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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EMERGENTSurgery/ID

Necrotizing Fasciitis / Gas Gangrene

Rapidly progressive soft tissue infection. Every hour to the operating room matters: delay beyond 24 hours carries roughly a 9-fold higher mortality. Pain OUT OF PROPORTION to exam is the hallmark. Surgical debridement IS the treatment. CT can miss early cases.

Overview

Classification

Type	Organisms	Risk Factors
Type 1 (Polymicrobial)	Mixed aerobic + anaerobic	Diabetes, post-surgical, immunocompromised
Type 2 (Monomicrobial)	Group A Strep	Young, healthy, minor trauma
Gas Gangrene	C. perfringens	Trauma, surgical wounds

Clinical Features

Pain OUT OF PROPORTION to exam, hallmark
Rapidly spreading erythema, crepitus, bullae, dusky/necrotic skin
Systemic toxicity: sepsis, shock. LRINEC ≥6 suggestive

If you suspect nec fasc, go to the OR. Do NOT wait for imaging. CT can MISS early disease. The “finger test” (bedside incision, tissue planes dissect easily) is diagnostic. Delay to debridement beyond 24 hours is the threshold most consistently linked to death (relative risk ~9.4 Wong, 2003), so the clock starts the moment you suspect it.

Workup

Clinical diagnosis, do NOT delay for imaging
Labs: CBC, BMP (Na often low), CRP, lactate, CK, coags, blood cultures
LRINEC score ≥6 suspicious, ≥8 highly suggestive
Finger test: bedside incision, easy tissue dissection = nec fasc

Management

SURGICAL DEBRIDEMENT IS THE TREATMENT, antibiotics are adjunct
Second-look operation 24–48h. Often serial debridements needed
ICU for sepsis management
IVIG for streptococcal toxic shock (1–2 g/kg, controversial but used)

🔄 Updated Practice: Old teaching: obtain CT or MRI to confirm necrotizing fasciitis before consulting surgery. Current practice: if you suspect nec fasc clinically (pain out of proportion, rapidly spreading, systemic toxicity, crepitus), take the patient to the OR immediately. CT can MISS early disease, sensitivity is only ~80%. Delay to debridement beyond 24 hours is independently associated with roughly 9-fold higher mortality (Wong 2003), and the EAST 2018 practice guideline recommends operating as soon as the diagnosis is suspected rather than waiting on imaging. The 'finger test' (bedside wound exploration, if tissue planes dissect easily with blunt finger) is faster and more reliable than imaging.

Medications

Antibiotic Regimen

Drug	Dose	Role
Vancomycin	25–30mg/kg load, 15–20mg/kg q8–12h	MRSA coverage
Piperacillin-Tazobactam	4.5g IV q6h	Broad GN + anaerobe coverage
Clindamycin	900mg IV q8h	TOXIN SUPPRESSION

Clindamycin for TOXIN SUPPRESSION, not just coverage. GAS and Clostridium produce exotoxins driving shock. Clindamycin (protein synthesis inhibitor) stops toxin production. Beta-lactams do NOT suppress toxins.

On Rounds

Why add clindamycin?

Toxin suppression. GAS and Clostridium make exotoxins (superantigens) driving shock. Clindamycin inhibits protein synthesis → stops toxin production. Beta-lactams target cell wall, not protein synthesis.

Can CT rule out nec fasc?

No. CT can miss early disease. Gas/fascial thickening are late findings. If clinical suspicion high, go to OR. Finger test or intraop exploration is diagnostic.

Clinical Examples

📋 Case 1, Type I Polymicrobial Necrotizing Fasciitis

Patient: 62M with T2DM, presents with rapidly expanding erythema and exquisite pain on left lower leg after minor skin break. Temp 39.8°C, HR 128, BP 88/52. WBC 24K, lactate 5.4, Cr 2.8. Skin: dusky discoloration, hemorrhagic bullae, crepitus on palpation.

Key findings: Crepitus = subcutaneous gas (Clostridium or mixed anaerobes). Pain out of proportion to exam appearance. Hemodynamic instability. LRINEC score > 6 (high risk). Type I = polymicrobial (diabetics, immunocompromised).

Management:

Emergent surgical debridement, this is the ONLY definitive treatment. Do NOT delay for imaging
Vancomycin + piperacillin-tazobactam + clindamycin (triple therapy: MRSA + GNR/anaerobes + toxin suppression)
Aggressive IVF resuscitation, vasopressors for septic shock, ICU admission
Plan for re-look debridement in 24-48h (often need multiple OR trips, "second look")
Wound VAC after debridement stabilizes; delayed closure or skin grafting

Teaching point: "When in doubt, cut it out." Delay to debridement is the modifiable driver of mortality, and going past 24 hours raises it roughly 9-fold. CT and MRI can miss early disease, if clinical suspicion is high, the patient goes to the OR, not radiology.

