Beyond the Basics: Preeclampsia and Eclampsia

     You arrive on the scene to find a 25-year-old pregnant patient complaining of sudden weight gain and a new onset of nausea, vomiting, blurred vision and headache. She tells you she noticed swelling to her hands when she was unable to remove her wedding ring. She also states that she has not been urinating as usual, but thought it was due to dehydration from vomiting. During your history, you gather that she is in her 28th week of pregnancy, has no known allergies, no pertinent past medical history, and is only taking prenatal vitamins. She had some tea and toast about four hours prior to your arrival; however, she vomited most of it up shortly after eating. She has not changed her activity throughout the pregnancy and does not recall any events that were unusual.

     Your partner obtains a set of vital signs as you continue to gather information regarding the current complaints. The BP is 152/98 mmHg, heart rate 92 bpm, respirations 22 per minute with an adequate tidal volume, and the skin is a normal color, warm and dry. Her SpO₂ reading is 97% on room air. The ECG monitor shows a normal sinus rhythm. During the physical exam, you note edema to the face and hands and a tender right upper quadrant.

     Based on the presentation, one might consider the complaints to parallel those of a normal pregnant patient. By using your critical thinking skills, this assumption becomes less likely. Weight gain occurs throughout pregnancy; it is not sudden in any one trimester. Nausea and vomiting are most likely to occur during the first trimester from hormonal changes and are less likely in the third trimester. Edema is not uncommon, especially in the third trimester, as the weight of the fetus compresses the pelvic and femoral vessels, causing impaired venous return. However, it is important to note that the edema is typically found in the lower extremities and most notably in the ankles and feet. This patient experienced a sudden onset of edema to the hands and face. Urinary frequency is common in the first trimester and returns to normal in the second trimester. In the third trimester, the large uterus compresses the bladder, once again increasing the frequency of urination. This patient experienced a decrease in urine output. The blood pressure decreases slightly during the first and second trimester, but returns to nonpregnant levels during the third trimester. This patient is presenting with a relatively elevated blood pressure. The heart rate appears to be slightly elevated, taking into consideration that a pregnant patient will experience an increase in heart rate of approximately 10 to 15 bpm. The respiratory rate is slightly elevated, but this is also expected in pregnancy.

     When you view the complaints and physical assessment findings cumulatively, there are some imperative indicators that are outside of what would be considered normal for a pregnant patient. Even though the signs and symptoms are somewhat subtle and do not overtly make one suspect an immediately life-threatening condition, there are consistent findings pointing to preeclampsia, which could be life-threatening for the fetus and mother.

     Preeclampsia develops after the 20th week of gestation and can manifest signs and symptoms up to the first few days after delivery. Preeclampsia was formerly known as toxemia of pregnancy due to the theory that a poison or toxin produced the condition. It is also frequently referred to as pregnancy-induced hypertension, since the condition is manifested by an elevated systolic and diastolic blood pressure. The terms are often used interchangeably; however, there are variations among the two.

     Interestingly, preeclampsia was so named because it was recognized historically as occurring prior to eclampsia. Eclampsia is considered a complication of severe preeclampsia and may occur if preeclampsia is unrecognized or left untreated. Approximately 25% of cases develop in the postpartum period, with approximately 98% occurring on the first postpartum day, while the other cases occur during the pregnancy following the 20th week of gestation. Eclampsia is distinguished by convulsive activity that mimics a generalized tonic-clonic seizure and coma. This condition puts the mother and fetus at increased risk for morbidity and mortality.

     Preeclampsia occurs in approximately 5% of all pregnancies in the United States, which represents an incidence of 23.6 cases per 1,000 deliveries. Eclampsia occurs in 0.05% to 0.2% of all pregnancies. Preeclampsia is the third-leading cause of death related to pregnancy, with hemorrhage and embolism ranking first and second, respectively. It accounts for approximately 790 maternal deaths per 100,000 live births. The maternal mortality rate for eclampsia is 8%–36%. Maternal morbidity and mortality from preeclampsia and eclampsia are related to organ ischemia associated with vasospasm and small vessel thrombosis, coagulation disorders, kidney damage, stroke, cerebral hemorrhage, seizures and abruptio placentae. Fetal morbidity and mortality may result from premature delivery, abruption placentae infarction of the placenta, ischemic encephalopathy and intrauterine growth retardation.

     African-American women have a higher mortality rate compared with Caucasians, with some literature suggesting the mortality risk is two times greater. Preeclampsia and eclampsia occur most often in women who became pregnant at both reproductive age extremes. Pregnant women younger than 20 years of age are at highest risk, especially if pregnant for the first time. Women older than 35 years are also at a high risk.

