Necrotizing Fasciitis Report of 39 Pediatric Cases

STUDY 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, Results: We examined 39 patients with NF (0.018% of life-threatening soft tissue infection. General features all hospitalized patients). Twenty-one patients (54%) were and risk factors for fatal outcome in children are not boys. Mean age was 4.4 years. Single lesions were seen in well known. 30 (77%) of patients, with 21(54%) in extremities. The most frequent preexisting condition was malnutrition in 14 pa- Objective: To characterize the features of NF in chil- tients (36%). The most frequent initiating factor was vari- dren and the risk factors for fatal outcome. cella in 13 patients (33%). Diagnosis of NF at admission was made in 11 patients (28%). Bacterial isolations in 24 Design: Retrospective, comparative, observational, and patients (62%) were polymicrobial in 17 (71%). Pseudo- longitudinal trial. monas aeruginosa was the most frequently isolated bacteria; gram-negative isolates, the most frequently associated Setting: Dermatology department of a tertiary care pe- bacteria. Complications were present in 33 patients (85%), diatric hospital. mortality in 7 (18%), and sequelae in 29 (91%) of 32 sur- viving patients. The significant risk factor related to a fatal Patients: All patients with clinical and/or histopatho- outcome was immunosuppression. logical diagnosis of NF seen from January 1, 1971, through December 31, 2000. Conclusions: Necrotizing fasciitis in children is frequently misdiagnosed, and several features differ from those Main Outcome Variables: Incidence, age, sex, num- of NF in adults. Immunosuppression was the main factor ber and location of lesions, preexisting conditions, ini- related to death. Early surgical debridement and antibi- tiating factors, clinical and laboratory features, diagno- otics were the most important therapeutic measures. sis at admission, treatment, evolution, sequelae, and risk factors for fatal outcome. Arch Dermatol. 2002;138:893-899

ECROTIZING fasciitis streptococcal gangrene, synergistic necro- (NF) is a rare, rapidly tizing cellulitis, Meleney cellulitis, and oth- progressive, and poten- ers. In addition, Wilson8 differentiated NF tially fatal infection of the from disorders like erysipelas, cellulitis, superficial fascia and and clostridial myonecrosis with muscle subcutaneous cellular tissue.1,2 Necrotiz- involvement. At present, a popular syn- N 9 ing fasciitis is frequently polymicrobial, onym is flesh-eating bacteria disease. and the combination of aerobic and an- Series of NF in children are scarce and aerobic bacteria contributes to the quick include few cases,1,10-14 with less than 100 progression and severity of the disorder.3 in the literature.1,2,10-24 The present series Necrotizing fasciitis has been known of 39 cases is, to our knowledge, the larg- since antiquity.4,5 In 1871, Jones6 gave the est reported. From the Departments of first clinical description of “hospital gan- Pediatric Dermatology 7 grene.” In 1924, Meleney wrote a classic RESULTS (Drs Fustes-Morales, report on NF, emphasizing the impor- Duran-Mckinster, tance of early diagnosis and surgical treat- We found 39 patients with a diagnosis of Orozco-Covarrubias, ment to reduce mortality. In 1952, Wil- NF during the 30-year study period, rep- Tamayo-Sanchez, and 8 Ruiz-Maldonado) and Research son proposed the term necrotizing fasciitis resenting 0.018% of all hospitalized pa- (Dr Gutierrez-Castrellon), to replace terms like gangrenous erysip- tients. Of these, 21 (54%) were boys, and National Institute of Pediatrics, elas, hospital gangrene, acute cutaneous gan- 18 (46%) were girls. Ages ranged from 10 Mexico City, Mexico. grene, nonclostridial crepitant cellulitis, days to 15.5 years (mean ± SD age, 4.4

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©2002 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021 (44%), ie, septicemia in 10 (59%) of these and humeral osteomyelitis, febrile neutropenia, hemorrhagic vari- PATIENTS AND METHODS cella, septic arthritis, malnutrition, acute diarrhea, and disseminated intravascular coagulation in 1 patient each STUDY DESIGN of the remaining 7. Initial antibiotic treatment included amikacin sul- We performed a retrospective, observational, com- fate, clindamycin phosphate, and gentamicin sulfate. A parative, and longitudinal study. single antibiotic was used in 5 patients (13%); 2 antibiotics in 30 (77%); and 3 antibiotics in 4 (10%). The most SAMPLE POPULATION frequent antibiotic combinations (22 patients [56%]) were an aminoglycoside or third-generation cephalosporin plus We included all clinical records of patients hospital- clindamycin, antistaphylococcal penicillin, and a first- ized in the