Michael A. Frölich
Mali Mathru
Major scientific advances have occurred in virtually all areas of patient care. One of the major changes in obstetrics has been the recognition of the specialty nature of medical complications related to pregnancy. The physiologic alterations that accompany pregnancy may have profound effects on a variety of pathologic conditions. In addition, maternal disease or its therapy may adversely affect the fetus, which makes these considerations unique to the obstetric patient.
The intensivist must be knowledgeable of the considerations specific to pregnant patients and should also understand the pathophysiologic alterations associated with high-risk conditions such as preeclampsia. Obstetricians have done a remarkably good job in managing common diseases such as diabetes, asthma, and chronic hypertension with great sophistication. Nevertheless, life-threatening emergencies during pregnancy challenge the knowledge and skills of anyone who works with this group of patients. Clinicians have acquired considerable information about the management of critically ill obstetric patients; however, this information is not geared toward the critical care provider in most textbooks. This chapter is intended to fill this gap and provide the essential information about the most severe critical conditions that might arise during pregnancy.
An extensive review of all maternal high-risk conditions would go beyond the scope of this chapter. Therefore, we will limit our review to the discussion of physiologic changes of pregnancy that clearly have to be recognized when managing the critically ill pregnant patient. This review is focused mainly on the most life-threatening pathophysiologic processes, including thrombosis and thromboembolism, hypertensive disease of pregnancy, hemorrhage, and amniotic fluid embolism (Tables 97.1 and 97.2), but is inclusive of other more common pregnancy-related problems that come to the attention of the intensivist, such as peripartum cardiomyopathy and pulmonary edema.
Physiologic Changes Associated With Pregnancy
Several physiologic changes are associated with normal pregnancy. These adaptations are necessary to meet the demands of the growing fetus, and have to be considered when evaluating and managing pregnant patients.
Body Constitution
Optimal weight gain in pregnancy is currently a matter of debate (1,2,3). In general, an approximate weight gain of 6 kg is attributed to the fetus, placenta, and uterus, and the remainder of the weight gain to an increase in maternal blood, interstitial fluid volume, and fat. A gestational weight gain of more than 12 kg in women of normal pre-pregnant weight is related to the lowest risk for complications during delivery. Thorsdottir et al. (4) studied the relationship between gestational weight gain and complications during pregnancy, comparing pregnant women with normal weight gain with other higher gestational weight gain. They found that women who exceeded 18 kg of weight gain during pregnancy are considered at greater risk for maternal (pre-eclampsia, gestational diabetes) and fetal (increased incidence of operative delivery) complications.
Changes in maternal physiology occur normally during pregnancy, and have the potential to alter the absorption, distribution, and elimination of drugs used therapeutically in pregnant women (5).
Metabolisms and Respiration
Key physiologic changes of respiration that occur in pregnancy are an increased minute ventilation, which is caused by increased respiratory center sensitivity and drive; a compensated respiratory alkalosis; and a low expiratory reserve volume (6). The vital capacity and measures of forced expiration are well preserved. Patients who have severe lung diseases tolerate pregnancy well, with the exception of those with pulmonary hypertension or chronic respiratory insufficiency from parenchymal or neuromuscular disease.
Lung volumes have been measured in several case series of pregnant women and compared to nonpregnant women or those in the postpartum state (7), with body plethysmography being the preferred technique of measurement (8), and were found well preserved in the majority of cases. The residual volume tends to decrease slightly, which leads to a small increase or stability of the vital capacity (7,9,10,11,12). The most consistent change in static lung volumes with pregnancy is the reduction in the functional residual capacity (FRC) and expiratory reserve volume. As the uterus enlarges, FRC decreases by 10% to 25% of the previous value, starting about the 12th week of pregnancy (7). The normal reduction in FRC is accentuated further in the supine position (13). The reduction in FRC is due to a decrease in chest wall compliance, up to 35% to 40% (14). The lung compliance remains normal during pregnancy, whereas expiratory muscle strength is in the low-normal range (9). The decreased chest wall compliance is the result of the enlarging uterus increasing the abdominal pressure, which leads to a reduction of the FRC (15). The diaphragm elevates about 4 cm, and the circumference of the lower rib cage increases about 5 cm (16). The lower end-expiratory lung volume leads to an increased area of apposition of the diaphragm to the chest wall, which improves the coupling of the diaphragm and chest wall. Thus, the increased tidal volume of pregnancy is achieved without an increase in the respiratory excursions of the diaphragm.
