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Immediate Complications Following Abdominal Aortic Surgery
Immediate Complications Following Abdominal Aortic Surgery GEORGE E. WANTZ, M.D., F.A.C.S.* PETER M. GUIDA, M.D. ** S. W. MOORE, M.D., F.A.C.S.***
Some immediate postoperative complications of abdominal aortic surgery are common to all major surgical procedures; others, however, are unique. The latter differ from the former in that they are usually especially serious since, involving the cardiovascular system, they endanger both life and limb. Patients undergoing aortic surgery are likely to have generalized arteriosclerosis and their margin of safety is therefore reduced. The surgeon, if he intends to carry these patients through their operative procedures with a minimum of risk and discomfort, must be ever mindful of every possible complication and must diligently insure their precision management. Only by so doing will the mortality and morbidity be reduced.
INJURY TO ADJACENT STRUCTURES
Injury to the inferior vena cava, the iliac veins or the lumbar veins during resection of the abdominal aorta may cause troublesome and profuse hemorrhage. Often a dense, adhesive, arteriosclerotic inflammatory process binds the aortic bifurcation and bifurcation of the inferior vena cava together. Generally, however, the proximal aorta, just below the From the Department of Surgery, The New York Hospital-Cornell Medical Center, New York, New York * Clinical Associate Professor of Surgery, Cornell University Medical College; Associate Attending Surgeon, The New York Hospital ** Research Associate, Cornell University Medical College; Surgeon to Outpatients, The New York Hospital *** Clinical Professor of Surgery, Cornell University Medical College; Attending Surgeon, The New York Hospital
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Table 1. Immediate Complications in 118 Unselected Patients Undergoing Abdominal Aortic Surgery at the New York Hospital-Cornell Medical Center* NO. COMPLICATIONSt
Renal failure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 10 Retroperitoneal hemorrhage. . . . . . . . . . . . . . . . . . . . . . . . . . . .. 5 Hemorrhage from ruptured aortic aneurysm.. . . . . . . . . . . . .. 3 Bleeding marginal ulcer. . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Myocardial infarction. . . . . . . . . . . . . . . . . . . . . . . . . . . .. 5 Cardiac arrhythmia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 1 Infected aortic prosthesis or homograft. . . . . . . . . . . . . . . . . .. 2 Wound infection........ . ... .. ..... . .... ... . ........ ... 3 Furunculosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 1 Thrombophlebitis, lower extremities. . . . . . . . . . . . . . . . . . . 8 Thrombophlebitis with pulmonary infarction. . . . . . . . . . . . .. 2 Acute cystitis and urethritis.. . . . . . . . . . . . . . . . . . . 12 Thrombosis of distal artery. . . . . . . . . . . . . . . . . . . . . . . . . . . .. 2 Thrombosis of arterial prosthesis or homograft. . . . . . . . 6 Pneumonia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Ischemic colitis with rectal stricture. . . . . . . . . . . . . . . . 1 Bladder and rectal incontinence.... . . . . . . . . . . . . . . . . . . . . .. 1 Mental disturbances.... . . . . . . .......... . . . . . . .. 2 TOTAL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
NO. DEATHS
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1
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* Includes operations for aorto-iliac occlusive disease, abdominal aortic aneurysms and ruptured aortic aneurysms. t The 67 complications occurred in 58 patients. renal arteries, can easily be encircled since it is usually not adherent to the inferior vena cava. However, there is frequently an extra large lumbar vein passing under the aorta a short distance below the renal arteries, which may also be adherent to the arteriosclerotic aorta and can be inadvertently lacerated. Before dissecting the proximal aorta, the left renal vein should always be identified since in about 4 per cent of patients it passes posterior to the aorta and, if its posterior position is not recognized, it may be injured. Freeing the aortic bifurcation may be especially difficult, and even with the greatest of care the inferior vena cava or one of the common iliac veins may be torn. If this occurs, the laceration should be repaired with one or two figure-of-8 sutures of arterial silk. The repair will be simplified if the laceration is excluded by a clamp which partially occludes the vein. Injury to the common iliac veins and inferior vena cava can be minimized if blind instrumentation is avoided, dissection is confined to the subadventitial layer, and the distal common iliac arteries or even the external iliac arteries are mobilized first. Then, after dividing the iliac arteries, excision of the aneurysm can be facilitated by reflecting it upward as the dissection proceeds cephalad. Sometimes even the subadventitial plane is obliterated by the inflammatory process, and cleavage of the fused aortic bifurcation and adjacent veins is impossible. In such instances the aneurysm can be opened and that portion of the arterial wall which is adherent to inferior
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vena cava left behind. All other atheromatous debris, clot and nonviable tissue must be completely extirpated for fear of subsequent infection. The ureters are in intimate contact with the iliac arteries and one or both of them may be displaced laterally by large aneurysms. Rarely, however, are they involved in the arteriosclerotic inflammatory process and their identification and displacement from the operative field, if necessary, is easily accomplished. Injury to the ureter is more likely to occur in the event of a secondary operation for arterial prosthetic failure. By immediately identifying the prosthesis and confining the dissection to it or the subadventitial layer of the involved arteries, the chance of injury to the ureter and adjacent vital vessels will be minimal. Should the ureter be injured, it must be immediately repaired with sutures of 4-0 chromic catgut, the ureteral anastomosis supported, and ureter and renal pelvis decompressed by the limbs of aT-tube. ARTERIAL THROMBOSIS AND PROSTHETIC FAILURE
Thrombosis of the aortic prosthesis or of one of the major distal arteries is one of the most discouraging and serious complications following abdominal aortic surgery. Thrombosis, if unilateral, will endanger the viability of the extremity, and, if bilateral, may be followed by ascending aortic thrombosis and death. There are a variety of ways that this event can come about. One cause of thrombosis of the prosthesis is an inadequate "run-off" in the distal vessels. Patients with diffuse thrombo-obliterative disease in the arteries of the lower extremities, of course, are not candidates for reconstructive aortic surgery; however, segmental occlusion can often be bypassed to insure an adequate outflow tract. The problem is less likely to occur in patients with abdominal aortic aneurysm since their vessels are, in general, universally dilated. However, distal segmental occlusive disease occasionally coexists with aneurysmal dilatation of the aorta, presenting difficult problems if the aneurysm is expanding and requires excision. The state of the distal vessels can be evaluated by arteriography, by direct inspection and palpation, by the degree of retrograde bleeding from a divided iliac artery and by the ease with which saline can be injected lower in that artery. If an obstruction is identified in an iliac artery, it is safer to bypass it by making the distal anastomosis to the side of the external iliac or common femoral arteries in the groin than hope that the "run-off" is adequate. Because such a possibility is ever present, the anterior thighs should always be prepared and draped along with the abdominal operative site. It is probably unwise to make the distal anastomosis to the popliteal artery at the same time as the insertion of an aortic prosthesis. However, this may be necessary in the rare event that the superficial femoral arteries are occluded and "run-off" into the deep femoral and internal iliac arteries is insufficient.
