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214 V. Dudeja and W. R. Jarnagin
5 Key Points to Manage
Complications
1. In case of intra-operative hemorrhage during
liver resection, inflow control, if not already
underway, should be obtained with Pringle
maneuver. If present, separate control of an
accessory/replaced left hepatic artery should
also be obtained.
2. In the presence of low CVP, bleeding from hepatic veins or retro-hepatic veins can generally
be controlled by pressure followed by suture
control. Rarely, in the face of massive hepatic
venous blood loss and hemodynamic instability, placement of abdominal packs is the only
means of achieving temporary control.
3. Control of catastrophic bleeding from hepatic
veins or retro-hepatic vena cava may require
increased exposure, by carrying the incision
into the right chest, by incising diaphragm or
with a median sternotomy and control of the
infra- and supra-hepatic vena cava.
4. In case of bleeding from the retro-pancreatic
PV, division of pancreas provides good exposure to the injury and allows for suture control. Proximal and distal control and control of
splenic vein may need to be obtained.
5. Bleeding from the lateral branches of SMV
and PV can be controlled by placing a hand
behind the head of the pancreas and duodenum and applying pressure, thereby allowing
localization and suture control.
References
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Am Coll Surg. 1998;187:620–5.
2. Correa-Gallego C, Gonen M, Fischer M, Grant F,
Kemeny NE, Arslan-Carlon V, Kingham TP, Dematteo
RP, Fong Y., Allen PJ, D’Angelica MI, Jarnagin WR.
Perioperative complications influence recurrence and
survival after resection of hepatic colorectal metastases. Ann Surg Oncol. 2013;20:2477–84.
3. Madjdpour C, Spahn DR. Allogeneic red blood cell
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Blumgart LH, Fong Y. Influence of transfusions on
perioperative and long-term outcome in patients following hepatic resection for colorectal metastases.
Ann Surg. 2003;237:860–9. Discussion 869–70.
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13. Jarnagin WR, Gonen M, Maithel SK, Fong
D’Angelica MI, Dematteo RP, Grant F, Wuest D,
Kundu K, Blumgart LH, Fischer M. A prospective
randomized trial of acute normovolemic hemodilution compared to standard intraoperative management in patients undergoing major hepatic resection.
Ann Surg. 2008;248:360–9.
14. Weiskopf RB. Hemodilution and candles. Anesthesiology. 2002;97:773–5.
15. Frankel TL, LaFemina J, Bamboat ZM, D’Angelica
MI, DeMatteo RP, Fong Y, Kingham TP, Jarnagin
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1210-1191.
Intraoperative Injury to Hepatic Arterial Structures
Vinod P. Balachandran and Michael I. D’Angelica
21
Introduction
Hepatic arterial branches serve as important
anatomic landmarks in surgery of the liver,
pancreas, and biliary tree. Their close proximity to the common bile duct (CBD) and portal
vein (PV), as well as anatomic variations in
20–50 % of patients [1, 2], make them susceptible to inadvertent injury during hepatopancreatobiliary (HPB) surgery. Hence, a thorough
understanding of normal and variant anatomy,
clinical scenarios permitting sacrifice or dictating preservation of hepatic arterial branches,
and techniques to anticipate, prevent, and safely navigate intraoperative injury are essential
components of the armamentarium of every
HPB surgeon.
Normal Anatomy of the Hepatic Arterial Vasculature
The celiac trunk, arising off the aorta below the
aortic hiatus of the diaphragm, provides blood
supply to the liver and upper abdominal viscera.
M. I. D’Angelica ()
Department of Surgery, Hepatopancreatobiliary Division,
Memorial Sloan Kettering Cancer Center, 1275 York
Avenue, New York, NY 10065, USA
e-mail: dangelim@mskcc.org
V. P. Balachandran
Department of Surgery, Memorial Sloan Kettering
Cancer Center, New York, NY, USA
e-mail: balachav@mskcc.org
After a short course, it trifurcates into the splenic
artery, left gastric artery (LGA), and common hepatic artery (CHA) (Fig. 21.1). The CHA curves
to the right along the superior border of the pancreas and gives off the gastroduodenal artery
(GDA) as it crosses anterior to the PV. The GDA
runs inferiorly, giving rise to superior pancreaticoduodenal arteries (SPDA) that anastomose
to branches of the inferior pancreaticoduodenal
artery (IPDA) from the superior mesenteric artery (SMA). This collateral circulation between
the SPDA and IPDA contributes to a rich arterial
plexus supplying the head of the pancreas and
duodenum and allows for preservation of flow to
upper abdominal viscera in the setting of pathologic decreased flow through the celiac trunk.
