CASE REPORT aortic occlusion; trauma, blunt
Aortoiliac Occlusion Secondary to Atherosclerotic Plaque Rupture as the Result of Blunt Trauma Abdominal aortic injuries secondary to blunt trauma are uncommon, particularly without associated visceral injury or external signs of localized trauma. Blunt trauma-induced abdominal aortic injuries most frequently result in intimal tearing. The most common mechanism is localized impact over the lower abdomen from sudden deceleration against a fixed object. We present the case of a patient with atheromatous plaque rupture in the distal abdominal aorta associated with acute aortoiliac occlusion as the result of a fall. Atherosclerotic disease m a y be present in young asymptomatic individuals and may be a predisposing factor for aortic intireal tearing. A high degree of suspicion and periodic reassessment of peripheral circulation in trauma patients are required to ensure early diagnosis of this injury. {Beless D J, Muller DS, Perez H: Aortoiliac occlusion secondary to atherosclerotic plaque rupture as the result of blunt trauma. Ann Emerg Med August 1990;19:922-924.]
INTRODUCTION Blunt abdominal aortic injuries are relatively rare, especially w h e n there is l i m i t e d injury to other a b d o m i n a l organs. A review of the literature reveals a u t o m o b i l e accidents as the m o s t c o m m o n cause of these injuries. The m o s t c o m m o n m e c h a n i s m of injury is rapid deceleration w i t h i m p a c t against the steering w h e e l or seat belt. In the m a j o r i t y of cases, m u l t i p l e abdominal organs are also injured. We report the case of a y o u n g m a n w h o fell and presented w i t h signs of acute i s c h e m i a of his leg w i t h o u t evidence of other i n t r a - a b d o m i n a l injury.
Daniel J Beless, MD, FACEP' Donna Sue Muller, MD, MPH Henry Perez, MD Attanta, Georgia From the Division of Emergency Medicine, Emory University School of Medicine, Atlanta, Georgia. Received for publication July 10, 1989. Revision received November 6, 1989. Accepted for publication November 20, 1989 Address for reprints: Daniel J Beless, MD, FACER Emergency Department, Crawford Long Hospital of Emery University, 550 Peachtree Street NE, Atlanta, Georgia 30365.
CASE REPORT A 34-year-old male construction w o r k e r fell from a b e a m 15 ft high and landed on his a n t e r i o r chest and a b d o m e n . H e suffered no loss of consciolisness and was i m m o b i l i z e d and transported to the emergency departm e n t by ambulance. On arrival, he was alert, oriented, and c o m p l a i n e d of anterior chest pain, left upper a b d o m i n a l pain, and n u m b n e s s in his left foot. Vital signs were blood pressure of 131/103 m m Hg; pulse, 72; respirations, 20; and temperature, 37.5 C. His medical h i s t o r y was significant only for s m o k i n g two packs of cigarettes per day for 22 years. Initial physical e x a m i n a t i o n revealed a m a n w h o was fully i m m o b i l i z e d on a long board. The p a t i e n t was s p o n t a n e o u s l y m o v i n g all e x t r e m i t i e s and denied n e c k tenderness. His pupils were equal and reactive, and his head was atraumatic. Bilateral breath sounds were clear. Abrasions were apparent on his right anterior chest wall and left upper abdomen. T h e abdomen was soft and nondistended, w i t h n o r m a l bowel sounds and m i l d left upperquadrant tenderness. His pelvis was stable and rectal e x a m i n a t i o n was guaiac-negative. The back was nontender, and the femoral and dorsalis pedis pulses were easily palpable bilaterally. E x t r e m i t y strength was normal, and sensation was intact to touch but subjectively d i m i n i s h e d in the left foot. Initial laboratory results included a h e m a t o c r i t of 42%, w i t h a WBC of 22,500/mm 3. The a m y l a s e was 102 somogyi units, and serum cholesterol was !85 mg/100 mL. S e r u m e l e c t r o l y t e s were n o r m a l , as was the urinalysis. Arterial blood gases on r o o m air were Pao z of 61; Pacoz, 25; and pH, 7.54. A n ECG showed a sinus r h y t h m of 90 w i t h small Q waves inferiorly b u t no acute ST-T wave changes. A portable chest radiograph showed
19:8 August 1990
Annals of Emergency Medicine
922/115
AORTOILIAC OCCLUSION Beless, Muller & Perez
FIGURE. Aortogram demonstrating