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Another cause for graft failure is spontaneous thrombosis in the distal vessels during aortic occlusion when the blood within these vessels lies relatively dormant. This usually can be avoided by periodically filling the distal vessels with a dilute heparin-saline solution (10,000 units of heparin per liter of saline), avoiding undue prolonged occlusion of the arteries, and making sure that good retrograde bleeding occurs before the distal anastomoses are completed. The period of occlusion in one of the extremities can be shortened advantageously by re-establishing blood flow to it while the anastomosis to the other is being completed. Should clots form in the distal vessels, however, they can be extracted by suction through a catheter passed gently down the vessels; this is aided by massage of the thigh and groin. Thrombosis of the graft may occur secondary to a hinged flap of intima which, by projecting into the vessel, either occludes it or acts as a nidus on which a thrombus forms. Disruption and fracture of the intima may occur when the occluding clamps are applied too tightly. Resumption of blood flow then dissects the intima from the media, creating a hinged flap. In such an instance, an additional segment of iliac artery should be resected and the anastomosis made at a healthier site. The same event can occur following endarterectomy and can be prevented by avoiding blind endarterectomies, continuing an endarterectomy to a point where there is normal appearing intima, and suturing the intima to the media. Less frequent causes of prosthetic graft failure are related to technique. A poorly constructed anastomosis can result in partial constriction of the artery with the possibility of thrombosis. Accordion-pleated prostheses should be stretched fairly taut or else buckling and kinking will occur either immediately or months later as the effects of blood pressures and blood flow tend to straighten out the pleats and elongate the prosthesis. Another error often committed by novices is making the aortic limb of the prosthesis too long, thereby causing a widening of the limbs of the bifurcation and kinking at the origin of each limb of the prosthesis. The aortic portion of the prosthesis should be short so that there is a narrow angle made by the limb of the bifurcation.
HEMORRHAGE Hemorrhage can occur from anyone of the arterial anastomoses, through pores in the arterial prosthesis, or from untied vessels. Usually an arterial anastomosis will leak upon release of the occluding clamps. Such hemorrhage usually ceases promptly upon the application of light pressure with a saline gauze, Gelfoam or hemostatic sponges. If the bleeding is excessive, one or more interrupted or figure-of-8 anastomotic sutures may be required. Leaky anastomoses can be avoided by accurately trimming
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and matching the prosthesis to size to prevent pleating and buckling of the anastomotic line, avoiding wide distances (more than 2 mm.) between bites of the suture, and maintaining an even tension to avoid slack in the continuous suture so that the anastomosis does not loosen excessively upon resumption of blood flow. It is advisable to make sure that the aortic anastomosis is leak-proof before proceeding to the distal anastomoses; the posterior aspect of the aortic anastomosis may otherwise be difficult to visualize and repair when the aortic prosthesis is held in position by a completed distal anastomosis. Even then, hemorrhage from the posterior suture line of the aortic anastomosis may be particularly distressing since this part of the aorta is frequently quite thin and is susceptible to laceration if the needle and sutures are not passed through with care. Placing the sutures in the posterior wall is facilitated if the pair of lumbar arteries just below the renal arteries are divided. Hardly ever is there any difficulty with the control of hemorrhage from the anterior portion of the aortic anastomosis or from the distal anastomosis since both are accessible. Hemorrhage through the pores of a woven aortic prosthesis is rarely a problem. Only a few drops of blood exude through the pores of the woven Teflon prosthesis when blood flow is resumed. Considerable hemorrhage may occur, however, through the pores of knitted prostheses and through defects in the material of any type of prosthesis. Defective prostheses, of course, should not be used, or, if the defects are small, they can be repaired with one or more Dacron sutures. Woven prostheses can be preclotted with 5 to 10 cc. of blood. If there is still significant bleeding after pre-clotting, the occluding clamps should be reapplied for one minute. This process should be repeated as often as necessary until the bleeding ceases. However, to leave the occluding clamps on longer than one minute risks the possibility of a thrombus developing in the stagnant blood sequestrated within the graft. All bleeding vessels should, of course, be ligated. Particular attention should be paid to securing the lumbar arteries as encountered and identifying the lumbar veins in the dissection of the aortic aneurysm. Large, unligated vessels may go unrecognized while the occluding clamps are in place, only to cause life-endangering hemorrhage after the resumption of blood flow, either immediately or in the early postoperative period. Hemorrhage into the loose tissues of the retroperitoneal space can also follow overanticoagulation or the premature use of anticoagulant drugs in the postoperative period. Generally anticoagulation is not indicated in patients with aneurysmal disease, but sometimes this state may be advisable in patients with occlusive disease or in patients who sustain postoperative myocardial infarctions, cerebral thromboses or thrombophlebitis. If anticoagulant drugs are indicated following abdominal aortic surgery, the safest policy is to permit at least 36 hours to elapse before the full levels of therapeutic anticoagulation are reached.
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RENAL FAILURE Renal failure is a fairly common and an especially serious complication of abdominal aortic surgery.2 It occurred in 8.5 per cent of our patients, with a mortality of 90 per cent. This figure includes patients who were operated upon for ruptured abdominal aortic aneurysms, in whom there is a notoriously high frequency of renal failure. Renal insufficiency, as manifested by oliguria for one to a few days postoperatively, is an even more frequent complication than renal failure. In many instances the etiology of the renal failure can be attributed to one or more of such well known causes as hemorrhage, hypotension, transfusion reactions, or trauma. These causes of renal failure may occur during or after any operative procedure of the magnitude of abdominal aortic resections, but they are very likely to induce renal failure in the patients underoing aortic surgery since they, with their generalized arteriosclerosis, tend to have diminished renal reserve and function from nephrosclerosis. While nephrotoxic causes are not likely to be present in these patients, the problem of renal failure can be magnified if the patient develops gangrene of an extremity. The massive necrosis of the gangrene, in a manner similar to crush injuries, may directly cause and most certainly aggravate renal dysfunction. The most common cause of the ischemia which produces renal failure is infarction. This was present in 78.8 per cent of the patients who died from renal failure. This may be the result of ascending aortic thrombosis due to inadequate "run-off." Usually, however, it is specifically related to the aortic surgery and is due to cross-clamping the abdominal aorta below the origin of the renal arteries. The aortic occluding clamps may fracture atheromas with the result that liberated atheromatous debris along with any clots that have formed on the galled atheromatous plaques or in the blind aortic pouch is churned and then whirled into the renal arteries. The renal arteries and their major branches may even be patent and the cause of the infarction not apparent unless the kidney is studied histologically. In these instances the renal arterioles are plugged by embolic cholesterol crystals. There is also always a danger of atheromatous debris and clots emboli zing to the renal arteries as well as the creation of a hinge flap of renal arterial intima when an endarterectomy in aortic occlusive disease must be continued upward and beyond the renal arteries. Temporary occlusion of the renal arteries is advisable under these circumstances. Excessive manipulation of the renal arteries should be avoided since this may induce thrombosis. Kidneys do not tolerate prolonged ischemia. If severe hypotension is a possibility, or if occlusion of the renal arteries, either directly or indirectly by cross-clamping the aorta above their origin in excess of 30 minutes, is anticipated, hypothermia should be induced, which will prolong the safe period of renal ischemia. Although disputed by some investigators,4 there is some evidence5 to indicate that cross-clamping the aorta causes diminished plasma renal flow and dimin-
