Necrotizing Fasciitis: What I do and When William Obremskey MD MPH - - PowerPoint PPT Presentation

necrotizing fasciitis what i do and when william
SMART_READER_LITE
LIVE PREVIEW

Necrotizing Fasciitis: What I do and When William Obremskey MD MPH - - PowerPoint PPT Presentation

Necrotizing Fasciitis: What I do and When William Obremskey MD MPH MMHC Vanderbilt University Medical Center Disclosures Board SEFC OTA EBQVS Chair No Industry Conflicts Necrotizing Fasciitis Basem Attum, MD Addison K. May, MD,


slide-1
SLIDE 1

Necrotizing Fasciitis: What I do and When William Obremskey MD MPH MMHC

Vanderbilt University Medical Center

slide-2
SLIDE 2

Disclosures

  • Board SEFC
  • OTA EBQVS Chair
  • No Industry Conflicts
slide-3
SLIDE 3

Necrotizing Fasciitis

Basem Attum, MD Addison K. May, MD, FACS, FCCM John Schoenecker MD PhD Megan Mignemi MD William Obremskey, MD, MPH, MMHC

Vanderbilt University Medical Center

Created August 2017

slide-4
SLIDE 4

Necrotizing Fascitis

  • JAAOS Article

– Coming Soon

slide-5
SLIDE 5

William T Obremskey MD MPH MMHC Vanderbilt Orthopedic Trauma

“My Summer Vacation with Necrotizing Fasciitis”

slide-6
SLIDE 6
slide-7
SLIDE 7

Necrotizing Fasciitis

slide-8
SLIDE 8

Classification of SSTIs

1) superficial cellulitis 2) superficial abscesses 3) deep abscesses 4) necrotizing cellulitis 5) necrotizing fasciitis 6) myonecrosis

DEPTH

slide-9
SLIDE 9

“Many were attacked by the erysipelas all over the body…Flesh, sinews and bones fell away in large quantities…The flux which formed was not like pus but a different sort of putrefaction with a copius and varied flux…There were many deaths.”

Hippocrates, ~5th Century BC

slide-10
SLIDE 10

Frank Meleney ‘Infections of Skin and the Subcutaneous Tissue’ in 1930, published in the Bulletin of the New York Academy of Medicine.

  • Page 370 ‘Hemolytic streptococcus

gangrene’ which is a classic description of what we call ‘necrotizing fasciitis’

  • ‘We do not know the cause of this

unusually rapid development of necrosis in these cases; whether it is due to a peculiar quality of the infecting organisms or the hypersensitive state of the patient.’

slide-11
SLIDE 11

Pallin DJ : Annals of Emergency Med – 2008

Frequency of soft tissue infections increasing

slide-12
SLIDE 12

Goals and objectives

  • Necrotizing Fasciitis: What I do and When
  • 1) Diagnosis
  • 2) Operate Early
  • 3) Transfer if needed AFTER surgery
  • 4) Know Pathogens and AB selection
  • 5) Avoid Transmission
slide-13
SLIDE 13

Diagnosis of Necrotizing SSTI:

  • “Hard signs” for the presence of a necrotizing process:

1) presence of bullae 2) skin ecchymosis that precedes skin necrosis 3) presence of gas in tissues by exam or on radiographs 4) cutaneous anesthesia – Present in 7- 44% of cases

  • Other suggestive signs:

5) pain disproportionate to examination (Like Compartment Syndrome!!) 6) edema extending beyond skin erythema 7) systemic toxicity 8) progression of infection despite antibiotic therapy

slide-14
SLIDE 14

Risk Factors

+/- history of trauma Diabetes Obesity Vascular Disease IV drug use ETOH abuse Malnutrition Smoking Cardiac disease Steroid use Immunosuppression Cancer Age

slide-15
SLIDE 15

Risk Factors

  • 50% No Trauma
  • Diabetes present in 18-60%
  • > 50% Healthy Pts
slide-16
SLIDE 16

Mortality from necrotizing SSTI remains high

  • 67 retrospective reports since 1980
  • 3302 patients
  • Overall

– Amputation 33% – mortality – 23.5%

May AK. Surg Clin N Am. 2009; 89:403–420

Necrotizing skin and soft tissue infections

(SSTI)

slide-17
SLIDE 17

Most common in necrotizing SSTI

May AK. Surg Clin N Am. 2009. 89: 403–420

slide-18
SLIDE 18

Clinical Findings

Mild skin changes

slide-19
SLIDE 19

Clinical Findings

Mild skin changes Rapid progression

slide-20
SLIDE 20

Clinical Findings

Mild skin changes Rapid progression

slide-21
SLIDE 21

Clinical Findings

Mild skin changes Rapid progression

slide-22
SLIDE 22

Mild skin changes Rapid progression Blisters/Bullae Bruising Necrotic Skin

Clinical Findings

slide-23
SLIDE 23

Clinical Findings

Mild skin changes Rapid progression Blisters/Bullae Bruising Necrotic Skin Systemic changes: Hypotension Tachycardia AMS Pain

