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Abstract
Introduction
Case Report
Discussion
Conclusion
References

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  Table of Contents 
CASE REPORT
Year : 2016  |  Volume : 17  |  Issue : 1  |  Page : 10-13
 

Anesthetic management of lower segment cesarean section with postpartum hemorrhage in two patients with tetralogy of Fallot


Department of Anaesthesia, Krishna Institute of Medical Sciences, Hyderabad, Telangana, India

Date of Submission04-Feb-2016
Date of Acceptance17-Mar-2016
Date of Web Publication17-Jun-2016

Correspondence Address:
Jayashree Patki
Swagat, 2-1-437/5, Street No. 5, Nallakunta, Hyderabad - 500 044, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-0311.183577

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  Abstract 


Pregnant patient with heart disease is a unique challenge to the obstetrician and anesthesiologist, and requires a thorough understanding of the impact of pregnancy on the haemodynamic response in view of existing cardiac lesion. Among the congenital heart diseases causing right to left shunt, Tetralogy of Fallot (TOF) is commonest congenital heart disease. Symptoms of TOF may get worsened during pregnancy and if neglected, it causes significant morbidity and mortality to the patient as well as to fetus. Uncorrecrected TOF parturient posted for LSCS poses an unique challenge to the anesthesiologist. We present 2 case reports of patients of TOF with BT shunt who underwent caesarean section under general anaesthesia. Both the patients had post partum hemorrhage (PPH) which was treated successfully without further complications


Keywords: Blalock-Taussig shunt, congenital heart disease, lower segment cesarean section, postpartum hemorrhage, tetralogy of Fallot


How to cite this article:
Patki J, Reddy N. Anesthetic management of lower segment cesarean section with postpartum hemorrhage in two patients with tetralogy of Fallot. Indian Anaesth Forum 2016;17:10-3

How to cite this URL:
Patki J, Reddy N. Anesthetic management of lower segment cesarean section with postpartum hemorrhage in two patients with tetralogy of Fallot. Indian Anaesth Forum [serial online] 2016 [cited 2023 May 30];17:10-3. Available from: http://www.theiaforum.org/text.asp?2016/17/1/10/183577



  Introduction Top


Among the congenital heart diseases (CHDs) causing right to left shunt, tetralogy of Fallot (TOF) is the most common heart defect and accounts for 5–6% of congenital heart malformations.[1] The anterior and superior infundibular septal displacement results in formation of the tetrad of ventricular septal defect (VSD), aortic override, infundibular obstruction, and right ventricular (RV) hypertrophy.[2] If uncorrected, TOF causes significant morbidity and mortality to the patient and have a poor pregnancy outcome. Symptoms of TOF get worsened during pregnancy which poses a major risk to the mother as well as the baby. Major concern during peripartum period is cardiac decompensation due to inability to meet the additional demands imposed by the physiological changes of pregnancy and parturition. Anesthetic management in such a patient requires clear understanding of anatomical defects, its physiological adaptations, events, and drugs that can alter the magnitude of the shunt.


  Case Report Top


We are reporting two cases of pregnancy with TOF who presented within a span of 1 month for lower segment cesarean section (LSCS) in our hospital. Incidentally, both the patients had postpartum hemorrhage (PPH) which was treated successfully.

Both of these patients were primigravidae with the age of 24–22 years, respectively carrying 36 weeks of pregnancy. One was admitted for elective LSCS and the other one for emergency LSCS.

