Core EM - Emergency Medicine Podcast

Group A strep in the pediatric ED: from strep throat to invasive disease and toxic shock. Host: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Group_A_Strep.mp3 Download Leave a Comment Tags: Infectious Diseases, Pediatrics Show Notes Background 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. Clinical Presentation Core findings: tonsillar inflammation/exudate, tender anterior cervical lymphadenopathy, fever. Classic strep tells to hunt for: Palatal petechiae Strawberry tongue Perioral pallor 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 headache even when the throat looks unimpressive. Low threshold to test with fever + abd pain or fever + headache. Diagnosis / Workup Centor / Modified (McIsaac) Score Centor Score (Modified/McIsaac) — MDCalc One point each: fever, tonsillar exudates, tender anterior cervical lymphadenopathy, absence of cough. The Modified (McIsaac) version adds age. Developed and validated in adults (≥16). It is not reliable in young children — don’t lean on it in peds the way you would in an adult. For reference, McIsaac culture-positive probabilities: ~2.5% (0 criteria), 6.5% (1), 15% (2), 32% (3), 56% (4). Testing 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. Complications Suppurative: peritonsillar abscess, sinusitis, meningitis, bacteremia. Non-suppurative: Acute rheumatic fever — typically 1–5 wks post-infection; Jones criteria (AHA 2015 revision · ACC summary · CDC). 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. The spectrum STSS, necrotizing fasciitis, meningitis, bacteremia, peritonitis. 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. Links & References Calculators Centor Score (Modified/McIsaac) for Strep Pharyngitis — MDCalc Guidelines 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” CDC Group A Strep Disease Surveillance and Trends (invasive disease rising since 2014; 2023 20-year high) MMWR — Increase in Pediatric Invasive Group A Streptococcus Infections, Colorado and Minnesota, Oct–Dec 2022 Diagnosing Acute Rheumatic Fever (clinician guidance) Read More

A guide to diagnosing, imaging, and managing acute renal colic and nephrolithiasis in the ED. Hosts: Brian Gilberti, MD Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nephrolithiasis.mp3 Download Leave a Comment Tags: Kidney Stones, Urology Show Notes 1. CLINICAL CORE & PHYSIOLOGIC FRAMEWORK Epidemiologic Risk Profiles 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. Pathophysiologic Symptom Complexes Acute, sudden-onset, maximum-intensity (10/10) unilateral flank pain. Classic structural radiation vector tracking downward toward the ipsilateral groin/genitourinary dermatomes. 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. 4. IMAGING MODALITIES & ALGORITHMIC CLINICAL SELECTION Non-Contrast CT Diagnostics 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. 5. Ultrasonography versus Computed Tomography for Suspected Nephrolithiasis Core Trial Architecture 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. 9. SPONTANEOUS PASSAGE PROBABILITIES Size-Dependent Passage Vectors Stones <5 mm: 70% to 90% spontaneous passage rate. Managed conservatively. Stones 5–10 mm: 50% to 60% spontaneous passage rate. Candidates for MET. Stones >10 mm: <10% spontaneous passage rate. Spontaneous transit is rare; requires urologic intervention. Anatomical Location Passage Vectors Distal Ureter (UVJ area): ~75% spontaneous passage likelihood. Mid-Ureter (Crossing point of iliac vessels): ~60% spontaneous passage likelihood. Proximal Ureter (UPJ to upper third): ~48% spontaneous passage likelihood. Transit Timeline Dynamics Mean passage window spans 2 to 4 weeks for complete structural clearance. Temporal Risk Threshold: Unremitting ureteral obstruction lasting >4 weeks carries an elevated risk of irreversible renal parenchymal injury, persistent AKI, and permanent loss of nephron function. 10. ADMISSION ARCHITECTURE & UROLOGIC CONSULTATION CRITERIA Mandatory Surgical Emergency Decompression Criteria 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. 11. OUTPATIENT DISCHARGE MATRICES & SAFETY NETTING Discharge Criteria Checklists 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. 12. CLINICAL PEARLS & QUICK-REFERENCE SUMMARY NOTES 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. Read More

Diagnosis, workup, and the four-step treatment protocol for thyroid storm. Hosts: Annaliese Elam, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Thyroid_Storm.mp3 Download Leave a Comment Tags: Critica Care, Endocrine, Thyroid Storm Show Notes I. Pathophysiology & Diagnosis 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 Warm, moist skin Precipitating Events: Infection, trauma, or surgery Parturition Abrupt cessation of antithyroid medications Burch-Wartofsky Point Scale (BWPS): ≥ 45: Highly suggestive of Thyroid Storm 25–44: Suggestive of impending storm < 25: Storm unlikely Note: High sensitivity but low specificity; can be skewed by unrelated febrile illness. II. Laboratory & Ancillary Findings Thyroid Panel: Characteristically low TSH with elevated free T₄ and T₃. Metabolic Abnormalities: Mild hyperglycemia (catecholamine-induced insulin inhibition) Mild hypercalcemia Elevated LFTs and leukocytosis Cardiovascular: EKG may show sinus tachycardia or atrial fibrillation with rapid ventricular response. III. Management: The Four-Step Blocking Strategy Step 1: Sympathetic Blockade (Beta Blockers) Agent of Choice: Propranolol Mechanism: Non-selective blockade; in high doses, inhibits peripheral conversion of T₄ to T₃. Dosing: PO: 60–80 mg every 4–6 hours IV: 0.5–1 mg over 10 minutes Critical Pitfall: Avoid in patients with acute decompensated heart failure with systolic dysfunction; risk of cardiovascular collapse. Step 2: Inhibition of Hormone Synthesis (Thionamides) Agent of Choice: Propylthiouracil (PTU) preferred over Methimazole in life-threatening storm. Mechanism: Blocks synthesis of new hormone and inhibits peripheral T₄-to-T₃ conversion (decreases T₃ by ~45% in 24 hours). Dosing: 200–250 mg PO every 4 hours Step 3: Inhibition of Hormone Release (Iodine) Agents: Potassium iodide (SSKI) or Lugol’s solution Critical Timing: Must wait at least 60 minutes AFTER thionamide administration. Rationale: Immediate iodine administration provides substrate for new hormone synthesis (Wolff-Chaikoff effect bypass), potentially worsening thyrotoxicosis. Step 4: Inhibition of Peripheral Conversion & Adrenal Support Agent: Glucocorticoids (Hydrocortisone) Mechanism: Inhibits peripheral T₄ to T₃ conversion and treats potential relative adrenal insufficiency. Dosing: 300 mg IV loading dose, followed by 100 mg IV every 8 hours IV. Supportive Care & Avoidance Measures Hyperpyrexia Management: Acetaminophen is the standard of care Avoid Aspirin: Salicylates displace thyroid hormone from thyroid-binding globulin (TBG), increasing free T₄/T₃ levels Volume Resuscitation: 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. Read More

Angioedema – Recognition and Management in the ED Hosts: Maria Mulligan-Buckmiller, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Angioedema.mp3 Download Leave a Comment Tags: Airway Show Notes Definition & Pathophysiology Angioedema = localized swelling of mucous membranes and subcutaneous tissues due to increased vascular permeability. Triggers increased vascular permeability → fluid shifts into tissues. Etiologies Histamine-mediated (anaphylaxis) Associated with urticaria/hives, pruritus, and redness. Triggered by allergens (foods, insect stings, medications). Rapid onset (minutes to hours). Bradykinin-mediated Hereditary angioedema (HAE): C1 esterase inhibitor deficiency (autosomal dominant). Acquired angioedema: Associated with B-cell lymphoma, autoimmune disease, MGUS. Medication-induced: Most commonly ACE inhibitors; rarely ARBs. Typically lacks urticaria and itching. Gradual onset, can last days if untreated. Idiopathic angioedema Unknown cause; diagnosis of exclusion. Clinical Presentations Swelling Asymmetric, non-pitting, usually non-painful. May involve lips, tongue, face, extremities, GI tract. Respiratory compromise Upper airway swelling → stridor, dyspnea, sensation of throat closure. Airway obstruction is the most feared complication. Abdominal manifestations Bowel wall angioedema can mimic acute abdomen: Nausea, vomiting, diarrhea, severe pain, increased intra-abdominal pressure, possible ischemia. Key Differentiating Features Histamine-mediated: rapid onset, hives/itching, resolves quickly with epinephrine, antihistamines, and steroids. Bradykinin-mediated: slower onset, lacks urticaria, prolonged duration, less responsive to standard anaphylaxis medications. Diagnostic Approach in the ED Focus on airway (ABCs) and clinical assessment. Labs (e.g., C4 level) useful for downstream diagnosis (esp. HAE) but not for acute management. Imaging: only if symptoms suggest abdominal involvement or to rule out other causes. Treatment Strategies Airway protection is always priority: Early consideration of intubation if worsening obstruction or inability to manage secretions. Histamine-mediated (anaphylaxis): Epinephrine (IM), antihistamines, corticosteroids. Bradykinin-mediated: Epinephrine may be tried if unclear etiology (no significant harm, lifesaving if histamine-mediated). Targeted therapies: Icatibant: bradykinin receptor antagonist. Ecallantide: kallikrein inhibitor (less available). C1 esterase inhibitor concentrate: replenishes deficient protein. Fresh frozen plasma (FFP): contains C1 esterase inhibitor. Tranexamic acid (TXA): off-label, less evidence, considered if no other options. Complications to Watch For Airway compromise: rapid deterioration possible. Abdominal compartment syndrome from bowel edema (rare, surgical emergency). Take-Home Points Secure the airway if in doubt. Differentiate histamine-mediated vs bradykinin-mediated by presence/absence of hives/itching and speed of onset. Use epinephrine promptly if suspecting histamine-mediated angioedema or if uncertain. Consider bradykinin-targeted therapies for confirmed hereditary, acquired, or ACE-inhibitor–related angioedema. Recognize ACE inhibitors as the most frequent medication trigger; ARBs rarely cause it. Labs and imaging generally don’t change initial ED management but aid diagnosis for follow-up care. Read More

Granulomatosis with Polyangiitis (GPA) – Recognition and Management in the ED Hosts: Phoebe Draper, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/GPA.mp3 Download One Comment Tags: Rheumatology Show Notes Background A vasculitis affecting small blood vessels causing inflammation and necrosis Affects upper respiratory tract (sinusitis, otitis media, saddle nose deformity), lungs (nodules, alveolar hemorrhage), and kidneys (rapidly progressive glomerulonephritis) Can lead to multi-organ failure, pulmonary hemorrhage, renal failure Red Flag Symptoms: Chronic sinus symptoms Hemoptysis (especially bright red blood) New pulmonary complaints Renal dysfunction Constitutional symptoms (fatigue, weight loss, fever) Workup in the ED: CBC, CMP for anemia and AKI Urinalysis with microscopy (hematuria, RBC casts) Chest imaging (CXR or CT for nodules, cavitary lesions) ANCA testing (not immediately available but important diagnostically) Management: Stable patients: Outpatient workup, urgent rheumatology consult, prednisone 1 mg/kg/day Unstable patients: High-dose IV steroids (methylprednisolone 1 g daily x3 days), consider plasma exchange, cyclophosphamide or rituximab initiation, ICU admission Conditions that Mimic GPA: Goodpasture syndrome (anti-GBM antibodies) TB, fungal infections Lung malignancy Other vasculitides (EGPA, MPA, lupus) ANCA Testing Utility: C-ANCA/PR3-ANCA positive in 80-90% of GPA cases P-ANCA/MPO-ANCA more common in MPA Don’t delay treatment while awaiting results if suspicion is high Outcomes: Without treatment: Fatal within a year (renal failure, respiratory complications) With treatment: 5-year survival ~75-90%, but ~50% relapse rate Long-term rheumatology follow-up is essential Take-Home Points: Always include vasculitis in the differential for unexplained respiratory, renal, or systemic symptoms. Recognize pulmonary-renal syndromes early. Initiate high-dose steroids immediately for unstable patients without waiting for ANCA results. GPA is rare but life-threatening – early recognition saves lives. Read More

We discuss capacity assessment, patient autonomy, safety, and documentation. Hosts: Anne Levine, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Capacity_Assessment.mp3 Download One Comment Show Notes The Importance of Capacity Assessment Arises frequently in the ED, even when not formally recognized Carries both legal implications and ethical weight Failure to appropriately assess capacity can result in: Forced treatment without justification Missed opportunities to respect autonomy Increased risk of litigation and poor patient outcomes Defining Capacity Capacity is: Decision-specific: varies based on the medical choice at hand Time-specific: can fluctuate due to medical conditions, intoxication, delirium Distinct from competency, which is a legal determination Relies on a patient’s ability to: Understand relevant information Appreciate the consequences Reason through options Communicate a clear choice Real-World ED Examples Intoxicated patient with head trauma refusing CT Unreliable neuro exam Potentially time-sensitive intracranial injury Elderly patient with sepsis refusing admission due to caregiving responsibilities Balancing autonomy vs. beneficence Patient with gangrenous diabetic foot refusing surgery Demonstrates logic and consistency despite high-risk decision The 4 Pillars of Capacity Assessment Understanding Can the patient explain: Their condition Recommended treatments Risks and benefits Alternatives and outcomes? Sample prompts: “What are the options for your situation?” “What might happen if we do nothing?” Appreciation Does the patient grasp the personal relevance of the information? Sample prompts: “Why do you think we’re recommending this?” “How do you think this condition could affect you?” Reasoning Can the patient logically explain their choice? Must demonstrate a rational process, even if the outcome seems unwise Sample prompts: “What factors are you considering in making this decision?” “What led you to this conclusion?” Choice Is the patient able to clearly communicate a decision? Any modality acceptable: verbal, written, gestural Sample prompts: “We’ve discussed several options. What do you want to do?” “Have you decided what option is best for you?” Common ED Challenges & Solutions Time Pressure Capacity assessments can be time-consuming Yet, patients leaving AMA without proper evaluation are at higher risk: ↑ 30-day mortality ↑ 30-day readmission Communication Barriers Language differences → use certified interpreters Cognitive impairment or psych illness → clarify baseline status Noisy ED environment → relocate to quiet space Use simple language, avoid jargon Ethical Dilemmas Providers may disagree with patient choices Ensure decision-making process—not the choice itself—is being judged Use tools like the Aid to Capacity Evaluation (ACE) When uncertain, consult Psychiatry or Risk Management Best Practices in Documentation Clearly document: The patient’s understanding, appreciation, reasoning, and choice Information delivered: Condition Treatment recommendations Alternatives and risks Patient’s responses and logic Witnesses to the conversation Any discharge instructions, including: Follow-up plans Prescriptions provided Return precautions Also document: If patient refused treatment, document: That risks and benefits were clearly explained That refusal was voluntary If treatment was administered despite objection: Document rationale for presumed lack of capacity Legal/ethical justification for action Involvement of other services (e.g., Psychiatry, Risk) Read More

