Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3594_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
29.08.2026
Размер:
89 Мб
Скачать
10 • Stent-Grafts, Coils, and Plugs 115
https://t.me/medicina_free
Table 10.1 Commonly Used Embolization Agents for Trauma
Embolization
Agent Size Vessel Tips
Temporary
Gelfoam Large or
Fibrillated collagen
Permanent
Coils Large Microcoils are also available
Amplatz Vascular Plug
Particles Small Limited role in trauma
Liquid adhesive Small Risk of gluing catheter to vessel
Thrombin Small May cause nontarget
small
Small Recanalization of vessels in 2–3
Large Multiple different shapes and
Gelfoam slurry can be used for
large vessels
Gelfoam powder can be used for
small vessels
Recanalization is highly variable
months
Concern for distal embolization if
not anchored or when used for arteriovenous fistula
lengths available
Can be used to make a backstop
for coils
Tends to cause more ischemia
and necrosis than large vessel occlusion
wall
Delivery can be challenging with
mixing of glue
embolization
Most commonly used for narrow
neck pseudoaneurysms
embolization of proximal vessels by administering puffs of the slurry under uoroscopy. The contrast medium in the slurry allows for visualization of the Gelfoam cast in the target vessel. Once vessel occlusion is achieved, no addi­tional agent is injected, as it may reux into a more cen­tral vessel and cause unintended embolization elsewhere. Recanalization typically occurs within 3 weeks but may take up to 3 months. The rate of recanalization is very unpredictable with Gelfoam. A powdered form of Gelfoam is also available but has a small diameter of only 10 to 100 µm. This and other small diameter temporary occlusive such as starch microspheres and brillated collagen tend to travel more distally, increasing the likelihood of tissue ischemia, and have limited utility in controlling the injured larger parenchymal vessels in solid organ trauma.
PERMANENT EMBOLIZATION AGENTS
Permanent embolization agents include coils, plugs, and particles. The decision of which agent to use is based on the size of the target vessel, the blood supply to the affected organ, and if ischemia is desired. In the setting of severe injury, tissue ischemia should be minimized, which makes the use of a large number of permanent small-particle embolic agents less desirable. Polyvinyl alcohol (PVA) par­ticles, tris-acryl gelatin (TAGM), and other types of micro­spheres, and liquid adhesives or sclerosants are frequently
used for elective vessel ablation and embolization of targeted tissue. Experience in trauma is currently limited for these agents, given the delivery systems can be difcult to control, resulting in unintended distal ischemia or reux into central vessels delivering embolization agent to other unintended locations. They are not without advantages, however, as liquid adhesives function independent of the clotting cas­cade and can occlude a vessel of a coagulopathic patient. In the setting of trauma, large-vessel embolic agents are most commonly used. In this setting, large vessels are considered any vessel that can be seen on angiography.
Thrombin
Although not commonly used for catheter-directed therapy, thrombin is used routinely for treatment of pseudoaneu­rysms at arterial access sites. Thrombin directly acts on brinogen, converting it to brin monomers thereby allowing it to cross-link and polymerize. This reaction results in almost immediate clot production with administration of thrombin. It is approved as a topical agent, and intraarterial use is off­label, though there has been extensive experience using this
4–6
agent.
When treating a postcatheterization pseudoaneu­rysm or posttraumatic peripheral pseudoaneurysm, the tar­get is accessed by direct puncture and a small syringe is used to administer small aliquots of thrombin until thrombosis of pseudoaneurysm is achieved. This generally takes less than 1000 units (1 mL of 1000 unit per mL preparation). Extreme care must be taken when injecting thrombin, as emboliza­tion of an unintended target can have severe consequences, including irreversible ischemia. Although there are reports of using thrombin to treat posttraumatic solid organ pseu­doaneurysms, we do not advocate this practice.
7
Coils
Coils are the most common agent for permanently embo­lizing large vessels, given their ease of use and availabil­ity. They may be used alone or in combination with other agents that provide scaffolding for coils and prevent distal embolization. When selecting a coil for embolization, the size of the target vessel, sheath size, and ow in the target vessel must be considered. Coils were originally a curled seg­ment of steel guidewire. These needed to be tightly packed because they were minimally thrombogenic. Now coils have a thrombogenic adjunct attached, such as nylon ber, poly­ester, or biologically active material that promotes clotting and allows for fewer coils needed for the desired effect. Mod­ern coils are made mostly of a platinum alloy, as it is more malleable than steel and easier to see under uoroscopy. To achieve their nal conguration, coils may have a built-in “memory” to which they assume after being released. There is also a class of surface-modied coils that have a coating, that when hydrated, expands and congures the wire and increases the diameter of the coil for more efcient pack­ing. The deployment method is also variable among differ­ent coils and commercial brands. Some coils may be pushed through the deployment catheter, chased with a saline ush, or advanced on a deployment system from which the coils must be detached. Detachable coils offer the greatest control and offer the possibility of repositioning prior to nal deployment to prevent migration in high-ow systems.
Multiple diameters from 0.010- to 0.052-inch are
available for different applications. The combination of coil
116 SECTION 3 Emerging Technologies and New Approaches to Vascular Trauma and Shock
https://t.me/medicina_free
composition and diameter will determine the stiffness of the coil, often reported as “softness.” Manufacturers also report the recommended catheter inner diameter, number of loops, extended coil length, and coiled diameter. This allows for appropriate/accurate selection based on vessel size. Correct sizing is crucial. Stiffer coils should not be oversized more than 1 mm, whereas softer coils can be oversized by 20% to 30%. Oversizing of coils prevents distal migration, especially in young patients who are vasoconstricted at the time of the procedure. The drawback to oversizing is that too large of a coil can push the delivery catheter backward, leading to unintended proximal embolization or dislodgement from the target vessel or failure of the coil to assume its intended shape. In lower-volume trauma centers or if a dedicated team is not available 24 hours a day, we favor selecting one size of macrocoils and microcoils that works with the diag­nostic catheters that are pulled for the trauma setup. This prevents having to nd additional delivery catheters dur­ing the procedure. For simplicity, 0.035-inch coils can be deployed through 4- or 5-Fr diagnostic catheters without difculty. If smaller vessels are being selected, microcoils are available that can be deployed through a 0.014- or
0.021-inch lumen (i.e., through a microcatheter). Micro­coils may jam or start to form their deployed conguration in a larger catheter, leading to obstruction of the catheter.
