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Necrotizing Fasciitis
Report of 39 Pediatric Cases
Antonio Fustes-Morales, MD; Pedro Gutierrez-Castrellon, MD; Carola Duran-Mckinster, MD;
Luz Orozco-Covarrubias, MD; Lourdes Tamayo-Sanchez, MD; Ramon Ruiz-Maldonado, MD
Background: Necrotizing fasciitis (NF) is a severe,
life-threatening soft tissue infection. General features
and risk factors for fatal outcome in children are not
well known.
Objective: To characterize the features of NF in chil-
dren and the risk factors for fatal outcome.
Design: Retrospective, comparative, observational, and
longitudinal trial.
Setting: Dermatology department of a tertiary care pe-
diatric hospital.
Patients: All patients with clinical and/or histopatho-
logical diagnosis of NF seen from January 1, 1971, through
December 31, 2000.
Main Outcome Variables: Incidence, age, sex, num-
ber and location of lesions, preexisting conditions, ini-
tiating factors, clinical and laboratory features, diagno-
sis at admission, treatment, evolution, sequelae, and risk
factors for fatal outcome.
Results: We examined 39 patients with NF (0.018% of
all hospitalized patients). Twenty-one patients (54%) were
boys. Mean age was 4.4 years. Single lesions were seen in
30 (77%) of patients, with 21(54%) in extremities. The most
frequent preexisting condition was malnutrition in 14 pa-
tients (36%). The most frequent initiating factor was vari-
cella in 13 patients (33%). Diagnosis of NF at admission
was made in 11 patients (28%). Bacterial isolations in 24
patients (62%) were polymicrobial in 17 (71%). Pseudo-
monas aeruginosa was the most frequently isolated bacte-
ria; gram-negative isolates, the most frequently associated
bacteria. Complications were present in 33 patients (85%),
mortality in 7 (18%), and sequelae in 29 (91%) of 32 sur-
viving patients. The significant risk factor related to a fatal
outcome was immunosuppression.
Conclusions: Necrotizing fasciitis in children is fre-
quently misdiagnosed, and several features differ from those
of NF in adults. Immunosuppression was the main factor
related to death. Early surgical debridement and antibi-
otics were the most important therapeutic measures.
Arch Dermatol. 2002;138:893-899
N
ECROTIZING fasciitis
(NF) is a rare, rapidly
progressive, and poten-
tially fatal infection of the
superficial fascia and
subcutaneous cellular tissue.
1,2
Necrotiz-
ing fasciitis is frequently polymicrobial,
and the combination of aerobic and an-
aerobic bacteria contributes to the quick
progression and severity of the disorder.
3
Necrotizing fasciitis has been known
since antiquity.
4,5
In 1871, Jones
6
gave the
first clinical description of “hospital gan-
grene.” In 1924, Meleney
7
wrote a classic
report on NF, emphasizing the impor-
tance of early diagnosis and surgical treat-
ment to reduce mortality. In 1952, Wil-
son
8
proposed the term necrotizing fasciitis
to replace terms like gangrenous erysip-
elas, hospital gangrene, acute cutaneous gan-
grene, nonclostridial crepitant cellulitis,
streptococcal gangrene, synergistic necro-
tizing cellulitis, Meleney cellulitis, and oth-
ers. In addition, Wilson
8
differentiated NF
from disorders like erysipelas, cellulitis,
and clostridial myonecrosis with muscle
involvement. At present, a popular syn-
onym is flesh-eating bacteria disease.
9
Series of NF in children are scarce and
include few cases,
1,10-14
with less than 100
in the literature.
1,2,10-24
The present series
of 39 cases is, to our knowledge, the larg-
est reported.
