Acute Thrombosis of Abdominal Aortic Aneurysm

Transcription

1 Acute Thrombosis of Abdominal Aortic Aneurysm Francisco J. Criado, M.D. Ofall the complications ofabdominal aortic aneurysm (AAA), complete acute thrombosis has received the least attention in the literature. Its infrequent occurrence, no doubt, accounts for the paucity of reports. The management of a recent patient with an acutely thrombosed AAA prompted this review ofthe English-language literaturefor specific information regarding the diagnosis and treatment of AAA. Case Report A77-YEAR-OLD woman was admitted to our hospital with a long-standing history of well-compensated congestive heart failure and hypertension. Several minutes after sustaining a fall at home, she experienced acute low back pain and increasing "painful numbness" of the lower extremities, which gradually progressed to total anesthesia and motor paralysis. Upon first examination, she had mottled cyanosis from the umbilicus distally. The lower extremity pulses were absent bilaterally, including the femorals. There was no palpable abdominal mass. Neurological examination revealed flaccid paraplegia and no reflexes, with dissociated sensory loss. Once the diagnosis of acute aortic occlusion had been made clinically, the patient was given a bolus intravenous injection of 10,000 units of heparin. Abdominal ultrasound disclosed the presence of an infrarenal aortic aneurysm with no discernible lumen. Laparotomy was performed after a two-hour period of intensive fluid therapy and correction of the existing metabolic acidosis (ph 7.29 on admission). The operative findings consisted of a completely thrombosed AAA that measured 5 cm in transverse diameter. The aorta, which was proximal to the aneurysm, and both renal arteries were pulsatile. The iliac arteries were severely diseased and appeared occluded. The aneurysm was repaired with an aorto-bifemoral woven Dacron graft, a tongue of which was extended distally as onlay patch profundaplasties. The postoperative course was one of slow but steady recovery, and the patient was discharged on the fourteenth day. The neurological deficit improved partially, allowing her to ambulate with the aid of a walker by the time of discharge. Review of the Literature Unlike peripheral aneurysms, complete acute thrombosis of an AAA is distinctly unusual. Although Schumaker' briefly mentioned one instance of AAA in 1959, Janetta and Roberts2 reported the first welldocumented case in In 1974, Johnson and associates3 collected ten cases from the literature and added seven of their own. Since then, eight more cases have been reported.48 Including the above case report, a total of 26 patients are reviewed in this paper. From the Department of Surgery, Union Memorial Hospital, Baltimore, Maryland. Address for reprints: Francisco J. Criado, M.D., Union Memorial Hospital, 201 E. University Parkway, Baltimore, Maryland Texas Heart Institute Journal 367

2 Not unexpectedly, men outnumbered women; of 22 patients in which the sex was reported, 16 were men. Aneurysm size was recorded in 17 of the 26 patients. It ranged from 4 cm to 14 cm and was 7 cm or smaller in 13 instances. Most of the patients had a history of severe occlusive atherosclerosis. Coronary artery disease and cerebrovascular insufficiency were also prevalent. Clinical presentations were often dramatic and relatively easy to diagnose. In 14 of the reported cases, mottling was described to the level of the iliac crest or umbilicus. The absence of femoral pulses and manifestations of severe ischemia of the lower extremities (pain, pallor, coldness) were also common findings. Ten of the 17 patients reviewed byjohnson et a13 had paraplegia at the time of clinical examination. Generally, the aneurysm could not be palpated preoperatively and aortography was only rarely performed. Twelve of the 26 patients died, for a mortality of 46%. Prolonged low-flow state and myocardial infarction were the most frequent causes of death. Renal insufficiency, usually severe, was present in most of the non-survivors. Discussion There are three possible mechanisms that can precipitate acute, complete thrombosis of an AAA. Undoubtedly, the most, common causative factor is occlusive iliac artery disease, leading to aneurysm outflow obstruction (Fig. 1). Marked iliac atherosclerosis and occlusion have been almost invariably associated with the problem in the reported cases. The second possible causative mechanism involves cardioaortic embolization (Fig. 2), similar in all respects to the more common distal aortic occlusion by a saddle embolus. It is noteworthy that in the second reported instance of AAA thrombosis,9 the precipitating event was thought to be embolic iliac artery occlusion. Thirdly, the intrasaccular mural thrombus may become acutely obstructive to blood flow if a sudden change in position occurs (Fig. 3). It is tempting to postulate this latter mechanism in the preceding case report, Fig. 1 Aneurysm thrombosis secondary to iliac artery occlusion. where there was a clear temporal relationship between the patient's fall (which could have induced such a shift in position) and the onset of symptoms of aortic occlusion. In some cases, hypotension and hypercoagulability states can contribute to complete thrombosis when coexisting with severe stenosis of the aneurysm outlet.3 Additionally, in two of the 17 cases reviewed by Johnson and colleagues,3 there was an associated contained rupture of the aneurysm. The clinical picture of acute abdominal aortic occlusion is characterized by mottling from the umbilicus distally, intense pain, pallor, and coldness of the lower extremities, which are also pulseless. Paraplegia is present in as many as 50% of the cases. Less commonly, the paralysis may be a component of the anterior spinal artery syndrome consisting of paraplegia, loss of thermoalgesic and touch sensation with preservation of proprioception, and sphincter tone disturbances. This syndrome is believed to be a result of ischemia of the anterior two-thirds and the lower one-fourth of the spinal cord when one major anterior radicular artery originates from a lumbar artery.'0 The likelihood of cord damage is accentuated when a concomitant low-flow state exists. If the patient's outcome is otherwise successful, the neurological deficit can be expected to improve in approximately 50% of cases." 368 Vol. 9, No. 3, September 1982