National Institute of Pediatrics, Mexico generation cephalosporin or fosfomycin. Treatment City, Mexico, with a diagnosis of NF from January with clindamycin plus cefoperazone sodium is recom- 1, 1971, through December 31, 2000. We included all patients aged 1 day to 18 years of either sex with mended as soon as NF is diagnosed. a diagnosis of NF. Surgical debridement with the patient under general anesthesia was performed in 33 patients (85%). The STATISTICAL CONSIDERATIONS number of surgeries ranged from 1 to 13 (mean number per patient, 3.6). The number of days from admission to The sample size needed to be considered significant surgical debridement ranged from 1 to 29 (mean, 5.42; was calculated as 35 to 40 patients. We used a com- median, 2). In 18 patients (46%), skin grafts were used. mercial statistical software package (SPSS Base Sys- The number of days in the hospital ranged from 1 to 130 tem; SPSS Inc, Chicago, Ill) for data analysis. All stud- (mean, 41.1). Seven patients (18%) died. ied variables were analyzed in univariate form using To find risk factors for death, a comparative analy- t or ␹2 test (P≤.05 was considered significant). Sig- nificant factors in the univariate analysis to predict sis of the variables was performed. Immunosuppres- risk for death were included in a logistic regression sion, delayed capillary refill, hypotension, hypother- multivariate analysis. mia, disseminated intravascular coagulation, and hypovolemic shock were statistically significant factors that predicted the probability of death. Once risk factors identified in the bivariate analysis were included in years±4.7 months). The number and location of le- a multivariate analysis, hypothermia, hypotension, and sions, preexisting conditions, initiating factors, bacte- immunosuppression remained the significant predictor rial isolations, complications, evolution, and sequelae are factors of death (95% confidence intervals did not over- shown in the Table. lap 1; PϽ.001). The signs and symptoms at the time of diagnosis were fever in 36 patients (92%), vomiting in 21 (54%), hypo- COMMENT tension and irritability in 13 (33%) each, prostration in 11 (28%), hyporexia in 8 (21%), altered consciousness Necrotizing fasciitis is rare in children.10 It has been re- in 6 (15%), impaired peripheral perfusion in 5 (13%), ported in 0.03% of hospitalization causes25 and in 0.08 per hypothermia in 2 (5%), and hypertension in 1 (3%). Lo- 100000 children per year.13 Our 39 patients (1.34 cases per cal signs and symptoms were pain, hard edema, and ery- year) represented 0.018% of all our hospitalized patients. thema in all patients; local warmth in 33 (85%); and func- Necrotizing fasciitis is more common in middle- tional limitation in 29 (74%). Ecchymoses and necrosis aged adults, without sex, race, or geographic predilec- were each recorded in 28 patients (72%), hemorrhagic tion.26 In adults, the lower extremities are more fre- blisters in 25 (64%), purulent secretion in 16 (41%), se- quently affected, followed by the trunk and head.7,27 In rous blisters in 14 (36%), local delayed capillary refill in children, most lesions are reported in the trunk.1,10-13 In 7 (18%), and crepitus in 4 (10%). newborns, NF originates from omphalitis.28 In our se- Serum laboratory findings showed hemoglobin lev- ries, the lower extremities constituted the most com- els ranging from 4.0 to 14.8 g/dL (mean level, 9.5 g/dL); monly affected area (17 patients [44%]). hematocrit levels, 12% to 48% (mean level, 29%); white Necrotizing fasciitis in the genital area is known as blood cell count, 300 to 72000 cells/µL (mean, 16552 Fournier gangrene. It is more common in diabetic pa- cells/µL); neutrophil levels, 18% to 87% (mean level, 59%); tients and in immunosuppressed males29 or after genital lymphocyte levels, 8% to 70% (mean level, 32%); mono- surgical procedures30 or rectal perforation.31 Fournier gan- cyte and eosinophil levels, within the reference ranges; grene is seldom reported in children.32-34 In our series, 5 bands, 0% to 33% (mean, 4%); and platelet count, 10 to patients had genital involvement. Of these, involvment 400 ϫ103/µL (mean, 188.4 ϫ103/µL). was primarily genital in 2, owing to an inadequate set- Results of radiographic studies performed in 13 pa- ting of a Foley catheter tube in one and after an orchio- tients (33%) showed soft tissue swelling in all and gas pexy in the other. The remaining 3 cases resulted from in 3 (8%). the extension of neighboring lesions (abdomen and thigh). Diagnoses at admission were cellulitis in 23 pa- In this group, 1 patient with immunosuppression died. tients (59%), NF in 11 (28%), and gangrene in 5 (13%). Location in the neck is a rare but severe presenta- Concomitant diagnoses were recorded in 17 patients tion associated with high mortality,35,36 owing to carotid