When deploying coils, it is important to ensure the deliv­ery system is well-positioned and stable. This allows for pre­cise deployment without proximal migration of the catheter and coil. The authors recommend that the catheter being used for delivery of the coil be placed through a sheath or an additional catheter that will not be moved during deploy­ment. This gives the operator the ability to remove the entire deployment catheter without losing purchase. Testing the stability can be performed by advancing a wire several cm from the tip of the delivery catheter to ensure the system remains in place. There are several techniques for emboli­zation. The two most common are the “anchor” technique, which involves anchoring the end of the coil in a small branching vessel, with the body of the coil remaining in the target vessel preventing migration of subsequently placed coils. The second is the “scaffold” technique, which initially uses a large coil to create a scaffold so that smaller coils can subsequently be packed proximally to form a dense coil nest. If no branching vessel, is present, or it is a high-ow sys­tem and there is concern for embolization of the initial coil, a plug device can be deployed. Detachable coils afford the operator greater control/accuracy for deployment. These systems allow for advancement, retraction, and reposition­ing of the coil before it is nally released from the delivery wire. This can be an advantage when in a high-ow system or if an arterial venous stula (AVF) is present that would allow for a misplaced coil to migrate to the venous system and cause a pulmonary embolus. Detachable coils are released by an electrical current, a mechanical switch, or a wire to break the bond of the coil to the deployment device.
Plugs
When no branching vessel is present to place an “anchor” coil, or in a high-ow system where there is concern for embolization of the initial coil, a plug device can be deployed. A commerically available vascular plug is Amplatzer Vascular Plugs (AVPs) (St. Jude Medical, AGA
Medical Corporation). AVPs are a series of four different generations of self-expanding occlusive devices made of nitinol mesh available in several shapes so that emboliza­tion/occlusion may be achieved in a variety of target ves­sels. These devices are available in a variety of diameters. There are four distinct plugs. The AVP, AVP II, AVP III, and AVP 4 have different numbers of segments, sizes of deliv­ery catheter, and deployed sizes ranging from 3 to 22 mm. When choosing a device, it should be oversized by 30% to 50% to the target vessel diameter. The AVPs are deployed by unsheathing and can be withdrawn into the sheath for repositioning if necessary. Once in position, the device is detached by unscrewing the plug device from the delivery system. The large nature of AVPs makes it ideal for large vessels such as the proximal splenic artery or for AVF, where there is concern for embolizing into the systemic system. The size and stiffness of the system does make it challenging to deploy after an acute angle or in a tortuous vessel.
Stents-Grafts
When the injured or target vessel provides inline ow to a vital structure without good collateral circulation, occlu­sion with an embolization device is often not a viable option. In many of these scenarios, such as with an injured periph­eral vessel, there is minimal morbidity associated with an open surgical approach to primary repair, or placement of an interposition or bypass graft. In contrast, open surgical repair of injured vessels in the chest, abdomen, or pelvis is associated with a greater degree of morbidity, which may be particularly precarious in severely injured patients with compromised physiology. As such, the use of catheter-based reconstructive options such as covered stents (i.e., stent­grafts) to manage vascular disruption in these anatomic locations is often benecial. Deployed inside of the injured vessel, covered stents or stent-grafts exclude or “seal” the vascular disruption, while maintaining antegrade ow in the affected artery or vein. Historically, stents could be mod­ied by the surgeon by using vein to make a covered stent from a bare metal stent. Currently, there is a wide range of commercially available balloon-expandable and self­expanding covered stents that can be used for the manage­ment of vascular trauma.
BALLOON-EXPANDING STENTS
Balloon-expandable stents are stored in a crimped state in the delivery catheter and are expanded by inating a bal­loon within the stent, expanding it to the vessel diameter or slightly larger. These stents are often stainless steel and have higher radial stiffness. Radial stiffness describes how much the diameter of the stent is reduced by a certain amount of external pressure. Balloon-expanding stents have greater degrees of radial stiffness or “hoop strength” and there­fore require a higher amount of force to buckle. However, balloon-expandable stents often lack the flexibility or elasticity to recover once buckling occurs.8 The deployment of balloon-expandable stents tends be more precise than self-expanding stents, though the technology for accurately deploying all types of stents continues to improve. The higher radial stiffness of balloon-expandable stents tends to
10 • Stent-Grafts, Coils, and Plugs 117
https://t.me/medicina_free
be ideal for preventing migration, and this feature coupled with the precise delivery capability make them preferred for placement in the ostia of large branch vessels. Due to their relative inexibility, balloon-expandable stents are less commonly used in tortuous vessel or in vessels located in highly mobile anatomic areas (e.g., behind the knee).
SELF-EXPANDING STENTS
Self-expanding stents are manufactured at the desired size and are then collapsed or constrained using a covering delivery device. When the constraining or covering device is removed, the stent expands and reconforms to its original manufactured shape. This physical property is accomplished through a spring mechanism inherent to the structure of the stent, or by using a temperature-driven method using the “shape memory” of the metal.9 Self-expanding stents are most commonly made from the metallic alloy called Nitinol, and they tend to have less radial stiffness than bal­loon-expandable stents. However, self-expanding Nitinol stents or stent-grafts have greater degrees of elasticity to recover their original conguration when the external force is removed. These qualities make self-expanding stents ideal to use in tortuous or exible anatomic areas, such as those crossing joints, or in areas of movement, such as the cervical vessels. An additional consideration is accurate placement or deployment of the self-expanding stents. As it resumes the manufactured shape upon removal of the covering or constraining deployment device, self-expanding stents may migrate or “jump,” thus making their precise placement more challenging. Newer deployment systems used with the most modern self-expanding stents or stent-grafts have improved the ability to accurately land the proximal extent of these devices in the desired location.
Management of Solid Organ Injury
Starting in the 1980s, there was a push for the nonopera­tive management of intraabdominal solid organ injuries in patients who were hemodynamically stable on presentation or who responded appropriately to resuscitation. protocols for nonoperative management included catheter­based contrast arteriography for hemodynamically stable patients with an injury to the spleen, kidney, or liver on CT imaging. If extravasation was observed at the time of arte­riography, an embolic agent could be deployed to increase the likelihood of splenic salvage or the nonoperative man­agement of splenic injury (versus open splenectomy). The management of solid organ injury has evolved as newer CT imaging technology provides quick, contrast-enhanced imaging during the immediate diagnostic phase of care. Advances in diagnostic imaging allow for a more selective use of catheter-based arteriography in certain patients with extravasation, high-grade injuries, and/or hemoperito­neum on the initial CT scan (Table 10.2).
12
SPLENIC INJURY
The spleen is the second most commonly injured abdomi­nal organ but the most common source of massive bleeding in blunt trauma.
