Year : 2014 | Volume
: 4 | Issue : 2 | Page : 78--80
Anesthetic management of cesarean section with mitral stenosis and respiratory tract infection
Madagondapalli Srinivasan Nataraj, Venkateshaiah Giri
Department of Anaesthesiology, Employees State Insurance Medical College, Bengaluru, Karnataka, India
Madagondapalli Srinivasan Nataraj
Department of Anaesthesiology, Employees State Insurance Medical College, Bengaluru, Karnataka
Mitral stenosis in pregnancy is poorly tolerated because of the pregnancy induced physiological changes in the cardiovascular system. Our patient had presented with cardiac failure in 5 th month of gestation due to valve area of 0.8 cm 2 . She underwent commissurotomy and was asymptomatic with valve area of 1.6 cm 2 until term when she developed lower respiratory tract infection. Anesthetic management of emergency caesarean section in this patient is discussed where neuraxial block is not well-tolerated, and general anesthesia is associated with increased morbidity in the presence of reactive airways.
|How to cite this article:|
Nataraj MS, Giri V. Anesthetic management of cesarean section with mitral stenosis and respiratory tract infection
.J Obstet Anaesth Crit Care 2014;4:78-80
|How to cite this URL:|
Nataraj MS, Giri V. Anesthetic management of cesarean section with mitral stenosis and respiratory tract infection
. J Obstet Anaesth Crit Care [serial online] 2014 [cited 2019 Aug 20 ];4:78-80
Available from: http://www.joacc.com/text.asp?2014/4/2/78/143877
Mitral stenosis of rheumatic origin is the most frequent valvular heart disease in pregnancy.  The ideal anesthetic technique based on the severity of the valvular lesion, maternal preference and safety out-come remains controversial. Presence of active lower respiratory tract infection in these patients can further complicate the anesthetic management. We present a case of moderate mitral stenosis with active respiratory tract infection for emergency caesarean section.
A 23-year-old primi-gravida at term was scheduled for emergency caesarean section in view of nonprogress of labor. At 4 months of gestation, she had presented with severe breathlessness at rest. Clinical examinations and investigations revealed severe mitral stenosis with valve area of 0.8 cm 2 . Echocardiography showed pulmonary artery systolic pressure (PASP) of 100 mmHg and mean left atrial pressure (LAP) of 27 mmHg. She underwent percutaneous transvenous mitral commissurotomy (PTMC) under conscious sedation with midazolam in 5 th month of pregnancy. Two dilatations were done using size 24 Accura balloon across mitral valve. Post PTMC, echocardiography showed mitral valve area had increased to 1.6 cm 2 , PASP decreased to 60 mmHg and LAP decreased to 16 mmHg. She was prescribed oral furosemide 20 mg and metoprolol 25 mg daily and discharged from hospital.
She presented to the hospital at 37 weeks gestation with complains of fever, cough, thick yellowish expectoration and breathlessness. On auscultation, bilateral lung fields had coarse crepitations and scattered ronchi. Lab investigations showed raised leucocyte count that was 18,500 cells/mm 3 . A diagnosis of lower respiratory tract infection was made, and she was started on injection Augmentin 1.2 g and salbutamol nebulization twice daily. Electrocardiogram (ECG) showed biphasic P wave in lead V1. Repeat echocardiogram revealed post PTMC status, mitral valve orifice area of 1.6 cm 2 , moderate mitral regurgitation, PASP of 42 mmHg and an ejection fraction 58%.
