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ABDOMINAL AORTA

HISTORY

The anatomic and surgical history of the abdominal aorta is the history of the vascular system. It is presented in Table 12-1.

Table 12-1. Anatomic and Surgical History of the Vascular System

Aretaeus (A.D. ca. 81 -ca. 138)

Considered phlebitis a septic process secondary to infection

Galen (A.D. ca. 130 -ca. 200)

Believed blood pass es from veins to arteries through small pores in various parts of body.

First to describe ductus arteriosus.

Antyllus A.D.350

Ligated above and below to o pen aortic aneurysm

Canano mid-1500s

Demonstrated valves of veins to Vesalius

Harvey 1628 Understood role of veins in circulation.

1651 Cannulated inferior vena cava to prove pulmonary circulation in postmortem heart-lung complex.William Hunter 1757 Described traumatic a rte riovenous communica tion

Hallowell 1759 Success fu lly closed brach ia l a rte ry by un iting edges o f wound with peg, around which he twis ted a th read

W hite 1784 De scrib ed "milk le g." Fa vo re d lymp ha tic o bs tructio n the ory o ve r ro le o f thro mb os is .

John Hunte r 1786 In troduced proximal ligation a lone in upper th igh for pop liteal aneurysm

Laennec 1819 Described "pulmonary apoplexy" (pulmonary embolism)

Cruveilhier 1829 Observed that arterial branches leading to lesions are "filled with clots that branched according to the vascular tree"

Lobstein 1829 First used term "arteriosclerosis"

Virchow 1846 Recognized role of clot in phlebitis and embolism

Cohnheim 1872

Welch 1899

Brodie 1846 Re cognize d inte rmitte nt cla udica tion in huma ns simila r to tha t of horse s

Ra yna ud 1862 De fine d va sospa stic dise as e tha t be ars his na me (Ra yna ud's dise ase )Friedlnder, vonWiniwarter

1870s Described arteritis obliterans

Von Eck 1879 P erformed a nastomosis of portal vein and inferior vena cava

Se ve re anu 1880 Atte mp te d a rte ria l thro mb ecto my to ma na ge o cclus ive d is ea se

Gluck 1881 Repaired arterial wounds with small ivory clamps

Matas 1888 Described endoaneurysmorrhaphy for management of aneurysms

Connheim 1889 Studied ischemic tissues

Jassinow sky 1889 Repaired a rterial w ounds with sutures

Trendelenburg 1890 Understood hemodynamics of varicosities and venous stasis of lower extremities and pulmonary embolism. Removed pulmonaryembolism.

Murphy 1896 Performed first successful arterial anastomosis

C arre l 1902 E xp erime nte d with arte ria l re pla ce me nts . P ub lis he d te chniq ue o f circula r s uture o f b lo od ve ss els .

Exner 1903 Transplanted autogenous venous graft

P ayr 1904 De vis ed me tho d to unite divid ed ve ss els b y inva gina ting e nd s into a n a bs orb ab le ma gne sium cylind er

Carrel & Guthrie 1906 Reported arteriovenous anastomoses and transplantat ion of organs

Delbet 1906 Attempted arterial thrombe ctomy to manage occlusive dise ase

1911

Lexer 1907 Successfully used free vein graft on axillary artery

Buerger 1908 Expanded description of thromboangiit is obliterans, showing that it and periarterit is nodosa cause only a small proport ion of cases of arterial obstruction in leg

Jianu 1909 Attempted arterial thrombectomy to manage occlusive disease

Pirovano 1910 Firs t clin ica l transplanta tion of homologous a rtery from one human to ano ther (unsuccess fu l)

La be y-Mo sny 1911 Succe ss fully p erfo rme d a rte ria l e mb ole cto my

Warthmulle r 1917 Succe ss fully tre ate d tra uma tic ane urys m u sing ve in g ra fts


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,

Orrin 1920 Published anatomic atlas of postmortem arteriograms

Osborne et al. 1923 Devised concept of angiography with sodium iodide, without films (USA)

Sicard & Forestier 1923 Experimented with venography and arteriography with Lipiodol in animals and in clinical trials in man

Dnner & Calm 1923 Visua lized subclavian ve in us ing sod ium iodide (one case)

Berberich & Hirsch 1923 Performed first successful arteriography in man with water-soluble contrast material (strontium bromide) and first gooddemonstration of peripheral veins w ith valves

Holman 1924 Described increase in b lood vo lume and card iac output with occasiona l ca rd iac fa ilu re in a rte riovenous fis tu las

Kirschner 1924 Performed successful pulmonary embolectomy

Moniz 1927 Devised carotid arteriography

Homans 1928 Prevented pulmonary embolism by venous ligation1934

dos Santos et al. 1928 Experimented with percutaneous aortography with sodium iodide

dos Sa ntos 1929 De ve lop ed te chnique of tra nslumba r a rte riogra phy

dos Santos et al. 1931 Introduced Thorotrast for angiography. Developed mechanical injector with preset pressure.

Gurin e t a l. 1935 Firs t surg ica l a tt empt to correct aneurysm of the aorta by d issection

Gibbon 1937 Devised heart-lung apparatus for use on animals

Mu rra y 1937 C on ce ptua liz ed va rico se ve ins a s a d is ea se o f d ee p ve no us s ys te m fo llo wing p hle bitis .

Prevented pulmonary embolism with anticoagulants.

Leriche 1937 Described arteriectomy for chronic arterial insufficiency

Castellanos & Pereiras 1938-1939

Performed inferior vena cavograp hy

Farias 1941 Performed abdominal aortography with catheterization through surgical cutdown of femoral artery and introduction throughtrocar

Crafoord 1944 Corrected coarctation of aorta

Alexander & Byron 1944 Performed first successful proximal and distal ligation of thoracic aorta for removal of fusiform aneurysm

dos Santos 1947 In troduced th romboendarte rectomy to disob lit era te occluded a rte ria l segments

Kunlin 1948 Introduced bypass principle for treatment of arterial occlusion

Gro ss 1949 P erfo rme d s ucce ss ful ho mo lo go us g ra ft to b rid ge a ortic d efe ct fo r co arcta tio n o f a orta

Linton 1949 Performed successful aneurysmectomy

So uz a P ere ira 1949 Inje cte d s up erio r me se nte ric ve in fo r p orto gra phy

Elkin & Cooper 1949 Described limited experience with Leriche terminal aortectomy

Oudot 1950 P erforme d first re se ction a nd homogra ft of a thrombos ed a ortic bifurca tion

Bigelow 1950 Published effect s o f hypothermia on lowering of oxygen consumption and it s impact on blood flow th rough heart

Peirce 1951 Performed thoracic aortography th rough femora l a rtery need le by inse rting polye thylene ca thete r without gu ide wire

Ponsdomenech & Beato-Nunez

1951 Performed left ventricular angiography with direct needle puncture

Thompson & Smithwick 1952 Performed first revascularization of kidney (unsuccessful)

Dubost et al. 1952 Dubost reported first successful resection of abdominal aortic aneurysm and use of preserved human arterial graft for continuity.Several other surge ons repo rted similar successful results.Szilagyi et al.

Shumacker & King

Julian e t al.

Voorhees, Jaretzki, andBlakemore

1952 Successful use in animal experiments of Vinyon-N tubes made of porous, biologically inert material that remained patent

De Ba ke y 1953 Firs t s ucce ss ful o pe n thro mb oe nd arte re cto my o f ca ro tid b ifurca tio n

DeBakey & Cooley 1953 First successful resection of aneurysm of thoracic aorta and replacement by graft

Se ldinge r 1953 Introduce d te chnique of pe rcuta ne ous arte ria l ca the te riza ton

Gibbon 1953 Applie d he art-lung appa ra tus to close an a tria l se pta l de fe ct in a young woma n

Edw ards 1953 Toge the r w ith che mist Ta pp, introduce d va scula r gra ft inno va tions

Shumway et al. 1955 Experimented with rolled sheets of polyvinyl sponge (Ivalon)

Shaw & Maynard 1958 Firs t superio r mesente ric endarte rectomy

Mikke lsen & Zaro 1959 Firs t to transect and re implant SMA

Palma & Esperon 1960 Treated postphlebit ic syndrome using venous transplant and grafts

Strm & Winberg 1962 Selective infe rio r mesenteric a rte riography

Boijsen e t al. 1963 Selective s imultaneous ce liac axis and superio r mesente ric arte riogram

Fogarty e t a l. 1963 Balloon ca thete rizat ion fo r extract ion of in travascu la r emboli

Golomb et al. 1964 Selective visceral catheterization of arteries for infusion cancer chemotherapy

Waldhausen &

Nahrwold

1966 Introduced subclavian flap angioplasty

Ha rrison e t a l. 1967 Introduce d e ve rsion e nd arte re ctom


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Connolly & Stemmer 1970

Be nta ll 1968 Intro duce d d ire ct re atta chme nt o f co ro na ry a rte ry o rig ins to co mp os ite va lve gra ft

Ochsner et a l. 1970 Reported 286 cases of IVC ligation with only 4% postph lebit ic sequelae

Amgwerd & Sege 1975 First clinical experience with modified heteroplastic arterial grafts from calf arteries

Rob et al. 1976 Studied chronic intestinal ischemia. Performed intraluminal wire reinforcement of symptomatic aortic aneurysm.

