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The management of localized abdominal aortic dissections
The management of localized abdominal aortic dissections Debra Graham, M D , J. Jeffrey Alexander, M D , Dido Franceschi, M D , and F o u a d Rashad, M D , Cleveland, Ohio Aortic dissections limited to the abdominal aorta occur infrequently. We have identified four cases of abdominal aortic dissection and have reviewed these in combination with 43 previously reported cases to identify factors that influence the prognosis and management of this disease. Abdominal aortic dissections are similar to thoracic dissections in their presentation, with acute shearing pain and systolic hypertension occurring commonly. A/though the diagnosis may be made by ultrasonography or CT scanning, angiography is the definitive diagnostic study. Factors found to be associated with high mortality include presentation with acute pain (p < 0.0003), involvement of visceral vessels (p < 0.02), and rupture (p < 0.000002). Chronicity appears to be protective (p < 0.04), although chronic dissections may present acutely. Although prosthetic replacement of the involved aorta is the treatment of choice in most cases, nonoperative management with regular follow-up can be considered in asymptomatic chronic dissections. (J VASC SURG 1988;8:582-91.)
Aortic dissection was first described by Morgagni in 1760 (cited in Hirst et al3 and Gore and Seiwart 2) and its pathophysiology accurately characterized by Maunoir in 1802 (cited in Sherman 3 and Anagnostopoulos et al.4). Laennec used the term "aneurysme dissdquant" to depict this condition in which the circulating blood penetrated into the arterial wall with extension of the effused blood between its layers. DeBakey et al.s later classified aortic dissections according to their location mad to the extent of dissection--factors that proved to be determinants of both the prognosis and treatment of this disease. Not included in the classification by DeBakey et al. are dissections limited to the infradiaphragmatic aorta, which comprise an estimated 2% to 4% of all aortic dissections) -a Dissection of the abdominal aorta was initially described by Shekelton6 in 1822. Since that time, it has been infrequently reported, and its optimal management has not been clearly defined. In this study, four new cases of documented, localized abdominal aortic dissection have been added to 43 cases previously reported and analyzed From the Departmentof Surgery,ClevelandMetropolitanGeneral Hospital, CaseWesternReserveUniversitySchoolof Medicine (Drs. Graham,Alexander,and Franceschi)and the Department of Radiology,ClevelandMetropolitan General Hospital (Dr. Rashad), Reprint requests: I. JeffreyAlexander, MD, Dept. of Surgery, ClevelandMetropolitanGeneralHospital, 3395 ScrantonRd., Cleveland, OH 44109. 582
to determine those factors that influence its natural histo~ and to ascertain its proper treatment. METHOD Medical and radiographic records at Cleveland Metropolitan General Hospital for the 10-year period from 1977 to the present were reviewed and revealed four cases of infradiaphragmatic aortic dissection. Angiograms and other radiographic studies were reevaluated to confirm the diagnosis. The entire thoracoabdominal aorta was visualized in all cases. An extensive search of the literature yielded an additional 43 cases, T M in which the diagnosis of isolated abdominal aortic dissection was documented by imaging studies, surgical exploration, or autopsy findings, and where adequate information regarding clinical presentation, management, and outcome was provided (Table I). Data were analyzed by means of the Fisher exact test. Values for p of less than 0.05 were considered significant. CASE REPORTS
Case 1. A 65-year-old normotensive white man was admitted to the hospital for evaluation of amaurosis fugax. He had a history of coronary artery occlusive disease and myocardial infarction and had undergone cardiac catheterization via the femoral artery several years previously, Attempts to pass a catheter through either femoral vessel were unsuccessful. As a result, carotid aalgiography was performed through an axillary artery approach. Concurrent
Volume 8 Number 5 November1988
.Abdominal aortic dissections 583
Fig. 1. Ukrasonogram of the abdominal aorta, transverse view, shows mural thrombus vs false lumen (arrow).
Fig. 2. CT scan of abdominal aorta shows contrast material within false lumen (arrow).
evaluation of the aorta revealed a normal thoracic aorta and an infrarenal aortic dissection extending into the right common iliac artery with reentry of the false lumen at that point. The patient had carotid endarterectomy for a critical left internal carotid stenosis. The aortic dissection, believed m be a complication of the initial cardiac catheterization, was not treated. The patient was asymptomatic for 2 years after endarterectomy. Case 2. A 59-year-old black man who had a history
of smoking was admitl:ed to the coronary care unit with chest pain. His medical history included pulmonary and meningeal tuberculosis, peptic ulcer disease, syphilis, pancreatitis, chronic obstructive pulmonary disease, and coronary occlusive disease, Physical examination was unremarkable. Although no evidence of myocardial infarction was found by electrocardiography or serial enzyme determinations, a gastric ulcer was shown with upper gastrointestinal endoscopy. Abdominal ultrasonography (Fig. 1)
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T a b l e I. D o c u m e n t e d cases o f localized a b d o m i n a l aortic dissections Author
Year
No. cases
Age (yr)
Sex
Symptoms
Cambria et al.7 Arendrup et al.8 Adar et al.9
1987 1983 1969
1 1 1
53 43 58
M F F
Low back pain Acute L flank pain Acute R thigh pain w/cold foot
BP 180/110 mm Hg Shock; rigid RLQ BP 290/110 mm Hg leg, ischemia~ $ femoral
Youngson et al) °
1983
1
67
F
Sniderman et alY
1978
1
56
M
Low abdominal/back pain None
BP 220/110 mm Hg; tender tortuous aorta None
Bradbrook et al)2
1974
i
46
M
Sharp upper abd. pain
Johns is
1953
1
50
M
LLQ pain
DeAngelis14
1943
1
64
M
Weston & Ardagh ~s
1975
3
69 67
M M
45
F
$ L femoral pulse; abdominal bruit BP 30/10 mm Hg; distended abd. BP 250/70 mm Hg; epigastric mass w/bruit None Diminished femoral pulses bilaterally Diminished R leg pulses
Ludin et al26
1961
1
60
F
Wallwork~z
1943
1
57
M
Abdominal pain 3 yr; mass 18 mo None Acute onset bilateral claudication Acute cold, painful, numb R leg Severe back and abdominal pain Back pain
BuckieyI8
1941
1
61
M
L lumbar pain
Cormier & Benhamida~9
1977
3
68
F
Acute worsening of claudication Acute onset claudication Epigastric pain 1 yr before R abdominal pain
58 52 Lodwick2°
1953
1
68
Amer et al.2~
1952
1
57
Goldsmith & Steinberga2 Glendy et al.23
I964
1
63
F
Bilateral LE pain and numbness None
1937
2
70
M
Vague abdominal pain
72
M
None Chronic abdominal pain Acute abdomen/leg pain None
Holland & Bayley24
1940
1
65
M
Bauersfeld2s
1947
1
60
F
Wood et al.26
1932
1
41
M
Physicalfindings
pulses
BP 55/25 mm Hg; pulsatile massBP 260/140 mm Hg; tender epigastrium w/thrill BP 190/110 mm Hg; tender L flank BP 180/100 mm Hg None None Rigid RUQ, pulsatile epigastric mass $ Femoral pulses; bilatera[ neurol deficit Diminished leg pulses bilaterally Distended abdomen; tender RLQ BP 190/100 mm Hg Tender abdomen/prostate Shock, systolic BP 84 mm Hg BP 210/165 mm Hg
A/C, Acute/chronic; AR, above renals; BR, below renals; LLQ, left lower quadrant; RLQ, right lower quadrant; RUQ, right upper quadrant; LE, lower extremity; RLE, right lower extremity; IMA, inferior mesenteric artery; MVA, motor vehicle accident; GI, gastrointestinal. + W I - Visceral vessel involvement
showed thrombus in the distal aorta, which was seen again with CT scanning (Fig. 2). A n aortogram (Fig. 3) showed an aortic dissection extending from the level of the inferior mesenteric artery to the iliac arteries. Initial operative repair o f the aortic dissection was refused by the patient. H e was readmitted one year later with recurrent chest pain. Repeat angiography at that time showed n o change in the dissection. Surgical treatment was n o t offered again because of the patient's deteriorating medical condition.
