When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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ℹ️ About

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High-YieldID / Wards

Herpes Simplex (HSV)

HSV-1 and HSV-2 cause lifelong latent infections with episodic reactivation. Primary genital herpes is a clinical diagnosis, treat empirically, confirm with PCR. Acyclovir is the backbone of treatment. HSV encephalitis is a medical emergency requiring immediate IV acyclovir, do NOT wait for PCR results.

🔍 Overview

HSV-1 vs HSV-2

Feature	HSV-1	HSV-2
Primary site	Orolabial (cold sores), keratitis, encephalitis	Genital herpes (but HSV-1 now causes 50%+ of new genital herpes in young adults)
Latency	Trigeminal ganglia	Sacral ganglia (S2–S4)
Seroprevalence	~50–80% of adults	~12–16% of adults (higher in HIV+, MSM)
Reactivation frequency	Less frequent genitally; orolabial ∼1–3/year	More frequent genitally (avg 4–5/year in year 1, decreasing over time)
Transmission	Oral contact, saliva	Sexual contact; asymptomatic shedding drives most transmission

Clinical Syndromes

Syndrome	Presentation	Key Points
Primary genital herpes	Painful grouped vesicles on erythematous base → shallow ulcers. Bilateral. Inguinal lymphadenopathy. Dysuria. Systemic symptoms (fever, malaise, myalgias) common.	Worst episode, lasts 2–3 weeks untreated. Often confused with chancroid, syphilis, or contact dermatitis. Primary HSV-1 genital is increasingly common.
Recurrent genital herpes	Unilateral grouped vesicles, fewer lesions, shorter duration (5–10 days). Often preceded by prodrome (tingling, burning, itching).	Less severe than primary. HSV-2 recurs more often than HSV-1 genitally. Frequency decreases over years.
Orolabial herpes (cold sores)	Painful vesicles at vermilion border of lip. Prodrome of tingling 24h before.	Usually HSV-1. Treat with topical or oral antivirals if caught early (within 72h of onset).
HSV keratitis	Eye pain, photophobia, tearing, decreased vision. Dendritic ulcer on slit-lamp fluorescein exam.	OPHTHALMOLOGY EMERGENCY, can cause corneal scarring and blindness. Treat with topical ganciclovir or trifluridine. Do NOT give topical steroids (worsens viral keratitis).
HSV encephalitis EMERGENCY	Fever, headache, altered mental status, seizures, focal neurologic deficits. Temporal lobe predilection on MRI.	Mortality 70% untreated. Start acyclovir 10 mg/kg IV q8h IMMEDIATELY if suspected, do NOT wait for CSF PCR. MRI: temporal lobe hyperintensity on T2/FLAIR. CSF: lymphocytic pleocytosis, elevated protein, RBCs.
Herpes whitlow	Painful vesicles on finger/thumb. Healthcare workers, thumb-sucking children.	Do NOT incise (not an abscess). Treat with oral acyclovir/valacyclovir. Self-limited in 2–3 weeks.
Eczema herpeticum	Widespread HSV over areas of eczema/atopic dermatitis. Punched-out erosions, fever.	Medical emergency in severe cases, IV acyclovir. Can be life-threatening in infants/immunocompromised.
Neonatal herpes	Skin/eye/mouth (SEM), CNS disease, or disseminated. Presents at 1–3 weeks of life.	Highest risk: primary maternal genital HSV near delivery. C-section if active lesions at labor. Mortality high if disseminated.

HSV encephalitis is the #1 treatable cause of fatal sporadic encephalitis. Temporal lobe involvement on MRI is classic. Start IV acyclovir BEFORE lumbar puncture results, delay increases mortality from 30% to 70%. Treat for 14–21 days minimum.

