:

Click Here to Register and Begin Module 1 The Clinical Case

Differential Diagnosis for the Hypoxic/Tachypneic Patient

What is SCAPE?Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is characterized by a sudden, massive sympathetic surge leading to intense vasoconstriction and a precipitous rise in afterload.

Bedside Diagnosis: POCUS vs. CXRPOCUS is the gold standard for rapid bedside diagnosis.

Management Strategy 1. NIPPV (CPAP or BiPAP)Start NIPPV immediately to reduce preload/afterload and recruit alveoli.

2. High-Dose NitroglycerinThe goal is to drop SBP to < 140–160 mmHg within minutes.

3. Refractory HypertensionIf SBP remains > 160 mmHg despite NIPPV and aggressive NTG, add a second vasodilator:

Troubleshooting & Pitfalls The “Mask Intolerant” PatientHypoxia is the primary driver of agitation. NIPPV is the best sedative. * Pharmacology: If needed, use small doses of benzodiazepines (Midazolam 0.5–1 mg IV).

The Role of DiureticsIn SCAPE, diuretics are not first-line.

Disposition

Take-Home Points

The post PODCAST: Sympathetic Crashing Acute Pulmonary Edema (SCAPE) first appeared on האיגוד הישראלי לרפואה דחופה.

Mike Weinstock on medmal cases: upper back pain (1:29)

Andrew Petrosoniak on traumatic pneumothorax and hemothorax decision making (27:55)

Justin Morgenstern on brain injury guidelines: risk stratification for neurosurgical consult, imaging and admission (38:23)

Andrew Tagg on management of post-circumcision bleeding  (47:32)

Hans Rosenberg & Ariel Hendin on evaluation and management of CT contrast allergy  (50:30)

Shawn Seregren on emotional contagion in resuscitation teams  (59:30)

Podcast production, editing and sound design by Anton Helman

Podcast content, written summary & blog post by Anton Helman, January, 2026

Cite this podcast as: Helman, Petrosoniak, A. Morgenstern, J. Tagg, A. Rosenberg, H. Hendin, A. Seregren, S. EM Quick Hits 70 – MedMal Case Upper Back Pain, Traumatic Pneumothorax/Hemothorax Decision Making, Risk Stratification of ICH for Consultation, Post-Circumcision Bleeds, IV Contrast Allergy, Emotional Contagion. Emergency Medicine Cases. January, 2026. https://emergencymedicinecases.com/em-quick-hits-70-jan-2026/. Accessed January 14, 2026.

This is Part 1 of a 2-part EM Quick Hits series on traumatic pneumothorax/hemothorax

This determines urgency, imaging, and tube selection for traumatic pneumothorax.

Peri-arrest or unstable patients with suspected traumatic pneumothorax: Immediate decompression is required—often before imaging. Finger thoracostomy followed by large-bore surgical chest tube placement prioritizes speed, reliability, and maximal drainage.

Stable patients allow for nuance. Imaging-based thresholds for traumatic pneumothorax help guide decisions:

Chest X-ray: pneumothorax >38 mm or >20% hemithorax

CT chest: pneumothorax >35 mm (largest lung-to-chest-wall distance)

For hemothorax, CT is preferred as size is difficult to quantify on ultrasound and chest X-ray; roughly 300 mL or pleural thickness >1.5 cm is a practical cutoff for drainage.

Stable patients generally benefit from CT imaging, which improves diagnostic certainty and decision-making.

*These thresholds apply primarily to patients without hemothorax and without significant oxygen requirements.

*Decisions should integrate imaging findings with respiratory status and work of breathing.

Evidence supports pigtail catheters for stable patients with traumatic pneumothorax and hemothorax, with similar outcomes to large-bore tubes. However, large-bore surgical tubes remain preferred in unstable patients, those with suspected pleural adhesions, significant subcutaneous emphysema, or complex injury patterns.

The AAST Brain Injury Guidelines (BIG 1–3) stratify traumatic intracranial hemorrhage by clinical risk and bleed characteristics to reduce unnecessary neurosurgery consults, repeat CTs and admissions while maintaining patient safety. Risk assignment is based on neurologic exam, intoxication status, anticoagulation, and bleed characteristics.

BIG 1 (low risk): small, simple bleeds, perfect neuro exam, no intoxication, no anticoagulants → in the study there were no neurosurgical interventions and very low rates of progression, but the data are still limited and confidence intervals wide.

BIG 2 (moderate risk): normal exam but larger bleeds or higher‑risk features → admit, repeat exam and CT; neurosurgical consultation is not mandatory up front, as neurosurgery interventions were 0% in this group despite ~7% radiographic progression.

