Pediatrics Cardioconference Vsd

8/11/2019 Pediatrics Cardioconference Vsd

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CARDIOLOGY CONFERENCEVALDEZ, Christel

VALENZUELA, Erlyn Joy

VERALLO, Sean Fergie

VERGARA, Tyrone

YOUNG, Julia


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VENTRICULAR SEPTAL DEFECT

INTRODUCTION


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INTRODUCTION

Henri Roger was the firstman to describe a

ventricular septal defect,in 1879 he wrote:

A developmental defect of

the heart occurs from whichcyanosis does not ensue inspite of the fact that a

communication exists betweenthe cavities of the two

ventricles and in spite of thefact that the admixture of

venous blood and arterialblood occurs. This congenitaldefect, which is even

compatible with long life, is asimple one. It comprises a

defect in the interventricularseptum


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EPIDEMIOLOGY

Most common CHD in children (25%)

Isolated VSD found in only 10% of adults

with CHD

75-80% of small VSDs close spontaneously by

late childhood

10-15% of large VSDs close spontaneously

60% of defects close before age 3,

90% close before age 8


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ANATOMY

A VSD is a

developmental

defect of the

interventricular

septum, wherein

communication

between thecavities of the 2

ventricles is

observed.


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TYPES

PERIMEMBRANOUS VSD:(70-80%) located in the leftventricle outflow tract beneath the aortic valve; mostcommon, highest rate of spontaneous closure

MUSCULAR VSD: (5-20%)second most common type of VSD,occurring in 5-20% of most cases. High rates of spontaneousclosure unless multiple

AV-CANAL TYPE VSD: (5-8%) rarely close spontaneously;

commonly seen in Trisomy 21

SUPRACRISTAL VSD:(5-7%) lie beneath the pulmonic valveand communicate with the RV outflow tract; least common.


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PATHOPHYSIOLOGY

Patent communication between systemic and pulmonary

circulations: Left-to-right shunt

Blood flow through the defect results inoxygenated blood entering the pulmonary artery

Increased blood flow to the lungs

Increased pulmonary venous return to the LA,

then subsequently to the LV

Increased LV volume LV dilatation and then

hypertrophy


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PATHOPHYSIOLOGY

Increased pulmonary blood flow

Increased pulmonary capillary

pressure

Increased pulmonary interstitial

fluid: PULMONARY EDEMA


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PATHOPHYSIOLOGY

Blood shunted by VSD away

from aorta

Cardiac output decreases

Compensatory mechanisms

stimulated to maintain adequate

organ perfusion (e.g. catecholamine

release, RAAS)


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LEFT-TO-RIGHT SHUNT


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PATHOPHYSIOLOGY

During systole, blood leaks from left to right, passes

through the lungs, and re-enters the LV via PV and LA:

2 net effects:

Circuitous refluxing of blood causes volume overload

of LV

Because LV normally has higher pressure (120mmHg)

than RV (20mmHg), leakage of blood elevates RV

pressure and volume: PULMONARY HYPERTESNSION

When PAP reaches levels equal to or higher than systemic

pressure, there is reversal of shunt: EISENMENGER

SYNDROME


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EISENMENGER SYNDROME

PAP equal to or higher than the systemic

pressure, there is reversal of shunt from left-to

right, it becomes right-to left

Blood flows from RV to LV causing cyanosis, asthe blood is by-passing the lungs for

oxygenation.

Too late to surgically repair: irreversible damage to

the lung arteries has occurred.


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LEFT-TO-RIGHT SHUNT

Pulmonary Flow (Qp) and Systemic Flow(Qs)ratio is normally equal to 1

The amount of blood that is pumped to the

lungs is equal to the blood that goes to thebody

GRADING

Qp:Qs ratio 2LARGE


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SIGNS AND SYMPTOMS

Initially cyanotic. Presence of shunt reversal eventually

leads to cyanosis.

Pansystolic/Holosystolic murmur along LLSB

+/- palpable thrill

Heart sounds normal

LARGE VSDs: parasternal heave, displaced apex beat

On PE:

Failure to thrive, sweating, tachypnea


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DIAGNOSIS

Cardiac auscultation

Considered as sufficient for detection

Echocardiography

May be used to determine the size and location of

VSD; may also provide semi-quantitative informationabout shunt volume

MRI

Useful adjunct tool, but infrequently required for thediagnosis of VSD

ECG

Ventricular hypertrophy

Chest Radiography


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VSD REPAIR

Repair is in the first two years of life:

asymptomatic adult survival

normal growth and development

Repair in older children:

late post operative increase in LV chamber size

decreased systolic function is seen

Risk of SBE persists and requires prophylaxis


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VSD REPAIR

Development of late postoperative PHTN islargely determined by the age at surgery andpreoperative PVR

