SAEM Clinical Images Series: Leg Rash

ulcer

A 42-year-old male with no significant medical problems presented to the Emergency Department with a 5-week history of abdominal pain and bloody diarrhea. He also reported painful intraoral blisters and ulcerative lesions on the bilateral lower extremities and scrotum. The patient had been self-managing his symptoms with over-the-counter antidiarrheal medications and has unsuccessfully attempted to establish care with a gastroenterologist. He denied any history of intravenous drug use, cutaneous injections, or previous skin infections and has no other complaints at this time.

Vitals: BP 125/85; HR 97; R 22; T 99.2°F; O2 sat; 100% on room air

General: Overall well-appearing but uncomfortable.

HEENT: Dry mucous membranes, no lesions seen.

Respiratory: Clear to auscultation.

Cardiovascular: Regular rhythm without murmurs, rubs, or gallops.

Abdominal: Mild diffuse tenderness on palpation of abdomen without rebound or guarding. Bowel sounds mildly hyperactive.

Genitourinary: External purulent lesion on anus. Gross bright red blood on digital rectal exam.

Skin: Overall pallor, there are Scattered purulent ulcers on bilateral lower extremities and scrotum. Image 1 shows a lesion on the inner right thigh. Image 2 shows a second lesion on the right inner buttock. The right inner thigh lesion has been present longer.

WBC: 17.9

Hgb: 10.6

Plt: 654,000

ESR: 112

CRP: 21.8

This rash is consistent with ulcerative pyoderma gangrenosum (PG), a rare inflammatory condition which may occur in isolation or in association with systemic diseases. PG typically manifests as an erythematous nodule or pustule that progresses to form a purulent or necrotic ulcerative base. The lower extremities are the most frequently affected sites. In this patient, the presence of abdominal pain, hematochezia, and elevated inflammatory markers raises suspicion for an underlying diagnosis of ulcerative colitis. Measurement of fecal calprotectin may provide additional diagnostic support. Management of mild flares in an outpatient setting may include rectal or oral mesalamine (5-ASA) in combination with oral prednisone. Severe exacerbations often require hospitalization for systemic glucocorticoid therapy and gastroenterology consultation. The patient was started on IV glucocorticoids and during his admission had resolution of his rectal bleeding and improvement in his rash. Colonoscopy results confirmed the underlying diagnosis of ulcerative colitis. The patient was discharged in stable condition with outpatient gastroenterology follow-up.

Take-Home Points

  • Pyoderma gangrenosum features erythematous nodules and pustules that progress to form a purulent or necrotic base, and is associated with inflammatory bowel diseases.

  • Severe cases of PG generally require glucocorticoid therapy.

  • Ruocco E, Sangiuliano S, Gravina AG, Miranda A, Nicoletti G. Pyoderma gangrenosum: an updated review. J Eur Acad Dermatol Venereol. 2009 Sep;23(9):1008-17. doi: 10.1111/j.1468-3083.2009.03199.x. Epub 2009 Mar 11. PMID: 19470075.
  • Ko CW, Singh S, Feuerstein JD, Falck-Ytter C, Falck-Ytter Y, Cross RK; American Gastroenterological Association Institute Clinical Guidelines Committee. AGA Clinical Practice Guidelines on the Management of Mild-to-Moderate Ulcerative Colitis. Gastroenterology. 2019 Feb;156(3):748-764. doi: 10.1053/j.gastro.2018.12.009. Epub 2018 Dec 18. PMID: 30576644; PMCID: PMC6858922.



SAEM Clinical Images Series: First a Splash and then a Rash

rash

The patient is a 25-year-old female with no significant past medical history who presents to the Emergency Department with a pruritic rash. She reported three days of progressive pruritus with an associated diffuse rash extending from the lower extremities to the proximal upper extremities with involvement of the chest and back. She denies fevers, chills, difficulty breathing, nausea, vomiting, or history of similar rash. She has no history of dermatologic or immunologic conditions. She has had no new exposures to new soaps or chemicals. She has no known allergies, is up to date on all vaccinations, and has not traveled in the last year other than a day trip to an indoor water park three days ago.

