University of Saint Louis

Tuguegarao City, Philippines

SCHOOL OF HEALTH AND ALLIED

SCIENCES

MATERNAL AND CHILD

HEALTH NURSING
Prepared by: Jonalyn P. Santos, MSN
Lesson 7.
ACUTE CONDITIONS OF
THE NEWBORN
MECONIUM ASPIRATION
SYNDROME
• (MAS) is a respiratory distress in an
infant born through Meconium
stained amniotic fluid (MSAF) whose
symptoms cannot be otherwise
explained.
Incidence
• MSAF observed in (8-20)% of all births.
• MAS occurs in 5% of newborns delivered
through MSAF.
• It is a disease of Term or Post-term Infant.
Causes of MSAF
• The passage of meconium from the fetus into
amnion is prevented by lack of peristalsis(low
motilin level) , tonic contraction of the anal
sphincter, terminal cap of viscous meconium.
• Fetal maturation post term(high motilin level)
• Vagal stimulation by cord or head
compression in absence of fetal distress.
• In utero stress(hypoxia, acidosis)producing
relaxation of anal sphincter.
Risk Factors of MSAF
• Maternal HT
• Maternal DM
• Maternal heavy cigarette smoking
• Maternal chronic respiratory or Cardio
vasculardisease
• Post term pregnancy
• Pre-eclampsia/eclampsia
• Oligohydramnios
• IUGR
• Abnormal fetal HR pattern
Pathophysiology of MAS
• Mechanical Obstruction
• Thick and viscous meconium lead to
complete or partial airway obstruction.
• With onset of respiration – meconium
migrates from central to peripheral airways.
• Complete obstruction – atelectasis
• Partial obstruction –
• Ball-valve – air trapping.
• Risk of pneumothorax - 15 – 33%
Pathophysiology of MAS
• Chemical pneumonitis
• with distal progressing of meconium
chemical pneumonitis develop resulting
bronchiolar edema and narrowing of the
small airway.
• Surfactant inactivation
• Bilirubin, fatty acid, triglycerides,
cholesterol content of meconium inhibit
surfactant function and inactivation.
Pathophysiology of MAS
• Pulmonary hypertension
• meconium in lungs stimulate release of
proinflammatory cytokines and vasoactive
substance which cause pulmonary
vasoconstriction
• Also hypoxia, acidosis, and hyperinflation
contribute to pulmonary hypertension.
Clinical Features
• HISTORY
• Infants with MAS must have a history of MSAF.
• They often are Term or post-term
• IUGR.
• Many are depressed at birth.
Clinical Manifestations
• Evidence of postmaturity: peeling skin, long
fingernails, and decreased vernix.
• The vernix, umbilical cord, and nails may be
meconium-stained, depending upon how long
the infant has been exposed in utero.
• In general, nails will become stained after 6
hours and vernix after 12 to 14 hours of
exposure .
• Umbilical cord staining (thick-15min, thin-
1hour)
Meconium Stained Umbilical
Cord and Nails
Clinical Manifestations
• Affected patients typically have respiratory
distress with marked tachypnea and
cyanosis.
• Use of accessory muscles of respiration are
evidenced by intercostal and subcostal
retractions and abdominal (paradoxical)
breathing, often with grunting and nasal
flaring.
Clinical Manifestations
• The chest typically appears barrel-shaped,
with an increased anterior-posterior diameter
caused by overinflation.
• Auscultation reveals rales and rhonchi
immediately after birth.
• Some patients are asymptomatic at birth and
develop worsening signs of respiratory
distress as the meconium moves from the
large airways into the lower tracheobronchial
tree.
Barrel Chest
Diagnostic Examinations
• Arterial blood gas measurements typically
show hypoxemia and hypercarbia.
• Infants with pulmonary hypertension and
right-to-left shunting may have a gradient
in oxygenation between preductal and
postductal samples.
• Echocardiogram for evaluation of PPH.
Management: Prenatal
• Key management lies in prevention during
prenatal period.
• Identification of high risk pregnancies and
close monitoring.
• Pregnancy that continue past due date,
induction as early as 41 weeks may help
prevent meconium aspiration.
