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Instructional Course Lectures, The American Academy of Orthopaedic Surgeons - Neurovascular Injury Associated with Hip Arthroplasty*

DAVID G. LEWALLEN, M.D., ROCHESTER, MINNESOTA

An Instructional Course Lecture, The American Academy of Orthopaedic Surgeons

	Introduction

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Neurological and vascular complications following hip arthroplasty are uncommon, and their impact ranges from transient and trivial to permanent and devastating. The proximity of neurological and vascular structures to the hip makes any operation on the hip potentially hazardous. Direct and indirect injury of these structures may occur during the operative exposure and the subsequent procedure. The important features of the neurological and vascular structures that are at risk during a hip arthroplasty, especially the pertinent anatomy, etiology of injuries, and treatment options, provide a foundation of information that can assist the physician who encounters neurological or vascular complications clinically.

	Neurological Complications

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Neurological dysfunction following hip arthroplasty can be due to central neurological injury or to a peripheral-nerve lesion. Peripheral-nerve lesions during hip arthroplasty may be categorized according to severity, location, and onset of symptoms relative to the index procedure. Central neurological injury may occur as a result of prolonged hypoxia, a cerebrovascular accident, or fat embolism secondary to the operation. Careful treatment by the anesthesiology team during procedures on the hip is necessary to avoid hypoxia or anoxia, to reduce major fluctuations in blood pressure that may contribute to the risk of a cerebrovascular accident, and to assist in careful positioning of the patient in order to prevent a peripheral-nerve lesion (such as brachial plexus stretch). Embolization of fat and marrow elements is one factor directly related to the operative procedure that can have an important central neurological effect and is somewhat under the control of the operating surgeon.

Neurological Sequelae of Fat Embolism
Embolization of fat and marrow elements from the femur and, to a lesser degree, the acetabulum has been shown to occur during all primary total hip arthroplasties and to peak during portions of the procedure that involve maximum manipulation of bone, such as reaming and particularly cementing of a component^{19,24,30,43,51}. Most patients seem to tolerate the passage of this embolic material through the right side of the heart and into the pulmonary vessels without apparent signs or sequelae¹⁹. Rarely, marked intraoperative hypotension, hypoxia, and even cardiac arrest and death occur as a result of those emboli, usually immediately after cementing of an implant^{13,15,29,34,45}. A patent foramen ovale, which was documented in approximately 25 per cent of 965 hearts of normal adults in an autopsy study, allows for the potential of paradoxical embolization of this material with passage from the right side of the heart to the left side and subsequent widespread systemic delivery^7,19,21. Paradoxical embolization has been estimated to be possible in 10 per cent of normal patients⁷. The passage of this material into the left-sided circulation may cause focal neurological deficits, perioperative delirium, and even death during the postoperative period. In individuals who do not have the potential for right-to-left shunting, the pulmonary vessels function as a filter, entrapping the material and limiting the risk that it poses to the central nervous system (Fig. 1). The use of transesophageal echocardiography intraoperatively has allowed documentation of the passage of fat and marrow elements through the right atrium and the right ventricle and has also allowed direct observation of paradoxical embolization in individuals who have right-to-left shunting at the atrial level¹⁹ (Fig. 2). Focal cerebral infarcts can be observed on computerized tomography scans (Fig. 3), and they can be seen directly in pathological specimens when perioperative death results from paradoxical embolization.

View larger version (138K): [in this window] [in a new window]   Fig. 1 Histological autopsy specimen of a pulmonary vessel from a patient who died intraoperatively immediately after cementing of a component. Intravascular fat and marrow elements are visible (hematoxylin and eosin, approximate magnification x 100).

View larger version (133K): [in this window] [in a new window]   Fig. 2 Intraoperative transesophageal echocardiogram of the heart, made just after insertion of a femoral component with cement. The right atrium (RA), left atrium (LA), and right ventricle (RV) are visible. There are bright-speckled echogenic material in the right atrium and paradoxical emboli (arrows) in the left atrium.

