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Acute abdominal aortic occlusion
TheJournalof
Emergency
Medicme,
Vol IO, pp 139-145,
PrInted an the USA
1992
ACUTE ABDOMINAL Steven Frost, Reprint
Address:
Division of Emergency Steven Frost, MD, Division
MD,
Copyrtght
F 1992 Pwgamon
Press Ltd
AORTIC OCCLUSION
and Robert C. Jorden,
Medicine, University of Mississippi of Emergency Medicine, University
0 Abstract-Acute occlusion of the infrarenal abdominal aorta is a catastrophic event requiring early recognition and intervention if permanent disability is to be decreased or avoided. While traditional causes of occlusion (saddle embolus and thrombosis) are the most frequent, vasculitis and hypercoagulable states have recently been suggested as etiologies. This article presents three casesof acute abdominal aortic occlusion from different mechanisms and reviews the literature concerning presentation and management.
MD,
FACEP
Medical Center, Jackson, Mississlppl of Mississippi Medical Center, Jackson.
MS 39216-4505
CASE REPORTS Case 1 A 36-year-old woman was transported
from an outside hospital after presenting with complaints of increasing difficulty breathing and acute onset of paraplegia. Treatment, at the referring hospital, was directed at the evident pulmonary edema and hypoxemia and included nasotracheal intubation and administration of intravenous furosemide. The patient’s vital signs were as follows: pulse, 126 beats/min; blood pressure, 106/80 torr; and respiratory rate, 36 breaths/min. Physical examination revealed an alert, cooperative patient with bilateral rales on auscultation of the chest and cold, rigid, pulseless lower extremities with complete loss of sensation and motor function. A chest x-ray study revealed moderate enlargement of the cardiac silhouette and pulmonary edema. The electrocardiogram showed a normal sinus rhythm with poor R wave progression in the anterior leads and right atrial enlargement. Laboratory results included hematocrit, 47.5%; WBC, 14,630/mm3; prothrombin time, 12.6 set; and partial thromboplastin time, 27.1 sec. Electrolytes, BUN, and creatinine were normal. After high-dose heparin was initiated, the patient was taken to the operating room where bilateral femoral embolectomies using Fogarty catheters were performed. Total time of ischemia had been approximately 15 hours. At this point, the patient sustained a cardiac arrest requiring multiple defibrillation attempts. A suspicion of reperfusion hyperkalemia was confirmed when a potassium of 7.3 mEq/L was re-
q Keywords-acute abdominal aortic occlusion; saddle embolus; aortic thrombosis; blunt abdominal trauma; abdominal aortic aneurysm
INTRODUCTION
Acute infrarenal abdominal aortic occlusion is an infrequent but catastrophic event. Because it causes neurologic dysfunction, these symptoms often predominate and cause the aortic lesions to be overlooked. Frequently traumatic spinal cord injury or prolapsed intervertebral disk are inappropriately diagnosed. Proper management depends on prompt recognition if permanent disability is to be decreased or avoided. Most often, the appropriate diagnosis is suggested by taking a thorough history and conducting a proper examination for distal pulses and neurologic deficits. During a 2-month period, 3 cases of acute abdominal aortic occlusion presented to our emergency department. Each case was caused by a different mechanism. This prompted a review of the literature to determine the pathophysiology and proper management of this disorder.
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ported. The wounds were reopened and the femoral vessels cross-clamped. Sinus rhythm was returned and after stabilization the patient was taken to the intensive care unit. The patient had a complicated hospital course requiring bilateral above the knee amputations, multiple debridements, and bilateral hemipelvectomy secondary to ascending gangrene. This was followed by excision of the sacrum. Her hospital course was also complicated by myoglobinuria and sepsis. She expired in septic shock after a prolonged hospitalization. Pathologic examination was consistent with extensive thromboemboli involving the aortic bifurcation, as well as the femoral and popliteal arteries.
Case 2 A 54-year-old man was transferred from an outside hospital for evaluation of a possible prolapsed intervertebral disk. After a recent drinking binge, the patient reported an episode of repeated vomiting followed by a sudden onset of pain in the lower back and legs followed by loss of sensation and motor function. The patient’s vital signs were as follows: pulse, 116 beats/min; blood pressure, 190/100 torr; and respiratory rate, 20 beats/min. The physical examination was significant for coolness and cyanosis extending distally from the inguinal ligaments. In addition, both lower extremities were pulseless, and there was a T12 complete sensory and motor deficit. Chest x-ray study and electrocardiogram were normal; abdominal aortogram revealed complete obstruction of the aorta just below the level of the renal arteries. Laboratory results included hematocrit, 49.3%; WBC, 13,960/mm3; glucose, 199 mg/dL; and ETOH, zero. Electrolytes, BUN, and creatinine were normal. The patient was taken to the operating room with a diagnosis of probable acute thrombotic aortic occlusion and high-dose heparin was initiated. Removal of thrombus from the aortoiliac femoral profunda and superficial femoral systems was accomplished with Fogarty catheters via bilateral femoral arteriotomies. The hospital course was complicated by bilateral compartment syndromes requiring fasciotomies, eventual bilateral above the knee amputations, myoglobinuria, right gluteal abscess requiring surgical drainage, and stump infections. Pathology reported organizing thrombus with underlying atherosclerosis of the femoral arteries. He regained only limited motor function in the stumps and was transferred to
Steven Frost and Robert C. Jorden
another hospital closer to his home for rehabilitation.
Case 3 A 54-year-old man fell asleep while driving and struck a tree head-on. He awoke with the steering wheel wedged into his lap. After pulling himself from the car, he stood up but then fell to the ground due to lower extremity weakness, He was seen initially at a local hospital and then transferred to our facility. On arrival, vital signs were as follows: pulse, 96 beats/min; blood pressure, 136/ 80 torr; and respiratory rate, 20/min. Heart and lung examinations were unremarkable. The abdomen was soft and nontender. Neurologic examination revealed a complete loss of motor function in the left leg and a sensory deficit to pin prick at the L2 level on the left. Some crude touch remained below this level. There were no deficits on the right side. There was no sphincter tone on rectal examination. Femoral pulses were detected by Doppler examination, but distal pulses were absent bilaterally. A chest x-ray study revealed fractures of the left 4th through 7th ribs laterally but no pneumothorax; radiographs of the neck, pelvis, and lumbrosacral spine were normal. An arteriogram revealed occlusion of the abdominal aorta just below the level of the superior mesenteric artery. An electrocardiogram was within normal limits. Laboratory results included hematocrit, 36.1%; WBC, I 1,560/mm3; prothrombin time, 11.6 set; partial thromboplastin time, 26.1 set; and ETOH, 38 mg/dL. Electrolytes, BUN, and creatinine were normal. The patient was taken to the operating room and high-dose heparin was started. On exploratory celiotomy there was an obvious severe contusion of the abdominal aorta with adventitial hematoma that began 3 to 4 cm below the renal arteries and extended beyond the bifurcation into both iliac arteries. Full thickness injury of the anterior and posterior aortic walls was apparent; extensive thrombus occluded the lumen. Both iliac arteries were also noted to be severely diseased with atheromatous thickening. A dacron bifurcation graft was placed. Total time of ischemia had been approximately 12 hours. The patient had return of distal pulses and neurologic function postoperatively. Except for myoglobinuria and bilateral compartment syndromes requiring fasciotomies, the patient had an unremarkable hospital course and was discharged with no limitation of activity.
