Stage 4: Individuating-reflexive—Adolescence beco- me more sceptical and begin to compare the religious
2. Labour and Delivery Conditions (i) Forceps or vacuum extraction
(ii) Abnormal presentation or breech (iii) Caesarean section
(iv) Cephalo-pelvic disproportion
(v) Maternal hypotension or haemorrhage 3. Foetal Conditions
(i) Premature or post mature birth
(ii) Meconium in amniotic fluid (iii) Foetal growth retardation (iv) Foetal malformation (v) Hydrops foetalis
(vi) Oligo- or polyhydramnios (vii) Multiple births
(viii) Sepsis (ix) Birth trauma (x) Difficult birth Pathophysiology
l Hypoxia and hypercarbia—leads to respiratory acidosis.
l Hypoxia—causes metabolic acidosis.
l Acidosis—leads to mixed respiratory and metabolic acidosis.
l Acidosis and hypotension of asphyxia stimulates chemoreceptors and baroreceptors causing constriction of the arterioles and a shunting of blood to the brain, heart and adrenals at the expense of the other organs of the body.
Essential Precautions Assessment and Management 1. Assessment of apnoea
(i) Heart rate
(ii) Response to stimulation
(iii) Need for positive pressure ventilation 2. Initial treatment goal
(i) Eliminate hypoxic environment
(ii) Correct metabolic and respiratory acidosis (iii) Stabilize blood pressure to maintain adequate
cardiac output.
3. Neonates at risk immediate and initiation of care plan.
Resuscitation Purpose or Indication
l To provide an adequate air way with expansion of the lungs to decrease the PCO2, increase the PO2.
l To support adequate cardiac output.
l To minimize oxygen consumption by reducing heat loss.
ABCD approach A—Air way B—Breathing
C—Circulation D—Drugs
Assessment of newborn after birth, depends on the APGAR score, of the asphyxia are classified and management provided to the infant.
If APGAR score is:
l 7 to 10—No or mild depression/asphyxia
l 4 to 6—Moderate depression/asphyxia
l Below 3—Severe asphyxia
Severe Moderate Mid depression asphyxia asphyxia or none
Suction Suction Suction
Oral air way O2 stream Mild to face stimulation
O2 bage and No improvement O2 Stream mask ventilation 30–60 sec to face
(if necessary)
No improvement Air way 30–60 sec
Intubation and O2 by bage and continue ventilation ventilation
No improvement Naloxone for 2 minutes injection
(Narcan) (if indicated)
External cardiac massage
Pharmacological assistance
Reevaluate APGAR score at 5 minutes If it is severe asphyxia immediate cardio pulmonary resuscitation.
Medication
l Injection naloxone 0.25 ml/kg IV or IM or ETT
l Injection adrenaline 0.25 ml/kg at 1 : 10,000 solution
l Injection sodium bicarbonate slowly—5 ml of 4%, sodium bicarbonate through umbilical vein
l Dextrose water IV 5 ml slowly.
Nursing Management
l Early assessment by APGAR score to identify the problem.
l Suctioning to the baby immediately after birth to remove the secretion.
l Maintain the thermoregulation by drying the baby and cover or keep the baby in a warmer or incubator.
l Administer oxygen to the baby.
l Assist for intubations.
l Assist in resuscitation.
l Insert the nasogastric tube for aspiration of stomach content.
l Administer the drugs prescribed to the infant.
l Monitor the vital signs and record.
l Secure the intravenous line, administer the dextrose intravenously as per order.
RESPIRATORY DISTRESS SYNDROME (RDS)
Respiratory Distress Syndrome (RDS) also known as hyaline membrane disease, is the commonest respiratory disorder in preterm infants. It is characterized by increased pulmonary vascular resistance and decreased or absent of surface-active substance resulting in stiff lungs. Cause is unknown.
Predisposing Factors
l Preterm infant
l Infant born to diabetic mother
l Infant born by cesarean section
l Perinatal asphyxia
l Non-immune hydrops fetalis
l Low birth weight babies.
