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. 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. 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 Surg
Am 2003; 85A:1454–1460.
5. Common diagnosis in our ward
Last 6 months data
Commonest pathogen Staph aureus
Others
Enterobacter / acinetobacter / proteus /e coli
Streptococcus interestingly not reported! Fallacies?
Total cases Male Female Mortality
51 30 21 1
Cultures sterile Monomicrobial Polymicrobial SNR
12 34 8 8
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. 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 Staphylococcus
aureus in Los Angeles. N Engl J Med 2005; 352:1445–53.
9. Blunt or penetrating trauma
Soft tissue infections
Surgery
Intravenous drug use
Childbirth
Burns
Muscle injuries
Minor trauma
Insect bite,
Pustule
Minor operations,
Anorectal abscess,
Instrumentation,
Septic abortion,
Genitourinary infection
10. Gram positive aerobic
bacteria
Group A ß haemolytic
streptoccoci
Group B streptococci
Enterococci
Coagulase negative
staphylococci
Staphylococcus aureus
Bacillus species
Gram negative aerobic
bacteria
Escherichia coli
Pseudomonas aeruginosa
Proteus species
Serratia species
Anaerobic bacteria
Bacteroides species
Clostridium species
Peptostreptococcus species
Fungi
Zygomycetes
Aspergillus
Candida
Other
Vibrio species
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.
13. 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
14. Bacteria proliferate within the superficial
fascia 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.
15. Necrosis of the superficial fascia
Polymorphonuclear infiltration of
the deep dermis and fascia
Thrombosis and suppuration of
the veins and arteries coursing
through the fascia
Microorganism proliferation
within the destroyed fascia.
16. Occlusion of perforating nutrient vessels
to the skin causes progressive skin
ischemia.
Initially, horizontal phase predominates with rapid
spread 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
17. one microorganism produces the
enzymes necessary to cause
coagulation of the nutrient vessels
tissue oxygen tension falls
tissue 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
18. 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!
19. 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
20. Early findings
Pain
Cellulitis
Pyrexia
Tachycardia
Swelling
Induration
Skin anaesthesia
Late findings
Severe pain
Skin discoloration (purple or
black)
Blistering
Haemorrhagic bullae
Crepitus
Discharge of “dishwater”
fluid
Severe sepsis or SIRS
Multiorgan failure
21. Stage I Stage II Stage III
Tenderness to
palpation(exending beyond
the apparent area of skin)
Blister or bullae formation
(serous fluid)
Hemorrhagic bullae
Erythema Skin fluctuance Skin Anesthesia
Swelling Skin induration Crepitus
Warm to palpation Skin necrosis with dusky
discoloration prgressing to
frank gangrene
22. Wong CH, Khin LW, Heng KS, Tan KC, Low CO., Journal of critical care medicine The LRINEC (Laboratory Risk Indicator for Necrotizing
Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections.epartment of Plastic Surgery, Singapore
General Hospital, Singapore.
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/
dL)
<1.6 >1.6
Glucose (g/dL) <180 >180
•PPV of 92%
• NPV of 96%.
Laboraotry Risk Indicator for Necrotising fasciitis
23. 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
24. 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
25.
26.
27. 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 excision
McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA. Determinants of mortality for necrotizing soft-tissue infections. Ann Surg 1995; 221:
558–63; discussion 563–5
Bilton BD, Zibari GB, McMillan RW, Aultman DF, Dunn G, McDonald JC. Aggressive surgical management of necrotizing fasciitis serves to
decrease mortality: a retrospective study. Am Surg 1998; 64:397–400;discussion 400–1.
28. 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
29. 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 necrotizing
fasciitis 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 J
Surg 2005; 189:462–6.
30. 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
31. 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
Diagnosis is often delayed because of the paucity of
symptoms and the unfamiliarity of the condition
among clinicians
32. 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.
Hinweis der Redaktion
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 NSTI
is to have a high index of suspicion. Unfortunately, true risk
factors for NSTI have not been identified. However, some conditions
appear to be more commonly associated with NSTI and
are worth considering when dealing with any kind of soft-tissue
infection. These include injection drug use and chronic debilitating
comorbidities (e.g., diabetes mellitus, immune suppression,
and obesity) [8–10]. Patients that have any of these characteristics
and present with soft-tissue infection should be
evaluated to confirm or rule out NSTI. Other than injection
drug use, the precipitating factor of NSTI does not appear
helpful for establishing the likelihood of NSTI versus nonnecrotizing
soft-tissue infection
The first and most important tool for early diagnosis of NSTI
is to have a high index of suspicion. Unfortunately, true risk
factors for NSTI have not been identified. However, some conditions
appear to be more commonly associated with NSTI and
are worth considering when dealing with any kind of soft-tissue
infection. These include injection drug use and chronic debilitating
comorbidities (e.g., diabetes mellitus, immune suppression,
and obesity) [8–10]. Patients that have any of these characteristics
and present with soft-tissue infection should be
evaluated to confirm or rule out NSTI. Other than injection
drug use, the precipitating factor of NSTI does not appear
helpful for establishing the likelihood of NSTI versus nonnecrotizing
soft-tissue infection
No specific combination of bacterial species is either diagnostic
of NSTI or found in all cases. A wide spectrum of organisms
are commonly recovered (table 3). In a relatively recent series,
approximately two-thirds of cases were polymicrobial, and onethird
were monomicrobial, with the great majority of monomicrobial
cases 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, ulceration
and 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, ulceration
and skin necrosis