Blunt vascular trauma

June 24, 2017 | Autor: Laurel Omert | Categoria: Humans, Clinical Sciences, Blood Vessels
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BLUNT

VASCU

TRAUMA

IN BFUEP The mixture of high, and increasing, roadway speeds, mounting highway congestion, and a general intensification of life’s pace has an unfortunate consequence: the inevitable occurrence of highspeed vehicular crashes. The people injured in such crashes, or in any traumatic event, are now more likely than ever before to enter a system of emergency care that brings rescuers to the scene and gets the stabilized patient to a hospital or trauma center in the shortest possible time. More severely injured patients are reaching definitive medical care while time still remains in the “golden hour.” The increased accuracy and definition in diagnostic techniques allow clinicians to find even occult injuries and appropriately intervene in lifethreatening processes. Our intent in writing this monograph is to cover the full spectrum of one type of potentially devastating injury-blunt vascular trauma. The diagnosis and treatment of vascular injuries resulting from blunt impact can be particularly challenging because the patient may have no external signs of injury or only minimal evidence of the internal damage. Furthermore, the tremendous force necessary to produce a vascular lesion usually causes associated injuries, which may be dramatic in appearance and thus divert attention from the vascular derangement. These associated injuries may also demand alterations in the usual treatment algorithms, as for a patient with a ruptured aorta and a severe head injury. Throughout recorded history, humans have sustained injuries to major vessels as a result of military conflicts as well as intentional and unintentional trauma (assaults and “accidents”). A large body of literature has accumulated based on the discovery, diagnosis, and treatment of these injuries. But most patients described in those accounts incurred penetrating trauma. Clinicians and institutions have far less often reported their experience with blunt vascular trauma. The approaches and conclusions contained in this monograph are based primarily on the experience gained at the Shock Trauma Center of the Maryland Institute for Emergency Medical Services Systems (MIEMSS). Here, approximately 3,500 patients are treated 286

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each year. More than &5W oi these patients have sustained blunt trauma, and 3% have sustained injury to the vascular system. The Shock Trauma Center is tke clinical hub of a statewide network of emergency communications, transportation (ambulances and stateoperated helicopters), and medical facilities. This comprehensive system of emergency care extends from on-the-scene, prehospi stabilization and immobil n, to definitive medical treatment the most appropriate hospi or trauma center. The MIEMSS Shock Tra Center is Maryland’s level I trauma center designated to eive adults with the most life-threatening injuries (including mu1 e-system trauma, head and spinal cord injuries, and conditions quiring hyperbaric oxygen therapy). Patient information is maintained within a clinical trauma registry, which details the history physical findings, and hospital course as well as the management decisions based on the suspicion and documentation of injuries. Data fer this monograph, reporting one of the largest experiences with blunt vascular trauma from one institution, were retrieved from that clinical trauma registry. The event that induces most blunt vascular injuries is a motor vehicle crash. The mechanism of injury is usually associated with deceleration and compression forces. We believe that a better understanding of these mechanisms, and thus heightened suspicion for resultant vascular disrup ns, allow for earlier diagnosis and treatment of these subtle, n devastating injuries. This increased awareness of patterns of injuries could lead to the design of safer vehicles and roadways. Although this monograph oes not focus on the technical aspects of the repair of blunt vascul injuries, we have extended those parameters in one particular area, that is, the surgical management of the traumatically ruptured aorta. Our recommendations regarding the treatment of an aortic injury are based on our extensive experience with many patients with this injury seen at the MIEMSS Shock Trauma Center. In addition to the review of ruptured aortas and other thoracic injuries, we discuss trauma to other anatomic regions: the neck, abdomen, a d upper and lower extremities. Blunt injuries to the vess of the neck are among the most cult to diagnose and can be lethal. A high index of suspicion and a low threshold for performing angiography are paramount for m the diagnosis. Once the diagnosis is made, the decisions regarding treatment may be difficult. The clinical status of the patient may complicate the choice of therapy. A thorough understanding of the current literature is ~eces~a~ to guide the clinician to the best decision. Traumatic injuries to the major thoracic vessels often represent dramatic clinical problems that demand rapid diagnosis and aggressive treatment Aortic dis~~t~on is among the most serious of these

injuries. This is an injury with which our institution has had an unusually large experience. The development of emergency medical systems has improved the early diagnosis and treatment of these injuries. The key to making the diagnosis is a high index of suspicion in any patient involved in a rapid deceleration accident, a good history and physical examination, and a baseline chest radiograph made with the patient upright. It is imperative that early evaluation be accomplished with minimal delay. Aortography remains the “gold standard” for making the diagnosis. However, we point out situations where chest computed tomography may be helpful in the diagnosis and management. The combination of injured thoracic vessels and either abdominal or head injury remains a difficult problem. Guidelines regarding the timing and order of repair are given. Blunt vascular injuries to the abdomen are commonly accompanied by other significant intraabdominal injuries. Consequently, the diagnosis of these injuries is made more difficult and the morbidity and mortality are increased. Rapid evaluation and prompt exploration to achieve control of the hemorrhage and to restore the blood flow are imperative. We believe a’“second-look” procedure is necessary if there is any question about the gastrointestinal vasculature. Historically, loss of a limb was a common outcome of both military and civilian injuries. Major improvements in both reconstruction techniques and graft material led to decreased amputation rates between World War II and the Vietnam conflict. However, blunt vascular trauma of the extremities continues to cause significant morbidity and mortality. The reason is twofold. First, vascular injuries of the extremities can be subtle, obscuring the diagnosis. Second, associated injuries often make the diagnosis and management difficult and increase the morbidity and mortality. A coordinated multidisciplinary approach, including the judicious use of fasciotomy and early orth.opedic stabilization, can further reduce the residual functional limitations experienced by the patients who sustain blunt vascular injuries of the extremities. An important concept derived from our review of the hospital course of patients with injured extremity vessels is that the allowable ischemic time for penetrating injuries (4-6 hours) is too long for blunt trauma. Because the outcome is affected by the duration of ischemia, every effort should be made to minimize the ischemic period. The care of the patient who suffers blunt vascular trauma remains a formidable challenge. Controversies regarding the optimal management of these patients persist. We trust that this report of our diagnostic and therapeutic experience will continue the discussion of the appropriate clinical approach to these patients as well as illuminate some effective treatment modalities. 288

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B., is a senior fellow in trauma surgery Carnell Cooper, and critic& care at the Shock Trauma Center of the Maryergency Medical Sem’ces Systems. He ency at the University of Minnesota Dr. Cooper’s scientific interests ree metabolic and immune responses to trauma.

B., F2LC.S., graduated from San Marma, Peru, with a B.S. degree, and redegree from the same inst~t~t~~~ in in the Peruvian Navy as a medical ofr. Rodriguez initiated his surgical internship in the United States at the University of ~i~ci~~at~ under the tutelage of Dr. William Aitemier. He continued his surgical trainin& at Henry Ford Hospital and Pontiac General Hospital. After 2 year offellowship in trauma and critical care at the Shock Trauma Center of the Maryland Znstitute for Eme~.~e~cy Medical Service Systems (‘~Z~~~S~~, he completed 2 years of cardiothoracic surgical residency at Wayne State %Jniversity. Dr. Rodriguez has been a senior attending tra~m~t~zogist and thdracic surgeon at the MZEMSS Shock Trauma Center for the past 12 years. He. has written e~t~~s~ve~yon trauma subjects arid coedited a B-chapter book on cardiothoracic trauma. Dr. Rodriguez is the fQund~~ and first president of the Panamerican .Trauma Society and currently is its executive director. He has served as a visiting professor at numerous institutions in ~~S~~~o~Arner~ca. In addition to cardiovascular trauma, Dr. Ro uez’s interests encompass ~rnpr~~.n~ trauma care on Americtin continent, new frontiers in the use of h ermia, ind new modalities of eva~~ati~~ of the abdomen in trauma, such as sonography and laparoscopy.

Laurel Omert, M.D., a graduate of Yale University, completed her surgical residency at Michael Reese Hospital and Medical Center in Chicago and a Z-year fellowship in trauma and critical care at the Maryland Institute for Emergency Medical Services Systems Shock Trauma Center. At present, Dr. Omert is assistant professor of surgery in the Section of Trauma/Emergency Surgery at the West Virginia University Health Science Center in Morgantown. She is board-ceFt$ed in general surgery and holds added qualifications in surgical critical care. Dr. Omert is also an instructor at the Paramedic/Emergency Medical Technician School in Web-ton, West Virginia, and an Advanced Trauma Life Support instructor. Her research interests focus on nutritional support of the critically ill surgical patient as well as the treatment of multisystem organ failure. 290

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Trauma is a disease without geographic boundaries. It has been stated that “injuries are the most serious public health problem facing developed societies.“” Violence, whether accidental or i~te~ti~~ally produced by man’s i~b~rnani~, is not the province of any race or nation. Increasingly crowded, high-speed roadways have placed more drivers, passengers, and pedestrians at risk of injuries. Despite the improvements in prehospital management and the advances in diagnostic and therapeutic modalities, blunt vascular trauma continues to pose a significa.nt threat to the life and limbs of the injured patient. In this monograph our intent is to cover the full spectrum of blunt vascular trauma, including biomechanics, patho~hysio~o~~ and current techniques for diagnosis and treatment. Also, this monograph focuses on the technical aspects of repairing blunt aortic injuries. Our approac is founded on experience gained at the Shock Trauma Center of Maryland Institute for Emergency Medical Services Systems SSI.” At tbis level I trauma facility ore than 3,500 patients are t d each year. Eighty-six percent of ese patients sustain blunt trauma and 3% have vascular injuries.” 3 Our endeavor is to present objectively this controversial topic and to provide surgeons with inf~~ation that might be useful in managing these challenging injuries.