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Table 97.1 Direct maternal deaths, 2000–2002a |
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The rib cage undergoes structural changes during pregnancy (17). Progressive relaxation of the ligamentous attachments of the ribs causes the subcostal angle of the rib cage to increase early in pregnancy. This change persists for months into the postpartum period. The increased elasticity of the rib cage is mediated by the polypeptide hormone, relaxin, which is increased during pregnancy and is responsible for the softening of the cervix and relaxation of the pelvic ligaments (18,19). Changes in pulmonary function during pregnancy are summarized in Figure 97.1.
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Table 97.2 Indirect maternal deaths, 2000–2002a |
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Changes in Arterial Blood Gases
The hormonal changes of pregnancy lead to remarkable respiratory changes throughout its course. The resulting changes of arterial blood gas values have been measured by Templeton et al. (20,21), who obtained serial measurements of maternal blood gases during pregnancy. The same investigators also measured serial alveolar-to-arterial oxygen tension differences (PAO2-PaO2), and calculated the pulmonary venous admixture (physiologic shunt), dead space-to-tidal volume ratio (VD/VT), and respiratory minute volume (Table 97.3). The mean arterial PO2 during pregnancy was found to be consistently greater than 100 mm Hg throughout pregnancy, with no alterations of dead space-to-tidal volume ratio (VD/VT) and shunt.
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Figure 97.1. Pregnancy—pulmonary changes. FVC, forced vital capacity; FEV1, forced expiratory volume in 1 second; RV, plethysmographic residual volume; FRC, plethysmographic functional residual capacity; TLC, plethysmographic total lung capacity. (Data from Garcia-Rio F, Pino-Garcia JM, Serrano S, et al. Comparison of helium dilution and plethysmographic lung volumes in pregnant women. Eur Respir J. 1997;10:2371–2375.) |
Cardiovascular System
Management of pregnancy, especially for women with heart disease, requires an understanding of the hemodynamic stress that occurs during gestation. The most important hemodynamic change in the maternal circulation during pregnancy is an increase in the cardiac index of 30% to 40% (22), which can be primarily attributed to an increase in stroke volume, while heart rate and blood pressure do not change significantly (Fig. 97.2).
This alteration has several unique features: (a) the augmentation occurs relatively early in pregnancy (20–24 weeks), (b) it cannot be explained entirely on the basis of fetal needs, and (c) fluctuations in cardiac output occur with changes in body position as the gravid uterus impinges in varying degrees on the inferior vena cava, thus altering systemic venous return (23).
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Table 97.3 Blood gas analysis in late pregnancya |
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Figure 97.2. Pregnancy—cardiovascular changes. HR, heart rate (bpm); B/Ps, systolic blood pressure (mm Hg); B/Pm, mean blood pressure (mm Hg); B/Pd, diastolic blood pressure (mm Hg); CI, cardiac index (L/min/m2); SV, stroke volume (mL); EDV, end-diastolic volume (mL). (Data from Circulation. 1978;58:434–441.) |
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Red Blood Cell, Plasma, and Blood Volume
An increase of plasma volume is evident by the sixth week of gestation, reaching a value by the end of the first trimester of 15% above nonpregnant women. There is subsequently a steep increase of this parameter until 28 to 30 weeks of gestation, followed by a more gradual rise, to a final volume at term of 55% above the nonpregnant level (24). Red blood cell mass decreases during the first 8 weeks of gestation, but increases to nearly 30% above the nonpregnant level at term. These physiologic changes result in a 45% increase of total blood volume and a reduction of the hemoglobin concentration and hematocrit to values of approximately 11.6 g/100 mL and 35.5 volume %, respectively (Fig. 97.3). Estrogens, progesterone, and placental lactogen elevate aldosterone production either directly or indirectly, and are responsible for the increase of plasma volume during pregnancy. The hyperaldosteronism of pregnancy can result in retention up to 500 to 900 mEq of sodium and an increase of 6,000 to 8,000 mL of total body water, 70% of which is extracellular. The elevated red blood cell volume after 8 to 12 weeks can be attributed to increased serum erythropoietin. Erythropoiesis may also be stimulated by prolactin, progesterone, and placental lactogen. Changes of blood counts during pregnancy are summarized in Figure 97.3.
