Author: Jamie Santistevan, MD (ED Quality and Administrative Fellow, University of Wisconsin, @jamie_rae_EMdoc) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital)

A wide range of benign and dangerous pathology can present with a rash. It is wise to develop a systematic approach to rashes in the ED, one that helps you recognize the deadly causes of rash while narrowing the differential diagnosis.

Key elements from the history include the distribution and progression of the skin lesions, recent exposures (sick contacts, foreign travel, sexual history and vaccination status), and any new medications. On physical exam, pay specific attention to vital signs. A rash associated with fever or hypotension should make you worry about potentially deadly diagnoses. Perform a careful physical exam, including undressing the patient to fully examine the trunk and the extremities as well as the palms, soles and mucous membranes. Touch the skin with a gloved hand to determine if the lesions are flat or raised and press on lesions to see whether they blanch. Rub erythematous skin to see if it sloughs. Historical and physical “red flags” in a patient with an unknown rash include:[1]

Fever

Toxic appearance

Hypotension

Mucosal lesions

Severe pain

Very old or young age

Immunosuppressed

New medication

For an organized approach to dangerous rashes, this post will focus on four broad categories based on visual and tactile characteristics:[2]

Petechial/Purpuric

Erythematous

Maculopapular

Vesiculobullous

Next, rashes in each category will be further categorized based on clinical features such as the presence or absence of fever. This post will focus on life threatening causes of rash, but you may notice some benign etiologies in the flow diagrams pictured.

Petechial/purpuric rashes

Petechiae are small, red lesions caused when capillaries leak blood into the skin. They do not blanch when pressure is applied and usually begin on the dependent areas of the body, such as the legs. Petechiae larger than 0.5 cm are purpura. Sometimes these lesions will be raised (palpable). Palpable petechiae and purpura are a result of either perivascular inflammation (vasculitis) or infection. Non-palpable petechiae usually occur in low platelet states such as ITP and DIC.

There are two defining features that help narrow the diagnosis for patients with a petechial rash. The most important is whether or not the patient is febrile or toxic appearing. To further narrow the diagnosis, ask yourself, is the rash palpable or flat?

Approach to the petechial/purpuric rash[2]

Febrile & Palpable: Patients with a petechial rash plus fever or toxic appearance should be considered sick because the rashes in this category are life threatening. In fact, fever plus petechial/purpuric rash equals meningococcemia until proven otherwise and the patient should be placed on respiratory and contact isolation immediately.

Meningococcemia and meningococcal meningitis: are caused by Neisseria meningitidis, an encapsulated gram-negative diplococcus. Meningococcemia is disseminated infection whereas meningitis is infection of the CNS. Untreated, both are fatal and even with treatment mortality remains between 10-20%.[1] Patients present with fever, chills, malaise, myalgias, headaches, nausea, and vomiting. The rash is initially erythematous, maculopapular and appears first on the wrist and ankles, then becomes palpable petechiae, mimicking Rocky Mountain spotted fever. The rash quickly spreads to the rest of the body coalescing into palpable purpura. Diagnosis is confirmed by positive cultures of the skin, blood or CSF. Treatment should begin immediately with ceftriaxone if suspecting this disease. Vancomycin should be added to cover resistant strep pneumoniae. Prophylaxis is necessary for anyone potentially exposed to respiratory secretions with Rifampin, Ciprofloxacin or Ceftriaxone.

Rocky Mountain spotted fever (RMSF): is a tick-borne illness caused by Rickettsia rickettsii. Mortality exceeds 30% and increases when untreated or when treatment is delayed. The skin lesions begin as a maculopapular rash on wrists and ankles before becoming palpable petechiae and then spreads to the rest of the body. Patients are febrile and toxic appearing and often have a history of travel to southeastern or south central US. Patients complain of fever, headaches, myalgias, and malaise. Calf and abdominal pain is also common. A patient with a history of travel to an endemic area between April to September who presents with fever, headaches, and a rash should be treated for RMSF.[2] Treatment is with doxycycline in all non-pregnant patients, even children.[3]

Endocarditis: is an infection of the heart valves commonly caused by streptococcus viridans or staphylococcus aureus. Patients present with vague constitutional symptoms that mimic other common infections. Symptoms include fever, malaise, fatigue and a new heart murmur. Skin findings include palpable petechiae, splinter hemorrhages (nail bed lesions), Janeway lesions (painless, macular spots on the palms and soles) and Osler’s nodes (painful, purple nodules on the pads of the finger and toes). Diagnosis is confirmed by finding valvular vegetations on ultrasound and positive blood cultures. If suspecting endocarditis, obtain at least three sets of blood cultures.

