Although vascular injuries constitute between 0.25% to 3.

7% of all trauma (civilian and military)(Caps  

1998), morbidity from the resultant limb-threatening ischaemia and life-threatening haemorrhage is high.
Mortality rates range from 13 to 25% and in one series was more than twice that of patients without
vascular injuries (Oller et al. 1992). Patients also tend to have higher injury severity scores, longer hospital
stays and incur a greater economic burden.

Penetrating vascular injuries account for 50% to 90% of all vascular trauma (Frykberg 1995). The majority
of penetrating civilian vascular injuries are caused by low-velocity weapons (handguns, knives, picks).
High velocity missile penetration results in injuries of greater severity largely due to cavitation effect (Holt
and Kostohryz, 1983). This pattern is commonly seen on the battlefield although the increasing use of
military weapons in the civilian sector has resulted in the rising incidence of such injuries seen in civilian
hospitals.

Blunt vascular trauma is frequently associated with more severe injuries and higher kinetic forces. There is
a higher incidence of blunt vascular trauma in a civilian setting, mainly due to the higher incidence of motor
vehicle accidents and falls from heights. Certain orthopaedic injuries, e.g. joint dislocations, pelvic
fractures, are also associated with a higher incidence of blunt vascular injury. For instance, 23% of patients
with knee dislocation have been found to have blunt popliteal artery injury on angiography (Trieman et al.
1992). Vascular injuries resulting from blunt trauma also have poorer outcomes because of the greater
extent of associated injury to surrounding tissue. The spectrum of vascular injuries is shown in Fig. 12.1.

Iatrogenic vascular trauma is on the rise due to the increasing number of invasive diagnostic, monitoring
and therapeutic procedures being performed (Nehler et al. 1998). Also becoming more common are
vascular injuries in intravenous drug abusers, which range from arterial and venous thromboembolism,
false and mycotic aneurysms to arteriovenous fistulae (Yellin et al. 1995).

Initial assessment

History
In major trauma, the history is often not available or given by a witness or emergency medical technician.
However, the mechanism of injury gives valuable clues to the extent and pattern of trauma and has
important prognostic implications. Shear forces from deceleration can result in significant lacerations of
major visceral vessels. The energy dissipated by a projectile is proportional to its velocity and therefore
one can expect extensive tissue damage with high velocity missiles. Because of the effects of cavitation,
injuries may be produced in a remote site. In contrast, most of the damage caused by low velocity injuries
is confined to the tract of the weapon.

The time of injury should be noted as the incidence of limb loss has been shown to be related to the
duration of ischaemia. The classic experiment conducted by Miller and Welch (1949) where they ligated
the femoral artery in dogs and restored perfusion at different time intervals, showed the limb salvage rate
to be 90% with an ischaemic time of less than 6 hours, 50% from 12 – 18 hours, and only 20% when
circulation was interrupted for more than 24 hours Debakey and Simeone also showed a rising amputation
rate with delays in definitive treatment of vascular injuries beyond 10 hours sustained by casualties during
World War II. These and other empirical observations indicate that the critical period of limb ischaemia
from vascular injury should not exceed 6 to 8 hours for the results of revascularization to be optimal
(Fletcher 1992).
It should also be noted that some vascular injuries may not present immediately and may be delayed for
anything from a few days to months. False aneurysms may present months or even years later and it is
prudent to inform the patient suspected of sustaining vascular trauma of this possibility.

Physical examination.
A good clinical examination is still paramount in the diagnosis of vascular injuries. One study of 2,674
patients evaluated a year after the initial trauma showed that physical examination yielding hard signs of
vascular injury (Table 12.1) had a positive predictive value of nearly 100% of penetrating vascular trauma
requiring surgery, with a false negative rate of 0.7% missing only two vascular injuries (Frykberg et al.
1991).

During the secondary survey, the extent of the vascular injury should be carefully documented. Dressings
and bandages controlling actively haemorrhaging wounds should only be taken down in the operating
room. In missile injuries, the entry point and exit wound should be examined and the path of the missile
determined if any major vascular structures are at risk of being traversed. Bear in mind possible ricochet
effects and shrapnel can also result in vascular injury in sites outside the path of trajectory.

