Newborn Jaundice Malpractice
As soon as a child is born, their body undergoes several important changes. One of these changes is a rapid rise in the level of oxygen in their blood. That oxygen then produces many changes, including a rapid rise in red blood cells that contain hemoglobin, which is the part of blood cells that carries oxygen around the body. When red blood cells with hemoglobin are naturally broken down by the body, the process creates bilirubin.
Bilirubin is the reason that bruises look yellow, and is typically the cause of jaundice. In healthy adults, bilirubin is typically cleared by the liver, and thus is rarely a problem unless a person has liver disease. Newborn infants, however, produce two to three times as much bilirubin as adults do, because they have a higher proportion of red blood cells and because their red blood cells don’t last as long as the red blood cells in an adult. Newborn infants also can’t clear bilirubin as quickly, because newborns have just one percent as much of the enzyme in the liver that clears bilirubin (called “UGT1A1”). A newborn infant won’t have as much UGT1A1 as an adult until they reach 14 weeks of age.
Jaundice is very common in newborns. In fact, most newborns — up to 80% — develop jaundice. The rate is even higher in preemies and infants with bruising, like cephalohematomas. Jaundice is usually treatable with a simple and safe therapy discovered back in 1956: light. (1) Hospitals typically treat jaundice with phototherapy, which causes the bilirubin to break down into water-soluble compounds that the body can remove more easily. If the phototherapy isn’t working fast enough to get bilirubin levels down to a safe level, then an exchange transfusion can help clear bilirubin from the newborn’s body.
The biggest danger from bilirubin comes from its ability to cross the “blood-brain barrier,” which allows bilirubin — which is toxic — to come into contact with the newborn’s brain, which is still in a sensitive developing state. There are three main terms for the types of brain damage caused by excessive bilirubin levels:
Bilirubin-Induced Neurological Dysfunction (“BIND”) refers to a wide range of neurological, cognitive, and mental injuries caused by bilirubin. The original “BIND” diagnosis came with a scale, Stage 1A (Early), Stage 1B (Moderate), and Stage II (Severe). A patient’s place on the scale was determined by looking at:
- Mental Status (sleepy, difficult to awaken, lethargic, apnea, convulsions, or coma)
- Muscle Tone (slightly decreased, neck or back arching, strong “posturing” with back, legs, or arms)
- Cry (high pitched, shrill, piercing)
- Suck (weak, absent)
- Feeding (decreased, poor, absent)
- Yellowness (eyes and face, trunk and chest, abdomen and below)
Recently, several medical researchers have argued for a more precise system that incorporated upward gaze and other factors, taking the scale from three levels to twelve.(2)
Acute bilirubin encephalopathy is the name given to acute clinical signs and symptoms of bilirubin-induced neurological dysfunction. In other words, this is the term given in the hospital, when the brain injury has just happened.
Kernicterus is the name for the chronic and permanent damage after excessive bilirubin levels, and is usually diagnosed in the first year or two after birth. The features of kernicterus often include choreoathetoid cerebral palsy (including termors and dystonia), hearing loss or other auditory neuropathy, problems with eye gaze (particularly limitations of upward gaze), and dental enamel dysplasia. a type of brain injury caused by too much bilirubin.
In this day and age, most cases of kernicterus are inexcusable. Excessive bilirubin levels (“hyperbilirubinemia”) don’t happen instantly, but rather happen as bilirubin accumulates. There are more than a few signs that doctors and nurses should follow — whether in a pediatric ward or in the neonatal intensive care unit — to check for excessive bilirubin.
A comprehensive study in 2009 (3) identified the twelve most common “breakdowns in health systems” that caused infants to develop kernicterus, and these are the same problems we see in the medical malpractice lawsuits we pursue:
Failure to recognize the clinical significance of jaundice within the first 24 h after birth.
Failure of clinicians to recognize the limitations of visual recognition of jaundice.
Failure of clinicians to recognize the onset and progression of clinical jaundice and document its severity by bilirubin measurement before discharge from the hospital.
Failure to ensure post-discharge follow-up based on the severity of pre-discharge hyperbilirubinemia.
Failure to respond to parental concerns of newborn jaundice, poor feeding, lactation difficulties and change in newborns behavior and activity in a timely manner.
Failure to provide ongoing effective lactation support in breast-feeding babies to ensure adequacy of intake.
Failure to recognize the impact of skin, color race, ethnicity and family history on severity of newborn jaundice.
Failure to monitor the progressive hyperbilirubinemia prior to onset of ABE
Failure to institute interventional strategies to prevent severe hyperbilirubinemia when bilirubin is rising more rapidly than expected.
Failure to aggressively treat severe hyperbilirubinemia with intensive phototherapy or exchange transfusion for hazardous bilirubin levels.
Failure to communicate with parents and educate them about the potential irreversible risks of jaundice during the newborn period and infancy.
Failure to recognize the need to identify post-icteric sequelae following hazardous bilirubin exposure.
These failures are all preventable with appropriate training and systems in place at the hospital, and it is malpractice for hospitals to allow these problems to continue in the wake of decades of research showing how to detect excessive bilirubin levels and how to treat them. For more than a decade, the American Academy of Pediatrics has had clear guidelines for how to properly diagnose and treat high bilirubin levels.(4)