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Necrotising fasciitis
Saiidy Hasham, Paolo Matteucci, Paul R W Stanley and Nick B Hart

BMJ 2005;330;830-833
doi:10.1136/bmj.330.7495.830

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Clinical review

Necrotising fasciitis
Saiidy Hasham, Paolo Matteucci, Paul R W Stanley, Nick B Hart

Necrotising fasciitis is a rare but life threatening condition that requires immediate action, but
uncertainties still hamper prompt diagnosis and treatment

Department of Despite the impression that may have been gained

Plastic
Reconstructive and from the British media, necrotising soft tissue
Hand Surgery, infections have been recognised and reported for cen-
Castle Hill Hospital,
Cottingham, East
turies, the earliest dating back to Hippocrates in the 5th
Yorkshire century BC.1 Such infections represent a large
HU16 5JQ spectrum of clinical entities, ranging from mild
Saiidy Hasham
research registrar in
pyodermas to life threatening necrotising fasciitis.
plastic surgery Although these infections are most commonly caused
Paolo Matteucci by streptococcal and staphylococcal species, a multi-
specialist registrar in
plastic surgery tude of other organisms have also been implicated.2
Paul R W Stanley The term necrotising fasciitis was first used by
consultant plastic Wilson3 in 1952 to describe the most consistent feature
surgeon
of the infection, necrosis of the fascia and subcutaneous
Nick B Hart
consultant plastic tissue with relative sparing of the underlying muscle. It
surgeon can progress rapidly to systemic toxicity and even death
Correspondence to: if not promptly diagnosed and treated. Once suspected,
S Hasham
management should consist of immediate resuscitation,
saiidyhasham@
hotmail.com early surgical debridement, and administration of broad
spectrum intravenous antibiotics.
BMJ 2005;330:830–3 As plastic surgeons, we receive several referrals
each year from other specialties to diagnose or exclude
the possibility of necrotising fasciitis. Since it is part of
a spectrum of necrotising soft tissue infections, diagno-
sis can certainly be difficult for people who are
unfamiliar with the condition and treatment may be
delayed. This may be compounded by the relative lack
of clinical signs and symptoms during the early course
of the infection and because surgical consultation is
sought only once the diagnosis is obvious and the signs
of sepsis are readily apparent. Unfortunately, most
adverse outcomes result from this delay in diagnosis.4
Fortunately, necrotising fasciitis is rare. The actual
incidence in the United Kingdom is estimated at 500
new cases each year but is difficult to record. This in
part is due to the confusion that arises by the
numerous eponyms given to describe the same condi-
tion. A further attempt to classify it according to
location (for example, Fournier’s gangrene), clinical
presentation, or bacteriology only complicates the
issue since there is little to distinguish between these
entities, and their initial management is the same.5 6
This article aims at eradicating this confusion and
looks at the measures that can be taken to increase
awareness of necrotising fasciitis among clinicians, with
the hope that this will result in earlier referral of
patients and improve their overall survival.
Summary points
Necrotising fasciitis is an uncommon but
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
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
We obtained the information for this article from
various sources. References came from medical journal
databases such as Medline and PubMed. Clinical pho-
tographs came from PRWS and NBH and their vast
personal archives.
Aetiology and predisposing factors
The aetiology of necrotising fasciitis is not fully under-
stood, and in many cases no identifiable cause can be
found. However, patients often have some prior history
of trauma (which may even be trivial), such as an insect
bite, scratch, or abrasion.7 The disease does not seem to
have any predilection for age but occurs slightly more
often in male patients.8 9 Most patients who develop
necrotising fasciitis have pre-existing conditions that
render them susceptible to infection. Conditions that
result in immunosuppression, such as advanced age,
chronic renal failure, peripheral vascular disease,
diabetes mellitus, and drug misuse seem to be risk fac-
tors (box 1).9

