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272 Part II Abdominal Wall
obstruction. Management of these patients is directed at
overall cardiovascular support, treatment of the underlying
acute condition(s), and broad-spectrum antibiotics. Intraarterial papaverine may be administered to relieve vascular
spasm, although this is not always eective and may be complicated by systemic hypotension. NOMI usually portends
a bad outcome in general, which is related as much to the
underlying illness as to mesenteric compromise. Laparotomy
should be reserved for patients in whom intestinal infarction
is suspected and often will not inuence the outcome in this
disease.
Mesenteric venous thrombosis may result in acute intestinal
ischemia, although this accounts for only about 5% of all
cases. Patients are a distinct subgroup, being younger (30–50
24–27
years) and predominantly female.
Associated hypercoagulable state can be identied in more than three quarters
of patients and a history of prior venous thrombosis is not
uncommon. Common inherited states include deciencies
of protein C, protein S, and antithrombin III; activated
protein C resistance; factor V Leiden mutation; and meth-
27
ylenetetrahydrofolate mutations.
Acquired prothrombotic
states include profound dehydration, polycythemia, cancer, pelvic or abdominal inammation, and hormone use.
Mesenteric venous occlusion is most readily diagnosed by
venous-phase CT angiography, which can demonstrate
thrombus in the superior mesenteric vein and portal system
(Fig. 13-13). Operative ndings suggestive of this condition are edematous beefy red bowel with thrombus in veins
of the mesentery. e primary mode of therapy is anticoagulation, operative intervention is rarely indicated. Most
patients can be managed supportively, although signicant
volume resuscitation may be required. ere are anecdotal
reports of mesenteric and portal vein thrombectomy and
FIGURE 13-13 CT scan demonstrating thrombus in the superior
mesenteric vein. CT scan is the most accurate diagnostic study in this
condition.
28–30
thrombolysis,
but these do not reect the standard of
care for most patients.
DETERMINING INTESTINAL VIABILITY:
THE ROLE OF “SECOND-LOOK” SURGERY
A major challenge in managing patients with intestinal
ischemia is assessing the need for, and extent of, intestinal
resection. Preoperatively, colonoscopy can be used to assess
the viability of the large intestine in questionable situations.
Friable red mucosa suggests viability and a grey mucosa that
readily sloughs indicates the need for resection. Viability of
the large bowel is dicult to judge from external appearance
at the time of laparotomy and in general it is preferable to
err on the side of resection in questionable circumstances,
because maintaining large bowel length is not an absolute
requirement for survival. Primary repair should not be undertaken after large bowel resection, as diversion with secondary
reconstruction is preferred.
When the small intestine is involved, the problem becomes
31–33
more complex.
Every eort should be made to preserve
as much small bowel as possible. Clearly necrotic segments
of bowel and areas of perforation are resected or excluded
immediately to prevent contamination during vascular reconstruction. Evaluation of the remainder of the small bowel is
done after blood ow to the intestine is restored. e bowel
is usually observed for 15–20 minutes after revascularization
and warm lap pads are applied to the intestines to reduce any
vasospasm. External inspection, with attention to color and
peristalsis, is more helpful than in the large bowel. Doppler
interrogation of the antimesenteric border for arterial ow
is useful when positive. Use of uorescein (1 ampule given
intravenously) followed by inspection with a Wood’s lamp,
is the most sensitive means of determining perfusion. Viable
bowel will be uorescent yellow while nonperfused bowel will
appear dark purple. When the extent of resection is minimal and the remaining bowel is clearly viable, anastomosis
and abdominal closure is appropriate. When there are large
areas of questionable bowel that might mandate extensive
resection, an alternative approach is undertaken. Under these
conditions, marginal segments of bowel are left in situ and
their ends are simply closed over and returned to the abdomen. Plans for a second operation are made. Stomas are not
performed at this stage to preserve intestinal length. Fluorescein is not used at this time but reserved for the second procedure. e abdomen is temporarily closed using a “Bogotá
bag,” polytetrauoroethylene (PTFE) patch, or other temporary appliance (to minimize the chance of abdominal compartment syndrome) and the patient is returned to the ICU
where resuscitation continues. A subsequent laparotomy is
performed at 18–24 hours after the patient has been stabilized. At this point uorescein is injected and nonviable bowel
is resected. Intestinal continuity is restored unless it is unsafe
to do so. e abdomen often cannot be closed primarily at
this point because of the danger of compartmental hypertension, and an “open abdomen” approach with delayed closure
may be needed. Any deterioration in the patient’s subsequent
Chapter 13 Abdominal Vascular Emergencies 273
hospital course should suggest breakdown of an anastomosis
and prompt the appropriate therapy.
Despite increased clinical awareness and advances in
diagnostic modalities and perioperative care, management
of intestinal ischemia remains a signicant challenge to the
most experienced surgeon with continued high mortality and
morbidity.
Management of Abdominal
Vascular Trauma
Vascular injuries occur in 10–15% of cases of blunt and penetrating trauma.
over 90% of patients with vascular trauma, most commonly
small bowel, colon, and liver.
lethal when they occur and remain the most common cause
of death following penetrating abdominal trauma. Arterial
and venous injuries occur with equal frequency. e pattern
of injury diers between blunt and penetrating injuries. In
penetrating injuries, the most commonly injured vessels are
the vena cava, followed by the aorta, iliac arteries and veins,
and the SMA, and vein and multiple vascular injuries are
common.
involved in blunt trauma. is section provides principles for
management of injuries to the major arteries and veins of the
abdomen and retroperitoneum. e reader is referred to the
prior sections on vascular exposure for a description of how
to obtain control of these vessels. e discussion here centers
on management of specic injuries.
