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Acute manifestation of bilirubin toxicity occurring in the first weeks after birth
Agglutination and hemolysis of fetal erythrocytes caused by incompatibility between the maternal and fetal blood types, such as when the fetus is Rh+ and mom is Rh-
condition in which the esophagus is separated from the stomach and ends in a blind pouch
protrusion of the intestines through a defect in the abdominal wall.
the intestines are not covered by a peritoneal sac or skin
heart failure and generalized edema in the fetus secondary to severe anemia resulting from destruction of erythrocytes
protrusion of the meninges through a defect in the vertebrae; a form of neural tube defect
protrustion of the meninges and spinal cord through a defect in the vertebrae
a form of neural tube defect
neonatal abstinence syndrome
a cluster of physical signs exhibited by newborns exposed in utero to maternal use of substances such as heroin
protrusion of the intestines into the base of the umbilical cord
the intestines are covered by a peritoneal sac
persistent pulmonary hypertension
vasoconstriction of the infants pulmonary vessels after birth
may result in right-to-left shunting of blood flow through the ductus arteriosus, the foramen ovale, or both
defective closure of the bony spine that encloses the spinal cord
type of neural tube defect
transient tachypnea of the newborn
condition of rapid respirations caused by inadequate absorption of fetal lung fluid
Maternal events that cause Asphyxia (6)
Equipment needed for an asphyxia emergency (6)
laryngoscope with working light
ET tube of different sizes
TTN- transient tachypnea of newborn (2)
self limiting disease in which there is an excess of lung fluid and/or failure to clear normal lung fluid
issue is not low surfactant
Dx/Tx of TTN (3)
if interventions are working RR wnl and color would improve
When should you collaborate with medicine re: TTN (3)
When an intervention is done and/or no longer working
look at WBC in case of sepsis
o2 hood (4)
Monitor % of o2
Temp of hood
o2 needs to be humidified
monitor infants response: blood gas results., respiratory system
Intrauterine stress may lead to (2)
passage of meconium in utero and MAS "Meconium Aspiration Syndrome"
Hypoxic incident -->vagal response -->poop
MAS is most common in infants
with asphyxia and in postterm infants who are SGA and have decreased amniotic fluid
which makes them prone to cord compression
signs of mild to severe respiratory distress:
tachypnea, cyanosis, retractions, nasal flaring, grunting, rales, rhonchi, and is severe cases a barrel-shaped chest from hyper inflation
Radiography shows patchy infiltrates, atelectasis, and hyperexpansion from air trapping
The infants nails, skin and umbilical cord may be stained a yellow-green color
ECMO Extracorporeal membrane oxygenation
used for infants >34wks >2000grams
Parental support needed
Oxygenates blood while bypassing the lungs, allows infants lungs to rest temporarily and recover
ECMO is used for (6)
Persistent pulmonary HTN
Life support w/ heart surgery
Nursing Dx for infants with Respiratory Disorders
Ineffective airway clearance
Ineffective breathing patterns
Risk for injury
Imbalanced nutrition less than body requirements
Risk for impaired parent-infant attachment
Pathologic jaundice is a concern because (2)
it may lead to acute bilirubin encephalopathy, the acute manifestation of bilirubin toxicity. Leads to kernicterus (brain damage)
- don't want 20 bili value in 1st two days of life
Hyperbilirubinemia is caused by (3)
Incompatibility of mom & baby's blood
Rh- mom with Rh+ infant,
O mom with A, B, or AB infant (rare)
5 types of antibodies
IgG (crosses placenta)
IgE (<1% allergies)
IgM (10% autoimmune)
IgD (<1% modifies IgG)
How many RBC antigens are there?
>400 RBC antigens
Most rare, low immunogenicity (C,c,E,e,Kell-K1(severe), Duffy)
40 specific antigens have causes hemolytic disease of the fetus/newborn
What happens when a Rh+ enders the Rh- persons blood?
