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Chapter Chapter Neonatal disorder Neonatal disorder Dr. Areefa Albahri Dr. Areefa Albahri

Chapter Neonatal disorder Dr. Areefa Albahri. Normal neonatal care Immediate care of newborn Immediate care of newborn Clear airway Clear airway Dry

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ChapterChapterNeonatal disorderNeonatal disorder

Dr. Areefa AlbahriDr. Areefa Albahri

Normal neonatal careNormal neonatal care Immediate care of newbornImmediate care of newborn Clear airwayClear airway Dry the infant wellDry the infant well Caring of umbilical cord. Caring of umbilical cord. Caring of the infant’s eyes that Caring of the infant’s eyes that

prophylactic treatment prophylactic treatment Administer 1 mg of vitamin K in the Administer 1 mg of vitamin K in the

deliverydelivery Check infant’s weight, height and Check infant’s weight, height and

circumferences of head and chest. circumferences of head and chest. Apply ID band to infant’s armApply ID band to infant’s arm Record your observations during labour:Record your observations during labour:

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

chartchart : :

Preterm InfantPreterm Infant

The preterm infant is a viable infant born The preterm infant is a viable infant born before the 37 weeks’ gestation, regardless of before the 37 weeks’ gestation, regardless of birth weight. birth weight.

Prematurity accounts for the largest number Prematurity accounts for the largest number of admission to neonatal intensive care units. of admission to neonatal intensive care units.

The incidence of neonatal complications is The incidence of neonatal complications is highest in the highest in the preterm infants preterm infants and infants with and infants with high-risk factors (high-risk factors (congenital defectscongenital defects) often ) often found in association with prematurity found in association with prematurity

Preterm InfantPreterm Infant A low-birth-weight (LBW) infant is A low-birth-weight (LBW) infant is

one whose birth weight is less than one whose birth weight is less than 2500 gm regardless of gestational age. 2500 gm regardless of gestational age.

LBW is divided into: very low birth LBW is divided into: very low birth weight (VLBW) as expressed by the weight (VLBW) as expressed by the percentage of infants who were percentage of infants who were weighting less than 1500 grams at birth weighting less than 1500 grams at birth

extremely low birth weight (ELBW) as extremely low birth weight (ELBW) as expressed by the percentage of infants expressed by the percentage of infants who were weighting less than 1000 who were weighting less than 1000 grams at birth grams at birth

EtiologyEtiologyThe exact cause is unknown, but there are some The exact cause is unknown, but there are some

factors: factors: 1. 1. Maternal factors: Maternal factors: - Poor nutrition - Diabetes - Multiple pregnancy. - Poor nutrition - Diabetes - Multiple pregnancy. - Drug abuse - IUD in gravid uterus - Drug abuse - IUD in gravid uterus - Chronic disease (heart disease, kidney disease, - Chronic disease (heart disease, kidney disease,

infection).infection). Complications of pregnancy (PIH, bleeding, placenta Complications of pregnancy (PIH, bleeding, placenta

previa…, previa…, 2. Fetal factors: 2. Fetal factors: - Chromosomal abnormalities - Chromosomal abnormalities - Feto-placental dysfunction. - Feto-placental dysfunction. - Anatomic abnormalities- Anatomic abnormalities

Altered physiologyAltered physiology Respiratory system: Respiratory system: Alveoli begins to form at 26-28 weeks’ Alveoli begins to form at 26-28 weeks’

gestation gestation Respiratory muscles are poorly developed. Respiratory muscles are poorly developed. Production of surfactant is reduced. Production of surfactant is reduced. Breathing may be difficult and irregular Breathing may be difficult and irregular

with periods of apnea and cyanosis. with periods of apnea and cyanosis. Infant is prone with atelectasis. Infant is prone with atelectasis. Gag and cough reflexes are poor (aspiration Gag and cough reflexes are poor (aspiration

is a problem). is a problem).

Digestive system: Digestive system: Stomach is small, vomiting is likely to occur. Stomach is small, vomiting is likely to occur. Tolerance is decreased related to decreased Tolerance is decreased related to decreased

enzymes. enzymes. Lack of bile salts that aid digestion of fats Lack of bile salts that aid digestion of fats

and absorption of vitamin D and other fat-and absorption of vitamin D and other fat-soluble vitamins. soluble vitamins.

Limited ability to convert glucose to Limited ability to convert glucose to glycogen and break down of glycogen to glycogen and break down of glycogen to glucose. glucose.

