Category Archives: Dermatology

Moffitt Pearls 10/30/17 – Palpable Purpura + AKI

Thank you, Lily for presenting a case this morning of a middle-aged woman from Mexico being treated for a metastatic GI malignancy p/w flank pain, AKI and palpable purpura found to have obstructive nephropathy and candiduria .

Key Pearls:

  1. Classic approach to AKI: pre-, intrinsic-, post-renal hold-up even when the patient becomes more complicated. Always remember to consider carefully a patient’s volume status and run the med list.
  2. The DDx for purpura can be broken down first by whether or not the lesions are palpable. If NOT palpable, we call these petechiae or ecchymoses based on the size (<3mm = petechiae). This should prompt consideration of the coagulation cascade, platelets, uremia. If palpable, this suggests inflammation and a possible vasculitis. See an approach to palpable purpura below.
  3. Yeast in urine is usually a colonizer and not a pathogen. However, treatment for funguria is indicated in patients with renal transplant and immunosuppression. See link for more info
Candiduria: A Review of Clinical Significance and Management – Zakeya Abdulbaqi Bukhary

Selected Highlights:

  • Treatment of Candida can be guided by in vitro susceptibility testing (although all labs do not send these).
  • Fluconazole gains high concentrations of active drug in the urine, is better tolerated and is less likely to be associated with the emergence of resistance during therapy.
  • The greatest concern for fluconazole resis­tance is related to C. glabrata and C. krusei isolates which require maximal doses of amphotericin B.
  • As HH mentioned – Echi­nocandin anti fungal agents (caspofungin, micafungin, and anidulafungin) can be used although low sub-therapeutic levels are achieved in the urine because the drug has poor glomerular filtration with subsequent diminished tubular secretion. 

More Info at:


Causes of Non-Palpable Purpura based on size of lesion

  • Remember these lesions are macular and are typically NOT inflammatory
  • Petechiae (small lesions < 3 mm)
    • Abnormal palatele function
    • Increased intravascular pressures
    • Thrombocytopenia
      • Idiopathic
      • Drug-induced
      • Thrombotic
    • DIC and infection
  • Ecchymoses (larger lesions > 5 mm)
    • Coagulation defects
    • DIC and infection (purpura fulminas)
    • External trauma
    • Hypergammaglobulinemic purpura

See the following link for more information in a case based ppt from the American Academy of Dermatology Titled “Petechiae, Purpura and Vasculitis.”

Break down Vasculitis based on vessel size




Moffitt Pearls 8.15.17 – Anaphylaxis and Drug Reactions

Case Summary:

Thank you to Karen for presenting a mystery case of a young man with hx of asthma, seasonal allergies and eczema p/w perioral edema, itching and profound hypotension concerning for anaphylaxis! We discussed the importance of early therapy for anaphylaxis, drug reaction patterns and the possibility of serum sickness in the setting of Bactrim exposure and the atypical nature of her presentation.


Key Pearls

  1. Anaphylaxis is a Type 1 IgE mediated hypersensitivity reaction that usually occurs within in minutes of an allergen exposure.
    • Volume and IM epinephrine are mainstays of therapy and should NOT be delayed.
  2. Drug reactions are often delayed days to weeks from drug exposure (make sure to review a log) and are mediated by Type IV hypersensitivity.
  3. Angioedema may be manifested by IgE mediated (Type I Hypersensitivity) drug reaction
    • IgE-mediated reactions tend to become more severe & progress toward anaphylaxis (Bactrum as in our case) upon re-exposure to causative agent


Classification of Allergic Reactions

Type Description Mechanism Clinical Features
I Anaphylactic Usually IgE dependent release of vasoactive substances (histamine, prostaglandins and leukotrienes) Anaphylaxis (definition below), Angioedema, urticarial, GI Sx and bronchospasm
II Antibody (AB)-dependent cytotoxicity Antigen/Haptan associated with cell binds AB -> cell/tissue damage Hemolytic anemia, Interstitial nephritis
III Immune Complex Disease Formation of Antigen-Antibody (AB) Complexes Causes damage Serum Sickness
IV Cell-mediated or Delayed Hypersensitivity Antigen sensitizes T cells, then mediates tissue injury Delayed dermatitis or drug reaction

Drug Reaction Patterns Discussed

SJS (< 10 % body surface area)/TEN (>30% body surface area)

  • Mucosal involvement required, occurs usually within 8 weeks of drug exposure


  • Systemic involvement (fever, adenopathy elevated LFTs) driven by eosinophilia; Reaction begins 2-6 weeks after exposure to offending drug


  • Reaction often occurs 48-72 hours after drug exposure

Fixed Drug Eruption

  • Usually without mucosal involvement, occurs anytime – days to weeks after drug exposure


  • >90% of body surface area involved; ddx wide and includes drugs ~ 20% cases and malignancy (Cutaneous T-cell lymphoma)



ZSFG Pearls: Anemia+DVT ddx, SCARs

Today, we discussed the case of a previously healthy young man who was found to have a DVT as an outpatient and prior to initiating anti-coagulation, was noted to have significant microcytic anemia. Ultimately, his work-up revealed a metastatic malignant process, likely GI primary.

