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1 - Paeds AE > Neonatal medicine > Flashcards

Neonatal medicine Flashcards

1
Q

What drug can be given to reverse neonatal respiratory depression caused by maternal opiate analgesia?

A

Naloxone

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2
Q

How do you decrease the risk of hypothermia is preterm neonates?

A

Infants, with the exception of the face, should be placed into a plastic bag or wrapped in plastic sheeting.

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3
Q

What is asymmetrical FGR and what does it mean?

A

The weight or abdominal circumference lies on a lower centile than that of the head. Usually caused by placental dysfunction, these infants rapidly put on weight after birth

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4
Q

What is symmetrical FGR?

A

The head circumference is equally reduced compared to the abdomen. It is usually a normal, small baby but may be due to a fetal chromosomal disorder or syndrome, they are likely to stay small after birth

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5
Q

What is a IUGR fetus at risk of?

A

Intrauterine hypoxia and ‘unexplained’ intrauterine death
Asphyxia during labour and delivery
Hypothermia due to their relatively large surface area
Hypoglycaemia from poor fat and glycogen stores
Hypocalcaemia
Polycythaemia

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6
Q

What are the problems associated with large for gestational age babies?

A

Birth asphyxia from a difficult delivery
Birth trauma, especially should dystocia
Hypoglycaemia due to hyperinsulinism
Polycythaemia

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7
Q

What do you look at on the routine examination of a newborn infant?

A 
Birthweight (weight and centile) and gestational age 
General observation: appearance, posture and movements
Head circumference
Fontanelle
The face
If plethoric or pale
Jaundice
The eyes
The palate
Breathing and chest wall movement
Auscultate the heart
Palpate the abdomen, femoral pulses
Genitalia and anus
Muscle tone
The whole of the back and spine
The hips
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8
Q

Why do you look at the fontanelle in a newborn examination?

A

A tense fontanelle when the baby is not crying may be due to raised intracranial pressure (cranial US needed). A tense fontanelle is also a late sign for meningitis

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9
Q

Why do you take the femoral pulses in a newborn examination?

A

The pulse pressure reduced in coarctation of the aorta. This can be confirmed be measuring the BP in the arms and legs. The pulse pressure is increased if there is a patent ductus arteriosus

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10
Q

What are some lesions in newborns that resolve spontaneously?

A

Peripheral cyanosis of the hands and feet
Traumatic cyanosis
Swollen eyelids and distortion of the head
Subconjunctival haemorrhage
Cysts of the gum
Breast enlargement
White vaginal discharge or small withdrawal bleed
Umbilical hernia

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11
Q

What are some significant abnormalities detected on the newborn screening examination?

A

Port-wine stain
Strawberry naevus
Natal teeth consisting of the front lower incisors (should be removed)
Extra digits
Heart murmur
Midline abnormality over the spine or skull
Palpable or large bladder

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12
Q

What are the risk factors of DDH?

A

Female sex (six fold)
Positive family history (20% of affected)
Breech presentation (30% of affected)
Neuromuscular disorder

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13
Q

What can Vitamin K deficiency result in?

A

Haemorrhagic disease of the newborn. In most, the haemorrhage is mild, such as bruising, haematemesis and melaena, or prolonged bleeding of the umbilical stump or after a circumcision. However, it can cause intracranial haemorrhage, half of whom are permanently disabled or die.

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14
Q

When does vitamin K deficiency present?

A

During the first week of life or late, from 1 to 8 weeks of age

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15
Q

Is breast milk or formula milk better for vitamin K deficiency.

A

Formula milk, breast milk is a poor source of vitamin K.

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16
Q

Are there any medications that the mother is taking whilst breast feeding that may worsen vitamin K deficiency?

A

Anti-convulsants, they impair the synthesis of vitamin K

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17
Q

How is vitamin K deficiency prevented?

A

All newborn infants are given an IM injection of vitamin K.

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18
Q

What is the routine biochemical screening of the newborn called?

A

Guthrie test

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19
Q

What is screened for in the Guthrie test?

