OVERVIEW: What every practitioner needs to know
Are you sure your patient has Omphalitis? What are the typical findings for this disease?
Drainage from the umbilical stump in a newborn may be indicative of serious infection. Bacteria colonize the umbilical stump soon after birth; during tissue necrosis, bacterial growth is promoted and the vessels provide a portal for bacteria to directly enter the bloodstream.
While rare in developed countries, omphalitis occurs in approximately 0.7% of term infants and carries a mortality rate as high as 15%. Omphalitis can progress to necrotizing fasciitis, which carries a mortality rate reported as high as 85%. Early recognition and treatment may prevent the development of necrotizing fasciitis and improve outcome. Symptoms must be distinguished from other conditions that result in drainage from the umbilical cord.
The localized symptoms of omphalitis include (see Figure 1):
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1. Erythema of periumbilical skin
2. Tenderness
3. Induration
4. Purulent discharge
5. Umbilical stump bleeding
What other disease/condition shares some of these symptoms?
Patent urachus presents with drainage from the umbilicus. In this condition, the urachus fails to involute into a fibrous cord, allowing the bladder to drain out the umbilicus. The drainage is urine and non-purulent. Patent urachus does not cause induration, tenderness, or bleeding. The skin may appear erythematous and irritated from exposure to urine. Urinary tract infection may ensue; systemic symptoms are otherwise rare.
Persistent omphalomesenteric duct presents with drainage from the umbilicus as well. In complete patency, the terminal ileum communicates with the umbilicus; the drainage contains intestinal secretions and is not purulent. The surrounding tissue is not tender or indurated. This condition is associated with intestinal obstruction and Meckel’s diverticulum. Rectal bleeding is common.
Excessive granulation tissue may persist at the base of the umbilicus after cord separation; this can also result in umbilical stump drainage. The drainage is serosanguineous, non-purulent. There is no associated tenderness, erythema, or induration.
What caused this disease to develop at this time?
The umbilical cord contains two umbilical arteries, the umbilical vein, the remnant of the omphalomesenteric (vitelline) duct, the rudimentary allantois, and a gelatinous encasing of Wharton’s jelly. At birth, the umbilical cord has a bluish-white hue. Soon after birth, the Wharton’s jelly dehydrates, and the umbilical cord begins to mummify and turn black. This process leads to eventual separation of the cord from the abdominal insertion site and is thought to involve autolysis from leukocyte-mediated lysosomal enzymatic activity. A small amount of purulent material at the base of the cord may be normal during this process.
Separation usually occurs within the first three weeks. The timing is influenced by a number of factors, including the cord care regimen. Immediately following birth, the umbilicus is colonized with skin flora.
The onset of omphalitis is typically 5-7 days after birth. Initially, the skin at the base of the cord becomes erythematous, warm, and tender, resembling cellulitis. As the infection evolves, the discharge becomes purulent and malodorous. Left untreated, the bacteria spreads to the subcutaneous tissue, and the abdomen becomes extremely tender to palpation. Crepitus may be appreciated. The skin becomes ecchymotic and violaceous, and the infant become systemically ill, including fever and lethargy. These are signs of necrotizing fasciitis. Necrotizing fasciitis is a surgical and medical emergency.
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
The physical findings of erythema, induration, tenderness, and purulent discharge at the umbilicus are pathognomonic for omphalitis. When suspected, a full septic work-up should be performed, including surface cultures, a complete blood count, C-reactive protein, blood culture, urinalysis, urine culture, and a lumbar puncture.
Would imaging studies be helpful? If so, which ones?
When necrotizing fasciitis develops, a radiograph may demonstrate subcutaneous air. A computed tomography (CT) scan may show fluid and air accumulation between the subcutaneous fat and muscle.
If you are able to confirm that the patient has omphalitis, what treatment should be initiated?
Prompt treatment when omphalitis is suspected is imperative. Omphalitis is a polymicrobial infection; some of the most likely offending organisms include Staphylococcus aureus, Escherichia coli, and streptococcal species. Treatment is therefore directed against Gram-positive and Gram-negative organisms. Most experts also include treatment against anaerobes (antistaphylococcal penicillins and aminoglycosides or third generation cephalosporins and clindamycin or metronidazole). Consider vancomycin if the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) is high. A surgery consult should be obtained if the patient has necrotizing fasciitis; wound debridement is necessary. Suspected necrotizing fasciitis is an emergency.
What are the adverse effects associated with each treatment option?
What are the possible outcomes of omphalitis?
