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Perinatal: Labour, Delivery and Newborn Care
Hyperbilirubinemia or neonatal jaundice is a commonly occurring condition in newborns with varying severities and treatment options depending on the timing of the first onset of symptoms. The condition affects up to 60% of full-term newborns and can vary in severity, with differing symptoms and requires the understanding of physiology, risk factors, available tests and screening as well as support and nursing interventions (Porter, & Dennis, 2002). By failing to understand the Hyperbilirubinemia mechanisms the risk of seizures and brain damage in newborns increases (Porter, & Dennis, 2002). New parents have a variety of resources available ranging from education, screening, and emotional support. In addition to this, considerations for discharge and follow ups can be given to new parents as well as having resources in the community for support. Clinical guidelines recommend early detection of infants at risk of hyperbilirubinemia in order prevent the associated burden (Barrington, & Sankaran, 2007). Early detection is the key in selecting the appropriate treatment and ensuring the proper transitioning and discharge into the community.
Jaundice is one of the most common clinical conditions encountered in full term or late preterm newborns. It is especially common for newborns within the first week of life and depending on the timing of first symptoms can determine the severity of the illness (Maisels, 2015). Jaundice is also known as hyperbilirubinemia which is defined as an elevated level of serum bilirubin concentration in newborns. With newborns, Jaundice can become severe advancing to acute bilirubin encephalopathy or kernicterus and a significant risk of neonatal mortality (Porter, & Dennis, 2002). Hyperbilirubinemia is a multifactorial disorder with many symptoms and can be a life-threatening condition. Jaundice can be defined as yellowing of the skin and whites of the eyes and other mucous membranes and is usually caused by hyperbilirubinemia. Hyperbilirubinemia is defined as a bilirubin level that is greater than 5mg per dL (Maisels, 2015). Bilirubin is defined as the yellow biproduct from the breakdown of old red blood cells. Some of the major signs and symptoms of Hyperbilirubinemia include yellowing of the skin and eyes, lethargy, poor intake and not gaining weight (Porter, & Dennis, 2002). Approximately, 60% of term newborns and 80% of premature babies develop jaundice by the second through fifth day of life. As previously mentioned, Jaundice which appears in the first 24 hours of life or the total serum bilirubin level is greater than 17mg per dL could suggest a serious illness and may require immediate attention and treatment. Subsequently, Jaundice which appears toward the end of the first week is usually as a result of an infection and if properly identified may be easier to treat and less severe (American Academy of Paediatrics, 2004). Diabetic mothers or those with Rh disease have an increased likeliness of offspring developing hyperbilirubinemia and jaundice (Porter & Dennis, 2002). Generally, the physiological jaundice is the most prevalent type and is considered a normal process which usually will not need treatment. There are different types of jaundice which include physiologic, breastfeeding, breast milk and pathologic. Physiological jaundice is the most commonly occurring and benign form and through proper testing can be separate from serious and ongoing cases. The baby’s limited ability to excrete bilirubin in the first days of life can be viewed as normal and is referred to as Physiological jaundice (Ontario Ministry of Health, 2017). Reabsorption of bilirubin through the intestinal tract is assumed to be caused by a substance in breast milk and is know as Breast milk jaundice. Jaundice as a result of breast milk develops in approximately 2 percent of babies after the first week of life and peaks about two weeks of age (Ontario Ministry of Health, 2017). Jaundice can also be caused by a failure to start breastfeeding. This causes dehydration, decreased urine production and an accumulation of bilirubin. Infants who are born 34 weeks to 36 weeks have an increased susceptibility to breastfeeding failure as a result of lack of coordination and strength to maintain successful breastfeeding. Jaundice may also occur as a result of breakdown of red blood cells due to newborn hemolytic disease. An abundance of red blood cells which then naturally break down and release bilirubin also causes hemolysis jaundice (Ontario Ministry of Health, 2017).