Vitals: Normal

General: No acute distress but uncomfortable from itching.
HEENT: Oropharynx clear without edema, erythema, or mucosal lesions.
Respiratory: Clear to auscultation bilaterally.
Skin: Key findings as shown in the image provided. There is a diffuse papular rash extending from the bilateral distal lower extremities up to level of the sternum with uniform involvement of the abdomen, chest, back, and upper extremities. Negative Nikolsky’s sign. No involvement of the head, neck, palms of the hands, or soles of the feet.

Pseudomonas aeruginosa folliculitis (“Hot Tub folliculitis”)

This patient presented with a history and exam classic for Pseudomonas aeruginosa folliculitis, or “hot tub” folliculitis. The primary risk factor for this condition is exposure to contaminated water, typically via public swimming pools or hot tubs with inadequate chlorine levels. Longer durations of exposure, female gender, and underlying skin trauma are additional risk factors. The infection is associated with a tender and pruritic rash which begins as papules and can progress to papulopustular or nodular lesions. The rash may develop on any body part that is exposed to the contaminated water. Symptoms classically begin within 8 to 48 hours of the initial exposure, however can develop up to five days later. A subset of patients may develop systemic symptoms of malaise and fever. Most cases are self-limited, resolving without treatment in one to two weeks. However, patients with significant cutaneous involvement or discomfort, systemic symptoms, or immunocompromised state should be treated empirically with an oral fluoroquinolone. Symptomatic

Take-Home Points

  • In patients presenting with follicular rashes, be sure to ask about public pool or hot tube exposures.
  • Hot tub folliculitis is a pseudomonas infection and can be treated with oral fluroquinolones.

1. Centers for Disease Control and Prevention (CDC). Pseudomonas dermatitis/folliculitis associated with pools and hot tubs–Colorado and Maine, 1999-2000. MMWR Morb Mortal Wkly Rep. 2000;49(48):1087-1091.

2. Tate D, Mawer S, Newton A. Outbreak of Pseudomonas aeruginosa folliculitis associated with a swimming pool inflatable. Epidemiol Infect. 2003;130(2):187-192. doi:10.1017/s0950268802008245

3. Jacob JS, Tschen J. Hot Tub-Associated Pseudomonas Folliculitis: A Case Report and Review of Host Risk Factors. Cureus. 2020;12(9):e10623. Published 2020 Sep 23. doi:10.7759/cureus.10623

4. Silverman AR, Nieland ML. Hot tub dermatitis: a familial outbreak of Pseudomonas folliculitis. J Am Acad Dermatol. 1983;8(2):153-156. doi:10.1016/s0190-9622(83)70017-4

5. Luelmo-Aguilar J, Santandreu MS. Folliculitis: recognition and management. Am J Clin Dermatol. 2004;5(5):301-310. doi:10.2165/00128071-200405050-00003

By |2025-10-27T08:34:29-07:00Oct 24, 2025|Dermatology, SAEM Clinical Images|

SAEM Clinical Images Series: Tropical Rash

rash

The patient is a 30-year-old female with no past medical history who presents to the Emergency Department with 2 months of non-healing ulcers on multiple parts of her body. She reports getting bitten by flies while traveling in wooded trails from Venezuela through Mexico. She reports the bites started as small scabs that have since enlarged, but they are non-painful or pruritic. She has ulcerative lesions on her left hand, right arm, back, and gluteal areas. She has taken multiple antibiotics from a doctor in Mexico including clindamycin, ceftriaxone, nitrofurantoin, flagyl, and doxycycline. She denies any fevers, chills, nausea, vomiting, weight loss, or night sweats, but given the persistence of the lesions, she comes in for evaluation.

Vitals: BP 143/91 HR 60 R 17 T 98.4 O2sat 100% room air.

General: Well-appearing, breast-feeding her child.

