Pitfalls in the Diagnosis of Abdominal Aortic Aneurysm Robert F. Merchant, Jr., MD, Reno, Nevada H. Treat Cafferata, MD, Reno, Nevada Ralph G. DePalma, MD, Reno, Nevada
Abdominal pain in a patient with a known abdominal aortic aneurysm is readily accepted as signalling a potentially lethal outcome. In these cases timely diagnosis is essential because delayed treatment of a ruptured aneurysm increases morbidity and mortality. The appearance or change in status of a groin hernia, or neuritic symptoms thought to be related to hernia, may herald lethal progression of aneurysma1 disease. This report draws attention to a group of elderly men in whom hernias and aneurysms progress synchronously. Possible biochemical abnormalities are discussed. Material
and Methods
In three of the following cases symptomatic changes in groin hernias detracted attention from the recognition of progressive changes in concomitant abdominal aortic aneurysms. The fourth case of femoral neuropathy was associated with a chronically leaking aneurysm which was diagnosed as a recurrent femoral hernia. Case 1. An 86 year old white man who was a nonsmoker but had a history of 40 pack-years of cigarette smoking was admitted to University Hospitals in Cleveland complaining of a large hernia in the right groin. The hernia had been present for years but in the past month became irreducible. An incarcerated and edematous combined inguinal hernia was repaired with the use of local anesthesia. Pain was relieved but vague abdominal complaints persisted postoperatively. An elevated blood urea nitrogen level of 47 mg/IOO ml prompted intravenous pyelography, which showed a retroperitoneal mass consistent with an aortic aneurysm. An upper gastrointestinal series showed a hiatal hernia, and a barium enema showed diverticular disease of the sigmoid colon. He was readmitted 5 weeks later with
symptoms of a painful hernia in the left groin and pain in the thigh. A left inguinal hernia was then repaired.
Two weeks later he had back pain. The aneurysm had enlarged and the patient was admitted for repair. On the night of admission he had a sudden increase in back pain and hypovolemia. The ruptured aneurysm was repaired within hours of admission; however, the patient died. Case 2. A 75 year old white man, a heavy cigarette smoker, was admitted to Washoe Medical Center, Reno, Nevada for repair of a previously asymptomatic left groin hernia. He complained of discomfort in the left groin of 4 weeks’ duration and recent onset of periodic emesis without nausea. In addition to a large combined left inFrom the Department of Surgery, School of Medicine, University of Nevada, and the Veterans Administration Medical Center, Rena, Nevada. Requests for reprints should be addressed to Robert F. Merchant, MD, 855 Mill Street, #l-S, Rena. Nevada 89502. Presented at the 33rd Annual Meeting of the Southwestern Surgical Congress, Monterey, California, May 4-7, 1981.
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guinal hernia, physical examination revealed a nontender 7 cm aortic aneurysm. An upper gastrointestinal barium examination (Figure 1) demonstrated partial duodenal obstruction due to an aortic aneurysm. Within 2 days, while the patient was undergoing these studies, the aneurysm became palpably larger, measured 9 cm and was tender. Immediate operation was done and a bilateral infrarenal aortoiliac aneurysm was repaired with an aortobifemoral bypass graft. A 2 cm hemosiderin-stained region of thinned adventitia was noted on the anterior surface of the aneurysm and appeared to represent a site of insidious leakage through a weakened area of the aneurysm wall. The left inguinal hernia was repaired transabdominally. The patient’s postoperative recovery was uneventful. Case 3. A 75 year old white man with a 57 pack-year history of smoking presented to the Reno Veterans Administration Medical Center with an 8 week history of severe “gas-like,” crampy lower abdominal pain. Several weeks before admission, a hernia in the left groin, previously repaired in 1975, recurred. The groin hernia was easily reduced on admission and the abdominal pain resolved, but vague abdominal complaints continued. Blood pressure was 156/90 mm Hg. A slightly tender, pulsatile 7 by 4 cm abdominal mass was noted on physical examination; distal pedal pulses were normal. Ultrasound examination revealed an 8 by 4.8 by 2.2 cm abdominal aortic aneurysm with intraluminal clot (Figure 2). The aneurysm, which measured 8 by 5 cm, was repaired using a woven Dacron@ tube graft. The left femoral hernia was repaired transabdominally. The patient recovered uneventfully. Case 4. A 64 year old white man with a 70 pack-year history of smoking presented to the Reno VA Medical Center Outpatient Department with a 5 week history of episodic pain in the left groin. Two days before admission he had had an abrupt increase in pain in the left groin and medial upper thigh. The pain radiated down the anterior aspect of the leg to the ankle and occurrred mainly on flexion of the hip. A previous repair of a left groin hernia, done in 1972, prompted referral to the surgical clinic with a tentative diagnosis of a recurrent left femoral hernia. Two days later he was unable to initiate flexion of the left hip without excruciating pain. On admission to the Center, physical examination showed an isolated left femoral neuropathy. Left psoas stress caused severe pain in the left groin and upper thigh. An 8 by 16 cm ecchymotic indurated area in the region of the left medial thigh was evident on inspection. There was slight tenderness over the left femoral artery, which measured about 2 cm in diameter. A 4 cm aneurysm on the right popliteal artery was present. Findings on abdominal examination were negative. Plain abdominal roentgenography showed no abnormality; however, ultrasound examination (B-mode and real-time) demonstrated a 5.3 by 8 cm abdominal aneurysm not evident on physical examination. The femoral and iliac arteThe American Journal of Surgery
AbdominalAortic Aneurysm
F@re 2. Case 3. B-modeabrknninaf ultrasound sttiy of the dtstal aorta. Note the anterior wall of the 8 by 4.8 cm aortic aneurysm and the intraluminal echo representing laminated thrombus. Figure 1. Case 2. Upper gastrointestinal bar/urn study demonstrating distortion of the third and fourth parts of the duodenum. Note the outline of the aortk aneurysm (arrows).