A study in Canada concluded that approximately 20 percent of infants in a year with a live birth rate of approximately 300 000 had acute bilirubin. As a result, 4 out of 10 000 live births had developed hyperbilirubinemia (Sgro, Campbell, & Shah, 2006). Incidence of neonatal hyperbilirubinemia has a higher occurrence rate in Asians as opposed to Caucasians. Additionally, low- and middle-income countries have the greatest burden of sever neonatal hyperbilirubinemia (Sgro, Campbell, & Shah, 2006). There are at least eight known risk factors which include breast feeding, premature birth, cephalohematoma, birth infection, asphyxia, ABO compatibility, glucose-6-phosphate deficiency and variant UDP-glucuronosyltransferase 1A1 gene. Babies born prior to 38 weeks of gestation may have inability with bilirubin processing in comparison to full term babies. Babies born prematurely may also feed less and have reduced bowel movements which subsequently results in less bilirubin being eliminated through stool (Sgro, Campbell, & Shah, 2006). Babies are also at higher risk for developing jaundice if they have difficulty nursing or getting enough nutrition from breast feeding. A baby may receive antibodies through the placenta which could cause abnormal rapid breakdown of red blood cells if the mother’s blood type is different from her baby’s. Additionally, other risk factors exist such as maternal age, occupation, drug usage during pregnancy, siblings previously treated with jaundice, low birth weight (Sgro, Campbell, & Shah, 2006). A case-control study revealed that neonates carrying the 211 and 388 variants of the UGT1A1 gene as well as being fed with breastmilk carry a higher risk of developing hyperbilirubinemia (Maisels, 2015). Additionally, risks associated with maternal factors exist, these include primiparity and place of delivery as well as risks with blood group incompatibilities. Infants with a gestational age of less than 36 weeks, infections or elevated bilirubin levels within the first hours of life should be considered for increased monitoring (Porter & Dennis, 2002).
The physiology of Hyperbilirubinemia has set of processes and mechanisms which result in identifiable signs and symptoms. Some of these processes include, increased production, decreased hepatic uptakes, decreased conjugation, impaired excretion, impaired bile flow and increased enterohepatic circulation (Porter & Dennis, 2002). The breakdown of red blood cells produces the majority of bilirubin and becomes unconjugated bilirubin and other substances. To make bilirubin water soluble and excretable unconjugated bilirubin binds to albumin and is transported to the liver where it is absorbed by hepatocytes and conjugated with glucuronic acid by the enzyme uridine diphosphogluconurate glucuronosyltransferase (Sgro, Campbell, & Shah, 2015).
There are several methods for diagnosing and screening for hyperbilirubinemia. These include measuring a red blood cell count, testing the blood type and testing for RH incompatibility as well as performing direct and indirect bilirubin level tests (American Academy of Paediatrics, 2004). Furthermore, several screening techniques available which correlate to a hyperbilirubinemia diagnosis. By performing timed TSB measurements, the chances of developing severe hyperbilirubinemia can be predicted. In addition to these, several other screening tests are available and include, umbilical cord blood TSB, universal hemoglobin assessment, blood group and Coombs testing (Porter & Dennis, 2002). A setback to testing and diagnosing is the occurrence of peak TSB concentration usually occurs between days three to five of life. During this time the majority of babies are being discharged from a hospital. Additionally, mothers should be tested for ABO and Rh(D) blood types and be screen for red cell antibodies during pregnancy (Muchowski, 2014).