They had history of cyanotic heart disease and were diagnosed as having TOF and underwent Blalock-Taussig shunt (BT shunt) during childhood. There was history of breathlessness on mild exertion, otherwise well-adjusted to normal course of life. They presented regularly for antenatal checkups and were advised bed rest and medications. On examination, both the patients had almost similar findings. They had cyanosis, peripheral, as well as central, and clubbing of fingers. Cardiovascular system revealed a pansystolic murmur of Grade 3 in the pulmonary as well as aortic areas, radiating all over the precordium. Rest of the examination was unremarkable. Their blood investigations were in normal range except hemoglobin values of 18 and 16 g%. SpO2 was 86–88% on room air. Electrocardiographies (ECGs) showed sinus tachycardia and RV hypertrophy. Two-dimensional echo showed post-BT shunt status with good functioning, high RV outflow obstruction gradient, large VSD with good left ventricular-RV function. On preanesthetic examination, they were found to be dyspneic with sigma of central cyanosis.

General anesthesia was planned for both of them. Informed high-risk consents were obtained and nil by mouth status was confirmed before surgery. They received aspiration prophylaxis and prophylactic antibiotics in the preoperative room. The patients were preloaded with 500 ml Ringer lactate. Patients were wheeled in the operating room and baseline monitors were attached Injection phenylephrine and metoprolol were kept ready for emergency. Under strict asepsis, right internal jugular vein was cannulated under local anesthesia. After preoxygenation, patients were induced with Inj. glycopyrolate 0.2 mg iv was given and they were induced with inj Ketamine 1-2mg/kg endotracheal intubation was performed under succinylcholine. Anesthesia was maintained with O2, N2O with vecuronium. ECG, noninvasive blood pressure, pulse oximetry, central venous pressure, and EtCO2 were monitored intraoperatively. Low birth weight babies were delivered with adequate APGAR scores. Injection fentanyl 2 microgram/kg and injection midazolam 2 mg were administered along with injection oxytocin 10 U IV infusion after delivery of the babies. Both the patients had atonic PPH. The first patient had a severe PPH with blood loss of more than 1.5 L within 30 min immediately after shifting to recovery room. The second patient had PPH intraoperatively which was controlled immediately. PPH was treated with uterine massage, extra doses of injection oxytocin infusion, with adequate quantities of blood, blood products, and IV fluids. At the end of surgery, neuromuscular blockade was reversed with IV neostigmine 0.05mg/kg and glycopyrolate 0.01 mg/kg and the trachea was extubated. Patients were shifted to surgical intensive care unit. IV paracetamol 1 g was administered for postoperative analgesia. As one patient was not maintaining O2 saturation in spite of O2 supplementation, labetalol infusion was given for a day. Their subsequent course in hospital was uneventful.


  Discussion Top


CHD is one of the most common inborn defects, occurring in approximately 0.8% of newborn infants.[3] Among the CHDs causing right to left shunt, TOF is most common. It accounts for 5–6% of cases of CHD. The dramatic success in pediatric cardiac surgery has created an ever-increasing population of young adults with grown-up CHD. The greatest example of this is the long-term survival of a patient who has undergone surgical treatment of TOF. The most widely performed palliative procedure for TOF is BT shunt or its modification in which the subclavian artery is connected to the pulmonary artery.

With uncorrected TOF, pregnancy presents serious risks including maternal mortality. In pregnant patients with TOF, the decrease in peripheral resistance that accompanies pregnancy augments right to left shunt and may exaggerate maternal cyanosis, which poses risks for both mother and fetus.[4] Preexisting pulmonary hypertension and elevated cardiac output leading to increased venous return to hypertrophic right ventricle result in further increase in the right to left shunt. However, the risk to the fetus is largely proportional to the degree of maternal hypoxia. Presbitero et al. demonstrated that the most important risk factor for adverse fetal outcome in cyanotic patients was the degree of cyanosis. These authors suggested that an arterial oxygen saturation (SaO2) >85% and a hemoglobin concentration <18 g/dl were more likely to result in live birth, whereas hemoglobin concentrations >20 g/dl were associated with adverse fetal outcome.[5]

In addition to right to left shunt, the problems in such patients are due to chronic hypoxia, polycythemia and coagulopathy, CHF, embolism, episodic and reactive pulmonary vasoconstriction, and altered acid-base status.[6]

