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Care of High Risk Newborn/Infants

Risk Newborns
1. Premature Babies – those born before the 38th week of gestation.
a. Terminologies
i. Small-for-gestational age (SGA) – birth weight is less than expected for the
specific gestational age. E.g. baby born on the 38th week of gestation who weighs
5lbs.
Risk Factors:
1. Adolescent pregnancy
2. Placental anomaly
3. Diabetes Mellitus
4. Pregnancy-induced-hypertension
5. Smokers
6. Alcoholic

ii. Appropriate-for-gestational age (AGA) – birth weight expected for the specific
gestational age. E.g. Baby born on the 34th week of gestation who weighs 5lbs.

iii. Large-for-gestational age (LGA) – birth weight more than expected for the specific
gestational age. E.g. Baby born on the 36th week of gestation who weighs 8lbs.
Risk Factors:
1. Diabetes mellitus
2. Multiparous
3. TOGA
4. Omphalocele

b. Characteristics:
i. Have underdeveloped subcutaneous tissues and less fat to act as insulator; thin
skinned.
Need: Place inside an incubator with temperature regulated to 33.3-34.4 C,
humidity of 55-65%; and frequent positioning on the right side to promote closure
of the foramen ovale.
ii. Poikilothermic (easily takes on temperature of environment). Temperature
stabilizes at a lower rate (35-36C).
Need: Take temperature by axilla to avoid crying.
iii. Physiologic weight loss is exaggerated.
iv. General activity is feeble and weak. (square sign = elbow passes the midline of the
body; square window wrist = wrist at a 90 angle; Recoil of extremities = less or
minimal)
v. Underdeveloped CNS centers for respiration.
Need: Oxygen inhalation.
Danger: O2 concentration should not exceed 40%; may lead to retrolental
fibrolasias = an overgrowth of retinal blood vessels causing blindness.
vi. High nutritional requirement – to maintain rapid growth appropriate for age.
(Required caloric intake as much as 200-220 cal/kg)
Need: Feeding done by OGT since premies have ineffective sucking not
coordinated with swallowing; plus minimal handling is necessary to conserve
energy.

c. Special Problems
i. Hyperbilirubinemia – because of the immaturity of the liver.
Management: Phototherapy – photooxidation by the use of artificial light in order
to convert bilirubin into excretable form.
ii. Infection – Premises are more susceptible due to general immaturity of the immune
system. Premies could not receive (they are born too early) the natural protection
given by mothers to their babies.
iii. Anemia – exaggerated of the physiologic anemia of full-term newborn – due to less
iron stores and smaller RBC mass.

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iv. Respiratory Distress Syndrome/Hyaline Membrane Disease
- due to lack of surfactant.
Pathophysiology:
Low pulmonary surfactant  increased surface tension  alveolar ventilation 
inadequate exchange of O2 & CO2  HYPOXIA  increased capillary
permeability, causing effusion from the pulmonary capillaries into the alveoli and
terminal bronchioles  HYALINE MEMBRANE found in the alveoli &
bronchioles  ATELECTASIS

Signs & Symptoms:


a. Expiration grunting (pathognomonic sign)
b. Increased RR
c. Flaring alae nasi
d. Cyanosis, retractions, rales
e. Respiartory acidosis
f. ABG: low pH level, low pO2 level, high pCO2

Management:
1. Monitor vital signs, ABG, skin color, muscle tone.
2. Proper positioning, NPO, IVF, OGT care.
3. Suction PRN.
4. O2 inhalation, high humidity, warmth
5. Sodium bicarbonate – for acidosis, CPAP
2. Postterm/Postmature Babies – born after the 42nd week of gestation.
a. Classic signs – “old man face” – evidence of intrauterine weight loss, dehydration, and
chronic hypoxia.
* Long and thin * Long nails, firm skull
* Cracked skin – loose, wrinkled, stained w/ greenish-yellow, no vernix nor lanugo.
* Wide-eyed alertness of a one-month old baby
*Hypoglycemia
b. Management: *Monitor V/S * IV as ordered

3. Neuromusculoskeletal Birth Injuries


a. Facial paralysis – asymmetry face due to damage to facial nerves from a difficult forceps
delivery; usually temporary, may disappear in a few days; no necessary treatment.
b. Erb-Duchenne paralysis (brachial paralysis) – caused by a difficult forceps or breech
extraction birth; treatment depends on severity of paralysis: Massage & exercise of arm to
prevent contractures, application of splints/braces as used in severe paralysis.
c. Dislocations and Fractures – diagnosed by crepitation, immobility, variations in ROM.
Treatment: Depends on site of fracture, may include application of swadling, splints,
slings, or casts and positioning.

