SAEM Clinical Images Series: A Rash You Don’t Want to Miss

rash

A 54-year-old female with a past medical history of diabetes presented to the Emergency Department (ED) for evaluation of unresponsiveness. The patient was found unresponsive by her spouse, who notes she had missed several doses of insulin over the past few days. EMS notes the glucometer read ‘HIGH’ on fingerstick. The patient remains unresponsive on presentation and is unable to contribute further history.

Vital Signs: BP 148/105; HR 120; RR 24; Pulse Oximetry 98% on room air; Temperature 97.7°F

Constitutional: Patient is morbidly obese, unresponsive, and toxic-appearing.

Cardiovascular: Regular rhythm with tachycardia. No murmur.

Pulmonary: Pulmonary effort is normal. Lungs clear to auscultation bilaterally.

Abdomen: Abdomen is soft and non-distended. Unable to assess for tenderness given unresponsiveness.

Skin: Cool, pale, mottled. Large gangrenous, draining, foul-smelling wound on proximal left thigh. There is necrotic, malodorous, black skin noted over the left lower abdomen and left upper thigh.

Neurological: Unresponsive. GCS 3.

White blood cell (WBC) count: 20.5

Comprehensive metabolic panel (CMP): K 5.8; Cr 2.06; BUN 86; Glucose >600

Venous blood gas (VBG): pH<7; lactate 3.4; bicarbonate 7

These photographs show advanced Fournier’s Gangrene, a form of necrotizing fasciitis located in the genitals, perineum, or perianal region. Rapid involvement of our surgical colleagues is crucial, as these patients will not recover without the debridement of affected tissues. Aggressive fluid resuscitation and broad-spectrum antibiotics can be initiated after a surgical consult is made.

This patient presented with impressive visual evidence of advanced disease including severe ecchymosis, but our clinical suspicion must be high as Fournier’s is rapidly progressing and carries a high mortality rate (may be upwards of 30%). Earlier symptoms are genital or perineal pain which may be associated with itching, lethargy, or fever. The biggest exam finding to keep in mind is ‘pain out of proportion to the exam’ as up to 40% of these patients may present without localized symptoms. Advanced disease, as seen in this patient, can present with crepitus and severe ecchymosis of tissue involved. This patient was also found to be in DKA, as evidenced by her laboratory findings. This case should serve as a reminder that it is vital to perform a proper skin examination in patients presenting with hyperglycemia. Ultimately in this case, the patient was intubated for airway protection and started on vasopressors for cardiovascular support in the setting of septic shock. She went into VTach arrest and was successfully defibrillated before further decompensating and becoming asystolic.

Take-Home Points

  • The first task after suspected diagnosis of Fournier’s Gangrene is a page to your surgery service for evaluation and emergent debridement in the OR (depending on your institution this may be general surgery, urology, or both). After your patient is on the path to definitive management, you can begin aggressive fluid administration and broad-spectrum antibiotics (gram-positive, gram-negative, and anaerobic coverage needed).
  • Fournier’s Gangrene is a clinical diagnosis. Imaging may assist in atypical or borderline cases, but should never result in delay of surgical evaluation and treatment. Crepitus and ecchymotic tissue are very late findings; have high clinical suspicion inpatients with signs of swelling, erythema, and pain.

  • Shyam DC, Rapsang AG. Fournier’s gangrene. Surgeon. 2013 Aug;11(4):222-32. doi: 10.1016/j.surge.2013.02.001. Epub 2013 Apr 8. PMID: 23578806.
  • Ustin JS, Malangoni MA. Necrotizing soft-tissue infections. Crit Care Med. 2011 Sep;39(9):2156-62. doi: 10.1097/CCM.0b013e31821cb246. Erratum in: Crit Care Med. 2011 Nov;39(11):2592. Dosage error in article text. PMID: 21532474.
  • Harbrecht BG, Nash NA. Necrotizing Soft Tissue Infections: A Review. Surg Infect (Larchmt). 2016 Oct;17(5):503-9. doi: 10.1089/sur.2016.049. Epub 2016 Aug 2. PMID: 27483003.
  • Singh A, Ahmed K, Aydin A, Khan MS, Dasgupta P. Fournier’s gangrene. A clinical review. Arch Ital Urol Androl. 2016 Oct 5;88(3):157-164. doi: 10.4081/aiua.2016.3.157. PMID: 27711086.
  • Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing fasciitis: current concepts and review of the literature. J Am Coll Surg. 2009 Feb;208(2):279-88. doi: 10.1016/j.jamcollsurg.2008.10.032. Epub 2008 Dec 12. PMID: 19228540.
  • Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. p.592- 593.

