Module 8 Neonatal complications: Complex care 1

Question 1

Respiratory disorders

Answer 1

Choanal artresia
Asphyxia
Meconium aspiration syndrome
Transient tachypnoea
Respiratory distress syndrome
Apnoea
Chronic lung disease
Diaphragmatic hernia

Question 2

What is asphyxia

Answer 2

Oxygen deprivation. Failure of initiation of respiration in the newborn. Blood oxygen levels are low and CO2 is high.

Question 3

Asphyxia results in a sequence of events what are these

Answer 3

1. A brief period of hyperventilation
2. Primary apnoea - respiratory effort ceases, heart rate falls, blood pressure rises, tone decreases
3. Deep, irregular gasping respirations, getting progressively weaker, further decrease in heart rate, falling bp, the baby is flaccid and takes a final gasp
4. Terminal (secondary apnoea) - the baby is unresponsive and the heart rate, bp, and oxygen levels in the blood continue to fall.

Question 4

Causes of asphyxia

Answer 4

Preterm birth
Obstruction
Certain drugs
Congenital anomalies
Cerebral damage
Infection
Haemorrhage
Pneumothorax
Pharyngeal suctioning

Question 5

Antenatal risk factors for asphyxia

Answer 5

Maternal diabetes
Pre-eclampsia
Anaemia or isoimmunisation
Previous fetal or neonatal death
Maternal infection
Polyhydramnios
Oligohydramnios
PROM/PPROM
APH
Post term
Multiple gestation
IUGR/SGR
Drug therapy
Drug abuse
Congenital abnormalities
Dminished fetal activity
No A/N care

Question 6

Intrapartum risk factors for asphyxia

Answer 6

LSCS
Breech/Malpresentation
Premature labour
Prolonged ROM
Precipitous labour
Prolonged labour >24 hours
Prolonged second stage >2 hours
Non reassuring CTG
Use of GA
Uterine tetany
Narcotics within 4 hours of delivery
Mec stained liquor
Cord prolapse
Placental abruption
Placenta previa

Question 7

Meconium aspiration syndrome incidence and mechanism

Answer 7

Evident in around 10-15% of all labours, but MAS occurs in <1% of live births. Mec is rarely passed in utero prior to 36 weeks.

Mechanism: Fetal hypoxia - causes increased gut paralysis, relaxes the anal sphincter - passage of meconium - fetal gasping occurs under stress - meconium becomes trapped in the airways allowing air in but not out - air accumulates behind the blockage - alveoli rupture - pneumothorax occurs and possible pneumonitis

Question 8

Treatment for meconium aspiration syndrome

Answer 8

Babies need full NICU care and ventilation to minimise further deterioration.
Oxygen therapy and antibiotics may be needed to avoid pneumonia.
Surfactant therapy commenced within 6 hours of birth may reduce severity of respiratory problems

Question 9

Transient tachypnoea of the newborn (TTN)

Answer 9

Commonly found in otherwise healthy, near term or term babies
Due to mild surfactant deficiency or failure to adequately absorb lung fluid
Increased risk in babies delivered by Caesarean, or those experiencing perinatal hypoxia

Question 10

Signs and symptoms of Transient tachypnoea

Answer 10

Tachypnoea >60 up to 120
Nasal flaring
Sternal recession
Expiratory grunting
Possible cyanosis
Do not suction if not obstructed
Observe every 15 minutes for colour, resp, tone, heart rate.

Question 11

Transient tachypnoea management

Answer 11

Pead review
Symptoms usually resolve within 24 hours although tachypnoea may persist longer
Important to rule out infection via chest x-ray, blood gases and cultures
Possible short NICU/SCN admission with possible oxygen
No long-term complications associated

Question 12

Respiratory distress syndrome

Answer 12

A condition seen in preterm infants caused by a lack of surfactant. The baby becomes exhausted by the efforts of breathing and there is characteristic flaring of the nares, expiratory grunt, sternal recission, intercostal recession, cyanosis and a low oxygen saturation.
Must go to NICU

Question 13

Respiratory distress syndrome incidence

Answer 13

Causes more neonatal deaths than any other condition. Occurs in 70% of neonates born at 29 weeks, declines sharply to near 0% at 39 weeks and is rarely seen after 37 weeks.
Fairly common in term infants born to mothers suffering from diabetes.

