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Omphalitis is the medical term for infection of the umbilical cord stump in the neonatal newborn period.1 While currently an uncommon anatomical location for infection in the newborn in the United States, it has caused significant morbidity and mortality both historically and in areas where health care is less readily available.
The current incidence in the United States is somewhere around 0.5% per year; overall, the incidence rate for developed world falls between 0.2–0.7%. In developing countries, the incidence of omphalitis varies from 2 to 7 for 100 live births.2 There does not appear to be any racial or ethnic predilection.
Like many bacterial infections, omphalitis is more common in those patients who have a weakened or deficient immune system or who are hospitalized and subject to invasive procedures. Therefore, infants who are premature, sick with other infections such as blood infection (sepsis) or pneumonia, or who have immune deficiencies are at greater risk. Infants with normal immune systems are at risk if they have had a prolonged birth, birth complicated by infection of the placenta (chorioamnionitis), or have had umbilical catheters.
Clinically, neonates with omphalitis present within the first two weeks of life with signs and symptoms of infection (cellulitis) around the umbilical stump (redness, warmth, swelling, pain), pus from the umbilical stump, fever, fast heart rate (tachycardia), low blood pressure (hypotension), somnolence, poor feeding, and yellow skin (jaundice). Omphalitis can quickly progress to sepsis and presents a potentially life-threatening infection. In fact, even in cases of omphalitis without evidence of more serious infection such as necrotizing fasciitis, mortality is high (in the 10% range).
Omphalitis is most commonly caused by bacteria. The culprits usually are Staphylococcus aureus and Streptococcus, Escherichia coli, and Klebsiella pneumoniae. The infection is typically caused by a combination of these organisms and is a mixed Gram-positive and Gram-negative infection. Anaerobic bacteria can also be involved.3
Diagnosis is usually made by the clinical appearance of the umbilical cord stump and the findings on history and physical examination. There may be some confusion, however, if a well-appearing neonate simply has some redness around the umbilical stump. In fact, a mild degree is common, as is some bleeding at the stump site with detachment of the umbilical cord. The picture may be clouded even further if caustic agents have been used to clean the stump or if silver nitrate has been used to cauterize granulomata of the umbilical stump. Leukocyte Adhesion Deficiency is a rare (autosomal recessive disease) in which there is an absence of CD18.
Treatment consists of antibiotic therapy aimed at the typical bacterial pathogens in addition to supportive care for any complications which might result from the infection itself such as hypotension or respiratory failure. A typical regimen will include intravenous antibiotics such as from the penicillin-group which is active against Staphylococcus aureus and an aminoglycoside for activity against gram-negative bacteria. For particularly invasive infections, antibiotics to cover anaerobic bacteria may be added (such as metronidazole). Treatment is typically for two weeks and often necessitates insertion of a central venous catheter or peripherally inserted central catheter.
Each hospital/birthing center has its own recommendations for care of the umbilical cord after delivery. Some recommend not using any medicinal washes on the cord. Other popular recommendations include triple dye, betadine, bacitracin, or silver sulfadiazine. There is little data to support any one treatment (or lack thereof) over another.
- Jones, Kevin, MD, Neayland, Beverly, MD. "Brief Review of Omphalitis". UNSOM Department of Pediatrics. Retrieved 23 July 2013.
- Bugaje, Mairo Adamu, et al. "Omphalitis". Paediatric Surgery: A Comprehensive Text For Africa. Retrieved 23 July 2013.
- Fleisher, Gary R. Textbook of Pediatric Emergency Medicine. Philadelphia: Lippincott Williams & Wilkins, 2006, p. 928.