Omphalitis

Author: Patrick G Gallagher, MD, Assistant Fellowship Program Director, Associate

Professor, Department of Pediatrics, Division of Neonatal-Perinatal Medicine, Yale
University and Yale-New Haven Children's Hospital
Coauthor(s): Samir S Shah, MD, Staff Physician, Departments of Pediatrics and
Immunologic and Infectious Diseases, The Children's Hospital of Philadelphia
Contributor Information and Disclosures
Updated: Jan 16, 2009

Introduction
Background
Omphalitis is an infection of the umbilical stump.1 Omphalitis typically presents as a
superficial cellulitis that may spread to involve the entire abdominal wall and may
progress to necrotizing fasciitis, myonecrosis, or systemic disease. Omphalitis is
uncommon in industrialized countries; however, it remains a common cause of neonatal
mortality in less developed areas. Omphalitis is predominantly a disease of the neonate.
Only a few cases have been reported in adults.
Approximately three fourths of omphalitis cases are polymicrobial in origin. Aerobic
bacteria are present in approximately 85% of infections, predominated by Staphylococcus
aureus, group A Streptococcus, Escherichia coli, Klebsiella pneumoniae, and Proteus
mirabilis.2,3 In the past, studies emphasized the importance of gram-positive organisms
(eg, S aureus and group A Streptococcus) in the etiology of omphalitis. This was followed
by a series of reports that highlighted the role of gram-negative organisms in the etiology
of omphalitis. These studies suggested that the change in etiology may have been caused
by the introduction of prophylactic umbilical cord care using antistaphylococcal agents,
such as hexachlorophene and triple dye (a widely adopted practice in the 1960s), with a
subsequent increase in gram-negative colonization of the umbilical stump.
Monitoring the microbial etiology of omphalitis is important, as recent trends have
moved back to dry cord care without routine application of topical antiseptic agents. This
trend has been widely accepted and is supported by the American Academy of Pediatrics
(AAP), which supports dry cord care of the umbilicus after birth. Dry cord care leads to
earlier separation of the cord after birth. It also leads to reports of wetter, odoriferous
cords (described by some parents as nasty, smelly, or yucky) and higher, sometimes
dramatic, colonization rates with S aureus and other bacteria.
Whether this increased colonization rate is, or will be, associated with higher rates of
omphalitis or other neonatal infection is controversial. Some studies have suggested that
higher colonization rates are associated with increased infection, whereas others have not.
Discontinuation of routine application of topical agents may not be prudent in certain

populations. A study from Nepal demonstrated that early chlorhexidine application

reduced omphalitis and overall neonatal mortality.4
When techniques adequate for the recovery of anaerobic bacteria are used in studying
newborns with omphalitis, anaerobes are recovered from one to two thirds of patients.5,6
The predominant anaerobic isolates include Bacteroides fragilis, Peptostreptococcus
species, and Clostridium perfringens. Several mothers whose newborns had omphalitis
caused by B fragilis also had amnionitis caused by this organism. Isolated cases due to
other anaerobic organisms, including Clostridium sordellii, also are reported. Neonatal
tetanus (with or without omphalitis) caused by Clostridium tetani usually results from
contamination of the umbilical cord during improperly managed deliveries outside of a
medical facility or the cultural practice of placing cow dung on the umbilical stump after
delivery. Neonatal tetanus is rare in the United States but is common in developing
countries.

Pathophysiology
The umbilical stump represents a unique but universally acquired wound, in which
devitalized tissue provides a medium that supports bacterial growth. Normally, the cord
area is colonized with potential bacterial pathogens during or soon after birth. These
bacteria have the potential to invade the umbilical stump, leading to omphalitis. If this
occurs, the infection may progress beyond the subcutaneous tissues to involve fascial
planes (necrotizing fasciitis), abdominal wall musculature (myonecrosis), and the
umbilical and portal veins (phlebitis). The factors that cause colonization to progress to
infection are not well understood.

