1. Trang chủ
  2. » Giáo Dục - Đào Tạo

LATE PREGNANCY COMPLICATIONS ppsx

42 133 0

Đang tải... (xem toàn văn)

Tài liệu hạn chế xem trước, để xem đầy đủ mời bạn chọn Tải xuống

THÔNG TIN TÀI LIỆU

Nội dung

325 THIRD TRIMESTER HEMORRHAGE DEFINITION AND ETIOLOGY The only bleeding that normally occurs during late pregnancy is a very small amount (Ͻ15 mL), with loss of the mucous plug prior to delivery. All other bleeding is abnormal and merits investigation. A useful list of the causes of third trimester bleeding is contained in Table 11-1. The health care provider must distinguish between obstetric and nonobstetric bleeding (the two major classifications). Nonobstet- ric causes are much less common in pregnancy and generally are less hazardous. Of the obstetric causes, various forms of placen- tal bleeding account for the vast majority. The most frequent are placenta previa or premature separation of a normally implanted placenta. Rupture of the uterus, rare without previous uterine sur- gery, occurs in up to 1% of patients previously delivered by ce- sarean section. Uterine rupture may cause vaginal bleeding, but most of the loss will be concealed. Nonplacental bleeding, rare during pregnancy, may be due to blood dyscrasia or lower genital tract disorders (e.g., cervical or vaginal infections, neoplasms, or varices). Generally, the bleeding is slight, even with carcinoma of the cervix. INCIDENCE AND IMPORTANCE Second trimester vaginal bleeding of obstetric origin is more com- mon in multiparous women and those with a history of prior preterm delivery. Second trimester bleeding is ominous, being associated with an increased risk of preterm delivery (relative risk 1.9), fetal 11 LATE PREGNANCY COMPLICATIONS CHAPTER Copyright 2001 The McGraw-Hill Companies. Click Here for Terms of Use. BENSON & PERNOLL’S 326 HANDBOOK OF OBSTETRICS AND GYNECOLOGY death (relative risk 5.4), and perinatal death (5-fold increase). If sonography reveals an intrauterine clot, membrane separation, or placenta previa, there is further risk and in these patients, perinatal mortality exceeds 250 per 1000. The etiologies of second trimester bleeding include: circumvallate placenta, early abruptio placenta, and placenta previa. Currently, expectant management is the most common treatment option for pregnancies complicated by second trimester bleeding. Significant vaginal bleeding occurs in 5%–10% of third tri- mester pregnancies and must be carefully evaluated because ob- stetric hemorrhage is the largest cause of maternal morbidity and mortality. Two of the major causes of late pregnancy hemorrhage (placenta previa and placenta abruption) are associated with ciga- rette smoking. Additionally, it is a significant factor in perinatal morbidity and mortality. Most patients have Ͻ500 mL bleeding, but serious hem- orrhage .500 mL will occur in 2%–3% of pregnancies. Overall, mul- tiparas are more commonly affected. TABLE 11-1 ETIOLOGIC CLASSIFICATION OF THIRD TRIMESTER BLEEDING Causes Risk Obstetric Nonobstetric High Placenta previa Coagulopathies Abruptio placentae Cervicouterine Uterine rupture neoplasms Vasa previa Lower genital with fetal malignancies bleeding Moderate Circumvallate Vaginal varices placenta Marginal sinus Vaginal lacerations rupture Low Cervical mucous Cervicitis, eversion, extrusion erosion, polyps (bloody show) DIAGNOSIS OF THE CAUSE OF BLEEDING INITIAL EXAMINATION There are three principles of investigation of third trimester hem- orrhage. ● Because of the extreme hazard of uncontrollable bleeding with placenta previa, vaginal or rectal examination must be avoided until that diagnosis can be excluded. ● All third trimester vaginal bleeding must be investigated in a hospital with the capability of dealing with maternal hem- orrhage and perinatal compromise. ● Immediate assessment of blood loss and hemodynamic sta- tus guides the earliest stage of therapy. Recall that the signs and symptoms of hypovolemic shock include pallor with clammy skin, orthostatic hypotension, syncope, thirst, dys- pnea, restlessness, agitation, anxiety, confusion, declining blood pressure, tachycardia, and oliguria. CRITICAL HEMORRHAGE (HEMODYNAMICALLY UNSTABLE PATIENTS) Antishock therapy must be immediately instituted in all hemodynam- ically unstable patients. The following is one method of initiating that therapy. The patient is placed in the Trendelenburg position. Care is taken that this is not so steep that respiration is compromised. An ad- equate airway is guaranteed by a plastic oral airway, or endotracheal tube. A large-bore (Ն18 gauge) IV is inserted for crystalloid re- placement (saline or lactated Ringer’s solution). Blood is obtained from another vein for