Dilatation And Curettage In A Patient Of Eisenmenger’s Syndrome: Anaesthesia Implications

Author Information

Fernandes  S*, Mali A**, Ritika***, Deo R****.

(Additional Professor, Assistant  Professor, Second Year Resident,

Department ofAnaesthesia, T N Medical College and BYL Nair Hospital, Mumbai, India.)

Abstract

The Eisenmenger’s syndrome consists of pulmonary hypertension with a reversed or bidirectional shunt at the atrioventricular or aortopulmonary level. The pathophysiological effects usually worsen during pregnancy increasing the risk of a poor maternal outcome.^[1] There are numerous reports of patients with Eisenmenger’s syndrome posted for non-cardiac surgeries. Both general and regional anaesthesia have been successfully used in these patients. We discuss the  anaesthetic goals and  intra-operative management of a primigravida undergoing dilatation and curettage under total intravenous anaesthesia.

Introduction

Maternal mortality in patients with Eisenmenger’s syndrome is as high as 30-50% and these women are usually advised to avoid conception. The increased blood volume of pregnancy is accommodated due to vasodilation in the pulmonary and the systemic vascular bed. Patients with Eisenmenger’s are at risk of right ventricular strain due to the irreversible increase in pulmonary vascular resistance. The decrease in systemic vascular resistance that normally occurs during pregnancy can exaggerate the right to left shunt thus worsening the hypoxemia.

Case-Report

A 23year old  female gravida 1,para 0 , weighing 30 kg, known case of Eisenmenger’s syndrome was admitted with pain in the abdomen since 3 days and bleeding per vaginum since 8days.She gave history of consuming an abortifacient at a private clinic two weeks ago. At three years of age she was advised surgery for ventricular septal defect but did not undergo the procedure due to financial constraints. She had been advised to avoid strenuous work as she suffered  dyspnoea Grade II . She was hospitalised for chest pain, syncope and dyspnoea Grade IV  two years ago. Electro-encephalography did not reveal any epileptiform focus. She was advised Tab Sildenafil 25 mg BD.

Pre-operative physical examination revealed Grade II clubbing, pulse rate of 90/min with occasional missed beats, blood pressure of 100/70mmHg and room air saturation of 95% .No cyanosis, peripheral oedema or rise in jugular venous pressure was observed. Lungs were clear to auscultate, there was a pansystolic murmur  over the left sternal border and a loud P2. ECG showed rSR ^| in I, aVL, R in V1 and RS in V1-V3 with occasional ventricular premature complexes. Two dimensional echocardiography with colour Doppler revealed a large midmuscular VSD with bidirectional shunt, good biventricular function and Pulmonary artery systolic pressure (PASP) by Tricuspid regurgitation (TR) jet of 110mmHg. Her haemoglobin was 12.5 g/dL with a hematocrit of 40% and a platelet count of 212000/cmm. Prothrombin time 19.6 sec, Prothrombin index 71.43 and International Normalised Ratio  (INR) 1.51. Ultrasonography  showed a intrauterine sac but no yolk sac or foetal pole. She had received Tab Misoprost 200mcg sublingually 4 hourly. Infective endocarditis prophylaxis was given. Monitoring included Electrocardiography, Noninvasive  Blood Pressure, Capnometry and Pulse-oximetry.  Intravenous line was secured with a 18 G intracath  with special precaution to avoid any air entrapment that could predispose to paradoxical air embolism. We did not place an arterial line and central venous catheter since it was a minor procedure. The  obstetrician had planned dilatation and endometrial curettage  under a paracervical  block but the patient was extremely anxious.She was given i.v midazolam 0.5mg, i.v fentanyl 70 μg and i.v. ketamine 30 mg. She maintained a saturation of 99% breathing spontaneously with face mask. Intra-operatively she continued to have Venticular Premature Contractions (VPCs) but remained hemodynamically stable. Post-operative course was uneventful and patient was discharged on day 3.