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Figure 97.3. Changes of blood count during pregnancy. RCM, red cell mass in mL/10; Bvol, blood volume in mL/kg; Hb, hemoglobin in g/100 mL; Hct, hematocrit in %; BL, pre-pregnant data; early, 8th week of pregnancy; mid, 14th week of pregnancy; late, 20th week of pregnancy. (Data from Metcalfe J, Ueland K. A study of pregnancy in Pygmy goats. Prog Cardiovasc Dis. 1974;16:363.) |
Plasma Proteins and Colloid Osmotic Pressure
The total serum protein concentration decreases from a nonpregnant value of 7.3 g/100 mL to 6.5 g/100 mL at term gestation. The change is due primarily to a decline of the albumin concentration, which decreases from a nonpregnant level of 4.4 g/100 mL to 3.4 g/100 mL at term. Although the concentration of globulins declines by 10% during the first trimester, the level rises subsequently to a value at term that is 5% to 10% above the nonpregnant level. These changes result in a progressive decrease in the albumin-to-globulin ratio from approximately 1.5 during pregnancy to 1.1 at term gestation. Maternal colloid osmotic pressure decreases in parallel with the decline in serum albumin concentration from nonpregnant values of 25 to 26 mm Hg to approximately 22 mm Hg at term.
Aortocaval Compression
Angiographic studies show that the aorta and inferior vena cava can be significantly compressed by the gravid uterus in the supine position. In fact, Kerr et al. (25) observed a complete obstruction of the inferior vena cava at the level of the bifurcation in 80% of patients in late pregnancy. Partial obstruction of the aorta at the level of the lumbar lordosis (L3–L5) has also been demonstrated in patients between the 27th week of pregnancy and term gestation (26,27).
The pregnant subject at term, when placed in the lateral decubitus position, exhibits a right ventricular filling pressure (central venous pressure) similar to that of a nonpregnant woman (28). This observation suggests that venous return in this position is maintained by the collateral circulation despite partial caval obstruction (25). In the plain supine position, however, right atrial pressure falls substantially, demonstrating that collateral circulation cannot compensate for complete or nearly complete caval obstruction (26). The fall in the cardiac filling pressure that follows this position change, which is evident by 20 to 28 weeks of gestation, results in a decrease of stroke volume and cardiac output of approximately 25% and a 20% reduction of uterine blood flow (22), and is reliably improved by a tilt to the left of at least 25 degrees (29).
Despite the reduction of cardiac output and stroke volume, a position change from lateral to supine can be associated with elevation of blood pressure. This results from an increase of systemic vascular resistance (30) due to compression of the aorta by the gravid uterus and enhanced sympathetic nervous system outflow. In approximately 5% of women, however, a substantial drop in blood pressure occurs (“supine hypotensive syndrome”), which is associated with bradycardia (usually following a transient tachycardia) and maternal symptoms, low systemic perfusion such as of pallor and sweating, possibly followed by cardiocirculatory collapse. This occasional but profound drop of venous return may be exacerbated by neuraxial block, the preferred method of providing anesthesia in pregnant patients (31). In conclusion and based on the observations above, the intensivist should always consider in his or her emergency treatment plan the proper positioning of the pregnant patient and its influence on hemodynamics.
Thrombosis and Thromboembolism in Pregnancy
Venous thromboembolism (VTE), which includes deep venous thrombosis (DVT) and pulmonary embolism, occurs in approximately 1 in 1,000 pregnancies (32). Women are five times more likely to develop VTE during pregnancy than during a nonpregnant state (33). Fatal pulmonary embolism (PE), a possible sequela of VTE, remains a leading cause of maternal mortality in the Western world (34). The rate of PE in pregnancy is five times greater than that for nonpregnant women of the same age, and is about 1 in 100 deliveries; the risks are even higher in the puerperium.
Risk Factors and Predisposition to Venous Thrombosis
Compared to nonpregnant females, pregnant women have a 10-fold risk of a thrombotic episode. Risk factors for VTE other than pregnancy are increased maternal age (>35 years), previous cesarean delivery, obesity, multiparity, and a history of DVT (Table 97.4).
Pregnancy is associated with an increased clotting potential, decreased anticoagulant properties, and decreased fibrinolysis. Pregnancy is accompanied by a two- to threefold increased concentration of fibrinogen and a 20% to 1,000% increase in factors VII, VIII, IX, X, and XII, all of which peak at term (35). Levels of von Willebrand factor (vWF) increase up to 400% by term (35). Free protein S levels decline significantly (up to 55%) during pregnancy due to increased circulating levels of its carrier molecular, complement 4 binding protein (35). As a consequence, pregnancy is associated with an increase in resistance to activated protein C (35,36). Levels of plasminogen activation inhibitor-1 increase three- to fourfold during pregnancy, while plasma plasminogen activation inhibitor-2 values, which are negligible before pregnancy, reach concentrations of 160 mg/L at delivery (30).
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Table 97.4 Risk factors for venous thromboembolism (VTE) during pregnancy |
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Pregnancy is also associated with venous stasis in the lower extremities due to compression of the inferior vena cava and pelvic veins by the enlarging uterus and hormone-mediated increases in deep vein capacitance secondary to increased circulating levels of estrogen and local production of prostacyclin and nitric oxide.
