EM@3AM: Cellulitis

Author: Seth Cohen, MD (@secohen11, EM Resident Physician, UTSW, Dallas, TX); Joshua Kern, MD (EM Attending Physician, UTSW, Dallas, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 56-year-old male with a history of type 2 diabetes presents to the ED with a rash on his right shin that started two days ago and has progressively worsened. He has associated mild pain but has not taken any analgesics. He denies any other associated symptoms; has had no history of a similar rash; and denies recent travel, surgeries, cancer history, or known trauma to the leg.

Vital signs include HR 90 bpm, BP 148/100, RR 16, T 100.2F, and SPO2 96%. Examination is significant for an obese disheveled male in no acute distress. His right shin has a large area of erythema with indistinct margins and increased warmth, as well as associated mild tenderness to palpation. He has 2+ dorsalis pedis pulses, sensation is intact to BLE, and strength is 5/5 in BLE.

What is the most likely diagnosis?

Answer: Cellulitis



  • Cellulitis is more commonly seen in middle aged and older adults.
  • Incidence is 200/100,000 person-years.1
  • Risk factors: Edema secondary to impaired lymphatic drainage or venous insufficiency, obesity, skin inflammation (eczema, radiation therapy, psoriasis), skin trauma (abrasion/laceration, ulcers, bites, intravenous drug use), immunosuppression, and pre-existing skin conditions2



  • Acute infection of the dermis and subcutaneous tissue caused by bacterial breach of the skin.3
  • Two bacteria are typically implicated in the infection: beta hemolytic streptococcus (approximately 73% of nonpurulent cellulitis cases) and Staphylococcus aureus (including methicillin resistant staph aureus; uncommon in cases of nonpurulent cellulitis).4
  • Streptococcus pneumoniae, Neisseria meningitidis, Clostridia (seen with crepitant and gangrenous cellulitis), and Haemophilus influenzae type b are less common causes of cellulitis but are more prevalent in those who are immunocompromised.


Clinical Presentation:

  • Most commonly presents as a unilateral rash with indistinct margins and local erythema, warmth, and swelling.5
  • Purulence may or may not be present.
  • Petechiae, vesicles, hemorrhage, and/or bullae can be present.
  • May have tenderness to palpation over the rash.
  • May be associated with systemic symptoms including fever, chills, lymphadenopathy, malaise, headache, nausea/vomiting.



  • If left untreated, complications can include sepsis/bacteremia, endocarditis, septic arthritis or osteomyelitis, and toxic shock syndrome.
  • There are multiple types of cellulitis aside from the commonly seen cellulitis on an extremity, with some having their own distinct complications.
    • Abdominal wall cellulitis
    • Buccal cellulitis (less common secondary to H influenzae vaccine)
    • Perianal cellulitis – anal scarring, fistula, or abscess
    • Orbital cellulitis – septic cavernous thrombosis



  • Cellulitis is a clinical diagnosis; laboratory evaluation is nonspecific.
  • CBC – leukocytosis may be present
  • ESR/CRP – possible elevation
  • Ultrasound can be used as cobblestoning of the subcutaneous fat due to the inflammation may be visualized.
  • If there is concern for necrotizing fasciitis, utilize imaging modalities such as CT to obtain a diagnosis.


Differential Diagnoses:

  • Erysipelas
  • Lymphangitis
  • Folliculitis
  • Abscess
  • Necrotizing infection
  • Stasis dermatitis
  • Sporotrichosis
  • Osteomyelitis
  • Deep venous thrombosis
  • Pyomyositis
  • Bug bites



  • Treatment includes antibiotics
  • Treatment groups divided into two groups, outpatient vs. inpatient (mg/kg is for pediatric dosing)
    • Oral therapy
      • Cover primarily for strep
      • Treatment is typically for 5 days but can be extended up to 10 days if warranted for slow response to treatment
      • Antibiotics
        • Cephalexin 500mg (6.25mg/kg) PO four times daily OR
        • If penicillin allergic – Clindamycin 450mg PO three times daily
      • MRSA should be suspected if there are systemic signs of toxicity (febrile, hypotensive, tachycardic), prior episode of MRSA infection, no improvement of the cellulitis while on an antibiotic regiment that does not currently include activity against MRSA, and/or there are one or more risk factors for MRSA (recent hospitalization, residence in long term care facility, recent surgery, hemodialysis, HIV infection, cellulitis over a joint that holds a prosthesis or overlying a vascular graft). If there is suspicion for MRSA, start:
        • TMP/SMX (DS) 1-2 tablets (5 mg/kg) PO twice daily6 OR
        • Clindamycin 450 mg (10 mg/kg) PO three times daily
    • Intravenous therapy
      • Parenteral therapy should be utilized when not tolerating PO antibiotics, rapid progression of erythema, and/or progression of erythema 48 hours after starting PO antibiotics.
      • Antibiotics
        • Cefazolin 1-2 g (30 mg/kg) IV three times daily OR
        • Clindamycin 600 mg (10 mg/kg) IV three times daily
      • If MRSA is suspected (see outpatient MRSA guidelines), start:
        • Daptomycin 4 mg/kg IV once daily OR
        • Vancomycin 20 mg/kg IV twice daily7,8
  • Pain control can be managed using NSAIDs as long as there are no contraindications (risk of bleeding, pregnancy, kidney disease). One study showed that NSAIDs shortened the time to regression of inflammation and resolution of the cellulitis.9
  • Steroids should not be routinely given for cellulitis in the emergency department. Steroids show no decrease in percent relapse of cellulitis.10 However, one study does suggest a one-day length of stay reduction for those given prednisolone in patients receiving parenteral antibiotics. More research is needed on whether outpatient steroids should be utilized.11


