Level 2 - Neonates Flashcards

1
Q

Define HIE?

A
  • Gas exchange is compromised resulting in cardiorespiratory depression
  • Brain injury secondary to hypoxia
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2
Q

Mortality of HIE?

A
  • Severe HIE has 30-40% mortality rate and 80% of survivors have learning impairments, particularly cerebral palsy
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3
Q

Aetiology of HIE? (4)

A

o Failure of gas exchange across placenta (excessive or prolonged contractions)
o Interruption of umbilical blood flow (cord compression, prolapse)
o Inadequate maternal perfusion
o Inadequate postnatal cardiopulmonary circulation

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4
Q

Symptoms of mild, moderate and severe HIE? General features?

A

Mild HIE
- Irritable, excessive response to stimulation, hyperventilation, impaired feeding
Moderate HIE
- Abnormal tone, movement, cannot feed and seizures
Severe HIE
- No normal spontaneous movements or response to pain, abnormal tone, prolonged seizure, multi-organ failure
Cyanosis, low heart rate, acidosis

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5
Q

Describe the signs in HIE?

A
Abnormal neurological signs and seizures
Persistent pulmonary hypertension
Hypotension
DIC
Renal Failure
Low glucose, Ca, Na
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6
Q

Investigations in HIE?

A
Blood gas
-	Acidosis
aEEG
-	Used to confirm encephalopathy or identify seizures
CT/MRI
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7
Q

Management of HIE?

A
Resuscitation
-	Baby will have respiratory depression
Hypothermia
Anticonvulsants
Fluid Restriction
Treat electrolyte imbalances
-	Low glucose, calcium, sodium
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8
Q

Define birthmarks?

A
  • Birthmarks are coloured marks that are visible on the skin. They’re often present at birth or develop soon afterwards
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9
Q

Two types of birthmarks?

A

o vascular birthmarks (often red, purple or pink) caused by abnormal blood vessels in or under the skin
o pigmented birthmarks (usually brown) caused by clusters of pigment cells

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10
Q

Name the common vascular birthmarks?

A

Salmon patches
Infantile haemangioma
Port-Wine stain

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11
Q

Name common pigmented birth marks?

A

Cafe-au-lait spots
Mongolian spot
Congenital melanocytic nevus

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12
Q

What is Salmon patch? How common? What happens to them?

A

o Flat red or pink patches that can appear on a baby’s eyelids, neck or forehead at birth
o They’re the most common type of vascular birthmark and occur in around half of all babies
o Most salmon patches will fade completely within a few months, but if they occur on the forehead they may take years
o Often more noticeable when a baby cries because they fill with blood and become darker

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13
Q

What is an infantile haemangioma? How common and who do they tend to affect? Any treatment?

A

o Red to purple papules or plaques with a normal epithelial surface
o Compression leads to partial emptying and the colour becomes less prominent
o Haemangiomas are common, particularly in girls, and affect around 5% of babies soon after birth
o If they get bigger rapidly, or those that interfere with vision or feeding may need treatment

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14
Q

What are Port-wine stains?

A

o Deep pink or red patch present at birth and grows as the child grows
o May darken to purple, is flat; the overlying skin is normal. Later in life more papular lesions can occur within the patch
o Present for life and has no tendency toward involution
o Usually unilateral with a clear demarcation at the midline

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15
Q

Investigations in Port wine stain?

A

o If Sturge-Weber syndrome is suspected, MRI scan of the brain is required
o Optical coherence tomography
o Regular ophthalmic checks to exclude glaucoma should be carried out in the first three years of life

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16
Q

Management of Port wine stains?

A

o Refer as young as possible, usually around 1 year old, to a centre which has the laser and anaesthetic facilities
o Tunable pulsed dye laser (PDL)
o Surgical excision with or without cosmetic reconstruction may be required for lesions resistant to laser therapy

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17
Q

What are Cafe-au-lait spots? When should you see your GP? What could it be linked with?

A

o Caused by an increase in melanin content, often with the presence of giant melanosomes
o Coffee-coloured skin patches
o Common but if >six have developed by the time the child is five, you should see your GP
o Could be due to neurofibromatosis 1

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18
Q

What are mongolian spots?

A

o Caused by melanin within the deep layer of the skin (dermis)
o A benign, flat, congenital birthmark, with wavy borders and an irregular shape
o More commonly seen in darker-skinned people and usually covers the lumbosacral, buttocks, sides and shoulders

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19
Q

Colour and prognosis of Mongolian spot? What must happen?

A

o Normally disappears three to five years after birth and almost always by puberty
o Colour is blue, although they can be blue-grey, blue-black or deep brown
o They’re completely harmless and don’t need treatment
o May sometimes be mistaken for a bruise so NEED to be documented in notes if found

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20
Q

What are congenital melanocytic nevus?

