PATIENT POSITIONING AND NERVE INJURY

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PATIENT POSITIONING AND NERVE INJURY Mark A. Warner, MD

Nerve injuries represent approximately one sixth of all anesthesia closed claims in this ~0untry.l~ Of these, claims of ulnar nerve injury are the most common, followed by claims of injury of the brachial plexus, lumbosacral nerve roots, and other specific peripheral nerves of the upper and lower extremities. Of special interest, all claims of perioperative neuropathy are related to injuries to adults; there are very few reports of perioperative nerve injury in children. In this article, the pathology of neuropathies, patient characteristics and risk factors associated with common perioperative neuropathies, and the inherent difficulty with assigning fault for these events are discussed.

What Causes a Neuropathy? There are four underlying basic pathologic forces responsible for a neuropathy: stretch, compression, generalized ischemia, and metab~lic.~ Ultimately, all of these forces cause sufficient ischemia within a nerve to result in transient or permanent nerve structural or functional damage. Perioperative nerve damage is often caused by the acute application of one of these forces. It is common, however, for perioperative nerve damage to occur in nerves that have chronic dysfunction. The acute application of one of these forces upon a dysfunctional but asympto-

From Mayo Medical School and Mayo Clinic, Rochester, Minnesota

ANESTHESIOLOGY CLINICS OF NORTH AMERICA VOLUME 14 * NUMBER 3 * SEPTEMBER 1996

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matic nerve often results in a symptomatic injury to large peripheral nerves.

Upper Extremity Neuropathy

Any nerve that passes into the upper extremity may sustain an injury or convert from an abnormal but asymptomatic state to a symptomatic state during the perioperative period. Of the major nerve structures of the upper extremity, the ulnar nerve and brachial plexus nerves are the most likely to become symptomatic and be associated with major disability during the perioperative period. Although the discussion in this article concentrates on ulnar and brachial plexus neuropathies, several other neuropathies that frequently appear during the perioperative period should be mentioned. The median nerve may be injured during an anesthetic or in the postoperative period if it is stretched.2, This injury anecdotally occurs most often in muscular young to middle-aged men. These individuals often are unable to completely extend their arms at the elbows because their large biceps muscles are inflexible and the bicipital tendons are contracted. When anesthetized and paralyzed, the arms may be extended flat onto armboards and the median nerves stretched. Appropriate padding placed under the arms and hands of these individuals may prevent stretch of these nerves. In a recent prospective study of perioperative neuropathy performed at Mayo Clinic (Rochester, MN), investigators found 47 of 1506 patients to have mild to moderate carpal tunnel symptoms during the perioperative period (Warner MA, personal communication, April 1996). Patients with carpal tunnel syndromes often had these symptoms appear during the day of surgery. A high percentage of these patients had a previous history of carpal tunnel syndrome or symptoms suggestive of the syndrome. It may be that immobilization and intravenous fluids during the immediate operative period may result in sufficient edema under the transcarpal ligament to cause symptoms in previously asymptomatic patients. The symptoms were transient in all 47 of the patients in this study. Ulnar Neuropathy

Improper anesthetic care and patient malpositioning have been implicated as causative factors in the development of ulnar neuropathies since reports by Biidinge$ and Garriques9 in the 1890s. These factors likely play an etiologic role for this problem in some surgical patients.