The Rh- person develops antibodies against rh+
IgG crosses placenta, and they destroy Rh+ RBCs
Rhesus (Rh) incompatibility requires
Only causes harm to fetus, not mother
(15% of white population is Rh-, lower in african american and asian population)
Rh sensitization process
Rh- pts immune system makes antibodies against Rh+
Sensitization can occur during spontaneous or elective abortion, amnio, CVS, trauma, birth, or thinning of placental membranes (>28wks)
Most exposures occur during birth
Requires only 0.1cc of Rh+ blood
1st child is not affected, no antibodies have been formed yet to cross the placenta and enter into fetal circulation
RhoGAM prevents sensitization
Classification: IgG antibodies +RBC
Action: Passive immunity for Rh- patients who have been exposed to +RBC
Dosage: 1 standard vial (300mcg) IM deltoid
Administer to women exposed to Rh+ blood via delivery, abortion, CVS, amnio, abd trauma, transfusion error
When to administer RhoGAM
28 wks pg- to prevent possible sensitization during 3rd trimester
Within 72hrs of exposure to Rh positive RBC
If IgG-+RBC antibodies are present in maternal blood
they will cross placental barrier and attach to +RBCs
Why do fetal bilirubin leveins increase?
Icterus Gravis (RBC breakdown), which can cause Kernicterus (neurologic disease and encephalopathy)
Hemolytic process proceeds to Erythroblastosis fetalis
Erythroblastosis Fetalis (4)
Rapid production of erythroblasts (immature RBCs) which are unable to carry o2
Fetus is so anemic that generalized fetal edema results (hydrops fetalis)
Can progress to CHF
EFM will show sinusoidal pattern= poor prognosis.
The fetus is so hypoxic that the Autonomic nervous system is unable to function
If Rh- an indirect Coombs test is drawn the 1st prenatal visit to see if..
The Rh- woman has Rh+ antibodies.
If the test is negative she has not developed them and no sensitization has occurred
repeated at 25-28wks-anticipate negative and if so give Rhogam at 28wks to protect Moms immune system and future babies
If Positive indirect Coombs
maternal sensitization or isoimmunization (alloimmunization) has occured.
Do not give Rhogam-
Once sensitization has occurred its too late. You can not reverse sensitization.
Repeat test throughout pg to evaluate rising maternal titer (>1:16 severe, but differs from lab to lab)
Postpartum management for all Rh- moms
Umbilical cord blood is collected to determine fetal blood type and Rh factor
If the baby is Rh+ the umbilical cord blood is used for a Direct Coombs also called a DAT= direct antibody test) detects antibodies attached to fetal RBCs
Mothers with type O blood have natural antibodies to type A and B blood so...
The antibodies cross the placenta and cause hemolysis of fetal RBCs.
Less severe than Rh incompatibility
Primary antibodies of the ABO system are IgM, which do NOT cross the placenta
No specific prenatal care required, but the nurse must monitor for hyperbilirubinemia
Postdelivery cord blood may be obtained to determine blood type and DIRECT Coombs test also called DAT
occurs within first 24hrs- notify doctor
Get blood bili or transQ bili, then get bili prn
Most common cause of pathological jaundice
hemolytic disease of newborn
assess infants intake, infant may be lethargic.
Most common tx of jaundice & how it works
changes physical nature of bilirubin from fat soluble to water soluble so it can be excreted
How does phototherapy work?
Bilirubin in the skin absorbs the light and changes into water-soluble products, the most important of which is lumirubin
These products do not require conjugation by the liver and can be excreted in the bile and urine
Side effects of phototherapy
frequent, loose, green stools that result from increased bile flow and peristalsis
this causes more rapid excretion of the bilirubin but may be damaging to the skin and result in fluid loss
Erythematous macular skin rash
African american babes can experience a tanning effect
If bronzing occurs you may continue phototherapy, it is not contraindicated
is for otherwise healthy babies, to decrease hospital stay
check T q3-4hrs, can cause an increased temp
Provide adequate fluids
change position every 2hrs so the light reaches all areas of the body
Promoting bonding with phototherapy
the infant may be removed from phototherapy for feedings, diaper changes and other general care, but should remain under the lights most of the time to decrease the jaundice as fast as possible.
Hold and cuddle the infant during the time the infant is not under the lights. When the baby is under the lights you can talk to them. The sound of the parents voice is comforting
Performed when phototherapy cannot reduce dangerously high bilirubin levels quickly enough.
Removes maternal antibodies, unconjugated bilirubin, and antibody-coated (sensitized) RBCs.
It provides fresh albumin with binding sites for bilirubin and corrects severe anemia.
When an immediate transfusion is needed for RH incompatibility, type O- packed RBCs with type AB plasma are used so that circulating antibodies will not detroy erythrocytes and there are no antiA or antiB antibodies present.
