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Chapter 57Intensive Care Monitoring of the CriticallyIll Pregnant Patient Stephanie Rae Martin, DO, and Michael Raymond Foley, MDLess than 1% of pregnant women will become critically ill and require Mortality rates have declined precipitously in the United Statesadmission to an intensive care unit (ICU).1-8 Between 47% and 93% over the past century, but a slight increase has been observed in moreof ICU admissions result from an obstetric complication, primarily recent years, as shown in Figure 57-2.11 Some of this increase has beenhemorrhage and hypertensive disorders. Other common causes include attributed to better ascertainment of data collected prospectively andrespiratory failure and sepsis. Common non-obstetric indications for to the use of multiple source documents. Although this trend is exhib-ICU admission include maternal cardiac disease, trauma, anesthetic ited for all races, wide discrepancies still exist between white and non-complications, cerebrovascular accidents, and drug overdosage. In white populations, even when controlling for age and use of prenatalmany series, most obstetric ICU admissions occur in the immediate care (Fig. 57-3).12 The reasons for this discrepancy remain unclear.postpartum period and are most likely caused by complications of Geographic differences in maternal mortality rates are also apparentacute hemorrhage.1,4-6,9 and are likely inﬂuenced by racial disparities. States with higher per- An intimate understanding of the physiologic changes of pregnancy centages of births to African-American women are also those with theis essential in managing critically ill patients. This chapter addresses highest maternal mortality rates. The data on pregnancy-related mor-basic critical care monitoring in obstetrics and discusses conditions in tality in the United States between 1990 and 1997 indicate a ratewhich more intensive management of the pregnant patient may be of 11.8 deaths per 100,000 pregnant women (8.1 deaths per 100,000indicated. whites, 30.0 deaths per 100,000 African Americans).12 Advancing maternal age and lack of education are also associated with an increased risk for death in pregancy.12 Potential explanations for this increased risk include a higher incidence of underlying or undiagnosed chronicMaternal Mortality disease.EpidemiologyMaternal mortality is deﬁned as the number of maternal deaths (direct Prediction of Maternal Mortalityand indirect) per 100,000 live births. Direct obstetric deaths result pri- Predicting the risk of mortality for pregnant patients remains a chal-marily from thromboembolic events, hemorrhage, hypertensive dis- lenge. The overall maternal mortality rate for critically ill gravidasorders of pregnancy, and infectious complications. Indirect obstetric admitted to an ICU ranges from 0% to 20%, with most series reportingdeaths arise from preexisting medical conditions, including diabetes, maternal mortality rates of less than 5% for all obstetric ICU admis-systemic lupus erythematosus, pulmonary disease, and cardiac disease sions.1,3-5,8 Several scoring systems are routinely employed in criticalaggravated by the physiologic changes of pregnancy. Figure 57-1 shows care settings in an attempt to objectively describe the severity of thespeciﬁc causes of pregnancy-related mortality for three time periods as critical illness and accurately predict mortality risks. The Acute Physi-reported by the Centers for Disease Control and Prevention.10-12 ologic and Chronic Health Evaluation (APACHE) scoring system,14,15 Maternal mortality rates are periodically surveyed by various local, Simpliﬁed Acute Physiologic Score (SAPS),16 and Mortality Predictionstate, and national agencies. Because these data are primarily collected Model (MPM)17 are three widely used methods that track a variety offrom death certiﬁcates, some have suggested that the numbers under- variables in nonpregnant patients.estimate the mortality rate by as much as 20% to 50%.13 Variations in Several authors have evaluated the applicability of the scoringthe deﬁnition of maternal death, medicolegal concerns, and physicians systems in critically ill pregnant patients.18-20 In a study of obstetricuntrained in the proper completion of death certiﬁcates further ICU patients, the APACHE III score did not accurately predict mater-confuse these investigations. To address these concerns, the Division nal mortality.18 In the largest series, 93 gravidas were compared withof Reproductive Health at the Centers for Disease Control and Preven- 96 nonpregnant women. The overall mortality rate in the obstetriction, in collaboration with the American College of Obstetricians and population was 10.8%. The APACHE II, SAPS II, and MPM II scoringGynecologists (ACOG) and state health departments, began in 1987 systems each performed well in predicting mortality (14.7%, 7.8%,to systematically collect these data in the Pregnancy-Related Mortality and 9.1%, respectively).19 The predicted mortality rate was signiﬁ-Surveillance System. cantly higher among obstetric patients compared with non-obstetric
1168 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 180 160 140 White 120 Black 100 Ratio 80 60 40 20 0 19 20–24 25–29 30–34 35–39 40 Age group (yrs) FIGURE 57-3 Pregnancy-related mortality ratios by age and race in the United States for 1991 to 1999. The mortality ratios are theFIGURE 57-1 Causes of maternal mortality for three time number of deaths per 100,00 live births.periods. Obstetric deaths are caused by thromboembolic events,hemorrhage, hypertension, infections, and preexisting medicalconditions, such as diabetes, systemic lupus erythematosus,pulmonary disease, and cardiac disease aggravated by the physiologic to the obstetric population, they have the potential to overestimate thechanges of pregnancy. CVA, cerebrovascular accident; HTN, mortality risk for critically ill gravidas.hypertension. (From Berg CJ, Chang J, Callaghan WM, et al:Pregnancy-related mortality in the United States, 1991-1997. ObstetGynecol 101:289-296, 2003.) Invasive Central Hemodynamic Monitoring 30 Background and Insertion Technique 25 Placement of a central venous catheter may be indicated to provide 20 central venous access for ﬂuid replacement, medication administra- tion, or hemodynamic measurements. Since its introduction in theRatio 15 early 1970s,21 invasive hemodynamic monitoring with a pulmonary 10 artery catheter (PAC) has become quite common in critically ill patients. The most commonly available Swan-Ganz catheters are 5 multilumen devices that enable direct monitoring of central venous pressure (CVP, right ventricular preload), pulmonary capillary wedge 0 pressure (PCWP, left ventricular preload), cardiac output (CO), sys- 67 69 71 73 75 77 79 81 83 85 87 89 91 93 95 temic vascular resistance (SVR, left ventricular afterload), pulmonary 19 19 19 19 19 19 19 19 19 19 19 19 19 19 19 Year artery pressures, and mixed venous oxygen saturation. CO and mixed venous oxygen saturation can be measured in the conventional mannerFIGURE 57-2 Maternal mortality ratios in the United States by by thermodilution and direct distal port aspiration, respectively, or byyear for 1967 to 1996. Ratios are the number of maternal deaths newer ﬁberoptic technology that allows continuous monitoring of COper 100,000 live births. The term ratio is used instead of rate because and mixed venous oxygen saturation.the numerator includes some maternal deaths that were not related PACs (i.e., Swan-Ganz catheters) are typically inserted percutane-to live births and therefore were not included in the denominator. ously through an introducer sheath and in a sterile manner through(From Centers for Disease Control and Prevention: Maternal the left subclavian or right internal jugular veins and advanced intoMortality—United States, 1982-1996. MMWR Morb Mortal Wkly Rep the right heart. The right internal jugular vein is usually preferred47:705-707, 1998.) because it offers the shortest and most direct entry into the right heart. Access through the femoral vein offers the advantage of com- pressibility in a patient with a coagulopathy, but it is most distantpatients for each of the three scoring tools, despite no difference in from the right heart and may require ﬂuoroscopic guidance. As theactual mortality between the two groups (10.8 versus 10.4%). catheter is advanced, characteristic oscilloscopic pressure waveforms None of the scoring systems includes adjustments for normal are used to establish the catheter’s location within the heart. A 1.5-mLobstetric physiologic changes such as decreased blood pressure and balloon is positioned close to the tip of the catheter. Inﬂation of theincreased respiratory rate. Laboratory abnormalities such as elevated balloon allows the catheter to be carried through the heart by ﬂowingliver function test results and low platelet counts, which are common blood.in obstetric disorders such as HELLP syndrome (hemolysis, elevated After the inﬂated balloon reaches the pulmonary artery, it travelsliver enzymes, and low platelets), are not included in the assessments distally until it wedges in a smaller-caliber artery and occludes bloodand may limit their potential applicability. In summary, although the ﬂow. This results in a nonpulsatile waveform from which the PCWPavailable critical care mortality scoring systems can possibly be applied is measured. When the balloon is deﬂated, return of an identiﬁable
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1169pulmonary artery systolic and diastolic pressure tracing should occur. TABLE 57-1 POTENTIAL PULMONARY ARTERYA portable chest radiograph is indicated after placement of a PAC to CATHETER COMPLICATIONSverify appropriate catheter positioning and exclude pneumothorax. At Insertion After PlacementIndications for Pulmonary Pneumothorax Pulmonary infarctionArtery Catheterization Thrombosis Pulmonary artery rupture Arterial puncture InfectionThe most common indications for PAC placement in the obstetric Air embolization Balloon rupturepopulation include the following22: Catheter knotting Endocardial or valvular damage Cardiac arrhythmias (transient, Hypovolemic shock unresponsive to initial volume sustained) resuscitation attempts Septic shock with refractory hypotension or oliguria Severe preeclampsia with refractory oliguria or pulmonary edema complication rates decline as operator experience increases, and only Ineffective intravenous antihypertensive therapy properly trained personnel should insert catheters for invasive hemo- Adult respiratory distress syndrome (ARDS) dynamic monitoring.38 Several studies have also demonstrated that Intraoperative or intrapartum cardiac failure ultrasound-guided placement results in fewer failed attempts at place- Severe mitral or aortic valvular stenosis ment, fewer complications such as hematoma or arterial puncture, and New York Heart Association (NYHA) class III or IV heart less time for placement.39 disease in labor Complications encountered at initial insertion include arterial Anaphylactoid syndrome of pregnancy (i.e., amniotic ﬂuid puncture, pneumothorax, and air embolism. Pneumothorax risks are embolism) highest with a subclavian approach. Transient cardiac arrhythmias are commonly encountered during placement and advancement of the Although use of the PAC in nonpregnant critically ill patients is PAC. The majority consist of premature ventricular contractions orwidespread, until recently, randomized trials demonstrating a clear nonsustained ventricular tachycardia, and they resolve with withdrawalbeneﬁt of PAC-directed care were lacking. Several small studies or advancement of the catheter. The overall incidence of transientsuggested a decrease in mortality when PACs are used to direct thera- minor arrhythmias during advancement of a PAC exceeds 20% in mostpies,23-25 while others reported an increase in mortality associated with studies.37 Signiﬁcant arrhythmias such as sustained ventricular tachy-the use of PACs26-29 or no beneﬁt.30-32 The large Canadian Critical Care cardia or ﬁbrillation are less common, occurring in less than 4% ofClinical Trials Group study prospectively randomized 1994 high-risk patients in most series, and they are more likely to be encountered insurgical patients to receive a PAC to direct therapy or standard therapy patients with cardiac ischemia.37and reported no survival beneﬁt when therapy was directed by Infections related to central venous catheters are common anda PAC (7.8% versus 7.7% for controls).33 A British trial randomized may involve a superﬁcial skin infection, colonization, or a moremore than 1000 critically ill patients to management with or without serious bacteremia. Skin ﬂora, particularly Staphylococcus species, area PAC and failed to demonstrate a survival beneﬁt (68.4% versus most commonly involved. Positive cultures from the tip of a PAC are65.7% for controls).34 The Evaluation Study of Congestive Heart common and are considered evidence of colonization. However, forFailure and Pulmonary Artery Catheterization Effectiveness (ESCAPE bacteremia or sepsis to be diagnosed, the patient must also have posi-trial) also demonstrated no difference in mortality or length of stay for tive blood cultures with the same organism and clinical evidence of433 patients with congestive heart failure randomized to PAC or no systemic infection, such as fever or hypotension.40 The risk of bactere-catheter.35 mia is approximately 0.5% per catheter day, and the risk increases with A meta-analysis of 13 trials published since 1985 included 5051 each day the catheter remains indwelling. Bacteremia resulting frompatients randomized to a PAC or to no PAC to guide management. central venous catheters accounts for 87% of bloodstream infectionsNo difference was identiﬁed in mortality or length of hospital stay. in critically ill patients.41 Infectious complications can be minimizedConversely, the use of a PAC was signiﬁcantly associated with more by adherence to strict sterile technique, placement in the subclavianfrequent use of inotropes and vasodilators.36 In summary, although site, use of antimicrobial-coated catheters, avoiding antibiotic oint-placement of PACs remain widespread, the available data do not ments that can increase fungal colonization, avoiding empiric cathetersupport the routine use of PACs for all critically ill patients. Data changes, and removing the catheter as soon as possible.42addressing the role of PACs in pregnant critically ill patients are Venous thrombosis risk can be minimized by placement at the sub-lacking. clavian site and by limiting the duration of catheter placement. Pulmo- nary infarction may occur as a result of direct occlusion of a pulmonary artery branch caused by drifting of the catheter or thromboembolicComplications of Central events. Catheter knotting can be avoided during placement if the opera-Venous Catheters tor remains aware of the centimeter markings on the advancing cathe- ter. The right ventricle usually is reached when the catheter has beenCommon complications associated with initial venous access, advance- inserted 25 to 30 cm from the jugular vein site. Few patients requirement, and maintenance of a PAC are listed in Table 57-1.37 Some more than 50 cm of catheter to reach the pulmonary artery. Inﬂatedcomplications, such as pulmonary infarction and pulmonary artery catheter balloons should be checked before insertion to reduce the riskrupture, are speciﬁc to placement of a PAC and do not occur with of air leakage and balloon rupture. Overinﬂation of the balloon withcentral venous access alone. Minimal available data address speciﬁc air (>1.5 mL) should be avoided. A pressure-release balloon has beencomplication rates associated with PAC use in pregnant women. Initial described that limits overinﬂation and thereby minimizes pulmonary