Overall, principles of trauma management including initial
resuscitation of the patient, rapid evaluation and triage, and
expeditious operation when indicated should prevail. Stable
patients, particularly those with blunt trauma, may undergo
one or more diagnostic tests, including peritoneal lavage,
“FAST” ultrasound examination, and, with increasing frequency, CT scan.
are taken directly to the operating room without further
diagnostic evaluation. Consequently, in a signicant proportion of cases, the extent of vascular trauma is not known
preoperatively and must be assessed by the surgeon in the
operating room.
Intraperitoneal hemorrhage is easily recognized and
should be expeditiously controlled, by application of external pressure, vascular clamps, or intravascular balloon occlusion catheters. Once active hemorrhage is controlled, any
visceral perforation is controlled by exclusion to prevent
ongoing peritoneal contamination and any remaining solidorgan injuries (ie, liver, spleen, and pancreas) should be
stabilized by packing. Denitive treatment of the vascular
injuries should then receive priority over denitive visceral
repair. e adaptation of a “damage control” approach to
abdominal trauma has improved outcomes in abdominal
trauma.
major venous injuries by ligation or packing and placement
of temporary shunts to restore arterial continuity when arterial
ligation will not be tolerated.
34–38
Associated nonvascular injuries are seen in
37
Vascular injuries can be highly
10
Vessels of the mesentery are the most commonly
39
Many patients with penetrating trauma
40,41
Vascular “damage control” involves the control of
42,43
Shunts are most often used to
temporarily restore ow to the extremities but areused less
often in management of visceral injuries. In general, visceral
vessels are either repaired or ligated during the initial operation. e end organ will either tolerate ligation because of
collateral circulation or be sacriced. e “damage control”
concept combined with endovascular techniques may be
of particular use when open vascular repair is exceedingly
complex and associated with signicant morality. is is particularly true of contained retroperitoneal or hepatic injuries.
Denitive treatment can be deferred at initial laparotomy in
these cases and attempted in an imaging suite using endovascular techniques after the patient is stabilized. Examples of
this include embolization of intrahepatic arterial injury and
treatment of some contained retroperitoneal hematomas.
is approach is in evolution and holds signicant promise.
ere are a number of situations in which the surgeon
must make a decision about whether to explore a contained
hematoma. In these cases, the risk of missing a major vascular injury is balanced against the morbidity of operative
exploration. Classic trauma training requires exploration
of all contained hematomas that result from penetrating
injury. In the case of blunt trauma, central hematomas
(zone 1) are explored because of the risk of injury to the
aorta or vena cava, while lateral and pelvic hematomas
are explored only if there is active bleeding or expansion
36
under observation.
If exploration occurs, it is important
to obtain proximal and, whenever possible distal, arterial
control outside the area of hematoma before proceeding.
Venous control above and below the area of injury is desirable but may not always be obtainable. Approaches to vascular control, including endovascular techniques in various
locations, have already been described. Intravascular occlusion catheters should be readily available for additional
control as needed. Only after every attempt to control the
arterial and venous ingress and egress to the hematoma has
been made should it be entered.
e advent of endovascular techniques may be changing
the classic paradigm of managing contained hematoma from
either blunt or penetrating cause. e rationale for exploring
nonexpanding hematomas of any type was based on the concern for occult vascular or visceral injury. e advent of CT
angiography and the existence of sophisticated intravascular
imagining in the operating room can facilitate evaluation of
nonexpanding hematomas from both penetrating and blunt
trauma without the need for operative exposure and its attendant blood loss. Furthermore, endovascular techniques such
as covered stents or coil embolization will allow treatment
of many vascular injuries from remote access with reduced
44,45
risk of blood loss.
Such treatments are in fact preferred
for trauma to branch vessels in the visceral, renal, or pelvic
circulations. is potential change in paradigm suggests
that the surgeon consider a form of vascular “damage control” in the case of contained hemorrhage, by considering
an “endovascular rst” approach for diagnosis and treatment of contained hematomas regardless of location. is
area is currently evolving, and there is no consensus onthe
role endovascular techniques should and will eventually
274 Part II Abdominal Wall
play. With these general comments in mind, a discussion of
specic vascular injuries and their management follows.
INJURIES TO THE SUPRARENAL AORTA
AND VENA CAVA
ese injuries as a group are highly lethal and management
is dicult. ey should be suspected in any patient with a
central hematoma from either blunt or penetrating trauma.
In the stable patient, CT scan with intravenous contrast can
help to identify the area of injury. If CT scan is not possible
preoperatively, a clear plan of exposure and management is
crucial before commencing any attempt at repair. Because
of the advances made in endovascular techniques, patients
should be treated in an operating room that has the capability of intraoperative uoroscopic imaging and angiography
whenever possible. If an injury to the aorta or vena cava is
suspected and the patient is not exsanguinating, the surgeon
should consider intraoperative angiography through the femoral artery or vein as appropriate to evaluate the location and
extent of vascular injury and consider intravascular control.
Following this, proximal and distal control should be established. Open exposure of the aorta at the diaphragmatic hiatus
3,4
or endoluminal balloon control,
both described previously,
can be performed. Injuries to the vena cava can initially be
controlled by balloon tamponade, although this may reduce
venous return to the right side of the heart. Open control of
the vena cava is described in the following text.
OPEN REPAIR OF THE SUPRARENAL AO RTA
e visceral aorta is exposed by a left medial visceral rotation described previously. If access to the posterior aspect of
the aorta is required, the left kidney should be elevated along
with the other viscera; if access to the anterior aorta is needed,
the kidney is left in its bed. Direct suture repair is undertaken whenever possible. Direct repair that does not narrow
the lumen of the aorta more than 50% or impinge on a visceral vessel is well tolerated. Larger defects may require patch
angioplasty using prosthetic material, arterial autograft, or
arterial homograft. In the absence of signicant contamination, prosthetic material provides a readily available, strong,
and durable material for repair. In the presence of gross fecal
contamination, biologic materials should be used if possible.