lumenal narrowing at the aortic bifurcation with diminished iliac flow. a right upper-lobe contusion but was otherwise normal. A portable crosstable lateral cervical-spine film was also normal. During the ED evaluation, the patient's vital signs remained stable; however, he complained of increasing pain in both lower extremities. A repeat examination of the extremities p e r f o r m e d a p p r o x i m a t e l y 15 minutes after the initial examination revealed diminished capillary refill and absent distant pulses bilaterally and a cool, pale left foot. Femoral pulses were also diminished as compared with the initial examination. Emergency general surgery and vascular surgery consultations were obtained. An emergency aortogram was performed through the brachial artery. The thoracic and upper abdominal aorta were normal, as were the renal arteries. Just above the bifurcation of the aorta, there was a lumenal irregularity and thrombus formation (Figure). The assessment was made of presumed traumatic dissection with thrombotic obstruction to the iliac arteries. The patient was taken directly to surgery. Surgical findings showed no rctroperitoneal hematoma or injuries to the abdominal organs. There was di = minished pulsation of both iliac vessels but no external sign of dissection or contusion of the aorta. When the vessels were opened, no intimal tears were n o t e d , but t h e r e was pronounced atherosclerotic plaque formation in the distal aorta and iliac vessels. A disrupted calcified plaque with fresh clot formation was found to significantly reduce the diameter of the bifurcation. A Dacron graft was placed, and bilateral femoral t h r o m b e c t o m i c s wcre performed, w h i c h restored distal pulses. The pathologic e x a m i n a t i o n of the resected segment demonstrated atheromatous plaque disruption resulting in a 60% reduction in the aortic lumen and adjacent clot formation. During the patient's hospital stay, serial ECGs were obtained that revealed Q waves inferiorly, but these remained unchanged from the initial ED recording. Creatinine phosphokinase i n i t i a l l y was 2,930 sigma 116/923
units/mL with MB 6%; later determinations had an MB index of less than 1. The transient elevation in creatinine phosphokinase and lack of change in serial ECGs suggested that the patient had not suffered an acute myocardial infarction; the elevation was attributed to muscle trauma and lower limb ischemia. Later in the hospitalization course, the patient began experiencing episodic chest pains. A cardiac catheterization was performed because of his k n o w n p e r i p h e r a l v a s c u l a r atherosclerosis and abnormal ECG. Angiography demonstrated a 100% occlusion of the right coronary artery, a 45% narrowing of the left anterior descending coronary artery, 100% occlusion of the first marginal branch, inferior apical hypokinesis, and an ejection fraction of 65%. Although the age of the inferior wall injury was indeterminate, it was presumed that the patient had suffered a previously unrecognized infarction unrelated to the fall. The patient was readmitted two months later and underwent sucAnnals of Emergency Medicine
cessful coronary artery bypass. DISCUSSION Blunt abdominal aortic injury occurs infrequently. This is probably due to the protected retroperitoneal position of this vessel. In two studies of large population samples, the abdominal aortic segment was involved in only 4.6% of all nonpenetrating aortic injuries in trauma fatalities.~,2 A review of the literature by Lass o n d e and L a u r e n d e a u in 1981 showed that 70% of these injuries were the result of automobile accidents, with acute arterial insufficiency being the most common presentation. 3 Late clinical presentat i o n s of b l u n t a b d o m i n a l a o r t i c injury include persistent abdominal pain or ciaudication occurring from weeks to months after the initial injury. 4 Our patient, a l t h o u g h only 34 y e a r s old, had s i g n i f i c a n t atherosclerotic lesions in his distal abdominal aorta and iliac vessels. Blunt t r a u m a in individuals with aortic 19:8 August 1990
