- Email: [email protected]
A Pregnant Woman with Edema: Conclusion
Case Review
Bryan Woodford, RN, MSN, MBA, NREMT-P, CMTE
A Pregnant Woman with Edema: Conclusion A mobile intensive care unit was dispatched to a suburban hospital for a 26-year-old woman who was 26 weeks pregnant and had been diagnosed with preeclampsia. The report from the referring facility indicated that the patient was stable without complaints but needed transported for further evaluation to a tertiary care center that specializes in high-risk obstetrics. The referring facility asked the transport crew to bring a fetal heart monitor because the fetus had demonstrated sporadic episodes of bradycardia. The history obtained indicated this patient was a gravida 1 para 0 who had developed some very mild elevations in her blood pressure (BP) accompanied by swelling of her face, feet, and hands beginning at 18 weeks’ gestation She had been admitted to the obstetric unit 24 hours before transport, complaining of a headache associated with a blood pressure of 144/100 mmHg, which was the highest reading that she had experienced during her pregnancy. The 24-hour urine protein was 333 mg/day (normal, 44-225). Initial suspicion of the attending obstetrician was pregnancy-induced hypertension (PIH), also referred to as preeclampsia.
Transport crew evaluation showed the maternal BP to be 121/70 mmHg (mean arterial pressure [MAP] 87), heart rate (HR) 78 beats/min with a sinus rhythm, and a respiratory rate (RR) of 20 breaths/min. The oxygen saturation was 98% on room air. Lung sounds were clear and equal bilaterally with symmetric chest wall expansion. Examination of the patient revealed marked edema of the face, hands, ankles, and feet, which had progressively worsened since onset. The edema to the lower extremities was symmetric, and the patient denied any complaints of pain associated with the swelling. The abdominal examination showed a symmetric abdomen that was free from surgical scars and a normal fundal height of 27 cm. Deep tendon reflexes were normal without any signs of clonus. Before departure, online medical command was contacted to discuss the case. The medical command physician was comfortable with the current treatment and did not feel the need for additional interventions. The crew was instructed to recontact medical command if changes were noted in the patient’s condition or if frequent fetal decelerations were observed. Total transport time to the tertiary center was 90 minutes; 25 minutes into the transport, the patient complained of nausea associated with a very mild frontal headache and dizziness. Repeat vital signs were BP 98/52 (MAP 67), HR 84 sinus rhythm, RR 20. The patient was placed on her left side and started on 3 L/min of nasal oxygen; 4 mg odansetron was administered intravenously, and a crystalloid infusion of 0.9% normal saline at 100 mL/hour was started. A short time later, the patient complained of right upper abdominal pain and became anxious. Repeat vital signs were BP 164/110 (MAP 128), HR 112, RR 24. No changes were noted on the fetal heart monitor, and the fetal heart rate was 170. The patient was placed on 15 L oxygen via a nonrebreather mask. Medical command was contacted again. Orders were received for nifedipine 20 mg orally, but this medication was not carried by the crew. The physician then requested labetalol 10 mg intravenously, 172
followed by a repeat of labetalol 20 mg intravenously in 10 minutes if MAP remained greater than 130. Magnesium sulfate 4 g intravenously as a bolus over 5 to 10 minutes was commenced and followed by an infusion of 2 g/hour. Ten minutes after administering the first dose of labetalol, the patient’s condition remained unchanged. Labetalol 20 mg intravenously was given without improvement. Shortly after this, the ground unit arrived at the receiving facility, and the care of the patient was turned over to a team of high-risk obstetricians and neonatologists. On arrival to the tertiary care center, the patient was taken to the emergency department (ED) and met by obstetric team, who quickly determined that she was suffering from severe preeclampsia and required an emergency cesarean section. She remained in the ED for another 10 minutes while additional attempts were made to treat her hypertension. None of the interventions were successful, however, and she was immediately transported to the labor and delivery unit for the cesarean section. Approximately 40 minutes after the patient arrived at the tertiary care facility, her preterm infant was born. The 25?week-old infant weighed 698 g, required immediate endotracheal intubation, and presented with APGAR scores of 5 (1 minute) and 7 (5 minutes). The infant then was taken to the neonatal intensive care unit, where he underwent aggressive lifesaving interventions. He remained hospitalized for the next 3 months and was discharged to home with low-flow oxygen. The child is now 5 years old and remains healthy without any residual complications as a result of his prematurity. Days after the delivery of her son, the mother was diagnosed with a thrombophilia known as factor V Leiden. This particular thrombophilia is an inherited disorder of blood clotting and is the name of a specific Air Medical Journal 28:4
