Unit 5

HIGH RISK NEWBORN

Concept
High risk infant can be defined as any neonate, regardless of birth weight, size, or gestational
age, who has a greater than average chance of morbidity or mortality, specially within the
first 28 days of life.
Risk factors
Include preconceptual, prenatal, natal, or postnatal condition or circumstances that interfere
with the normal birth process or impede adjustment to extrauterine growth and development.
Predictable risk factor include
1) Low socioeconomic level of the mother, poor nutrition
2) Exposure to poor environment conditions such as toxic chemicals
3) Pre-existing maternal morbidity such as heart disease, diabetes
4) Obstetric factors such as age or parity, other premature births.
Goals
1) Perinatal prevention
2) Resuscitation and stabilization
3) Evaluate and manage
4) Monitoring and therapeutic modalities
5) Family-centered care
Aim of nursing care
1) To ensure a physiologically stable infant
2) To prepare the family who can provide the necessary care with appropriate support
services in the community.
Assessment
The average healthy new-born undergoes three predictable periods of responsiveness:
Initial assessment include
1) A period of reactivity: In the first 15-60 minutes after birth, the normal infant will be
highly responsive to many different stimuli. There is a lot sniffing, grimacing, sucking,
chewing, crying, hiccupping and trembling

2) A relatively unresponsive interval: The next 60 minutes are characterized by a lack of

responsiveness and a lower rate of metabolism although there may be a few spontaneous
jerks during sleep

3) A second period of reactivity: Between 2-6 hours, responsiveness returns and there may
be periods of rapid respiration, gagging and vomiting and the passing of meconium. New-
borns continue to be very responsive during this period.
Other assessment include
Clinical, transitional, behavioural, physical, reflexes.
Understanding these distinct periods of reactivity will help nurse with initial expectations. Early
identification and prompt management are imperative in treating new-borns with complications.
Medical conditions related to pregnancy such as PIH, PROM, infection etc. are to be explored and
prompt management to be done.
Principles

POSTMATURE INFANTS

MEANING

Baby born after 42 weeks AOG/ 294 days past 1st day of mother‘s LMP; regardless of birth
weight is referred to as postmature infants.

OTHER NAMES -Post term, post maturity, prolonged pregnancy, post datism

INCIDENCE

 7% (3.5 -15%) of all pregnancies

CAUSES

1) Unknown
2) History of >/= 1 previous post term pregnancies
3) Miscalculated due date (not sure of LMP)
4) Fetal Risk
 Progressive placental dysfunction ±placenta (supplies nutrient & oxygen) ages toward the end of
pregnancy ---may not function efficiently
 Amniotic fluid volume decreases, fetus may stop gaining weight/ weight loss§
 Decreased amniotic fluid may lead to cord compression during labour
 Increased risk of MAS and hypo-glycemia
 Increasing size (mainly length) & hardening of skull may contribute to CPD
 GRE ATEST RISK: during stresses of labor & delivery especially in infants of primi-
gravidas.

CHARACTERISTICS OF INFANTS
  Absent lanugo,
 Little if any vernix caseosa,
 Abundant scalp hair,
 Overgrown nails
 Dry, peeling skin (cracked, parchmentlike & desquamating
 Wasted physical appearance (reflects intrauterine deprivation)
 Minimal fat deposit (depleted subcutaneous fat) thin, elongated appearance
 Meconium staining - seen in skin folds w/ vernix caseosa
 Visible creases palms/ soles

DIAGNOSIS:

 Physical Examination
 Ultrasound Scanning
 Non -stress testing
 Estimate amniotic fluid volume

MANAGEMENT

 Check respiratory problems related to meconium

 Suctioning Blood test for hypoglycemia

NURSING MANAGEMENT

 Provide care individually according to each newborn’s needs.

 Observe signs and symptoms of respiratory distress.
 Take temperature.
 Monitor serum glucose.
 Observe signs and symptoms of hypoglycemia because of limited glycogen stores.
 Monitor serum calcium.
 If oral calcium is ordered, give the medication with enteral feeding because it may cause
gastric irritation.

 Post-Term Newborn – If calcium is ordered IV, monitor the heart rate during
administration, administer slowly, and stop it if bradycardia or arrhythmia occurs.
 Provide skin care, wash with non- alkaline soap or water only and allow skin to slough
naturally.

PREVENTION

 Accurate due date and Ultrasound Scanning

 Caesarean section/ induction of labor -recommended.

Infant of diabetic mother (IDM)

Definition
Any offspring of a gestational or insulin dependent diabetic woman
Diabetes- WHO –Classification:-
1. Type 1- insulin dependent
2. Type 2 – insulin resistance
3. Gestation Diabetes Mellitus***- Impaired Glucose Tolerance during pregnancy
4. other rare types of DM ( CF , drug-induced DM.)
• Women with diabetes mellitus during pregnancy (Type 1, Type 2, and gestational) are all at
increased risk for adverse pregnancy outcomes.
• Adequate glycaemic control before and during pregnancy is crucial for improving outcome.
• Most infants born to diabetic mothers are large for gestational age.
• If the diabetes is complicated by vascular disease, infants may have growth restriction, especially
those born after 37 wk gestation.
• The neonatal mortality rate is over 5 times that of infants of non diabetic mothers

INCIDENCE
 3% to 10% of pregnancies are complicated by abnormal glycemic control.
 Of these, 80% are caused by gestational diabetes mellitus

Problems of Infants of Diabetic Mothers

1. Birth trauma
2. Birth asphyxia
3. Hypoglycemia
4. Hypocalcemia
5. Hypomagnesemia
6. Hyperbilirubinemia
7. Surfactant deficiency, related respiratory distress syndrome (hyaline membrane disease)
8. Polycythemia
9. Renal vein thrombosis
10. Cardiac septal hypertrophy and cardiomyopathy
11. Congenital malformations
Diabetic mothers have a high incidence of;

1. polyhydramnios
2. preeclampsia
3. pyelonephritis
4. preterm labor
5. chronic hypertension
6. High fetal mortality rate at all gestational ages, especially after 32 wk

Pathophysiology of GDM

During pregnancy, insulin resistance is increased due to production of placental hormones that
antagonize insulin action. when insulin release is inadequate, hyperglycemia occurs (gestational
diabetes mellitus) and an excess amount of glucose is transferred via the placenta to the embryo.
Neither maternal nor embryo insulin crosses the placenta.

PATHOPHYSIOLOGY OG IDM
 Effects of poor glycemic control in pregnant diabetic women

CLINICAL MANIFESTATIONS
• Infants tend to be large and plump as a result of increased body fat and big viscera.
• They have puffy, plethoric facies.
• These infants if delivered before term or the mother had associated vascular disease, then
may have normal or low birth-weight.

 Hypoglycemia
• Develops in 25–50% of infants of diabetic mothers
• Occurs in 15–25% of infants of gestational diabetes mothers, and only small percentage of
these infants become symptomatic.
• The nadir in an infant's blood glucose concentration is usually reached between 1 - 3 hr after
birth; and spontaneous recovery may begin by 4–6 hr after birth.
• The infants tend to be jumpy, tremulous, and hyper-excitable during the 1st 3 days of life,
although hypotonia, lethargy, and poor sucking may also occur.

 Tachypnea
• Develops in many infants of diabetic mothers during the 1st 2 days of life.
• Infants of diabetic mothers have a higher incidence of respiratory distress syndrome may be
related to the antagonistic effect of insulin on stimulation of surfactant synthesis by cortisol.

Cardiomegaly
• Cardiomegaly is common in 30% of IDM
• Heart failure occurs in 5–10% of infants of diabetic mothers.
• Congenital heart disease is more common in infants of diabetic mothers.
• Asymmetric septal hypertrophy may occur, and inotropic agents worsen the obstruction and
so are contraindicated.

Birth trauma is also a common sequel of fetal macrosomia.

Neurologic development and ossification centers tend to be immature and correlate with brain
size (which is not increased) and gestational age rather than total body weight.
Hyperbilirubinemia, polycythemia, and renal vein thrombosis; are increased, and the incidence
of the latter should be suspected in infants with a flank mass, hematuria, and thrombocytopenia.

Congenital anomalies
• The incidence is 3X in infants of diabetic mothers;
• cardiac malformations (VSD, ASD, TGA, coarctation of the aorta, others)
• lumbosacral agenesis are most common.
• neural tube defects
• hydronephrosis, other renal anomalies.

TREATMENT:

1. Prenatal evaluation of all pregnant women with overt or gestational diabetes, and
planning the delivery in hospitals where expert obstetric and pediatric care is available.
2. Preconception glucose control reduces the risk of anomalies and other adverse outcomes,
and glucose control during labor reduces the incidence of neonatal hypoglycemia.
3. Regardless of size, all infants of diabetic mothers should initially receive intensive care.
4. Hypoglycemia is defined; plasma glucose of 30 to 45 mg/dl (25 to 40 mg/dl in whole blood)
in term infants.
5. The best treatment of mild, transient neonatal hypoglycemia is early feeding, whether the
neonate is an IDM or not.
6. A plasma or blood glucose level of less than 20 or 25 mg/dl, respectively, requires
intravenous glucose administration unless the infant readily takes a good feeding and
remains normoglycemic.
7. Asymptomatic infants should have a blood glucose determination within 1 hr of birth and
then every hour for the next 6–8 hr;
8. If clinically well and normoglycemic, oral or gavage feeding with breast milk or formula
should be started as soon as possible and continued at 3 hr intervals. If any question
arises about an infant's ability to tolerate oral feeding, the feeding should be discontinued
and glucose is given by peripheral intravenous infusion at a rate of 4–8 mg/kg/min.
9. Hypoglycemia should be treated, even in asymptomatic infants, by frequent feeding
and/or intravenous infusion of glucose.  Bolus injections of hypertonic glucose should be
avoided because they may cause further hyperinsulinemia and potentially produce
rebound hypoglycemia

Substance use mothers

Overview
The fetus grows and develops due to the nourishment from the mother via the placenta. Along with
nutrients, any toxins in the mother's system may be delivered to the fetus. These toxins often cause
damage to the fragile, developing fetal organs. Depending on the organs affected, long-term
effects may be severe, including mental problems such as retardation and seizures.

Maternal substance use may consist of any combination of drug, chemical, alcohol, and tobacco use during
the pregnancy.

While in the womb, a fetus grows and develops due to nourishment from the mother via the placenta.
However, along with nutrients, any toxins in the mother's system may be delivered to the fetus. These toxins
may cause damage to the developing fetal organs. A baby also may become dependent on substances used
by the mother.

SIGNS AND SYMPTOMS

Babies born to substance-using mothers may have short- or long-term effects.

 Short-term withdrawal symptoms may consist only of mild fussiness.

 More severe symptoms may include irritable or jittery behavior, feeding problems, and diarrhea.
Symptoms vary depending on which substances were used.

 The diagnosis for babies with signs of withdrawal may be confirmed with drug tests of the baby's urine
or stool. The mother's urine will also be tested. However, if urine or stool is not collected soon enough,
the results may be negative. A sample of the umbilical cord may be tested.

More significant long-term developmental problems may be seen in babies who are born
with growth failure or various organ problems.

 Infants born to mothers who drink alcohol, even in modest amounts, are at risk for fetal
alcohol syndrome (FAS). This condition consists of growth problems, unusual facial
features, and intellectual disability. It may not be detected at the time of birth.
 Other drugs may cause birth defects involving the heart, brain, bowel, or kidneys.

 Babies who have been exposed to drugs, alcohol, or tobacco are at higher risk for SIDS
(sudden infant death syndrome).

TREATMENT FOR AN INFANT OF A SUBSTANCE-USING MOTHER

The baby's treatment will depend on the drugs the mother used. Treatment may involve:

 Limiting noise and bright lights

 Maximizing "TLC" (tender loving care) including skin-to-skin care and breastfeeding
with mothers who are in treatment/no longer using illicit substances (including
marijuana)

 Using medicines (in some cases)

In the case of babies whose mothers used narcotics, the baby is most often given small doses
of a narcotic at first. The amount is slowly adjusted as the baby is weaned off of the
substance over days to weeks. Sedatives are sometimes used as well.

Infants with organ damage, birth defects or developmental issues may need medical or
surgical therapy and long-term therapies.

These infants are more likely to grow up in homes that do not promote healthy emotional,
social, and mental development. They and their families will benefit from long-term support.

Alternative Names:--- IUDE; Intrauterine drug exposure; Maternal drug abuse; Maternal substance use;
Maternal drug use; Narcotic exposure - infant; Substance use disorder - infant
Respiratory conditions
ASPHYXIA NEONATORUM
Definition

Asphyxia neonatorum is a condition that occurs when a baby doesn’t get enough oxygen during the
birth process. It can be fatal. Another more common name for it is perinatal asphyxia,
or birth asphyxia.Hypoxic-ischemic encephalopathy may be a result of severe asphyxia neonatorum.
Incidence
The frequency of perinatal asphyxia is approximately 1% to 5 %of live birth in the western
countries.
Etiology
a) Factors that increase the risk of perinatal asphyxia include the following
i) Impairment of maternal oxygenation

ii) Decreased blood flow from mother to placenta

iii) Decreased blood flow from placenta to fetus
iv) Impaired gas exchange across the placenta or at the Fetal tissue level
v) Increased Fetal O2 requirement

b) Etiologies of perinatal hypoxia- ischemia include the following

i) Maternal factors: hypertension, infection, diabetes, hypotension

ii) Placenta; factors: infarction, fibrosis, abruption, hydrops
iii) Uterine rupture
iv) Umbilical cord accidents: prolapsed, compression
v) Abnormalities of umbilical vessels
vi) Fetal factors: anemia, infection, cardiomyopathy

Pathophysiology
Baby fails to initiate and maintain respiration

leads to hypoventilation, aerobic to anaerobic metabolism, glycolysis and lactic acidosis

baby fails to cry, an attempt is made to breath, but there is primary gasps and subsequent raise in heartbeat
and blood pressure

after 1 minute there is primary apnea.

