Early recognition of neonatal hyperbilirubinemia and its emergent management

Hannah Smitherman1, Ann R Stark, Vinod K Bhutani

  • 1Department of Pediatrics, Section of Emergency Medicine, Baylor College of Medicine, Houston, TX, USA. hfsmithe@texaschildrenshospital.org

Hyperbilirubinemia and kernicterus are re-emerging as prominent clinical concerns and have been hypothesized to be secondary to increased breast-feeding rates, early hospital discharges and overall lack of concern for the potential impact of severe hyperbilirubinemia on healthy term newborns. Although the clinical symptoms can be non-specific and vague, they could be early, insidious and heralding signs of acute bilirubin encephalopathy (ABE) or acute stage kernicterus. Because it is highly prevalent, evaluation of a jaundiced neonate requires detailed questions about specific signs, review of birth and postnatal histories, evaluation of predischarge data, and possibly an emergency clinical evaluation of the neurological status of the infant. Medical urgency to evaluate, investigate and monitor such a newborn ensues from the possibility of rapid progression that might lead to permanent sequelae of bilirubin-induced neurologic dysfunction (BIND). Early recognition of the urgency and rapid transition to treatment seem to be the major barriers leading to delay in therapy. However, because there is a well-established and relatively safe treatment for neonatal jaundice, there should be zero tolerance for kernicterus, and BIND prevention has become a national priority in the USA. This paper reviews the clinical signs and epidemiology of ABE and BIND and presents a system-based strategy for preventing their occurrence, focusing particularly on the transition from recognition of clinical jaundice to actual treatment. A novel emergency-room-based protocol is presented as an example of how to expedite and facilitate rapid progression to treatment.

Related Concept Videos

Jaundice01:25

Jaundice

Jaundice, or icterus, is the yellow discoloration of the skin, sclerae, and mucous membranes. It happens when plasma bilirubin levels rise above 2.5-3 mg/dL, leading to bilirubin deposition in tissue.Bilirubin is a byproduct of hemoglobin degradation. In macrophages, hemoglobin breaks down into globin and heme. Globin is converted into amino acids, while heme is turned into biliverdin by heme oxygenase, which is then reduced to unconjugated bilirubin by biliverdin reductase.Unconjugated...
Esophageal Varices-II: Clinical Features and Management01:28

Esophageal Varices-II: Clinical Features and Management

Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps.
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol abuse, or...
Acute Pancreatitis II: Clinical Manifestations and Management01:30

Acute Pancreatitis II: Clinical Manifestations and Management

Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...