4. Hemolytic Disease
a. Rh incompatibility - occurs when an Rh (-) woman is sensitized to an Rh (+) fetus,
develops antibodies against Rh (+) blood.
Consequences:
* Erythroblastosis fetalis – occurs in subsequent pregnancies when the antibodies are
transferred through the placental barrier to the fetus = agglutination and destruction of
RBC.
Prevention:
* RhoGAM (D antigen) immunization [Anti-Rh immunoglobulin] given to Rh (-) mother
on the 28th week of pregnancy & 72 hours after birth/abortion.
b. ABO incompatibility – occurs when the fetal blood type is A, B, or AB and the mother is
type O; mother’s anti-A or anti-B antibodies are transferred through the placental barrier to
the fetus, causing hemolysis = anemia, jaundice, & kernicterus; 1st pregnancy can be
affected.

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Manifestations:
1. Jaundice and increasing bilirubin levels during the 1st 24 hours
2. Lethargy or irritability
3. Poor feeding pattern
4. Hepatosplenomegaly
5. Signs of anemia
6. Signs of kernicterus:
a. (-) moro reflex, severe lethargy, apnea, high-pitched cry, assumption of
opisthotonus position, tremors, & seizures
Therapeutic interventions:
1. During pregnancy, amniotic fluid determinations are done; elevation readings warrant
either intrauterine transfusion or induction of labor, depending on AOG.
2. Phototherapy – in an attempt to reduce mild to moderate kernicterus.
3. Exchange transfusions – on severely affected infants to decrease antibody level &
increase infant’s RBCs & Hgb levels.

5. Cardiac Malformations
Classification:
a. Acyanotic – Shunt from left to right side of the heart.
- No abnormal communication between pulmonary & systemic circulation.
- If connection within the heart chambers exist, pressure forces blood from the
arterial (left) to the venous (right) side of the heart, where it is reoxygenated.

i. Ventricular Septal Defect (VSD)


- Abnormal opening between the two ventricles.
- High pressure in right ventricle causes hypertrophy; low harsh murmur
heard throughout systole;\
- Mortality Rate: >5%
Specific therapeutic intervention:
1. Closure of the opening at the septum.

ii. Atrial Septal Defect (ASD)


- Abnormal opening between the two arteries
- Murmur heard high on the chest with fixed splitting of the heart sound.
- Mortality rate: >1%
Specific therapeutic intervention:
1. Closure of the opening at the septum.

iii. Patent Ductus Arteriosus (PDA)


- Failure of the fetal connection between the aorta & pulmonary artery to
close.
- Shunting of blood  pulmonary hypertension  cardiomegaly.
- Machine type murmur heard throughout the heartbeat in the left 2nd to 3rd
interspace.

Specific therapeutic intervention:


1. Closure of the opening between aorta & pulmonary artery.

iv. Coarctation of the Aorta


- In utero, failure of the aorta to develop completely; with stricture below
level of the aortic arch.
- Increased systemic circulation above stricture: bounding radial & carotid
pulses, headache, dizziness, epistaxis.
- Decreased systemic circulation below stricture: absent femoral pulses, cool
lower extremities.
- Increased pressure in aorta above the defect: left ventricular hypertrophy.
Specific therapeutic intervention:
1. Resection of the defect and anastomosis of ends of aorta.

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v. Aortic Stenosis
- Narrowing of the aortic valve.
- Causes increased workload on the left ventricle, and the lowered pressure in
aorta reduces coronary artery flow.
Specific therapeutic intervention:
1. Division of the stenotic valves of the aorta.

vi. Pulmonary stenosis


- Narrowing of the pulmonic valve.
- Causes decreased blood flow to the lungs and increased pressure to the right
ventricle.
Specific therapeutic intervention:
1. Valvotomy or balloon angioplasty

b. Cyanotic – shunt from the right to left side of the heart.


- Abnormal connection between the pulmonary & systemic circulations.
- Venous (unoxygenated) blood enters systemic circulation.
- Polycythemia occurs as body compensate for inadequate supply of oxygen.
- Squatting or knee chest position is preferred because it decreases venous return by
constricting femoral veins, among other physiologic actions.

i. Tetralogy of Fallot (TOF)

* Four Associated Defects:


1. Pulmonary valve stenosis
2. Ventricular septal defect
3. Overriding of aorta, receiving blood from both ventricles, or an aorta
arising from the right ventricle.
Specific therapeutic intervention:
1. Blalock-Taussig procedure: subclavian artery to pulmonary artery anastomosis.
2. Complete Repair: Closure of ventricular septal defect and resection of the
infundibular stenosis.