View larger version (134K): [in this window] [in a new window]   Fig. 3 Computerized tomography scan of the head, showing dark areas of focal cerebral infarction (arrowheads) in a patient who went into a coma immediately after a bipolar arthroplasty with cement and subsequently died. The presence of a previously undiagnosed major right-to-left shunt at the atrial level on an echocardiogram led to the diagnosis of intraoperative paradoxical embolization.

	Peripheral-Nerve Complications

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Injuries of peripheral nerves can be categorized according to location, severity, and etiology. The prevalence of neurological injuries in the upper extremity following hip arthroplasty is approximately 0.15 per cent, as documented in a review of more than 7000 replacements⁴¹; such injuries are usually due to problems with positioning of the patient and are much more likely to occur in patients who have rheumatoid arthritis^41,61. Neurological injury involving the contralateral lower extremity is also rare, occurring in five of 919 arthroplasties in one review, and is also due mainly to problems with positioning; these injuries most frequently manifest as a transient hypoesthesia or less often as motor dysfunction⁶¹. Most peripheral-nerve lesions associated with hip arthroplasty involve the treated limb and may be due to direct injury, positioning problems, or excessive retraction.

The severity of peripheral-nerve lesions was categorized by Seddon according to the degree of anatomical disruption⁵⁵. Neurapraxia involves an intact neurological structure with decreased function due to local pressure producing ischemia and contusion of the nerve. Axonotmesis involves axonal disruption with distal degeneration of the myelin but with no disruption of the endoneural tube. A return of nerve function is possible with neurapraxia or axonotmesis. Neurotmesis involves complete disruption of the nerve, such as is seen in complete transection, and results in a permanent loss of nerve function unless an operative repair is performed⁵⁵. Clinical discrimination between neurapraxia and neurotmesis is difficult, especially initially.

Prevalence
Peripheral-nerve lesions have been clinically evident after 0.6 to 1.3 per cent of primary total hip arthroplasties, according to reports of series involving 600 to more than 2000 patients^{16,28,63,66,68}. Neural injury has been observed after as many as 7.5 per cent of revision arthroplasties, according to series ranging in size from eighty-eight to more than 3000 patients^2,39,53. However, subclinical neural injury demonstrable on electromyographic or nerve-conduction studies is actually quite common after hip arthroplasty. In one prospective study, it was detected in 70 per cent of thirty hips⁶⁸. In two series of 614 and 7133 hips, more than 90 per cent of the observed nerve palsies involved the sciatic nerve, with half of these involving only the peroneal division^16,41. The femoral nerve is the next most commonly injured nerve, but such injury is rarely noted clinically and even more rarely involves prolonged dysfunction or disability⁶⁰. Injury of the obturator nerve, at least by clinical criteria, is infrequent but can be due to intrapelvic extrusion of cement⁵⁹. The prevalence of injury of the superior gluteal nerve, especially that associated with the Hardinge or transgluteal approach, is not clear. While they are thought to be uncommon, these injuries may occur more often than is recognized as weakness of the abductors is common at least temporarily after most operations on the hip and may be attributed to a variety of causes other than intraoperative neural injury. Splitting of the gluteus medius more than six centimeters proximal to the tip of the greater trochanter (or four centimeters proximal to the acetabular rim) places the superior gluteal nerve at risk^23,27. Palsy of the lateral femoral cutaneous nerve is also observed occasionally and may be due to pressure from hip rests or supports used to position the patient during the procedure. This problem is often transient, and the etiology usually is not clearly defined.

Risk factors for peripheral-nerve lesions have been examined by several authors. Female gender has repeatedly emerged as an important variable, with 80 per cent or more of the nerve palsies in three different studies of 825 to 2012 patients occurring in women^28,62,68. It has been postulated that this increased prevalence in women is due to the fact that, compared with men, they have reduced muscle bulk, smaller size, shorter limbs, and possible differences in local vascular anatomy^62,68. Experimental models have shown that neural injury will occur if the nerve is elongated more than 6 per cent of its length. Given this 6 per cent stretch limit, smaller individuals with shorter limbs, and thus much shorter nerves, have less of a potential for absolute neural retraction than do much larger individuals^28,62. This factor may help to explain partially the difference in prevalence between the genders.

