When bacteria go bad

2,083 views

Published on

it's a presentation that includes general description , pathophysiology and management of Necrotising Fasciitis

Published in: Health & Medicine, Technology
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
2,083
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
154
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide
  • Necrotizing fasciitis has been recognized for centuries dating back to Hippocratus in the 5th century BC1. Necrotizing fasciitis was first described in 1871 by Confederate Army Surgeon Joseph Jones during the American civil war as ‘hospital gangrene’ and then by Meleny as ‘haemolytic streptococcal gangrene’4. In 1883,Fournier5 described a fulminating genital gangrene affecting healthy men, and named the process ‘idiopathic gangrene of the scrotum’2. In 1952, Wilson6 used the term necrotizing fasciitis to describe the same disease in other parts of the body.
  • The first and most important tool for early diagnosis of NSTIis to have a high index of suspicion. Unfortunately, true riskfactors for NSTI have not been identified. However, some conditionsappear to be more commonly associated with NSTI andare worth considering when dealing with any kind of soft-tissueinfection. These include injection drug use and chronic debilitatingcomorbidities (e.g., diabetes mellitus, immune suppression,and obesity) [8–10]. Patients that have any of these characteristicsand present with soft-tissue infection should beevaluated to confirm or rule out NSTI. Other than injectiondrug use, the precipitating factor of NSTI does not appearhelpful for establishing the likelihood of NSTI versus nonnecrotizingsoft-tissue infection
  • The first and most important tool for early diagnosis of NSTIis to have a high index of suspicion. Unfortunately, true riskfactors for NSTI have not been identified. However, some conditionsappear to be more commonly associated with NSTI andare worth considering when dealing with any kind of soft-tissueinfection. These include injection drug use and chronic debilitatingcomorbidities (e.g., diabetes mellitus, immune suppression,and obesity) [8–10]. Patients that have any of these characteristicsand present with soft-tissue infection should beevaluated to confirm or rule out NSTI. Other than injectiondrug use, the precipitating factor of NSTI does not appearhelpful for establishing the likelihood of NSTI versus nonnecrotizingsoft-tissue infection
  • No specific combination of bacterial species is either diagnosticof NSTI or found in all cases. A wide spectrum of organismsare commonly recovered (table 3). In a relatively recent series,approximately two-thirds of cases were polymicrobial, and onethirdwere monomicrobial, with the great majority of monomicrobialcases being a result of gram-positive cocci.
  • As this process progresses, occlusion of perforating nutrient vessels to the skin causes progressive skin ischemia.Initially a horizontal phase predominates with rapid spread through the fascia with extensive undermining of the apparently normal looking skin. As the condition evolves, ischemic necrosis of the skin ensues with gangrene of the subcutaneous fat, dermis and epidermis, manifesting progressively as bullae formation, ulcerationand skin necrosis
  • As this process progresses, occlusion of perforating nutrient vessels to the skin causes progressive skin ischemia.Initially a horizontal phase predominates with rapid spread through the fascia with extensive undermining of the apparently normal looking skin. As the condition evolves, ischemic necrosis of the skin ensues with gangrene of the subcutaneous fat, dermis and epidermis, manifesting progressively as bullae formation, ulcerationand skin necrosis
  • When bacteria go bad