Important hereditary risk factors that can increase DVT risk are antithrombin III deficiency, protein S and C deficiency, a G1691A mutation of the factor V gene (37), and a G20210A mutation of the factor II gene (38).
Diagnosis of Venous Thromboembolism during Pregnancy
Bates and Ginsberg have recently addressed the diagnosis of VTE during pregnancy in detail (39). In pregnant women presenting with lower extremity edema, back pain, and/or chest pain, the prevalence of VTE is less than in the general population because of the high frequency of these complaints in the pregnant woman. D-dimer assays, which can be used to exclude VTE in healthy nonpregnant individuals, usually become positive late in pregnancy, which decreases the utility of this assay in pregnancy (40). Radiologic studies used to diagnose VTE in the nonpregnant individual have not been validated in pregnancy, and potential risks to the fetus, particularly in terms of ionizing radiation exposure, need to be considered (41). Compression ultrasonography (CUS) of the proximal veins has been recommended as the initial test for suspected DVT during pregnancy (39). When results are equivocal or an iliac vein thrombosis is suspected, magnetic resonance venography (MRV) can be used. MRV does not carry the radiation risk of contrast venography, and is becoming increasingly available in the United States. The approach to the diagnosis of PE is similar in the pregnant and nonpregnant individual. Ventilation/perfusion (V/Q) scanning confers relatively low radiation exposure to the fetus, a risk less than that of missing a diagnosis of PE in the mother. However, when a V/Q study is indeterminate in a pregnant patient without demonstrated lower extremity thrombosis, it is usually followed by angiography. A brachial approach carries less radiation exposure to the fetus than spiral computed tomography (CT).
Prevention of Thrombosis during Pregnancy
The optimal anticoagulation regimen has not been established. Low-molecular-weight heparins (LMWHs) have become the anticoagulant of choice because, like unfractionated heparin (UFH), they do not cross the placenta, have better bioavailability, and carry less risk of osteoporosis and heparin-induced thrombocytopenia than UFH (42). A recent review of published data on the use of LMWHs in pregnancy supports their use as safe alternatives to UFH as anticoagulants during pregnancy (43).
A more recent practice trend, especially in the United States, has been to switch patients to the longer-acting, subcutaneous UFH a few weeks before delivery to allow the use of activated partial thromboplastin time (aPTT) as a diagnostic test to assess anticoagulation pre- and post labor. (44)
Another means of providing VTE prophylaxis is with elastic compression stockings, which may be used for the entire pregnancy period. Elastic stockings are appropriate for in-hospital patients at increased risk of VTE, and may be combined with the use of LMWH. Vena cava filter placement represents a potentially important but poorly evaluated therapeutic modality in the prevention of pulmonary emboli. Randomized trials to establish the appropriate role of vena cava filters in the treatment of venous thromboembolic disease are lacking (45).
Thrombolytic Therapy for Pulmonary Embolism
The indications for thrombolytic therapy for PE remain controversial. The incidence of intracranial hemorrhage may be as high as 2% to 3% with systemic thrombolytic therapy (46), although rates were lower in a recent trial (47). Fatality rates in patients with PE presenting in cardiogenic shock may be as high as 30% (46); thrombolytic therapy should be considered in this circumstance, although evidence for this subgroup is limited (48). Approximately 10% of symptomatic pulmonary emboli are rapidly fatal (49,50). The International Cooperative Pulmonary Embolism Registry, established to ascertain PE mortality, reported that 2% of patients were first diagnosed with PE at autopsy (51). Of patients diagnosed with PE before death, 5% to 10% have shock at presentation, which is associated with a mortality of 25% to 50% (51,52,53). Echocardiographic evidence of right ventricular dysfunction at presentation also has been suggested as an indication for thrombolytic therapy (47); however, a recent randomized trial failed to demonstrate a survival benefit with thrombolysis in patients with this finding (47), and mortality rates with conventional therapy are conflicting (46). At the time of this writing, routine thrombolysis cannot be justified in all patients.
Hemorrhage
Peripartum hemorrhage remains a significant cause of maternal and fetal morbidity and mortality. In the United States and other industrialized nations, massive obstetric hemorrhage has generally ranked among the top three causes of maternal death despite modern improvements in obstetric practice and transfusion services.
