You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 138 No. 7, July 2002 TABLE OF CONTENTS
  Archives
  •  Online Features
  Study
 This Article
 •Abstract
 •PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (28)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Topic Collections
 •Diagnosis
 •Alert me on articles by topic
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

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

Arch Dermatol. 2002;138:893-899.

ABSTRACT

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 children and the risk factors for fatal outcome.

Design  Retrospective, comparative, observational, and longitudinal trial.

Setting  Dermatology department of a tertiary care pediatric hospital.

Patients  All patients with clinical and/or histopathological diagnosis of NF seen from January 1, 1971, through December 31, 2000.

Main Outcome Variables  Incidence, age, sex, number and location of lesions, preexisting conditions, initiating factors, clinical and laboratory features, diagnosis 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 patients (36%). The most frequent initiating factor was varicella 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%). Pseudomonas aeruginosa was the most frequently isolated bacteria; 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 surviving patients. The significant risk factor related to a fatal outcome was immunosuppression.

Conclusions  Necrotizing fasciitis in children is frequently misdiagnosed, and several features differ from those of NF in adults. Immunosuppression was the main factor related to death. Early surgical debridement and antibiotics were the most important therapeutic measures.



INTRODUCTION
 Jump to Section
 •Top
 •Introduction
 •Patients and methods
 •Results
 •Comment
 •Conclusions
 •Author information
 •References

NECROTIZING fasciitis (NF) is a rare, rapidly progressive, and potentially fatal infection of the superficial fascia and subcutaneous cellular tissue.1-2 Necrotizing fasciitis is frequently polymicrobial, and the combination of aerobic and anaerobic bacteria contributes to the quick progression and severity of the disorder.3

Necrotizing fasciitis has been known since antiquity.4-5 In 1871, Jones6 gave the first clinical description of "hospital gangrene." In 1924, Meleney7 wrote a classic report on NF, emphasizing the importance of early diagnosis and surgical treatment to reduce mortality. In 1952, Wilson8 proposed the term necrotizing fasciitis to replace terms like gangrenous erysipelas, hospital gangrene, acute cutaneous gangrene, nonclostridial crepitant cellulitis, streptococcal gangrene, synergistic necrotizing cellulitis, Meleney cellulitis, and others. In addition, Wilson8 differentiated NF from disorders like erysipelas, cellulitis, and clostridial myonecrosis with muscle involvement. At present, a popular synonym is flesh-eating bacteria disease9.

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 largest reported.


PATIENTS AND METHODS
 Jump to Section
 •Top
 •Introduction
 •Patients and methods
 •Results
 •Comment
 •Conclusions
 •Author information
 •References

STUDY DESIGN

We performed a retrospective, observational, comparative, and longitudinal study.

SAMPLE POPULATION

We included all clinical records of patients hospitalized 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 commercial statistical software package (SPSS Base System; SPSS Inc, Chicago, Ill) for data analysis. All studied variables were analyzed in univariate form using t or {chi}2 test (P<=.05 was considered significant). Significant factors in the univariate analysis to predict risk for death were included in a logistic regression multivariate analysis.


RESULTS
 Jump to Section
 •Top
 •Introduction
 •Patients and methods
 •Results
 •Comment
 •Conclusions
 •Author information
 •References

We found 39 patients with a diagnosis of NF during the 30-year study period, representing 0.018% of all hospitalized patients. 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 years ± 4.7 months). The number and location of lesions, preexisting conditions, initiating factors, bacterial isolations, complications, evolution, and sequelae are shown in Table 1.


View this table:
[in this window]
[in a new window]
Features in 39 Patients With Necrotizing Fasciitis*


The signs and symptoms at the time of diagnosis were fever in 36 patients (92%), vomiting in 21 (54%), hypotension 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%). Local signs and symptoms were pain, hard edema, and erythema in all patients; local warmth in 33 (85%); and functional limitation in 29 (74%). Ecchymoses and necrosis were each recorded in 28 patients (72%), hemorrhagic blisters in 25 (64%), purulent secretion in 16 (41%), serous blisters in 14 (36%), local delayed capillary refill in 7 (18%), and crepitus in 4 (10%).