Skin Findings in Endocarditis

Disseminated gonococcal infection: is caused by widespread infection with Neisseria gonorrhoeae. It typically causes urethritis and cervicitis but can also cause pharyngitis, proctitis, and conjunctivitis. If untreated, the infection can disseminate, occurring in about 3% of patients.[4] Systemic infection can lead to septic arthritis alone without a rash, or the triad of tenosynovitis, polyarthritis and rash.[5] Patients generally complain of fever, chills, arthralgias, and malaise. The rash consists of few skin lesions only, usually on the distal extremities, and may be missed. The lesions begin as petechial macules which progress to form papules and pustules as microabscesses form around embolized bacteria. They later develop a necrotic center. Diagnosis is made with positive cultures of blood, cervical or urethral secretions or skin lesions. Cultures of synovial fluid may also be positive in the case of septic arthritis. Patient should be tested for other sexually transmitted infections. Treatment is with IV Ceftriaxone for 7 days and add Azithromycin or Doxycycline to cover for Chlamydia.[4]

Skin Findings in Disseminated Gonorrhea

Henoch-Schonlein Purpura (HSP): is an autoimmune vasculitis that primarily affects children causing palpable purpura, GI hemorrhage and nephritis. HSP is an acute, self-limited disease characterized by IgA and C3 deposition preceded by an infection or drug exposure. Patients usually present with palpable purpura on the legs and buttocks and complain of joint and abdominal pain. Some children will develop intussusception as a complication and may appear toxic. Nephritis (hematuria and proteinuria) occurs in about 40% of patients, but only 1% will develop end-stage renal disease.[6] Most patients require admission and consultation with a nephrologist, and treatment is with corticosteroids and/or IVIG.

Febrile & Nonpalpable: Patients in this category are also likely to have a life-threatening diagnosis. Again, beware fever plus petechial rash!

Thrombotic Thrombocytopenic Purpura (TTP): is a disease of abnormal platelet aggregation and activation leading to micro-thrombus formation, hemolysis and end organ damage. Consumption of platelets and subsequent thrombocytopenia leads to a nonpalpable, petechial rash. The classic pentad is fever, thrombocytopenia, hemolytic anemia, renal failure, and altered mental status. However, the occurrence of the entire pentad is rare. The combination of thrombocytopenia plus hemolytic anemia is sufficient to suspect TTP and initiate treatment.[2,7] Unlike patients with DIC, patients with TTP will have normal PT, PTT and fibrin levels. Hematology consultation is warranted and treatment is with plasmapheresis. Without treatment mortality exceeds 90%.[2] Platelets should not be transfused because they will precipitate additional thrombus formation.

Disseminated Intravascular Coagulation (DIC): is a pathologic activation of the coagulation cascade leading to thrombin and fibrin clot formation, microvessel occlusion and end organ damage. This is followed by activation of the fibrinolytic system, including endogenous TPA, and subsequent bleeding. Patients are toxic appearing, often with fever and shock and develop a non-palpable petechial/purpuric rash. Laboratory findings include thrombocytopenia, increased PT and PTT, increased D-dimer and fibrin degradation products and decreased fibrinogen. Causes include pregnancy, massive trauma, transfusion reactions, or sepsis from Gram-negative bacteremia. Treat the underlying cause and reverse coagulopathy with FFP, platelets, cryoprecipitate and RBCs as needed. Patients require emergent hematologic consultation and ICU admission.

Purpura fulminans: is basically end-stage DIC. Patients develop shock and rapid subcutaneous hemorrhage often forming large purpura, hemorrhagic bullae, tissue necrosis, widespread bleeding from multiple sites and multi-organ failure.

Afebrile & Palpable: Patients with palpable petechiae or purpura who are not febrile nor toxic appearing are more likely to be suffering from some form of vasculitis.

