Surgical outcome of congenital heart defects with pulmonary hypertension in infants

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Акилов, Х., Хамраева , Г., Саитазизов, Х., & Чориев, Х. (2024). Surgical outcome of congenital heart defects with pulmonary hypertension in infants. in Library, 3(3), 8–13. извлечено от https://inlibrary.uz/index.php/archive/article/view/36902
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Аннотация

Background: Congenital heart diseases with large left-to-right shunt often have signs of pulmonary artery hypertension. It is an important determinant of morbidity and mortality in patients without educate surgical treatment especially in infants. Methods: Ninety patients with congenital cardiac septal defects and pulmonary arterial hypertension had operation to close their septal defects. All the patients have been checked by Chest X-ray, EchoCG, ECG, selectively performed the cardiac catheterization and lung biopsy. Before and after surgery the PA pressure was compared to systemic by needle puncture measurement. Results: Twenty patients died in the hospital after operation and there were no later deaths in follow-up. Hemodynamic changes after operation included a significant decrease in pulmonary artery pressure (mean pulmonary artery pressure, 28.3± 2.4 mm Hg versus 58.45± 1.69 mm Hg before repair). The follow-up period was from 3 months to 4 years (mean 1.3 +0.6 years). Conclusion: Studies from developed countries have shown that in term infants, young age is not a risk factor for adverse postoperative outcome after surgical closure of septal left-to-right defects. The data presented in this study shows that operations to close cardiac septal defects in the presence of severe pulmonary hypertension are effective, but must be done during first 6 month.


background image

International Journal of Education, Social Science & Humanities.
Finland Academic Research Science Publishers

ISSN: 2945-4492 (online) | (SJIF) = 7.502 Impact factor

Volume-11| Issue-7| 2023

Published:

|22-07-2023|

8

Publishing centre of Finland

SURGICAL OUTCOME OF CONGENITAL HEART DEFECTS WITH PULMONARY

HYPERTENSION IN INFANTS

https://doi.org/10.5281/zenodo.8133405

Kh.A.Akilov

G.Sh.Khamraeva

Center for the development of professional qualification of medical workers;

Kh.B.Saitazizov

Kh.T.Choriev

IHLOS Doctor MT” medical center


Background:

Congenital heart diseases with large left-to-right shunt often have signs

of pulmonary artery hypertension. It is an important determinant of morbidity and
mortality in patients without educate surgical treatment especially in infants.

Methods: N

inety patients with congenital cardiac septal defects and pulmonary

arterial hypertension had operation to close their septal defects. All the patients have been
checked by Chest X-ray, EchoCG, ECG, selectively performed the cardiac catheterization
and lung biopsy. Before and after surgery the PA pressure was compared to systemic by
needle puncture measurement.

Results:

Twenty patients died in the hospital after operation and there were no later

deaths in follow-up. Hemodynamic changes after operation included a significant decrease
in pulmonary artery pressure (mean pulmonary artery pressure, 28.3

2.4 mm Hg versus

58.45

1.69 mm Hg before repair). The follow-up period was from 3 months to 4 years

(mean 1.3

0.6 years).

Conclusion:

Studies from developed countries have shown that in term infants,

young age is not a risk factor for adverse postoperative outcome after surgical closure of
septal left-to-right defects. The data presented in this study shows that operations to close
cardiac septal defects in the presence of severe pulmonary hypertension are effective, but
must be done during first 6 month.

Key words

bypass, pulmonary hypertension, infants

Congenital heart defects (CHD) with left-to-right shunt carry high mortality in

infancy due to development of pulmonary arterial hypertension. The natural
mortality during the first year of life is about 8-11%. There are some reasons of high
mortality: development of pulmonary arterial hypertension with congestive right
heart failure, pulmonary hypertensive crisis, difficult for curing pneumonia,


background image

International Journal of Education, Social Science & Humanities.
Finland Academic Research Science Publishers

ISSN: 2945-4492 (online) | (SJIF) = 7.502 Impact factor

Volume-11| Issue-7| 2023

Published:

|22-07-2023|

9

Publishing centre of Finland

hypotrophy and septic conditions. In 30- 50% of this condition complicated with
severe pulmonary arterial hypertension, which has a progressive character [1].
Pulmonary artery pressure is hyperkinetic in early phase but may eventually
become a fixed elevation associated with fixed increase of pulmonary vascular
resistance [2].

CHD with pulmonary hypertension requires urgent surgical treatment, which

is caused by development of irreversible changes of in-lungs and critical condition
of patients [3, 4]. This need requires surgical intervention in the first year of life.

During the past years many world leading hospitals have been excellently

performing surgical interventions in infants. This report documents the experience
and results of septal defects repair in a group of patients with pulmonary
hypertension in infancy.

