Geronimo Rodriguez Md ,Joseph Y Li ,Michael Gurevitch and pseudo experts of the RNB and MBC take a look over this article and try, to learn.PLEASE!!

Aggressive Management of Hellp Syndrome and Eclampsia
Judith H. Poole, RNC, MN, FACCE
Hypertensive disorders are the most common medical complication of pregnancy.^1,2 A significant contributor to maternal and perinatal morbidity and mortality,^3,4 hypertension is estimated to complicate approximately 7% to 10% of all pregnancies.⁵ In the United States, preeclampsia ranks second only to embolic events as a major cause of maternal mortality and is directly responsible for approximately 18% of maternal deaths.³ Eclampsia is responsible for approximately 50,000 maternal deaths worldwide each year.⁶ The prevalence of pregnancy-related hypertension has not varied markedly since 1989, when data for this medical risk factor were first available from vital statistics.⁷

Pregnancy-induced hypertension (PIH) is a subtle and insidious disease process. The signs and symptoms of PIH become apparent relatively late in the course of the disease, usually during the third trimester of pregnancy. However, the underlying pathophysiology may be present as early as the eighth week of gestation.^8,9 This delay between the clinical manifestation of signs and symptoms and the onset of the hypertensive pathology can place the woman and fetus at increased risk for nonoptimal outcomes before the care provider is aware of a problem. Therefore, the health care provider must be aware of subtle changes that may be indicative of impending disease.

Historically, several well-defined risk factors have been identified for the development of PIH (Table 1).^10,11 Although risk factors are identified, the individual predictive value of the risk factors for screening and for risk identification has not been verified.

Classification of Disease
Terminology used to describe the hypertensive disorders of pregnancy is imprecise, causing confusion for the provider caring for women with hypertensive complications during pregnancy and childbirth. The American College of Obstetricians and Gynecologists' (ACOG) technical bulletin no. 219, Management of Preeclampsia, outlines the current accepted terminology for the hypertensive disorders of pregnancy.⁵

Two basic types of hypertension occur during pregnancy: chronic hypertension and pregnancy-induced hypertension. The difference is the time of onset in relation to the pregnancy. Chronic hypertension is that which predates the pregnancy or continues beyond 42 days postpartum. Pregnancy-induced hypertension, with onset generally after the 20th week of pregnancy, is a marker for a pregnancy-specific vasospastic condition. Clinically, chronic hypertension and PIH may coexist or occur as separate disease processes.⁵

Once PIH is recognized, it is further classified according to the maternal organ systems affected. Preeclampsia is the progression of PIH, characterized by renal pathology as evidenced by the onset of proteinuria. Pre-eclampsia is either mild or severe, based on maternal or fetal clinical findings. The HELLP syndrome, a form of severe preeclampsia, is a laboratory diagnosis characterized by hepatic pathology as evidenced by hemolysis (H), elevated liver enzymes (EL), and low platelets (LP). Eclampsia is the onset of seizure activity in the woman diagnosed with PIH who has no history of a neurologic or metabolic derangement.⁵

Table 1. Risk Factors for Pregnancy-Induced Hypertension

· First pregnancy or pregnancy of new genetic make-up · Multifetal gestation · The presence of preexisting diabetes, collagen vascular disease, hypertension, or renal disease · Hydatidiform mole · Fetal hydrops · Maternal age (<18 y or >35y) · Maternal weight (<100 lbs or obese) · African-American race · Family history of pregnancy-induced hypertension · Antiphospolipid syndrome · Low socioeconomic status · Late entry or no prenatal care

Pathophysiology of Preeclampsia
Preeclampsia has been called the "disease of theories." There is no single agreed-upon etiology, but ongoing research is attempting to identify the pathophysiology of this process. Although the exact mechanism is unknown, preeclampsia is thought to occur secondary to alterations of the normal physiologic adaptations of pregnancy. Arterial vasospasm, endothelial damage, and platelet aggregation with resultant tissue hypoxia are underlying mechanisms for the clinical manifestation of preeclampsia. In Table 2, the normal hemodynamic values of pregnancy are shown.

Table 2. Normal Hemodynamic Values for Pregnancy



Easterling et al.^12,13 propose that preeclampsia is a hyperdynamic condition, in which the characteristic findings of hypertension and proteinuria result from an increase in cardiac output above normal pregnancy values and renal hyperperfusion. To control the hyperperfusion, renal vasospasms are initiated as a protective mechanism, but the vasospasms eventually produce endothelial damage, proteinuria, and hypertension characteristic of preeclampsia. In several other studies, investigators have proposed that preeclampsia results from endothelial cell injury; increased platelet activation, with platelet consumption in the microvasculature; and excessive clotting activity.^8,14-16 In addition to endothelial damage, arterial vasospasm may contribute to the increase in capillary permeability and red blood cell (RBC) destruction. Endothelial damage and increased capillary permeability allow for increased edema and further depletion of intravascular volume and reduction in colloid osmotic pressure.

The destruction of red blood cells is of concern in women with severe preeclampsia. In the report of a recent study, it is suggested that severe preeclampsia is a state of fixed oxygen extraction.¹⁷ Women with severe preeclampsia demonstrate an abnormally low oxygen consumption, even at high oxygen-delivery levelsùa finding that may prove clinically significant. With a tissue-level oxygen extraction defect, the maternal end-organs and the utero-placental-fetal units will not be adequately perfused.

