Dermatologic Emergencies

Brief H&P

A 68 year-old male with hypertension and gout presents with rash for 2-3 weeks. He note some subjective fevers but is otherwise asymptomatic. He denies recent travel or sick contacts. When asked about his medications, he reports that his primary care provider started him on allopurinol approximately two months ago.

He first noted the rash on his face, characterizing it as “pimples” which were slightly pruritic. The lesions subsequently spread to his trunk and extremities and have been growing in size.

Objectively, vital signs were notable for fever (38.2°C) and tachycardia (108bpm). Examination demonstrated diffuse blanching erythema most prominent on the trunk and extremities. The remainder of the physical examination was normal. Laboratory studies were obtained and notable for a complete blood count (CBC) with peripheral eosinophilia, as well as mildly elevated serum transaminases.

The patient was diagnosed with Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), likely owing to the initiation of a xanthine oxidase inhibitor. He improved after withdrawal of the drug and a brief course of systemic corticosteroids.

Principles of Dermatologic Emergencies

Critical dermatologic processes can be broadly divided into two categories:

1. Cutaneous manifestation of critical illness

The presence of a dermatologic abnormality does not itself represent a life-threat. Instead, the skin lesion is a signal suggestive of the presence of an underlying critical process. The prototypical example would be the petechiae/purpura in meningococcemia.

2. Acute Skin Failure

As with any other organ system failure, Acute Skin Failure carries significant morbidity and mortality and is characterized by derangements in normal skin function.

Critical functions of skin
Temperature regulation
Protection against excess fluid loss
Mechanical barrier to prevent penetration of foreign materials
Important pathophysiologic changes in ASF
Increased peripheral vasodilation (dramatic increase in cardiac output to low-resistance circuits) and increased vascular permeability resulting in relative hypovolemia and shock.
Increased blood flow and dysfunction of eccrine sweat glands results in altered temperature regulation (usually hypothermia)
Fluid imbalances occur, similar to burns (transepidermal water loss) which varies in quality somewhat between “dry” (erythroderma) and “wet” (vesiculobullous) diseases
Electrolytes: increased basal metabolic rate, hyperglycemia (insulin resistance), hypophosphatemia, protein depletion
Barrier dysfunction: increased risk of infection
Intensive Care Unit: Dermatologic (DICU) or Burn Center preferred
Treatment: Temperature management, early enteral nutrition, fluid/electrolyte management, local wound care, disease-specific management
Complications: Sepsis/shock, ARDS, high-output CHF, known complications of critical illness (multi-organ failure, GI ulcers, VTE)
Long-term complications: occular (ectropion, keratitis, ulcer), esophageal (stricture), GU (urethral stricture, phimosis, vaginal stenosis), Integumentary (scarring, alopecia)

Skin Lesions and their Pathophysiology

The objective of this algorithm is to develop a systematic approach to the evaluation of dermatologic processes with a focus on the identification of dermatologic emergencies. The foundation of this approach is an understanding of the underlying pathophysiologic mechanisms for each of four broad categories of dermatologic processes which guide the resultant differential diagnosis.


Extensive cutaneous capillary dilation, results in widespread exfoliation of the epidermis
Inflammatory mediators result in dramatic increase of epidermal turnover rate, accelerated mitotic rate, increased number of germinative skin cells.
Exfoliative toxin
Skin-homing T-cells

View Erythroderma Algorithm


Represent the passage of erythrocytes from the intravascular to extravascular compartment
May be the result of disruption of vascular integrity (trauma, infection, vasculitis) or disorders of primary or secondary hemostasis
If lesions are palpable, this may suggest a more prominent underlying inflammatory process such as vasculiitis.
When cutaneous manifestations are identified, other small vessels may be affected (commonly renal and pulmonary

View Petechiae/Purpura Algorithm


Pustules more commonly suggest an infectious process (bacterial, fungal)
Vesiculobullous lesions are generally more concerning
Loss of basic structural elements maintaining cohesion between keratinocytes in the epidermis, or between the epidermal layer and the dermis (near basement membrane zone).
Intraepidermal blisters tend to be flaccid, fragile and thin-roofed.
Subepidermal blisters have a thick roof and can remain intact when compressed
Often due to autoantibodies targeting structural proteins in the skin.

