Acute Treatment of Penetrating Popliteal Artery Trauma: The Importance of Soft Tissue Injury

Acute Treatment of Penetrating Popliteal Artery Trauma: The Importance of Soft Tissue Injury

Acute Treatment of Penetrating Popliteal Artery Trauma: The Importance of Soft Tissue Injury Willis H. Wagner, MD, Albert E. Yellin, MD, Fred A. Weave...

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Acute Treatment of Penetrating Popliteal Artery Trauma: The Importance of Soft Tissue Injury Willis H. Wagner, MD, Albert E. Yellin, MD, Fred A. Weaver, MD, Steven C. Stain, MD, and Anne E. Siegel, Rig, Los Angeles, California

During a 20-year period from 1973 to 1992, 109 patients underwent early operation for acute popliteal artery trauma. Clinical variables were analyzed for their association with amputation. Gunshot wounds accounted for the majority of injuries (73%), followed by shotgun wounds (18%), stab wounds (6%), iatrogenie injuries (2%), and lacerations (1%). Fasciotomies were performed selectively in 41% of patients. Seven patients (6%) lost the injured extremity despite arterial repair. The mean time from injury to arterial repair was not significantly different for patients with or without subsequent amputation (8.6 _+ 3.6 and 9.7 _+ 7.4 hours, respectively; p = 0.69). Delay in diagnosis longer than 6 or 12 hours after the injury did not increase the risk of amputation. Other factors not associated with limb loss were preoperative ischemic neurologic deficit or compartmental hypertension, concomitant fracture, and popliteal vein injury. Severe soft tissue injury (p <0.0001) or postoperative wound sepsis (p <0:0001) substantially increased the risk of amputation. Delayed fasciotomies were uncommon (4%) but were associated with a significantly increased risk of amputation (p < 0.0001). Vein grafting for arterial repair (p = 0.0017) and shotgun injuries (p <0.0001) were associated with amputation to the extent that they were related to severe soft tissue injury. The degree of soft tissue trauma and subsequent infection of devitalized tissue limits the success of popliteal arterial repair. Changes in the mechanism of trauma, liberal use of four-compartment fasciotomies, and aggressive management of soft tissue injury resulted in a significant decline in the amputation rate from 21% (4/19) in the first 5 years to 0% (0/39) in the last 5 years of the study. (Ann Vasc Surg 1994;8:557-565.)

Improvement in the treatment of arterial trauma depends on identification and correction of the factors related to limb loss and prolonged disability. Amputation rates for extremity vascular trauma vary substantially depending on the location of the injury. Since the techniques of arterial repair have been standard since the Korean War, other factors specific to the sites of injury deterFrom the Division of Vascular Surgery, University of Southern California, Los Angeles, California. Presented at the Twelfth Annual Meeting of the Southern California Vascular Surgical Society, Coronado, Calif., September 17-19, 1993. Reprint requests: Willis H. Wagner, MD, 8631 W. Third St., Ste. 615-E, Los Angeles, CA 90048.

mine the outcome of vascular injury. Comparison of treatment protocols between institutions is obscured by differences in the study groups relating to mechanism and anatomic location of the arterial injury. Variables such as delay in treatment, methods of arterial reconstruction and orthopedic stabilization, use of arteriography and fasciotomies, and repair of venous injuries have been related to limb salvage in patients with lower extremity arterial trauma. In an attempt to analyze the influence of these variables on outcome we have focused our review on one arterial segment. Popliteal artery injuries continue to be associated with a significant risk of limb loss. Within the past 10 years the amputation rate reported with popliteal artery 557

Annals of Vascular Surgery

558 Wagner et al.

trauma has ranged from 0% to 28%. T M To a large degree, variation in results relates to the mechanism of injury. Blunt trauma to the knee is generally associated with more soft tissue damage and disruption of collateral circulation than penetrating trauma. We previously reviewed the management of 100 consecutive popliteal artery injuries due to blunt t r a u m a ) 2 Over the course of the study period, experience in treating these challenging injuries resulted in a decline in the rate of limb loss from 23% to 6%. Early systemic anticoagulation to prevent distal small vessel thrombosis and aggressive management of severe soft tissue damage were found to have a significant hnpact on limb salvage. We now review our 20-year experience with early operative management of penetrating injuries of the popliteal artery. The factors influencing amputation risk and the functional status after discharge are analyzed.