1170 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 24 TABLE 57-2 FORMULAS FOR CALCULATING HEMODYNAMIC VARIABLES 22 SVR = [(MAP − RAP)]/CO × 80 20 PVR = (PAP − PCWP/CO) × 80 18 CO = VO2/(CaO2 − CvO2) DO2 = CO × CaO2 × 10 PCWP (mm Hg) 16 VO2 = (CaO2 − CvO2) × CO × 10 CaO2 = (1.34 × Hb × SaO2) + (0.003 × PaO2) 14 CvO2 + (1.34 × Hb × SvO2) + (0.003 × PvO2) 12 O2 extraction = VO2/ DO2 Qs/Qt = CcO2 − CaO2/CcO2 − CvO2 10 CaO2, arterial oxygen concentration; CcO2, end capillary O2 content; 8 CO, cardiac output; CvO2, venous oxygen concentration; DO2, oxygen 6 delivery; Hb, hemoglobin; MAP, mean arterial pressure; O2, oxygen; PaO2, arterial partial pressure of oxygen; PAP, pulmonary artery 4 pressure; PCWP, pulmonary capillary wedge pressure; PvO2, venous partial pressure of oxygen; PVR, pulmonary vascular resistance; 2 Qs/Qt, shunt fraction; RAP, right atrial pressure; SaO2, arterial oxygen saturation; SvO2, venous oxygen saturation; SVR, systemic vascular –2 0 2 4 6 8 10 12 14 16 18 resistance; VO2, oxygen consumption. CVP (mm Hg)FIGURE 57-4 Relationship of central venous pressure (CVP)to pulmonary capillary wedge pressure (PCWP) in severe obtained. Table 57-2 lists formulas for calculating selected hemody-pregnancy-induced hypertension. If an accurate assessment of left namic variables.ventricular preload is deemed important in the management of the Hemodynamic variables often are expressed in an “indexed” fashionpatient’s cardiovascular complications, insertion of a pulmonary artery (i.e., cardiac index). To do this, the original nonindexed CO value mustcatheter may be indicated. (From Cotton DB, Gonik B, Dorman K,et al: Cardiovascular alterations in severe pregnancy-induced be divided by body surface area. Because standard body surface areahypertension: Relationship of central venous pressure to pulmonary calculations have never been established speciﬁcally for pregnancy, thiscapillary wedge pressure. Am J Obstet Gynecol 151:762, 1985.) traditional way of expressing hemodynamic data is somewhat contro- versial in obstetrics. Those who argue for its use point out that index- ing allows direct comparison of hemodynamic parameters for pregnantvessel injury. Pulmonary artery rupture is a rare but often fatal compli- women of different sizes, a critical issue when interpreting thesecation that occurs more commonly in patients with pulmonary artery values.hypertension or who are anticoagulated. Valvular damage can occur Mean hemodynamic measurements for pregnant and nonpregnantfrom chronic catheter irritation or during insertion when the catheter patients are presented in Table 57-3. They are paired data from 10balloon is not deﬂated before retrograde movement. healthy subjects, taken between 36 and 38 weeks’ gestation and between CVP monitoring alone should not be considered equivalent to PAC 11 and 13 weeks after delivery.45 Using the noninvasive technique ofmonitoring. Preeclampsia and its complications, such as oliguria M-mode echocardiography, other investigators have demonstratedand pulmonary edema, may prompt central venous access. However, that many of these physiologic alterations in hemodynamics begin inseveral investigators have described poor correlation between the the early phases of pregnancy.46 Position changes late in pregnancycentral venous catheter and PCWP in gravidas with pregnancy-induced signiﬁcantly inﬂuenced central hemodynamic stability. The standinghypertension (Fig. 57-4).43,44 If an accurate assessment of left ventricu- position increased pulse by 50%, left ventricular stroke work index bylar preload is deemed important in the management of the patient’s 21%, and pulmonary vascular resistance by 54%.47 Compared with thecardiovascular complications, insertion of a PAC may be indicated. nonpregnant state, the pregnant state seemed to result in a bufferingWhether this holds true for pregnant women with critically ill disease of orthostatic-related hemodynamic changes. The investigators specu-states other than pregnancy-induced hypertension remains unknown. lated that the increased intravascular volume during pregnancy accounted for this stabilizing effect.Hemodynamic ConsiderationsWith a PAC, the following hemodynamic variables can be directlymeasured in the patient: Hemodynamics of Speciﬁc Conditions during Pregnancy Heart rate (beats/min) CVP (mm Hg) Mitral Valve Stenosis Pulmonary artery systolic and pulmonary artery diastolic Mitral stenosis is the most common rheumatic valvular lesion encoun- pressures (mm Hg) tered in pregnancy (see Chapter 39). When the valve area falls below PCWP (mm Hg) 1.5 cm2, ﬁlling of the left ventricle during diastole is severely limited, CO (L/min) resulting in a ﬁxed CO. Prevention of tachycardia and maintenance of Mixed venous oxygen saturation (%) adequate left ventricular preload is essential in these patients. As the heart rate increases, less time is allowed for the left atrium to ade- By use of a sphygmomanometer or by peripheral artery catheteriza- quately empty and ﬁll the left ventricle during diastole. The left atriumtion, direct measurements of systemic arterial pressures can also be may become overdistended, resulting in dysrhythmias (primarily atrial
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1171 TABLE 57-3 NORMAL CENTRAL HEMODYNAMIC PARAMETERS IN HEALTHY NONPREGNANT AND PREGNANT PATIENTS Hemodynamic Parameter Nonpregnant Values Pregnant Values Cardiac output (L/min) 4.3 ± 0.9 6.2 ± 1.0 Heart rate (beats/min) 71 ± 10 83 ± 10 Systemic vascular resistance (dyne × cm × sec−5) 1530 ± 520 1210 ± 266 Pulmonary vascular resistance (dyne × cm × sec−5) 119 ± 47 78 ± 22 Colloid oncotic pressure (mm Hg) 20.8 ± 1.0 18.0 ± 1.5 Colloid oncotic pressure − pulmonary capillary wedge pressure (mm Hg) 14.5 ± 2.5 10.5 ± 2.7 Mean arterial pressure (mm Hg) 86.4 ± 7.5 90.3 ± 5.8 Pulmonary capillary wedge pressure (mm Hg) 6.3 ± 2.1 7.5 ± 1.8 Central venous pressure (mm Hg) 3.7 ± 2.6 3.6 ± 2.5 Left ventricular stroke work index (g × m × m−2) 41 ± 8 48 ± 6 From Clark SL, Cotton DB, Lee W, et al: Central hemodynamic assessment of normal term pregnancy. Am J Obstet Gynecol 161:1439, 1989.ﬁbrillation, which increases the risk of thromboembolic complica- for patients with primary pulmonary hypertension; mean survival istions) or pulmonary edema. Adequate preload, however, is essential to 2.8 years from the diagnosis. Maternal mortality rates for patients withmaintain left ventricular ﬁlling pressure. Alternatively, if preload pulmonary hypertension have been as high as 50%.48-50 These patientsis excessive, pulmonary edema and atrial dysrhythmias may result. are at increased risk for complications from placement of a PAC.Medical management of these patients involves activity restriction, Pulmonary hypertension may also result from unrepaired congenitaltreatment of dysrhythmias, β-blockers to control heart rate, and careful intracardiac shunts such as a ventricular septal defect, atrial septaldiuretic use. The goal of diuretic therapy is to treat pulmonary edema, defect, or patent ductus arteriosus, which lead to chronic over-with care not to overly reduce left ventricular preload. Adequate anal- perfusion of the pulmonary vasculature. Over time, pulmonary arterialgesia and anesthesia during labor and delivery also reduce excessive pressures may become signiﬁcant enough to reverse the direction ofcardiac demands associated with pain and anxiety. ﬂow across the shunt. This reversal of shunt ﬂow to a right-to-left The other important hemodynamic consideration for patients pattern deﬁnes Eisenmenger syndrome. The estimated maternal mor-with mitral valve stenosis relates to the potential for misinterpretation tality rate for Eisenmenger syndrome is between 30% and 40%.50,51 Inof the invasive monitoring data. Because of the stenotic mitral valve, a review of 73 patients with Eisenmenger syndrome, the overall mor-PCWP readings do not accurately reﬂect left ventricular diastolic tality rate was 36%, which has been essentially unchanged during thepressure. In some instances, very high PCWP values are recorded (and past 2 decades.50are needed to maintain an adequate CO). Overt pulmonary edema is The underlying problem in patients with this condition is obstruc-usually not associated with these high readings. During attempts at tion to right ventricular outﬂow caused by a ﬁxed and elevatedmaintaining a relatively constricted intravascular volume, the CO pulmonary vascular resistance. This can ultimately lead to right-to-leftshould be concomitantly monitored and maintained. For each indi- shunting of deoxygenated blood with resultant hypoxemia. Reductionsvidual patient, optimal PCWP and CO values (i.e., values that maintain in blood return to the heart can decrease right ventricular preload soblood pressure and tissue perfusion) should be determined. that the pulmonary vasculature is further hypoperfused. The resultant hypoxemia has been associated with sudden death. Intrapartum man-Aortic Stenosis agement requires maintenance of a relatively hypervolemic state, andThe major problem encountered with aortic stenosis is the patient’s any interventions that may lead to signiﬁcant reduction in preload orpotential inability to maintain CO because of severe obstruction or in decrease in SVR should be avoided. Placement of a PAC may be quitethe setting of decreasing left ventricular preload (see Chapter 39). challenging in these patients, and many experts believe the risks ofUnlike mitral valve stenosis, aortic valve stenosis requires that attempts placement may outweigh any potential beneﬁt.be made to maintain the patient in a relatively hypervolemic state,although the ﬁxed CO may lead to pulmonary edema. The time sur- Anaphylactoid Syndrome of Pregnancyrounding labor and delivery is particularly risky for these patients. To Anaphylactoid syndrome of pregnancy (i.e., amniotic ﬂuid embolus)maintain an adequate CO, adequate venous return to the heart is is a rare but devastating complication of pregnancy characterized bycrucial. Decreased venous return can result from excess blood loss, acute onset of hypoxia, hypotension or cardiac arrest, and coagulopa-hypotension, and ganglionic blockade from a regional anesthetic or thy occurring during labor, during delivery, or within 30 minutes aftereven vena caval occlusion in the supine position. Pulmonary artery delivery.52,53 This same constellation of ﬁndings may have other causes,catheterization may be indicated in patients with signiﬁcant aortic such as hemorrhage, uterine rupture, or sepsis, and each should bestenosis to accurately estimate intravascular volume and guide ﬂuid excluded before assigning a diagnosis of amniotic ﬂuid embolism. Thereplacement. combination of sudden cardiovascular and respiratory collapse with a coagulopathy is similar to that observed in patients with anaphylacticPulmonary Hypertension or septic shock. In each of these settings, a foreign substance (e.g.,Pulmonary artery hypertension may arise as a primary lesion or result endotoxin) is introduced into the circulation. This initiates a cascadefrom an underlying cardiac abnormality (see Chapter 39). Primary of events resulting in activation and release of mediators such as his-pulmonary hypertension is characterized by an unexplained elevation tamines, thromboxane, and prostaglandins, which lead to dissemi-in pulmonary artery pressures (>25 to 30 mm Hg). Prognosis is grim nated intravascular coagulation (DIC), hypotension, and hypoxia. The
1172 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patientinciting factor is presumed to be present in amniotic ﬂuid that is 120introduced into the maternal circulation, but the precise factor thatinitiates the sequence have not been identiﬁed. It is a commonly held 110misconception that the presence of fetal debris in the pulmonary cir-culation is diagnostic of an amniotic ﬂuid embolus. Fetal debris can 100 Left ventricular stroke work indexbe found in the pulmonary circulation in most normal laboringpatients, and it is identiﬁed only in 78% of patients who meet the 90criteria for the diagnosis of amniotic ﬂuid embolism.52,53 Management of amniotic ﬂuid embolism is entirely supportive. 80 (gm m m 2)Replacement of blood and clotting factors, adequate hydration andblood pressure support, ventilatory support, and invasive cardiac mon- 70itoring in addition to resuscitation efforts usually are required for thesepatients. The data suggest mortality rates approach 61% or higher. 60Most patients do not survive the initial course and die within 5 days.For those who survive, neurologic impairment is common.52 50 40Hypertensive Disorders of PregnancyMost clinical hemodynamic monitoring studies in obstetrics have 30enrolled patients with hypertensive disorders of pregnancy (see Chapter35). From a purely clinical perspective, clear indications for this inva- 0sive technology have not been established. Arguments for its use center 0 5 10 15 20 25 30on reports demonstrating a broad spectrum of hemodynamic ﬁndings Pulmonary capillary wedge pressurein this group of patients. For patients identiﬁed to be relatively hypo- (mm Hg)volemic, optimizing intravascular volume status should improveuteroplacental perfusion, reduce SVR, and blunt hypotensive compli- FIGURE 57-5 Ventricular function in pregnancy-inducedcations associated with conduction anesthesia and antihypertensive hypertensive patients. On plots of ventricular function curves thattherapy. Oliguria (particularly if unresponsive to ﬂuid therapy) and correlate pulmonary capillary wedge pressure with left ventricularrefractory pulmonary edema, both recognized complications of severe stroke work index, most preeclamptic and eclamptic patients fall intopreeclampsia, may also be better deﬁned and managed with invasive a relatively hyperdynamic range. (Combined data from Benedetti TK, Cotton DB, Read JC, et al: Hemodynamic observations in severemonitoring. pre-eclampsia with a ﬂow-directed pulmonary artery catheter. Am J Vasospasm is a central feature of preeclampsia. In one series of 51 Obstet Gynecol 136:465, 1980; Hankins GDV, Wendel GP,untreated preeclamptic patients, an elevated SVR value was identiﬁed Cunningham FG, et al: Longitudinal evaluation of hemodynamicwith invasive monitoring.54 Preeclampsia likely represents an overall changes in eclampsia. Am J Obstet Gynecol 15:506, 1984; Phelanvasoconstrictive condition that is frequently inﬂuenced by underlying JP, Yurth DA: Severe preeclampsia. I. Peripartum hemodynamicdisease processes such as chronic hypertension, duration and severity observations. Am J Obstet Gynecol 144:17, 1982; and Rafferty TD,of illness, and various therapeutic modalities. Berkowitz RL: Hemodynamics in patients with severe toxemia during Using ventricular function curves that correlate PCWP (i.e., left labor and delivery. Am J Obstet Gynecol 138:263, 1980.)ventricular preload) with left ventricular stroke work index (i.e., myo-cardial contractility), investigators found that most preeclamptic andeclamptic patients fall into a relatively hyperdynamic range.55 The nine or fractional excretion of sodium. Although these urinary param-values shown in Figure 57-5 are superimposed on ventricular function eters are routinely used in non-obstetric patients to differentiategraphs derived from nonpregnant subjects. The preeclamptic patient prerenal and renal causes of oliguria, they have proved to be unreliableprobably has at least a normal and probably a somewhat hyperdynamic in patients with preeclampsia. In preeclampsia complicated by oliguria,functioning heart during pregnancy. As expected, this cardiac function, urinary diagnostic indices may suggest a prerenal cause despite normalas estimated by CO, appears to be inversely related to SVR. intravascular volume, demonstrated by invasive pressure measurement Some investigators have recommended that patients with preg- determinations. From a physiologic standpoint, it is postulated that thenancy-induced hypertension be classiﬁed by different hemodynamic kidney misinterprets local renal artery vasospasm to indicate a volume-subsets so that management protocols can be tailored to individual depleted state.needs. Clark and associates56 ﬁrst reported the use of this approach fordealing with the oliguric preeclamptic patient. They found that these Septic Shockpatients had low PCWP values (i.e., hypovolemic) and elevated SVR Septic shock refers to the systemic inﬂammatory response syndrome(i.e., severe vasoconstriction) or were volume replete with normal to associated with infection, persistent hypotension, and major organelevated vascular resistances. A third group had markedly elevated dysfunction despite initial ﬂuid resuscitation.57 Although the hemody-PCWP and SVR readings with depressed cardiac function.56 Manage- namic effects of septic shock have been well described in the non-ment of these groups of oliguric patients varies. In the ﬁrst subset, obstetric literature, limited information is available for obstetricpatients respond favorably to volume expansion therapy. The next two patients. One study described the hemodynamic proﬁles of 10 obstet-groups of patients are best managed with vasodilators and aggressive ric patients at various gestational ages, who were identiﬁed to haveafterload reduction therapy. septic shock and required invasive monitoring. In this small series, SVR Another important issue in the management of oliguric patients and myocardial function were depressed but improved with therapy.58with preeclampsia is the use of standard urinary diagnostic indices, Mabie and coworkers59 described similar ﬁndings in a more recentsuch as urine-to-plasma ratios of osmolality, urea nitrogen, and creati- series of 18 obstetric patients with septic shock. The main hemody-