Frequency
International
Overall incidence varies from 0.2-0.7% in industrialized countries.7 Incidence is higher in
hospitalized preterm infants than in full-term infants. Episodes of omphalitis are reported
and are usually sporadic, but, rarely, epidemics occur (eg, due to S aureus or group A
Streptococcus).8,9,10

Mortality/Morbidity
Outcome is usually favorable in infants with uncomplicated omphalitis associated with
cellulitis of the anterior abdominal wall. In a study by Sawin and colleagues, no deaths
occurred among 32 infants with omphalitis in the absence of necrotizing fasciitis and
myonecrosis.11 The mortality rate among all infants with omphalitis, including those who
develop complications, is estimated at 7-15%. The mortality rate is significantly higher
(38-87%) after the development of necrotizing fasciitis or myonecrosis. Suggested risk
factors for poor prognosis include male sex, prematurity or being small for gestational
age, and septic delivery (including unplanned home delivery); however, data are limited
and conclusions cannot be drawn regarding the role of these factors in the mortality rate.

Sequelae of omphalitis may be associated with significant morbidity and mortality,

including necrotizing fasciitis, myonecrosis, sepsis, septic embolization, intra-abdominal
complications, and death (see Complications).

Sex
No sex predilection has been reported, although males may have a worse prognosis than
females.

Age
In full-term infants, the mean age at onset is 5-9 days. In preterm infants, the mean age at
onset is 3-5 days.

Clinical
History

A detailed review of the pregnancy, labor, delivery, and the neonatal course is
important when assessing omphalitis. A history of poor feeding or feeding
intolerance may be an early indication of infection. A history of change in mental
status, such as irritability, lethargy, and somnolence, or a history of a decreased
level of activity may be an important indicator of systemic dissemination of the
infection.
Anaerobic bacteria are part of the normal flora of the female genital tract and are
commonly involved in ascending infections of the uterus and in septic
complications of pregnancy; therefore, the higher incidence of omphalitis caused
by anaerobes (especially B fragilis) in infants with adverse perinatal histories,
such as premature or prolonged rupture of membranes and amnionitis, may relate
to exposure to maternal infection.
History of urine or stool discharge from the umbilicus suggests an underlying
anatomic abnormality.

Physical

Local disease: Physical signs vary with the extent of disease. Signs of localized
infection include the following:
o Purulent or malodorous discharge from the umbilical stump
o Periumbilical erythema (Recently, algorithms that attempt to standardize
the clinical diagnosis of omphalitis have been developed, emphasizing
extent of periumbilical erythema and absence or presence of pus.)
o Edema
o Tenderness
Extensive local disease, with extension: The following signs indicate more
extensive local disease, such as necrotizing fasciitis or myonecrosis, which are

typically found in a periumbilical location but may spread across the abdominal
wall, onto the flanks and back, and into the scrotum. These signs may also suggest
infection by both aerobic and anaerobic organisms and include the following:
o Ecchymoses, violaceous discoloration
o Bullae
o Peau d'orange appearance
o Crepitus
o Petechiae
o Progression of cellulitis despite antimicrobial therapy
Systemic disease: Signs of sepsis or other systemic disease are nonspecific and
include disturbances of thermoregulation or evidence of dysfunction of multiple
organ systems. Examples include the following:
o Disturbances of thermoregulation - Fever (temperature >38C),
hypothermia (temperature <36C), or temperature instability
o Cardiovascular disturbances - Tachycardia (pulse >180 beats per minute
[bpm]), hypotension (systolic blood pressure <60 mm Hg in full-term
infants), or delayed capillary refill (<2-3 s)
o Respiratory disturbances - Apnea, tachypnea (respirations >60/min),
grunting, flaring of the alae nasi, intercostal or subcostal retractions, or
hypoxemia
o GI tract disturbances - Rigid or distended abdomen or absent bowel
sounds
o Cutaneous abnormalities - Jaundice, petechiae, or cyanosis
o Neurologic abnormalities - Irritability, lethargy, weak sucking, hypotonia,
or hypertonia