PATIENTS A N D M E T H O D S All patients were treated at the Los Angeles County-University of Southern California Medical Center, a level 1 university trauma center. The records of 109 patients undergoing early repair of popliteal artery injuries caused by penetrating trauma from 1973 until 1992 were reviewed retrospectively. All patients were diagnosed within 24 hours of their injury and were operated on within 36 hours. Operations that occurred after this interval were not included in our review since they were generally performed for repair of stable, minor injuries that did not constitute a risk of limb loss. Patients with nonocclusive intimal injuries and small pseudoaneurysms who were observed rather than undergoing early operation have been previously reported 13 and were also excluded from this series. Most of the patients were young (mean age 26.7 years, median age 24.0 years, range I0 to 62 years) and male (N = 99, 91%). The majority of injuries were the result of civilian violence (Table I). The two iatrogenic injuries resulted from an arthroscopic meniscectomy and a hamstring muscle release. Forty-five (41%) arterial injuries were associated with fractures (Table II). Twenty-three (2I%) patients had 30 significant associated injuries: musculoskeletal in 14, intra-abdominal in 7, urologic in 3, pulmonary in 3, craniofacial in 2, and spinal cord in 1. Pedal pulses were normal in 12%, diminished

Table I. Cause of 109 penetrating popliteal artery injuries Mechanism of injury

No. of patients

%

Gunshot* Shotgun Stab wound Iatrogenic Accidental laceration Total

79 20 7 2 1 109

73 18 6 2 1 100

*Handgun or rifle.

Table II. Associated skeletal trauma Fracture

No. of patients

%

Distal femur Proximal tibia-fibula Proximal fibula Proximal tibia Total

30 6 5 4 45

27 5 5 4 41

in 15%, and absent in 73% of limbs. The presence of distal limb ischemia was subjectively determined by the physical examination. Clinical ischemia was present in 55% of limbs preoperatively, as defined by neurologic deficit, cyanosis, or profound temperature differential relative to the contralateral extremity. Capillary refill was considered an unreliable measurement of distal perfusion. Ankle-brachial indices, which are now routinely recorded, 14 were not obtained during most of the study period. Arteriograms were obtained in the radiology suite in 51% of patients. The remainder had preoperative arteriograms obtained in the operating room (7%) or underwent exploration alone (42%). The mean time from injury to arterial repair was 9.6 hours (median 8.1 hours, range 1 to 30.5 hours). Patients who presented with ischemic neurologic deficits were taken to the operating room in less than half the average time of those patients whose limbs were neurologically intact (6.0 and 14.1 hours, respectively). The time delay was largely beyond our control. Fifty (46%) patients were first evaluated at other emergency departments and then transferred, resulting in an initial mean delay of 3.9 hours. The institution of

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a county-wide trauma system has reduced the transfers of patients with serious injuries. During the second decade of the study the percentage of patients transferred from other facilities declined from 63% to 33%. At operation 56 (51%) of the injured popliteal arteries were transected (44%) or thrombosed (7%). Fifty-three (49%) of the popliteal arteries were patent despite intimal injuries (3%) or fullthickness defects (46%). The trifurcation of the popliteal artery was involved in 8%. There were 50 (46%) popliteal vein injuries: 24 (22%) transected/thrombosed and 23 (24%) transmural injuries in patent veins. The degree of soft tissue damage was graded intraoperative as minimal or none in 63 (58%), moderate in 31 (28%), and severe in 15 (14%). Compartmental hypertension of the injured leg was noted preoperatively in 18 (17%) patients. Patients were systemically anticoagulated (94%) unless severe musculosketetal or other associated injuries limited the use of heparin to local infusion (6%). The majority of arteries were repaired primarily by debridement and end-to-end anastomosis (N -- 70, 64%) or lateral repair (N = 4, 4%). Autogenous vein (usually contralateral saphenous) was used for either a short interposition graft (N = 32, 29%) or a bypass conduit (N -- 3, 3%) in the remainder. Reconstruction of 40 of the 50 injured popliteal veins was performed using either lateral repair (17), end-to-end anastomosis (16), or interposition vein grafting (7). Ten popliteal veins were ligated. Four-compartment fasciotomies were selectively performed at the time of the vascular repair in 45 (41%) patients. During the second decade of the study, skin grafts were placed at the time of decompression if the underlying muscle was clearly viable. Six tibial or peroneal nerves were repaired at the time of vascular reconstruction. Concomitant procedures for fixation of associated fractures were performed in 34 (3{%) patients, all following the vascular repairs. During the second decade of the study there was a transition from traction as primary therapy to open reduction and internal fixation or external fixation if w o u n d coverage or contamination obviated a definitive open procedure. Comparisons of the means of continuous data was performed using an unpaired, two-tailed t test. The Pearson chi-square test was used for subgroup analysis of the rate of amputation for individual risk factors.

