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Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights:
Credit: 12.5 AMA PRA Category 1 Credits™
Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
Acute is <2 weeks, persistent is 2–4 weeks, chronic is >30 days. Most acute diarrhea is self-limited and needs only supportive care.
Stool cultures are positive in only 2–6% of unselected patients. Yield rises with >4 stools/day and longer duration.
The ED job is not to name the organism. It is to find volume depletion, rule out the dangerous mimic, and decide who needs testing, antibiotics, or admission.
Don’t-Miss Mimics
Diarrhea is a symptom, not a diagnosis. In anyone who looks sick, gastroenteritis is a diagnosis of exclusion.
Abdominal catastrophes: mesenteric ischemia (pain out of proportion, vascular risk factors), early appendicitis, partial obstruction with overflow stool, diverticulitis.
Systemic disease presenting through the gut: sepsis from another source, DKA, adrenal insufficiency.
Fulminant C. diff or toxic megacolon: distension, fever, tachycardia, peritonitis. The diarrhea may actually stop as the colon dilates.
GI bleeding masquerading as dark diarrhea, and in women of childbearing age, ectopic pregnancy.
History & Exam
Duration, frequency, and appearance. Watery and high-volume suggests small bowel. Small, painful, frequent stools suggest colon.
Exam: volume status plus a real abdominal exam. A soft belly does not end the evaluation.
Who Gets Testing
Ask first whether the result will change anything. If the patient is going home on supportive care, a stool study often just generates a callback.
Test when the patient is likely to be admitted or is higher risk: febrile, hypovolemic, elderly (roughly >70), known cardiac disease, immunocompromised, IBD, or pregnant.
Bloodwork is not routine. Send a BMP and CBC for significant hypovolemia, persistent vomiting, bloody stool, or the elderly and comorbid.
Routine cultures cover Salmonella, Campylobacter, Shigella. Ask the lab specifically for Vibrio, Yersinia, Aeromonas, or Listeria.
Know your multiplex GI PCR panel. At many shops it already includes C. diff, so ordering it separately is redundant. One call to your lab settles this.
Bloody diarrhea plus anemia, thrombocytopenia, or a rising creatinine → think HUS, especially in young children.
Antibiotics or hospitalization within 3 months → C. diff moves up the differential.
Neutropenic patient on active chemotherapy → consider typhlitis (enterocolitis of the cecum).
CT only for peritoneal signs or focal tenderness. It is not part of the routine workup.
Management
Oral rehydration solution is the mainstay for anyone tolerating PO — water, salt, sugar. Preferred over sports drinks and flavored electrolyte powders, which are not ORS-formulated. A commercial ORS packet is ideal, and the home recipe works when you do not have one. One liter of water, six level teaspoons of sugar, half a teaspoon of salt.
IV fluids for severe hypovolemia, intractable vomiting, or if labs are being drawn anyway.
Most non-bloody, non-traveler’s diarrhea does not need antibiotics.
Suspected Shiga toxin E. coli: no antibiotics. Lysing the organism releases toxin and raises HUS risk.
When empiric coverage is warranted: azithromycin for severe inflammatory diarrhea, fever, dysentery risk, or fluoroquinolone resistance. Otherwise cipro or levofloxacin, and IV ceftriaxone if PO is not tolerated.
Traveler’s diarrhea: most cases are self-limited. Reserve antibiotics for moderate to severe illness, and reach for azithromycin given widespread quinolone resistance in South and Southeast Asia.
Confirmed C. diff: oral vancomycin 125 mg four times daily for 10 days, or fidaxomicin. Stop the inciting antibiotic where you can.
Loperamide: generally avoid. If diarrhea is mild and the patient is afebrile, let it run.
Bismuth subsalicylate is an option — avoid in younger patients (Reye’s syndrome) and in salicylate allergy or intolerance.
Diet: eat what is tolerated. Early refeeding is fine and BRAT is not required. Dairy can transiently make things worse. Probiotics are unlikely to change the course.
Disposition
Set expectations: we often never identify the organism, and in a stable acute patient there is no routine test and no routine cure.
Food handlers and healthcare workers may need occupational clearance before returning to work.
Return precautions: bloody stools, fever, falling urine output, or an inability to keep fluids down.
No improvement past 1–2 weeks warrants re-evaluation for parasitic or non-infectious causes, including IBD.
Cyclospora
Protozoan with no person-to-person spread — transmission is poop to produce to person. Humans are the only natural host.
Oocysts need days to weeks to sporulate, so long-shelf-life produce is the culprit: berries, basil, cilantro, and leafy greens.
Incubation is about a week. Presents as watery, explosive diarrhea, typically non-bloody and afebrile.
Untreated, it drags on for weeks and tends to relapse, often with profound fatigue, anorexia, and weight loss.
Included on many multiplex GI PCR panels. Microscopy requires a special stain or it will be missed.
Treatment is Bactrim (TMP-SMX), one DS tablet twice daily for 7–10 days, which disrupts the parasite’s folate synthesis. Azithromycin does not cover Cyclospora — this is the exception to the usual workhorse. Ciprofloxacin is the fallback for sulfa allergy, and it is less effective.
Washing produce does not kill it. Only heat does.
Take Home Points
Most acute diarrhea is self-limited. If the patient tolerates PO, is afebrile, and the course is short, supportive care and discharge is the right answer.
Before you call it gastroenteritis, make sure it is not mesenteric ischemia, DKA, or a surgical abdomen.
Bloody diarrhea with concern for Shiga toxin gets no antibiotics.
For Cyclospora, wash and cook your produce — and remember it is Bactrim, not azithro.
Group A strep = Streptococcus pyogenes — gram-positive organism that colonizes the pharynx, but also the perianal and genital mucosa (worth remembering when the source isn’t the throat).
Extremely common. The episode cites an estimated ~289 million cases/yr of strep pharyngitis in children 5–14 (NIH). For a U.S.-specific, verifiable anchor: the CDC estimates strep throat drives ~5.2 million outpatient visits/yr in people <65.
No true beta-lactam resistance. GAS remains uniformly susceptible to penicillin and amoxicillin. Note this is not true for macrolides/clindamycin — roughly 1 in 3 invasive isolates are now erythromycin/clindamycin resistant.
Pathophysiology — the throughline
Exotoxins (superantigens) tie the whole spectrum together — they drive scarlet fever, streptococcal toxic shock syndrome (STSS), and are implicated in the Kawasaki overlap discussed below.
The organism is the same from a sore throat to a life-threat; what changes is host response and toxin burden.
Scarlet fever — fine, sandpapery rash, typically starts on the trunk and spreads outward; later desquamation of the fingers and toes.
Extrapharyngeal clues: kids commonly present with abdominal pain or headacheeven when the throat looks unimpressive. Low threshold to test with fever + abd pain or fever + headache.
Rapid PCR — high sensitivity and specificity; increasingly the front-line test.
Rapid antigen detection test (RADT) — highly specific but less sensitive. Per IDSA, a negative RADT in a child/adolescent should be backed up with a throat culture (culture is the more sensitive gold standard). Backup culture is not required in adults.
Who not to test
Generally don’t test/treat children <3 — acute rheumatic fever is rare in this group.
Exception: the symptomatic young child with a close contact recently diagnosed with strep.
Management
First-line: amoxicillin 50 mg/kg once daily, max 1 g/dose. GAS stays beta-lactam susceptible (penicillin and amoxicillin remain treatments of choice per IDSA 2012).
IM penicillin G / benzathine (bicillin) for kids who can’t tolerate oral meds — one shot, done.
Return to school: after one full day of treatment (~12–24 h), provided afebrile and feeling well.
Contact prophylaxis:
Pharyngitis — routine prophylaxis of asymptomatic contacts is not standard; consider it for households with recurrent infection or a history of rheumatic fever.
Invasive GAS — more aggressive. Prophylaxis is recommended for household contacts who are immunosuppressed, pregnant, post-recent-surgery, or have an open wound (CDC).
The Bounce-Back / Treatment Failure
The kid who finishes amox and is back a week later. Sort into three buckets:
Chronic carrier — GAS carriage in children runs 2–20%. Carriers test positive but are asymptomatic, with low risk of transmission or complications. Don’t chase them.
New infection.
True treatment failure → ask why:
The shield effect — the throat is co-colonized with beta-lactamase producers (Staph aureus, H. influenzae, Moraxella) that degrade amoxicillin before it can act, effectively shielding the GAS.
This is NOT true resistance — the strep is still beta-lactam susceptible; the neighbors are the problem.
Fix: switch to a beta-lactamase–stable agent — amoxicillin-clavulanate or a first-generation cephalosporin.
Post-infectious glomerulonephritis (PIGN) — several weeks out; hematuria / “Coca-Cola” urine. Note strep impetigo can also seed PIGN.
The pearl: we treat strep to prevent rheumatic fever — but treatment does NOT prevent PIGN.
Invasive Group A Strep (iGAS)
Why it’s on the radar
Rates have been climbing since 2014, and preliminary 2023 data hit a 20-year high (CDC). A CDC/ABCs analysis flagged a roughly 3-fold pediatric increase in Colorado/Minnesota in late 2022 (MMWR).
Keep it in mind when a child isn’t following the typical strep course or just looks sicker than expected.
Increasingly common and worth highlighting: bone and joint disease — septic arthritis, osteomyelitis — often traveling with pyomyositis.
The trap — nonspecific early presentation
Symptoms are often nonspecific: fever, “not acting like themselves,” localized pain.
Septic joint/osteo may show a limp or focal pain — but not always.
When your gut fires, cast a wide net.
Workup
Blood cultures, CBC, chemistries, CRP, ESR.
Imaging — tailor to the suspected site:
Suspected joint → start with X-ray + ultrasound.
Worried about osteomyelitis or pyomyositis → MRI (the recommended modality for pyomyositis per IDSA SSTI).
Management
Broad-spectrum: vancomycin + piperacillin-tazobactam (concordant with IDSA SSTI).
In shock / STSS: ADD clindamycin or linezolid for toxin suppression — this is on top of vanc/zosyn, not a coverage swap. (IDSA: penicillin plus clindamycin for documented GAS necrotizing infection; consider IVIG in STSS.)
The Kawasaki overlap
Meaningful overlap between iGAS and Kawasaki disease.
Proposed mechanism: strep superantigens activate a shared inflammatory (T-cell) pathway that may contribute to KD; some data suggest kids with iGAS may be at higher risk of developing Kawasaki.
Get rheumatology involved early — they’ll want those inflammatory markers and can help sort KD from mimics.
Take-Home Points
Adult tools don’t translate to peds. Centor was built for ≥16 and is unreliable in young kids — diagnose on exam, the eponyms, and testing. Low threshold to swab the febrile kid with abdominal pain or headache.
The bounce-back is a triage problem — carrier (2–20%) vs. new infection vs. true failure. True failure is usually the shield effect (beta-lactamase co-colonizers, not resistance) → switch to amox-clav or a first-gen cephalosporin.
Treatment prevents rheumatic fever, NOT PIGN — and impetigo can cause PIGN too.
iGAS is rising and hides behind nonspecific symptoms. When your gut fires, work it up broadly and escalate to MRI for osteo/pyomyositis. Treat with vanc + pip-tazo, and in shock add clindamycin/linezolid for toxin suppression. Keep Kawasaki in the differential and call rheum early.
Shulman ST, et al. Clinical Practice Guideline for the Diagnosis and Management of Group A Streptococcal Pharyngitis: 2012 Update. IDSA / Clin Infect Dis. 2012;55(10):e86–e102. — IDSA · Full text
Stevens DL, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update. IDSA / Clin Infect Dis. 2014;59(2):e10–e52. (necrotizing infection, STSS, clindamycin adjunct, MRI for pyomyositis) — IDSA · Full text
Gewitz MH, et al. Revision of the Jones Criteria for the Diagnosis of Acute Rheumatic Fever in the Era of Doppler Echocardiography. AHA / Circulation. 2015;131:1806–1818. — Circulation · ACC “10 Points to Remember”
Lifetime incidence parameters hover around 1 in 11, presenting with a prominent male sex skew.
Peak demographic manifestation concentrated within the 30–60 age band.
High-yield temporal parameter: 50% recurrence vector within a 5-year post-initial-insult window.
Mineralogical Composition Vectors
Calcium oxalate crystals represent the predominant structural matrix.
Struvite configurations (magnesium ammonium phosphate matrix) account for 1–2% of cohorts.
Struvite stones function explicitly as infection-driven configurations secondary to upper tract proliferation; higher distribution index noted in female cohorts.
Etiological & Modifiable Relational Dynamics
Profound systemic dehydration or low baseline fluid throughput states.
High-sodium diet structures and heavy animal-protein consumption loads.
Positive genetic/familial history variables.
Relative risk modulation: Each variable independently operates to expand baseline risk by a factor of 2x to 3x.
Distinctive behavioral marker: Renal colic pacing/writhing behavior with zero antalgic position availability.
Concomitant autonomic triggers: Nausea and emesis manifest in 50% of acute presentations.
Physical Exam Discordance Metrics
Severe subjective distress contrasted with a characteristically soft, completely non-tender abdominal palpation exam.
CVA tenderness is completely variable and lacks reliable negative predictive value.
Atypical Presentation Classifications
Vague, poorly localized abdominal pain presentations occurring in up to 20% of active cases.
Isolated lower urinary tract irritative signs including acute frequency or severe urgency.
Incidental & Asymptomatic Dynamics
Silent intrarenal or ureteral stones found incidentally.
Longitudinal tracking demonstrates up to 33.3% of initially asymptomatic cohorts convert to fully symptomatic renal colic within a multi-year tracking window.
2. EXCLUSION DIAGNOSES & CRITICAL PATHWAY RED FLAGS
Vascular Mimics: AAA rupture/expansion. This is a mandatory exclusion pathway in elderly cohorts presenting with acute flank or back pain. Physical tracking requires active exploration for an expansile, pulsatile abdominal mass.
