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19 • Inferior Vena Cava, Portal, and Mesenteric Venous Systems 235
https://t.me/medicina_free
the venous injury site. Indiscriminate clamping of the porta
hepatis and portal vein should be avoided to prevent injury
to delicate structures in the region.
4,14,52
Proximal and distal
control of the portal vein is obtained with the assistance of
direct compression while dissecting the vein free from the
hepatic artery and bile duct. Working back from the effective application of manual pressure with one’s ngers or
hand can be accomplished with gentle application of small
sponge sticks or lower prole Kittner dissecting sponges.
Once the injury is visualized, it can be gently grasped with
Judd-Allis clamps and mobilized to allow suture closure or
passage of vascular control tapes.
Endovascular options are limited in controlling hemorrhage
from a portal vein injury. A Fogarty balloon catheter may be
introduced at the site of portal vein injury to occlude the vessel
and its inow/outow.34 Access from more distal sites, such as
femoral access, is not practical for portal vein injuries.
Repair of Portal Venous Injuries
Repair of the portal vein follows the principles outlined for
the vena cava and other large venous injuries. After the
edges of the injured vein have been débrided, the surgeon
must decide if a primary repair is possible. Simple repairs
should be performed using 5-0 or 6-0 monolament suture,
often in an interrupted fashion. If the portal vein has been
divided, an end-to-end anastomosis may be accomplished if
there is minimal tension between the two ends. Behind the
pancreas, small medial tributaries entering the portal vein
may be ligated and divided to achieve additional length.
Additionally, if it has not already been done to achieve control, partial division of the pancreas and ligation of small
medial tributaries may provide further mobilization to make
an anastomosis possible. Placement of a reverse saphenous
vein interposition graft is possible if a large segment of the
portal vein has been injured; however, few patients with this
signicant an injury are stable enough to permit this kind
of reconstruction. In cases in which repair is not feasible,
the only alternative is ligation.
Portal Vein Ligation
Patients with portal venous injuries usually sustain massive
blood loss, have associated injuries, and present in a state of
extremis which precludes an extensive venous repair. From a
review of 18 patients with portal vein injuries between 1958
and 1980, only 13% survived when ligation was used as a
last-ditch salvage option.
13,53
However, when the portal vein
was ligated earlier in the course of operative management
(i.e., before cardiovascular collapse), the rate of survival
improved to 80%.
53,54
Because of the detrimental effects associated with abrupt occlusion of splanchnic outow, portal
vein ligation is less well tolerated than ligation of the vena
cava and carries a survival rate ranging from 10% to 85%.
5,51
If portal vein ligation is required, the anesthesia team must
be made aware as up to 50% of a patient’s blood volume may
be sequestered in the splanchnic circulation.5 Ligation of
the portal vein results in decreased venous return with subsequent splanchnic hypertension and systemic hypoperfusion.55 Aggressive uid administration, both intraoperatively
and in the ICU, is required. Patients develop massive visceral
swelling due to the portal venous congestion; therefore, the
abdomen should be left open to prevent abdominal hypertension and compartment syndrome.
The excessive mortality associated with portal vein
ligation is likely attributable to unintentional “underresuscitation.” Resuscitation of patients with this injury
pattern should adhere to the 1:1:1 strategy during the
acute phase of care. However, this population of patients
is likely to continue to have a signicant requirement for
crystalloid and colloid infusion even after the bleeding has
been controlled. Many reports of high mortality following
portal vein ligation were made prior to the understanding of
intraabdominal hypertension and compartment syndrome
and the benets of temporary abdominal closure. Contemporary, blood-component based resuscitation along with
temporary abdominal closure strategies are likely to improve
outcomes of patients who require portal vein ligation.
Delayed complications specic to portal vein ligation are
common. Low mesenteric ow combined with shock may
lead to venous thrombosis, bowel ischemia, and necrosis.16 The degree of bowel infarction may vary from patchy
necrosis of small segments of bowel to near total small
bowel infarction. Additionally, portal vein thrombosis and
portal hypertension may occur as sequelae in this setting.
The complications of portal vein ligation are sobering but
unavoidable when ligation is the only option to control
bleeding and provide immediate patient survival.
THE SUPERIOR MESENTERIC VEIN
It is uncommon to manage a patient with an SMV injury as
they account for less than 1.0% of all trauma admissions.15
When present, mesenteric vein injuries most likely occur
from penetrating mechanisms. However, blunt trauma can
result in a high degree of shear force exerted on the mobile
mesentery, which can cause tearing or avulsion of the mesenteric vein. Due to its anatomic association with the SMA,
the two vessels are often injured in tandem. Found to the
patient’s right of the mesenteric artery, the vein provides
outow for the jejunum, ileum, appendix, and the colon to
the mid-transverse segment. Portions of the pancreas and
duodenum are also dependent on the SMV for outow.
Due to the central location of the SMV, associated injuries are common. In a study focusing on 51 patients with
3.5.16 As with all the major abdominal veins, mortality is
high with reported rates varying between 50% and 71%,
depending on the number of associated vascular and solid
organ injuries.