Arterial homograft provides the most expeditious alternative
both for size and durability, if available. Saphenous vein is
inappropriate in this circumstance due to concerns about
strength and durability; deep veins of the leg have proven reliable substitutes for in situ aortic reconstruction in infected
46
If appropriate, the aortic repair can be buttressed by
elds.
an apron of omentum of some paraspinous muscle, to separate the suture line from any visceral vessels. is should be
done in the presence of associated visceral injury, particularly
injury to the pancreas. Drainage is established as needed. If
the damage involves the origins of one or more of the visceral
vessels, these are ligated. Revascularization of these vessels
can be performed as described in the following text. Damage
control of the suprarenal aorta is not possible because of the
mesenteric ischemia that would attend any such attempt.
ENDOVASCULAR REPAIR OF THE AORTA
is emerging alternative should be considered in selected
circumstances. In a stable patient with a contained injury,
placement of a suitable covered stent can be combined with
extra-anatomic debranching of one or two visceral vessels, as
has been described for treatment of thoracoabdominal aneu-
47
rysms.
is is most suitable when a single mesenteric vessel
is involved, because the bowel will tolerate more prolonged
ischemia than the kidney. Modication of the stent graft
(“fenestrations”), to allow continued visceral perfusion, is
48
possible.
is is most feasible when the aortic defect is posterior and relatively remote from the visceral orices. More
precise fenestrations, as required in suprarenal aortic repair,
are currently beyond the capability of most surgeons in an
acute setting. If a stent graft is selected, its diameter should be
110–115% of the normal aorta to allow for secure xation.
A variety of o-the-shelf aortic cus are available and their
successful use has been reported in conjunction with thoracic
aortic transection.
OPEN REPAIR OF THE SUPRARENAL
INFERIOR VENA CAVA
Open repair of injuries to the suprarenal vena cava is one of
the most dicult of all abdominal vascular operations. Exposure of the infrahepatic suprarenal IVC is achieved by an
extended Kocher maneuver and right medial visceral rotation.
One cannot overemphasize the utility of intravascular balloon
control in these cases to avoid hemorrhage. Balloon control
can be combined with external pressure and the application
of partial occlusion clamps to provide hemostasis. Fine Allis
clamps are useful in coapting and controlling the cut ends
of the IVC and are preferable to more traumatic attempts at
control. Wounds of the infrahepatic suprarenal IVC are usually managed by lateral venorrhaphy with running vascular
suture. Narrowing the IVC 50–60% is often acceptable. If
lateral venorrhaphy is not possible, patch repair using prosthetic or biologic material is acceptable. e use of anticoagulation in these circumstances is unsettled and is likely to
remain individualized. Ligation of the suprarenal IVC should
be avoided. Injuries to the retrohepatic vena cava, especially
those that accompany blunt trauma, usually involve avulsion
of the hepatic veins. Such injuries are highly lethal. Exposure
of the retrohepatic IVC involves mobilization of the liver and
49–51
anterior medial rotation of the right lobe.
Repair of retrohepatic venous injuries may require hepatic isolation (control
of the aorta at the hiatus as well as the vena cava above and
below the injury and occlusion of the portal triad), placement of an intraluminal shunt between the right atrium and
infrarenal IVC or veno venous bypass with hepatic isolation.
ese techniques are only used in desperate circumstances
when bleeding persists despite adequate perihepatic packing.
In general, injuries in this area should initially be treated by
Chapter 13 Abdominal Vascular Emergencies 275
packing, nonexpanding hematomas should not be opened,
and the extent of injury should be dened and denitive
repair planned after the patient has been stabilized.
ENDOVASCULAR TECHNIQUES IN THE
SUPRARENAL IVC
At this point, any endovascular approach would be considered experimental. e complexities of and poor results with
open surgery in this area make an endovascular approach
to suprarenal IVC injuries an attractive potential alternative. Remote access and control, facilitating exposure, along
with limited occlusion of the IVC, are all points in favor
of an endovascular approach. e size and distensibility of
the IVC complicate the selection of an appropriate diameter
endovascular graft. Patients with caval injury are often in
shock and there may be external pressure on the vessel, both
factors that cloud the estimation of caval diameter. No stent
grafts have been made for caval use, and it is likely that aortic
cus or short segment of grafts used for thoracic aortic repair
would be most useful. Inadvertent coverage of the renal
orhepatic veins represents a further potential complicating
factor. ere have been no reports of endovascular treatment
of hepatic vein injuries. Nonetheless, the potential treatment
of these injuries by remote rather than direct access is appealing enough that it will undoubtedly be investigated in the
future.
REPAIR OF THE INFRARENAL AO RTA AND
ILIAC ARTERIES
unifemoral bypass is possible. Incases where the aortic bifurcation is not salvageable, primary end-to-end anastomosis of
the proximal ends of the common iliac arteries can be performed, followed by axillo-unifemoral bypass. If this is not
possible, axillo-bifemoral bypass may be required.
Unilateral common iliac artery injuries may be ligated with
subsequent cross femoral reconstruction using a prosthetic
graft. Isolated external iliac artery injuries can be repaired in
most cases with saphenous vein interposition. Internal iliac
artery injuries should be ligated. In the absence of signicant contamination, interposition graft replacement of the
damaged vessel with a prosthetic graft is preferred. ere are
advocates of in situ prosthetic bypass, even in the face of more
52
signicant contamination.
We prefer not to do this unless
the situation is life threatening and prefer temporary placement of a shunt.