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ished renal function. This has been attributed to a renovascular reflex since in experimental animals the effect is abolished by ganglionic blocking agents and by the infiltration of a local anesthetic into the renal pedicle. In man, oliguria invariably accompanies and follows for a short period thereafter the occlusion of the aorta below the renal vessels. In combination with the other factors, this reflex renal insufficiency may be important as a cause of renal failure. Since renal failure carries a grave prognosis, every effort should be made to prevent its possible causes from developing. Irredeemable gangrenous extremities should be amputated early; blood loss should be determined accurately and replaced with carefully cross-matched and compatible whole blood; and blood loss should be kept at a minimum to avoid the danger attendant upon the administration of multiple transfusions. Hypotension should be diligently prevented, even momentary hypotension being sufficient at times to cause irreversible renal failure. Vasopressor drugs, however, should be used with caution, since they will only further reduce renal blood flow while falsely producing a sense of security by elevating systemic blood pressure. Hypovolemia and hypotension can develop when circulation is restored to the extremities. This is a critical moment since not only may the kidneys be adversely affected, but thromboses of the coronary and cerebral vessels may also occur. The occluding clamps should, therefore, always be removed very slowly to permit sufficient time for the circulatory system and blood volume to readjust. Usually the administration of a unit of blood is advisable at this moment. The intravenous administration of mannitol during and immediately after the operation has been advocated as a means of enhancing or maintaining renal plasma flow and glomerular filtration and reducing the oliguria which occurs with aortic cross-clamping. 1 Mannitol, like urea, is an osmotic diuretic. It is more efficient than urea and, of course, will not cause misleading elevations of blood urea nitrogen. Our experience with the use of mannitol or urea has been minimal and we have not routinely used either one. Of course, the operative procedure should proceed expeditiously to avoid prolonged aortic occlusion. Aortic occlusion clamps should be applied decisively, only once if possible, and never too tightly. Debris should be flushed from the blind aortic pouch and prolonged aortic occlusion avoided by re-establishing circulation to one of the extremities while the other distal anastomosis is completed. The treatment of renal insufficiency and renal failure is beyond the scope of this discussion. Usually renal insufficiency responds to conservative management. Frank renal failure often requires repeated and frequent dialyses. Prompt renal arterial embolectomy or thrombectomy is indicated if renal arterial occlusion is the cause of renal failure. An arteriogram will make the diagnosis if the condition is suspected. Unfortunately there is
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usually also parenchymal arterial thrombosis and embolization and the kidneys may, therefore, be irretrievable. THROMBOPHLEBITIS
Deep thrombophlebitis is an especially common complication of abdominal aortic surgery. It occurred in 8.5 per cent of our patients. Thrombophlebitis is a potentially serious complication because of the ever present danger of pulmonary embolism and because the patient may be disabled by subsequent development in the lower extremities of pain, varicose veins, brawny edema, stasis dermatitis and stasis ulcerations. The etiology of the thrombophlebitis is probably related to bed rest, inactivity, venous stagnation and the increased coaguability of the blood following the stress of the surgical procedure. Perhaps the unavoidable manipulation and trauma of the inferior vena cava, the iliac veins or other venous tributaries may contribute to its development. There is no certain prophylaxis for thrombophlebitis, although early active motion of the lower extremities and early ambulation, provided they are not contraindicated, are probably helpful. Compressive bandages will also aid in preventing venous stagnation and should always be applied to postoperative patients who have simple varicose veins. The manifestations of thrombophlebitis are pain and tenderness along the course of the inflamed vein, edema of the involved extremity and a low-grade fever. Ambulatory patients often call the surgeon's attention to it by complaining of a pain or cramp in their legs. Sometimes a pulmonary infarction is the first indication of a deep thrombophlebitis, especially when the thrombophlebitis is restricted to the pelvic veins or the inflammatory element is otherwise minimal. Superficial thrombophlebitis in the lower extremities is also a frequent complication. It usually is secondary to prolonged intravenous canalization of one of the saphenous veins. Intravenous fluids and drugs are administered preferably in the veins of the upper extremities rather than in the veins of the lower extremities. Superficial thrombophlebitis is readily recognizable and generally is not a serious complication, although it may become serious by extending into the deep veins of the lower extremity. In general, deep thrombophlebitis readily responds to anticoagulation and bed rest. The extremity should be elevated and wrapped with elastic compressive bandages to control the edema, compress the superficial veins, and promote venous circulation. Moist heat, provided arterial circulation is adequate, is also sometimes beneficial, although it almost always is curiously accompanied by furunculosis. Superficial phlebitis resolves quickly without bed rest, elevation or other adjunctive therapy, by the simple procedure of wrapping the extremity evenly with an adherent compressive bandage such as Elastoplast. Venous thrombectomy may at times be
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indicated, especially if there have been multiple pulmonary emboli. Thrombectomy is preferable to ligation of the superficial femoral vein since the thrombophlebitis may involve the veins of the pelvis. It may also be preferable to ligation of the inferior vena cava since the latter procedure may be difficult to execute after aortic resection and since it is regularly followed by severe postphlebitic lower extremities.
INTESTINAL ISCHEMIA Intestinal ischemia, fortunately, is an uncommon complication following abdominal aortic surgery.6 Usually collateral circulation through the marginal artery of Drummond is adequate to supply the sigmoid and the rectum after the inferior mesenteric artery is interrupted. Indeed, the inferior mesenteric artery is more often occluded than patent, allowing the rectum and colon to become dependent on the internal iliac and marginal arteries for their blood supply. However, if the collateral arteries are underdeveloped and it is necessary to sacrifice both internal iliac arteries, ischemic colitis and proctitis may very likely ensue. While it is not always possible to preserve even one of the internal iliac arteries, the incidence of intestinal ischemia can be minimized by avoiding trauma to the left colonic and sigmoid arterial arcades, by employing retractors gently, and by dividing the inferior mesenteric artery as close as is feasible to the aorta before any of its branches arise. The latter is especially important if the main stem of the inferior mesenteric artery is patent and contains a pulse. The manifestations of ischemic colitis and proctitis are protean. It may begin at any time during the postoperative period and last for only one to two days or persist for many weeks. Sometimes the only evidence of its presence is mild left lower quadrant pain with perhaps several episodes of diarrhea. At other times the gangrenous bowel develops suddenly with classical and unmistakable signs and symptoms. Often the clinical picture resembles either pseudomembranous enterocolitis or ulcerative colitis and consists of a protracted period of bloody diarrhea, abdominal cramps and tenderness, leukocytosis and fever. The diagnosis can be confirmed by sigmoidoscopy and barium enema. In the former the bowel will appear cyanotic early, with obvious ulcerations apparent later. In the latter examination mUltiple lesions resembling ulcerative colitis are typical. There is no specific remedy for this complication. Rarely is it possible to restore or increase circulation to the ischemic bowel since the arteries supplying it are too small and too arteriosclerotic. Gangrenous bowel of course requires immediate resection. However, less severe cases may resolve with conservative management. The bowel should be placed at rest by a clear liquid diet and infection controlled by antibiotics. The outcome, however, is unpredictable and the ischemic colitis and proctitis
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may at any time progress to gangrene. While mild cases usually heal completely without residual stigmata, those with more severe involvement terminate with strictures which, if symptomatic, will require additional surgery. If conservative management is pursued, the patient must be observed closely so that an immediate laparotomy can be carried out should it become necessary.
ISCHEMIC NEUROLOGIC COMPLICATIONS Ischemic neurologic complications following infrarenal aortic surgery are very rare. We have observed only one patient in whom urinary and rectal incontinence developed after resection of an abdominal aortic aneurysm. Others,a however, have reported a variety of motor, sensory and reflex deficits varying from mild vesicorectal disturbance to paraplegia and loss of sensation extending to the level of the umbilicus. In some instances, the neurologic complications are the result of ischemia to the peripheral nerves, due either to thrombosis of a distal artery, to thrombosis of the prosthesis, or to prolonged aortic occlusion. Peripheral nerves are extremely susceptible to hypoxia and ischemic neuropathy may develop quickly and in the acsence of other evidences of arterial occlusion. Probably most of the reported neurologic complications are due to spinal cord damage. The spinal cord ends at the level of the first lumbar vertebra and its principal blood supply is derived from branches of the aorta arising above the renal arteries. Consequently, the spinal cord is protected from infrarenal aortic occlusion. Nevertheless, anatomic studies have shown that the major radicular artery, which is vital for the blood supply of the spinal cord, may arise from one of the first or second lumbar arteries instead of the usual site in the lower thoracic aorta. In such cases and in the absence of adequate collateral circulation, irreparable damage to the spinal cord can follow infrarenal aortic resection.