3
Exposure and Mobilization
Although relatively more accessible than the portal vein, the
proximal portions of the SMV may require division of the
pancreas for successful access. Adjacent to the SMA and
the other major visceral and vascular structures, exposure of
the vein is complicated when other injuries are present in the
region. The SMV is quite accessible in its distal portion compared to the other major abdominal veins and is approached
operatively in the same manner as the SMA (Fig. 19.6). A
direct approach at the base of the mesentery may be appropriate if the injury occurs several centimeters distal to the
inferior border of the pancreas. Medial visceral rotation may
be necessary to access the root of the mesentery. If very proximal control of the SMV is required, then the operative exposure mirrors that used for the portal vein with mobilization
236 SECTION 4 • The Management of Vascular Trauma
Ascending
Descending
Celiac
https://t.me/medicina_free
Hepatic
proper a.
Portal v.
Bile duct
Duodenum
Right kidney
Pancreas
colon
Fig. 19.6 Superior mesenteric vein in situ. a, Artery, IMA, inferior mesenteric artery; IMV, inferior mesenteric vein; IVC, inferior vena cava; SMA, superior
mesenteric artery; SMV, superior mesenteric vein; v, vein.
SMV
SMA
IVC
trunk
Splenic a.
Splenic v.
Spleen
Left kidney
IMV
colon
Aorta
IMA
of the right colon and performance of a Kocher maneuver to
provide access. As mentioned, the body of the pancreas may
need to be divided to gain proximal control of the SMV.
4,16
Bleeding Control and Repair
A distal SMV injury that is out in the mesentery of the
bowel may be rst controlled with manual compression and
then ligated. Dissection of the injury at this level can allow
placement of small vessel loops, clamps, or clips to obtain
control. In contrast, and as noted previously, the more proximal SMV injury will require pancreatic division to access.
Bleeding is more signicant with more proximal SMV
injuries and poor exposure of the vessel can lead to blind
placement of suture ligatures, incomplete hemostasis, and
iatrogenic injury to neighboring structures. In these cases,
bleeding can be temporarily controlled by occlusion of the
distal SMV and a Pringle maneuver, though back-bleeding
from the splenic vein may still complicate the eld to some
extent. These maneuvers may be adequate to slow hemorrhage and allow mobilization of the proximal SMV. Primary
repair of the SMV may be accomplished with interrupted
5-0 or 6-0 monolament suture. In cases where signicant
tissue loss precludes primary repair, a saphenous vein interposition graft may be required.
Ligation of the Superior Mesenteric Vein
Patients who require SMV ligation fare better than those
requiring portal vein ligation. Various studies describe a 15%
to 33% mortality associated with SMV ligation, as opposed
to 36% to 43% mortality in the repair group.
13,56
Asensio
et al. found no difference in mortality in 84 patients with
SMV injury, 53 of whom underwent ligation.57 These reports
indicate that patients requiring ligation of the SMV will likely
tolerate the procedure and may fare as well as those having
venous repair. The possibility of splanchnic hypertension and
bowel ischemia exist with ligation, as they do with ligation of
the portal vein. Those surviving SMV ligation should undergo
temporary abdominal closure and second look operations
to evaluate viability of the intestines prior to denitive closure. Whether it be the SMV, the portal vein, or the IVC, ligation should not necessarily be viewed as a last-ditch option.
In many scenarios of abdominal venous injury, early and
controlled ligation – in communication with the anesthesia
team – is preferable to prolonged attempts at repair that can
be associated with large volume blood loss and irrecoverable
shock. Judgment and composure are required to recognize
the need for early ligation and to accomplish it quickly, prior
to massive blood loss and futile attempts at repair.
Temporary shunts should be considered for portal and superior mesenteric venous injuries in the setting of an unstable
patient whose injury anatomy is amenable to shunting. The
relative low ow in the venous compared to the arterial system
may result in a higher rate of thrombosis with venous shunts.
However, this approach may provide options for reconstruction during a second-look laparotomy. In many regards, if
shunt thrombosis does occur, it will result in a situation similar
to ligation of the vein.
Endovascular Options
Endovascular techniques are now more commonly used to
manage vascular injury and a new generation of trauma surgeons are familiar and facile with these less invasive options.
19 • Inferior Vena Cava, Portal, and Mesenteric Venous Systems 237
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Although denitive data regarding the effectiveness of
endovascular balloon occlusion or stent grafts for major
venous injury is lacking, their practical utility is clear in
many cases. An increasing number of reports, primarily
case reports and small single-center series, now show that
catheter-based techniques are useful to temporize and, in
some cases, denitively treat these complex injuries.
Although both interventional radiology and vascular
and endovascular surgery are available in most trauma
centers, several variables should be considered before a
trauma surgeon opts for this management strategy. First,
practitioners who are skilled in these techniques must be
readily available. In many centers, trauma surgeons are
able to perform endovascular interventions. However, if
this is not an option, the patient's hemodynamic status may
preclude waiting for the vascular surgery or interventional
radiology specialist to arrive. Additionally, a hybrid operative suite should be available to accommodate the multiple
demands of resuscitation, open operative exploration, and
uoroscopic imaging needed for the endovascular methods.
An extensive inventory of guidewires, catheters, and grafts
of various sizes is also required, although recent efforts have
been made to rene a more manageable, trauma- specic
endovascular inventory.