Serum laboratory findings showed hemoglobin levels 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 72 000 cells/µL (mean, 16 552 cells/µL); neutrophil levels, 18% to 87% (mean level, 59%); lymphocyte levels, 8% to 70% (mean level, 32%); monocyte and eosinophil levels, within the reference ranges; bands, 0% to 33% (mean, 4%); and platelet count, 10 to 400 x103/µL (mean, 188.4 x103/µL).

Results of radiographic studies performed in 13 patients (33%) showed soft tissue swelling in all and gas in 3 (8%).

Diagnoses at admission were cellulitis in 23 patients (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 varicella, septic arthritis, malnutrition, acute diarrhea, and disseminated intravascular coagulation in 1 patient each of the remaining 7.

Initial antibiotic treatment included amikacin sulfate, clindamycin phosphate, and gentamicin sulfate. A single antibiotic was used in 5 patients (13%); 2 antibiotics 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 recommended as soon as NF is diagnosed.

Surgical debridement with the patient under general 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 analysis of the variables was performed. Immunosuppression, delayed capillary refill, hypotension, hypothermia, 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 a multivariate analysis, hypothermia, hypotension, and immunosuppression remained the significant predictor factors of death (95% confidence intervals did not overlap 1; P<.001).


COMMENT
 Jump to Section
 •Top
 •Introduction
 •Patients and methods
 •Results
 •Comment
 •Conclusions
 •Author information
 •References

Necrotizing fasciitis is rare in children.10 It has been reported in 0.03% of hospitalization causes25 and in 0.08 per 100 000 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 predilection.26 In adults, the lower extremities are more frequently 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 series, the lower extremities constituted the most commonly affected area (17 patients [44%]).

Necrotizing fasciitis in the genital area is known as Fournier gangrene. It is more common in diabetic patients and in immunosuppressed males29 or after genital surgical procedures30 or rectal perforation.31 Fournier gangrene 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 setting of a Foley catheter tube in one and after an orchiopexy 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 presentation associated with high mortality,35-36 owing to carotid artery and mediastinal dissemination.37 Four of our patients 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 failure, obesity, alcoholism, and malnutrition, are important underlying factors.39 Nonsteroidal anti-inflammatory drugs have been implicated as a predisposing factor,11 although the relationship remains controversial.40 Some cases in children have been associated with immunosuppressive diseases such as acute lymphoblastic leukemia.10, 17, 20 In our series, half of the patients presented 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, initiating factors cannot be identified.7, 26-27 In newborns, omphalitis,1 circumcision,1, 44 and placement of electrodes for the monitoring of vital signs1 have been reported as initiating factors. In our series, initiating factors were determined 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 discoloration (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 lesion turns black with a necrotic crust (Figure 3). Removal of the crust shows fascial tissue and a brown grayish secretion.7 Subcutaneous cellular tissue is friable and easily removable. Sometimes the presence of gas (produced by aerobic and anaerobic bacteria) is recognized through tissue crepitation. This sign, although infrequent, is highly suggestive of NF.45 Necrosis of the superficial fascia is always more extensive than that indicated by the extension of skin necrosis.46



View larger version (45K):
[in this window]
[in a new window]
Figure 1. Necrotizing fasciitis on the third day shows erythema and edema.




View larger version (45K):
[in this window]
[in a new window]
Figure 2. Necrotizing fasciitis on the fifth day shows initial epidermal necrosis and hemorrhagic and serous blisters.




View larger version (74K):
[in this window]
[in a new window]
Figure 3. Necrotizing fasciitis on the seventh day shows well-defined necrosis.


Systemic signs and symptoms are a consequence of the toxic process and septicemia. A high fever is disproportionate in relation to the size of cutaneous lesion.7 Consciousness 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 pericardium may develop.7, 27 Tissue edema may deplete the vascular volume and provoke hemoconcentration, hypotension, obnubilation, and shock. Tachypnea, hyperglycemia (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 documented.26, 50 In our series, the isolates in 17 (71%) of 24 cases were polymicrobial.