We dive into the recognition and management of blast crisis. Hosts: Sadakat Chowdhury, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Blast_Crisis.mp3 Download 2 Comments Tags: Hematology, Oncology Show Notes Topic Overview Blast crisis is an oncologic emergency, most commonly seen in chronic myeloid leukemia (CML). Defined by: >20% blasts in peripheral blood or bone marrow. May include extramedullary blast proliferation. Without treatment, median survival is only 3–6 months. Pathophysiology & Associated Conditions Usually occurs in CML, but also in: Myeloproliferative neoplasms (MPNs) Myelodysplastic syndromes (MDS) Transition from chronic to blast phase often reflects disease progression or treatment resistance. Risk Factors 10% of CML patients progress to blast crisis. Risk increased in: Patients refractory to tyrosine kinase inhibitors (e.g., imatinib). Those with Philadelphia chromosome abnormalities. WBC >100,000, which increases risk for leukostasis. Clinical Presentation Symptoms often stem from pancytopenia and leukostasis: Anemia: fatigue, malaise. Functional neutropenia: high WBC count, but increased infection/sepsis risk. Thrombocytopenia: bleeding, bruising. Leukostasis/hyperviscosity effects by system: Neurologic: confusion, visual changes, stroke-like symptoms. Cardiopulmonary: ARDS, myocardial injury. Others: priapism, limb ischemia, bowel infarction. Rapid deterioration is common — early recognition is critical. Diagnostic Workup CBC with differential: assess blast % and cytopenias. Peripheral smear and manual diff: confirm immature blasts. CMP: screen for tumor lysis syndrome: Elevated potassium, phosphate, uric acid. Low calcium. LDH & uric acid: markers of high cell turnover. Coagulation studies (PT, PTT): assess for DIC. Definitive tests (done inpatient): bone marrow biopsy, flow cytometry. Emergency Department Management Resuscitation & ABCs: oxygen, IV fluids, vitals monitoring. Avoid aggressive transfusions: Risk of hyperviscosity with PRBCs and platelets. Initiate broad-spectrum antibiotics early: High suspicion for sepsis in functionally neutropenic patients. Consider antifungals for prolonged febrile neutropenia. Cytoreduction strategies: Hydroxyurea to lower WBCs quickly. Tyrosine kinase inhibitors (TKIs). High-dose chemotherapy. Early consultation with hematology/oncology is essential. Mutation testing may guide targeted therapy. Prognosis Without treatment: median survival ~3 months. With treatment: Potential survival >1 year. Best outcomes in patients who enter a second chronic phase and undergo allogeneic stem cell transplant. Ethical & Logistical Considerations Treatment may involve aggressive interventions with serious side effects. Important to assess: Patient goals of care. Capacity for informed consent. Resource limitations: Not all hospitals have oncology services. Patients may require transfer over long distances. Emphasize early, transparent discussions with patients and families. Top 3 Take-Home Points Recognize early: Look for cytopenias, leukostasis, and rapid clinical decline. Resuscitate appropriately: Start antibiotics; be cautious with transfusions. Call for help: Early hematology/oncology involvement is essential for definitive care. Read More

We explore the expanding field of Geriatric Emergency Medicine. Hosts: Ula Hwang, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Geriatric_Emergency_Medicine.mp3 Download One Comment Tags: Geriatric Show Notes Key Topics Discussed Importance and impact of geriatric emergency departments. Optimizing care strategies for geriatric patients in ED settings. Practical approaches for non-geriatric-specific EDs. Challenges in Geriatric Emergency Care Geriatric patients often present with: Multiple chronic conditions Polypharmacy Functional decline (mobility issues, cognitive impairments, social isolation) Adapting Clinical Approach Core objective remains acute issue diagnosis and treatment. Additional considerations for geriatric patients: Review and caution with medications to prevent adverse reactions. Address functional limitations and cognitive impairments. Emphasize safe discharge and care transitions to prevent unnecessary hospitalization. Identifying High-Risk Geriatric Patients Screening tools: Identification of Seniors at Risk (ISAR) Frailty screens Alignment with the “Age-Friendly Health Systems” initiative focusing on: Mentation Mobility Medications Patient preferences (what matters most) Mistreatment (elder abuse awareness) Minimizing Hospital-Related Harms Involvement of multidisciplinary teams: Social workers and care managers for care transitions Geriatric-certified pharmacists for medication review Coordination with outpatient services post-discharge Implementing Geriatric Care in All EDs Basic geriatric care achievable even in resource-limited or rural EDs. Level 3 Geriatric ED Accreditation can be achieved through: Improved care transitions Staff education enhancements Age-friendly environments (comfort, nutrition, hydration) Future of Geriatric Emergency Medicine Vision: Universal integration of geriatric-focused care. Goals: Enhanced patient experience Improved care transitions Alignment of treatments with patient goals Broader enhancement of emergency care quality for all patient populations Read More

We discuss the injuries sustained from smoke inhalation. Hosts: Sarah Fetterolf, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Smoke_Inhalation.mp3 Download Leave a Comment Tags: Environmental, Toxicology Show Notes Table of Contents 00:37 – Overview of Smoke Inhalation Injury 00:55 – Three Key Pathophysiologic Processes 01:41 – Physical Exam Findings to Watch For 02:12 – Airway Management and Early Intervention 03:23 – Carbon Monoxide Toxicity 04:24 – Workup and Initial Treatment of CO Poisoning 06:14 – Cyanide Toxicity 07:19 – Treatment Options for Cyanide Poisoning 09:12 – Take-Home Points and Clinical Pearls Physiological Effects of Smoke Inhalation: Thermal Injury: Direct upper airway damage from heated air or steam. Leads to swelling, inflammation, and possible airway obstruction. Chemical Irritation: Causes bronchospasm, mucus plugging, and inflammation in the lower airways. Increases capillary permeability, potentially causing pulmonary edema. Systemic Toxicity: Primarily involves carbon monoxide and cyanide poisoning. Clinical Signs and Symptoms: Physical Exam: Facial burns, singed nasal hairs Hoarseness, stridor (upper airway swelling) Carbonaceous sputum (lower airway edema) Systemic Symptoms: Headache, dizziness, nausea Syncope, seizures, altered mental status Airway Management Considerations: Not every patient requires immediate intubation. Intubation should be performed early if airway compromise is suspected, as swelling can rapidly progress. Close airway monitoring recommended for all patients. Carbon Monoxide Poisoning: Common cause of death post-smoke inhalation (50–75% of fire-related injuries). Hemoglobin affinity 250 times greater for CO than oxygen, impairing tissue oxygenation. Diagnosis: Carboxyhemoglobin level via VBG (ensure proper lab ordering). Pulse oximetry unreliable; falsely high readings. Treatment: Immediate high-flow oxygen administration. Consider hyperbaric oxygen therapy for severe cases to reduce delayed neurocognitive sequelae. Cyanide Poisoning: Blocks cytochrome oxidase in electron transport chain, halting aerobic ATP production. Patients present critically ill; notable features include: Elevated lactate levels (>8–10 mmol/L) Arterialization of venous blood Treatment: First-line therapy: hydroxocobalamin (Cyanokit) binds cyanide forming vitamin B12 for renal excretion. Alternative: Cyanide antidote kit (amyl nitrite, sodium nitrite, sodium thiosulfate); induces methemoglobinemia and requires monitoring. Important note: hydroxocobalamin turns blood and urine bright red; draw labs beforehand. Key Takeaways: Assess for airway compromise and signs of inhalation injury early. Maintain a high index of suspicion for CO and cyanide poisoning in smoke inhalation victims. Immediate, aggressive oxygen therapy and early antidote administration can significantly impact outcomes. Read More

We discuss the evaluation of and treatment options for acute back pain. Hosts: Benjamin Friedman, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Back_Pain.mp3 Download Leave a Comment Tags: Musculoskeletal, Orthopaedics Show Notes **Please fill out this quick survey to help us develop additional resources for our listeners: Core EM Survey** Clinical Evaluation: 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. Read More

We discuss the impact of family presence during resuscitations. Hosts: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Family_Presence_During_Resuscitation.mp3 Download Leave a Comment Tags: Critical Care, Pediatrics Show Notes Overview 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. Evidence from the Literature New England Journal of Medicine study on Family Presence During Cardiopulmonary Resuscitation (Jabre et al., 2013): 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. Read More

We discuss the recognition and treatment of necrotizing fasciitis. Hosts: Aurnee Rahman, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Necrotizing_Fasciitis.mp3 Download Leave a Comment Tags: Critical Care, General Surgery Show Notes Table of Contents 0:00 – Introduction 0:41 – Overview 1:10 – Types of Necrotizing Fasciitis 2:21 – Pathophysiology & Risk Factors 3:16 – Clinical Presentation 4:06 – Diagnosis 5:37 – Treatment 7:09 – Prognosis and Recovery 7:37 – Take Home points Introduction Necrotizing soft tissue infections can be easily missed in routine cases of soft tissue infection. High mortality and morbidity underscore the need for vigilance. Definition A rapidly progressive, life-threatening infection of the deep soft tissues. Involves fascia and subcutaneous fat, causing fulminant tissue destruction. High mortality often due to delayed recognition and treatment. Types of Necrotizing Fasciitis Type I (Polymicrobial) Involves aerobic and anaerobic organisms (e.g., Bacteroides, Clostridium, Peptostreptococcus). Common in immunocompromised patients or those with comorbidities (e.g., diabetes, peripheral vascular disease). Type II (Monomicrobial) Often caused by Group A Streptococcus (Strep pyogenes) or Staphylococcus aureus. Can occur in otherwise healthy individuals. Vibrio vulnificus (associated with water exposure) is another example. Fournier’s Gangrene (Subset) Specific to perineal, genital, and perianal regions. Common in diabetic patients. Higher mortality, especially in females. Pathophysiology Spread Along Fascia Poor blood supply in fascial planes allows infection to advance rapidly. Tissue ischemia worsened by vascular thrombosis → rapid necrosis. High-Risk Patients Diabetes with vascular compromise. Recent surgeries or trauma (introducing bacteria into deep tissue). Immunosuppression (e.g., cirrhosis, malignancy, or immunosuppressive meds). NSAID use may mask symptoms, delaying diagnosis. Clinical Presentation Early Signs & Symptoms Severe Pain out of proportion to exam findings. Erythema (often with indistinct borders). Fever, Malaise (systemic signs of infection). Rapid progression with possible color changes (red → purple). Bullae Formation (fluid-filled blisters) and skin necrosis/gangrene. Crepitus in polymicrobial cases (gas production in tissue). Late-Stage Signs Systemic toxicity: hypotension, multi-organ failure if untreated. Diagnosis Clinical Suspicion Is Key Pain out of proportion, rapid progression, systemic signs. The “finger test” (small incision to explore fascial planes). Surgical Consultation Early surgical exploration is often the definitive diagnostic step. Lab Tests LRINEC Score (CRP, WBC, Hemoglobin, Sodium, Creatinine, Glucose) to stratify risk. Not definitive but can guide suspicion. Imaging CT scan may reveal gas in tissues, fascial edema, or muscle involvement. Must not delay surgical intervention if clinical suspicion is high. Treatment Principles Immediate & Aggressive Surgical Debridement Often multiple surgical procedures are required as necrosis progresses. Debridement back to healthy tissue margins. Empiric Broad-Spectrum Antibiotics Cover gram-positive (including MRSA), gram-negative, and anaerobes. Examples include: Vancomycin or Linezolid (for MRSA). Piperacillin-tazobactam or Carbapenems (for gram-negative & anaerobes). Clindamycin (to inhibit bacterial toxin production). Adjust based on culture results later. Adjunct Therapies Hyperbaric Oxygen Therapy (if available) for resistant cases. Evidence is mixed; not universally accessible. Supportive Care Intensive monitoring, often in an ICU setting. Fluid resuscitation & vasopressors for septic shock. Prognosis & Disposition High Mortality Rate Influenced by infection site, patient’s baseline health, and speed of intervention. Importance of Rapid Intervention Early recognition, aggressive surgery, and antibiotics improve survival. Long-Term Considerations Patients may require extensive rehabilitation. Reconstructive surgery often needed for tissue deficits. Disposition Operative management is mandatory; patients do not go home. Critical care admission is typical for hemodynamic monitoring and support. Five Key Take-Home Points High Suspicion Saves Lives: Recognize severe pain out of proportion as a critical red flag. Know Your NF Types & Risk Factors: Type I polymicrobial vs. Type II monomicrobial, plus subsets (Fournier’s). Clinical Diagnosis Above All: LRINEC and imaging help, but timely surgical exploration is paramount. Combined Surgical & Medical Therapy: Early debridement + broad-spectrum antibiotics (including toxin inhibition) is lifesaving. Extended Recovery & Mortality Risks: High mortality if missed or delayed. Expect prolonged rehab and possible multiple surgeries. Resources & Further Reading LRINEC Score Calculator  EMCrit – Necrotizing Fasciitis Read More

We sit down with one of our toxicologists to discuss acetaminophen toxicity. Hosts: Marlis Gnirke, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acetaminophen_Toxicity.mp3 Download One Comment Tags: Toxicology Show Notes Table of Contents 0:35 – Hidden acetaminophen toxicity in OTC products 3:24 – Pharmacokinetics and toxicokinetics  6:06 – Clinical Course 9:22 – The antidote – NAC 11:02 – The Rumack-Matthew Nomogram  17:36 – Treatment protocols 22:34 – Monitoring and Lab Work 23:23 – Considerations when treating pediatric patients 23:57 – IV APAP overdose, fomepizole  25:42 – Take Home Points Acetaminophen vs. Tylenol: The importance of recognizing that acetaminophen is found in many products beyond Tylenol. Common medications containing acetaminophen, such as Excedrin, Fioricet, Percocet, Dayquil/Nyquil, and others. The risk of unintentional overdose due to combination products. Prevalence of Acetaminophen Toxicity: Widespread availability and under-recognition contribute to its prevalence. The potential for unintentional overdose when taking multiple medications containing acetaminophen. Pharmacokinetics and Metabolism: Normal metabolism pathways of acetaminophen and the role of glutathione. Formation of the toxic metabolite NAPQI during overdose situations. Saturation of safe metabolic pathways leading to hepatotoxicity. Pathophysiology of Liver Injury: How excessive NAPQI leads to hepatocyte death, especially in zone III of the liver. The difference between therapeutic dosing and overdose metabolism. Clinical Stages of Acetaminophen Toxicity: Stage 1: Asymptomatic or nonspecific symptoms (first 24 hours). Stage 2: Onset of hepatic injury (24-72 hours), elevated AST/ALT. Stage 3: Maximum hepatotoxicity (72-96 hours), signs of liver failure. Stage 4: Recovery phase, complete hepatic regeneration if survived. Antidote – N-Acetylcysteine (NAC): Mechanisms of NAC in replenishing glutathione and detoxifying NAPQI. The importance of early administration, ideally within 8 hours post-ingestion. NAC’s role even in late presenters and in fulminant hepatic failure. The Rumack-Matthew Nomogram: How to use the nomogram for acute overdoses to determine the need for NAC. Limitations in chronic overdoses and late presentations. Emphasis on obtaining accurate time of ingestion and acetaminophen levels. Treatment Protocols: Standard 21-hour IV NAC protocol and dosing specifics. Managing anaphylactoid reactions associated with IV NAC. Criteria for extending NAC therapy beyond 21 hours. Monitoring and Laboratory Work: Importance of trending AST/ALT, INR, creatinine, lactate, and phosphate. Use of the King’s College Criteria for potential liver transplant evaluation. Special Considerations: Adjustments in pediatric patients regarding NAC dosing volumes. Awareness of IV acetaminophen overdoses and their management. Emerging discussions on the use of fomepizole in massive overdoses. Take-Home Points: Comprehensive Medication History: Always inquire about all medications taken to assess for potential acetaminophen exposure. Early Recognition and Treatment: Due to often silent initial stages, maintain a high index of suspicion and measure acetaminophen levels promptly. Understanding Metabolism and Toxicity: Recognize how overdose alters metabolism, leading to toxic NAPQI accumulation. N-Acetylcysteine Efficacy: NAC is most effective when administered early but remains beneficial even in advanced stages. Proper Use of the Nomogram: Utilize the Rumack-Matthew Nomogram appropriately for acute ingestions and consult toxicology when in doubt. Monitoring and Continuing Care: Be vigilant in monitoring laboratory values and prepared to extend NAC therapy as needed. Consultation and Resources: Engage with poison control centers and utilize available resources for complex cases.   Resources Mentioned Rumack-Matthew Nomogram  Rumack-Matthew Nomogram, credit: MDCalc King’s College Criteria King’s College Criteria for Acetaminophen Toxicity 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. Read More

