An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
Keratitis and Corneal Ulcers
Keratitis and corneal ulcers can scar the visual axis, perforate the cornea, and blind a patient if treatment is delayed. Contact lens–associated infections are common, aggressive, and easy to under-triage.
A 29-year-old contact lens wearer sits under the triage fluorescent lights, one eye half-closed, tearing so hard the cheek is wet. He says the pain started as “grit” after an overnight shift, but now even the dim hallway light feels like a spotlight. The sclera is red, the eyelid keeps fluttering, and he can barely keep the lens story straight because he forgot to take them out. The eye looks angry in a way that makes you stop scrolling and lean in.
— What’s your move? Read on.
Before you read
Which finding separates simple abrasion from ulcerative infection?
What is the one mistake that risks permanent vision loss?
When to Think of It
Think of this when there is painful red eye + photophobia + foreign body sensation + decreased vision or a corneal opacity/infiltrate on exam. Contact lens use, trauma with vegetative matter, topical steroid use, or immunocompromise should push this to the top of the list.
Sick or Not Sick
The fork is simple epithelial defect vs. sight-threatening corneal infection/perforation risk. Any decreased vision, corneal infiltrate/opacity, hypopyon, central ulcer, contact lens wear, or severe pain/photophobia is “treat as ulcerative keratitis until proven otherwise.”
The First Fifteen Minutes
Topical anesthetic for exam only if needed: tetracaine 0.5% 1–2 drops in the ED to permit fluorescein/slit-lamp exam, because you need a real corneal look; do not prescribe for home use.
Pain control: ibuprofen 400–600 mg PO or acetaminophen 650–1,000 mg PO/IV if needed, because it improves comfort without obscuring exam findings.
Cycloplegic if significant ciliary spasm/photophobia: cyclopentolate 1% 1 drop or homatropine 2% 1 drop in the affected eye, because it relieves painful spasm and photophobia.
Suspected bacterial keratitis/corneal ulcer, especially contact lens wearer → start topical fluoroquinolone: moxifloxacin 0.5% 1 drop q1h while awake or ciprofloxacin 0.3% 1–2 drops q1h initially, because high local antibiotic levels are needed to suppress corneal pathogens.
If severe ulcer, central lesion, or ophthalmology directs fortified therapy: fortified tobramycin 14 mg/mL and cefazolin 50 mg/mL or vancomycin-based drops per ophthalmology protocol; dosing varies meaningfully, so check local/ophthalmology guidance.
If concern for herpetic keratitis (dendrites, reduced corneal sensation) → do not start topical steroids; urgent ophthalmology, because steroids can worsen HSV corneal disease.
Remove contact lenses immediately and bring the case/lens/case if available, because it reduces ongoing inoculation and helps identify pathogens.
Definitive Care & Disposition
Urgent ophthalmology consultation is required for any ulcer/infiltrate, visual change, hypopyon, central or large lesion, corneal thinning, immunocompromise, or inability to ensure follow-up. Small peripheral abrasions can sometimes be outpatient, but true corneal ulcer/keratitis generally gets same-day ophthalmology and often admission if severe, bilateral, atypical, or fungal/amoebic disease is suspected. Continue topical antibiotics as directed; later therapy may include culture-directed treatment, antifungals (e.g., natamycin for fungal keratitis), or anti-amoebic regimens.
How This One Kills
The fatal error is treating an infectious corneal ulcer like a routine abrasion and sending the patient away with no urgent follow-up—this can progress to corneal melt, perforation, endophthalmitis, and permanent vision loss.
The Differential — What Else Looks Like This
Corneal abrasion — epithelial defect without stromal infiltrate/opacity; confusing it for ulcer delays antibiotics and ophthalmology.
Acute glaucoma — severe pain, halos, mid-dilated fixed pupil, high IOP; confusing it for keratitis delays pressure-lowering therapy and threatens the optic nerve.
Anterior uveitis/iritis — consensual photophobia and ciliary flush with a quiet cornea; missing it can lead to synechiae and chronic vision loss.
Endophthalmitis — profound vision loss, hypopyon, post-op/injection history; missing it is catastrophic because it needs immediate intraocular therapy.
The Second-Day Story
Older adults, diabetics, and steroid-treated patients may have less dramatic pain but worse disease, and contact lens users may present late with just “irritation” and blurry vision. Any unilateral red eye with decreased visual acuity deserves fluorescein staining and slit-lamp inspection; if you see a focal infiltrate or corneal haze, assume infection until an eye specialist says otherwise.