Acute Abdominal Aortic Occlusion
141
DISCUSSION
is provided by two longitudinal systems: the paired posterolateral longitudinal arterial trunks and the single anterior median longitudinal arterial trunk (8,9). The posterior system is supplied by numerous medullary feeder arteries and is seldom compromised
Presentation and Pathophysiology Acute aortic occlusion occurs as a sudden event without previous history of claudication. Symptoms are variable depending on completeness of obstruction, but the most common symptoms are pain, pallor, pulselessness, paresthesia, and paralysis (1). If preexisting aortoiliac atherosclerotic disease is present, the degree and severity of symptoms may be lessened due to development of collateral circulation. In the absence of collateral circulation, the patient experiences sudden onset of severe low back, buttocks, and lower extremity pain. This is accompanied by a flaccid paralysis of the lower extremities if spinal cord infarction occurs, or by the gradual onset of lower extremity weakness if ischemia of peripheral nerves or the cauda equina occurs. The skin is cool and pale distal to the occlusion. This may occur at the umbilicus or at the level of the iliac crests. Waxy, white skin indicates viable arterioles supplying blood to the skin (2). When nonblanching, blotchy cyanosis occurs, it indicates thrombosed capillaries and skin necrosis (2). Skin may withstand severe ischemia for as long as 24 hours; however, muscle sustains permanent damage after 8 to 12 hours (1,2). As cellular edema increases, the ischemic muscle takes on a doughy, firm consistency indicating early necrosis (1,2). The presence of rigidity is a reliable sign of nonviability (l-4). In almost all cases of acute aortic occlusion the neurological deficits appear to be caused by ischemia of the cauda equina or peripheral nerves; thus, recovery is likely with timely intervention. However, spinal cord infarction, while rare, may occur and is nearly always irreversible. Peripheral nerves may withstand ischemia for 12 to 24 hours with complete return of function (5). Sensory deficits begin with severe burning pain and paresthesias, followed by complete loss of all sensory modalities, while motor deficits begin distally and progress proximally; both can be delayed in onset (6). Spinal cord infarction with paralysis occurs suddenly, and since the spinal cord is extremely sensitive to ischemia, irreversible damage occurs in 18 to 60 minutes (7). Knowledge of the normal vascular supply of the spinal cord in the thoracolumbar region is necessary to understand the neurologic manifestations and implications for recovery in patients with acute abdominal aortic occlusion. The superior portion of the spinal cord is afforded an ample blood supply. Whether spinal cord infarction occurs depends on the highly variable vascular supply to the distal spinal cord that
W).
The anterior system supplies most of the ventral two-thirds of the spinal cord that includes the pyramidal tracts; thus, with occlusion of this system, a flaccid paralysis occurs with initially absent deep tendon reflexes that become hyperactive over time. Bowel and bladder incontinence are also characteristic (10). Loss of pain and temperature is part of the clinical picture, but proprioception and vibratory sensation are preserved since the dorsal columns are supplied by the posterior system. The supply to the anterior system is variable and has only a few medullary feeders. The anatomy has been meticulously described by Dommisse in a series of cadaveric dissections supplemented by microangiograms (11). He found great variability in the size of the anterior trunk and the number of medullary feeders. A large medullary feeder in this region, referred to as the artery of Adamkiewicz, may be the only supplier to the anterior system. Dommisse (11) found it occurring on the left in 77% of cadavers and originating anywhere from T7 to L4; an origin as low as LS has also been reported (12). Dommisse also found as many as three large vessels in a single cadaver. The infrequency of spinal infarction may be explained by two factors: 1. The artery of Adamkiewicz most often arises above the Ll vertebral level and is thus above the site of most occlusion (11,13). 2. Even when arising below L 1, collateral circulation is usually adequate or other medullary feeders arise more proximally and supply the cord (11). Etiologies of Acute Aortic Occlusion There are several causes of acute occlusion of the abdominal aorta, including saddle embolism, acute thrombosis with or without preexisting aortoiliac atherosclerotic disease, thrombosis of an abdominal aortic aneurysm, aortic dissection, and posttraumatic abdominal aortic occlusion. Acute thrombosis resulting from a hypercoagulable state or vasculitis has also been implicated. Occlusion by Saddle Embolus An embolus occluding the aortic bifurcation (saddle embolus) is the most frequent cause of acute abdomi-
142
nal aortic occlusion. However, it only accounts for about 10% of all emboli to the extremities (4,14). Rheumatic heart disease, formerly the most common source of emboli, has been supplanted in that role by atherosclerotic coronary artery disease. Despite the low incidence of embolism following myocardial infarction (less than lCro), the frequency of coronary artery disease makes this a common cause (15). In a review of postmortem studies, Arvan (16) reported the incidence of postinfarction mural thrombus to range 17% to 66%. The median interval from onset of infarction to embolism is 10 days, while two-thirds of emboli occur less than 3 weeks postinfarction (15,17). Atria1 fibrillation has been reported in 40% to 100% of patients with abdominal aortic saddle embolus (4,15,17,18). Besides myocardial infarction, other common sources of saddle embolus include prosthetic valves and dilated cardiomyopathy. At postmortem examination, left mural thrombus has been found in up to 60% of cases of dilated cardiomyopathy and in 50% of cases of left ventricular aneurysm (19). When echocardiography is performed, large mural thrombi (larger than 2 cm) are more commonly seen in dilated cardiomyopathy than in coronary artery disease complicated by segmental wall abnormalities or left ventricular aneurysm (19,20). Because an embolus is the most common cause of acute abdominal aortic occlusion, it is presumed whenever a predisposing factor such as a recent myocardial infarction, cardiomyopathy, or atria1 fibrillation exists (4,14).