Pulses should be ascertained but the presence of a pulse does not exclude vascular injury. In one study,
64% of patients with proximal thoracic vascular injuries had palpable peripheral pulses (Calhoon et al.
1992). Capillary refill and skin temperature are unreliable signs as patients may be vasoconstricted from
shock or exposure to cold. An expanding haematoma and the presence of a pulsatile mass are hard signs
of vascular injury (see Table 12.1) (Frykberg et al. 1991).

Auscultation may reveal a bruit – a systolic bruit suggests a false aneurysm, and a continuous bruit
suggests an arteriovenous fistula.
A neurological examination is not only important to document associated peripheral neural injury, but may
also reveal signs suggestive of compartment syndrome (paraesthesia, paralysis). It is especially important
in evaluating injuries to the head and neck region where blunt carotid artery trauma may result in
hemiparesis or even hemiplegia.

Where a joint dislocation has occurred, the dislocated joint should first be reduced as far as possible and
the arterial circulation re-assessed. If a pulse deficit still persists, then the patient should proceed to further
diagnostic imaging. It should be noted that vasospasm my take several hours to resolve following
reduction of a dislocated joint, and as such, it may be prudent to re-assess the patient for distal pulses
later, especially if other hard signs of vascular injury are not present. (Fig. 12.2)
In some patients, assessment of the pulses may be difficult due to tissue swelling. The highest systolic
pressure in the pedal arteries should be obtained and its ratio to the brachial pressure, called the ankle-
brachial index (ABI), calculated. It should be remembered that the mere presence of a pulse on Doppler
does not exclude vascular injury.

Investigations
Angiography has been the gold standard in the evaluation of patients suspected of possible traumatic
vascular injury. However, angiography is not without its attendant risks, increases the cost of trauma care,
and may also delay definitive treatment. Careful selection of patients for angiography is needed. In the
absence of objective clinical findings, angiography for “proximity” wounds reveal arterial injury in less than
10% of patients (Weaver et al. 1990).

Non-invasive vascular testing has been found to be reliable in excluding occult extremity arterial trauma.
Johansen et al found that an ankle-brachial index (ABI) of less than 0.9 had a sensitivity and specificity of
detecting major arterial trauma of 95% and 97% respectively (Johansen et al. 1991). Conversely, the
negative predictive value of an ABI greater than 0.9 was 99% in excluding major vascular injury.

Hood and Weaver (Hood et al. 1998) have proposed an algorithm (Fig. 12.3) based on the use of the
ankle-brachial index to stratify patients according to their risk of vascular injury. In their analysis of 514
patients who had penetrating extremity trauma, patients with hard signs of vascular injury (Table 12.1)
proceeded to operative repair and on-table angiography. Those with “soft” or no signs of vascular injury
were classified as either of intermediate risk (ABI < 1.0 or pulse deficit) or low risk (ABI > 1.0, no pulse
deficit).

Those at low risk of injury were managed by close observation and did not develop further signs of
vascular injury in the first 24 hours of observation and on follow-up. The intermediate risk group proceeded
to angiography, and the sensitivity of an ABI of less than 1.0 in predicting major arterial injury was 96%.
The negative predictive value of an ABI greater than 1.0 was 99%. The authors concluded that patients
who have a normal pulse and an ABI of greater than 1.0 do not require angiographic evaluation. All
clinically occult injuries requiring intervention were found in extremities with a distal pulse deficit or an ABI
of less than 1.0 or both.

Duplex ultrasound has emerged as a useful modality for screening and follow-up of patients with vascular
injury. Indeed, definitive diagnosis is often possible in the vessels of the extremity and the neck region.
Several studies have correlated its accuracy with angiography and operative findings, yielding sensitivities
of between 90-100% and specificities of 98-100% (Brynoe et al. 1991, Fry et al. 1993, Kuzniec et al.
1998). It is particularly useful for distinguishing pseudoaneurysms from haematomas (Jargiello et al. 1998).
Intimal flaps and arteriovenous fistulae can be identified on B-mode and colour-flow duplex. Arterial
occlusion gives a characteristic “thump” on pulsed wave

Doppler. Associated venous thrombosis and isolated venous injuries can also be detected (Gagne et al.
1995). Some centres are now utilizing duplex ultrasound as the primary modality of imaging for detecting
vascular injuries, which has the advantage of lower cost as well as virtually nil procedural complication rate
(Fry et al. 1993).