We generated a short starter list (not exhaustive) for entities whose illness script includes anemia (w/o obvious signs of blood loss) and DVT. A few pathophysiologic explanations follow the syndromes. Feel free to add/comment with more!

Anemia + DVT ddx
-Fe-deficiency anemia*
-Sideroblastic anemia, thalassemia**
-Myeloproliferative neoplasms, PNH
-Malignancy NOS
Post-splenectomy ***
-Nephrotic syndrome

*From the Annals of Hematology: while concomitant thrombocytosis tends to be involved in iron-related thrombosis, iron-deficiency on its own may contribute to a hypercoagulable state through anemic hypoxia or by affecting blood flow patterns within the vessels because of reduced deformability and increased viscosity of microcytic red blood cells

fe def anemia

**Patients with thalassemia (mild, intermediate, or major clinical phenotype) have chronically activated platelets, enhanced platelet aggregation, and have higher levels of pro-coagulant microparticles of RBC, leukocytes, and endothelial membrane compared to controls. Per the Mediterranean Journal of Hematology and ID which has many more touches with thalassemia than us, “the presence of other peripheral blood elements in [patients with thalassemia] such as E-selectin (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), von Willebrand factor (VWF) and vascular cell adhesion molecule-1 (VCAM-1) indicates that endothelial injury or activation may be an aspect of the disease, aiding in the recruitment of white blood cells and RBCS, promoting thrombosis.”
thal outline

***In patients who have undergone splenectomy (see blood smear below with H-J bodies 🙂, there are more exposed pro-coagulant phospholipids on altered membranes of the abnormal erythrocytes–and these are no longer removed by splenic macrophages. Studies suggest that in patients who are post-splenectomy, there is a higher number of negatively charged RBCs and increased thrombin generation!
h-j body


At a recent intern report, we discussed the entity of DRESS or drug reaction with eosinophilia and systemic symptoms AKA drug-induced hypersensitivity syndrome (DISH). This diagnosis is under the larger umbrella of severe cutaneous adverse reactions to drugs (SCARs).


  • While adverse cutaneous reactions to drugs affect 2% to 3% of all hospitalized patients, only 2% of these are considered severe
  • Spectrum of SCARs:
    • Acute Generalized Exanthematous Pustulosis (AGEP)
    • Drug reaction with eosinophilia and systemic symptoms (DRESS) or Drug-induced Hypersensitivity Syndrome (DISH)
    • Epidermal necrolysis (Stevens-Johnson syndrome-SJS, toxic epidermal necrolysis –TEN)

There is a nice review of SCARs in NEJM from 2012: Features of Selected Severe Cutaneous Adverse Reactions to Drugs.” A few key points and classy comparison table are below.

  • Exanthematous drug eruptions, also called morbilliform or maculopapular drug rashes, occur in 1 to 5% of first-time users of most drugs (whoa!)
  • Identifying and discontinuing the causative drug are the most important steps in management
    • Symptomatic treatment with antipruritic agents and potent topical glucocorticoids may be helpful.
  • Signs and symptoms that should alert the clinician to the possibility of a severe cutaneous reaction (SCARs): mucous-membrane involvement, temperature above 38.5°C, blisters, facial edema and erythema, and lymphadenopathy.


dish dress 3

Despite the ambiguities among all the severe cutaneous adverse reactions to drugs (SCARs), there is actually minimal overlap in diagnoses as discussed in this article from the Journal of Rare Diseases (no joke!) looking retrospectively at 216 cases of SCARs: 


  • Franchini M, Targher G, Montagnana M, Lippi G. Iron and thrombosis. Annals of Hematology. 2008;87(3):167-173. doi:10.1007/s00277-007-0416-1.
  • Succar J, Musallam KM, Taher AT. Thalassemia and Venous Thromboembolism. Mediterranean Journal of Hematology and Infectious Diseases. 2011;3(1):e2011025. doi:10.4084/MJHID.2011.025.
  • Byrne MT, Bergman AK, Ruiz AI, Silver BJ, Maciejewski JP, Tiu RV. Postsplenectomy thromboembolic disease in congenital sideroblastic anaemia. BMJ Case Reports. 2010;2010:bcr1220092514. doi:10.1136/bcr.12.2009.2514.
  • Stern RS. Features of Selected Severe Cutaneous Adverse Reactions to Drugs N Engl J Med 2012;366:2492-2501.
  • Bouvresse S, Valeyrie-Allanore L, Ortonne N, et al. Toxic epidermal necrolysis, DRESS, AGEP: Do overlap cases exist? Orphanet Journal of Rare Diseases. 2012;7:72. doi:10.1186/1750-1172-7-72.