Etiology
In general, neural injury may occur as a result of traction, compression, or ischemia⁶⁴. Neural injury following arthroplasty may be due to direct damage occurring acutely during the procedure or to indirect damage occurring in a delayed fashion, as may be seen with problems with positioning postoperatively or the formation of deep hematomas. However, several specific factors have been associated with an increased risk of neural injury. A previous operative procedure on the hip is one such factor¹⁶. Revision of a failed implant is associated with a 1.4 to 7.5 per cent rate of postoperative nerve palsy according to reviews of series including eighty-eight to 3126 patients^2,39,53. This increased risk may be due to the more extensive and difficult dissection required with revision procedures and perhaps, in some patients, to uncertainty regarding the location of major neurological and vascular structures when a previous operative exposure has been performed. In addition, tethering by scar tissue may predispose the nerve to stretch with retraction, dislocation of the hip, or limb-lengthening. During isolated revision of the acetabular component through a posterior approach, retraction of the intact femoral component anteriorly may increase the risk of compression of the femoral nerve.

Acute limb-lengthening of more than two to four centimeters during arthroplasty has been associated with an increased risk of neural injury^16,28,56. In a study of 100 patients who had a total hip replacement for the treatment of dysplasia of the hip, nerve palsy occurred in thirteen (28 per cent) of the forty-six patients who had more than four centimeters of limb-lengthening and no nerve palsy occurred in the fifty-four who had less than four centimeters of lengthening²⁸. The peroneal division of the sciatic nerve may be particularly at risk during limb-lengthening maneuvers because tethering at both the sciatic notch and the fibular head makes the effective length of the nerve less than that of the over-all limb.

Altered anatomy in the region of the hip has been considered a factor that increases the potential for neural injuries³⁹ (Figs. 4-A, 4-B, and 4-C). Congenital dysplasia of the hip, for example, results in abnormal anatomy because not only is lengthening sometimes attempted but also the severity of the dysplasia inherently alters the relationship of the nearby neurological structures. This may help to explain rates of nerve palsy ranging from 5.2 to 13 per cent in series of 100 to 172 patients who had dysplasia of the hip treated with arthroplasty^28,53,56.

View larger version (124K): [in this window] [in a new window]   Figs. 4-A, 4-B, and 4-C: A patient who had severe dysplasia and intermittent sciatic nerve sensory symptoms preoperatively as well as pain in the hip. The patient had had a previous femoral osteotomy. Fig. 4-A: Preoperative radiograph.

View larger version (157K): [in this window] [in a new window]   Fig. 4-B Preoperative computerized tomography scan.

View larger version (134K): [in this window] [in a new window]   Fig. 4-C Despite derotation and shortening, anterior translation of the hip to allow articulation with a cup placed in the anatomical location resulted in a transient motor loss in the peroneal distribution. Persistent sensory symptoms and causalgia-like pain in the leg were still present one year after the operation.

The formation of a hematoma can produce delayed-onset nerve palsy subsequent to hip arthroplasty and has been associated with excessive anticoagulation for prophylaxis against venous thrombosis^8,20. When the hematoma involves the gluteal compartment, the sciatic nerve is at risk^11,20. A hematoma involving the iliacus muscle can produce femoral nerve palsy and may be the result of perforation of the medial wall of the acetabulum during the arthroplasty⁶⁹. Hematoma of the iliacus muscle has been noted on postoperative computerized tomography scans, and computerized tomography may sometimes facilitate the diagnosis and treatment if the exact etiology and timing of onset of the nerve palsy are unclear. Symptoms associated with the formation of a hematoma and secondary nerve palsy include not only neurological dysfunction but also excessive pain exacerbated by passive stretch of the involved compartment¹¹. Other causes of delayed-onset nerve palsy that are not directly related to the initial operative procedure include dislocation, late ischemia from stretch neurapraxia after lengthening, positional effects as seen with direct compression of the peroneal division at the fibular head¹⁴, and late migration of hardware such as trochanteric wires³. Prominence of an implant or associated cement spurs can also produce irritation of adjacent neurological structures and the delayed onset of neural symptoms¹⁷.