Material

90 patients with congenital cardiac defects and pulmonary hypertension had

been operated in three institutions during the period from January 2, 2000, to May,
2008. There were 69 patients with isolated ventricular septal defects, 2 patients
with ventricular septal defects with interrupted aortic arch, 2 cases of ventricular
septal defect with coarctation of aorta, 4 patients with complete endocardial
cushion defects, 5 patients with total anomalous pulmonary venous return, 3
patients with double outlet of right ventricle, 2 patients with truncus arteriosus and
1 patient with transposition of great arteries. The age ranged from 4 days to 36
months (average, 12.29 ± 1.63 months). All the patients had complains on often
colds, lack of physical growing, strengthless, heart beating. All patients had
hypotrophy about 30%. A systolic murmur was audible in 28 patients. The murmur
was only of grade I in 8 patients and it was absent in 6 patients. The second heart
sound was increased at the left base in all the patients.

Methods

All the patients had been examined on ECG, Chest X-ray, Echocardiography.

Some patients were selectively chosen for cardiac catheterization before surgery
and lung biopsy during surgery. Anesthesia was induced by fentanyl and
intermittent positive pressure ventilation with isoflurane. Ketamine was used for
premedication. Pressure in pulmonary artery was measured by needle puncture
before repair of the septal defect and at completion of operation before closure of
the wound. Systemic blood pressure and central venous pressure were monitored
in the radial artery and femoral vein. We used hollow fiber oxygenators, the bypass
performed on continuous and intermittent flow, with conventional and modified


background image

International Journal of Education, Social Science & Humanities.
Finland Academic Research Science Publishers

ISSN: 2945-4492 (online) | (SJIF) = 7.502 Impact factor

Volume-11| Issue-7| 2023

Published:

|22-07-2023|

10

Publishing centre of Finland

ultrafiltration for all the patients. For myocardial protection we used cristalloid
cardioplegia (Stanford University formula) for the first time 20ml/kg and for
additional infusions blood cardioplegia.

Results

During the preoperative examination we found that:
The electrocardiogram showed mostly right axis deviation. There were right

ventricular hypertrophy in 35 patients and 7 showed biventricular hypertrophy.
Chest roentgenogram showed dilation of main pulmonary artery in all the patients.
The mean cardiothoracic ratio number is 0.64

0.10. The pressure gradient through

the intracardiac or extracardiac defect was present in all the patients by
echocardiography and ranged from 45 to 5 mmHg (mean, 18

8 mmHg ). Cardiac

catheterization was performed in 4 patients. We found that 3 patients had
bidirectional shunt, and 1 patient with left to right shunt. The pulmonary artery
pressure was relatively close to systemic arterial pressure. The angiography shows
the same picture as on echo. Biopsy of the lung was performed in 10 consecutive
patients. Pulmonary vascular disease was graded by Heath - Edwards’
classification [4]. There were 4 patients in grade III, and 6 had grade IV pulmonary
vascular disease. The results of biopsy were different than the results of echo and
tensiometry. This means that the lung biopsy could present the real PH picture in
infants. Pulmonary artery pressure to systemic pressure value before surgery was
85± 1.87% and 50.73± 2.11% after correction by intraoperative tensiometry. The
defect was repaired via right atrium in most cases, but in 5 cases through right
ventricle incision. We used Dacron, Teflon, Double Velour, Gore-Tex and
glutaldehide treated pericardial patches. For the suture technique in most cases we
used continuous suture, less interrupted sutures and in some cases combine
method. We didn’t find any differences and complication of two bypass techniques.
The mean bypass time was 94.67 ±3.63 minutes and cardiac arrest time was 60.68
±2.87 minutes. All the patients were checked intraoperative by TEE after correction
for the prevention of air embolization and for checking of correction and cardiac
performance after bypass weaning. The early postoperative period was
complicated, because the most of the patients required urgent surgery or indicated
for surgery by vital signs. After the surgery all the patients transferred to HICU and
managed postoperatively. All the patients received dopamine, epinephrine,
dobutamine, milrinone in sub- or maximal therapeutic dosage, in all cases partial
parenteral nutritions were infused on the second postoperative day. The dynamics
of pulmonary hypertension was estimated with echocardiography by the tricuspid
and pulmonary regurgitation method before and during follow-up after operation.


background image

International Journal of Education, Social Science & Humanities.
Finland Academic Research Science Publishers

ISSN: 2945-4492 (online) | (SJIF) = 7.502 Impact factor

Volume-11| Issue-7| 2023

Published:

|22-07-2023|

11

Publishing centre of Finland

Sedation and oxygen supplement were considered to be important to these patients
in postoperative care. The patients had been ventilated for 109

8.68 hours and

extubated after complete recovering of vital signs. The inotrops has been infused
during 145.66± 8.14 hours and stopped after complete cardiac performance
improving. The average postoperative stay in HICU was 12.04± 2.39days. The
patients transferred to the general ward for continuous follow up of PH regress and
improving patients’ condition. The mean in hospital stay after operation was 16.25±
2.20 days.