RESULTS
We found 39 patients with a diagnosis of
NF during the 30-year study period, rep-
resenting 0.018% of all hospitalized pa-
tients. Of these, 21 (54%) were boys, and
18 (46%) were girls. Ages ranged from 10
days to 15.5 years (mean ± SD age, 4.4
STUDY
From the Departments of
Pediatric Dermatology
(Drs Fustes-Morales,
Duran-Mckinster,
Orozco-Covarrubias,
Tamayo-Sanchez, and
Ruiz-Maldonado) and Research
(Dr Gutierrez-Castrellon),
National Institute of Pediatrics,
Mexico City, Mexico.
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years±4.7 months). The number and location of le-
sions, preexisting conditions, initiating factors, bacte-
rial isolations, complications, evolution, and sequelae are
shown in the
Table.
The signs and symptoms at the time of diagnosis were
fever in 36 patients (92%), vomiting in 21 (54%), hypo-
tension and irritability in 13 (33%) each, prostration in
11 (28%), hyporexia in 8 (21%), altered consciousness
in 6 (15%), impaired peripheral perfusion in 5 (13%),
hypothermia in 2 (5%), and hypertension in 1 (3%). Lo-
cal signs and symptoms were pain, hard edema, and ery-
thema in all patients; local warmth in 33 (85%); and func-
tional limitation in 29 (74%). Ecchymoses and necrosis
were each recorded in 28 patients (72%), hemorrhagic
blisters in 25 (64%), purulent secretion in 16 (41%), se-
rous blisters in 14 (36%), local delayed capillary refill in
7 (18%), and crepitus in 4 (10%).
Serum laboratory findings showed hemoglobin lev-
els ranging from 4.0 to 14.8 g/dL (mean level, 9.5 g/dL);
hematocrit levels, 12% to 48% (mean level, 29%); white
blood cell count, 300 to 72000 cells/µL (mean, 16552
cells/µL); neutrophil levels, 18% to 87% (mean level, 59%);
lymphocyte levels, 8% to 70% (mean level, 32%); mono-
cyte and eosinophil levels, within the reference ranges;
bands, 0% to 33% (mean, 4%); and platelet count, 10 to
400 ⫻10
3
/µL (mean, 188.4 ⫻10
3
/µL).
Results of radiographic studies performed in 13 pa-
tients (33%) showed soft tissue swelling in all and gas
in 3 (8%).
Diagnoses at admission were cellulitis in 23 pa-
tients (59%), NF in 11 (28%), and gangrene in 5 (13%).
Concomitant diagnoses were recorded in 17 patients
(44%), ie, septicemia in 10 (59%) of these and humeral
osteomyelitis, febrile neutropenia, hemorrhagic vari-
cella, septic arthritis, malnutrition, acute diarrhea, and
disseminated intravascular coagulation in 1 patient each
of the remaining 7.
Initial antibiotic treatment included amikacin sul-
fate, clindamycin phosphate, and gentamicin sulfate. A
single antibiotic was used in 5 patients (13%); 2 antibi-
otics in 30 (77%); and 3 antibiotics in 4 (10%). The most
frequent antibiotic combinations (22 patients [56%]) were
an aminoglycoside or third-generation cephalosporin plus
clindamycin, antistaphylococcal penicillin, and a first-
generation cephalosporin or fosfomycin. Treatment
with clindamycin plus cefoperazone sodium is recom-
mended as soon as NF is diagnosed.
Surgical debridement with the patient under gen-
eral anesthesia was performed in 33 patients (85%). The
number of surgeries ranged from 1 to 13 (mean number
per patient, 3.6). The number of days from admission to
surgical debridement ranged from 1 to 29 (mean, 5.42;
median, 2). In 18 patients (46%), skin grafts were used.
The number of days in the hospital ranged from 1 to 130
(mean, 41.1). Seven patients (18%) died.
To find risk factors for death, a comparative analy-
sis of the variables was performed. Immunosuppres-
sion, delayed capillary refill, hypotension, hypother-
mia, disseminated intravascular coagulation, and
hypovolemic shock were statistically significant factors
that predicted the probability of death. Once risk fac-
tors identified in the bivariate analysis were included in
a multivariate analysis, hypothermia, hypotension, and
immunosuppression remained the significant predictor
factors of death (95% confidence intervals did not over-
lap 1; P⬍.001).