Gynecologic Emergencies: Ruptured ectopic pregnancy. Demands universal screening protocols via rapid beta-hCG testing in all female patients of childbearing potential presenting with lower abdominal/pelvic localization.
Infectious Upper Tract Decompensation: Acute uncomplicated pyelonephritis. Differentiated via persistent high spikes, high fevers, systemic shaking chills, and profound pyuria.
Genitourinary Structural Crises: Acute testicular torsion. Mandates a thorough, explicit scrotal/testicular structural exam if the flank pain radiates into the scrotum.
Gastrointestinal and Adnexal Torsional Confounds: Acute appendicitis variants, acute mesenteric/bowel ischemia, and ovarian torsion syndromes.
3. LABORATORY TESTING & PHYSIOLOGIC EVALUATION
Urinalysis Interpretation Nuances
Microscopic or gross hematuria presents in approximately 66% to 90% of acute cases.
Critical Pathological Caveat: Complete absence of hematuria documented in 20% to 33.3% of confirmed, acute obstructing ureteral stones.
Diagnostic rule: A pristine urinalysis with zero red blood cells is entirely insufficient to exclude acute ureterolithiasis.
Urinary pH as a Composition Clue
Consistently low urinary pH parameters (pH < 5.5) point strongly toward a uric acid crystalline composition.
Elevated urinary pH parameters (pH > 7.5) indicate the presence of urease-producing microbial pathogens, pointing toward a struvite infection stone.
Infectious Screening Metrics
Active tracking for marked pyuria, positive leukocyte esterase, and bacterial nitrites to rule out an obstructed, infected upper urinary tract system.
BMP
Immediate quantification of baseline serum creatinine to establish accurate eGFR values.
Targeting detection of post-renal AKI from bilateral obstruction, unilateral obstruction in a single functioning kidney, or severe volume depletion.
CBC
Evaluation for marked leukocytosis.
Physiologic Nuance: Mild-to-moderate white blood cell count elevations frequently represent non-specific stress demargination driven by severe pain and repetitive vomiting.
High-grade white blood cell shifts demand immediate exclusion of systemic bacteremia or an infected, obstructed urinary system.
Adjunctive Lab Pathways
Rapid qualitative urine hCG testing.
Reflex urine culture execution whenever urinalysis metrics display significant inflammatory profiles or clinical suspicion of UTI is high.
Gold standard; diagnostic sensitivity and specificity parameters exceed 95% for stones >2 mm.
Provides precise quantification of stone diameter (mm), exact localization (proximal, mid, or distal ureter), and degree of secondary hydronephrosis.
Excellent structural visualization for detecting or ruling out alternate retroperitoneal, vascular, or intra-abdominal pathologies.
Contrast-Enhanced CT Protocols
Indicated when alternative intra-abdominal surgical pathology is highly suspected over isolated renal colic.
Retains diagnostic capability to identify urinary tract stones >3 mm even within contrast-enhanced phases.
NCCT Structural Architecture Limitations
Standard stone protocol CT scans are executed in a prone position without IV contrast enhancement. It does not opacify the ureteral lumen.
Presents a cumulative radiation exposure penalty when utilized serially across recurrent ED presentations.
POCUS / Radiology Ultrasound
Direct stone visualization capabilities are modest, operating at approximately 50% to 60% sensitivity, and is highly dependent on anatomical positioning at the extreme proximal ureter or the UVJ.
Secondary obstruction tracking: Demonstration of hydronephrosis operates at a high sensitivity of approximately 80%.
POCUS Clinical Utility Metrics
Eliminates ionizing radiation exposure and allows immediate, rapid real-time execution directly at the patient’s bedside.
Confirmation of significant hydronephrosis within a classic clinical presentation yields high post-test probability for stone presence while lowering suspicion for vascular catastrophes like a AAA.
KUB Radiography
Extremely poor overall diagnostic sensitivity, hovering around 57%.
Fails to image radiolucent configurations (pure uric acid matrices) or small stones measuring <5 mm.
Avoided in acute ED diagnostic pathways; selectively considered as a low-radiation tracking step in pediatric cohorts or pregnant populations.
Large-scale multi-center randomized controlled trial assessing POCUS first vs. Radiology US first vs. NCCT first pathways in acute ED cohorts.
Primary Clinical Outcomes
No statistically significant variations in missed high-risk alternative diagnoses (AAA, appendicitis, bowel ischemia, or adnexal torsion rates remained rare at ~0.4%).
No differences noted in serious adverse event rates, subjective pain-control scores, return ED visits, or overall hospitalization frequencies.
Radiation Modulation Impact
An ultrasound-first initial strategy reduced cumulative, downstream radiation exposure by approximately 50%.
Algorithmic Selection Guidelines
Establishes the clinical premise that raw diagnostic sensitivity does not automatically equate to superior clinical utility or better patient outcomes.
An ultrasound-first diagnostic pathway paired with selective escalation to NCCT is safe and indicated for recurrent, young, clinically stable cohorts.
6. IMAGING SELECTION MATRIX
Indications Favoring an Ultrasound-First Approach
Age parameters <35 years to mitigate lifetime cumulative radiation risks.
Confirmed, well-documented history of recurrent nephrolithiasis presenting with identical symptoms to prior events.
Hemodynamic stability paired with reassuring, classic clinical tracking.
Indications Favoring Immediate NCCT Imaging
Advanced age parameters.
First-time presentation with zero history of stone disease.
Atypical clinical presentation or diagnostic uncertainty.
Persistent, unmitigated symptoms refractory to standard ED interventions.
High pre-test probability of immediate surgical or urological decompression.
7. EMERGENCY PHARMACOTHERAPY & COLIC MANAGEMENT
First-Line Analgesic Paradigms
NSAIDs: Specifically Ketorolac (Toradol) titrated at 15–30 mg.
High-Yield Data Marker: Multiple trials confirm IV NSAIDs provide equivalent pain reduction scores to titrated IV opioids in acute renal colic.
Mechanism: Targets localized ureteral smooth muscle spasms and downregulates prostaglandin-mediated hyper-filtration and local tissue inflammation.
NSAID Absolute/Relative Contraindications
Significantly depressed GFR or active acute renal failure states.
Active gastrointestinal hemorrhage risks or history of severe peptic ulcerations.
Third-trimester pregnancy.
Second-Line Analgesic Titration
Intermittent titration of IV opioids (e.g., Morphine) indicated if the NSAID maximum ceiling effect is reached or if explicit contraindications prevent NSAID administration.
Antiemetic Adjuvant Therapy
Concomitant use of Ondansetron (Zofran) to manage reflex nausea and vomit-induced dehydration.
Fluid Resuscitation Realities
Targeted IV fluids to correct explicit volume deficits driven by emesis or reduced oral intake.
Physiologic Caveat: Aggressive, high-volume fluid hydration does not accelerate stone transit speed or improve the spontaneous passage rate.
8. MEDICAL EXPULSIVE THERAPY (MET) CLINICAL PARAMETERS
Pharmacologic Agent
Tamsulosin (Flomax) dosed at 0.4 mg orally once daily for a maximum duration of 28 days.
Target Efficacy Window
Highly specific for distal ureteral stones measuring between 5 mm and 10 mm.
Yields modest improvements in spontaneous clearance rates within this specific size band.
Literature Controversies
A 2015 Lancet randomized controlled trial demonstrated neutral primary endpoints.
Subsequent large-scale meta-analyses and network meta-analyses identify a significant signal for benefit, particularly for combinations.
Stones Measuring <5 mm
MET is generally not indicated or cost-effective.
Spontaneous passage rates are high, making the side effect profile of alpha-blockade unjustifiable.
Side Effect Profile
Orthostatic hypotension, transient dizziness, and retrograde ejaculation.
Obstructed Urinary Tract + Concomitant Infection: Co-existence of an obstructing stone and upper tract infection (fever, systemic chills, pyuria, nitrites, leukocytosis) is a urologic emergency. It carries a high risk for rapid progression to pyonephrosis, perinephric abscess, overwhelming urosepsis, and cardiovascular collapse. Requires emergent urologic consultation for surgical retrograde stent placement or percutaneous nephrostomy tube insertion.
Refractory Symptom Complexes
Intractable pain scores or persistent emesis failing aggressive ED parenteral therapies.
High-Risk Patient Anatomy / Physiology
Solitary functioning kidney or renal transplant anatomy presenting with acute obstruction (high risk for sudden anuric renal failure).
Complete clinical anuria.
High-grade, progressive acute kidney injury (AKI) that fails to stabilize following targeted volume resuscitation.
Acute obstructing ureterolithiasis manifesting within a pregnant patient.
High Structural Stone Burden
Stone diameter >10 mm. Spontaneous resolution is unlikely; needs shockwave lithotripsy, ureteroscopy, or specialized stenting.
Prolonged Structural Symptoms
Documented stone impaction or symptom tracking extending past a 4-week timeline without clear passage.
Pain score controlled with oral medications; tolerating adequate PO oral fluids; stable renal function panel; zero systemic or local signs of infection.
Outpatient Prescribing Packets
Scheduled or high-dose PRN oral NSAIDs plus short-course rescue oral opioids for breakthrough colic episodes.
Tamsulosin 0.4 mg once daily if stone localization is distal and diameter measures 5–10 mm.
Oral anti-emetics for home management.
Discharge Guidance and Counseling
Vigorous oral hydration to maintain constant, high volumetric urine throughput.
Provide a urine strainer to capture the stone matrix for metabolic and chemical composition testing.
Explicit Return Precautions
Instruct the patient to return to the ED for temperature spikes, shaking chills, or unmanageable pain spikes.
Instruct the patient to return for relentless vomiting preventing fluid retention.
Clinical Follow-up Tracking
Ensure structured outpatient urology follow-up within a 1- to 2-week window.
The Hematuria Diagnostic Confound: Up to 33% of patients with a confirmed obstructing stone will exhibit a completely normal urinalysis with zero RBCs. Never drop nephrolithiasis from the differential based on a negative dipstick.
Leukocytosis Interpretation: Severe colic and violent vomiting induce physiological demargination. Treat the overall clinical presentation and temperature curve; do not over-interpret an isolated WBC.
Hydrative Fluid Mechanics: Fluids address dehydration from emesis. Over-hydrating a patient in acute colic does not push the stone out faster and may worsen pain by increasing renal capsular hydrostatic pressure.
The 4-Week Functional Boundary: Ureteral obstruction lasting longer than 4 weeks requires specialized intervention to prevent permanent nephron damage.
Size and Anatomy Rules: A 3 mm stone at the UVJ passes spontaneously in ~90% of cases. An 11 mm stone in the proximal ureter has a <10% clearance rate and requires early urologic involvement.
Definition: Life-threatening hypermetabolic state resulting from decompensated thyrotoxicosis.
Hormonal Profile: Absolute levels of total T₄/T₃ often mirror uncomplicated thyrotoxicosis; storm is driven by rapid rate of rise, increased catecholamine sensitivity, or increased free T₄/T₃ concentrations.
Clinical Presentation:
Hyperpyrexia (e.g., 104.2°F)
Tachycardia/Arrhythmias (e.g., 155 bpm)
Altered Mentation: Agitation, delirium, or psychosis; often the primary differentiator between “storm” and “compensated” hyperthyroidism
Aggressive IV fluids; patients are often profoundly dehydrated
May require 3–5 liters of isotonic crystalloid per 24 hours
Take Home Points
I. Diagnostic Essentials
Clinical Diagnosis: Based on hyperpyrexia, cardiovascular dysfunction, and altered mentation.
Key Differentiator: Altered mentation (agitation, delirium, psychosis) is often the sole finding distinguishing “storm” from “compensated” thyrotoxicosis.
Burch-Wartofsky Point Scale (BWPS):
≥ 45: Highly suggestive of storm.
25–44: Suggests impending storm.
< 25: Storm unlikely.
Note: High sensitivity, low specificity (e.g., hyperthyroid + flu can score > 45).
Triggers: Infection, trauma, parturition, or abrupt cessation of antithyroid drugs.
II. The Four-Step Blocking Strategy
Beta Blockade (Propranolol):
Dose: 60–80 mg PO q4–6h or 0.5–1 mg IV over 10 min.
Action: Blocks symptoms and inhibits peripheral T4 to T3 conversion.
Caution: Avoid in acute decompensated heart failure with systolic dysfunction.
Thionamides (PTU):
Dose: 200 to 250 mg every four hours. (note: some resources suggest a loading dose beforehand)
Action: Preferred over methimazole; blocks new hormone synthesis and peripheral T4 to T3 conversion.
Iodine (SSKI/Lugol’s):
Timing: Must wait ≥ 60 minutes AFTER thionamide dose.
Action: Blocks hormone release.
Pitfall: Early iodine provides substrate for new hormone synthesis, worsening the condition.
Glucocorticoids (Hydrocortisone):
Dose: 300 mg IV load, then 100 mg IV q8h.
Action: Blocks conversion and provides adrenal support.
III. Critical Supportive Care
Hyperpyrexia: Use Acetaminophen.
NEVER Use Aspirin: Displaces thyroid hormone from binding proteins, acutely increasing free T4/T3 levels.
Volume: Aggressive fluid resuscitation; patients may require 3–5 L/day due to profound dehydration.
Definition: Systemic toxicity secondary to local anesthetic (LA) via accidental intravascular injection or excessive systemic absorption.
Threshold: Occurs when plasma concentration exceeds the safety threshold for cardiac and neural tissue.
Agent Profile: Bupivacaine (High Risk)
Highly lipophilic with high protein binding.
“Fast-on, Slow-off” Kinetics: Strong Na+ channel binding with extremely slow dissociation during diastole.
Myocardial Depression: Direct inhibition of Ca2+ release from the sarcoplasmic reticulum, impairing contractility.
Low CC:CNS Ratio: The dose required for cardiac collapse is very close to the dose that triggers seizures (narrow safety margin).
Contributing Factors:
Acidosis/Hypercapnia: Increases the fraction of free drug and promotes ion trapping in the brain/heart; shifts the LA-binding curve toward higher toxicity.