Limited and immature ability to release Limited and immature ability to release insulin in response to glucose. insulin in response to glucose.

Poor thermal stability: Poor thermal stability: Has very little subcutaneous fat with no heat Has very little subcutaneous fat with no heat

storage or insulation, and poor glycogen and storage or insulation, and poor glycogen and lipid stores. lipid stores.

Limited ability to shiver has poor vasomotor Limited ability to shiver has poor vasomotor control of blood flow to skin capillaries. control of blood flow to skin capillaries.

There is a relatively large surface area in There is a relatively large surface area in comparison to body weight. comparison to body weight.

Sweat glands are decreased; infant cannot Sweat glands are decreased; infant cannot perspire under 32 weeks’ gestation. perspire under 32 weeks’ gestation.

Usually less active. Usually less active. Posture flaccid (increased surface area Posture flaccid (increased surface area

exposed). exposed).

Renal function: Renal function: Sodium excretion is probably increased which Sodium excretion is probably increased which

may lead to hyponatremia. There is difficulty in may lead to hyponatremia. There is difficulty in excreting potassium. excreting potassium.

Decreased ability to concentrate urine, which Decreased ability to concentrate urine, which may result in dehydration. may result in dehydration.

Decreased ability to acidify urine. Decreased ability to acidify urine. Glomerular tubular imbalance accounts for Glomerular tubular imbalance accounts for

sugar, protein and sodium present in urine. sugar, protein and sodium present in urine. Nervous system: Nervous system: Response to stimulation is slow. Response to stimulation is slow. Suck, swallow and gag reflexes are poor Suck, swallow and gag reflexes are poor

(aspiration). (aspiration). Cough reflex is weak or absent. Cough reflex is weak or absent. Centers that control respiration, temperature Centers that control respiration, temperature

and other vital functions are poorly developed. and other vital functions are poorly developed.

Infection: Infection: Actively found antibodies are lacking at birth (active Actively found antibodies are lacking at birth (active

immunity). immunity). No IgM is present at birth (passive immunity). No IgM is present at birth (passive immunity). Decreased opsonization (preparation of cells to Decreased opsonization (preparation of cells to

phagocytosis).phagocytosis). Liver function: Liver function: Does not have a good ability to handle and conjugate Does not have a good ability to handle and conjugate

bilirubin. bilirubin. Does not store or release sugar well (hypoglycemia). Does not store or release sugar well (hypoglycemia). Steady decrease in Hb and production of blood Steady decrease in Hb and production of blood

(anemia). (anemia). Does not make or store vitamin K (hemorrhage). Does not make or store vitamin K (hemorrhage).

Eyes: Eyes: Oxygen given beyond the point of infant need may Oxygen given beyond the point of infant need may

result in retinal artery constriction and anoxic result in retinal artery constriction and anoxic damage. damage.

The retina detaches from the posterior chamber, The retina detaches from the posterior chamber, fibrous mass forms leading to inability to receive fibrous mass forms leading to inability to receive visual stimulation (retrolental fibroplasia). visual stimulation (retrolental fibroplasia).

The exact amount and level of oxygen needed to The exact amount and level of oxygen needed to produce retrolental fibroplasia are unknown. produce retrolental fibroplasia are unknown.

Skin: Skin: Sensitive because of permeability and decreased Sensitive because of permeability and decreased

thickness of stratus corneum (outer layer of thickness of stratus corneum (outer layer of epidermis). epidermis).

Delayed skin pH recovery to acidity following Delayed skin pH recovery to acidity following washing with alkaline based soap. washing with alkaline based soap.

Post mature infantPost mature infant

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

Predisposing factors: Predisposing factors: Primigravida and high parity at any age. Primigravida and high parity at any age. History of prolonged gestation in the previous History of prolonged gestation in the previous

pregnancies pregnancies Altered physiology: Altered physiology: The postmature infant appear to have suffered The postmature infant appear to have suffered

from intrauterine malnutrition and hypoxia, before from intrauterine malnutrition and hypoxia, before termination of pregnancy but at the point when termination of pregnancy but at the point when birth should have occurred the placental function birth should have occurred the placental function begins to diminish resulting in impaired oxygen begins to diminish resulting in impaired oxygen exchange and inadequate nutrient transfer to the exchange and inadequate nutrient transfer to the fetus. fetus.