Twenty patients died in the hospital after operation. The most common reason

of mortality was heart failure, residual PH, respiratory failure. None of survived
patients required reoperation. 6 patients were under the 6 months and other in age
more than 1 year.

The follow-up period was from 3 months to 4 years (mean 1.3

0.6 years).

Symptoms of dyspnea on exertion were relieved, and physical growing improved.
Hemodynamic changes after operation included a significant decrease in
pulmonary artery pressure (mean pulmonary artery pressure, 28

2.4 mm Hg

versus 58.45

1.69 mm Hg before repair)

.

Arterial oxygen saturation increased

significantly after operation (mean, 98%

1% versus 90

4% before operation). The

follow-up echocardiography showed the residual shunt in 6 patients which doesn’t
significantly changes hemodynamic and need reoperation.

Comments

The surgical treatment of congenital heart defects with pulmonary

hypertension is controversial. Perioperative mortality to close septal defects is high
(22.7% to 50%) [5-8]. Acute congestive heart failure, residual pulmonary
hypertensive crisis, acute respiratory failure are the principal causes of
perioperative deaths. Many authors reported that operations to close septal defects
were carried out cautiously when the ratio of pulmonary to system flow was less
than 1.5, and the arterial oxygen saturation is near to or less than 90% [2,9,10].

Pulmonary arterial pressure usually falls down in the first 3 months of age. If

the congenital heart defect with left-to-right shunt present the pulmonary
hypertension could progressively increase. Pulmonary artery pressure and
pulmonary vascular resistance has always significantly elevated in patients with
Eisenmenger's syndrome. Operations to correct congenital cardiac defects require
the use of cardiopulmonary bypass, infusion of protamine, and other factors that
could cause release of vasoactive substances such as thromboxane A2 and
catecholamines, resulting in pulmonary vasoconstriction and acute pulmonary


background image

International Journal of Education, Social Science & Humanities.
Finland Academic Research Science Publishers

ISSN: 2945-4492 (online) | (SJIF) = 7.502 Impact factor

Volume-11| Issue-7| 2023

Published:

|22-07-2023|

12

Publishing centre of Finland

hypertension [11-14]. Pulmonary hypertensive crisis can be associated with acute
congestive heart failure and death after operation in some of these patients.

The data presented in this study show that operations to close cardiac septal

defects in the presence of severe pulmonary hypertension are effective. Even if our
22.2 % overall mortality rate is much higher than the rates reported recently from
the leading centers (0% to 5%) [13, 16]. In our point of view the surgical treatment
of this category of patients must be done before 6 months, but it depends on the
level of cardiology service developing.

Studies from developed countries [13,16]

have shown that in term infants,

young age is not a risk factor for adverse postoperative outcome after surgical
closure of septal left-to-right defects. Also in this study, patients did not have
significant impacts on mortality rates. However, younger patients had longer
postoperative recovery periods (duration of mechanical ventilation, ICU stay, and
hospital stay). Their slower recovery may have resulted, in part, from longer
durations of CPB.

REFERENCES:


1.

S.V. Gorbachevskiy- Pulmonary Hypertension in Ventricular Septal Defect.:

J. Grudnya Hirurgiya. Moskow, 1990.

2.

Arciniegas E. Ventricular septal defect. In: Glen WWL, ed. Thoracic and

cardiovascular surgery. East Norwalk: Appleton-Century-Crofts, 1983:745-56.

3.

V.I. Burakovskiy, L.A.Bokeriya- Serdechno- Sosudistaya Hirurgiya. Moskow

“Medicine”, 1989.

4.

Heath D, Edwards JE. The pathology of hypertensive pulmonary vascular

disease: a description of six grades of structural changes in the pulmonary artery
with special reference to congenital cardiac septal defects. Circulation 1958;18:533-
47.

5.

Hallman GL, Cooley DA, Wolfe RR, McNamara DG. Surgical treatment of

ventricular septal defect associated with pulmonary hypertension. J Thorac
Cardiovasc Surg 1964; 48:588-600.

6.

Cartmail TB, Dushane JW, McGoon DC, Kirklin JW. Results of repair of

ventricular septal defect. J Thorac Cardiovasc Surg 1966;52:486-9.

7.

Friedli BG, Kidd BSL, Mustard WT, Keith JD. Ventricular septal defect

with increased pulmonary vascular resistance. Am J Cardiol 1974;33:403-9.

8.