Endovascular repair of injured aorta and iliac vessels
can be performed using techniques applied for repair of
endovascular infrarenal aortic aneurysm repair. One must
remember, however, that many of these patients are young
and the durability of these repairs is unknown. In addition most patients will require laparotomy for associated
injuries. ese two factors suggest a limited role for stent
grafts in the treatment of traumatic lesions of the aortoiliac
system. Endovascular repair has been used in treatment of
53
traumatic dissection of the aorta or iliac arteries.
As previously noted, endovascular balloon tamponade is a valuable
technique and endovascular coil embolization of dicultto-access hypogastric artery branches can be employed with
great success.
Injuries to the infrarenal aorta and iliac arteries can be managed by a combination of open and endovascular techniques.
Use of an endovascular balloon to achieve proximal arterial
control, described for ruptured aortic aneurysm, should
be considered as a part of management. ese techniques
require access to intraoperative uoroscopy and familiarity
with endovascular techniques. e balloon should be placed
in the operating room before celiotomy if possible, either
through the femoral artery with a supporting sheath or the
3,4
left brachial artery, as previously described.
e balloon
does not need to be inated if the patient remains stable.
Because concurrent visceral injury is common, laparotomy
is almost universally required. After “damage control” of any
gross intestinal spillage, attention is turned to the arterial
injuries. Exposure of the aorta and iliac arteries has been
described. When there is minimal enteric spillage, irrigation and repair with an in situ prosthetic bypass of appropriate diameter is the most expeditious approach. e repair
should be wrapped in omentum if possible to separate it
from the viscera. In the presence of signicant contamination, the infrarenal aorta and/or iliac vessels should either be
repaired primarily, ligated, or a temporary shunt inserted as
42
part of a “damage control “strategy.”
If ligation is required,
extra-anatomic (eg, axillofemoral or femoral) bypass with
prosthetic material can be used to restore perfusion to the
lower extremities. If the aortic bifurcation is preserved, a
INFRARENAL IVC AND ILIAC VEIN
e principles of controlling venous injuries, including use
of balloon tamponade and external pressure, have been previously described. e infrarenal IVC, iliac conuence, and
right iliac vein are exposed through a right medial visceral
rotation (see Fig. 13-7). e conuence of the iliac veins is
obscured by the aortic bifurcation and right common iliac
artery. If the aortic bifurcation cannot be suciently mobilized to provide exposure, the right common iliac artery
should be mobilized or even transected for additional exposure. is is often required in any event because concomitant
arterial injury is common. e more distal left iliac vein is
approached on either side of the descending/sigmoid colon
depending on the location of the injury.
As with the suprarenal IVC, lateral venorrhaphy is the
preferred approach, with autogenous vein patch or ligation as alternatives. If needed, the infrarenal IVC and iliac
veins can be ligated, due to the rather extensive collateral
network that can develop within hours. While this may
cause uid sequestration in the lower legs, it is usually tolerated in the short term and is preferable to an attempt at
repair in an unstable patient. In the rare case that ligation
results in extreme distal venous hypertension, a bypass
graft is indicated. In patients who have been stabilized, we
prefer venous repair, either with a vein patch or, when an
276 Part II Abdominal Wall
interposition graft is required, a ringed prosthetic conduit.
Successful venous repair must use a conduit of equal or
slightly greater diameter than the native vein and should
avoid any tension. Saphenous vein is of insucient diameter for replacement of the iliac vessels and must be modied to be useful (“panel” grafts”). We nd such panel grafts
excessively time consuming to construct in these critically
ill patients and prefer externally supported PTFE of suitable diameter and length. is is usually done in situ but
may be performed using an extra anatomic route. When
short segments of prosthesis are used in the presence of
distal venous hypertension, ow is usually sucient to
maintain patency without the need for anticoagulation or
an adjunctive stula. In our experience, when thrombosis
of a prosthetic vein graft does occur, adequate collateral
venous ow has been invariably present. e indication
for caval lters in patients with venous injury is not clearly
established and remains a manner of individual clinical
judgment.
TREATMENT OF TRAUMATIC
ARTERIOVENOUS FISTULA
Fistula between the major arteries and veins can occur at any
level, because the vessels are in close proximity throughout
their course. It is important to realize that, while this may
occur acutely, such a stula rarely represents a true vascular emergency. Exsanguinating hemorrhage does not occur,
because the arterial blood is decompressed into the venous
system. Most of these patients present months to years after
their initial injury. ese patients may present with a continuous bruit, signs of lower extremity edema, and high-output
54
cardiac failure.
Management depends on an accurate history of trauma, including prior surgery (particularly lumbar
disc surgery) or endovascular manipulation. Detailed vascular
imaging is essential. ese patients are rarely in extremis, and
an eort to delineate the problem and develop a careful plan
of correction is time well spent. Repair can usually be delayed
until the patient is stabilized and other acute problems are
corrected.
Treatment is directed at repair of both the arterial and
54,55
venous defect.
is is most often done by primary suture
closure, although patch closure is sometimes required. Proximal and distal arterial control is essential and is obtained
using open or endovascular techniques as described previously. Proximal and distal venous control should be obtained
when possible before opening the stula. is can be done by
external dissection, compression, or an intraluminal balloon.
Central venous occlusion is important to prevent air embolization when the vein is opened. We generally avoid extensive venous dissection in close proximity to the stula. On
occasion, venous control can be obtained by placing a balloon catheter through the stula from within the artery and
then closing the communication with interrupted or running
sutures (Fig. 13-14). In the acute circumstance, the artery and
vein may be separated, but this is more dicult in the case of
a more chronic stula and closure of the communication, by
FIGURE 13-14 Control of the aorta by nger dissection. e aortic
neck can be elevated o the spine and a clamp applied.
primary suture or patch, can be done from within the vessel.