Distal to the GDA origin, the CHA becomes the
proper hepatic artery (PHA), courses superiorly,
and bifurcates into the right hepatic artery (RHA)
and left hepatic artery (LHA). The PHA gives
off a smaller right gastric artery (RGA) from its
anterior surface that supplies the lesser curvature
of the distal stomach. The origin of the RGA is
variable, occasionally arising from the CHA,
RHA, or LHA. The LHA gives rise to a middle
hepatic artery (MHA) supplying segment IV of
the liver, smaller branches to the caudate lobe,
and a separate branch feeding segments II and III
of the liver. The MHA occasionally arises from
the proximal RHA. The arterial branches to the
left liver then join the left PV and left hepatic
duct in the umbilical fissure invaginating Glisson’s capsule and forming the left inflow pedicle.
Shortly after its origin, the RHA gives off a cystic
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_21,
© Springer Science+Business Media New York 2015
217
218 V. P. Balachandran and M. I. D’Angelica
Fig. 21.1 Normal arterial anatomy of upper abdomi-
nal viscera. RH right hepatic artery, MH middle hepatic
artery, LH left hepatic artery, PV portal vein, RGA right
gastric artery, GDA gastroduodenal artery, SPDA superior
pancreaticoduodenal artery, Post PDA poster branch of
the superior pancreaticoduodenal artery, Ant PDA anterior
branch of the superior pancreaticoduodenal artery, GEA
artery supplying the gallbladder and continues to
supply segments V, VI, VII, VIII, and the caudate
process [3]. In 80 % of patients, the RHA runs
posterior to the common hepatic duct before entering the substance of the right liver along with
the right portal and biliary branches as the right
portal pedicle. The RHA commonly branches
into posterior and anterior sectoral vessels, which
can often be dissected extrahepatically. Overall,
the hepatic arteries supply 25 % of blood flow to
the liver and 50 % of the liver’s oxygen content,
while the remainder is derived from the PV [4].
The blood supply to the CBD arises from the
RHA and the retroduodenal branches of the GDA
(Fig. 21.1). The most important vessels lie at the
3 o’clock and 9 o’clock locations. Approximately
40 % of the blood supply runs downward from
branches of the RHA [3, 5].
Variant Anatomy of the Hepatic Arterial Vasculature
Anatomic variations of the hepatic arterial vasculature are common, and a thorough knowledge
of these anomalies is essential to preventing
gastoepiploic artery, IPDA inferior pancreaticoduodenal
artery, SMV superior mesenteric vein, SMA superior mesenteric artery, MCV middle colic vein, MCA middle colic
artery, SA splenic artery, DP dorsal pancreatic artery, LGA
left gastric artery, HA hepatic artery (proper hepatic artery). (With permission from [82] © Springer 2012)
injury. Although Haller first published his treatise on variant hepatic arterial anatomy in 1756, a
systematic analysis of hepatic arterial variations
was not undertaken until 1966 when Michels
described 10 anatomic variants based on 200
cadaveric dissections [6]. Following Michels,
Hiatt and colleagues classified hepatic arterial
variations into six types (Fig. 21.2) based on
1000 patients who underwent liver harvest for
transplantation [7]. Numerous other groups have
since reported on variant hepatic arterial vasculature, based on cadaveric dissections, liver harvest
for transplantation, and angiographic evidence
(Table 21.1) [8–11]. A hepatic arterial branch is
termed replaced when it does not arise off the
PHA but supplies a hemi-liver. A hepatic arterial
branch is termed accessory when it supplies part
of a hemi-liver in addition to an arterial branch
off the PHA. The most common variations are
a replaced RHA (RRHA) arising from the SMA
(3–15 %), replaced LHA (RLHA) arising off the
LGA (2–10 %), normal anatomy with an accessory LHA (ALHA) off the LGA (≤ 10 %), and normal anatomy with an accessory RHA (ARHA)
off the SMA (≤ 7 %) (Table 21.1) [6, 9–16].