Key points

• Note duration of ischaemia

• Reduce fractures/dislocations first before assessment

• Check peripheral pulses of ALL limbs

• Look for “soft” and “hard” signs

• Obtain ankle (or wrist) - brachial systolic pressure index

• Vasospasm may occur in blunt injury - reassess later if limb not threatened

General principles of management

The principles of resuscitation must be upheld – securing the airway is a priority. Providing supplementary
oxygen via face mask or nasal prongs ensures optimal oxygenation of blood in both haemorrhage and
ischaemia .

Active haemorrhage should be controlled by direct pressure and packing. The use of tourniquets and blind
arterial clamping should be avoided. Appropriate fluid resuscitation should be administered according to
the severity of the injury.

The stable patient suspected of arterial injury should be managed according to the algorithm above. Not all
vascular injuries require surgical intervention and some can be observed (Table 12.2) (Stain et al. 1989). If
a non-operative strategy is adopted, close monitoring of vital signs and the affected extremity, with repeat
assessment of the injury for progression by angiography or duplex ultrasound, is mandatory.

The haemodynamically unstable patient should be brought to the operating room without delay. Undue
delays in obtaining angiography should be avoided as this can be performed on the operating table if
necessary (Fletcher and Little 1981).

The management plan and priorities in treatment for the patient must be decided and agreed upon in the
presence of all the various teams involved. The patient should be positioned to allow both vascular and
orthopaedic surgical approaches. A radiolucent operating table should be utilized as far as possible to
facilitate imaging. Autotransfusion devices (e.g. Cell-Saver®) and a full range of vascular instruments
(Fogarty balloon catheters, arterial clamps, shunts, etc.) should be available.

The uninjured lower limb should also be prepared for saphenous vein harvesting if required.

The preferred surgical incision in the extremity would be along the injured vessel’s anatomical course, as
in an elective procedure. Existing open wounds may be extended in the line of the vessel. Care should be
taken to preserve as many collateral vessels as possible during dissection. The injured vessel is explored
to expose a normal segment proximally and distally. It should be remembered that thrombosis can and will
usually extend well proximal to the point of injury, and every attempt should be made to expose healthy
artery distally.

Systemic heparinization may increase the risk of bleeding in multitrauma patients and should be used
cautiously. It is generally best avoided except in isolated penetrating injuries. Most patients with significant
haemorrhage would already be in a mild coagulopathic state and local administration of heparinized saline
usually suffices.

Vasospasm is common in trauma but may also mask underlying intimal damage. A segment in spasm can
be treated with topical papaverine and flow reassessed. An embolectomy catheter should be used to
gently retrieve any clot from the distal arteries until good backflow is seen.

The intima of the injured vessel should be inspected carefully, and preferably with the aid of magnifying
loupes. Any segment of artery with damaged intima should be resected, other than a simple flap, which
can be successfully tacked. End-to-end anastomosis of transected vessels should only be attempted if
tension-free with adjacent joints in full extension.

Where an interposition graft is required, autogenous saphenous vein is the conduit of choice. Size
discrepancy is usually well-tolerated and is not an issue in vessels of the extremity. The ends are
spatulated, stay sutures may be used for approximation, and either continuous or interrupted
polypropylene sutures are used for the anastomosis. In children, interrupted sutures are used to permit
radial growth of the vessel. The proximal end is best constructed first to allow an accurate estimation of the
length when the vein graft is distended with arterial inflow. When vein is not available, prosthetic material
has been used with good results and low infection rates. Soft tissue cover is desirable to protect the
anastomoses regardless of the material used.

Postoperative monitoring of the peripheral circulation is mandatory. Early thrombosis is usually technical
and should be re-explored. The use of anticoagulation or rheologic agents should only be used as an
adjunct in carefully selected cases. The early signs of compartment syndrome (see section on reperfusion
injury) should be recognized and fasciotomy undertaken if any concern arises.
Management of concomitant orthopaedic injuries

The question of whether concomitant orthopaedic injuries should be stabilized first or vascular repair
proceeded with initially remains controversial. In broad terms, the vascular injury takes priority because of
ongoing limb ischaemia or haemorrhage. But where there is an unstable fracture, e.g. an open book
fracture of the pelvis, this should be stabilized first. A dislocated joint should also be first reduced before
arterial injuries are assessed and managed. With all other stable orthopaedic fractures without gross
deformity, the vascular injuries should be repaired first to minimize ischaemic time. The fear of disrupting
an initial vascular repair by orthopaedic manipulation is largely unfounded (Winkelaar and Taylor 1998).