Pathophysiology
Surfactant is a surface-active phospholipid secreted by the alveolar epithelium. It acts as a detergent, this
substance reduces the surface tension of fluid that lines the alveoli and respiratory passages resulting in uniform expansion and maintenance of lung expansion
In preterm babies
Surfactant decreased Structurally or deficiency occurs immature lung
Infant unable to keep the lung inflated or inability to maintain lung expansion
Atelactasis, hypoxemia and hypercapnia
Prolonged hypoxemia Atelactasis
Activates anaerobic glycolysis Atelactatic lung produces increased produces excess CO2 amount of lactic acid
Respiratory acidosis
Metabolic acidosis Lower pH causes vasoconstriction pulmonary circulation (↓ deficiency and Hypoxemia alveolar perfusion)
Transduction of fluid Blood O2 concentration ↓ into the alveoli
Respiratory difficulty due
to diminished lung Surfactant production distensibility are not circulated to the
alveoli Lungs are stiffer
Clinical Manifestations
l Tachypnea (> 60 breaths/minute)
l Chest retraction
l Nasal flaring
l Grunting
l Cyanosis
l Poor air entry
l Later stage—abdominal distension
l Bowel sounds are poor or absent
l Oedema is common in hands and feet.
Diagnostic Test Findings
l Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with RDS), but 24 hours after birth X-rays show ground glass appearance and air filled bronchi.
l Arterial Blood Gas analysis (ABG)—Increased PCO2, decreased PO2, decreased arterial blood pH (from respiratory or metabolic acidosis both).
l Chest auscultation reveals normal or diminished air entry and crackles (rare in early stages).
Medical Management
l Provides effective respiratory support
m Warm, humidified oxygen is administered by oxygen hood, or if such treatment fails, by continuous positive airway pressure (administered by nasal prongs or mechanical ventilation).
m Special ventilation techniques are used on infants who don’t respond to conventional mechanical ventilation.
n High-frequency ventilation.
n Nasal continuous positive airway pressure (CPAP) is used in less severe cases.
n High-frequency oscillatory ventilation.
m Extra corporeal membrane oxygenation
n The last choice for ventilation.
n Keep the baby in controlled ventilation usually positive end expiratory pressure (PEEP) if CO2 is increased.
l Keep the baby in a radiant infant warmer or isolate for thermoregulation.
l Secure intravenous line to maintain fluid and electrolyte balance.
l Administer sodium bicarbonate 5 ml of 4% to control acidosis.
l Nasogastric tube feeding or TPN if the neonate is too weak to suck the breast or oral feeding.
l Administration of surfactant by an ET tube with in the first 24 hours after birth.
m Time of surfactant administration—two approaches have been used for surfactant delivery:
n Prophylactic and rescue treatment.
n Prophylactic administration involves giving surfactant soon after birth, as soon as the infants has been stabilized.
n Rescue administration involves giving surfactant to infants who have established RDS and require mechanical ventilation and supplemental oxygen.
m Administration and dose of surfactant
n Normally single dose therapy is administrated but several studies have shown that two doses therapy is better.
n The dose of surfactant is Infasurf–3 ml/kg Survanta–4 ml/kg.
Note: Surfactant therapy is a very costly therapy, it needs mechanical ventilation. It is available in certain specialized institutions.
Complications
l Pneumothorax
l Risk of Retinopathy of prematurity
l Bronchopulmonary dysplasia
l Respiratory insufficiency
l Death
Preventive Measures
l Prevention of premature delivery
l Avoid elective caesarean section, to expanding the alveoli and replacing the lung fluid with air.
l Amniocentesis and ultrasound are used to find out the maturity of foetus.
l Administration of corticosteroids is done to mothers for 24 hours to 7 days prior to delivery.
It stimulates surfactant production in the foetus and decreases the incidence of hyaline membrane disease.
Nursing Intervention
l Expect the neonate to be on a ventilator or nasal CPAP to keep the alveoli open.
m Administer oxygen as needed.
m In neonates, mechanical ventilation is usually done in a pressure-limited mode rather than the volume-limited mode used in adults.
m Watch for signs of barotraumas
n Increase in respiratory distress
n Subcutaneous emphysema.
l Organize care to ensure minimal handling.
l Control the neonate’s temperature to reduce stress and decrease additional energy use.
l Use aseptic technique to reduce the risk of infection.
l Administer I.V. fluids to ensure adequate hydration, but withhold oral food and fluid, if the neonate has a high respiratory rate; anticipate possible nasogastric tube feeding.
l Turn the neonate every 2 hours; raise the head of the bed; perform chest percussion before suctioning.
l Closely monitor blood gas as well as fluid intake and output.
m If the neonate has an umbilical catheter, check for arterial hypertension or abnormal central venous pressure.
m Watch for complication, such as infection, thrombosis, or decreased circulation to the legs.
m If the neonate has a transcutaneous oxygen monitor, change the site of the lead placement every 2 to 4 hours to avoid burning the skin.
l Weigh the neonate once or twice daily
l To evaluate the neonate’s progress, assess skin colour, rate and depth of respirations, severity of retractions, nasal flaring, frequency of expiratory grunting, frothing at the lips and restlessness.
l Teach the parents about their neonate’s condition and let them participate in his care (using aseptic technique) to encourage normal parent neonate bonding.
l Advise parents that full recovery may take up to one year; when the prognosis is poor, prepare the parents for the neonates impending death and offer emotional support.
