High-Pressure Injection Injury of the Hand: The Tiny Wound That Isn't Tiny

Case presentation (composite)

A man in his mid-thirties arrives after "a little poke" from an airless paint spray gun at work. The nondominant index fingertip has a pinpoint volar puncture with a speck of paint. The finger is mildly swollen and looks almost normal. Heart rate is 108, he is diaphoretic, and he is holding the hand very still. Capillary refill is brisk. Sensation is intact but he will not let you move the finger.

The first guess, and why it is tempting

The first guess is a puncture wound: irrigate, bandage, tetanus, an NSAID, discharge. It is tempting because the skin is the least informative organ here. The entry wound is often a few millimeters across, bleeding is minimal, and early on the patient may report surprisingly little pain. The injury is defined by what happens below the skin, not by the wound you can see.

What does not fit

Two findings should break the anchor.

1. The mechanism. A pressurized source. Pressures above roughly 100 psi are commonly cited as enough to breach skin [2, 10]. Equipment pressures range from about 100 psi (grease gun) to about 10,000 psi (hydraulic systems) [5], and a recent practice review for emergency physicians cites pressures up to 12,000 psi [1].
2. The disproportion. Pain, guarding, and autonomic signs that exceed a pinpoint wound. The opposite trap also exists: these wounds are often punctate with minimal pain early on, which is exactly why severity is underestimated [7]. Do not let a quiet first hour talk you out of the mechanism.

The typical patient is a working man in his thirties with an injury to the nondominant index finger; the nondominant hand and the index finger are the most commonly reported sites in case series and reviews [2, 5, 10].

Why the wound lies

The fluid (paint, grease, hydraulic fluid, solvent) is forced through a tiny opening and then spreads along tendon sheaths, neurovascular bundles, and fascial planes, sometimes well into the palm or forearm. Harm comes from several mechanisms at once: mechanical dissection, vascular compression and spasm, chemical inflammation from the injectate, and later infection. Swelling then compounds ischemia in a digit that is already at risk. Compartment syndrome can follow [5].

Differential

• Simple puncture or laceration, with or without retained foreign body
• Flexor tenosynovitis or early deep space infection (timing and mechanism differ)
• Compartment syndrome from another cause
• Injection of a small volume of benign material (for example air or certain veterinary vaccines), which can sometimes be observed [4]
• Chemical or solvent toxicity, including systemic effects from large exposures

Workup

• History. What was injected (ask for the product name or safety data sheet), the estimated pressure, the distance, the time of injury, hand dominance, last oral intake, tetanus status.
• Exam. Full neurovascular assessment, tendon function, swelling extent, tenderness along the flexor sheath and proximal to the wound. Mark the margin of swelling and recheck.
• Plain radiographs. Some injected materials (some paints, for example) may show on X-ray and help map the extent of spread, but whether a given modern latex or oil-based paint is visible is uncertain, and some material is radiolucent, in which case subcutaneous air or soft-tissue swelling may be the only sign [2, 5]. A normal film does not exclude injury. Soft-tissue gas or lucency may be the only clue.
• Labs. Baseline CBC, renal function, inflammatory markers as a trend; these do not make or exclude the diagnosis.
• Advanced imaging is rarely needed and should never delay the hand surgeon.

Management

Think "limb-threatening injury with a clock."

• Call hand surgery (or the regional center) early, before imaging is finished.
• Do not be falsely reassured by a small wound, a comfortable-looking finger, or a normal radiograph.
• Keep the patient NPO, elevate the limb, update tetanus, and start broad-spectrum antibiotics per local protocol [4, 5, 6, 10].
• Analgesia is appropriate. Pain relief is not a sign of safety.
• Perform and document serial neurovascular checks (color, capillary refill, sensation, swelling, tense compartments), and mark the margin of swelling.
• Commonly taught cautions, not formal guideline rules: many authors advise avoiding a digital block (it may add to swelling and vasospasm) and avoiding ice, and leaving the wound open rather than closing it or applying a tight dressing [2, 5, 10]. These come from expert review and case-series experience, not from controlled trials; confirm with the receiving hand surgeon.
• Do not try to squeeze, flush, or chase the material in the ED. If irrigation is done in the operating room, organic solvents should not be used to remove the injected material [2, 5]. A small cadaveric study (two hands) suggested that adding a detergent (for example 10% povidone-iodine or a shampoo) cleared paint better than saline alone, but this is weak evidence and not an ED decision [8].
• Consider poison center input when a toxic solvent or large exposure is involved.
• Definitive care is wide surgical exploration and debridement, often with decompression, and frequently with repeat operations [4, 5, 6].
• Admit. Even a good-looking digit needs inpatient observation and surgical decision-making.

Steroids

Steroids have been used to limit inflammation, but they remain controversial: the pooled literature does not show a benefit for amputation or infection [3], some surgical series report selected use for solvent injuries [9], and recent reviews describe their role as uncertain [2, 6]. Not an ED decision; defer to the surgeon.

Disposition and consults

Emergent hand surgery consultation and operative exploration. Transfer if there is no hand surgeon or operating room available; do not hold the patient for observation "to see if it declares itself." Admit even if the finger looks good.

The evidence, in context

• A literature review of 435 upper-extremity cases (Hogan and Ruland, 2006) reported an overall amputation rate of 30% (the figure is stated in the abstract and applies to that pooled, largely historical series). Risk was highest with organic solvent injected into the fingers and lower with thumb or palm injuries. For paint, thinner, gasoline, oil, or jet fuel, amputation risk was lower when wide debridement occurred within 6 hours. Steroids did not change the amputation rate [3]. This is a pooled review of case reports and series, so confounding is substantial.
• A 2013 review reached a similar practical conclusion: emergent debridement, with the best outcomes when treated within 6 hours, and observation only for small-volume air, gas, or vaccine injections without concern for compartment syndrome [4].
• Amputation rates appear to be lower in some contemporary series; the authors of the series below note that older reports put the figure at roughly 30% to 40%, and cite other recent series reporting 3.1% and 0%. A single-center retrospective review of 53 cases (2007 to 2023) found one amputation among the 53 patients, in a patient with end-stage liver disease, which the authors report as a 2.2% rate (one of 53 is about 1.9%, so the published percentage does not exactly match the count) [7]. The authors describe fewer reoperations and complications with latex-based paint injuries, but their own analysis found no statistically significant differences between injected materials, and the groups were small [7]. Better outcomes do not mean an option to wait: amputation is only one outcome, and stiffness, chronic pain, and reoperation remain common concerns [2].

Clinical pearls

• A pressurized tool plus a hand wound is an injection injury until a surgeon says otherwise.
• The patient who looks comfortable at hour one may not at hour six.
• "What was in the gun?" is part of the triage question, not a detail.
• Solvent-based injectate into a finger carries the highest risk [3].
• Treat "pain out of proportion" as a sign of ischemia or compartment syndrome until proven otherwise.

Common pitfalls

• Anchoring on "puncture wound" and discharging with an NSAID.
• Digital block for exam or repair (commonly taught as a caution).
• Closing the wound, or applying a tight dressing (commonly taught as a caution).
• Waiting for a normal-looking film to "rule out" injection; a normal film does not exclude injury.
• Counting hours after the patient arrives, not after the injury.

Teaching points

• Small hole, big force: mechanism beats appearance.
• Pressurized source plus pain that does not match the exam means hand surgery now.
• Commonly taught cautions: avoid digital block, ice, closure, and tight dressings. Do not discharge.
• Earlier debridement (ideally within about 6 hours) is associated with lower amputation risk, especially with solvents.
• Steroids are controversial; leave that to the surgeon.

References

1. Cornely RM, et al. Recognising high-pressure injection injuries to the hand: a practice review with guidance for emergency physicians. Emerg Med J. 2026;43(2):122-127. doi:10.1136/emermed-2024-214689 | PMID 40588328
2. Rosenwasser MP, Wei DH. High-pressure injection injuries to the hand. J Am Acad Orthop Surg. 2014;22(1):38-45. doi:10.5435/JAAOS-22-01-38 | PMID 24382878
3. Hogan CJ, Ruland RT. High-pressure injection injuries to the upper extremity: a review of the literature. J Orthop Trauma. 2006;20(7):503-511. doi:10.1097/00005131-200608000-00010 | PMID 16891944
4. Amsdell SL, Hammert WC. High-pressure injection injuries in the hand: current treatment concepts. Plast Reconstr Surg. 2013;132(4):586e-591e. doi:10.1097/PRS.0b013e31829f4bb4 | PMID 24076706
5. Azevedo JM, et al. High-pressure injection injuries of the hand: a report of three cases presenting with acute compartment syndrome. Cureus. 2024. doi:10.7759/cureus.72786 | PMID 39618598
6. Cejin MC, Koyfman A, Long B. High risk and low incidence diseases: high-pressure injection injury. Am J Emerg Med. 2025;88:120-125 (published online November 2024). doi:10.1016/j.ajem.2024.11.066 | PMID 39615434
7. Jakkaraju SK, Sager BW, Brady CI. Revisiting amputation rates in high-pressure injection injuries. J Hand Surg Glob Online. 2024;6(4):540-544. doi:10.1016/j.jhsg.2024.04.007 | PMID 39166208
8. Bascone CM, et al. Optimal irrigant in high pressure paint injection injuries of the hand. Plast Reconstr Surg Glob Open. 2022;10(1):e4064. doi:10.1097/GOX.0000000000004064 | PMID 35083106

9. Gutowski KA, Chu J, Choi M, Friedman DW. High-pressure hand injection injuries caused by dry cleaning solvents: case reports, review of the literature, and treatment guidelines. Plast Reconstr Surg. 2003;111(1):174-177. doi:10.1097/01.PRS.0000038024.90426.CA | PMID 12496578

10. Pertea M, Luca S, Benamor M, et al. High-pressure injection injury of the hand: a rare but true surgical emergency. J Clin Med. 2024;14(1):72. doi:10.3390/jcm14010072 | PMID 39797154

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Occlusion MI Hiding Behind a "Nonspecific" EKG

Case presentation (composite)

A man in his late fifties presents with forty minutes of crushing substernal pressure. He is pale and diaphoretic. Vitals are unremarkable apart from mild tachycardia. The first EKG is read as nonspecific. The first troponin is pending. The room's working impression drifts toward anxiety versus reflux; a GI cocktail is discussed, along with a repeat troponin and possible observation admission for rule-out.

The first guess, and why it is tempting

The machine read and the absence of ST elevation give a false sense of resolution. Troponin is pending, which feels like a safety net. The pathway says "rule out," so the plan becomes waiting. The anchoring error is treating "does not meet STEMI criteria" as "does not have a coronary occlusion."

The key idea: STEMI is a proxy, not the disease

STEMI criteria were built to identify acute coronary occlusion. They do it imperfectly. A meta-analysis of seven studies (40,777 patients with NSTEMI) found that 25.5% had an occluded culprit artery at angiography, with higher short-term all-cause mortality (RR 1.67) and MACE (RR 1.41) than NSTEMI patients with a patent culprit [1]. A 2025 narrative review cites that 25% to 34% of NSTEMI may include acute coronary occlusion [2].

In a retrospective case-control study of 808 patients with suspected ACS (Pendell Meyers et al., Int J Cardiol Heart Vasc 2021), for the first interpreter, formal STEMI criteria had sensitivity of 41% and specificity of 94% for occlusion MI, compared with 86% and 91% for that interpreter's read using predefined "OMI" ECG findings. A second interpreter, reading a 250-patient subset, had sensitivity of 36% versus 80% with specificity of 91% versus 92% [3]. STEMI-negative OMI patients had similar infarct size and mortality as STEMI-positive OMI patients, but longer delays to angiography [3]. Caveats: retrospective, enriched case-control design; the interpreters were authors and proponents of the paradigm; and the work has not been validated in a prospective reperfusion-outcome trial. The 2025 ACC/AHA/ACEP/NAEMSP/SCAI ACS guideline keeps STEMI/NSTEMI terminology and does not formally adopt the OMI paradigm [9]. The OMI paradigm is promising and widely discussed, but it is not yet the guideline standard [2, 3, 9].

What does not fit

• The patient. Ongoing pain, diaphoresis, pallor, a story that sounds ischemic. Gestalt of a sick patient is data.
• The tracing, on second look. Findings that are easy to label "nonspecific":
  • Hyperacute T waves: broad-based, bulky, symmetric T waves, large relative to the QRS, often in contiguous leads; may precede ST elevation.
  • Reciprocal change: for example, subtle ST depression or T-wave inversion in aVL with a hyperacute inferior T wave. Reciprocal findings may be the first thing you notice. In a single-center series of 107 consecutive patients with a first acute inferior MI, reciprocal ST depression was found more often in aVL than in any other lead, all but 3 patients had it, and in 8 patients (7.5%) it was the only early ECG sign of the infarction [12]. That series is from 1993 and small, so use it as a reason to look at aVL, not as a sensitivity figure for any one tracing.
  • Subtle ST depression in V1 to V3: posterior occlusion until proven otherwise; obtain posterior leads (V7 to V9).
  • De Winter pattern: upsloping ST depression of about 1 mm or more at the J point, continuing into tall, symmetric T waves in the precordial leads, without classic ST elevation. It was described by de Winter et al. (N Engl J Med 2008;359:2071-3) [10] and in 35 of 1,890 (2%) primary PCI patients with LAD occlusion by Verouden et al. (Heart 2009;95:1701-6) [11], who found it mostly with proximal LAD occlusion. It is treated as a STEMI-equivalent pattern in the OMI literature [2].
  • Dynamic change between serial tracings or compared with an old ECG.

The Fifth Universal Definition of Myocardial Infarction (Mills et al., 2026) is the current reference for formal ECG criteria [4]. The working diagnosis of STEMI requires new ST elevation at the J point in at least two contiguous leads: 1 mm or more in all leads other than V2 to V3, where the thresholds are 2.5 mm or more in men under 40, 2 mm or more in men 40 and older, and 1.5 mm or more in women, in the absence of left ventricular hypertrophy or left bundle branch block [4]. The document notes that up to 1 in 4 patients managed as NSTEMI without classical ST elevation have an acute occlusion of the culprit artery, and that in the right clinical setting other patterns may be considered equivalent to STEMI, including new or presumed-new bundle branch block when accompanied by other signs of ischemia [4]. It lists further patterns that suggest acute coronary occlusion: marked ST depression or hyperacute T waves in V1 to V2 with reciprocal changes elsewhere, the de Winter pattern, Wellens syndrome, the Aslanger pattern, the "South African flag" sign, and the Sgarbossa criteria in LBBB or paced rhythm [4]. A posterior MI is suggested by ST depression of 1 mm or more in V1 to V3, particularly with a dominant R wave in V1 or V2, confirmed by ST elevation in posterior leads V7 to V9 [4]. It is not a blanket "new LBBB alone" rule: the 2025 ACS guideline states that new or presumed-new LBBB in isolation should not be considered diagnostic of acute MI [9].

Differential

Acute coronary occlusion (including circumflex and posterior territories), NSTEMI without occlusion, unstable angina, aortic dissection (consider before anticoagulation), PE, pericarditis, myocarditis, takotsubo, and non-cardiac chest pain such as reflux or musculoskeletal pain. Anxiety is a diagnosis of exclusion in a patient who looks this sick.

Workup

• EKG within 10 minutes of arrival and immediate physician review, not reliance on the machine read [5].
• Serial EKGs when the first tracing is nondiagnostic and suspicion stays high or symptoms continue. The 2025 ACC/AHA/ACEP/NAEMSP/SCAI ACS guideline gives a Class 1 recommendation (level of evidence B-NR) for serial ECGs after a nondiagnostic initial ECG, timed by symptoms and clinical change with no fixed interval [9]. The 2021 chest pain guideline also supports serial ECGs without specifying an interval [5]. The commonly cited repeat interval of 15 to 30 minutes over the first hour comes from the earlier 2014 NSTE-ACS guideline, for symptomatic patients with a nondiagnostic initial ECG [6], not from the 2021 or 2025 documents.
• Compare with old ECGs whenever available.
• Posterior leads (V7 to V9) when there is ST depression in V1 to V3 and a circumflex or posterior occlusion is possible [4]; consider right-sided leads for inferior changes.
• Bedside echocardiography for regional wall motion abnormality can support the diagnosis. In one retrospective series of 256 OMI patients who had formal echocardiography, regional wall motion abnormalities (RWMA) were present in 82% of STEMI-negative OMI cases (90% of STEMI-positive OMI). Among patients with an RWMA, the location matched the ECG territory in 82% of STEMI-negative OMI (102 of 124) versus 93% of STEMI-positive OMI (87 of 94) [7]. It supports, but does not replace, angiography.
• High-sensitivity troponin is necessary but can lag in the first hours and can be normal or only mildly elevated early in occlusion. A single troponin does not exclude an evolving infarct. Elevated troponin does not distinguish occlusion from non-occlusion MI.

The GI cocktail trap

A GI cocktail response is not diagnostic. A descriptive single-center study of 97 patients found that relief with the cocktail was frequent (and similar in admitted and discharged patients), and that it was hard to separate the cocktail's effect from coadministered drugs such as morphine and nitroglycerin [8]. Do not use response to a cocktail to risk-stratify chest pain.

Management and disposition

• If STEMI criteria are met: standard STEMI pathway, activate the cath lab.
• If STEMI criteria are not met but the clinical picture and ECG suggest occlusion (ongoing ischemic pain, hyperacute T waves, posterior pattern, dynamic changes): discuss early with cardiology and request emergent angiography, rather than waiting for a troponin trend. Follow your institution's protocol for how these cases are activated.
• Start standard ACS therapy per local protocol. Consider aortic dissection before anticoagulation if pain is tearing, pulses are unequal, or the mediastinum is wide.
• Refractory pain, arrhythmia, hemodynamic instability, or heart failure shifts to immediate invasive strategy.
• Repeat the ECG with any change in symptoms, and on every reassessment.

Clinical pearls

• Read the ECG yourself, every time, before you read the machine.
• Ask of each EKG: is this T wave too big for this QRS?
• ST depression in V1 to V3 is ST elevation until proven otherwise (posterior leads).
• A normal or nonspecific EKG does not rule out acute MI, and a normal troponin early does not either.
• If the patient looks ischemic and the tracing "does not show it," repeat the tracing, not just the troponin.

Common pitfalls

• Waiting for a textbook ST elevation before calling cardiology.
• Treating the troponin as the test that decides, and treating "pending" as reassurance.
• Labeling pain as reflux or anxiety based on response to antacids.
• Not asking for old tracings.
• Forgetting posterior and right-sided leads.

Teaching points

• STEMI criteria miss a large share of occlusion MI; the ECG is an imperfect proxy.
• Hyperacute T waves, reciprocal change, and posterior patterns are the classic subtle signs.
• Repeat the ECG during ongoing symptoms; compare with old tracings.
• Clinical gestalt and dynamic change can justify early cardiology involvement before criteria are met.
• No GI cocktail for risk stratification.

References

1. Khan AR, Golwala H, Tripathi A, et al. Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. Eur Heart J. 2017;38(41):3082-3089. doi:10.1093/eurheartj/ehx418 | PMID 29020244
2. Ricci F, Martini C, Scordo DM, et al. ECG patterns of occlusion myocardial infarction: a narrative review. Ann Emerg Med. 2025;85(4):330-340. doi:10.1016/j.annemergmed.2024.11.019 | PMID 39818676
3. Pendell Meyers H, Bracey A, Lee D, et al. Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction. Int J Cardiol Heart Vasc. 2021;33:100767. doi:10.1016/j.ijcha.2021.100767 | PMID 33912650
4. Mills NL, Newby LK, Zaman S, et al. Fifth Universal Definition of Myocardial Infarction (2026). J Am Coll Cardiol. 2026;88(11):1314-1368 (also Eur Heart J, Circulation and Glob Heart 2026). doi:10.1016/j.jacc.2026.07.025 | PMID 42663357
5. Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR guideline for the evaluation and diagnosis of chest pain. Circulation. 2021;144(22):e368-e454 (also J Am Coll Cardiol. 2021;78(22):e187-e285). doi:10.1161/CIR.0000000000001029 | PMID 34709879
6. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228 (also Circulation. 2014;130(25):e344-e426). doi:10.1016/j.jacc.2014.09.017 | PMID 25260718
7. Bracey A, Meyers HP, Watkins C, et al. Comparison of regional wall motion abnormalities in patients with occlusion myocardial infarction with and without ST-elevation myocardial infarction. Clin Exp Emerg Med. 2025;12(4):342-349. doi:10.15441/ceem.24.373 | PMID 40803357
8. Wrenn K, Slovis CM, Gongaware J. Using the "GI cocktail": a descriptive study. Ann Emerg Med. 1995;26(6):687-690. doi:10.1016/s0196-0644(95)70038-270038-2) | PMID 7492037
9. Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for the management of patients with acute coronary syndromes. J Am Coll Cardiol. 2025;85(22):2135-2237 (also Circulation. 2025;151:e771-e862). doi:10.1016/j.jacc.2024.11.009 | PMID 40013746
10. de Winter RJ, Verouden NJ, Wellens HJ, Wilde AA. A new ECG sign of proximal LAD occlusion. N Engl J Med. 2008;359(19):2071-2073. doi:10.1056/NEJMc0804737 | PMID 18987380
11. Verouden NJ, Koch KT, Peters RJ, et al. Persistent precordial "hyperacute" T-waves signify proximal left anterior descending artery occlusion. Heart. 2009;95(20):1701-1706. doi:10.1136/hrt.2009.174557 | PMID 19620137
12. Birnbaum Y, Sclarovsky S, Mager A, Strasberg B, Rechavia E. ST segment depression in aVL: a sensitive marker for acute inferior myocardial infarction. Eur Heart J. 1993;14(1):4-7. doi:10.1093/eurheartj/14.1.4 | PMID 8432289

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Masquerading as ACS: Hold the Heparin

Case presentation (composite)

A man in his early sixties describes sudden tearing chest pain radiating to the back. He is diaphoretic. BP is 180/110. The first troponin is mildly elevated and rising. The ACS pathway is already running: aspirin, heparin, call cardiology. On re-examination there is a pulse deficit in one arm, and a new murmur is heard. The pain reached maximal intensity at onset, rather than building over minutes.

