Chapter 12 Great Vessels in The Abdomen

5/24/2014
Print: Chapter 12. Great Vessels in the Abdomen

Print | C lose Window
Note: Large images and tables on this page may necessitate printing in landscape mode.
Skandalakis' Surgical Anatomy > Chapter 12. Great Vessels in the Abdomen >
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 passes 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 open aortic aneurysm
Canano
mid1500s
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 arteriovenous communication
Hallowell
1759
Successfully closed brachial artery by uniting edges of wound with peg, around which he twisted a thread
White
1784
Described "milk leg." Favored lymphatic obstruction theory over role of thrombosis.
John Hunter
1786
Introduced proximal ligation alone in upper thigh for popliteal 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
Recognized intermittent claudication in humans similar to that of horses
Raynaud
1862
Defined vasospastic disease that bears his name (Raynaud's disease)
Friedlnder, von
Winiwarter
1870s
Described arteritis obliterans
Von Eck
1879
Performed anastomosis of portal vein and inferior vena cava
Severeanu
1880
Attempted arterial thrombectomy to manage occlusive disease
Gluck
1881
Repaired arterial wounds with small ivory clamps
Matas
1888
Described endoaneurysmorrhaphy for management of aneurysms
Connheim
1889
Studied ischemic tissues
Jassinowsky
1889
Repaired arterial wounds with sutures
Trendelenburg
1890
Understood hemodynamics of varicosities and venous stasis of lower extremities and pulmonary embolism. Removed pulmonary
embolism.
Murphy
1896
Performed first successful arterial anastomosis
Carrel
1902
Experimented with arterial replacements. Published technique of circular suture of blood vessels.
Exner
1903
Transplanted autogenous venous graft
Payr
1904
Devised method to unite divided vessels by invaginating ends into an absorbable magnesium cylinder
Carrel & Guthrie
1906
Reported arteriovenous anastomoses and transplantation of organs
Delbet
1906
1911
Lexer
1907
Successfully used free vein graft on axillary artery
Buerger
1908
Expanded description of thromboangiitis obliterans, showing that it and periarteritis nodosa cause only a small proportion of
cases of arterial obstruction in leg
Jianu
1909
Pirovano
1910
First clinical transplantation of homologous artery from one human to another (unsuccessful)
Labey-Mosny
1911
Successfully performed arterial embolectomy
Warthmuller
1917
Successfully treated traumatic aneurysm using vein grafts
Heuser
1919
Developed concept of angiography with sodium iodide on basis of personal experience, without films (Argentina)
http://web.uni-plovdiv.bg/stu1104541018/docs/res/skandalakis'%20surgical%20anatomy%20-%202004/Chapter%2012_%20Great%20Vessels%20in%20the%2
1/36
5/24/2014
Heuser
1919
Developed concept of angiography with sodium iodide on basis of personal experience, without films (Argentina)
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
Visualized subclavian vein using sodium iodide (one case)
Berberich & Hirsch
1923
Performed first successful arteriography in man with water-soluble contrast material (strontium bromide) and first good
demonstration of peripheral veins with valves
Holman
1924
Described increase in blood volume and cardiac output with occasional cardiac failure in arteriovenous fistulas
Kirschner
1924
Performed successful pulmonary embolectomy
Moniz
1927
Devised carotid arteriography
Homans
1928
Prevented pulmonary embolism by venous ligation
1934
dos Santos et al.
1928
Experimented with percutaneous aortography with sodium iodide
dos Santos
1929
Developed technique of translumbar arteriography
dos Santos et al.
1931
Introduced Thorotrast for angiography. Developed mechanical injector with preset pressure.
Gurin et al.
1935
First surgical attempt to correct aneurysm of the aorta by dissection
Gibbon
1937
Devised heart-lung apparatus for use on animals
Murray
1937
Conceptualized varicose veins as a disease of deep venous system following phlebitis.
Leriche
1937
Described arteriectomy for chronic arterial insufficiency
Castellanos & Pereiras
19381939
Performed inferior vena cavography
Farias
1941
Performed abdominal aortography with catheterization through surgical cutdown of femoral artery and introduction through
trocar
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
Introduced thromboendarterectomy to disobliterate occluded arterial segments
Kunlin
1948
Introduced bypass principle for treatment of arterial occlusion
Gross
1949
Performed successful homologous graft to bridge aortic defect for coarctation of aorta
Linton
1949
Performed successful aneurysmectomy
Souza Pereira
1949
Injected superior mesenteric vein for portography
Elkin & Cooper
1949
Described limited experience with Leriche terminal aortectomy
Oudot
1950
Performed first resection and homograft of a thrombosed aortic bifurcation
Bigelow
1950
Published effects of hypothermia on lowering of oxygen consumption and its impact on blood flow through heart
Peirce
1951
Performed thoracic aortography through femoral artery needle by inserting polyethylene catheter without guide wire
Ponsdomenech &
Beato-Nunez
1951
Performed left ventricular angiography with direct needle puncture
Prevented pulmonary embolism with anticoagulants.
Thompson & Smithwick 1952
Performed first revascularization of kidney (unsuccessful)
Dubost et al.
Dubost reported first successful resection of abdominal aortic aneurysm and use of preserved human arterial graft for continuity.
Several other surgeons reported similar successful results.
1952
Szilagyi et al.
Shumacker & King
Julian et al.
Voorhees, Jaretzki, and 1952
Blakemore
Successful use in animal experiments of Vinyon-N tubes made of porous, biologically inert material that remained patent
DeBakey
1953
First successful open thromboendarterectomy of carotid bifurcation
DeBakey & Cooley
1953
First successful resection of aneurysm of thoracic aorta and replacement by graft
Seldinger
1953
Introduced technique of percutaneous arterial catheterizaton
Gibbon
1953
Applied heart-lung apparatus to close an atrial septal defect in a young woman
Edwards
1953
Together with chemist Tapp, introduced vascular graft innovations
Shumway et al.
1955
Experimented with rolled sheets of polyvinyl sponge (Ivalon)
Shaw & Maynard
1958
First superior mesenteric endarterectomy
Mikkelsen & Zaro
1959
First to transect and reimplant SMA
Palma & Esperon
1960
Treated postphlebitic syndrome using venous transplant and grafts
Strm & Winberg
1962
Selective inferior mesenteric arteriography
Boijsen et al.
1963
Selective simultaneous celiac axis and superior mesenteric arteriogram
Fogarty et al.
1963
Balloon catheterization for extraction of intravascular emboli
Golomb et al.
1964
Selective visceral catheterization of arteries for infusion cancer chemotherapy
Waldhausen &
1966
Introduced subclavian flap angioplasty
1967
Introduced eversion endarterectomy
Nahrwold
Harrison et al.
2/36
5/24/2014
Harrison et al.
1967
Connolly & Stemmer
1970
Bentall
1968
Introduced direct reattachment of coronary artery origins to composite valve graft
Ochsner et al.
1970
Reported 286 cases of IVC ligation with only 4% postphlebitic 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.
Greenfield
1976
Published excellent monographs on pulmonary embolism and IVC filters
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 separate small Dacron tube graft
Crawford
1984,
1986
Performed graft replacement of aneurysm in descending thoracic aorta without 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
1992,
1993
Outlined conservative treatment of chronic and acute dissection of descending thoracic aorta
Miller
Introduced eversion endarterectomy
History table compiled by David A. McClusky III and John E. Skandalakis.

