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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Cellulitis & Skin Infections

The most overdiagnosed infection in medicine -up to 30% of "cellulitis" admissions are actually stasis dermatitis, DVT, gout, or contact dermatitis. Purulent vs non-purulent determines whether you cover MRSA. Mark the borders with a pen.

🔍 Overview

Purulent vs Non-Purulent -This Drives Treatment

Type	Features	Organism	Treatment
Non-purulent cellulitis	Diffuse erythema, warmth, tenderness. No abscess, no pus, no drainage. Clear borders.	Beta-hemolytic strep (Group A strep) is the most common cause. NOT usually MRSA.	Cefazolin (Ancef) 2g IV q8h (inpatient) or cephalexin 500 mg QID (outpatient). 5–6 days is sufficient IDSA, 2014. No MRSA coverage needed.
Purulent cellulitis / abscess	Fluctuant, drainable collection. Pus expressed. Central pustule or wound.	S. aureus (MSSA or MRSA) -especially CA-MRSA (USA300).	I&D is the primary treatment (antibiotics alone are less effective). Talan et al. (NEJM), 2016 Antibiotics: TMP-SMX (Bactrim) DS BID or doxycycline (Vibramycin) 100 mg BID × 5–7 days. IV: vancomycin if severe.
Necrotizing fasciitis SURGICAL EMERGENCY	Pain out of proportion, crepitus, rapid spread, bullae, skin necrosis, hemodynamic instability. LRINEC score ≥ 6 → high suspicion.	Type I: polymicrobial. Type II: Group A strep (monomicrobial).	Emergent surgical debridement (do NOT wait for imaging). Vanc + pip-tazo + clindamycin (clindamycin inhibits toxin production). ICU.

Cellulitis mimics (up to 30% of admissions): stasis dermatitis (bilateral, chronic, hemosiderin staining -#1 mimic), DVT (unilateral leg swelling → get duplex US), gout (peri-articular), contact dermatitis, erythema migrans (Lyme -single expanding ring), lipodermatosclerosis (woody induration).

Key Principles

Mark the borders with a pen and date/time it -this is how you track whether it's improving or spreading on antibiotics
Blood cultures are NOT recommended for uncomplicated cellulitis (positive in < 2%). IDSA SSTI Guidelines, 2014 Only get if: sepsis, immunocompromised, animal/water bite, or unusual exposures.
Elevate the affected limb -reduces edema and speeds resolution
Bilateral "cellulitis" is almost never cellulitis -think stasis dermatitis, HF, venous insufficiency
Not improving at 48–72h? Consider: wrong diagnosis (mimic), abscess needing drainage, resistant organism, deeper infection (osteomyelitis, septic joint), necrotizing fasciitis

🧪 Workup

Workup -Cellulitis & Skin Infections

CBC with differential -leukocytosis supports infection, but WBC is often normal in uncomplicated cellulitis. Bandemia or left shift suggests more severe/systemic infection.
BMP -baseline Cr (for antibiotic dosing), glucose (uncontrolled DM worsens outcomes and increases recurrence risk)
Blood cultures -only if systemic signs/sepsis (fever > 38.5°C, tachycardia, hypotension, immunocompromised). NOT routine for simple cellulitis -yield is < 2% IDSA, 2014 Perl et al., 1999
Wound culture -only if abscess drained (send purulent material) or open wound present. Swab of intact skin over cellulitis is useless -do not send.
Ultrasound -if abscess suspected but not clinically obvious. Bedside US has excellent sensitivity for detecting drainable fluid collections. A missed abscess is the #1 reason cellulitis "fails" antibiotics.
Mark borders with skin marker -draw along the leading edge of erythema and write the date/time. This is the most important bedside tool to objectively track response at 48h.

Cellulitis is a clinical diagnosis. Imaging is for ruling out abscess (US) or necrotizing fasciitis (CT with gas), NOT for confirming cellulitis. If bilateral → think stasis dermatitis. If unilateral with edema → consider DVT (get duplex US). Up to 30% of "cellulitis" admissions are misdiagnosed.