Major vascular injuries have been a problem for all cultures and civilizations. Althoug a wide variety of surgical procedures were available centuries ago, few techniques were effective for the repair of major vascular injury. The beginning of vascular surgery is credited to Sushruta, the great surgeon who lived in India between 800 and 600 B.C. and practiced vessel ligation.’ During the first half of the 18th century, chemical styptic was the preferred treatment for minor bleeding, cauterization was used for moderate hemorrhage, and ligature was employed almost exclusively for controlling blood flow in large vessels Cur-r

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during amputations. In 1759, Hollowell performed the first lateral arteriorrhaphy while repairing a brachial artery.5 Despite his clinical success, results in the laboratory were not as promising. Consequently, this technique fell into disfavor. Sepsis was a major problem and widespread use of Hollowell’s technique awaited the contribution of Joseph Lister’s articles on antisepsis in surgery in 1867.6’ 7 A benchmark in vascular surgery took place in 1879 in Pavlov’s laboratory in Leningrad. There, Nicolai Eck devised the first portocaval shunt using a continuous row of silk sutures to anastomose the veins. Performed in dogs, it was the first documented anastomosis of two blood vessels.” ’ The first vascular anastomosis for trauma-an end-to-end anastomosis of the femoral arterytook place at Cook County Hospital in Chicago in 1896.l’ Many prominent surgeons of the period (Car~l,~~,~~ Matas,13 and Guthrie*4) began intense work in their laboratories and clinical practices utilizing this new technique. In 1916, Makins,” in a review of the British experience during World War I, recognized that a potential life-for-limb trade-off occurred when vascular repair was attempted. Consequently, ligation became the treatment of choice for traumatic vascular injuries. As a result, the amputation rate in World War II approached 75%, Subsequently, Hughes documented a high amputation rate (32.4%) with extremity vascular ligation during the Korean War.16-ls He also demonstrated that the amputation rate was 12% to 16% when arteries were repaired. These poor results fostered a new approach for the Vietnam era, resulting in a reduction of the amputation rate to approximately 13% .20 Rapid evacuation of casualties, improved resuscitation techniques, and advances in surgical technique are other important principles gained from the Vietnam experience. Advances in technology such as digital subtraction angiography, computed tomography (CT), and prosthetic graft materials have enhanced surgeons’ ability to identity and treat vascular trauma.

MECHANISMS

OF INJURY

Blunt vascular injury is most commonly caused by motor vehicle crashes. The injuries that result from these events are generally caused by rapid deceleration or compression. In accordance with Newton’s first law of motion, when a vehicle traveling at a high speed collides with a slower moving or stationary object, the occupant will continue to move forward along a vector that is in proportion to the opposing force. Therefore, if the vehicle stops suddenly against a tree, wall, or another car, an unrestrained occupant will continue to move forward at the same speed until acted on by a stationary object. Two types of forces result: compression and deceleration. 292

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Mechanisms of blunt injury to the neck are varied and include motor vehicle accidents, Is, chiropractic manipulation, strangulation, boxing matches and diagnostic carotid compressionzl The majority of cases described in the literature occurred as a result of a direct blow to the neck. The forces can be transmitted directly to the internal carotid artery or the artery can be compressed against the cervical vertebrae. A blow to the side of the head, resulting in byperextension, rotation, and stretching of the internal carotid artery across the third cervical vertebra, is the second most common mechanism of injury. A mechanism, intraoral trauma, is ally seen in children wh while carrying foreign objects in mouths .” ull fracture can result in injury t intrapetrous portion of the internal carotid artery. Protected in a bony canal, the cervical portion of the vertebral artery is relatively resistant to trauma. Most blunt vertebral artery injuries are associated with motor vehicle accidents. However, injury has also been associated iropractic manipulationz3 The usual mechanism of injury is rextension and rotation of the neck. Blunt traumatic aorti ture is closely linked to high-speed accidents and the resultant trauma. There is considerable debate over the precise mechanism of injury in traumatic aortic rupture. Two factors are important. First, the descending aorta is relatively fured, compared with the aortic arch and the ascending aorta. This fixation is primarily through the ~ig~e~tum arteriosum of the aortic isthmus Second, the descending thoracic aorta is a rigid structure since it is filled with a column The resulting difference in the rate of deceleration of the rtic arch and of the less mobile descending aorta places max ress on the aortic isthmus, the point of attachment etween these two aortic segments. Most traumatic ruptures occur at this point.z5 Similar mechanisms can affect the ascending aorta, where tear s can extend into the sin.us of the aortic valve or branches of the aortic arch.26 Extension of a periaortic hematoma into the pericardi sac can cause a fatal cardiac tamponade. When involved in a head-on collision, the occupants of the vehicle often hit the steering wheel or dashboard. This can cause significant damage to the organs of the chest. If escaping air is blocked by a closed glottis, intrabroncbial pressures rise, resulting in the blowQ~t of a large bronchus or even the tracbea.z7 Other contents of t chest are also affected. This mechanism of injury can result in fractures, flail chest, pulmonary contusion, lung laceration, and massive hemothorax. The abdominal organs are also subject to deceleration and compression forces. Wit& deceleration, severe stretching forces on tethered organs such as be tidney, spleen, and bowel can result in vascular intimal tears. is can lead to thrombosis and organ isch-

emia.“’ ” The vasculature of these organs can also be avulsed, leading to hemorrhage. Compression forces most commonly result in lacerations to the liver, spleen, pancreas, and bowel and associated vascular injuries to these organs are common. Isolated vascular injuries resulting from compression are rare unless associated with skeletal fractures. Shearing off of the portal vein secondary to compression is a rare exception. Compression injuries that cause pelvic fractures can result in significant vascular injuries and lead to Hypogastric vessel injuries are large retroperitoneal hematomas.30 associated with pelvic fractures. An abdominal aortic intimal tear can occur in association with a spine fracture. Most blunt arterial injuries to the upper extremity are caused by traffic or industrial accidents; motorcyclists appear to be particularly susceptible.31 The mechanism by ich the brachial and axillary arteries are injured is twofold. Aside from laceration by bony fragments, overstretching of the artery can lead to rupture, especially in

Thrombus

FIG 1. Three major forms of traumatic vascular injury that can accompany blunt trauma-induced long-bone fracture. Top, complete transection. Middle, partial transection. Bottom, intimal tear. (From Yaremchuk MJ: Special injuries, in Yaremchuk MJ, Burgess AR, Brumback RJ [eds]: Lower Extremity Salvage and Reconstruction: Orthopedic and Plastic Surgical Management. New York, Elsevier, 1989, p 47. Used by permission.)

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so, acute compression and stretching can an atheromatous artery. result in an intimal tear, ing to rupture, dissection, or throm sis (Fig 11. Ischemic con ures associated with supracondylar fractures of the elbow are Blunt trauma to the f the lawer extremity commonly occurs with both deceleration and compression accidents. In isions, the knees are p ed into the dashboard, resulting in terior dislocation at the knee and hip as well as fraccause of the tight attachments of the poplires of the femur.l’ teal artery just inferior and superior to the knee, dislocation of this joint frequently leads to stretching and disruption of the artery intima. NECK VESSELS

Carotid artery injuries account for 10% of all vascular trauma.“’ Blunt injuries to this vessel are uncommon, constituting 3% to 5% of all carotid trauma; boweve~, they present interesting and challenging diagnosis and manageress issues.32-38 Ninety percent of blunt injuries occur in the internal carotid artery or at the bifurcation as compared with penetrating injuries, which involve the common carotid artery 75% of the time.“’ Blunt carotid trauma is o en difficult to diagnose in the presence of other injuries, es cially a closed head injury) which may To complicate matters elude an accurate p sical examination. ther, patients frequently present without neurologic signs of injury. Indeed, in series by Pearce and Whitehil13’ and Krajewski and Hertzer,35 only 10% of patients manifested neurologic signs of injury in the first hour and 27% of patients ecame symptomatic longer than 24 hours after the injury occurre . In several reported cases, the injured patient was as tomatic and the diagnosis delayed for signs do appear, they most comweeks or even months.3s monly include aphasia, resis, or hemiparesis. Patients with carotid-cavernous sinus fistulas may develop abnormalities of CFSnial nerves III, IV, V, and VI. Blunt carotid injuries can be separated into four distinct groups. Type I injuries result from a direct blow to the neck and may result in hemorrhage, thrombosis, or pseudoaneurysm. In type 11 injuries, b,vperextension of the neck causes compression of the carotid artery vessel between the mandible and upper cervical vertebrae and can result in intim&l disruption creation of a flap,35 and thrombus formation Once initiated, ~bro~b~s may7 propagate proximally distally within the vessel Type III injuries typically occur secondary Curr

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23%

to intraoral trauma, and type IV injuries are carotid-cavernous sinus fistulas, which usually occur in conjunction with a basilar skull fracture.32’ 35 Typ e I m ’ j uries are by far the most common. If a patient with neck or cervical trauma develops or manifests lateralizing neurologic signs, the initial study should be a CT scan of the brain, followed by four-vessel cervical angiography.4” The examination should be thorough because bilateral and multiple-vessel injuries can occur.41-43 In patients who present with no neurologic deficits but with a worrisome mechanism of injury, an arteriogram is warranted. The spectrum of injuries that can occur as a result of blunt traumatic episodes includes spasm, intimal disruption, dissection, pseudoaneurysm, thrombosis, and complete transection (Figs 2-4).

FIG 2. A selectwe internal blunt trauma. 296

carotid

arteriogram,

demonstrating

an lnrirnal

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19%~

A selective !eft internal carotid artenosran?, showing portion (arrow) and a distal intimal dissection. The skull base and led to left middie cerebral infarction.

a pseudoaneurysm injury was caused

of the caverneus by a fracture at the

Once a carotid jnjury is diagnosed, the mode of treatment can be Most physicians agree that patients either surgical or nonsurgic with accessible lesions and normal neurologic function should undergo revascularization.44 Surgical! jntervention should be considered in those patients with carotid injury who present with transient ischemic attacks, a ing and waning neurologic status, or progressive neurologic deterioration. Even patients with mild neurologic deficits deserve surgica‘r consideration because a clot from the site of injury can embolize, leading to additional neurologic de% tits. 34,45 The issue of optimal management in comatose patients is unresolved. Most clinicians believe that there is little to gain by surgery,

FIG 4. A right internal

common carotid

carotid artenogram, demonsrrattng artery (arrow) following blunt trauma.

complete (Courtesy

thrombosis of the proximal of S. Mirvis, M.D.)

so nonsurgical management is the treatment of choice.35 However, matters are usually not so well efined, and considerable clinical judgment is required. Carotid-cavernous sinus fistulas are usually treated by angiographic occlusion techniques. In a retrospective review of 484 patients with blunt vascular trauma at the MIEMSS Shock Trauma Cenclosure. It is ter,46 1 of the 2 patients with fistulas had spontaneous important to insert the balloon and inflate it while the patient is observed for neurologic deterioration. If neurologic deterioration occurs, the patient may require extracranial-intracranial bypass prior to the balloon-induced occlusion. If the patient tolerates occlusion, the balloon is left inflated for 8 weeks, by which time the fistula has usually thrombosed. On occasion, it has been necessary to ligate the internal carotid artery proximal and distal to the fistula.40’47,48 238

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The mortality sate fro blunt carotid trauma has ranged from 23% to 40% .4g In one seriesi3’ death or severe neurologic damage was the result of nonoperative treatment in 86% of patients, while those who underwent arterial reco~~t~~c~~~~ had a 53% rate of mortality or severe neurologic deficit During the time of the MHEMSS Shock Trauma Center study of blunt vascular trauma,4s five patients were admitted with blunt carotid artery injury. One was neurologically intact at diagnosis; a vein graft interposition was performed, and the patient was discharged in good neurologic condition. TWQ hemiparetic patients were treated differently. One, a tr ferred patient, was admitted to the instit more than 48 hours er injury. This patient was systemically he rinized fm 3 weeks discharged with hemiparesis and receptive aphasia. The second patie ad a severe head injury, which precluded anticoagulation. The carotid artery was ligated, and no progressive postoperative deterioration was noted. Two patients with carotid-cavernous sinus fistulas were identified. One patient was observed, and the fistula closed spontaneously. The other patient was treated successfully with balloon embolization.

