Necrotizing Fasciitis & Septic Shock

1. Necrotizing Fasciitis & Septic Shock Rapid identification and rapid treatment is essential for recovery from this aggressive disease.

2. Is is new??? NO... • Hippocrates in the 5th century BC noted it • known as malignant ulcer, gangrenous ulcer putrid ulcer, and hospital gangrene in the 18th century • in 1871 after the Civil War was called hospital gangrene by a war surgeon • in 1924 called hemolytic streptococcal gangrene • in 1952 called “necrotizing fasciitis”

3. Is there an epidemic? • “killer bug”, “flesh eating bacteria” in the media • 1989 toxic shock syndrome and strep A necrotizing fasciitis reported • 1990-1992 estimated 10,000-15,000 strep A infections with 5% of patients developing necrotizing fasciitis • stable numbers in Wales and England • SO is it just media interest?

4. What causes it? • group A streptococcus bacteria • but often polymicrobial • anaerobes and aerobic bacteria present • prediposing factors • IV drug use, immunosuppression, trauma • diabetes • obesity • atherosclerosis • alcoholism

5. What bugs cause it? • mainly virulent group A beta hemolytic streptococcus • enterobacteriaceae • anaerobes include: • bacteroides fragilis • peptostreptococcus • clostridium species • aerobes include: • staph aureus • escherichia coli

6. Another cause • third type • caused by the marine vibrios(gram negative rods) • Vibrio vulnificus, Vibrio parahemolyticus, Vibrio damsela, Vibrio alginolyticus • puncture wound from fish, cut or insect bite exposed to sea water, shellfish or fish in tropical water • synthesize an extracellular toxin

7. toxins=host releases cytokines, including interleukin-2, tumor necrosis factor and gamma-interferon. resulting in shock substances cause vascular thrombosis and ischemic gangrene tissue is consumed at 1 inch per hour innoculation from subcutaneous tissue hematogenous spread from distant site ie., strep throat found in post op complications of fecal contaminated wound shock & multi system organ failure, ARDS Why is it so aggressive?

8. incubation- 1-7 days onset - acute pain - severe skin- cellulitis like eventually becoming blistered with sero-sanguinous fluid exudate-dishwater pus gas formation deep tissue necrosis low grade fever sometimes cool (cold sepsis) tachycardia increased WBC shift to left hematocrit decreased ABG- metabolic acidosis increased CPK hypocalcemia from fat necrosis Labs & Symptoms

9. Distinguishing between cellulitis and necrotizing fasciitis • cellulitis is red, hot, tender area of skin • streptococcal necrotizing fasciitis is diffuse swelling followed by appearance of bullous lesions filled with fluid in 30% of cases • severe systemic toxicity, and pain out of proportion to the degree of skin involvement • leakage into perineum results in anerobic Fournier’s gangrene of the male genitals

10. Diagnosis • gram stain, blood cx • elevated serum creatine kinase(CPK) • CT and MRI in advanced cases • surgical biopsy • decreased mortality rate for surgical intervention prior to 24 hrs. **high index of suspicion is necessary and should be included in differential diagnosis whenever patient looks acutely ill or toxic.

11. Treatment • surgical debridement • possible amputation • antibiotics • penicillin • clindamycin • fluids & pressors for septic symptoms • hyperbaric oxygen therapy • immunoglobulin

12. Why Immunoglobulin? • an attempt to reduce hyperproliferation of T cells • inhibit production of tumor necrosis factor

13. Prognosis • aggressive treatment- mortality 30% • delayed treatment - mortality 92% • patients with predisposing factors mortality 80% • ineffective debridement or repeated surgical interventions mortality 83% • death caused by sepsis and multi system organ failure.

14. reports of association in healthy individuals because of billions of instances where medication is taken question if cause and effect or correlation however-advocate no use in soft tissue inflammation if an infection don’t give ibuprofen to patients with chicken pox NSAIDS & Necrotizing Fasciitis

15. NSAIDS working by dampening inflammation response inflammation response works by: macrophages produce tumor necrosis factor TNF reaches brainstem brain produces prostoglandins prostoglandins produce fever they tell macrophages to stop producing TNF NSAIDS block production of prostaglandin and TNF is not turned off therefore, NSAIDS mask clinical symptoms overproduction of TNF permits rapid spread of bacteria NSAIDS MASK Symptoms

16. Septic Shock • bacteremia • endotoxins • hypothalmus and fever • interleukins • TNF activates coagulation cascade, tissue repair • produce vasodilation, edema, leukocytosis, coagulation creating hypotension • platelet activation factor • decreased coronary blood flow, pulmonary edema, decreased renal perfusion, decreased CO

17. Septic Shock • all leading to: • hypoxia • oliguria • metabolic failure • acidosis • organ dysfunction • multi organ system failure