Robert L. Cloutier
Cellulitis is a common, acute, rapidly spreading, nonsuppurative inflammation of the epidermis, dermis, and subcutaneous fat that is usually caused by bacterial infection. The age of the patient, the history, and the location of the infection all serve as important determinants of the most likely causative bacterial organisms. Cellulitis may occur by local tissue invasion after minor traumatic skin breaks and bite wounds or by hematogenous dissemination of a pathogenic organism. It may also be the presenting sign of disease states such as septic arthritis, osteomyelitis, sinusitis, or pyomyositis (1). Neonatal omphalitis (infection of the umbilical stump and surrounding tissues) and neonatal mastoiditis are unique to the newborn period.
Recent studies have demonstrated a dramatic increase in the incidence of soft-tissue infections in the United States and concomitant emergency department visits (2). These increasing infection rates are due to the emergence of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA), which affect otherwise healthy children (3,4). Most of the culture-proven CA-MRSA infections present as superficial abscesses or and carbuncles.
In most instances, children with cellulitis recover uneventfully. However, the recent resurgence of invasive group A β-hemolytic Streptococcus (GABHS) infection, characterized by bacteremia, toxic shock, and necrotizing fasciitis, emphasizes both the potential for serious complications and the need for accurate diagnosis and appropriate management of pediatric cellulitis.
EPIDEMIOLOGY
During the course of normal play, children routinely incur minor injuries with breaks of the skin. Any injury or skin opening that disrupts the protective barrier of the skin can serve as a portal of entry for pathogens, most commonly GABHS or Staph aureus. The role of MRSA in cellulitis without obvious purulence is unclear because cultures are rarely obtained from children with these infections, but CA-MRSA has emerged as an increasing cause of purulent soft-tissue infections in children (4). The incidence and prevalence of CA-MRSA vary geographically. In surveillance conducted in areas of Maryland, Georgia, and Minnesota in 2001 and 2002, the proportion of all MRSA infections that were caused by CA-MRSA ranged from 8% to 20% (4). Factors common in outbreaks of CA-MRSA include crowding; frequent skin-to-skin contact between people; participation in activities that result in abraded or compromised skin surfaces; sharing of potentially contaminated personal items such as towels, sporting equipment, and razors; and limited access to health care. One explanation for these increased infection rates is related to virulence characteristics that are more common in this organism. One such factor is thought to be a cytotoxin, Panton-Valentine leukocidin, that destroys leukocytes by creating pores in the cell membranes. CA-MRSA should be considered a potential cause of every infection presenting to the hospital or clinic, emphasizing the need for practitioners to be aware of local antibiotic resistance patterns.
Puncture wounds by a contaminated object such as a nail penetrating a shoe may predispose to infections with pathogens such as Pseudomonas species. Likewise, animal and human bites are associated with an increased likelihood of Pasteurella multocida and Eikenella corrodens infections, respectively.
Omphalitis, infection of the umbilicus, with accompanying erythema of the abdomen, is a diagnosis unique to the newborn period that usually occurs in the first few weeks of life. Neonatal mastitis is an infection of the breast tissue in prepubertal children, limited to the first 2 to 5 weeks of life (5). Female infants are affected twice as often as males. Hormonally induced hypertrophy of the glandular tissue facilitates bacterial entry and abscess formation. The most common pathogen is Staph. aureus, including CA-MRSA; however, occasionally gram-negative enteric organisms are involved.
