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16 • Cardiac, Great Vessel, and Pulmonary Injuries 195
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control. Phelan et al. have reviewed these principles as summarized in Box 16.3.
106
COMPLICATIONS
Air Leak
An air leak that persists after pulmonary injury is caused
by necrosis of the parenchyma at the site of sutures or staples, failure of an injured lung to heal, or a missed bronchial injury. Once technical problems have been excluded
including leaks in the thoracostomy tube circuit outside of
the chest, some centers choose to lower suction pressure
on the underwater seal system or even take the patient's
thoracostomy tube off suction. Failure of this approach
after 5 to 7 days is followed by wedge resection of the
remaining lung, pleural abrasion, or chemical pleurodesis
by thoracoscopy with a double-lumen endotracheal tube
in place with timing depending on the cause of the pneumothorax.
Ventilator-Associated Pneumonia
Ventilator-assisted pneumonia (VAP) is a nosocomial complication seen in both trauma and nontrauma patients in
the ICU. New onset purulent sputum, elevation of temperature, leukocytosis (occasional leukopenia), inltrate on
chest x-ray, and an increasing oxygen requirement are suggestive, but not diagnostic of VAP. Fiberoptic bronchoscopy
with lavage or protected specimen brush for culture is the
Box 16.3 Damage Control for Thoracic Trauma
Heart
Sauerbruch maneuver to control hemorrhage
Inflow occlusion to control hemorrhage
Restore rhythm before suture repair
Leave pericardial sac open/leave incision open.
Great Vessels
Foley balloon catheter tamponade
Claviculectomy for injury to subclavian vessels
Insertion of temporary intraluminal shunt
Ligation of major injured veins
Lungs
Hilar twist to control hemorrhage
Pulmonotomy (pulmonary tractotomy) for through-and-through
or deep lobar injuries
Simultaneously stapled pneumonectomy
Pack pleural cavity/leave incision open
best diagnostic. Starting empiric antibiotic therapy based
on risk factors and local patterns of infection while patientspecic cultures are pending is an accepted standard.
Pulmonary Pseudocyst
A posttraumatic pulmonary pseudocyst is a parenchymal
cavity that may have an air-uid level. A chest x-ray or
thoracic CT scan conrms the diagnosis. Observation and
serial imaging studies are appropriate in asymptomatic
patients, although antibiotics and even catheter drainage may be needed for an infected pseudocyst (pulmonary
abscess).
107
Retained Hemothorax
A retained hemothorax greater than an estimated 300 mL
after thoracic trauma or after a trauma thoracotomy should
be evacuated to reduce the incidence of empyema.
108
When
a suspected retained hemothorax is present, a chest CT scan
should be performed to assess the location, volume, and
presence of an adjacent signicant injury to the lung. After
a double lumen endotracheal tube is inserted, the patient
is placed in a full lateral position. The 30-degree thoracoscope is inserted through a previous tube thoracostomy site,
the collection is visualized, and the sites for insertion of two
more trocars selected. The retained hemothorax is evacuated with a combination of manual traction using thoracoscopic graspers, irrigation, and suction. Most current
reviews recommend that video-assisted thoracoscopic surgery (VATS) evacuation of a retained hemothorax be performed in the rst 4 to 7 days after injury.
109–111
In contrast,
the “management of post-traumatic retained hemothorax”
study of the AAST (2012) demonstrated “no relationship
between timing of VATS and success rate.”
108
Of interest,
the same study noted that 26% of patients undergoing
VATS required a second procedure and that thoracotomy
was ultimately required in 20% of patients.
Empyema
In one multicenter study, empyema or a purulent infection of the pleural space developed in 27% of patients with
a retained traumatic hemothorax.
112
As the overlapping
stages of empyema include exudative, brinopurulent, and
organizing, both VATS and thoracotomy with decortication
have a role depending on the stage encountered. Should
thoracotomy be necessary, goals of the procedure include
evacuation of purulent collections, division of pleural adhesions, decortication of any entrapped lung, and drainage of
the pleural space with thoracostomy tubes.