🔄 Updated Practice: Old teaching: draw blood cultures for all cellulitis. Current practice: blood cultures are positive in <2-5% of uncomplicated cellulitis and do not change management. Only draw blood cultures if: systemic signs of sepsis (fever, tachycardia, hypotension), immunocompromised, facial cellulitis, animal/water exposure, or failed outpatient therapy (IDSA 2014). Similarly, wound cultures are only useful from abscess drainage or open wounds, surface swabs grow contaminants.

🚨 Management

Management by Severity

Severity	Treatment	Duration	Key Points
Mild (outpatient) Non-purulent, no systemic signs	Cephalexin (Keflex) 500 mg PO QID	5–7 days Hepburn et al., 2004	Covers Group A strep. No MRSA coverage needed. Elevate limb, mark borders, follow-up in 48h.
Moderate (inpatient) Systemic signs, rapid spread, failed PO	Cefazolin (Ancef) 2g IV q8h	Transition to PO at 48–72h	Admit if: fever, tachycardia, WBC > 15K, rapidly spreading, immunocompromised, facial/periorbital/hand cellulitis.
Purulent / Abscess Fluctuance, drainable collection	I&D primary + TMP-SMX DS PO BID or doxycycline 100 mg PO BID	5–7 days	I&D is the definitive treatment, antibiotics alone are inferior. Daum et al. (NEJM), 2017 Send wound culture. Pack wound, recheck in 48h.
Severe / Necrotizing Fasciitis SURGICAL EMERGENCY	Vancomycin + pip-tazo 4.5g IV q6h + clindamycin 900 mg IV q8h	Until surgical debridement + clinical improvement	Pain out of proportion, crepitus, bullae, rapid spread → call surgery immediately. Clindamycin inhibits toxin production. Do NOT delay for imaging.

IV → PO Transition Criteria

Afebrile × 24 hours
WBC trending down
Erythema receding past marked borders (the most objective criterion)
Tolerating oral intake
Systemically well (no ongoing tachycardia, hypotension)

Transition typically at 48–72h. Switch cefazolin IV → cephalexin PO. Total antibiotic course: 5–7 days (including IV days). Longer courses (10–14 days) only for immunocompromised or slow response. Eron et al., 2003

Recurrence Prevention

Treat tinea pedis (interdigital cracking is the #1 portal of entry), topical terbinafine × 2–4 weeks
Compression stockings for chronic venous insufficiency and lymphedema
Skin care, moisturize dry skin, avoid trauma, treat eczema and dermatitis
Weight loss, obesity and lymphedema are major risk factors for recurrence
Prophylactic antibiotics, consider penicillin V 250 mg PO BID for ≥ 3 episodes/year PATCH I, 2013

📋 On Rounds

Why is non-purulent cellulitis usually strep and not staph?

Non-purulent (diffuse) cellulitis is caused by bacteria that spread through tissue planes via hyaluronidase and streptokinase -enzymes that break down connective tissue and dissolve clots, allowing rapid lateral spread. Beta-hemolytic streptococci (especially Group A) excel at this. S. aureus, by contrast, tends to form localized, walled-off collections (abscesses) because it produces coagulase (promotes clot formation around the infection).

How do you distinguish cellulitis from DVT, and why does it matter?

Both present with a red, swollen, warm leg -and misdiagnosis is common. Key distinguishers: Cellulitis = fever, leukocytosis, skin warmth with clear border, often portal of entry (wound, tinea pedis), bilateral involvement suggests stasis dermatitis not cellulitis. DVT = unilateral leg edema, calf tenderness on palpation, risk factors (immobility, cancer, surgery), usually no fever or skin erythema early on.

How do you decide between IV and PO antibiotics for cellulitis?

Outpatient PO: Non-purulent, no systemic toxicity (afebrile, non-toxic), small area, immunocompetent, reliable follow-up. Drug: cephalexin 500 mg QID × 5-7 days. Inpatient IV: Rapidly spreading (beyond marked borders), systemic toxicity (fever, tachycardia, WBC > 15K), failed outpatient PO after 48h, immunocompromised, facial cellulitis, periorbital cellulitis, hand cellulitis, concern for deeper infection. Drug: cefazolin 2g IV q8h.

What are the red flags that suggest necrotizing fasciitis instead of simple cellulitis?

