Sepsis in pediatric burn patients

Robert L. Sheridan, MD

Objective: To review the specific infections common in pediatric

burns, including their categorization, diagnosis, and treatment.
Design: Review of the literature and expert opinion.
Results: Children with serious burns are prone to a host of
septic complications. This proclivity to infection is secondary to
the immunosuppressive effect of burn injury, the loss of the skin
and mucosal physical barriers, and the requirement for invasive
support devices.

Conclusion: Sepsis is common in the pediatric burn patient and

can markedly increase morbidity and mortality. Anticipation,
prompt diagnosis of infection, and effective therapy can result in
successful outcomes for many of these children. (Pediatr Crit Care
Med 2005; 6[Suppl.]:S112S119)
KEY WORDS: burns; infection; sepsis; pneumonia; critical illness;
multiple organ failure

urn patients die for three

main reasons: burn shock
during the first few hours after injury, respiratory failure
in the following days, and septic complications and organ failures during the
subsequent weeks (1). Fluid resuscitation
formulas, developed initially in the 1930s
and 1940s (2, 3) and subsequently refined
(4, 5), have markedly reduced the prevalence of death due to resuscitation failure
(6). The development and refinement of
techniques of positive-pressure ventilation have sharply reduced the prevalence
of respiratory death (7, 8). Paradoxically,
the reduced rates of early death from
burn shock and respiratory failure have
resulted in an increasing prevalence of
infection as a cause of late mortality and
morbidity in the burn unit (9, 10).
In times past, the dominant infection
in burn units was found in the wounds
themselves. However, since the wide
adoption of early excision of deep wounds
in the 1980s and 1990s, wound sepsis is
much less frequent (1113). As early
burn excision and closure has reduced
the incidence of burn-wound infection

(14), the occurrence of other more complex infectious complications has increased. These infections not only cause
direct morbidity and mortality, but even
when successfully treated, they may trigger systemic inflammation and organ
failures (10, 15). Infection is the single
biggest killer in the burn unit (16).
Existing incidence data for pediatric
burn infections, although scanty and
compromised by variability in definitions
and reporting, seems to suggest that specific infection rates in children hospitalized for burns at the present time are
higher than in critically ill nonburn patients. Infection rates are similar to other
immunocompromised groups and include: (1) central catheter infection rate
of 4.9/1000 central venous catheter days,
(2) burn-wound infection rate of 5.6/1000
patient days, (3) ventilator-related pneumonia rate of 11.4/1000 ventilator days,
and (4) urinary catheterrelated urinary
tract infection rate of 13.2/1000 urinary
catheter days (17). Burn unit based infection surveillance programs can help to
decrease the rate of infection in these
children (18) and should be a part of all
organized burn programs.

From the Department of Surgery, Division of Burns,

Shriners Hospital for Children, Massachusetts General
Hospital, Harvard Medical School, Boston, MA.
This work was supported by the Mannion Family
FundCenter for the Critically Ill Child, Division of
Critical Care Medicine at Childrens Hospital Boston,
the PALISI Network, and the ISF.
Copyright 2005 by the Society of Critical Care
Medicine and the World Federation of Pediatric Intensive and Critical Care Societies

Pathogenesis of Infection

DOI: 10.1097/01.PCC.0000161577.27849.BE

S112

Serious burns render children markedly susceptible to a variety of infectious

complications (19, 20). Both local and
systemic factors contribute to this susceptibility. Local factors include the open
wounds, an incompetent gut barrier, and
exposure of the globe, bones, cartilage,
and joints. As long as wounds are open,

underlying tissues are at risk of contamination and infection (21). The invasive
devices required to support these children also add new potential portals of
entry for infection. Central venous and
arterial catheters, endotracheal tubes,
bladder catheters, and transnasal tubes
all increase the exposure of injured children to potential infection. These critically important tools should be promptly
discontinued when they are no longer
needed. Prompt and effective wound excision and closure will decrease the
childs dependence on invasive devices.
Systemic factors are also important
contributors to the increased susceptibility to infection. There is a well-documented global decrease in cellular immune function associated with burns
(2224). Neutropenia is common, neutrophil function is depressed (25), and
T-cell transcription is altered (22). Increased gut permeability has been documented (26, 27). Burn patients experience occult bacteremia with wound
manipulations (28, 29). Data suggest that
excessive transfusion of blood products
may exacerbate global immunosuppression (30). In ways that are not yet understood, these factors combine to result in
an increased susceptibility to infection
(31).

Prevention of Infection
Quick and effective closure of deep
burns is the cornerstone of infection prevention. Other methods include prophylactic antibiotics, topical antimicrobial
agents, and infection control practices.
Pediatr Crit Care Med 2005 Vol. 6, No. 3 (Suppl.)