mutation that results in thrombophilia (blood clotting). Factor V Leiden mutation is associated with an increased risk of miscarriage, PIH (preeclampsia), slow fetal growth, and early separation of the placenta from the uterine wall (placental abruption).1 Initially, the highrisk obstetricians believed the presence of factor V Leiden caused micro clot formation within the placenta, decreasing blood flow to the fetus and causing the severe preeclampsia. This theory was proved inaccurate once the placenta pathology report was obtained, and the results showed no signs of micro clot formation within the placenta. Even days after delivery, the mother’s blood pressure remained slightly elevated. She was discharged to home with a prescription for an oral antihypertensive and was ordered to follow up with her obstetrician at the tertiary care center to discuss her newly diagnosed thrombophilia and to evaluate her mildly elevated blood pressure. At the time of discharge, it was still unclear what caused the mother to experience severe preeclampsia.
1. What is the likely cause of this patient’s deteriorating clinical picture and severe pain while in transport? The patient was diagnosed with preeclampsia after testing positive for proteinuria, hypertension, and elevated uric acid levels at the referring facility. The condition worsens in a small percentage of women (10%) diagnosed with preeclampsia, causing them to develop HELLP Syndrome. HELLP stands for hemolysis, elevated liver enzymes, and low platelet count, and it carries a very high mortality rate. When women who are diagnosed with HELLP are not treated aggressively during the early onset, studies have shown that up to 25% will suffer serious complications.2 A small number of women may even die if their signs and symptoms are not treated. In this case, the patient’s symptoms developed very rapidly without warning and required emergency surgery to extract the fetus. This is the only definitive treatment for the mother who has developed HELLP syndrome, because liver function rapidly worsens and causes significant complications for the mother and the fetus.3,4 Although the maternal laboratory values from the tertiary care facility are not available, the development of HELLP syndrome was likely. Once the mother arrived in the ED at the tertiary care center, a group of high-risk obstetricians performed a rapid physical assessment. Their findings included severe hypertension, headache, right upper quadrant abdominal pain with hepatomegaly, epigastric pain, and blurred vision. Recent literature regarding efforts at determining a laboratory diagnosis of HELLP syndrome based on elevations of various liver enzymes (aspartate aminotransferase [AST], alanine aminotransferase, and lactate dehydrogenase [LDH]) is variable and inconsistent, because interlaboratory differences are a major problem. July-August 2009
2. What might have been done differently in the transport of this patient and the treatment provided? As evidenced in this particular transport, it is clear that the symptoms associated with preeclampsia may worsen very rapidly, requiring immediate lifesaving interventions. The mother was diagnosed with a mild case of preeclampsia at the referring facility, which rapidly progressed to severe preeclampsia during transport. Severe preeclampsia has been associated with increased rates of maternal mortality (0.2%) and morbidity (5%), which is why transport personnel need to continuously reassess their patient for worsening symptoms.2 Potential life-threatening conditions include convulsions, pulmonary edema, acute renal or liver failure, liver hemorrhage, disseminated intravascular coagulopathy, and stroke.2 Each of these complications is typically seen in women who develop severe preeclampsia before their 32nd week of gestation. It is important for critical care transport personnel to obtain “what if” orders from medical command if they do not have a liberal set of protocols that allow them to readily treat signs and symptoms related to certain disease processes. The transport personnel failed to obtain these “what if” orders from the medical command physician during the consult that was performed before leaving the referring facility. The transport program did not have a protocol that allowed them to treat the aforementioned signs and symptoms without contacting the medical command physician. Transport personnel must demonstrate meticulous behavior while taking all the necessary steps possible to ensure a safe and efficient transport. As previously noted, a mother’s symptoms may worsen very rapidly with little warning, thus requiring immediate interventions. The transport personnel in this case had little difficulty contacting medical command; however, delays were possible and might have caused undue harm. Many patients may not have been able to tolerate the acute onset of severe preeclampsia as the mother did in this case. Maternal and perinatal outcomes largely depend on issues such as gestational age, disease severity, presence of multifetal gestation, and the presence of preexisting medical conditions such as diabetes and renal disease.1,5
