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(BQ) Part 2 book Civetta, taylor, & kirby’s manual of critical care has contents: Special patient population, respiratory disorders, neurologic disease and dysfunction, renal disease and dysfunction, endocrine disease and dysfunction,.... and other contents.
P1: Trim: 8.375in × 10.875in LWBK937-61-65 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 SECTION X August 12, 2011 ■ SPECIAL PATIENT POPULATION CHAPTER 61 ■ THE OBSTETRIC PATIENT: GENERAL sReview is focused mainly on the most life-threatening patho- sWomen who exceed 18 kg of weight gain during pregnancy are considered at greater risk for maternal (preeclampsia, gestational diabetes) and fetal (increased incidence of operative delivery) complications physiologic processes (Tables 61.1 and 61.2): sThrombosis and thromboembolism sHypertensive disease of pregnancy sHemorrhage sAmniotic fluid embolism sPeripartum cardiomyopathy sPulmonary edema Metabolism and Respiration sKey physiologic changes of respiration in pregnancy are: sIncreased minute ventilation—caused by increased respira- PHYSIOLOGIC CHANGES ASSOCIATED WITH PREGNANCY tory center sensitivity and drive sCompensated respiratory alkalosis sLow expiratory reserve volume sVital capacity and measures of forced expiration are well Body Constitution preserved sWomen with severe lung diseases tolerate pregnancy well sExcept for those with pulmonary hypertension or chronic sOptimal weight gain in pregnancy is currently a matter of debate sGenerally, weight gain of kg attributed to fetus, placenta, and uterus sRemainder attributed to increase in maternal blood, interstitial fluid volume, and fat sGestational weight gain of more than 12 kg in women of normal prepregnant weight is related to the lowest risk for complications during delivery respiratory insufficiency from parenchymal or neuromuscular disease sLung volumes measured in pregnant women and compared to nonpregnant women or those in the postpartum state sWell preserved in the majority of cases sResidual volume tends to decrease slightly, which leads to a small increase or stability of the vital capacity TA B L E DIRECT MATERNAL DEATHS, 2000–2002a Cause of death Thrombosis and thromboembolism Hypertensive disease of pregnancy Hemorrhage Amniotic fluid embolism Deaths in early pregnancy: Total Ectopic Spontaneous miscarriage Legal termination Other Genital tract sepsis Other direct total Genital tract trauma Fatty liver Other Anaesthetic Total number of deaths 1985–87 1988–90 1991–93 1994–96 1997–99 2000–02 32 27 10 22 16 6b 27 6 15 139 33 27 22 11 24 15 7b 17 145 35 20 15 10 18 9b 14 8 128 48 20 12 17 15 12 14c 134 35 15 17 13 2 14c 106 30 14 17 15 11 11c 106 a Deaths reported to the Enquiry only and excluding other deaths identified by ONS Excluding early pregnancy deaths due to sepsis Including early pregnancy deaths due to sepsis From Confidential Enquiry into Maternal and Child Health (CEMACH), Chiltern Court (Lower ground floor), 188 Baker Street, London Publication 2004: Why Mothers Die 2000–2002 b c 383 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 384 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Section X: Special Patient Population TA B L E INDIRECT MATERNAL DEATHS, 2000–2002a Causes of indirect deaths Cardiac Psychiatric Other indirect Indirect malignancies Total number of indirect deaths 1985–87 1988–90 1991–93 1994–96 1997–99 22 N/A 62 N/A 84 18 N/A 75 N/A 93 37 N/A 63 N/A 100 39 86 N/A 134 35 15 75 11 136 2000–02 44 16 90 155 N/A, not available Deaths reported to the Enquiry only and excluding other deaths identified by ONS From Confidential Enquiry into Maternal and Child Health (CEMACH), Chiltern Court (Lower ground floor), 188 Baker Street, London Publication 2004: Why Mothers Die 2000–2002 a sMost consistent change in static lung volumes with pregnancy is the reduction in the functional residual capacity (FRC) and expiratory reserve volume ❝ As uterus enlarges, FRC decreases by 10% to 25% of the previous value, starting about the 12th week of pregnancy ❝ Normal reduction in FRC is accentuated further in the supine position ❝ Reduction in FRC is due to a decrease in chest wall compliance, up to 35% to 40% sLung compliance remains normal sExpiratory muscle strength is in the low-normal range sDecreased