Case 3. A 56-year-old white w o m a n was initially seen in the emergency ward with mottled discoloration and pain of both lower extremities. H e r medical history included mitral valve commissurotomy 12 years earlier, which was complicated by a right hemispheric stroke. I n addition, she had chronic atrial fibrillation and recurrent episodes of congestive heart failure. The patient was found to be normotensive and the heart was in normal sinus rhythm. Both legs were cool and mottled below the midthigh and lacked palpable pulses
Volume 8 Number 5 November 1988
Location
Abdominal aortic dissections
Evaluation of thoracic aorta
Reentry
WI
Rupture
A /C
+ +
-
+ +
A A A
Angiogram Autopsy Angiogram
BR to R common lilac
-
-
A
At operation
Celiac to common lilac
-
-
C
Angiogram
1-2 cm AR to birfurcation IMA to lilacs
+
-
A
Angiogram
-
-
+
A
Autopsy
Anglo for known AAA R renal arteq, involvement --
-
-
+
C
Autopsy
--
-
-
C A
Angiog;cam Angiogram
---
-
-
A
Angiogram
--
BR to L lilac Below celiac-lilacs BR to R lilac
AR to above bifurcation BR BR BR to lilacs
Remarks --Contained rupture R groin --
BR to L common lilac
-
+
+
A
Autopsy
Celiac to R iliac
+
-
-
C
Autopsy
AR
-
+
A
Autopsy
AR to L lilac
-
-
A
Angiogram
BR to R common lilac
+
-
A
Angiogram
AR to iliacs
-
-
C
Angiogram
--
BR to bifurcation
-
+
A
Autopsy
--
SMA to lilacs
-
-
A
Autopsy
--
BR to R. common lilac
-
-
A
Operation
BR to above bifurcation
-
+
C
Autopsy
BR to lilacs
-
-
C
Autopsy
Mesenteric involvement Died 4 yr postop, unrelated --IMA involved
Dissection witnessed in O R --
Confined to abdomen
+
-
-
C
Autopsy
Death from head injury Death from sepsis
AR to R common lilac
-
-
+
A
Autopsy
--
-
-
C
Autopsy
Death from pneumonia
Just below diaphragm
585
Continued
a n d m o t o r f u n c t i o n . E x a m i n a t i o n o f the a b d o m e n w a s n o r m a l . A n g i o g r a p h y d e m o n s t r a t e d total o c c l u s i o n o f t h e infrarenal aorta, w h i c h w a s believed to be e m b o l i c in origin. A bilateral f e m o r a l t h r o m b o e m b o l e c t o m y w a s perf o r m e d w i t h r e e s t a b l i s h m e n t o f b l o o d f l o w to the legs. O n the s e c o n d p o s t o p e r a t i v e day the p a t i e n t c o m p l a i n e d o f severe a b d o m i n a l pain. E x a m i n a t i o n o f the a b d o m e n w a s u n r e v e a l i n g and, in t h e p r e s e n c e o f a w o r s e n i n g acidosis, acute m e s e n t e r i c insufficiency w a s suspected. R e p e a t ang i o g r a p h y (Fig. 4) s h o w e d a posterior-lateral dissection o f t h e a b d o m i n a l a o r t a f r o m the celiac axis t o the iliac arteries,
w i t h a p p a r e n t r e e n t r y at t h e level o f the aortic bifurcation. T h r o m b o s i s w a s seen in the distal aorta. T h e disscction w a s f o u n d t o involve the r i g h t renal a n d s u p e r i o r m e s e n teric arteries. T h e p a t i e n t w a s taken to the o p e r a t i n g r o o m w h e r e a necrotic s i g m o i d c o l o n w a s resected, a n d an ext r a a n a t o m i c axillobifemoral b y p a s s w a s p e r f o r m e d . N o att e m p t w a s m a d e to repair t h e aorta directly. T h e p a t i e n t r e m a i n e d h y p o t e n s i v e a n d acidotic; h e r c o n d i t i o n deterio r a t e d , w i t h w o r s e n i n g renal a n d cardiac failure. She died o n t h e sixth p o s t o p e r a t i v e day. P e r m i s s i o n for a u t o p s y w a s denied. C a s e 4. A 72-year-old h y p e r t e n s i v e , diabetic black m a n
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Graham et al.
T a b l e I. C o n t ' d
Author
Year
No. cases
Age (yr)
Sex.
Symptoms
Puderbach2r
1954
1
73
M
Tender abdomen
Kocandrle et al.28
1970
1
48
M
Gaylis & Laws29
1956
2
58
M
Abdominal pain/yoreking After anglo, L leg pain & paresthesia None
62
M
None
None
42
M
BP 260/130 mm Hg
62
M
Cardiac arrest after anglo After anglo, cold LE
51
M
GI bleed, after anglo
Rectal necrosis Tender lower abdomen; absent LE pulses
Wolfman & Boblitt3°
1959
3
Tomatis et al.3~
1968
1
27
F
David & Blumenberga2
1970
1
54
F
Bilateral leg pain & numbness from MVA MVA
Welborn & Sawyers3a
I969
1
33
F
MVA; nmaab feet
Nunn34
1973
1
58
M
MVA; paralysis LE
Ngu & Konstam35
1965
1
37
F
Surfboard to abdomen
Hewitt & Grablowsky 36
1970
1
65
M
MVA; paralysis LE
Jackson & Slavin37
1953
1
74
M
Shormess of breath
Faivre et al.s8
1962
4
72
F
70
M
Low back/abdominal pain Low back pain
74
M
75
M
Abdominal/back pain; melena Abdominal pain 2 mo
J.J. B.P.
58 65
M M
Chest/epigastric pain None
B.C.
56
F
C.N.