3. What is the best treatment for this disease? Two different algorithms may be followed when treating a mother suspected of having HELLP syndrome. The first involves the mother who remains clinically stable and presents with minimal or no stress to her or the fetus. This patient requires immediate hospitalization with continual observation in the labor and delivery unit. This patient should be treated for severe preeclampsia and should receive magnesium sulfate prophylactically to prevent seizures.6 The next step is to confirm or exclude the diagnosis of HELLP syndrome from the other conditions that mimic HELLP. Laboratory tests should include a complete blood count, peripheral smear, coagulation studies, serum AST levels, creatinine, glucose, bilirubin, and LDH levels. If 173
the diagnosis of HELLP is confirmed, the next decision is to decide how soon the fetus will need to be delivered. If the mother is at less than 35 weeks’ gestation, she will require immediate transportation to a tertiary care facility that specializes in high-risk obstetrics. If the clinical condition of the mother and fetus is determined to be stable, a decision must be made as to whether the delivery should occur immediately or whether both the mother and fetus could tolerate waiting up to 48 hours for corticosteroid therapy. The second algorithm follows the path experienced by the woman in this case study. The mother’s clinical condition rapidly deteriorated during transport to the tertiary care facility. Aggressive attempts at lowering her life-threatening blood pressure were unsuccessful. On arrival to the tertiary care facility, it was quickly determined that the mother was not clinically stable and showed no signs of improvement. The decision was made to perform an emergency cesarean section, which would ultimately save the life of this mother and her fetus.
small clots to form inside the placenta, which in turn causes the HELLP syndrome and accounts for a 60% reoccurrence of preeclampsia in future pregnancies. The highrisk obstetricians ordered a pathology study on the placenta, which did not reveal any blood clots within the placenta. This enabled them to rule out the factor V Leiden as the cause but made it unclear as to what was indeed the cause for this preterm delivery. It is likely that if the patient in this case study were to become pregnant again, she would require daily anticoagulant therapy such as enoxaparin (Lovenox) to further prevent clot formation. Studies have shown that women with preeclampsia have a recurrence risk of 7.5% to 18%.15-18 For women with severe preeclampsia during the second trimester, such as the one in this case study, the recurrence risk is 65%.19 If a woman is actually diagnosed with HELLP syndrome, her risk of recurrence is between 2% and 6%.20-22 Several studies also suggest that women who develop preeclampsia during pregnancy are more likely to develop cardiovascular complications later in life.23-27
4. What is the most common complication associated with preeclampsia?
6. What infrequent complication of preeclampsia is associated with high mortality?
The most common complication of preeclampsia is eclampsia, the development of convulsions or unexplained coma during pregnancy in patients who display signs and symptoms of preeclampsia.7 The incidence of eclampsia is reported to range from 1:2,000 pregnancies to 1:3,448 pregnancies, with the higher incidence in geographic locations with little or no prenatal care, multi-fetal gestation, and tertiary referral centers.8-10 Eclampsia is also known for having a very high mortality rate and often requires a magnesium sulfate infusion to help stop the seizure activity. In this case, a magnesium sulfate infusion was started during the transport phase to prevent any seizures from occurring and was continued postoperatively until the mother’s blood pressure stabilized. Eclampsia can occur during the antepartum, intrapartum, or postpartum periods.10-13 Most cases of postpartum eclampsia occur within the first 48 hours after delivery, but some cases have been reported between 48 hours and 23 days postpartum.11,13,14 In cases that occur days to weeks after the delivery, it is important for the mother to undergo a comprehensive neurologic evaluation to rule out any other possible cerebral pathologic conditions.13,14
One of the most infrequent complications of preeclampsia is the development of HELLP syndrome. HELLP syndrome occurs in only 3% of women who are diagnosed with preeclampsia or eclampsia but results in a much higher mortality rate—25% of women who are not treated early will develop serious complications and even death.
