eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Omphalitis: Follow-up

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

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:
    • Triple dye applied once daily until cord separation
    • Triple dye applied once, then alcohol applied daily until cord separation
    • Triple dye applied once, then no further antimicrobial treatment
    • Povidone-iodine applied daily until cord separation
    • Silver sulfadiazine applied daily until cord separation
    • Bacitracin ointment applied daily until cord separation
    • Chlorhexidine 4% applied once, with no further antimicrobial treatment
    • Chlorhexidine 4% applied daily until cord separation
    • 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.
    • 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.
    • 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.
    • 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.
    • 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.
 


More on Omphalitis

Overview: Omphalitis
Differential Diagnoses & Workup: Omphalitis
Treatment & Medication: Omphalitis
Follow-up: Omphalitis
References
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References

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Further Reading

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Keywords

omphalitis, umbilicus, umbilical cord, umbilical stump, umbilicus infection, umbilical infection, umbilical stump infection, necrotizing fasciitis, myonecrosis, Staphylococcus aureus, group A Streptococcus, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, fragilis, Peptostreptococcus species, Clostridium perfringens, tetanus, sepsis, septic embolization, jaundice, cellulitis, petechiae, crepitus, bullae, leukocyte adhesion deficiency, LAD, patent urachus, patent omphalomesenteric duct, urachal cyst, disseminated intravascular coagulation, DIC, hypoglycemia, hypocalcemia, metabolic acidosis

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Contributor Information and Disclosures

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
Patrick G Gallagher, MD is a member of the following medical societies: American Society of Hematology and American Society of Human Genetics
Disclosure: Nothing to disclose.

Coauthor(s)

Samir S Shah, MD, Staff Physician, Departments of Pediatrics and Immunologic and Infectious Diseases, The Children's Hospital of Philadelphia
Samir S Shah, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Shelley C Springer, MD, MBA, MSc, FAAP, JD LS-3, Clinical Instructor, Department of Pediatrics, University of Wisconsin; Neonatologist, Pediatrix Medical Group; Assistant Clinical Professor, Department of Pediatrics, University of North Texas Science Center; Assistant Clinical Professor, Department of Pediatrics, Texas A & M University
Shelley C Springer, MD, MBA, MSc, FAAP, JD LS-3 is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Minnesota Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Brian S Carter, MD, FAAP, Professor of Pediatrics (Neonatology), Vanderbilt University School of Medicine; Co-director, Pediatric Advance Comfort Team, Monroe Carell Jr Children's Hospital at Vanderbilt
Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, National Hospice and Palliative Care Organization, and National Perinatal Association
Disclosure: Nothing to disclose.

CME Editor

Carol L Wagner, MD, Professor of Pediatrics, Medical University of South Carolina
Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD, Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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