The most common coagulation abnormality seen in preeclampsia is platelet consumption that results in thrombocytopenia. Arterial vasospasms damage the endothelial lining of blood vessels, activating the hemostatic system and causing platelet aggregation and the formation of a fibrin network.^18,19 Platelet aggregation reduces available circulating platelets and causes a narrowing of the vessel lumen. As RBCs are forced through the fibrin network under high pressure, hemolysis occurs.^18,19

As preeclampsia worsens, renal involvement leads to changes in urinary output and in serum chemistries. Renal blood flow and glomerular filtration are decreased, resulting in oliguria, decreased urine creatinine clearance, and increased blood urea nitrogen, serum creatinine, and serum uric acid.²⁰

Preeclampsia affects the central nervous system (CNS) by inducing cerebral edema and increased cerebral resistance.²⁰ Complications may include headaches, seizures, or cerebral vascular accidents. As CNS involvement worsens, the patient will complain of headaches and visual disturbances or exhibit changes in mentation and level of consciousness. A life-threatening complication of preeclampsia is the development of eclampsia.

The CNS effects of preeclampsia may be responsible for an increase in systemic vascular resistance and hypertension. Recent research suggests that preeclampsia is a state of sympathetic overactivity²¹ that causes an increase in sympathetic-mediated vasoconstrictor activity.

Clinical Manifestations of Preeclampsia
Historically, the classic triad of symptoms for preeclampsia includes hypertension, proteinuria, and edema. However, all of these parameters need not be present for a diagnosis of preeclampsia. (Hypertension alone is diagnosed as PIH.) Hypertension and proteinuria are the most significant indicators of preeclampsia. Edema is significant only if hypertension, proteinuria, or signs of multisystem organ involvement are present. The clinical manifestations of preeclampsia are directly related to the presence of vascular vasospasms. These vasospasms result in endothelial injury, RBC destruction, platelet aggregation, increased capillary permeability, and increased systemic vascular resistance, leading to tissue hypoxia and multiorgan system dysfunction.

Hypertension
Although controversy exists about the most appropriate definition of hypertension, current ACOG⁵ criteria define hypertension as a sustained blood pressure elevation of 140/90 mmHg after the 20th week of gestation, as recorded on two or more measurements taken at least 6 hours apart. An elevation of 30 mmHg in systolic or 15 mmHg in diastolic pressure above first trimester or prepregnancy baseline values is of questionable use for defining hypertension during pregnancy. MacGillivary et al.²² reported that 73% of nulliparous women with normal pregnancy outcomes demonstrated an increase in diastolic blood pressure of more than 15 mmHg during pregnancy, whereas 57% of these women demonstrated an increase in diastolic pressure of more than 20 mmHg. Results of later studies have confirmed these findings.^22-24

Proteinuria
Proteinuria is the excretion of 0.1 g/L (100 mg/L) protein in a random urine specimen, or 0.3 g/L in a 24-hour specimen (300 mg/L), or 1 to 2+ on dipstick. The presence of proteinuria indicates a worsening of the disease process increasing the risk to the woman and the fetus.^25,26

In a recent study, the accuracy of routine dipstick analysis to diagnose proteinuria in hypertensive patients is questioned. Meyer et al.²⁷ reported that among negative or trace readings on urinary protein dipstick determinations, clinically significant proteinuria of 300 mg or more per 24 hours was confirmed by 24-hour urine collections. Furthermore, the negative predictive value for urinary protein dipstick determinations was stated to be 34%. Based on the results reported by Meyer²⁷ asymptomatic women with early renal changes consistent with preeclampsia may be inappropriately diagnosed as disease free.

Edema
Edema is a common finding of pregnancy and is not necessary for the diagnosis of preeclampsia. Intracellular and extracellular edema is present, representing a generalized and excessive accumulation of fluid in tissue. As vasospasms worsen, capillary endothelial damage increases systemic capillary permeability (leakage), leading to hemoconcentration and an increased risk of pulmonary edema.

Severe Preeclampsia
To identify the progression of preeclampsia from mild to severe disease, nursing management requires accurate and thorough observation and assessments. Criteria for severe preeclampsia are in Table 3, and the potential maternal and fetal complications of severe preeclampsia are in Table 4. Table 5 shows laboratory values typical in women with severe preeclampsia or the HELLP syndrome. Severe preeclampsia and the HELLP syndrome are multiorgan system disease processes. The wide range of symptoms and multiple organ system involvement can result in misdiagnosis or delay in treatment. Cocaine intoxication, lupus nephritis, chronic renal failure, and acute fatty liver of pregnancy are examples of conditions that may mimic preeclampsia and eclampsia.^28-32

HELLP Syndrome
HELLP syndrome^19,33, a multisystem disease, is a form of severe preeclampsia in which the woman reports a variety of complaints and exhibits common laboratory markers for a syndrome of hemolysis (H), elevated liver enzymes (EL), and low platelets (LP). This subset of women progress from preeclampsia to the development of multiple organ system compromise. The complaints range from malaise, epigastric pain, and nausea and vomiting to nonspecific viral syndrome-like symptoms. Symptoms generally develop in these patients in the second or early third trimester of pregnancy; initially, they may show few signs of preeclampsia. Because of the symptomatology these patients often receive a nonobstetric diagnosis, delaying treatment and increasing maternal and perinatal morbidity and mortality.^18,19,33,34 Assessments and management of the woman diagnosed with HELLP syndrome are the same as for the woman with severe preeclampsia.