If there is no resuscitation, there will be secondary gasps, a flat heartbeat and a rapid drop in blood pressure
and in 5 to 8 minutes slight brain damage begins.
 There will be long gasps and long apneas and the baby will be acidotic due to low levels of pH in the blood,
hypoxia and hypercapnia.

Brain damage becomes more severe,

There is cerebral edema and rupture of small blood vessels resulting in cerebral hemorrhage.

There is ischemia of brain cells resulting in severe brain damage.

(Signs are convulsions, inability to suck, baby is more flaccid, cerebral palsy)

Death results of failure to resuscitate.

SYMPTOMS
1.Skin that appears pale or blue
2.Difficulty breathing, which may cause symptoms such as nasal flaring or abdominal breathing
3.A slow heart rate
4.Weak muscle tone

DIAGNOSTIC EVALUATION

a) Perinatal assessment of risk: includes awareness of pre-existing maternal or fetal problems that may
predispose to perinatal asphyxia and of changing placental and fetal conditions ascertained by USG,

biophysical profile, nonstress test

b) Clinical presentations: can be variable. Common clinical scenarios include a postdates infant With asphyxia,
meconium aspiration, pulmonary hypertension, pneumothorax or birth trauma

c) Low apgar score: apgar score <3>5 minutes

d) Umbilical cord or first blood gas determination

MANAGEMENTA.

A. PERINATAL MANAGEMENT OF HIGHRISK PREGNANCIES

 Fetal HR rhythm abnormalities may provide supporting evidence of asphyxia, especially if
accompanied by presence of thick meconium
 Measurement of fetal scalp pH is a better determinant of fetal oxygenation than Po2
 Close monitoring of progress of labor with awareness of other sign of in utero stress.
 B. DELIV ER Y R OOM MANAGEM ENT
i) A=Establish open airway: Suctioning, if necessary endotracheal intubation
ii) B= Breathing: Through tactile stimulation, PPV, bag and mask, or through endo tracheal
tube
iii. C= Circulation: Through chest compressions and medications if needed
iv) D= Drugs: Adrenaline .01 of .1 solution
v) Hypothermia treatment to reduce the extent of brain injury
vi) Epinephrine 1:1000 (0.1-0.3ml/kg) IV
vii) Saline solution for hypovolemia

C. POSTNATAL MANAGEMENT OF NEUROLOGIC EFFECTS OF ASPHYXIA

 Ventilation: CO2 should be maintained in the normal range. Hypercapnia can cause cerebral
acidosis and cerebral vasodilation
 Oxygenation: Oxygen levels should be maintained in the normal range,although poor
peripheral perfusion may limit the accuracy of continuous non invasive monitoring
 Temperature: should be maintained in the normal range and hyperthermia should
be avoided
 Maintain physiologic metabolic state
i. Hypocalcaemia is a common metabolic alteration after neonatal asphyxia. It is
important to maintain calcium in the normal range
ii. Hypoglycaemia is often seen in asphyxiated infants: blood glucose level should be
maintained in the normal range for term infants
iii. Judicious fluid management: I s needed and fluid over load should be avoided
iv. Control of seizures: use anticonvulsants

D. MANAGEMENT OF OTHER TARGET ORGAN INJURY

E.
 Cardiac dysfunction should be managed with correction of hypoxemia, acidosis and
hypoglycaemia and avoidance of fluid over load
 Arterial BP should be maintained
 CVP should be monitored
 Renal function should be monitored
 Feeding should be withheld until good bowel sounds are heard and stools are negative for
blood
NURSING ASSESSMENT AND DIAGNOSIS
i) Communication between the obstetric office or clinic and the birthing area helps the
birthing area nurse identify new-borns who may need resuscitation.
ii) When the woman arrives in the birthing area, have the antepartal record ready.
iii. Note any contributory perinatal history factors and assess present fetal status.
iv. As labor progresses, continue ongoing monitoring of fetal heartbeat and its response to
contractions, assist with fetal scalp blood sampling, and observe for the presence of
meconium in the amniotic fluid to assess for fetal asphyxia.
v. Alert the resuscitation team and the pracitioner responsible for the newborn’s care of any
potential high-risk laboring women.
PLANNING AND IMPLEMENTATION
Hospital-Based Nursing Care
i)In the high-risk nursery, resuscitation may be needed at any time. Check and maintain equipment to
ensure its reliability at all times. Inspect all equipment, bag and mask, oxygen and flow meter,
laryngoscope, and suction machine for damaged or non-functioning parts before a birth or when setting up
an admission bed. Sterilize resuscitative equipment in the birthing room after each use
ii) A systematic check of the emergency cart and equipment is a routine responsibility of each shift. It is a
good idea to be prepared by assembling equipment for pH and blood gas determination.
iii)During resuscitation it is essential to keep the new born warm. Dry the new born quickly with warmed
towels or blankets to prevent evaporative heat loss, remove the wet blankets, and place him or her under
the radiant warmer
iv. This device provides an overhead radiant heat source (a thermostatic mechanism taped to the infant’s
abdomen triggers the radiant warmer to turn on or off to maintain consistent temperature). Set the servo
control at 36.5 C(97.7 F). Cover the newborn’s head with a hat as the head is a major source of heat
loss
v. ) An open bed is necessary for easy access to the new born. Training and knowledge about
resuscitation are vital to personnel in the birth setting for both normal and at-risk births. Since
resuscitation must be a two-person effort for high-risk new borns, call for additional support as needed.

vi. One member must have the skill to perform airway management and ventilation. Record resuscitative
efforts on the newborn’s chart so that all members of the healthcare team have access to the information.
Parent Teaching
i)The new CPR guidelines favor family members being present during resuscitation in the birthing room
and in the neonatal intensive care unit (NICU), but the procedure is particularly distressing for parents.
ii) Advise parents that a support person will be available for them if resuscitation is necessary
.iii) As soon as the infant’s condition has stabilized, a member of the interdisciplinary team needs to discuss
the newborn’s condition with the parents.
iv) The parents may have many fears about the reasons for resuscitation and the condition of their baby
after resuscitation.
EVALUATION
Expected outcomes of nursing care include the following:
i)The new born requiring resuscitation is promptly identified, and intervention is started early
.ii) The newborn’s metabolic and physiologic processes are stabilized, and recovery is proceeding without
complications.
iii)The parents can verbalize the reason for resuscitation and what was done to resuscitate their new born.
iv)The parents can verbalize their fears about the resuscitation process and potential implications for their
baby’s future.
Nursing diagnoses that may apply to the new born with asphyxia and the newborn’s parents include
the following
:1. Ineffective Breathing Pattern related to lack of spontaneous respirations at birth secondary to in utero
asphyxia
2. Decreased Cardiac Output related to impaired oxygenation
3. Ineffective Family Coping: Compromised related to baby’s lack of spontaneous respirations at birth and
fear of losing their new born

Neonatal apnoea
Definition
Neonatal apnea happens when a new born baby pauses while breathing. These pauses can stop their
breathing for 10 to 15 seconds or longer. The baby also has a rapid heart rate and a bluish tint to their skin.
This is one of the more common conditions diagnosed in the neonatal intensive care units of hospitals. It's
unclear whether neonatal apnea, even when it goes away and comes back, is harmful to the baby. Often, it's
just a matter of the child developing their ability to control their breathing.
Neonatal Apnea :- Preterm infants respond to a fall in inspired oxygen with a transient hyperventilation
followed by hypoventilation and sometimes apnea.

Incidence
• As many as 25% of all preterm infants who weigh <1800 g (34 Week) have at least one apneic
episode. Essentially all infants <28 Week have apnea.
Types of neonatal apnea
The three main types of neonatal apnea include:
1. Central apnea - there's no signal going from the brain to the baby's diaphragm to make their lungs
breathe.
2. Obstructive apnea - this can happen when the baby's pharynx collapses or when certain lung
muscles are too weak.
3. Mixed apnea - a mixture of central and obstructive apnea.

Causes of neonatal apnea

Causes of neonatal apnea may include:

1. Premature birth
2. Heart or blood vessel problems
3. Immature nervous system
4. Bleeding or tissue damage in the brain
5. Respiratory disease
6. CNS: (Abnormality, Encephalitis, Meningitidis, ICH,)
7. Upper & lower Air way: (choanal A., congestion, RDS, pneumonia,)
8. Cardiovascular: (Malformation, hypotension, hypertension,)
9. Digestive system:(GER, NEC, Distention,)
 10. Other:(Sepsis, Anemia, Hypothermia, Hyperthermia, pain, metabolic disorder,)

Risk factors for neonatal apnea

The most common cause of neonatal apnea is premature birth. Other risk factors that contribute to neonatal
apnea include:
1. Infections
2. Poor temperature regulation
3. Mothers who are exposed to certain drugs before their babies are born
4. Other conditions like labored breathing or problems with heart functioning
Symptoms of neonatal apnea
Symptoms of neonatal apnea include:
1. Periods of absent breathing for 20 seconds or more
2. Rapid heartbeat
3. Blue coloring around the lips or nose
4. Severe decrease in heart rate (bradycardia)
Diagnosis of neonatal apnea
Once the baby shows symptoms, the doctor will try to determine the underlying cause. Diagnostic
procedures may include:
1. Blood tests - these are done to check for blood counts, electrolyte levels, and infection.
2. Measurement of the levels of oxygen - the doctor will measure the amount of oxygen in the baby's
body during an apnea episode.
3. Apnea study - a machine known as an "apnea monitor" can work as an alarm for any abnormal
breathing patterns.
Treatments for neonatal apnea
Doctors first try to treat any underlying conditions that cause neonatal apnea. They often use a medicine
called caffeine citrate. This drug relaxes smooth muscles, such as lungs. It also stimulates the baby's
central nervous system and cardiac muscles to create breathing.

Other treatment options include:

Gently running the baby's feet during mild and intermittent breathing episodes
Positioning the baby to ensure their head and neck are in neutral positions so breathing is easier
Using suction to open the baby's airways. If this isn't effective, the baby may need to use a machine that
puts air into their lungs until they breathe again
If these treatments don't work, doctors can use a high-flow nasal cannula. This device puts air through the
baby's nostrils. A doctor may opt for a mechanical ventilation machine to breathe for the baby in more
extreme cases.
Apneic Spells
Cessation of airflow for at least 20 seconds or accompanied by bradycardia or cyanosis. Bradycardia and
cyanosis are usually present after 20 sec. of apnea. After 30 to 45 sec., pallor and hypotonia are seen, and
infant may be unresponsive to tactile stimulation.
Apnea is Associated with Many Clinical Conditions:
1. Intraventricular bleed
: - may see hypoventilation, apnea or respiratory arrest
• Subtle seizures
: - along with fluttering eyelids, drooling or sucking, tonic posturing
• Sepsis
Bacterial (GBS, staph. Proteus, Listeria, Coliforms
Viral (RSV, paraflu, herpes, CMV
Chlamydial
NEC
2. Congestive Heart Failure
• PDA and CHD
• Due to decreased lung compliance
• Respiratory muscle fatigue
• Chest wall distortion
• Hypoxemia

Respiratory Distress Syndrome

 Due to atelectasis, increase work of breathing, fatigue
 May lead to chronic lung disease
Anemia
• oxygen carrying capacity of blood decreases
• Arterial pressure perfusing CNS decreases
Polycythemia
• Increase blood viscosity and decrease blood flow to CNS
• begins at 2-4 hours of age
 High temperature of environment
 Feeding problems
• overdistention of stomach
• aspiration
• GER (gastroesphogeal reflux) with or without aspirations
• due to laryngospasm
• stimulation of irritant receptors in lower esophagus causing ‘reflux apnea’
• some reflux is common (laundry issue only?)
  Metabolic conditions
• Hypoglycemia
• Hypocalcemia
• Hypernatremia
• Alkalosis

 Others
• Myelomeningocele
• Meningitis

Periodic Breathing
• Recurrent sequences of pauses in respiration lasting for 5-10 seconds and followed by 10-15
seconds of rapid respiration.

Monitoring
• All preterm infants below 35 WG must be monitored for at least the first week after birth.
Monitoring should continue until no significant apneic episode has been detected for at least 5
days.
• Because impedance apnea monitors may not distinguish respiratory efforts during airway
obstruction from normal breaths, heart rate should be monitored in addition to, or instead of,
respiration.
• BP should be measured frequently and hypotension with oliguria< 2 mL/kg/h should be treated
accordingly
• Hct should be> 45%

Care of the infants

1. Prevent hyperflexion of the neck
2. Nurse the baby in prone position
3. Set the thermal environment to obtain a central temperature of 36.5-37⁰ C
4. Minimize the duration and rate of pharyngeal suction
5. Place the orogastric tube carefully
6. Avoid sudden gastric distension
7. Continuous gastric feeding if apnea occurs with gavage
8. Warm air and oxygen to incubator temperature
Nursing Management During Apneic Episode
1. Check infant at once
2. Cancel alarm
3. Stimulate if there is no obvious vomit
4. Suction
5. Give O2 via face mask in same concentration as infant had been receiving
6. Summon help if infant does not respond
7. Document and report
8. Intubation if indicated
Management of Idiopathic Apnea
• When apneic spells are repeated and prolonged, (i.e., more than 2 to 3 times/h.) or when they
require frequent bag and mask ventilation, treatment should be initiated.
• Diagnosis and treatment of specific causes
• Nursing care • Nasal CPAP (4-6 cm H2O)
• Methylxanthine therapy
• Increased environmental O2 only as necessary to maintain adequate baseline O2 saturation.
Often associated with treatment of anemia
• Assisted ventilation if all else fails

A. General measures
1. Diagnosis and treatment of specific causes
2. SO2 : 85-95%
3. Avoid reflexes that may trigger apnea. Suctioning of the pharynx should be done carefully,
and oral feeding should be avoided.
4. Position of extreme flexion or extension of the neck should be avoided, to reduce the
likelihood of airway obstruction.
5. Avoid swings in environmental temperature.
6. Consider a transfusions of PRBCs if the Hct is <25% and the infant has episodes of apnea and
bradycardia that are frequent or severe while methylxanthine levels are therapeutic.