View Fluid-filled Algorithm


Catch-all term with a wide range of potential pathophysiologic mechanisms and causative etiologies.
Any process that results in erythroderma, petechiae, or fluid-filled lesions may start as a macule or papule.
Pathophysiology is of little guidance in this category where we must instead rely on the patient’s history and identification of red-flags to exclude dermatologic emergencies.
High-risk Features (Identified by dermatologists to stratify urgency of inpatient consultations):
Ill-appearing, vital sign instability
New-onset fever with rash
Mucocutaneous or ocular lesions
Recent introduction of anti-convulsant or sulfa-drug
Skin pain

View Maculopapular Algorithm

Algorithm for the Evaluation of Dermatologic Processes

Algorithm for the Evaluation of Dermatologic Processes
An algorithm for the evaluation of dermatologic processes was developed initially by Lynch in 1984. Since then, several modified Lynch algorithms have emerged. The concept of an algorithmic approach to dermatologic diagnosis was further expanded with the development of VisualDx, a decision-support application. There is evidence to suggest that the use of algorithms and decision support tools like VisualDx (and by extension this algorithm) may aid with the development of more thorough differential diagnoses and improve diagnostic accuracy.



  1. Wolf R, Parish LC, Parish JL. Emergency Dermatology, Second Edition. August 2017:1-369.
  2. Usatine RP, Sandy N. Dermatologic emergencies. Am Fam Physician. 2010;82(7):773-780.
  3. Shilpi Khetarpal MD, Anthony Fernandez MP. Dermatological Emergencies. Cleveland Clinic. Published August 2014. Accessed August 5, 2017.
  4. McQueen A, Martin SA, Lio PA. Derm emergencies: detecting early signs of trouble. J Fam Pract. 2012;61(2):71-78.
  5. Browne BJ, Edwards B, Rogers RL. Dermatologic emergencies. Prim Care. 2006;33(3):685–95–vi. doi:10.1016/j.pop.2006.06.002.
  6. Drage LA. Life-threatening rashes: dermatologic signs of four infectious diseases. Mayo Clinic Proceedings. 1999;74(1):68-72. doi:10.4065/74.1.68.
  7. Baibergenova A, Shear NH. Skin conditions that bring patients to emergency departments. Arch Dermatol. 2011;147(1):118-120. doi:10.1001/archdermatol.2010.246.


  1. Tan TL, Chung WM. A case series of dermatological emergencies – Erythroderma. Med J Malaysia. 2017;72(2):141-143.
  2. Karakayli G, Beckham G, Orengo I, Rosen T. Exfoliative dermatitis. Am Fam Physician. 1999;59(3):625-630.


  1. Stevens GL, Adelman HM, Wallach PM. Palpable purpura: an algorithmic approach. Am Fam Physician. 1995;52(5):1355-1362.


  1. Lynch PJ, Edminster SC. Dermatology for the nondermatologist: a problem-oriented system. YMEM. 1984;13(8):603-606.
  2. Nguyen T, Freedman J. Dermatologic Emergencies: Diagnosing And Managing Life-Threatening Rashes. Emergency Medicine Practice. 2002;4(9):1-28.
  3. Murphy-Lavoie H, LeGros TL. Emergent Diagnosis of the Unknown Rash: an Algorithmic Approach-Rash Is Among the Top 20 Reasons for ED Visits in the United States. Certain Rashes …. Emergency Medicine; 2010.
  4. Dean S. Emergency Medicine Dermatology. 2017:1-20. doi:10.21980/J8DW21.
  5. Talley NJ, O’Connor S. Clinical Examination. Elsevier Health Sciences; 2013.
  6. Jack AR, Spence AA, Nichols BJ, Peng DH. A simple algorithm for evaluating dermatologic disease in critically ill patients: a study based on retrospective review of medical intensive care unit consults. J Am Acad Dermatol. 2009;61(4):728-730. doi:10.1016/j.jaad.2008.12.025.