Autoimmune vasculitis: is a disease in which the blood vessels come under attack of the immune system. Involvement of the small, cutaneous vessels leads to inflammation and capillary leakage producing palpable petechiae. There are many rheumatologic causes, including systemic lupus erythematosus (SLE), rheumatoid arthritis and Sjogren’s syndrome. Systemic vasculitides include Wegener’s granulomatosis, Churg-Strauss syndrome or microscopic polyangiitis. Other causes include chronic hepatitis C or B and medications such as penicillins, cephalosporins, sulfonamides, phenytoin and many more.

Afebrile & Nonpalpable: patients who are not febrile nor toxic appearing with a non-palpable petechial rash are likely suffering from isolated thrombocytopenia.

Idiopathic thrombocytopenic purpura (ITP): is a syndrome of isolated thrombocytopenia, which leads to bleeding diathesis. Most commonly, it occurs in children and is self-limited. Often, patients report a preceding viral illness. Rarely, intracranial hemorrhage can occur, often when platelets drop below 10 x 10 ^3/uL and happens in 0.5-1% of cases.[8] The rash of ITP develops as nonpalpable petechiae first in dependent areas such as the ankles or buttocks and can spread to the rest of the body. Patients may have petechiae of the face after coughing or vomiting, but are generally well appearing. Labs show thrombocytopenia but with normal coagulation studies. Treatment is with steroids.

Erythematous Rashes

Erythematous rashes are characterized by diffuse red skin from capillary congestion, mimicking a bad sunburn. These rashes can occur in a variety of inflammatory and infectious conditions, some of which can be rapidly fatal.

When evaluating the bright red patient, first try applying lateral pressure to the skin and see if it sloughs (Nikolsky’s sign). Then to further narrow the differential, consider wither or not the patient is febrile or toxic in appearance. Patients with an erythematous rash plus fever are also at high risk for having a deadly diagnosis.

Approach to the erythematous rash[2]

Febrile & Positive Nikolsky’s Sign: Patients in this group have the potential to be sick (Fever + Rash= Badness). But thy also have the potential to lose large amounts of skin which lead to fluid loss and electrolyte imbalances!

Staphylococcal Scalded Skin Syndrome (SSSS): occurs in children <5 years old and presents as a red rash with eventual sloughing of the epidermis. It is caused by certain strains of Staphylococcus aureus, which release an exfoliative toxin.[9] Symptoms include abrupt fever, diffuse, blanching skin erythema usually beginning on the neck, axillae and groin associated with skin tenderness. Mucous membranes are NOT involved. Patients may develop flaccid, loose bullae, but because epidermal cleavage is very superficial, these fragile bullae often are not intact at the time of presentation. If suspecting SSSS, cultures should be obtained from blood, urine, nasopharynx, umbilicus or any suspected focus of infection. Culture from fluid within any intact bullae will not be helpful as they contain sterile fluid. Treatment includes antistaphylococcal antibiotics (nafcillin or oxacillin), and Vancomycin in areas with a high prevalence of CA-MRSA. Patients will require diligent fluid and electrolyte management and wound care, generally in a burn unit.

Toxic Epidermal Necrolysis (TEN): TEN is a serious drug reaction commonly associated with sulfa drugs, anticonvulsants and antivirals, but other drugs may be involved. Other causes include Mycoplasma pneumonia and CMV infections.[10] TEN presents with sudden onset diffuse erythema with painful skin and eventual sloughing. Patients are usually febrile and toxic appearing. Skin cleavage is full thickness and occurs in massive large sheets and the mucous membranes will have painful, erosive and crusting lesions. Mortality is as high as 30-35%.[2] Treatment includes discontinuation of offending medication and IV fluid management and wound care, usually in a burn unit.

Febrile & Negative Nikolsky’s Sign: Patients in this group still have potential to be sick. Again, Fever + Rash = Badness. Although their skin is diffusely red, it will not slough with lateral pressure. Patients in this group can have eventual sloughing of the skin, but this is generally isolated to the hands and feet.