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Other factors, however, may contribute to the development of postoperative ulnar neuropathies. In a series of 12 inpatients with newly acquired ulnar neuropathy, Wadsworth and Williams27determined that external compression of an ulnar nerve during surgery was a factor in only two patients. Interestingly, a number of their nonsurgical patients developed ulnar neuropathies during both inpatient and outpatient treatment. Typically, anesthesia-related ulnar nerve injury is thought to be associated with external nerve compression or stretch caused by malpositioning. Although this implication may be true for some patients, three factors suggest that other factors may contribute. First, Warner et alZ9 found several patient-related characteristics to be associated with these ulnar neuropathies, including the following: Male gender Very thin patients (body mass index < 24) Very heavy patients (body mass index > 24) Prolonged immobilization postoperatively Second, a high incidence of contralateral ulnar nerve conduction dysfunction in patients with postoperative ulnar neuropathies suggests that many of these patients likely have asymptomatic but abnormal ulnar nerves prior to the administration of anesthetics.' These abnormal nerves may become symptomatic during the perioperative period. Third, many patients do not notice or complain of ulnar nerve symptoms until more than 24 hours after their surgical procedures.', 3, 29 As noted previously, investigators at Mayo Clinic have just completed a prospective study of ulnar neuropathy performed on 1506 adult patients who underwent noncardiac surgical and diagnostic procedures with and without anesthetics (Warner MA, personal communication, April 1996). In this study, all patients were assessed preoperatively and daily for 1 week after their procedures to determine if and when they developed symptoms or signs of ulnar neuropathy. Seven patients (1:215) developed an ulnar neuropathy. Three of these patients remained symptomatic for at least 2 months. Interestingly, when prospectively questioned and tested, none of these patients noted or was found to have any ulnar neuropathy symptoms or signs until at least 2 days after their procedures (mean 4.4 days, range 2-7 days). This finding is supported by previous retrospective data (Fig. 1).When asked 6 to 16 weeks later to remember the onset of their symptoms, 2 of the 7 patients strongly believed that their symptoms were present immediately after their procedures. This finding of a difference between documented events and recall may have significant medicolegal impact.

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Figure 1. Distribution of patients with ulnar neuropathy by time from conclusion of the procedure to notation of first symptoms. The onset of symptoms was first noted more than 24 hours after the procedure in more than one half of all patients. PARU = postanesthetic recovery unit. (From Warner MA, Warner ME, Martin JT: Ulnar neuropathy: Incidence, outcome, and risk factors in sedated or anesthetized patients. Anesthesiology 81 :13321340, 1994; with permission.)

Brachial Plexus Neuropathy Brachial plexus neuropathies may masquerade as ulnar neuropathies or have symptoms that suggest injuries to other nerve structures. In general, brachial plexus neuropathies are associated with median sternotomy*O, 21, 22, 24, 25, 32 or the use of head-down positions in which shoulder braces are used for support and ~tabilization.~, 8, 17, 31 Rarely, they may be found in patients in a prone position who have their arm hyperabducted, especially when the humeral heads are externally rotated. Neuropathy associated with median sternotomy often involves stretch or compression of the brachial plexus during sternal separation.B Other potential mechanisms of injury include direct trauma from fractured first ribs. Brachial plexus nerve injury during sternal retraction is most common during internal mammary artery dissection. The mechanism is assumed to be asymmetric retraction of the rib cage. This brachial plexus neuropathy may be difficult to delineate from peripheral ulnar neuropathy . Sternal retraction posteriorly displaces the upper rib cage and may stretch or compress the brachial plexus's inferior trunk (C8-Tl) or medial cord. These nerve structures later join to form the major contribution to the ulnar nerve. Regardless of which of these mechanisms is present, brachial plexus neuropathy does not appear to be related to a patient's arm position or padding during the sternotomy and related procedures.

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Brachial plexus neuropathy associated with procedures that are performed on patients in steep head-down (Trendelenburg) postures and who are restrained with shoulder braces may be caused by direct compression or stretch of the brachial plexus. Shoulder braces, if used, should be properly placed over the acromioclavicular join+) to prevent patients who are placed in steep head-down postures from slipping downward and, potentially, off operating tables. In general, the use of nonslip operating table mattresses has eliminated the need to use shoulder braces, but they are still used for steep head-down postures in some medical communities. If a shoulder brace is placed medial to the acromioclavicular joint, downward slide of a patient may cause direct compression of the ipsilateral brachial or cervical plexus by the brace. If placed laterally, downward slide of a patient may cause the shoulder and arm to be displaced caudally and stretch the fixated brachial plexus. The potential for injury from this mechanism may increase when the ipsilateral arm is abducted to 90 degrees or more (eg., when placed on a side armboard).I7 Lower Extremity Neuropathy