References:
Doby T. Development of Angiography and Cardiovascular Catheterization. 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 Saunders, 1986.
Shumacker HB Jr. Extraperitoneal approach for vascular operation: 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 address: the foundations of modern aortic surgery. J Vasc Surg 27:7-15, 1998.
Warren R. Surgery. Philadelphia: WB Saunders, 1963.
Yao JST, Pearce 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 truncus
arteriosus 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. Although
hypertension 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 Kelly6 associated coarctation of the abdominal aorta with concomitant narrowing of the origins of major visceral arteries as a
rare 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 Suwanwela7 have observed
geographic 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 practical
purposes this is really a bifurcation, as the middle sacral artery represents a small median branch emerging between the two common iliacs.
Fig. 12-1.
3/36
5/24/2014
The diaphragmatic openings for the inferior vena cava, esophagus, and aorta as seen 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 the abdominal aorta extends approximately from a point 2 cm below
the 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 connecting
the 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 diameter
is 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. At
the 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 a
position 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 cava
assumes a position dorsal to the aorta, dividing at the level of L5.
Fig. 12-2.
4/36
5/24/2014
The apertures of the diaphragm seen from below and the structures traversing them. A = aorta, IVC = inferior vena cava. (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 contributes visceral branches that serve intraperitoneal and retroperitoneal organs, and parietal branches that support the roof and
walls of the abdomen. Grant and Basmajian12 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 are
often referred to as the unpaired, visceral branches.)
Fig. 12-3.
The branches of the abdominal aorta arranged according to the planes they occupy (diagrammatically depicted in Fig. 12-4). The branches supply the following
territories: 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; with
permission.)
Fig. 12-4.
5/36
5/24/2014
The three vascular planes of the collateral branches of the abdominal 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 visceral
branches.)
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) beautifully demonstrate the arterial distribution and the territories 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 umbilicus
and 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 the
common 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 aortic
bifurcation to the femoral point. This point is midway between the anterior superior iliac spine and the pubic symphysis. The course of the common iliac
occupies 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 4
cm, 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 the
bifurcation 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 anatomic
entities they supply and the vessels responsible for their 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 usually
about 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) hepatic
artery. Its third branch, the left gastric artery, is a mobile vessel whose origin may slide between the aorta (leaving a hepatosplenic trunk) all over
the 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 its
branches 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 artery
does 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 the
hepatic and splenic artery. The most common collateral of the celiac trunk is a single or double inferior phrenic artery.
Fig. 12-5.
6/36
5/24/2014
The division of the celiac trunk. (Lit.), reported in medical literature. (Modified from Van Damme JPJ, Bonte J. Arteria splenica and the blood supply
of the 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 gastric arises early from celiac, followed by hepatosplenic bifurcation: 49 percent
"Typical" trifurcation of celiac trunk: 25 percent
Hepatosplenic trunk: 5 percent. (Left gastric arises independently from aorta.)
Gastrosplenic trunk: 3 percent. (Common hepatic arises separately from aorta.)
Gastrohepatic trunk: 1 percent. (Splenic arises separately from aorta.)
Gastrohepatosplenomesenteric 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 Damme16 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 level
the 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 superior
mesenteric artery in cases of intestinal ptosis. After the origin of the ileocolic artery, the superior mesenteric artery gives off ileal branches only. It
is 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, the superior mesenteric artery gives pancreatic and duodenal branches also (pancreaticoduodenal arcades, the
artery for the neck, the transverse pancreatic artery, a branch for the duodenojejunal angle). Aberrant branches from the superior mesenteric
artery 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.
7/36
5/24/2014
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 from
the 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 injury19 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
Grade 2 Moderate
Major segment, small bowel and/or right colon
Grade 3 Minimal
Minor segment or segments, small bowel or right colon
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 permission.
Table 12-3. Superior Mesenteric Artery Injury Classification by Anatomy
Zone
Segment of SMA Involved
Trunk proximal to first major branch
II
Trunk between pancreaticoduodenal and middle colic
8/36
5/24/2014
II
Trunk between pancreaticoduodenal and middle colic
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 permission.
Fig. 12-8.
Artist's conception of SMA circulation, showing the classification by anatomic zones. IPD = Inferior pancreaticoduodenal artery, R. col. = Right colic artery. (Modified
from 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 at
the 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 Damme16 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 these
two vessels. Only those important vessels that mainly supply the sigmoid colon and have a direct origin from a main stem (inferior mesenteric
artery, colosigmoid, or left colic artery) are considered as sigmoid branches. The inferior mesenteric artery is a short artery that irrigates a very
long 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 a
fan-like course.
Fig. 12-9.
9/36
5/24/2014
The inferior mesenteric artery and its branches: origin distance in millimeters. If the inferior mesenteric artery is divided at "a," above the last full
anastomosis, collateral circulation toward the rectum is still possible. Division at "b" would interrupt the collateral circulation. (Modified from Van
Damme JP, Bonte J. Vascular Anatomy in Abdominal Surgery. Stuttgart: 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 to
infarction.
The spinal cord is supplied dependably neither by a continuous longitudinal vessel nor by strictly segmental arteries. The anterior spinal artery (Figs. 1210, 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 odontoid
process. Passing down the ventral sulcus, the anterior spinal artery normally receives input from a branch of the left thyrocervical trunk, which enters the
3rd or 4th cervical intervertebral foramen. This branch can be injured by cervical surgical procedures. This upper part of the artery continues down to
about the level of T4, giving off circumferential vessels to a plexus on the surface of the cord; the vessels anastomose with the paired posterior spinal
arteries.
http://web.uni-plovdiv.bg/stu1104541018/docs/res/skandalakis'%20surgical%20anatomy%20-%202004/Chapter%2012_%20Great%20Vessels%20in%20the%
10/36
5/24/2014
Fig. 12-10.
The anterior and posterior spinal arteries. (Modified from Decker GAG, duPlessis DJ (eds). Lee McGregor's Synopsis of Surgical Anatomy. Bristol: Wright, 1986; with
permission.)
Fig. 12-11.
The distribution of a lumbar or intercostal artery. The anterior and posterior radicular arteries are branches of 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.
11/36
5/24/2014
The blood supply of the spinal cord. The main radicular arteries are shown. (Modified from Decker GAG, duPlessis DJ (eds). Lee McGregor's Synopsis of Surgical
Anatomy. 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. Some
variable input to the spinal cord occurs by way of radicular branches of cervical, intercostal, or lumbar arteries that enter the spinal canal on the spinal
nerve roots. We have also seen large contributions to the cauda equina nerve roots and the longitudinal anastomotic network of the cord derived from the
median 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 branch
is 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 also
be 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 level23 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 retention
and 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 Geertruyden24 recognized the importance of the arteria radicularis magna and emphasized that
neurologic 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 on
one of the upper lumbar nerve roots. When the vascular supply to the lumbar segments of the spinal cord and nerve roots is occluded (an infrequent
occurrence), 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 spinal
artery and the anterior radicular arteries supply blood to the gray matter (anterior and intermediate portions), the base of the posterior gray column, the
white matter of the anterior funiculus, and the deeper portion of the lateral funiculus (Figs. 12-12 and 12-13).
Fig. 12-13.
12/36
5/24/2014
The anterior and posterior radiculo-medullary branches.
In summary, the posterior spinal arteries and posterior radicular arteries supply blood to the posterior funiculus, most of the posterior gray columns, and
the superficial part of the lateral funiculus.
Approximately eight anterior and 12 posterior radicular arteries pass along the spinal nerve rami and nerve roots to reach and supply, variably, the
vertebrae, meninges, and cord. The most important radicular artery is, as noted above, the arteria radicularis magna. It produces the anatomic
complication of paraplegia (transverse myelitis) when violated.
Medical causes of vascular impairment to the spinal cord include atherosclerosis, diabetes mellitus, thromboses, dissecting aneurysms of the aorta, and
others.
Collateral Arterial Branches