🧪 Workup

Diagnostic Testing

Test	When to Use	Key Points
HSV PCR (swab)	Active vesicles/ulcers, preferred test	Gold standard for genital/mucosal lesions. More sensitive than viral culture (3–5x). Swab base of unroofed vesicle. Can distinguish HSV-1 vs HSV-2.
HSV PCR (CSF)	Suspected HSV encephalitis or meningitis	Sensitivity 96–98%. Can be false-negative in first 72h, if high suspicion and initial PCR negative, repeat at 3–7 days. Do NOT stop acyclovir based on a single negative PCR early on.
Viral culture	Active vesicles (if PCR not available)	Sensitivity depends on lesion stage: highest in vesicles (> 90%), drops rapidly in crusted lesions (< 30%). Swab base of unroofed vesicle. Takes 2–5 days.
Type-specific serology (IgG)	No active lesions; screening; confirm past infection	HSV-1 IgG and HSV-2 IgG (glycoprotein G-based assays). Seroconversion takes 2–12 weeks after primary infection. IgM is NOT useful, cross-reacts, false positives, does not distinguish primary from recurrent. Do not order HSV IgM.
Tzanck smear	Bedside, rapid (if PCR unavailable)	Multinucleated giant cells = herpesvirus (HSV or VZV, cannot distinguish). Low sensitivity (60%). Largely replaced by PCR.

Do NOT order HSV IgM. It has poor sensitivity and specificity, cross-reacts between HSV-1 and HSV-2, cannot distinguish primary from recurrent infection, and frequently gives false-positive results causing unnecessary anxiety. Use type-specific IgG (glycoprotein G-based) instead.

HSV Encephalitis Workup

MRI brain with contrast, temporal lobe hyperintensity on T2/FLAIR (unilateral or bilateral) is classic. Sensitivity > 90%. CT misses early disease.
LP with CSF studies, HSV PCR, cell count (lymphocytic pleocytosis), protein (elevated), glucose (usually normal), RBCs (often present from hemorrhagic necrosis)
EEG, periodic lateralized epileptiform discharges (PLEDs) from temporal lobe. Helps if MRI equivocal.
Start acyclovir 10 mg/kg IV q8h BEFORE results, empiric treatment is the standard of care. Duration: 14–21 days.

🚨 Management

Treatment by Syndrome

Scenario	Treatment	Duration	Notes
Primary genital herpes	Valacyclovir (Valtrex) 1g PO BID or Acyclovir (Zovirax) 400 mg PO TID	7–10 days	Start as soon as possible (best within 72h of onset). Reduces duration by 3–5 days and viral shedding. Extend if lesions not healed at day 10.
Recurrent genital herpes (episodic)	Valacyclovir 500 mg PO BID × 3 days or Valacyclovir 1g PO daily × 5 days or Acyclovir 800 mg PO TID × 2 days	Valacyclovir 500 mg BID: 3 days Valacyclovir 1g daily: 5 days Acyclovir 800 mg TID: 2 days	Most effective if started during prodrome or within 24h of lesion onset. Patient-initiated therapy, prescribe in advance so patient can start at first sign.
Suppressive therapy	Valacyclovir 500 mg PO daily (if ≤9 episodes/yr) Valacyclovir 1g PO daily (if ≥10 episodes/yr)	Ongoing (reassess annually)	Reduces outbreaks by 70–80% and transmission to seronegative partners by ~50%. Recommend if: ≥6 episodes/year, severe episodes, serodiscordant couple, significant psychological impact.
Orolabial herpes	Valacyclovir 2g PO q12h × 1 day or topical penciclovir (Denavir) cream q2h × 4 days	Valacyclovir: 1 day Penciclovir cream: 4 days	Start at prodrome (tingling). Systemic therapy more effective than topical. Sunscreen on lips prevents UV-triggered recurrences.
HSV encephalitis EMERGENCY	Acyclovir 10 mg/kg IV q8h	14–21 days	Start empirically, do NOT wait for CSF PCR. Adjust for renal function (CrCl). Aggressive IV hydration to prevent acyclovir crystalluria/nephrotoxicity. Repeat CSF PCR near end of treatment to confirm clearance.
HSV in immunocompromised	Valacyclovir 1g PO BID (mild) Acyclovir 5–10 mg/kg IV q8h (severe)	7–14 days (or until lesions healed)	Higher doses, longer courses. Consider acyclovir resistance if lesions not improving after 10 days, send for resistance testing. Treat resistant HSV with foscarnet 40 mg/kg IV q8h.
Neonatal herpes	Acyclovir 20 mg/kg IV q8h	14 days (SEM) or 21 days (CNS/disseminated)	Neonatology/ID consult. High-dose acyclovir. Follow with suppressive oral acyclovir × 6 months after IV course.

