CASE STUDY
Ruptured Splenic Artery Aneurysm in Pregnancy: A Case Series Mary Lou Garey, MSN, RN, CNP,1 Sarah Greenberger, MD,2 and Howard A. Werman, MD, FACEP1,2
Rupture of a splenic artery aneurysm (SAA) is a rare and often catastrophic complication in pregnancy. Maternal and fetal mortality in the spontaneous rupture of a splenic artery aneurysm during pregnancy have been reported as high as 75% and 95%, respectively.1,2 We present 2 patients with SAA rupture in pregnancy who were transported by our critical care transport program. Both patients were transported from the same 100-bed community hospital within a 25-month period. The implications for critical care transport are discussed.
Case Reports Case 1 A 26-year-old woman presented to the regional emergency department by local emergency medical services after experiencing 2 generalized seizures at home. The patient was gravida 2 para 3 with triplets during her first pregnancy. She had a previous obstetric history of the delivery of triplets by cesarean section 3 years earlier. Notably, the patient was treated for pre-eclampsia during her previous pregnancy and had required magnesium infusion. At the time of the current presentation, she was at 36 weeks’ gestation with a single fetus. This pregnancy had thus far been uncomplicated. The patient did not report any other medical or surgical history. On the night of admission, the patient presented with seizures after an episode of nausea, vomiting, bowel incontinence, and diarrhea. The patient was responsive and answering questions slowly. She complained of headache and left upper quadrant pain. Her presenting blood pressure was 66/30 with a heart rate of 101. The fetal heart rate was 152. The patient had 2 intravenous lines placed, she received 4 g magnesium sulfate, and she was quickly transferred to the obstetric unit where her obstetrician was waiting. Her blood pressure on arrival to the unit was 160/116 with her heart rate unchanged. She then had 2 more episodes of hypotension that quickly rebounded to the range of 140/70 with intravenous
1. MedFlight, Columbus, OH, USA 2. Department of Emergency Medicine, The Ohio State University, Columbus, OH, USA 1067-991X/$36.00 Copyright 2014 by Air Medical Journal Associates http://dx.doi.org/:10.1016/j.amj.2014.05.006 214
fluid administration. Her abdomen was soft. The fetal heart rate was in the 140s but with minimal reactivity. Subsequently, an emergent cesarean section was performed using a transverse suprapubic incision under spinal anesthesia. Delivery of a 2,760-g female followed with a 1-minute Apgar of 3; the 5and 10-minute Apgar scores were 6 and 7, respectively. Upon handing off the infant, large pools of clotted blood as well as fresh active bleeding were noted in the left upper abdomen. The uterus was intact on examination. However, the patient’s mentation and blood pressure began to deteriorate, and she was intubated for airway protection. Postintubation blood gases revealed a pH of 7.15, paO2 of 516, pCO2 of 34, and bicarbonate of 11.5. Additional laboratory values drawn included a white blood cell count of 14.7 with a hemoglobin level of 10.6 and platelets of 63,000. She had an international normalized ratio of 1.5 and a fibrinogen level of 116 mg/dL (normal 200-400 mg/dL). A general surgeon arrived to assist the obstetric team. A ruptured spleen was believed to be the cause of the hemorrhage, although a distinct source could not be identified. The limited blood supply of the community hospital was rapidly being exhausted. By this point, the patient had received 4,500 mL crystalloids and 7 units of packed cells, including 2 units of O-negative blood. Her systolic blood pressure was initially 80 mm Hg at the start of the case and increased to 120 mm Hg intraoperatively but was trending downward by the end of the procedure. The patient’s abdomen was packed, and preparations were made to transport her by helicopter to a tertiary care center because of the lack of available blood products as well as the need for advanced surgical care. Upon leaving the community hospital, her systolic blood pressure remained around 80 mm Hg, and the last of the available units of blood (units #8 and #9) were infusing along with crystalloids. During flight, the patient’s blood pressure dropped below 50 mm Hg as determined by Doppler measurement. Her heart rate remained in the 120s with short runs of ventricular tachycardia. She remained intubated. The pulse oximetry would not register because of her poor peripheral perfusion. Her pupils were sluggish to react, and she would turn her head in response to loud verbal stimulation. On arrival to the receiving facility, the patient was taken directly to the operating suite for an exploratory laparotomy. A midline incision was made with profuse bleeding noted. Blood products and crystalloid fluid infusions continued. On further exploration, a ruptured SAA was discovered. She underwent a splenectomy, after which her abdomen was packed because of hemodynamic instability. Two days after Air Medical Journal 33:5
her transfer, she returned to the operating room for the removal of packing and final closure. There were no additional sources of bleeding found. At the time of her final surgery, the patient had received a total of 38 units of packed red blood cells (PRBCs), 22 units of fresh frozen plasma, 8 units of platelets, and 5 units of cryoprecipitate. The patient made a slow but steady recovery and was discharged to home 11 days after admission. Her recovery course was complicated by a low-grade pancreatic fistula, which resolved with percutaneous drainage and antibiotics. Her newborn daughter was waiting for her at home, having been discharged on the third postpartum day.