She developed labor pains on the 3 rd day of admission. She was offered epidural analgesia for alleviation of her labor pains, and her labor was augmented with oxytocin infusion. However, before epidural analgesia could be instituted, the fetal cardiotocograph showed decelerations, and she was scheduled for emergency caesarean section. She was afebrile, but cough with expectoration persisted with bilateral crepitations and ronchi. Aspiration prophylaxis with injection ranitidine 50 mg and metaclopramide 10 mg intravenous (IV) was given. Considering her clinical condition, epidural anesthesia with invasive monitoring was planned. She was shifted to the operating room in a lateral propped up position with oxygen supplementation as the room air saturation was 92%. An 18 g IV access was secured in the left upper arm. Five electrode ECG monitoring lead II and V5, noninvasive blood pressure (NIBP) and pulse oximeter were connected. Her baseline vitals were heart rate 84/min, NIBP 104/72 mmHg, respiratory rate 26/min, and SpO 2 of 92%. As the radial artery could not be cannulated due to technical reason, the right dorsalis pedis artery was cannulated with a 20 g canula and a 15 cm 7Fr triple lumen central venous catheter was inserted into right subclavian vein using Seldinger's technique for invasive pressure monitoring. The baseline central venous pressure (CVP) recorded was 6 mmHg. Under aseptic precautions between L1-L2 inter-space epidural catheter was inserted using 18G Tuohy needle. 5 ml of 2% plain lignocaine was used for test dose for confirming negative response for subarachnoid and venous placement. Incremental doses of 2% lignocaine (4 ml) and 0.5% bupivacaine (4 ml) were administered over 30 min to achieve a segmental block up to T6 at the end of 45 min. Hemodynamically she was stable during the period with systolic blood pressure above 100 mmHg and heart rate maintained between 70/min and 80/min. Prophylactic phenylephrine infusion was started (dose of 20 μg/min) to prevent peri-operative reduction of blood pressure. No preloading was done earlier, and a total of 850 ml of Ringer's lactate was administered monitoring and maintaining (CVP) within 6-8 mmHg the bladder was catheterized and the total urine output measured in 1 h was 120 ml. After delivery of the baby, oxytocin 10 units in 500 ml Ringer's lactate infusion started at a rate of 100 ml/h. A bolus dose of oxytocin was avoided, and prophylactic phenylephrine infusion was continued for half an hour after baby extraction. During the intraoperative period there were no episodes of hypotension, tachycardia, bronchospasm, desaturation or pulmonary edema. Surgery lasted for 45 min, and the total blood loss was 800 ml. After the surgery, she was monitored in a high dependency unit (HDU). IV fluids 60 ml/h of 5% dextrose in saline was continued, and oral furosemide and metoprolol were resumed after 6 h. Her blood pressure was maintained above 110 mmHg systolic and heart rate between 60 and 70/min. Total dose of phenylephrine used was 250 μg. Postoperative pain was managed with epidural infusion of 0.1% bupivacaine with 1 μg/cc of fentanyl at 6 ml/h for next 24 h. She was shifted out of HDU on the second day with a healthy baby.
Mitral stenosis of rheumatic etiology is the commonest valvular heart disease in women of reproductive age especially in developing countries.  The physiological changes that occur in pregnancy can be detrimental to patients with mitral stenosis. When valve area is reduced to <2.0 cm 2 , a pressure gradient develops across the valve. This increase in LAP is reflected back into the pulmonary venous circulation and increases the risk of pulmonary edema. Untreated, this results in pulmonary arterial hypertension that may lead to increase in right ventricular pressures and possibly, to right ventricular failure.  For symptomatic patients with moderate to severe mitral stenosis and severe pulmonary hypertension, percutaneous mitral balloon valvuloplasty or mitral valve surgery should be considered before pregnancy to reduce the need for gestational treatment and to improve pregnancy out-comes.  Beta blockers and diuretics remain the main stay of medical management for symptomatic patients in pregnancy.  Mitral valve surgery is reserved for those refractory to medical therapy who are not suitable candidates for vavuloplasty because cardiovascular surgery during pregnancy is associated with increased fetal mortality.  Our patient with a valve area of 0.8 cm 2 presented with features of pulmonary edema and right ventricular failure in 5 th month of pregnancy and underwent percutaneous mitral valve commissurotomy. After the procedure, she was on beta blockers and diuretics and was symptom-free till term when she developed respiratory tract infection. Even though the features resembled pulmonary edema, the diagnosis of an infectious cause was made based on the presence of fever and raised leucocyte count. Presence of respiratory tract infection complicates the management of caesarean section in patients with mitral stenosis. The bronchodilators used can cause tachycardia decreasing time for left ventricular filling. In the presence of infection, general anesthesia carries significant morbidity. Neuraxial block in patients with mitral stenosis reduces systemic vascular resistance, cardiac preload and causes reflex tachycardia. A single-shot spinal anesthesia is not recommended for the pregnant patients with significant mitral stenosis.  A well-controlled, individualized epidural neuraxial block using incremental dosing of local anesthetic with invasive monitoring of arterial and cardiac filling pressures may be beneficial even for the most severe cardiac disease.  In the present case a mixture of 2% lignocaine and 0.5% bupivacaine was chosen to provide a quicker and longer duration of block.  Segmental epidural block with incremental doses of local anesthetic were well tolerated in our patient without any hemodynamic disturbances. We had prophylactically used a small dose of phenylephrine infusion as it has been shown to prevent oxytocin induced tachycardia and hypotension. , Invasive monitoring like CVP and intra-arterial BP readings are required to detect and treat sudden changes in hemodynamics that can occur in these patients. Even though CVP does not reflect the actual LAP, it can be used as a rough guide for fluid management.
This report describes an uneventful management of a patient with respiratory tract infection in patients with mitral stenosis for emergency caesarean section.
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