5. Does the presence of PIH in this patient make her more susceptible for reoccurrence in future pregnancies? Yes! After the patient recovered from her emergency cesarean section, an array of laboratory tests were performed on an outpatient basis in hope of coming up with a cause for her preeclampsia. Studies have shown that the exact cause of preeclampsia is unknown, but some of the likely suspects are clotting disorders and chromosomal abnormalities. In this case, the detailed laboratory studies revealed that the patient indeed had a thrombophilia disorder called factor V Leiden. This disorder often causes 174
References 1. Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol 2003;103:181-92. 2. Diagnosis and management of preeclampsia and eclampsia. ACOG Practice Bulletin No. 33. American College of Obstetricians and Gynecologists. Obstet Gynecol 2002;99:159-67. 3. Weinstein L. Syndrome of hemolysis, elevated liver enzymes, and low platelet count: A severe consequence of hypertension in pregnancy. Am J Obstet Gyncecol 1982;142:159-67. 4. Rath W, Loos W, Kuhn W, Graeff H. The importance of early laboratory screening methods for maternal and fetal outcome in cases of HELLP syndrome. Eur J Obstet Gynecol Reprod Biol 1990;36:43-51. 5. Sibai B, Dekker G, Kupferminc M. Preeclampsia. Lancet 2005;365:785-99. 6. Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Obstet Gynecol 2004;103:981-91. 7. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol 2005;105:402-410. 8. Saftlas AF, Olson DR, Franks AC, Atrash HK, Polaras, R. Epidemiology of preeclampsia and eclampsia in the United States: 1979-1986. Am J Obstet Gynecol 1990;163:460-5. 9. Moller B, Lindmark G. Eclampsia in Sweeden, 1976-1980. Acta Obstet Gynecol Scand 1986;65:307-14. 10. Douglas KA, Redman CW. Eclampsia in the United Kingdom. BMJ 1994;309:1395-400. 11. Matter F, Sibai BM. Eclampsia VIII: Risk factors for maternal morbidity. Am J Obstet Gyncecol 2000;182:307-12. 12. Katz VL, Farmer R, Kuller J. Preeclampsia into eclampsia: toward a new paradigm. Am J Obstet Gynecol 2000;182:1389-96. 13. Chames MC, Livingston JC, Invester TS, Barton JR, Sibai BM. Late postpartum eclampsia: A preventable disease? Am J Obstet Gynecol 2002;186:1174-7. 14. Lubarsky SL, Barton JR., Friedman SA, Nasreddine S, Ramaddan MK, Sibai, BM. Late postpartum eclampsia revisited. Obstet Gynecol 1994;83:502-5. 15. Campbell DM, MacGillivray I, Carr-Hill R. Preeclampsia in second pregnancy. B J OG 1985;92:131-40. 16. Hjartardottir S, Leifsson BG, Geirsson RT, Steinthorsdottir V. Recurrence of hypertensive disorder in second pregnancy. Am J Obstet Gynecol 2006;194:916-20.