Table 3. Criteria for Severe Preeclampsia

· Systolic blood pressure of 160 mmHg or diastolic blood pressure of 110 mmHg on two occasions at least 6 hours apart with the patient on bedrest · Proteinuria of 5 g or greater in 24 hours, or 3-4+ on dipstick · Oliguria, less than 400-500 mL of urine output over 24 hours, or altered renal function tests · Elevated serum creatinine > 1.0 mg/dL · Intrauterine growth restriction · Cerebral or visual disturbances including but not limited to altered level of consciousness, headache, scotomata, or blurred vision · Impaired liver function demonstrated by right upper quadrant or epigastric pain and/or altered liver function · Thrombocytopenia: platelet count < 150,000 · Pulmonary or cardiac involvement: may present as pulmonary edema, cyanosis, chest pain, cardiac dysrhythmias

Table 4. Potential Maternal and Fetal Complications of Severe Preeclampsia

· Cardiovascular: severe hypertension, hypertensive crisis, pulmonary edema · Renal: oliguria, acute renal failure · Hematologic: hemolysis, decreased oxygen-carrying capacity, thrombocytopenia, coagulation defects including disseminated intravascular coagulation · Neurologic: eclampsia, cerebral edema, cerebral hemorrhage, cerebral vascular accidents, amaurosis (blindness) · Hepatic: hepatocellular dysfunction, hepatic rupture, hypoglycemia · Uteroplacental: abruptio placentae, fetal growth retardation, fetal intolerance to labor, fetal death

Table 5. Laboratory Findings With Severe Preeclampsia and the HELLP Syndrome



Eclampsia
Eclampsia is the development of convulsions, coma, or both in a woman with signs and symptoms of preeclampsia. Other causes of seizures must be excluded. Eclampsia can occur antepartum, intrapartum, or postpartum; approximately 50% of cases occur antepartum.³⁵

The immediate care during a convulsion is to ensure a patent airway. Once this has been attained, adequate oxygenation must be maintained by use of supplemental oxygen. MgSO₄ (and amobarbital sodium for recurrent convulsions) is given according to institution protocol.^5,36 Suggested management of an eclamptic seizure is as follows:^2,36

· Do not attempt to shorten or abolish the initial convulsion. Attempts to administer anticonvulsants intravenously without secure venous access can lead to phlebitis and venous thrombosis.

· Prevent maternal injury during the convulsion. Because the woman may have vomiting, the airway must be protected.

· Maintain adequate oxygenation. Once the convulsion has stopped and the woman has begun spontaneous respirations, oxygenation status is monitored. If spontaneous respirations are not present, ventilatory support will be required.

· Minimize the risk of aspiration. The woman should be positioned to facilitate drainage from the mouth. Suction equipment should be readily available and in working order. Also, if supplemental oxygen is being administered by face mask, be aware of the possibility of vomiting and aspiration. After a convulsion, a chest radiograph may be ordered to rule out aspiration.

· Give adequate magnesium sulfate to control the convulsion. As soon as possible after the convulsion venous access should be secured and a 4- to 6-g loading dose of MgSO₄ given in a 15- to 20-minute period. If the woman convulses after the loading dose, another 2-g bolus may be given intravenously, in 3 to 5 minutes.

· Correct maternal acidemia. Blood gas analysis will allow monitoring of oxygenation and pH status. Respiratory acidemia is possible after convulsion, but sodium bicarbonate is not administered unless the pH is less than 7.10.² Ensuring adequate respiratory status is essential.

· Avoid polypharmacy. Maternal respiratory depression, respiratory arrest, or cardiopulmonary arrest is more likely in women receiving polytherapy to arrest convulsion. Remember that anticonvulsant drugs are respiratory depressants and may interact.

Rapid assessments of uterine activity, cervical status, and fetal status are performed. During the convulsion, membranes may rupture and the cervix may dilate because the uterus becomes hypercontractile and hypertonic. If birth is not imminent the timing and route of delivery (induction of labor versus cesarean delivery) depend on maternal and fetal status. All medications and therapy are merely temporary measures.

Medical Management for Severe Preeclampsia: The HELLP Syndrome
The only definitive therapy for preeclampsia is delivery. Objectives of medical management for any pregnancy complicated by severe preeclampsia or the HELLP syndrome are termination of pregnancy with the least possible trauma to mother and fetus, birth of an infant who subsequently thrives, and complete restoration of health to the mother.³⁷ For the woman with mild disease, these objectives are reasonable.

For the woman with severe preeclampsia, HELLP syndrome or eclampsia, especially at preterm gestation, these objectives are often unrealistic. In this situation, delivery may be the most appropriate management decision. Suggested management for the woman with severe preeclampsia includes:³⁶

· On diagnosis, admit to the hospital and initiate parenteral magnesium sulfate prophylaxis and antihypertensive therapy if diastolic blood pressure is higher than 110 mmHg for maternal pharmacologic management of severe preeclampsia-HELLP syndrome is described in Table 6.

· If there is evidence of maternal or fetal jeopardy, if gestational age is more than 34 weeks, or if labor has begun, deliver.

· If hospital admission results in stabilization of the woman and if gestational age is more than 28 weeks, consider expectant management; timing and route of delivery depend on evaluation of maternal or fetal assessments for reassuring findings and gestational age.

· If gestational age is 24 to 28 weeks, begin maternal counseling, institute prophylactic magnesium sulfate therapy and antihypertensive therapy as indicated, and monitor maternal and fetal status daily. Deliver if there is evidence of fetal lung maturity and maternal or fetal deterioration.

· If gestational age is less than 24 weeks, consider termination of pregnancy.

Additional management decisions include assessment of maternal central hemodynamic status and the treatment of persistent oliguria. Routine use of a pulmonary artery (PA) catheter in uncomplicated, severe preeclampsia is not recommended. Use of a PA catheter may be indicated if there are complications related to central volume status, including pulmonary edema, persistent oliguria unresponsive to traditional management, or intractable severe hypertension unresponsive to first-line antihypertensive agents.^38,39

Management of persistent oliguria is based on the understanding that three hemodynamic subsets of preeclamptic eclamptic patients have been identified.^40,41

· Hypovolemic oliguria is the most common clinical occurrence. Symptoms include low pulmonary capillary wedge pressure, hyperdynamic left ventricular function, and mild to moderate increased systemic vascular resistance. The condition is thought to be secondary to intravascular volume depletion and generally responds to fluid volume replacement.

