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18 • Abdominal Aortic Trauma, Iliac and Visceral Vessel Injuries 225
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been championed again, with several reports in the literature. Gaining access via the femoral vessels, the resuscitative endovascular balloon occlusion of the aorta (REBOA)
is placed either in the thoracic aorta, or just above the aortic bifurcation depending on the zone of injury. Despite
some promising results, no clear mortality benet has
been shown in a systematic review,33 with some reporting
adverse outcomes.34 Further evidence is likely to be required
before there is widespread adoption of the technique, and
randomized trials are undwerway.
35
References
1. Tyburski JG, Wilson RF, Dente C, Steffes C, Carlin AM. Factors affect-
ing mortality rates in patients with abdominal vascular injuries.
JTrauma Acute Care Surg. 2001;50(6):1020–1026.
2. Heuer M, Hussmann B, Kaiser GM, et al. Abdominal vascular
trauma in 760 severely injured patients. Eur J Trauma Emerg Surg.
2013;39(1):47–55.
3. Demetriades D, Inaba K. Vascular trauma: abdominal. In: Sidawy AN,
Perler BA, eds. Rutherford’s Vascular Surgery and Endovascular Therapy.
Philadelphia: Elsevier; 2019:2391–2409.e2.
4. Williams TK, Fox C, Rasmussen TE. Epidemiology and natural history
of vascular trauma. In: Sidawy AN, Perler BA, eds. Rutherford’s Vas-
cular Surgery and Endovascular Therapy. Philadelphia: Elsevier; 2019.
2350-2364.e3.
5. Perkins ZB, De’Ath HD, Aylwin C, Brohi K, Walsh M, Tai NRM. Epide-
miology and outcome of vascular trauma at a british major trauma
centre. Eur J Vasc Endovasc Surg. 2012;44(2):203–209.
6. DuBose JJ, Savage SA, Fabian TC, et al. The American Associa-
tion for the Surgery of Trauma PROspective Observational Vascular Injury Treatment (PROOVIT) registry. J Trauma Acute Care Surg.
2015;78(2):215–223.
7. Asensio JA, Chahwan S, Hanpeter D, et al. Operative manage-
ment and outcome of 302 abdominal vascular injuries. Am J Surg.
2000;180(6):528–533, discussion 533.
8. DeBakey ME, Simeone FA. Battle injuries of the arteries in World War
II; an analysis of 2,471 cases. Ann Surg. 1946;123:534–579.
9. White JM, Stannard A, Burkhardt GE, Eastridge BJ, Blackbourne LH,
Rasmussen TE. The epidemiology of vascular injury in the wars in
Iraq and Afghanistan. Ann Surg. 2011;253(6):1184–1189.
10. Asensio JA, Forno W, Roldán G, etal. Abdominal vascular injuries:
injuries to the aorta. Surg Clin. 2001;81(6):1395–1416.
11. Demetriades D, Theodorou D, Murray J, et al. Mortality and prog-
nostic factors in penetrating injuries of the aorta. J Trauma.
1996;40(5):761–763.
12. Lichte P, Oberbeck R, Binnebösel M, Wildenauer R, Pape H-C, Kobbe P.
A civilian perspective on ballistic trauma and gunshot injuries. Scand
J Trauma Resusc Emerg Med. 2010;18:35.
13. Tresson P, Touma J, Gaudric J, etal. Management of vascular trauma
during the Paris terrorist attack of November 13, 2015. Ann Vasc
Surg. 2017;40:44–49.
14. Botha A, Brooks A, Loosemore T, eds. Gunshot, Fragment and Blast
Injuries. London: Royal College of Surgeons of England; 2002.
15. Mokoena T, Robbs JV. Surgical management of mycotic aneurysms.
SAfr J Surg. 1991;29(3):103–107.
16. Robbs J. Abdominal Vascular Injuries. 2nd ed. London: Hodder Arnold;
2005.
17. Davis TP, Feliciano DV, Rozycki GS, Bush JB. Results with abdomi-
nal vascular trauma in the modern era/Discussion. Am Surg.
2001;67(6):565.
18. Burdick TR, Hoffer EK, Kooy T, etal. Which arteries are expendable?
The practice and pitfalls of embolization throughout the body. Semin
Intervent Radiol. 2008;25(3):191–203.
19. Mehta M, Darling III RC, Taggert JB, et al. Outcomes of planned
celiac artery coverage during TEVAR. J Vasc Surg. 2010;52(5):
1153–1158.
20. Mattox KL, Feliciano DV, Burch J, Beall AC, Jordan GL, De Bakey
ME. Five thousand seven hundred sixty cardiovascular injuries in
4459 patients. Epidemiologic evolution 1958 to 1987. Ann Surg.
1989;209(6):698–705, discussion 706.
21. Clark DE, Georgitis JW, Ray FS. Renal arterial injuries caused by blunt
trauma. Surgery. 1981;90(1):87–96.
22. Springer F, Schmehl J, Heller S, Claussen CD, Brechtel K. Delayed
endovascular treatment of renal artery dissection and reno-vascular hypertension after blunt abdominal trauma. Cardiovasc Intervent
Radiol. 2011;34(5):1094–1097.
23. Haas CA, Spirnak JP. Traumatic renal artery occlusion: a review of
the literature. Tech Urol. 1998;4:1–11.
24. Shoobridge JJ, Corcoran NM, Martin KA, Koukounaras J, Royce PL,
Bultitude MF. Contemporary management of renal trauma. Rev Urol.
2011;13(2):65–72.
25. Burch JM, Richardson RJ, Martin RR, Mattox KL. Penetrating iliac
vascular injuries: recent experience with 233 consecutive patients.
JTrauma. 1990;30(12):1450–1459.
26. Zealley IA, Chakraverty S. The role of interventional radiology in
trauma. BMJ. 2010;340:c497.
27. Borger van der Burg BLS, van Dongen TTCF, Morrison JJ, etal. A sys-
tematic review and meta-analysis of the use of resuscitative endovascular balloon occlusion of the aorta in the management of major
exsanguination. Eur J Trauma Emerg Surg. 2018;44(4):535–550.