Air Medical Journal 28:4
17. Caritis S, Sibai BM, Hauth J, Lindheimer MD, Klebanoff M, Thom E, et al. Low-dose aspirin to prevent preeclampsia in women at high risk. N Engl J Med 1998;338:701-5. 18. Sibai BM, El-Nazer A, Gonzalez-Ruiz A. Severe preeclampsia-eclampsia in young Primigravida women: Subsequent pregnancy outcome and remote prognosis. Am J Obstet Gynecol 1986;155:1011-16. 19. Sibai BM, Mercer B, Sarinoglu C. Severe preeclampsia in the second trimester: Recurrence risk and long-term prognosis. Am J Obstet Gynecol 1991;165:1408-12. 20. Sibai BM, Ramadan MK, Chari RS, Friedman SA. Pregnancies complicated by HELLP syndrome: subsequent pregnancy outcome and long-term prognosis. Am J Obstet Gynecol 1995;172:125-9. 21. Van Pampus MG, Wolf H, Mayruhu G, Treffers PE, Bleker OP. Long-term follow-up in patients with a history of (H) ELLP syndrome. Hypertens Pregn 2001;20:15-23. 22. Chames MC, Haddad B, Barton JR, Livingston JC, Sibai BM. Subsequent pregnancy outcome in women with a history of HELLP syndrome at 28 weeks of gestation. Am J Obstet Gynecol 2003;188:1504-8. 23. Ramsey JE, Stewart P, Greer IA, Sattar N. Microvascular dysfunction: A link between preeclampsia and maternal coronary heart disease. Br J OG 2003;110:2029-31. 24. Wilson RJ, Watson MS, Prescott GI, Sunderland S, Campbell DM, et al. Hypertensive disease of pregnancy and risk of hypertension and stroke in later life: results from cohort study. Br Med J 2003;326:1-7. 25. Haukkamaa L, Salminen M, Laivuori H, Leinonen H, Hiilesma V, Kaaja R. Risk For subsequent coronary artery disease after preeclampsia. Am J Cardial 2004;93:805-8. 26. Wikstrom AK, Haglund B, Olovsson M, Lindberg SN. The risk of ischemic heart disease after gestational hypertensive disease. B J OG 2006;116:185-91. 27. Brown DW, Dueker N, Jamieson DJ, Cole JW, Wozniak MA, et al. Preeclampsia and the risk of ischemic stroke among young women: results from the stroke prevention in young women study. Stroke 2006;37:1055-9.
Bryan Woodford, RN, BSN, NREMT-P, is a flight nurse at STAT MedEvac in Pittsburgh, PA, and a firefighter/paramedic with Cumberland Trail Fire District in St. Clairsville, OH. He also is a coauthor and editor of Critical Care Paramedic Transport and an editor of Air and Surface Patient Transport Principles and Practice. He can be reached at [email protected]. David W. Ross, DO, FACEP, Carol Wichman, BSN, MSN, and Mike MacKinnon, BSN, CEN, CCRN, CCFRN, are section editors. They can be reached at [email protected]. 1067-991X/$36.00 Copyright 2009 by Air Medical Journal Associates doi:10.1016/j.amj.2009.04.016
July-August 2009
175
Bryan Woodford, RN, MSN, MBA, NREMT-P, CMTE
A Pregnant Woman with Edema: Conclusion A mobile intensive care unit was dispatched to a suburban hospital for a 26-year-old woman who was 26 weeks pregnant and had been diagnosed with preeclampsia. The report from the referring facility indicated that the patient was stable without complaints but needed transported for further evaluation to a tertiary care center that specializes in high-risk obstetrics. The referring facility asked the transport crew to bring a fetal heart monitor because the fetus had demonstrated sporadic episodes of bradycardia. The history obtained indicated this patient was a gravida 1 para 0 who had developed some very mild elevations in her blood pressure (BP) accompanied by swelling of her face, feet, and hands beginning at 18 weeks’ gestation She had been admitted to the obstetric unit 24 hours before transport, complaining of a headache associated with a blood pressure of 144/100 mmHg, which was the highest reading that she had experienced during her pregnancy. The 24-hour urine protein was 333 mg/day (normal, 44-225). Initial suspicion of the attending obstetrician was pregnancy-induced hypertension (PIH), also referred to as preeclampsia.