113
Adapted from Phelan HA, Patterson SG, Hassan MO, et al. Thoracic
damage-control operation: principles, techniques, and definitive
repair. J Am Coll Surg. 2006;203:933–941.
Table 16.8 Survival After Injuries to the Lungs.
Author Suture/Wedge Pulmonotomy Lobectomy Pneumonectomy
Thompson et al., 1988
Wall et al., 1998
Karmy-Jones et al., 2001
Huh et al., 2003
100
99
97
SURVIVAL
Survival gures in large series of patients with injuries to
the lungs since 1980 are listed in Table 16.8.
97% — 45% 0%
82
— 83% — —
91%/70% 87% 57% 50%
76.1/80% 90.9% 65% 30.3%
196 SECTION 4 • The Management of Vascular Trauma
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17
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Blunt Thoracic Aortic Injury
DEMETRIOS DEMETRIADES, PEEP TALVING, and KENJI INABA
Introduction
The screening, denitive diagnosis, and the method and
timing of definitive management of blunt thoracic aortic
injuries (BTAI), have undergone revolutionary changes
over the last few years. A routine chest CT scan has
replaced plain x-rays for screening purposes; CT angiography (CTA) has replaced formal angiography as a
method of definitive diagnosis; semielective definitive
repair of BTAI instead of emergency repair has now
become the new standard; endovascular stent grafts have
largely replaced open surgical repair. All these changes
have resulted in a significant reduction of early mortality
and complications.
History
The rst case of blunt thoracic aortic injury was reported
by the anatomist Andreas Vesalius in a man who fell from
a horse in 1557.1 The rst reported repair of an acute
repair of a BTAI occurred in the late 1950s.2 In the 1970s,
there was the development and widespread use of various
shunting techniques and graft materials.1 In the 1990s,
we saw the rst reports supporting routine use of CT scan
as a screening method in patients with a suspicious mechanism of injury3, and soon afterward CTA was advocated
as the preferred method of denitive diagnosis of BTAI. In
1997, the rst endovascular repair of a patient with BTAI
was reported4 and in the 2000s endovascular aortic repair
(EVAR) became the new preferred therapeutic approach.
the scene and are not captured in hospital-based datasets.
The incidence of aortic injuries in fatal trafc injuries is
very high. In a recent analysis of 304 deaths due to blunt
trauma in the county of Los Angeles, 102 patients (33%)
had a rupture of the thoracic aorta. About 80% of the
deaths occurred at the scene and only 20% in the hospital10
(Fig. 17.1).
In another autopsy analysis of 25 fatalities in a 2008 train
crash in Los Angeles, thoracic aortic rupture was found in
eight cases (33%). All mortalities occurred at the scene.
The incidence of aortic trauma increases with age, and
it is rare to nd this injury in the pediatric population. In a
National Trauma Databank analysis, the incidence of thoracic aortic injury in children younger than 16 years old
was seven times lower than in adults (0.03% vs. 0.21%).12
In an analysis of 5838 auto versus pedestrian injuries,
there were no aortic injuries in the age group 14 years or
younger. The incidence increased to 0.2% in the group
15 to 65 years, 0.5% in the group 56 to 65 years, and 1.5%
in the group older than 65 years.
7
11
Epidemiology
It is estimated that 8000 to 9000 blunt trauma victims
suffer thoracic aortic injury every year in the United States.5
The majority of these injuries are due to motor vehicle
collisions (approximately 70%) followed by motorcycle collisions (13%), fall from height (7%), auto versus pedestrian
(7%), and other mechanisms.6 The overall incidence of thoracic aortic injuries in patients reaching the hospital alive
is less than 0.5%. In a series of 5838 pedestrian injuries
reaching hospital care, the incidence of BTAI was 0.3%.7 In
another study of 613 admissions following high-level falls,
the incidence of BTAI was 0.1%.8 The presence of a pelvic
fracture is a marker of an associated thoracic aortic injury.