Prophylactic antimicrobials have been

used in burn patients in four settings: 1)
antistreptococcal drugs to prevent burnwound cellulitis, 2) oral and enteral administration of antifungal agents to prevent candidiasis or antibiotics to prevent
bacterial infection, 3) perioperative administration of antibiotics, and (4) broadspectrum antibiotics pending return of
culture information in febrile or hypotensive patients.
Before early excision and closure of
deep wounds was common practice,
group A streptococcal burn-wound cellulitis was common and was often fatal.
This prompted routine administration of
penicillin to burn patients. However, this
practice was associated with its own set of
problems and expense (32) without data
to support its efficacy. In a recent study of
917 children admitted for burn care during a 6-yr interval, it was documented
that group A streptococcal infection was
infrequent and was not further reduced
by prophylactic penicillin as long as those
who had group A streptococcal at admission or on surveillance cultures were
treated (33). This is no longer part of the
general standard of care.
Oral and enteral administration of antifungal agents to prevent candidiasis
(34) or of antibiotics to decontaminate
the gut (3537) has been periodically recommended, although neither practice is
part of the standard of care. Available data
suggest that enteral antifungals are not
effective in reducing the prevalence of
fungal infection (38). Selective decontamination of the gut has not been
adopted, either, because data simply are
not sufficient to support the practice, and
generation of resistant organisms is
feared (39).
Perioperative antibiotics are commonly administered to decrease the prevalence of graft or donor-site infection,
although there are no data to support the
efficacy of this practice (40). In acute
burns, antibiotics are chosen to suppress
the known or suspected wound flora. It
has been well documented that burnsurgery wound manipulations are associated with a substantial rate of bacteremia
(41, 42), and perioperative antibiotics
may protect against intravascular catheter contamination.
Prophylactic antimicrobials are commonly administered to the febrile or hypotensive child in the burn unit. However, children with significant burns are
commonly febrile in the absence of infection (43), and overuse of broad-spectrum
Pediatr Crit Care Med 2005 Vol. 6, No. 3 (Suppl.)

antibiotics may be harmful. The newly

febrile child in the burn unit should have
a careful history and physical examination. Intravascular catheter sites should
be evaluated. Often, this will bring to
light a potential or actual focus on occult
infection. Cultures of blood, urine, sputum, and wounds should be sent. If the
child is toxic, with significant change in
mental status, hypotension, thrombocytopenia, neutropenia, or new leukocytosis, it is not unreasonable to administer
broad-spectrum antibiotics pending return of culture information. If no infectious focus is identified, these can be
stopped in 48 or 72 hrs. Overuse of broadspectrum antibiotics may generate resistant organisms, and this tendency should
be resisted.
A wide variety of topical antimicrobials are commonly applied to burn
wounds. The general objectives are: 1) to
decrease water vapor loss, 2) to prevent
desiccation of exposed viable tissues, 3) to
contribute to pain control, and 4) to inhibit bacterial and fungal growth. Periodic gentle cleaning of wounds to remove
accumulated topical agent and wound exudate seems important. This can generally be done using light sedation at the
bedside. Immersion hydrotherapy has
been traced as a source of cross-infection
and is less commonly used (44). Silver
sulfadiazine is the most common topical
in general use. It is an opaque, white
cream that is painless on application, has
fair to poor eschar penetration, has no
metabolic side effects, and has a broad
antibacterial spectrum. Mafenide acetate
is painful on application and a carbonic
anhydrase inhibitor, but it penetrates eschar and has a broad antibacterial spectrum. Aqueous 0.5% silver nitrate is also
painless on application, but it has poor
eschar penetration and leeches electrolytes. However, it has a broad spectrum of
activity (including fungi) and can be used
on adjacent wounds, grafts, and donor
sites. Superficial burns can be treated
with a number of occlusive, viscous antibiotic ointments.
A number of temporary membranes
are available for use on superficial
wounds or donor sites to decrease infection and facilitate comfort (45). Among
them are fresh or reconstituted porcine
xenograft, synthetic bilaminates, hydrofibers, semipermeable membranes, hydrocolloid dressings, and human allograft.
Some of these membranes are impregnated with silver to reduce bacterial and
fungal growth. All are useful in the man-

agement of selected wounds. When using

wound membranes, it is essential that the
wounds be regularly evaluated, as an occlusive dressing over eschar can lead to
enclosed infection and serious problems
(46). An increasing variety of other topical antimicrobials and membranes exist.
All have advantages and disadvantages,
making them useful in specific clinical
situations. Regardless of the specific topical agent used, regular assessment of all
wounds for early signs of infection is essential.
Burns are tetanus-prone wounds. If
immune status is questionable, children
should undergo active immunization
with tetanus toxoid. If children have not
been immunized, or their tetanus immune status is unknown, both active
with tetanus toxoid and passive immunization with tetanus hyperimmune globulin is appropriate. This is particularly true
if burns are extensive, deep, or heavily
contaminated.
Infection control programs play an
important role in infection prevention
(47). The primary objectives of these programs include: 1) protection of patients
and staff from resistant bacterial species
(48), 2) surveillance of patients and the
environment, 3) education of staff and
family members, 4) monitoring staff performance of universal precautions, and 5)
identifying and eliminating potential
sources of cross-infection (49). These
programs have been shown to be highly
effective in reducing the spread of resistant species (50, 51).

Diagnosis and Management of

Bacterial Infections
Most infections in burned children are
bacterial. Infections can be very subtle
and diagnosis elusive in this setting. Localizing signs are commonly obscured by
wounds, operative sites, dressings,
wound-associated fever, and drug-induced analgesia. A high index of suspicion and very careful history and physical
examination are essential. Virtually all
burn patients are febrile. Injudicious use
of antibiotics may facilitate emergence of
resistant bacterial strains or fungi that
can be very difficult to treat. Also, the
pharmacokinetics of many antibiotics,
particularly the aminoglycosides, are altered in burned children (52), so dose
adjustment based on serum levels is often
necessary.
Wound Infections. Wound sepsis was a
very common cause of death before the
S113

Table 1. Clinically focused set of burn-wound infectionsa

Infection
Burn impetigo
Burn-related surgical wound
infection
Burn-wound cellulitis

Invasive burn-wound infection

Diagnostic Points
Y Loss of epithelium from previously epithelialized surface
Y Not related to local trauma
Y Infection in surgically created wound that has not yet
epithelialized
Y Includes loss of any overlying graft or membrane
Y Infection occurs in uninjured skin surrounding a wound
Y Signs of local infection progress beyond what is expected
form burn-related inflammation
Y Infection occurs in unexcised burn and invades viable
underlying tissue
Y Diagnosis may be supported by histologic examination or
quantitative cultures

