|Year : 2014 | Volume
| Issue : 1 | Page : 41-44
Presentation of undiagnosed mixed mitral valve disease during caesarean section
Michelle R. Cole
Department of Anaesthetic, Frimley Park Hospital, Frimley, Surrey GU16 7UJ; St. Georges Hospital, Tooting, London SW17 0QT, UK
|Date of Web Publication||20-May-2014|
Michelle R. Cole
70 Ladds Way, Swanley, Kent BR8 8HW, UK
Source of Support: None, Conflict of Interest: None
This report describes a woman presenting for an elective caesarean section, with undiagnosed valvular heart disease. She had recent hospital admissions for respiratory dysfunction. Soon after the initial surgical incision, she became asystolic for 20-30 s with an un-recordable blood pressure. She was treated with anticholinergics and became cardiovascularly stable enough for the procedure to continue. However, she had deteriorating respiratory function. A transthoracic echocardiogram in recovery demonstrated mixed mitral valve (MV) disease, moderate mitral stenosis, and severe mitral regurgitation with evidence of severe pulmonary hypertension. She had a dilated left atrium, dilated right ventricle with pulmonary artery systolic pressures of 100 mmHg. She underwent a period of medical optimization followed by a mechanical MV replacement 6 weeks postdelivery. This case attempts to highlight the diagnostic dilemma of unknown maternal cardiac disease. The growing popularity of echocardiography as a diagnostic tool among anaesthetists and critical care physicians proved pivotal in this case.
Keywords: Cesarean section, mitral stenosis, mitral regurgitation
|How to cite this article:|
Cole MR. Presentation of undiagnosed mixed mitral valve disease during caesarean section. J Obstet Anaesth Crit Care 2014;4:41-4
|How to cite this URL:|
Cole MR. Presentation of undiagnosed mixed mitral valve disease during caesarean section. J Obstet Anaesth Crit Care [serial online] 2014 [cited 2022 Sep 30];4:41-4. Available from: https://www.joacc.com/text.asp?2014/4/1/41/132824
| Introduction|| |
Undiagnosed mixed mitral valve disease (MVD) in women may become unmasked during the hemodynamic stresses involved during pregnancy and labour. Maternal heart disease complicates 0.2-3% of pregnancies,  the majority of which have an underlying cause of rheumatic heart disease, endocarditis, or congenital heart disease. Cardiac disease in pregnancy is associated with high maternal and foetal morbidity.
In this report, we describe a case of a young woman's first presentation of acute mixed mitral value disease, predominantly mitral regurgitation, during an elective cesarean section.
| Case report|| |
The case we present here is about a 28-year-old woman (gravida 6 and para 2), presented for her third elective cesarean section. She has a past medical history of depression and asthma, the latter of which was described as becoming increasingly symptomatic during the current pregnancy. At 22 weeks gestation, she presented to hospital with dyspnoea and left sided pleuritic chest pain and underwent a V/Q scan, which showed an intermediate probability of a pulmonary embolism. She was subsequently started on therapeutic dose low molecular weight heparin to be continued until delivery. At 36 weeks gestation, she was re-admitted with dyspnea, wheeze, reduced exercise tolerance, and blood stained sputum. She was treated with antibiotics for infected exacerbation of asthma.
At 39 weeks gestation, she was admitted for her elective cesarean section. Her preoperative assessment was unremarkable albeit precordial auscultation was not documented. She had an uneventful spinal producing a bilateral block to T4, with no hemodynamic compromise. Soon after surgery commenced she became drowsy, lost verbal contact and became bradycardic at 30 beats/min with a blood pressure of 77/41 mmHg. This rapidly progressed to approximately 20-30 s of asystole. Her observations at the time of this event are displayed in [Figure 1].
|Figure 1: Observations postinitial surgical incision (SBP: Systolic blood pressure, DBP: Diastolic blood pressure, HR: Heart rate, Sats: Oxygen saturations)|
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Cardiopulmonary resuscitation was not commenced as on palpation she had a carotid pulse albeit bradycardic with an un-recordable blood pressure. She was given 200 μg of glycopyrrolate, which alleviated her bradycardia and she became cardiovascularly stable. It was decided to continue with surgery because should the patient undergo another cardiovascular collapse, resuscitation would be more effective postdelivery. The operation remained uncomplicated resulting in the delivery of a healthy infant.
Her respiratory function slowly became impaired, with a decline in saturations and consequently and increase in oxygen requirement, delivered through a non-rebreathe face mask. She did not require support in ventilation or vasopressor agents. She was given a total of 2000 ml of crystalloids intraoperatively. Differential diagnosis included a pulmonary embolism or a high spinal, but in the absence of sensory loss above T4, this seemed less likely.
In postanesthetic care unit (PACU) her observations were: Heart rate (HR) 109 beats/min, blood pressure 100/57 mmHg, respiratory rate 25 breaths/min and oxygen saturations ranging from 85-92% on 15 L/min of oxygen. Consequently an urgent computed tomography pulmonary angiography and transthoracic echocardiogram (TTE) were requested.
