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.

Ebola Virus Disease -Recognition, Isolation, Supportive Care & 2026 Bundibugyo Outbreak -RoundsRx

Ebola Virus Disease

A filovirus causing severe viral hemorrhagic fever with case-fatality 25 to 90% by species. The intern’s job is recognition, isolation, and calling the right people. Aggressive supportive care saves lives independent of any drug. Inmazeb, Ebanga, and Ervebo are Zaire-ebolavirus-only, the active 2026 outbreak is Bundibugyo virus, so the approved drugs do not apply.

Species	Geography	Case Fatality	Approved MCM	Approved Vaccine
Zaire ebolavirus	DRC, West Africa (2014–16 epidemic), most US-imported cases	40–90% (untreated); ~28–35% with MCM + supportive care	Inmazeb (atoltivimab/maftivimab/odesivimab); Ebanga (ansuvimab)	Ervebo (rVSV-ZEBOV-GP), single dose, ages ≥12
Sudan ebolavirus	Uganda, Sudan/South Sudan	40–60%	None approved. cAd3-EBO-S and ChAd3-SUDV candidates deployed under trial protocols during outbreaks.	None approved.
Bundibugyo ebolavirus 2026 OUTBREAK	DRC, Uganda (2007, 2012, 2026)	25–50%	None approved. Investigational MCMs case-by-case via NIH/CDC; cross-reactivity of Zaire-targeted antibodies is incomplete and not a substitute.	None approved.
Tai Forest ebolavirus	Côte d’Ivoire (single human case, 1994)	Single survivor	None approved.	None approved.
Reston ebolavirus	Philippines, China (in non-human primates and swine)	No human disease documented	Not applicable	Not applicable

Species

Geography

Case Fatality

Approved MCM

Approved Vaccine

Zaire ebolavirus

DRC, West Africa (2014–16 epidemic), most US-imported cases

40–90% (untreated); ~28–35% with MCM + supportive care

Inmazeb (atoltivimab/maftivimab/odesivimab); Ebanga (ansuvimab)

Ervebo (rVSV-ZEBOV-GP), single dose, ages ≥12

Sudan ebolavirus

Uganda, Sudan/South Sudan

40–60%

None approved. cAd3-EBO-S and ChAd3-SUDV candidates deployed under trial protocols during outbreaks.

None approved.

Bundibugyo ebolavirus 2026 OUTBREAK

DRC, Uganda (2007, 2012, 2026)

25–50%

None approved. Investigational MCMs case-by-case via NIH/CDC; cross-reactivity of Zaire-targeted antibodies is incomplete and not a substitute.

None approved.

Tai Forest ebolavirus

Côte d’Ivoire (single human case, 1994)

Single survivor

None approved.

Reston ebolavirus

Philippines, China (in non-human primates and swine)

No human disease documented

Not applicable

Phase	Days	Features	Why It Matters
1. Early febrile (“dry”)	Days 1–3	Abrupt fever, severe fatigue, myalgia, headache, sore throat, conjunctival injection. Looks like flu or malaria.	Most cases get missed here. Travel history within 21 days is the single most important screening question. Pretest probability is everything.
2. GI (“wet”)	Days 3–10	Severe vomiting, profuse watery diarrhea (5–10 L/day), abdominal pain, anorexia, hiccups. Maculopapular rash in ~25% (often missed on darker skin).	This is where supportive care saves lives. Hypovolemic shock and electrolyte derangements (hypokalemia, hypomagnesemia, hypocalcemia) are the proximate killers, not the virus itself. IV fluids and electrolyte repletion are the highest-yield interventions.
3. Critical / shock	Days 7–12	Hypovolemic and/or distributive shock, AKI, hepatitis (AST > ALT, often 5–10× ULN), encephalopathy, hemorrhage in ~20% (GI bleeding, petechiae, gingival, conjunctival, IV-site oozing).	Hemorrhage is not universal and not required for diagnosis. The classic “hemorrhagic fever” image is overstated, most patients die from shock and multi-organ failure, not exsanguination.
4. Recovery or death	Days 8–16	Death typically days 8–16. Survivors enter prolonged convalescence with fatigue, arthralgias, uveitis, hearing loss, neurocognitive symptoms.	Post-Ebola syndrome is real and underrecognized. Survivors need ophthalmology, audiology, and mental health follow-up; CNS, ocular, and genital tract are sanctuary sites where virus can persist.

Phase

Days

Features

Why It Matters

1. Early febrile (“dry”)

Days 1–3

Abrupt fever, severe fatigue, myalgia, headache, sore throat, conjunctival injection. Looks like flu or malaria.

Most cases get missed here. Travel history within 21 days is the single most important screening question. Pretest probability is everything.

2. GI (“wet”)

Days 3–10

Severe vomiting, profuse watery diarrhea (5–10 L/day), abdominal pain, anorexia, hiccups. Maculopapular rash in ~25% (often missed on darker skin).

This is where supportive care saves lives. Hypovolemic shock and electrolyte derangements (hypokalemia, hypomagnesemia, hypocalcemia) are the proximate killers, not the virus itself. IV fluids and electrolyte repletion are the highest-yield interventions.

