|Year : 2014 | Volume
| Issue : 4 | Page : 557-560
Anesthesia in an adult patient with patent ductus arteriosus
Hemlata Kapoor, Mohan K Terdal, Meenal Zamre
Department of Anaesthesiology, Kokilaben Dhirubhai Ambani Hospital and Medical Research Institute, Andheri (west), Mumbai, India
|Date of Submission||28-Jan-2014|
|Date of Acceptance||05-Aug-2014|
|Date of Web Publication||28-Nov-2014|
Department of Anaesthesiology, Kokilaben Dhirubhai Ambani Hospital and Medical Research Institute, Four Bungalows, Andheri (west), Mumbai 53
Source of Support: None, Conflict of Interest: None
The survival rate of neonates with congenital heart disease has increased manifold due to advancement in both surgical and medical management. A small percentage of adults present with unrepaired or inadequately repaired congenital cardiac defects. They pose a challenge on the operation table due to altered hemodynamics. A comprehensive understanding of the congenital defect and an apt plan of anesthesia are essential for successfully managing such patients.
Keywords: adult congenital heart disease, anesthesia, patent ductus arteriosus
|How to cite this article:|
Kapoor H, Terdal MK, Zamre M. Anesthesia in an adult patient with patent ductus arteriosus. Ain-Shams J Anaesthesiol 2014;7:557-60
|How to cite this URL:|
Kapoor H, Terdal MK, Zamre M. Anesthesia in an adult patient with patent ductus arteriosus. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2021 May 6];7:557-60. Available from: http://www.asja.eg.net/text.asp?2014/7/4/557/145727
| Introduction|| |
The incidence of congenital heart disease (CHD) has been reported to be six per thousand live births . With advancement in pediatric cardiac surgery and other modalities of medical management, the percentage of infants reaching adulthood has jumped from 20% to more than 85% . This set of population is referred to as grown-up congenital heart disease patients . The group includes small percentage of unoperated patients who either have trivial malformation or rarely a naturally compensated complex cardiac lesion. The blood flow through the cardiac defect depends on the difference in the pressure on either side of the defect. Usually, the pressure is higher on the left side of the heart and the blood flows to the right side. The left-to-right shunt sends oxygenated blood to the pulmonary circulation. As deoxygenated blood does not enter systemic circulation, there is no cyanosis. This occasionally causes delay in medical management of these patients.
Majority of the grown-up congenital heart disease patients have undergone some form of surgical intervention. Nevertheless, the basic anomaly, comorbidities, surgical outcome, residual defect, and operative complications are of prime importance in these patients. Some of the issues pertaining specifically to these patients are arrhythmias, heart failure, bacterial endocarditis, cyanosis, polycythemia, malfunctioning of intracardiac devices, and alteration in pulmonary vascular status. A regular follow-up is of help when considering these patients for any concomitant surgery later in life.
We describe a patient with patent ductus arteriosus (PDA) who had to be administered anesthesia twice under different circumstances. Regional anesthesia was found to be suitable for the first surgery; however, the second time only general anesthesia could be administered.
| Case history|| |
A 69-year-old man was admitted for transurethral resection of the prostate. He was a known diabetic for the last 12 years and was well controlled with oral hypoglycemic agents. He was diagnosed to have PDA - an acyanotic CHD at birth; however, no surgical correction was carried out. At the age of 54 years, the patient was admitted for giddiness, palpitation, and sweating. The two-dimensional (2D) echocardiogram before correction showed a large PDA with continuous left-to-right shunt. The pulmonary artery pressure was found to be mildly elevated. The arch aortogram showed the ductal length to be 1 cm with a diameter of 4-5 mm. The coronary angiogram showed single vessel coronary disease and a PDA. He underwent PDA ligation but had incomplete closure with residual left-to-right shunt. However, his symptoms of recurrent productive cough were resolved after the surgery.
All hematological parameters were reported to be within normal limits. Chest Radiograph showed prominent bronchovascular markings and cardiomegaly. The ECG showed left ventricular hypertrophy and left anterior fascicular block with elevated ST segment in chest leads V2, V3, and V4. The 2D echocardiogram reported ejection fraction to be 50%, no regional wall motion abnormality, mild mitral regurgitation, and a small PDA showing left to right flow. A continuous Doppler showed a 98 mmHg gradient across the PDA. The pulmonary artery pressure was noted to be 30 mmHg. The blood pressure was 140/80 mmHg, heart rate was 76 beats/min, and the SpO 2 was 100%. A pan systolic murmur was present on auscultation. A cardiologist's opinion was sought before taking up the patient for surgery. Intravenous fluids were initiated preoperatively to keep the patient well hydrated. In the operation theater, ECG (lead II and V5), noninvasive blood pressure, and SpO 2 were monitored. The patient was given subarachnoid block in the left lateral position at the intervertebral space between lumbar three and lumbar four vertebrae with 2.8 ml of 0.5% heavy bupivacaine. The level of block was achieved up to the eighth thoracic dermatome. Intraoperatively, there was no incidence of hypotension, and blood pressure remained stable at around 130/70 mmHg and the heart rate around 68 beats/min. Infective endocarditis prophylaxis was carried out as per the protocol set by the hospital infection control committee. The surgery got over in 45 min and no immediate complications were noted. Intravenous paracetamol was given for postoperative pain relief, and the patient was shifted to the ICU for postoperative monitoring and management.