Gre enfie ld 1976 P ub lis he d exce lle nt mo no gra phs on pulmo na ry emb olis m a nd IVC filte rs

Shumacker 1982 For selected patients, advocated extraperitoneal surgery of abdominal aorta, iliac arteries, and aortic visceral branches

Cabrol 1981,1986

Reattached coronary artery origins to composite valve graft using se parate small Dacron tube g raft

Crawford 1984,1986 Performed graft replacement of aneurysm in descend ing thoracic aorta w ithout bypass or shunting.

1992,1993

"Open button" technique for composite valve graft replacement of proximal aorta.

1993 Report on 1509 patients who underwent treatment for thoracoabdominal aortic aneurysm

Miller 1992,1993

Outlined conservative treatment of chronic and a cute dissection of descending thoracic aorta

History table compiled by David A. McClusky III and John E. Skandalakis.

References:

Doby T. Development of Angiograp hy and Cardiovascular Cathe terization. Littleton MA: Publishing Sciences Group, 1976.

Greenfield LJ. Surgery: Scientific Principles and Practice. Philadelphia: JB Lippincott, 1993.

Haimovici H (ed). Haimovici's Vascular Surgery (4th ed). Cambridge MA: Blackwell, 1996.

Heberer G, van Dongen RJAM. Vascular Surgery. Berlin: Springer-Verlag, 1989.Sabiston DC Jr. Textbook of Surgery. Philadelphia: WB Saunde rs, 1986.

Shumacker HB Jr. Extraperitoneal a pproach for vascular ope ration: retroperitoneal review. South Med J 75(12):1499-1516, 1982.

Shumacker HB Jr. Little used surgical techniques of value. Am J Surg 144:186-190, 1982.

Smith RB III. Presidential ad dress: the foundations of modern aortic surgery. J Vasc Surg 27:7-15, 1998.

Warren R. Surgery. Philadelphia: WB Saund ers, 1963.

Yao JST, Pea rce WH (eds). Progress in Vascular Surgery. Stamford CT: Appleton & Lange , 1997.

EMBRYOGENESIS

Normal Development

The aortic sac is responsible for the embryologic development of the aorta. The sac is the terminal portion of the truncus arteriosus. The truncusarteriosus represents the distal portion of the bulbus cordis. All these complex embryologic entities are related to the formation of the cardiac loop. (The

interested reader is encouraged to read Embryology For Surgeons2).

Congenital Anomalies

As compared with the thoracic aorta, the abdominal aorta has few congenital anomalies. Its branches, however, are subject to numerous variations.

Coarctation of the abdominal aorta constitutes a rare group of vascular abnormalities, including segmental stenoses and extended hypoplasia. Althoughhypertension is usually the only clinical finding, there is considerable diversity of both anatomic lesions and surgical techniques used for their

treatment. 3,4,5 Smith and Kelly 6 associated coarctation of the abdominal aorta with concomitant narrowing of the origins of major visceral arteries as arare cause of life-threatening hypertension.

It is often difficult to determine whether aortic coarctation is congenital in origin or due to Takayasu's arteritis. 3 Piyachon and Suwanwela 7 have observedgeographic differences in frequency according to gender, anatomic distribution, and the type of lesion observed in association with Takayasu's arteritis.

In a case reported by Takeshita et al., 8 the abdominal aorta was divided into two abnormal vessels. One vessel was the celiac artery, while the other was

considered to be the abdominal aorta. These authors presented their findings and discussed the embryologic basis of this rare anomaly.SURGICAL ANATOMY

Topography and Branches

The abdominal aorta (Fig. 12-1), extending downward from T12 as a continuation of the thoracic aorta, is approximately 10 cm long. It terminates at the

lower one-third of the body of L4 (60% of cases). 9 Here it trifurcates as the right and left common iliac arteries and the middle sacral artery. For practicalpurposes this is really a bifurcation, as the middle sac ral artery represents a small median branch emerging between the two common iliacs.

Fig. 12-1.


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The diaphragmatic openings for the inferior vena cava, es ophagus , and a orta as see n from the left. (Modified from Skandalakis LJ, Colborn GL, Skandalakis JE.Surgical anatomy of the diaphragm. In: Nyhus LM, Baker RJ, Fischer JE. Mastery of Surgery, 3rd ed, Vol 1. Boston: Little, Brown & Co, 1997; with permission.)

The abdominal aorta traverses approximately 3 vertebrae. The surface anatomy of t he abdominal aorta extends approximately from a point 2 cm belowthe tip of the xiphoid process to a point usually averaging 1 cm below and slightly to the left of the umbilicus, near the midpoint of the line connectingthe summits of the iliac crests (the intercristal plane).

The aorta decreases markedly in diameter as it descends within the abdomen, due to the large size of its principal branches. At the 11th rib, the diameteris about 25 mm; above the origin of the renal arteries, 22 mm; below the renals, 20 mm; and at the bifurcation, 19 mm. 10

Yahel and Arensburg reported that the length of the total descending aorta does not correlate with stature, and prediction of its length is not possible. 11

The aorta is closely related to the right and left diaphragmatic crurae. It passes by means of the aortic hiatus (Fig. 12-1, Fig. 12-2) behind the diaphragm,not through a hiatus of the diaphragm, as do the inferior vena cava and esophagus. Therefore the aortic hiatus does not open within the diaphragm. Atthe diaphragm, the aorta is separated from the inferior vena cava and the right celiac ganglion by the right crus. Here, the inferior vena cava assumes aposition ventral to the aorta as the cava angles forward to pierce the diaphragm to enter the right atrium. At the aortic bifurcation the inferior vena cavaassumes a position dorsal to the aorta, dividing at the level of L5.

Fig. 12-2.


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The ape rtures of the diap hragm seen from below and the structures traversing the m. A = aorta, IVC = inferior vena cava. (Modified from Skandalakis LJ, ColbornGL, Skandalakis JE. Surgical anatomy of the diaphragm. In: Nyhus LM, Baker RJ, Fischer JE. Mastery of Surgery, 3rd ed, Vol 1. Boston: Little, Brown & Co, 1997;with permission.)

The abdominal aorta contributes visceral branches that serve intraperitoneal and retroperitoneal organs, and parietal branches that support the roof and

walls of the abdomen. Grant and Basmajian 12 present these as collateral branches as follows.

The celiac trunk, superior mesenteric artery, and inferior mesenteric artery provide for the G-I canal and the 3 unpaired glands (Fig. 12-3A). (These areoften referred to as the unpaired, visceral branches.)

Fig. 12-3.

The branches o f the ab dominal aorta arranged according to the plane s they occupy (diagrammatically depicted in Fig. 12-4). The branches s upply the followingterritories: A, GI canal and 3 unpaired glands ; B, 3 paired glands; C, roof and walls of abdomen. CA = celiac artery, SMA = superior mesenteric artery, IMA =inferior mesenteric artery, A = adrenal gland, AA = adrenal artery, K = kidney, RA = renal artery, T = testis, TA = testicular artery, PhA = phrenic artery, LA =lumbar arteries, MSA = median sacral artery. (Modified from Grant JCB, Basmajian JV. Grant's Method of Anatomy, 7th ed. Baltimore: Williams & Wilkins, 1965; withpermission.)

Fig. 12-4.


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The three vascular planes of the collateral branches of the a bdominal aorta (see Fig. 12-3A, B, C). (Modified from Grant JCB, Basmajian JV. Grant's Method of Anatomy, 7th ed. Baltimore: Williams & Wilkins, 1965; with permission.)

The adrenal arteries, renal arteries, and gonadal (ovarian or testicular) arteries go to the 3 paired glands (Fig. 12-3B) (These are the three paired visceralbranches.)

As parietal branches, the (inferior) phrenic arteries, lumbar arteries, and median sacral artery provide circulation to the roof and walls of the abdomen (Fig.12-3C).

To the above-named parietal branches, we would include the right and left common iliac arteries.

Grant and Basmajian's diagrammatic figures (Figs. 12-3, 12-4) beaut ifully demonstrate the arterial distribution and the t erritories supplied.

The two principal terminal branches of the abdominal aorta, the common iliac arteries, arise from the aortic bifurcation, about 1 cm inferior to the umbilicusand to the left of the midline. Ending at the level of the sacroiliac joints, they divide into the internal iliac and external iliac arteries. The courses of thecommon iliac and external iliac arteries can be shown on the surface of the body by a somewhat laterally convex line drawn from the point of aorticbifurcation to the femoral point. This point is midway between the anterior superior iliac spine and the pubic symphysis. The course of the common iliacoccupies the proximal third of the line, and the external iliac occupies the distal two thirds.

Because the aortic bifurcation occurs to the left of the median plane, the right common iliac is somewhat longer than the left, approximately 5 cm and 4cm, respectively. The course of the right common iliac artery is from 1 cm left and inferior to the umbilicus to a point 3 cm from the midline at the level of the intertubercular plane. In a relatively thin, supine patient whose pelvis is elevated slightly to displace the viscera upward, the aortic pulse at thebifurcation and the pulses in the common and external iliac arteries can be palpated along the lines described.

