POST TERM

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POST MATURE INFANT, BABY OF DIABETIC

MOTHER AND SUBSTANCE USE MOTHERS


POST TERM NEONATE :-
The normal length of pregnancy is from 37 weeks to 42 weeks
Prolonged pregnancy is also referred to as post term, post
maturity and postdates pregnancy
and is said to be the one that exceeds 42 weeks of gestation
Prolonged pregnancy and post term are used synonymously
and relate to the duration of
pregnancy and not a maternal condition ( Fraser et.al,
2006).The most frequent cause of post
term pregnancy is inaccurate dating.
Prolonged pregnancy is the most common reason for induction
of labour.
The post newborn is at high risk for morbidity and has a
mortality rate two to three times
greater than that of term infants.
DEFINITIONS
• Prolonged pregnancy; Defined as a pregnancy
that exceeds 42 weeks gestation or 294 days
• past the first day of the mothers last normal
menstrual period (Marcia et al, 2007).
• Post term; Any newborn born after 42 weeks
of gestation (Joel et al, 2007).
• Incidence:- 12% of all births.
CAUSES
• The cause of prolonged pregnancy is
unknown.
RISK FACTORS
• Miscalculation or inaccurate last menstrual period.
• Lack of stimulation factors such as oxytocin and
prostaglandins e.g. in women who take
• high doses of aspirin or like compounds, which are known
to inhibit the synthesis of prostaglandins.
• Prime gravidae
• High parity ( five or more pregnancies)_ the recurrence risk
of post term birth increases with parity.
• Previous post term pregnancy
• Advanced maternal age is a strong risk factor (over 35
years)
DIAGNOSIS
• The accurate diagnosis of postdates pregnancy
can be made on by proper dating.
• The estimated date of delivery is most
accurately determined early in pregnancy.
However,
• the following aid in diagnosis.
History taking
Establish the first day of the last normal
menstrual period. Then calculate the expected
date of delivery. For the EDD to be accurate:
The woman should be sure of her LMP
• The period must have been of normal length
and regular.
• Not having been on oral contraceptives pill.
• Quickening; maternal perception of first fetal
movements at about 16-20 weeks.
Abdominal examination
• On abdominal inspection the pregnancy
appears bigger than the gestational age.
• Abdominal palpation for height of fundus
which will be more than 40 weeks.
Ultra sound scanning
• In patients without reliable clinical data,
ultrasound is beneficial. However, ultrasonography
is most accurate in early gestation (before
12weeks).
After 12weeks,the crown-rump length becomes
less accurate in determining gestational age
because the fetus begins to curve.
• Ultra sound can also show placental calcification
and the amount of amniotic fluid at term which is
reduced in postterm.
RISKS AND CLINICAL IMPLICATIONS OF POST-TERM PREGNANCY.
FETAL RISKS

• AT the end of pregnancy, the placenta which supplies the fetus


with oxygen, nutrients and removal of wastes begins to fail to
function properly due to aging or infarction. Therefore, the
baby’s health may be at risk of :-
• Asphyxia
• respiratory distress syndrome and
• meconium aspiration. In addition, the following occurs;
• Fetal distress syndrome due to insufficient oxygen supply to the
fetus
• Oligohydraminious occurs due to reduced urine output by the
fetus
• Hypoglyceamia due to too little glucose producing in stores.
Clinical manifestation :-
• Wasted physical appearance
• Little subcutaneous fat
• Long thin appearance
• Long finger and toenails
• Minimum vernix caseosa
• Abundant scalp hair
• Skin frequently cracked and desquamating
parchment paper like pale skin
• Absence of lanugo hair
Diagnostic evalution :-
• General appearance
• Gestational age
• APGAR score
• Blood gases
PROBLEMS ASSOCIATED WITH POST
MATURITY
• FETAL DISTRESS :- The effect of uterine
contractions on an already compromised
placenta may cause fetal hypoxia causing the
fetus to be distressed.
MECONIUM ASPIRATION.
• Hypoxia and distress may cause relaxation of
the anal sphincter leading to the passage of
meconium while in utero.
• The fetus can aspirate the meconium stained
liquor into the lungs either in utero or during
delivery.
HYPOGLYCEAMIA
• May result from nutritional deprivation and
resultant depleted glycogen stores.
HYPOTHERMIA
• • This is due to decreased liver glycogen and
brown fat stores.
• • This is due to reduced fats which act as an
insulator.
POLYCYTHEMIA
• This is the increase in the red blood cell
production coming in as a result of hypoxia.
BIRTH INJURIES
• There will complete ossification of the skull
bones leading to poor moulding which
contributes to birth injuries.
SEIZURES
• The neonate can have episodes of seizures
which can come as a result of the hypoxia
experienced during intra uterine
INTRA UTERINE DEATH
• This can result from acute fetal hypoxia while
it is in uterus and this can lead to fetal death
MANAGEMENT OF A POST MATURE BABY