Refer to Peck et al. (57) for a full definition of burn-wound infections.

wide introduction of early wound excision (53). Although much less common
today, it remains a serious threat and is
regularly seen. The most common organisms are Staphylococcus aureus and
Pseudomonas aeruginosa. Vaccination
against the latter organism has been explored (54, 55) but has not been widely
used because early identification, excision, and closure of wounds is more effective (56). A variety of classification
schemes have been used for burn-wound
infections. A recently developed set of
clinically focused definitions, including
1) burn impetigo or superficial infection with loss of epithelium, 2) open
burn-related surgical wound infection, 3)
burn-wound cellulitis, and 4) invasive
burn-wound infection, will be used here
(Table 1) (57). Like impetigo in unburned
skin, burn impetigo is usually associated
with S. aureus or Streptococcus pyogenes. Often, only S. aureus is isolated.
This is particularly common in burns of
the scalp. Treatment requires wound
cleansing, which often mandates shaving
of nearby hair-bearing areas. Topical
treatment with antistaphylococcal medications, such a mupirocin (58), is generally sufficient, although systemic treatment may be required in some cases. On
occasion, skin grafting of denuded areas
is required for healing to occur.
Open burn-related surgical wound infection describes purulent infection that
develops in excised wounds and donor
sites. These infections usually drain fluid
containing white cells and are commonly
associated with systemic toxicity, such as
fever and hypotension, and loss of skin
grafts. In many situations, these infections are associated with inadequately excised wounds, the unexcised necrotic
skin and subcutaneous tissue being the
nidus of infection. Treatment requires
S114

debridement of necrotic and infected material with delayed wound closure. Staphylococcal toxic shock syndrome has been
reported in children with superficial
burns and donor sites and is a risk, particularly when occlusive dressings are
employed over deep burns in young children (46).
Burn-wound cellulitis (Fig. 1) refers to
spreading dermal infection in uninjured
skin around a burn wound or donor site.
This can vary from an early subtle erythema a centimeter or so around the
wound to a brawny erythema involving
an entire limb or torso. It is often asymmetric in pattern, and it is usually difficult to recover an organism from wound
swabs or dermal aspirates because infection typically spreads in dermal lymphatics of unburned skin around the wound.
This is most commonly seen in the first
few days after a burn or as a postoperative
donor-site complication (59). In the past,
prevention of such infections was a principal reason for the administration of
prophylactic penicillin. When deep burns
undergo prompt excision and closure,
this should infrequently occur (60). Burn
cellulitis is commonly caused by S. pyogenes, and the diagnosis is usually based
on clinical examination.
Invasive burn-wound infection (Fig. 2)
is a clear threat to life. Children with
invasive burn-wound infection are systematically toxic with high fever and a
hyperdynamic circulatory state. Subsequently, bacteremia, hypotension, and
cardiovascular collapse occur (48). There
has been a great deal of controversy over
how a diagnosis of invasive burn-wound
infection is appropriately established.
Three methods have been advocated by
various authors: 1) clinical examination
(61), 2) quantitative cultures of a burnwound biopsy (60), and 3) burn-wound

histology (62). Clinical signs of invasive

infection include a change in the appearance of the wound in the setting of a toxic
patient. Typical changes include punctate
hemorrhage, change in color, new drainage, and rapidly progressive liquefaction.
Quantitative cultures require a 1-g specimen of eschar, which is homogenized
and cultured. If 105 colony-forming
units per gram of tissue are cultured,
infection is diagnosed. Histologic diagnosis of infection can be done by frozen or
permanent section, the latter being perhaps more accurate. A grading system
has been reported (62), with a diagnosis
of invasive infection supported by bacteria invading viable tissue. Both quantitative culture and histologic examination
are subject to sampling error and can
cause clinical delays in treatment. When
compared with burn-wound biopsy,
quantitative cultures have been demonstrated to overdiagnose infection (63).
From a practical perspective, clinical diagnosis of these infections suffices for the
vast majority of situations.
Prompt treatment of invasive burnwound infection is essential because
these are life-threatening events. Although subeschar infiltration of antibiotics has been advocated (64), most of these
infections are best managed with parenteral antibiotics, resuscitation from septic shock, and wound excision and closure (65). Heavily contaminated wounds,
particularly in septic patients, are often
more appropriately allografted and later
autografted. On occasion, unusual organisms related to the mechanism of injury
will cause invasive infection. In these circumstances, knowledge of the likely organisms based on history and surveillance cultures can guide effective
antibiotic therapy. An example is early
wound infection with waterborne organisms, such as Aeromonas or Flavobacteria, when burns are extinguished with
contaminated water (66, 67).
Otolaryngologic Infections. The supporting cartilage of the ear is almost avascular and is therefore highly susceptible
to infection when the overlying delicate
skin is deeply burned. Auricular chondritis presents with pain, fever, and rapidly
progressive edema of the ear and is followed by liquefaction of the cartilage.
This sequence of events can be effectively
prevented with topical mafenide acetate.
This agent has a broad antibacterial spectrum and readily penetrates eschar (68).
When established, auricular chondritis
Pediatr Crit Care Med 2005 Vol. 6, No. 3 (Suppl.)

Figure 1. Burn-wound cellulitis refers to spreading dermal infection in uninjured skin around a burn
wound or donor site. Erythema is demonstrated by the blanched finger impressions.

Figure 2. Invasive burn-wound infection is a highly lethal complication.

requires operative debridement of infected, liquefying cartilage.