Peripartum hemorrhage includes a wide range of pathophysiologic events. Antepartum bleeding occurs in nearly 4% of pregnant women (54). The causes of serious antepartum bleeding are abnormal implantation (placenta previa, accreta), placental abruption, or uterine rupture. The latter is often caused by a dehiscence of a pre-existing uterine scar. The main reason for postpartum bleeding is uterine atony when myometrial contraction is inadequate. It is not surprising that uterine bleeding may be fatal when considering the massive amount of blood flow perfusing the uterus at term (up to 600 mL/minute).
Patients with hemodynamic instability or massive hemorrhage require prompt resuscitative measures, including the administration of supplemental oxygen, placement of two intravenous lines, intravenous hydration, and blood typing and cross-matching for the replacement of packed red blood cells (Table 97.5). A delay in the correction of hypovolemia, diagnosis and treatment of impaired coagulation, and surgical control of bleeding are the avoidable factors in most maternal mortality cases caused by hemorrhage. If a transfusion must be given before full cross-matching is finished, type-specific uncross-matched blood can be used (55).
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Table 97.5 Management of severe postpartum hemorrhage |
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If the placenta has not been delivered when hemorrhage begins, it should be removed, if necessary by manual exploration of the uterine cavity. Placenta accreta is diagnosed if the placental cleavage plane is indistinct. In this situation, the patient should be prepared by the intensivist or the anesthesiologist for probable urgent hysterectomy. Firm bimanual compression of the uterus (with one hand in the posterior vaginal fornix and the other on the abdomen) can limit hemorrhage until help can be obtained. Hemorrhage after placental delivery should prompt vigorous fundal massage while the patient is rapidly given 10 to 30 units of oxytocin in 1 L of intravenous crystalloids. Uterotonic agents such as oxytocin are routinely used in the management of uterine atony (56). This synthetic nonpeptide is a first-line therapeutic agent because of the paucity of side effects and the absence of contraindications. If the fundus does not become firm, uterine atony is the presumed (and most common) diagnosis. While fundal massage continues, the patient may be then given 0.2 mg of methylergonovine (Methergine) intramuscularly, with this dose to be repeated at 2- to 4-hour intervals if necessary. Methylergonovine, an ergot alkaloid, is used as a second-line uterotonic agent in the setting of massive obstetric hemorrhage due to uterine atony. It may cause undesirable adverse effects such as cramping, headache, and dizziness. Coexisting severe hypertension is an absolute contraindication to its use. Injectable prostaglandins may also be used when oxytocin fails. Both prostaglandin E and prostaglandin F2 stimulate myometrial contractions, and have been used intramuscularly or intravenously for refractory hemorrhage due to uterine atony.
In particular, carboprost (Hemabate), 15-methyl prostaglandin F2-α, may be administered intramuscularly or intramyometrially in a dosage of 250 µg every 15 to 90 minutes, up to a maximum dosage of 2 mg. Sixty-eight percent of patients respond to a single carboprost injection; 86% respond to a second dose (57). Since oxygen desaturation has been reported with the use of carboprost (58), patients should be monitored by pulse oximetry.
The use of a hydrostatic balloon has been advocated as an alternative to uterine packing for controlling hemorrhage due to uterine atony (59). The inflated Rusch balloon can conform to the contour of the uterine cavity and provides an effective tamponade. Life-threatening hemorrhage can also be treated by arterial embolization by interventional radiology (60). Finally, in cases of continuing hemorrhage, a variety of surgical techniques can be used to avoid a hysterectomy, such as bilateral uterine artery ligation or internal iliac artery ligation (61).
Amniotic Fluid Embolism
Morgan published the first major review on amniotic fluid embolism in 1979 (62), although the entry of amniotic fluid into the maternal circulation was already recognized in 1926 (63). He reviewed 272 cases reported in the English literature up to date. While the true incidence of this disease entity is not known, most authors estimate it to be between 1 in 8,000 and 1 in 80,000 pregnancies.
Clinical Presentation
The classic presentation of amniotic fluid embolism is described as a sudden, profound, and unexpected cardiovascular collapse followed, in many cases, by irreversible shock and death (64). The only known predisposing factor to this life-threatening complication appears to be multiparity, which accounts for 88% of the cases (62). In a smaller percentage of cases (51%), the presenting symptom was respiratory related. Hypotension is present in 27% of surviving cases, with coagulopathy comprising 12% and seizures 10%. Fetal bradycardia (17%) and hypotension (13%) are the next most common presenting features (Table 97.6).
Etiology and Pathophysiology
It has been a common misperception in the literature that the entry of amniotic fluid into maternal circulation is a routine event. This belief arises from the recognized presence of squamous cells in the pulmonary vasculature as a marker signaling the entry of amniotic fluid into the maternal circulation.
