Newborn Issues

Chapter 67 Newborn Issues



Michael Giuliano



The Jaundiced Newborn



ETIOLOGY



What Causes Jaundice?


Jaundice is the term used to describe the clinical appearance of a patient who has elevated indirect or direct bilirubin. Almost half of all newborns develop jaundice in the first week of life, in most cases as a physiologic process caused by elevation of indirect bilirubin. This “physiologic jaundice” develops when indirect bilirubin levels reach a peak of 8 mg/dl by the fourth day of life. Elevated direct bilirubin is uncommon, reflects a pathologic process, and usually does not become clinically apparent until several weeks of age.



What Causes Elevated Indirect Bilirubin?


Bilirubin is a breakdown product of hemoglobin. The red blood cells (RBCs) of newborns have a short life span, which means that a relatively large amount of hemoglobin is released into the circulation as the cells break down. Hemoglobin is converted first to biliverdin and then to indirect bilirubin, which is insoluble in water and must be conjugated by the liver into water-soluble direct bilirubin for excretion into the gut. Each of these steps is immature in the newborn, leading to an expected or physiologic elevation of indirect bilirubin.



What Else Causes Indirect Bilirubin to Rise?


Anything that leads to increased destruction of red blood cells, such as bruising, a cephalohematoma, or hemolysis, will result in hemoglobin breakdown and cause an abnormal elevation of bilirubin levels. Breast-feeding, dehydration, and anything that slows gastrointestinal motility can also cause elevated bilirubin levels. Rarely, infection or inborn errors of metabolism can be the cause.



What Are the Effects of Elevated Indirect Bilirubin?


Indirect bilirubin is a neurotoxin that causes central nervous system (CNS) damage when high levels cross the blood-brain barrier and produce kernicterus. The healthy full-term newborn has no risk of kernicterus at bilirubin levels below 25 mg/dl. A newborn infant with hemolysis, acidosis, hypoxia, or dehydration, however, has a high risk of kernicterus at much lower bilirubin levels. For example, if hemolysis is present and the bilirubin level is rising quickly, a level of 20 mg/dl appears to be the threshold at which kernicterus becomes possible. The fear of kernicterus drives almost all of the diagnostic and treatment decisions related to elevated bilirubin levels. It is important to note that premature infants may develop kernicterus at bilirubin levels much lower than for full-term newborns.



What Causes Direct Bilirubin to Become Elevated?


Direct bilirubin elevation can be seen with congenital infections, inborn errors of metabolism, liver dysfunction, and obstruction of the bile duct system. Each of these problems has a characteristic clinical presentation and associated findings that usually make the diagnosis straightforward. Direct bilirubin does not cause kernicterus, but the underlying diseases can lead to significant morbidity and mortality.



EVALUATION



How Do I Determine the Cause of Newborn Jaundice?


First, you must determine if the bilirubin is indirect or direct: Measuring total and direct bilirubin will allow calculation of the indirect fraction and immediately tell you the type of bilirubin causing the problem. The total bilirubin concentration and the age of the infant in hours can be used to predict risk for development of kernicterus using the Bhutani curve (see the Jaundice section of the Bibliography). Timing of the bilirubin elevation also helps identify the cause: If indirect bilirubin rises in the first 24 hours of life, you should suspect hemolysis caused by conditions that sensitize fetal RBCs, such as ABO incompatibility and Rh incompatibility. Elevation of indirect bilirubin after 48 hours of life is most commonly seen with physiologic jaundice, a condition that may last several days. Physical examination will often reveal bruising or a large cephalhematoma as a possible cause of jaundice. Breast-fed infants who experience difficulties with fluid intake in the first few days of life can also have elevated bilirubin, so-called breast-feeding jaundice. If indirect bilirubin rises in the second week of life, it may reflect “breast-milk jaundice,” a condition thought to be caused by factors in human milk that inhibit conjugation of bilirubin. Other risk factors for elevated indirect bilirubin include prematurity, a previous sibling requiring treatment for jaundice, or East Asian race. If the cause of indirect bilirubin elevation is unclear, complete blood count (CBC), reticulocyte count, review of the peripheral blood smear, and direct Coombs’ test will usually clarify the etiology. Direct bilirubin elevation is always pathologic and demands careful evaluation, although the cause is usually obvious from the history or physical examination findings.