The first guess, and why it is tempting

Chest pain plus diaphoresis plus troponin elevation is a pattern every clinician has been trained to act on quickly. Door-to-treatment metrics reward speed. The ACS order set is fast, and heparin feels like a low-risk default. Dissection is rare in a chest pain population (an incidence on the order of 5 to 30 per million per year is cited in the 2022 ACC/AHA aortic guideline [1]), so base rates favor ACS. That is exactly why dissection gets missed.

In a single tertiary center cohort of 66 consecutive acute aortic syndrome patients, 39% were initially misdiagnosed. Acute coronary syndrome was the most common wrong diagnosis. Those who received antithrombotic agents inappropriately had more major bleeding (38% vs 13%), and a trend toward higher in-hospital mortality (27% vs 13%; the authors report p = 0.02 for the combined end point) [2]. It is a small single-center study, but the direction makes physiologic sense.

What does not fit

• Pain character and onset. Sudden onset of severe pain was the single most common presenting complaint in IRAD [3]. Plaque rupture usually builds. In a systematic review, the absence of sudden-onset pain lowered the likelihood of dissection (negative LR 0.3) [4].
• Pulse or blood pressure differential. Pulse deficit or BP differential raised the likelihood of dissection (positive LR 5.7) [4]. But only about 15% of IRAD patients had a pulse deficit, so absence is not reassuring [3].
• A new aortic regurgitation murmur. Found in about a third of IRAD patients [3]; a diastolic murmur by itself changes pretest probability little (positive LR 1.4) [4]. Its value is in combination.
• Neurologic deficit, syncope, or limb ischemia: strong clues when present [4].
• ECG and chest radiograph. In IRAD, the initial chest radiograph and ECG were frequently not helpful: 12.4% of chest radiographs and 31.3% of ECGs had no abnormality [3]. A normal film does not exclude dissection, and a normal ECG is common. Ischemic ECG changes do not exclude it either; coronary involvement (most often the right coronary artery) can occur. In a review of IRAD data, ischemic ECG abnormalities were recorded in about 17% of type A dissections and findings of myocardial infarction (new Q waves or ST changes) in about 7%, and coronary malperfusion was estimated at 10% to 15% of type A cases [12]. STEMI can be the presenting picture: in one single-center series of 1,576 STEMI patients taken for PCI, 0.51% (8 patients) had type A dissection, predominantly with right coronary involvement; 3 of the 8 died, including patients treated with thrombolysis or PCI before the dissection was recognized [11]. These are small or secondary sources and the exact frequency varies by series.

Troponin can be elevated in dissection. A positive troponin does not mean the ACS pathway is the only pathway.

Differential

ACS (including STEMI), pulmonary embolism, pericarditis or myopericarditis, esophageal rupture, pneumothorax, musculoskeletal pain, and other acute aortic syndromes (intramural hematoma, penetrating ulcer, contained rupture). Risk factors: hypertension, known aortopathy or bicuspid valve, Marfan or related connective tissue disease, prior aortic surgery, cocaine or stimulant use, pregnancy or peripartum state, and recent instrumentation.

Workup

1. Think of it. Pretest probability drives everything. The Aortic Dissection Detection Risk Score (ADD-RS) counts high-risk conditions, high-risk pain features (abrupt, severe, ripping or tearing), and high-risk exam features (pulse deficit, systolic BP differential, focal neurologic deficit with pain, new AR murmur, hypotension or shock). In the IRAD analysis of 2,538 patients with confirmed dissection, 4.3% (108 patients) scored 0 [5].
2. Risk-stratified D-dimer. In the prospective ADvISED study (1,850 outpatients), a D-dimer below 500 ng/mL was called negative. An ADD-RS of 0 with a negative D-dimer had a failure rate of 0.3% (1 missed case in 294 patients; 95% CI 0.1% to 1.9%), and an ADD-RS of 1 or less with a negative D-dimer also had 0.3% (3 missed cases in 924 patients; 95% CI 0.1% to 1%), with the latter ruling out about half of the cohort (efficiency 49.9%). A positive D-dimer (500 ng/mL or higher) had an overall sensitivity of 96.7% and specificity of 64% for acute aortic syndromes [6]. This is for low-risk patients only. A high-risk ADD-RS (2 or more) goes directly to imaging, regardless of D-dimer.
3. Definitive imaging: CT angiography of the aorta (ECG-gated when available) for high-risk patients. TEE and MRI are alternatives in specific situations.
4. Bedside echo (effusion, AR, aortic root dilation, flap) can support but does not exclude the diagnosis.
5. Blood pressure in both arms. Do it early; it is cheap.

Management

• Before imaging, if suspicion is moderate to high, hold antithrombotics and thrombolytics until dissection is reasonably excluded. If ACS and dissection are both plausible, the question "what happens if I am wrong?" favors imaging first. In the author's clinical judgment, the harm from a short delay in heparin in a true NSTEMI is small compared with the harm of heparin in a type A dissection (not a trial-derived statement).

• Anti-impulse therapy. The 2022 ACC/AHA guideline recommends treating acute aortic syndrome to a heart rate of 60 to 80 bpm and a systolic BP below 120 mm Hg (or the lowest pressure that maintains end-organ perfusion), with an intravenous beta-blocker first unless contraindicated, and an IV vasodilator added if BP remains uncontrolled [1, 7]. Control heart rate before adding a vasodilator, so reflex tachycardia does not increase aortic wall stress. Use an arterial line and titratable agents; follow your local protocol for agent selection and dosing. Doses are intentionally not given in this article.
• Analgesia is part of hemodynamic control.
• Early surgical involvement. Stanford type A dissection is a surgical emergency. The 2022 ACC/AHA guideline states that mortality in acute aortic syndromes can be as high as 1% to 2% per hour without prompt diagnosis and treatment (Section 7.1), and gives about 1% per hour for unoperated acute type A dissection (Section 7.4.1.1) [1]. Acute type A dissection with malperfusion needs immediate repair, with one exception: in clinically significant mesenteric malperfusion, immediate mesenteric revascularization may precede ascending aortic repair [1].

• Type B: initial medical therapy for uncomplicated cases, with endovascular or surgical intervention for malperfusion, rupture, or refractory pain/hypertension [1, 7].
• Disposition: ICU or cardiac surgery service; transfer early to a center with aortic surgery if you do not have it. Activate the transfer before the scan is final if the clinical picture is strong.

Evidence in context

IRAD (464 patients, 12 centers, 1996 to 1998) found in-hospital mortality of 27.4%; type A managed surgically had 26% mortality versus 58% when surgery was not performed; uncomplicated type B managed medically had 10.7% [3]. A later IRAD analysis identified delays in diagnosis in patients with atypical symptoms (not abrupt, no chest/back/any pain), no pulse deficit or hypotension, fever, female sex, and presentation to a non-tertiary hospital [8]. In that analysis (patients enrolled 1996 to 2007; 894 with timing data; the paper's focus is type A dissection), the median time from ED arrival to diagnosis was 4.3 hours (interquartile range 1.5 to 24 hours) [8]. In the 2016 systematic review, patients were typically aged 60 to 70 years [10], and in an earlier IRAD analysis 63 of 977 patients (6.4%) had painless dissection, who more often presented with syncope, heart failure, or stroke [9]. These are registry data from referral centers and reflect selection.

Clinical pearls

• Sudden and maximal at onset is a dissection feature; building over minutes is more plaque-like. Both have exceptions.
• Always ask: "Could this be dissection?" before the anticoagulant is hung.
• Do not let a mildly positive troponin end the conversation.
• Check bilateral arm pressures, pulses, and the heart sounds.
• A normal chest radiograph does not exclude dissection.
• Keep D-dimer for the low-risk patient, not the one with tearing pain and a pulse deficit.

Common pitfalls

• Ordering the ACS bundle before considering dissection.
• Using D-dimer in high-risk patients.
• Relying on chest X-ray or ECG to exclude.
• Giving a thrombolytic for an ECG that shows ST elevation in a patient with features of dissection.
• Dropping BP with a vasodilator alone, causing reflex tachycardia.
• Missing less classic presentations (painless, syncope, neurologic, abdominal).

Teaching points

• Sudden maximal tearing pain plus unequal pulses: pause the ACS autopilot.
• ADD-RS plus D-dimer is a validated rule-out for low-risk patients only.
• Initial anti-impulse therapy: heart rate first, then pressure.
• Antithrombotics in unrecognized dissection are associated with bleeding.
• Type A is an immediate surgical call.

References

1. Isselbacher EM, Preventza O, Hamilton Black J 3rd, et al. 2022 ACC/AHA guideline for the diagnosis and management of aortic disease. Circulation. 2022;146(24):e334-e482. doi:10.1161/CIR.0000000000001106 | PMID 36322642
2. Hansen MS, Nogareda GJ, Hutchison SJ. Frequency of and inappropriate treatment of misdiagnosis of acute aortic dissection. Am J Cardiol. 2007;99(6):852-856. doi:10.1016/j.amjcard.2006.10.055 | PMID 17350381
3. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903. doi:10.1001/jama.283.7.897 | PMID 10685714
4. Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA. 2002;287(17):2262-2272. doi:10.1001/jama.287.17.2262 | PMID 11980527
5. Rogers AM, Hermann LK, Booher AM, et al. Sensitivity of the aortic dissection detection risk score, a novel guideline-based tool for identification of acute aortic dissection at initial presentation: results from the International Registry of Acute Aortic Dissection. Circulation. 2011;123(20):2213-2218. doi:10.1161/CIRCULATIONAHA.110.988568 | PMID 21555704
6. Nazerian P, Mueller C, Soeiro AM, et al. Diagnostic accuracy of the aortic dissection detection risk score plus D-dimer for acute aortic syndromes: the ADvISED prospective multicenter study. Circulation. 2018;137(3):250-258. doi:10.1161/CIRCULATIONAHA.117.029457 | PMID 29030346
7. American College of Cardiology. 2022 ACC/AHA aortic disease guideline key perspectives, part 2 of 2 (Ten Points to Remember). acc.org
8. Harris KM, Strauss CE, Eagle KA, et al. Correlates of delayed recognition and treatment of acute type A aortic dissection: the International Registry of Acute Aortic Dissection (IRAD). Circulation. 2011;124(18):1911-1918. doi:10.1161/CIRCULATIONAHA.110.006320 | PMID 21969019
9. Park SW, Hutchison S, Mehta RH, et al. Association of painless acute aortic dissection with increased mortality. Mayo Clin Proc. 2004;79(10):1252-1257. doi:10.4065/79.10.1252 | PMID 15473405
10. Mussa FF, Horton JD, Moridzadeh R, et al. Acute aortic dissection and intramural hematoma: a systematic review. JAMA. 2016;316(7):754-763. doi:10.1001/jama.2016.10026 | PMID 27533160
11. Zhu QY, Tai S, Tang L, et al. STEMI could be the primary presentation of acute aortic dissection. Am J Emerg Med. 2017;35(11):1713-1717. doi:10.1016/j.ajem.2017.05.010 | PMID 28511806
12. Berretta P, Trimarchi S, Patel HJ, et al. Malperfusion syndromes in type A aortic dissection: what we have learned from IRAD. J Vis Surg. 2018;4:65. doi:10.21037/jovs.2018.03.13 | PMID 29682475

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Thunderclap Headache Is Not a Migraine Until Proven Otherwise

Case presentation (composite)

A woman in her early forties arrives with a severe headache that started at rest and peaked within seconds. She vomited once. She is uncomfortable but conversant, with a normal mental status. BP is 160/90. She reports photophobia and, on exam, true resistance to neck flexion. She says it is the worst headache of her life, and unlike any she has had. A migraine cocktail and a dark room are proposed, with reassessment in an hour.

The first guess, and why it is tempting

Migraine is common, the patient is awake and talking, the neurologic exam is nonfocal, and nausea and photophobia are features of migraine too (and are not, on their own, reliable discriminators). A treat-and-reassess approach also “works” in the sense that many patients improve with antiemetics and analgesics, which creates a false sense of diagnostic confirmation. Improvement with migraine therapy does not exclude SAH.

The data on misdiagnosis are sobering. In a cohort of 482 patients with SAH, 12% were initially misdiagnosed, including 19% of those with normal mental status at first contact. Migraine or tension headache was the most common incorrect diagnosis (36%), and failure to obtain a CT scan was the most common error (73%). Neurologic complications occurred in 39% of misdiagnosed patients before correct diagnosis, including rebleeding in 12 patients (21%). Among those with normal mental status, misdiagnosis was associated with worse outcomes at 12 months [1]. Patients who look well are the ones at risk of being missed.

What does not fit

• Instant onset. Pain that peaks within seconds to a minute (thunderclap; the headache classification, ICHD-3, defines it as reaching maximum intensity in less than 1 minute) is the classic feature [9]. In practice the cutoff should not be applied rigidly: the Ottawa rule enrolled patients whose headache peaked within 1 hour, and it lists thunderclap onset as only one of several criteria [3] (clinical judgment).
• “Worst ever.” In the 2011 Canadian CT cohort, most enrolled patients (82%) reported worst-ever headache, yet only 7.7% had SAH. The phrase raises concern but is not specific [2].
• Neck stiffness or limited neck flexion. Both were predictors in the Ottawa SAH rule [3]. The 2019 ACEP policy notes that neck pain and stiffness are strongly associated with SAH but that no single sign or symptom should be used to rule it out (Level B) [6].
• No comparable headache history. A new pattern matters more than any label.
• Vomiting, hypertension, brief loss of consciousness, exertional onset add weight.

Differential

Aneurysmal SAH, perimesencephalic and other non-aneurysmal SAH, reversible cerebral vasoconstriction syndrome (RCVS), cervical artery dissection, cerebral venous thrombosis, intracerebral hemorrhage, pituitary apoplexy, hypertensive emergency, meningitis or encephalitis (neck stiffness, fever), colloid cyst, spontaneous intracranial hypotension, primary thunderclap headache (a diagnosis of exclusion), and migraine.

Workup

Who needs testing: the Ottawa SAH rule

The Ottawa SAH rule applies to alert adults (age 15 or older) with new severe nontraumatic headache reaching maximum intensity within 1 hour, and no neurologic deficit. It is positive (investigate) if any of: age 40 or older, neck pain or stiffness, witnessed loss of consciousness, onset during exertion, thunderclap headache (instantly peaking), or limited neck flexion on examination. In the validation and refinement cohort of 2,131 patients (6.2% with SAH), the rule had 100% sensitivity (95% CI 97.2% to 100%) and 15.3% specificity [3]. In a later prospective implementation study (3,672 patients, 188 with SAH), sensitivity remained 100% (95% CI 98.1% to 100%) [4]. It is a rule to reduce testing in low-risk patients, not to add an exclusion to a high-risk one: this patient meets several items (age 40 or older, neck stiffness, thunderclap) and needs imaging. The rule was also tested in a separate 2017 multicenter validation (1,153 patients, 67 with SAH; sensitivity 100%, 95% CI 94.6% to 100%; specificity 13.6%) [8]. The 2023 AHA/ASA guideline gives the rule a weak recommendation (Class 2b, B-NR) as a reasonable option [7].

Noncontrast head CT

• In a prospective cohort of 3,132 neurologically intact patients at 11 Canadian EDs, CT sensitivity overall was 92.9% (95% CI 89.0% to 95.5%), and for the 953 scanned within 6 hours of onset, 100% (95% CI 97.0% to 100%), all 121 SAH cases detected [2]. The conditions matter: third-generation scanner, scan within 6 hours of onset, interpretation by a qualified radiologist.
• A meta-analysis limited to modern (16-slice or greater) scanners within 6 hours pooled sensitivity at 98.7% (95% CI 97.1% to 99.4%) and a negative likelihood ratio of 0.010 [5].
• The 2023 AHA/ASA guideline is slightly more cautious: within 6 hours of onset, in a patient with no new neurologic deficit, a noncontrast CT on a high-quality scanner read by a board-certified neuroradiologist is considered reasonable (Class 2a, B-NR); beyond 6 hours, or with a new deficit, CT followed by LP if negative is recommended (Class 1, B-NR) [7]. The 2019 ACEP clinical policy gives a Level B recommendation that a normal noncontrast head CT performed within 6 hours of symptom onset, in a patient with a normal neurologic exam, may be used to rule out nontraumatic SAH [6]. The key caveats: normal neurologic exam, modern scanner, and a qualified reader. The patient’s “time of onset” must be reliable.
• Beyond 6 hours, CT sensitivity falls as blood clears, and further testing is required.
• Profound anemia is a recognized way to miss SAH on CT (one such miss was reported in the 6-hour rule implementation study [4]).

After a negative CT, when suspicion persists or CT was delayed

• Lumbar puncture: look for xanthochromia (spectrophotometry where available) and red cell counts, with the usual issue of traumatic tap.
• CT angiography of the head: avoids an LP and can find an aneurysm, but may detect incidental unruptured aneurysms, exposes the patient to radiation and contrast.
• ACEP gives a Level C recommendation to perform either LP or CTA after a negative CT, with shared decision making between the two [6]. The 2023 AHA/ASA guideline favors LP after a negative CT outside the 6-hour window, with CTA as an alternative, and notes that no study has directly compared the two [7]. The evidence comparing them is limited.
• If the patient also has fever, altered mental status, or meningismus that raises concern for meningitis, LP serves a second purpose.

Management and disposition

• Positive CT: emergent neurosurgery/neurointerventional involvement, transfer if needed, and management in a neurocritical care setting.
• Blood pressure: the 2023 AHA/ASA guideline recommends frequent monitoring and control with short-acting agents to avoid severe hypertension, hypotension, and BP variability in patients with unsecured aneurysms; there is insufficient evidence for a specific target before aneurysm treatment [7]. This is a Class 1 recommendation with level of evidence C-EO [7].
• Nimodipine: the 2023 guideline recommends early enteral nimodipine (Class 1, level of evidence A) to prevent delayed cerebral ischemia and improve functional outcome [7]. Dosing per pharmacy and neurocritical care.
• Reverse anticoagulation if applicable; avoid antiplatelets and anticoagulants in suspected SAH.
• Symptom treatment: analgesia and antiemetics are reasonable while the workup is ongoing. They do not substitute for the workup.
• Airway and neuro checks at intervals; any decline prompts repeat imaging.
• Negative workup: discharge only with a clear return plan. Consider other causes (RCVS, dissection, CVT) based on the picture and obtain vessel imaging when suspicious.

Clinical pearls

• Thunderclap plus neck stiffness in a person over 40: image first, cocktail second.
• Time from onset is a required input, not a detail. Document it.
• The 6-hour CT rule works under specific conditions. Outside them, use LP or CTA.
• Improvement after a migraine cocktail does not lower the probability of SAH. The 2019 ACEP policy advises that response to therapy should not be used as the sole indicator of the underlying cause of an acute headache (Level C) [6].
• An awake, talking patient with a mild-looking presentation is the one most likely to be sent home.
• Look beyond aneurysm: dissection, CVT, and RCVS can present identically.

Common pitfalls

• Treating before imaging, then reassessing on the basis of symptom relief.
• Using CT beyond 6 hours as a rule-out.
• Applying the Ottawa SAH rule to patients with neurologic deficits, recurrent headaches of a known pattern, or trauma.
• Relying on LP with a traumatic tap and ignoring the clinical picture.
• Not repeating the neurologic exam.
• Missing non-aneurysmal causes after a negative SAH workup.

Teaching points

• “Worst headache of life” is a prompt for a workup, not a diagnosis.
• CT within 6 hours on a modern scanner, read by a radiologist, in a neurologically intact patient has very high sensitivity.
• After 6 hours, or if the CT is indeterminate, use LP or CTA and share the decision with the patient.
• Misdiagnosis is most likely in patients who look well, and delay causes rebleeding.
• Early nimodipine and blood pressure control matter once SAH is confirmed.

References

1. Kowalski RG, Claassen J, Kreiter KT, et al. Initial misdiagnosis and outcome after subarachnoid hemorrhage. JAMA. 2004;291(7):866-869. doi:10.1001/jama.291.7.866 | PMID 14970066
2. Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011;343:d4277. doi:10.1136/bmj.d4277 | PMID 21768192
3. Perry JJ, Stiell IG, Sivilotti ML, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-1255. doi:10.1001/jama.2013.278018 | PMID 24065011
4. Perry JJ, Sivilotti MLA, Émond M, et al. Prospective implementation of the Ottawa subarachnoid hemorrhage rule and 6-hour computed tomography rule. Stroke. 2020;51(2):424-430. doi:10.1161/STROKEAHA.119.026969 | PMID 31805846
5. Dubosh NM, Bellolio MF, Rabinstein AA, Edlow JA. Sensitivity of early brain computed tomography to exclude aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. Stroke. 2016;47(3):750-755. doi:10.1161/STROKEAHA.115.011386 | PMID 26797666
6. American College of Emergency Physicians Clinical Policies Subcommittee on Acute Headache. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med. 2019;74(4):e41-e74. doi:10.1016/j.annemergmed.2019.07.009 | PMID 31543134
7. Hoh BL, Ko NU, Amin-Hanjani S, et al. 2023 guideline for the management of patients with aneurysmal subarachnoid hemorrhage: a guideline from the American Heart Association/American Stroke Association. Stroke. 2023;54(7):e314-e370. doi:10.1161/STR.0000000000000436 | PMID 37212182
8. Perry JJ, Sivilotti MLA, Émond M, et al. Prospective validation of the Ottawa Subarachnoid Hemorrhage Rule: a multicenter observational study. CMAJ. 2017;189(45):E1379-E1385. doi:10.1503/cmaj.170072 | PMID 29133539
9. Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211 (criterion 4.4, primary thunderclap headache: abrupt onset, maximum intensity in under 1 minute).