Because iliac arteries can pose formidable obstacles to successful treatment of infrarenal abdominal aortic aneurysms, Henretta et al. report that at

Southern Illinois University all patients are treated with a bifurcated, modular graft that can be tailored to the patient's aortic and iliac anatomy. 13,14,15

Numerous other chapters include detailed material about the visceral and parietal branches of the aorta including discussions of the various anatomicentities they supply and the vessels responsible for t heir blood supply. However, we briefly summarize some of them here.

Celiac Axis

The celiac trunk often arises at the lower margin of T12, but it may originate between this point and the lower margin of L1. Its site of origin is usuallyabout 1 cm above that of the superior mesenteric artery. Van Damme, the modern student of abdominal vascular anatomy, states the following about the

celiac axis in his beautiful paper Behavioral Anatomy of the Abdominal Artery .16

The celiac trunk does not trifurcate into its three main branches as is usually depicted, but it bifurcates into the splenic and the (common) hepaticartery. Its third branch, the left gastric artery, is a mobile vessel whose origin may slide between the aorta (leaving a hepatosplenic trunk) all overthe celiac trunk up to a real trifurcation. The complete celiac trunk can fuse with the superior mesenteric artery (celiacomesenteric trunk). One of the three constituent branches of the celiac trunk can have a separate origin from the superior mesenteric artery or from the aorta. If two of itsbranches have a separate origin, there is no celiac trunk left (Fig. 12-5). The hepatic artery pulls the celiac trunk to the right. If the hepatic arterydoes not arise from the celiac trunk, the remaining gastrosplenic trunk is directed to the left and seems to continue into the splenic artery.Variations in the origin of the splenic artery are unusual. The left gastric vein is usually found in the fork where the celiac trunk bifurcates into thehepatic and splenic artery. The most common collateral of the celiac trunk is a single or double inferior phrenic artery.

Fig. 12-5.


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The division of the ce liac t runk. (Lit. ), reported in medical literature. (Modified from Van Damme JPJ, Bonte J. Arteria splenica and the blood supplyof t he spleen (splen). Probl Gen Surg 1990;7:18-27; with permission.)

avdar et al. 17 reported a case of celiacomesenteric trunk, a variation found in only 1 percent to 2.7 percent of the population.

Of the three principal unpaired visceral branches of the aorta, the celiac trunk is the most prone to variations. As reviewed by Lippert et al., 18 some of these and their percentages of occurrence in the population are:

Origin of inferior phrenic artery from celiac trunk: 50 percent

Left ga stric arises ea rly from celiac, followe d by hepato splenic bifurcation: 49 percent

"Typical" trifurcation of celiac trunk: 25 percent

Hepatos plenic trunk: 5 percent. (Left gastric arises independ ently from aorta.)

Gastrosplenic trunk: 3 percent. (Common he patic arises sepa rately from aorta.)

Gastrohepa tic trunk: 1 pe rcent. (Splenic arises se parate ly from aorta.)

Gastrohepa tosplenomesente ric trunk: 2 percent. (Celiac and superior mesenteric combined)

Hepatomesenteric trunk: 3 percent. (Splenic and left gastric form common stem.)

Superior Mesenteric Artery

We are grateful to Dr. Jean- Pierre J. Van Damme 16 for permitting us to reprint his excellent description of the superior mesenteric artery.

The superior mesenteric artery (SMA) is the axis around which the rotation of the gut takes place. The left renal vein is found between the origin of the superior mesenteric artery and the aorta. The superior mesenteric artery and vein run between the duodenum and the pancreas; at this levelthe artery runs to the left of the vein. The horizontal part of the duodenum may become compressed in the fork between the aorta and the superiormesenteric artery in cases of intestinal ptosis. After the origin of the ileocolic artery, the superior mesenteric artery gives off ileal branches only. Itis a continuous vessel that progressively decreases in diameter and anastomoses with the ileal branch of the ileocolic artery. Except from its

jejunal, ileal, and colic branches, t he superior mesenteric artery gives panc reatic and duodenal branches also (pancreat icoduodenal arcades, theartery for the neck, the transverse pancreatic artery, a branch for the duodenojejunal angle). Aberrant branches from the superior mesentericartery are the common hepatic artery, an aberrant right hepatic branch, or exceptionally the splenic artery or a cystic artery (Figs. 12-6, 12-7).

Fig. 12-6.


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The origin of anomalous hepatic arteries. (Modified from Brantigan OC. Clinical Anatomy. New York: McGraw-Hill, 1963; with permission.)

Fig. 12-7.

The collaterals of the superior mesenteric artery. (Modified from Van Damme JPJ, Van der Schueren G. A reevaluation of the colic irrigation fromthe superior mesenteric artery. Acta Anat 1976;95:588-688; with permission.)

Injuries to the superior mesenteric artery are rare, but when they occur the mortality rate is very high. Classifications of SMA injury by ischemic extent

and anatomic injury 19 are presented in Fig. 12-8 and Tables 12-2 and 12-3 respectively.

Table 12-2. Superior Mesenteric Artery Injury Classification by Ischemic Extent

Ischemic Category Bowel Segments Affected

Grade 1 Maximal Jejunum, ileum, right colon

Gra de 2 Mo de ra te Ma jo r s eg me nt, sma ll bo we l a nd /o r rig ht co lo n

Gra de 3 Minima l Min or s eg me nt or s eg me nts , s ma ll b ow el o r rig ht co lo n

Grade 4 None No ischemic bowel

Source: Fullen WD, Hunt J, Altemeier WA. The clinical spectrum of penetrating injury to the superior mesenteric arterial circulation. J Trauma 12(8):656-664, 1972;with pe rmission.

Table 12-3. Superior Mesenteric Artery Injury Classification by Anatomy

Zone Segment of SMA Involved

I Trunk proximal to firs t major b ranch

II Trunk between ancreaticoduodenal and middle colic


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III Trunk distal to middle colic

IV Segmental branches, jejunal, ileal, or colic

Source: Fullen WD, Hunt J, Altemeier WA. The clinical spectrum of penetrating injury to the superior mesenteric arterial circulation. J Trauma 12(8):656-664, 1972;with pe rmission.

Fig. 12-8.

Artist's conception of SMA circulation, showing the classification by anatomic zones. IPD = Inferior pancreaticoduodenal artery, R. col. = Right colic artery. (Modifiedfrom Fullen WD, Hunt J, Altemeier WA. The clinical spectrum of penetrating injury to the superior mesenteric arterial circulation. J Trauma 12(8):656-664, 1972;with permission.)

According to Komori et al., 20 who reported the successful resection of a superior mesenteric artery aneurysm with reconstruction of the superior

mesenteric artery by aortic anastomosis, only 8% of all visceral artery aneurysms occur at the superior mesenteric artery. They conclude, "Aneurysms atthe site are very susceptible to rupture, irrespective of size, and may be difficult to manage even in the case of elective surgery. In the absence of

serious complicating factors, the treatment of choice is excision of the aneurysm and reconstruction of the artery, if necessary, to maintain patency."

Inferior Mesenteric Artery

We are grateful to Dr. Jean- Pierre J. Van Damme 16 for permitting us to reprint his excellent description of the inferior mesenteric artery:

The inferior mesenteric artery (IMA) is a straight vessel that gives collaterals only from its left side while it runs to the dorsal side of the rectum,where it ends by dividing into two superior rectal arteries (Fig. 12-9). The first collateral is the left colic artery. At the colosigmoidal transition zone,where the descending colon changes into sigmoid colon by the development of a meso [mesentery], a very constant and extremely important

colosigmoidal vessel can be identified. 21 It arises in the angle between the left colic artery and the inferior mesenteric artery or from one of thesetwo vessels. Only those important vessels t hat mainly supply the sigmoid colon and have a direct origin from a main stem (inferior mesentericartery, colosigmoid, or left colic artery) are considered as sigmoid branches. The inferior mesenteric artery is a short artery that irrigates a verylong territory from the splenic angle of the colon to the midrectum. Because it acts like too short a string for too long a bowel, its branches have afan-like course.

Fig. 12-9.


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The inferior mesenteric artery and its branches: origin distance in millimeters. If the inferior mesenteric artery is divided at "a," above the last fullanastomosis, collateral circulation toward the rectum is still possible. Division at "b" would interrupt the collateral circulation. (Modified from VanDamme JP, Bonte J. Vascular Anatomy in Abdominal Surgery. Stut tgart: Thieme Verlag, 1990; with permission.)

Normal and Altered Spinal Cord Blood Supply

The following brief description of the blood supply of the spinal cord is presented for the reader's understanding of the complication of paraplegia due toinfarction.

The spinal cord is supplied dependably neither by a continuous longitudinal vessel nor by strictly segmental arteries. The anterior spinal artery (Figs. 12-10, 12-11, 12-12) arises by the merger of two vessels. These arteries arise from the vertebral arteries at the foramen magnum adjacent to the odontoidprocess. Passing down the ventral sulcus, the anterior spinal artery normally receives input from a branch of the left thyrocervical trunk, which enters the3rd or 4th cervical intervertebral foramen. This branch can be injured by cervical surgical procedures. This upper part of the artery continues down toabout the level of T4, giving off circumferential vessels to a plexus on the surface of the cord; the vessels anastomose with the paired posterior spinalarteries.