Case 2 A 26-year-old woman presented to the regional obstetric unit with complaints of abdominal pain and cramping. She was assessed as gravida 2 para 1 at 34 weeks’ gestation with a single fetus. Her past medical and surgical history was negative, and her previous pregnancy had been uncomplicated. Fetal monitoring showed the fetal heart rate was in the 160s. During the initial evaluation, the patient suddenly sat upright and developed projectile vomiting. She became pale and diaphoretic. The fetal monitor showed profound persistent bradycardia. The maternal patient became less responsive, and an emergent cesarean section using a midline laparotomy incision was performed. A 2,800-g infant was delivered and resuscitated with some difficulty. The Apgar score was 0 upon delivery, 3 at 1 minute, 6 at 5 minutes, and 8 at 10 minutes. September-October 2014
The infant was later transferred to a level 3 nursery for neonatal intensive care. After handing off the infant, the patient was found to have 2,000 mL of both clotted and unclotted blood in the left upper abdominal quadrant. A general surgeon had been called in to assist the obstetric staff. The patient had a blood pressure of 110/60 and a heart rate of 120. Laboratory values sent from the operating room revealed a white blood cell count of 16.8, hemoglobin of 8.9, and platelets of 159,000. On exploration, a rupture of a dilated splenic artery wall was found just distal to its branching from the celiac artery. A repair was performed with appropriate hemostasis achieved after the administration of 4,600 mL crystalloid and 6 units of PRBCs including 2 units of O-negative blood. The abdomen was packed, and the patient was transferred directly from the operating room to a tertiary care center by the ground mobile intensive care unit for definitive care. She remained hemodynamically stable during transport, with crystalloids infusing at a maintenance rate and continued administration of her seventh unit of PRBCs. At the receiving facility, the patient’s hemoglobin repeatedly decreased. An exploratory laparotomy was performed 12 hours after admission. She was found to have a large amount of fresh and clotted blood in the peritoneal cavity (estimated 2,000 mL). Blood was found to be leaking from the repaired SAA and the uterine sutures. A splenectomy was performed as well as a suture repair of the uterus. The patient’s recovery course was uncomplicated, and she was discharged to home 6 days after admission. Unfortunately, 215
the infant did not survive the event, with death attributed to significant neurologic and end-organ damage.
Discussion SAA remains relatively uncommon, with a reported incidence of 0.01% to 0.98%3,4; a retrospective review found only 217 cases of SAA documented at the Mayo Clinic over the period of 1980 to 1998.5 SAA rupture occurs in 2% to 3% of all cases and with increased frequency (estimated at 20%40%) in otherwise healthy pregnant women or during the recent postpartum period.3,4,6,7 At least 3 cases of SAA have been reported to occur as early as the first trimester of pregnancy.8,9 Because of the infrequency of SAA complicating pregnancy, there is a relative paucity of literature about this condition. To our knowledge, this is the first time SAA rupture in pregnant patients has been reported in the critical care transport literature. An SAA usually is asymptomatic until rupture occurs.10 Even then, the diagnosis of severe abdominal pain and hypotension in pregnancy may be attributed to a variety of potential working diagnoses such as ruptured ectopic pregnancy, placental abruption, uterine rupture, amniotic fluid embolism, pulmonary thromboembolism, cholecystitis, appendicitis, or perforation of a peptic ulcer.7-9,12 The use of ultrasound to detect free fluid may help with early, and often lifesaving, diagnosis of hemoperitoneum in a stable pregnant patient presenting with abdominal pain. The mortality from a ruptured SAA has been reported to be as high as 36% to 40% in the general population and up to 70% for pregnant women specifically, with mortality for the fetus upward of 90%.3,4,13 The literature contains more than 100 cases of SAA rupture in pregnancy but only 17 other cases of maternal and fetal survival.7,13,14 Both mothers survived their diagnosis in our cases, but, unfortunately, subsequent fetal mortality was 50%. There is no clear