The severity of the associated problems is The severity of the associated problems is determined by length of gestation ―the longer the determined by length of gestation ―the longer the gestation, the more severe the problems‖. gestation, the more severe the problems‖.

Clinical manifestations: Clinical manifestations: Wasted physical appearance, little Wasted physical appearance, little

subcutaneous fat ― long, thin appearance‖. subcutaneous fat ― long, thin appearance‖. Long fingernails and toenails. Long fingernails and toenails. Reduced amount of vernix caseosa Reduced amount of vernix caseosa Abundant scalp hair. Abundant scalp hair. Skin frequently cracked and desquamating, Skin frequently cracked and desquamating,

parchment – like pale skin parchment – like pale skin Absence of lanugo hair. Absence of lanugo hair.

Diagnostic evaluation: Diagnostic evaluation: Evaluate general appearance. Evaluate general appearance. Determine gestational age, APGAR scoring and Determine gestational age, APGAR scoring and

blood gas analysis. blood gas analysis.

Complications: Complications: Meconium aspiration. Meconium aspiration. Hypoglycemia, hypocalcaemia and polycythemia. Hypoglycemia, hypocalcaemia and polycythemia. Pulmonary hemorrhage, pneumonia and Pulmonary hemorrhage, pneumonia and

pneumothorax. pneumothorax.

Infant of diabetic mother Infant of diabetic mother (IDM)(IDM) Is the infant born to a mother with diabetes. The Is the infant born to a mother with diabetes. The

mother may be an chronic diabetic or gestational mother may be an chronic diabetic or gestational diabetic. The severity of infant problems depends on diabetic. The severity of infant problems depends on the severity of maternal diabetes. the severity of maternal diabetes.

Altered physiology: hyperinsulinemia in utero Altered physiology: hyperinsulinemia in utero secondary to decreased epinephrine and glucose secondary to decreased epinephrine and glucose response result in the following in the infant: response result in the following in the infant:

Increased amount of body fat Increased amount of body fat Hypoglycemia: occurs within first 2-12 hours of Hypoglycemia: occurs within first 2-12 hours of

life (may occur within minutes). IDM may be life (may occur within minutes). IDM may be symptomatic or asymptomatic with blood glucose symptomatic or asymptomatic with blood glucose below 20 mg/dl. below 20 mg/dl.

Hypocalcemia: associated with prematurity, Hypocalcemia: associated with prematurity, difficult labor or/and asphyxia at birth. Generally difficult labor or/and asphyxia at birth. Generally occurs during first 24-48 hours after birth. occurs during first 24-48 hours after birth.

Infant of diabetic mother Infant of diabetic mother (IDM)(IDM) Prematurity, difficult labor or/and asphyxia at birth. Prematurity, difficult labor or/and asphyxia at birth.

Generally occurs during first 24-48 hours after birth. Generally occurs during first 24-48 hours after birth. Hyperbilirubinemia: most likely to occur within 48-Hyperbilirubinemia: most likely to occur within 48-

72 hours after birth. 72 hours after birth. Prematurity: may be premature or SGA when Prematurity: may be premature or SGA when

associated with placental insufficiency. associated with placental insufficiency. Respiratory function is similar to that of Respiratory function is similar to that of

premature infants. premature infants. Polycythemia: HCT greater than 65% or Polycythemia: HCT greater than 65% or

hemoglobin 22 gm/dl. This increases the risks of hemoglobin 22 gm/dl. This increases the risks of renal vein thrombosis, respiratory distress, renal vein thrombosis, respiratory distress, hypoglycemia and hypocalcemia. hypoglycemia and hypocalcemia.

Congenital anomalies: Congenital anomalies: Infection: prematurity lowered passive immunity. Infection: prematurity lowered passive immunity.

Diagnostic evaluation: Diagnostic evaluation: Maternal history of diabetes. Maternal history of diabetes. Physical assessment of infant and determination Physical assessment of infant and determination

of gestational age. of gestational age. Blood studies: Glucose, HCT, Hb, blood gas Blood studies: Glucose, HCT, Hb, blood gas

analysis, bilirubin, electrolytes (calcium) analysis, bilirubin, electrolytes (calcium) Clinical manifestations: Clinical manifestations: Macrosomia, cardiomegaly, hepatomegaly Macrosomia, cardiomegaly, hepatomegaly Abundant fat, hair and vernix caseosa. Abundant fat, hair and vernix caseosa. Tendency to be large for gestational age, some Tendency to be large for gestational age, some

may be AGA or SGA. may be AGA or SGA. Intrauterine growth retardation when mother Intrauterine growth retardation when mother

has had long standing insulin dependency. has had long standing insulin dependency.