  1. McQueen A, Martin SA, Lio PA. Derm emergencies: detecting early signs of trouble. J Fam Pract. 2012;61(2):71-78.
  2. Cardoso CS, Vieira AM, Oliveira AP. DRESS syndrome: a case report and literature review. BMJ Case Rep. 2011;2011. doi:10.1136/bcr.02.2011.3898.

Evidence-Based Algorithms

  1. David CV, Chira S, Eells SJ, et al. Diagnostic accuracy in patients admitted to hospitals with cellulitis. Dermatol Online J. 2011;17(3):1.
  2. Chou W-Y, Tien P-T, Lin F-Y, Chiu P-C. Application of visually based, computerised diagnostic decision support system in dermatological medical education: a pilot study. Postgrad Med J. 2017;93(1099):256-259. doi:10.1136/postgradmedj-2016-134328.

Kawasaki Disease

Brief H&P:

An 8-month old male is brought to the emergency department with fever. He has had four days of fever (temperature ranging from 37-40°C), rash on trunk and extremities, white-colored tongue discoloration, and irritability with decreased oral intake. Temperature on presentation was 39.4°C, examination revealed an erythematous maculopapular rash on the extremities and trunk including soles of the feet. Mucous membrane involvement was noted with oropharyngeal erythema and bilateral conjunctival injection. Neck examination demonstrated right-sided cervical adenopathy.


  • WBC: 23.4 (N: 59%, B: 21%)
  • ESR: 100mm/hr
  • CRP: 7.59mg/dL
  • Albumin: 3.3g/dL
  • AST/ALT: 78U/L, 65U/L
  • UA: 7WBC, no bacteria

Hospital Course

The patient was admitted with a diagnosis of Kawasaki Disease and was treated with IVIG and high-dose aspirin. The patient demonstrated marked improvement with treatment and had a normal echocardiogram. He was discharged on hospital day three.


  • Age: 6 months to 5 years
  • Northeast Asian
  • Possible heritable component
  • Seasonal (winter/spring)


  • Acute febrile (T > 39°C refractory to anti-pyretics)
  • Subacute (coronary vasculitis)
  • Convalescent


  • Fever >5d
  • Criteria (4/5)
    • Conjunctivitis (bilateral, non-exudative)
    • Oropharynx changes (strawberry tongue, erythema, perioral)
    • Cervical lymphadenopathy (unilateral, >1.5cm)
    • Rash
    • Extremity changes (erythema, edema, palm/sole involvement)
  • Incomplete (2-3 criteria)


  • CBC: Elevated WBC (neutrophil predominant)
  • Urinalysis: Sterile pyuria
  • Acute phase reactants: Elevated ESR (>40-60mm/hr), CRP (>3.0-3.5mg/dL)
  • CMP: Hyponatremia, hypoalbuminemia, hypoproteinemia, elevated transaminases
  • ECG: AV block, ischemia/infarction (aneurysm/thrombosis)
  • Echocardiography: Decreased LVEF, MR, pericardial effusion


  • Hospital admission
  • IVIG (2g/kg)
  • Aspirin (80mg/kg/day)