Risks for treatment failure:

  • Antibiotic failure can be defined as hospitalization, change in class of oral antibiotic, or switch to parenteral therapy, after 48 hours.
  • Approximately 30% of patients in one study had oral antibiotic failures.12
  • Indicators for failure of outpatient management include:
    • Tachypnea at triage
    • History of MRSA
    • Cellulitis in the past 12 months
    • Chronic ulcers12
    • Fever at triage
    • Chronic edema or lymphedema
    • Prior cellulitis in the same area
    • Cellulitis at a wound site13



  • Most patients can be discharged.
    • Discharge instructions
      • Take the entire course of the prescribed antibiotic.
      • NSAIDs and acetaminophen for pain relief.
      • The infection may continue to worsen for up to 48 hours even while on antibiotics. If the infection continues to worsen past then, return to the ED.
  •  Admit for the following:
    • Outpatient treatment failure
    • Significant comorbidity including immunocompromised state or poorly controlled diabetes
    • Sepsis
    • Significant hand, face, or genitalia infection
    • Reason for parenteral therapy


Key Points:

  • Cellulitis is a clinical diagnosis, but if there is concern for necrotizing fasciitis or other diagnoses, imaging modalities such as ultrasound or CT can be utilized.
  • Start parenteral therapy when the patient is not tolerating PO antibiotics, there is rapid progression of erythema, and/or progression of erythema 48 hours after starting PO antibiotics.
  • Admit the patient for sepsis, hand/face/genitalia cellulitis, or there is another reason for parenteral therapy (failed outpatient therapy).


  1. Ataro P, Mushatt D, Ahsan S. Tetanus: a review. Southern Medical Journal. 2011;104(8):613-7. DOI: 10.1097/SMJ.0b013e318224006d.
  2. Rushdy AA, White JM, Ramsay ME, et al. Tetanus in England and Wales, 1984-2000. Epidemiol Infect. 2003;130(1):71-77.
  3. Chambers, HF. Skin and Soft Tissue Infections in Persons Who Inject Drugs. Infectious Disease Clinics of North America. 2021;35(1): 169-181.
  4. Lu P, et al. Adult Vaccination Disparities among Foreign Born Populations in the United States, 2012. American Journal of Preventive Medicine. 2014;47(6):722-733.
  5. Tejpratap SP, Tiwari MD, et al. Tetanus. Pinkbook. Centers of Disease Control and Prevention (CDC): Epidemiology and Prevention of Vaccine Preventable Diseases. 2020;13.
  6. Hassel B. Tetanus: Pathophysiology, Treatment, and the Possibility of Using Botulinum Toxin against Tetanus-Induced Rigidity and Spasms. Toxins. 2013;5(1):73-83. DOI: 10.3390/toxins5010073.
  7. Birch T, Bleck T. Tetanus (Clostridium tetani). Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, Ninth edition. 2019;9(244):2948-2953.e2.
  8. Thwaites, Louise, MD. Tetanus. UpToDate. 11 November 2021. https://www.uptodate.com/contents/tetanus#H29. Accessed January 7, 2022.
  9. Lavender TW, McCarron B. Acute infections in intravenous drug users. Clin Med (Lond). 2013;13(5):511-3. DOI: 10.7861/clinmedicine.13-5-511.
  10. Ganesh Kumar AV. Benzathine penicillin, metronidazole and benzyl penicillin in the treatment of tetanus: a randomized, controlled trial. Ann Trop Med Parasitol. 2004;98(1):59-63.
  11. Fernandez-Frackelton M: Bacteria, in Marx JA, Hockberger RS, Walls RM, et al (eds). Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc.; 2010;121:1579-1588.
  12. Finkelstein, P, et al. Tetanus: A Potential Public Health Threat in Times of Disaster. Prehospital and Disaster Medicine. 2017;32(3):339-342.

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