In an analysis of 1450 pelvic fractures, aortic injury was
diagnosed in 1.4%.9 However, it seems that this is the tip of
the iceberg and the real incidence of BTAI is much higher.
The vast majority of patients with this type of injury die at
Fig. 17.1 Transected thoracic aorta noted at autopsy.
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Approximately 40% of patients with aortic rupture have
at least one very severe associated injury (body area abbreviated injury Score of 4 of greater), the most common being the
head and the abdomen. The mean injury severity score is 40,
a strong indicator of the grave condition of the victims.
6
Site and Type of Aortic Injury
The most common anatomical site of the aortic injury is
the medial aspect of the lumen, distal to the left subclavian
artery (Fig. 17.2). In a prospective analysis of 185 cases of
thoracic aortic injuries, the rupture involved the isthmus
in 75%, followed by the descending aorta in 22% and the
ascending aorta in 4%.6 Computer simulation and cadaver
studies have shown that the combination of increased
intraaortic pressure (mean 1149 mm Hg) and rotational
forces exerts a highly focused stress at the isthmus. In addition, the tensile strength at the isthmus was found to be
only 63% of that of the proximal aorta.
13,14
The most common type of injury is a false aneurysm (58%), followed by
dissection (25%) and intimal tear (20%)6 (Fig. 17.3).
Natural History of BTAI
The majority of patients with BTAI die at the scene, before
reaching hospital care. In an analysis of 242 fatal BTAI,
Burkhart et al. reported that 57% of the deaths occurred at
the scene or on arrival to hospital, 37% died within the rst
4 hours of admission, and 6% died more than 4 hours after
admission.15 In another autopsy study of 102 victims with
BTAI, about 80% of the deaths occurred at the scene and
only 20% in the hospital.
10
Fig. 17.2 Classic site of the blunt thoracic aortic injury: medial aspect of
the aorta, distal to the left subclavian artery.
Screening and Diagnosis
The supine chest x-ray has been extensively used as the
initial screening tool for the diagnosis of BTAI. Numerous
radiological ndings have been described as suspicious
markers for aortic trauma. They include a widened upper
A B
Fig. 17.3 (A) Aortography: traumatic false aneurysm of the proximal descending aorta (see circle) is the most common type of injury. (B) CT angiogram:
sagittal view of blunt thoracic aortic injury with extensive dissection (see arrows).
17 • Blunt Thoracic Aortic Injury 201
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mediastinum (greater than 8 cm on an anterior-posterior
supine chest lm at the level of the aortic knob) (Fig. 17.4A)
obliteration of the aortic contour, loss of the perivertebral
pleural stripe, depression of the left mainstem bronchus,
deviation of the nasogastric tube to the right, a left apical
pleural hematoma (apical cap), a massive left hemothorax, and the presence of fractures of the sternum, scapula,
upper ribs, or clavicle in a multitrauma patient.
5,16–18
The
widened mediastinum is the most common nding but it
still has a low sensitivity and specicity. Many conditions,
such as a fracture of the sternum or the thoracic spine or
supine position in an obese patient, may cause a widened
mediastinum. The most specic signs are loss of the aortic knob, abnormality of the aortic arch, and deviation of
the nasogastric tube, but the sensitivity is very low. Traditionally, a normal chest x-ray had been considered reliable
in excluding BTAI.
19,20
However, numerous studies have
shown that chest radiography is a poor screening tool and
a signicant number of aortic injuries may not show any
mediastinal abnormalities
3,21,22
(Fig. 17.4B,C). On the basis
of these chest x-ray limitations, many centers now use CT
scan of the chest as the primary screening tool for BTAI,
irrespective of x-ray ndings.
tive predictive value of the CT scan in the diagnosis of BTAI
approaches 100%.
