complications of newborn Flashcards
RDS
○ Due to lung prematurity
○ 60-80% of <28 weekers will develop
■ Due to lack of production of surfactant
○ CXR shows atelectasis (hazy lung fields)
common predictors of RDS
■ Prematurity
■ C-section without labor
■ IDM
■ 2nd twin
antepartum complications with RDS
■ Hemorrhage
■ Asphyxia
Consequences of RDS
■ Lung scarring ■ Increased risk of asthma ■ Bronchopulmonary dysplasia (BPD) ● High O2 for long periods of time ● Chronic lung condition ● Greater risk for URIs and permanent bronchial changes
S/S of respiratory distress with RDS
RETRACTIONS!
complications associated with premature infant
○ Defined as an infant that is delivered at less than 37 weeks gestation
○ Infant’s ability to survive is dependent on degree of prematurity and infant’s own strengths and weaknesses
○ In general, infants born at less than 24 weeks are not viable
○ At delivery, if eyes are fused and infant weighs less than 500g, generally resuscitation is not done
■ Eyes fused= extreme prematurity
○
○ Alteration in thermoregulation
■ Hypothermia
○ Alteration in GI physiology
○ Alteration in renal physiology
○ Alteration in immunologic physiology
■
prematurity alterations in respiratory and cardiac physiology
Alteration in respiratory and cardiac physiology
■ Apnea of prematurity
● > 20 sec → leads to bradycardia → color changes
■ Patent ductus arteriosus (PDA)
■ Respiratory distress syndrome (RDS)
■ Bronchopulmonary dysplasia (BPD)
■ Intraventricular hemorrhage (IVH)
■ Anemia of prematurity
● Exaggerated response from hypoxic state in utero to hyperoxic state after birth
● Normocytic, normochromic, hyporegenerative
● Low serum erythropoietin
● Spontaneously resolves in 3-6 months
■ Aspiration
prematurity alterations in GI
Hypoglycemia
■ Necrotizing enterocolitis
● Baby is fed, sweet component to food is not moving through GI system as it should → bacteria accumulate → gas formation → abdominal distention
● Gas bubbles in lining of intestine → risk of perforation
● Shows bradycardia, periods of bradypnea, color changes
● High dose antibiotic- no more feedings
● Caused by feedings too close together
alteration in immunologic physiology
Neonatal infection
○ Alteration in neurological physiology
■ Reactivity periods and behavioral states
○ Alteration in ocular physiology
■ Retinopathy of prematurity
● Vessels grow into vitreous humor → fingerlike projections → engorgement
● Rupture → blindness?
phototherapy risks
- positive combs test –> phototherapy needed, lots of bilirubin as byproduct
- can cause permanent bronzing
- can develop a dark grey-brown discoloration of the skin, urine and serum
- development of purpura or bullae in infants with cholestatic jaundice or congenital erythropoietic porphyria
- infants who have familial history of porphyria this is an ABSOLUTE CONTRAINDICATION!
Hyperbilirubinemia (jaundice)
○ The yellowing of the skin d/t the accumulation of bilirubin in the skin and the brain
○ Bilirubin is the byproduct of heme from the breakdown of hemoglobin
○ One of the components of bile, yellow in color
○ Occurs when the breakdown of RBCs happens faster than the liver and GI tract can remove them
○ 60-70% of term and near term infants will become visibly jaundiced
○ 100% of preterm infants will become jaundiced
○ The leading cause of hospital readmission in the first 2 weeks of life
○ Major reason for prolonged hospitalization in otherwise healthy newborn
causes of hyperbilirubinemia
physiologic
hemolytic
physiologic causes of hyperbilirubinemia
● Increased load of RBC breakdown ○ Cephalohematoma ○ Suction or forceps delivery ○ Other bruising ● Liver immaturity ● Breast feeding ● Infant of diabetic mother ● Hepatic or bowel abnormalities
hemolytic causes of hyperbilirubinemia
● Blood group incompatibilities
● Rh negative moms
● ABO incompatibility
● Glucose-6-phosphate dehydrogenase (D6PD) deficiency
○ Helps body process carbs and protects RBCs
○ → inherited condition passed on X chromosome
complications of extreme jaundice
■ Neurological complications ■ Seizures ■ Poor suck reflex ■ Irritability ■ Abnormal muscle tone
what happens if bilirubin passes BBB
