Necrotizing Fasciitis

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
Why is it so aggressive?

• toxinshost 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

8
Labs Symptoms

• 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

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
  Fourniers 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
NSAIDS Necrotizing Fasciitis

• 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

• dont give ibuprofen to patients with chicken pox

15
NSAIDS MASK Symptoms

• 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

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