BIG 3 (high risk): any neuro abnormality, anticoagulation/antiplatelet use (including aspirin), or larger/more complex bleeds → neurosurgery consult, admission and repeat CT; this group had high rates of clinical deterioration, progression and neurosurgical intervention.

Pragmatic approach:

BIG 1 (low risk): consider observation + reassessment; discharge only if your local system supports it and follow-up is reliable.

BIG 2 (moderate risk): admission often reasonable; consider repeat imaging selectively (progression isn’t zero).

BIG 3 (high risk): neurosurgical consult + admission + repeat imaging.

First10EM deeper dive into AAST Brain Injury Guidelines

Modern iodinated and gadolinium contrast agents are remarkably safe. Contrast agents used after 2000 are significantly safer than older formulations.

True contrast hypersensitivity is rare, most “contrast allergies” are misclassified, and routine steroid premedication should be abandoned.

How common are true allergic reactions?

Shellfish or iodine allergies are not contrast allergies.

Many “contrast allergies” represent physiologic or non-allergic reactions.

Longstanding steroid premedication protocols persist despite weak, outdated evidence derived from older high-osmolar contrast agents. Contemporary data show:

Contrast switching

Which antihistamines are best for treatment of true mild IV contrast allergy?

Poor documentation is the biggest barrier to safe imaging—always record the exact contrast agent, reaction type (immediate vs delayed), severity, treatment required, and outcome.

Bottom line: switch contrast agents, document accurately, and stop reflex steroid premedication.

Resuscitations are not emotionally neutral environments. Emotional contagion describes how tone, pace, and affect spread unconsciously through teams, shaping the emotional climate of the room. The emotional tone of a resuscitation is strongly influenced by the team leader. Leaders often underestimate how their tone affects team performance. A rushed or sharp tone amplifies anxiety, cognitive overload, and error. Calm, firm leadership steadies performance—even when decisions are complex or stakes are high. Simple, trainable behaviors help regulate the room:

Importantly, leadership is shared. Nurses, recorders, and respiratory therapists can actively dampen rising tension with neutral phrasing and steady updates. Leadership skills require deliberate practice, often recognized after simulation.

Bottom line: emotional regulation is not “soft skills”—it is a patient safety intervention.

The post PODCAST: EM Quick Hits 70 MedMal Cases Upper Back Pain, Traumatic Pneumothorax/Hemothorax Decision Making, Risk Stratification of ICH for Consultation, Post-Circumcision Bleeds, IV Contrast Allergy, Emotional Contagion first appeared on האיגוד הישראלי לרפואה דחופה.

Roy Perlis, MD, MSc1; Yulin Hswen, ScD, MPH2

In this episode of JAMA+ AI Conversations, we review the past year in AI and health, and talk about what we hope to see this coming year. We discuss our favorite articles and what they might mean for the future of medicine.

This interview is part of a series in which JAMA Network editors and expert guests explore issues surrounding the rapidly evolving intersection of AI and medicine.

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Nondisabling stroke is where Emergency Medicine earns its keep. The threats are quieter, the windows are wider, and the misses—especially in younger and female patients—are more common. In this Part 2 or our 2-part podcast update on ED stroke management with Dr. Katie Lin and Dr. Walter Himmel we explore non-disabling strokes, where symptoms are mild enough that patients can continue daily activities if deficits persist. Yet, non-disabling does not mean benign. Nondisabling strokes occupy the same ischemic continuum as high risk TIAs and carry a substantial risk of early recurrent disabling stroke. In this EM Cases podcast we answer questions such as: Which patients with non-disabling stroke can safely be discharged from the ED with prompt follow-up and which require urgent investigation or admission? Which stroke mimics do we need to be on the look out for and how do we identify them at the bedside? How dangerous is thrombolysis in a patient with presumed stroke who turns out to be a stroke mimic? What are the key distinguishing features between a stroke and functional neurologic disorder? What are the most common causes of stroke in young people that we commonly miss? How does stroke etiology dictate the management pathway? What are the indications for carotid endarterectomy in patients with nondisabling stroke and what is the ideal timing of the endarterectomy? When is dual antiplatelet therapy vs single antiplatelet therapy vs anticoagulant therapy indicated? What is the best medication strategy for the patient on a DOAC for atrial fibrillation who presents to the ED with a nondisabling stroke? For patients not on a DOAC for atrial fibrillation who come in with a stroke, when is it safe to start anticoagulation? and many more…

Podcast production, sound design & editing by Anton Helman; Voice editing by Braedon Paul

Written Summary and blog post by Anton Helman, edited by Katie Lin, November, 2025

Cite this podcast as: Helman, A. Himmel, W. Lin, K. Nondisabling Strokes Recognition and Management. Emergency Medicine Cases. November, 2025. https://emergencymedicinecases.com/nondisabling-strokes-recognition-management. Accessed November 15, 2025

Nondisabling stroke accounts for a substantial proportion of ED cerebrovascular presentations. Although clinical deficits are mild, the 30-day risk of neurologic deterioration or disabling stroke is about 4-5%. ED priorities include precise phenotyping, urgent vascular imaging when indicated, early secondary prevention, and reliable short-interval follow-up. The key operational pivot is from “major/minor” toward disabling vs nondisabling—a distinction that determines whether to activate reperfusion pathways or pursue prevention-first pathways. Nondisabling stroke is where quiet presentations carry big stakes. Deficits may be subtle, windows feel wider, and the risk of being lulled into false reassurance is real—especially in younger patients and women.

