Chapter Neonatal disorder Dr Areefa Albahri Normal neonatal

Chapter Neonatal disorder Dr. Areefa Albahri

Normal neonatal care n n n n n Immediate care of newborn Clear airway �Dry the infant well �Caring of umbilical cord. �Caring of the infant’s eyes that prophylactic treatment �Administer 1 mg of vitamin K in the delivery �Check infant’s weight, height and circumferences of head and chest. �Apply ID band to infant’s arm �Record your observations during labour:

Evaluate infant’s condition by Apgar scoring at one and five minutes, Be ready to rescue the infant if required, after birth by using the next Apgar chart:

Preterm Infant n n n The preterm infant is a viable infant born before the 37 weeks’ gestation, regardless of birth weight. �Prematurity accounts for the largest number of admission to neonatal intensive care units. �The incidence of neonatal complications is highest in the preterm infants and infants with high-risk factors (congenital defects) often found in association with prematurity

Preterm Infant �A low-birth-weight (LBW) infant is one whose birth weight is less than 2500 gm regardless of gestational age. n LBW is divided into: very low birth weight (VLBW) as expressed by the percentage of infants who were weighting less than 1500 grams at birth n extremely low birth weight (ELBW) as expressed by the percentage of infants who were weighting less than 1000 grams at birth n

Etiology The exact cause is unknown, but there are some factors: n 1. Maternal factors: n - Poor nutrition - Diabetes - Multiple pregnancy. n - Drug abuse - IUD in gravid uterus n - Chronic disease (heart disease, kidney disease, infection). n Complications of pregnancy (PIH, bleeding, placenta previa…, n 2. Fetal factors: n - Chromosomal abnormalities n - Feto-placental dysfunction. n - Anatomic abnormalities

Altered physiology n n n n Respiratory system: �Alveoli begins to form at 26 -28 weeks’ gestation �Respiratory muscles are poorly developed. �Production of surfactant is reduced. �Breathing may be difficult and irregular with periods of apnea and cyanosis. �Infant is prone with atelectasis. �Gag and cough reflexes are poor (aspiration is a problem).

n n n Digestive system: �Stomach is small, vomiting is likely to occur. �Tolerance is decreased related to decreased enzymes. �Lack of bile salts that aid digestion of fats and absorption of vitamin D and other fat-soluble vitamins. �Limited ability to convert glucose to glycogen and break down of glycogen to glucose. �Limited and immature ability to release insulin in response to glucose.

n n n n Poor thermal stability: �Has very little subcutaneous fat with no heat storage or insulation, and poor glycogen and lipid stores. �Limited ability to shiver has poor vasomotor control of blood flow to skin capillaries. �There is a relatively large surface area in comparison to body weight. �Sweat glands are decreased; infant cannot perspire under 32 weeks’ gestation. �Usually less active. �Posture flaccid (increased surface area exposed).

n n n n n Renal function: �Sodium excretion is probably increased which may lead to hyponatremia. There is difficulty in excreting potassium. �Decreased ability to concentrate urine, which may result in dehydration. �Decreased ability to acidify urine. �Glomerular tubular imbalance accounts for sugar, protein and sodium present in urine. �Nervous system: �Response to stimulation is slow. �Suck, swallow and gag reflexes are poor (aspiration). �Cough reflex is weak or absent. �Centers that control respiration, temperature and other vital functions are poorly developed.

n n n n n Infection: �Actively found antibodies are lacking at birth (active immunity). �No Ig. M is present at birth (passive immunity). �Decreased opsonization (preparation of cells to phagocytosis). �Liver function: �Does not have a good ability to handle and conjugate bilirubin. �Does not store or release sugar well (hypoglycemia). �Steady decrease in Hb and production of blood (anemia). �Does not make or store vitamin K (hemorrhage).

n n n n Eyes: �Oxygen given beyond the point of infant need may result in retinal artery constriction and anoxic damage. �The retina detaches from the posterior chamber, fibrous mass forms leading to inability to receive visual stimulation (retrolental fibroplasia). �The exact amount and level of oxygen needed to produce retrolental fibroplasia are unknown. �Skin: �Sensitive because of permeability and decreased thickness of stratus corneum (outer layer of epidermis). �Delayed skin p. H recovery to acidity following washing with alkaline based soap.