HEENT: Oropharynx is clear, moist mucous membranes, nares clear.
Cardiovascular: Regular rate and rhythm, no murmur.

Skin: There are multiple lesions as shown in the images provided. These
are annular ulcerated pink plaques with erythematous indurated borders
and are located diffusely. The larger lesion shown is on her right arm and
is newer than the other lesions shown on her hand and trunk.

CBC: WBC: 7.6 Hgb 12.2

CRP: 0.3

Hep C/HIV/syphilis/GCCT: negative

This patient has cutaneous leishmaniasis.

Cutaneous leishmaniasis (CL) is caused by the protozoan parasite Leishmania and is transmitted through the bite of an infected female sandfly. CL is commonly diagnosed in travelers and immigrants who are susceptible to exposure. The lesions of CL usually begin as small erythematous papules that increases in size and eventually ulcerate and crust over. Lesions generally have distinct borders that are raised and erythematous. The diagnosis can be made based on travel history, lesion appearance, skin biopsy, and serology. Without treatment, the ulcers heal slowly but can leave disfiguring scars. Treatment modalities include pentamidine, amphotericin B, antimoniate, paromomycin, imiquimod, thermotherapy and cryotherapy. Visceral leishmaniasis (VL) is the most serious form of infection and is almost always fatal if untreated. With VL, the parasites directly infect organs including the spleen, liver, bone marrow, and other viscera. Common signs and symptoms of VL include fever, weight loss, fatigue, weakness, night sweats, hepatosplenomegaly, and pancytopenia.

Take-Home Points

  • Cutaneous Leishmaniasis should be suspected in travelers who have been to endemic areas and present with non-healing skin ulcerations. Visceral Leishmaniasis is the most severe form of disease and carries an extremely high mortality rate if untreated.
  • The vector for this disease is the sandfly; diagnosis is made through skin biopsy and direct microscopy of the parasite.

1. Eiras DP, Kirkman LA, Murray HW. Cutaneous Leishmaniasis: Current Treatment Practices in the USA for Returning Travelers. Curr Treat Options Infect Dis. 2015;7(1):52-62. doi:10.1007/s40506-015-0038-4

2. Chappuis, F., Sundar, S., Hailu, A. et al. Visceral leishmaniasis: what are the needs for diagnosis, treatment and control?. Nat Rev Microbiol 5, 873–882 (2007). https://doi.org/10.1038/nrmicro1748

By |2025-10-27T08:26:58-07:00Oct 3, 2025|Dermatology, SAEM Clinical Images|

SAEM Clinical Images Series: When in Doubt, Swab It Out

eczema

A 26-year-old female with a history of atopic dermatitis presents with one week of rash that began on her lower lip but spread over her face, eyelids, and neck, plus one day of fevers and headache. She was seen at an urgent care and referred to the emergency department for evaluation and management of “impetigo.” On presentation, she endorsed nausea, headache, and mild neck pain.

Vitals: Temp 100.7° F; BP 134/85; HR 121; SpO2: 100%

General: Uncomfortable appearing.

Cardiovascular: Tachycardia

Neurological: AOx3. CN II-XII grossly intact. Moves all extremities equally and spontaneously.

Skin: Upper cutaneous lip – eroded plaque with yellow crust. Bilateral jaw line, cheek, neck, eyelids – eroded papules. Lichenified patches in antecubital fossa bilaterally.

CBC: WBC 10.7; PLT 244

Lactate: 1.31

CSF: Colorless, clear; WBC 1; RBC<1; Protein 23; Glucose 55, Gram Stain Negative

Given the patient’s history of atopic dermatitis and evidence of crusted over papules/pustules on exam, this patient’s presentation was most consistent with diagnosis of eczema herpeticum (EH).