Sinusitis and otitis media are complications of transnasal gastric and endotracheal tubes. The tubes, or secondary mucosal edema, obstruct the eustachian
tubes or sinus orifices. Diagnosis can be
difficult in the critically ill child who will
not complain of ear or sinus pain. A high
index of suspicion and regular examination, supplemented by radiographs and
sinus aspiration, will allow the diagnosis
to be made. Treatment requires moving
the offending tubes, if possible, out of the
nares. Topical decongestants, antibiotics,
and occasionally, surgical drainage of infected closed spaces are important ancillary treatments.
Ophthalmic Infections. The avascular
corneal stroma is protected from invading
bacteria only by a fragile layer of corneal
Pediatr Crit Care Med 2005 Vol. 6, No. 3 (Suppl.)

epithelium. If this thin protective layer is

damaged by direct thermal injury, chemical burn, or ectropion and desiccation, the
underlying cornea can quickly become infected with disastrous results. Corneal exposure and infection can cause permanent
scarring only repairable with corneal transplantation. Infected corneal ulcers can perforate and result in herniation of the lens
and loss of the eye (Fig. 3) (69). These
complications are best avoided by early and
ongoing examination of the eye. Direct corneal burns are treated with vigilant eye
lubrication using topical ophthalmic antibiotic ointments applied every 2 to 4 hrs.
Globe exposure secondary to progressive
contracture of burned eyelids and facial
skin is managed with acute eyelid release
(Fig. 4).
Pulmonary Infections. Children who
have serious burns are at high risk for

pulmonary infections for several reasons

(70), and this causes significant morbidity and mortality in burn units (71). Children with inhalation injury demonstrate
loss of ciliary clearance from necrosis of
respiratory epithelium and small airway
obstruction from sloughed endobronchial debris. Children requiring endotracheal intubation have the upper airway
protective mechanisms compromised.
Hematogenous seeding of the lungs can
occur from wound or other infectious
foci.
There are two common types of pulmonary infection seen: pneumonia and
tracheobronchitis. Pneumonia or tracheobronchitis occurs in up to 35% of
those with inhalation injury. A diagnosis
of pulmonary infection is made when the
child develops a fever, a change in quantity and character of sputum, a Gram
stain revealing abundant polymorphonuclear leukocytes and bacteria, and a sputum culture revealing a dominant organism. If the chest radiograph is consistent
with a diffuse or lobar process, the diagnosis of pneumonia is made. If there are
no such radiographic abnormalities, purulent tracheobronchitis is the likely diagnosis. Although bronchoscopy can be
used to support a diagnosis of tracheobronchitis, bronchoalveolar lavage and
protected brush specimens are of no established utility (72). Treatment consists
of antibiotics directed by the sensitivities
of recovered organisms and pulmonary
toilet. Pulmonary toilet, regular suctioning of endobronchial secretions, is of particular value given the common loss of
native clearance mechanisms secondary
to necrosis of respiratory epithelium in
those with inhalation injury with consequent loss of ciliary clearance. Toilet
bronchoscopy can be useful in older children.
Chest tubes in children with chest
wall burns can lead to empyema if the
tube must be placed through a wound.
Chest tubes should be removed as soon as
practical. It goes without saying that subclavian catheter placement in such children carries added hazard because a complicating hemopneumothorax may
require chest tube placement through eschar. In this setting, subclavian catheterization should be done by experienced
people with great care. If empyema is
established, treatment is surgical if antibiotics and drainage fail.
Endovascular Infection. Endovascular
infections are uncommon but cause significant morbidity and mortality when
S115

Figure 3. Infected corneal ulcers can perforate and result in herniation of the lens and loss of the eye.

Figure 4. Globe exposure secondary to progressive contracture of burned eyelids or facial skin is
managed with acute eyelid release.

they arise. Before the wide use of central

venous catheters in the critically ill, suppurative peripheral vein thrombophlebitis was a common cause of systemic sepsis. The use of percutaneous central
venous catheters has reduced this complication. Endovascular infections generally present with fever and bacteremia in
the absence of localizing signs of infection. Both diagnosis and therapy can be
very difficult. Septic peripheral thromboS116

phlebitis is diagnosed by careful examination of all sites of previous cannulation

and treated by excision of the thrombosed
purulent vein to normal vein. Septic central thrombophlebitis can be diagnosed
by physical examination and imaging
studies such as ultrasound. Treatment of
central septic phlebitis requires prolonged antibiotic therapy and systemic
anticoagulation, when safe in light of potential bleeding from burn wounds. Car-