a t h e r o m a can r e s u l t i n s u b i n t i m a l d i s s e c t i o n a n d e m b o l i z a t i o n of p l a q u e s or t h r o m b u s f o r m a t i o n . 5 Lassonde and Laurendeau found atherosclerosis to be a predisposing factor in b l u n t abdominal aortic inj u r y , w i t h i n t i m a l d i s r u p t i o n acc o u n t i n g for most of the pathologic lesions. 3 Atherosclerotic changes m a y be associated w i t h a weakening of t h e i n t i m a , a n d cases of n o n t r a u m a t i c distal dissections appeari n g to arise from an a t h e r o m a t o u s p l a q u e p e r f o r a t i o n h a v e b e e n reported. 6 It would be reasonable to ass u m e then that this w e a k e n i n g of the i n t i m a ] l a y e r by a t h e r o s c l e r o s i s would m a k e this site more susceptible to injury through trauma or sudden increases i n intra-aortic pressure. The m e c h a n i s m of injury resulting in i n t i m a l disruption, dissection, and thrombosis is unclear. Thal et al postulated sudden increases i n intra-aort i c p r e s s u r e as a p o s s i b l e factor. 7 T h e y also proposed t h a t rapid deceleration, w i t h the aorta mobile bet w e e n two relatively fixed points (the d i a p h r a g m and iliac arteries), produces shearing forces that could rupture the vessel. 7 This view was shared by Matelo et al, who added that atherosclerosis also contributes by causing the abdominal aorta to become semirigid and more susceptible to rupture and dissection. 8 A n o t h e r theory, p r o m u l g a t e d by Dajee et al, postulated that longitudin a l stress on the i n t i m a of the abd o m i n a l aorta caused by the "shock w a v e s m o v i n g along the aorta" resuited i n dissection. 9 Lassonde and L a u r e n d e a u d i s c o u n t e d the s h o c k wave theory and suggested that injury to the abdominal aorta usually involves a more direct force one t h a t c r u s h e s the aorta a g a i n s t the l u m b a r spine. 3 They believed that indirect forces such as the differing rate of deceleration between the aorta and its b r a n c h e s played o n l y a " m i n o r role" in a b d o m i n a l aortic injuries. 3 Finally, citing a case involving a seatbelt i n j u r y to a 36-year-old w o m a n with atheromatous plaques, Warrian et al supported the opinion that a di-
19:8 August 1990
rect insult crushes the intimal p l a q u e s and r e s u l t s in t e a r i n g and dissection. Lo In each of the previously reported cases, i m p a c t was against the relatively small surface area of a seat belt or steering wheel. In all cases, the patient had external signs of injury on the lower a b d o m i n a l walt. Our pat i e n t showed no signs of lower abd o m i n a l i n j u r y yet s u s t a i n e d distal aortic plaque r u p t u r e and t h r o m b u s formation. The i n j u r i n g forces were also d i s t r i b u t e d over the larger surface area of the anterior trunk, as evidenced by the patient's chest and abdominal wall abrasions. We postulate that direct crush was n o t responsible for this injury as the forces of direct i m p a c t should have been dissipated over the entire aorta and not concentrated at one point. It is probable that the atheromatous plaque was initially injured secondary to the b e n d i n g stress of deceleration as p o s t u l a t e d by Tha] et al. 7 I n a d d i t i o n , i n c r e a s e d i n t r a thoracic pressure generated during the deceleration may have been t r a n s m i t t e d down the blood c o l u m n in the aorta. The hydraulic r a m effect caused by this m a y have contributed to the final plaque rupture, as suggested by Dajee et al. 9 T h r o m b u s form a t i o n , l u m e n a l occlusion, and leg ischemia then occurred. Lack of sign i f i c a n t i n i t i a l pulse deficit i n the p a t i e n t i n d i c a t e d that the aortic t h r o m b u s c o n t i n u e d to p r o p a g a t e w h i l e the p a t i e n t was being evaluated. Although an emergency physician certainly would not overlook absent or s i g n i f i c a n t l y d i m i n i s h e d pulses, this case demonstrates the need for c o n t i n u e d assessment of the peripheral vascular status. It may have been easy to assign the patient's n u m b n e s s and pain to spinal nerve root injury or compression had repeat examinations of the circulation not been performed. Our patient underwent p r o m p t aortography and surgery. M a n y medical centers currently use c o m p u t e d t o m o g r a p h y to e v a l u a t e stable patients with possible abdomi-
Annals of Emergency Medicine
nal aortic injury. Computed tomography, while shown to accurately diagn o s e 9 0 % of a o r t i c d i s s e c t i o n s , would n o t have revealed the plaque rupture in this patient. In addition, it cannot provide additional information c o n c e r n i n g the peripheral vasculature status.