Livedo reticularis and livedo racemosa

We’ve had a purple, net-like week here at ZSFG. At both M&M and intern report we talked about livedo rashes. After both conferences, I was still confused. So I looked it up in a dermatology textbook. Here’s what I learned.
Top pearls
  • Livedo reticularis can be primary and benign or secondary and very bad
  • Livedo racemosa is morphologically different and always bad
  • There’s a lot of conflicting information out there about the distinction between these two conditions!
Pathophysiology of livedo rashes
  • both racemosa and reticularis arise from deoxygenation or dilation of the venous plexus in the skin
  • veno-dilation can be benign (due to cold, called cutis marmorata) or from one of the following pathologic processes
    • small vessel sludging/clotting (due to coagulopathy)
    • vasospasm
    • vasculopathy
Livedo reticularis
  • the rash of classic Livedo reticularis  is “fishnet-like, red or purple mottling [that] surrounds a pallorous conical core.” The rings are closed/complete circles and relatively symmetric
  • Here’s a good picture from the mayo clinic. The circles can definitely bigger/more netlike.
Livedo racemosa
The rash of livedo racemosa is the same color, but tends to be more broken and asymmetric. It partially goes away with warming, but not completely.
Screen Shot 2017-02-17 at 10.59.24 AM.png
  • Livedo reticularis can be primary or secondary. 
    • primary is caused by cold or is idiopathic and requires no special management other than cold avoidance.
  • Livedo Racemosa is always secondary and bad.
    • Always, always test patients with racemosa for APLS.
  • The DDX for secondary reticularis and racemes is super broad, and can be categorized using the clotting, vasospasm, vasculopathy framework above. See a full differential below.
Let me know if you have a different framework for thinking about these! Every paper had a different definition and very strong opinions =)
Chadachan V, Dean SM, Eberhardt RT. Chapter 173. Cutaneous Changes in Peripheral Arterial Vascular Disease. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K. eds. Fitzpatrick’s Dermatology in General Medicine, 8e New York, NY: McGraw-Hill; 2012. Accessed February 17, 2017.
Gunderson CG, Federman DG. Web of confusion Am J Med. 2011 Jun;124(6):501-4. (this is where the table comes from)

MOFFITT AM REPORT PEARLS 10/24/16: Sweet Syndrome!

Hi Everyone! Thanks to Kenny for presenting a SWEET case of a young woman with multiple prior malignancies presenting with monoarticular swelling and erythema, possibly concerning for Sweet syndrome! There were 30148592 other things we could have talked about in this case, but we’ll focus on Sweet syndrome for today.


Top pearls:

  • Sweet syndrome is acute febrile neutrophilic dermatosis
  • Characterized by abrupt onset painful palpable skin lesions
  • 3 types: Classical, Malignancy-associated, and Drug-associated
  • Treatment is corticosteroids (topical or systemic based on severity)


For those who want more info:

Abrupt appearance of painful papules, plaques, or nodules, with fever and leukocytosis

Inflammation of eyes, MSK system, and internal organs may occur

According to some authors, there are 3 types:

  • Classical Sweet syndrome (idiopathic), majority of cases
    • 1-3 weeks after URI or GI infection
    • IBD-associated
    • Pregnancy-associated
  • Malignancy-associated Sweet syndrome
  • Drug-induced Sweet syndrome

Dx criteria.jpg

The first two criteria (major criteria) are necessary for the diagnosis, in addition to two of the remaining (minor) criteria.

Criteria for drug-induced Sweet syndrome are similar but involve establishing a temporal relationship between the culprit drug and symptom onset/resolution.

Malignancy-associated Sweet syndrome is more likely with hematologic malignancies than with solid tumors (approx. 85% vs 15% of cases). AML is the most common associated malignancy.

The list of drugs associated with Sweet syndrome is long, but commonly used drugs include furosemide, hydralazine, diazepam, TMP-SMX, nitrofurantoin, carbamazepine, abacavir, PTU, azathioprine, and G-CSF, among several others.

Epidemiology: Adults aged 30-60 is most common age group, 80% women for classical Sweet syndrome, 50-60% women for malignancy-associated Sweet syndrome.

Skin lesions most common on upper extremities, head, neck, trunk, and back.

