מתמחים - האיגוד הישראלי לרפואה דחופה

Welcome to the Rebel Core Content Blog, where we delve into crucial knowledge for emergency medicine. Today, we share insightful tips from PEM specialist Dr. Elise Perelman, shedding light on respiratory challenges in infants, toddlers, and young children during the viral season. Understanding that most cases involve typical viruses, we aim to equip you with diagnostic pearls to identify more serious pathologies.

Pearl #1: Look at Your Patient

Begin exams from the doorway. Observing patterns such as accessory muscle usage can reveal a patient’s respiratory effort. Specify whether the work of breathing occurs during inspiration, expiration, or both. Inspiratory work indicates difficulty getting air in, while expiratory work suggests trouble pushing air out. Silent tachypnea may point to other issues, like acidemia or pneumothorax.

Pearl #2: Localize the Sound

Breathing noises signal varied respiratory issues. Stridor, often heard on inspiration, results from obstructions above the thoracic inlet. Conversely, wheezing, generally linked to exhalation, indicates obstructions in the lower airways. Watch for signs like ‘silent chest’—a dangerous, severe obstruction, and distinguish grunting as a bodily mechanism to prevent alveolar collapse. Correctly identifying the sound assists in determining the appropriate intervention.

Once a sound is localized, treatments vary. We explore Soder from nasal congestion, typically needing supportive care and suctioning. Stridor from conditions like croup is eased with interventions to reduce airway swelling, such as steroids or inhaled epinephrine. Conversely, wheezing in infants is often due to bronchiolitis—not bronchospasms—and over-treatment is to be avoided. Supportive measures including suction, hydration, and oxygen are preferred unless improvement warrants bronchodilators.

In severe cases of asthma or bronchiolitis, where standard at-home treatments fail, immediate adjunct therapies like intramuscular epinephrine become essential. Administering this quickly can alleviate obstruction when inhalants aren’t effective due to low air movement.

When recognizing Zebras—uncommon cases overshadowed by routine diagnoses—remain vigilant for histories or presentations that don’t conform. Conditions like pneumonia, bacterial tracheitis, and even myocarditis may mimic more common issues.

As attending physicians, our role extends beyond conventional treatment—it’s about discerning the atypical from the typical. Dr. Perelman urges continual reassessment, emphasizing reliance on observational skills as much as technological aid. Keeping keen on respiratory nuances ensures we catch those outlier cases, paving the way for adept medical care despite the overwhelming prevalence of viral infections.

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Deborah Schonfeld on pediatric urinary retention & acute transverse myelitis (01:27)

Jesse McLaren on Occlusion MI Diagnosis (24:44)

Matthew McArthur on post-dural puncture headache (31:34)

Joseph Yasmeh on Med Mal Cases: clenched fist injury (42:42)

Brit Long on IV thrombolysis for minor strokes (59:27)

Victoria Myers & Lauren Westafer on mentorship and what it means to be a physician leader (1:11:34)

Podcast production, editing and sound design by Anton Helman

Podcast content, written summary & blog post by Brandon Ng, edited by Anton Helman, December, 2025

Cite this podcast as: Helman, A. Schonfeld, D. McLaren, J. McArther, M. Yasmeh, J. Long, B. Myers, V. Westafer, L. EM Quick Hits 69 – Pediatric Urinary Retention & Acute Transverse Myelitis, Post-Dural Puncture Headache, Med Mal Cases: Clenched Fist Injury, IV Thrombolysis for Minor Stroke, EM Leadership Spotlight #4. Emergency Medicine Cases. December, 2025. https://emergencymedicinecases.com/em-quick-hits-month-year/. Accessed December 3, 2025.

Inability to void at least 12 hours, no urine output for 12 hours, greater volume of urine in the bladder expected for age, or palpable bladder distension.

Bottom line: Urinary retention may present variably in pediatric patients. In pediatric patients with otherwise unexplained urinary retention, consider neurogenic causes of urinary retention in patients.

Bottom line: ECG represents only one aspect of the clinical picture. Do not interpret ECGs using STEMI criteria alone. Consider POCUS to enhance diagnosis of OMI.

Deeper Dive and practice ECGs: ECG Cases 57 Art of Occlusion MI Part 5 – Clinical-ECG-POCUS Triptych

Register for Dr. McLaren’s HEARTS ECG Course to master your ECG interpretation skills.

Consider post-dural puncture headache in any patient with new positional headache that occurs within five days of a dural puncture.