Nursing Interventions exist to reduce the occurrence of severe hyperbilirubinemia and to decrease the risks of unintended harm including but not limited to maternal anxiety, breast feeding decrease, reduce costs or treatments Ministry of Ontario, 2017). The key ideas behind the prevention and management of hyperbilirubinemia are the promotion and support of successful breast-feeding regime (American Academy of Paediatrics, 2004). As well as providing a systematic pre-discharge assessment for the risk of hyperbilirubinemia. As a result of this assessment it is possible to provide an early and focused follow up. When required provide support in regards to obtaining treatments such as phototherapy or exchange transfusion. Proper screening, education and awareness of family history also helps plan for pregnancy and any complication which may arise related to the jaundice (Ministry of Ontario, 2017). Additionally, clinicians should interpret and record all bilirubin levels according to the infants age and hours. It is also necessary to recognize that those infants which are breastfed and with less than 36 weeks’ gestation are at a higher risk of developing hyperbilirubinemia and as a result should have higher surveillance and monitoring (Ministry of Ontario, 2017). As a result of reduced caloric intake or subpar breastfeeding, nursing clinicians should inform mothers to increase the frequency of infant nursing to at least eight times per day. Nurses should pay close attention in regards to infant skin and eye care as a result of phototherapy. It is important to observe the skin color, check for rashes and clean the skin with warm water especially after stooling. It is necessary to monitor the infant’s temperature at least every four hours. Eye pads should be provided over the infant’s eyes during phototherapy to reduce the possibility of retinal damage (Ministry of Ontario, 2017).
Specific treatments exist for hyperbilirubinemia and are determined by the baby’s gestational age, overall health and medical history. In addition to these, the extent of the disease, the baby’s tolerance for medications and available therapies play a role in selecting an appropriate treatment to ensure highest success rates. The cause of hyperbilirubinemia and the level of bilirubin are key factors in determining the best treatment options early in the diagnosis (Muchowski, 2014). In terms of treatments, the main goal is to prevent the level of bilirubin from increasing to dangerous levels. Some treatment options include Phototherapy, Fiberoptic blanket, Exchange transfusion to replace the baby’s damaged blood with fresh blood. Adequate hydration with breastfeeding or pumped breast milk or treating any underlying cause such as infection is important (Porter & Dennis, 2002). Phototherapy is the process of exposing a baby to a special blue light spectrum. As a result, bilirubin will absorb the light which will result in a decrease in bilirubin and jaundice. In addition to using regular phototherapy a fiberoptic blanket may be placed under the baby which provides additional blue light spectrum. Another available treatment is exchange transfusion of damaged blood with fresh blood. This increases the red blood cell count and lowers the bilirubin. If bilirubin levels remain high the exchange transfusion process may be repeated (Porter & Dennis, 2002). Furthermore, it is recommended that babies be breastfed while receiving any of the aforementioned therapies to reduce dehydration and weight issues (Muchowski, 2014). Special Considerations should be given to parents which speak different languages to ensure that the information is properly interpreted and understood. Also increased awareness should be exercised when treating an underlying illness due to the possibility of damaging the infant’s liver and subsequently increasing the chances of developing jaundice (Ministry of Ontario, 2017). Providing community care after discharge is essential in ensuring ongoing care is successful. It is also necessary to increase the communication between hospitals and community care centers when consultation with a paediatrician or a neonatologist is required (Ministry of Ontario, 2017).
Patient education is a key factor in early detection especially for cases which have already been discharged from the hospital. Some of the signs of jaundice returning or worsening include the skin or whites of the eyes turning yellow (Maisels, 2015). In worsening cases the yellowing from the eyes will move to the face and subsequently travel further downwards towards the feet. Most babies with jaundice improve after eating for several days as a result of bilirubin being removed from the body through stool processes. It is necessary to inform the baby’s health care provider about feedings if the primary feeding method is bottle-feeding (Ministry of Ontario, 2017). Patients should be informed about the availability to use ‘bili lights’ in their home which can aid the baby’s body in properly breaking down the bilirubin. Information should also be provided to patients regarding seeking medical attention if the baby’s condition worsens. Some of these worsening symptoms may include lack of feeding, pale skin, pale or gray stool, worsening jaundice as mentioned above, fever and or vomiting (Ministry of Ontario, 2017).
