Published online March 27, 2006
PEDIATRICS Vol. 117 No. 4 April 2006, pp. e796-e805 (doi:10.1542/peds.2005-1074)
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Clostridium septicum Infections in Children: A Case Report and Review of the Literature

Candra L. Smith-Slatas, MD, PhDa,b, Michael Bourque, MDc,d and Juan C. Salazar, MD, MPHb,e

a ProHealth Physicians, Wethersfield, Connecticut
b Pediatrics
c Surgery, University of Connecticut School of Medicine, Farmington, Connecticut
d Surgery
e Pediatric Infectious Diseases, Connecticut Children's Medical Center, Hartford, Connecticut


   ABSTRACT
TOP
 ABSTRACT
CASE REPORT
 REVIEW OF PUBLISHED PEDIATRIC...
 DISCUSSION
 CONCLUSION
 REFERENCES
 
Clostridium myonecrosis is a rare and deadly infection that progresses very rapidly; thus, prompt diagnosis and treatment is vital. In adults, clostridial myonecrosis used to be a well-known complication of war wounds. Today, it is usually seen in settings of trauma, surgery, malignancy, skin infections/burns, and septic abortions. More recently, cases of nontraumatic or spontaneous clostridial myonecrosis have been reported in both adults and children. Clostridium perfringens and Clostridium septicum are responsible for the majority of the clinically relevant infections. Higher mortality rates are seen when C septicum is the causative agent.

Here we present a child who survived a severe case of C septicum myonecrosis involving both abdominal and thoracic cavities. This rare infection has a high mortality rate and might be easily misdiagnosed in children, even by experienced clinicians, because of its nonspecific presentation. We also review all reported pediatric cases of C septicum infection and myonecrosis and discuss the surgical and medical interventions associated with improved survival.

We identified a total of 47 cases of C septicum infection; of these, 22 (47%) were cases of C septicum associated with myonecrosis. Several factors, if available, were analyzed for each case: age, gender, infection location, previous diagnoses, presenting signs and symptoms, neutropenia, gross pathology of the colon, antibiotic use, surgical intervention, and final outcome.

We found that conditions related with C septicum infection in children can be grouped into 3 major categories: patients with neutrophil dysfunction; patients with associated bowel ischemia; and patients with a history of trauma. Malignancies were found in 49% of the cases, cyclic or congenital neutropenia in 21%, hemolytic-uremic syndrome in 11%, structural bowel ischemia in 4%, and local extremity trauma in 6%. In addition, 6% of the cases had no known underlying disorder. Abdominal symptoms including vomiting, diarrhea, blood per rectum, abdominal pain, anorexia, and/or acute abdomen, were reported in 85% of the children. Fever was also a common finding.

The mainstay of treatment for C septicum infection was parenteral antibiotics and/or surgical intervention. The mortality rate for children with C septicum infection and myonecrosis was 57% and 59%, respectively. Although 82% of all cases received antibiotics, only 43% underwent therapeutic surgical intervention. Several clinical factors were found to be associated with improved survival. Only 35% of the children with gastrointestinal tract involvement survived, compared with 86% of the children without gastrointestinal tract involvement. The survival rates for other conditions ranged from 0% to 50%. One hundred percent survival was reported in patients with no previously diagnosed conditions and those with infections resulting from trauma to the extremities. All survivors received antibiotic treatment, compared with only 68% of the nonsurvivors. Most survivors (84%) underwent therapeutic surgical intervention, compared with only 12% of nonsurvivors. Other treatments were used adjunctively, including hyperbaric oxygen, granulocyte colony-stimulating factor, granulocyte transfusions, and intravenous immunoglobulin.

C septicum infections in children are often fatal; thus, one needs to have a high index of suspicion in at-risk patients. This review describes who these patients are, their clinical presentation, and the therapeutic strategies associated with improved survival.