• • The management is directed at


differentiating the fetus that has post maturity
syndrome from the one who is large, well
nourished and tolerated the prolonged
pregnancy.
• The goal of management is to identify and
manage the post mature newborn’s potential
problems.
Nursing Management
• Respiratory assessment
• Airway management
• Thermoregulations
• Fluid and electrolyte management
• Potential nutritional support
PSYCHOLOGICAL SUPPORT
• Provide emotional support to the parents to
encourage them as the neonate may appear
with dry cracking skin and possible aspiration
of meconium.
• Explain all the procedures in order to obtain
co- operation.
MAINTAINING A CLEAR AND PATENT AIR
WAY
• If the amniotic fluid is meconium stained the
baby’s nose and mouth should be wiped
before the baby takes its first breath to
minimize the chances of meconium aspiration
syndrome . After birth the direct suctioning of
the trachea is needed.
OBSERVATION
• Observe the cardiopulmonary function of the neonate because of
the stress of labour which is poorly tolerated by the post mature
infant and may lead to severe birth asphyxia.
• Monitor the apical beat of the neonate which should be in the range
of 120b/m to 160b/m as well as the respirations which should be
between 30 to 60 b/m.
• Monitor the skin colour as these neonates tend to be cyanosed as
well as jaundiced.
• There is also need to observe for the occurrence of convulsions
which are likely to be experienced by the neonate.
• Observe for any injury the neonate can sustain such cephalo
heamatoma and caput succedenum.
• Other observations are as for any normal neonate.
PROVISION OF WARMTH
• • The post mature neonate tends to suffer from hypothermia
because of their reduced fat stores.
• • The neonate can be nursed together with the mother
through skin to skin contact hence provision of warmth from
the mother more especially if the condition is stable.
• • If the condition of the neonate needs interventions from
neonatal intensive care unit then the neonate can be nursed
in the pre warmed incubator with an incubator temperature
of (32.5 to 37.7 degrees Celsius).
• The environment should be warm enough to provide enough
heat to the neonate as this baby has low glycogen and brown
fat stores
PREVENTION OF HYPOGLYCAEMIA
• If the neonate is unable to suck. Intravenous fluid of
10 % of dextrose can be given.
• This can be followed by breast feeding either
expressed or cup and spoon type of feeding until such
a time a baby can breast feed on its own.
• Early initiation of feeding is very important to prevent
hypoglycaemia (within 1 hour) after delivery.
• Frequent monitoring of blood glucose is very cardinal
to ensure that the neonate is not in a state of
hypoglycaemia.
The Infant of a Diabetic Mother
• Is infant born to a mother with diabetes or gestational
diabetes, severity of the problem depend on the severity of
maternal diabetes.
• Altered physiology: hyperinsulinemia in utero secondary to
decreased epinephrine and glucose response result in the
following in the infant: Altered physiology
• Amount of body fat.
• Hypoglycemia can occur immediately or within 2-12 hours
post delivery.
• IDM may symptomatic or not with blood glucose below 20
mg/dl.
• Hypocalcemia: associated with prematurity, difficult labor
and or asphyxia at birth, can occur during first 24-48 h after
birth.
• Birth trauma such as cephallhematom due to large size of
infant.
• Hyperbilirubinemia: occur 48-72 h due to immature liver
and inability to conjugate bilirubin.
• Prematurity or SGA associated with placental insufficiency.
• Respiratory problems may occur.
• Polycythemia: HCT more than 65% or Hb% 22gm/dl, which
the risk of thrombosis, RDS, hypoglycaemia & hypocalcemia.
• Congenital anomalies: (cardiac & skeletal).
• Infection.
Diabetes Mellitus
• A chronic metabolic disorder involving
complete or decreased insulin secretion or
other insulin dysfunction resulting in increased
serum glucose concentration.
Diagnostic criteria
• Family or mother history of DM.
• Determine gestational age.
• Blood studies:
• Blood glucose, HCT, Hb%, blood gases,
bilirubin, electrolytes.
Clinical manifestations:
Marcosomia, cardiomegaly, hepatomegaly,
abundent fatty, hair, vernix caseosa
• May SGA
Diabetes- ADA Classification
• • Type 1: IDDM (Juvenile diabetes)- early
onset, lack of insulin, presence of antibodies
against B-cells; insulin needed, ketoacidosis
seen.
• Type 2: NIDDM (Adult diabetes, Maturity
