Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 4 PAEDS > Neonatal and Newborn 2 > Flashcards

Neonatal and Newborn 2 Flashcards

1
Q

What is a cephalohaematoma?

A

Bleeding between periosteum and skull causes a haematoma, usually in the parietal region and occasionally in the occipital region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the location of a cephalohaematoma

A

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

Don’t cross the midline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a risk of a large cephalohaematoma?

A

Anaemia and potentially hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can occur as the a cephalohaematoma resolves?

A

Breakdown of haemoglobin can cause hyperbilirubinaemia that may need urgent treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What else may be present with a cephalohaematoma?

A

Underlying skull fracture

May beed CT / MRI and surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some RF for developing a cephalohaematoma?

A

Prolonged or instrumental labour
LGA
Malpresentation
Shoulder dystocia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List some ddx for a cephalohaematoma

A

Caput succudaneum - can cross midline

Subaponeurotic haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the management of a cephalohaematoma?

A

Do not attempt to needle aspirate due to high risk of infection and abscess formation

Phototherapy for jaundice

Exchange transfusion to treat anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the prognosis of a cephalohaematoma?

A

Majority resolve spontaneously within days / weeks however some may calcify

Rarely require surgical removal for cosmetic reasons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is haemolytic disease of the newborn? What are the two most common causes?

A

Maternal antibodies react with antigen on the fetal RBC, most commonly:

1) Rhesus incompatibility
2) ABO blood group incompatibility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the pathophysiology of rhesus haemolytic disease?

A

Mother is rhesus negative and fetus is rhesus positive

Mother has been sensitised to rhesus-positive cells in previous pregnancies (during which fetal cells cross into maternal circulation)

Mother develops anti-rhesus antibodies, which cross the placenta and cause haemolysis of fetal RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is rhesus haemolytic disease prevented?

A

Rhesus negative women are immunised with anti-D antibody at 28wks

This ‘mops up’ fetal RBC before they stimulate maternal IgG production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the pathophysiology of ABO haemolytic disease?

A

The mother is most commonly group O and the baby is most commonly group A

mOther and bAby

The mother’s natural anti-A antibodies react with the fetal cells causing haemolysis and jaundice

Condition cannot be detected antenatally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does haemolytic disease of the newborn present?

A

Antenatal:

  • Foetal anaemia
  • Hydrops foetalis

Postnatal:

  • Hydrops foetalis
  • Early jaundice (within first 24hrs)
  • Kernicterus
  • Cutaneous hemopoietic lesions
  • Hepatosplenomegaly
  • Coagulopathy
  • Thrombocytopenia
  • Leucopenia

Late:

  • Anaemia
  • Inspissated bile syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What cause of haemolytic disease of the newborn is more likely to cause RDS?

A

Rhesus disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the management of haemolytic disease of the newborn?

A

Aim is to deliver baby before severe haemolysis has occurred and then undertake a serious of exchange transfusions to wash out the antibodies as well as toxic bilirubin

In-utero blood transfusions can now be given via the umbilical cord in severe cases of haemolytic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What antenatal investigations are performed for rhesus haemolytic disease?

A

Indirect Coomb’s test at first antenatal visit

Anetanal USS - detect hydrops fetalis

Fetal blood sampling

  • Anaemia
  • High reticulocyte count
  • If DIC = schistocytes and burr cells can be seen and neutoropenia and thrombocytopenia can occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What postnatal investigations are performed for haemolytic disease?

A

Immediately after birth of any baby to a rhesus-negative woman, blood form the umbilical cord or from the baby should be checked for:

  • ABO and Rh blood group
  • Direct Coomb’s test
  • Hb
  • Baseline bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is hydrops fetalis?

A

Abnormal accumulation of fluid in two or more fetal compartments, including ascites, pleural effusion, pericardial effusion, and skin oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

List some brain complications of prematurity (4)

A

1) Intraventricular haemorrhage
2) Posthaemorrhagic hydrocephalus
3) Periventricular leucomalacia
4) Increased risk of cerebral palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is an eye complication of prematurity and how is it managed?

A

Retinopathy of prematurity due to abnormal vascularisation of the developing retina

Requires laser treatment to prevent retinal detachment and blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

List some respiratory complications of prematurity (4)

A

1) RDS - surfactant deficiency
2) Apnoea and bradycardia
3) Pneumothorax
4) Chronic lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List some CV complications of prematurity (2)

A

1) Hypotension

2) Patent ductus arteriosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

List some GI complications of prematurity (3)

A

1) Necrotising enterocolitis
2) GOR
3) Inguinal hernias (with high risk of strangulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why do premature babies have problems regulating temperature? (3)

A

1) Increased SA:V leads to loss of heat
2) Immature skin cannot retain heat and fluid efficiently
3) Reduced SC fat reduces insulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What metabolic problems do premature babies face?