· In renal artery spasm, normal or increased pulmonary capillary wedge pressure, normal cardiac output, normal systemic vascular resistance, and uroconcentration. Oliguria is thought to be secondary to intrinsic renal arterial spasm out of proportion to systemic vasospasm. Low-dose dopamine infusion (1- to 5-mg/kg per minute) may be used.

· Hypervolemic oliguria causes symptoms of elevated pulmonary capillary wedge pressure and systemic vascular resistance, with depressed ventricular function. Incipient pulmonary edema may be the first sign in this subset of patients with oliguria. Aggressive afterload reduction and diuresis should be used.

If urinary output is less than 25 mL/hour for 2 consecutive hours, a medical plan of care should be established. A fluid challenge of 500 to 1,000 mL of normal saline or lactated Ringer's solution is usually ordered to be infused in a 30-minute period. If urine output does not respond, and if the woman is not expected to deliver in a reasonable time, a PA catheter should be considered if more aggressive medical management is attempted.^39,40


Table 6. Pharmacological Management of Severe Preeclampsia/HELLP Syndrome




Controversial Management Protocols
Several management protocols are considered to be inappropriate or controversial in the care of the woman with severe preeclampsia or eclampsia. Diuretics and the administration of high concentrations of colloid solutions (albumin, hetastarch) should not be used to decrease peripheral edema caused by further depletion of intravascular volume and an increased risk of pulmonary edema and uteroplacental insufficiency.^20,42 Valium is no longer the first-line agent to stop seizure activity related to the depressant effect on the fetus and mother.² If diazepam is ordered, a rapid bolus may lead to apnea, cardiac arrest, or both. Diazepam should not be administered intravenously unless someone skilled in intubation is immediately available.² Seizure precautions, including administration of intravenous magnesium sulfate, should be followed according to institution protocol. Finally, heparin should not be administered as prophylaxis against coagulopathy because of the compromise in the maternal vascular system.⁴³

Nursing Implications
Nursing care involves very accurate and astute observations and assessments. A comprehensive knowledge base regarding pharmacologic therapies, management regimes, and possible complications is also required.

Assessments
Preeclampsia can occur without warning or with the gradual development of symptoms. Systematic assessments are critical, with the frequency of assessments dictated by the patient's (maternal or fetal) condition and response to therapy.

History. Obtain a thorough medical and perinatal history on all women diagnosed with PIH. The medical history includes the presence of underlying cardiovascular disease, diabetes, systemic lupus erythematosus, renal disease, pulmonary disease, migraine headaches, or seizure disorders. Perinatal history includes the presence of PIH, abruptio placentae, fetal demise, or fetal growth restriction in any previous pregnancy; also, include past pregnancy outcomes. Current pregnancy history includes prepregnancy blood pressure, presence of proteinuria, hypertension, amniotic fluid volume, fetal growth, fetal assessment test results, and current fetal status. It is also important to note whether the woman complains of unusual, frequent, or severe headaches, visual disturbances, or epigastric pain.

Cardiovascular Assessment. The cardiovascular assessment is performed to identify signs of cardiac decompensation. Assessments include the following parameters: auscultation of heart sounds, lungs, and breath sounds; edema, increases or changes every shift; early signs or symptoms of pulmonary edema, including tachycardia and tachypnea; daily weight; skin color, temperature, and turgor; capillary refill. Oxygen saturation monitoring (pulse oximetry) and cardiac monitoring are performed if indicated by clinical condition; however, neither should replace clinical assessment.

Accurate and consistent blood pressure assessment is important for establishing a baseline and for monitoring subtle changes throughout the pregnancy. Blood pressure readings are affected by maternal position and measurement techniques. Consistency in obtaining readings must be ensured, including proper equipment and cuff size, correct position of the woman, a rest period before recording the pressure, and use of Korotkoff phase IV sounds.^44-47 Debate remains within the medical community regarding which Korotkoff sound (phase IV or V) should be used for evaluating diastolic blood pressure. Korotkoff sound phase IV is characterized by a muffling of the sound, whereas phase V is the disappearance of the sound. The World Health Organization (WHO), The British Hypertension Society, and the International Society for the Study of Hypertension in Pregnancy (ISSHP) all recommend that phase IV be used in recording diastolic blood pressure. Phase IV measurement is more reproducible during pregnancy, but when compared with intraarterial catheters, phase IV may overestimate diastolic pressures by as much as 15 mmHg.^48,49 Phase V measurement can be more accurately determined than phase IV, but women demonstrate an extremely wide variation in phase V readings because of the hyperkinetic circulation of pregnancy.⁴⁷ It is not unusual in pregnancy to obtain a phase V measurement of 0.

If the initial blood pressure measurement indicates an elevation, the woman should be allowed to relax and have a repeat measurement performed, maintaining position used for initial measurement.⁵ In using electronic blood pressure devices, there is a normal widening of the pulse pressure compared with that in manual readings; however, the mean arterial pressure is unchanged.^50,51 The main point to remember is that blood pressure measurements should be taken in a consistent manner, because assessments focus on blood pressure trends that develop with passing time, not a single reading.

The presence of edema plus hypertension or proteinuria warrants additional investigation. Edema is assessed by distribution and degree. Assessments are directed at signs of cardiopulmonary and renal involvement, indicating worsening of disease.