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1173namic characteristics of those who succumbed to septic shock includedlower blood pressure, stroke volume, and left ventricular stroke workindex than survivors.59 Sepsis and septic shock are addressed in more Respiratory Failuredetail later in this chapter. Substantial anatomic and physiologic changes occur over the course of pregnancy that impact respiratory function (see Chapter 7). Minute ventilation increases in a normal pregnancy and is determined byNoninvasive Hemodynamic respiratory rate and tidal volume. The 40% increase in tidal volumeAssessment (i.e., amount of air exchanged during a cycle of inspiration and expira- tion) primarily drives the increase in minute ventilation. As a result,The PAC is the gold standard for measurement of hemodynamic status the levels of CO2 decline, creating an alkalotic state. To accommodatein the critically ill patient. However, according to available data, use of for the decrease in CO2, the kidneys excrete bicarbonate (HCO3−). Anthe PAC to guide therapy does not favorably affect survival and carries arterial blood gas determination in a normal pregnant woman there-substantial risks. fore reﬂects a slightly increased pH, decreased PCO2, and decreased Transesophageal echocardiography (TEE) has emerged as a nonin- serum HCO3− (i.e., respiratory alkalosis with compensatory metabolicvasive tool for the bedside assessment of the hemodynamic status of acidosis), as outlined in Table 57-5. As the pregnancy progresses,nonpregnant, critically ill adults. In an anesthetized patient, a small increasing abdominal girth leads to an upward displacement of thetransducer is introduced into the esophagus and real-time data diaphragm, widening of the subcostal angle by 50%, and increasedcollected. TEE can accurately measure left ventricular preload, left chest circumference. The end result is a decrease in the functionalventricular ﬁlling pressure, CO, left ventricular ejection fraction, and residual capacity by 20%. The functional residual capacity reﬂects thesevere right ventricular dysfunction.60-62 TEE is often used in hypoten- amount of air remaining in the alveoli at the completion of expiration.sive patients to determine the cause of the hypotension, such as inad- As the functional residual capacity decreases, the alveoli collapse, andequate ﬁlling or depressed contractility (Table 57-4). TEE can detect gas exchange decreases.67other abnormalities, including left ventricular obstruction, structural Common causes for respiratory failure in pregnancy includeabnormalities, proximal pulmonary emboli, and valvular disease. It is pulmonary edema, asthma, infection, and pulmonary embolus.68,69also useful in evaluating the left atrium and mitral valve because of the In a series of 43 gravidas requiring mechanical ventilation whileproximity of these structures to the transducer, and it appears to be undelivered, 86% delivered during the admission, and of these,superior in evaluating congenital cardiac defects. 65% underwent cesarean section, with an associated mortality rate Only a few small series have compared data derived from a PAC of 36% for those delivered by cesarean section. Overall maternalwith two-dimensional transthoracic and Doppler echocardiography in and perinatal mortality rates were high (14% and 11%,obstetric patients. In one report of 12 patients requiring PAC for pre- respectively).68eclampsia management, CO measured by Doppler echocardiography Debate continues about whether delivery improves respiratorycorrelated well with CO assessed by thermodilution using a PAC.63 status in these patients. Tomlinson and coworkers70 described theirAnother study of 16 obstetric patients found good correlation between experience with 10 patients who delivered while mechanically venti-thermodilution assessment of CO and Doppler echocardiography.64 lated. In all but one patient, the cause of respiratory failure was pneu-In a study of 11 critically ill obstetric patients, Belfort and colleagues65 monia.70 The only demonstrable beneﬁt after delivery was a 28%demonstrated no difference between Doppler echocardiographic and reduction in FIO2 in the ensuing 24 hours. The investigators concludedPAC-derived estimation of stroke volume, CO, cardiac index, left ven- that routine delivery of these patients was not recommended. This istricular ﬁlling pressure, pulmonary artery systolic pressure, and right the only study published that was designed speciﬁcally to address thisatrial pressure.65 The data from these reports are encouraging, but question. However, data from other series support the conclusion thatechocardiographic estimation of pulmonary artery pressure was sig- delivery does not uniformly result in signiﬁcant maternal improve-niﬁcantly overestimated in 32% of obstetric patients with suspected ment. Mortality rates after delivery while requiring ventilatory supportpulmonary artery hypertension.66 The technique appears to be well- range from 14% to 58%, and cesarean section may further increase thistolerated, but further study is warranted. risk.68,69,71 TABLE 57-5 CHANGES IN ARTERIAL BLOOD TABLE 57-4 ORIGIN OF HYPOTENSION GAS MEASUREMENTS IN End-Diastolic PREGNANCY Cross-Sectional Area Ejection Fraction Cause Measurements Pregnant Values Nonpregnant Values Decreased >0.8 Hypovolemia pH 7.4-7.46 7.38-7.42 Increased <0.2 Left ventricular failure PCO2 (mm Hg) 26-32 38-45 Normal >0.5 Low SVR or severe MR, PO2 (mm Hg) 75-106 70-100 AR, or VSD HCO3− (mEq/L) 18-21 24-31 O2 saturation (%) 95-100 95-100 AR, aortic regurgitation; MR, mitral regurgitation; SVR, systemic vascular resistance; VSD, ventricular septal defect. Modiﬁed from Dildy G, Clark SL, Phelan JP, et al: Maternal-fetal blood From Cahalan MK: Intraoperative Transesophageal Echocardiography: gas physiology. In Critical Care Obstetrics, 4th ed. New York, An Interactive Text and Atlas. New York, Churchill Livingstone, 1996. Blackwell, 2004.
1174 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient ventilator-associated pneumonia was observed. However, no differenceAcute Respiratory Distress Syndrome in mortality was demonstrated by prone positioning.76 Only one studyAcute respiratory distress syndrome (ARDS) is characterized by rapid has shown a mortality beneﬁt with early and prolonged prone posi-onset of progressive respiratory distress. Evaluation reveals bilateral tioning of ARDS patients. The major difference in this study was thepulmonary inﬁltrates without evidence of cardiac failure or increased length of time patients were maintained prone—on average 17 hourshydrostatic pressure (i.e., PCWP < 18 mm Hg). These patients require daily for a mean of 10 days. The 136 patients were randomized withinhigh concentrations of oxygen and frequently need intubation. ARDS 48 hours of intubation.77is also deﬁned by a diminished ratio of the partial pressure of oxygen Prone positioning can be accomplished manually or with a specialto the fraction of inspired oxygen (PaO2/FIO2 200). If the ratio falls bed designed to rotate the patient. Complications related to pronebetween 200 and 300, acute lung injury is present that is not severe positioning include pressure sores, endotracheal tube displacement orenough to be called ARDS. obstruction, loss of venous access, vomiting, and edema. Data on prone In pregnant women, infections with varicella or herpes simplex ventilation in the pregnant patient are lacking. Anticipated problemsvirus, severe preeclampsia, eclampsia, and hemorrhage most com- include the gravid abdomen and difﬁculties in accomplishing fetalmonly precipitate respiratory failure.68,72 Septic patients are at par- monitoring while prone.ticular risk for developing acute pulmonary injury and ARDS as aconsequence of pulmonary vascular damage that facilitates the leakageof intravascular ﬂuid into the pulmonary interstitial spaces. Mortality Pulmonary Edemarates are quite high, and patients who survive often have pulmonary Pregnant women are predisposed to developing pulmonary edema forfunction compromised by ﬁbrosis and scarring of pulmonary tissue. various reasons, including increased plasma volume and CO in con- The treatment of ARDS focuses on identifying and treating under- junction with decreased colloid oncotic pressure (COP), which occurslying causes such as infection and then providing respiratory, hemo- normally over the course of pregnancy. Alterations in the balance ofdynamic, and nutritional support to facilitate lung healing. Respiratory hydrostatic and oncotic pressure between the pulmonary vessels andsupport may precipitate additional lung injury, and efforts to maintain the interstitial spaces can lead to an egress of ﬂuid from the vascularadequate oxygen delivery should also minimize lung trauma in an space into the interstitium and manifest clinically as pulmonary edema.effort to facilitate healing of the lungs. Approximately 1 in 1000 pregnancies is complicated by pulmonary Management of respiratory failure in nonpregnant, critically ill edema. In a review of almost 63,000 pregnancies, Sciscione andpatients has historically used a goal of maintaining a tidal volume of coworkers78 reported pulmonary edema occurring most often during10 to 15 mL/kg. In ARDS, high tidal volumes may lead to alveolar the antepartum period (47%), with 39% occurring in the postpartumoverdistention or repeated recruitment and collapse of alveoli, predis- period and the remaining 14% in the intrapartum period.78 In thisposing to alveolar damage and release of inﬂammatory mediators that series, the two most common attributable causes of pulmonary edemaworsen pulmonary damage. In 2000, the ARDSNet published results were cardiac disease and tocolytic use (25.5% each). The remainingof 861 patients with ARDS randomized to traditional tidal volumes cases of pulmonary edema were caused by ﬂuid overload (21.5%) and(12 mL/kg) or to a low tidal volume of 6 mL/kg.73 The traditional tidal preeclampsia (18%). The management of patients with pulmonaryvolume group also maintained a goal of 50 cm of H2O or less, com- edema is focused on establishing the diagnosis, determining the cause,pared with lower peak pressures of 30 cm of H2O in the low tidal and improving oxygenation.volume group. Low tidal volumes and lower peak pressures were asso-ciated with lower mortality rates (31% versus 40%) and shorter periodsof intubation compared with conventional tidal volumes and peak Colloid Oncotic Pressurepressure goals. Increased tidal volume and other normal changes in Abnormalitiespulmonary physiology may affect the utility of this approach in preg- Four forces affect ﬂuid balance between vascular and interstitial spaces.nant women. The COP is the force exerted primarily by albumin and other proteins within the capillary, which holds ﬂuid within the vascular space. The oncotic pressure within the interstitial space also works to hold ﬂuidProne Ventilation in the interstitium. Hydrostatic forces within the vessel and the inter-Mechanical ventilation in the prone position has improved oxygen- stitium exert the opposite effect.ation in up to 80% of patients with ARDS and acute lung injury. COP decreases over the course of pregnancy, and by term, itApproximately 50% of patients maintain improved oxygenation after approximates 22 mm Hg.79 This is approximately 3 mm Hg lower thanthey return to the supine position.74 Mechanical ventilation in the pre-pregnancy values as a result of the dilutional effect from plasmaprone position is believed to achieve several beneﬁcial physiologic expansion. An isolated decrease in oncotic pressure, as may occur inchanges: improved aeration of well-perfused dorsal atelectatic lung pregnancy or in patients with nephrotic syndrome, is usually wellareas, improved alveolar recruitment, relief of cardiac compression on compensated and does not lead to pulmonary edema unless compli-the lung posteriorly, and improved mobilization of secretions. cated by additional factors such as increased intravascular pressure or Several randomized trials have compared supine with prone posi- pulmonary injury resulting in vascular permeability.80 Excessive intra-tioning in nonpregnant patients with ARDS and acute lung injury. In venous ﬂuids, blood loss, decreasing COP after delivery, and the post-one randomized trial of 304 patients, prone positioning maintained partum autotransfusion effect can place patients at further increasedfor an average of 7 hours daily was not associated with a decrease in risk for pulmonary edema.mortality, but signiﬁcant improvement in oxygenation was observedin 70% of patients, with most of the beneﬁt occurring in the ﬁrst hourof prone positioning.75 Another multicenter, randomized trial of Hydrostatic or Cardiogenic791 patients with hypoxemic respiratory failure with multiple causes, Pulmonary Edemaincluding ARDS, found similar results. In addition to improved oxy- Pulmonary edema due to primary cardiac issues with or without alter-genation with prone positioning at least 6 hours daily, a decrease in ations in COP is referred to as hydrostatic or cardiogenic pulmonary
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1175edema. CO is controlled through continuous adjustments in heart states and neurogenic shock. In obstetric patients, shock mostrate and stroke volume. At some point, the heart is no longer able commonly results from hemorrhage and sepsis. Regardless of theto increase the CO in response to increasing preload because of intrin- cause, therapy is directed at restoring tissue oxygenation by eliminatingsic cardiac abnormalities or excessive ﬂuid administration, resulting in the originating cause, providing adequate volume replacement, andoverload. If left ventricular outﬂow is restricted, blood intended to improving cardiac function and circulation. Difﬁculty in reversing thisempty into the left atrium remains in the pulmonary vasculature, phenomenon explains the high mortality rates for patients withwhich is reﬂected by the increased PCWP, left ventricular end-diastolic shock.pressure, and pulmonary artery pressure. The net result is an increasein the pulmonary intravascular hydrostatic pressure. When this pres-sure exceeds the interstitial pressures, ﬂuid is forced out of the pulmo- Sepsis and Septic Shocknary vasculature into the interstitial spaces, resulting in pulmonaryedema. Incidence and Mortality A transthoracic or transesophageal echocardiogram can distinguish Sepsis accounts for 9.3% of deaths occurring in the United States andwhether pulmonary edema is cardiogenic in origin. Evidence of poor complicates approximately 1 in 8000 deliveries.86 Fortunately, only aventricular systolic function is identiﬁed by a decreased ejection frac- small percentage of these deaths can be attributed to gynecologic ortion, as seen in patients with a cardiomyopathy. Echocardiography may obstetric problems. Bacteremia is not uncommon in obstetric pati-also identify valvular abnormalities that may lead to compromised ents, but these patients appear to be less likely to progress to septiccardiac function and predispose patients to pulmonary edema, such as shock.59,87,88 An epidemiologic review of sepsis in the United Statesaortic or mitral stenosis. gathered discharge data on more than 10 million cases of sepsis over a 22-year period ending in 2000.89 According to this study, the inci- dence of sepsis in the population is increasing at a rate of 8.7% annu-Pulmonary Edema in the Setting ally. However, the percentage of pregnant women diagnosed withof Preeclampsia sepsis in that period decreased by 50%, from 0.6% to 0.3%. AfricanPulmonary edema develops in approximately 2.5% of patients with Americans and men appear to be at higher risk for developing sepsis,preeclampsia, most commonly in the postpartum period.43,81,82 The but mortality rates did not appear to differ from those of whites andcause is not completely understood, but it likely results from a combi- women, respectively.nation of problems. Impaired left ventricular function may be a result Mortality rates overall have declined signiﬁcantly to approximatelyof chronic hypertension, particularly if it develops in the antepartum 17%, but the marked increase in sepsis diagnosis in the populationperiod. Substantially increased SVR may also impair left accounts for tripling of the rate of hospital death from sepsis. Betweenventricular function and lead to pulmonary edema, especially in the 1987 and 1997, infectious causes accounted for 13% of maternalsetting of iatrogenic ﬂuid overload. Preeclamptic patients often lose deaths.10,11 Mortality rates associated with septic shock in pregnancysigniﬁcant amounts of albumin through the urine and exhibit decreased are uncertain and are derived primarily from older, small series ofalbumin production, both of which can lower the COP. In preeclamp- cases, but they generally appear to be much lower than for the non-tic patients, the COP can decrease to 18 mm Hg by term and drop pregnant population. Estimates range from 12% to 28% for obstetricfurther after delivery to 14 mm Hg.43 Endothelial damage also leads to septic patients58,59,87,90 to 40% to 80% for the nongravid population.91increased capillary permeability. Preeclamptic patients with pulmo- Improved outcomes for pregnant patients have been attributed to anary edema that fails to respond to oxygen, diuresis, and ﬂuid restric- younger patient population, type of organisms, sites of infection moretion, especially when combined with oliguria, may require pulmonary easily accessed and treated, and lower rates of coexistent diseases.artery catheterization to guide further therapy. In a series of 10 patientswith severe preeclampsia who underwent placement of a PAC, the Deﬁnitionsﬁndings varied. Five patients demonstrated a decreased gradient The American College of Chest Physicians and the Society of Criticalbetween the COP and PCWP, but two patients had a cardiac explana- Care Medicine published consensus guidelines in 1991 that weretion for the pulmonary edema, and three patients had increased pul- designed to create consistency in the deﬁnitions used to describe septicmonary vascular permeability.83 conditions. Updated guidelines were published in 2003.57 These deﬁni- tions represent the understanding that these conditions exist along a continuum of increasing severity while sharing a common patho-Tocolytic-Induced Pulmonary Edema physiology. This continuum begins after the body develops a systemicIn the past, the use of parenteral β-agonists such as terbutaline and response to an infection and may progress to multiorgan dysfunctionritodrine was more common and became associated with the develop- with hemodynamic instability and even death.ment of pulmonary edema.78,84 However, as the use of intravenous The later classiﬁcation system questions the utility of the diagnosisβ-agonists for tocolysis has decreased, the incidence of pulmonary of systemic inﬂammatory response syndrome (SIRS), suggesting thatedema related to tocolytic use appears to have diminished. Magne- the criteria previously set forth are too sensitive and nonspeciﬁc. SIRSsium does not appear to independently increase the risk of pulmo- was deﬁned as the clinical response to infection manifested by twonary edema.85 or more of the following: temperature of 38° C or higher or 36° C or lower; pulse of 90 beats/min or higher; respiration rate of 20 breaths/ min or higher or a PaCO2 less than 32 mm/Hg; or a white blood cellShock count of 12,000 or more or 4000 or less or more than 10% immature neutrophils. When SIRS criteria are met and infection is conﬁrmed orShock is the physiologic response to impaired tissue oxygenation. suspected, the patient is then considered to be septic. The latest guide-Oxygen deﬁciency at the cellular level may result from inadequate lines expanded on this concept in the deﬁnitions (Table 57-6). Thesedelivery of oxygen, such as in hypovolemic states, cardiac failure, and deﬁnitions do not take into account the physiologic changes of preg-hemorrhage or from improper uptake or use of oxygen, as in septic nancy and therefore may overdiagnose sepsis.