INFECTION
Infection of an aortic prosthesis, of an arteriotomy or of an arterial anastomosis is obviously a very hazardous complication of aortic surgery. Such infections are manifested by septicemia, septic emboli to one or both of the lower extremities, fever, chills and malaise. Localizing signs, however, are often minimal unless the infection is superficial, as in the groin. Infection of an arteriotomy or of an arterial anastomosis interferes with healing, and infected hematomas or serious hemorrhage are inevitable consequences. Even after drainage and repair of the arteries, breakdown of the suture margin often recurs because of continued infection or the inability of the arterial sutures to hold. Infected arteries become friable, soft, and their vasa vasorum may be thrombosed; indeed they are often nonviable, which contributes to some of the difficulties attending this complication. The most efficient and safest method of eradicating such an infection is to evacuate the pus, to ligate the involved artery in a healthy site, and to drain the infected area. However, the viability of the corresponding
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extremity will be jeopardized unless a developed collateral circulation pre-exists as a result of underlying occlusive aortic disease for which the aortic surgery was performed. When the aortic surgery is for aneurysmal disease, collateral circulation will be inadequate. To preserve the extremity in these circumstances it is often necessary, in addition, to bypass the infected area completely with a prosthetic graft placed preferably in a noninfected area. Infection within or surrounding an interpolated aortic bifurcation prosthesis presents an even more difficult problem. Fortunately aortic prosthetic grafts will continue to function for many months without rejection and extrusion by the host because they are composed of such inert and nonreactive materials that they induce little, if any, foreign body reaction. Consequently, an infected prosthesis may lie relatively indolent and may not be immediately obvious for weeks, even though the infection may have begun in the early postoperative period. Nevertheless the prosthesis is a foreign body which will perpetuate the infection until it is removed completely. Because a new prosthesis must be inserted immediately in the bed of the old one, it is important that pus be evacuated, infected and necrotic tissues excised and the new prosthesis sutured with Dacron to freshened and viable arterial walls. In every instance the organism should be identified and massive quantities of the appropriate antibiotic administered preoperatively and for prolonged periods postoperatively. There is no conclusive evidence that the prophylactic postoperative administration of antibiotics reduces the incidence of infection and for several years now we have not routinely given them to patients undergoing aortic surgery unless they develop an infection. Rather, every effort should be made at reducing the possibility of a potentially catastrophic infection by meticulous and careful surgical technique, by the avoidance of hematomas and necrotic tissue and, above all, by the complete extirpation of all atheromatous debris, clot and nonviable arteriosclerotic arterial wall when for technical reasons the aneurysm has been opened. Wound infections are usually dw') to a hemolytic Staphylococcus aureus. They present no special problem but should be treated promptly and adequately so that the infection does not spread nor metastasize to the prosthesis.
OTHER GENERAL COMPLICATIONS Cardiac complications are serious and are fairly common after abdominal aortic surgery. This is not surprising since these patients with their advanced arteriosclerosis tend also to have coronary and cerebral arterial disease, hypertension, or significant cardiac arrhythmia; indeed, many will have already sustained myocardial infarctions while others may be taking digitalis preparations or other cardiac drugs. Thus, every effort should be
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made to avoid states which are conducive to myocardial damage. Deep planes of anesthesia are inadvisable. Hypoxia, hypovolemia and hypotension should be strictly prevented, since their momentary occurrence is all that is necessary to cause cardiac arrhythmia, cardiac arrest or myocardial infarction. Likewise, hypervolemia from excessive blood and fluid replacement must be carefully avoided for fear of inducing pulmonary edema. Dangerous cardiac arrhythmias and myocardial infarctions often originate during or immediately after the operation; consequently, it has been our policy to monitor the electrocardiogram of most of the patients during the operation so that, if required, therapy can be instituted properly. Pulmonary complications are rare despite the fact that many of the patients undergoing aortic surgery are cigarette smokers and will have some degree of pulmonary insufficiency, emphysema and bronchitis. Those patients with advanced pulmonary disease should be carefully prepared for operation by the use of bronchial dilators, expectorants, the cessation of smoking, postural drainage and antibiotics. Sedatives and other respiratory depressants should be used sparingly after the operation. Abdominal binders will permit the patient to cough more efficiently and aerosol therapy will loosen tenacious bronchial secretions. Tracheal suctions will help by aspirating secretions and stimulating the patient's cough reflex. If atelectasis nevertheless occurs and secretions cannot be eliminated by conservative measures, bronchoscopy or tracheostomy may be indicated. Pneumonia generally will respond to antibiotic therapy and other conventional measures. Oxygen therapy is sometimes necessary and the use of a positive pressure demand-assist respirator will aid ventilation. Pyuria from acute urethritis and cystitis inevitably follows prolonged use of a urinary catheter. While it is not always possible or even advisable not to employ a urethral catheter, its use should never be extended unnecessarily. Periodic irrigations of the bladder with saline or various antiseptic solutions are ineffective in the prevention of this complication and, although frequently recommended, they are a waste of time and may actually introduce infection. Mental abnormalities developed in two of our patients and consisted of periods of disorientation and confusion which lasted one week. Such disturbances are not unlikely in any elderly patient who undergoes a major surgical procedure, but they are usually only transient and subside spontaneously. Sedatives, especially the barbiturates, can cause bizarre mental behavior in older patients and, if used, should be administered cautiously. I Finally paralytic ileus, wound dehiscence and gastrointestinal hemorrhage are always possible complications. The prevention of paralytic ileus, like its treatment, consists of gastrointestinal decompression via a nasogastric tube. Peristalsis always ceases for a variable period following major abdominal operations.~The period of bowel inactivity, however, will be shortened if the bowel is handled gently and oral fluids are not reinstituted I
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prematurely. JVound dehiscence should be treated by immediate resuture. Even when healing is delayed and tension on the wound is increased by abdominal distention and coughing, the incidence of wound dehiscence will be minimized if the wound is closed meticulously in layers with nonabsorbable sutures, and with enough stay sutures to reduce strain on the suture line. Any major operation can induce acute peptic ulcers and exacerbate those that are long-standing and chronic. Hemorrhage from these stress ulcers is always serious, and fatal exsanguination common. Thus it is generally safer to intervene surgically than to manage the hemorrhage expectantly by conservative means.