Although injuries to the nerves of the lower extremities may occur in a variety of patient postures, most reported neuropathies occur in patients who are undergoing procedures while placed in one of the lithotomy positions. These neuropathies often have been considered to be preventable and to occur because of poor intraoperative care (e.g., improper positioning or padding) or judgment (e.g., excessively prolonged use of lithotomy position).6This perception has significant impact on the outcomes of medicolegal cases involving these types of problem^.^ A number of studies have suggested that there are many factors other than improper intraoperative care that may contribute to the risk of lower extremity nerve injury.'*, IR, 30 In 1994 Warner et aI2* retrospectively reviewed the rate and type of motor neuropathies that occurred in 198,461 consecutive patients who underwent procedures while they were in a lithotomy position. These authors found that prolonged duration in lithotomy (Fig. 2) and patient-specific risk factors such as a very thin body habitus (Fig. 3) and smoking in the preoperative period were associated with the development of these neuropathies. These findings suggest that patient characteristics contribute to the risk of neuropathy and that not all neuropathies should be assumed to be the result of improper positioning or judgment during the care of patients who develop a neuropathy. In this study, the most commonly involved nerves were the common peroneal (81Y0), sciatic (15%), and femoral (4%). The potential risk factors for each of these nerves are discussed here.

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Figure 2. Distribution of duration in lithotomy for patients with neuropathies and control subjects. Patients with neuropathies generally had a longer duration in lithotomy than controls ( P <0.001). Fifteen patients with neuropathies spent more than 4 hours in lithotomy; no control patient spent more than 4 hours in lithotomy. Dark bar = cases in which lithotomy position lasted 4 hours or more. (From Warner MA, Martin JT, Schroeder DR, et al: Lower-extremity motor neuropathy associated with surgery performed on patients in a lithotomy position. Anesthesiology 81 :6-12, 1994; with permission.)

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Body mass index (kglrnz) Figure 3. Distribution of body mass index (BMI) for patients with neuropathies and control subjects Patients with neuropathies generally had lower BMls The majority of patients with neuropathies had a BMI of 20 or less no control subject had a BMI of 20 or less cases in which BMI was 20 or less (From Warner MA, Martin JT, Schroeder Dark bar DR, et a1 Lower-extremity motor neuropathy associated with surgery performed on patients in d Itthotomy position Anesthesiology 81 6-12, 1994, with permission ) ~

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Common Peroneal Neuropathy

The common peroneal nerve is very superficial as it wraps around the head of the fibula. Because it is quite exposed at this level, it may be easily compressed and injured. This risk may be increased in very thin people.28Direct compression of the peroneal nerve by leg holders has commonly been considered the primary mechanism of injury in peroneal neuropathy.2, There are no data, however, that support this claim. A large variety of leg holders have been implicated by anecdote to increase the risk of direct nerve compression, but none has been shown in comparison to others to increase the risk of this neuropathy. Intuitively, legs supported by these devices should be padded, especially at the level of the fibular head, if they lay in direct contact with a leg holder. Regardless of the type of leg holder used, the position of the legs within leg holders should be frequently assessed during the intraoperative period to confirm that no change in position or padding has occurred and that the position and padding, if needed, are appropriate. Sciatic Neuropathy

The same forces that contribute to stretch injuries of the hamstring group muscles (e.g., biceps femoris muscle) may stretch the sciatic nerve. Simultaneous hyperflexion of the hip and extension of the knee will stretch and possibly injure the sciatic nerve. This set of actions can occur during the establishment and maintenance of the lithotomy position. A patient in a lithotomy position may passively shift toward the caudal end of an operating table when placed in a head-up posture or be actively shifted caudally by a member of the operating team in an attempt to obtain increased exposure of the perineum. This movement may increase the flexion of the hips and extension of the legs if the legs are already fixated within leg holders. It would seem prudent to frequently confirm that the flexor muscles of the knee (e.g., hamstring group) are not taut after placing a patient’s legs into any lithotomy position. Femoral Neuropathy