Causes

Omphalitis is a polymicrobial infection typically caused by a mixture of aerobic

and anaerobic organisms. Associated risk factors include the following:
o Low birth weight (<2500 g)
o Prior umbilical catheterization
o Septic delivery (as suggested by premature rupture of membranes,
nonsterile delivery, or maternal infection)
o Prolonged rupture of membranes
Omphalitis occasionally manifests from an underlying immunologic disorder.12
Leukocyte adhesion deficiency (LAD) is most prominent among the
immunodeficiency syndromes.13,14,15,16 Numerous infants with acute or chronic
omphalitis have been diagnosed with LAD, a rare immunologic disorder with an
autosomal recessive pattern of inheritance. These infants typically present with
the following:
o Leukocytosis
o Delayed separation of the umbilical cord, with or without omphalitis
o Recurrent infections
Omphalitis may also be the initial manifestation of neutropenia in the
neonate.17,18,19 Infants with neonatal alloimmune neutropenia have presented with

omphalitis. Neonatal alloimmune neutropenia is a disease analogous to Rhhemolytic disease and results from maternal sensitization to fetal neutrophils
bearing antigens that differ from the mother's. Maternal immunoglobulin G
antibodies cross the placenta and result in an immune-mediated neutropenia that
can be severe and last for several weeks to 6 months. Affected infants may present
with other cutaneous infections, pneumonia, sepsis, and meningitis. Since
omphalitis complicated by sepsis also can be associated with neutropenia, the
underlying immune-mediated neutrophil destruction may not be immediately
appreciated in affected newborns.
Rarely, an anatomic abnormality such as a patent urachus, patent
omphalomesenteric duct, or urachal cyst may be present.20,21,22,23,24

Differential Diagnoses
Other Problems to Be Considered
The clinical picture of omphalitis is sufficiently characteristic that diagnosis can be made
with fair certainty on clinical grounds. Determining whether associated complications
such as necrotizing fasciitis, myonecrosis, sepsis, septic embolization, or intraabdominal
complications are present is important. In neonates with omphalitis and either delayed
separation of the umbilical cord or neutropenia, the presence of a predisposing anatomic
abnormality (eg, patent urachus) or an immunologic problem (eg, leukocyte adhesion
deficiency [LAD] or neonatal alloimmune neutropenia) must be considered.
Persistence of a portion of the embryonic tract between the bladder and the umbilicus
results in various urachal anomalies. A patent urachus, a free communication between the
bladder and umbilicus, may result in persistent drainage from the umbilicus, which can
be mistaken as a sign of infection. Incomplete obliteration of the urachal remnant may
lead to the formation of an isolated extraperitoneal cyst, which can present with a
secondary bacterial infection mimicking omphalitis. However, these cysts rarely present
with secondary infections in the neonatal period.

Workup
Laboratory Studies
The following studies are indicated in omphalitis:

Routinely obtain specimens from umbilical infection and submit specimens for
Gram stain and culture for aerobic and anaerobic organisms. If myonecrosis is
suspected, obtain specimens from the involved muscle rather than the wound
surface.
Obtain a blood culture for aerobic and anaerobic organisms.
Obtain a CBC count with manual differential.

Neutrophilia or neutropenia may be present in acute infection. An

immature-to-total neutrophil ratio greater than 0.2 may be a useful
indicator of systemic bacterial infection in the first few days of life.
o Thrombocytopenia may be present.
Other nonspecific laboratory tests, either alone or in combination with a defined
scoring system, have been evaluated for their usefulness in rapid detection of
bacterial infection in neonates, although none has demonstrated sensitivity or
specificity sufficiently high to dictate clinical care. The tests include the
following:
o C-reactive protein levels
o Erythrocyte sedimentation rate
o Limulus lysate test, which detects endotoxin
The following laboratory studies are suggested in neonates in whom sepsis and
disseminated intravascular coagulation (DIC) are suspected:
o Peripheral blood smear
o Prothrombin time
o Activated partial thromboplastin time
o Fibrinogen
o Fibrinogen split products or D-dimer
Other abnormalities associated with serious systemic infection include the
following:
o Hypoglycemia
o Hypocalcemia (often related to saponification with fatty acids released by
bacterial lipases in subcutaneous tissue)
o Metabolic acidosis
o

Imaging Studies

Abdominal radiography may reveal intra-abdominal wall gas.

Ultrasonography may reveal fascial thickening and fluid accumulation between
subcutaneous fat and muscle in cases with fascial involvement. It may also be
useful in the detection of anatomic abnormalities.
CT scanning of the abdomen may determine the presence and extent of muscle
and/or fascial involvement and potentially aid in detection of anatomic
abnormalities.