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

When the Belly Is Soft and the Gut Is Dying

Case presentation (composite)

A woman in her mid-seventies with atrial fibrillation presents with sudden severe abdominal pain. The abdomen is soft with mild tenderness and no peritoneal signs. The lactate is only starting to rise. The differential offered by the room is gastroenteritis, constipation, or early diverticulitis, with analgesia and serial abdominal exams. On questioning, the pain was abrupt, "like a switch flipped," and seems far greater than the exam would suggest. She has a vascular history.

The first guess, and why it is tempting

Abdominal pain in older adults is often benign, and a soft abdomen with mild tenderness is reassuring in most settings. In the early phase of mesenteric ischemia, the bowel is ischemic but not yet infarcted and peritoneal irritation has not yet developed. Peritonitis is a late finding: by the time the exam is "surgical," the bowel may be necrotic. Waiting for the exam to declare itself means waiting for the disease to progress.

What does not fit

• Pain out of proportion to the exam. The classic teaching. It reflects visceral ischemic pain without parietal peritoneal involvement. It is a prompt rather than a validated rule: no pooled likelihood ratio was identified for this sign in the sources checked, so treat it as gestalt. The 2022 WSES guideline nonetheless advises that severe abdominal pain out of proportion to the examination should be assumed to be acute mesenteric ischemia until disproven (strong recommendation, low-quality evidence) [2].
• Abrupt onset. Consistent with an embolic event.
• A source of emboli. Atrial fibrillation, valvular disease, and recent MI with LV thrombus. A review of superior mesenteric artery embolism states that patients with atrial fibrillation, valvular disease, or atherosclerosis should be considered for this diagnosis, and that SMA embolism is the main cause of acute mesenteric ischemia [1]. Other subtypes include arterial thrombosis (often on chronic atherosclerotic stenosis), non-occlusive mesenteric ischemia (low-flow states, vasopressors), and mesenteric venous thrombosis [2].
• Risk context. Older age, vascular disease, low-flow states, sepsis, cardiac failure, vasopressors, recent cardiac surgery.
• Vomiting or diarrhea can occur early and mimic gastroenteritis.

The 2022 WSES guideline gives the incidence as roughly 0.09% to 0.2% of acute surgical admissions (the Background text says acute admissions to emergency departments), increasing with age, and states that mortality remains in the range of 50% if untreated (elsewhere "exceeding 50%"); it cites delay in diagnosis as the dominant factor behind mortality of 30% to 70% [2]. It gives the etiologies as arterial embolism about 50%, arterial thrombosis 15% to 25%, venous thrombosis 5% to 15%, and non-occlusive ischemia in approximately 20% of cases; the non-occlusive figure appears in the body text rather than the summary sentence, and the categories are not presented as a formal partition [2].

Differential

Gastroenteritis, constipation, diverticulitis, small bowel obstruction, perforated viscus, pancreatitis, biliary disease, ruptured or leaking abdominal aortic aneurysm, aortic dissection, renal colic or infarct, ischemic colitis, volvulus, incarcerated hernia, and inferior MI. In a patient with atrial fibrillation and sudden severe pain, also consider splenic or renal embolic infarcts.

Workup

Labs: supportive, not decisive

A meta-analysis of 23 studies (1,970 patients) found: lactate pooled sensitivity 86% and specificity 44%; D-dimer pooled sensitivity 96% and specificity 40%. The authors concluded that signs, symptoms, and laboratory testing are insufficiently diagnostic, and that only CT angiography had adequate accuracy to establish the diagnosis in lieu of laparotomy [3]. Practical implications:

• A normal lactate does not exclude early ischemia. Lactate rises when the bowel is already in trouble.
• A negative D-dimer makes the diagnosis less likely in a low-probability setting, but the quality of the evidence is variable and specificity is low. D-dimer is not a substitute for imaging when clinical suspicion is moderate to high (clinical judgment).
• Leukocytosis, metabolic acidosis, and elevated amylase are nonspecific.
• Labs to send: CBC, BMP, lactate, liver enzymes, lipase, coagulation studies, type and screen, troponin, and an ECG (rhythm, MI).

Imaging: CT angiography

The 2022 WSES guideline gives a strong recommendation, graded 1A (high-quality evidence), that CT angiography be performed without delay in any patient in whom AMI is suspected. The suggested protocol is a biphasic CTA with a non-contrast phase, then arterial and venous phases, and multiplanar reformats. Oral contrast is not indicated. The guideline advises performing CTA despite acute kidney injury, because the consequences of delayed or missed diagnosis outweigh the contrast risk [2].

Test characteristics: a 2025 meta-analysis of 81 studies found CTA sensitivity of 92.0% and specificity of 98.8%, lower for non-CTA protocols (75.8% and 90.5%) [4]. The 2013 meta-analysis pooled CT at 94% sensitivity and 95% specificity [3]. A non-angiographic, portal-venous-phase CT of the abdomen, the default in many ED abdominal pain pathways, may therefore under-call arterial occlusion. Tell the radiologist what you are looking for, and order the protocol by its clinical question, not just "CT abdomen/pelvis with contrast." Protocol names vary by institution. The 2022 WSES guideline recommends CT angiography without delay and advises against oral contrast [2].

Nonvascular signs (bowel wall thickening, pneumatosis, portal venous gas, free fluid) are nonspecific and often late. Absent bowel wall enhancement had a pooled sensitivity of 57.9% and specificity of 90.1% [4]. Do not wait for them.

Management

• Resuscitate. IV crystalloid, correction of electrolytes, oxygen as needed, rate control or rhythm management as appropriate. Minimize vasopressors where possible: the 2022 WSES guideline lists vasopressor elimination as an important primary measure in non-occlusive disease, citing experimental data that some vasopressors may impair mucosal perfusion [2].
• Anticoagulation. The WSES guideline states that full-dose anticoagulation with unfractionated heparin should be initiated in all patients prior to surgical procedures (the 2017 version said "unless contraindicated"), and that continuous unfractionated heparin infusion is the first-line treatment for mesenteric venous thrombosis [2]. This is the mirror image of Case 03: here heparin is part of the treatment. Confirm the diagnosis and discuss with surgery and vascular, as the decision is individualized (bleeding risk, planned intervention).
• Antibiotics. The 2022 WSES update recommends immediate broad-spectrum antibiotics for suspected acute mesenteric ischemia, continued for at least 4 days in stable immunocompetent patients [2]. (The guideline labels this a strong recommendation but the printed grade, 1C, sits oddly beside its "moderate-quality evidence" description, so the grade is not relied on here.) The recommendation was also in the 2017 version [6].
• Early surgical and vascular involvement. Call general/vascular surgery when you order the CTA, not after the result. Revascularization may be open (embolectomy, bypass) or endovascular, and laparotomy is used to assess bowel viability and resect necrotic bowel. The WSES guideline describes a multidisciplinary approach and the increasing role of endovascular techniques [2].
• Non-occlusive and venous forms are treated differently (treat the low-flow state; anticoagulate for MVT) [2].
• Disposition: operating room or hybrid suite, then ICU. Transfer early to a center with vascular and surgical capability. Discuss goals of care in frail patients, since mortality is high even with optimal care.

Evidence in context

The pooled operative mortality for mesenteric ischemia in the 2013 meta-analysis was 47% (95% CI 40% to 54%) [3]. The same analysis calculated a test threshold of 2.1% (below which no further testing) and a treatment threshold of 74%. In a retrospective study of 212 patients who had surgery for acute mesenteric ischemia, delayed revascularization (late vascular consultation or vascular surgery not performed at the first operation) was associated with higher 30-day mortality (OR 2.09, 95% CI 1.4 to 4.9) and 2-year mortality (HR 1.55), a longer length of bowel resection and more short bowel syndrome [7]. This is observational, single-system data, so it supports urgency but does not give a precise cost per hour of delay. A 2016 NEJM review provides a general overview of the topic [5]. Quality of the underlying literature is variable, mostly retrospective.

Clinical pearls

• Sudden severe abdominal pain plus atrial fibrillation is mesenteric ischemia until you show otherwise.
• Peritonitis is the late sign, not the warning sign.
• The test is a CT angiogram, not a lactate.
• A negative D-dimer or a normal lactate does not make you safe when the story is classic.
• Order the CTA as a mesenteric CTA, and call surgery at the same time.
• Every hour of delay is bowel.

Common pitfalls

• Serial abdominal exams as a diagnostic strategy for an older patient with a high-risk story.
• Analgesia and discharge because the pain improved.
• Delaying CTA over a borderline creatinine.
• Ordering a portal-venous-phase CT only.
• Withholding heparin by reflex (carried over from dissection thinking) once dissection has been excluded and mesenteric ischemia is confirmed.
• Missing non-occlusive ischemia in patients on vasopressors or in low-flow states.

Teaching points

• In early mesenteric ischemia, the abdomen can be soft. Believe the pain.
• Risk factors: atrial fibrillation, vascular disease, low-flow states, older age.
• Labs do not rule out; CTA is the diagnostic test of choice.
• Resuscitate, anticoagulate (unless contraindicated), and involve surgery early.
• Delay in diagnosis drives mortality.

References

1. Liao G, Chen S, Cao H, Wang W, Gao Q. Review: acute superior mesenteric artery embolism: a vascular emergency cannot be ignored by physicians. Medicine (Baltimore). 2019;98(6):e14446. doi:10.1097/MD.0000000000014446 | PMID 30732209
2. Bala M, Catena F, Kashuk J, et al. Acute mesenteric ischemia: updated guidelines of the World Society of Emergency Surgery. World J Emerg Surg. 2022;17(1):54. doi:10.1186/s13017-022-00443-x | PMID 36261857
3. Cudnik MT, Darbha S, Jones J, Macedo J, Stockton SW, Hiestand BC. The diagnosis of acute mesenteric ischemia: a systematic review and meta-analysis. Acad Emerg Med. 2013;20(11):1087-1100. doi:10.1111/acem.12254 | PMID 24238311
4. Reintam Blaser A, Koitmäe M, Laisaar KT, et al. Radiological diagnosis of acute mesenteric ischemia in adult patients: a systematic review and meta-analysis. Sci Rep. 2025;15(1):9875. doi:10.1038/s41598-025-94846-w | PMID 40119151
5. Clair DG, Beach JM. Mesenteric ischemia. N Engl J Med. 2016;374(10):959-968. doi:10.1056/NEJMra1503884 | PMID 26962730
6. Bala M, Kashuk J, Moore EE, et al. Acute mesenteric ischemia: guidelines of the World Society of Emergency Surgery. World J Emerg Surg. 2017;12:38. doi:10.1186/s13017-017-0150-5 | PMID 28794797 (2017 version; source of the antibiotic recommendation noted above)
7. Tran LM, Andraska E, Haga L, Sridharan N, Chaer RA, Eslami MH. Hospital-based delays to revascularization increase risk of postoperative mortality and short bowel syndrome in acute mesenteric ischemia. J Vasc Surg. 2022;75(4):1323-1333.e3. doi:10.1016/j.jvs.2021.09.033 | PMID 34634418

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Syncope in a Young Woman: What Is Behind a Single Faint That Does Not Quite Add Up?

Case presentation (composite)

A woman in her late twenties has a brief loss of consciousness while stepping out of a car after a long day. She recovers within moments and is awake on arrival, with mild shortness of breath. Heart rate is 110, oxygen saturation 94% on room air, blood pressure about 112/70 mmHg, no fever, no chest pain. The room's working diagnosis is a vasovagal episode with dehydration; IV fluid is started with the expectation of reassurance and discharge.

Two history items arrive late: a cross-country flight about a week ago, and a combined oral contraceptive. After the fluids, her heart rate is still around 105 to 110.

(Composite. Blood pressure, temperature, and absence of chest pain are illustrative details added for teaching.)

The first guess, and why it is tempting

Vasovagal syncope is common in healthy young people, and a quick, full recovery after standing fits the story. Mild tachycardia is easy to attribute to dehydration or anxiety, and a saturation of 94% is easy to read as "basically normal." Each finding alone is a defensible rounding error. Together, in the right host, they change the pretest probability. The trap is anchoring on the syncope label and then explaining every finding as its consequence. A better habit is to ask which findings the label cannot explain.

What does not fit

• Tachycardia that persists after volume. Dehydration should respond to fluids; a rate that stays near 110 is a prompt to look further (clinical judgment). Sinus tachycardia is nonspecific: the ESC guideline notes that in milder PE it may be the only ECG abnormality, present in about 40% of patients [1].
• Borderline saturation with dyspnea. PERC requires SaO2 above 94%, so 94% fails that item [1,8].
• Syncope itself. The ESC guideline lists syncope among presentations that should prompt thought of PE and notes it is associated with more hemodynamic instability and RV dysfunction [1].
• Two recognized risk factors. Estrogen-containing contraception and recent prolonged travel.

The risk factors, with their actual size

• Combined oral contraceptives. The ESC guideline lists oral contraceptive therapy as a moderate risk factor (OR 2 to 9) and describes an approximately two- to six-fold increase in VTE risk, with low absolute risk in most users [1]. A network meta-analysis found a relative risk of 3.5 (95% CI 2.9 to 4.3) versus non-use, against baseline incidences of 1.9 and 3.7 per 10,000 woman-years; estimates were unadjusted and varied with progestogen and ethinylestradiol dose [13].
• Travel. A meta-analysis of 14 studies found a pooled relative risk of 2.0 (1.5 to 2.7), or 2.8 (2.2 to 3.7) excluding studies with referred controls, with 18% higher risk per 2 hours of travel and 26% per 2 hours of air travel [14]. In a cohort of 8,755 employees, absolute risk was about one event per 4,656 long-haul (4 hours or more) flights, highest in the first 2 weeks and back to baseline by about 8 weeks; risk was particularly high in women using oral contraceptives [15]. The ESC table classes prolonged sitting (car or air travel) as a weak factor (OR below 2) [1]. Estimates differ by design and definition, so travel is best treated as a modest, additive factor.

Differential

Vasovagal or orthostatic syncope, hypovolemia, arrhythmia (including preexcitation and long QT), pregnancy-related causes (so a pregnancy test belongs in the workup), blood loss or anemia, structural heart disease such as hypertrophic cardiomyopathy, myocarditis, acute coronary or aortic pathology (low probability here), hypoglycemia, seizure, toxic or medication effects, and pulmonary embolism.

Workup

Pretest probability first

The ESC guideline describes pretest probability by implicit judgment or by a rule (Wells, revised Geneva); roughly 10%, 30%, and 65% of low-, intermediate-, and high-probability patients have PE, and about 12% of "PE unlikely" versus 30% of "PE likely" patients [1]. Syncope is not a scored Wells item. The derivation paper lists heart rate above 100 (1.5 points) and "no alternative diagnosis" (3.0), among others, with "PE unlikely" defined as 4.0 or less [10]. Here, tachycardia gives 1.5; whether the clinician judges PE the most likely diagnosis is the swing item (4.5, PE likely, versus 1.5). With the simplified revised Geneva rule, a heart rate of 95 or more scores 2 points, already in the intermediate band (2 to 4) [1].

PERC: what it does and does not do

PERC has eight criteria: age under 50, pulse under 100, SaO2 above 94%, no unilateral leg swelling, no hemoptysis, no recent trauma or surgery, no history of VTE, and no oral hormone use [1,8]. The derivation authors noted that its utility was limited by low specificity [8]. The PROPER trial (1,916 patients, 14 French EDs) found a PERC strategy noninferior for 3-month thromboembolic events, but only in patients whose gestalt probability was low (below 15%) [9]. The ESC guideline cautions that the low overall PE prevalence in these studies limits generalizability [1]. This patient fails three criteria (heart rate, saturation, hormone use) and does not have a low gestalt, so PERC does not apply.

D-dimer depends on probability

A quantitative ELISA-type D-dimer has sensitivity of at least 95% and can exclude PE in low or intermediate pretest probability; it cannot confirm PE, and is more often falsely positive in cancer, hospitalization, infection, inflammation, and pregnancy [1]. The 3-month thromboembolic risk after a negative result in such patients was under 1% [1]. YEARS (DVT signs, hemoptysis, PE most likely) uses 1000 ng/mL with no items and 500 ng/mL with one or more; of 2,946 patients left untreated, 0.61% (95% CI 0.36 to 0.96) had VTE at 3 months, and CTPA was avoided in 48% [11]. Age-adjusted cutoffs apply only above age 50 [1]. In a high-probability patient, the next step is imaging, not a D-dimer.

Imaging and the rest

CTPA is the imaging method of choice [1]. In PIOPED II, multidetector CTA had sensitivity of 83% and specificity of 96%; predictive values were 96% with concordantly high or low clinical probability, and further testing is needed when probability and imaging disagree [12]. For young women the ESC guideline lists CTPA radiation of 3 to 10 mSv with significant breast exposure, and describes V/Q scanning as lower in radiation but inconclusive in about half of cases [1]. If pregnancy is possible, test first. Also: ECG (RV strain patterns such as T-wave inversion in V1 to V4, S1Q3T3, or right bundle branch block are usually seen in more severe cases [1]), glucose, hemoglobin, troponin if indicated, and a look at the legs.

The syncope and PE controversy

In PESIT, 560 patients hospitalized for a first syncope (mean age 76) were systematically evaluated; overall PE prevalence was 17.3% (95% CI 14.2 to 20.5), including 12.7% (45 of 355) of those with an alternative explanation for syncope and 25.4% (52 of 205) of those without [2]. The ESC guideline cites the 17% figure [1].

Other work is far lower. Across five databases covering 1,671,944 ED syncope patients, coded PE prevalence ranged from 0.06% to 0.55% overall, and 0.15% to 2.10% in hospitalized patients [3]. In the prospective BASEL IX cohort (1,397 ED patients), PE was found at presentation in 1.4% (0.87 to 2.11), and the authors concluded systematic screening does not seem warranted [4]. A systematic review pooled 0.8% (0.5 to 1.3) in ED patients and suggested PESIT may reflect site effect, accrual bias, or investigation strategy [5].

A reasonable reading (judgment): routine PE testing for every faint is not supported; PE should be considered when the story does not fit a benign cause (persistent tachycardia, hypoxemia, dyspnea, leg symptoms, strong risk factors); and PESIT's older, hospitalized population should not be applied to a young woman in the ED. Her risk comes from her risk factors and vital signs more than from the faint.

Why syncope matters once PE is found

A meta-analysis of 29 studies (21,956 PE patients, 3,706 with syncope) linked syncope to hemodynamic instability (OR 3.50; 2.67 to 4.58), RV dysfunction (OR 2.10), early death (OR 1.73), and PE-related adverse outcomes (OR 2.00), but in normotensive-only studies the absolute risk difference for death was -1% (-2% to +1%) [6]. Another meta-analysis found mortality OR 1.82 and concluded the association was explained by differences in hemodynamic instability [7]. The takeaway: syncope in confirmed PE is a reason to look hard at hemodynamics and the RV, not an independent mandate for aggressive therapy in a stable patient (judgment).

Management

• Risk-stratify. High-risk PE is cardiac arrest, obstructive shock, or persistent hypotension (systolic BP below 90 mmHg, or a drop of 40 mmHg or more for over 15 minutes, not due to arrhythmia, hypovolemia, or sepsis) [1]. This patient is normotensive.
• Normotensive severity. The simplified PESI scores 1 point for pulse of 110 or more; 30-day mortality was 1.0% for a score of 0 versus 10.9% for 1 or more [1]. RV dysfunction plus elevated troponin classes a normotensive patient as intermediate-high risk, with close monitoring recommended [1].
• Anticoagulation while testing. For high or intermediate probability, the ESC guideline states anticoagulation should be initiated while awaiting test results (low-molecular-weight heparin, fondaparinux, or unfractionated heparin; LMWH and fondaparinux are preferred over UFH), and that oral anticoagulants are the first choice in eligible patients [1]. Bleeding risk and local pathways individualize the decision.
• Fluids. For acute right ventricular failure in high-risk PE, the guideline suggests only cautious volume loading (up to 500 mL over 15 to 30 minutes) and warns that it can over-distend the RV [1]. A normotensive patient does not need repeated boluses chasing the heart rate.
• Disposition. Depends on risk class; early discharge is for carefully selected low-risk patients [1]. Decisions about estrogen-containing contraception belong to the treating team and patient (general principle; no grade verified).

Clinical pearls

• A faint plus tachycardia that does not respond to fluids is not a simple faint until shown otherwise.
• Syncope is not a Wells item; the vital signs and risk factors are.
• PERC rules out only in low-probability patients; this patient does not qualify.
• D-dimer is for low or intermediate probability; a likely PE goes to imaging.
• Syncope in confirmed PE: look at hemodynamics and the RV.

Common pitfalls

• Anchoring on "vasovagal" and reading the heart rate as dehydration.
• Applying PERC without a low gestalt.
• Acting on a D-dimer in a high-probability patient.
• Testing everyone who faints; the evidence does not support it.
• Missing the pregnancy test.