A 
Phenylketonuria
Hypothyroidism
Haemoglobinopathies (sickle cell, thalassaemia)
Cystic fibrosis
MCAD deficiency (mitochondrial disease)
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20
Q

What is neonatal hypoxic-ischaemic encephalopathy?

A

In perinatal asphyxia, gas exchange, either placental or pulmonary, is compromised, resulting in respiratory depression. Hypoxia, hypercarbia and metabolic acidosis follow. Compromised cardiac output diminishes tissue perfusion, causing hypoxic-ischaemic injury to the brain and other organs

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21
Q

What are some significant hypoxic events immediately before or during labour or delivery that can cause hypoxic-ischaemia encephalopathy?

A

Before labour: maternal hypo- or hypertension, fetal anaemia or IUGR
During labour: excessive or prolonged uterine contractions, placental abruption, ruptured uterus, cord compression (prolapse or shoulder dystocia)
After delivery: failure to breathe

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22
Q

What are the clinical manifestations of hypoxic-ischaemic encephalopathy?

A

Mild - irritable, responds excessively to stimulus, hyperventilation, impaired feeding
Moderate - marked abnormalities of tone and movement, cannot feed, seizures
Severe - no normal movements or response to pain, fluctuating tone (hypo/hyper), prolonged seizures, multi-organ failure

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23
Q

How would you manage hypoxic-ischaemic encephalopathy?

A 
Respiratory support
aEEG (a - amplitude integrated)
Treatment of seizures
Fluid restriction (transient renal impairment)
Treat hypotension
Monitor and treat electrolyte imbalances
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24
Q

What is the prognosis of hypoxic-ischaemic encephalopathy?

A

Mild - expect complete recovery
Moderate - may be better by 2 weeks but if not full recovery is unlikely
Severe - mortality is 30-40%, over 80% of survivors have neurodevelopment disabilities

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25
Q

What are some soft tissue injuries that can occur during delivery?

A

Oedema and bruising (caput succedaneum [extending beyond the margins of the skull bones], chignon [from ventouse delivery])
Haematoma (cephalhaematoma [below the periosteum, confined within the margins of the skull sutures])
Abrasions
Forceps marks on face

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26
Q

What causes brachial nerve palsy and in what conditions is it more common?

A

It results from traction to the brachial plexus nerve roots. It may occur at breech deliveries or with shoulder dystocia

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27
Q

What would an upper nerve root (C5/6) injury result in?

A

Erb palsy

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28
Q

Do nerve palsies recover?

A

Most resolve completely by 2 years but they should be referred to an orthopaedic or plastic surgeon if not resolved by 2-3 months

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29
Q

What fractures can occur during delivery?

A

Clavicle (shoulder dystocia, good prognosis, no specific treatment)
Humerus/femur (usually mid-shaft, occurring at breech deliveries, or fracture of the humerus at shoulder dystocia, heal rapidly with immobilisation)

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30
Q

What are some medical problems of preterm infants?

A 
Resuscitation at birth
Respiratory (respiratory distress, pneumothorax, apnoea and bradycardia)
Hypotension
Patent ductus arteriosus
Temperature control
Metabolic (hypo- glycaomia and calcaemia, electrolyte imbalance)
Nutrition
Infection
Jaundice
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31
Q

What is the pathophysiology of respiratory distress syndrome?

A

Deficiency of surfactant, which lowers surface tension, leading to widespread alveolar collapse and inadequate gas exchange.

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32
Q

Is respiratory distress syndrome more severe in boys or girls?

A

Boys

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33
Q

In which neonates is respiratory distress syndrome more common?

A

It is common in infants born before 28 weeks gestation. It is rare at term but may occur in mothers with DM.

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34
Q

What are the clinical features of RDS?

A 
At delivery or within 4 hours of birth:
Tachypnoea > 60 breaths/min
Laboured breathing with chest wall recession (sternal and subcostal indrawing) and nasal flaring
Expiratory grunting
Cyanosis
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35
Q

Why does expiratory grunting take place in RDS?

A

In order to try to create positive airway pressure during expiration and maintain functional residual capacity

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36
Q

What does a characteristic X-ray of RDS show?