Group A {beta}-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 involved.10, 23, 29, 46, 49, 51, 56-65 Fungi such as Aspergillus,64 Mucoraceae,46 and Candida albicans65 rarely are etiologic agents. Pseudomonas has been implicated as an important causal agent in patients with neutropenia.16 In our series, Pseudomonas 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 unresponsive 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 include necrosis of the superficial fascia; leukocytic infiltrates with polymorphonuclear cells predominant in fascia, subcutaneous fat tissue, and dermis; arterial and venous fascial thrombosis; angiitis with fibrinoid necrosis; 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 clinical diagnosis of NF.

Anemia, found in 29 (74%) of our cases and reported in 70% to 90% of cases in the literature,10, 26 is probably due to hemolysis. Leukocytosis was present in 25 (64%) and leukopenia in 5 (13%) of our cases. Trombocytopenia,10, 48 longer coagulation time, hypofibrinogenemia, and circulating fibrin degradation products can be a marker of disseminated intravascular coagulation.26 Disseminated intravascular coagulation was a complication in 11 (28%) of our cases and was fatal in 5 of them. Abnormal results of liver function tests,66 prerenal azotemia, hypocalcemia, hypoalbuminemia,48 and an increased creatine phosphokinase level47 may be present.

A differential diagnosis should be made with other infectious or necrotic processes with similar appearance. 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 toxicity.24 Gaseous gangrene produces a quickly progressive myonecrosis that involves deep fascia with early crepitation, severe local pain, and few cutaneous changes.67 Pyoderma gangrenosum has a slow evolution and is frequently associated with ulcerative colitis, rheumatoid arthritis, and myeloma.68 In cutaneous necrosis caused by the extravasation of intravenous drugs, the positive history 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 fulminans often appears after varicella and starts with ecchymotic areas in the extremities with inflammation, hemorrhage, and necrosis.71 In our series, cellulitis and purpura fulminans were the most frequent initial diagnoses.

Once vital signs are stable and the hydroelectrolytic balance is stabilized, extensive debridement of necrotic tissue must be performed (Figure 4), and the procedure must be repeated as many times as needed. Sudarsky et al39 reported a decrease in mortality from 50% to 0% in selected patients with appropriate early treatment. Freischlag et al72 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 administered accordingly. Antibiotics alone, because of their inability to reach the poorly vascularized and necrotic fascia, 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 Table 1), 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 appears.26, 48, 51 When indicated, total parenteral nutrition must be given.21



View larger version (49K):
[in this window]
[in a new window]
Figure 4. Necrotizing fasciitis after extensive surgical debridement of necrotic tissue.


The benefit of hyperbaric oxygen in NF remains controversial.73 Other poorly tested therapies include high doses of intravenous immune globulin, granulocyte transfusion, granulocyte colony-stimulating factor (in granulocytopenic 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, sepsis, septic hepatitis, and pneumonia) or volemic alterations (disseminated intravascular coagulation and hypovolemic shock). One patient died owing to tracheal compression, and another, owing to carotid rupture.

In the multivariate analysis, immunosuppression, hypothermia, and hypotension were the significant risk factors for death. Hypotension and hypothermia were considered 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 stenosis in 1 (3%), and toe amputation in 1 (3%).


CONCLUSIONS
 Jump to Section
 •Top
 •Introduction
 •Patients and methods
 •Results
 •Comment
 •Conclusions
 •Author information
 •References

Necrotizing fasciitis is a severe multisystemic disorder with prominent cutaneous features that can compromise 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 immunosuppression. 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.


AUTHOR INFORMATION
 Jump to Section
 •Top
 •Introduction
 •Patients and methods
 •Results
 •Comment
 •Conclusions
 •Author information
 •References

Accepted for publication June 29, 2001.