72
M
Acute bilateral LE ischemia None
Present series
1988
was admitted for angiographic evaluation of rest pain in the left foot. The blood pressure was 156/76 man H g during examination. The abdomen was normal. The lower extremities showed clinical evidence of chronic arterial insufficiency. Doppler studies indicated bilateral occlusive disease o f the superficial femoral and popliteal arteries with severe ischemia o f the left leg. Angiography showed dissection of the infrarenal aorta, with marked arterial occlusive disease of the left leg. In retrospect, the patient recalled being involved in a mine collapse 45 years earlier, causing severe back pain that subsided 3 to 4 years later. Because this was thought to
Physicalfindings
After anglo; loss of LE pulses bilaterally Diminished R femoral pulse
No LE pulses
Absent LE pulses w/sensorimotor deficit Loss of LE pulses; sensorimotor deficit Absent pulses; legs cold, mottled, sensoqr deficit Tender abdomen; absent LE pulses w/neuro deficit Absent LE pulses; mottled and cold LLQ pulsatile mass Shock, systolic BP 80 mm Hg Systolic BP 60 mm Hg; no femoral pulses None BP 200/100 mm Hg; abdominal bruit Epigastric tenderness None; equal pulses bilaterially Absent LE pulses; sensorimotor deficit None
be the cause of his apparent chronic aortic dissection, therapy for this incidental finding was n o t recommended. The patient had successful distal arterial reconstruction of the left leg. RESULTS
Presentation. T h e m e a n age o f all p a t i e n t s at t h e t i m e o f d i a g n o s i s was 5 8 . 6 years ( r a n g e 2 7 to 75 years). Sex, r e p o r t e d i n 4 3 cases, s h o w e d a m a l e pred o m i n a n c e ( 6 7 % ) . R a c e was i n d i c a t e d i n o n l y 2 0 cases; m o s t o f these p a t i e n t s w e r e w h i t e ( 7 5 % ) . T h e m o s t c o m m o n p r e s e n t i n g s y m p t o m , p r e s e n t i n 19
~=
Volume 8 Number 5 November 1988
Abdominal aortic dissections
Location
Reentry
AR Below IMA to lilacs
-
Evaluation of thoracic aorta
VVI
Rupture
A /C
+
+
A
Autopsy
-
-
A
At operation
-
-
A
Angiography
A
Angiography
A
Autopsy
587
Remarks R renal a r t e q ~ , involved Secondary to a n g l o
Above bifurcation
BRtoRcommon
i~ac
BR to R common lilac
-
-
3 cm AR to 7 cm BR
-
+
A
Autopsy
AR to lilacs
-
+
A
Autopsy
Distal 5 cm aorta, lilacs
-
-
A
At operation
+
A
Autopsy
-
+
A
At operation
BR to above bifurcation
-
-
A
At operation
Below IMA to above bifurcation
-
-
A
At operation
A
Autopsy
C
Autopsy
SMA to L COlnmon iliac /MA, above bifurcation
-
-
m
L
m
IMA to lilacs Above bifurcation
m
Below SMA
+
A
Autopsy
Below diaphragm to bifurcation Confined to abdomen
+
A
Autopsy
+
A
Autopsy
A
Autopsy
+
Confined to abdomen L-3 to lilacs BR to R iliac
+ +
-
C C
Angiogram Angiogram
L-3 to L iliac
+
+
A
Angiogram
BR to bifurcation
-
-
C
Angiogram
patients, was pain of acute onset (less than 2 weeks) (Table II). This was frequently described as sharp, severe or knife-like, and radiated between the abdomen and back. Acute leg ischemia, in the absence of previous arterial insufficiency, was also a common finding. Other presenting symptoms included chronic (greater than 2 weeks' duration) abdominal pain, hematuria, melena, and shock. In most cases (70%), symptoms were of acute onset. Medical histories were often incompletely reported. A history o f hypertension was present in 18
SecondaDr to lumbar anglo for claudication Secondary. to lumbar anglo for claudication
Bilateral renals involved IMA & renals involved Traumatic
IMA & R renal involved IMA involved
Death from to sepsis
Mesenteric involvement
Seconda U to anglo SMA, IMA and L renal involved --
of 34 cases (53%), and atherosclerosis was evident in 31 of 40 cases (78%). Medial arterial disease and syphilis were rarely reported. No patients had Marfan's syndrome, congenital cardiovascular anomalies, or were pregnant. Dissection was asymptomatic in nine cases. Physical findings included systolic hypertension in 15 patients (38%) (Table II). Abdominal tenderness was present in 13 of 37 patients, whereas other findings were the presence of a pulsatile abdominal mass, an abdominal bruit, diminution of lower ex-
588
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Journal of VASCULAR SURGERY
Fig. 3. Abdominal aortogram demonstrates dissection extending from infrarenal aorta to iliac arteries (arrow).
Fig. 4. Abdominal aortogram demonstrates dissection from supraceliac aorta to lilac arteries (black arrow) and thrombus within distal aorta (white arrow).
tremity pulses, and loss of sensation or motor function. Rupture of the dissection occurred in 13 cases (28%) and was associated with a 92% mortality rate (p < 0.000002). In seven cases, dissection of the abdominal aorta was iatrogenic--a complication of translumbar or transfemoral aortography. Dissection was the result of blunt abdominal trauma in seven others. In the remaining 33 cases (70%), no obvious etiologic factor could be ascertained. Diagnosis. The means of diagnosis of abdominal aortic dissections varied considerably according to the period of presentation. Early cases were often diagnosed by abdominal exploration or at autopsy. More recently, such imaging modalities as ultrasonography, CT scanning, and angiography have been used to establish the diagnosis. In this series, the diagnosis was made by angiography in 17 cases (36%) and ultrasonography in one case (2%). Dissection was diagnosed clinically in three cases, at surgical exploration in nine, and at autopsy in 17. Most dissections of this type were located below the renal arteries (Table III). The site of the intimal
tear, reported in 20 cases, was below the renal arteries (n = 12), between the renal arteries and the superior mesenteric artery (n = 6), or between the superior mesenteric artery and diaphragm (n = 2). Visceral vessel involvement, whether an extension of the dissection process or branch occlusion, was present in 10 cases (21%). Reentry tears were present in 33% of cases adequately examined and were more frequently associated with chronic rather than acute dissections (p < 0.02). Twenty-eight patients (68%) had continued flow in the false lumen. Rupture occurred more frequently in this group (p < 0.003). Management. Management options have evolved considerably over the period included in this study. Twenty-six patients (55%) received no specific treatment, often because current methods of assessment and treatment of these lesions were not available. The remaining 21 patients were managed surgically. Most of these patients had the affected aorta replaced with a prosthesis (n = I4). Other procedures included the creation of an outflow (reentry) channel from the false lumen (n = 2), oversewing the dissection channel (fenestration) (n = 1), suture
Volume8 Number5 November1988
repair of an external rupture (n = 2), endarterectomy (n = 1), and extraanatomic bypass without direct aortic repair (n = 1). Overall survival (64%) was influenced by several factors (Table IV). Those patients who were hemodynamically unstable (p < 0.002) or who presented with acute pain (p < 0.0003) were more likely to die as a result of their dissection than those who did not. Rupture was associated with death in 92% of cases. Dissections involving the suprarenal aorta or visceral vessels were also more frequently linked with a poor outcome than those limited to the infrarenal aorta. Although operative treatment significantly improved survival in acute dissections (p < 0.002), it had no effect on outcome in chronic cases. When all cases were considered, chronicity appeared to be protective (p < 0.04). Twelve major perioperative complications occurred in 10 patients. Renal insufficiency, varying from a transient azotemia to progressive renal failure, occurred in seven patients, five of whom died. In two cases, acute renal failure was attributed to renal hypoperfusion during shock. Five patients had dissections involving the visceral vessels (p < 0.003) and five had dissections involving the suprarenal aorta (20 < 0.05). Gastrointestinal ischemia occurred in four patients. None of these survived despite resection of the involved bowel in three. Paraplegia was reported in one patient, who died of associated injuries. DISCUSSION Although aortic dissection has been found to occur in 1 of 363 autopsies, those limited to the abdominal aorta contribute only 2% to 4% of all cases) 3 In many respects, localized dissections of the abdominal aorta are similar to their thoracic counterparts. Both occur in middle age and affect men three times more frequently than women. 1,4 Hypertension is common to both, occurring in 54% of patients in this series as compared with 58% to 90% of those with thoracic dissections. 2,39Atherosclerosis was also a common finding in this series (76%) and was often found in the region of the dissection, although its significance is unlmown. Medial dysplasia, frequently associated with thoracic aortic dissections, 1-4was rarely reported in this group of patients. Marfan's syndrome, congenital cardiovascular lesions, and pregnancy were notably absent in this series. Presentation with acute, shearing pain and systolic hypertension appears to be common to both abdominal and thoracic aortic dissections. Limb isch-
Abdominal aortic dissections 589
Table II. Symptoms and physical findings Symptoms (n = 47) Acute pain, abdomenor back Chronic pain Acute lower extremityischemia Hematuria Melena Asymptomatic Physicalfindings Blood pressure (n = 40) Shock (systolicBP ~ 90 mm Hg) Hypertension (systolicBP />180 mm Hg) Abdomen (n = 38) Tenderness Pulsatile mass Nonpulsatile mass Bruit Extremities (n = 42) Diminished pulses Sensory impairment Loss of motor fi.mction Bruits
No.