A

o Initially appear as flat, pigmented lesions
o As the lesion ages, it tends to become raised and may become hairy
o Located in the area of the head and neck 15% of the time

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21
Q

Management of melanocytic nevus?

A

o Need to be aware of ABCD changes in malignant melanoma
o Typical small/medium lesions with no suspicious features usually require no investigation
o Dermoscopy and biopsy of suspicious lesions
o No treatment usually but can have done if suspicious

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22
Q

What is Sturge-Weber syndrome?

A

Neurocutaneous disorder classically presenting with:
Facial port wine stain affecting facial skin
Vascular abnormalities
Ipsilateral occipital leptomeningeal angioma
Venous hypertension

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23
Q

What complications of Sturge-Weber syndrome?

A

Develop progressive problems including glaucoma, seizures, stroke, and intellectual disability

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24
Q

How is diagnosis of SWS made?

A

Diagnosis of SWS is made if the cutaneous port-wine stain is associated with either brain or eye involvement (USS then MRI/CT needed)

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25
Q

Management of SWS?

A

Cosmetic camouflage creams can be used to help to conceal the port-wine stain
Carbamazepine
Pulsed dye laser (PDL) treatment is used for port-wine stain

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26
Q

General management of birthmarks?

A

Most haemangiomata require no treatment unless the patient is concerned about their appearance
Port-wine stains are usually treated by camouflage but the patient may wish to be referred for laser therapy

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27
Q

Definiton of cephalohaematoma?

A
  • Subperiosteal swelling on foetal head and its boundaries

- Spread is restricted by suture lines that are adherent, so it is limited to the surface of one cranial bone

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28
Q

Where is cephalohaematoma most common?

A
  • Commonest over parietal bones
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29
Q

Risk factors of cephalohaematoma?

A
o	Malposition
o	Large infant
o	Instrumental delivery (forceps/Ventouse)
	Ventouse more likely to cause injury
o	Breech delivery
o	Prematurity
o	Primagravida
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30
Q

Symptoms and signs of cephalohaematoma?

A
  • Centre feels soft
  • Blood loss can cause anaemia and even hypotension
  • Could have jaundice following blood breakdown
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31
Q

DDx of cephalohaematoma?

A
Caput succedaneum (extends beyond bone margins)
Chignon (following forceps delivery)
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32
Q

Investigations of cephalohaematoma?

A
  • Underlying skull fracture may be present. If suspected and thought to be depressed, CT or MRI scanning is required and surgery may be indicated
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33
Q

Management of cephalohaematoma?

A
  • Usually resolves over several weeks
  • Rarely this may require surgical removal for cosmetic reasons
  • Jaundice needs treatment
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34
Q

Types of haemolytic disease in neonate?

A
Rhesus haemolytic disorder
ABO incompatibility
G6PD deficiency
Spherocytosis
Sickle Cell Disease
Thalassaemia
35
Q

What is Rhesus haemolytic disorder?

A
  • Usually identified antenatally
  • Presents with anaemia, hydrops, hepatosplenomegaly with rapidly developing jaundice
  • Usually anti-D
  • Antibodies may develop to rhesus antigens other than D and to the Kell and Duffy blood groups
36
Q

What is ABO incompatibility?

A
  • Now more common than Rhesus incompatibility
  • Most ABO antibodies are IgM and do not cross placenta, but some blood group O women have IgG anti-A-haemolysin which haemolyses red blood cells of a group A infant
  • Occasionally group B infants affected by anti-B haemolysins
37
Q

Features of ABO incompatibility?

A
  • Can cause jaundice – peaks 12-72 hours
  • Anaemia is less severe and no hepatosplenomegaly
  • Coombs test positive
38
Q

What is G6PD deficiency?

A
  • Mainly from Mediterranean, Middle-East and Far East
  • Males mostly, develop severe jaundice
  • Drugs need to be avoided
39
Q

What is spherocytosis? Features? Diagnosis? Treatment?

A
  • Autosomal dominant inheritance with FHx in 75%
  • Early, severe jaundice in newborn infants
  • May cause anaemia, jaundice, splenomegaly, aplastic crisis and gallstones
  • Diagnosed on blood film
  • Treatment with folic acid, splenectomy if symptomatic
40
Q

Diagnostic clues towards haemolytic disease?

A

Increased reticulocyte count

Increased unconjugated bilirubin

41
Q

Definition of prematurity?

A
  • Infants born <37 weeks gestation
42
Q

Epidemiology of prematurity?

A
  • Leading cause of perinatal mortality
  • 50% of perinatal deaths
  • Prevalence 6% in singletons, 46% of twins, 79% of triplets
43
Q

Risk factors for premature birth?

