Approach to skin and soft tissue Infection.pptx

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1. Approach to skin and soft tissue Infection Presenter: Dr Abebe (ECCMR1) Moderator: Dr Nathan(Assistant professor in ECCM Pagume 2014 1

2. Course Outlines Introduction Types of skin and soft tissue infections Etiology,Pathogenesis of different skin and soft tissue infections Principles of management Dispostion 2

3. Introduction The skin is the largest organ of the body;with atotal area of 15% of body wt. It protects us from microbes;regulates body temperature and permits the sensation of touch,heat,and cold. It is composed of 3 layers; Epidermis Dermis and Subcutaneous tissues. 3

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5. Physiologic functions Protection Micro organisms thermal Chemical UV radiation Homeostatic Thermoregulatio Immunologic Synthetic function. Eg vit D,melanin 5

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7. Cellulitis and erysipelas Cellulitis accounts for approximately 1.3% of all ED visits . Cellulitis observed more frequently among middle-aged and elderly patients, whereas erysipelas is common among children and elderly patients. Majority involve either the lower or upper extremities . 10% of patients with cellulitis are hospitalized, and the majority are over age 64 years. 7

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9. Etiology G - positive bacteria(80%). MRSA is most common cause of skin and soft tissue infections. MRSA is likely to be the causative agent in purulent cellulitis. For nonpurulent cellulitis, β- hemolytic streptococcal infection . Gram-negative aerobic bacilli are the third most common etiology. Erysipelas is usually caused by β- hemolytic streptococci. 9

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11. PATHOPHYSIOLOGY Break in the skin such as fissure,cut , lacerations,insect bite or puncture wounds cause entry of bacteria into subcutaneous tissue. Deep inflammation of subcutaneous tissue from enzyme produced by bacteria. Most symptoms are secondary to a complex set of immune and inflammatory reactions . 11

12. CLINICAL FEATURES Cellulitis T ender , warm, erythematous ,swollen skin does not have a sharp demarcation from uninvolved skin . Lymphangitis and lymphadenopathy are seen occasionally but purely local inflammation is much more common. In cases of purulent cellulitis, exudate drains from the wound; an abscess may or may not subsequently form. 12

13. cont;d Systemic signs of fever, leukocytosis, and bacteremia are more typical in the immunosuppressed . Repeated infection may cause chronic changes and predispose patients to further attacks of cellulitis. 13

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15. Erysipelas The prodromal phase is usually abrupt, with fever, chills, malaise . Over the next 1 to 2 days, a small area of erythema with a burning sensation develops. Then affected skin has raised border that is “distinctly demarcated from the normal skin”. A classic description is a “butterfly” pattern over the face . 15

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17. cont;d “ Milian ear sign ” is a distinguishing feature of erysipelas. Lymphatic inflammatory changes and local lymphadenopathy are common . Purpura , bullae, and small areas of necrosis warrant a search for possible necrotizing soft tissue infections. On resolution of the infection, desquamation of the site often occurs. 17

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19. DIAGNOSIS The diagnosis of cellulitis and erysipelas is clinical. In mild infection, lab test are not recommended . Pts with drainable abscess should undergo I &D with culture. Areas with abscess formation have significantly higher yields . wound culture is recommend when the decision has been made to place the patient on antibiotics for purulent cellulitis . 19

20. Blood Cultures Blood cultures are positive in only 5% of cases. patients with systemic toxicity , extensive skin involvement, underlying comorbidities , immunodeficiency, immersion injuries , failed initial therapy. 20

21. Radiography Should be considered if osteomyelitis or necrotizing soft tissue infections are suspected . POCUS is useful to exclude occult abscess. Doppler U/S may be indicated to distinguish DVT from cellulitis. The most important diagnosis to exclude is necrotizing soft tissue infection. 21

22. Management Elevation of the affected area , helps drainage of edema. Incision and drainage of any abscess antibiotics treatment of underlying conditions. Treat predisposing conditions such as tinea pedis . 22

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24. Indications of MRSA coverage Diabetic Immunosuppressed Peripheral vascular disease History of IV drug abuse require hospitalization who have failed initial non-MRSA therapy previous history of or risks for MRSA who live in an area with a high prevalence of community-associated MRSA infections. 24

25. Surgical management Consider surgical consultation in patients with bullae, crepitus, pain out of proportion to examination, or rapidly progressive erythema with signs of systemic toxicity, because these signs and symptoms suggest necrotizing infection. 25

26. Follow up Admit patients with cellulitis or erysipelas and evidence of systemic toxicity and C omorbidities like DM, alcoholism, or immunosuppression . patients without systemic toxicity can be discharged to home with close follow-up in 2 to 3 days . Mark the patient’s skin along the perimeter of infection so healing can be determined at follow-up ; also aid the patient to evaluate worsening of infection. 26

27. NECROTIZING SOFT TISSUE INFECTIONS These infections are characterized clinically by fulminant,extensive tissue destruction, systemic signs of toxicity and high mortality . Terms to describe NSTI; necrotizing fasciitis, necrotizing soft tissue infection , or gas gangrene . It involves epidermis;dermis;subcutaneous tissue;fascia and muscle. 27

