Diagnostics
Splenic Artery Aneurysm Rupture DANIEL MINES, MD Splenic artery aneurysms are rare and usually asymptomatlc. However, rupture can produce severe abdominal paln and prove lethal. Two cases of ruptured rplenlc arlery aneurysm are presented. In one, cocaine lnjecllon occurred Immedlataly prior to the onset of symptoms and may have praclpltated the event. (Am J Emerg Med 1##1;#:74-76. Copyright 0 1991 by W.B. Saunders Company) Although splenic artery aneurysms (SAAs) are uncommon and usually asymptomatic, their ruptures can cause severe abdominal pain and death. The diagnosis of ruptured SAA can be difficult because it is rare and because its presentation mimics more common ailments. From 1988 to 1989 two patients with this condition presented to the emergency department (ED) at Pennsylvania Hospital. CASE REPORTS Case1 A 46-year-old man with a history of reflux esophagitis complained of severe abdominal pain following a single episode of forceful vomiting. The pain localized to his left upper quadrant, and radiated to the left side of his chest, shoulder, and neck. He acknowledged drinking heavily in the days prior to his illness. He denied fever, dyspnea, pleuritic pain, trauma, bloody emesis, melena, or prior abdominal surgery. Physical examination showed a man in mild distress with a blood pressure of 170/80 mm Hg and pulse of 76 beats/min, without orthostatic changes; oral temperature, 37.2”C; respirators, 20 breaths/ min. The heart and lungs were unremarkable. The abdomen was soft with normal bowel sounds and no organomegaly or mass. Tenderness was elicited in the epigastrium and left upper quadrant, but there was no rebound. The stool was negative for occult blood. The hemoglobin was 145 g/L, and the white blood cell (WBC) count 9.5 x 109/L. Electrolytes, glucose, blood urea nitrogen, and amylase results were all normal. Obstruction series showed neither free air nor abdominal calcifications. The electrocardiogram showed no abnormalities. The diagnostic impression was gastritis with musculoskeletal pain secondary to retching. He was treated with antacids and advised to decrease his intake of alcohol. Twelve hours later the patient returned with intensified abdominal pain after vomiting again. The pain now was more diffuse, worse
From the Department of Medicine, Emergency Services, Hospital of the University of Pennsylvania, Philadelphia, PA. Address reprint requests to Dr Mines: Emergency Department, Ground Silverstein, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104-4283. Key words: Splenic artery, aneurysm, rupture, cocaineadverse effects. Copyright 0 1991 by W.B. Saunders Company 0735-6757/91/0901-0021$5.00/O
74
supine and with movement. The chest, shoulder, and neck pain had resolved. The patient appeared very uncomfortable and was diaphoretic. The vital signs were essentially unchanged. Abdominal examination showed voluntary guarding and marked left upper quadrant tenderness but no rebound. Normal bowel sounds were present. The remainder of the physical examination was unchanged. A second hemoglobin was 130 g/L and the WBC count was 16.3 x lO?L, without a left shift. Second chemistries and roentgenograms were unchanged. Pain diminished markedly after liquid antacid was administered. While the impression remained gastritis or other peptic process, the emergency physician recommended a surgical consultation, which the patient declined because he was feeling so much better. Antacids were continued. When he followed up with his internist the next day, 36 hours after initial presentation, pain had diminished but continued to be worse with motion. Examination now showed percussion tenderness in the epigastrium. An abdominal ultrasound demonstrated free peritoneal fluid; the spleen, pancreas, and hepato-biliary tree appeared normal. The patient was admitted to a surgical service with the presumptive diagnoses of a wailed-off perforated ulcer. He was treated with intravenous fluids and ranitidine. The next morning an upper gastrointestinal series showed a normal esophagus and no evidence of ulcer. A subsequent hemoglobin returned at 90 g/L. Abdominal paracentesis recovered grossly bloody fluid. At exploratory laparotomy, bleeding appeared to originate from the splenic hilum; a splenectomy was performed. On pathological review, an aneurysm, 1 cm in diameter, was found at the first bifurcation of the splenic artery. The patient recovered uneventfully.