SAEM Clinical Images Series: An Enlarging Scalp Mass

scalp mass

A 27-day-old female infant born at 34 weeks 4 days with a prenatal history of maternal syphilis treated with penicillin presented with an enlarging scalp mass since birth. Since birth, the patient has had a 1 cm erythematous and flat lesion on her scalp. Since that time, the lesion has continued to grow and develop scales. On the day of presentation, the lesion was noted to be 7-8cm in diameter with multiple surrounding smaller lesions. There is some clear to bloody drainage coming from the main lesion. The patient has otherwise been growing and developing normally. No fevers or other sick symptoms. Feeding well. Mom has no concerns with bowel movements or voiding habits.

General: She is active. She is not in acute distress. She is well-developed.

HEENT: No congestion or rhinorrhea. Mucous membranes are moist. No posterior oropharyngeal erythema.

Cardiovascular: Normal rate and regular rhythm. Normal pulses. No murmur heard.

Pulmonary: Respiratory effort is normal. No retractions. Normal breath sounds. No wheezing.

Skin: Skin is warm. Capillary refill takes less than 2 seconds. On the left side of the scalp, there is a large raised keratinized plaque with a stuck-on appearance. Some red blood is noted when tapped with a white sheet. The plaque is firm and non-tender. On the rest of the scalp, there are several peeling flat lesions with hair attached, and intermittent alopecia.

Neurological: No focal deficit present. She is alert. Suck is normal.

Scalp ultrasound: Posteriorly exophytic left parietal lesion is peripherally echogenic, possibly representing a calcified lesion or cephalohematoma. CT or MRI may be useful for further evaluation, as clinically indicated.

a. Seborrheic Dermatitis: A common, self-limiting eruption consisting of erythematous plaques with greasy, yellow-colored scales that distribute to the areas of the body with sebaceous glands.

b. Atopic Dermatitis: Erythematous, scaly, crusted lesions that are poorly demarcated. It is pruritic and commonly involves the cheeks, scalp, and extensor surfaces.

c. Psoriasis: Uncommon in infants, but can mimic seborrheic dermatitis with sharply demarcated, shiny, erythematous plaques with fine silvery scales in non-intertriginous regions.

d. Tinea Capitis: While rare, tinea can present with a scaly scalp rash in infants. There may be a mild to moderate inflammatory reaction associated as well as hair loss.

e. Langerhans Cell Histiocytosis (LCH): LCH can present as refractory seborrheic dermatitis. There may also be papules or reddish-brown nodules that appear with the rash.

Pityriasis Amiantacea secondary to Seborrheic Dermatitis with a significant build-up of crust and scale. Pityriasis amiantacea is an exaggerated inflammatory response to regional dermatitis, most often seborrheic dermatitis. Treatment consists of a keratinolytic and antibacterial ointment. In this patient, 1:4 part vinegar and water soaks were recommended twice daily, followed by mupirocin ointment until the resolution of the lesions.

Take-Home Points

  • Seborrheic dermatitis is a commonly presenting rash in infancy.
  • When rashes are refractory to conservative management, additional diagnoses and sequelae need to be considered.

  • Amorim GM, Fernandes NC. Pityriasis amiantacea: a study of seven cases. An Bras Dermatol. 2016 Sep-Oct;91(5):694-696. doi: 10.1590/abd1806-4841.20164951. PMID: 27828657; PMCID: PMC5087242.
  • Olanrewaju O. Falusi; Seborrhea. Pediatr Rev February 2019; 40 (2): 93–95. https://doi.org/10.1542/pir.2017-0215. PMID: 30709979.

SAEM Clinical Images Series: Localized Weakness

sturge-weber

A 69-year-old Caucasian female with a past medical history of seizures, cerebral vascular accident, and Parkinson’s disease presents by EMS for evaluation of a 30-minute episode of left upper and lower extremity weakness and left facial drooping. The patient complains of a right-sided “migraine-type” headache similar to that experienced with her prior stroke.

Vitals: Temp 36.5°C; BP 186/74; P 74; RR 18; O2 Sat 95%

General: Alert; no acute distress

Skin: Warm; dry; dark red discoloration localized to the left side of face, neck, chest, and upper extremity

HEENT: Normocephalic; left-sided facial droop; pupils are equal round and reactive to light

Cardiovascular: Regular rate and rhythm; no murmurs or gallops

Neurological: Alert and oriented x 4; CN II-XII grossly intact; slow and sluggish speech with left-sided facial droop; motor strength 4/5 LUE and LLE; tremor consistent with Parkinson’s disease

Comprehensive Metabolic Panel (CMP) and Complete Blood Count (CBC) are within normal limits.