Nec fasc mimics cellulitis early but kills fast. Red flags: (1) Pain out of proportion to exam (the hallmark, disproportionate pain = alarm), (2) Rapid progression (spreading beyond marked borders within hours, not days), (3) Systemic toxicity (high fever, tachycardia, hypotension out of proportion to skin findings), (4) Crepitus (gas in tissues, palpable or visible on imaging), (5) Hemorrhagic bullae or skin necrosis (dusky, purple discoloration = fascial ischemia), (6) Lab flags (WBC > 25K, Na < 135, Cr elevated, CRP > 150, calculate LRINEC score ≥ 6). Call surgery immediately, do NOT delay for imaging. Negative CT does not rule it out.

A patient with a skin abscess asks if antibiotics alone can treat it. What do you tell them?

Incision and drainage (I&D) is the primary treatment for cutaneous abscesses. The LOOP trial and a landmark NEJM trial by Rajendran et al. (2017) confirmed that I&D alone cures most uncomplicated abscesses. Adding TMP-SMX or clindamycin after I&D modestly improves cure rates (~7% absolute benefit) per the IDSA 2014 guidelines, but antibiotics WITHOUT drainage have unacceptably high failure rates. Talan et al., 2016

Why do you mark the borders of cellulitis with a skin marker?

Marking the leading edge of erythema with date/time is the most objective way to assess treatment response at 48h. Cellulitis erythema that remains within or recedes past the marks = responding. Spreading beyond marks = failing therapy. Without marks, subtle progression or improvement is impossible to detect, especially with shift changes. This simple bedside tool prevents unnecessary antibiotic escalation and catches true treatment failures early.

What is the most common cause of recurrent lower extremity cellulitis and how do you prevent it?

Tinea pedis (athlete's foot) with interdigital cracking is the #1 portal of entry for recurrent leg cellulitis. Other risk factors: lymphedema, chronic venous insufficiency, obesity, prior cellulitis. Prevention: treat tinea pedis (topical terbinafine x 2-4 weeks), moisturize dry skin, compression stockings for edema, weight loss. For >= 3 episodes/year, consider prophylactic penicillin V 250 mg BID. PATCH I, 2013 PATCH II, 2020

When should you suspect necrotizing fasciitis and what is the LRINEC score?

Suspect nec fasc when pain is OUT OF PROPORTION to skin findings, rapid spread, crepitus, hemorrhagic bullae, skin necrosis, or hemodynamic instability. LRINEC score uses 6 labs: CRP (>150 = 4 pts), WBC (>15k = 1, >25k = 2), Hgb (<11 = 2, <13.5 = 1), Na (<135 = 2), Cr (>1.6 = 2), glucose (>180 = 1). Score >= 6 = high suspicion. BUT a low score does NOT rule it out. Clinical suspicion trumps any score. Call surgery immediately - do NOT wait for imaging. Wong et al., 2004

A patient's cellulitis is not improving after 48 hours of cefazolin. What is your differential?

Five things to consider: (1) Wrong diagnosis - stasis dermatitis, DVT, gout, contact dermatitis (up to 30% of cellulitis admissions are misdiagnosed). (2) Missed abscess - get bedside ultrasound (a missed drainable collection is the #1 reason cellulitis 'fails'). (3) Resistant organism - broaden to vancomycin for MRSA coverage. (4) Deeper infection - osteomyelitis, septic joint, pyomyositis (get MRI). (5) Necrotizing fasciitis - pain out of proportion, crepitus, rapid spread = emergent surgery.

Case 1: Non-Purulent Cellulitis

Presentation: 58M with HTN and chronic venous insufficiency presents with 2 days of progressive left lower leg redness, warmth, and pain. He noticed a small crack between his toes (tinea pedis) last week. Exam shows well-demarcated unilateral erythema from mid-shin to ankle, warmth, tenderness, no fluctuance or crepitus. No purulence or drainable collection. T 38.2°C, HR 88, BP 142/86. WBC 13.2.