13–15
Nonoperative management of splenic
10,11
Initial
injuries in hemodynamically normal patients has been pur­sued as a standard of care since the 1990s, with a goal of preserving splenic function and lowering the risk of post­splenectomy spesis.16 Although nonoperative management is well-accepted, the optimal application of splenic angio­embolization (SAE) remains unsettled.
12,16,17
The Eastern Association for the Surgery of Trauma (EAST) guideline on splenic trauma recommends angiogra­phy for patients with Association for the Surgery of Trauma (AAST) grade III or higher injury, contrast extravasation, moderate hemoperitoneum, or ongoing splenic bleeding.12 This guideline is in agreement with a large metaanalysis showing a decrease in the failure of nonoperative manage­ment when SAE was used as an adjunct in patients with grade IV or V injuries. In this report, SAE had a failure rate of 12% for grade IV or V injuries, whereas nonoperative management alone failed 50% of the time. The benecial effect of SAE was not observed in the lower, grade I to III groups, although there was likely selection bias, as many of these patients had a separate indication for arteriography and/or embolization.16 The authors’ practice is to perform catheter-directed arteriography for stable patients or tran­sient responders with extravasation on initial CT imaging (Fig. 10.1A), or those with a moderate hemoperitoneum and a grade IV or higher splenic injury. Embolization is only performed at the time of arteriography if there is evidence of bleeding (see Fig. 10.1B), pseudoaneurysm, or a concern for secondary rupture (Fig. 10.2).
Once the decision is made to proceed with SAE, the next step is selecting where, along the course of the splenic artery, embolization should occur. Anatomically, the options include the proximal splenic artery, distal arteries near or in the hilum of the spleen, or a combined proximal and distal approach. There is no consensus as to the opti­mal technique, but there are recognized patterns of success and failure.
18,19
For example, proximal SAE is likely a bet­ter approach in patients with multiple areas of extravasa­tion, a high risk of secondary splenic rupture, or as a rapid intervention if the patient has hemodynamic deterioration during the procedure. Proximal embolization also allows collateral ow from the short gastric, gastroepiploic, and pancreatic arteries to maintain some degree of splenic per­fusion and function. In the case of proximal, large-vessel embolization, the driving pressure of the main artery is attenuated, which promotes hemostasis and decreases the rate of splenic rupture, while allowing for some degree of splenic function via small-vessel collateral ow.
The splenic artery is 5.6 mm ± 1.3 mm for both adult men and women, and embolization is best achieved with appro­priately sized coils or plugs.20 Distal embolization is indicated in patients with a single or several small parenchymal inju­ries. This allows for preservation of antegrade ow from the splenic artery to the remainder of the spleen and pres­ervation of functional parenchyma. Distal embolization has higher rates of infarction, abscess, and cyst formation.18 The authors do not recommend the technique of distal subselec­tive embolization followed by proximal embolization, with or without use of a particulate embolization agent between the coils, except in patients who are rebleeding after distal embo­lization and in whom the proximal embolization is being performed as a salvage maneuver. Combining proximal and distal embolization has the highest complication rate, with
118 SECTION 3 Emerging Technologies and New Approaches to Vascular Trauma and Shock
https://t.me/medicina_free
Table 10.2 AAST Organ Injury Scale Imaging Criteria (CT Findings)
Injury
Grade Spleen Liver Kidney
I
II
III
IV
V
AAST, American Association for the Surgery of Trauma; CT, computed tomography.
Subcapsular hematoma <10% surface area
Parenchymal laceration <1 cm depth
Capsular tear
Subcapsular hematoma 10%–50% surface area; intrapa­renchymal hematoma <5 cm
Parenchymal laceration 1–3 cm
Subcapsular hematoma >50% surface area; ruptured subcap­sular or intraparenchymal hema­toma 5 cm
Parenchymal laceration >3 cm depth
Any injury in the presence of a splenic vascular injury or active bleeding confined within splenic capsule
Parenchymal laceration involving segmental or hilar vessels producing >25% devascularization
Any injury in the presence of splenic vascular injury with active bleeding extending beyond the spleen into the peritoneum
Shattered spleen
Subcapsular hematoma <10% surface area
Parenchymal laceration <1 cm in depth
Subcapsular hematoma 10%–50% surface area; intraparenchymal hematoma <10 cm in diameter
Laceration 1–3 cm in depth and 10 cm length
Subcapsular hematoma >50% surface area; ruptured subcapsular or parenchymal hematoma
Intraparenchymal hematoma >10 cm
Laceration >3 cm depth
Any injury in the presence of a liver vas­cular injury or active bleeding contained within liver parenchyma
Parenchymal disruption involving 25%–75% of a hepatic lobe
Active bleeding extending beyond the liver parenchyma into the peritoneum
Parenchymal disruption >75% of hepatic lobe
Juxtahepatic venous injury to include retrohepatic vena cava and central major hepatic veins
Subcapsular hematoma and/or parenchymal contusion without laceration
Perirenal hematoma confined to Gerota fascia
Renal parenchymal laceration 1 cm depth with­out urinary extravasation
Renal parenchymal laceration >1 cm depth without collecting system rupture or urinary extravasation
Any injury in the presence of a kidney vascular injury or active bleeding contained within Gerota fascia
Parenchymal laceration extending into urinary col­lecting system with urinary extravasation
Renal pelvis laceration and/or complete uretero­pelvic disruption
Segmental renal vein or artery injury
Active bleeding beyond Gerota fascia into the retroperitoneum or peritoneum
Segmental or complete kidney infarction(s) due to vessel thrombosis without active bleeding
Main renal artery or vein laceration or avulsion of hilum
Devascularized kidney with active bleeding
Shattered kidney with loss of identifiable paren­chymal renal anatomy
Fig. 10.1 (A) High-grade splenic injury with active arterial extravasation seen on CTA. (B) The same patient with contrast extravasation seen on angiography.