830 BMJ VOLUME 330 9 APRIL 2005 bmj.com

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Fig 1 Young woman presenting with cellulitis of her lower abdomen
after a caesarean section five days earlier. Small areas of skin
necrosis are clearly visible
Clinical features
Necrotising fasciitis can affect any part of the body but
the extremities, the perineum, and the truncal areas are
the most commonly involved. Most patients present
with signs of inflammation such as erythema, swelling,
and pain at the affected site.7 9 Severe pain dispropor-
tionate to local findings and in association with
systemic toxicity should raise the suspicion of necrotis-
ing fasciitis (box 2). However, these symptoms may be
non-specific at first, which often causes the diagnosis to
be missed (fig 1). As the infection progresses, the skin
becomes increasingly tense and erythematous with
indistinct margins. It may change colour sequentially
from a red-purple to a dusky blue before progressing
to necrosis and formation of bullae and eventually
becoming haemorrhagic (box 2, fig 2). Crepitus of the
affected area may be palpated and may even be seen as
soft tissue air on a plain radiograph. Symptoms may
develop over a period of hours to several days, and
presentations are varied. Patients presenting at an
advanced stage may show signs of systemic shock and
sepsis, and it is these patients that often pose diagnos-
tic difficulties since they may be confused, agitated, or
even have a reduced level of consciousness.
Box 1: Predisposing factors for necrotising
fasciitis
Comorbid conditions
Immunosuppression
Diabetes
Chronic disease
Drugs—for example, steroids
Malnutrition
Age > 60
Intravenous drug misuse
Peripheral vascular disease
Renal failure
Underlying malignancy
Obesity
Aetiological factors
Blunt or penetrating trauma
Soft tissue infections
Surgery
Intravenous drug use
Childbirth
Burns
Muscle injuries
BMJ VOLUME 330 9 APRIL 2005 bmj.com
Clinical review
Box 2: Clinical findings in necrotising fasciitis
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 systemic inflammatory response
syndrome
Multiorgan failure
Diagnosis
Certain diagnostic signs that we have come to associate
with necrotising fasciitis are not always present. The find-
ings of crepitus and soft tissue air on plain radiograph
are seen in only 37% and 57% of patients, respectively.9
However, great caution should be taken. Even though
they are pathognomonic for the disease, their absence
should not exclude the diagnosis. This is an important
point to make since many referrals by other specialties
are made only once these signs become apparent.
Other findings that are common in necrotising fas-
ciitis include a raised white cell count as well as raised
concentrations of glucose, urea, and creatinine.
Hypoalbuminaemia, acidosis, and an altered coagula-
tion profile may also be present (box 3).7 9 10 Other
tests, such as fine needle aspiration and incisional
biopsy (which can be performed on the ward), have
been used to aid diagnosis since they provide
tissue samples for culture and histological analysis,
respectively. However, their usefulness is limited by
false negative results and the small cohort of patients
in completed trials.11 Similarly, computed tomography
and magnetic resonance imaging are useful in cases
where signs are equivocal or the diagnosis is in
doubt.12 13 Both have their roles in delineating the
extent of the infection and showing soft tissue gas, but
the critical condition of patients often precludes their
use and may even delay treatment.
Fig 2 Late signs of necrotising fasciitis with extensive cellulitis,
induration, skin necrosis, and formation of haemorrhagic bullae
831
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Clinical review
The diagnosis therefore remains a clinical one, and
the information drawn from all the investigations should
be used in conjunction; clinicians should not rely on
individual tests. Clinicians should have a high index of
suspicion and a low threshold for surgical referral.
Microbiology
Most studies have shown that necrotising fasciitis is
polymicrobial in nature, with most cultures yielding a
mixture of aerobic and anaerobic organisms.6 10 Those
that are isolated reflect their distribution as normal