Occlusion by Acute Thrombosis Acute thrombosis should not be confused with the Leriche syndrome. This is a slowly progressing disease due to atherosclerotic lesions of the aortic wall that reduces the diameter of the lumen until it reaches a critical stenosis of 80% of the cross-sectional area (21). In the absence of this critical stenosis, acute thrombosis produces sudden and severe effects (22). Thrombosis usually occurs in the setting of preexisting atherosclerotic disease, as in case 2. However, the possibility of a hypercoagulable state should be considered, especially in the younger patient. While these syndromes usually affect the venous system, cases of arterial occlusion have been reported. Hypercoagulable states may play an increasing role in aortic occlusive disease, especially when they are superimposed on preexisting arteritis or atherosclerotic disease.
Steven Frost and Robert C. Jorden
Primary causes of hypercoagulability include antithrombin III deficiency or a lower functional level of the inhibitor, protein C and S deficiency, prostacyclin deficiency, disorders of the fibrinolytic system including low or abnormal plasminogen states and deficiency of plasminogen activator, dysfibrinogenemia, and the presence of lupus anticoagulant factor (23). Secondary causes include malignancy, pregnancy, heparin-induced thrombocytopenia with arterial thrombosis, homocystinuria, nephrotic syndrome, diabetes, hyperlipidemia, use of oral contraceptives, and vasculitis (23-25). Thus far the data linking acute aortic thrombosis with a hypercoagulable state are sparse. There have been two cases reported with an antithrombin III deficiency and one case associated with a prostacyclin deficiency (26,27). Although not acute, a case of aortic occlusion has been reported in a patient with systemic lupus erythematosus with positive antibodies to cardiolipin and positive lupus anticoagulant (28). Although the coagulopathy-associated cases are rare, the incidence of this association is probably higher than reported because it is frequently not considered.
Occlusion in Abdominal Dissection
Aortic Aneurysm and
Sudden complete thrombosis of an abdominal aortic aneurysm is a rare but catastrophic event. It presents with the same symptoms as a saddle embolus or acute atherosclerotic thrombosis of the abdominal aorta. In fact, it is difficult to distinguish it from these two entities, particularly if the aneurysm is overlooked or not apparent on physical examination (29). Ultrasound remains the diagnostic method of choice, with accuracy approaching 100% and bedside availability for the unstable patient (30-32). Computed tomography (CT scan) may allow the upper limits of the aneurysm to be more clearly identified, especially if the presence of bowel gas interferes with ultrasound, but it requires intravenous contrast that adds an additional burden to the kidneys. It also requires moving the patient to the scanner. Aortography should be reserved for those patients thought to have aortic dissection (18,33). Real-time ultrasonography may occasionally detect the motion of an intimal flap or the presence of a double lumen, but usually a CT scan or angiography is necessary to confirm the diagnosis (32,34,35). These patients often have the symptoms of acute thoracic aortic occlusion as well as symptoms of compromise of the visceral vasculature (33). They usually complain of
143
Acute Abdominal Aortic Occlusion
tearing chest and back pain, but at least three cases of painless aortic dissections with decreased lower extremity motor function have been reported (34,36). Although rare, isolated abdominal aortic dissection with aortic occlusion has been reported (37-39). An unusual case of acute thrombosis of an abdominal aortic aneurysm subsequent to a Heimlich maneuver has also been reported (40).
Posttraumatic
Occlusion of the Abdominal
Aorta
Occlusion of the abdominal aorta following blunt abdominal trauma is seen occasionally. The mechanism is one of compression of the aorta between the lumbar spine and either a seat belt or steering wheel; the presence of atherosclerosis predisposes to this injury. Typically, the patient presents with abdominal tenderness, low back pain, absent or decreased pulses below the site of occlusion, and cool lower extremities. Neurologic manifestations are common. A review of the literature revealed 19 cases of abdominal aortic occlusion with lower extremity motor deficits following blunt abdominal trauma (6,41-58). Case 3 is typical. Of the cases previously reported, occlusion was caused by intimal dissection in 17 cases, and 8 of these were accompanied by thrombosis. In 2 cases thrombosis alone was found. The intima may be dissected in a circumferential manner and rolled downward causing complete or partial occlusion. Fluctuating or progressing symptoms are common, probably secondary to movement of the intimal flaps. Motor deficits reported included 14 cases with paraplegia, 3 with paraparesis, 1 with hemiparesis below the knee, and 1 with right hemiplegia associated with left hemiparesis below the knee. Of the 19 patients, 7 died, 8 had complete recovery of motor function, 2 had partial recovery (1 of these patients required a unilateral below the knee amputation), and the outcomes in 2 patients were undocumented. Two of the patients who died had recovery of motor function prior to expiring. It is apparent that, while mortality is high, there is a good chance of neurologic recovery in survivors.