ries were ectatic. Because of the ultrasound findings, arteriography was done immediately. This demonstrated a 7.5 by 9 cm abdominal aneurysm with ectatic femoral arteries. No leak was seen. The patient was taken to surgery. The left femoral region was explored first. Green hemosiderin-like pigmentation was noted in the periarterial tissue planes; the edematous appearance suggested recent diffusion of degenerated blood products into the femoral sheath. The source of neuropathy was not locally evident, and there was no disease involving the femoral artery. The abdomen was explored; no retroperitoneal hematoma was apparent. On exposure of the abdominal aortic aneurysm by division of the retroperitoneal tissues, a telltale red flame area of hemorrhage was seen anteriorly over the body of the aneurysm. A small hematoma was present in the left periaortic tissues. The aneurysm was repaired with a 16 mm woven Dacron tube graft. The pain in the left leg was immediately relieved postoperatively. Ten months postoperatively the patient remained free of pain and had returned to his preoperative activity without further symptoms. The right popliteal artery aneurysm was subsequently repaired without incident.
Comments The expansion of an aneurysm in these patients occurs as a slow, subtle phenomenon until the aneurysm ruptures. There may be periods of chronic leakage lasting weeks or months. Symptoms in previously stable hernias may be related to expansion and increased abdominal pressure, which probably occurred in cases 1 and 3. In case 2 enlargement of the aneurysm or vomiting secondary to the duodenal obstruction, or both, could have prompted the hernia symptoms. In addition, small chronic leaks into the retroperitoneum can cause neuritic symptoms related to groin hernias. This combination of presenting symptoms has been observed and reported to us in four additional cases not documented here; this condition may be more common than hitherto beVolume 142, December 1991
lieved. There may be a biochemical association between acquired groin hernias in elderly men and abdominal aortic aneurysms. If a biologic or biochemical association exists, there should be a higher incidence of groin hernias in patients with aneurysms or, conversely, an abnormally high incidence of aneurysms in patients presenting with herniations in the fifth decade or later. The present experience is too small to examine these questions; a larger series of patients should be studied prospectively. The clinical picture encountered here may be entirely coincidental. However, there are reports demonstrating defects in fascial integrity and collagen in older men, especially smokers who are veterans. These men develop late inguinal herniation. Biochemical and ultrastructural evidence of collagen deficiency in the fascia of the abdominal wall’has been obtained in these men [1,2]. At the same time, as pointed out by Peacock and Van Winkle [3], patients with aneurysms probably have a connective tissue abnormality. There is a loss of the normal cross-linked collagen and elastin in the medial layer of the vessel wall, primarily in the vulnerable abdominal aorta. This loss is related either to inhibition of collagen synthesis, excessive collagenolysis, or a combination of the two. Busuttil et al [4] postulated that such a deficit of aortic wall collagen may be the cause of aneurysmal expansion. They compared collagenase activity in the walls of aneurysms with that in patients with ecclusive disease and found increased collagenase activity that correlated directly with the size of the aneurysm. The highest values were found in ruptured aneurysms. Of note is the ubiquity of cigarette smoking in these patients. Read and Cannon [2] documented two biochemical abnormalities in the blood of male patients with hernias. They found increased collagenolytic activity combined with decreased alpha-l antitrypsin activity; most abnormal values occurred in smokers with hernias. They postulated that these 757
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diagnosis of expanding or ruptured aneurysms. The prolonged time frame of symptom progression and coincidental hernias and neuritis tended to obscure the true diagnosis. Patients with this constellation of symptoms, especialy men with risk factors for atherosclerosis, must be viewed with a high index of suspicion. When the hernia is the presenting symptom and the aneurysm is palpable, the aneurysm must be repaired without delay. If the aneurysm is not palpable, but suspected, then abdominal roentgenography, ultrasonic scanning, computed axial tomographic scanning or arteriography might detect its presence. When the aneurysm is detected it also should be repaired urgently. In addition, if groin hernias become symptomatic in patients of extreme age who ordinarily are not candidates for aneurysm repair, then these patients should be considered for urgent surgical repair before rupture. Figure 3. Diagram of the anatomic relafions of an aotiic aneurysm, the psoas muscle, femoral nerve and lumbar nerve roots. The nerve is composed of the posterior portions of ihe second, third and fourth krmbar nerve roofs. it courses deep fo the psoas muscle and emerges laterally af the level of the first saccral vertebra.