Takeaways

• Consider PE in syncope when something does not fit, not for every faint.
• Build pretest probability from heart rate, saturation, hormone use, travel, and leg findings.
• PERC for low probability; D-dimer for low or intermediate; imaging when probability is high.
• Start anticoagulation while awaiting the scan when probability is high or intermediate and bleeding risk allows.
• Stratify by hemodynamics and RV findings, not by the faint alone.

References

1. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J. 2020;41(4):543-603. doi:10.1093/eurheartj/ehz405 | PMID 31504429
2. Prandoni P, Lensing AWA, Prins MH, et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med. 2016;375(16):1524-1531. doi:10.1056/NEJMoa1602172 | PMID 27797317
3. Costantino G, Ruwald MH, Quinn J, et al. Prevalence of pulmonary embolism in patients with syncope. JAMA Intern Med. 2018;178(3):356-362. doi:10.1001/jamainternmed.2017.8175 | PMID 29379959
4. Badertscher P, du Fay de Lavallaz J, Hammerer-Lercher A, et al. Prevalence of pulmonary embolism in patients with syncope. J Am Coll Cardiol. 2019;74(6):744-754. doi:10.1016/j.jacc.2019.06.020 | PMID 31395124
5. Oqab Z, Ganshorn H, Sheldon R. Prevalence of pulmonary embolism in patients presenting with syncope. A systematic review and meta-analysis. Am J Emerg Med. 2018;36(4):551-555. doi:10.1016/j.ajem.2017.09.015 | PMID 28947223
6. Barco S, Ende-Verhaar YM, Becattini C, et al. Differential impact of syncope on the prognosis of patients with acute pulmonary embolism: a systematic review and meta-analysis. Eur Heart J. 2018;39(47):4186-4195. doi:10.1093/eurheartj/ehy631 | PMID 30339253
7. de Winter MA, van Bergen EDP, Welsing PMJ, et al. The prognostic value of syncope on mortality in patients with pulmonary embolism: a systematic review and meta-analysis. Ann Emerg Med. 2020;76(4):527-541. doi:10.1016/j.annemergmed.2020.03.026 | PMID 32461009
8. Kline JA, Mitchell AM, Kabrhel C, Richman PB, Courtney DM. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost. 2004;2(8):1247-1255. doi:10.1111/j.1538-7836.2004.00790.x | PMID 15304025
9. Freund Y, Cachanado M, Aubry A, et al. Effect of the pulmonary embolism rule-out criteria on subsequent thromboembolic events among low-risk emergency department patients: the PROPER randomized clinical trial. JAMA. 2018;319(6):559-566. doi:10.1001/jama.2017.21904 | PMID 29450523
10. Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer. Thromb Haemost. 2000;83(3):416-420. PMID 10744147 (no DOI listed in PubMed)
11. van der Hulle T, Cheung WY, Kooij S, et al. Simplified diagnostic management of suspected pulmonary embolism (the YEARS study): a prospective, multicentre, cohort study. Lancet. 2017;390(10091):289-297. doi:10.1016/S0140-6736(17)30885-130885-1) | PMID 28549662
12. Stein PD, Fowler SE, Goodman LR, et al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med. 2006;354(22):2317-2327. doi:10.1056/NEJMoa052367 | PMID 16738268
13. Stegeman BH, de Bastos M, Rosendaal FR, et al. Different combined oral contraceptives and the risk of venous thrombosis: systematic review and network meta-analysis. BMJ. 2013;347:f5298. doi:10.1136/bmj.f5298 | PMID 24030561
14. Chandra D, Parisini E, Mozaffarian D. Meta-analysis: travel and risk for venous thromboembolism. Ann Intern Med. 2009;151(3):180-190. doi:10.7326/0003-4819-151-3-200908040-00129 | PMID 19581633
15. Kuipers S, Cannegieter SC, Middeldorp S, Robyn L, Büller HR, Rosendaal FR. The absolute risk of venous thrombosis after air travel: a cohort study of 8,755 employees of international organisations. PLoS Med. 2007;4(9):e290. doi:10.1371/journal.pmed.0040290 | PMID 17896862

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Sudden Back and Flank Pain in an Older Smoker: Is It Really a Strain?

Case presentation (composite)

A man in his late sixties with a long smoking history reports that he "threw his back out." The pain began suddenly in the low back and flank and was at its worst from the start. He is sweating and looks pale and gray. Blood pressure is 150/90 mmHg. The abdomen is soft. He asks for a muscle relaxant. The room's plan is musculoskeletal strain or sciatica, ketorolac and cyclobenzaprine, and discharge with primary care follow-up.

(Composite case. No real patient is described. Heart rate and other vital signs are not specified in this teaching case.)

The first guess, and why it is tempting

Back pain is among the most common ED complaints, and the large majority is benign. A soft abdomen, a normal-looking blood pressure, and a patient who is walking and talking support the strain story. A blood pressure of 150/90 invites the thought that a leaking aorta is not present, because a leak should mean hypotension.

That reasoning is the trap. The classic triad is often incomplete, and a contained or slowly leaking rupture can be normotensive or even hypertensive, particularly in someone with baseline hypertension and a pain response (judgment). The ESVS 2024 guideline states that the classic triad (hypotension, abdominal and/or back pain, pulsatile abdominal mass) is present in about 50% of patients with ruptured AAA, and that misdiagnosis may occur in 32% to 39% of patients, particularly those presenting without hemodynamic shock [1].

What does not fit

• Sudden onset, maximal at the start. Abrupt, maximal pain in an older patient is not typical of mechanical strain (clinical judgment, not a validated rule).
• Risk profile. Smoking is the strongest risk factor for AAA, with an odds ratio above 3 per the ESVS guideline [1]. USPSTF screening recommendations target men aged 65 to 75 who have ever smoked (B recommendation) [10].
• Appearance. Sweating and a gray look are signs that the body is under physiologic stress. They are not specific to AAA but do not belong to a muscle strain (judgment).
• Soft abdomen. A soft abdomen does not argue against AAA. In a meta-analysis of 9 studies (1,109 patients), abdominal pain, shock, and a pulsatile mass were present in 61%, 46%, and 45% of ruptured AAAs, respectively [2].
• A mimic that fits the story. In that same meta-analysis, the most common wrong diagnoses were ureteric colic and myocardial infarction [2]. Flank pain with restlessness is easy to label as renal colic.

How often it is missed

A systematic review and meta-analysis found an initial misdiagnosis rate of 42% (95% CI 29% to 55%) across 9 studies, and 32% (16% to 49%) in studies after 1990 [2]. A Swedish registry-based cohort of 261 patients found 33% initially misdiagnosed, with a median additional delay to surgery of 4.8 hours; 30-day mortality did not differ (27.9% vs. 28.0%), though only patients who reached surgery were included, so this cannot be taken as evidence that delay is harmless [3]. In a population-based Stockholm study of 216 patients, only 13% had all three signs of the standard triad as defined in that study (abdominal pain, syncope, pulsatile mass), whereas 35% met a broader set of pain, hypovolemia-related signs, and pulsatile mass or ultrasound finding; abdominal pain was recorded in 84% and dizziness in 50% [4]. In a US Medicare cohort, about 3.4% of ruptured AAA presentations (95% CI 2.9% to 4.0%) ended in ED discharge without diagnosis [5].

Differential

Renal or ureteric colic, musculoskeletal strain, lumbar disc disease or sciatica, pyelonephritis, pancreatitis, diverticulitis, mesenteric ischemia (see Case 05), aortic dissection, inferior MI, spinal epidural abscess or hematoma, retroperitoneal hemorrhage from another cause, symptomatic but unruptured AAA, and infected or inflammatory aneurysm.

Workup

Bedside ultrasound

A systematic review of ED bedside ultrasound for suspected AAA (7 studies, 655 patients) reported pooled sensitivity of 99% (95% CI 96% to 100%) and specificity of 98% (97% to 99%) for aneurysm of at least 3 cm in symptomatic patients; abdominal palpation sensitivity rose with aneurysm diameter, and 50% of AAA patients lacked the classic triad [6]. The ESVS guideline adds two limits: ultrasound has low sensitivity for retroperitoneal hemorrhage and cannot identify a leak, but the presence of an AAA in an unstable patient is very suggestive of rupture [1]. A palpation exam has sensitivity of 33% to 100% and specificity of 75% to 100% across studies and should not be relied on [1].

CT angiography

The ESVS 2024 guideline states that an immediate CTA of the thoraco-abdominal aorta and iliac vessels is the key imaging modality for all patients with suspected ruptured AAA, noting that most patients who reach hospital alive are sufficiently stable to undergo it. It defines hemodynamic instability as reduced or lost consciousness or systolic BP below 80 mmHg, and notes that very unstable patients may go directly to the operating room for intra-operative imaging [1].

Other tests

Type and crossmatch, CBC, chemistry, lactate, and an ECG (myocardial infarction is a documented mimic [2]). These are supportive; none rules out AAA (judgment).

Management

• Call vascular surgery now, in parallel with imaging. The ESVS 2024 guideline recommends endovascular repair as the first-line option for ruptured AAA with suitable anatomy (Class I, Level A) [1]. In the IMPROVE randomized trial (613 patients), 30-day mortality was 35.4% with an endovascular-first strategy and 37.4% with open repair (OR 0.92; 95% CI 0.66 to 1.28), with more patients discharged directly home after the endovascular strategy (94% vs. 77%) [8]. Transfer early to a center with vascular capability if needed.
• Permissive hypotension. The ESVS guideline recommends a policy of permissive hypotension for ruptured AAA (Class I, Level C, downgraded from B), for example by restricting fluid resuscitation, using consciousness and the ability to speak as markers of adequate cerebral perfusion. It describes a target systolic pressure of 70 to 90 mmHg as the traditional range, while noting that no direct comparative study exists and that the ideal target is debatable [1]. In IMPROVE, the lowest systolic BP was independently associated with 30-day mortality (51% among those with pressure below 70 mmHg), and the authors suggested that 70 mmHg is too low a threshold [9].
• Resuscitate with blood, not large volumes of crystalloid. The guideline states that vigorous fluid replacement may exacerbate bleeding, and suggests blood and blood products with a plasma-to-red-cell ratio close to 1:1 [1].
• Blood pressure "control." The guideline notes that whether pharmacological lowering of blood pressure is beneficial remains unclear, and that adequate pain management contributes to keeping BP down [1]. For a patient like this one with a hypertensive reading and a suspected contained leak, the aim is to avoid surges while arranging definitive care, with the exact plan set with vascular surgery (judgment).
• Avoid delay for tests that do not change management. Muscle relaxants and further observation have no role once rupture is suspected (judgment).

Evidence in context

A systematic review of 24 population-based cohort studies (1977 to 2012) estimated total mortality from ruptured AAA at 81% (95% CI 78% to 83%), 74% (72% to 77%) in high-quality studies since 1990, with 32% (27% to 37%) of cases ending before the patient reached hospital; the studies were retrospective and of varying quality [7]. The ESVS guideline similarly describes rupture as fatal in more than 80% of cases [1]. These figures are population-wide; outcomes for patients who reach a vascular center alive are better, as in IMPROVE [8].

Clinical pearls

• Sudden back or flank pain in an older smoker is a ruptured AAA until a plan rules it out.
• A normal or high blood pressure does not exclude a contained leak.
• A soft abdomen and the absence of a pulsatile mass do not help.
• Ultrasound can find the aneurysm; CTA shows the rupture and the anatomy for repair.
• Permissive hypotension means not chasing the blood pressure with fluid.

Common pitfalls

• Treating a flank pain as renal colic without considering the aorta.
• Relying on the triad; it is present in about half.
• Using ultrasound to exclude a leak; it cannot.
• Discharging after analgesia improves the pain.
• Aggressive crystalloid resuscitation.
• Waiting for hypotension before calling vascular surgery.

Takeaways

• Misdiagnosis of ruptured AAA is frequent (about one in three after 1990 in one meta-analysis).
• Risk (age, male sex, smoking) and the pain pattern matter more than a reassuring blood pressure.
• Bedside ultrasound is highly accurate for AAA; CTA is the key study for rupture in a patient stable enough to scan.
• Early vascular surgery involvement, blood-based resuscitation, and permissive hypotension are the guideline-supported pillars.

References

1. Wanhainen A, Van Herzeele I, Bastos Goncalves F, et al. Editor's Choice: European Society for Vascular Surgery (ESVS) 2024 clinical practice guidelines on the management of abdominal aorto-iliac artery aneurysms. Eur J Vasc Endovasc Surg. 2024;67(2):192-331. doi:10.1016/j.ejvs.2023.11.002 | PMID 38307694
2. Azhar B, Patel SR, Holt PJ, Hinchliffe RJ, Thompson MM, Karthikesalingam A. Misdiagnosis of ruptured abdominal aortic aneurysm: systematic review and meta-analysis. J Endovasc Ther. 2014;21(4):568-575. doi:10.1583/13-4626MR.1 | PMID 25101588
3. Smidfelt K, Drott C, Törngren K, Nordanstig J, Herlitz J, Langenskiöld M. The impact of initial misdiagnosis of ruptured abdominal aortic aneurysms on lead times, complication rate, and survival. Eur J Vasc Endovasc Surg. 2017;54(1):21-27. doi:10.1016/j.ejvs.2017.03.022 | PMID 28526396
4. Bergmark P, Sadeghi M, Talvitie M, et al. Initial signs in patients with ruptured abdominal aortic aneurysms: time for an expanded triad? Scand J Trauma Resusc Emerg Med. 2024;32:94. doi:10.1186/s13049-024-01268-0 | PMID 39313802
5. Waxman DA, Kanzaria HK, Schriger DL. Unrecognized cardiovascular emergencies among Medicare patients. JAMA Intern Med. 2018;178(4):477-484. doi:10.1001/jamainternmed.2017.8628 | PMID 29482196
6. Rubano E, Mehta N, Caputo W, Paladino L, Sinert R. Systematic review: emergency department bedside ultrasonography for diagnosing suspected abdominal aortic aneurysm. Acad Emerg Med. 2013;20(2):128-138. doi:10.1111/acem.12080 | PMID 23406071
7. Reimerink JJ, van der Laan MJ, Koelemay MJ, Balm R, Vahl AC. Systematic review and meta-analysis of population-based mortality from ruptured abdominal aortic aneurysm. Br J Surg. 2013;100(11):1405-1413. doi:10.1002/bjs.9235 | PMID 24037558
8. IMPROVE Trial Investigators; Powell JT, Sweeting MJ, Thompson MM, et al. Endovascular or open repair strategy for ruptured abdominal aortic aneurysm: 30 day outcomes from IMPROVE randomised trial. BMJ. 2014;348:f7661. doi:10.1136/bmj.f7661 | PMID 24418950
9. IMPROVE Trial Investigators; Powell JT, Hinchliffe RJ, Thompson MM, et al. Observations from the IMPROVE trial concerning the clinical care of patients with ruptured abdominal aortic aneurysm. Br J Surg. 2014;101(3):216-224. doi:10.1002/bjs.9410 | PMID 24469620
10. US Preventive Services Task Force; Owens DK, Davidson KW, Krist AH, et al. Screening for abdominal aortic aneurysm: US Preventive Services Task Force recommendation statement. JAMA. 2019;322(22):2211-2218. doi:10.1001/jama.2019.18928 | PMID 31821437

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

"He's Just Drunk": When Alcohol Explains the Smell but Not the Neurologic Exam

Case presentation (composite)

A man in his mid-fifties is brought in after being found down outside a bar. He smells of alcohol and groans in response to pain but does not otherwise engage. Fingerstick glucose is 110 mg/dL. His friends say he "always drinks like this." Nobody saw what happened before he was found. The room's plan is to board him for sobering, watch the airway, and hold off on imaging.

Over the next hour, his pupils are noted to be slightly unequal and he vomits once without waking.

(Composite case. No real patient is described. Vital signs and the trauma history are not specified in this teaching case.)

The first guess, and why it is tempting

Intoxication is the most common reason for altered mental status in this setting, the smell is real, and a negative glucose removes the first reversible cause. A patient who is repeatedly the same "regular" is easy to anchor on. Waiting also feels low-risk, because sobering is expected to improve the exam over hours.

The trap is that the alcohol is a true finding that explains only part of the picture, and that waiting is not neutral if something structural is present. The most useful question is not "is he drunk?" but "does the exam fit the amount of alcohol, and can I explain every finding?"

What does not fit

• Depth of reduced responsiveness. Groaning only to pain implies a markedly reduced Glasgow Coma Scale (GCS) score (clinical estimate). In a retrospective registry of 1,075 blunt traumatic brain injury patients, alcohol intoxication (mean blood alcohol 202 mg/dL) lowered GCS by less than one point in nearly all injury types (1.4 points in the most severe injuries), and the authors concluded that GCS changes after head injury should not be attributed to alcohol, because doing so can delay monitoring and treatment [5].
• Unequal pupils. Physiologic anisocoria is common: 19% of 128 healthy volunteers had at least 0.4 mm of anisocoria at any given exam [6], and 13.7% of 708 healthy subjects in another study [7]. In that study, bedside clinical assessment missed more than half of true anisocoria (sensitivity 0.46, specificity 0.91), and the authors suggested that patients at risk of uncal herniation may benefit from routine pupillary assessment with a portable pupillometer [7]. So the finding is real but nonspecific: a new or changing asymmetry, especially with a sluggish larger pupil and reduced consciousness, is a worrying sign, while a stable, brisk asymmetry in an awake patient is often benign (judgment).
• Vomiting. In the Canadian CT Head Rule derivation, vomiting (more than 2 episodes in the abstract; two or more as the rule is commonly cited) was one of five high-risk factors [3]. In a systematic review of minor head trauma, two or more vomiting episodes carried a likelihood ratio of 3.6 for severe intracranial injury [4]. One episode does not meet either threshold, but in a patient who does not wake it adds to the picture (judgment).
• No witness and no mechanism. An unwitnessed event means trauma cannot be excluded. A found-down patient with intoxication has a plausible fall, assault, or both.

Differential

Acute alcohol intoxication, traumatic intracranial hemorrhage (subdural, epidural, contusion, subarachnoid), spontaneous intracerebral hemorrhage, ischemic stroke, hypoglycemia (excluded by the fingerstick), other toxic ingestions or co-ingestants, Wernicke encephalopathy, postictal state or nonconvulsive seizure, hypothermia, sepsis or meningitis, hyponatremia or other metabolic derangements, carbon monoxide, hepatic encephalopathy, and cervical spine or other injuries.

Workup

Imaging

A noncontrast head CT is the study. The 2022 AHA/ASA guideline for spontaneous intracerebral hemorrhage gives a Class 1 recommendation to obtain rapid CT or MRI to confirm the diagnosis in patients presenting with stroke-like symptoms, and a Class 2a recommendation that serial head CT is useful in the first 24 hours to evaluate hematoma expansion, and in patients with low GCS or neurologic deterioration to evaluate for expansion, hydrocephalus, edema, or herniation [1,8]. Hematoma expansion occurs in up to a third of patients after ICH and is associated with poor outcome [8]. (This guideline addresses spontaneous ICH; the principle of early imaging with repeat imaging for deterioration also applies to traumatic hemorrhage, but the details differ.)

Why the head-CT rules need care here

The ACEP 2023 clinical policy recommends the Canadian CT Head Rule (Level A) and, at Level B, the NEXUS Head CT or New Orleans Criteria, for adults with minor head injury [2]. Three cautions apply:

1. The policy defines minor head injury as a GCS of 14 or 15 [2]. The original Canadian CT Head Rule included patients with GCS of 13 to 15 [3]. A patient who groans only to pain is outside both.
2. The New Orleans Criteria list drug or alcohol intoxication as a higher-risk feature [2].
3. In the policy's discussion of a prospective cohort of 283 intoxicated adults with minor head injury, the Canadian CT Head Rule had a sensitivity of 70% (95% CI 47% to 87%) and NEXUS Head CT 83% (61% to 95%), and the policy concluded that the absence of high-risk criteria cannot alone eliminate the need for CT in intoxicated patients [2].

So intoxication is not a reason to skip imaging and, in a patient this obtunded, is not a setting for a decision rule at all.

Other tests

The AHA work-up for suspected ICH includes CBC (platelets), coagulation studies (PT/INR, aPTT), glucose, renal and liver function, urine toxicology, pregnancy test where relevant, ECG, and troponin; thrombocytopenia, hyperglycemia, acute kidney injury, and elevated troponin are listed as indicators of increased morbidity and mortality, and anticoagulant-related hemorrhage and anemia as indicators of increased hematoma expansion [8]. Alcohol use disorder is listed among the factors associated with ICH [8]. Add a blood alcohol level for context only: it neither confirms nor excludes a structural lesion.

Management

• Airway first. Protect the airway in a patient who does not wake and has vomited. GCS of 8 or less is the conventional teaching threshold for definitive airway management (general teaching; not verified from a guideline in this pass).
• Image early, without waiting for him to sober up. See above.
• Look for anticoagulant or antiplatelet use and reverse when indicated. In anticoagulant-related spontaneous ICH, the AHA guideline gives a Class 1 recommendation to discontinue anticoagulation immediately and to perform rapid reversal as soon as possible, with agent-specific options; for antiplatelet-related ICH, platelet transfusion is potentially harmful unless neurosurgery is needed (Class 3: Harm, versus 2b if emergent neurosurgery is required) [8].
• Blood pressure. In mild-to-moderate spontaneous ICH presenting with systolic pressure of 150 to 220 mmHg, acute lowering to a target of 140 mmHg with a goal of maintaining 130 to 150 mmHg is safe and may be reasonable (Class 2b), and lowering below 130 mmHg is potentially harmful (Class 3: Harm) [8]. Traumatic hemorrhage and patients with suspected raised intracranial pressure need individualized targets with neurosurgery and critical care.
• Neurosurgery and disposition. Obtain neurosurgical input for any hemorrhage. The guideline recommends a specialized inpatient unit with a multidisciplinary team, and transfer to a center with neurosurgical capability for hydrocephalus (Class 1) [8].