VERTEB

AR’TEAb/

R/lost vertebral

artery

mju&s

are secondary

to blunt

;rau

some occur following c iropractic manipulation and yoga exercises. 32,34J5o The mechanism of injury appears to involve neck hy-

perextension and rotation, which can result in an intimal tear, section, pseudoaneurysm, or arteriovenous fistula.51 In the ME Shock Trauma Center series4” three patients incurred vertebral artery injuries accsmpa . ce~cal spine fractures. No patient underwent surgical repa no further neurologic deterioration occurred. In general, injury to the vertebral artery is usually well tolerated, and ischemia of the midbrain or cerebellum does not occur as long as the contralateral vertebral artery is normal and flow in the ipsilatera1 posterior inferior cerebellar artery PICA) is preserved. However, 3.1% of left vertebral arteries and 1.8% of right vertebral arteries do not communicate with the asilar arteries.“2 Additionally, 15% of the population has one hyvpo lastic vertebral artery.53 Patients with these anomalies are at high risk for midbrain and cerebellar ischemia following a vertebral artery injury. This heightened risk underscores the need for a preoperative arteriogram. The clinical ma~ifesta~i~~~ of vertebral artery trauma are frequently delayed. They include headache, nausea, ataxia, dy~a~l~ri~, and cranial nerve p ies. Patients may present with a classic Wallenberg’s syndrome ficits involving cranial nerves V, IX, X, and XI curi- Probl surg, May 1992

xx3

and a contralateral loss of pain and temperature) or with the “locked-in” syndrome (respiratory failure and quadriplegia with intact cognition) .32S53 The diagnosis of vertebral artery injury can be difficult and a high index of suspicion is necessary. Appropriate signs and symptoms found in patients with cervical spine or neck trauma should be investigated with four-vessel cervical angiography (Figs 5- 7) unless the patient appears to have had a cerebellar infarction (which can be documented by CT). Patients with an infarction may require emergency suboccipital decompression of the posterior fossa mass. In general, vertebral artery injuries do not require treatment unless the opposite vertebral artery is hypoplastic. If the injured vessel ends in a PICA or contributes substantial blood supply to the spinal cord, ischemia can result a.nd the patient might benefit from revascularization.54 Pseudoaneurysms and arteriovenous fistulas can be embolized angiographically, but if this is not technically feasible, operative intervention is necessary.53

FIG 5. A selective left vertebral arteriogram, demonsrratlng ing blunt trauma. (Courtesy of S. Mirvis, M.D.) 300

occlusion

of the artery

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lntimal dissection of the horizontai qoition OI tne ngh: chiropractic manipulation. The patient deve!oped laterai syndrome). (Courtesy Of S. Mirvis, M.D.;

verteDral medullary

artery (arrows) fQiiGWiflg infarction (Wallenberg’s

Blunt chest trauma can restiit in a variety of vascular injuries.“” These injuries are most corn~~~nly incurred in high-speed motor vehicle crashes. The most common vascular injury due to blunt thoracic trauma is aortic rupture. The rupture usually occurs just distal to the origin of the left subclavian artery. The next most frequently injured vessels are the subclavian and innominate arteries. The dktribution of thoracic vascular injuries seen at the MIEMSS Shock Trauma Center is presented in Figure 8.

Traumatic injuries to tire major thoracic vessels often represent dramatic clinical prob?ems that demand rapid diagnosis and decision making as well as aggressive management. Aortic disruption remains one of the most devastating injuries seen in blunt chest

FIG 7. A selective bral artery M.D.)

left subclavian arteriogram, demonstrating proxlmai occlusion of the ieft verteiarrow). The patient sustained a lateral medullary infarct. (Courtesy of 0. Pais,

trauma.3’ 56 However, the development of emergency medical systems has improved the early diagnosis and treatment of this injury.57-61 Aortic injury, initially described by Versalius in ~5.57,~~ became better understood during World War I, when it was seen relatively frequently in the crew members of crashed planes.63 The first extensive report came in 1957, when Parmley and coworkers from the Armed Forces Institute of Pathology reported on 296 cases of nonpenetrating injuries to the aorta.64 302

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The distribution (1983-1988). WC = superior vein.

of thoracic blunt vascular injuries at the MIEMSS Shock Trauma Center SA = subclavian artery, SV = subclavian vein; IVC = Inferior vena cava; vena cava; IC = internai carotld; PA = pulmonary artery; PV = puimorlary

Greendyke, in a 1966 review, tound that I in 6 people killed in vehicular crashes sustained an aortic rupture.‘” He also noted that aortic rupture was more common among occupants ejected from the vehicles. As described by Parmley and associates,“” 80% to 90% of those who sustain blunt traumatic thoracic aortic rupture die prior to reaching a medical facility. Ap ~~x~rnat~ly 25% of the remaining eurvivors die in the following 24 ours. Another third of the initial survivors die during the first 2 weeks, leavi approximately 6% of the total number of victims alive. Although ronic traumatic thoracic aortic aneurysms have been observed, their stability is doubtful and delayed ruptures do occur without surgical intervention (Fig 57,6G--69 9 1. The most common setting for aortic disruption is rapid deceleration, resulting in extreme force along a horizontal or vertical plane. As discussed earlier, such ct intrathoracic organs differently, depending on their ocation, and attachments and the direction of the force. raclc aorta is relatively mobile except at the isthmus, where it is tacbed at the level of the ~~g~rne~turn arteriosum. This is by far most common location for trau-

SCHEMATIZED BLUNT

COMPOSITE NATURAL TRAUMATIC THORACIC

SURVIVAL CURVE AORTIC RUPTURE

FOR

FIG 9. A hypothetic composite survival curve of untreated blunt traumatic aortic rupture, with estimated uncertainty limits, based on published autopsy and clinical series and the resuscitation outcome experience at the Shock Trauma Center.57, 66-6s (From Turney SZ, Rodriguez A: Injury to the great thoracic vessels, in Turney SZ, Rodriguez A, Cowley RA [eds]: Management of Cardiothoracic Trauma. Baltimore, Williams & Wilkins, 1990, p 231. Used by permission.)

matic rupture of the aorta (Fig 10). Tears of the descending thoracic aorta, arch, and abdominal aorta are far less common, but they do occur. The clinical presentation of rupture of the thoracic aorta is variable. Upper-extremity hypertension (‘“pseudocoarctation syndrome”) or a pulse pressure difference between the right and left arms should immediately arouse suspicion, but these are relatively uncommon findings. A high index of suspicion of rupture in any patient involved in a rapid deceleration accident enhances the clinician’s ability to make the diagnosis. A baseline chest radiograph should be obtained on admission6”’ 7o Signs of aortic rupture such as a widened mediastinum or an obscured aortic knob require further investigation. Since the initial. chest film is usually obtained with the patient supine, a 304

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Schematic views of the aortic arch and descending aorta from the left lateral perspective. showing common variations of an acute traumatic rupture of the descending aorta. (From Turney SZ, Rodriguez A: Injuries to the great thoracic vessels, in Turney SZ, Rodriguez A, Cowley RA [eds]: Managemen? of Caro’iolhoracic Trauma. Baltimore, Wlliams & Wilkins, 1990, p, 243. Used by permission.)

radiograph made with the patient upright may be all that is required for clarifkation (Figs 11-13). 11 uestions still exist, then ao~ogr~~by is indicated. The variety of rad logic appearances can be diagnostically challenging. These radio1 presentations vary with t es of hematomas and lacerations t have been incurred. A continuously growing body of literature describes experiences

FIG Il. An anteropostenor chest radiograph made with the patient upnght, showing widening of the mediastinum bilaterally, loss of the aortic arch contour, and an apical pleural cap (arrow). Note the marked left supraclavicular hematoma. The patient had an aortic rupture. (Courtesy of S. Mirvis, M.D.)

An anieroposterior c17es1 raoiograp,“:aae with astinal widening and ioss of the aor!!c contour. (Courtesy of S. Mirvis, M.D.)

ihe oatienr upright, showing gross mealThe patient sustained an aorlic rupture.

FiG 13. ‘An anteropostenor cnest radlogiap;l 3ade witn !he patient in an uprlgl? posiliori, showq a relatively narrow mediastinum but loss of the sot-tic arch contour. The nasogastric tube is oowed slightly to the right !arrowsi. The patient had an aortic rupture. (Courtesy of S. Mirvis, MD.)

FIG 14. An axral CT scan pseudoaneurysm

wrth intravenous projects toward

contrast the right

material, (arrow).

revealing (Courtesy

a ruptured thoracic of S. Mirvis, M.D.)

aorta.