%
19 4 16 3 2 8
40 9 34 6 4 17
6
15
i5
32
13 3 1 3
34 8 3 8
i9 6 5 2
45 14 I2 5
emia is often associated with abdominal aortic dissections. Although rupture can occur with both, cardiac tamponade may predominate with thoracic dissections and hypovolemic shock with abdominal dissections. Presenting signs and symptoms may be nonspecific. Numerous imaging modalities have been helpful in establishing or confirming the clinical diagnosis. B-mode ultrasonography has been used to demonstrate an echogenic, intimal flap, but this finding can be easily missed in a nondilated aorta. 4° Realtime abdominal ultrasonography can more clearly show the intimal flap moving with aortic flow and, if combined with Doppler flow studies, can readily evaluate flow in the false and true lumens. 41'42 CT scanning may show a double aortic lumen, nonopacification or poor opacification of a portion of the aorta, aortic widening, or inward displacement ofintimal calcifications.43.44As with ultrasonography, dissections can be misinterpreted as intraluminal thrombus. Such modalities are often unable to provide sufficient information regarding the point of initiation, the extent of the dissection, and the presence or absence of visceral vessel involvement. Angiography remadns the definitive diagnostic study in abdominal aortic dissection. Specific signs of aortic dissection include visualization of a double channel, the presence of a linear radiolucency within the aortic lumen, demonstration of entry or reentry tears, and branch involvement. Indirect signs include compression of the true aortic lumen by the false
590
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Table III. Characteristics o f dissection Location (n = 51) Below renais Above rends Extent unclear Site of tear (n = 20) Level of celiac Between rends and SMA Between rends and bifurcation Reentry tear (n = 21) Flow in false lumen (n = 41) Visceral vessel involvement(n = 47) Rupture (n = 47) Acuity (n = 47) Acute Chronic
No.
%
Survivo,x
%
28 16 3
85 31 6
23 5 2
82 31 67
2 6 12 7 28 10 i3
10 30 60 33 68 21 28
2 1 8 5 15 3 1
100 17 67 71 54 30 8
33 14
70 30
18 12
55 86
Table IV. Factors adversely affecting outcome p Value*
Presentation Acute pain, abdomen or back Shock Characteristics of dissection Location above rends Visceral vessel involvement Rupture Acute dissection Management Nonopcrative, all cases Nonopcrative, with acute pain
0.0003 0.002 0.003 0.02 0.000002 0.05 0.03 0.05
~Fisher's exact test. lumen, thickening o f the aortic wall, irregular projection o f the dye column, or abnormal catheter position. False-negative findings can result from simultaneous opacification o f both lumens, total aortic occlusion, or limited radiographic projections. 4s,46 Because abdominal aortic dissections may represent the extension o f a thoracic aortic dissection, the thoracic aorta must be evaluated in all patients. Few recommendations for the management o f abdominal aortic dissections have been made. Recent reports recommend repair or replacement, 7'2° but this has not been shown to bc necessary in all cases. Although nonsurgical management has been found to be appropriate for type III thoracic aortic dissections, 47 its role in the treatment of dissections limited to the abdominal aorta is unclear. EightT-one percent o f patients treated operatively in this series survived, including 13 o f 14 who had prosthetic replacement o f the aorta, two who had reentry, procedures, one who had a fenestration, and one who had an endarterectomy. Suture o f an external rupture was per-
formed in two patients, both o f w h o m died. An extraanatomic bypass was done in one case without direct repair o f the aorta and this patient died. Although the data presented here support the idea that operative treatment o f dissections results in a better outcome, there appears to be a role for nonoperative management in selected patients. Patients who require surgical intervention include those with signs o f rupture, visceral vessel involvement, or acute limb ischemia. The presence o f acute abdominal pain or suprarenal aortic involvement is also associated with a high mortality rate if left untreated and so should be considered indications for surgical therapy. Patients in w h o m nonoperative management can be considered are those with chronic dissections without symptoms. Survival in this group was not significantly altered by operation. However, those patients with chronic dissections who have acute symptoms require surgical treatment. Chronic dissections not repaired should be observed closely with CT scanning or angiography. Signs o f progression o f the dissection or the development o f a saccular aneurysm should prompt surgical treatment. CONCLUSION Aortic dissection timitcd to the abdomen is rare. Several characteristics o f the disease, such as presentation and risk factors, are similar to those o f thoracic dissections. Although the diagnosis may be made by CT scanning or tdtrasonography, angiography should always bc performed to document the extent o f the dissection and the presence o f major branch involvement and to rule out thoracoabdominal dissection. In most cases, prosthetic replacement o f the aorta is the treatment of choice. However, in selected patients with asymptomatic chronic dissections, ob-
Volume 8 Number 5 November 1988
servation and close follow-up with either CT scanning or angiography may be sufficient. REFERENCES 1. Hirst AE, Johns VJ, Kime SW. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine 1958;37:217-79. 2. Gore I, Seiwart VJ. Dissecting aneurysm of the aorta. Arch Pathol 1952;53:121-41. 3. Shennan T. Dissecting aneurysm. Medical Research Council Special Report Series No. 193. London: His Majesty's Stationery Office, 1934. 4. Anagnostopoulos CE, Prabhakar MJS, Kirtle CF. Aortic dissections and dissecting aneurysms. Am J Cardiol 1972; 30:263-73. 5. DeBakey ME, Henly SW, Cooley DA, Morris GC, Crawford ES, Beall AC. Surglcal management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965;49:130-49. 6. Shekelton J. Dissections and aneurism. Dublin Hosp Rep !822;3:231-40. Cited in Peacock TB. Report on cases of dissecting aneurism. Tr Path Soc London 1863;14:87-99. 7. Cambria R_P, Morse S, August D, Gusberg R. Acute dissection originating in the abdominal aorta. J VAsc SuR~ 1987;5:495-7. 8. Arendrup H, Frimodt-Moeller PC, Christensen JEJ. Acute dissection confined to the abdominal aorta. Scand J Thorac Cardiovasc Surg 1983;17:121-3. 9. Adar R, Nazarian M, Salzman EW. Abdominal aortic dissection presenting as femoral artery Occlusion. Isr J Med Sci 1969;5:407-10. 10. Youngson G, Engeset J, Hussey J, Smith G. Dissecting aneurysm of infrarenal abdominal aorta. Surgery 1983;94: 521-3. 11. Sniderman KW, Sos TA, Gay WA, Subramanian VA. Aortic dissection beginnning in the abdomen. M R 1978;130: I15-8. 12. Bradbrook RA, Marshall AJ, Spreadbury PL. Hypertension with dissecting abdominal aortic aneurysm. Br Med J 1974;4:23-4. 13. Johns TNP. Dissecting aneurysm of the abdominal aorta. Ann Surg 1953;137:232-5. 14. DeAngelis E. Dissecting aneurysm of the abdominal aorta. Am Heart J 1943;26:124-8. 15. Weston TS, Ardagh JW. Infrarenat dissection of the aorta. N Z Med J 1975;82:302-4. 16. Ludin H, Waibel P, Scheidegger S. Medionecrotic dissecting aneurysm of the abdominal aorta. Acta Radiol (Stockh) 196i;55:177-85. 17. Wallwork DW. Survival for four years following dissecting aneurysm of the abdominal aorta. N Engl J Med 1943 ;228:451-2. 18. Buckley TI. Hematuria associated with dissecting aneurysms of the abdominal aorta. J Urol 1941;44:816-20. 19. Comfier JM, Benhamida F. H6matomes dissdquants de l'aorte abdominale sous-rdnale. Nouv Presse Mdd 1977;6:2137-41. 20. Lodwick GS. Dissecting aneurysms of the thoracic and abdominal aorta. Am J Roentgenol 1953;69:907-25. 21. Amer NC, Schaeffer HC, Domingo RT, Sawyer PN, Wesolowski SA. Aortic dissection presenting as iliac artery occlusion. N Engl J Med I962;266:1040-2. 22. Goldsmith EL, Steinberg I. Spontaneous dissecting hematoma (aneurysm) of the abdominal aorta in the Leriche syndrome. Circulation 1964;30:230-3. 23. Glendy RE, Castleman B, White PD. Dissecting aneurysm of the aorta. Am Heart J 1937;13:129-62.