Anesthetic management of pregnant patients with TOF requires thorough understanding of anatomical defects and its physiological adaptations and perioperative factors that can alter the magnitude of right-to-left shunt.[7] Conventional anesthetic management can be appropriate for patients having good outcome from cardiac surgery with no evidence of late deterioration. Women who had undergone repair and in whom cyanosis did not reappear do well in pregnancy.[8]

Major goals of anesthesia in TOF are to maintain intravascular volume and systemic vascular resistance, minimize pulmonary vascular resistance, and provide mild myocardial depression. Most of the patients have a dynamic RV outflow obstruction which may be worsened by sympathetic stimulation during anesthesia.[9] The main goals of managing these patients are:

  • To maintain normal intravascular volume to avoid hypovolemia and hypotension and to avoid decrease in systemic vascular resistance
  • Which leads to worsening of right to left shunt
  • Epidural analgesia early in labor
  • To improve arterial blood SaO2 and to maintain cardiovascular stability.[10]


Various reports have mentioned that no specific technique is suggested for such patients and both general and regional techniques have been employed successfully in parturient with TOF. We preferred general anesthetic with endotracheal intubation as it provides airway protection, eliminates work of breathing, and assures good oxygenation. However, systemic vasodilatation may occur during general anesthesia and exacerbate the shunting and intensify the resultant hypoxia. Hence, dehydration should be avoided in these patients. Preloading should be done to improve the circulating volume and decrease the blood viscosity as acute hypovolemia tends to increase right to left intracardiac shunt. Preloading also helps in preventing cyanotic spells which are treated with volume and phenylephrine (5 μg/kg).

Both, IV and inhalational drugs have been used successfully for induction. Of note, the right to left shunt tends to slow the rate of rise of inhalational agents. The patients need a higher dial concentration which might result in myocardial depression. Conversely, the right to left shunt may speed the onset of IV agents. Ketamine has been found to be the excellent induction agent as it increases the systemic vascular resistance [11] and does not increase the right to left shunting. Adding N2O along with O2 can be beneficial while keeping a watch on O2 saturation. Although N2O increases pulmonary vascular resistance, this potentially adverse effect is more than offset by its beneficial effects on systemic vascular resistance (no change or modest increase) in comparison with other inhalation agents.

Bolus IV dose of oxytocin should not be administered as that would affect peripheral vascular resistance; however, IV infusion of 10–15 U of oxytocin in 500 ml of Ringer lactate can be administered over a period. However, methergine is more preferred than oxytocin in these patients.

Regional anesthesia with careful titration of agents and attention to hemodynamic stability is acceptable.[12] A gradual epidural anesthesia rather than a single prick spinal is more preferable as it will prevent acute fall in SVR precipitating right to left shunt.

The need for invasive monitoring depends upon the nature of the surgery. Previous BT shunt placement requires arterial pressure monitoring on the contralateral side. Central venous canulae pose a significant thromboembolic risk and yet the information they provide may be extremely valuable. Capnography significantly under-reads PaCO2 in the presence of right-to-left shunting, and the degree of discrepancy will change as the extent of shunting changes.[13]

CHD is an important risk factor for the development of infective endocarditis, being responsible for 9% of all cases recently reported in Japan.[14] Both the American Heart Association and the European Society of Cardiology clearly recommend that for patients at high and moderate risk, antibiotic prophylaxis should be used when performing procedures associated with a risk of bacteremia.

The majority of patients who have undergone repair of TOF are asymptomatic. Approximately 10% of patients may require late re-intervention. Most problems encountered during late follow-up relate to abnormalities of RV physiology and include exercise intolerance, ventricular arrhythmias, and sudden death secondary to chronic pulmonary regurgitation. With the introduction of “Arogya Sri” health scheme in the State of Andhra Pradesh and Telangana wherein the expenditure for surgeries of congenital cardiac lesions is being financed by government scheme, after a decade, we would notice more number of surgically corrected CHD cases.