If time allowed Rh- blood of the infants blood type should be used
Infection is acquired in utero from Mom to Baby
Infections should be considered a teratogen
Neonatal infections (4)
immune system is immature and untried
breastmilk supplies antibodies, some maternal antibodies are received thru placental transfer
Handwashing is important
Cytomegalovirus (CMV) (4)
Most common congenital infection
CMV is a herpes virus
Its widespread- infects most humans
Transmitted by contact with contaminated urine, saliva, blood, cervical mucus, semen, breast milk, transplacental and stool
Neotanal effects of CMV
Leading cause of hearing loss
Baby needs ISOLATED
Most severe affects associated with primary maternal infection during the 1st trimester. Causes deafness, mental retardation, seizures, blindness, and dental abnormalities
Viral transmission via droplets, direct contact with nasopharyngeal secretions or transplacental
Maternal effects of Rubella
Maculopapular rash that begins on face and migrates over the body and lasts 3 days
Lymph node enlargement
Rubella Maternal issues
Prevent by immunization
Rubella Titer: 1:10 or > indicates immunity
Women with rubella require no special therapy other than analgesics
If receive Rubella vaccine DO NOT GET PREGNANT FOR 4 weeks!! Vaccine contains live virus, risk to developing baby. Document this discussion along with the type of birth control parents plan on using
Rubella Fetal Effects
SERIOUS- greatest risks in 1tri
1/3 will spontaneously abort
50-70% have cataracts, deafness, mental retardation, cardiac defects, IUGR, microcephaly
If multisystem involvement mortality is 80%
Congenital Rubella Syndrome (CRS)
Chicken pox- member of herpes virus family
Transmission: direct contact or through respiratory tract, transplacental
Contagious for 48 hrs prior to the onset of vesicular rash
Incubation 10-21 days
becomes latent in the nerve ganglia of spinal cords, can become reactivated as herpes zoster (shingles)
Maternal Effect of Varicella Zoster virus
generalized pruritic rash, preterm labor, encephalitis, varicella pneumonia
If moms rash onset is 5 days prior to delivery to 48hrs postpartum SEVERE DISSEMINATED NEONATAL DISEASE MAY DEVELOP 1/3 DIE
Congenital varicella syndrome- only occurs if exposed <20wks gestations, rare only 2% of exposures
-limb reduction anomalies
How do you prevent VZV?
-No pgcy within 3 months, know pts status, if no known disease draw blood titers.
If pt nonimmune teach her to call clinic if been exposed. Give VZIG(varicella-zoster immune globulin)
What do you do if the mother contracts VZV 5-7days or less before deliver?
Administer VZIG! may prevent newborn infection
If the mom has VZV you must teach her about the potention severe illness-ER
If mom HBsAG+ (dx acute or chronic infection)
incubation period 50-180 days
Baby needs HBIG and HepB vaccine within 12hrs of birth
If no protection 90% have chronic infection and of those with chronic infection 15-25% die of HBV related disease as adults (liver cancer)
Breastmilk contains HBsAg but
does not increase or decrease rate of transmission.
AAP says it is okay for moms with HepB to feed their baby
Herpes Simplex Virus (HSV)
Lifelong infection- active lesions/dormant
If chart says hx of herpes, BE CAREFUL, lays dormant in the dorsal nerve ganglion.
30% of women have +antibodies for HSV
Stress brings on outbreaks and labor and pregnancy are stressful
Direct contact of skin/mucous membrane with lesion
Lesions develop at site of contact, begin as painful papules, progress to vesicles, shallow ulcers, pustules and crusts
The virus is shed until lesions are COMPLETELY HEALED and 24-48hrs BEFORE the outbreak
Fetal transmission of HSV
Vertical (in utero) transmission from mom to baby occus:
-after ROM virus ascends, FECG
-During birth, contact with lesions
-Rarely transplacentally with primary outbreak (spont ab, PTL, IUGR)
Dx= positive culture from lesions or antibody titer
Complications are rare with recurrent infection
(rare if pt had HSV prior to becoming pregant)
No known cure
Antiviral chemotherapy- Acyclovir
Reduces symptoms and shortens duration
Controversial med during pg to prevent outbreaks
What if mom has HSV but no active lesions?
Can deliver vaginally
There is no increase in perinatal mortality
What if mom has active/prodromal HSV
must do C/S
Ask mom before delivery what to tell family if they are asked.