    1. 1. Necrotising Fasciitis Dr Anang Pangeni 068.09.
    2. 2.  Recognized and reported for centuries Hippocrates in the 5th century BC Joseph Jones in 1871 : „hospital gangrene‟ Meleny , 1924 , Beijing outbreak “hemolytic streptococcal gangrene” Wilson , 1952, coined the term  infection, necrosis of the fascia and subcutaneous tissue with relative sparing of the underlying muscle
    3. 3. A rapidly progressive tissue infection characterized by extensive necrosis of the subcutaneous fat and fascia with secondary involvement of skin and rarely muscles Necrotizing fasciitis is a severe, insidiously advancing, soft-tissue infection characterized by widespread fascial necrosis
    4. 4.  High mortality  Reported incidence 6 to 76%  Studies* :Delay in diagnosis and consequent delayed debridement is often the cause A common admission in our facility.McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA. Determinants of mortality in necrotizing soft tissue infections. Ann Surg 1995; 221:558–563.Wong CH, Chang HC, Pasupathy S, et al. Necrotizing fasciitis: clinical presentation, microbiology and determinants of mortality. J Bone Joint SurgAm 2003; 85A:1454–1460.
    5. 5.  Common diagnosis in our ward Last 6 months data Total cases Male Female Mortality 51 30 21 1 Cultures sterile Monomicrobial Polymicrobial SNR 12 34 8 8 Commonest pathogen Staph aureus Others  Enterobacter / acinetobacter / proteus /e coli  Streptococcus interestingly not reported! Fallacies?
    6. 6.  Not fully understood, and in many cases no identifiable cause can be found. True risk factors for NSTI have not been identified Agreed : pre-existing conditions that render them susceptible to infection  injection drug use  chronic debilitating comorbidities (e.g.,diabetes mellitus, immune suppression,and obesity)
    7. 7.  Cases without a recognized precipitating factor are more likely to be caused by group A streptococcal infection, and community-acquired MRS infection**Miller LG, Perdreau-Remington F, Rieg G, et al. Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcusaureus in Los Angeles. N Engl J Med 2005; 352:1445–53.
    8. 8.  Diabetes Chronic disease  Age > 60  Intravenous drug misuse Drugs—for example, steroids  Peripheral vascular disease Malnutrition Immunosuppression  Renal failure  Underlying malignancy  Obesity
    9. 9.  Blunt or penetrating trauma  Minor trauma Soft tissue infections  Insect bite, Surgery  Pustule Intravenous drug use  Minor operations, Childbirth  Anorectal abscess, Burns  Instrumentation, Muscle injuries  Septic abortion,  Genitourinary infection
    10. 10.  Gram positive aerobic  Gram negative aerobic bacteria bacteria  Group A ß haemolytic  Escherichia coli streptoccoci  Pseudomonas aeruginosa  Group B streptococci  Proteus species  Enterococci  Serratia species  Coagulase negative  Anaerobic bacteria staphylococci  Bacteroides species  Staphylococcus aureus  Clostridium species  Bacillus species  Peptostreptococcus species  Fungi  Zygomycetes  Aspergillus  Candida  Other  Vibrio species
    11. 11.  Type 1  Polymicrobial (aerobic and anaerobic bacteria)  Occur most commonly after surgery or in individuals with diabetes and peripheral vascular disease.  Primarily includes 3 categories (locations) of infection  Diabetes Mellitus- infections of the feet  Cervical necrotizing fasciitis- infection of the neck  Fournier’s Gangrene- infection of the perineum
    12. 12.  Type 2  A monomicrobial infection caused primarily by group A streptococcus (GAS), although it is occasionally caused by community-associated methicillin-resistant Staphylococcus aureus (MRSA) Type 3 (not usually described)  Clostridial gas gangrene / Vibrio spp infection
    13. 13. Bacteria proliferate within the superficialfascia and elaborate enzymes and toxins Expression of bacterial enzymes such as hyaluronidase, which degrades the fascia Angiothrombotic microbial invasion and liquefactive necrosis of the superficial fascia.
    14. 14. Necrosis of the superficial fasciaPolymorphonuclear infiltration ofthe deep dermis and fascia Thrombosis and suppuration ofthe veins and arteries coursingthrough the fasciaMicroorganism proliferationwithin the destroyed fascia.
    15. 15. Occlusion of perforating nutrient vessels to the skin causes progressive skin ischemia. Initially, horizontal phase predominates with rapidspread through the fascia with extensive undermining of the apparently normal looking skin. Ischemic necrosis of the skin ensues with gangrene of the subcutaneous fat, dermis and epidermis, manifesting progressively as bullae formation, ulceration and skin necrosis
    16. 16. one microorganism produces the enzymes necessary to cause coagulation of the nutrient vessels  tissue oxygen tension fallstissue hypoxia allows growth of facultative anaerobes and microaerophilic organisms produce enzymes (eg, lecithinase, collagenase), which lead to digestion of fascial barriers, thus fueling the rapid extension of the infection
    17. 17.  Early on in the evolution, the disease is clinically indistinguishable from severe soft tissue infection such as cellulitis and erysipelas presenting with only pain, tenderness and warm skin. Blistering or bullae formation is rarely seen in erysipelas or cellulitis and should raise the suspicion of necrotizing soft tissue infection!!Unfortunately these ‘HARD SIGNS’ are late!
