Infection in Unusual Spaces
Certain pediatric infections are noteworthy for their presence in unusual body
spaces. These may be rarely seen but when present require rapid diagnosis and
therapy. This chapter provides a discussion of such infections, including
necrotizing fasciitis, omphalitis, endophthalmitis, peritonitis secondary to
ruptured appendicitis, and retropharyngeal abscess.
Necrotizing Fasciitis
Necrotizing fasciitis is an infection involving the subcutaneous tissues and
deep fascia. It can affect any portion of the body, although the lower
extremities are the most commonly involved. First described by Hippocrates in
the 5th century, this condition has been reported under a variety of names,
including
“hospital gangrene” and “malignant ulcer.” The term necrotizing fasciitis was first used in the 1950s and accurately
describes the location of infection.
Etiology
The infection begins with the introduction of the pathogen into the subcutaneous
tissues. Many mechanisms of this introduction have been reported, including
insect bites, minor trauma, preceding varicella infection, and surgical
incisions. Hematogenous spread has also been reported as a means of
inoculation. A variety of toxins, cytokines, and inflammatory mediators are
thought to be involved in the progression of the infection.
Necrotizing fasciitis has been divided into distinct groups based on causative
organism. Type 1 refers to a polymicrobial infection usually caused by non
–group A streptococcus and other aerobic and anaerobic bacteria. Type II
necrotizing fasciitis usually is caused by group A streptococcus alone or with
staphylococcus. The etiologic agents of necrotizing fasciitis cannot be
determined from clinical presentation alone. During the past decade, the most
common cause of necrotizing fasciitis has remained group A streptococcus
following varicella infection. It is thought that the group A streptococcus is
inoculated directly into the skin when the child scratches the varicella
lesions.
Presentation
A major challenge for the pediatrician is to separate necrotizing fasciitis from
a routine cellulitis. Clinical examination is the mainstay of diagnosis. A
major clue on physical examination involves severe pain, often out of
proportion to the physical findings. As the infection progresses, one finds
worsening erythema and edema. Later, the skin may develop blisters, and bullae
may form (Fig. 16.1). The formation of bullae is thought to be an important
diagnostic finding that should always raise the suspicion for necrotizing
fasciitis. Later in the progression of the disease, the bullae become
hemorrhagic and are often accompanied by crepitus.
Diagnosis
Several tests have been used in an attempt to document the progression of
cellulitis to necrotizing fasciitis. The presence of leukocytosis and acidosis
has been used to identify patients with progressive disease. The appearance of
gas on plain radiograph is an inconsistent finding and is seen in less than 20%
of cases. Magnetic resonance imaging (MRI) has been reported to detect
extension of the inflammatory process into the subcutaneous tissue. High signal
intensity of the fascia in the T2-weighted images strongly suggests the
diagnosis.
The gold standard of diagnosis for necrotizing fasciitis is surgical biopsy;
biopsies reveal acute inflammation of the dermis and fascia with accompanying
thrombosis of blood vessels.
Management
The management of necrotizing fasciitis involves aggressive medical and surgical
therapy. Optimal medical treatment includes a third-generation cephalosporin
and anaerobic coverage, usually with clindamycin. Complete d
ébridement of all devitalized tissue is required. A repeat second-look surgery
after 24 hours is often needed to determine whether remaining devitalized
tissue is present. Adjunctive therapies include hyperbaric oxygen and
intravenous immunoglobulin, although definitive data of the efficacy of these
measures is lacking (Table 16.1).
Omphalitis
Omphalitis, or infection of the umbilicus, remains a major cause of morbidity
and mortality in developing countries. In a poorly understood process,
omphalitis is thought to arise from bacterial colonization occurring at the
time of delivery. This colonization becomes invasive and can proceed to
funisitis(a term given to mild cellulitis or inflammation of the periumbilical skin) or
to omphalitis, in which the umbilical stump and surrounding tissues are
involved.
Etiology
Omphalitis has been traditionally caused by Staphylococcus aureus and Streptococcus pyogenes (group A streptococcus.) Modern cord care with triple-dye antimicrobial soap and
alcohol has reduced the frequency of omphalitis in developed countries;
however, it may also have changed the microbiology of omphalitis. During the
past 10 years, reports of omphalitis have emphasized the role of additional
pathogens, particularly gram-negative and anaerobic bacteria.