The most common complication of omphalitis is sepsis. Additional complications include septic thrombophlebitis, hepatic abscess, portal vein thrombosis, peritonitis resulting in intra-abdominal abscess, spontaneous evisceration of small bowel resulting in intestinal gangrene, and necrotizing fasciitis.
Necrotizing fasciitis in neonates causes septic shock. The mortality from necrotizing fasciitis is reported to be as high as 85%. Treatment includes rapid surgical debridement of nonviable tissue, broad-spectrum antibiotics, and supportive care. Even with surgery, mortality remains extremely high.
What causes this disease and how frequent is it?
The incidence of omphalitis ranges from 0.7% to 7%; developing nations have the highest incidence.
Omphalitis has an associated mortality rate of 7%-15%; if omphalitis progresses to necrotizing fasciitis the mortality can be as high as 85%.
Risk factors include nonsterile delivery, home birth, prolonged labor, prolonged rupture of membranes, umbilical catheterization, prematurity, low birthweight, and non-aseptic cord care. Abnormalities of the immune system are also thought to put an infant at risk for omphalitis. (For example, leukocyte adhesion defects delay cord separation, allowing pathogenic bacteria to multiply.)
The umbilicus undergoes polymicrobial colonization after birth. Bacteria propagate in the devitalized tissues of the umbilical cord stump; this infection prevents obliteration of the umbilical vessels, which allows microorganisms direct entry into the blood, potentially leading to sepsis.
How do these pathogens/genes/exposures cause the disease?
Other clinical manifestations that might help with diagnosis and management
What complications might you expect from the disease or treatment of the disease?
Complications include septic thrombophlebitis, hepatic abscess, portal vein thrombosis, peritonitis resulting in intra-abdominal abscess, spontaneous evisceration of small bowel resulting in intestinal gangrene, myonecrosis of the abdominal wall musculature, and necrotizing fasciitis.
Are additional laboratory studies available; even some that are not widely available?
How can omphalitis be prevented?
According to the American Academy of Pediatrics, no single cord care regimen has been shown to be more effective than any other in preventing infection.
In developed countries the stump should be left to dry after birth. Topical antibiotics and alcohol are no longer recommended because they may prolong cord separation. In addition, they have not been found to be effective in preventing infection.
Because necrotic tissue in the drying umbilical stump provides rich media for bacterial growth, it is readily colonized following birth. Pathogenic bacteria can infect and enter the blood stream through the umbilical vessels. In developing countries, hygienic cord care reduces colonization, tetanus, infection, and sepsis.
What is the evidence?
Cord care:
Zupan, J, Garner, P, Omari, AA. “Topical umbilical cord care at birth”. Cochrane Database Syst Rev. 2004. This meta-analysis of 10 studies in developed countries compared umbilical cord care treatments. There was no significant difference in mortality or the incidence of omphalitis between any of the cord care regimens (dry cord care, antiseptic topical agents including chlorhexidine, triple dye, alcohol, or silver sulfadiazine).
Mullany, LC, Darmstadt, GL, Khatry, SK. “Topical applications of chlorhexidine to the umbilical cord for prevention of omphalitis and neonatal mortality in southern Nepal: a community-based, cluster-randomised trial”. Lancet. vol. 367. 2006. pp. 910-8. To determine how cord care impacts outcomes in developing countries where aseptic technique may be less available, this community-based, cluster-randomized trial assigned one of three cord care regimens to 413 different Nepalese communities. It was shown that antiseptic topical care of the umbilicus significantly reduces the risk of omphalitis and neonatal mortality.
•Chlorhexidine compared to dry cord care reduced the incidence of severe omphalitis (0.2 versus 1.1 percent) and mortality (72 versus 98 deaths per 1000 live births; RR 0.76, 95% 0.55 to 1.04).
•Infants who had early cord care (<24 hours of life) had a lower mortality rate compared to the overall group. In infants who received early cord care, chlorhexidine reduced the mortality rate compared to dry cord care (14 versus 21 deaths per 1000 live births; RR 0.66, 95% 0.46 to 0.95).
•There was no difference in the incidence of omphalitis or mortality rate between cord care with soap/water and dry cord care.
“Neonatal tetanus–Montana, 1998”. MMWR Morb Mortal Wkly Rep. vol. 47. 1998. pp. 928-30. Inappropriate cord care can result in umbilical infections. As an example, neonatal tetanus has been reported as a complication of inappropriate application of cow dung or bentonite clay.
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