Abdominal aortic dissections 591
24. Holland LF, Bayley RLH. Dissecting aneurysm. Am Heart J 1940;20:223-35. 25. Bauersfeld SR. Dissecting aneurysm of the aorta: a presentation of fifteen cases and a review of the recent literature. Ann Int Med 1947:26:873-89. 26. Wood FC, Pendergrass EC, Ostrum HW. Dissecting aneurysm of the aorta with special reference to ~ts roentgenographic features. Am J Roentgenol 1932:28:437-65. 27. Puderbach WJ. Dissecting aneurvsm of the aorta and its relation to the acute condition of the abdomen. Am J Surg 1954:87:887-90. 28. Kocandde V, Kittle CF, Petasnick J. Percutaneous retrograde abdominal aorrography complication: intimal dissection. Arch Surg 1970:100:611-3. 29. Gaylis H, Laws JW. Dissection of aorta as a complication of translumbar aortography. Br Med J 1956:2:1141-6. 30. Wolfman EF, Boblitt DE. Intramural aortic dissection as a complication of translumbar aortography. Arch Surg 1959: 78:629-38. 31. Tomatis LA, Doornbos FA~ Beard JA. Circumferential inti: real tear of aorta with complete occlusion due to blunt trauma. J Trauma 1968:8:1096-1101. 32. David D, Blumenberg RM. Subintimal aortic dissection with occlusion after blunt abdominal trauma. Arch Surg 1970;100:302-4. 33. Welborn MB, Sawyers JL. Acute abdominal aortic occlusion due to nonpenetrating trauma. Am J Sutg 1969;118:112-6. 34. Nunn DB. Abdominal aortic dissection following nonpenetrating abdominal trauma. Am Surg 1973;39:177-9. 35. Ngu VA, Konstam PG. Traumatic dissecting aneurysm of the abdominal aorta. Br J Surg 1965;52:981-2. 36. Hewitt RL, Grablowsky OM. Acute traumatic dissecting aneurysm of the abdominal aorta. Ann Surg 1970;171:160-2. 37. Jackson A, Slavin M. Dissecting aneurysm of the aorta. Angiology 1953;4:357-73. 38. Faivre G, Gilgenkrantz JM, Cherrier FM, Tenett EC. Aspects cliniques de la m4dionecrose aortique apropos de 15 observations. Arch Mal Coeur 1962;55:1264-73. 39. Roberts WC. Aortic dissection: anatomy, consequences, and causes. Am Heart J 1981;101:195-214. 40. Bresnihan ER~ Keates PG. Ultrasound and dissection of the abdominal aorta. Clin Radiot 1980;31:105-8. 41. Conrad MR, Davis GM, Green CE, Curry TS. Real time ultrasound in the diagnosis of acute dissecting aneurysm of the abdominal aorta. AJR 1979;132:115-6. 42. Kumari SS, Pillari G, Mandon V, Bank S. Occult aortic dissection: diagnosis by ultrasound. Br J Radiol 1980;53: 1093-5. 43. Thorsen MK, SanDretto MA, Lawson TL, Foley WD, Smith DF, Berland LL. Dissecting aortic aneurysms: accuracy of computed tomography diagnosis. Radiology 1983;148:
773-7. 44. Oudkerk M, Overbosch E, Dee P. CT recognition of acute aortic dissection. AJR 1983;141:671-6. 45. Beachley MC, Ranninger K, Roth FJ. Roentgenographic evaluation of dissecting aneurysm of the aorta. Am J Roentgenol 1974;121:617-25. 46. Hayaski K, Meaney TF, Zelch JV, Tarar R. Aortographic analysis of aortic dissection. AmJ Roentgeno11974;122:76982. 47. Wheat MW. Current status of medical therapy of acute dissecting aneurysms of the aorta. World J Surg 1980;4:503-9.
Aortic dissection was first described by Morgagni in 1760 (cited in Hirst et al3 and Gore and Seiwart 2) and its pathophysiology accurately characterized by Maunoir in 1802 (cited in Sherman 3 and Anagnostopoulos et al.4). Laennec used the term "aneurysme dissdquant" to depict this condition in which the circulating blood penetrated into the arterial wall with extension of the effused blood between its layers. DeBakey et al.s later classified aortic dissections according to their location mad to the extent of dissection--factors that proved to be determinants of both the prognosis and treatment of this disease. Not included in the classification by DeBakey et al. are dissections limited to the infradiaphragmatic aorta, which comprise an estimated 2% to 4% of all aortic dissections) -a Dissection of the abdominal aorta was initially described by Shekelton6 in 1822. Since that time, it has been infrequently reported, and its optimal management has not been clearly defined. In this study, four new cases of documented, localized abdominal aortic dissection have been added to 43 cases previously reported and analyzed From the Departmentof Surgery,ClevelandMetropolitanGeneral Hospital, CaseWesternReserveUniversitySchoolof Medicine (Drs. Graham,Alexander,and Franceschi)and the Department of Radiology,ClevelandMetropolitan General Hospital (Dr. Rashad), Reprint requests: I. JeffreyAlexander, MD, Dept. of Surgery, ClevelandMetropolitanGeneralHospital, 3395 ScrantonRd., Cleveland, OH 44109. 582
to determine those factors that influence its natural histo~ and to ascertain its proper treatment. METHOD Medical and radiographic records at Cleveland Metropolitan General Hospital for the 10-year period from 1977 to the present were reviewed and revealed four cases of infradiaphragmatic aortic dissection. Angiograms and other radiographic studies were reevaluated to confirm the diagnosis. The entire thoracoabdominal aorta was visualized in all cases. An extensive search of the literature yielded an additional 43 cases, T M in which the diagnosis of isolated abdominal aortic dissection was documented by imaging studies, surgical exploration, or autopsy findings, and where adequate information regarding clinical presentation, management, and outcome was provided (Table I). Data were analyzed by means of the Fisher exact test. Values for p of less than 0.05 were considered significant. CASE REPORTS
Case 1. A 65-year-old normotensive white man was admitted to the hospital for evaluation of amaurosis fugax. He had a history of coronary artery occlusive disease and myocardial infarction and had undergone cardiac catheterization via the femoral artery several years previously, Attempts to pass a catheter through either femoral vessel were unsuccessful. As a result, carotid aalgiography was performed through an axillary artery approach. Concurrent
Volume 8 Number 5 November1988
.Abdominal aortic dissections 583
Fig. 1. Ukrasonogram of the abdominal aorta, transverse view, shows mural thrombus vs false lumen (arrow).