If this approach is chosen, it is important to be sure that the
communication has been completely interrupted at the end
of the procedure by use of intraoperative ultrasound or angiography. Appropriate ushing of both the arterial and venous
sides is important to avoid embolization of debris or air into
the central venous circulation.
Arterial-venous communications can also be approached
56
endovascularly using covered stents.
e stent can be
placed only on the arterial side of the defect if the site of
injury is in a main artery and can be accurately identied.
However, it is important to remember that the arterial
injury may be in a branch of one of the iliac vessels, in
which case placement of a stent graft in the main artery
will not correct the abnormality. Detailed description of
repair of these branch stulae is complex and beyond the
scope of this chapter. Suce it to say that coil embolization
can be particularly dangerous in these cases due to the high
ow in the venous system and chance of central venous
embolization. A variety of techniques can be employed to
reduce this possibility. Endovascular treatment of these
lesions should only be undertaken by those with signicant
experience in endovascular techniques. As with open repair,
it is important to be sure that complete interruption of the
stulous communications has occurred using completion
angiography.
Chapter 13 Abdominal Vascular Emergencies 277
TRAUMA TO THE MESENTERIC
ARTERIES AND VEINS
e origin of the celiac axis is exposed through the gastrohepatic ligament or by a left medical visceral rotation as described
earlier. While a short bypass from the aorta to the bifurcation
of the splenic and hepatic arteries can be performed, the origin
of the celiac artery can be ligated safely, if necessary, in most
cases. is is preferable to attempting repair in a relatively
conned space in an unstable patient. Collaterals through the
pancreaticoduodenal and gastroduodenal are usually sucient
to preserve foregut ow. If there is any doubt, a bypass can
beperformed from the aorta to the common hepatic artery.
e splenic artery can be ligated, as can the splenic vein. In the
case of proximal injuries to these vessels, the short gastric vessels provide adequate collateral ow. When the splenic vessels
are injured close to the hilum, a splenectomy is usually the
best approach. Injuries to the common hepatic artery may be
ligated because of collateral circulation, while injuries to the
proper hepatic artery are more likely to require repair. In order
of preference, techniques are primary repair, interposition vein
graft, and aortomesenteric graft using either saphenous vein or
prosthetic. Two-thirds or more of hepatic ow is supplied by
the portal vein, and, if this is intact, proper hepatic artery ligation is an acceptable option. Intrahepatic arterial lesions are
generally treated with angiographically directed coil embolization unless massive exsanguination requires resection of the
damaged area of the liver.
Injuries to the main trunk of the SMA should be repaired
because signicant loss of small bowel may result from sacrice of the vessel. Ligation of proximal SMA aneurysms can be
performed with acceptable results, due to the presence of collaterals from the celiac and inferior mesenteric arteries. However, in the trauma setting, integrity of collateral pathways
from the pancreaticoduodenal and middle colic vessels is not
easily ascertained and repair should be performed. Lesions at
the origin of the vessel are best exposed by left medial visceral
rotation and repaired with a short bypass originating from the
aorta. More distal lesions are exposed through the base of the
small bowel mesentery and can be repaired by patch angioplasty, interposition graft using saphenous vein, or proximal
ligation and distal bypass arising from the aorta. In the trauma
setting, the infrarenal aorta is preferred as inow for the more
distal SMA because supraceliac exposure and control is best
avoided in patients who may be unstable and have multiple
injuries. Saphenous vein is the preferred conduit. e details
of SMA bypass have been described, including the need for
proper length and orientation to prevent kinking. Trauma to
the branches of the SMA is usually treated by vessel ligation
and any nonviable bowel is resected. Attempts to repair distal
arterial and venous injuries in the mesentery are not rewarding. Mesenteric hematomas that are not expanding and are
not associated with compromised bowel should be observed
initially with angiography as necessary to identify vascular
lesions. Attempts to explore stable mesenteric hematomas can
lead to excessive blood loss and vascular compromise, resulting in more bowel ischemia.
Injuries to the splenic vein are treated by ligation, with or
without splenectomy. ere is often an accompanying injury
to the splenic artery. In the rare instance of isolated splenic
vein injury, consideration should be given to concomitant
splenic artery ligation or splenectomy. Acute ligation of the
splenic vein alone may result in sequestration of signicant
amounts of blood within the spleen and left-sided portal
hypertension. is can be ameliorated by ligating the main
arterial inow to the spleen. Injuries to the main trunk of
superior mesenteric vein should be repaired to avoid bowel
ischemia secondary to mesenteric venous obstruction. If
the vein cannot be repaired using a patch angioplasty or
short interposition graft, a bypass from the superior mesenteric vein to the portal vein should be performed. is
probably will require a large (6- to 8-mm) conduit of either
reinforced PTFE or deep vein (jugular or femoral). Injuries
to the portal vein should be repaired if possible, by lateral
venorrhaphy, patch angioplasty, or interposition grafting, if
the patient isstable enough to undergo repair. e retropancreatic portal vein is best exposed by transection of the
pancreas (Fig. 13-15). Isolated injuries of the portal vein,
with an intact hepatic artery, may be ligated if necessary
to save the life of the patient, although signicant hepatic
dysfunction and acute massive bowel edema can be anticipated. is leads to signicant uid sequestration and may
even result in bowel necrosis. Lesions of the hepatic artery
FIGURE 13-15 Exposure of the retropancreatic portal vein by
division of the pancreas.
278 Part II Abdominal Wall
and portal vein that are not immediately lethal should be
repaired if possible.
Injuries to the inferior mesenteric artery can usually be
ligated, because adequate collaterals will exist from the
arc of Riolan, the marginal artery of Drummond, and the
hemorrhoidal vessels. Ifit appears that ligation will not be
tolerated, reimplantation or a short bypass with saphenous
vein is indicated.