CBC, platelets, fibrinogen, PT and PTT, fibrin split products, type and crossmatch for 4–6 units of whole blood or packed red blood cells. In severe cases, it may also be necessary to obtain fresh frozen plasma, platelet packs, electrolytes, and blood gases. The necessity of hemodynamic monitoring is considered. The use of vasoactive drugs is weighed. They are desirable for their phar- macologic effects (e.g., increasing myocardial contractility) or if vol- ume expansion is ineffective. One effective agent is dopamine, 200 mg in 500 mL saline at 2–5 mg/kg/min increasing to 20–50 mg/kg/min. Once the acute measures are taken, an indwelling Foley catheter may be inserted to measure urinary output and obtain details of the acute episode. CHAPTER 11 LATE PREGNANCY COMPLICATIONS 327 BENSON & PERNOLL’S 328 HANDBOOK OF OBSTETRICS AND GYNECOLOGY Use the clot fragility observation test if serial determinations of fibrinogen levels are not immediately available. This is performed by drawing venous blood (2–3 mL) into a clean test tube q 1h. If clot formation fails to occur within 5–10 min or if dissolution of a formed clot follows gentle shaking, a clotting deficiency due pri- marily to lack of fibrinogen and platelets is likely. Examination of the abdomen is gently conducted and the fun- dus measured or the uterine apex marked. The fetal heart rate is frequently recorded and electronic fetal monitoring initiated. Uter- ine tone, fetal presentation, and possible engagement of the pre- senting part (engagement largely excludes total placenta previa) are all observed. Next, it is decided whether the patient must be taken to surgery immediately or if blood transfusions and stabilization must be accomplished first. The patient is readied for surgery (prepare abdomen, obtain in- formed consent, notify the operating room, anesthesia department, and neonatal–pediatrics). Frequent vital signs and FHR (every 2–15 min depending on status) are continued until definitive therapy is accomplished. Delivery and control of hemorrhage are accom- plished as soon as practical. In postpartum hemorrhage, it is evaluated whether selective arterial embolization, prophylactic uterine, or hy- pogastric artery ligation will be of assistance. In all cases of hem- orrhage, erythropoietin use after the acute episode is considered. LESS THAN CRITICAL HEMORRHAGE (HEMODYNAMICALLY STABLE PATIENTS) The patient is placed at bedrest and the history of the acute episode obtained. Also, the obstetric history is obtained and the patient’s vi- tal signs ascertained. A gentle abdominal examination is conducted and the fundus measured or the uterine apex marked. Fetal heart rate is ascertained and electronic fetal monitoring initiated. If elec- tronic fetal monitoring is not available, the FHR is frequently recorded. Uterine tone, uterine irritability, fetal presentation, and the likely station of the presenting part are determined. A large-bore (Ն18 gauge) IV is started to initiate crystalloid maintenance re- placement (saline or lactated Ringer’s solution). Venous blood is obtained for CBC, platelets, fibrinogen, PT and PTT, fibrin split products, type and crossmatch for 2–4 units of whole blood or packed red blood cells from another vein. A gentle vaginal exami- nation is considered. Vaginal examination is indicated before ultra- sonic examination only if delivery may be imminent, the present- ing part is unquestionably engaged, or the patient is in active labor. If vaginal delivery is not imminent, an ultrasound examination as- sists in determination of placental location (possible placenta pre- via) and status (perhaps abruptio placenta). Additionally, the ultra- sound examination should include assessment of fetal well being, estimation of gestational age, and amount and localization of am- niotic fluid. In cases of borderline maturity when a few days delay (if possible) may mean the avoidance of respiratory distress, am- niocentesis and subsequent fetal maturity determination may be use- ful. At this time, sufficient information has usually been obtained to assist in determining which of the three general management options is most desirable based on the maternal status, fetal status, and probable cause of the bleeding. ● Immediate delivery is indicated when there is fetal or ma- ternal compromise, or persistent heavy bleeding. ● Continued labor is warranted with a mature fetus, active la- bor (.4 cm), ruptured membranes, bleeding at a controllable rate, or if there are additional complications making vagi- nal delivery desirable. ● Expectant management is possible in almost 90% of cases because third trimester bleeding will usually subside within 24 h. By saving all pads, a