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35 Cards in this Set
- Front
- Back
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respiratory distress
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"fair" glucose control,
unknown Group B strep status, prematurity, and C-section Maternal diabetes is a risk factor for respiratory distress syndrome and other difficulties. Maternal group B strep infection is a risk factor for neonatal sepsis. Prematurity predisposes to respiratory distress syndrome (RDS) caused by lung immaturity and lack of surfactant, but most infants born at 36 weeks' gestational age do not have RDS. C-section delivery predisposes to transient tachypnea of the newborn. Additional risk factors that were NOT present in this case include - Premature rupture of membranes ≥ 18 hours, a risk factor for neonatal sepsis - Meconium in the amniotic fluid, a risk factor for meconium aspiration syndrome. |
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not causes of infant resp distress
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Asthma is not a diagnoses in the neonatal period, making this diagnosis unlikely.
Pulmonary embolism is very rare in children and usually is a result of a clotting disorder. Pulmonary embolism is only seen in neonates who have a predisposing condition such as the placement of a central venous catheter. |
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Transient Tachypnea of the Newborn or TTN
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delayed clearance of lung fluid following birth.
risk factors: diabetc moms and C-sections disease of term infants but can occur in preterm This fluid is thought to leave the lungs by a combination of being squeezed out during uterine contractions with vaginal delivery, and absorption by the pulmonary lymphatics. Delayed absorption of pulmonary fluid results in a condition known as Transient Tachypnea of the Newborn (TTN), also referred to as persistent postnatal pulmonary edema. |
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Respiratory distress syndrome
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lung-surfactant deficiency and is the most common cause of respiratory distress in premature infants.
infant of diabetic mom= delay in lung maturation can occur as late as 37wks |
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Congestive Heart Failure (CHF)
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most often caused by a congenital heart defect
risk factor: diabetic mom no murmur, normal pulses and normal oxygen saturation. This constellation of symptoms rules out most major cardiac causes of congestive heart failure. |
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hypothemia
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causes tachypnea
premie more likely to get hypothermic Hypothermia can cause tachypnea and may be associated with neonatal sepsis. Small for gestational age and premature infants are at increased risk to develop hypothermia. Adam’s temperature is normal and he is an LGA infant making this diagnosis unlikely. |
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pneumothorax
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more likely in premature infant with RDS
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neonatal sepsis
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can present initially with tachypnea and progress to more severe illness rapidly.
Risk factors: Prolonged rupture of the membranes often due to Group B Beta Strep, usually transmitted from the mother during labor unlikely b/c normal temperature, blood pressure and perfusion. In addition, his mother is well without fever suggesting she does not have chorioamnionitis. |
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How does the Apgar score help the physician manage a newborn infant?
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Apgar score reflects the infant's transition from intrauterine to extrauterine life.
describes the condition of the newborn infant immediately after birth and, when properly applied, is a tool for standardized assessment. It provides a mechanism to record fetal-to-neonatal transition. correlates poorly with the future neurological outcome of the term infant Apgar score is affected by gestational age, maternal medications, resuscitation, and cardiorespiratory and neurologic conditions that may be present in the infant. Low Apgar scores at 1 and 5 minutes alone are not conclusive markers of an acute intrapartum hypoxic event. Poor neurologic outcome is better associated with documented asphyxia, and that is why it is important to obtain arterial blood gases to look for metabolic acidosis. |
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LGA
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birth weight above the 90th percentile.