📋 Case 2, Type II (Group A Strep) Necrotizing Fasciitis

Patient: 35F previously healthy. Severe left arm pain after minor cut while gardening 48h ago. Now with rapidly spreading purple discoloration, bullae. Temp 40.1°C, HR 135, BP 78/42. WBC 2.8K (leukopenia), platelets 68K. Blood cultures: GPC in chains.

Key findings: Type II = monomicrobial GAS (Streptococcus pyogenes). Can occur in healthy young adults. Streptococcal toxic shock syndrome (STSS): hypotension + organ failure + soft tissue infection. Leukopenia paradoxically indicates severe disease.

Management:

Emergent radical surgical debridement, may require amputation if limb-threatening
Penicillin G 4 million units IV q4h + clindamycin 900 mg IV q8h (clindamycin stops exotoxin production)
IVIG 1-2 g/kg × 1 dose (neutralizes streptococcal superantigens in STSS)
ICU: vasopressors, ventilator support, blood products for DIC
Notify public health, GAS necrotizing fasciitis is reportable in many jurisdictions

Teaching point: GAS necrotizing fasciitis can kill a healthy young adult in 24-48h. The clue is "pain out of proportion" + rapid systemic deterioration. IVIG is specifically beneficial for streptococcal toxic shock, it binds superantigens that drive the immune storm.

📋 Case 3, Fournier Gangrene

Patient: 58M with poorly controlled T2DM (A1c 11), presents with severe perineal pain, scrotal swelling, and foul-smelling discharge × 2 days. Temp 39.4°C, HR 130. Exam: scrotal erythema extending to perineum with crepitus. WBC 28K, lactate 4.8.

Key findings: Fournier gangrene = necrotizing fasciitis of the perineum/genitalia. Same pathophysiology as extremity necrotizing fasciitis. Diabetes is the #1 risk factor. Mortality 20-40% even with aggressive treatment.

Management:

Emergent surgical debridement of all necrotic tissue (urology + general surgery)
Same antibiotic regimen: vancomycin + piperacillin-tazobactam + clindamycin
Fecal diversion (colostomy) if perineal wound is extensive (prevents fecal contamination)
Suprapubic catheter if urethral involvement
Daily wound care, re-look in 24-48h, wound VAC once clean, delayed reconstruction

Teaching point: Fournier gangrene follows the same treatment principles as all necrotizing fasciitis: emergent surgical debridement is the ONLY life-saving intervention. Antibiotics without surgery = death. The threshold for surgical exploration should be very low.

Monitoring

Parameter	Frequency
Wound	q4–6h. Advancing necrosis = return to OR
Hemodynamics	Continuous ICU. MAP >65
CBC, CRP, lactate	q6–12h

Summary

The Hallmark Is the Mismatch

Pain out of proportion to the exam in a limb that looks deceptively unimpressive early. Later signs, skin necrosis, bullae, crepitus and anesthesia over the involved skin, mean the disease is already advanced. Systemic toxicity out of keeping with a cellulitis is the other tell.

Surgery Is the Treatment

Antibiotics do not cure necrotizing fasciitis; debridement does. Thrombosed perforating vessels mean the drug never reaches the dying fascia. Delay to debridement beyond 24 h carries roughly a 9-fold higher mortality, so surgical consultation happens at the moment of suspicion.

Do Not Wait for Imaging

Old teaching was CT or MRI first; current practice is straight to the operating room on clinical suspicion. CT can miss early disease, and a normal scan does not exclude it. If imaging is obtained it must not delay surgery.

The Bedside Test That Settles It

The finger test: a small incision under local anesthetic down to fascia. Tissue planes that separate with minimal resistance, dishwater-gray fluid and non-bleeding fascia are diagnostic. This is faster and more reliable than any scan.

Antibiotics: Broad, Plus a Toxin Blocker

Vancomycin 25 to 30 mg/kg load then 15 to 20 mg/kg q8-12h for MRSA, plus piperacillin-tazobactam 4.5 g IV q6h for gram-negatives and anaerobes, plus clindamycin 900 mg IV q8h. Narrow only after cultures and source control.

Why Clindamycin Is Not Optional

It is there for toxin suppression, not for coverage. Group A Strep and Clostridium drive shock through exotoxins, and clindamycin blocks their production by inhibiting protein synthesis. Beta-lactams do not suppress toxin, and they lose potency against a high-inoculum stationary-phase organism (the Eagle effect).

Know the Two Types and Gas Gangrene

Type 1 is polymicrobial, aerobes plus anaerobes, in diabetics, post-surgical and immunocompromised patients. Type 2 is monomicrobial Group A Strep in young healthy people after minor trauma. Gas gangrene is C. perfringens after trauma or surgical wounds. LRINEC can support the suspicion but a low score never rules it out.

Expect to Go Back

Plan a second look in 24 h and reassess the wound every 4 to 6 h. Advancing necrosis means a return to the operating room; most patients need several debridements. Support with ICU-level care, MAP above 65, and consider IVIG in streptococcal toxic shock.

📄 One Pager

Necrotizing Soft-Tissue Infection one-page infographic. The surgical emergency · cut, don't wait. Tap to open the full-size printable PDF.

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