John S, Korula R, Jairaj PS, Muralidharan S, et al. Results of surgical

treatment of ventricular septal defect with pulmonary hypertension. Thorax


background image

International Journal of Education, Social Science & Humanities.
Finland Academic Research Science Publishers

ISSN: 2945-4492 (online) | (SJIF) = 7.502 Impact factor

Volume-11| Issue-7| 2023

Published:

|22-07-2023|

13

Publishing centre of Finland

1983;38:279-83.

9.

Kirklin JW, Barratt-Boyes BG. Cardiac surgery. New York: John Wiley &

Sons, 1986:599.

10.

Guo JQ, Xue GX, Zhu XD, et al. Surgical treatment of congenital

ventricular septal defect: a 21 years experience in 1187 patients. Chin Med J
1983;96:323-9.

11.

De Souza CA, Spyt TJ. Release of vasoactive substance during

cardiopulmonary bypass. Ann Thorac Surg 1992;56: 397-8.

12.

Komai H, Yamamoto F, Tanaka K, et al. Increased lung injury in

pulmonary hypertensive patients during open heart operations. Ann Thorac Surg
1993;55:1147-52.

13.

Nuttall GA, Murray MJ, Bowie EJW. Protamine-heparininduced

pulmonary hypertension in pigs: effects of treatment with a thromboxane receptor
antagonist on hemodynamics and coagulation. Anesthesiology 1991;74:138-45.

14.

Montalescot G, Lowenstein E, Ogletree ML, et al. Thromboxane

receptor blockade prevents pulmonary hypertension induced by heparin-
protamine reactions in awake sheep. Circulation 1990;82:1765-77.

15.

Steele PM, Ruster V, Cohen M, Ritter DG, McGoon DC. Isolated atrial

septal defect with pulmonary vascular obstructive disease: long-term follow-up
and prediction of outcome after surgical correction. Circulation 1987;76: 1037-42.

16.

Kirkling/Barrat-Boyes. Cardiac Surgery, third edition, Volume II, 2003.

Библиографические ссылки

l.S.V. Gorbachevskiy- Pulmonary Hypertension in Ventricular Septal Defect.: J. Grudnya Hirurgiya. Moskow, 1990.

Arciniegas E. Ventricular septal defect. In: Glen WWL, ed. Thoracic and cardiovascular surgery. East Norwalk: Appleton-Century-Crofts, 1983:745-56.

V.I. Burakovskiy, L.A.Bokeriya- Serdechno- Sosudistaya Hirurgiya. Moskow "Medicine", 1989.

Heath D, Edwards JE. The pathology of hypertensive pulmonary vascular disease: a description of six grades of structural changes in the pulmonary artery with special reference to congenital cardiac septal defects. Circulation 1958;18:533-47.

Hallman GL, Cooley DA, Wolfe RR, McNamara DG. Surgical treatment of ventricular septal defect associated with pulmonary hypertension. J Thorac Cardiovasc Surg 1964; 48:588-600.

Cartmail ТВ, Dushane JW, McGoon DC, Kirklin JW. Results of repair of ventricular septal defect. J Thorac Cardiovasc Surg 1966;52:486-9.

Friedli BG, Kidd BSL, Mustard WT, Keith JD. Ventricular septal defect with increased pulmonary vascular resistance. Am J Cardiol 1974;33:403-9.

John S, Korula R, Jairaj PS, Muralidharan S, et al. Results of surgical treatment of ventricular septal defect with pulmonary hypertension. Thorax 1983;38:279-83.

Kirklin JW, Barratt-Boyes BG. Cardiac surgery. New York: John Wiley & Sons, 1986:599.

Guo JQ, Xue GX, Zhu XD, et al. Surgical treatment of congenital ventricular septal defect: a 21 years experience in 1187 patients. Chin Med J 1983;96:323-9.

De Souza CA, Spyt TJ. Release of vasoactive substance during cardiopulmonary bypass. Ann Thorac Surg 1992;56: 397-8.

Komai H, Yamamoto F, Tanaka K, et al. Increased lung injury in pulmonary hypertensive patients during open heart operations. Ann Thorac Surg 1993;55:1147-52.

Nuttall GA, Murray MJ, Bowie EJW. Protamine-heparininduced pulmonary hypertension in pigs: effects of treatment with a thromboxane receptor antagonist on hemodynamics and coagulation. Anesthesiology 1991;74:138-45.

Montalescot G, Lowenstein E, Ogletree ML, et al. Thromboxane receptor blockade prevents pulmonary hypertension induced by heparinprotamine reactions in awake sheep. Circulation 1990;82:1765-77.

Steele PM, Ruster V, Cohen M, Ritter DG, McGoon DC. Isolated atrial septal defect with pulmonary vascular obstructive disease: long-term follow-up and prediction of outcome after surgical correction. Circulation 1987;76:1037-42.

Kirkling/Barrat-Boyes. Cardiac Surgery, third edition, Volume II, 2003.

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