3. Definition
Life-threatening bacterial soft tissue infection that spreads along soft tissue planes
rapidly.
Rapidly progressive inflammatory infection of the fascia, with secondary necrosis
of the subcutaneous tissues.
9. Pathophysiology
1) Bacteria inoculation
2) GAS-virulence factors
-polysaccharides capsule
-M-protein-impede phagocytosis
-enzymes- degrade host tissue
-toxins(strep pyrogenic exotoxin) - overstimulate immune systems
3) Spread from subcutaneous tissue along superficial and deep fascial plane
-facilitated by bacterial toxins
10. 4) Deep infection - vascular occlusion, ischaemia and tissue necrosis
-damage to superficial nerves-localized anaesthesia
5) Systemic infection
6) Facultative anaerobic organism grow
-dt polymorphonuclear leukocytes reduce in function under hypoxic wound
condition
-further lower the oxidation
-enabling anaerobic proliferation-accelerating disease progress
11.
12.
13. Clinical features
Symptoms :
Early : localized abscess/cellulitis with rapid progression
Minimal swelling
No trauma/discolouration
Late : severe pain
High fever, chills & rigors
Systemic toxicity ( fever, tachycardia, hypotension)
15. Stage 1 (Early stage)
Tenderness to palpation (extending beyond
the
apparent area of skin involvement)
Erythem
Swelling
Warm on palpation
Stage 2 (Intermediate)
Blister or bullae formation(serous fluid)
Skin fluctuance
Skin induration
Stage 3 (Late)
Hemorrhagic bullae
Crepitus
Skin anesthesia
Skin necrosis with dusky discoloration
progressing
to frank gangrene
16. Disease progression
Hyperacute variant
The patient with a hyperacute course presents with sepsis and rapidly
progresses to multiorgan failure
Vibrio species are notable causative agents of hyperacute necrotizing fasciitis.
Subacute variant
Patient demonstrate a slow indolent course with an absence of systemic
disturbance
Gradual tissue necrosis with progressive cutaneous changes over the affected
site
Progression of disease despite use of antimicrobial medications followed by a
sudden deterioration with rapid progression of NF or systemic features of sepsis
17. Differential diagnosis
Gas gangrene
Usually caused by Clostridium Perfringens
Has sweet smelling odor
Erysipelas
An infection of the superficial dermis and superficial lymphatics
Has well-defined borders and might blister profoundly
Lesions are raised above the level of surrounding skin
Cellulitis
Infection of the deeper dermis and subcutaneous fat tissue
Expect erythema with lymphangitis
Minimal blistering
21. Radiological investigation
Plain x-ray
Specific but not sensitive (positive in 25% of cases)
Demonstrate subcutaneous gas
CT scan
Sensitivity 80%
Demonstrate assymetrical fascial thickening,fat stranding ang gas tracking along the fascial plane
MRI
Deep fascia involvement with fluid collection,thickening and enhancement after contrast administration
Sensitivity 100%,specificity 86%
22.
23.
24. Surgical diagnosis
• Tissue biopsy
Taken during wound debridement
• Tissue integrity and depth
Present of fascial necrosis and myonecrois
Loss of fascial intergrity
Presence of dusky gray subcutaneous fat and fascia, dishwater pus, lack of bleeding
• Probe test (finger test)
2cm incision down to deep fascia is made unde LA
Level of superficial fascia probed with gloved finger
Positive :lack of bleeding,foul smelling dishwater pus,minimal tissue resistance to finger dissection
27. 2. INTRAVENOUS ANTIBIOTIC5
Infection/condition &
Likely Organism
Suggested treatment Comment
Preferred treatment Alternative
treatment
Necrotising Fasciitis
Type 1
Polymicrobial infection
Primarily occurs in patients who
are immunocompromised or have
certain chronic diseases such as
diabetes
Piperacillin / tazobactam
4.5g IV q6-8H
PLUS/ MINUS
Clindamycin 600 –
900mg IV q8H
Cefotaxime 2gm IV q8H
PLUS
Metronidazole 500mg IV
q8H
OR
Clindamycin 600-900mg
IV q8H
OR
Ampicilin /Sulbactam 3g,
IV q6-8H
PLUS/MINUS
Clindamycin 600 – 900mg
IV q8H
Piperacillin/tazobactam : if given
as q8H to be given as extended
infusion (over 3-4 hours)
Clindamycin : only necessary if
risk of group A streptococcus /
presenceof gas crepitus
Immediate aggressive surgical
debridement is the primary
treatment modality
Repeated surgical debridement
for source control are normally
necessary
Urgent gram stain
Based on intraoperative C&S ,
antibiotic should be streamlined
28.
29. 3. SURGICAL DEBRIDEMENT AND
WOUND CARE
Surgical emergency
Immediate aggressive surgical debridement within
24 hours-mortality rate 4.2%
Delayed treatment-mortality rate 38%
Remove all non viable tissues
30. WOUND CARE
Hyperbaric oxygen therapy 4
increase tissue oxygen tension->bacteriostasis of clostridia,halting
production alpha-toxin
Induced fibroblast proliferation and angiogenesis-promote wound
closure
Vacuum assisted closure
Wound Closure
Skin grafts/flaps
31. 4. OTHERS
Nutritional support
To promote wound healing
IVIG4
for pt with toxic shock syndrome-neutralizing superantigen activity of GAS
Amputation
Irreversible necrotic changes following sepsis
Failed multiple debridement
Low threshold for amputation when life threatening
33. REFERENCES
1. Morgan MS,Diagnosis and management of necrotisisng fasciitis : a
multiparametric approach,Journal of Hospital infection ,2010,75 :249-
257
2.Jamalludden NM,microbiology of musculoskeletal infections,Donnish
journal of medicine and medical sciences,2014,1:1
3. hwps://www.orthobullets.com/trauma/1007/Necrotizing-fasciitis
4. Cheung JPY,Fung B,Tang WM,Ip WY,A review of necrotizing fasciitis
in the extremities,Hong Kong Medical Journal,2009,15 : 44-52
5. National antibiotic guideline 2019,third edition