58
Catheter-based options offer the greatest potential for
vena cava injuries which often occur in anatomic locations
that are difcult to access. The anatomy of the portal and
superior mesenteric veins precludes conventional endovascular treatments although use of balloons and stents introduced into the vessels at the time of open operation can be
used in select cases.
Occlusion Balloons: The use of endovascular occlusion balloons to control bleeding is one of the most appealing applications of endovascular technology. As means to maintain
central aortic pressure and perfusion, REBOA may be indicated for patients who are in extremis or who have uncontrolled or unidentied intraabdominal hemorrhage. Balloon
occlusion techniques can also be used in the venous system
to control/isolate areas of laceration or avulsion. As an
example, in the setting of an IVC injury, an occlusive balloon
can be introduced into the venous system via femoral vein
access to control inow into the injured segment. In some
instances, a second balloon can be placed through a transjugular approach (i.e., from above) to isolate the injury and
facilitate management more completely. Depending on operative circumstances, an endovascular or Foley balloon can be
inserted directly through the venous injury to control bleeding while proximal and distal control are obtained. As with
proximal control obtained with a vascular clamp, occluding
the vena cava with a balloon results in loss of right heart lling and potentially lethal hypotension.38 In cases in which a
caval injury is identied or occlusion of the vena cava can be
anticipated, large bore vascular access in the upper extremities or internal jugular veins should be secured.
Stent Grafts: Endovascular covered stents (i.e., stent grafts)
can provide an effective approach for managing select retrohepatic and suprahepatic IVC injuries. Multiple reports
describe the use of stent grafts in conjunction with laparotomy to manage IVC injuries.
39,40,50,59,60
If the patient is
stable enough to undergo immediate endovascular access,
direct stent repair may be a superior option for retrohepatic and suprahepatic IVC lacerations.61 Accommodations
for hepatic vein inow by fenestrating the graft prior to
placement has even been performed.47 Concerns exist that
stent grafts may be thrombogenic during the early/immediate phases after deployment, especially in a low-ow venous
system.39 As such, and in cases in which the patient’s injury
pattern allows it, the use of anticoagulation to prevent
thrombus formation should be considered, although this
is controversial and should be considered on a case by case
47,58
basis.
ALTERNATIVE MANAGEMENT OPTIONS
Temporary Venous Shunts: The use of temporary prosthetic shunts in the management of venous injuries is
increasing. Military operations in Iraq and Afghanistan initially raised the prole of temporary shunts used for damage control vascular surgery, though the vast majority of
this evidence is from extremity injuries. A 2009 review of
64 extremity arterial injuries in US troops demonstrated
38% with concomitant venous injuries. These authors note
that several of the patients in their study cohort underwent
venous shunting and subsequent restoration of venous
continuity.45 Though carotid shunts, such as the Javid or
Argyle shunt, are the most widely used for arterial shunting, the larger luminal size of the major abdominal veins
renders a small caliber chest tube a better match. The use of
venous shunts for abdominal trauma may facilitate damage
control surgery via improved hemorrhage control and by
allowing time for patient resuscitation, operative planning,
or, potentially, transfer to a higher level of care.
Whereas the patency rates of temporary arterial shunts
are encouraging, reports of temporary venous shunting
remain largely limited to small series and limited objective data exists on patency rates in these cases. Rasmussen
et al. note in a 2006 review that four venous injuries were
shunted in combat troops and all remained patent.44 As
dwell times for shunts in theater are limited by transport
policy, however, it remains unclear how damage control
venous shunts would fare over longer time periods, in light
of lower ow rates and pressures. From a practical standpoint, if hemorrhage is controlled but the patient’s physiologic status mandates damage control surgery, a temporary
prosthetic shunt is a reasonable alternative to ligation. The
shunt should be secured with ligatures at both the proximal
and distal end to prevent dislodgment during transport and
subsequent ICU care. Denitive operative choices may then
be made during a second look, when the patient’s status
accommodates potential reconstruction. Venous shunts are
an acceptable choice when damage control is required, but
surgeons must remain mindful that patency times are not
well-dened.
Atriocaval Shunt: First described by Schrock in 1968,
this shunt functionally bypasses the site of a retrohepatic
caval injury. A large diameter chest tube is introduced via
an incision in the right atrial appendage. With the tube
outow protruding from the right atrium and clamped, fenestrations in the tube are positioned in the intrapericardial
IVC and below the site of injury, usually the infrarenal cava
(Fig. 19.7). Vessel loops or Rommel tourniquets are used
to secure the vessel around the tube.
survival following the atriocaval shunt is poor. Burch et al.
had only 6 of 31 patients survive with the shunt; all were
41,42,62
Unfortunately,
238 SECTION 4 • The Management of Vascular Trauma
Rommel tour
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Right atrium
and repaired, bloodlessly, on a back table. Potentially, a second team may address remaining vascular or other visceral
injuries in vivo. The transplant option is extremely rare and
feasible in only extraordinary circumstances, in part due to
lack of organ availability and the presence of other injuries
that occurred at the time of the hepatic/caval trauma.
63
Chest tube
niquet
Fig. 19.7 Atriocaval shunt. IVC, Inferior vena cava.