COMMENT
Necrotizing fasciitis is rare in children.
10
It has been re-
ported in 0.03% of hospitalization causes
25
and in 0.08 per
100000 children per year.
13
Our 39 patients (1.34 cases per
year) represented 0.018% of all our hospitalized patients.
Necrotizing fasciitis is more common in middle-
aged adults, without sex, race, or geographic predilec-
tion.
26
In adults, the lower extremities are more fre-
quently affected, followed by the trunk and head.
7,27
In
children, most lesions are reported in the trunk.
1,10-13
In
newborns, NF originates from omphalitis.
28
In our se-
ries, the lower extremities constituted the most com-
monly affected area (17 patients [44%]).
Necrotizing fasciitis in the genital area is known as
Fournier gangrene. It is more common in diabetic pa-
tients and in immunosuppressed males
29
or after genital
surgical procedures
30
or rectal perforation.
31
Fournier gan-
grene is seldom reported in children.
32-34
In our series, 5
patients had genital involvement. Of these, involvment
was primarily genital in 2, owing to an inadequate set-
ting of a Foley catheter tube in one and after an orchio-
pexy in the other. The remaining 3 cases resulted from
the extension of neighboring lesions (abdomen and thigh).
In this group, 1 patient with immunosuppression died.
Location in the neck is a rare but severe presenta-
tion associated with high mortality,
35,36
owing to carotid
PATIENTS AND METHODS
STUDY DESIGN
We performed a retrospective, observational, com-
parative, and longitudinal study.
SAMPLE POPULATION
We included all clinical records of patients hospital-
ized in the National Institute of Pediatrics, Mexico
City, Mexico, with a diagnosis of NF from January
1, 1971, through December 31, 2000. We included
all patients aged 1 day to 18 years of either sex with
a diagnosis of NF.
STATISTICAL CONSIDERATIONS
The sample size needed to be considered significant
was calculated as 35 to 40 patients. We used a com-
mercial statistical software package (SPSS Base Sys-
tem; SPSS Inc, Chicago, Ill) for data analysis. All stud-
ied variables were analyzed in univariate form using
t or
2
test (P≤.05 was considered significant). Sig-
nificant factors in the univariate analysis to predict
risk for death were included in a logistic regression
multivariate analysis.
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Features in 39 Patients With Necrotizing Fasciitis*
Patient
No./Sex Age
Location/No.
of Lesions
Underlying
Factors Initiating Factors Tissue Bacteriology
Blood
Bacteriology Complications Outcome Sequelae
1/F 11 y UE and LE/2 None None Morganella morganii None Sepsis, Ost Survived US, FJL, D
2/F 1 y Trunk/1 None Varicella None None Sepsis, RF Survived D
3/M 7 y LE/2 ALL BMB, chemotherapy None None Sepsis, DIC, Ost,
pneumonia
Survived US, FJL, D
4/F 4 y LE/1 Malnutrition Close injury None None Sepsis Survived US
5/M 1 y UE/1 None None None None Sepsis Survived US, FJL, D
6/M 2 y LE/1 None Varicella None None None Survived US
7/M 8 mo Trunk/1 None Surgery† GABHS, Staphylococcus
aureus
None Sepsis Survived D
8/F 4 y LE/1 Malnutrition Varicella ␣-Hemolytic
streptococcus
None None Survived None
9/F 1 y Neck/1 Malnutrition Varicella None None Sepsis Survived D, US
10/F 5 y Head/1 None Varicella Streptococcus faecium S faecium Sepsis, pneumonia Survived D, US
11/M 15 y Trunk/1 Aplastic
anemia
Steroidal therapy None None Sepsis, HS, DIC Died . . .
12/F 6 y UE/1 None Traumatic wound None None Sepsis, DIC, SH, HS Died . . .
