1. 3 년차 이준배

2.  The emergency physician is more likely to encounter the life-threatening rashes INTRODUCTION

3. Differential Diagnosis And Terminology  Lesion a general term for a single, small area of skin disease  Rash the result of a more extensive process and generally involves many lesions  Transform primary lesions into secondary lesions various external factors such as scratching, healing, medications, and infections

5. Macule Papule Nodule Plaque Pustule Vesicle Bulla Petechiae Purpura Scales

7. Excoriation Lichenification ErosionUlcer Crust Atrophy

8. Head-To-Toe Examination  Head: patient’s scalp, conjunctiva, and oral mucosa  Neck: check for nuchal rigidity and other meningeal signs  Lymph nodes: Adenopathy  Lung: signs of bronchial constriction and edema, such as tachypnea, wheezing, and retractions

9. Head-To-Toe Examination  Cardiovascular: heart murmurs (endocarditis)  Abdominal: hepatosplenomegaly (drug hypersensitivity or viral illness)  Trunk and chest: Most viral exanthems start on the trunk and then spread to the extremities  Genital: Look in the mucosal areas of the anus and scrotum or vulva

10. Head-To-Toe Examination  Extremities: Palpable purpura and petechiae, The petechial rash of Rocky Mountain spotted fever spreads from the wrists and ankles  Joints: Arthralgias (sign of serum sickness)  Palms and soles: The classic target lesions of erythema multiforme are often found on the palms and soles  Nails and fingers: endocarditis (Splinter hemorrhages are found under the nails)

11. Diagnostic Decision Making

15. Maculopapular Rashes

16. Cutaneous Drug Reactions  Etiology The most commonly involved drugs are sulfonamides, penicillins, anticonvulsants, and nonsteroidal-anti- inflammatory drugs  Epidemiology 1%-3% of hospitalized patients and 1% of outpatients Most drug reactions are not serious The most severe reactions  the hypersensitivity syndrome, Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN)

17. Cutaneous Drug Reactions  Clinical Presentation Most cutaneous drug eruptions are morbilliform (meaning it looks like measles) or exanthematous

18. Cutaneous Drug Reactions  Diagnosis clinical

19. Cutaneous Drug Reactions

21.  Treatment Removing the drug If possible, all drug therapy should be stopped Routine use of corticosteroids is not indicated Oral antihistamines (diphenhydramine 25-50 mg PO q6h prn) may alleviate pruritus

22. Erythema Multiforme, Stevens-Johnson Syn drome, And Toxic Epidermal Necrolysis

23. Erythema Multiforme  Etiology EM is a common acute inflammatory disease that is usually self-limited in up to 50% of cases no etiologic agent can be identified

24. Erythema Multiforme

25.  Pathophysiology Not clearly understood  Epidemiology The true incidence of EM is not known  Morbidity And Mortality Rare If patients have ocular involvement, disabling and permanent visual sequelae may occur

26. Erythema Multiforme  Clinical Presentation Chief complaint : rash  malaise, fever, and arthralgias Target lesions are the hallmark of EM minor and major EM minor  mucous membrane involvement is absent  bullae and systemic symptoms do not develop  becomes EM major if a single mucous membrane is involved

27. Erythema Multiforme  Diagnosis Clinical classic target lesions if the patient looks toxic, has systemic complaints, or has abnormal vital signs, consider an alternative diagnosis

28. Erythema Multiforme  Management EM minor and major generally resolve without treatment in 2-3 weeks underlying infection should be treated Based on a review of the literature, there is no strong evidence that steroids are beneficial in EM minor or major systemic antihistamines and possibly analgesia

29. Erythema Multiforme  Disposition All patients diagnosed with EM minor or major can be safely discharged home Follow-up with the primary medical doctor or dermatologist Patients must return to the ED if there is rapid progression Follow-up with an ophthalmologist

30. Vesiculo-Bullous Rashes  Stevens-Johnson Syndrome (SJS),Toxic Epidermal Necrolysis (TEN), and pemphigus vulgaris (PV) Potentially life-threatening

31. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Etiology SJS and TEN are related to the use of certain medications

32. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)

33.  Pathophysiology Not completely understood  Epidemiology 0.4-1.2 cases per million per year

34. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Morbidity And Mortality The leading causes of death in TEN are sepsis from Staphylococcus aureus or Pseudomonas aeruginosa and fluid/electrolyte abnormalities The mortality rate  5%-10% for SJS  23%-30% for TEN  Higher in elderly

35. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Morbidity And Mortality Variables associated with a poor prognosis  increased age, extent of disease, extent of disease at time of transfer to a burn center, azotemia, multiple medication use, thrombocytopenia, and neutropenia Ophthalmologic sequelae  keratitis and corneal ulcerations, cornel scarring  blindness occur in 40%-50% of patients

36. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Clinical Presentation Rash, myalgias, fever, cough, or sore throat If a new drug is the cause, the prodrome usually begins within days of ingestion Skin lesions then develop suddenly, after 1-2 weeks of prodromal symptoms

37. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Clinical Presentation SJS  atypical target lesions or purpuric macules on the trunk  oropharyngeal lesions causing an erosive stomatitis  purulent conjunctivitis can lead to ocular erosions and blindness  SJS is a selflimited disease

38. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Clinical Presentation TEN  skin tenderness, pruritus, and pain  Onset is more rapid with repeated ingestion of the inciting agent  warm and tender erythema that first affects the face around the eyes, nose, and mouth  Lateral pressure on normal skin adjacent to a bullous lesion dislodges the epidermis (This is known as Nikolsky’s sign)

39. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Clinical Presentation The clinically distinguishing features of SJS and TEN is the degree of epidermal detachment  SJS involves mucosal erosions and less than 10% of epidermal detachment  TEN is defined by more than 30% of epidermal detachment  Between 10%-30% is considered the overlap zone of SJS and TEN

40. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Diagnosis Clinical Biopsy

41. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Treatment supportive removal of the offending agent replacement of fluid losses similar to burn victims analgesics all drugs started within the past month should be discontinued avoid Silvadene (silver sulfadiazine)

42. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Treatment the role of corticosteroids in SJS and TEN is highly controversial  Based on a review of the literature, there does not appear to be a consensus on the use of steroids in the treatment of SJS and TEN aseptic technique to avoid infection use of adhesive material, ointments, and creams should be avoided  Patients should be covered in a clean white sheet

43. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Treatment Debridement of necrotic tissue may be necessary Prophylactic antibiotic therapy is no longer given  Crossreactivity with the drug that initiated the TEN  the risk of selecting for resistant organisms

44. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Disposition Some patients diagnosed with SJS can be safelydischarged from the ED  1) the patient is non-toxic and has stable vital signs  2) the patient is tolerating oral fluids  3) the rash is not rapidly progressing  4) the patient is not immunocompromised  5) close follow-up is ensured Ophthalmologist f/u

45. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Disposition If these criteria are not met, patients with SJS should be admitted  24-hour observation  IV hydration  local skin care  nutritional support If there is any progression of lesions, transfer to a burn or intensive care unit should be considered

46. Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)  Disposition All patients suspected of having TEN should be admitted to an intensive care unit early transfer to a burn unit may be necessary  patients who were treated in a burn unit had lower rates of bacteremia, septicemia, and mortality if transfer was done early in the hospital course (less than seven days)

47. Pemphigus Vulgaris  Etiology rare but potentially lethal autoimmune disease Erosions and blistering of epithelial surfaces of the oral mucosa and skin  Epidemiology 4500 cases a year

48. Pemphigus Vulgaris  Pathophysiology circulating IgG autoantibodies that bind to the surface of the keratinocytes blisters form within in the epidermal layer of the skin

49. Pemphigus Vulgaris  Clinical Presentation Initially, blisters localize to the oral mucosa weeks to months before the skin blisters appear Over several weeks, non-pruritic skin blisters erupt over the rest of the body  head and trunk first Ruptured blisters develop into painful erosions that may become secondarily infected

50. Pemphigus Vulgaris  Clinical Presentation the mortality is approximately 10%-20% Most of the complications are due to infections Some patients can develop extensive fluid, protein, and electrolyte loss in association with extensive blistering

51. Pemphigus Vulgaris  Diagnosis Biopsy Immunofluorescence demonstrates IgG on the surface of keratinocytes emergency physician must act based on the clinical scenario

52. Pemphigus Vulgaris

53.  Treatment A low daily dose of prednisone (1 mg/kg/d) is the initial treatment Steroids are given until remission  no new blisters for one week Most cases of PV can be treated at home as long as the patient is not toxic-appearing and has only a few blisters

54. Pemphigus Vulgaris  Treatment Patients with extensive blisters, erosions of the skin, or who are toxic-looking should be admitted  monitored and treated for fluid or electrolyte imbalances and observed for potential infection  if there are overt signs of infection in the ED, start antibiotics immediately

55. Petechial/Purpuric Rashes

56. Meningococcemia  Neisseria meningitidis  colonization of the nasopharynx and then progress to systemic invasion bacteremia, sepsis, CNS invasion  Untreated, meningococcemia is invariably fatal Even with prompt treatment, the mortality rate is about 10%-20%

57. Meningococcemia  Clinical Presentation usually begins 3-4 days after exposure fever, chills, malaise, myalgias, headaches, nausea, and vomiting A rash is seen in more than 70% of people with meningococcemia  Petechiae, which develop on the wrist and ankles Look for signs of meningeal irritation—neck soreness or stiffness, photophobia, and headaches

