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144 terms

2155 #2 HR Newborn: Aquired and Congenital Conditions

STUDY
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Asphyxia
Insufficient O2 and excess CO2 in the blood and tissues
Bilirubin encephalopathy
Acute manifestation of bilirubin toxicity occurring in the first weeks after birth
erythroblastosis fetalis
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-
esophageal atresia
condition in which the esophagus is separated from the stomach and ends in a blind pouch
gastroschisis
protrusion of the intestines through a defect in the abdominal wall.

the intestines are not covered by a peritoneal sac or skin
hydrops fetalis
heart failure and generalized edema in the fetus secondary to severe anemia resulting from destruction of erythrocytes
meningocele
protrusion of the meninges through a defect in the vertebrae; a form of neural tube defect
myelomeningocele
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
omphalocele
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
spina bifida
defective closure of the bony spine that encloses the spinal cord

type of neural tube defect
tracheoesophageal fistula
abnormal connection between the esophagus and trachea
transient tachypnea of the newborn
condition of rapid respirations caused by inadequate absorption of fetal lung fluid
Maternal events that cause Asphyxia (6)
HTN
Abruption
prolapse cord
Uterine rupture
Infection
Drug use
In utero causes of asphyxia (3)
Abrupto placenta

Placenta previa

Post maturity
Fetal causes of asphyxia (4)
Cord problems

Infection

Premature birth

Multifetal gestation
Equipment needed for an asphyxia emergency (6)
Prepared warmer

o2 mask/bag

laryngoscope with working light

ET tube of different sizes

suctioning equiptment

blankets
Asphyxia: Hypoxic-Ischemic Encephalopathy (3)
seizures

decreased muscle tone and reflexes

50% die
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
Risk factors for TTN (3)
C/S birth

Breech birth

Precipitous birth
s/s TTN (3)
RR >60
can be 100-120

Do not give nipple feedings unless under 60 resps a minute
Dx/Tx of TTN (3)
Chest xray

supportive care

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
condition worsening
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
MAS results in
obstruction of the airways

chemical pneumonitis

air trapping
s/s MAS
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)
RDS
MAS
Persistent pulmonary HTN
Diaphragmatic Hernia
Sepsis
Life support w/ heart surgery
Nursing Dx for infants with Respiratory Disorders
Ineffective airway clearance
Ineffective thermoregulation
Ineffective breathing patterns

Risk for injury

Imbalanced nutrition less than body requirements
Risk for impaired parent-infant attachment
PC hypovolemia
PC hypoglycemia
Total serum bilirubin reaches 5-7
jaundice is visible in the face
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
Kernicterus
The chronic and permanent brain damage result of bilirubin toxicity
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)
Antigens trigger
antibody production in a healthy immune system
What is an antigen
anything that is foreign to the body

such as a germ
5 types of antibodies
IgG (crosses placenta)

IgA (breastmilk)

IgE (<1% allergies)
IgM (10% autoimmune)
IgD (<1% modifies IgG)
Which antibodies cross into the placenta?
IgG
What do antibodies do?
attack antigens
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
Type A blood
A antigen on RBC

B antibodies in plasma
Type B blood
B antigen on RBC

A antibodies in plasma
Type AB blood
A and B antigen on RBC

NO antibodies in plasma
Type O blood
NO antigens on RBC

A and B antibodies in plasma
Universal Donor
Type O
Universal Receiver
Type AB
Rh positive
has Rh antigen on RBC
Rh negative
does not have antigen on RBC
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
Mother Rh-
Fetus Rh+

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
RhoGAM indications
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
Antigen-antibody complexes destroyed by immune system leads to
Fetus anemia -> hypoxia
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)
Amniocentesis is performed to determine fetal Rh
to see if there is a need for Rhogam
Ultrasound is used to evaluate
fetus for edema, ascites and an enlarged heart
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
Reason to give Rhogam
Rh- mom with Rh+ baby and no sensitization
Reasons not to give Rhogam
Rh- mom with Rh- baby

Prior Rh+ sensitization
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
DAT
Direct antibody test
Notify MD if
positive Coombs test

Pathological Jaundice
Pathological Jaundice
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
phototherapy
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
Protect the eyes and genitals
because the light could cause burns
Home phototherapy
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
Exchange transfusion
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
Vertical infection
Infection is acquired in utero from Mom to Baby

Infections should be considered a teratogen
Horizontal infection
infection acquired after birth
TORCH test-
Toxoplasmosis, other, rubella, cytomegalovirus, herpes
Neonatal infections (4)
immune system is immature and untried

breastmilk supplies antibodies, some maternal antibodies are received thru placental transfer

Iatrogenic influences

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
Maternal effects with CMV
most are asymptomatic
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
Rubella
Viral transmission via droplets, direct contact with nasopharyngeal secretions or transplacental
Maternal effects of Rubella
Fever
General Malaise
Maculopapular rash that begins on face and migrates over the body and lasts 3 days
Lymph node enlargement
Headache
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)
Varicella-Zoster Virus
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
-IUGR
-Cataracts
-Microcephaly
-Skin scarring
How do you manage VZV with newborn?
STRICT ISOLATION
How do you prevent VZV?
Vaccination
-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
Hepatitis B
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)
HSV1 oral
HSV2 genital

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
HSV transmission
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)
HSV tx
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
HIV
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
s/s GBS in infant
Temp instability
Resp distress
Color change
feeding poorly
lethargy
tremors
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
Influenza
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
Handwashing

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.
Hyperbilirubinemia
PTL/birth
More likely admitted to NICU
What tests would you anticipate during pg with mom with diabetes?
Glucose levels
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
irritability
jitteriness
tremors
restless
difficult to console
rigid muscle tone
high pitched cry
difficult to feed
vomiting
diarrhea
SEIZURES
APNEA
**** 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)
Cocaine-neurotoxicity issue

Swaddle infant to maintain flexion- do not over stimulate. Balance with need to attach to a loving caregiver
Can we get a drug screen on the infant without moms consent?
Yes, meconium
Congenital Anomalies
Cardiac
Cleft lip and palate (May not be revealed on US)
Esophageal Atresia
TEF Transesophageal Fistula
Omphalocele
Gastroschisis
Diaphragmatic Hernia
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
Polyhydramnios is associated with?
GI and/or CNS malformations
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:
Genetics
Teratogens
Maternal Diabetes
Rubella
Recognition and Tx of cardiac defects
Neonatology consult
Cardiac consult
Chest Xray
Echocardiogram
CBC
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.
Acyanotic defects-
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
ASD Atrial septal defect
Incompetent or malformed foramen ovale
Tetralogy of Fallor - 4 characteristics
4 Characteristics:
Ventricular septal defect
Aorta positioned over the ventricular defect
Pulmonary Stenosis
Hypertrophy of the right ventricle
High risk infants for ALL cardiac defects (5)
IDM
Downs Syndrome
Mother had rubella while pg
Fetal alcohol syndrome
Genetics
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
Diaphragmatic Hernia
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
Stat evaluation/tx
Hydrocephalus
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
Folic acid
helps prevent neural tube defects