Damaged IVC
gunshot wounds to the retroperitoneal IVC.62 Advances in
endovascular technology will likely make atriocaval shunts
obsolete.
Venovenous Bypass, Circulatory Arrest, and Trans-
plantation: The profound hemorrhage from major
abdominal vein injuries, combined with a young, otherwise healthy trauma patient, may place the trauma
surgeon in the position of attempting truly heroic measures. Falling into the camp of uncommon measures for
hemorrhage control, venovenous bypass or circulatory
arrest have intermittently been described in case reports
with marginal success. To entertain these options, a
trauma center must have personnel experienced in placing patients on bypass, experience managing a pump, and
cannula availability.35 Cannula placement includes open
approaches via the right atrium or left pulmonary artery
(benecial in preventing right heart overload and tricuspid
regurgitation), or percutaneous placement in the femoral,
subclavian, or internal jugular veins.
23,32
Once on bypass,
repair in a fairly bloodless eld may commence. Hypothermic circulatory arrest is appealing for the potential tissue
protective effects of profound hypothermia. Practically
speaking, achieving venovenous bypass or circulatory
arrest is logistically difcult in the unplanned case for a
patient in extremis.
There are reports of liver explantation or transplantation
for severe IVC injuries combined with profound hepatic disruption. Isolated reports of liver explantation with back-table
repair and autotransplantation exist, with poor survival. If
total hepatic isolation can be achieved, the liver is explanted
Pitfalls and Points
n Ligation of the infrarenal IVC is well-tolerated and the
preferred management strategy for patients in extremis.
Suprahepatic IVC ligation, however, is uniformly lethal.
n Endovascular options may be superior to address injuries
to the retrohepatic IVC.
n Portal vein and SMV ligation is a reasonable bail-out
option when catastrophic bleeding is present.
n Division of the head of the pancreas should not be
delayed when improved portal vein exposure is needed.
n Ligation of the IVC, portal vein, or SMV requires second-
look laparotomy to ensure viability of bowel.
n Both the atriocaval shunt and resuscitative thoracotomy
have extremely poor outcomes and are to be avoided.
REBOA should be considered for aortic occlusion for
patients in extremis.
POSTOPERATIVE CARE AND COMPLICATIONS
Patients who survive large intraabdominal venous trauma
are prone to develop a few early and late complications
unique to these injury patterns. Stenosis and/or thrombosis at the venous repair sites may occur after primary repair
or other types of venous reconstruction (e.g., patch angioplasty or interposition graft). Varying degrees of lower
extremity swelling, which can improve or be self-limited
over time, occur in nearly all instances of IVC ligation.
Vigilance for the development of lower extremity compartment syndrome resulting from acute venous hypertension
must be maintained in these situations and in rare cases
fasciotomies performed. Splanchnic hypertension with
portal and superior mesenteric venous narrowing or ligation may also occur.
Long-term outcomes following IVC repair are generally
favorable. However, concern remains regarding the possibility of complications, primarily thrombosis, and the potential
for embolism. Though there are isolated reports of sudden
death from pulmonary embolism in patients having undergone IVC ligation, the literature is scarce regarding venous
thromboembolism following repair. Postoperative screening with duplex ultrasonography is warranted to monitor
the cava following repair, especially in patients with lower
extremity edema or other symptoms. In symptomatic or
high-risk patients, consideration may be given to a caval
lter or extended oral anticoagulation.36 Finally, in some
instances of blunt caval injury, late development of thrombosis and Budd-Chiari syndrome have been observed.
32,36
22
Conclusion
Despite advances in prehospital care, resuscitation, and intensive care, and the development of endovascular techniques,
19 • Inferior Vena Cava, Portal, and Mesenteric Venous Systems 239
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the mortality associated with intraabdominal large-vein
injuries has changed little over the last several decades.
9,13,36
In a trend that likely reects more effective prehospital care
and operating on more severely injured patients, the mortality associated with these injuries may have even increased
compared to series reported in the 1980s and 1990s.9 More
effective, blood component-based resuscitation and an
emphasis on permissive hypotension will like prove especially
benecial in the management of these low pressure venous
injuries. Abdominal venous injuries must be evaluated on a
case-by-case basis, as no one algorithm is adequate to guide
all the steps in managing these cases. One will be well served
by the principles of adequate operative exposure, intentional
vascular control, and implementation of damage control or
repair techniques while limiting time in the operating room.
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42. Rosenthal D, Wellons ED, Shuler FW, Levitt AB, Henderson VJ. Retro-
hepatic vena cava and hepatic vein injuries: a simplied experimental
method of treatment by balloon shunt. J Trauma. 2004;56(2):450–452.
43. Votanopoulos KI, Welsh FJ, Mattox KL. Suprarenal inferior vena cava
ligation: a rare survivor. J Trauma. 2009;67(6):E179–E180.
44. Matsumoto S, Jung K, Smith A, Coimbra R. Management of infe-
rior vena cava injury: repair or ligation? A propensity score matching analysis using the National Trauma Data Bank. J Am Coll Surg.
2018;226(5):752–759.
45. Droz NM, Bini JK, Jafree KA, Matsuura JH. Staged reconstruction of
the inferior vena cava after gunshot injury. J Vasc Surg Cases Innov
Tech. 2017;3(3):136–138.