Hypoxemia: Exacerbates myocardial depression and lowers seizure threshold.
II. Risk Assessment & Prevention
Patient-Specific Risk Factors
Extremes of Age: Neonates (low α-1-acid glycoprotein) and elderly (reduced clearance).
Body Composition: Low muscle mass/frailty (decreased volume of distribution).
Organ Dysfunction:
Hepatic: Reduced metabolism of amide LAs.
Renal: Accumulation of metabolites; risk of metabolic acidosis lowering seizure threshold.
Cardiac: Reduced cardiac output slows hepatic delivery/clearance; heart failure patients are more sensitive to Na+ channel blockade.
Pregnancy: Increased sensitivity to cardiotoxicity.
Procedural Risk Factors
Vascularity of Site (Highest to Lowest Risk):
Intercostal blocks (highest absorption rate).
Caudal/Epidural.
Interfascial plane blocks (e.g., TAP block).
Psoas compartment/Sciatic.
Brachial plexus.
Technique: Large volume infiltration, lack of ultrasound, lack of incremental injection.
Prevention Mandates
Weight-Based Dosing:
Lidocaine (Plain): Max 4.5 mg/kg.
Lidocaine (with Epi): Max 7 mg/kg.
Bupivacaine: Max 2.5–3 mg/kg.
Incremental Injection: 3–5 mL aliquots with frequent aspiration.
Intravascular Marker: Use Epinephrine (1:200,000) to detect accidental IV placement (HR increase >10 bpmor SBP increase >15 mmHg).
III. Clinical Presentation
Neurologic Phase (Early to Late)
Unexpected Agitation: In a patient who just received a block, don’t assume “anxiety.”
Wide QRS: Any widening of the QRS complex post-injection is LAST until proven otherwise.
Refractory Arrest: Standard ACLS failing in a patient who received LA. Lipid must be given.
Critical Note: LAST is a clinical diagnosis. Do not wait for serum lidocaine levels or laboratory confirmation to initiate Lipid Emulsion Therapy. Immediate correction of pH and PaCO2 is as vital as the lipid itself.
Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.
Course Highlights:
Credit: 12.5 AMA PRA Category 1 Credits™
Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.
Course Highlights:
Credit: 12.5 AMA PRA Category 1 Credits™
Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
High-Risk Period: Rearrest rates reach 30% within the first minutes post-ROSC.
Shock Incidence: Two-thirds of patients develop profound hypotension/shock as initial resuscitative efforts subside.
Catecholamine Washout: Super-physiologic “code-dose” epinephrine (1mg IV) typically wears off within ~3 minutes post-ROSC, leading to predictable hemodynamic collapse.
Diagnostic Yield: 50% for clinically significant findings (causes or consequences of arrest).
Contrast Risk: Negligible (1–2% increase in AKI risk) compared to the high diagnostic utility.
Avoid Anchoring: Do not assume ischemic EKG changes are the cause; they are frequently a consequence of the global arrest-induced ischemia.
III. Hemodynamic & Respiratory Targets
Mean Arterial Pressure (MAP)
Autoregulation Shift: In acute brain injury/post-arrest, the lower limit of cerebral autoregulation shifts right, often requiring MAPs of 110–120 mmHg for adequate perfusion.
Clinical Target: Aim for MAP >80 mmHg.
The BOX Trial Nuance: While the BOX trial showed no difference between MAP 63 vs. 77, its cohort (Denmark) had exceptionally high survival rates (70% back to work) and short response times, which may not generalize to North American populations with lower shockable rhythm incidence.
Permissive Hypertension: If the patient is “self-driving” to higher pressures, do not aggressively lower them, as this may be a physiologic demand for cerebral blood flow.
Ventilation and Oxygenation
PaCO2 Management:
Target: High-normal to slightly hypercarbic (45–55 mmHg).
Rationale: Avoid accidental hyperventilation (PaCO2 <30), which can cut cerebral blood flow by 50%.
PaO2 Management: Maintain normoxia; avoid extreme hyperoxia, though trial data (BOX trial) suggests small variances (70 vs 90 mmHg) are likely neutral.
IV. Neurological Prognostication & Communication
The “Stunned” Brain
Anoxic Depolarization: Occurs within ~2 minutes of pulselessness as ATP-dependent ion pumps fail.
Clinical Pitfall: Early neurological exams (absent pupils, no motor response) are unreliable in the first hours as they reflect global neuronal “stunning” rather than definitive permanent injury.
Time Horizon: Meaningful recovery is measured in days/weeks, not minutes/hours.
Family Engagement
Presence: Bring family to the bedside immediately, including during procedures or continued resuscitation.
Psychological Impact: Significantly reduces PTSD, anxiety, and depression in survivors’ families.
Prognostic Honesty: Explicitly state “I don’t know” regarding etiology and outcome.
Framing: Define “No News” as the best possible early outcome (preventing rearrest and stabilization).
Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.
Course Highlights:
Credit: 12.5 AMA PRA Category 1 Credits™
Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
Clinical Evolution: Initial assessment noted cachexia and a large ventral hernia. Following initial workup, the patient became acutely altered (A&O x0) and febrile to 102.9°F.
Physical Exam Findings:
Brudzinski Sign: Positive (knees flexed upward upon passive neck flexion).
Kernig Sign: Discussed as highly specific (resistance/pain during knee extension with hip flexed at 90°).
Meningeal Triad: Fever, nuchal rigidity, and AMS (present in 40% of cases; 95% of patients have at least two of the four cardinal symptoms including headache).
Imaging:
Chest X-ray: Scattered opacities (pneumonia) and a small pneumothorax.
CT Abdomen/Pelvis: Confirmed asplenia (secondary to 2011 GSW/exploratory laparotomy).
Head CT: Ventricle enlargement concerning for obstructive hydrocephalus and diffuse sulcal effacement.
CSF Analysis & Microbiology
Bacterial Meningitis
Opening Pressure: Elevated (Normal is <170 mm H2O).
Color: Cloudy or turbid.
Gram Stain: Positive in 60%–80% of cases before antibiotics; drops to 7%–41% after antibiotics.
Cell Count: Very high (>1000–2000/mm3 WBC); dominated by neutrophils (>80% PMN).
Glucose: Low (<40 mg/dL); CSF/blood glucose ratio is <0.3–0.4.
Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.
Course Highlights:
Credit: 12.5 AMA PRA Category 1 Credits™
Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is characterized by a sudden, massive sympathetic surge leading to intense vasoconstriction and a precipitous rise in afterload.
Pathophysiology: Unlike HFrEF, these patients are often euvolemic or even hypovolemic. The primary issue is fluid maldistribution (fluid shifting from the vasculature into the lungs) due to extreme afterload.
Bedside Diagnosis: POCUS vs. CXR
POCUS is the gold standard for rapid bedside diagnosis.
Lung Ultrasound: Look for diffuse B-lines (≥3 in ≥2 bilateral zones).
Cardiac: Assess LV function and check for pericardial effusion.
Why not CXR? A meta-analysis shows LUS has a sensitivity of ~88% and specificity of ~90%, whereas CXR sensitivity is only ~73%. Importantly, up to 20% of patients with decompensated HF will have a normal CXR.
Management Strategy
1. NIPPV (CPAP or BiPAP)
Start NIPPV immediately to reduce preload/afterload and recruit alveoli.
Settings: CPAP 5–8 cm H₂O or BiPAP 10/5 cm H₂O. Escalate EPAP quickly but keep pressures to avoid gastric insufflation.
The goal is to drop SBP to < 140–160 mmHg within minutes.
No IV Access: 3–5 SL tabs (0.4 mg each) simultaneously.
IV Bolus: 500–1000 mcg over 2 minutes.
IV Infusion: Start at 100–200 mcg/min; titrate up rapidly (doses > 800 mcg/min may be required).
Safety: ACEP policy supports high-dose NTG as both safe and effective for hypertensive HF. Use a dedicated line/short tubing to prevent adsorption issues.
3. Refractory Hypertension
If SBP remains > 160 mmHg despite NIPPV and aggressive NTG, add a second vasodilator:
Clevidipine: Ultra-short-acting calcium channel blocker (titratable and rapid).
Nicardipine: Effective alternative for rapid BP control.
Enalaprilat: Consider if the above are unavailable.
Troubleshooting & Pitfalls
The “Mask Intolerant” Patient
Hypoxia is the primary driver of agitation. NIPPV is the best sedative. * Pharmacology: If needed, use small doses of benzodiazepines (Midazolam 0.5–1 mg IV).
AVOID Morphine: Data suggests higher rates of adverse events, invasive ventilation, and mortality. A 2022 RCT was halted early due to harm in the morphine arm (43% adverse events vs. 18% with midazolam).
The Role of Diuretics
In SCAPE, diuretics are not first-line.
The problem is redistribution, not volume excess. Diuretics will not help in the first 15–30 minutes and may worsen kidney function in a (relatively) hypovolemic patient.
Delay Diuretics until the patient is stabilized and clear systemic volume overload (edema, weight gain) is confirmed.
Disposition
Admission: Typically requires CCU/ICU for ongoing NIPPV and titration of vasoactive infusions.
Weaning: As BP normalizes and work of breathing improves, infusions and NIPPV can be gradually tapered.
Take-Home Points
Recognize SCAPE: Hyperacute dyspnea + severe HTN. Trust your POCUS (B-lines) over a “clear” CXR.
NIPPV Immediately: Don’t wait. It saves lives and prevents tubes.
High-Dose NTG: Use boluses to “catch up” to the sympathetic surge. Don’t fear the dose.
Avoid Morphine: Use small doses of benzos if the patient is struggling with the mask.
Lasix Later: Prioritize afterload reduction over diuresis in the hyperacute phase.
Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.
Course Highlights:
Credit: 12.5 AMA PRA Category 1 Credits™
Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
It typically affects infants <1 year of age and is characterized by a sudden, brief, and now resolved episode of one or more of the following:
Cyanosis or pallor
Irregular, absent, or decreased breathing
Marked change in tone (hypertonia or hypotonia)
Altered level of responsiveness
Crucial Caveat: BRUE is a diagnosis of exclusion. If the history and physical exam reveal a specific cause (e.g., reflux, seizure, infection), it is not a BRUE.
Risk Stratification: Low Risk vs. High Risk
Risk stratification is the most important step in management. While only 6-15% of cases meet strict “Low Risk” criteria, identifying these patients allows us to avoid unnecessary invasive testing.
Low Risk Criteria
To be considered Low Risk, the infant must meet ALL of the following:
Age: > 60 days old
Gestational Age: GA > 32 weeks (and Post-Conceptional Age > 45 weeks)
Frequency: This is the first episode
Duration: Lasted < 1 minute
Intervention: No CPR performed by a trained professional
Clinical Picture: Reassuring history and physical exam
Management for Low Risk:
Generally do not require extensive testing or admission.
The Threat: Marburg Virus Disease is from the same family as Ebola and has historically had a reported fatality rate as high as 90%.
The Outbreak (Sept. 2024): Rwanda declared an MVD outbreak. The initial cases involved a miner, his pregnant wife (who fell ill and died after having a baby), and the baby (who also died).
Healthcare Worker Impact: The wife was treated at an epicenter hospital. Eight HCWs were exposed to a nurse who was coding in the ICU; all eight developed symptoms, tested positive within a week, and four of them died.
The Turning Point: The outbreak happened in city referral hospitals where advanced medical interventions (dialysis, mechanical ventilation) were available.
Rapid Therapeutics Access: Within 10 days of identifying Marburg, novel therapies (experimental drugs and monoclonal antibodies) and an experimental vaccine were made available through diplomacy with the US government/CDC and agencies like WHO, Africa CDC, CEPI and more.
The Outcome: This coordinated effort—combining therapeutics, widespread testing, and years of investment in a resilient healthcare system—helped curb the fatality rate down to 23%.
Barriers and Enablers in Outbreak Preparedness
Fragmented Systems: Emergency and surveillance functions often operate in silos, leading to delayed or missed outbreak identification (e.g., inconsistent travel screening at JFK during early COVID-19 vs. African countries).
Solution: Empowering Emergency Departments and the community as the sentinel site can bridge this gap.
Limited Frontline Capacity and Protection: Clinicians are often undertrained and underprotected and are frequently not part of the decision-making for surveillance.
Weak Governance and Accountability: Unclear command structures and lack of feedback discourage early reporting.
Enabler: Strong governance and accountability in Rwanda helped contain the virus.
Dependence on External Programs: Many low-income countries rely on outside sources for vaccines and therapeutics, slowing response.
Solution: Invest in local production (e.g., Rwanda’s pre-outbreak investment in developing its own mRNA vaccines).
Lack of Resource-Smart Innovation: Gaps exist in things like integrating digital triage tools and surveillance systems.
Four Pillars of a Responsive and Equitable Emergency System
Workforce: Invest in pre-service and in-service training, mentorship, and fair compensation to ensure a skilled, protected, and motivated team.
Integration into the Health System: Emergency care (including pre-hospital services) must not operate in silos; it needs to be embedded in national health strategies and linked to surveillance, referral, and financing systems.
Equity in Design and Policy: The system must address the needs and protection of vulnerable groups and work closely with policymakers.
Data: Utilize real-time data and dashboards to provide a feedback loop between clinicians and policymakers, enabling tailored and innovative interventions.
Advice for Clinicians in Global Health Work
Start Small and Build Trust: Meaningful work requires humility and relationship over scale or visibility. Focus on local priorities and sustainable change through long-term partnership, not just presence. Avoid the “savior mindset”.
Be T-Shaped: Be deep in one specialty (e.g., EM) but fluent across other critical areas like policy, finance, and data, as these drive decision-making.
Focus on Knowledge Transfer: True impact means making yourself less essential over time. Prioritize mentorship, co-creation, and sharing leadership opportunities.
Looking Ahead: Global Threats Shaping the Next Decade
The future of EM will be shaped by the convergence of several complex challenges:
Climate and Environmental Crisis: Extreme heat, floods, and vector-borne illnesses will strain emergency systems.