A

Diffuse granular or ‘ground glass’ appearance of the lungs and an air bronchogram, where the larger airways are outlined. The heart border becomes indistinct or obscured completely with severe disease

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37
Q

How do you treat RDS?

A

Raised ambient oxygen, supplemented with continuous positive airway pressure (delivered via nasal cannulae) or artificial ventilation via a tracheal tube

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38
Q

How is RDS prevented?

A

Steroids in high risk pregnancies

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39
Q

How does RDS lead to pulmonary interstitial emphysema?

A

Air from the over distended alveoli may track into the interstitial, resulting in PIE

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40
Q

How does PIE lead to pneumothorax?

A

Air leaks into the pleural cavity and causes a pneumothorax

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41
Q

How is a neonatal pneumothorax detected?

A

Breath sounds and chest movement on the affected side are decreased but it is difficult to detect clinically. Transillumination with a bright fiberoptic light source applied to the chest wall may show a pneumothorax

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42
Q

How do you prevent a pneumothorax?

A

Infants are ventilated with the lowest pressures that provide adequate chest movement and satisfactory blood gases.

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43
Q

When are episodes of apnoea, bradycardia and desaturation common?

A

In very low birthweight infants until they reach about 32 weeks gestational age.

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44
Q

Acutely, when does bradycardia occur?

A

It may occur when an infant stops breathing for over 20-30 secs or when breathing continues against a closed glottis.

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45
Q

What may be the causes of neonatal bradycardia?

A

In many cases immaturity of central respiratory control. Must rule out hypoxia, infection, anaemia, electrolyte disturbances, hypoglycaemia, seizures, heart failure or aspiration due to reflux

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46
Q

How would you treat neonatal bradycardia?

A

Breathing will often start again after gentle physical stimulation. Caffeine often helps. Continuous positive airway pressure (CPAP) may be needed if episodes are frequent

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47
Q

What are the consequences of hypothermia in a neonate?

A

Increased energy consumption, resulting in hypoxia and hypoglycaemia, failure to gain weight and increased mortality.

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48
Q

Why are neonates particularly susceptible to hypothermia?

A

Large SA:volume ratio
Thin skin that is very heat permeable
Little subcutaneous fat for insulation

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49
Q

How can you prevent the heat loss in newborn infants?

A

Convection: raise temperature of ambient air in incubator, clothe (including head), avoid draughts.
Radiation: cover baby, double wall for incubators
Evaporation: dry and wrap at birth, humidify incubator
Conduction: nurse on heated mattress

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50
Q

In which neonates in patent ductus arteriosus most common?

A

In infants with RDS

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51
Q

What are the clinical features on a PDA?

A

May be asymptomatic but may cause apnoea and bradycardia, increased oxygen requirement and difficulty in weaning the infant from artificial ventilation. With increasing circulatory overload, signs of heart failure may develop

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52
Q

What would you find on examination of PDA?

A

‘Bounding’ pulses from an increased pulse pressure, the precordial impulse becomes prominent and a systolic murmur may be audible

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53
Q

How would you treat PDA?

A

If symptomatic, prostaglandin synthesise inhibitor, indomethacin or ibuprofen is used. If this fail, surgical libation will be required

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54
Q

How do you feed ‘healthy’ neonates?

A

Infants of 35/36 weeks are mature enough to suck and swallow milk. Less mature infants will need to be fed via an oro- or nasogastric tube.

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55
Q

How would feed very immature or sick neonates?

A

Parenteral nutrition through a central venous catheter, inserted peripherally (PICC lines, peripherally inserted central catheters).

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56
Q

What are the risk factors of PICC lines?

A

Significant risk of septicaemia (use aseptic technique). Other risks include thrombosis of a major vein

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57
Q

What condition does cow’s milk formula increase the risk of in neonates?

A

NEC

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58
Q

Why are preterm infants at increased risk of infection?

A

IgG is mostly transferred across the placenta in the last trimester and no IgA or IgM is transferred.

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59
Q

Are brain haemorrhages common in neonates and how are the screened for?

A

They occur in 25% of very low birthweight infants and are easily recognised on cranial US scans. Most occur in the first 72hours of life.