INJURIES TO THE RENAL ARTERY AND VEIN
Management of renal artery lesions is dictated by the overall
status of the patient, duration of ischemia, and presence or
absence of a contralateral kidney. It is important to remember
that after 60 minutes of warm ischemia time, most of the
kidney’s excretory function is lost. While some authors
advocate renal vascular repair within the rst 3–6 hours after
injury, preservation of long-term renal function in these
57,58
cases has been poor.
erefore, situations in which there
is nonvisualization of one kidney on a preoperative CTA or
intravenous pyelogram (IVP) suggests that renal function will
not be salvaged by revascularization. In most cases of arterial
transection, ligation with nephrectomy is indicated. In cases
of blunt trauma observation is usually indicated. In circumstances where the status of the kidney is unknown or when
there is not a contralateral kidney, attempts at revascularization should be undertaken. e most expeditious approach
is aortorenal bypass for lesions of the main renal artery, using
saphenous vein with PTFE as a second choice. Lesions of the
more distal renal artery, at or beyond branch points, are best
ligated in the acute situation, unless they can be repaired with
a simple vein patch, or if the injury is to a solitary functioning kidney. If there is doubt about contralateral renal function, the ipsilateral (damaged kidney) ureter can be clamped
and indigo carmine administered intravenously. Appearance
of dye in the urine conrms contralateral kidney function.
Renal artery thrombosis due to blunt trauma, diagnosed as
lack of perfusion on CT scan, can be treated by endovascu-
59
lar placement of a stent
if the patient is otherwise stable.
However, salvage of a renal vessel in a patient with a contralateral functioning kidney remains a secondary priority in the
trauma patient’s overall management.
Lesions of the proximal renal veins may be ligated, as
long as collateral ow through the gonadal, adrenal, and
hypogastric veins is preserved. is works best on the left
side. While it is known that some transitory renal dysfunction will occur after renal vein ligation, it is generally well
tolerated. If inadequate venous collaterals exist or have been
damaged during the course of the injury, a short bypass
between the renal vein and the vena cava with 8- to 10-mm
PTFE can be performed, although ligation and nephrectomy is appropriate if the patient is unstable. Under rare
circumstances of injuries to the renal hilum, for example
with a solitary kidney, nephrectomy with ex vivo repair and
autotransplantation may be indicated. is extensive reconstructive surgery, however, is unwise in an unstable patient
with a contralateral functioning kidney.
TREATMENT OF RUPTURED
ABDOMINAL AND VISCERAL
ANEURYSMS
In the patient presenting with abdominal pain, pathology
of the abdominal aorta and its branches should always be
included within the dierential diagnosis. Because of their
rapidly catastrophic potential, prompt diagnosis and timely
treatment for ruptured abdominal aneurysms are mandatory
for patient survival and a successful outcome. While the most
common aneurysms of the abdomen involve the abdominal
aorta and iliac arteries, aneurysms of the visceral vessels may
also rupture and present as abdominal emergencies.
Ruptured Aneurysms of the
Aorta and Iliac Arteries
Although historically called atherosclerotic aneurysms, the
etiology of abdominal aortic aneurysms (AAAs) has come
to be recognized as multifactorial.
which includes elastin degradation, increased proteolytic
activity, inammation, matrix metalloproteinases, and other
factors, leads to the ultimate development of aortic expan-
61–63
sion and degeneration.
It is for this reason that the term
degenerative aneurysm better describes the pathophysiology of
64
AAAs. Familial
and sex-linked65 factors also likely contribute:
the incidence is several times higher in men, and the relative
risk for development of AAA among rst-degree relatives of
aected individuals is increased 11-fold. e infrarenal aorta
is the most common intra-abdominal location for aneurysmal
degeneration; aneurysmal degeneration of the suprarenal aorta
is much less common.
Despite advances in treatment and early diagnosis, AAAs
continue to be a signicant cause of death. In the United
States, AAAs are the 15th cause of death overall and the
10th leading cause among men older than 55 years.
improvements in the operative and perioperative management
of elective AAAs, coupled with the introduction and renement of endovascular techniques, ruptured AAAs overwhelmingly account for most of these deaths. Even among specialized centers, the operative mortality for ruptured AAAs is at
least 40%, a number that has remained constant over the past
67
three decades.
When one also considers the proportion of
patients who die without reaching the hospital, the mortality rate approaches 75%.
68
are notoriously asymptomatic until ruptured, much clinical
research has centered on the natural history of the disease, specically focused toward identiable risk factors for rupture.
e absolute diameter of the aneurysm is the principal determinant of rupture risk. As the diameter increases,
the risk of rupture increases nonlinearly, such that larger
aneurysms have a signicantly higher rupture rate. For
example, AAAs 5–5.5 cm have an annual rupture risk of less
than 5%, whereas those 6–7 cm in diameter have a 10–15%
69
annual risk of rupture.
ese “hinge points,” in which the
60
is complex interplay,
66
With
Accordingly, and because AAAs
Chapter 13 Abdominal Vascular Emergencies 279
rupture risk rises dramatically, are the basis for recommending elective repair for asymptomatic AAAs based on size alone
70
(in general, >5.5 cm in average risk patients).