Treatment of penetrating popliteal artery trauma

559

RESULTS Of the 109 repairs, I06 (97%) arterial repairs remained patent without revision. Three arterial repairs were revised. One repair thrombosed due to occlusion of the distal arterial runoff. Intraarterial streptokinase was infused in the operating room after vein graft thrombectomy. Postoperative intra-arterial infusion of a vasodilator (tolazoline) was unsuccessful in maintaining arterial patency and an amputation followed. One arterial repair thrombosed in the immediate postoperative period due to an unstable femur fracture that was treated with tibial pin traction. Graft thrombectomy alone and revision of the traction provided successful long-term reconstruction. A third repair was revised because of a missed pseudoaneurysm due to a shotgun pellet. Clinically evident deep vein thrombosis was confirmed by duplex scan in three patients: one had repair of an injured popliteal vein, one had ligation of the popliteal vein, and one had no known venous injury. Four patients had delayed fasciotomies for postoperative compartmental hypertension, all during the first decade of the study. Three patients with delayed fasciotomies ultimately had amputations, two with patent arterial repairs. Superficial or deep infection complicated w o u n d care of 23 (21%) injured limbs. One patient who arrived at~ the hospital in shock from exsanguinating chest and extremity injuries died 3 weeks later from anoxic encephalopathy and multiorgan system failure. Seven (6%) patients had major amputations after arterial reconstruction. Only one patient had postoperative arterial occlusion, which was believed to be due to thrombosis of the runoff bed. The remainder of the amputations were required because of extensive soft tissue damage and infection. The amputations were below-knee in three, above-knee in three, and through-knee in one. The clinical characteristics of each patient are given in Table III. The rate of limb loss declined significantly over the study period (p -- 0.02 by chi-square analysis; Fig. 1). During the four successive pentads since I973, the rate of amputation has been 21%, 7%, 4%, and most recently 0%. The mean time from injury to arterial repair was not significantly different in patients who had amputation (8.6 • 3.6 hours) compared to those whose limbs were salvaged (9.7 • 7.4 hours) (p -- 0.69). The time interval was likewise

560

Annals of Vascular Surgery

Wagner et al.

T a b l e I I I . Major a m p u t a t i o n following acute t r e a t m e n t of p e n e t r a t i n g popliteal artery injuries No.

Mech.

Soft tissue injury

Ischemic

Compartment HTN

Injury to OR (hr)

Popliteal vein injury/repair

1

GSW

Severe

Yes

Yes

10.5"

No injury

2

SGW

Severe

No

No

9.0*

No injury

3

SGW

Severe

Yes

No

8.2*

Lateral injury/repaired

4

SGW

Severe

Yes

No

4.0

Transected/ligated

5 6

SGW SGW

Severe Severe

Yes Yes

No No

8.5* 5.0"

Transected/repair Transected/repair

7

SGW

Severe

No

No

i5.0"

Transected/repair

*Transferred from outside hospital. Mech. = mechanism of injury; HTN = hypertension; GSW = gunshot wound; SGW = shotgun wound,

45

35 30

~. 2s E

J~

l

20-

39

ii l i 27 ~ m

/

19

24

///;

v//, i///. ,//.

/ / 1 1

Y/

/ /.,,,

15-

S

10-

/.

,///

F "///. r "/// /

~A,//"///~ 2

,'/

/

'73-'77

[]

Amputations

--_

,//, ///,

v A~.