SUMMARY The case of a p a t i e n t w i t h b l u n t abdominal aortic injury is presented. The patient's acute lower leg ischem i a was s u c c e s s f u l l y r e v e r s e d b y p r o m p t s u r g i c a l r e p a i r of an aortoiliac obstruction resulting from atherosclerotic plaque disruption. Persons presenting w i t h deceleration injuries are at a small but real risk of a b d o m i n a l aortic injuries. Periodic reassessment of the peripheral circulation should be routine in the evalu a t i o n of the trauma patient. Lowerleg i s c h e m i a w i t h o u t a p p a r e n t injuries below the costal margin in p a t i e n t s who e x p e r i e n c e rapid deceleration should mandate prompt exclusion of aortic injury.
REFERENCES
1. Parmley LF, Mattingly TW, Manion WC, et al: Nonpenctrating traumatic injury of the aorta. Circulation 1958;17:1086q101. 2. 8trassmann G: Traumatic rupture of the aorta. Am He¢lrt ] 1947;33:508 515. 3. Lassonde J, LaurendeauF: Blunt injury of the abdominal aorta. Ann Surg 1981;194:745-748. 4. Campbell D, Austin RF: Seatbelt injury: In jury of the abdominal aorta. Radiology 1969; 92:123-124. 5. Hertzer NR: Peripheral atheromatous cmbolization followingblunt abdominaltrauma. Surgery 1977;82:244-247. 6. DeSanctis RW, Doroghazi RM, Austen WG, et al: Aortic dissection. N Engl J M e d 1987; 317:1060-1066. 7. Thai ER, Perry MO, Crighton I: Traumatic abdominal aortic occlusion. South Med l 1971; 64:653 655. 8. Matolo NM, Danto LA, WolfmanEF Jr: Traumatic aneurysm of tile abdominal aorta. Arch SuzX 1974;108:867-869. 9. Dajee H; Richardson iW, lype MO: Seatbelt aorta: Acute dissection and thrombosis of the abdominal aorta. Surgery 1979;85:263-267. 10. Warrian RK, Shoenut JP, Iannicello CM, et ah Seatbelt injury to the abdominal aorta. ] Trmtmn 1988;28:1505-1507.
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Aortoiliac Occlusion Secondary to Atherosclerotic Plaque Rupture as the Result of Blunt Trauma Abdominal aortic injuries secondary to blunt trauma are uncommon, particularly without associated visceral injury or external signs of localized trauma. Blunt trauma-induced abdominal aortic injuries most frequently result in intimal tearing. The most common mechanism is localized impact over the lower abdomen from sudden deceleration against a fixed object. We present the case of a patient with atheromatous plaque rupture in the distal abdominal aorta associated with acute aortoiliac occlusion as the result of a fall. Atherosclerotic disease m a y be present in young asymptomatic individuals and may be a predisposing factor for aortic intireal tearing. A high degree of suspicion and periodic reassessment of peripheral circulation in trauma patients are required to ensure early diagnosis of this injury. {Beless D J, Muller DS, Perez H: Aortoiliac occlusion secondary to atherosclerotic plaque rupture as the result of blunt trauma. Ann Emerg Med August 1990;19:922-924.]