10 • Stent-Grafts, Coils, and Plugs 119
https://t.me/medicina_free
Fig. 10.3 High-grade liver injury involving the medium-sized ves-
Fig. 10.2 Delayed splenic rupture after a high-grade blunt splenic injury
that was not managed with endovascular adjuncts.
sels. Extravasation seen on CTA and was subsequently treated with embolization.
embolization is performed, it is not uncommon to see
up to one in three patients having infarction, abscess, or cyst.21 Other complications include splenic atrophy, postpro­cedure bleeding, pleural effusion, and splenic abscess.22 The authors favor the use of coils over particulate in most cases of splenic embolization, as there tends to be less reaction and pain with coils alone. Additionally, if proximal coils are used to attenuate antegrade ow, the operator should expect to see a pseudoaneurysm on subsequent imaging with CT and should have a plan with that in mind.
revascularization from distal branches. For this reason, if super-selective embolization distal and proximal to the injury with microcoils is not possible, Gelfoam may be needed to control the distal bleeding and coil embolization used to control the proximal or inow artery. Embolization of the liver is generally well tolerated, given the dual arte­rial and portal venous blood supply. With this in mind, Gel­foam or particle embolization should be avoided proximal or just distal to the cystic artery, as there is concern for reuxing of the agent into the cystic artery causing infarc-
LIVER
The liver is the most commonly injured intraabdominal organ, and severe liver injury carries mortality rates of up to 40%. has been a standard method of treatment since a 1996 review of 13 level I trauma centers in the United States reported high rates of success with this approach.24 As with splenic injury, patients who are hemodynamically unstable with evidence of severe liver injury or those who have dif­fuse peritonitis should undergo surgical exploration. In the early days of nonoperative management, high-grade injuries (AAST IV or V), altered neurologic status, contrast extravasation on CT, moderate- to large-volume hemoperi­toneum, or age greater than 55 were seen as an indica­tion for operative exploration. still contribute to decision making, none are considered a contraindication to nonoperative management, and over 85% of liver trauma is now managed without open opera­tive intervention. endovascular embolization after open surgical intervention, as a number of patients who undergo damage control lapa­rotomy for hepatic injury continue to have bleeding after leaving the operating room.
having an AAST grade I or II injury, with the average liver grade of patients undergoing angioembolization being 3.7.29 These tend to be parenchymal injuries involv­ing small or medium branches (Fig. 10.3). If proximal
14,15,23
Nonoperative management of liver injuries
24,25
Although these factors
26,27
At least one study describes the use of
28
The majority of livery injuries are minor, with 68%
tion of the gallbladder. Although the common or proper hepatic arteries may be embolized, stent-graft placement to exclude the injury is often a better option that main­tains inline arterial ow to the liver parenchyma.
There should be a high index of suspicion for a concomi­tant venous injury in patients with high-grade liver injury who require continued uid resuscitation after embolization. These injuries are often difcult to visualize on angiogra­phy and may require operative exploration and packing. For patients who have undergone successful embolization of liver bleeding, there are several mid- and long-term complications which need to be considered, if not anticipated. These include hepatic necrosis, abscess formation (Fig. 10.4), gallblad der infarction, bile leak, and hemobilia (i.e., bleeding into the bile system) after a combined ductal and vascular injury. Although abscess and necrosis are most common, the rate attributable to the embolization procedure itself is not clear, as the liver injury alone contributes to a signicant portion of this complication. With no intervention, these complication rates have ranged from 5% to 24% for simple nonoperative management and from 0 to 40% in patient’s managed with angiography.
23,29
RENAL
The kidneys are the most commonly injured genitourinary organ in trauma. selective nonoperative management of blunt renal injury is well-tolerated, and the majority of all kidney injuries are
14,15,30
Similar to other solid organ injuries,
120 SECTION 3 Emerging Technologies and New Approaches to Vascular Trauma and Shock
https://t.me/medicina_free
traversed with a wire. If the area of injury is able to be crossed, a balloon-expandable stent-graft can be deployed. In these cases, balloon-expandable stents are preferred because of their radial force and because they tend to be deployed with greater degrees of control and precision. Fol­lowing renal stent-grafting, thrombosis of the repair can occur resulting in kidney loss.37 If concomitant injuries do not preclude, it is the authors’ practice to give the patient an antiplatelet medication at the time of the procedure, and for a number of weeks afterwards as a way to assist stent-graft patency. However, successful stent patency has also been reported in patients who are unable to receive antiplatelet agents or coagulation.38 Complications related to endovas­cular management of renal trauma include impaired renal function, urinoma, persistent hematuria, abscess, renal failure, AVF, pseudoaneurysm, and urinary tract infection.
Fig. 10.4 Liver abscess that occurred after angioembolization of medium sized hepatic arteries for high-grade blunt liver injury.
The rates of complication between patients undergoing nonoperative management with and without angioembo­lization have been reported to be similar.
32
managed nonoperatively. Patient selection for nonoperative management is similar to other intraabdominal solid organ injuries, and is based on the patient’s physiology, associated injuries, and anatomy. One unique factor of the kidney is its retroperitoneal location, which makes the nding of hemo­peritoneum less common, as Gerota fascia may tampon­ade bleeding from the injury. The majority of blunt renal injuries are the result of sudden deceleration which applies sheer forces to the renal pelvis or pedicle, as it is the only xed attachment point of the kidney.
Renal injuries that are amenable to angioemboliza­tion include parenchymal injury with arterial contrast extravasation, pseudoaneurysms, arteriovenous stulas, and nonself-limiting gross hematuria.31 Successful use of embolization in the setting of blunt kidney injury ranges from 63% to 100%. not mandate operative intervention, and a second attempt may prove successful.
31–34
Initial failure of embolization does
32,35
If embolization of the injury is to be undertaken, a super-selective approach should be under­taken to limit scarring and to preserve renal function. The use of microcoils is preferred in these cases, as embolic agents are prone to reux into neighboring arteries and adversely affect uninjured parts of the kidney. If an emboli­zation or sclerosing agent is to be used, we recommend using a balloon catheter to deliver the agent, as it can be inated to occlude the injured branch and prevent reux of mate­rial. Blind angioembolization or more proximal emboliza­tion should be avoided, as this will result in necrosis of the renal parenchyma and other complications.36 If during the endovascular procedure the patient becomes unstable or the injury is deemed to require operative intervention, balloon occlusion of the main renal artery is a useful maneuver to reduce bleeding until open surgical control can be achieved.
Injuries to the renal artery or vein in hemodynamically stable patients may be managed with revascularization maneuvers including placement of a covered stent across the area of vascular disruption to preserve ow to the renal parenchyma. Unlike other solid organs of the abdomen, there is no collateral ow to the kidney and the organ does not tolerate proximal, large-vessel embolization/occlusion. In order to place a covered stent in the main renal artery, the injured portion of the vessel must be able to be safely
POSTINTERVENTION MANAGEMENT
After successful embolization of an abdominal solid organ injury, close monitoring is necessary to assess for rebleed­ing. Up to 13% of patients will require either additional embolization or splenectomy after initial SAE for splenic trauma.39 Similar rates exist for patients undergoing embo­lization for liver or renal injury. No consensus exists at this time for a monitoring algorithm after the procedure. We rec­ommend trending hemoglobin/hematocrit every 6 to 8 hours and monitoring in an ICU for at least the rst 24 hours after the procedure. Once discharged from the ICU, these patients remain in the hospital for a minimum length of stay of at least 3 days while we continue to trend hemoglobin and hemato­crit at less frequent intervals. There is no evidence to suggest pharmacologic prophylaxis for venous thromboembolism (VTE) increases failure of nonoperative management of solid organ injuries. We initiate VTE prophylaxis after two consecutive stable hemoglobin checks and if there is no other evidence of bleeding.