Hyperbilirubinemia occurrence rate amongst newborns makes it an illness which can stress new parents and clinicians. The lack and availability of universal pre-screening techniques and measures makes it harder to prevent (American Academy of Paediatrics, 2004). Additionally, treating and preventing the illness is difficult as a result of the short amount of time between birth and discharge. In those Baby’s where bruising occurs it may be harder to observe the yellowing of skin and as such a proper diagnosis may be missed (Maisels, 2015). Even though jaundice is commonly occurring in newborns it has been shown that having proper awareness and clinical processes in place for neonatal care results in decreased complications of existing conditions related to jaundice and other symptoms (Ministry of Ontario, 2017). Robust epidemiological studies on the profile of infants with or at risk of hyperbilirubinemia are needed to further help understand and expand the incidence and occurrence levels. It is also necessary to recognize the hemolytic disease in fetus and newborn or other neonatal jaundice as separate and important diseases so that it may become easier to study, discuss and inform patients (Barrington, & Sankaran, 2007). Creating new studies and investing in research could lead to a quicker and more readily available diagnostic approach. Newborns in hospitals should receive Routine laboratory investigation for sepsis and bilirubin levels as a form of standard of care. It is also crucial to provide immediate identification of underweight infants, with or without visual evidence of weight loss on admission should be incorporated into the clinical protocol for management of neonatal hyperbilirubinemia (American Academy of Paediatrics, 2004). Through out this paper an onus has been placed on identifying setbacks and deficiencies of the current understanding of hyperbilirubinemia. One of these deficiencies is resource constraints which prevent the ability of universal screening for newborns and accepting that it should be routinely provided to all secondary and tertiary points of care for neonatal jaundice. As a result of this treatments and care plans should become standardized especially for those cases which are identified prior to discharge (Ministry of Ontario, 2017). One of the more difficult components of hyperbilirubinemia is that it is difficult to isolate and firmly trace a root cause of the issue amongst certain newborns compared to others. Even though risk factors may provide a general understanding of a more susceptible group of individuals and babies it is still difficult to specifically understand the affects the mechanisms have in relation to the elapsing of time after birth (Porter & Dennis, 2002). In conclusion, even though the illness affects those who are most vulnerable it is possible to provide proper care, and treatment so that baby’s can continue their discharge process and transition into community and parental care.
- American Academy of Pediatrics (2004) Management of Hyperbilirubinemia in the newborn infant 35 or more weeks of Gestation. Subcommittee on Hyperbilirubinemia. Clinical Practice Guideline. 114(1), 297-316. Doi: 10.1542/peds.114.1.297
- Barrington, K.J., & Sankaran, K. (2007). Guidelines for detection, management and prevention of hyperbilirubinemia in term and late preterm newborn infants. Canadian Paediatric Society: Fetus and Newborn Committee.12(Suppl B), 1B-12B. Retrieved from https://www.cps.ca/en/documents/position/hyperbilirubinemia-newborn
- Maisels, M.J. (2015). Managing the Jaundiced newborn: A Persistent challenge. Canadian Medical Association Journal. 187(5), 335-343. Doi:https://doi.org/10/10.1503/cmaj.122117
- Muchowski, K.E. (2014). Evaluation and Treatment of Neonatal Hyperbilirubinemia. American Family Physician. 89(11), 873-878. Retrieved from http://www.aafp.org/ afp/2010/0815/p336.html.
- Porter, M.L., & Dennis, B.L. (2002). Hyperbilirubinemia in the Term Newborn. American Family Physician. 65(4), 599-606. Retrieved from https://www.aafp.org/afp/2002/0215/p599.html
- Ontario Ministry of Health (2017). Clinical Pathway Handbook for Hyperbilirubinemia in term and late pre-term infants (> 35 weeks). Provincial council for Maternal and child health and Ministry of Health and Long-term Care. Pp.1-33.Retrieved from http://www.health.gov.on.ca/en/pro/programs/ecfa/docs/qbp_jaundice.pdf
- Sgro, M., Campbell, D., & Shah, V. (2006). Incidence and causes of Severe neonatal hyperbilirubinemia in Canada. Canadian Medical Association Journal. 175(6), 587-590. Doi:https://doi.org/10.1503/cmaj.060328
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