Swabs of the upper lip lesion were positive for HSV1 DNA, which confirmed the diagnosis. Early identification and treatment of EH is critical to preventing dangerous complications including ocular involvement, viremia, meningoencephalitis, hepatitis, or secondary infection with S. aureus resulting in bacteremia. Patients with EH involving the face, periocular areas, or systemic symptoms should be admitted for intravenous antiviral therapy and supportive care.

Take-Home Points

  • The diagnosis of EH is primarily based on history and physical, but the presence of HSV in skin lesions can be confirmed by PCR.
  • Delayed treatment is associated with increased risk of complications and prolonged hospitalization.

1.Wollenberg A, Wetzel S, Burgdorf WH, Haas J. Viral infections in atopic dermatitis: pathogenic aspects and clinical management. J Allergy Clin Immunol. 2003 Oct;112(4):667-74. PMID: 14564342.

2.Aronson PL, Yan AC, Mittal MK, Mohamad Z, Shah SS. Delayed acyclovir and outcomes of children hospitalized with eczema herpeticum. Pediatrics. 2011 Dec;128(6):1161-7. PMID: 22084327.

By |2025-10-27T08:24:25-07:00Sep 29, 2025|Dermatology, SAEM Clinical Images|

SAEM Clinical Images Series: Unusual Presentation of an Exophytic Tumor

cutaneous horn

A 60-year-old African American female without a past medical history presented to the emergency department with a complaint of a “hard, yellowish brown, growth” on her right upper abdomen. The patient reported that it had been present and slowly enlarging over a two-year period and was now causing pain when it “snags on clothing”.

Skin: 9.5 cm, firm, curved, exophytic, keratotic, tumor protruding from the right upper abdominal wall.

Non-contributory

Histopathology confirmed a diagnosis of a benign Cutaneous Horn a.k.a. Cornu Cutaneum (latin). Cutaneous horns are yellow or white exophytic hyperkeratotic projections formed in reaction to a number of physical and disease processes. Defined by having a height more than one-half the size of their base in diameter, they are slow-growing and found in conical, cylindrical, pointed, or curved configurations. Their exact pathogenesis is unknown, they occur equally among genders, are more common in the elderly and fair-skinned individuals, and are predominant in sun-exposed areas of the body.

Cutaneous horns are formed in reaction to a number of underlying conditions and are most commonly (>60%) benign, however underlying premalignant and malignant diseases may exist. Histopathologic evaluation of the skin at the base of the lesion is necessary to establish any associated disease. Benign cutaneous horns may form from chronic irritation and are affiliated with numerous skin conditions, most commonly seborrheic keratosis. Links to multiple other skin diseases including psoriasis, discoid lupus erythematosus, sarcoidosis, molluscum contagiosum, and Bowen’s disease exist. Actinic keratosis is the most common premalignant etiology. Cutaneous horns reflecting a malignancy are predominantly associated with wider and erythematous bases in sun-exposed areas of the body in elderly males. Cutaneous horns arising from malignancy tend to occur from squamous cell carcinoma although associations with at least nine other malignancies including basal cell carcinoma, malignant melanoma, Paget’s disease of the breast, Kaposi’s sarcoma, and renal cell carcinoma exist.

Take-Home Points

  • Cutaneous horns occur most frequently with aging in fair-skinned individuals on areas exposed to ultraviolet radiation.

  • Cutaneous horns are hyperkeratotic epithelial lesions formed in reaction to multiple conditions.

  • Complete excisional biopsy including full thickness skin from the base is the treatment of choice and is required for histopathologic analysis.

  • Cutaneous horns, although most commonly benign, may reflect a premalignant or malignant disease process requiring further evaluation and surveillance.

  • Cohen PR. Cornu Cutaneum: Case Reports of Patients With a Cutaneous Horn Associated With Either a Verruca Vulgaris or an Inverted Follicular Keratosis and a Review of the Etiologies of Cutaneous Horns. Cureus. 2023 Oct 9;15(10):e46747. doi: 10.7759/cureus.46747. PMID: 38022343; PMCID: PMC10631572.

  • Thiers BH, Strat N, Snyder AN, Zito PM. Cutaneous Horn. 2023 Mar 7. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 33085427.