A

FIG 15. An axial CT scan with intravenous contrast material, revealrng an anterior mediastinal hemorrhage. Note the straightening of the panetal pleura (arrowsJ The aorta and great vessels were intact, as determined by angiography. (Courtesy of S. Mirvis, M.D.) 308

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with CT in diagnosin am-tic ~~sr~~tion Wig 14). owever, the lack of experience with this ~ad~o~~a~b~c modality at many medical facilities has raised questions about its sensitivity and specificity. Hn many situations, the i~te~retation of CT results is dependent on a radiologist who in~eq~e~tly sees traumatic aortic lesions. Additionally, mediastinal hematoma may arise from a source other than a ruptured aorta (Fig 15). Despite these drawbacks, in the follower groups of patients, CT has valuable applications: 1. In patients with fracture QT possible neck injury, who cannot be safely oned upright for a chest radiograph and whose chest film in a su ine position shows equivocally abnsrmal mediastinaf contours; 2. Hn patients who require a head an&or abdominal CT scan an

A suggested algorithm for the evaluation of patients sustaining significant blunt deceleratng thoracic trauma. If chest radiograph can be obtained only with the patient supine (1) tne choice of angiography or dynamic enhanced CT should be based on a clinical level of susprcion for injury. When a chest radiograph of the patient upright is equivocal or unsatisfactory (2) the choice of angiography or CT may be influenced by a clinical level of suspicion for injury. AP = anteroposterior; CXR = chest radiograph. (From Richardson P, Mirvis SE, Scorpio R, et al: AJR 1991; !56:273-279. Used by permission.) Curr

Probl

Surg,

May

1992

am

FIG 17. A digital subtraction aortogram, descending aorta (arrows). Note rysm producing acute coarctatlon. 310

demonstrating the narrowing (Courtesy

a large pseudoaneurysm of the aortic lumen below of 0. Pais, M.D.) Curr

Probl

of the proximal the pseudoaneu-

Surg,

May

1992

who have an ~n~at~~fa~to~~ c normal mediastinal contour).

iograph

(equivocaiiy

ab-

thenvise, if a patient demo~$trates unequivocal signs of me nal hemorrhage on a chest diograph, time should not be wasted chest: An immediate a~el~~og~arn is on obtaining a CT scan of warranted71 (Figs 16-21). Ultimately, aortic rupture must be diagnosed by aortograpby prior to a thoracotomy. The most common site of disruption in most seaorta just distal to t ries, including our own, ” is the descending left subclavian artery. Intraabdominal injury in conjunction with a ruptured aorta is frequently seens7 It occurred in 15 of the 41 patients with aortic injury in the MIEMSS Shock Trauma Center series reported by Omert and colleagues.7” Diagnostic and treatment priorities were not well es-

i? digital thoracic lng aorta (arrows). Curr

Probl

Surg,

aortogram, (Courtesy May

1992

demonstrating a pseudoaneurysm of 0. Pais, M.D.)

of tl?e Droxirnai

aescend-

311

FIG 19. A digital subtraction aortogram, rior aspects of the aortic arch

showing (arrows).

a pseudoaneurysm involving (Courtesy of 0. Pais, M.D.)

the dorsal

and

infe-

tablished for this subset of patients until 1982.73 Turney and coworkers74 described 10 patients who underwent both laparotomy and thoracotomy; in 6 of these patients, laparotomy was performed first. These patients were all in shock, had unequivocally positive findings on diagnostic peritoneal lavage, and responded well to the administration of fluid. They were taken to the angiograpby suite and then to the operating room. The average laparotomy time was 1.5 hours; none of the patients developed aortic rupture within this period. Reporting a similar sequence of events in patient management, Fickard and associates7” concluded that hypovolemic shock in the absence of free aortic rupture or external blood loss is most likely caused by intraabdominal bleeding. Eight of the 15 patients in the MIEMSS Shock Trauma Center series with combined abdominal injury and aortic disruption underwent laparotomy prior to thoracotomy;72 no free ruptures occurred during the initial procedure. Two of the remaining 7 patients became significantly hypotensive at the start of laparotomy, during ef312

Cur-r

Probl

Surg,

May

1992

A digital proximai

arteriogram descending

of the thoracic aorta (arrow).

agr[a, showing a small pseudoaneurysm (Courtesy of 0. Pais, M.D.)

oi :he media,

forts to controol the ~ntraab~~~~~~ hemorrhage. They bot oped multiple-organ failure ~o~to~erative~y and were paralyzed despite a Z&minute cross~cla~~~ time. Accordingliy, we recommend tbat a patient in hypovolemic shock, with positive findings on lavage and a distended abdomen, and without evidence of a free aortic rupture or external bleeding undergo laparotomy first, followed by aortogram and thoracotomy. Patients with combined aortic and abdominal injuries have a high mortality rate. In the recent ~~~~~~ study,7Z 9 (69.2%) of the 13 patients who died in the operating room or postoperatively be to this subset Surgical repair is p ed through a posterior left thoracotomy, foFollowing proximal an lstal control of blood flow. A tube graft is most commonly used for re jr. Direct repair is rarely done.76 The use of a shunt to s the area of injury during aortic occlusion is controversial.77 e clinicians advocate the use of simle cross-clamping acic aorta during re -25); others documented a significant decrease i Cum

Probl

Surg,

May

1992

313

FIG 21. A digital subtraction aspect of the aortic ductus divertwlum.

aortogram, revealing a smoothly contoured arch (arrowsj. No intimal tear IS observed. (Courtesy of 0. Pais, M.D.)

defect along the inferior This finding represents a

paraplegia with the use of a shunt iFig 261.77 The centrifugal pump (Bio Medicus Inc., Eden Prairie, Minnesota) utilized with a shunt from the left atrium to the femoral artery was recently demonstrated to be extremely effective”, 8x (Fig 271; cardiopulmonary bypass has been virtually abandoned, except for the repair of ascending aorta or arch injuries. In the MIEMSS series described by Omert and associates7’ 10 injuries (26.3%) were repaired with a shunt and 22 (73%) by simple cross-clamping. Three of the 25 survivors had postoperative paraplegia. A shunt was utilized in 1 paralyzed patient, and the aortic occlusion time averaged 3.5 minutes for the subset. One paraplegic patient had complete paralysis; the other 2, with partial deficits, markedly improved during rehabilitation. One of these 2 latter patients had an associated spine fracture, in addition to other injuries, which might have been responsible for the deficit. The most remark314

Cur

Pi-obl

Surg,

May

1992

The maneuver !o org&ly ~o~s~ti~t 31~ &die .1 :,e,-~aort~c :~:lnel dlouna :ne aomc arcn oeiween the left common carotid artery and the ‘eft subclav~an artery in the presence of an acute traumatic rupture at the aortic isthmus. The extent of the stall-intact hematoma surrounding the rupture site IS rilustrated. It IS tmporiant to avoid entering ihe hematoma while tnaking a generous tunnel for the prox!mal aortrc cross-clamp. (From Turney SZ, Rodriguez A: Injuries to the great thoracic vessels, In Turney SZ, Rodriguez A, Cowley RA [eds]: Management of Cardioli?orac:c Trauma. Baltimore, Wil!rams & Wilkins, 1990, p 239. *Used by permission.)

FIG 23. The typical sites for applying clamps to achieve hemostasis in a traumatic rupture at the aortic isthmus. The preferred cannulation sites for aortic-aortic bypass are outlined by the dashed circles. The pericardial reflection is shown. (From Turney SZ, Attar S, Ayella R, et al: J Thorac Cardiovasc Surg 1976; 721727-732. Used by permission.)

able finding in this group of patients was the association between paraplegia and hypotension (systolic blood pressure < 70 mm Hg): All 3 paraplegic patients became hypotensive during the declamping period. Many factors can cause postoperative paraplegia;58, 73-75,77,7&, 82 this complication is not dependent solely on the clamp time or the use of shunting. Important contributors to a successful outcome include reduction in transfer delays, expeditious diagnosis and preoperative preparation, aggressive hemodynamic support from admission through operation, efficient treatment of any associated injuries, and good communication with the anesthesiologists during surgical procedures. The group of patients with aortic rupture treated at the MIEMSS Shock Trauma Center developed additional complications of hypertension (the most frequent), renal failure, sepsis, multiple-organ fail316

Curr

Probl

Surg,

May

1992

FIG 24. The techniques to gain extra length of the proximal stump. “Walking” the proximal clamp from position 1 to 2 or to position 3 may gain more stump length on the convexity than on the concavity of the aortic arch. In position 3. the left common carotid artery is occluded, a potentially dangerous but sometimes necessary maneuver. Also shown is the gent/e application of traction (in the direction of the arrow) while the proximal cross-clamps are repositioned. (From Turney SZ, Rodriguez A: !n,iuries to the great ihoracic vessels, in Turney SZ, Rodriguez A, Cowley RA [eds]: Management of Cerdiothoracic Trauma. Baltimore, Williams & Wilkins, 1990, p 242. Used by permission.)

ure, and aortoesophageal fistula.7” Twelve patients (48%) had at least one episode of hypertension, anct several became refractory to conventional therapy. In general, the judicious use of sodium nitroprusside and nitroglycerin infusions effectively controlled the blood pressure.83J 84

Despite an increasing incidence of vascular trauma in the United States of America, there are only a few reports of significant experience with nonpenetrating injuries of the subclavian artery. The three Curr

Probl

Surg,

May

1992

311

FIG 25. A, the technique of suture placement in the fragrle posteromedrai proximal aortic stump. The lateral aortic wail facing the surgeon is retracted gently by the first assistant. Clamps are shown on the aortic arch proximal to the left subclavian artery and on the artery (large arrowj. The recurrent laryngeal branch of the left vagus nerve (small arrows) is shown passing behind the ligamentum arteriosum, which :s still attached to the proximal aortic stump. (From Turney SZ, Rodriguez A: Injuries to the great thoracic vessels, in Turney SZ, Rodriguez A, Cowley RA [eds]: Management of Cardiothoracic Trauma. Baltimore, Williams & Wilkins, 1990, p 245. Used by permission.) B, the appearance of the aorta following reconstruction wrth a tubular synthetic graft correctly sized to the aortic diameter and to the length of the rupture defect. A simple running suture technique was used, taking wider and deeper bites than illustrated here. Aortic cannulation sites, if used, are shown having been closed using tied-down felt pledget-reinforced horizontal mattress sutures taken superficially in the aortic wall. (From Turney SZ, Attar S, Ayella R, et al: J Thorac Cardiovasc Surg 1976; 721727-732. Used by permrssion.)