--> kernicterus ■ Long term complication ■ Seizures ■ Hearing loss ■ Motor deficits ■ Vision loss ■ Learning difficulties ■ Death
when to treat jaundice
■ Premature infants need to be treated at lower levels than term infants
■ The total bilirubin level must be evaluated in reference to how old the infant is, in terms of hrs
■ Complicating factors, such as hypoglycemia and sepsis, will affect the decision to treat
how to test jaundice infants
■ Observation ● Cephalocaudal progression ● Easy, but unreliable ■ Transcutaneous bilirubinometry ■ Blood draws from a heal stick (definitive way) ● Neonatal or total bilirubin level ● Direct bilirubin level ● Measured in mg/dL
treatment options for jaundice
■ Phototherapy ● High direct - cannot be done ● Can cause permanent bronzing ■ Hydration ■ Feeding- breast or bottle ■ IV ● Hydrated to pass the stool ■ Exchange transfusion ● Partial- blood is removed, saline put in to dilute blood ● Full- take blood out, put blood in, take blood out ○ PKU test before ○ Have 75% of blood or more exchanged
complications associated with SGA <10%tile
■ Asphyxia ■ Aspiration syndrome ■ Hypothermia ■ Hypoglycemia ■ Polycythemia
asphyxia
chronic hypoxia in utero - little reserve during delivery
■ Test the cord blood
■ Cord pH < 7.2 = increased morbidity
aspiration syndrome
- utero hypoxia can cause infant to gasp → aspiration of amniotic fluid
■ Relaxation of anal sphincter → passage of meconium → aspiration
hypothermia
less brown fat which is thermal subQ fat that helps keep them warm - poor thermoregulation
■ Stay in flexed position to decrease surface area
hypoglycemia
working harder to stay warm → increased metabolic demand (already have inadequate glycogen stores in the liver)
polycythemia
increased RBCs with high HCT d/t hypoxia in utero
HCT > 65%
intrauterine growth retardation (IUGR) SGA plus additional complications
congenital malformations intrauterine infections continued growth difficulties cognitive difficulties symmetrical/asymmetrical
congenital malformations
impaired ability of cells to divide and replicate
intrauterine infections
rubella, cytomegalovirus
cytomegalovirus –> likes to hide in granulocytes and macrophages –> direct effect on brain and organs
continued growth difficulties
● Asymmetrical- catch up with good optimal environment
● Symmetrical- do not usually catch up (too little for too long)
symmetrical (proportional)
○ Caused by long term conditions (chronic HTN, severe malnutrition)
○ Head, body all small
asymmetrical (disproprtional)
○ Acute compromise of uteroplacental blood flow not evident before 3rd trimester
○ Head larger than abdominal circumference
○ Subnormal liver growth, decreased glycogen stores
○ Can happen because of infarct in placenta, preeclampsia, poor maternal weight gain
cognitive difficulties
hyperactivity short attention span fine motor coordination hearing loss speech deficits
nursing diagnosis for SGA/IUGR
○ Risk for imapred gas exchange r/t meconium aspiration
○ Risk for ineffective thermoregulation s/t decreased subcutaneous fat
○ Altered nutrition: less than body requirements r/t increased metabolic needs in the infant
○ Risk for altered parenting r/t lack of knowledge of infant care and prolonged separation of infant and parents s/t illness
Characteristics of a diabetic infant
■ Macrosomia or SGA
● SGA bc mom is insulin-dependent, not enough nutrient for infant
● Macrosomia (>9 lbs)
■ Ruddy in color
■ Excessive adipose tissue
■ Large umbilical cord and placenta
■ Decreased total body water
● More fat
■ Excessive fetal growth from exposure to high levels of maternal glucose
● Beta cells of the fetus will release a lot of insulin
● Cells are fed too much everyday → excessive growth
■ At risk infants- requires close observation for first hours and days possibly
complications of diabetic infant
■ Hypoglycemia ● High glucose from placenta → still secreting high insulin → severe hypoglycemic ● Often need bolus 10% dextrose ■ Hyperbilirubinemia ● d/t polycythemia ■ Birth trauma ● Shoulder dystocia ● Erb’s palsy ■ Polycythemia ■ Respiratory distress syndrome ■ Congenital birth defects: cardiac anomalies, GI anomalies, sacral agenesis ■ Poor eaters
symptoms of a diabetic bb????