We review Sexually Transmitted Infections and pertinent updates in diagnosis and management. Hosts: Avir Mitra, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Sexually_Transmitted_Infections_2_0.mp3 Download Leave a Comment Tags: gynecology, Infectious Diseases, Urology Show Notes Table of Contents (1:49) Chlamydia  (3:31) Gonorrhea (4:50) PID (6:14) Syphilis (8:08) Neurosyphilis  (9:13) Tertiary Syphilis (10:06) Trichomoniasis  (11:13) Herpes (12:49) HIV (14:10) PEP (15:13) Mycoplasma Genitalium  (18:00) Take Home Points Chlamydia: Prevalence: Most common STI. High percentage of asymptomatic cases (40% to 96%). Presentation: Urethritis, cervicitis, pelvic inflammatory disease (PID), prostatitis, proctitis, pharyngitis, arthritis. Importance of considering extra-genital sites (oral and rectal infections). Testing: Gold Standard: Nucleic Acid Amplification Test (NAAT) via PCR. Sampling Sites: Endocervical or urethral swabs preferred over urine samples due to higher sensitivity. Triple-site testing (genital, rectal, pharyngeal) recommended for comprehensive detection. Treatment Updates: Previous Regimen: Azithromycin 1 g orally in a single dose. Current First-Line Treatment: Doxycycline 100 mg orally twice daily for 7 days. Alternatives: Azithromycin remains an option for patients unlikely to adhere to a 7-day regimen or for pregnant patients. Note: PID treatment differs and will be discussed separately. Gonorrhea: Presentation: Similar to chlamydia; can be asymptomatic. Symptoms include urethritis, cervicitis, PID, prostatitis, proctitis, pharyngitis. Testing: Gold Standard: NAAT. Sampling Sites: Endocervical swabs are more sensitive than urine samples. Triple-site testing is crucial to avoid missing infections. Treatment Updates: Previous Regimen: Ceftriaxone 250 mg IM plus azithromycin 1 g orally. Current Recommendation: Ceftriaxone 500 mg IM single dose. Adjusted due to rising azithromycin resistance and updated pharmacokinetic data. Co-Infection Considerations: High rates of chlamydia and gonorrhea co-infection (20% to 40%). CDC recommends empiric treatment for chlamydia when treating gonorrhea to prevent complications like PID and infertility. Pelvic Inflammatory Disease (PID): Etiology: Not solely caused by chlamydia and gonorrhea; about 50% of cases involve other pathogens like bacterial vaginosis (BV) organisms and anaerobes. Treatment Changes: Expanded Coverage Regimen: Ceftriaxone 500 mg IM once. Doxycycline 100 mg orally twice daily for 14 days. Metronidazole 500 mg orally twice daily for 14 days. Inclusion of metronidazole addresses anaerobic bacteria contributing to PID. Syphilis: Stages and Presentation: Primary Syphilis: Painless chancre on genitals. Treatment: Penicillin G 2.4 million units IM single dose. Secondary Syphilis: Rash (often diffuse), mucocutaneous lesions, nonspecific joint pain. Treatment: Same as primary syphilis. Latent Syphilis: Asymptomatic phase; divided into early (<1 year) and late (>1 year). Treatment for Late Latent: Penicillin G 2.4 million units IM once weekly for 3 weeks. Recommended when the timing of infection is unclear. Neurosyphilis: Can occur at any stage. Symptoms include visual changes, severe headaches, neurological deficits. Diagnosis: Requires lumbar puncture (LP) for confirmation. Treatment: Admission for intravenous penicillin G. Tertiary Syphilis: Rare, advanced stage with severe manifestations (e.g., gummas, cardiovascular complications, neurological signs). Treatment: Extended penicillin therapy similar to late latent syphilis. Trichomoniasis: Presentation: Often asymptomatic. In women: Vaginal discharge. In men: Urethritis. Testing: Shift from wet mount microscopy to NAAT for improved detection. Swab samples preferred over urine for higher sensitivity. Treatment Updates: Previous Regimen: Metronidazole 2 g orally in a single dose. Current Recommendations: Women: Metronidazole 500 mg orally twice daily for 7 days. Men: Single 2 g dose remains acceptable. Herpes Simplex Virus (HSV): Types and Transmission: HSV-1 and HSV-2: Both can cause oral and genital infections. Increasing crossover between oral and genital sites. Testing: Serum IgG testing not useful for acute diagnosis due to widespread prior exposure. Preferred Method: PCR testing from lesion swabs. Clinical Tip: If the lesion is characteristic, clinicians may start treatment without waiting for test results. Treatment: Preferred Medication: Valacyclovir (Valtrex) for ease of dosing. Dosage: Initial episode: 1 g orally twice daily for 7 to 10 days. Recurrence: 1 g daily for 5 days. Alternative: Acyclovir for cost considerations. Human Immunodeficiency Virus (HIV): Testing Limitations: Window Periods: Fourth-generation tests have a window period of 2 to 4 weeks. Negative results during this period may not rule out recent infection. Acute HIV Infection: Presents with flu-like symptoms: malaise, joint pains, fatigue. Diagnosis Challenges: Standard HIV tests may be negative during the window period. Options: Empiric treatment with follow-up testing. Order an HIV viral load test (more sensitive but expensive and delayed results). Post-Exposure Prophylaxis (PEP): Timing: Initiate ideally within 72 hours of potential exposure. Duration: 28-day regimen. Pre-Treatment Testing: Baseline HIV test to rule out existing infection. Renal and hepatic function tests to monitor for medication side effects. Follow-Up: Reassess renal/hepatic function in 2 weeks. Mycoplasma genitalium: Recognition: Newly recognized STI by the CDC in 2021. Causes cervicitis and urethritis. Possible associations with PID and proctitis, but not definitively established. Testing: When to Test: Only in patients with persistent symptoms after standard STI testing and treatment. Not recommended for initial screening. Method: NAAT. Treatment: Step 1: Doxycycline 100 mg orally twice daily for 7 days. Step 2: Moxifloxacin 400 mg orally once daily for 7 days. Addresses antibiotic resistance concerns and ensures comprehensive treatment. General Management and Patient Counseling: Partner Notification: Encourage patients to inform sexual partners for testing and treatment. Medication Adherence: Emphasize the importance of completing the full course of prescribed medications. Prevention Measures: Discuss the use of barrier protection (e.g., condoms) to prevent transmission and reinfection. Follow-Up Care: Advise patients to return if symptoms persist, indicating possible infections like Mycoplasma genitalium. Key Take-Home Points: Chlamydia Treatment Update: Doxycycline 100 mg orally twice daily for 7 days is now first-line treatment for cervical infections. For epididymitis, extend doxycycline to 10 days. Gonorrhea Treatment Update: Treat with a single 500 mg IM dose of ceftriaxone. PID Management Update: Expanded antimicrobial coverage includes: Ceftriaxone 500 mg IM once. Doxycycline 100 mg orally twice daily for 14 days. Metronidazole 500 mg orally twice daily for 14 days. Mycoplasma genitalium Recognition: Test in patients with persistent symptoms after standard treatment. Treat with doxycycline followed by moxifloxacin. HIV Testing and PEP: Be aware of HIV test window periods; negative results may not rule out recent infection. Consider HIV viral load testing if acute infection is suspected. Initiate PEP within 72 hours for a 28-day course, ensuring clear discharge planning and patient support. Read More

We discuss migraines with one of the authorities in the field. Hosts: Benjamin Friedman, MD of Montefiore Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Migraines.mp3 Download Leave a Comment Tags: Neurology Show Notes Initial Approach to Diagnosing Migraines: 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. Read More

We discuss a new class of medications, Immune Checkpoint Inhibitors, and their side effects. Hosts: Avir Mitra, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Immune_Checkpoint_Inhibitors.mp3 Download Leave a Comment Tags: Oncology Show Notes Overview of Immune Checkpoint Inhibitors (ICIs) 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. Read More

We discuss a case of ataxia in children and how to approach the evaluation of these pts. Hosts: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Ataxia_in_Children.mp3 Download Leave a Comment Tags: Neurology, Pediatrics Show Notes Introduction 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. Read More

We discuss the approach to diagnosing and managing hypernatremia in the emergency department. Hosts: Abigail Olinde, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hypernatremia.mp3 Download One Comment Tags: Electorlye Show Notes Episode Overview: Introduction to Hypernatremia Definition and basic concepts Clinical presentation and risk factors Diagnosis and management strategies Special considerations and potential complications Definition and Pathophysiology: Hypernatremia is defined as a serum sodium level over 145 mEq/L. It can be acute or chronic, with chronic cases being more common. Symptoms range from nausea and vomiting to altered mental status and coma. Causes of Hypernatremia based on urine studies: Urine Osmolality > 700 mosmol/kg Causes: Extrarenal Water Losses: Dehydration due to sweating, fever, or respiratory losses Unreplaced GI Losses: Vomiting, diarrhea Unreplaced Insensible Losses: Burns, extensive skin diseases Renal Water Losses with Intact AVP Response: Diuretic phase of acute kidney injury Recovery phase of acute tubular necrosis Postobstructive diuresis Urine Osmolality 300-600 mosmol/kg Causes: Osmotic Diuresis: High glucose (diabetes mellitus), mannitol, high urea Partial AVP Deficiency: Incomplete central diabetes insipidus Partial AVP Resistance: Nephrogenic diabetes insipidus Urine Osmolality < 300 mosmol/kg Causes: Complete AVP Deficiency: Central diabetes insipidus Complete AVP Resistance: Nephrogenic diabetes insipidus Urine Sodium < 25 mEq/L Causes: Extrarenal Water Losses with Volume Depletion: Vomiting, diarrhea, burns Unreplaced Insensible Losses: Sweating, fever, respiratory losses Urine Sodium > 100 mEq/L Causes: Sodium Overload: Ingestion of salt tablets, hypertonic saline administration Salt Poisoning: Deliberate or accidental ingestion of large amounts of salt Mixed or Variable Urine Sodium Causes: Diuretic Use: Loop diuretics, thiazides Adrenal Insufficiency: Mineralocorticoid deficiency 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. Read More

We discuss an approach to the acutely agitated patient and review medications commonly used. Hosts: Jonathan Kobles, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Agitation.mp3 Download Leave a Comment Tags: Agitation, psychiatry, Toxicology Show Notes Background/Epidemiology •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. •IV/IM Regimens: •Medications: Droperidol, haloperidol, midazolam, ketamine. •ACEP 2023 Guidelines: Recommend droperidol with midazolam or an atypical antipsychotic for severe agitation. •Pharmacokinetics (IM): •Haloperidol: IM onset in 15, time to sedation ~25 minutes, can last for 2 hours •Droperidol: IM onset in 5-10 minutes, duration 2-4 hours but can last as long as 12 hours •Midazolam: IM onset ~15 minutes, , duration 20 minutes – 2 hours. •Lorazepam: IM onset ~15-30 minutes, , duration up to 3 hours •Ketamine: IM onset in ~5 minutes, duration 5-30 minutes. Special Situations •Elderly/Dementia: Optimize environment, use non-pharmacologic measures, avoid benzodiazepines to reduce delirium risk. •Parkinson’s Disease: Avoid antipsychotics that can precipitate a Parkinsonian crisis. •Autism/Pediatrics: Engage caregivers, create a calming environment, avoid aggressive measures. •Alcohol Withdrawal: Utilize benzodiazepines and phenobarbital. Re-dosing and Physical Restraints •Re-dosing: Use the lowest effective dose, consider continuous monitoring, and reassess frequently. •Physical Restraints: Employ as a last resort, ensuring close monitoring for any adverse effects. Final Points •Clinical Leadership: Physicians should lead with clear communication, planning, and support for the team. •Continuous Learning: Regular debriefing and assessment after each incident to improve future responses.   Read More

We discuss an approach to the critically ill infant. Hosts: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/The_Critically_Ill_Infant.mp3 Download Leave a Comment Tags: Pediatrics Show Notes The Critically Ill Infant: THE MISFITS Trauma ‘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).   Read More

We review Acute Respiratory Distress Syndrome Hosts: Sadakat Chowdhury, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/ARDS.mp3 Download Leave a Comment Tags: Critical Care, Pulmonary Show Notes Definition of ARDS: 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. Pathophysiology: Exudative phase: Immune-mediated alveolar damage, pulmonary edema, cytokine release. Proliferative phase: Reabsorption of edema fluid. Fibrotic phase: Potential for prolonged ventilation. Etiology: Direct lung injury (pneumonia, toxins, aspiration, trauma, drowning) and indirect causes (sepsis, pancreatitis, transfusion reactions, certain drugs). Diagnostics: Comprehensive workup including imaging (chest X-ray, CT), laboratory tests (complete blood count, basic metabolic panel, blood gases), and specialized tests depending on suspected etiology. Management Strategies: Steroids: Beneficial in certain etiologies of ARDS, with specifics on dosing and duration. Fluid Management: Conservative fluid strategy, diuresis guided by patient condition. Ventilation: Non-invasive ventilation (NIV) preferred in specific cases; mechanical ventilation strategies to ensure lung-protective ventilation. Proning: Used in severe ARDS to improve oxygenation. Inhaled Vasodilators: Used for refractory hypoxemia and specific complications like right heart failure. Extracorporeal Membrane Oxygenation (ECMO): Considered for severe ARDS as salvage therapy. Supportive Care: Includes monitoring and management of complications, nutrition, and physical therapy. Ventilation Specifics: Tidal volume and pressure settings aim for lung-protective strategies to prevent ventilator-induced lung injury. Permissive hypercapnia, plateau pressure, PEEP, and ventilation mode adjustments based on patient response. ARDSnet Table: ventilator_protocol_2008-07 Read More

We review Nitrous Oxide Toxicity: Symptoms, diagnosis, and treatment overview Hosts: Stefanie Biondi, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nitrous_Oxide_Toxicity.mp3 Download Leave a Comment Tags: Toxicology Show Notes Patient Case Illustration 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/ Khin-Htun S, Tan H, Aung T. “Approach to a Patient With Weakness” 2021 Feb 15. Youtube. https://www.youtube.com/watch?v=3WQvtCuC4Fo&t=922s  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. Lim PAC. Transverse Myelitis. Essentials of Physical Medicine and Rehabilitation. 2020:952–9. doi: 10.1016/B978-0-323-54947-9.00162-0. Epub 2019 Apr 17. PMCID: PMC7151963. 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&sectionid=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.  https://www.nytimes.com/2021/01/30/style/nitrous-oxide-whippets-tony-hsieh.html  Read More

We review threatened abortion and the complexities in its care. Hosts: Stacey Frisch, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Threatened_Abortion.mp3 Download One Comment Tags: OBGYN Show Notes Background 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. Read More

We review a general approach to syncope in children. Hosts: Brian Gilberti, MD Ellen Duncan, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Syncope_in_Children.mp3 Download Leave a Comment Tags: Cardiology, Pediatrics Show Notes Initial Evaluation and Management: 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. Condition Characteristic ECG Findings Congenital/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 Read More