58. Meningococcemia  Clinical Presentation septic shock, with acute renal failure, hypoxia, hypotension, multi-organ failure, and disseminated intravascular coagulopathy Early diagnosis and treatment are crucial  Biopsy and Gram stain

59. Meningococcemia

60.  Treatment Ceftriaxone (2 g q12h)  bacterial causes of purpuric disease  N. meningitidis, H. influenzae, and S. pneumoniae IV penicillin G (4 million units q4h) ampicillin (2 g q6h) In cases of severe penicillin allergy, IV chloramphenicol 4 g/d is indicated

61. Meningococcemia  Treatment Supportive care involving IV fluids is crucial in the patient with overt or incipient shock Close contacts, such as daycare center personnel, household members, or ED personnel  antibiotic prophylaxis  ciprofloxacin 500 mg PO  rifampin 600 mg q12h PO for two days or ceftriaxone 250 mg IM

62. Rocky Mountain Spotted Fever  Rickettsia rickettsii the bites of several species of ticks  The mortality rate for the untreated exceeds 30% Risk factors for mortality include delay in treatment and advanced age

63. Rocky Mountain Spotted Fever  Clinical Presentation The rash typically appears on the fourth day after the bite (range, 1-15 days)  erupting first on the wrist and ankles In severe cases of RMSF, multiple organs can be involved  CNS involvement may range from headaches (very common) to coma and even seizures  Disseminated intravascular coagulopathy is a predictor for mortality

64. Rocky Mountain Spotted Fever  Clinical Presentation The diagnosis of RMSF is empiric and is initially based on clinical and epidemiologic findings  triad of fever, rash, and a history of tick bite

65. Rocky Mountain Spotted Fever  Treatment Adults : doxycycline 100 mg BID PO or IV for seven days or for two days after temperature has normalized Young children  Chloramphenicol or doxycycline pregnant women  chloramphenicol 500 mg QID PO or IV for seven days or for two days after the temperature has normalized

66. Rocky Mountain Spotted Fever  Treatment The need for hospitalization depends on the severity of the illness Long-term sequelae  hearing loss, peripheral neuropathy, bladder and bowel incontinence, and cerebellar, vestibular, and motor dysfunction

67. Diffuse Erythematous Rashes  The differential diagnosis for diffuse erythematous rashes is broad  rapidly lethal the toxic shock syndromes (TSS) necrotizing fasciitis

68. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Etiology exotoxin-mediated diseases fever, rash, mucous membrane involvement, and hypotension  Pathophysiology colonization of toxin-producing strains of S. aureus

69. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Epidemiology In TSS  young, healthy women who used hyper-absorbent tampons vaginal colonization of toxin-producing strains of S. aureus increased patient and physician awareness, along with removal of these tampons from the market, has decreased the incidence of TSS in menstruating women

70. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Epidemiology In TSS  abscesses, bursitis,surgical wounds, indwelling foreign bodies such as nasal packing, and in post-partum patients In STSS  soft-tissue infection or minor skin trauma

71. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Morbidity And Mortality the morbidity and mortality are higher in STSS than TSS shock, renal failure, sepsis, and adult respiratory distress syndrome The overall mortality is 30%, and mortality rates can reach 80% in the elderly

72. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Clinical Presentation low-grade fever, malaise, myalgias, and vomiting Symptoms may occur within 2-3 days of tampon use, soft- tissue infection, or within a week of other inciting factors high fever, rash, and hypotension begins abruptly after the prodrome

73. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Clinical Presentation Hypotension develops rapidly, leading to tissue ischemia and subsequent multisystem involvement Rash is a characteristic feature of TSS  usually develops 1-3 days after other major symptoms If the patient is thrombocytopenic, purpura may develop

74. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Clinical Presentation A key distinguishing factor of STSS, present in 85% of patients, is extreme localized pain at the site of infection that is out of proportion to physical findings

75. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Diagnosis Clinical  TSS  STSS Soft-tissue infection may progress to necrotizing fasciitis or myositis

76. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)

77.  Treatment Aggressive resuscitation  vasopressors, inotropic agents, and mechanical ventilation In TSS, remove the source of staphylococcal colonization, such as vaginal tampons, nasal packing, or breast implants

78. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Treatment In TSS, antibiotic therapy with anti-staphylococcal coverage is recommended  oxacillin, nafcillin, cefoxitin, vancomycin, or clindamycin  decrease the rate of recurrence The use of steroids in TSS and STSS is controversial

79. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Treatment In STSS, antibiotic treatment is essential broad-spectrum antibiotic coverage  penicillin G or ampicillin, plus clindamycin, and possibly an aminoglycoside

80. Staphylococcal Toxic Shock Syndrome (TSS) and Streptococcal Toxic Shock Syndrome (STSS)  Disposition All patients who are suspected of having TSS or STSS should be admitted