maternal diabetes mellitus - Large infants often must be delivered by C-section, by forceps, or vacuum extraction (all of which have associated complications) - Birth injuries are more common, such as fractured clavicle, brachial plexus injury, and facial nerve palsy - Hypoglycemia is especially common in LGA infants born to diabetic mothers |
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AGA
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birth weights between the 10th and 90th percentiles
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small gestational age (SGA) or intrauterine growth restricted (IUGR)
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birth weights below the 10th percentile
- Temperature instability (hypothermia) - Hypoglycemia because of inadequate glycogen stores - Polycythemia and hyperviscosity |
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fetal circulation/respiration
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Oxygenation changes dramatically at birth from a passive, placenta-provided source to an active respiration-based process. In utero, oxygenated blood from the placenta is transported to the fetus by the umbilical vein. A portion of this blood perfuses the liver. The remainder bypasses the liver through the ductus venosus and enters the inferior vena cava. One-third of this vena caval blood crosses the patent foramen ovale (PFO) to the left atrium and is pumped to the coronary, cerebral and upper body circulations. The remaining two-thirds combines with venous blood from the upper body in the right atrium, and is directed to the right ventricle and out the pulmonary artery. In utero, vasoconstriction of the pulmonary arterioles produces high pulmonary vascular resistance, allowing only 8-10% of the blood from the right ventricle to flow through the pulmonary vasculature. The remainder, 90-92%, is shunted through the patent ductus arteriosus (PDA) to the descending aorta.
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At birth, successful transition to extrauterine life involves:
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- Removal of the low-resistance placental circulation by cutting the umbilical cord.
- Initiation of air breathing by the newborn infant. - Reduction of the pulmonary arterial resistance. - Closure of the PFO and PDA. |
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In the first hour of life, as transition occurs, the respiratory and heart rates are often elevated:
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In the first hour of life, as transition occurs, the respiratory and heart rates are often elevated: The heart rate is often 160-180 per minute, and the respiratory rate is often 60-80 per minute. In an infant with a successful transition, by the age of 2 hours the heart rate is usually 120-160 per minute, and the respiratory rate is usually 40-60 per minute.
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Persistent pulmonary hypertension of the newborn (PPHN)
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is the result of elevated pulmonary vascular resistance to the point that venous blood is diverted to various degrees through fetal channels (the ductus arteriosus and foramen ovale) into the systemic circulation and bypasses the lungs, resulting in systemic arterial hypoxemia.
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PPHN can result from several conditions,
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including meconium aspiration syndrome, diaphragmatic hernia, hypoplastic lungs, and in utero asphyxia.
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The following findings may indicate that an infant has PPHN:
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- Tachypnea
- Tachycardia - Respiratory distress, with findings such as expiratory grunting and nasal flaring - Generalized cyanosis - Low oxygen levels, even while receiving 100% oxygen |
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ddx for cyanotic infant
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Respiratory:
Common - transient tachypnea of the newborn, respiratory distress syndrome. Uncommon - pneumothorax, diaphragmatic hernia, choanal atresia, pulmonary hypoplasia. Cyanotic congenital heart defects: Common - Tetralogy of Fallot, transposition of the great arteries. Uncommon - truncus arteriosus, tricuspid atresia, total anomalous pulmonary venous return, pulmonary atresia. CNS: hypoxic-ischemic encephalopathy, intraventricular hemorrhage, sepsis/meningitis. Infectious: septic shock, meningitis |
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test for cyanotic individual
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Arterial blood gases help in determining the oxygenation, ventilation, and acid-base status of the infant. Knowing the pCO2 is very helpful in understanding the cause of the cyanosis.
The CBC with differential count is useful to rule out neutropenia, leukopenia, abnormal immature-to-total-neutrophil ratio, and thrombocytopenia as signs of sepsis. A chest radiograph is an integral part of the initial assessment of the newborn with respiratory distress. The size and the shape of the heart may yield some clues to the diagnosis. The appearance of the lungs may suggest pneumonia, meconium aspiration, RDS, etc. Normal inspiratory films should have eight or more intercostal spaces of lung fields on both sides. An echocardiogram is the gold standard in the diagnosis of congenital cardiac lesions and persistent pulmonary hypertension of the newborn. An echocardiogram is indicated when there is persistent cyanosis and no indication of lung disease, or when there are other signs suggesting a heart defect, such as a murmur, an abnormal ECG or a chest X-ray showing an abnormal cardiac contour. An oxygen challenge test (hyperoxia test) is a valuable tool that can help differentiate between cardiac and pulmonary etiology in infants who are cyanotic. In brief, oxygen will increase the PaO2 of an infant whose cyanosis is caused by a respiratory condition, but will not significantly increase the PaO2 if a cardiac lesion causes cyanosis. This test is described in some detail in the article by Sasidharan. Physical examination is critical to identify heart murmurs and respiratory findings that might be the cause of the cyanosis. Remember, however, that some murmurs may not be present early in life because of the elevated pulmonary vascular pressure. Pulse oximetry detects the oxygen saturation in the blood. |
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recommended in 2010 that screening of newborns for the following cyanotic congenital cardiac disorders be implemented:
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1) hypoplastic left heart syndrome, 2) pulmonary atresia, 3) Tetralogy of Fallot, 4) total anomalous pulmonary venous return, 5) transposition of the great arteries, 6) tricuspid atresia, and 7) truncus arteriosus.