Case2 A 43 year-old-male intravenous drug abuser with diabetes mellitus presented complaining of severe thoracic back pain and shortness of breath that began shortly after injecting cocaine. The patient was very agitated and combatative; no additional history could be obtained. The patient appeared acutely ill, pale, and diaphoretic. The blood pressure was initially palpated at 70 mm Hg in the right arm. Pulse was 120 beats/min; respirations, 26 breathslmin; temperature 35.7”C. A distant S-l and S-2 were heard, without murmur or gallop.
The abdomen was obese, soft, nontender, and without palpable mass. The only arterial pulses palpated were the carotids. The electrocardiogram showed sinus tachycardia with nonspecific ST-T wave changes. The chest roentgenogram showed normal heart and lung fields, with a suggestion of mediastinal widening. Hemoglobin was % g/L and the WBC count 15.2 x 10% Arterial blood gas on nasal oxygen at 2 Wmin was pH 7.32, Pco, 21 mm Hg, PO, 97 mm Hg, HCO, 11.2 mmol/L. Serum sodium was 141 mmoYL; potassium, 4.1 mmol/L; chloride, 112 mmoYL; bicarbonate 16 mmol/L. Glucose, blood urea nitrogen; and creatinine levels were normal. Shortly after arrival the patient became profoundly hypotensive
DANIEL MINES n SPLENIC
ARTERY ANEURYSM
RUPTURE
and unresponsive. He was treated with intravenous saline and dopamine, as well as naloxone, thiamine, and dextrose. He was intubated and mechanically ventilated. Although the diagnosis was unclear, the leading concern was a thoracic aortic dissection. Surgical consultation and echocardiogram were requested. The patient became progressively acidotic, and hypotension was refractory to therapy. Bicarbonate, norepinephrine, and blood were administered. After infusion of several liters of fluid, the abdomen became distended and rigid. At this point focus shifted to a ruptured viscus or abdominal aortic aneurysm. The patient died before he could be taken to the operating room. An autopsy showed cirrhosis of the liver, splenomegaly and massive bleeding into the peritoneal cavity. Part of the splenic artery formed atherosclerotic aneurysm, measuring 5 cm in diameter, with a small defect that was believed to be the source of bleeding. Cocaine was detected in the blood.
DISCUSSION Splenic artery aneurysms are rare, but exactly how rare is not known, because most patients do not have symptoms and are diagnosed incidentally.’ The reported incidence of SAA ranges from 0.16%* to 0.78%3 to 10.4%,4 depending on the age and sex of the group studied and the intensity with which it was sought.5 The true incidence in the overall population is probably less than 1%. Following the aorta and iliac arteries, the splenic artery is the third most common location for intraabdominal aneurysms.6 Unlike aortoiliac aneurysms, however, SAAs occur two to five times more frequently in women, in multiparous women in particular, and in younger patients-not uncommonly in the third through fifth decades.‘,‘*’ The rupture of SAAs in pregnant women is more likely to occur late in the third trimester or in the early postpartum period,‘-” and is associated with a 71% maternal and 95% fetal mortality.’ Rupture in nonpregnant patients is less lethal, with morality rates ranging from 10% to 50%.‘,5,7*9 The leading causes of SAA are atherosclerosis and medial degeneration of the arterial wall, a poorly understood phenomenon associated with multiparity.‘*” Injury to the arterial wall, as a result of pancreatitis, septic emboli, or trauma, less commonly produces SAA. Interestingly, after he was shot in an assassination attempt, President Garfield developed a SAA and died when it ruptured. SAAs are also associated with portal hypertension,‘,” and may occur congenitally or as part of a disease causing multiple vascular aneurysms.’ Patients with SAAs are usually asymptomatic, although some may report vague left upper quadrant discomfort radiating to the left subscapular area. The physical examination rarely detects a bruit or mass and is almost always unrevealing. ’ Patients generally come to medical attention in one of two ways. Most are discovered incidentally, when plain abdominal roentgenograms, done for other reasons, demonstrate characteristic “egg-shell” calcifications in the left upper quadrant.‘*5 Others present with symptoms at the time of rupture. Patients describe the sudden onset of left upper quadrant pain radiating to the back, left flank, or shoulder.‘,‘* There may be vomiting, abdominal distension, tenderness, and signs of hypovolemic shock.‘* A SAA ruptures usually into one of two places, the peritoneal cavity or the lesser sac. In the former situation, hemodynamic collapse occurs quickly. Rupture into the lesser