Algorithm for the Evaluation of Kawasaki and Incomplete Kawasaki Disease3,4

Algorithm for the Evaluation of Kawasaki and Incomplete Kawasaki Disease


  1. Shiari R. Kawasaki Disease; A Review Article. Arch Pediatr Infect Dis. 2014;2(1 SP 154-159).
  2. Yu JJ. Diagnosis of incomplete Kawasaki disease. Korean J Pediatr. 2012;55(3):83-87. doi:10.3345/kjp.2012.55.3.83.
  3. Newburger JW, Takahashi M, Gerber MA, et al. Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Pediatrics. 2004;114(6):1708-1733. doi:10.1542/peds.2004-2182.
  4. Yellen ES, Gauvreau K, Takahashi M, et al. Performance of 2004 American Heart Association recommendations for treatment of Kawasaki disease. Pediatrics. 2010;125(2):e234-e241. doi:10.1542/peds.2009-0606.


Source: Mulpuru, S., Touchie, C., Karpinski, J., & Humphrey-Murto, S. (2010). Coexistent Wegener“s granulomatosis and Goodpasture”s disease. The Journal of rheumatology, 37(8), 1786–1787. doi:10.3899/jrheum.091404

Linear IgG deposits consistent with anti-GBM disease.


“bad cough”


61yo African American female w/hx of HTN presenting with 1mo of persistent cough productive of green-yellow sputum, noticed streaks of blood for the past 5 days. She came to the ED today because she has been feeling increasingly fatigued. She reports subjective fevers at the onset of symptoms which has resolved. She denies shortness of breath, chest pain, chills, night sweats. She sought medical care for this problem 2wk ago and was treated with amoxicillin and a cough suppressant. She recalls a coworker was ill one month ago. She is US-born, had a negative PPD in the past and has no known exposures to tuberculosis.

Of note, the patient reports her urine had a foamy appearance and has been darker in color beginning 3 weeks ago, but this had resolved. She denied dysuria, or frank hematuria.


  • HTN
  • Asthma – last required medications >30yrs ago


  • None


  • Non-contributory


  • No t/e/d
  • Works as librarian


  • benazepril
  • amlodipine
  • amoxicillin
  • promethazine


  • NKDA

Physical Exam:

VS: T 99.4 HR 97 BP 132/60 RR 20 O2 92%
Gen: Well-appearing, pleasant, speaking in complete sentences
HEENT: PERRL, MMM no lesions, no cervical lymphadenopathy
CV: RRR, normal S1/S2, no murmur appreciated
Lungs: Crackles in posterior: right middle/inferior and left inferior fields, no wheezing, no dullness to percussion
Abd: +BS, soft, non-tender, no CVAT
Ext: Warm, well-perfused, 2+ peripheral pulses, 1+ pitting edema to knee
Skin: No lesions on exposed skin
Neuro: AAO


  • CBC: 12.3/6.7/19.8/52.3 (S: 94, B: 1, L: 4, M: 1, MCV: 92.3); baseline Hb/Hct (1/11/2012) 13.4
  • BMP: 136/3.6/101/25/46/3.43/126; baseline creatinine (1/11/2012) 1.18
  • UA: brown, trace LE, – nitrites, 2+ protein, 81 RBC



  • Right mid-lung zone consolidation is present, suggests pneumonia if acute.
  • Mild asymmetric right parenchymal increased density is seen diffusely as well.


65AAF w/hx HTN presents with persistent productive cough, recently with hemoptysis.

# Cough: Symptoms and physical findings of abnormal breath sounds (crackles, though no strict consolidation) concerning for community-acquired pneumonia. Addition of hemoptysis raises concern for TB, particularly when taking into consideration the duration of cough and presence of constitutional symptoms. CBC shows leukocytosis with left shift, CXR with right mid/lower lob infiltrates consistent with pneumonia. Recommend admission and isolation to rule out TB, start empiric therapy for community acquired pneumonia with ceftriaxone, azithromycin. Obtain induced sputum samples for culture, AFB smear and culture.