The epidemiology of childhood facial cellulitis has changed dramatically since the introduction of the Haemophilus influenzae type B vaccine in 1985. H. influenzae type B (HIB) had been the cause of more than 50% of cases of facial cellulitis but, in the post-vaccine era, it has become rare. In fact, there has been an approximately 90% decrease in the incidence of HIB disease (6). Any child who has received the second dose of HIB vaccine more than 7 days prior is unlikely to have HIB disease. Currently, common organisms for facial cellulitis include Streptococcus pneumoniae, GABHS, and Staph. aureus. As more children become completely immunized with the conjugated pneumococcal vaccine it is anticipated there will be a decrease in cellulitis due to Strep. pneumoniae vaccine and nonvaccine serotypes. Facial and periorbital infections caused by HIB and Strep. pneumoniae are usually spread hematogenously and hence can be isolated by blood cultures. Primary dental infection may also lead to bacterial seeding of adjacent facial soft tissues by a variety of aerobic and anaerobic bacteria such as Bacteroides, Prevotella, Fusobacterium, and Peptostreptococcus (7).
Important pre-existing conditions that may predispose to cellulitis include other traumatic injuries, particularly crush injuries, pre-existing vascular or lymphatic compromise, chronic cutaneous conditions such as eczema, and immunocompromised states. More recently, there has been an increase in case reports of necrotizing fasciitis due to GABHS infection occurring in conjunction with varicella infection (8).
CLINICAL PRESENTATION
The most reliable way to diagnose cellulitis is to recognize the characteristic clinical features: Localized erythema, warmth, edema, and pain. Demarcation between involved and adjacent normal skin may be indistinct. Most often, cellulitis involves the extremities, with the leg affected three times as often as the arm (1). There may be associated lymphangitis, appearing as red streaks radiating from the margin of the lesion, and also enlargement and tenderness of regional lymph nodes, particularly with streptococcal infection. The white blood cell (WBC) count is usually normal. In 10% to 20% of cases, cellulitis is associated with fever and other systemic symptoms such as chills, malaise, myalgias, and emesis. When fever is present, a concomitant bacteremia should be presumed leukocytosis is expected.
More recently, increasing childhood purulent infection rates due to CA-MRSA, and the inability to distinguish these infection from methicillin-sensitive strains, have necessitated the development of new evaluation and management schemata for these infections, such as that recommended by the American Academy of Pediatrics (Fig. 277.1) (9).
FIGURE 277.1 Initial outpatient management of suspected CA-MRSA skin and soft-tissue infections schematically illustrated. Assumes CA-MRSA strains are prevalent in a community.
Erysipelas is a superficial cellulitis predominantly affecting the upper dermis. It is characterized by tender, rapidly enlarging, erythematous, indurated plaques with sharply demarcated borders, with extensive lymphatic involvement. Patients tend to be young children, and most cases involve the legs and feet (10,11). Symptoms also include toxic appearance with fever and chills (12). Facial erysipelas may occur after streptococcal upper respiratory tract infection (10). GABHS is the most common cause of erysipelas, in addition to other streptococcal groups including groups B, C, and G. Historically, erysipelas has rarely been linked to staphylococci. Current investigations still acknowledge the possibility of CA-MRSA as a causative agent but data supporting its existence remains weak (13).
Buccal cellulitis presents as a tender mildly erythematous swelling of the cheek in children between 6 and 24 months, most often not associated with previous trauma. Hematogenous seeding by oropharyngeal or middle-ear bacteria is suggested as the pathogenesis (6). Previously, HIB was by far the most common etiologic agent, with rare cases caused by Staph. aureus and Strep. pneumoniae. As a result of routine immunization with HIB vaccine, the incidence of buccal cellulitis has decreased (12). Of note, in infants younger than 3 months of age, facial cellulitis may be the only presenting sign of GBS bacteremia.
Ludwig angina is a cellulitis of the submandibular and sublingual space. Patients often present with rapidly progressive, tense, and painful induration of the submental area and neck, along with drooling, dysphonia, high fever, and leukocytosis. It is important to recognize the potential for airway compromise in such patients (12). Predisposing factors include poor dental hygiene, recent dental extractions, and impacted foreign bodies in the oral cavity. Infections tend to be polymicrobial, involving oral flora.