Placement of a passive aortic-aortic shunt IO bypass a rraumatic rupture of the descendng thoracic aorta. The shunt tubing, in!tiaily primed with heparinized saline solution and clamped, was unclamped as the aortic ciamps were applied. (From Turney SZ, Attar S, Ayella R, et al: J Thorac Cardiovasc Surg 1976; 72:727-732. Used by permission.)

largest series, which enco ass a C-year span, were repolted by Richardson and colleague 115 patients), Sturm and Cicenos5 113 patients), and Zelenock and coworkers86 16 patients). The se Omert and associates,72 covering over a &year period, inclu arterial lesions and one venous lesion. Injuries of the subclavian vessels constitute 1% to 5% of all vascular injuries; the ratio of ~~ne~rati~g to blunt trauma has been reported to be 50 : 1 .85' 86 ~ig~ifi~a~t force is required to injure the anatomically well-protected subclavian vessels. Therefore it is not surprising that more than half of these patients have associated injuries. Most are injured in high-speed motor ve icie crashes or falls. 61,85,86 Clinical suspicion for a subclavian artery injury should be raise

FIG 27. The

Bio-Medicus

centrifugal

pump

when a patient presents with a history of high-speed deceleration and when the physicat examination reveals a hematoma or swelling over the upper part of the thorax and an upper-extremity pulse deficit. A nemolo@? 85 deficit in the involved extremity and a widened mediastinum may be present. Omert and colleagues7’ found a pulse deficit in 5 patients (100%) and a neurologic deficit in 1 patient (20%). The method of choice for the diagnosis and localization of the injury is angiography (Figs 28 and 29). Absolute indications for angiography include a pulse deficit or a widened mediastinum.85J 87 Relative indications are brachial plexus fnjury, apical hematoma, and first-rib fracturess5, 87 A notable finding on review of the literature is the frequency with which subclavian artery injuries are missed at the time of presenta320

Cut-r

Probl

Surg,

May

1992

iG 28. A selective right suoclavkan of the proximal subclavian bral and internal mammary

artenogram {digita! subiraction), revea!ing artery with marked contrast extravasation arteries are intact. (Courtesy of S. Mirvis,

complete (arrows). M.D.)

OCWSIO~

The

verte-

tiorxs8 There are three major reasons for alais aversight: First, the boundaries of the fibrous a bony compa~me~~ through which the artery runs can confine a matoma and cause bleeding to stop. Second, the signs of distal ischemia are often absent because of extensive collateral circulation around the shoulder joint. And last, the urgency to treat other ace-threatening injuries might divert akte~tio~ from less obvious injuries. The subtlety of some subclavian artery injuries is exemplified by the emi8 called “scapulothoracic dissociation” by Oreck and coworkers?” and by Ebraheim and associates.90 Patients with this injury have massive soft tissue swelling over the shoulder, lateral displacement of the scapula, injured bony elements of the shoulder, and severe dam e to the brachial plexus and subclavian vessels. The mechanism of injury is traction on the vessels, caused by blunt trauma to the shoulder, Early surgical management of subclavian lesions is recommended Curr

Probl

Surg,

May

1992

324

FIG 29. A digital thoracic arteriogram, revealing an intimai Injury of the proximal right subclavian artery and pseudoaneurysm formation at the base of the thyrocervical trunk and internal mammary artery (arrows). (Courtesy of S. Mirvis, M.D.)

because of the danger of delayed hemorrhage. The surgical approach to these lesions depends on the site of the injury. A simple transverse supraclavicular incision is adequate for most distal subclavian artery injuries. If extension is necessary, clavicle resection or disarticulation can also be done. The proximal left subclavian artery is best approached through a left anterior-lateral thoracotomy. The proximal right subclavian artery is best approached through a sternotomy or a “trapdoor” incision; either approach could require an extended supraclavicular incision. The choice of graft material is relatively unimportant since these short conduits with relatively high flow rates should have excellent long-term patency. In the series at the MIEMSS Shock Trauma Center,72 two arteries were repaired with reverse saphenous vein grafts, while polytetrafluoroethylene grafts were used in the other four re322

Cur-r

Probi

Surg,

May

1992

roup was done in a patient with pairs. The only amputation in a venous injury, necessitating iigation, o also sustained a severe brachiaf plexus crush injury resulting in an insensate extremity. When severe damage to the brachial plexus complicates a subclavian artery injury, we believe that the correct approach is to repair the vessel and give the patient the “benefit of the doubt.” At this early stage, it is very difficult to evaluate the magnitude of neurologic damage. In concurrence with other reported series,881 ” associated injuries were common in the group ed by Omert and colleagues.72 Head trauma was found in all 6 tients (100%); 5 (83%) of the 6 had upper-rib fractures; 4 (67%) had clavicle fractures; and 2 133%) bad brachial plexus injuries.

Blunt trauma of the ~~~~rn~~~at~ artery, altbough rare, is seeond most common mediastinclk vascular injury. Fisher and orkinnominate arteries em, ” in a radiologic review! identified ruptured in 20 (4% 1 of 510 patients nderwent aortic and brachiocephalic surgical literature, Castagna and Nelarteriograms. By reviewing t brachiocephalic artery injuries; 2.2 of song3 found 36 case reports them described injuries of the innominate artery. Both §ymbass4 experiences from major and Omert and associates,7Z presenting trauma centers, reported only four cases. Various mechanisms of injury have been postulated, including deceleration, chest compression, and hyperextension of the neck.s3’ ” The diagnosis is based on clinical and radiologic manifestations. al pulses can be present in more than 50% of patients with this ry. A chest radiograph disclosing a wide mediastinum mandates aortography. The aortogram might reveal a variety of abnormalities, from filling defects to complete obstruction (Fig 30). Although the natural history of innominate artery injury is not completely known, if we extrapolate from our knowledge of aortic ruptures, prompt surgical repair is indicated. A median sternotomy with extension into the neck gives excellent access to the innominate artery. For lesions at the antericpr take-off, if side-clamping is not adequate, some form of cardiopulmonary bypass is recornmended. However, some surgeons repair the lesion by interposing a synthetic graft with or wit out a temporary aortocarotid shunt. When we repair injured ~n~~rn~~ate arteries, we do not touch the injured area until a synthetic Dacron) graft has been placed from the ascending aorta to the distal innominate artery. After this bypass has been established (Fig 311, the hematoma can be entered.

FIG 30. An arteric Igram frc ,rn the aortic arch, demonstrating a pseudoaneurysm the base of the ini nominate artery extending into the right subclavian Mirvis, M .D.)

(arrows) invc blving of s. a& 3-y. (Courtesy

SUPERIOR AND INFERIOR VENAE CAVAE Few cases of superior and inferior venae cavae disruptions have been reported. Patients with these injuries typically have a very high mortality rate. Five of the 7 patients with these injuries in the MIEMSS review7’ had an associated atrial laceration, and only 1 patient survived. Patients with this injury can be salvaged only by prompt thoracotomy for hemorrhage or cardiac tamponade, combined with rapid isolation and repair. 324

Cur-r Probl

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1992

1. The surgical artery using

oi the ,nnominate artery repair of concomitant !njurles bifurcated Dacron graft. (Courtesy of S. Mirvis, M.D.)

and

right

subcIavian

CONCLUSIONS

Thoracic trauma alone is responsible for 25% of deaths among vehicular crash victims. Injuries of the thoracic uasculature subsequent to blunt impact present diagnostic and surgical challenges to surgeons and emergency medicine physicians, particularly when those injuries are part of multitrauma constellations. Traumatic rupture of the thoracic aorta and other great vessels is receiving considerable attention in the medical and legal literature. Physicians must be aware of the potential for these intrathoracic disruptions, based on the mechanism of injury and p sical findings. Proper radiologic evaluations are essential for a precise diagnosis and definitive surgical management. Controversies regarding surgical modalities of repair persist: shunt versus no shunt, pump versus no pump. However, we believe that good outcomes are predicated on the essentials enumerated below: 1. 2. 3. 4.

Minimization of interhospital transfer delays; Expeditious definitive diagnosis through arteriography; Prevention of perioperative hypotensive episodes; and Mastery of surgical techniques, which will minimize clamping time and avoid surgical mishaps.

ABDOMEN Often complicated by urgency, blunt trauma to the abdomen can present major diagnostic difficulties. Shock, secondary to blood loss, is the rate-setting condition in the management of abdominal trauma. If the patient is stable at the time of presentation, one can then proceed with an algorithmic workup of the patient’s problem. When shock is present (blood pressure < 90 mm Hg), resuscitation takes precedence over all other considerations. At least two large-bore intravenous lines (one above and one below the diaphragm), a Foley catheter, and a nasogastric or orogastric tube should be inserted. One hundred percent oxygen should be provided, and a low threshold for intubation maintained. Peritoneal lavage or abdominal CT with contrast media is largely used to evaluate intraabdominal injuries. Recently, sonography was recommended as a screening modality for the detection of intraabdominal fluid.s6-ss If tbe results of these procedures are positive, then the patient should be taken immediately to the operating room for exploratory laparotomy.

326

Curr

mob1

Surg,

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1992

Injuries of the main superior mesenteric artery an for approximately 0.2% of all ab~omin~ blunt vascul ihough injury to these specific vessels may be uncommon, when considered in combination with respective peripheral branch inju::ies, the superior mesenteric system is the most common site of vassular injury in patients who have sustained blunt abdominal trauma Fig 32). Because the mesentery is freely mobile, its vessels are s ject to stretching and shearing wing deceleration. Resultant i ries to the main trunk or large ranches must be repaired expediliously to prevent bowel is~be~~.a, The clinical indication of these disruptions is usually a exsanguinating hemorrhage discovered ’ has also been evmg vascular con;-eported.lol Recommen rrol include direct digital pressure during dissection,102, lo3 disseerion through the lesser sac or root of the mesentery,‘04 or the Ndattox maneuver.‘Ol In our experience, the Mattox maneuver, in which all left-sided abdominal viscera are rotated medially, allows the most

%e distribution of abdominal blunt vascular injuries at the !UIEMSS Shock Trauma Center (19831988). SMA = superior mesenteric artery; SAW = superior mesenteric vein; /Li = iliac vessels; IMA = inferior mesen!eric artery; IMV = inferior mesenteric vein; CEL = ceiiac axis; IVC = inferior vena cava; RA = renal artery; HV = hepatic vein, RV = renai vein; AOR = aorta.

expeditious control of the injured vessels. When there are both arterial and venous injuries, the vein should be repaired first to prevent bowel engorgementlo5 and because arterial occlusion is tolerated When the laparotomy time must be longer than venous occlusion.*‘” kept short, as in patients who are extremely unstable, the superior mesenteric vein can be ligated; however, this procedure should be avoided if at all possible because it usually leads to bowel ischemia. Graft placement was not required in any of the 88 patients with superior mesenteric vascular injury in the series of Omert and coworkers.72 This repair is necessary, however, in some patients with extensive vessel contusion or disruption. In these cases, all suture lines must be “re-peritonealized” as thoroughly as possible to prevent vascular-enteric fist&as. Courcy and colleagues,*o4 describing an earlier shock trauma patient group, found a 57% mortality rate associated with superior mesenteric main-trunk arteriovenous injuries. The mortality rate for the corresponding group in Omert’s study7’ was 26% (Table 1); the rate in Accola’s serieslo was 68%. The low mortality in Omert’s series may be related to the improvement in postoperative critical care and the routine “second-look” operations done on these patients. The follow-up assessment provides an opportunity to ensure patency of the repair and to check for ischemic bowel. Two patients in Omert’s series required additional small-bowel resection; both survived. INFERIOR MESENTERZC ARTERY iWD VEZN Because the the abdomen, eight injuries ers.lo7 When