1176 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient TABLE 57-6 DIAGNOSTIC CRITERIA OF SEPSIS summarized in Table 57-7. The initial phase is characterized by vaso- SYNDROMES dilation, increased capillary permeability, and endothelial damage. Clinically, the patient may have evidence of infection or fever and may Condition Deﬁnition have positive blood cultures. Peripheral vasodilation causes ﬂushing and warm extremities. It also leads to a decrease in blood pressure with Infection Pathologic process caused by the invasion of diminished cardiac preload, which leads to a tachycardic response in normally sterile tissue or ﬂuid or body cavity by pathogenic or potentially pathogenic an effort to maintain or increase the CO. Initial laboratory ﬁndings microorganisms vary. An elevated white blood cell count may be followed by neutro- Bacteremia Presence of bacteria in the bloodstream penia. Hyperglycemia is typical as a result of altered adrenal respon- Sepsis Systemic inﬂammation accompanied by infection siveness, insulin resistance, and increased levels of catecholamines and Severe sepsis Sepsis complicated by major organ dysfunction cortisol. Septic shock Persistent unexplained arterial hypotension in the If uninterrupted, sepsis progresses and is characterized by intense setting of severe sepsis vasoconstriction. This leads to poor perfusion, which is manifested by cool extremities and altered organ function as a result of inadequate Data from Levy MM, Fink MP, Marshall JC, et al: 2001 SCCM/ESICM/ ACCP/ATS/SIS International Sepsis Deﬁnitions Conference. Crit Care oxygenation (i.e., cold shock). Oliguria is typical, as are respiratory Med 31:1250-1256, 2003. failure and ARDS. The CO decreases as a result of inadequate venous return and increasing peripheral resistance. In the advanced stages of septic shock (i.e., secondary or irreversible shock), symptoms progress Gram-positive organisms have surpassed gram-negative organisms and reﬂect the global effects of inadequate tissue perfusion and oxy-as the most common cause of sepsis in the general population, unlike genation: hypotension, respiratory failure, renal failure, DIC, myocar-the situation for pregnant patients. Common organisms isolated from dial depression, electrolyte disturbances, obtundation, and metabolicpregnant patients in septic shock include Escherichia coli, groups A and acidosis.B streptococci, Klebsiella species, and Staphylococcus aureus.59 Thesource of infection in pregnant women is typically the genitourinary Managementtract and includes lower urinary tract infections, pyelonephritis, cho- If the patient is at a viable gestational age and is undelivered with evi-rioamnionitis, endometritis, and rarely, septic abortion, necrotizing dence of sepsis or septic shock, the fetal status should be monitoredfasciitis, and toxic shock syndrome.58,59,87,88,92 closely with continuous fetal heart rate monitoring and ultrasound evaluation to estimate fetal weight, assess amniotic ﬂuid volume,Pathophysiology of Sepsis and conﬁrm gestational age. Uterine perfusion and oxygenation areSepsis is a complex phenomenon that originates with invasion of the adversely affected as the sepsis progresses. Contractions are oftenhost by an offending organism. After infection, macrophages are encountered, possibly as a result of decreased uterine perfusion andrecruited, bind to the organism, and initiate a collection of responses decreased oxygen delivery to the myometrium. Tocolysis should beresulting in the activation of the inﬂammatory and coagulation cas- undertaken with caution because the side effects of the medicationscades. Initially, the sepsis response was postulated to be the result (e.g., tachycardia, vasodilation) may impair physiologic adaptations toof an exaggerated inﬂammatory response. Initial pharmacologic sepsis. If maternal status can be corrected and fetal status remainsapproaches therefore targeted suppression of the inﬂammation process, reassuring, delivery can be avoided. The decision about whether toincluding corticosteroids and agents to block cytokines such as proceed with delivery may be challenging, particularly if maternaltumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β).93 These status is deteriorating. The fetus may not tolerate labor because of poorapproaches have been largely unsuccessful, a testament to the uterine perfusion and maternal hypoxemia; conversely, the mothercomplexity of the sepsis syndromes. The roles of anti-inﬂammatory may be too unstable to safely undergo a surgical procedure. If themediators and genetics in the sepsis cascade has been increasingly source of infection is the uterus, as in septic abortion or chorioamnio-appreciated.94 Activation of the inﬂammatory cascade after infection nitis, evacuation of the uterus is necessary.causes release of interleukins, tumor necrosis factors, interferons, pros- Sepsis management has several goals:taglandins, platelet-activation factor, oxygen free radicals, nitric oxide,complement, and ﬁbrinolysins.95 Identiﬁcation of the source of infection Hemostatic mechanisms are also affected in severe sepsis. Initiation Institution of empiric antibiotic therapyof the clotting cascade results from macrophages and monocytes Early, aggressive improvement in circulating volumeinvolved in production of inﬂammatory mediators. Endothelial damage Optimization of hemodynamic performancealso contributes to the procoagulant effect, causing platelet activation Maintenance of oxygenationand suppression of protein C activity. These derangements in the Volume resuscitationhemostatic balance lead to clotting factor consumption, ﬁbrin deposi-tion, thrombin generation, and decreased platelet levels.96 The resultant Aggressive ﬂuid replacement to improve circulating intravascularmicrothrombi are thought to negatively affect end-organ damage and volume is a mainstay of sepsis management and has improved CO,contribute to the clinical features of severe sepsis and septic shock, such oxygen delivery, and survival. Studies have demonstrated a survivalas oliguria, ARDS, and hepatic dysfunction. In severe cases, consump- beneﬁt for patients with septic shock managed with protocol-driven,tion of clotting factors is substantial enough to cause hemorrhagic early, aggressive volume resuscitation. Early goal-directed therapycomplications from DIC. Figure 57-6 outlines the sepsis cascade. (EGDT) involves tailoring treatments and resuscitative efforts to achieve speciﬁed endpoints, which include normal mixed venousClinical Manifestations oxygen saturation, arterial lactate concentration, base deﬁcit, and pHSeptic shock has been classiﬁed as three progressive clinical stages: in an effort to reduce end-organ dysfunction and ultimately reducewarm shock, cold shock, and irreversible (secondary) shock, which are mortality.
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1177 Bacterial products and components Macrophage TNF-a Activation of coagulation IL-1 and complement system IL-6 Tissue factor release PAF Fibrinolytic activity NO etc. Neutrophil activation, Platelet activation, Metabolism of T-cell release of aggregation, aggregation arachidonic acid IL-2, INF-g, degranulation Release of GM-CSF Release of O2 radicals thromboxane A, and proteases PGS, LTS Endothelial damage Tissue injury Organ dysfunction FIGURE 57-6 The sepsis cascade. Hemostatic mechanisms are affected in patients with severe sepsis, and derangements in the hemostatic balance lead to clotting factor consumption, ﬁbrin deposition, thrombin generation, decreased platelets, tissue injury, and organ dysfunction. GM-CSF, granulocyte-macrophage colony-stimulating factor; IL, interleukin; LTS, leukotrienes; NO, nitric oxide; PAF, platelet-activating factor; PGS, prostaglandin synthesis; TNF-α, tumor necrosis factor α. (Modiﬁed from Bone RC: The pathogenesis of sepsis. Ann Intern Med 115:457-469, 1991.) TABLE 57-7 STAGES OF SHOCK Warm (Early) Shock Cold (Late) Shock Secondary (Irreversible) Shock Flushing Cyanosis Renal failure Warm extremities Cool extremities Disseminated intravascular coagulopathy Rapid capillary reﬁll Delayed capillary reﬁll Myocardial failure Decreased mental status Increased vascular resistance Refractory hypotension Hypotension Decreased cardiac output Obtundation Increased cardiac output Respiratory failure or adult respiratory distress syndrome Tachycardia Oliguria Tachypnea In 2001, Rivers and colleagues97 published the results of a prospec- 12 mm Hg. The volume of ﬂuid administered to both groups oftive, randomized trial of EGDT compared with standard therapy for patients was similar in the ﬁrst 72 hours (>13 L), but the EGDT grouppatients in septic shock in a single institution. Therapy for patients received more volume in the initial 6 hours of therapy (5 versusin the EGDT group was initiated in the emergency room setting 3.5 L). This aggressive approach decreased the mortality rate by 16%before transfer to the intensive care unit and included placement (30.5% versus 46.5%).of central venous catheters with the ability to measure continuous Clinicians have questioned whether modiﬁcation of this protocol,venous oxygen saturation (SCvO2). An elevated SCvO2 value reﬂects particularly elimination of continuous venous oxygen saturationinadequate perfusion and uptake of oxygen in the tissues. Red blood (SCvO2), could produce similar results. In 2006, Lin and coworkers98cell transfusions were administered to maintain the hematocrit at randomized patients to EGDT without measurement of SCvO2 and30% or higher, and inotropic agents were added if the SCvO2 level was conﬁrmed survival beneﬁt. Patients randomized to receive modiﬁedinadequately corrected (<70%). The protocol called for a 500-mL EGDT were signiﬁcantly less likely to die (71.6% versus 53.7%), spentcrystalloid bolus every 30 minutes until the CVP reached 8 to fewer days in the hospital, were intubated for a shorter time, and were
1178 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patientat less risk for developing sepsis-associated central nervous system and infection are the uterus and genitourinary tract, and gram-negativerenal dysfunction compared with controls. bacteria constitute the primary organisms. In the non-obstetric popu- Because of the encouraging survival and morbidity data, EGDT is lation, gram-positive organisms represent most of the organisms iso-being widely adopted in the management of severe sepsis, but it remains lated in septic patients, followed closely by gram-negative bacteria.89to be conﬁrmed whether this approach will produce similarly improved Cultures should be collected from blood and any suspected site, includ-outcomes in a pregnant population. The precise goals to appropriately ing the uterus if necessary, for identiﬁcation of the organism andguide therapy in a pregnant population also must be deﬁned. determination of antibiotic sensitivities. Empiric antimicrobial therapy targeted at the suspected organism should not be delayed pendingOptimization of Hemodynamic Performance culture results.100-103In addition to replacing intravascular volume to improve perfusion In an obstetric and postpartum population, antibiotic coverageand cardiac preload, early pharmacologic interventions to improve usually consists of β-lactam antibiotics (i.e., penicillins, cephalospo-vascular tone, cardiac contractility, and cardiac preload confer a rins, carbapenems, and monobactams) with or without an aminogly-considerable survival advantage.97,98 If the patient fails to respond coside (see Chapter 38). Monotherapy with a carbapenem or third- orappropriately to aggressive ﬂuid resuscitation efforts, vasopressors are fourth-generation cephalosporin is as effective as a β-lactam antibioticindicated to improve vascular tone, resulting in improved cardiac in combination with an aminoglycoside in non-neutropenic patientsreturn and CO, peripheral perfusion, and oxygen delivery. In the initial with severe sepsis.104 In undelivered patients, tetracycline derivativespublication on EGDT, the requirement for vasopressors was signiﬁ- and quinolones should be avoided. When culture results become avail-cantly diminished by early, aggressive ﬂuid resuscitation (37% versus able, antibiotic therapy can be adjusted if necessary.51%), but there was no difference in the requirement for inotropic After appropriate antibiotic therapy has been initiated and theagents between the two groups (9% versus 15%).97 In this study, vaso- process of stabilization of the patient has begun, attention should bepressors were initiated to maintain mean arterial pressure above directed to source control. This entails removal of indwelling lines and65 mm Hg. Use of a similar protocol minimized the delay in initiation catheters, with replacement if necessary. Indications for more aggres-of vasopressors and reduce mortality.98 sive surgical approaches are less clearly deﬁned. Generally, more inva- Dopamine hydrochloride is the most commonly employed ﬁrst- sive surgical approaches are not emergent and can be accomplishedline vasopressor in the intensive care setting. Dopamine’s α- and β- after the condition of the patient has stabilized.105 Exceptions are infec-adrenergic effects are dose dependent. Low doses (<10 μg/kg/min) tions involving clostridia and group A streptococci, such as necrotizingimprove myocardial contractility, CO, and renal perfusion without fasciitis. In this scenario, delay in excision of affected tissues can havenegatively affecting myocardial oxygen consumption. As the dose a dramatic negative effect on the patient’s condition.106 Evaluation ofincreases (>20 mg/kg/min), α-adrenergic effects predominate, result- the abdomen by ultrasound or computed tomography (CT) can assisting in increasing SVR in addition to increased CO. In a viable gestation in identiﬁcation of an intra-abdominal abscess. When drainage of anrequiring vasopressor support, fetal monitoring is essential because intra-abdominal abscess is necessary, the percutaneous approach isdopamine has decreased uterine perfusion in an animal model.99 preferable. In obstetric conditions, evacuation of the uterus by suctionDobutamine is similar to dopamine, but it has primarily β1-adrenergic curettage in septic abortion or delivery of the neonate in viable gesta-effects. Dobutamine therefore improves CO with minimal impact on tions should occur after initiation of antibiotics and stabilization ofheart rate or vascular resistance. In the EGDT protocol, dobutamine the patient. Postpartum hysterectomy may be necessary if the patientwas used to improve oxygen consumption in patients who failed to fails to respond to antibiotics and the uterus is the suspected source.respond to ﬂuid resuscitation, dopamine infusion to improve meanarterial pressure, and red cell transfusion to correct anemia.97 Table Adjunctive Therapies in Sepsis Management57-8 lists other commonly used vasopressor agents for the manage- INSULIN THERAPYment of severe sepsis and septic shock. In the critically ill population, hyperglycemia is a common phe- nomenon attributable to insulin resistance and escalations in glucagon,Source Control and Antimicrobial Therapy cortisol, and catecholamine levels, which promote glycogenolysis andPrompt identiﬁcation of the probable source of infection is essential gluconeogenesis.107 In 2001, Van den Berghe and colleagues108 pub-to initiate appropriate antimicrobial therapy and improve outcomes lished a large, prospective, randomized trial that demonstrated thatfor septic patients. In an obstetric population, common sources of tight glycemic control (blood glucose level of 80 to 110 mg/dL) in critically ill patients decreased overall mortality by 34%. Septic patients exhibited an even more impressive 76% reduction in mortality as a TABLE 57-8 INOTROPIC DRUGS FOR result of aggressive euglycemia with insulin therapy.108 Other signiﬁ- MANAGEMENT OF SHOCK cant beneﬁts of tight glycemic control included fewer ventilator days, less time in the ICU, decrease risk for developing septicemia, and a Agent Dose Hemodynamic Effect reduced need for dialysis. Dopamine Pregnant women demonstrate insulin resistance and to have higher Low dose <10 μg/kg/min ↑ CO, vasodilation of renal circulating insulin levels than their nonpregnant counterparts. They arteries are also predisposed to developing fasting hypoglycemia because of High dose 10-20 μg/kg/min ↑ CO, ↑ SVR higher levels of insulin and continuous delivery of glucose to the fetus. Dobutamine 2.5-15 μg/kg/min ↑ CO, ↓ SVR or ↑ SVR However, the impact of aggressive euglycemia in the critically ill preg- Phenylephrine 40-180 μg/min ↑ SVR nant patient remains to be studied. Norepinephrine 2-12 μg/min ↑ CO, ↑ SVR Isoproterenol 0.5-5 μg/min ↓ CO, ↑ SVR CORTICOSTEROIDS CO, cardiac output; SVR, systemic vascular resistance; ≠, increase; Ø, Empiric administration of corticosteroids in high doses does not decrease. improve survival of unselected septic patients and may worsen out-