This case involves an young adult male who presents with an injured hand that occurred when “messing around with some friends” when a brick “fell directly onto the back of his left hand”. The case highlights the importance of spotting the disconnect between the patient’s story and the presenting wound.

Clenched Fist Injury (Fight Bite) = consider in any laceration over the dorsal aspect of MCP or PIP joints, usually in the dominant hand.

Pathophysiology of clenched fist injury (fight bite)

Red-flag exam: Pain with passive finger motion = deep infection (infectious tenosynovitis/septic arthritis) until proven otherwise.

Investigations for suspected clenched fist injury (fight bite)

Critical Error #1: During wound care (including anesthetizing, irrigation and exploration), the tendon sheath was “frayed”, but the wound was closed with sutures.

Critical Error #2: Cefazolin/cephalexin were given for the skin and soft tissue injury.

Critical Error #3: Patient was discharged with a splint and told to follow-up with a plastic surgeon in several days.

Additional considerations: An accurate diagnosis and reasonable plan may fail if the patient can’t access treatment.

Bottom line: Trust the injury pattern not the story, injury over the knuckles of young person = clenched fist injury until proven otherwise. For bite wounds: irrigate thoroughly, do not suture primarily, splint hand in position of function, follow-up within 24-48 hours, and preferred antibiotic is amoxicillin-clavulanate. Acknowledge and address barriers of care to help ensure that patient gets the treatment you prescribe.

*This case was obtained from Dr. Mike Weinstock’s EM Boucebacks series of closed legal cases

To address an EM Caser’s concern about the questionable evidence for IV thrombolysis in patients who present within 4.5 hours of symptom onset with a minor stroke (defined as NIHSS ≤5) but their stroke is deemed disabling, we asked Brit Long for an evidence-based deep dive…

Current Guidelines

Literature on IVT in disabling strokes:

·       NINDS II (1995): n = 333, 12% benefit with IVT in 3 hours.

·       ECASS III (2008): n = 821, 8% benefit with IVT in 3-4.5 hours.

Literature on IVT in non-disabling stroke:

Optimizing practice:

Bottom line: Evidence overall suggests that risk of IVT may outweigh benefits in patients with minor stroke, however for disabling minor strokes, IVT should be offered. Consider legal implications of not giving IVT in disabling minor strokes. Reference your local institutional protocols on IVT for stroke.

For further listening on referenced EMCases episodes and Dr. Katie Lin’s take on the evidence for thrombolysis is disabling minor stroke in the comments sections: Ep 208 Paradigm Shift in Ischemic Stroke Management Part 1: Disabling Strokes and Ep 209 Nondisabling Stroke Recognition and Management.

The post PODCAST: EM Quick Hits Pediatric Urinary Retention & Acute Transverse Myelitis, Post-Dural Puncture Headache, Med Mal Cases: Clenched Fist Injury, IV Thrombolysis for Minor Stroke, EM Leadership Spotlight #4 first appeared on האיגוד הישראלי לרפואה דחופה.

The QT interval is a vital part of ECG interpretation, reflecting the heart’s electrical recovery after each beat. When prolonged, it can set the stage for torsades de pointes. Understanding how to measure and correct the QT interval, identify high-risk medications, and act quickly when TdP occurs is essential for every clinician. This guide walks you through the physiology, interpretation, common causes, and emergency management of QTc prolongation to keep your patients safe.

The post PODCAST: Understanding QTc Prolongation: Causes, Risks, and Management first appeared on האיגוד הישראלי לרפואה דחופה.

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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Date: October 10, 2025

Guest Skeptic: Dr. Sergey Motov is an Emergency Physician in the Department of Emergency Medicine, Maimonides Medical Center in New York City. He is also one of the world’s leading researchers on pain management in the emergency department. 

Case: A 37-year-old man presents to the emergency department (ED) with severe right-sided flank pain.  The pain started about eight hours ago as a vague discomfort in his right flank, but it has gotten progressively worse and now is radiating to his groin. Patient reports nausea, an increased urge to urinate and noticing blood in his urine on one occasion. The patient denies prior medical or surgical history.

Upon ED arrival, his vital signs are normal. Physical examination revealed a stated age patient in distress due to severe right flank pain, prominent right-sided costovertebral angle tenderness, and absence of abdominal tenderness or guarding. While strongly considering renal colic in differential diagnosis and reaching for the bedside ultrasound, you are wondering if a single dose of a non-steroidal anti-inflammatory (NSAID) will be enough to relieve this patient’s pain, or should you add Magnesium or Lidocaine?