Presentation
Neonates typically present with purulent discharge of the umbilical cord with
rapidly progressing cellulitis of the abdominal wall.
Diagnosis
The diagnosis is based largely on the history and clinical examination. It is
generally thought that any abdominal wall cellulitis surrounding the umbilical
structures is consistent with the diagnosis of omphalitis.
Management
Due to the potential life-threatening complications of an umbilical cord infection, neonates presenting with any evidence of inflammation around the umbilical cord should be managed aggressively. This includes admission and
treatment with broad-spectrum antibiotics, usually a third-generation
cephalosporin and clindamycin. Surface cultures should be obtained, although it
should be stressed that these may not represent the entire spectrum of bacteria
involved in the deeper fascial planes. As in necrotizing fasciitis, surgical
resection is a major part of therapy, and early involvement with experienced
pediatric surgeons is mandatory.
Continued concern regarding omphalitis has led to an ongoing evaluation of
optimal umbilical cord care. Some hospitals have abandoned triple-dye alcohol
regimens for a regimen of dry cord care consisting of gentle cleaning with soap
and water and allowing the area to air dry. A prospective study evaluating this
approach in nearly 800 infants found a single case of omphalitis in the dry
care group. In the dry care group, infants were more likely to be colonized
with group B streptococcus,
S. aureus, and gram-negative bacteria. Whether this colonization ultimately leads to an
increase in invasive infection will need to be the subject of further studies
(Table 16.2).
Endophthalmitis
Endophthalmitis refers to infection within the ocular structures. There are two
mechanisms for this infection. In endogenous (hematogenous) endophthalmitis,
bacteria are seeded within the eye following a bacteremic or septicemic
illness. Exogenous endophthalmitis refers to infection within the eye following
direct inoculation from a surgical procedure or traumatic event.
Etiology
Organisms that can seed the ocular structures following a bacteremic or
septicemic illness include
Bacillus cereus, Candida species, and Neisseria meningitidis. B. cereus infection is associated with the use of intravenous drugs. Organisms of
exogenous disease include
Staphylococcus epidermidis, Streptococcus species, and S. aureus.
Presentation
Patients have decreased vision and proptosis, often accompanied by periocular
inflammation and edema. Visual acuity is usually markedly decreased. This
process should be suspected in any bacteremic patient who, during the course of
illness, develops ocular complaints. Exogenous endophthalmitis is particularly
important in pediatrics because ocular trauma may not be immediately reported.
Diagnosis
The diagnosis of endophthalmitis should be done in conjunction with an experienced ophthalmologist. Ophthalmologic examination may reveal corneal haziness and a purulent exudate (hypopyon) in the anterior chamber of the eye.
Typically, anterior chamber and vitreous aspiration should be performed in an
effort to identify the responsible pathogen. The yield of Gram stain or culture
approaches 60%.
Treatment
Therapy is difficult, given the low rate of positive cultures and the poor
penetration of systemic antibiotics into the eye. Initial antibiotic choices
are often based on the most likely pathogen. It is recommended that, following
the aspiration of fluid, antibiotics be instilled directly into the vitreous
cavity. Intraocular vancomycin,
1 mg, and ceftazidime, 2.25 mg, are frequently used. Amikacin, 400 µg, is used in some centers as an alternative to ceftazidime for gram-negative
coverage.
Intravenous antibiotics are considered to have poor penetration into the aqueous
humour. Adjunctive therapy with intravenous vancomycin, ceftazidime, and
amikacin is frequently employed, although their usefulness remains unclear.
Ciprofloxacin has been reported to achieve levels above the minimal inhibitory
concentration (MIC) for coagulase-negative staphylococcus; some centers use
this medication if this pathogen is identified. Intraocular and systemic
steroids, in conjunction with vitrectomy, have been used for progressive
disease (Table 16.3).
Peritonitis Secondary to Ruptured Appendicitis
Etiology
Children with appendicitis often have perforation at the time of diagnosis. This
perforation leads to the seeding of the peritoneal cavity with the multitude of
aerobic and anaerobic organisms found in the gastrointestinal tract. This
seeding serves as a risk factor for the development of intra-abdominal
abscesses. During recent years, there has been a great interest in the proper
management of patients with peritonitis following a perforated appendicitis.
Presentation
Although adults frequently present with periumbilical pain and subsequent
migration of point tenderness to the right lower quadrant, up to one half of
young children present with the appendicitis already ruptured. These children
often present with fever, diffuse abdominal tenderness, and rebound tenderness
indicating peritoneal irritation.