    18. 18.  Although the following features can occur with cellulitis, they may instead suggest necrotizing fasciitis:  Rapid progression  Poor therapeutic response  Blistering necrosis  Cyanosis  Extreme local tenderness  High temperature  Tachycardia  Hypotension  Altered level of consciousness
    19. 19.  Early findings  Late findings  Pain  Severe pain  Cellulitis  Skin discoloration (purple or  Pyrexia black)  Tachycardia  Blistering  Swelling  Haemorrhagic bullae  Induration  Crepitus  Skin anaesthesia  Discharge of “dishwater” fluid  Severe sepsis or SIRS  Multiorgan failure
    20. 20. Stage I Stage II Stage III Tenderness to Blister or bullae formation Hemorrhagic bullaepalpation(exending beyond (serous fluid)the apparent area of skin) Erythema Skin fluctuance Skin Anesthesia Swelling Skin induration Crepitus Warm to palpation Skin necrosis with dusky discoloration prgressing to frank gangrene
    21. 21. Laboraotry Risk Indicator for Necrotising fasciitis Variables 0 1 2 3 4 WCC /mm3 <15 15-25 >25 CRP (mg/L) <150 >150 Hb (g/dl) >13.5 11-13.5 <11 Na (mmol/L) >135 <135 Creatinine(mg/ <1.6 >1.6 dL) Glucose (g/dL) <180 >180 •PPV of 92% • NPV of 96%.Wong CH, Khin LW, Heng KS, Tan KC, Low CO., Journal of critical care medicine The LRINEC (Laboratory Risk Indicator for NecrotizingFasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections.epartment of Plastic Surgery, Singapore General Hospital, Singapore.
    22. 22.  Laboratory investigations  Leucocytosis  Acidosis  Altered coagulation profile  Hypoalbuminaemia  Abnormal renal function Plain radiography  Soft tissue gas CT/MRI  May delineate extent of disease  Soft tissue gas Incisional exploration or biopsy (can be done at bedside)  Histological confirmation of diagnosis  Tissue culture to identify pathogens and sensitivities
    23. 23.  Gray necrotic tissue Lack of bleeding Thrombosed vessels “Dishwater” pus, Non-contracting muscle Positive “finger test” result  characterized by lack of resistance to finger dissection in normally adherent tissues
    24. 24.  Preoperative resuscitation  Should be aggressive!  Surgical Wound excision  As soon as confirmed.  Some advocate surgery as a means for diagnosis  Clinical and laboratory findings are still not conclusive  Diagnosis of NSTI is still a possiblity  Aggressive Is Better!  Researches have clearly shown the impact of early and complete debridement on final outcome in patients with NSTI *  Earlier and Complete Vs Delayed or Incomplete excisionMcHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA. Determinants of mortality for necrotizing soft-tissue infections. Ann Surg 1995; 221:558–63; discussion 563–5Bilton BD, Zibari GB, McMillan RW, Aultman DF, Dunn G, McDonald JC. Aggressive surgical management of necrotizing fasciitis serves todecrease mortality: a retrospective study. Am Surg 1998; 64:397–400;discussion 400–1.
    25. 25.  Extent of Excision  Generous incision at outset  Increase as demanded by the nature of tissue beneath  Macroscopic findings are used as guide  Occasionally, amputation of a limb is necessary to achieve this goal and is encouraged if that is the case.  Healthy, viable, bleeding tissue should be present at the edges of the excision site
    26. 26.  We have not seen these! Advocated by different groups that argue for a decreased number of debridements and decreased mortality*  increases the normal oxygen saturation in the infected wounds by 1000-fold leading to  Bacteriocidal effect,  Improves neutrophil function,  Enhanced wound healing Results are contradictory! Where available  Should not jeopardize the standard therapy — adequate and timely debridements*Riseman JA, Zamboni WA, Curtis A, Graham DR, Konrad HR,Ross DS. Hyperbaric oxygen therapy for necrotizingfasciitis reduces mortality and the need for debridements. Surgery 1990; 108:847–50.Jallali N, Withey S, Butler PE. Hyperbaric oxygen as adjuvant therapy in the management of necrotizing fasciitis. Am JSurg 2005; 189:462–6.
    27. 27.  Defined as infections of any of the layers within the soft tissue compartment (dermis,subcutaneous tissue, superficial fascia, deep fascia, or muscle) that are associated with necrotizing changes. Different terms are used to define and classify STIs, leading to confusion when referring to infections that have common pathophysiological and clinical characteristics and, most importantly, share a common management strategy
    28. 28.  Necrotising fasciitis is potentially fatal condition and can affect any part of the body . The aetiology is not fully understood but most patients who develop necrotising fasciitis have pre- existing conditions that render them susceptible to infection Diagnosisis often delayed because of the paucity of symptoms and the unfamiliarity of the condition among clinicians
    29. 29.  Laboratory findings and other diagnostic tests may be useful adjuncts, but the diagnosis is still primarily a clinical one and a high index of suspicion is required Management should consist of immediate resuscitation, early surgical debridement, and administration of broad spectrum intravenous antibiotics. ‘Necrotising soft tissue infection’ can be used as a standard term to designate these infections, so as to help in correct data interpretation.

    ×