Several other
factors also independently predict rupture risk. e strongest
risk factors are hypertension, chronic obstructive pulmo-
71,72
nary disease (COPD), and family history of AAA.
possible risk factors include rapid expansion (>0.4 cm annu-
73
female gender,74 and current smoking history.
ally),
Other
75
A
e classic presentation for ruptured AAA is abdominal
or back pain, pulsatile mass, and hypotension; however, this
complete triad is present in only a minority of patients. A
large pannus or abdominal girth may preclude appreciation
for a pulsatile mass; similarly, a blood pressure of 100 mm Hg
systolic in an otherwise hypertensive individual may be mistakenly interpreted as “normotensive.” Pain is almost always
a presenting symptom, and may include abdominal or back
pain, groin pain, testicular pain, or ank pain. Less commonly, a patient with a large ruptured AAA may be obtunded
and can present with hypotension only. e diagnosis of rup-
FIGURE 13-16 CT scan of ruptured abdominal aortic aneurysm
(AAA) with retroperitoneal hematoma.
tured AAA must be included among the dierential in every
patient older than 50 years presenting with abdominal pain,
abdominal pain and hypotension, or hypotension alone.
When a pulsatile mass is also appreciated, the diagnosis of
ruptured AAA is almost certain.
Much less commonly, an aortocaval stula may arise from
rupture into the adjacent IVC; signs and symptoms may
include a bruit, distended veins, and acute heart failure. In
general, these patients may be hypotensive but can usually be
is contemplated. e newer-generation multislice scanners allow for complete chest and abdominal imaging to be
completed in less than 5 minutes. Although intravenous contrast is very helpful in the planning for elective AAA repair,
it is not required for diagnosis in the patient with suspected
rupture and may exacerbate postoperative renal dysfunction.
Even with an endovascular approach, thin slice (2 mm) noncontrast CT can provide sucient information for repair.
resuscitated. Because their treatment is dierent from that of a
ruptured aneurysm, careful examination of the abdomen, with
an eort to identify a thrill or bruit, will help in diagnosis.
DIAGNOSTIC IMAGING
Ultimately, the role of imaging should depend on the
patient’s hemodynamic stability. In the patient with abdominal pain and hypotension and a pulsatile abdominal mass,
immediate transport to the operating room without imaging
is indicated. In the more stable patient, in whom the diagnosis is in question, abdominal ultrasound may be performed
rapidly in the emergency room to identify AAAs. When performed expeditiously by an experienced ultrasonographer,
the diagnosis of ruptured AAA may be rapidly conrmed.
However, the technique is operator-dependent and accuracy
may be limited by excessive bowel gas and obesity.
CT scanning is the most accurate and useful radiographic
method in the evaluation of ruptured AAA (Fig. 13-16).
e most common ndings are retroperitoneal hematoma,
an aneurysmal aorta, and retroperitoneal stranding of blood.
76
With 100% specicity and a very high sensitivity,
CT can
reliably conrm or rule out the diagnosis of ruptured AAA as
well as identify alternative nonvascular causes of the patient’s
symptoms. It also yields important anatomical information
about adjacent structures (such as a retroaortic left renal vein,
horseshoe kidney, or concomitant iliac aneurysms) and about
the aneurysm itself (such as an inammatory AAA). CT
scanning is particularly important if endovascular repair
FIGURE 13-17 Control of lumbar vessels from within the aneurysm
using mattress sutures to encircle the vessel.
280 Part II Abdominal Wall
PREOPERATIVE MANAGEMENT
Once the diagnosis of ruptured AAA is made, either by
clinical presentation or radiographically, the patient should
be taken immediately to the operating room. Large-bore
intravenous access in the upper extremities (or central
venous access), indwelling urinary catheter, type and crossmatch for at least 6 units of packed cells, and chemistry
and coagulation studies should all be performed. Because
elevated blood pressure may lead to frank rupture of an
otherwise contained leak, a strategy of permissive preoperative hypotension with minimal uid resuscitation has been
recommended. Although no rigid blood pressure parameter
exists, most vascular surgeons would favor a minimum systolic pressure to maintain consciousness (usually around
80mm Hg systolic).
OPEN REPAIR
Open repair remains the most common and versatile
approach to ruptured AAA. Because general anesthesia will
lead to both generalized vasodilatation and relaxation of the
abdominal musculature, both of which can produce abrupt
hypotension; the patient must be prepped and draped (“nipples to knees”) and the surgical team scrubbed prior to induction. A cell saver device should be set up and used when possible. A midline incision is performed for rapid access to the
supraceliac aorta. After induction, the abdomen is opened
from xiphoid to pubis. e abdomen and retroperitoneum
are inspected. If a small or moderate retroperitoneal hematoma is found without intraperitoneal blood, the supraceliac
aorta is controlled, as described earlier, but the artery is not
clamped. If the juxtarenal aorta is spared of hematoma, this
area may be dissected and a clamp applied directly below the
renal arteries. Should bleeding develop during the course of
this dissection, the supraceliac clamp is applied.
If intraperitoneal blood is present, rapid supraceliac aortic control is obtained, usually by manual compression at the
diaphragmatic hiatus while the anesthesiologist rapidly continues resuscitation. e supraceliac aorta is then exposed
as previously described and occluded with a vascular clamp.
Once the cross clamp is placed, the distal aorta is palpated to
conrm obliteration of the pulse and attention is turned to
the aneurysm. In patients with massive rupture, bleeding, or
hypothermia, in which coagulopathy is almost certainly present, heparin is not given. In such cases, thrombectomy of the
distal vessels and vigorous ushing of the graft are necessary
prior to restoring ow. In all other cases, we give a small dose
of heparin, 40–50 U/kg.
ere is an increasing tendency to obtain intravascular
supraceliac balloon control of the aorta prior to celiotomy.