Brain Computed Tomography demonstrates chronic atrophy, subcortical calcification, and microvascular ischemia.

Port-wine stain birthmark. This birthmark typically occurs on the forehead, scalp, or around the eye, and is unilateral. It is a manifestation of an overabundance of capillaries near the surface of the skin and exhibits a classic light pink to dark red discoloration.

When located around the eye, port wine stains have been associated with an increased incidence of glaucoma. Large port wine stains on the arm or leg have been associated with extra growth in that limb known as Klippel-Trenaunay syndrome. Port wine staining of the face, forehead, and scalp, when associated with cerebral leptomeningeal angiomas that elicit migraine headaches, seizures, strokes, and intellectual impairment as in this patient, are the classic findings of Sturge-Weber syndrome.

Take-Home Points

  • Sturge-Weber syndrome is the third most prevalent neurocutaneous disorder impacting 1 in 20,000 live births. It is a sporadic congenital neurocutaneous disorder that is caused by somatic activating mutations in the GNAQ gene.
  • Sturge-Weber syndrome is characterized by a facial port-wine stain, leptomeningeal angiomatosis, and glaucoma. Brain involvement can begin early in infancy, and manifests as seizures, strokes, stroke-like episodes, and a variety of neurological impairments.
  • Anticonvulsants, low-dose aspirin, and glaucoma medications are often employed in the management of Sturge-Weber syndrome as well as skin pulse dye laser therapy as desired for cosmesis. The prognosis of this condition depends on the extent of leptomeningeal involvement and the severity of glaucoma.

  • Comi AM. Sturge-Weber syndrome. Handb Clin Neurol. 2015;132:157-68. doi:10.1016/B978-0-444-62702-5.00011-1. PMID: 26564078.
  • Higueros E, Roe E, Granell E, Baselga E. Sturge-Weber Syndrome: A Review. ActasDermosifiliogr. 2017 Jun;108(5):407-417. English, Spanish. doi: 10.1016/j.ad.2016.09.022. Epub2017 Jan 23. PMID: 28126187.

By |2022-08-18T21:54:43-07:00Aug 22, 2022|Dermatology, Neurology, SAEM Clinical Images|

SAEM Clinical Images Series: A Backpacker’s Rash

rash

A 33-year-old female presented with a progressively worsening rash for one week. The patient just finished hiking the John Muir Trail, a backpacking trip that encompassed three weeks and over 240 miles. On the last days of the trip, the patient started to develop a severely itchy, red rash on both feet. She tried using a topical anti-fungal, which seemed to make the rash worse. She now has swelling and difficulty walking. The rash does not involve the hands or other parts of the body. She denies fever, open wounds, nausea, vomiting, or systemic symptoms, and has never had a similar rash before.

Skin: Diffuse edema and erythematous maculopapular rash to both feet, with vesicles and bullae overlying the dorsal and plantar surfaces of toes and feet. No rash proximal to the ankles. No petechiae or purpura noted. Normal hands and palms.

Non-contributory

The rash has both vesicles and bullae which narrow the differential to contact dermatitis and dyshidrotic eczema. Without petechiae or purpura, it is less likely vasculitis (such as exercise-induced vasculitis). There is no fever, spreading redness, or systemic signs, and it is bilateral, making cellulitis less likely. There were no known exposures to poison oak and the patient never walked without shoes or socks. There were no known tick bites, the hike was in California, and the rash did not involve the palms, making an infectious cause such as Rocky Mountain Spotted Fever unlikely. The rash became worse with topical anti-fungal cream, making fungal infection less likely.

The most concentrated areas of the rash are on the plantar surface of the foot and toes. Upon further inspection, it appears in a pattern that may be consistent with sports tape being used during hiking for blisters and plantar fasciitis pain. The patient later received patch testing by dermatology and was diagnosed with a colophony allergy. In this case, colophony was found in the sports tape causing severe allergic contact dermatitis on the feet. This is a T-cell-mediated reaction caused by repeated exposure to an allergen on the skin. Colophony is a mixture of many different compounds that are all derived from pine trees and is a common ingredient in medical and sports tapes. It is also sometimes used in making shoes.

Take-Home Points

  • The presence of vesicles and bullae narrow differential to contact dermatitis or dyshidrotic eczema. Both of these should respond to topical and/or oral steroids.
  • Look for patterns on the highest concentrated area of the rash to suggest allergic contact dermatitis.
  • Repeated lengthy exposure over a short course of time can cause allergic contact dermatitis to develop.