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Patient Location/No. Underlying Blood No./Sex Age of Lesions Factors Initiating Factors Tissue Bacteriology 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, Survived US, FJL, D pneumonia 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 None Sepsis Survived D aureus 8/F 4 y LE/1 Malnutrition Varicella ␣-Hemolytic None None Survived None streptococcus 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 Steroidal therapy None None Sepsis, HS, DIC Died . . . anemia 12/F 6 y UE/1 None Traumatic wound None None Sepsis, DIC, SH, HS Died . . . 13/F 4 y Neck, UE, Malnutrition None Gram-positive cocci S aureus Sepsis, SH, Died . . . LE/3 pneumonia, CR 14/M 1 y LE/1 Malnutrition Diarrhea Proteus morganii, None Sepsis, DIC, SH, HS Died . . . Enterobacter cloacae 15/M 10 d Trunk/1 MR Abdominal surgery Gram-positive cocci None Sepsis, DIC, HS Died . . . 16/M 2 y Head and None Traumatic wound None None Tracheal Died . . . neck/1 compression 17/M 12 y Trunk, Spondylitis, Steroidal therapy Pseudomonas aeruginosa, None Sepsis, DIC, MOF Died . . . genitalia/2 JRA E cloacae 18/M 10 y Genitalia/1 ALL Chemotherapy, S aureus None Sepsis, HS Survived D, US Foley catheter tube 19/F 9 mo Neck, trunk/2 Malnutrition Diarrhea P aeruginosa, E cloacae, None Sepsis, pneumonia, Survived US, LS Klebsiella pneumoniae 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 None Sepsis, DIC, SH Survived D, US, FJL coli 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, None None Survived D, US Salmonella typhi, GABHS 32/F 11 y LE/1 Malnutrition Diarrhea Serratia marcescens, None Sepsis Survived LFU GABHS, P aeruginosa, K pneumoniae 33/M 3 y LE, genitalia/2 Malnutrition Varicella Neisseria species, GABHS, None Sepsis Survived US S aureus 34/F 9 mo Trunk, LE/2 None None K pneumoniae, None Ost Survived D, US, FJL E cloacae 35/M 10 mo Trunk/1 Malnutrition Diarrhea P aeruginosa, Proteus None Sepsis Survived LFU species 36/M 1 y Trunk/1 Malnutrition Varicella S aureus, Haemophilus None None Survived US species 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, K pneumoniae, Sepsis, DIC Survived D E cloacae E cloacae 39/M 2 y Genitalia/1 None Surgery‡ S aureus, group D None Sepsis, pneumonia Survived D streptococcus

*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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©2002 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021 Figure 1. Necrotizing fasciitis on the third day shows erythema and edema. Figure 3. Necrotizing fasciitis on the seventh day shows well-defined necrosis.

termined in 85% of patients, the most frequent being varicella. Clinical manifestations in NF start around a week after the initiating event, with induration and edema, followed 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 results in hyposensitivity or anesthesia. Forty-eight to 72 hours later, the skin turns smooth, bright, and serous, or hemorrhagic blisters develop (Figure 2). Without treatment, necrosis develops, and by the fifth or sixth day, the Figure 2. Necrotizing fasciitis on the fifth day shows initial epidermal lesion turns black with a necrotic crust (Figure 3). Re- necrosis and hemorrhagic and serous blisters. moval of the crust shows fascial tissue and a brown gray- ish secretion.7 Subcutaneous cellular tissue is friable and artery and mediastinal dissemination.37 Four of our pa- easily removable. Sometimes the presence of gas (pro- tients presented with NF in the neck. Of these, one died duced by aerobic and anaerobic bacteria) is recognized of tracheal compression and another of carotid rupture through tissue crepitation. This sign, although infre- (both causes were diagnosed at autopsy). The patient with quent, is highly suggestive of NF.45 Necrosis of the super- tracheal compression presented with severe respiratory ficial fascia is always more extensive than that indicated failure. At admission, intubation was unsuccessful, and by the extension of skin necrosis.46 tracheostomy could not be performed due to severe Systemic signs and symptoms are a consequence of edema. the toxic process and septicemia. A high fever is dispro- Predisposing factors vary with age. Diabetes is the portionate in relation to the size of cutaneous lesion.7 Con- main factor in adults,38 but other chronic diseases, such sciousness disturbance correlates with the severity of the as hypertension, peripheral vascular disease, renal fail- process.47 Multiple organs and systems can be involved, ure, obesity, alcoholism, and malnutrition, are impor- and abscesses of the liver, lungs, spleen, brain, and peri- tant underlying factors.39 Nonsteroidal