Corresponding author and reprints: Ramon Ruiz-Maldonado, MD, Insurgentes Sur 3700-C, Colonia Insurgentes Cuicuilco, Mexico City, Mexico CP 04530 (e-mail: rrm{at}servidor.unam.mx).

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.


REFERENCES
 Jump to Section
 •Top
 •Introduction
 •Patients and methods
 •Results
 •Comment
 •Conclusions
 •Author information
 •References

1. Kosloske AM, Cushing AH, Borden TA, et al. Cellulitis and necrotizing fasciitis of the abdominal wall in pediatric patients. J Pediatr Surg. 1981;16:246-251. FULL TEXT | ISI | PUBMED
2. Goldwag DA, Purcell TB. Necrotizing fasciitis in the pediatric age group: report of a case. J Emerg Med. 1990;8:299-304. FULL TEXT | PUBMED
3. Giuliano A, Lewis F Jr, Hadley K, Blaisdell FW. Bacteriology of necrotizing fasciitis. Am J Surg. 1977;134:52-57. FULL TEXT | ISI | PUBMED
4. Hippocrates. Works. Jones WHS, trans. Vol 2. New York, NY: GP Putnam's Sons; 1933:46-49.
5. Finegold SM. Anaerobic infections. Surg Clin North Am. 1980;60:49-64. ISI | PUBMED
6. Jones J. Investigations Upon the Nature, Causes, and Treatment of Hospital Gangrene as It Prevailed in the CONFEDERATE Armies, 1861-1865. New York, NY: US Sanitary Commission, Surgical Memoirs of The War of Rebellion: 1871. Cited by: Meleney FL. Treatise on Surgical Infections. New York, NY: Oxford University Press; 1948:15.
7. Meleney FL. Hemolytic streptococcus gangrene. Arch Surg. 1924;9:317-364. FREE FULL TEXT
8. Wilson BL. Necrotizing fasciitis. Am Surg. 1952;18:416-431. PUBMED
9. Morantes MC, Lipsky BA. "Flesh-eating bacteria": return of an old nemesis. Int J Dermatol. 1995;34:461-463. ISI | PUBMED
10. Wilson HD, Haltalin KC. Acute necrotizing fasciitis in childhood: report of 11 cases. AJDC. 1973;125:591-595.
11. Rimailho A, Riou B, Richard C, Auzepy P. Fulminant necrotizing fasciitis and nonsteroidal anti-inflammatory drugs. J Infect Dis. 1987;155:143-146. PUBMED
12. Moss RL, Musemeche CA, Kosloske AM. Necrotizing fasciitis in children: prompt recognition and aggressive therapy improve survival. J Pediatr Surg. 1996;31:1142-1146. FULL TEXT | ISI | PUBMED
13. Laupland KB, Davies HD, Low DE, Schwartz B, Green K, McGeer A and the Ontario Group A Streptococcal Study Group. Invasive group A streptococcal disease in children and association with varicella-zoster virus infection. Pediatrics. 2000;105:e60.
14. Hsieh T, Samson LM, Jabbour M, Osmond MH. Necrotizing fasciitis in children in eastern Ontario: a case-control study. CMAJ. 2000;163:393-396. FREE FULL TEXT
15. Goldberg GN, Hansen RC, Lynch PJ. Necrotizing fasciitis in infancy: report of three cases and review of the literature. Pediatr Dermatol. 1984;2:55-63. PUBMED
16. Murphy JJ, Granger R, Blair GK, Miller GG, Fraser GC, Magee JF. Necrotizing fasciitis in chilhood. J Pediatr Surg. 1995;30:1131-1134. FULL TEXT | ISI | PUBMED
17. Lou J, Low CH. Necrotising fasciitis in leukaemic children. Ann Acad Med Singapore. 1990;19:290-294. PUBMED
18. Collette CJ, Southerland D, Corrall CJ. Necrotizing fasciitis associated with Haemophilus influenzae type b. AJDC. 1987;141:1146-1148.