We go over the treatment of rapid atrial fibrillation (afib with RVR). Hosts: Brian Gilberti, MD Jonathan Kobles, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Rapid_Atrial_Fibrillation.mp3 Download One Comment Tags: Cardiology Show Notes Understanding AF with RVR Categories General AF with RVR: Definition and basic understanding. Rapid AF with Pre-excitation: Characteristics and complications. Chronic AF in Critical Illness: Identification and special considerations. Stability Assessment in AF with RVR ACLS Protocols: Distinction between unstable and stable patients. Unstable Patients: Immediate need for synchronized cardioversion, standard dose at 200 J for adults. Stable Patients: Rate vs. rhythm control strategies, consideration of underlying etiology. Limitations in Chronic AF: Challenges in patients with AF secondary to critical illness. ACLS Guidelines and ECG Findings Tachycardia with a Pulse Approach: Initial assessment guidelines. ECG Interpretation: Irregularly Irregular Rhythm: Absence of discernible P waves. Ventricular Rate: Typically over 100 bpm. QRS Complexes: Usually narrow, alterations in the presence of bundle branch block or ventricular rate-related aberrancy. Identifying Pre-Excitation Syndromes: Signs of shortened PR interval and slurred QRS, indication of Wolff-Parkinson-White Syndrome. AF with Pre-Excitation (WPW Syndrome) Risk Assessment: Dangers of using AV nodal blockers (BB/CCB, digoxin, adenosine). Alternative Management: Utilization of procainamide for stable patients, synchronized electrical cardioversion for unstable patients. Treatment Approaches for AF Types General Rapid AF: First Line Agents: Metoprolol vs. Diltiazem. Metoprolol Considerations: Dosing (5 mg every 10-15 minutes, max 15 mg), benefits in CAD and HF, limitations in asthma/COPD patients. Diltiazem Advantages: Faster action, suitability in asthma/COPD, typical dosing (0.25 mg/kg initial, followed by 0.35 mg/kg if needed). Critically Ill Patients: Tailoring treatment to underlying pathology, avoiding typical AF pharmacologic treatments. Systematic Evaluation of Tachycardia Causes (TACHIES Mnemonic) Thyrotoxicosis, Alcohol withdrawal, Cardiac issues, Hemorrhage, Intervals (WPW), Embolus, Sepsis. Application of the mnemonic for a comprehensive approach to differential diagnosis. Ultrasound in Diagnostic Assessment Application in Undiagnosed Tachycardia: Identifying EF, pericardial effusion, valvular pathology, and signs of pulmonary embolism. Fluid Status Evaluation: Use of ultrasound for assessing b-lines in lung scans. Management of Chronic AF with HD Instability Assessment of Hemodynamic Impact: Effects of extreme tachycardia on cardiac output, preload and afterload considerations. Chronic vs. Paroxysmal AF: Differentiation in clinical presentation and treatment response. Approaches in Complex AF Cases Addressing RVR of Unclear Etiology: Targeted therapies based on suspected underlying causes. Medication Strategies: Amiodarone: Bolus and drip approach, slow AV nodal without significant impact on contractility. Esmolol: Titration for heart rate control, short-acting nature allowing for rapid cessation if adverse effects are observed. Comprehensive Patient Disposition Considerations: Hemodynamic stability, underlying cause, comorbidities, outpatient follow-up feasibility. 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. Read More

We discuss Electrical Storm (VT storm) and how to care for the very irritable heart. Hosts: Brian Gilberti, MD Reed Colling, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Electrical_Storm.mp3 Download Leave a Comment Tags: Cardiology Show Notes Background/Overview of VT: Definition: What makes it a storm  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. Read More

We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma) Hosts: Brian Gilberti, MD Jonathan Kobles, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3 Download 2 Comments Tags: Renal Colic Show Notes Introduction Background Physiology: Normal range and the significance of deviations (>5.5 mEq/L) Epidemiology: Prevalence of hyperkalemia in the ER ESRD missed HD → ECG, monitor Causes / Risk Factors Causes Kidney Dysfunction, Medications,  Cellular Destruction,  Endocrine Causes, Pseudohyperkalemia High-Risk Medications: Antibiotics: Bactrim, antifungals Calcineurin inhibitors Beta-blockers ACE/ARB K+ Sparing diuretics NSAIDs Digoxin SUX – high risks in neuromuscular disease Lab errors, hemolysis in samples VBG vs Chem accuracy  When to repeat a hemolyzed sample  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) Consider evaluation for adrenal insufficiency Waiting for labs may not be an option Renal dysfunction + consistent ECG findings → prompt treatment before chem results 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 Read More

We go over the essential and complex topic of vasopressors in the ED. Hosts: Brian Gilberti, MD Catherine Jamin, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Vasopressors.mp3 Download Leave a Comment Tags: Critical Care Show Notes Introduction Host: Brian Gilberti, MD Guest: Catherine Jamin, MD Associate professor of Emergency Medicine at NYU Langone Health Vice Chair of Operations Triple-boarded in Emergency Medicine, Internal Medicine, and Critical Care Medicine Topic: Vasopressors: Essential agents for supporting critically ill patients in the ED What Are Vasopressors and When to Use Them Two primary mechanisms to increase blood pressure: Increasing systemic vascular resistance via vasoconstriction Increasing cardiac output via augmenting inotropy and chronotropy Indicators for vasopressor use: MAP <65, systolic BP <90, or significant drop from baseline BP Signs of organ dysfunction like altered mental status, decreased urine output, elevated lactate Fluid resuscitation either ineffective or contraindicated (e.g., in CHF patients) Commonly Used Vasopressors in the ED Norepinephrine Epinephrine Vasopressin Phenylephrine Norepinephrine Mechanism: Stimulates alpha-1 (vasoconstriction) and beta-1 receptors (increases inotropy & chronotropy) Starting Dose: 10 mcg/min, titrate to MAP >65 Max Dose: No strict limit but usually add a 2nd pressor at 15-20 mcg/min Situational Preference: First-line for most cases of shock (septic, undifferentiated, hypovolemic, cardiogenic) Pros: Can be infused peripherally via large bore IV Vasopressin Mechanism: Activates V1a receptors causing vasoconstriction Dose: Fixed, non-titratable dose of 0.04 units/min Situational Preference: Second-line in septic shock Concerns: Potential for peripheral ischemia Phenylephrine Mechanism: Stimulates alpha-1 receptors causing vasoconstriction Starting Dose: 100 mcg/min, titrate to MAP >65 Situational Preference: High cardiac output states, tachyarrhythmias, peri-intubation Concerns: Increases afterload, can worsen low cardiac output states Epinephrine Mechanism: Stimulates alpha-1, beta-1 and beta-2 receptors Starting Dose: 5-10 mcg/min, titrate to MAP >65 Situational Preference: Anaphylactic shock, septic cardiomyopathy Limitations: Can induce tachycardia, may elevate lactate levels Escalation Strategy in Refractory Shock Norepinephrine -> Vasopressin (with stress dose steroids) -> Epinephrine 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/ Read More

We discuss the diagnosis and management of septic arthritis in the pediatric population. Hosts: Brian Gilberti, MD Ellen Duncan, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Septic_Joint_in_Children.mp3 Download 2 Comments Tags: Infectious Diseases, Pediatrics Show Notes General 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 Read More

A quick primer on hypocalcemia in the ED. Hosts: Joseph Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/hypocalcemia.mp3 Download 4 Comments Tags: calcium, Critical Care, Endocrine Show Notes Swami’s CoreEM Post Hypocalcemia Repletion: 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: Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ 2008; 336:1298. ​​Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med 1988; 84:209. Goltzman, D. Diagnostic approach to hypocalcemia. UpToDate. UpToDate; Jul 17, 2020. Accessed April 29, 2022. https://www.uptodate.com/contents/plantar-fasciitis Kelly A, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med 2013; 28:166. Pfenning CL, Slovis CM: Electrolyte Disorders; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 125: p 1636-53. Swaminathan, A. (2016, January 27). Hypocalcemia. CoreEM. Retrieved April 29, 2022, from https://coreem.net/core/hypocalcemia/ 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. Read More

How and when to reverse anticoagulation in the bleeding EM patient. Hosts: Joe Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/AC_reversal.mp3 Download 3 Comments Tags: Anticoagulation, Critical Care, Resuscitation Show Notes Coagulation Cascade:   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 Eikelboom JW, Quinlan DJ, van Ryn J, Weitz JI. Idarucizumab: The Antidote for Reversal of Dabigatran. Circulation. 2015 Dec 22;132(25):2412-22. doi: 10.1161/CIRCULATIONAHA.115.019628. PMID: 26700008. 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 Siegal DM, Curnutte JT, Connolly SJ, Lu G, Conley PB, Wiens BL, Mathur VS, Castillo J, Bronson MD, Leeds JM, Mar FA, Gold A, Crowther MA. Andexanet Alfa for the Reversal of Factor Xa Inhibitor Activity. N Engl J Med. 2015 Dec 17;373(25):2413-24. doi: 10.1056/NEJMoa1510991. Epub 2015 Nov 11. PMID: 26559317. Read More

A primer on this airway/ ID/ ENT emergency. Hosts: Joe Offenbacher MD, A Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/ludwigs_2.mp3 Download 2 Comments Tags: Airway, ENT, Infectious Diseases Show Notes References: Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s Angina. Ann Maxillofac Surg 2015; 5:168. Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis 2009; 13:327. Brook I. Microbiology and principles of antimicrobial therapy for head and neck infections. Infect Dis Clin North Am. 2007 Jun;21(2):355-91, vi. doi: 10.1016/j.idc.2007.03.014. PMID: 17561074. Chong W, Hijazi M, Abdalrazig M, Patil N. Respect the Floor of the Mouth. J Emerg Med. 2020 Jul;59(1):e27-e29. doi: 10.1016/j.jemermed.2020.04.015. Epub 2020 May 19. PMID: 32439254. http://www.emdocs.net/ludwigs-angina-2/ 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. Read More

A quick overview of pneumothorax for the EM physician: the what, why, diagnosis, and treatment. Hosts: Joe Offenbacher, MD Audrey Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumothorax_CoreEM_podcast.mp3 Download One Comment Tags: #pneumothorax #FOAMed Show Notes Shownotes: CoreEM Pulmonary Ultrasound Post References: 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. Brown SGA, Ball EL, Perrin K, Asha SE, Braithwaite I, Egerton-Warburton D, Jones PG, Keijzers G, Kinnear FB, Kwan BCH, Lam KV, Lee YCG, Nowitz M, Read CA, Simpson G, Smith JA, Summers QA, Weatherall M, Beasley R; PSP Investigators. Conservative versus Interventional Treatment for Spontaneous Pneumothorax. N Engl J Med. 2020 Jan 30;382(5):405-415. doi: 10.1056/NEJMoa1910775. PMID: 31995686. 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. Chan KK, Joo DA, McRae AD, et al. Chest ultrasonography versus supine chest radiography for diagnosis of pneumothorax in trauma patients in the emergency department. Cochrane Database Syst Rev 2020; 7:CD013031. 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. Gobbel Jr WG, Rhea Jr WG, Nelson IA, Daniel RA. Spontaneous pneumothorax. J Thorac Cardiovasc Surg 1963; 46:331. Lesur O, Delorme N, Fromaget JM, et al. Computed tomography in the etiologic assessment of idiopathic spontaneous pneumothorax. Chest 1990; 98:341. 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. Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med 2000; 342:868.   Read More

An interesting back story on this must-not-miss EKG finding in the ED! Hosts: Joseph Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/CoreEM_Wellens.mp3 Download One Comment Tags: #FOAMed, #wellens, Cardiology, EKG, STEMI Show Notes Hosts: Joe Offenbacher MD, Audrey Bree Tse MD EKG Findings in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. Table 1 in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. REFERENCES: de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. Lee, M., & Chen, C. (2015). Myocardial Bridging: An Up-to-Date Review. Journal of Invasive Cardiology, 27(11), 521–528.  https://lifeinthefastlane.com/ecg-library/wellens-syndrome/ Lin AN, Lin S, Gokhroo R, Misra D. Cocaine-induced pseudo-Wellens’ syndrome: a Wellens’ phenocopy. BMJ Case Rep. 2017 Dec 14;2017:bcr2017222835. doi: 10.1136/bcr-2017-222835. PMID: 29246935; PMCID: PMC5753703. Rhinehardt, J., Brady, W. J., Perron, A. D., & Mattu, A. (2002). Electrocardiographic manifestations of Wellens’ syndrome. The American Journal of Emergency Medicine, 20(7), 638–643. https://doi.org/10.1053/ajem.2002.34800 Tandy, TK; Bottomy DP; Lewis JG (March 1999). “Wellens’ syndrome”. Annals of Emergency Medicine. 33 (3): 347–351. PMID 10036351. doi:10.1016/S0196-0644(99)70373-2. (via Wikipedia) Read More

We discuss EM presentation, diagnosis, and management of subarachnoid hemorrhage. Hosts: Mark Iscoe, MD Brian Gilberti, MD Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/SAH.mp3 Download One Comment Tags: Critical Care, Neurology, Subarachnoid Hemorrhage Show Notes 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. Read More

We discuss the (F)utility(?) of ED Utox screens with our very own Dr. Phil DiSalvo. Hosts: Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Urine_Drug_Screen_final.mp3 Download Leave a Comment Tags: Toxicology Show Notes Special Thanks To: Dr. Philip DiSalvo, MD 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 Table 2: Approximate Drug Detection Time in the Urine Table 4: Summary of Agents Contributing to Results by Immunoassay Read More

EM management of the rare but potentially complicated precipitous vaginal breech delivery. Hosts: Audrey Bree Tse, MD Masashi Rotte, MD MPH https://media.blubrry.com/coreem/content.blubrry.com/coreem/Breesashi_Breech_CoreEM.mp3 Download One Comment Tags: Obstetrics, Precipitous Deliveries, Pregnancy Show Notes Frank Breech Presentation: Complete Breech Presentation: Incomplete Breech (“Footling”) Presentation:   Pinard Maneuver:   Mauriceau Maneuver: References: Cunningham FG et al.  Breech Presentation and Delivery.  Williams Obstetrics, 22nd ed. 2005. Desai S, Henderson SO. Labor and Delivery and Their Complications. Rosen’s Emergency Medicine, 8e. 2014. Chapter 181. Gabbe SG et al.  Obstetrics: Normal and Problem Pregnancies, 2nd e. 1991. p.479. Stitely ML, Gherman RB. Labor with abnormal presentation and position. Obstet Gynecol Clin North Am. 2005; 32: 165. VanRooyen MJ, Scott J.  Emergency Delivery.  Tintanelli’s Emergency Medicine, 7th e.  2011.  Chapter 105. http://www.emdocs.net/the-complicated-delivery-what-do-you-do/#:~:text=Deliveries%20that%20occur%20in%20the,in%20denial%20of%20their%20pregnancies. https://ranzcog.edu.au/womens-health/patient-information-resources/breech-presentation-at-the-end-of-your-pregnancy https://wikem.org/wiki/Breech_delivery Read More

The speech given by Dr. Goldfrank at the 2020 NYU / Bellevue Emergency Medicine Graduation Ceremony https://media.blubrry.com/coreem/content.blubrry.com/coreem/Goldfrank_Graduation_Speech_2020.mp3 Download Leave a Comment Tags: Graduation. Goldfrank Show Notes Graduation 2020 Lewis R. Goldfrank, MD June 17, 2020 WELCOME TO THE GRADUATES 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. THANK YOU AND CONGRATULATIONS! Read More