Evidence in context

The AHA/ASA guideline summary notes about 79,000 ICH cases per year among roughly 795,000 US strokes, with early mortality of 30% to 40% [8]. These figures describe spontaneous ICH, not traumatic hemorrhage in a found-down patient, and are given for scale only. Most data on decision rules come from patients who are awake and oriented; there is little prospective evidence on the specific question of the unwitnessed, obtunded, intoxicated patient, so the strongest recommendations rest on the principle that GCS should not be attributed to alcohol [5].

Clinical pearls

• Alcohol explains the smell. It does not, by itself, explain a depressed exam.
• GCS is not meaningfully shifted by alcohol in head injury, so low GCS should be explained by something else.
• Pupil asymmetry is common in healthy people, so look for change over time and for other signs.
• Head-CT rules are for minor head injury in awake patients; intoxication erodes their sensitivity.
• "Frequent flyer" is a social label, not a diagnosis.

Common pitfalls

• Boarding a patient for sobering without a defined reassessment plan.
• Treating a blood alcohol level as a stand-in for the neurologic exam.
• Applying a minor head-injury rule to a patient with a GCS below 13.
• Assuming the first fingerstick glucose ends the metabolic search.
• Missing anticoagulant use and platelet or coagulation abnormalities.
• Leaving imaging until the morning.

Takeaways

• Treat "found down" with alcohol as altered mental status until proven otherwise.
• Do not attribute reduced responsiveness to alcohol; image early.
• Secure the airway, check glucose and coagulation, and look for anticoagulant use.
• Re-examine pupils and GCS serially and involve neurosurgery early if a hemorrhage is found.

References

1. Greenberg SM, Ziai WC, Cordonnier C, et al. 2022 guideline for the management of patients with spontaneous intracerebral hemorrhage: a guideline from the American Heart Association/American Stroke Association. Stroke. 2022;53(7):e282-e361. doi:10.1161/STR.0000000000000407 | PMID 35579034 (full text not opened; see ref 8 and the log)
2. American College of Emergency Physicians Clinical Policies Subcommittee on Mild Traumatic Brain Injury; Valente JH, Anderson JD, Paolo WF, et al. Clinical policy: critical issues in the management of adult patients presenting to the emergency department with mild traumatic brain injury. Ann Emerg Med. 2023;81(5):e63-e105. doi:10.1016/j.annemergmed.2023.01.014 | PMID 37085214
3. Stiell IG, Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001;357(9266):1391-1396. doi:10.1016/S0140-6736(00)04561-X04561-X) | PMID 11356436
4. Easter JS, Haukoos JS, Meehan WP, Novack V, Edlow JA. Will neuroimaging reveal a severe intracranial injury in this adult with minor head trauma? The Rational Clinical Examination systematic review. JAMA. 2015;314(24):2672-2681. doi:10.1001/jama.2015.16316 | PMID 26717031
5. Sperry JL, Gentilello LM, Minei JP, Diaz-Arrastia RR, Friese RS, Shafi S. Waiting for the patient to "sober up": effect of alcohol intoxication on Glasgow Coma Scale score of brain injured patients. J Trauma. 2006;61(6):1305-1311. doi:10.1097/01.ta.0000240113.13552.96 | PMID 17159670
6. Lam BL, Thompson HS, Corbett JJ. The prevalence of simple anisocoria. Am J Ophthalmol. 1987;104(1):69-73. doi:10.1016/0002-9394(87)90296-090296-0) | PMID 3605282
7. George AS, Abraham AP, Nair S, Joseph M. The prevalence of physiological anisocoria and its clinical significance: a neurosurgical perspective. Neurol India. 2019;67(6):1500-1503. doi:10.4103/0028-3886.273623 | PMID 31857545
8. American Heart Association. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage: Clinical Update slide set (adapted from ref 1; recommendation classes quoted from this AHA-authored summary). heart.org PDF

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Everyone at Home Has the Flu, the Dog Included: What Is the Normal Oximetry Missing?

Case presentation (composite)

A 35-year-old woman presents with several days of headache, nausea, and aching. Heart rate is 98. She has no fever, and pulse oximetry reads 98% on room air. The working diagnosis is a viral illness or migraine, with fluids and discharge home.

On further history, her husband and both children feel the same. The family dog has been sluggish. Everyone is better at work and school, and worse at home.

(Composite case. No real patient or family is described. Ages, vital signs, and household details are fictional. Blood pressure, respiratory rate, and the season are not specified in this teaching case.)

The first guess, and why it is tempting

Headache, nausea, and myalgias in an afebrile adult with a normal saturation fit a viral syndrome or a primary headache disorder, and both are far more common than poisoning. The symptoms of carbon monoxide (CO) poisoning are described in the ACEP clinical policy as vague complaints of headache, dizziness, nausea, vomiting, shortness of breath, and chest pain [1]. CDC states that the symptoms are often described as "flu-like" [9], and a professional reference notes that many mild cases are mistaken for viral syndromes [10]. A reassuring oximeter reading closes the loop in the clinician's mind. That reading is the trap.

What does not fit

• A cluster. The Merck Manual advises considering CO when people from the same dwelling have nonspecific flu-like symptoms [10]. In a small 1987 study of 37 adults with headache seen in an ED during the heating season, 7 (18.9%) had a COHb above 10%. Three of those seven had cohabitants with headache, versus none of the 30 with lower levels (P = .0045). None of the seven had been suspected of CO poisoning before the level returned [6]. A second study of 89 patients with headache or dizziness found that concurrently symptomatic cohabitants were a significant predictor of the COHb level [7]. Both studies are small and old, and both enrolled selected patients with headache or dizziness, so treat them as pattern recognition rather than a decision rule.
• Location-dependent symptoms. A review of out-of-hospital diagnostic errors lists several epidemiologic clues: multiple people in a confined space, all family members with flu symptoms but without fever, early symptoms in small pets, and diminution of symptoms outside a specific environment [8]. That review is secondary and draws these clues from earlier sources that I did not open, so they are descriptive rather than validated.
• Animals. CDC notes that CO can build up indoors and affect both people and animals [9].
• No fever. Consistent with a non-infectious process, but it is also common in viral illness and should not be over-read.
• A normal saturation. See below.

Why the oximeter reading is normal

Carboxyhemoglobin and oxyhemoglobin absorb light similarly at the wavelength used by standard two-wavelength pulse oximeters, so the device reports their sum as saturation [8]. In a retrospective review of 124 patients with CO poisoning who had both an arterial blood gas and pulse oximetry, measured oxyhemoglobin saturation fell linearly with rising COHb (mean 88.7%), while the pulse oximetry reading stayed at a mean of 99.2% (range 92% to 100%); the "gap" approximated the COHb level [2]. The authors concluded that pulse oximetry should be considered unreliable until a COHb level has been measured [2]. The Merck Manual adds that blood gases alone are also inadequate, because the oxygen value they report represents dissolved oxygen and is unaffected by COHb [10].

Differential

Viral syndromes (influenza, COVID-19, other respiratory viruses), primary headache disorders, gastroenteritis or a shared-meal food-borne illness, anemia, and other toxic exposures. A shared meal can explain a group with gastrointestinal symptoms, and the review of diagnostic errors specifically lists food poisoning, tension headache or migraine, and viral illness among commonly mistaken diagnoses [8]. Methylene chloride exposure can also cause delayed CO poisoning through its metabolism [10]. Features that argue against infection include improvement away from the home, household members with identical symptoms, and animal illness (clinical reasoning).

Workup

The diagnostic test

Order a blood carboxyhemoglobin level measured by CO-oximetry. Venous samples are acceptable because arteriovenous differences are trivial [10]. ACEP describes this as the traditional approach: co-oximeter analysis of venous or arterial blood [1]. Typical nontoxic levels are 3% or less in nonsmokers, with smokers up to 10% [1].

Interpretation pitfalls

• A low level does not exclude exposure. COHb falls quickly after exposure ends, especially after supplemental oxygen such as in an ambulance [10]. The half-life is about 4 to 5 hours on room air and about 85 minutes with high-flow oxygen [1]. Draw the level early and record the time since the last exposure and any oxygen given (clinical practice).
• Handheld pulse CO-oximeters are not a substitute. ACEP gives a Level B recommendation against using noninvasive COHb measurement to diagnose CO toxicity, citing a sensitivity of 48% in one ED study [1]. A 2023 meta-analysis of six studies (1,734 patients) found a pooled sensitivity of 0.65 and a pooled specificity of 0.93 at a 10% cutoff, and concluded the devices cannot be used as a screening tool in the ED [5].
• Symptoms and level correlate loosely. The Merck Manual notes headache and nausea can begin at COHb levels of 10% to 20%, with vague dizziness, weakness, and poor concentration more common above 20% [10]. A review of prehospital errors cautions that the percentage does not reliably track severity or prognosis, especially with chronic exposure [8].

Other testing

For moderate to severe poisoning, ACEP recommends an ECG and cardiac biomarkers (Level B) because acute myocardial injury predicts a worse outcome [1]. Other testing is guided by symptoms (for example CT or MRI for neurologic findings) [10].

Management

• Remove from the source and give high-flow oxygen. Merck advises removing the patient from the source and giving 100% oxygen by non-rebreather mask [10]. ACEP's Level B recommendation is to use either hyperbaric oxygen (HBO2) or high-flow normobaric oxygen, and notes that it remains unclear whether HBO2 is superior for long-term neurocognitive outcomes [1].
• Hyperbaric oxygen: sometimes used, benefit debated. In the 2002 double-blind randomized trial, cognitive sequelae at 6 weeks occurred in 25.0% (19 of 76) with three HBO2 sessions versus 46.1% (35 of 76) with normobaric oxygen (P = 0.007); the trial was stopped early at an interim analysis [3]. ACEP's review describes the trials as inconsistent, with differences in timing, dose, and outcome definitions, and lists three studies finding no benefit and two finding benefit [1]. A 2026 systematic review and meta-analysis of six randomized trials found no significant benefit of HBO2 for mortality or neurological outcomes, with low to very low certainty of evidence, and concluded that efficacy remains unproven [4]. A correction notice for that article was published later [4]; its content was not reviewed here. The Merck Manual says HBO2 typically should be considered for patients with life-threatening cardiopulmonary complications, ongoing chest pain, altered or lost consciousness, or a COHb above 25%, and for pregnant patients, while noting its use is "becoming increasingly controversial" and recommending consultation with a poison control center or hyperbaric expert [10]. Whether to transfer for HBO2 is an individualized decision (clinical judgment).
• Evaluate everyone exposed. In a cluster, the other household members, children, and pets are part of the case (clinical reasoning). Merck advises ventilation, evacuation of the dwelling, and evaluation for the source [10].
• Follow-up. Neurologic sequelae, either persistent or delayed by 2 to 21 days, have been described in 12% to 68% of poisoned patients in the studies cited by ACEP, typically memory loss, impaired concentration, or mood changes [1]. Tell patients to return for new cognitive or neurologic symptoms (clinical practice).
• Prevention. CDC recommends battery-operated or battery back-up CO detectors near every sleeping area, checking batteries regularly, and annual servicing of fuel-burning appliances [9]. This is education for the discharge conversation, not a substitute for treatment.

Evidence in context

Diagnostic data on household cohorts are limited to small, older, single-center studies [6,7]. The best-supported tests and treatments come from a clinical policy by ACEP [1] and a limited number of randomized trials with conflicting results [1,3,4]. In the United States, CDC reports more than 100,000 emergency department visits and more than 14,000 hospitalizations per year from unintentional CO poisoning [9]. The true burden is probably higher because of misdiagnosis [1].

Clinical pearls

• Several people at one address with the same flu-like illness: ask about CO before settling on a virus.
• Symptoms that improve away from home and return on re-entering the home are a major clue.
• Pulse oximetry cannot rule out CO poisoning; a venous COHb on a co-oximeter can confirm it.
• A normal COHb late in the course or after oxygen does not exclude significant exposure.
• Treat the household, not just the patient in front of you.

Common pitfalls

• Reassurance from a normal SpO2.
• Using a handheld SpCO device as a screening test.
• Drawing the level hours after exposure and after oxygen, then calling it normal.
• Discharging one family member without considering the rest.
• Forgetting follow-up for delayed neurologic symptoms.

Takeaways

• Think CO when a household is sick together and better apart from home.
• A normal pulse oximeter reading does not exclude it.
• Send a blood carboxyhemoglobin level; treat with high-flow oxygen.
• Hyperbaric oxygen is a debated adjunct; discuss selected cases with poison control or a hyperbaric expert.
• Evaluate the others in the home.

References

1. Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD; American College of Emergency Physicians Clinical Policies Subcommittee. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute carbon monoxide poisoning. Ann Emerg Med. 2017;69(1):98-107.e6. doi:10.1016/j.annemergmed.2016.11.003 | PMID 27993310
2. Bozeman WP, Myers RA, Barish RA. Confirmation of the pulse oximetry gap in carbon monoxide poisoning. Ann Emerg Med. 1997;30(5):608-611. doi:10.1016/s0196-0644(97)70077-5 | PMID 9360570
3. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347(14):1057-1067. doi:10.1056/NEJMoa013121 | PMID 12362006
4. Fujita M, Todani M, Ajimi Y, et al. Evaluating the efficacy of hyperbaric oxygen therapy for acute carbon monoxide poisoning: a systematic review and meta-analysis. Acute Med Surg. 2026;13(1):e70114. doi:10.1002/ams2.70114 | PMID 41624627
5. Ramponi G, Gianni F, Karlafti E, et al. The diagnostic accuracy of carbon monoxide pulse oximetry in adults with suspected acute carbon monoxide poisoning: a systematic review and meta-analysis. Front Med (Lausanne). 2023;10:1250845. doi:10.3389/fmed.2023.1250845 | PMID 38223786
6. Heckerling PS. Occult carbon monoxide poisoning: a cause of winter headache. Am J Emerg Med. 1987;5(3):201-204. doi:10.1016/0735-6757(87)90320-2 | PMID 3580051
7. Heckerling PS, Leikin JB, Maturen A. Predictors of occult carbon monoxide poisoning in patients with headache and dizziness. Ann Intern Med. 1987;107(2):174-176. doi:10.7326/0003-4819-107-2-174 | PMID 3605895
8. Fucili G, Brauzzi M. Tips for avoiding common mistakes in out-of-hospital diagnosis of carbon monoxide poisoning. J Anesth Analg Crit Care. 2022;2:14. doi:10.1186/s44158-022-00041-y | PMID 37386527
9. Centers for Disease Control and Prevention. Carbon monoxide poisoning basics. Updated January 12, 2026. cdc.gov/carbon-monoxide/about
10. O'Malley GF, O'Malley R. Carbon monoxide poisoning. Merck Manual Professional Edition. Full review April 2025. merckmanuals.com

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Sore Throat, Negative Strep Test, Getting Worse: What Is the Swab Not Telling You?

Case presentation (composite)

A man in his late thirties has a severe sore throat and fever that have worsened over the past day. His voice sounds muffled and he is drooling a little. Heart rate is 120. He looks anxious and prefers to sit leaning forward, and he will not lie flat. A rapid strep test is negative. The oropharynx looks only mildly red, and the pain seems far greater than the exam would suggest. The initial plan is viral pharyngitis, ketorolac, a topical throat preparation, and discharge to primary care.

(Composite case. No real patient is described. Other vital signs are not specified in this teaching case.)

The first guess, and why it is tempting

Sore throat is one of the most common complaints in emergency medicine, and the large majority of cases are viral or benign. A negative rapid strep test appears to lower the stakes, and a pharynx that looks only mildly inflamed supports the story. The error is letting the strep result stand in for an airway assessment. A rapid antigen test answers one question, whether group A streptococcus is likely, and says nothing about the supraglottic airway (clinical reasoning).

What does not fit

• Drooling and a muffled voice. The 2022 emergency medicine review lists drooling, muffled voice, and dyspnea among the symptoms of adult epiglottitis, and notes that adults commonly present with severe dysphagia in a subacute manner [1]. In a Spanish single-center series of 88 adults, muffled voice (41%) and respiratory distress (38%) were the commonest presenting symptoms, and hypersalivation was independently associated with airway intervention (p = 0.027) [4].
• Pain out of proportion to the pharyngeal exam. This is a recognized clinical teaching point because the inflammation is supraglottic and below what the mouth shows (clinical judgment; not a validated rule). In a Finnish series of 308 adults, sore throat and odynophagia were the commonest symptoms and inflammation usually involved more than the epiglottis alone [6].
• Posture. Refusing to lie flat and sitting forward is a classic sign of upper-airway compromise (teaching point; no study of its accuracy in adults was found in this pass).
• Course. Half of the patients in a nine-year U.S. series had symptoms for 48 hours or longer, so an indolent course does not exclude it [2].

Note what is not reliably present. In that same series of 70 adults, only 12.9% were febrile in the ED and 13.1% had stridor, and 38.6% had voice changes [2]. A normal temperature does not argue against the diagnosis.

Differential

Viral or bacterial pharyngitis, peritonsillar or retropharyngeal abscess, parapharyngeal or deep neck space infection (including Ludwig angina), epiglottic abscess, croup-like conditions, foreign body, angioedema (hereditary or drug-related), thermal or caustic injury, laryngeal trauma, and, rarely, laryngeal tumor. Viral, fungal, caustic, thermal, and autoimmune causes are also described [1].

Workup

Visualize the airway, with the right team

The 2022 review states that visualization of the epiglottis is the key to diagnosis, and that airway assessment and management are paramount, with a shift in practice from direct laryngoscopy to flexible intubating endoscopy and video laryngoscopy with the assistance of anesthesia and/or otolaryngology if available [1]. Early involvement of ENT and anesthesia, before the patient deteriorates, is the priority (judgment). Avoid anything that agitates the patient or forces a supine position, such as repeated tongue-blade examinations, until the plan and equipment are ready (teaching point).

Where imaging fits

A lateral neck radiograph may help but can be falsely negative [1]. In a Korean case-control study of 91 laryngoscopy-confirmed adults and 91 controls, the radiographic parameters had sensitivities of 33.0% to 80.2% and specificities of 64.8% to 100%; the best was an epiglottis width above 6.3 mm (sensitivity 75.8%, specificity 97.8%), and the false-negative rate of radiograph-based diagnosis was 31.9%, with prior oral antibiotic use an independent risk factor for a false-negative result [7]. A normal film therefore does not close the question. Imaging is reasonable only in a patient who is stable and attended; it should never delay the airway plan or move an unstable patient away from resuscitation resources (judgment).

Labs

Labs rarely change the immediate plan. Blood cultures, a CBC, and glucose are reasonable once the airway is addressed; diabetes was associated with airway intervention in a meta-analysis (below) [3].

Which patients need an airway intervention?

Estimates vary by cohort. A meta-analysis of 30 studies (10,148 patients) found that the rate of airway intervention fell from 18.8% before to 10.9% after Haemophilus influenzae type b vaccine introduction, and that epiglottic abscess (RR 2.45), stridor (RR 7.15), and diabetes (RR 2.15) were associated with the need for an airway intervention [3]. In a nine-year U.S. academic series of 70 adults, 17.1% had an acute airway intervention, including three emergent cricothyroidotomies and one tracheostomy; two patients died and one suffered an anoxic brain injury after difficult airway management [2]. In the Spanish series, 17% received an airway intervention (10% intubated, 7% tracheotomy) [4]. In a Danish series of 34 adults, 29% needed an artificial airway, and respiratory distress was associated with intervention [5]. In the Finnish series of 308 adults, 45 patients needed an airway intervention and mortality was 0.6% [6].

The take-away is not a number but a pattern: most patients can be managed without a surgical airway, but a minority deteriorate quickly and the consequences of a failed airway are severe. Stridor, abscess, diabetes, hypersalivation, and respiratory distress mark higher risk [3,4,5].

Management

• Airway first. Prepare for a difficult airway with the most experienced operator, a double set-up, and anesthesia/ENT presence where possible. Keep the patient upright in a position of comfort and observe continuously (clinical practice; see ref 1).
• Antibiotics. The 2022 review states that antibiotics should be administered with the airway assessment [1]. In the Finnish series, intravenous cephalosporins were the commonest empiric regimen, and streptococcus was the commonest organism in throat cultures [6]. Local resistance and allergy guide the choice.
• Corticosteroids and nebulized epinephrine. The 2022 review calls both controversial but to be considered [1]. A 2026 retrospective cohort of adult ED epiglottitis (TriNetX database, propensity-matched) found early corticosteroids associated with a lower risk of intubation (RR 0.48; 95% CI 0.26 to 0.88) and ICU admission (RR 0.71), and early antibiotics similarly (intubation RR 0.54), but this is observational and cannot establish causation [8].
• Disposition. The review recommends admission to an intensive care setting for close airway observation or ventilatory management if intubated [1].