slide-24
SLIDE 24

Bullae, ecchymosis, loss of sensation

slide-25
SLIDE 25
slide-26
SLIDE 26
slide-27
SLIDE 27

Necrotizing Streptococcal Cellulitis

slide-28
SLIDE 28

Staphyloccal Toxic Shock

slide-29
SLIDE 29

Staphyloccal Toxic Shock

slide-30
SLIDE 30

Sensitivity (%) Specificity (%) Positive Predictive Value (%) Negative Predictive Value (%) Tense Edema 38 100 100 62 Gas on XR 39 95 88 62 Bullae 24 100 100 57 WBC > 14 x 109/L 81 76 77 80 Sodium < 135 mmol/L 75 100 100 77 Chloride < 95 mmol/L 30 100 100 55 BUN > 15 mg/dL 70 88 88 71

Objective Criteria to Distinguish Necrotizing from Non-necrotizing Infection

Wall DB et al. Am J Surg. 2000;179:17-21.

slide-31
SLIDE 31

31

31

Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) Score

Modified from Abrahamian FM, et al. Infect Dis Clin North Am. 2008;22:89-116; Wong CH, et al. Crit Care Med. 2004;32:1535-1541.

Laboratory parameter, units LRINEC points Laboratory parameter, units LRINEC points CRP, mg/L Sodium, mmol/L <150 ≥135 ≥150 4 <135 2 Total WBC, k/mm3 Creatinine, mg/dL <15 ≤1.6 15-25 1 >1.6 2 >25 2 Glucose, mg/dL Hb, g/dL ≤180 >13.5 >180 1 11–13.5 1 <11 2

slide-32
SLIDE 32

32

32

LRINEC Score: Corresponding Risk and Probability of Necrotizing SSTI

Finding abnormalities that make up the LRINEC score in patients with SSTI should increase suspicion of a necrotizing infection such that further observation and evaluation should be considered

Wong CH, et al. Crit Care Med. 2004;32:1535-1541. Abrahamian FM, et al. Infect Dis Clin North Am. 2008;22:89-116, vi.

LRINEC Score LRINEC score Risk category Probability of necrotizing SSTI ≤5 Low <50% 6–7 Intermediate 50%–75% ≥8 High >75%

10 20 30 40 50 60 70 80 90 100 110 1 2 3 4 5 6 7 8 9 10 11 12 13

LRINEC Score Probability of Necrotizing Fasciitis (%)

slide-33
SLIDE 33

Treatment

  • Fluid support
  • Ventilatory support
  • OPERATE EARLY

– Treat like CPS – ABOS Q’s – Recert exam – JAAOS – Coming soon

  • Antibiotics –

– multiple broad – Culture directed

  • Steroids - ? If “toxic”
slide-34
SLIDE 34
slide-35
SLIDE 35
slide-36
SLIDE 36

Clostridial Myonecrosis: 36 Hrs-Untreated Stab Wound

slide-37
SLIDE 37

Retrospective reviews identify several factors:

  • Time to first debridement
  • Inadequate first debridement
  • Extent of tissue involvement
  • Age > 60 years
  • Bacteremia
  • # Failed organs on admission
  • Elevated lactate

Independent Predictors for Mortality

Bosshardt TL. Arch.Surg. 1996;131:846-52 Elliott DC. Ann.Surg. 1996; 224:672-83 Bilton BD. Am.Surg. 1998; 64:397-400

slide-38
SLIDE 38

Treatment of necrotizing SSTI

  • Surgical debridement is mainstay of therapy
  • Aggressive debridement of all involved tissues
  • Average number of débridements 3-4 / patient
  • STSG or flap coverage most commonly used for

coverage of tissue defects

  • Studies suggest that early and aggressive surgical

therapy can reduce mortality to < 10%

Bosshardt TL. Arch.Surg. 1996;131:846-52 Elliott DC. Ann.Surg. 1996; 224:672-83 Gunter OL Surg. Infect. 2008; 9:443-450 Bilton BD. Am.Surg. 1998; 64:397-400

slide-39
SLIDE 39

Summary of surgical approach

  • HARD signs = necrotizing infection and require OR

– Bullae, cutaneous anesthesia, ecchymosis, tense edema, gas

  • Early and aggressive surgical debridement improves
  • utcome with achievable mortality of < 10%
  • Carefully consider factors that suggest necrotizing

process

  • Empiric surgical exploration if in doubt!
slide-40
SLIDE 40

How to Avoid Transmission?

slide-41
SLIDE 41

Index patient: 34 yo M LE nec fasc, taken to OR for debridement

48 h postop HCW 1 (resp therapist): + GAS pharyngitis

slide-42
SLIDE 42

Transmission through aerosols: Open wounds Secretions

slide-43
SLIDE 43

The best treatment places healthcare workers at risk Protect your oropharynx!

slide-44
SLIDE 44

Enjoy this!