chest wall compliance is the result of the enlarging uterus increasing the abdominal pressure, leading to reduced FRC sDiaphragm elevates about cm, and the circumference of the lower rib cage increases about cm sDecreased FRC leads to an increased area of apposition of the diaphragm to the chest wall, which improves the coupling of the diaphragm and chest wall ❝ Thus, increased tidal volume of pregnancy achieved without an increase in the respiratory excursions of the diaphragm sRib cage undergoes structural changes sProgressive relaxation of the ligamentous attachments of the ribs causes the subcostal angle of the rib cage to increase early in pregnancy ❝ Persists for months into the postpartum period ❝ Increased elasticity mediated by the polypeptide hormone, relaxin, increased during pregnancy and responsible for the softening of the cervix and relaxation of the pelvic ligaments Cardiovascular System sMost important hemodynamic change in the maternal circulation during pregnancy is an increase in the cardiac index of more than 30% (Tables 61.4 and 61.5) Red Blood Cell, Plasma, and Blood Volume sIncreased plasma volume evident by sixth week of gestation sBy the end of the first trimester of 15% above nonpregnant women sSubsequently a steep increase of this parameter until 28 to 30 weeks of gestation to a final volume at term of 55% above the nonpregnant level sRed blood cell mass decreases during first weeks of gestation sIncreases to nearly 30% above the nonpregnant level at term sResult in 45% increase of total blood volume and a reduction of the hemoglobin concentration and hematocrit to values of approximately 11.6 g/100 mL and 35.5%, respectively sEstrogens, progesterone, and placental lactogen elevate aldosterone production either directly or indirectly, and are responsible for the increase of plasma volume during pregnancy sHyperaldosteronism of pregnancy can result in retention up to 500 to 900 mEq of sodium and an increase of 6,000 to 8,000 mL of total body water, 70% of which is extracellular sElevated red blood cell volume after to 12 weeks can be attributed to increased serum erythropoietin sErythropoiesis may also be stimulated by prolactin, progesterone, and placental lactogen TA B L E BLOOD GAS ANALYSIS IN LATE PREGNANCYa Changes in Arterial Blood Gases sHormonal changes of pregnancy lead to remarkable respiratory changes throughout its course (Table 61.3) sMean arterial PO2 during pregnancy consistently >100 mm Hg sNo alterations of dead space-to-tidal volume ratio (VD /VT ) and shunt pH 7.44 HCO3 – (mMol / L) 20 PaO2 (mm Hg) PaCO2 (mm Hg) 103 30 BE (mMol / L) 2.5 a Averages Data from Templeton A, Kelman GR Maternal blood-gases, PAO2 –PaO2 , physiological shunt and VD /VT in normal pregnancy Br J Anaesth 1976;48:1001 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Chapter 61: The Obstetric Patient: General 385 TA B L E HEMODYNAMIC CHANGES IN PREGNANCY % Changea Cardiac output Heart rate Stroke volume Blood volume Plasma volume Red cell volume Oxygen consumption Systemic vascular resistance Systemic blood pressure: Systolic Diastolic Pulmonary vascular resistance Pulmonary artery occlusion pressure (PAOP) Colloid oncotic pressure (COP) COP—PAOP a b Pregnancy Labor and delivery Postpartum +30–50 +10–15 +20–30 +20–80 +44–55 +20–30 +20 –10–25 +50–65b +10–30b +40–70 — — — +40–100b — +60–80 –10–15 +60–80 +0–10 +0–30 –10 –10–15 — –5 –10 –30 –10 –25 +10–30b +10–30b — — — — +10 +10 — — — — Percentage change from nonpregnant state Percentage change without regional anesthesia (local anesthetic) Plasma Proteins and Colloid Osmotic Pressure sTotal serum protein concentration decreases from a nonpregnant value of 7.3 to 6.5 g/100 mL at term gestation sChange due primarily to a decline of the albumin concentration sDecreases from a nonpregnant level of 4.4 to 3.4 g/ 100 mL at term sMaternal colloid osmotic pressure decreases in parallel with the decline in serum albumin concentration from nonpregnant values of 25 to 26 to approximately 22 mm Hg at term Aortocaval Compression sAngiographic studies show that the aorta and inferior vena cava can be significantly compressed by the gravid uterus in the supine position sComplete obstruction of the inferior vena cava at the level of the bifurcation in 80% of patients in late pregnancy sPartial