Back to Our Patient
Back to our patient: the 29-year-old contact lens wearer with tearing, photophobia, and blurry unilateral pain gets a slit-lamp exam showing a corneal infiltrate with fluorescein uptake, so this is infectious keratitis/corneal ulcer, not a simple abrasion. Because contact lens use and decreased vision make him high risk, he goes straight into the First Fifteen with topical fluoroquinolone drops, no contact lens use, and pain control after exam, then same-day ophthalmology for culture consideration and close follow-up, with admission if the lesion is central or severe.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“29-year-old man with contact lens use presents with one day of severe left eye pain, tearing, photophobia, and blurred vision. He says it started like a scratch after a night shift, but it has worsened and he can barely tolerate light; no trauma with metal, no chemical exposure, and no headache or neurologic symptoms. On exam he has conjunctival injection, obvious discomfort, and decreased visual acuity in the affected eye; fluorescein shows a focal corneal epithelial defect with surrounding infiltrate, and I don’t see a mid-dilated fixed pupil or elevated IOP features to suggest acute glaucoma. This is most concerning for infectious keratitis/corneal ulcer, likely bacterial given the contact lens history. I’ve removed the lens, started topical fluoroquinolone drops, given analgesia, and I’m calling ophthalmology now for urgent evaluation and disposition.”
Study Directive
Draw the red painful eye algorithm from memory: abrasion vs keratitis vs glaucoma vs uveitis.
Practice naming the bedside discriminators: visual acuity change, fluorescein uptake pattern, corneal opacity, pupil shape, and IOP clues.
Write out the first-hour orders for a contact lens wearer with suspected ulcer: exam, lens removal, topical fluoroquinolone, analgesia, ophthalmology call.
Review when steroids are harmful in eye disease, especially HSV keratitis and microbial ulcers.
A broad clinical review of infectious keratitis that reinforces the ED priorities: suspect it in painful red eyes with corneal staining or contact lens use, start prompt topical antimicrobial therapy when indicated, and arrange urgent ophth
Optic neuritis can be the first manifestation of multiple sclerosis or another demyelinating disease. Missing it delays neurologic evaluation and can blur...
A 33-year-old woman closes one eye against the hallway light and says the world on the right is “washed out,” like someone turned the color down. She had a retro-orbital ache yesterday, and now the pain flares when she looks side to side. The pupils seem nearly equal until you swing the flashlight and one eye suddenly behaves as if the bulb has gone dim. She’s asking whether this will go away, and you’re still deciding whether this is the nerve, the retina, or something else.
Before You Read
What bedside sign most strongly points to optic nerve disease?
When is this an emergency versus an urgent outpatient workup?
What associated pattern should make you think of multiple sclerosis?
Why It Matters
Optic neuritis can be the first manifestation of multiple sclerosis or another demyelinating disease. Missing it delays neurologic evaluation and can blur the line between reversible inflammation and permanent visual loss.
When to Think of It
Think of optic neuritis with subacute unilateral vision loss, pain with eye movement, color desaturation, and a relative afferent pupillary defect (RAPD). It is classically a young adult, often female, with normal-appearing external eye exam.
Sick or Not Sick
The key decision is simple suspected optic neuritis vs. atypical optic neuropathy needing emergent alternate workup. Red flags for not-the-usual include bilateral simultaneous loss, very severe vision loss, no pain, marked disc edema with hemorrhage, immunocompromise, fever, trauma, or other focal neurologic deficits.
The First Fifteen Minutes
Check visual acuity, color vision, pupils, and RAPD because the diagnosis is primarily clinical and you need a baseline.
Pain control: ibuprofen 400–600 mg PO or acetaminophen 650–1,000 mg PO if needed.
If optic neuritis is strongly suspected and there are no atypical red flags, urgent ophthalmology and neurology consultation; ED meds do not reverse the disease immediately, but prompt steroid planning matters.
High-dose steroids are commonly used for typical acute optic neuritis after specialist involvement or per protocol: methylprednisolone 1,000 mg IV daily for 3 days, because it speeds visual recovery; dosing and whether to transition to oral prednisone should be coordinated with neurology/ophthalmology.