Key Words: Clostridium septicum • myonecrosis • gas gangrene • necrotizing enterocolitis • hyperbaric oxygenation • granulocyte colony-stimulating factor • intravenous immunoglobulin • neutropenia • malignancy • hemolytic-uremic syndrome

Abbreviations: ED, emergency department • OR, operating room • WBC, white blood cell • CT, computed tomography • IVIg, intravenous immunoglobulin • HUS, hemolytic- uremic syndrome • G-CSF, granulocyte colony-stimulating factor

Clostridium myonecrosis is a rare and often fatal infection resulting from rapid invasion and destruction of muscle tissue. Only 1000 to 3000 cases per year are reported in the United States, most of which occur in adults with severe underlying medical conditions.1,2 Nontraumatic or "spontaneous" clostridial infections account for ~10% of all reported cases in both adults and children.1,3–44 This form of the disease is more deadly than wound-related myonecrosis because of its insidious onset with subsequent rapid clinical deterioration.4

Clostridia are large, Gram-positive, anaerobic bacilli that are nonpathogenic in normal gut flora but can cause infection quickly if gut tissue becomes necrotic or inflamed.2,45 Although clostridial species are frequently found in the gastrointestinal tract, Clostridium septicum is only grown from feces in 2.8% of the healthy adult population; thus, it is somewhat rare.46 Because clostridia can reproduce readily in low-oxygen conditions, infections are usually seen in the setting of decreased blood supply. In fact, most cases are seen in patients with a history of trauma, recent surgery, complicated peripheral vascular disease, diabetes, colon cancer, skin infections/burns, and septic abortions, among others.3,4,47,48 Only 6 members of the clostridial species can invade muscle and cause myonecrosis in humans,45,47,49,50 and of those, Clostridium perfringens and C septicum are responsible for the majority of clinically relevant infections.3,5–7,45,47 Higher mortality rates are seen when C septicum is the causative agent: a mortality rate of 79% in adults with C septicum myonecrosis versus a mortality rate of 32% in adults with C perfringens myonecrosis.3,45,51

C septicum infections are rarely seen in children and therefore might not be easily recognized even by experienced clinicians. In this article we present the successful management of a child with a severe C septicum infection involving both abdominal and thoracic cavities and evaluate the reported pediatric cases of C septicum infection. In doing so we intend to clarify the causes of this disease in children and discuss the surgical and medical interventions associated with improved survival.


   CASE REPORT
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 CASE REPORT
REVIEW OF PUBLISHED PEDIATRIC...
 DISCUSSION
 CONCLUSION
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A previously healthy 5-year-old girl was brought to the Connecticut Children's Medical Center's emergency department (ED) with a complaint of abdominal pain and blood-tinged fluid leaking from her rectum. In addition, there was a 6-day history of fever and poor appetite, a 2-day history of crampy abdominal pain, a 1-day history of decreased urine output, and 1 episode of coffee-ground emesis. There was no history of trauma, foreign travel, animal exposures, ingestion of raw foods, recent antibiotic use, or sick contacts.

Initial physical examination in the ED revealed that she was listless but responsive to verbal stimuli. Her vital signs were significant for a temperature of 38.2°C, a pulse rate of 184 beats/minute, a respiratory rate of 38/minute, and a blood pressure of 120/65 mm Hg. She had dry mucous membranes and a capillary refill time of 2 to 3 seconds. Her abdomen was diffusely tender with hypoactive bowel sounds, but there was no organomegaly, mass, guarding, or rebound tenderness. There was a 0.5-cm area of rectal mucosa intermittently prolapsing. An abdominal radiograph showed minimal air-fluid levels and no free air. A chest radiograph was normal. Her initial laboratory results showed anion-gap acidosis (venous pH: 7.19; anion gap: 24 mEq/L) with an elevated serum lactate level at 7.5 mmol/L (reference: 0.5–2.2 mmol/L). She had a white blood cell (WBC) count of 5600 cells per mm3 with a left shift (44% bands, 41% neutrophils) and had evidence of hemoconcentration (hematocrit: 46%). A platelet count was within the normal range at 417000 cells per mm3. Serum urea nitrogen and creatinine were within the reference range with values of 16 and 0.9 mg/dL, respectively. She had a minimally elevated C-reactive protein (2.34 mg/dL; reference: 0–0.5 mg/dL) but a normal erythrocyte sedimentation rate (3 mm/hour). Amylase and lipase were found to be normal. Results from coagulation studies including prothrombin time and partial thromboplastin time were normal. Stool and blood cultures were sent. No urine was available for analysis.