Studies have now shown that squamous cells can appear in the pulmonary blood of heterogenous populations of both pregnant and nonpregnant patients who have undergone pulmonary artery (PA) catheterization (65,66,67,68,69). The presence of these cells is probably the result of contamination by epithelial cells derived from the cutaneous entry site of the PA catheter (65,66). Since it is difficult to differentiate adult from fetal epithelial cells, the isolated finding of squamous cells in the pulmonary circulation of pregnant patients, with or without coexisting thrombotic pulmonary embolism, should be seen as a contaminant and not indicative of maternal exposure to amniotic fluid (70,71,72).
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Table 97.6 Clinical presentation of amniotic fluid embolism |
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Table 97.7 Differential diagnosis of amniotic fluid embolus: Exclusion criteria |
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Recently, it has been hypothesized that amniotic fluid could act as a direct myocardial depressant. In vitro observation documented that amniotic fluid can cause a decrease in myometrial contractility (73). Other humoral factors, including proteolytic enzymes, histamine, serotonin, prostaglandins, and leukotrienes, may contribute to the hemodynamic changes and consumptive coagulopathy associated with amniotic fluid embolus, with a pathophysiologic mechanism similar to distributive or anaphylactic shock (73,74).
Diagnosis and Management
Amniotic fluid embolus syndrome is a diagnosis of exclusion (Table 97.7), and the treatment is essentially supportive. Hemodynamic instability should be treated with optimization of preload by rapid volume infusion. An α-receptor agonist such as phenylephrine may be useful to maintain adequate aortic perfusion pressure (90 mm Hg systolic) while volume is infused. Coagulopathy associated with amniotic fluid embolus should be treated with aggressive administration of blood component therapy. If maternal cardiopulmonary resuscitation (CPR) must be initiated, and the fetus is sufficiently mature and is undelivered at the time of the cardiac arrest, a perimortem cesarean section should be immediately instituted (74,75).
Peripartum Cardiomyopathy
Peripartum cardiomyopathy is a rare disease of unknown cause that strikes women in the childbearing years, and is associated with a high mortality rate.
Definition
Peripartum cardiomyopathy (PPCM) is defined by the development of left ventricular or biventricular failure in the last month of pregnancy or within 5 months of delivery in the absence of other identifiable cause (76). Peripartum cardiomyopathy in the United States can affect women of various ethnic backgrounds at any age, but is more common in women 30 years of age. The strong association of PPCM with gestational hypertension and twin pregnancy should raise the level of suspicion for this condition in pregnant patients who develop symptoms of congestive heart failure (77).
Etiology and Diagnosis
A number of possible causes have been proposed for PPCM, including myocarditis (78), abnormal immune response to pregnancy, maladaptive response to the hemodynamic stresses of pregnancy (79), stress-activated cytokines, and prolonged tocolysis. A genetic tract is probable, as there have been reported few cases of familial PPCM. The diagnosis of PPCM requires the exclusion of more common causes of cardiomyopathy, and should be confirmed by standard echocardiographic assessment of the left ventricular systolic dysfunction, including depressed fractional shortening and ejection fraction documentation.
Treatment and Prognosis
Therapy should be initiated using standard clinical protocols for heart failure. However, angiotensin-converting enzyme inhibitors should be avoided prenatally.
Long-term clinical prognosis is usually defined within 6 months after delivery. In one study, approximately half of 27 women studied had persistent left ventricular dysfunction beyond 6 months, with a cardiac mortality rate of 85% over 5 years, as compared with the group in whom cardiac size returned to normal by the same time interval, with no mortality (76). The identification of the underlying cause of heart failure in the pregnant patient is another important factor that influences long-term survival (80).
Hypertensive Disease of Pregnancy
Diagnosis
Hypertensive disorders of pregnancy include chronic hypertension, preeclampsia/eclampsia, preeclampsia superimposed on chronic hypertension, and gestational hypertension (81). Pre-eclampsia is a pregnancy-specific, multisystem disorder that is characterized by the development of hypertension and proteinuria after 20 weeks of gestation. The disorder complicates approximately 5% to 7% of pregnancies (82), with an incidence of 23.6 cases per 1,000 deliveries in the United States (83). Chronic hypertension is defined by elevated blood pressure that predates the pregnancy, and is documented before 20 weeks of gestation or is present 12 weeks after delivery. Eclampsia, a severe complication of preeclampsia, is a new onset of seizures in a woman with preeclampsia.