Transport crew evaluation showed the maternal BP to be 121/70 mmHg (mean arterial pressure [MAP] 87), heart rate (HR) 78 beats/min with a sinus rhythm, and a respiratory rate (RR) of 20 breaths/min. The oxygen saturation was 98% on room air. Lung sounds were clear and equal bilaterally with symmetric chest wall expansion. Examination of the patient revealed marked edema of the face, hands, ankles, and feet, which had progressively worsened since onset. The edema to the lower extremities was symmetric, and the patient denied any complaints of pain associated with the swelling. The abdominal examination showed a symmetric abdomen that was free from surgical scars and a normal fundal height of 27 cm. Deep tendon reflexes were normal without any signs of clonus. Before departure, online medical command was contacted to discuss the case. The medical command physician was comfortable with the current treatment and did not feel the need for additional interventions. The crew was instructed to recontact medical command if changes were noted in the patient’s condition or if frequent fetal decelerations were observed. Total transport time to the tertiary center was 90 minutes; 25 minutes into the transport, the patient complained of nausea associated with a very mild frontal headache and dizziness. Repeat vital signs were BP 98/52 (MAP 67), HR 84 sinus rhythm, RR 20. The patient was placed on her left side and started on 3 L/min of nasal oxygen; 4 mg odansetron was administered intravenously, and a crystalloid infusion of 0.9% normal saline at 100 mL/hour was started. A short time later, the patient complained of right upper abdominal pain and became anxious. Repeat vital signs were BP 164/110 (MAP 128), HR 112, RR 24. No changes were noted on the fetal heart monitor, and the fetal heart rate was 170. The patient was placed on 15 L oxygen via a nonrebreather mask. Medical command was contacted again. Orders were received for nifedipine 20 mg orally, but this medication was not carried by the crew. The physician then requested labetalol 10 mg intravenously, 172
followed by a repeat of labetalol 20 mg intravenously in 10 minutes if MAP remained greater than 130. Magnesium sulfate 4 g intravenously as a bolus over 5 to 10 minutes was commenced and followed by an infusion of 2 g/hour. Ten minutes after administering the first dose of labetalol, the patient’s condition remained unchanged. Labetalol 20 mg intravenously was given without improvement. Shortly after this, the ground unit arrived at the receiving facility, and the care of the patient was turned over to a team of high-risk obstetricians and neonatologists. On arrival to the tertiary care center, the patient was taken to the emergency department (ED) and met by obstetric team, who quickly determined that she was suffering from severe preeclampsia and required an emergency cesarean section. She remained in the ED for another 10 minutes while additional attempts were made to treat her hypertension. None of the interventions were successful, however, and she was immediately transported to the labor and delivery unit for the cesarean section. Approximately 40 minutes after the patient arrived at the tertiary care facility, her preterm infant was born. The 25?week-old infant weighed 698 g, required immediate endotracheal intubation, and presented with APGAR scores of 5 (1 minute) and 7 (5 minutes). The infant then was taken to the neonatal intensive care unit, where he underwent aggressive lifesaving interventions. He remained hospitalized for the next 3 months and was discharged to home with low-flow oxygen. The child is now 5 years old and remains healthy without any residual complications as a result of his prematurity. Days after the delivery of her son, the mother was diagnosed with a thrombophilia known as factor V Leiden. This particular thrombophilia is an inherited disorder of blood clotting and is the name of a specific Air Medical Journal 28:4
mutation that results in thrombophilia (blood clotting). Factor V Leiden mutation is associated with an increased risk of miscarriage, PIH (preeclampsia), slow fetal growth, and early separation of the placenta from the uterine wall (placental abruption).1 Initially, the highrisk obstetricians believed the presence of factor V Leiden caused micro clot formation within the placenta, decreasing blood flow to the fetus and causing the severe preeclampsia. This theory was proved inaccurate once the placenta pathology report was obtained, and the results showed no signs of micro clot formation within the placenta. Even days after delivery, the mother’s blood pressure remained slightly elevated. She was discharged to home with a prescription for an oral antihypertensive and was ordered to follow up with her obstetrician at the tertiary care center to discuss her newly diagnosed thrombophilia and to evaluate her mildly elevated blood pressure. At the time of discharge, it was still unclear what caused the mother to experience severe preeclampsia.