TABLE Treatment

inferior mesenteric vessels are well protected within they are rarely injured. Over a l5-year period, only to these vessels were seen by Graham and coworkthe mesentery is torn during rapid deceleration,

1. and Mortality:

Vessel Main SMA/SMY Main IMNIMV Renal arteryhiein Aorta IVC Hepatic vein Iliac arterymein

Blunt Injuries 21 10 16 3 11 8 17

Abdominal

Vascular

Trauma*

MO. of Patients 15

8 14 3 11 8 15

“From Omert L, Rodriguez A, Simon B, et al: Panam J Trauma, SMA = superior mesenteric artery; SMV = superior mesenteric IMV = inferior mesenteric vein; IVC = inferior vena cava. 328

Repair

Mortality

1017 l/O 4/3 3 3 17

26 62 35 66 72 88 47

in press. Used by permission. vein; IMA = inferior mesenteric

Curr

(‘3%I

Probl

Surg,

May

artery;

1992

branches of the inferior mesentatic artery and veiein can be avulsed; truncal injuries are usually caused major compressive forces. Further illustration of the severe f impact these patients receive to their lower torso is provi by the fact that 50% of those with inferior mesenteric artery or vein injuries also have pelvic ring disruptions. Large, ing midline hematomas are the most common indicators e injuries. Direct access to the inferior mesenteric artery can be obtained through the sigmoid mesocolon, but hemorrhage often prompts occlusion of the supraceliac aorta prior to dissection through the hematoma. Ligation of the inferior mesenteric artery is tolerated well in most patients because multiple collateral vessels can maintain adequate blood flow. Although 5 of the 32 patients with inferior mesenteric vessel injuries in Omert’s series died,72 none of the deaths was directly attributable to blood loss or bowel ischemia. NAL ARTEISY AND VEllV Injury to the renal artery is uncommon. RO successful repair of a blunt renai artery injury in 1971. Renal vascular injury can be induced by two mechanisms: One is deceleration, during which the relatively mobile kidney moves forward while the aorta remains stationary, resulting in intimaf disruption. Because the left pedicle is longer, left-sided renal vascular injuries are likely caused by deceleration. The second mechanism is a direct blow resulting in contusion.. Ky either mechanism, the renal vessels can be avulsed or torn or an intimal flap or complete thrombosis can develop. Hematuria is usually the first stion of a urinary tract injury. Unfortunately, about 20% of pat with renal injuries do not exhibit this sign. When present, gross or microscopic evidence of blood in the urine is an indication for further workup of the genitourinary tract. Obtaining an intravenous pyelogram (MJ) is generally the next step in stable patients. Patients who are unstable and need urgent laparotomy should be taken to the operating room. Once the tient is stable, an IVP or arteriogram can be done in the operating The amount of tvarm ischemia time the kidney will tolerate is unclear. Although more than 2 hours of warm ischemia can lead to irreversible renal dysfunction,5” collateral circulation may preserve function for several hours nlore.109 By reviewing reports on the treatment of blunt renal artery thrombosis, Spirnak and Kesnick”’ determined that the best results were achieved when blood flow was reestablished within 4 hours after isruption. Yet, in a few patients, revascularization up to 12 hours after injury was successfu1111 (Figs 33-36). Curr

k’robl

Surg,

May

19%

329

FIG 33. A nephrotomogram Pais; M.D.)

showing

complete

nonfuncbon

of the

right

kidney.

(Courtesy

of 0.

Blunt renovascular trauma can be treated nonoperatively.llO’ II23 ‘13 Some patients with perirenal hematomas have clinically verified, intact genitourinary systems or a low suspicion of genitourinary disruption. The authors who described nonoperative management in these patients noted that time and blood can be saved by not unroofing the perirenal hematoma. Even after revascularization, many patients have poor renal function as a result of long periods of ischemia or technical problems is reasonable to perwith the repair.l13 Therefore, revascularization form only if a short period has passed since the time of injury, the patient is stable hemodynamically and has no significant associated injuries, or the other kidney is absent or abnormal. A dysfunctional kidney can be removed later if problems occur. If vascularization is attempted, the damaged arterial segment should be excised, followed by primary repair or bypass, The patient must be closely monitored postoperatively for changes in creatinine clearance and the onset of hypertension. Renal artery injury was diagnosed in 11 (7%) of the 163 patients in Omert’s series.72 Two thirds (7 of 11) of these patients had solitary injuries. Renal venous injury was rare, occurring in 3% (5 of 163) of the patients. Two patients had combined arterial and venous lesions. Associated visceral injuries were common, occurring in 11 of 330

Gun- Probl

Surg,

May

1992

IG 34. A fractured Pais, M.D.)

opper

pole

of the

righ!

kidney

with

actwe

b!eedmg

(arrow).

[Courtesy

of 0.

14 patients. Remarkably, renal ~a~e~~b~~ injuries were detected in only 3 (27%) of the 11 patients with vascular injuries. Two of the patients with renal artery injuries were observed. The following surgical interventions were completed: three direct repairs, one bypass, one ligation, an four nephrectomies. Three of the nephrectomies were necessitated by severe parenchymal disruption.

t&e

The exact incidence of injury ea the infrarenat is unknown, since many patients witb these

aorta and vena eava disruptions do not

FIG 35. A digital subtraction per pole, with gross

arteriogram extravasation

of the ieft kidney, demonstrating of blood (arrows). (Courtesy

fractures through of 0. Pais, M.D.)

the up-

reach the hospital alive. Only 1 of 1,320 blunt abdominal trauma patients in Killen’s seriesloo had an aortic injury. The mechanism of injury is compression of the aorta or vena cava between the steering wheel or lap-type seat belt and the lumbar spine.114-116 Findings at presentation are ecchymosis and abrasions of the abdominal wall at the level of the umbilicus. There may be decreased or no pulses in the lower extremity secondary to aortic dissection or thrombosis. Diagnosis is usually based on clinical suspicion, CT, and aortography. In the operating room, the large midline retroperitoneal hematoma that accompanies abdominal aortic disruption often makes proximal and distal control of blood flow difficult. Aortic occlusion at the diaphragm may be helpful until control is gained. Intimal dis332

Curr

Probl

Surg,

May

1992

le; 36. Occlusion of left renal artery at the :unctlon of the proximal and mrddle tiwds clusion of this type usually resuits from thrombosis after a spiral intimal tear. 0. Pais, M.D.)

~avow). (Courtesy

Ocof

ruption often necessitates resection and placement of an ~nte~~siZion synthetic (Dacron or ~~l~~etrafluoroethyle~e) graft. The survival rate of patients with infraren aortic injuries caused by penetrating or blunt trauma is approximately 45% .ll’ The extrahepatic suprarenal vena cava can be exposed by a generous Kocher maneuver. Injuries of this vessel are difficult to treat. The intrahepatic vena cava is notoriously inaccessible. Injuries of this structure require placement of an intracaval shunt for vascular isolation. Intrahepatic caval injuries are frequently accompanied by beCur-r Probl

Surg,

May

1992

333

patic vein avulsions. Mobilization of the liver in an attempt to visualize the area usually results in massive bleeding. Injuries to the inferior vena cava and hepatic veins are the most lethal abdominal vascular lesions. In the MIEMSS series,72 abdominal aortic injury was rare, occurring in only 2% (31163) of patients and usually as an isolated injury. In contrast, inferior vena cava injuries were seen much more frequently, in 7% (11 of 163) of patients. Seventy-two percent of the patients with caval injuries died, almost all of whom had associated severe hepatic parenchymal disruption. Disruptions of the main iliac artery require operative repair. However, if a bowel injury causes fecal contamination, ligation may be a safer option, coupled with axillofemoral or femoral bypass to relieve lower-extremity ischemia. Most published reports of iliac artery injuries are based on penetrating trauma. The survival rate for patients with isolated iliac lesions has been reported to be 87%;l17 for those with combined penetrating arterial and venous injuries, the rate is 55% .l18 The survival rate of 53% in Omert’s series7’ reflects the severe vascular disruptions that usually result from blunt trauma.

CONCLUSIONS Blunt abdominal vascular injuries are among the most lethal, with mortality rates as high as 30% in some series.llg’ lzo The explanation is threefold. First, the forces necessary to produce serious abdominal vascular injuries by a blunt mechanism frequently cause other major organ injuries. These associated injuries have a significant impact on morbidity and mortality. Second, such rapid bleeding is associated with these injuries that exsanguination can occur quickly. The mesenteric vessels are the most commonly injured, probably because of their anterior position in the abdomen. They are also notorious for massive bleeding. Third, blunt trauma to the abdomen may present major diagnostic difficulties, often complicated by the urgency of the situation in the unstable patient without an obvious source of bleeding. Diagnostic peritoneal lavage remains the most rapid means of evaluation. In the stable patient without an obvious source for blood loss, the workup can employ several modalities. These include CT, ultrasound, laparoscopy, diagnostic peritoneal lavage, and angiography. Rapid evaluation and prompt exploration to achieve control of the hemorrhage are imperative. Vascular repair can usually be done primarily, but graft replacement may occasionally be necessary. ‘Second-look” procedures should be employed early and literally to ensure optimal care of patients with blunt vascular trauma. 334

Cum

Probl

Surg,

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1992

ination was a cornmorn outHistorically, loss of limb or exsa come of both military and civilian ries to the extremities. ever, with an improvement in vascular reconstruction techn and materials, coupled with a better understanding of the biomechanics of vascular trauma, the amputation rate decrease from 75%t18 during World War II to between 10% and 15% during tbe Vietnam era.”