An exception could be made if the degree of limb ischaemia is mild. For instance, in patients with vascular
injuries of upper limb, where the collateral circulation is usually adequate, it may be expedient to stabilize
any associated orthopaedic injury first. The patient in Fig. 12.4 a & b sustained open humeral and
radial/ulnar fractures resulting in a ‘floating’ elbow following a motor vehicle accident. He had lost his distal
arterial pulses and angiography was performed. The bony injuries were fixed first and the brachial artery
explored and repaired with an interposition vein graft. The postoperative angiogram is shown in Fig. 12.4c
& d demonstrating good restoration of perfusion to the distal forearm and hand, preserving limb viability.

Where the collateral circulation is deemed inadequate or where limb viability is threatened, and
orthopaedic stabilization is imperative, the use of temporary plastic or silastic shunts (e.g. Javid®) may be
employed to re-establish perfusion to the distal extremity. Definitive vascular repair can then be safely
undertaken later once the orthopaedic injury has been fixed.

Key points

• Control active haemorrhage with direct pressure.

• DO NOT APPLY A TOURNIQUET

• Supplemental oxygen by face mask

• Unstable fractures usually stabilised first

• Surgical approach to expose healthy artery proximally and distally

• Defects > 2 cm should be repaired with interposition vein grafts

• Assess for compartment and reperfusion syndromes

Specific vascular injuries

Cervico-thoracic vascular injuries

Monson and Freeark (1969) divide the neck into three anatomical zones for managing penetrating cervical
trauma. Zone I extends from the sternal notch to 1 cm above the clavicular head, zone II from this point to
the angle of the mandible and zone III from the angle of the mandible to the base of the skull. He proposed
that stable patients with injuries in zone I and III should be evaluated with angiography, a view which is
generally held today. Controversy surrounds the management of zone II injuries, which Monson proposes
warrant mandatory exploration. However, several series of mandatory exploration yielded a negative rate
of 40-60% (Byrne 1995), and one study showed that physical examination alone is a good predictor of
arterial injury (Beitsch et al. 1994). The use of duplex ultrasound has also made it possible to accurately
diagnose zone II vascular injuries without the risk of angiography.

High cervical (Zone III) injuries of the internal carotid artery, if stable, should be managed conservatively or
with angiographic embolization (with either coils or detachable balloons) (Ditmars et al. 1997). Surgery is
reserved for patients who are actively bleeding, or require surgical exploration for associated injuries.

Surgical exposure of Zone II injuries is best achieved with an oblique incision along the anterior border of
the sternomastoid, and if a high carotid injury is suspected, adjunctive measures such as nasotracheal
intubation, division of the posterior belly of the digastric muscle and jaw subluxation may be necessary for
access. A Fogarty balloon catheter may be useful in controlling bleeding from the distal internal carotid
arteries. Primary repair may be attempted but seldom achieved. Patch angioplasty or interposition graft
using autogenous saphenous vein is usually necessary. The branches of the external carotid may be
ligated with impunity.

Blunt carotid trauma constitutes between 3 to 10% of all carotid artery injuries (McIntyre and Ballard 1998).
It can arise from a direct blow to the neck, from hyperextension injury, intraoral trauma (in children) and
skull-base fractures (Beitsch et al. 1994). There is a high association with other injuries. More than half of
these patients may develop neurological signs ranging from transient ischaemic attack to dense
hemiplegia. There is usually a characteristic delay in the onset of symptoms. The usual arterial lesion is a
dissection or intimal flap resulting in thrombosis. The prognosis is generally poor and in this situation
conservative management is recommended. Surgical thrombectomy has not resulted in improved
outcomes in patients who have neurological deficits compared with anticoagulation alone (Teehan et al.
1997, Englund et al. 1988). Patients are anticoagulated for 3 to 6 months. Some thrombosed arteries do
recanalize on follow-up.

Management of arterial injuries at the root of the neck and thoracic outlet (Zone I) involving the subclavian,
common carotid and innominate arteries presents a major challenge to the surgeon. These arteries are
well-protected within the thoracic cavity and their injury reflect the magnitude of the incident forces.
Claviculectomy, median sternotomy, and trap door incisions may be required for proximal vascular control
and repair. Outcomes are generally poor due to the high incidence of associated head and major truncal
and soft tissue injury (Fletcher 1988).
Injuries of the thoracic aorta are dealt with in the chapter on chest trauma.

