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130 Necrotising Fasciitis
Table 21.1: Clinical (pathophysiological) stages and features of NF. often not cultured. Vincent’s organisms and bacteroides are commonly
Clinical stage Pathology Clinical features isolated in noma. Recently described are new varieties of NF caused
18
by Photobacterium damsela; halophilic marine vibrios, especially
Pain and tenderness in affected area Vibrio fulnificus; 19,20 and phycomycoses, especially Rhizopus arrhi-
22
zus and Cryptococcus neophormans. Approximately 70–80% of NF
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Oedema and shininess (hyeraemia in is polymicrobial.
I Acute inflammation
light-skinned) of affected area
Pathophysiology
Aerobic pathogens are usually the primary tissue invaders. They
Systemic features (fever, anaemia)
destroy tissues and create an anaerobic environment conducive for
anaerobic or microaerophilic organisms, which are secondary invad-
Discharge of infected fluid/pus (may 2,3,7,13
be offensive) ers. The primary pathogens produce exotoxins, such as strepto-
Progressive lysin, streptodornase, streptokinase, and many other proteases and
necrosis of skin
II Necrosis and sloughing of affected cholagenases, which result in extensive tissue destruction and necrosis.
and subcutaneous The infection is commonly polymicrobial and synergistic, and the
tissue area, resulting in tissue defects
resultant damage is usually more extensive than that attributable to
Systemic features may appear any individual pathogen. Most bacteria, especially facultative gram-
2,3
negative rods such as E. coli, produce insoluble gases whenever sub-
Disappearance of acute inflammatory jected to anerobic metabolism. Because human tissue cannot survive
4
features in an anaerobic environment, gas associated with infection implies the
Healing and tissue presence of dead tissues.
III
repair Appearance of granulation tissue Streptococcal NF associated with toxic shock syndrome
(StrepTSS) has been on the increase in the past two decades and is
Gradual healing of affected area
observed in previously normal children. Caused by a highly invasive
strain of group-A streptococcus, the pathogenesis is related to
Contractures
Maturation and streptococcal pyrogenic exotoxins (SPE) produced by specific strains
IV 23
contraction of scar of Streptococcus pyogenes.
Disfigurement
Natural History (Clinical Stages)
The different pathophysiological stages observed (Table 21.1) include
inflammation (stage I), necrosis (stage II), repair (stage III), and
sequelae (stage IV). 2,3,7,13
Inflammation (stage I)
The prominent feature of NF is the stage of acute inflammation and
results from the effects of the exotoxins, which lead to the release of
cytokines, with local and systemic effects. 4,23 The local features are
mainly those of hyperaemia (or shiny skin), oedema (Figure 21.3)
and pain. Systemic toxaemia commonly results in death if appropriate
resuscitative measures are not put in place. The process can be arrested
at this stage if appropriate antibiotics are given early.
Necrosis (stage II)
Tissue destruction results either from the direct effect of the enzymes
or from vascular thrombosis involving the nutrient vessels serving the
area. There is enough evidence to suggest that stages I and II may occur
2,3
simultaneously in most cases. In addition, tissue oedema that results
Figure 21.3: Inflammatory phase of necrotising fasciitis. from inflammation could increase the pressure within the tight fascial
compartment, further reducing blood supply to the tissues in the area.
laparotomy, or dental extraction; or it can follow infections such as This destruction is rapidly progressive and could occur within 3–5 days.
chicken pox, gingivitis, boil, or perineal abscess. 9,13–15 Extensive subcutaneous/fascial necrosis may proceed with minimal
3. General illness could be in the form of malaria or measles, skin involvement, giving rise to significant undermining. Although rare
23
especially in developing countries. in NF, true muscle necrosis occurs in patients with StrepTSS. This
Microbiology condition, known as gangrenous streptococcal myositis, is similar to
clostridial myonecrosis (gas gangrene) but differs from it in the absence
Necrotising fasciitis could result from a variety of microorganisms,
of gas in the tissues. 4
particularly bacteria and occasionally fungi. Initially thought to be
caused mainly by non-group-A beta-haemolytic streptococci, there is Repair (stage III)
now enough evidence that NF results mostly from synergy between Healing takes place by rejection of the slough, appearance of healthy
gram-positive cocci (such as non-group-A beta-haemolytic strep- granulation tissue, and, subsequently, scar tissue formation.
tococci and staphylococci) and gram-negative organisms such as Sequelae (stage IV)
Bacteroides fragilis, peptostreptococci, Proteus sp., Pseudomonas sp.,
Disfigurement, contractures and trismus may result from tissue loss
or Enterobacter sp. 3,4,16,17 Much less common is a pure group-A strep-
and scar formation after months to years if no appropriate preventive
tococcal infection. Anaerobic bacteria may also be involved, although
measures are taken.