diac valvular endocarditis is diagnosed by

cardiac ultrasound. Endocarditis may occur more frequently in children with pulmonary arterial catheters (73). Endocarditis is treated with protracted antibiotic
courses and, in selected cases, valve replacement.
Central venous catheter sepsis is the
most common endovascular infection in
the burn unit, presenting with bacteremia and fever. It is diagnosed by examination of the catheter site, peripheral
blood culture, and semiquantitative culture of the catheter tip. Treatment requires catheter removal and antibiotics.
Scheduled rotation of central vein catheters may reduce the prevalence of this
infection (74). Although prophylactic
catheter rotation policies remain controversial (75), they are probably effective in
high-risk populations (76). A policy including weekly central venous catheter
rotation is associated with a rate of catheter sepsis of about 10% (74, 77). Arterial
catheters rarely become infected (75),
probably because of the high flow rates
around the catheters.
Intraabdominal Infection. On occasion, serious intraabdominal infections
will arise in burn patients, often presenting an occult focus on sepsis. Acute cholecystitis can occur in older children and
adolescents, particularly if protracted periods pass without enteral nutrition. This
presents with fever, cholestatic chemistries, and often no localizing signs in
obtunded patients. It can mimic sepsisinduced cholestatic liver dysfunction. Diagnosis is made by bedside ultrasound.
Treatment can be by percutaneous transhepatic drainage (78) or surgery with adjunctive antibiotics. Acute pancreatitis
can complicate severe burns and is managed with bowel rest. Secondary pancreatic abscess may require percutaneous
drainage or surgery, with adjunctive antibiotics (79). Appendicitis is seen with
some regularity in the burn unit, and this
diagnosis can be difficult to make in the
heavily sedated child. A high index of
suspicion and liberal use of imaging are
useful.
Splanchnic ischemia occurs in critically ill children and can be followed by
peritonitis in severe cases (80). Diagnosis
is by examination and radiography, and
treatment is surgical. Thankfully this is a
rare problem in the well-resuscitated
child. Clostridium difficile colitis presents with fever and diarrhea. Diagnosis
is by clinical picture and C. difficile stool
titer. Treatment is enteral vancomycin or
Pediatr Crit Care Med 2005 Vol. 6, No. 3 (Suppl.)

metronidazole, the latter being less expensive and equally effective. Gastrointestinal permeability increases with inadequate splanchnic perfusion, burn size,
and infection (27) and is likely related to
splanchnic ischemia caused by inadequate resuscitation. Translocation may
contribute to the inflammatory state and
may be the cause of overt infection.
Musculoskeletal Infection. Intracompartmental sepsis can follow missed or occult compartment syndromes with subsequent hematogenous seeding of necrotic
muscle (81). It is not difficult to miss an
evolving compartment syndrome early in
the course of a large burn because most of
the signs are obscured in the obtunded
child. Diagnosis requires a high index of
suspicion, serial physical examination, and
liberal surgical exploration. Compartment
pressure measurement can supplement diagnosis in selected children. Treatment is
surgical, and many such limbs can be salvaged (Fig. 5).
Suppurative costal chondritis and osteomyelitis can occur when bone or costal
cartilage is exposed and becomes desiccated
and superinfected. Diagnosis is by examination and radiography; bone scans can be
overly sensitive. Treatment is by debridement of necrotic tissue with adjunctive antibiotics. Intraarticular sepsis can occur
over deeply burned major joints. Diagnosis
is by examination. Treatment requires
drainage and antibiotic administration.
Abscesses can develop beneath hypertrophic scars in the later phase of recovery
in some patients, presenting with fever and
minor local tenderness. Frequently, the
thickness and stiffness of the tissue makes
it a surprisingly difficult diagnosis. Treatment is by surgical exploration, drainage,
and often, excision, release, and grafting.

infection have been reported in burned

children (87 89) (Fig. 6). Specific defects
in the processing of herpes virus by the
immune system have been described after
thermal injury (90, 91). Reactivation of latent herpetic infection commonly causes
rapidly progressive perioral and intraoral
lesions (92). Morbidity from cytomegalovirus infection in burn units is extremely
rare, despite the relative infrequency of cytomegalovirus immunity in young children
and the common use of blood transfusions.
Human allograft is a potential source of
cytomegalovirus transmission, but infection is essentially nonexistent in clinical
practice (93).
Varicella pneumonitis can be particularly virulent in immunocompromised
burned children (51), although woundrelated morbidity is rare. Prophylactic
acyclovir or varicella zoster immune

globulin may be appropriate in recently

exposed children with serious injuries.
Exposed children should be placed in
strict isolation to prevent cross-infection
in other susceptible children during the
incubation period.
Fungal Infections. Candida and Aspergillus are the dominant pathogens in
this setting. They do not seem to carry a
higher mortality, in themselves, than the
bacterial infections that so often occur
simultaneously. Candidemia is seen particularly in the setting of prolonged exposure to broad-spectrum antibiotics in
the face of heavily colonized open wounds
(38). Wound closure and avoidance of injudicious broad-spectrum antibiotic use
will minimize the occurrence of candida
infection. Prophylactic enteral administration of antifungal agents has been used
to reduce the prevalence of this compli-

Figure 5. Intracompartmental sepsis can follow occult compartment syndrome with hematogenous
seeding of necrotic muscle.

Diagnosis and Management of

Nonbacterial Infections
The large majority of infectious complications in burned children are bacterial. However, there are some important
viral and fungal infections that are seen
regularly. These infections are less frequently lethal but cause significant morbidity and occasional mortality.
Viral Infections. Burn patients have reduced cellular immune function (24, 82),
and viral infections are more common in
burned children than is generally appreciated (83, 84). Herpes simplex virus, cytomegalovirus, and varicella are of particular
importance. Herpes simplex virus tracheobronchitis, pneumonia (85, 86), and wound
Pediatr Crit Care Med 2005 Vol. 6, No. 3 (Suppl.)

Figure 6. Herpetic burn-wound infection can often be traced to preinjury exposures.

S117

cation (34), but this is not in general use,

as data do not consistently support the
effectiveness of the practice (38). Treatment requires administration of systemic
antifungal agents and the eradication of
the source, when possible. Infected
wounds should be excised and closed (65,
94), and infected catheters should be removed.
When in the wound, Aspergillus
causes discreet areas of indolent, burrowing wound invasion (95). Pulmonary aspergillus infections are usually seen only
in very compromised patients (96).
Wound infections are best managed with
excision and with topical and systemic
antifungal agents. Pulmonary infection is
treated with pulmonary toilet and systemic antifungal agents.