Preparation: Invest in climate-resilient infrastructure for both EDs and the community.
Outbreaks and Biosecurity: Future outbreaks will emerge faster than current systems can handle, coupled with challenges from anti-microbial resistance.
Conflict, Displacement, and Urbanization: Mass migration and overcrowded cities will require new models of emergency care that are mobile, scalable, and inclusive.
Preparation: Building resilient healthcare systems ready for crisis mental health and cross-border coordination.
Digital Tools and AI: These can augment solutions, but investment is needed in data governance and ethical AI that preserves local control and adapts to local capacity.
Definition: Obstruction of pulmonary arteries, usually from a DVT in the proximal lower extremity veins (iliac/femoral), but may be tumor, air, or fat emboli.
Incidence & Mortality: 300,000–370,000 cases/year in the USA, with 60,000–100,000 deaths annually.
Mantra: “Don’t anchor on the obvious. Always risk stratify and resuscitate with precision.”
Risk Factors: Broad, including older age, inherited thrombophilias, malignancy, recent surgery/trauma, travel, smoking, hormonal use, and pregnancy.
Clinical Presentation and Risk Stratification
Presentation: Highly variable, showing up as anything from subtle shortness of breath to collapse.
Acute/Subacute:Dyspnea (most common), pleuritic chest pain, cough, hemoptysis, and syncope. Patients are likely tachycardic, tachypneic, hypoxemic on room air, and may have a low-grade fever.
Chronic: Can mimic acute symptoms or be totally asymptomatic.
Pulmonary Infarction Signs: Pleuritic pain, hemoptysis, and an effusion.
High-Risk Red Flags: Signs of hypotension (systolic blood pressure < 90 mmHg for over 15 minutes), requirement of vasopressors, or signs of shock → activate PERT team immediately.
History/Scoring: Ask about prior clots, recent surgeries, hospitalizations, travel. Use Wells/PERC criteria to assess pretest probability.
Labs:
D-dimer: A good test to rule out PE in a patient with low probability. If suspicion is high, proceed directly to imaging.
Troponin/BNP: Act as RV stress gauges. Elevated levels are associated with increased risk of a complicated clinical course (25-40%).
Lactate: Helpful in identifying patients in possible cardiogenic shock.
EKG: Most common finding is sinus tachycardia. Classic RV strain patterns (S1Q3T3, T-wave changes/inversions) are nonspecific.
Imaging:
CXR: Usually normal, but quick and essential to rule out other causes.
CTPA: The usual standard and gold standard for stable patients. High sensitivity (> 95%) and can detect RV enlargement/strain.
V/Q Scan: Option for patients with contraindications to contrast (e.g., severe contrast allergies).
POCUS (Point-of-Care Ultrasound): Useful adjunct for unstable patients.
Bedside Echo: Can show signs of RV strain (enlarged RV, McConnell sign).
Lower Extremity Ultrasound: Can identify a DVT in proximal leg veins.
Treatment & Management
Resuscitation (Reviving the RV):
Oxygenation: Give supplementally as needed (nasal cannula, non-rebreather, high flow).
Intubation:Avoid if possible; positive pressure ventilation can worsen RV dysfunction.
Fluids:Be judicious; even the smallest amount can worsen RV overload.
Vasopressors:Norepinephrine is preferred as first-line for hypotension/shock.
Anticoagulation (Start Immediately):
Initial choice is UFH or LMWH (Lovenox).
Lovenox is preferred for quicker time to therapeutic range, but is contraindicated in renal dysfunction, older age, or need for emergent procedures.
DOACs can be considered for stable, low-risk patients as an outpatient.
Escalation for High-Risk PE
Systemic Thrombolytics: Consider for very sick patients with shock/cardiac arrest (e.g., Alteplase 100 mg over two hours or a bolus in cardiac arrest). High risk of intracranial hemorrhage; weigh risks versus benefits.
PERT Activation: Engage multidisciplinary teams (usually including ICU, CT surgery, and interventional radiology).
Interventions: Consult specialists for catheter-directed thrombolysis or suction embolectomy. Surgical embolectomy can also be considered.
Bridge to Care: Activate the ECMO team early for unstable patients to buy valuable time.
Prognosis & Disposition
Mortality: Low risk < 1%; intermediate 3-15%; high risk 25-65%.
Complications: 3-4% of patients develop Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Others may have long-term RV dysfunction and chronic shortness of breath.
Recurrence: ∼ 30% chance in the next few weeks to months, if not treated correctly.
Disposition:
ICU: All high-risk and some intermediate-high risk patients.
Regular Floor: Intermediate-low risk patients.
Outpatient Discharge:Low-risk patients can be sent home on anticoagulation. Use PSI or HESTIA scores to risk stratify suitability, typically starting a DOAC.
Shared Decision-Making: Critical to ensure care is safe and consistent with the patient’s wishes.
Primary Goal: Distinguish benign musculoskeletal pain from serious pathology.
Red Flags: Look for indicators of spinal infection, spinal bleed, or space-occupying lesions (e.g., tumors, large herniated discs).
Assessment: A thorough history and neurological exam (strength testing, gait) is essential.
Additional Tools: Use bedside ultrasound for post-void residual assessment in suspected cauda equina syndrome
Imaging Guidelines:
Routine Imaging: Generally not indicated for young, healthy patients without red flags.
ACEP Recommendations: Avoid lumbar X-rays in patients under 50 without risk factors, as they do not change management and may increase costs and ED time.
Advanced Imaging: Reserve MRI for patients with red flags, neurological deficits, or suspected cauda equina syndrome; CRP may be a part of your calculus when evaluating for infectious causes of back pain
Treatment Options:
Evidence-Based First-Line:
NSAIDs offer modest benefit.
Skeletal muscle relaxants can be used but require caution due to side effects.
Ineffective Therapies:
Acetaminophen shows no benefit for back pain.
Steroids are not recommended for non-radicular pain, with only limited benefit in sciatica.
Topical treatments, lidocaine patches, and opioids are not supported by evidence and may pose additional risks.
Alternative and Experimental Interventions:
Nerve Blocks: Current evidence is limited; more research is needed on trigger point injections and erector spinae plane blocks.
Severe Pain Management:
A single opioid dose (preferably codeine or oral morphine) may be considered to facilitate discharge when necessary.
Use diazepam sparingly for immediate mobilization.
Onsite physical therapy in the ED can be beneficial when available.
Preventing Chronic Pain:
Research Focus: Ongoing studies are evaluating whether duloxetine (Cymbalta) can prevent the transition from acute to chronic back pain.
Non-Pharmacologic Measures: Consider spinal mobilization, physical therapy, acupuncture, and cognitive behavioral therapy (CBT) as adjuncts in management.
Take-Home Points:
Most acute back pain is benign, but watch for red flags like IV drug use, anticoagulation, or neurological symptoms (e.g., weakness, bladder dysfunction) that may indicate serious conditions like spinal infections, bleeds, or cord compression.
Avoid unnecessary lumbar X-rays in young, healthy patients without red flags—MRI is preferred only for those with risk factors, neurological deficits, or suspected cauda equina syndrome.
Use NSAIDs and skeletal muscle relaxants for acute musculoskeletal back pain, as they offer modest benefits. Avoid opioids, acetaminophen, and steroids for non-radicular pain, as they lack evidence.
For severe, uncontrolled pain, consider a single opioid dose (e.g., codeine) or diazepam sparingly
Encourage patients to engage in non-pharmacologic therapies like yoga, massage, or cognitive behavioral therapy to aid recovery and prevent chronic pain.
Historical Context: The conversation around allowing family members in the room during resuscitation events began gaining attention in 1987. Since then, the practice has been increasingly encouraged.
Current Practices in Pediatrics:
Family presence during pediatric resuscitations remains inconsistent, with healthcare provider acceptance ranging from 15% to 85%.
Many subspecialists and consultants still request that families step out, often due to outdated concerns.
Common Concerns & Myths:
Interference in resuscitation → Studies show minimal disruption.
Legal risks → No increased litigation risk has been demonstrated.
Family trauma → Research suggests that presence may help with grieving and reduce PTSD symptoms.
In a randomized controlled trial of 570 relatives, PTSD-related symptoms were significantly higher in family members who were not offered the opportunity to be present during resuscitation.
79% of relatives in the intervention group witnessed CPR compared to 43% in the control group.
Family members who did not witness CPR had a higher likelihood of PTSD symptoms (adjusted OR 1.7, p=0.004).
Anxiety and depression symptoms were also higher in those who did not witness CPR.
Impact on Medical Teams:
The study found no evidence that family presence affected resuscitation success rates, medical team stress levels, or led to legal consequences.
Health professionals’ concerns over interference were largely unfounded.
Guideline Support & Barriers to Implementation
Professional recommendations from pediatric societies support family presence during resuscitations.
Barriers include:
Lack of institutional policies ensuring family inclusion.
Lack of formal training for providers on how to support families during these critical moments.
Final Takeaways
Encouraging institutional policy changes and training providers is key to implementing family presence during codes.
Medical teams should challenge outdated practices and prioritize family-centered care in the emergency department.
Family-witnessed resuscitation does not increase stress, legal risk, or compromise medical care—but it can significantly improve bereavement outcomes.
Use this tool to assess the need for liver transplant evaluation in cases of acetaminophen-induced hepatic failure. Includes criteria for pH, INR, creatinine, and more.
Poison Control Center (available 24/7 for consultation): 1-800-222-1222
References
Goldfrank’s Toxicologic Emergencies, 9th Edition was consulted for information on the pharmacokinetics and clinical presentation of acetaminophen toxicity.
For more details, see: Nelson, L. S., Howland, M. A., Lewin, N. A., Smith, S. W., Goldfrank, L. R., & Hoffman, R. S. (Eds.). (2011). Goldfrank’s toxicologic emergencies (9th ed.). McGraw-Hill Education.
Differentiating between primary headaches (migraine, tension-type, cluster) and secondary causes (e.g., subarachnoid hemorrhage).
The importance of patient history and reevaluation after initial treatment.
Recognizing the unique presentation of cluster headaches and their management implications.
Effective Acute Migraine Treatments:
First-line treatments including anti-dopaminergic medications like metoclopramide (Reglan) and prochlorperazine (Compazine), and parenteral NSAIDs like ketorolac (Toradol).
The limited role of triptans in the ED due to side effects and less efficacy compared to anti-dopaminergics.
The use of nerve blocks (greater occipital nerve block and sphenopalatine ganglion block) as effective treatments without systemic side effects.
Treatments to Avoid or Use with Caution:
Diphenhydramine (Benadryl): Studies show it does not prevent akathisia from anti-dopaminergics nor improve migraine outcomes.
IV Fluids: Routine use is not supported unless the patient shows signs of dehydration.
Magnesium: Conflicting evidence with some studies showing no benefit or even harm.
Managing Refractory Migraines:
Second-line treatments including additional doses of metoclopramide combined with NSAIDs or dihydroergotamine (DHE).
Considering opioids as a last resort when other treatments fail.
The potential use of newer medications like lasmiditan and CGRP antagonists.
Preventing Recurrence of Migraines:
Administering a single dose of dexamethasone (4 mg IV) to reduce the risk of headache recurrence after discharge.
Prescribing NSAIDs or triptans upon discharge for outpatient management.
Recognizing and addressing chronic migraine, and initiating preventive therapies like propranolol when appropriate.
Key Takeaways
Differentiate Primary from Secondary Headaches and Reassess After Treatment:
Use patient history and reevaluation post-treatment to distinguish migraines from more serious conditions, reducing unnecessary imaging and procedures.
First-Line Treatments Are Effective:
Anti-dopaminergic medications and NSAIDs are the mainstay of acute migraine treatment in the ED.
Reserve opioids for cases unresponsive to multiple lines of treatment.
Avoid Unnecessary Interventions:
Diphenhydramine and routine IV fluids do not have proven benefits and can be excluded to streamline care.
Utilize Nerve Blocks for Refractory Cases:
Greater occipital nerve blocks and sphenopalatine ganglion blocks are effective alternatives for patients not responding to medication.
Prevent Recurrence with Dexamethasone and Outpatient Planning:
A single IV dose of dexamethasone can help prevent recurrence.
Provide prescriptions and consider preventive therapies to reduce future ED visits.
ICIs are a relatively new class of oncologic drugs that have revolutionized cancer treatment.
Unlike chemotherapy, ICIs help the immune system develop memory against cancer cells and adapt as the cancer mutates.
Since their release in 2011, ICIs have expanded to 83 indications for 17 different cancers, with approximately 230,000 patients using them.
Mechanism of Action
Cancer cells can evade the immune system by binding to T cell receptors that downregulate the immune response.
ICIs work by blocking these receptors or ligands, preventing the downregulation and allowing T cells to proliferate and attack cancer cells.
Common ICIs
Risks and Toxicities of ICIs
ICIs can lead to autoimmune attacks on healthy cells due to immune system upregulation.
Immune-related adverse effects (irAEs) include colitis, pneumonitis, dermatitis, hepatitis, and endocrine issues (e.g., hypothyroid, hypocortisolemia, hypophysitis).
These toxicities can present as infections, making diagnosis challenging in the emergency room.
Management of ICI Toxicities in the ER
Diagnosis: Look for signs that mimic infections (e.g., cough and fever in pneumonitis).
Diagnostic Imaging in pneumonitis: If CXR is normal but suspicion is high, consider CT scans to differentiate conditions like pneumonitis from other issues such as malignancy-associated pleural effusion or acute pulmonary embolism.
Treatment: The primary treatment for irAEs is steroids (e.g., prednisone 1 mg/kg). Start steroids early and hold the ICI to manage symptoms effectively and increase the likelihood of resuming ICI therapy later.
Consider using antibiotics in combination with steroids if there is uncertainty about whether symptoms are due to infection or ICI toxicity.
Coordinate care with the patient’s oncologist if possible
Disposition Decisions
Patient disposition (admit vs. discharge) should depend on clinical presentation and severity.