75
sac may allow for temporary tamponade of bleeding, and pain may abate. Without treatment, however, free rupture into the peritoneal cavity occurs minutes to days later, and is usually catastrophic. ‘J’ The patient described in case 1 probably first bled into the lesser sac. Less commonly rupture results in bleeding into the gastrointestinal tract or pancreas. ’ 7’ ’ The differential diagnosis of a ruptured SAA is broad, and includes perforated peptic ulcer, acute pancreatitis, strangulated bowel, ruptured abdominal aortic aneurysm, acute mesenteric ischemia, ‘* myocardial infarction,’ splenic infarct, renal colic, and, as the cases presented here illustrate, gastritis and thoracic aortic dissection. In the obstetrical patient it can mimic ruptured uterus, cholecystitis,” placental abruption with concealed bleeding or massive pulmonary embolus.13 Once one suspects a splenic artery aneurysm, urgent surgical consultation is recommended. Left upper quadrant calcifications on abdominal roentgenogram support the diagnosis but are absent in about a quarter of patients,’ and are not specific for SAA. While computed tomography and ultrasound with Doppler have been used to diagnose SAA,‘4*‘5 their ability to reliably exclude small leaking aneurysms is unclear and thus the gold standard remains arteriography.5*‘6 The severity of illness may not permit enough time for this study, however. If ultrasound is readily available, detection of unexpected peritoneal fluid may lead to the correct diagnosis. The demonstration of nonclotted blood by paracentesis implies intraabdominal bleeding and necessitates exploratory laparotomy,‘* as does unexplained abdominal pain with shock. Diagnosis at the time of laparotomy is not unusual. Of 16 recently reported cases,‘*’ 5 were diagnosed in this manner. Cocaine may have precipitated the rupture of the SAA described in case 2, in which the onset of symptoms immediately followed injection of the drug. Cocaine is known to cause a surge in blood pressure due to sympathetically mediated tachycardia and vasoconstriction.” While cocaine has been implicated in thoracic aortic dissection” and subarachnoid hemorrhage,” visceral aneurysmal rupture associated with cocaine has not been reported previously. SUMMARY When SAAs rupture, patients present with collapse or left upper quadrant pain that can radiate to the back or shoulder. Given such a history, the diagnosis should be suspected, particularly when characteristic calcifications are seen on roentgenograms, and in patients who have portal hypertension, are multiparous, or present peripartum. Cocaine use may precipitate rupture. REFERENCES 1. Trastek VF, Pairolero PC, Joyce JW, et al: Splenic artery aneurysms. Surgery 1982;91:894-899 2. Scheps SG, Spittell JA Jr, Fairbairn JF II, et al: Aneurysms of the splenic artery with special reference to bland aneurysms. Prof Staff Meet Mayo Clinic 1958;33:381-390 3. Stanley JC, Fry WJ: Pathogenesis and clinical significance of splenic artery aneurysms. Surgery 1974;76:898-909 4. Bedford PD, Lodge 6: Aneurysms of the splenic artery. Gut 1960;1:312-320
76
AMERICAN
JOURNAL