Conclusions
Infection remains the largest single
cause of morbidity and mortality in
acutely burned children (21). Anticipation of the common burn-related infections facilitates early and more effective
treatment. If infection can be controlled
and wounds closed, most seriously
burned children will have very satisfying
outcomes (97, 98).

REFERENCES
1. Jackson DM: The evolution of burn treatment in the last 50 years. Burns 1991; 17:
329 334
2. Underhill FP: The significance of anhydremia
in extensive superficial burns. JAMA 1930;
95:852 857
3. Saffle JR: The 1942 fire at Bostons Cocoanut
Grove nightclub. Am J Surg 1993; 166:
581591
4. Moore FD: The body-weight burn budget:
Basic fluid therapy for the early burn. Surg
Clin North Am 1970; 50:1249 1265
5. Artz CP, Moncrief JA: The burn problem. In:
The Treatment of Burns. Artz CP, Moncrief
JA (Eds). Philadelphia, WB Saunders, 1969,
pp 122
6. Saffle JR, Davis B, Williams P: Recent outcomes in the treatment of burn injury in the
United States: A report from the American
Burn Association Patient Registry. J Burn
Care Rehabil 1995; 16(3 Pt 1):219 232
7. Sheridan R: Specific therapies for inhalation
injury. Crit Care Med 2002; 30:718 719
8. Sheridan RL, Weber JM, Schnitzer JJ, et al:
Young age is not a predictor of mortality in
burns. Pediatr Crit Care Med 2001;
2:223224
9. Weber JM, Sheridan RL, Pasternack MS, et
al: Nosocomial infections in pediatric patients with burns. Am J Infect Control 1997;
25:195201

S118

10. Sheridan RL, Ryan CM, Yin LM, et al: Death

in the burn unit: Sterile multiple organ failure. Burns 1998; 24:307311
11. Burke JF, Quinby WC Jr, Bondoc CC: Primary excision and prompt grafting as routine
therapy for the treatment of thermal burns
in children: 1976. Hand Clin 1990;
6:305317
12. Burke JF, Quinby WC Jr, Bondoc CC: Primary excision and prompt grafting as routine
therapy for the treatment of thermal burns
in children. Surg Clin North Am 1976; 56:
477 494
13. Herndon DN, Gore D, Cole M, et al: Determinants of mortality in pediatric patients
with greater than 70% full-thickness total
body surface area thermal injury treated by
early total excision and grafting. J Trauma
1987; 27:208 212
14. Merrell SW, Saffle JR, Larson CM, et al: The
declining incidence of fatal sepsis following
thermal injury. J Trauma 1989; 29:
13621366
15. Sittig K, Deitch EA: Effect of bacteremia on
mortality after thermal injury. Arch Surg
1988; 123:13671370
16. Peck MD, Heimbach DM: Does early excision
of burn wounds change the pattern of mortality? J Burn Care Rehabil 1989; 10:710
17. Weber JM, Sheridan RL, Pasternack MS, et
al: Nosocomial infections in pediatric patients with burns. Am J Infect Control 1997;
25:195201
18. Sheridan RL, Tompkins RG, Burke JF: Prophylactic antibiotics and their role in the
prevention of surgical wound infection. Adv
Surg 1994; 27:43 65
19. Pruitt BA Jr: Infection and the burn patient
[see comments]. Br J Surg 1990; 77:
10811082
20. Pruitt BA Jr, McManus AT: Opportunistic infections in severely burned patients. Am J
Med 1984; 76:146 154
21. Peck MD, Heimbach DM: Does early excision
of burn wounds change the pattern of mortality? J Burn Care Rehabil 1989; 10:710
22. Horgan AF, Mendez MV, ORiordain DS, et al:
Altered gene transcription after burn injury
results in depressed T-lymphocyte activation.
Ann Surg 1994; 220:342351
23. Yurt RW, Pruitt BA Jr: Decreased wound
neutrophils and indiscrete margination in
the pathogenesis of wound infection. Surgery 1985; 98:191198
24. OMahony JB, Palder SB, Wood JJ, et al:
Depression of cellular immunity after multiple trauma in the absence of sepsis.
J Trauma 1984; 24:869 875
25. Solomkin JS: Neutrophil disorders in burn
injury: Complement, cytokines, and organ
injury. J Trauma 1990; 30(12 Suppl):
S80 S85
26. Ziegler TR, Smith RJ, ODwyer ST, et al:
Increased intestinal permeability associated
with infection in burn patients. Arch Surg
1988; 123:13131319
27. Ryan CM, Bailey SH, Carter EA, et al: Additive effects of thermal injury and infection on

28.

29.

30.

31.

32.

33.

34.

35.

36.

37.

38.

39.

40.

41.

42.

43.

44.

gut permeability. Arch Surg 1994; 129:

