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With DIC, anticoagulation and procoagulation factors are activated simultaneously. DIC develops when the clotting factor thromboplastin is released into the maternal bloodstream as a result of placental bleeding and consequent clot formation. The circulating thromboplastin may activate widespread clotting in small vessels throughout the body. This process consumes, or "uses up," other clotting factors such as fibrinogen and platelets. The condition is further complicated by activation of the fibrinolytic system to lyse, or destroy, clots. The result is a simultaneous decrease in clotting factors and increase in circulating anticoagulants, which leaves the circulating blood unable to clot. This situation allows bleeding to occur from any area, such as IV sites, incisions, or the gums or nose, as well as from expected sites such as the site of placental attachment during the postpartum period.

In DIC, fibrinogen and platelets are usually decreased, prothrombin and partial thromboplastin times may be prolonged, and fibrin degradation products, the most sensitive measurement, are increased. The D-dimer serum assay, which is normally negative, is a specific measurement of fibrin degradation activity that may be ordered.

The priority in treating DIC is delivery of the fetus and placenta to stop the production of thromboplastin, which is fueling the process. In addition, blood replacement products, such as whole blood, packed red blood cells, and cryoprecipitate, are administered to maintain the circulating volume and to transport oxygen to body cells.
•Amount and nature of bleeding: Time of onset, estimated blood loss before admission to hospital, and description of tissue or clots passed. Peripads and underpads should be saved so that blood loss can be estimated more accurately.
•Pain: Type (constant, intermittent, sharp, dull, severe), onset (sudden, gradual), and location (generalized over abdomen, localized). Is the uterus tender or irritable when palpated gently?
•Maternal vital signs: To identify hypertension or hypotension and tachycardia that occur with hypovolemia. A normal blood pressure can be misleading in a woman with abruptio placentae because she may have been hypertensive before the blood loss caused her blood pressure to fall to normal or hypotensive levels. An indwelling catheter helps identify reduced urine output that may occur before hypotension is evident.
•Condition of the fetus: Application of an electronic monitor to identify trends and patterns in fetal heart rate, baseline variability, and fetal response to uterine activity (late decelerations or loss of baseline variability are of particular concern).
•Uterine contractions: If the membranes are ruptured, placement of an intrauterine pressure catheter allows more precise evaluation of baseline pressure and contraction intensity. Inadequate uterine relaxation, uterine irritability, and high baseline pressures (greater than 20 mm Hg) are common.
•Obstetric history: Gravida, para, previous abortions, preterm infants, previous pregnancy outcomes. History of abruptio placenta.
•Length of gestation: Date of last menstrual period, fundal height, correlation of fundal height with estimated gestation, results of ultrasound examinations performed during pregnancy. With bleeding into the myometrium, the fundus enlarges rapidly as bleeding progresses. A piece of tape can be used to mark the top of the fundus at a given time and then to observe and report increasing fundal size, which suggests that bleeding into uterine muscles is occurring.
•Laboratory data: Laboratory studies include a complete blood count and blood typing and screening. Blood crossmatching is done if transfusion is likely. Type and Rh factor identify possible need for RhoGAM. Other tests may be done serially to identify whether the abruption is stable or worsening. The K-B test identifies fetal blood cells in the maternal circulation. Coagulation studies include fibrinogen, fibrin split products (FSPs), prothrombin and partial thromboplastin times (PT/PTTs), and D-dimer to identify fibrin degradation fragments. A drug screen is done if illegal drug use is suspected or if the woman had no prenatal care.
•Decreased renal perfusion reduces the glomerular filtration rate. Consequently, blood urea nitrogen, creatinine, and uric acid levels rise.
•Glomerular damage secondary to reduced renal blood flow allows protein to leak across the glomerular membrane.
•Loss of protein from the kidneys reduces colloid osmotic pressure and allows fluid to shift to interstitial spaces. This fluid shift may result in relative hypovolemia, which causes increased viscosity of the blood and a rise in hematocrit. Generalized edema often occurs.