12,40
Repeat imaging during the patient’s hospital course should be guided by clinical status. Some groups advocate for reimaging of the solid organ 48 to 72 hours after the injury to assess for latent pseudoaneu­rysms or AVF that may benet from intervention, but this practice is clinician and institution-dependent.
Pelvic Bleeding
Pelvic injuries with associated bleeding present a chal­lenge for surgeons and the resuscitation team. It takes a signicant amount of energy to cause a pelvic fracture, and as such, these injuries are often associated with other life-threatening ndings requiring acute intervention. Of these patients, 15% will have an associated injury in the chest, 32% an intraabdominal injury, and 40% a long bone fracture.41 A multiplicity of injuries can confound the initial workup and management of these critically ill patients, whose risk of death is as high as 40%.42 A rel­atively small proportion of bleeding associated with pel­vic fractures is secondary to an arterial source (15%). In contrast, venous or osseous sources are responsible for up
10 • Stent-Grafts, Coils, and Plugs 121
https://t.me/medicina_free
to 85% of the bleeding that occurs in conjunction with this injury pattern.42 When arterial bleeding is present, it is most commonly from a named branch vessel of the internal iliac artery, such as the superior gluteal, internal pudendal, lateral sacral, iliolumbar, or inferior gluteal. Arterial bleeding is present in more than 60% of patients who die from pelvic fractures.43 It is important to remem­ber that the volume of the pelvis can increase by 20% with a 5-cm pubic diastasis, allowing for potentially fatal hem­orrhage in what is normally a conned space.
44
As with the management of other injury patterns, patient selection is important to optimize success. Hemo­dynamically unstable patients should be initially managed by advanced trauma life support guidelines including pel­vic x-ray, external reduction of the pelvic fracture using a binder or sheet, and performance of a focused assessment with sonography for trauma (FAST) examination to assess for hemoperitoneum. If the patient is hypotensive, and there is no hemoperitoneum, the patient should undergo arteriography if the capability exists in that given medical center. In settings where these capabilities are not pres­ent or there is a signicant hemoperitoneum, the patient should undergo preperitoneal packing and laparotomy. If hemorrhage continues with preperitoneal packing, angi­ography/angioembolization may be used as an adjunct for hemostasis after open surgery (Fig. 10.5).
If on initial presentation the patient is hemodynami­cally normal, he or she may undergo the usual trauma evaluation including contrast-enhanced CT imaging of the abdomen and pelvis, with a delayed phase to assess for bleeding and injuries to pelvic or genitourinary structures. If contrast extravasation is identied on CT imaging, diag­nostic and potentially therapeutic arteriography should be performed. This should be undertaken as quickly as
possible, as each hour of delay has been shown to be asso­ciated with increased mortality.
45
If obtained prior to the pelvic arteriogram, CT imaging can direct or help improve the efciency of the catheter­based intervention. It is important to understand the vas­cular anatomy of the pelvis, including collateral pathways that may contribute to bleeding. These include the contra­lateral internal iliac, lumbar, inferior mesenteric, inferior epigastric, medial and lateral circumex, median sacral, and deep circumex iliac arteries. This anatomy is variable, and beginning the procedure with a pelvic arteriogram is often benecial if there has been no preceding CT imaging. Next, selective catheterization of the internal iliac artery is performed and digital subtraction angiography obtained to delineate the vascular anatomy. Once the bleeding source is localized, embolization may be performed.
In these cases, selective embolization of the bleeding arteries is ideal and can be achieved using either coil embo­lization which causes permanent occlusion or a temporary agent such as Gelfoam. Angioembolization in the pelvis is a risk factor for orthopedic interventions to the pelvic ring to have higher complications rates.46 However, in hemody­namically unstable patients, less selective embolization is often employed, including Gelfoam, which can be used as an embolic agent for larger portions of the internal iliac artery circulation. Because of extensive collateral circula­tion, it is often necessary to complete embolization of ves­sels in the contralateral internal iliac system to achieve a more complete hemostasis. If the patient continues to have evidence of bleeding after initial selective embolization maneuvers, occlusion of bilateral internal iliac arteries may be performed in an attempt to decrease ow (i.e., pressure head) through the system and allow for tamponade of small arterial and venous bleeding.
Fig. 10.5 (A) Patient with active extravasation of contrast from the mid left internal iliac artery that was not controlled with per-peritoneal packing (retractor and radio-opaque laparotomy pads seen in negative on digital subtraction angiography). Laparotomy was performed and proximal control of distal aorta (zone III) was performed while awaiting endovascular support. (B) Image after embolization without additional extravasation.
122 SECTION 3 Emerging Technologies and New Approaches to Vascular Trauma and Shock
https://t.me/medicina_free
In certain hemodynamically unstable patients, when sur­gical xation of the pelvic fracture is necessary, temporary balloon occlusion of the internal iliac arteries may be per­formed to slow bleeding. Denitive angioembolization may then be performed after the anatomy of the bony pelvis is restored. These interventions are not without complica­tions. The most common complications are at the vascular access site or involve contrast-induced nephropathy. Com­plications related to the embolization include pelvic infec­tion, poor bone healing, skin sloughing, skin or muscle necrosis, rectal ischemia, and neurologic effects on the bladder and/or sexual function.
43,44,47
Cervical Vascular Injury
Trauma to vessels at the thoracic outlet and in the cervical region may be preferentially managed with endovascular techniques depending on the size of the vessel and its acces­sibility via an open surgical approach. In hemodynamically stable patients with penetrating neck injuries or a concern for blunt cerebral injury, the workup begins with contrast­enhanced CT imaging to assess for extravasation, vessel dis­ruption, dissection, intimal ap, pseudoaneurysm, AVF, or thrombosis. Once the defect is identied in this scenario, the choice of management is based on the anatomic location of the injury. The location of neck injuries is described in one of three zones reported by Monson et al. in 1969. Zone I is below the cricoid cartilage, zone II is located between the cri­coid cartilage and the angle of the mandible, and zone III is above the angle of the mandible.48 Zone II injuries are readily accessible via a cervical incision, which has the added ben­et of direct visual inspection of adjacent aerodigestive tract structures. This accessibility and the low morbidity of a cervi­cal incision make open repair the approach of choice for zone II injuries. Patients with hard signs of vascular injury includ­ing expanding hematoma, pulsatile bleeding, neurologic
changes, or loss of distal pulse require operative exploration irrespective of the zone of injury. Although not the primary therapy, endovascular adjuncts such as proximal balloon occlusion may be used to gain temporary bleeding control of the great vessels or at the skull base.