TREATMENT



How Do I Treat a Jaundiced Baby?


Most infants with physiologic hyperbilirubinemia do not need treatment. Phototherapy is the most common treatment for elevated bilirubin. It uses light energy to change the shape of the bilirubin molecule, making indirect bilirubin water soluble so that it can be excreted into the urine. Indications for phototherapy are based on the cause of hyperbilirubinemia, the level of bilirubin, and the infant’s age in hours, all of which contribute to risk of kernicterus (see the Jaundice section of the Bibliography). The uncommon infant with extremely elevated levels of indirect bilirubin must be treated aggressively to prevent kernicterus. This requires a double-volume exchange transfusion, a procedure that reduces bilirubin to nontoxic levels, but it is invasive and can have serious complications. Full-term newborns with hemolysis undergo exchange transfusion when indirect bilirubin levels are greater than 20 mg/dl, whereas those without hemolysis can tolerate 25 mg/dl before needing this procedure. Premature and ill infants may require aggressive treatment at lower levels. A new medication, tin mesoporphyrin, blocks hemoglobin breakdown, which limits bilirubin production and may decrease the need for exchange transfusion. The treatment of direct hyperbilirubinemia must address the underlying process.



THE BLUE/CYANOTIC AND TACHYPNEIC NEWBORN



ETIOLOGY



What Causes Newborn Cyanosis and Tachypnea?


The blue or cyanotic newborn represents a medical emergency, with or without respiratory distress. First, you must decide if the infant is really blue or just bruised. Facial bruising may sometimes mimic cyanosis, but the two conditions can be distinguished by examining the mucous membranes and the rest of the body. Many problems in the newborn can cause cyanosis, but the key distinction is between cardiac and pulmonary disease. Congenital cyanotic heart disease will often present shortly after birth, although cyanosis may be delayed several days in some cases. Pulmonary disease is by far the most common cause of cyanosis and respiratory distress in the newborn.



What Are the Cardiac Causes of Cyanosis?


Lesions can range from transposition of the great vessels to hypoplasia of the right or left side of the heart. Patients with many of these lesions depend on a patent ductus arteriosus (PDA) to bring blood to the lung or body. Without a PDA these patients quickly decompensate and die, but a PDA may delay the appearance of cyanosis, making the infant look amazingly “normal.”



What Pulmonary Conditions Cause Cyanosis?


Cyanosis and respiratory distress may be caused by retained fetal fluid, aspiration of meconium or blood, pneumonia, pneumothorax, surfactant deficiency, or congenital structural abnormalities of the lungs. Infants with any of these conditions will usually have tachypnea and increased work of breathing, with “grunting,” intercostal space retractions, nasal flaring, and prominent abdominal breathing. Transient tachypnea of the newborn (TTN) results from retained fetal fluid and usually resolves within 24 hours, although oxygen may be needed.



EVALUATION



How Should I Evaluate a Cyanotic Infant?


Give oxygen immediately and move the baby to an environment where the temperature can be controlled and the infant can be monitored. Assess the response of the infant to the oxygen. Look for persistence or improvement of cyanosis while monitoring oxygen saturation with pulse oximetry: If administration of 100% oxygen brings the oxygen saturation to 100%, the infant probably has a pulmonary process. If oxygen saturation remains low despite 100% O2, congenital cyanotic heart disease must be considered. The history, physical examination, and a chest radiograph will often be the only diagnostic tests that you need to determine the cause of cyanosis. The gestational age of the newborn is important: A premature infant will be at risk for surfactant deficiency, whereas an infant born after 40 weeks’ gestation or who is meconium-stained will more likely have meconium aspiration syndrome. A history of resuscitation in the delivery room using positive pressure ventilation or a physical examination that demonstrates asymmetrical breath sounds would argue for a pneumothorax. Blood culture and CBC should be done routinely and antibiotics should be started while the diagnostic evaluation continues because sepsis and pneumonia can be overwhelming in the newborn. A maternal history suggestive of infection would add to this concern. The arterial blood gas (ABG) is most useful for detection of metabolic or respiratory acidosis.