Evidence in context

Adult epiglottitis is uncommon and has been described as a disease whose incidence in adults has remained stable or risen as childhood disease declined with vaccination. In Denmark, adult incidence was constant at a mean of 1.9 per 100,000 per year [5]; in Finland, it rose from 1.88 to 4.73 per 100,000 between decades (P = .05) [6]; in a U.S. network database, annual incidence proportion rose from 0.002% in 2014 to 0.005% in 2024 [8]. Mortality estimates in adults range widely, from 0.6% in the Finnish series [6] to a quoted range of 1% to 20% [2], reflecting differences in population, era, and airway practice. Almost all data are retrospective, single-center, or database-derived, and no randomized trial of steroids, epinephrine, or airway strategy was identified.

Clinical pearls

• A negative rapid strep test does not evaluate the airway.
• Drooling, a muffled voice, and an inability to lie flat shift the question from "which pharyngitis" to "how safe is the airway."
• A normal temperature or a normal film does not rule it out.
• Look at the epiglottis with the right team and equipment; the sicker the patient, the more this should happen in a controlled setting.
• Stridor, abscess, diabetes, and hypersalivation signal higher-risk disease.

Common pitfalls

• Discharging on a negative strep test with a worrying voice and posture.
• Relying on a lateral neck film to exclude the diagnosis.
• Sending an unstable patient to radiology without an airway plan.
• Agitating the patient with repeated oral exams or forcing him supine.
• Treating the infection but not planning the airway.

Takeaways

• Severe sore throat with a muffled voice, drooling, or an inability to lie flat is an airway problem until the epiglottis has been seen.
• Neck films miss a third of cases in one series; direct or flexible visualization by the right team is the diagnostic step.
• Antibiotics matter, but the airway plan comes first.
• Plan for ICU-level observation.

References

1. Bridwell RE, Koyfman A, Long B. High risk and low prevalence diseases: adult epiglottitis. Am J Emerg Med. 2022;57:14-20. doi:10.1016/j.ajem.2022.04.018 | PMID 35489220
2. Felton P, Lutfy-Clayton L, Smith LG, et al. A retrospective cohort study of acute epiglottitis in adults. West J Emerg Med. 2021;22(6):1326-1334. doi:10.5811/westjem.2021.8.52657 | PMID 34787558
3. Sideris A, Holmes TR, Cumming B, Havas T. A systematic review and meta-analysis of predictors of airway intervention in adult epiglottitis. Laryngoscope. 2020;130(2):465-473. doi:10.1002/lary.28076 | PMID 31173373
4. Penella A, Mesalles-Ruiz M, Portillo A, et al. Acute infectious supraglottitis in adult population: epidemiology, management, outcomes and predictors of airway intervention. Eur Arch Otorhinolaryngol. 2022;279(8):4033-4041. doi:10.1007/s00405-022-07365-z | PMID 35396955
5. Guldfred LA, Lyhne D, Becker BC. Acute epiglottitis: epidemiology, clinical presentation, management and outcome. J Laryngol Otol. 2008;122(8):818-823. doi:10.1017/S0022215107000473 | PMID 17892608
6. Bizaki AJ, Numminen J, Vasama JP, Laranne J, Rautiainen M. Acute supraglottitis in adults in Finland: review and analysis of 308 cases. Laryngoscope. 2011;121(10):2107-2113. doi:10.1002/lary.22147 | PMID 21898436
7. Lee SH, Yun SJ, Kim DH, Jo HH, Ryu S. Do we need a change in ED diagnostic strategy for adult acute epiglottitis? Am J Emerg Med. 2017;35(10):1519-1524. doi:10.1016/j.ajem.2017.04.039 | PMID 28460811
8. O'Brien J, Muccio DR, Schrock JW. Association of early steroid and antibiotic therapy with airway outcomes in adult epiglottitis: a 10-year multicenter retrospective cohort study. Acad Emerg Med. 2026;33(4):e70285. doi:10.1111/acem.70285 | PMID 42023439

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Severe Headache, Nausea, and Halos Around Lights: Is It Really Migraine?

Case presentation (composite)

A 58-year-old woman has a severe left-sided headache with nausea, and she has vomited twice. Heart rate is 92 and blood pressure is 148/90. The neurologic exam is normal. The initial plan is migraine: a dark, quiet room, ketorolac, an antiemetic, and discharge with neurology follow-up.

On a closer history, she sees rainbow-colored rings around lights, and vision in the left eye is hazy. The left pupil sits half-open and barely reacts. The episode began in a dim theater, after she took an over-the-counter cold medicine.

(Composite case. No real patient is described. Visual acuity, eye redness, and other findings are not specified in this teaching case.)

The first guess, and why it is tempting

Severe unilateral headache with nausea and vomiting in a middle-aged woman fits migraine, and a normal neurologic examination reinforces that. Migraine is common, and the eye is easy to leave out of a headache workup. The mistake is stopping when the neurologic exam is normal. Eye pain, headache, nausea, and vomiting are the characteristic symptoms of acute angle-closure crisis (AACC), as described in the American Academy of Ophthalmology (AAO) Preferred Practice Pattern (PPP) [1]. A published case of angle-closure crisis illustrates the pattern: a patient was initially labeled with sinusitis-related headache, and the authors concluded that periocular pain always deserves visual acuity assessment and intraocular pressure (IOP) measurement [4].

What does not fit

• Halos and blurred vision. The PPP lists blurred vision with halos among the characteristic symptoms of AACC, with corneal edema as the underlying cause [1]. Halos are not part of a typical migraine description (clinical judgment; migraine aura is a different phenomenon).
• A mid-dilated, sluggish pupil. The PPP lists a mid-dilated pupil among the clinical signs, along with markedly elevated IOP, corneal edema, and conjunctival and episcleral congestion [1]. A UpToDate summary describes a mid-dilated pupil of 4 to 6 mm that reacts poorly to light or is fixed [6].
• The dim theater. The UpToDate emergency overview states that episodes are often triggered by sudden pupillary dilation from darkness, such as when the lights go down in a theater, and by sympathetic arousal or medications [6].
• The cold medicine. The PPP warns that medicines with anticholinergic properties, including over-the-counter decongestants, cold and flu medications, allergy medications, and sleeping aids, could cause pupil dilation and induce AACC in people at risk [1]. A published case report and review describes bilateral AACC triggered by a single dose of pseudoephedrine and states that even a single dose of an implicated medication may trigger an attack [3].
• Risk profile. The PPP lists older age, female sex, family history, Asian or Inuit descent, hyperopia, and a shallow anterior chamber as risk factors [1].

Why it happens

Pupillary block is a key element in most cases. In a predisposed eye, the pressure gradient between the posterior and anterior chambers is high because aqueous flow at the pupil is impaired. The iris bows forward and crowds the angle, which can be worsened by pupil dilation and an aging lens. In a minority of cases, this happens acutely, producing AACC [1]. Said simply, the fluid in the eye cannot drain, and the pressure rises. The PPP states that, untreated, the condition may rapidly cause permanent vision loss, and that the fellow eye is also at high risk [1]. About 90% of AACC episodes are unilateral [1].

Differential

Migraine and other primary headaches (cluster headache, which commonly involves the eye and can mimic this picture; clinical reasoning), other painful red-eye conditions such as uveitis, keratitis, or scleritis, optic neuritis or ischemic optic neuropathy including giant cell arteritis, subarachnoid hemorrhage or an expanding aneurysm, and sinusitis. A neurovascular cause should not be dismissed when imaging has not been done, but none of these explains halos with a mid-dilated pupil (clinical reasoning).

Workup

The check that changes it

Measure the intraocular pressure and get emergency ophthalmology involved. The UpToDate rapid overview lists a typical IOP of 40 to 70 mmHg in a severe attack, against a normal of about 8 to 21 mmHg, and advises obtaining emergency ophthalmology consultation [6]. The PPP describes assessment by applanation tonometry and gonioscopy [1]. Gonioscopy and definitive diagnosis are the ophthalmologist’s domain. In the ED, the practical checks are visual acuity, pupil size and reactivity, a look for redness and a cloudy cornea, and tonometry if available (clinical practice).

Examine both eyes

The UpToDate overview notes that usually one eye is affected at a time, but both eyes must be carefully examined [6].

Other testing

Neuroimaging or other testing is guided by the whole picture. If halos, a fixed mid-dilated pupil, and elevated pressure are present, the diagnosis is made at the eye, not the scanner (clinical judgment).

Management

The treatments below are described for education. Selection, dosing, and timing are decisions for the treating clinician, in consultation with ophthalmology.

• Medical lowering of pressure first. The PPP states that in AACC, medical therapy is usually initiated first to lower the IOP to reduce pain and clear corneal edema, and that laser peripheral iridotomy (LPI) should then be performed as soon as safely feasible [1]. Agents described include aqueous suppressants (beta-adrenergic antagonists, carbonic anhydrase inhibitors), parasympathomimetics, and, when needed, systemic hyperosmotic agents such as mannitol [1]. The UpToDate overview lists a staged sequence of topical timolol, apraclonidine, and pilocarpine followed by acetazolamide (intravenous, or by mouth if intravenous is not available) when an ophthalmologist is not available within an hour and vision has declined significantly, with attention to contraindications such as a beta blocker in severe bronchospasm, high-grade AV block, or uncompensated heart failure [6].
• Why the drops can underperform at first. The PPP notes that aqueous suppressants may be ineffective initially if the ciliary body is ischemic at severely elevated pressure, and that pressure-induced ischemia of the pupillary sphincter can make the pupil unresponsive to miotics [1]. That is one reason ophthalmology involvement is urgent.
• Symptom relief. The UpToDate overview recommends analgesics and antiemetics for associated symptoms [6].
• Definitive treatment. LPI is the preferred surgical treatment because it has a favorable risk-benefit ratio. It relieves pupillary block and can prevent or slow the formation of peripheral anterior synechiae [1]. If LPI is not possible or the attack cannot be broken medically, laser peripheral iridoplasty, paracentesis, and incisional iridectomy remain alternatives [1].
• Lens extraction. A 2023 Cochrane review of two small randomized trials (99 eyes, high risk of bias) found low-certainty evidence that phacoemulsification may give better IOP control than LPI at 18 to 24 months (RR 1.66; 95% CI 1.28 to 2.15) [2]. The PPP also describes early lens extraction as a discretionary recommendation after the attack is medically broken [1].
• The other eye. The PPP advises evaluating the fellow eye, since approximately half of fellow eyes of acute angle-closure patients can develop an attack within 5 years, and prompt prophylactic LPI if the angle is anatomically narrow [1].
• Medication review. Medicines with pupil-dilating or anticholinergic properties are a recognized trigger, and the PPP advises counseling patients at risk about this [1].

Evidence in context

Primary angle-closure disease is a major cause of blindness. The PPP estimates that 0.7% of people over 40 worldwide have angle-closure glaucoma, with most cases in Asia, and that Inuit, Chinese, and other Asian populations have the highest rates [1]. Most of the treatment guidance rests on observational data, small trials, and expert consensus. Pharmacologic dilation of narrow angles carries a low absolute risk: in a Singapore study of 471 Asian subjects aged over 50 with narrow angles, 3 (0.64%) developed acute angle closure within 6 hours after tropicamide dilation, despite oral acetazolamide pretreatment [5]. That study supports the PPP’s statement that dilation can rarely precipitate AACC [1,5], and it should not be extrapolated to people with unrecognized disease who take systemic medications.

Clinical pearls

• Headache plus nausea plus halos or blurred vision is an eye problem until pressure has been measured.
• A mid-dilated pupil that reacts poorly is a sign, not a variant.
• Dim light and cold-and-flu medicines are classic triggers.
• A normal neurologic examination does not address the eye.
• Treat the pressure, call ophthalmology early, and think about the fellow eye.

Common pitfalls

• Treating a one-sided headache as migraine without looking at the eye.
• Dilating the pupil of a patient with a suspected attack to “see better”.
• Waiting on neuroimaging when the pupil and corneal findings already explain the picture.
• Discharging without tonometry or ophthalmology input.
• Forgetting the fellow eye and the triggering medication.

Takeaways

• Severe headache with nausea, halos, blurred vision, and a half-open, sluggish pupil suggests acute angle closure.
• Measure the eye pressure and call ophthalmology without delay.
• Medical lowering of pressure comes first; laser iridotomy is the preferred definitive treatment.
• Cold-and-flu medicines and dim light can precipitate attacks in susceptible eyes.

References

1. Gedde SJ, Chopra V, Vinod K, et al.; American Academy of Ophthalmology Preferred Practice Pattern Glaucoma Committee. Primary angle-closure disease Preferred Practice Pattern. Ophthalmology. 2026;133(4):P153-P201. doi:10.1016/j.ophtha.2025.12.030 | PMID 41665581
2. Ong AY, McCann P, Perera SA, et al. Lens extraction versus laser peripheral iridotomy for acute primary angle closure. Cochrane Database Syst Rev. 2023;3:CD015116. doi:10.1002/14651858.CD015116.pub2 | PMID 36884304
3. Spencer BG, Baskin J, Giarola BF, Craig JE. Single dose of pseudoephedrine induces simultaneous bilateral acute angle closure crisis. Case Rep Ophthalmol. 2019;10(3):365-368. doi:10.1159/000503854 | PMID 31762769
4. Lee NS, Woo TL, Agar A, Francis IC. Acute angle closure glaucoma misdiagnosed as sinusitis. Pract Neurol. 2023;23(6):527-529. doi:10.1136/pn-2023-003864 | PMID 37679039
5. Lavanya R, Baskaran M, Kumar RS, et al. Risk of acute angle closure and changes in intraocular pressure after pupillary dilation in Asian subjects with narrow angles. Ophthalmology. 2012;119(3):474-480. doi:10.1016/j.ophtha.2011.08.033 | PMID 22118999
6. UpToDate. Severe acute angle-closure glaucoma: rapid overview of emergency management (Graphic 74621, version 9.0). Accessed 2026. uptodate.com

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Two Days of Vomiting and Fast, Deep Breathing in a Young Woman: Is It Really Gastroenteritis?

Case presentation (composite)

A 22-year-old woman has had two days of nausea, vomiting, and abdominal pain. She has no fever and her lungs are clear. Heart rate is 112. The working diagnosis is viral gastroenteritis: ondansetron, clear liquids, and rest at home.

On a closer look, she is breathing fast and deep at 28 breaths a minute, without a cough, and her breath has a fruity smell. For several weeks she has had constant thirst and weight loss.

(Composite case. No real patient is described. Blood pressure, mental status, and laboratory values are not specified in this teaching case.)

The first guess, and why it is tempting

Vomiting and abdominal pain in a young adult are most often a self-limited gastrointestinal illness, and an afebrile, otherwise well-appearing patient does not prompt a broader workup. The consensus report of the American Diabetes Association and partner societies notes that nausea, vomiting, and abdominal pain are common in DKA (more than 50%) [1]. The report also cautions that abdominal pain in DKA may be a result of the DKA or an indication of a precipitating cause, and that further evaluation is needed if it does not resolve with the resolution of dehydration and acidosis [1]. The error is anchoring on the gastrointestinal complaint and not asking what else explains the vomiting.

What does not fit

• Fast, deep breathing without a respiratory cause. The respiratory compensation for metabolic acidosis in DKA is manifest by Kussmaul breathing, which consists of deep breaths with a fruity odor from acetone [1]. A respiratory rate of 28 with clear lungs and no cough points to a metabolic explanation (clinical reasoning).
• Weeks of thirst and weight loss. Both DKA and the hyperglycemic hyperosmolar state may present with polyuria, polydipsia, weight loss, vomiting, and dehydration [1]. A history of weeks of symptoms before two days of vomiting suggests a diabetes prodrome (clinical reasoning).
• No fever. The report identifies infection as the most common precipitant of DKA worldwide, in 14% to 58% of cases [1], but a first presentation of diabetes may occur without an identifiable trigger, and a normal temperature does not make DKA less likely (clinical reasoning).
• Tachycardia. The report notes that tachycardia and hypotension correlate with severe hypovolemia, although some patients maintain hemodynamic stability because of the hypertonicity of hyperglycemia [1].

How common is it as a first presentation?

The consensus report states that between 6% and 21% of adults present with DKA as their initial diagnosis of type 1 diabetes [1]. It also notes that over half of Black and Hispanic adults with newly diagnosed diabetes presenting with unprovoked DKA have type 2 diabetes ("ketosis-prone" or "atypical" diabetes), who often can later reduce or stop insulin after stabilization [1]. A review of ketosis-prone diabetes describes the syndrome as diabetes commencing with ketoacidosis in individuals who are antibody-negative and have no known precipitating cause [4]. Age and sex do not exclude DKA. In a U.S. analysis cited by the report, most DKA events occur in young adults aged 18 to 44 years with type 1 diabetes [1].

Differential

Gastroenteritis, pregnancy-related nausea and vomiting (pregnancy testing is reasonable in any person who can become pregnant; clinical practice), cyclic vomiting or cannabinoid hyperemesis, pancreatitis, appendicitis or other surgical abdomen, urinary tract infection, and other causes of high anion gap metabolic acidosis such as toxic ingestion, lactic acidosis, and alcoholic or starvation ketosis (clinical reasoning). The consensus report specifically lists starvation ketosis, alcoholic ketoacidosis, and the ketosis of pregnancy and hyperemesis in the differential of elevated ketones [1].

Workup

The first quick tests

A fingerstick glucose is the fastest first check (clinical practice). The consensus report advises that when DKA is suspected, initial samples should be taken for glucose, electrolytes, venous blood gas, complete blood count, and blood or urine ketones, and that an ECG should be performed to look for hyperkalemic or ischemic changes [1].

Diagnostic criteria

The consensus report defines DKA by three criteria that must all be present: hyperglycemia (glucose of 200 mg/dL or higher, or a prior history of diabetes irrespective of the glucose), elevated ketones, and metabolic acidosis [1]. Blood β-hydroxybutyrate of 3.0 mmol/L or higher correlates with acid-base changes with greater than 90% sensitivity and specificity for DKA [1]. The Joint British Diabetes Societies (JBDS) guideline uses a similar framework with different thresholds: glucose above 11.0 mmol/L or known diabetes, capillary or blood ketones above 3.0 mmol/L or significant ketonuria (2+ or more), and bicarbonate below 15.0 mmol/L and/or venous pH below 7.3 [2]. The two documents differ on the acidosis cutoff (ADA bicarbonate under 18 mmol/L vs JBDS under 15), so local protocol matters (clinical practice).

Prefer blood ketones

The consensus report recommends direct measurement of venous or capillary β-hydroxybutyrate for diagnosis and monitoring, because the nitroprusside reaction in urine measures acetoacetate, not β-hydroxybutyrate, and can underestimate the severity of ketonemia early in the course [1]. A systematic review of nine observational studies reported that capillary β-hydroxybutyrate has high sensitivity, specificity, and predictive values for identifying DKA compared with urinary ketone testing [3]. JBDS likewise states that blood ketones, not urine ketones, should be measured [2].

Anion gap and mixed disorders

Most patients with DKA have a high anion gap metabolic acidosis. About one-third have mixed acid-base disorders, because vomiting can add a metabolic alkalosis and hyperventilation a respiratory alkalosis [1]. The report does not recommend the anion gap as a first-line diagnostic or resolution criterion [1].

Management

The treatments below are described for education, drawn from published consensus guidance. Doses, fluids, and sequencing are decisions for the treating team under local protocols.

• Setting and severity. The report classifies DKA as mild, moderate, or severe by pH, bicarbonate, β-hydroxybutyrate, and mental status. Severe DKA, an altered mental status, or critical illness as a precipitating cause should be treated in the ICU, while uncomplicated mild or moderate DKA can be treated in the ED or a step-down unit with close monitoring [1].
• Fluids first. The mainstays of treatment are fluid replacement, insulin therapy, electrolyte repletion, and treatment of the underlying precipitating event [1]. For adults without renal or cardiac compromise, the report recommends isotonic saline or a balanced crystalloid at an initial rate of 500 to 1,000 mL per hour during the first 2 to 4 hours, with caution in those at risk of fluid overload [1]. It notes that balanced crystalloids have been associated with faster DKA resolution and less hyperchloremic acidosis than saline in several studies, but that most guidelines still recommend isotonic saline as the default [1].
• Check potassium before insulin. Most patients with DKA present with normal or high serum potassium despite total-body depletion, because acidosis and insulin deficiency shift potassium out of cells [1]. The report states that if potassium is below 3.5 mmol/L on admission (5% to 10% of patients), potassium replacement should begin and insulin should be delayed until the level is above 3.5 mmol/L, to avoid life-threatening arrhythmias and respiratory muscle weakness. It recommends starting potassium replacement once the level is below 5.0 mmol/L [1]. JBDS advises adding potassium to fluids unless the level is above 5.5 mmol/L, and reviewing the regimen if potassium falls below 3.5 mmol/L [2].
• Insulin. Short-acting insulin by continuous intravenous infusion is the preferred choice, started as soon as possible after diagnosis (with the potassium caveat above); the report describes a fixed-rate infusion of 0.1 units/kg/h [1]. JBDS describes the same fixed-rate approach [2]. Mild or moderate uncomplicated DKA may be treated with subcutaneous rapid-acting analogs in selected settings [1]. The report’s physiology section notes that fluid resuscitation alone can lower plasma glucose by roughly 50 to 70 mg/dL per hour and improves insulin sensitivity, which is part of the rationale for fluids first [1].
• Dextrose. Once glucose is below 250 mg/dL, the report advises adding 5% to 10% dextrose to fluids and reducing the insulin infusion rate to continue treating ketosis while avoiding hypoglycemia [1].
• Bicarbonate. Routine bicarbonate is not recommended, though it may be considered if pH is below 7.0 [1].
• Monitoring and resolution. Capillary glucose is checked every 1 to 2 hours, and electrolytes, β-hydroxybutyrate, and venous pH about every 4 hours until resolution [1]. DKA is considered resolved when ketones are below 0.6 mmol/L and venous pH is 7.3 or higher or bicarbonate 18 mmol/L or higher [1]. JBDS uses ketones below 0.6 mmol/L and venous pH above 7.3 [2].
• Find the trigger and plan the transition. The report advises identification and treatment of the precipitating cause, a transition to subcutaneous basal-bolus insulin with an overlap of 1 to 2 hours, and education before discharge [1]. For a first presentation, diabetes type and autoimmunity are addressed by the diabetes team (clinical judgment).
• Complications to watch for. Hypoglycemia and hypokalemia during treatment are common; cerebral edema is rare in adults [1].