,

,///

,///

4

0-

Total patients

2

k

5-

[]

'78-'82

'83-'87

0

'88-'92

Years

Fig. 1. Total patients and associated major amputations during 5-year periods from 1973 to 1992.

n o t significantly associated w i t h o u t c o m e in patients w h o p r e s e n t e d w i t h clinical signs of ische m i a ( m e a n 7.2 _+ 2.7 h o u r s for a m p u t a t i o n vs. 5.9 _+ 4.4 h o u r s for l i m b salvage; p = 0.52). Univariate analysis of individual risk factors for a m p u t a t i o n is given in Table IV. Subgroup analysis c o m p a r i n g the risk of t i m e delay in patients w i t h p r e o p e r a t i v e limb i s c h e m i a or severe soft tissue

injury does not s h o w an influence of t i m e factor (Table V). M u l t i v a r i a t e analysis by s t e p w i s e logistic regression w a s n o t included in the results since the end p o i n t of a m p u t a t i o n w a s so infreq u e n t t h a t o u t c o m e prediction using this technique is limited. Data r e g a r d i n g f u n c t i o n a l status after discharge is available for 94 of the 102 (92%) pa-

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Treatment of penetrating popliteal artery trauma

Arterial repair

Primary/delayed fasciotomy

Postop. infection

Interposition vein graft

Primary

Deep

Interposition vein graft

Delayed

None

Interposition vein graft

Primary

Deep

Interposition vein graft

Primary

Deep

Interposition vein graft Interposition vein graft

Delayed Primary

Deep None

Primary repair

Delayed

Deep

tients whose limbs were salvaged. The mean period of follow-up was 4.7 months (median 3.0 months, range 1 to 36 months). Twenty-four (26%) patients had peroneal nerve dysfunction: 63% temporary and 37% persistent during linlited follow-up. Seventy-five (80%) patients were walking without limitation. Eleven (12%) patients noted minor disability and six (6%) were walking with a cane or other support. Two (2%) patients were nonambulatory because of conditions unrelated to their vascular trauma. One patient who sustained an iatrogenic arterial injury during a hamstring release had cerebral palsy from birth and was nonambulatory before surgery. The second patient was a T-10 paraplegic from an associated gunshot wound. There have not been any known late arterial complications.

DISCUSSION Recommendations for management of m a n y aspects of extremity vascular trauma, specifically popliteal artery injuries, are based on opinion and anecdotal evidence. This review was intended to provide insight into the cause of past failures with the goal of improving future therapy. We recognize the limitations of a retrospective study that evaluates nonrandomized treatment options. Many of the classifications used to evaluate risk

561

Comments Postop. anglo. • 2; patent repair, no runoff/extensive necrosis & infection Postop. vein thrombosis/reop, for arterial occlusion/intraop, streptokinase & postop. tolazoline/arterial repair failure Massive soft tissue injury & infection/patent arterial repair Extensive muscle necrosis, infection, & foot gangrene with palpable pedal pulse Clostridial sepsis/patent arterial repair Postop. anglo.; patent repair, no runoff/extensive necrosis with palpable pedal pulse/tolazoline infusion postop. 2nd arterial injury found postop./arterial repair revised/erosion of graft by external fixator/extensive necrosis & infection

factors such as the degree of soft tissue injury were subjectively allocated. Furthermore, several of the variables were interrelated, not independent. However, while accepting these shortcomings, the data suggest that m a n y long-standing assumptions may not be valid. The most significant factor in determining outcome for penetrating popliteal artery injuries is the severity of soft tissue damage related to the mechanism of injury. Shotguns produce a spectrum of arterial and soft tissue injury that depend primarily on proximity. Pellets released at less than 3 meters act as a single projectile and uniformly result in massive soft tissue destruction) ~ Barrel length, lack of constriction of the muzzle ("choke"), gauge or bore caliber, and the size of the shot also affect the extent of injury. ~518 During the 1970s and early 1980s a common form of retribution between gang members in Los Angeles was a close-range shotgun blast referred to as "knee-capping." This type of injury accounted for six of the seven amputations in our series. In contrast, popliteal artery injuries from remote shotgun blasts produce small pseudoaneurysms that can frequently be safely observed nonoperatively) x~9 A shift in armamentarium from shotguns to firearms with lower kinetic energy contributed to the improved results with popliteal artery injuries during the past decade.

562

Annals of Vascular Surgery

Wagner et al.