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Congenital diaphragmatic hernia
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is a congenital malformation resulting from a defect in the development of the diaphragm. It occurs in 1 out of every 2,200 to 5,000 live births. The most common type is the Bochdelek hernia (a posterolateral hernia) that accounts for the majority (> 95%) of cases. This defect allows the passage of organs from the abdomen into the chest cavity and severely impairs lung development. Most defects occur on the left side. Absent breath sounds or presence of bowel sounds on one side of the chest are important diagnostic clues. Adam’s physical examination with the presence of bilateral normal breath sounds makes this diagnosis unlikely.
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Pneumothorax
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is caused by a collection of gas in the pleural space with resultant collapse of lung tissue. Common risk factors are mechanical ventilation or underlying lung disease (especially meconium aspiration or severe infant respiratory distress syndrome). Absence of breath sounds on one side of the chest in combination with respiratory distress is an important diagnostic clue. Adam’s physical examination with the presence of bilateral normal breath sounds makes this diagnosis unlikely.
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Transposition of the Great Arteries (TGA)
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is a congenital heart defect in which the aorta and pulmonary arteries are transposed resulting in respiratory distress and severe cyanosis at shortly after birth as the patent ductus arteriosus closes. One risk factor for transposition of the great arteries is being born to a diabetic mother. TGA is often associated with other congenital heart defects such as a VSD so a murmur may be heard on physical examination. Adam’s normal cardiovascular examination and absence of cyanosis makes this diagnosis unlikely.
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Severe Coarctation of the Aorta
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may cause respiratory distress if there is severe left ventricular outflow tract obstruction. Classically, diminished pulses in the lower extremities or asymmetric blood pressure readings suggest the diagnosis. In severely ill neonates, there may be no differences in the pulses because cardiac output is so poor. Adam’s general appearance and normal pulses in all extremities argues against this diagnosis.
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hypoglycemia
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infants of diabetic mothers due to the chronic hyperinsulinemic state that occurred during gestation. Hypoglycemia may be more pronounced in premature infants. Tachypnea is a non specific response to this metabolic derangement. This diagnosis remains a possibility for Adam and could be investigated by a serum glucose readin
High levels of maternal serum glucose during pregnancy result in hyperglycemia in the fetus. This stimulates the fetal pancreatic beta cells and the development of hyperinsulinemia. Maternal insulin does not cross the placenta. Insulin is the primary anabolic hormone for fetal growth. High levels in the third trimester result in increased growth of the insulin-sensitive organ systems (heart, liver and muscle) and a general increase in fat synthesis and deposition. This combination of increased body fat, muscle mass, and organomegaly produces a macrosomic (LGA) infant. Insulin-insensitive organs, such as the brain and kidneys, are not affected by the elevated insulin levels, and have appropriate size for gestational age. |
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Control of diabetes during pregnancy is an important predictor of fetal outcome, especially with regard to the risk of
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birth defects. The incidence of major malformations is directly related to the First-Trimester HbA1C level: Infants born to women with HbA1C levels >12 have at least a 12-fold increase in major malformations.
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breastfeeding a child in resp distress
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Many infants with respiratory rates of 60-80 per minute tolerate oral feeds, but some may need nasogastric feeding or IV fluids if respiratory distress worsens with feeding. Many infants with respiratory rates of > 80 per minute will have difficulty with both oral and nasogastric feedings and will often require intravenous fluid support.