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1179comes because of secondary infection.109,110 However, as the patho- trial, a multicenter, randomized trial, APC administration to patientsphysiology of sepsis has become more clearly understood, the in septic shock decreased the 28-day mortality rate from 30.8% in thecontribution of relative adrenal insufﬁciency in critically ill patients placebo group to 24.7% (P = .005) in the study group. This representsand the potential beneﬁt of lower-dose, selective corticosteroid replace- a 6.1% absolute reduction in overall mortality due to septic shock andment have reemerged. a 13% reduction in the groups with the highest predicted mortality Stresses such as pain, fever, hypovolemia, or severe illness normally based on APACHE II scores.120 A subsequent single-arm trial (Extendedstimulate marked increases in cortisol levels. In the patient with septic Evaluation of Recombinant Human Activated Protein C [ENHANCE]shock, the adrenal gland may not respond to adrenocorticotropic trial) using APC in severe sepsis patients demonstrated a mortality ratehormone (ACTH) stimulus appropriately and fail to mount adequate (25.3%) similar to that seen in the PROWESS trial (24.7%). Patientscorticosteroid production. In the setting of septic shock, however, the who received the therapy in the ﬁrst 24 hours after diagnosis of majorlevels of cortisol may be increased overall, but the magnitude of organ dysfunction had the lowest mortality rate (22.9%).121increase after ACTH administration may be blunted. This phenome- The most signiﬁcant complication resulting from the use of APCnon is described as relative adrenal insufﬁciency.111,112 This group of is hemorrhage. In the PROWESS trial, 3.5% of patients receivingpatients is being evaluated for potential beneﬁt from lower doses of APC suffered a signiﬁcant hemorrhagic event such as intracranialcorticosteroids. A randomized trial conducted by Annane and col- hemorrhage or need for transfusion, compared with a 2% incidenceleagues113 demonstrated a survival beneﬁt (mortality rate of 37% versus in the control group. The risk of bleeding appears to be greatest during47% for controls) for patients with septic shock treated with low-dose the infusion period, because APC has a very short half-life. Because ofhydrocortisone and ﬂudrocortisone. Patients who had documented this risk, APC is not indicated for all patients with septic shock, andblunted adrenal responsiveness also beneﬁted from a reduced need for its use should be limited to patients with greatest risk of mortality (i.e.,vasopressor support. All of these patients had elevated baseline cortisol APACHE II scores 25 and one major organ dysfunction). APC islevels. A 2004 meta-analysis of 16 trials that included more than 2000 contraindicated if the risk of bleeding is increased (i.e., active internalpatients suggested similar beneﬁt from lower-dose steroid replace- bleeding, hemorrhagic stroke in the preceding 3 months, intracranialment in patients with severe sepsis and septic shock.114 Steroids did not or intraspinal surgery, severe head trauma in the preceding 2 months,appear to confer a mortality beneﬁt when all data were included. trauma, or epidural catheter). The role of APC in managing obstetricHowever, inclusion of only studies utilizing low-dose (300 mg of patients has not been established. Signiﬁcant changes in the coagula-hydrocortisone or an equivalent), longer-duration (5 to 11 days) tion cascade occur, including elevated factor VIII levels. The impact oftherapy did demonstrate a decrease in overall mortality rates. The these changes on the responsiveness to APC is unknown; however,investigators recommended initiation of low-dose glucocorticoid pregnancy is not a contraindication to its use.replacement in septic patients with blunted adrenal responsivenessconﬁrmed by an ACTH stimulation test. The degree of adrenal suppression in pregnant or postpartum Hemorrhagic Shockseptic shock patients and the effect of low-dose steroids on outcomesin this population are unknown. If the patient remains undelivered, Incidence and Etiologycare should be taken in the choice of corticosteroids. Betamethasone Obstetric hemorrhage is the leading cause of maternal death after anand dexamethasone cross the placenta and have improved neonatal intrauterine gestation. The overall incidence of maternal death fromoutcomes for premature infants. However, both can negatively impact hemorrhage is 1.4 per 100,000 live births. When ectopic gestations areneonatal outcomes when administered in large doses.115 excluded, placental abruption is the most common cause of death (18.5%).122 The cause of hemorrhage varies by pregnancy outcome; ACTIVATED PROTEIN C THERAPY FOR maternal deaths after a live birth are most likely associated with post-SEVERE SEPSIS partum hemorrhage. Stillbirths are most likely to be associated with One of the pathophysiologic mechanisms thought to contribute to death from placental abruption, and undelivered pregnancies occurmorbidity and mortality in sepsis patients is inappropriate activation most often with lacerations or uterine ruptures.122 A signiﬁcant increaseof the coagulation system. As a result, many trials have been performed in risk of death from hemorrhage is seen in nonwhite women and withinvolving various antithrombotic agents, including antithrombin III advancing age. In an analysis of maternal morbidity and mortality,and tissue factor-pathway inhibitor, without successfully identifying a hemorrhage accounted for 39% of near-miss morbidities. The inves-treatment to reduce mortality among septic shock patients.116 In con- tigators estimated that 46% of these near-miss events were preventabletrast, activated protein C (APC, drotrecogin alfa) has been approved and were related to communication issues, policies and procedures,by the U.S. Food and Drug Administration (FDA) for use in severely failure to identify high-risk status, failure to transfer to a higher levelseptic patients at high risk for death as evidenced by an APACHE II of care, or inappropriate care. The presence of a signiﬁcant diseasescore greater than 25. state, such as preeclampsia, was also a contributor.123 Patients with severe sepsis have an acquired deﬁciency of protein C Causes of obstetric hemorrhage associated with an intrauterineand are limited in their ability to convert protein C to its active form. gestation include placental abruption or previa, uterine rupture, surgi-These low protein C levels have been associated with poorer outcomes cal lacerations, invasive placentation, uterine inversion, and postpar-for severe sepsis patients.117,118 APC is believed to mediate the effects of tum hemorrhage, usually caused by atony or retained products ofsevere sepsis in several ways. APC stimulates ﬁbrinolysis and inacti- conception. The source of hemorrhage can usually be determined byvates factors Va and VIIIa, resulting in inhibition of thrombin forma- assessment of the patient. Concealed hemorrhage (e.g., abruption, livertion.94,119 Decreased thrombin formation then leads to decreased capsule rupture in HELLP syndrome) is also possible and should beinﬂammation by inhibiting platelet activation, neutrophil recruitment, considered in a patient with evidence of shock and no obvious sourceand mast cell degranulation. Two trials have evaluated APC’s effect on of hemorrhage.mortality in patients with severe sepsis. In the Recombinant Human Obstetric hemorrhage has been arbitrarily deﬁned as an estimatedActivated Protein C Worldwide Evaluation in Severe Sepsis (PROWESS) blood loss of more than 500 mL in a vaginal delivery and greater than
1180 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient TABLE 57-9 CLINICAL STAGING OF HEMORRHAGIC SHOCK BY VOLUME OF BLOOD LOSS Severity of Shock Findings Blood Loss (%) Volume (mL)* None None Up to 20 Up to 900 Mild Tachycardia (<100 beats/min) 20-25 1200-1500 Mild hypotension Peripheral vasoconstriction Moderate Tachycardia (100-120 beats/min) 30-35 1800-2100 Hypotension (80-100 mm Hg) Restlessness Oliguria Severe Tachycardia (>120 beats/min) >35 >2400 Hypotension (<60 mm Hg) Altered consciousness Anuria *Based on an average blood volume of 6000 mL at 30 weeks’ gestation.1000 mL for cesarean section.124 Other deﬁnitions describe a decrease TABLE 57-10 COLLOID INFUSIONSin the hematocrit by 10% or the need for transfusion.125 However,estimates of blood loss are inaccurate and can vary widely. The true Crystalloid Volume Estimatedincidence of obstetric hemorrhagic shock is unknown. Expansion Duration of Colloid Dose (mL) Equivalent Effect (hr)Clinical Staging of Hemorrhage AlbuminBecause of the normal blood volume expansion in pregnancy, clinical 5% solution 500-700 Similar to crystalloid 24evidence of hypovolemia becomes evident much later than expected. 25% solution 100-200 3.5 times crystalloid 24Relatively minor symptoms such as orthostatic hypotension and tachy- Hetastarch 500-1000 Similar to crystalloid 24-36cardia typically do not appear until at least 20% to 25% of the blood Dextran (70) 500 1050 mL over 2 hours 24volume is lost. Table 57-9 outlines the clinical staging of hemorrhagicshock, depending on severity.Management resuscitation may destabilize clot formation and stability, worsenThe goal of management of hemorrhagic shock is to identify and hypothermia, and contribute to hemodilution without providing thecontrol the bleeding source while restoring circulating blood volume expected beneﬁt in survival. Some physicians recommend resuscita-and clotting factors. Baseline laboratory evaluation is recommended tion to allow for permissive hypotension (i.e., systolic blood pressureon recognition of the hemorrhage and should include a complete >80 mm Hg).127blood cell count, blood type and crossmatch, ﬁbrinogen level, pro-thrombin time (international normalized ratio), and activated partial COLLOID SOLUTIONSthromboplastin time. A basic metabolic panel is potentially useful to Colloid solutions are intravenous ﬂuids containing particles largerassess renal function and electrolyte disturbances. These laboratory than 10,000 daltons. Packed red cells are considered a colloid, but thistests should be repeated at regular intervals until the situation is discussion focuses on additional colloid products. The major advan-resolved. The Lee-White whole-blood clotting time test can be used as tage provided by a colloid solution is the signiﬁcant increase in plasmaa crude method to assess for the presence of DIC. Whole blood is col- volume compared with a crystalloid solution. Colloid solutions increaselected in an unheparinized tube and observed. A stable clot should intravascular COP and draw ﬂuid into the intravascular space. Inform between 5 and 15 minutes. achieving this effect, extravascular volume can become depleted, and ﬂuid resuscitation should include adequate administration of crystal- VOLUME REPLACEMENT THERAPY loids. The degree of plasma expansion depends on the availability of Adequate and timely replacement of circulating volume is essential extravascular ﬂuid. In certain clinical settings such as sepsis, surgicalin the management of hemorrhagic shock. This is accomplished by trauma, or preeclampsia, vascular permeability is altered, and colloidadministering crystalloid solutions such as normal saline or colloids solutions can escape into extravascular spaces, particularly the lungs,such as albumin or blood products. Controversy exists about the most and lead to pulmonary edema. Available colloid solutions includeappropriate combination of ﬂuids to replace circulating volume. albumin, dextran, and hetastarch. Table 57-10 compares the effects ofCrystalloid solutions appear to be as effective as colloid solutions in these agents.most settings.126 The Advanced Trauma Life Support (ATLS) course Albumin solutions are available in concentrations of 5% or 25%. Ahas proposed widely accepted standards for management of the trauma 25-g infusion of albumin temporarily increases intravascular volumepatient. For the patient in hemorrhagic shock, initial resuscitation with by roughly 450 mL over 60 minutes as a result of its considerable2 L of crystalloid solution is followed by packed red cell transfusions.127 oncotic activity. Albumin is cleared rapidly from the circulation, par-The degree of volume resuscitation is also a matter of debate. Histori- ticularly in patients with shock or sepsis.cally, aggressive, early ﬂuid resuscitation was thought to result in Dextran solution contains large glucose polymers with meanimproved outcomes. However, later data suggest that excessive ﬂuid molecular weights of 40,000 daltons (dextran 40) or 70,000 daltons
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1181(dextran 70). Dextran 40 is rarely used for the purposes of volume administration of clotting factors after every 4 to 6 units of packed redexpansion. A 500-mL infusion of 6% dextran 70 should rapidly expand blood cells has not been demonstrated to improve outcomes.129intravascular volume by more than 1000 mL. Adverse effects of dextran A single unit of packed red cells has a hematocrit of approximatelyadministration include increased bleeding risk and allergic reaction. 80% and can increase the hemoglobin level by 1 g/dL in a 70-kg indi-Anaphylactic reactions affect 1 in 3300 patients receiving dextran. In vidual. Removal of white blood cells from the unit of blood (i.e., leu-higher doses (>20 mL/kg/24 hr), dextran may negatively affect platelet kocyte-poor blood) decreases the risk of febrile transfusion reactions.function and clotting factor activation, and it may interfere with ﬁbrin Patients with evidence of acute hemorrhage (>30% blood volumefunction. It also may interfere with laboratory cross-matching of loss), hemoglobin level between 6 and 10 g/dL with evidence of tachy-blood. Dextran should be used cautiously in patients with hypovole- cardia and hypotension, or hemoglobin concentration less than 6 g/dLmia due to hemorrhage who may already have a coagulopathy and should be considered candidates for transfusion.130,131require further cross-matching of blood. Dilutional thrombocytopenia can occur as a result of massive Hydroxymethyl starch (i.e., hetastarch) is a synthetic molecule transfusion in a hemorrhaging patient. After replacement of oneavailable in a 6% solution in normal saline (Hespan) or lactated elec- blood volume, 35% to 40% of a patient’s platelets usually remain, andtrolyte solution (Hextend). Like the other available colloid solutions of platelet replacement is recommended in the setting of bleeding andalbumin and dextran, hetastarch also induces intravascular volume signiﬁcant thrombocytopenia. Platelet counts equilibrate within 10expansion by increasing oncotic pressure. The effects of hetastarch can minutes and can be assessed immediately after completion of thepersist for 24 to 36 hours. As with dextran, hetastarch may negatively transfusion.affect the clotting system. Hetastarch can prolong prothrombin and Fresh-frozen plasma (FFP) is plasma that is extracted from wholepartial thromboplastin times, decrease platelet counts, and reduce clot blood within 6 hours of collection and frozen. A single unit of FFPtensile strength, and it should be used with caution in patients who contains 700 mg of ﬁbrinogen in addition to factors II, V, VII, IX, X,may have a coagulopathy. Hextend is a newer hetastarch formulation and XI. It is indicated for the replacement of multiple clotting factorswith smaller-molecular-weight particles in addition to electrolytes and in patients with acute hemorrhage and evidence of DIC. The goal is tolactate similar to plasma levels. It may have less effect on the coagula- correct clotting factor deﬁciencies and to achieve a post-transfusiontion proﬁle compared with other colloids and therefore offer a theo- serum ﬁbrinogen level of approximately 100 mg/dL.retical advantage in the setting of hemorrhage.128 Cryoprecipitate is obtained from FFP and contains factor VIII (80 to 120 units), ﬁbrinogen (200 mg), von Willebrand factor, and factor BLOOD COMPONENT THERAPY XIII. One unit of cryoprecipitate and one unit of FFP have similar Blood product replacement is the cornerstone of successful manage- effects on the ﬁbrinogen level (increase of 10 to 15 mg/dL). However,ment of hemorrhagic shock. The variety of blood product components because of its smaller volume, cryoprecipitate more efﬁciently raisesavailable for transfusion is summarized in Table 57-11, along with the ﬁbrinogen level compared with FFP.anticipated effects. Whole blood has not been separated into the variouscomponents and therefore offers a theoretical advantage because it COMPLICATIONS OF TRANSFUSIONcontains clotting factors and platelets in addition to red blood cells. The Complications resulting from blood component transfusion varymajor limitation to the use of whole blood is the inability to store the from infections to immunologic responses. Table 57-12 outlines theproduct beyond 24 hours. After 24 hours of extravascular storage, plate- frequency of various transfusion-related complications.lets and granulocytes are completely lost and 2,3-diphosphoglycerate is Minor transfusion reactions are relatively common occurrencesdepleted, signiﬁcantly compromising the oxygen carrying capacity of and are not caused by hemolysis. Common clinical ﬁndings includethe red blood cells. Prolonged storage results in depletion of clotting low-grade fever, urticaria, or hives, and they result from exposure tofactors and increasing levels of potassium and ammonia. For these incompatible platelet or white blood cell antigens. The use of leuko-reasons, whole blood is typically separated into its individual compo- cyte-poor packed red cells minimizes these types of reactions. Nonhe-nents and stored for later use; it is essentially unavailable in the United molytic reactions do not require discontinuation of the transfusion.States. Individual components can then be administered to address Symptoms can be managed with antipyretic agents and antihistamines,speciﬁc derangements according to clinical indications. The routine as needed. TABLE 57-11 BLOOD COMPONENTS Component Contents Indications Volume Shelf Life Expected Effect Packed RBCs Red cells, some Correct anemia 300 mL 21 days Increase HCT 3%/unit, Hgb 1 g/unit plasma, few WBCs Leukocyte-poor blood RBCs, some plasma, Correct anemia, reduce 250 mL 21-24 days Increase HCT 3%/unit, Hgb 1 g/unit few WBCs febrile reactions Platelets Platelets, some plasma, Bleeding due to 50 mL Up to 5 days Increase total platelet count RBCs, few WBCs thrombocytopenia 7500 μL/unit Fresh-frozen plasma Plasma, clotting factors Treatment of coagulation 250 mL 2 hours thawed, Increase total ﬁbrinogen V, XI, XII disorders 12 months 10-15%/unit frozen Cryoprecipitate Fibrinogen, factors V, Hemophilia A, von 40 mL 4-6 hours Increase total ﬁbrinogen VIII, XIII, von Willebrand disease, thawed 10-15 mg/dL per unit Willebrand factor ﬁbrinogen deﬁciency HCT, hematocrit; Hgb, hemoglobin; RBCs, red blood cells; WBCs, white blood cells.