reasonably accurate estimate of blood loss can be made. Generally, the patient is observed for 24 h. If bleed- ing materially decreases or ceases, and she is not near term, she may be transferred for less intensive observation. If placenta pre- via can be excluded, a gentle cervical visualization and pelvic examination may be performed to assist in ascertaining the cause of bleeding. ABRUPTIO PLACENTAE (PREMATURE SEPARATION OF THE PLACENTA, ABLATIO PLACENTAE, AND ACCIDENTAL HEMORRHAGE) DEFINITIONS AND INCIDENCE Abruptio placenta is defined as placental separation from a normal implantation site before delivery of the fetus. It occurs in 1:86 to 1:206 advanced pregnancies, depending on the diagnostic criteria employed, and is responsible for ϳ30% of all late antepartal bleed- CHAPTER 11 LATE PREGNANCY COMPLICATIONS 329 BENSON & PERNOLL’S 330 HANDBOOK OF OBSTETRICS AND GYNECOLOGY ing. About 50% of abruptions occur before labor, but 10%–15% are not diagnosed before the second stage of labor. Abruptio pla- centa may be classified into three groups by clinical and laboratory findings (Table 11-2). ETIOLOGY AND IMPORTANCE The exact cause of placental separation is usually unknown, al- though there are a number of common associations. A previous pla- cental separation carries a recurrence rate of 10%–17%; following TABLE 11-2 GRADES OF ABRUPTIO PLACENTAE Grade Clinical Finding 1 2 3 Vaginal bleeding Uterus Maternal pulse Maternal blood pressure Fetal status Fibrinogen level % of total (approxi- mate) Slight Irritable, Normal Normal Normal Normal 15 Mild to moderate Irritable tetanic Increased Maintained, but postural hypotension Fetal compromise (FHR criteria) Reduced (150–250 mg%) 20–40 Moderate to severe, (but may be concealed) Tetanic, painful Elevated Hypotension to shock Fetal death Ͻ150 mg% and thrombocyto- penia or factor depletion Ͼ45 two previous separations, the incidence is Ͼ20%. The hypertensive states of pregnancy impose a 2.5%–17.9% incidence of abruptio placenta. However, of those cases severe enough to cause fetal de- mise, ϳ50% are associated with hypertensive states of pregnancy (with one half associated with chronic hypertension and one half associated with pregnancy-induced hypertension). Other frequent predispositions to placental separation include high parity, smok- ing, uterine over distention (e.g., multiple pregnancy, hydramnios), vascular disease (e.g., diabetes mellitus, collagen disorders), mi- croangiopathic hemolytic anemia, Factor V Leiden mutation, co- caine usage, and uterine anomalies or tumors. There are direct pre- cipitating causes (in only 1%–5%) of abruptio placenta, including circumvallate placenta, direct uterine trauma (e.g., external ver- sion, automobile and other accidents), sudden reduction of amni- otic fluid, or short cord. DIAGNOSIS The symptoms and signs are variable and are largely predicated on the extent of the problem (Table 11-2). However, the usual symp- toms of abruptio placenta are dark red vaginal bleeding (80%), uter- ine irritability (two thirds), and lower abdominal or back pain (two thirds). The erroneous diagnosis of premature labor will be assigned to about 20%. Fetal compromise (determined by electronic-fetal heart rate criteria) is present in .50% of cases. Because of the protective factors in healthy gravidas, there may be a considerable acute blood loss before anemia develops. Thus, with abruptio placenta, the amount of blood loss is all too frequently out of proportion to the degree of anemia. A peripheral blood smear may reveal schistocytes (suggesting disseminated intravascular co- agulation, DIC). Reduced platelet counts and fibrinogen depletion are common in more severe cases. With DIC, elevated levels of fib- rin split products will be present. Thrombomodulin, a marker of en- dothelial cell damage, has been localized to the placental syncy- tiotrophoblast. It is a highly sensitive and specific marker for acute placental separation. To date, it has not been of value in detection of those where abruption is imminent. PATHOLOGY AND PATHOPHYSIOLOGY Various pathophysiologic mechanisms have been suggested as be- ing operative in abruptio placenta, including local vascular injury leading to decidua basalis vessel disruption, an abrupt rise in uter- ine venous pressure leading to intervillous space engorgement and CHAPTER 11 LATE PREGNANCY COMPLICATIONS 331 BENSON & PERNOLL’S 332 HANDBOOK OF OBSTETRICS AND GYNECOLOGY separation, mechanical factors (e.g., short cord, trauma, sudden loss of amniotic fluid), and possible extrinsic initiation of the coagula- tion cascade (e.g., trauma with the release of tissue thromboplastin). Hemorrhage may occur into the decidua basalis or directly