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ii. Transposition of the Great Vessels (TOGA)
- Aorta arises from the right ventricle, and pulmonary artery arises from the
left ventricle (incompatible with life).
Specific therapeutic interventions:
1. Palliative treatment procedures performed to prevent pulmonary vascular
resistance and CHF until child is able to tolerate complete repair.
a. Rashkind procedure – enlargement of an existing atrial sepetal defect by
pulling a balloon through the defect during a cardiac catheterization.
b. Pulmonary artery banding – to decreased blood flow to lungs & increase
shunting of oxygenated blood intraventricularly of the aorta.
c. Pharmacologic dilation of Prostaglandin
d. Blalock-Hanlon operation: surgical creation of an ASD.
2. Complete repair
a. Rastell’s procedure: closure of VSD>
b. Mustard or Senning Procedure: removing an entire atrial septum &
creating a new atrial septum from existing pericardium.
c. Jatene operation: transposing the great vessels to the correct anatomic
placement with reimplantation of the coronary arteries.

iii. Tricuspid Atresia


- Absence of the tricuspid valve; (incompatible with life unless there is ASD,
VSD, or PDA.
Specific therapeutic intervention:
1. Palliative treatment procedure: same as for TOF
2. Complete repair: Modified Fontan procedure, conversion of the right atrium
into an outlet for the pulmonary artery.
iv. Truncus Arteriosus
- Single great vessel arising from the base of the heart, serving as a
pulmonary and aorta.
- Systolic murmur is heard with a loud second that is not split.
Specific therapeutic intervention:
1. Palliative: banding of pulmonary arteries to decrease blood flow to lungs.
2. Completer repair: Rastelli’s procedure – excising pulmonary arteries from
aorta & attaching them to the right ventricle by means of a prosthetic valve.

General Clinical Findings:


1. Dyspnea, especially on exertion.
2. Feeding diffculty & failure to thrive (often 1st sign)
3. Stridor or choking spells
4. HR more than 200, RR = 60
5. Recurrent respiratory tract infections.
6. In older children: poor physical development, delayed milestones, & decreased
exercise tolerance.
7. Cyanosis, squatting, clubbing of fingers & toes.
8. Heart murmurs
9. Excessive perspiration.

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6. Neurologic Malformations
a. Spina Bifida

- Malformation of the spine in which the posterior portion of the laminae of


the vertebrae fails to close; usually in the lumbosacral area.

Classification:
1. Spina bifida occulta – defect only of the vertebrae; spinal cord & meninges are intact.
2. Meningocele – meninges protrude through the vertebral defect.
3. Meningomyelocele – meninges & spinal cord protrude through the defect.

Clinical Findings:
1. Degree of neurologic dysfunction directly related to level of defect.
2. Defective nerve supply to bladder affects sphincter & muscle bone.
3. Frequently poor anal sphincter control

Treatment
1. Surgical repair of sac.

7. Gastrointestinal Malformations
a. Cleft lip – failure of median maxillary nasal process to fuse by 5-8 weeks of pregnancy.
- Cause: UNKNOWN
- Predisposing Factors:
1. Hereditary.
2. Maternal smoking

Chances of Having the Defect:


1. If history of either anomaly present in one parent = 4% chance that 1st infant will have
the defect.
2. If one infant is born with a cleft lip/palate but no hx of anomaly in family, then chance
of occurrence in next infant is 4%.
3. More common in males.

Clinical Findings:
1. Difficulty feeding because infant cannot form a vacuum with the mouth to suck.
2. Mouth breathing, resulting in increased swallowed air causing a distended abdomen.
3. Pressure against the diaphragm
4. Drying up of mucous membranes in oropharynx.

Treatment:
1. Surgical repair – Cheiloplasty (1-3 month)

Pre-op feeding technique:


1. Feed in an upright position.
2. Feed with a soft large-holed nipple or rubber tipped syringe.
3. Burp frequently.
4. Give water after each feeding for cleansing.
5. To prevent infection from irritation: restraint’s arm; provide pacifier.
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Post-op Care:
1. Maintain a patent airway.
2. Cleanse suture line to prevent crust formation & eventual scarring.
3. Prevent crying.
4. Place infant in supine position with arm or elbow restraints.
5. Feed
6. Logan bar – ½ strength H2O2 & saline solution

b. Cleft Palate – failure of the palate to fuse by 9-12 weeks of pregnancy.


