Case Study
A 36-year-old nulliparous woman who was previously healthy presented at 38 weeks’ gestation to the delivery suite. She was contracting twice in 10 minutes. On examination, she was hypertensive (170/90 mmHg) with 3+ proteinuria, her cervix was dilated 4 cm, and cardiotocography (CTG) of the fetus was reassuring. The midwife altered the multidisciplinary team (duty obstetrician and anesthetist). An IV cannula was inserted, and blood was taken for a full blood examination (hemoglobin, platelet count, and blood film), liver function tests, and determination of urea, creatinine, and electrolyte levels. Then 1,000 ml of 0.9% saline was started, and 20 mg IV labetalol was administered to reduce the blood pressure to 150/90 mmHg. Shortly after this, the patient requested pain relief. After checking the results of the blood tests (platelet count 110,000 × 109/liter), an uncomplicated lumbar epidural was inserted, and effective analgesia was achieved with patient-controlled epidural analgesia using 0.2% ropivacaine with 2 µg/ml fentanyl, a 5-ml bolus every 15 minutes as required.
Two hours later, the patient developed a severe headache and hyperreflexia with blood pressure 180/100 mmHg. Infusions of magnesium sulfate, for seizure prophylaxis, and hydralazine, for blood pressure control, were started. There was no change in cervical dilatation, so augmentation of labor was undertaken with an oxytocin infusion. A nonreassuring CTG combined with limited labor progress led to the decision to deliver by cesarean delivery. Surgery was uncomplicated, and a healthy baby girl was born after an effective epidural top-up dose of 15 ml 2% lidocaine with 1:100,000 epinephrine and 100 µg fentanyl. IV fluid was limited to 500 ml intraoperatively, and the magnesium sulfate and hydralazine infusions continued during surgery. At the end of surgery, the epidural catheter was removed, and the patient was started on regular acetaminophen and oral slow- and intermittent-release opioid analgesia. A low-dose, high-concentration oxytocin infusion (40 units oxytocin in 40 ml 0.9% saline over 4 hours) was started to maintain uterine contractions, and the patient was returned to the delivery suite for close clinical monitoring and continuing magnesium sulfate and hydralazine infusions.
Eighteen hours later, a medical emergency team (MET) call was made when the patient developed critically high blood pressure (190/110 mmHg) followed rapidly by shortness of breath (respiratory rate of 26 breaths/min with lung crackles on auscultation) with reduced oxygen saturation (90 percent on room air). These clinical findings were consistent with pulmonary edema indicating heart failure. In order to determine whether this was reduced ejection fraction heart failure or preserved ejection fraction heart failure, bedside transthoracic echocardiography was performed. This investigation revealed a nondilated left ventricle (left ventricle end-diastolic diameter of 5.1 cm – normal nonpregnant female reference range 3.8–5.2 cm), normal fractional shortening of 38 percent (preserved ejection fraction), mitral valve E/septal e′ ratio of 15 (normal nonpregnant reference value ≤ 8) consistent with diastolic dysfunction and a moderate pericardial effusion. These findings indicated that the patient had preserved ejection fraction heart failure. A bolus dose of hydralazine and furosemide was administered, and continuous positive airway pressure (CPAP) noninvasive ventilation was started. Over the next 15 minutes, her blood pressure decreased to 160/90 mmHg, respiratory rate decreased to 20 breaths/min, and oxygen saturation increased to 96 percent. Over the next hour, urine output increased to 150 ml, and the patient was weaned from noninvasive ventilation. After 24 hours, the magnesium sulfate and hydralazine infusions were ceased, and her blood pressure remained between 130 and 140/80 and 90 mmHg with no cerebral symptoms or signs.
The remainder of her hospital stay was uncomplicated, and she was discharged home on day 5. A follow-up transthoracic echocardiogram at 6 weeks, when she was normotensive, demonstrated normal cardiac structure and function with normal diastolic function evidenced by a mitral valve E/e′ ratio of 7. She was advised to undergo yearly cardiovascular system follow-up with her general practitioner.
Key Points
This patient developed severe intrapartum preeclampsia and underwent an emergency cesarean delivery. This was recognized early, and the multidisciplinary team was alerted.