obstruction of the aorta at the level of the lumbar lordosis (L3–L5) demonstrated in patients between the 27th week of pregnancy and term gestation sTerm pregnant woman, when placed in the lateral decubitus position, exhibits a right ventricular filling pressure (central venous pressure) similar to that of a nonpregnant woman sSuggests that venous return in this position is maintained by the collateral circulation despite partial caval obstruction sIn plain supine position right atrial pressure falls substantially, demonstrating that collateral circulation cannot compensate for complete or nearly complete caval obstruction sEvident by 20 to 28 weeks of gestation sResults in a decrease of stroke volume and cardiac output of approximately 25% s20% reduction of uterine blood flow sReliably improved by a tilt to the left of at least 25 degrees sDespite the reduction of cardiac output and stroke volume, a position change from lateral to supine can be associated with elevation of blood pressure sResults from an increase of systemic vascular resistance sDue to compression of the aorta by the gravid uterus sEnhanced sympathetic nervous system outflow TA B L E NORMAL CARDIAC SYMPTOMS AND SIGNS IN PREGNANCY Symptoms Fatigue Dyspnea Decreased exercise tolerance Light-headedness Syncope Signs General: Distended neck veins Peripheral edema Hyperventilation Heart: Loud S1 ; increased split S1 Loud S3 Systolic ejection murmur Continuous murmurs (venous hum, mammary souffle) Chest radiograph: Increased pulmonary vasculature Horizontal position of heart Electrocardiogram: Left axis deviation Nonspecific ST-T–wave changes Mild sinus tachycardia 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 386 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Section X: Special Patient Population sIn approximately 5% of women a substantial drop in blood pressure occurs (“supine hypotensive syndrome”) ❝ Associated with bradycardia (usually following a transient tachycardia) and maternal symptoms, low systemic perfusion such as of pallor and sweating, possibly followed by cardiocirculatory collapse ❝ May be exacerbated by neuraxial block, the preferred method of providing anesthesia in pregnant women sBased on the observations above, the intensivist should always consider in his or her emergency treatment plan the proper positioning of the pregnant patient and its influence on hemodynamics THROMBOSIS AND THROMBOEMBOLISM IN PREGNANCY sVenous thromboembolism (VTE) sIncludes deep venous thrombosis (DVT) and pulmonary embolism, occurs in approximately in 1,000 pregnancies sWomen five times more likely to develop VTE during pregnancy than during a nonpregnant state sFatal pulmonary embolism (PE) remains a leading cause of maternal mortality in the Western world sRate of PE in pregnancy is five time greater than that for nonpregnant women of the same age ❝ Seen in about in 100 deliveries ❝ Risks even higher in the puerperium Risk Factors and Predisposition to Venous Thrombosis sCompared to nonpregnant females, pregnant women have a 10-fold risk of a thrombotic episode (Table 61.6) sPregnancy associated with increased clotting potential, decreased anticoagulant properties, and decreased fibrinolysis sAccompanied by two to three times increased concentration of fibrinogen s20% to 1,000% increase in factors VII, VIII, IX, X, and XII, all of which peak at term sLevels of von Willebrand factor (vWf) increase up to 400% by term sFree protein S levels decline significantly (up to 55%) during pregnancy due to increased circulating levels of carrier molecular, complement four binding proteins TA B L E RISK FACTORS FOR VENOUS THROMBOEMBOLISM (VTE) DURING PREGNANCY Cesarean delivery History of prior VTE Family history of VTE Inherited or acquired thrombophilia Obesity Older maternal age Higher parity Prolonged immobilization sThus pregnancy associated with increase in resistance to activated protein C sLevels of plasminogen activation inhibitor-1 increase three to four times during pregnancy sPlasma plasminogen activation inhibitor-2 values-– negligible before pregnancy-–reach concentrations of 160 mg/L at delivery sPregnancy also associated with venous stasis in the lower extremities due to compression of the inferior vena cava and pelvic veins by the enlarging uterus and hormone-mediated