Fig. 2. CT scan of abdominal aorta shows contrast material within false lumen (arrow).
evaluation of the aorta revealed a normal thoracic aorta and an infrarenal aortic dissection extending into the right common iliac artery with reentry of the false lumen at that point. The patient had carotid endarterectomy for a critical left internal carotid stenosis. The aortic dissection, believed m be a complication of the initial cardiac catheterization, was not treated. The patient was asymptomatic for 2 years after endarterectomy. Case 2. A 59-year-old black man who had a history
of smoking was admitl:ed to the coronary care unit with chest pain. His medical history included pulmonary and meningeal tuberculosis, peptic ulcer disease, syphilis, pancreatitis, chronic obstructive pulmonary disease, and coronary occlusive disease, Physical examination was unremarkable. Although no evidence of myocardial infarction was found by electrocardiography or serial enzyme determinations, a gastric ulcer was shown with upper gastrointestinal endoscopy. Abdominal ultrasonography (Fig. 1)
584
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T a b l e I. D o c u m e n t e d cases o f localized a b d o m i n a l aortic dissections Author
Year
No. cases
Age (yr)
Sex
Symptoms
Cambria et al.7 Arendrup et al.8 Adar et al.9
1987 1983 1969
1 1 1
53 43 58
M F F
Low back pain Acute L flank pain Acute R thigh pain w/cold foot
BP 180/110 mm Hg Shock; rigid RLQ BP 290/110 mm Hg leg, ischemia~ $ femoral
Youngson et al) °
1983
1
67
F
Sniderman et alY
1978
1
56
M
Low abdominal/back pain None
BP 220/110 mm Hg; tender tortuous aorta None
Bradbrook et al)2
1974
i
46
M
Sharp upper abd. pain
Johns is
1953
1
50
M
LLQ pain
DeAngelis14
1943
1
64
M
Weston & Ardagh ~s
1975
3
69 67
M M
45
F
$ L femoral pulse; abdominal bruit BP 30/10 mm Hg; distended abd. BP 250/70 mm Hg; epigastric mass w/bruit None Diminished femoral pulses bilaterally Diminished R leg pulses
Ludin et al26
1961
1
60
F
Wallwork~z
1943
1
57
M
Abdominal pain 3 yr; mass 18 mo None Acute onset bilateral claudication Acute cold, painful, numb R leg Severe back and abdominal pain Back pain
BuckieyI8
1941
1
61
M
L lumbar pain
Cormier & Benhamida~9
1977
3
68
F
Acute worsening of claudication Acute onset claudication Epigastric pain 1 yr before R abdominal pain
58 52 Lodwick2°
1953
1
68
Amer et al.2~
1952
1
57
Goldsmith & Steinberga2 Glendy et al.23
I964
1
63
F
Bilateral LE pain and numbness None
1937
2
70
M
Vague abdominal pain
72
M
None Chronic abdominal pain Acute abdomen/leg pain None
Holland & Bayley24
1940
1
65
M
Bauersfeld2s
1947
1
60
F
Wood et al.26
1932
1
41
M
Physicalfindings
pulses
BP 55/25 mm Hg; pulsatile massBP 260/140 mm Hg; tender epigastrium w/thrill BP 190/110 mm Hg; tender L flank BP 180/100 mm Hg None None Rigid RUQ, pulsatile epigastric mass $ Femoral pulses; bilatera[ neurol deficit Diminished leg pulses bilaterally Distended abdomen; tender RLQ BP 190/100 mm Hg Tender abdomen/prostate Shock, systolic BP 84 mm Hg BP 210/165 mm Hg
A/C, Acute/chronic; AR, above renals; BR, below renals; LLQ, left lower quadrant; RLQ, right lower quadrant; RUQ, right upper quadrant; LE, lower extremity; RLE, right lower extremity; IMA, inferior mesenteric artery; MVA, motor vehicle accident; GI, gastrointestinal. + W I - Visceral vessel involvement
showed thrombus in the distal aorta, which was seen again with CT scanning (Fig. 2). A n aortogram (Fig. 3) showed an aortic dissection extending from the level of the inferior mesenteric artery to the iliac arteries. Initial operative repair o f the aortic dissection was refused by the patient. H e was readmitted one year later with recurrent chest pain. Repeat angiography at that time showed n o change in the dissection. Surgical treatment was n o t offered again because of the patient's deteriorating medical condition.
Case 3. A 56-year-old white w o m a n was initially seen in the emergency ward with mottled discoloration and pain of both lower extremities. H e r medical history included mitral valve commissurotomy 12 years earlier, which was complicated by a right hemispheric stroke. I n addition, she had chronic atrial fibrillation and recurrent episodes of congestive heart failure. The patient was found to be normotensive and the heart was in normal sinus rhythm. Both legs were cool and mottled below the midthigh and lacked palpable pulses
Volume 8 Number 5 November 1988
Location
Abdominal aortic dissections
Evaluation of thoracic aorta
Reentry
WI
Rupture
A /C
+ +
-
+ +
A A A
Angiogram Autopsy Angiogram
BR to R common lilac
-
-
A
At operation
Celiac to common lilac
-
-
C
Angiogram
1-2 cm AR to birfurcation IMA to lilacs
+
-
A
Angiogram
-
-
+
A
Autopsy
Anglo for known AAA R renal arteq, involvement --
-
-
+
C
Autopsy
--
-
-
C A
Angiog;cam Angiogram
---
-
-
A
Angiogram
--
BR to L lilac Below celiac-lilacs BR to R lilac
AR to above bifurcation BR BR BR to lilacs
Remarks --Contained rupture R groin --
BR to L common lilac
-
+
+
A
Autopsy
Celiac to R iliac
+
-
-
C
Autopsy
AR
-
+
A
Autopsy
AR to L lilac
-
-
A
Angiogram
BR to R common lilac
+
-
A
Angiogram
AR to iliacs
-
-
C
Angiogram
--
BR to bifurcation
-
+
A
Autopsy
--
SMA to lilacs
-
-
A
Autopsy
--
BR to R. common lilac
-
-
A
Operation
BR to above bifurcation
-
+
C
Autopsy
BR to lilacs
-
-
C
Autopsy
Mesenteric involvement Died 4 yr postop, unrelated --IMA involved
Dissection witnessed in O R --
Confined to abdomen
+
-
-
C
Autopsy
Death from head injury Death from sepsis
AR to R common lilac
-
-
+
A
Autopsy
--
-
-
C
Autopsy
Death from pneumonia
Just below diaphragm
585
Continued
a n d m o t o r f u n c t i o n . E x a m i n a t i o n o f the a b d o m e n w a s n o r m a l . A n g i o g r a p h y d e m o n s t r a t e d total o c c l u s i o n o f t h e infrarenal aorta, w h i c h w a s believed to be e m b o l i c in origin. A bilateral f e m o r a l t h r o m b o e m b o l e c t o m y w a s perf o r m e d w i t h r e e s t a b l i s h m e n t o f b l o o d f l o w to the legs. O n the s e c o n d p o s t o p e r a t i v e day the p a t i e n t c o m p l a i n e d o f severe a b d o m i n a l pain. E x a m i n a t i o n o f the a b d o m e n w a s u n r e v e a l i n g and, in t h e p r e s e n c e o f a w o r s e n i n g acidosis, acute m e s e n t e r i c insufficiency w a s suspected. R e p e a t ang i o g r a p h y (Fig. 4) s h o w e d a posterior-lateral dissection o f t h e a b d o m i n a l a o r t a f r o m the celiac axis t o the iliac arteries,
w i t h a p p a r e n t r e e n t r y at t h e level o f the aortic bifurcation. T h r o m b o s i s w a s seen in the distal aorta. T h e disscction w a s f o u n d t o involve the r i g h t renal a n d s u p e r i o r m e s e n teric arteries. T h e p a t i e n t w a s taken to the o p e r a t i n g r o o m w h e r e a necrotic s i g m o i d c o l o n w a s resected, a n d an ext r a a n a t o m i c axillobifemoral b y p a s s w a s p e r f o r m e d . N o att e m p t w a s m a d e to repair t h e aorta directly. T h e p a t i e n t r e m a i n e d h y p o t e n s i v e a n d acidotic; h e r c o n d i t i o n deterio r a t e d , w i t h w o r s e n i n g renal a n d cardiac failure. She died o n t h e sixth p o s t o p e r a t i v e day. P e r m i s s i o n for a u t o p s y w a s denied. C a s e 4. A 72-year-old h y p e r t e n s i v e , diabetic black m a n
586
Journal of VASCULAR SURGERY
Graham et al.
T a b l e I. C o n t ' d
Author
Year
No. cases
Age (yr)
Sex.