A

1) Hypoglycaemia is common:
- Symptomatic hypoglycaemia must be treated promptly
- Blood glucose should be maintained >2.6mmol/L
2) Hypocalcaemia
3) Electrolyte imbalance
4) Osteopenia of prematurity with risk of fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What infections are common in prematurity?

A

1) Increased risk of sepsis - esp group B strep and coliforms
2) Pneumonia is common
3) Infection is a common complication of central venous lines required for feeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What nutritional requirements may a premature baby have?

A

May require parenteral nutrition
NG feeds until sucking reflex develops at 32-34wks

NB it is difficult to achieve in utero-growth rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What blood complications may be associated with prematurity? (2)

A

1) Anaemia of prematurity

2) Neonatal jaundice

30
Q

What gestation is defined as:

1) Extremely preterm
2) Very preterm
3) Moderate to late preterm

A

1) Extremely preterm = <28wks
2) Very preterm = 28-32wks
3) Moderate to late preterm = 32-37wks

31
Q

What are the most common long-term complications of prematurity?

A

1) Chronic lung disease = bronchopulmonary dysplasia
- Results from disrupted lung development
- May require long-term oxygen treatment for months / years

2) Neurological sequelae
- Significant risk of hydrocephalus developing secondary to an intraventricular haemorrhage
- Shunt may need to be inserted to relieve pressure
- Hypotension may be sustained which can lead to periventricular leucomalacia. This carries risk of cerebral palsy (esp diplegic type)

3) Blindness

4) Poor growth
- Esp if catch up growth is not achieved

32
Q

What is periventricular leucomalacia?

A

White-matter brain injury, characterised by necrosis of white matter near the lateral ventricles

Premature infants are at greatest risk

Leads to problems with motor control and developmental delay, often developing CP or epilepsy later in life

33
Q

What is the antenatal management of a premature infant?

A

IM corticosteroids to women expecting delivery <34wks

2 doses, 12-24hrs apart

Betamethasone or dexamethasone

34
Q

What is the postnatal management of a premature infant?

A

Most require stabilisation and support (not resuscitation)

<28 weeks need senior paediatrician

Delay cord clamping for 1 min if infant not compromised

Keep warm

Provide resp support if needed:

  • Positive end experiratoy pressure = PEEP (CPAP)
  • Consider intubation

Monitor and maintain blood glucose

Encourage mother to express breast milk

If ?infection - start broad spectrum abx

35
Q

What are some causes of respiratory distress syndrome (RDS)? (5)

A

1) Surfactant deficiency = by far most common
2) Pneumonia
3) Pneumothorax
4) Cardiac failure
5) Congenital lung malformation

36
Q

What are the risk factors for surfactant deficiency?

A
  • Premature birth - main risk factor
  • Genetic predisposition
  • Elective C-section - uterine contractions during normal labour increase levels of glucocorticoids that aid lung maturation
  • Maternal diabetes - insulin inhibits surfactant synthesis - main cause of RDS in term babies
  • Hydrops fetalis
  • Multiple pregnancy
37
Q

How may RDS present?

A 
Tachypnoea - RR > 60
Nasal flaring
Intercostal recession
Cyanosis 
Expiratory 'grunting'
38
Q

What may a CXR show in RDS?

A

‘Ground glass’ appearance due to alveolar collapse with an air-bronchogram

= bilateral and relatively symmetric diffuse ground glass lungs with low volumes and a bell-shaped thorax

Generalised atelactasis = complete of partial collapse of a lung or lobe of the lung

39
Q

What is surfactant?

A

A phospholipid which reduces alveolar surface tension to prevent them from collapsing

Produced by lamellar bodies of type II alveolar cells

40
Q

When is surfactant production mature?

A

Surfactant production occurs at 20 weeks’ gestation but distribution throughout the lungs begins around 28-32 weeks and reaches sufficient concentration at 35 weeks

However, the stress of labour usually stimulates production, and thus RDS is usually self-limiting, lasting 5-7 days

41
Q

What can be administered antenatally to at risk mothers?

A

24mg IM betamethasone (2 doses of 12mg 24h apart) to stimulate surfactant production

1-7 days before birth

42
Q

Why do IUGR babies tend to get less severe RDS?

A

They are physiologically ‘stressed’ and thus tend to get less severe RDS due to endogenous corticosteroid release

43
Q

What is the management of RDS?

A

Optimising oxygenation and supporting respiration - either with CPAP via nasal prongs, or by mechanical ventilation

Surfactant can be administered via an endotracheal tube

Abx - penicillin or gentamycin until congenital pneumonia has been excluded (can mimic or coexist with RDS)

Nutrition - IV fluids until stable, then start NG tube feeds

44
Q

What is a long-term complication of RDS?

What is the prognosis?

A

20% develop chronic lung disease of prematurity = bronchopulmonary dysplasia

If severe may require home oxygen therapy

Generally good prognosis, 5-10% mortality

45
Q

What is necrotising enterocolitis (NEC)?