Procedures

Lumbar puncture may be warranted in infants in whom sepsis is suspected.

Histologic Findings

Analysis of biopsy specimens may reveal necrotizing fasciitis, which is an acute

inflammatory infiltrate found in subcutaneous fat and connective tissue, or

myonecrosis, which is an acute inflammatory process surrounding muscle

bundles, many of which are no longer viable.

Treatment
Medical Care
Treatment of omphalitis (periumbilical edema, erythema, and tenderness) in the newborn
includes antimicrobial therapy and supportive care.

Antimicrobial therapy
o Include parenteral antimicrobial coverage for gram-positive and gramnegative organisms. A combination of an antistaphylococcal penicillin and
an aminoglycoside antibiotic is recommended.
o Some believe that anaerobic coverage is important in all patients.
Omphalitis complicated by necrotizing fasciitis or myonecrosis requires a
more aggressive approach, with antimicrobial therapy directed at
anaerobic organisms as well as gram-positive and gram-negative
organisms. Metronidazole or clindamycin may provide anaerobic
coverage.
o Pseudomonas species have been implicated in particularly rapid or
invasive disease.
o As with antimicrobial therapy for other infections, consider local antibiotic
susceptibility patterns, particularly patterns of S aureus and enterococcal
susceptibility.
o Additional topical therapy with triple dye, bacitracin, and other
antimicrobials has been suggested in addition to parenteral antibiotic
therapy, but such treatment is unproven.
Supportive care: In addition to antimicrobial therapy, supportive care is essential
to survival. These measures include the following:
o Provide ventilatory assistance and supplementary oxygen for hypoxemia
or apnea unresponsive to stimulation.
o Administer fluid, vasoactive agents, or both (as indicated) for hypotension.
o Administration of platelets, fresh frozen plasma, or cryoprecipitate for
disseminated intravascular coagulation (DIC) and clinical bleeding is
suggested.
o Treat infants at centers capable of supporting cardiopulmonary function.
Other treatment considerations
o Monitor patients for progression of disease. Early surgical intervention
may be lifesaving.
o In uncomplicated cases, expect erythema of the umbilical stump to
improve within 12-24 hours after the initiation of antimicrobial therapy.
Failure to respond may suggest disease progression, presence of an
anatomic defect, or an immunodeficiency state.

The role of hyperbaric oxygen in treatment of patients with anaerobic

necrotizing fasciitis and myonecrosis is controversial because no
prospective controlled data are available and pediatric data are scarce. In
the treatment chambers, tissue levels of oxygen are maximized when the
patient breathes 100% oxygen at 2-3 atm. The delivery of high
concentrations of oxygen to marginally perfused tissues may have a
detrimental effect on the growth of anaerobic organisms and improve
phagocyte function. However, surgical therapy has the highest priority,
and initiation of hyperbaric oxygen therapy should not delay transport to a
facility with staff capable of performing surgical debridement.

Surgical Care
Management of necrotizing fasciitis and myonecrosis involves early and complete
surgical debridement of the affected tissue and muscle.25,26

Although the extent of debridement depends on the viability of tissue and muscle,
which is determined at the time of surgery, excision of preperitoneal tissue
(including the umbilicus, umbilical vessels, and urachal remnant) is critically
important in the eradication of the infection.
These tissues can harbor invasive bacteria and provide a route for progressive
spread of infection after less extensive debridement.
Delay in diagnosis or surgery allows progression and spread of necrosis, leading
to extensive tissue loss and worsening systemic toxicity.
Several surgical procedures may be required before all nonviable tissue is
removed.

Consultations

Infectious disease specialist - For appropriate antimicrobial selection, particularly

if necrotizing fasciitis or myonecrosis occurs
Surgeon - If necrotizing fasciitis or myonecrosis is suspected (consult early in the
disease course)

Diet

Once omphalitis is suspected, do not feed the infant enterally. Enteral feedings
may be resumed once the acute infection resolves.
Parenteral nutrition is required in infants with omphalitis.