increases in deep vein capacitance secondary to increased circulating levels of estrogen and local production of prostacyclin and nitric oxide sImportant hereditary risk factors that can increase DVT risk are: sAntithrombin III deficiency sProtein S and C deficiency sG1691A mutation of the factor V gene sG20210A mutation of the factor II gene Diagnosis of VTE During Pregnancy sIn pregnant women presenting with: sLower extremity edema sBack pain sAnd/or chest pain sPrevalence of VTE is less than in the general population because of the high frequency of these complaints in the pregnant woman sD-dimer assays-–used to exclude VTE in healthy nonpregnant individuals-–usually positive late in pregnancy sRadiologic studies not been validated in pregnancy sPotential risks to the fetus, particularly in terms of ionizing radiation exposure, need to be considered sCompression ultrasonography (CUS) of the proximal veins has been recommended as the initial test for suspected DVT during pregnancy sWhen results equivocal or an iliac vein thrombosis is suspected, magnetic resonance venography (MRV) can be used sApproach to the diagnosis of PE is similar in the pregnant and nonpregnant sVentilation/perfusion (V/Q) scanning confers relatively low radiation exposure to the fetus, a risk less than that of missing a diagnosis of PE in the mother sWhen V/Q study is indeterminate in a pregnant woman without demonstrated lower extremity thrombosis, it is usually followed by angiography sBrachial approach carries less radiation exposure to the fetus than spiral CT Prevention of Thrombosis During Pregnancy sOptimal anticoagulation regimen not established sLow-molecular-weight heparins (LMWHs) the anticoagulant of choice sThey not cross the placenta (like unfractionated heparin [UFH]) sHave better bioavailability 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Chapter 61: The Obstetric Patient: General sCarry less risk of osteoporosis and heparin-induced thrombocytopenia than UFH sLMWHs safe alternatives to UFH as anticoagulants during pregnancy sRecent practice trend to switch patients to the longer-acting, subcutaneous UFH a few weeks before delivery to allow use activated partial thromboplastin time as a diagnostic test to assess anticoagulation pre- and postlabor sVTE prophylaxis with elastic compression stockings may be used for entire pregnancy sAppropriate for in-hospital patients at increased risk of VTE, and may be combined with the use of LMWH sVena cava filter placement a potentially important but poorly evaluated therapeutic modality in the prevention of pulmonary emboli sRandomized trials to establish the appropriate role of vena cava filters in the treatment of venous thromboembolic disease are lacking Thrombolytic Therapy for Pulmonary Embolism sIndications for thrombolytic therapy for PE controversial sIncidence of intracranial hemorrhage as high as 2% to 3% with systemic thrombolytic therapy sFatality rates in patients with PE presenting in cardiogenic shock as high as 30% ❝ Thrombolytic therapy should be considered in this circumstance, although evidence is limited sApproximately 10% of symptomatic pulmonary emboli are rapidly fatal ❝ 2% of patients were first diagnosed with PE at autopsy ❝ Of patients diagnosed with PE before death, 5% to 10% have shock at presentation – Associated with a mortality of 25% to 50% ❝ Echocardiographic evidence of right ventricular dysfunction at presentation – Suggested as indication for thrombolytic therapy – Recent randomized trial failed to demonstrate a survival benefit with thrombolysis in patients with this finding – Mortality rates with conventional therapy are conflicting sRoutine thrombolysis cannot be justified in all patients HEMORRHAGE sPeripartum hemorrhage remains a significant cause of maternal and fetal morbidity and mortality sIn industrialized nations, massive obstetric hemorrhage ranks among the top three causes of maternal death despite modern improvements in obstetric practice and transfusion services sPeripartum hemorrhage includes a wide range of pathophysiologic events sAntepartum bleeding occurs in nearly 4% of pregnant women sCauses of serious antepartum bleeding are: ❝ Abnormal implantation (placenta previa, accreta) 387 TA B L E MANAGEMENT OF SEVERE POSTPARTUM HEMORRHAGE Conservative Management