The collateral circulation between the arterial branches to the abdominal viscera is excellent and surgically important. Communications exist between
branches of the celiac axis itself; between the branches of the celiac axis and the superior mesenteric artery (Fig. 12-14); between the branches of the
superior 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 with the superior mesenteric artery. (Modified from Brantigan OC. Clinical Anatomy. New York: McGrawHill, 1963; with permission.)
13/36
5/24/2014
Fig. 12-15.
The collateral circulation of the branches of the superior mesenteric artery and inferior mesenteric artery. (Modified from Brantigan OC. Clinical Anatomy. New
York: McGraw-Hill, 1963; with permission.)
The names of three researchers are associated with mesenteric circulation: Bhler, Riolan, and Drummond.
Arc of Bhler. The arc of Bhler is an artery connecting the common hepatic or gastroduodenal artery with the SMA and forming an anastomotic network
between the SMA and celiac artery (Fig. 12-16).
Arc of Riolan. Another anastomotic network is the arc of Riolan, between the SMA and IMA (Fig. 12-17).
Marginal artery of Drummond. The best known of the three is the marginal artery of Drummond, also communicating between the SMA and IMA (Fig. 12-17).
Fig. 12-16.
14/36
5/24/2014
The arc of Bhler forming a direct anastomotic communication between the celiac and the SMA. (Modified from Rosenblum JD, Boyle CM, Schwartz LB. The
mesenteric 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, Boyle
CM, 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 Table
12-4.
Table 12-4. Normal and Variant Vascular Anatomy
Vessel
Incidence
Celiac
Three branches (classic)
65-75%
Four branches including dorsal pancreatic artery
5-10%
15/36
5/24/2014
Celiacomesenteric trunk

<1%
Hepatic
Common hepatic from celiac artery
75%
Common hepatic from SMA
2.5%
Replaced right hepatic artery
17-18%
From SMA
10-18%
From aorta
<2%
Replaced left hepatic artery
15-18%
From left gastric
11-12%
From SMA
2.5%
Accessory right hepatic artery
7-8%
Accessory left hepatic artery
2.5%
Gastric
Left gastric artery
From celiac artery
90%
From aorta
3%
Accessory branches from or to left hepatic artery 23%

Right gastric artery
From proper hepatic artery
40%
From left or middle hepatic artery
40%
From right hepatic artery
10%
From gastroduodenal artery
8%
SMA, superior mesenteric artery.

Source: Rosenblum JD, Boyle CM, Schwartz LB. The mesenteric circulation: anatomy and physiology. Surg Clin North Am 77(2):289-306, 1997; with permission.
Anatomic Entities Related to Abdominal Aorta (and Some Surgical Applications)