A TTE was performed by an ITU consultant who by chance was present in the department. This showed signs of significant mitral stenosis and regurgitation. Following this, she was reviewed by a consultant cardiologist where on examination she had signs of a loud pansystolic murmur and fine crepitations to the midzones. A repeat TTE showed similar findings of mixed MVD and dilated left atrium (LA) and right ventricle (RV) suggestive of significant pulmonary hypertension. She was started on regular intravenous furosemide, continuous oxygen via Hudson mask and remained in PACU overnight. All hematological and biochemical tests were normal except for hemoglobin 7.1 g/dl. Serial arterial blood gases revealed an improving Type I respiratory failure and metabolic acidosis.
Day 1 postoperative, she had symptoms consistent with New York Heart Association (NYHA) Class III, orthopnea and hemoptysis. A retrospective history revealed no evidence of rheumatic or congenital heart disease. She was started in ivarbradine (I f current inhibitor at the sinoatrial node) for HR control, given contraception advise and referred to cardiothoracic surgery.
Her repeat TTE 3 days postdelivery showed moderate mitral stenosis with valve area 1.5 cm 2 and severe mitral regurgitation into a severely dilated LA. Severe pulmonary hypertension was demonstrated, with RV systolic pressure 95 mmHg and pulmonary artery systolic pressures of 100 mmHg. RV and LV systolic function were preserved.
Two weeks postdelivery, she had symptomatically improved with reduced pulmonary artery systolic pressures of 60 mmHg. She was discharged after 17 days and underwent an elective mechanical mitral valve replacement 6 weeks later. [Figure 2], [Figure 3], [Figure 4] display the pre- and postoperative TTE findings.
|Figure 2: Preoperative transthoracic echocardiographic images: (a and b) Mitral valve stenosis showing typical hockey stick appearance, (c) mitral valve planimetry, (d) mitral valve regurgitation|
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|Figure 3: Preoperative transthoracic echocardiographic dynamic measurements (MV: Mitral valve, Vmax: Maximal velocity, Vmean: Mean velocity, PGmax: Maximal pressure gradient, PGmean: Mean pressure gradient, VTI: Velocity time integral, HR: Heart rate)|
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|Figure 4: Postoperative transthoracic echocardiographic dynamic measurements (MV: Mitral valve, Vmax: Maximal velocity, Vmean: Mean velocity, PGmax: Maximal pressure gradient, PGmean: Mean pressure gradient, VTI: Velocity time integral, HR: Heart rate)|
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| Discussion|| |
The objective of writing this report is to highlight that maternal cardiac disease may only become evident in the late stages of pregnancy, after which the patient can easily decompensate with the additional hemodynamic stresses such as neuroaxial anaesthesia. It is well accepted that maternal cardiac disease may also mimic the normal physiological changes that occur during pregnancy, complications of the pregnant state or preexisting medical co-morbidity.
Valvular heart disease in young women is most commonly due to rheumatic heart disease;  however, a recent study shows MVD is also associated with advanced maternal age, Jewish ethnicity, hypertensive disorders and recurrent abortions,  the latter of which pertains to this patient.
In general, regurgitant lesions are well-tolerated during pregnancy because the reduction in systemic vascular resistance (SVR) reduces the regurgitant flow. Conversely stenotic lesions have a greater potential to decompensate, as this case demonstrates. Those with significant mitral stenosis fail to tolerate the cardiovascular demands of pregnancy (increase volume loads and tachycardia) leading to pulmonary hypertension and an advancing NYHA class. The reduction in SVR postspinal normally causes a compensatory tachycardia, however in the presence of mitral stenosis, this leads to a reduction of LV filling and increased LA pressure, leading to reduction and cardiac output and pulmonary congestion respectively.
Within the literature, it is suggested for women with a diagnosis of moderate to severe mitral stenosis and/or evidence of severe pulmonary hypertension, percutaneous mitral balloon valvuloplasty or open cardiac surgery should be strongly considered before pregnancy. ,,
When considering delivery by cesarean section, expert opinion recommends anaesthetic technique should be individualized.  Epidural anesthesia is preferred in patients with mitral stenosis as the on-set of blockade is slow.  Likewise a cardio-stable induction of general anesthesia, with blunting the vasopressor effect of laryngoscopy, can be equally safe.  The use of remifentanil infusion is gaining popularity among specialist in this respect. A general anaesthetic also provides the opportunity to use trans-oesophageal echocardiography intra-operatively.
Maternal cardiac disease is a high risk phenomena warranting invasive monitoring, stable haemodynamics, involvement of senior clinicians early and a multidisciplinary approach.
With retrospect, this patients' respiratory symptoms were likely secondary to pulmonary hypertension, highlighting the diagnostic difficulty of maternal cardiac disease. A TTE at her second hospital presentation may have been appropriate, or one can argue perhaps prior to proceeding with the cesarean section following her cardiovascular collapse. One can assume precordial auscultation did not occur as it was not documented, however had this been the case, detection of a loud murmur may have changed her perioperative course.
There is a growing interest in echocardiography amongst anaesthetists and critical care physicians, which proved to be of great value in this case. This diagnostic tool as demonstrated by the intensive care consultant present in PACU by simple chance highlighted the true underlying pathology in this case, which expedited cardiology review and subsequent definitive management.
| References|| |
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]