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46. Tulip HH, Smith SV, Valentine RJ. Delayed reconstruction of the
superior mesenteric vein with autogenous femoral vein. J Vasc Surg.
2012;55:1773–1774.
47. Rasmussen TE, Clouse WD, Jenkins DH, Peck MA, Eliason JL, Smith
adjunct in the management of wartime vascular injury. J Trauma.
2006;61:8–15.
48. Gifford SM, Aidinian G, Clouse WD, etal. Effect of temporary shunting
on extremity vascular injury: an outcome analysis from the Global War
on Terror vascular injury initiative. J Vasc Surg. 2009;50(3):549–555.
49. Mansukhani NA, Havelka GE, Helenowskin IB, Rodriguez HE, Hoel
AW, Eskandari MK. The enduring patency of primary inferior vena
cava repair. Surgery. 2017;161:1414–1422.
50. Watarida S, Nishi T, Furukawa A, et al. Fenestrated stent-graft for
traumatic juxtahepatic inferior vena cava injury. J Endovasc Ther.
2002;9:134–137.
51. Jurkovich GJ, Hoyt DB, Moore FA, etal. Portal triad injuries. J Trauma.
1995;39(3):426–434.
52. Emmiler M, Kocogullari CU, Yilmaz S, Cekirdekci A. Repair of the
inferior vena cava with autogenous peritoneo-fascial patch graft
following abdominal trauma: a case report. Vasc Endovascular Surg.
2008;42(3):272–275.
53. Stone HH, Fabian TC, Turkleson ML. Wounds of the por tal venous sys-
tem. World J Surg. 1982;6(3):335–340.
54. English WP, Johnson MB, Borman KR, Turner Jr WW. Mesenteric
ischemia: an unusual presentation of traumatic intrahepatic arterioportal stula. Am Surg. 2001;67(9):865–867.
55. Sabat J, Hsu CH, Chu Q, Tan TW. The mortality for surgical repair is
similar to ligation in patients with traumatic portal vein injury. J Vasc
Surg Venous Lymphat Disord. 2018:1–6.
56. Donahue T, Strauch G. Ligation as denitive management of injury to
the superior mesenteric vein. J Trauma. 1988;28(4):541–543.
57. Asensio JA, Britt LD, Borzotta A, etal. Multiinstitutional experience
with the management of superior mesenteric artery injuries. J Am
Coll Surg. 2001;193(4):354–365.
58. Sam 2nd AD, Frusha JD, McNeil JW, Olinde AJ. Repair of blunt trau-
matic inferior vena cava laceration with commercially available endografts. J Vasc Surg. 2006;43(4):841–843.
59. Hommes M, Kazemier G, van Dijk L, etal. Complex liver trauma with
bilhemia treated with perihepatic packing and endovascular stent in
the vena cava. J Trauma. 2009;67(2):E51–E53.
60. Denton JD, Moore EE, Coldwell DM. Multimodality treatment for grade
V hepatic injuries: perihepatic packing, arterial embolization and
venous stenting. J Trauma. 1997;42(5):964–968.
61. de Naeyer G, Degrieck I. Emergent infrahepatic vena cava stenting for
life-threatening perforation. J Vasc Surg. 2005;41(3):552–554.
62. Burch JM, Feliciano DV, Mattox KL. The atriocaval shunt. Facts and
ction. Ann Surg. 1988;207(5):555–568.
63. Boggi U, Vistoli F, Del Chiaro M, etal. Extracorporeal repair and liver
autotransplantation after total avulsion of hepatic veins and retrohepatic inferior vena cava injury secondary to blunt abdominal trauma.
J Trauma. 2006;60(2):405–406.
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Neck and Thoracic Outlet
GREGORY A. MAGEE and FRED A. WEAVER
Introduction
Perhaps no other anatomic region contains so many vital
structures in such a compact space as the neck and thoracic
outlet. Injuries in this region can result in hemorrhage,
stroke, upper and/or lower extremity paralysis, loss of airway, and digestive tract injury. Consequently, the clinician
must adopt a thorough approach and maintain a high
index of suspicion when caring for patients with injuries in
this area. The spectrum of vascular trauma in the cervical
region ranges from exsanguinating hemorrhage to subtle
imaging ndings with a seemingly innocuous examination
that can lead to delayed hemispheric stroke. The variation
in presentation and potentially devastating nature of neck
and thoracic outlet injuries has led to an increased awareness and screening for patients with penetrating wounds
and those at risk for blunt vascular injury.
The surgical management of carotid artery injuries dates
back to 1552, when Ambroise Paré reported the successful management of a common carotid artery and jugular
vein injury by ligation.1 The patient developed aphasia and
hemiplegia but survived. Fleming later reported a favorable
outcome after ligating an injured common carotid artery,
and this became the standard surgical management until
the Korean War.2 In his review of the management of arterial injuries during World War II, DeBakey found that arterial repair was associated with higher mortality rates, and
based on this report, the US military abandoned arterial
repair.3 Frank Spencer is credited with bringing back arterial injury repair during the Korean War with improved
results, including injuries to the carotid.4 Subsequently,
these reconstructive techniques were applied to civilian
carotid and subclavian artery injuries. More recently, endovascular techniques have been applied to selected injuries
of the neck and thoracic outlet vessels.