• If there is sign of fetal distress corrective
measure should be undertaken or infant
should be delivered in timely manner.
Management: Intrapartum
Management: Intrapartum
When the infant is not vigorous:
• Clear airways as quickly as possible.
• Free flow 02.
• Radiant warmer but drying and stimulation
should be delayed.
• Direct laryngoscopy with suction of the mouth
and hypopharynx under direct visualization,
followed by intubation and then suction directly
to the ET tube .
• The process is repeated until either ‘‘little
additional meconium is recovered, or until the
baby’s heart rate indicates that resuscitation
must proceed without delay’’.
Management: Postnatal
• Most of them do not require any
interventions besides close monitoring for RD.
• Most infants who develop symptoms will do
so in the first 12 hours of life.
• Approach to the ill newborns:
• Transfer to NICU.
• Monitor closely.
• Full range of respiratory support should be given.
• Sepsis w/up and ABx indicated.
Management: Postnatal
• Goals of Management:
• Increased oxygenation while minimizing
the barotrauma (may lead to air leak).
• Prevent pulmonary hypertension.
• Successful transition from intrauterine to
extrauterine life with a drop in pulmonary
arterial resistance and an increase in
pulmonary blood flow.
SUDDEN INFANT DEATH
SYNDROME
• Sudden infant death syndrome (SIDS) is the
sudden, unexplained death of an infant
younger than one year old.
• Some people call SIDS "crib death" because
many babies who die of SIDS are found in their
cribs.
• SIDS is the leading cause of death in children
between one month and one year old.
• Most SIDS deaths occur when babies are
between two months and four months old
Symptoms of SIDS
• Almost all SIDS deaths happen without any
warning or symptoms
• Death occurs when the infant is thought to
be sleeping
Etiology
• A combination of physical and sleep
environmentalfactors can make an infant
more vulnerable to SIDS.
• These factors may vary from child to child.
• Brain abnormalities
• Low birth weight
• Respiratory infection
Risk Factors
• Sleep environmental factors
• Sleeping on the stomach or side. Babies
who are placed on their stomachs or sides
to sleep may have more difficulty
breathing than those placed on their
backs.
Risk Factors
• Sleep environmental factors
• Sleeping on a soft surface. Lying face down
on a fluffy comforter or a waterbed can
block an infant's airway. Draping a blanket
over a baby's head also is risky.
Risk Factors
• Sleep environmental factors
• Sleeping with parents. While the risk of
SIDS is lowered if an infant sleeps in the
same room as his or her parents, the risk
increases if the baby sleeps in the same
bed — partly because there are more soft
surfaces to impair breathing.
Fetal Risk Factors
• Sex
• Age.
• Race.
• Family history
• Secondhand smoke
• Being premature
Maternal Risk Factors
• Is younger than 20
• Smokes cigarettes
• Uses drugs or alcohol
• Has inadequate prenatal care
HYPERBILIRUBINEMIA/
JAUNDICE
• Jaundice is the yellow
color of the skin and
sclerae caused by
deposits of bilirubin
Incidence
• Term : Occurs in 60%
• Preterm : 80% of preterm neonates
• Jaundice is the most common condition
that requires medical attention in
newborns.
Types of Bilirubin
Unconjugated Conjugated bilirubin
bilirubin (Direct )
(Indirect )
• Bind to albumen • Conjugated with
• Fat soluble glucoronic acid
• Can cross blood • Water soluble
brain barrier • Excreted in urine
• Toxic in high level to and stool
brain • Not toxic
Mechanisms of Neonatal
Jaundice
• Increased Bilirubin Load
• due to a high hemoglobin concentration.
• The normal newborn infant
• Hemolysis
• Cephalhematoma or bruising , Polycythemia
• Decreased Bilirubin Conjugation in the liver
• Decreased uridine glucuronyl transferase Activity
• Glucuronyl Transferase Deficiency Type 1 (Crigler
Najar Syndrome)
• Defective Bilirubin Excretion
Etiology
Physiological Jaundice
• Increased bilirubin
load
• Defective conjugation
• Increased entero-
hepatic circulation
• Incidence
• Term in 60%
• Preterm 80%
Breast Milk Jaundice
• It is caused by prolonged
increased enterohepatic
circulation of bilirubin.