Only a few reports devoted to blunt vascular trauma of the upper extremity have been published.1”‘-1Z4 Most articles combine blunt and penetrating vascular injuries; several allow the blunt injuries to be separated from the penetrating ones.125-127 Between 2% and 16% of u er-extremity vascular injuries are caused by blunt trauma.lz8’ I’9 No single causative mechanism tes. The injurious events include vehicular crashes, industrial acents, falls, and crushes. These mechanisms generate direct blows, stretching forces, and bony injuries (i.e., fractures or dislocations) to the vessels. One case report suggested that atherosclerotic pl may have predisposed an elderly patient to vascular injury seemingly minor blunt trauma.121 Early diagnosis is the most important factor affecting successfuful care of patients with blunt vascuPar trauma to the upper extremities. Unfortunately, the presentation of the injuries may be subtle. Patients might exhibit only soft tissue damage, bony injury, or ~~~gb~ly decreased pulses. However, they can have pronounced signs, preng with an expanding hematoma, loss of distal pulses, or evie of severe ischemia. Clinical signs suggestive of vascular injury in the upper extremity are listed in Table 2. Certain fractures and dislocations are associated with vascular injuries. Axillary artery injury is associated with fracture of the proximal

Ciinical Signs of Vascular Upper Extremity

Injury

Decreased or absent distal pulse Active bleeding Bematoma Bruit Associated nerve injury Associated fracture or dislocation Proximal wound

of the

part of the humerus but is infrequently seen. Supracondylar fractures of the humerus are associated with brachial artery injury.13’ The presence of a pulse does not exclude vascular injury. Specifically, a pulse may initially be present in a patient with an intimal disruption, but it may be absent later when the vessel thromboses. Additionally, there is a rich collateral circulation around the shoulder and, depending on the level of the injury to the axillary artery, distal circulation may remain adequate and the patient asymptomatic. If such an injury is suspected, and if time and the patient’s stability permit, angiography should be performed. In some situations, the treatment of upper-extremity vascular disruption may need to be postponed until other injuries are evaluated or repaired. The sequence of intervention is determined by the threat to life presented by those other injuries and the potential for disability. One controversy that may arise is the management of an associated major venous injury. The shoulder possesses a rich venous collateral system. Therefore, if attempted repair of the axillary vein significantly increases the patient’s risk of morbidity and mortality, it should be avoided. In a recent review of patients treated at the MIEMSS Shock 13 patients with 15 blunt injuries of Trauma Center,46 we identified the upper-extremity vasculature: 1 axillary, 7 brachial, and 7 radial and/or ulnar arterial injuries (Fig 37). The majority (12 of 15) was diagnosed by angiography (Figs 38 and 39). Twelve (92.3%) of the 13 patients had associated fractures and/or dislocations (Table 31.

TABLE3. Association of Upper-Extremity Iniuries and Bonv Iniuries

Arterial Bony

Artery

Axillary Brachial Proximal NIid Distal Radial Proximal Mid Distal Ulnar Proximal Mid Distal Total

NO.

Dislocations

Injuries Fractures

1

1

0

1 2 4

0 0 1

1 2 2

0 0

2 1

1 0 0 3

1 1 1 11

0 2 1 2 1 1 15

-

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1992

es

_II

.-.

FIG 37. The distribution of blunt vascular injuries of the upper extremity among patients treated at the MIEMSS Shock Trauma Center (1983-1988). N = number of injuries at each anatomic site.

The axillary artery injury was repaired with an interposition polytetrafluoroethylene graft. Unfortunately, postoperative neurologic function was not improved due to a brachial plexopathy. Two of the 7 patients with brachiad artery injuries required upper-limb amputation because of severe nerve and soft tissue damage. In the remainCUFF Probl

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337

FIG 38. Left axillary blood flow

arteriogram, distally. Note

showing an lntimal Injury of the axillary the fracture of the left clavicle. (Courtesy

artery marrow) with of 0. Pais, M.D.)

good

ing patients, revascularization was successful with reverse saphenous vein grafts. Three isolated ulnar artery injuries, 2 radial artery injuries, and 1 combined radial and ulnar injury were identified. Patients with isolated radial OF ulnar artery injuries and normal findings on sensory and motor examinations at admission were treated with ligation or were treated nonoperatively. The vascular complications in the patient with a combined radial and ulnar injury were treated via thrombectomy, resection of the injured areas, and end-to-end anastomoses. Four of the 7 patients who required restoration of the vascular flow underwent fasciotomies when the clinical examination indi338

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IG 39. 4 left-upper-extremity arteriogram, revealing row) with poor collateral blood flow. (Courtesy

thrombosis of the proximal of 0. Pais, M.D.]

axrllary

artery

;a/--

cated compartment syndr note, 10 surgical vasculiar repairs were done before art mani ations ~ Radial and ulnar artery resulting from blunt trauma are ite rare. Only 6 patients se injuries were identified among 196 blunt trauma ~drn~ssi~~~ to the MIEMSS Shock Trauma Center. ollateral flow in the forearm is excellent, so, unless both arteries are compromised, ischemia is rare. The interosseous artery also assists in supplying blood to the and via connections with other arteries of the wrist. The connection the radial artery through the palmar arch is intact in a~~r~~rnat 95% of the population. Evidence of ischemia should be evaluated with arteriogra XIost patients with radial and/or ulnar artefy injuries do not require surgical intervention. In e who do, primary repair with saphenous veins or prosthetic s is usually successful.

Although the management ;PB‘vascular mjuries of the lower extremities has always been surgic ly challenging, mortality and morbidity rates have improved over the years as experience has been gained with various inte~e~tio~~. The Vietnam experience demon-

strated the importance of expeditious, definitive treatment of both blunt and penetrating vascular trauma of the lower extremities.131 Since then, studies have concluded that blood flow to an ischemic extremity should be reestablished within 6 hours after the injury occurred.132J133 In addition to time, factors that have been correlated with salvage of an extremity are early fasciotomy, reestablishing blood flow prior to orthopedic stabilization, using a temporary shunt while preparing anastomotic sites or stabilizing fractures, systemic heparinization, repairing concomitant venous injuries, primary repair, and use of completion angiography.87, 134-*3s Femoral Artery The overall incidence of injury to the common femoral, superficial femoral, and profunda femoral arteries is 15%.14' Blunt injury of these particular vessels is even less common. Injury is usually diagnosed based on absent or decreased pulses. Once the suspicion of an injury is established in a stable patient, an arteriogram is performed. Patients who are unstable secondary to bleeding from this site should be taken expeditiously to the operating room. Proximal and distal control should be obtained. For proximal control, the inguinal ligament may need to be partially transected or an extraperitoneal (transplant) abdominal incision may be required. The repair can be done primarily or might require an interposition graft using prosthetic material or saphenous vein from the opposite leg. If the repair is done primarily, it is important that enough vessel be mobilized proximally and distally to ensure that the anastomosis is tension-free. A completion angiogram as well as assessment of the need for fasciotomy should be done intraoperatively. If there is a concurrent injury to the common femoral vein or deep femoral vein, it should also be repaired. Ligation of these particular vessels can result in massive edema, potentially leading to tissue necrosis. Nerves should be repaired at a later date. Prophylactic antibiotic administration is considered appropriate in most patients with blunt vascular trauma. No controlled study has precisely defined the benefits of antibiotics in patients with isolated vascular trauma. Several studies, however, have shown that antibiotics should be given perioperatively so that peak blood levels coincide with the surgical procedure”’ and antibiotic coverage continues thereafter for at least 48 hours. Obviously, in blunt vascular trauma, contamination naturally precedes surgical intervention. One rational approach to antibiotic prophylaxis was outlined by KeighleyT4’ Essentially, the administration of antibiotics is appropriate when the risk of infection is high, when the risk of bacterial contamination is high, when contamination is unlikely but infection would have disastrous consequences, or when contamination is unlikely but the host is compromised. 340

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Studies have examined contaminated field an thetic grafts in most s taminated tissues and mount in the prevention

the

graii material to be used in a ave proved superior to uate debridement of ge of the repair are

of infections.

opliteal Artery The difficulty of s~v~g~r~ .t3e lower extremity after injury was well documente ation rates as high as view of the World War II 73% were associated with ry. Although most vascular wounds are caused by penetrating trauma, there is a bigh incidence of associated liteal artery injury in patients with disloca1 and tibial fractures.““6-148 tions of the knee a urred by passengers or pedestrians in The injuries are vehicular or mot0 hes. The impact results in a crush inion of the popliteal artery. jury, stretching injury or trat Presenting symptoms incl absent or decreased pulses, exanding hematoma, and dist chemia. if the patient is stable, angiography should be evolved !Fig 40). If the patient is unstable secondary to bleeding from ssel, then emergent operative intervention is necessary to ob proximal and distal control. wben there is no sign of injur er reduction of the fracture o location, we suggest liberal use of a~giogra~by. Being relatively

A, radiograph of a knee dislocauon. :F:oni Yaremchuk V 2 Specia, injuries, in varemc’nw MJ, Burgess AR, Brumback RJ feds]. Lower Extremity S&age and Reconstructton: Orthomedic and Piastic Surgical Management New York, Elsevier, 1989, p 48. Used by permission.) B, complete occlusion of the proximal popliteal artery. (Cour:esy of 0. Pais, M.D.) CUPS Probl

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341

proximally to the adductor magnus an distally by the soleus, the popliteal artery is particularly vulnerable to blunt trauma. Thus, a high index of suspicion is warranted. Exploration through a medial incision gives good exposure. If an orthopedic repair is necessary, a shunt bypass should be employed until a definitive procedure can be done. Repair usually involves a saphenous vein from the opposite leg or ‘ringed” prosthetic grafts. Completion angiography is imperative. Fasciotomy is used more often in this setting than any other and it should be used liberally. In the MIEMSS series, 50 multiple-trauma patients had 53 lowerextremity injuries (Fig 41). Fasciotomy was performed on 52% of the injured limbs. Five of the 7 patients who required amputation, despite attempts to reestablish blood flow, underwent fasciotomy prior rocedure, as did 9 of the 11 patients in whom revascularization was successful. The decision to perform fasciotomy was based on clinical judgment and findings on repeated physical examinations.

level of lngulnal ligament

N=3

IrWenlng adductor magnu* tendon N = 21

N = 11

N=a

FIG 41. The distribution of blunt vascular injuries of the lower extremities the MIEMSS Shock Trauma Center (1983-1988). N = number anatomic site. Five patients had 11 distal artery injuries.