23
3,21,22
The sensitivity and nega-
Aortography remained the gold standard for the definitive diagnosis of BTAI until the late 1990s. However, it
is invasive, takes time, and the angiographic team is not
always readily available after hours. In the last few years,
CT scan has replaced formal angiography for the denitive
diagnosis of BTAI. The new generation multislice CT
scanners with 3-D reformation have been shown to have
almost 100% sensitivity and specificity, a 90% positive and 100% negative predictive value, and an overall
diagnostic accuracy of 99.7%,
20,24
and allow classification of the type of injury (Figs. 17.5 and 17.6). Formal
angiography still has a limited diagnostic role in the rare
cases where the CT scan findings are suspicious but not
diagnostic.
Transesophageal echocardiography (TEE) is another
diagnostic modality in the evaluation of suspected BTAI.
25–27
The initial enthusiasm for this imaging modality has been
replaced by skepticism. It has failed to gain popularity
because of conicting reports about its accuracy and concerns regarding its availability 24 hours a day.28 The dramatic shifting from angiography and TEE to CT scanning
in the diagnosis of BTAI is demonstrated by a multicenter
study sponsored by the American Association for the Surgery of Trauma (AAST).6 The use of angiography and TEE
for the diagnosis of thoracic aortic injuries decreased from
87% and 12%, respectively, in 1997 to only 8% and 1% in
20076 (Table 17.1).
Other diagnostic modalities such as magnetic resonance
imaging (MRI) or intravascular ultrasound may be useful in
rare patients where the CTA ndings are not denitive.
In summary, the new generation scanners have made
CTA the standard modality for screening and denitive
diagnosis of BTAI. Formal aortography may have a rare
diagnostic role in patients undergoing angiography for
other injuries such as pelvic fractures, comple x liver inju-
A B
Fig. 17.4 (A) Chest x-ray shows a very widened mediastinum due to blunt thoracic aortic injury. (B) Chest x-ray with a normal mediastinum in an occult
blunt thoracic aortic injury. (C) CT-angiography in the same patient demonstrating blunt thoracic injury.
202 SECTION 4 • The Management of Vascular Trauma
ABSENT EXTERNAL CONTOUR ABNORMALITY PRESENT EXTERNAL CONTOUR ABNORMALITY
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Type of aortic injury Definition Example Type of aortic injury Definition Example
Intimal tear
No aortic external
contour abnormality:
tear and/or associated
thrombus is <10mm
Pseudoaneurysm
Aortic external contour
abnormality: contained
Large intimal flap
Fig. 17.5 Classification of blunt thoracic injury. (From Starnes, BW, Lundgren RS, Gunn M, et al. A new classification scheme for treating blunt aortic injury.
J Vasc Surg. 2012;55:47–54.)
No aortic external
contour abnormality:
tear and/or associated
thrombus is >10mm
Rupture Aortic external contour
abnormality: not
contained, free rupture
Table 17.1 Changing Perspectives: Diagnostic
Modalities for Blunt Thoracic Aortic Injury: AAST1 (1997)
vs. AAST2 (2007).
AAST
1
n 253 193
Aortogram 207 (87%) 16 (8.3%) <.001
CT scan 88 (34.8%) 180 (93.3%) <.001
TEE 30 (11.9%) 2 (1.0%) <.001
From Demetriades D, et al. Diagnosis and treatment of blunt thoracic
aortic injuries: changing perspectives. J Trauma. 2008;64;1415–1419.
AAST, American Association for the Surgery of Trauma; CT, computed
tomography; N, number; TEE, transesophageal echography.
AAST
2
P-value
Fig. 17.6 CT angiogram with 3-D reconstruction provides reliable and
detailed information about the site, size, and type of aortic injury.
ries, etc. TEE might be useful in critically ill patients in the
intensive care unit who cannot be transferred safely to the
radiology suite for CT scan.