19. Ramamurthy RS, Srinivasan G, Jacobs NM. Necrotizing fasciitis and necrotizing 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;27:668-671. ISI | PUBMED
21. Kosloske AM. Surgical infections in children. Curr Opin Pediatr. 1994;6:353-359. PUBMED
22. Dolmans S, Bostoen H, Allegaert W. Necrotizing fasciitis: an unusual soft tissue infection. Acta Chir Belg. 1974;73:563-572. ISI | PUBMED
23. Bomar WE, Ferlauto JJ, Wells DH. An unusual presentation of a {beta} hemolytic group B streptococcal infection. J Pediatr Surg. 1980;15:683-685. FULL TEXT | ISI | PUBMED
24. Barton LL, Jeck DT, Vaidya VU. Necrotizing fasciitis in children: report of two cases and review of the literature. Arch Pediatr Adolesc Med. 1996;150:105-108. FREE FULL TEXT
25. Fujisawa N, Yamada H, Kohda H, Tadano J, Hayashi S. Necrotizing fasciitis caused by Vibrio vulnificus differs from that caused by streptococcal infection. J Infect. 1998;36:313-316. FULL TEXT | ISI | PUBMED
26. Rea WJ, Wyrick WJ. Necrotizing fasciitis. Ann Surg. 1970;172:957-964. ISI | PUBMED
27. Freeman HP, Oluwole SF, Ganepola GA, Dy E. Necrotizing fasciitis. Am J Surg. 1981;142:377-383. FULL TEXT | ISI | PUBMED
28. Ryan CA, Fischer J, Gayle M, Wenman W. Surgical and postoperative management of two neonates with necrotizing fasciitis. Can J Surg. 1993;36:337-341. ISI | PUBMED
29. Hirn M, Niinikoski J. Management of perineal necrotizing fasciitis (Fournier's gangrene). Ann Chir Gynaecol. 1989;78:277-281. ISI | PUBMED
30. Walther PJ, Andriani RT, Maggio MI, Carson CC. Fournier's gangrene: a complication of penile prosthetic implantation in a renal transplant patient. J Urol. 1987;137:299-300. ISI | PUBMED
31. Khan SA, Smith NL, Gonder M, Ravo B, Siddharth P. Gangrene of male external genitalia in a patient with colorectal disease: anatomic pathways of spread. Dis Colon Rectum. 1985;28:519-522. ISI | PUBMED
32. Adeyokunnu AA. Fournier's syndrome in infants: a review of cases from Ibadan, Nigeria. Clin Pediatr (Phila). 1983;22:101-103.
33. Heemann KF, Homann W, Pistor K. Fournier's gangrene in a 2-month-old infant. Klin Padiatr. 1984;196:392-393. ISI | PUBMED
34. Sanjeev Rai B, Baliga BV, Shenoy MR, Pai KR, Krishnamurthy PN. Fournier's gangrene in an infant. Indian J Pediatr. 1984;51:99-100. PUBMED
35. Brenner BE, Vitullo M, Simon RR. Necrotizing fasciitis. Ann Emerg Med. 1982;11:384-386. FULL TEXT | ISI | PUBMED
36. Langenbrunner DJ, Dajani S. Pharyngomaxillary space abscess with carotid artery erosion. Arch Otolaryngol. 1971;94:447-457. FREE FULL TEXT
37. Mathieu D, Neviere R, Teillon C, Chagnon JL, Lebleu N, Wattel F. Cervical necrotizing fasciitis: clinical manifestations and management. Clin Infect Dis. 1995;21:51-56. ISI | PUBMED
38. Oh C, Lee C, Jacobson JH. Necrotizing fasciitis of the perineum. Surgery. 1982;91:49-51. ISI | PUBMED
39. Sudarsky L, Laschinger JC, Coppa GF, Spencer FC. Improved results from a standardized approach in treating patients with necrotizing fasciitis. Ann Surg. 1987;206:661-665. ISI | PUBMED
40. Zerr DM, Rubens CE. NSAIDS and necrotizing fasciitis. Pediatr Infect Dis J. 1999;18:724-725. FULL TEXT | ISI | PUBMED