Toxic shock syndrome: TSS is a toxin-mediated illness, which occurs secondary to staph or strep infection. The majority of cases are due to methicillin-susceptible aureus (MSSA), but TSS due to methicillin-resistant S. aureus (MRSA) is increasing.[11] Classically TSS has been associated with high absorbent tampon use, however nasal packing, surgical wounds, postpartum infection and abscesses are other causes. Patients are febrile and toxic appearing and have hypotension refractory to fluids due to massive vasodilation. They have a diffuse erythematous rash, which eventually desquamates on the hands and feet. Treatment involves rapid removal of the infected material, IV antibiotics (Clindamycin and Vancomycin), and hemodynamic resuscitation with fluids often requiring vasoactive medications and ICU admission.

Kawasaki disease: is a vasculitis of unknown etiology that manifests in childhood. Patients present with diffuse red rash and fever with lymphadenopathy, strawberry tongue, conjunctivitis, edema of the extremities and peeling skin of the fingers and toes. Symptoms generally follow a nonspecific respiratory or GI illness. Other nonspecific symptoms can also occur including abdominal pain, joint pain, cough, vomiting, irritability or decreased PO intake. The worrisome complication is development of coronary artery aneurysm and myocardial infarction. Treatment is with high dose aspirin and IVIG.

Fever lasting at least five days without any other explanation combined with at least four of the five following criteria: Bilateral conjunctivitis Oral mucous membrane changes: red, fissured lips or strawberry tongue Peripheral extremity changes: erythema of palms or soles, edema of hands or feet, and periungual desquamation Polymorphous rash Cervical lymphadenopathy (at least one lymph node >1.5 cm in diameter)

Table 1: Diagnostic criteria for Kawasaki Disease[12]

Mucocutaneous Findings Kawasaki’s Disease

Afebrile & Negative Nikolsky Sign: Most rashes in this category are benign, including scombroid, medication side effect (Vancomycin, Niacin) and alcohol use, but there is one that you don’t want to miss!

Anaphylaxis: is a life threatening, generalized allergic reaction. The diagnosis should be highly suspected in an acute illness (developing over minutes to hours) involving the skin and mucosal tissue. The patient may have diffuse hives, pruritus or generalized skin flushing, swollen mucous membranes (lips, tongue, or uvula) and at least one of the following: respiratory compromise (dyspnea, wheezing, stridor, hypoxia) OR symptoms of hypoperfusion (hypotension, syncope, altered mental status). Patients may also have abdominal pain and vomiting as signs of GI tract involvement. Treatment is with prompt delivery of epinephrine, volume resuscitation and management of airway compromise or respiratory distress. Adjunctive agents (antihistamines and glucocorticoids) may be given, but should NOT be used as initial or sole treatment because they do not relieve respiratory tract obstruction, hypotension, or shock and are NOT life saving.[13]

Maculopapular Rashes

The most common types of rashes are maculopapular and they have the broadest differential diagnosis. They are usually seen with viral illnesses but can also be seen in certain bacterial infections, drug reactions, and immune-mediated syndromes. These rashes are characterized by a combination of two types of lesions: macules, which are flat, red splotches and papules, which are solid, raised lesions.

To narrow the differential, first ask yourself if this patient looks ill (febrile and toxic appearing). Then ask where the lesions are concentrated. Are they central (chest, abdomen or back) or peripheral (on the extremities)?

Approach to the maculopapular rash[2]

Febrile/Toxic & Central: This category generally encompasses viral exanthems, but Lyme disease should also be considered.

Lyme disease: is a tick-borne illness caused by Borrelia burgdorferi. Initially patients will have a large, targetoid lesion with central clearing at the site of the tick bite (erythema migrans). This initial lesion characterizes early, localized Lyme disease and is often found in the axilla, inguinal region, popliteal fossa, or at the belt line. It is not particularly painful, although the lesion may burn or itch, and is hot to the touch. Over the next few weeks, patients may develop systemic symptoms such as diffuse dermatitis, meningitis, fever, AV nodal blocks, arthralgias and myalgias (early disseminated Lyme disease). Late Lyme disease is typically associated with intermittent or persistent arthritis involving one or a few large joints and rare neurologic problems, primarily a subtle encephalopathy or polyneuropathy. Serologic testing for antibodies to burgdorferi should be seen as an adjunct to the clinical diagnosis and can neither establish nor exclude the diagnosis of Lyme disease. A positive or negative serologic test for Lyme disease simply changes the probability of actually having the disease. The use of serologic testing in populations with a low pre-test probability of Lyme disease results in a greater likelihood of false positive test results than true positive test results.[14] Doxycycline is the first line treatment in nonpregnant adults and children can be treated with amoxicillin. Patients with EM who reside in or have recently traveled to an endemic area should be treated for Lyme disease without serologic testing.