She was given a 40 mL/kg fluid bolus and admitted with a diagnosis of severe gastroenteritis and dehydration 2 hours after presenting to the ED. Over the next 2 hours, she had worsening abdominal pain with guarding and coffee-ground emesis. She remained tachycardic and became hypotensive despite aggressive fluid management, requiring transfer to the pediatric intensive care unit (PICU) with a diagnosis of septic shock and infectious enterocolitis. On arrival in the PICU she was febrile (40°C), tachycardic (204 beats/minute), tachypneic (30 breaths/minute), and hypotensive (73/27 mm Hg). Repeat abdominal radiographs were unchanged. Two hours later, an abdominal ultrasound showed diffuse bowel wall edema. Repeat laboratory studies 9 hours after presentation revealed that she had developed a coagulopathy (prothrombin time: 18.1 seconds; partial thromboplastin time: 42.7 seconds), anemia with evidence of hemolysis (hematocrit: 30% with Burr cells, polychromasia, increased aspartate aminotransferase and lactate dehydrogenase), neutropenia (WBC count: 1000 cells per mm3 with 4% metamyelocytes, 12% bands, 4% neutrophils, and 80% lymphocytes), and thrombocytopenia (platelet count: 159000 cells per mm3). She initially received 2 units of packed red blood cells and 2 units of fresh-frozen plasma.

Her course rapidly deteriorated and required mechanical ventilation. A repeat abdominal radiograph 11 hours after presentation showed a paucity of bowel gas and early pneumatosis in the left upper quadrant. An emergent abdominal computed tomography (CT) scan that was done within the hour showed pneumatosis in the colon near the splenic flexure and both intraperitoneal and retroperitoneal free air that tracked up the iliopsoas to the level of the kidney and down into the pelvis (Fig 1). At that time she was also noted to have developed an ecchymotic discoloration on her left abdomen and flank.


Figure 1
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  		FIGURE 1 The scout film from the emergent CT scan illustrates the extent of the infection. Free air is seen tracking down the left psoas muscle into the pelvis, and pneumatosis is seen in the bowel wall in the left upper quadrant.

 
Once hemodynamically more stable, she was taken to the operating room (OR) for surgical resection of necrotic bowel. The transverse and descending colon were removed after they were found to be grossly infarcted, necrotic, and perforated. Subsequent pathologic examination of resected tissue revealed edema, hemorrhage, and necrosis with a striking paucity of WBCs (neutropenic colitis).5,8,12,18 In addition, a large torsed juvenile polyp was seen near the splenic flexure, which was felt to be the entry site of the infection. The repair of her gastrointestinal tract was complicated by the congenital absence of a marginal arterial arcade of Drummond,52,53 necessitating the removal of the ascending colon and cecum. In addition, her left psoas, iliacus, paraspinal and abdominal wall muscles were found to be necrotic and thus were resected.

Broad-spectrum antibiotics (meropenem, metronidazole, and clindamycin) were started before surgery along with 1 dose of intravenous immunoglobulin (IVIg) at 400 mg/kg. She received 4 additional doses of IVIg over the next several days. Within 48 hours from presentation, a pan-sensitive C septicum was isolated from blood cultures, peritoneal fluid cultures, and necrotic muscle tissue samples. Thus, meropenem was discontinued, and penicillin G (6 million U/day [300000 U/kg per day]) was added to the antibiotic regimen. She remained on this therapy for 21 days. Daily blood and surgical-site cultures became negative within 48 hours of antibiotic treatment.

A repeat CT on the second day of hospitalization showed that the pneumatosis had spread to her left thigh and left diaphragm. She went to the OR daily for 2 weeks for repeated exploration and further resection of necrotic tissue. Ultimately, much tissue was resected, including her left back and flank musculature, left groin muscles, 80% of the left diaphragm, sections of the left lower ribs along with the intercostal muscles, the transverse processes of several lumbar vertebrae, the skin on the left flank, the left kidney, and left ureter.

Many medical problems complicated her postsurgical course including acute renal failure, pneumonia, seizures, and hypertension. Over time, she showed remarkable improvement and began to ambulate after split-thickness skin grafts were placed on her abdomen and left flank. She was discharged from the hospital 7 and a half months after admission and was doing well at the time of this writing.