28. Risk factors Trauma,laceration ,recent surgery D iabetes mellitus, A lcoholism , P eripheral vascular disease , Heart disease, renal failure , HIV, cancer, NSAID use, decubitus ulcers, chronic skin infections, IV drug abuse, and immune system impairment. However , infections also occur in young and healthy individuals. 28

29. Epidemiology The incidence is increasing, but mortality has decreased in the USA from 25% to 10% over the past 20 years. Bacteremia is reported in 25% to 30% of cases and is a strong predictor of mortality. Other factors that increase mortality are age <1 year old or > 60 years old; IV drug use; comorbid conditions, and certain characteristics such as positive blood cultures, trunk or perineal involvement, infection related to peripheral vascular disease, and delayed time to diagnosis or treatment. 29

30. MICROBIOLOGY Type I polymicrobial infections include 55% to 75% of all NSTIs and a combination of gram-positive cocci , gram-negative rods, and anaerobes . Type II (20 to 30%) monomicrobial infections are mostly caused by group A Streptococcus. occur on an extremity who often has a history of trauma or a recent operative procedure at the site of the infection . Community-acquired MRSA is a cause of type II infection, particularly in IV drug abusers , athletes, and institutionalized patients. 30

31. cont;d type III infection . caused by Vibrio vulnificus This infection may occur in patients who have an apparently insignificant break in their skin in a seawater environment. Type IV Associated with fungal infections, primarily in immunocompromised patients. 31

32. pathogenesis The rapid necrotizing process typically begins with direct invasion of subcutaneous tissue from external trauma . Bacteria proliferate, invade subcutaneous tissue and deep fascia, and release exotoxins that lead to tissue ischemia, liquefaction necrosis, and systemic toxicity. Infection , which can spread as fast as 1 inch/h. 32

33. CLINICAL FEATURES Classic symptoms of are severe pain, anxiety, and diaphoresis. Pain often out of proportion to physical findings with tenderness beyond the area of erythema . Usually trauma or a break in the skin roughly 48 hours before onset of symptoms. Late in the course of the infection,bronze or brownish discoloration with a malodorous serosanguineous discharge, and bullae may be present . Systemic manifestations include a low-grade fever with tachycardia out of proportion to the fever . 33

34. P/E The painful area may demonstrate a brawny edema . crepitus caused by bacterial gas production may be present/50%/. >50% of pts present with erythema, tenderness, or marked edema beyond the area of redness . In fulminant NSTIs patients may have cardiovascular collapse due to release of bacterial toxins; cytokines, and may be confused, irritable, or have a rapid deterioration of mental status. 34

35. cont;d Marked edema may produce compartment syndrome requiring fasciotomy . Subcutaneous tissue may be firm and indurated so that underlying muscle groups cannot be palpated distinctly. With in 3 to 5 days from onset;skin breakdown with bullae and frank cutaneous gangrene can be seen. 35

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37. DIAGNOSIS C linical in combination with laboratory tests and imaging when the clinical picture is unclear. One or more “hard” signs of necrotizing fasciitis—crepitus, skin necrosis, bullae, hypotension, or gas on radiograph—are present in less than half of patients. laboratory abnormalities like laboratory risk indicator for necrotizing fasciitis (LRINEC score ) are helpful LRINEC score of ≥6 is associated with increased risk of necrotizing fasciitis but misses many cases and therefore should not be used in isolation for the diagnosis and management. 37

38. cont;d possible debridement early is being considered rather than waiting for confirmatory studies that may yield equivocal results. There is no single test or sign that can reliably confirm the early diagnosis of necrotizing fasciitis. The finger test has been advocated, which involves making a 2-cm incision . A positive test is lack of normal bleeding, or friable tissue to minimal finger pressure. However, its use has never been studied formally. 38

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41. Principles of management Immediate surgical intervention remain the cornerstone of successful management. Surgery is the gold standard for diagnosis and treatment ; include fasciotomy , debridement, and/or amputation . Mortality is high if debridement is delayed >24 hours . Antibiotics alone are not effective. fluid resuscitation immediately as well as transfusion of packed RBC as needed . Provide tetanus prophylaxis as indicated. 41

42. Factors associated with increased mortality; WBC greater than 30,000/ microL Creatinine greater than 2 mg/dl Age greater than 60 yrs Streptococcal toxic shock syndrome Clostridial infection Delay surgery more than 24 hrs Infection involving head;neck;thorax or abdomen 42

43. Toxic shock syndromes/TSS The main systemic,toxin mediated bacterial skin syndromes are: Streptococcal toxic shock syndrome Staphylococcal toxic shock Syndrome Staphylococcal Scalded syndrome These are caused by bacterial exotoxins known as super antigens. Systemic diseases result from immune system’s response to the toxins. 43