13/F 4 y Neck, UE,
LE/3
Malnutrition None Gram-positive cocci S aureus Sepsis, SH,
pneumonia, CR
Died . . .
14/M 1 y LE/1 Malnutrition Diarrhea Proteus morganii,
Enterobacter cloacae
None Sepsis, DIC, SH, HS Died . . .
15/M 10 d Trunk/1 MR Abdominal surgery Gram-positive cocci None Sepsis, DIC, HS Died . . .
16/M 2 y Head and
neck/1
None Traumatic wound None None Tracheal
compression
Died . . .
17/M 12 y Trunk,
genitalia/2
Spondylitis,
JRA
Steroidal therapy Pseudomonas aeruginosa,
E cloacae
None Sepsis, DIC, MOF Died . . .
18/M 10 y Genitalia/1 ALL Chemotherapy,
Foley catheter tube
S aureus None Sepsis, HS Survived D, US
19/F 9 mo Neck, trunk/2 Malnutrition Diarrhea P aeruginosa, E cloacae,
Klebsiella pneumoniae
None Sepsis, pneumonia,
LS
Survived US, LS
20/M 3 y UE/1 None Varicella None None None Survived US
21/M 2 y Head/1 None Varicella S faecium None None Survived D, US
22/F 5 y Head, trunk/2 None Varicella P aeruginosa, S faecium None Sepsis, DIC, HS Survived D, US
23/F 1 y LE, genitalia/2 None IMI None None Ost Survived US
24/F 1 y LE/1 None Varicella P aeruginosa, Escherichia
coli
None Sepsis, DIC, SH Survived D, US, FJL
25/M 2 y Head/1 None Varicella S aureus, P aeruginosa P aeruginosa Sepsis, DIC, SH Survived US
26/M 10 y LE/1 Malnutrition Traumatic wound None None Toe necrosis Survived Toe amp
27/F 3 mo LE/1 None Burn S aureus, E cloacae None Sepsis, DIC Survived US, FJL
28/M 4 y Trunk/1 Malnutrition Varicella None None Sepsis, MOF Survived D, US
29/F 9 y LE/1 Malnutrition None None None Sepsis Survived D, US
30/M 4 y LE/1 ALL 1 Bacillus megaterium None Sepsis, pneumonia Survived LFU
31/M 11 mo Head/1 None None Shigella flexneri,
Salmonella typhi,
GABHS
None None Survived D, US
32/F 11 y LE/1 Malnutrition Diarrhea Serratia marcescens,
GABHS, P aeruginosa,
K pneumoniae
None Sepsis Survived LFU
33/M 3 y LE, genitalia/2 Malnutrition Varicella Neisseria species, GABHS,
S aureus
None Sepsis Survived US
34/F 9 mo Trunk, LE/2 None None K pneumoniae,
E cloacae
None Ost Survived D, US, FJL
35/M 10 mo Trunk/1 Malnutrition Diarrhea P aeruginosa, Proteus
species
None Sepsis Survived LFU
36/M 1 y Trunk/1 Malnutrition Varicella S aureus, Haemophilus
species
None None Survived US
37/M 8 y LE/1 None Close injury None None Sepsis Survived D, US
38/F 1 y LE/1 Malnutrition Insect bites K pneumoniae, E coli,
E cloacae
K pneumoniae,
E cloacae
Sepsis, DIC Survived D
39/M 2 y Genitalia/1 None Surgery‡ S aureus, group D
streptococcus
None Sepsis, pneumonia Survived D
*UE indicates upper extremities; LE, lower extremities; Ost, osteomyelitis; US, unslightly scar; FJL, functional joint limitation; D, deformity; RF, respiratory failure;
ALL, acute lymphoblastic leukemia; BMB, bone marrow biopsy; DIC, disseminated intravascular coagulation; GABHS, group A -hemolytic streptococcus;
HS, hypovolemic shock; SH, septic hepatitis; CR, carotid rupture; MR, myelomeningocele rupture; JRA, juvenile rheumatoid arthritis; MOF, multiple organ failure;
LS, laryngeal stenosis; IMI, intramuscular injection; amp, amputation; and LFU, lost to follow-up.