Key Actions:
• Draw borders with skin marker and document date/time for 48h reassessment
• Start cefazolin (Ancef) 2g IV q8h, no MRSA coverage needed for non-purulent cellulitis
• Elevate the affected limb above heart level to reduce edema
• Rule out DVT with duplex ultrasound if significant unilateral swelling or risk factors
• Transition to cephalexin (Keflex) 500 mg PO QID once afebrile × 24h, WBC trending down, and erythema receding past marked borders
• Treat underlying tinea pedis with topical antifungals to eliminate portal of entry and prevent recurrence
• Total antibiotic course: 5–7 days

Case 2: Purulent MRSA Abscess

Presentation: 28F, otherwise healthy, presents with 4 days of a painful, enlarging left axillary lump with overlying redness. She shaves her axillae regularly. Exam shows a 3 cm fluctuant, tender, erythematous mass with a central area of pointing. No surrounding induration or tracking lymphangitis. Afebrile, vitals stable, WBC 9.8. No systemic signs of infection.

Key Actions:
• I&D is the primary treatment, antibiotics alone are inferior for drainable abscesses
• Send wound culture from purulent material (not a surface swab) to confirm MRSA and guide therapy
• Start TMP-SMX (Bactrim) DS 1 tab PO BID × 7 days or doxycycline (Vibramycin) 100 mg PO BID × 7 days for MRSA coverage
• No IV antibiotics needed, patient is non-toxic, afebrile, and abscess is well-localized
• Pack wound loosely with iodoform gauze, arrange follow-up in 48h for repacking and wound check
• Educate on wound care: keep clean, avoid shaving the area until healed, no sharing towels or razors

Case 3: Necrotizing Fasciitis Concern

Presentation: 65M with poorly controlled diabetes (A1c 10.2) and PVD presents with 1 day of rapidly worsening right lower leg pain, erythema, and swelling. Exam shows dusky erythema extending from foot to knee with hemorrhagic bullae, crepitus on palpation, and pain dramatically out of proportion to visible skin findings. T 39.4°C, HR 122, BP 88/52, WBC 22.1, lactate 3.8, Cr 1.9.

Key Actions:
• Emergent surgical consult, do NOT delay for imaging. Necrotizing fasciitis is a clinical and surgical diagnosis
• Calculate LRINEC score (WBC, Hgb, Na, glucose, Cr, CRP), score ≥ 6 is highly suspicious
• Start broad-spectrum empiric coverage immediately: vancomycin (Vancocin) 25 mg/kg IV + piperacillin-tazobactam (Zosyn) 4.5g IV q6h + clindamycin (Cleocin) 900 mg IV q8h
• Clindamycin is added specifically to inhibit toxin production (protein synthesis inhibitor), critical in GAS necrotizing fasciitis
• Aggressive IV fluid resuscitation, vasopressors if needed, ICU admission
• CT may show fascial gas but a negative CT does NOT rule out nec fasc, surgery decides
• Mortality 20–40% even with optimal care; delay in debridement is the strongest predictor of death

📣 Sample Presentation

One-Liner

"Mr. Williams is a 56-year-old diabetic presenting with left lower leg erythema, warmth, and swelling × 3 days. No abscess or purulence. Tinea pedis noted on foot exam. Non-purulent cellulitis."

Key Points to Cover on Rounds

Non-purulent cellulitis -likely strep (Group A). Portal of entry: tinea pedis (interdigital cracking). Borders marked with skin marker + time. Treatment: cefazolin 2g IV q8h (first-line for non-purulent). No I&D needed (no abscess on exam, no fluctuance). US: no fluid collection. Blood cultures not sent (low yield unless septic/immunocompromised). Leg elevated. Response at 48h: erythema receding from marked borders. Plan: transition to cephalexin 500 QID PO to complete 5-7 day course. Treat tinea pedis (terbinafine cream) to prevent recurrence.

Monitoring Parameters -Cellulitis & Skin Infections

Parameter	Frequency	Target / Action
Demarcation line progression	Mark and remeasure daily (at least q12h if concern for rapid spread)	Erythema receding past marked borders = responding. Spreading beyond marks at 48h → broaden antibiotics, image for abscess, or consider necrotizing fasciitis.
WBC	Daily while on IV antibiotics	Trending down = responding. Rising or persistently elevated → consider treatment failure, abscess, deeper infection, or wrong diagnosis.
Fever curve	q4h (Tmax documented daily)	Afebrile × 24h is one criterion for IV → PO transition. Persistent fever > 48h on appropriate antibiotics → re-evaluate diagnosis and coverage.
IV → PO transition criteria	Assess daily starting at 48h	Transition to oral when: afebrile × 24h, WBC trending down, erythema receding past marked borders, tolerating PO, systemically well. Usually at 48–72h.
Wound check (if I&D performed)	Daily until packing removed	Wound packing removed or changed at 48h. Assess for re-accumulation, ongoing drainage, surrounding cellulitis. Consider wound culture if not improving.