Isolation from mom is NOT indicated.
Teach mom about proper handwashing and to avoid infant contact with active lesions..
Dont kiss the baby if you have an active oral lesion
Neonatal effects HSV
Uncommon but potentially devastating
May be limited to skin lesions or disseminated
DEATH RATE IS 50% IF DISSEMINATED DISEASE
HIGHER RISK IF MOTHER HAS PRIMARY INFECTION DURING PREGNANCY
Symptoms develop within the 1st week in infant and progress rapidly
risk of transmission to fetus/neonate is 25% without tx!
Decreases to 2% if treated with combination antiretroviral therapy
Offer HIV testing to all pg women
Pregnancy does not accentuate HIV
Possible scheduled C/S @ 38wks if viral load >1000ml before ROM
Mom needs antibx bc she is at risk for complications of C/S than non HIV mom d/t impaired immune system
DO NOT BREASTFEED WITH HIV
HIV infected newborns
Rare 2% with mom being treated
All babies born to mom with HIV will have antibodies in blood for 18months bc it crosses placenta
If HIV+/perinatal infection=complex therapy, regiment of nutritional supplements to px weight loss, vaccines to px infections, antiviral and antibx to tx HIV and px opportunistic infections
GBS- Group B Strep Early onset disease
Must assess maternal status during labor admission, if unknown check protocol, Tx as + if any/all high risk infection situations
Tx Newborn GBS
Observation of all at risk infants
Blood cultures, CBC, possible urine culture, even spinal tap ALWAYS DONE FIRST BEFORE ANTIBX GIVEN
What is the antibiotic therapy for GBS?
Ampicillin, Gentamycin IV
Always check patent IV site because if it goes subQ it can cause tissue slough
Always check dose mg/kg/dose
Supportive care PRN
Pg woman are much greater risk of morbidity and mortality because their immune system is altered "asleep". Also have increased cardiac output and the decreased lung capacity increases their risk
Vaccination is recommended by AWHONN and it is safe in all trimesters and even when breast feeding
INHALED FLU VACCINE IS CONTRAINDICATED
Px of influenza in infants
Breastfeeding- IgA gives baby immunitys
Limit contact with potential infective sources, screen all contacts, appropriate cough and sneeze etiquette.
All contacts must wash hands for 20 seconds with warm water
Or alcohol based gel NOT watered down and Rub hands until its dry
Infant of Diabetic Mother IDM
Intrauterine environment of the A1 or A2 (both gestational) have possible hyperglycemia, no danger of vascular compromise therefore expect a LGA baby
Intrautering environment with Class B or C or D or R expect a SGA baby
If there is vascular involvement for IDM what are potential fetal effects?
SGA, because decreased placental blood flow causes IUGR. HTN occurs more often in DM mom and further compromises uteroplacental flow
IDM has higher risk of asphyxia and RDS. RDS occurs bc increased levels of insulin block the effect of cortisol on stimulation of surfactant production.
Hypocalcemia, and low mag levels
Polycythemia may occur as a response to chronic hypoxia in utero.
More likely admitted to NICU
Nursing Dx: PC Hypoglycemia
What other infants at risk for this? SGA, postterm, RDS, sepsis
S/s hypoglycemia in infant? lethargy, tremors, weakness
Whats the worst that can happen? death
How often should u monitor infants blood sugar?
Within the 1st hr after birth
Then q2h x 2
Then q4h x 2 if wnl
If BS less than 40-45 report to MD and verify with lab analysis
Feed baby if low BS, may need IV glucose to maintain glucose level balance and to prevent injury to the brain
Drug exposed infants
Denial is one of the hallmark signs of addiction so be alert to the s/s the infant may manifest
Maternal hx cues- late or no prenatal care, skips appointments, didnt gain enough weight, dishevelled appearance
s/s of drug exposed infants
difficult to console
rigid muscle tone
high pitched cry
difficult to feed
**** Assess with NAS (neonatal abstinence syndrome)
Look at handout scoring key
Tx drug exposed infants
Urine and Meconium drug screen
Social Service Consult
Possibly medications to wean infant from drugs (Methadone)
Swaddle infant to maintain flexion- do not over stimulate. Balance with need to attach to a loving caregiver
Cleft lip and palate (May not be revealed on US)
TEF Transesophageal Fistula
Neural Tube Defects
If you see a small defect such as a pilonidal dimple or FLK you should
keep looking for more types of defects and inform the MD
May do more "investigation" to r/o other anomalies
Oligohydramnios is associated with?