28. Kessel D, Robertson I. Embolization. In: Kessel D, Robertson I, eds.
Interventional Radiology: a Survival Guide. Philedelphia: Elsevier; 2005.
29. Thorson CM, Ryan ML, Otero CA, etal. Operating room or angiog-
raphy suite for hemodynamically unstable pelvic fractures? J Trauma
Acute Care Surg. 2012;72(2):364–372.
30. Yao DC, Jeffrey RB, Mirvis SE, et al. Using contrast-enhanced heli-
cal CT to visualize arterial extravasation after blunt abdominal
trauma: incidence and organ distribution. AJR Am J Roentgenol.
2002;178(1):17–20.
31. Schnüriger B, Inaba K, Konstantinidis A, Lustenberger T, Chan LS,
Demetriades D. Outcomes of proximal versus distal splenic artery
embolization after trauma: a systematic review and meta-analysis.
JTrauma Acute Care Surg. 2011;70(1):252–260.
32. Chabrot P, Cassagnes L, Aldja A, et al. Revascularization of trau-
matic renal artery dissection by endoluminal stenting: three cases.
Acta radiol. 2010;51(1):21–26.
33. Morrison JJ, Galgon RE, Jansen JO, Cannon JW, Rasmussen TE,
Eliason JL. A systematic review of the use of resuscitative endovascular balloon occlusion of the aorta in the management of hemor rhagic
shock. J Trauma Acute Care Surg. 2016;80(2):324–334.
34. Joseph B, Zeeshan M, Sakran JV, etal. Nationwide analysis of resusci-
tative endovascular balloon occlusion of the aorta in civilian trauma.
JAMA Surg. 2019;154(6):500–508.
35. Jansen JO, Pallmann P, MacLennan G, Campbell MK. Investigators
U-RT. Bayesian clinical trial designs: another option for trauma trials?
J Trauma Acute Care Surg. 2017;83(4):736–741.
19
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Inferior Vena Cava, Portal, and
Mesenteric Venous Systems
TIMOTHY FABIAN and STEPHANIE SAVAGE
Introduction
Injury to the large veins of the abdominal cavity, including
the inferior vena cava (IVC) and the portal and the superior
mesenteric veins is uncommon occurring in 5% of penetrating and 1% of blunt trauma cases.1 Because prehospital
mortality associated with injury to these large veins ranges
between 30% and 50%, there are relatively few patients
who survive to have surgical repair. As such, even experienced trauma and vascular surgeons have a relatively limited practice with the operative management of these injury
patterns.2 The literature has consistently reported mortality
rates of 50% to 70% for injuries to the superior mesenteric
vein (SMV), portal vein, and IVC.
have been unchanging over several decades and thought
to be refractory because of the difculty in accessing the
venous injury, both exposing and controlling, as well as
the likelihood of torrential hemorrhage from these lowpressure, high-ow structures.
exposure and repair that will be reviewed in this chapter
have remained fairly consistent, though newly developed
endovascular techniques offer promise in creating more
effective approaches to certain of these highly lethal patterns of vascular trauma.
Historical references to abdominal venous injuries are
limited mostly to case reports and oblique references in
clinical series of combat injured.
comprehensive reviews among civilian patients have been
published from the Baylor College of Medicine registry. In a
1982 review of 312 patients with vascular injury, venous
injuries most commonly occurred to the internal jugular
vein (5.7% of vascular injuries), with the SMV injured 2%
of the time and the IMV injured in 0.4% of patients.
additional review of 4459 patients over 30 years found
that 34% of the vascular injuries were to the abdominal
vasculature and roughly 4% of these were to the mesenteric
11
vessels.
As noted, the mortality associated with abdominal
venous injuries has changed little in the last 30 years,
despite advances in other areas of trauma care. Though
comprehensive reviews are uncommon, case reports of
heroic efforts to save patients using specialized techniques
have been published. The military’s experience using temporary vascular shunts has become a standard in civilian
practice, providing a unique opportunity to control and
temporize certain forms of venous injury while componentbased resuscitation occurs. At the same time, resuscitative
endovascular balloon occlusion of the aorta (REBOA) has
become more common as an adjunct to quickly restore central aortic pressures (i.e., coronary and cerebral pressures)
and stem bleeding in certain patterns of torso venous injury
3–6
The mortality gures
4,7
The principles of operative
4,8,9
Some of the most
4,10
An
and shock. Aggressive options such as venovenous bypass
and liver explantation are mostly anecdotal and uncommon, often impractical, methods to manage the bleeding
patient.
The infrequent nature of abdominal venous injury is due
to the relatively small size of the vessels and the fact that
they are hidden or protected by the surrounding inferior
costal margin, the viscera, and the retroperitoneum. Penetrating trauma accounts for 95% of injury to intraabdominal veins, with outcomes following stab wounds slightly
better than those following injury from rearms or blunt
mechanisms.
gery of Trauma (AAST) includes injuries to the major
abdominal veins in the Organ Injury Scale for Abdominal
Vascular Trauma (Table 19.1). Not surprisingly, the most
common cause of death in these situations is exsanguination, whether in the prehospital setting or in the resuscitation or operating room.
Patients with major venous injuries who survive to the
hospital often present in shock, although some will have
reached a precarious state of equilibrium as the hypotension will have reduced the rate of bleeding. In situations in
which permissive hypotension is effective, the patient may
appear relatively stable. One report of patients sustaining
these types of injuries documented an average hospital
admission systolic blood pressure of 90 mm Hg and heart
rate of 95 beats per minute.14 In addition to lower blood
pressure, those who died also had higher overall injury
severity (i.e., ISS), a greater number of associated injuries,
were older, and had more blood loss at the time of laparotomy.13 A 7-liter blood loss has been shown as a threshold
associated with higher mortality, while patients with major
venous injuries require an average of 19 units of packed red
blood cells and 7 liters of crystalloid.
ing numbers, one should be in a damage control mindset
when tackling this type of vascular trauma, looking for
ways to expeditiously control or temporize bleeding while
coordinating with the resuscitation team to maintain key elements of the patient’s overall physiology (e.g., temperature,
acid/base status, coagulation prole, oxygenation).