Do not start low-dose oral prednisone alone as monotherapy for typical optic neuritis, because it may increase recurrence risk without the benefit of high-dose IV therapy.
If signs suggest infection, compressive lesion, giant cell arteritis, or another alternate diagnosis, treat that pathway instead; for example, in older patients with headache/jaw claudication, send ESR/CRP and start GCA therapy as indicated.
Definitive Care & Disposition
Typical optic neuritis needs urgent outpatient or inpatient neuro-ophthalmic evaluation, MRI brain/orbits with contrast, and MS risk assessment. Admit if the diagnosis is uncertain, vision loss is severe, there are neurologic deficits, or follow-up is unreliable. Later therapy may include MRI-based demyelinating workup, disease-modifying MS treatment, and a steroid taper strategy if guided by consultants.
How This One Kills
The dangerous miss is assuming every painful monocular vision loss is “just optic neuritis” and overlooking retinal detachment, CRAO, GCA, orbital cellulitis, or compressive mass lesions.
The Atypical Presentation
Not all optic neuritis is the classic young woman with eye pain. Older patients, men, and immunocompromised patients may present with less pain, bilateral symptoms, or a swollen disc that looks more inflammatory than demyelinating; if the story is off, do not anchor. Any mismatch between symptoms and exam, or any systemic neurologic symptom, should push you toward MRI and specialty consultation rather than reassurance.
Back to Our Patient
Back to our patient: the 33-year-old woman with unilateral color desaturation, pain on eye movement, and a positive RAPD has typical optic neuritis until proven otherwise. She is not crashing, so the move is to document vision and pupils carefully, involve neurology/ophthalmology, and arrange MRI brain/orbits with contrast; if consultants agree and no alternate diagnosis emerges, she receives high-dose IV methylprednisolone and close follow-up, with admission if her workup or social situation makes outpatient care unsafe.
Patient Presentation to Attending
“33-year-old woman with one day of unilateral blurry vision and retro-orbital pain worse with eye movements. She describes color desaturation in the affected eye, and on exam her visual acuity is decreased with a relative afferent pupillary defect; external exam is otherwise unremarkable and I don’t see the fixed mid-dilated pupil or severe headache pattern that would push me toward acute glaucoma. No fever, trauma, or orbital swelling, and no flashes or curtain symptoms to suggest retinal detachment. This is most consistent with optic neuritis, likely demyelinating, so I’m checking a neuro exam, arranging MRI brain and orbits with contrast, and involving neurology/ophthalmology for steroid planning and disposition.”
Study Directive
Practice swinging-flashlight testing on a partner and identify RAPD from memory.
Make a one-page “painful monocular vision loss” comparison with optic neuritis, glaucoma, GCA, CRAO, and retinal detachment.
Memorize the typical MRI workup and the high-dose steroid regimen used for classic cases.
Review which historical features should trigger a broader neurologic or vascular workup.
Key Medications
Methylprednisolone 1,000 mg IV daily x 3 days for typical acute optic neuritis, usually with specialist guidance.
Acetaminophen 650–1,000 mg PO/IV for pain.
Ibuprofen 400–600 mg PO for pain if appropriate.
Steroid regimen specifics vary by institution; check local neurology/ophthalmology protocol.
High-Yield Pearls
RAPD is the bedside clue that the problem is afferent, not just “blur.”
Pain with eye movement + color desaturation is the optic neuritis signature until proven otherwise.
If the patient is >50 or atypical, think beyond demyelination before giving the optic neuritis label.
The Mimics
Acute angle-closure glaucoma — high IOP, halos, mid-dilated fixed pupil; confusing it wastes the narrow window to lower pressure.
Retinal detachment — flashes/floaters and curtain over vision with painless field loss; missing it can cost central vision.
Central retinal artery occlusion — sudden painless profound vision loss; missing it delays stroke-level evaluation.
Giant cell arteritis — age >50, headache, jaw claudication, scalp tenderness; missing it can blind the other eye.
Board Question
A 27-year-old woman has unilateral vision loss, pain with eye movement, decreased color vision, and a relative afferent pupillary defect. What is the most likely diagnosis?
AOptic neuritis
BCentral retinal artery occlusion
CAcute angle-closure glaucoma
DVitreous hemorrhage
Reveal answer
Correct: A
Pain with eye movement, color desaturation, and RAPD are classic for optic neuritis. CRAO and vitreous hemorrhage are typically painless, while acute angle-closure glaucoma usually has a red eye with high IOP, halos, and a fixed mid-dilated pupil.