Pitfall: a common pitfall is getting lulled into a false sense of reassurance for expedited workup when a patient presents with a nondisabling stroke. While nondisabling strokes do not require as rapid workup and treatment as disabling strokes, urgent workup and management should still be a priority.

As discussed in Part 1, The very first decision is whether the symptoms are disabling vs nondisabling, not whether the presentation is consistent with a “major vs minor” stroke. Disabling means the deficit(s)—if persisted—would compromise independence: language that prevents functional communication, dominant-hand motor weakness that prevents ADLs or work, gait failure, major visual field loss, or depressed consciousness. Nondisabling implies that, even if the deficit remained, independent living would still be possible (e.g., mild facial droop, subtle sensory change, small visual field cut that doesn’t affect reading/driving, mild dysarthria without aphasia). The classification determines tempo: disabling strokes get immediate CT and stroke-protocol CTA to consider reperfusion; nondisabling strokes still demand urgent prevention—non-contrast CT now to screen for intracranial hemorrahge, CTA soon thereafter—but the pathway is focused on stopping the next event.

Source: Dr. Katie Lin’s SYNAPSE: EM Neuro Essentials Course (www.SynapseCourse.com)

Emergency physicians miss approximately 1 in 10 strokes. Short term morbidity and mortality are 8 fold higher in missed strokes. Conversely, a similar proportion of “strokes” turn out to be mimics. Recognizing the difference is critical for avoiding both under- and overtreatment.

Functional presentations can mimic stroke. The key is inconsistency and distractibility.

Pitfall: Functional ≠ feigned. Up to 60% of patients with functional presentations have underlying organic disease—always rule out stroke first. Avoid diagnosing a “functional condition” in a patient without prior objective testing and/or neurologic consultation. Err on the side of stroke until proven otherwise. FND features do not exclude stroke.

Data show very low rates of hemorrhage (0–1%) when thrombolytics are given to stroke mimics as compared to the 3–5% seen in true strokes.
Thus, for disabling presentations, it’s safer to err on the side of treating as a potential true stroke when in doubt, including shared decision-making, informed consent when possible, and timely specialist consultation.

Strokes in the young are rare but can be devastating when missed. Approximately 13–18% of all strokes in North America occur in individuals under the age of 50. This proportion has increased over the past two decades. Younger patients are more likely to be labeled migraine, anxiety, or “functional”—particularly women—despite a vascular event. Etiologies also differ: dissection, PFO-related emboli, hypercoagulable states, and intracranial disease figure more prominently, yet we often default to “too young for stroke.”

Bottom line: Any sudden focal neurological deficit in a young person should be treated as a stroke until proven otherwise.

Non-disabling strokes and TIAs share pathophysiology, prognosis and treatments. The DOUBT study found that 13% of TIA presentations as short as 5 minutes in duration are subsequently found to have evidence of stroke lesions on MRI. 2-17% of patients with TIA or minor stroke suffer a subsequent disabling stroke within 90 days, most within 48 hours.

The ABCD2 score lacks sufficient sensitivity and specificity to reliably stratify short-term stroke risk after TIA, particularly for identifying patients at very low or very high risk. The score does not account for critical high-risk features such as ipsilateral large artery stenosis, atrial fibrillation, recurrent or crescendo TIAs, or imaging evidence of acute infarction, all of which substantially increase early stroke risk independent of ABCD2 score. As a result, patients with low ABCD2 scores may still harbor significant vascular pathology and face substantial risk, undermining the score’s utility for disposition or management decisions. Instead, current best practice focuses on clinical features to risk stratify patients. These are the features that predict a subsequent disabling stroke and mandate urgent imaging and treatment:

Persistent nondisabling deficits and resolved high-risk features share the same message: active cerebrovascular pathology with high risk for early subsequent stroke. A persistent deficit—even when “mild”—raises the pretest probability of a treatable lesion such as symptomatic carotid stenosis, intracranial atherosclerosis, or cervical artery dissection, and the opportunity for secondary prevention. Resolved high-risk features—true motor weakness (often described as heaviness), speech or language disturbance, major visual field loss, or depressed consciousness—suggest potentially high risk vascular territory at risk for susequent stroke from ongoing vascular pathology. Either scenario should trigger urgent head CT to exclude hemorrhage, early CTA head and neck to define the vasculature, and immediate antithrombotic decisions. The goal is to prevent the next stroke event, which is at highest risk within the first 48 hours to one week.