Diagnosis
Although the hallmark of infectious disease evaluation is obtaining appropriate
cultures, there remains debate about the clinical usefulness of obtaining
intraoperative peritoneal cultures in patients with perforated appendicitis.
Some studies have demonstrated that culture results do not alter therapy or
outcome in patients with peritonitis. This appears to be particularly true when
Pseudomonas aeruginosa is isolated; in this patient population, P. aeruginosa is not considered a clinically important pathogen. Other authors cite
alternative studies in which complications were more common in patients whose
intraoperative cultures grew an organism that was not covered by the initial
antibiotic regimen. One explanation for these discrepancies is that peritoneal
cultures are often obtained in children with perforated but not abscessed
appendicitis. The potential for abscess formation is extremely low in this
population.
Management
In 2003, the Infectious Disease Society of American (IDSA) published guidelines
for the selection of antibiotics for complicated intra-abdominal infections.
The study reported the clinical usefulness of cultures, particularly in
complicated (i.e., those processes associated with peritonitis or abscess
formation) intra-abdominal infections. The IDSA recommended that culture and
susceptibility be done against the isolated gram-negative bacilli because there
is increasing resistance among these organisms. Based on published reports of
increasing resistance in the
Bacteroides fragilis group of organisms, it recommended that empiric use of clindamycin, cefoxitin,
and quinolones for treatment of
B. fragilis not be used.
The polymicrobial nature of intra-abdominal infections requires consideration of
a broad-spectrum regimen. Coverage against any enteric gram-negative organisms,
such as
Escherichia coli, and anaerobes, such as Bacteroides species, is crucial. For this reason, ampicillin, gentamycin, and clindamycin,
the traditional
“surgical triples,” were often used in the past for intra-abdominal infections. As a result of
increasing resistance among the gram-negative enteric bacteria and
B. fragilis, newer regimens are increasingly used. A single combination agent such as
ampicillin-sulbactam (Unasyn) or piperacillin-tazobactam (Zosyn), is often used
to treat community-acquired intraabdominal infections of mild to moderate
severity. Carbapenems, which include imipenem and meropenem, can also be used
as single agents because these drugs provide broad-spectrum gram-negative and
anaerobic coverage. Combination regimens based on
β-lactam antibiotics include third- or fourth-generation cephalosporins such as
cefotaxime, ceftriaxone, and cefepime, combined with metronidazole (Flagyl).
The latter provides good coverage against
Bacteroides species, which may be resistant to clindamycin.
Enterococcus is a common organism found in the intestinal tract. In the past,
the regimens used to treat complicated intraabdominal infections have provided
coverage for this organism. A review of previous studies done by the IDSA found
that coverage against enterococci does not provide an advantage and is not
necessary in treatment of community-acquired intra-abdominal infection. Similar
recommendations can be found for
Candida albicans, which is isolated in a good percentage of patients who have perforation of the
gastrointestinal tract. Unless the patient is receiving immunosuppressive
therapy or has recurrent disease, antifungal therapy is not required.
Antibiotic Duration
The duration of antibiotic treatment and the ability to transition to oral
antibiotics have also been studied. These studies usually reflect the child
with noncomplicated appendicitis in whom there is no extensive infection or
abscess in the peritoneal cavity; these are the children most frequently seen
by pediatricians. One recent study observed that intravenous antibiotics can be
discontinued when the patient is afebrile for 24 hours and the white blood cell
count shows less than 3% band forms.
Typically, the duration of therapy following this protocol was between 3 and 14
days.
Other investigators have evaluated programs in which patients are transitioned
to oral amoxicillin-clavulanate (Augmentin) plus metronidazole to complete a
10-day total course. In the patients studied, there was no difference between
children who had received oral antibiotic therapy and those who had prolonged
intravenous treatment (Table 16.4).
Retropharyngeal Abscess
Etiology
Retropharyngeal abscess is a deep neck infection that can obstruct the upper
airway. Most cases occur in patients younger than 5 years of age. These
infections are the result of bacteria in the nasopharynx or middle ear
infecting the lymph nodes that lie between the posterior pharyngeal wall and
the prevertebral fascia. These nodes are thought to atrophy during childhood,
which may explain the age distribution seen. Traumatic retropharyngeal abscess
is the result of penetrating trauma and can occur at any time in life.