   REVIEW OF PUBLISHED PEDIATRIC CASES
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 ABSTRACT
 CASE REPORT
 REVIEW OF PUBLISHED PEDIATRIC...
DISCUSSION
 CONCLUSION
 REFERENCES
 
All published, English-language, Medline-reported pediatric cases (≤18 years old) of C septicum infection and C septicum myonecrosis were included in this review. Several factors, if available, were analyzed for each case: age, gender, infection location, previous diagnoses, presenting signs and symptoms, neutropenia, gross pathology of the colon, antibiotic use, surgical intervention, and final outcome. As seen in Table 1, we identified a total of 47 cases of C septicum infection; of these, 22 (47%) were cases of C septicum associated with myonecrosis. Cases were distributed equally between males and females. Because no major differences were found for reported cases with or without myonecrosis, we elected to combine both entities for this analysis.


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  		TABLE 1 Clostridium septicum Infections in Children

 
In our review of published pediatric literature, we found that conditions related with C septicum infection in children can be grouped into 3 major categories: patients with neutrophil dysfunction (including malignancies, congenital or cyclic neutropenia, aplastic anemia); patients with associated bowel ischemia (hemolytic-uremic syndrome [HUS], intussusception, torsed polyp); and patients with a history of trauma (Tables 1 and 2). Malignancies were found in 49% of the cases of C septicum infection, with acute myelocytic and lymphocytic leukemias as the most common diagnoses. This link between C septicum infection and malignancy in children was first established by Alpern and Dowell in 196914 and corroborated by a more recent study38 in which 79% of pediatric patients with C septicum infection had an associated malignancy. Others have reported a similar association in children.*


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  		TABLE 2 Clostridium septicum Infection: Clinical Features and Survival

 
Cyclic and congenital neutropenia was present in 21% of the published pediatric cases.10,12,15,18,31,38,39,44 In other cases, neutropenia was observed only at the time of presentation with C septicum infection (Table 1)5,17,33,35,37–39,41. In most of the cases in which neutropenia was first seen at the time presentation, there was an underlying malignancy,5,17,33,35,37,38,41 and the neutropenia was likely secondary to this disease process or its treatment (ie, chemotherapy or radiation). Eleven percent of cases were reported in pediatric patients with complicated HUS.29,30,32,36,42 Structural bowel ischemia also predisposed 2 additional patients, including our patient, to C septicum infection.14 Three cases were associated with local trauma to the extremities,43,55,56 and only 3 children had no known underlying disorder.11,38,43

Several clinical features are described in pediatric C septicum infections.40 In our review, abdominal symptoms including vomiting, diarrhea, blood per rectum, abdominal pain, anorexia, and/or acute abdomen were reported in 85% of the children (Tables 1 and 2). Fever was also a common finding. The mainstays of treatment for C septicum infection are surgical intervention and parenteral antibiotics. As seen in Table 1, most of the patients (82%) received antibiotic treatment, but only 43% underwent therapeutic surgical intervention. All of the patients that received surgical intervention had also received antibiotics. Adjunctive therapy with hyperbaric oxygen and granulocyte colony-stimulating factor (G-CSF) was also used in some patients.15,44

In our review we found mortality rates of 57% for children with C septicum infection and 59% for children with C septicum myonecrosis (Table 1). Previously published pediatric mortality rates for C septicum infection with or without myonecrosis were higher (71–75%), but these rates were calculated in smaller case series.38,40

Due to the retrospective nature of this review, we can't causally link associated clinical features, location of the infection, previous diagnoses, and treatments to improved survival rates in pediatric C septicum infection. However, our review demonstrates an association between improved survival rates and various clinical factors (Tables 2 and 3). The highest survival rates were seen in patients with no previously diagnosed conditions or those with local trauma to an extremity (100% survival). The combined overall survival rate for patients with a history of cancer was 30%, but only 20% of the patients with HUS survived. Patients with cyclic or congenital neutropenia had a survival rate of 50%. The presence of neutropenia at the time of diagnosis did not vary between survivors and nonsurvivors; however, 94% of the nonsurvivors had abnormal pathological findings in the colon as compared with only 47% of the survivors. This finding underscores the significant impact that infection location has on survival, especially if myonecrosis is present. In fact, only 35% of the children with gastrointestinal tract involvement survived, compared with 86% of the children without gastrointestinal tract involvement. The vast majority of the pediatric survivors of C septicum myonecrosis described in the literature suffered from metastatic spread to an extremity, requiring amputation,10,11,15,38,43 or to the abdominal wall, requiring resection.15 C septicum infection with demonstrated myonecrosis in the gastrointestinal tract is quite devastating, and until the case reported here, there was only 1 other survivor reported.44 Our case represents the first time that a child has been reported to survive C septicum infection with myonecrosis in both the gastrointestinal tract and the thoracic cavity.