among patients treated at of injuries at each specific

342

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1992

~~~~~~~~e-tranrna patients who are anesthetized early for the repair of other injuries, those tith ead injury, and those who are heavily sedated will not be able to express subjective complaints of pain. Therefore, the clinician must rely on other clinical manifestations such as swelling over the camp ment or, more precisely, compartment pressure measurements to determine the need for fasciotomy. Despite the controversy in the literature regarding the central pressure threshold, studies have shown myoneural necrosis to be present when the interstitial ressure is as low as 30 mm Hg.14s’15Q Therefore, we recommend I unconscious or uncooperative trauma patients with a highfracture, a tense and swollen extremity, or a compartment over 30 mm Hg should have an immediate four-compartment fasciotomy. We prefer the doubleincision technique (Figs 42-441.

42. Double-incision technique of ieg fasc~oiomy. f cross-sectional diagram depicting the medial and laterai incisions and the release of the myofascial compartments, L3, anatomic tocation of the medial and lateral skin incisions. Note that the medial incision is more distal than the midcalf iateral incision. (From Brumback RJ, Blick SS: Compartment syndrome, in Yaremchuk MJ, Burgess AR, Brumback RJ [eds]: Lower Extremity Salvage and Reconstruction: Orthopedic and Plastic Surgical Management, New York, Elsevier, 1989, p 64. Used by permission.) Cum

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FIG 43. A, location

of the anterolateral skin incision for fasciotomy of the anterior and lateral muscle compartments of the leg. B, visualization of the fascia of the leg musculature after the skin is incised. Once the intermuscular septum separating the anterior from the lateral compartments is palpated, a transverse incision is made, confirming the locale of both compartments. C, fascial incisions carried longitudinally in the proximal and distal directions, forming a divergent “H” and releasing the two compartments. D, cross-sectional depiction of release of the anterior and lateral muscle compartments. (From Brumback RJ, Blick SS: Compartment syndrome, in Yaremchuk MJ, Burgess AR, Brumback RJ [eds]: Lower Extremity Salvage and Reconstruction: Orthopedic and Plastic Surgical Management. New York, Elsevier, 1989, p 64, Used by permission.)

Also in the MIEMSS series, orthopedic stabilization preceded vascular repair in all but one of the patients with bony injuries. The time between injury and vascular repair averaged 12.8 hours for limbs that were eventually amputated and 5.4 hours for salvaged limbs. Although bony stabilization extends the duration of limb ischemia, it frequently was performed as the initial procedure in our patient population due to instability and foreshortening of the extremity. The use of temporary shunts may have improved limb salvage. As a result of our findings, temporary shunts are now used at the MIEMSS Shock Trauma Center if the time since injury approaches 5 or 6 hours or if a limb appears ischemic. Several authors advocated repair of concomitant venous injufies.134,136 Our own experience is too small to allow us to make con344

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1992

FIG 44. A, location of the skin incision of the superfrcra and deep posterior compartments. gitudrnal incision, after the skin is incised. of the investing fascia of the superficial p compartment, exposing the soleus muscle beneath. C, the oblique tibia1 attachment of the soleus muscle, superiicial to the deep posterior compartment. D, incision of the fascia overlying the deep posterior compartment, and release (arrows) of the tibia1 attachment of the soleus muscle to guarantee decompression of the deep posterior compartment, (From Brumback RJ, Blrck SS: Compartment syndrome, in Yaremchuk MJ, Burgess AR, Brumback RJ [eds]: Lower Extremity Salvage and Reconstruction: Orthopedic and Plastic Surgical Management. New York, Elsevier, 1989, p 64 Used by permission.)

elusive statements regarding repair of these injuries: We identified only 8 popliteal vein injuries, and we repaired 3. One of the venous repairs was unsuccessful, and the extremity had to be amputated despite a patent arterial bypass graft. The remaining 5 patients with venous injury required amputation at admission because their extremities were not salvageable. Blunt trauma usually causes arterial edema and contusion as well as intimal disruption. The distinct severance of vessels induced by penetrating trauma is rarely seen in blunt trauma patients. Properly performed primary repair or resection with a bypass and grafting are the best means of achieving t~n~io~-~ee a~a$tomose~ iFig 451. Primary repair was successful in only 2 of the 6 patients in whom i.t was attempted in the MIEMSS s Technical success should be cumented by completion angiogcwr Probl surg, May xE?z

345

FIG 45. Restoring arterial continuity may require (A) direct repair (note triangulation technique), (B) interposition vein graft, or (C) vein patch angioplasty. (From Yaremchuk MJ: Special injuries, in Yaremchuk MJ, Burgess AR, Brumback RJ [eds]: Lower Extremity Salvage and Reconstruction: Orthopedic and Plastic Surgical Management. New York, Elsevier, 1989, p 50. Used by permission.)

raphy.135 At the MIEMSS Shock Trauma Center, completion angiography was not used routinely, primarily because some patients had multiple injuries and required other emergency surgical intervention. In addition, patients who required surgical mediastinal or abdominal evaluation had already received large doses of intravenous contrast material. However, completion angiography is warranted whenever graft patency is in question and should be routine if the patient’s condition permits. The seriousness of popliteal artery injuries and the attendant difficulties in their management have been discussed by other authorS~87,1S1-l~3 In the recent MIEMSS Shock Trauma Center series, 60% of the patients with popliteal injuries required amputation. Forty-four percent of those amputations were done immediately when operative examination revealed extensive nerve destruction or substantial loss of bone and tissue. Eleven limbs were judged salvageable and were revascularized; however, 4 subsequently became necrotic and were therefore amputated. All of the popliteal injuries in the series were associated with one or more of the following: grade III tibial or fibular fracture, knee dislocation, or tibial plateau fracture (Table 4). The mortality rate was 23.8%. One death was associated with sepsis from the injured extremity. 346

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Lower-Extremity

Blunt

Vascular

Trauma:

“Arterial

Injlrry

Versus Orthopedic

Orthopedic

Injwy’

Injury

No. of Injuries

Knee Dislocation

Femoral Popliteal Anterior tibial Posterior tibial Peroneal Combined distal

3 21 8 11 3 11

-

Total

57

10

Tib/Fib

Closed T&/Fib Fracture -

8 1 1

Open Tib/Fib Fracture -

1 2 3 6

Tibial Plateau Fracture -

12

5

5 8 2

1 1 -

5

-

32

7

= tibiaUfibdar.

Anterior

Tibia&,

PosteriQ~ Ti~i~~~s, and Peroneal

Vessels

Most blunt injuries to the vessels below the trifurcation occur in association with bony injuries. Fortunately, simultaneous injury of more than one vessel at this hew1 is rare. The presence of major osa clinical presentation of a pulseseous involvement a arteriogram, prioritized less or ischemic leg to the circumstances (Figs 46 and 47). The surgical i should be individualized, pa icularly in the young, multiple-trauma patient with a number of othe ’ ‘uries that demand more immediate attention. Although having or three patent vessels is ideal, if at least one vessel is patent nischemic leg, we do not pursue further revascularization. A routine completion arteriogram and a low threshold for fasci re optimal limb salvage. Some authors believed that an re is less likely to be complicated by compartment syndrome owever, in a study of 198 patients s at the MIEMSS Shock Trauma Center, 9.1% with open tibial frac bad an accompa ment syndrome.155 This complication parallels the tissue and bony injuries. Unlike ligation of the p or femoral veins, no adverse e are reported after ligation of tibial or peroneal veins.156 The ferred surgical modality h or an interposition vein graft; polytetrafluoroethylene ided because of thromboge~ic~ ity.157

In the MIEMSS series, 8 pa with isolated anterior tibial artery injuries were identified. Five Gents had open tibial or fibular fractures in proximity to the inju and 3 bad closed fractures. The clinical presentation of diminishe ulses or an ischemic extremity dethese lesions was repaired. Seven manded an arteriogram 1 course for a G-month follow-up period. patients had an uneven CUFF

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FIG 46. A distal extremity arteriogram obtained after tibia1 and fibular fractures, demonstrating occlusion of the posterior tibia1 artery. There is reconstitution of the peroneal artery (arrows). The anterior tibia1 artery is intact. 348

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199.2

FIG 47. A lower-extremity arteriogram following proximal oblique tibia1 fracture, demonstrating occlusion at the origin of the anterior tibia1 artery with a small focal pseudoaneurysm (arrow), The tibioperoneal trunk is intact.

One developed complications of an infected fasciotomy and multiple-system organ failure. Eleven isolated posterior tibi artery injuries were identified in this series. Eight of tbe 11 pati ts bad open fractures, and 3 bad closed tibial or fibular fractures. Five patients were treated nonsurgitally and did well. In 2 patients, the posterior tibial artery wa gated without complications. In 3 of the remaining patients, the 1 was revascularized during orthopedic procedures due to surgical accessibility of the injury; 2 of these repairs were successful (Fig 481, and 1 was not. Despite good vascular repair, the 11th patient’s extremity was amputated due to extensive muscle and soft tissue damage (Table 51. Three patients in Omert’s series bad isolated peroneal vessel injuand ries. One injury was repaired by ligation 1 patient was observed, the third patient, with a severe crush injury, required amputation. Curr

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FIG 48. Interposition reversed vein graft reconstruction of the posterior tibia1 artery transected by blunt trauma. Note the good match in size of the lesser saphenous donor vein (large arrow) and the posterior tibia1 artery (small arrows). (From Yaremchuk MJ: Special injuries, in Yaremchuk MJ, Burgess AR, Brumback RJ [eds]: Lower Extremity Salvage and Reconstruction: Orthopedic and Plastic Surgical Management. New York, Elsevier, 1989, p 51. Used by permlssion.)

Five patients in the series had 11 combined distal vessel injuries. All had grade III tibial or fibular fractures. In 3 patients, repair was attempted either primarily or using a reverse saphenous vein graft. Only one repair was successful. The remaining 2 patients required amputation, one due to a nonfunctional extremity 3 months after admission. The combined lower-extremity injuries in the other 2 patients were not repaired: 1 patient died of irreversible brain damage and the other had a patent anterior tibial vessel. CONCLUSIONS

Undoubtedly, the high morbidity and mortality rates related to blunt vascular injuries of the extremities will continue to provoke considerable debate in regard to diagnostic workup and management. In parallel with the development of emergency medical systems, physicians have a responsibility to perfect diagnostic techniques, such as quick imaging of the vascular tree, to eliminate “missed injuries.” In addition, patients will certainly benefit from a 350

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Contraindications to Attempted Revascdaeization Massive crush injury to the leg and/or thigh Severe degloving injury to the plantar surface of the foot or completely crushed foot Anesthetic extremity secondary to multiple nerve injuries &morbid, advanced peripheral vascular disease Other injuries that would pose a threat to life if lengthy revascularization procedures were undertaken

coordinated multidisci~~i~a~ vascular reconstruction, from the jum early orthopedic stabilization. dicious use of fasciotomy, and The widely accepted “golden” safe ischemic time for penetrating vascular injuries is 4 to 6 hours; we believe this is too long for blunt injuries of the vasculature, which are commonly associated with major soft tissue and osseous injuries. Consequently, the elapsed time between injury and repair ~rnai~s one of the most important determinants of outcome.

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