Coordination with oncology is crucial; they are often comfortable with starting steroids even if there is a potential infection.
Patients can be discharged if symptoms are mild, but sicker patients with more complex presentations may require admission.
Take-Home Points
ICIs are a new class of cancer drugs that effectively target cancer cells but come with unique immune-related toxicities.
Diagnosing irAEs can be challenging due to symptom overlap with infections.
The cornerstone of treatment is early administration of steroids and temporarily holding the ICI.
Close collaboration with oncology teams is essential for optimal patient management.
The episode focuses on ataxia in children, which can range from self-limiting to life-threatening conditions.
Pediatric emergency medicine specialist shares insights on the topic.
The Case
An 18-month-old boy presented with ataxia, unable to keep his head up, sit, or stand, and began vomiting.
Previously healthy except for recurrent otitis media and viral-induced wheezing.
The decision to take the child to the emergency department (ED) was based on acute symptoms.
Differential Diagnosis
Common causes include acute cerebellar ataxia, drug ingestion, Guillain-Barre syndrome, and basilar migraine.
Less common causes include cerebellitis, encephalitis, brain tumors, and labyrinthitis.
Importance of History and Physical Examination
A detailed history and physical exam are essential in diagnosing ataxia.
Key factors include time course, recent infections, signs of increased intracranial pressure, and toxic exposures.
Look for signs such as bradycardia, hypertension, vomiting, and overall appearance.
Diagnostic Workup
Initial tests include point-of-care glucose and neuroimaging for concerns about trauma or increased intracranial pressure.
MRI is preferred for posterior fossa abnormalities, but non-contrast head CT is commonly used due to accessibility.
Lumbar puncture may be needed if meningismus is present.
Treatment Approach
Treatment depends on the underlying cause:
Acute cerebellar ataxia is self-limiting and typically resolves with time.
Antibiotics are required for meningitis or encephalitis.
Steroids may be useful for cerebellitis and acute disseminated encephalomyelitis (ADEM).
Specialist consultations are necessary for severe diagnoses like intracranial masses.
Outcome of the Case Study
The child had a normal fast T2 MRI and improved during the ED stay.
Diagnosed with a combination of cerebellar ataxia and labyrinthitis.
Received myringotomy tubes and experienced no further neurologic changes or otitis media episodes.
Take-Home Points
Diverse Etiologies: Ataxia in children can have various causes that range from self-limiting to life-threatening
Comprehensive Assessment: History and physical exams guide diagnosis and workup direction, focusing on symptom time course, infections, and toxic exposures.
Physical Examination Clues: Vital signs and appearance offer clues; increased ICP may present with bradycardia, hypertension, and vomiting.
Diagnostic Imaging: Point-of-care glucose testing and neuroimaging are key; MRI is preferred for posterior fossa abnormalities.
Tailored Treatment: Treatment varies by cause; acute cerebellar ataxia typically resolves over time without specific intervention.
Osmotic Diuresis with Renal Water Losses: High glucose, mannitol
Risk Factors:
Patients with impaired thirst response or those unable to access water (e.g., altered or ventilated patients) are at higher risk.
Important to consider underlying conditions affecting thirst mechanisms.
Diagnosis:
Initial assessment includes history, physical examination, and laboratory tests.
Key tests: urine osmolality and urine sodium levels.
Lab errors should be considered if the clinical picture does not match the lab results.
Management Strategies:
Calculate the Free Water Deficit (FWD) to guide treatment.
Administration routes include oral, NGT, G-tube, or IV with D5W for larger deficits.
Safe correction rate is 10-12 mEq/L per day or 0.5 mEq/L per hour to avoid cerebral edema.
Address hypovolemia with isotonic fluids before correcting sodium.
Monitoring and Follow-Up:
Monitor sodium levels every 4-6 hours.
Assess urine output and adjust free water administration as needed.
Admission to ICU for symptomatic patients or those with severe hypernatremia (sodium >160 mEq/L).
Decision to discharge vs admit is a complicated one that factors in symptoms, etiology, degree of hypernatremia, patient preference, access to follow up, etc.
Take Home Points:
Hypernatremia is a serum sodium level over 145 mEq/L, with symptoms ranging from nausea to coma.
It is primarily caused by water loss exceeding intake due to various factors like sweating, vomiting, diarrhea, and renal issues.
Correcting hypernatremia too quickly can lead to cerebral edema, so a safe correction rate is essential.
Initial treatment involves calculating the Free Water Deficit and selecting the appropriate administration route.
Monitor sodium levels frequently and decide on admission or discharge based on symptoms, sodium levels, and patient’s ability to follow up.
•Definition and Scope: Agitation encompasses behaviors from restlessness to severe altered mental states. It’s a common emergency department presentation, often linked with acute medical or psychiatric emergencies.
•Significance: Patients with agitation are at high risk for morbidity and mortality, necessitating prompt and effective management to prevent harm to themselves and healthcare providers.
A Changing Paradigm in Describing Agitation
•Terminology Shift: Move away from terms like ‘excited delirium’ due to their politicization and stigmatization. Focus on describing agitation by severity and underlying causes.
Agitation as a Multifactorial Process
•Complex Nature: Recognize agitation as a result of various factors, including medical, psychiatric, and environmental influences.
Recognizing Agitation
•Signs and Symptoms: Identify agitation early by monitoring for behaviors such as hostility, pacing, non-compliance, and verbal aggression.
Initial Evaluation
•Severity Assessment: Determine the severity of agitation and prioritize reversible causes and life-threatening conditions.
•Diagnostic Steps: Perform vital signs check, blood glucose levels, ECG, and a targeted medical screening exam.
Life Threats
•Immediate Concerns: Identify and address immediate life threats such as hypoxia, hypoglycemia, trauma, and acute neurological emergencies.
Forming a Differential Prior to Treatment
•Prioritization: Severe agitation requires immediate treatment to facilitate further evaluation and reduce risk of harm.
Physician/Staff Safety
•Safety Measures: Ensure personal and team safety by maintaining a calm environment and preparing for potential violence.
Multimodal Approach
•Self-check In: Physicians should mentally prepare and approach the situation calmly to ensure effective management.
•Verbal De-escalation: Use techniques focused on safety, therapeutic alliance, and patient autonomy to manage agitation non-pharmacologically.
Medication Administration
•Oral/Sublingual Medications: Consider oral medications for less severe cases to maintain patient autonomy and avoid invasive procedures.
•IM or IV Medications: Use intramuscular or intravenous medications for rapid control in severe cases.
Specific Medication Regimens
•PO Regimens:
•Medications: Antipsychotics like Zyprexa (olanzapine) 5-10 mg, benzodiazepines like Ativan (lorazepam) 1-2 mg.
•Benefits: Empower patients with a sense of autonomy, avoid injection-related trauma.
•Pharmacokinetics:
•Olanzapine: Onset in 15-45 minutes, peak effect in 1-2 hours, duration 12-24 hours.
•Lorazepam: Onset in 30-60 minutes, peak effect in 2 hours, duration 6-8 hours.
‘T’ in the mnemonic stands for trauma, which includes both accidental and intentional causes.
Considerations for Non-accidental Trauma:
Stresses the importance of considering non-accidental trauma, especially given that it may not always present with obvious external signs.
Anatomical Vulnerabilities:
Highlights specific anatomical considerations for infants who suffer from trauma:
Infants have proportionally larger heads, increasing their susceptibility to high cervical spine (c-spine) injuries.
Their liver and spleen are less protected, making abdominal injuries potentially more severe.
Heart
5 T’s of Cyanotic Congenital Heart Disease: Introduces a mnemonic to help remember key right-sided ductal-dependent lesions:
Truncus Arteriosus: Single vessel serving as both pulmonary and systemic outflow tract.
Transposition of the Great Arteries: The pulmonary artery and aorta are switched, leading to improper circulation.
Tricuspid Atresia: Absence of the tricuspid valve, leading to inadequate development of the right ventricle and pulmonary circulation issues.
Tetralogy of Fallot: Comprises four defects—ventricular septal defect, pulmonary stenosis, right ventricular hypertrophy, and an overriding aorta.
Total Anomalous Pulmonary Venous Connection (TAPVC): Pulmonary veins do not connect to the left atrium but rather to the right heart or veins, causing oxygen-rich blood to mix with oxygen-poor blood.
Other Significant Conditions:
Ebstein’s Anomaly: Malformation of the tricuspid valve affecting right-sided heart function.
Pulmonary Atresia/Stenosis: Incomplete formation or narrowing of the pulmonary valve obstructs blood flow to the lungs.
Left-sided Ductal-Dependent Lesions:
Conditions such as aortic arch abnormalities (coarctation or interrupted arch), critical aortic stenosis, and hypoplastic left heart syndrome are highlighted. These generally present with less obvious cyanosis and more pallor.
Diagnostic and Management Considerations:
Routine prenatal ultrasounds detect most cases, but conditions like coarctation of the aorta and TAPVC might not be apparent until after birth when the ductus arteriosus closes.
Emphasizes the importance of a thorough physical exam: checking for murmurs, assessing hepatosplenomegaly, feeling for femoral pulses, measuring pre- and post-ductal saturations, and taking blood pressures in all four limbs.
Treatment Recommendations:
Early initiation of alprostadil (a prostaglandin) for patients with suspected ductal-dependent lesions to maintain ductal patency.
Preparedness for potential complications from alprostadil treatment, such as apnea and hypotension, which may necessitate intubation and hemodynamic support.
Endocrine
Focuses on acute salt-wasting crisis in undiagnosed Congenital Adrenal Hyperplasia (CAH).
Electrolyte imbalances: ↓Na, ↑K, ↓HCO3, ↓Glu.
Treatment: hydrocortisone (25mg for babies, 50mg for kids, 100mg for adults).
Metabolic
Electrolyte abnormalities such as hypoglycemia (values: <60 in infants, <40 in neonates).
Broad differential.
Rule of 50s for correction: D% x #ml/kg fluid = 50.
Inborn Errors of Metabolism
Major classes include organic acidurias (profound anion gap metabolic acidosis) and urea cycle defects (hyperammonemia)
Recommendation: Draw gas and ammonia level.
Sepsis
Emphasized as a critical condition in the differential diagnosis for ill infants, though placed later in the mnemonic for easier recall.
Presentation and Diagnosis:
Sepsis in infants often presents nonspecifically, making early detection challenging.
Immediate drawing of blood cultures upon suspicion of sepsis.
Initial Treatment:
Prompt initiation of antimicrobials and fluids.
Use of vancomycin for gram-positive and MRSA coverage, a third-generation cephalosporin or pip-tazo for broad bacterial coverage, and acyclovir for HSV. (tailor based on age and institutional guidelines)
Supportive Care:
Highlights the necessity of fluid resuscitation to stabilize the patient.
Formula
Formula-Related Electrolyte Imbalances:
Incorrect mixing of infant formula can cause hypo- or hypernatremia.
Consequences of Electrolyte Imbalances:
Both conditions can lead to severe outcomes including altered mental status, seizures, coma, and potentially death.
Management Strategies:
Treatment varies based on the sodium levels:
Symptomatic hyponatremia is treated with hypertonic saline.
Hypernatremia requires fluid resuscitation.
Intestinal Catastrophe
Specific Conditions:
Malrotation with Midgut Volvulus: Twisting of the intestines that can obstruct blood flow.
Necrotizing Enterocolitis (NEC): Can occur in both full-term and preterm infants, involves inflammation and bacterial infection that can destroy bowel tissue.
Hirschsprung-associated Enterocolitis: Complication of Hirschsprung’s disease involving blockage and infection.
Intussusception: Older infants might only show altered mental status instead of the typical intermittent pain and lethargy.
Symptoms:
Common symptoms include bilious emesis (green vomit) or hematemesis (vomiting blood).
Emergency Response:
Urges early mobilization of pediatric surgery and radiology teams upon suspicion of these conditions.
Toxins
Includes intentional or unintentional ingestion.
One pill killers include: calcium channel blockers (CCB), tricyclic antidepressants (TCA), opiates, sulfonylureas, Class 1 antiarrhythmics, antimalarials, camphor, oil of wintergreen.
Seizures
The second ‘S’ in the mnemonic refers to seizures, which can be triggered by various conditions such as hypoglycemia, sepsis, inborn errors of metabolism, and trauma.
First-Line Treatment:
Actively seizing patients should initially be treated with benzodiazepines.
Second-Line Medications:
Includes fosphenytoin, phenobarbital, levetiracetam (Keppra), and valproic acid.
Management of Reversible Causes:
Urges prompt treatment of any identifiable causes like hypoglycemia or electrolyte imbalances.
Special Consideration:
Notes the possibility of pyridoxine-dependent epilepsy in neonates, recommending pyridoxine (vitamin B6) for intractable seizures unresponsive to multiple antiepileptic drugs (AEDs).
Non-cardiogenic pulmonary edema characterized by acute respiratory failure.
Berlin criteria for diagnosis include acute onset within 7 days, bilateral pulmonary infiltrates on imaging, not fully explained by cardiac failure or fluid overload, and impaired oxygenation with PaO2/FiO2 ratio <300 mmHg, even with positive end-expiratory pressure (PEEP) >5 cm H2O.
Severity based on oxygenation (Berlin criteria):
Mild: PaO2/FiO2 200-300 mmHg
Moderate: PaO2/FiO2 100-200 mmHg
Severe: PaO2/FiO2 <100 mmHg
Epidemiology:
Occurs in up to 23% of mechanically ventilated patients.
Mortality rate of 30-40%, primarily due to multiorgan failure.
Differentiation from Cardiogenic Pulmonary Edema:
Chest CT shows diffuse edema and pleural effusion in cardiogenic edema; patchy edema, dense consolidation in ARDS.
Ultrasound may show diffuse B lines in cardiogenic edema; patchy B lines and normal A lines in ARDS.