biochemical abnormalities were related to the release of enzymes into the bloodstream from the lung. This biochemical abnormality might be the cause of both aneurysm and late hernia formation. The basis for such an abnormality was reviewed recently [5]. Apart from these speculative considerations, the surgeon must be alerted to the fact that hernias can present as the first symptom of an expanding aneurysm. This type of chronic expansion or rupture exhibits a treacherous clinical course because the hernia symptoms may antedate rupture and herald this event by many weeks. The outcome will be poor if these hernias are treated rather than the aneurysm. In fact, the operative procedure to repair the hernia might predispose to rupture by causing a negative nitrogen balance and collagenolysis ]6]. Another pitfall in diagnosis is femoral or obturator neuropathy, which can mimic groin pain due to hernia. The mechanism of neuropathy is retroperitoneal bleeding, which is also seen in coagulation disorders [ 71. The fourth case demonstrates an unusual isolated femoral neuropathy previously reported [B]. It occurred because the femoral nerve is confined in a fixed compartment bounded by iliacus fascia and bone. Figure 3 illustrates these anatomic relations. Even a small leak or diffusion of blood products into this closed space can provoke severe symptoms. The chronicity of this process is remarkable. When the aneurysm is not palpable, as in case 4, diagnosis is difficult. In that case a popliteal aneurysm and ectatic femoral arteries prompted diagnostic studies resulting in timely aneurysm repair. The association of popliteal and abdominal aortic aneurysm was noted by Evans and Steele [9] and the significance of arteriomegaly noted by Tilson and Dang 1101. This experience demonstrates difficulties in the 758
Summary The lethal progression of expanding aneurysms may present as a confusing clinical picture. Four cases are reported in which the diagnosis was masked and treatment delayed by symptoms thought to be related mainly to inguinal hernias. It is concluded that there is a subset of patients with aneurysmal progression in whom symptoms are related mainly to the groin. Exhaustive diagnostic methods will detect this condition when the aneurysm is not palpable. The ability to recognize these unique symptoms and signs in elderly men presenting with enlarging inguinal hernias and neuropathy is essential. Biologic and biochemical relations between inguinal hernias and aneurysms may exist.
References 1. Wagh PV, Leverich AP, Sun CN, White HJ, Read RC. Direct inguinal herniation in men: a disease of collagen. J Surg Res 1974;1:425-33. 2. Read RC, Cannon DJ. Metastatic emphysema, a mechanism for acquiring inguinal herniation. Ann Surg 1981; 194: 270-8. 3. Peacock EE, Van Winkel W Jr. Wound repair. Philadelphia: WB Saunders, 1976:47 1. 4. Busuttil RW, Abou-Zamzam AM, Machleder HI. Collagenase activity of the human aorta: a comparison of patients with and without abdominal aortic aneurysms. Arch Surg 1980; 1151373-8. 5. DePalma RG. Biochemical abnormalities and atherosclerotic aneurysms. In: Bergan JJ, Yao JST, eds. Aneurysms: their surgery and treatment. New York: Grune & Stratton (in press). 6. Swanson RJ, Littooy FN, Hunt TK, Stoney RJ. Laparotomy as a precipitating factor in the rupture of intraabdominal aneurysms. Arch Surg 1980;115:299-304. 7. Willbanks WL, Fuller CH. Femoral neuropathy due to retroperitoneal bleeding. Arch Intern Med 1973;132:83-6. 8. Merchant RF Jr, Cafferata HT, DePalma RG. Abdominal aortic aneurysms presenting solely as acute femoral neuropathy. Arch Surg (in press). 9. Evans WE, Steele G Jr. Peripheral artery aneurysms. In: Rutherford RB, ed. Vascular surgery. Philadelphia: WB Saunders, 1977:687-94. 10. Tilson MD, Dang C. Generalized arteriomegaly: a possible predisposition to the formation of abdominal aortic aneurysms. Arch Surg 1981; 8:1030-2.
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