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Fig. 12-10.

The an terior and posterior sp inal arteries. (Modified from Decker GAG, duPles sis DJ (eds). Lee McGregor's Synopsis of Surgical Anatomy. Bristol: Wright, 1986; withpermission.)

Fig. 12-11.

The distribution of a lumbar or intercostal a rtery. The a nterior and p osterior radicular arteries are branches o f the intercostal artery. (Modified from Decker GAG,duPlessis DJ (eds). Lee McGregor's Synopsis of Surgical Anatomy. Bristol: Wright, 1986; with permission.)

Fig. 12-12.


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The blood supply of the spinal cord. The main radicular arteries are s hown. (Modified from Decker GAG, duPlessis DJ (eds). Lee McGregor's Synopsis of SurgicalAnatomy. Bristol: Wright, 1986; with permission.)

The posterior spinal arteries (Figs. 12-10, 12-11, 12-12) arise from the posterior inferior cerebellar arteries or, occasionally, from the vertebrals. Somevariable input to the spinal cord occurs by way of radicular branches of cervical, intercostal, or lumbar arteries that enter the spinal canal on the spinalnerve roots. We have also seen large contributions to the cauda equina nerve roots and the longitudinal anastomotic network of the cord derived from themedian and lateral sacral arteries in latex-injected cadaveric specimens.

The thoracic segment of the spinal cord (Fig. 12-12) receives important supply by a variable branch of the left fifth or sixth intercostal artery. This branchis vulnerable to operative procedures through the bed of the sixth rib. Perhaps even more important is the supply derived from the "arteria magna of

Adamkiewicz," a branch arising in 65% of cases from lower left intercostal arteries (T10-T12). 22 The "great radicular artery," as it is also called, can alsobe injured in thoracic procedures or left lumbar sympathectomy, left nephrectomy, splenectomy, adrenalectomy, or intercostal nerve blocks. Such a

vascular lesion can lead to possible infarction of the cord up to the T3 or T4 level 23 and paraplegia. A lesion involving segments T4-T6 (the most common

site) results in infarction of the entire anterior half of the spinal cord, according to Patten. 23 This produces an acute flaccid paraplegia with urine retentionand spinothalamic sensory loss to the level of the lesion, but with preservation of touch and joint position sense. Severe localized back pain usually

accompanies occlusion of the artery. Adams and van Geertruyden 24 recognized the importanc e of the arteria radicularis magna and emphasized thatneurologic sequelae follow injury to this vessel.

The lower spinal cord and the nerve roots comprising the cauda equina receive a variable source of supply from an artery that enters the spinal canal onone of the upper lumbar nerve roots. When the vascular supply to the lumbar segments of the spinal cord and nerve roots is occluded (an infrequentoccurrence), it leads to a condition termed claudication of the cauda equina. Severe pain, weakness, and numbness in one or both lower limbs

accompanies this condition.

In a general way, the anterior spinal artery is responsible for the blood supply of approximately the anterior 4/5 of the spinal cord. The anterior spinalartery and the anterior radicular arteries supply blood to the gray matter (anterior and intermediate portions), the base of the posterior gray column, thewhite matter of the anterior funiculus, and the deeper portion of the lateral funiculus (Figs. 12-12 and 12-13).

Fig. 12-13.


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The ante rior and po sterior radiculo-medullary branches.

In summary, the posterior spinal arteries and post erior radicular arteries supply blood to t he post erior funiculus, most of t he posterior gray c olumns, andthe superficial part of the lateral funiculus.

Approximately eight anterior and 12 posterior radicular arteries pass along the spinal nerve rami and nerve roots to reac h and supply, variably, thevertebrae, meninges, and cord. The most important radicular artery is, as noted above, the arteria radicularis magna. It produces the anatomiccomplicat ion of paraplegia (t ransverse myelitis) when violated.

Medical causes of vascular impairment to the spinal cord include atherosclerosis, diabetes mellitus, thromboses, dissecting aneurysms of the aorta, andothers.

Collateral Arterial Branches

The collateral circulation between the arterial branches to the abdominal viscera is excellent and surgically important. Communications exist betweenbranches of the celiac axis itself; between the branches of the celiac axis and the superior mesenteric artery (Fig. 12-14); between the branches of thesuperior and inferior mesenteric arteries (Fig. 12-15); and between the inferior mesenteric artery and the middle rectal branch of the internal iliac.

Fig. 12-14.

The celiac axis, its branches, and the collateral circulation w ith the superior mesente ric artery. (Modified from Brantigan OC . Clinical Anatomy. New York: McGraw-Hill, 1963; with permission.)


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Fig. 12-15.

The collateral circulation of the branches of the superior mesente ric artery and inferior mesente ric artery. (Modified from Brantigan OC . Clinical Anatomy. NewYork: McGraw-Hill, 1963; with permission.)

The names of three researc hers are assoc iated with mesenteric c irculation: Bhler, Riolan, and Drummond.

Arc of Bhler. The arc of Bhler is an a rtery connecting the common hepatic or gastroduo dena l artery with the SMA and forming an anas tomotic networkbetwe en the SMA and celiac artery (Fig. 12-16).

Arc of Riolan. Another ana stomotic netwo rk is the arc of Riolan, betw een the SMA and IMA (Fig. 12-17).

Marginal artery of Drummond. The be st known of the three is the marginal artery of Drummond, also communicating betwe en the SMA and IMA (Fig. 12-17).

Fig. 12-16.


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The arc of Bhler forming a direct anastomotic communication between the celiac and the SMA. (Modified from Rosenblum JD, Boyle CM, Schwartz LB. Themesenteric circulation: anatomy and physiology. Surg Clin North Am 77(2): 289-306, 1997; with permission.)

Fig. 12-17.

The marginal artery of Drummond and the arc of Riolan, which form anastomotic communications between the SMA and IMA. (Modified from Rosenblum JD, BoyleCM, Schwartz LB. The mesenteric circulation: anatomy and physiology. Surg Clin North Am 77(2):289-306, 1997; with permission.)

The normal and variant anatomy of the celiac artery, hepatic artery, and left and right gastric arteries as reported by Rosenblum et al. 25 is shown in Table12-4.

Table 12-4. Normal and Variant Vascular Anatomy

Vessel Incidence

Celiac

Three branches (classic) 65-75%

Four branches including dorsal pancreatic artery 5-10%


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Celiacomesenteric trunk


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The attachments of the muscles of the diaphragm see n from below. A = aorta, E = esophag us, IVC = inferior vena cava. (Modified from Skandalakis LJ, ColbornGL, Skandalakis JE. Surgical anatomy of the diaphragm. In Nyhus LM, Baker RJ, Fischer JE. Mastery of Surgery, 3rd ed, Vol 1. Boston: Little, Brown & Co, 1997;with permission.)

The median arcuate ligament passes in front of the aorta at the level of L1, just above the origin of the celiac trunk (Fig. 12-18). The celiac ganglia lie inintimate juxtaposition to the lateral aspects of the celiac trunk. Together with the profuse celiac neural network, they conceal the origin of the artery andmuch of the length of the trunk. The median arcuate ligament and the origin of the celiac artery descend slightly with increasing age. In 16 percent of

patients, 26 a low median arcuate ligament covers the celiac artery and can compress it. At angiography, such compression can simulate atheroscleroticplaques. Lack of symptoms arising from the vascular compression indicates that such patients have adequate collateral circulation. The median arcuateligament has been implicated in abdominal angina in instances when substantial tense fibromuscular tissue at the hiatus exerted a constrictive effect onthe celiac trunk or the aorta.

Bech27 stated that in rare cases compression of the visceral arteries produces true mesenteric ischemia. Some authors believe that the left crus of thediaphragm generates the c eliac artery compression syndrome (also referred to as ce liac axis compression, celiac band syndrome, and Dunbar's syndrome).It is our opinion that in most cases the median arcuate ligament is responsible for this syndrome despite the anatomic variation of the entities of the aortic"hiatus."

The question remaining is the cause. Is it caused by high origin of the celiac axis, low insertion of the diaphragmatic crura, or the topography of the celiac

plexus? Harjola, 28 first to present a case of mesenteric ischemia, thought that perhaps it was caused by extrinsic pressure to the celiac axis by the celiacplexus.

Diagnosis of t he median arcuate ligament syndrome may be est ablished by elimination of other causes for abdominal pain as Bec h 27 stated. T he surgeonshould remember that this syndrome is real, not imaginary, and t hat s imple division of the median arcuate ligament may c ure the patient. Occ asionallyrevascularization of the celiac axis may also be necessary.

If there is no true median arcuate ligament and the muscular arms of the crura are thinned by posterior extension of the esophageal hiatus, the aortic andesophageal openings can become practically confluent. Some connective tissue is always present between them, however.