mechanism by which pregnancy increases the incidence of SAA rupture. Risk factors postulated in this population include increased portal venous pressure; increased cardiac output during pregnancy; and higher estrogen, progesterone, and relaxin levels contributing to elastin disruption in the tunica media of the vasculature.3,4,15 Of note, approximately 40% of women with splenic artery aneurysms are reported to be grand multiparous (ⱖ 5 births)16; additional risk factors predisposing to SAA include a history of cirrhosis or liver transplant.17 Given a prevalence of SAA of less than 0.1%, routine radiologic screening of all women of childbearing age has not been recommended.18 However, if an SAA is detected in an asymptomatic patient, elective repair via endovascular stent graft, embolization, or ligation is recommended in the settings of pregnancy and/or size ⬎ 2 cm.3,4 When these approaches fail, laparoscopic aneurysm resection with splenectomy has been successful, even when performed as late as the third trimester of pregnancy.19 The symptoms of an SAA rupture are vague and varied. The patient may have mild epigastric pain or referred left 216
shoulder pain that is followed by an increasing intensity in the severity of abdominal pain and shock. In 25% of the cases, a double rupture phenomenon has been described with the initial hemorrhage being controlled by tamponade mediated by clot formation in the lesser sac followed by further clinical deterioration after the first event as blood flows into the greater intraperitoneal sac.1,14,15 Emergent splenectomy remains the most common form of surgical therapy for SAA rupture.17 Hypotension secondary to acute blood loss is treated in the usual manner with crystalloid and blood product administration until definitive surgical repair is undertaken. The role of massive transfusion protocols and tranexamic acid has not been previously addressed but should be considered in these cases. Critical care transport is often the best means of transporting patients with splenic artery rupture to a referral center capable of managing complex complications of pregnancy. In such cases, patients require careful management of hypovolemic shock as well as detailed attention to fetal and maternal well-being. When longer distances are involved, air transport is often used to minimize the time to definitive care.
Conclusion These case studies emphasize that ruptured splenic artery aneurysm should be considered in the differential diagnosis of the pregnant patient who presents with abdominal pain and hypotension; evidence of hemoperitoneum, as detected by bedside ultrasound for example, should further heighten concern for this diagnosis. Prompt recognition of the problem with rapid transport to a tertiary center with appropriate surgical and obstetric intervention may be key factors in maternal and fetal survival. Otherwise, high maternal and fetal mortality may result.
References 1. Hillemanns P, Knitza R, Muller-Hocker J. Rupture of splenic artery aneurysm in a pregnancy patient with portal hypertension. Am J Obstet Gynecol. 1996;174:16651666. 2. Shahabi S, Jani J, Masters L, Cobin L, Greindl J. Spontaneous rupture of a splenic artery aneurysm in pregnancy: report of two cases. Acta Chir Belg. 2000;100:231233. 3. Oakley E, Ho J, Johnson V, VanCamp J, Melson T, Hick J. Splenic artery aneurysm: an important cause of hemoperitoneum and shock. J Emerg Med. 2014;46:e65-e67. 4. Pasha SF, Gloviczki P, Stanson A, Kamath P. Splanchnic artery aneurysms. Mayo Clin Proc. 2007;82:472-479. 5. Abbas M, Stone W, Fowl R, et al. Splenic artery aneurysms: two decades experience at Mayo Clinic. Ann Vasc Surg. 2002;16:442-449. 6. Williams JJ. Splenic artery aneurysm rupture: an uncommon obstetrical catastrophe. J Fam Pract. 1998;25:73-75. 7. Bettendorf O, Falbrede J, Eltze E. Letter to the editor—brief communication. Eur J Obstet Gynecol Reprod Biol. 2004;117:119-120. 8. Groussolles M Jr, Merveille M, Alacoque X, Vayssiere C, Reme JM, Parant O. Rupture of a splenic artery aneurysm in the first trimester of pregnancy. J Emerg Med. 2011;41:313-316. 9. Pavlis T, Seretis C, Gourgiotis S, Aravosita P, Mystakelli C, Aloizos S. Spontaneous rupture of splenic artery aneurysm during the first trimester of pregnancy: report of an extremely rare case and review of the literature. Case Rep Obstet Gynecol. 2012;2012:528051.