MANAGEMENT
Management of acute aortic occlusion in the emergency department consists of prompt recognition, provision of supportive care, immediate surgical consultation, and initiation of a limited diagnostic workup. Since outcome is time dependent, early rec-
ognition and referral are essential elements of management. As in the cases presented, supportive care varies depending on the specific needs of each patient and the etiology of the occlusion. The most difficult aspect of management relates to the diagnostic evaluation. A bedside ultrasound is the best first step; its availability, ease of performance, and sensitivity make it ideally suited for this situation. If ultrasound is not available or is technically inadequate, a CT scan should be considered. The indications for angiography in acute aortic occlusion are limited. It should be considered when there is a history of trauma and when aortic dissection or occlusion of the renal arteries is suspected (4,18,33,59). An antecedent history of claudication may also necessitate an angiogram to determine the presence of collaterals and the distal runoff. Even though on retrospective analysis the information gained by angiography is not helpful, most surgeons routinely obtain it preoperatively (4,18,33). This is probably reflective of the need for this study in many types of vascular disease and injury. It may also be difficult to prospectively select cases that do not require angiography. Given this uncertainty it is probably best to rely on the preference of the surgeon. Nevertheless, emergently needed surgery should not be deferred until angiography is performed. Ultimately the treatment of acute aortic occlusion is surgery. Prior to the introduction of the Fogarty arterial balloon catheter, operative mortality was approximately 75% (18,60). With the advent of this catheter in 1963, embolectomy via common femoral arteriotomy became possible. Embolectomy in combination with early high-dose heparin has resulted in mortalities as low as 14% in some series (4,15). However, overall mortality remains at approximately 50% (18). If acute occlusion from embolism or thrombosis is suspected, high-dose heparin should be initiated in the emergency department and the patient taken for emergent embolectomy (1,2,61). Initially, aortoiliac embolectomy via bilateral common femoral arteriotomies should be attempted (4,14,15,60). Intraoperative angiography or Doppler scan may be used to assessdistal patency (1,14,61). This procedure can be performed under local anesthesia, a distinct advantage in the unstable patient. If vigorous systolic flow cannot be obtained by this method, then bilateral axillofemoral grafting should be performed (22,33). This approach has a lower operative mortality than aortobifemoral bypass in the unstable patient. While embolectomy within 8 to 12 hours after onset of is-
144
Steven Frost and Robert C. Jorden
chemia is optimal, limb viability should determine whether the procedure is performed (14). Embolectomy is contraindicated for thrombosed abdominal aortic aneurysms. Fortunately, these are usually palpable or readily diagnosed by ultrasound. Emergent aneurysmectomy with graft replacement is indicated in these patients, especially if there is renal involvement (59). If the patient is unstable, a bilateral axillofemoral bypass graft may be used (22,61). Aortic bypass grafting is the procedure of choice in cases of dissection or posttraumatic occlusion. Following revascularization, patients should be monitored in an intensive care setting. Patients may suffer from myoglobinuria, lactic acidosis, and severe reperfusion hyperkalemia, as encountered in case 1. In the presence of hyperkalemia and renal failure, hemodialysis may be necessary. It has been suggested by some authors that phlebotomy of the initial venous effluent via the common femoral vein at the time of embolectomy may prevent the initial surge of dangerous metabolites and thrombotic debris from an ischemic extremity that may contribute to an adult respiratory distress syndrome (1,61). Pa-
tients should also be carefully monitored for compartment syndromes for which aggressive use of fasciotomies may be limb saving. SUMMARY
The patient with acute abdominal aortic occlusion presents as a true surgical emergency. Unnecessary diagnostic tests are time-consuming and often involve transporting a critical patient. A careful examination and history suggest the correct diagnosis in most cases. Because of the rarity of this disorder, confusion may exist concerning diagnosis and management. Even with proper management, mortality remains high. A decrease in mortality and morbidity has been seen with the use of anticoagulation and embolectomy with Fogarty arterial catheters. Further decreases in mortality and morbidity may be realized with advances in fibrinolytic therapy as has been used in selected pediatric patients (62). Much research continues with respect to hypercoagulable states and the mechanisms by which they predispose certain patients to thrombosis.
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14. Haimovici H. Arterial embolism of the extremities and technique of embolectomy. In: Haimovici H, ed. Haimovici’s vascular surgery: principles and techniques, 3rd ed. Norwalk, Connecticut: Appleton and Lange; 1989:330-53. 15. Thompson JE, Weston AS, Sigler L, Raut PS, Austin DJ, Patman RD. Arterial embolectomy after acute myocardial infarction: a study of 31 patients. Ann Surg. 1970;171:979-86. 16. Arvan S. Mural thrombi in coronary artery disease: recent advances in pathogenesis, diagnosis, and approaches to treatment. Arch Intern Med. 1984;144:113-16. 17. Santiani B, Gross WS, Evans WE. Improved limb salvage after arterial embolectomy. Ann Surg. 1978;188:153-7. 18. Littooy FN, Baker WH. Acute aortic occlusion-a multifaceted catastrophe. J Vast Surg. 1986;4:211-16. 19. Reeder GS, Tajik AJ, Seward JB. Left ventricular mural echocardiographic diagnosis. thrombus: two-dimensional Mayo Clin Proc. 1981;56(2):82-6. 20. Ports TA, Cogan J, Schiller NB, Rapaport E. Echocardiography of left ventricular masses. Circulation. 1978;58:528-36. 21. Haimovici H, Escher DJW. Aortoiliac stenosis: diagnostic significance of vascular hemodynamics. Arch Surg. 1956;72:107-17. 22. Haimovici H. Acute arterial thrombosis. In: Haimovici H, ed. Haimovici’s vascular surgery: principles and techniques, 3rd ed. Norwalk, Connecticut: Appleton and Lange; 1989:354-60. 23. Schafer AI. The hypercoagulable states. Ann Intern Med. 1985;102:814-28. 24. Gruber HE, Weisman MH. Aortic thrombosis during sigmoidoscopy in Behcet’s syndrome. Arch Intern Med. 1983;143:3435. 25. King DJ, Kelton JG. Heparin-associated thrombocytopenia. Ann Intern Med. 1984;100:535-40. 26. Shapiro ME, Rodvien R, Bauer KA, Salzman EW. Acute aortic thrombosis in antithrombin III deficiency. JAMA. 1981; 245:1759-61.
Acute Abdominal Aortic Occlusion 27. Lanham JG, Levin M, Brown Z, Gharavi AE, Thomas PA, Hanson GC. Prostacyclin deficiency in a young woman with recurrent thrombosis. Br Med J. 1986;292:435-6. 28. Drew P, Asherson RA, Zuk RJ, Goodwin FJ, Hughes GRV. Aortic occlusion in systemic lupus erythematosus associated with antiphospholipid antibodies. Ann Rheum Dis. 1987;46: 612-16. 29. Cervantes J, Martinez R, Perez-Garcia D. Acute thrombosis of abdominal aortic aneurysm. J Cardiovasc Surg. 1985;26:598-601. 30. Lee KR, Walls WJ, Martin NL. A practical approach to the diagnosis of abdominal aortic aneurysms. Surgery. 1975;78: 195-201. 31. Bluth EI. Ultrasound of the abdominal aorta. Arch Intern Med. 1984;144:377-80. 32. Godwin JD, Korobkin M. Acute disease of the aorta: diagnosis by computed tomography and ultrasonography. Radio1 Clin North Am. 1983;21:551-74. 33. Drager SB, Riles TS, Imparato AM. Management of acute aortic occlusion. Am J Surg. 1979;138:293-5. 34. Rosen SA. Painless aortic dissection presenting as spinal cord ischemia. Ann Emerg Med. 1988;17:840-2. 35. Conrad MR, Davis GM, Green CE, et al. Real time ultrasound in the diagnosis of acute dissecting aneurysm of the abdominal aorta. AJR. 1979;132:115-16. 36. Gerber 0, Heyer EJ. Painless dissections of the aorta presenting as acute neurologic syndromes. Stroke. 1986;17:644-7. 37. Adler J, Robey G. Acute aorto-iliac thrombosis in a young man shown on unenhanced computed tomography. Br J Radiol. 1989;62:627-8. 38. Weston TS, Ardagh JW. lnfrarenal dissection of the aorta. N Z Med J. 1975;82:302-4. 39. Sutton D. Arteriography in the diagnosis of dissecting aneurysm. Clin Radiol. 1960;11:85-92. 40. Kirshner RL, Green RM. Acute thrombosis of abdominal aortic aneurysm subsequent to Heimlich maneuver: A case report. J Vast Surg. 1985;2:594-6. 41. Welborn MB, Sawyers JL. Acute abdominal aortic occlusion due to nonpenetrating trauma. Am J Surg. 1969;118:112-16. 42. Nunn DB. Abdominal aortic dissection following nonpenetrating abdominal trauma. Am Surg. 1973;39:177-9. 43. Angel RT, Crosthwait RW. Acute traumatic dissecting aneurysm of the abdominal aorta. Tex Med. 1972;68:82-5. 44. Borja AR, Lansing AM. Thrombosis of the abdominal aorta caused by blunt trauma. J Trauma. 1970;10:499-501. 45. Sumpio BE, Gusberg RJ. Aortic thrombosis with paraplegia: an unusual consequence of blunt abdominal trauma. J Vast Surg. 1987;6:412-14.