~¼ Large-artery atherosclerosis (carotid/intracranial):

~¼ Lacunar/small-vessel:

~¼ Other/cryptogenic (dissection, thrombophilia, hyperviscosity; higher in young):

Etiology is not an academic afterthought—it determines secondary prevention timelines, including both medications and interventional procedures. Large-artery atherosclerosis (carotid or intracranial) may require a surgical approach when symptomatic ICA stenosis is present; pre-op therapy is typically single antiplatelet, and the procedural window is early (after the first 48 hours, but ideally within the first couple of weeks). Lacunar or small-vessel disease typically requires an antiplatelet-based prevention strategy with aggressive risk-factor control; thrombolysis is reserved for disabling presentations within the treatment window. Cardioembolic sources (most commonly atrial fibrillation, but also structural heart disease) shift the plan toward oral anticoagulation once it is safe, so an ECG at the time of presentation and arrangements for rhythm monitoring and echocardiography matter even in nondisabling stroke or high risk TIA cases. Cervical artery dissection and other “cryptogenic/other” mechanisms are proportionally more common in younger patients; they necessitate CTA head/neck to confirm the diagnosis and typically lead to a short course of dual antiplatelets for TIA/nondisabling stroke presentations while awaiting confirmatory testing for underlying stroke etiology.

The appropriate acute imaging study in suspected ischemic stroke is a stroke-protocol CTA performed immediately, not a delayed “carotid stenosis” CTA intended for elective surgical planning. The stroke-protocol CTA provides time-sensitive information essential to emergency management: identifying the site of occlusion, assessing collateral circulation, and detecting stenosis or dissection that may alter acute therapeutic decisions.

A normal early CT or CTA does not exclude ischemic stroke. Lacunar infarcts, distal vessel occlusions, and small ischemic cores can be radiographically occult in the hyperacute phase. Clinicians should treat the clinical syndrome, and when imaging findings appear discordant with the patient’s presentation, pursue specialist advice rather than prematurely excluding the diagnosis.

Carotid and vertebral Doppler ultrasonography remain useful for secondary prevention and pre-operative assessment, but they do not substitute for CTA when available to inform real-time decisions in the ED.

Carotid endarterectomy remains one of the few surgical interventions in stroke care that meaningfully alters outcomes. Patients with symptomatic internal carotid artery stenosis of 70–99% derive the greatest absolute risk reduction in recurrent stroke with early CEA. Selected patients with 50–69% stenosis may also benefit, depending on plaque/composition/stability, comorbidities, and symptoms.

Timing is critical: CEA is typically deferred for the first 48 hours following ischemic stroke to avoid reperfusion injury in the “hot brain” phase, then performed as soon as safely feasible—ideally within 7–14 days of the index event. The benefit declines substantially with delay beyond two weeks.

Emergency clinician priorities:

Once intracranial hemorrhage is ruled out:

High-risk TIA and nondisabling stroke live on the same continuum and should be managed with the same urgency. Load antiplatelets in the ED and tailor the regimen to mechanism. Most patients without endarterectomy plans or atrial fibrillation benefit from a short course of dual antiplatelet therapy (DAPT)—typically  21 days—then de-escalation to monotherapy. Pragmatically, aspirin 160–325 mg loading then 81 mg daily combined with clopidogrel 300 mg loading then 75 mg daily is common; aspirin with ticagrelor 180 mg loading then 90 mg twice daily is a reasonable alternative. Benefit is front-loaded in the first three weeks; bleeding risk rises after, which is why DAPT is not continued indefinitely as a standard. Use single antiplatelet therapy if carotid surgery is anticipated, extend dual antiplatelet therapy when intracranial atherosclerosis is the culprit per local protocol, and/or transition to anticoagulation when cardioembolic sources such as atrial fibrillation are identified and it is safe to do so. For symptomatic cervical artery dissection with TIA or nondisabling stroke, treatment typically involves a short course of DAPT, while asymptomatic dissection commonly receives single-agent therapy for months in coordination with the stroke team.

Single antiplatelet medication options:

DAPT (short course ~21–28 days):

Etiology-specific nuances:

Cardioembolic sources (e.g., AF): oral anticoagulation for secondary prevention; initiation/timing individualized (consider infarct size, hemorrhagic risk, and neurology guidance) but typically within 4 days; the trend as of 2025 is to start a DOAC as soon as 24 hrs after the stroke initiation for smaller infarcts with low hemorrhagic transformation risk.