Air Medical Journal 33:5
10. Ha, J, Phillips M, Faulkner K. Splenic artery aneurysm rupture in pregnancy. Eur J Obstet Gynecol Reprod Biol. 2009;146:133-137. 11. Lowry SM, Shanley CJ. Visceral artery aneurysm. Surg Clin North Am. 1997;77:425-442. 12. Barrett J, Caldwell BH. Association of portal hypertension and ruptured splenic artery aneurysm in pregnancy. Obstet Gynecol. 1981;57:255-256. 13. Selo-Ojeme D, Welch C. Review: spontaneous rupture of splenic artery aneurysm in pregnancy. Eur J Obstet Gynecol Reprod Biol. 2003;109:124-127. 14. Khurana J, Spinello IM. Splenic artery aneurysm rupture: a rare but fatal cause for peripartum collapse. J Intensive Care Med. 2013;28:131-133. 15. Sadat U, Dar O, Walsh S, Varty K. Splenic artery aneurysms in pregnancy—a systematic review. Int J Surg. 2008;6:261-265. 16. Stanley JC, Fry WJ. Pathogenesis and clinical significance of splenic artery aneurysm. Surgery. 1974;76:889-909.
September-October 2014
17. Jack S, Hammond R, James DK. Diagnosis and treatment of ruptured splenic artery aneurysm in pregnancy. J Obstet Gynaecol. 1997;18:86-87. 18. McMahon DP, Ward WH, Harwood JL, Moore EM. An institutional review of splenic artery aneurysm in childbearing-aged females and splenic artery aneurysm rupture during pregnancy. Is screening justified? Mil Med. 2012;177:96-98. 19. Samame J, Kaul A, Garza U, Echeverria A, Galvani C. Laparoscopic aneurysm resection and splenectomy for splenic artery aneurysm in the third trimester of pregnancy. Surg Endosc. 2013;27:2988-2991. 20. Liu C, Kung C, Liu B, Ng S, Huang C, Ko S. Splenic artery aneurysms encountered in the ED: 10 years’ experience. Am J Emerg Med. 2007;25:430-436.
217
Ruptured Splenic Artery Aneurysm in Pregnancy: A Case Series Mary Lou Garey, MSN, RN, CNP,1 Sarah Greenberger, MD,2 and Howard A. Werman, MD, FACEP1,2
Rupture of a splenic artery aneurysm (SAA) is a rare and often catastrophic complication in pregnancy. Maternal and fetal mortality in the spontaneous rupture of a splenic artery aneurysm during pregnancy have been reported as high as 75% and 95%, respectively.1,2 We present 2 patients with SAA rupture in pregnancy who were transported by our critical care transport program. Both patients were transported from the same 100-bed community hospital within a 25-month period. The implications for critical care transport are discussed.
Case Reports Case 1 A 26-year-old woman presented to the regional emergency department by local emergency medical services after experiencing 2 generalized seizures at home. The patient was gravida 2 para 3 with triplets during her first pregnancy. She had a previous obstetric history of the delivery of triplets by cesarean section 3 years earlier. Notably, the patient was treated for pre-eclampsia during her previous pregnancy and had required magnesium infusion. At the time of the current presentation, she was at 36 weeks’ gestation with a single fetus. This pregnancy had thus far been uncomplicated. The patient did not report any other medical or surgical history. On the night of admission, the patient presented with seizures after an episode of nausea, vomiting, bowel incontinence, and diarrhea. The patient was responsive and answering questions slowly. She complained of headache and left upper quadrant pain. Her presenting blood pressure was 66/30 with a heart rate of 101. The fetal heart rate was 152. The patient had 2 intravenous lines placed, she received 4 g magnesium sulfate, and she was quickly transferred to the obstetric unit where her obstetrician was waiting. Her blood pressure on arrival to the unit was 160/116 with her heart rate unchanged. She then had 2 more episodes of hypotension that quickly rebounded to the range of 140/70 with intravenous
1. MedFlight, Columbus, OH, USA 2. Department of Emergency Medicine, The Ohio State University, Columbus, OH, USA 1067-991X/$36.00 Copyright 2014 by Air Medical Journal Associates http://dx.doi.org/:10.1016/j.amj.2014.05.006 214
fluid administration. Her abdomen was soft. The fetal heart rate was in the 140s but with minimal reactivity. Subsequently, an emergent cesarean section was performed using a transverse suprapubic incision under spinal anesthesia. Delivery of a 2,760-g female followed with a 1-minute Apgar of 3; the 5and 10-minute Apgar scores were 6 and 7, respectively. Upon handing off the infant, large pools of clotted blood as well as fresh active bleeding were noted in the left upper abdomen. The uterus was intact on examination. However, the patient’s mentation and blood pressure began to deteriorate, and she was intubated for airway protection. Postintubation blood gases revealed a pH of 7.15, paO2 of 516, pCO2 of 34, and bicarbonate of 11.5. Additional laboratory values drawn included a white blood cell count of 14.7 with a hemoglobin level of 10.6 and platelets of 63,000. She had an international normalized ratio of 1.5 and a fibrinogen level of 116 mg/dL (normal 200-400 mg/dL). A general surgeon arrived to assist the obstetric team. A