145 46. Dajee H, Richardson IW, Iype MO. Seat belt aorta: acute dissection and thrombosis of the abdominal aorta. Surgery. 1979;85:263-7. 47. David D, Blumenberg RM. Subintimal aortic dissection with occlusion after blunt abdominal trauma. Arch Surg. 197O;lOO: 302-4. 48. Hewitt RL, Grablowsky OM. Acute traumatic dissecting aneurysm of the abdominal aorta. Ann Surg. 1970;171:160-2. 49. Macbeth A, Malone JM, Norton LW, Peltier LF. Paralysis and aortic thrombosis following blunt abdominal trauma. J Trauma. 1982;22:591-4. 50. Ngu VA, Konstam PG. Traumatic dissecting aneurysm of the abdominal aorta. Br J Surg. 1965;52:981-2. 51. Mangiante EC, Voeller GR, Kidsk KA, Fabian TC. Blunt injury of the abdominal aorta. J Ten Med Assoc. 1989;82:2556. 52. Thal ER, Perry MO, Crighton J. Traumatic abdominal aortic acclusion. South Med J. 1971;64:653-6. 53. Rybak JJ, Thomford NR. Acute occlusion of the infrarenal aorta from blunt trauma. Am Surg. 1%9;35:444-7. 54. Kleinert HE, Romero J. Blunt abdominal trauma: review of cases admitted to a general hospital over a 10 year period. J Trauma. 1961;1:226-40. 55. Tomatis LA, Doornbos FA, Beard JA. Circumferential intima1 tear of aorta with complete occlusion due to blunt trauma. J Trauma. 1968;8:1096-101. 56. Potter DJ, Hopkins JG. Reversible paraplegia and acute renal failure due to occlusive disease of the abdominal aorta. Ann Intern Med. 1968;69:777-80. 57. Blute R, Ray F. Traumatic dissecting aneurysm of the abdominal aorta. J Maine Med Assoc. 1973;64:164-6. 58. Van Reedt Dorland RWH, Clevers GJ. Crush accident resulting in isolated abdominal aortic injury. Neth J Surg. 1988; 40(4): 108-9. 59. Haimovici H. Metabolic complications of acute arterial occlusion and related conditions: role of free radical (myonephropathic-metabolic syndrome). In: Haimovici H, ed. Haimovici’s vascular surgery, 3rd ed. Norwalk, Connecticut: Appleton and Lange; 1989:386-408. 60. Porter JM, Acinapura AJ, Silver D. Aortic saddle embolectomy. Arch Surg. 1966;93:360-4. 61. Gordon RD, Fogarty TJ. Peripheral arterial embolism. In: Rutherford RB, ed. Vascular surgery, 2nd ed. Philadelphia: WB Saunders; 1984:449-59. 62. LeBlanc JG, Culham JAG, Chan KW. et al. Treatment of grafts and major vessel thrombosis with low-dose streptokinase in children. Ann Thorac Surg. 1986;41:630-5.
Emergency
Medicme,
Vol IO, pp 139-145,
PrInted an the USA
1992
ACUTE ABDOMINAL Steven Frost, Reprint
Address:
Division of Emergency Steven Frost, MD, Division
MD,
Copyrtght
F 1992 Pwgamon
Press Ltd
AORTIC OCCLUSION
and Robert C. Jorden,
Medicine, University of Mississippi of Emergency Medicine, University
0 Abstract-Acute occlusion of the infrarenal abdominal aorta is a catastrophic event requiring early recognition and intervention if permanent disability is to be decreased or avoided. While traditional causes of occlusion (saddle embolus and thrombosis) are the most frequent, vasculitis and hypercoagulable states have recently been suggested as etiologies. This article presents three casesof acute abdominal aortic occlusion from different mechanisms and reviews the literature concerning presentation and management.
MD,
FACEP
Medical Center, Jackson, Mississlppl of Mississippi Medical Center, Jackson.
MS 39216-4505
CASE REPORTS Case 1 A 36-year-old woman was transported
from an outside hospital after presenting with complaints of increasing difficulty breathing and acute onset of paraplegia. Treatment, at the referring hospital, was directed at the evident pulmonary edema and hypoxemia and included nasotracheal intubation and administration of intravenous furosemide. The patient’s vital signs were as follows: pulse, 126 beats/min; blood pressure, 106/80 torr; and respiratory rate, 36 breaths/min. Physical examination revealed an alert, cooperative patient with bilateral rales on auscultation of the chest and cold, rigid, pulseless lower extremities with complete loss of sensation and motor function. A chest x-ray study revealed moderate enlargement of the cardiac silhouette and pulmonary edema. The electrocardiogram showed a normal sinus rhythm with poor R wave progression in the anterior leads and right atrial enlargement. Laboratory results included hematocrit, 47.5%; WBC, 14,630/mm3; prothrombin time, 12.6 set; and partial thromboplastin time, 27.1 sec. Electrolytes, BUN, and creatinine were normal. After high-dose heparin was initiated, the patient was taken to the operating room where bilateral femoral embolectomies using Fogarty catheters were performed. Total time of ischemia had been approximately 15 hours. At this point, the patient sustained a cardiac arrest requiring multiple defibrillation attempts. A suspicion of reperfusion hyperkalemia was confirmed when a potassium of 7.3 mEq/L was re-
q Keywords-acute abdominal aortic occlusion; saddle embolus; aortic thrombosis; blunt abdominal trauma; abdominal aortic aneurysm
INTRODUCTION
Acute infrarenal abdominal aortic occlusion is an infrequent but catastrophic event. Because it causes neurologic dysfunction, these symptoms often predominate and cause the aortic lesions to be overlooked. Frequently traumatic spinal cord injury or prolapsed intervertebral disk are inappropriately diagnosed. Proper management depends on prompt recognition if permanent disability is to be decreased or avoided. Most often, the appropriate diagnosis is suggested by taking a thorough history and conducting a proper examination for distal pulses and neurologic deficits. During a 2-month period, 3 cases of acute abdominal aortic occlusion presented to our emergency department. Each case was caused by a different mechanism. This prompted a review of the literature to determine the pathophysiology and proper management of this disorder.