1182 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient TABLE 57-12 TRANSFUSION-RELATED RISKS decreased risk of infectious morbidity, alloimmunization, and immu- nologic complications. Adverse fetal effects have not been described Disease or Disorder Risk during this process.138,139 Acute normovolemic hemodilution is a time- consuming process and is not appropriate for an acutely hemorrhaging Hepatitis B 1/137,000 Hepatitis C <1/1,000,000 patient. Suggested criteria for acute normovolemic hemodilution Human immunodeﬁciency virus type 1 <1/1,900,000 include an increased likelihood of transfusion; preoperative hemoglo- (HIV-1) bin level of 12 g/dL or higher; absence of clinically signiﬁcant coronary, Bacterial contamination 1/38,565 pulmonary, renal, or liver disease; absence of severe hypertension; and Acute hemolytic reaction 1/250,000-1/1,000,000 absence of infection and risk of bacteremia.140 Delayed hemolytic reaction 1/1,000 Other Measures. Supplemental oxygenation and elevation of Transfusion-related acute lung injury 1/5,000 the lower extremities are recommended for patients with hemorrhage. The use of antishock (MAST) trousers has fallen out of favor after Adapted from Goodnough LT, Brecher ME, Kanter MH, et al: Transfusion medicine. Part 1. Blood transfusion. N Engl J Med 340:438- publication of a randomized trial that failed to demonstrate survival 447, 1999; and the American Association of Blood Banks 2002. beneﬁt.141 Available at www.aabb.org. Massive transfusion and blood loss place the patient at signiﬁcant risk for concomitant abnormalities that can compromise successful resuscitation. Maintenance of the airway and ventilation cannot be Severe reactions after transfusion are usually the result of a hemo- ignored. Management of the hemorrhaging patient should includelytic reaction to the administration of an incompatible unit of blood. regular assessment for coagulation abnormalities and recurrent bleed-Historically, administration of ABO-incompatible blood was thought ing, correction of electrolyte abnormalities, particularly calcium andto occur at a rate of 1 in 600,000 units, but a later report suggests it potassium, and maintenance of temperature above 35° C. After controloccurs with much greater frequency (1 in 25,000 units). Administrative of bleeding is achieved, resuscitation is considered complete if theerror is the culprit in most of these events, underscoring the need for following goals are met142:accurate accounting of transfused units, particularly in an emergentsituation.132 Cardiovascular decompensation with DIC, fever, and renal Normal or hyperdynamic vital signsfailure usually develop rapidly after initiation of an incompatible Hematocrit higher than 20% (transfusion thresholdtransfusion. Treatment entails immediate discontinuation of the trans- determined by the patient’s age)fusion and supportive care. Normal serum electrolyte levels Normal coagulation function, with a platelet count of at least ADDITIONAL SUPPORTIVE MEASURES 50,000 Red Blood Cell–Saving Devices. In patients anticipated to be at Restoration of adequate microvascular perfusion, as indicatedrisk for excessive intraoperative blood loss, such as suspected placenta by a pH of 7.40 with a normal base deﬁcit, normalized serumaccreta, use of an autologous transfusion device (Cell Saver) should be lactate level, normal mixed venous oxygenation, normal orconsidered.124,133 Theoretical risks of inducing amniotic ﬂuid embolism high CO, and normal urine output.have caused some concern regarding the use of intraoperative cellsalvage during cesarean section. However, several reports have vali- DEFINITIVE THERAPY FOR HEMOSTASISdated its safety in this arena.134-137 After delivery of the fetus and clear- Control of obstetric hemorrhage must take into consideration theing the operating ﬁeld of amniotic ﬂuid, the suction device is changed, apparent cause of the hemorrhage. For example, the most likely causeand blood is collected into the Cell Saver. In approximately 3 minutes, of postpartum hemorrhage is uterine atony, which would be expecteda unit of blood with a hematocrit of 50% is generated. In one study to respond to uterine massage and uterotonic agents as ﬁrst-linecomparing patients who received blood salvage and autotransfusion therapy. Hemorrhage due to placenta accreta or previa requires surgi-during cesarean section with those receiving allogeneic blood transfu- cal intervention. Recombinant factor VIIa (rFVIIa, NovoSeven) issions, no differences in the rates of infection, coagulation abnormali- approved for the management of bleeding in hemophiliacs, but its roleties, or respiratory problems could be identiﬁed.135 This technology is emerging as an off-label adjunctive therapy for the control of cata-may be particularly valuable for patients who have the potential for strophic, coagulopathic bleeding. Recombinant factor VIIa functionssevere blood loss or who have religious preferences mandating the by activating factor X, thereby enhancing thrombin production andavoidance of transfused blood products. formation of a stable clot. It is not intended as ﬁrst-line therapy for Acute Normovolemic Hemodilution. Acute normovolemic control of hemorrhage, and most physicians recommend use of rFVIIahemodilution offers an additional option for patients at signiﬁcant risk only after other attempts to control hemorrhage have failed. Thisfor intraoperative hemorrhage. The principle behind this approach is includes any necessary surgical approach, appropriate replacementto dilute the patient’s circulating volume so that when bleeding occurs, of blood products, and correction of severe acidosis, hypothermia,it has a lower hematocrit. This is accomplished by collecting blood and hypocalcemia.143,144 rFVIIa has been employed for the control offrom the patient preoperatively and placing it into special storage bags obstetric hemorrhage.145-148 Table 57-13 outlines pharmacologic agentsthat can be obtained from the blood bank. Simultaneously, the patient useful in controlling hemorrhage from an atonic uterus.is given crystalloid solution in a 3 : 1 ratio, resulting in a dilutional Hemorrhage after a vaginal delivery should prompt a thorougheffect and a decrease in the maternal hematocrit. Intraoperatively, after evaluation for and repair of cervical or vaginal lacerations, particularlyachieving control of the blood loss, or at the discretion of the surgeon, if an instrumented delivery was performed. If uterine atony fails tothe patient’s blood is then reinfused, resulting in an increase in the respond to uterine massage and uterotonic agents, evaluation forhematocrit. potential retained placental fragments should be performed. Ultra- Potential advantages include preservation of clotting factors, a sound may be of assistance in this assessment process, particularly ifdecreased likelihood of allogeneic transfusion, and therefore a uterine curettage is necessary. Intrauterine pressure packs to control
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1183 TABLE 57-13 PHARMACOLOGIC AGENTS USEFUL FOR CONTROLLING UTERINE ATONY Agent Dose Considerations/Side Effects Oxytocin (Pitocin) 10-40 units/L IV IV bolus may cause PVCs and hypotension 10 units IM Methylergonovine (Methergine) 0.2 mg IM every 2-4 hours, Increased SVR, increased MAP, increased CVP maximum of 5 doses Side effects include pulmonary edema, seizures, intracranial hemorrhage, retinal detachment, and coronary vasospasm. Avoid in patients with hypertension Prostaglandin 15-methyl F2α 0.25 mg IM every 15-90 minutes, Diarrhea (Hemabate) maximum dose of 2 mg Bronchoconstriction Increased CO, increased heart rate, and increased right heart pressure Increased PVR Decreased SVR Decreased coronary artery perfusion Avoid in patients with asthma Dinoprostone (prostaglandin E2) 20 mg per rectum or vagina every Diarrhea, nausea, vomiting 2 hours Tachypnea, pyrexia, tachycardia Decreased SVR Decreased MAP Increased CO Misoprostol (Cytotec, 800-1000 μg per rectum Diarrhea, vomiting prostaglandin E1) Abdominal pain Headache Recombinant factor VIIa 200 μg/kg initial dose; may repeat Indicated with persistent bleeding despite adequate ﬁrst-line therapies (NovoSeven) with 100 μg/kg at 1 and 3 hours May increase risk for thromboembolic events after the ﬁrst dose CVP, central venous pressure; CO, cardiac output; IM, intramuscular; IV, intravenous; MAP, mean arterial pressure; PVC, premature ventricular contraction; PVR, pulmonary vascular resistance; SVR, systemic vascular resistance.life-threatening postpartum hemorrhage have been successful accord- obstruct blood ﬂow to the lower extremity. If possible, ligation of theing to some reports.149,150 However, the technique used to place the vessel should occur below the branch of the superior gluteal artery, aspacking is integral to its success and can be challenging. Other physi- demonstrated in Figure 57-9. Because of the technical challenges andcians have attempted to provide packing by modifying various questionable efﬁcacy of the procedure (hemorrhage controlled ininﬂatable devices such as Foley catheters or Sengstaken-Blakemore approximately 40% of cases), hypogastric artery ligation is not com-tubes.151,152 The SOS Bakri tamponade balloon has been introduced monly performed.159speciﬁcally to provide intrauterine compression in the management of The incidence of emergent peripartum hysterectomy for obstetricpostpartum hemorrhage.153 The SOS Bakri tamponade balloon has hemorrhage is less than 0.8%.160-164 Cesarean delivery, prior cesareanbeen placed vaginally and at cesarean section. delivery, and multiple gestation are signiﬁcant risk factors.164,165 Other Surgery to Control Obstetric Hemorrhage. If uterine hemor- indications for peripartum hysterectomy include uterine rupture,rhage after vaginal delivery fails to respond to the previously described extension of the uterine incision, infection, and myomas. A studymeasures, exploratory laparotomy should be performed. If the bleed- reported peripartum hysterectomy data from a national databaseing is encountered at cesarean section, the same techniques for control between 1998 and 2003 and included more than 18,000 hysterectomies.of hemorrhage may be applied. The B-Lynch uterine body compres- Although some case series have suggested that invasive placentationsion suture has been performed successfully to control hemorrhage appears to be supplanting uterine atony as the leading indication fordue to unresponsive uterine atony, and it is demonstrated in Figure peripartum hysterectomy, other data suggest they may be equally57-7.154,155 The B-Lynch suture has been performed in conjunction with common.160,161,164,166 Complications from emergency peripartum hys-placement of an SOS Bakri balloon to achieve hemostasis.156 terectomy include excessive blood loss and the need for blood product Suture ligation of the ascending uterine arteries (i.e., O’Leary replacement, fever, wound infection, ureteral injury, thromboembolicsuture) is another option and is technically straightforward to perform events, cardiac arrest, and death.160,162,163,166 Supracervical and totalin most scenarios. O’Leary and O’Leary157,158reported the successful use hysterectomy have been described for the management of obstetricof this technique (Fig. 57-8) in controlling postpartum and postcesar- hemorrhage, although data are lacking to determine whether oneean bleeding. The uterine artery can be visualized and accessed ante- approach is superior to the other.riorly or posteriorly. The uterine arteries are readily accessible with Pelvic Artery Embolization. Interventional radiologists haveuterine manipulation, and minimal or no vessel dissection is necessary become proﬁcient in arteriography for a variety of diagnostic andfor uterine artery ligation. Hypogastric artery ligation is more techni- therapeutic approaches. It is no surprise then that selective pelviccally challenging, requiring dissection of the retroperitoneal space artery embolization for the management of obstetric hemorrhage isthrough the broad ligament. Bilateral ligation usually is necessary to gaining in experience. Many case series have described its effectivenessachieve adequate reduction in pulse pressure. The surgeon must be in this scenario, with success rates exceeding 90%.167-170 In addition tofamiliar with pelvic vascular anatomy to avoid ureteral injury or in- avoiding the added morbidity of surgical exploration, it preservesadvertent ligation of the common or exterior iliac artery, which will future fertility.170,171
1184 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient Fallopian Ovarian Cervical branch Round tube Round ligament Fallopianligament ligament tube Uterine artery Broad ligament Ureter A B FIGURE 57-8 Anterior approach to the uterine artery ligation technique for postpartum obstetric hemorrhage. External iliac artery Ureter Common Obturator iliac artery artery CFIGURE 57-7 B-Lynch surgical technique. A, Anterior view of theB-Lynch stitch placement. B, Posterior view of the B-Lynch stitch Aorta Superiorplacement. C, Anterior view of the completed procedure. (From gluteal arteryB-Lynch C, Coker A, Lawal AH, et al: The B-Lynch surgical techniquefor the control of massive postpartum haemorrhage: An alternative to Hypogastric arteryhysterectomy? Five cases reported. BJOG 104:372, 1997. Reprinted ligation sitewith permission.) Uterine artery Internal pudendal trunk FIGURE 57-9 Localization of the hypogastric artery along the The procedure is performed in the interventional radiology suite. right pelvic side wall.The femoral artery is accessed and diagnostic arteriography performedwith ﬂuoroscopic imaging to localize the target arteries for emboliza-tion. A variety of options are available for arterial occlusion, including pregnant women, followed by domestic violence, assault, and suicidean absorbable gelatin sponge (Gelfoam) or another type of particulate attempts.172,176-178 Domestic violence escalates during pregnancy andmaterial. is estimated to affect as many as 20% of pregnant patients.179 A high Potential adverse results from the procedure include ischemia or index of suspicion for domestic violence is warranted for any pregnanttissue necrosis, infection, nephrotoxicity due to contrast medium, and woman presenting for evaluation after a traumatic event.bleeding at the access site or failure of the embolization. Failure ofthis approach does not preclude a subsequent surgical attempt athemorrhage control. Conversely, after hypogastric artery ligation is Blunt Abdominal Traumaperformed, successful arteriographic embolization is much more dif- The gravid uterus is particularly vulnerable to blunt trauma fromﬁcult to achieve. motor vehicle accidents, assaults, and falls. When a pregnant woman is injured severely, it most likely involved a motor vehicle accident. Three-point restraint seatbelts are safe for use by pregnant women,Trauma in Pregnancy they signiﬁcantly decrease the risk of serious maternal injury and fetal loss, and they are recommended by ACOG.180-183 Proper use of seatbeltsTrauma is a leading cause of non-obstetric deaths in the United States, appears to be a signiﬁcant predictor of maternal and fetal out-and it is estimated to complicate 6% to 7% of all pregnancies.172 About comes.181,184 Approximately one third of pregnant women do not wear4000 fetuses are lost annually due to complications from trauma in seat belts because of discomfort, inconvenience, or fears about hurt-pregnancy.173 Most incidents are considered minor, and less than 0.4% ing the fetus. Prenatal education regarding seat belt use signiﬁcantlyof patients require hospitalization. Of those requiring admission, 24% improves proper seat belt use.173 The addition of airbags does notproceed to delivery during the hospitalization.174,175 Motor vehicle appear to be problematic for pregnant patients and may further reduceaccidents and falls account for most traumatic events affecting risk of injury.182