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  		TABLE 3 Clostridium septicum Infection: Characteristics of Survivors Versus Nonsurvivors

 
Not surprisingly, both surgical intervention and antibiotic use were also found to be associated with improved survival (Tables 1 and 3). All survivors (100%) received antibiotic treatment, compared with only 68% of nonsurvivors, and none of the patients who didn't receive antibiotics survived. Most survivors (84%) underwent therapeutic surgical intervention, compared with only 12% of the nonsurvivors. This is in accord with the report by Bratton et al,38 who noted that a higher percentage of the survivors had early surgical intervention than the nonsurvivors. Although the use of antibiotics was shown to decrease mortality in adult patients with clostridial infections,14,54 it has never expressly been shown to affect outcome in pediatric patients; however, one can surmise this from the literature.14,38,40


   DISCUSSION
TOP
 ABSTRACT
 CASE REPORT
 REVIEW OF PUBLISHED PEDIATRIC...
 DISCUSSION
CONCLUSION
 REFERENCES
 
This case report and comprehensive examination of the pediatric literature reviews the associated conditions, common clinical presentation, and therapeutic strategies used in children diagnosed with severe C septicum infections. We have shown here that most reported pediatric cases are not related to trauma and instead result from metastatic or local spread of C septicum. The large intestine is probably the site of entry for nontraumatic, "spontaneous" clostridial infections in both adults and children.10,24,38 In our patient, no malignancies or hematologic abnormalities were found. Instead, the location of a torsed colonic juvenile polyp suggests that this was the site of her initial infection. Torsion could have caused a decrease in local oxygen tension, proliferation of C septicum, toxin production, destruction of the gut mucosa, and extensive compromise of adjacent and distant anatomic structures.

Typhlitis or necrotizing enterocolitis of the colon with massive involvement of the cecum and ileocecal area is typically seen in cases of C septicum infection.5,15,16,18,27,38,57 In this review we found that 70% of the reported patients had abnormal pathological findings in the colon, including the patient presented here. Several factors may play a role in the predisposition of this site for infection. Poor vascular supply,52,53 local redox potential, pH, and osmotic and electrolyte environment allow for C septicum to thrive in the ileocecal area.57 Because C septicum is seen in immunodeficient patients, it is possible that the malignancy itself or its treatment might impair the immune function of the gastrointestinal mucosa enough to allow for colonization by C septicum.3,5,7,14

C septicum then may gain access to the circulation via mucosal ulcerations resulting from neoplastic lesions, cytotoxic drugs, irradiation, and immunosuppressive drugs.9,27 Neutropenia alone can also increase mucosal ulceration in the colon, thus allowing for metastatic spread of C septicum infection.15,18 Inflamed, necrotic areas of colon have been seen in leukemic patients,21,49 with associated areas of C septicum proliferation.5,17 In 1 study, 100% of leukemic patients with clostridial septicemia were neutropenic, and 89% were thrombocytopenic.54 Because platelets function to maintain endothelial integrity, it is possible that increased vascular permeability to bacteria also plays a role in the metastatic spread of C septicum infection.54

The period between clostridial contamination to myonecrosis ranges from 6 to 48 hours.26,45,47 In anaerobic settings the bacilli proliferate, producing a bevy of exotoxins. The most important of these is the {alpha} toxin, which causes intravascular hemolysis and necrosis of host tissue.7,9,24,49 Clinically, this process is characterized by pain that is often described as heaviness or pressure that is out of proportion to the physical findings. The {alpha} toxin also increases capillary permeability, producing marked tachycardia and hypotension.7 Further destruction of tissue results in edema and ischemia generating an overwhelming metabolic acidosis, fever, disseminated intravascular coagulation, and renal failure.3,49,58 Clostridial proliferation generates carbon dioxide and hydrogen gases. These gases will move along tissue planes, separating them and producing the characteristic feature of palpable emphysema. A magenta-bronze discoloration of the skin and bulla filled with a foul-smelling, serosanguinous fluid may appear secondary to the necrosis beneath the surface. Despite all of this, the patient's mental status remains surprisingly intact.3,50