Evidence in context

Recommendations for DKA are largely based on consensus and opinion rather than rigorous outcomes research, as the consensus report itself acknowledges [1]. Reported inpatient mortality for DKA admissions ranges from 0.20% in type 1 diabetes to 1.04% in type 2 diabetes in recent U.S. estimates, and appropriate treatment has reduced mortality to under 1% [1]. The report also describes a 55% increase in DKA hospitalization rates in the recent past, especially in adults under 45 [1]. Mortality is much higher in low- and middle-income countries, which the report attributes potentially to delayed diagnosis and treatment [1].

Clinical pearls

• Vomiting with fast, deep breathing and a clear chest: think metabolic acidosis.
• Check glucose and ketones before calling it a stomach bug.
• Weeks of thirst, urination, and weight loss are the prodrome.
• Measure blood β-hydroxybutyrate when you can; urine ketones can mislead.
• Potassium is checked before insulin starts.

Common pitfalls

• Anchoring on gastroenteritis in an afebrile patient.
• Discharging after antiemetics without a glucose check.
• Starting insulin before knowing the potassium.
• Relying on urine ketones to judge severity or resolution.
• Treating the acidosis but not looking for the trigger or arranging diabetes education.

Takeaways

• DKA can be the first sign of diabetes, in 6% to 21% of adults with type 1 diabetes in the studies cited by the consensus report.
• Fast, deep breathing with vomiting and no fever warrants glucose, ketones, and a blood gas.
• Fluids come first; insulin follows once potassium is known to be safe.
• Look for the trigger and arrange diabetes care before discharge.

References

1. Umpierrez GE, Davis GM, ElSayed NA, et al. Hyperglycemic crises in adults with diabetes: a consensus report. Diabetes Care. 2024;47(8):1257-1275. doi:10.2337/dci24-0032 | PMID 39052901
2. Dhatariya KK; Joint British Diabetes Societies for Inpatient Care. The management of diabetic ketoacidosis in adults: an updated guideline from the Joint British Diabetes Society for Inpatient Care. Diabet Med. 2022;39(6):e14788. doi:10.1111/dme.14788 | PMID 35224769
3. Brooke J, Stiell M, Ojo O. Evaluation of the accuracy of capillary hydroxybutyrate measurement compared with other measurements in the diagnosis of diabetic ketoacidosis: a systematic review. Int J Environ Res Public Health. 2016;13(9):837. doi:10.3390/ijerph13090837 | PMID 27563914
4. Lebovitz HE, Banerji MA. Ketosis-prone diabetes (Flatbush diabetes): an emerging worldwide clinically important entity. Curr Diab Rep. 2018;18(11):120. doi:10.1007/s11892-018-1075-4 | PMID 30280274

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Restless, Sweaty, Shaky, and Febrile on a New Medication: Is It Really a Panic Attack?

Case presentation (composite)

A 34-year-old man presents with restlessness, sweating, and shakiness that began this morning. Heart rate is 122, temperature is 101 °F (38.3 °C), and blood pressure is 142/88. The working diagnosis is a panic attack: lorazepam, reassurance, breathing exercises, and discharge.

On examination, his ankle twitches on its own in a steady rhythm. His reflexes are brisk and his pupils are wide. A second prescription was added to his daily medication last night.

(Composite case. No real patient is described. The specific drugs, respiratory rate, mental status, tone, and laboratory values are not specified in this teaching case.)

The first guess, and why it is tempting

Restlessness, sweating, tremor, and tachycardia are the textbook description of acute anxiety, and a patient who is on a daily medication for a mood or pain condition has a plausible psychiatric story. Two features of serotonin toxicity make it easy to miss. First, the mental-status and autonomic findings are nonspecific: Isbister and colleagues note they are indistinguishable from those seen with other causes of an agitated delirium [3]. Second, the nonspecific side effects of a newly started serotonergic drug can look like anxiety on their own. Foong and colleagues note that it is normal for nontoxic increases in serotonin to cause anxiety, restlessness, and irritability for 1 to 2 weeks after starting a drug or increasing a dose [4]. The error is labeling the picture as psychiatric without a neuromuscular examination and a medication timeline.

What does not fit

• Fever. A temperature of 38.3 °C is unusual for panic. It is also below the severe range in a primary care review, which defines severe symptoms as a temperature above 38.5 °C (101.3 °F), confusion, delirium, sustained clonus or rigidity, and rhabdomyolysis [4]. A mild fever here argues for looking further, not for reassurance.
• Spontaneous clonus. The Hunter criteria list spontaneous clonus as sufficient on its own in a patient exposed to a serotonergic agent [1][2]. Chiew and Isbister describe neuromuscular excitation, especially clonus (spontaneous, inducible, and ocular), as far more indicative of serotonin toxicity than the autonomic and mental state changes [2]. An anxiety state does not produce it.
• The ankle. Isbister and colleagues report that sustained clonus is usually found at the ankle, and that the lower limbs usually have a much greater degree of hyperreflexia and clonus than the upper limbs [3]. Foong and colleagues make the same point about the legs [4].
• Brisk reflexes and wide pupils. Hyperreflexia and mydriasis (dilated pupils) are both listed among the signs of serotonin toxicity [4]; pupil size and reaction are part of the focused examination [3].
• The timeline. Chiew and Isbister report that symptoms typically start shortly after the intake of a serotonergic agent, becoming apparent within an hour in about 30% of patients and within 6 hours in 60% [2]. A second prescription added last night and symptoms the next morning is a plausible sequence.

Differential

The primary care review and the Australian practical approach both list the main alternatives [3][4]:

• Anticholinergic toxicity. Dilated pupils, fever, agitation, and delirium overlap, but muscle tone and reflexes are normal, and skin is dry rather than sweaty [4].
• Neuroleptic malignant syndrome. Idiosyncratic rather than dose-related, with onset over days, and distinguished by bradykinesia and lead-pipe or cogwheel rigidity rather than hyperkinesia, hyperreflexia, and clonus [3][4].
• Malignant hyperthermia. Triggered by specific volatile anesthetics during or shortly after surgery [4].
• Antidepressant discontinuation. Symptoms start within days of stopping or tapering a drug and are usually self-limited [4].
• Withdrawal states, infection, and other causes of agitated delirium. Alcohol or benzodiazepine withdrawal, meningitis or encephalitis, and drug overdose are listed as similar-looking conditions [4]. Non-convulsive seizures and acute baclofen withdrawal are also described [3].
• Sympathomimetic toxicity and thyrotoxicosis. These produce tachycardia, sweating, and agitation. Clonus and hyperreflexia are the discriminating features (clinical reasoning; neither condition is covered in the sources opened).

Workup

There is no confirmatory test. Chiew and Isbister state that the diagnosis of serotonin toxicity is clinical and that there are no useful laboratory or neurophysiological tests to confirm excess synaptic serotonin [2].

• Focused neurological examination. Isbister and colleagues consider this the most important step: mental state; upper- and lower-limb tone, clonus, and reflexes; and pupillary size, reaction, and extraocular movements [3]. Vital signs are usually enough to document the autonomic features [3].
• Medication history. Include over-the-counter products, herbals, and recreational drugs. Foong and colleagues list the main serotonergic classes: monoamine oxidase inhibitors (MAOIs), serotonin reuptake inhibitors (SSRIs, SNRIs, tramadol, some other opioids, dextromethorphan, some antihistamines, St John’s wort), and serotonin releasers (amphetamine, MDMA) [4]. The CMAJ summary adds often-overlooked agents such as lithium, methadone, fentanyl, and methylene blue [5]. Several drugs on regulatory interaction lists are unlikely to cause toxicity (for example ondansetron and triptans), so a drug appearing on a checker is not enough [2][4].
• Hunter criteria. In the presence of a serotonergic agent, any one of the following is sufficient: spontaneous clonus; inducible clonus with agitation or diaphoresis; ocular clonus with agitation or diaphoresis; tremor with hyperreflexia; or hypertonia with temperature above 38 °C and ocular or inducible clonus [1][2]. The criteria were derived from 473 single-SSRI overdoses and tested in 2222 serotonergic overdose admissions, where they were more sensitive (84% vs 75%) and more specific (97% vs 96%) than Sternbach’s criteria [1]. Among these criteria, temperature above 38 °C enters only the hypertonia criterion; this case meets the spontaneous clonus criterion regardless of temperature.
• Caveat on validation. Chiew and Isbister point out that the Hunter criteria were validated in the overdose setting and have been extrapolated to patients on stable therapeutic doses, which can over-diagnose toxicity [2]. A new drug added to an existing one is a drug-interaction scenario, the moderate-to-high-risk setting in which the criteria are better used [2].
• Other testing. Glucose, electrolytes, creatine kinase, renal function, and a urine drug screen when the history is unclear are reasonable (clinical judgment; the opened sources do not prescribe a test panel). A creatine kinase and renal function check matters if rigidity or rising temperature appears, because rhabdomyolysis, renal failure, and disseminated intravascular coagulation are the complications of severe toxicity [2][3].

Management

The following describes approaches reported in the cited literature for education. It is not a treatment protocol, and doses are not provided. Management in a real patient is decided by the treating team, often with a poison centre or medical toxicologist.

Grade severity first. Isbister and colleagues describe three groups: mild (features that may or may not trouble the patient), moderate (significant distress, deserving treatment but not life-threatening), and severe (a rapidly rising temperature with muscle rigidity, a medical emergency that can progress to multiorgan failure if not treated within hours) [3]. Chiew and Isbister add that the focus should be on identifying those developing worsening toxicity, characterized by a rapidly rising temperature above 39 °C and muscle rigidity [2].

All grades: stop the serotonergic agents. The CMAJ summary advises discontinuing all serotonergic medications, and notes that in mild cases discontinuation of the causative agent may be sufficient [5]. Chiew and Isbister report that toxicity often resolves within 24 hours of stopping the agent and starting supportive care, but that drugs with long half-lives or active metabolites can cause persistent symptoms [2].

Mild to moderate: supportive care and benzodiazepines. Benzodiazepines are described as commonly used for their anxiolytic and sedating properties and are useful for symptomatic treatment of mild to moderate toxicity, where anxiety and agitation are the main features [2]. The CMAJ summary describes benzodiazepines and intravenous fluids as the mainstay [5]. The patient in this case would likely have received a benzodiazepine under the panic label. What was missed was not the drug but the diagnosis and the offending medication. Isbister and colleagues suggest observing moderate toxicity for about 6 hours, longer with slow-release formulations [3] (the observation period is taken from that source; local practice varies).

Moderate to severe: serotonin antagonists as an adjunct, with limited evidence. The CMAJ summary says cyproheptadine may be used as an adjunct to benzodiazepines in moderate cases, that evidence is limited, and advises consulting a regional poison centre or medical toxicologist [5]. The evidence base:

• Chiew and Isbister state that definitive evidence of effectiveness is lacking, with data limited to case reports and series, and that there is no clear association between cyproheptadine and improved outcomes or shorter symptom duration [2]. It is available only orally [2].
• In a California Poison Control System review of 288 probable cases, 68 received cyproheptadine; there were no significant differences in serious outcomes or hospitalization, and the authors concluded its benefits and indications are uncertain [6].
• Isbister and colleagues note that case-report "responses" are hard to separate from natural resolution, and that no controlled trials demonstrate effectiveness [3].
• Chiew and Isbister go further: confirming the diagnosis and giving serotonin antagonists are not lifesaving, and the cornerstone of treating severe cases is early resuscitative and supportive care [2].

Severe: hyperthermia and rigidity. The management of toxin-induced hyperthermia is described as sedation with intravenous benzodiazepines, active cooling (fans with water sprays, ice packs, cooling blankets, or ice-water submersion), and in severe cases paralysis and ventilation [2]. Chiew and Isbister state that paralysis and intubation are essential when the temperature is above 39 °C with agitation, altered consciousness, rigidity, or no response to initial cooling [2]. The CMAJ summary says that if the temperature cannot quickly be reduced below 39 °C, paralysis and intubation may be necessary [5]. The same source stresses that hyperthermia in serotonin toxicity is a medical emergency [5]. The script’s "rising fever and stiffness mean intensive care" is consistent with these sources.

Evidence in context

The evidence is mostly observational. The Hunter criteria derive from a single toxicology service’s overdose data [1]. The ToxIC registry review cited by Chiew and Isbister included 1010 patients: most received benzodiazepines (67%), 15% received cyproheptadine, and hyperthermia above 40 °C was documented in only 3% [2]. Chiew and Isbister note that mild toxicity, or simply side effects, can occur on starting any serotonergic agent but is highly unlikely to cause severe toxicity [2]. The true incidence is unknown, and severe, life-threatening toxicity occurs almost exclusively with an MAOI plus another serotonergic agent [2]. About 15% of single-SSRI overdoses develop toxicity, mild to moderate, with no severe cases in the cited studies [2][3]. This matters for counselling: most patients with a new serotonergic combination will not become critically ill, but the same examination that finds clonus is the one that identifies the rare patient who will. Animal data suggest 5-HT2A antagonism can prevent hyperthermia only at high doses, and its clinical meaning remains uncertain [2].

Clinical pearls

• Examine the ankles. Sustained clonus is usually found at the ankle, and the legs are affected more than the arms [3].
• Spontaneous clonus in a patient on a serotonergic agent meets the Hunter criteria by itself [1][2].
• Ask what changed in the last day or two: a new drug, a higher dose, a supplement, or a recreational drug [2][4].
• Tone and reflexes are normal in anticholinergic toxicity; they are increased in serotonin toxicity [4].
• Temperature and rigidity decide severity. Watch the trend, not a single reading [2][3].

Common pitfalls

• Closing on "panic" without examining tone, reflexes, and clonus.
• Treating the agitation with sedation while the serotonergic agent continues.
• Assuming a drug on an interaction checker explains the picture, or that a drug absent from the list cannot (for example, regulatory lists include agents unlikely to cause toxicity) [4].
• Reaching for an antagonist as an "antidote" before airway, cooling, and sedation are addressed [2].
• Applying the Hunter criteria to a patient on a stable dose with a competing explanation, which can over-diagnose toxicity [2].
• Missing rigidity because clonus and hyperreflexia may not be elicitable in extreme muscle rigidity [2].

Takeaways

• Fever, sweating, agitation, and tachycardia on a new or added medication call for a clonus and reflex examination.
• Spontaneous clonus plus a serotonergic agent establishes the diagnosis in the Hunter criteria.
• Stopping the serotonergic agent and supportive care with benzodiazepines are the foundation. Cyproheptadine has limited evidence.
• Rising temperature (above about 39 °C) with rigidity is an emergency that needs active cooling and early airway control.
• Ask the patient to tell every prescriber and pharmacist about every medicine, and not to change doses on their own.

References

1. Dunkley EJ, Isbister GK, Sibbritt D, Dawson AH, Whyte IM. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM. 2003;96(9):635-642. doi:10.1093/qjmed/hcg109 | PMID 12925718
2. Chiew AL, Isbister GK. Management of serotonin syndrome (toxicity). Br J Clin Pharmacol. 2025;91(3):654-661. doi:10.1111/bcp.16152 | PMID 38926083
3. Isbister GK, Buckley NA, Whyte IM. Serotonin toxicity: a practical approach to diagnosis and treatment. Med J Aust. 2007;187(6):361-365. doi:10.5694/j.1326-5377.2007.tb01282.x | PMID 17874986
4. Foong AL, Grindrod KA, Patel T, Kellar J. Demystifying serotonin syndrome (or serotonin toxicity). Can Fam Physician. 2018;64(10):720-727. PMID 30315014 (PMC6184959; no DOI in PubMed)
5. Beamish IV, Austin E, Kent JT. Managing serotonin toxicity. CMAJ. 2026;198(29):E1158. doi:10.1503/cmaj.260159 | PMID 42637246
6. Nguyen H, Pan A, Smollin C, Cantrell LF, Kearney T. An 11-year retrospective review of cyproheptadine use in serotonin syndrome cases reported to the California Poison Control System. J Clin Pharm Ther. 2019;44(2):327-334. doi:10.1111/jcpt.12796 | PMID 30650197

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Sudden Lower Abdominal Pain Waking a 19-Year-Old at 3 a.m.: Is the Examination Actually Complete?

Case presentation (composite)

A 19-year-old man woke at about 3 a.m. with sudden lower abdominal pain. He has been nauseated and has vomited twice. He has no diarrhea and no fever. Heart rate is 110 and the abdomen is soft. He is pale, curled up, and quiet.

The working diagnosis is gastroenteritis or early appendicitis: an antiemetic, laboratory tests, and observation with a recheck. The examination stopped at the abdomen.

(Composite case. No real patient is described. Blood pressure, laboratory values, and any genital findings are not specified in this teaching case.)

The first guess, and why it is tempting

Sudden abdominal pain with vomiting in a young man is common, and most such patients have a gastrointestinal cause. Lower abdominal pain with a soft abdomen and normal temperature fits a self-limited illness or early appendicitis, and observation is a reasonable strategy for both. The error is not the differential. It is closing the examination before the genitals have been looked at, in a patient who is also in the age group where torsion is most common.

The Irish Association for Emergency Medicine (IAEM) guideline lists nausea and vomiting among the classic features of torsion, and states that up to 20% of patients with torsion can present with isolated lower abdominal pain, which is more common in paediatric cases [2]. The European Association of Urology (EAU) paediatric guideline describes sudden severe pain with a vagal reaction (nausea, vomiting) as typical [1]. Embarrassment can work in both directions. The national audit of torsion in England found that adolescent delays in seeking care may reflect a "watch and wait" approach, a lack of public awareness, and an unwillingness to trouble services for fear of embarrassment or raising a false alarm [4]. A busy clinician can share the same hesitation.

What does not fit

• Sudden onset that wakes the patient. The EAU describes sudden onset of severe pain as typical [1]. Onset from sleep is a common teaching feature of torsion, but none of the opened sources states it as a criterion (clinical reasoning). One case vignette in the national audit describes a patient who woke from sleep in pain [4].
• Vomiting without diarrhea. Nausea and vomiting are part of the TWIST score [6][7]. The absence of diarrhea removes a common clue toward gastroenteritis (clinical reasoning).
• No fever. Fever occurs more often in epididymitis (11% to 19%) in the EAU chapter [1]. A normal temperature is a mild pointer rather than an exclusion; fever and urinary symptoms can occur in torsion as nonspecific features [5].
• Pale, curled up, and quiet. Severe pain is the dominant feature of torsion [1][2]. A patient who looks in more pain than a soft abdomen explains is a prompt to broaden the examination (clinical reasoning).
• A missing examination. Guidance in the United Kingdom states that children with abdominal pain should always have a testicular examination [3]. Applying that principle to an adult is an extension of the paediatric guidance (clinical reasoning).

Differential

• Epididymo-orchitis. More often has a tender epididymis, a longer duration of symptoms (31% presenting within 12 hours vs 69% for torsion), and fever more often [1].
• Torsion of the appendix testis. Isolated tenderness at the upper pole, sometimes a "blue dot" (found in only 10% to 23%) [1][5]. It is managed conservatively [1].
• Appendicitis, gastroenteritis, and other abdominal causes. Incarcerated hernia and appendicitis are listed by the EAU and the IAEM as mimics of acute scrotal pain, and the reverse is also true [1][2].
• Other scrotal causes. Hydrocele, trauma, mumps orchitis, and idiopathic scrotal oedema are listed in the same sources [1][2].
• Renal colic and testicular tumor. Referred pain from the renal tract and mass lesions can mimic or accompany acute scrotal pain (clinical reasoning). The IAEM guideline includes creatinine in its laboratory panel for renal outflow obstruction as a source of referred pain [2].

Workup

Examination. Torsion is a clinical diagnosis [5]. The classic findings are a tender testicle, a high-riding testis with a horizontal lie, and an absent cremasteric reflex, with scrotal swelling or redness variable and not specific [2][5]. The EAU reports that absence of the cremasteric reflex has 100% sensitivity and 66% specificity [1], while the IAEM notes that the presence of the reflex does not rule out torsion, citing studies that report sensitivities as low as 60% [2]. The family medicine review states that the reflex's presence suggests but does not confirm the absence of torsion [5]. Comparison with the other side helps, and a normal-appearing scrotum on a hurried examination does not close the question (clinical reasoning). Sources suggest asking about trauma, urinary symptoms, and sexual health, since these shape the differential [2].

TWIST score. The Testicular Workup for Ischemia and Suspected Torsion score assigns testicular swelling (2), hard testis (2), high-riding testis (1), absent cremasteric reflex (1), and nausea or vomiting (1) [6][7]. A pediatric study in which emergency medical technicians scored it found that low-risk patients did not need ultrasound and high-risk patients could proceed to surgery [6]. A systematic review of 13 studies concluded that the Barbosa risk bands (0 to 2, 3 to 4, 5 to 7) were the most accurate, with a modeled missed torsion rate of 1.6 per 100 acute scrotum presentations [7]. A small adult study (68 patients, median age 24.9 years, half with torsion) reported a score of 2 or less in 23 patients with no torsion, and 100% positive predictive value at 6 or more [8]. The limitations matter: the EAU states that scores do not conclusively prove or refute the diagnosis and should not be solely relied on [1], and the 2026 national pathway notes that a score of 0 to 4 does not exclude torsion, and that its own preliminary meta-analysis found about 1 in 3 torsions with a score of 0 to 4 and about 1 in 25 with a score of 0 to 2 [3]. Note also that the score can only be calculated if the genitals have been examined.