- may involve the soft or hard palate & may extend into nose, forming an
oronasal passageway
- More common in females
Clinical Findings:
1. Infection, especially aspiration pneumonia.
2. Defective speech – nasal speech
3. Excessive dental caries
4. Malocclusion from displacement of maxillary arch
5. Eating difficulty

Treatment:
1. Surgical repair – Uranoplasty  done between 4-6 months

c. Tracheoesophageal Anomalies
Classification:
1. Absence of esophagus
2. Tracheoesophageal fistula – abnormal connection between the trachea & esophagus.
3. Atresia – failure of the esophagus to form a continuous passage from the pharynx to the
stomach during embryonic development.
a. Atresia of esophagus without tracheal fistula.
b. Proximal esophageal atresia combined with distal tracheoesophageal fistula.

Cause: UNKNOWN
Clinical Findings:
1. 3C’s: coughing, choking, & cyanosis
2. Excessive drooling
3. Excessive mucus in nasopharynx causing cyanosis, reversible by suctioning.
4. Choking, sneezing, & coughing during feeding, with regurgitation of formula through
mouth & nose.
5. Inability to pass a catheter in the stomach

Treatment:
1. Surgical repair – Fistula division & gastrostomy, esophageal anastomosis or colonic
transplant.

d. Intestinal Obstruction
Classification:
1. Mechanical: constricted or occluded lumen.
2. Muscular: Interference with normal muscular contraction.

Clinical Findings:
1. Abdominal distention
2. Absence of stools esp. meconium in the newborn (meconium ileus)
3. Vomiting of bile-stained material; may be projectile
4. Cyanosis & weak grunting respirations.
5. Paroxysmal pain.
6. Weak, thready pulse.

Treatment:
Surgical Repair
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e. Anorectal Anomalies (Imperforate Anus)
Classification:
1. Low anomalies
2. Intermediate anomalies
3. High anomalies

Clinical Findings:
1. Failure to pass meconium stool.
2. Inability to insert a thermometer, catheter or small finger into rectum.
3. Abdominal distention

Treatment:
1. Surgical correction; possible colostomy with multistaged surgical repair.

f. Pyloric Stenosis
- Congenital hypertrophy of muscular tissue of the pyloric sphincter, usually
asymptomatic until 2-4 weeks after birth.
- 5 times more common in males than females.

Characteristics:
1. Grossly enlarged circular muscle of pylorous.
2. Narrowed opening between stomach & duodenum.
3. Inflammation & edema that cause total obstruction.

Clinical Findings:
1. Vomiting, progressively projectile, non-bile stained vomitus.
2. Constipation
3. Dehydration & weight loss
4. Olive shape mass in the RUQ – pathog sign
5. Distention of the epigastrum
6. Vesible peristalsis

Treatment:
1. Surgical Repair – Fredet-Ramstedt procedure

g. Megacolon (Hirschsprung’s Disease)


- Absence of parasympathetic ganglion cells in a portion of the bowel, which
causes enlargement of the bowel proximal to the defect.
- 4 times more common in males than females.

Characteristics:
1. Length of involved bowel varies from only internal sphincter to entire colon.
2. Rectosigmoid colon involvement – most commonly affected

Clinical Findings:
1. Constipation of passage of ribbon-like or pellet-like stools.
2. Intestinal obstruction.
3. Abdominal distention.

Treatment:
1. Surgical repair

h. Diaphragmatic Hernia
- Failure of pleuroperitoneal cavity to close completely during embryonic
life.

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Characteristics:
1. Most of abdominal organs maybe found in the thorax.
2. Respirations are compromised by increased contents of thechest – interferes with
normal diaphragmatic breathing.

Clinical Findings:
1. Severe respiratory difficulty with cyanosis.
2. Relatively large chest, especially on affected side.
3. Failure of affected side to expand during respiration, absence of breath sounds.
4. Relatively small abdomen.

Treatment:
1. Respiratory support (upright position).
2. Surgical Repair
a. Diaphragmatic repair within 24 hours.

8. Substance Dependence (Neonatal Abstinence Syndrome)


- infant born with physiologic dependence on alcohol or drugs as a result of
maternal drug use and/or abuse.
- Common Drugs: Alcohol, Methadone, Heroin, Cocaine

Withdrawal Symptoms:
1. Hyperactivity
2. Shrill cry
3. Tremors
4. Sneezing
5. Yawning
6. Disturbed sleep
7. Seizures
8. Tachypnea
9. Drooling
10. Poor sucking reflex
11. Vomiting
12. Stuffy nose
13. Excoriated buttocks
14. Facial scratches

Signs:
1. Respiratory distress
2. Jaundice
3. Congenital anomalies
4. Behavioral alterations

Treatment:
1. Supportive Treatment

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