skin commensals that are found adjacent to the site of
infection—for example, anaerobic bacteria are usually
isolated in necrotising fasciitis affecting the perineum.
Infection with a single pathogen is reported in about
15% of cases.4 Overall, streptococcus is the most
common causative organism (box 4).7 9 Much concern
has arisen in recent years with the emergence of toxic
shock strains of streptococcus (group A
haemolytic
streptococci) leading to fasciitis with organ dysfunc-
tion. This virulent organism received much press
coverage as the “flesh eating bacterium.” This relates to
the fact that group A streptococci can cause
necrotising fasciitis and associated toxic shock syn-
drome with profound discoloration and sloughing of
the skin. However, in a recent study, group A
streptococci (GAS) were isolated in only 15% of
individuals with necrotising fasciitis.6 Most cases are
caused by M types 1 and 3 and produce exotoxin A
and streptolysin O.14 In a process similar to necrotising
fasciitis resulting from a polymicrobial aetiology, the
production of these M proteins inhibits phagocytosis
and, along with the exotoxins, the proteins act as
superantigens, which leads to the liberation of
cytokines and a toxic shock-like syndrome.
As most cases of necrotising fasciitis are polymicro-
bial, empirical broad spectrum antibiotic coverage
should be administered. Although subsequent antibi-
otic management will be guided by sensitivities of cul-
tures taken intraoperatively, initial treatment should
provide effective cover against Gram positive cocci,
facultative anaerobic Gram negative rods, and anaer-
obes. In our unit, we use a combination of penicillin,
gentamicin (if renal function permits), plus metronida-
zole or clindamycin to cover against the three principal
Box 3: Adjuncts to help diagnosis
Laboratory investigations
Leucocytosis
Acidosis
Altered coagulation profile
Hypoalbuminaemia
Abnormal renal function
Plain radiography
Soft tissue gas
Computed tomography or magnetic resonance
imaging
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
832
Box 4: Organisms identified in necrotising soft
tissue infections
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
groups of organisms, but consultation with the on-call
microbiologist should be sought before starting
treatment with antibiotics.
Management
Having established the diagnosis, treatment should be
instituted immediately. The patient should be resusci-
tated according to his or her clinical state and may even
require intensive care support. Intravenous antibiotics
should be started at the same time and be changed
according to sensitivities. Patients should be taken to
theatre without delay and have aggressive surgical
debridement. Surgeons should make incisions to the
deep fascia (this may reveal the presence of “murky
dishwater fluid” in the wound), and all non-viable tissue
including fascia should be excised. Further surgical
exploration 24-48 hours later is mandatory to ensure
that the infectious process has not extended. Repeated
debridements may be necessary (as dictated by the
state of the wound) until the infection has been
controlled adequately. Haemorrhage is not uncom-
mon after debridement, and in cases of disseminated
intravascular coagulation such bleeds can be difficult to
control. Having whole blood and clotting products
available for the patient before surgery is essential.
Reconstructive surgery should be considered only
once the patient has been stabilised and the infection
fully eradicated. Sterile dressings may be used to cover
the wound in the interim. Wound coverage can be
achieved by either split thickness skin grafting or tissue
transfer (fig 3). Vacuum assisted closure (VAC) therapy
may be employed to promote healing and help close
wounds, and this has helped in reducing the size of
larger defects that would have been difficult to deal
with simply on their own. Other forms of surgery, such
as amputation, may be necessary for necrotising infec-
tions of the extremities, and a defunctioning colostomy
should be considered if wounds are regularly contami-
nated with faeces.
BMJ VOLUME 330 9 APRIL 2005 bmj.com
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Clinical review