ruptured spleen was believed to be the cause of the hemorrhage, although a distinct source could not be identified. The limited blood supply of the community hospital was rapidly being exhausted. By this point, the patient had received 4,500 mL crystalloids and 7 units of packed cells, including 2 units of O-negative blood. Her systolic blood pressure was initially 80 mm Hg at the start of the case and increased to 120 mm Hg intraoperatively but was trending downward by the end of the procedure. The patient’s abdomen was packed, and preparations were made to transport her by helicopter to a tertiary care center because of the lack of available blood products as well as the need for advanced surgical care. Upon leaving the community hospital, her systolic blood pressure remained around 80 mm Hg, and the last of the available units of blood (units #8 and #9) were infusing along with crystalloids. During flight, the patient’s blood pressure dropped below 50 mm Hg as determined by Doppler measurement. Her heart rate remained in the 120s with short runs of ventricular tachycardia. She remained intubated. The pulse oximetry would not register because of her poor peripheral perfusion. Her pupils were sluggish to react, and she would turn her head in response to loud verbal stimulation. On arrival to the receiving facility, the patient was taken directly to the operating suite for an exploratory laparotomy. A midline incision was made with profuse bleeding noted. Blood products and crystalloid fluid infusions continued. On further exploration, a ruptured SAA was discovered. She underwent a splenectomy, after which her abdomen was packed because of hemodynamic instability. Two days after Air Medical Journal 33:5
her transfer, she returned to the operating room for the removal of packing and final closure. There were no additional sources of bleeding found. At the time of her final surgery, the patient had received a total of 38 units of packed red blood cells (PRBCs), 22 units of fresh frozen plasma, 8 units of platelets, and 5 units of cryoprecipitate. The patient made a slow but steady recovery and was discharged to home 11 days after admission. Her recovery course was complicated by a low-grade pancreatic fistula, which resolved with percutaneous drainage and antibiotics. Her newborn daughter was waiting for her at home, having been discharged on the third postpartum day.
Case 2 A 26-year-old woman presented to the regional obstetric unit with complaints of abdominal pain and cramping. She was assessed as gravida 2 para 1 at 34 weeks’ gestation with a single fetus. Her past medical and surgical history was negative, and her previous pregnancy had been uncomplicated. Fetal monitoring showed the fetal heart rate was in the 160s. During the initial evaluation, the patient suddenly sat upright and developed projectile vomiting. She became pale and diaphoretic. The fetal monitor showed profound persistent bradycardia. The maternal patient became less responsive, and an emergent cesarean section using a midline laparotomy incision was performed. A 2,800-g infant was delivered and resuscitated with some difficulty. The Apgar score was 0 upon delivery, 3 at 1 minute, 6 at 5 minutes, and 8 at 10 minutes. September-October 2014
The infant was later transferred to a level 3 nursery for neonatal intensive care. After handing off the infant, the patient was found to have 2,000 mL of both clotted and unclotted blood in the left upper abdominal quadrant. A general surgeon had been called in to assist the obstetric staff. The patient had a blood pressure of 110/60 and a heart rate of 120. Laboratory values sent from the operating room revealed a white blood cell count of 16.8, hemoglobin of 8.9, and platelets of 159,000. On exploration, a rupture of a dilated splenic artery wall was found just distal to its branching from the celiac artery. A repair was performed with appropriate hemostasis achieved after the administration of 4,600 mL crystalloid and 6 units of PRBCs including 2 units of O-negative blood. The abdomen was packed, and the patient was transferred directly from the operating room to a tertiary care center by the ground mobile intensive care unit for definitive care. She remained hemodynamically stable during transport, with crystalloids infusing at a maintenance rate and continued administration of her seventh unit of PRBCs. At the receiving facility, the patient’s hemoglobin repeatedly decreased. An exploratory laparotomy was performed 12 hours after admission. She was found to have a large amount of fresh and clotted blood in the peritoneal cavity (estimated 2,000 mL). Blood was found to be leaking from the repaired SAA and the uterine sutures. A splenectomy was performed as well as a suture repair of the uterus. The patient’s recovery course was uncomplicated, and she was discharged to home 6 days after admission. Unfortunately, 215
the infant did not survive the event, with death attributed to significant neurologic and end-organ damage.