Serologic testing should be performed in patients who meet all of the following criteria: A recent history of having resided in or traveled to an area endemic for Lyme disease AND A risk factor for exposure to ticks AND Symptoms consistent with early disseminated disease or late Lyme disease (eg, meningitis, radiculopathy, mononeuritis, cranial nerve palsy, arthritis, carditis) Serologic testing for Lyme disease should NOT be performed in the following settings: In patients with an erythema migrans (EM) rash. For screening of asymptomatic patients living in endemic areas. For patients with non-specific symptoms only (eg, fatigue, myalgias/arthralgias)

Table 2: Indications for serologic testing for Lyme disease.[14]

Febrile/Toxic & Peripheral: Patients in this group can be further differentiated based on the presence or absence of characteristic targetoid lesions. It is important to note that patients who are febrile with peripheral maculopapular lesions that aren’t targetoid require emergent evaluation for meningococcemia and RMSF because both of these infections can begin with rashes that are in the maculopapular form before becoming petechial.

Erythema Multiforme (EM): is a condition that can either present as a self-limited rash (EM minor) or progress to include the mucous membranes and become life threatening (EM major). EM is an autoimmune process that follows infection with herpes simplex, mycoplasma or fungal diseases or drug exposure such as sulfa drugs, anticonvulsants and antibiotics.[15] EM minor presents as pruritic targetoid lesions on the extremities that then resolve in 1-2 weeks. Target lesions involve the palms, soles, dorsa of hands and feet, face, extensor surfaces of the extremities. EM minor requires only symptomatic treatment. EM major, on the other hand, is life threatening and is defined by mucous membrane involvement. EM major requires discontinuing the offending agent and fluid management, analgesics, wound care. Although often given, systemic steroids are of unproven benefit. Dermatology consult should be obtained and diagnosis is confirmed with skin biopsy.

Mucocutaneous findings in Erythema Multiforme

Stevens-Johnson Syndrome (SJS): is a mucocutaneous reaction triggered by medications characterized by detachment of the epidermis. SJS and TEN are in one disease continuum and are distinguished by severity. SJS involves <10% body surface area whereas TEN involves >30%. Patients with skin detachment of 10-30% are described as having “SJS/TEN overlap syndrome”.[16] There are two different ways that these patients present: either with macular (flat), targetoid lesions, which coalesce into large erythematous areas, OR with sudden, diffuse skin erythema and pain (as described above for TEN). The mucous membranes are involved patients have sloughing of large areas of skin. Patients are febrile and may complain of general malaise and other constitutional symptoms. Treatment involves discontinuation of the offending medication and optimizing fluid and electrolyte levels. The use of steroids is controversial.

Afebrile/Nontoxic: Patients with a maculopapular rash, whether central or peripheral, who are afebrile and well appearing are much less likely to have a life threatening diagnosis. Things to consider in these patients are drug reactions, pityriasis, scabies, eczema and psoriasis.

Vesiculobullous rashes

Vesiculobullous disorders are characterized by involvement of the dermal-epidermal junction causing fluid-filled lesions to form. Vesicles are small, <1cm, in size whereas bullae are larger than 1cm.

As with the other forms of rashes, you must first consider whether or not the patient has a fever or is toxic appearing, because this points to a deadly diagnosis. Next look at the distribution of the lesions: are they diffuse or concentrated to a single area of the body?

Approach to the vesiculobullous rash[2]

Febrile and Diffuse: As always, fever and rash should get your attention. In this category of vesucolobullous rashes, one disease is common in childhood and the other is basically extinct.