1. What is the likely cause of this patient’s deteriorating clinical picture and severe pain while in transport? The patient was diagnosed with preeclampsia after testing positive for proteinuria, hypertension, and elevated uric acid levels at the referring facility. The condition worsens in a small percentage of women (10%) diagnosed with preeclampsia, causing them to develop HELLP Syndrome. HELLP stands for hemolysis, elevated liver enzymes, and low platelet count, and it carries a very high mortality rate. When women who are diagnosed with HELLP are not treated aggressively during the early onset, studies have shown that up to 25% will suffer serious complications.2 A small number of women may even die if their signs and symptoms are not treated. In this case, the patient’s symptoms developed very rapidly without warning and required emergency surgery to extract the fetus. This is the only definitive treatment for the mother who has developed HELLP syndrome, because liver function rapidly worsens and causes significant complications for the mother and the fetus.3,4 Although the maternal laboratory values from the tertiary care facility are not available, the development of HELLP syndrome was likely. Once the mother arrived in the ED at the tertiary care center, a group of high-risk obstetricians performed a rapid physical assessment. Their findings included severe hypertension, headache, right upper quadrant abdominal pain with hepatomegaly, epigastric pain, and blurred vision. Recent literature regarding efforts at determining a laboratory diagnosis of HELLP syndrome based on elevations of various liver enzymes (aspartate aminotransferase [AST], alanine aminotransferase, and lactate dehydrogenase [LDH]) is variable and inconsistent, because interlaboratory differences are a major problem. July-August 2009
2. What might have been done differently in the transport of this patient and the treatment provided? As evidenced in this particular transport, it is clear that the symptoms associated with preeclampsia may worsen very rapidly, requiring immediate lifesaving interventions. The mother was diagnosed with a mild case of preeclampsia at the referring facility, which rapidly progressed to severe preeclampsia during transport. Severe preeclampsia has been associated with increased rates of maternal mortality (0.2%) and morbidity (5%), which is why transport personnel need to continuously reassess their patient for worsening symptoms.2 Potential life-threatening conditions include convulsions, pulmonary edema, acute renal or liver failure, liver hemorrhage, disseminated intravascular coagulopathy, and stroke.2 Each of these complications is typically seen in women who develop severe preeclampsia before their 32nd week of gestation. It is important for critical care transport personnel to obtain “what if” orders from medical command if they do not have a liberal set of protocols that allow them to readily treat signs and symptoms related to certain disease processes. The transport personnel failed to obtain these “what if” orders from the medical command physician during the consult that was performed before leaving the referring facility. The transport program did not have a protocol that allowed them to treat the aforementioned signs and symptoms without contacting the medical command physician. Transport personnel must demonstrate meticulous behavior while taking all the necessary steps possible to ensure a safe and efficient transport. As previously noted, a mother’s symptoms may worsen very rapidly with little warning, thus requiring immediate interventions. The transport personnel in this case had little difficulty contacting medical command; however, delays were possible and might have caused undue harm. Many patients may not have been able to tolerate the acute onset of severe preeclampsia as the mother did in this case. Maternal and perinatal outcomes largely depend on issues such as gestational age, disease severity, presence of multifetal gestation, and the presence of preexisting medical conditions such as diabetes and renal disease.1,5
3. What is the best treatment for this disease? Two different algorithms may be followed when treating a mother suspected of having HELLP syndrome. The first involves the mother who remains clinically stable and presents with minimal or no stress to her or the fetus. This patient requires immediate hospitalization with continual observation in the labor and delivery unit. This patient should be treated for severe preeclampsia and should receive magnesium sulfate prophylactically to prevent seizures.6 The next step is to confirm or exclude the diagnosis of HELLP syndrome from the other conditions that mimic HELLP. Laboratory tests should include a complete blood count, peripheral smear, coagulation studies, serum AST levels, creatinine, glucose, bilirubin, and LDH levels. If 173
the diagnosis of HELLP is confirmed, the next decision is to decide how soon the fetus will need to be delivered. If the mother is at less than 35 weeks’ gestation, she will require immediate transportation to a tertiary care facility that specializes in high-risk obstetrics. If the clinical condition of the mother and fetus is determined to be stable, a decision must be made as to whether the delivery should occur immediately or whether both the mother and fetus could tolerate waiting up to 48 hours for corticosteroid therapy. The second algorithm follows the path experienced by the woman in this case study. The mother’s clinical condition rapidly deteriorated during transport to the tertiary care facility. Aggressive attempts at lowering her life-threatening blood pressure were unsuccessful. On arrival to the tertiary care facility, it was quickly determined that the mother was not clinically stable and showed no signs of improvement. The decision was made to perform an emergency cesarean section, which would ultimately save the life of this mother and her fetus.