325328
Mozingo DW, McManus AT, Kim SH, et al:
Incidence of bacteremia after burn wound
manipulation in the early postburn period.
J Trauma 1997; 42:1006 1010
Vindenes H, Bjerknes R: The frequency of
bacteremia and fungemia following wound
cleaning and excision in patients with large
burns. J Trauma 1993; 35:742749
Graves TA, Cioffi WG, Mason AD Jr, et al:
Relationship of transfusion and infection in a
burn population. J Trauma 1989; 29:
948 952
Pruitt BA Jr: Host opportunist interactions
in surgical infection. Arch Surg 1986; 121:
1322
Durtschi MB, Orgain C, Counts GW, et al: A
prospective study of prophylactic penicillin
in acutely burned hospitalized patients.
J Trauma 1982; 22:1114
Sheridan RL, Weber JM, Pasternack MM, et
al: Admission streptococcal screening allows
elimination of burn wound prophylaxis.
J Burn Care Rehabil 1999; 20:S146
Desai MH, Rutan RL, Heggers JP, et al: Candida infection with and without nystatin prophylaxis: A 11-year experience with patients
with burn injury. Arch Surg 1992; 127:
159 162
Mackie DP, van Hertum WA, Schumburg T,
et al: Prevention of infection in burns: Preliminary experience with selective decontamination of the digestive tract in patients with
extensive injuries. J Trauma 1992; 32:
570 575
Zobel G, Kuttnig M, Grubbauer HM, et al:
Reduction of colonization and infection rate
during pediatric intensive care by selective
decontamination of the digestive tract. Crit
Care Med 1991; 19:12421246
Koruda MJ: Gut sterilization to prevent
nosocomial infection. New Horiz 1993;
1:194 201
Sheridan RL, Weber JM, Budkevich LG, et al:
Candidemia in the pediatric patient with
burns. J Burn Care Rehabil 1995; 16:
440 443
van Saene HK, Stoutenbeek CC, Stoller JK,
et al: Selective decontamination of the digestive tract in the intensive care unit: Current
status and future prospects. Crit Care Med
1992; 20:691703
Rodgers GL, Fisher MC, Lo A, et al: Study of
antibiotic prophylaxis during burn wound
debridement in children. J Burn Care Rehabil 1997; 18:342346
Sasaki TM, Welch GW, Herndon DN, et al:
Burn wound manipulation-induced bacteremia. J Trauma 1979; 19:46 48
Beard CH, Ribeiro CD, Jones DM: The bacteraemia associated with burns surgery. Br J
Surg 1975; 62:638 641
Parish RA, Novack AH, Heimbach DM, et al:
Fever as a predictor of infection in burned
children. J Trauma 1987; 27:69 71
Tredget EE, Shankowsky HA, Joffe AM, et al:
Epidemiology of infections with Pseudomo-

Pediatr Crit Care Med 2005 Vol. 6, No. 3 (Suppl.)

45.
46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

60.

61.

62.

nas aeruginosa in burn patients: The role of

hydrotherapy. Clin Infect Dis 1992; 15:
941949
Sheridan RL, Tompkins RG: Skin substitutes
in burns. Burns 1999; 25:97103
Bacha EA, Sheridan RL, Donohue GA, et al:
Staphylococcal toxic shock syndrome in a
paediatric burn unit. Burns 1994; 20:
499 502
Weber JM, Tompkins DM: Improving survival: Infection control and burns. AACN Clin
Issues Crit Care Nurs 1993; 4:414 423
Sheridan RL, Weber JM, Petras M, et al: Implications of delayed definitive management
of serious burns in children. J Burn Care
Rehabil In Press
Lee JJ, Marvin JA, Heimbach DM, et al: Infection control in a burn center. J Burn Care
Rehabil 1990; 11:575580
Sheridan RL, Weber J, Benjamin J, et al:
Control of methicillin-resistant Staphylococcus aureus in a pediatric burn unit. Am J
Infect Control 1994; 22:340 345
Sheridan RL, Weber JM, Pasternak MM, et al:
A 15-year experience with varicella infections
in a pediatric burn unit. Burns 1999; 25:
353356
Glew RH, Moellering RC Jr, Burke JF: Gentamicin dosage in children with extensive
burns. J Trauma 1976; 16:819 823
Kagan RJ, Matsuda T, Hanumadass M, et al:
Serious wound infections in burned patients.
Surgery 1985; 98:640 647
Jones RJ, Roe EA, Gupta JL: Controlled trial
of Pseudomonas immunoglobulin and vaccine in burn patients. Lancet 1980;
2:12631265
Roe EA, Jones RJ: Active and passive immunization against Pseudomonas aeruginosa
infection of burned patients. Burns Incl
Therm Inj 1983; 9:433 439
McManus AT, Mason AD Jr, McManus WF, et
al: Twenty-five year review of Pseudomonas
aeruginosa bacteremia in a burn center. Eur
J Clin Microbiol 1985; 4:219 223
Peck MD, Weber J, McManus A, et al: Surveillance of burn wound infections: A proposal for definitions. J Burn Care Rehabil
1998; 19:386 389
Strock LL, Lee MM, Rutan RL, et al: Topical
Bactroban (mupirocin): Efficacy in treating
burn wounds infected with methicillinresistant staphylococci. J Burn Care Rehabil
1990; 11:454 459
Griswold JA, Grube BJ, Engrav LH, et al:
Determinants of donor site infections in
small burn grafts. J Burn Care Rehabil 1989;
10:531535
Dodd D, Stutman HR: Current issues in burn
wound infections. Adv Pediatr Infect Dis
1991; 6:137162
Sheridan RL, Tompkins RG, Burke JF: Management of burn wounds with prompt excision and immediate closure. J Intensive Care
Med 1994; 9:6 19
Kim SH, Hubbard GB, McManus WF, et al:
Frozen section technique to evaluate early
burn wound biopsy: A comparison with the

Pediatr Crit Care Med 2005 Vol. 6, No. 3 (Suppl.)

63.

64.

65.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

77.

78.