  • Vanik S, Mehta S, Shah R, Trivedi P, Rathod P, Bhatt S. Giant Cutaneous Horn: Is It a Tip of An Iceberg? Two Case Reports and a Review of Literature. Indian J Otolaryngol Head Neck Surg. 2022 Dec;74(Suppl 3):5432-5435. doi: 10.1007/s12070-021-02719-1. Epub 2021 Jul 6. PMID: 36742859; PMCID: PMC9895721.

  • Copcu E, Sivrioglu N, Culhaci N. Cutaneous horns: are these lesions as innocent as they seem to be? World J Surg Oncol. 2004 Jun 3;2:18. doi: 10.1186/1477-7819-2-18. PMID: 15176977; PMCID: PMC421749.

By |2025-01-21T09:36:34-08:00Jan 31, 2025|Dermatology, SAEM Clinical Images|

SAEM Clinical Images Series: Painful Weeping Scalp

An otherwise healthy 11-year-old female presented to the Emergency Department (ED) with one week of scalp pain and discharge. Her symptoms began as a dry and itchy rash in the scalp area that was unresponsive to triamcinolone 0.1% ointment. She was initially seen in clinic and was diagnosed with an abscess of the scalp and treated with Trimethoprim/ Sulfamethoxazole (TMP-SMX) for seven days. Two days before her presentation to ED, the rash started to increase in size and pain, and her mother noticed a purulent oozing coming from her scalp. The patient denied any trauma to her head or scalp. There is no history of rashes or other skin infections on her scalp. Review of systems is negative for any systemic symptoms including fever, chills, nausea, vomiting or diarrhea.

Vitals: BP 105/68; HR 113; T 99.7°F; RR 16, O2 sat 98%, RA

General: Patient has an irritable mood and scratches her head.

Head: Normocephalic, matted hair with dried yellow drainage at crown of scalp visible, no occipital lymphadenopathy.

Skin: Inspection reveals an erythematous, crusted, scaly, boggy plaque at the vertex of the patient’s scalp with significant yellow serosanguinous drainage and tenderness to palpation (Figure 1).

Eyes: Conjunctivae clear, EOM intact, PERRL, fundi normal.

Ears: External ears and canals normal, TM’s normal landmarks bilaterally.

Nose: Nares normal, mucosa normal, no drainage.

Mouth/Throat: Moist mucosa without lesions.

Neck: Supple, no cervical lymphadenopathy.

Bacterial aerobic swab with sensitivities

Fungal smear and sensitivities

Kerion is an inflammatory type of tinea capitis characterized by swelling and alopecia of the scalp, which could be mistaken as bacterial infection. It is caused by dermatophyte fungi found on animals and in the soil such as Trichophyton spp. and Microsporum spp. It occurs almost exclusively in children and is more common in patients of African descent and males. Secondary bacterial infection needs to be suspected if there is associated fever, pain, or occipital lymphadenopathy. If left untreated, scarring, and permanent alopecia can develop. Location and the presence of other signs of a fungal infection, such as scaling can distinguish it from cellulitis [1]. The diIerential diagnosis includes bacterial abscess, psoriasis, seborrheic dermatitis, contact dermatitis, pseudolymphoma and dissecting cellulitis of the scalp. The patient’s clinical image demonstrates a boggy, suppurative plaque consistent with kerion (Figure 2).