MEDIAN ARCUATE LIGAMENT, THORACIC DUCT, AZYGOS VEIN, AND AORTIC HIATUS
The aorta follows an oblique course behind the diaphragm rather than traveling through it (Fig. 12-1). At the level of T12, the anterior border of the
opening is provided by the median arcuate ligament. Laterally the diaphragmatic crura form its margins. The thoracic duct accompanies the aorta.
The azygos vein often also accompanies the aorta, but its course can vary. It can pass behind the diaphragm with the aorta, or to the right of the right
crus, or it can pierce the right crus. Also passing through the crura are the greater, lesser, and least thoracic splanchnic nerves (Fig. 12-2).
The esophageal hiatus is separated from the aortic hiatus by the fusing of the arms of the left and right crura. If the tendinous portions of the crura are
fused, the median arcuate ligament (Fig. 12-18) is present as a fibrous arch passing over the aorta, connecting the right and left crura. If the fusion is
muscular only, the ligament is ill-defined or absent.
Fig. 12-18.
16/36
5/24/2014
The attachments of the muscles of the diaphragm seen from below. A = aorta, E = esophagus, IVC = inferior vena cava. (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 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 in
intimate juxtaposition to the lateral aspects of the celiac trunk. Together with the profuse celiac neural network, they conceal the origin of the artery and
much 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 atherosclerotic
plaques. Lack of symptoms arising from the vascular compression indicates that such patients have adequate collateral circulation. The median arcuate
ligament has been implicated in abdominal angina in instances when substantial tense fibromuscular tissue at the hiatus exerted a constrictive effect on
the 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 the
diaphragm generates the celiac artery compression syndrome (also referred to as celiac 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 celiac
plexus.
Diagnosis of the median arcuate ligament syndrome may be established by elimination of other causes for abdominal pain as Bech27 stated. The surgeon
should remember that this syndrome is real, not imaginary, and that simple division of the median arcuate ligament may cure the patient. Occasionally
revascularization 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 and
esophageal 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 surgical
repair of the esophageal hiatus. In the remainder, there was enough preaortic fascia lateral to the celiac trunk to perform a posterior fixation of the
gastroesophageal junction. In hiatal hernia procedures, the celiac ganglia, located just below the arcuate ligament (or its expected position), must be
avoided.
ABDOMINAL AORTIC NERVE PLEXUSES
The celiac plexus (Fig. 12-19) is formed by a retroperitoneal network of several sympathetic ganglia, together with sympathetic and parasympathetic
nerves and many afferent fibers. These interconnect with each other and envelop the celiac axis and the superior mesenteric artery. This plexus receives
input 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.
17/36
5/24/2014
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 mesenteric
plexus, 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 near
its 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 splits
into right and left pelvic plexuses.) The preaortic nerve plexus and the hypogastric plexus receive two or more bilateral contributions from the lumbar
segments of right and left sympathetic chains. Numerous fibers, which contain pelvic splanchnic parasympathetic fibers and afferent neurons, ascend into
the 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 wall
or 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, but
these are rare occurrences. More likely, trauma or a ruptured splenic artery aneurysm may cause an arteriovenous fistula between the splenic artery and
splenic vein.
18/36
5/24/2014
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 from
this, 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 inferior
mesenteric 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 the
duodenum 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 ROOT
The 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 the
aorta and behind the pancreas and splenic vessels, the left renal vein may be fused tightly with an aortic aneurysm. The possible involvement of the left
adrenal and left gonadal veins is variable, depending on the size of the aneurysm.
LEFT LUMBAR VEINS
When repairing an aortic aneurysm, the 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 retroperitoneal
anatomic 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 cardiac
systole. 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 and
irregular smooth muscle cells (most arranged in circumferential fashion) and collagenous 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 layers
containing collagen fibers, elastic fibers, and smooth muscle cells.
Davies and Hagen35 reported that the surface area of the vascular endothelium is approximately 5000 m2, 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 the
surgeon today. The endothelium influences blood vessel tone, permeability, cell adhesion, coagulation, and growth by regulating molecules and proteins
expressed 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 essential.
Ballard38 advised ultrasound evaluation for patients with asymptomatic abdominal aortic aneurysms of 4.0-5.5 cm, and surgical intervention for rapidly
growing or larger aneurysms.
According to Davis et al.39 the pathways of rupture of aortoiliac aneurysms are into the:
retroperitoneal spaces
peritoneal 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
19/36
5/24/2014
Based upon a retrospective review of 25 patients, Weinstein et al.40 indicated that patients with normal blood pressure who have "stable" ruptured
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 tremendous
morbidity 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 potential
anatomic complications, the repair of aortic aneurysms is presented strictly from an anatomic standpoint. We consider transabdominal and retroperitoneal
approaches.
Surgical Approaches
TRANSABDOMINAL APPROACH
An aortic aneurysm can be attacked by the transabdominal approach of the surgeon's choice, using a long ventral midline incision or a transverse
midabdominal incision. Keep in mind the following anatomic entities or landmarks during such procedures.
Ligament of Treitz at the duodenojejunal flexure
Retroperitoneum
Mesentery of the small bowel (the radix)
Inferior mesenteric vein and inferior mesenteric artery
Paths of both the right and left renal veins (remember the possibility of retroaortic left renal vein)
Both right and left external and internal iliac arteries (remember to preserve one of the internal iliac arteries for the pelvic blood supply through collateral
circulation)
Right and left femoral arteries (as necessary)
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 aorta and inferior mesenteric artery
Marino et al.,42 who studied the proximal abdominal aorta and especially the celiac region, recommended left subpancreatic transplexus exposure of the
celiac axis and the superior mesenteric artery. They reported finding two types of nerve plexuses: the totally covering plexus and the partly covering
plexus. 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 thin
covering 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. This
left 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 approach risks intercostal neuralgia secondary to injury of intercostal nerves.
Using the thoracoabdominal approach, denervation of the flat abdominal muscles can result in flank bulge secondary to atrophy.
Arterial or venous bleeding is possible.
Ischemia of the lower extremity may occur. The best treatment includes palpation, Doppler examination, or angiography, done in the operating room during the
aneurysmectomy.
Colonic ischemia (a threat especially to patients with previous left colectomy) can be avoided by reimplanting the inferior mesenteric artery during the resection
of the aneurysm. If postoperative bloody diarrhea occurs, the surgeon should consider repeated colonoscopic examinations and, depending on the findings,
exploratory laparotomy with colectomy and transverse colostomy if necessary.
Ischemia of the distal part of the spinal cord may result in very grave complications with high mortality secondary to ligation of both internal iliac (hypogastric)
arteries. Postoperatively, the patient may have motor and sensory loss in both lower extremities, incontinence, and mottling and necrosis of gluteal muscles. To
minimize the chance of ischemia, reimplant one internal iliac if at all possible.
Use renal scan and ultrasound examination to diagnose renal artery occlusion and/or ureteric ligation. Early correction is essential to avoid high mortality.
One of the most tragic complications in thoracic and abdominal aorta surgery is paraplegia or paraparesis. Connolly43 stated that such a catastrophe occurs with
surgery at the top and bottom of the aorta in under 1% of cases, but exceeds 10% in operations just above the diaphragm. Figure 12-13 demonstrates the spinal
blood supply.
Read an Editorial Comment
20/36
5/24/2014

Based on a nationwide study in Finland, Jrvinen et al.44 reported that 27 patients out of 1752 who underwent aortoiliac surgery suffered with intestinal
ischemia 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.
Transverse colon-rectum
43
Sigmoid colon only
Jejunum-transverse colon
24
Ileum only
10
Ileum + sigmoid colon
Ileum + sigmoid colon + rectum
14
Single infarction
Inferior mesenteric artery
Superior mesenteric artery
Multiple infarctions
Source: Jrvinen O, Laurikka J, Salenius J-P, Lepntalo M, Finnvasc Study Group. Mesenteric infarction after aortoiliac surgery on the basis of 1752 operations from
the national vascular registry. World J Surg 1999;23:243-247; with permission.
We quote from du Toit and Saaiman45:

An important Achilles heel of endovascular repair of abdominal aortic aneurysms is back bleeding or endoleak formation due to incomplete sealing or
bridging of aortic branches ostia by endoluminal stents. Significant, recurrent, and persistent retroleaks, a topic of clinical interest, are related to
either incompletely sealed-off inferior mesenteric and/or lumbar arteries. The optimal method to diagnose and manage these endoleaks is currently
in a state of evolution. In the process of stent-graft treatment of abdominal aortic aneurysms, other important aortic branches are also bridged
that may potentially present with the sequelae of peripheral ischemia.
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 Development
The right common cardinal vein and the proximal part of the right anterior cardinal (right precardinal) vein are responsible for development of the inferior
vena cava (Fig. 12-20).
Fig. 12-20.
21/36
5/24/2014
Schematic diagrams showing some of the steps in the development of the inferior vena cava. A to F, stages in ventral (anterior) view; G to I, cross-sectional
views. Cardinal veins are shown in blue; subcardinal veins are red; supracardinals are yellow. Vessels arising independently of these three systems are indicated
by small crosses. , mesenteric portion of inferior vena cava; Sub., subcardinal vein; Umb., umbilical vein; V.V., vitelline vein; Meson. or Mes., mesonephros; Ob.,
oblique vein of left atrium; subcl., subclavian vein; *, left superior intercostal; Supr., suprarenal. (From Carlson BM. Patten's Foundations 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 portion comes from an anastomosis of the right subcardinal and supracardinal veins.
The sacrocardinal or postrenal section 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. The
congenital 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 at First Appearance (or Other

Onset
Diagnostic Clues)
Sex Chiefly
Affected
Relative
Frequency
Absence of hepatic segment of inferior

vena cava
6th week
Symptoms related to associated

cardiac defects only
Equal
Uncommon
Double inferior vena cava; left-sided

inferior vena cava
7th week
None
Equal
Common
Preureteral vena cava
7th week
At any age
Equal
Rare
Remarks
Compression of ureter
products symptoms
Source: Skandalakis JE, Gray SW (eds). Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with permission.
ABSENCE
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 the
22/36
5/24/2014
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 the
6th 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 below
the level of the renal veins, and they have connections with other veins. All these variations are asymptomatic.
Fig. 12-21.
23/36
5/24/2014
The inferior vena cava at the diaphragm. A, Relations. B, Anomalous double inferior vena cava. In this illustration, the right vessel is larger and receives all the
lumbar veins. C, Relations to other vessels. (Modified from Gray SW, Skandalakis JE, McClusky DA. Atlas of Surgical Anatomy for General Surgeons. Baltimore:
Williams & Wilkins, 1985; with permission.)
24/36
5/24/2014
Inferior vena cava duplication has been reported by Colborn46 and Shingleton et al.47 The former has recently observed (in unpublished observations) the
occurrence 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 ureter
with 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 surgical
intervention.
Nakatani et al.48 described a patient with an anomalous triad of a single left-sided inferior vena cava, a retroesophageal right subclavian artery, and
bilateral 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-Sided
IVC
Double IVC
Gladstone, 1929 (D)
0.11 (1/876)
0.2 (2/876)
Seib, 1934 (D)
0.57 (1/176)
2.8 (5/176)
Adachi, 1940 (D)
0.26 (3/1176) 1.4