General Measures Administration of supplemental oxygen Placement of adequate intravenous access lines Intravenous hydration Blood typing and cross-matching Placement of arterial line for repeated blood sampling Pharmacologic Measures Oxytocin Methylergonovine 15-Methyl prostaglandin F2 -α Surgical Management Vascular Ligation Uterine artery Hypogastric artery Ovarian artery Hysterectomy Supracervical Total ❝ Placental abruption ❝ Uterine rupture sMain reason for postpartum bleeding: sUterine atony when myometrial contraction is inadequate sBlood flow perfusing the uterus at term is up to 600 mL/minute sPatients with hemodynamic instability or massive hemorrhage require prompt resuscitative measures (Table 61.7): sAdministration of supplemental oxygen sPlacement of two large-bore intravenous (IV) lines sIV hydration sBlood typing and cross-matching for the replacement of packed red blood cells (PRBCs) sDelay in the correction of hypovolemia, diagnosis and treatment of impaired coagulation, and surgical control of bleeding are avoidable factors in most maternal mortality cases caused by hemorrhage sIf transfusion must be given before full cross-matching, typespecific uncross-matched blood can be used sIf placenta not delivered when hemorrhage begins, it must be removed sPlacenta accreta diagnosed if placental cleavage plane indistinct sIn this situation, the patient should be prepared by the intensivist or the anesthesiologist for probable urgent hysterectomy sFirm bimanual compression of uterus (with one hand in the posterior vaginal fornix and the other on the abdomen) can limit hemorrhage until help obtained sHemorrhage after placental delivery: sShould prompt vigorous fundal massage while the patient is rapidly given 10 to 30 units of oxytocin in L of intravenous crystalloids ❝ Uterotonic agents such as oxytocin routinely used in management of uterine atony ❝ If fundus does not become firm, uterine atony is the presumed (and most common) diagnosis 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 388 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Section X: Special Patient Population – While fundal massage continues – Patient may be then given 0.2 mg of methylergonovine (Methergine) intramuscularly (IM), with dose repeated at 2- to 4-hour intervals if necessary sMay cause undesirable adverse effects such as cramping, headache, and dizziness sCoexisting severe hypertension is an absolute contraindication to its use – Injectable prostaglandins may also be used when oxytocin fails – Prostaglandin E and prostaglandin F2 stimulate myometrial contractions sHave been used IM or IV for refractory hemorrhage due to uterine atony sCarboprost (Hemabate), 15-methyl prostaglandin F2 -α, may be administered IM or intramyometrially in dose of 250 μg every 15 to 90 minutes, to a maximum dose of mg s 68% of patients respond to a single carboprost injection; 86% respond to a second dose s Oxygen desaturation has been reported with the use of carboprost, so patients should be monitored by pulse oximetry ❝ Use of a hydrostatic balloon has been advocated as an alternative to uterine packing for controlling hemorrhage due to uterine atony – Inflated Rusch balloon can conform to the contour of the uterine cavity and provides an effective tamponade – Life-threatening hemorrhage can also be treated by arterial embolization by interventional radiology – Finally, in cases of continuing hemorrhage, surgical techniques can be used to avoid a hysterectomy, such as bilateral uterine artery ligation or internal iliac artery ligation AMNIOTIC FLUID EMBOLISM (AFE) sEntry of amniotic fluid into the maternal circulation recognized in 1926 sTrue incidence of AFE not known, estimated to be between in 8,000 and in 80,000 pregnancies Clinical Presentation sClassic presentation of amniotic fluid embolism is described as a sudden, profound, and unexpected cardiovascular collapse followed, in many cases, by irreversible shock and death sOnly known predisposing factor to this life-threatening complication is multiparity, which accounts for 88% of the cases sA smaller percentage of cases (51%) had respiratory-related presenting symptom sHypotension is present in 27% of surviving cases sCoagulopathy comprising 12% sSeizures 10% sFetal bradycardia (17%) and hypotension (13%) the