Management
INITIAL MANAGEMENT OF THORACIC AORTIC
INJURIES
Prompt diagnosis and early appropriate treatment
remain the cornerstone for survival of patients with
BTAI. Prevention of free rupture of a contained BTAI
until definitive repair is performed is the most urgent
priority. The risk of free rupture is highest in the first
few hours after the injury, with more than 90% of ruptures occurring within the first 24hours. In an AAST
multicenter study by Fabian et al.,5 24 (8.8%) of the 274
patients in the study population progressed to free rupture. However, rigorous blood pressure control reduces
the risk of rupture to about 1.5%.29 Blood pressure control is best achieved with a combination of judicious fluid
restriction and pharmacological intervention. The systolic blood pressure should be kept as low as tolerated,
which in most patients will range from 90 to 110 mm
Hg. In elderly patients the optimal systolic pressure may
be slightly higher. Cautious restriction of intravenous
fluids and administration of beta-blockers such as an
esmolol drip are the most commonly used modalities for
blood pressure control. In the presence of an associated
severe brain or spinal cord injury, the systolic blood pressure should be maintained at a slightly higher level (110
to 120 mm Hg) in order to reduce the risk of secondary
neurological damage.
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TIMING OF DEFINITIVE MANAGEMENT
Untreated, the risk of rupture of a BTAI is highest in the
rst 24 hours after injury although it does not disappear
altogether, with late rupture a possibility weeks later.30 In
the AAST multicenter study by Fabian et al.,5 24 (8.8%)
patients of the study population progressed to free rupture.
Ninety-two percent of the ruptures died within 24 hours
of the injury, one at 30 hours, and one at 6 days. In the
group of 13 free ruptures with precise time of rupture, 46%
occurred within 4 hours and another 38% within 8 hours.
For these reasons, the denitive management of BTAI has
been considered as an emergency and this policy remained
the standard of care for many years. However, subsequent
studies showed that the early initiation of vigorous blood
pressure control via restrictive uid resuscitation and pharmacological agents decreases wall stress in the region of
the injury
mately 1.5%.29 For patients with contained ruptures who
survive out past 4 hours, with medical treatment, in-hospital free rupture and death are now rare.29 The successful
management of these injuries therefore hinges on the early
diagnosis and careful blood pressure control.
In the late 1990s and early 2000s, some studies suggested that selected patients with major associated injuries
could safely be managed with delayed repair until after stabilization of other major trauma, provided that the blood
pressure was adequately controlled.
delayed repair was subsequently applied more liberally in
patients with no severe associated injuries or major comorbidities.
The safety of delayed repair of BTAI and its effect on outcomes remained controversial for many years. Most studies
included in their analysis only patients with major associated injuries and reported contradictory results. Some studies showed improved outcomes with delayed repair, whereas
others failed to show any benets. Wahl et al.,35 in a retrospective review of 48 cases, reported that delayed aortic
repair (more than 24 hours) was safe, but it was associated
with a longer hospital stay and direct costs than early repair.
A similar study of 78 cases by Hemmila et al.29 reported a
higher complication rate and a longer hospital stay in the
delayed (more than 16 hours) group. However, other studies
suggested that delayed repair was associated with improved
outcomes.
analyzed outcomes in 178 patients with BTAI, according
to the timing of denitive repair (early less than 24 hours,
delayed more than 24 hours).6 The two groups were similar
with regards to injury severity, major associated injuries,
type of aortic injury, and type of aortic repair (operative
vs. endovascular). The mean time from injury to repair was
10.2 hours in the early group and 126.2 hours in the delayed
group. The overall mortality in the delayed repair group
was signicantly lower than the early repair group (5.8%
vs. 16.5%, P = .034). Multivariate analysis adjusting for
injury severity, severe extrathoracic injuries, Glasgow coma
scale (GCS), hypotension on admission, age, and method of
aortic injury repair, showed a signicantly increased risk of
death in the early repair group (adjusted odds ratio [95%
condence interval] 7.78 [1.69–35.70], adjusted P-value =
.008). The survival benets in the delayed repair group were
conrmed in the subanalysis of the groups with or without
29,31,32
and reduces the risk of rupture to approxi-
29,31,33,34
33,36
An AAST multicenter, prospective study
The concept of
major associated injuries (see Table 17.4). The incidence of
paraplegia was similar in the two groups (early repair 1.8%,
delayed repair 1.4%).