†Indicates herniorrhaphy.
‡Indicates orchiopexy.
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artery and mediastinal dissemination.
37
Four of our pa-
tients presented with NF in the neck. Of these, one died
of tracheal compression and another of carotid rupture
(both causes were diagnosed at autopsy). The patient with
tracheal compression presented with severe respiratory
failure. At admission, intubation was unsuccessful, and
tracheostomy could not be performed due to severe
edema.
Predisposing factors vary with age. Diabetes is the
main factor in adults,
38
but other chronic diseases, such
as hypertension, peripheral vascular disease, renal fail-
ure, obesity, alcoholism, and malnutrition, are impor-
tant underlying factors.
39
Nonsteroidal anti-inflamma-
tory drugs have been implicated as a predisposing
factor,
11
although the relationship remains controver-
sial.
40
Some cases in children have been associated with
immunosuppressive diseases such as acute lymphoblas-
tic leukemia.
10,17,20
In our series, half of the patients pre-
sented predisposing factors, the most frequent being
malnutrition in 14. Immunosuppression was a factor in
6 patients, due to acute lymphoblastic leukemia in 3
and drug-induced in 3.
Initiating factors reported in the literature include
minor injuries,
3,7,8,26,27,38
surgical and traumatic wounds,
21,26
contusion,
41
and varicella.
42,43
In a number of cases, ini-
tiating factors cannot be identified.
7,26,27
In newborns, om-
phalitis,
1
circumcision,
1,44
and placement of electrodes for
the monitoring of vital signs
1
have been reported as ini-
tiating factors. In our series, initiating factors were de-
termined in 85% of patients, the most frequent being vari-
cella.
Clinical manifestations in NF start around a week af-
ter the initiating event, with induration and edema, fol-
lowed 24 to 48 hours later by erythema or purple discol-
oration (
Figure 1) and increasing local fever.
7
Pain is
important in the early stages, and sometimes crepitation
can be found.
3
Tissue necrosis with nerve involvement re-
sults in hyposensitivity or anesthesia. Forty-eight to 72
hours later, the skin turns smooth, bright, and serous, or
hemorrhagic blisters develop (
Figure 2). Without treat-
ment, necrosis develops, and by the fifth or sixth day, the
lesion turns black with a necrotic crust (
Figure 3). Re-
moval of the crust shows fascial tissue and a brown gray-
ish secretion.
7
Subcutaneous cellular tissue is friable and
easily removable. Sometimes the presence of gas (pro-
duced by aerobic and anaerobic bacteria) is recognized
through tissue crepitation. This sign, although infre-
quent, is highly suggestive of NF.
45
Necrosis of the super-
ficial fascia is always more extensive than that indicated
by the extension of skin necrosis.
46
Systemic signs and symptoms are a consequence of
the toxic process and septicemia. A high fever is dispro-
portionate in relation to the size of cutaneous lesion.
7
Con-
sciousness disturbance correlates with the severity of the
process.
47
Multiple organs and systems can be involved,
and abscesses of the liver, lungs, spleen, brain, and peri-
cardium may develop.
7,27
Tissue edema may deplete the
vascular volume and provoke hemoconcentration, hy-
potension, obnubilation, and shock. Tachypnea, hyper-
glycemia (with osmotic diuresis), and fever aggravate the
hypovolemic state.
48
Tissue bacteria are isolated in about 76% of cases.
49
In our series, positive tissue cultures were found in 24
cases (62%). A polybacterial cause of NF is well docu-
mented.
26,50
In our series, the isolates in 17 (71%) of 24
cases were polymicrobial.
Group A  -hemolytic streptococcus has been the
most frequently incriminated agent since Meleney’s
findings,
4,8,38,39,51
and a recent increase in its frequency
has been reported.