Smoking cessation, diabetes optimization, physical activity, and diet counselling—all should begin in the ED discharge summary or follow-up instructions.

Disposition decisions for patients presenting with acute nondisabling stroke should be individualized, guided by risk stratification and institutional resources. Admission to a specialized stroke unit is associated with improved outcomes even in nondisabling presentations and should be prioritized when high-risk features are present or reliable outpatient follow-up cannot be assured.

Hospital admission or observation is recommended for patients with any of the following:

Selected patients with nondisabling stroke can be discharged safely from the ED when all of the following are satisfied:

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In this episode of the Rebel Core Content podcast, Swami provides crucial tips on using tourniquets. Highlighting the significance of these life and limb-saving devices, the discussion focuses on the optimal placement of tourniquets, emphasizing placing them 2-3 inches (5-6 cm) above the bleeding source and avoiding joints. Swami also advises on the correct way to tighten the tourniquet using the Velcro strap first, followed by minimal use of the windless. The importance of noting the application time to avoid prolonged arterial flow interruption is also discussed. The episode concludes with a reminder to visit the podcast’s website for more valuable content.

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Try Alex (chatbot in right lower corner of the website)

Published on September 1, 2025

Written by Vivian Lei

Mindful Intubation

How does this change my practice?

Source

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Massive hemorrhage is one of the most time-critical, high-stakes scenarios in Emergency Medicine. Every minute matters. Every decision counts. But more blood is not always better—what saves lives is systematic, team-based, goal-directed care. In this update to the 7 T’s of Massive Hemorrhage Protocols with Dr. Jeannie Callum and Dr. Andrew Petrosoniak, we explore the most current, evidence-informed strategies for bleeding patients, from polytrauma to obstetrical, drawing on the latest clinical trial data, provincial MHP 2.0 rollouts, and real-world experience. We answer the questions: What is the evidence based alternative to FFP in EDs where FFP is not readily available? How accurate are decision scores in helping decide the trigger for MHP activation? Why is testing fibrinogen levels and giving fibrinogen concentrates so important in massive hemorrhage? How should we tailor our MHP to the GI bleed patient? To the obstetrical patient? and many more….

Podcast production, sound design & editing by Anton Helman; Voice editing by Braedon Paul

Written Summary and blog post by Matthew McArther, edited by Anton Helman August, 2025

Cite this podcast as: Helman, A. Callum, J. Petrosoniak, A. Massive Hemorrhage Protocols 2.0 – Update on the 7 Ts. Emergency Medicine Cases. August, 2025. https://emergencymedicinecases.com/massive-hemorrhage-protocols-2-0/. Accessed August 5, 2025

Determining when to activate MHP can be challenging. Overactivating MHP can cause harm by clogging up hospital resources as well as adverse sequelae from overtreatment. But even small delays in transfusing critically bleeding patients is associated with increased mortality. Rather than calling an MHP immediately based on EMS report or on arrival in the ED, our experts suggest a critical administration threshold approach to MHP.

In general, the literature suggests there is little downside to giving a 2-3 units of RBCs up front, so have RBCs ready for any patient who has hypotension in the field with a concerning mechanism, or any other suspicion of hemorrhagic shock. Once the patient arrives and you begin your primary survey, have a low threshold to administer those first 1-3 units if you are still concerned for hemorrhagic shock. In trauma, this strategy aligns with observational evidence that early red cell transfusion improves outcomes while minimizing premature plasma exposure.

Predicting upfront which bleeding patients will go on to need massive transfusion is challenging. Even our best clinical scoring tools are only 60-80% accurate. Trauma scores such as the Assessment of Blood Consumption (ABC), Shock Index, Revised Assessment of Bleeding and Transfusion score (RABT) and Resuscitation Intensity (RI) have been used to predict need for MHP. However, their sensitivity and specificity are modest. Instead, seeing how a patient responds after those first few units during the initial resuscitation will be most useful for you to decide when to activate MHP.

MHP Mnemonic: “Easy as ABC After 3”

It is useful to conceptualize the MHP as a “full court press” for patients with massive hemorrhage, designed to:

Dr. Andrew Petrosoniak proposes a two-step decision-making model: first, administer two or three units of uncrossmatched red cells to the bleeding patient. Then, reassess. This “ABC after 3” rule—standing for “Activate MHP, Balance products, Consider calcium and concentrates (fibrinogen)”—anchors the transition point between supportive transfusion and full protocol activation. If, after three RBCs, the patient remains unstable, coagulopathic, or is likely to require operative or angiographic intervention, then activation is warranted.