Periorbital or preseptal cellulitis is an infection presented anterior to the orbital septum and is usually seen in children younger than 5 years old (6,14). It typically presents with sudden onset of unilateral eyelid and periorbital tenderness, swelling, and erythema; extraocular eye movements and visual acuity are preserved and there is no evidence of proptosis (12). More than half cases are secondary to local extension from a nearby facial wound infected with either GABHS or Staph. aureus. In general, children appear nontoxic, but bacteremia and leukocytosis may occur, particularly when infection is due to H. influenzaeor Strep. pneumoniae infections.
In contrast, orbital cellulitis, which is less common than periorbital cellulitis, is postseptal and involves the orbit itself (14) (see Chapter 253). Ethmoid sinusitis is most commonly the source of infection as the ethmoid sinus is separated from the orbit by the rather thin bony structure known as the lamina papyracea (14).
Omphalitis presents in the newborn as purulent, foul-smelling discharge from the umbilical stump and as erythema of the abdominal wall. However, both of these clinical findings may occur without infection, thus making the diagnosis challenging at times. Suggestive findings include anterior abdominal erythema and circumferential erythema of the umbilicus (5). The cord stump may serve as a portal of entry for Staph. aureus, CA-MRSA, GABHS, group B Streptococci (GBS), or gram-negative enteric organisms. Infection is clinically diagnosed when induration and erythema of the anterior abdominal wall are present. Fever, temperature instability, lethargy, and irritability may be seen late as signs of sepsis. Laboratory studies such as WBC count may be normal in early localized infections. Omphalitis is rare in developed countries where the usual cord care in the neonatal period avoids most infections.
Neonatal mastitis presents as enlargement of the breast bud with associated tenderness, warmth, erythema, and purulent nipple discharge (5). Hormonally induced hypertrophy of the breast tissue does not present as erythema or tenderness and is associated only with a milky white discharge. About one-fourth of infants will present with fever and ill appearance. Since the infection tends to be well localized, the WBC is normal in most cases, and blood cultures are negative.
Wound-related cellulitis is the most common cause, of cellulitis of the extremities, especially in older children and adolescents (12). The involved area is red, warm, and tender, and systemic signs of fever, chills, and leukocytosis are often present. Lymphangitic streaking and regional lymphadenopathy are more common than in cases of erysipelas. Children with cellulitis of an extremity may have limitation of movement of the affected limb or refusal to walk because of pain. Infections tend to be polymicrobial and are age related, with GBS more common in infants younger than 3 months old, Strep. pneumoniaeand HIB in patients aged 6 to 24 months (still undergoing primary vaccination series), and Staph. aureus, CA-MRSA, and GABHS most likely in children older than 24 months (1). With GBS, Strep. pneumoniae, and HIB, high fever, WBC above 15,000, and bacteremia are not uncommon.
Necrotizing fasciitis (NF) is an uncommon but potentially devastating infection of the subcutaneous and fascial tissues (11). Children may be predisposed as a result of traumatic skin lesions, or those of varicella zoster infection, eczema, or burns (12,15,16). Necrotizing fasciitis may initially present as a cellulitis, but develops rapidly into dusky, painful, indurated plaques and progresses to purpura, blistering, and necrosis. Crepitance may develop within the tissues. The infection spreads rapidly along fascial planes between subcutaneous tissue and superficial muscle fascia (15). The initial diagnosis may be difficult to make because there are often only modest skin changes early in the course of disease. However, extreme pain that is out of proportion to examination findings is very suggestive. Patients may present with fever and marked fussiness and may refuse to bear weight or move the affected limb. Severe systemic toxicity with tachycardia, hypotension, and multiorgan system failure are common in fulminant cases. The child may be lethargic, disoriented, and in profound septic shock. When necrotizing fasciitis occurs in conjunction with streptococcal toxic shock syndrome (STSS), the mortality rate is particularly high (15).
STSS may be associated with NF in as many as 50% of cases (10). The syndrome presents with a generalized, fine, scarlatiniform rash and hyperemia of the conjunctivae or other mucous membranes, along with fever, tachycardia that out of proportion to fever, hypotension, and possibly altered mental status and respiratory distress, vomiting, diarrhea, and renal and hepatic dysfunction are often present (10,15).