Not improving at 48h? Differential: (1) missed abscess (get US), (2) wrong diagnosis (stasis dermatitis, DVT, gout), (3) resistant organism (broaden to vancomycin), (4) deeper infection (osteomyelitis, septic joint → MRI), (5) necrotizing fasciitis (pain out of proportion, crepitus, rapid spread → emergent surgery).

💊 Medications

Antibiotic Selection -Cellulitis & Skin Infections

Scenario	Drug (Brand)	Dose	Notes
Non-purulent cellulitis (outpatient) 1ST LINE	Cephalexin (Keflex)	500 mg PO QID × 5–7 days	Covers beta-hemolytic strep (Group A). No MRSA coverage needed. Shorter courses (5 days) are effective IDSA, 2014.
Non-purulent cellulitis (inpatient) 1ST LINE	Cefazolin (Ancef)	2g IV q8h	Transition to cephalexin PO when afebrile × 24h, WBC trending down, erythema receding past marked borders.
Purulent / abscess (MRSA coverage)	TMP-SMX (Bactrim) DS or Doxycycline (Vibramycin)	TMP-SMX DS 1 tab PO BID × 5–7 days Doxycycline 100 mg PO BID × 5–7 days	I&D is the primary treatment for abscess -antibiotics are adjunctive. Both cover CA-MRSA. TMP-SMX: avoid in pregnancy, check K⁺ (can cause hyperkalemia). Doxycycline: photosensitivity, avoid in pregnancy.
Severe / necrotizing fasciitis EMERGENT	Vancomycin + piperacillin-tazobactam (Zosyn) + clindamycin (Cleocin)	Vanc: 15–20 mg/kg IV q8–12h (target AUC/MIC 400–600) Pip-tazo: 4.5g IV q6h Clindamycin: 900 mg IV q8h	Clindamycin inhibits toxin production (ribosomal suppression) -critical for toxin-mediated disease (GAS, S. aureus). Broad coverage for polymicrobial (Type I) and monomicrobial (Type II) nec fasc. Emergent surgical debridement is definitive treatment.

PCN allergy? Non-purulent: clindamycin 300–450 mg PO TID (but 15–20% MRSA resistance in some areas). Severe: vancomycin alone covers both MRSA and most strep. For true anaphylaxis to penicillin, avoid all cephalosporins (although cross-reactivity is < 2% with cephalexin).

⚡ Summary

Summary

Non-Purulent

Likely strep (Group A). Cephalexin 500 QID × 5-7 days (outpatient) or cefazolin 2g IV q8h (inpatient). No I&D needed.

Purulent/Abscess

Likely MRSA. I&D is primary treatment. TMP-SMX or doxycycline for surrounding cellulitis. Clindamycin alternative.

Mark Borders

Skin marker + date/time at periphery of erythema. Objective assessment of response at 48h. If spreading past lines → broaden or image.

Admit Criteria

Systemic toxicity (fever, tachycardia, WBC > 15K), rapid spread, failed outpatient PO, immunocompromised, facial/periorbital/hand.

IV → PO Switch

Afebrile × 24h, WBC trending down, erythema receding past marked borders (usually 48-72h). Transition to oral equivalent.

Nec Fasc Red Flags

Pain out of proportion, rapid spread, crepitus, hemorrhagic bullae, skin necrosis, systemic toxicity. Emergent surgical exploration.

📄 One Pager

Cellulitis & Skin Infections -Quick Reference Card

Print this page (Ctrl/Cmd + P) for a condensed reference card. All tabs will print on the same page for a complete topic summary.

CELLULITIS & SKIN INFECTIONS -AT A GLANCE

📋 Diagnose: See Overview tab for criteria
🧪 Workup: Focused labs + imaging → see Workup tab
⚡ Treat: Evidence-based algorithm → see Management tab
💊 Drugs: Key medications with dosing → see Medications tab
📣 Present: One-liner + key points → see Rounds tab