NEONATAL PNEUMONIA
Pneumonia is very common in the neonates.
Pneumonia is an inflammation of the pulmonary parenchyma which occurs more frequently in infants.
Such infection, be it bacterial or viral in origin, may be acquired before or at the time of birth or in the early postnatal period. The bacterial pneumonia carries a substantial mortality in the neonates.
Etiology
l Congenital bacterial pneumonia—acquired by transplacental route.
l Ascending infection from the genital tract before or during labour.
m Prolonged rupture of membranes (exceeds 24 hours).
m Bacteria may gain access to the foetus even with intact membrane.
m Bacterial colonization of the infant always occurs during vaginal delivery.
m Foetal asphyxia (gasping during delivery—
the infant aspirates contaminated amniotic fluid).
l Nosocomial infection within the hospital environment.
l Pathogens like Group B streptococci are the major organisms that cause neonatal pneumonia, and
l Other organisms are:
m Escherichia
m Klebsiella
m Staphylococcus
m Chlamydia trachomatis
m Group D streptococci
m Listeria organisms and pneumococci
m Staphylococcus and pseudomonas organisms,
m Fungi.
l Viral pneumonia can be acquired by the foetus from transplacental passage of organisms—
TORCH syndromes.
Clinical Manifestations
l Non-specific nature of the clinical signs.
l There are characteristics of neonatal sepsis in early diagnosis.
l In some cases it causes severe pneumonia.
l Other features include thermal instability, apneic spells, abdominal distension or jaundice.
l Tachypnea.
l Cyanosis or other signs of respiratory distress.
Investigation
l Chest roentgenogram—findings show unilateral or bilateral streaky densities.
l Blood and urine examination—for detection of Group B streptococcal antigen in urine and blood.
l Cerebrospinal fluid examination—for latex particle agglutination may facilitate the rapid diagnosis of group B streptococcal sepsis.
l Direct culture of blood, urine and nasopharyngeal or tracheobronchial secretions.
l Serological tests.
l Cord blood immunoglobulin to be measured—
In intrauterine pneumonia, we can see elevated IgM levels.
Treatment
l Identification of organisms and its antibiotic sensitivities determined.
l Administration of antibiotics for 10 days or longer depend upon the infant condition.
l Chlamydial pneumonia—administration of oral erythromycin for 14 days course.
l Good supportive care is essential like fluid management, blood gas monitoring and ventilator assistance for the baby.
Complications
l Primary pulmonary hypertension.
l Decreased cardiac output.
l Pulmonary vascular injury.
l Death.
Nursing Management
l Maintain the airway pattern:
m Administer oxygen as needed.
m In neonates, mechanical ventilation is usually done in a pressure-limited mode rather than the volume-limited mode used in adults.
m Watch for signs of barotraumas:
n Increase in respiratory distress.
n Subcutaneous emphysema.
l Organize care to ensure minimal handling.
l Control the neonate’s temperature to reduce stress and decrease additional energy use.
l Use aseptic technique to reduce the risk of infection.
l Administer I.V. fluids to ensure adequate hydration, but withhold oral food and fluid, if the neonate has a high respiratory rate; anticipate possible nasogastric tube feeding.
l Turn the neonate every 2 hours; raise the head of the bed; perform chest percussion before suctioning.
l Closely monitor blood gas as well as fluid intake and output.
m If the neonate has an umbilical catheter, check for arterial hypertension or abnormal central venous pressure.
m Watch for complication, such as infection, thrombosis, or decreased circulation to the legs.
m If the neonate has a transcutaneous oxygen monitor, change the site of the lead placement every 2 to 4 hours to avoid burning the skin.
l To evaluate the neonate’s progress, assess skin colour, rate and depth of respirations, severity of retractions, nasal flaring, frequency of expiratory grunting, frothing at the lips and restlessness.
l Teach the parents about their neonates condition and let them participate in his care (using aseptic technique) to encourage normal parent neonate bonding.