A similar toxin-mediated syndrome affecting young children is staphylococcal scalded skin syndrome (SSSS). Skin manifestations are age related and include the spectrum of bullous impetigo, scarlatiniform eruption, and widespread exfoliation (11). Generalized SSSS, called Ritter disease, usually occurs in patients younger than 5 years of age; older children tend to have more localized infections. Following a purulent conjunctivitis, upper respiratory infection, or localized superficial skin infection, a generalized orange-red macular erythema resembling sunburn develops. During the subsequent scarlatiniform phase, the skin becomes extremely tender. Within 1 to 3 days, the skin becomes wrinkled, and large flaccid bullae develop in flexural areas or around orifices. During this phase, Nikolsky sign is present—the epidermis pulls away from the dermis with gentle traction, leaving raw, weeping, and denuded skin underneath (12). As the skin dries, large flakes are formed, leading to widespread desquamation with complete recovery in 10 to 14 days. Dehydration and superinfection may occur due to loss of the dermal barrier during exfoliation.
DIFFERENTIAL DIAGNOSIS
Any tender, erythematous swelling of the skin and subcutaneous soft tissue may resemble cellulitis. Trauma, insect bites or stings, localized urticarial eruptions, lymphadenitis, swelling overlying a sprain or fracture, or a joint with septic arthritis may all be mistaken for cellulitis. Mosquito bites may induce significant lymphedema surrounding the bite site, which develops over hours. The bites are usually described as pruritic rather than painful. Bee stings and spider bites may also cause significant lymphedema, warmth, and even tenderness and therefore may be more difficult to distinguish from cellulitis.
“Popsicle panniculitis” can mimic facial cellulitis. Thought to be a cold-induced histamine response from drinking ice water, typically the skin involvement begins at the labial crease and spreads outward with a warm, mildly tender cheek. Insect bites and stings, panniculitis, and orthopedic injuries all lack accompanying systemic signs such as fever or ill appearance.
Localized specific soft-tissue infections, such as folliculitis (infection of a hair follicle), furuncles and carbuncles (deep follicular abscess, either solitary or multiseptate and loculated), impetigo (vesiculopustular lesions), ecthyma (impetigo involving the dermis), and others, should be differentiated from cellulitis by their characteristic clinical appearances.
Extremity cellulitis, as mentioned earlier, may limit range of motion of the affected limb; making it difficult to distinguish deeper tissue infections (such as osteomyelitis or septic arthritis) from cellulitis.
ED EVALUATION
In most cases, cellulitis is a clinical diagnosis. Blood culture and WBC counts should be reserved for immunocompromised patients or those presenting with fever or other signs of systemic illness. Clinical judgment and patient age should be used to determine the need for lumbar puncture for culture, particularly with cellulitic infections of the head and neck region (6). In infants with facial cellulitis who have not been fully immunized a lumbar puncture should be strongly considered (6).
Many clinical features are specific enough for clinical decisions to be made based on appearance alone; however, given the rapid increase in frequency of CA-MRSA, cultures may become more necessary. Erysipelas, with its characteristic rapidly advancing, raised, sharply demarcated margin, is usually caused by GABHS. A bluish or violaceous discoloration of the affected area suggests infection by H. influenzae or Strep. pneumoniae. Cellulitis in the perineal or buccal area, or cellulitis in an area involving devitalized or necrotic tissue should raise concern for polymicrobial anaerobic organisms or CA-MRSA. Cellulitis caused by pet bites is often associated with P. multocida,whereas human bite infections are often associated with E. corodens. Cellulitis due to water-contaminated wounds is usually caused by Mycobacterium marinum or Aeromonas and Vibrio species (17). Systemic symptoms in any patient with cellulitis should suggest the possibility of concurrent bacteremia. Immunocompromised states should alert the clinician to the possibility of atypical infectious agents and to neutropenia potentially masking the actual depth and extent of infection.