In patients with proximal zone I injuries, the area of injury may be accessible through a cervical incision. How­ever, many patients with zone I injuries will need a median sternotomy to obtain proximal control to perform a repair. If the patient’s physiology permits and there are endovascular capabilities, a transfemoral approach with balloon occlusion using a compliant balloon may spare the patient the morbid­ity of a thoracic exposure. Once the balloon is in place, angi­ography may be performed to locate the injury for surgical planning. If there is adequate proximal vessel length after open exposure, the balloon may be replaced with a clamp. If proximal length is not adequate, the balloon can be main­tained for proximal control during the repair.
Zone III injuries located above the angle of the mandible are often difcult to expose and control. The use of self­expanding covered stents has been described to treat acute injuries that are not amenable to open exposure.49 Zone III is also the most common site for blunt carotid artery injury. Blunt cerebrovascular injury (BCVI) occurs in 3% of trau­mas and is the result of hyperextension or hyperexion of the neck in the setting of a high-speed deceleration injury.50 The Denver group proposed screening criteria in the 1990s and revised them in 2012. The new guidelines contain indication for screening as well as a grading sys­tem (Table 10.3). The mainstay of treatment for low-grade BCVI is anticoagulation. For patients who are not eligible for anticoagulation due to other injuries, either bare or cov­ered stents have been used as an alternate therapy for these injures.51 Pseudoaneurysms may result from blunt or pen­etrating trauma. When present, they can be treated using endovascular coiling or exclusion with a covered stent.
52–54
Studies reporting the use of stents for BCVI have reported
Table 10.3 Blunt Cerebral Vascular Injury (BCVI)
Denver Screening Criteria for BCVI Denver Grading Scale for BCVI
Signs/Symptoms of BCVI
Arterial hemorrhage
Cervical bruit
Expanding cervical hematoma
Focal neurologic deficit
Neurologic examination incongruous with CT scan findings
Stroke on secondary CT scan
Risk factors for BCVI
High-energy transfer mechanism with:
– LeForte II or III fracture
– Cervical-spine fracture patterns: subluxation, fractures
extending into the transverse foramen, and fractures of C1–C3
– Basilar skull fracture with carotid canal involvement
– Petrous bone fracture
– Diffuse axonal injury with GCS score <6
– Near hanging with anoxic brain injury
Adapted from Burlew et al. Blunt cerebrovascular injuries: redefining screening criteria in the era of noninvasive diagnosis. J Trauma Acute Care Surg. 2012;72(2):330–337.
Grade I: Irregularity of the vessel wall or a dissection/intramural hematoma with
<25% luminal stenosis
Grade II: Intraluminal thrombus or raised intimal flap is visualized, or dissection/
intramural hematoma with 25% or more luminal narrowing
Grade III: Pseudoaneurysm
Grade IV: Vessel occlusion
Grade V: Vessel transection
10 • Stent-Grafts, Coils, and Plugs 123
https://t.me/medicina_free
a stroke rate of 0% to 5%, but the rate of cerebrovascular events may be higher given the paucity of quality long-term follow-up data with this injury pattern.
54,55
Vertebral arteries may also be injured from penetrating or blunt trauma resulting in free hemorrhage, pseudoaneu­rysm, AVF, dissection, or occlusion. Encompassing only 0.5% of vascular trauma, the rarity of injury and the relationship to the cervical spine can make treatment a challenge.56 The rst portion of the vertebral artery may be readily accessible via open exposure, whereas the second and third portions are within the cervical spine foramina and skull base, respec­tively, making endovascular intervention preferred. In a ret­rospective review of 101 patients with extracranial vertebral artery injuries (95 of which were penetrating injuries), 81 patients were treated with endovascular intervention, with the majority being coil embolization. Of these, six patients had failed intervention and required open surgery. Primary open surgery was performed in 20 patients, with 10 of those patients subsequently undergoing endovascular procedure for bleeding or AVF.57 Embolization of the vertebral arteries has a complication rate of 0% to 5%, with the most feared complication being stoke, reported at less than 1%.
57
Junctional Vascular Trauma
Junctional trauma includes injury to vessels in the axillo­subclavian and iliac/femoral regions. Injuries to these vessels are not amenable to tourniquet control and are dif­cult, if not impossible, to control with direct pressure. As such, patients with these injuries are at high risk of bleed­ing to death.58 The challenge of managing injuries in the thoracic outlet is obtaining proximal control. Using the open surgical approach requires a median sternotomy to control the innominate and right subclavian arteries or high, left anterolateral thoracotomy with or without cla­vicular resection for left subclavian artery. Even with the associated morbidity of exposure, open surgery remains a standard for hemodynamically unstable patients with junctional hemorrhage. outlet junctional trauma is less problematic for the general or vascular surgeon, as it is accomplished via laparotomy.
Penetrating injury to the axillo-subclavian vasculature often has the added morbidity associated with injury to the brachial plexus that runs adjacent to the artery and vein. Blunt injury to this region is similarly challenging due to the shear and/or traction forces applied to the vessels and nerve bundles. When evaluating vascular injury in the axillo­subclavian (i.e., junctional) region, it is especially important to consider concomitant nerve, aero-digestive tract, boney, or lymphatic injury.61 In stable patients, CT angiography can aid in identifying the location and extent of vascular injury. Once the area of injury is identied, an operative plan can be formulated based on accessibility of the vessel and if balloon proximal control is needed to prevent exsan­guination. One advantage of the hybrid operating room is being able to place a proximal occlusion balloon to provide hemostasis while open exposure of the vessel is obtained by a second team for repair. This allows for an arteriogram to be performed under a controlled setting, preventing exsan­guination of the whole area of injury, to identify the injured segment of the vessel. Once the injury is identied, it can
59,60
Proximal control for pelvic
safely be repaired endovascularly with a covered stent or open if easily accessible. This hybrid approach reduces the morbidity of an open repair for this pattern of injury.
62
While experience using stent-grafts for axillo-subclavian pseudoaneurysm, iatrogenic injury, and trauma extends back to the 1990s, its overall use in trauma remains
59,61,63
low.