NEONATAL HYPOGLYCAEMIA
Background and Pathophysiology
Glucose is the major energy source for foetus and neonate. The newborn brain depends upon glucose almost exclusively. Upto 90% of total glucose used is consumed by the brain. Alternate fuels (e.g., ketones, lactate) are produced in very low quantities. The usual rate of glucose utilization is 4–8 mg/kg/minute. Glucose regulatory mechanisms are sluggish at birth. At birth the infant must rely on the glycogen stores deposited in the liver, heart and skeletal muscle during the last trimester of pregnancy for full time babies. It provides adequate source of energy for first 2 to 3 days of life.
Thus, the infant is susceptible to hypoglycaemia when glucose demands are increased or when exogenous or endogenous glucose supply is limited. Severe or prolonged hypoglycaemia may result in long-term neurologic damage.
Definition
Hypoglycaemia in the first few days after birth is defined as blood glucose < 40 mg/dl. In preterm infants, repeated blood glucose levels below 50 mg/dl may be associated with neurodevelopmental delay.
Etiology
Conditions associated with an increased risk for neonatal hypoglycaemia include:
Decreased Substrate Availability
l Intrauterine growth retardation
l Inborn errors (e.g., fructose intolerance)
l Prolonged fasting without IV glucose
l Glycogen storage diseases
l Prematurity/small for gestation age
l Postmature
l Prolong labour/difficult labour
l Mother did not receive supplementary glucose during pregnancy
l Infant of a pair of twins
l Infant born of toxaemic mother Hyperinsulinemia
l Infant of diabetic mother
l Erythroblastosis foetalis
l Beckwith-Wiedemann Syndrome
l High umbilical arterial Catheter
l Exchange transfusion
l Abrupt cessation of IV glucose Other Endocrine Abnormalities
l Pan-hypopituitarism
l Adrenal insufficiency
l Hypothyroidism Increased Glucose Utilization
l Cold stress
l Sepsis
l Increased work of breathing
l Perinatal asphyxia Miscellaneous Conditions
l Polycythemia
l CNS abnormalities
l Congenital heart diseases Clinical Manifestations
Clinical signs and symptoms of hypoglycaemia are non-specific and include:
l Jitteriness, tremors
l Irritability, lethargy
l Weak or high–pitched cry
l Seizures
l Apnea, grunting and sweating (uncommon).
l Hypoglycaemic infants may not always be symptomatic.
l Other clinical features like cyanosis, irregular respiration, sweating, eye rolling and refusal to take feeds, the routine glucose monitoring for at- risk infants is mandatory.
Investigations
l Routine blood glucose monitoring is obtained from heel stick.
Management of Hypoglycaemia
l Take care to prevent hypothermia.
l Commence feed within 1 hour of birth and regularly 2–3 hours at breast or at least 80–90 ml/kg/day with EBM or formula milk.
l Measure blood glucose within 2 hours of birth if high risk, otherwise before the second feed.
l Glucometer reading > 40 mg/dl means infant is feeding normally. Follow the usual nursery protocol.
l Glucometer reading 20–40 mg/dl, infant is term and is able to feed:
m Draw blood for stat blood glucose.
m Give 5 ml/kg of D5W orally.
m Repeat blood glucose or glucometer 20 min after feeding.
l Glucometer reading: If the reading is as given below treatment should be given as follows:
(a) < 20 mg/dl or
(b) < 40 mg/dl and NPO or preterm or (c) < 40 mg/dl after feeding or
(d) < 40 mg/dl and symptomatic Treatment
l Draw blood for stat glucose measurement.
l Give IV bolus of 2–3 ml/kg/minute.
l Begin continuous infusion of D10W at 4–6 mg/
kg/minute.
l If infant is of diabetic mother, begin D10W at 8–10 mg/kg (100–125 ml/kg/dl).
Nursing Care
l Identification of problem of the baby, prepare the baby to feed immediately.
l Observe the signs and symptoms.
l Encourage the mother to feed the baby, educate the mother about correct position and good attachment (feeding technique).
l Secure the IV with aseptic manner and administer dextrose infusion.
ANAEMIA IN NEWBORN
Definition
The cord blood haemoglobin level of 14 gm% or lesser is considered to be anaemic.
Causes
1. Blood loss 2. Prematurity
3. Haemlytic disease of the newborn.
4. Delivery of the baby by caesarean section after cutting through the placenta in anterior placenta previa.
5. Unnoticed scalp injuries inflicted during caesarean section.
6. Ruptured vase previa.
7. Torn cord as in precipitated labour.
8. One baby is monozygotic twin (twin transfusion syndrome).
9. Excessive feto-maternal blood.
Anaemia Developing within First Week
l Slipping ligature (Improper ligature )
l Haemlytic disease.
l Hemorrhagic disease of the newborn.
l Secondary haemorrhage from the cord.
l Visceral trauma.
l Large cephlohaematoma.