5
Indications
Patients with neck/thoracic outlet vessel injury frequently
have concomitant injuries. The use of advanced trauma
life support protocol is crucial to recognize and treat lifethreatening injuries rst and then thoroughly evaluate for
other possible injuries. The secondary survey of the patient
should include a neurologic examination, auscultation
for bruits, and assessment of carotid and upper extremity
pulses, and blood pressure in both arms. Pressure differentials or decreased pulses may suggest a thoracic outlet
injury.
Patients with carotid injuries may present with contralateral extremity decit, aphasia, or Horner's syndrome.
Vertebral artery injuries rarely present with neurological
symptoms, but posterior cerebral symptoms such as ataxia,
dizziness, vomiting, facial and body analgesia, or visual
eld decits mandate evaluation of their cerebral vasculature. Complaints of headache, neck, ear, face, or periorbital
pain may indicate intramural hemorrhage or dissection.6
Because of the frequent association of blunt cerebrovascular injuries (BCVI) with closed head injury, many patients
have a decreased Glasgow Coma Scale (GCS) on arrival,
which makes physical examination–directed diagnosis a
challenge. Patients with BCVI may also arrive at the emergency department (ED) with no neurological decit and
then develop a delayed neurologic decit 10 to 72 hours
later.7 Penetrating subclavian artery injuries are particularly lethal due to severe noncompressible hemorrhage with
over half who survive to the hospital requiring resuscitative
thoracotomy.
also have associated brachial plexus injuries, which cause
signicant postoperative morbidity.
Physical examination is extremely important in the
evaluation of penetrating injuries, including the number,
location, and possible trajectory of wounds. Hard signs of
vascular injury are pulsatile hemorrhage, expanding hematoma, absent distal pulses, and palpable thrill, all of which
mandate exploration. Soft signs include peripheral nerve
decit, signicant hemorrhage at the scene, nonexpanding hematoma, and decreased distal pulse, which should
be evaluated by computed tomography angiography (CTA)
or other imaging modality. Minor vascular injuries do not
always require repair and can be followed by serial physical examination with or without duplex ultrasound, an
approach that has 95% sensitivity for detecting injuries that
require repair.
Because most blunt cerebrovascular injuries are clinically
occult, screening CTA of the neck should be performed on
patients with risk factors such as: (1) head and neck trauma
associated with severe neck hyperextension and rotation
or hyperexion; (2) a Lefort II or III fracture; (3) a basilar
skull fracture involving the carotid canal; (4) a closed head
injury consistent with diffuse axonal injury presenting with
GCS score less than 6; (5) a cervical vertebral body or transverse foramen fracture, subluxation, or ligamentous injury
at any level or any fracture of C1–C3; or (6) a seat-belt or
other clothesline-type injury with signicant cervical pain,
swelling, or altered mental status.
Denitive repair of penetrating carotid injuries in patients
with a neurologic decit has been controversial. In the
1970s, Cohen and Bradley raised the concern that repair
of a carotid injury in a patient with a neurologic decit may
lead to intracranial hemorrhage.24 However, subsequent
studies found that regardless of the initial neurologic decit, mortality and nal neurologic status was improved if
carotid repair was performed.
8–12
More than a third of those who survive
13,14
14–22
7,23
25–27
A comprehensive review
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of the US military’s experience with cervical carotid injury
during the wars in Afghanistan and Iraq showed that common and internal carotid artery repair resulted in lower
rates of stroke and death when compared to ligation.
28
Relative contraindications to repair include surgically
inaccessible lesions, a delay of more than 3 to 4 hours from
establishment of coma, large areas of cerebral infarct on
admission CT, and absence of retrograde back-bleeding
from the distal arterial segment after operative exposure
and open thrombectomy.
29
Nonoperative management of neurologically intact
patients with penetrating injuries is occasionally warranted. For patients with a carotid or vertebral artery
occlusion and normal neurologic examination, observation and anticoagulation with heparin is an acceptable
approach. Likewise, minimal arterial injuries, dened as
non–ow-limiting intimal aps and pseudoaneurysms less
than 5 mm in size, can be safely observed, based on series
with follow-up extending to 10 years.
30,31
These injuries
should be evaluated by repeat CTA or duplex prior to discharge to conrm they have not progressed. The current
grading system for BCVI is: grade I, intimal injury with
less than 25% luminal narrowing; grade II, dissection
or hematoma with more than 25% luminal narrowing;
grade III, pseudoaneurysm; grade IV, occlusion; and grade
V, vessel transection.
BCVI are almost always managed nonoperatively based on
Fabian’s nding that antithrombotic therapy improved survival (P < .02) and neurologic outcome (P < .01) in patients
with this injury pattern, a result that has been conrmed
in several subsequent reports.