52-55
Many other bacteria may be in-
volved.
10,23,29,46,49,51,56-65
Fungi such as Aspergillus,
64
Muco-
raceae,
46
and Candida albicans
65
rarely are etiologic agents.
Pseudomonas has been implicated as an important causal
Figure 1. Necrotizing fasciitis on the third day shows erythema and edema.
Figure 2. Necrotizing fasciitis on the fifth day shows initial epidermal
necrosis and hemorrhagic and serous blisters.
Figure 3. Necrotizing fasciitis on the seventh day shows well-defined
necrosis.
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agent in patients with neutropenia.
16
In our series, Pseu-
domonas was the main causal agent, always in association
with other bacteria. The results of gram stain should not
be used as a guide to therapy because of the polymicro-
bial nature of NF.
48
The diagnosis of NF was suspected initially in only
11 (28%) of our patients. Cellulitis was the most fre-
quent initial diagnosis, made in 23 (59%) of our pa-
tients. These findings suggest that the diagnosis of NF is
often overlooked and, consequently, that specific thera-
peutic measures are delayed. Over time, the trend in our
series was toward an improvement of the survival rate.
In the presence of a soft tissue infection unrespon-
sive to treatment and with rapid health deterioration, NF
should be suspected. The diagnosis is confirmed during
surgical debridement by the presence of liquid necrosis
of the superficial fascia.
46
In doubtful cases, the results
of a frozen-section biopsy during surgery may confirm
the diagnosis.
63
Elements for histological diagnosis in-
clude necrosis of the superficial fascia; leukocytic infil-
trates with polymorphonuclear cells predominant in fas-
cia, subcutaneous fat tissue, and dermis; arterial and
venous fascial thrombosis; angiitis with fibrinoid necro-
sis; visible bacteria in the fascia and dermis on results of
gram stain; and absence of muscular damage.
63
A skin
biopsy was performed in 16 (41%) of our patients, and
the findings were in all cases compatible with the clini-
cal diagnosis of NF.
Anemia, found in 29 (74%) of our cases and re-
ported in 70% to 90% of cases in the literature,
10,26
is prob-
ably due to hemolysis. Leukocytosis was present in 25
(64%) and leukopenia in 5 (13%) of our cases. Trombo-
cytopenia,
10,48
longer coagulation time, hypofibrinogen-
emia, and circulating fibrin degradation products can be
a marker of disseminated intravascular coagulation.
26
Dis-
seminated intravascular coagulation was a complication
in 11 (28%) of our cases and was fatal in 5 of them. Ab-
normal results of liver function tests,
66
prerenal azote-
mia, hypocalcemia, hypoalbuminemia,
48
and an in-
creased creatine phosphokinase level
47
may be present.
A differential diagnosis should be made with other
infectious or necrotic processes with similar appear-
ance. Among the more benign infectious processes, early
cellulitis may present in a form similar to NF, but the
edema in NF is harder. Cellulitis and NF present with
signs of toxicity, but cellulitis responds to conventional
treatment in 24 to 48 hours, whereas in NF, necrosis will
progress if surgical treatment is not initiated. Erysipelas
presents with well-defined erythematous edges, soft
edema, and the absence of necrosis and systemic toxic-
ity.
24
Gaseous gangrene produces a quickly progressive
myonecrosis that involves deep fascia with early crepi-
tation, severe local pain, and few cutaneous changes.
67
Pyoderma gangrenosum has a slow evolution and is fre-
quently associated with ulcerative colitis, rheumatoid ar-
thritis, and myeloma.
68
In cutaneous necrosis caused by
the extravasation of intravenous drugs, the positive his-
tory findings are helpful.
69
Ecthyma gangrenosum is due
to Pseudomonas aeruginosa and consists of pustules with
an erythematous base that burst in hours and turn into
punched, quickly progressive lesions with purpuric raised
edges, more frequently located in the anogenital region,
axillae, abdomen, and legs of children.