     The etiology of both preeclampsia and eclampsia remains unclear. It is thought that the underlying factor is hypoperfusion of the placenta. This may be due to the abnormal formation of uteroplacental spiral arteries, making them highly susceptible to vasoconstriction. Preeclampsia is described as a condition where there is an abnormally high peripheral vascular resistance with a relatively normal or low intravascular volume. Thus, even though the patient may present with hypertension upon assessment of vital signs, she may actually be volume-depleted. Vasoconstriction of the placental vessels promotes ischemia or infarction. The hypoperfusion state of the placenta is thought to lead to the release of vasoactive substances causing an inflammatory response, vasoconstriction, coagulation disorders, an increase in capillary permeability and platelet dysfunction. All of these will contribute to organ dysfunction and clinical signs of the disease process.

     Hypertension is one of the primary manifestations of preeclampsia. Hypertension in preeclampsia is defined as a systolic blood pressure greater than 140 mmHg and a diastolic blood pressure greater than 90 mmHg in a pregnant patient who was normotensive in her prepregnant state or prior to the 20th week of gestation. The blood pressure must remain elevated on two successive measurements 4 to 6 hours apart. If preexisting hypertension was present prior to the pregnancy or 20th week of gestation, an increase of greater than 30 mmHg systolic and 15 mmHg diastolic is used as a guide in determining preeclampsia. Severe preeclampsia is associated with a systolic blood pressure greater than 160 mmHg and a diastolic blood pressure greater than 110 mmHg that is measured on two occasions at least six hours apart while the patient is on bedrest. Unless the patient has been measuring and tracking her blood pressure prior to your arrival, it is not possible for EMS to adhere strictly to this diagnostic criterion in making a field differential diagnosis; however, you must have a high index of suspicion and consider preeclampsia in a pregnant patient in her 20th week of gestation or further along who presents with a blood pressure greater than 140/90 mmHg, or 30/15 mmHg greater than what was normal in the prepregnancy state, and other clinical signs and symptoms such as headache and visual disturbances.

     Proteinuria that develops after the 20th week of gestation is another major clinical diagnostic criterion. There is, however, no test administered in the prehospital environment that can determine the level of protein in the urine.

     Most women who develop preeclampsia can deliver a healthy baby. However, the more severe the preeclampsia and the earlier it occurs in the pregnancy, the greater the risk for both patient and fetus. Complications associated with preeclampsia include eclampsia, HELLP syndrome, placental hypoperfusion and abruptio placentae.

     Eclamptic seizures, which represent the hallmark progression from preeclampsia to eclampsia, are also not well understood. These are seizures that occur without any evidence of other underlying metabolic or structural conditions. It is thought that the seizures result from the same pathology as what is occurring in the placenta. Cerebral vasospasm, edema, ischemia, infarction, hemorrhage and ionic shifts are thought to incite seizure activity. If a seizure occurs in the first trimester or well into the postpartum period, you should suspect and assess for other central nervous system causes.

     Although the relationship is not clearly understood, approximately 10% of preeclamptic and 30%–50% of eclamptic patients develop HELLP—a syndrome associated with hemolysis, elevated liver enzymes and a low platelet count. Patients with both conditions develop liver dysfunction, which is associated with a higher mortality rate. In addition, the low platelet count can be problematic because it can increase the risk of bleeding into the brain, especially when it exists in eclamptic hypertension.

     Constriction of the uteroplacental arteries creates a hypoperfused placenta. The reduced blood flow delivers less oxygen and nutrients to the fetus, which may retard fetal growth or precipitate low-birth-weight babies, preterm birth or stillbirth.

     Another complication of preeclampsia is an increased risk of abruptio placentae, when the placenta prematurely separates from the uterine wall. Depending on the degree of separation, this puts the pregnant patient at great risk for severe hemorrhage. Separation of the placenta may also significantly reduce fetal blood flow and increase the risk of fetal mortality.

     Mild to moderate preeclampsia may go unnoticed by the patient, since it remains relatively asymptomatic. This is especially true of the pregnant patient often seen in the prehospital environment who has had no prenatal care or very inconsistent or sporadic prenatal care. Routine prenatal screening would be necessary to identify patients with mild to moderate preeclampsia. Thus, if a patient presents with a more severe case of preeclampsia or eclampsia and does not report any past medical history of such, she may have not been aware that she actually had a milder form of the condition if prenatal care was inconsistent or absent. Most often, you will be responding for a patient who is experiencing a more severe form of preeclampsia and has end-organ effects that are producing abnormal signs and symptoms that are recognized by the patient. In the most severe cases, the patient may be seizing. It is then important to determine if she has a preexisting medical condition that makes her prone to seizures, if the seizure is a manifestation of eclampsia, or if she is experiencing some other central nervous system pathology, such as a hemorrhagic stroke, that is causing her to seize. Pregnant patients who seize due to a preexisting condition would not typically present with hypertension and some of the following complaints upon assessment. History is very important in making a differential field diagnosis in this case.