•In response to hypovolemia, additional angiotensin II and aldosterone are secreted to trigger the retention of both sodium and water. The pathologic processes spiral: additional angiotensin II results in further vasospasm and hypertension; aldosterone increases fluid retention, and edema is worsened.
•Decreased circulation to the liver impairs liver function and leads to hepatic edema and subcapsular hemorrhage, which can result in hemorrhagic necrosis. This process is manifested by elevated liver enzyme levels in maternal serum. Epigastric pain is a common symptom.
•Vasoconstriction of cerebral vessels leads to pressure-induced rupture of thin-walled capillaries, resulting in small cerebral hemorrhages. Signs and symptoms of arterial vasospasm include headache and visual disturbances, such as blurred vision and "spots" before the eyes, as well as hyperreflexia.
•Decreased colloid oncotic pressure can lead to pulmonary capillary leaks that result in pulmonary edema. Dyspnea is the primary symptom.
•Decreased placental circulation results in infarctions that increase the risk for abruptio placentae and HELLP (which stands for hemolysis, elevated liver enzymes, and low platelets) syndrome (see p. 600). In addition, the fetus may experience IUGR and persistent fetal hypoxemia.
Classification: Miscellaneous anticonvulsant.
Action: Decreases acetylcholine released by motor nerve impulses, thereby blocking neuromuscular transmission. Depresses the central nervous system (CNS) to act as an anticonvulsant; also decreases frequency and intensity of uterine contractions. Produces flushing and sweating as a result of decreased peripheral blood pressure.
Indications: Prevention and control of seizures in severe preeclampsia. Prevention of uterine contractions in preterm labor.
Dosage and Route: A common intravenous (IV) administration protocol for preeclampsia includes a loading dose and a continuous infusion. The loading dose is 4 to 6 g magnesium sulfate administered in 100 mL IV fluid over 15 to 20 minutes. The continuing infusion to maintain control is commonly 2 g/hr. Doses are individualized as needed. Deep intramuscular (IM) injection is acceptable but is painful.
Magnesium sulfate may also be administered in a similar dose profile to stop preterm labor contractions because of the relaxant effects on smooth muscle.
Absorption: Immediate onset following IV administration.
Excretion: Excreted by the kidneys.
Contraindications and Precautions: Contraindicated in persons with myocardial damage, heart block, myasthenia gravis, or impaired renal function. Magnesium toxicity, possibly related to incomplete renal drug excretion, may be evidenced by thirst, mental confusion, or decrease in reflexes.
Adverse Reactions: Result from magnesium overdose and include flushing, sweating, hypotension, depressed deep tendon reflexes, and CNS depression, including respiratory depression.
Nursing Implications: Monitor blood pressure closely during administration. Assess woman for respiratory rate of at least 12 breaths per minute, oxygen saturation of 95% or higher; presence of deep tendon reflexes, and urinary output greater than 30 mL/hr before administering magnesium. Place resuscitation equipment (suction, oxygen) in the room. Keep calcium gluconate, which acts as an antidote to magnesium, in the room along with syringes and needles.
Magnesium is usually administered by intravenous infusion, which allows for immediate onset of action and does not cause the discomfort associated with IM administration. Intravenous magnesium is administered via a secondary ("piggyback") line so that the medication can be discontinued at any time while the primary line remains functional.
Daily weight

Provides estimate of fluid retention.

Blood pressure

To determine worsening condition, response to treatment, or both.

Respiratory rate, pulse oximeter readings

Drug therapy (magnesium sulfate) causes respiratory depression, and drug should be withheld and the physician notified if respiratory rate is 12 breaths/min or as specified by hospital policy. Pulse oximeter readings 95% or greater.

Breath sounds

To identify sounds of excess moisture in lungs associated with pulmonary edema.

Deep tendon reflexes

Hyperreflexia indicates increased cerebral irritability and edema; hyporeflexia is associated with magnesium excess.

Edema

For estimation of interstitial fluid.

Urinary output

Output of at least 30 mL/hr indicates adequate perfusion of the kidneys (25 mL/hr is used by some authorities). Magnesium levels may become toxic if urinary output is inadequate.