REFERENCES 1. Barry, K. G., Cohen, A., Knochel, J. P., Whelan, T. J., Jr., Beisel, W. R., Vargas, C. A. and LeBlanc, P. C., Jr.: Mannitol infusion: II. Prevention of acute functional renal failure during resection of aneurysm of abdominal aorta. New England J. Med. 264: 967, 1961. 2. Doolan, P. D., Wiggins, R. A., Thiel, G. B., Lee, K. J. and Martinez, E.: Acute renal insufficiency after aortic surgery. Am. J. Med. 28: 895, 1960. 3. Mehrez, I. 0., Nabseth, D. C., Hogan, E. L. and Deterling, R. A., Jr.: Paraplegia following resection of abdominal aortic aneurysm. Ann. Surg. 156: 890, 1962. 4. Mowlem, A., McClintock, J. T. and Campbell, G. S.: Effect on renal function of occlusion of aorta inferior to renal vessels. Surg. Gynec. & Obst. 111: 423, 1960. 5. Whitley, J. E., Witcofski, R. L., Feltz, J. H. and Meschan, I.: Investigation of renal complications of aortic clamping. Surgery 50: 673, 1961. 6. Young, J. R., Humphries, A. W., deWolfe, V. G. and LeFevre, F A.: Complications of abdominal aortic surgery. II. Intestinal ischemia. A.M.A. Arch. Surg. 86: 51. 1963. 525 East 68th Street New York, N. Y.
Some immediate postoperative complications of abdominal aortic surgery are common to all major surgical procedures; others, however, are unique. The latter differ from the former in that they are usually especially serious since, involving the cardiovascular system, they endanger both life and limb. Patients undergoing aortic surgery are likely to have generalized arteriosclerosis and their margin of safety is therefore reduced. The surgeon, if he intends to carry these patients through their operative procedures with a minimum of risk and discomfort, must be ever mindful of every possible complication and must diligently insure their precision management. Only by so doing will the mortality and morbidity be reduced.
INJURY TO ADJACENT STRUCTURES
Injury to the inferior vena cava, the iliac veins or the lumbar veins during resection of the abdominal aorta may cause troublesome and profuse hemorrhage. Often a dense, adhesive, arteriosclerotic inflammatory process binds the aortic bifurcation and bifurcation of the inferior vena cava together. Generally, however, the proximal aorta, just below the From the Department of Surgery, The New York Hospital-Cornell Medical Center, New York, New York * Clinical Associate Professor of Surgery, Cornell University Medical College; Associate Attending Surgeon, The New York Hospital ** Research Associate, Cornell University Medical College; Surgeon to Outpatients, The New York Hospital *** Clinical Professor of Surgery, Cornell University Medical College; Attending Surgeon, The New York Hospital
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Table 1. Immediate Complications in 118 Unselected Patients Undergoing Abdominal Aortic Surgery at the New York Hospital-Cornell Medical Center* NO. COMPLICATIONSt
Renal failure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 10 Retroperitoneal hemorrhage. . . . . . . . . . . . . . . . . . . . . . . . . . . .. 5 Hemorrhage from ruptured aortic aneurysm.. . . . . . . . . . . . .. 3 Bleeding marginal ulcer. . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Myocardial infarction. . . . . . . . . . . . . . . . . . . . . . . . . . . .. 5 Cardiac arrhythmia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 1 Infected aortic prosthesis or homograft. . . . . . . . . . . . . . . . . .. 2 Wound infection........ . ... .. ..... . .... ... . ........ ... 3 Furunculosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 1 Thrombophlebitis, lower extremities. . . . . . . . . . . . . . . . . . . 8 Thrombophlebitis with pulmonary infarction. . . . . . . . . . . . .. 2 Acute cystitis and urethritis.. . . . . . . . . . . . . . . . . . . 12 Thrombosis of distal artery. . . . . . . . . . . . . . . . . . . . . . . . . . . .. 2 Thrombosis of arterial prosthesis or homograft. . . . . . . . 6 Pneumonia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Ischemic colitis with rectal stricture. . . . . . . . . . . . . . . . 1 Bladder and rectal incontinence.... . . . . . . . . . . . . . . . . . . . . .. 1 Mental disturbances.... . . . . . . .......... . . . . . . .. 2 TOTAL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
NO. DEATHS
9 4 3 1 4
1
22
* Includes operations for aorto-iliac occlusive disease, abdominal aortic aneurysms and ruptured aortic aneurysms. t The 67 complications occurred in 58 patients. renal arteries, can easily be encircled since it is usually not adherent to the inferior vena cava. However, there is frequently an extra large lumbar vein passing under the aorta a short distance below the renal arteries, which may also be adherent to the arteriosclerotic aorta and can be inadvertently lacerated. Before dissecting the proximal aorta, the left renal vein should always be identified since in about 4 per cent of patients it passes posterior to the aorta and, if its posterior position is not recognized, it may be injured. Freeing the aortic bifurcation may be especially difficult, and even with the greatest of care the inferior vena cava or one of the common iliac veins may be torn. If this occurs, the laceration should be repaired with one or two figure-of-8 sutures of arterial silk. The repair will be simplified if the laceration is excluded by a clamp which partially occludes the vein. Injury to the common iliac veins and inferior vena cava can be minimized if blind instrumentation is avoided, dissection is confined to the subadventitial layer, and the distal common iliac arteries or even the external iliac arteries are mobilized first. Then, after dividing the iliac arteries, excision of the aneurysm can be facilitated by reflecting it upward as the dissection proceeds cephalad. Sometimes even the subadventitial plane is obliterated by the inflammatory process, and cleavage of the fused aortic bifurcation and adjacent veins is impossible. In such instances the aneurysm can be opened and that portion of the arterial wall which is adherent to inferior
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vena cava left behind. All other atheromatous debris, clot and nonviable tissue must be completely extirpated for fear of subsequent infection. The ureters are in intimate contact with the iliac arteries and one or both of them may be displaced laterally by large aneurysms. Rarely, however, are they involved in the arteriosclerotic inflammatory process and their identification and displacement from the operative field, if necessary, is easily accomplished. Injury to the ureter is more likely to occur in the event of a secondary operation for arterial prosthetic failure. By immediately identifying the prosthesis and confining the dissection to it or the subadventitial layer of the involved arteries, the chance of injury to the ureter and adjacent vital vessels will be minimal. Should the ureter be injured, it must be immediately repaired with sutures of 4-0 chromic catgut, the ureteral anastomosis supported, and ureter and renal pelvis decompressed by the limbs of aT-tube. ARTERIAL THROMBOSIS AND PROSTHETIC FAILURE
Thrombosis of the aortic prosthesis or of one of the major distal arteries is one of the most discouraging and serious complications following abdominal aortic surgery. Thrombosis, if unilateral, will endanger the viability of the extremity, and, if bilateral, may be followed by ascending aortic thrombosis and death. There are a variety of ways that this event can come about. One cause of thrombosis of the prosthesis is an inadequate "run-off" in the distal vessels. Patients with diffuse thrombo-obliterative disease in the arteries of the lower extremities, of course, are not candidates for reconstructive aortic surgery; however, segmental occlusion can often be bypassed to insure an adequate outflow tract. The problem is less likely to occur in patients with abdominal aortic aneurysm since their vessels are, in general, universally dilated. However, distal segmental occlusive disease occasionally coexists with aneurysmal dilatation of the aorta, presenting difficult problems if the aneurysm is expanding and requires excision. The state of the distal vessels can be evaluated by arteriography, by direct inspection and palpation, by the degree of retrograde bleeding from a divided iliac artery and by the ease with which saline can be injected lower in that artery. If an obstruction is identified in an iliac artery, it is safer to bypass it by making the distal anastomosis to the side of the external iliac or common femoral arteries in the groin than hope that the "run-off" is adequate. Because such a possibility is ever present, the anterior thighs should always be prepared and draped along with the abdominal operative site. It is probably unwise to make the distal anastomosis to the popliteal artery at the same time as the insertion of an aortic prosthesis. However, this may be necessary in the rare event that the superficial femoral arteries are occluded and "run-off" into the deep femoral and internal iliac arteries is insufficient.