79.

rapid section technique. J Trauma 1985; 25:

1134 1137
McManus AT, Kim SH, McManus WF, et al:
Comparison of quantitative microbiology
and histopathology in divided burn-wound
biopsy specimens. Arch Surg 1987; 122:
74 76
McManus WF, Goodwin CW Jr, Pruitt BA Jr:
Subeschar treatment of burn-wound infection. Arch Surg 1983; 118:291294
Spebar MJ, Walters MJ, Pruitt BA Jr: Improved survival with aggressive surgical
management of noncandidal fungal infections of the burn wound. J Trauma 1982;
22:867 868
Sheridan RL, Ryan CM, Pasternack MS, et al:
Flavobacterial sepsis in massively burned pediatric patients. Clin Infect Dis 1993; 17:
185187
Barillo DJ, McManus AT, Cioffi WG, et al:
Aeromonas bacteraemia in burn patients.
Burns 1996; 22:48 52
Mills DC Jr, Roberts LW, Mason AD Jr, et al:
Suppurative chondritis: Its incidence, prevention, and treatment in burn patients.
Plast Reconstr Surg 1988; 82:267276
Asch MJ, Moylan JA Jr, Bruck HM, et al:
Ocular complications associated with burns:
Review of a five-year experience including
104 patients. J Trauma 1971; 11:857 861
Rue LW III, Cioffi WG, Mason AD Jr, et al:
The risk of pneumonia in thermally injured
patients requiring ventilatory support.
J Burn Care Rehabil 1995; 16(3 Pt 1):
262268
Hollingsed TC, Saffle JR, Barton RG, et al:
Etiology and consequences of respiratory
failure in thermally injured patients. Am J
Surg 1993; 166:592596
Niederman MS, Torres A, Summer W: Invasive diagnostic testing is not needed routinely to manage suspected ventilatorassociated pneumonia. Am J Respir Crit Care
Med 1994; 150:565569
Munster AM, DiVincenti FC, Foley FD, et al:
Cardiac infections in burns. Am J Surg 1971;
122:524 527
Goldstein AM, Weber JM, Sheridan RL: Femoral venous access is safe in burned children:
An analysis of 224 catheters. J Pediatr 1997;
130:442 446
Sheridan RL, Weber JM, Tompkins RG: Femoral arterial catheterization in paediatric
burn patients. Burns 1994; 20:451 452
Gregory JA, Schiller WR: Subclavian catheter
changes every third day in high risk patients.
Am Surg 1985; 51:534 536
Sheridan RL, Weber JM, Peterson HF, et al:
Central venous catheter sepsis with weekly
catheter change in paediatric burn patients:
An analysis of 221 catheters. Burns 1995;
21:127129
Sheridan RL, Ryan CM, Lee MJ, et al: Percutaneous cholecystostomy in the critically ill
burn patient. J Trauma 1995; 38:248 251
Ryan CM, Sheridan RL, Schoenfeld DA, et al:
Postburn pancreatitis. Ann Surg 1995; 222:
163170

80. Desai MH, Herndon DN, Rutan RL, et al:

Ischemic intestinal complications in patients
with burns. Surg Gynecol Obstet 1991; 172:
257261
81. Sheridan RL, Tompkins RG, McManus WF, et
al: Intracompartmental sepsis in burn patients. J Trauma 1994; 36:301305
82. Merrell SW, Shelby J, Freeman TR, et al:
Effect of exchange transfusion on cellmediated immune function following thermal injury. J Trauma 1988; 28:184 189
83. Linnemann CC Jr, MacMillan BG: Viral infections in pediatric burn patients. Am J Dis
Child 1981; 135:750 753
84. Foley FD, Greenawald KA, Nash G, et al:
Herpesvirus infection in burned patients.
N Engl J Med 1970; 282:652 656
85. Nash G, Foley FD: Herpetic infection of the
middle and lower respiratory tract. Am J Clin
Pathol 1970; 54:857 863
86. Prellner T, Flamholc L, Haidl S, et al: Herpes
simplex virus: The most frequently isolated
pathogen in the lungs of patients with severe
respiratory distress. Scand J Infect Dis 1992;
24:283292
87. Brandt SJ, Tribble CG, Lakeman AD, et al:
Herpes simplex burn wound infections: Epidemiology of a case cluster and responses to
acyclovir therapy. Surgery 1985; 98:338 343
88. Bisno AL: Cutaneous infections: Microbiologic and epidemiologic considerations.
American Journal of Medicine 1985; 76:
172179
89. Garcia H, Edwards MS: Herpes simplex infection of burn wounds. South Med J 1981;
74:991992
90. Klimpel GR, Herndon DN, Fons M, et al:
Defective NK cell activity following thermal
injury. Clin Exp Immunol 1986; 66:384 392
91. Kohl S, Ericsson CD: Cellular cytotoxicity to
herpes simplex virus-infected cells of leukocytes from patients with serious burns. Clin
Immunol Immunopathol 1982; 24:171178
92. Kagan RJ, Naraqi S, Matsuda T, et al: Herpes
simplex virus and cytomegalovirus infections
in burned patients. J Trauma 1985; 25:
40 45
93. Kealey GP, Aguiar J, Lewis RW Jr, et al:
Cadaver skin allografts and transmission of
human cytomegalovirus to burn patients.
J Am Coll Surg 1996; 182:201205
94. Spebar MJ, Pruitt BA Jr: Candidiasis in the
burned patient. J Trauma 1981; 21:237239
95. Bruck HM, Nash G, Foley D, et al: Opportunistic fungal infection of the burn wound
with phycomycetes and Aspergillus: A clinical-pathologic review. Arch Surg 1971; 102:
476 482
96. Becker WK, Cioffi WG Jr, McManus AT, et al:
Fungal burn wound infection: A 10-year experience. Arch Surg 1991; 126:44 48
97. Sheridan RL: The seriously burned child: Resuscitation through reintegration. 1. Curr
Probl Pediatr 1998; 28:105127
98. Sheridan RL: The seriously burned child: Resuscitation through reintegration. 2. Curr
Probl Pediatr 1998; 28:139 167

S119