Medication
A combination of parenterally administered antistaphylococcal penicillin and an
aminoglycoside antibiotic is recommended for uncomplicated omphalitis. Some believe
that anaerobic coverage also should be considered in all infants with omphalitis.

Omphalitis complicated by necrotizing fasciitis or myonecrosis requires a more

aggressive approach, and antimicrobial therapy directed at anaerobic organisms, as well
as gram-positive and gram-negative organisms, is suggested. Metronidazole may be
added to the combination of antistaphylococcal penicillin and aminoglycoside to provide
anaerobic coverage, or clindamycin may be substituted for antistaphylococcal penicillin.
As with antimicrobial therapy for other infections, consider local antibiotic susceptibility
patterns and results of blood and biopsy specimen culturing.
Blood products (eg, packed RBCs, platelets, fresh frozen plasma) and other medications
(eg, inotropic agents, sodium bicarbonate) may be required for supportive care.

Antibiotics
Empiric antimicrobial therapy must be comprehensive and should cover all likely
pathogens in the context of the clinical setting.27
Gentamicin (Garamycin)
Aminoglycoside antibiotic for gram-negative coverage. Used in combination both with
an agent against gram-positive organisms and with an agent that covers anaerobes.

Dosing
Interactions
Contraindications
Precautions

Adult
Pediatric
Neonatal dosage dependent on PMA and postnatal age
PMA <29 weeks and postnatal age 0-7 days: 5 mg/kg/dose IV q48h
PMA <29 weeks and postnatal age 8-28 days: 4 mg/kg/dose IV q36h
PMA <29 weeks and postnatal age >29 days: 4 mg/kg/dose IV q24h
PMA 30-34 weeks and postnatal age 0-7 days: 4.5 mg/kg/dose IV q36h
PMA 30-34 weeks and postnatal age >8 days: 4 mg/kg/dose IV q24h
PMA >35 weeks (any postnatal age): 4 mg/kg/dose IV q24h

Dosing
Interactions
Contraindications
Precautions

Amphotericin B, cyclosporine, cephalosporins, or furosemide may increase the risk of

renal toxicity; coadministration with other aminoglycosides, cephalosporins, penicillins,
and amphotericin B may increase nephrotoxicity; because aminoglycosides enhance

effects of neuromuscular blocking agents, prolonged respiratory depression may occur;

coadministration with loop diuretics may increase auditory toxicity of aminoglycosides;
possible irreversible hearing loss of varying degrees may occur (monitor regularly)

Dosing
Interactions
Contraindications
Precautions

Documented hypersensitivity

Dosing
Interactions
Contraindications
Precautions

Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions
Nephrotoxicity and ototoxicity may be associated with prolonged elevated trough
concentrations; monitor levels to minimize risk of toxicity and to optimize therapy (ie,
peak 6-10 mg/L, trough <2 mg/L); caution in renal failure (not on dialysis), myasthenia
gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust
dose in renal impairment

Oxacillin (Bactocill)
Antistaphylococcal penicillin. Bactericidal antibiotic that inhibits cell wall synthesis.
Used in the treatment of infections caused by penicillinase-producing staphylococci. May
be used to initiate therapy when staphylococcal infection is suspected.

Dosing
Interactions
Contraindications
Precautions

Adult
Pediatric

Neonatal dosing adjusted by PMA and postnatal age

PMA <29 weeks and postnatal age 0-28 days: 25 mg/kg/dose IV/PO q12h
PMA <29 weeks and postnatal age >28 days: 25 mg/kg/dose IV/PO q8h
PMA 30-36 weeks and postnatal age 0-14 days: 25 mg/kg/dose IV/PO q12h
PMA 30-36 weeks and postnatal age >14 days: 25 mg/kg/dose IV/PO q8h
PMA 37-44 weeks and postnatal age 0-7 days: 25 mg/kg/dose IV/PO q12h
PMA 37-44 weeks and postnatal age >7 days: 25 mg/kg/dose IV/PO q8h
PMA >45 weeks (any postnatal age): 25 mg/kg/dose IV/PO q6h

Dosing
Interactions
Contraindications
Precautions

Probenecid decreases elimination

Dosing
Interactions
Contraindications
Precautions

Documented hypersensitivity; patients with combined renal and hepatic impairment

Dosing
Interactions
Contraindications
Precautions

Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in
animals

Precautions
May cause rash and bone marrow suppression; caution in renal insufficiency (decrease
dose)

Clindamycin (Cleocin)
Used to treat infections caused by anaerobic bacteria. Lincosamide for treatment of
serious skin and soft tissue staphylococcal infections. Also effective against aerobic and
anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by

blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein

synthesis to arrest.