need to look up
hypoglycemic baby
○ Blood sugar decreases to low w/in 1-2 hours after clamping
○ Failure to increase blood sugar concentration at 4 hours is pathologic
■ Term infants can usually compensate
■ Preterm infants do not have the stores to compensate
■ Preterm infants cannot tolerate early feedings sufficient to maintain blood sugar levels alone
○ Less than 40 mg/dL needs intervention
■ Feeding, IV, or both
causes of hypoglycemic bb
■ Prematurity ● Greater need for more calories per kilo weight ■ IUGR ■ Delayed feedings ■ Increased need for glucose ■ Increased uptake of glucose ■ Inborn errors
s/s for hypoglycemic bb
■ May not see any s/sx, therefore need to check chemstrip if indicated by history
■ Tremors/jittery → seizures
■ Abnormal cry (high pitched or weak)
● Cat-like cry- cocaine addiction
■ Respiratory distress → apnea, irregular resp, tachypnea, cyanosis
■ Stupor, hypotonia, refusal to eat
prevention and treatment of hypoglycemic bb
■ Early feeding ■ Frequent monitoring ■ Prevention of causative factors ● Temperature stability ● Treat respiratory difficulties ● Early IV
meconium aspiration syndrome
○ Affects term and near term infants
■ Meconium made up of broken down red cells, green in color, sticky and tarry
■ Green stained amniotic fluid → passed first stool in utero
○ Complete or partial airway obstruction
○ Can cause atelectasis or hyperinflation
○ Can cause pneumonitis
○ Requires intubation directly after birth to suction meconium from airway
■ No stimulation whatsoever
■ Do not want them to take first breath
■ Suction at level of vocal cords → then stimulate first breath
■ Too late to do once they take first breath
common predictors of meconium aspiration syndrome
■ Term or post term infants
■ Rarely seen <36 weeks gestation (not ready to pass meconium)
complications of meconium aspiration syndrome
■ Pneumothorax ■ Pneumonia ■ Persistent pulmonary HTN ■ Bronchopulmonary dysplasia ■ Neurologic complications ■ Possible death
transient tachypnea of the newborn (TTNB)
○ Occurs in term and near term infants- amniotic fluid in the lung ■ “Wet lungs” ○ Lasts 1 to 5 days ○ Minimal hypoxia ○ Respiratory rates generally > 100 ○ First phase: grunting phase to open alveoli ○ Second phase: tachypnea ○ Support w IV, introduce food slowly
Common predictors of TTNB
■ C-section w/o labor ■ Precipitous delivery ■ Prolonged labor ■ Male ■ 2nd twin
Consequences of TTNB
■ Cannot nipple feed with a respiratory rate >70 ● → can aspirate breast milk ■ IV or NG feed ■ No long term consequences ■ Self-limiting
Persistent pulmonary hypertension (persistent fetal circulation)
○ Occurs in near term, term, and post term infants
○ History of hypoxia at birth
■ Must have oxygenated systems
■ Hypoxia in pulmonary circulation → vasoconstriction
○ Common to have other delivery problems such as abruption, meconium staining, etc
Consequences of persistent pulmonary hypertension (persistent fetal circulation)
■ Pneumothorax ■ Hypotension and CHF ■ Impaired kidney function ■ DIC ■ Seizures
polycythemia
increased RBCs with high HCT d/t hypoxia in utero
HCT > 65%
higher HCT, blood is hype viscous → harder to pump → decreased nutrient delivery
MORE RBCS THAN NORMAL!
polycythemia causes
- baby’s body makes more RBCs than it should
- if baby was a twin and got extra RBCs from another source
- just after birth, too many RBCs traveled from the umbilical cord to the baby before the cord was clamped
- maternal substance use such as smoking
- maternal diabetes
- large for gestational age infant
- chromosomal abnormality
- placental insufficiency
- placental red cell transfusion
polycythemia symptoms
Lethargy Irritability Jitteriness Tremors Seizures Cerebrovascular accidents Oliguria and/or hematuria Respiratory distress Cyanosis Apnea
potential complications of polycythemia
increased blood thickness and decreased blood flow
CNS abnormalities
Cardiopulmonary complications (Cardiomegaly, increase in pulmonary vascular resistance and decrease in cardiac output) with tachycardia and tachypnea may develop
- decreased blood flow to organ systems
Shoulder dystocia newborn complications
brachial plexus (most common complication) palsy injuries fractures hypoxia death
cerebral hemorrhage in the newborn
- cerebral vessels are very fragile, which can lead to bleeding into the ventricles –> intraventricular hemorrhaging
- higher incidence less than 30 weeks
- can be caused by birth asphyxia or birth trauma
persistent pulmonary HTN
- occurs in near term, term and post term infants
- history of hypoxia at birth
- must have oxygenated systems
- hypoxia in pulmonary circulation –> vasoconstriction
- common to have other delivery problems such as abruption, meconium staining, etc
consequences of persistent pulmonary HTN
- pneumothorax
- hypotension and CHF
- impaired kidney function
- DIC
- seizures
cause of persistent pulmonary HTN
RV –> PA –> DUCTUS ARTERIOSUS –> AORTIC ARCH –> BODY
- only 5-10% of R & L ventricular output goes to the pulmonary vessels… the rest bypasses the lungs
- at birth there is a rapid fall in pulmonary vascular resistance and pulmonary artery pressure accompanied by a 10 fold increase in pulmonary blood flow
complications associated with SGA baby
- asphyxia
- hypothermia
- hypoglycemia
- aspiration syndrome
- polycythemia
complications associated with IUGR infant
SGA COMPLICATIONS PLUS
- congenital malformations
- intrauterine infections
- continued growth difficulties
- cognitive difficulties
two types of patterns of continued growth difficulties
symmetrical
asymmetrical
symmetrical
caused by long term conditions (chronic HTN, severe malnutrition)
head, body all small
do not usually catch up (too little for too long)
asymmetrical
acute compromise of uteroplacental blood flow not evident before 3rd trimester
head larger than abdominal circumference
subnormal liver growth, decreased glycogen stores
can happen because of infarct in placenta, preeclampsia, poor maternal weight gain
