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Jesse Keller, MD

Assistant Professor

Oregon Health & Science University

Disclaimer� I did not come up with the name for this talk

Outline� Topical steroid management

� Infection mimics

� Psoriasis/eczema mimic

� Paraneoplastic process

� Slow but life threatening condition

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Topical steroids� 7 different strengths

� Ointments, creams, lotions, gels, foams, shampoos, sprays

� Tubes come in different sizes depending on the steroid

� Insurance coverage, especially Medicaid, is tricky

Topical steroids - simplifiedStrength Potent Medium Weak

Thick plaques of psoriasis

Hand/foot eczema

Lichen planus

Most rashes

Full body rashes *Comes in a one POUND jar

Facial rashes

Topical steroids - simplifiedStrength Potent Medium Weak

Clobetasol 0.05% ointment

*if Medicaid, then use augmentedbetamethasone diproprionate0.05% cream

Triamcinolone 0.1% ointment

Hydrocortisone 2.5% ointment

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Topical steroids simplified� Always use ointment

� If your patient will not use ointment, then use cream

� Safe if used twice daily for 2-3 weeks

� For chronic rashes, use twice weekly for maintenance

Clinical pearl� To increase potency of topical steroids, have the

patient sleep in a sauna suit at night, wear gloves at night

� Occlusion enhances penetration of the topical

+

Topical steroids – what not to do� Common mistakes include:

� Underprescribing quantity in grams

� Using triamcinolone on the face – can trigger severe rosacea

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Infection mimics

Pop quiz� Dolor

� Rubor

� Calor

� Tumor

Pop quiz� Dolor - Pain

� Rubor

� Calor

� Tumor

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Pop quiz� Dolor - Pain

� Rubor - Redness

� Calor

� Tumor

Pop quiz� Dolor - Pain

� Rubor - Redness

� Calor - Heat

� Tumor

Pop quiz� Dolor - Pain

� Rubor - Redness

� Calor - Heat

� Tumor - Swelling

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Pop quiz� Dolor - Pain

� Rubor - Redness

� Calor - Heat

� Tumor – Swelling

� The four cardinal signs of inflammation

Pop quiz� Dolor - Pain

� Rubor - Redness

� Calor - Heat

� Tumor – Swelling

� The four cardinal signs of inflammation

� Not necessarily infection

Cellulitis vs ?� Inpatient dermatology consultation aids diagnosis of cellulitis among hospitalized patients: A multi-institutional analysis.

� BACKGROUND:

� Given its nonspecific physical examination findings, accurately distinguishing cellulitis from a cellulitis mimicker (pseudocellulitis) is challenging.

� OBJECTIVE:

� We sought to investigate the national incidence of cellulitis misdiagnosis among inpatients.

� METHODS:

� We conducted a retrospective review of inpatient dermatology consultations at Massachusetts General Hospital, University of Alabama at Birmingham Medical Center, University of California Los Angeles Medical Center, and University of California San Francisco Medical Center in 2008. All consults requested for the evaluation of cellulitis were included. The primary outcomes were determining the incidence of cellulitis misdiagnosis, evaluating the prevalence of associated risk factors, andidentifying common pseudocellulitides.

� RESULTS:

� Of the 1430 inpatient dermatology consultations conducted in 2008, 74 (5.17%) were requested for the evaluation of cellulitis. In all, 55 (74.32%) patients evaluated for cellulitis were given a diagnosis of pseudocellulitis. There was no statistically significant difference in the rate of misdiagnosis across institutions (P = .12). Patient demographics and associated risk factor prevalence did not statistically vary in patients given a diagnosis of cellulitis versus those with pseudocellulitis (P > .05).

� LIMITATIONS:

� This study was unable to evaluate all patients admitted with cellulitis and was conducted at tertiary care centers, which may affect the generalizability of the results.

� CONCLUSIONS:

� Cellulitis is commonly misdiagnosed in the inpatient setting. Involving dermatologists may improve diagnostic accuracy and decrease unnecessary antibiotic use.