Discussion

Eisenmenger’s syndrome a term coined by Paul Wood is defined as Pulmonary Vascular Obstructive Disease that develops as a consequence of a large pre-existing left to right shunt such that pulmonary artery pressures  approach systemic levels and the direction of flow becomes bilateral  or right to left. Congenital heart defects that can result in Eisenmenger’s syndrome include simple defects such as Atrial septal defect (ASD), Ventricular septal defect (VSD)  and Patent ductus arteriosus (PDA) as well as complex defects such as Atrioventricular septal defect, truncus arteriosus, aortopulmonary window and univentricular heart. The high pulmonary vascular resistance (PVR)  is usually established   by the age of  2 years  except in ASD and is sometimes present from birth.^[2]  In the absence of  complications, un-operated patients generally have an excellent to good functional capacity up to their third decade and thereafter usually experience a progressive decline in their physical abilities.  Most patients survive to adulthood with a reported 77% and 42% survival rate at 15 and 25 yr of age respectively.^[3]

Thromboembolic phenomena are responsible for as many as 43% of all maternal deaths with many occurring as late as 4-6 weeks after delivery.^[4] These women are often unable to respond to the increased demands for oxygen during pregnancy. The decrease in PVR seen in normal pregnancy does not occur in these women because PVR is fixed. The decrease in Systemic vascular resistance (SVR) associated  with pregnancy tends to exacerbate the severity of the right to left shunt. The pregnancy associated decrease in Functional residual capacity (FRC) also may predispose to hypoxemia.^[5]

Primary goals of anesthesia management are: to maintain adequate SVR, maintain intravascular volume and venous return, avoid aortocaval compression, prevent pain,myocardial depression, hypoxemia, hypercarbia and  acidosis which may cause an increase in PVR. Several disadvantages are associated with the use of general anesthesia. Positive pressure ventilation results in decreased venous return which compromises cardiac output.The volatile anesthetic agents can cause myocardial depression and decreased SVR. Hofland et al have successfully conducted a laproscopic cholecystectomy by the use of xenon anaesthesia and obtained cardiovascular stability.^[6]   Induction agents such as thiopental or propofol  decrease both contractility and SVR which may exacerbate a right to left shunt.  Ketamine  has been recommended as drug of choice for induction because it has little effect on pulmonary and  systemic vascular resistance,  maintains spontaneous respiration and intact  laryngopharygeal reflexes.^[7]

Pretreatment with phenylephrine to prevent changes in SVR is also recommended although it may cause similar vasoconstriction in both pulmonary and systemic circulations and therefore have only little effect on shunt direction.^[8] Increase in SVR will cause increased left to right shunting with a further increase in pulmonary pressure and right ventricular failure. Volume overload has the same effect and hence fluids have to be administered judiciously.^[9] Tsutsumi et al performed a paracervical block using 1% lidocaine 12ml under 6 L oxygen inhalation through a face mask.^[10]

Although some physicians have stated that a Pulmonary artery catheterisation (PAC) is essential for the management of pregnant women with eisenmengers,^[11] there are some who believe that a PAC may be relatively contraindicated for several reasons.^[12]   In the presence of a large intracardiac shunt, measurement of cardiac output by thermodilution may not be accurate, these patients may not tolerate arrhythmias , Pulmonary artery pressure (PAP) monitoring rarely yields useful information in the presence of severe fixed pulmonary hypertension and the PAC may predispose to pulmonary thromboembolism. To avoid to the risk of invasive cardiac output monitoring in Eisenmenger syndrome, transthoracic bioimpedence cardiography has been used.^[13] Weber et al discussed the role of low dose heparinization to prevent thromboembolism,^[14] however this was not considered  in our patient as it was a short procedure and she was ambulatory soon.

A multidisciplinary approach, judicious perioperative monitoring and knowledge of pathophysiology of Eisenmenger’s syndrome is essential for a successful outcome.

References

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Citation

Fernandes  S, Mali A, Ritika Deo R. Dilatation And Curettage In A Patient Of Eisenmenger’s Syndrome: Anaesthesia Implications. JPGO 2015. Volume 2 No. 3. Available from: http://www.jpgo.org/2015/03/dilatation-and-curettage-in-patient-of.html