Background: Renal colic is a common and extremely painful emergency department (ED) complaint encountered in the ED that frequently recurs. The nonsteroidal anti-inflammatory drugs (NSAIDs) given intravenously or intramuscularly (IM) are frequently used as first-line therapy. However, about 30% of ED patients receiving NSAIDS require rescue analgesia in the form of opioids. Opioid use, though effective, is limited at times due to the potentially dangerous adverse effects. Thus, there might be a role for other non-opioid classes of drugs to be co-administered with NSAIDs for relief of renal colic.

Magnesium sulfate (MgSO₄) has been suggested as a possible treatment option. It may blunt ureteral smooth muscle spasm by antagonizing calcium influx in smooth muscle and by N‑methyl‑D‑aspartate (NMDA) receptor antagonism. These are mechanisms that can reduce visceral pain and augment other analgesics. Small ED trials and meta‑analyses suggest MgSO₄ can reduce pain scores and opioid use in renal colic, though the evidence base has been limited and heterogeneous [1].

Another suggested treatment modality for renal colic is intravenous lidocaine. We looked at this treatment on SGEM#202 and were unimpressed with the efficacy. Systemic lidocaine blocks voltage‑gated sodium channels and appears to modulate central sensitization and visceral pain pathways. In ED populations, systematic reviews indicate IV lidocaine offers variable analgesia with a mixed signal for benefit, and renal colic–specific RCTs suggest it may be inferior to ketorolac and best considered (if at all) as part of a multimodal strategy rather than as monotherapy [2].

Reference: Toumia M, Sassi S, Dhaoui R, et al. Magnesium Sulfate Versus Lidocaine as an Adjunct for Renal Colic in the Emergency Department: A Randomized, Double-Blind Controlled Trial. Ann Emerg Med 2024

Authors’ Conclusions: “Adding intravenous MgSO4, but not lidocaine, to IM diclofenac offered superior pain relief but at levels below accepted thresholds for clinical importance.” 

Quality Checklist for Randomized Clinical Trials:

Results: They screened 1,321 patients and included 840 who were randomized (280 per arm). The mean age is in the mid 40s with a fairly even male/female split. The mean baseline NRS ~8.5–8.7. Ultrasound showed stones in ~20% and pyelocaliceal dilation in over one-third of patients.

Comment on Authors’ Conclusion Compared to SGEM Conclusion: We would have tweaked the conclusion to say: Adding intravenous MgSO₄, but not lidocaine, to IM diclofenac MAY offer superior pain relief, but at levels below accepted thresholds for clinical importance.

Case Resolution: You proceeded with administration of 10mg of IV Ketorolac as a single agent, and upon assessment of the patient at 20 minutes, the patient verbalized significant pain relief without experiencing any adverse effects. Urinalysis is positive for blood, while complete blood count, complete metabolic panel, and the remainder of the urinalysis are normal.  A non-contrast CT scan reveals a 4 mm non-obstructing stone in the right distal ureter.

Dr. Sergey Motov

Clinical Application: Intravenous adjunctive MgSO₄ does not seem to provide clinically meaningful pain relief in patients with renal colic but leads to frequent development of facial flashing. This precludes if from routine use in the ED for patients with renal colic. Similarly, IV lidocaine combined with parenteral NSAIDs does not provide clinically meaningful pain relief in patients with renal colic, and the evidence doesn’t support its use at this time.

What Do I Tell the Patient?  It looks like you have classic kidney‑stone pain. I will order an IV analgesic called ketorolac that should reduce your pain and make you more comfortable. However, if you are still in pain in 15-20 minutes after receiving this medication, I will proceed with ordering intravenous morphine.

Keener Kontest: Last week’s winner was Dr. Steven Steltz from NZ. He knew it was called Cable Beach in Broome, Western Australia, because it was the site where an undersea telegraph cable came ashore in 1889, connecting Australia to the rest of the world via Java.

Listen to the SGEM podcast this week to hear the trivia question. If you know the answer, send an email to [email protected] with “keener” in the subject line. The first correct answer will receive a cool skeptical prize.

Other SGEM Episodes:

References: 

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Reference: Jessen et al. Pharmacological interventions for the acute treatment of hyperkalaemia: A systematic review and meta-analysis. Resuscitation 2025

Date: August 6, 2025

Guest Skeptic: William Toon is a paramedic who, this past May achieved over 50 years of continuous EMS certification. His professional path has taken him from front-line paramedic to national presenter, expert witness, flight medic, EMS program director, and senior training executive with a doctorate in Higher Education.