(16/1176)
Pick and Anson, 1940a, b (D)
Retrocaval
Ureter
0.2 (1/500)
Davis and Lundberg, 1968 (D)
1.8 (5/270)
2.2 (11/500)
0.35 (1/289)
1.7 (3/176)
9.3 (16/176)
3.4 (7/202)
16.8 (34/202)
2.4 (12/500)
6.0 (30/500)
Azygos
Continuation
1.5 (4/270)
Hoeltl et al., 1990 (D)

Bartle et al., 1987 (O)
Circumaortic Venous
Ring
0.17 (2/1176)
0.18 (1/570)
Reise and Esenther, 1959 (D)
Retroaortic Left Renal

Vein
0.35 (1/289)
Hoeltl et al., 1990 (O)
1.1 (4/354)
0.56 (1/289)
0.35 (1/289)
0.35 (1/289)
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)
Mayo et al., 1983 (CT)
0.35 (4/1140) 0.44

(5/1140)
Ueda et al., 1983 (CT)
1.0 (9/874)
Kokubo et al., 1988 (CT)
0.18 (2/1100) 1.1

(12/1100)
Hoeltl et al., 1990 (CT)
0.04 (2/4520) 0.02

(1/4520)
0.08 (1/1200)
0.25 (3/1200)
0.09 (1/1140)
0.09 (1/1140)
0.09 (1/1140)
0.18 (2/1100)
0.36 (4/1100)
0.55 (6/1100)
0.64 (29/4520)
0.09 (4/4520)
0.69 (6/874)
0.08 (1/1260)
D, dissection; O, operation; CT, computed tomography.
All 2,500 cases have congenital heart diseases. The azygos continuation was commonly associated with congenital heart disease.
Source: Nakatani T, Tanaka S, Mizukami S. Anomalous triad of a left-sided inferior vena cava, a retroesophageal right subclavian artery, and bilateral superficial
brachial arteries in one individual. Clin Anat 11:112-117,1998; with permission.
Fig. 12-22.
25/36
5/24/2014
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 renal
vein; 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, left
ureter; 10, left-sided inferior vena cava; 11, inferior mesenteric artery; 12, left ovarian vein; 13, left common iliac vein; and 14, hypogastric plexus. (Modified from
Nakatani T, Tanaka S, Mizukami S. Anomalous triad of a left-sided inferior vena cava, a retroesophageal right subclavian artery, and bilateral superficial brachial
arteries 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 left
IVC 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 prerenal
IVC passes posterior to the diaphragmatic crura to enter the thorax as the axygos vein. In circumaortic left renal vein, one left renal vein crosses
anterior to the aorta and another crosses posterior to the aorta. In retroaortic left renal vein, the left renal vein passes posterior to the aorta. In
circumcaval 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 Tributaries