T a b l e IV. U n i v a r i a t e a n a l y s i s of p a t i e n t - r e l a t e d v a r i a b l e s Grouping

No. of patients

Gunshot Shotgun Stab Other No Yes Normal Diminished Absent No Yes No Yes No Yes No Yes No Yes No Yes Primary Vein graft None Repaired Ligated Regional Systemic Minimal Moderate Severe No Yes No Yes None Superficial Deep

79 20 7 3 64 45 13 16 80 9I 18 49 60 42 67 72 37 58 51 59 50 74 35 59 40 10 7 102 63 31 15 64 45 105 4 86 13 l0

Variable Mechanism of injury

Associated fracture Preop. pedal pulse

Preop. compartment hypertension Clinical ischemia Preop. delay >6 hr Preop. delay > 12 hr Artery occluded preop. Popliteal vein injury Arterial repair Vein repair

Intraop. anticoagulation Soft tissue injury

Concomitant fasciotomy Delayed fasciotomy Postop. infection

No. of amputations 1 6 0 0 2 5 0 1 6 6 1 2 5 2 5 6 1 4 3 2 5 1 6 2 4 1 1 6 0 0 7 3 4 4 3 2 0 5

(1%) (30%) (0%) (0%) (3%) (ll%) (0%) (6%) (8%) (7%) (6%) (4%) (8%) (5%) (7%) (8%) (3%) (8%) (5%) (3%) (10%) (1%) (17%) (3%) (10%) (10%) (14%) (6%) (0%) (0%) (47%) (5%) (9%) (4%) (75%) (2%) (0%) (50%)

p Value < 0.0001

0.094 0.59

0.87 0.37 0.58 0.26 0.83 0.16 0.0017 0.37

0.38 < 0.0001

0.38 <0.0001 <0.0001

NOTE:p value derived from Pearson chi-square test for significance probability.

T a b l e V. S u b g r o u p a n a l y s i s of t i m e d e l a y a n d a m p u t a t i o n r i s k Variable Clinical ischemia & preop, delay > 6 hr Clinical ischemia & preop, delay > 12 hr Severe soft tissue injury & preop, delay > 6 hr Severe soft tissue injury & preop, delay > 12 hr

Grouping

No. of patients

No Yes No Yes No Yes No Yes

34 26 54 6 6 9 13 2

Nor~: p value derived from Pearson chi-square test for significance probability.

No. of amputations 2 3 5 0 2 5 6 1

(6%) (12%) (9%) (0%) (33%) (56%) (46%) (50%)

p Value 0.43 0.44 0.40 0.92

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The adverse influence on outcome of prolonged delay from injury to repair is suspected by most authors but is inconsistently supported by d a t a ) '4-6'~'2~ Time delay has not been uniformly associated with amputation risk since patients with the most severely injured limbs are frequently taken to the operating room in the shortest time period. ~~ Our o w n results did not show a relationship between amputation and time delay. However, we advocate prompt revascularization for all patients with moderate to severe soft tissue injury or clinical evidence of ischemia. Small vessel thrombosis and infection of devitalized tissue in these high-risk patients may possibly be prevented by expeditious vascular reconstruction and soft tissue debridement. Peroneal nerve dysfunction, which commonly results from ischemic injury and limits postoperative recovery, can also be minimized. Since the development of a regional trauma system, transfer of patients with the most severely injured limbs from other facilities and thus the overall time delay have been sharply curtailed. Many patients with occluded popliteal arteries and minimal soft tissue disruption have no clinical signs of distal limb ischemia. These patients constitute a low-risk subgroup that is not affected by the timing of arterial repair. Arteriograms obtained in the radiology suite add an average of 2 to 3 hours to the delay in arterial repair. Patients with penetrating injuries around the knee and a cool, neurologically impaired foot or active bleeding belong in the operating room. If necessary, an arteriogram can be obtained in the operating room. This might be most helpful in patients with shotgun wounds and numerous scattered arterial injuries in w h o m localization of the arterial defect is important. The role of arteriography in the stable patient without hard signs of arterial injury is still evolving. The yield of arteriograms for proximity alone is low. 22-25 Dennis et al. 23 found that only 1.8% of 3 18 penetrating injuries resulted in major arterial defects requiring operative repair. The routine acquisition of Doppler-derived ankle-brachial indices in our recent experience has reduced the number of unnecessary arteriograms. A pulse deficit and an ankle-brachial index of < 1.0 identified all major vascular injuries in a series of 469 consecutive patients with penetrating trauma. ~4 Color-flow duplex ultrasonography may further refine the indications for arteriography in patients with abnormal pulses or diminished Doppler pressures. 2~-28 Because of the tethering of the popliteal artery by geniculate branches, Lim et al. 29 have advo-