Post mature infant n �Infants born after completed 42 weeks of gestation, as calculated from the mother’s last menstrual period are considered to be post mature or post-term regardless of birth weight.

n n n Predisposing factors: �Primigravida and high parity at any age. �History of prolonged gestation in the previous pregnancies �Altered physiology: �The postmature infant appear to have suffered from intrauterine malnutrition and hypoxia, before termination of pregnancy but at the point when birth should have occurred the placental function begins to diminish resulting in impaired oxygen exchange and inadequate nutrient transfer to the fetus. �The severity of the associated problems is determined by length of gestation ―the longer the gestation, the more severe the problems‖.

n n n n �Clinical manifestations: �Wasted physical appearance, little subcutaneous fat ― long, thin appearance‖. �Long fingernails and toenails. �Reduced amount of vernix caseosa �Abundant scalp hair. �Skin frequently cracked and desquamating, parchment – like pale skin �Absence of lanugo hair.

n n n n Diagnostic evaluation: �Evaluate general appearance. �Determine gestational age, APGAR scoring and blood gas analysis. �Complications: �Meconium aspiration. �Hypoglycemia, hypocalcaemia and polycythemia. �Pulmonary hemorrhage, pneumonia and pneumothorax.

Infant of diabetic mother (IDM) n n n Is the infant born to a mother with diabetes. The mother may be an chronic diabetic or gestational diabetic. The severity of infant problems depends on the severity of maternal diabetes. �Altered physiology: hyperinsulinemia in utero secondary to decreased epinephrine and glucose response result in the following in the infant: �Increased amount of body fat �Hypoglycemia: occurs within first 2 -12 hours of life (may occur within minutes). IDM may be symptomatic or asymptomatic with blood glucose below 20 mg/dl. �Hypocalcemia: associated with prematurity, difficult labor or/and asphyxia at birth. Generally occurs during first 24 -48 hours after birth.

Infant of diabetic mother (IDM) n n n n Prematurity, difficult labor or/and asphyxia at birth. Generally occurs during first 24 -48 hours after birth. �Hyperbilirubinemia: most likely to occur within 48 -72 hours after birth. �Prematurity: may be premature or SGA when associated with placental insufficiency. �Respiratory function is similar to that of premature infants. �Polycythemia: HCT greater than 65% or hemoglobin 22 gm/dl. This increases the risks of renal vein thrombosis, respiratory distress, hypoglycemia and hypocalcemia. �Congenital anomalies: �Infection: prematurity lowered passive immunity.

n n n n n Diagnostic evaluation: �Maternal history of diabetes. �Physical assessment of infant and determination of gestational age. �Blood studies: Glucose, HCT, Hb, blood gas analysis, bilirubin, electrolytes (calcium) �Clinical manifestations: �Macrosomia, cardiomegaly, hepatomegaly �Abundant fat, hair and vernix caseosa. �Tendency to be large for gestational age, some may be AGA or SGA. �Intrauterine growth retardation when mother has had long standing insulin dependency.

n n n �Complications: �Hypoglycemia - Hypocalcemia - Hyaline membrane disease �Infection - hyperbilirubinemia - Congenital anomalies �Birth injuries - prematurity - organomegaly �Asphyxia neonatorum: it results in primary to secondary apnea or failure to breath or death if not promptly treated.

Nursing interventions n n n Observe closely for hypoglycemia. �Monitor infant closely for changes in acid-base status, respiratory distress temperature, hypocalcaemia, sepsis, cardiac anomalies and hyperbilirubinemia. �Assist in the prevention of dehydration and maintenance of fluid and electrolyte balance.

Hypoglycemia n n Abnormal serum levels of glucose can have life threatening implications for the neonate. Since the brain is dependent upon a constantly circulating supply of glucose, neurological impairment may occur if hypoglycemia is left untreated. �Hypoglycemia during the first 72 hours of life in the term infant is defined as a serum glucose level equal to or below 35 mg/dl or in the low birth weight infant as equal to or below 25 mg/dl. After 72 hours of life, hypoglycemia is a serum glucose level less than 45 mg/dl.

n n Incidence: �In full term, AGA infants approximately 10%. �In full term, SGA infants approximately 25%. �In preterm, SGA infants approximately 67%

Altered physiology: n n n �Under normal conditions, the concentration of serum glucose declines during the first 24 hours after birth with the lowest level usually reached (Nadir) 2 hours after delivery, followed by a subsequent rise. �Per Kilogram of body weight the glucose requirement of the neonate is twice that of the adult. �Ability to produce glucose from glycogen or from alternate substrates (gluconeogenesis) is limited. �Pathogenesis may involve one or both of these mechanisms: 1. Decreased source of serum glucose. 2. Increased rate of serum glucose removal.

n n Patient care management: �Blood glucose monitoring is performed hourly during the first 4 to 6 hours of life and then every 4 hours for 24 hours, or per agency protocol. Blood is generally obtained by heel stick �An intravenous infusion of glucose may be necessary if early feeding does not keep the blood glucose at 45 mg/d. L or above. �Diet A feeding of 5% glucose water may be given soon after birth, followed in 1 hour by a breast or formula feeding, which is continued on a regular basis.