Comprehensive, current framework for distinguishing typical MS-associated optic neuritis from NMOSD/MOGAD and other autoimmune optic neuropathies, guiding ED decisions on urgent MRI, antibody testing, and high-dose steroid treatment.
3 of 4
Complications of Tracheostomies
Tracheostomy problems can cause rapid hypoxia, loss of airway access, and death if handled like routine tube troubleshooting. The ED must distinguish...
A 68-year-old man with a trach from last winter is sitting upright, anxious, and gripping the bedrail while thin secretions hiss around the tube. His caregiver says the inner cannula looked “sticky” this morning, and now he’s making a high-pitched noise with each breath. The skin around the stoma is wet and red, the suction catheter won’t pass smoothly, and everyone in the room has gotten very quiet. The question isn’t what disease he has; it’s whether the airway is about to fail in front of you.
Before You Read
Which tracheostomy complication is an airway emergency first, diagnosis second?
What do you do when the tube is blocked, displaced, or cuffed incorrectly?
When is the stoma a usable backup airway?
Why It Matters
Tracheostomy problems can cause rapid hypoxia, loss of airway access, and death if handled like routine tube troubleshooting. The ED must distinguish obstruction from displacement and act before the patient decompensates.
When to Think of It
Think of this with respiratory distress, noisy breathing, inability to pass suction catheter, air leak, bleeding, subcutaneous emphysema, or sudden desaturation in a patient with a tracheostomy. Early post-op tubes are especially dangerous because the tract may not be mature.
Sick or Not Sick
The fork is can oxygen still move through the tube/stoma or not. If the patient is unstable, assume tube obstruction or displacement with impending airway loss and manage as an airway emergency.
The First Fifteen Minutes
High-flow oxygen to both face and trach/stoma because you may still ventilate through either route while you troubleshoot.
Suction the trach and attempt to pass a suction catheter; inability to pass suggests obstruction or malposition.
Remove and replace the inner cannula if present, because mucus plugging is common and immediately reversible.
If tube is cuffed and ventilation is needed, inflate cuff to seal; if cuff failure or major leak persists, replace the tube.
If the patient is in distress and the tube is obstructed or displaced, remove the tracheostomy tube and ventilate with mask over mouth/nose or stoma as appropriate; a patent upper airway can often be used if the tract is mature.
If the tube was placed recently and the tract may be immature, call airway/anesthesia/ENT immediately and avoid blind reinsertion if resistance is met, because false passage can be fatal.
If bleeding is brisk or pulsatile, apply local pressure and activate ENT/surgical help urgently; concern for tracheo-innominate fistula is a surgical catastrophe.
Nebulized saline or humidification may help after initial stabilization if secretions are thick, because it loosens mucus plugging.
IV access and monitoring are mandatory while definitive airway decisions are made.
Definitive Care & Disposition
Definitive management depends on the complication: tube exchange, bronchoscopy, ENT evaluation, stoma revision, or operative repair for fistula/false passage. Most true tracheostomy complications require ICU-level monitoring or admission, especially if there is respiratory distress, recent trach placement, infection, or bleeding.
How This One Kills
The catastrophic miss is assuming a trach patient “has a secure airway” and delaying intervention while oxygenation silently worsens—especially with mucus plugging, decannulation, or tracheo-innominate fistula.
The Atypical Presentation
Some patients look only mildly uncomfortable until they suddenly are not, especially those with a partially obstructed tube or a mature stoma that still allows minimal airflow. Small leaks, changing voice, increasing work of breathing, or frequent suctioning needs may be the only clues; if a trach patient says “this tube feels wrong,” take it seriously and inspect the airway early.
Back to Our Patient
Back to our patient: the 68-year-old man with hissing secretions and a suction catheter that won’t pass is most likely obstructed by a mucus plug or malpositioned trach. He gets oxygen to both face and stoma, the inner cannula is removed and exchanged, suction is attempted, and because he is working harder to breathe the tube is removed and airway support is prepared while ENT/anesthesia are called; if the tract is mature and the tube replacement is straightforward, he stabilizes and is admitted for observation and trach care, but if bleeding or false passage is suspected he goes to ICU/OR immediately.