# Abnormal urine: Patient describes changes in urine suggestive of proteinuria and hematuria. Acuity of onset and apparent spontaneous resolution suggests a chronic kidney injury 2/2 hypertension is unlikely. Absence of dysuria, or tenderness (suprapubic, costovertebral) suggests complicated UTI unlikely. Urinalysis notable for 2+ protein and significant RBC’s, possible nephritic syndrome. In the setting of hemoptysis, this raises concern for anti-GBM disease vs. vasculitis.

# Anemia: Normocytic anemia. No evidence of acute, life-threatening hemorrhage as patient is currently hemodynamically stable. Possible sites of blood loss include alveoli, glomeruli. Given that patient sought care today for worsening fatigue, will monitor hemoglobin closely and consider transfusion. Obtain iron studies.

# HTN: BP stable, hold home medications.

Interval History:

The patient was admitted for management of community-acquired pneumonia and isolation to rule out TB. Empiric therapy with CTX + azithromycin was continued. On HOD1, the patient was transfused two units of PRBC’s. On HOD2, the patient underwent CT chest/abdomen/pelvis due to worsening respiratory status despite antimicrobial therapy. On HOD3, the patient went into atrial fibrillation with RVR which was converted to sinus rhythm with metoprolol 5mg IV x3. On HOD5, nephrology consult recommended starting steroid therapy, plasmapheresis and obtaining a renal biopsy, however the biopsy was delayed due to worsening respiratory status.

Interval Labs:

  • Iron studies: Fe 8, TIBC 203, Ferritin 468, haptoglobin 333, retics 2.7
  • Inflammatory markers: ESR 120, CRP 34
  • Micro: BCx NGTD, RCx moderate Candida, sputum AFB smear negative x3
  • LFT: AST 34, ALT 29, ALP 52, protein 6.3, albumin 2.4, T.bil 0.8, D.bil 0.2
  • Quant-gold: negative
  • Anti-GBM 1.2 (nl <1.0)
  • p-ANCA: positive 1:640, [ELISA pending]
  • ANA: positive 1:320, speckled
  • HIV: negative

Interval Imaging:

CT Chest

  • Diffuse right lung, tree and bud opacities, ground-glass opacities and areas of confluence with scattered air bronchograms. Less severe similar pattern in the left lung as well particular at the base.
  • Right paratracheal, subcarinal and perihilar LAD.
  • Findings concerning for primary TB in the right clinical setting. DDx nonspecific bacterial PNA and fungal PNA.

CT Abdomen/Pelvis

  • Mild nonspecific R > L perinephric stranding.

Interval Assessment/Plan:

# Acute respiratory failure: Unlikely simple CA-PNA given worsening status while on appropriate antibiotic therapy. Active tuberculosis possible given history of chronic productive cough with hemoptysis, constitutional symptoms and imaging findings. IGRA’s of limited utility in diagnosis of active disease, further, while three negative sputum AFB smears decreases the likelihood of TB, additional testing with NAAT and culture is required. Another possibility is a vasculitic process given concomitant hematuria and acute renal failure, with respiratory symptoms now 2/2 alveolar hemorrhage. This was evaluated with ANCA assay which was positive for p-ANCA with high titer. This is often suggestive of primary vasculitis (in this case likely microscopic polyangiitis vs. Churg-Strauss), however ELISA for target antigen is of particular importance as p-ANCA with specificity for antigens other than MPO can be associated with another condition on the differential: Goodpasture’s syndrome. This patient was found to have elevated anti-GBM antibodies which are highly suggestive of Goodpasture’s syndrome, and can be associated with ANCA-positivity (often suggesting a poorer prognosis with decreased likelihood of recovery of renal function).1

# Acute kidney injury: The patient had significant elevation of serum creatinine compared to last-recorded baseline. She also described darkening and foamy appearance of urine 3 weeks prior to admission, suggestive of proteinuria/hematuria of relatively acute onset. This was supported by urinalysis findings of protein and RBC’s (with casts). Given presence of anti-GBM antibodies, high specificity of such findings, and correlation with glomerulonephritis with evidence of pulmonary alveolar hemorrhage, this appears to be the most likely cause at this time. Definitive diagnosis with renal biopsy to be obtained following stabilization of respiratory status. Patient will be started on plasmapheresis and immunosuppressive therapy (corticosteroids, cyclophosphamide).