Varicella: is an infection primarily in children caused by Varicella-Zoster Virus (a herpesvirus) and is transmitted by aerosolized droplets from nasal secretions. The illness begins with a prodrome of fever, malaise and pharyngitis followed by a generalized vesicular rash. The rash appears in crops over several days. The lesions are initially macular, but evolve to become papular, vesicular and then eventually crust over. Lesions have an erythematous base and are present in a variety of stages at one time. Since the introduction of the varicella vaccine in 1995, the overall incidence of complications has declined. The most common complications include: soft tissue infections (42%), dehydration (11%) and neurologic complications such as encephalitis and Reye syndrome (9%).[17]

Smallpox: is a deadly disease caused by variola virus and is highly contagious. If you are seeing Smallpox in your emergency department, then we are all doomed, because the disease was pronounced eradicated in 1979 (one of the greatest achievements of modern medicine).[18] However, it is considered among the highest priority agents for biological weapons. Category A agents (including smallpox and anthrax) are of concern because they can be grown easily in large quantities, are resistant to destruction and well-suited for airborne dissemination allowing for infection of large numbers of people.[19] Smallpox presents with sudden onset high fever, headache, malaise and myalgias followed by the development of mucous membrane lesions and cutaneous rash. The rash begins as papules then develops into vesicles involving the face, proximal extremities and trunk then spreading distally. A key finding is skin lesions that are all at the same stage of development. Unvaccinated patients had a mortality rate of 30-50%, but vaccination decreased mortality rate to <1%.[20]

Febrile and localized: Ppatients with localized skin blistering can have a variety of diagnoses, but remember, if they have a fever or look sick, they probably are.

Necrotizing fasciitis: is a severe soft tissue infection characterized by tissue destruction, systemic toxicity and high morbidity and mortality. It can occur anywhere on the body but most commonly affects the extremities, perineum and genitalia and rarely arises on the trunk.[21] Early in the infection, skin findings may be mild. About one third of patients are misdiagnosed as having cellulitis.[22] Symptoms that should heighten your suspicion include fever, hypotension or toxic appearance, pain out of proportion to the skin findings, pain beyond the margins of erythema, indistinct margins of involvement and edema beyond the margins of erythema.[23] Later in the course of the disease more ominous signs can appear including skin bullae, skin necrosis and crepitus. Aggressive resuscitation and broad-spectrum antibiotics should be given, but definitive treatment is with immediate surgical debridement.

Hand foot and mouth (HFM) disease: is an illness affecting children, which presents with fever, oral vesicles and skin lesions. The oral vesicles are present on the buccal mucosa and tongue. On the skin, small blistering lesions are distributed on the hands and feet but also can occur on the buttocks and less commonly on the genitalia.[24] The infection is spread by contact with nasal discharge, saliva, blister fluid or stool. Coxsackie A is the etiologic agent. Management is primarily supportive consisting of oral analgesics and encouraging adequate fluid intake.

Mucocutaneous findings in Hand Foot and Mouth Disease

Afebrile and Diffuse: There are only two rashes in this category to consider and both are caused by auto-antibodies.

Bullous pemphigoid: is an autoimmune disease characterized by skin blisters and occurring in the elderly (age 65 and older). Patients present with prodrome phase lasting weeks to months characterized by eczematous, papular or urticarial skin lesions. Following this phase, tense blisters and bullae develop most commonly on the trunk, extremity flexures and axillary and inguinal folds. It is the tense quality of the bullae, which differentiate bullous pemphigoid from pemphigus vulgaris. Mucosal lesions are present in 10-30% of patients.[25] First line treatment is with topical or oral corticosteroids with the addition of other immunosuppressive therapies if needed.[26]

Pemphigus vulgaris: is also an autoimmune, blistering skin disease, but with an average age of onset between 40-60 years old.[27] In PV, bullae are flaccid and superficial and they coalesce to produce large areas of skin sloughing. Positive Nikolsky sign can also be elicited on physical exam and painful mucosal erosions will be present. Patients may require fluid and electrolyte control similar to burn care, requiring pain control, prevention of secondary infection, treatment with steroids and occasionally other immunosuppressant medications.

Afebrile and localized: The patients in this group generally do not have a life threatening diagnosis. Localized burns and contact dermatitis to are included in this category. But there is one important diagnosis to consider.