The use of a nasogastric feeding tube will avoid use of a bottle, which may facilitate Ms. Mason's wish to breastfeed.. (After feeding from a bottle, some babies may get frustrated when they breastfeed because the milk does not flow as fast from the breast as from a bottle.) |
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glucose
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Glucose is the primary substrate for brain metabolism in the neonate, and even asymptomatic hypoglycemia may have negative consequences for long-term neurodevelopment.1,2 The precise definition of hypoglycemia in the neonate has been difficult to establish because plasma glucose levels often do not correlate with symptoms and long-term outcome. A newborn can be hypoglycemic yet be entirely asymptomatic. This is why it is important to screen all newborns for glucose level and to monitor closely the glucose levels of infants of diabetic mothers.
n utero, glucose crosses the placenta, maintaining the fetal blood glucose at approximately two-thirds of maternal levels. At birth, separation from the placenta results in a decline in the infant's glucose levels over the first 1-2 hours of life. Levels then increase and stabilize by 3-4 hours at mean levels of 65-71 mg/dL. The infant of a diabetic mother has hyperinsulinemia and the glucose level declines precipitously at birth. Prompt intervention is required to raise glucose levels. Both the definition of hypoglycemia and identification of a threshold value (below) that signals intervention is indicated have been revised. Currently, most neonatologists attempt to maintain glucose levels between 41-50 mg/dL. Proposed Threshold Values for initial intervention depend on the clinical situation4: - Asymptomatic infants and infants at risk for hypoglycemia: <35 mg/dL3 - Symptomatic infants: <45 mg/dL |
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glucometer test
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is a screening test only, and must not be used to confirm hypoglycemia. Glucose oxidase reagent strips are read by meter (glucometer) or by eye (Dextrostix, Chemstrip) and measure whole blood glucose, which is 10-15% lower than plasma glucose levels. These reagent strips are widely used as screening tools for hypoglycemia and may also be used for ongoing monitoring of glucose levels. Any reagent-strip reading of whole blood glucose <40 mg/dL must be confirmed by laboratory analysis of serum or plasma glucose. Treatment should be started immediately, not delayed until laboratory results are available.
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remember that the very young infant with sepsis and/or meningitis may have no localizing signs and only subtle clinical symptoms, such as temperature instability, lethargy, and poor feeding.
Determination of serum electrolytes and calcium is not recommended early after birth because the newborn's levels reflect the mother's status as well as the effect of medications administered to the mother during labor. Results at age 12-24 hours are more indicative of the infant's status. F - A urine culture in the early neonatal period (birth to 3 days old) is of little value. It may be more useful for an infant 4 days or older who is suspected of having late-onset sepsis. |
Many neonatologists will start an intravenous infusion because it guarantees a more stable source of glucose. The choice of breastfeeding, bottle feeding of formula or breast milk, or use of a feeding tube to provide formula or breast milk depends on the ability of the infant to take feedings orally. Most pediatricians would not give 5% glucose in water to a hypoglycemic infant, and if they do, the infant would be fed with breast milk or formula as soon as possible after the glucose. Glucose water does raise the serum glucose level, but only transiently. Rebound hypoglycemia often develops 1-2 hours after feeding glucose water if the infant is hyperinsulinemic (i.e. IDM). Milk feeding (formula or breast) raises glucose levels, maintains stable levels, and avoids rebound hypoglycemia.
Once feeds have been initiated, glucose levels should be closely monitored until levels are stable (>40 mg/dL). The frequency of monitoring will depend on the severity of the hypoglycemia and may range from every 30 minutes to every 3 hours prior to feeds. If the blood glucose is not >40 mg/dL with the first enteral feeding, most pediatricians would initiate IV dextrose infusions. Breast milk is the ideal nutrient for the newborn human. It provides a lower renal solute load than formula, has several anti-infective and anti-allergic properties, and fosters mother-infant bonding. Separation of mother and infant poses a challenge for the successful establishment of breastfeeding. This most often happens with the birth of a premature infant, or an infant requiring special care, such as Adam. Adam's ability to breastfeed will be determined by letting his mother put him to the breast as soon as possible. If he cannot successfully breastfeed because of his tachypnea, it will be important that Ms. Mason begin pumping her breasts as soon as possible after delivery. This will initiate milk production and ensure an adequate supply when Adam is able to feed at the breast. In the meantime, Adam would be fed expressed breast milk, supplemented with formula as needed while breast milk volumes are low in the first 2-48 hours after birth. Pumping breast milk is also psychologically helpful for mothers at a very stressful time: Breast milk is the single thing that no one else can provide for their infants. |
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In 1970, the earliest system for evaluating gestational age was developed by Dubowitz1. This was a detailed scoring system based on the infant's external physical characteristics and neurologic findings. The Dubowitz system requires that the infant be alert and active, and In very immature or sick infants, results were often skewed due to low neurologic scores.