# Normocytic Anemia: Likely combination of acute blood loss (2/2 hematuria, pulmonary alveolar hemorrhage) and chronic disease. Normocytic anemia with some reticulocytosis suggestive of acute blood loss, however iron studies with low Fe, TIBC and elevated ferritin suggest chronic disease as an associated factor.

Differential Diagnosis of Hemoptysis: 2, 3

A System for Hemoptysis

A System for the Diagnosis of Tuberculosis: 4, 5

A System for the Diagnosis of Tuberculosis


A System for Vasculitides: 8, 9

A System for Vasculitidies


Vasculitis Mimics: 9

Vasculitis Mimics


Interpretation of antineutrophil cytoplasmic autoantibodies (ANCA): 10

Pattern Target Associated vasculitis Other diseases
  • Granulomatosis with polangiitis (Wegener’s)
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
  • Microscopic polyangiitis
  • Pauci-immune glomerulonephritis
C-ANCA (atypical) BPIMPO
  • IBD
  • Cystic fibrosis


  • Microscopic polyangiitis
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
  • Pauci-immune glomerulonephritis
  • Autoimmune hepatitis
  • IBD, PSC
  • SLE, RA
  • Drugs
  • Infection (HIV, fungal)

Differential Diagnosis of Anemias: 11

A System for Anemias


  1. Levy, J. B., Hammad, T., Coulthart, A., Dougan, T., & Pusey, C. D. (2004). Clinical features and outcome of patients with both ANCA and anti-GBM antibodies. Kidney international, 66(4), 1535–1540. doi:10.1111/j.1523-1755.2004.00917.x
  2. Bidwell, J. L., & Pachner, R. W. (2005). Hemoptysis: diagnosis and management. American family physician, 72(7), 1253–1260.
  3. Hirshberg, B., Biran, I., Glazer, M., & Kramer, M. R. (1997). Hemoptysis: etiology, evaluation, and outcome in a tertiary referral hospital. Chest, 112(2), 440–444. doi:10.1378/chest.112.2.440
  4. Campbell, I. A., & Bah-Sow, O. (2006). Pulmonary tuberculosis: diagnosis and treatment. BMJ (Clinical research ed.), 332(7551), 1194–1197. doi:10.1136/bmj.332.7551.1194
  5. Zumla, A., Raviglione, M., Hafner, R., & Reyn, von, C. F. (2013). Tuberculosis. The New England journal of medicine, 368(8), 745–755. doi:10.1056/NEJMra1200894
  6. Diagnostic Standards and Classification of Tuberculosis in Adults and Children. American journal of respiratory and critical care medicine. doi:10.1164/ajrccm.161.4.16141
  7. Laraque, F., Griggs, A., Slopen, M., & Munsiff, S. S. (2009). Performance of nucleic acid amplification tests for diagnosis of tuberculosis in a large urban setting. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 49(1), 46–54. doi:10.1086/599037
  8. Gross, W. L., Trabandt, A., & Reinhold-Keller, E. (2000). Diagnosis and evaluation of vasculitis. Rheumatology (Oxford, England), 39(3), 245–252.
  9. Suresh, E. (2006). Diagnostic approach to patients with suspected vasculitis. Postgraduate medical journal, 82(970), 483–488. doi:10.1136/pgmj.2005.042648
  10. Rus, V., & Handwerger, B. S. (2000). Clinical value of antineutrophil cytoplasmic antibodies. Current rheumatology reports, 2(5), 383–389.
  11. Goljan, E. (2011). Pathology. Philadelphia, PA: Mosby/Elsevier.