In approximately one-half of the cadavers with hiatal hernia examined by Gray et al., 2,29,30 the ligament was sufficiently well developed to use in surgicalrepair of the esophageal hiatus. In the remainder, there was enough preaortic fascia lateral to the celiac trunk to perform a posterior fixation of thegastroesophageal junction. In hiatal hernia procedures, the celiac ganglia, located just below the arcuate ligament (or its expected position), must beavoided.

ABDOMINAL AORTIC NERVE PLEXUSES

The celiac plexus (Fig. 12-19) is formed by a retroperitoneal network of several sympathetic ganglia, together with sympathetic and parasympatheticnerves and many afferent fibers. These interconnect with each other and envelop the celiac axis and the superior mesenteric artery. This plexus receivesinput especially from the greater and lesser thoracic splanchnic nerves and the celiac branch of the posterior vagal trunk. It is infused with sensory fibers

of all kinds that pass to the plexus in retrograde fashion along the visceral arterial branches.

Fig. 12-19.


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The celiac plexus, celiac ganglia, and adrenal glands. (Modified from Grant JCB. An Atlas of Anatomy, 4th ed. Baltimore: Williams & Wilkins, 1956; with permission.)

The ganglionated celiac network is continuous inferiorly as the preaortic or intermesenteric plexus. This is succeeded, in turn, by the inferior mesentericplexus, which is associated with the origin and course of that artery. That part of the nerve plexus upon the distal segment of the aorta, especially nearits bifurcation, is referred to as the hypogastric plexus, or superior hypogastric plexus. (The first term is used if it is assumed that this nerve plexus splitsinto right and left pelvic plexuses.) The preaortic nerve plexus and the hypogastric plexus receive two or more bilateral contributions from the lumbarsegments of right and left sympathetic chains. Numerous fibers, which contain pelvic splanchnic parasympathetic fibers and afferent neurons, ascend intothe hypogastric plexus from the pelvic nerve plexuses.

T2-L4 VERTEBRAE

An aneurysm of the abdominal aorta can cause erosion of the left lateral surfaces of the lumbar vertebrae.

Spontaneous rupture of an aortic aneurysm into the inferior vena cava is a complication of this aortic pathology. Skinner et al. 31 present such a case,observing that more than 200 cases have been reported since Syme's first description in 1831.

LESSER SAC AND STOMACH

The lesser omental bursa (lesser sac) is located between the abdominal aorta and the posterior wall of the stomach. Tumors of the posterior gastric wallor an aortic suprarenal aneurysm may partially or completely obliterate the lesser sac. Erosion of the gastric wall may result in gastrointestinal bleeding.Such pathologic entities and their complications are extremely rare.

BODY OF THE PANCREAS

An aortic aneurysm may fuse closely with the body of the pancreas.

SPLENIC VEIN

Pathology of either the splenic vein or the aorta can produce dense fixation between the two and perhaps cause a fistula to form between them, butthese are rare occurrences. More likely, trauma or a ruptured splenic artery aneurysm may cause an arteriovenous fistula between the splenic artery andsplenic vein.


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TRANSVERSE COLON AND MESOCOLON

Pathology of the transverse colon and mesocolon can cause fixation. The middle colic artery is the first vessel affected. Again, fistulas can result fromthis, and colonic bleeding may occur.

THIRD PART OF THE DUODENUM

A portion of the third part of the duodenum typically lies between the superior mesenteric artery and the aorta; it also covers the origin of the inferiormesenteric artery. Most cases of superior mesenteric artery syndrome or vascular compression of the duodenum result from extrinsic compression of the

third part of the duodenum between the aorta and the superior mesenteric artery. 32 Aneurysms of the abdominal aorta can erode the wall of theduodenum and rupture into the duodenum, resulting in severe or fatal gastrointestinal bleeding. Another clinical entity is the formation of hernias into the

paraduodenal fossae and into the fossae of Waldeyer. 33,34

MESENTERIC ROOTThe aorta may be tightly adherent to the root of the mesentery if aortic or mesenteric pathologies (aneurysm or mesenteric cyst) are present.

GREATER SAC, JEJUNUM, AND ILEUM

Loops of small bowel may be tethered or they may be adherent to an aortic aneurysm.

LEFT RENAL VEIN

Always remember that the left renal vein usually crosses the aorta just beyond the origin of the superior mesenteric artery. At its crossing in front of theaorta and behind the pancreas and splenic vessels, the left renal vein may be fused tightly with an aortic aneurysm. The possible involvement of the leftadrenal and left gonadal veins is variable, depending on the size of the aneurysm.

LEFT LUMBAR VEINS

When repairing an aortic aneurysm, t he left or right lumbar veins may be ligated, if necessary, with impunity.

AORTIC LYMPH NODES

The lymph nodes related to the abdominal aorta are of several periaortic groups that accept lymph from several intraperitoneal and retroperitonealanatomic entities. These lymph nodes are described in the lymphatic discussion of each organ. In general the nodes are described as preaortic,retroaortic, and paraaortic.

HISTOLOGY AND PHYSIOLOGY

From outside to inside, the aortic wall is composed of three layers: the tunica adventitia, tunica media, and tunica intima.

The relatively thin tunica adventitia is formed by connective tissue, including collagenous fibers that protect the wall from overexpansion during cardiacsystole. The tunica adventitia contains vasa vasorum (tiny blood vessels) and nervi vascularis (thin nerves).

The tunica media, a thick layer of the aortic wall, is constructed of 50 to 65 fenestrated, interconnected sheets of elastic tissue containing flattened andirregular smooth muscle cells (most arranged in circumferential fashion) and c ollagenous fibers.

The tunica intima is not as thick as the tunica media. It is lined by an endothelium of simple squamous epithelium. Deep to the endothelial layer are layerscontaining collagen fibers, elastic fibers, and smooth muscle cells.

Davies and Hagen 35 reported that the surface area of the vascular endothelium is approximately 5000 m 2, comprising only 1% of the total body weight.

According to Cain et al. 36 the vascular endothelium is the autocrine and paracrine control center for much of the disease responses confronting thesurgeon today. The endothelium influences blood vessel tone, permeability, cell adhesion, coagulation, and growth by regulating molecules and proteinsexpressed at the cell surface.

The aorta is an elastic conduction tube responsible for the movement of oxygenated blood throughout its branches.

AORTIC ANEURYSMS

The most common location of aortic aneurysms is the infrarenal portion of the aorta including its bifurcation and extending to the iliac arteries. To avoid

rupture, which has nearly 90% mortality, 37 early diagnosis and surgery are essent ial.

Ballard 38 advised ultrasound evaluation for patients with asymptomatic abdominal aortic aneurysms of 4.0-5.5 cm, and surgical intervent ion for rapidlygrowing or larger aneurysms.

According to Davis et al. 39 the pathways of rupture of aortoiliac aneurysms are into the:

retroperitoneal spaces

pe ritoneal cavity

iliac veins

inferior vena cava

intestinal lumina

They advised early diagnosis and stated that IVC interruption is seldom warranted.

Based upon a retrospective review of 25 patients, Weinstein et al.40

indicated that patients with normal blood pressure who have "stable" ruptured


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5/24/2 014 Print: Chapter 12. Great Vessels in the Abdomen


abdominal aortic aneurysm give physicians a false sense of security; the authors recommended emergency surgery.

Surowiec et al. 41 reported that acute aortic occlusion, which commonly is secondary to saddle embolus or atherosclerotic thrombosis, has tremendousmorbidity and mortality.

It is not within the scope of this book to describe in detail the surgical techniques to correct aortic aneurysm. However, to illustrate the potentialanatomic complications, the repair of aortic aneurysms is presented strictly from an anatomic standpoint. We consider transabdominal and retroperitonealapproaches.

Surgical ApproachesTRANSABDOMINAL APPROACH

An aortic aneurysm can be attacked by the transabdominal approach of the surgeon's choice, using a long ventral midline incision or a transversemidabdominal incision. Keep in mind the following anatomic entities or landmarks during such procedures.

Ligament of Treitz at the duodenojejuna l flexure

Retroperitoneum

Mesentery of the small bowe l (the radix)

Inferior mesenteric vein and inferior mesente ric artery

Pa ths of both the right and left renal veins (remember the poss ibility of retroaortic left renal vein)

Both right and left external a nd internal iliac arteries (remember to preserve one of the internal iliac arteries for the pe lvic blood supply through collateralcirculation)

Right and left femoral arteries (as necess ary)

Right and left ureters

Right and left common iliac veins (remember that the left common iliac vein is crossed and compressed by the right common iliac artery)

Intraaortic orifices of lumbar a orta a nd inferior mesenteric artery

Marino et al., 42 who studied the proximal abdominal aorta and especially the celiac region, recommended left subpancreatic transplexus exposure of theceliac axis and the superior mesenteric artery. They reported finding two types of nerve plexuses: the totally covering plexus and the partly coveringplexus. In 70% of cases, the nerve plexus completely covers the first centimeters of the branches of the aorta. In 30%, the nerve plexus forms only a thincovering from which the large aortic branches emerge.

RETROPERITONEAL APPROACH

Using the retroperitoneal approach, two anatomic entities are involved: the inferior mesenteric artery and any lumbar vein draining into the renal vein. Thisleft flank incision can be extended to a thoracoabdominal incision through the 10th or 11th interspace, but without thoracotomy.

The inferior mesenteric artery must be ligated and may be reimplanted using the button technique by reimplanting the vessel orifice together with a piece,about 1.8 cm across, of the aortic wall sutured into the graft. Ligate the lumbar vein draining into the left renal vein.

ANATOMIC COMPLICATIONS

The thoracoabdominal approa ch risks intercostal neuralgia secondary to injury of intercostal nerves.

Using the tho racoabdominal approach, dene rvation of the flat abdominal muscles can res ult in flank bulge s econdary to a trophy.

Arterial or venous b leeding is poss ible.

Ischemia of the lower extremity may occur. The be st treatment includes palpation, Doppler examination, or angiography, done in the ope rating room during theaneurysmectomy.

Colonic ischemia (a threat e specially to patients with previous left colectomy) can be avoided b y reimplanting the inferior mesenteric artery during the resectionof the aneurysm. If postope rative bloody diarrhea occurs, the surgeon should consider repe ated colonoscopic examinations and , depend ing on the findings,exploratory laparotomy with colectomy and transverse colostomy if necessary.

Ischemia of the d istal part of the spinal cord may result in very grave complications w ith high mortality secondary to ligation of both internal iliac (hypogastric)arteries. Postop eratively, the pa tient may have motor and se nsory loss in both lower extremities, incontinence, and mottling and ne crosis of gluteal muscles. Tominimize the chance of ischemia, reimplant one internal iliac if at all possible.

Use re nal scan and ultrasound examination to diagnos e rena l artery occlusion and/or ureteric ligation. Early correction is esse ntial to avoid high mortality.

One of the most tragic complications in thoracic and abd ominal aorta surgery is parap legia or pa rapares is. Connolly 43 stated tha t such a catastrophe occurs withsurgery at the top and b ottom of the aorta in under 1% of cases, but exceeds 10% in operations just above the diaphragm. Figure 12-13 demonstrates the spinalblood supply.
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Based on a nationwide study in Finland, Jrvinen et al. 44 reported that 27 patients out of 1752 who underwent aortoiliac surgery suffered with intestinalischemia and 1.2% had intestinal infarction. Table 12-5 describes the distribution of this lesion by location.

Table 12-5. Distribution of Mesenteric Infarction as Defined at Laparotomy or at Autopsy in 21 Patients

Patients

Location of Mesenteric Infarction No. %

Single infarction

Inferior mesenteric artery

Transverse colon-rectum 9 43

Sigmoid colon only 1 5

Superior mesenteric artery

Jejunum-transverse colon 5 24

Ileum only 2 10

Multiple infarctions

Ileum + sigmoid colon 1 5

Ileum + sigmoid colon + rectum 3 14

Source: Jrvinen O, Laurikka J, Salenius J-P, Lepntalo M, Finnvasc Study Group. Mesenteric infarction after aortoiliac surgery on the basis of 1752 op erations fromthe na tional vascular registry. World J Surg 1999;23:243-247; with p ermission.

We quote from du Toit and Saaiman 45 :

An important Achilles heel of endovascular repair of abdominal aortic aneurysms is back bleeding or endoleak formation due to incomplete sealing orbridging of aortic branches ostia by endoluminal stents. Significant, recurrent, and persistent retroleaks, a topic of clinical interest, are related toeither incompletely sealed-off inferior mesenteric and/or lumbar arteries. The optimal method t o diagnose and manage these endoleaks is currentlyin a state of evolution. In the process of stent-graft treatment of abdominal aortic aneurysms, other important aortic branches are also bridgedthat may potentially present with the sequelae of peripheral ischemia.

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INFERIOR VENA CAVA

HISTORY

The anatomic and surgical history of the inferior vena cava is the history of the vascular system. It is presented in Table 12-1.

EMBRYOGENESIS

Normal DevelopmentThe right common c ardinal vein and t he proximal part of the right anterior cardinal (right precardinal) ve in are responsible for development of the inferiorvena cava (Fig. 12-20).

Fig. 12-20.
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Schematic diagrams showing so me of the ste ps in the development of the inferior vena cava. A to F, stag es in ventral (anterior) view; G to I, cross-sectionalviews. Cardinal veins are shown in blue; subcardinal veins are red; supracardinals are yellow. Vesse ls arising indepe ndently of these three systems are indicatedby small crosses . , mesente ric portion of inferior vena cava; Sub. , subcardinal ve in; Umb. , umbilical vein; V.V. , vitelline vein; Meson. or Mes. , mesone phros; Ob. ,oblique vein of left atrium; subcl. , subclavian vein; *, left superior intercostal; Supr. , suprarena l. (From Carlson BM. Patten's Found ations of Embryology, 5th ed.New York: McGraw-Hill, 1988; with permission.)

The following three embryonic networks are, most likely, the principal contributors to parts of the inferior vena cava.

The hepatic portion derives from the omphalomesenteric vein (right vitelline vein).

The renal po rtion comes from an ana stomosis of the right subcardinal and supracardinal veins.

The s acrocardinal or postrenal s ection comes from the right sacrocardinal or supracardinal vein. 46

Congenital Anomalies

Anomalies of the IVC can include absence or duplication; abnormalities of location, length, or connections and drainage; and membranous obstruction. Thecongenital anomalies of the inferior vena cava are summarized in Table 12-6. Here we discuss only a few.

Table 12-6. Anomalies of the Inferior Vena Cava

Anomaly Prenatal Age atOnset

First Appearance (or OtherDiagnostic Clues)

Sex ChieflyAffected

RelativeFrequency

Remarks

Absence of hep atic segment of inferiorvena cava

6th w ee k Symp to ms re la te d to a ss ocia te dcardiac defects only

Equal Uncommon

Double inferior vena cava; left-sidedinferior vena cava

7th week None Equal Common

Preureteral vena cava 7th week At any age Equal Rare Compression of ureterproducts symptoms

Source: Skandalakis JE, Gray SW (eds). Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with permission.

ABSENCE


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Absence of the hepatic segment of the IVC is secondary to failure of the right subcardinal vein tributaries to connect with the hepatic veins during the6th week.

DUPLICATION

The presence of both a right and a left IVC below the renal veins is not an unusual variation (Fig. 12-21B). Usually the right and left cava join at or belowthe level of the renal veins, and they have connections with other veins. All these variations are asymptomatic.

Fig. 12-21.


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The inferior vena cava at the diaphragm. A, Relations. B, Anomalous double inferior vena cava. In this illustration, the right vessel is large r and re ceives all thelumbar veins. C, Relations to other vessels. (Modified from Gray SW, Skandalakis JE, McClusky DA. Atlas of Surgical Anatomy for General Surgeons. Baltimore:


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, .

Inferior vena cava duplication has been reported by Colborn 46 and Shingleton et al. 47 The former has recently observed (in unpublished observations) theoccurrence of bilateral inferior venae cavae in a female cadaver with total situs inversus.

PREURETERIC IVC (RETROCAVAL URETER)

Preureteric inferior vena cava, or retrocaval ureter, occurs on the right only. The right ureter passes behind and around the IVC. Obstruction of the ureterwith possible hydronephrosis may be present (see chapter on kidneys).

Most of the anomalies of the inferior vena cava are totally asymptomatic. A few do present symptoms and sequelae, and, of course, they need surgicalintervention.

Nakatani et al. 48 described a patient with an anomalous triad of a single left-sided inferior vena cava, a retroesophageal right subclavian artery, andbilateral superficial brachial arteries (Fig. 12-22). The same authors present the frequency of abnormalities of the inferior vena cava in Table 12-7.

Table 12-7. Frequency of Abnormalities of Inferior Vena Cava (IVC)

Type of Abnormality

Frequency (%) (No. of Abnormality/Size of Study)

Authors, Year (Methods of Examination) a

Left-SidedIVC

Double IVC RetrocavalUreter

Retroaortic Left RenalVein

Circumaortic VenousRing

AzygosContinuation

Gladstone, 1929 (D) 0.11 (1/876) 0.2 (2/876)

Seib, 1934 (D) 0.57 (1/176) 2.8 (5/176) 1.7 (3/176) 9.3 (16/176)

Adachi, 1940 (D) 0.26 (3/1176) 1.4(16/1176)

0.17 (2/1176)

Pick and Anson, 1940a, b (D) 0.18 (1/570) 3.4 (7/202) 16.8 (34/202)Reise and Esenther, 1959 (D) 0.2 (1/500) 2.2 (11/500) 2.4 (12/500) 6.0 (30/500)

Davis and Lundberg, 1968 (D) 1.8 (5/270) 1.5 (4/270)

Hoeltl et al., 1990 (D) 1.1 (4/354) 0.56 (1/289)

Bartle et al., 1987 (O) 0.35 (1/289) 0.35 (1/289) 0.35 (1/289) 0.35 (1/289)

Hoeltl et al., 1990 (O) 2.8 (6/215) 0.93 (2/215)

Anderson et al., 1961 (CT) 0.6 (15/2500) b

Alexander et al., 1982 (CT) 0.08 (1/1200) 0.08(1/1200)

0.08 (1/1200) 0.25 (3/1200)

Mayo et al., 1983 (CT) 0.35 (4/1140) 0.44(5/1140)

0.09 (1/1140) 0.09 (1/1140) 0.09 (1/1140)

Ueda et al., 1983 (CT) 1.0 (9/874) 0.69 (6/874) 0.08 (1/1260)

Kokubo et al., 1988 (CT) 0.18 (2/1100) 1.1(12/1100)

0.18 (2/1100) 0.36 (4/1100) 0.55 (6/1100)

Hoeltl et al., 1990 (CT) 0.04 (2/4520) 0.02(1/4520)

0.64 (29/4520) 0.09 (4/4520)

a D, dissection; O, opera tion; CT, computed tomography.

bAll 2,500 cases have congenital heart disea ses. The azygos continuation was commonly associated with congenital heart disea se.