Given the intimate anatomic proximity, patients with
central venous trauma commonly have injuries to other
intraabdominal structures such as viscera, solid organ, or
ductal structures of the hepatobiliary or urogenital tracts.
The liver and stomach are most commonly associated with
intraabdominal venous trauma, although patients with
injury to the vena cava or portal or superior mesenteric
veins have, on average, between two and four additional
injuries, including those to other large vessels.
tant liver injuries are especially challenging as attempts
to mobilize the organ can place torque on the vena cava
4,12,13
The American Association for the Sur-
12,15
Given these daunt-
4,5
Concomi-
226
19 • Inferior Vena Cava, Portal, and Mesenteric Venous Systems 227
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Table 19.1 American Association for the Surgery of
Trauma: Organ Injury Scale for Abdominal Vascular Injury.
Grade Description
Grade 1 Non-named superior mesenteric artery or superior mesen-
Grade 2 Right, left or common hepatic artery
Grade 3 Superior mesenteric vein, trunk
Grade 4 Superior mesenteric artery, trunk
Grade 5 Portal vein
a
This classification system is applicable to extraparenchymal vascular
injuries. If the vessel injury is within 2 cm of the organ parenchyma, refer
to specific organ injury scale. Increase one grade for multiple grade III or
IV injuries involving >50% vessel circumference. Downgrade one grade if
<25% vessel circumference laceration for grades IV or V.
From Moore EE, Cogbill TH, Malangoni M, Jurkovich GJ, Champion
HR. Scaling systems for organ specific injuries. Curr Opin Crit Care.
1996;2(6):450–462.
teric vein branches
Non-named inferior mesenteric artery or inferior mesenteric
vein branches
Phrenic artery or vein
Lumbar artery or vein
Gonadal artery or vein
Ovarian artery or vein
Other non-named small arterial or venous structures requir-
ing ligation
Splenic artery or vein
Right or left gastric arteries
Gastroduodenal artery
Inferior mesenteric artery or inferior mesenteric vein, trunk
Primary named branches of mesenteric artery or vein
Other named abdominal vessels requiring ligation or repair
Renal artery or vein
Iliac artery or vein
Hypogastric artery or vein
Vena cava, infrarenal
Celiac axis proper
Vena cava, suprarenal and infrahepatic
Aorta, infrarenal
Extraparenchymal hepatic vein
Vena cava, retrohepatic or suprahepatic
Aorta, suprarenal, subdiaphragmatic
a
and/or portal vein and extend or worsen the primary venous
injury. Injury to a major venous structure is frequently
accompanied by damage to the adjacent artery, including
the aorta and the hepatic and superior mesenteric arteries
5
(SMA).
In a review by Coimbra, 94% of patients with portal
and superior mesenteric venous trauma had associated
intraabdominal injuries, with 61% of these being to other
major blood vessels (most commonly the IVC and SMA).3
Just over one-third of SMA injuries (35%) have an associated injury to the of SMV.16 Additional ndings from that
clinical experience showed the impact of multiple vascular
injuries on survival. From a cohort of 302 patients with
abdominal vascular trauma, a single vessel injury had a
mortality rate of 45%; when two vessels were injured, the
mortality increased to 60%, and 73% when three vessels
were injured. Injury to more than three intraabdominal
vessels was uniformly fatal.
17
Complication rates are also high in the setting of intraabdominal venous trauma. The genesis of these is multifactorial, attributable to associated injuries, patient age and
comorbidities, and severity of blood loss and shock. Common complications include but are not limited to pulmonary
failure, renal failure, wound infection and dehiscence, and
sepsis. Intraabdominal complications include thrombosis
of the venous repair, abdominal compartment syndrome,
reoperation for bleeding, a prolonged intensive care unit
stay, including need for vasopressor support and gastrointestinal complications. In those who survive operative
repair, delayed gut or liver ischemia resulting from vessel
ligation or thrombosis (or just prolonged ischemia prior to
the vessel repair) can result in postoperative complications
and prolonged intensive care unit admissions.
4,18
Preoperative Preparation
The most important component of preoperative preparation
is beginning the operation with a thorough understanding of anatomy and knowledge about how to expose and
control the abdominal vascular injury. In many instances
of central venous trauma, preoperative imaging is limited
to only a focused assessment with sonography for trauma
(FAST) examination as the unstable patient must be taken
directly to the operating room. In these cases, it is often useful to enter the operation in a damage control mindset, looking for opportunities to expeditiously control bleeding and
ways to restore ow, but also a willingness to ligate or shunt
vessels and stage operations to optimize the patient’s resuscitation and physiological condition. In many instances a
“second look” operation 12 to 24 hours after the rst surgery is needed to assess for bleeding, viability of the viscera,
and the need to perform denitive vascular repair.
Not all patients with intraabdominal venous trauma are
hemodynamically unstable. The hematoma surrounding
the injury may be contained within the retroperitoneum
resulting in tamponade and a patient with normal vital
signs or one who responds to small amounts of resuscitation.19 The utility of computed tomography (CT) depends on
the nature and mechanism of injury. CT scan has less of
a role in the immediate management of patients who have
sustained penetrating abdominal trauma, especially those
in who are hemodynamically normal or lacking peritoneal
signs and in whom the penetrating injury is thought to be
extraperitoneal. In contrast, CT is invaluable in the diagnosis and management of patients with signicant blunt
trauma, especially those with injury to a major abdominal
vein such as the IVC. In the appropriate patient, detailed CT
imaging allows the surgeon to gauge the need for an aggressive resuscitation and to develop a treatment plan that may
range from nonoperative management, to a damage control
operation, to the use of endovascular techniques.
Identifying an injury to the vena cava on CT may be challenging as contrast extravasation is often not seen, especially in the patient with relatively normal vital signs. The
most common radiographic nding associated with a large
vein injury is a retroperitoneal hematoma. Between 75%
and 91% of retroperitoneal hematomas develop in zone I
228 SECTION 4 • The Management of Vascular Trauma
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of the abdomen (i.e., central or midline), whereas 18% of
patients will have a zone II hematoma (i.e., lateral spaces).