5. Trastek VF, Pairolero PC, Beratz PE: Splenic artery aneurysms. World J Surg 1985;9:376-383 6. Spittel JA: Aneurysms of the splenic artery. JAMA 1961 ;175:452-456 7. Greene DR, Gorey TF, Tanner WA, et al: The diagnosis and management of splenic artery aneurysms. J R Sot Med 1988; 81:387-388 8. Martinez E, Menendez AR, Ablanedo P: Splenic artery aneurysms. Int Surg 1986;71:95-99 9. Sabiston DC: Visceral artery aneurysms, in Sabiston DC (ed): Textbook of Surgery (ed 13). Philadelphia, PA, Saunders, 1986, pp 1826-1828 10. Lowry SM, O’Dea TP, Gallagher DI, et al: Splenic artery aneurysm rupture: The seventh instance of maternal and fetal survival. Obstet Gynecol 1986;67:291-292 11. Sheldon GF, Croom RD, Meyer AA: The spleen. In Sabiston DC (ed): Textbook of Surgery (ed 13). Philadelphia, PA, Saunders, 1986, pp 1228-1230 12. Adams JT: Aneurysms of the splanchnic arteries. In
OF EMERGENCY
MEDICINE
n Volume 9, Number
1 n January
1991
Schwartz SI, Shires GT, Spencer FC (eds): Principles of Surgery, (ed 5). New York, NY, McGraw Hill, 1989, pp 1511-1512 13. Williams JJ: Splenic artery aneurysm rupture: An uncommon obstetrical catastrophe. J Fam Practice i988;26:73-75 14. Derchi LE. Biaai E. Cicio GR. et al: Aneurvsms of the splenic artery: nonin&ive diagnosis’by pulsed Doppler sonography. J Ultrasound Med 1984;3:41-44 15. Ueda J, Kobayashi Y, Hara K, et al: Giant aneurysm of the splenic artery and huge varix. Gastrointest Radio1 1985;10:55-57 16. Jeffrey RB Jr: CT and Sonography of the Acute Abdomen. New York, NY, Raven Press, 1989, pp 102-104 17. Ritchie JM, Greene NM: Local Anesthetics. In Gilman AG, Goodman LS, Rail TW, et al (eds): Goodman and Gillman’s The Pharmacological Basis of Therapeutics (ed 7). New York, NY, Macmillan, 1985, pp 309-310 18. Gadaleta D, Hall Ml-f, Nelson RL: Cocaine-induced acute aortic dissection. Chest 1989;96:1203-1205 19. Jacobs, IG, Roszler Ml-f, Kelly JK, et al: Cocaine abuse: Neurovascular complications. Radiology 1989;170:223-227
Splenic Artery Aneurysm Rupture DANIEL MINES, MD Splenic artery aneurysms are rare and usually asymptomatlc. However, rupture can produce severe abdominal paln and prove lethal. Two cases of ruptured rplenlc arlery aneurysm are presented. In one, cocaine lnjecllon occurred Immedlataly prior to the onset of symptoms and may have praclpltated the event. (Am J Emerg Med 1##1;#:74-76. Copyright 0 1991 by W.B. Saunders Company) Although splenic artery aneurysms (SAAs) are uncommon and usually asymptomatic, their ruptures can cause severe abdominal pain and death. The diagnosis of ruptured SAA can be difficult because it is rare and because its presentation mimics more common ailments. From 1988 to 1989 two patients with this condition presented to the emergency department (ED) at Pennsylvania Hospital. CASE REPORTS Case1 A 46-year-old man with a history of reflux esophagitis complained of severe abdominal pain following a single episode of forceful vomiting. The pain localized to his left upper quadrant, and radiated to the left side of his chest, shoulder, and neck. He acknowledged drinking heavily in the days prior to his illness. He denied fever, dyspnea, pleuritic pain, trauma, bloody emesis, melena, or prior abdominal surgery. Physical examination showed a man in mild distress with a blood pressure of 170/80 mm Hg and pulse of 76 beats/min, without orthostatic changes; oral temperature, 37.2”C; respirators, 20 breaths/ min. The heart and lungs were unremarkable. The abdomen was soft with normal bowel sounds and no organomegaly or mass. Tenderness was elicited in the epigastrium and left upper quadrant, but there was no rebound. The stool was negative for occult blood. The hemoglobin was 145 g/L, and the white blood cell (WBC) count 9.5 x 109/L. Electrolytes, glucose, blood urea nitrogen, and amylase results were all normal. Obstruction series showed neither free air nor abdominal calcifications. The electrocardiogram showed no abnormalities. The diagnostic impression was gastritis with musculoskeletal pain secondary to retching. He was treated with antacids and advised to decrease his intake of alcohol. Twelve hours later the patient returned with intensified abdominal pain after vomiting again. The pain now was more diffuse, worse
From the Department of Medicine, Emergency Services, Hospital of the University of Pennsylvania, Philadelphia, PA. Address reprint requests to Dr Mines: Emergency Department, Ground Silverstein, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104-4283. Key words: Splenic artery, aneurysm, rupture, cocaineadverse effects. Copyright 0 1991 by W.B. Saunders Company 0735-6757/91/0901-0021$5.00/O