Unlike most other neuropathies in which the anesthesia provider is often considered to have acted improperly for the neuropathy to occur, those involving the femoral nerve and its cutaneous branches are often considered to result from improper placement of abdominal wall retractors and direct compression of the nerve.I9When related to retractors, the assumption is that retractors place continuous pressure on the iliopsoas muscle and either stretch the nerve or cause it to become ischemic by

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Figure 4. Relationship of iliopsoas muscle, iliac muscle, femoral nerve, and external iliac artery within the pelvis. Note the probable location of a displacing and compressing retractor blade that would be used for an abdominal surgical approach to the pelvis. Note the formation of the femoral nerve from the lumbar plexus and its course in the iliopsoas muscle. Because the origin of the netve branch to the iliopsoas muscle is proximal to the location of the retractor blade, an injury caused by this mechanism would not affect the function of the iliopsoas muscle. In contrast, any injury mechanism that would involve the lumbosacral nerve plexus likely would affect the function of this muscle. (From Rosenblum J, Schwarz GA, Bendler E: Femoral neuropathy-a neurological complication of hysterectomy. JAMA 195:409-414, 1966; with permission.)

occluding the external iliac artery or penetrating vessels of the nerve as it passes through the muscle (Fig. 4). Rosenblum at all9have speculated that self-retaining retractors placed in the abdomen that exert continuous pressure are more likely to produce a femoral neuropathy than handheld retractors that usually exert pressure intermittently. Vaginal retractors in n o n p a r t ~ r i e n tand s ~ ~forceps in parturients" also have been implicated in femoral neuropathies. There may be factors other than retractors associated with perioperative femoral neuropathies.26As noted previously, a variety of patient factors, such as very thin body habitus and smoking in the perioperative period, may be associated with lower extremity neuropathies.28Extremes of either hip flexion or extension also may be associated with femoral 2o Hemorrhage in the iliopsoas muscle and subsequent ne~ropathies.'~, compression or ischemia of the femoral nerve also have been reported to occur during the perioperative peri0d.3~ Cutaneous branches of the femoral nerve appear to be particularly

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susceptible to compression injury during labor and childbirth. O’Donnell et all6 prospectively evaluated the peripartum care of 412 parturients. They found that 21% of these women had sensory loss detectable by careful postpartum neurologic examination. Most of this sensory loss was in the distribution of the lateral and anterior femoral cutaneous nerves, and 94% of these neuropathies were transient. In general, these neuropathies occurred in heavy women with large fetuses who required prolonged pushing while in a lithotomy position. The authors did not speculate whether the neuropathy resulted from trauma to the femoral nerve by the fetus within the pelvis during the prolonged labor or whether the prolonged duration in lithotomy during labor increased the risk of femoral cutaneous nerve branches being pinched at the level of the inguinal ligament. Practical Considerations

Efforts to prevent perioperative neuropathies are frequently debated, and there often is confusion on how to handle a neuropathy once it has occurred. In general, there are no data to support rigid opinions on any of these issues. Most opinions related to these issues have been formulated by personal experience and seasoned or supported with speculation raised in anecdotal case reports. Therefore, the following represent my ”best guess” opinions on how to handle the following issues. Padding Exposed Peripheral Nerves. There are many types of padding materials that are advocated to protect exposed peripheral nerves. These materials often consist of cloth (e.g., blankets and towels), foam sponges (e.g., ”eggcrate” foam), and gel pads. There are no data to suggest that any of these materials is more effective than any other or better than no padding at all. A good rule-of-thumb would be to use positioning and padding of an exposed peripheral nerve to (1)prevent stretch of the nerve beyond normal tolerable limits, (2) avoid direct compression of the nerve, if possible, and (3) distribute any compressive forces that must be place on the nerve over as large an area as possible. Prolonged Duration in One Position. Most everyone would agree that prolonged duration in one position increases the risk of neuropathy and other superficial integumentary damage. For example, prolonged duration in lithotomy positions has been well-documented to greatly increase the risk of lower extremity neuropathy.28Alopecia and occipital neuropathy can occur from prolonged immobilization in the supine position, especially in patients undergoing cardiopulmonary bypass who might have reduced perfusion pressure to the occiput. When possible, it would appear prudent to limit as much as practical the time the patient spends in any one position. For example, simply turning the head from