Causalgia-like pain or reflex sympathetic dystrophy may complicate recovery from a neural injury and can compromise the end result even if the final motor and sensory deficits are minimum (Fig. 4-C). This problem was seen in as many as 29 per cent of twenty-eight patients following an arthroplasty²⁸, and it can be the main cause of a poor result in some instances.

Prevention
Prevention of a nerve palsy is clearly preferable to treatment of an already established neurological problem. Careful operative technique and avoidance of direct injury of the nerve during exposure, retraction, and placement of the implant are important. Operative techniques that emphasize the use of instruments and sharp dissection away from rather than toward important neurological or vascular structures are suggested. Such techniques make it possible to avoid neural injury when (not if) those instruments slip. Limiting one-stage limb-lengthening efforts to four centimeters or 6 per cent of the calculated length of the nerve, whichever is less, should help to reduce the risk of associated nerve palsy. Identification and protection of the sciatic nerve in some high-risk situations, such as when there are major alterations in local anatomy, is probably indicated. Maintenance of the knee in flexion during retraction for exposure about the acetabulum through a posterior approach can reduce tension on the sciatic nerve and reduce the risk of nerve palsy. Avoidance of screw placement on the acetabular side into the anterior-superior and anterior-inferior quadrants is recommended. Careful subperiosteal circumferential exposure of the femoral shaft during placement of the cerclage wires, with protection of the sciatic nerve if it is immediately adjacent, is also recommended,

Intraoperative neural monitoring has been explored as a potential means to reduce the risk of neural injury^6,32,40,48. It is possible to document intraoperative irritation of the nerves and, if necessary, to alter the operative technique or the position of the limb. Such monitoring has been recommended as a surveillance method during revision total hip arthroplasty or when major limb-lengthening efforts are planned⁴⁸. Simultaneous changes in amplitude and latency appear to be predictive of an alteration in the function of the sciatic nerve postoperatively⁴⁸. However, the actual reduction in the risk of nerve palsy due to intraoperative neural monitoring has not been well established, and thus the ability of this method to actually prevent neural injury remains controversial^6,32,40,48. While routine use of this method for primary or even revision total hip arthroplasties may be difficult to support on the basis of current data, judicious use in situations involving increased risk due to distorted anatomy or anticipated major limb-lengthening seems reasonable.

Treatment
While prevention is better than treatment, it is critically important to assess the neurological and vascular status of all patients carefully in the postoperative period, with good written documentation that this has been done. Observation with serial examinations and sequential electromyographic and nerve-conduction studies are helpful for the follow-up of individuals in whom neurological dysfunction is detected. Direct operative intervention is clearly indicated in patients in whom a postoperative hematoma has produced nerve palsy. The clinical hallmark of this problem is delayed onset or late progression of a neurological deficit associated with evidence of local hematoma about the hip on examination. Decompression of the hematoma reduces the risk of long-term neurological sequelae^8,20,62. When an immediate postoperative nerve palsy is discovered, exploration of the nerve is indicated only when there is reason to believe that a major direct injury, such as complete transection or encirclement of the nerve with cerclage wires, has occurred as these problems are associated with a poor prognosis unless exploration and appropriate repair are carried out. Routine operative exploration of nerve palsies after an arthroplasty is not indicated. Late exploration has been suggested when there has been no sign of nerve regeneration²², but, at present, exploration is rarely performed unless complete disruption is strongly suspected.

Prognosis
Neurological recovery is variable and is related to the severity of the initial injury. The prognosis is better for femoral nerve palsy than for sciatic palsy and is better for isolated peroneal palsy than for complete sciatic palsy¹⁶. A satisfactory functional outcome, with some residual neurological loss, is achieved in many patients. Johanson et al. reported that 79 per cent of thirty-four patients who had nerve palsy had incomplete recovery, and fifteen of the twenty-eight patients who had sufficient follow-up had both motor and sensory deficits at the most recent examination²⁸. Good prognostic signs include retention of motor function with isolated sensory loss or recovery of motor function during the initial days after the operation. Both of these situations are associated with a high rate of good results and over-all recovery⁵³. It is important, when counseling patients, to state that improvement may continue for at least one year after the injury but the status is unlikely to change after eighteen months.