Suspected necrotising fasciitis

History and examination

Full blood count, urea and electrolytes, C reactive protein

Blood cultures
Wound swab
Plain x ray

Intravenous access
Fluid resuscitation
Intravenous antibiotics
Regular review

Fig 3 Split thickness skin grafting can be used successfully to cover

large defects after surgical debridement Early surgical consultation
Consult microbiology/infectious diseases
The role of hyperbaric oxygen in the treatment of
necrotising fasciitis remains controversial. Authors Improvement
have advocated its practice in addition to operative Yes No
debridement in improving overall survival. The princi-
Continue therapy Deterioration
ple behind its use is to increase the tissue oxygen Repeated assessment
tension in zones of infected hypoxic areas. This
Yes No
prevents extension of the disease and the need for
further debridements.15 Conversely, others have shown Surgical consultation: Consider further investigation
no survival benefit.4 Further studies are therefore • Transfer to theatre or surgical ward Computed tomography/magnetic resonance
• May require support in intensive care or imagery
required before this treatment can be recommended. high dependency unit Exploratory surgery
• Urgent radical debridement
• Frequent reassessment
Prognosis
Necrotising fasciitis is an uncommon, but life threaten- Patient will also require:
ing, condition with a high associated mortality and • Nutritional support
• Physiotherapy/occupational therapy
morbidity. Reported mortality varies from 6% to 76%, • Psychological support
but more recent studies report this to be much lower, at • Reconstructive surgery
around 25%.7 9 10 This is partly the result of early recog-
nition and improved supportive measures that are
Fig 4 Algorithm for assessment and treatment of suspected necrotising fasciitis
multidisciplinary in origin.
5 Dellinger EP. Severe necrotizing soft tissue infections: multiple disease
entities requiring a common approach. JAMA 1981;246:1717-21.
Summary 6 Eke N. Fournier’s gangrene: A review of 1726 cases. Br J Surg 2000;
87:718-28.
Because of the potential fatal course of necrotising 7 Singh G, Sinha SK, Adhikary S, Babu KS, Ray P, Khanna SK. Necrotising
fasciitis, prompt diagnosis is the key to a favourable infections of soft tissues—a clinical profile. Eur J Surg 2002;168:366-71.
8 Hsieh WS, Yang PH, Chao HC, Lai JY. Neonatal necrotizing fasciitis: A
outcome. Laboratory findings and other diagnostic report of three cases and review of the literature. Paediatrics 1999;
tests may be useful adjuncts, but the diagnosis is still 103:e53.
9 Elliott DC, Kufera JA, Myers RAM. Necrotizing soft tissue infections: Risk
primarily a clinical one, and suspicion alone warrants factors for mortality and strategies for management. Ann Surg 1996;
early surgical referral. The mainstay of treatment is 224:672-83.
10 McHenry CR, Piotrowski JJ, Teprinic D, Malangoni MA. Determinants of
immediate resuscitation of the patient, followed by mortality for necrotizing soft tissue infections. Ann Surg 1995;221:558-65.
aggressive surgical debridement. Further explorations 11 Majeski J, Majeski E. Necrotising fasciitis: Improved survival with early
recognition by tissue biopsy and aggressive surgical treatment. Southern
may be necessary before soft tissue coverage is under- Med J 1997;90:1065-8.
taken. Intravenous treatment with broad spectrum 12 Wykosi MG, Santora TA, Shah RM, Friedman AC. Necrotising fasciitis:
CT characteristics. Radiology 1997;203:859-63.
antibiotics should also be implemented. We have 13 Rahmouni A, Chosidow O, Mathieu D, Gueorguieva E, Jazaerli N, Radier C,
devised an algorithm that we hope will improve the et al. MR imaging in acute infectious cellulitis. Radiology 1994;192:493-6.
14 Hackett SP, Stevens DL. Streptococcal toxic shock syndrome: Synthesis of
referral service in suspected cases of necrotising tumour necrosis factor and interleukin-1 by monocytes stimulated with
fasciitis and avoid unnecessary delays in treatment pyrogenic exotoxin A and streptolysin O. J Infect Dis 1992;165:879-85.
(fig 4). Initial responses from the different specialties 15 Riseman JA, Zamboni WA, Curtis A, Graham DR, Konrad HR, Ross DS.
Hyberbaric oxygen therapy for necrotising fasciitis reduces mortality and
in our hospital have been good, but the algorithm the need for debridements. Surg 1990;108:847-50.
requires formal evaluation to identify any benefit. (Accepted 22 February 2005)

The experience of PRWS and NBH, along with help from other
specialist professionals (such as N Sohal, consultant microbiol-
ogist) allowed SH to set out an article that will hopefully benefit Endpiece
others.
Competing interests: None declared. Not old
A person is not old until regrets take the place of
1 Descamps V, Aitken J, Lee MG. Hippocrates on necrotising fasciitis. Lancet
1994;344:556. hopes and plans.
2 File TM Jr, Tan JS. Treatment of skin and soft-tissue infections. Am J Surg
1995;169(5A suppl.):27S.
Scott Nearing, American writer (1883-1983)
3 Wilson B. Necrotising fasciitis. Am Surg 1952;18:416-31. Fred Charatan, retired geriatric physician, Florida
4 Lille ST, Sato TT, Engrav LH, Foy H, Jurkovich GJ. Necrotizing soft tissue
infections: obstacles in diagnosis. J Am Coll Surg 1996;182:7-11.