onset)- older patients, insulin resistance
common, decreased insulin sensitivity,
overweight patients, significant genetic
component.
• • Gestational Diabetes : Carbohydrate intolerance with onset
or first recognition during pregnancy
• Morbidities in Infants of Diabetic Mothers
• Macrosomia
• Hypoglycemia
• RDS
• IUGR
• Hypocalcemia
• Hyperbilirubinemia
• Congenital Anomalies
• Polycythemia
• Hyper viscosity
• Cardiomyopathy
• Increased fetal death
• Postnatal problems
Macrosomia
• Common Definition: Infant with Bwt >4000 grams
and/or Head Circumference & Length > 90th percentile .
• IDMs have increased fat cells and fat cell hypertrophy.
• Excess non-fatty tissue in shoulders and scapular areas.
Macrosomia ¼ th of insulin dependent mothers have
Macrosomic infants.
• Excess growth happens in 3rd trimester.
• GDM mothers have same incidence of Macrosomic
infants as other diabetics.
Macrosomia- Complications
. Birth Injuries- Brachial Plexus injury, Fracture Clavicle or
Humerus, Facial nerve injury, Cephalhematoma.
• Shoulder Dystocia (2-4 fold more)
• Hypoglycemia
• Increased risk for asphyxia
• Increased recurrence risk in mother.
Morbidities- Congenital Anomalies
• Upto 4-fold increase in infants of IDDMs
• Malformations shown to occur before 8th week of gestation.
• Most common are CV, Musculo-Skeletal & CNS.
• Incidence decreased with tight glucose control in mothers.
Respiratory Distress Syndrome
• Increased risk of RDS in IDMs <37 weeks GA
• Possible insulin interference with surfactant
composition and delayed maturation of
surfactant system
• Metabolic Complications
• Hypoglycemia
• Hypocalcemia
• Hypomagnesemia
• Hypoglycemia
Occurs in up to 25 % of IDMs.
• Half of hypoglycemia occurs in first 24 hours.
• Less likely when mother’s glucose tightly controlled.
• May be asymptomatic.
• Hypocalcemia & Hypomagnesemia Occur in 50% or more of IDMS
born to mothers who are IDDM.
• Decreased parathormone or parathyrin hormon (PTH) secretion in
IDMs
• IDMs may have decreased calcium transfer
• Decreased Mg++ levels in mothers
• ? Decreased Mg++- Decreased PTH
Polycythaemia/ Hyperbilirubinemia
• Fetal hypoxia Polycythemia hyperbilirubinemia
• Ineffective RBC Production
Management of IDMs
• Delivery:
Consider as high risk. (mother & infant)
Follow basic steps of resuscitation for infant.
• Nursing Management
• Respiratory assessment
• Airway management
• Thermoregulations
• Hypoglycemia
• Fluid and electrolyte management
• Potential nutritional support
Post-delivery Observe / Evaluate for:
• Asphyxia.
• Birth injury.
• Malformations.
• Macrosomia.
• Hypoglycemia.
• Respiratory Distress.
Management of Hypoglycemia
• May be asymptomatic
• Can occur within 30 minutes.
• May last up to 48 hrs or more.
• Check Blood Glucose as soon as possible
after birth and at regular intervals for 48 hrs.
• Early feeds.
• Blood Glucose < 30 mg/dl IV dextrose
recommended.
Prognosis
• IDMs 10 x more likely to be obese.
• Macrosomic infants 6 X likely to be obese at
age 7 (Vohr 1980)
• Increased risk for teenage obesity
• Increased risk for glucose intolerance as young
adults (19%)
• No developmental problems noted in
asymptomatic hypoglycemic infants.
Follow up for the IDM
• Developmental risk:
• CP , seizures 3-5 X common. SGA IDM infants
have increased risk for cognitive delay at 3-5
years.
• Metabolic Risk:
• IDMs with 1 parent Type 2DM have 1-6 % risk
of DM themselves
• INFANT OF SUBSTANCE ABUSED MOTHER :-
An infant of a substance-abusing
Mother (ISAM) is one whose mother has
taken drugs that may potentially cause
neonatal withdrawal symptoms. The
constellation of signs and symptoms
associated with withdrawal is called the
neonatal withdrawal syndrome.
Pathophysiology of specific drugs are as
follows:
• Opiates. Opiates bind to opiate receptors in the CNS; part of the clinical
manifestations of narcotic withdrawal result from α2-adrenergic supersensitivity
(particularly in the locus ceruleus).
• Cocaine. Cocaine prevents the reuptake of neurotransmitters (epinephrine,
norepinephrine, dopamine, and serotonin) at nerve endings and causes a
supersensitivity or exaggerated response to neurotransmitters at the effector organs.
Cocaine is a CNS stimulant and a sympathetic activator with potent vasoconstrictive
properties. It causes a decrease in uterine and placental blood flow with consequent
fetal hypoxemia. It causes hypertension in the mother and the fetus with a reduction
in fetal cerebral blood flow.