next most common presenting features (Table 61.8) TA B L E CLINICAL PRESENTATION OF AMNIOTIC FLUID EMBOLISM Acute cardiorespiratory collapse Acute respiratory distress Hypotension Hemorrhage/coagulopathy Seizures Fetal distress Etiology and Pathophysiology sSquamous cells can appear in the pulmonary blood of heterogenous populations of both pregnant and nonpregnant patients who have undergone pulmonary artery (PA) catheterization sPresence of these cells probably the result of contamination by epithelial cells derived from the cutaneous entry site of the PA catheter sIsolated finding of squamous cells in the pulmonary circulation of pregnant patients, with or without coexisting thrombotic pulmonary embolism, seen as a contaminant and not indicative of maternal exposure to amniotic fluid sAmniotic fluid could act as a direct myocardial depressant sIn vitro observation document that amniotic fluid decreases myometrial contractility sHumoral factors, including proteolytic enzymes, histamine, serotonin, prostaglandins, and leukotrienes, may contribute to the hemodynamic changes and consumptive coagulopathy associated with AFE sPathophysiologic mechanism similar to distributive or anaphylactic shock Diagnosis and Management sAFE syndrome a diagnosis of exclusion (Table 61.9) sTreatment is essentially supportive sHemodynamic instability treated with optimization of preload by rapid volume infusion TA B L E DIFFERENTIAL DIAGNOSIS OF AMNIOTIC FLUID EMBOLUS: EXCLUSION CRITERIA Thrombosis Air embolus Septic shock Acute myocardial infarction Peripartum cardiomyopathy Anaphylaxis Aspiration Placental abruption Transfusion reaction Local anesthetic toxicity 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Chapter 62: Cardiac Disease and Hypertensive Disorders in Pregnancy sα-receptor agonist such as phenylephrine useful to maintain adequate aortic perfusion pressure (90 mm Hg systolic) while volume is infused sCoagulopathy treated with aggressive administration of blood component therapy sIf maternal cardiopulmonary resuscitation (CPR) must be initiated, and the fetus is sufficiently mature and is undelivered at the time of the cardiac arrest, a perimortem cesarean section should be immediately instituted 389 Etiology and Diagnosis sPossible causes proposed for PPCM sMyocarditis sAbnormal immune response to pregnancy sMaladaptive response to the hemodynamic stresses of pregnancy sStress-activated cytokines sProlonged tocolysis sDiagnosis of PPCM requires the exclusion of more common PERIPARTUM CARDIOMYOPATHY (PPCM) sA rare disease of unknown cause that strikes women in the childbearing years and is associated with a high mortality rate causes of cardiomyopathy sConfirmed by standard echocardiographic assessment of left ventricle systolic dysfunction sIncluding depressed fractional shortening and ejection fraction documentation Treatment and Prognosis Definition sPPCM defined by the development of left ventricular or biventricular failure in the last month of pregnancy or within months of delivery in the absence of other identifiable cause sIn the United States can affect women of various ethnic backgrounds at any age sMore common in women 30 years of age sStrong association of PPCM with gestational hypertension and twin pregnancy sRaise level of suspicion for this condition in pregnant women who develop symptoms of congestive heart failure sInitiated using standard clinical protocols for heart failure sAngiotensin-converting enzyme inhibitors should be avoided prenatally sLong-term clinical prognosis is usually defined within months after delivery sApproximately half of 27 women studied had persistent left ventricular dysfunction beyond months, with a cardiac mortality rate of 85% over years sAs compared with the group in whom cardiac size returned to normal by the same time interval, with no mortality sIdentification of the underlying cause of heart failure in the pregnant patient is important factor influencing long-term survival CHAPTER 62 ■ CARDIAC DISEASE AND HYPERTENSIVE DISORDERS IN PREGNANCY HYPERTENSIVE DISEASE OF PREGNANCY Diagnosis sHypertensive disorders of pregnancy include: sChronic hypertension sPreeclampsia/eclampsia sPreeclampsia superimposed on chronic hypertension sGestational hypertension sPreeclampsia is a pregnancy-specific, multisystem