Clostridium myonecrosis progresses very rapidly, with death usually occurring in 24 to 48 hours8,17,22,26,54,57–59; thus, prompt diagnosis and treatment is vital. Unfortunately, the initial clinical features are nonspecific. Because the early diagnosis of clostridium myonecrosis is difficult, yet critical to the patient's outcome, Cline and Turnbull48 recommend making the diagnosis solely on 4 early clinical findings: (1) pain disproportionate to clinical findings or injury; (2) marked tachycardia; (3) discolored and edematous skin; and (4) Gram-stain of the bulla/drainage showing a preponderance of Gram-positive bacilli without spores47 and few leukocytes.3,8,22,60 In the case presented here, the first 3 of Cline and Turnbull's clinical findings were noted; however, the discolored skin didn't present until pneumatosis was found. Thus, in children with clostridium myonecrosis, early diagnosis is even more difficult secondary to the nonspecific nature of the clinical presentation.41

Clinical diagnosis should be corroborated with additional radiologic and laboratory studies. Unfortunately, standard cultures are impractical for immediate diagnosis, secondary to the time required for growth and the clostridial species' fastidiousness.61 Despite this, both aerobic and anaerobic cultures should be sent to secure future antibiotic sensitivities. Radiographs will often reveal soft tissue gas before it is palpable,9 which is particularly helpful for clostridial infections that originate in the gastrointestinal tract,3,62 but tissue emphysema is a late sign of infection. Once clostridial infection is suspected, however, radiographs and/or CT scans can help to understand the extent of infection, as was done in our case. Laboratory studies are not specific enough alone but can be supportive of a clinical diagnosis of clostridial infection. Typical early laboratory results include a normal to slightly increased WBC count, decreased hematocrit, and metabolic acidosis.3,48 In our patient, metabolic acidosis was present with an initial anion gap of 24 mEq/L, portending the severity and extent of the infection before it was clinically apparent.

Initial management of presumed clostridium myonecrosis includes supportive measures and broad-spectrum antibiotics, covering Gram-negative and Gram-positive organisms with a third- or fourth-generation cephalosporin or meropenem and anaerobes with metronidazole. Patients generally are intubated and given blood and plasma products to stabilize the patient during shock and disseminated intravascular coagulation. Vasopressors should be avoided if possible because of the theoretical risk of a further decrease in tissue perfusion to an already ischemic area.47 In our case, hypotension that was unresponsive to aggressive fluid therapy necessitated vasopressor use. Patients need to be started on antibiotics immediately, as was our patient, because antibiotic treatment consistently and significantly improves survival.14,54 Once the diagnosis of a clostridial infection is confirmed, the treatment of choice is high-dose penicillin G (20–40 million U/day intravenously).{dagger} A second agent usually is added to provide proper coverage against mixed infections. Cephalosporins should not be used alone for prophylaxis or treatment of known clostridial infections.28,38

A patient with clostridium myonecrosis also needs an urgent surgical evaluation. In adults, the mortality rate increases substantially in the absence of surgical treatment.57 We also have found that surgical intervention is important in treating children with C septicum infections. In this review, 84% of the pediatric survivors of C septicum infection had received therapeutic surgical intervention, whereas only 12% of the patients that died had received therapeutic surgeries. Surgery can range from a small area of debridement and fasciotomy to limb amputation or bowel resection. Oftentimes, blood flow to the infected site is poor, making it difficult for systemically administered antibiotics to have an effect.6 Thus, surgery that removes the bacteria-contaminated, toxin-laden, necrotic tissue and subsequent disruption of the anaerobic environment is critical in the treatment of clostridial infections.13,37 After thorough debridement, wounds should be packed open and kept moist with saline. The patient should return to the OR in 24 hours for more exploration and debridement. Additional daily exploration is required for infections involving the trunk,60 as was done for our patient.

Early surgical intervention with resection of inflamed or perforated bowel can increase overall survival in adults5,8,20,26 and children.38 This was observed even when the patients were critically ill and required both fluid and vasopressor support. Thus, shock is not an absolute contraindication for surgery. On the basis of our findings, we suggest that surgical exploration of the abdomen is imperative in children with presumed C septicum infection when abdominal symptoms are present.