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Table 97.8 Physical examination of the severely preeclamptic patient |
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Diagnostic criteria for preeclampsia include new onset of elevated blood pressure and proteinuria after 20 weeks of gestation. Severe preeclampsia is indicated by more substantial blood pressure elevations and a greater degree of proteinuria. Other features of severe preeclampsia include oliguria, cerebral or visual disturbances, and pulmonary edema or cyanosis (81,84) (Table 97.8).
Therapy
Initial therapeutic goals during labor are focused on preventing seizures and controlling hypertension (84). Magnesium sulfate is the medication of choice to prevent eclamptic seizures for either preeclampsia or eclamptic seizures (85). Magnesium sulfate has been shown to be superior to phenytoin (Dilantin) and diazepam (Valium) for the treatment of eclamptic seizures, although they do not prevent the progression of the disorder (86,87). Women with systolic blood pressures of 160–180 mm Hg or higher diastolic blood pressures of 105–110 mm Hg should receive immediate antihypertensive therapy. The treatment goal is to lower systolic pressure to 140–150 mm Hg and diastolic pressure to 90–100 mm Hg. Hydralazine (Apresoline) and labetalol (Normodyne, Trandate) are the antihypertensive drugs most commonly used. Nifedipine (Procardia) and sodium nitroprusside (Nitropress) are potential alternatives, but their use is associated with significant adverse effects and risk of overdose. Similarly, labetalol should not be used in women with asthma or congestive heart failure. Angiotensin-converting enzyme inhibitors are also contraindicated in this group of patients. In women with preeclampsia, blood pressure usually normalizes within a few hours after delivery but may remain elevated for 2 to 4 weeks (88).
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Table 97.9 Antihypertensive therapy in pre-eclampsia |
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Care and Management of the Hypertensive Parturient
Some patients with severe preeclampsia will require admission in the intensive care setting for invasive monitoring and close supervision. Typical indications include (a) a severe increase in blood pressure, with diastolic blood pressures greater than 115 to 120 mg/dL or a systolic blood pressure greater than 200 mm Hg refractory to initial antihypertensive therapy; (b) oliguria refractory to repeated fluid challenges; (c) eclamptic seizures; or (d) respiratory insufficiency with pulmonary edema. The initial physical examination should include a neurologic assessment, funduscopic examination, auscultation of the heart and lungs, and palpation of the abdomen (Table 97.8). If magnesium sulphate is given, it should be continued for 24 hours following delivery or at least 24 hours after the last seizure. Regular assessment of urine output, maternal reflexes, respiratory rate, and oxygen saturation is paramount while magnesium is infused. A loading dose of 4 g should be given by infusion pump over 5 to 10 minutes, followed by a further infusion of 1 g/hour maintained for 24 hours after the last seizure. Gradual antihypertensive therapy can be accomplished with a 25% reduction of mean arterial pressure within minutes to 2 hours, to 160/100 mm Hg (89) (Table 97.9).
Most patients satisfying the criteria for intensive care unit admission should be monitored with central venous access and an arterial catheter. The use of invasive monitoring facilitates the therapeutic goals and can clarify the suspected diagnosis. Occasionally, the use of a pulmonary artery catheter facilitates cardiovascular management by monitoring cardiac output and systemic oxygen delivery while gradually reducing systemic vascular resistance and restoring preload. Other indications for placement of a pulmonary artery catheter include underlying or complicating cardiac diseases with suspected pulmonary hypertension or the progression of respiratory failure to acute lung injury or acute respiratory distress syndrome.
Fetal Monitoring in The Intensive Care Setting
Electronic fetal monitoring (EFM) is used in the management of labor and delivery in nearly three of four pregnancies in the United States. The apparent contradiction between the widespread use of EFM and expert recommendations to limit its routine use indicates that a reassessment of this practice is warranted (90). Even more difficult is the question of whether fetal monitoring is of any substantial use in the critically ill mother or the mother undergoing surgery. Continuous cardiotocography (CTG) during labor is associated with a reduction in neonatal seizures, but no significant differences in cerebral palsy, infant mortality, or other standard measures of neonatal well-being. On the contrary, this monitoring technique was associated with an increase in cesarean sections and instrumental vaginal births. When considering the use of EFM, the intensivist should consider the effects of many sedative, hypnotic, or analgesic drugs routinely used in the critical care setting on fetal heart rate variability (91,92,93). At this time, no systematic studies have been performed concerning the value of CTG during general anesthesia for nonobstetric surgery; it is assumed that uneventful sedation and analgesia provide adequate oxygenation and circulatory stability without having any influence on the fetus (91,92,93).