Respiratory Assessment. Respiratory assessments are performed to identify signs of pulmonary edema, respiratory compromise, or magnesium toxicity. Respiratory rate is evaluated for rate, quality, and pattern, especially if receiving magnesium sulfate, to identify early signs of toxicity. Labored respirations or use of the accessory muscles are assessed. Breath sounds are auscultated every shift, or more often if indicated, to identify diminished breath sounds, crackles, or wheezes; pulmonary edema can develop very quickly. Tachypnea and tachycardia are early signs of evolving pulmonary edema. Skin color and mucous membranes are assessed for the presence of cyanosis, which may indicate problems with oxygenation or perfusion. Monitoring oxygenation status with pulse oximetry is performed as indicated by the woman's clinical condition and response to therapy. However, pulse oximetry should not replace clinical assessments.

Renal Assessment. Renal assessments are performed to identify signs of renal failure. The volume of urinary output is evaluated every 1 to 4 hours. The output should be at least 25 to 30 mL/hour or 100 mL/4-hour period. If oliguria is present (less than 25 mL/hour) or serum creatinine is elevated, the woman is at increased risk for magnesium toxicity. Urine is evaluated for protein by dipstick analysis. However, testing proteinuria by dipstick analysis may be a poor substitute for a 24-hour urine in women with preeclampsia or the HELLP syndrome.²⁷ A 24-hour urine collection for total protein and creatinine clearance is a more accurate measure of renal function.

Laboratory evaluation of renal function includes electrolytes, blood urea nitrogen (BUN), serum creatinine, serum protein, and uric acid determinations. A normal serum creatinine value during pregnancy is less than 1 mg/dL and a normal creatinine clearance is 115 to 150 mL/minute.⁵² As serum creatinine increases or creatinine clearance declines, the woman is at increased risk for magnesium toxicity or renal impairment. Creatinine clearance approximates glomerular filtration rate and may be calculated by the following formula:⁵³

CrCl = (140 - age) X weight(kg) X 0.85
72 X serumCr
Placement of an indwelling Foley catheter with urometer facilitates accurate assessment of fluid balance and early signs of renal compromise. The presence of oliguria in the woman laboring with a Foley catheter may indicate fetal descent, causing a mechanical obstruction of the catheter.

Hematologic Assessment. Hematologic assessments are monitored to identify signs of hemolysis, coagulation defects, and decreased oxygen carrying capacity. Monitoring of RBC count can identify anemia or the presence of hemolysis, both of which decrease oxygen-carrying capacity. Morphologic study of RBC will also indicate the presence of hemolysis, in that Burr cells and schistocytes will be present. Determining the status of platelet number and function identifies an evolving coagulopathy. Women are at increased risk of hemorrhage once platelet counts fall below 100,000 X 10⁹/L.⁵⁴

Central Nervous System Assessment. Assessments of the CNS are performed to identify signs of hypoxemia, increasing CNS irritability, increasing intracranial pressure, cerebral hemorrhage, and magnesium toxicity. For the woman receiving magnesium sulfate, deep tendon reflexes (DTRs) are assessed and the findings recorded. The most frequent DTRs evaluated are knee-jerk response. Deep tendon reflexes should be present, but not hyperactive (1+ to 2+). The evaluation of DTR is especially important if the woman is being treated with magnesium sulfate; absence of DTR is an early indication of impending magnesium toxicity. Assess the woman's level of consciousness and identify changes in behavior or the presence of apprehension, anxiety, or restlessness. Such findings may be early indications of evolving pulmonary edema or hypoxemia. The presence of a headache, visual changes or changes in behavior or level of mentation may be early signs of increasing intracranial pressure.

Fetal Assessments. An important ongoing assessment is determination of fetal status. Uteroplacental perfusion is decreased in women with preeclampsia, thereby placing the fetus in jeopardy. The spiral arteries of the placental bed are subject to vasospasm. When this occurs, perfusion between maternal circulation and the intervillous space is compromised, decreasing blood flow and oxygenation to the fetus. Oligohydramnios, intrauterine growth restriction, fetal stress, and intrauterine fetal death are all associated with preeclampsia. The fetal heart rate is assessed for baseline rate, variability, and reassuring versus nonreassuring patterns. The presence of abnormal baseline rate, decreased or absent variability, or late decelerations are indications of fetal intolerance to its intrauterine environment. The presence of variable decelerations are suggestive of decreased amniotic fluid volumes (oligohydramnios), increasing the risk of umbilical cord compression and fetal compromise. Biophysical or biochemical monitoring for fetal well-being may be ordered: fetal movement counts, nonstress testing, contraction stress testing, biophysical profile, and serial ultrasonographic scanning.^2,43

Uterine tonicity is evaluated for signs of labor and abruptio placentae. If labor is suspected, a vaginal examination for cervical changes is indicated. Early signs of abruptio placentae are uterine tenderness and fetal tachycardia; the presence of vaginal bleeding is not necessary for diagnosis.

Laboratory Tests
The nurse assists in obtaining a number of blood and urine specimens to aid in the diagnosis and management of severe preeclampsia, HELLP syndrome, or eclampsia. At present, no known laboratory tests predict the development of preeclampsia or eclampsia. Baseline laboratory test information is useful in the early diagnosis of preeclampsia and for comparison with results obtained to evaluate progression and severity of disease. See Table 5 for common laboratory values assessed in the woman with hypertension during pregnancy.

Pharmacologic Therapies
Pharmacologic therapies are used for seizure prophylaxis and antihypertensive management. (See Table 6 for common pharmacologic therapies for the hypertensive disorders of pregnancy).

