Derm Dx: Pus blisters on the leg evolve into ulcers

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  • Ecthyma 1_0112 Derm Dx 2

  • Ecthyma 2_0112 Derm Dx 2

A 56-year-old woman presents complaining of painful and foul-smelling crusted ulcers on her leg and thigh. The patient reported developing several “pus blisters” on her leg and thigh 10 days prior that had enlarged over the course of several days and subsequently developed a black crust.

The patient endorses mild to moderate pain, but denies fevers. Symptom review is otherwise negative. She is uncertain if there was trauma to her legs. She stated that her cat may have scratched her, and she may have cut herself shaving. Past medical history is significant for hepatitis C and manic-depressive disorder. Her medications include lithium daily and acetaminophen as needed.

On exam the patient is afebrile with normal BP and heart rate. She is alert, oriented and appears non-toxic. There is a 3 cm round shallow ulceration on her left anterior leg that is covered by a thick eschar-like black crust. Beneath the crust, the tissue appears necrotic and there is a purulent and foul-smelling exudate. Surrounding the ulceration is 1 cm rim of erythema. The patient has several similar but smaller lesions on her medial thigh. There is no lymphadenopathy.

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Ecthyma is considered to be an ulcerated variant of non-bullous impetigo. It is most frequently caused by Streptococcus pyogenes and less frequently Staphlococcus aureus. Lesions commonly occur on the legs or dorsal feet. There may be a history of preceding...

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Ecthyma is considered to be an ulcerated variant of non-bullous impetigo. It is most frequently caused by Streptococcus pyogenes and less frequently Staphlococcus aureus. Lesions commonly occur on the legs or dorsal feet. There may be a history of preceding trauma, but frequently patients develop lesions primarily.

Initially, a vesicle or vesiculopustule develops, which enlarges over several days and progresses into a shallow ulceration with a thick black crust. When the crust is removed, the base of the ulcer appears necrotic and purulent. Lesions are localized to the skin without further extension into soft-tissue or bone (i.e. cellulitis or osteomyelitis), and there is usually no progression to systemic infection (i.e. sepsis). Ecthyma generally heals over the course of several weeks and produces scarring. Risk factors include poor hygiene, lymphedema, trauma, immunosupression, young age and neglect.1, 2

Diagnosis

Diagnosis is clinically based on history and physical exam. Skin biopsy, deep-tissue culture and gram stain may aid diagnosis. 

Ecthyma gangrenosum is a similarly named entity, but should not be confused with ecthyma.  Ecthyma gangrenosum occurs in the setting of Pseudomonas aeruginosa septicemia. Patients with ecthyma gangrenosum are generally quite ill with fever, hypotension and tachycardia and require hospitalization.

Skin findings in ecthyma gangrenosum consist of hemorrhagic vesicles or bullas that rupture and develop into a necrotic ulcer with black eschar. Ecthyma gangrenosum ulcerations are due to P. aeruginosa septic emboli, which invade the walls of cutaneous blood vessels causing a necrotizing hemorrhagic vasculitis. While the individual lesions of ecthyma and ecthyma gangrenosum may appear similar, these entities occur in distinct clinical settings with different etiologies and prognoses.1, 2     

Treatment

Ecthyma treatment consists of cleansing the wounds, gently debriding the crust, applying topical antibiotics such as mupirocin, retapamulin or bacitracin, and initiating oral antibiotics to cover S.  pyogenes. Hospital admission is generally not indicated.1, 2

Adam Rees, MD, is a graduate of the University of California Los Angeles School of Medicine and a resident in the Department of Dermatology at Baylor College of Medicine in Houston.

References

1. Bolognia J, Jorizzo JL, Rapini RL. “Chapter 73: Bacterial Diseases.” Dermatology. St. Louis, Mo.: Mosby/Elsevier; 2008.
2. James WD, Berger TG, Elston DM et al. “Chapter 14: Bacterial Infection.” Andrews’ Diseases of the Skin: Clinical Dermatology. Philadelphia: Saunders Elsevier; 2006.

 

 

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