INTRODUCTION Blunt abdominal aortic injuries are relatively rare, especially w h e n there is l i m i t e d injury to other a b d o m i n a l organs. A review of the literature reveals a u t o m o b i l e accidents as the m o s t c o m m o n cause of these injuries. The m o s t c o m m o n m e c h a n i s m of injury is rapid deceleration w i t h i m p a c t against the steering w h e e l or seat belt. In the m a j o r i t y of cases, m u l t i p l e abdominal organs are also injured. We report the case of a y o u n g m a n w h o fell and presented w i t h signs of acute i s c h e m i a of his leg w i t h o u t evidence of other i n t r a - a b d o m i n a l injury.
Daniel J Beless, MD, FACEP' Donna Sue Muller, MD, MPH Henry Perez, MD Attanta, Georgia From the Division of Emergency Medicine, Emory University School of Medicine, Atlanta, Georgia. Received for publication July 10, 1989. Revision received November 6, 1989. Accepted for publication November 20, 1989 Address for reprints: Daniel J Beless, MD, FACER Emergency Department, Crawford Long Hospital of Emery University, 550 Peachtree Street NE, Atlanta, Georgia 30365.
CASE REPORT A 34-year-old male construction w o r k e r fell from a b e a m 15 ft high and landed on his a n t e r i o r chest and a b d o m e n . H e suffered no loss of consciolisness and was i m m o b i l i z e d and transported to the emergency departm e n t by ambulance. On arrival, he was alert, oriented, and c o m p l a i n e d of anterior chest pain, left upper a b d o m i n a l pain, and n u m b n e s s in his left foot. Vital signs were blood pressure of 131/103 m m Hg; pulse, 72; respirations, 20; and temperature, 37.5 C. His medical h i s t o r y was significant only for s m o k i n g two packs of cigarettes per day for 22 years. Initial physical e x a m i n a t i o n revealed a m a n w h o was fully i m m o b i l i z e d on a long board. The p a t i e n t was s p o n t a n e o u s l y m o v i n g all e x t r e m i t i e s and denied n e c k tenderness. His pupils were equal and reactive, and his head was atraumatic. Bilateral breath sounds were clear. Abrasions were apparent on his right anterior chest wall and left upper abdomen. T h e abdomen was soft and nondistended, w i t h n o r m a l bowel sounds and m i l d left upperquadrant tenderness. His pelvis was stable and rectal e x a m i n a t i o n was guaiac-negative. The back was nontender, and the femoral and dorsalis pedis pulses were easily palpable bilaterally. E x t r e m i t y strength was normal, and sensation was intact to touch but subjectively d i m i n i s h e d in the left foot. Initial laboratory results included a h e m a t o c r i t of 42%, w i t h a WBC of 22,500/mm 3. The a m y l a s e was 102 somogyi units, and serum cholesterol was !85 mg/100 mL. S e r u m e l e c t r o l y t e s were n o r m a l , as was the urinalysis. Arterial blood gases on r o o m air were Pao z of 61; Pacoz, 25; and pH, 7.54. A n ECG showed a sinus r h y t h m of 90 w i t h small Q waves inferiorly b u t no acute ST-T wave changes. A portable chest radiograph showed
19:8 August 1990
Annals of Emergency Medicine
922/115
AORTOILIAC OCCLUSION Beless, Muller & Perez
FIGURE. Aortogram demonstrating
lumenal narrowing at the aortic bifurcation with diminished iliac flow. a right upper-lobe contusion but was otherwise normal. A portable crosstable lateral cervical-spine film was also normal. During the ED evaluation, the patient's vital signs remained stable; however, he complained of increasing pain in both lower extremities. A repeat examination of the extremities p e r f o r m e d a p p r o x i m a t e l y 15 minutes after the initial examination revealed diminished capillary refill and absent distant pulses bilaterally and a cool, pale left foot. Femoral pulses were also diminished as compared with the initial examination. Emergency general surgery and vascular surgery consultations were obtained. An emergency aortogram was performed through the brachial artery. The thoracic and upper abdominal aorta were normal, as were the renal arteries. Just above the bifurcation of the aorta, there was a lumenal irregularity and thrombus formation (Figure). The assessment was made of presumed traumatic dissection with thrombotic obstruction to the iliac arteries. The patient was taken directly to surgery. Surgical