Seizure Prophylaxis
Magnesium sulfate. Magnesium sulfate (MgSO₄) is the drug of choice in the management of preeclampsia to prevent seizure activity. MgSO₄ is always administered as a secondary infusion, through an infusion-controlled device to achieve serum levels of approximately 5 to 8 mg/dL (4 to 7 mEq/dL). The loading dose is a 4-to 6-g bolus administered intravenously in 15 to 30 minutes; followed by a maintenance infusion of 2 to 3 g/hour.^2,5,36

The action of magnesium sulfate as an anticonvulsant is controversial, but it is thought to decrease neuromuscular irritability and block the release of acetylcholine at neuromuscular junctions, depressing the vasomotor center, thereby depressing central nervous system irritability.

Side effects of magnesium sulfate are dose dependent and include: flushing, nausea, vomiting, headache, lower maternal temperature, blurred vision, respiratory depression, and cardiac arrest. The effect of magnesium sulfate on fetal heart baseline variability is controversial; a decrease in baseline variability may be seen.

Nursing responsibilities and assessments for the woman receiving magnesium sulfate include assessment of maternal baseline vital signs, deep tendon reflexes, and urinary output before initiation of therapy and reassessment according to institution protocol; preparation of MgSO₄ according to protocol; establishment of primary intravenous infusion and administration of MgSO₄ as a secondary infusion through an infusion-control device; documentation of MgSO₄ infusion in grams per hour; accurate fetal assessment; keeping calcium gluconate at bedside (antidote for magnesium toxicity); exercising caution in concurrent administration of narcotics, CNS depressants, calcium channel blockers, and beta blockers; and discontinuation of MgSO₄ and notification of primary care provider if signs of toxicity develop (loss of knee-jerk reflexes, respiratory depression, oliguria, respiratory arrest, cardiac arrest) or if the woman complains of shortness of breath or chest pain. If signs of magnesium toxicity occur, be prepared to give 1 g of calcium gluconate (10 mL of a 10% solution), as a slow intravenous bolus.

Phenytoin. Phenytoin has limited use for eclampsia prophylaxis; however, it is not a first-line therapy in the United States.⁵⁵ Clinical studies have not demonstrated better results with phenytoin when compared with those obtained with magnesium sulfate. Because of the lack of obstetric experience with phenytoin and significant maternal side effects, magnesium sulfate remains the first-line drug in the United States.

Antihypertensive Therapy
Pharmacologic therapies directed at the control of significant hypertension include a variety of agents. There are several general precautions to be considered when antihypertensive agents are ordered during pregnancy: When blood pressure is sustained at or greater than 160 mmHg systolic or 110 mmHg diastolic, antihypertensive therapy is initiated to prevent maternal cerebral vascular accident; effect of the agent may depend on intravascular volume status and hypovolemia, secondary to increased capillary permeability and hemoconcentration, which may need correction before the initiation of therapy; and diastolic blood pressure should be maintained between 90 to 100 mmHg to sustain uteroplacental perfusion.

Hydralazine hydrochloride. Hydralazine hydrochloride (Apresoline) is considered by many to be the first-line agent to decrease hypertension. Dosage regimens vary, but intermittent intravenous boluses (5 to 10 mg repeated every 15 to 20 minutes) are generally as effective as continuous infusions; there is also less chance of rebound hypotension with intermittent boluses. Side effects of hydralazine include flushing, headache, maternal and fetal tachycardia, palpitations, uteroplacental insufficiency with subsequent fetal tachycardia, and late decelerations. Because hydralazine increases maternal cardiac output and heart rate, hypertension may worsen.

Labetalol. Labetalol has recently been used in place of hydralazine for the management of hypertension. If hydralazine is used as a first-line antihypertensive agent, labetalol is then given as a second-line drug. Dosage regimes vary, based on physician experience and preference. Labetalol is contraindicated in women with asthma and in those with greater than first-degree heart block.⁵⁶ Rebound hypotension is less common with labetalol than with hydralazine hydrochloride.⁵⁶ Because of labetalol's alpha and beta adrenergic blockade, transient fetal and neonatal hypotension, bradycardia, and hypoglycemia are possible.

Nifedipine. Nifedipine (Procardia) may be used as a third line agent in the treatment of hypertension. Again, protocols vary. With the administration of nifedipine, a calcium channel blocker, care must be taken with concomitant administration with magnesium sulfate and beta blockers, in that these drugs may potentiate each other.

Other Antihypertensive Agents. For women experiencing a hypertensive crisis or for those in whom traditional therapy fails, alternative antihypertensive agents may be used. Nitroglycerin is used for hypertension refractory to conservative pharmacologic therapy. It works to relax predominantly venous but also arterial vascular smooth muscle and will decrease preload at low doses and afterload at high doses. Side effects include hypotension, tachycardia, nausea, vomiting, pallor, sweating, headache, flushing, and methemoglobinemia (intravenous doses greater than 7 mg/kg per minute). Fetal stress may occur with a mean arterial pressure less than 106 mmHg and fetal heart rate variability may be diminished. Sodium nitroprusside (Nipride) is indicated for severe hypertension or hypertensive crisis. Nipride is a potent vasodilator with direct effect on arterial and venous smooth muscle. Side effects include nausea, diaphoresis, anxiety, headache, bradycardia, changes in electrocardiograph, tachycardia, raised intracranial pressure, decreased reflexes, blurred vision, and cyanide toxicity. Fetal side effects are possible because sodium nitroprusside crosses the placental barrier.

Postpartum Management
After birth, most women will stabilize within 48 hours. However, because of the risk of eclampsia during the first 24 to 48 hours, careful monitoring of vital signs, level of consciousness, and DTRs and laboratory assessments are continued. Additional assessments focus on identifying the development of postpartum hemorrhage, disseminated intra-vascular coagulopathy, pulmonary edema, HELLP syndrome, increased intracranial pressure, and intracranial hemorrhage. Intravenous MgSO₄ is continued for at least the first 24 hours after birth. Immediate postpartum curettage has been associated with a more rapid recovery in cases of severe preeclampsia, although more research is needed in this area.^57,58 Efforts are made to initiate maternal-newborn attachment by bringing the newborn, if stable, to visit the mother. Photographs of the newborn can be taken and provided to the woman if either maternal or newborn condition prevents visitation.