An overview and management tips of hemoptysis in the ED. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hemoptysis.mp3 Download One Comment Tags: Critical Care, Pulmonary Show Notes OVERVIEW: Definition: expectoration/ coughing of blood originating from tracheobronchial tree Sources: Bronchial arteries (90%): under systemic circulatory pressure to supply supporting structures of the lung → heavier bleeding Pulmonary arteries (5%): under low pressure to supply alveoli → milder bleeding Nonbronchial arteries (5%): intercostal arteries, coronary arteries, thoracic/ upper/ inferior phrenic arteries Quantification: Mild: <20mL/ 24h Massive defined anywhere from >300mL-1L/ 24hr Mortality: 38% for massive (>500mL/ 24hr) vs 4.5% for nonmassive Etiology (in adults): Infectious (most common): Bronchitis PNA (necrotizing, lung abscess) TB Viral Fungal Parasitic Malignancy: Primary lung cancer vs metastatic disease Pulmonary: Bronchiectasis COPD PE/ infarction Bronchopleural fistula Sarcoidosis Cardiac: Mitral stenosis Tricuspid endocarditis CHF Rheumatological: Goodpasture Syndrome SLE Vasculitis (Wegener’s, HSP, Behcet) Amyloidosis Hematological: Coagulopathy/ thrombocytopenia/ platelet dysfunction DIC Vascular: Pulmonary HTN AA Pulmonary artery aneurysm Aortobronchial fistula Pulmonary angiodysplasia Toxins: Anticoagulation/ aspirin/ antiplatelets Penicillamine, amiodarone Crack lung Organic solvents Trauma: Tracheobronchial rupture Pulmonary contusion Other: bronchoscopy/ lung biopsy Pulmonary artery or central venous catheterization Foreign body aspiration Pulmonary endometriosis (catamenial hemoptysis) Idiopathic (up to 25% of cases) Pseudohemoptysis:  Sinusitis Epistaxis Rhinorrhea Pharyngitis URI Aspiration GIB WORKUP: HPI: CP, SOB B symptoms: fever, weight loss, chills, night sweats Lymphadenopathy Timeframe: acute vs chronic Prior lung/ renal/ cardiac disease Recreational drug/ cigarette/ chemical exposures travel/ infectious exposure Medications Any other sites of bleeding Precipitating factors Description of blood clots Patients are unable to accurately estimate degree of bleeding PE: Petechiae, edema, ecchymosis, ulcers, clubbing (chronic lung disease) Cardiopulmonary Sputum samples Labs: CBC w/ diff, BMP, LFTs, coags, T&S ABG UA Infectious workup if suspected: cultures, grain stains Imaging: CXR: 20% will be normal.  May see tumour, cavity, effusion, infiltrate, PTX.  Early pulmonary hemorrhage may present as infiltrate CT: only for stable patients!  May see bronchiectasis, cavitary lesions, acinar nodules, tumours CTA: bronchial arteries, aneurysms, PE ECHO: identify valvular abnormalities, signs of PE, aortic aneurysm Bronchoscopy: Not often performed in ED, but therapeutic & diagnostic Allows direct visualization of tumours, foreign bodies, granulomas, infiltration, as well as local therapy (vasoconstrictive agents, stent/ balloon tamponade, electrocautery, procoagulants) MANAGEMENT: Goals: Control airway Protect healthy lung Identify and treat underlying cause Stabilize hemodynamics with volume resuscitation Provider precautions (respiratory & contact) ABCs, close monitoring Early airway management: massive hemoptysis, respiratory compromise, hypoxia, risk factors (elderly, AMS, coagulopathic) 2 x suction, preoxygenation, patient positioned upright, >8Fr ETT to facilitate suctioning/ bronch If bleeding side can be identified, consider “selective intubation” into nonbleeding lung to minimize further aspiration of blood and to provide ventilation Life threat = asphyxiation, not exsanguination.  ~Only 150cc anatomic dead space in major airways 2 x large bore IVs MTP prn vs volume resuscitation “Bad lung down” in lateral position: theoretical belief to minimize reflux of blood into normal lung Correct coagulopathy Consider nebulized TXA for nonmassive hemoptysis (500mg w/ NS per neb) Double-blind, randomized controlled trial in 2018 Nebulized TXA (500mg TID) vs placebo (normal saline) in hemodynamically stable adult patients admitted with mild hemoptysis (<200 mL/ 24hr) and no respiratory instability Additional exclusion criteria included those with renal failure, hepatic failure, or coagulopathy Assessed mortality and hemoptysis recurrence rate at 30 days and 1 year 25 patients randomized to receive TXA nebs, 22 randomized to receive normal saline nebs Results: Resolution of hemoptysis within 5 days of admission was significantly higher in TXA-treated patients than placebo patients (96% vs 50%; P < 0.0005) Mean hospital length of stay was shorter for TXA group (5.7 +- 2.5 days vs 7.8 +- 4.6 days; P = 0.046) Fewer patients in TXA group required invasive procedures to control bleeding vs placebo group (0% vs 18.2%; P = 0.041) No side effects were noticed in either group Antibiotics if infectious Bronchoscopy: local therapy (vasoconstrictive agents, stent/ balloon tamponade, electrocautery, procoagulants) Rigid bronch for unstable patients to evacuate clots vs fiberoptic bronch for stable patients Bronchial artery embolization (call IR early!) May require lobectomy or pneumonectomy (consult thoracic surgery) DISPOSITION: Low threshold for higher level of care: only mild, hemodynamically stable hemoptysis on floor Discharge: only if certain regarding etiology in healthy, hemodynamically stable patients with scant, resolved hemoptysis, no coagulopathy, and reassuring workup Ensure patients have reliable follow up and avoid smoking. Strict return precautions!   REFERENCES: Kiraly A, Pang P, Cheema N.  Hemoptysis.  In: Schaider J, Barkin R, Hayden S, Wolfe R, Barkin A, Shayne P, Rosen P.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult.  5th Edition.  Philadelphia, PA: Wolters Kluwer; 2015; 504-505. Nickson, C.  Haemoptysis. Life in the Fastlane.  [litfl.com/haemoptysis/]. Updated April 9, 2019.  Retrieved February 10, 2020. Wand O, Guber E, Guber A, Schochet GE, Israeli-Shani L, Shitrit D.  Inhaled Tranexamic Acid for Hemoptysis Treatment: A Randomized Controlled Trial.  Chest. December 2018; 154(6): 1379-1384. Young WF.  Hemoptysis.  In: Cline, David,eds. Tintinalli’s Emergency Medicine Manual. 7th Edition.  New York : McGraw-Hill Medical; 2011; 473-476. Read More

We go over the recent updates in the workup and management of pneumonia. Hosts: Brian Gilberti, MD Audrey Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumonia_Updates.mp3 Download Leave a Comment Tags: Infectious Diseases, Pulmonary Show Notes 2007 Infectious Diseases Society of America/American Thoracic Society Criteria for Defining Severe Community-acquired Pneumonia Validated definition includes either one major criterion or three or more minor criteria Minor criteria Respiratory rate > 30 breaths/min PaO2/FIO2 ratio<250 Multilobar infiltrates Confusion/disorientation Uremia (blood urea nitrogen level > 20 mg/dl) Leukopenia* (white blood cell count , 4,000 cells/ml) Thrombocytopenia (platelet count , 100,000/ml) Hypothermia (core temperature , 368 C) Hypotension requiring aggressive fluid resuscitation Major criteria Septic shock with need for vasopressors Respiratory failure requiring mechanical ventilation A special thanks to our Infectious Diseases Editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine Read More

Diagnosing and managing one of our critical diagnoses - posterior stroke. Hosts: Mukul Ramakrishnan, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/final_posterior_stroke_podcast_post_edit.mp3 Download 2 Comments Tags: Neurology, Posterior Stroke Show Notes See Dr. Newman-Toker demonstrate the HINTS exam here Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009 Nov;40(11):3504-10   Read More

We discuss one of the most complex problems we face – Homelessness Hosts: Kelly Doran, MD Audrey Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Homelessness.mp3 Download One Comment Tags: Social Emergency Medicine Show Notes Special Thanks To: Dr. Kelly Doran, MD MHS Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue ___________________________ References: Doran, K.M.  Commentary: How Can Emergency Departments Help End Homelessness?  A Challenge to Social Emergency Medicine. Ann Emerg Med. 2019;74:S41-S44. Doran, K.M., Raven, M.C. Homelessness and Emergency Medicine: Where Do We Go From Here? Acad Emerg Med. 2018;25:598-600. Salhi, B.A., et al. Homelessness and Emergency Medicine: A Review of the Literature. Acad Emerg Med. 2018;25:577-93. U.S. Department of Housing and Urban Development, Annual Homeless Assessment Report to Congress. Available at: https://www.hudexchange.info/resource/5783/2018-ahar-part-1-pit-estimates-of-homelessness-in-the-us/ U.S. Interagency Council on Homelessness. Home, Together Federal Strategic Plan to Prevent and End Homelessness. https://www.usich.gov/resources/uploads/asset_library/Home-Together-Federal-Strategic-Plan-to-Prevent-and-End-Homelessness.pdf Read More

We go into one of the more complex injuries – blunt neck trauma. Hosts: Audrey Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Blunt_Neck_Injuries.mp3 Download One Comment Tags: Trauma Show Notes Overview Blunt neck trauma comprises 5% of all neck trauma Mortality due to loss of airway more so than hemorrhage Mechanism MVCs with cervical hyperextension, flexion, rotation during rapid deceleration, direct impact   Strangulation: hanging, choking, clothesline injury (see section on strangulation in this chapter) Direct blows: assault, sports, falls Initial Management/Primary Survey Airway Evaluate for airway distress (stridor, hoarseness, dysphonia, dyspnea) or impending airway compromise Early aggressive airway control: low threshold for intubation if unconscious patient, evidence of airway compromise including voice change, dyspnea, neurological changes, or pulmonary edema Assume a difficult airway  Breathing Supplemental oxygen Assess for bilateral breath sounds  Can use bedside US to evaluate for pneumothorax or hemothorax Circulation Assess for open wounds, bleeding, hemorrhage  IV access Disability Maintain C-spine immobilization  Calculate GCS Look for seatbelt sign Secondary Survey Evaluate for specific signs of vascular, laryngotracheal, pharyngoesophageal, and cervical spinal injuries with inspection, palpation, and auscultation Perform extremely thorough exam to evaluate for any concomitant injuries (e.g. stab wounds, gunshot wounds, intoxications/ ingestions, etc.) Types of Injuries Vascular injury Overview Carotid arteries (internal, external, common carotid) and vertebral arteries injured Mortality rate ~60% for symptomatic blunt cerebral vascular injury Mechanism Hyperextension and lateral rotation of the neck, direct blunt force, strangulation, seat belt injuries, and chiropractic manipulation Morbidity due to intimal dissections, thromboses, pseudoaneurysms, fistulas, and transections Clinical Features Most patients are asymptomatic and do not develop focal neurological deficits for days if Horner’s syndrome, suspect disruption of thoracic sympathetic chain (wraps around carotid artery) specific screening criteria are used to detect blunt cerebrovascular injury in asymptomatic patients (see below) Tintinalli 2016 Diagnostic Testing Gold standard for blunt cerebral vascular injury = MDCTA (multidetector four-vessel CT angiography) <80% sensitive but 97% specific Also images aerodigestive tracts and C-spine (unlike angiography) Followed by Digital Subtraction Angiography (DSA) for positive results or high suspicion  Angiography is invasive, expensive, resource-intensive, and carries a high contrast load Management Antithrombotics vs. interventional repair based on BCVI grading system Involve consultants early: trauma surgery, neurosurgery, vascular surgery, neurology All patients with blunt cerebral vascular injury will require admission Tintinalli 2018 Pharyngoesophageal injury   Overview Rare in blunt neck trauma Includes hematomas and perforations of both pharynx and esophagus Mechanism Sudden acceleration or deceleration with hyperextension of the neck Esophagus is thus forced against the spine Clinical Features Dysphagia, odynophagia, hematemesis, spitting up blood Tenderness to palpation SC emphysema Neurological deficits (delayed presentation) Infectious symptoms (delayed presentation) Diagnostic Testing Esophagography with water-soluble contrast (e.g. Gastrograffin) If negative contrast esophagography, obtain flexible endoscopy (most sensitive) Combination of contrast esophagography + esophagoscopy has sensitivity close to 100% Swallow studies with water-soluble agent MDCTA Plain films of neck and chest  Findings such as pneumomediastinum, hydrothorax, or retropharyngeal air may suggest perforation but are not sensitive Management All pharyngoesophageal injuries receive IV antibiotics with anaerobic coverage Parenteral/ enteral nutrition NGT should only be placed under endoscopic guidance to avoid further injury Medical management vs. surgical repair depending on extent of injury Surgical repair for esophageal perforations or pharyngeal perforations >2cm Involve consultants early: trauma surgery, vascular surgery, otolaryngology, gastroenterology All patients with blunt cerebral vascular injury will require admission Laryngotracheal injury   Overview Occurs in >0.5% of blunt neck trauma Includes hyoid fractures, thyroid/ cricoid cartilage damage, cricotracheal separation, vocal cord disruption, tracheal hematoma or transection Mechanism Assault, clothesline injuries, direct blunt force from MVCs compressing the larynx between a fixed object and the spine Clinical Features Patients are often asymptomatic at first and then develop airway edema and/or hematoma resulting in airway obstruction Children are at higher risk for airway compromise due to less cartilage calcifications Diagnostic Testing Flexible fiberoptic laryngoscopy (FFL) to assess airway patency and extent of intraluminal injury MDCTA Obtain 1-mm cuts of larynx and perform multiplanar reconstructions  Consider POCUS to detect laryngotracheal separation Plain films of neck and chest Poor sensitivity for penetrating neck trauma injuries Can show extraluminal air, fracture or disruption of cartilaginous (e.g. larynx) structures  Management When securing airway, use an ETT that is one size smaller due to likelihood of airway edema Conservative management (IV antibiotics, steroids, observation) vs. surgical repair Grades III, IV, and V laryngotracheal injuries as defined by Schaefer and Brown’s classification system require OR Tintinalli 2018 Involve consultants early: trauma surgery, neurosurgery, vascular surgery, neurology, otolaryngology  Cervical spine/ spinal cord injury   See chapter for spinal trauma Disposition Admit symptomatic patients to monitored setting Given delayed symptoms, consider monitoring patients who are asymptomatic on arrival Serial exams for worsening dyspnea, dysphonia, stridor, drooling, bruits, focal neuro deficits Only discharge after ruling out airway threat, neurological deficit, vascular injury, or suicidal/ homicidal ideation Monitor asymptomatic patients on home anticoagulation in ED for at least 6 hours from trauma to rule out delayed neck hematoma Social work and/or psychiatry for patients in whom you suspect suicide risk or domestric violence, look for other signs of self harm Take Home Points Aggressive early airway management for unconscious patient, evidence of airway compromise including voice change, dyspnea, neurological changes, or pulmonary edema Involve consultants early: trauma surgery, neurosurgery, vascular surgery, neurology, otolaryngology  Victims of blunt cerebral vascular injury may present completely asymptomatic but develop delayed neurological symptoms; close observation and monitoring is recommended especially for patients on home anticoagulation Remember to evaluate for concomitant injuries Psychiatric evaluation for all attempted suicides References Bromberg, William. et al. Blunt Cerebrovascular Injury Practice Management Guidelines: The Eastern Association for the Surgery of Trauma. J Trauma. 68 (2): 471-7, Feb 2010.  Cothren CC, Moore EE, Biffl WL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. 2004;139:540–545; discussion 545–546. Joshua AA.  Neck Trauma, Blunt, Anterior.  In: Schaider J, Barkin R, Hayden S, Wolfe R, Barkin A, Shayne P, Rosen P.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult. 5th Edition. Philadelphia, PA: Wolters Kluwer; 2015; 738-739. Tintinalli, J., Stapczynski, J. Stephan, editor, Ma, O. John, editor, Yealy, Donald M., editor, Meckler, Garth D., editor, & Cline, David, editor. (2018). Tintinalli’s emergency medicine : A comprehensive study guide (9th ed.). Walls, R., Hockberger, Robert S., editor, & Gausche-Hill, Marianne, editor. (2018). Rosen’s emergency medicine : Concepts and clinical practice (Ninth ed.). Advanced trauma life support. (2018). 10th ed. Chicago, IL: American College of Surgeons. Special thanks to Sana Maheshwari, MD  NYU Bellevue Emergency Medicine Residency PGY3   Read More