Valacyclovir vs acyclovir: Valacyclovir is the prodrug of acyclovir with 3–5x better oral bioavailability (55% vs 15–20%). Allows less frequent dosing and equivalent efficacy. Use valacyclovir for oral therapy; reserve IV acyclovir for severe disease (encephalitis, disseminated, immunocompromised).

Pregnancy Considerations

Primary genital herpes near delivery (<6 weeks before) → highest risk of neonatal transmission (30–50%) → C-section recommended
Recurrent genital herpes at delivery → much lower transmission risk (1–3%) → C-section if active lesions present at onset of labor
Suppressive therapy from 36 weeks: Acyclovir 400 mg PO TID or Valacyclovir 500 mg PO BID starting at 36 weeks gestation to reduce outbreaks at delivery and avoid unnecessary C-sections ACOG, 2020
Acyclovir/valacyclovir are safe in pregnancy (Category B), extensive safety data with no increased risk of birth defects

💊 Medications

Antiviral Medications for HSV

Drug (Brand)	Mechanism	Dosing	Key Considerations
Acyclovir (Zovirax)	Nucleoside analog, activated by viral thymidine kinase → inhibits viral DNA polymerase	Oral: 200–800 mg, 2–5x daily (varies by indication) IV: 5–10 mg/kg q8h	Poor oral bioavailability (15–20%). Nephrotoxic (crystalluria), aggressive IV hydration, dose-adjust for CrCl. IV formulation for severe disease only.
Valacyclovir (Valtrex)	Prodrug of acyclovir, converted to acyclovir in gut/liver. Same mechanism.	500 mg–2g PO, 1–2x daily (varies by indication)	Preferred oral agent, better bioavailability (55%) = less frequent dosing. Same efficacy as acyclovir. Dose-adjust for renal impairment. Rare: TTP/HUS at very high doses in immunocompromised.
Famciclovir (Famvir)	Prodrug of penciclovir, similar mechanism to acyclovir	250–500 mg PO BID-TID	Third-line option. Similar efficacy. No IV formulation. Use if intolerant to valacyclovir.
Foscarnet (Foscavir)	Directly inhibits viral DNA polymerase (no thymidine kinase activation needed)	40 mg/kg IV q8h	For acyclovir-resistant HSV (usually in immunocompromised). Highly nephrotoxic. Electrolyte wasting (Ca²⁺, Mg²⁺, K⁺). Painful genital ulcers as side effect. Monitor renal function and electrolytes closely.

Acyclovir resistance: Suspect if lesions not improving after 10 days of appropriate-dose acyclovir in immunocompromised patient. Caused by thymidine kinase mutations (most common). Treat with foscarnet (does not require TK activation). Send viral culture with resistance testing. Resistance is rare in immunocompetent patients.

📋 On Rounds

What is the most important step in managing suspected HSV encephalitis?

Start IV acyclovir 10 mg/kg q8h immediately, do NOT wait for CSF PCR results or MRI. Mortality is 70% untreated vs ~20% with early acyclovir. Every hour of delay worsens outcomes. Treat for 14–21 days. Temporal lobe involvement on MRI is classic but not required to initiate treatment.

Why should you never order HSV IgM?

HSV IgM has poor sensitivity and specificity, cross-reacts between HSV-1 and HSV-2, cannot distinguish primary from recurrent infection, and frequently gives false-positive results. It causes unnecessary anxiety and does not change management. Use type-specific IgG (glycoprotein G-based) for serologic diagnosis or HSV PCR swab for active lesions.