disorder that is characterized by the development of hypertension and proteinuria after 20 weeks of gestation (Table 62.1) sComplicates approximately 5% to 7% of pregnancies sIncidence of 23.6 cases per 1,000 deliveries in the United States sDiagnostic criteria for preeclampsia include: sNew onset of elevated blood pressure and proteinuria after 20 weeks of gestation sSevere preeclampsia indicated by more substantial blood pressure elevations and a greater degree of proteinuria ❝ Other features of severe preeclampsia include oliguria, cerebral or visual disturbances, and pulmonary edema or cyanosis (Tables 62.2 through 62.4) sChronic hypertension defined by elevated blood pressure that predates the pregnancy sIs documented before 20 weeks of gestation or is present 12 weeks after delivery 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 390 August 12, 2011 Section X: Special Patient Population TA B L E RISK FACTORS FOR PREECLAMPSIA Maternal Fetal s First pregnancy s New partners s Age younger than 18 y or s Multiple gestations s Molar pregnancies (can older than 35 y s Chronic hypertension s Prior history of preeclampsia s Family history of preeclampsia s Pregestational diabetes s Obesity s Thrombophilias s Systemic erythematosus s Renal disease cause preeclampsia at 200 mm Hg refractory to initial antihypertensive therapy sOliguria refractory to repeated fluid challenges sEclamptic seizures sRespiratory insufficiency with pulmonary edema sInitial physical examination should include a neurologic assessment, funduscopic examination, auscultation of the heart and lungs, and palpation of the abdomen (Tables 62.2 and 62.3) sIf magnesium sulphate is given, it should be continued for 24 hours following delivery or at least 24 hours after the last seizure sRegular assessment of urine output, maternal reflexes, respiratory rate, and oxygen saturation is paramount while magnesium is infused sLoading dose of g should be given by infusion pump over to 10 minutes, followed by a further infusion of g/hour maintained for 24 hours after the last seizure sGradual antihypertensive therapy can be accomplished with a 25% reduction of mean arterial pressure within minutes to hours, to 160/100 mm Hg (Table 62.5) The Role of Arterial Lines, Central Venous Pressure Monitors, and Pulmonary Artery Catheters in Preeclamptic Patients sMost severe preeclamptic patients have normal or hyperdynamic left ventricular (LV) function with normal pulmonary artery pressure sCentral venous pressure (CVP) monitoring is usually adequate to assess volume status and LV function 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 August 12, 2011 Chapter 62: Cardiac Disease and Hypertensive Disorders in Pregnancy 391 TA B L E CLINICAL FEATURES OF PREECLAMPSIA Symptoms Headache Visual phenomena Epigastric pain Edema Signs Hypertension >140/ 90 mm Hg Epigastric or right upper quadrant tenderness Hyperreflexia Retinal artery vasospasm on funduscopy The headache that characterizes preeclampsia is typically frontal in location, throbbing in character, persistent, and not responsive to mild analgesia The visual disturbances that characterize preeclampsia are presumed to be caused by cerebral vasospasm and are typically scintillations or scotomas Longer-lasting visual field deficits and rarely transient blindness can result from edema, posterior reversible encephalopathic syndrome, and even infarction in the occipital region of the brain Serous retinal detachments can also occur in preeclampsia and are related to retinal edema Magnesium, which is commonly used to prevent seizures in preeclamptic women, can cause mild visual blurring or double vision but should not cause scotomas, scintillations, or visual loss The epigastric or right upper quadrant discomfort that occurs in preeclampsia can be marked and may be out of proportion to the degree of liver enzyme abnormalities It is believed to be caused by edema in the liver that stretches the hepatic capsule In rare cases, it may be caused by hepatic infarction or rupture Edema is present in more than 30% of normal pregnancies and is thus not a reliable sign of preeclampsia Rapid weight gain (more than pound per week in the third trimester) or edema in the hands or facial area (nondependent edema) is best viewed as a sign that should lead the