Almost a week after the surgery, the patient had repeated episodes of breathlessness on exertion and orthopnea. His heart rate was 142 beats/min, blood pressure was 162/100 mm of Hg, and respiratory rate was 48/min. He was diagnosed to have urosepsis leading to cardiogenic shock and pulmonary edema. The patient was intubated. On auscultation, crepts were found on both sides of the chest and blood investigations revealed a raised troponin I. A 2D echocardiogram showed an ejection fraction of 30% with anteroseptal wall hypokinesia. An angiogram revealed a stenosis in proximal left anterior descending coronary artery and in right coronary artery. PDA was found to be patent. PTCA was performed to right coronary artery and left anterior descending. The patient was initiated on ecosprin, clopidogrel, furosemide, digoxin in addition to his other medications and was eventually discharged.
Two months after the surgery, patient was admitted for incision and drainage and bilateral orchiectomy for severe scrotal infection. Regional anesthesia was ruled out because of the antiplatelets and sepsis. The effort tolerance was found to be reduced. On auscultation, there were no crepts; however, the murmur could be auscultated. The 2D echocardiogram showed increase in left atrial and ventricular size, regional wall motion abnormalities, and an ejection fraction of 40-45%. The PDA showed left to right flow, and there was no significant pulmonary hypertension.
General anesthesia was planned for the patient. Right radial artery was cannulated for continuous blood pressure monitoring. In addition, ECG, SpO 2 , and EtCO 2 were monitored. Anesthesia was induced with fentanyl and sevoflurane. A size 4 proseal LMA was inserted and anesthesia was maintained with a mixture of oxygen, air, and sevoflurane. Muscle relaxation was attained with boluses of atracurium. The blood pressure before induction was 130/50 mmHg and during the surgery ranged between 110/50 and 98/47 mmHg. The pulse rate varied between 62 and 68 beats/min. The surgery was uneventful and the patient was extubated after reversing muscle relaxation with neostigmine and glycopyrrolate. Intravenous paracetamol was given before extubation and further pain management was carried out in the ICU where the patient was shifted for postoperative management.
| Discussion|| |
PDA comprises ~5-10 % of CHD . PDA was first described by Galen and is due to failure of closure of the duct between aorta and pulmonary artery. The first successful surgical repair was carried out by Gross . PDA is often easily detected in childhood and the surgical rectification has good results; it is rarely seen in adults. However, life expectancy with PDA has been reported to be significantly reduced . The detrimental effect of PDA depends on the extent of the shunt, which in turn is determined by various factors including the size of the duct and the pressure gradient across the shunt . Various techniques such as balloon occlusion, ligation, and patch repair are used to surgically repair adult PDA.
Although PDA is not an intracardiac left-to-right shunt, pathophysiologically it behaves like a left-to-right cardiac abnormality comparable to a mild form of atrial septal defect. Similar to other left-to-right shunts, in PDA also some amount of oxygenated blood is directed toward the pulmonary circulation. Hence, there is a perpetual increase in the amount of blood flowing through the pulmonary circulation. This leads to an increase in the thickening of arteriolar walls and decrease in the size of the lumen, and therefore an increase in pulmonary vascular resistance. Gradually, pulmonary artery hypertension develops, which can eventually lead to heart failure . Cardiomegaly, arrhythmias, and myocardial ischemia are also known complications of left-to-right shunts. Long-standing pulmonary hypertension can reverse the direction of flow of blood through the shunt converting it to a right-to-left shunt. Hence, an acyanotic congenital defect becomes a cyanotic condition known as Eisenmenger syndrome.
Patients with small PDAs are often asymptomatic. Large PDA shunt patients are prone to lower respiratory tract infection, exertional dyspnea, tachypnea, atelectasis, tachycardia, CHF, and poor weight gain. These patients develop hypertrophy of the left atrium and both left and right ventricles. Chest radiograph shows cardiomegaly and a 2D echocardiogram is often diagnostic. The size of the shunt can be estimated by the dimensions of the left atrium and ventricle. These patients have bounding peripheral pulses and a continuous machinery murmur at the left upper sternal border. According to Ohye and Bove , PDA should be closed in all patients in whom it can be identified on physical examination. In our case, the patient had his PDA repaired at the age of 54 years. However, the closure was incomplete and a residual defect still remained.