Initial management in the ER should focus on adequate pain control, debridement and obtaining bacterial and fungal cultures. Our patient was given ibuprofen and oxycodone for pain control and the area was cleansed and gently debrided. After irrigation and removal of matted hair, there was an erythematous boggy plaque with scaling and associated overlying hair loss (Figure 3). Fungal culture of hairs or biopsy will provide speciation but will take several weeks. In the ED setting, potassium hydroxide (KOH) preparation of infected plucked hairs or skin scrapings under the microscope can provide early diagnosis. When the diagnosis is uncertain, early antibiotics are prudent to prevent exacerbation and systemic spread. Treatment of suspected kerion should also include oral antifungal medication [2]. Our patient was transitioned from TMP-SMX to cefadroxil for better streptococcus coverage. Pediatric dermatology recommended dilute acetic acid soaks, oral terbinafine and ketoconazole shampoo for 12 weeks, and a one-week course of prednisone. Bacterial culture returned positive for three colonies of Streptococcus dysgalactiae, Acinetobacter parvus, and Staphylococcus epidermidis. Fungal cultures grew a filamentous fungus – Trichophyton verrucosum.

Take-Home Points

  • Superimposed bacterial infection should be suspected if a scalp lesion is painful and there is discharge.

  • Treatment should consist of both, an antifungal, and antibiotics.

  • Pain control and gentle debridement constitute the initial management of a suppurative scalp lesion.

  • Bacterial and fungal cultures should be obtained in the ER to optimize the management in outpatient setting.

  • John AM, Schwartz RA, Janniger CK. The kerion: an angry tinea capitis. Int J Dermatol. 2018 Jan;57(1):3-9. doi: 10.1111/ijd.13423. Epub 2016 Oct 1. PMID: 27696388.

  • Leung AKC, Hon KL, Leong KF, Barankin B, Lam JM. Tinea Capitis: An Updated Review. Recent Pat Inflamm Allergy Drug Discov. 2020;14(1):58-68. doi: 10.2174/1872213X14666200106145624. PMID: 31906842.

By |2025-01-06T21:27:38-08:00Jan 17, 2025|Dermatology, SAEM Clinical Images|

SAEM Clinical Images Series: Not Your Average Eczema

eczema

A 3-year-old male with a history of severe atopic dermatitis presented for facial rash and hand pain. Mom had been applying Aquaphor and Vaseline several times a day. On the day of presentation, he woke up with a new rash over his face and hands which prompted the ED visit. He is up to date on childhood immunizations and is not prescribed any oral medications.

Vitals: BP 103/61; HR 156; Temp 102.9°F; RR 30; SpO2 99%.

General: He appears in no acute distress, acting appropriately for age. Interacts and follows commands. Scratching himself all over.

Skin: Diffuse, itchy, dry skin throughout and findings noted in the attached images most notably erythematous pustules on the dorsal hands and peri-oral lesions in addition to punched-out ulcerations on the philtrum. Lesions are tender to palpation and spare mucous membranes and palms/soles. Nikolsky sign negative.

WBC: 12.96

Skin scraping: +VZV

This patient has Eczema herpeticum as demonstrated by multiple grouped pustules on an erythematous base.

Ophthalmology should be consulted to rule out ocular involvement most notably herpes zoster ophthalmicus.

Take-Home Points

  • Eczema herpeticum is typically caused by superinfection of Herpes Simplex Virus due to a diminished skin barrier from atopic dermatitis. It is commonly misdiagnosed as impetigo. Grouped vesicles/pustules on an erythematous base and tenderness to palpation should prompt the physician to suspect herpetic skin infection.
  • Eczema herpeticum may be potentially life-threatening if it has spread to multi-system involvement such as HSV keratitis or encephalitis.
  • Treatment includes acyclovir in addition to gram positive coverage such as TMP/SMX or cephalexin.

  • American Academy of Pediatrics: Herpes simplex. In: Kimberlin DW, Brady MT, Jackson MA, Long SS, eds. Red Book: 2015 Report of the Committee on Infectious Diseases. 30th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2015:432–445.
  • Studdiford JS, Valko GP, Belin LJ, Stonehouse AR. Eczema herpeticum: making the diagnosis in the emergency department. J Emerg Med. 2011 Feb;40(2):167-9. doi: 10.1016/j.jemermed.2007.11.049. Epub 2008 Jun 27. PMID: 18584994.

By |2024-12-02T22:01:54-08:00Dec 20, 2024|Dermatology, SAEM Clinical Images|
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