urogenital malformations, such as a kidney block
this causes probs with lung development
Congenital heart defects are
the leading cause of death from congenital anomalies
possible factors are:
Recognition and Tx of cardiac defects
ABGs or CBGs (capillary blood gasses)
May need corrective surgery
May need to be transferred to the NICU
VSD Ventral septal defect (5)
Most common type of congenital heart defect
Opening in the septum that may range from size of a pin to very large
Many small defects close spontaneously
When the pressure in the left ventricle increases after birth, oxygenated blood is shunted through a large ventricular septal defect into the right ventricle and recirculated to the lungs. (left-to-right shunt)
Increased pulmonary resistance may cause pulmonary HTN, hypertrophy of the right ventricle and heart failure. Surgery needed if large opening
PDA Patent Ductus Arteriosis (4)
Vessel joining pulmonary arteries to aorta.
If left open after birth= increased blood volume to lungs leads to pulmonary congestions, leads to increases o2 consumptions.
Premature infants are especially at risk
Symptoms vary to none to early CHF
Coarctation of the Aorta (2)
narrowing of the aorta near the ductus arteriosus
BP elevated in upper extremities- carotid, brachial and radial pulses are bounding and pulses in legs are weak or absent
Transposition of the great arteries (3)
Incompatible with life if another defect is not also present
Positions of the aorta and pulmonary artery are reversed. The aorta carries venous blood from the right ventricle back to the general circulation. The pulmonary artery returns oxygenated blood from the left ventricle to the lungs. Unless there is another sourve for mixing oxygenated and venous blood, the infant cannot survive.
A septal defect, open foramen ovale, or patent ductus arteriosis may be present. Prostaglandins may be given to keep the ductus open and surgical correction is performed.
an obstruction of blood flow from the left to right, or a defect that causes increased blood flow to the lungs occurs.
increases work of heart, increased pressure in lungs
Cyanotic defects (3)
blood flow to the lungs decreases or venous blood and oxygenated blood are mixed in the general systemic circulation or both. Decreasing the o2 carried to tissues resulting in cyanosis.
Right to left shunt
The presence of cyanosis depends on the severity and combination of defects and the childs ability to compensate, some babies may be pic, and some with acyanotic heart defects may be cyanotic.
cyanosis caused by mixing of oxygenated and unoxygenated blood (2)
will not improve with o2 therapy. cyanosis will increase with crying, feeding, or other activity.
Pallor, mottling, or gray color may be present in infants who do not have cyanosis
Tetralogy of Fallor - 4 characteristics
Ventricular septal defect
Aorta positioned over the ventricular defect
Hypertrophy of the right ventricle
High risk infants for ALL cardiac defects (5)
Mother had rubella while pg
Fetal alcohol syndrome
Cleft lip and Palate (4)
Associated with increased risk of other defects
Unilateral/bilateral, lip alone, palate alone, or both
Tx with corrective surgery
May be upsetting to family
EA esophageal atreasia and TEF tracheal esophageal fistula
5 variations of disease
-Most common is EA with distal TEF
Tx is corrective surgery
Increased risk for other anomalies
Infants 1st feeding- assess for patency
Early symptom excessive oral secretions, drooling
Omphalocele (base of cord) (4)
Herniation of intestine and liver into base of umbilical cord at 11-12 wks when the alimentation tract should have withdrawn back into the abdomen
20% will also have cardiac defects
Surgery needed, cover with sterile saline dressing
Should be diagnosed prenatally with US
Gastroschisis (abd wall defect) (3)
Herniation of bowel and other viscera through defect in abd wall
Freq associated with intestinal atresias. 40% born preterm, all have shortened intestines
No coverings on organs-need sterile saline dressing stat and corrective surgery
Herniation of abd organs into thorax related to defect in diaphragm
Mortality rate 50%
Left side 90% fetal compression causes hypoplasia of the lungs
Severe resp distress
state of progressive ventricular enlargement with increased volume of CSF- neural tube defect
surgical placement of shunt
Bulging fontanels, wide sutures, enlarged head
Head circumference would increase, compare to normal size heads and baseline head measurements
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