74
supine and with movement. The chest, shoulder, and neck pain had resolved. The patient appeared very uncomfortable and was diaphoretic. The vital signs were essentially unchanged. Abdominal examination showed voluntary guarding and marked left upper quadrant tenderness but no rebound. Normal bowel sounds were present. The remainder of the physical examination was unchanged. A second hemoglobin was 130 g/L and the WBC count was 16.3 x lO?L, without a left shift. Second chemistries and roentgenograms were unchanged. Pain diminished markedly after liquid antacid was administered. While the impression remained gastritis or other peptic process, the emergency physician recommended a surgical consultation, which the patient declined because he was feeling so much better. Antacids were continued. When he followed up with his internist the next day, 36 hours after initial presentation, pain had diminished but continued to be worse with motion. Examination now showed percussion tenderness in the epigastrium. An abdominal ultrasound demonstrated free peritoneal fluid; the spleen, pancreas, and hepato-biliary tree appeared normal. The patient was admitted to a surgical service with the presumptive diagnoses of a wailed-off perforated ulcer. He was treated with intravenous fluids and ranitidine. The next morning an upper gastrointestinal series showed a normal esophagus and no evidence of ulcer. A subsequent hemoglobin returned at 90 g/L. Abdominal paracentesis recovered grossly bloody fluid. At exploratory laparotomy, bleeding appeared to originate from the splenic hilum; a splenectomy was performed. On pathological review, an aneurysm, 1 cm in diameter, was found at the first bifurcation of the splenic artery. The patient recovered uneventfully.
Case2 A 43 year-old-male intravenous drug abuser with diabetes mellitus presented complaining of severe thoracic back pain and shortness of breath that began shortly after injecting cocaine. The patient was very agitated and combatative; no additional history could be obtained. The patient appeared acutely ill, pale, and diaphoretic. The blood pressure was initially palpated at 70 mm Hg in the right arm. Pulse was 120 beats/min; respirations, 26 breathslmin; temperature 35.7”C. A distant S-l and S-2 were heard, without murmur or gallop.
The abdomen was obese, soft, nontender, and without palpable mass. The only arterial pulses palpated were the carotids. The electrocardiogram showed sinus tachycardia with nonspecific ST-T wave changes. The chest roentgenogram showed normal heart and lung fields, with a suggestion of mediastinal widening. Hemoglobin was % g/L and the WBC count 15.2 x 10% Arterial blood gas on nasal oxygen at 2 Wmin was pH 7.32, Pco, 21 mm Hg, PO, 97 mm Hg, HCO, 11.2 mmol/L. Serum sodium was 141 mmoYL; potassium, 4.1 mmol/L; chloride, 112 mmoYL; bicarbonate 16 mmol/L. Glucose, blood urea nitrogen; and creatinine levels were normal. Shortly after arrival the patient became profoundly hypotensive
DANIEL MINES n SPLENIC
ARTERY ANEURYSM
RUPTURE
and unresponsive. He was treated with intravenous saline and dopamine, as well as naloxone, thiamine, and dextrose. He was intubated and mechanically ventilated. Although the diagnosis was unclear, the leading concern was a thoracic aortic dissection. Surgical consultation and echocardiogram were requested. The patient became progressively acidotic, and hypotension was refractory to therapy. Bicarbonate, norepinephrine, and blood were administered. After infusion of several liters of fluid, the abdomen became distended and rigid. At this point focus shifted to a ruptured viscus or abdominal aortic aneurysm. The patient died before he could be taken to the operating room. An autopsy showed cirrhosis of the liver, splenomegaly and massive bleeding into the peritoneal cavity. Part of the splenic artery formed atherosclerotic aneurysm, measuring 5 cm in diameter, with a small defect that was believed to be the source of bleeding. Cocaine was detected in the blood.