Treatment of penetrating popliteal artery trauma

563

cated routine vein interposition for arterial reconstruction. Our series as well as others ~'6'~~ have actually demonstrated an increased risk of limb loss when vein grafts are required. A tension-free anastomosis between the debrided ends of the popliteal artery was accomplished in 68% of our patients. None of the amputations was related to a technical problem with the arterial reconstruction, The increased frequency of limb loss with vein interposition graft is not related to the vein graft but to the severe underlying trauma that necessitated more extensive arterial resection. Repair of injured popliteal veins remains controversial. The goals of reconstruction are improved early hemodynamics and avoidance of the late sequelae of chronic venous insufficiency. Experimental canine studies show a significant reduction in femoral artery flow with ligation of the accompanying vein. 3~ The results of clinical series have been equivocal. Snyder 32 found a lower amputation rate in patients whose popliteal vein injuries were reconstructed. However, vein ligation was reserved for more severely injured patients with hemodynamic instability and extensive adjacent trauma. Consequently, the higher rate of amputation associated with popliteal vein ligation was related to the severity- of the underlying trauma. Many series, including our own, have shown no influence of venQus reconstruction on limb salvage) ~ However, venous reconstruction significantly reduces venous pressure and may prevent myofascial compartment hypertension and the long-term disability associated with chronic venous insufficiency, s'35-3. Because significant collaterals about the knee are lacking, the hemodynamics of the leg are particularly disturbed by ligation of the popliteal vein. Ligation of other major veins of the lower extremity does not consistently produce late morbidity. 39"4~Because of the possibility of delayed morbidity, we currently repair injured popliteal veins in all hemodynamically stable patients. During the limited follow-up period we have not encountered severe limb edema in any patient with a popliteal vein injury. Routine fasciotomies are not mandatory for limb salvage. 29 The indications for selective fasciotomies must be sufficiently liberal so that all delayed fasciotomies are prevented. The diagnosis of postoperative compartment syndrome is usually not made until nerve and muscle damage have occurred. The myonecrosis associated with delayed treatment of compartmental hypertension increases the risk of invasive wound sepsis and amputation. 2~ During the past decade late fasciotomies have been prevented by decompres-

564 Wagner et al.

sion at the time of vascular repair in patients w i t h severe soft tissue t r a u m a , preoperative signs of limb ischemia, evidence of leg e d e m a either before or after revascularization, or c o m b i n e d arterial a n d venous injuries. According to these guidelines, approximately 60% of patients should have c o n c o m i t a n t fasciotomies, similar to rates reported by o t h e r s ) '7 Severe soft tissue d a m a g e a n d secondary infection of devitalized tissue were the p r i m a r y indications for a m p u t a t i o n . During the past 10 years a n aggressive a p p r o a c h to d e b r i d e m e n t of nonviable tissue and early w o u n d closure has been implemented. Local rotational and free muscle flaps are n o w used to provide closure of large defects. During the first decade of the study, d e r m o t o m y - f a s c i o t o m y w o u n d s were always left open w i t h skin grafting or delayed p r i m a r y closure performed 1 to 2 weeks later. The open d e r m o t o m y was frequently a site of superficial infection. Exposure of u n d e r l y i n g m a r g i n a l l y viable tissue to this bacterial insult resulted in deep w o u n d sepsis in several patients. 4~ This is currently prevented b y closure of the d e r m o t o m y f a s c i o t o m y w o u n d w i t h a c o m b i n a t i o n of p r i m a r y lateral d e r m o t o m y closure a n d medial skin grafting at the time of decompression. W o u n d s are left open only if there is significant concern about the viability of the u n d e r l y i n g muscle, in w h i c h case patients are r e t u r n e d to the operating r o o m in 2 to 3 days for either further muscle d e b r i d e m e n t or w o u n d closure. All patients w i t h persistent, unexplained sepsis should u n d e r g o reexploration. Nearly all patients w h o s e limbs are salvaged r e s u m e normal, active life-styles w i t h i n 6 m o n t h s to a year of surgery. M o s t nerve deficits associated w i t h p e n e t r a t i n g popliteal artery injuries are transient, p r e s u m a b l y related to the initial ischemic insult or to nerve contusion. The use of ankle-foot orthotics and occasionally ankle fusion have allowed i n d e p e n d e n t a m b u l a t i o n in patients w i t h persistent peroneal nerve damage.