Ask three questions after 3 units RBCs (the “ABC after 3” rule):

Most of the evidence around MHP activation is in trauma. But not all bleeding patients share the same physiology: what about other causes of hemorrhagic shock?

Importantly, bleeding patients differ in fundamental ways depending on etiology. Trauma-induced coagulopathy occurs in approximately 25% of trauma patients and arises from complex endothelial dysfunction and fibrinolysis. In contrast, gastrointestinal bleeds—particularly variceal bleeds—typically involve a paradoxical mix of hypercoagulability and active bleeding. Postpartum hemorrhage, on the other hand, is most often caused by uterine atony, with hypofibrinogenemia as a late and ominous sign.

Accordingly, thresholds for MHP activation must be tailored. In trauma, early red cells followed by reassessment offers a reasonable approach. In GI bleeding, full activation is rarely needed, with only 5% of patients requiring more than red cells alone, and FFP may even be harmful. In contrast, obstetric hemorrhage demands a low threshold for activation. With blood flow to the gravid uterus at term reaching 1.5L/min, complete exsanguination can occur in minutes. Thus, any signs of instability in postpartum patients should prompt immediate protocol initiation.

These patients have very different physiology than bleeding trauma patients and rarely need MHP activation. A combination of crystalloid volume resuscitation and red cell transfusions to a hemoglobin target of 70-80mg/dL should be adequate for the vast majority of patients with variceal bleeds (Baveno VII consensus guidelines). Activating consultants early for endoscopic management is key. Giving plasma, as in MHP protocols, could increase portal venous pressures and increase bleeding.

Pitfall: Do not trust the INR in cirrhotic patients. These patients have alterations in both pro-thrombotic and anti-thrombotic protein synthesis, so they may have an overall pro-thrombotic state despite having an elevated INR. Focus your management on resuscitation, decreasing portal pressures, and hemorrhage source control, rather than trying to correct coagulopathy. TXA has been shown to increase thrombotic complications in these patients with no mortality benefit (HALT-IT trial).

Because of the high uterine blood flow of 1.5L/min of pregnancy, these patients have the potential to exsanguinate rapidly. Have a very low threshold to activate MHP for any post partum hemorrhage (PPH) patient who is showing signs of hemorrhagic shock in order to mobilize blood products quickly. Rapid source control of uterine atony, with medications and operative management if needed, is critical for these patients.

The first “T,” trigger, remains perhaps the most critical. Without timely activation of the MHP, the rest of the pathway simply doesn’t unfold. Traditionally, we’ve relied on a mix of gestalt, shock index, and trauma scores like ABC or REBT to guide activation. But the latest thinking encourages a more pragmatic, flexible approach.

Ratio-based Resuscitation

2:1 ratio of RBC to FFP is recommended by our experts which corresponds with multiple consensus guidelines. PROPER trial did not show a benefit of 1:1 compared to 2:1.

If FFP is unavailable, after the first 4 units of RBCs, give 2000 units of PCC and 4g of fibrinogen in lieu of FFP. You can repeat this once after the second pack of 4 RBCs.

Don’t overuse O negative – it’s a very limited resource. Women under 45 of childbearing potential should get O negative Kell negative blood. Everyone else gets O positive.

MHPs require seamless collaboration between emergency, surgical, nursing, transfusion, and laboratory services. High-performance teams emphasize clear role allocation, defined hemodynamic goals, and shared mental models.

Delegating transfusion logistics to two team members operating a rapid infuser is another high-yield move. Once MHP is activated, the transfusion sequence can be semi-automated: start with four units of RBCs, then alternate between RBC and FFP to approach a 2:1 ratio, with the team leader monitoring for signs of over- or under-transfusion. Regular check-ins—every 30 minutes or after each pack—allow for reassessment and recalibration. Shared situational awareness is critical. Reminders like “pause the transfusion if systolic >140 or <70” empower the team to speak up and support dynamic decision-making.

Despite its importance, lab testing is often overlooked in the midst of resuscitation. Yet timely, repeated laboratory data are essential for guiding goal-directed therapy. Trauma-induced coagulopathy can occur due to the release of natural heparins and tPA from damaged endothelial cells. Clinical signs of trauma-induced coagulopathy include excessive oozing from IV sites as well as mucosal bleeding.

Serial labs should be repeated every hour or after every 4 units of red cells, whichever comes first. Anchoring lab draws to clinical actions—such as after each MHP pack—makes this easier to remember.

Labs at baseline and minimum q60min (or after every pack/4 units):

A PTT should be included at baseline but only repeated if elevated or if the patient is on heparin or dabigatran.

 Pitfall: Forgetting fibrinogen. It’s important and often missed.

In Small Centers:

No fibrinogen testing? For hospitals lacking fibrinogen testing, empirical administration  of fibrinogen concentrates 4 g IV is recommended after two MHP packs in patients with ongoing bleeding.