A

Life-threatening complication in which there is impaired blood flow to the bowel

Mucosal ischaemia allows gut microorgnaisms to penetrate the bowel wall causing severe hemorrhagic colitis

46
Q

What are some RF and protective factors for necrotising enterocolitis?

A

Breast milk = protective

But increasing milk feeds (esp formula feeds) too quickly is a risk factor for NEC

Prematurity

47
Q

How may NEC present?

A

Acute collapse
Abdo distension
Bilious vomiting
Fresh red blood in stools

48
Q

What 3 abdo XR views are required to diagnose NEC? What would be seen on AXR

A

Supine position
Lateral position
Lateral decubitus position

Distended loops of bowel with thickening of bowel wall
Gas in bowel wall = pneumatosis intestinalis
Possible pneumoperitoneum if perforation has occurred

49
Q

What is the management of NEC?

A

Gut rest - nil by mouth with IV fluids and TPN and NG tube

Broad spectrum antibiotics - 10 days metronidazole

Laparotomy - surgical emergency

  • Resection of dead bowel tissue
  • Temporary stoma if significant bowel removed
50
Q

What can be given antenatally as prophylaxis for NEC?

A

Erythromycin

51
Q

What is the management of ROP?

A

Most cases require no treatment but causes blindness in 1%

Laser ablation to prevent risk of retinal detachment and blindness

52
Q

What causes ROP?

A

Proliferation of new blood vessels in an area of relative ischaemia in the developing retina

Oxygen toxicity and genetic predisposition are two causes - at risk infants should be screened by an opthalmologist

53
Q

What is an intraventricular haemorrhage (IVH)?

A

A haemorrhage develops in the floor of the lateral ventricle and ruptures into the ventricle

In a small minority the haemorrhage involves the white matter around the ventricle by a process of obstructive venous infarction = high risk of hemiplegic cerebral palsy

Can be asymptomatic and diagnosed by asymptomatic USS

Occurs in 30% of very low birth weight babies

54
Q

What can occur as a complication of severe IVH?

A

Posthaemorrhagic hydrocephalus

Occurs in 15% of severe IVH

55
Q

What is posthaemorrhagic hydrocephalus?

A

Progressive dilation of the ventricular system

56
Q

How is posthaemorrhagic hydrocephalusmanaged?

A

May require insertion of a ventriculo-peritoneal shunt

57
Q

How common is periventricular leucomalacia (PVL)?

A

Less common than IVH but is the most common cause of cerebral palsy in surviving infants

58
Q

What increases risk of PVL?

A

Chorioamnionitis
Severe hypotension
Monozygotic twins

59
Q

What worsens the prognosis in PVL?

A

Cystic change = 80% develop CP

60
Q

Babies with severe IUGR should be screened for TORCH. What is TORCH?

A 
Toxoplasmosis
Other = syphilis
Rubella
CMV
Hepatitis and HIV
61
Q

What is the risk of over-feeding during infancy?

A

Excessive weight gain can lead to HTN, IHD and DM later in life

62
Q

What is a neonatal club foot called?

A

Tallipes equinovarus

63
Q

In which group is tallipes more common?

A

Males 2 x more likely

64
Q

What % of tallipes are bilateral?

A

50%

65
Q

What are the 2 types of talipes?

A

Talipes equinovarus = club foot - feet are hyper-inverted and plantar-flexed

Talipes calcaneovalgus = ankles are hyperflexed

66
Q

What are the five deformities in talipes equinovarus?

A
  1. Equinus foot position - short Achilles tendon fixes the foot in plantar flexion so dorsiflexion beyond 90 degrees is not possible
  2. Varus position - supination of calcaneus
  3. Adductus - medial deviation of the toes
  4. Supinatus - inversion of forefoot
  5. Distinct arching of foot
67
Q

What can tallipes be associated with? (3)

A

1) Oligohydraminous
2) Uterine anomalies
3) Multiple surgeries

= restrictive uterine environment

68
Q

Describe the findings when trying to passively move the ankle in an infant with tallipes

A

The foot cannot be passively everted and dorsiflexed through the normal range

69
Q

What is the treatment of tallipes?

A

Ponseti-method - manual correction with serial casting that should be initiated within 24 hours of birth

Foot is manipulated and placed in a long leg plaster cast on repeat occasions - important that the deformity correction is gradual

If this does not work, operations on soft tissues and/or bones may be carried out later (from 2yrs)

70
Q

What are the main features of congenital rubella?

A
  • IUGR
  • Sensorineural deafness
  • Bilateral cataracts
  • Microcephaly
  • PDA
71
Q

What are the main features of congenital CMV?

A
  • IUGR
  • Periventricular calcifications
  • Pin point petechial ‘blueberry muffin’ skin lesions

remember CMV infection would have been asymptomatic in the mother so no history of maternal illness

72
Q

What are the main features of congenital toxoplasmosis?

A

Classic triad:

1. Chorioretinitis
2. Hydrocephalus
3. Diffuse intracranial calcifications

Year 4 PAEDS (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions