Paediatrics- cardiology Flashcards
1
Q
Henoch schonlein purpura and hypertension in children
A
The most common small vessel vasculitis in children. It most commonly affects children aged 3-5.
Hypertension in children= Hypertension is defined as BP ≥95th centile for age, sex and height centile on three or more occasions, with maximum of ≥140/90 which is the adult definition of hypertension.
2
Q
Henoch schonlein purpura- presentation
A
- Abdominal pain
- Arthralgia- joint pain and swelling
- Nephritis (haematuria +/- proteinuria)
- May be pyrexial
- HSP is commonly preceded by a viral upper respiratory tract infection
3
Q
HSP- management
A
- NSAIDs for analgesia and their anti-inflammatory effect
- Antihypertensives may be needed to control blood pressure
- After an episode of HSP, children should have regular urine dips for 12 months to check for renal impairment.
4
Q
HSP-prognosis
A
- The majority of cases of HSP recover completely
- 1/3 of patients have a second episode of HSP
- Long-term renal impairment occurs in about 1/5 patients with significant proteinuria
5
Q
HSP- complications
A
- Hypertension
- Oedema
- Orchitis- inflammation of the testicles causing pain and swelling
- Intussusception- blockage in the bowel
6
Q
Acyanotic cardiac lesion include:
A
- Ventricular septal defects (VSD)
- Atrial septal defects (ASD)
- Patent ductus arteriosis (PDA)
7
Q
Acyanotic cardiac lesions have the following features
A
- Left to right shunting, mixing of oxygenated blood with deoxygenated blood
- Increased pulmonary blood flow → risk of pulmonary hypertension and untreated acyanotic heart disease can lead to Eisenmenger syndrome
- Lesions that are above the level of the nipple usually give rise to ejection systolic murmurs while lesions below the level of the nipple typically cause pan systolic murmurs
8
Q
Ventricular septal defect: symptoms
A
- Small- asymptomatic, normal growth
- Moderate- poor feeding, failure to thrive (FTT), short of breath (SOB)
- Large- poor feeding, FTT (falls down centiles), SOB, sweaty and pale with feeds
- Most common congenital heart defect, associated with downs syndrome, all require echo
9
Q
Ventrical septal defect: Time of presentation
A
- Antenatal diagnosis at 16-18 weeks
- Presentation at 6-8 weeks
- Defect in the membranous portion of the ventricular septum is more common than the muscular portion
- Congestive heart failure typically presents after 4-6 weeks
- Persistent pulmonary hypertension of the newborn (PPHN) may become established by 6-12 months
10
Q
Ventricular septal defect- clinical findings
A
- Palpate: Check for the presence of a thrill, Might be useful to palpate the liver (enlarged in heart failure)
- Auscultate: Pan-systolic murmur heard loudest at the lower left sternal border (LLSB). Typically grade 3-4. Loud P2 suggests the presence of pulmonary hypertension
11
Q
Ventricular septal defect: Investigations
A
- Pulse oximetry – to determine the level of oxygen saturation
- Echocardiography – visualise defect directly
- CXR – cardiomegaly and pulmonary oedema (increased pulmonary vascular markings) if severe VSD (presence of heart failure), enlarged pulmonary artery
- ECG: In patients with moderate or large VSD, the ECG may demonstrate LV hypertrophy (LVH) manifesting as increased voltage in V5 and V6 or leads II, III, and aVF
- ECG: In patients with elevated RV pressure, the ECG demonstrates RV hypertrophy (RVH), often manifesting as tall R waves in leads V4R and V1, or upright T waves in these leads beyond the first 24 hours of life, in addition to LVH
12
Q
Ventricular septal defect: Management
A
- Small lesion: < 5mm usually close spontaneously, no repair required (30-40%)
- Moderate lesion: Diuretic therapy (furosemide and spironolactone). Feeding with high caloric feeds (Infantrini)
- Large lesion: Manage as per moderate lesion. Optimise weight gain for surgery. Schedule for surgery before 12 months to prevent persistent pulmonary hypertension of the newborn (PPHN)
13
Q
Atrial septal defect: symptoms
A
- Typically asymptomatic, some children will have recurrent chest infections
- The mean age of diagnosis is 4.5 years from an incidental finding of a murmur. Symptomatic presentation is usually before the age of 40 with arrhythmias, dyspnoea
14
Q
Atrial septal defect: Ausculate
A
- Ejection systolic murmur heard loudest at the upper-left sternal border (ULSB)
- Widely fixed splitting of the second heart sound (L→ R shunting increases RV filling, thus RV ejection time is increased and pulmonary valve closure is delayed for a significant amount of time after aortic valve closure)
15
Q
Atrial septal defect: Investigations
A
- Pulse oximetry
- ECHO – visualise defect directly, shows dilated RV and increased RV filling and ejection time
- CXR – usually no findings
- ECG – incomplete RBBB
16
Q
Atrial septal defect: Management
A
- Most children are asymptomatic and rarely require congestive heart failure (CHF) therapy
- Spontaneous closure in lesions smaller than 7-8mm
- Large defects require repair – percutaneous (catheter closure) or surgery using median sternotomy incision
17
Q
Patent ductus arteriosus: symptoms
A
- Small – asymptomatic
- Moderate – congestive heart failure with failure to thrive (poor feeding)
- Large – poor feeding, severe failure to thrive, recurrent lower respiratory tract infections (preterm infants may experience failure to wean from ventilation)
- More common in preterm infants
- Symptoms usually present 3-5 days after birth when the duct begins to close
18
Q
Patent ductus arteriosus: clinical features
A
- Palpate: Might be useful to palpate the liver (enlarged in heart failure). Bounding pulses and wide pulse pressure
- Auscultate: Continuous machinery murmur typically heard at the upper-left sternal border (best heard below left the clavicle). Check for the presence of a thrill at the upper left sternal border
19
Q
Patent ductus arteriosus: investigations
A
- 2D echocardiography and Doppler
- CXR and ECG are less useful in diagnosing PDA
20
Q
Patent ductus arteriosus: Management
A
- If preterm – good probability of spontaneous closure
- If term – less likely to close spontaneously
- Medical – indomethacin/ibuprofen (not effective in term infants)
- Surgical – catheter closure or PDA ligation (left lateral thoracotomy incision) when weight is at least 5kg
21
Q
Outflow tract obstruction: Coarctation of the aorta
A
- Obstruction to the left ventricles outflow tract leads to an increase in left ventricular afterload which causes left ventricular hypertrophy
- Neonates with severe aortic coarctation can develop heart failure.
- Associated with Turners syndrome
- Symptoms present 3-5 days after birth when the duct begins to close as the PDA and foramen ovale allows blood to bypass the outflow obstruction
- Narrowing usually after the branches supplying the head and arm, prevents blood from circulating in the lower half of the body