retro- placental, from rupture of a spiral artery. In either case, bleeding oc- curs, a clot forms, and the placental surface cannot provide exchange between mother and placenta. The clot compresses the adjacent pla- centa, and nonclotted blood courses from the site. In either concealed FIGURE 11-1. Types of premature separation of the placenta. (Redrawn from Beck and Rosenthal, Obstetrical Practice, 7th ed. Williams & Wilkins, 1957.) CHAPTER 11 LATE PREGNANCY COMPLICATIONS 333 or external (apparent) bleeding (Fig. 11-1), blood may rupture through the membranes or placenta. The latter has grave significance, for it may lead to maternal–fetal hemorrhage, fetomaternal hemor- rhage, maternal bleeding into the amniotic fluid, or amniotic fluid embolus. Occasionally, extensive intramyometrial hemorrhage leads to a purplish, ecchymotic, and indurated uterus (uteroplacental apoplexy, Couvelaire uterus) and loss of contractility. With severe placental separation there may be DIC. Clinically, the hemorrhagic diathesis consists of widespread petechiae, active bleeding, hypovolemic shock, and failure of the clotting mecha- nisms. Although not directly observable, fibrin is being deposited in small capillaries, resulting in dire complications, for example: renal cortical and tubular necrosis, acute cor pulmonale, and ante- rior pituitary necrosis (Sheehan’s syndrome). DIFFERENTIAL DIAGNOSIS ● Nonplacental causes of bleeding. These usually are non- painful. Rupture of the uterus may cause vaginal bleeding but, if extensive, is associated with pain, shock, and death of the fetus. ● Placental causes of bleeding. Placenta previa is associated with painless hemorrhage and is commonly diagnosed by sonography. ● Undetermined causes of bleeding. In at least 20% of cases, the cause of antepartum bleeding cannot be determined. If serious problems can be ruled out, however, undiagnosed bleeding rarely is critical. TREATMENT EMERGENCY MEASURES If deficient, the clotting mechanism must be restored before any at- tempt is made to deliver the infant. Administer cryoprecipitate, fresh frozen plasma, or fresh blood. Institute antishock therapy. Monitor the fetus continuously. Rupture the membranes, if possible, irre- spective of the probable mode of delivery. SPECIFIC MEASURES Grade 1. When the patient is not in labor, watchful expectancy is indicated, because bleeding ceases spontaneously in many cases. When labor begins, prepare for vaginal delivery in the absence of further complications. BENSON & PERNOLL’S 334 HANDBOOK OF OBSTETRICS AND GYNECOLOGY Grade 2. Anticipate vaginal delivery if labor is expected within about 6 h, especially if the fetus is dead. Cesarean section should be performed if there is persistent evidence of fetal compromise, and the infant is likely to survive. Grade 3. The patient is always in shock, the fetus has died, the uterus is tetanic, and a coagulation defect may be present. After correction of the coagulopathy, deliver the patient vaginally if this can be done within about 6 h. Vaginal delivery is probably best for the multiparous patient. Otherwise, do a cesarean section. SURGICAL MEASURES Cesarean section is indicated when labor is expected to be of long duration (over 6 h), when hemorrhage does not respond to am- niotomy and cautious administration of dilute oxytocin, and when early (not prolonged) fetal compromise is present and the fetus is likely to survive. Hysterectomy rarely is indicated. Even a Couve- laire uterus will contract, and bleeding will almost always cease when the coagulation defect is corrected. PROGNOSIS Worldwide maternal mortality rates are currently between 0.5% and 5%. Most women die of hemorrhage (immediate or delayed) or car- diac or renal failure. Early diagnosis and definitive therapy should reduce maternal mortality rates to 0.3%–1%. Fetal mortality rates range from 50% to 80%. About 30% of patients with premature separation of the placenta are delivered at term. Almost 20% of those with abruptio placenta have no fetal heartbeat on admission to the hospital, and in another 20%, fetal compromise is soon noted. When maternal transfusion is urgently required, the fetal mortality rate will probably be at least 50%. Birth is preterm in 40%–50% of cases of premature separation of the pla- centa. Infants die of hypoxia, prematurity, or delivery trauma. PLACENTA PREVIA Placenta previa occurs when the placenta develops implants low, within the zone of dilatation–effacement of the lower uterine seg- ment. Thus, the placenta precedes the fetus and can block vaginal delivery. Placenta previa complicates 1:200–1:250 pregnancies that continue beyond the 28th week. There is a strong association be- tween previous lower uterine segment cesarean section and subse- [...]