While varicella is relatively rare because of routine immunizations against it, invasive GABHS should be considered in children with varicella who have fever on or beyond the fourth day of the exanthem (8). With the re-emergence of suppurative GABHS infections, it is vital to distinguish early streptococcal necrotizing fasciitis from cellulitis. Although the combination of clinical features and epidemiologic considerations may suggest the etiology of cellulitis, definitive bacteriologic diagnosis requires isolation of the causative organism. In the past, because of the high prevalence of H. influenzae, bacteremia, blood cultures were routinely obtained in children with cellulitis. In the post-HIB vaccine era, however, the association of bacteremia with cellulitis in children has been dramatically reduced, and recent studies indicate that it is not necessary to obtain blood cultures routinely (18). Of note, positive blood cultures are most commonly associated with younger age, active varicella, and deeper tissue infections such as osteomyelitis or septic arthritis.
Needle aspiration of the cutaneous lesion, accompanied by gram stain and culture, is a rapid and specific tool for establishing a bacteriologic diagnosis. Aspiration is performed by inserting a 22-gauge needle attached to a 1-cc syringe into the advancing edge of the cellulitis. If no material is aspirated, 0.1 mL of normal saline may be injected into the area, followed by immediate aspiration. The yield of needle aspiration, however, can be modest; positive aspiration rates vary from 5% to 50%.
If underlying deeper trauma or infection is suspected, appropriate imaging should be ordered, especially in patients with suspected orbital cellulitis (19). Patients with cellulitis involving the midface are also susceptible to cavernous sinus thrombosis.
Complications of cellulitis may result from direct extension, seeding of an underlying joint space, or hematogenous spread. Meningitis, endocarditis, or other serious complications, although rare, may develop, especially in immunocompromised patients.
KEY TESTING
• CBC, blood culture, and wound cultures in patients with atypical presentations, ill appearance, or immunocompromise
• CT scan for patients with suspected orbital cellulitis
• CT, MRI, or ultrasonography to investigate potential joint infections or osteomyelitis
ED MANAGEMENT
Antibiotic therapy is warranted in most cases, except in the mildest forms of cellulitis. See Figure 277.1 for management of purulent infections (9). Given the low yield of microbiologic testing, in most situations antibiotic therapy is empiric but should be based on sound clinical judgment.
The presence of pus should prompt a high index of suspicion for CA-MRSA, and incision and drainage with packing should be performed. Any fluid aspirated should be cultured, including MRSA typing. Hospital admission and parenteral antibiotic therapy should be strongly considered in any febrile child. Application of warm compresses and elevation of the affected limb are useful adjunctive therapies. Analgesics may be necessary for pain control, and antipyretics for relief of fever.
All neonates with suspected omphalitis or mastitis should be promptly admitted and started empirically on parenteral antibiotics for Staph. aureus and CA-MRSA, GABHS, GBS, and gram-negative enteric organisms. In infants younger than 3 months of age with facial or extremity cellulitis should be admitted and treated with parenteral penicillin and an aminoglycoside. Between 3 months and 3 years of age, Staph. aureus, H. influenzae, or Strep. pneumoniae may be causative organisms, and third-generation cephalosporins (ceftriaxone or cefotaxime) should be administered, as well as clindamycin. In ill-appearing children, clinicians should consider the possibility of a more invasive infection and have an increased suspicion for CA-MRSA (16). Vancomycin is required if meningitis is suspected.
Patients with orbital cellulitis require hospital admission. Multispecialty involvement by otorhinolaryngology, infectious diseases, and ophthalmology is warranted, since surgical drainage of an abscess or a sinuses may be required. Patients should be started empirically on intravenous antibiotics to cover respiratory pathogens; ampicillin–sulbactam is a reasonable choice (14). Intravenous antibiotics for a total of 7 days, followed by a course of oral antibiotics for 14 days, are recommended.