findings showed no rctroperitoneal hematoma or injuries to the abdominal organs. There was di = minished pulsation of both iliac vessels but no external sign of dissection or contusion of the aorta. When the vessels were opened, no intimal tears were n o t e d , but t h e r e was pronounced atherosclerotic plaque formation in the distal aorta and iliac vessels. A disrupted calcified plaque with fresh clot formation was found to significantly reduce the diameter of the bifurcation. A Dacron graft was placed, and bilateral femoral t h r o m b e c t o m i c s wcre performed, w h i c h restored distal pulses. The pathologic e x a m i n a t i o n of the resected segment demonstrated atheromatous plaque disruption resulting in a 60% reduction in the aortic lumen and adjacent clot formation. During the patient's hospital stay, serial ECGs were obtained that revealed Q waves inferiorly, but these remained unchanged from the initial ED recording. Creatinine phosphokinase i n i t i a l l y was 2,930 sigma 116/923
units/mL with MB 6%; later determinations had an MB index of less than 1. The transient elevation in creatinine phosphokinase and lack of change in serial ECGs suggested that the patient had not suffered an acute myocardial infarction; the elevation was attributed to muscle trauma and lower limb ischemia. Later in the hospitalization course, the patient began experiencing episodic chest pains. A cardiac catheterization was performed because of his k n o w n p e r i p h e r a l v a s c u l a r atherosclerosis and abnormal ECG. Angiography demonstrated a 100% occlusion of the right coronary artery, a 45% narrowing of the left anterior descending coronary artery, 100% occlusion of the first marginal branch, inferior apical hypokinesis, and an ejection fraction of 65%. Although the age of the inferior wall injury was indeterminate, it was presumed that the patient had suffered a previously unrecognized infarction unrelated to the fall. The patient was readmitted two months later and underwent sucAnnals of Emergency Medicine
cessful coronary artery bypass. DISCUSSION Blunt abdominal aortic injury occurs infrequently. This is probably due to the protected retroperitoneal position of this vessel. In two studies of large population samples, the abdominal aortic segment was involved in only 4.6% of all nonpenetrating aortic injuries in trauma fatalities.~,2 A review of the literature by Lass o n d e and L a u r e n d e a u in 1981 showed that 70% of these injuries were the result of automobile accidents, with acute arterial insufficiency being the most common presentation. 3 Late clinical presentat i o n s of b l u n t a b d o m i n a l a o r t i c injury include persistent abdominal pain or ciaudication occurring from weeks to months after the initial injury. 4 Our patient, a l t h o u g h only 34 y e a r s old, had s i g n i f i c a n t atherosclerotic lesions in his distal abdominal aorta and iliac vessels. Blunt t r a u m a in individuals with aortic 19:8 August 1990
a t h e r o m a can r e s u l t i n s u b i n t i m a l d i s s e c t i o n a n d e m b o l i z a t i o n of p l a q u e s or t h r o m b u s f o r m a t i o n . 5 Lassonde and Laurendeau found atherosclerosis to be a predisposing factor in b l u n t abdominal aortic inj u r y , w i t h i n t i m a l d i s r u p t i o n acc o u n t i n g for most of the pathologic lesions. 3 Atherosclerotic changes m a y be associated w i t h a weakening of t h e i n t i m a , a n d cases of n o n t r a u m a t i c distal dissections appeari n g to arise from an a t h e r o m a t o u s p l a q u e p e r f o r a t i o n h a v e b e e n reported. 6 It would be reasonable to ass u m e then that this w e a k e n i n g of the i n t i m a ] l a y e r by a t h e r o s c l e r o s i s would m a k e this site more susceptible to injury through trauma or sudden increases i n intra-aortic pressure. The m e c h a n i s m of injury resulting in i n t i m a l disruption, dissection, and thrombosis is unclear. Thal et al postulated sudden increases i n intra-aort i c p r e s s u r e as a p o s s i b l e factor. 7 T h e y also proposed t h a t rapid deceleration, w i t h the aorta mobile bet w e e n two relatively fixed points (the d i a p h r a g m and iliac arteries), produces shearing forces that could rupture the vessel. 