Currently, hyperbaric oxygen therapy is thought of as a useful adjunct to the standard medical and surgical management of clostridium myonecrosis.1,63 Although no adequately controlled trials of hyperbaric oxygen exist,3,13,48,60 its use is widely accepted.15,43,58,62–64 In some adult case series, morbidity and mortality were reduced significantly by the addition of hyperbaric oxygen therapy to antibiotics and surgery.2,43,50,63 It is generally recommended that the patient receive 1 hyperbaric oxygen treatment before surgical debridement43,48,62 to allow the devitalized tissue to revitalize, clearly demarcating the necrotic tissues that need to be removed.8,63 Because of the fulminant and frequently fatal nature of clostridial myonecrosis, physicians often find themselves in a bind: do we transfer a critically ill patient to a hyperbaric facility or start with immediate surgical debridement? In our case, transport to a hyperbaric facility was not possible secondary to the level of critical care that the patient required. In addition, C septicum may not be as responsive to hyperbaric oxygen as other species.8,65 Thus, a rapid case-by-case assessment that weighs the pros and cons of hyperbaric oxygen therapy is important.

Adjunctive therapies for treating clostridial infections include G-CSF,15,22,23,44,59 granulocyte transfusions,23,38,54 and IVIg.44,66 Although no case-controlled studies have been done, a brief look at some of these therapies is warranted. Bar-Joseph et al15 and Barnes et al44 describe the successful treatment of C septicum infection and neutropenia with the adjunctive use of G-CSF in several pediatric patients. IVIg has been used successfully in settings of pediatric septic shock and multiple organ failure67; however, this is only the second report of IVIg use in C septicum infection. In the previously reported case the patient died,44 and it is unclear if IVIg played a significant role in our patient's successful outcome. IVIg has been used along with vancomycin to treat recurrent Clostridium difficile diarrhea.66,68,69 Pooled human immunoglobulins contain significant titers of anti–C difficile antibodies,68,69 thus IVIg administration will bolster the patient's ability to fight off this infection. It is not known if IVIg contains anti–C septicum antibodies or other cross-reacting antibodies that might have provided some passive protection in our patient. This area needs additional investigation.

In the case presented here, our patient had no known underlying malignancy, blood disorder, or trauma. However, she did have a torsed juvenile polyp in her colon, which occurs in 1 in 1000 children.70 Our patient also defied the odds by having C septicum in her gastrointestinal tract, which is normally seen in only 2.8% of the population.46 Finally, a congenitally diminished or absent marginal arterial arcade, which occurs in 5% of the population, complicated the picture further.52,53 This unfortunate combination of events can be expected to occur in 1.4 individuals per million, and all of this led to a very severe case of C septicum myonecrosis with extensive abdominal and thoracic cavity involvement. Our patient received both appropriate antibiotics and surgical intervention in a timely fashion, just 13 hours from the ED to the OR. Her survival, no doubt, is a result of this multidisciplinary management and the dedication of everyone involved in her care.


   CONCLUSION
TOP
 ABSTRACT
 CASE REPORT
 REVIEW OF PUBLISHED PEDIATRIC...
 DISCUSSION
 CONCLUSION
REFERENCES
 
C septicum infections in children have a high mortality rate; thus, one needs to have a high index of suspicion in at-risk patients. Abdominal symptoms (including vomiting, diarrhea, blood per rectum, abdominal pain/acute abdomen, anorexia), and fever were found to be present in the vast majority of children with C septicum infections; however, these symptoms are nonspecific. Because prompt diagnosis is critical to the patient's outcome, one must watch for early clinical signs including pain out of proportion to objective findings, marked tachycardia, discolored skin, and bulla. Antibiotic coverage needs to be initiated immediately, and surgical consultation should be obtained early, especially for patients with gastrointestinal tract involvement. Hyperbaric oxygen can be a useful adjunctive treatment when it is directly available. In addition, newer treatment modalities such as G-CSF, granulocyte transfusions, and IVIg (as used for our patient) may also play an expanding role in the treatment of pediatric C septicum infections.


   FOOTNOTES
 
Accepted Oct 18, 2005.

Address correspondence to Candra L. Smith-Slatas, MD, PhD, ProHealth Physicians, 1331 Silas Deane Hwy, Wethersfield, CT 06109. E-mail: candra1{at}comcast.net

The authors have indicated they have no financial relationships relevant to this article to disclose.

* Refs 5, 14, 16, 17, 19, 20, 33, 35, 37, 41, and 54. Back

{dagger} Refs 1, 2, 13, 24, 47–50, 58, and 62. Back


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 DISCUSSION
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 REFERENCES
 

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