In 1979, Ballard et al.2 developed a shortened version of the Dubowitz exam. This score recently has been modified to allow assessment in extremely premature infants.3 |
Gestational age assessment should be performed on every neonate within 12-24 hours of life. Accuracy of results of each system is +/- 2 weeks.
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TTN CXR
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CXR findings are typical of TTN, with "wet" looking lungs, no consolidation, and no air bronchograms (which would indicate respiratory distress syndrome). There is no evidence for a diaphragmatic hernia. A repeat chest X-ray will not be needed as long as Adam shows continued clinical improvement.
X-ray findings similar to those on Adam's films may also be seen with neonatal pneumonia, but this diagnosis is unlikely in the absence of other clinical signs of sepsis. If respiratory symptoms do not improve, a repeat chest X-ray should be ordered and intravenous antibiotics should be initiated. An infant with respiratory distress syndrome (RDS) would have radiographic findings that typically include a diffuse reticulogranular appearance of the lung fields ("ground glass appearance") and air bronchograms. Diaphragmatic hernia most commonly develops on the left side. A radiograph shows air-filled loops of bowel in the left side of the chest, displacing the heart and mediastinum to the contralateral side. - Significant perihilar streaking: interstitial fluid and engorged lymphatics. - Coarse, fluffy densities that represent fluid-filled alveoli. - Fluid in the pleural space and a small amount of fluid in the fissures on the lateral view. |
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Developmental Dysplasia of the Hip (DDH),
previously known as Congenital Dislocation of the Hip |
Clinical features:
partial or complete dislocation, or instability of the femoral head. Risk factors: - Breech position: 30-50% of DDH cases occur in infants born in the breech position. - Gender: 9:1 female predominance. - Family history. developmental process that is not always detectable at birth. In spite of newborn screening programs we continue to see dislocated hips being diagnosed later in infancy. recognition of risk factors and regular hip examinations up to age 18 months. |
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factors for discharge
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Physical examination without major defects
Minimal or no jaundice No blood group incompatibility Breastfeeding well every 2-4 hours (10-15min each side) 6 or more wet diapers daily Transition from meconium to seedy, soft, tan-yellow stools Weight loss <10% Car seat available Good support for mother at home Back-to-Sleep program reviewed Prescription for Vitamin D completed Follow-up arranged with an identified primary care physician Infant Co-bedding reviewed infant discharged from the nursery before 48 hours of life must be evaluated by a health care practitioner within 48 hours. exclusively breastfed infants receive a daily dose of 200 IU of Vitamin D, because human milk does not provide adequate intake if it is the sole source of nutrition. This supplementation should continue until the infant is weaned to a formula containing vitamin D. Standard formulas all contain at last 400 IU of vitamin D and meet the infant's needs. The Back to Sleep program has resulted in a significant decrease in the incidence of Sudden Infant Death Syndrome. Co-bedding of an infant with an adult increases the risk of death by suffocation should the adult accidentally roll onto the infant. The AAP recommends that infants not bed share during sleep. Infants may be brought into bed for nursing or comforting but should be returned to their own bassinet or crib when the parent is ready to return to sleep. The infant should not be brought into bed when the parent is excessively tired or using medications or substances that could impair his or her alertness. The task force recommends that the infant’s bassinet or crib be placed in the parent’s bedroom, which will allow for convenient breastfeeding and contact. Infants also should not bed share with other children. |