Complications: Complications: Hypoglycemia - Hypocalcemia - Hyaline Hypoglycemia - Hypocalcemia - Hyaline

membrane disease membrane disease Infection - hyperbilirubinemia - Congenital Infection - hyperbilirubinemia - Congenital

anomalies anomalies Birth injuries - prematurity - organomegaly Birth injuries - prematurity - organomegaly Asphyxia neonatorum: it results in primary to Asphyxia neonatorum: it results in primary to

secondary apnea or failure to breath or death if not secondary apnea or failure to breath or death if not promptly treated. promptly treated.

Nursing interventionsNursing interventions

Observe closely for hypoglycemia. Observe closely for hypoglycemia. Monitor infant closely for changes in acid-base status, Monitor infant closely for changes in acid-base status,

respiratory distress temperature, hypocalcaemia, sepsis, respiratory distress temperature, hypocalcaemia, sepsis, cardiac anomalies and hyperbilirubinemia. cardiac anomalies and hyperbilirubinemia.

Assist in the prevention of dehydration and maintenance Assist in the prevention of dehydration and maintenance of fluid and electrolyte balance. of fluid and electrolyte balance.

HypoglycemiaHypoglycemia

Abnormal serum levels of glucose can have life threatening Abnormal serum levels of glucose can have life threatening implications for the neonate. Since the brain is dependent implications for the neonate. Since the brain is dependent upon a constantly circulating supply of glucose, upon a constantly circulating supply of glucose, neurological impairment may occur if hypoglycemia is left neurological impairment may occur if hypoglycemia is left untreated. untreated.

Hypoglycemia during the first 72 hours of life in the term Hypoglycemia during the first 72 hours of life in the term infant is defined as a serum glucose level equal to or below 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 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 below 25 mg/dl. After 72 hours of life, hypoglycemia is a serum glucose level less than 45 mg/dl. serum glucose level less than 45 mg/dl.

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

Altered physiologyAltered physiology : : Under normal conditions, the concentration of Under normal conditions, the concentration of

serum glucose declines during the first 24 hours after serum glucose declines during the first 24 hours after birth with the lowest level usually reached (Nadir) 2 birth with the lowest level usually reached (Nadir) 2 hours after delivery, followed by a subsequent rise. hours after delivery, followed by a subsequent rise.

Per Kilogram of body weight the glucose Per Kilogram of body weight the glucose requirement of the neonate is twice that of the adult. requirement of the neonate is twice that of the adult.

Ability to produce glucose from glycogen or from Ability to produce glucose from glycogen or from alternate substrates (gluconeogenesis) is limited. alternate substrates (gluconeogenesis) is limited.

Pathogenesis may involve one or both of these Pathogenesis may involve one or both of these mechanisms: mechanisms:

1. Decreased source of serum glucose. 1. Decreased source of serum glucose. 2. Increased rate of serum glucose removal. 2. Increased rate of serum glucose removal.

Patient care management: Patient care management: Blood glucose monitoring is performed hourly during the Blood glucose monitoring is performed hourly during the

first 4 to 6 hours of life and then every 4 hours for 24 first 4 to 6 hours of life and then every 4 hours for 24 hours, or per agency protocol. Blood is generally obtained hours, or per agency protocol. Blood is generally obtained by heel stick by heel stick

An intravenous infusion of glucose may be necessary if An intravenous infusion of glucose may be necessary if early feeding does not keep the blood glucose at 45 mg/dL early feeding does not keep the blood glucose at 45 mg/dL or above. or above.

Diet A feeding of 5% glucose water may be given soon Diet A feeding of 5% glucose water may be given soon after birth, followed in 1 hour by a breast or formula after birth, followed in 1 hour by a breast or formula feeding, which is continued on a regular basis. feeding, which is continued on a regular basis.

Septicemia NeonatorumSepticemia Neonatorum

Septicemia is the systemic invasion of pathogenic Septicemia is the systemic invasion of pathogenic bacteria into the blood stream. In the newborn it is known bacteria into the blood stream. In the newborn it is known as sepsis neonatorum. as sepsis neonatorum.