Prognosis: degree of pulmonary vascularresistance elevation before the operation

< or = 1/3 of systemic: pulmonary disease progressionunusual


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MANAGEMENT

Medical

Increased caloric density of feedings

Diuretics

ACE Inhibitors

Digoxin


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Transcatheter Closure

Muscular VSDs have been closed with transcatheter

devices for the past 15 years. The Amplatzer membranous VSD occluder (AGA Medical

Corporation; Golden Valley, Minnesota), has undergone

phase I trials in the United States

Current recommendations are to use this device in olderpatients who weigh more than 8 kg and who have a

subaortic rim of more than 2 mm.


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Transcatheter Versus Surgical Closure of

Perimembranous Ventricular Septal

Defects in Children

JOURNAL PRESENTATION


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Clinical Question

Is a transcatheter approach safer and more

efficient than a surgical approach in the closure

of perimembranous ventricular septal defect in

children ages 3-12 years old?


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P: children ages 3-12 years old with perimembranous

ventricular septal defect

I: open heart surgery versus transcatheter closure

O: safe and efficient closure of perimembranous

ventricular septal defect

M: prospective, randomized, controlled clinical trial


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Population

January 2009 - July 2010: 465 children age 3 to 12 years

with pmVSD from 3 major medical centers in northwest

China.

After clinical and transthoracic echocardiographic (TTE)

assessment for eligibility:

236: excluded from the study.

229: randomly allocated to either the surgical or

transcatheter group.


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Methodology

ECG.Performed prior to operation or intervention and at each

follow-up visit.

Catheterization. Each patient underwent catheterizaion

before surgery or transcatheter intervention.

Occluding Device. The Shanghai pmVSD occluder was used.

Transcatheter device implantation.


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Methodology

Surgical Procedure.

Follow-up protocol.All patients were followed up for 2 years.

Each patient underwent serial follow-up at 3 days, 3 months, 6

months, 1 year, and 2 years following intervention or surgery.

Laboratory tests


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Results

Patients

- followed-up until June 2012

- median follow-up of 2 years (2 to 40 months).

29 patients withdrew from the study.

Patients who completed follow-up:

101 patients in the transcatheter group

99 patients in the surgery group

Safety and efficacy are considered in terms of success of theprocedure, complications, cost, hospital stay, and time to

return to normal activities.


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Conclusion

Transcatheter device closure and surgical repair are both

effective treatments.

Transcatheter device closure is more practical with fewer

complications.

Transcatheter device closure is the treatment of choice

for pmVSD.


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Application in Clinical Setting

Preference of transcatheter approach due to

financial considerations.

Less stressful to patients and staff.


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Repetitive Delay in Diagnosisof Ventricular Septal Defect

JOURNAL PRESENTATION


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P: patients with ventricular septal defect

I: color doppler echocardiogram, cardiac

catheterization, angiography

O: diagnosis of ventricular septal defect

M: cross-sectional study

PIOM


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CLINICAL QUESTION

Does early diagnosis of ventricular septal defect

(VSD) using color doppler echocardiogram,

cardiac catheterization, angiography will lead to

better outcome?


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POPULATIONThe study included 145 patients with VSD identified throughclinical findings, color Doppler echocardiogram, cardiac

catheterization, and angiography.

METHODOLOGYThis study was across-sectional study done on 145 patients

with VSD during 54 months in Isfahan. The disease wasidentified through color Doppler echocardiogram, cardiac

catheterization and angiography. The required data were

collected at the time of definite diagnosis.


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RESULTS

Studying 145 cases of VSD indicated that although

the mean age at initial diagnosis was 17months

(16.7713.70), the mean age at definite diagnosis

was 4months(43.5829.06).

Heart murmur led to the initial diagnosis

in123(85%)cases.


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CONCLUSION

Diagnosis of VSD at the age of 44 months is too

late and this might lead to irreparable

complications. It would be appropriate that 88%

and 96% of the patients be diagnosed during thefirst and fourth year of life, respectively.


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Will the results of the study change our approach in the

management of the patient?

ANSWER: YES because early diagnosis will lead to early

management and avoidance of irreparable complications.

ANSWER:We recommend that as early as 17 months,

with clinical findings of VSD, diagnostic exam should be

done for confirmation of the disease. (our setting here in

UST, we can do ECHOCARDIOGRAM

around 2,600pesos)

CLINICAL APPLICATION

Pediatrics Cardioconference Vsd

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