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Another cause for graft failure is spontaneous thrombosis in the distal vessels during aortic occlusion when the blood within these vessels lies relatively dormant. This usually can be avoided by periodically filling the distal vessels with a dilute heparin-saline solution (10,000 units of heparin per liter of saline), avoiding undue prolonged occlusion of the arteries, and making sure that good retrograde bleeding occurs before the distal anastomoses are completed. The period of occlusion in one of the extremities can be shortened advantageously by re-establishing blood flow to it while the anastomosis to the other is being completed. Should clots form in the distal vessels, however, they can be extracted by suction through a catheter passed gently down the vessels; this is aided by massage of the thigh and groin. Thrombosis of the graft may occur secondary to a hinged flap of intima which, by projecting into the vessel, either occludes it or acts as a nidus on which a thrombus forms. Disruption and fracture of the intima may occur when the occluding clamps are applied too tightly. Resumption of blood flow then dissects the intima from the media, creating a hinged flap. In such an instance, an additional segment of iliac artery should be resected and the anastomosis made at a healthier site. The same event can occur following endarterectomy and can be prevented by avoiding blind endarterectomies, continuing an endarterectomy to a point where there is normal appearing intima, and suturing the intima to the media. Less frequent causes of prosthetic graft failure are related to technique. A poorly constructed anastomosis can result in partial constriction of the artery with the possibility of thrombosis. Accordion-pleated prostheses should be stretched fairly taut or else buckling and kinking will occur either immediately or months later as the effects of blood pressures and blood flow tend to straighten out the pleats and elongate the prosthesis. Another error often committed by novices is making the aortic limb of the prosthesis too long, thereby causing a widening of the limbs of the bifurcation and kinking at the origin of each limb of the prosthesis. The aortic portion of the prosthesis should be short so that there is a narrow angle made by the limb of the bifurcation.
HEMORRHAGE Hemorrhage can occur from anyone of the arterial anastomoses, through pores in the arterial prosthesis, or from untied vessels. Usually an arterial anastomosis will leak upon release of the occluding clamps. Such hemorrhage usually ceases promptly upon the application of light pressure with a saline gauze, Gelfoam or hemostatic sponges. If the bleeding is excessive, one or more interrupted or figure-of-8 anastomotic sutures may be required. Leaky anastomoses can be avoided by accurately trimming
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and matching the prosthesis to size to prevent pleating and buckling of the anastomotic line, avoiding wide distances (more than 2 mm.) between bites of the suture, and maintaining an even tension to avoid slack in the continuous suture so that the anastomosis does not loosen excessively upon resumption of blood flow. It is advisable to make sure that the aortic anastomosis is leak-proof before proceeding to the distal anastomoses; the posterior aspect of the aortic anastomosis may otherwise be difficult to visualize and repair when the aortic prosthesis is held in position by a completed distal anastomosis. Even then, hemorrhage from the posterior suture line of the aortic anastomosis may be particularly distressing since this part of the aorta is frequently quite thin and is susceptible to laceration if the needle and sutures are not passed through with care. Placing the sutures in the posterior wall is facilitated if the pair of lumbar arteries just below the renal arteries are divided. Hardly ever is there any difficulty with the control of hemorrhage from the anterior portion of the aortic anastomosis or from the distal anastomosis since both are accessible. Hemorrhage through the pores of a woven aortic prosthesis is rarely a problem. Only a few drops of blood exude through the pores of the woven Teflon prosthesis when blood flow is resumed. Considerable hemorrhage may occur, however, through the pores of knitted prostheses and through defects in the material of any type of prosthesis. Defective prostheses, of course, should not be used, or, if the defects are small, they can be repaired with one or more Dacron sutures. Woven prostheses can be preclotted with 5 to 10 cc. of blood. If there is still significant bleeding after pre-clotting, the occluding clamps should be reapplied for one minute. This process should be repeated as often as necessary until the bleeding ceases. However, to leave the occluding clamps on longer than one minute risks the possibility of a thrombus developing in the stagnant blood sequestrated within the graft. All bleeding vessels should, of course, be ligated. Particular attention should be paid to securing the lumbar arteries as encountered and identifying the lumbar veins in the dissection of the aortic aneurysm. Large, unligated vessels may go unrecognized while the occluding clamps are in place, only to cause life-endangering hemorrhage after the resumption of blood flow, either immediately or in the early postoperative period. Hemorrhage into the loose tissues of the retroperitoneal space can also follow overanticoagulation or the premature use of anticoagulant drugs in the postoperative period. Generally anticoagulation is not indicated in patients with aneurysmal disease, but sometimes this state may be advisable in patients with occlusive disease or in patients who sustain postoperative myocardial infarctions, cerebral thromboses or thrombophlebitis. If anticoagulant drugs are indicated following abdominal aortic surgery, the safest policy is to permit at least 36 hours to elapse before the full levels of therapeutic anticoagulation are reached.
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RENAL FAILURE Renal failure is a fairly common and an especially serious complication of abdominal aortic surgery.2 It occurred in 8.5 per cent of our patients, with a mortality of 90 per cent. This figure includes patients who were operated upon for ruptured abdominal aortic aneurysms, in whom there is a notoriously high frequency of renal failure. Renal insufficiency, as manifested by oliguria for one to a few days postoperatively, is an even more frequent complication than renal failure. In many instances the etiology of the renal failure can be attributed to one or more of such well known causes as hemorrhage, hypotension, transfusion reactions, or trauma. These causes of renal failure may occur during or after any operative procedure of the magnitude of abdominal aortic resections, but they are very likely to induce renal failure in the patients underoing aortic surgery since they, with their generalized arteriosclerosis, tend to have diminished renal reserve and function from nephrosclerosis. While nephrotoxic causes are not likely to be present in these patients, the problem of renal failure can be magnified if the patient develops gangrene of an extremity. The massive necrosis of the gangrene, in a manner similar to crush injuries, may directly cause and most certainly aggravate renal dysfunction. The most common cause of the ischemia which produces renal failure is infarction. This was present in 78.8 per cent of the patients who died from renal failure. This may be the result of ascending aortic thrombosis due to inadequate "run-off." Usually, however, it is specifically related to the aortic surgery and is due to cross-clamping the abdominal aorta below the origin of the renal arteries. The aortic occluding clamps may fracture atheromas with the result that liberated atheromatous debris along with any clots that have formed on the galled atheromatous plaques or in the blind aortic pouch is churned and then whirled into the renal arteries. The renal arteries and their major branches may even be patent and the cause of the infarction not apparent unless the kidney is studied histologically. In these instances the renal arterioles are plugged by embolic cholesterol crystals. There is also always a danger of atheromatous debris and clots emboli zing to the renal arteries as well as the creation of a hinge flap of renal arterial intima when an endarterectomy in aortic occlusive disease must be continued upward and beyond the renal arteries. Temporary occlusion of the renal arteries is advisable under these circumstances. Excessive manipulation of the renal arteries should be avoided since this may induce thrombosis. Kidneys do not tolerate prolonged ischemia. If severe hypotension is a possibility, or if occlusion of the renal arteries, either directly or indirectly by cross-clamping the aorta above their origin in excess of 30 minutes, is anticipated, hypothermia should be induced, which will prolong the safe period of renal ischemia. Although disputed by some investigators,4 there is some evidence5 to indicate that cross-clamping the aorta causes diminished plasma renal flow and dimin-