     Common signs and symptoms of preeclampsia are:

•      Hypertension

       A blood pressure greater than 140/90 mmHg or 30/15 mmHg over preexisting blood pressure is cause for concern.

•      Edema

       A certain amount of swelling is absolutely normal for the pregnant patient; however, a sudden increase in edema or edema involving the face or eyes that is consistent with preeclampsia is not considered normal.

•      Proteinuria

       This is a result of protein spilling into the urine due to small vessel damage in the kidney. Although proteinuria is a major diagnostic criterion, it is unfortunately not tested for in the prehospital environment.

•      Sudden weight gain

       A gain of more than 2 lbs. in one week or greater than 6 lbs. in a month may be concerning. Again, if the patient has not been tracking weight gain through consistent prenatal care, it will be very difficult for the prehospital provider to make any judgments on the relationship between weight gain and the possibility of preeclampsia.

•      Headache

       Headache is often described as dull, throbbing, migraine-like and persistent.

•      Nausea and vomiting

       Nausea and vomiting that presents suddenly, especially in the second and third trimester, is significant.

•      Visual disturbances

       Visual disturbances may include temporary loss of vision, flashing lights, light sensitivity, blurred vision or seeing spots. An unusual improvement in vision in some farsighted women has been noted.

•      Right upper quadrant and/or right shoulder pain (largely due to compression of the optic nerve from cerebral edema)

       Right upper quadrant pain and referred pain to the right shoulder are indicative of liver involvement, which may also be a sign of HELLP syndrome. The patient will often complain of tenderness to the RUQ or midepigastric region upon palpation.

•      Lower back pain

       Lower back pain is another common complaint in pregnancy due to strain on the lower back muscles. However, when other signs of preeclampsia exist, lower back pain may be another indication that the liver is involved.

     Other signs and symptoms include:

• Tachycardia
• Altered mental status
• Increased sense of anxiety
• Dyspnea
• Weakness or a feeling of malaise
• Hyperreflexia
• Focal neurologic deficits
• Seizure
• Petechiae (pinpoint hemorrhages to the skin) and bruising
• Oliguria (decreased urine output).

     Preeclampsia may require only routine or supportive emergency medical care, but severe preeclampsia and eclampsia require more aggressive intervention. Consider the following emergency medical care when managing a patient who presents with preeclampsia or eclampsia:

     If the patient presents with an altered mental status, seizures, or is comatose, it may be necessary to establish an airway manually or with a mechanical device, including endotracheal intubation in severely altered mental states.

     If the patient's respiratory rate or tidal volume is inadequate, it is necessary to provide positive-pressure ventilation.

     Assess the patient for evidence of hypoxia. Apply a pulse oximeter and determine the SpO₂ reading. If there is clinical evidence of hypoxia or the SpO₂ reading is less than 95% on room air, administer a high concentration of oxygen via a nonrebreather mask. Although the SpO₂ reading may be within a normal range, the fetus may be experiencing significant fetal hypoxia due to vasoconstriction of the uteroplacental arteries. It would be prudent to place the patient presenting with preeclampsia on a nonrebreather mask at 15 lpm in order to maximize fetal oxygenation, even if signs of maternal hypoxia are not present or the SpO₂ reading remains within a normal range.

     As with any woman in her third trimester of pregnancy, place the patient in a left lateral recumbent position to avoid supine hypotensive syndrome and further reduction of placental perfusion due to a drop in maternal preload and cardiac output. Any decrease in cardiac output in light of the high peripheral vascular resistance could be detrimental to placental perfusion and fetal oxygenation.

     Preeclamptic and eclamptic patients may suffer cardiac events due to extreme vasoconstriction and multisystem organ involvement.

     Preeclamptic patients are often volume-depleted, but, due to the extremely high peripheral vascular resistance, the patient presents with hypertension. For this reason, do not consider using diuretics to reduce blood pressure. Aggressive volume infusion may lead to increased blood pressure and may cause pulmonary edema, which increases the mortality risk. Keep the intravenous line at a keep-open rate.