B. Nasal CPAP (4-6 cm H2O) can reduce the number of mixed and obstructive apneic spells.
C. Methylxanthine (caffeine of theophylline) therapy, commencing with a loading dose followed
by maintenance therapy, and serum level monitoring, especially for theophylline.
D. Assisted ventilation if all else fails

Meconium aspiration syndrome

INCIDENCE
a. Meconium-stained amniotic fluid (MSAF) complicates delivery in approximately 8% to 15%
of live birth.
b. The incidence of MSAF in preterm infant is very low .
c. Most babies with MSAF are 37 weeks or older and most meconium-stained infants are post
mature and small for gestational age.
d. Approximately 5% of neonates born through MSAF develop meconium aspiration syndrome
(MAS).
e. MSAF is associated with an increased risk of respiratory disorder and approximately 50% of
these infants require mechanical ventilation
CAUSES
i) Acute or chronic hypoxia
ii) Infection: can result in the passage of meconium in utero.
iii) In this setting gasping by the fetus or newly born infant can cause aspiration of amniotic fluid
contaminated by meconium.
iv) Meconium aspiration before or during birth can obstruct airways interfere with gas exchange
and cause severe respiratory distress

PATHOPHYSIOLOGY
 Meconium in the lungs

a ball-valve action (air is allowed in but not exhaled)

alveoli over distend and rupture

pulmonary air leaks (pneumomediastinum or pneumothorax)

meconium triggers a chemical pneumonitis

oxygen and carbon dioxide trapping

lungs to hyper inflate

CLASSIFICATION OF RESPIRATORY DISEASE

1.Mild MAS is a disease requiring <40% oxygen for <48 hours.
2. Moderate MAS is a disease requiring >40% oxygen for >48 hours without air leak.
3. Severe MAS is a disease requiring assisted ventilation for >48 hours, often
associated with PPHN.

CLINICAL MANIFESTATION
1) Fetal hypoxia: in utero a few days or a few minutes before birth, indicated by a sudden increase
in fetal activity followed by diminished activity, slowing of FHR or weak and irregular
heartbeat, loss of beat-to-beat variability, and meconium staining of amniotic fluid

2)Signs of distress at birth: such as pallor, cyanosis, apnea, slow heart-beat, and low Apgar
scores (below 6) at 1 and 5 minutes. New borns with intrauterine asphyxia, meconium-
stained new borns, or new borns that have aspirated meconium are depressed at birth and
require resuscitation to establish adequate respiratory effort

PREVENTION OF MAS
1) Prevention of passage of meconium in utero: Mothers at risk for uteroplacental insufficiency
include those with preeclampsia or increased blood pressure, chronic respiratory or cardiovascular
disease, poor uterine growth post-term pregnancy and heavy smokers. These women should be
carefully monitored during pregnancy. During labor the fetal heart rate should be monitored, with
fetal scalp blood samples obtained for PH determination when indicated.
2) Amnioinfusion: The use of amnioinfusion in women whose labor is complicated by MSAF does
not reduce neonatal morbidity related to meconium aspiration although the technique effectively
treats repetitive variable fetal heart rate decelerations by relieving umbilical cord compression in
labor. A large randomized trial of amnioinfusion for women with thick meconium-stained fluid with
or without variable fetal heart rate decleration showed no reduction of the risk of moderate or severe
MAS perinatal death, or caesarean delivery. How ever the study did not have adequate power to
determine definitively if amnioinfusion may benefit the group with variable decelerations.
3) Timing and mode of delivery: In pregnancies that continue past the due date, induction as early
as 41 weeks may help prevent MAS by avoiding passage of meconium. Delivery mode does not
appear to significantly impact the risk of aspiration.

MANAGEMENT OF INFANTS DELIVERED THROUGH MECONIUM-

STAINED FLUID
Oro-pharyngeal and nasopharyngeal suctioning on the perineum and routine tracheal intubation and
aspiration of meconium in vigorous infants are not effective in preventing MAS. Infants should be
assessed and intervention reserved for infants who are depressed or have respiratory distress.
A. Initial assessment: At a delivery complicated by MSAF the clinician should determine whether
the infant is vigorous, demonstrated by heart rate >100 beats per minute spontaneous and good tone
(spontaneous movement or some degree of flexion) The infant will be depressed approximately
20% to30% of the time.
1. If the infant appears vigorous routine care should be provided regardless of the consistency
of the meconium.
2. If respiratory distress develops or the infant becomes depressed the trachea should be
incubated under direct laryngoscopy and intra tracheal suctioning performed. Visualization of the
cords without suctioning is not adequate because significant meconium may be present below the
cords.
3. In questionable cases it is safer to incubate and suction as MAS can occur in infants
delivered through thinily stained amniotic fluid.
B. Suctioning technique
1.The infant should be placed on a radiant warmer and given free-flow oxygen.
2. Delay drying and stimulation and postpone emptying of any gastric contents until the infant
has stabilized.
3. A clinician (e.g., Paediatrician, Anesthesiologist, advanced practice nurse) should incubate
the trachea under direct laryngoscopy preferably before inspiratory efforts have been initated. A 3.0
mm or 3.5 mm internal – diameter endotracheal tube is used in term infants.
4. After incubation the tube is attached to wall suction at a pressure of 80 to100 mm Hg by
means of a plastic adapter (Neotech Meconium Aspirator, Neotech product Chatsworth CA)
Continuous suction is applied as the tube is being withdrawn: the procedure is repeated until the
trachea is cleared or resuscitation needs to be initiated.
5.Avoid positive pressure ventilation, if possible until tracheal suctioning is accomplished.
C. Complications of intubation
Include bleeding, laryngospasm stridor apnea and cyanosis. This procedure should be
accomplished rapidly and ventilation with oxygen should be initiated before significant bradycardia
occurs. The infant’s general condition must not be ignored in persistent attempts to clear the trachea.
Because a few inspiratory efforts by the infant will move the meconium from the trachea to the
smaller airways. exhaustive attempts to remove it are unwise.

MANAGEMENT OF MAS
A. Observation: Infants who are depressed at birth and have had meconium suctioned from the
trachea are at risk for meconium aspiration pneumonia and should be observed closely for
respiratory distress.
1. A chest radiograph may help determine those infant who are most likely to develop
respiratory distress although a significant number of asymptomatic infant will have an abnormal
appearing chest film. The classic roentgenographic finding are diffuse asymmetric patcy infiltrates
areas of consolidation and hyperinflation.
2. Monitoring of oxygen saturation during this period aids assessment of the severity of the
infant’s condition and avoids hypoxemia.
B. Routine care
1. The infant should be maintained in a neutral thermal environment and tractile stimulation
should be minimized
2. Blood glucose and calcium levels should be assessed and corrected if necessary. Severely
depressed infants may have severe metabolic acidosis that may need to be corrected.
3. Fluids should be restricted as much as possible to prevent cerebral and pulmonary edema.
4. Infants may also require specific therapy for hypotension and poor cardiac output including
cardiotonic medications such as dopamine.
5. Circulatory support with normal saline or packed red blood cells should be provided in
patients with marginal oxygenation. In infants with substantial oxygen and ventilator requirements.
We usually maintain a haemoglobin concentration above 15 g (hematocrit above 40%)
6. Renal function should be continuously monitored
C. Oxygen therapy: Management of hypoxemia should be accomplished by increasing the inspired
oxygen concentration and by monitoring blood gases and PH. An indwelling arterial catheter is
usually required for blood sampling. It is crucial to provide sufficient oxygen because repeated
hypoxic insults may result in ongoing pulmonary vasoconstriction and contribute to the
development of PPHN.
D. Assisted in ventilation
Continuous positive airway pressure
Mechanical ventilation
E.Medications
1. Antibiotics
2. Surfactant
3. Corticosteroids

COMPLICATIONS
a. Pulmonary air leaks
b. anoxic cerebral injury manifested by convulsions
c. myocardial injury evidenced by congestive heart failure or cardiomegaly
d. disseminated intravascular coagulation (dic) resulting from hypoxic hepatic damage
e. Anoxic renal damage demonstrated by hematuria, oliguria, or anuria;
f. Fluid overload
g. Sepsis secondary to bacterial pneumonia

h. intestinal necrosis from ischemia

i. gastrointestinal obstruction
j. hemorrhage

NURSING MANAGEMENT
Assessment
1. During the intrapartum period, observe for signs of fetal hypoxia and meconium staining of
amniotic fluid.
2. At birth assess the new-born for signs of distress.
3. Carefully observe for complications

Nursing diagnoses
1.Impaired Gas Exchange related to aspiration of meconium and amniotic fluid during birth
2.Altered Nutrition: Less than Body Requirements related to respiratory distress and increased
energy requirements
3.Ineffective Family Coping: Compromised related to life threatening illness in term new-born

Planning and implementation

Hospital-Based Nursing Care
i) Initial interventions are aimed at preventing aspiration by helping remove the meconium from
the infant’s oropharynx and nasopharynx before the first extra uterine breath.
ii) When significant aspiration occurs, the primary goals of therapy are to maintain appropriate gas
exchange and minimize complications
iii) Nursing interventions after resuscitation should include maintaining adequate oxygenation and
ventilation, regulating temperature, performing glucose testing by glucometer at 2 hours of age to
check for hypoglycemia, observing intravenous fluids administration, calculating necessary fluids
(which may be restricted in the first 48 to 72 hours due to cerebral edema) providing caloric
requirements, and monitoring intravenous antibiotic therapy
Evaluation
Expected outcomes of nursing care include the following:
1) The new-born at risk of MAS is promptly identified, and early intervention is initiated.
2) The new-born is free of respiratory distress and metabolic alterations.
3) The parents verbalize their concerns about their baby’s health problem and survival and
understand the rationale behind the management of their new-born

Pneumothorax
Definition of pneumothorax
Accumulation of air in the pleural cavity causing lungs to collapse

Incidence
 Global health problem
 The estimated annual incidence of one type (primary spontaneous) pneumothorax is 7.4-
18/100,000 in men 1.2-6/100,000 in women
 The incidence of pneumothorax in mechanically ventilated patients is approximately 4-15%

Types of Pneumothorax
 Spontaneous
 Primary
• No predisposing lungs disease
 Secondary
• COPD
• Cystic Fibrosis
 • Pneumonia
 Traumatic
 Open- Gunshot, stab
 Close- Fracture ribs
 Iatrogenic
Diagnostic
Therapeutic
 Tension
  Fatal- emergency decompression

Classification

Pathophysiology
 Normally intra-pleural pressure is negative

Open trauma Close trauma

Air accumulation in pleural cavity (Built up positive pressure)

Compression and collapse of lung

Decrease vital capacity of lungs and mediastinal shift

Clinical features
Depends on types, size and extent of pneumothorax
 Tachypnea
 Tachycardia
 Dyspnea
 Shortness of breath
 Pleuritic chest pain
 Cyanosis
 Hypotension
 Shock

Physical examination
 Inspection
 Tracheal deviation
 Distended neck vein
 Unilateral chest movements
 Palpation
 Absent tactile fremitus
 Percussion
 Hyperresonance
 Hyper tympanic sound over the affected side
 Auscultation
 Absent/Reduced breath sound on affected side

Investigations
 Chest X-ray
 No pleural marking
 Hyperlucency
 Chest Ultrasonography
 Accurate size
 Chest computed tomography scanning
 Prompt and high-quality images

Treatment
Goal- to evacuate air promptly and allow the lung to re-inflate
 Supplemental oxygen- to treat hypoxia
 Conservative management- resolve at a rate of approximately 1.25-2.2% of the volume per
day
 Simple aspiration
 First line treatment (50-83% success rate)
 Chest tube drainage
If simple aspiration fails
 Emergency decompression for tension pneumothorax (66-97% success rate)

Treatment
 Pharmacotherapy
 Antibiotics (Cephalosporin)
 Opioids (Fentanyl, morphine)
 Surgery
 Open thoracotomy and pleurectomy
  Video-assisted thoracoscopic.
 Pleurodesis or sclerotherapy
 To create adhesion between visceral and parietal pleura
 Talc
 Tetracycline
 Doxycycline

Chest drainage
 Underwater seal drainage- 3 chambers
 Water seal
 Suction
 Drainage.
 Role of Nurse during insertion
 Informed Consent
 Positioning
 Assist in insertion and securing
 Close monitoring and documentation.
 Complications
 Lung infection
 Lung infarction
 Re-expansion pulmonary oedema
 Haemothorax
 Dislodgement

Role of nurse in managing chest drainage

 Maintain patency
 Maintain UWSD
 Suction
 Position
 Pain management
 Observations
• Oscillation
• Bubbling
• Air leak
• Dressing site
PNEUMOMEDIASTINUM
Introduction
Is a condition in which air is present in the mediastinum. This condition can result from physical
trauma or other situations that lead to air escaping from the lungs, airways or bowel into the chest
cavity.
rare situation and occurs when air leaks into the mediastinum.
diagnosis can be confirmed via chest X-ray or CT scanning of the thorax.
main symptom -- severe central chest pain.
Other symptoms --laboured breathing, voice distortion (as with helium) and subcutaneous
emphysema, specifically affecting the face, neck, and chest.
Characterized by the shortness of breath, a respiratory system problem.
on auscultation --"crunching" sound timed with the cardiac cycle (Hamman’s crunch).
May also present with symptoms mimicking cardiac tamponade as a result of the increased
intrapulmonary pressure on venous flow to the heart. The tissues in the mediastinum will slowly
resorb the air in the cavity so most pneumomediastinums are treated conservatively.