In 2012, it was reported that 9% of subclavian arterial trauma cases were managed using endovascular techniques.64 In a 2017 multicenter trial, 17% of patients with axillo-subclavian injuries were treated with endovas­cular intervention alone, and an additional 6% had hybrid procedures.59 As hybrid operating rooms become more common, we anticipate an increasing role for endovascular therapy in the management of junctional vascular injuries. This may assist in both proximal and denitive control of the injury. At this time, endovascular intervention offers hope of decreasing the morbidity of a thoracotomy or ster­notomy in patients appropriate for endovascular hemor­rhage control. Postprocedure, there are reports of using anticoagulation or antiplatelet agents over variable time periods to maintain stent patency.55 No consensus exists at this time, and it is our practice to use antiplatelet therapy with 81 mg aspirin daily for life in these patients.
Lower extremity junctional trauma often requires intraabdominal proximal control which is easily obtained by vascular or general surgeons at the infrarenal aorta or through endovascular techniques such as REBOA. With this injury pattern, the transabdominal approach is often used, as there is concern for concomitant intraabdominal injuries. If the injury is more distal, a single iliac artery may be isolated with a retroperitoneal dissection via hockey stick incision or bilateral iliac vessels may be exposed via mid­line extraperitoneal incision.65 An exception is in military trauma, as these patients are wearing body armor that may protect from intraabdominal injuries, while still leaving the wearer susceptible to lower extremity junctional injury.
58
Extremity Vascular Trauma
Extremity vessel trauma is almost always amenable to control with manual pressure or a tourniquet. A proximal tourniquet is generally easily placed for the majority of these injuries and may be replaced with a pneumatic tourniquet on arrival to the hospital. This allows full workup of life-threatening torso, junctional, thoracic, abdominal, or pelvic sources of bleeding while the tourniquet is in place. Extremity vascular injuries causing exsanguination or profound ischemia should be man­aged in an open fashion. There is a limited role for endovas­cular interventions for extremity vascular trauma. Delayed sequalae from extremity vascular trauma such as pseudoan­eurysms or AVF may be managed with open, endovascular, or, in the case of pseudoaneurysms with a small neck, with ultrasound-guided thrombin injection.
References
1. Callcut RA, Kornblith LZ, Conroy AS, et al. The why and how our
trauma patients die: a prospective multicenter Western Trauma Asso­ciation study. J Trauma Acute Care Surg. 2019;86(5):864–870.
2. Romagnoli AN, Zeeshan M, Joseph B, Brenner ML. Utilization of
endovascular and open surgical repair in the United States: a 10-year analysis of the National Trauma Databank (NTDB). Am J Surg. 2019;218(6):1128–1133.
124 SECTION 3 Emerging Technologies and New Approaches to Vascular Trauma and Shock
https://t.me/medicina_free
3. Bass EM, Crosier JH. Percutaneous control of post-traumatic hepatic
hemorrhage by Gelfoam embolization. J Trauma. 1977;17(1):61–63.
4. Taylor BS, Rhee RY, Muluk S, et al. Thrombin injection versus
compression of femoral artery pseudoaneurysms. J Vasc Surg. 1999;30(6):1052–1059.
5. Edgerton JR, Moore DO, Nichols D, et al. Obliteration of femoral
artery pseudoaneurysm by thrombin injection. Ann Thorac Surg. 2002;74(4):1413–1415.
6. Kurzawski J, Janion-Sadowska A, Zandecki L, Sadowski M. Compari-
son of the efcacy and safety of two dosing protocols for ultrasound guided thrombin injection in patients with iatrogenic femoral pseu­doaneurysms. Eur J Vasc Endovasc Surg. 2020;59(6):1019–1025.
7. Francisco LE, Asunción LC, Antonio CA, Ricardo RC, Manuel RP,
Caridad MH. Post-traumatic hepatic artery pseudoaneurysm treated with endovascular embolization and thrombin injection. World J Hepatol. 2010;2(2):87–90.
8. Duerig TW, Wholey M. A comparison of balloon- and self-expanding
stents. Minim Invasive Ther Allied Technol. 2002;11(4):173–178.
9. Grenacher L, Rohde S, Gänger E, Deutsch J, Kauffmann GW, Richter
GM. In vitro comparison of self-expanding versus balloon-expandable stents in a human ex vivo model. Cardiovasc Intervent Radiol. 2006;29(2):249–254.
10. Sclafani SJ. The role of angiographic hemostasis in salvage of the
injured spleen. Radiology. 1981;141(3):645–650.
11. Sclafani SJ, Shaftan GW, Scalea TM, etal. Nonoperative salvage of
computed tomography-diagnosed splenic injuries: utilization of angiography for triage and embolization for hemostasis. J Trauma. 1995;39(5):818–825; discussion 826–827.
12. Stassen NA, Bhullar I, Cheng JD, etal. Selective nonoperative manage-
ment of blunt splenic injury: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 Suppl 4):S294–300.
13. Clancy TV, Gary Maxwell J, Covington DL, Brinker CC, Blackman D.
A statewide analysis of level I and II trauma centers for patients with major injuries. J Trauma. 2001;51(2):346–351.
14. Arumugam S, Al-Hassani A, El-Menyar A, et al. Frequency, causes and pattern of abdominal trauma: a 4-year descriptive analysis. J Emerg Trauma Shock. 8(4):193–198.
15. Smith J, Caldwell E, D’Amours S, Jalaludin B, Sugrue M. Abdominal
trauma: a disease in evolution. ANZ J Surg. 2005;75(9):790–794.
16. Crichton JCI, Naidoo K, Yet B, Brundage SI, Perkins Z. The role of
splenic angioembolization as an adjunct to nonoperative manage­ment of blunt splenic injuries: a systematic review and meta-analysis. J Trauma Acute Care Surg. 2017;83(5):934–943.
17. Cirocchi R, Boselli C, Corsi A, etal. Is non-operative management safe
and effective for all splenic blunt trauma? A systematic review. Crit Care. 2013;17(5):R185.
18. Foley PT, Kavnoudias H, Cameron PU, Czarnecki C, Paul E, Lyon SM.
Proximal versus distal splenic artery embolisation for blunt splenic trauma: what is the impact on splenic immune function? Cardiovasc Intervent Radiol. 2015;38(5):1143–1151.
19. Schnüriger B, Inaba K, Konstantinidis A, Lustenberger T, Chan LS,
Demetriades D. Outcomes of proximal versus distal splenic artery embolization after trauma: a systematic review and meta-analysis. J Trauma - Inj Infect Crit Care. 2011;70(1):252–260.