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ported. The wounds were reopened and the femoral vessels cross-clamped. Sinus rhythm was returned and after stabilization the patient was taken to the intensive care unit. The patient had a complicated hospital course requiring bilateral above the knee amputations, multiple debridements, and bilateral hemipelvectomy secondary to ascending gangrene. This was followed by excision of the sacrum. Her hospital course was also complicated by myoglobinuria and sepsis. She expired in septic shock after a prolonged hospitalization. Pathologic examination was consistent with extensive thromboemboli involving the aortic bifurcation, as well as the femoral and popliteal arteries.
Case 2 A 54-year-old man was transferred from an outside hospital for evaluation of a possible prolapsed intervertebral disk. After a recent drinking binge, the patient reported an episode of repeated vomiting followed by a sudden onset of pain in the lower back and legs followed by loss of sensation and motor function. The patient’s vital signs were as follows: pulse, 116 beats/min; blood pressure, 190/100 torr; and respiratory rate, 20 beats/min. The physical examination was significant for coolness and cyanosis extending distally from the inguinal ligaments. In addition, both lower extremities were pulseless, and there was a T12 complete sensory and motor deficit. Chest x-ray study and electrocardiogram were normal; abdominal aortogram revealed complete obstruction of the aorta just below the level of the renal arteries. Laboratory results included hematocrit, 49.3%; WBC, 13,960/mm3; glucose, 199 mg/dL; and ETOH, zero. Electrolytes, BUN, and creatinine were normal. The patient was taken to the operating room with a diagnosis of probable acute thrombotic aortic occlusion and high-dose heparin was initiated. Removal of thrombus from the aortoiliac femoral profunda and superficial femoral systems was accomplished with Fogarty catheters via bilateral femoral arteriotomies. The hospital course was complicated by bilateral compartment syndromes requiring fasciotomies, eventual bilateral above the knee amputations, myoglobinuria, right gluteal abscess requiring surgical drainage, and stump infections. Pathology reported organizing thrombus with underlying atherosclerosis of the femoral arteries. He regained only limited motor function in the stumps and was transferred to
Steven Frost and Robert C. Jorden
another hospital closer to his home for rehabilitation.
Case 3 A 54-year-old man fell asleep while driving and struck a tree head-on. He awoke with the steering wheel wedged into his lap. After pulling himself from the car, he stood up but then fell to the ground due to lower extremity weakness, He was seen initially at a local hospital and then transferred to our facility. On arrival, vital signs were as follows: pulse, 96 beats/min; blood pressure, 136/ 80 torr; and respiratory rate, 20/min. Heart and lung examinations were unremarkable. The abdomen was soft and nontender. Neurologic examination revealed a complete loss of motor function in the left leg and a sensory deficit to pin prick at the L2 level on the left. Some crude touch remained below this level. There were no deficits on the right side. There was no sphincter tone on rectal examination. Femoral pulses were detected by Doppler examination, but distal pulses were absent bilaterally. A chest x-ray study revealed fractures of the left 4th through 7th ribs laterally but no pneumothorax; radiographs of the neck, pelvis, and lumbrosacral spine were normal. An arteriogram revealed occlusion of the abdominal aorta just below the level of the superior mesenteric artery. An electrocardiogram was within normal limits. Laboratory results included hematocrit, 36.1%; WBC, I 1,560/mm3; prothrombin time, 11.6 set; partial thromboplastin time, 26.1 set; and ETOH, 38 mg/dL. Electrolytes, BUN, and creatinine were normal. The patient was taken to the operating room and high-dose heparin was started. On exploratory celiotomy there was an obvious severe contusion of the abdominal aorta with adventitial hematoma that began 3 to 4 cm below the renal arteries and extended beyond the bifurcation into both iliac arteries. Full thickness injury of the anterior and posterior aortic walls was apparent; extensive thrombus occluded the lumen. Both iliac arteries were also noted to be severely diseased with atheromatous thickening. A dacron bifurcation graft was placed. Total time of ischemia had been approximately 12 hours. The patient had return of distal pulses and neurologic function postoperatively. Except for myoglobinuria and bilateral compartment syndromes requiring fasciotomies, the patient had an unremarkable hospital course and was discharged with no limitation of activity.
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DISCUSSION
is provided by two longitudinal systems: the paired posterolateral longitudinal arterial trunks and the single anterior median longitudinal arterial trunk (8,9). The posterior system is supplied by numerous medullary feeder arteries and is seldom compromised
Presentation and Pathophysiology Acute aortic occlusion occurs as a sudden event without previous history of claudication. Symptoms are variable depending on completeness of obstruction, but the most common symptoms are pain, pallor, pulselessness, paresthesia, and paralysis (1). If preexisting aortoiliac atherosclerotic disease is present, the degree and severity of symptoms may be lessened due to development of collateral circulation. In the absence of collateral circulation, the patient experiences sudden onset of severe low back, buttocks, and lower extremity pain. This is accompanied by a flaccid paralysis of the lower extremities if spinal cord infarction occurs, or by the gradual onset of lower extremity weakness if ischemia of peripheral nerves or the cauda equina occurs. The skin is cool and pale distal to the occlusion. This may occur at the umbilicus or at the level of the iliac crests. Waxy, white skin indicates viable arterioles supplying blood to the skin (2). When nonblanching, blotchy cyanosis occurs, it indicates thrombosed capillaries and skin necrosis (2). Skin may withstand severe ischemia for as long as 24 hours; however, muscle sustains permanent damage after 8 to 12 hours (1,2). As cellular edema increases, the ischemic muscle takes on a doughy, firm consistency indicating early necrosis (1,2). The presence of rigidity is a reliable sign of nonviability (l-4). In almost all cases of acute aortic occlusion the neurological deficits appear to be caused by ischemia of the cauda equina or peripheral nerves; thus, recovery is likely with timely intervention. However, spinal cord infarction, while rare, may occur and is nearly always irreversible. Peripheral nerves may withstand ischemia for 12 to 24 hours with complete return of function (5). Sensory deficits begin with severe burning pain and paresthesias, followed by complete loss of all sensory modalities, while motor deficits begin distally and progress proximally; both can be delayed in onset (6). Spinal cord infarction with paralysis occurs suddenly, and since the spinal cord is extremely sensitive to ischemia, irreversible damage occurs in 18 to 60 minutes (7). Knowledge of the normal vascular supply of the spinal cord in the thoracolumbar region is necessary to understand the neurologic manifestations and implications for recovery in patients with acute abdominal aortic occlusion. The superior portion of the spinal cord is afforded an ample blood supply. Whether spinal cord infarction occurs depends on the highly variable vascular supply to the distal spinal cord that
W).