7 This view was shared by Matelo et al, who added that atherosclerosis also contributes by causing the abdominal aorta to become semirigid and more susceptible to rupture and dissection. 8 A n o t h e r theory, p r o m u l g a t e d by Dajee et al, postulated that longitudin a l stress on the i n t i m a of the abd o m i n a l aorta caused by the "shock w a v e s m o v i n g along the aorta" resuited i n dissection. 9 Lassonde and L a u r e n d e a u d i s c o u n t e d the s h o c k wave theory and suggested that injury to the abdominal aorta usually involves a more direct force one t h a t c r u s h e s the aorta a g a i n s t the l u m b a r spine. 3 They believed that indirect forces such as the differing rate of deceleration between the aorta and its b r a n c h e s played o n l y a " m i n o r role" in a b d o m i n a l aortic injuries. 3 Finally, citing a case involving a seatbelt i n j u r y to a 36-year-old w o m a n with atheromatous plaques, Warrian et al supported the opinion that a di-
19:8 August 1990
rect insult crushes the intimal p l a q u e s and r e s u l t s in t e a r i n g and dissection. Lo In each of the previously reported cases, i m p a c t was against the relatively small surface area of a seat belt or steering wheel. In all cases, the patient had external signs of injury on the lower a b d o m i n a l walt. Our pat i e n t showed no signs of lower abd o m i n a l i n j u r y yet s u s t a i n e d distal aortic plaque r u p t u r e and t h r o m b u s formation. The i n j u r i n g forces were also d i s t r i b u t e d over the larger surface area of the anterior trunk, as evidenced by the patient's chest and abdominal wall abrasions. We postulate that direct crush was n o t responsible for this injury as the forces of direct i m p a c t should have been dissipated over the entire aorta and not concentrated at one point. It is probable that the atheromatous plaque was initially injured secondary to the b e n d i n g stress of deceleration as p o s t u l a t e d by Tha] et al. 7 I n a d d i t i o n , i n c r e a s e d i n t r a thoracic pressure generated during the deceleration may have been t r a n s m i t t e d down the blood c o l u m n in the aorta. The hydraulic r a m effect caused by this m a y have contributed to the final plaque rupture, as suggested by Dajee et al. 9 T h r o m b u s form a t i o n , l u m e n a l occlusion, and leg ischemia then occurred. Lack of sign i f i c a n t i n i t i a l pulse deficit i n the p a t i e n t i n d i c a t e d that the aortic t h r o m b u s c o n t i n u e d to p r o p a g a t e w h i l e the p a t i e n t was being evaluated. Although an emergency physician certainly would not overlook absent or s i g n i f i c a n t l y d i m i n i s h e d pulses, this case demonstrates the need for c o n t i n u e d assessment of the peripheral vascular status. It may have been easy to assign the patient's n u m b n e s s and pain to spinal nerve root injury or compression had repeat examinations of the circulation not been performed. Our patient underwent p r o m p t aortography and surgery. M a n y medical centers currently use c o m p u t e d t o m o g r a p h y to e v a l u a t e stable patients with possible abdomi-
Annals of Emergency Medicine
nal aortic injury. Computed tomography, while shown to accurately diagn o s e 9 0 % of a o r t i c d i s s e c t i o n s , would n o t have revealed the plaque rupture in this patient. In addition, it cannot provide additional information c o n c e r n i n g the peripheral vasculature status.
SUMMARY The case of a p a t i e n t w i t h b l u n t abdominal aortic injury is presented. The patient's acute lower leg ischem i a was s u c c e s s f u l l y r e v e r s e d b y p r o m p t s u r g i c a l r e p a i r of an aortoiliac obstruction resulting from atherosclerotic plaque disruption. Persons presenting w i t h deceleration injuries are at a small but real risk of a b d o m i n a l aortic injuries. Periodic reassessment of the peripheral circulation should be routine in the evalu a t i o n of the trauma patient. Lowerleg i s c h e m i a w i t h o u t a p p a r e n t injuries below the costal margin in p a t i e n t s who e x p e r i e n c e rapid deceleration should mandate prompt exclusion of aortic injury.
REFERENCES
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