� JAAD 2015

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Chronic venous insufficiency

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� Mechanism:

� Pressure of too much pooling of blood in veins over the years causes veins to stretch irreversibly and valves to eventually break down

Chronic venous insufficiency

� Mechanism:� Pressure of too much pooling of blood in veins over the years

causes veins to stretch irreversibly and valves to eventually break down

� Even more blood pooling occurs� Excess fluid leaks out of vessels, into surrounding tissue� Hemosiderin (iron) deposition from red blood cells gets

deposited, causes rust color on ankles

� Risk factors: � Age� Obesity� Standing long periods of time� Sitting long periods of time

Chronic venous insufficiency

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� Mechanism:

� Pressure of too much pooling of blood in veins over the years causes veins to stretch irreversibly and valves to eventually break down

� Even more blood pooling occurs

� Excess fluid leaks out of vessels, into surrounding tissue

� Hemosiderin (iron) deposition from red blood cells gets deposited, causes rust color on ankles

� Fluid gets into epidermis, which triggers eczema

Stasis dermatitis

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� Mechanism:

� Pressure of too much pooling of blood in veins over the years causes veins to stretch irreversibly and valves to eventually break down

� Even more blood pooling occurs

� Excess fluid leaks out of vessels, into surrounding tissue

� Hemosiderin (iron) deposition from red blood cells gets deposited, causes rust color on ankles

� Excess fluid causes poor blood and nutrient exchange to skin, causes necrosis and ulceration

� Most common on medial and lateral ankles along the veins

Stasis ulcer

� Mechanism: ???

� Venous stasis

� Spontaneous scar

tissue of the

underlying fat

Lipodermatosclerosis

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� Thought to resemble an upside down champagne bottle

Lipodermatosclerosis

� Chronic venous insufficiency

� Stasis dermatitis

� Acute, chronic

� Venous ulcers

� Lipodermatosclerosis

Venous disease approach…

� Concept is to encourage blood flow back up towards the heart

� Elevation above the level of the heart all night � Stack pillows under the ankles

� Compression with 30-40mmHg compression stockings worn all day

� Topical steroids if stasis eczema develops� Wound care for ulcers� Intralesional steroids at the first sign of

lipodermatosclerosis� Endovenous ablation procedure for severe or refractory

cases

Venous treatment

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� Avoid adding an allergic contact dermatitis

� Use only steroid ointments or Vaseline

� Allergy can be caused by Neosporin, Bacitracin, triple antibiotic ointment, lanolin or propylene glycol (inactive ingredients in many over the counter creams or lotions)

Venous treatment continued

� Gentle debridement of excess fibrin

� Moisture with white petrolatum, Xeroform, silver cream

� Daily dressing changes

� Monitor for superinfection

� Smell

� Pain

Wound care – venous ulcer

� Sluggish or damaged lymphatics

� Risk factors:� Age

� Obesity

� Scar tissue from previous bacterial infections (cellulitis, lymphangitis)

� Lymphatic removal from surgery (mastectomy)

� Parasitic infection in 3rd world countries

� Genetic lymphedema diseases (rare)

Lymphedema

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Lymphedema

“Squared toes” of lymphedema

Elephantiasis verrucosa nostra

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� Prevention of infection (cellulitis)

� Hygiene – chlorhexidine wash of entire foot, toes, calves

� Keep nails trimmed

� Antifungal cream in between toes

� Elevation (avoid sitting or standing long period of time)

� Compression

� Unna boots acutely

� Compression stockings for maintenance

Lymphedema treatment

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� Definition: Bacterial infection of the subcutaneous tissues

� Usually Strep� Not worth culturing – surface swabs are not representative of

the deep infection, deeper tissue cultures are negative half of the time. Lower leg wounds heal poorly.