The anterior system supplies most of the ventral two-thirds of the spinal cord that includes the pyramidal tracts; thus, with occlusion of this system, a flaccid paralysis occurs with initially absent deep tendon reflexes that become hyperactive over time. Bowel and bladder incontinence are also characteristic (10). Loss of pain and temperature is part of the clinical picture, but proprioception and vibratory sensation are preserved since the dorsal columns are supplied by the posterior system. The supply to the anterior system is variable and has only a few medullary feeders. The anatomy has been meticulously described by Dommisse in a series of cadaveric dissections supplemented by microangiograms (11). He found great variability in the size of the anterior trunk and the number of medullary feeders. A large medullary feeder in this region, referred to as the artery of Adamkiewicz, may be the only supplier to the anterior system. Dommisse (11) found it occurring on the left in 77% of cadavers and originating anywhere from T7 to L4; an origin as low as LS has also been reported (12). Dommisse also found as many as three large vessels in a single cadaver. The infrequency of spinal infarction may be explained by two factors: 1. The artery of Adamkiewicz most often arises above the Ll vertebral level and is thus above the site of most occlusion (11,13). 2. Even when arising below L 1, collateral circulation is usually adequate or other medullary feeders arise more proximally and supply the cord (11). Etiologies of Acute Aortic Occlusion There are several causes of acute occlusion of the abdominal aorta, including saddle embolism, acute thrombosis with or without preexisting aortoiliac atherosclerotic disease, thrombosis of an abdominal aortic aneurysm, aortic dissection, and posttraumatic abdominal aortic occlusion. Acute thrombosis resulting from a hypercoagulable state or vasculitis has also been implicated. Occlusion by Saddle Embolus An embolus occluding the aortic bifurcation (saddle embolus) is the most frequent cause of acute abdomi-
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nal aortic occlusion. However, it only accounts for about 10% of all emboli to the extremities (4,14). Rheumatic heart disease, formerly the most common source of emboli, has been supplanted in that role by atherosclerotic coronary artery disease. Despite the low incidence of embolism following myocardial infarction (less than lCro), the frequency of coronary artery disease makes this a common cause (15). In a review of postmortem studies, Arvan (16) reported the incidence of postinfarction mural thrombus to range 17% to 66%. The median interval from onset of infarction to embolism is 10 days, while two-thirds of emboli occur less than 3 weeks postinfarction (15,17). Atria1 fibrillation has been reported in 40% to 100% of patients with abdominal aortic saddle embolus (4,15,17,18). Besides myocardial infarction, other common sources of saddle embolus include prosthetic valves and dilated cardiomyopathy. At postmortem examination, left mural thrombus has been found in up to 60% of cases of dilated cardiomyopathy and in 50% of cases of left ventricular aneurysm (19). When echocardiography is performed, large mural thrombi (larger than 2 cm) are more commonly seen in dilated cardiomyopathy than in coronary artery disease complicated by segmental wall abnormalities or left ventricular aneurysm (19,20). Because an embolus is the most common cause of acute abdominal aortic occlusion, it is presumed whenever a predisposing factor such as a recent myocardial infarction, cardiomyopathy, or atria1 fibrillation exists (4,14).
Occlusion by Acute Thrombosis Acute thrombosis should not be confused with the Leriche syndrome. This is a slowly progressing disease due to atherosclerotic lesions of the aortic wall that reduces the diameter of the lumen until it reaches a critical stenosis of 80% of the cross-sectional area (21). In the absence of this critical stenosis, acute thrombosis produces sudden and severe effects (22). Thrombosis usually occurs in the setting of preexisting atherosclerotic disease, as in case 2. However, the possibility of a hypercoagulable state should be considered, especially in the younger patient. While these syndromes usually affect the venous system, cases of arterial occlusion have been reported. Hypercoagulable states may play an increasing role in aortic occlusive disease, especially when they are superimposed on preexisting arteritis or atherosclerotic disease.
Steven Frost and Robert C. Jorden
Primary causes of hypercoagulability include antithrombin III deficiency or a lower functional level of the inhibitor, protein C and S deficiency, prostacyclin deficiency, disorders of the fibrinolytic system including low or abnormal plasminogen states and deficiency of plasminogen activator, dysfibrinogenemia, and the presence of lupus anticoagulant factor (23). Secondary causes include malignancy, pregnancy, heparin-induced thrombocytopenia with arterial thrombosis, homocystinuria, nephrotic syndrome, diabetes, hyperlipidemia, use of oral contraceptives, and vasculitis (23-25). Thus far the data linking acute aortic thrombosis with a hypercoagulable state are sparse. There have been two cases reported with an antithrombin III deficiency and one case associated with a prostacyclin deficiency (26,27). Although not acute, a case of aortic occlusion has been reported in a patient with systemic lupus erythematosus with positive antibodies to cardiolipin and positive lupus anticoagulant (28). Although the coagulopathy-associated cases are rare, the incidence of this association is probably higher than reported because it is frequently not considered.