Summary
The most common medical complication of pregnancy is hypertension. Women diagnosed with the HELLP syndrome or eclampsia present a variety of management issues and problems for the health care provider. Regardless of the diagnosis, severe pre-eclampsia, the HELLP syndrome, or eclampsia can profoundly affect the woman and her fetus. The underlying pathophysiology must be evaluated and treated with both patients in mind at all times. Nurses caring for the woman diagnosed with severe preeclampsia, the HELLP syndrome, and eclampsia must be fully aware of the risk factors, diagnostic criteria, appropriate management regimes, and the potential complications for both the woman and her fetus.

References
1. Poole J. Legal and professional issues in critical care obstetrics. Crit Care Nurs Clin North Am 1992;4:687-690.
2. Sibai B. Hypertension in pregnancy. In Gabbe S, Niebyl J, Simpson J, eds. Obstetrics: Normal & Problem Pregnancies. 3rd ed. New York: Churchill Livingstone; 1996: 935-996.
3. Berg C, Atrash H, Koonin L, Tucker M. Pregnancy-related mortality in the United States, 1987-1990. Obstet Gynecol 1996;88: 161-167.
4. Wilcox L, Marks J. From Data to Action: CDC's Public Health Surveillance for Women, Infants, and Children. Washington, DC,: US Department of Health & Human Services, Public Health Services, Centers for Disease Control and Prevention; 1994:412.
5. American College of Obstetricians and Gynecologists. Management of preeclampsia. ACOG Tech Bull 1996;219.
6. Duley L. Maternal mortality associated with hypertensive disorders of pregnancy in Africa, Asia, Latin America and the Caribbean. Br J Obstet Gynaecol 1992;99:547-553.
7. Ventura S, Martin J, Taffel S, Mathews T, Clarke S. Advance Report of Final Natality Statistics, 1993. Monthly Vital Statistics Report. Hyattsville, MD: National Center for Health Statistics; 1995:1-88.
8. Friedman SA, Taylor RN, Roberts JN. Pathophysiology of preeclampsia. Clin Perinatol 1991;18:661-682.
9. Robertson WB, Khong TY. Pathology of the uteroplacental bed. In Sharp F, Symonds EM, eds. Hypertension in Pregnancy. Ithaca, NY: Perinatology Press; 1987:101.
10. Davies AM, Czaczkes JW, Sadovsky E. Toxemia of pregnancy in Jerusalem. I. Epidemiological studies of a total community. Isr J Med Sci 1970;6:253.
11. Davies AG. Geographical Epidemiology of the Toxemias of Pregnancy. Springfield IL: Charles C Thomas; 1971.
12. Easterling TR, Benedetti TJ. Preeclampsia: A hyperdynamic disease model. Am J Obstet Gynecol 1989;160:1447-1453.
13. Easterling TR. The maternal hemodynamics of preeclampsia. Clin Obstet Gynecol 1992;35: 375-386.
14. Roberts J, Taylor R, Goldfien A. Endothelial cell activation as a pathogenetic factor in preeclampsia. Semin Perinatol 1991;15:86-93.
15. Taylor RN, Casal DC, Jones LA. Selective effects of preeclamptic sera on human endothelial cell procoagulant protein expression. Am J Obstet Gynecol 1991;165:1705-1710.
16. Zeeman GG, Dekker GA. Pathogenesis of preeclampsia: A hypothesis. Clin Obstet Gynecol 1992;35:317-337.
17. Belfort M, Anthony J, Saade G, et al. The oxygen consumption/oxygen delivery curve in severe preeclampsia: Evidence for a fixed oxygen extraction state. Am J Obstet Gynecol 1993;169:1448-1455.
18. Sibai BM. The HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets): Much ado about nothing? Am J Obstet Gynecol 1990;162:311-316.
19. Weinstein L. Syndrome of hemolysis, elevated liver enzymes, and low platelet count: A severe consequence of hypertension in pregnancy. Am J Obstet Gynecol 1982;142: 159-163.
20. Dildy GA, Phelan JP, Cotton DB. Complications of pregnancy-induced hypertension. In Clark SL, Cotton DB, Hankins GDV, Phelan JP, eds. Critical Care Obstetrics. 2nd ed. Boston: Blackwell Scientific Publications; 1991: 251-288.
21. Schobel H, Fischer T, Heuszer K, Geiger H, Schmieder R. Preeclampsia: A state of sympathetic overactivation. N Engl J Med 1996;335: 1480-1485.
22. MacGillivary I, Rose GA, Rowe D. Blood pressure survey in pregnancy. Clin Sci 1969;37: 395-407.
23. Moutquin JM, Fainville RN, Raynauld P. A prospective study of blood pressure in pregnancy: Prediction of preeclampsia. Am J Obstet Gynecol 1985;151:191-196.
24. Villar MA, Sibai BM. Clinical significance of elevated mean arterial blood pressure in second trimester and threshold increase in systolic and diastolic blood pressure during third trimester. Am J Obstet Gynecol 1989;160: 419-423.
25. Mabie WC, Pernoll ML, Biswas MK. Chronic hypertension in pregnancy. Obstet Gynecol 1986;67:197-205.
26. MacGillivary I. Some observations on the incidence of pre-eclampsia. Br J Obstet Gynecol 1958;65:536-543.