Hypothetical case: 21-year-old male with no previous medical history, experiencing a month of progressively worsening numbness, tingling, and weakness. Initially starting in his toes and spreading to his hips, and later involving his hands, the symptoms eventually escalated to the point of immobilization. Despite initially denying drug use, the patient admitted to using 40-60 canisters of nitrous oxide (whippets) every weekend for the last three months.
Background and Recreational Use of Nitrous Oxide
Nitrous oxide, a colorless, odorless gas with anesthetic properties.
Synthesized in the 18th century.
Its initial medical purpose expanded into recreational use due to its euphoric effects.
Resurgence as a recreational drug during the COVID-19 lockdowns.
Accessibility and legal status.
Public Misconceptions and Health Consequences
There are widespread misconceptions about nitrous oxide
Particularly the belief in its safety and lack of long-term health risks.
Contrary to popular belief, frequent use of nitrous oxide can lead to significant, sometimes irreversible, health issues.
Neurological Examination and Diagnosis
Key components of the examination include assessing strength, sensation, cranial nerves, and proprioception, with specific abnormalities such as symmetrically decreased strength in a stocking-glove pattern, upgoing Babinski reflex, and positive Romberg sign being indicative of potential toxicity.
Physical Exam Findings: Upper vs Lower Motor Neuron Lesions
Localize the Lesion- Differential Diagnoses for Extremity Weakness
Localize the Lesion- Differential Diagnoses for Extremity Weakness
Localize the Lesion- Differential Diagnoses for Extremity Weakness
MRI Findings and Subacute Combined Degeneration
The MRI displayed symmetric high signal intensity in the dorsal columns, a diagnostic feature identified as the inverted V sign or inverted rabbit ear sign.
Significance of the Inverted V Sign: This MRI sign is pathognomonic for subacute combined degeneration, indicating it is a distinct marker for this condition.
T2 Weighted Axial Images: The inverted V sign is observed in T2 weighted axial MRI images, which are used to evaluate the presence and extent of demyelination within the spinal cord.
Interpretation of Hyperintense Signals: Hyperintense signals on T2 weighted images generally indicate demyelination, where the protective myelin sheath around nerve fibers is damaged or destroyed.
Anatomical Location: The dorsal columns, located anatomically dorsal (toward the back) within the spinal cord, will appear toward the bottom of the screen in an axial (cross-sectional) view on the MRI.
Demyelination Appearance: Demyelination in the dorsal columns, typically situated in the thoracic spine, manifests as an upside-down V shape on the MRI, correlating with the described inverted V or rabbit ear sign.
Pathophysiology of SCD due to Nitrous Oxide
Nitrous Oxide’s Effect on Vitamin B12: Nitrous oxide inactivates vitamin B12 by oxidizing a cobalt component within the molecule, rendering the vitamin functionally ineffective despite adequate consumption and absorption.
Impact on Methionine Synthase: The oxidation of vitamin B12 by N2O prevents it from activating methionine synthase, an enzyme critical for important biochemical processes.
Folate to Tetrahydrofolate Conversion: Inactive methionine synthase cannot convert folate into tetrahydrofolate, which is necessary for DNA synthesis. This disruption can lead to megaloblastic anemia, a condition associated with N2O-induced subacute combined degeneration.
Conversion of Homocysteine to Methionine: Methionine synthase is also responsible for converting homocysteine to methionine. Methionine is essential for the maintenance of myelin integrity, the protective sheath around nerve fibers.
Demyelination and Neurological Symptoms: The inability to maintain myelin integrity due to disrupted methionine production leads to the demyelination of dorsal columns and peripheral motor/sensory nerves, characteristic of N2O-SCD.
Normal B12 Levels with Functional Deficiency: Blood levels of vitamin B12 can appear normal in individuals affected by N2O exposure, as the issue lies in the vitamin’s inactivation rather than its absence, creating a functional deficiency.
Diagnosis of N2O-SCD: To diagnose N2O-induced SCD, healthcare providers need to check for elevated levels of methylmalonic acid and homocysteine. These substances are typically metabolized with the help of vitamin B12, and their elevated levels indicate a functional deficiency of B12 due to N2O exposure.
Treatment and Management
Lack of Standardized Treatment: There is no universally accepted treatment protocol for N2O induced SCD, but common practices exist based on neurologist recommendations.
B12 Injection Protocol: A common approach involves administering vitamin B12 injections daily or every other day until there is noticeable improvement in symptoms. Once symptoms start to improve, the frequency of injections can be reduced to once a week.
Importance of Abstinence from N2O: For recovery to be possible, it is crucial that the patient completely abstains from using whippets (recreational N2O canisters). Continuing to use N2O can inactivate the administered vitamin B12, undermining the treatment efforts.
Recovery Process: Recovery from N2O induced SCD is typically slow and may not be complete. While remyelination and neurological function can gradually improve, the process is lengthy and may not fully return to baseline.
Recovery Statistics: Approximately 80% of individuals with N2O-SCD experience some improvement after a year of consistent B12 treatment. However, only between 10% and 20% of patients fully recover to their pre-condition baseline.
Risk Factors and Prevalence: The risk of developing SCD correlates with the frequency and quantity of N2O use. About 3.4% of individuals who use whippets will develop SCD, with the risk increasing to 8.5% among those who use more than 100 canisters per session. The case in point involved a patient using 20-40 canisters per session.
Increased Risk with Preexisting Conditions: Individuals who already have a vitamin B12 deficiency are at a greater risk of experiencing SCD symptoms, even with minimal use of whippets. This highlights the importance of understanding individual health conditions and potential vulnerabilities when assessing risk.
Conclusion and Preventive Measures
Providers should be vigilant in screening for nitrous oxide use among patients presenting with unexplained neurological symptoms. The goal is to enhance early detection and treatment of N2O-induced SCD and to educate patients on the potential long-term health consequences of recreational nitrous oxide use.
References
Neurology. Mumenthaler M, Mattle H, Taub E, ed. 4th Edition. Stuttgart: Thieme; 2003. doi:10.1055/b-005-148905
Zayia LC, Tadi P. Neuroanatomy, Motor Neuron. [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554616/
Bhattacharyya S.Spinal Cord Disorders: Myelopathy, The American Journal of Medicine, Volume 131, Issue 11, 2018, Pages 1293-1297, ISSN 0002-9343,https://doi.org/10.1016/j.amjmed.2018.03.009.
Garg RK, Malhotra HS, Kumar N. Approach to a case of myeloneuropathy. Ann Indian Acad Neurol. 2016 Apr-Jun;19(2):183-7. doi: 10.4103/0972-2327.182303. PMID: 27293327; PMCID: PMC4888679.
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Jayarangaiah A, Lui F, Theetha Kariyanna P. Lambert-Eaton Myasthenic Syndrome. [Updated 2023 Oct 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507891/
Nguyen TP, Taylor RS. Guillain-Barre Syndrome. [Updated 2023 Feb 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532254/
Froese DS, Fowler B, Baumgartner MR. Vitamin B12 , folate, and the methionine remethylation cycle-biochemistry, pathways, and regulation. J Inherit Metab Dis. 2019 Jul;42(4):673-685. doi: 10.1002/jimd.12009. Epub 2019 Jan 28. PMID: 30693532.
Guo CJ, S. Kaufman B. Inhalational Anesthetics. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank’s Toxicologic Emergencies, 11e. McGraw-Hill Education; 2019. Accessed February 27, 2024. https://accessemergencymedicine-mhmedical-com.ezproxy.med.nyu.edu/content.aspx?bookid=2569§ionid=210274345
Lin JP, Gao SY, Lin CC. The Clinical Presentations of Nitrous Oxide Users in an Emergency Department. Toxics. 2022 Feb 26;10(3):112. doi: 10.3390/toxics10030112. PMID: 35324737; PMCID: PMC8950993.
Qudsiya Z, De Jesus O. Subacute Combined Degeneration of the Spinal Cord. [Updated 2023 Feb 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559316/
Hemmer B, Glocker FX, Schumacher M, et alSubacute combined degeneration: clinical, electrophysiological, and magnetic resonance imaging findingsJournal of Neurology, Neurosurgery & Psychiatry 1998;65:822-827.
Shah K, Murphy C. Nitrous Oxide Toxicity: Case Files of the Carolinas Medical Center Medical Toxicology Fellowship. J Med Toxicol. 2019 Oct;15(4):299-303. doi: 10.1007/s13181-019-00726-x. Epub 2019 Aug 6. PMID: 31388940; PMCID: PMC6825085.
Kalmoe MC, Janski AM, Zorumski CF, Nagele P, Palanca BJ, Conway CR. Ketamine and nitrous oxide: The evolution of NMDA receptor antagonists as antidepressant agents. J Neurol Sci. 2020 May 15;412:116778. doi: 10.1016/j.jns.2020.116778. Epub 2020 Mar 19. PMID: 32240970.
Defined as vaginal bleeding during early pregnancy (before 20 weeks) with a closed cervical os, no passage of fetal tissue, and IUP on ultrasound
Occurs in 20-25% of all pregnancies.
Initial Assessment and Management
Priority is to assess patient stability, establish good IV access, FAST may be helpful in identifying some ruptured ectopics early
Broad differential diagnosis is crucial to avoid mistaking conditions like ectopic pregnancy for other emergencies.
Importance of a detailed history and physical examination.
Diagnostic Approach
Essential tests include HCG level, urinalysis, and possibly CBC + blood type/Rh status.
Rhogam’s use is well-supported in second and third trimester bleeding; however, data is less robust for first trimester bleeding in preventing sensitization
Importance of interpreting b-HCG with caution and understanding HCG discriminatory zones.
Use of ultrasound imaging, both bedside and formal, to assess the pregnancy’s status.
Patient Counseling and Management
Open and honest communication about the prognosis of threatened abortion.
Addressing psychosocial aspects, including dispelling guilt and myths, and screening for intimate partner violence and mental health issues.
Recommendations against bedrest and certain activities
Lack of evidence supporting restrictions on sexual activity.
Standard pregnancy guidelines: avoiding smoking, alcohol, drug use, and starting prenatal vitamins.
Follow-up and Precautions
Adopting a wait-and-see approach for stable patients, with scheduled follow-ups for ultrasounds and beta-HCG tests.
Educating patients on critical warning signs that require immediate medical attention.
Emphasizing the importance of returning to the hospital if experiencing significant bleeding or other severe symptoms.
Take Home Points
Threatened Abortion is defined as Experiencing abdominal pain and/or vaginal bleeding during early pregnancy (before 20 weeks), characterized by a closed cervical os and no expulsion of fetal tissue. In these cases, it is important to assess patient stability promptly.
Keep your differential broad in these cases. The evaluation will in most cases involve a combination of labs and ultrasound imaging.
Understand that the Rhogam certainly has a role in second and third trimester vaginal bleeding in the Rh-negative patient, and that there is a dearth of good data on its role in the first trimester – it will ultimately be a decision that is made by you, OBGYN, and the patient.
Approach the interpretation of HCG levels with caution and remember that ectopic pregnancies might not adhere to conventional HCG levels.
Established follow up and discharge instructions are crucial. Manage stable patients with a watchful waiting approach, scheduling subsequent visits for continuous ultrasounds and HCG testing. Clearly outline the importance of immediate medical attention for symptoms such as intense bleeding, significant abdominal pain, fever, or feelings of insecurity at home.
Finally, we play an important role wherein we must ensure that the patient is medically stable and psychosocially safe. Here, compassionate communication is crucial when discussing what the diagnosis might entail, alleviate any feelings of blame or shame, and remain vigilant for signs of intimate partner violence or mental health issues. As emergency medicine physicians, it’s crucial for us to approach these cases with a comprehensive mindset.
Similar initial workup for children and adults: checking glucose levels for hypoglycemia and conducting an EKG.
The history and physical exam are crucial.
Dextrose Administration in Children:
Explanation of the ‘rule of 50s’ for determining the appropriate dextrose solution and dosage for children.
ECG Analysis:
Importance of ECG in diagnosing dysrhythmias like long QT syndrome, Brugada syndrome, catecholamine polymorphic V tach, ARVD, ALCAPA, and Wolff-Parkinson-White syndrome.
Younger children’s dependency on heart rate for cardiac output and the risk of arrhythmias in kids with congenital heart disease.
ConditionCharacteristic ECG FindingsCongenital/Acquired
Long QT Syndrome (LQTS)
Prolonged QT interval
Congenital/Acquired
Wolff-Parkinson-White Syndrome (WPW)
Short PR interval, Delta wave
Congenital
Brugada Syndrome
ST elevation in V1-V3, Right bundle branch block
Congenital
Atrioventricular Block (AV Block)
PR interval prolongation (1st degree), Missing QRS complexes (2nd & 3rd degree)
Congenital/Acquired
Supraventricular Tachycardia (SVT)
Narrow QRS complexes, Absence of P waves, Tachycardia
Congenital/Acquired
Ventricular Tachycardia
Wide QRS complexes, Tachycardia
Congenital/Acquired
Arrhythmogenic Right Ventricular Dysplasia (ARVD/C)
Epsilon waves, V1-V3 T wave inversions, Right bundle branch block
Congenital
Hypertrophic Cardiomyopathy (HCM)
Left ventricular hypertrophy, Deep Q waves
Congenital
Pulmonary Hypertension
Right ventricular hypertrophy, Right axis deviation
Acquired
Athlete’s Heart
Sinus bradycardia, Voltage criteria for left ventricular hypertrophy
Acquired
Catecholaminergic Polymorphic VT (CPVT)
Bidirectional or polymorphic VT, typically normal at rest
Congenital
Anomalous Origin of Left Coronary Artery from Pulmonary Artery (ALCAPA)
May be normal, signs of ischemia or infarction in severe cases
Congenital
History Taking:
Key aspects include asking about syncope with exertion, syncope after being startled, and syncope after pain or emotional stress.
Prolonged loss of consciousness may indicate seizures, and emotional stress and pain can trigger breath-holding spells.
Breath-Holding Spells:
Clarification of misconceptions about breath-holding spells, discussing their causes and characteristics, like cyanotic and pallid types.