• Bilirubin peaks at 10-15
days of age.
• The level of
unconjugated bil. is at
10-30 mg/dL
• If nursing is interrupted
for 24 hours, the
bilirubin level falls
quickly
Pathological Jaundice
• Appears age Appears within 24 hours of
age
• Increase of bilirubin > 5 mg / dl / day
• Serum bilirubin > 15 mg / dl
• Jaundice days Jaundice persisting after 14
days
• Stool clay / white colored and urine
staining yellow staining clothes
• Direct bilirubin > 2 mg / dl
Pathologic Jaundice: Types
• Unconjugated (Indirect) hyperbilirubinemia
• Hemolysis
• Rh , ABO and other blood group incompatibilities
• spherocytosis , elliptocytosis, Alpha thalassemia
• Sepsis ,DIC
• Hematomas
• Polycythemia
• Non hemolytic
• Breast milk jaundice
• Crigler-Najjar syndrome, types I and II
• Gilbert syndrome
Hemolytic Diseases of
Newborn
• It is an
isoimmunity
hemolysis
associated with
• Rh incompatibility
or
• ABO
Hemolytic Diseases of
Newborn: Rh Incompatibility
Hemolytic Diseases of
Newborn: ABO Incompatibility
• Mothers with type O blood may have
circulating antibodies of Ig G class to other
red cell antigens that can cross the
placenta and cause hemolytic disease in a
baby with a different blood type, such as
blood type A or B.
• The baby develop jaundice in the 1st day
of life
Hemolytic Diseases of
Newborn: ABO Incompatibility
Pathologic Jaundice: Types
• Conjugated (direct) hyperbilirubinemia
• Hepatic
• Idiopathic neonatal hepatitis
• Infections - TORCH, sepsis
• Inborn errors of metabolism
• Galactosemia
• Tyrosinemia
• Post hepatic
• Biliary atresia, choledochal cyst
Risk Factors
• J - jaundice within first 24 hrs of life or
premature
• A - a sibling who was jaundiced as neonate
• U - unrecognized hemolysis (ABO)
• N nursing – non-optimal sucking/nursing
• D - deficiency of G6PD , DRUGS , Ceftriaxone,
• I - infection
• C – Cephalhematoma /bruising
• E - East Asian/North Indian
Approach to Jaundice
Management
• Determine birth weight, gestation and
postnatal age
• Assess clinical condition (well or ill)
,degree of jaundice
• Decide whether jaundice is physiological
or pathological
• Look for evidence of kernicterus in deeply
jaundiced NB
Assessment of Jaundice
Assessment of Jaundice
• Measurement of
bilirubin by
jaundice meter
Diagnostic Examination
• Total & direct bilirubin
• Blood group and Rh for mother and baby
• Hematocrit, retic count and peripheral smear
• G6PD assay
• Coomb’s test
• Sepsis screen
• Liver and thyroid function
• TORCH titers
• Liver scan when conjugated hyperbilirubinemia
• Ultrasonography of the liver and bile ducts in
cholestatsis
Management
• Phototherapy
• intravenous immune globulin (IVIG)
• Exchange transfusion
• Drugs
Phototherapy
• Perform hand wash
• Place baby naked in cradle or incubator
• Fix eye shades
• Keep baby at least 45 cm from lights
• Start phototherapy
• Frequent extra breast feeding every 2 hourly
• Turn baby after each feed
• Temperature record 2 to 4 hourly
• Weight record- daily
• Monitor urine frequency
• Monitor bilirubin level
Phototherapy
Phototherapy
Side Effects:
• Increased insensible
water loss
• Loose stools
• Skin rash
• Bronze baby
syndrome
• Hyperthermia
• May result in
hypocalcemia
Intravenous Immunoglobulins
• IVIG in infants with Rh or ABO
isoimmunization can significantly reduce
the need for exchange transfusions.
• Now IVIG has replaced exchange
transfusion as the second-line treatment in
infants with isoimmune jaundice.