Approximately 1 in 10 patients with abdominal venous
injury will have radiographic evidence of a zone III or pelvic hematoma.
4,14
The presence of retroperitoneal blood
should raise suspicion for injury to a large abdominal vessel, remembering that the zone of the hematoma may not
correspond anatomically to the injured vessel. One consistent anatomic association is that between a right lateral retroperitoneal hematoma (zone II) near the ascending colon
and duodenum and an injury to the IVC. As noted previously, the retroperitoneum and surrounding visceral or
solid organ structures often serve to contain and tamponade low-pressure venous bleeding.
Another CT nding that points to, or should raise suspicion regarding, a large venous injury is “at” IVC which is
an indicator of hypovolemia. A at IVC is dened as having
a maximal transverse-to-anteroposterior ratio of less than
4:1. The at IVC can also be detected in the trauma bay
using ultrasound and is a useful indicator of caval injury
and/or pending hemodynamic collapse. Subtle ndings,
particularly in relation to IVC injury, include an irregular
contour to the cava or a lling defect within the lumen on
CT imaging.
fat into the lumen of the vena cava may be present as an
indication of vessel laceration.
20,21
In rare cases, herniation of surrounding
20,22
Nonoperative management (i.e., observation) of some retroperitoneal hematomas
is indicated as open exposure of these injuries can release
the tamponade and result in torrential hemorrhage.
23
The most hemodynamically depleted patients with
abdominal venous trauma may deteriorate too rapidly for
CT or ultrasound imaging or even transport to the operating room. In these cases, a resuscitative thoracotomy,
either in the emergency department or in the operating
room, should be considered as means to restore central
aortic pressure and coronary and cerebral perfusion.
This maneuver reduces or stops bleeding below the aortic
clamp and maintains left ventricular afterload, preventing
cardiac arrest until hemostasis can be obtained and the
clamp slowly removed. Indications for thoracotomy are
limited because of the low likelihood of survival in these
scenarios. However, thoracotomy should be considered in
patients who have penetrating trauma and a witnessed
cardiac arrest (pre- or in-hospital), and in those having
sustained blunt injury and who arrest after arrival to
the hospital. One literature review on the topic showed
a 10.5% (4 of 38) survival rate in patients undergoing
resuscitative thoracotomy in the setting of abdominal vascular injury.
13,24,25
Although a left thoracotomy provides relatively easy
access to the aorta for clamping, the exposure comes at a
cost to the patient’s temperature, pulmonary function, and
acid-base status, not to mention the morbidity of the incision itself. One alternative is a midline laparotomy with
supraceliac clamping of the aorta at the diaphragmatic
crus. This approach can be more anatomically constrained
and difcult for those not familiar with the supraceliac
exposure, but if performed quickly, it does accomplish the
desired effects of resuscitative aortic occlusion and avoids
opening the thoracic cavity.
REBOA is an appealing, less-invasive alter native to resuscitative thoracotomy for unstable patients or those progressing
to a terminal degree of shock. Endovascular access to place
the balloon catheter is achieved using a percutaneous or
open femoral artery approach. In either instance, ultrasound can be used to identify the common femoral artery
just below the inguinal ligament. The length of REBOA
catheter to be inserted is estimated by placing the catheter
on the outside of the patient and measuring the distance
between the femoral artery and the desired aortic occlusion
zone. For a suspected subdiaphragmatic, intraabdominal
aortic zone 1 which is between the origin of the left subclavian and the celiac arteries (i.e., supraceliac aorta).26 Zone
III balloon positioning and ination is indicated for patients
with a pelvic bleeding source (e.g., severe pelvic fracture),
and occurs between the renal arteries and the aortic bifurcation (i.e., infrarenal aorta).
Signicantly less invasive than resuscitative thoracotomy,
ination of the REBOA balloon has the same hemodynamic
and bleeding control effects as cross-clamping the aorta.
REBOA limits or stops bleeding below or distal to the inated
balloon and increases central aortic pressure and perfusion to the coronary arteries and brain. Like other forms
of external aortic cross-clamping, REBOA is only a temporizing maneuver that can be applied for 20 to 30 minutes
until resuscitation can begin and efforts made at denitive
hemorrhage control. Preclinical, large-animal studies have
shown that REBOA is effective in decreasing blood loss, stabilizing central venous pressures, and improving survival in
the setting of major venous injury.
27
Operative Management
THE INFERIOR VENA CAVA
Of the three major abdominal veins discussed in this chapter, the IVC is the most frequently injured and requires
some of the most complex decision-making. The incidence
of IVC injury ranges from 0.5% to 5% of penetrating injuries and 0.6% to 1% of blunt trauma.9 Approximately
30% to 50% of patients with this injury pattern die prior
to reaching the hospital, either from exsanguination or
associated injuries.
tal, 20% to 57% will not survive to discharge, dying from
bleeding in the operating room or during the early postoperative period.
Penetrating injury to the vena cava is slightly more common. However, the vena cava is relatively xed in the retroperitoneum and in the setting of blunt trauma, there
is torque and tearing of the vessel at one or more of the
venous tributaries attached to the IVC. The retrohepatic
cava is especially xed in place, protected by the hepatic ligaments, the retroperitoneum, and the hepatic parenchyma.
Signicant force is required to tear or avulse the vena cava
in this location, often resulting in a catastrophic injury.
Of all major abdominal veins, injury to the IVC, whether
blunt or penetrating, is the most amenable to nonoperative
management. As the IVC is a low-pressure (3–5 mm Hg)
retroperitoneal structure, bleeding is initially contained
within the connes of the retroperitoneum, allowing for
tamponade of bleeding. Studies with swine have found that
nonoperative management of IVC lacerations is effective in
2,9
Of those who survive to the hospi-
2
28
19 • Inferior Vena Cava, Portal, and Mesenteric Venous Systems 229
Suprahepatic
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selective circumstances, especially instances in which the
hematoma is contained and the patient’s hemodynamic
status is stable.