Occlusion in Abdominal Dissection
Aortic Aneurysm and
Sudden complete thrombosis of an abdominal aortic aneurysm is a rare but catastrophic event. It presents with the same symptoms as a saddle embolus or acute atherosclerotic thrombosis of the abdominal aorta. In fact, it is difficult to distinguish it from these two entities, particularly if the aneurysm is overlooked or not apparent on physical examination (29). Ultrasound remains the diagnostic method of choice, with accuracy approaching 100% and bedside availability for the unstable patient (30-32). Computed tomography (CT scan) may allow the upper limits of the aneurysm to be more clearly identified, especially if the presence of bowel gas interferes with ultrasound, but it requires intravenous contrast that adds an additional burden to the kidneys. It also requires moving the patient to the scanner. Aortography should be reserved for those patients thought to have aortic dissection (18,33). Real-time ultrasonography may occasionally detect the motion of an intimal flap or the presence of a double lumen, but usually a CT scan or angiography is necessary to confirm the diagnosis (32,34,35). These patients often have the symptoms of acute thoracic aortic occlusion as well as symptoms of compromise of the visceral vasculature (33). They usually complain of
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tearing chest and back pain, but at least three cases of painless aortic dissections with decreased lower extremity motor function have been reported (34,36). Although rare, isolated abdominal aortic dissection with aortic occlusion has been reported (37-39). An unusual case of acute thrombosis of an abdominal aortic aneurysm subsequent to a Heimlich maneuver has also been reported (40).
Posttraumatic
Occlusion of the Abdominal
Aorta
Occlusion of the abdominal aorta following blunt abdominal trauma is seen occasionally. The mechanism is one of compression of the aorta between the lumbar spine and either a seat belt or steering wheel; the presence of atherosclerosis predisposes to this injury. Typically, the patient presents with abdominal tenderness, low back pain, absent or decreased pulses below the site of occlusion, and cool lower extremities. Neurologic manifestations are common. A review of the literature revealed 19 cases of abdominal aortic occlusion with lower extremity motor deficits following blunt abdominal trauma (6,41-58). Case 3 is typical. Of the cases previously reported, occlusion was caused by intimal dissection in 17 cases, and 8 of these were accompanied by thrombosis. In 2 cases thrombosis alone was found. The intima may be dissected in a circumferential manner and rolled downward causing complete or partial occlusion. Fluctuating or progressing symptoms are common, probably secondary to movement of the intimal flaps. Motor deficits reported included 14 cases with paraplegia, 3 with paraparesis, 1 with hemiparesis below the knee, and 1 with right hemiplegia associated with left hemiparesis below the knee. Of the 19 patients, 7 died, 8 had complete recovery of motor function, 2 had partial recovery (1 of these patients required a unilateral below the knee amputation), and the outcomes in 2 patients were undocumented. Two of the patients who died had recovery of motor function prior to expiring. It is apparent that, while mortality is high, there is a good chance of neurologic recovery in survivors.
MANAGEMENT
Management of acute aortic occlusion in the emergency department consists of prompt recognition, provision of supportive care, immediate surgical consultation, and initiation of a limited diagnostic workup. Since outcome is time dependent, early rec-
ognition and referral are essential elements of management. As in the cases presented, supportive care varies depending on the specific needs of each patient and the etiology of the occlusion. The most difficult aspect of management relates to the diagnostic evaluation. A bedside ultrasound is the best first step; its availability, ease of performance, and sensitivity make it ideally suited for this situation. If ultrasound is not available or is technically inadequate, a CT scan should be considered. The indications for angiography in acute aortic occlusion are limited. It should be considered when there is a history of trauma and when aortic dissection or occlusion of the renal arteries is suspected (4,18,33,59). An antecedent history of claudication may also necessitate an angiogram to determine the presence of collaterals and the distal runoff. Even though on retrospective analysis the information gained by angiography is not helpful, most surgeons routinely obtain it preoperatively (4,18,33). This is probably reflective of the need for this study in many types of vascular disease and injury. It may also be difficult to prospectively select cases that do not require angiography. Given this uncertainty it is probably best to rely on the preference of the surgeon. Nevertheless, emergently needed surgery should not be deferred until angiography is performed. Ultimately the treatment of acute aortic occlusion is surgery. Prior to the introduction of the Fogarty arterial balloon catheter, operative mortality was approximately 75% (18,60). With the advent of this catheter in 1963, embolectomy via common femoral arteriotomy became possible. Embolectomy in combination with early high-dose heparin has resulted in mortalities as low as 14% in some series (4,15). However, overall mortality remains at approximately 50% (18). If acute occlusion from embolism or thrombosis is suspected, high-dose heparin should be initiated in the emergency department and the patient taken for emergent embolectomy (1,2,61). Initially, aortoiliac embolectomy via bilateral common femoral arteriotomies should be attempted (4,14,15,60). Intraoperative angiography or Doppler scan may be used to assessdistal patency (1,14,61). This procedure can be performed under local anesthesia, a distinct advantage in the unstable patient. If vigorous systolic flow cannot be obtained by this method, then bilateral axillofemoral grafting should be performed (22,33). This approach has a lower operative mortality than aortobifemoral bypass in the unstable patient. While embolectomy within 8 to 12 hours after onset of is-
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chemia is optimal, limb viability should determine whether the procedure is performed (14). Embolectomy is contraindicated for thrombosed abdominal aortic aneurysms. Fortunately, these are usually palpable or readily diagnosed by ultrasound. Emergent aneurysmectomy with graft replacement is indicated in these patients, especially if there is renal involvement (59). If the patient is unstable, a bilateral axillofemoral bypass graft may be used (22,61). Aortic bypass grafting is the procedure of choice in cases of dissection or posttraumatic occlusion. Following revascularization, patients should be monitored in an intensive care setting. Patients may suffer from myoglobinuria, lactic acidosis, and severe reperfusion hyperkalemia, as encountered in case 1. In the presence of hyperkalemia and renal failure, hemodialysis may be necessary. It has been suggested by some authors that phlebotomy of the initial venous effluent via the common femoral vein at the time of embolectomy may prevent the initial surge of dangerous metabolites and thrombotic debris from an ischemic extremity that may contribute to an adult respiratory distress syndrome (1,61). Pa-
tients should also be carefully monitored for compartment syndromes for which aggressive use of fasciotomies may be limb saving. SUMMARY
The patient with acute abdominal aortic occlusion presents as a true surgical emergency. Unnecessary diagnostic tests are time-consuming and often involve transporting a critical patient. A careful examination and history suggest the correct diagnosis in most cases. Because of the rarity of this disorder, confusion may exist concerning diagnosis and management. Even with proper management, mortality remains high. A decrease in mortality and morbidity has been seen with the use of anticoagulation and embolectomy with Fogarty arterial catheters. Further decreases in mortality and morbidity may be realized with advances in fibrinolytic therapy as has been used in selected pediatric patients (62). Much research continues with respect to hypercoagulable states and the mechanisms by which they predispose certain patients to thrombosis.
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