Patient Presentation to Attending
“68-year-old man with a chronic tracheostomy presents with acute dyspnea and noisy breathing from the trach. Caregiver reports thick secretions and inability to pass the suction catheter, and on exam he has increased work of breathing, wet erythematous stoma tissue, and a poor air leak around the tube; I’m very concerned about tube obstruction versus displacement rather than a primary pulmonary process. I’ve put oxygen to both the face and trach, tried suctioning, and removed the inner cannula. I’m calling ENT/anesthesia now because if he worsens or the tube cannot be cleared, this is an airway emergency and may need tube exchange or advanced airway management.”
Memorize which complication is most associated with each timing: early post-op, mature trach, bleeding, mucus plugging.
Practice a two-minute oral presentation of a trach emergency with an explicit airway plan.
Review your institution’s trach replacement and emergency airway cart contents.
Key Medications
Oxygen: high-flow via face and trach/stoma as needed.
Nebulized normal saline: commonly used for thick secretions; dosing varies by setup.
Topical vasoconstrictor or packing agents for bleeding may be used per ENT protocol; specifics vary and should follow local guidance.
Medication is secondary here; airway maneuvers and tube management are the treatment.
High-Yield Pearls
In a trach emergency, “can I pass the suction catheter?” is the first yes/no question.
Recent tracheostomy = immature tract; blind reinsertion can create a false passage.
Small bleeding can precede catastrophic tracheo-innominate fistula hemorrhage — never dismiss sentinel bleeding.
The Mimics
Asthma/COPD exacerbation — wheeze and dyspnea without trach obstruction; confusing it delays a life-saving tube check.
Panic attack — tachypnea with normal airflow and oxygenation; confusing it can miss an actual obstructed airway.
Mucus plug without displacement — inability to pass suction catheter; missing it delays the simplest fix.
Tracheo-innominate fistula — sentinel bleed may be small before exsanguination; missing it is often fatal.
Board Question
A patient with a mature tracheostomy becomes acutely dyspneic, and suction catheter cannot be passed through the tube. What is the best immediate next step?
ADischarge with antibiotics for presumed tracheitis
BRemove the inner cannula and attempt suctioning/airway troubleshooting
CGive oral steroids and observe for improvement
DDelay intervention until a chest radiograph confirms the problem
Reveal answer
Correct: B
Inability to pass a suction catheter strongly suggests obstruction or malposition, often from mucus plugging. Immediate bedside troubleshooting—especially inner cannula removal and suction—comes before imaging; waiting can allow rapid airway failure.
Practical ED approach to life-threatening tracheostomy problems—obstruction, dislodgement/false passage, bleeding, and ventilation failure—with bedside algorithms for securing oxygenation first.
4 of 4
Post-Tonsillectomy Hemorrhage
Post-tonsillectomy hemorrhage is a true airway and hemorrhagic emergency; swallowed blood can hide severity, and even minor-appearing bleeding can herald...
A 12-year-old boy is sitting bolt upright in the chair, pale and quiet, with a red stain spreading through the tissues in his fist. His mother says he woke up tasting blood and then started spitting “just a little” into the sink, but now the saliva is pink and his throat keeps making him swallow. He won’t lie flat, keeps pointing to his mouth, and there’s a raw metallic smell in the room. No one has seen him vomit, but the sink has a dark clotted ring and he looks more drained than he wants to admit.
Before You Read
What is the first priority when the post-tonsillectomy patient is bleeding?
Which bleeding pattern is dangerous even if the amount looks small?
What bedside move can worsen the hemorrhage?
Why It Matters
Post-tonsillectomy hemorrhage is a true airway and hemorrhagic emergency; swallowed blood can hide severity, and even minor-appearing bleeding can herald major vessel exposure. Children can deteriorate quickly from aspiration, shock, or obstruction.
When to Think of It
Think of this diagnosis with any oral bleeding, frequent swallowing, hematemesis, hemoptysis-like spitting, or clot in the tonsillar fossa after tonsillectomy. It is classically within 24 hours (primary) or 5–10 days (secondary) after surgery.
Sick or Not Sick
The key fork is active bleeding / clot present / unstable vs. no active bleeding and fully stopped. Any ongoing hemorrhage, repeated swallowing, tachycardia, pallor, or difficulty managing secretions is high risk and needs immediate ENT involvement.