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1185 Placental abruption is a particularly serious complication after Fetal red blood cells MBV maternal Hct % fetal cells (KB)blunt trauma and motor vehicle accidents, because it may lead to pre- Newborn Hctmature labor and delivery, concealed hemorrhage, consumptive coagu-lopathy, fetomaternal hemorrhage, fetal distress, and death. Detection If KB result is 0.9% : 0.9% of maternal blood volume (MBV) is fetalof an abruption in the patient without vaginal bleeding presents a origin.challenge. Abruption occurs in approximately 7% of patients after MBV is assumed to be 5000 mL for an average-size woman at term. Maternal hematocrit (Hct) should be measured; assumetrauma, but the severity of the injury does not appear to correlate with approximately 35%.the presence of an abruption or to predict outcome. Most Normal Hct for term newborn infant can be assumed to be 50%, ifplacental abruptions occur in patients after relatively minor trauma the patient is undelivered.without evidence of serious injury.172,178,185-187 Unfortunately, a negativeultrasound result does not reliably exclude the possibility of a placental Fetal red blood cells 5000 0.35 0.009 31.5 mLabruption. At best, the sensitivity of ultrasound to detect abruption is 0.525%.188 However, the sonographic identiﬁcation of an abruption cor- Therefore, the fetus has hemorrhaged 31.5 mL of red cells into therelates with a higher likelihood of adverse outcome.188,189 maternal circulation. At term, the neonatal blood volume is 125 mL/kg. The Injury Severity Score (ISS) is often used to quantify the risk of If the Hct is assumed to be approximately 50% at term, the actualadverse outcomes for nonpregnant patients.190 Unfortunately, the ISS amount of blood lost is 63 mL. In a term infant assumed to weighdoes not translate well to the pregnant population and has not been 3500 g, the blood volume is approximately 438 mL, and the fetusshown to reliably predict outcomes in this group. El-Kady and col- has lost 7% of its blood volume.leagues174 published a large, population-based study of more than FIGURE 57-10 Calculation of the volume of fetomaternal10,000 trauma evaluations in pregnant women.174 Patients were divided hemorrhage using the Kleihauer-Betke results.into those delivering during the admission for trauma and those dis-charged to deliver at a later date. Falls were most common amongwomen requiring delivery, followed by motor vehicle accidents. Thelikelihood of abruption, uterine rupture, maternal death, and adverse recommend at least 24 hours because most serious complicationsneonatal outcomes, including fetal and neonatal death, was signiﬁ- occur shortly after the traumatic event.cantly higher for the group that delivered during the trauma admis- Fetomaternal hemorrhage is another potential concern after bluntsion. Those women discharged undelivered after trauma had improved trauma in pregnancy. A Kleihauer-Betke test can provide an estimatematernal outcomes compared with the delivered patients, but they of the amount of fetal blood within the maternal circulation, which isremained at increased risk for preterm delivery, abruption, and the particularly important in determining if additional doses of RhoGAMneed for blood products compared with uninjured controls. These are necessary in Rh-negative women. The test is based on the detectionrisks could not accurately be predicted by the ISS. Adverse fetal and of fetal hemoglobin. If the presence of fetal hemoglobin within mater-neonatal outcomes were not increased after discharge. In contrast, for nal red cells, such as in a hemoglobinopathy, is detected, the result willthe group of patients who delivered during the trauma admission, a be falsely elevated. Figure 57-10 describes how to interpret a Kleihauer-high ISS (>10) was associated with the highest risk for adverse out- Betke result and calculate volume of fetomaternal hemorrhage. Spon-comes. However, a lower ISS score (<10) was still associated with a taneous fetomaternal hemorrhage can occur throughout pregnancy insigniﬁcant increase in serious adverse events, including abruption, the absence of any identiﬁed precipitating event, but the volumesuterine rupture, and maternal or fetal death. The Revised Trauma appear to be low.193 Fetomaternal hemorrhage is thought to occur withScore (RTS), which includes the Glasgow Coma Scale, also appears to greater frequency after blunt trauma, and Kleihauer-Betke testing isbe limited in its ability to accurately predict pregnancy outcome after often recommended. However, the available data suggest that a positivetrauma.191 Kleihauer-Betke result does not alter management. In four studies of External monitoring of the fetal heart rate and contraction moni- 730 pregnant women who had Kleihauer-Betke testing performed aftertoring are recommended after blunt trauma in a viable gestation. blunt trauma, 95 (13%) had evidence of fetomaternal hemor-Pearlman and associates178 performed a prospective study monitoring rhage.172,178,192,194 Of these, in only two cases (0.02%) did the resultpatients for a minimum of 4 hours after blunt trauma. Eighty-eight potentially alter management; one patient had signiﬁcant hemorrhagepercent of the patients had no visible trauma; 2.4% were critically requiring delivery as a result of fetal distress, and one underwentinjured. Most patients had contractions, and 70% required admission umbilical cord blood sampling but did not require transfusion orbeyond the initial 4-hour observation period. Of these, 19% went on delivery. For the remainder, the result did not appear to affect manage-to deliver, with one fetal death. The abruption incidence in this sub- ment. In another study, no difference was found in the frequency ofgroup was 9.4%. No adverse events occurred in the group of patients positive Kleihauer-Betke tests between normal controls and pregnantfor whom contractions did not occur more frequently than every 15 women being evaluated for trauma.194minutes. However, all women suffering an adverse perinatal outcome Because of the gravid uterus, patterns of traumatic injury are some-had contractions every 2 to 5 minutes at some point during the initial what different in pregnant patients after blunt abdominal trauma,4-hour observation period. The severity of injury did not predict particularly motor vehicle accidents. Upper abdominal injury to theabruption or adverse outcomes.178 Other investigators have since vali- spleen and liver are more common, whereas bowel injuries occur lessdated the concept that less than one contraction every 15 minutes is frequently.192,195 Traumatic uterine rupture has been reported, but it isnot associated with adverse outcomes after blunt trauma in pregnant rare with minor trauma.174,196 The risk increases with increasing sever-patients.172,185,192 A minimum of 4 hours of fetal heart rate and contrac- ity of trauma and the size of the uterus. Most ruptures occur in thetion monitoring is recommended after blunt trauma in pregnant fundal or posterior regions. With traumatic rupture of the uterus, fetalwomen, regardless of injury severity. Beyond the initial observation mortality approaches 100%.period, the recommended duration for monitoring is not clear, par- Pelvic fractures are typically related to trauma as a result of a motorticularly for patients with evidence of contractions. Most physicians vehicle accident. The presence of a pelvic fracture should raise concern
1186 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patientabout signiﬁcant bleeding risk and coexistent intra-abdominal trauma, TABLE 57-14 ESTIMATES OF FETAL RADIATIONsuch as splenic or hepatic laceration or urinary tract injury. Pelvic EXPOSURE FROM COMMONfracture is not a contraindication to vaginal delivery. The decision RADIOLOGIC PROCEDURES IN Ashould be based on the stability of the fracture and presence of pelvic TRAUMA PATIENTdeformities. Fetal head injuries are also more common if a pelvicfracture is sutained.197 Fetal Radiation Exposure Radiologic Examination (cGy)Penetrating Abdominal Trauma Chest (posteroanterior, lateral) <<0.1 Abdomen 0.15-0.26Gunshot and stab wounds are the most common penetrating injuries Pelvis 0.2-0.35in pregnant women, usually as a result of assault or suicide attempt. Hip 0.13-0.2The enlarged uterus increases the likelihood that the uterus and fetus Computed tomography of head <<0.1will sustain injury, and the prognosis is generally less favorable for the Computed tomography of abdomen 0.04fetus. Penetrating trauma to the lower abdomen carries a lower likeli- Computed tomography of pelvis 2.5hood of maternal bowel injury. The impact of gunshot wounds is lesspredictable and varies according to the entry site and angle, size ofuterus and distance from the gun. Visceral injuries occur in 19%of pregnant patients, compared with 82% in nonpregnant patients. as a result of consumption. In pregnancy, ﬁbrinogen levels are substan-Mortality rates are correspondingly lower in pregnant victims (3.9% tially elevated, and low and even normal-range ﬁbrinogen should raiseversus 12.5%).198 Stab wounds are more likely to involve the upper concern about the pregnant patient.abdomen during pregnancy, and in these cases, bowel injury should be Delivery timing and route are dictated by maternal and fetal statusconsidered.198,199 and need to be individualized. If laparotomy is necessary, hysterotomy Evaluation of the patient after penetrating abdominal trauma is not automatically indicated. If there is evidence of uterine injury,should include an assessment of the likelihood of intra-abdominal delivery may be necessary. Pregnancy should not preclude the use ofbleeding. Ultrasound and CT are useful in this regard, and exploratory diagnostic testing thought to be otherwise indicated for a pregnantlaparotomy is recommended if there is suspicion of bowel perforation trauma patient. No single diagnostic radiologic imaging study existsor active hemorrhage. Diagnostic peritoneal lavage can help determine that can provide enough radiation exposure to adversely affect a devel-if bleeding is likely in hemodynamically stable patients with equivocal oping fetus. Radiation exposure of less than 5 rads has not been associ-ﬁndings on abdominal ultrasound or CT. Lavage is performed by ated with fetal abnormalities or pregnancy loss, and the radiationentering the abdomen through a small incision and infusing a saline associated with abdominal and pelvic CT scans falls substantiallywash. The presence of blood in the recovered lavage ﬂuid supports the below this threshold.200 Magnetic resonance imaging (MRI) does notpresence of intra-abdominal bleeding and warrants exploration. produce ionizing radiation, and no adverse fetal effects have beenTetanus toxoid prophylaxis should be used for the same indications as reported from in utero exposure. However, because of theoretical con-in the nonpregnant patient. cerns, ACOG states that the “National Radiological Protection Board arbitrarily advises against its use in the ﬁrst trimester.”200 Table 57-14 lists anticipated dose of radiation exposure to the fetus from examina-Trauma Management Issues tions commonly required for a trauma patient.On initial presentation, the pregnant trauma patient should be evalu-ated similar to the nonpregnant patient. Assessment and stabilizationof the airway, breathing, and circulation are the primary steps, followedby systematic evaluation for evidence of traumatic injuries. If the Burns in Pregnancypatient is pregnant, rapid conﬁrmation of gestational age and assess-ment of fetal well-being are necessary. This evaluation can be per- Backgroundformed simultaneous to any required maternal stabilization efforts. According to the American Burn Association, 40,000 people require Care should be taken to provide displacement of the gravid uterus hospitalization because of burns each year. Of these, 60% are admittedoff the aorta and vena cava. Compression of the great vessels occurs to one of the 125 specialized burn centers in the United States. Theseafter the uterus reaches a size consistent with 20 weeks’ gestation, and centers admit 200 patients per year on average, compared with theit decreases the CO. Displacement can be accomplished manually, by average of three burn admissions to nonspecialized burn centers.201,202moving the patient to a lateral position, or by placing a wedge under Although current U.S. statistics are not available, burn injuries appearthe hip. to be more common in developing countries, as evidenced by fewer case Evaluation of a pregnant trauma patient must take into consider- reports from the United States In two larger series of burns in pregnancyation the physiologic changes of pregnancy that affect the clinical pre- collected in India and Iran, approximately 7% of burn victims weresentation. Pregnant women near term have expanded their circulating pregnant patients. Burns resulting from ﬂames or scalds account forblood volume by 40% to 50%. As a result, signiﬁcant intra-abdominal 78% of cases; the remainder resulted from hot object contact (8%) oror intrauterine blood loss can occur with minimal change in maternal electrical (4%), chemical (3%), or other (6%) causes.203vital signs. Prognosis is worse if the patient develops hypotension andtachycardia.187 In a viable gestation, a reassuring fetal heart rate tracingdemonstrates adequate uterine perfusion and acts as a barometer of Classiﬁcationmaternal status. As maternal cardiovascular status deteriorates, uterine Burns are characterized by the depth and size of the involved area.perfusion suffers and manifests as contractions and fetal heart rate Partial-thickness burns (formerly classiﬁed as ﬁrst-degree and second-abnormalities. Fibrinogen levels decrease in the setting of hemorrhage degree burns) involve superﬁcial skin layers and are capable of re-