anti-inflamma- cardium may develop.7,27 Tissue edema may deplete the tory drugs have been implicated as a predisposing vascular volume and provoke hemoconcentration, hy- factor,11 although the relationship remains controver- potension, obnubilation, and shock. Tachypnea, hyper- sial.40 Some cases in children have been associated with glycemia (with osmotic diuresis), and fever aggravate the immunosuppressive diseases such as acute lymphoblas- hypovolemic state.48 tic leukemia.10,17,20 In our series, half of the patients pre- Tissue bacteria are isolated in about 76% of cases.49 sented predisposing factors, the most frequent being In our series, positive tissue cultures were found in 24 malnutrition in 14. Immunosuppression was a factor in cases (62%). A polybacterial cause of NF is well docu- 6 patients, due to acute lymphoblastic leukemia in 3 mented.26,50 In our series, the isolates in 17 (71%) of 24 and drug-induced in 3. cases were polymicrobial. Initiating factors reported in the literature include Group A ␤-hemolytic streptococcus has been the minor injuries,3,7,8,26,27,38 surgical and traumatic wounds,21,26 most frequently incriminated agent since Meleney’s contusion,41 and varicella.42,43 In a number of cases, ini- findings,4,8,38,39,51 and a recent increase in its frequency tiating factors cannot be identified.7,26,27 In newborns, om- has been reported.52-55 Many other bacteria may be in- phalitis,1 circumcision,1,44 and placement of electrodes for volved.10,23,29,46,49,51,56-65 Fungi such as Aspergillus,64 Muco- the monitoring of vital signs1 have been reported as ini- raceae,46 and Candida albicans65 rarely are etiologic agents. tiating factors. In our series, initiating factors were de- Pseudomonas has been implicated as an important causal

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©2002 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021 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 polymicrobial nature of NF.48 The diagnosis of NF was suspected initially in only 11 (28%) of our patients. Cellulitis was the most frequent initial diagnosis, made in 23 (59%) of our patients. These findings suggest that the diagnosis of NF is often overlooked and, consequently, that specific therapeutic 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 Figure 4. Necrotizing fasciitis after extensive surgical debridement should be suspected. The diagnosis is confirmed during of necrotic tissue. surgical debridement by the presence of liquid necrosis of the superficial fascia.46 In doubtful cases, the results axillae, abdomen, and legs of children.70 Purpura fulmi- of a frozen-section biopsy during surgery may confirm nans often appears after varicella and starts with ecchy- the diagnosis.63 Elements for histological diagnosis in- motic areas in the extremities with inflammation, hem- clude necrosis of the superficial fascia; leukocytic infil- orrhage, and necrosis.71 In our series, cellulitis and purpura trates with polymorphonuclear cells predominant in fas- fulminans were the most frequent initial diagnoses. cia, subcutaneous fat tissue, and dermis; arterial and Once vital signs are stable and the hydroelectro- venous fascial thrombosis; angiitis with fibrinoid necro- lytic balance is stabilized, extensive debridement of ne- sis; visible bacteria in the fascia and dermis on results of crotic tissue must be performed (Figure 4), and the gram stain; and absence of muscular damage.63 A skin procedure must be repeated as many times as needed. biopsy was performed in 16 (41%) of our patients, and Sudarsky et al39 reported a decrease in mortality from the findings were in all cases compatible with the clini- 50% to 0% in selected patients with appropriate early cal diagnosis of NF. treatment. Freischlag et al72 concluded that mortality Anemia, found in 29 (74%) of our cases and re- doubles when surgery is delayed for more than 24 ported in 70% to 90% of cases in the literature,10,26 is prob- hours. Initially, the combination of clindamycin and a ably due to hemolysis. Leukocytosis was present in 25 third-generation cephalosporin that covers P aeruginosa (64%) and leukopenia in 5 (13%) of our cases. Trombo- seems adequate. Once culture findings and bacterial cytopenia,10,48 longer coagulation time, hypofibrinogen- sensitivity are obtained, antibiotics should be adminis- emia, and circulating fibrin degradation products can be tered accordingly. Antibiotics alone, because of their in- a marker of disseminated intravascular coagulation.26 Dis- ability to reach the poorly vascularized and necrotic fas- seminated intravascular coagulation was a complication cia, have little effect if surgery is not performed.10 In our in 11 (28%) of our cases and was fatal in 5 of