27. Meyer N, Mercer B, Friedman S, Sibai B. Urinary dipstick protein: A poor predictor of absent or severe proteinuria. Am J Obstet Gynecol 1994;170:137-141.
28. O'Brien WF. Predicting preeclampsia. Obstet Gynecol 1990;75:445û=-456.
29. O'Brien WF. The prediction of preeclampsia. Clin Obstet Gynecol 1992;35:351-364.
30. Poole JH. Getting perspective on HELLP syndrome. Am J Matern Child Nurs 1988;13: 432-437.
31. Poole JH. HELLP syndrome and coagulopathies of pregnancy. Crit Care Nurs Clin North Am 1993;5:475-487.
32. Simpson K. Acute fatty liver of pregnancy. J Obstet Gynecol Neonat Nurs 1993;22: 213-219.
33. Weinstein L. Preeclampsia/eclampsia with hemolysis, elevated liver enzymes, and thrombocytopenia. Obstet Gynecol 1985;66: 657-661.
34. Martin JN, Blake PG, Perry KG, McCaul J, Hess L, Martin R. The natural history of HELLP syndrome: Patterns of disease progression and regression. Am J Obstet Gynecol 1991; 164:1500-1513.
35. Fairlie FM, Sibai BM. Hypertensive diseases in pregnancy. In Reece EA, Hobbins JC, Mahoney MJ, Petrie RH, eds. Medicine of the Fetus and Mother. Philadelphia: J.B. Lippincott; 1993.
36. Sibai B. Treatment of hypertension in pregnant women. N Engl J Med 1996;335:257-265.
37. Cunningham FG, MacDonald PC, Gant NF, Leveno KJ, Gilstrap LC, III. Williams Obstetrics. 19th ed. Norwalk, CT: Appleton & Lange; 1993.
38. American College of Obstetricians and Gynecologists. Invasive hemodynamic monitoring in obstetrics and gynecology. ACOG Tech Bull 1992;175.
39. Clark SL, Cotton DB, Hankins GDV, Phelan JP. Handbook of Critical Care Obstetrics. Boston: Blackwell Scientific Publications; 1994.
40. Clark SL, Greenspoon JS, Aldahl D, Phelan JP. Severe preeclampsia with persistent oliguria: Management of hemodynamic subsets. Am J Obstet Gynecol 1986;154:490-494.
41. Lee W, Gonik B, Cotton DB . Urinary diagnostic indices in preeclampsia-associated oliguria: Correlation with invasive hemodynamic monitoring. Am J Obstet Gynecol 1987;156: 100-103.
42. Repke JT. Hypertension and preeclampsia. In Moore TR, Reiter RC, Rebar RW, Baker VV, eds. Gynecology & Obstetrics: A Longitudinal Approach. New York: Churchill Livingstone; 1993:463-477.
43. Cunningham F, MacDonald P, Gant N, et al. Williams Obstetrics. 20th ed. Stamford, CT: Appleton & Lange; 1997.
44. Redman CWG, Beilin LJ, Bonner J. Treatment of hypertension in pregnancy with methyldopa: Blood pressure control and side effects. Br J Obstet Gynecol 1977;84:419-422.
45. Reiss RE, Tizzano TP, O'Shaughnessy RW. The blood pressure course in primiparous pregnancy. A prospective study of 383 women. J Reprod Med 1987;32:523-526.
46. Sibai BM. Pitfalls in diagnosis and management of preeclampsia. Am J Obstet Gynecol 1988;159:1-5.
47. Wichman K, Ryden G, Wichman G. The influence of different positions and Korotkoff sounds on blood pressure measurements in pregnancy. Acta Obstet Gynecol Scand 1984; 118(suppl):25-28.
48. Lindheimer M, Katz A. Renal physiology and disease in pregnancy. In Seldin D, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. 2nd ed. New York: Raven Press; 1992:3371-3431.
49. Wallenburg HCS. Hemodynamics in hypertensive pregnancy. In Rubin PC, ed. Hypertension in Pregnancy: Handbook of Hypertension. Amsterdam: Elsevier; 1988:66-101.
50. Cashion K, Schulz K, Sibai BM, Anderson GD. Consistency of Blood Pressure Measurement and Recording during Pregnancy. 5th Congress ISSHP. Nottingham, England; 1986.
51. Marx GF, Schwalbe SS, Cho E, Whitty JE. Automated blood pressure measurements in laboring women: Are they reliable? Am J Obstet Gynecol 1993;168:796-798.
52. Ramsay M, James D, Steer P, Weiner C, Gonik B. Normal Values in Pregnancy. Philadelphia: WB Saunders; 1996.
53. Schoolwerth A, Gehr T. Clinical Assessment of Renal Function. In Ayres S, Grenvik A, Holbrook P, Shoemaker W, eds. Textbook of Critical Care. 3rd ed. Philadelphia: WB Saunders; 1995:1018-1029.
54. Leduc L, Wheeler JM, Kirshon B, Cotton DB. Coagulation profile in severe preeclampsia. Obstet Gynecol 1992;79:14-18.
55. Repke JT, Friedman SA, Kaplan PW. Prophylaxis of eclamptic seizures: Current controversies. Clin Obstet Gynecol 1992;35:365-374.
56. Chez R, Sibai BM. Labetalol for intrapartum hypertension. Contemp Obstet Gynecol 1994;39:37-38.
57. Magann E, Martin J, Isaacs J, Perry K, Martin R, Meydrech E. Immediate postpartum curettage: Accelerated recovery from severe preeclampsia. Obstet Gynecol 1993;81:502-506.
58. Magann E, Martin JJ. Complicated postpartum preeclampsia/eclampsia. Obstet Gynecol Clin North Am 1995;22:337-356.