21921 Intraoperative Injury to Hepatic Arterial Structures
Fig. 21.2 Hiatt’s classification of hepatic arterial varia-
tions. Dotted lines indicate that the variant artery may be
accessory (if branch shown by dotted line is present) or
replaced (if absent). Type I: normal anatomy; Type II: re-
placed or accessory left hepatic artery; Type III: replaced
or accessory right hepatic artery; Type IV: replaced or
Replaced and Accessory Right Hepatic Arteries
Aberrant RHA anatomy is the most common and
surgically relevant variant. Both a RRHA and
ARHA arise from the SMA, travel posterior to
the pancreatic head, and enter the hepatoduodenal ligament posterolateral to the CBD. Although
many anatomic courses including through the
pancreatic parenchyma have been reported, including through the pancreatic parenchyma [1],
a dissectable groove usually exists between these
vessels and the pancreas (Table 21.1, Fig. 21.2).
accessory right hepatic artery + replaced or accessory left
hepatic artery; Type V: Common hepatic artery from the
superior mesenteric artery; Type VI: Common hepatic artery from the aorta (not shown). (With permission from
[7] © Lippincott Williams and Wilkins 1994)
Replaced and Accessory Left Hepatic Arteries
Replaced and accessory LHAs arise from the
LGA, run in the substance of the lesser omentum
anterior to the caudate lobe, and join the left PV
and left hepatic duct on the left side of the base
of the umbilical fissure (Table 21.1, Fig. 21.2).
Replaced Common Hepatic Artery
A replaced CHA (RCHA), referred to as the hepatomesenteric trunk, most commonly arises from
the SMA posterior to the pancreatic head [17], but
also can run through the pancreatic parenchyma
220 V. P. Balachandran and M. I. D’Angelica
Table 21.1 Variant hepatic arterial anatomy [6, 9–16]
Arterial anatomy Frequency (%)
Proper hepatic artery branching into
right and left hepatic arteries
Replaced arteries
Left hepatic artery from left gastric
artery
Right hepatic artery from superior
mesenteric artery
Left hepatic artery from left gastric,
right hepatic from superior mesenteric artery
Common hepatic artery from superior
mesenteric artery
Common hepatic artery from left
gastric artery
Common hepatic artery from the
aorta
Accessory arteries
Left hepatic artery from left gastric
artery
Right hepatic artery from superior
mesenteric artery
Left hepatic artery from left gastric,
right hepatic from superior mesenteric artery
Replaced and accessory arteries
Replaced right hepatic artery (from
superior mesenteric artery), accessory
left hepatic artery (from left gastric
artery)
Replaced left hepatic artery (from
left gastric artery), accessory right
hepatic artery (from superior mesenteric artery)
52–80
2–10
3–15
3
<
1–5
< 1
<
1
≤ 10
7
≤
< 1
<
2 %
2 %
<
(Table 21.1, Fig. 21.2) [18–20]. Rare variants include RCHA off the LGA, or off the aorta [17].
Celiac Artery Stenosis
Although not an anatomic variant, celiac artery
stenosis (CAS) is an important vascular abnormality in HPB surgery. Blood supply through the
celiac trunk is impaired, leading to retrograde
flow from the SMA through the pancreaticoduodenal arcades, dorsal pancreatic artery, and arc of
Buhler (an embryonic communication between
the celiac and SMA observed in 2 % of population) [21]. In patients with CAS, retrograde flow
through the GDA is the primary source of arterial
blood to the liver and commonly manifests as an
unusually large GDA or pancreatic collateral vessel. The incidence of CAS ranges from 10 to 25 %
of the population [21]. The pathophysiology may
be divided into the following three categories:
• Extrinsic compression: It is commonly due
to the median arcuate ligament, an enlarged
celiac ganglion, or fibroinflammatory tissue.