	Vascular Complications

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Vascular injuries associated with hip arthroplasty may present either with acute hemorrhage during the procedure or with delayed, postoperative bleeding problems. Other potential sequelae include thrombosis of arterial or venous structures, formation of an arteriovenous fistula or false aneurysm, and embolic events (both venous and arterial)^25,26. Symptoms that may be noted days or years after the index arthroplasty include pain from pressure by a pseudoaneurysm, ischemia due to occlusion or embolization, and bleeding at the time of subsequent revision procedures⁵. Structures at risk include the femoral artery and vein; the obturator artery and venous branches; the external iliac, common iliac, and profunda femoris vessels; and the superior gluteal artery and vein.

Prevalence
The over-all risk of vascular complications associated with hip arthroplasty is small, with an estimated prevalence of approximately 0.25 per cent³⁸. The external iliac artery and the common femoral artery are the most often injured structures⁵⁸. One review of the literature revealed that thirty-six of sixty-eight reported vascular complications involved the external iliac artery and seventeen, the common femoral artery; two-thirds of the injuries were observed on the left side⁵⁸. Vascular injury is more common in previously treated hips or after revision hip arthroplasty than during primary hip replacement^37,58. The exact prevalence depends somewhat on how the investigator defines an important vascular problem. For example, excessive bleeding was reported in association with 1 per cent (nineteen) of 2012 arthroplasties, with six of the nineteen patients needing a reoperation; however, not all of them were thought to have had an injury of a major named vascular structure¹². Shoenfield et al., in a review of the results of sixty-eight arthroplasties complicated by vascular injury necessitating operative treatment, found a 7 per cent mortality rate and a 15 per cent rate of subsequent amputation⁵⁸.

Etiology
The etiology of vascular injuries may be either direct damage to the vessel or indirect injury from stretch, tearing, or compression. Direct injury may occur from sharp instruments, such as scalpels or osteotomes, and may involve any of the adjacent vascular structures depending on the area and the direction of the dissection. Direct injury of the common iliac vein from excessive acetabular reaming with violation of the medial wall has been reported³⁵. Damage caused by Hohmann or other sharp-tipped retractors is one of the more common mechanisms of vascular injury and tends to occur in two locations: over the anterior aspect of the acetabular rim and medial to the femoral neck. The common femoral artery and the medial and lateral circumflex femoral vessels are involved, with presentation in the form of bleeding, ischemia due to occlusion, or the late formation of a pseudoaneurysm necessitating operative repair^4,33,38,52. Nachbur et al. reported six such cases related to use of a Hohmann retractor, with injury of the external iliac, common femoral artery, or circumflex vessels³⁸. One of those cases resulted in amputation.

Vascular injury due to placement of a screw during fixation, without cement, of an acetabular component has received attention recently because of reports of major hemorrhage and even death³¹. Anatomical studies by Keating et al.³¹ and by Wasielewski et al.⁶⁷ clearly demonstrated the close proximity of the external iliac vessels, obturator nerve and vessels, and superior and inferior vesicular venous plexus to the medial aspect of the acetabulum (Fig. 5). Wasielewski et al. described a four-quadrant system for the safe placement of acetabular screws (Fig. 6). The anterior-superior and anterior-inferior quadrants are the zones in which there is a major risk of vascular injury by screws. Because the mechanical strength or quality of screw fixation in these anterior zones is inferior anyway, there is little reason to subject a patient to the risk of an attempted placement in those regions during primary arthroplasty. In revision arthroplasties in which anterior bone fixation may be desired because of bone loss elsewhere, palpation of drill-bits and screws after dissection of the anterior column can facilitate safe placement of the screw. The potential risk associated with such screws does not end after successful placement, however. In one report, a death occurred as a result of bleeding from a vascular injury associated with a traumatic acetabular fracture adjacent to a cup inserted without cement and fixed with screws; the cup and screws displaced medially, injuring the external iliac vessels⁴⁷.