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ished renal function. This has been attributed to a renovascular reflex since in experimental animals the effect is abolished by ganglionic blocking agents and by the infiltration of a local anesthetic into the renal pedicle. In man, oliguria invariably accompanies and follows for a short period thereafter the occlusion of the aorta below the renal vessels. In combination with the other factors, this reflex renal insufficiency may be important as a cause of renal failure. Since renal failure carries a grave prognosis, every effort should be made to prevent its possible causes from developing. Irredeemable gangrenous extremities should be amputated early; blood loss should be determined accurately and replaced with carefully cross-matched and compatible whole blood; and blood loss should be kept at a minimum to avoid the danger attendant upon the administration of multiple transfusions. Hypotension should be diligently prevented, even momentary hypotension being sufficient at times to cause irreversible renal failure. Vasopressor drugs, however, should be used with caution, since they will only further reduce renal blood flow while falsely producing a sense of security by elevating systemic blood pressure. Hypovolemia and hypotension can develop when circulation is restored to the extremities. This is a critical moment since not only may the kidneys be adversely affected, but thromboses of the coronary and cerebral vessels may also occur. The occluding clamps should, therefore, always be removed very slowly to permit sufficient time for the circulatory system and blood volume to readjust. Usually the administration of a unit of blood is advisable at this moment. The intravenous administration of mannitol during and immediately after the operation has been advocated as a means of enhancing or maintaining renal plasma flow and glomerular filtration and reducing the oliguria which occurs with aortic cross-clamping. 1 Mannitol, like urea, is an osmotic diuretic. It is more efficient than urea and, of course, will not cause misleading elevations of blood urea nitrogen. Our experience with the use of mannitol or urea has been minimal and we have not routinely used either one. Of course, the operative procedure should proceed expeditiously to avoid prolonged aortic occlusion. Aortic occlusion clamps should be applied decisively, only once if possible, and never too tightly. Debris should be flushed from the blind aortic pouch and prolonged aortic occlusion avoided by re-establishing circulation to one of the extremities while the other distal anastomosis is completed. The treatment of renal insufficiency and renal failure is beyond the scope of this discussion. Usually renal insufficiency responds to conservative management. Frank renal failure often requires repeated and frequent dialyses. Prompt renal arterial embolectomy or thrombectomy is indicated if renal arterial occlusion is the cause of renal failure. An arteriogram will make the diagnosis if the condition is suspected. Unfortunately there is
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usually also parenchymal arterial thrombosis and embolization and the kidneys may, therefore, be irretrievable. THROMBOPHLEBITIS
Deep thrombophlebitis is an especially common complication of abdominal aortic surgery. It occurred in 8.5 per cent of our patients. Thrombophlebitis is a potentially serious complication because of the ever present danger of pulmonary embolism and because the patient may be disabled by subsequent development in the lower extremities of pain, varicose veins, brawny edema, stasis dermatitis and stasis ulcerations. The etiology of the thrombophlebitis is probably related to bed rest, inactivity, venous stagnation and the increased coaguability of the blood following the stress of the surgical procedure. Perhaps the unavoidable manipulation and trauma of the inferior vena cava, the iliac veins or other venous tributaries may contribute to its development. There is no certain prophylaxis for thrombophlebitis, although early active motion of the lower extremities and early ambulation, provided they are not contraindicated, are probably helpful. Compressive bandages will also aid in preventing venous stagnation and should always be applied to postoperative patients who have simple varicose veins. The manifestations of thrombophlebitis are pain and tenderness along the course of the inflamed vein, edema of the involved extremity and a low-grade fever. Ambulatory patients often call the surgeon's attention to it by complaining of a pain or cramp in their legs. Sometimes a pulmonary infarction is the first indication of a deep thrombophlebitis, especially when the thrombophlebitis is restricted to the pelvic veins or the inflammatory element is otherwise minimal. Superficial thrombophlebitis in the lower extremities is also a frequent complication. It usually is secondary to prolonged intravenous canalization of one of the saphenous veins. Intravenous fluids and drugs are administered preferably in the veins of the upper extremities rather than in the veins of the lower extremities. Superficial thrombophlebitis is readily recognizable and generally is not a serious complication, although it may become serious by extending into the deep veins of the lower extremity. In general, deep thrombophlebitis readily responds to anticoagulation and bed rest. The extremity should be elevated and wrapped with elastic compressive bandages to control the edema, compress the superficial veins, and promote venous circulation. Moist heat, provided arterial circulation is adequate, is also sometimes beneficial, although it almost always is curiously accompanied by furunculosis. Superficial phlebitis resolves quickly without bed rest, elevation or other adjunctive therapy, by the simple procedure of wrapping the extremity evenly with an adherent compressive bandage such as Elastoplast. Venous thrombectomy may at times be
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indicated, especially if there have been multiple pulmonary emboli. Thrombectomy is preferable to ligation of the superficial femoral vein since the thrombophlebitis may involve the veins of the pelvis. It may also be preferable to ligation of the inferior vena cava since the latter procedure may be difficult to execute after aortic resection and since it is regularly followed by severe postphlebitic lower extremities.
INTESTINAL ISCHEMIA Intestinal ischemia, fortunately, is an uncommon complication following abdominal aortic surgery.6 Usually collateral circulation through the marginal artery of Drummond is adequate to supply the sigmoid and the rectum after the inferior mesenteric artery is interrupted. Indeed, the inferior mesenteric artery is more often occluded than patent, allowing the rectum and colon to become dependent on the internal iliac and marginal arteries for their blood supply. However, if the collateral arteries are underdeveloped and it is necessary to sacrifice both internal iliac arteries, ischemic colitis and proctitis may very likely ensue. While it is not always possible to preserve even one of the internal iliac arteries, the incidence of intestinal ischemia can be minimized by avoiding trauma to the left colonic and sigmoid arterial arcades, by employing retractors gently, and by dividing the inferior mesenteric artery as close as is feasible to the aorta before any of its branches arise. The latter is especially important if the main stem of the inferior mesenteric artery is patent and contains a pulse. The manifestations of ischemic colitis and proctitis are protean. It may begin at any time during the postoperative period and last for only one to two days or persist for many weeks. Sometimes the only evidence of its presence is mild left lower quadrant pain with perhaps several episodes of diarrhea. At other times the gangrenous bowel develops suddenly with classical and unmistakable signs and symptoms. Often the clinical picture resembles either pseudomembranous enterocolitis or ulcerative colitis and consists of a protracted period of bloody diarrhea, abdominal cramps and tenderness, leukocytosis and fever. The diagnosis can be confirmed by sigmoidoscopy and barium enema. In the former the bowel will appear cyanotic early, with obvious ulcerations apparent later. In the latter examination mUltiple lesions resembling ulcerative colitis are typical. There is no specific remedy for this complication. Rarely is it possible to restore or increase circulation to the ischemic bowel since the arteries supplying it are too small and too arteriosclerotic. Gangrenous bowel of course requires immediate resection. However, less severe cases may resolve with conservative management. The bowel should be placed at rest by a clear liquid diet and infection controlled by antibiotics. The outcome, however, is unpredictable and the ischemic colitis and proctitis
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may at any time progress to gangrene. While mild cases usually heal completely without residual stigmata, those with more severe involvement terminate with strictures which, if symptomatic, will require additional surgery. If conservative management is pursued, the patient must be observed closely so that an immediate laparotomy can be carried out should it become necessary.