BMJ VOLUME 330 9 APRIL 2005 bmj.com 833

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Commentary: Excellent review scheme for critical incidents but
insufficient for revalidation
Mayur Lakhani
I want to consider the potential use of the Scottish Audit
of Surgical Mortality (SASM)1 scheme for revalidation of
surgeons. Revalidation is an important policy initiative
in the United Kingdom from the medical profession’s
regulatory body, the General Medical Council.2 It is
aimed at ensuring that doctors remain up to date and fit
to practise, and is also a way of restoring and retaining
the public’s trust in doctors. The policy is in some
difficulty, and the government has ordered a review of
how revalidation can be made to work.
The Royal College of Surgeons of England and the
Senate of Surgery recommend that surgeons include
results of clinical outcomes and record of audits
(including morbidity and mortality) in their evidence
for revalidation.3 To this end, the SASM scheme, which
looks at avoidable deaths, seems to be a potentially
valuable contribution to the process.
The SASM scheme can be regarded as a peer
review of critical incidents. Peer review is an important
component of revalidation. The clinical ownership and
engagement in the SASM scheme is striking, and there
is evidence of the iterative development of standards.
There is also clear evidence of improvement resulting
from collaboration between clinicians and hospitals.
The disadvantages are that no benchmark is
established because the denominator is not known and
outliers would not be detected. The analysis concerns
itself with the process of surgical care that involved
individual surgeons, teams, and the institution, whereas
revalidation is an assessment of the individual doctor
concerned.
Although patients are involved at a strategic (board)
level, lay involvement does not seem to exist at other lev-
els. Surgeons elect members of the management group;
this generic procedure (as used by the GMC) was
criticised by Dame Jane Smith in her fifth report on the
case of the general practitioner Harold Shipman (who
was convicted of killing some of his patients and is
thought to have killed hundreds more.)4 Although no
evidence exists, this might suggest that the procedure is
perceived as a relatively closed process and that it may
not meet the modern day requirements of principles of
assessment5, transparency, and lay involvement.
Revalidation is more than just a record of continu-
ing professional development or taking part in clinical
audit. The doctor must also show that his or her clini-
cal performance is not unacceptable—the “patient
safety” test. It is significant that participation in SASM
is voluntary and that a small number of surgeons do
not participate. The reasons for this are not clear, but
for the purposes of revalidation a proved and
consistent refusal to participate in a national clinical
audit scheme focusing on outcomes for surgeons could
be a cause for concern.
In conclusion, participation in the critical incident
scheme described would be insufficient by itself to
revalidate a surgeon. Revalidation should not be its
primary purpose. Instead, it is an important and
BMJ VOLUME 330 14 MAY 2005 bmj.com
Education and debate
thoughtful scheme with the potential to develop into a Royal College of
General
more robust and widespread confidential reporting Practitioners,
and learning system to tackle patient safety by focusing London SW1 7PU
on systems improvement. Mayur Lakhani
chairman of council
This is a personal analysis and does not represent a formal view
MLakhani@rcgp.
of the Royal College of General Practitioners. org.uk
Competing interests: None declared
1 Thompson AM, Stonebridge PA. Building a framework for trust: critical
event analysis of deaths in surgical care. BMJ 2005;330:1139-42.
2 General Medical Council. Licensing and revalidation formal guidance for
doctors (draft). London: GMC, 2004.
3 Royal College of Surgeons. Guidance on surgical practice—criteria, standards
and evidence. 2004. www.rcseng.ac.uk/services/publications/publications/
pdf/cse.pdf (accessed 12 Apr 2005).
4 Fifth report. Safeguarding patients: lessons from the past—proposals for the
future. Report of the Judicial Inquiry into Harold Shipman. 2004.
www.the-shipman-inquiry.org.uk/home.asp (accessed 12 Apr 2005).
5 Postgraduate Medical Training Board. Principles for an assessment system for
postgraduate medical training. 2004. www.pmetb.org.uk/pmetb/
publications/principles.pdf (accessed 12 Apr 2005).
Corrections and clarifications
Necrotising fasciitis
An error occurred in the placement of the three
photographs accompanying this Clinical Review
article by Saiidy Hasham and colleagues (BMJ
2005;330:830-3, 9 Apr), with the result that each is
accompanied by the wrong caption. The photograph
labelled figure 1 should be accompanied by the
caption that was used for figure 2 (“Late signs of
necrotising fasciitis . . . ”); the photograph labelled
figure 2 should be accompanied by the caption that
was used for figure 3 (“Split thickness skin grafting . .
.”); and the photograph labelled figure 3 should be
accompanied by the caption that was used for figure 1
(“Young woman presenting with
cellulitis . . .”).
Regulator restricts use of SSRIs in children
This News article by Lynn Eaton (BMJ 2005;330:984,
30 Apr) contained two inaccuracies about the drug
atomoxetine. The manufacturer, Lilly, points out that
we wrongly suggested that atomoxetine is an
antidepressant (whereas it has no antidepressant
activity). Also, atomoxetine is not associated with an
increased incidence of suicide related behaviour (as we
implied), although it is associated with an increased
risk of hostility (as we stated) and emotional lability.
Interactive case report: Postoperative hypoxia in a woman
with Down’s syndrome
The table in the first part of this report by A K Siotia
and colleagues (BMJ 2005;330:834, 9 Apr) was
inadvertently given the wrong title during editing. As
the text suggests, the table shows the patient’s
postoperative (not preoperative) results.
Reader’s guide to critical appraisal of cohort studies: 1. Role
and design
At the final page proof stage of this Education and
Debate article, some sort of glitch—the cause of which
we have yet to fathom—resulted in the first author’s
name jumping to the end of the authorship line (BMJ
2005;330:895-7, 16 Apr). Paula A Rochon (not Jerry H
Gurwitz), therefore, is the first (not the last) author of
this paper. This has already been changed on bmj.com.
1143