20. Machálek L, Holibková A, Tůma J, Houserková D. The size of the
splenic hilus, diameter of the splenic artery and its branches in the human spleen. Acta Univ Palacki Olomuc Fac Med. 1998;141: 45–48.
21. Ekeh AP, Khalaf S, Ilyas S, Kauffman S, Walusimbi M, McCarthy MC.
Complications arising from splenic artery embolization: a review of an 11-year experience. Am J Surg. 2013;205(3):250–254.
22. Wu SC, Chen RJ, Yang AD, Tung CC, Lee KH. Complications associ-
ated with embolization in the treatment of blunt splenic injury. World J Surg. 2008;32(3):476–482.
23. Duane TM, Como JJ, Bochicchio GV, Scalea TM. Reevaluating the
management and outcomes of severe blunt liver injury. J Trauma - Inj Infect Crit Care. 2004;57(3):494–500.
24. Pachter HL, Knudson MM, Esrig B, etal. Status of nonoperative man-
agement of blunt hepatic injuries in 1995: a multicenter experience with 404 patients. J Trauma. 1996;40(1):31–38.
25. Fang JF, Chen RJ, Wong YC, etal. Pooling of contrast material on
computed tomography mandates aggressive management of blunt hepatic injury. Am J Surg. 1998;176(4):315–319.
26. Stassen NA, Bhullar I, Cheng JD, etal. Nonoperative management
of blunt hepatic injury: an Eastern Association for the Surgery of
Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 SUPPL.4):S288–293.
27. Tinkoff G, Esposito TJ, Reed J, et al. American Association for the
Surgery of Trauma organ injury scale i: spleen, liver, and kidney, validation based on the National Trauma Data Bank. J Am Coll Surg. 2008;207(5):646–655.
28. Matsushima K, Hogen R, Piccinini A, etal. Adjunctive use of hepatic
angioembolization following hemorrhage control laparotomy. J Trauma Acute Care Surg. 2020;88(5):636–643. 2020.
29. Green CS, Bulger EM, Kwan SW. Outcomes and complications of
angioembolization for hepatic trauma: a systematic review of the literature. J Trauma Acute Care Surg. 2016;80(3):529–537.
30. Erlich T, Kitrey ND. Renal trauma: the current best practice. Ther Adv
Urol. 2018;10(10):295–303.
31. Coccolini F, Moore EE, Kluger Y, etal. Kidney and uro-trauma: WSES-
AAST guidelines. World J Emerg Surg. 2019;14(1):54.
32. van der Wilden GM, Velmahos GC, Joseph DK, etal. Successful non-
operative management of the most severe blunt renal injuries: a multicenter study of the research consortium of New England Cen­ters for Trauma. JAMA Surg. 2013;148(10):924–931.
33. Mohsen T, El-Assmy A, El-Diasty T. Long-term functional and mor-
phological effects of transcatheter arterial embolization of traumatic renal vascular injury. BJU Int. 2008;101(4):473–477.
34. Sarani B, Powell E, Taddeo J, etal. Contemporary comparison of sur-
gical and interventional arteriography management of blunt renal injury. J Vasc Interv Radiol. 2011;22(5):723–728.
35. Huber J, Pahernik S, Hallscheidt P, etal. Selective transarterial embo-
lization for posttraumatic renal hemorrhage: a second try is worth­while. J Urol. 2011;185(5):1751–1755.
36. Breyer BN, McAninch JW, Elliott SP, Master VA. Minimally invasive
endovascular techniques to treat acute renal hemorrhage. J Urol. 2008;179(6):2248–2253.
37. Breyer BN, Master VA, Marder SR, McAninch JW. Endovascular man-
agement of trauma related renal artery thrombosis. J TraumaInj Infect Crit Care. 2008;64(4):1123–1125.
38. Lee JT, White RA. Endovascular management of blunt traumatic
renal artery dissection. J Endovasc Ther. 2002;9(3):354–358.
39. Zarzaur BL, Dunn JA, Leininger B, et al. Natural history of
splenic vascular abnormalities after blunt injury: A Western Trauma Association multicenter trial. J Trauma Acute Care Surg. 2017;83(6):999–1005.
40. Eberle BM, Schnüriger B, Inaba K, et al. Thromboembolic prophy-
laxis with low-molecular-weight heparin in patients with blunt solid abdominal organ injuries undergoing nonoperative manage­ment: current practice and outcomes. J Trauma Inj Infect Crit Care. 2011;70(1):141–147.
41. Heetveld MJ, Harris I, Schlaphoff G, Balogh Z, D’Amours SK, Sugrue
M. Hemodynamically unstable pelvic fractures: recent care and new guidelines. World J Surg. 2004;28(9):904–909.
42. White CE, Hsu JR, Holcomb JB. Haemodynamically unstable pelvic
fractures. Injury. 2009;40(10):1023–1030.
43. Salazar GMM, Walker TG. Evaluation and management of acute vas-
cular trauma. Tech Vasc Interv Radiol. 2009;12(2):102–116.
44. Salcedo ES, Brown IE, Corwin MT, Galante JM. Pelvic angioemboliza-
tion in trauma – indications and outcomes. Int J Surg. 2016;33(Part B):231–236.
45. Matsushima K, Piccinini A, Schellenberg M, etal. Effect of door-to-
angioembolization time on mortality in pelvic fracture: every hour of delay counts. J Trauma Acute Care Surg. 2018;84(5):685–692.
46. Ding A, O’Toole RV, Castillo R, etal. Risk factors for early reoperation
after operative treatment of acetabular fractures. J Orthop Trauma. 2018;32(7):E251–E257.
47. Rehwald R, Schönherr E, Petersen J, etal. Prognostic factors in endo-
vascular treated pelvic haemorrhage after blunt trauma. BMC Surg. 2017;17(1):1–13.
48. Monson DO, Saletta JD, Freeark RJ. Carotid vertebral trauma. J Trauma.
1969;9(12):987–999.
49. Wang K, Peng X, Liu A, etal. Covered stenting is an effective option
for traumatic carotid pseudoaneurysm with promising long-term out­come. J Korean Neurosurg Soc. 2020:1–8.
50. Grigorian A, Kabutey NK, Schubl S, et al. Blunt cerebrovascular
injury incidence, stroke-rate, and mortality with the expanded Denver criteria. Surg (United States). 2018;164(3):494–499.
51. Arthurs ZM, Sohn VY, Starnes BW. Vascular trauma: endovas-
cular management and techniques. Surg Clin North Am. 2007; 87(5):1179–1192.