41. Svensson LG, Brookstone AJ, Wellested M. Necrotizing fasciitis in contused areas. J Trauma. 1985;25:260-262. ISI | PUBMED
42. Brook I. Aerobic and anaerobic microbiology of necrotizing fasciitis in children. Pediatr Dermatol. 1996;13:281-284. ISI | PUBMED
43. Kyong CU, Smith CD, Othersen HB. Necrotizing fasciitis of the abdominal wall as a complication of chickenpox. Pediatr Infect Dis. 1985;4:420-421. FULL TEXT | ISI | PUBMED
44. Fisher RG. Plastibell circumcision: a novel complication [letter]. J Pediatr. 1998;133:468. ISI | PUBMED
45. Fisher JR, Conway MJ, Takeshita RT, Sandoval MR. Necrotizing fasciitis: importance of roentgenographic studies for soft-tissue gas. JAMA. 1979;241:803-806. FREE FULL TEXT
46. Stone DR, Gorbach SL. Necrotizing fasciitis. The changing spectrum. Dermatol Clin. 1997;15:213-220. FULL TEXT | ISI | PUBMED
47. Misago N, Narisawa Y, Ryu S, et al. Necrotizing fascitis due to group A streptococci: a clinicopathological study of six patients. J Dermatol. 1996;23:876-882. PUBMED
48. Addison WA, Livengood CH, Hill GB, Sutton GP, Fortier KJ. Necrotizing fasciitis of vulvar origin in diabetic patients. Obstet Gynecol. 1984;63:473-479. ISI | PUBMED
49. Choudhri SH, Brownstone R, Hashem F, Magro CM, Crowson AN. A case of necrotizing fascitis due to Streptococcus pneumoniae. Br J Dermatol. 1995;133:128-131. FULL TEXT | ISI | PUBMED
50. Brown DR, Davis NL, Lepawsky M, Cunningham J, Kortbeek J. A multicenter review of the treatment of major truncal necrotizing infections with and without hyperbaric oxygen therapy. Am J Surg. 1994;167:485-489. FULL TEXT | ISI | PUBMED
51. Farrell LD, Karl SR, Davis PK, Bellinger MF, Ballantine TVN. Postoperative necrotizing fasciitis in children. Pediatrics. 1988;82:874-879. FREE FULL TEXT
52. Stevens DL, Tanner MH, Winship J, et al. Severe group A streptococcal infections associated with a toxic shock–like syndrome and scarlet fever toxin A. N Engl J Med. 1989;321:1-7. ABSTRACT
53. Wolf JE, Rabinowitz LG. Streptococcal toxic shock–like syndrome. Arch Dermatol. 1995;131:73-77. FREE FULL TEXT
54. Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med. 1996;334:240-245. FREE FULL TEXT
55. Feingold DS, Weinberg AN. Group A streptococcal infections: an old adversary reemerging with new tricks? Arch Dermatol. 1996;132:67-70. FREE FULL TEXT
56. Casali RE, Tucker WE, Petrino RA, Wastbrook KC, Read RC. Postoperative necrotizing fasciitis of the abdominal wall. Am J Surg. 1980;140:787-790. FULL TEXT | ISI | PUBMED
57. Crawford SA, Evans JA, Crawford GE. Necrotizing fasciitis of the upper extremity associated with Haemophilus achrophilius: report of a case. Arch Intern Med. 1978;138:1714-1715. FREE FULL TEXT
58. Tang WM, Wong JWK. Necrotizing fasciitis caused by Vibrio damsela. Orthopedics. 1999;22:443-444. ISI | PUBMED
59. Webb, R, Berg E. Symbiotic gangrene due to Pseudomonas pyocyanea and E coli. Aust N Z J Surg. 1966;36:159-160. PUBMED
60. Roberts DB. Necrotizing fasciitis of the vulva. Am J Obstet Gynecol. 1987;157:568-571. ISI | PUBMED
61. Steel A. An unusual case of necrotizing fasciitis. Br J Oral Maxillofac Surg. 1987;25:328-333. FULL TEXT | ISI | PUBMED