Low temperature is also a sign for sepsis. Low temperature is also a sign for sepsis. It is a generalized infection, which may occur in the It is a generalized infection, which may occur in the

neonate and is characterized by the proliferation of neonate and is characterized by the proliferation of bacteria in the blood stream and frequently involves the bacteria in the blood stream and frequently involves the meninges. meninges.

Incidence: Incidence: 1 in 1000 live full term births. 1 in 1000 live full term births. I in 250 live premature births. I in 250 live premature births.

Etiology: The etiologic agents varies from year to year and from institution to Etiology: The etiologic agents varies from year to year and from institution to another. another.

Common offending organisms: Escherichia coli ( E. Coli), Listeria, klebsiella, Group B Common offending organisms: Escherichia coli ( E. Coli), Listeria, klebsiella, Group B hemolytic streptococci, staphylococcus aureus, Pseudomonas, and Hemophilus influenza hemolytic streptococci, staphylococcus aureus, Pseudomonas, and Hemophilus influenza

Portal of entry may be nasopharynx, skin, eye, umbilicus or Aspiration of infected Portal of entry may be nasopharynx, skin, eye, umbilicus or Aspiration of infected amniotic fluid. amniotic fluid.

Predisposing factors: Predisposing factors: 1. Perinatal factors: 1. Perinatal factors: Maternal complications e.g. prolonged rupture of membranes, prolonged and difficult Maternal complications e.g. prolonged rupture of membranes, prolonged and difficult

labor, UTI, endometritis, chorioamnionitis, maternal illness, and abruption placenta labor, UTI, endometritis, chorioamnionitis, maternal illness, and abruption placenta

2. Infant complications e.g. prematurity, LBW, congenital heart disease and RDS 2. Infant complications e.g. prematurity, LBW, congenital heart disease and RDS 3. Iatrogenic or environmental factors e.g. unclean equipment, surgical procedures, 3. Iatrogenic or environmental factors e.g. unclean equipment, surgical procedures,

obstetric and nursery practice obstetric and nursery practice Complications: Complications: Meningitis and neurological damage. – shock - Pneumonia. Meningitis and neurological damage. – shock - Pneumonia. Congestive heart failure. – DIC - high mortality rate. Congestive heart failure. – DIC - high mortality rate.

Assessment: Assessment: 1. Clinical presentation 1. Clinical presentation a. Signs and symptoms: a. Signs and symptoms: The early signs of sepsis usually vague and subtle. The infant is often described as 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, not doing well. The signs often include: poor feeding, gastric retention, lethargy, meconium stained, and temperature alteration, usually hypothermia but may have meconium stained, and temperature alteration, usually hypothermia but may have hyperthermia. hyperthermia.

Later signs and symptoms: pallor, cyanosis, apneic episodes, jaundice, abdominal Later signs and symptoms: pallor, cyanosis, apneic episodes, jaundice, abdominal distention, vomiting, diarrhea, hepatosplenomegaly, bulging fontanels, hypotonia, distention, vomiting, diarrhea, hepatosplenomegaly, bulging fontanels, hypotonia, fever or seizures. fever or seizures.

b. History of predisposing factors. b. History of predisposing factors. 2. Laboratory: presence of organism in the blood culture must be obtained for a 2. Laboratory: presence of organism in the blood culture must be obtained for a

diagnosis of sepsis neonatorum. diagnosis of sepsis neonatorum. Cultures to detect specific organism: blood, urine, umbilical stump, skin lesions, Cultures to detect specific organism: blood, urine, umbilical stump, skin lesions,

nose, throat, rectum, CSF, external auditory canal or/and gastric fluid. nose, throat, rectum, CSF, external auditory canal or/and gastric fluid. WBC, Hb and HCT WBC, Hb and HCT Blood chemistry, bilirubin and blood gas analysis. Blood chemistry, bilirubin and blood gas analysis. Medical management: Medical management: Antibacterial: Ampicillin and aminoglycoside or according to culture and Antibacterial: Ampicillin and aminoglycoside or according to culture and

sensitivity. sensitivity. Supportive therapy: as oxygen therapy, fluid and caloric maintenance. Supportive therapy: as oxygen therapy, fluid and caloric maintenance.