The importance of fibrinogen and calcium

Among all these tests, fibrinogen is one of the most crucial—and the most frequently missed. Hypofibrinogenemia is a strong predictor of transfusion need and poor outcomes, particularly in obstetric and liver disease–associated bleeding. A declining fibrinogen level is a key indicator of worsening coagulopathy, and replacement must be timely and targeted. Calcium levels must also be vigilantly monitored, as hypocalcemia reduces cardiac contractility and interferes with coagulation factor activity. In cirrhotic patients with variceal bleeds, fibrinogen remains important. While their INRs may appear deranged, many are in a tenuous hemostatic balance. However, if fibrinogen is critically low, even expert endoscopists will struggle to achieve source control of bleeding.

CRASH-2 study showed that TXA has a time-sensitive mortality benefit if given in the 1st hour, so remember to give it ASAP for trauma patients with severe bleeding. Give the entire 2g upfront as a bolus- no need for an infusion as described in earlier protocols.

Tranexamic acid (TXA) is one of the few medications in hemorrhage resuscitation that has been shown to confer a mortality benefit—when used correctly. For trauma patients, their is an associated reduced mortality benefit with a 2-gram dose given within the first hour of injury. The key is speed. Delayed administration beyond 3 hours confers no benefit and may cause harm. In the chaos of resuscitation, having a timekeeper or checklist item reminding the team to administer TXA early is crucial. In prehospital settings, a 1 g dose by EMS can be followed by an additional 1 g in the ED.

In postpartum hemorrhage, our experts recommend 1 gram as soon as bleeding begins, followed by a second gram if bleeding persists after 30–60 minutes. This is supported by the WOMAN trial and WHO guidelines.

However, in gastrointestinal bleeding, TXA is no longer recommended. The HALT-IT trial demonstrated no mortality benefit and an increased rate of thromboembolic events in patients who received TXA. This underscores the importance of tailoring adjunctive therapy to the bleeding context.

Caution is advised in patients with recent thromboembolic disease (<3 months), although anticoagulated patients may still benefit from TXA given the overriding risk of hemorrhagic death.

Hypothermia is one-third of the deadly trauma triad, yet it’s often overlooked in the early stages of care. Hypothermia exacerbates coagulopathy by impairing platelet function and fibrinogen polymerization. Every 1°C drop is associated with a 20% increase in transfusion needs. There is also a potential psychologic benefit to our patients: patients who are kept warmer in the trauma bay often feel safer during their resuscitation.

A systems-based approach is needed. Warm IV fluids, forced-air warming, and heated resuscitation rooms should be standard. Temperature monitoring should begin immediately upon arrival, as anesthesia and operating room teams do routinely.

Tips to avoid hypothermia in trauma patients:

Target a temperature of 37 degrees celsius.

The initial 1-2 hours of the resuscitation is guided by hemodynamics and the overall clinical impression rather than lab parameters. The ongoing resuscitation is then guided by lab testing.

Pitfall: The treatment dose of fibrinogen is 4g which will increase the serum fibrinogen by approximately 1g/L. A common pitfall is to underdose fibrinogen.

Recommendations for platelet transfusion are based on expert opinion without RCT-level evidence of benefit. Studies in multiple patient populations (ICH on antiplatelet, dengue patients, neonatal patients) show a signal for harm with platelet transfusion, so be cautious to not over-transfuse platelets even in bleeding patients.

In the context of MHP, our experts recommend using a platelet treatment threshold of 50 × 10⁹/L, and increase to 100 × 10⁹/L if significant brain or spinal cord injury.

Transfusion decisions during massive hemorrhage must evolve from fixed-ratio empiricism to goal-directed, personalized care. While initial resuscitation can follow predefined ratios, once lab results are available, therapy should be adjusted based on specific targets.

For hemoglobin, a threshold of 70–90 g/L is adequate post-stabilization, according to a large cluster-randomized Japanese trial. During early resuscitation, however, red cells are given to maintain perfusion rather than based on hemoglobin levels.

Fibrinogen should be maintained above 1.5–2.0 g/L. If replacement is required, fibrinogen concentrate is preferred over cryoprecipitate where available. Unfortunately, underdosing is common; less than four grams is often ineffective. A full four-gram dose increases fibrinogen by approximately 1 g/L.

INR should be kept below 1.8, although this threshold is based on consensus rather than high-level evidence. Calcium (ionized) should be monitored and maintained above 1.15 mmol/L. A major trial in progress (CAVALIER) may soon provide more clarity on prehospital calcium administration.