DISCUSSION Splenic artery aneurysms are rare, but exactly how rare is not known, because most patients do not have symptoms and are diagnosed incidentally.’ The reported incidence of SAA ranges from 0.16%* to 0.78%3 to 10.4%,4 depending on the age and sex of the group studied and the intensity with which it was sought.5 The true incidence in the overall population is probably less than 1%. Following the aorta and iliac arteries, the splenic artery is the third most common location for intraabdominal aneurysms.6 Unlike aortoiliac aneurysms, however, SAAs occur two to five times more frequently in women, in multiparous women in particular, and in younger patients-not uncommonly in the third through fifth decades.‘,‘*’ The rupture of SAAs in pregnant women is more likely to occur late in the third trimester or in the early postpartum period,‘-” and is associated with a 71% maternal and 95% fetal mortality.’ Rupture in nonpregnant patients is less lethal, with morality rates ranging from 10% to 50%.‘,5,7*9 The leading causes of SAA are atherosclerosis and medial degeneration of the arterial wall, a poorly understood phenomenon associated with multiparity.‘*” Injury to the arterial wall, as a result of pancreatitis, septic emboli, or trauma, less commonly produces SAA. Interestingly, after he was shot in an assassination attempt, President Garfield developed a SAA and died when it ruptured. SAAs are also associated with portal hypertension,‘,” and may occur congenitally or as part of a disease causing multiple vascular aneurysms.’ Patients with SAAs are usually asymptomatic, although some may report vague left upper quadrant discomfort radiating to the left subscapular area. The physical examination rarely detects a bruit or mass and is almost always unrevealing. ’ Patients generally come to medical attention in one of two ways. Most are discovered incidentally, when plain abdominal roentgenograms, done for other reasons, demonstrate characteristic “egg-shell” calcifications in the left upper quadrant.‘*5 Others present with symptoms at the time of rupture. Patients describe the sudden onset of left upper quadrant pain radiating to the back, left flank, or shoulder.‘,‘* There may be vomiting, abdominal distension, tenderness, and signs of hypovolemic shock.‘* A SAA ruptures usually into one of two places, the peritoneal cavity or the lesser sac. In the former situation, hemodynamic collapse occurs quickly. Rupture into the lesser
75
sac may allow for temporary tamponade of bleeding, and pain may abate. Without treatment, however, free rupture into the peritoneal cavity occurs minutes to days later, and is usually catastrophic. ‘J’ The patient described in case 1 probably first bled into the lesser sac. Less commonly rupture results in bleeding into the gastrointestinal tract or pancreas. ’ 7’ ’ The differential diagnosis of a ruptured SAA is broad, and includes perforated peptic ulcer, acute pancreatitis, strangulated bowel, ruptured abdominal aortic aneurysm, acute mesenteric ischemia, ‘* myocardial infarction,’ splenic infarct, renal colic, and, as the cases presented here illustrate, gastritis and thoracic aortic dissection. In the obstetrical patient it can mimic ruptured uterus, cholecystitis,” placental abruption with concealed bleeding or massive pulmonary embolus.13 Once one suspects a splenic artery aneurysm, urgent surgical consultation is recommended. Left upper quadrant calcifications on abdominal roentgenogram support the diagnosis but are absent in about a quarter of patients,’ and are not specific for SAA. While computed tomography and ultrasound with Doppler have been used to diagnose SAA,‘4*‘5 their ability to reliably exclude small leaking aneurysms is unclear and thus the gold standard remains arteriography.5*‘6 