Jaundice in the newborn Jaundice in the newborn “Hyperbilirubinemia“Hyperbilirubinemia ” ”

The infant’s immature liver is often unable to conjugate all of the The infant’s immature liver is often unable to conjugate all of the bilirubin released by the destroyed RBCs, and this is evident as bilirubin released by the destroyed RBCs, and this is evident as jaundice. The jaundice usually peaks at 72 hours and then disappears in jaundice. The jaundice usually peaks at 72 hours and then disappears in a couple of weeks a couple of weeks

Hyperbilirubinemia is an excess of bilirubin (unconjugated bilirubin) Hyperbilirubinemia is an excess of bilirubin (unconjugated bilirubin) in the blood, may be related to physiologic jaundice or pathologic in the blood, may be related to physiologic jaundice or pathologic jaundice. Physiologic jaundice occurring after the first 24 hours of life jaundice. Physiologic jaundice occurring after the first 24 hours of life is related to the normal destruction of the excess red blood cells (RBCs) 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 in the newborn. With direct oxygenation of the blood in the newborn’s lungs, the extra RBCs of the fetus are no longer needed. lungs, the extra RBCs of the fetus are no longer needed.

Pathologic jaundice appears in the first 24 hours and may lead to Pathologic jaundice appears in the first 24 hours and may lead to kernicterus (deposits of bilirubin causing yellow staining in the brain). kernicterus (deposits of bilirubin causing yellow staining in the brain). The exact level of total bilirubin when kernicterus occurs is not known The exact level of total bilirubin when kernicterus occurs is not known but may occur at 20 mg/dL in full-term infants and at a lower level in but may occur at 20 mg/dL in full-term infants and at a lower level in preterm neonates. Kernicterus is a chronic, serious neurological preterm neonates. Kernicterus is a chronic, serious neurological impairment result of bilirubin toxicity. Preterm infants are at a greater impairment result of bilirubin toxicity. Preterm infants are at a greater risk of developing kernicterus, and the most common cause is Rh risk of developing kernicterus, and the most common cause is Rh incompatibility and severe dehydration incompatibility and severe dehydration

Incidence: Occurs in 50% of term infants, 80% of preterm. Incidence: Occurs in 50% of term infants, 80% of preterm. Predisposing factors: Predisposing factors: Blood group incompatibility with mother. Blood group incompatibility with mother. Prematurity, Infection, Birth trauma and Polycythemia Prematurity, Infection, Birth trauma and Polycythemia Maternal or neonatal metabolic or endocrine disorders. Maternal or neonatal metabolic or endocrine disorders. Malfunction of gastrointestinal tract. Malfunction of gastrointestinal tract. Altered physiology: Altered physiology: Bilirubin is released (result from RBC destruction) into the circulation Bilirubin is released (result from RBC destruction) into the circulation

where it combines with albumin (unconjugated or indirect bilirubin). where it combines with albumin (unconjugated or indirect bilirubin). Once the unconjugated bilirubin is in the liver, it is converted into direct 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 or conjugated water-soluble bilirubin with the aid of enzymes, one of which is glucuronyl transferase and excreted via the bile into the intestine 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 and is excreted in the stool or is hydrolyzed to unconjugated bilirubin in the intestine and reabsorbed across the intestinal mucosa into the the intestine and reabsorbed across the intestinal mucosa into the circulation (enterohepatic circulation). circulation (enterohepatic circulation).

Signs and symptoms may include: Signs and symptoms may include: Sclera appearing yellow before skin. Sclera appearing yellow before skin. Skin appearing light to bright yellow. Skin appearing light to bright yellow. Lethargy, poor feeding and dark stool. Lethargy, poor feeding and dark stool. Dark amber, concentrated urine. Dark amber, concentrated urine. Diagnostic evaluation: Diagnostic evaluation: Maternal blood and Rh type. Maternal blood and Rh type. Infant screening: total and direct bilirubin, CBC, blood and Infant screening: total and direct bilirubin, CBC, blood and

Rh type, Albumin or total proteins, glucose, pH, blood culture Rh type, Albumin or total proteins, glucose, pH, blood culture if sepsis indicated as cause. if sepsis indicated as cause.

Treatment: Treatment: 1. Phototherapy – to allow for utilization of alternate pathways 1. Phototherapy – to allow for utilization of alternate pathways

for bilirubin excretion. for bilirubin excretion. 2. Exchange transfusion: during this procedure, 5 mL to 10 mL 2. Exchange transfusion: during this procedure, 5 mL to 10 mL

of blood are removed from the infant and replaced with a like of blood are removed from the infant and replaced with a like amount of donor blood. amount of donor blood.

Thank You AllThank You All

Any Question ??????Any Question ??????