44. Streptococcal Toxic shock syndrome It is a clinical illness characterized by shock and multi organ failure. Streptococcal TSS consists of isolation of GAS from normal sterile body site togather with hypotension;tachycardia and evidence of multi organ failure such as; 1.ARDS 2.Coagulopathy 3.liver failure 4. renal failure Streptococcal TSS occurs most frequently in setting of severe soft tissue infection due to GAS(streptococcus pyogenes ). 44

45. Epidemiology Invasive infections associated with GAS TSS have been increasesd in frequency in USA. One third of pts with invasive GAS diseases developed TSS. The rate of TSS among pts with necrotizing fasciitis is approximately 50 %. 3.5 cases of invasive GAS per 100,000 persons with fatality rate 30 to 60%. 45

46. Risk factors GAS TSS occurs in all age groups. Most pts were either less than 1 yrs or greater than 60 yrs and had underlying disease such as cancer;renal failure;leukemia;severe burns and were receiving steroid therapy. Minor trauma Use of NSAID Recent surgery Viral infections Post partal state 46

47. Microbiology and pathogenesis GAS is aerobic gram positive coccus . Invasive GAS infection with M type isolates with exotoxin A and B. It causes capillary leak and tissue damage due to release of inflammatory cytokines induced by streptococcal toxins. Act as super antigens which causes release of exotoxins. 47

48. Clinical manifestations Shock-due to capillary leak and vasodilation. Most often associated with severe pain and tenderness signifying infection at site of trauma. Fever is common/hypothermia may be present in shock. Altered mental status in 50% of pts. Pain is often out of proportion to physical findings. At the site of minor trauma such as bruise;strained muscle;sprained ankle;pts may develop deep infections such as necrotizing fasciitis with in 24 to 72 hrs . 48

49. cont;d Clinical signs of soft tissue infections consists ; Localized swelling and erythema Ecchymoses and sloughing of skin Progression to necrotizing fascitis in 70 to 80% of cases. In 20% of cases influenza like illness such as; fever;chills ; myalgia;Nausea;Vomiting;diarrhea 49

50. Complications of GAS TSS Bacteremia ARDS 55% Renal failure Disseminated intravascular coagulation/DIC Waterhouse- Friderichsen syndrome 50

51. Staphylococcal Toxic Shock Syndrome/STSS It is life threatening systemic illness caused by S.aures exotoxins. The classic presentation is fever ,rash and hypotension often in patients who were previously healthy. Menses associated tampon use continues to remain arisk factor. 51

52. Risk factors Menstrual associated use of tampons Non menstrual cases occurs in 50 % includes: Surgical procedures like rhinoplasty,abortion Nasal packing Burns,osteomyelitis Injection drug use Postpartum state 52

53. pathogenesis S.aures exotoxins TSST1 53

54. Clinical manifestations Pts often have acute onset of fever,chills , malaise,myalgia . Diffuse blanching macular rash that is not pruritic and desquamation eventually occurs 7 to 14 days after onset. There may be nausea,vomiting or diarrhea. Patiens may have altered mental status. V/S show hypotension and fever. 54

55. Staphylococcal Scalded Syndrome/SSSS It is adesquamating skin disorder caused by exfoliating toxins produed by S.aures . S.aures produces epidermolytic toxin A or B w/c act proteases that target protein desmoglein 1 on epidermis. In this condition the skin changes resemble a scald. Erythema and tenderness are followed by the loosening of large areas of overlying epidermis. This is in contrast to toxic epidermal necrolysis , which is usually drug-induced. 55

56. Clinical features Common in age less than 5 yrs. Begins with minimal infection in extracutaneous foci. Diffuse erythema formation One or 2 days later extensive bullows lesions appear w/c easily broken allowing serous fluid to escape. There are high grade fever and malaise “ Nikolsky sign positive”. There is noticeable desquamation. 56

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58. Diagnosis GAS TSS Isolation of GAS from sterile sites( blood,CSF,pleural;wound ) ,hypotension and 2 of thefollowing : Renal dysfunction( Cr greater than or equal 2mg/dl Coagulopathy(thrombocytopenia or DIC Liver dysfunction(liver enzymes or greater than or equal to 2x ULN ARDS Erythematous macular rash;may desquamate Soft tissue necrosis 58

59. cont,d STSS should be considered in any pt presenting diffuse rash and hypotension. Dx made on the basis of clinical presentation. The characterstic rash often raises suspicion and ultimately aids Dx . Isolation of S.aures is not required for dx to be made. 59

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62. Management principles treatment of septic shock Large amount of IV fluid is necessary to maintain perfusion(10 to 20 L/day Vasopressors may be required Surgical debridement Early aggressive surgical intervention is critical in necrotizing fascitis or myonecrosis Antibiotic therapy Empiric antibiotic therapy should be started Vancomycin and Clindamycin for STSS. 62

63. Disposition Patients suspected TSS should be admitted to ICU. Pts with NSTIs associated Strept.TSS usually require surgical debridement. Children with mild SSSS may be considered out pt with PO medication. 63

64. Referrences Tintinalis 9 th edition Rosons 9 th edition Uptodate 21.1 Tropical Dermatology 64