NECROTIZING SOFT TISSUE INFECTION

1. NECROTISING SOFT TISSUE
INFECTION WITH INFECTIVE
ENDOCARDITIS
DR. MANISH KUMAR
SR, SURGERY
UNIT IV
VMMC & SAFDARJUNG HOSPITAL,
NEW DELHI

2. NECROTIZING SOFT TISSUE INFECTIONS (NSTI)
• NSTI are rapidly progressing skin and soft tissue infections associated with necrosis of the
dermis, subcutaneous tissue, superficial fascia, deep fascia, or muscle.
• This definition includes a variety of conditions, such as Fournier gangrene affecting the
perineum and genitalia, Meleney streptococcal gangrene, and clostridial myonecrosis.

3. ANATOMY
• Most bacteria and fungi can multiply within viable tissue, but fibrous
attachments or “boundaries” between subcutaneous tissues and fascia (e.g., scalp,
hands) can help limit the spread of infection.
• The natural lack of fibrous attachments in the larger areas of the body (e.g.,
trunk, extremities) facilitates widespread infection.

4. • From the surface down and forming concentric circles, we find the skin (epidermis
and dermis), superficial fascia or subcutaneous tissue (hypodermis), the deep fascia,
and muscles.
• The deep fascia continues with the epimysium (connective tissue surrounding
muscles), and sends prolongations (intermuscular septa) that divide the different
muscle compartments.

5. • Since the fascia is a continuum from the surface to the endomysium muscles, it is
the route by which a surface process spreads to muscles or bones and vice versa.
Diagram showing the names of
the infections corresponding to
the different layers from the skin
to the muscle. NSTI necrotizing
soft tissue infections

6. • NSTIs are rarely “idiopathic”; a minor wound or injury almost always
precedes the devastating infection, often by several weeks.

7. RISK FACTORS AND PRECIPITATING EVENTS
RELATED TO NECROTIZING SOFT TISSUE
INFECTIONS (NSTI)
Risk factors Precipitating events
Diabetes Surgery
Alcohol abuse Minor invasive procedures
Immunosuppression Intravenous drug use
Malnutrition/obesity Penetrating injuries
Age >60 years Soft tissue infection
Peripheral vascular disease
Underlying malignancy
Intravenous drug misuse

8. • Streptococci and clostridia - fulminant course with rapid onset of symptoms and
worsening over days or even hours and may be rapidly progressing to death if
untreated.
• Infections caused by mixed flora, staphylococcus, and gram-negative organisms -
indolent course over days to weeks, which may mislead clinicians into not
considering the diagnosis of NSTI.

10. PATHOPHYSIOLOGY
• Microbial invasion of the subcutaneous tissues (SCT) occurs either through
external trauma or from direct spread from perforated viscera.
• After that, microorganisms proliferate and generate toxins and enzymes like
hyaluronidase, enabling horizontal extension through deep fascial planes.

11. • As this process progresses, thrombosis of the perforating nutrient vessels causes
progressive dermis and skin ischemia, leading to bullae formation, ulceration,
and skin necrosis. Ischemia and necrosis generate an inflammatory response and
cytokine

13. DIAGNOSIS
• The gold standard modality for the diagnosis of NSTI remains operative exploration, and it
is also the mandatory live-saving treatment.
• Erythema, warmth, and pain - 90% of cases
• Crepitus, skin necrosis, and bullae are much more specific to NSTI - less than 40% (1)
• Signs and symptoms of systemic illness (i.e., sepsis)
• Fever, hypotension, organ failure such as renal failure or hypoxia

15. Imaging
Plain radiography
Most radiographic findings are similar to those for cellulitis, with increased soft-tissue
thickness and opacity.
Frequently, films are unremarkable until the infection and necrosis are advanced and
subcutaneous air can be identified.
Radiographic evidence of air in the soft tissue may be present before clinical crepitus is
detected [34].

16. Plain X-ray film of the
pelvis with NF showing
ectopic air in the
subcutaneous tissue of the
right thigh (arrow)

17. USG
• Suggestive ultrasound features are thickening and distortion of the deep fascia (>4 mm;
fasciitis), turbid fluid collections along the deep fascia, features of myositis, i.e., muscle
hypo- or hyperechogenic swelling, findings of cellulitis, i.e., swelling of the
subcutaneous tissue, including cobblestone appearance (hyperechogenic subcutaneous
tissue traversed by hypoechoic strands of fluid).

18. • Increased Doppler hyperemia or thrombosed small blood vessels [36, 37] can also be seen.
• In the case of Fournier gangrene, the main ultrasound findings are a thickened edematous
scrotal wall that may contain hyperechoic foci with reverberation artifacts (gas). The testes
and epididymis are often normal in size and echotexture owing to their direct aorta branch
blood supply.

19. CT - gas in the soft tissues (the easiest finding for nonradiologists to diagnose and the most
specific), multiple fluid collections, absence or heterogeneity of tissue enhancement by
intravenous (IV) contrast, and significant inflammatory changes under the fascia.

20. a. Stranding of the fat of the
subcutaneous tissue and skin
thickening (cellulitis; asterisk),
thickening and blurring of the
left sternocleidomastoid and
platysma muscles (myositis;
thick arrow).
b. Asymmetrical thickening of the
superficial and deep fascial
layers (fasciitis; thin arrow) and
stranding of the fat of the
subcutaneous tissue and skin
thickening (cellulitis; asterisk).