... Adolescent pregnancy (younger maternal age) Previous pregnancy Multiple induced abortions Cervical or uterine laceration Onset of pregnancy within four months of prior delivery Current or previous pregnancy Chronic hypertension Severe pregnancy- induced hypertension CHAPTER 11 LATE PREGNANCY COMPLICATIONS 353 TABLE 11-3 (Continued) Current pregnancy Malnutrition Severe anemia Inadequate weight gain during pregnancy. .. CHAPTER 11 LATE PREGNANCY COMPLICATIONS 337 FIGURE 11-4 Normal placenta SONOGRAPHY Sonography is the modality of choice for the diagnosis of placenta previa False negative reports of placenta previa with sonography in early pregnancy are uncommon However, there are enough false positives to warrant confirmatory sonography at 26–30 weeks if placenta previa is suspected in mid -pregnancy Late in pregnancy, ... benefit PROLONGED PREGNANCY (POSTDATES) There is no accurate end point of pregnancy; however, prolonged pregnancy is defined as one that has continued for $294 days, or 14 days beyond the EDC, as calculated from the LMP or other means (280 ϩ 14 ϭ 294 days, or 42 weeks.) About 5% of all pregnancies go beyond 294 days Prolonged pregnancy may be recidive (a woman who has had one postdate pregnancy has 2... resuscitation CHAPTER 11 LATE PREGNANCY COMPLICATIONS 349 with crystalloids and colloids and the utilization of plasma-poor red cells With this therapy, plasma content is minimal; thus, deficits of plasma and coagulation factors develop earlier than with whole blood and packed red blood cells Characteristically, hypofibrinogenemia develops first followed by other coagulation factor deficits and later by thrombocytopenia... previa in many hospitals in the United States before expectant treatment was approximately 15%, or more than 10 times that of normal term pregnancy This has dropped, and the rate probably can be reduced to , 10% with current management CHAPTER 11 LATE PREGNANCY COMPLICATIONS 341 PLACENTA ACCRETA When the placenta directly adheres to, penetrates into, or entirely traverses the myometrium, it is termed... CHAPTER 11 LATE PREGNANCY COMPLICATIONS 355 TABLE 11-4 RELATIVE CONTRAINDICATIONS TO LABOR SUPPRESSION Mature fetus Probable lethal fetal defects Fetal death Fetal compromise (including that occurring with tocolysis) Chorioamnionitis Ruptured membranes Bulging membranes Cervical dilation of Ͼ4 cm and effacement Ͼ80% Polyhydramnios Erythroblastosis fetalis Severe intrauterine growth retardation Severe pregnancy- induced... Pelvic drainage may be necessary Abscesses may require surgical drainage CHAPTER 11 LATE PREGNANCY COMPLICATIONS 345 PROGNOSIS The maternal mortality rate due to puerperal sepsis in the United States is about 0.2%, but in some areas of the world, the mortality rate is vastly greater The morbidity of severe sepsis is related to the multiple organ dysfunction syndrome manifest by disseminated intravascular... levels often heralds shock (Also see p 350.) TREATMENT Shock is an acute emergency that takes precedence over all other problems except acute hemorrhage, cardiac arrest, and respiratory CHAPTER 11 LATE PREGNANCY COMPLICATIONS 347 failure To act effective, the primary cause of shock must be determined promptly A brief history (if available) and the gross physical findings often permit the differentiation...CHAPTER 11 LATE PREGNANCY COMPLICATIONS 335 quent risk of placenta previa Moreover, the risk increases with the number of previous cesarean sections: one cesarean increases the risk 2.2-fold, two cesareans increase the... inserted and volume expansion continued until the pulmonary capillary wedge pressure (PCWP) is Ն14–16 mm Hg Should the blood pressure fail to respond to volume expansion and if the left CHAPTER 11 LATE PREGNANCY COMPLICATIONS 351 ventricular function curve is depressed, begin inotropic therapy with dopamine and digoxin If there is no improvement in left ventricular function curve, add dobutamine or isoproterenol . on the diagnostic criteria employed, and is responsible for ϳ30% of all late antepartal bleed- CHAPTER 11 LATE PREGNANCY COMPLICATIONS 329 BENSON & PERNOLL’S 330 HANDBOOK OF OBSTETRICS AND. sonography in early pregnancy are uncommon. However, there are enough false positives to warrant confirmatory sonography at 26–30 weeks if placenta previa is suspected in mid -pregnancy. Late in pregnancy, it. investigational circum- stances) has been reported to be safe and to prolong pregnancy in CHAPTER 11 LATE PREGNANCY COMPLICATIONS 339 BENSON & PERNOLL’S 340 HANDBOOK OF OBSTETRICS AND GYNECOLOGY selected

Ngày đăng: 05/08/2014, 16:20

TỪ KHÓA LIÊN QUAN

TÀI LIỆU CÙNG NGƯỜI DÙNG

TÀI LIỆU LIÊN QUAN