• 1 gm/kg/dose IV
Exchange Transfusion
HEMORRHAGIC DISEASE OF
NEWBORN
• Any haemorraghic manifestation due to
deficiency of vitamin K dependent clotting
factors is known as Haemorraghic disease
of newborn (HDN).
• Coagulation factors II, VII, IX, X and other
Gla-proteins ( protein C, protein S, protein
Z) also depend on the presence of vitamin K
for their activity.
Role of Vitamin K
• The following forms of vitamin K are known:
• K 1: Phylloquinone is predominantly found in green leafy
vegetables, vegetable oils, and dairy products. Vitamin K given to
neonates as a prophylactic agent is an aqueous, colloidal solution
of vitamin K 1.
• K 2: Menaquinone is synthesized by gut flora.
• K 3: Menadione is a synthetic, water soluble form.
• Vitamin K is an essential cofactor for γ-glutamyl
carboxylase enzymatic activity that catalyses the γ-
carboxylation of specific glutamic acid residues in a
subclass of proteins.
Role of Vitamin K
• New born babies are predisposed to
develop vitamin K deficiency.
• Minimal transplacental passage of vitamin K
• Limited hepatic storage of vitamin k in
newborn
• Low concentration of vitamin k in breast milk
• Absence of the bacterial intestinal flora
normally responsible for the synthesis of
vitamin K
Hemorrhagic Disease of
Newborn (HDN)
• Haemorrhagic disease of the newborn
resulting from severe transient deficiencies in
vitamin K–dependent factors is characterized
by bleeding that tends to be gastrointestinal,
nasal, subgleal, intracranial, or post-
circumcision.
• Classification:
• Early-HDN
• Classical-HDN
• Late-HDN
Early HDN
• Onset: 0-24 hr
• Incidence:Rare
• Site:Cephalohematoma, Subgaleal, Intracranial,
Gastrointestinal, Umbilicus, Intra-abdominal.
• Etiology:Maternal drugs (phenobarbital,
phenytoin, warfarin, rifampin, isoniazid) that
interfere with vitamin K.
• Risk factor:Inherited coagulopathy.
Classical HDN
• Onset: 2-7 days
• Incidence: ≈2% if infant not given vitamin
K.
• Site: Gastrointestinal, Ear-nose-throat-
mucosal, Intracranial, Circumcision,
Cutaneous, Injection sites.
• Etiology: Vitamin K deficiency, Breast-
feeding.
Late HDN
• Onset:1-6 mo
• Incidence:Dependent on primary disease.
• Site:Intracranial, Gastrointestinal, Cutaneous,
Ear-nose-throatmucosal, Injection sites,
Thoracic.
• Etiology:Cholestasis—malabsorption of vitamin
K (biliary atresia, cystic fibrosis, hepatitis)
• Risk factor:Abetalipoprotein deficiency,
Idiopathic in Asian breastfed infants,Warfarin
ingestion.
Clinical Presentation
• Gastrointestinal
haemorrhage
• Prolonged bleeding after
circumcision
• Epistaxis
• Ecchymosis (bruising)
• Intracranial haemorrhage
• Bleeding from umbilicus
• Cephalohematoma
Prevention
• Early-HDN: Administrations of vitamin K to
infant at birth or to mother (20 mg) before
birth.
• Classical-HDN: Parenteral vitamin K at
birth.
• Late-HDN: Parenteral and high-dose oral
vitamin K during periods of malabsorption
or cholestasis.
Management
• Intramuscular administration of 1 mg of
vitamin K at the time of birth prevents the
decrease in vitamin K–dependent factors in
full-term infants, but it is not uniformly
effective in the prophylaxis of haemorrhagic
disease of the newborn, particularly in breast-
fed and in premature infants.
• The disease may be effectively treated with a
slow intravenous infusion of 1-5 mg of vitamin
K1.
Management
• Serious bleeding, particularly in premature
infants or those with liver disease, may require a
transfusion of fresh frozen plasma or whole
blood.
• Hematomas, melena, and post-circumcision and
umbilical cord bleeding may be present; only 5-
35% of cases of factor VIII and IX deficiency
become clinically apparent in the newborn
period. Treatment of the rare congenital
deficiencies of coagulation factors requires fresh
frozen plasma or specificfactor replacement.
Questions?