Treatment is based on severity but is always steroids:

  • Mild (<5% BSA involvement and mild systemic sx): high potency topical steroids or intralesional steroid injections
  • Moderate-severe: Systemic steroids. Alternative therapies include colchicine, dapsone, or potassium iodide
  • Refractory cases: IV steroid pulse or other immunomodulation therapy

Some pictures of classic skin findings (Remember, these are painful! Itching is rare.):

*Photos from VisualDx and Uptodate


Have a great day everyone!



Erythema Multiforme

Thanks to Kenny and Chloe for bringing a case earlier this week to ID report of a woman with an HSV infection who had a rash that was either leukocytoclastic vasculitis, erythema multiforme, or maybe both.
Some pearls about EM, something we see rarely in in the inpatient setting.
What is EM?
  • classically a targetoid rash with mucosal involvement. Has a benign clinic course.
  • Called “multiforme” because the rash has protean manifestations. But it classically looks like this:
erythema multiforme.png
  • Rare, most common in children and adults age 20-40.
  • Some more pictures of classic lesions


What causes EM?
  • most commonly HSV-related.
    • rash begins 2-17 days after HSV outbreak
    • recurrent EM is usually HSV-related.
  • Other causes
    • mycoplasma (and other bacterial infections but mycoplasma is common)
    • other viruses
    • malignancy
    • autoimmune disease
    • radiation
    • sarcoid
    • medications
  • Because of the mucosal involvement, it is important to distinguish EM from it’s more life threatening cousin – SJS. Here are some distinguishing feature
    • SJS can atypically have target lesions. The targets of EM are papular, while the targets of SJS are macular
    • Medications rarely cause EM and commonly cause SJS
    • skin sloughing should always make you concerned for SJS
  • Other things on the ddx for targetoid skin lesions
    • urticaria and urticarial vasculitis
    • fixed drug eruption
    • bullous pemphigoid
    • sweets syndrome
    • Rowell syndrome (EM in the setting of cutaneous lupus)
    • cutaneous small vessel vasculitis.
  • Antivirals are helpful if started early in the course of an HSV-mediated outbreak
  • Antivirals do prevent recurrent EM in patients with >6 outbreaks/year
  • topical glucocorticoids (for skin) and glucocorticoid gels (for mucosal involvement) are key for symptomatic relief
  • people with debilitating recurrent EM sometimes need systemic immune suppression. This is rare.
Lamoreux MR1Sternbach MRHsu WT.Erythema multiforme. Am Fam Physician. 2006 Dec 1;74(11):1883-8.

Impromptu derm report: SDRIFE and intertriginous rashes

Thank you to Chuka and Kenny for spearheading an impromptu and super interesting dermatology report.
From the pearl archives: the 6 A’s of drug reactions
 6 “A” Classes of Common Drug Reactions – always take a history of these drugs!
  • Allopurinol
  • NS(A)IDs
  • Anti-epileptic Drugs
  • ARVs
  • Sulf(A)
  • Antibiotics
Uncomplicated (non-lifethreatening) drug reactions
  • Most drug reactions (90%) are uncomplicated exanthems, classically maculopapular, sparing the palms and soles
    • usually within 5-14 days of starting the offending drug
    • can have rare bullae or pustules like this patient did
This patient had a reaction in an intertriginous distribution after surgery. Ddx for intertriginous eruptions includes
  • Common
    • contact dermatitis (irritant or allergic)
    • intertrigo (usually staph, strep or corynebacterium)
    • tine cruris
  • can’t miss
    • inverse psoriasis
    • early Acute Generalized Exanthematous pustulosis
    • staph scalded skin syndrome
  • Zebras
    • Systemic drug-related intertrigenous and flexural exanthema (SDRIFE)
    • eccrine shamus syringometaplasia
    • pemphigus vegetans
    • Hailey-Hailey disease
Systemic, drug-related intertriginous and flexural exanthema AKA SDRIFE
  • SDRIFE is a drug reaction that has a predilection for the buttocks and inguinal area. It is relatively rare, but has a classic distribution.
  • usually morbiliform, sometimes with bullae or pustules. While it’s rare, this is one of those diagnoses the dermatologists can make from the door.
  • it looks like this:
  • SDRIFE used to be called baboon syndrome due to the red buttocks. But that’s not a very nice thing to call a person, so the name was changed.
  • Treatment is supportive with topical corticosteroids and discontinuation of the offending agent.
Winnicki M1Shear NH. A systematic approach to systemic contact dermatitis and symmetric drug-related intertriginousand flexural exanthema (SDRIFE): a closer look at these conditions and an approach to intertriginous eruptions. Am J Clin Dermatol. 2011 Jun 1;12(3):171-80.