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 Leave a 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.

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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.

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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.

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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.

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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

1. Diverse Etiologies:  Ataxia in children can have various causes that range from self-limiting to life-threatening
2. Comprehensive Assessment: History and physical exams guide diagnosis and workup direction, focusing on symptom time course, infections, and toxic exposures.
3. Physical Examination Clues: Vital signs and appearance offer clues; increased ICP may present with bradycardia, hypertension, and vomiting.
4. Diagnostic Imaging: Point-of-care glucose testing and neuroimaging are key; MRI is preferred for posterior fossa abnormalities.
5. Tailored Treatment: Treatment varies by cause; acute cerebellar ataxia typically resolves over time without specific intervention.

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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 Leave a 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.

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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.

 

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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).

 

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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

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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 

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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

1. 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.
2. Keep your differential broad in these cases. The evaluation will in most cases involve a combination of labs and ultrasound imaging. 
3. 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. 
4. Approach the interpretation of HCG levels with caution and remember that ectopic pregnancies might not adhere to conventional HCG levels.
5. 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.
6. 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.

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