Abdominal vascular injuries

Whether retroperitoneal haematomas should be explored would depend on the mechanism of injury. As a
rule, all penetrating injuries should be explored as the extent of vascular disruption is usually limited and
amenable to direct repair. The exception would be with stable perinephric haematoma, where preoperative
CT evaluation has excluded major pedicle injury or extravasation of urine, it would be permissible to follow-
up the patient with serial imaging (see section on Renal Trauma).

Injuries of the abdominal aorta may present as a central retroperitoneal haematoma. Depending on the
level of injury, a left medial visceral rotation may be necessary to obtain full exposure of the aorta. This will
also expose the coeliac axis, proximal superior mesenteric artery and the left renal artery. Isolated
lacerations of the aorta may be repaired primarily. More extensive injuries may require the use of
prosthetic graft material. To minimize the risk of prosthetic graft infection in the presence of concurrent
bowel injury, rifampicin-soaked gelatin-sealed grafts may be used together with meticulous debridement of
all devitalized tissue and copious irrigation of the peritoneal cavity. In extreme contamination, aortic ligation
below the renals with axillobifemoral bypass may be performed.

Exploration of haematomas associated with pelvic fractures should be avoided, unless the patient is
exsanguinating. The pelvic fracture should be stabilized before assessment of ongoing haemorrhage is
made. Bleeding is best controlled via angiographic embolization.

Injuries of the inferior vena cava may also produce a central retroperitoneal haematoma. Exposure is
obtained by a right medial visceral rotation (Kocher manoeuvre). Control is best obtained by the use of
sponge sticks or using a side-biting Satinsky clamp. Up to 50% reduction in the diameter of the cava
following repair is well tolerated.

Wherever possible, the splanchnic vessels should be repaired. The superior mesenteric artery if injured in
its proximal segment should be reconstituted due to the high incidence of bowel necrosis with ligation. The
coeliac and inferior mesenteric arteries can be ligated if necessary as long as the superior mesenteric
artery is intact, as the collateral supply through the gastroduodenal or marginal arteries is usually
adequate. Injuries to the liver , hepatic vasculature and the retrohepatic cava are dealt with elsewhere in
this book.

It may be necessary to monitor the intraabdominal pressure postoperatively to detect abdominal

compartment syndrome. This is characterized by a tense abdomen, oliguria/anuria, increased airway
pressure and ventilatory requirements, and decreased cardiac output (Schien et al. 1995). Prompt reversal
of these manifestations are obtained with decompression. An intraabdominal pressure of greater than 30-
35 mmHg mandates surgical re-exploration (Kron et al. 1994).

Venous injuries

Venous injuries constitute about 35-63% of all extremity vascular trauma (Frykberg 1995), the majority of
which are associated with major arterial injury (Rich et al. 1992). The management of venous injury has
been embroiled in controversy over the past few decades. Ligation used to be favoured over repair due to
the high incidence of thrombosis of such repairs and the fear of thromboembolism, which is probably
unfounded. The impetus for venous repair is derived from experimental and clinical studies showing that
ligation is associated with increased morbidity from high venous pressures following venous ligation
leading to oedema, compartment syndrome and even impaired arterial inflow threatening limb viability
(Rich 1992). However, venous repair is associated with a high rate of thrombosis, which does not appear
to affect limb salvage. Recanalization may subsequently occur in these thrombosed segments (Nypaver et
al. 1992). Recent clinical data now suggests that adverse long term sequelae from extremity venous
ligation are minimal, and most complications that arise are transient, and often manageable with
conservative measures such as limb elevation and compression (Meyer et al. 1992).

Major proximal extremity venous injuries should only be repaired if the patient is stable, and can be
performed primarily with lateral suture or end-to-end anastomosis. In unstable patients with multiple
injuries or in venous injury in the distal extremity, ligation should be performed. Where major arterial and
venous injuries coexist, it is recommended that venous repair be performed first to facilitate venous outflow
upon revascularization, avoiding severe limb oedema. A temporary shunt can be used to restore arterial
perfusion in the interim.