Herpes Zoster: also known as shingles, is caused by varicella-zoster virus and results from reactivation of latent VZV infection in the sensory nerve ganglia. The rash is characterized by a painful eruption of vesicular lesions that do not cross midline and are localized to a single dermatome (most commonly the thoracic and lumbar). Severe pain associated with the acute neuritis may actually precede the rash.[28] The rash begins as erythematous papules, which then progress into grouped vesicles on an erythematous base. There are a number of complications associated with herpes zoster in immunocompetent hosts, the most common of which is postherpetic neuralgia (about 8% of patients).[29] Other complications include bacterial skin infection (2.3%), uveitis or keratitis (1.6%), motor neuropathy (about 1%), meningitis (0.5%) and herpes zoster oticus (0.2%).[29] In immunocompromised patients, those with HIV, organ transplant recipients, those on chemotherapy or with congenital immunodeficiency, VZV can cause severe complications including cutaneous dissemination or end organ involvement. Cutaneous dissemination presents with generalized vesicular skin lesions affecting multiple dermatomes, which do cross the midline. Visceral organ involvement can present as pneumonia, hepatitis or VZV meningoencephalitis. Additionally, pregnant patients are at risk for congenital varicella syndrome (limb hypoplasia, skin lesions, neurologic abnormalities and structural eye damage). All patients with suspected VZV infection should be placed on droplet precautions.

Well that’s all for now. I hope you enjoyed this review on an approach to dangerous rashes. Remember, all patients with a rash who also have fever have the potential to have a life threatening condition, but further differentiating the causes can be done by categorizing the rash into one of four morphologies to help narrow your diagnosis.

References / Further Reading

Nguyen T and Freedman J. Dermatologic Emergencies: Diagnosing and Managing Life-Threatening Rashes. Emergency Medicine Practice. September 2002 volume 4 no 9. Murphy-Lavoie H and Leigh LeGros T. Emergent Diagnosis of the Unknown Rash: An Algorithmic Approach. Emergency Medicine Magazine. March 2010. emedmag.com American Academy of Pediatrics. Rocky Mountain Spotted Fever. In: Red Book: 2012 Report of the Committee on Infectious Diseases, 29th ed, Pickering LK. (Ed), American Academy of Pediatrics, Elk Grove Village, IL 2012. Goldenberg D and Sexton D. Disseminated gonococcal infection. This topic last updated: Jun 11, 2015. Accessed June 19, 2016 at https://www-uptodate-com.ezproxy.library.wisc.edu/contents/disseminated-gonococcal-infection?source=machineLearning&search=disseminated+gonorrhea&selectedTitle=1%7E150§ionRank=2&anchor=H6#H6 O’Brien JP, Goldenberg DL, Rice PA. Disseminated gonococcal infection: a prospective analysis of 49 patients and a review of pathophysiology and immune mechanisms. Medicine (Baltimore). 1983;62(6):395. Scheinfeld NS. Langman CB (Ed). Henoch Schonlein purpura. eMedicine. http://emedicine.medscape.com/article/984105-overview. Last updated Sept 28, 2016. Accessed June 20, 2016 George JN and Cuker A. Acquired TTP: Clinical manifestations and diagnosis. This topic last updated: Nov 25: 2015. Accessed July 7, 2016 at https://www-uptodate-com.ezproxy.library.wisc.edu/contents/acquired-ttp-clinical-manifestations-and-diagnosis?source=search_result&search=ttp&selectedTitle=1%7E150#H10434276 Kessler CM, and Nagalla S (ED). Immune Thrombocytopenic Purpura. eMedicine. http://emedicine.medscape.com/article/202158-overview Patel GK, Finlay AY. Staphylococcal scalded skin syndrome: diagnosis and management. American Journal of Clinical Dermatology. 2003;4(3):165 Mukasa Y, Craven N. Management of toxic epidermal necrolysis and related syndromes. Postgrad Med J. 2008;84(988):60-65. Durand G, Bes M, Meugnier H, Enright MC, Forey F, Liassine N, Wegner A, Kikuchi K, Lina G, Vandenesch F, Etienne J. Detection of new methicillin-resistant Staphylococcus aureus clones containing the toxic shock syndrome toxin 1 gene responsible for hospital- and community-acquired infections in France. Journal of Clinical Microbiology. 2006;44(3):847. Ayusawa M, Sonobe T, Uemura S, Ogawa S, Nakamura Y, Kiyosawa N, Ishii M, Harada K. Revision of diagnostic guidelines for Kawasaki disease (the 5th revised edition). Kawasaki Disease Research Committee. Pediatric Int. 2005;47(2):232. Campbell RL and Kelso JM. Anaphylaxis: Emergency treatment. This topic last updated Jun 07, 2016. 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