Discussion SAA remains relatively uncommon, with a reported incidence of 0.01% to 0.98%3,4; a retrospective review found only 217 cases of SAA documented at the Mayo Clinic over the period of 1980 to 1998.5 SAA rupture occurs in 2% to 3% of all cases and with increased frequency (estimated at 20%40%) in otherwise healthy pregnant women or during the recent postpartum period.3,4,6,7 At least 3 cases of SAA have been reported to occur as early as the first trimester of pregnancy.8,9 Because of the infrequency of SAA complicating pregnancy, there is a relative paucity of literature about this condition. To our knowledge, this is the first time SAA rupture in pregnant patients has been reported in the critical care transport literature. An SAA usually is asymptomatic until rupture occurs.10 Even then, the diagnosis of severe abdominal pain and hypotension in pregnancy may be attributed to a variety of potential working diagnoses such as ruptured ectopic pregnancy, placental abruption, uterine rupture, amniotic fluid embolism, pulmonary thromboembolism, cholecystitis, appendicitis, or perforation of a peptic ulcer.7-9,12 The use of ultrasound to detect free fluid may help with early, and often lifesaving, diagnosis of hemoperitoneum in a stable pregnant patient presenting with abdominal pain. The mortality from a ruptured SAA has been reported to be as high as 36% to 40% in the general population and up to 70% for pregnant women specifically, with mortality for the fetus upward of 90%.3,4,13 The literature contains more than 100 cases of SAA rupture in pregnancy but only 17 other cases of maternal and fetal survival.7,13,14 Both mothers survived their diagnosis in our cases, but, unfortunately, subsequent fetal mortality was 50%. There is no clear mechanism by which pregnancy increases the incidence of SAA rupture. Risk factors postulated in this population include increased portal venous pressure; increased cardiac output during pregnancy; and higher estrogen, progesterone, and relaxin levels contributing to elastin disruption in the tunica media of the vasculature.3,4,15 Of note, approximately 40% of women with splenic artery aneurysms are reported to be grand multiparous (ⱖ 5 births)16; additional risk factors predisposing to SAA include a history of cirrhosis or liver transplant.17 Given a prevalence of SAA of less than 0.1%, routine radiologic screening of all women of childbearing age has not been recommended.18 However, if an SAA is detected in an asymptomatic patient, elective repair via endovascular stent graft, embolization, or ligation is recommended in the settings of pregnancy and/or size ⬎ 2 cm.3,4 When these approaches fail, laparoscopic aneurysm resection with splenectomy has been successful, even when performed as late as the third trimester of pregnancy.19 The symptoms of an SAA rupture are vague and varied. The patient may have mild epigastric pain or referred left 216
shoulder pain that is followed by an increasing intensity in the severity of abdominal pain and shock. In 25% of the cases, a double rupture phenomenon has been described with the initial hemorrhage being controlled by tamponade mediated by clot formation in the lesser sac followed by further clinical deterioration after the first event as blood flows into the greater intraperitoneal sac.1,14,15 Emergent splenectomy remains the most common form of surgical therapy for SAA rupture.17 Hypotension secondary to acute blood loss is treated in the usual manner with crystalloid and blood product administration until definitive surgical repair is undertaken. The role of massive transfusion protocols and tranexamic acid has not been previously addressed but should be considered in these cases. Critical care transport is often the best means of transporting patients with splenic artery rupture to a referral center capable of managing complex complications of pregnancy. In such cases, patients require careful management of hypovolemic shock as well as detailed attention to fetal and maternal well-being. When longer distances are involved, air transport is often used to minimize the time to definitive care.