The 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 IVC
is 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 be
treated 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 after
traversing 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 vena
cava 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 the
infradiaphragmatic 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.
26/36
5/24/2014
The inferior vena cava and its tributaries. (Modified from Gray SW, Skandalakis JE, McClusky DA. Atlas of Surgical Anatomy for General Surgeons. Baltimore:
Topographicoanatomically the posterior wall of the suprahepatic IVC is anchored by a thin, but strong "ligament" to the diaphragmatic hiatus, to the
posterior 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 posterolateral
abdominal 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
common iliac artery. The apparent compression can result in the formation of an iliac or iliofemoral thrombosis.
27/36
5/24/2014
common iliac artery. The apparent compression 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 readily
injured 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 phrenic
veins. 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 is
possible 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 the
anterior 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 most
important 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 is
possible in extremely rare cases. Of course, we remind the reader to avoid suprarenal ligation of the IVC if at all possible.
Remember
The suprahepatic 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. Portal
hypertension, in some cases with secondary varices, may result from suprahepatic obstruction of the hepatic veins (Budd-Chiari syndrome).
The inferior vena caval diaphragmatic opening at T8, a hiatus shaped like a square, is located in the right hemidiaphragm, close to the midline.
The right adrenal vein is short and very fragile as it passes to drain into the posterolateral caval wall above the renal vein.
The IVC passes 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 and
the flexor surface is related to the hepatic triad.
The right renal artery is located behind the IVC and right renal vein (Fig. 12-21C). It is related dorsally to the right psoas muscle and the right diaphragmatic crus.
Ventrally, the IVC and the right renal vein separate the artery from the common bile duct, pancreatic head, and the second part of the duodenum.
The first part of the duodenum is related posteriorly to the IVC and gastroduodenal artery. The third part of the duodenum 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 of the pancreas during pancreatic and duodenal
surgery should be done carefully to avoid anatomic complications.
The distal part of the root of the mesentery of the small bowel crosses the IVC, right ureter, and right gonadal vein.
The right gonadal artery originates below the renal artery and crosses the IVC to come to rest on the psoas muscle. (For all practical purposes the psoas muscle
is the only muscular entity related to the IVC, because the IVC lies on the ventral surface of the muscle.)
There are several other anatomic relationships to remember. The right sympathetic chain is located just posterior to the IVC. On the ventral surface of the psoas
muscle are two other parallel anatomic entities to recognize: the right genitofemoral nerve and the upper one-half of the right ureter. The ureter lies behind the
right gonadal vessels.
Caval lymph nodes are divided into: precaval, retrocaval, and paracaval.
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 deep venous thrombosis of the pelvis or the lower
extremities that does not respond to conservative treatment (anticoagulants). The preferred method is to insert an intraluminal filter (Figs. 12-24, 12-25). This
permits the upward flow of blood but not the upward transmission of the embolus. Another method of interrupting the IVC is to narrow it below the renal veins
using a serrated or non-serrated clip and ligating the left gonadal vein. Prior to the IVC interruption, cavography is essential for identification of variations and
anomalies of this vessel (Figs. 12-21B and 12-26).
28/36
5/24/2014
Fig. 12-24.
Surgical prevention of pulmonary embolism. Large emboli can be trapped by partial interruption of the inferior vena cava. A, Serrated Teflon (Miles) clip. B, Smooth
Teflon (Moretz) clip. These should be placed just distal to the renal veins, and the gonadal veins should be ligated. C, Greenfield filter, which is inserted
transvenously through a jugular or femoral approach. Some surgeons prefer to simply ligate the cava. (Modified from Miller TA. Physiologic Basis of Modern
Surgical Care. St. Louis: CV Mosby, 1988; with permission.)
Fig. 12-25.
29/36
5/24/2014
Diagrammatic illustration of surgical approaches for interruption of the inferior vena cava in prevention of pulmonary embolism. The clips shown are constructed of
plastic material. (Modified from Sabiston DC Jr. Textbook of Surgery, 13th ed. Philadelphia: WB Saunders, 1986; with permission.)
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:
30/36
5/24/2014
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 approaching it through a right flank incision or through the abdomen using a long midline incision or a right subcostal incision.
Retroperitoneal malignant tumors may compress the IVC and produce unilateral or, rarely, bilateral varicosities of the lower extremities and swelling. A gravid
uterus or giant fibroid may compress the IVC and produce edema or varicosities of one or both lower limbs.
In treating injuries of the inferior vena cava that require it to be clamped, use a vein of the upper extremity for intravenous fluids or blood administration. The
infrarenal portion of the IVC is injured most often. For any suspected injury of the IVC, perform abdominal exploration through a long midline incision to
immediately arrest the bleeding and repair the vessel.
With cirrhosis of the liver or Budd-Chiari syndrome, hepatic segments I and VIII may be enlarged. This results in segmented external compression of the vena
cava followed by elevation of the venous pressure. According to Turcotte et al.,54 this entrapment of the IVC by the ligament and enlarged hepatic segments
precludes construction of a standard portosystemic shunt. Schwartz 55 advised that in some patients resection of the caudate lobe will permit a shunt (Fig. 12-27).
The IVC may be injured with fatal results during surgery for lumbar intervertebral disc herniation.
An inferior vena cava lacerated iatrogenically or by trauma should be repaired primarily by one of the following procedures:
Closure of laceration
Closure of defect by a vein patch
Reconstruction by saphenous vein panel graft
Reconstruction by synthetic graft
Ligation below the renal 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 part of the IVC involved with malignant
process. Ohwada et al.56 advised the following:
If involvement of the wall of the IVC is minimal, excision must be done and the defect can be closed with sutures without obstructing the upward venous flow.
The suprarenal IVC can be ligated safely if collaterals are well developed (azygos-hemiazygos, etc.)
Huguet et al.57 recommended reconstruction of the IVC after hepatectomy to avoid acute renal failure.
Several surgical innovations should be considered individually for major resection of a cirrhotic liver for hepatic malignancies involving the IVC or the hepatic
venous confluence. Although aggressive hepatectomy and IVC reconstruction can be used in a cirrhotic liver, evaluation of the functional hepatic reserve and
ischemic injury remain problematic.
Bianchi et al.58 reported that long-term survival is low when resections for carcinoma are associated with major vessel infiltration or a complication that
necessitates a vascular procedure as an emergency.
Occasionally after repair a pulmonary embolus may follow, but this is infrequently a sequela of the procedures on the IVC. Venous hypertension and renal
impairment may occur following ligation of the IVC above the renal veins.
Injury of the retrohepatic vena cava in adults may require a right hepatic lobectomy or placement of a retrohepatic venous shunt to maintain cavo-venous flow
while repairing the venous injury. In children, the extrahepatic joining of the hepatic veins and the inferior vena cava permits access to the veins and aids repair.
However, these injuries are frequently lethal.
Khaneja et al.59 reported management of penetrating juxtahepatic IVC injuries by total vascular occlusion with selective use of aortic cross-clamping. They
reported 70% survival.
Visceral mobilization and rotation to the left exposes the right kidney, IVC, and lower aorta. Visceral mobilization to the right exposes the left kidney and aorta.
In cases of blunt abdominal trauma the abdominal veins may be involved, but rarely the abdominal aorta.60 With aortic injury the mortality is very high.
Fletcher et al.61 reported that obstruction of the intrahepatic IVC secondary to metastasis from hepatic malignant process (IVC syndrome, including ascites,
anasarca, etc.) can be palliated by placement of percutaneous stents via the femoral vein.
Babu et al.62 advised an aggressive approach when renal or adrenal neoplasms extend intraluminally into the IVC. Fig. 12-28 demonstrates the level of
extension.
Staehler and Brkovic63 concluded that when a tumor thrombus does not extend cranially beyond the level of the diaphragm, radical surgery for renal cell
carcinoma extending to the vena cava is justified.
31/36
5/24/2014
McLoughlin and Rankin 64 evaluated 100 CT scans and reported that the distance between the IVC and main portal vein is less than 1 cm in most cases. If the
main portal vein is subdivided into 3 parts upper, middle, and lower the anatomic entities between the IVC and the main portal vein are as follows:
Upper: liver
Middle: in most cases, 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 pancreas
Lower: pancreas, duodenum, celiac axis
Fig. 12-27.
32/36
5/24/2014
Anatomic location of the retrohepatic inferior vena cava compression in a lateral, inferior, and posterior projection. (Modified from Greenfield LJ (ed). Complications
in Surgery and Trauma. Philadelphia: JB Lippincott, 1984; with permission.)
Fig. 12-28.
Involvement of inferior vena cava in renal cancer is usually intraluminal extension of tumor mass. The superior margin of the tumor in inferior vena cava defines
the level and surgical approach. Level I: Tumor is in the suprarenal cava, but infrahepatic. Level II: Tumor extends into the retrohepatic cava with or without
occluding 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, Eshghi