TREATMENT



What Should I Do First for a Cyanotic Infant?


Provide 100% oxygen and monitor with pulse oximetry. No matter the cause of cyanosis, the overarching goal in treatment is to maintain oxygenation. If congenital cyanotic heart disease is diagnosed, intravenous administration of prostaglandin will often be needed to maintain the patency of the ductus arteriosus until corrective surgery can be done. For all pulmonary causes of cyanosis, the cornerstone of therapy is oxygen, which may require endotracheal intubation and mechanical ventilation. Close monitoring of arterial blood gas levels will be necessary in this setting. Each etiology has a specific treatment: Pneumothorax will often need to be evacuated, surfactant deficiency can be treated with surfactant replacement, pneumonia is treated with antibiotics, and the aspiration syndromes require supportive therapy. Many of the congenital structural abnormalities of the lung will require surgical treatment. Examples include diaphragmatic hernia, pulmonary sequestration, and congenital cystic adenomatoid malformation.



THE NEWBORN WITH A MURMUR



ETIOLOGY



What Causes a Heart Murmur in a Newborn Infant?


Most murmurs heard in the immediate newborn period are caused as the PDA closes in response to increasing oxygen tension and decreasing prostaglandin levels, usually in the first 3 days of life. As the PDA closes, it creates turbulent blood flow that can be heard as a murmur. A murmur may also indicate an underlying cardiac defect such as a ventricular septal defect, pulmonary stenosis, coarctation of the aorta, aortic stenosis, or tricuspid regurgitation. Newborns with congenital cyanotic heart disease can also present with a murmur, although the cyanosis is usually the first indication of heart disease.



EVALUATION



How Can I Determine the Cause of a Heart Murmur?


You should make every effort to describe the murmur that you hear. Although certain heart diseases have characteristic murmurs, both the quality and the location of murmurs in newborns may be difficult to characterize. Because most newborn murmurs result from the physiologic closing of the PDA, the initial evaluation involves a check of the oxygen saturation and four-extremity blood pressures. If the murmur persists on follow-up examinations, an electrocardiogram (ECG) will help identify the lesions of acute concern: Healthy full-term newborns have a right axis on ECG; infants with a lesion obstructing flow from the left ventricle will have a left axis on ECG. Infants with suspected aortic stenosis or coarctation of the aorta should be evaluated promptly with an echocardiogram. Careful palpation of femoral pulses will aid in detection of coarctation of the aorta. Most other infants can be followed and evaluated by echocardiogram at a later date if the murmur persists.



TREATMENT



How Is Congenital Heart Disease Treated?


Most newborns with heart murmurs do not need special treatment in the nursery. Support, monitoring, and, occasionally, oxygen usually suffice while the diagnostic evaluation is being done. An infant who has a persistently open PDA will need surgery or catheter ablation to close the PDA because of the high risk of developing bacterial endocarditis. Most infants with ventricular septal defect need no treatment unless congestive heart failure develops. Pulmonary stenosis must be followed closely to monitor the adequacy of blood flow to the pulmonary circuit. In time, this lesion may also require treatment via a catheter. Coarctation of the aorta and aortic stenosis require surgical repair. The congenital cyanotic heart lesions require complex surgical repair. Guidelines for SBE prophylaxis have been changed (see Chapter 56).

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Jun 19, 2016 | Posted by in PEDIATRICS | Comments Off on Newborn Issues

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