We dissect one of the most common injuries we see in the ER -- ankle sprains Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Ankle_Sprains.mp3 Download 3 Comments Tags: Orthopedics Show Notes Background Among most common injuries evaluated in ED A sprain is an injury to 1 or more ligaments about the ankle joint Highest rate among teenagers and young adults Higher incidence among women than men Almost a half are sustained during sports Greatest risk factor is a history of prior ankle sprain Anatomy Bone: Distal tibia and fibula over the talus → constitutes the ankle mortise Aside from malleoli, ligament complexes hold joint together Medial deltoid ligament Lateral ligament complex Anterior talofibular ligament Most commonly injured Weakest 85% of all ankle sprains  Posterior talofibular ligament Calcaneofibular ligament Syndesmosis Mechanism of Injury Lateral ankle sprains  Most common among athletes ATFL most commonly injured Combined with CFL in 20% of injuries 2/2 inversion injuries Medial ankle sprains Less common than lateral because ligaments stronger and mechanism less frequent More likely to suffer avulsion fracture of medial malleolus than injure medial ligament 2/2 eversion +/- forced external rotation Typically landing on pronated foot -> external rotation High Ankle sprains Syndesmotic injury More common in collision sports (football, soccer, etc) Grade I Mild Stretch without “macroscopic” tearing Minimal swelling / tenderness No instability No disability associated with injury     Grade II Moderate Partial tear of ligament Moderate swelling / tenderness Some instability and loss of ROM Difficulty ambulating / bearing weight     Grade III Severe Complete rupture of ligaments Extensive swelling / ecchymosis / tenderness Mechanical instability on exam Inability to bear weight Examination     Beyond visual inspection for swelling, ecchymoses, abrasions, or lacerations Palpation  Pain when palpating ligament is poorly specific but may indicate injury to structure Check sites for Ottawa ankle rules to evaluate if there may be an associated fracture with injury Posterior edge or tip of lateral malleolus (6 cm) Posterior edger or tip of medial malleolus (6 cm) Base of fifth metatarsal Navicular bone Acute ATFL rupture / Grade III Sprain 90% chance of this injury if hematoma and localized tenderness with palpation present on exam over this ligament  Anterior drawer test Assess for anterior subluxation of talus from the tibia Ankle in relaxed position, distal extremity is stabilized with one hand while the other cups the heel to apply anterior force Compare to contralateral side Difficult to determine if there is an acute rupture at this point and may be more easily diagnosed in subacute phase (4-5 days after injury) Ability to perform exam adequately limited by pain, swelling and potential muscle spasm Talar tilt test If applying inversion force to ankle and there is excessive mobility → calcaneofibular ligament Thompson test Can be performed if there is concern for concomitant Achilles tendon injury  Do not miss a Maisonneuve fracture by palpating proximally about the fibular ahead as forces may be transmitted through the syndesmosis  Squeeze test – pressure just proximal to ankle If elicits pain → concern for syndesmotic injury Diagnostics     X-rays indicated if unable to rule out using Ottawa Ankle Rules Sn (Up to 99.6) (one of the best validated tools we use in the ER) May have trouble applying rule if there is question of patients ability to sense pain (diabetic neuropathy), in which case obtain radiographs Treatments     RICE Crutch train so they can be weight bearing a tolerated Ideally initiate within first 24 hours of injury Ice 15-20 minutes q2-3h over the first 48 hours or until swelling improves     NSAIDs Topical and PO are better than placebo  We do not know if PO is superior to topical NSAIDs     Early mobilization / Functional Rehab (sample patient instructions here) Work to restore range of motion, strength, proprioception For Grade I and II, can begin as soon as the patient can tolerate and ideally within 1 week of the injury Patients return to work sooner, decreased chronic instability, less recurrent injuries Dorsiflexion, plantarflexion, and perform foot circles as well as toe curls, inversion and eversion as tolerated Proprioception Balancing on wobble board Continue exercises until patient is able to return to activities at full capacity, without pain Immobilization High re-injury rates and important to protect against this Grade I No immobilization required +/- Ace wrap Grade II Aircast brace Ensure patient understands that they should still partake in rehabilitation exercises Grade III Data conflicts RCT, multicenter study comparing aircast brace, compression bandage, Bledsoe immobilization boot and below-knee cast for 10 days Ankle function at 3 months Cast group had most improvement No difference at 9 months in function or complications May be institution-dependent and a cast can be offered initially Prognosis Acute inflammation → reduction in swelling → development of new tissue → strengthening of tissue  Return of basic function, though limited, occurs over 4-6 weeks depending on severity of sprain Try to limit strain put on joint (no heavy lifting, walking on uneven surfaces, try to limit standing while at work) Follow up: If pain or instability does not improve over 4-6 weeks Grade III sprains Medial ankle sprains (may have underlying fracture that was undetected in ED on XR) Syndesmosis injuries (protracted recovery course) Injuries associated with fractures or dislocation / subluxation   Read More

An overview of Vaping Associated Lung Injury (VALI) Hosts: Audrey Bree Tse, MD Larissa Laskowski, DO Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Vaping_Associated_Lung_Injury.mp3 Download 2 Comments Tags: Pulmonary, Toxicology Show Notes Why this matters As of Oct 15, vaping has been associated with acute lung injury in over 1400 people 33 deaths have been confirmed in 24 states 70+% of those with VALI are young men A large number of patients are requiring ICU/ intubation/ ECMO 4 main ingredients in solvent +/- Flavor additives +/- Nicotine or THC (Tetrahydrocannabinol) Propylene Glycol (PG) Vegetable Glycerin (VG) CDC definition of VALI (Vaping Associated Lung Injury) Using an e-cigarette (“vaping”) or dabbing* in 90 days prior to symptom onset AND Pulmonary infiltrate, such as opacities, on plain film chest radiograph or ground-glass opacities on chest CT AND Absence of pulmonary infection on initial work-up.  No evidence in the medical record of alternative plausible diagnoses (e.g., cardiac, rheumatologic, or neoplastic process). *Dabbing allows the user to ingest a high concentration of THC.  Butane Hash Oil (BHO), an oil or wax-like substance extracted from the marijuana plant, is placed on a “nail” attached to a specialized glass bong called a “rig.” A blow torch is used to heat the wax, which produces a vapor that can then be inhaled to supposedly produce an instantaneous effect. Pathophysiology At present, no single compound or ingredient has emerged as the cause, and there may be more than one cause The only common thread among the cases is that ALL patients reported using e-cig or vaping products Leading potential toxins: Vaping products containing THC concentrates: most cases are linked to THC concentrates that were either purchased on the street or from other informal sources (meaning not from a dispensary) Vitamin E acetate: nutritional supplement safe when ingested or applied to the skin (but likely not when inhaled) has been found in nearly all product samples of NY state cases of suspected VALI vitamin E acetate is NOT an approved additive at least by NYS Medical Marijuana program Other potential toxins: IT CANNOT BE UNDERSTATED that a small percentage of persons w/ VALI have reported exclusive use of nicotine-containing vape products, such as JUUL; as such, we must consider the potential toxicity of standard e-liquid or vape juice Flavor additives, that exists as chemical aldehydes: irritating and potentially damaging to lung tissue PG/VG: shown not only to break down to formaldehyde which is a known carcinogen, but also to produce lipoid pneumonia in rat lungs Some devices are easily manipulated to increase the capacity to produce vapor; increasing these settings may impact heating temperature, metabolic breakdown, and release of microscopic metal particles Lungs are multifunctional, including serving as an immune organ: lungs cleave proteins of all of the bacteria, viruses and other pathogens we are exposed to and inhale daily human studies on those that are chronic e-cig users or vapers have revealed that these products are shifting the balance of proteases and antiproteases in our lungs such that the proteases are destroying native lung tissue similar to how traditional cigarettes cause COPD Many potential reactions: NEJM article in references: details four radiographic phenotypes essentially reflecting different pathologic changes Long-term Effects Long term effects are unknown (some pts have required home oxygen on discharge) Risk for recurrence or relapse, especially if repeat exposure Presentation 95% of pts have had pulmonary sxs (cough, cp, dyspnea) 77% of pts have had GI sxs (abd pain, n/v/d) 85% of pts w/ constitutional sxs (f/c, weight loss) 57% w/ hypoxia (O2 < 95%) Unfortunately auscultation has been unreliable and poorly sensitive Workup There is no specific test or marker for dx, so VALI is still considered a dx of exclusion Labs: CBC ESR/CRP (93% w/ elevated ESR) LFTs (50% w/ transaminitis) ABG: hypoxia Imaging: CXR: typically shows bilateral infiltrates, although not always and there have even been some cases w/ unremarkable chest XR (so high degree of clinical suspicion in any person p/w hypoxia) CT: ground glass opacities, typically bilaterally  Management Dispo: 96% of cases required hospitalization Any pt w/ hypoxia, respiratory distress, or comorbidities Outpatient only if: no hypoxia or respiratory distress, reliable followup within 48h and good social support (keep in mind that some patients w/ mild symptoms of first presentation deteriorated rapidly within 48h) Empiric treatments for pneumonia inc abx, antivirals Steroids (methylpred 60mg q6h, based on how index cases in Illinois were managed) Case reports have documented improvement Mechanism: blunting of inflammatory response Aggressive supportive care Special Thanks To: Dr. Larissa Laskowski, DO Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue New York City Poison Control Center References: Outbreak of Lung Injury Associated with E-Cigarette Use, or Vaping.  https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html Carlos WG, Crotty Alexander LE, Gross JE, Dela Cruz CS, Keller JM, Pasnick SP, Jamil S.  Vaping-associated Pulmonary Illness (VAPI). Public Health Information Series. Am J Respir Crit Care Med Vol. 200, 13-15, 2019.  www.atsjournals.org/doi/pdf/10.1164/rccm.2007P13 Henry TS, Kanne JP, Kilgerman SJ.  Images of Vaping-Associated Lung Disease — Correspondence.  N Engl J Med. 2019 Oct 10; 381;15.   Layden JE, Ghana I, Pray I, Kimball A, Layer M, Tenforde M, Navon L, Hoots B, Salvatore PP, Elderbrook M, Haupt T, Kanne J, Patel MT, Saathaff-Huber L, King BA, Schier JG, Mikosz CA, Meiman J.  Pulmonary Illness Related to E-Cigarette Use in Illinois and Wisconsin – Preliminary Report.  N Engl J Med. 2019 Sep 6. doi: 10.1056/NEJMoa1911614. [Epub ahead of print].  https://www.ncbi.nlm.nih.gov/pubmed/31491072?dopt=AbstractPlus Siegel DA, Jatlaoui TC, Koumans EH, et al. Update: Interim Guidance for Health Care Providers Evaluating and Caring for Patients with Suspected E-cigarette, or Vaping, Product Use Associated Lung Injury — United States, October 2019. MMWR Morb Mortal Wkly Rep 2019;68:919–927. DOI: http://dx.doi.org/10.15585/mmwr.mm6841e3external icon. https://www.health.ny.gov/press/releases/2019/2019-09-05_vaping.htm Read More