Late Anaemia
Haemlytic disease Increased RBC Destruction Intrinsic Causes
Hereditary RBC disorders (rare) including
l RBC enzyme defect
l RBC membrane defects
l Hemoglobinopathies (e.g., Meriitt syndrome) Extrinsic Causes
l Haemlytic disease (Immune haemolysis)
m Rh incompatibility
m ABO incompatibility
m Minor blood group incompatibility (e.g., kell, duffy)
l Acquired haemolysis
m Infection
m Vitamin E deficiency (very rare)
m Drugs.
Clinical Findings
Clinical features vary with the severity of anaemia and other associated conditions. There may be no signs with mild anaemia with more severe anaemia, findings includes:
l Pallor
l Tachypnea
l Tachycardia
l Apnea
l Poor feeding
l Lethargy
l Jaundice
l Hepatosplenomegaly
l Wide pulse pressure
l Hypotension
l Metabolic acidosis with severe anaemia.
History
l Family history: Anaemia, ethnicity
l Maternal and perinatal: Blood type and Rh;
anaemia; complications of labour or delivery
l Neonatal: Age of onset; presence of other physical findings.
Laboratory Evaluation
l CBC with platelets, smear and reticulocyte count
l Blood glucose and type, direct antiglobulin test (Coomb’s test)
l Bilirubin test (total and direct)
l Kleihauer-Betke test (to identify feto-maternal haemorrhage)
l Ultra sonogram for internal bleeding (head, abdomen)
Treatment
It will depend on cause and severity:
l Prenatal case diagnosis of significant fatal anaemia is usual except in haemolytic disease of the newborn and B-19 infection. Fetal transfusion may be needed for severe anaemia.
l Postnatal
Anaemia of prematurity
The main methods of management are:
l Limit blood drawing for laboratory tests.
l In emergency transfusion of packed cell 10–15 ml/kg body weight should be given.
l Oral Iron in suspension may have to be continued for a longer period.
INJURIES OF THE NEWBORN (BIRTH INJURY)
The injuries are common in newborns during delivery, due to mismanagement during delivery. It causes injuries to infant’s at birth. Various types of soft tissue injuries may be sustained during the process of birth, primarily in the forms of bruises and/or abrasions secondary to dystocia. Soft tissue injuries usually occur when there is some degree of disproposition between the presenting part and the maternal pelvis.
Discolouration or abrasion occurs due to application of forceps. Petechiae or ecchymoses occurs due to pressure on the presenting part after a breech or brow delivery. Nerve injuries due to pulling the baby in breech delivery, even rarely, laceration occurs during caesarean section.
The injuries are described under two headings:
1. Injuries to the head 2. Other injuries.
Injuries to the Head Cephalohaematoma
It is a collection of blood in-between the pericranium (periosteum) and the flat bone of the skull, usually unilateral and over a parietal bone.
Causes
l Forceps delivery.
l Ventose application.
Clinical Manifestations
l It is never present at birth but gradually develops after 12–24 hours.
l The swelling is limited by the suture lines.
l The blood is usually not significant.
Treatment
l No active treatment is necessary, the blood collection subsides itself within 2 weeks to 3 months.
l Do not aspirate the blood collection, it causes infection to infants.
Caput Succedaneum
The most commonly observed scalp lesion is Caput succedaneum, a vaguely outlined area of oedematous tissue situated over the portion of the scalp that presents in a vertex delivery.
Clinical Manifestations
l The swelling consists of serum or blood or both, accumulated in the tissues above the bone, and it often extends beyond the bone margins.
l The swelling may be associated with overlying petechiae or ecchymoses.
Treatment
l No specific treatment is needed, and the swelling subsides within a few days.
Subgaleal Haemorrhage
It subgaleal haemorrhage is bleeding into the subgaleal compartment. The subgaleal compartment is a potential space that contains loosely arranged connective tissues; it is located beneath the galea aponeurosis, the tendinous sheath that connects the fontal and occipital muscles and forms the inner surface of the scalp.
Causes
l Forceps delivery due to compression.
l Using vacuum extractor at birth.
Clinical Manifestations
l Increased head circumference.
l Increased oedema in the back of the neck and a firm mass.
Investigation
l Intranatal history-mode of delivery.
l Physical examination.
l X-ray.
l Computerized tomography or magnetic resonance image to conform the diagnosis.