CONCLUSION C o m p a r i s o n of patient variables w i t h a m p u t a t i o n risk have helped identify factors that have significant i m p a c t on o u t c o m e in p e n e t r a t i n g popliteal artery trauma. The m e t h o d of popliteal arterial r e c o n s t r u c t i o n is less i m p o r t a n t t h a n creation of a tension-free a n a s t o m o s i s to an uninjured segm e n t of the artery. A l t h o u g h there does not appear to be an influence on a m p u t a t i o n , popliteal veins should be repaired to prevent severe leg e d e m a a n d possible postphlebitic syndrome. Fas-

Annals of Vascular Surgery

ciotomies can be p e r f o r m e d selectively, but the indications m u s t be liberal. Despite optimal m a n a g e m e n t of these injuries, the m e c h a n i s m of injury a n d the degree of soft tissue d a m a g e appeared to determine the need for s u b s e q u e n t a m p u t a t i o n in a small group of patients w i t h intact arterial repairs. Because we are unable to reliably predict w h i c h individual patient could be spared a n u n s u c c e s s f u l a t t e m p t at limb salvage a n d w o u l d be best served by a p r i m a r y a m p u t a t i o n , we c o n t i n u e to reconstruct virtually all patients. Aggressive m e a n s of w o u n d coverage, including m y o c u t a n e o u s flaps and s i m u l t a n e o u s skin grafting at the time of p e r f o r m i n g fasciotoroles, have improved our results in treating the m o s t severely injured limbs. Progress in m a n a g ing popliteal artery t r a u m a has resulted in a decline in a m p u t a t i o n rate from 2 I % to 0% despite a doubling in the n u m b e r of patients treated f r o m the first to the last 5-year period.

REFERENCES 1. Orcutt MB, Levine BA, Root HD, et al. The continuing challenge of popliteal vascular injuries. Am J Surg 1983;146: 758-761. 2. MendoncaJM, de Matos AN. Arterial injuries associated with trauma to the knee. Am J Surg 1984;147:210-211. 3. Shah DM, Naraynsingh V, Leather RP, et al. Advances in the management of acute popliteal vascular blunt injuries. J Trauma 1985;25:793-797. 4. Downs AR, MacDonald P. Popliteal artery injuries: Civilian experience with sixty-three patients during a twenty-four year period {1960 through 1984). J Vasc Surg 1986;4:55-62. 5. Krige JEJ, Spence RAJ. Popliteal artery trauma: A high risk injury. Br J Surg 1987;74:91-94. 6. Armstrong K, Sfeir R, Rice J, et al. Popliteal vascular injuries and war: Are Beirut and New Orleans similar? J Trauma 1988;28:836-839. 7. Gnanadev DA, Fandrich BL. Popliteal artery trauma: Update and recent advances in management. Ann Vasc Surg ,1988; 2:332-335. 8. Thomas DD, Wilson RE Wiencek RG. Vascular injury about the knee. Am Surg 1989;55:370-377. 9. Hamza N, Marath A, A1-Fakhry MR. The management of aneurysms and arteriovenous fistulae of the popliteal artery arising from war trauma. J Cardiovasc Surg 1990;31:457-461. 10. Peck JJ, Eastman AB, Bergan JJ, et al. Popliteal vascular trauma. Arch Surg 1990;125:1339-1344. 11. Sfeir RE, Khoury GS, Haddad FF, et al. Injury to the popliteal yessels: The Lebanese War experience. World J Surg 1992;16: 1156-1159. 12. Wagner WH, Calkins ER, Weaver FA, et al. Blunt popliteal artery trauma: One hundred consecutiveinjuries. J Vasc Surg 1988;7:736-748. 13. Stain SC, Yellin AE, Weaver FA, et al. Selectivemanagement of nonocclusive arterial injuries. Arch Surg 1989;124:11361141. 14. Schwartz MR, Weaver FA, Bauer M, et al. Refining the indications for arteriography in penetrating extremity trauma: A prospective analysis. J Vasc Surg 1993;17:116-124.