There is growing interest in viscoelastic assays (TEG/ROTEM) for fine-tuned coagulation guidance. While the ITACTIC trial did not show mortality benefit in trauma, widespread adoption is limited by cost, complexity, and clinician unfamiliarity. Cardiac surgery data suggest these tools improve outcomes when used in experienced hands.

Deciding when to terminate an MHP is as important as when to initiate. The risks of over-transfusion include volume overload, alloimmunization, and product wastage. Therefore, the protocol should not run on autopilot.

Continuously Assess the Need for Ongoing MHP

Automate: reassess the need for MHP every 30 minutes or after every pack.

Use protocolized prompts: e.g., blood bank asks if MHP can be discontinued after 1 hour of inactivity.

Post-MHP, continue 4–6 hours of vigilant monitoring:

Development of antibodies is a real risk, so make sure the patient knows about what they have received and is informed of subsequent risks. For every unit there is 1/13 chance of making antibodies, but these are usually fleeting. Women of childbearing potential who received MHP should undergo a group and screen q3months. They should go into any future pregnancy aware of the increased risk of complication, as antibody-related transfusion complications can profoundly impact pregnancies.

In resource-limited settings where fresh frozen plasma (FFP) is unavailable, a validated alternative approach is to administer 2000 IU of prothrombin complex concentrate (PCC) along with 4 grams of fibrinogen concentrates. This replacement strategy has been shown to be safe and effective, was validated in the FIRST2 trial, and aligns with European guidelines.

PCC 2000 IU + fibrinogen concentrates 4 g per four units of RBCs

These centers typically deliver two such packs (PCC + fibrinogen) alongside RBCs before transferring the patient. Even without lab capacity to measure fibrinogen, empirical dosing in this context is justified and often lifesaving.

The MHP must also be modified for anticoagulated patients. Rapid identification is crucial, particularly in elderly patients presenting with trauma or GI bleeding.

For patients taking warfarin, administer 2000 IU of PCC along with vitamin K. For direct oral anticoagulants (DOACs), the same 2000 IU dose of PCC is given initially, and a second 2000 IU may be administered after one hour if bleeding continues. This simplified approach reduces delay and aligns with recent expert consensus.

MHP 2.0 emphasizes clinical judgment, early red cells, goal-directed therapy, and avoidance of over-activation. The 7 T’s remain our framework, but we now understand that:

Massive hemorrhage protocols have evolved. What began as a reactionary, one-size-fits-all approach has matured into a tailored, systematic framework grounded in physiology, evidence, and team dynamics. The 7 T’s offer a cognitive scaffold, but MHP 2.0 demands clinical judgment, humility, and leadership. As practice evolves, focus must shift from fixed-ratio empiricism to goal-directed transfusion guided by physiology, laboratory data, and systems-level readiness.

The post PODCAST: Massive Hemorrhage Protocols 2.0 – Update on the 7 TsMassive Hemorrhage Protocols 2.0 – Update on the 7 Ts first appeared on האיגוד הישראלי לרפואה דחופה.

Date: June 2, 2025

Dr. Andrew Tagg

Guest Skeptic: Dr. Andrew (Andy) Tagg is an Emergency Physician with a special interest in education and lifelong learning. He is the co-founder and website lead of Don’t Forget the Bubbles.

This is another SGEM Xtra that talks about what we can learn about being physicians from certain pop culture (TV and Movies). Past episodes include:

The SGEM will return with a structured critical appraisal of a recent publication. We will continue to strive to reduce the Knowledge Translation (KT) window from over ten years to less than one year, leveraging the power of social media.

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Dr. Wm. Ken Milne Emergency Medicine Physician Researcher/EBM Skeptic

The post PODCAST: Your Mission, Should You Choose to Accept It – To Be an EM Doc first appeared on האיגוד הישראלי לרפואה דחופה.

Date: May 14, 2025

Dr. Ross Prager

Guest Skeptic: Dr. Ross Prager is an Intensivist at the London Health Sciences Centre and an adjunct professor at Western University. His expertise in critical care medicine is complemented by his research interests in critical care ultrasound and evidence-based knowledge translation.

This is an SGEM Xtra episode. The inspiration was a thread Ross posted on X: Here are 10 lessons they don’t teach in medical school (but should) that I’ve learned the hard way over the years. He shared ten hard-earned lessons from his clinical life that never made it into the standard curriculum. These lessons are rooted in humility, human connection, and the everyday realities of medical practice.

Final Thought from Dr. Prager: “Medicine is not just about answers, it’s about presence. Our best tool is our humanity.”

The SGEM will be back next episode with a structured critical appraisal of a recent publication. Trying to cut the knowledge translation window from over ten years to less than one with the power of social media.

The post PODCAST: Ten Lessons They Don’t Teach in Medical School (But Should) first appeared on האיגוד הישראלי לרפואה דחופה.