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side to side in a supine patient who is undergoing a prolonged procedure may intermittently increase perfusion of the occiput and reduce the risk of alopecia and occipital neuropathy. What To Do if Your Patient Develops a Neuropathy. Although each situation is unique and will require careful individual assessment, the following guidelines may suggest a basic course of action:

Is the neuropathy sensory or motor? Sensory lesions are more frequently transient than motor lesions.29If the symptoms are numbness or tingling only, it may be appropriate for you to inform the patient that most of these neuropathies will resolve over a period of 5 days. You should instruct the patient to avoid postures that would compress the involved nerve. Arrangements should be made to frequently contact the patient. A call to alert your local neurologist would be appropriate. If the symptoms still persist on day 5, the neurologist should be consulted. If the neuropathy has a motor component, a neurologist should be consulted from the start. Electromyographic studies may be needed to assess the level of any acute lesion. This knowledge may direct an appropriate treatment plan. The studies may also demonstrate chronic abnormalities of the nerve or, if applicable, the contralateral nerve.

SUMMARY

The etiology of perioperative neuropathies is often multifactorial, and this realization hampers efforts to eliminate their occurrence. Although some of these neuropathies may be associated with various intraoperative positions, many perioperative neuropathies appear to develop during an extended period after surgery and anesthesia. Documentation of the absence of any symptoms of neuropathy in the preoperative and early postoperative periods will delineate the onset of perioperative neuropathies. Strategies to decrease the incidence of these injuries should include resources to teach postoperative nursing staff and patients preventive measures to avoid stretch or prolonged compression to peripheral nerves while in the hospital and at home.

References 1. Alvine FG, Schurrer ME: Postoperative ulnar-nerve palsy: Are there predisposing factors? J Bone Joint Surg 69:255-259, 1987 2. Britt BA, Gordon RA: Peripheral nerve injuries associated with anaesthesia. Can Anaesth SOCJ 11:514-536, 1964