70
Purpura fulmi-
nans often appears after varicella and starts with ecchy-
motic areas in the extremities with inflammation, hem-
orrhage, and necrosis.
71
In our series, cellulitis and purpura
fulminans were the most frequent initial diagnoses.
Once vital signs are stable and the hydroelectro-
lytic balance is stabilized, extensive debridement of ne-
crotic tissue must be performed (
Figure 4), and the
procedure must be repeated as many times as needed.
Sudarsky et al
39
reported a decrease in mortality from
50% to 0% in selected patients with appropriate early
treatment. Freischlag et al
72
concluded that mortality
doubles when surgery is delayed for more than 24
hours. Initially, the combination of clindamycin and a
third-generation cephalosporin that covers P aeruginosa
seems adequate. Once culture findings and bacterial
sensitivity are obtained, antibiotics should be adminis-
tered accordingly. Antibiotics alone, because of their in-
ability to reach the poorly vascularized and necrotic fas-
cia, have little effect if surgery is not performed.
10
In our
series, the median time from admission to surgery was 2
days. Owing to severe multiple organ failure treated in
the intensive care unit in a 4-year-old boy (patient 28 in
the Table), the time from admission to surgery was 29
days. Skin grafts should be applied as soon as there is no
evidence of infection and granulation tissue ap-
pears.
26,48,51
When indicated, total parenteral nutrition
must be given.
21
The benefit of hyperbaric oxygen in NF remains
controversial.
73
Other poorly tested therapies include high
doses of intravenous immune globulin, granulocyte trans-
fusion, granulocyte colony-stimulating factor (in gra-
nulocytopenic patients),
20
and bovine thymic extract
(Thymostimulin).
74
Mortality rates in adults range from 8% to 100%.
8,26,67
In newborns, the mortality rate can be as high as 87.5%.
75
The average mortality in children ranges from 10% to 60%,
with a mean of 20%.
18
Most deaths are due to sepsis or
multiorgan failure. In our series, mortality was average
(18%), mostly owing to infectious complications (eg, sep-
sis, septic hepatitis, and pneumonia) or volemic alter-
ations (disseminated intravascular coagulation and hy-
povolemic shock). One patient died owing to tracheal
compression, and another, owing to carotid rupture.
In the multivariate analysis, immunosuppression, hy-
pothermia, and hypotension were the significant risk fac-
Figure 4. Necrotizing fasciitis after extensive surgical debridement
of necrotic tissue.
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tors for death. Hypotension and hypothermia were con-
sidered terminal events.
Sequelae were present in 29 (91%) of 32 survivers,
most frequently unsightly scars (23 patients [72%]) and
deformity (18 [56%]). Other observed sequelae included
joint function limitation in 6 patients (19%), laryngeal ste-
nosis in 1 (3%), and toe amputation in 1 (3%).
CONCLUSIONS
Necrotizing fasciitis is a severe multisystemic disorder
with prominent cutaneous features that can compro-
mise life if diagnosis and treatment are delayed. After
the first month of life, the location of lesions is the same
in adults and children. The most frequent predisposing
factor in our patients was malnutrition. In 19 children
(49%), predisposing factors were not identified. The
most frequent initiating factor was varicella. The most
important risk factor for death in our series was immu-
nosuppression. On the basis of our findings, antibiotic
treatment with clindamycin plus cefoperazone sodium
is recommended as soon as NF is diagnosed. According
to the findings of bacterial cultures and antibiograms,
this regimen may be modified. Surgical debridement
should be performed as soon as the patient’s condition
is stabilized.
Accepted for publication June 29, 2001.
Corresponding author and reprints: Ramon Ruiz-
Maldonado, MD, Insurgentes Sur 3700-C, Colonia Insur-
gentes Cuicuilco, Mexico City, Mexico CP 04530 (e-mail:
rrm@servidor.unam.mx).
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