Symptoms
Puderbach2r
1954
1
73
M
Tender abdomen
Kocandrle et al.28
1970
1
48
M
Gaylis & Laws29
1956
2
58
M
Abdominal pain/yoreking After anglo, L leg pain & paresthesia None
62
M
None
None
42
M
BP 260/130 mm Hg
62
M
Cardiac arrest after anglo After anglo, cold LE
51
M
GI bleed, after anglo
Rectal necrosis Tender lower abdomen; absent LE pulses
Wolfman & Boblitt3°
1959
3
Tomatis et al.3~
1968
1
27
F
David & Blumenberga2
1970
1
54
F
Bilateral leg pain & numbness from MVA MVA
Welborn & Sawyers3a
I969
1
33
F
MVA; nmaab feet
Nunn34
1973
1
58
M
MVA; paralysis LE
Ngu & Konstam35
1965
1
37
F
Surfboard to abdomen
Hewitt & Grablowsky 36
1970
1
65
M
MVA; paralysis LE
Jackson & Slavin37
1953
1
74
M
Shormess of breath
Faivre et al.s8
1962
4
72
F
70
M
Low back/abdominal pain Low back pain
74
M
75
M
Abdominal/back pain; melena Abdominal pain 2 mo
J.J. B.P.
58 65
M M
Chest/epigastric pain None
B.C.
56
F
C.N.
72
M
Acute bilateral LE ischemia None
Present series
1988
was admitted for angiographic evaluation of rest pain in the left foot. The blood pressure was 156/76 man H g during examination. The abdomen was normal. The lower extremities showed clinical evidence of chronic arterial insufficiency. Doppler studies indicated bilateral occlusive disease o f the superficial femoral and popliteal arteries with severe ischemia o f the left leg. Angiography showed dissection of the infrarenal aorta, with marked arterial occlusive disease of the left leg. In retrospect, the patient recalled being involved in a mine collapse 45 years earlier, causing severe back pain that subsided 3 to 4 years later. Because this was thought to
Physicalfindings
After anglo; loss of LE pulses bilaterally Diminished R femoral pulse
No LE pulses
Absent LE pulses w/sensorimotor deficit Loss of LE pulses; sensorimotor deficit Absent pulses; legs cold, mottled, sensoqr deficit Tender abdomen; absent LE pulses w/neuro deficit Absent LE pulses; mottled and cold LLQ pulsatile mass Shock, systolic BP 80 mm Hg Systolic BP 60 mm Hg; no femoral pulses None BP 200/100 mm Hg; abdominal bruit Epigastric tenderness None; equal pulses bilaterially Absent LE pulses; sensorimotor deficit None
be the cause of his apparent chronic aortic dissection, therapy for this incidental finding was n o t recommended. The patient had successful distal arterial reconstruction of the left leg. RESULTS
Presentation. T h e m e a n age o f all p a t i e n t s at t h e t i m e o f d i a g n o s i s was 5 8 . 6 years ( r a n g e 2 7 to 75 years). Sex, r e p o r t e d i n 4 3 cases, s h o w e d a m a l e pred o m i n a n c e ( 6 7 % ) . R a c e was i n d i c a t e d i n o n l y 2 0 cases; m o s t o f these p a t i e n t s w e r e w h i t e ( 7 5 % ) . T h e m o s t c o m m o n p r e s e n t i n g s y m p t o m , p r e s e n t i n 19
~=
Volume 8 Number 5 November 1988
Abdominal aortic dissections
Location
Reentry
AR Below IMA to lilacs
-
Evaluation of thoracic aorta
VVI
Rupture
A /C
+
+
A
Autopsy
-
-
A
At operation
-
-
A
Angiography
A
Angiography
A
Autopsy
587
Remarks R renal a r t e q ~ , involved Secondary to a n g l o
Above bifurcation
BRtoRcommon
i~ac
BR to R common lilac
-
-
3 cm AR to 7 cm BR
-
+
A
Autopsy
AR to lilacs
-
+
A
Autopsy
Distal 5 cm aorta, lilacs
-
-
A
At operation
+
A
Autopsy
-
+
A
At operation
BR to above bifurcation
-
-
A
At operation
Below IMA to above bifurcation
-
-
A
At operation
A
Autopsy
C
Autopsy
SMA to L COlnmon iliac /MA, above bifurcation
-
-
m
L
m
IMA to lilacs Above bifurcation
m
Below SMA
+
A
Autopsy
Below diaphragm to bifurcation Confined to abdomen
+
A
Autopsy
+
A
Autopsy
A
Autopsy
+
Confined to abdomen L-3 to lilacs BR to R iliac
+ +
-
C C
Angiogram Angiogram
L-3 to L iliac
+
+
A
Angiogram
BR to bifurcation
-
-
C
Angiogram
patients, was pain of acute onset (less than 2 weeks) (Table II). This was frequently described as sharp, severe or knife-like, and radiated between the abdomen and back. Acute leg ischemia, in the absence of previous arterial insufficiency, was also a common finding. Other presenting symptoms included chronic (greater than 2 weeks' duration) abdominal pain, hematuria, melena, and shock. In most cases (70%), symptoms were of acute onset. Medical histories were often incompletely reported. A history o f hypertension was present in 18
SecondaDr to lumbar anglo for claudication Secondary. to lumbar anglo for claudication
Bilateral renals involved IMA & renals involved Traumatic
IMA & R renal involved IMA involved
Death from to sepsis
Mesenteric involvement
Seconda U to anglo SMA, IMA and L renal involved --
of 34 cases (53%), and atherosclerosis was evident in 31 of 40 cases (78%). Medial arterial disease and syphilis were rarely reported. No patients had Marfan's syndrome, congenital cardiovascular anomalies, or were pregnant. Dissection was asymptomatic in nine cases. Physical findings included systolic hypertension in 15 patients (38%) (Table II). Abdominal tenderness was present in 13 of 37 patients, whereas other findings were the presence of a pulsatile abdominal mass, an abdominal bruit, diminution of lower ex-
588
Graham et al.
Journal of VASCULAR SURGERY
Fig. 3. Abdominal aortogram demonstrates dissection extending from infrarenal aorta to iliac arteries (arrow).
Fig. 4. Abdominal aortogram demonstrates dissection from supraceliac aorta to lilac arteries (black arrow) and thrombus within distal aorta (white arrow).