Pathogens
Microbiology of retropharyngeal abscess has been the focus of considerable
study. Group A streptococcus is the usual pathogen, although numerous
investigators believe there may be a large polymicrobial component. Organisms
that have been isolated in children with retropharyngeal abscess include
S. aureus and anaerobic species such as Bacteroides and Peptostreptococcus species.
Presentation
Patients often present with a history of sore throat which progresses to
increasing neck swelling, drooling, or dysphagia. Affected children may also
exhibit decreased neck mobility to such an extent that meningitis is frequently
considered and lumbar puncture performed. Increasing stridor has been reported
as a classic clinical sign of retropharyngeal abscess, although recent reviews
have not found this to be a consistent symptom.
Diagnosis
Diagnosis of retropharyngeal abscess begins with appropriate clinical suspicion
in the right clinical setting. Lateral neck films can show an increased
retropharyngeal soft tissue space, although interpretation of these plain films
may be dependent on patient positioning. Computed tomography of the neck can be
extremely helpful in documenting infection in the retropharyngeal space (Fig.
16.2). Evaluation by computed tomography is not without difficulty. There are
limitations in the ability of computed tomography to determine definitively
whether a well-defined abscess is present; a retropharyngeal cellulitis (or
phlegmon) may be difficult to distinguish on computed tomography from a frank
abscess. Numerous reports have stated that clinical correlation should be used
in making decisions regarding the presence of a true abscess.
Management
Treatment of retropharyngeal cellulitis or abscess always involves the use of
appropriate antimicrobials. Ampicillin-sulbactam (Unasyn) offers an advantage
in that it has broad-spectrum coverage against not only group A streptococcus
and
S. aureus but also a variety of anaerobic organisms. A combination of clindamycin and a
third-generation cephalosporin will also provide coverage for the probable
organisms involved. The adjunctive surgical management of retropharyngeal
abscess remains controversial. Some reviews and textbooks state that the
treatment always includes drainage; many otolaryngologists feel that a trial of
antibiotics can be used initially. Failure to respond clinically to medical
management alone warrants surgical therapy (Table 16.5).
Selected Readings
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(1):105–108.
Brook I. Microbiology of retropharyngeal abscesses in children. Am J Dis Child 1987;141(2):202–204.
Craig FW, Schunk JE. Retropharyngeal abscess in children: clinical presentation,
utility of imaging, and current management.
Pediatrics 2003;111(6 Pt 1):1394–1398.
Gollin G, Abarbanell A, Moores D. Oral antibiotics in the management of
perforated appendicitis in children.
Am Surg 2002;68(12):1072–1074.
Hoelzer DJ, Zabel DD, Zern JT. Determining duration of antibiotic use in
children with complicated appendicitis.
Pediatr Infect Dis J 1999;18(11):979–982.
Hsieh WS, Yang PH, Chao HC, et al. Neonatal necrotizing fasciitis: a report of
three cases and review of the literature.
Pediatrics 1999;103(4):E53.
Janssen PA, Selwood BL, Dobson SR, et al. To dye or not to dye: a randomized,
clinical trial of a triple dye/alcohol regimen versus dry cord care.
Pediatrics 2003;111(1):15–20.
Mason WH, Andrews R, Ross LA, et al. Omphalitis in the newborn infant. Pediatr Infect Dis J 1989;8(8):521–525.
Solomkin J, Mazuski J, Baron E, et al. Guidelines for the selection of
anti-infective agents for complicated intra-abdominal infections.
Clin Infect Dis 2003;37:997–1005
Vural C, Gungor A, Comerci S. Accuracy of computerized tomography in deep neck
infections in the pediatric population.
Am J Otolaryngol 2003;24:143–148.
Wong CH, Chang CH, Pasupathy S, et al. Necrotizing fasciitis: clinical
presentation microbiology, and determinants of mortality.
J Bone Joint Surg Am 2003;85A(8):1454–1460.
Pictures
Book Source Details
- Book Title: Pediatric Infectious Disease
- Author(s): Donald Janner MD
- Year of Publication: 2004
- Copyright Details: Pediatric Infectious Disease, Copyright © 2004 Lippincott Williams & Wilkins.
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Copyright Details: Pediatric Infectious Disease, Copyright © 2008 Williams & Wilkins.
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Title: Pediatric Infectious Disease
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Copyright: 2004
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