77
is is performed by passing a wire and then a balloon into
the supraceliac aorta via either a retrograde transfemoral or a
prograde transbrachial approach, as described earlier in the
chapter, before induction of anesthesia. is requires intraoperative uoroscopic capabilities and catheter/guidewire skills.
is approach provides less invasive and more rapid control
of the supraceliac aorta and can facilitate resuscitation of the
patient in circumstances of profound shock.
e aneurysm is approached by evisceration of the transverse colon and omentum cephalad and the small bowel to
the right. Care is taken not to injure the IVC or the inferior
mesenteric, gonadal, or left renal veins. In most cases, the
retroperitoneal hematoma facilitates the dissection. Eorts
are made to identify an infrarenal neck of the aneurysm and
place a clamp at this level. When there is a free rupture of the
aorta, the surgeon can pass the ngers of one hand through
the rupture into the aorta (after application of the supraceliac clamp) to help locate the proximal neck of the aneurysm.
Bimanual palpation can facilitate the placement of a clamp
above the aneurysm without extensive dissection. Once
the aortic neck is controlled, the iliac vessels are dissected
to allow for clamping and control. Because the iliac veins
often adhere to the artery, circumferential dissection around
the iliac arteries should be avoided to prevent vein injury.
In most cases, the iliac arteries may be readily clamped with
minimal dissection. However, if the dissection is dicult,
as with a large distal hematoma, endoluminal control may
be obtained using a number 5 occlusion balloon, placed in
each iliac artery after opening the sac. Once the aneurysm
has been isolated proximally and distally, the sac is opened
longitudinally and thrombus evacuated. Bleeding from the
lumbar vessels is controlled with direct suture ligation using
a mattress suture (Fig. 13-17). Venous bleeding encountered
inside the sac suggests an aorto caval stula. In those cases
the patient should be placed in mild Trendelenburg’s position to reduce the chance of air embolus and the venous
bleeding controlled by pressure. e defect is oversewn from
within the aneurysm sac, with gentle digital or spongestick
compression of the cava proximally and distally (Fig. 13-18).
No attempt is made to clamp or mobilize the cava.
Because of the signicant risk of colon ischemia following
ruptured AAA repair, reimplantation of the IMA should be
77
considered in cases of ruptured AAA.
Brisk back bleeding
suggests adequate SMA collaterals and implantation is not
required. If the IMA is patent and back bleeding is absent or
sluggish, reimplantation of the IMA should be planned after
aortic repair. In these cases, the IMA is controlled just outside
the aneurysm sac with a small bulldog clamp, and after the
aortic repair the IMA is reimplanted on the aortic graft using
a Carrel spatulated patch. An IMA that is obviously occluded
at its origin is not reimplanted.
With the aneurysm opened and bleeding controlled, the
graft may be sewn in place. When possible, this is done with
an infrarenal clamp in place. It is absolutely mandatory that
the proximal anastomosis be sewn meticulously into relatively healthy (nonaneurysmal) aorta. Poorly placed sutures
in friable aorta will lead to proximal suture line bleeding
once clamps are removed. If a secure anastomosis cannot
be performed with an infrarenal clamp, the proximal anastomosis should be done with a suprarenal clamp in place.
Tamponade of visceral back bleeding may be required while
this is performed by placing an inated balloon catheter
through the aneurysm neck into the visceral aorta. Sutures
Chapter 13 Abdominal Vascular Emergencies 281
FIGURE 13-18 Repair of an aortocaval stula from within the
aneurysm. Venous back bleeding is controlled with sponge sticks. is
avoids dangerous dissection of the vena cava.
must be placed in the aorta precisely and without tension or
torsion of the needle. e proximal anastomosis may be reinforced with a Teon felt pledget. Once the proximal anastomosis is completed and judged to be satisfactory, heparinized
saline (5000 U/1000 mL saline) is ushed into the graft and
the graft clamped. e distal anastomosis is then performed
in a similar fashion. If heparin had not been given, a number 4 balloon thrombectomy catheter is gently passed down
each iliac artery to extract thrombus. e graft should also be
ushed to ensure adequate forward ow and the anastomosis
is then completed (Fig. 13-19).
e anesthesiologist should be notied before release of
the distal clamps. One leg should be perfused gradually, once
the pressure has stabilized, the contralateral leg may be perfused. Pulses are checked at the femoral level and should be
palpable; if not, thrombus or emboli are likely present and
should be treated with thromboembolectomy. With the
blood pressure stabilized and following a period of adequate
perfusion, both feet should be assessed. Although palpable
pulses may not be present, the feet should appear viable with
reasonable capillary rell with Doppler ow.
Once adequate perfusion to the lower extremities has been
achieved, the colon should be assessed. e colon should
appear pink and Doppler ow should be present ideally at the
antimesenteric border. If the colon appears ischemic, IMA
reimplantation should be performed if not already done.
FIGURE 13-19 Aortic tube graft in place for treatment of aortic
aneurysm.
Hemostasis should be assured as best as possible prior to closure, and this may require infusion of additional clotting factors
and protamine if heparin were given. e aneurysm sac is closed
snugly around the graft with a running suture to obliterate the
dead space and provide some hemostasis. e intestines should
be excluded from contact with the graft as best as possible, usually by closing the proximal retroperitoneum or occasionally
with a mobilized segment of omentum.
If the abdomen can be closed without tension, the linea
alba is approximated and closed with a running suture.
However, in many cases, the substantial hematoma precludes
closure, and to prevent the development of abdominal
compartment syndrome, the abdomen is left open with
subsequent delayed closure several days later.
ENDOVASCULAR REPAIR
e rationale for endovascular repair (EVAR) for ruptured
AAAs is extrapolated from data showing less blood loss
and improved outcomes in patients undergoing elective
78
endovascular AAA repair
and from direct data from spe-
cialized centers demonstrating encouraging results with
79,80
ruptured AAAs.
EVAR requires accurate assessment of
aneurysm geometry using either CT scan or intraoperative calibrated angiography. Accepted anatomic criteria for
EVAR include (1) aortic neck diameter between 18 and