� Strep bacteria live in between the toewebs, and gain entry through the skin barrier because of cuts or macerations caused by athlete’s foot

� For this reason, bilateral cellulitis is extremely rare

Cellulitis

� Can be very difficult to tell from stasis dermatitis

Cellulitis

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Cellulitis Stasis dermatitis

Warmth X X

Swelling X X

Elev. WBC, ESR, CRP X X

Color Red-orange Pink-red

Symptom Extremely tender “Burning” or “Itchy”

How many legs Always unilateral Usually bilateral

Cellulitis compared to stasis

dermatitis

If there are red legs bilaterally then it cannot be cellulitis

� Cellulitis causes scarring of lymphatic tissue � which makes you more likely to get:

-repeat cellulitis

-lymphedema

Complications of cellulitis

� Antibiotics – with Strep coverage

� Those with diabetes may need broader coverage

� Treat risk factors

� If athlete’s foot present, treat with lifelong antifungals

� Portal of infection? Look between the toes

Treatment of cellulitis

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Neutrophilic dermatoses

Neutrophilic dermatoses� Definition: Noninfectious, autoimmune skin rash full

of neutrophils on biopsy

� Examples:

� Sweet’s syndrome

� Pyoderma gangrenosum

� Neutrophilic dermatosis of the dorsal hands (NDDH)

� Crohn’s associated dermatosis

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Case 1� Exam findings

� Healthy appearing 39 yo man

� 12-13cm solitary round ulcer with violaceous rim on left lower leg

Case 1 � History

� Pt with history of Crohn’s disease

� Self discontinued Enbrel, found it was unhelpful

� No GI symptoms currently

� “Small bug bite or pimple that I decided to squeeze” turned into the current ulcer over 3 days

� Imaging showed signs of periosteal inflammation

Pyoderma gangrenosum� Commonly mimics infection, esp. necrotizing fasciitis

� Sterile osteomyelitis may be seen in underlying bone, further raising the question of infectious osteomyelitis and suspicion of infection

� Pathergy phenomenon leads to spreading and potential loss of limb if/when surgery takes place

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Pyoderma gangrenosum� Biopsies are usually nonspecific and therefore not

helpful

� Tissue cultures can be useful to rule out infection

� Clinical appearance is distinctive – deeply violacousborders

� History that is important:

� Pathergy – did it get worse after a debridement, surgical procedure, or biopsy?

� Steroid responsiveness – systemic, intralesional kenalog, clobetasol

Pyoderma gangrenosum� Demographics

� Young patients with Crohn’s disease, ulcerative colitis

� Middle aged Caucasian patients with metabolic syndrome, CKD, tobacco use

� Treatment� Combination of high dose steroids, dapsone,

mycophenolate, IVIG if refractory

� Infliximab if inflammatory bowel disease

� Frequent superinfections of chronic wounds may necessitate prophylactic antibiotics and/or surgical grafting as inpatient with high dose IV steroids on board

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Case 1 (continued)� Despite high dose oral steroids, our patient’s ulcer

continued to enlarge

� Needed a telemetry bed and 1 gram IV methylprednisolone x 3 consecutive days

� Pain control important

� Colonoscopy was scheduled in-house, showed extensive/severe Crohn’s involvement despite lack of clinical symptoms

� Started on infliximab and methotrexate as an outpatient, healed completely without recurrence

More pyoderma gangrenosum� Pt with 2 year history of chronic ulcer on the thigh not

responding to wound care for “venous ulcer”

� Pt had vascular procedure 2 years ago, ulcer formed in the scar after the surgery

� Surgery debrided the wound – it quadrupled in size

� This illustrates the role of pathergy and its usefulness as a clue in diagnosing PG

� Skin biopsy is usually nonspecific

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Case 2

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Case 2 (continued)� Inpatient case� Well appearing 53yo man with myelodysplastic

syndrome/AML� Derm consulted for “skin biopsy to prove diagnosis of

anthrax”

� Anthrax grows well on standard culture media, but -� Wound culture, tissue culture negative x 3� Biopsy was nonspecific� Broad range highly sensitive PCR sequencing at UW was

negative for DNA of any bacterial, fungal, tuberculous or atypical mycobacterial organisms

Diagnosis?