The First Fifteen Minutes
Suction the oropharynx gently and have the patient spit blood into a basin if able, because swallowed blood obscures severity and increases aspiration risk.
Position upright, leaning forward, because this reduces aspiration and helps visualize the source.
Two large-bore IVs and monitor vitals; if unstable, begin resuscitation with balanced crystalloid 20 mL/kg IV and blood products as needed, because children can hide shock until late.
ENT emergently for any active bleed or clot.
Ice water gargle or swish/spit may be used in a cooperative, stable patient while awaiting ENT, because cold vasoconstriction can temporize minor bleeding.
If active bleeding is present and the child can cooperate, topical vasoconstrictor/pressure measures may be used by ENT; ED should not aggressively manipulate the tonsillar fossa unless directed.
Antiemetic if needed: ondansetron 0.15 mg/kg IV/PO (max 8 mg) for vomiting/retching, because retching can worsen bleeding and aspiration risk.
If severe bleeding with shock or airway compromise, prepare for airway management and massive transfusion; intubation is difficult and should involve the most experienced operator available.
Definitive Care & Disposition
All patients with true post-tonsillectomy bleeding need ENT evaluation and usually observation or admission. Active bleeds, recurrent bleeds, significant anemia, or unstable patients require operative control and inpatient monitoring; even if bleeding stops, many need prolonged observation because rebleeding can occur.
How This One Kills
The classic failure is dismissing “just a little blood” while the child is repeatedly swallowing it—this can mask ongoing hemorrhage until the patient suddenly aspirates or decompensates.
The Atypical Presentation
Some children do not vomit blood at all; they simply swallow, become pale, or refuse to talk because talking hurts. Teenagers and adults may be more articulate but still underestimate the amount because blood is diluted in saliva; any persistent swallowing, throat clearing, or taste of blood after tonsillectomy should be treated as hemorrhage until proven otherwise.
Back to Our Patient
Back to our patient: the 12-year-old boy with persistent swallowing, blood-streaked saliva, and a clot in the tonsillar fossa has post-tonsillectomy hemorrhage until proven otherwise. He stays upright, gets suction and IV access, and because even “small” bleeding can be significant, ENT is called immediately for bedside and likely operative control; if he is tachycardic, pale, or actively bleeding, he gets resuscitation and admission after hemostasis, with airway planning kept front and center.
Patient Presentation to Attending
“12-year-old boy status post tonsillectomy with concern for postoperative bleeding. His mother reports recurrent swallowing and blood-tinged saliva, and on exam he is pale, spitting blood, and has a clot in the tonsillar fossa; I’m concerned this is active post-tonsillectomy hemorrhage rather than routine postoperative irritation. I’ve kept him upright, avoided aggressive manipulation, placed IV access, and am calling ENT emergently. Depending on his ongoing bleeding and vitals, he may need resuscitation, operative hemostasis, and admission for observation.”
Study Directive
Rehearse the first-five-minute tonsillectomy bleed algorithm from memory.
Memorize primary vs secondary timing and what each implies about risk.
Practice a focused oral presentation that includes airway, hemodynamics, and ENT disposition.
Review pediatric resuscitation fluid dosing and the threshold for blood product escalation.
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Mechanism Pearl of the Day: Several of today’s problems hinge on a hidden lumen becoming dangerous because you can’t see the damage from the outside: corneal infection beneath a red eye, optic nerve inflammation behind a normal-appearing globe, a trach tube failing inside a “secure” airway, and tonsillar bleeding masked by swallowed blood. In each, bedside discrimination beats reassurance.
Key Medications
Ondansetron 0.15 mg/kg IV/PO (max 8 mg) for vomiting/retching.
0.9% normal saline or balanced crystalloid 20 mL/kg IV bolus for resuscitation if unstable.
Acetaminophen dosing is weight-based in children; use institutional pediatric dosing.
Specific hemostatic/topical measures are usually ENT-directed and vary by institution.
High-Yield Pearls
Swallowing blood is the clue — many children don’t spit it out.
A tonsillar clot is not reassuring; it can be the tamponading edge of active hemorrhage.
Post-tonsillectomy bleeding is an airway problem before it is a “bleeding history” problem.
The Mimics
Epistaxis with swallowed blood — nasal source and posterior drainage; confusing it misses a surgical throat source.
Postoperative nausea/vomiting — can be from swallowed blood, but if you treat it as simple vomiting you miss hemorrhage.