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60
Q

What are some risk factors for neonatal brain haemorrhage?

A

Perinatal asphyxia, severe RDS, pneumothorax

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61
Q

What is necrotising enterocolitis?

A

Bacterial invasion of ischaemia bowel wall

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62
Q

What are the clinical features of NEC?

A

Feeding stops, milk is aspirated from the stock and there may be bile-stained vomiting. The abdomen becomes distended and the stool sometimes contains fresh blood. The infant may rapidly become shocked and require artificial ventilation due to abdo distention and pain

63
Q

What does the X-ray show on NEC?

A

Distended loops of bowel and thickening of the bowel wall with intramural gas, there may be gas in the portal tract.

64
Q

How would you treat NEC?

A

Stop oral feeding and give broad-spectrum antibiotics. Parenteral nutrition is always needed and artificial ventilation and circulatory support are often needed.

65
Q

What are the long term consequences of NEC?

A

Development of strictures and malabsorption

66
Q

What is retinopathy of prematurity?

A

Vascular proliferation, which may progress to retinal detachment, fibrosis and blindness.

67
Q

Which blood vessels does retinopathy of prematurity affect?

A

Developing blood vessels at the junction of the vascular and non-vascularised retina

68
Q

What increase the risk of retinopathy of prematurity?

A

Uncontrolled use of high concentrations of oxygen

69
Q

How do you treat retinopathy of prematurity?

A

Laser therapy reduces visual impairment

70
Q

What is bronchopulmonary dysplasia?

A

Infants who still have an oxygen requirement at a post-gestational age of 36 weeks. The lung damage comes from pressure and volume trauma from artificial ventilation, oxygen toxicity and infection

71
Q

What does the X-ray show in bronchopulmonary dysplasia?

A

Widespread areas of opacification, sometimes with cystic changes.

72
Q

How would you treat bronchopulmonary dysplasia?

A

Some need prolonged artificial ventilation, but most are weaned onto CPAP followed by additional ambient oxygen. Corticosteriod therapy may facilitate earlier weaning from the ventilation but has neurological side effects so it’s use is limited

73
Q

How is anaemia following discharge prevented?

A

Additional iron as supplementation or in preterm formula is given until 6 months corrected age, when iron becomes available from solid foods

74
Q

Why are over 50% of newborn infants born jaundiced?

A

There is marked physiological release of haemoglobin from the breakdown of red cells because of the high Hb concentration at birth.
The red cell life span of newborn infants is shorter than that adults.
Hepatic bilirubin metabolism is less efficient in the first few days of life.

75
Q

Why is neonatal jaundice important?

A

It may be a sign of another disorder (haemolytic anaemia, infection, metabolic disease, liver disease)
Unconjugated bilirubin can be deposited in the brain, particularly in the basal ganglia, causing kernicterus

76
Q

What is Kernicterus?

A

Encephalopathy resulting from the deposition of unconjugated bilirubin in the basal ganglia and brainstem ganglia and brainstem nuclei.

77
Q

Why does Kernicterus occur?

A

Because the level of unconjugated bilirubin exceeds the albumin-binding capacity of bilirubin in the blood. As this free bilirubin is fat-soluble, it can cross the blood-brain barrier.

78
Q

What are the clinical manifestations of Kernicterus?

A

They may vary from transient disturbance to severe damage and death.
Acute: lethargy and poor feeding
Severe: irritability, increased muscle tone (arched back), seizures and coma.

79
Q

What are the long term complications of Kernicterus?

A

Infants who survive may develop choreoathetoid cerebral palsy, learning difficulties and sensorineural deafness

80
Q

What does the management of newborn jaundice depend on?

A

Infant’s gestational age, age at onset, bilirubin level and rate of rise, and the overall clinical condition.

81
Q

What are the causes of neonatal jaundice?

A

<24h after birth: haemolytic disorders (rhesus, ABO incompatibility, G6PD deficiency), congenital infection
24h-2wks after birth: physiological, breast milk, infection (UTI), haemolysis, bruising, polycythaemia
>2 weeks after birth: physiological, breast milk, infection (UTI), hypothyroidism, haemolytic anaemia, GI obstruction. Conjugated: bile duct obstruction, neonatal hepatitis

82
Q

How do you test for ABO incompatibility?