A
  • History of preterm births
  • Multiple pregnancy
  • Cervical surgery
  • Uterine anomalies
  • Pre-existing medical conditions
  • Pre-eclampsia
  • IUGR
44
Q

Symptoms of very preterm infant?

A
  • Low birthweight
  • Very skin thin
  • Dark red colour
  • No palpable breast tissue
  • Males
    o Scrotum smooth, no testes in scrotum
  • Females
    o Prominent clitoris, labia minora protruding
45
Q

Associated features of a preterm infant?

A
  • Apnoeas common
  • No coordinated sucking and often need TPN
  • Jerky movements, startled easily
46
Q

Investigations of premature baby?

A
  • Monitor observations (HR, BP, RR, SpO2, To), weight, etc
  • FBC (Haemoglobin, neutrophils, platelets), CRP, U&Es, lactate, glucose
  • Blood cultures
  • Mid-stream urine
  • Speculum to rule out PROM
47
Q

Management to delay delivery in preterm labour?

A
  • Tocolytics could be used to delay and allow corticosteroids to work
48
Q

Management of preterm infant?

A
  • Transfer to NICU
    o Early contact with mother
    o Handling kept to a minimum as painful and affect oxygenation
    o Airway/Breathing
     Oxygen, High-flow humidified oxygen, CPAP
     Mechanical Ventilation
    o Keep warm
     Heat lamp, wrapped in plastic wrap
    o Arterial line for IV access
     Circulatory support via transfusion, saline, inotropic drugs
    o CXR all NICU infants for respiratory distress
    o IV Antibiotics
49
Q

Prognosis of preterm briths?

A
  • Prognosis good after 32 weeks gestation

o Increased risk in Cerebral palsy

50
Q

Define respiratory distress syndrome? Pathology? (RDS)

A
  • Inadequate surfactant production causes air sacs to collapse on expiration and greatly increases the energy required for breathing
  • Most alveolar surfactant produced >30 weeks
  • Interstitial oedema makes the lung even less compliant which leads to hypoxia and retention of carbon dioxide
51
Q

Epidemiology of RDS?

A
  • Incidence and severity inversely proportional to gestational age
  • Affects ½ of infants born at 28-32 weeks
52
Q

Pathology of RDS?

A
  • Caused by the inadequate production of surfactant in the lungs. Surfactant is normally produced by type II pneumocytes and has the property of lowering surface tension
53
Q

Risk Factors of RDS?

A
o	Premature delivery
o	Males
o	C-Section
o	Hypothermia
o	Maternal Diabetes
54
Q

Secondary surfactant deficiency caused by what?

A

o Pulmonary infection, haemorrhage

o Meconium aspiration

55
Q

Symptoms and signs of RDS?

A
-	At delivery or within 4 hours:
o	Preterm delivery
o	Tachypnoea (>60/min), expiratory grunting, subcostal and intercostal retractions, diminished breath sounds, cyanosis and nasal flaring
o	Progress to apnoea, fatigue and hypoxia rapidly
o	Decreased cardiac output, hypotension, acidosis and renal failure
56
Q

DDx of RDS?

A
  • Pneumothorax, pneumomediastinum
  • Infection (group-B strep), aspiration
  • Transient tachypnoea of newborn
    o Due to excess lung fluid
  • Congenital lung/heart defects
57
Q

Investigations in RDS?

A
-	Blood gases
o	Respiratory and metabolic acidosis
-	Pulse oximetry
o	Aim for 91-95%
-	Chest X-ray
o	Diffuse ground glass appearance
o	Air bronchograms
-	Monitor FBC, electrolytes, glucose, renal and liver function
-	Echo and cultures
58
Q

Prevention of RDS?

A

o Dexamethasone offered to at risk women of preterm delivery from 23-25 weeks

59
Q

Management of RDS?

A

o Delay clamping of cord to promote placental-fetal transfusion
o Wrap up baby warmly and take to NICU
o Oxygen
 Via oxygen-air blender and can use CPAP
 Mechanical ventilation if needed
o Surfactant replacement
 Via endotracheal tube
 Inositol is essential nutrient promoting surfactant maturation
o Fluids
 10% glucose IVI if needed
o Antibiotics
 Start antibiotics in all infants who present with respiratory distress at birth, after obtaining blood cultures

60
Q

Complications of RDS?

A

o Alveolar rupture, intracranial haemorrhage, PDA, pulmonary hypertension
o Chronic lung disease, retinopathy of prematurity, neurological impairment if severe hypoxia

61
Q

Define IUGR?

A
  • Where a baby’s growth slows or ceases when it is in the uterus
  • Part of wider group of SGA foetuses and often used synonymously
  • Clinical definition and applies to neonates born with clinical features of malnutrition and in-utero growth restriction, irrespective of their birth weight percentile
62
Q

Definition of SGA?