An overview of septic arthritis. Hosts: Audrey Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Septic_Arthritis.mp3 Download One Comment Tags: Infectious Diseases, Orthopedics Show Notes Episode Produced by Audrey Bree Tse, MD Background Bacteria enters the joint by hematogenous spread due to absence of basement membrane in synovial space from invasive procedures, contiguous infection (e.g. osteomyelitis, cellulitis), or direct inoculation (e.g. plant thorns, nails) WBCs migrate into joint → acute inflammatory process → synovial hyperplasia, prevents new cartilage from forming, pressure necrosis on surrounding joint, purulent effusion Why do we care?  irreversible loss of function in up to 10% & mortality rate as high as 11% Cartilage destruction can occur in a matter of hours Complications include bacteremia, sepsis, and endocarditis Etiology Risk factors: extremes of age, RA, DJD, IVDA, endocarditis, GC, immunosuppression, trauma, or prosthesis Organisms:  Staph: staph aureus (most common), MRSA, Staph epidermis N gonorrhea: young healthy sexually active adults Strep: group A & B GNRs: IVDA, diabetics, elderly Salmonella: sickle cell disease Cutibacterium acnes: prosthetic shoulder infection Consider mycobacterial & fungal in more indolent courses Presentation Typically a single, warm, erythematous, tender joint (#1: knee (50% of cases) → hip, shoulder, ankle) *Any joint can be involved! IVDA can involve sacroiliac, costochondral, & sternoclavicular joints  Classic teaching: very painful with ROM, but this is not always present! Joint usually held in position of maximum joint volume Prosthetic joints may have less pain than expected for a septic joint given changed anatomy and disrupted nerve endings In 10-20% of cases, can see polyarticular involvement GC typically monoarticular but commonly polyarticular Often have fever & separate infection as well (only see fever in ~60% of cases) Diagnostics Arthrocentesis:  Gold standard  Tap joint even if acceptable ROM: septic joints can have normal motion so it does not exclude the diagnosis! Use ultrasound if possible Relative contraindications: overlying cellulitis (risk of seeding joint) or severe coagulopathies (weigh risk of creation or worsening of iatrogenic hemarthrosis) Keep in mind that a “dry tap” may occur due to incorrect needle placement, absent/ minimal joint effusion, ort mechanical obstruction Note: talk to ortho colleagues if prosthesis present prior to performing arthrocentesis  Ortho team may want to perform the arthrocentesis themselves because scar tissue formation and altered anatomic relationships make the procedure more challenging Usually want to perform washout in OR plus/ minus antibiotic spacer Send fluid for protein, glucose, cell count with differential, gram stain, culture, and crystals Often see decreased glucose and elevated protein The presence of crystals does not rule out septic arthritis No clear number of synovial WBCs to define septic arthritis, but in general: >30 to 50K/ mm3 synovial WBCs with PMN predominance (>75%) seen in septic arthritis A 2011 meta-analysis suggests +LRs of 4.7 (95% CI = 2.5 to 8.5) and +LR of 13.2 (95% CI = 3.6 to 51.1) for a sWBC count of >50L × 109 or >100K, respectively Use the synovial WBC count plus the whole clinical picture to rule in or out the diagnosis of septic arthritis (do not use the synovial WBC in isolation) Different threshold for prosthetic joints: WBC > 1100 or >64% PMNs = septic arthritis Gram stains only identify causative organisms 1/3 of the time Culture negative arthrocentesis can be seen in cases where abx have been given prior to arthrocentesis, or in TB/ brucella/ nocardia/ other indolent organisms like fungi Labs: No studies have demonstrated an acceptable sensitivity or overall diagnostic accuracy of peripheral WBC count for SA, but usually see leukocytosis with left shift ESR and CRP are reasonably sensitive but there is no cutoff that significantly increases or decreases the pretest probability UA, urine cultures, blood cultures: send even if no fever Blood cultures are positive in 50-70% of nonGC SA If GC suspected, do GC NAAT from throat/ rectal/ urethral/ cervical discharge Imaging: XRs: effusion, baseline status of joint, contiguous osteomyelitis, fractures, foreign body US: effusion CT, MRI: not really used in ED Differential Viral arthritis RA gout/ pseudogout HIV associated arthritis Reactive arthritis Lyme Osteo Septic bursitis Trauma Treatment Septic arthritis is an orthopedic emergency! Needs IV abx + often washout of the joint Hold abx as much as possible prior to tap unless pt is unstable or tap cannot be performed easily Initiate empiric IV antibiotic therapy prior to definitive cultures based Transition to organism-specific antibiotic therapy once culture sensitivities result Start empiric abx based on gram stain if available (in non-=GC SA, grain stain is positive in 50% of cases), age group, & risk factors Empiric abx: Vancomycin 15mg/kg q12h (to cover MRSA) + cefepime 2gr IV q8h (to cover gram-negatives) If gram stain with GPC = Vancomycin 15mg/kg q12h If gram stain with GN diplococci = ceftriaxone 1gr IV q24h + Azithromycin 1gr q24h If gram stain with GN rods = cefepime 2gr IV q8h If penicillin allergy: ciprofloxacin 500mg q12h or aztreonam 2gr q8h No need to cover anaerobes unless human/dog/cat bite (then use Unasyn to cover eikenella, pastereulla, capnocytophaga, anaerobes, etc.) They usually need antibiotics for 2-6 weeks: 2 weeks for strep, up to 6 weeks if S aureus   Pain control: consider moderately flexed splinting Admit all patients with suspected septic arthritis until SA is ruled out, abx, monitoring, likely operative intervention Take-Home Points Patients may present with either a single affected joint or polyarticular; they may or may not have a fever Have a high index of suspicion for SA, and a low threshold to tap: pts do not necessarily present w/ “classic” findings and it is difficult to distinguish SA from crystal arthropathy ESR, CRP, serum WBC are not definitive diagnostic tools for septic arthritis There is no exact cutoff for synovial WBCs for diagnosis: use whole clinical picture & keep 50K in mind for native joints, and >1100 for prostheses Treat with empiric abx after tap then narrow accordingly, & admit all patients with septic arthritis Involve your ortho colleagues early especially for prosthesis References Carpenter CR, Schuur JD, Everett WW, et al.  Evidence-based diagnostics: Adult septic arthritis.  Acad Emerg Med.  2011;18:781-796. Jones D, Clements C.  Physical exam and bloodwork do not adequately differentiate infectious from inflammatory arthritis.  In: Mattu A, Chanmugam A, Swadron S, Woolridge D, Winters M.  Avoiding Common Errors in the Emergency Department. 2nd Edition.  Philadelphia, PA: Wolters Kluwer; 2017; 412-414.   Kazzi A, Zaghrini E.  Septic Arthritis.  In: Schaider J, Barkin R, Hayden S, Wolfe R, Barkin A, Shayne P, Rosen P.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult.  5th Edition.  Philadelphia, PA: Wolters Kluwer; 2015; 102-103. Osmon D, Berbari E, Berendt A, Lew D, Zimmerli W, Steckelberg J, Rao N, Hanssen A, Wilson W.   Diagnosis and Management of Prosthetic Joint Infection: Clinical Practice Guidelines by the Infectious Diseases Society of America, Clinical Infectious Diseases, Volume 56, Issue 1, 1 January 2013, Pages e1–e25, https://doi.org/10.1093/cid/cis803 Mlynarek C, Sullivan A.  Arthrocentesis Tips.  In: Mattu A, Chanmugam A, Swadron S, Woolridge D, Winters M.  Avoiding Common Errors in the Emergency Department. 2nd Edition.  Philadelphia, PA: Wolters Kluwer; 2017; 684-686. Purcell D, Terry B, Sharp B.  Joint Arthrocentesis.  In: Purcell D, Chinai S, Allen B, Davenport M.  Emergency Orthopedics Handbook. 1st Edition. Cham, Switzerland: Springer; 2019; 87-104. Sheth U, Moore D.  Septic Arthritis — Adult.  OrthoBullets.  [https://www.orthobullets.com/trauma/1058/septic-arthritis–adult].  Updated 1/9/19.  Accessed 8/2/19.   A special thanks to our Infectious Diseases Editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine   A special thanks to our Orthopedics Editor: Daniel Purcell, MD Emergency Medicine NYU Langone Brooklyn   Read More

A look at the most common type of seizures in the young pediatric population. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Febrile_Seizures.mp3 Download Leave a Comment Tags: Pediatrics Show Notes Background The most common type of seizure in children under 5 years of age Occur in 2-5% of children In children with a fever, aged 6 months to 5 years of age, and without a CNS infection Risk Factors 4 times more likely to have a febrile seizure if parent had one Also increase in risk if siblings or nieces / nephews had one Common associated infections Human Herpesvirus 6 Human Herpesvirus 7 Influenza A & B Simple Febrile Seizure Generalized tonic-clonic activity lasting less than 15 minutes in a child 6 months to 5 years of age Complex Febrile Seizure Lasts longer than 15 minutes, occurs in a child outside of this age range, are focal, or that recur within a 24-hour period. Diagnostics / Workup Gather thorough history and perform thorough physical exam Most cases will not require labs, imaging or EEG If e/o meningitis, perform LP AAP suggests considering LP in: Children 6-12 months who are not immunized for H flu type B or strep pneumo Children who had been on antibiotics For complex seizures, clinician may have a lower threshold for obtaining labs Hyponatremia is more common in this group than in the general population. LPs are more commonly done by providers, but these are low yield with one study showing bacterial meningitis being diagnosed in just 0.9% (Kimia 2010), all of whom did not have a normal exam or negative cultures. Neuroimaging is also exceedingly low yield if the patient returns to baseline (Teng 2006) One study that showed that the duration of complex febrile seizure, being greater than 30 minutes, was associated with a higher incidence of bacterial meningitis. (Chin 2005) Of they have history and exam concerning for meningitis, they should get an LP If they look dehydrated or edematous, you would have more of a reason to get a chemistry Treatment Benzodiazepine if seizure lasted for >5 minutes, either IV or IN Supportive care Tylenol or motrin if febrile Fluids if signs of dehydration Antipyretics “around the clock” A majority of data show no benefit in preventing recurrence of seizure One study (Murata 2018) found that giving tylenol q6h at 10 mg/kg for the first 24 hours following the initial seizure decreased the rate of recurrence when compared to children who did not receive antipyretics. NNT here was 7 Questionable whether we can generalize these findings from a single ED in Japan. No role for antiepileptics Prognosis High rate of recurrence (~1/3) within 1 year of initial seizure Risk increases for Younger age at which they had initial seizure Lower temperature at which they had seizure If initial febrile seizure was prolonged, more likely that the next will be prolonged 1-2% develop epilepsy for simple febrile seizure, slightly above risk of general population 5-10% develop epilepsy for complex febrile seizure Follow up with PMD Generally, peds neuro follow up is not necessary References Chin RF, Neville BG, Scott RC. Meningitis is a common cause of convulsive status epilepticus with fever. Arch Dis Child. 2005;90(1):66-9. Kimia A, Ben-Joseph EP, Rudloe T, Capraro A, Sarco D, Hummel D, et al. Yield of lumbar puncture among children who present with their first complex febrile seizure. Pediatrics. 2010;126(1):62-9. Murata S, Okasora K, Tanabe T, Ogino M, Yamazaki S, Oba C, et al. Acetaminophen and Febrile Seizure Recurrences During the Same Fever Episode. Pediatrics. 2018;142(5). Patel N, Ram D, Swiderska N, Mewasingh LD, Newton RW, Offringa M. Febrile seizures. BMJ. 2015;351:h4240. Pavlidou E, Panteliadis C. Prognostic factors for subsequent epilepsy in children with febrile seizures. Epilepsia. 2013;54(12):2101-7. Stapczynski, J. S., & Tintinalli, J. E. (2016). Tintinalli’s emergency medicine: A comprehensive study guide, 8th Edition. New York: McGraw-Hill Education. Subcommittee on Febrile S, American Academy of P. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011;127(2):389-94. Teng D, Dayan P, Tyler S, Hauser WA, Chan S, Leary L, et al. Risk of intracranial pathologic conditions requiring emergency intervention after a first complex febrile seizure episode among children. Pediatrics. 2006;117(2):304-8. Warden CR, Zibulewsky J, Mace S, Gold C, Gausche-Hill M. Evaluation and management of febrile seizures in the out-of-hospital and emergency department settings. Ann Emerg Med. 2003;41(2):215-22. A special thanks to our editors: Michael A. Mojica, MD Director, Pediatric Emergency Medicine Fellowship Bellevue Hospital Center Christie M. Gutierrez, MD  Pediatric Emergency Medicine Fellow Columbia University Medical Center Morgan Stanley Children’s Hospital New York Presbyterian   Read More

A review for the emergency physician of this common tick-borne illness. Hosts: Audrey Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Lyme_Disease.mp3 Download Leave a Comment Tags: Infectious Diseases Show Notes Episode Produced by Audrey Bree Tse, MD Background Most common tick-born illness in North America Endemic in Northeast, Upper Midwest, northwest California 80% to 90% in summer months Pathophysiology Ixodes tick (deer tick) has a 3-stage life cycle (larvae, nymph, adult) & takes 1 blood meal per stage Deer tick feeds on an infected wild animal (infected with spirochete Borrelia burgodrferi) then bites humans On humans, they typically move until they encounter resistance (e.g. hairline, waistband, elastic, skin fold).  It takes 24-48 hrs for B. Burgdorferi to move from the tick to the host Pathogenesis: organism induced local inflammation, cytokine release, autoimmunity No person to person transmission Clinical Presentation Stage 1: Early Symptom onset few days to a month after tick bite Erythema migrans rash: bulls eye rash seen in more than 90% of patients with Lyme disease (Irregular expanding annular lesion(s)) Regional adenopathy, intermittent fevers, headache, myalgias, arthralgia, fatigue, malaise Stage 2: disseminated/ secondary Days to weeks after tick bite Intermittent fluctuating sx that eventually resolve Triad of aseptic meningitis, cranial neuritis, and radiculoneuritis: bell palsy most common Cardiac symptoms: tachycardia, bradycardia, AV block, myopericarditis Stage 3: tertiary/ late Symptoms occur >1 year after tick bite Acrodermatitis chronic atrophicans: Atrophic lesions on extensor surfaces of extremities (resembles scleroderma) Monoarthritis, oligoarthritis (knee > shoulder > elbow) GI: Hepatitis, RUQ pain Ocular: keratitis, uveitis, iritis, optic neuritis Neurological: Chronic axonal polyneuropathy or encephalopathy Chronic Lyme disease (versus well-accepted Lyme disease sequelae): Continuation of symptoms after antibiotics Current recommendation for management is supportive care only Pediatric considerations: More likely to be febrile than adults Facial palsy accompanied by aseptic meningitis in 1/3 Untreated kids can develop keratitis Excellent prognosis if appropriately treated History Travel, camping, woods, playing under leaves or in wood piles Living in endemic area (Northeastern area: Maine to Virginia; upper Midwestern: Wisconsin, Minnesota; Northwest California) Endemic in Northern Europe and Eastern Asia as well History of tick bite (- 30-50% of patients recall tick bite) Flu like illness in summer Rash: https://www.cdc.gov/lyme/signs_symptoms/rashes.html Joint complaints Cardiac complaints Neurologic complaints Careful search for tick Diagnosis Labs CBC (leukocytosis, anemia, thrombocytopenia) ESR: most common lab abnormality (>30 mm/hr) Chem 7 LFTs: commonly elevated especially GGT Cultures not typically indicated LP when meningeal signs (CSF: pleocytosis, elevated protein, CSF spirochete ABs).  LP function is more to rule out other etiologies of meningitis rather than diagnose Lyme meningitis given that lyme PCR and lyme Ab index are not very accurate. Serological Testing Serological testing is not always warranted because of the very high incidence of false positive results Serologies are not useful in acute phase (<30 days of infection) because they are negative; it takes several weeks to develop enough antibodies for either test below (ELISA or Western Blot) Acute Lyme is a clinical diagnosis and does not need laboratory testing, especially in endemic areas such as NY If pretest probability is high (symptoms consistent with Lyme + epidemiological background), say patients with CN palsy, meningitis, carditis, or migratory large joint arthritis, then serologies can be very helpful Do not test if patients in endemic areas with potential tick exposure present with EM — just treat with antibiotics Do not test if patients in endemic areas present with no history of tick exposure or only nonspecific symptoms Test if you have high suspicion of lyme without EM PCR is highly specific and sensitive but not available for routine use.  There are two tests you need to use together: 1) ELISA: this detects antibodies to lyme bacteria (borrelia burgdorferi)  in your blood, BUT it can’t distinguish between borrelia and similar bacteria (even sometimes normal flora that lives in you).  In addition, IgM response takes 1-2 weeks while IgG response takes 2-4 weeks. If ELISA is positive or equivocal, then you move onto the: 2) Western blot test: this looks for antibodies not to the whole organism, but to the basic building blocks of the lyme bacteria — the individual proteins, BUT many types of bacteria use the same building blocks. So the CDC says that the Western Blot test must detect IgG antibodies to 5 out of the 10 proteins. See figure 2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918152/ Two-tiered testing has sensitivity between 70-100% and specificity ~95% in late stages Interpretation of Lyme serologies should be done by an ID specialist because they can be confusing and can lead to wrong conclusions if unfamiliar with them NYC is an endemic region where 5% of the population can have a positive without symptoms! If somebody who HAD Lyme disease but successfully treated it with doxycycline tested themselves years later, they could still have the antibodies and therefore it would look like they still had Lyme disease (despite being cured) Positive serology or previous Lyme disease not ensure protective immunity Other tests: Arthrocentesis for acute arthritis: elevated cryoglobulin XRs: may show soft tissue, cartilaginous, osseous changes ECG Differential Diagnosis Tick-borne diseases: Rocky Mountain Spotted fever, tularemia, relapsing fever, Colorado tick fever, tick-bite paralysis, babesiosis, anaplasmosis, powassan virus Remember that doxycycline covers anaplasmosis and lyme but not babesiosis, which requires Atovaquone Rheumatic fever (usually presents with erythema marginatum rash, valvular involvement rather than heart block, TM joint arthritis) Viral meningitis Septic arthritis Syphilis Parvovirus B19 Infectious endocarditis Juvenile rheumatoid arthritis Reiter syndrome Brown recluse spider bite Fibromyalgia Chronic fatigue syndrome Treatment Remove tick: disinfect site then with blunt instrument, grasp tick proximal to skin and pull upward with gentle constant traction.  Mouthparts will release after about a minute. If residual mouthparts are left in skin, leave them alone to avoid infection (they will extrude from skin naturally over time).  Since ticks that have not attached or are moving on the skin cannot transmit Lyme, they can just be brushed off. NS IVF bolus, supportive care Cardiac monitoring, temporary pacemaker for heart block Beware Jarisch Herxheimer reaction: worsening of sx a few hours after treatment initiated Aspirin for cardiac involvement, NSAIDs for arthralgias/ arthritis Prophylaxis: Per the IDSA, give a single dose of 200 mg PO doxycycline to patients who meet all of the following criteria: Deer tick has been attached for 36 hours or more  (the rationale for time of attachment relates to the fact that the spirochetes live in the tick’s gut so they need a long time to multiply and travel to the salivary glands (event that’s triggered by a blood meal) and later overcome the salivary gland  (which only a few do) and finally reach the patient’ skin Prophylaxis can be provided within 72 hours of tick removal Local rate of B. Burgdorferi infection in ticks exceeds 20% (in the northeast USA, the prevalence of infected ticks is between 15-20%) Doxycycline can be used (children >8 years old, non-pregnant females) A 2001 study examined doxycycline vs placebo prophylaxis.  A single dose of 200 mg of oral doxycycline or placebo was given to persons presenting within 72 hours of removal of an I scapularis tick. One of 235 persons in the doxycycline group developed erythema migrans (EM) versus 8 of 247 in the placebo group, for treatment efficacy of 87% (95% CI, 25%–98%; P<0.04) (9). Reasonable alternative strategy: monitor for EM or other signs of infection then initiate treatment if they develop Lyme disease (excellent outcomes in patients treated during early EM stage of disease) Antibiotics: Antibiotics can speed resolution of arthritis and cardiac conduction delays, but not necessarily facial palsy Doxycycline has the best bioavailability and CNS penetration Always check with your ID colleagues to determine appropriate duration of treatment in more serious cases of Lyme disease Stage 1: Amoxicillin (500 mg PO TID) or cefuroxime (500 mg PO BID) or doxycycline (100 mg PO BID; > 8 years old & not pregnant) x 21 days; azithromycin (500 mg PO qday x 14-21 days) IV therapy in pregnant patients Stage 2: PO antibiotics for isolated Bell palsy and mild involvement Amoxicillin with probenecid (500 mg PO TID) x 30 days or doxycycline (100 mg PO BID; > 8 years old & not pregnant) x 10-21 days IV ceftriaxone (2 g IV qday) x 14-21 days, or penicillin G (20-24 million units IV q4-6h x 14-28 days) for meningitis, carditis, severe arthritis Stage 3: Penicillin G (20-24 million units IV q4-6h) x 14-21 days or ceftriaxone (2 g IV qday x 14-28 days) Dispotition Admit unstable or sick patients, those with meningoencephalitis, & carditis (telemetry/ ICU admission) DC patients treated with PO therapy Future prevention strategies: wear long pants & shirts, light-colored clothing (easier to spot crawling ticks), tuck pants into socks, DEET spray, clothing impregnated with permethrin References Baker C et al, Lyme Disease Review Panel of the Infectious Diseases Society of America (IDSA).  Final report of the lyme disease review panel of the infectious diseases society of America (IDSA). 2006.  https://www.idsociety.org/globalassets/idsa/topics-of-interest/lyme/idsalymediseasefinalreport.pdf (22 July 2019, date last accessed) Centers for Disease Control and Prevention.  CDC — Lyme. 2019. https://www.cdc.gov/lyme/index.html (22 July 2019, date last accessed) Hilton E, DeVoti J,, Benach JL, Halluska ML, White DJ, Paxton H, Dumler JS.  Seroprevalence and seroconversion for tick-borne diseases in a high-risk population in the northeast United States.  Am J Med. 1999 Apr;106(4):404-9. Hu LT.  Lyme Disease.  Ann Intern Med.  2016;164:ITC65-ITC80.  Doi: 10.7326/AITC201605030 Lee, M.  Lyme Disease.  Rosen and Barkin’s 5-Minute Emergency Medicine Consult.  2015; 664-665. Nadelman RB, Nowakowski J, Fish D et al., Tick Bite Study Group.  Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after an Ixodes scapularis tick bite.  N Engl J Med.  2001;345:79-84. Sanders, L.  (2009). Every patient tells a story: Medical mysteries and the art of diagnosis. A special thanks to our Infectious Diseases Editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine Read More