  • Litchman G, Nair PA, Atwater AR, Bhutta BS. Contact Dermatitis. 2022 May 8. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 29083649.

ACMT Toxicology Visual Pearl: Hypertension and Rash

mercury poisoning toxicity

Which toxic exposure can present with the pictured rash along with hypertension and tachycardia mimicking pheochromocytoma?

  1. Arsenic
  2. Lead
  3. Mercury
  4. Silver
  5. Thallium

(more…)

SAEM Clinical Image Series: Eye Pain

necrotizing

A 59-year-old gentleman experiencing homelessness with a history of hepatocellular carcinoma, hepatitis C, alcohol use disorder, and tobacco dependence presented to the emergency department (ED) with severe, worsening right eye pain, blurry vision, swelling, redness, and purulent discharge after scraping his upper face on concrete during a mechanical fall two weeks prior. Of note, his partner presented to the ED at the same time with a necrotic infection of the breast as well as multiple skin lesions reportedly due to insect bites.

Vitals: T 102.4°F; HR 108; BP 121/94

Head: Lice nits visible in his hair

Eye: Unable to open right eye without assistance; eyelids crusted and necrotic with underlying orbicularis oculi muscle visible; EOM full but painful in all fields of gaze; visual acuity 20/60 in each eye; pupils 2 mm, equal and minimally reactive.

White blood cell (WBC) count: 27,600/μl

Comprehensive metabolic panel (CMP): Na 121; K 2.8; Cl 83; AST 113; ALT 45

Wound culture: Positive for MRSA, Streptococcus pyogenes, Enterobacter cloacae, and Staphyloccocus epidermis

This patient’s presentation is consistent with periorbital necrotizing fasciitis complicated by severe sepsis.

This patient had type 1 necrotizing fasciitis given the polymicrobial source of infection with both aerobic and anaerobic organisms growing from his wound culture. Type 2 necrotizing fasciitis is attributable to streptococcal and/or staphylococcal infection alone. Group A strep is the most common organism responsible for necrotizing fasciitis, found in about 50% of cases.

Independent risk factors for necrotizing fasciitis include advanced age, diabetes mellitus, heart disease, liver cirrhosis, alcohol use disorder, and trauma. Furthermore, persons who experience homelessness are at risk of skin lesions due to insect bites, burns, and physical trauma which predispose them to secondary bacterial infections because of inadequate hygiene resources.

A systematic review of periorbital necrotizing fasciitis showed that 35% of cases were triggered by trauma, while 14% were caused by other infections such as acute dacryocystitis, sinus infections, and infections of the parotid glands.  Thus, it is likely that the patient’s contact with his partner who had a necrotic soft tissue infection secondary to insect bites, as well as his recent trauma to the eye, predisposed his development of this condition.

Initiation of broad-spectrum intravenous (IV) antibiotics with vancomycin, piperacillin/tazobactam, and clindamycin, as well as IV fluids.

In this case, the patient received the above antibiotics, underwent operative debridement, frequent wound care including dilute hypochlorous acid, local vancomycin administered via intra-orbital catheter, as well as lid reconstruction with glabellar flap. He was ultimately discharged on a two-week course of oral moxifloxacin and linezolid, healing well at his one-month follow-up appointment.

 

Take-Home Points

  • Skin problems are a common reason that persons experiencing homelessness seek medical care, given their risk factors for both primary insults and subsequent superinfection.
  • Common sources of infection for periorbital necrotizing fasciitis include trauma, surgery, and other infections of the upper face.
  • The standard of care for periorbital necrotizing fasciitis consists of IV and local antibiotics, and operative debridement.

  • Amrith S, Hosdurga Pai V, Ling WW. Periorbital necrotizing fasciitis — a review. Acta Ophthalmol. 2013 Nov;91(7):596-603. doi: 10.1111/j.1755-3768.2012.02420.x. Epub 2012 Apr 20. PMID: 22520175.

 

SAEM Clinical Image Series: Pediatric Rash

pediatric rash

A 17-month-old girl with a history of eczema presents to the pediatric emergency department for evaluation of a rash. The rash is different from her usual eczema, developed three days prior to presentation, and is described as red with yellow crusting. Her mother also noticed blistering in her groin and under her axilla. She has associated fussiness and decreased feeding, but no fever.