A

Coombs’ test: direct antibody test, which demonstrates the antibody on the surface of red cells

83
Q

How can jaundice be tested for clinically?

A

Blanching the skin with one’s finger

84
Q

How does jaundice tend to spread?

A

Tends to start on the head and face and then speeds down the trunk and limbs.

85
Q

How is jaundice investigated?

A

The bilirubin should be check with a transcutaneous bilirubin meter or blood sample.

86
Q

How does jaundice tend to change over time?

A

The rate of rise tends to be linear until a plateau is reached, so serial measurements can be polluted on a chart and used to anticipate the need for treatment before it rises to a dangerous level.

87
Q

How does gestation affect jaundice treatment?

A

Preterm infants are more susceptible to damage from raised bilirubin, so the intervention threshold is lower

88
Q

How do you treat jaundice?

A

Increase milk intake and hydration. Phototherapy is used widely, with exchange therapy transfusion used for severe cases

89
Q

How does phototherapy work?

A

Light from the blue-green band of the visible spectrum converts unconjugated bilirubin into a harmless water-soluble pigment excreted predominantly in the urine. The infants eyes are covered, as bright light is uncomfortable

90
Q

What are the side effects of phototherapy?

A

It can result in temperature instability as the infant is undressed, a macular rash and bronze discolouration of the skin if the jaundice is conjugated.

91
Q

When is exchange transfusion used and what is it?

A

Twice the infant’s blood volume is exchanged with donor blood if the bilirubin rises to levels which are considered potentially dangerous.

92
Q

What may cause jaundice after 2 weeks of age?

A

Prolonged neonatal jaundice may be caused by biliary atresia, which needs to be diagnosed and treated promptly, as delay adversely affects outcome. Most cases are caused by ‘breast milk’ jaundice.

93
Q

How do you differentiate conjugated and unconjugated jaundice in neonates?

A

Conjugated hyperbilirubinaemia is suggested by the baby passing dark urine and unpigmented stools. Hepatomegaly and poor weight gain are other clinical signs that may be present.

94
Q

What are the causes of respiratory distress?

A

Pulmonary
Common: transient tachypnoea
Less common: meconium aspiration, pneumonia, RDS, pneumothorax
Rare: diaphragmatic hernia, airways obstruction
Non-Pulmonary: congenital heart disease, intracranial birth trauma/encephalopathy, severe anaemia

95
Q

What is transient tachypnoea of the newborn?

A

Delay in the resorption of the lung liquid and is more common after birth by C section.

96
Q

What would an X-ray show in transient tachypnoea of the newborn?

A

It may show fluid in the horizontal fissure.

97
Q

How do you treat transient tachypnoea of the newborn?

A

It is a condition that usually settles within the first day of life but can take several days to resolve completely.

98
Q

What may cause meconium aspiration?

A

It may be passed in response to hypoxia. At birth these infants may inhale thick meconium. Asphyxiated infants may start gasping and aspirate meconium before delivery

99
Q

Why is meconium aspiration bad?

A

Meconium is a lung irritant and results in both mechanical obstruction and a chemical pneumonitis, as well as pre-disposing to infection.

100
Q

What happens to the lungs after meconium aspiration?

A

The lungs are over-inflated, accompanied by patches of collapse and consolidation. There is a high incidence of air leak, leading to pneumothorax and pneumomediastinum.

101
Q

How do you treat meconium aspiration?

A

Artificial ventilation is often required.

102
Q

What are some predisposing factors for pneumonia?

A

Prolonged rupture of the membranes, chorioamionitis and low birthweight.

103
Q

How would you treat pneumonia?

A

Broad-spectrum antibiotics are started early until the results of the infection screen are available.

104
Q

What are some risk factors for milk aspiration?

A

It occurs more frequently in preterm infants and those with respiratory distress or neurological damage. Bronchopulmoary dysplasia and cleft palate are also risk factors

105
Q

What is persistent pulmonary hypertension of the newborn associated with?