Dosing
Interactions
Contraindications
Precautions

Adult
Pediatric
Neonatal dosage dependent on PMA and postnatal age
PMA <29 weeks and postnatal age 0-28 days: 5-7.5 mg/kg/dose IV/PO q12h
PMA <29 weeks and postnatal age >28 days: 5-7.5 mg/kg/dose IV/PO q8h
PMA 30-36 weeks and postnatal age 0-14 days: 5-7.5 mg/kg/dose IV/PO q12h
PMA 30-36 weeks and postnatal age >14 days: 5-7.5 mg/kg/dose IV/PO q8h
PMA 37-44 weeks and postnatal age 0-7 days: 5-7.5 mg/kg/dose IV/PO q12h
PMA 37-44 weeks and postnatal age >7 days: 5-7.5 mg/kg/dose IV/PO q8h
PMA >45 weeks (any postnatal age): 5-7.5 mg/kg/dose IV/PO q6h

Dosing
Interactions
Contraindications
Precautions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium;

erythromycin may antagonize effects; antidiarrheals may delay absorption

Dosing
Interactions
Contraindications
Precautions

Documented hypersensitivity; meningitis

Dosing
Interactions
Contraindications
Precautions

Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in
animals

Precautions
May cause diarrhea, rash, granulocytopenia, thrombocytopenia, and Stevens-Johnson
syndrome; adjust dose in severe hepatic dysfunction; no adjustment necessary in renal
insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of
Clostridium difficile

Metronidazole IV (Flagyl)
Anaerobic antibiotic that also has amebicide and antiprotozoal actions.

Dosing
Interactions
Contraindications
Precautions

Adult
Pediatric
Neonatal dosing adjusted by PMA and postnatal age
Loading dose: 15 mg/kg IV/PO
Maintenance doses: 7.5
PMA <29 weeks and postnatal age 0-28 days: 7.5 mg/kg/dose IV/PO q48h
PMA <29 weeks and postnatal age >28 days: 7.5 mg/kg/dose IV/PO q24h
PMA 30-36 weeks and postnatal age 0-14 days: 7.5 mg/kg/dose IV/PO q24h
PMA 30-36 weeks and postnatal age >14 days: 7.5 mg/kg/dose IV/PO q12h
PMA 37-44 weeks and postnatal age 0-7 days: 7.5 mg/kg/dose IV/PO q24h
PMA 37-44 weeks and postnatal age >7 days: 7.5 mg/kg/dose IV/PO q12h
PMA >45 weeks (any postnatal age): 7.5 mg/kg/dose IV/PO q8h

Dosing
Interactions
Contraindications
Precautions

May increase levels or toxicity of phenytoin, lithium, and warfarin; phenobarbital and
rifampin may increase metronidazole metabolism; disulfiram reaction may occur with PO
ingested ethanol (caution with elixir preparations)

Dosing
Interactions
Contraindications
Precautions

Documented hypersensitivity; liver disease

Dosing
Interactions
Contraindications
Precautions

Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in
animals

Precautions
Requires dose adjustment in patients with renal and liver disease; may cause CNS
toxicity (eg, seizures, neuropathy, headache, vomiting)

Ampicillin
Broad-spectrum penicillin. Interferes with bacterial cell wall synthesis during active
replication, causing bactericidal activity against susceptible organisms. Bactericidal for
organisms, such as GBS, Listeria, nonpenicillinase-producing staphylococci, some
strains of Haemophilus influenzae, and meningococci.