21. Axial images of a CT of
a. the pelvis and b. the lower
extremities show stranding of
the fat of the subcutaneous
tissue, thickening of the skin
(cellulitis), and thickening of
the superficial and deep fascial
layers (fasciitis; asterisk).
Subcutaneous emphysema
(thick arrow) is also noted.
A continuity solution in the
right gluteus is seen, indicating
a decubitus ulcer (thin arrow)

22. MRI
• Hyperintense signal in subcutaneous tissue in fluid-sensitive sequences (cellulitis),
deep fascial thickening (fasciitis), deep fascial fluid collections, and hyperintense T2
signal within the muscles [11-16].
• The involvement of three or more compartments in one extremity has also been
described as an NSTI indicator [15].

23. • Gas in the deep fascial planes is inconstant and characterized by signal voids, is
best seen on gradient echo sequences, and is a hallmark of NF [12, 13, 15, 17].
• A thick (>3 mm) abnormal perifascial signal hyperintensity on fat-suppressed (FS)
T2-weighted images is seen more frequently in NSTI and explained as purulent
perifascial fluid and edema [15].
• This feature, independent of the thickness, has been described as a sensitive, albeit
nonspecific, feature [12].

24. a.Fatsuppressed T2-weighted axial image shows
areas of high signal intensity in nearly all fasciae
surrounding the muscles of the antero-medial and
posterior compartments (fasciitis±fluid collections;
thin arrows), hyperintensity in the subcutaneous
tissue (cellulitis; asterisk) and within the muscles
(myositis; thick arrow).
b. Fatsuppressed T1-weighted axial image shows
the same findings as T2, stranding of subcutaneous
tissue (cellulitis) and the thickness of the deep
fasciae (fasciitis and fluid collections).
c. Post-contrast fat-suppressed T1-weighted axial
image and
d. post-contrast subtraction T1-weighted axial
image show enhancement in some of the
hyperintense fasciae seen in a (arrows)

25. Local Exploration
• A 2-cm elliptical excision on an extremity will usually suffice and can be
performed under local anesthesia at the bedside.
• Visually inspect for tissue necrosis, dishwater fluid or purulence, greyish
discoloration of tissues.

26. • The tissue at the edges of the incision should be firm and resist pressure—the
“push” test.
• If the surgeon is able to dissect more than a centimeter subcutaneously with blunt
finger pressure alone, this is considered a positive finding and wide debridement
in the operating room is indicated.

27. • Any fluid encountered should be collected and sent for immediate Gram stain
and culture in addition to at least 1 cm3 of skin and subcutaneous tissue and
samples from fascia and muscle.

28. TREATMENT OF NECROTIZING SOFT
TISSUE INFECTIONS
Surgery
• All affected tissue should be sharply excised with at least 1 cm rim of normal tissue
• Bleeding is not an indication of tissue viability, since the presence of active infection will
often cause these areas to be hyperemic.
• All questionable tissue should be resected at the initial operation; the need for multiple
operations and the spread of infection both increase the risk of mortality.(2)

29. Antibiotics
• Broad-spectrum antibiotics - effective against most gram-positive and gram-negative
organisms and ensure Methicillin-resistant S. aureus coverage and good anaerobic
coverage.
• Clindamycin has toxin-neutralization properties, especially in streptococcal and
clostridial infections.

30. Resuscitation
• Sepsis and septic shock should be managed in an intensive care unit (ICU)
• Goal-directed resuscitation with isotonic fluids, vasopressor support as needed with
norepinephrine and vasopressin, and control of hyperglycemia
• Recent studies suggest that IV thiamine, vitamin C, and hydrocortisone in
combination might improve outcomes in sepsis.(3)

31. Adjunctive treatment
Hyperbaric oxygen treatment (HBO)
• Patient is placed in a high-pressure chamber, resulting in delivery of oxygen at 2-3
times atmospheric pressure.
• This leads to arterial oxygen tension as high as 2000 mm Hg with resulting tissue
oxygen tension of 300 mm Hg.
• This compares with arterial oxygen tension of 300 mm Hg and tissue oxygen tension
of 75 mm Hg when breathing 100% oxygen at normal atmospheric pressure.

32. • The use of HBO is based on animal and human studies showing that elevated
levels of oxygen at the tissue level reduce edema, stimulate fibroblast growth,
increase the killing ability of leukocytes by augmenting the oxidative burst, have
independent cytotoxic effects on some anaerobes, inhibit bacterial toxin
elaboration and release, and enhance antibiotic efficacy.4-8

33. • Multiple studies have examined the use of HBO in the treatment of NSTIs with
mixed results.
• its use should only be considered in hemodynamically stable patients in whom
HBO therapy will not delay surgical debridement.

35. Intravenous immunoglobulin (IVIg)
• Involves the administration of pooled IVIg from human donors.
• Its use in the treatment of NSTI is based on the theory that it binds exotoxins
produced by staphylococcal and streptococcal bacterial infections and subsequently
limits systemic inflammatory response.9,10
• Consideration of IVIg therapy be limited to critically ill patients with only
staphylococcal or streptococcal NSTIs or both.

36. Wound Care and Reconstruction
• Once the infection is resolved - negative pressure vacuum dressing and reconstructive
procedures, usually a skin graft, is planned in 2 to 4 weeks.
• Rehabilitation with physical therapy and optimal nutrition.
• The inclusion of tissue substitutes such as acellular dermal matrix and regeneration
templates in reconstruction may improve cosmetic and functional outcomes, although this
increases cost significantly.

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46. THANK YOU