Question 14

Respiratory distress syndrome management

Answer 14

Correct diagnosis - exclude other diagnosis
Blood cultures and blood gases
Surfactant therapy - within 15 min of birth
Oxygen therapy and ventilation support for severely affected
Intermittent and continuous observations
Support for parents
Documentation

Question 15

Apnoea

Answer 15

Cessation of respiratory effort for 20 seconds or more, requires constant monitoring
More common in preemies
Physiology: immature respiratory centre and immaturity of chemoreceptor response to hypoxia and acidosis
Can be the first sign of sepsis, pneumonia, NEC or meningitis

Question 16

Chronic lung disease

Answer 16

Seen in the preterm neonate who continues to require supplemented oxygen supply at 36 weeks post conceptual age or beyond the 28th day of life.
Risk factors: prematurity, endotracheal intubation, high level ventilator PIP, oxygen toxicity

Question 17

Pneumothorax

Answer 17

Occurs when the alveoli rupture causing air to enter the pleural cavity
Spontaneous: at birth on initial inspiration or following mec aspiration
Induced: by high ventilator settings, maldistribution of ventilated gas in the lungs, neonate-ventilator breathing interactions
Baby’s condition suddenly deteriorates

Question 18

Congenital diaphragmatic hernia

Answer 18

Incidence of CDH rare 1:2200-4000 live births
Usually known from the anatomical scan and offered TOP
Historically have had a poor prognosis due to pulmonary hypertension and pulmonary hypoplasia.

Question 19

Sources of neonatal infection

Answer 19

Skin, eyes, mouth and cord
Inutero acquired infections TORCH, HIV, CMV

Question 20

Prenatal infections

Answer 20

TORCH viruses - Toxoplasmosis, other viruses, rubella, cytomegalovirus, Herpes
Varicella zoster
Listeriosis
Hepatitis

Question 21

Intrauterine infection

Answer 21

Chorioamnionitis is diagnosed after the event. Fetal losses between 16-22 weeks were studied, 77.2% had histological chorioamnionitis.
At least 40% of preterm birth were associated with intrauterine infections

Question 22

Pathogenesis of intrauterine infection

Answer 22

Ascending infection from the lower genital tract
Retrograde passage of organisms from the peritoneal cavity via the fallopian tubes
From the maternal circulation
From invasive antenatal diagnostic procedures

Question 23

Risk factors for neonatal infection

Answer 23

Transplacental infection
Preterm birth
Low birth weight
Prolonged ROM
Hypothermia
Some congenital malformations
Birth trauma

Question 24

Prevention of infection

Answer 24

Inutero
Handwashing
Equipment
Environment
Invasive procedures
Nosocomial visitors

Question 25

Types of neonatal infections

Answer 25

Mild eye infection - in the first 1-2 days often due to chemical irritation and clears spontaneously, treat by wiping away secretions with cotton wool-soaked sterile water

Conjunctivitis - purulent discharge, relatively common, clean eyes as above and 1 drop of chloramphenicol QID for 5 days.

Coagulase Negative staphylococcus

Omphalitis - infection of the periumbilical skin, risks the spread via the umbilical vain

General skin sepsis - need to culture and treat. Minor lesions use antiseptic powder, don’t overdo antibiotics as encourages MRSA.

Upper respiratory tract infections

Scalp infections

Gastroenteritis or necrotising enterocolitis - inflammation of the gut wall as a result of infection. Blood in the stools and vomiting.

Question 26

Signs of neonatal infection

Answer 26

Lethargy
Vomiting
Diarrhea
Jaundice
Mild respiratory difficulty
Pyrexia
Hypothermia
Hypotonia
Irritability
Poor feeding
Weak cry
Abdominal distension
Failure to thrive
Rashes
Purpura
Respiratory distress
Shock
Bulging fontanelle (with RDS)
Pustular areas

Question 27

Investigation of neonatal infection

Answer 27

Full blood count and blood gases
Blood culture
Urine or meconium culture
Swabs
Lumbar puncture
Chest X-ray
C-reactive protein
Culture of amniotic fluid, placental tissue and cord blood

Question 28

Sepsis

Answer 28

Early onset (first few days) often caused by GBS, E.coli, blood born
Late onset over half caused by coagulsae negative staph
Treatment IV antibiotics will commence prior to ID of causative organism. Combination of ampicillin, gentamicin or cefotaxime, drugs may change when causative organism is identified.

Question 29

Group B haemolytic streptococcus

Answer 29

If mum is a carrier 10% neonates acquire GBS through vertical transmission at birth, causes early (within 12 hours-6 days) or late onsent (4-5 weeks). Deadly in 20% of cases
Rate of infection in neonates is <1 per 1000 live births.