Reperfusion syndromes

Much of the morbidity from vascular injury occurs with re-establishment of flow to ischaemic tissue.
Compartment syndrome is the term given to the pathophysiological effects of elevated tissue pressure.
The muscle compartments most susceptible to damage are those in the calf and the forearm. Following
successful revascularization, if prophylactic fasciotomy has not already been done, monitoring of
compartmental tissue pressure by clinical observation is mandatory looking out for pain and pain on
passive stretching of the muscles within the compartment. The tissues most sensitive to tissue hypoxia are
the type C sensory fibres carrying fine touch. A later symptom of compartment syndrome is the
development of previously undocumented paraesthesia.

Where compartment syndrome is suspected, intracompartmental pressures may be obtained using a

simple manometric device shown in Fig. 12.5. Normal tissue compartmental pressure should be less than
8 mmHg (Whitesides et al. 1975). Fasciotomy is clinically indicated when the tissue compartment pressure
exceeds 30 mmHg. Other experimental means of detecting the clinicopathological effects of raised
intracompartmental pressure include the detection of abnormal venous haemodynamics on duplex
ultrasound (Ombrellaro et al. 1996), and diminished somatosensory evoked potentials (Present et al.
1993).

Complete fasciotomy in the leg consists of release of all four compartments: the anterior, lateral (peroneal),
and the superficial and deep posterior compartments. This can be achieved through either a single lateral
incision or more commonly through two separately placed skin incisions (Gulli and Templeman 1994). (Fig.
12.6.) The incisions made laterally should extend from the fibular head to the malleolus. Access to the
deep posterior (soleal) compartment may be difficult and the best strategy is to start at the distal tendinous
portion of the gastrocnemial-soleal muscle complex. If there is any doubt, a complete decompression of
the deep compartment can be achieved with a middle third fibulectomy.

Closure of fasciotomy may be performed once tissue swelling subsides, usually within 7 to 14 days. The
problem of skin retraction can be countered by threading a soft vessel loop through strategically placed
skin staples in a “shoelace” fashion and tightened daily (Berman et al. 1994). Commercial devices are also
available to facilitate skin apposition. If two incisions are made, one can be closed primarily and the other
grafted with a split-skin graft.

Other compartments that may be affected include the forearm, where decompression of both
compartments may be achieved through a single incision on the volar aspect of the forearm starting from
the elbow down to the wrist, including the carpal tunnel. The muscles of the foot may sometimes be
affected, characterized by pain and swelling in the plantar region following revascularization, and may
have to be decompressed as well with incisions over the dorsum and over the medial plantar aspects of
the foot.

The other consequence of revascularization of ischaemic skeletal muscle tissue is the myonephropathic
syndrome (Haimovici 1973). The breakdown of a large mass of ischaemic muscle tissue leads to
metabolic abnormalities such as hyperkalemia, metabolic acidosis, elevated creatine kinase, lactate
dehydrogenase and myoglobinuria. Myoglobin precipitation within the tubules may result in acute tubular
necrosis and renal failure. In severe cases the adult respiratory distress syndrome and even cardiac arrest
may ensue. Recent evidence suggest that mannitol, besides its diuretic effect, also acts as a scavenger of
free oxygen radicals generated during ischaemia, which have been implicated in the pathogenesis of
reperfusion syndrome (Shah et al. 1996). Alkalinization of the urine is beneficial and diuretics such as
frusemide which acidify the urine should be avoided. Patients should also be adequately hydrated to
replace the diuretic loss. Metabolic acidosis and other electrolyte derangements should be treated
aggressively.

Endovascular treatment

Angiographic intervention in the treatment of vascular injuries is not new but its indications are expanding.
Major pelvic bleeding is often difficult to control surgically and has traditionally been treated by
embolization, particularly in the unstable patient.
Injuries of arteries not surgically accessible (e.g. distal internal carotid artery and carotid-cavernous
fistulae) may also be treated by embolization with coils or detachable balloons.
There are reports of successful obliteration of false aneurysms of the aorta using stents covered with vein,
polytetrafluoroethylene, or polyester (White et al. 1997, Scharrer et al. 1998, Parodi et al. 1999).
Traumatic arteriovenous fistulae may also be treated in the same way. Initial results have been good, but
the long-term patency and function of these stent-grafts remain to be evaluated (Parodi et al. 1999).

An endovascular approach to the treatment of vascular injuries has the advantage of being minimally
invasive and is able to treat vessels which are difficult to access through conventional surgery.