29,30
When the retroperitoneum is violated,
the tamponade can be released into the peritoneal cavity
resulting in much higher rates of bleeding and shock.
To minimize the likelihood of releasing the retroperitoneal tamponade, one should opt for permissive hypotension and avoid over resuscitation and arbitrarily increasing
the patient’s blood pressure. Administering large volumes
of resuscitation uid (blood or crystalloid) will increase
the venous pressure, enlarge the vena cava, including the
injured segment, and increase the likelihood of bleeding.
Similarly, patients with penetrating injuries are likely to
benet from uid restriction and hypotensive resuscitation, a strategy which reduces the chances that hydro-
Retrohepatic
static pressure will force the clot off the tear in the vena
cava. Patients in whom there is a suspicion for vena cava
(or other major abdominal vein) injury, should not have
resuscitation uids administered through femoral venous
or other lower extremity sites. Overt signs of deteriora-
Suprarenal
tion, including worsening shock, peritonitis, and ominous
changes in acid base status, indicate the need for surgical
exploration.
29
The distal IVC arises from the conuence of the common
iliac veins and as it courses cephalad through the right retroperitoneum, it receives venous ow from several tribu-
Infrarenal
taries including lumbar and the right gonadal veins, both
renal veins, the right adrenal vein, and the inferior phrenic
veins. More cephalad, the vena cava traverses posterior to
the liver parenchyma (i.e., retrohepatic). In many cases, the
liver completely engulfs the vena cava, making retrohepatic
exposure more challenging. At, or immediately below, the
diaphragmatic hiatus, the hepatic veins feed into the cava,
including small branches entering the lateral retrohepatic
cava from the liver. After traversing the diaphragm, the
proximal IVC enters the pericardium and drains into the
right atrium.
For operative considerations, the IVC is divided into four
Fig. 19.1 Inferior vena cava anatomy with subsegments—infrarenal,
suprarenal, retrohepatic, and suprahepatic.
anatomic segments: infrarenal, suprarenal, retrohepatic,
and suprahepatic (Fig. 19.1). Injuries to the infrarenal IVC
have the highest likelihood of survival, due to the relative
ease of access and tolerance to ligation, when necessary.
The suprarenal IVC remains relatively accessible but is more
intimately associated with structures such as the kidneys,
the pancreatic head, and portal structures. Suprarenal ligation of the IVC is poorly tolerated.12 The retrohepatic IVC
is approximately 7 cm in length and is directly behind, or
within, the liver parenchyma. Injury to this segment almost
invariably includes damage to the liver parenchyma, allowing free bleeding from the vein into the peritoneum via the
injury tract through the liver. Exposure of the retrohepatic
IVC is difcult, and survival from injuries in this location less
likely.31 The suprahepatic IVC includes the course of the vessel from the dome of the liver to the right atrium, including
the hepatic veins and the transition across the diaphragm.
Mortality from injuries in this region approaches 100%,
due to difculty gaining proximal and distal control in this
high-ow region. Due to the large diameter of the IVC in
this location and difculty of surgical access, in the rare
circumstances when this injury is identied preoperatively,
percutaneous endovascular techniques will likely provide
better salvage than open approaches.
Exposure and Mobilization
Access to the IVC depends on the anatomic segment that
is injured. Upon identication of a retroperitoneal hematoma suspicious for caval injury, the vena cava should
be approached from the patient’s right side. Specically,
the white line of Toldt is divided along its length and the
ascending colon, hepatic exure, and transverse colon are
mobilized and reected cephalad and to the patient’s left
side or midline. An extensive Kocher maneuver is then performed, mobilizing the duodenum and pancreatic head to
the patient’s left, using visualization of the left renal vein
as the cue that mobilization is adequate (Fig. 19.2). Often,
these maneuvers will expose a hematoma overlying the
area of injury. Although proximal and distal control of the
IVC is advisable in most cases, this is not always possible.
Even in instances where proximal and distal control can
be achieved, signicant bleeding may occur from lumbar
veins and other posterior tributaries. When hemorrhage is
encountered, direct pressure on the area of injury should be
applied. Control may then be achieved by starting proximal
and distal to this region and “marching” toward the defect.
In this manner, the site of injury may be localized without
230 SECTION 4 • The Management of Vascular Trauma
Gallbladder
intestine
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Liver
IVC
Right kidney
Posterior duodenum
Small
Ascending
colon
Fig. 19.2 Medial visceral rotation exposing
the inferior vena cava (IVC) in situ.
intermittent episodes of profuse bleeding. A common
mistake is in not dissecting down to the actual substance
of the IVC and attempting to sew the peritoneal tissues that
overlie the vena cava in a hurried effort to achieve hemostasis. Division of the overlying lmy retroperitoneal tissues
will expose the actual wall of the IVC that needs to be seen
to be débrided and repaired.
Control of the retrohepatic and suprahepatic portions of
the IVC is particularly difcult to achieve given their friable
nature and their anatomic location.32 Cephalad retraction
of the liver will allow access to the most proximal portion
of the infrahepatic IVC.33 Complete mobilization of the liver
by division of the suspensory ligaments, including the right
triangular, coronary, and falciform ligaments, will provide
mobility to access the retrohepatic portion of the cava.
However, attempts to mobilize the liver in this region often
result in increased bleeding from the retrohepatic wound,
as torque on the liver and IVC can increase the size of the
laceration. Though lobar resection may seem appropriate, especially in cases of damaged liver parenchyma, this
maneuver is discouraged and should be one of last resort.
Removal of the overlying liver removes the possibility of
tamponade by the organ and adds disrupted liver parenchyma as a source of bleeding. Endovascular approaches,
including balloon occlusion of the IVC through remote
femoral and/or jugular venous access, can offer a quick and
safe alternative for temporary hemostasis to facilitate repair
of caval injury in any of its anatomic segments.
15,34
Approach to the suprahepatic IVC will almost always
require division of the diaphragm for exposure. Additionally, a sternotomy to access the intrapericardial IVC may be
indicated for proximal control, as the infradiaphragmatic
section of the IVC is not amenable to easy clamping and
repair.35 Care must be taken when working in this region
to avoid dislodging thrombus from the injury or disrupting the thin-walled hepatic veins inserting into the cava.