Definition
is the term which defines the presence of air in the mediastinum. It has also been described as
mediastinal emphysema

Classification
Pathophysiology
Increase of alveolar pressure

causes them to rupture

therefore releasing air

which in turn migrates through the peri-bronchial and perivascular

sheaths to the mediastinum

Incidence
 Rare
 more frequent in children
  common in males
Clinical presentation
 Hamman’s sign (it is the presence of mediastinal crunch or click present on auscultation
over the cardiac apex and the left sternal border synchronous with the heart beat)
 chest pain
 asthma
 dyspnea
 coughing spells
 neck pain
 dysphagia
 Subcutaneous emphysema
 Rhinolalia
 hoarseness and neck swelling,
 tachycardia
 tachypnea
 Malignant pneumomediastinum is considered the accumulation of a significant amount of
air in the mediastinum, causing vessel or tracheal obstruction and inducing respective
symptoms and signs of tamponade and decreased venous return.
 Pneumothorax (presenting sign)

Diagnosis –

showing lucent streaks, bubbles of air outlining mediastinal structures and visible mediastinal
pleura
CT scan
chest X-ray
patient’s previous health status
Ultrasound

Investigations
Rising white blood cells
ECG abnormalities
pulmonary function tests

Management
Physical activity should be discouraged and bed rest must be ensured.
Pain – analgesics
Anti-anxiety drugs
Coughing should be suppressed with antitussives.
O2 administration
airway compression - thoracotomy for decompression

Complications
extensive subcutaneous emphysema
pneumothorax
pneumorrhachis
ICTERUS NEONATORUM
INTRODUCTION
Jaundice is a yellow discoloration of the skin, sclera and mucus membrane caused by
hyperbilirubinemia.
The newborn appear jaundice when level is>5mg/dl.
Jaundice usually becomes visible at
 Sclera -2 to 3 mg/dL
 Face - 4 to 5 mg/dL
 Umbilicus -15 mg/dL
 Feet - 20 mg/dL.
INCIDENCE
 25-60 % of full-term newborns develop clinical jaundice
 75-85% of preterm infants
 3% of normal term infants show bilirubin levels > 15mg/dl
FETAL BILIRUBIN METABOLISM
 Bilirubin can be detected in normal amniotic fluid from 12 weeks of GA and
disappears by 36 to 37 weeks.
 Uridine diphosphoglucoronosyl transferace activity in 0.1 % fetal liver, reaches to 1%
of adult value by term gestation.
 The major route of fetal bilirubin excretion is across the placenta.

BILIR IN META OLISM

TYPES
 Physiological jaundice
 Pathological jaundice
 Breast feeding jaundice
 Breast milk jaundice
 Comparison of major types of unconjugated hyperbilirubinemia
Physiological jaundice Breastfeeding- Breast milk jaundice Haemolytic disease
associated jaundice
(early onset)
Causes Decreased milk intake Possible factors in Blood antigen
Immature hepatic related to fewer calories breast milk that prevent incompatibility causes
function plus increased consumed by infant bilirubin conjugation. hemolysis of large
bilirubin load from before mothers’ milk is Less frequent stooling number of RBCs.
hemolysis of red blood well established, Liver unable to
cells enterohepatic shunting conjugate and excrete
excess bilirubin from
hemolysis
nd th th th
Onset 2 to 4 day 5 to 7 day During 1st 24 hrs
After 24 hrs (preterm (levels increase faster
infants, prolonged) than 5mg/dl/day)
Peak 3rd to 5th day 10th to 15th day variable
72-90 hours
Duration variable May remain jaundiced Dependent on severity
Declines on fifth to for 3-12 weeks or more and treatment
seventh day
Therapy Frequently Increase the frequency Phototherapy in
Phototherapy if breastfeeding (10-12 to breast feeding; use severe cases exchange
bilirubin levels increase times/day) no supplementation transfusion is done.
significantly (rise in Phototherapy for such as glucose water; Prenatal-transfusion of
bilirubin is greater than bilirubin 17-22 mg/dl in cessation of breast fetus.
5mg/dl/day) healthy term infants and feeding is no longer Prevent sensitization
continue breastfeeding; recommended. (Rh incompatibility)
possibly alternate If bilirubin levels reach of Rh -ve mother with
formula feeding; avoid 16mg/dl, may RhIG (RHOGAM)
glucose water and water discontinue
supplementation breastfeeding for 12hrs;
if bilirubin levels
decrease, breast feeding
can be resumed

Physiological jaundice
In term neonates: TSB reaches to 5-6 mg/dl by 48 to 120 hours of age.
10-14 mg/dl at 72-120 hours of age.
Rapid decline to approx. 3mg/dl by fifth day of life.
 This is designated as a phase I physiological jaundice.

From the 5-10th day of life TSB concentration decline slowly reaching the normal adult
value of less than2mg/dl phase 2 physiological jaundice.
In preterm neonate: jaundice is more severe with mean peak TSB concentration reaching
10 to 12mg/dl by the fifth day of life
Pathological jaundice
Clinical jaundice appearing in the first 24 hours. It increases in the level of TSB by more
than 0.5 mg/dl /hr or 5mg/dl/24 hours

CAUSES
 Feto-maternal blood group incompatibility –Rh, ABO
 Hereditary spherocytosis
 G6PD deficiency
 Vitamin induced hemolysis
 Sepsis
 Enterohepatic circulation
 Pyloric stenosis
 Large bowel obstruction
 Hypothyroidism

Breast feeding jaundice

Occur in the I week of life in the breast feed neonates.
Maternal factors like lack of proper technique, breast engorgement, cracked nipple.
Neonatal factors like ineffective and some congenital anomalies like cleft lip and palate.
All these leads to dehydration and delayed passage of meconium. Leads to increase in
enterohepatic reuptake of bilirubin leading to unconjugated hyperbilirubinemia.

BREAST MILK JAUNDICE

 Occur during 2-3 weeks of life beyond up to 3 months of age.
 Usually, TSB reaches a peak of 5 to 10mg/dl at approximately 2 weeks of life or
beyond up to 3 months of age.
 Pregnadiol a progestrone metabolism found in the breast milk was thought to be the
cause of the disorder.

RULE OF FIVE TO ASSESS JAUNDICE

1. I - 5mg/dl
2. II-10 mg/dl
3. III- 12 mg/dl
4. IV- 15 mg/dl
5. V- >15 MG/dl
 KERNICTERUS (CHRONICBILIRUBIN ENCEPHALOPATHY
Kern: nuclear region of the brain and
Icterus – jaundice
Kernicterus is brain damage caused by unconjugated bilirubin deposition in basal ganglia
and brain stem nuclei, caused by either acute or chronic hyperbilirubinemia.
Causes
Bilirubin can cross the blood-brain barrier in certain situations:
When serum bilirubin concentration is markedly elevated >20mg/dl
When serum albumin concentration is markedly low (e g, in preterm infants)
When bilirubin is displaced from albumin by competitive binders (e g, sulfisoxazole,
ceftriaxone, aspirin and free fatty acids and hydrogen ions e g, in fasting, septic, or acidotic
infants).

Clinical features
Extrapyramidal disturbances especially athetosis (slow, purposeless, and involuntary
movements of the hands, feet, face, tongue, and neck as well as other muscle groups).
Auditory abnormalities especially sensory neural hearing loss
Gaze palsies especially upward gaze
Dental dysplasia

Clinical Features of Bilirubin Encephalopathy

1. Initial phase

●slight stupor
● (lethargy, sleep)
●Slight hypotonia
●Poor sucking

2. Intermediate phase

●Moderate stupor
●Tone variable, opisthotonos
●Minimal feeding

3. Advanced phase

●Deep stupor to coma

●Tone usually increased
●No feeding shrill cry
INVESTIGATIONS

1. History
2. Transcutaneous bilirubinometer
3. Total serum bilirubin
4. Blood type and Rh
5. Direct antiglobulin test (DAT) in the
6. infant (direct Coombs test)
7. Hb, PCV
8. Serum albumin levels
9. Liver function tests
10. Nomogram for hour-specific bilirubin values
11. Measurement of End-tidal carbon monoxidein breath (ETCO
12. Peripheral blood film for erythrocyte morphology
13. Reticulocyte count
14. Conjugated bilirubin levels:
15. Thyroid function test
16. Ultrasonography
17. Radionuclide scanning
18. Tests for viral and/or parasitic infection

MANAGEMENT
PHYSIOLOGIC JAUNDICE
 no specific treatment required
 continue breast feeding
 watch for sudden rise in bilirubin levels
 treat any exaggerating factors.

PATHOLOGIC JAUNDICE
 Increase feeds in volume and calories. Early feeding lowers serum bilirubin level by
stimulating the peristalsis.
 Stop drugs interfering with bilirubin metabolism.
 Correct hypoxia, infection, and acidosis.
 Phototherapy
Prophylactic: in LBW or bruised neonate.
Therapeutic.
 Exchange transfusion.
  Phenobarbital
 Agar-Agar
 Albumin infusion
 Tin protoporphyrin

Phototherapy
It consists of the application of fluorescent light (blue or white) to the newborns skin. Light
causes break down of bilirubin by the process of photo oxidation.
Indications of phototherapy:
It is used when bilirubin level is:
 5-9 mg/dl at the 1st day of life.
 9-15 mg/dl at the 2nd day of life

Side effects of phototherapy:

 Dehydration due to increased insensible water loss.
 Watery diarrhoea.
 Hypocalcemia.
 Retinal damage.
 Erythema and skin rashes.
 Bronze baby syndrome.
 Maternal newborn interaction is affected.
 Dark yellow urine.

Nurse’s responsibility in phototherapy:

 The lamp should be 5-8 cm over the incubator.
 Continue the feeding.
 Shield the newborn’s eyes, genetalia
 change position frequently.
 Cleanse skin frequently to prevent irritation.
 prevent dehydration and calculate intake and output.
 Check newborn’s body temperature every four hours.
 Weight newborn daily.
 Observe skin, mucous membranes, and stool.
 Bilirubin levels should be followed for at least 24hours after discontinuing
phototherapy.

EXCHANGE TRANSFUSION
It is an ideal dilution of S. Bilirubin and antibodies. A catheter is introduced into the
umbilical vein after cutting the cord. Through a special valve, the umbilical catheter is
connected with the donor blood. Exchange is carried out over 45-60 min period by
alternating aspiration of 20 ml of newborn’s blood and infusions of 20 ml of the donor blood.
Exchange transfusion Indication
 Despite phototherapy progressive rise of bilirubin>1mg/dl/hr
 To improve anaemia and CCF of neonate
 Serum bilirubin ≥ 20mg/dl
 Cord blood B < 12 mg/dl &bilirubin> 5mg/dl

Complications:
 Embolism, thrombosis, infarction.
 Arrhythmias, heart failure, arrest.
 Electrolyte disturbances.
 Thrombocytopenia.
 Infections
 Hypo and hyperthermia.

Nursing responsibilities:
 Keep the newborn NPO for 2-4 hours before exchange to prevent aspiration.
 Check donor blood charts compatibility.
 Keep resuscitation equipment at bedside: oxygen, ambubag, endotracheal tubes, and
laryngo-scope.
 Assist physician with exchange transfusion procedure.
 Track amount of blood withdrawn and transfused to maintain balanced blood
volume.
 Maintain body temperature to avoid hypothermia and cold stress.
 Monitor vital signs and observe for rash.
 After transfusion, continue to monitor vital signs and check umbilical cord for
bleeding or signs of infection.

PHENOBARBITAL
 Mechanism of Action: induces activity of enzyme glucoronyl transferase and
increases bilirubin conjugation and excretion.
 Dosage: therapeutic- 5-8mg/kg/day to newborn indicated only in Crigler Najjar
syndrome type II & type II & other conjugated hyperbilirubinemia.
 Side-Effects: drowsy child, slow feeding.

AGAR
 Mechanism of Action: binds bilirubin to gut and diminishes enterohepatic circulation.
Dosage: 125mg/ 3 hrly in mild to moderate hyper bilirubinaemia.
 TIN PROTOPORP YRIN: - heme oxygenase enzyme inhibitor.
ALBUMIN INFUSION
 Mechanism of Action: raises bilirubin binding capacity.
 Dosage: 1mg/kg of salt free albumin can be used as an alternative for exchange
transfusion.
BREAST MILK JAUNDICE
Interruption of breastfeeding for 24-48hours and feeding with breast milk
substitutes often helps to reduce the bilirubin level.