  Conclusion Top


A patient with uncorrected TOF coming for LSCS is a great challenge to an anesthetist. They need to be managed at tertiary care hospital for safe surgical delivery. Meticulous multidisciplinary care by a team of experts including anesthesiologist, intensivist, obstetrician, and cardiologist will be considered for core management of such particular patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Hoffman JI. Incidence of congenital heart disease: I. Postnatal incidence. Pediatr Cardiol 1995;16:103-13.  Back to cited text no. 1
    
2.
Anderson RH, Allwork SP, Ho SY, Lenox CC, Zuberbuhler JR. Surgical anatomy of tetralogy of Fallot. J Thorac Cardiovasc Surg 1981;81:887-96.  Back to cited text no. 2
[PUBMED]    
3.
Perloff JK, Warnes CA. Challenges posed by adults with repaired congenital heart disease. Circulation 2001;103:2637-43.  Back to cited text no. 3
    
4.
Mann DL, Zipes DP, Libby P, Bonow RO. Braunwald's Heart Disease. A Textbook of Cardiovascular Medicine. 8th ed.. Philadelphia, PA: Saunders Publishers; 2007. p. 1971.  Back to cited text no. 4
    
5.
Presbitero P, Somerville J, Stone S, Aruta E, Spiegelhalter D, Rabajoli F. Pregnancy in cyanotic congenital heart disease. Outcome of mother and fetus. Circulation 1994;89:2673-6.  Back to cited text no. 5
    
6.
Srivastava A, Chaturvedi A, Sinha G. Pregnancy with uncorrected tetralogy of fallot: Anaesthetic management of a case for LSCS. Internet J Anesthesiol 2008;21(1). Available from: http://ispub.com/IJA/21/1/8333. [Last accessed on 2016 Mar 15].  Back to cited text no. 6
    
7.
Robert KS. Congenital heart disease. In: Stoelting RK, Dierdorf SF, editors. Anesthesia and Co-existing Disease. 3rd ed. Churchill Livingstone; 1993. p. 42-5.  Back to cited text no. 7
    
8.
Cunningham FG. Cardiovascular disease. In: Cunningham FG, editor. Williams Obstetrics. 22nd ed. McGraw Hill Publishers; 2005. p. 1028.  Back to cited text no. 8
    
9.
Lovell AT. Anaesthetic implications of grown-up congenital heart disease. Oxford Journals, BJA 2004;93 (1): 129-39.  Back to cited text no. 9
    
10.
Laishley RS, Burrows FA, Lerman J, Roy WL. Effect of anesthetic induction regimens on oxygen saturation in cyanotic congenital heart disease. Anesthesiology 1986;65:673-7.  Back to cited text no. 10
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11.
Naqash I, Ahad B, Zargar J, Kirmani A, Wani A. Anaesthetic management of a case of tetrology of fallot for drainage of brain abscess: A Case Report. The Internet Journal of Anesthesiology 2002:7(1). Available from: http://ispub.com/IJA/7/1/7487. [Last accessed on 2016 Mar 15].  Back to cited text no. 11
    
12.
Solanki SL, Jain A, Singh A, Sharma A. Low-dose sequential combined-spinal epidural anesthesia for Cesarean section in patient with uncorrected tetrology of Fallot. Saudi J Anaesth 2011;5(3):320-2.  Back to cited text no. 12
    
13.
Lovell AT. Anaesthetic implications of grown-up congenital heart disease. Br J Anaesth 2004;93:129-39.  Back to cited text no. 13
    
14.
Nakatani S, Mitsutake K, Hozumi T, Yoshikawa J, Akiyama M, Yoshida K, et al. Current characteristics of infective endocarditis in Japan: An analysis of 848 cases in 2000 and 2001. Circ J 2003;67:901-5.  Back to cited text no. 14
    




 

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