Conclusion These case studies emphasize that ruptured splenic artery aneurysm should be considered in the differential diagnosis of the pregnant patient who presents with abdominal pain and hypotension; evidence of hemoperitoneum, as detected by bedside ultrasound for example, should further heighten concern for this diagnosis. Prompt recognition of the problem with rapid transport to a tertiary center with appropriate surgical and obstetric intervention may be key factors in maternal and fetal survival. Otherwise, high maternal and fetal mortality may result.
References 1. Hillemanns P, Knitza R, Muller-Hocker J. Rupture of splenic artery aneurysm in a pregnancy patient with portal hypertension. Am J Obstet Gynecol. 1996;174:16651666. 2. Shahabi S, Jani J, Masters L, Cobin L, Greindl J. Spontaneous rupture of a splenic artery aneurysm in pregnancy: report of two cases. Acta Chir Belg. 2000;100:231233. 3. Oakley E, Ho J, Johnson V, VanCamp J, Melson T, Hick J. Splenic artery aneurysm: an important cause of hemoperitoneum and shock. J Emerg Med. 2014;46:e65-e67. 4. Pasha SF, Gloviczki P, Stanson A, Kamath P. Splanchnic artery aneurysms. Mayo Clin Proc. 2007;82:472-479. 5. Abbas M, Stone W, Fowl R, et al. Splenic artery aneurysms: two decades experience at Mayo Clinic. Ann Vasc Surg. 2002;16:442-449. 6. Williams JJ. Splenic artery aneurysm rupture: an uncommon obstetrical catastrophe. J Fam Pract. 1998;25:73-75. 7. Bettendorf O, Falbrede J, Eltze E. Letter to the editor—brief communication. Eur J Obstet Gynecol Reprod Biol. 2004;117:119-120. 8. Groussolles M Jr, Merveille M, Alacoque X, Vayssiere C, Reme JM, Parant O. Rupture of a splenic artery aneurysm in the first trimester of pregnancy. J Emerg Med. 2011;41:313-316. 9. Pavlis T, Seretis C, Gourgiotis S, Aravosita P, Mystakelli C, Aloizos S. Spontaneous rupture of splenic artery aneurysm during the first trimester of pregnancy: report of an extremely rare case and review of the literature. Case Rep Obstet Gynecol. 2012;2012:528051.
Air Medical Journal 33:5
10. Ha, J, Phillips M, Faulkner K. Splenic artery aneurysm rupture in pregnancy. Eur J Obstet Gynecol Reprod Biol. 2009;146:133-137. 11. Lowry SM, Shanley CJ. Visceral artery aneurysm. Surg Clin North Am. 1997;77:425-442. 12. Barrett J, Caldwell BH. Association of portal hypertension and ruptured splenic artery aneurysm in pregnancy. Obstet Gynecol. 1981;57:255-256. 13. Selo-Ojeme D, Welch C. Review: spontaneous rupture of splenic artery aneurysm in pregnancy. Eur J Obstet Gynecol Reprod Biol. 2003;109:124-127. 14. Khurana J, Spinello IM. Splenic artery aneurysm rupture: a rare but fatal cause for peripartum collapse. J Intensive Care Med. 2013;28:131-133. 15. Sadat U, Dar O, Walsh S, Varty K. Splenic artery aneurysms in pregnancy—a systematic review. Int J Surg. 2008;6:261-265. 16. Stanley JC, Fry WJ. Pathogenesis and clinical significance of splenic artery aneurysm. Surgery. 1974;76:889-909.
September-October 2014
17. Jack S, Hammond R, James DK. Diagnosis and treatment of ruptured splenic artery aneurysm in pregnancy. J Obstet Gynaecol. 1997;18:86-87. 18. McMahon DP, Ward WH, Harwood JL, Moore EM. An institutional review of splenic artery aneurysm in childbearing-aged females and splenic artery aneurysm rupture during pregnancy. Is screening justified? Mil Med. 2012;177:96-98. 19. Samame J, Kaul A, Garza U, Echeverria A, Galvani C. Laparoscopic aneurysm resection and splenectomy for splenic artery aneurysm in the third trimester of pregnancy. Surg Endosc. 2013;27:2988-2991. 20. Liu C, Kung C, Liu B, Ng S, Huang C, Ko S. Splenic artery aneurysms encountered in the ED: 10 years’ experience. Am J Emerg Med. 2007;25:430-436.
217