The median arcuate ligament joins the left and
right diaphragmatic crura, contacting the aorta
cephalad to the celiac trunk. However, it can
pass anterior to the celiac artery in up to 25 %
of individuals. Extrinsic compression is the
most common cause of CAS in Asian populations (55 %) [21, 22].
• Intrinsic stenosis: Intrinsic stenosis is second-
ary to atherosclerotic disease and is the most
frequent cause of CAS in Western countries
[21, 23].
• Other etiologies: These include neoplastic
invasion, pancreatitis, acute or chronic dissection, or intimal disruption [21].
Preoperative Radiographic Assessment
Careful radiographic assessment allows for the
identification and anticipation of anatomic and
pathologic factors such as variant anatomy or
malignant vascular invasion that may increase
susceptibility to injury, necessitate ligation, or
require reconstruction. For preoperative evaluation prior to pancreas resections, the best imaging
modality is a pancreas protocol CT scan, which
includes contrast-enhanced thin-cut arterial and
venous phase imaging through the pancreas [24].
Although direct angiography remains the gold
standard for assessing vascular anatomy and is
the only modality that identifies directional flow,
it is rarely used as arterial phase CT angiography,
with or without angiographic reconstruction has
a reported accuracy of 98 % for detecting arterial anatomic variations [25, 26], and has the advantage of delineating the relationship of arteries
to adjacent organs or tumor [27]. The advent of
multidetector-row CT scanners has further enhanced pancreatic imaging, enabling prediction
of visceral vessel involvement and resectabil-
21 Intraoperative Injury to Hepatic Arterial Structures
221
ity in 80–90 % of pancreas resections [28]. MRI
typically includes arterial and portal phase imaging and is comparable with CT in predicting
vascular invasion and local tumor extension. It
is particularly useful when patients are intolerant
to intravenous contrast agents and when greater
soft-tissue contrast or visualization of the pancreatic duct and biliary tree is desired, such as while
evaluating cystic pancreatic neoplasms [29]. Arterial reconstruction is also possible with MR imaging (MR angiography). Endoscopic ultrasound
(EUS), an operator-dependent modality, has not
been shown to be superior to CT in determining
arterial involvement [30]. We do not routinely use
EUS to assess resectability or vascular anatomy.
For radiographic evaluation prior to liver resection, CT scans using a triphasic protocol (noncontrast, arterial, and portal venous phase) are
helpful in assessing hepatic parenchymal disorders such as steatosis, cirrhosis, lobar/segmental
atrophy, as well as normal and variant hepatic
anatomy. CT angiography can also be used and
is a valuable tool in facilitating surgical planning
and avoiding iatrogenic injury [31]. MRI/MRCP
is considered by many to be superior to CT in assessing the liver and biliary tree and can be combined with MR arteriography to simultaneously
assess vascular structures [29].
Preoperative Considerations
Preoperative management focuses on recognizing clinical scenarios where hepatic artery injury
and subsequent arterial compromise can lead to
liver and biliary ischemia/necrosis. The hepatic
arteries contribute to 25 % of hepatic blood flow
and 50 % of oxygen delivery [4]. Ligation of hepatic arterial branches was historically a feared
complication due to the consequent risk of liver
necrosis and death. These beliefs were based on
very early experiences with hepatic arterial ligation—in 1933, Graham and Cannell reported a
mortality rate of approximately 60 % in a review
of 28 cases where the CHA, PHA, RHA, or LHA
was ligated [32]. Mortality in that era, however,
was heavily influenced by deficiencies in perioperative care, including anesthetic techniques,
antibiotics, and transfusion medicine. In 1964,
Starzl and colleagues observed in four patients
that ligation of the CHA, PHA, RHA, and LHA
in patients with normal liver function only resulted in mild transaminitis and not death [33].