Case: A 65-year-old patient presents to the emergency department (ED) with general weakness, mild abdominal cramping, and nausea over the past 12 hours. The patient has poorly controlled type 2 diabetes, heart failure with reduced ejection fraction, and chronic kidney disease stage 4 on hemodialysis. The patient missed their last dialysis appointment two days ago. The patient takes several medications for kidney disease and blood pressure, including a potassium-sparing diuretic. His ECG shows peaked T-waves. Stat chemistry reveals a serum potassium of 6.5 mmol/L. He is not yet oliguric and is hemodynamically stable. The team must initiate pharmacologic treatment immediately while preparing for possible escalation to dialysis.

Background: Hyperkalemia is a potentially life-threatening electrolyte abnormality frequently encountered in the ED. It’s common in patients with chronic kidney disease, diabetes, or those on renin-angiotensin-aldosterone system (RAAS) inhibitors. While treatments like insulin, beta-agonists, and calcium gluconate are well-known, the comparative efficacy and safety of pharmacologic agents used to rapidly reduce serum potassium remain uncertain.

Clinicians must balance rapid action with safety when choosing treatment for hyperkalemia. Understanding which pharmacologic interventions work best and how quickly they act is vital to optimizing care. Unfortunately, much of the existing data on hyperkalemia treatment is derived from small or methodologically limited trials.

Reference: Jessen et al. Pharmacological interventions for the acute treatment of hyperkalaemia: A systematic review and meta-analysis. Resuscitation 2025

Authors’ Conclusions: “Evidence supports treatment with insulin in combination with glucose, inhaled or intravenous salbutamol, or the combination. No evidence supporting a clinical effect of calcium or bicarbonate for hyperkalaemia was identified.”

Quality Checklist for Therapeutic Systematic Reviews:

Results: Studies included adult patients with hyperkalemia from EDs, inpatient wards, and dialysis units. Ages ranged widely, with a predominance of patients with chronic kidney disease (CKD) and cardiovascular comorbidities.

Comment on Authors’ Conclusion Compared to SGEM Conclusion: We agree with the authors’ conclusions but would emphasize the limited certainty and highlight the need for better patient-oriented outcome data before changing practice broadly. 

Case Resolution: You administer 10 units of IV insulin with an amp of D50 and initiate inhaled albuterol. You consult nephrology and start sodium zirconium cyclosilicate, which is available in your ED. Repeat potassium at four hours drops to 5.4 mmol/L. No dialysis is needed.

William Toon

Clinical Application: This SRMA reaffirms insulin-glucose as the first-line treatment for hyperkalemia in the ED. It also supports adding beta-agonists when needed, de-emphasizing bicarbonate and sodium polystyrene sulfonate in acute settings, and suggests newer agents like SZC for future integration into your ED’s hyperkalemia protocol.

However, it does not mean we should not use calcium gluconate or chloride in patients with hyperkalemia. These agents are not meant to lower potassium levels, and it would be inappropriate to have expected them to do so. The SRMA did not demonstrate a patient-oriented outcome (POO) of benefits. We should interpret the findings cautiously. The absence of evidence of benefit is not the same as evidence of no benefit. Therefore, calcium should not be abandoned for the acute treatment of hyperkalemia solely based on this SRMA.

What Do I Tell the Patient? We’re treating your high potassium levels quickly to protect your heart. We’ve given insulin and another medicine to bring the levels down safely. We’ll keep monitoring you closely over the next few hours.

Keener Kontest: Last week’s winner was David Michaelson. He knew that TENS units are thought to reduce pain through the gate control mechanism and the release of endorphins.

Listen to the SGEM podcast for this week’s question. If you know, then send an email to [email protected] with “keener” in the subject line. The first correct answer will receive a shoutout on the next episode.

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Limping is a common complaint in pediatric emergency care, but the differential is broad and the stakes are high. In this episode, we walk through a detailed, age-based approach to the evaluation of the limping child. You’ll learn how to integrate the Kocher criteria, when imaging and labs are truly necessary, and how to avoid being misled by small joint effusions on ultrasound. We also highlight critical mimics like appendicitis, testicular torsion, and malignancy—and remind you why watching a child walk is one of the most valuable parts of the exam. Whether it’s transient synovitis, septic arthritis, or something much more concerning, this episode gives you the tools to manage pediatric limps with confidence.

Mastodon: @[email protected]

PEMBlog: PEMBlog.com

Blue Sky: @bradsobo

X (Twitter): @PEMTweets

Instagram: Brad Sobolewski

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Written by Amanda Mathews

Update your pharmacopia 

How does this change my practice?

Source

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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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