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15. Sherman RT, Parfish RA. M a n a g e m e n t of s h o t g u n ir~juries. J Trauma 1963;3:76-85. 16. Roberts RiM, String ST. Arterial injuries in extremity s h o t g u n wounds: Requisite ['actors for successful m a n a g e m e n t . Surgery 1984;96:902-907. 17. Meyer JP, Lim LT, Schuler JJ, et al. Peripheral vascular t r a u m a from close-range s h o t g u n injuries. Arch Surg 1985; 120:1126-1131. 18. Walker ML, Poindexter JM, Stovall I. Principles of s h o t g u n wounds. Surg Gynecol Obstet 1990;170:97-105. 19. Frykberg ER, Crump JM, Dennis JW, et aL Nonoperative observation of clinically occult arterial injuries: A prospective evaluation. Surgery 1991;109:85-96. 20. Jaggers RC, Feliciano DV, Mattox KL, et al. hrjury to popliteal vessels. Arch Surg 1982;117:657-66l. 2I. Alexander J J, Piotrowski J J, Graham D, et al. Outcome of complex vascular injuries of the lower extremity. Am J Surg t991;162:111-116. 22. Reid JDS, Weigelt JA, That ER, et al. A s s e s s m e n t of proximity of a w o u n d to major vascular structures as an indication for arteriography. Arch Surg 1988;123:942-946. 23. Dennis JW, Frykberg ER, Crump JM, et al. New perspectives on the m a n a g e m e n t of penetrating trauma in proximity to major limb arteries. J Vasc Surg 1990; 1 1:85-93. 24. Weaver FA, Yellin AE, Bauer M, et al. Is arterial proximity a valid indication for arteriography in penetrating extremity trauma. Arch Surg 1990;125:1256-1260. 25. Gillespie DL, Woodson J, K a u f m a n J, et al. Role of arteriography for blunt or penetrating injuries in proximity to major vascular structures: An evolution in m a n a g e m e n t . A n n Vasc Surg 1993;7:145-149. 26. Bynoe RE Miles WS, Bell RM, et al. Noninvasive diagnosis of vascular t r a u m a by duplex ultrasonography. J Vase Surg 1991; 14:346-352. 27. Schwartz M, Weaver E Yellin A, et al. The utility of color flow Doppler e x a m i n a t i o n in penetrating extremity arterial trauma. Am Surg 1993;59:375-378.

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28. Anderson RJ, ttobson RW, Lee BG, et al. Reduced dependency on arteriography for penetrating extremity trauma: Influence of w o u n d location and noninvasive vascular studies. J Trauma 1990;30:i059 1065. 29. Lira LT, Michuda MS, Flanigan P, et al. Popliteal artery trauma. Arch Surg i980;115:1307-1313. 30. Barcia PJ, Nelson T G , W h e l a n TJ. hnportance of venous occlusion in arterial repair failure: An experimental study. Ann Surg 1972;175:223-237. 31. Hobson RW, Howard EW, Wright CB, et al. Hemodynamics of canine femoral venous ligation: Significance in combined arterial and venous injuries. Surgery 1973;74:824-829. 32. Snyder WH. Vascular injuries near the knee: An updated series and overview of the problem. Surgery 1982;91:502-506. 33. McCabe CJ, Ferguson CM, Ottinger LW. Improved limb salvage in popliteal artery injuries. J Trauma 1983;28:982985. 34. Odland MD, Gisbert VL, Gustilo RB, et al. Combined orthopedic and vascular injury in the lower extrenrities: Indications for amputation. Surgery 1990;108:660-666. 35. Sharma PVP, Ivatury RR, Simon RJ, et al. Central and regional h e m o d y n a m i c s determine optimal m a n a g e m e n t of major venous injuries. J Vasc Surg 1992;16:887-894. 36. Rich NM, Hobson RW, Collins GJ, et al. The effect of acute popliteal venous interruption. A n n Surg 1976;183:365-368. 37. Nypaver TJ, Schuler JJ, McDonnell P, et al. Long-term results of venous reconstruction after vascular trauma in civilian practice. J Vase Surg 1992;16:762-768. 38. Shah PM, Wapnir I, Babu S, et al. Compartmental syndrome in combined arterial and venous injuries of the tower extremity. Am J Surg 1989;158:136-141. 39. Mullins RJ, Lucas CE, Ledgerwood AM. The natural history following venous ligation for civilian injuries. J Trauma 1980;20:737-743. 40. Timberlake GA, O'Connell RC, Kerstein MD:Venous injury: To repair or ligate, the dilemma. J Vasc Surg 1986;4:553-558. 41. J o h n s o n SB, Weaver FA, Yeltin AE, et al. Clinical results of decompressive dermotomy-fasciotomy. Am ,J Surg 1992;164: 286-290.