NURSING DIAGNOSIS
 Risk for injury from breakdown products of red blood cells in greater numbers than
normal and functional immaturity of liver
 Altered family processes related to maturational crisis, birth of term infant, change in
family unit

BIRTH INJURIES
INTRODUCTION
Birth injury is damage that occurs as a result of physical pressure during the birthing process,
usually during transit through the birth canal. Many newborns have minor injuries during birth.
Infrequently, nerves are damaged or bones are broken. Most injuries resolve without treatment. A
difficult delivery, with the risk of injury to the baby, may occur with extremely large fetuse. Injury
is also more likely when the fetus is lying in an abnormal position in the uterus before birth.
INCIDENCE
India showed incidence of 3.2/1000 live birth during 2009- 2010.Significant birth injuries
accounts for fewer than 2 % of neonatal death and stillbirth. Injuries may occur during intra- natal,
antenatal, during resuscitation and may be avoidable or unavoidable. Global neonatal mortality
rate is 19 per 1000 in 2016. Incidence of birth injuries was 2.2%. in vaginal delivery it is 3.6% and
in CS 1.2%.
MEANING
Birth injuries is an impairment of the infant’s body function or structure due to adverse
influences that occurred at birth. Injuries to the newborn from the forces of labour and birth are
categorized as birth trauma. The injuries commonly occur during labour or delivery.
HIGH RISK FACTORS FOR BIRTH INJURIES
 Primigravida
 Prolonged or obstructed labor
 Fetal macrosomia
 Cephalo-pelvic disproportion
 Very low birth weight infant
 Abnormal presentation (breech)
  Instrumental delivery (forceps or ventouse)
 Difficult labor
 Shoulder dystocia
 Inadequate maternal pelvis
 Oligohydramnios
 Precipitate labor
TYPE OF INJURY ORGANS AFFECTED
Soft Tissue Skin - Lacerations, abrasions, fat necrosis, petechiae

Muscle sternocleidomastoid

Nerve Facial nerve, Brachial plexus, Spinal cord, Phrenic

nerve (C3, C4 or C), Horner’s syndrome, recurrent
laryngeal nerve

Eye Hemorrhages: Sub-conjunctiva, vitreous, retina

Viscera Rupture of liver, adrenal gland, spleen testicular injury

Scalp Laceration, abscess, hemorrhage, caput succedaneum

Dislocation Hip, shoulder, cervical vertebrae

Skull Cephalohematoma, subgaleal hematoma, fractures

Intracranial Hemorrhages—Intraventricular, Subdural, subarachnoid

Bones Mandible, Clavicle, Humerus, Femur, Skull and Nasal bone

EXTRACRANIAL INJURIES
1 •Cephalo-hematoma
2 •Caput Succedaneum
3 •Subgaleal Haemorrhage
FEATURES OF CEPHALO-HEMATOMA
 It is never present at birth but gradually develops after 12- 24 hrs.
 The swelling is limited by the suture’s lines of the skull as the pericranium is fixed to the
margins of the bones.
 Well circumscribed, soft, fluctuant and incompressible (irreducible fullness of
cephalohematoma) does not pulsate or bulge when the infant cries.
 There may be underlying fracture of the skull.
 A hard sharp edge can be felt surrounding the swelling due to organization of the blood.
 A cephalohematoma is usually largest on 2nd or 3rd day.
MANAGEMENT OF CEPHALO-HEMATOMA
 No active treatment is needed.
  The fullness of a cephalo-hematoma spontaneously resolves in 3 to 6 weeks.
 Only observation in most cases.
 Incision and aspiration of a cephalo-hematoma may introduce infection so it is
contraindicated.
 Symptomatic treatment of anaemia and jaundice.

FORMATION OF CAPUT SUCCEDANEUM

With vertex presentation the sustained pressure of the occiput against the cervix results in
compression of local vessels, thereby slowing venous return. The slower venous return causes an
increase in tissue fluids within the skin of the scalp and an edematous swelling develops.
FEATURES
 Poorly defined margins.
 Baby’s head - swelling, puffiness, and bruising present at birth extends across suture lines
of the fetal skull and disappears spontaneously within 3-4 days. These are hallmark
symptoms of caput succedaneum.
 Can extend over the presenting portion of the scalp and usually associated with molding.
 Usually present after birth and resolves spontaneously without first few days after birth.
SUBGALEAL HEMORRHAGE
 A Subgaleal hemorrhage is bleeding between the galeaaponeurosis of the scalp and the
periosteum.
Causes:
 Forces that compress and then drag the head through the pelvic outlet
 Increased use of the vacuum extractor at birth
FEATURES
 Presents as a firm-to-fluctuant mass that crosses suture lines.
 A boggy scalp, pallor, tachycardia, and increasing head circumference – early signs.
 Forward and lateral positioning of the infant’s ear because hematoma extends posteriorly.
 The mass is typically noted within 4 hours of birth.
 The bleeding extends beyond bone, often posteriorly into neck and continues after birth.
DIAGNOSIS
 Serial hemoglobin and hematocrit monitoring- decrease in hematocrit level.
 Monitor for level of consciousness.
 Coagulation profile to investigate for the presence of a coagulopathy.
 Bilirubin levels also need to be monitored- increased as a result of degrading blood cells.
 CT / MRI for confirming the diagnosis.
TREATMENT
 Supportive.
 Replacement of lost blood and clotting factors is required in acute cases of hemorrhage.
 Transfusions may be required if blood loss is significant.
 In severe cases, surgery may be required to cauterize the bleeding vessels.
 These lesions typically resolve over a 2–3 week period.
SCALP INJURIES
  Minor injuries of the scalp are abrasion over the scalp.
Causes:
 Forceps delivery
 Incised wound inflicted during cesarean section
 Scalp electrodes placement
 Episiotomy
Signs: on occasion, the incised wound may cause brisk hemorrhage which requires stitches.
Care: wound may bleed require stitches and which should be dressed with antiseptic solution.
SKULL FRACTURE
 Fracture of the vault of the skull (frontal or anterior part of the parietal bone) may be linear
or depressed type.
Causes:
 Effect of difficult forceps delivery in disproportion or due to wrong application of the
forceps (blades not placed over the bi-parietal diameter).
 Projected sacral promontory of the flat pelvis may produce depressed fracture even though
the delivery is spontaneous.
Features:
 It may be associated with cephalo-hematoma, extradural or subdural hemorrhage or a
hematoma or brain contusion.
 Depressed fractures cases some pressure effect.
 Neurological manifestation- occur later due to compression effect.
Treatment:
 Conservative in symptomless cases.
 Antibiotic is started.
 The depressed bone has to be elevated or subdural hematoma may have to be aspirated or
excised surgically.
 Follow-up imaging should be performed at 8-12 weeks to evaluate any cyst formation.
INTRACRANIAL HEMORRHAGE
 An intracranial hemorrhage is a type of bleeding that occurs inside the skull (cranium).
 Intracranial hemorrhage may be –
External to the brain( epidural, subdural or subarachnoid spaces)
In the parenchyma of brain (cerebrum or cerebellum) and
Into the ventricles from sub-pendymal germinal matrix or choroid plexus.
Causes:
 Traumatic
 Anoxic
 Primary hemorrhagic disease
SUBDURAL HAEMORRHAGE
 Slight haemorrhage may occur following:
  Fracture of skull bone,
 Rupture of the inferior sagittal sinus,
 Rupture of small veins leaving the cortex.
 The hemorrhage, so occurring, produces hematoma which may remain stationary or
increase in size.
 Neurological symptoms may appear acutely or may have insidious onset, like vomiting,
irritability and failure to gain weight.
 Hydrocephalus and mental retardation may be a latesequelae.
MASSIVE HAEMORRHAGE
 Massive subdural haemorrhage usually results from
 Tear of the tentorium cerebella thereby opening up the straight sinus or rupture of the vein
of galen or its distribution.
 Injury to the superior sagittal sinus.
ANOXIC
Intracerebral intraparenchymal hemorrhage( Intracerebral):
It is also known as periventricular hemorrhagic infarction (PVHI. It was seen following perinatal
hypoxic ischemic event as small petechial haemorrhage in the brain substance due to anoxia. It
usually occurs in mature babies following prolonged labor. The features are vague- loss of weight,
flaccid limbs and anxious expression.
Intraventricular Hemorrhage (IVH)/Germinal Matrix Hemorrhage (GMH)—
The pathogenesis of IVH in the term infant is more likely due to trauma (difficult delivery) or
perinatal asphyxia. In the preterm infant GMH/IVH is mainly due to ischemia/reperfusion.
Clinical presentation is extremely diverse: clinically silent, seizures, apnea, irritability, lethargy,
vomiting or a full fontanel.
INVESTIGATION:
 Ultrasonography is used to detect intraventricular haemorrhage.
 Doppler Ultrasonography can detect any change in cerebral circulation.
 CT scan is useful to detect cortical neuronal injury.
 MRI is used to evaluate any hypoxic ischemia brain injury.
 CSF- elevated RBCs, WBCs and protein.
MANAGEMENT:
Prevention: antenatal glucocorticoids reduce GMH/ IVH.
Supportive care: to maintain normal circulatory volume, cerebral perfusion, serum electrolytes
and blood gases, packed red blood cells transfusion may be needed where IVH is large.
Thrombocytopenia and coagulation parameters should be corrected.
TREATMENT
 Follow up- serial neuroimaging cranial ultrasound (CT)- Detect any progressive
hydrocephalus.
 Anticonvulsant –
Phenobarbitone- 3-5 mg/kg/day- 12 hrs interval – oral/ IM
Phenytoin- 20mg/kg- IV (Loading dose) – rate – 1mg/ kg/ min- followed -5mg/kg/day-
cardiac monitoring.
Diazepam- 0.1 mg/kg – IV- thrice daily.
SUBDURAL HAEMATOMA
 Subdural tap: Aspiration of the blood through lateral angles of the anterior fontanelle.
 Open surgical evacuation: Serial CT is indicated before surgical intervention. The infant
should be monitored for any hydrocephalus. Surgical removal of the clot including the
capsule may have to be done to prevent developmental of neurological sequelae.
 Rarely subdural-peritoneal shunting may be needed.
 Prevention: Comprehensive antenatal and intranatal care is the key to success in the
reduction of intracranial injuries.
ANTENATAL PREVENTION OF IVH/ GMH:
 Tocolysis with indomethacin should be avoided.
 In utero transfer of preterm labor to a centre with NICU.
 Caesarean delivery before active phase of labor in preterm infant.
 Antenatal steroids can reduce the risk by three fold.
 To prevent or to detect at the earliest, intrauterine fetal asphyxia by intensive fetal
monitoring
 To avoid traumatic vaginal delivery in preference to caesarean section. difficult forceps
should be avoided.
 Administration of vitamin K 1 mg IM soon after birth in susceptible babies.
 POSTNATAL PREVENTION: Avoid birth asphyxia, fluctuation of blood pressure, correct
acid base abnormalities, surfactant therapy is found helpful.
SUBARACHNOID HEMORRHAGE
 Is an accumulation of blood between the arachnoid and the pia matter.
Causes:
 Excessive molding in deflexed vertex with gross disproportion;
 Rapid compression of the head during delivery of the after coming head of breech or in
precipitate labor and
 Forcible forceps traction following wrong application of the blades (other than bi parietal
diameter).
Clinical features:
 Hemorrhage is fetal and baby is delivery dead.
 Baby will have respiratory depression.
 Cerebral irritation (Frequent high pitch cry, neck retraction, incoordination ocular
movements, convulsion, vomiting and bulging of the anterior fontanel)
FACIAL FRACTURES
 Facial fractures can be caused by numerous forces including natural passage through the
birth canal, forceps use or delivery of the head in breech presentation.
Features: It is presented with facial asymmetry, ecchymosis, edema and crepitus or respiratory
distress with poor feeding.
Treatment:
 Treatment should be started promptly because maxillary and lacrimal fractures begins to
heal within 7-10 days and mandibular fractures starts to repair at 10-14 days.
 Airway patency should be closely monitored.
 Anti-biotic is started if sinus and middle ear is involved.
SKIN AND SUBCUTANEOUS INJURIES
 Bruises and lacerations on the face are usually caused by forceps blades. These are treated
with application of 1% lotion mercurochrome.
 Buttocks in breech presentation, or eyelids, lips or nose in face presentation, similarly
become edematous and congested. No treatment is required.
 Scalpel cut or laceration injury may occur during cesarean section. They usually occur on
the buttocks, scalp or thigh.
 Small cut heals spontaneously. Laceration injury may need repair by stitches with 7-0
nylon. Healing is usually rapid.
MUSCLES INJURIES
 Sternomastoid hematoma usually appears about 7–10 days after birth and is usually
situated at the mid-position of the muscle. It is caused by rupture of the muscle fibers and
blood vessels, followed by a hematoma and cicatrical contraction.
 It is seen in difficult breech delivery or in attempted delivery of shoulder dystocia or
excessive lateral flexion of the neck even during the normal delivery.
 There is transient torticollis and it is wise not to massage.
 Stretching of the involved muscles should be done several times a day. Recovery is rapid
in most of the cases (3 months). Surgery is needed is it persist after 6 months of physical
therapy.
 Necrosis of the subcutaneous tissue: may occur while the superficial skin is intact. After
few days, a small hard subcutaneous nodule appears. It is result of the fat necrosis due to
pressure and takes many weeks to disappears. No treatment is needed.

Hypoxic ischemic encephalopathy

Definition
Refers to CNS dysfunction or encephalopathy associated with Perinatal asphyxia.
Potential to cause mortality and long term sequele like disabilities and cerebral palsy.
Etiology
 Pathologically, any factors which interfere with the circulation between maternal and
fetal blood exchange
 maternal factor, delivery factor and fetal factor.
Etiology—High Risk Factors
 Maternal factor:
hypoxia, anemia, diabetes, hypertension, smoking, nephritis, heart disease, too old or
too young etc
 Delivery condition: Abruption of placenta, placenta previa, prolapsed cord, premature
rupture of membranes, etc
 Fetal factor: Multiple birth, congenital or malformed fetus, etc
Pathophysiology
Asphyxia

self-defensive mechanism

redistribution of blood flow to vital organs ( brain, heart and adrenal) to prevent from hypoxic
damage. ‘Diving Reflex’
Pathophysiology
Hypoxic cellular damages:
a. Reversible damage (early stage): Hypoxia may decrease the production of ATP, and result in
the cellular dysfunctions. But this change can be reversible if hypoxia is reversed in short time.
b. Irreversible damage: Longer hypoxia irreversible cellular damage
Pathophysiology
 Cerebral blood flow Early stage: normal (intraorgans shunt) then slow down (selective
vulnerability) finally ischemia – Watershed regions
 Cerebral metabolism – altere
 Cellular electrolyte alteration- Na, Ca

Neuropathological lesions in HIE

 Term infant
 Parasagittal injury, Selective neuronal necrosis, focal/multifocal ischemia, status
marmoratus
 Proximal spastic quardiparesis. Spastic CP, Spastic hemiparesis, Cognitive defects,
Seizures, EP cerebral palsy.

