Core EM - Emergency Medicine Podcast

Superwarfarin toxicity: recognition, reversal, and prolonged vitamin K therapy. Hosts: Mac Josh Reandelar, DO Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Superwarfarin_Toxicity.mp3 Download Leave a Comment Tags: Toxicology Show Notes Toxicology & Pathophysiology Long-acting vitamin K antagonists (LA-VKAs), developed as potent rodenticides Examples: brodifacoum, bromadiolone, difenacoum, chlorophacinone Much more potent + far longer acting than warfarin MOA: inhibits VKORC1 → ↓ vitamin K recycling → impaired γ-carboxylation ↓ factors II, VII, IX, X + proteins C/S Highly lipophilic → extensive tissue/fat sequestration + slow redistribution Effect can persist weeks-months; occasionally much longer Not dialyzable Exposure: large acute ingestion OR repeated low-dose exposure Source may be unclear, concealed, or initially unknown Presentation Often delayed + insidious Severe coagulopathy may precede obvious bleeding Early: epistaxis, gingival bleeding, bruising/ecchymoses, hematuria Classic clue: well-appearing pt + extraordinarily abnormal coagulation studies Severe bleeding: RP hemorrhage, ICH, spinal hemorrhage, tamponade, major GI/GU bleeding RP bleed → flank/back pain ± CVA tenderness Labs & Diagnosis PT/INR: profoundly elevated, sometimes beyond assay range aPTT: may also be markedly prolonged with severe factor depletion CBC/plts: often initially preserved unless major blood loss/other process LFTs: often relatively normal Profound INR + no warfarin + preserved liver function → think superwarfarin CT based on bleeding site; CT A/P for suspected RP hemorrhage Confirm: specialized serum/blood testing for long-acting anticoagulants, typically chromatography/mass spec Do NOT delay resuscitation/treatment for confirmatory testing Elevated INR: Differential Superwarfarin exposure Warfarin toxicity Severe vitamin K deficiency: malnutrition, malabsorption, prolonged abx Liver failure/cirrhosis DIC Acquired factor deficiency/inhibitor Helpful discriminators Liver dz → abnormal hepatic profile/clinical context DIC → ↓ plts, ↓ fibrinogen, ↑ D-dimer No warfarin + massive INR + relatively normal LFTs/plts → superwarfarin rises on the differential ED Management Major/Life-Threatening Bleeding Goal: replace factors NOW + restore endogenous synthesis 4F-PCC = preferred factor replacement Fast, predictable correction Small volume No thawing/type matching FFP if PCC unavailable Slower + large volume/TACO risk Give IV vitamin K concurrently PCC = immediate bridge; vitamin K = sustained factor synthesis Recheck INR + clinical bleeding response Repeat PCC generally not routine; reassess before redosing No Major Bleeding, Critical INR Vitamin K is primary therapy High-dose PO vitamin K often preferred when clinically stable Avoid unnecessary PCC/FFP if no major bleeding Serial INR monitoring essential Poison Control Call early Helps with: Confirmatory testing Vitamin K dosing Duration of therapy Monitoring/taper strategy Outpatient planning The Long Game This is NOT standard warfarin toxicity Vitamin K requirements may persist for months Discharge only when bleeding controlled + clinically stable on oral regimen Close serial INR follow-up mandatory Slowly taper vitamin K under laboratory guidance Stopping too early → rebound INR elevation + recurrent bleeding Take Home Points Massive unexplained INR + relatively normal liver function → think superwarfarin Major bleeding → 4F-PCC + IV vitamin K Expect prolonged vitamin K therapy + meticulous INR follow-up Read More

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

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

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

We discuss the evaluation of and treatment options for acute back pain. Hosts: Benjamin Friedman, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Back_Pain.mp3 Download Leave a Comment Tags: Musculoskeletal, Orthopaedics Show Notes **Please fill out this quick survey to help us develop additional resources for our listeners: Core EM Survey** Clinical Evaluation: Primary Goal: Distinguish benign musculoskeletal pain from serious pathology. Red Flags: Look for indicators of spinal infection, spinal bleed, or space-occupying lesions (e.g., tumors, large herniated discs). Assessment: A thorough history and neurological exam (strength testing, gait) is essential. Additional Tools: Use bedside ultrasound for post-void residual assessment in suspected cauda equina syndrome Imaging Guidelines: Routine Imaging: Generally not indicated for young, healthy patients without red flags. ACEP Recommendations: Avoid lumbar X-rays in patients under 50 without risk factors, as they do not change management and may increase costs and ED time. Advanced Imaging: Reserve MRI for patients with red flags, neurological deficits, or suspected cauda equina syndrome; CRP may be a part of your calculus when evaluating for infectious causes of back pain Treatment Options: Evidence-Based First-Line: NSAIDs offer modest benefit. Skeletal muscle relaxants can be used but require caution due to side effects. Ineffective Therapies: Acetaminophen shows no benefit for back pain. Steroids are not recommended for non-radicular pain, with only limited benefit in sciatica. Topical treatments, lidocaine patches, and opioids are not supported by evidence and may pose additional risks. Alternative and Experimental Interventions: Nerve Blocks: Current evidence is limited; more research is needed on trigger point injections and erector spinae plane blocks. Severe Pain Management: A single opioid dose (preferably codeine or oral morphine) may be considered to facilitate discharge when necessary. Use diazepam sparingly for immediate mobilization. Onsite physical therapy in the ED can be beneficial when available. Preventing Chronic Pain: Research Focus: Ongoing studies are evaluating whether duloxetine (Cymbalta) can prevent the transition from acute to chronic back pain. Non-Pharmacologic Measures: Consider spinal mobilization, physical therapy, acupuncture, and cognitive behavioral therapy (CBT) as adjuncts in management. Take-Home Points: Most acute back pain is benign, but watch for red flags like IV drug use, anticoagulation, or neurological symptoms (e.g., weakness, bladder dysfunction) that may indicate serious conditions like spinal infections, bleeds, or cord compression. Avoid unnecessary lumbar X-rays in young, healthy patients without red flags—MRI is preferred only for those with risk factors, neurological deficits, or suspected cauda equina syndrome. Use NSAIDs and skeletal muscle relaxants for acute musculoskeletal back pain, as they offer modest benefits. Avoid opioids, acetaminophen, and steroids for non-radicular pain, as they lack evidence. For severe, uncontrolled pain, consider a single opioid dose (e.g., codeine) or diazepam sparingly Encourage patients to engage in non-pharmacologic therapies like yoga, massage, or cognitive behavioral therapy to aid recovery and prevent chronic pain. Read More

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

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