62. Cornu E, Christides C, Lacroix Ph, et al. Fasciite necrosante: une urgence médicale et chirurgicale: a propos d'un cas. J Chir (Paris). 1992;129:169-171.
63. Stamenkovic I, Lew PD. Early recognition of potentially fatal necrotizing fasciitis: the use of frozen-section biopsy. N Engl J Med. 1984;310:1689-1693. ABSTRACT
64. Johnson MA, Lyle G, Hanly M, Yeh KA. Aspergillus: a rare primary organism in soft-tissue infections. Am Surg. 1998;64:122-126. ISI | PUBMED
65. Gaukroger MC. Cervicofacial necrotizing fasciitis. Br J Oral Maxillofac Surg. 1992;30:111-114. FULL TEXT | ISI | PUBMED
66. White W. Hemolytic streptococcal gangrene. Plast Recontr Surg. 1980;11:1-14.
67. Barzilai A, Zaaroor M, Toledano C. Necrotizing fasciitis: early awareness and principles of treatment. Isr J Med Sci. 1985;21:127-132. ISI | PUBMED
68. Koehn GG. Necrotizing fasciitis. Arch Dermatol. 1978;114:581-583. FREE FULL TEXT
69. Brown A, Hoelzer DJ, Piercy SA. Skin necrosis from extravasation of intravenous fluids in children. Plast Reconstr Surg. 1979;64:145-150. ISI | PUBMED
70. Heffner RW, Smith GF. Ecthyma gangrenosum in pseudomonas septicemia. AJDC. 1960;99:524-528.
71. Smith EW, Garson A Jr, Boyleston JA, Katz SL, Wilfert CM. Varicella gangrenosa due to group A beta-hemolytic streptococcus. Pediatrics. 1976;57:306-310. FREE FULL TEXT
72. Freischlag JA, Ajalat G, Busuttil RW. Treatment of necrotizing soft tissue infections: the need for a new approach. Am J Surg. 1985;149:751-755. FULL TEXT | ISI | PUBMED
73. Feldmeier JJ, Workman WT. The USAF Hyperbaric Center: a look through the porthole. Mil Med. 1983;148:118-121. ISI | PUBMED
74. Lin CY, Hsu CH, Liu KC, Chen CL, Hsu HC. Serial immunologic and histopathologic studies in the treatment of necrotizing fasciitis with combined immunodeficiency by a bovine thymic extract (Thymostimulin). J Pediatr Surg. 1986;21:1000-1004. ISI | PUBMED
75. Lally KP, Atkinson JB, Woolley MM, Mahour GH. Necrotizing fasciitis: a serious sequela of omphalitis in the newborn. Ann Surg. 1984;199:101-103. ISI | PUBMED


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

CD46 Transgenic Mouse Model of Necrotizing Fasciitis Caused by Streptococcus pyogenes Infection
Matsui et al.
Infect. Immun. 2009;77:4806-4814.
ABSTRACT | FULL TEXT  

Necrotizing fasciitis
Puvanendran et al.
cfp 2009;55:981-987.
ABSTRACT | FULL TEXT  

Necrotizing Fasciitis in a Young Girl With Atopic Eczema
Brady and Levin
CLIN PEDIATR 2007;46:181-183.
 

Abdominal cellulitis due to Escherichia coli in a two month old premature newborn.
Dauger et al.
Arch. Dis. Child. Fetal Neonatal Ed. 2006;91:F442-F442.
FULL TEXT  

Clostridial Myonecrosis in an Adolescent Male
Langhan and Arnold
Pediatrics 2005;116:e735-e737.
ABSTRACT | FULL TEXT  

Acute Bullous Eruption With Compartment Syndrome Due to Intravenous Infiltration
Spenny et al.
Arch Dermatol 2004;140:798-800.
FULL TEXT  

Musculoskeletal Infections in Children. Basic Treatment Principles and Recent Advancements
McCarthy et al.
JBJS 2004;86:850-863.
FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2002 American Medical Association. All Rights Reserved.