Management of severe preeclampsia involved biochemical investigations to determine the derangement in organ systems, close clinical monitoring, a magnesium sulfate infusion for seizure prophylaxis, and a hydralazine infusion for blood pressure control.
After excluding contraindications, epidural analgesia was started that could be extended to anesthesia for cesarean delivery.
Postoperatively, the patient developed pulmonary edema in the presence of hypertension. Bedside transthoracic echocardiography demonstrated preserved ejection fraction heart failure. Treatment involved reduction of blood pressure with hydralazine and redistribution of fluid away from the lungs using noninvasive positive end-expiratory pressure ventilation and a diuretic.
Discussion
Cardiovascular disease is a leading cause of maternal mortality worldwide.1–3 Preeclampsia is a cardiovascular condition of pregnancy and is one of the hypertensive disorders of pregnancy. It is defined as new-onset repeatedly high blood pressure (≥140 mmHg systolic and/or ≥90 mmHg diastolic) developing after 20 weeks’ gestation and associated with another organ system involvement. It is not necessary to have proteinuria although this is a common manifestation of organ dysfunction in preeclampsia.4–6
Preeclampsia is frequently subclassified into mild and severe, with severe preeclampsia often defined as critically high blood pressure (≥160/110 mmHg) associated with significant derangement of organ function (e.g., 3+ proteinuria, liver enzymes twice the upper limit of normal, platelet count < 100,000/ml, headache, seizures, pulmonary edema).7
Anesthetists are frequently involved in the multidisciplinary management of women with severe preeclampsia because these women often require analgesia for labor, anesthesia for surgery (cesarean delivery), critical care management of hypertension, management of hemorrhage including antepartum hemorrhage, and management of life-threatening complications such as eclampsia, pulmonary edema, renal failure, or hepatic failure.8 In addition, anesthetists need to consider other causes of hypertension when managing a woman with new-onset hypertension in pregnancy, especially when the presentation is atypical. The recent MBRRACE-UK perinatal mortality surveillance report on maternal deaths in the United Kingdom reported two deaths due to pheochromocytoma in women whose hypertension was inadequately investigated and managed.1
Coordinated management of a woman with severe preeclampsia is important because both stabilization of the condition and risk-reduction strategies to prevent complications need to occur simultaneously8–11 (Table 22.1).
| Key management strategy | General considerations |
|---|---|
| Multidisciplinary team involvement | Obstetrician, anesthetist, midwife, neonatologist, obstetric physician |
| Close monitoring | Maternal monitoring and fetal monitoring; activation of emergency response when observations become abnormal |
| Management of hypertension | Reduce blood pressure to safe levels (140–150/90–100 mmHg) |
| Prevention of neurologic complications | Magnesium sulfate bolus and infusion |
| Restrictive fluid therapy | Minimal IV fluid administration – low volume, high concentration oxytocin infusion if required |
| Analgesia | Neuraxial analgesia is safe, provided that there are no contraindications (thrombocytopenia) |
| Anesthesia | Neuraxial anesthesia is safe (assuming no contraindications); if general anesthesia is required, ablate the response to tracheal intubation using most familiar technique |
| High-acuity postpartum care | Monitor of complications and deterioration |
| Postpartum follow-up | Further investigations of hypertension and its resolution are required; lifelong regular review for early detection of cardiovascular system complications such as hypertension |
Echocardiography, especially transthroaicic echocardiography (TTE), is an important diagnostic and management tool in women with severe hypertension and complications related to hypertension such as acute pulmonary edema, aortic dissection, and myocardial ischemia, and international guidelines recommend its use in these situations.12–16 In pregnancy, favorable characteristics such as anterior and lateral displacement of the heart, the requirement to lie in the left lateral position to avoid aortocaval compression, the noninvasive safe nature of ultrasound, and its high accuracy and validity mean that it is ideal for use in women with obstetric critical illness.17, 18
Acute pulmonary edema is a dangerous complication of preeclampsia, and the reasons for its development are often multifactorial.19 Transthoracic echocardiography can be performed at the point in patient care, often at the bedside, in the situation of breathlessness, desaturation, and hypertension, in order to determine the hemodynamic mechanism for pulmonary edema (Figures 22.1 and 22.2).