Question 30

Physiology of bilirubin metabolism

Answer 30

When RBCs age, are immature or malformed they are removed from the circulation and broken down in the reticuloendothelial system (liver, spleen and macrophages). Haemoglobin is broken down to form haem which is converted to unconjugated bilirubin, globin and iron.

Question 31

What are the two forms of bilirubin

Answer 31

Unconjugated bilirubin - can’t be easily excreted from the body by urine or bile as it is fat soluble. Deposited in the connective tissue of the skin in excess causing yellow. Transported to the liver. Has the potential to cross the blood brain barrier as it is fat soluble causing kernicterus.

Conjugated bilirubin - has been processed by the liver to become water soluble and then can be easily excreted from the body, mainly through faeces and urine.

Question 32

How is bilirubin processed

Answer 32

Through 3 stages:
Transport
Conjugation
Excretion

Question 33

What is jaundice

Answer 33

Yellow discoloration of the skin, mucous membranes and sclera due to hyperbilirubinemia.
One of the most common neonatal disorders.

Question 34

Cause of jaundice in neonates

Answer 34

Early neonatal jaundice is usually caused by the physiological destruction of red blood cells in the infants, and its importance lies in the ability of the bilirubin pigment to cross the blood brain barrier resulting in neurotoxicity.

In a baby it is primarily due to an immature liver system and not effectively coping with RBC destruction and the decreased hepatic blood flow. During the first 3-4 months destruction og RBCs exceeds production.

Question 35

Incidence of jaundice in neonates

Answer 35

60% of term babies develop jaundice in the first week of life
85% of preterm babies develop jaundice in the first week of life
10% breast fed babies are still jaundiced at 1 month

Question 36

Risk factors for jaundice

Answer 36

Gestational age
Delivery trauma - bruising
Hypoxia
Hypothermia
Hypoglycemia
Delayed or poor feeding, or delayed passage of meconium - decreased bilirubin excretion
Decreased albumin binding capacity - eg if receiving ampicillin
Urinary infection
ABO incompatibility
Rhesus incompatibility

Question 37

Rhesus incompatibility

Answer 37

Process of antibody formation is called maternal sensitisation - causes haemolysis in the fetus, fetal haemolytic anaemia, and inutero jaundice usually not evident - may lead to hydrops fetalis - increases RBC destruction and more circulating unconjugated bilirubin - may require intrauterine exchange transfusion with rhesus negative blood or premature delivery and exchange transfusion

Question 38

Exchange transfusion

Answer 38

Baby’s blood is gradually removed and replaced with fresh Rh negative ABO compatible blood. Rh nehative blood is used so that there is no Rh antigen to attract the antibodies - this washes out excess bilirubin and the unwanted antibodies but also increases haemoglobin level. An amount equivalent to twice the babies blood volume needs to be used.

Question 39

Physiological jaundice

Answer 39

In the term neonate jaundice presents when Serum bilirubin concentration is 85-120 umol/l. Never appears before 24 hours of life. Peaks of day 3 and usually fades by 1 week. Bilirubin levels never exceed 200-215 umol/l

Question 40

Breast milk jaundice

Answer 40

Low fluid and calorie intake during colostrum production causes a slower intestinal transit time, this in turn adds more unconjugated bilirubin to the system.

Lipoprotein lipase in the breast milk of some women and progesterone inhibits the action of glucuronyl transferase which is responsible for the conjugation and subsequent excretion of bilirubin

Question 41

Physiological jaundice diagnosis

Answer 41

Visual inspection of the skin, sclera and mucous membranes in natural light.
TCB can be used - if a the concentration is >250 umol/l on day 3 check the result by taking a SBR

Other diagnostic methods - U/S scans can be done, liver biopsy or exploratory surgery

Question 42

Pathological jaundice

Answer 42

Occurs when additional factors are superimposed on the basic mechanisms that result in physiological jaundice. Most likely due to haemolytic disease, ABO incompatibility. Occurs within 24 hours of birth and is characterised by a rapid rise in serum bilirubin. Persistence of clinical jaundice for 7-10 days in term babies or 2 weeks in preterm babies. Prolonged neonatal jaundice may be an indication of an underlying liver disorder.

Question 43

Kernicterus

Answer 43

Bilirubin hyperpigmentation of the basal ganglia of the brain with destruction of nerves cells see as a complication of severe neonatal jaundice caused by Rh isoimmunisation.

Healthy term neonates have a potential for kernicterus if SBR is >340 umol/l.

50% of affected babies die, survivors may develop some level of brain damage.