• Alcohol. Ethanol is an anxiolytic-analgesic with a depressant effect on the CNS. Both
ethanol and its metabolite, acetaldehyde, are toxic. Alcohol crosses the placenta and
also impairs its function. The risk of affecting the fetus is related to alcohoigns and
symptoms for specific
drugs are as follows:
SIGNS AND SYMPTOMS OF NEONATAL
ABSTINENCE
• Opiates. Infants born to opiate-addicted mothers show an
increased incidence of IUGR andperinatal distress.The
clinical course may be protracted, with exacerbations or
recurrence of symptoms afterdischarge. Restlessness,
agitation, tremors, wakefulness, and feeding problems may
persist for 3–6 months. There is a reduced incidence of both
RDS and hyperbilirubinemia.
• CocaineSymptoms seen in neonates exposed to cocaine in
utero. Irritability, tremors, hypertonia, a high-pitched cry,
hyperreflexia, frantic fist sucking, feeding problems,
sneezing, tachypnea, and abnormal sleep patterns period of
irritability and overactivity, a period of lethargy and
decreased tone has been described.
SIGNS AND SYMPTOMS OF NEONATAL
ABSTINENCE
• Alcohol. Probably the foremost drug of abuse
today. The risk that an alcoholic woman will
have a child with fetal alcohol syndrome (FAS)
is ∼ 35–40%. However, even in the absence of
FAS, and also with lower alcohol intakes, there
is an increased risk of congenital anomalies
and impaired intellect. It is estimated that
alcohol is the major cause of congenital
mental retardation today. FAS consists of the
following:
• Prenatal or postnatal growth retardation, CNS involvement such as
irritability in infancy or hyperactivity in childhood, developmental delay,
hypotonia, or intellectual impairment.
• Facial dysmorphology. Microcephaly, microphthalmos, or short palpebral
fissures, a poorly developed philtrum, a thin upper lip (vermilion border),
and hypoplastic maxilla.
• benzodiazepines. Symptoms are indistinguishable from those of narcotic
withdrawal, including seizures. The onset of symptoms may be shortly
after birth.
• Phencyclidine (PCP). Symptoms usually begin within 24 hours of birth, and
the infant may show signs of CNS “hyperirritability” as in narcotic
withdrawal. Gastrointestinal symptoms of withdrawal are less common.
• Selective serotonin reuptake inhibitors (SSRIs). Symptoms, occurring in up
to 30% of exposed infants, may include irritability, seizures, myoclonus,
hyperreflexia, jitteriness, persistent crying, shivering, increased tone,
feeding difficulties, tachypnea, and temperature instability.
Nursing Management
• Respiratory assessment • Airway management • Thermoregulations
• Fluid and electrolyte management
• Potential nutritional support
• Supportive care
• Minimal stimulation. Attempt to keep the infant in a darkened, quiet environment.
Reduce
• other noxious stimuli. Swaddling and positioning. Use gentle swaddling with positioning
that encourages flexion
• rather than extension. Prevent excessive crying with a pacifier, cuddling, and so on.
Feedings should be on
• demand if possible, and treatment should be individualized based on the infant's level of
• tolerance. General drug treatment. Warning: Naloxone (Narcan) may precipitate acute
drug
• withdrawal in infants exposed to narcotics. It should not be used in infants born to
mothers
• suspected of abusing opiates.
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• History. Many, if not most, drug abusers withhold this information. Details of the
extent, quantity, and duration of abuse are unreliable. However, the history is the
simplest and most convenient means of diagnosis.
• Laboratory tests. The most commonly used tests to detect drugs of abuse are
immunoassays (enzymatic assays or radioimmunoassays).
• Urine. Easily obtained and is the most common substance used for drug testing. It
reflects intake only in the last few days before delivery. Urine may be obtained from
both the mother and the infant (in whom the substance may persist for a longer
time).
• Meconium. Easily obtained, and drugs may be found up to 3 days after delivery. It
reflects drug use after the first trimester, has a lower rate of false negatives, is a
more sensitive test than urine for detecting drug abuse, and reflects usage over a
longer period than is detectable by urine testing. stools.
• Hair. This is by far the most sensitive test available for detection of drug abuse. Hair
grows at 1–2 cm/mo; hence maternal hair can be segmented and each segment
analyzed for drugs.

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