As mentioned, percutaneous approaches that involve use
of compliant endovascular balloons for inow and outow
occlusion may be helpful in visualizing and repairing injuries to this portion of the IVC.
Bleeding Control
If massive hemorrhage is encountered at the time of laparotomy, temporary aortic occlusion may be required to support left ventricular afterload, avoid end stage shock, and
prevent onset of a terminal cardiac rhythm. This can be
accomplished by compressing or clamping the supraceliac
aorta at the diaphragmatic hiatus or using REBOA inserted
through one of the femoral arteries. The principles of proximal and distal control apply, regardless of size and location
of the vessel injury. Initial manual compression of the IVC
allows visualization of the eld of injury, to begin dissection.
The traditional teaching is to apply sponge sticks above and
below the venous injury for proximal and distal control.
2,12
This technique can be problematic if not accomplished
with great care as forceful application may widen or create
an iatrogenic injury or avulse a venous branch. Applying
direct pressure with one’s ngers is often gentler and easier
to control while localization of the injury is underway.
After localization of the injury, proximal and distal control with atraumatic blunt instruments should be achieved
to free one’s hands for more detailed dissection of the vessel and eventual repair. Transitioning smaller, more focal
instruments such as the low-prole Kittner dissectors (i.e.,
“peanut”) to compress proximal and distal to the injury
is less likely to obscure or block key parts of the operative
eld from view. The smaller Kittner dissectors are a reasonable choice for control, as they can be gently placed directly
19 • Inferior Vena Cava, Portal, and Mesenteric Venous Systems 231
udd-Allis clamp
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on top of, or above and below, the source of bleeding. The
objective in this setting is to work back from the use of one’s
ngers or hand to a visible and workable operative space
to allow clearer dissection, visualization, and repair of the
injury. The initial use of one’s hand, the sponge stick, or
the Kittner dissectors avoids having to place larger metallic
clamps in the eld before the vena cava or the edges of the
injury have been clearly dened.
The importance of good lighting, well-set and wide
retraction, and multiple suction devices cannot be overstated in accomplishing these steps. In the case of linear
injuries to the major abdominal veins, the vein edges may
IVC
J
be grasped with Judd-Allis clamps and closed with either a
Satinsky clamp or 4-0 polypropylene sutures (Fig. 19.3A).
A simple stitch placed at the proximal and distal extent of
the laceration, with accompanying gentle upward traction, will also elevate and collapse the laceration. This
controls the bleeding and facilitates exposure for primary
suture closure.
36
Another consideration when going to repair the IVC or
other large venous injuries is to use a larger noncutting
needle (e.g., 4-0 polypropylene on an SH needle). A larger
needle is easier to visualize and direct in the presence of considerable amounts of blood. Although well-intended, too
small of a needle is often submerged in blood and not able
to be seen or appropriately guided which can prolong the
A
repair and potentially extend the original injury. Another
common misstep is in not dissecting down to the actual substance of vein wall and attempting to blindly place a clamp
Liver
or to sew the overlying peritoneal tissues in an attempt to
achieve hemostasis. Division of the overlying lmy tissues
leads to identication of the substance of the wall of the IVC
and allows for control and suture repair of the injury.
IVC
Hemorrhage control presents unique challenges in the
case of blunt retrohepatic and suprahepatic IVC injuries.
The IVC injury is usually combined with signicant hepatic
parenchymal disruption. Hemorrhage results from both
the disrupted liver and from the retroperitoneum. Visualization and identication of the exact area of injury is
difcult. In this circumstance, direct pressure consists of
compressing the liver parenchyma to reapproximate its
anatomic form and pressuring posteriorly onto the injured
and underlying vena cava as a means of tamponade until
anesthesia can catch up with blood loss. A Pringle maneu-
Left renal vein
ver, in which a nger is introduced into the foramen of
Winslow to encircle and occlude the structures of the porta
hepatis, should be utilized if the liver parenchyma is contributing to the bleeding.
19
Complete mobilization of the liver, including division of
the triangular and coronary ligaments and retroperitoneal
attachments, should be carefully weighed in the circum-
Fig. 19.3 (A) Judd-Allis clamps approximating an inferior vena cava
(IVC) laceration. (B) Intraluminal repair of a backwall, IVC laceration.
stance of retrohepatic caval injuries. When hematoma is
identied behind the hepatic suspensory ligaments, division of the ligaments should be avoided. With the liver completely mobile, existing tamponade is released and will not
be possible to reestablish with a freely oating liver.
37
Control by direct pressure may be difcult or incomplete
and adjunctive endovascular techniques may be benecial
in these circumstances. Specically, the use of endovascular
occlusion balloons may provide a better option for bleeding
control. Ination of the balloons proximal and distal to the
injury site can provide a bloodless eld, allowing time to
obtain more direct proximal and distal control of the vessel
with loops or clamps, or even allow immediate primary
repair. If circumstances permit, occlusive balloons should
be introduced and positioned via percutaneous access from
above (i.e., transjugular) and below (i.e., transfemoral) prior
to exposing the caval injury to lessen bleeding and keep the
site free for repair. The balloon catheters may be introduced
through both femoral veins, or using a combined femoral
232 SECTION 4 • The Management of Vascular Trauma
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and internal jugular vein approach.38 In some cases, insertion and ination of a balloon through the site of injury
may be more expeditious. Endovascular stent grafts (i.e.,
covered stents) are also an option for hemorrhage control
in the multiply injured patient. In these cases, the stent graft
may be inserted to cover or seal the injury from within and
control bleeding while other injuries are addressed.
39,40
In the setting of profound bleeding from the perihepatic IVC or liver parenchyma, total vascular exclusion
may be necessary. This maneuver requires control of the
supra- and infrahepatic IVC which may require a partial
sternotomy or right thoracoabdominal incision to expose
and clamp the limited length of vena cava between the diaphragmatic cruse and the liver itself.23 A Pringle maneuver
to occlude portal vein and hepatic artery inow completes
vascular isolation and should stop all bleeding. In reality,
total hepatic isolation may only stem the bleeding by 40%
to 60%, but it should allow enough control to facilitate
parenchymal or vascular injury repair.41 Because this series
of operative steps induces warm ischemia, they can only be
held for 45 to 60 minutes before inducing irreversible damage to the liver and hepatic failure.