The severity of illness may not permit enough time for this study, however. If ultrasound is readily available, detection of unexpected peritoneal fluid may lead to the correct diagnosis. The demonstration of nonclotted blood by paracentesis implies intraabdominal bleeding and necessitates exploratory laparotomy,‘* as does unexplained abdominal pain with shock. Diagnosis at the time of laparotomy is not unusual. Of 16 recently reported cases,‘*’ 5 were diagnosed in this manner. Cocaine may have precipitated the rupture of the SAA described in case 2, in which the onset of symptoms immediately followed injection of the drug. Cocaine is known to cause a surge in blood pressure due to sympathetically mediated tachycardia and vasoconstriction.” While cocaine has been implicated in thoracic aortic dissection” and subarachnoid hemorrhage,” visceral aneurysmal rupture associated with cocaine has not been reported previously. SUMMARY When SAAs rupture, patients present with collapse or left upper quadrant pain that can radiate to the back or shoulder. Given such a history, the diagnosis should be suspected, particularly when characteristic calcifications are seen on roentgenograms, and in patients who have portal hypertension, are multiparous, or present peripartum. Cocaine use may precipitate rupture. REFERENCES 1. Trastek VF, Pairolero PC, Joyce JW, et al: Splenic artery aneurysms. Surgery 1982;91:894-899 2. Scheps SG, Spittell JA Jr, Fairbairn JF II, et al: Aneurysms of the splenic artery with special reference to bland aneurysms. Prof Staff Meet Mayo Clinic 1958;33:381-390 3. Stanley JC, Fry WJ: Pathogenesis and clinical significance of splenic artery aneurysms. Surgery 1974;76:898-909 4. Bedford PD, Lodge 6: Aneurysms of the splenic artery. Gut 1960;1:312-320
76
AMERICAN
JOURNAL
5. Trastek VF, Pairolero PC, Beratz PE: Splenic artery aneurysms. World J Surg 1985;9:376-383 6. Spittel JA: Aneurysms of the splenic artery. JAMA 1961 ;175:452-456 7. Greene DR, Gorey TF, Tanner WA, et al: The diagnosis and management of splenic artery aneurysms. J R Sot Med 1988; 81:387-388 8. Martinez E, Menendez AR, Ablanedo P: Splenic artery aneurysms. Int Surg 1986;71:95-99 9. Sabiston DC: Visceral artery aneurysms, in Sabiston DC (ed): Textbook of Surgery (ed 13). Philadelphia, PA, Saunders, 1986, pp 1826-1828 10. Lowry SM, O’Dea TP, Gallagher DI, et al: Splenic artery aneurysm rupture: The seventh instance of maternal and fetal survival. Obstet Gynecol 1986;67:291-292 11. Sheldon GF, Croom RD, Meyer AA: The spleen. In Sabiston DC (ed): Textbook of Surgery (ed 13). Philadelphia, PA, Saunders, 1986, pp 1228-1230 12. Adams JT: Aneurysms of the splanchnic arteries. In
OF EMERGENCY
MEDICINE
n Volume 9, Number
1 n January
1991
Schwartz SI, Shires GT, Spencer FC (eds): Principles of Surgery, (ed 5). New York, NY, McGraw Hill, 1989, pp 1511-1512 13. Williams JJ: Splenic artery aneurysm rupture: An uncommon obstetrical catastrophe. J Fam Practice i988;26:73-75 14. Derchi LE. Biaai E. Cicio GR. et al: Aneurvsms of the splenic artery: nonin&ive diagnosis’by pulsed Doppler sonography. J Ultrasound Med 1984;3:41-44 15. Ueda J, Kobayashi Y, Hara K, et al: Giant aneurysm of the splenic artery and huge varix. Gastrointest Radio1 1985;10:55-57 16. Jeffrey RB Jr: CT and Sonography of the Acute Abdomen. New York, NY, Raven Press, 1989, pp 102-104 17. Ritchie JM, Greene NM: Local Anesthetics. In Gilman AG, Goodman LS, Rail TW, et al (eds): Goodman and Gillman’s The Pharmacological Basis of Therapeutics (ed 7). New York, NY, Macmillan, 1985, pp 309-310 18. Gadaleta D, Hall Ml-f, Nelson RL: Cocaine-induced acute aortic dissection. Chest 1989;96:1203-1205 19. Jacobs, IG, Roszler Ml-f, Kelly JK, et al: Cocaine abuse: Neurovascular complications. Radiology 1989;170:223-227
