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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. jlkj • Mm,m ,m • 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.