them. Ab- series, the median time from admission to surgery was 2 normal results of liver function tests,66 prerenal azote- days. Owing to severe multiple organ failure treated in mia, hypocalcemia, hypoalbuminemia,48 and an in- the intensive care unit in a 4-year-old boy (patient 28 in creased creatine phosphokinase level47 may be present. the Table), the time from admission to surgery was 29 A differential diagnosis should be made with other days. Skin grafts should be applied as soon as there is no infectious or necrotic processes with similar appear- evidence of infection and granulation tissue ap- ance. Among the more benign infectious processes, early pears.26,48,51 When indicated, total parenteral nutrition cellulitis may present in a form similar to NF, but the must be given.21 edema in NF is harder. Cellulitis and NF present with The benefit of hyperbaric oxygen in NF remains signs of toxicity, but cellulitis responds to conventional controversial.73 Other poorly tested therapies include high treatment in 24 to 48 hours, whereas in NF, necrosis will doses of intravenous immune globulin, granulocyte trans- progress if surgical treatment is not initiated. Erysipelas fusion, granulocyte colony-stimulating factor (in gra- presents with well-defined erythematous edges, soft nulocytopenic patients),20 and bovine thymic extract edema, and the absence of necrosis and systemic toxic- (Thymostimulin).74 ity.24 Gaseous gangrene produces a quickly progressive Mortality rates in adults range from 8% to 100%.8,26,67 myonecrosis that involves deep fascia with early crepi- In newborns, the mortality rate can be as high as 87.5%.75 tation, severe local pain, and few cutaneous changes.67 The average mortality in children ranges from 10% to 60%, Pyoderma gangrenosum has a slow evolution and is fre- with a mean of 20%.18 Most deaths are due to sepsis or quently associated with ulcerative colitis, rheumatoid ar- multiorgan failure. In our series, mortality was average thritis, and myeloma.68 In cutaneous necrosis caused by (18%), mostly owing to infectious complications (eg, sep- the extravasation of intravenous drugs, the positive his- sis, septic hepatitis, and pneumonia) or volemic alter- tory findings are helpful.69 Ecthyma gangrenosum is due ations (disseminated intravascular coagulation and hy- to Pseudomonas aeruginosa and consists of pustules with povolemic shock). One patient died owing to tracheal an erythematous base that burst in hours and turn into compression, and another, owing to carotid rupture. punched, quickly progressive lesions with purpuric raised In the multivariate analysis, immunosuppression, hy- edges, more frequently located in the anogenital region, pothermia, and hypotension were the significant risk fac-

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©2002 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/28/2021 tors for death. Hypotension and hypothermia were con- 16. Murphy JJ, Granger R, Blair GK, Miller GG, Fraser GC, Magee JF. Necrotizing sidered terminal events. fasciitis in chilhood. J Pediatr Surg. 1995;30:1131-1134. 17. Lou J, Low CH. Necrotising fasciitis in leukaemic children. Ann Acad Med Sin- Sequelae were present in 29 (91%) of 32 survivers, gapore. 1990;19:290-294. most frequently unsightly scars (23 patients [72%]) and 18. Collette CJ, Southerland D, Corrall CJ. Necrotizing fasciitis associated with Hae- deformity (18 [56%]). Other observed sequelae included mophilus influenzae type b. AJDC. 1987;141:1146-1148. joint function limitation in 6 patients (19%), laryngeal ste- 19. Ramamurthy RS, Srinivasan G, Jacobs NM. Necrotizing fasciitis and necrotizing nosis in 1 (3%), and toe amputation in 1 (3%). cellulitis due to group B streptococcus. AJDC. 1977;131:1169-1170. 20. Duncan BW, Adzick NS, deLorimier AA, et al. Necrotizing fasciitis in two children with acute lymphoblastic leukemia. J Pediatr Surg. 1992;27:668- CONCLUSIONS 671. 21. Kosloske AM. Surgical infections in children. Curr Opin Pediatr. 1994;6:353- Necrotizing fasciitis is a severe multisystemic disorder 359. with prominent cutaneous features that can compro- 22. Dolmans S, Bostoen H, Allegaert W. Necrotizing fasciitis: an unusual soft tissue infection. Acta Chir Belg. 1974;73:563-572. mise life if diagnosis and treatment are delayed. After 23. Bomar WE, Ferlauto JJ, Wells DH. An unusual presentation of a ␤ hemolytic group the first month of life, the location of lesions is the same B streptococcal infection. J Pediatr Surg. 1980;15:683-685. in adults and children. The most frequent predisposing 24. Barton LL, Jeck DT, Vaidya VU. Necrotizing fasciitis in children: report of two cases factor in our patients was malnutrition. 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