 Preterm infant
 Periventricular leukomalacia, IVH
 Spastic diplegia, visual impairment.
  Status Marmoratus: basal ganglia lesion resulting from asphyxia. The lesions have a
marbled appearance caused by neuronal loss and an overgrowth of myelin in the
putamen, caudate, and thalamus.

 Selective vulnerability - The hippocampal pyramidal cells of CA1, pyramidal

neocortical neurons (layers 3, 5, and 6), Purkinje cells, and striatal neurons have the
highest vulnerability.
Clinically, more term babies suffered from this disease than premature babies.
Pathologically, more premature babies suffered from this disease than term babies.

Clinic Manifestation The clinic features of HIE are mainly symptoms of consciousness in two
types-

1.Excitation: hyperalert, irritable, hypertonia, tachycardia, tachypnea, seizure, etc

2. Depressing: coma, hypotonia, bradycardia, bradypnea, unresponsibility, etc

Classification—Clinical
 Mild (stage I): hyperalert, irritable, normal muscular tone & reflex, no seizure, normal
EEG
 Moderate (stage II): lethargy, hypotonia, weak sucking & Moro response, often
seizure, EEG+
 Severe (stage III): coma, absent muscular tone & reflex, persistent seizure, EEG++

HIE: Classification

 Sarnat and Sarnat Staging

Stage I , II and III
 Thompson Scoring: For HIE progression and prognostic scoring- quantitative
Management
 Monitoring
 Vitals
 Urine output
 Blood sugar monitoring
 Hematocrit /PCV
 Electrolytes
 Assessment of Neurological status- 6 hourly
 Tone: Hypotonia
 Seizure – may be subtle to frank
Management
Generalized treatment:
 Ventilation: CPAP, CMV, HFOV
 Perfusion/Circulation: Dopamine/Dobutamine
 Energy: normal glucose level maintained ( 50- 110mg/dl) : Hypo and hyperglycemia
avoided
 Fluid: 60-80ml/kg/d - restriction if SIADH
 Electrolytes- Na and Calcium should be monitored.
 Avoid Polycythemia: If Hct>65-70 , partial exchange transfusion is done to bring Hct
level to 55.
Control of seizures: HIE seizures are difficult to control
 Phenobarbital loading dose 15-20mg/kg, iv maintenance dose 3-5mg/kg, iv
 Phenytoin loading dose 15-20mg/kg, iv maintenance dose 5mg/kg, iv
 Midazolam: 0.1-0.3mg/kg, iv
 Leveracetam, Topiramate
Special Investigations
 EEG
Routine EEG does not help
Continous aEEG- Amplified EEG used for cerebral function monitoring
 Detects voltage pattern- burst, low voltage, isoelectric
 Detects electrical seizure activity
 Cranial Ultrasound:
Not good modality
Preterm – IVH, Periventricular leukomalacia
Severe cases- hypoechoic areas.
CFM - aEEG
 CT scan: only indicated in emergency
 Generalized low attenuation of brain parenchyma in acute stage.
 local or patchy hypodensity, extensive & generalized hypodensity, usually
combined with brain hemorrhage

 MRI
 Time consuming
 DWI ( Diffusion weighted imaging) is helpful in early stage.
 Within hours shows restricted diffusion to hypoxic areas.
Recent advances in Management
 Cerebral Hypothermia
 Selective head cooling ( CoolCap trial ) vs Whole body cooling
 Decreases brain metabolism and injury.
 >=36 weeks and >=2000gm
 Cooling upto 33-34 C.
 Provided for 72 hours
 Seen to have better outcomes specially for moderate HIE cases.
Drugs under trial
 Allopurinol
 blocks free radical generation
 Scavenging free radicals
 Superoxide dismutase, N acetyl cysteine, alpfa tocopherol
 NMDA receptor blocker
 Mg, MK80
 Calcium channel blockers
 Nimodipine, Flunarizine
 Prophylactic phenobarbitone?
 Prognosis
Depend on the severity of brain damage & medical treatment, usually:
Mild or moderate cases could be cured completely, but severe cases represent poor
prognosis with high mortality or cerebral complications such as mental retardation & cerebral
palsy.
Overall mortality – 20%
Overall incidence of sequele - 30%
Mild: 100% good prognosis
Mod: 80% normal
Severe: 50% death, 50% sequele

Presence of seizure increases chance of Cerebral palsy by 50-70 times.

Prevention
 Better Obstetric care
 Skilled resuscitation teams and neonatal fascilities.

Congenital anomalies
Definition
Structural deformities existing at birth are known as congenital anomalies
Etiology
1. Genetic factors:
Any abnormalities in the genes transferred from parents to the offspring as well as new
mutations in germ cells leads to congenital defects. E.g., colour blindness, thalassemia etc.
any abnormalities in chromosomal structure or number which may occur during cell division
of zygote also results in congenital anomalies. E.g., down’s syndrome resulting from trisomy
21 (i.e., chromosome number 21), Edwards syndrome due to trisomy 18.

2. Abnormal intrauterine environment:

I. Maternal infection: few infections pass from mother to the fetus via placenta
resulting in serious malformations. For e.g., rubella infection to mother can lead to
congenital heart diseases and measles infection in mother can lead to congenital
deafness in baby.
II. Exposure to radiation: exposure to pregnant female to radiation especially during
first trimester of pregnancy may lead to gene mutation in zygote or fetus which
may cause congenital malformation like skeletal defects, microcephaly, etc.
III. Use of certain drugs by mother during first trimester o pregnancy can lead to
congenital malformation in baby like use of radioactive iodine ca cause goiter,
thalidomide can cause mental retardation
IV. Mechanical factor: presence of factors like hydramnios, oligohydramnios, ectopic
pregnancies, bicornuate uterus and fibroid in uterus may cause abnormal positions
or posture of fetus or pressure on fetal parts that may result into malformation
 V. Ingestion of harmful substances by mother e.g., alcohol and mercury can result in
development of congenital malformation in baby
VI. Dietary deficiencies in mother can result in fetal malformations, e.g., folic acid
deficiency in mother is associated with spina bifida in baby

It has been seen that the cause of 40-60% of congenital anomalies is unknown. These are
referred to as “sporadic” a term that implies an unknown cause. For 20-25% of anomalies,
there seems to be “multifactorial” Etiology, meaning a complex interaction of multiple minor
genetic anomalies with environmental risk factor. Another 10-13% of anomalies have a purely
environmental cause (e.g., infections, illness or drug abuse in mother). Only 12-25% of
anomalies have purely genetic cause.
Occurrence rate
About 3% of newborns have a “major physical anomaly” meaning a physical anomaly or
defect that has cosmetic or functional significance. Congenital anomalies involving brain are
the most common, with a rate of 10/1,000 live births, compared to heart defects with a rate of
8/1,000, kidneys 4/1,000 and limbs 1/1,000. All other physical anomalies have a combined
incidence of 6/1,000 live births.
Common congenital malformation
Skeletal defects
A limb anomaly is called dysmelia. It includes:
1. Amelia (absence of arm or leg)
2. Ectrodactyly (absence of one or more central digits of hand or foot)
3. Phocomelia (hand or feet attached to abbreviated arms and legs)
4. Polymelia (more than normal number of limbs)
5. Polydactyly (having more digits or fingers in hand or feet)
6. Syndactyly (two or more digits are fused together)
7. Achondroplasia (disorder of bone growth leading to dwarfism)
8. Aplasia (absence of an organ or tissue)
Central nervous system defects
1.Neural tube defects like spina bifida (failure of formation of bony arch around spinal cord)
which includes meningocele (failure of formation of bony arch around spinal cord without
defective development of spinal cord) and myelomeningocele (failure of formation of bony
arch around spinal cord with protrusion of cord through the defect)
2. Encephalocele (protrusion of brain and meninges through opening in the skull)
3. Anencephaly (absence of large part of brain and skull)
4. Hydrocephalus (enlargement of skull due to accumulation of CSF)
5. Microcephaly (abnormally small head and brain)
6. Megalencephaly (abnormally large brain)
7. Arnold-Chiari malformation
8. Dandy-walker malformation

Gastrointestinal defects
It includes
1. Cleft lip (failure of fusion of maxillary processes with nose elevation on frontal prominence)
2. Cleft palate (failure of fusion of secondary palate with each other and with primary palate)
3. Esophageal atresia (failure of esophagus to form a continuous passage from pharynx to
stomach)
4. Pyloric stenosis (narrowing of pylorus)
5. Anorectal malformation (malformed structure of anus and rectum)
6. Exomphalos (herniation of abdominal organs into umbilical cord with evisceration into the sac)
7. Megacolon (enlarged colon due to absence of ganglionic cells)

Respiratory system defects

1. Choanal atresia (back of nasal passage is blocked)
2. Tracheoesophageal fistula or TEF (abnormal connection between trachea and esophagus)
3. Diaphragmatic hernia (protrusion of abnormal organs trough a defect in diaphragm into the
thoracic cavity)

Cardiovascular defects
Neonates may be born with cyanotic and acyanotic cardiac defects like:
1. Atrial septal defects (abnormal communication between right and left atrium)
2. Ventricular septal defect (abnormal communication between right and left ventricle)
3. Aortic stenosis (obstructive lesion in aorta that interferes with outflow of blood from the left
ventricle)
4. Pulmonary stenosis (obstructive lesion in pulmonary artery that interferes with outflow of
blood from right ventricle)
5. Tetralogy of Fallot (includes four defects – ventricular sepal defect, aortic overriding,
pulmonary stenosis and right ventricular hypertrophy)
6. Dextroposition (heart on right side)

Genitourinary system defects

1. Atrophy of bladder (failure of abdominal wall to close resulting in exposed urinary bladder)
2. Hypospadias (urethral meatus on ventral penile surface)
3. Epispadias (urethral meatus on dorsal penile surface)
4. Phimosis (foreskin is narrowed and cannot be retracted over the glans)
5. Wilms’ tumor (malignant tumor of kidney)
6. Polycystic kidneys (presence of multiple cysts in the kidneys)

Blood disorders
1. Thalassemia (defective hemoglobin production)
2. Haemophilia (deficiency of clotting factor)
3. Sickle cell anemia (RBCs are sickle-shaped so breakdown is rapid, resulting in anemia)
4. Hereditary spherocytosis (disorder of RBCs membrane that leads to spherical RBCs which
break prematurely)
 Metabolic disorders
1. Cystic fibrosis (thick sticky mucus in lungs, digestive tract and pancreas, due to a defective
gene)
2. Phenylketonuria (inability to metabolize the amino acid phenylalanine)
3. Galactosemia (inability of the body to metabolize galactose)
4. G6PD deficiency (deficiency if enzyme results in hemolysis of RBCs)
5. Glycogen storage disease (defect in processing or glycogen synthesis or breakdown of
glycogen in muscles and liver)
6. Mucopolysaccharidosis (absence or malfunctioning of lysosome enzyme needed for
carbohydrate metabolism)
7. Tay – Sachs disease (disease of nervous system characterized by deafness, decreased eye
contact, blindness and decreased muscle tone)

Endocrinal abnormalities

1. Congenital dwarfism (deficiency of growth hormone)

2. Cushing’s syndrome (elevated cortisol level)
3. Cretinism (congenital hypothyroidism)
4. Goiter (diffuse or nodular enlargement of thyroid)
5. Juvenile diabetes mellitus (autoimmune destruction of insulin producing beta-cells resulting in
hyperglycemia)

Chromosomal anomalies
1. Down’s syndrome (trisomy 21)
2. Patau’s syndrome (trisomy 13)
3. Edwards’ syndrome (trisomy 18)
4. Turner’s syndrome (X,0)
5. Klinefelter’s syndrome (XXY, XXXY)
6. Cri-du-chat syndrome (partial deletion of short arm of chromosome 5)
7. Prader-willi syndrome (deletion on long arm of paternal chromosome 15)
8. Noonan’s syndrome (abnormality on long arm of chromosome 12)
9. Rett’s syndrome (X-linked dominant abnormality)

Diagnostic evaluation
1. Possible to diagnose in fetus, prior to the baby’s birth
2. Various prenatal and postnatal investigations are required for diagnosis
3. Prenatal diagnosis of genetic disorder has been possible because of great advances in
techniques of obtaining fetal tissue, as well as developed in cytogenetics, biochemical
techniques and recombinant DNA technology

Prenatal diagnosis
1. Chorionic villus sampling: it is a technique for obtaining fetal cells from placenta for prenatal
diagnosis. The procedure is usually done transabdominally after 10 weeks of pregnancy
2. Amniocentesis: it is withdrawal of amniotic fluid from amniotic sac surrounding the fetus.
Early amniocentesis, done between 11 and 15 weeks, is useful for cytogenetic study. Early in
pregnancy amniocentesis is used for diagnosis of down’s syndrome, trisomy 13, trisomy 18,
fragile X syndrome, and rare metabolic disorders.
3. Cordocentesis: withdrawing blood from umbilical vein under ultrasound guidance is called
cordocentesis. It helps in prenatal diagnosis of genetic disorder and understanding fetal
physiology, development and metabolism
4. Fetoscopy: a fine endoscope is inserted into the uterus for direct visualization of fetus and
fetal blood sampling can be done.
5. Embryoscopy: this is an experimental technique used in first trimester of pregnancy. A rigid
endoscope is inserted through the cervix into the space between amnion and chorion; to
visualize the embryo and diagnose any structural malformations.
6. Fluorescence in situ hybridization (FISH): molecular cytogenetics has given rise to powerful
new technology or FISH. This method is useful in detecting chromosomal abnormalities
both numerical and microdeletion syndromes.
7. Ultrasonography: it is done to visualize the fetus in mother’s womb
8. Blood test: an elevated level of alpha-fetoprotein in maternal blood indicates neural tube
defect in the baby
9. Radiography: it is use to diagnose anencephaly, hydrocephaly and skeletal defects, fetal X-ray
can be done in last trimester of pregnancy.