Association with iron deficiency and the fact that most children outgrow these spells by age 8.
Physical Examination and History:
A cardiac exam is vital, with specific signs to look for, like murmurs in hypertrophic cardiomyopathy.
History can help identify the etiology of syncope, such as vasovagal responses or orthostatic hypotension.
Vasovagal Syncope:
Common in kids, especially teenagers, typically presenting with a prodrome of lightheadedness, diaphoresis, and pallor.
Normal glucose and EKG are expected in these cases.
Additional Lab Tests:
Pregnancy tests in reproductive-age women, and checking for less common causes like pulmonary embolism, subarachnoid hemorrhage, and toxic exposures.
Take Home Points:
Immediate assessments for syncope in children should include a FS to evaluate for hypoglycemia and an ECG to evaluate any cardiac rhythm or conduction abnormalities.
Apply the “Rule of 50s” for hypoglycemic patients to suggest which fluids should be used.
Refer to our table for ECG findings to look out for when reviewing ECG tracings for these patients.
Pay particular attention to clues in the history that would suggested HCOM or seizures.
Breath-holding spells usually resolve by eight
HCOM murmurs will increase with Valsalva maneuver
Always keep your differential broad when approaching these patients given the heterogeneity of potential pathology that could lead to this chief complaint
Decision-Making Process: Balancing acute management with long-term treatment strategies.
Take Home Points
Differentiation in AF with RVR Types: It’s essential to distinguish between primary AF with RVR, chronic AF with RVR related to other health issues, and new-onset AF (NOAF) with RVR in critically ill patients, as each type necessitates a unique approach to treatment.
ACLS Guidelines for AF with RVR: The ACLS guidelines provide a treatment framework, particularly recommending immediate synchronized cardioversion for unstable patients. However, these guidelines may have limited effectiveness for chronic AF with RVR patients suffering from underlying critical illnesses.
ECG Diagnosis in AF: Identifying AF on an ECG is crucial, with key indicators being an irregular rhythm without clear P waves and a ventricular rate exceeding 100 bpm. Accurate ECG interpretation guides effective treatment planning.
Special Cases like WPW Syndrome: WPW syndrome and similar conditions require careful treatment consideration, as standard AF treatments can worsen these conditions. Alternatives like procainamide or amiodarone are often more appropriate.
Patient-Centered Management of AF with RVR: Management should account for the patient’s overall health, underlying conditions, the chronicity of AF, and other comorbidities. Drugs like metoprolol and diltiazem offer benefits and risks, demanding personalized treatment plans.
Pathophysiology in Critical AF Patients: Understanding the underlying pathophysiology in critically ill patients is vital. Tachycardia in these cases might be compensatory, necessitating an investigation into causes like myocarditis, dehydration, or GI bleeding.
Systematic Evaluation with TACHIES Mnemonic: The mnemonic TACHIES (Thyrotoxicosis, Alcohol withdrawal, Cardiac issues, Hemorrhage, Intervals [WPW], Embolus, Sepsis) aids in systematically assessing and addressing emergent tachycardia causes in critically ill patients.
Three or more sustained episodes of VF, VT, or appropriate ICD shocks in a 24-hour period
Pathophysiology: Understanding the origin and mechanism
Sympathetic drive/adrenergic surge
Underlying pathology: Sodium channelopathies, infiltrative disease like cardiac sarcoidosis, etc.
RF’s / trigger / population (reversible cause in ~25% of patients)
MI
Electrolyte Derangements (emphasis on potassium and magnesium)
New/worsening heart failure
Catecholamine Surge
Drugs (stimulants, cocaine, amphetamines, etc)
QT Prolongation
Thyrotoxicosis
Clinical Presentation:
Symptoms of VT: spectrum of symptoms – from palpitations to syncope to cardiac arrest
Differentiating VT from other potential ER presentations.
Diagnostics in ER:
Electrocardiogram (ECG): Recognizing VT patterns.
Monomorphic vs polymorphic (Torsades) may change management
Wide QRS
Fusion best
Capture beats
Concordance
AV-dissociation
Lab tests: Potassium, magnesium, troponins, TFTs, etc.
Acute Management in the ER:
Hemodynamically stable vs. unstable V
Unstable = cardioversion
Sedation
Catecholamine surge should be considered
No ideal agent
Etomidate or propofol can be considered
Ketamine may worsen irritability
Pharmacological treatments:
Amiodarone
Class III antiarrhythmic
Most studied in VT storm
First line
Beta Blockers
Propranolol
B1 and B2 activity
Non-pharmacological approaches:
Immediate synchronized cardioversion
IABP / ECMO considered for HD unstable patient
Cath lab if ischemic etiology suspected
Stellate Ganglion Block
Take Home Points
Definition: VT Storm is commonly defined as three or more sustained episodes of ventricular fibrillation, ventricular tachycardia, or appropriate ICD shocks within a 24-hour period.
Varied Presentation: Patients may experience a range of symptoms from palpitations to severe hemodynamic instability.
ECG and Diagnosis: Initial ECG may not show VT; continuous cardiac monitoring or device interrogation may be required for diagnosis.
VT Identification: Look for wide QRS, rate over 100, fusion beats, capture beats, and AV dissociation to identify VT.
Management in Hemodynamic Instability: Cardiovert if the patient shows signs of hemodynamic instability.
Sedation Considerations: Be cautious with sedation, especially with ketamine, as it may worsen cardiac irritability in these already adrenergic state patients.
Medication Choices: Typically, amiodarone and propranolol are used to manage VT Storm.
Cardiology Involvement: Involve cardiology early on, as treatment may extend beyond medications.
2023 study: Of the 145 children with hemolyzed hyperkalemia, 142 (97.9%) had a normal repeat potassium level. Three children (2.1%) had true hyperkalemia: one had known chronic renal failure and was referred to the ED due to concern for electrolyte abnormalities; the other 2 patients had diabetic ketoacidosis (DKA).
Clinical Presentation / eval
Symptomatic vs. Asymptomatic:
“First symptom of hyperkalemia is death”
If severe, ascending muscle weakness → paralysis
Point at which patients experience symptoms depends on chronicity
>7 mEq/L if chronic and can be lower if acute
Hyperkalemia can be a cause of non-specific GI symptoms
EKG Changes:
ECG findings may be the first marker the ER doc gets that something is wrong
Typical changes:
Peaked T-waves, shortened QT
Lengthening of PR interval and QRS duration
Bradycardia / Junctional rhythm
Hyperkalemia can produce bradycardia without other ECG findings
Ones associated with VT/VF/code, death in one study: QRS widening (RR = 4.74), Junctional Rhythm (RR = 7.46), HR <50 (RR = 12.29) while no adverse outcomes with just peaked T waves or PR prolongation (Durfey, 2017)
Don’t be fooled by a normal ECG, may be normal, but it’s also on case report level to have K > 9 and a normal ECG
Series of 127 patient (K 6-9.3), no serious arrhythmia noted, only 46% had ECG changes, (Acker, 1998)
ECG changes are not linear, there is no exact association between K+ levels and ECG changes
ECG changes may be hidden and subtle in patients with underlying inter-ventricular conduction delay (BBBs)
Be suspicious of the patient with LBBB > 160 ms or RBBB > 140 ms
BRASH Syndrome
Synergism between hyperkalemia, renal failure/injury and AV nodal blocking agents -> may produce ECG changes out of proportion to serum potassium levels.
Labs
Chem, VBG, +/- CK if you think muscle breakdown is at play (Tintinalli talks about looking at urine K, but this is not most people’s practice)
Realistically 2 hours to get back chemistry in most settings ≈ eternity
Management in the ER
Discontinue/hold any nephrotoxins or medications in suspected medication-induced hyperkalemia
A. Acute Management Strategies:
Cardiac protection with calcium
1g over 5-10 mins
Lasts 30-60 mins, may have to redose
Dose considerations if on digoxin
AEs: Calciphylaxis and hypercalcemia
Fast pushes can result in hypotension, arrhythmia
Calcium chloride vs calcium gluconate
Caution in patients taking Digoxin
IVF choice – NS vs LR
Caution/Avoid fluid in patients with ESRD/CHF or signs of VOL
Shifting potassium:
insulin/glucose
5 units vs 10 units
5 similar effect, less hypoglycemic episodes (LaRue 2017)
If doing 10 units, start D10W at 50-75 cc/h after amp of d50 but be mindful that anuric patient who missed HD may not have much room for volume
Decrease but about 0.5-1.2 mEq/L
Effect starts 10-20 mins after administration and can last 4-6 hours
Albuterol
10-20 mg over 10 mins (NB: higher dose than for asthma)
Peak effect at 90 mins
Decreases by 0.5 – 1.0 mEq/L alone
With insulin, ~1.2 mEq/L, additive effect
Bicarbonate
Controversy. Useless in hyperkalemic, nonacidotic patient. Useful as drip but takes hours to work, again, volume in anuric patient an issue
May be most useful in patients with renal failure and hyperkalemia 2/2 volume loss
Hypertonic Bicarb is ineffective – More potassium is pulled out of cells due to osmotic shift.
Removal:
Lokelma (Sodium Zirconium cyclosilicate)
Luckily residents have never had to use Kayexalate
Can start working in 1-2 hours of administration
0.37 mEq/L reduction at 4 hours after 10 g
Not a magic bullet in patients who need dialysis
Diuretics
No studies that demonstrate effectiveness in this ED setting
May be effective in patients with normal renal function
If patient not anuric, may be worth using, can give 40 mg, but again, should not be the only attempted method of removing K
Nephron BOMB
Loop Diuretic (160-250 mg IV Lasix or 4-5 mg IV Bymex)
Thiazide (500-1000 mg IV chlorothiazide or 5-10 mg metolazone)
+/- Acetazolamide
+/- Fludrocortisone
May help stimulate the kidneys to secrete potassium
Primarily helpful in patients with mineralocorticoid deficiencies
Dialysis
Involve renal early because it takes a while to call in an HD nurse sometimes
If no access and emergent HD is required → HD catheter placement
Strategies for suspected Brash syndrome
Epinephrine/Levo (if hypotensive/bradycardic)
Calcium gtt
Disposition/wrap up
Many factors at play here – patient preference, access, degree of hyperkalmia, identifiable / corrected cause
Take Home points
Hyperkelamia causes can be put into three categories, pseudohyperkalemia, due to redistribution, and due to total body increase in potassium. Check out the show notes for a more complete list
Hyperkalemia can be difficult to pick up on before the labs come back because it can lurk without symptoms or even ECG changes
If a patient does have ECG changes, they may not follow that linear pattern that is traditionally taught and ECGs can be poorly sensitive. Now, if you do see changes, the ones that are more commonly associated with adverse events are QRS widening, junctional rhythm, and bradycardia
Treatment is a numbers game, calcium for cardiac stabilization can last just 30-60 minutes, insulin will be the fastest way to shift potassium back into cells, but be mindful that 10 units is associated with increased episodes of hypoglycemia whereas 5 units may have the same effect in reducing potassium. And albuterol is at a much higher dose than what is given for asthma
Lokelma is now a pillar of treatment for removal of potassium.
Diuretics with the goal of kiuresis may have a role in the oliguric patient, and increased doses along with other agents may buy time in patients with severe hyperK when HD is not readily available
Involve renal early if you think that the patient will require HD
Consider POCUS, lactate, central venous saturation, and acid-base status
Peripheral Pressors
Can safely be administered peripherally via large bore IVs in proximal upper extremity
Sites: Cephalic or basilic veins
Adverse Events: Low at 1.8% based on meta-analysis
Actions in case of extravasation: Phentolamine injection, nitroglycerin paste
Push-Dose Pressors
Primarily Phenylephrine (peri-intubation, during procedures)
Also Epinephrine for peri-code situations
Doses: Epi – 5-20 mcg every 2-5 min
Take-Home Points
Most used medications are going to be norepinephrine, vasopressin, phenylephrine, and epinephrine.
Consider these medications if there are signs of end-organ dysfunction, there is a considerable delta in baseline BP, systolic is less than 90 and/or MAP is less than 65
Norepinephrine is a good pressor for a lot of the situations that we encounter in the emergency department, such as septic shock, undifferentiated shock and hypovolemic shock.
Vasopressin is commonly the second we reach for in most of these scenarios
Epinephrine will be first for anaphylactic shock and may be the third agent in septic shock
Think about phenylephrine in high-output states (patients with tachydysrhythmias), or with AS, though be cautious in patient with low cardiac output
The benefits outweigh risks for peripheral pressors in situations where you promptly have to increase blood pressure while you work on central access
Push-dose pressures can help you in a peritinbatuion or pericode situation because it is going to be one of the fastest ways we can boost BP while we work on other measures to stabilize the patient
Additional References
Importance of RUSH (Rapid Ultrasound in SHock) exam for diagnosis and treatment planning: https://emcrit.org/rush-exam/
Pain in joint for pediatric patient has a broad differential, including transient synovitis and septic arthritis
Transient synovitis, also known as toxic synovitis, is a common condition affecting kids aged 3-10 and often occurs after a viral infection. It is typically self-limiting and not considered a serious condition.
Septic arthritis is an infection in the joint space, typically affecting only one joint. It is often difficult to diagnose due to the fact that many patients, particularly under the age of 3, may not be able to localize their pain to a specific joint.
Workup
Diagnostic work-up for septic arthritis begins with blood work, which includes a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures. Lyme disease studies may also be necessary since Lyme disease can cause joint pain.
Patients with transient synovitis typically have mild elevation in inflammatory markers, while those with septic arthritis usually show a significant elevation.
Imaging studies, including X-rays, ultrasound to evaluate for a joint effusion, and MRI to assess for associated osteomyelitis, are also part of the diagnostic approach.
The Kocher criteria, developed specifically for septic arthritis of the hip, are a useful tool for clinical decision-making. The criteria include fever above 38.5 C, inability to bear weight, ESR above 40, and a white blood cell count above 12,000.