Fig. 5 Diagram of the intrapelvic vascular structures adjacent to the inner surface of the anterior column and medial wall of the acetabulum. The arrows indicate long rods extending from the anterior screw-holes of an acetabular component and marking the intrapelvic trajectory of any screws placed in those positions. (Reprinted from: Keating, E. M.; Ritter, M. A.; and Faris, P. M.: Structures at risk from medially placed acetabular screws. J. Bone and Joint Surg., 72-A: 510, April 1990.)

View larger version (28K): [in this window] [in a new window]   Fig. 6 Diagram of the four acetabular quadrants created by two intersecting lines from the anterior and posterior superior iliac spines. Placement of the screw in the anterior-superior or anterior-inferior quadrant should be avoided because of the risk of vascular injury. (Adapted from: Wasielewski, R. C.; Cooperstein, L. A.; Kruger, M. P.; and Rubash, H. E.: Acetabular anatomy and the transacetabular fixation of screws in total hip arthroplasty. J. Bone and Joint Surg., 72-A: 502, April 1990.)

Prevention
Careful operative exposure and technique are important to avoid damage of adjacent vascular structures. The technique of sharp dissection and the use of sharp instruments away from, rather than toward, adjacent vascular structures should be encouraged. Careful placement of the retractor intraoperatively is important especially over the anterior aspect of the acetabular rim. Preoperative vascular evaluation is reasonable for patients who have severe pre-existing peripheral vascular disease. Preoperative arteriography may be indicated for high-risk situations, such as those involving intrapelvic migration of a failed acetabular component or intrapelvic extravasation of cement^{1,9,25,26,50,54}. Planned intrapelvic, medial exposure with mobilization or repair of the iliac vessel may be indicated in such patients to avoid injury during removal of the cup¹. A thorough knowledge of the vascular anatomy in the region of the hip helps the surgeon to avoid vascular injuries. In particular, it is essential that acetabular screws not be placed into hazardous zones, as determined by the adjacent vascular anatomy medial to the acetabulum^31,66,67.

Treatment
Contingency planning for the treatment of a potentially catastrophic vascular injury can facilitate an effective and rapid response. Prompt recognition of vascular injury is important. When such an injury is identified intraoperatively, the initial essential step is to control the bleeding. Standard measures of coagulation or ligation may be effective. Packing of the wound may provide temporary control or, in some instances, result in hemostasis as a result of thrombosis. However, injury of a major vessel can necessitate operative repair. The operating orthopaedic surgeon must have a thorough knowledge of pertinent regional vascular anatomy, and familiarity with adjunctive operative approaches, such as the ilioinguinal approach or the McBurney incision for retroperitoneal or intrapelvic exposure, facilitates emergent proximal vascular control and may be life-saving. The immediate availability of a vascular surgeon or a surgeon who has comparable expertise is essential in the event of a major injury necessitating vascular repair. Preoperative consultation with a vascular surgeon and intraoperative assistance may be considered when there is a risk of an intraoperative vascular injury, as in patients who have a markedly distorted anatomy, a history of previous vascular injury or repair, or intrapelvic migration of the components and cement.

	Overview

Top Introduction Neurological Complications Peripheral-Nerve Complications Vascular Complications Overview References

 
Neurovascular injuries associated with hip arthroplasty are uncommon but may be catastrophic. A thorough knowledge of local anatomy, careful consideration of the structures at risk, and avoidance of maneuvers that increase the risk of these injuries can help to reduce the chance of these problems⁴⁹. Should neurological or vascular injury occur, prompt recognition is essential to allow appropriate treatment in order to minimize the chance of permanent sequelae.

	Footnotes

 
*Printed with permission of The American Academy of Orthopaedic Surgeons. This article will appear in Instructional Course Lectures, Volume 47, The American Academy of Orthopaedic Surgeons, Rosemont, Illinois, March 1998.

No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

Department of Orthopedics, Mayo Clinic, 200 First Street S.W., Rochester, Minnesota 55905. E-mail address for Dr. Lewallen: lewallen.david@mayo.edu.

	References

Top Introduction Neurological Complications Peripheral-Nerve Complications Vascular Complications Overview References

 

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