Pulmonary Edema in Pregnancy
Pulmonary edema is a rare but well-documented complication of tocolytic therapy in pregnant patients (94,95,96). The incidence of pulmonary edema related to β-mimetic tocolysis is estimated to be 0.15% (97). The etiology of the pulmonary edema is unclear, but is likely multifactorial (98). Both cardiogenic and noncardiogenic mechanisms have been proposed. Possible cardiogenic causes include fluid overload, catecholamine-related myocardial necrosis, cardiac failure secondary to reduced diastolic compliance, and down-regulation of β-receptors (97,98,99,100,101).
Treatment
Immediate recognition and appropriate therapy can ameliorate the course of respiratory insufficiency in patients who develop pulmonary edema during tocolytic treatment. Therapy involves discontinuing the medication, ensuring adequate ventilation and oxygenation, correcting fluid imbalance and hypotension, and maintaining adequate cardiac output. Continuous assessment of the fetus' well-being is necessary.
Tocolytic Therapy
The development of pulmonary edema during the course of β-adrenergic agonist treatment for preterm labor is an indication for discontinuing the treatment and either switching to a different type of labor-inhibiting drug or terminating all efforts to prevent preterm delivery. Magnesium sulfate, calcium channel blockers, or oxytocin antagonists are the most frequently used alternatives.
Ventilatory Support
This topic is reviewed extensively in other sections of the book. Mechanical ventilation principles are not different for the pregnant patient, and are being standardized by evidence-based medicine and consensus conferences (101,102,103).
Fetal Considerations
In particular, fetal well-being must be interpreted within the context of maternal respiratory failure. At minimum, intermitted fetal monitoring is indicated. If refractory maternal hypoxemia and acidosis presents, and results in fetal distress, cesarean delivery to salvage the fetus should be considered.
Cardiopulmonary Resuscitation in Pregnancy
The major causes of maternal cardiac arrest are trauma, cardiac arrest, and embolism. Other causes are sepsis, magnesium overdose, complications of eclampsia, or the result of an unanticipated difficult intubation. The general treatment of the pregnant patient in cardiac arrest is no different than any other patient, including drug dosages and defibrillation settings. Chest compressions and ventilations should be performed with the recommended sequence. Because a slight left tilt of the pregnant patient during CPR enhances venous return after 24 weeks of gestation, this position is recommended. Because of the reduced pulmonary reserve, pregnant women do not tolerate hypoxia well. IV fluid should be running wide open on pressure bags, and blood products should be considered if hemorrhage is suspected. Once the age of the fetus is determined, a decision can be made whether to proceed with a perimortem cesarean section. The fetus can tolerate hypoxia longer than normal, but the decision to proceed with a cesarean delivery should be made within 4 minutes (102). In a recent retrospective review on cardiopulmonary resuscitation with perimortem cesarean section, authors found 35 reports with 20 potentially resuscitable causes, of which 13 women survived (103). While this recent review fell short of proving that perimortem cesarean delivery within 4 minutes of maternal cardiac arrest improves maternal and neonatal outcomes, it provided additional support for this procedure. An extensive review of this topic is also available on the American Society of Anesthesiologists (ASA) website.
Anesthesiologists have recognized that the management of the airway in the obstetric patient may be especially challenging. According to a closed claims analysis of the ASA, the main mechanisms for airway problems are inadequate ventilation, esophageal intubation, and difficult intubation (104). If the anesthesiologist encounters an unanticipated difficult airway, alternative airway management attempts may include the laryngeal mask airway or the Combitube. If cricothyrotomy becomes necessary, this maneuver should be initiated in a timely fashion to minimize the chance of maternal hypoxic brain damage.
Summary
The obstetric patient poses exceptional challenges in the intensive care unit. Knowledge of the physiologic changes of pregnancy and specific pregnancy-related disorders is necessary for optimal management. The critically ill obstetric patient is unique in terms of medical management and often requires the input of several specialties. These patients require specialized nursing care and aggressive monitoring of both mother and fetus, and often include invasive monitoring of the mother. Intensive care unit diagnoses may include preeclampsia, including the HELLP syndrome, pulmonary embolic disease, amniotic fluid embolism, status asthmaticus, respiratory infection, acute respiratory distress syndrome, and sepsis. There is little doubt that intensivists in an intensive care unit can best treat these patients. The management of mechanical ventilation is based on modern principles of avoiding lung injury, while hypercapnia may be tolerated even during the pregnancy. The maternal–fetal medicine physician should be included in the treatment team. Care must include the consideration of pregnancy-induced physiologic changes, normal laboratory alterations, and continued fetal well-being if antepartum. Ultimately, the goal of this interdisciplinary approach is to ensure cohesive coordinated care for the pregnant patient. The following chapter will review some of the topics discussed above in more detail.
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