Urine protein

Normal protein in a random dipstick urine sample is negative or trace. Higher protein levels suggest greater leaking of protein secondary to glomerular damage with worsening preeclampsia. A 24-hour urine sample is most accurate for quantitative urine protein level.

Level of consciousness

Drowsiness or dulled sensorium indicates therapeutic effects of magnesium; no responsive behavior or muscle weakness is associated with magnesium excess.

Headache, epigastric pain, visual problems

These symptoms indicate increasing severity of the condition caused by cerebral edema, vasospasm of cerebral vessels, and liver edema. Eclampsia may develop quickly.

Fetal heart rate and baseline variability

Rate should be between 110 and 160 beats per minute in a term fetus. Decreasing baseline variability may be caused by therapeutic magnesium level or by inadequate placental perfusion.

Laboratory data

Elevated serum creatinine, elevated liver enzymes, or decreased platelets (thrombocytopenia) are significant signs of increasing severity of disease. Serum magnesium levels should be in the therapeutic range designated by the physician.
The woman's blood volume is usually severely contracted in eclampsia, increasing the risk for poor placental perfusion. Fluid shifts from her intravascular space to the interstitial space, including the lungs, causing pulmonary edema and possibly heart failure as forward blood flow is impeded. Renal blood flow is severely reduced, with oliguria (less than 30 mL/hr urine output) and possible renal failure. Cerebral hemorrhage may accompany eclampsia because of the high blood pressure and coagulation deficits. The woman's lungs should be auscultated at regular intervals, usually hourly. A pulse oximeter provides continuous readings of oxygen saturation. Furosemide (Lasix) may be administered if pulmonary edema develops. Oxygen by facemask at 8 to 10 L/min improves maternal and fetal oxygenation. Digitalis may be needed to strengthen contraction of the heart if circulatory failure results. Urine output should be assessed hourly; if output drops below 30 mL/hr, renal failure should be suspected.

Because eclampsia stimulates uterine irritability, the woman should be monitored carefully for ruptured membranes, signs of labor, or abruptio placentae. While the woman is unresponsive, she should be kept on her side to prevent aspiration and to improve placental circulation. The side rails should be padded and raised to prevent an injury from a fall. When maternal and fetal vital signs have stabilized, delivery of the fetus should be considered.

Aspiration of gastric contents is a leading cause of maternal morbidity after an eclamptic seizure. After initial stabilization, the nurse should anticipate orders for chest radiography and arterial blood gas determination to identify aspiration.
Classification: Concentrated immunoglobulins directed toward the red blood cell antigen Rho(D).
Action: Prevents production of anti-Rho(D) antibodies in Rh-negative women who have been exposed to Rh-positive blood by suppressing the immune reaction of the Rh-negative woman to the antigen in Rh-positive blood. Prevents antibody response and subsequently prevents hemolytic disease of the newborn in future pregnancies of women who have conceived an Rh-positive fetus.
Indications: Administered to Rh-negative women who have been exposed to Rh-positive blood by:
•Delivering an Rh-positive infant
•Aborting an Rh-positive fetus
•Having chorionic villus sampling, amniocentesis, or intraabdominal trauma while carrying an Rh-positive fetus
•Accidental transfusion of Rh-positive blood to an Rh-negative woman
Dosage and Route: One standard dose administered intramuscularly:
•At 28 weeks of pregnancy and within 72 hours of delivery
•Within 72 hours following the termination of a pregnancy of 13 weeks or more of gestation
One microdose within 72 hours following the termination of a pregnancy of less than 13 weeks of gestation.
After accidental transfusion with Rh-positive blood, dosage is calculated based on the volume of blood erroneously administered.
Absorption: Well absorbed from intramuscular sites.
Excretion: Metabolism and excretion unknown.
Contraindications and Precautions: Women who are Rh-positive or women previously sensitized to Rho(D) should not receive Rho(D) immune globulin. Used cautiously for women with previous hypersensitivity reactions to immune globulins.
Adverse Reactions: Local pain at intramuscular site, fever, or both.
Nursing Implications: Type and screen of mother's blood and cord blood of the newborn must be performed to determine the need for the medication. The mother must be Rh-negative and negative for Rh antibodies; the newborn must be Rh-positive. If there is doubt regarding the fetal blood type following spontaneous or elective abortion, the medication should be administered. The drug is administered to the mother, not the infant. The deltoid muscle is recommended for intramuscular administration.
If the mother is Rh-negative, umbilical cord blood is taken at delivery to determine the baby's blood type, Rh factor, and antibody titer (direct Coombs test) of the newborn. Rh-negative, unsensitized mothers who give birth to Rh-positive infants are given an IM injection of RhoGAM within 72 hours after delivery. If RhoGAM is given to the mother in the first 72 hours after delivery of an Rh-positive infant, fetal Rh antigens present in her circulation are destroyed, and she does not form natural, permanent antibodies.