clinician to evaluate the patient for other, more specific, evidence of preeclampsia Hypertension in preeclampsia is due to vasospasm and can be very labile Ideally, blood pressure should be measured in the sitting position with a manual cuff, with the brachial artery at the level of the heart There is a literature suggesting that some automated blood pressure cuffs may be less reliable in preeclampsia and that either a manual cuff or arterial line should be used to verify blood pressure in preeclamptic patients with severe hypertension Although a rise in systolic/diastolic blood pressure of 30/15 mm Hg was once considered a criterion for diagnosing preeclampsia, it is now recognized that this definition lacks both sensitivity and specificity Abdominal pain in preeclampsia is attributed to hepatic capsular stretching from edema The degree of tenderness is often out of proportion to the degree of elevation of liver function tests Epigastric tenderness is suggestive of severe preeclampsia and is associated with an increased risk of both maternal and fetal adverse outcomes Clonus is an important sign of preeclampsia but should be distinguished from the very brisk reflexes commonly seen in normal pregnancies Retinal vasospasm, retinal edema (in the form of soft exudates), hemorrhage, and exudative retinal detachment are uncommon findings in preeclampsia Papilledema is rare sSeverely preeclamptic patients may develop cardiac failure, progressive and marked oliguria, or pulmonary edema sIn such cases, a pulmonary artery (PA) catheter may be helpful for proper diagnosis and treatment, because right and left ventricular pressures may not correlate ❝ The rather limited literature about their use in obstetric populations is questioned ❝ No clear consensus exists as to their role in the management of preeclampsia ❝ Risks—especially on labor and delivery units where the personnel have less experience in their placement and interpretation—seem to outweigh the evidence justifying their use ❝ An urgent bedside echocardiogram may guide care sAn arterial catheter monitor may be indicated for protracted severe hypertension during therapy with potent antihypertensive agents sMost patients satisfying the criteria for intensive care unit admission should be monitored with central venous access and an arterial catheter FETAL MONITORING IN THE INTENSIVE CARE SETTING sElectronic fetal monitoring (EFM) is used in the management of labor and delivery in nearly three of four pregnancies in the United States sApparent contradiction between the widespread use of EFM and expert recommendations to limit its routine use indicates that a reassessment of this practice is warranted sQuestion of whether fetal monitoring is of any substantial use in the critically ill mother or the mother undergoing surgery sContinuous cardiotocography (CTG) during labor is associated with a reduction in neonatal seizures, but no significant differences in cerebral palsy, infant mortality, or other standard measures of neonatal well-being sThis monitoring technique was associated with an increase in cesarean sections and instrumental vaginal births 21:9 P1: Trim: 8.375in × 10.875in LWBK937-61-65 Top: 0.375 in Gutter: 0.75 in LWBK937-Gabrielli-v1 392 August 12, 2011 Section X: Special Patient Population TA B L E LABORATORY FEATURES OF PREECLAMPSIA Complete blood count with elevated hemoglobin and/or thrombocytopenia Elevated serum creatinine Elevated serum uric acid Elevated liver enzymes Proteinuria DIC screen The “elevation of hemoglobin” seen with preeclampsia (which may manifest as a hemoglobin of 12 g/dL at 37 wk when it would be expected to be closer to 10 g/dL because of the physiologic dilutional anemia that is seen in pregnancy) is due to hemoconcentration Much less commonly, hemoglobin may fall with preeclampsia due to a microangiopathic hemolytic anemia Platelet consumption in preeclampsia can cause an increased mean platelet volume and thrombocytopenia and is an important manifestation of severe disease In severe cases of preeclampsia or HELLP (a subset of preeclampsia), schistocytes (fragmented red cells) may be seen on peripheral smear and can lead to a mild drop in hemoglobin Brisk hemolysis is rare, however, and should lead to the consideration of HUS or TTP Typically serum creatinine is