Dosing
Interactions
Contraindications
Precautions

Adult
Pediatric
Neonatal dosing adjusted by PMA and postnatal age
PMA <29 weeks and postnatal age 0-28 days: 25-50 mg/kg/dose IV/PO q12h
PMA <29 weeks and postnatal age >28 days: 25-50 mg/kg/dose IV/PO q8h
PMA 30-36 weeks and postnatal age 0-14 days: 25-50 mg/kg/dose IV/PO q12h
PMA 30-36 weeks and postnatal age >14 days: 25-50 mg/kg/dose IV/PO q8h
PMA 37-44 weeks and postnatal age 0-7 days: 25-50 mg/kg/dose IV/PO q12h
PMA 37-44 weeks and postnatal age >7 days: 25-50 mg/kg/dose IV/PO q8h
PMA >45 weeks (any postnatal age): 25-50 mg/kg/dose IV/PO q6h
Note: 100 mg/kg/dose may be considered for meningitis or group B streptococcal sepsis

Dosing

Interactions
Contraindications
Precautions

Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin

effects and has additive effects on ampicillin rash; may decrease effects of PO
contraceptives

Dosing
Interactions
Contraindications
Precautions

Documented hypersensitivity

Dosing
Interactions
Contraindications
Precautions

Pregnancy
Precautions
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction

Vancomycin (Vancocin, Vancoled)

Bacteriocidal agent against most aerobic and anaerobic gram-positive cocci and bacilli.
Especially important in the treatment of MRSA. Recommended therapy when coagulasenegative staphylococcal sepsis is suspected.

Dosing
Interactions
Contraindications
Precautions

Adult
Pediatric
Neonatal dosing adjusted by PMA and postnatal age
PMA <29 weeks and postnatal age 0-28 days: 10 mg/kg/dose IV/PO q18h
PMA <29 weeks and postnatal age >28 days: 10 mg/kg/dose IV/PO q12h

PMA 30-36 weeks and postnatal age 0-14 days: 10 mg/kg/dose IV/PO q12h
PMA 30-36 weeks and postnatal age >14 days: 10 mg/kg/dose IV/PO q8h
PMA 37-44 weeks and postnatal age 0-7 days: 10 mg/kg/dose IV/PO q12h
PMA 37-44 weeks and postnatal age >7 days: 10 mg/kg/dose IV/PO q8h
PMA >45 weeks (any postnatal age): 10 mg/kg/dose IV/PO q6h
Note: 15 mg/kg/dose may be considered for meningitis

Follow-up
Further Inpatient Care

Examine the patient with omphalitis frequently, and immediately debride any
tissue that shows signs of advancing infection or necrosis. Postoperatively, inspect
the gross appearance of the tissue on the perimeter of the debrided area several
times a day or more frequently if the infant has any unresolved signs of systemic
infection.
Monitor aminoglycoside levels, and adjust dose accordingly.
Monitor and manage metabolic abnormalities, which are common in any ill
neonate.

Further Outpatient Care

Routine postsurgical follow-up care is indicated.

Infants developing portal vein thrombosis require follow-up care for
complications associated with portal hypertension.

Inpatient & Outpatient Medications

Intravenous antimicrobial therapy with an antistaphylococcal penicillin,

aminoglycoside, and clindamycin or metronidazole if indicated, are administered
during hospitalization.

Transfer

Critically ill infants, including those who may require surgical intervention, may
require transfer to an ICU equipped to treat infants.
Transport the patient with advanced life support technology in place and qualified
personnel in attendance.
Options for further treatment or intervention must be immediately available. (See
Transport of the Critically Ill Newborn.)

Deterrence/Prevention

Antimicrobial agents have been applied to the umbilicus to decrease bacterial

colonization and to prevent omphalitis and associated complications. Several
effective umbilical cord care regimens are available, including the following:
o Triple dye applied once daily until cord separation
o Triple dye applied once, then alcohol applied daily until cord separation
o Triple dye applied once, then no further antimicrobial treatment
o Povidone-iodine applied daily until cord separation
o Silver sulfadiazine applied daily until cord separation
o Bacitracin ointment applied daily until cord separation
o Chlorhexidine 4% applied once, with no further antimicrobial treatment
o Chlorhexidine 4% applied daily until cord separation
o Salicylic sugar powder (97% powdered sugar, 3% salicylic acid) applied
daily until cord separation
Routine topical therapy may be indicated in developing countries where
omphalitis is more common.
Topical therapy is also commonly used in attempts to control outbreaks of
omphalitis.