18,23
Intermittent release
of the Pringle clamp to allow periods of perfusion should
be performed if the occlusion time must be longer. Broering
et al. have proposed extending a safe ischemic time period
by infusing cold preservation solution with or without topical cooling of the liver.18 However, in these unstable, often
hypothermic, patients such complex maneuvers are often
not possible and are rarely successful.
If hepatic isolation is inadequate to allow visualization
and repair, total abdominal vascular exclusion is required.
In addition to occlusion of the IVC and performance of a
Pringle maneuver, a supraceliac aortic clamp or REBOA is
placed to prevent all arterial inow into the abdomen and
distal structures. The loss of venous return in an already
hypotensive patient often leads to full arrest.
41,42
Although
mortality is very high, an occasional patient in this extreme
situation will survive.
Considerations for Venous Repair
After controlling the bleeding, attention is turned towards
repairing the vessel. Thorough exposure, proximal and distal control, and careful dissection of enough vessel length
on which to work are all important steps. Careful inspection for, and control of, branch vessels facilitates mobilization and prevents “back-bleeding” into the injured artery
or vein. In most cases, prior to repair, the vessel should
be opened with Potts scissors to inspect the backwall and
intima and débride injured parts of the wall. The intima of
the vessel should then be irrigated vigorously with heparinized saline to remove platelet aggregate and thrombus and
allow further inspection of the lumen.
Primary repair is one method should the vessel have a
sharp injury and maintained its length and diameter. If the
edges of the injured site are jagged or their viability in question, they should be débrided with Potts scissors to ensure
integrity of any subsequent suture line. Closing longitudinal tears transversely minimizes vessel narrowing. How-
which either need to be xed with patch angioplasty or
by placement of an interposition graft. Vessel repair is
done with ne monolament suture (4-0, 5-0, or 6-0
polypropylene) with enough purchase so that the suture
does not pull through the wall. If primary repair is going
to result in signicant luminal narrowing, then one should
consider using a synthetic or biologic patch angioplasty. As
previously noted, in a bloody eld, one should use a larger
needle with the monolament suture to be able to see and
effectively maneuver.
The type of vascular reconstruction (primary repair
versus patch angioplasty versus interposition graft) will
depend on the location and extent of the venous injury and
associated injuries. One should be mindful that in damage
control scenarios, venous ligation may be the most appropriate approach. Although repairing the venous injury to
maintain ow is appealing, any signicant vascular reconstruction will take time, resources and more resuscitation.
It is a difcult call to make, and one that should be made
in conjunction with the anesthesia or resuscitation team,
but in patients who are cold, coagulopathic, and acidotic,
foregoing venous repair in favor of ligation may be the better part of valor.
Ligation
As a rule, ligation of the infrarenal vena cava, and the iliac
and left renal veins, is well tolerated. In contrast, ligating
the portal or superior mesenteric veins is poorly tolerated
and ligating the right renal vein often results in loss of
kidney function.17 As expected, ligation is better tolerated
when there is an abundant collateral circulation.
As a damage control maneuver, ligation of the vena cava
has been well-described in clinical reports throughout the
literature. Although the operation is associated with a high
degree of mortality, death is often due to associated injuries
and the degree of shock in which patients present. Initially
described from wartime experiences in the 20th century,
ligation remains a contemporary option for managing these
complex injury scenarios.9 A few notable reports include
Navsaria et al. who used ligation in two-thirds of injuries, and Huerta et al. who described a 42% survival rate
among 36 patients with caval trauma, one-third of whom
underwent ligation.
12,36
Sullivan et al. reviewed 100 injuries over a 13-year period, noting that almost half (43%)
were ligated. In that report, patients undergoing ligation
had a 41% early and a 59% longer-term mortality. Whereas
patients in the repair group fared better, with a mortality of
21%, the patients in the ligation group were more severely
injured.9 Ligation of the suprarenal cava is poorly tolerated
and associated with higher mortality, unless the patient
happens to have existing generous collaterals via the azygous and lumbar systems.
12,43
Ligation of the vena cava at
or above the retrohepatic segment is uniformly fatal.
Hesitation to ligate the major abdominal veins stems
not only from mortality concerns but from the potential sequelae of ligation. A major consideration following ligation of the infrarenal IVC is swelling of the lower
extremities, potentially severe enough to cause compartment syndrome. Historically, prophylactic fasciotomy has
been recommended for patients undergoing ligation of the
cava.9 However, recent guidelines focus more on clinical
vigilance rather than prophylactic fasciotomy.
19,36,44
If the
IVC is ligated, one must closely monitor lower extremities
compartment and have a low threshold to measure compartment pressures and perform fasciotomy.
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19 • Inferior Vena Cava, Portal, and Mesenteric Venous Systems 233
Reconstructive Techniques
If the patient has sound hemodynamic and physiologic
measures, more complex repairs of the vena cava can
be considered. Though some degree of narrowing can
be expected or tolerated following primary venorrhaphy,
attempts to primarily close injuries of more than 50% circumference are likely to cause too much luminal compromise, clot formation, and even thrombosis.
The optimal reconstructive technique will depend on the
extent of venous injury. Those that involve both the anterior
and posterior wall of the cava are relatively common and
require comprehensive mobilization of the vessel and side
branches (e.g., lumbar veins) in order to gently rotate and
visualize the back wall. When possible, the knots of monolament repair sutures (e.g., Proline sutures) should be
extraluminal to avoid them becoming a nidus for thrombus
formation. In the cephalad position, the cava is more xed,
tethered by the renal and hepatic veins and liver parenchyma.
If there is an injury to the front and back walls of the cava
in these locations, the anterior venotomy can be extended to
Graft
allow repair of the posterior laceration from inside the lumen
(Fig. 19.3B). In this instance the monolament knots may be
left intraluminal as a matter of expediency.