In patients with PDA, during preanesthetic evaluation, the cardiac function and the hemodynamic parameters need to be assessed thoroughly. Patients undergoing major surgery or with severe cardiac defect need invasive monitoring such as central venous pressure, pulmonary capillary wedge pressure, and intra-arterial blood pressure. Transesophageal echocardiography is also frequently used.
Intraoperatively, the aim is to maintain cardiovascular stability, hence providing adequate perfusion and oxygenation of various organs. During the diastolic phase of the contraction of the heart, more blood tends to flow into the duct; hence, the coronary flow is decreased. A low diastolic blood pressure can effectively lead to myocardial ischemia as reported by Fluri et al. . Furthermore, high PaO 2 and low PaCO 2 are known to dilate pulmonary vessels; hence, 100% oxygen and hyperventilation should be avoided.
General anesthesia is frequently used in such patients with inhalation induction by sevoflurane being the mainstay. However, gradually intravenous induction with ketamine is gaining popularity because it causes bronchodilation and maintains systemic vascular resistance . Opioids do not affect the cardiac function but respiratory depression is of concern. Nitrous oxide is known to increase pulmonary vascular resistance and is avoided, as it can worsen pre-existing pulmonary hypertension, which can lead to congestive heart failure. Pulmonary vascular resistance also tends to increase acidosis, hypothermia, hypercarbia, hypoxia, high airway pressures, and bronchospasm due to excessive airway stimulation . Neuraxial anesthesia is known to decrease systemic vascular resistance, and hence decrease left-to-right shunt. However, in a hypovolemic patient, this can increase the blood flow through the shunt. In addition, the resultant tachycardia can be deleterious . Bacterial endocarditis is an important aspect in patients with CHD undergoing surgery, and appropriate antibiotic prophylaxis has to be carried out. Postoperative hemodynamic monitoring and adequate pain relief are of vital importance.
Considering the nature and duration of surgery in our patient in the first scenario, we preferred neuraxial blockade to general anesthesia. The patient was well hydrated to prevent any incidence of sudden hypotension. Furthermore, as large fluid shifts were not expected due to the surgical technique, central venous cannulation was not performed. Bacterial endocarditis prophylaxis was carried out as per the guidelines of the infection control committee of our hospital. As TURP is not a very painful procedure, adequate pain relief was achieved with intravenous paracetamol. The patient was shifted to the ICU postoperatively. In the second scenario, general anesthesia was the only option. Induction was performed with sevoflurane and fentanyl. Nitrous oxide was not used and other factors leading to increased pulmonary vascular resistance were avoided. Bacterial endocarditis prophylaxis was carried out and patient was shifted to ICU.
| Conclusion|| |
Anesthesiologists need a thorough understanding of the pathophysiology of various types of CHD and decide the anesthesia technique according to the type of surgery the patient is scheduled for. Patients with complex lesions undergoing major surgery should preferably be operated in centers having units for pediatric cardiac surgery. Vigilant hemodynamic management is the mainstay for successfully managing adult patients with CHD.
| Acknowledgements|| |
| References|| |
Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol 2002; 39:1890-1900.
Macmohan B, McKeown T, Record RG. The incidence and life expectation of children with heart disease. Br Heart J 1953; 15:121-129.
Daliento L, Mazzotti E, Mongillo E, Rotunda M, Dalla Volta S. Life expectancy and quality of life in adult patients with congenital hrast disease. Ital Heart J 2002; 3:339-347.
Mitchell SC, Korones SB, Berendes HW. Congenital heart disease in 56,109 births. Incidence and natural history. Circulation 1971; 43: 323-332.
Gross RE. Surgical management of the patent ductus arteriosus: with summary of four surgically treated cases. Ann Surg 1939; 110:321-356.
Marquis RM, Miller HC, McCormack RJ, Matthews MB, Kitchin AH. Persistence of ductus arteriosus with left to right shunt in older patient. Br Heart J 1982; 48:469-484.
Schnieder DJ, Moore JW. Patent ductus arteriosus. Circulation 2006; 114:1873-1882.
Kaye AD, Stout TB, Padnos IW, Schwartz BG, Baluch AR, Fox CJ, Liu H. Left to right shunt: perioperative anesthetic considerations. Middle East J Anesthesiol 2012; 21:793-806.
Ohye RG, Bove EL. Advances in congenital heart surgery. Curr Opin Pediatr 2001; 13:473-481.
Fluri S, Pavlovic M, Wagner BP. Patent arterial duct, bottlemeal, and fatal myocardial ischaemia. Cardiol Young 2010; 20:108-110.
Levin SK, Arslan-Carlon V. Tetralogy of Fallot. In: Yao FSFeds. Yao & Artusio's anesthesiology: problem-oriented patient management. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins 2003; ??:242-244.
Cosgrove MS. Anaesthesia for the adult patient with an unrepaired congenital cyanotic heart defect: a case report. AANA J 2012; 80:197-202.