Subsequent studies conrmed that delayed repair is an
independent factor protective against mortality.
37,38
The
current evidence supports that, with adequate medical
blood pressure control, delayed repair is not only safe but
may be preferable to emergent repair in select patients. This
allows for optimizing patient risk factors and operative conditions and ensures that other more life-threatening injuries can be prioritized. The practice management guidelines
from the Eastern Association for the Surgery of Trauma
suggest delayed repair of BTAI, with the stipulation of effective blood pressure control.
39
The optimal time from injury or admission to repair is
unknown and should be individualized, taking into account
many factors, such as the presence of other severe injuries or
comorbid conditions, the physiological status of the patient,
and the type and severity of the aortic injury. Delayed repair
should not be attempted in cases with active leaking from
the aortic injury (Fig. 17.7). Also, it might be advisable that
in cases with large contained injuries, the repair should be
done urgently, within a few hours of the diagnosis.
DEFINITIVE MANAGEMENT OF THORACIC AORTIC
INJURIES
Operative repair remained for many decades the only standard denitive management of all BTAI. However, in the
21st century there has been a dramatic shift to endovascular techniques. This shift is clearly demonstrated by two
large prospective studies by the AAST in 19975 (AAST1)
and 20076 (AAST2). In 1997, all 207 cases with BTAI were
managed with open repair, whereas in 2007, 65% of the
193 cases were managed with endovascular stent grafts and
only 35% with open repair (Table 17.2). Currently, the only
indication for open repair is an injury involving the aortic
arch, where placement of an endograft might be technically
Extravasation
Fig. 17.7 CT angiogram demonstrating active extravasation from a
traumatic throacic aortic aneurysm.
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Table 17.2 Changing Perspectives: Methods of Definitive Treatment of Thoracic Aortic Injuries: AAST1 (1997) vs. AAST2 (2007).
AAST
1
n 207 193
Open repair 207 (100%) 68 (35.2%) <.001
Clamp and sew 73/207 (35.3%) 11/68 (16.2%) 0.003
Bypass 134/207 (64.7%) 57/68 (83.8%) 0.003
Endovascular repair 0/207 (0%) 125/193 (64.8%) <.001
From Demetriades D, et al. Diagnosis and treatment of blunt thoracic aortic injuries: changing perspectives. J Trauma. 2008;64;1415–1419.
AAST, American Association for the Surgery of Trauma.
AAST
2
P-value
difcult or impossible. A third evolving therapeutic option
for selected cases with minor aortic injuries is observation
combined with medical therapy.
Open Surgical Repair
The rst successful surgical repair of BTAI was performed
by DeBakey and Cooley in 1953.40 The clamp-and-sew
technique, as it was known, became the standard of care
for many decades. Advantages of this technique included
a relatively expeditious repair and lack of requirement for
systemic heparinization. The clamp-and-sew technique
was initially practiced without distal aortic perfusion and
resulted in a signicant rate of paraplegia when aortic
cross-clamp times exceeded 30 minutes. In more recent
years, open surgical repair, performed with the use of roller/
an effort to reduce the risk of paraplegia, has become the
standard of care.
41,42
There are multiple techniques for active distal aortic perfusion during open repair and aortic cross-clamping. The
most common conguration is the left heart partial bypass
with the inow into the pump achieved through a cannula
inserted into the left atrium through the left atrial appendage or left pulmonary vein. The outow cannula is inserted
in the femoral artery or into distal aorta beyond the distal
aortic clamp using a purse-string controlled aortotomy.