When do you recommend suppressive therapy for genital herpes?

Suppressive therapy (valacyclovir 500 mg–1g daily) is recommended for: (1) ≥6 recurrences per year, (2) serodiscordant couples (reduces transmission by ~50%), (3) severe episodes causing significant morbidity, (4) significant psychological impact. Also start at 36 weeks gestation in pregnant women with history of genital herpes to reduce outbreaks at delivery.

What is the difference between HSV-1 and HSV-2 genital herpes?

HSV-1 now causes >50% of new genital herpes in young adults (via oral-genital contact). HSV-1 genital herpes recurs less frequently (avg 1/year vs 4–5/year for HSV-2). HSV-2 genital herpes recurs more often and has more asymptomatic shedding. Both respond to the same antivirals. Type-specific serology (IgG) or PCR swab can distinguish them, important for counseling on recurrence risk and transmission.

What is herpes whitlow and why should you NOT incise it?

Herpes whitlow is HSV infection of the finger, typically in healthcare workers (from contact with oral/genital secretions) or children who suck their thumbs. It presents as painful vesicles on the distal finger. Do NOT incise, it mimics a felon (bacterial abscess) but is viral. Incision can spread virus, cause secondary bacterial infection, and delay healing. Treat with oral antivirals (valacyclovir). Self-limited in 2–3 weeks.

📣 Sample Presentation

One-Liner

"Ms. Chen is a 24-year-old woman presenting with her first episode of painful genital vesicles and ulcers × 4 days, with inguinal lymphadenopathy and low-grade fever, consistent with primary genital herpes."

Key Points to Cover on Rounds

Primary genital herpes, clinical diagnosis with grouped vesicles on erythematous base. Sent HSV PCR swab for type-specific confirmation. Started valacyclovir 1g PO BID × 10 days. Counseling provided: lifelong infection, asymptomatic shedding, condom use, disclosure to partners, suppressive therapy options if frequent recurrences. Screened for other STIs (HIV, syphilis, gonorrhea, chlamydia). Not pregnant, no delivery planning needed. Follow-up with PCP for ongoing management.

⚡ Summary

Summary

Primary Genital

Valacyclovir 1g PO BID × 7–10 days. Start early. Most severe episode. Screen for STIs.

Recurrent Genital

Valacyclovir 500 mg BID × 3 days (episodic). Start at prodrome. Patient-initiated therapy.

Suppressive

Valacyclovir 500 mg–1g daily. For ≥6/year, serodiscordant couples, severe impact. Reduces transmission ~50%.

HSV Encephalitis

Acyclovir 10 mg/kg IV q8h × 14–21 days. START IMMEDIATELY. Temporal lobe on MRI. 70% fatal untreated.

Diagnosis

HSV PCR swab (gold standard for active lesions). Type-specific IgG for serology. NEVER order HSV IgM.

Pregnancy

Suppress from 36 weeks. C-section if active lesions at labor. Primary HSV near delivery = highest neonatal risk.

📄 One Pager

Herpes Simplex (HSV), Quick Reference Card

Print this page (Ctrl/Cmd + P) for a condensed reference card.

HERPES SIMPLEX (HSV), AT A GLANCE

📋 Diagnose: HSV PCR swab (active lesions), type-specific IgG (serology). Never IgM.
🧪 Workup: PCR swab unroofed vesicle. Encephalitis: MRI + CSF PCR + start acyclovir empirically.
⚡ Treat: Valacyclovir 1g BID × 7–10d (primary), 500 mg BID × 3d (recurrent), 500 mg–1g daily (suppressive).
💊 Encephalitis: Acyclovir 10 mg/kg IV q8h × 14–21d. DO NOT WAIT for results.
🤰 Pregnancy: Suppress from 36 wk. C-section if active lesions at labor.
⚠️ Resistance: Suspect if no improvement at 10d in immunocompromised → foscarnet.