M, 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 a
prominent 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, edema of the lower
extremities and varicosities may follow.
Another complication of filter insertion is wound hematoma due to early resumption of anticoagulants.65
Occlusion of the IVC by a very large embolus within the filter is recognizable by a sudden fall in blood pressure. Measuring PaO 2 and central venous pressure are
essential in differentiating between 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 Spencer66 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, Hafez A, Baudet E. Coarctation of the abdominal aorta. Ann Vasc Surg 2(2):138-144,
1988.
4. Palmaz JC, Carson SN, Hunter G, Weinshelbaum A. Male hypoplastic infrarenal aorta and premature atherosclerosis. Surgery 94(1):91-94, 1983.
5. van Meurs-van Woezik H, Wolff ED, Essed CE, Meradji M, Bos E, de Villeneuve VH. Tandem coarctation of the thoracic aorta with hypoplasia of the
abdominal aorta. Thorac Cardiovasc Surg 33(1):44-47, 1985.
6. Smith SH, Kelly DR. Coarctation of the abdominal aorta in a child: morphometric analysis of the arterial lesion. Pediatr Pathol 5:363-371, 1986. [PubMed:
3523454]
33/36
5/24/2014
7. Piyachon C, Suwanela N. Takayasu arteritis in Thailand. Heart Vessels Suppl 7:60-67, 1992. [PubMed: 1360974]
8. Takeshita T, Miyaji N, Kobayashi H, Inoue H, Yano T, Asato M, Ito Y, Shinohara S. [A case of a rare anomaly of the abdominal aorta: magnetic
resonance image and angiographic finding]. Nippon Igaku Hoshasen Gakkai Zasshi 50(3):258-261, 1990.
9. Anson BJ, McVay CB. Surgical Anatomy, 5th ed. Philadelphia: W.B. Saunders Co., 1971.
10. Meschan I. Anatomy Basic to Radiology. Philadelphia: W.B. Saunders Co., 1975.
11. Yahel J, Arensburg B. The topographic relationships of the unpaired visceral branches of the aorta. Clin Anat 11:304-309, 1998. [PubMed: 9725573]
12. Grant JCB, Basmajian JV. Grant's Method of Anatomy, 7th Ed. Baltimore: Williams & Wilkins, 1965, pp. 276-296.
13. Henretta JP, Karch LA, Hodgson KJ, Mattos MA, Ramsey DE, McLafferty R, Sumner DS. Special iliac artery considerations during aneurysm endografting.
Am J Surg 178:212-218, 1999. [PubMed: 10527442]
14. Allen RC, White RA, Zarins CK, Fogarty TJ. What are the characteristics of the ideal endovascular graft for abdominal aortic aneurysm exclusion? J
Endovasc Surg 4:195-202, 1997. [PubMed: 9185007]
15. Allen RC, Fogarty TJ. The Medtronic-AneuRx modular bifurcated graft. In: Yao JST, Pearce WH (eds). Techniques in Vascular and Endovascular
Surgery. Stamford, CT: Appleton & Lange, 1998, pp. 401-409.
16. Van Damme JPJ. Behavioral anatomy of the abdominal arteries. Surg Clin North Am 73(4):699-725, 1993.
17. avdar S, Sehirli , Pekin B. Celiacomesenteric trunk. Clin Anat 10:231-234, 1997.
18. Lippert H, Pabst R. Arterial Variations in Man. Classification and Frequency. Munchen: JF Bergmann, 1985.
19. 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.
20. Komori K, Mori E, Yamaoka T, Ohta S, Takeuchi K, Matsumoto T, Kume M, Sugimachi K. Successful resection of superior mesenteric artery aneurysm. A
case report and review of the literature. J Cardiovasc Surg 2000;41:475-478. [PubMed: 10952344]
21. Van Damme JP, Bonte J. Vascular Anatomy in Abdominal Surgery. Stuttgart: Thieme Verlag, 1990.
22. Williams PL (ed). Gray's Anatomy, 38th Ed. New York: Churchill Livingstone, 1995, p. 1218.
23. Patten J. Neurological Differential Diagnosis, 2nd Ed. New York: Springer, 1996.
24. Adams HD, van Geertruyden HH. Neurologic complications of aortic surgery. Ann Surg 144:574, 1956. [PubMed: 13373248]
25. Rosenblum JD, Boyle CM, Schwartz LB. The mesenteric circulation: anatomy and physiology. Surg Clin North Am 77(2):289-306, 1997.
26. 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, p. 661.
27. Bech FR. Celiac artery compression syndromes. Surg Clin North Am 77(2):409-424, 1997.
28. Harjola PT. A rare obstruction of the coeliac artery. Ann Chir Gynaec Fenniae 52:547, 1963. [PubMed: 14083857]
29. Gray SW, Skandalakis LJ, Skandalakis JE. Classification of hernias through the oesophageal hiatus. In Jamieson GG (ed). Surgery of the Oesophagus.
Edinburgh: Churchill Livingstone, 1988.
30. Gray SW, Rowe JS Jr, Skandalakis JE. Surgical anatomy of the gastroesophageal junction. Am Surg 45:575, 1979. [PubMed: 507565]
31. Skinner JA, Prabhakar G, Genecov DG, Granke K, McDowell DE. Presentation and treatment of spontaneous aortocaval fistula. South Med J 90(10):993996, 1997.
32. Akin JT Jr, Gray SW, Skandalakis JE. Vascular compression of the duodenum: presentation of ten cases and review of the literature. Surgery
79(5):515-522, 1976.
33. Sims WG, Skandalakis JE, Gray SW. Right paraduodenal hernia into the fossa of Waldeyer. J Med Assoc Georgia 60:105-108, 1971. [PubMed: 5554670]
34. Skandalakis JE, Gray SW, Harlaftis M, Collier HS. Hernia into the fossa of Waldeyer: Three cases of right paraduodenal hernia with emphasis on surgical
anatomy. In Honour of Thomas Doxiadis, Evangelismos Hospital, Athens, 1976.
35. Davies MG, Hagen PO. The vascular endothelium: a new horizon. Ann Surg 218:593-609, 1993. [PubMed: 8239773]
36. Cain BS, Meldrum DR, Selzman CH, Cleveland JC Jr, Meng X, Sheridan BC, Banerjee A, Harken AH. Surgical implications of vascular endothelial
physiology. Surgery 122(3):516-526, 1997.
37. Ouriel K, Green RM. Arterial disease. In: Schwartz SI (ed). Principles of Surgery, 7th Ed. New York: McGraw-Hill, 1999, p. 947.
34/36
5/24/2014
37. Ouriel K, Green RM. Arterial disease. In: Schwartz SI (ed). Principles of Surgery, 7th Ed. New York: McGraw-Hill, 1999, p. 947.
38. Ballard DJ, Fowkes FG, Powell JT. Surgery for small asymptomatic abdominal aortic aneurysm. Cochrane Database Syst Rev [computer file]
2000;2;CD001835.
39. Davis PM, Gloviczki P, Cherry KJ Jr, Toomey BJ, Stanson AW, Bower TC, Hallett JW Jr. Aorto-caval and ilio-iliac arteriovenous fistulae. Am J Surg
176:115-118, 1998. [PubMed: 9737613]
40. Weinstein ES, Cooper M, Hammond S, Carlson R, Guber M, Maloy J. The "stable" ruptured abdominal aortic aneurysm gives a false sense of security.
Am J Surg 1999;178:133-135. [PubMed: 10487265]
41. Surowiec SM, Isiklar H, Sreeram S, Weiss VJ, Lumsden AB. Acute occlusion of the abdominal aorta. Am J Surg 176:193-197, 1998. [PubMed: 9737631]
42. DiMarino V, Brunet C, Coppens R, Bonnoit J. Left subpancreatic transplexus exposure of the proximal abdominal aorta. Surg Radiol Anat 18:167-172,
1996.
43. Connolly JE. Prevention of spinal cord complications in aortic surgery. Am J Surg 176:92-101, 1998. [PubMed: 9737610]
44. Jrvinen O, Laurikka J, Salenius J-P, Lepntalo M, Finnvasc Study Group. Mesenteric infarction after aortoiliac surgery on the basis of 1752 operations
from the national vascular registry. World J Surg 1999;23:243-47. [PubMed: 16453391]
45. du Toit DF, Saaiman A. Anatomical importance of infrarenal aortic branches in conventional and endovascular surgery: a review. Clin Anat 2000;13:5462.
46. Colborn GL. A case of bilateral inferior vena cavae joined only at the iliac anastomosis. J Urol 91:478-481, 1966.
47. Shingleton WB, Hutton M, Resnick MI. Duplication of inferior vena cava: its importance in retroperitoneal surgery. Urology 1994;43:113-115. [PubMed:
8284871]
48. Nakatani T, Tanaka S, Mizukami S. Anomalous triad of a left-sided inferior vena cava, a retroesophageal right subclavian artery, and bilateral
superficial brachial arteries in one individual. Clin Anat 11:112-117, 1998. [PubMed: 9509924]
49. Bass JE, Redwine MD, Kramer LA, Huynh PT, Harris JH Jr. Spectrum of congenital anomalies of the inferior vena cava: cross-sectional imaging findings.
Radiographics 2000;20:639-652. [PubMed: 10835118]
50. Capellades J, Pellis F, Rovira A, Griv E, Pedraza S, Villanueva C. Magnetic resonance anatomic study of iliocava junction and left iliac vein positions
related to L5-S1 disc. Spine 2000;25:1695-1700. [PubMed: 10870145]
51. Nesbit RM, Wear JB Jr. Ligation of the inferior vena cava above the renal veins. Ann Surg 154 Suppl:332-344, 1961.
52. Gazzaniga AB, Colodny AH. Long-term survival after acute ligation of the vena cava above the renal veins. Ann Surg 175(4): 563-568, 1972.
53. Thomas JH, Cornell KM, Siegel EL, Sparks C, Rosenthal SJ. Vena caval occlusion after bird's nest filter placement. Am J Surg 176:598-600, 1998.
[PubMed: 9926797]
54. Turcotte JG, Raper SE, Eckhauser FE. Portal hypertension. In: Greenfield LJ (ed). Surgery: Scientific Principles and Practice. Philadelphia: JB Lippincott,
1993, p. 888.
55. Schwartz SI. Complications of portal decompressive surgery. In: Greenfield LJ (ed). Complications in Surgery and Trauma. Philadelphia: JB Lippincott,
1984, p. 567.
56. Ohwada S, Ogawa T, Kawashima Y, Ohya T, Kobayashi I, Tomizawa N, Otaki A, Takeyoshi I, Nakamura S, Morishita Y. Concomitant major hepatectomy
and inferior cava reconstruction. J Am Coll Surg 188(1):63-71, 1999.
57. Huguet C, Ferri M, Gavelli A. Resection of the suprarenal inferior vena cava. The role of prosthetic replacement. Arch Surg 130:793-797, 1995.
[PubMed: 7611873]
58. Bianchi C, Ballard JL, Bergan JH, Killeen JD. Vascular reconstruction and major resection for malignancy. Arch Surg 1999; 134:851-855.
59. Khaneja SC, Pizzi WF, Barie PS, Ahmed N. Management of penetrating juxtahepatic inferior vena cava injuries under total vascular occlusion. J Am Coll
Surg 184:469-474, 1997. [PubMed: 9145066]
60. Lassonde J, Laurendeau F. Blunt injury of the abdominal aorta. Ann Surg 194:745, 1981. [PubMed: 7305489]
61. Fletcher WS, Lakin PC, Pommier RF, Wilmarth T. Results of treatment of inferior vena cava syndrome with expandable metallic stents. Arch Surg
133:935-938, 1998. [PubMed: 9749843]
62. Babu SC, Mianoni T, Shah PM, Goyal A, Choudhury M, Eshghi M, Moggio RA, Sarabu MR, Lafaro RJ. Malignant renal tumor with extension to the inferior
vena cava. Am J Surg 176:137-139, 1998. [PubMed: 9737618]
63. Staehler G, Brkovic D. The role of radical surgery for renal cell carcinoma with extension into the vena cava. J Urol 2000;163: 1671-1675. [PubMed:
10799157]
35/36
5/24/2014
64. McLoughlin RF, Rankin RN. Portacaval space anatomy: potential implications for percutaneous portacaval shunts. J Vasc Intervent Radiol 7(5):761-767,
1996.
65. Greenfield LJ. Complications of venous thrombosis and pulmonary embolism. In: Greenfield LJ (ed). Complications in Surgery and Trauma. Philadelphia:
JB Lippincott, 1984, p. 412.
66. Sabiston DC Jr, Spencer FC. Surgery of the Chest, 6th Ed. Philadelphia: WB Saunders, 1996.
C opyright 2006 The McGraw-Hill C ompanies. All rights reserved.
Privacy Notice. Any use is subject to the Terms of Use and Notice. Additional C redits and C opyright Information.
36/36