1 criterion met = 3% probability of septic arthritis
2 criteria met = 40% probability of septic arthritis
3 criteria met = 93% probability of septic arthritis
4 criteria met = 99+% probability of septic arthritis
If septic arthritis is suspected, orthopedics should be consulted immediately. Joint fluid aspiration is necessary for diagnosis and should not be delayed. The fluid should be sent for cell count, gram stain, glucose, culture, and PCR if available.
Septic arthritis is most commonly caused by bacterial infections, with Staph aureus being the most common organism. In school-age children, other bacteria such as Strep pyogenes, Strep pneumoniae, and Haemophilus influenzae should also be considered. In preschool-aged children, K. kingae is also considered. In older children and neonates, the range of potential bacteria varies.
Management
Empiric antibiotic therapy should target the most likely organisms and should not be delayed. Antibiotics may be narrowed once culture results are obtained.
The choice of antibiotics is dependent on the age group, with specific combinations suggested for neonates, children between 1 month and 4 years, and children aged 5 and older.
Cultures are only positive in 50-60% of cases. Synovial fluid PCR studies can help narrow antibiotic treatment.
Take Home Points
Limp in the pediatric population can commonly be transient synovitis but we should always consider septic arthritis
Some clues in the history and physical that would point you towards septic arthritis include fever, refusal to bear weight, and limited range of motion on exam
We are going to have to get labs, including CBC, inflammatory markers, and preoperative labs, along with an XR and possibly an ultrasound
Kocher criteria is one tool that can help us determine if this is a patient that requires a joint tap.
Arthrocentesis is the gold standard for diagnosis, but antibiotics should be started promptly if the diagnosis is suspected.
The choice of antibiotics is dependent upon age group.
Neonates get vanc/cefepime, kids 1-4 yo get vanc / ceftriaxone
Older than 5 yo get vancomycin
Add ceftriaxone to them if patient has sickle cell disease, are immunocompromised, or Lyme or STI are suspected
Always cross check with institutional preferences / guidelines when choosing antibiotics
IV calcium supplementation with 100-300 mg Ca2+ raises serum Ca2+ by 0.5 – 1.5 mEq
For acute but mild symptomatic hypocalcemia: 200-1000mg calcium chloride IV or 1-2g IV calcium gluconate over 2 hours
For severe hypocalcemia: 1g calcium chloride IV or 1-2g IV calcium gluconate IV over 10 minutes repeated q 60 min until symptoms resolve
References:
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Vantour L, Goltzman D. Regulation of calcium homeostasis. In: rimer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 9th ed, Bilezikian JP (Ed), Wiley-Blackwell, Hoboken, NJ 2018. p.163.
Algorithm for Anticoagulated Bleeding Patient in the ED:
Indications for Anticoagulation Reversal:
References:
Baugh CW, Levine M, Cornutt D, et al. Anticoagulant Reversal Strategies in the Emergency Department Setting: Recommendations of a Multidisciplinary Expert Panel. Ann Emerg Med. 2020;76(4):470-485. doi:10.1016/j.annemergmed.2019.09.001
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Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515-523. doi:10.4103/0019-5049.144643
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Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s Angina. Ann Maxillofac Surg 2015; 5:168.
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Mohamad I, Narayanan MS. “Double Tongue” Appearance in Ludwig’s Angina. N Engl J Med 2019; 381:163.
Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J. 2004 Mar;21(2):242-3. doi: 10.1136/emj.2003.012336. PMID: 14988363; PMCID: PMC1726306.
Wolfe MM, Davis JW, Parks SN. Is surgical airway necessary for airway management in deep neck infections and Ludwig angina? J Crit Care. 2011 Feb;26(1):11-4. doi: 10.1016/j.jcrc.2010.02.016. PMID: 20537506.
Bense L, Lewander R, Eklund G, et al. Nonsmoking, non-alpha 1-antitrypsin deficiency-induced emphysema in nonsmokers with healed spontaneous pneumothorax, identified by computed tomography of the lungs. Chest 1993; 103:433.
Bense L, Wiman LG, Hedenstierna G. Onset of symptoms in spontaneous pneumothorax: correlations to physical activity. Eur J Respir Dis 1987; 71:181.
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Chardoli M, Hasan-Ghaliaee T, Akbari H, Rahimi-Movaghar V. Accuracy of chest radiography versus chest computed tomography in hemodynamically stable patients with blunt chest trauma. Chin J Traumatol 2013; 16:351.
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Ebrahimi A, Yousefifard M, Mohammad Kazemi H, et al. Diagnostic Accuracy of Chest Ultrasonography versus Chest Radiography for Identification of Pneumothorax: A Systematic Review and Meta-Analysis. Tanaffos 2014; 13:29.
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Lichtenstein DA, Mezière G, Lascols N, et al. Ultrasound diagnosis of occult pneumothorax. Crit Care Med 2005; 33:1231.
Melton LJ 3rd, Hepper NG, Offord KP. Influence of height on the risk of spontaneous pneumothorax. Mayo Clin Proc 1981; 56:678.
Ohata M, Suzuki H. Pathogenesis of spontaneous pneumothorax. With special reference to the ultrastructure of emphysematous bullae. Chest 1980; 77:771.
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Non-contrast head CT showing SAH (Case courtesy of Dr. David Cuete, Radiopaedia.org, rID: 22770)
Hunt-Hess grade and mortality (from Lantigua et al. 2015.)
Hunt-Hess grade
Mortality (%)
1. Mild Headache
3.5
2. Severe headache or cranial nerve deficit
3.2
3. Confusion, lethargy, or lateralized weakness
9.4
4. Stupor
23.6
5. Coma
70.5
Ottawa Subarachnoid Hemorrhage Rule, and appropriate population for rule application (from Perry et al. 2017)
Apply to patients who are:
Alert
≥ 15 years old
Have new, severe, atraumatic headache that reached maximum intensity within 1 hour of osnet
Do not apply to patients who have:
New neurologic deficits
Previous diagnosis of intracranial aneurysm, SAH, or brain tumor
History of similar headaches (≥ 3 episodes over ≥ 6 months)
SAH cannot be ruled out if the patient meets any of the following criteria:
Age ≥ 40
Symptom of neck pain or stiffness
Witnessed loss of consciousness
Onset during exertion
“Thunderclap headache” (defined as instantly peaking pain)
Limited neck flexion on examination (defined as inability to touch chin to chest or raise head 3 cm off the bed if supine)
___________________________
Special Thanks To:
Dr. Mark Iscoe, MD (Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue)
___________________________
References:
Bellolio MF, Hess EP, Gilani WI, et al. External validation of the Ottawa subarachnoid hemorrhage clinical decision rule in patients with acute headache. Am J Emerg Med. 2015;33(2):244-9.
Carstairs SD, Tanen DA, Duncan TD, et al. Computed tomographic angiography for the evaluation of aneurysmal subarachnoid hemorrhage. Acad Emerg Med. 2006;13(5):486-492.
Connolly ES, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012;43(6):1711-1737.
Czuczman AD, Thomas LE, Boulanger AB, et al. Interpreting red blood cells in lumbar puncture: distinguishing true subarachnoid hemorrhage from traumatic tap. Acad Emerg Med. 2013;20(3):247-256.
Dugas C, Jamal Z, Bollu PC. Xanthochromia. [Updated 2020 Aug 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526048/
Goldstein JN, Camargo CA, Pelletier AJ, Edlow JA. Headache in United States emergency departments: demographics, work-up and frequency of pathological diagnoses. Cephalalgia. 2006;26(6):684-90.
Kumar A, Niknam K, Lumba-brown A, et al. Practice Variation in the Diagnosis of Aneurysmal Subarachnoid Hemorrhage: A Survey of US and Canadian Emergency Medicine Physicians. Neurocrit Care. 2019.
Lantigua H, Ortega-Gutierrez S, Schmidt JM, et al. Subarachnoid hemorrhage: who dies, and why? Crit Care. 2015;19:309.
Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389(10069):655-666.
Mayer PL, Awad IA, Todor R, et al. Misdiagnosis of symptomatic cerebral aneurysm. Prevalence and correlation with outcome at four institutions. Stroke. 1996;27(9):1558-63.
Meurer WJ, Walsh B, Vilke GM, Coyne CJ. Clinical guidelines for the emergency department evaluation of subarachnoid hemorrhage. J Emerg Med. 2016;50(4):696-701.
Perry JJ, Spacek A, Forbes M, et al. Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid hemorrhage? Ann Emerg Med. 2008;51(6):707-713
Perry JJ, Stiell IG, Sivilotti MLA, et al. High risk clinical characteristics for subarachnoid haemorrhage in patients with acute headache: prospective cohort study. BMJ. 2010;341:c5204.
Perry JJ, Stiell IG, Sivilotti MLA, 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(jul18 1):d4277-d4277.
Perry JJ, Stiell IG, Sivilotti ML, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-55.
Perry JJ, Sivilotti MLA, Sutherland J, et al. Validation of the Ottawa Subarachnoid Hemorrhage Rule in patients with acute headache. CMAJ. 2017;189(45):E1379-E1385.
Vermeulen MJ, Schull MJ. Missed diagnosis of subarachnoid hemorrhage in the emergency department. Stroke. 2007;38(4):1216-21.
Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue
New York City Poison Control Center
References:
Christian MR, et al. Do rapid comprehensive urine drug screens change clinical management in children? Clin Toxicol (Phila). 2017;57:977-980.
Grunbaum AM, Rainey PM (2019). Chapter 7: Laboratory Principles. In Goldfrank’s toxicologic emergencies. New York, NY: McGraw-Hill Education.
Moeller K, Kissack J, Atayee R, Lee K. Clinical Interpretation of Urine Drug Tests: What Clinicians Need to Know About Urine Drug Screens. Mayo Clinic Proceedings Review. Volume 92, Issue 5, p774-796, May 1, 2017. https://www.mayoclinicproceedings.org/article/S0025-6196(16)30825-4/fulltext
Congratulations to a wonderful group of physicians. It is a pleasure to recognize your great accomplishments in the presence of your friends, families, loved ones and the residents and faculty who have learned so much from and with you. I would first like to recognize those of you who are members of the Gold Humanism Honor Society.
There are a remarkable number of awardees in our graduating class of 2020.
CLASS OF 2020
Joe Bennett (R)
Max Berger (R)
Ashley Miller (R)
Leigh Nesheiwat (S)
Kristen Ng (R)
Emily Unks (S)
AND
Arie Francis (R)
Nisha Narayanan (S)
FUTURE PGY-4
Elena Dimiceli (S)
Kamini Doobay (S)
Mark Iscoe (R)
FUTURE PGY-3
Stasha O’Callaghan (S)
Nicholus Warstadt (S)
FUTURE PGY-1
Aaron Bola (S)
Alison (Ali) Graebner (S)
Aron Siegelson (S)
Melissa Socarras (S)
Sarah Spiegel (S)
Thomas Sullivan (S)
Christy Williams (S)
GOLD HUMANISM CORE VALUES
Integrity, Excellence, Compassion, Altruism, Respect, Empathy, Service
These are the values you want as a doctor for yourself or a loved one,
to have outstanding listening skills with patients
to be at your side during a medical emergency,
to have exceptional interest in service to the community,
to have the highest standards of professionalism
to integrate a humanistic approach in patient care.
These values are what brought all of you to NYU-Bellevue and that you have honed throughout your training. The remainder of this talk shows how all of you have been successful and demonstrated these values some of you were elected to the Gold Humanism—all of you have achieved humanistic success.
Your personal efforts in the face of uncertainty of the evolution of the pandemic, the inadequate supplies, the hospital and governmental problematic decisions are remarkable. In our country, the President did not mourn the loss of more than a 100,000 human beings and the needs of society. Nor did he provide the leadership and moral support that the country desperately needed to optimally handle this unprecedented crisis. You, in contrast, demonstrate unflappable commitment to address and overcome obstacles to care for your patients, assist your peers, educate and care for your families and friends, while also caring for yourselves. This is a tribute to your humanism. You created essential ways to help patients who were isolated from families and friends during the critical phases of COVID-19. You utilized new tools to communicate your sorrow, your compassion and love, to maintain essential humanistic traditions of medicine while you could not talk, touch or utilize other essential skills to the fullest extent of a physician.
When you recognized that all your knowledge of the social determinants of medicine was playing out as COVID-19 assaulted the poorest in our country, the people of color, the people with essential jobs without personal protective equipment, the people crowded in apartments and subways and buses, you spoke up and acted with appreciation and understanding of these disparities. You recognized that our system of using medicine to correct the societal social institutionally entrenched disparities was inadequate. George Floyd’s death, and that of Breonna Taylor and innumerable others document the racism in America that destroys a part of us each and every day and by extension reinforces and normalizes white privilege. The ever increasing body of video evidence of the horrors of systemic racism is indisputable. You recognized that the American system of criminalization of social determinants is unacceptable. You spoke up and demonstrated that you saw our blind spots on policing and race. You protested to demand change in America.
Change for equity and justice must occur throughout our society. “Black Lives Matter” will only be realized when the social determinants are truly addressed through changes that impact every vulnerable person. We must recognize that person, institutional and societal failures will not be corrected by medicalizing or criminalizing of socially determined inequities. Racism is systemic. Today you are seeking to create essential changes in medicine that will only occur when all the workplaces and governmental sites across the country, are enriched to allow a full representation of all the voices of all the people.
You are leaders in the response to COVID-19 and the fight against racism. You will not only be remembered for having been present, but particularly for how you have responded. Thank you for your courage, creativity, resiliency and ability to transition and advance under duress. It was a privilege to watch you demonstrate the importance of your core values and the impact that your training here at NYU/Bellevue has had on your ability to integrate them into your practice.
You are truly individuals of immense potential, ideal for advancing our world. How you keep these values and grow them in the next developmental stage of your careers will be critical. Each of you will contribute according to your talent, resources and priorities whether in clinical practice, academics, advocacy or public health. Always in every encounter with patients and their families “Be the change that you wish to see in the world” Mahatma Ghandi.