Postnatal diagnosis
1. Detail history of mother and family
2. Physical examination of the newborn
3. Blood test
4. Cytogenetic study
5. Biochemical assay
6. Radiography
7. Ultrasonography

Nurse responsibility in prevention of congenital malformation

1. Primary prevention: it includes the action taken to prevent the development of congenital
anomalies. The nurse must educate the people regarding the following preventive
measures:
a) All the girls should be immunized with measles mumps-rubella (MMR) vaccine
b) Women of childbearing age group should not smoke
c) Avoiding late marriages and avoiding pregnancy after 35 yrs of age
d) Discouraging consanguineous marriage
e) Health promotion of girl child
f) Good antenatal care of pregnant female including iron and folic acid supplementation
g) Prevention of intrauterine infection and promotion of sexual hygiene
h) Genetic counselling of couple with family history of hereditary disorder
i) Avoiding drug intake without doctor’s prescription by pregnant lady
j) Pregnant female should not be exposed to X-rays during first trimester of pregnancy
k) Before marriage, boy and girl should be screened for thalassemia
 2. Secondary prevention:
It involves actions taken to identify the disorder as its onset so as to prevent its
extension. Actions taken for secondary prevention are:
a) Entire gestational period should be monitored. Regular ultrasonography pf pregnant
female helps in early diagnosis of congenital anomalies in fetus.
b) Serum alpha-fetoprotein estimation in 14-16 weeks of gestation helps in the diagnosis
of neural tube defect
c) Medical termination of pregnancy (MPT) is recommended in presence of gross
abnormality in fetus

3. Tertiary prevention:
It includes the action taken to limit disability due to existing condition. It includes
following actions:
a) Nurses must provide necessary information to parents
b) Guide the family about rehabilitation services available in community through welfare
agencies

Neonatal seizures
Introduction
Neonatal convulsion are common life-threatening emergency in the newborn due to cerebral or
biochemical abnormality. Preterm babies are more prone to this problem.

Incidence
Incidence being 0.2-2.7/1000live births in term babies and 57.5-132/1000 live births in preterm
babies.

Definition
A seizure is a paroxysmal behavior caused by hyper synchronous discharge of a group of
neurons. Neonatal seizures are the most common overt manifestation of neurological
dysfunction in the newborn.

It is a paroxysmal spell of altered neurological function (behavior, motor or autonomic function)

occurring during the first 28 days in term infants or 44weeks gestational age in pre-term infants.

Classification of neonatal seizures

Type characteristics
1. Clonic slow rhythmic jerky movements approximately 1-3 seconds

 Focal involves upper or lower extremities on one side of body.

Mainly involves neck or trunk. Infant is conscious during event.
 Multifocal may migrate from one part of the body to other.
Movements may start at other times.

2. Tonic extension/stiffening movements.

 Generalized extension of all four limbs ( similar to decerebrate rigidity)
Upper limbs are maintained in a stiffy flexed position
 Focal sustained posturing of limbs, Asymmetric posturing of
trunk or neck.
3. Subtle May develop in full term or pre-term . common in
preterm Eye deviation (Term)
Blinking, fixed stare (Preterm). Repetitive mouth & tongue
movements, Apnea, Pedaling, tonic posturing of limbs.

4. Myoclonic rapid jerks that involve flexor muscle group.

 Focal involves upper extremity flexor muscle group.
 Multifocal asynchronous twitching of several parts of the body.
 Generalized bilateral jerks of upper and lower limbs.

Causes of neonatal seizures

1. Metabolic problems
Hypoglycemia, Hypocalcaemia, Hyponatremia, Hypomagnesaemia, Pyridoxine
Deficiency

2. Developmental neurological problems

Congenital hydrocephalus, microcephaly, cerebral dysgenesis, porencephaly,,
Polymicrogyria, hydraencephaly, lissencephaly, Agenesis of corpus callosum

3. Toxic
Uremia, Bilirubin encephalopathy

4. Prenatal infections
Toxoplasmosis, syphilis, cytomegalovirus, herpes simplex, hepatitis

5. Postnatal complications
Bacterial meningitis, viral meningoencephalitis, sepsis, brain abscess

6. Trauma at birth
Hypoxic brain injury, intracranial hemorrhage, subarachnoid hemorrhage, subdural
hemorrhage, intraventricular hemorrhage

7. Miscellaneous conditions
a) Neonates born to narcotic withdrawal or abstinence syndrome: the babies born to
the mother addicted to heroin alcohol, diamorphine, methadone. May manifest with
characteristic withdrawal symptoms like irritability, high pitched cry, tremors,
hyper tonicity, vomiting diarrhea after 48 hours of birth.

b) Local anesthetics: During paracervical block inadvertent injection of local

anesthetics into fetal scalp may result in intractable convulsion.

c) Hypomagnesaemia
d) Pyridoxine dependency: prolonged maternal administration of vitamin B6during
pregnancy may predispose to this condition.

Benign seizures in neonates

1. Benign neonatal sleep myoclonus: It has onset during first week of life and occur as
synchronous myoclonic jerks during REM sleep. There are no seizures when the baby is
awake. EEG is normal and seizures spontaneously disappear by 2 months of age.

2. Benign familial neonatal convulsions occur as self-limiting isolated clonic seizures on

second and third day of life the recovery is within 1-6 months of life.

3. Benign idiopathic “fifth day seizures”: the multi focal clonic seizures occur on day 5 and
 usually, disappear on day 15 the cause is unknown though CSF zinc level is reported in
some cases.

Age of onset of convulsion

 First day: Hypoxic-ischemic encephalopathy, cerebral contusion, first day
hypocalcaemia, pyridoxine dependency accidental injections of local anesthesia

 Between 1-3 days: intracranial hemorrhage, hypoglycemia, narcotic withdrawal, inborn

error of metabolism.
 Fourth to seventh day: tetany, meningitis, torch infection developmental
malformation, kernicterus.

Investigations
 Family history of convulsion, history of maternal drug addiction and infections are
important aspect of investigation.
 Electroencephalography (EEG) is essential in diagnosis and management of neonatal
seizures.
 Neuroimaging: Imaging the brain is essential in determining the Etiology of neonatal
seizures. MRI scanning is very effective for determining the presence and extent of
hypoxic-ischemic injury and of parenchyma brain injury. If MRI scanning is not possible
acutely,
 CT scan is effective for determining the presence of hemorrhage and calcification (e.g.,
congenital infection, cortical dysplasia).
 Blood examination for calcium, sugar, phosphorus
 Lumbar puncture for CSF study
 Serology for STORCH

Management:
A. Infant should be nursed in thermoneutral environment and special attention should be
given to the baby’s perfusion and ventilation.

B. Stop feeds and start 10%dextrose

C. Treating the primary cause

 Hypoglycaemia – IV 10% dextrose 5ml-10 ml/kg as a bolus is given, then 2ml/kg
dextrose 10% strated. The blood glucose should be maintained between 70-120 mg/dl.
 Hypocalcemia (Ionised Ca <1.1) – IV 10% calcium gluconate 2ml/kg over 10mins
 Hypomagnesemia (<1.0) – IV/IM 50% MgSO4 0.2ml/kg over 10mins

D. Anticonvulsant therapy
a) Parenteral dose of phenobarbitone 20m/kg is administered slowly intravenously over
20 minutes. If no response in 15 minutes additional dose of phenobarbitone 10mg/kg
every 15 minutes is administered intravenously till seizures are controlled.

b) If convulsions are still uncontrolled phenytoin is administered intravenously in a

loading dose of 20 mg/kg.

c) The maintenance therapy with phenobarbitone and phenytoin is started after 12

hours of loading dose and given in a dose of 5mg/kg/day in two divided doses.

d) If convulsions are intractable and baby is in status convulssicus give lorazepam

50ug/kg IV slowly over 2-5 min. Alternately clonazepam 100-200 ug/kg can be
given IV 30 sec.

e) Specific situation :
a. Pyridoxine dependent seizures ; give 100mg IV under EEG control and close
observation

b. Exchange blood transfusion; In life threatening metabolic disorder , kernicterus,

accidental injections.

Nursing management
• Document any fits or abnormal movement in the baby on the fit chart.
• Raise any concerns with the doctors regarding any abnormal movement.
• Do observations as requested.
• Document any concerns which parents have and to inform to the doctors.

Prognosis
The outcome following neonatal seizures depends primarily on the underlying cause. The
presence of both clinical and electrographic seizures in the newborn often indicates some degree
of brain injury and may alter the prognosis of the underlying disorder (e.g., hypoxic-ischemic
injury) The prognosis is good in hypocalcemic convulsions. About one-fourth to 40 percent of
neonates with neonatal convulsions die. Birth trauma and hypoxia are having bad prognosis.
Among survivors, about 25 percent suffer from recurrent convulsions and neurodevelopmental
defects.

Neonatal HYPOGLYCEMIA
Introduction
Neonatal hypoglycemia is a common metabolic disorder which can cause unexplained death and
high mortality. Incidence and severity can be reduced by initiating appropriate feeding regimen
and timely administration of supplements.
Definition
Hypoglycemia in the newborn baby is termed when the blood glucose level is less than 40 mg/dl,
irrespective of period of gestational age. It may be asymptomatic or symptomatic.
Types
1. Increased or impaired glucose utilization :
Large or normal size infants who appears to suffer from hyperinsulinism, infant born to
women with diabetes, infants with increased metabolic demand such as cold stress, sepsis,
or after resuscitation, infants with enzymatic or metabolic endocrine defects.
2. Decreased glucose stores:
Small or growth restricted infant’s premature infants.
Causes of neonatal hypoglycemia
Transient hypoglycemia
1. Inadequate substrate
i. Premature and SGA infants
ii. Smaller of the twins
iii. Infants of diabetic mothers
2. Relative hyperinsulinism as in infants of diabetic mothers.
Persistent hypoglycemia
1. Hyper insulin states
i. Beta cell hyperplasia
ii. Adenoma of beta cells
iii. Leucine sensitivity
2. Deficiency of hormones such as glucagon ,adrenal and ACTH
3. Deficiency of substrate such as in ketotic hypoglycemia
4. Disorders of carbohydrate metabolism such as glycogen storage disease and fructose
intolerance.
Others
1. May be due to perinatal stress like asphyxia, hypothermia, infection, polycethemia,
respiratory distress and neurological disturbances.
2. Maternal tocolytic therapy like isoxusprine, salbutamol, etc.
Clinical manifestation
The clinical features are associated with release of epinephrine and activation of autonomic
nervous systems which may alter due to anoxia and intracranial injury.
 Cerebral Signs:
Limpness, jitteriness, tremors, twitching, pallor, hypothermia, high pitched cry, lethargy
or irritability, restlessness, convulsions and coma.
 Other signs:
Apnea with cyanosis, tachypnea with irregular breathing, sweating, eye rolling, poor
feeding.
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 6
Screening
Besides monitoring serum blood glucose should be done for all infants at risk.
 Infants who also may need screening include:
 Significant hypoxia, perinatal distress, or five-minute Apgar <5
 Infant with mother on terbutaline, beta-blockers, or oral hypoglycemic agents
 Infant with isolated hepatomegaly (rule out glycogen storage disease [GSD]);
microcephaly; anterior midline defects; gigantism
 Infants with macroglossia or hemi hypertrophy (rule out Beckwith-Wiedemann Syndrome)
 Infants you suspect have an inborn error of metabolism
Management
1. Hypoglycemia should be prevented by early initiation of breast feeding within first hour of
birth.
2. The baby should be nursed in warm or thermo neutral environment with careful
observation of at-risk situation and prevention of hypoxia and hypothermia.
3. In symptomatic infants with convulsions, 25 percent dextrose 2ml/ kg intravenously is
given as bolus. If there is no convulsion, 10 percent dextrose at a rate of 6-8 mg/kg/minute.
4. Blood glucose level to be checked every ½ hourly. Infusion rate to be reduced only if last
two glucose estimation is more than 60mg/dl.
5. Oral feeds are introduced gradually and glucose infusion is tapered off.
6. If blood glucose level is not corrected then bolus administration of dextrose can be
repeated and serum cortisol and insulin level is checked.
7. Glucogen and/or epinephrine, diazoxide may be given to the babies with maternal diabetes
mellitus or erythroblastosis.
8. Asymptomatic case with low blood sugar level should be treated as symptomatic cases.
Nursing management
 Identify infants at risk or with hypoglycemia
 Reduce environmental factors that predispose to hypoglycemia eg cold stress, respiratory
distress.
 Administer IV glucose as prescribed
 Initiate early feedings in healthy infant.
 Ensure adequate intake of carbohydrates ( breast milk or formula).
Prognosis
The prognosis of hypoglycemia is generally poor. Untreated symptomatic neonates usually have
fatal outcome. Among survivors of symptomatic cases, about 50 percent neonates may have
mental retardation or cerebral palsy with convulsions. In asymptomatic hypoglycemic babies of
diabetic mothers the prognosis is usually excellent.

Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 7

Neonatal HYPOCALCEMIA
Introduction
Hypocalcaemia is a common metabolic problem in newborns. Hypocalcemia occurs in 30% of
infants with very low birth weight (<1500 g) and 89% of infants whose gestational age at birth
was less than 32 weeks. A high incidence is also reported in infants of mothers with diabetes
mellitus and in infants with birth asphyxia.
Definition
Hypocalcaemia is defined as total serum calcium <7 mg/dl or ionized calcium < 4mg/dl.
Perinatal metabolism
During pregnancy, calcium is transferred actively from the maternal circulation to the fetus by a
transplacental Ca pump regulated by parathyroid hormone. The majority of fetal Ca accretion
occurs in the third trimester. This process results in higher plasma Ca concentrations in the fetus
than in the mother and leads to fetal hypercalcemia, with total and ionized Ca concentrations of
10
to 11 mg/dL (2.5 to 2.75 mmol/L) and 6 mg/dL (1.5 mmol/L), respectively, in umbilical cord
blood at term After the abrupt cessation of placental transfer of Ca at birth, total serum Ca
concentration falls to 8 to 9 mg/dL (2 to 2.25 mmol/L) and ionized Ca to as low as 4.4 to 5.4
mg/dL (1.1 to 1.35 mmol/L) at 24 hours.. Serum Ca concentration subsequently rises, reaching
levels seen in older children and adults by two weeks of age.
Calcium homeostasis in newborn
Body calcium exists in two major compartments; (a) Skeleton (99%) and (b)
Extracellular fluid (1%).
Both calcium and maternal parathyroid hormone cross the placenta
There is an active transport of calcium and phosphorus to fetus from maternal sources
Fetal concentrations are 1.0mg/dl higher than maternal
Placental transport of calcium takes place during last trimester of pregnancy
Paratharmone & 1,25 dihydroxy vitamin D3 are the principal calcium regulating hormones
Paratharmone mobilizes calcium from bones, increases calcium reabsorption in renal tubules
Serum calcium level falls after birth in preterm babies
Hypocalcaemia occurs during 24-36 hours of age
Due to reduced GFR and defective tubular reabsorption in the newborn kidney is unable to
excrete
phosphorus
During first days of life serum calcium falls and phosphorus level rises.
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 8
Types of hypocalcaemia
1. Early onset Neonatal Hypocalcaemia (ENH)
This condition is fairly common and seen within the first 3 days of life.
 Prematurity: Preterm babies born at a gestation £32 weeks are at an increased risk of
ENH in the first 3 days of postnatal life. This may be related to premature termination of
trans-placental supply, exaggeration of the postnatal drop to hypocalcemic levels and
diminished target organ responsiveness to parathyroid hormone.
 Infant of diabetic mother: (gestational and insulin dependent). This may be related to
increased calcium demands of a macrocosmic baby.
 Perinatal asphyxia: Hypocalcaemia and hyperphosphatemia in this condition may be
related to renal insufficiency, metabolic acidosis and diminished parathyroid hormone
secretion.
Screening is recommended in at-risk neonates:
1. Preterm infants (£32 weeks)
2. Infant of diabetic mothers
3. Severe perinatal asphyxia defined as Apgar score <4 at 1 minute of age. Screening for
hypocalcaemia is not needed in small for gestational age (SGA) infants unless additional risk
factors like asphyxia are present.
Time schedule for screening:
At 24 and 48 hours in high-risk babies
Clinical presentation:
 Early onset: jitteriness, apnea, cyanotic, episodes, high pitched cry, abdominal distension.
 Late onset: twitching, tremors, seizures.
Diagnosis
1. Clinical presentation
2. History: abnormal movements and lethargy may precede seizure activity rarely use of
goat’s milk or cow milk may be reported.
3. Laboratory: Total or ionized serum calcium (total <7 mg/dL or ionized <4.0 mg/dL).
Ionized calcium is the preferred mode for diagnosis of hypocalcaemia.
4. ECG
Treatment:
1. Patients at increased risk of hypocalcemia: Preterm infants, sick infants of diabetic mothers
and those with severe perinatal asphyxia should receive 40 mg/kg/day of elemental calcium (4
ml/kg/day of 10% calcium gluconate). Infants tolerating oral feeds may receive this calcium
orally
q 6 hourly. Therapy should be continued for 3 days.
2. Patients diagnosed to have asymptomatic hypocalcemia: Infants detected to have
hypocalcemia on screening and who are otherwise asymptomatic should receive 80-mg/kg/day
elemental calcium (8 ml/kg/day of 10% calcium gluconate) for 48 hours. This may be tapered to
50% dose for another 24 hours and then discontinued. Neonates tolerating oral feeds may be
treated with oral calcium (IV preparation may be used orally).
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 9
3. Patients diagnosed to have symptomatic hypocalcemia: These patients should receive a bolus
dose of 2 ml/kg/dose diluted 1:1 with 5% dextrose over 10 minutes, under cardiac monitoring.
This should be followed by a continuous IV infusion of 80-mg/kg/day elemental calcium for 48
hours. Continuous infusion is preferred to IV bolus doses (1ml/kg/dose q 6 hourly).
2. Late onset neonatal hypocalcemia (LNH)
This condition is rare as compared to ENH. It usually presents at the end of the first week It is
usually symptomatic in the form of neonatal tetany.
Causes of late onset hypocalcemia
1. Hypomagnesemia
2. Increased phosphate load: Cows milk
3. Hypoparathyroidism
 Idiopathic, transient
 Hypoplasia, aplasia of parathyroid glands. (DiGeorge’s syndrome)
 Pseudohypoparathyroidism
 Maternal hyperparathyroidism
4. Vitamin deficiency
 Maternal vitamin D deficiency
 Malabsorption
 Maternal anticonvulsant therapy
 Renal insufficiency
 Hepatobiliary disease
Investigations
These should be considered in LNH or if the hypocalcaemia does not respond to adequate
doses of calcium.
 Serum magnesium: Magnesium levels <1.2 mg/dL should be treated
 Serum phosphate (P): Phosphate levels are increased in renal failure, top feeding with
cow’s milk and hyperparathyroidism.
 Alkaline phosphates (ALP): ALP levels are increased in hyperparathyroidism
 PTH levels: PTH is decreased in hyperparathyroidism.
 Urine calcium/ creatinine ratio: Ratio >0.2 is suggestive of hyperparathyroidism
 Chest x-ray
 Maternal calcium, phosphate and alkaline phosphates levels: These would be helpful in
detection of maternal vitamin D deficiency
Treatment of LNH
The treatment of LNH is specific to etiology and may in certain diseases be life-long
1. Hypomagnesaemia: Symptomatic hypocalcaemia unresponsive to adequate doses of IV
calcium therapy is usually due to hypomagnesaemia. It may present either as ENH or later as
LNH. The neonate should receive 2 doses of 0.2ml/kg of 50% MgSO4 injection, 12 8 hours
apart,
deep IM followed by a maintenance dose of 0.2 ml/kg/day of 50% MgSO4, PO, 3 days.
2. High phosphate load: These infants have hyperphosphatemia with near normal
calcium levels. Exclusive breast-feeding should be encouraged and top feeding with
cow’s milk should be discontinued.
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 10
3. Hypoparathyroidism: These infants tend to be hyperphosphatemic and hypocalcemic
with normal renal functions. Elevated phosphate levels in the absence of exogenous
phosphate load (cow’s milk) and presence of normal renal functions indicates
parathormone inefficiency. These neonates need supplementation with calcium (50
mg/kg/day in 3 divided doses) and 1,25(OH)2 Vitamin D3 (0.5-1 mg/day). Syrup Shelcal
has 250 mg/5ml of calcium and Vitamin D3 (calcitriol) is available as 0.25 mg capsules.
Therapy may be stopped in hypocalcaemia secondary to maternal hyperparathyroidism
after 6 weeks.
4. Vitamin D deficiency states: These babies have hypocalcaemia associated with
hypophosphatemia due to an intact parathormone response on the kidneys. They benefit
from Vitamin D3 supplementation in a dose of 30-60 mg/kg/day
Nursing management
1. Identify infant at risk or with hypocalcaemia.
2. Provide calm environment to reduce stimuli that might precipitate a seizures or tremors.
3. Administer calcium as prescribed. Observe for sign of acute hypocalcaemia (eg
bradycardia, vomiting)
4. Precautions should be taken while administration of calcium
Bradycardia and arrhythmia are known side effects of bolus IV calcium administration
and bolus doses of calcium should be diluted 1:1 with 5% dextrose and given under
cardiac monitoring.
5. An umbilical venous catheter (UVC) may be used for administration of calcium only after
ensuring that the tip of the catheter is in the inferior vena cava.
6. Hepatic necrosis may occur if the tip of the UVC lies in a branch of the portal vein.
7. Umbilical artery catheter (UAC) should never be used for giving calcium injections.
8. Accidental injection into the UAC may result in arterial spasms and intestinal necrosis.
9. Skin and subcutaneous tissue necrosis may occur due to extravasation. Hence IV sites
where calcium is being infused should be checked at least q 6 hourly to monitor for
extravasation and avoid subcutaneous tissue necrosis.

Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 11

Neonatal Hypomagnesemia

Introduction
Hypomagnesemia is an electrolyte disturbance in which there is an abnormally low level of
magnesium in the blood. Usually a serum level less than 0.7 mmol/l is used as reference.
Hypomagnesaemia is not equal to magnesium deficiency. Hypomagnesaemia can be present
without magnesium deficiency and vice versa. Magnesium is the second most abundant
intracellular cation and the fourth most abundant cation overall. Almost all enzymatic processes
using phosphorus as an energy source require magnesium for activation
It is resorbed through the small intestine, and to a lesser degree in the colon. The rectum and
sigmoid colon can absorb magnesium Hypomagnesaemia stimulates and hypomagnesaemia
inhibits this absorption. The kidneys regulate the serum magnesium. About 2400 mg of
magnesium passes through the kidneys, of which 5% (120 mg) is excreted through urine. The
loop
of Henle is the major site for Mg-homeostasis, and 60% is resorbed.
Definition
Neonatal hypomagnesaemia is defined as total magnesium (TMg) ≤0.65 mmol/L (1.6 mg/dl
Normal plasma magnesium is 1.5-2.3mg/dl. Infants have slightly higher plasma magnesium
concentration than older children.
Human milk contains approximately 35mg/l of magnesium formula contains 40-70mg/l of
magnesium. Small intestine is the major site of magnesium absorption.
Causes
1. Gastrointestinal disorder
Diarrhea, nasogastric suction, emesis, pancreatitis, celiac disease, cystic firbrosis, protein
calorie malnutrition, hypomagnesaemia secondary to hypocalcaemia, chronic kidney
disease.
2. Renal disorders
Acute tubular necrosis, hypocalcaemia, genetic diseases, Bartter syndrome, autosomal
recessive renal magnesemia wasting.
3. Miscellaneous causes
Poor intake, hungry bone syndrome, pancreatitis, exchange transfusion, infant of diabetic
mother, IUGR.
Transient hypomagnesaemia in newborn
Commonly seen in infants of diabetic mother due to maternal depletion from osmotic losses.
Other
maternal diseases that cause magnesium losses predispose infants to hypomagnesaemia.
Hypomagnesaemia is more common in infants with intrauterine restriction.hyomagnesemia
develops in infants who require exchange transfusion because of magnesium removal in banked
blood.
Clinical manifestation
 Seizures
 Tetany
 Tremors
 Restlessness at 28 weeks of life due to severe hypomagnesemia
Neeta Rajesh Bhide, (M.Sc.N., M.A. Psyco., M.C.F.H., M.D.F.M. Page 12
 Depression
 ECG changes flattening of T waves and lengthening of ST segment
 Arrhythmias may occur
Diagnosis
 Clinical manifestation
 Serum magnesium: low serum magnesium level of < 1.6 mg/dl suggests
hypomagnesaemia.
Management
 Severe hypomagnesaemia treated with parenteral magnesium-
 Magnesium sulphate is given at dose of 25 -50 mg/kg/ 0.05-.1ml/kg og 50% solution
administered as I/V I/M in neonates. Dose is repeated every 8-12 hours in neonates.
 Exchange transfusion
Bibliography
1. Hockenberry J.Marilyn(2005)Wong’s Essentials of Pediatric Nursing, Edition -7
th
Missouri: Mosby pp272-282
2. Dutta Parul(2007) Pediatric Nursing, Edition-1
st New Delhi:Jaypee Brothers, pp 102-103
3. Marlow R Dorothy & Barbara .A Redding (2001).Textbook of Pediatric Nursing, Edition6
th
, Philadelphia: W.B.Saunders.pp 386-437.
4. Chloherty, Eichenwald,(2008) Manual of neonatal care,edition-6
th ,Lippincott Williams &
Wilkins : Philedephia,pp540,551
5. Kleigman, Behrman,(2008),Nelson’s Textbook of Peadiatircs,Edition- 18th ,Volume 2,
Elsevier: Saunders, pp-282
6. Dr.Meharban. Singh, (2004),Care of Newborn,edition-6
th ,Sagar
Publications:NewDelhi,pp-351-363
Internet
1. www.uptodate.com/patients/content/topic.do?topicKey=~M0SV9YKC...
2. www.newbornwhocc.org/pdf/Hypoglycemia.pdf
3. www.healthsystem.virginia.edu/uvahealth/peds_diabetes/hyponew.cfm
4. www.healthsystem.virginia.edu/uvahealth/peds_diabetes/hyponew.cfm
5. www.newbornwhocc.org/pdf/Hypocalcemia.pdf
6. www.healthsystem.virginia.edu/uvahealth/peds_hrnewborn/hypocal.cfm
7. www.ucsfhealth.org/childrens/health_professionals/.../48_Seizures.pdf