32–35
Antithrombotic therapy
consists of either therapeutic anticoagulation with heparin
followed by warfarin, or antiplatelet therapy with aspirin or
aspirin plus clopidogrel. A recent Cochrane meta-analysis
of antiplatelet therapy versus anticoagulation therapy for
carotid dissection showed no differences in stroke rate or
hemorrhagic complications between the two treatment
regimens.36 However, dual antiplatelet therapy may be preferred due to its safety and cost prole.7 A follow-up CTA is
recommended 7 to 10 days after injury because over 60%
of injuries will change in grade or severity during this time
interval. Grade I and II BCVI can often develop into grade
III pseudoaneurysms. Additionally, imaging 3 to 6 months
after the injury is warranted in these cases to exclude the
development of an enlarging pseudoaneurysm over time.
Current recommendations are that patients with grade
I–IV BCVI should be treated with antithrombotic therapy.
Grade V injuries are frequently associated with nonvascular injuries and may require operative intervention as a
life-saving maneuver. These injuries should be surgically
repaired, if possible, but in many instances they are surgically inaccessible and require ligation or embolization.
7,37,38
The natural history of BCVI is that 90% of stenotic lesions
will resolve and that 67% of occluded vessels will recanalize
with antithrombotic therapy only.39 Blunt vertebral artery
injuries tend to occur at junctions between xed and mobile
segments with the V2 segment most commonly affected in
adults, and the V3 and upper V2 segments more commonly
affected in children. Approximately one-third of patients
have bilateral injuries.40 The need for operative intervention
or endovascular repair is rare for both blunt and penetrating vertebral artery injuries.
Preoperative Preparation
The preoperative preparation of patients with a documented neck and thoracic outlet vascular injury depends
on the presence of active bleeding and the suspected location or zone of injury. Patients who have hard signs of
vascular injury should go directly to the operating room
(OR) for exploration, vascular control, and repair. Rapid
establishment of an oral or nasotracheal airway is critical.
Patients with soft signs of vascular injury require expeditious diagnostic imaging and, in select circumstances,
require formal catheter-based diagnostic angiography. This
approach is especially applicable for patients with zone
I and III injuries in which surgical access to the vessels in
question is difcult. Duplex ultrasonography can provide
a rapid, accurate, and noninvasive assessment of zone II
neck and thoracic outlet vasculature; however, it is often
not available in the ED, whereas CTA has become the diagnostic evaluation of choice.
and may be used as the basis for operative planning.
41–43
CTA ndings are accurate
19,44,45
Recently published recommendations specify that a 16-slice
or higher CTA is required for assessment of a possible blunt
vascular injury.
mented a sensitivity of 29% to 64%, and 51% to 54% with
16-slice and 64-slice scanners, respectively.
7,37
However, subsequent studies have docu-
46–48
Depending
on the mechanism, location, and type of injury, endovascular intervention at the time of diagnostic angiography may
be an appropriate and denitive treatment.
Pitfalls and Danger Points
n CTA: For stable patients without hard signs of vascu-
lar injury, it is advisable that a CTA be performed before
operative intervention in order to demonstrate the extent
and the zone of the injury. This information guides the
surgical eld(s) and exposure(s) required for proximal
and distal vascular control.
n Blunt cerebrovascular injuries (BCVI): Most of these
injuries should be managed by antithrombotic therapy
with either heparin followed by warfarin or by antiplatelet
therapy. Dual antiplatelet therapy may be preferable due to
a better safety and cost prole.7 Failure to screen for these
injuries and failure to treat with antithrombotic therapy
increase the risk of stroke and long-term morbidity.
n Exit and entry wounds: Although a penetrating
wound may be in a surgically accessible zone or segment
of a neck or thoracic outlet, the trajectory of the penetrating object should be considered when preparing the
operative eld. The surgeon must anticipate the need for
more proximal or distal exposure depending on the trajectory and the course of the penetrating object.
n Neurologic decit: Careful neurologic examination
of patients with a suspected or known cerebrovascular
injury is essential. Documentation of neurologic status
before an intervention is critical to anticipating and recognizing new neurologic changes postoperatively.
n Associated aerodigestive injuries: Surgical exposure
of a cervical wound includes careful inspection for injury
to the trachea and or esophagus before proceeding with formal carotid artery repair. If present, one should protect the
20 • Neck and Thoracic Outlet 243
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arterial repair by interposing muscle between the arterial
repair and aerodigestive tract injury and place at least one
drain near the injury before closing the wound. Vascular
reconstruction in a contaminated eld is best performed with
an autologous conduit to avoid prosthetic graft infection.
n Brachial plexus injury: The brachial plexus is fre-
quently injured in the setting of thoracic outlet injuries.
Consequently, a preoperative neurologic examination
of the affected extremity is important to establish the
degree of neurologic compromise. This allows for detection of evolving neurologic decits postoperatively due
to operative trauma or to the development of an upper
extremity compartment syndrome.
n Proximal vascular control: Essential to successful
repair and minimization of blood loss is proximal control
of the artery before exposure of the injury. This is particularly important for proximal subclavian injuries and zone
I carotid injuries, where a median sternotomy, proximal
endovascular balloon occlusion, or a third–fourth interspace left thoracotomy (in the case of a left subclavian
artery injury) may be required. The proximal left subclavian
artery is difcult to control through a median sternotomy.
n Venous injuries: Venous injuries are frequently asso-
ciated with cervical arterial injuries. Ligation usually
causes minimal morbidity; however, the more proximal
the injury, the greater the likelihood that the venous
injury requires operative repair. In the setting of bilateral
internal jugular vein injuries, repair of one is necessary
to prevent intracranial venous hypertension.