They went on to examine all reports of hepatic
artery branch ligation in patients without cirrhosis or hepatic artery aneurysms between 1933
and 1964. They concluded that ligation of any hepatic arterial branch (CHA, PHA, RHA, or LHA)
in patients with normal liver function results in
mild transient transaminitis and rarely leads to
liver necrosis and death. Flow through the PV
and arterial collaterals was sufficient to maintain
hepatic oxygenation, provided factors increasing
hepatic oxygen demand or decreasing PV blood
flow (shock, jaundice) were absent. These seminal early observations established the safety of
hepatic arterial branch ligation and served as the
basis for later investigations into its mechanisms
and therapeutic potential.
Following these data demonstrating its safety, Plengvanit demonstrated that ligation of the
CHA, RHA, or LHA resulted in collateral formation commonly through the right inferior phrenic
and subcostal arteries in addition to multiple other
collateral sources, which was evident angiographically as early as 1 week after ligation [34]. Mays
and Wheeler made similar observations, demonstrating collateral circulation could develop as
early as 10 h after ligation of the RHA or LHA
[35]. With these data and advances in perioperative care of the surgical patient, hepatic artery
ligation was used to control hemorrhage in the
setting of liver trauma [36, 37] and also as therapy for metastatic disease to the liver [38]. Ligation of the PHA was accompanied by a transient
increase in transaminases, alkaline phosphatase,
and bilirubin, confirming the earlier observations
by Brittain and Starzl [33, 39]. We employ these
principles of hepatic arterial branch ligation routinely in HPB surgery, particularly during placement of hepatic arterial pumps for regional chemotherapy [40, 41]. We have noted through dye
injection perfusion tests performed while placing
hepatic artery pumps that cross-perfusion after ligation of arterial branches occurs within minutes.
These principles have also been utilized for tu-
222 V. P. Balachandran and M. I. D’Angelica
Table 21.2 General principles of hepatic artery preservation
No jaundice or liver dysfunction
Ligation of the CHA and PHA has been shown to be safe; however, attempts at reconstruction are reasonable
Ligation of a hepatic arterial branch(es) is generally safe with one patent hepatic arterial branch
Ligation of all hepatic arterial branches is generally not advised although historical data have shown it to be safe
Jaundice or liver dysfunction
Ligation of any hepatic arterial branch is not advised due to the risk of hepatic ischemia/necrosis
Biliary anastomosis
Ligation of either RHA/RRHA or GDA alone is safe
Ligation of both RHA/RRHA and GDA is not advised due to the risk of anastomotic dehiscence or stricture
CHA common hepatic artery, PHA proper hepatic artery, RHA right hepatic artery, RRHA replaced right hepatic artery,
GDA gastroduodenal artery
mors of the body/tail of the pancreas involving
the celiac axis, where en-bloc resection of the celiac and CHA is performed (Appleby procedure)
after confirming adequate collateral flow through
the GDA [42, 43]. In summary, with respect to
the risk of clinically significant liver ischemia/
necrosis, ligation of hepatic arterial branch(es)
is safe in patients with normal liver function, no
jaundice, and hemodynamic stability, provided a
single remaining hepatic arterial branch is patent (Table 21.2). Ligation of the CHA or PHA in
patients with normal liver function, no jaundice,
and hemodynamic stability has also been shown
to be safe; however, avoiding injury is preferable and reconstruction of an injured CHA/PHA
is reasonable. In the setting of liver dysfunction
or jaundice, hepatic reliance on arterial supply
for oxygenation is increased, possibly due to
increased metabolic demand of hepatocytes and
greater susceptibility to hypoxia and decreased
intrahepatic portal flow due to local compression
from dilated bile ducts [44–46]. Ligation of any
hepatic arterial branch in these settings should be
avoided as it may worsen liver dysfunction and
precipitate liver failure.
A second concern with ligation of a hepatic
arterial branch, primarily the RHA/RRHA, is the
effect on the biliary tree. Isolated ligation of the
RHA/RRHA has not been shown to increase the
risk of biliary stricture formation or biliary anastomotic dehiscence, likely due to arterial crossperfusion at the hilar plate from the LHA, and intact blood supply from the GDA [47]. However,
interruption of both components of biliary blood
supply (RHA and GDA) in the setting of a biliary
reconstruction is associated with a risk of anastomotic dehiscence and stricture formation [48, 49].