3 Fig. 2 Cardioaortic embolism causing aneurysm outlet obstruction and subsequent thrombosis. Fig. 3 Shift in position of intrasaccular mural thrombus leading to obstruction and aneurysm thrombosis. When faced with such manifestations of distal aortic occlusion, the differential diagnosis should include four conditions: saddle embolus, acute atherosclerotic aortic thrombosis, acute aortic dissection, and acute thrombosis of an AAA. Saddle embolus is the most frequent cause of acute aortic occlusion and is relatively simple to diagnose when the patient has no significant peripheral arterial disease, and there is a cardiac source of embolization (atrial fibrillation, mitral stenosis, recent myocardial infarction). Acute aortic dissection can frequently be distinguished by the presence of severe chest or back pain, signs of major visceral artery occlusion, and an abnormal chest roentgenogram in a hypertensive patient. The most difficult differentiation lies between atherosclerotic aortic thrombosis and aneurysm thrombosis, particularly in view of the fact that a thrombosed aneurysm is frequently small and impalpable on physical examination. In delineating the presence and size of aortic aneurysms, ultrasound is expeditious, totally noninvasive, and very accurate. In fact, it is the most reliable diagnostic tool in diagnosing AAA,'2 and should be routinely employed in patients presenting with acute aortic occlusion, a recommendation not emphasized in any of the previous reports. One crucial diagnostic aspect focuses on the possibility of renal artery involvement by the thrombotic process. In this regard, the assessment of urinary output by indwelling bladder catheter and its response to parenteral fluid administration are of decisive importance. The presence of oligoanuria constitutes the only clear-cut indication for emergency aortography in this setting. Acute AAA thrombosis is a major surgical emergency with a mortality rate comparable to that reported in ruptured aneurysms. When the clinical diagnosis of acute aortic occlusion is made, the first therapeutic gesture should be rapid systemic anticoagulation by intravenous heparin bolus injection to halt further propagation of thrombosis in the distal vascular bed. Emergent surgical intervention is indicated to avoid an otherwise catastrophic outcome (death or limb loss). Some time should be allowed, however, for insertion of all the necessary lines for invasive cardiovascular monitoring and intensive correction of fluid and acid-base disturbances. Surgical strategy is influenced to a great extent by the specific underlying condition. There should no longer be an initial trialand-error approach of "blind" retrograde transfemoral embolectomy in a patient with acute abdominal aortic occlusion and no obvious aneurysm. Preoperative aortic ultrasound will assist in recognizing most, if not all, cases of thrombosed aneurysm. The preferred treatment involves aneurysmal Texas Heart Institute Journal 369