Peritonsillar abscess — muffled voice and sore throat without postoperative timing; confusing it misses bleeding control.
Upper GI bleeding — hematemesis history, abdominal symptoms; confusing it diverts attention from the oropharynx.
Board Question
A 9-year-old is 7 days post-tonsillectomy and presents with repeated swallowing, blood in the saliva, and a visible clot in the tonsillar fossa. What is the most appropriate next step?
AReassure and discharge if the bleeding is not brisk
BPlace the child supine for inspection and send labs only
CKeep upright, obtain IV access, and urgently consult ENT
DGive oral antibiotics and outpatient follow-up tomorrow
Reveal answer
Correct: C
A clot or recurrent swallowing after tonsillectomy is a bleed until proven otherwise and can worsen quickly. The correct move is immediate stabilization, upright positioning, IV access, and urgent ENT involvement; waiting for brisk bleeding is too late.
EM-focused review of post-tonsillectomy bleeding priorities: early ENT/anesthesia involvement, airway readiness, suction/positioning, IV access/resuscitation, and temporizing hemostatic measures such as topical or nebulized tranexamic acid.
Large pediatric database study relevant to analgesic choices after tonsillectomy, helping frame whether ketorolac exposure is associated with subsequent hemorrhage risk.
Yesterday’s Differential
The daily puzzle — from editions past
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
A 44-year-old woman treated with methadone and ondansetron becomes lightheaded, then briefly loses consciousness. The monitor shows a rapid wide-complex rhythm whose QRS axis appears to twist above and below the baseline. What’s the diagnosis, and the first move?
Check your answer
Torsades de Pointes. If pulseless or unstable, defibrillate. If perfusing, give magnesium sulfate 2 g IV, correct potassium/magnesium, stop QT-prolonging drugs, and consider overdrive pacing or isoproterenol for recurrent pause-dependent episodes.
From the June 18 edition
Today, three days ago: Phenylephrine. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
Infusion: 0.1–0.5 mcg/kg/min, titrate to MAP. Push-dose: commonly 50–200 mcg IV aliquots using institution-approved premixed concentration. Severe hypertension, ventricular tachycardia.
From the June 11 edition
A 72-year-old woman with a PEG tube placed 1 week ago develops fever, abdominal pain, and leakage around the tube shortly after tube feeds are restarted. She is tachycardic and has diffuse tenderness with guarding. What is the most appropriate next step?
AResume feeds at a slower rate and observe
BFlush the tube aggressively with warm water
CHold tube feeds, make the patient NPO, and obtain urgent imaging/consultation for possible intraperitoneal placement
DRemove the tube at bedside and replace it immediately
Reveal answer
Correct · C
Early after PEG placement, the tract is not mature, so dislodgement or malposition can lead to intraperitoneal feeding and peritonitis. The correct step is to stop feeds, keep the patient NPO, and urgently confirm position with imaging while involving GI/surgery.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
Journal Feed covers adenosine dosing for SVT, cath lab activation after OHCA ROSC, and calcium in whole blood resuscitation. The post Journal Feed Weekly Wrap-Up appeared first on emDocs .
In this episode, Sam Ashoo, MD and Dr. T.R. Eckler, MD discuss the April 2026 Emergency Medicine Practice article, Wide Complex Tachycardia in the Emergency Department: An Updated Approach to Diagnosis and Management . Introduction – 0:11 Article Overview – 2:02 Top 5 Bedside Steps – 7:54 Sodium Channel Blockade – 9:26 Hyperkalemia – 11:53 SVT with...
AHA Guidelines and some new studies strengthen the EMCrit recs for Sick PE management EMCrit Project by Scott Weingart, MD FCCM .
Pharmacology Corner
Two drugs for the shift
One antimicrobial and one other ED workhorse — selected daily, with sources and last-reviewed dates so every dose is cross-checkable.
Antimicrobial of the Day
Fosfomycin
Phosphonic acid urinary antibacterial
Indication
Single-dose treatment of uncomplicated cystitis, including many MDR uropathogens (ESBL-producing E. coli, VRE) in the lower urinary tract.
What’s your dose? — reveal dosing & cautions
ED Dose
3 g PO as a single dose, dissolved in water (sachet). Some complicated-cystitis regimens use 3 g q48–72h x3 doses.