A

Birth asphyxia, meconium aspiration, septicaemia or RDS.

106
Q

Why is persistent pulmonary HTN of the newborn bad?

A

As a result of the high pulmonary vascular resistance, there is right-to-left shunting within the lungs and at atrial and ductal levels. Cyanosis occurs soon after birth.

107
Q

How do you treat persistent HTN of the newborn?

A

Most infants require mechanical ventilation and circulatory support in order to achieve adequate oxygenation. Inhaled nitric oxide, a potent vasodilator, is often beneficial.

108
Q

How does diaphragmatic hernia often present?

A

It usually presents with failure to respond to resuscitation or respiratory distress.

109
Q

What are the symptoms of diaphragmatic hernia?

A

The apex beat and heart sounds will be displaced to the right side of the chest, with poor air entry in the left chest.

110
Q

How is diaphragmatic hernia diagnosed?

A

On X-ray

111
Q

How do you treat diaphragmatic hernia?

A

A large nasogastric tube is passed and suction is applied to prevent distension of the intrathoracic bowel. After stabilisation, the diaphragmatic hernia is repaired surgically. In lung hypoplasia has taken place, mortality is high

112
Q

What causes early onset (<48h after birth) infection?

A

In early-onset sepsis, bacteria have ascended from the birth canal and invaded the amniotic fluid. The fetus is secondarily infected because the fetal lungs are in direct contact with infected amniotic fluid.

113
Q

What are the risk factors for early-onset infection?

A

Prolonged or premature rupture of the membranes, chorioamionitis

114
Q

What are the clinical features of neonatal sepsis?

A 
Fever or temperature instability or hypothermia 
Poor feeding
Vomiting
Apnoea and bradycardia
Respiratory distress
Abdominal distension
Jaundice 
Neutropaenia
Hypo-/hyperglycaemia
Shock
Irritability
Seizures
Lethargy/drowsiness
115
Q

How do you treat early-onset infection?

A

IV Antibiotics are started immediately

116
Q

How can you prevent group B strep transmission from other to child?

A

Prophylactic intrapartum antibiotics can be given IV to the mother

117
Q

How is Listeria transmitted to the mother?

A

In food, such as unpasteurised milk, soft cheese and undercooked poultry.

118
Q

What can Listeria infection cause?

A

Spontaneous abortion, preterm delivery or fetal/neonatal sepsis.

119
Q

What are the characteristic features of Listeria infection?

A

Meconium staining of the liquor, unusual in preterm infants, a widespread rash, septicaemia, pneumonia and meningitis.

120
Q

Is conjunctivitis common in newborns?

A

Yes, sticky eyes are common in the neonatal period, starting on the 3rd or 4th day of life. Cleaning with saline or water is all that is required.

121
Q

What infection may cause neonatal conjunctivitis, are there any long term consequences?

A

Gonococcal infection, it can cause permanent loss of vision

122
Q

How would you treat umbilical infection?

A

If the skin surrounding the umbilicus becomes inflamed, systemic antibiotics are indicated

123
Q

What treatment should infants of hepatitis B surface antigen positive mothers get?

A

Hep B vaccination shortly after birth to prevent vertical transmission

124
Q

Which infants are at most risk of being hypoglycaemic in the first 24h of life?

A

IUGR babies, preterm, born to mother with DM, large for dates, hypothermic, polycythaemic or ill for any reason.

125
Q

What are the symptoms of hypoglyaemia?

A

Jitteriness, irritability, apnoea, lethargy, drowsiness and seizures

126
Q

How can you prevent neonatal hypoglycaemia?

A

Early and frequent milk feeding

127
Q

How would you treat neonatal hypoglycaemia?

A

Glucose can be given by IV infusion aiming to maintain the glucose >2.6mmol/L. If there is difficult or delay in starting the infusion, or a response is not achieved, glucagon or hydrocortisone can be given.

128
Q

How do neonatal seizures typically present?

A

There are repetitive, rhythmic (clonic) movements of the limbs, which persist despite restraint and are often accompanied by eye movements and changes in respiration

129
Q

What needs to be excluded after neonatal seizures?