An in depth review of this notorious parasite. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Malaria.mp3 Download Leave a Comment Tags: Infectious Diseases Show Notes Background In 2017, there were 219 million cases and 435,000 people deaths from malaria Five species: Falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi. Falciparum, Vivax and Knowlesi can be fatal History of recent travel to Africa (69% of cases in US), particularly to west-Africa should raise suspicion for malaria Clinical Manifestations Average incubation period for Falciparum is 12 days 95% will develop symptoms within 1 month Clinical findings with high likelihood ratios include periodic fevers, jaundice, splenomegaly, pallor. Can also have vomiting, headache, chills, abdominal pain, cough, and diarrhea Severe malaria has a mortality of 5% to 30%, even with therapy Diagnostic criteria for severe malaria: Ashley 2018 Most common manifestations of severe malaria affect the brain, lungs, and kidneys Patients with cerebral malaria can present encephalopathic or comatose, some severe enough to exhibit extensor posturing, or seizures Can have acute lung injury with a quarter of these patients progressing to ARDS Can have AKI from ATN and resultant acidosis Labs may be unremarkable but watch for anemia and thrombocytopenia Hgb <5 has an OR = 4.9 for death Severe thrombocytopenia has an OR = 2.8 Anemia + Thrombocytopenia has an OR = 13.8 (Lampah 2015, PMID 25170106) Watch for hypoglycemia Be mindful of co-infection with salmonella and HIV Obtain BCx, cover with ceftriaxone Diagnosis Blood smear Thick smear to increase sensitivity for detecting parasites Thin smear for quantifying parasitemia and species The first smear is positive in over 90% of cases, but if suspicion is high, it has to be repeated BID for 2-3 days for proper exclusion of malaria (CDC 2019) Management For uncomplicated, non-severe cases, most patients with falciparum should be admitted, especially those with no prior exposure to malaria parasites Malarone is one of the first line options Check out other suggested regimens from the CDC Important to note that when they take this, ensure they take with milk or food containing fat to enhance absorption Severe Malaria Resuscitative efforts directed at affected organ Can deteriorate rapidly Initiate IV Artesunate if high level of suspicion Requires call to CDC: CDC Malaria Hotline: (770) 488-7788 or (855) 856-4713 (toll-free) Monday–Friday 9am–5pm EST – (770) 488-7100 after hours, weekends, and holidays Benzodiazepines for seizures Be judicious with fluids as this can precipitate pulmonary edema and cerebral edema a/w increased mortality in children at 48 hour (Maitland 2011, PMID: 21615299; Hanson 2013, PMID: 23324951) Take Home Points This is going to be a diagnosis that is mainly made through a thorough history, and pay particular attention to those with recent travel to West-Africa The incubation period for falciparum is 12 days, but there is a range of weeks and we should consider Malaria when consistent symptoms develop within 1 month of travel to an endemic area Typical signs and symptoms for uncomplicated malaria are periodic fevers, jaundice, pallor Be mindful of end organ involvement, such as cerebral edema, ATN, and pulmonary edema; these cases are considered to be severe and treated differently than uncomplicated  malaria Uncomplicated cases should get Malarone or Coartem Severe cases require IV Artesunate Be judicious with your fluid resuscitation as this can harm our patients References Centers for Disease Control and Prevention. CDC Parasites – Malaria. 2019 https://www.cdc.gov/parasites/malaria/index.html (7 July 2019, date last accessed) Ashley EA, Pyae Phyo A, Woodrow CJ. Malaria. Lancet. 2018;391(10130):1608-21. Hanson JP, Lam SW, Mohanty S, Alam S, Pattnaik R, Mahanta KC, et al. Fluid resuscitation of adults with severe falciparum malaria: effects on Acid-base status, renal function, and extravascular lung water. Crit Care Med. 2013;41(4):972-81. Lampah DA, Yeo TW, Malloy M, Kenangalem E, Douglas NM, Ronaldo D, et al. Severe malarial thrombocytopenia: a risk factor for mortality in Papua, Indonesia. J Infect Dis. 2015;211(4):623-34. Lokken KL, Stull-Lane AR, Poels K, Tsolis RM. Malaria Parasite-Mediated Alteration of Macrophage Function and Increased Iron Availability Predispose to Disseminated Nontyphoidal Salmonella Infection. Infect Immun. 2018;86(9). Maitland K, Kiguli S, Opoka RO, Engoru C, Olupot-Olupot P, Akech SO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. 2011;364(26):2483-95. Park SE, Pak GD, Aaby P, Adu-Sarkodie Y, Ali M, Aseffa A, et al. The Relationship Between Invasive Nontyphoidal Salmonella Disease, Other Bacterial Bloodstream Infections, and Malaria in Sub-Saharan Africa. Clin Infect Dis. 2016;62 Suppl 1:S23-31. Tintanelli, Judith E., et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. Eighth edition. New York: McGraw-Hill Education, 2016: p.1070-1077 World Health Organization. Guidelines for the treatment of malaria. Third edition April 2015. WHO. 2015 https://www.who.int/malaria/publications/atoz/9789241549127/en/ (7 July 2019, date last accessed) A special thanks to our editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine   Read More

A look at this common and controversial topic. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Otitis_Media.mp3 Download Leave a Comment Tags: Pediatrics Show Notes Background: The most common infection seen in pediatrics and the most common reason these kids receive antibiotics The release of the PCV (pneumococcal conjugate vaccine), or Prevnar vaccine, has made a big difference since its release in 2000 (Marom 2014) This, along with more stringent criteria for what we are calling AOM, has led to a significant decrease in the number of cases seen since then 29% reduction in AOM caused by all pneumococcal serotypes among children who received PCV7 before 24 months of age The peak incidence is between 6 and 18 months of age Risk factors: winter season, genetic predisposition, day care, low socioeconomic status, males, reduced duration of or no breast feeding, and exposure to tobacco smoke. The predominant organisms: Streptococcus pneumoniae, non-typable Haemophilus influenzae (NTHi), and Moraxella catarrhalis. Prevalence rates of infections due to Streptococcus pneumoniae are declining due to widespread use of the Prevnar vaccine while the proportion of Moraxella and NTHi infection increases with NTHi now the most common causative bacterium Strep pneumo is associated with more severe illness, like worse fevers, otalgia and also increased incidence of complications like mastoiditis. Diagnosis The diagnosis of acute otitis media is a clinical one without a gold standard in the ED (tympanocentesis) Ear pain (+LR 3.0-7.3), or in the preverbal child, ear-tugging or rubbing is going to be the most common symptom but far from universally present in children. Parents may also report fevers, excessive crying, decreased activity, and difficulty sleeping. Challenging especially in the younger patient, whose symptoms may be non-specific and exam is difficult Important to keep in mind that otitis media with effusion, which does not require antibiotics, can masquerade as AOM AAP: Diagnosis of Acute Otitis Media (2013)* In 2013, the AAP came out with a paper to help guide the diagnosis of AOM Moderate-Severe bulging of the tympanic membrane or new-onset otorrhea not due to acute otitis externa (grade B) The presence of bulging is a specific sign and will help us distinguish between AOM and OME, the latter has opacification of the tympanic membrane or air-fluid level without bulging (Shaikh 2012, with algorithm) Bulging of the TM is the most important feature and one systematic review found that its presence had an adjusted LR of 51 (Rothman 2003) Classic triad is bulging along with impaired mobility and redness or cloudiness of TM Mild bulging of the tympanic membrane AND (grade C) Recent onset (48hrs) Ear pain (verbal child) Holding, tugging, rubbing of the ear (non-verbal child) OR Intense erythema of the tympanic membrane * The diagnosis should not be made in the absence of a middle ear effusion (grade B) Treatment Options A strategy of “watchful waiting” in which children with acute otitis media are not immediately treated with antibiotic therapy, has been endorsed by the American Academy of Pediatrics. Who gets antibiotics? Depends on age, temperature, duration of otalgia, laterality / otorrhea, and access to follow up Get’s antibiotics: <6 months: Treat 6 months to 2 years: Treat Exception, AAP permits initial observation: unilateral AOM with mild symptoms (mild ear pain, <48h, T <102.2) But know that there is a high rate of treatment failure (Hoberman 2013) >2: Treat Unless they have mild symptoms and it’s unilateral, you can observe for 48-72 hours Why do we give antibiotics? Demonstrated reduction in pain, TM perforations, contralateral episodes of AOM They are no walk in the park, with increased adverse events (vomiting, diarrhea, rash) Two well-designed clinical trials (2011) randomized approximately 600 children meeting strict diagnostic criteria for acute otitis media to receive Augmentin or placebo. These studies demonstrated a significant reduction in symptom burden and clinical failures in those who received antibiotics. The authors conclude that those patients with a clear diagnosis of acute otitis media would benefit from antibiotic therapy AAP AOM Treatment Algorithm Antibiotic Selection High-dose amoxicillin in most (for now) Amoxicillin should not be used if the patient has received Amoxicillin in the past 30 days, has concomitant purulent conjunctivitis (likely H flu) or is allergic to penicillin. beta lactamase resistant antibiotic should be used. Amoxicillin clavulanate or 2nd or 3rd generation cephalosporins (including intramuscular ceftriaxone). Patients with a history of type 1 hypersensitivity reactions to penicillin should be treated macrolides. Studies on duration of therapy have shown better results with 10-day duration in children younger than 2 years and suggest improved efficacy in those 2-5 years. For patients older than 5 years, shorter course therapy (5-7 days) can be utilized. Pain Control Motrin and APAP may have benefit with otalgia reduction Other Decongestants and antihistamines have been shown to not benefit patients in terms of duration of symptoms or complication rate. Not surprisingly, these agents increase the side-effects experienced by patients. Follow up If you chose to observe, let the parents know to return to ED or f/u with their provider in 48-72 hours if they symptoms do not improve. Providing a prescription to parents with clear instructions on when to fill it is also an acceptable option. Strict return precautions should be given if patient develops meningismus or facial nerve palsy. If antibiotics were initiated, and there isn’t improvement in 2-3 days, the diagnosis of AOM should be revisited and, if still suspected, we have to consider that the causative bug is resistant to the prescribed antibiotic. These patients should RTED or f/u with their pediatrician for escalation of care Amoxicillin → Augmentin Augmentin → Ceftriaxone IM Macrolide → no clear antimicrobial agent, consult pediatric ENT If antibiotics are initiated with resolution of symptoms, the patient should f/u in 2-3 months to ensure resolution of the middle ear effusion and ensure that there is no associated conductive hearing loss References: Coker TR, Chan LS, Newberry SJ, Limbos MA, Suttorp MJ, Shekelle PG, et al. Diagnosis, microbial epidemiology, and antibiotic treatment of acute otitis media in children: a systematic review. JAMA. 2010;304(19):2161-9. Hoberman A, Ruohola A, Shaikh N, Tahtinen PA, Paradise JL. Acute otitis media in children younger than 2 years. JAMA Pediatr. 2013;167(12):1171-2. Lieberthal AS, Carroll AE, Chonmaitree T, Ganiats TG, Hoberman A, Jackson MA, et al. The diagnosis and management of acute otitis media. Pediatrics. 2013;131(3):e964-99. Marom T, Tan A, Wilkinson GS, Pierson KS, Freeman JL, Chonmaitree T. Trends in otitis media-related health care use in the United States, 2001-2011. JAMA Pediatr. 2014;168(1):68-75. Rothman R, Owens T, Simel DL. Does this child have acute otitis media? JAMA. 2003;290(12):1633-40. Shaikh N, Hoberman A, Rockette HE, Kurs-Lasky M. Development of an algorithm for the diagnosis of otitis media. Acad Pediatr. 2012;12(3):214-8. Venekamp RP, Sanders S, Glasziou PP, Del Mar CB, Rovers MM. Antibiotics for acute otitis media in children. Cochrane Database Syst Rev. 2013(1):CD000219. See our core article on the topic by Dr. Deborah Levine and Dr. Michael Mojica here A special thanks to our editors: Michael A. Mojica, MD Director, Pediatric Emergency Medicine Fellowship Bellevue Hospital Center Christie M. Gutierrez, MD  Pediatric Emergency Medicine Fellow Columbia University Medical Center Morgan Stanley Children’s Hospital New York Presbyterian Read More