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3. Budinger K: Ueber Lahmungen nach chloroform-narkosen. Arch f Kin Chirc 47121145, 1894 4. Clausen EG: Postoperative (“anesthetic”) paralysis of the brachial plexus. Surgery 12~933-942,1942 5. Dawson DM, Krarup C: Perioperative nerve lesions. Arch Neurol 46:1355-1360, 1989 6. Dornette WHL: Compression neuropathies: Medical aspects and legal implications. Int Anesthesiol Clin 24:201-209, 1986 7. Dornette WHL Indentifying, moving, and positioning the patient. In Domette WHL (ed): Legal Issues in Anesthesia Practice. Philadelphia, FA Davis, 1991, pp 120-123 8. Ewing MR, Edin MB: Postoperative paralysis in the upper extremities: Report of five cases. Lancet 1:99-103, 1950 9. Carriques HJ: Anaesthesia-paralysis. Am J Med Sci 13381-89, 1897 10. Hickey C, Gugino LD, Aglio LS, et al: Intraoperative somatosensory evoked potential monitoring predicts peripheral nerve injury during cardiac surgery. Anesthesiology 78:29-35, 1993 11. Hill EC: Maternal obstetric paralysis. Am J Obstet Gynecol 83:1452-1460, 1962 12. Honet JC, Wajszczuk WJ, Rubenfire M, et al: Neurological abnormalities in the leg(s) after use of intraaortic balloon pump. Arch Phys Med Rehabil 56:346-352, 1975 13. James SE, Wade PJF: Lateral popliteal nerve palsy as a complication of the use of a continuous passive motion machine. Injury 18:72-73, 1987 14. Knoll DA, Caplan RA, Posner K, et al: Nerve injury associated with anesthesia. Anesthesiology 73:202-207, 1990 15. Miller EH, Benedict FE: Stretch of the femoral nerve in a dancer. J Bone Joint Surg Am 67315317,1985 16. O’Donnell D, Rottman R, Kotelko D, et al: Incidence of maternal postpartum neurologic dvsfunction. Anesthesiology 81:A1127, 1994 17. Romanowski L, Reich H, McClynn F, et a1 Brachial plexus neuropathies after advanced laparoscopic surgery. Fertility Sterility 60:729-732, 1993 18. Rose HA, Hood RW, Otic JC, et al: Peroneal nerve palsy following total knee arthroplasty. J Bone Joint Surg Am 64:347-351, 1982 19. Rosenblum J, Schwarz GA, Bendler E: Femoral neuropathy-a neurological complication of hysterectomy. JAMA 195:409-414, 1966 20. Rottenberg MF, DeLisa J A Severe femoral neuropathy with ”hanging leg” syndrome. Arch Phys Med Rehabil62:404-406,1981 21. Roy RC, Stafford MA, Charlton JE: Nerve injury and musculoskeletal complaints after cardiac surgery: Influence of internal mammary artery dissection and left arm position. Anesth Analg 67277-279 22. Seyfer AE, Grammer MY, Bogumill GP, et a]: Upper extremity neuropathies after cardiac surgery. J Hand Surg 10:1&19, 1985 23. Stoelting RK: Brachial plexus injury after median sternotomy: An unexpected liability for anesthesiologists. J Cardiothorac Vasc Anesth 8:2-4, 1994 24. Vahl CF, Carl I, Muller-Vahl H, et al: Brachial plexus injury after cardiac surgery. The role of internal artery preparation: A prospective study of 1000 consecutive patients. J Thorac Cardiovasc Surg 1023724-729, 1991 25. Vander Salm TJ, Cereda J-M, Cutler BS: Brachial plexus injury following median sternotomy. J Thorac Cardiovasc Surg 80:447-452, 1980 26. Vargo MM, Robinson LR, Nicholas JJ, et al: Postpartum femoral neuropathy: Relic of an earlier era? Arch Phys Med Rehabil71:591-596,1990 27. Wadsworth TG, Williams JR: Cubital tunnel external compression syndrome. Br Med J 1:662-666, 1973 28. Warner MA. Martin IT. Schroeder DR. et al: Lower-extremitv motor neurouathv associated with surgery performed on patients in a lithotomy pokition. Anesthesiology 81:6-12, 1994 29. Warner MA, Warner ME, Martin J T Ulnar neuropathy: Incidence, outcome, and risk factors in sedated or anesthetized patients. Anesthesiology 81:1332-1340, 1994 30. Weber ER, Daube JR, Coventry MB: Peripheral neuropathies associated with total hip arthroplasty. J Bone Joint Surg Am 58:6649, 1976 ,

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31. Westin B: Prevention of upper-limb nerve injuries in Trendelenburg position. Acta Chir Scand 108:61-67, 1959 32. Wey JM, Guinn GA: Ulnar nerve injury with open-heart surgery. Ann Thor Surg 39:358-360,1985 33. Wooten SL, McLaughlin R E Iliacus hematoma and subsequent femoral nerve palsy after penetration of the medial acetabular wall during total hip arthroplasty. Clin Orthop 191:221-223, 1984 Address reprint requests to Mark A. Warner, MD Department of Anesthesiology Mayo Clinic 200 First Street SW Rochester, MN 55905