small clots to form inside the placenta, which in turn causes the HELLP syndrome and accounts for a 60% reoccurrence of preeclampsia in future pregnancies. The highrisk obstetricians ordered a pathology study on the placenta, which did not reveal any blood clots within the placenta. This enabled them to rule out the factor V Leiden as the cause but made it unclear as to what was indeed the cause for this preterm delivery. It is likely that if the patient in this case study were to become pregnant again, she would require daily anticoagulant therapy such as enoxaparin (Lovenox) to further prevent clot formation. Studies have shown that women with preeclampsia have a recurrence risk of 7.5% to 18%.15-18 For women with severe preeclampsia during the second trimester, such as the one in this case study, the recurrence risk is 65%.19 If a woman is actually diagnosed with HELLP syndrome, her risk of recurrence is between 2% and 6%.20-22 Several studies also suggest that women who develop preeclampsia during pregnancy are more likely to develop cardiovascular complications later in life.23-27
4. What is the most common complication associated with preeclampsia?
6. What infrequent complication of preeclampsia is associated with high mortality?
The most common complication of preeclampsia is eclampsia, the development of convulsions or unexplained coma during pregnancy in patients who display signs and symptoms of preeclampsia.7 The incidence of eclampsia is reported to range from 1:2,000 pregnancies to 1:3,448 pregnancies, with the higher incidence in geographic locations with little or no prenatal care, multi-fetal gestation, and tertiary referral centers.8-10 Eclampsia is also known for having a very high mortality rate and often requires a magnesium sulfate infusion to help stop the seizure activity. In this case, a magnesium sulfate infusion was started during the transport phase to prevent any seizures from occurring and was continued postoperatively until the mother’s blood pressure stabilized. Eclampsia can occur during the antepartum, intrapartum, or postpartum periods.10-13 Most cases of postpartum eclampsia occur within the first 48 hours after delivery, but some cases have been reported between 48 hours and 23 days postpartum.11,13,14 In cases that occur days to weeks after the delivery, it is important for the mother to undergo a comprehensive neurologic evaluation to rule out any other possible cerebral pathologic conditions.13,14
One of the most infrequent complications of preeclampsia is the development of HELLP syndrome. HELLP syndrome occurs in only 3% of women who are diagnosed with preeclampsia or eclampsia but results in a much higher mortality rate—25% of women who are not treated early will develop serious complications and even death.
5. Does the presence of PIH in this patient make her more susceptible for reoccurrence in future pregnancies? Yes! After the patient recovered from her emergency cesarean section, an array of laboratory tests were performed on an outpatient basis in hope of coming up with a cause for her preeclampsia. Studies have shown that the exact cause of preeclampsia is unknown, but some of the likely suspects are clotting disorders and chromosomal abnormalities. In this case, the detailed laboratory studies revealed that the patient indeed had a thrombophilia disorder called factor V Leiden. This disorder often causes 174
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Bryan Woodford, RN, BSN, NREMT-P, is a flight nurse at STAT MedEvac in Pittsburgh, PA, and a firefighter/paramedic with Cumberland Trail Fire District in St. Clairsville, OH. He also is a coauthor and editor of Critical Care Paramedic Transport and an editor of Air and Surface Patient Transport Principles and Practice. He can be reached at [email protected]. David W. Ross, DO, FACEP, Carol Wichman, BSN, MSN, and Mike MacKinnon, BSN, CEN, CCRN, CCFRN, are section editors. They can be reached at [email protected]. 1067-991X/$36.00 Copyright 2009 by Air Medical Journal Associates doi:10.1016/j.amj.2009.04.016
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