A

Hypoglycaemia and meningitis

130
Q

What investigations are performed after neonatal seizures and what are they looking for?

A

A cerebral US is performed to identify haemorrhage or cerebral malformation

131
Q

How are seizures treated?

A

Treat cause. Recurrent seizures are treated with anticonvulsants but these are a lot less effective in young children.

132
Q

How does a neonatal cerebral infarct present?

A

It may present with seizures at 12-24h in a. term infant. There are no other abnormal clinical features.

133
Q

How is a neonatal cerebral infarct diagnosed?

A

It is confirmed on MRI

134
Q

What is the pathophysiology of neonatal cerebral infarct?

A

It is thought to be thrombotic, either thromboembolism from placental vessels or sometimes secondary to inherited thrombophilia.

135
Q

What is the prognosis of neonatal cerebral infarct?

A

Relatively good, only 20% have hemiparesis or epilepsy presenting later in infancy or in early childhood

136
Q

What is the pathophysiology of cleft lip and palate?

A

Cleft lip results from the failure of fusion of the frontonasal and maxillary processes.
Cleft palate results from failure of fusion to eh palatine processes and the nasal septum.

137
Q

What is an iatrogenic cause of cleft lip and palate?

A

Maternal anticonvulsant therapies

138
Q

How do you treat cleft lip and palate?

A

Surgical repair of the lip may be performed within the first week of life. The palate is usually repaired at several months of age.

139
Q

What are the consequences of cleft palate?

A

It can make feeding more difficult, but some affected infants can still breast-feed successfully.

140
Q

What ear condition is associated with cleft lip and palate?

A

Secretory otitis media is relatively common. Infants are also prone to acute otitis media.

141
Q

What is Pierre Robin sequence?

A

An association of micorognathia, posterior displacement of the tongue (glossoptosis) and midline cleft of theft palate. There may be difficulty feeding and cyanotic episodes due to the tongue falling back.

142
Q

What is oesophageal atresia?

A

Closure of the oesophagus, it is usually associated with a tracheotomy-oesophageal fistula

143
Q

What are the clinical features of oesophageal atresia?

A

If not diagnosed at birth, clinical presentation is with persistent salivation and drooling from the mouth after birth. If diagnosis is still not made, the infant with cough and choke when fed, and have cyanotic episodes

144
Q

How does small bowel obstruction present?

A

Can be recognised antenatally on US scanning. Otherwise, small bowel obstruction presents with persistent vomiting, which is bile-stained unless the obstruction is above the ampulla of Vater. Meconium may initially be passed, but subsequently its passage is usually delayed of absent.

145
Q

What would you find on examination of small bowel obstruction?

A

Abdominal distention becomes increasingly prominent the more distal the bowel obstruction

146
Q

What are the causes of small bowel obstruction?

A

Atresia or stenosis of the duodenum (associated with Downs)
Atresia or stenosis of the jejunum or ileum
Malrotation of the volvulus
Meconium ileus
Meconium plug

147
Q

How would you diagnose small bowel obstruction?

A

On clinical features and abdominal X-ray showing intestinal obstruction.

148
Q

How would you treat small bowel obstruction?

A

Atresia or stenosis of the bowel and malrotation are treated surgically. A meconium plus will usually pass spontaneously.

149
Q

What are the causes of large bowel obstruction?

A 
Hirschprunt disease (absence of the myenteric plexus)
Rectal atresia (absence of the anus at the normal site, treat surgically)
150
Q

What is bile-stained vomiting a sign of?

A

It is from intestinal obstruction until proved otherwise

151
Q

What is exomphalos?

A

The abdominal contents protrude through the umbilical ring, covered with a transparent sac formed by the amniotic membrane and peritoneum

152
Q

What is gastroschisis?

A

The bowel protrudes through a defect in the anterior abdominal wall, adjacent to the umbilicus, and there is no covering sac.

153
Q

What are the consequences of gastroschisis?

A

Dehydration and protein loss, so the infants should be wrapped in several layers of clingfilm to minimise fluid and heat loss

1 - Paeds AE (24 decks)

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