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1187 4.5 4.5 Outcomes Severe burns are morbid events with signiﬁcant short-term and long- term consequences. The pregnancy does not appear to negatively affect the outcome after a burn, but the burn has the potential to signiﬁcantly affect the pregnancy outcome. Maternal and fetal survival depends most on the severity of the burn itself.201,202,206 In one of the largest series of burns in pregnancy, Maghsoudi and colleagues202 prospec- 18 18 tively collected data on 51 pregnant burn victims admitted to a referral 4.5 4.5 4.5 4.5 burn center in Iran over a 9-year period. The overall maternal mortal- ity rate was 39%, and the fetal mortality rate was 45%. The most sig- niﬁcant predictor of maternal and fetal mortality was total body surface area involvement exceeding 40% and the presence of inhalation 9 9 9 9 injury. These patients suffered severe burns; the mean burn surface area was 38%. In nonsurvivors, the mean burn surface area was 69%. Other studies have found similar results.201 Management Management of the pregnant burn patient is similar to that of a nonpregnant patient. Acute management of the burn victim should address aggressive ﬂuid resuscitation, evaluation for inhalation injuryFIGURE 57-11 Body surface area diagram depicts the relative and airway maintenance, assessment of carbon monoxide poisoning,percentage of the total body surface area of deﬁned anatomic anemia, prevention of infection, and wound management.areas in nonpregnant adults. (From Wolf SE, Hernon DN: Burns. In The initial priority is recognition of smoke inhalation injury,Townsend CM, Beauchamp RD, Evers BM, et al [eds]: Sabiston’sTextbook of Surgery, 17th ed. Philadelphia, Elsevier Saunders, 2004.) carbon monoxide poisoning, and airway management. Carbon monoxide crosses the placenta easily, and fetal hemoglobin has a higher afﬁnity for carbon monoxide than adult hemoglobin. Hyper- TABLE 57-15 CLASSIFICATION OF BURN baric oxygen may play a role in treating carbon monoxide poison- SEVERITY ing.207 Early intubation should be considered to maximize oxygen delivery in a patient with inhalation injury and to protect against Classiﬁcation Deﬁned Body Surface Areas aspiration. Minor <15% partial thickness Fluid losses after a serious burn are substantial as a result of third <2% full thickness spacing due to edema and evaporative loss from damaged skin. The Moderate 15-25% ﬂuid deﬁcit is easily underestimated in a pregnant patient. The normal 2-10% full thickness physiologic adaptations of pregnancy, including up to 40% increase in Major >25% blood volume, 40% increase in CO, and 20% decrease in SVR, are not >10% full thickness reﬂected in the ﬂuid replacement strategies recommended for non- Any burn involving the face, eyes, ears, feet, or pregnant burn patients. One commonly used formula, the Parkland perineum formula, recommends replacement with Ringer’s lactate at a rate of Inhalation injury or electrical injury 4 mL/kg of body weight per percent of body surface area burned. Fifty percent of the calculated replacement volume is administered over the initial 8 hours and the remainder over the subsequent 16 hours. In oneepithelialization. These burns are painful, blistering injuries that can report, 208 the Parkland formula underestimated ﬂuid requirement inbe red, white, or pink. These wounds are usually managed with topical a pregnant burn patient by almost 10 L. Given the lack of guidelinesagents and dressings. If healing does not occur within 3 weeks, man- for pregnant patients, ﬂuid resuscitation should be individualized toagement converts to that for more serious burns. Full-thickness burns achieve hemodynamic stability, adequate urine output, and uterine(formerly called third-degree burns) are the most severe, and epithe- perfusion. Electrolyte disturbances should also be anticipated andlium does not regenerate. These burns are not blistering and are pain- addressed.less. They can be gray, white, or brown. Burns are associated with a signiﬁcant hypermetabolic state and Early surgical excision of the eschar is the standard of management markedly increased nutritional requirements. Hypermetabolism canin the United States. Full-thickness wounds hold the greatest potential be minimized by providing adequate pain relief; supplying aggressivefor scarring, contractures, and infection and should be referred to a wound management with excision, grafting, and occlusive dressings;burn center.204,205 The prognosis for pregnant and nonpregnant patients and managing temperature and adequate ﬂuid replacement. Attentionis directly related to the percentage of body surface area involved. to adequate nutrition is essential and usually requires enteral and par-Figure 57-11 shows one method of estimating the percentage of total enteral feeds.209body surface burned in nonpregnant adults. A modiﬁcation for the Wound infection and sepsis are signiﬁcant risks after burn injury.pregnant patient has not been created, but the gravid abdomen should Bacteremia results from colonization of the burn area. The mostbe taken into account when estimating body surface area involvement. common organisms encountered are S. aureus, Pseudomonas aerugi-The severity of the burn increases in proportion to the degree of nosa, and Candida albicans.210 Aggressive management of the woundinvolvement, as outlined in Table 57-15. with excision of the eschar, grafting, and occlusive dressings, in addi-
1188 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patienttion to topical and systemic antibiotics, helps to prevent infectious bonate to correct maternal acidosis should be undertaken with cautioncomplications. The patient may be at increased risk for venous throm- because of the potential for worsening fetal acidosis. Electrocardiover-boembolic events. sion can be performed in a pregnant patient; the recommendations are Assessment of fetal well-being in a viable gestation should not be the same as for nonpregnant patients.216overlooked. Intravascular depletion, hypoxemia, hypermetabolism, Rapid restoration of maternal circulation and reversal of hypoxiaand infection can adversely affect the fetus. Continuous monitoring is are the most effective ways to minimize negative effects on the fetus.recommended in a viable gestation, particularly during the early stages If this is not possible, attention must then be directed to evacuation ofof management. If the abdomen is involved with burn, direct ausculta- the uterus by cesarean section. Cesarean section in the setting of mater-tion may be limited and continuous fetal heart rate monitoring not nal cardiac arrest can improve the likelihood of an intact neonatalfeasible. Sterile coverings are available for the heart rate monitor and outcome and simultaneously improve maternal resuscitative efforts. Inultrasound probes to minimize infection risk. Vaginal ultrasound 1986, Katz and colleagues217 initially advocated performing a cesareanassessment may also be considered in some settings. section at 4 minutes after instituting CPR.217 This recommendation Contractions and preterm labor are to be expected, particularly in was based on the theory that emptying the uterus would improve COa severely burned pregnant patient, although the frequency is unknown. generated by chest compressions after the obstructing uterus wasFew data are available to guide the use of tocolytic medications. Tocoly- emptied. Maternal neurologic injury could be avoided if cerebral per-sis should therefore be undertaken cautiously and judiciously, with an fusion improved by 6 minutes, the time at which cerebral injury occursappreciation of the hemodynamic effects and other side effects of the after cessation of blood ﬂow. They then reviewed the literature anddrug. Hypovolemic patients may not tolerate β-agonists such as terbu- reported neonatal outcomes at various time intervals after delivery.taline, because they may already be in a high output state. Given the From these data, delivery within 5 minutes of arrest was most likely tohigh fetal mortality rates with severe burns, delivery may be the most result in good neonatal outcomes.52,217judicious alternative in a viable gestation. Most physicians recommend Subsequently, Katz and coworkers214 reviewed 34 published cases ofcesarean section for the usual obstetric indications. Delivery by cesar- perimortem cesarean section performed between 1985 and 2004 toean section through a burned abdomen and vaginal delivery through assess whether the “4-minute rule” was valid. In this series, 79% deliv-a burned perineum have been reported.208,211-213 ered live infants (30 of 38; 3 sets of twins and 1 set of triplets). Data were available regarding the arrest-to-delivery interval for 25 infants and are presented in Table 57-16. Similar to data presented in earlierCardiopulmonary series, prolonging the arrest-to-delivery interval decreased the likeli- hood of intact survival, although apparently normal neonates wereResuscitation delivered even after more than 15 minutes. Data were also provided about perimortem cesarean sectionand Perimortem potentially negatively impacting maternal survival. Twenty (59%) ofCesarean Section 34 cases provided information regarding maternal hemodynamic status and indicated a beneﬁcial effect on maternal resuscitation effortsCardiac arrest in a pregnant patient is a rare event. According to the after perimortem cesarean. None of the cases had worsening maternalmost recent available data on United States maternal mortality, themost likely neonatal outcome in the setting of a maternal death is alive birth.12 The data do not reﬂect the frequency of arrest occurring TABLE 57-16 PERIMORTEM CESAREANbefore delivery. In a review of 38 patients delivered perimortem by DELIVERIES WITH SURVIVINGcesarean section, the causes included trauma, cardiac abnormalities, INFANTS WITH REPORTS OF TIMEembolism, magnesium overdose, sepsis, intracranial hemorrhage, FROM MATERNAL CARDIACanesthetic complications, eclampsia, and uterine rupture.214 The causesof cardiac arrest in pregnant women are more likely to be acute and ARREST TO DELIVERY OF THEtherefore may be more amenable to aggressive interventions. Several INFANT, 1985-2004physiologic changes of pregnancy negatively affect attempts at cardio- Gestational Agepulmonary resuscitation (CPR): Time (min) (wk) Number of Patients Increased CO and requirement for uterine perfusion 0-5 25-42 8 (normal infant) Aortocaval compression by the gravid uterus in the supine 1 (retinopathy of prematurity and position hearing loss) 3 (condition not reported) Reduced functional residual capacity and increased oxygen 6-10 28-37 1 (normal infant) consumption 2 (neurologic sequelae) Reduced chest wall compliance 1 (condition not reported) Delayed stomach emptying and decreased esophageal sphincter 11-15 38-39 1 (normal infant) tone, which increase the aspiration risk 1 (neurologic sequelae) >15 30-38 4 (normal infants) Aortocaval obstruction should be relieved by placing the patient 2 (neurologic sequelae)in a more lateral recumbent position or by manually displacing 1 (respiratory sequelae)the uterus. CPR can provide only 30% of the CO when the patient is Total 25supine.215 The effectiveness of compressions increases dramatically From Katz V, Balderston K, DeFreest M: Perimortem cesarean delivery:when the patient is tilted in the lateral position.214 Early intubation is Were our assumptions correct? Am J Obstet Gynecol 192:1916-1920,recommended to minimize aspiration risk. The use of sodium bicar- 2005.
CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patient 1189status as a result of perimortem cesarean section; 12 women had tate a worse maternal outcome. If CPR is effective at restoring circula-“sudden” and “profound” improvement at the time of emptying the tion, perimortem cesarean section is not recommended.uterus.214 The following guidelines are being suggested for the managementof maternal cardiac arrest with a viable gestation: Brain Death and Somatic1.2. Begin maternal CPR immediately. Establish an airway. Support during Pregnancy3. Establish intravenous access simultaneously. Brain death is deﬁned as the complete absence of brain function, which4. Institute cesarean delivery if there is no evidence of a maternal pulse is determined clinically by lack of consciousness, movement, respira- by 4 minutes. tory effort, and most reﬂexes. It is conﬁrmed by the lack of activity on5. Sterile technique is not necessary, and the patient need not be electroencephalogram. It is considered distinct from coma and persis- moved to an operating room. tent vegetative state (Table 57-17).2186. Continue CPR efforts during and after delivery. Maternal brain death has been rarely reported in the obstetric and7. Continuous fetal monitoring is not possible because of interference critical care literature. Two reviews on the topic identiﬁed only 12 from resuscitative efforts. The maternal condition dictates whether reported cases since 1982.218,219 Two additional cases were identi- perimortem cesarean section is necessary. ﬁed.220,221 The most common reason for brain death was subarachnoid hemorrhage, followed by trauma and infection. Cesarean section is not recommended in an unstable patient After brain death occurs, the options include immediate delivery,because of anticipated cardiac arrest. This may inadvertently precipi- withdrawal of maternal support, or prolongation of maternal life to TABLE 57-17 FEATURES OF COMA, PERSISTENT VEGETATIVE STATE, AND BRAIN DEATH Feature PVS Coma Brain Death Self-awareness Absent Absent Absent Suffering No No No Motor function No purposeful movement No purposeful movement None or only reﬂex spinal movements Sleep-wake cycles Intact Absent Absent Respiratory function Normal Depressed, variable Absent Electroencephalographic activity Polymorphic delta or theta, Polymorphic delta or theta Electrocerebral silence sometimes slow alpha Cerebral metabolism Reduced by 50% or more Reduced by 50% or more, Absent variable Life expectancy Usually 2-5 yr Varies Death within 2-4 wk (Harvard criteria) Neurologic recovery Nontraumatic: rare after 3 mo Usually recovery, PVS, or No recovery Traumatic: rare after 12 mo death in 2-4 wk PVS, persistent vegetative state. Adapted from Ashwal S, Cranford R: Medical aspects of the persistent vegetative state—ﬁrst of two parts. The Multi-Society Task Force on PVS. N Engl J Med 330:1499-1508, 1994. TABLE 57-18 INTENSIVE CARE MANAGEMENT OF PREGNANT PATIENTS WITH SEVERE NEUROLOGIC INJURY Condition Therapy Physiologic Goal Respiratory failure Controlled hyperventilation, PEEP Physiologic hypercarbia, decrease intracranial pressure, avoid neurogenic pulmonary edema Fluid-resistant hypotension Left lateral position, vasopressors Maintain uteroplacental circulation Hypothermia Warming blankets Prevent fetal bradycardia and IUGR Hyperthermia Cooling blankets Prevent fetal death Nutritional support Enteral or parenteral insulin Maintain positive nitrogen balance (energy intake of 126-147 kJ/kg of ideal body weight), avoid hyperglycemia Panhypopituitarism DDAVP, thyroxine, cortisol Adjust for central diabetes insipidus and adrenocortical insufﬁciency Infection prevention Frequent cultures, catheter line changes Prevent sepsis Deep venous thrombosis prophylaxis Heparin Prevent pulmonary embolism Preterm labor Betamethasone or dexamethasone, consider Prolong gestation tocolysis General condition Expert nursing care DDAVP, L-deamino-8-D-arginine vasopressin; IUGR, intrauterine growth restriction; PEEP, positive end-expiratory pressure.
1190 CHAPTER 57 Intensive Care Monitoring of the Critically Ill Pregnant Patientimprove the neonatal prognosis by advancing gestational age. The 21. Swan HJ, Ganz W, Forrester J: Catheterization of the heart in man withchallenges in providing life support to the brain-dead gravida cannot use of a ﬂow-directed balloon- tipped catheter. N Engl J Med 283:447-451,be underestimated and include hemodynamic instability, panhy- 1970.popituitarism, ventilatory support, temperature regulation, nutrition, 22. American College of Obstetricians and Gynecologists (ACOG): Invasive hemodynamic monitoring in obstetrics and gynecology. ACOG technicalinfectious complications, hypercoagulability, and premature contrac- bulletin no. 175, December 1992. Int J Gynaecol Obstet 42:199-205,tions (Table 57-18).215 Given these challenges, it is surprising that two 1993.patients experienced a latency exceeding 100 days, with a mean latency 23. 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