Complications
The sequelae of omphalitis may be associated with significant morbidity and mortality.
These include necrotizing fasciitis; myonecrosis; sepsis; septic embolization; and,
particularly, endocarditis and liver abscess formation, abdominal complications (eg,
spontaneous evisceration, peritonitis, bowel obstruction, abdominal or retroperitoneal
abscess), and death.28,29,30

Necrotizing fasciitis: This is a florid bacterial infection of the skin, subcutaneous

fat, and superficial and deep fascia that complicates 8-16% of cases of neonatal
omphalitis.31,32,33,34,35,26,36 It is characterized by rapidly spreading infection and
severe systemic toxicity. Necrotizing fasciitis typically involves the abdominal
wall but may also involve the scrotum or penis.
o
Necrotizing soft tissue infections are caused by production of factors (by
single or multiple organisms) that lead directly to tissue cell death,
enzymatic destruction of supporting connective tissue, and destruction of
host humoral and cellular immune responses to infecting organisms.
o
Certain organisms are well known to invade tissue and proliferate in
necrotic areas. Group A Streptococcus, S aureus, and Clostridium species
may elaborate extracellular enzymes and toxins that can damage tissue,
may facilitate movement of organisms through soft tissue planes, and may
limit host defenses and penetration of systemic antimicrobial agents.3
Myonecrosis: This refers to infectious involvement of muscle.
o
In infants with omphalitis, development of myonecrosis usually depends
on conditions that facilitate the growth of anaerobic organisms. These
conditions include the presence of necrotic tissue, poor blood supply,
foreign material, and established infection by aerobic bacteria such as
staphylococci or streptococci. C perfringens, in particular, does not

replicate under conditions of an oxidation-reduction potential (Eh) greater

than -80 mV; the Eh of healthy muscle is 120-160 mV. In infections with
mixtures of facultative aerobes and anaerobes, the aerobic organisms use
oxygen available in tissue, thereby further reducing the Eh in tissues
inoculated by Clostridium species or other anaerobic bacteria, often to less
than -150 mV, allowing anaerobic bacterial growth.
o
The toxins produced in the anaerobic environment of necrotic tissue allow
rapid spread of organisms through tissue planes. Local spread of toxins
extends the area of tissue necrosis, allowing continued growth of
organisms and increasing elaboration of toxins. Because of progressive
deep tissue destruction and subsequent systemic spread of toxins,
anaerobic infections, in particular, may be fatal if not treated promptly. In
addition, rapid development of edema, which constricts the muscle within
its fascia, may lead to ischemic myonecrosis.
Sepsis: This is the most common complication of omphalitis. In a study by Mason
and colleagues, bacteremia was a complication in 13% of infants with omphalitis.
In these infants, disseminated intravascular coagulation (DIC) and multiple organ
failure may occur.37
Septic embolization: If septic embolization arises from infected umbilical vessels,
it may lead to metastatic foci in various organs, including the heart, liver, lungs,
pancreas, kidneys, and skin.
Abdominal complications: Abdominal complications include spontaneous
evisceration, peritonitis, bowel obstruction, abdominal abscess, retroperitoneal
abscess, or liver abscess.
Long-term or late complications of omphalitis: These may include nonneoplastic
cavernous transformation of the portal vein, portal vein thrombosis, extrahepatic
portal hypertension, and biliary obstruction.38,39,40

Prognosis

The prognosis for infants with omphalitis varies.

Patient Education

Referral for psychosocial counseling may assist the family in coping with a
critically ill infant.
For excellent patient education resources, visit eMedicine's Children's Health
Center. Also, see eMedicine's patient education article Umbilical Cord Care.

Miscellaneous
Medicolegal Pitfalls

Failure to recognize necrotizing fasciitis or myonecrosis may result in delay of

appropriate surgical intervention.

Special Concerns

The relatively high incidence of necrotizing fasciitis following omphalitis in the

newborn, with its attendant morbidity and mortality, requires close observation
and early surgical intervention if any question surrounds the diagnosis.

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