Vitals: T 37.7°C; HR 161; BP 115/75; RR 24; O2 sat 100% on room air

General: Fussy but consolable

Eyes: No conjunctival erythema or discharge

Mouth: Yellow crusting and fissuring surrounding mouth; no intra-oral lesions

Neck: No nuchal rigidity

Cardiovascular: Tachycardic with regular rhythm; no murmurs

Respiratory: Normal rate; normal breath sounds

Abdomen: Non-tender to palpation; non-distended; normal bowel sounds

Neurologic: Alert

Skin: Diffusely erythematous; scaling rash over the face with areas of yellow crusting; erythematous areas with blistering/desquamation to the anterior trunk, axilla, and inguinal regions

Complete blood count (CBC) and comprehensive metabolic panel (CMP) unremarkable.

Staphylococcal scalded skin syndrome caused by impetigo.

This case describes a patient with a rash, blistering/desquamation of axilla and groin, and systemic symptoms consistent with staphylococcal scalded skin syndrome (SSSS). Clinical features of SSSS include erythema to intertriginous areas, rapid progression of erythema, and systemic symptoms such as fever, irritability, and poor oral intake. Mucous membranes are not typically involved. Physical exam findings include perioral crusting and fissuring (seen in photo), blanching erythema, desquamation, shallow skin erosions, and a positive Nikolsky sign. SSSS is caused by exfoliative toxin A (ETA) and exfoliative toxin B (ETB), two exotoxins produced by certain strains of S. aureus. ETA and ETB cause the breakdown of keratinocyte adhesions within the epidermis, leading to desquamation. Infection with S. aureus at any site can cause SSSS, including bacterial conjunctivitis, wound/skin infection, staphylococcal pneumonia, pyomyositis, septic arthritis, and endocarditis. SSSS is more common in children, a phenomenon thought to be due to a lack of protective antibodies against staphylococcal antigens. The diagnosis of SSSS is clinical but can be confirmed with histopathology. In this case, the extensive yellow, crusting lesions of the face suggest impetigo, a superficial skin infection predominantly caused by S. aureus, as the etiology of SSSS. Children with eczema are at increased risk of impetigo due to disruption of the normal skin barrier. Complications of SSSS include fluid losses due to extensive skin breakdown, electrolyte abnormalities, sepsis, and death.

Penicillinase-resistant penicillins (oxacillin, nafcillin) or first- or second-generation cephalosporins. Clindamycin monotherapy should be avoided due to high rates of resistance. Management of SSSS in most cases also includes hospitalization for IV antibiotics and supportive care. In patients with significant skin involvement, admission to either an ICU or burn unit is warranted for close monitoring and wound care.

Take-Home Points

  • Staphylococcal scalded skin syndrome (SSSS) is caused by the release of S. aureus exfoliative toxins A and B into the bloodstream, thus SSSS can be caused by any infection caused by S. aureus.
  • Penicillinase-resistant penicillins are the first-line therapy in patients with SSSS. First- and second-generation cephalosporins, as well as vancomycin, can also be considered.
  • Treatment with clindamycin monotherapy should be avoided in patients with SSSS due to high levels of resistance among strains of S. aureus which cause SSSS.

  • Mishra AK, Yadav P, Mishra A. A Systemic Review on Staphylococcal Scalded Skin Syndrome (SSSS): A Rare and Critical Disease of Neonates. Open Microbiol J. 2016 Aug 31;10:150-9. doi: 10.2174/1874285801610010150. PMID: 27651848; PMCID: PMC5012080.
  • Paller A, Mancini, A. Hurwitz Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence. Edinburgh, Scotland: Elsevier; 2015.
  • Handler MZ, Schwartz RA. Staphylococcal scalded skin syndrome: diagnosis and management in children and adults. J Eur Acad Dermatol Venereol. 2014 Nov;28(11):1418-23. doi: 10.1111/jdv.12541. Epub 2014 May 20. PMID: 24841497.
  • Braunstein I, Wanat KA, Abuabara K, McGowan KL, Yan AC, Treat JR. Antibiotic sensitivity and resistance patterns in pediatric staphylococcal scalded skin syndrome. Pediatr Dermatol. 2014 May-Jun;31(3):305-8. doi: 10.1111/pde.12195. Epub 2013 Aug 23. PMID: 24033633; PMCID: PMC4349361.
  • Neubauer HC, Hall M, Wallace SS, Cruz AT, Queen MA, Foradori DM, Aronson PL, Markham JL, Nead JA, Hester GZ, McCulloh RJ, Lopez MA. Variation in Diagnostic Test Use and Associated Outcomes in Staphylococcal Scalded Skin Syndrome at Children’s Hospitals. Hosp Pediatr. 2018 Sep;8(9):530-537. doi: 10.1542/hpeds.2018-0032. PMID: 30139766; PMCID: PMC6317540.

 

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