ISCHEMIC NEUROLOGIC COMPLICATIONS Ischemic neurologic complications following infrarenal aortic surgery are very rare. We have observed only one patient in whom urinary and rectal incontinence developed after resection of an abdominal aortic aneurysm. Others,a however, have reported a variety of motor, sensory and reflex deficits varying from mild vesicorectal disturbance to paraplegia and loss of sensation extending to the level of the umbilicus. In some instances, the neurologic complications are the result of ischemia to the peripheral nerves, due either to thrombosis of a distal artery, to thrombosis of the prosthesis, or to prolonged aortic occlusion. Peripheral nerves are extremely susceptible to hypoxia and ischemic neuropathy may develop quickly and in the acsence of other evidences of arterial occlusion. Probably most of the reported neurologic complications are due to spinal cord damage. The spinal cord ends at the level of the first lumbar vertebra and its principal blood supply is derived from branches of the aorta arising above the renal arteries. Consequently, the spinal cord is protected from infrarenal aortic occlusion. Nevertheless, anatomic studies have shown that the major radicular artery, which is vital for the blood supply of the spinal cord, may arise from one of the first or second lumbar arteries instead of the usual site in the lower thoracic aorta. In such cases and in the absence of adequate collateral circulation, irreparable damage to the spinal cord can follow infrarenal aortic resection.
INFECTION
Infection of an aortic prosthesis, of an arteriotomy or of an arterial anastomosis is obviously a very hazardous complication of aortic surgery. Such infections are manifested by septicemia, septic emboli to one or both of the lower extremities, fever, chills and malaise. Localizing signs, however, are often minimal unless the infection is superficial, as in the groin. Infection of an arteriotomy or of an arterial anastomosis interferes with healing, and infected hematomas or serious hemorrhage are inevitable consequences. Even after drainage and repair of the arteries, breakdown of the suture margin often recurs because of continued infection or the inability of the arterial sutures to hold. Infected arteries become friable, soft, and their vasa vasorum may be thrombosed; indeed they are often nonviable, which contributes to some of the difficulties attending this complication. The most efficient and safest method of eradicating such an infection is to evacuate the pus, to ligate the involved artery in a healthy site, and to drain the infected area. However, the viability of the corresponding
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extremity will be jeopardized unless a developed collateral circulation pre-exists as a result of underlying occlusive aortic disease for which the aortic surgery was performed. When the aortic surgery is for aneurysmal disease, collateral circulation will be inadequate. To preserve the extremity in these circumstances it is often necessary, in addition, to bypass the infected area completely with a prosthetic graft placed preferably in a noninfected area. Infection within or surrounding an interpolated aortic bifurcation prosthesis presents an even more difficult problem. Fortunately aortic prosthetic grafts will continue to function for many months without rejection and extrusion by the host because they are composed of such inert and nonreactive materials that they induce little, if any, foreign body reaction. Consequently, an infected prosthesis may lie relatively indolent and may not be immediately obvious for weeks, even though the infection may have begun in the early postoperative period. Nevertheless the prosthesis is a foreign body which will perpetuate the infection until it is removed completely. Because a new prosthesis must be inserted immediately in the bed of the old one, it is important that pus be evacuated, infected and necrotic tissues excised and the new prosthesis sutured with Dacron to freshened and viable arterial walls. In every instance the organism should be identified and massive quantities of the appropriate antibiotic administered preoperatively and for prolonged periods postoperatively. There is no conclusive evidence that the prophylactic postoperative administration of antibiotics reduces the incidence of infection and for several years now we have not routinely given them to patients undergoing aortic surgery unless they develop an infection. Rather, every effort should be made at reducing the possibility of a potentially catastrophic infection by meticulous and careful surgical technique, by the avoidance of hematomas and necrotic tissue and, above all, by the complete extirpation of all atheromatous debris, clot and nonviable arteriosclerotic arterial wall when for technical reasons the aneurysm has been opened. Wound infections are usually dw') to a hemolytic Staphylococcus aureus. They present no special problem but should be treated promptly and adequately so that the infection does not spread nor metastasize to the prosthesis.
OTHER GENERAL COMPLICATIONS Cardiac complications are serious and are fairly common after abdominal aortic surgery. This is not surprising since these patients with their advanced arteriosclerosis tend also to have coronary and cerebral arterial disease, hypertension, or significant cardiac arrhythmia; indeed, many will have already sustained myocardial infarctions while others may be taking digitalis preparations or other cardiac drugs. Thus, every effort should be
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made to avoid states which are conducive to myocardial damage. Deep planes of anesthesia are inadvisable. Hypoxia, hypovolemia and hypotension should be strictly prevented, since their momentary occurrence is all that is necessary to cause cardiac arrhythmia, cardiac arrest or myocardial infarction. Likewise, hypervolemia from excessive blood and fluid replacement must be carefully avoided for fear of inducing pulmonary edema. Dangerous cardiac arrhythmias and myocardial infarctions often originate during or immediately after the operation; consequently, it has been our policy to monitor the electrocardiogram of most of the patients during the operation so that, if required, therapy can be instituted properly. Pulmonary complications are rare despite the fact that many of the patients undergoing aortic surgery are cigarette smokers and will have some degree of pulmonary insufficiency, emphysema and bronchitis. Those patients with advanced pulmonary disease should be carefully prepared for operation by the use of bronchial dilators, expectorants, the cessation of smoking, postural drainage and antibiotics. Sedatives and other respiratory depressants should be used sparingly after the operation. Abdominal binders will permit the patient to cough more efficiently and aerosol therapy will loosen tenacious bronchial secretions. Tracheal suctions will help by aspirating secretions and stimulating the patient's cough reflex. If atelectasis nevertheless occurs and secretions cannot be eliminated by conservative measures, bronchoscopy or tracheostomy may be indicated. Pneumonia generally will respond to antibiotic therapy and other conventional measures. Oxygen therapy is sometimes necessary and the use of a positive pressure demand-assist respirator will aid ventilation. Pyuria from acute urethritis and cystitis inevitably follows prolonged use of a urinary catheter. While it is not always possible or even advisable not to employ a urethral catheter, its use should never be extended unnecessarily. Periodic irrigations of the bladder with saline or various antiseptic solutions are ineffective in the prevention of this complication and, although frequently recommended, they are a waste of time and may actually introduce infection. Mental abnormalities developed in two of our patients and consisted of periods of disorientation and confusion which lasted one week. Such disturbances are not unlikely in any elderly patient who undergoes a major surgical procedure, but they are usually only transient and subside spontaneously. Sedatives, especially the barbiturates, can cause bizarre mental behavior in older patients and, if used, should be administered cautiously. I Finally paralytic ileus, wound dehiscence and gastrointestinal hemorrhage are always possible complications. The prevention of paralytic ileus, like its treatment, consists of gastrointestinal decompression via a nasogastric tube. Peristalsis always ceases for a variable period following major abdominal operations.~The period of bowel inactivity, however, will be shortened if the bowel is handled gently and oral fluids are not reinstituted I
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prematurely. JVound dehiscence should be treated by immediate resuture. Even when healing is delayed and tension on the wound is increased by abdominal distention and coughing, the incidence of wound dehiscence will be minimized if the wound is closed meticulously in layers with nonabsorbable sutures, and with enough stay sutures to reduce strain on the suture line. Any major operation can induce acute peptic ulcers and exacerbate those that are long-standing and chronic. Hemorrhage from these stress ulcers is always serious, and fatal exsanguination common. Thus it is generally safer to intervene surgically than to manage the hemorrhage expectantly by conservative means.
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