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Diagnosis?� Neutrophilic dermatosis of the dorsal hands (NDDH)

� Neutrophilic dermatosis

� Overlap between Pyoderma gangrenosum and Sweet’s syndrome

� Like Sweet’s, common in pts with AML/myelodysplasia

� Like Sweet’s, extremely responsive to prednisone

� Like PG, triggered by trauma

Case 3� 50 yo man with eczema x 6 years, never responds to

topical steroids

� Biopsied 3 times in the past, all showing “spongiotic” (eczematous) dermatitis

� Not really that itchy

� Plaques seem to be changing, more annular

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Case 3� Punch biopsy taken

� shows lymphocytes in the epidermis, suspicious for mycosis fungoides/CTCL

� The lymphocytes are atypical appearing

� Special stains show increased CD4 to CD8 ratio

� Special stains show loss of CD7 marker

� Referred to derm

� Flow cytometry looking for abnormal T-cell clones in blood

� 2 more biopsies for T-cell gene rearrangement testing on two separate sites. Clonal population seen in each; they are identical to one another

Mycosis fungoides� Hypothetical case

� Takes 6 years on average to make this diagnosis

� Can mimic psoriasis or eczema

� Can respond (partially) to topical steroids

� Annular sometimes scaly patches in “bathing suit” (sun protected areas) distribution

� Evolves slowly, may require biopsy several times

� Prednisone and topical steroids may mask the biopsy results

Case 4� 53yo woman admitted to the hospital for “cellulitis”

� Past medical history of diabetes, end stage renal disease s/p transplant complicated by failure of transplant, chronic DVT on warfarin

� Longstanding “venous disease” on legs for 2 years, not responding to wound care

� Legs have been progressively more painful to the point where she cannot walk

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Calciphylaxis� Risk factors

� ESRD

� Hypercalcemia/hyperphosphatemia

� Obese, Caucasian, females

� Warfarin use

� Diabetes

� Hypercoagulable state

� Steroid use

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Calciphylaxis� Risk factors

� ESRD

� Hypercalcemia/hyperphosphatemia

� Obese, Caucasian, females

� Warfarin use

� Diabetes

� Hypercoagulable state

� Iron use

� Steroid use

Calciphylaxis� Prognosis is not great

� 1 year mortality rate of 50% due to infections of ulcerations

� Treatment

� Stop warfarin

� Stop supplemental Vitamin D, Calcium, iron

� IV sodium thiosulfate

� Good evidence

� Mechanism unknown

Case 5

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Case 5� 52yo healthy man� 4 months progressive rash� 1 month severe dysphagia, weakness

� Visit 1: Urgent care: Gave him Claritin. No better.� Visit 2: PCP: Prednisone. No better.� Visit 3: ED: Diagnosis of allergic contact dermatitis from soap.

Prednisone. No better.� Visit 4: ED: Labs were taken, showed ESR 100, CRP 2, LFTS 335, 93, UA

with + proteinuria� Visit 5: ENT� Visit 6: PCP� Visit 7: Dermatology – Biopsies taken� Visit 8: OHSU ED

Dermatomyositis� Frequently missed by dermatologists and

nondermatologists alike� Important not to miss- this is a paraneoplastic syndrome

most of the time� Can be acute onset or more slow in appearance� Can appear a few years before, at the same time as, or a few

years after a new cancer� Classic rash is bright pink around the eyes, over the joints

(usu. Knuckles), and on the upper chest and back (“Shawl sign”)

� May also present with severe/refractory scalp dermatitis� Skin biopsy findings similar to lupus but more subtle

Case 5 (continued) � CK elevated at 7,000

� Skin biopsy was diagnostic

� Pt with severe weakness and dysphagia, required speech therapy and eventual PEG tube placement

� Prednisone, azathioprine, and IVIG were needed to control his disease

� Given lifetime smoking history, suspicion for lung cancer

� CT chest/abdomen/pelvis revealed incidental renal mass

� Found to have renal cell carcinoma

� Removal should cause the disease to remit