Perinatal meeting Flashcards

1
Q

What is the staging and prognostic factors for hypoxic ischemic encephalopathy?

A
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2
Q

Outline the multi-organ involvement of severe HIE

A
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3
Q

What are the types of decelerations in CTG?

A

Early: uniform in shape and occur with each contraction (mirror image), heart rate reaches its lowest point at the peak of contraction and recovered to baseline by the end of contraction
Late: uniform in shape and depth and occur after each contraction with lowest point occurs >15s after peak of contraction

Shouldering = The accelerations before and after a variable deceleration are known as the shoulders of deceleration. Their presence indicates the fetus is not yet hypoxic and is adapting to the reduced blood flow.

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4
Q

What is the etiologies of late decelerations in fetus?

A
  • Excessive uterine contractions, maternal hypotension, or maternal hypoxemia
  • Reduced placental exchange as in hypertensive disorders, diabetes, IUGR, abruption
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5
Q

What is the most common of type of decelerations in CTG?

A

Variable: inconsistent in shape and frequency

Typical: shoulders, acceleration on either side of deceleration. Could by physiological response to cord compression
Atypical: loss of shouldering, delayed recover of FHR< rebound tachycardia, reduction in variability during deceleration, biphasic deceleration

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6
Q

What is the NICE guideline for categorizing individual features of CTG?

A
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7
Q

What is DR C BRAVADO for CTG interpretation?

A

DR Define risk
C: contractions
BRa: baseline rate
V: variability
A: accelerations
D: decelerations
O: overall impression

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8
Q

What is present in left hypoplastic heart syndrome?

A
  • Mitral valve stenosis/atretic
  • Left ventricle: slit like cavity
  • Aortic valve: atretic
  • Ascending aorta: diminutive
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9
Q

What is the haemodynamics of left hypoplastic heart syndrome?

A
  • Blood in the left atrium flows to the right atrium through a patent oval foramen/ASD
  • No cardiac output from the left ventricle
  • Duct dependent systemic circulation
  • Ascending aorta and its branches are supplied by retrograde blood flow via PDA
  • Right ventricle supports borth pulmonary and systemic circulation
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10
Q

What is the management of left hypoplastic heart syndrome?

A
  • Immediate post delivery and resuscitation
  • Oxygen target spo2: 75-85% as supplying too much oxygen will cause dilatation of the pulmonary vessels which increases pulmonary blood flow –> respiratory compromise and subsequent dilatation and reduced RV function
  • Maintain patency of ductus arteriosus and optimize systemic perfusion
  • Commence prostaglandin infusion
  • Correction of metabolic acidosis
  • Corrective surgery vs palliative care
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11
Q

What is the 1st staged surgery for left hypoplastic heart syndrome?

A

1st stage neonatal period: Norwood operation
* Converts the right ventricle into the main ventricle pumping blood to both the lungs and the body
* Main pulmonary artery and the aorta are connected
* Main pulmonary artery is cut off from the 2 branching pulmonary arteries that direct blood to each side of the lung
* Shunt placed between the pulmonary arteries and the aorta to supply blood to the lung

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12
Q

What is the 2nd staged surgery for left hypoplastic heart syndrome?

A

Bidirectional Glenn operation: performed at about 6 months after Norwood to divert alf of the blood to the lungs when circulation through the lung no longer needs as much pressure from the ventrile
* Shunt to the pulmonary arteries is disconnected
* Right pulmonary artery is connected directly to the SVC: send half of the deoxygenated blood to the lungs without going through the ventricle

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13
Q

What is the 3rd staged surgery for left hypoplastic heart syndrome?

A

Fontan operation performed about 18-36 months after the Glenn operation
* Connects the IVC to pulmonary artery creating a channel to direct blood to the pulmonary artery
* All deoxygenated blood flows passively through the lungs

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14
Q

What is the surgical outcome of Fontan operation (3rd stage) for left hypoplastic heart syndrome?

A
  • Not curative
  • Good results in patients with ideal haemodynamics: many cases result in normal and near normal growth, development, excercise tolerance and good QoL
  • Long term complications: excercise intolerance, ventricular failure, right atrium dilatation and arrhythmia, systemic and hepatic venous hypertension, portal hypertension
  • Cardiac transplantation –> only definitive treatment for those failing Fontan operation
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15
Q

How can doppler flow be used to assess coarctation of aorta?

A
  • Reversed blood flow across the foramen ovale and retrograde flow in the aortic arch
  • Mainly observe during systole
  • Retrograde flow in the fetal aortic arch combined with a small left heart is suspicious for coarctation
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16
Q

How can the 3 vessel view on USG be used to assess coarctation of aorta?

A
  • Measurement of PA: Ao ratio diameter during diastole at 3V view at 3rd trimester
  • If PA: Ao ratio of 1.6 or more
  • Probably reltaed to blood flow redistribution due to increased resistance of the left ventricular outflow tract: can be temporary redistribution that normalizes after birth or a permanent redistribution
17
Q

What are the associated conditions of coarctation of aorta?

A
  • Bicuspid aortic valve, aortic valve stenosis, a large VSD and mitral stenosis
  • Chromosomal abnormalities: in 14% of patients with Turner syndrome, CoA is present
18
Q

How to define the VSD defect by anatomic size?
Size of the intracardiac shunt?

A
  • Small: <4mm
  • Moderate: 4-6mm
  • Large: >6mm

Size of the intracardiac shunt determined by the ratio of pulmonary to systemic blood flow
* Small: Qp: Qs <1.5
* Moderate: Qp: Qs 1.5 to 2.3
* Large: Qp: Qs >2.3

19
Q

What is the ddx for overgrowth syndromes?

A
  • Beckwith Wiedemann syndrome
  • Sotos syndrome
  • Perlman syndrome
  • Simpson Golabi Behmel syndrome
  • Costello syndrome
20
Q

What is the gene involved in Simpson Golabi Behmel syndrome type 1?
What clinical features

A

GPC3

21
Q

What is growth, head and neck, genitourinary features of Simpson Golabi Behmel syndrome?

A
22
Q

What is cardiovascular, abd, chest, respiratory features of Simpson Golabi Behmel syndrome?

A
23
Q

What is skeletal, skin, neurologic, neoplasia, prenatal manifestation features of Simpson Golabi Behmel syndrome?

A