Source: Nakatani T, Tanaka S, Mizukami S. Anomalous triad of a left-sided inferior vena cava, a retroe sophag eal right sub clavian a rtery, and bilateral supe rficialbrachial arteries in one individual. Clin Anat 11:112-117,1998; with permission.

Fig. 12-22.


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Illustration of the single left-sided inferior vena cava. AA, abdominal aorta; rA, right atrium; LSR, left adrenal gland; LK, left kidney; D, diaphragm; 1, right renalvein; 2, right ureter; 3, right ovarian vein; 4, right common iliac vein; 5, hepatic veins; 6, celiac trunk; 7, superior mesenteric artery; 8, left renal vein; 9, leftureter; 10, left-sided inferior vena cava; 11, inferior mesenteric artery; 12, left ovarian vein; 13, left common iliac vein; and 14, hypogastric plexus. (Modified fromNakatani T, Tanaka S, Mizukami S. Anomalous triad of a left-sided inferior vena cava, a retroe sophag eal right sub clavian a rtery, and bilateral supe rficial brachialarteries in one individual. Clin Anat 11:112-117, 1998; with permission.)

We quote from Bass et al. 49 :

A left IVC typically ends at the left renal vein, which crosses anterior to the aorta to form a normal right-sided prerenal IVC. In double IVC, the leftIVC typically ends at the left renal vein, which crosses anterior to the aorta to join the right IVC. In azygos continuation of the IVC, the prerenalIVC passes posterior to the diaphragmatic crura to enter the thorax as the axygos vein. In circumaortic left renal vein, one left renal vein crossesanterior to the aorta and another crosses posterior to the aorta. In retroaortic left renal vein, the left renal vein passes posterior to the aorta. Incircumcaval ureter, the proximal ureter courses posterior to the IVC. Other anomalies include absence of the infrarenal IVC or the entire IVC.

SURGICAL ANATOMY

Topography and TributariesThe paths of the inferior vena cava (IVC) and the abdominal aorta proceed parallel to the midline with a distance of 1 cm to 2 cm between them. The IVCis a good neighbor, but aneurysms of the aorta occasionally invade the IVC and form a fistula. Dense fixation of an aortic aneurysm to the IVC should betreated with special care. It may not be advisable to remove the aneurysmal sac.

The IVC results from the union of the left and right common iliac veins at L5 (Fig. 12-23). The IVC ascends to the right of the midline and terminates aftertraversing the central tendon of the diaphragm at T8. It enters the right atrium at the level of the 6th costal cartilage. The hiatus of the inferior venacava creates a quadrangular opening in the central tendon of the diaphragm (Fig. 12-21A). The supradiaphragmatic vena cava is 2 cm to 3 cm and theinfradiaphragmatic vena cava is 18 cm to 19 cm, together averaging approximately 21 cm (approximately 8''). The IVC does not have any valves.

Fig. 12-23.


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The inferior vena cava and its tributaries. (Modified from Gray SW, Skandalakis JE, McClusky DA. Atlas of Surgical Anatomy for General Surgeons. Baltimore:Williams & Wilkins, 1985; with permission.)

Topographicoanatomically the posterior wall of the suprahepatic IVC is anchored by a thin, but strong "ligament" to the diaphragmatic hiatus, to theposterior aspect of the caudate lobe, and to segment VIII of the right hepatic lobe. In the lab, usually we did not see a "ligament," but just a fixation of the posterior wall of the IVC to the above hepatic segments.

The IVC receives visceral veins from the intraretroperitoneal anatomic entities and parietal veins from the lower extremities, pelvis, and posterolateralabdominal wall. Because the IVC forms to the right of the midline and is relatively dorsal to the aorta, the left common iliac vein passes behind the right


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common iliac artery. T he apparent c ompression can result in the formation of an iliac or iliofemoral thrombosis.

The visceral venous tributaries moving upward from below are the right gonadal vein and the ureteric, renal, right adrenal, and hepatic veins (Fig. 12-23).The right adrenal vein and hepatic venous tributaries, especially direct contributants from the caudate lobe, often are very short and therefore readilyinjured and difficult to repair.

The parietal venous tributaries moving upward from below are the right and left common iliacs, lumbar veins, ascending lumbar vein, and inferior phrenicveins. The left gonadal and left adrenal veins drain directly to the left renal vein (Fig. 12-21C). The left inferior phrenic vein may also drain in this way or,variably, both to the left renal vein and to the IVC (Fig. 12-23).

There is great variability in the vascular anatomy of this region. Capellades et al. 50 reported that damage to the left iliac vein is a severe complication of anterior fusion of the L5-S1 disc. Low iliocava junction positions and medial location of the left common iliac vein reduce the size of the operative window,increasing the risk for vascular injury.

All these visceral and parietal veins are discussed in other chapters as they relate to the anatomy of the various intraperitoneal or retroperitoneal organs.

Collateral Venous Pathways

Generous anastomoses form a rich but complicated venous collateral circulation between the networks of the IVC and superior vena cava (SVC).Therefore, when infrarenal interruption of the IVC or thrombosis occurs, the blood is shunted upward to the SVC and the heart. For this reason, also, it ispossible to ligate the inferior vena cava after it has been injured without causing serious sequelae for venous drainage of the lower limbs.

The venous network includes the vertebral plexus, gonadal veins, ascending lumbar veins, and azygos and hemiazygos veins, as well as the veins of theanterior body wall (superficial epigastric, circumflex iliac, lateral thoracic, and intercostal). The thoracoepigastric veins provide a potentially rich linkage

between the femoral and axillary veins by way of superficial epigastric and axillary anastomosing tributaries. According to Nesbit and Wear, 51 the mostimportant vessels of collateral circulation in most cases of IVC obstruction are the lumbar, vertebral, and azygos.

The collateral circulation of the veins is much better than that of the arteries.

As reported by Gazzaniga and Colodny, 52 Nesbit and Wear, 51 and others, long-term survival after acute ligation of the IVC above the renal veins ispossible in extremely rare cases. Of course, we remind the reader to avoid suprarenal ligation of the IVC if at all possible.

Remember

The suprahep atic IVC is located within the vicinity of the bare area of the liver and to the left. It receives the three (or occasionally more) hepatic veins. Portalhypertension, in some case s w ith secondary varices, may result from suprahepatic obstruction of the hepatic veins (Budd-Chiari syndrome).

The inferior vena caval diaphragmatic opening at T8, a hiatus shape d like a sq uare, is located in the right hemidiaphragm, close to the midline.

The right adrenal vein is short and very fragile as it passe s to drain into the po sterolateral caval wall above the renal vein.

The IVC passe s behind the epiploic foramen. If the index finger is inserted into the foramen, the posterior surface of the distal phalanx is related to the IVC andthe flexor surface is related to the hep atic triad.

The right renal artery is located b ehind the IVC and right renal vein (Fig. 12-21C). It is related dorsa lly to the right psoas muscle a nd the right diaphragmatic crus.Ventrally, the IVC and the right renal vein sepa rate the a rtery from the common bile duct, pancreatic head, and the second pa rt of the duodenum.

The first part of the duo denum is related pos teriorly to the IVC and g astroduod enal artery. The third part of the d uodenum is anterior to the IVC. The posterior

surface of the pancreatic head is related to the IVC. Kocherization of the duodenum and elevation of the head o f the pancreas during pancreatic and duodena lsurgery should b e d one carefully to avoid anatomic complications.

The distal part of the root of the mese ntery of the small bowel crosses the IVC, right ureter, and right gonadal vein.

The right gonadal artery originates be low the rena l artery and crosses the IVC to come to rest o n the pso as muscle. (For all practical purposes the psoa s muscleis the only muscular entity related to the IVC, because the IVC lies on the ventral surface of the muscle.)

There are several othe r anatomic relationships to remember. The right sympathetic chain is located just p osterior to the IVC. On the ventral surface of the p soasmuscle are two other parallel anato mic entities to recognize : the right genitofemoral nerve and the upper one -half of the right ureter. The ureter lies behind theright gonadal vessels.

Caval lymph nodes a re divided into: precaval, retrocaval, and p aracaval.

HISTOLOGY AND PHYSIOLOGY

The wall of the IVC consists of three layers, similar to those of the aorta, but they are not well defined. The tunica adventitia forms the thickest layer,containing prominent longitudinal layers of smooth muscle and elastic networks in addition to loose connective tissue.