Alternatively, right atrial to distal aortic cannulation is used
in conjunction with an oxygenator; this requires full heparinization (i.e., bolus of 300 to 400 units/kg and maintenance of activated clotting time [ACT] above 400 seconds).
This conguration is used very infrequently in trauma settings due to the risk of hemorrhage from associated injuries (Fig. 17.8). Debate over the preferential distal perfusion
technique is still evolving.
In patients who present with free rupture, especially in
settings with limited resources, the clamp-and-sew technique might be the only option. In these cases, during
surgery, double-lumen intubation and independent lung
ventilation is instituted. The patient is placed in the right
lateral decubitus position and access to the aorta is obtained
through a left posterolateral thoracotomy in the fourth or
fth intercostal space. The proximal aorta above the area
of the injury and the left subclavian artery are identied,
isolated, and controlled with vessel loops. The thoracic aorta
distal to the injury is identied and likewise isolated with a
vessel loop. Aortic clamps are applied proximal and distal to
periaortic hematoma and the subclavian artery. Decisionmaking with regard to the location of clamp placement can
be greatly aided by the use of two-dimensional and threedimensional reconstructions of CTAs.43 When feasible, the
vascular clamp placed on the aortic arch is subsequently
transferred distal to the origin of the left subclavian artery
to minimize cardiac afterload and spinal cord ischemia
during cross-clamp time. The periaortic dissection plane
is identied and the aortic lesion is exposed. A transverse
aortotomy is performed to allow inspection of the aortic
tear and subsequently decide whether primary repair or
interposition graft placement is required. The intercostal
arteries in proximity of the aortic lesion are preferentially
not ligated nor oversewn, but incorporated into the tailored
aortic repair. A cell-saver device can be successfully utilized
for autotransfusion of blood from the chest in the case of
major hemorrhage. The aortic injury is repaired utilizing
2-0 or 3-0 polypropylene suture material and a collagencoated or preclotted Dacron interposition graft that reduces
bleeding from the graft. The size of the interposition graft
ranges from 22 to 40 mm and is chosen to match the size of
the aorta. Primary repair is utilized only in exceedingly rare
pediatric blunt aortic injuries to avoid coarctation with the
graft as the child grows.
In the AAST1-sponsored prospective multi-institutional
study of 1997, the clamp-and-sew technique (without
distal aortic perfusion) was performed in 35% (n = 73) of
all patients undergoing operative repair. In these instances,
the paraplegia rate was 16.4%. In comparison, in the 134
patients undergoing repair using distal aortic perfusion, the
paraplegia rate was signicantly lower at 4.5%. The most
important independent risk factor for paraplegia was crossclamp time of more than 30 minutes (odds ratio 15).
5
A decade later, a second AAST-sponsored multiinstitutional prospective study (AAST2), including 193 patients
subjected to denitive repair of BTAI, was published.6 The
incidence of clamp-and-sew technique without bypass
between 1997 and 2007 had decreased from 35% to 16%.
Likewise, the overall incidence of procedure-related paraplegia in patients undergoing open surgical repair had
fallen signicantly from 8.7% to 1.6% (P = .001). Currently,
approximately 85% of thoracic aortic injuries treated with
open surgery are managed with bypass techniques.
Numerous studies have demonstrated that active distal perfusion is superior to “passive perfusion” in reducing
the incidence of procedure-related paraplegia.
5,41,42,44,45
A
meta-analysis of mortality and risk of paraplegia following
repair of traumatic aortic rupture in 1492 patients showed
an overall postoperative paraplegia rate of 9.9%. Among
patients treated with simple aortic cross-clamping, case
fatality and incidence of paraplegia were reported as 16%
and 19.2%, respectively. With passive shunting, mortality
was 12.3% and the incidence of paraplegia 11.1%, and
with active perfusion the rate of paraplegia was 2.3%.
41,42
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