Septicemia Neonatorum n n n �Septicemia is the systemic invasion of pathogenic bacteria into the blood stream. In the newborn it is known as sepsis neonatorum. �Low temperature is also a sign for sepsis. �It is a generalized infection, which may occur in the neonate and is characterized by the proliferation of bacteria in the blood stream and frequently involves the meninges. Incidence: � 1 in 1000 live full term births. �I in 250 live premature births.

n n n Etiology: The etiologic agents varies from year to year and from institution to another. �Common offending organisms: Escherichia coli ( E. Coli), Listeria, klebsiella, Group B hemolytic streptococci, staphylococcus aureus, Pseudomonas, and Hemophilus influenza �Portal of entry may be nasopharynx, skin, eye, umbilicus or Aspiration of infected amniotic fluid. �Predisposing factors: 1. Perinatal factors: �Maternal complications e. g. prolonged rupture of membranes, prolonged and difficult labor, UTI, endometritis, chorioamnionitis, maternal illness, and abruption placenta 2. Infant complications e. g. prematurity, LBW, congenital heart disease and RDS 3. Iatrogenic or environmental factors e. g. unclean equipment, surgical procedures, obstetric and nursery practice �Complications: �Meningitis and neurological damage. – shock - Pneumonia. �Congestive heart failure. – DIC - high mortality rate.

n n n n Assessment: 1. Clinical presentation a. Signs and symptoms: �The early signs of sepsis usually vague and subtle. The infant is often described as not doing well. The signs often include: poor feeding, gastric retention, lethargy, meconium stained, and temperature alteration, usually hypothermia but may have hyperthermia. �Later signs and symptoms: pallor, cyanosis, apneic episodes, jaundice, abdominal distention, vomiting, diarrhea, hepatosplenomegaly, bulging fontanels, hypotonia, fever or seizures. b. History of predisposing factors. 2. Laboratory: presence of organism in the blood culture must be obtained for a diagnosis of sepsis neonatorum. �Cultures to detect specific organism: blood, urine, umbilical stump, skin lesions, nose, throat, rectum, CSF, external auditory canal or/and gastric fluid. �WBC, Hb and HCT �Blood chemistry, bilirubin and blood gas analysis. �Medical management: �Antibacterial: Ampicillin and aminoglycoside or according to culture and sensitivity. �Supportive therapy: as oxygen therapy, fluid and caloric maintenance.

Jaundice in the newborn “Hyperbilirubinemia” n n n The infant’s immature liver is often unable to conjugate all of the bilirubin released by the destroyed RBCs, and this is evident as jaundice. The jaundice usually peaks at 72 hours and then disappears in a couple of weeks �Hyperbilirubinemia is an excess of bilirubin (unconjugated bilirubin) in the blood, may be related to physiologic jaundice or pathologic jaundice. Physiologic jaundice occurring after the first 24 hours of life is related to the normal destruction of the excess red blood cells (RBCs) in the newborn. With direct oxygenation of the blood in the newborn’s lungs, the extra RBCs of the fetus are no longer needed. �Pathologic jaundice appears in the first 24 hours and may lead to kernicterus (deposits of bilirubin causing yellow staining in the brain). The exact level of total bilirubin when kernicterus occurs is not known but may occur at 20 mg/d. L in full-term infants and at a lower level in preterm neonates. Kernicterus is a chronic, serious neurological impairment result of bilirubin toxicity. Preterm infants are at a greater risk of developing kernicterus, and the most common cause is Rh incompatibility and severe

n n n n n Incidence: Occurs in 50% of term infants, 80% of preterm. �Predisposing factors: �Blood group incompatibility with mother. �Prematurity, Infection, Birth trauma and Polycythemia �Maternal or neonatal metabolic or endocrine disorders. �Malfunction of gastrointestinal tract. �Altered physiology: �Bilirubin is released (result from RBC destruction) into the circulation where it combines with albumin (unconjugated or indirect bilirubin). �Once the unconjugated bilirubin is in the liver, it is converted into direct or conjugated water-soluble bilirubin with the aid of enzymes, one of which is glucuronyl transferase and excreted via the bile into the intestine and is excreted in the stool or is hydrolyzed to unconjugated bilirubin in the intestine and reabsorbed across the intestinal mucosa into the circulation (enterohepatic circulation).

n n n Signs and symptoms may include: �Sclera appearing yellow before skin. �Skin appearing light to bright yellow. �Lethargy, poor feeding and dark stool. �Dark amber, concentrated urine. �Diagnostic evaluation: �Maternal blood and Rh type. �Infant screening: total and direct bilirubin, CBC, blood and Rh type, Albumin or total proteins, glucose, p. H, blood culture if sepsis indicated as cause. �Treatment: 1. Phototherapy – to allow for utilization of alternate pathways for bilirubin excretion. 2. Exchange transfusion: during this procedure, 5 m. L to 10 m. L of blood are removed from the infant and replaced with a like amount of

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