Chapter 12 Great Vessels in The Abdomen

Hochgeladen von

Dokumentinformationen

Originaltitel

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Chapter 12 Great Vessels in The Abdomen

Hochgeladen von

Copyright:

Verfügbare Formate

5/24/2014

Print: Chapter 12. Great Vessels in the Abdomen

Considered phlebitis a septic process secondary to infection

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

Ligated above and below to open aortic aneurysm

Demonstrated valves of veins to Vesalius

Understood role of veins in circulation.

Described traumatic arteriovenous communication

Introduced proximal ligation alone in upper thigh for popliteal aneurysm

Described "pulmonary apoplexy" (pulmonary embolism)

First used term "arteriosclerosis"

Recognized role of clot in phlebitis and embolism

Recognized intermittent claudication in humans similar to that of horses

Defined vasospastic disease that bears his name (Raynaud's disease)

Described arteritis obliterans

Performed anastomosis of portal vein and inferior vena cava

Attempted arterial thrombectomy to manage occlusive disease

Repaired arterial wounds with small ivory clamps

Described endoaneurysmorrhaphy for management of aneurysms

Studied ischemic tissues

Repaired arterial wounds with sutures

Performed first successful arterial anastomosis

Transplanted autogenous venous graft

Carrel & Guthrie

Reported arteriovenous anastomoses and transplantation of organs

Attempted arterial thrombectomy to manage occlusive disease

Successfully used free vein graft on axillary artery

Attempted arterial thrombectomy to manage occlusive disease

Successfully performed arterial embolectomy

Successfully treated traumatic aneurysm using vein grafts

Print: Chapter 12. Great Vessels in the Abdomen

Published anatomic atlas of postmortem arteriograms

Devised concept of angiography with sodium iodide, without films (USA)

Sicard & Forestier

Dnner & Calm

Visualized subclavian vein using sodium iodide (one case)

Berberich & Hirsch

Performed successful pulmonary embolectomy

Devised carotid arteriography

Prevented pulmonary embolism by venous ligation

Experimented with percutaneous aortography with sodium iodide

Developed technique of translumbar arteriography

dos Santos et al.

First surgical attempt to correct aneurysm of the aorta by dissection

Devised heart-lung apparatus for use on animals

Conceptualized varicose veins as a disease of deep venous system following phlebitis.

Described arteriectomy for chronic arterial insufficiency

Castellanos & Pereiras

Performed inferior vena cavography

Corrected coarctation of aorta

Alexander & Byron

Introduced thromboendarterectomy to disobliterate occluded arterial segments

Introduced bypass principle for treatment of arterial occlusion

Performed successful aneurysmectomy

Injected superior mesenteric vein for portography

Elkin & Cooper

Described limited experience with Leriche terminal aortectomy

Performed first resection and homograft of a thrombosed aortic bifurcation

Performed left ventricular angiography with direct needle puncture

Prevented pulmonary embolism with anticoagulants.

Thompson & Smithwick 1952

Performed first revascularization of kidney (unsuccessful)

First successful open thromboendarterectomy of carotid bifurcation