The inferior vena cava returns deoxygenated blood to the right atrium.

SURGICAL APPLICATIONS

The IVC may be interrupted totally or partially to prevent recurrent pulmonary embolism secondary to dee p venous thrombosis of the pelvis or the lowe rextremities that does not respo nd to conservative treatment (anticoagulants). The preferred method is to insert a n intraluminal filter (Figs. 12-24, 12-25). Thispermits the upw ard flow of blood but not the upwa rd transmission of the embolus. Another method of interrupting the IVC is to narrow it below the re nal veinsusing a s errated o r non-serrated clip and ligating the left gonada l vein. Prior to the IVC interruption, cavography is ess ential for identification of variations andanomalies of this vess el (Figs. 12-21B and 12-26).


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Fig. 12-24.

Surgical prevention of pulmonary embolism. Large emboli can be trapped by pa rtial interruption o f the inferior vena cava. A, Serrated Teflon (Miles) clip. B, SmoothTeflon (Moretz) clip. These sho uld be p laced just distal to the renal veins, and the go nadal veins s hould be ligated. C, Greenfield filter, which is insertedtransvenously through a jugular or femoral approach. Some surgeo ns pre fer to simply ligate the cava. (Modified from Miller TA. Physiologic Basis of ModernSurgical Care. St. Louis: CV Mosby, 1988; with permission.)

Fig. 12-25.


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Diagrammatic illustration of surgical approa ches for interruption of the inferior vena cava in prevention of pulmonary embolism. The clips show n are constructed of plastic material. (Modified from Sabiston DC Jr. Textbook of Surgery, 13th e d. Philadelphia: W B Saunders, 1986; with pe rmission.)

Fig. 12-26.

The inferior vena cava with measurements. (Modified from Gray SW, Skandalakis JE, McClusky DA. Atlas of Surgical Anatomy for General Surgeons. Baltimore:


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Williams & Wilkins, 1985; with permission.)

Thomas et al. 53 advised critical evaluation of IVC filters, since IVC thrombosis may occur in 6.5-7% of cases.

One may ligate the IVC by approa ching it through a right flank incision or through the a bdomen using a long midline incision or a right subcostal incision.

Retroperitoneal malignant tumors may compress the IVC a nd produce unilateral or, rarely, bilateral varicosities of the lower e xtremities and swe lling. A graviduterus or giant fibroid may compress the IVC and produce edema o r varicosities of one or both low er limbs.

In treating injuries of the inferior vena cava that require it to be clamped, use a vein of the upper e xtremity for intravenous fluids or blood a dministration. Theinfrarenal p ortion of the IVC is injured most often. For any suspe cted injury of the IVC, perform abdominal exploration through a long midline incision toimmediately arrest the bleeding a nd repair the ves sel.

With cirrhosis of the liver or Budd-Chiari syndrome, hepatic segments I and VIII may be enlarged. This results in se gmented external compression of the venacava followed by e levation of the venous pressure. According to Turcotte et al., 54 this entrapment of the IVC by the ligament and enlarged hepatic segmentsprecludes construction of a standa rd portosystemic shunt. Schwartz 55 advised tha t in some patients rese ction of the caudate lobe w ill permit a shunt (Fig. 12-27).

The IVC may be injured with fatal res ults during surgery for lumbar intervertebral disc herniation. An inferior vena cava lacerated iatroge nically or by trauma should be repaired p rimarily by one of the following procedures :

Closure of laceration

Closure of defect by a vein pa tch

Reconstruction by saphe nous vein pane l graft

Reconstruction by synthetic graft

Ligation below the rena l veins (avoid ligation above the renal veins)

Tumors can infiltrate the IVC, and resection and reconstruction of the IVC is a surgical decision determined by the pa rt of the IVC involved w ith malignantprocess. Ohwada et al. 56 advised the following:

If involvement of the w all of the IVC is minimal, excision must be done a nd the defect can be closed with sutures without obs tructing the upw ard venous flow.

The suprarena l IVC can be ligated safely if collaterals are we ll developed (azygos-hemiazygos, etc.)

Huguet et al. 57 recommended reconstruction of the IVC after hepate ctomy to avoid a cute renal failure.

Several surgical innovations should be conside red individually for major resection of a cirrhotic liver for hepatic malignancies involving the IVC or the hepaticvenous confluence. Although a ggressive he patectomy and IVC reconstruction can be use d in a cirrhotic liver, evaluation of the functional hep atic reserve andischemic injury remain problematic.

Bianchi et al. 58 reported that long-term survival is low w hen rese ctions for carcinoma a re ass ociated with major vessel infiltration or a complication thatnecessitates a vascular procedure as an emergency.

Occasionally after repair a pulmonary embolus may follow, but this is infrequently a seque la of the procedures o n the IVC. Venous hypertension and renalimpairment may occur following ligation of the IVC a bove the renal veins.

Injury of the retrohepatic vena cava in adults may require a right hep atic lobectomy or placement of a retrohe patic venous shunt to maintain cavo-venous flowwhile repairing the veno us injury. In children, the e xtrahepatic joining of the hepa tic veins and the inferior vena cava pe rmits access to the veins and a ids repair.However, these injuries are freque ntly lethal.

Khaneja et al. 59 reported management of p enetrating juxtahep atic IVC injuries by to tal vascular occlusion with s elective use o f aortic cross-clamping. Theyreported 70% survival.

Visceral mobilization and rotation to the left expose s the right kidney, IVC, and lower a orta. Visceral mobilization to the right exposes the left kidney and a orta.

In cases of blunt abdominal trauma the ab dominal veins may be involved, but rarely the a bdominal aorta. 60 With aortic injury the mortality is very high.

Fletcher et al. 61 reported that obs truction of the intrahepa tic IVC seconda ry to metastasis from hepatic malignant process (IVC syndrome, including ascites,anasa rca, etc.) can be palliated by placement of percutaneous stents via the femoral vein.

Babu et al. 62 advised a n aggres sive approa ch when rena l or adrenal neop lasms extend intraluminally into the IVC. Fig. 12-28 demonstrates the level of extension.

Staehler a nd Brkovic 63 concluded that w hen a tumor thrombus do es no t extend cranially beyond the level of the diaphrag m, radical surgery for renal cellcarcinoma extending to the vena cava is justified.


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McLoughlin and Rankin 64 evaluated 100 CT scans and reported tha t the distance be twee n the IVC and main portal vein is less than 1 cm in most cases . If themain portal vein is subdivided into 3 parts upp er, middle, and lower the anatomic entities be twee n the IVC and the main portal vein are as follows:

Upp er: liver

Middle: in most case s, none

Lower: nodes

McLoughlin and Rankin indicated that the most common structures related to the main portal vein at its three levels are:

Upper: liver; hepatic artery, and gallbladder

Middle: liver, stomach, and pa ncreas

Low er: pancreas, duod enum, celiac axis

Fig. 12-27.


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Anatomic location of the retrohepatic inferior vena cava compression in a lateral, inferior, and posterior projection. (Modified from Greenfield LJ (ed). Complicationsin Surgery and Trauma. Philade lphia: JB Lippincott, 1984; with permission.)

Fig. 12-28.

Involvement of inferior vena cava in renal cancer is usua lly intraluminal extension of tumor mass. The s uperior margin of the tumor in inferior vena cava de finesthe level and surgical approach. Level I: Tumor is in the sup rarenal cava, but infrahepatic. Level II: Tumor extends into the retrohepatic cava with or w ithoutoccluding the orifices of hepatic veins. Level III: Tumor extends into the right atrium. (Modified from Babu SC, Mianoni T, Shah PM, Goyal A, Choudhury M, EshghiM, Moggio RA, Sarabu MR, Lafaro RJ. Malignant renal tumor with extension to the inferior vena cava. Am J Surg 176:137-139, 1998; with permission.)

The same authors concluded that the middle part of the main portal vein appears to be a relatively safe cavo-portal route (if aberrant vessels and aprominent caudate lobe are excluded) and that perhaps percutaneous portacaval shunting may be worthy of further experimental study.

ANATOMIC COMPLICATIONS

The most common complication is misplacement of a vena caval filter, which occasionally migrates to the right atrium. In a minority of cases, ed ema of the low erextremities a nd varicosities may follow.

Another complication of filter insertion is wound hematoma due to ea rly resumption of a nticoagulants. 65

Occlusion of the IVC by a very large embolus within the filter is recognizable by a sud den fall in blood pressure. Measuring Pa O 2 and central venous pressure are

esse ntial in differentiating betw een functional hypovolemia and right ventricular overload. 65

Note

The inferior vena cava is, of course, part of both the abdominal and chest cavities. For more information about the inferior vena cava, we strongly

recommend that the reader consult Surgery of the Chest by Sabiston and Spencer 66 and Embryology for Surgeons by Skandalakis and Gray. 2

REFERENCES

1. Carrel A. The surgery of blood vessels. Bull Johns Hopk Hosp 19:18-27, 1906.

2. Skandalakis JE, Gray SW. Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994.

3. Roques X, Bourdeaud'hui A, Choussat A, Riviere J, Laborde N,

chapter 12 great vessels in the abdomen

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