Transected vessels may be amenable to an end-to-end
anastomosis, although it is rare that a patient with this
injury pattern would be stable enough to tolerate more than
IVC
ligation. End-to-end anastomosis is difcult in this location
due to tethering of the cava from visceral and lumbar tributaries making it difcult to mobilize the vessel for a tensionfree anastomosis. This is especially true when segments of
Fig. 19.4 Spiral vein graft used for inferior vena cava (IVC) repair.
the vessel wall have been lost or need to be débrided.
When primary repair of the vein is not possible, other
options include an interposition graft, patch angioplasty,
and placement of an endovascular stent graft. The vena
cava’s larger caliber is such that standard saphenous vein
interposition graft will not provide adequate luminal size.
If time permits and the expertise exists, the saphenous vein
can be harvested, opened along its length to create a long
panel that can then be sewn over a chest tube to create a
spiral vein graft (Fig. 19.4). The internal jugular or deep
femoral veins are larger-caliber options that may be considered as options for an interposition caval reconstruction. A
downside of using autologous vein for this type of reconstruction is the time and expertise required to harvest and
prepare the vein graft, requisites that may not be present
in resource-limited environments or with unstable patients.
Delayed reconstruction of the transected vena cava can
also be an option.
45,46
If the patient has severely compromised physiology mandating a damage control approach,
the vena cava can be shunted with a thoracostomy tube as a
way to quickly maintain ow for a short period of time. Once
the patient has been resuscitated, a “second look” operation
can be performed, typically within 12 to 36 hours, where
the temporary shunt can be removed and a more formal
vascular repair performed. Though temporary vascular
shunts are most often being used in instances of arterial
injury, reports of their effectiveness in the management of
venous injuries exist, including experience which conrms
acceptable patency when used in a damage control situa-
47,48
tion.
Even if the venous shunt occludes with thrombus,
the clot can almost always be cleared (i.e., thrombectomy)
at the time of the shunt removal. In the rare instance in
which the clot from a thrombosed venous shunt cannot be
removed, the patient is then essentially left with a functionally ligated venous injury.
Patch angioplasty is a reasonable option when injury to
the cava results in loss of part of the vessel wall or when
primary repair will cause more than 30% to 50% luminal
narrowing. Patches may be constructed from autologous
vein, polytetrauoroethylene (PTFE), or bovine pericardium.49 Each option has advantages and disadvantages and
patient physiology and local circumstances will inuence
the choice. Autologous vein has the lowest infection rate
and is usually available, but it does take additional time to
harvest and prepare and this method leaves the patient with
vein harvest incisions. PTFE is generally available but has
slightly higher rates of infection, especially if there are concerns of contamination in the eld. Bovine pericardium is a
biologic material, and has a slightly higher rate of infection
compared to autologous vein, but it is a good “off the shelf”
option if it is stocked in the operating room.
Endovascular options are appealing in situations when it
is difcult to access and control a vessel such as the proximal portions of the IVC. If radiographic evidence of this
injury pattern is present prior to laparotomy, endovascular balloons may be placed prior to making the incision to
prevent further hemorrhage. Increasingly, reports in the
literature detail the use of intravenous stents to seal or
repair injuries to the cava. Long-term outcomes are lacking
and stent grafts can be thrombogenic in low-ow vessels, a
property which could increase the risk of venous thromboembolism (VTE). However, initial reports on the use of stent
234 SECTION 4 • The Management of Vascular Trauma
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grafts for caval injuries are promising and an endovascular
approach may be the best option to manage these hard-
to-reach injury patterns that are associated with a persistently high mortality rate.
39,40,50
THE PORTAL VEIN
Injury to the portal vein is uncommon, documented in one
series at 0.1% of all injuries over 20 years.13 Morbidity and
mortality associated with portal vein injury is high, attributable to the frequency of signicant associated injuries
including those in the region of the portal triad.5 In a multicenter review of 99 portal triad injuries, survival was only
20% if more than one portal structure was damaged. Of
patients with portal triad injuries who died in the operating
room, 85% had at least one portal vein injury.
51
The portal vein is formed from the conuence of the
splenic vein and the SMV behind the neck of the pancreas
(Fig. 19.5). Contained within the hepatoduodenal ligament, the closely associated hepatic artery and bile ducts
are frequently injured at the same time. The average diameter of the portal vein is 2 cm and despite a high ow rate,
approaching 1 L/min, pressures within the vessel are low at
approximately 10 mm Hg or less.
5
Exposure and Mobilization
The portal vein is best approached through a midline laparotomy and from the right side of the abdomen. To expose
the portal vein, the ascending colon and hepatic exure are
mobilized and reected from right to left at least to the midline or even further into the left side of the abdominal cavity.
A wide Kocher maneuver is next performed with leftward
reection of the duodenum and head of the pancreas which
allows near complete exposure of the portal vein and associated structures. The common bile duct may be isolated
and retracted leftward as well, to provide additional access
to the anterior surface of the vein. Division of the pancreatic neck may be necessary to access more distal portions
of the portal vein. A Pringle maneuver, in which an atraumatic clamp, vessel loop, umbilical tape, or manual pressure
is used to occlude the portal structures, is often needed to
control hemorrhage while the portal structures are being
mobilized.
13
Bleeding Control
In the circumstance of massive hemorrhage, proximal control will consist of supraceliac aortic control with a clamp or
performance of zone 1 REBOA. This may be the only way to
reasonably control in-ow; both splenic ow from the celiac
axis and superior mesenteric ow. In less dire circumstances,
the Pringle maneuver is generally the most useful method of
controlling hemorrhage from suprapancreatic portal vein
injuries. However, the Pringle maneuver often obscures dissection and exposure of the injured portal vein. Even in the
setting of more limited injuries, the occlusive tape or clamp
placed around the porta hepatis prevents visualization of
colon
Duodenum
Liver
SMV
Gastric vein
Splenic vein
IMV
Pancreas
Descending
colon
Fig. 19.5 Anatomy of the portal vein in
situ. IMV, Inferior mesenteric vein; SMV,
superior mesenteric vein.
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