Preoperative interventions are therefore directed toward clinical situations that may violate
principles of hepatic artery preservation, thereby
increasing the risk of liver and biliary complications (Table 21.2). Three preoperative techniques have been described to minimize the risk
of liver ischemia when a hepatic artery branch is
at risk for injury. The first and most commonly
used technique is preoperative biliary drainage
in jaundiced patients. Although demonstrated to
increase overall perioperative complications for
pancreas resections [50, 51], preoperative biliary
drainage improves liver function and likely relieves pressure on the portal system from the bile
ducts, thereby minimizing the risk of postoperative liver ischemia [52]. We recommend preoperative biliary drainage in patients with obstructive
jaundice when a hepatic arterial branch is at risk
for injury or clearly requires ligation or reconstruction (and hence risks thrombosis) during surgery (Fig. 21.3). A second technique that has been
described but is less commonly used is embolization of the arterial branch to be sacrificed, to
preoperatively promote development of collateral flow to the corresponding hepatic segment(s),
thereby minimizing postoperative ischemia [53].
We have only occasionally used this technique
in our practice. A third preoperative technique
to minimize liver ischemia, used in patients with
CAS and expected GDA ligation at surgery, is celiac artery stent placement (Fig. 21.3). Stenting
of the celiac artery has been reported to decrease
the risk of biliary/pancreatic anastomotic disruption and liver ischemia [54–57], with 80–95 %
21 Intraoperative Injury to Hepatic Arterial Structures
223
Fig. 21.3 Preoperative vascular considerations in hepa-
tobiliary and pancreatic resections. RHA right hepatic
artery, RRHA replaced right hepatic artery, CAS celiac
artery stenosis, GDA gastroduodenal artery
success rates [21, 58, 59]. Anticoagulation to
prevent stent thrombosis and an adequate waiting
period to allow for collateral development are important considerations prior to staged resection.
If stenting is not possible, surgical bypass, either
at the time of or prior to planned resection, is the
only option.
Preoperative considerations to minimize the
risk of biliary ischemia are relevant in patients
with a RRHA and GDA that will be ligated or are
at risk for injury or thrombosis. In this setting,
embolization of the RRHA to allow for collateral
flow to develop to the bile duct prior to resection
and anastomosis has been reported (Fig. 21.3)
[60]. However, we rarely use this technique as
the RRHA can often be preserved without margin
compromise, or can be reconstructed [61, 62].
Intraoperative Considerations
Meticulous dissection with complete exposure
and identification of structures prior to division
is essential to prevent inadvertent hepatic artery
injury. The CHA can be identified by its relation-
ship to the hepatic artery lymph node (HALN),
located at the superior border of the pancreas,
medial to structures in the HD ligament. The
HALN abuts the superior wall of the CHA, just
proximal to the GDA origin and careful removal
exposes the CHA near the GDA origin. The CHA
can be mistaken for the RHA, the LHA, or even
the splenic artery and inadvertently ligated, underscoring the need for complete exposure and
identification as well as test clamping prior to
division of any structure. Injury to the CHA and
PHA can be difficult to successfully suture repair
primarily, although this has been described [63].
Reconstruction options include primary anastomosis, transposition of native arteries (splenic artery, right gastroepiploic artery, GDA) [64–68],
or interposition grafts with autologous tissue
such as the gonadal vein [69]. Vascular reconstruction of the hepatic artery is technically challenging and not commonly performed by HPB
surgeons; hence, assistance from a vascular or
transplant surgeon can be helpful and sought out
if necessary.
Specific Intraoperative Considerations
Pancreaticoduodenectomy (PD)
Replaced/Accessory Right Hepatic Artery
A RRHA/ARHA is in close proximity to the bile
duct and head of the pancreas (and therefore
close to tumors in the head of the pancreas) in the
posterolateral space of the hepatoduodenal ligament and is therefore at risk for injury during a
PD. If the patient is jaundiced, preoperative biliary drainage is indicated (Fig. 21.3). Meticulous
dissection during mobilization of the CBD, duodenum, and pancreatic head commonly allows
preservation of a RRHA/ARHA, without compromise of margin status or outcomes [61, 62].