tremity pulses, and loss of sensation or motor function. Rupture of the dissection occurred in 13 cases (28%) and was associated with a 92% mortality rate (p < 0.000002). In seven cases, dissection of the abdominal aorta was iatrogenic--a complication of translumbar or transfemoral aortography. Dissection was the result of blunt abdominal trauma in seven others. In the remaining 33 cases (70%), no obvious etiologic factor could be ascertained. Diagnosis. The means of diagnosis of abdominal aortic dissections varied considerably according to the period of presentation. Early cases were often diagnosed by abdominal exploration or at autopsy. More recently, such imaging modalities as ultrasonography, CT scanning, and angiography have been used to establish the diagnosis. In this series, the diagnosis was made by angiography in 17 cases (36%) and ultrasonography in one case (2%). Dissection was diagnosed clinically in three cases, at surgical exploration in nine, and at autopsy in 17. Most dissections of this type were located below the renal arteries (Table III). The site of the intimal
tear, reported in 20 cases, was below the renal arteries (n = 12), between the renal arteries and the superior mesenteric artery (n = 6), or between the superior mesenteric artery and diaphragm (n = 2). Visceral vessel involvement, whether an extension of the dissection process or branch occlusion, was present in 10 cases (21%). Reentry tears were present in 33% of cases adequately examined and were more frequently associated with chronic rather than acute dissections (p < 0.02). Twenty-eight patients (68%) had continued flow in the false lumen. Rupture occurred more frequently in this group (p < 0.003). Management. Management options have evolved considerably over the period included in this study. Twenty-six patients (55%) received no specific treatment, often because current methods of assessment and treatment of these lesions were not available. The remaining 21 patients were managed surgically. Most of these patients had the affected aorta replaced with a prosthesis (n = I4). Other procedures included the creation of an outflow (reentry) channel from the false lumen (n = 2), oversewing the dissection channel (fenestration) (n = 1), suture
Volume8 Number5 November1988
repair of an external rupture (n = 2), endarterectomy (n = 1), and extraanatomic bypass without direct aortic repair (n = 1). Overall survival (64%) was influenced by several factors (Table IV). Those patients who were hemodynamically unstable (p < 0.002) or who presented with acute pain (p < 0.0003) were more likely to die as a result of their dissection than those who did not. Rupture was associated with death in 92% of cases. Dissections involving the suprarenal aorta or visceral vessels were also more frequently linked with a poor outcome than those limited to the infrarenal aorta. Although operative treatment significantly improved survival in acute dissections (p < 0.002), it had no effect on outcome in chronic cases. When all cases were considered, chronicity appeared to be protective (p < 0.04). Twelve major perioperative complications occurred in 10 patients. Renal insufficiency, varying from a transient azotemia to progressive renal failure, occurred in seven patients, five of whom died. In two cases, acute renal failure was attributed to renal hypoperfusion during shock. Five patients had dissections involving the visceral vessels (p < 0.003) and five had dissections involving the suprarenal aorta (20 < 0.05). Gastrointestinal ischemia occurred in four patients. None of these survived despite resection of the involved bowel in three. Paraplegia was reported in one patient, who died of associated injuries. DISCUSSION Although aortic dissection has been found to occur in 1 of 363 autopsies, those limited to the abdominal aorta contribute only 2% to 4% of all cases) 3 In many respects, localized dissections of the abdominal aorta are similar to their thoracic counterparts. Both occur in middle age and affect men three times more frequently than women. 1,4 Hypertension is common to both, occurring in 54% of patients in this series as compared with 58% to 90% of those with thoracic dissections. 2,39Atherosclerosis was also a common finding in this series (76%) and was often found in the region of the dissection, although its significance is unlmown. Medial dysplasia, frequently associated with thoracic aortic dissections, 1-4was rarely reported in this group of patients. Marfan's syndrome, congenital cardiovascular lesions, and pregnancy were notably absent in this series. Presentation with acute, shearing pain and systolic hypertension appears to be common to both abdominal and thoracic aortic dissections. Limb isch-
Abdominal aortic dissections 589
Table II. Symptoms and physical findings Symptoms (n = 47) Acute pain, abdomenor back Chronic pain Acute lower extremityischemia Hematuria Melena Asymptomatic Physicalfindings Blood pressure (n = 40) Shock (systolicBP ~ 90 mm Hg) Hypertension (systolicBP />180 mm Hg) Abdomen (n = 38) Tenderness Pulsatile mass Nonpulsatile mass Bruit Extremities (n = 42) Diminished pulses Sensory impairment Loss of motor fi.mction Bruits
No.
%
19 4 16 3 2 8
40 9 34 6 4 17
6
15
i5
32
13 3 1 3
34 8 3 8
i9 6 5 2
45 14 I2 5
emia is often associated with abdominal aortic dissections. Although rupture can occur with both, cardiac tamponade may predominate with thoracic dissections and hypovolemic shock with abdominal dissections. Presenting signs and symptoms may be nonspecific. Numerous imaging modalities have been helpful in establishing or confirming the clinical diagnosis. B-mode ultrasonography has been used to demonstrate an echogenic, intimal flap, but this finding can be easily missed in a nondilated aorta. 4° Realtime abdominal ultrasonography can more clearly show the intimal flap moving with aortic flow and, if combined with Doppler flow studies, can readily evaluate flow in the false and true lumens. 41'42 CT scanning may show a double aortic lumen, nonopacification or poor opacification of a portion of the aorta, aortic widening, or inward displacement ofintimal calcifications.43.44As with ultrasonography, dissections can be misinterpreted as intraluminal thrombus. Such modalities are often unable to provide sufficient information regarding the point of initiation, the extent of the dissection, and the presence or absence of visceral vessel involvement. Angiography remadns the definitive diagnostic study in abdominal aortic dissection. Specific signs of aortic dissection include visualization of a double channel, the presence of a linear radiolucency within the aortic lumen, demonstration of entry or reentry tears, and branch involvement. Indirect signs include compression of the true aortic lumen by the false
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Graham et al.
Table III. Characteristics o f dissection Location (n = 51) Below renais Above rends Extent unclear Site of tear (n = 20) Level of celiac Between rends and SMA Between rends and bifurcation Reentry tear (n = 21) Flow in false lumen (n = 41) Visceral vessel involvement(n = 47) Rupture (n = 47) Acuity (n = 47) Acute Chronic
No.
%
Survivo,x
%
28 16 3
85 31 6
23 5 2
82 31 67
2 6 12 7 28 10 i3
10 30 60 33 68 21 28
2 1 8 5 15 3 1
100 17 67 71 54 30 8
33 14
70 30
18 12
55 86
Table IV. Factors adversely affecting outcome p Value*
Presentation Acute pain, abdomen or back Shock Characteristics of dissection Location above rends Visceral vessel involvement Rupture Acute dissection Management Nonopcrative, all cases Nonopcrative, with acute pain
0.0003 0.002 0.003 0.02 0.000002 0.05 0.03 0.05
~Fisher's exact test. lumen, thickening o f the aortic wall, irregular projection o f the dye column, or abnormal catheter position. False-negative findings can result from simultaneous opacification o f both lumens, total aortic occlusion, or limited radiographic projections. 4s,46 Because abdominal aortic dissections may represent the extension o f a thoracic aortic dissection, the thoracic aorta must be evaluated in all patients. Few recommendations for the management o f abdominal aortic dissections have been made. Recent reports recommend repair or replacement, 7'2° but this has not been shown to bc necessary in all cases. Although nonsurgical management has been found to be appropriate for type III thoracic aortic dissections, 47 its role in the treatment of dissections limited to the abdominal aorta is unclear. EightT-one percent o f patients treated operatively in this series survived, including 13 o f 14 who had prosthetic replacement o f the aorta, two who had reentry, procedures, one who had a fenestration, and one who had an endarterectomy. Suture o f an external rupture was per-
formed in two patients, both o f w h o m died. An extraanatomic bypass was done in one case without direct repair o f the aorta and this patient died. Although the data presented here support the idea that operative treatment o f dissections results in a better outcome, there appears to be a role for nonoperative management in selected patients. Patients who require surgical intervention include those with signs o f rupture, visceral vessel involvement, or acute limb ischemia. The presence o f acute abdominal pain or suprarenal aortic involvement is also associated with a high mortality rate if left untreated and so should be considered indications for surgical therapy. Patients in w h o m nonoperative management can be considered are those with chronic dissections without symptoms. Survival in this group was not significantly altered by operation. However, those patients with chronic dissections who have acute symptoms require surgical treatment. Chronic dissections not repaired should be observed closely with CT scanning or angiography. Signs o f progression o f the dissection or the development o f a saccular aneurysm should prompt surgical treatment. CONCLUSION Aortic dissection timitcd to the abdomen is rare. Several characteristics o f the disease, such as presentation and risk factors, are similar to those o f thoracic dissections. Although the diagnosis may be made by CT scanning or tdtrasonography, angiography should always bc performed to document the extent o f the dissection and the presence o f major branch involvement and to rule out thoracoabdominal dissection. In most cases, prosthetic replacement o f the aorta is the treatment of choice. However, in selected patients with asymptomatic chronic dissections, ob-
Volume 8 Number 5 November 1988
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