     Seizure activity may complicate the airway, ventilation, oxygenation and circulation, further increasing the hypoxic state of the fetus. Active seizures in an eclamptic patient should be immediately stopped with magnesium sulfate. Magnesium sulfate may also be used prophylactically to prevent seizure activity in severe preeclampsia. The adult dose is 4 to 6 grams intravenously over 20 minutes. If a long transport time is expected that will exceed 20 minutes for the initial dose, initiate a maintenance infusion of 1 to 2 grams/hour. Magnesium sulfate antagonizes calcium channels of smooth muscle and will depress the central nervous system and terminate electrical activity associated with seizures by inhibiting the release of acetylcholine. The effect of magnesium sulfate on vascular smooth muscle may reduce severe vasoconstriction and heightened peripheral vascular resistance, which in turn may improve uteroplacental blood flow and perfusion of the fetus, thereby reducing fetal hypoxia.

     Due to the serious consequences of seizures in the eclamptic patient, if magnesium sulfate is not effective in stopping seizure activity, administer your traditional benzodiazepine for seizure control. This may include diazepam, lorazepam or midazolam.

     Management of hypertension associated with preeclampsia is typically not performed in the prehospital environment.

     If the patient is experiencing severe preeclampsia or eclampsia, consider rapid transport to an appropriate medical facility. The one definitive procedure to reverse preeclampsia or eclampsia is to deliver the baby and placenta. Thus, careful consideration must be given to transporting to a medical facility that is able to manage acute obstetric emergencies.

     Recognition of any hypertensive disorder in pregnancy is extremely important. In patients with inconsistent or no prenatal care, it may be very difficult to establish a baseline blood pressure and the potential for preeclampsia or other hypertensive disorders associated with pregnancy. Emergency medical service personnel must be prepared to recognize the multitude of signs and symptoms, in addition to hypertension, in making a differential field diagnosis of preeclampsia.

     Dalton AL, Limmer DD, Mistovich JJ, Werman HA. Advanced Medical Life Support: A Practical Approach to Adult Medical Emergencies, 3rd ed. Upper Saddle River, NJ: Prentice Hall, 2007.

     Erogul M. Pregnancy, Preeclampsia. www.emedicine.com/emerg/topic480.htm.

     Fugate SR, Chow GC. Eclampsia. www.emedicine.com/med/topic1905.htm.

     Gaufberg SV. Abruptio Placentae. www.emedicine.com/emerg/topic12.htm.

     Guyton AC, Hall JE. Textbook of Medical Physiology, 10th ed. Philadelphia, PA: W.B. Saunders, 2001.

     Hamilton GC, Sanders AB, et al. Emergency Medicine: An Approach to Clinical Problem Solving, 2nd ed. Philadelphia, PA: W.B. Saunders, 2003.

     Huether SE, McCance KL. Understanding Pathophysiology, 3rd ed. St Louis, MO: Mosby, 2004.

     Marx JA, Hockberger RS, Walls RM. Rosen's Emergency Medicine: Concepts and Clinical Practice, 5th ed. St. Louis, MO: Mosby, Inc., 2002.

     Morris SC, Brooks MB. Pregnancy, Eclampsia. www.emedicine.com/emerg/topic796.htm.

     Warden M, Euerle B. Preeclampsia (Toxemia of Pregnancy). www.emedicine.com/med/topic1905.htm.

     Joseph J. Mistovich, MEd, NREMT-P, is a professor and chair of the Department of Health Professions at Youngstown (OH) State University.

     William S. Krost, MBA, NREMT-P, is director of Emergency Services & Health System Access for Blanchard Valley Health System in Findlay, OH.

     Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, ME.

     CONTINUING EDUCATION FROM EMS

     This CE activity is approved by EMS Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS), for 1.5 CEUs.

• Review pathophysiology of preeclampsia
• Discuss assessment findings
• Review emergency care of preeclampsia patient

• Family history of preeclampsia
• Young maternal age (less than 20 years)
• Older maternal age (older than 35 years)
• Nulliparity (woman who has not delivered a child)
• Multifetal pregnancy
• Preeclampsia in a previous pregnancy
• Multiparity and conception with a new partner
• African-American
• Obesity
• Gestational diabetes (15% increase in risk)
• Preexisting (pregestational) diabetes mellitus (30% increase in risk)
• Chronic hypertension
• Kidney disease
• Periodontal disease.

     Preeclampsia is only one of four disorders occurring in pregnancy that are related to hypertension. The other three are:

•      Gestational hypertension

       The patient develops hypertension after the 20th week of gestation; however, there is no increase in protein in the urine. Gestational hypertension may lead to the development of preeclampsia.

•      Chronic hypertension

       Chronic hypertension is often present, but undetected, prior to the pregnancy. It is defined as high blood pressure that occurs before the 20th week of gestation or lasts more than 12 weeks after delivery.

•      Preeclampsia superimposed on chronic hypertension

       The patient enters the pregnancy with chronic hypertension, which continues to worsen as the pregnancy progresses, and develops proteinuria.