Imaging. Doppler ultrasonography is the usual imaging study. The EAU quotes sensitivity of 63.6% to 100% and specificity of 97% to 100%, operator dependence, and that persistent arterial flow does not exclude torsion [1]. The 2026 pathway reports a pooled sensitivity of 92% and specificity of 98% in its preliminary analysis, and states that a negative ultrasound does not exclude torsion [3]. The family medicine review gives a sensitivity of 88.9% and a specificity of 98.8% [5]. The consistent message across the guidelines is that imaging is an adjunct and should not delay surgical intervention when suspicion is high [1][2][3][5].

Laboratory tests. A urine dipstick and basic blood tests may help with the differential but should not delay assessment and definitive treatment [2].

Management

The following describes approaches in the cited guidelines, for education. It is not a treatment protocol for individual care. Decisions are made by the treating surgical team.

Surgical exploration is the definitive step. The EAU recommends urgent surgical exploration in all cases of testicular torsion as soon as possible, and that Doppler ultrasound is useful but should not delay intervention (both strong recommendations) [1]. The IAEM advises urgent referral to urology or general surgery for all suspected cases and notes that the procedure is both diagnostic and therapeutic [2]. Where there is a torsion, the other testicle is fixed at the same time, and if the testicle cannot be saved, orchiectomy may be needed [1][2]. The family medicine review states that a negative exploration is preferable to a missed diagnosis [5], and the UK pathway accepts that some patients will have an unnecessary procedure as preferable to missing a torsion, while aiming to limit negative explorations through structured assessment [3].

Timing. The EAU describes a critical window of about 4 to 6 hours, with an evidence level of 3 for ideally operating within that time [1]. The IAEM reports a 97% salvage rate in the first 6 hours, decreasing to 61.3% beyond 12 hours [2]. The family medicine review gives salvage of 90% to 100% within 6 hours, about 50% after more than 12 hours, and typically under 10% at 24 hours or more, and says these figures are approximate [5]. The national audit notes that salvage is still possible after more than 14 hours, and, citing another source, that every additional hour of delay is associated with a 4% increase in the risk of orchiectomy [4]. The IAEM adds that the duration of symptoms should not guide urgency [2]. The EAU names the time to detorsion and the degree of cord twisting as the two most important determinants of early salvage [1]. The sources support "best salvage within about six hours", and none supports abandoning surgery after six.

Manual detorsion (clinician-performed, education only). The EAU states that manual detorsion can be attempted in the emergency room while awaiting surgery, should not delay surgery, and that residual torsion was found at exploration in 17 of 53 patients, including 11 who reported relief after manual detorsion [1]. The family medicine review (SORT level C) and a 2026 meta-analysis of eight retrospective studies (670 patients) describe it as a bridge; the meta-analysis authors support considering it as an initial strategy in selected scenarios, and found a pooled manual detorsion success rate of 75.7% with wide variation (15% to 76% across studies) and no statistically significant difference in orchiectomy rates [5][9]. Surgery remains required [1][5].

Supportive care. The patient is kept fasting, with analgesia and antiemetics while awaiting surgery [2]. The UK pathway sets an aim for review by a surgical decision-maker within 60 minutes of arriving in the emergency department, and for surgery within 1 hour of the decision when pain has lasted less than 48 hours (these are paediatric-pathway aims) [3].

Evidence in context

The guideline evidence is mostly level 3 and expert consensus [1][5]. The EAU chapter and the 2026 UK pathway were written for children and young people, and the national audit covered ages 2 to 24 years [3][4]. A 19-year-old is covered by the audit's age range but is at the edge of the paediatric guidance. Adult data are limited [8]. The national audit reviewed 635 cases: 73.0% had contacted a healthcare professional within 6 hours of symptoms, a delay in diagnosis was found in 18.3% (affecting care in 59.5% of those), and 37.3% of 573 patients underwent orchiectomy [4]. A 2026 meta-analysis of 176 studies found that misdiagnosis was associated with a longer delay (risk ratio for a delay above 12 hours of 1.52, 95% CI 1.27 to 1.83), and that abdominal pain was associated with a higher risk of delay above 12 hours (RR 1.19, 95% CI 1.04 to 1.37), but not above 6 or 24 hours [10]. These are observational associations. In a quality-improvement study of boys under 16 presenting with abdominal pain or a testicular problem, documentation of testicular examination was low before an educational intervention and improved afterwards, though that study measured documentation rather than outcomes [11].

Clinical pearls

• Lower abdominal pain with vomiting in a young male: examine the genitals as part of the abdominal examination [2][3].
• Up to 1 in 5 torsion cases present with isolated lower abdominal pain, more often in younger patients [2].
• A TWIST score can be calculated only after the scrotal examination, and a low score does not exclude torsion [1][3].
• Imaging is an adjunct. When suspicion is high, do not let it delay surgical review [1][2][3][5].
• Symptom duration should not decide urgency; salvage is possible later but declines with time [2][4].

Common pitfalls

• Stopping the examination at the abdomen.
• Relying on a normal temperature or a soft abdomen.
• Relying on the cremasteric reflex or a single negative ultrasound to exclude torsion [1][2][3].
• Waiting for imaging or laboratory results before calling for surgical review [2][5].
• Transferring a patient for ultrasound, which the UK pathway advises against when torsion is suspected [3].
• Withholding the genital examination because of the patient's or the clinician's embarrassment. A calm, matter-of-fact explanation and a chaperone offer are standard practice (clinical judgment).

Takeaways

• Finish the examination: in a young man with sudden lower abdominal pain, check the testicles.
• Up to 1 in 5 torsions present with only lower abdominal pain, mostly in younger patients.
• Urgent surgical review is the priority, and ultrasound is an adjunct.
• Salvage is best within about 6 hours and declines with time, but it should not be abandoned after that.
• Clear, kind communication reduces embarrassment and saves time.

References

1. European Association of Urology. EAU Guidelines on Paediatric Urology, Chapter 8: Acute Scrotum. uroweb.org/guidelines/paediatric-urology/chapter/acute-scrotum (accessed 2 Oct 2026; no PMID or DOI)
2. Irish Association for Emergency Medicine. Clinical Guideline: Testicular Torsion (Version 1, August 2022). iaem.ie (no PMID or DOI)
3. Getting It Right First Time (GIRFT), NHS England. Children and Young People: Testicular Torsion Pathway, Version 2.1, May 2026. gettingitrightfirsttime.co.uk (no PMID or DOI)
4. National Confidential Enquiry into Patient Outcome and Death (NCEPOD). Twist and Shout: a review of the pathway and quality of care provided to children and young people aged 2-24 years who presented to hospital with testicular torsion. 2024. ncepod.org.uk (no PMID or DOI)
5. Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician. 2013;88(12):835-840. PMID 24364548 (no DOI in PubMed)
6. Sheth KR, Keays M, Grimsby GM, et al. Diagnosing testicular torsion before urological consultation and imaging: validation of the TWIST score. J Urol. 2016;195(6):1870-1876. doi:10.1016/j.juro.2016.01.101 | PMID 26835833
7. Qin KR, Qu LG. Diagnosing with a TWIST: systematic review and meta-analysis of a testicular torsion risk score. J Urol. 2022;208(1):62-70. doi:10.1097/JU.0000000000002496 | PMID 35238603
8. Barbosa JABA, de Freitas PFS, Carvalho SAD, et al. Validation of the TWIST score for testicular torsion in adults. Int Urol Nephrol. 2021;53(1):7-11. doi:10.1007/s11255-020-02618-4 | PMID 32844355
9. Kılıç S. Effectiveness of manual detorsion in the treatment of testicular torsion: systematic review and meta-analysis. Can J Urol. 2026;33(3):505-514. doi:10.32604/cju.2025.072049 | PMID 42415571
10. Sun M, Yu C, Zeng Z, et al. Are we still too late to preserve the testes? A global survey of delayed consultation and risk factors for testicular torsion: a systematic review and meta-analysis. Front Reprod Health. 2026;8:1735652. doi:10.3389/frph.2026.1735652 | PMID 41815410
11. Cheng EM, Chui JN, Crowe M, et al. Improving testicular examinations on paediatric patients in the emergency department: a quality improvement study to improve early diagnosis of testicular torsion. Asian J Urol. 2022;9(2):152-156. doi:10.1016/j.ajur.2021.07.002 | PMID 35509479

Educational only. Not medical advice. Composite case. Seek care for real symptoms.

Low Back Pain Down Both Legs With Trouble Starting to Urinate: Is It Really Sciatica?

Case presentation (composite)

A 41-year-old man has had low back pain for three days. It now aches down both legs. His vital signs are normal, and he is asking for stronger pain medicine. The working diagnosis is sciatica: an NSAID, a muscle relaxant, physical therapy, and discharge with a back-care handout.

On further questioning, he has had trouble starting to urinate since yesterday. On examination, he has a numb patch in the area that would touch a saddle.

(Composite case. No real patient is described. Leg strength, reflexes, bladder scan result, and any imaging are not specified in this teaching case.)

The first guess, and why it is tempting

Low back pain with leg pain is among the most common reasons for an emergency department visit. In the United States, acute low back pain accounts for about 3% of emergency department visits, and uncomplicated acute low back pain with or without radiculopathy is a benign, self-limited condition for which the American College of Radiology advises against routine imaging [2]. A normal set of vital signs, a patient who is asking for analgesia, and a typical sciatica story all push toward a conservative plan. Cauda equina syndrome (CES) is rare. The English national pathway cites 1 to 3 cases per 100,000 population [1], so most clinicians will see few cases and many mimics.

The pitfall is the question that did not get asked. Urinary hesitancy and saddle numbness are easy to omit from a back pain history, and patients may not volunteer them. The national pathway states that CES has no set clinical pattern, that no single symptom or combination has good diagnostic accuracy, and that negative physical tests do not rule out CES if positive subjective symptoms are present [1].

What does not fit

• Trouble starting to urinate. The pathway lists difficulty initiating micturition or impaired sensation of urinary flow, in the context of back and/or leg pain with recent onset (14 days or fewer) or deterioration, as a trigger for emergency referral to a facility with emergency MRI [1].
• A numb saddle area. Altered perianal, perineal, or genital sensation (the S2 to S5 dermatomes) is a listed trigger. The pathway notes the area may be small or as large as a saddle, and may be reported by the patient or found on testing [1].
• Both legs. The pathway describes sudden-onset bilateral radicular leg pain, or unilateral pain that has progressed to bilateral, as a warning sign that CES may occur [1]. By itself, without CES symptoms, this prompts an urgent referral (to be seen within two weeks) to a musculoskeletal triage service, with safety netting. Once urinary or saddle symptoms appear, it becomes an emergency [1]. In this case, both are present.
• A pain-medicine request in a patient with normal vital signs. Normal vital signs are expected in CES. The syndrome is neurological and the vital signs are not part of the diagnosis (clinical reasoning).

Differential

• Lumbar radiculopathy without CES. The commonest alternative. Management is conservative if red flags are absent [2], with safety netting and urgent musculoskeletal triage when bilateral sciatica has appeared without CES symptoms [1].
• Other causes of compression. CES is most often due to a large lumbar disc prolapse, but can follow haematoma, trauma, infection, tumour, or spinal or epidural anaesthesia [1]. The ACR lists neoplasm, infection or inflammation, spinal stenosis, and haemorrhage as other etiologies [2].
• Urinary tract causes of urinary symptoms. The pathway advises that urinary incontinence without impaired sensation of urinary flow, and without saddle anaesthesia, should prompt consideration of other causes first, such as urinary tract infection, stress incontinence, or urge incontinence [1].
• Spinal cord disease. Multifocal or progressive neurologic deficits can be caused by noncompressive conditions with overlapping features; the ACR refers to its separate myelopathy guidance [2].
• Acute urinary retention from other causes (for example, medication-related). Plausible, but not addressed in the opened sources (clinical reasoning).

Workup

History and examination. The pathway symptoms that mandate emergency referral with back and/or leg pain are recent onset or deterioration of: difficulty initiating micturition or impaired sensation of urinary flow; altered perianal, perineal, or genital sensation; severe or progressive neurological deficit of both legs; loss of sensation of rectal fullness; or sexual dysfunction [1]. A digital rectal examination is not necessary, but subjective perianal sensation should be recorded [1]. Document power and sensation in the lower limbs, and the duration and progression of symptoms [1].

How well do red flags perform? Poorly, individually. A systematic review of seven studies (569 participants) comparing red flags with MRI found pooled sensitivities of 0.19 to 0.43 and pooled specificities of 0.62 to 0.88, concluding that red flags are more specific than sensitive, and that when present they should justify prompt diagnostic workup [4]. In a prospective study of 260 patients with suspected CES referred to a spinal unit, bilateral sciatica had a sensitivity of 32.4%, a positive predictive value of 17.2%, and a negative predictive value of 88.3% for compression on MRI [5]. Large cohort data show the presenting picture in confirmed CES is dominated by back pain (96%) and sciatica (93%), with urinary dysfunction in 83% and saddle numbness in 81% of 621 patients [3].

Bladder scan. The national pathway calls a bladder scan a useful adjunct that should not be used in isolation or as a discriminator in deciding whether to request an MRI or undertake surgery. It reports that 60% of patients who underwent emergency decompression had a post-void residual below 200 mL, and that a residual below 200 mL cannot exclude CES while a residual above 200 mL makes CES about 20 times more likely [1]. The data underneath:

• In a prospective study of 260 patients, a post-void residual of 200 mL or more had sensitivity of 94.1%, specificity of 66.8%, positive predictive value of 29.9%, and negative predictive value of 98.7%; the authors proposed that a low-risk residual could allow non-urgent MRI (13% of patients in that study, none with compression) [5].
• A meta-analysis of seven studies found that a 200 mL threshold had the best accuracy, with sensitivity of 82% [6].
• A series of 50 MRI-confirmed medicolegal cases found that of 26 who had a scan, 13 (50%) had a residual of 200 mL or less despite a clear clinical and MRI diagnosis, all with incomplete CES, all proceeding to emergency decompression; the authors concluded that clinical suspicion should always lead to an MRI [7].
• In a prospective cohort of 621 patients with CES, 59% of the 368 who had a pre-operative scan had a residual below 200 mL [3].

These studies differ in design, and none of them shows that a bladder scan can safely replace MRI in a patient with symptoms like this one. In this case, the presence of both a urinary symptom and a saddle sensory change makes the pre-test probability high enough that a scan result would not change the next step (clinical reasoning).

Imaging. In the United States, the ACR Appropriateness Criteria rate MRI of the lumbar spine without contrast (or without and with contrast) as usually appropriate for low back pain with suspected CES. They note that CT without contrast may be appropriate, and that a CT retrospective review of 151 patients found less than 50% thecal sac effacement reliably excluded impingement [2]. The English pathway states that an emergency MRI should be done as soon as possible and certainly within four hours of the request to radiology, that discussion with the spinal surgical team is not required before MRI and may cause delay, that the patient should be kept nil by mouth in case surgery is needed, and that CT or CT myelography may be used if MRI is contraindicated [1]. It also states that a sagittal T2-weighted sequence is the single sequence needed to screen for compression [1]. The four-hour target is a UK standard; the ACR criteria did not specify a time target in the text reviewed [2].

Management

The following describes approaches in the cited guidance, for education. It is not a treatment protocol for individual care. Decisions rest with the treating team.

Emergency imaging and referral. The pathway recommends an emergency referral to the nearest facility with emergency MRI for the symptom triggers above, and, if compression is confirmed, immediate referral to the spinal surgical service with the patient kept nil by mouth [1]. If there is no CES compression but there is neural compression explaining sciatica, the patient is safety-netted about progression and referred to an MSK service [1].

Surgery. Decompression is the definitive treatment [1]. The pathway says surgery for incomplete CES should be done as quickly as possible, as an NCEPOD E1/E2 emergency, noting that CES is time-sensitive and life-changing but not life-threatening [1]. For painless urinary retention with overflow incontinence, timing is at the discretion of the surgeon, but surgery should still occur within 24 hours of MRI, and about 70% of these patients are reported to benefit from decompression despite a poorer prognosis [1]. Catheterisation guidance in the pathway includes catheterising patients before surgery to avoid bladder distension, and, when a bladder scan is above 600 mL, catheterising and documenting sensation [1].

Pain control and supportive care. The pathway does not prescribe analgesic regimens. In this scenario, the patient would be fasted and treated for pain while he awaits imaging and surgical review (clinical reasoning). No doses are given here.

Evidence in context

The timing question is less settled than the pathway wording suggests. A 2026 meta-analysis of 15 comparative studies (26,627 adults) found that decompression within 48 hours of symptom onset was associated with better urinary recovery (pooled odds ratio about 2.3) and motor function than later surgery, with a strong timing effect in incomplete CES and no significant timing effect in retention-type CES. It found no consistent advantage for surgery within 24 hours compared with 24 to 48 hours, differences that attenuated at 12 months or more, and baseline bladder status as the dominant long-term prognostic factor [8]. The large prospective UK cohort found no association between time to surgery and outcome in multivariable analyses, but noted the observational limits: median time to surgery was 3 days and only 32% were operated on within 48 hours [3]. The same cohort found that function improved after surgery even in patients who presented with urinary retention [3]. The pathway's four-hour MRI standard is a consensus target rather than a randomized result. It follows from the aim of identifying patients before the bladder is affected (the pathway states that treatment before symptoms become severe can reduce the risk of permanent disability) [1].

Clinical pearls

• Ask every back pain patient about urinary flow, perineal sensation, and sexual function [1].
• Bilateral radicular pain alone is a warning sign (urgent triage); with urinary or saddle symptoms it becomes an emergency [1].
• Red flags are more specific than sensitive; absent flags do not exclude CES when subjective symptoms are present [1][4].
• A normal post-void residual does not exclude CES; do not let a bladder scan stand in for MRI [1][5][7].
• A numb saddle area may be small. Ask about toilet-paper sensation and perianal feeling [1].

Common pitfalls

• Discharging with a back-care handout without asking about bladder, bowel, and saddle sensation.
• Using a bladder scan as the reason not to image [1].
• Waiting for a spinal surgical opinion before requesting the MRI, when the pathway says this may delay care [1].
• Treating urinary hesitancy as a primary urological problem without back pain context.
• Calling it "sciatica" on the basis of leg pain without testing power and sensation in both legs.

Takeaways

• Back pain plus new urinary change or saddle numbness is an emergency until imaging says otherwise.
• Bilateral leg pain is a warning, not the full picture.
• Emergency MRI is the test. The UK pathway standard is within four hours of request.
• A bladder scan is an adjunct and a normal result does not exclude CES.
• Early decompression is the goal, particularly for incomplete presentations, though the timing evidence is mixed.

References

1. Getting It Right First Time (GIRFT), NHS England. National Suspected Cauda Equina Syndrome (CES) Pathway (February 2023; updated through March 2026). gettingitrightfirsttime.co.uk (no PMID or DOI)
2. Expert Panel on Neurological Imaging; Hutchins TA, Peckham M, Shah LM, et al. ACR Appropriateness Criteria Low Back Pain: 2021 update. J Am Coll Radiol. 2021;18(11S):S361-S379. doi:10.1016/j.jacr.2021.08.002 | PMID 34794594
3. Woodfield J, Hoeritzauer I, Jamjoom AAB, et al. Presentation, management, and outcomes of cauda equina syndrome up to one year after surgery, using clinician and participant reporting: a multi-centre prospective cohort study. Lancet Reg Health Eur. 2023;24:100545. doi:10.1016/j.lanepe.2022.100545 | PMID 36426378
4. Dionne N, Adefolarin A, Kunzelman D, et al. What is the diagnostic accuracy of red flags related to cauda equina syndrome (CES), when compared to magnetic resonance imaging (MRI)? A systematic review. Musculoskelet Sci Pract. 2019;42:125-133. doi:10.1016/j.msksp.2019.05.004 | PMID 31132655
5. Katzouraki G, Zubairi AJ, Hershkovich O, et al. A prospective study of the role of bladder scanning and post-void residual volume measurement in improving diagnostic accuracy of cauda equina syndrome. Bone Joint J. 2020;102-B(6):677-682. doi:10.1302/0301-620X.102B6.BJJ-2020-0195.R1 | PMID 32475252
6. Boktor J, Wong F, Joseph VM, et al. Predictive value of post-void residual volume as an adjunctive tool in the clinical evaluation of cauda equina syndrome. Bone Joint J. 2023;105-B(5):487-495. doi:10.1302/0301-620X.105B5.BJJ-2022-0739.R2 | PMID 37121596
7. Todd N, Dangas K, Lavy C. Post-void bladder ultrasound in suspected cauda equina syndrome: data from medicolegal cases and relevance to magnetic resonance imaging scanning. Int Orthop. 2022;46(6):1375-1380. doi:10.1007/s00264-022-05341-0 | PMID 35182176
8. Najjar E, Egu C, Akil H, et al. Reassessing the clock in cauda equina syndrome: a systematic review and meta-analysis of surgical timing and outcomes. Spine J. 2026;26:1653-1670. doi:10.1016/j.spinee.2026.04.013 | PMID 41991105

Educational only. Not medical advice. Composite case. Seek care for real symptoms.