We break down pneumothorax: risks, diagnosis, and management pearls.
Hosts:
Christopher Pham, MD
Brian Gilberti, MD



https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumothorax.mp3



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Tags: Chest Trauma, Pulmonary, Trauma





Show Notes

Risk Factors for Pneumothorax

* Secondary pneumothorax

* Trauma: rib fractures, blunt chest trauma (as in the case).
* Iatrogenic: central line placement, thoracentesis, pleural procedures.


* Primary spontaneous pneumothorax

* Young, tall, thin males (10–30 years).
* Connective tissue disorders: Marfan, Ehlers-Danlos.
* Underlying lung disease: COPD with bullae, interstitial lung disease, CF, TB, malignancy.


* Technically, anyone is at risk.


Symptoms & Differential Diagnosis

* Typical PTX presentation: Dyspnea, chest pain, pleuritic discomfort.
* Exam clues: unilateral decreased breath sounds, focal tenderness/crepitus.
* Red flags (suggest tension PTX):

* JVD
* Tracheal deviation
* Hypotension, shock physiology
* Severe tachycardia, hypoxia


* Differential diagnoses:

* Pulmonary: asthma, COPD, pneumonia, pulmonary edema (SCAPE), ILD, infections.
* Cardiac: ACS, CHF, pericarditis.
* PE and other acute causes of dyspnea.




Diagnostics

* Bloodwork: limited role, except type & screen if intervention likely.
* EKG: reasonable given chest pain/shortness of breath.
* Imaging:

* POCUS (bedside ultrasound)

* High sensitivity (86–96%) & specificity (97–100%).
* Signs:

* Seashore sign: normal lung sliding.
* Barcode sign: absent lung sliding.
* Lung point: most specific for PTX.




* CXR

* Sensitivity ~70–90% for small PTX.
* May show pleural line, hyperlucency.


* CT chest (gold standard)

* Defines size/severity.
* Rules out mimics (bullae, pleural effusion, hemothorax).
* Guides intervention choice.






Management

* First step for all: Oxygen supplementation (non-rebreather if possible).

* Accelerates resorption of pleural air.


* Stable vs. unstable decision point:

* Unstable/tension PTX

* Immediate needle thoracostomy (14-g angiocath, 2nd ICS midclavicular).
* Temporizing until chest tube/pigtail placed.


* Stable, small PTX (<2 cm on O₂)

* Observation, supplemental O₂, conservative management.


* Stable, larger PTX or symptomatic

* Chest tube or pigtail catheter insertion.
* Pigtail catheters: less invasive,

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



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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.

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



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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.



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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



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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,

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



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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.

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



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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






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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



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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 excre...

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



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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:

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



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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.

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



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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

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



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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:

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



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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.

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



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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 ...

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



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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 temp...

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



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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 ...

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



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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.

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



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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.

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



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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,

We review Acute Respiratory Distress Syndrome
Hosts:
Sadakat Chowdhury, MD
Brian Gilberti, MD



https://media.blubrry.com/coreem/content.blubrry.com/coreem/ARDS.mp3



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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,

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



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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,