Question 44

Pathological jaundice diagnosis

Answer 44

Jaundice within the first 24 hours of life
A rapid increase in TSB >85 umol/l per day
TSB > 200 umol/l in first 24 hours requires phototherapy
Persistence of clinical jaundice for 7-10 days in term babies or 2 weeks in preterm babies.

Question 45

Treatment of jaundice

Answer 45

Phototherapy - discovered in 1958 in England and the US in the 1960s

Types:
Fiberoptic systems - bilibed & Biliblanket
overhead single lights
overhead double lights
lights combined with a fiberoptic system
intermittent versus continuous treatment

Question 46

Action of phototherapy

Answer 46

Works through a process of isomerisation that changes trans-bilirubin into the water soluble cis-bilirubin isomer. The blue light oxidises the bilirubin to biliverdin that does not contribute to kernicterus. This lowers the SBR so that the water-soluble isomers can be eliminated without further metabolism by the liver.

Greatest impact in the first 24-48 hours.

Question 47

Specific cares for phototherapy

Answer 47

Temperature: Nurse in a warm environment, monitor for hypothermia or hyperthermia
Eyes: Protect with eye shiels, ensuring they don’t occlude the nose
Skin: Nurse baby naked or with just a nappy, observe for rashes, dryness and excoriation
Hydration: Fluid intake and stool and urine output are monitored. Potential need for extra fluids
Neurobehavioural status: Observe sleeping and waking states, feeding behaviours, responsiveness, response to stress and interaction with parents
Calcium levels: hypocalcaemia may be indicated by jitteriness, irritability rash, loose stools, fever, dehydration and convulsions
Bilirubin levels: usually estimated daily.

Question 48

Aim of resucitation

Answer 48

To promote and maintain adequate ventilation and oxygenation
To initiate and maintain adequate cardiac output and perfusion
To maintain temperature and blood glucose levels

Question 49

Naloxone (Narcan)

Answer 49

Use if there are clinical signs of maladaptation AND mum has been given opioids in labour
Dose: 400mcg per 1ml ampoule

Do not give to mothers of known drug abuse

Question 50

Types of respiratory support

Answer 50

Oxygen therapy
Incubator
Exogenous surfactant
Intermittent positive pressure (IPPV)
Continuous positive airway pressure (CPAP)
Synchronous intermittent mandatory ventilation (SIMV)
Nitric oxide
Caffeine
Extracorporeal membrane oxygenation (ECMO)

Question 51

Indications for intubation

Answer 51

Tracheal suction for meconium - if absent or depressed respirations at birth or obvious obstruction
Prolonged ventilation
Inability to ventilate with bag and mask
To give exogenous surfactant
Suspected or diagnosed CDH

Question 52

Cardiac compressions

Answer 52

Indicated when HR >60 after 30 seconds of effective ventilation
3 compressions to 1 breath
Rate 120 events/min
Re evaluate HR every 30 seconds
If HR < 60 after 30 seconds of chest compressions reassess ABC and consider drug therapy.

Question 53

Drugs in resucitation

Answer 53

Adrenaline used if HR < 60 after 30 seconds of initial assessment, 30 seconds of baby and mask, 30 seconds of CPR. Dose: 0.1-0.3 ml/kg of 1:10 000. Can repeat up to 3 doses

Other drugs, sodium bicarbonate, dextrose, saline.

Question 54

Ethical challenges and dilemmas in resuscitation

Answer 54

Unexpected stillbirths
Parental wishes
Withholding/withdrawing care
Health costs.

Question 55

Spina bifida

Answer 55

A congenital birth defect involving the development of a baby’s spine and spinal cord during the first month of pregnancy. The bony cavity around the spinal cord is not completely closed and so the meninges herniate through. Incidence around 150 babies in Australia each year.

Question 56

Omphalocele/exomphalos

Answer 56

Is a herniation of the abdominal viscera through the base of the umbilical cord and is covered in a sac formed by the peritoneum and amniotic membrane. 1-2000 births.

Question 57

Gastroschisis

Answer 57

A congenital fissure of the abdominal wall. Most common congenital abdominal wall defect. The contents of the abdomen protrude through a defect in the abdominal wall, lateral to and commonly to the right of the umbilicus. 5 per 1000 births.

Question 58

Congenital diaphragmatic hernia (CDH)

Answer 58

A life-threatening condition at birth. Should be detected at anatomy scan. The diaphragm does not form properly in pregnancy. A hole in the diaphragm allows organs to move up into the chest cavity. This encroaches on heart and lung growth and development. Requires tertiary referral and surgery after birth.