3. Critical / shock

Days 7–12

Hypovolemic and/or distributive shock, AKI, hepatitis (AST > ALT, often 5–10× ULN), encephalopathy, hemorrhage in ~20% (GI bleeding, petechiae, gingival, conjunctival, IV-site oozing).

Hemorrhage is not universal and not required for diagnosis. The classic “hemorrhagic fever” image is overstated, most patients die from shock and multi-organ failure, not exsanguination.

4. Recovery or death

Days 8–16

Death typically days 8–16. Survivors enter prolonged convalescence with fatigue, arthralgias, uveitis, hearing loss, neurocognitive symptoms.

Post-Ebola syndrome is real and underrecognized. Survivors need ophthalmology, audiology, and mental health follow-up; CNS, ocular, and genital tract are sanctuary sites where virus can persist.

Tier	Definition	Action
High risk	Percutaneous or mucous-membrane exposure to body fluids of a confirmed case; unprotected direct contact with a corpse in an outbreak area; lab handling without proper PPE.	Direct active monitoring × 21 days. Confine movement. Public health-supervised isolation if symptomatic.
Some risk	Household contact with confirmed case; direct contact with case while wearing PPE; healthcare worker in an outbreak setting with PPE breaches.	Active monitoring × 21 days. Restricted travel. Symptom-triggered isolation.
Low (but not zero) risk	Travel from outbreak country without specific contact; brief direct contact (e.g., handshake) with a symptomatic case while wearing PPE.	Passive self-monitoring × 21 days with reporting to public health if febrile.
No identifiable risk	Travel from non-outbreak countries adjacent to affected areas; contact with asymptomatic person who later tested negative.	No restrictions.

Tier

Definition

Action

High risk

Percutaneous or mucous-membrane exposure to body fluids of a confirmed case; unprotected direct contact with a corpse in an outbreak area; lab handling without proper PPE.

Direct active monitoring × 21 days. Confine movement. Public health-supervised isolation if symptomatic.

Some risk

Household contact with confirmed case; direct contact with case while wearing PPE; healthcare worker in an outbreak setting with PPE breaches.

Active monitoring × 21 days. Restricted travel. Symptom-triggered isolation.

Low (but not zero) risk

Travel from outbreak country without specific contact; brief direct contact (e.g., handshake) with a symptomatic case while wearing PPE.

Passive self-monitoring × 21 days with reporting to public health if febrile.

No identifiable risk

Travel from non-outbreak countries adjacent to affected areas; contact with asymptomatic person who later tested negative.

No restrictions.

Drug	Composition	Dose	Indication	Evidence
Inmazeb (REGN-EB3)	Cocktail of three human monoclonal antibodies (atoltivimab, maftivimab, odesivimab) targeting Ebola glycoprotein	50 mg/kg of each component (150 mg/kg total) IV ×1	Zaire ebolavirus only, adults and pediatric including neonates born to Ebola-positive mothers	PALM, 2019 reduced 28-day mortality to 33.5% vs 49.7% with ZMapp
Ebanga (ansuvimab, mAb114)	Single human monoclonal antibody against Ebola glycoprotein, derived from a 1995 Kikwit survivor	50 mg/kg IV ×1	Zaire ebolavirus only, adults and pediatric including neonates	PALM, 2019 28-day mortality 35.1%, comparable to Inmazeb

Drug

Composition

Dose

Indication

Evidence

Inmazeb (REGN-EB3)

Cocktail of three human monoclonal antibodies (atoltivimab, maftivimab, odesivimab) targeting Ebola glycoprotein

50 mg/kg of each component (150 mg/kg total) IV ×1

Zaire ebolavirus only, adults and pediatric including neonates born to Ebola-positive mothers

PALM, 2019 reduced 28-day mortality to 33.5% vs 49.7% with ZMapp

Ebanga (ansuvimab, mAb114)

Single human monoclonal antibody against Ebola glycoprotein, derived from a 1995 Kikwit survivor

50 mg/kg IV ×1

Zaire ebolavirus only, adults and pediatric including neonates

PALM, 2019 28-day mortality 35.1%, comparable to Inmazeb

2 a.m. page from the ED: “Hi, we have a 34-year-old man, returned from Kampala 5 days ago, came in with fever 38.9°C, vomiting, watery diarrhea ×2 days. He’s in fast-track right now. Can you come down?”

What you do in the next 5 minutes:

Stop the patient from moving. Ask the ED to mask him, place him in a private room with the door closed (any private room is better than fast-track). No more visitors. No more staff in/out.
Page charge nurse and ED attending, confirm the exposure history with the patient directly (Uganda travel within 21 days? contact with sick person? handling animals?).
Page hospital infection control immediately. They activate the institution’s Special Pathogens Response Team or equivalent.
State health department, then CDC EOC 770-488-7100.
Order malaria smear and RDT (single dedicated draw with full PPE), and start empiric artemether-lumefantrine if any delay in smear results.
No central line, no LP, no routine bloods until cleared. Bedside POCUS for volume status, peripheral IV by experienced nurse, IV fluids LR via syringe pump in sealed administration set.
Document exposure list, every staff member who has touched or been within 1 m of the patient since arrival, with timestamp. This is the contact-tracing dataset if the case turns positive.

The wrong move is to draw a CBC, BMP, blood cultures, and an ABG in the first 10 minutes “just to get them done”. Every needle stick before PPE and infection control are in place is a potential transmission event.