If the infant is Rh-negative, there is no antibody formation, and RhoGAM is not necessary. RhoGAM is also administered after abortion, chorionic villus sampling, and amniocentesis, when fetal-to-maternal transfusion is possible without knowing the fetal blood type, and at 28 weeks of gestation if the mother is Rh-negative and unsensitized. The drug may also be given after trauma if fetal-to-maternal hemorrhage is detected. More than the single 300-mcg dose may be needed for large fetal hemorrhages.

Families are often very concerned about the fetus. Nurses must be sensitive to clues and signals that indicate that the family is anxious, and must be able to offer honest reassurance. This is especially important if the pregnant woman is sensitized and fetal testing is necessary throughout pregnancy.

At birth, the physician or nurse should collect cord blood to determine the blood type and Rh factor of the newborn. During the postpartum period, nurses are responsible for follow-up to determine whether RhoGAM is necessary and to administer the injection within the prescribed time.
As a preventive measure, the fetus is considered Rh positive, and RhoGAM is administered to the unsensitized, Rh-negative woman at 28 weeks of gestation. RhoGAM is a commercial preparation of passive antibodies against Rh factor. It effectively prevents the formation of active antibodies if a small amount of fetal Rh-positive blood enters the circulation of an Rh-negative mother during the remainder of the pregnancy. RhoGAM is repeated after birth if the woman delivers an Rh-positive infant.

A positive indirect Coombs test result indicates maternal sensitization and the presence of antibodies against Rh-positive erythrocytes. The indirect Coombs test is repeated at frequent intervals throughout the pregnancy to determine whether the antibody titer is rising, which indicates that the process is continuing. The fetus will be in jeopardy because fetal erythrocytes are being attacked by maternal anti-Rh antibodies.

Amniocentesis may be performed to evaluate change in the optical density (delta [Δ] OD 450) of amniotic fluid. This measure reflects the amount of bilirubin (residue of red blood cell destruction) present in the amniotic fluid. If the fluid OD remains low, it may indicate that the fetus is Rh-negative or is in no jeopardy if Rh-positive. If the OD is elevated, the fetus is in jeopardy.

Ultrasound examination is used to noninvasively evaluate the condition of the fetus. Doppler studies allow evaluation of cardiac function and blood flow in fetal vessels. Generalized fetal edema, ascites, an enlarged heart, or hydramnios occurs when the fetus is very anemic. Percutaneous umbilical blood sampling (PUBS) or cordocentesis (see Chapter 15), allows invasive sampling of fetal blood from cord vessels to determine the degree of erythrocyte destruction. Because it is invasive, PUBS is reserved for the fetus thought to be significantly affected.

Intrauterine transfusion is the direct infusion of O-negative erythrocytes into the umbilical cord by percutaneous umbilical blood transfusion (see Chapter 15). The transfused erythrocytes must be compatible with maternal blood to avoid destruction by the woman's antibodies. Whole blood is usually used to replace fetal serum proteins. Erythrocytes may also be transfused into the fetal abdominal cavity, where they are gradually absorbed into the circulation.