A

Estimated fetal weight <10th centile for age or head circumference <10th centile

63
Q

Pathology of IUGR?

A
  • Any mismatch between the supply of nutrient by the placenta and the demand of the fetus also leads to IUGR
64
Q

Where is incidence highest in IUGR?

A

6x more common in developing countries

65
Q

Risk factors for IUGR?

A
o	Maternal age (<16, >35)
o	Twins 
o	Placental dysfunction/abruption
o	Chronic hypertension/pre-eclampsia
o	Diabetes
o	Previous SGA baby
o	Previous stillbirth Smoker
o	Cocaine use
66
Q

Classification of IUGR?

A
  • Symmetrical
    o Earlier in pregnancy
    o All antenatal and postnatal measurements are reduced proportionally
  • Asymmetrical
    o Later in pregnancy
    o Antenatal scans all normal but reduced postnatal measurements
  • Mixed
67
Q

Investigations in IUGR?

A
  • At booking, every woman should have growth chart considering maternal age, parity, BMI, ethnicity and birthweights of previous children
  • USS if:
    o SFH measurement <10th centile or static growth
  • Serial measurements of amniotic fluid volume, foetal movements, foetal tone, foetal breathing and heart activity
  • Umbilical artery doppler scan
68
Q

Management of IUGR?

A
  • If normal doppler aim for IOL at 37 weeks
  • If abnormal then may need LSCS earlier
  • Corticosteroids
    o Foetal lung maturation
  • Keep warm and feed early as prone to hypoglycaemia
69
Q

Complications of IUGR?

A

o Perinatal asphyxiation, meconium aspiration, persistent pulmonary hypertension, jaundice, NEC
o Poor growth and neurodevelopmental problems
o Obesity, metabolic syndrome, type 2 diabetes, CVD

70
Q

Definition of congenital talipes equinovarus?

A
  • Congenital talipes equinovarus is characterised by a permanent alteration of the morphology of the foot
  • The foot cannot be placed flat on the ground when in the physiological standing position
71
Q

Two types of talipes?

A

Positional

Congenital

72
Q

What is positional talipes? How common? Management?

A

 Normal foot that has been held in a deformed position in the uterus
 Postural talipes is correctable with gentle passive dorsiflexion of the foot
 This positional variant occurs about five times more often than congenital talipes equinovarus
 Passive exercises by physio can help

73
Q

What is congenital talipes? Types?

A

 A fixed condition, which may be idiopathic or teratological
 The idiopathic type is usually an isolated skeletal anomaly. It is usually bilateral, and has a higher response rate to conservative treatment
 Teratological associated with genetic syndromes, neurological disorders and myopathies

74
Q

Epidemiology of talipes?

A
  • 50% are bilateral

- Males 2x more common

75
Q

Aetiologies of talipes?

A

o Neuromuscular and anatomical causes (muscle fibre abnormalities, titling and rotation of the talus, hypoplasia of the anterior tibial artery)
o Polygenic multifactorial genetics
o Arrested fetal development

76
Q

What may lead to positional talipes?

A
  • Oligohydramnios, uterine anomalies and multiple pregnancy may lead to positional talipes due to fetal restriction
77
Q

Associated conditions with talipes?

A
  • Associations with spina bifida, cerebral palsy and arthrogryposis
78
Q

Symptoms of talipes?

A
  • Foot
    o Inverted
    o Adduction of forefoot relative to hindfoot
    o Equinus (plantarflexion) deformity
    o Sole of foot points medially
  • Heel is high and calf muscle is smaller
  • Affected foot is smaller
79
Q

Feature of congenital talipes?

A
  • Foot is fixed and cannot be corrected completely
80
Q

DDx of talipes?

A

Child with a limp

81
Q

Investigations of talipes?

A
  • Diagnosis made on clinical assessment
  • Classed using Pirani scoring system
  • Imaging helps class severity
    o Xray AP and lateral standing
    o USS
82
Q

What is Ponseti method in managing talipes?

A

o Used in children up to 2 years old
o Stretching – the foot is re-positioned, and a cast is applied
o Re-cast weekly for several months
o Towards the end, Achilles tenotomy usually performed to lengthen the tendon
 Botulinum toxin is sometimes used as an alternative to tenotomy
o The child wears special shoes or braces full-time for three months, then nightly for three years

83
Q

What is the French functional method in managing talipes?

A

o Done in young children by specialist physios, foot gradually stretched and held in correct place with tape

84
Q

Surgery in talipes?

A

o Not recommended as primary treatment
o Used when unbalanced growth
o Selective medial release, posteromedial release and cuboid subtraction osteotomy