n Cranial and phrenic nerves: The anatomic proxim-
ity of these nerves to the vasculature of the neck and
thoracic outlet place them at risk during exposure and
repair of vascular trauma in this region. Identication
and preservation of nerve structures are important to
minimize short- and long-term morbidity.
n Internal carotid repairs: Thrombosis of the internal
carotid artery due to either a blunt or penetrating injury
may extend intracranially. Gentle passage of a thrombectomy catheter from the cervical carotid may be necessary
to evacuate distal thrombus. However, it is important to
allow “back-bleeding” pressure to remove most of the
thrombus and not pass the thrombectomy catheter too
far up the carotid artery (e.g., into the cavernous portion
of the carotid). In the absence of back-bleeding, repair
and reperfusion of the distal internal carotid should not
be performed and the artery may be ligated. In patients
for whom back-bleeding is restored, intraoperative angiography should be used to document complete evacuation of distal thrombus before repair and reperfusion.
n Avoidance of hypotension and hypoxia: For patients
with a neurologic decit secondary to cortical brain
injury, maintenance of normal blood pressure and
avoidance of hypoxemia are essential to prevent secondary brain injury.
Operative Strategy and Technique
CAROTID
In 1969, Monson described three zones of the neck for guidance in diagnosis and treatment of carotid artery trauma49
Fig. 20.1 Carotid zones of the neck. Zone I extends from the sternal
notch to the cricoid cartilage. Zone II extends from the cricoid cartilage
to the angle of the mandible. Zone III extends from the angle of the
mandible to the base of the skull.
(Fig. 20.1). Zone I spans from the clavicle to the cricoid car-
tilage, zone II from the cricoid cartilage to the angle of the
mandible, and zone III from the angle of the mandible to
the skull base.50 The zone II carotid artery travels within the
carotid sheath, which also contains the vagus nerve and
internal jugular vein. The common carotid divides into the
internal and external within zone II, in most instances one
to two ngerbreadths below the angle of the mandible. An
awareness of carotid bifurcation anatomy is important in
preoperative planning, particularly for those injuries at the
junction of zones II and III.
The operative eld for repair of a carotid injury requires
preparation of the neck and chest as well as a thigh for possible great saphenous vein harvest. For patients with a zone
I carotid or innominate artery injury, median sternotomy
is required for proximal control (Fig. 20.2). Alternatively,
endovascular balloon occlusion can be used to establish
proximal control. After proximal control via median sternotomy, extension of the incision along the anterior border of the ipsilateral sternocleidomastoid provides excellent
exposure of the cervical carotid (Fig. 20.3). Opening of the
carotid sheath and retraction of the internal jugular vein
laterally exposes the facial vein, usually located near the
carotid bifurcation. The facial vein should be ligated and
divided allowing for lateral retraction of the internal jugular
vein and exposure of the cervical carotid artery. Care should
be taken to identify and protect the vagus nerve within the
carotid sheath. Cephalad dissection along the medial edge
of the internal jugular vein exposes the proximal internal carotid artery. Dissection along the lateral border of
III
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the internal carotid exposes the hypoglossal nerve, which
traverses across the supercial surface of the internal and
external carotid arteries. Identication of the hypoglossal
nerve can be facilitated by following the ansa cervicalis to its
junction with the hypoglossal trunk.
More distal exposure of the internal carotid artery at
the junction of zones II and III may require division of
the occipital artery and mobilization of the posterior belly
of the digastric muscle by release of its posterior fascial
investment. Care should be taken to identify and preserve
the glossopharyngeal and spinal accessory nerves, which
typically lie posterior and superior to the posterior belly of
the digastric muscle and are at risk during zone III exposure. Anterior displacement of the mandible with xation
by intraoral wires may provide additional exposure, but this
maneuver requires preoperative planning with placement
of a nasotracheal airway. In practice this maneuver is rarely
Fig. 20.2 (A) Photograph of a zone 1 gunshot wound. (B) Operative
photograph following resection of injured segment of innominate
artery from gunshot wound. (C) Operative photograph of innominate
artery repair with expanded polytetrafluoroethylene (ePTFE) interposition graft. (Operative photos courtesy Gregory A. Magee, University of
Southern California.)
helpful.51 Dividing the stylohyoid muscles and ligament as
well as the styloid process allows exposure of the internal
carotid distally to where it enters the skull base. Alternative
techniques such as mandibular subluxation and osteotomy
impart little additional advantage and are associated with
greater morbidity.
It is advisable to obtain proximal control prior to exposing
the injury to prevent substantial blood loss. After the injured
segment is exposed, a 2- or 3-Fr Fogarty balloon thrombectomy
catheter should be passed gently both proximally and distally to
remove thrombus. It is important to use an appropriately small
thrombectomy catheter and to not overinate the balloon in
the internal carotid artery in order to avoid arterial spasm,
dissection, or intimal injury that can lead to thrombosis, and
perforation. Both proximal and distal arterial lumens should be
ushed with heparinized saline solution (e.g., 2000 units heparin/1 L saline); and systemic heparin, if not contraindicated,
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