Patients suspected of a severe infection with GABHS should receive parenteral clindamycin in addition to penicillin, intravenous immunoglobulin, an immediate surgical consultation for emergent débridement, and close cardiorespiratory monitoring for signs of septic shock. Aggressive fluid resuscitation may be required. Surgical intervention must not be delayed by radiologic investigations when the clinical likelihood of sever disease is high (10,15,16).
Immunocompromised patients often develop cellulitis caused by atypical organisms such as Corynebacterium, Pseudomonas, atypical mycobacteria, and even fungi. A microbiologic diagnosis should be vigorously pursued in these patients, particularly when initial empirical therapy fails to produce a satisfactory response.
Beyond 3 years of age, patients with well-localized cellulitis and without fever or systemic illness may be treated as outpatients with antistaphylococcal and anti-GABHS oral agents. Consider the addition of anaerobic coverage with clindamycin for cases of bite wounds, oral infections, or wounds with devitalized tissue. Caregivers of children who are treated as outpatients require instruction about the necessity of close follow-up within 48 hours and about signs and symptoms that necessitate prompt return to the ED.
Susceptibility patterns of CA-MRSA to clindamycin and trimethoprim–sulfamethoxazole differ in various regions of the country. Generally, either of these agents can be used to treat mild-to-moderate cellulitis due to such MRSA. In the case of severe infection with CA-MRSA, empiric, parenteral vancomycin is recommended (20).
A patient with cellulitis who shows severe systemic toxicity or does not improve within 48 hours of oral antibiotic therapy should receive high-dose intravenous broad-spectrum antibiotic therapy covering both streptococci and staphylococci. Newer recommendations favor changing empiric therapy to include CA-MRSA coverage. Antibiotic recommendations for possible CA-MRSA infection are presented in Table 277.1.
TABLE 277.1
Antibiotic Doses for the Treatment of Infections Caused by CA-MRSA
Patients who respond promptly to parenteral antibiotics may be switched over to oral antibiotics but in most cases the total duration of therapy should be a full 10 days.
CRITICAL INTERVENTIONS
• Recognize that patients with necrotizing fasciitis present with pain out of proportion to physical examination findings.
• Arrange follow-up within 48 hours for patients with cellulitis who are treated on an outpatient basis.
• Recognize that patients with purulent infections should be cultured and treated as if they have CA-MRSA.
• Recognize that mastitis and omphalitis are serious forms of cellulitis in the neonatal period that mandate emergent evaluation and treatment.
DISPOSITION
Most children with simple cellulitis can be started on oral antibiotics on an outpatient basis, with follow-up arranged at 48-hour intervals. With the decreasing incidence of H. influenzae and Strep. pneumoniaecellulitis and the availability of potent oral antibiotics, more and more patients with cellulitis can be safely managed as outpatients.
Admission should be strongly considered in infants younger than 6 months old. Any child, who appears to be ill, has extensive lesions or is immunosuppressed should also be admitted. Patients with facial cellulitis and a fever of >38.5°C or those with extremity cellulitis and a fever of >39°C and a WBC count >15,000/mL are likely to require intravenous antibiotics.
Patients with necrotizing fasciitis require surgical débridement in the operating room. Children with severe systemic manifestations need aggressive treatment and admission to a pediatric intensive care unit. Wound management in cases of extensive SSSS may be best accomplished in a pediatric burn unit.
Common Pitfalls
• Failure to recognize that CA-MRSA infection in children without identified risk factors is increasing in prevalence
• Failure to include orbital cellulitis in the differential diagnosis of periorbital cellulitis
• Failure to recognize that in immunocompromised patients with cellulitis, atypical and opportunistic infections are common and that a microbiologic diagnosis should be actively pursued
ACKNOWLEDGMENTS
The author gratefully acknowledges the contributions of Christopher S. Kennedy and Mary E. Moffatt to the content of this chapter.
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