Altering the operative approach has also been
described as a technique to minimize the risk of
injury. The most common approach to a PD is
through an anterior approach, dissecting the head
and uncinate process off the PV, followed by dissection along the SMA. Although this may still
be safely feasible, a posterior or “artery first”
224 V. P. Balachandran and M. I. D’Angelica
approach should be considered when a RRHA/
ARHA is noted. A posterior approach allows for
early assessment of resectability, SMA identification, and proximal control [70–74]. If intraoperative injury or involvement by tumor necessitates ligation of a RRHA, reconstruction is recommended to prevent bilio-enteric anastomotic
and hepatic ischemia as the GDA is commonly
ligated in a PD. Reconstruction of an ARHA is
advised in jaundiced patients to prevent liver necrosis, as discussed earlier (Table 21.2). Injury
to the RRHA/ARHA can be repaired by primary
anastomosis, venous or prosthetic interposition,
or reconstruction using a ligated GDA stump [65,
75–77].
Replaced Common Hepatic Artery
A RCHA is a rare anatomic variant and of greatest significance during a PD. If identified on preoperative workup, a posterior approach is helpful, whereby the SMA and the RCHA takeoff is
identified first and GDA ligation is delayed until
the RCHA is clearly identified and noted to be
free of tumor. The anatomic course of a RCHA
is important in choosing the best operative strategy. If it courses through the pancreas, it can be
preserved by dividing the pancreas lateral to it—
this approach however may compromise margin
status. If it has an anastomotic connection to the
LGA or another accessory artery, ligation without compromise of arterial supply to the liver
and extrahepatic biliary tree has been reported.
Finally, if it is involved and must be sacrificed,
reconstruction is indicated and has been described using autologous vascular grafts such as
the GDA or saphenous vein [78].
Celiac Artery Stenosis
CAS is of significance in a PD if the liver is dependent on retrograde GDA flow for arterial supply. If test clamp of the GDA leads to loss of a
pulse in the porta hepatis, four options exist.
• Examination of the celiac axis for extrinsic
compression
Division of external compression due to
median arcuate ligament, fibrous tissue, or an
enlarged celiac ganglion can be effective at
immediately restoring arterial flow.
•
Preservation of GDA
GDA-preserving PD has been described and
technically demanding, however feasible [79].
It may be a less attractive option for patients
with malignant tumors due to an incomplete
nodal clearance and may be more appropriate
for benign or small tumors.
•
Revascularization
Revascularization can be achieved through
either
Bypass can be performed using autologous
vein or PTFE between the aorta and the
hepatic artery, middle colic artery to the GDA
stump, and venous bypass between the splenic
artery and iliac artery [21]. Arterial reimplantation can be achieved through reimplantation
of the celiac trunk into the aorta, or the splenic
artery into the SMA [21].
• Postpone procedure
Postponing the resection allows for celiac
stent placement or elective revascularization
followed by a delayed attempt at resection.
bypass or arterial reimplantation.
is
Hemi-hepatectomy
Preservation of arterial supply to the remnant
liver during a hemi-hepatectomy is crucial to
prevent liver ischemia to the regenerating future
liver remnant. As a general principle, we advocate complete arterial dissection and visualization of both right and left hepatic arteries, test
clamping of the ipsilateral artery to be ligated,
and confirmation of a contralateral pulse prior to
dividing any structures in the porta.
Right Hepatectomy For a right hepatectomy,
the RHA is most easily ligated to the right of the
common hepatic duct to protect the LHA from
inadvertent injury. Preservation can be confirmed by palpating a pulse at the base of the
umbilical fissure after temporary occlusion of the
RHA. Division of the RHA distal to the common
hepatic duct also allows for medial traction of the
proximal stump, which is useful in exposure of
the right PV. Injury to the LHA is rarely a concern during division of a RRHA/ARHA.
Left Hepatectomy During a left hepatectomy,
the LHA can occasionally be mistaken for the