Renal Adjustment
Single-dose cystitis generally does not require adjustment; limited data in advanced CKD.
Contraindications
Hypersensitivity to fosfomycin.
Interactions
Metoclopramide and other prokinetics reduce serum/urinary concentrations.
Monitoring
Clinical response; GI tolerance.
ED Pearl
A one-time 3 g sachet maximizes adherence and retains activity against many ESBL/MDR uropathogens — but it is a lower-UTI agent only and has no role in pyelonephritis.
Hyperkalemia intracellular shift with dextrose support, DKA/HHS insulin infusion after potassium assessment, and severe hyperglycemia protocols.
What’s your dose? — reveal dosing & cautions
ED Dose
Hyperkalemia: 5–10 units IV with dextrose unless already markedly hyperglycemic. DKA: 0.1 units/kg/h IV infusion after confirming K is adequate; some protocols omit bolus.
Renal Adjustment
Higher hypoglycemia risk in renal failure; consider lower hyperkalemia dose and prolonged glucose monitoring.
Contraindications
Hypoglycemia; DKA insulin should be delayed if K <3.3 mEq/L until potassium repletion begins.
Interactions
Beta-blockers mask hypoglycemia; other glucose-lowering drugs increase hypoglycemia risk.
Monitoring
Glucose q30–60 min after hyperkalemia therapy, potassium, anion gap/ketones in DKA, mental status.
ED Pearl
The dangerous part of insulin for hyperkalemia is delayed hypoglycemia after the ECG looks better — monitor glucose long enough, especially in renal failure.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Ischemia
Left Main Coronary Artery Occlusion / ST Elevation in aVR
Diffuse ST depression with ST elevation in aVR is global subendocardial ischemia until proven otherwise.
The Tracing
A 72-year-old man presents diaphoretic and hypotensive with chest pressure. The ECG does not meet classic STEMI criteria. Instead, it shows widespread horizontal ST depression in I, II, aVL, and V3 through V6 with 1.5 mm of ST elevation in aVR. He looks much sicker than the computer interpretation suggests.
Diffuse ST depression across multiple territories, often maximal in lateral precordial leads
ST elevation in aVR, sometimes also V1
Pattern suggests global subendocardial ischemia from left main, proximal LAD, severe triple-vessel disease, or supply-demand mismatch
Clinical instability, ongoing chest pain, or dynamic change increases concern for acute coronary occlusion or critical stenosis
May not meet classic STEMI criteria despite high-risk coronary anatomy
Pearls
aVR is not a trash lead. In the right pattern, it is the lead that tells you the whole heart is ischemic.
This pattern is not automatically left main occlusion, but it is automatically high-risk when paired with ACS symptoms or shock.
The differential includes severe anemia, hypoxia, hypotension, and tachydysrhythmia; treat supply-demand causes while involving cardiology.
Pitfalls
Do not call it NSTEMI-low-risk just because there is no regional ST elevation.
Do not overcall isolated aVR elevation without diffuse reciprocal depression and a fitting clinical picture.
Left main/prox LAD/triple-vessel physiology can deteriorate quickly; serial troponins alone are not the plan.
At the Bedside
Treat as high-risk ACS/global ischemia: resuscitate, correct supply-demand triggers, give ACS therapy per protocol, and obtain urgent cardiology consultation for possible emergent angiography.
For educational use only. Verify ECG interpretation against the LITFL entry and your institution’s practice before clinical decision-making.
Case of the Day
From the lead · Keratitis and Corneal Ulcers
Self-Examination
Test Your Understanding
A 24-year-old contact lens wearer presents with unilateral eye pain, photophobia, and decreased vision. Fluorescein staining shows a central corneal defect with stromal opacity. What is the best next step?
AReassure and discharge with lubricating drops
BStart topical fluoroquinolone and obtain urgent ophthalmology consultation
CPrescribe topical steroid drops and follow up in 1 week
DMeasure intraocular pressure and treat for angle-closure glaucoma
Reveal answer
Correct answer · B
This is infectious keratitis/corneal ulcer until proven otherwise, especially in a contact lens wearer with decreased vision and corneal opacity. The key is immediate topical antibiotic therapy and urgent ophthalmology; steroids can worsen infectious keratitis, and delays risk corneal perforation and vision loss.
Study Pace4 topics today; 92 remaining; Day 20 of 43Deadline · June 1, 2026