4 replacement with a prosthetic graft. Distal anastomoses frequently need to be made at the femoral artery level because of concomitant iliac artery disease. Furthermore, chronic superficial femoral artery occlusion and proximal profunda femoris artery disease are also likely to be encountered. This set of findings, whenever present, dictates the performance of bilateral profundaplasties if a durable aortofemoral reconstruction is to be achieved. Renal artery disobstruction is life-saving when the thrombotic process extends to a critical level. The presence of oliguria, unresponsive to fluid challenge, signifies renal involvement and should prompt the performance of preoperative aortography. In general, transaortic renal thrombectomy (or thromboendarterectomy), done before constructing the proximal aortoprosthetic anastomosis, will restore blood flow to the kidneys." In recent years, there has been a growing trend toward utilization of axillo-bifemoral bypass grafting as treatment of aortoiliac occlusion,7 and as a form of nonresective treatment of AAA in high-risk patients.'4-'1 The chief advantage of this approach is that the procedure can be carried out under local or light general anesthesia as a major intraabdominal aortic reconstruction is avoided; this lessens the risk of perioperative death. On the other hand, the disadvantages include a high rate of postoperative graft thrombosis and, even more critically, the failure to restore aortic continuity with the attendant risk of subsequent propagation of thrombosis to the renal arteries.'3 The current state-of-the-art of intraoperative monitoring and anesthesia should permit the performance of standard transabdominal aneurysm graft replacement within reasonable safety in most patients. Only in exceptional cases should a thrombosed AAA be left untouched and axillo-bifemoral grafting resorted to. Such a situation may arise when acute AAA thrombosis is concurrent with acute myocardial infarction. Even then, if there is renal artery thrombosis, the aneurysm must be dealt with directly. On the basis of these observations, we conclude that: 1. Acute complete thrombosis of AAA is a rare and catastrophic event carrying a mortality (46%) which approaches that of aneurysmal rupture. 2. The presentation is frequently dramatic, consisting of mottling from the umbilicus distally, severe ischemia of the lower extremities with no discernible pulses and, often, paraplegia. 3. Ultrasound is emphasized as the most expeditious, accurate means of disclosing the underlying aneurysm in this setting; when appropriate, preoperative aortography should be obtained to rule out renal artery involvement. 4. The treatment should be emergent, consisting of (a) immediate systemic heparinization; (b) preoperative evaluation of cardiorespiratory and metabolic disturbances in the intensive care setting, with rapid restoration of fluid deficits, correction of metabolic acidosis, and assessment of the renal response to intravascular fluid replenishment; and (c) emergency laparotomy with prosthetic graft replacement of the aneurysm. At the same time, the coexisting iliac artery disease should be bypassed by attaching the distal ends of the graft to the common femoral-profunda femoris arteries. Axillo-bifemoral grafting, instead of aneurysm replacement, should be considered when there is evidence of acute myocardial infarction, but only after the adequacy of blood flow to the kidneys has been ascertained. References 1. Schumaker HD. Surgical treatment of aortic aneurysms. Postgrad Med 1959; 25: Janetta PJ, Roberts B. Sudden complete thrombosis of an aneurysm of the abdominal aorta. N Engl J Med 1961; 264: Johnson JM, Gaspar MR, Movius HJ, Rosenthal JJ. Sudden complete thrombosis of aortic and iliac aneurysms. Arch Surg 1974; 108: Saha SP, Nunn DB. Sudden thrombotic occlusion of abdominal aortic aneurysm: A report of two patients. Am Surg 1974; 40: Vol. 9, No. 3, September 1982

5 5. Olcott C, Holcroft JW, Stoney RJ, Wylie EJ. Unusual problems of abdominal aortic aneurysms. Am J Surg 1978; 135: Kornmesser TW, Trippel OH, Haid SP. Acute occlusion of the abdominal aorta. In BerganJJ and Yao JST (eds): Surgery of the Aorta and Its Body Branches. New York, Grune & Stratton, Drager SB, Riles TS, Imparato AM. Management of acute aortic occlusion. Am J Surg 1979; 138: Bridges KG, DonnellyJCJr. Acute occlusion of an abdominal aortic aneurysm complicated by bilateral lower extremity venous thrombosis: A case report. Cardiovasc Dis Bull Texas Heart Inst 1981; 8: Seidenburg B, Stern J, Hurivitt ES. Thrombotic occlusion of abdominal aortic aneurysm following distal embolization. Circulation 1962; 25: Zuber WF, Gaspar MR, Rothschild PD. The anterior spinal artery syndrome: A complication of abdominal aortic surgery. Ann Surg 1970; 172: Johnson ND, Yao JST, Bergan JJ. Spinal cord ischemia after abdominal aortic surgery. In Bergan JJ and Yao JST (eds): Surgery of the Aorta and Its Body Branches. New York, Grune & Stratton, Leopold GR, Goldberger LE, Bernstein EF. Ultrasonic detection and evaluation of abdominal aortic aneurysms. Surgery 1972; 79: Starrett RP, Stoney RJ. Juxtarenal aortic occlusion. Surgery 1974; 76: Leather RP, Shah D, Goldman M, Rosenberg M, Karmody AM. Nonresective treatment of abdominal aortic aneurysms: Use of acute thrombosis and axillofemoral bypass. Arch Surg 1979; 114: Berguer R, Feldman AJ, Karmody AM. Intravascular thrombosis of abdominal aortic aneurysms in high-risk patients. Vasc Diag Therapy 1981; Dec/ Jan: p. 24. Texas Heart Institute Journal 371