When confronted with the complaint of pain and instability of the knee, the orthopedic surgeon frequently focuses on traumatic causes and searches for specific ligamentous laxity. The quadriceps mechanism is a major stabilizer of the knee, and weakness secondary to femoral nerve palsy results in symptomatic instability. l The etiologies of femoral nerve paralysis are numerous and include extrinsic compression by retroperitoneal masses2,3 (Table 1). The following case report is a classic representative example.
A 67-year-old black woman presented one year prior to admission to this institution with left distal anterior thigh pain and left hip pain with an event of giving way of her left knee. She was treated with nonsteroidal antiinflammatory drugs and a cane, with moderate relief. In light of her past history of cervical carcinoma in situ (1969) and Stage I cancer of the vagina (1979), bone and liver/spleen scans were ordered; these were negative except for findings consistent with mild degenerative changes at the hip and knee. Gynecologic reevaluation two months prior to admission revealed no evidence of local disease.
One month prior to admission, upon evaluation she was found to have left quadriceps atrophy and developed left upper quadrant pain. Sensory exam at that time was noted to be normal . Lumbar spine films showed disc space narrowing at L4-5 and slight anterior displacement of L4 on L5.
Fig. 1: CT reveals a large cystic mass displacing the retroperitoneal structures on the left.
CT of the pelvis revealed a large cystic retroperitoneal mass displacing the kidney and aorta (Fig. 1). The patient was admitted to the general surgery service for evaluation of this mass. Intravenous pyelography showed an enlarged left kidney with displacement and a large mass inferior to it (Fig. 2). At surgery a large retroperitoneal mass was exposed and drained of copious amounts of serous fluid, and pathology reported it as a benign cyst.
ETIOLOGlES OF NONTRAUMATIC FEMORAL NEUROPATHIES
Fig. 2: Intravenous pyelogram. Enlarged left kidney (arrows) and superior portion of the mass (arrowheads).
Fig. 3: Clinical exam demonstrated left quadriceps atrophy.
Orthopedic Service was consulted. Upon physical exam the patient was found to be a thin, short, black woman with her left knee held in 20° flexion and severe left quadriceps atrophy (Fig. 3). No demonstrable quadriceps muscle function could be elicited (Fig. 4) and there was no patellar tendon reflex. Hip flexors were present, but weak. Sensory loss, although reported to be all in the anterior thigh, was at this time restricted to the lateral femoral cutaneous nerve distribution.
Distal motor function was intact for plantar flexion, dorsiflexion, extensor hallucis longus, and eversión of the left foot. Sensation was intact, and Achilles tendon reflex was slight but present and comparable to the right Achilles reflex. The right lower extremity exam was unremarkable. Lab tests were BUN 8, serum creatinine 1.0, WBC8.7, bgb610.5, bet 32.7, and EMG/ NCS elicited L2, L3, IA, L5 neuropathies.
It was felt that the above deficits were secondary to compression on the left lumbar plexus involving L2, L3, L4 in particular by the retroperitoneal cyst. A knee-ankle-foot orthosis with drop-lock knee and free ankle was recommended, along wiüi range-of-motion exercises of hip and knee joint.
The patient was followed at her local hospital in our referral area. Upon evaluation there, two months after discharge, she was felt to have a recurrence of her left lower quadrant mass, with increasing pain and a 30-pound weight loss over that short period of time. She was again referred to our institution for further evaluation.
On the General Surgery service, another incisional biopsy and drainage of the cyst was undertaken. The biopsy revealed keratinizing squamous cell carcinoma consistent with her previous vaginal malignancy.
Chemotherapy was declined and the lesion was considered inoperable.
The patient was sent home and arrangements were made for her to have supporti ve care in the home environment. It should be noted that the patient's weakness of her left leg progressed and that her leg pain, presumably neuropathic in origin, was considerably improved with Dilantin, 100 mg p.o. , t.i.d. and Elavil, 25 mg q.a.m. and 50 mg q.h.s.
Currently she is in a weakened condition and bedridden at home.
The femoral nerve arises from the posterior divisions of lumbar nerve roots two, three and four. Most fibers derive from the mird and fourth roots of the lumbar plexus. In prefixed plexuses it may receive fibers from Ll, and with postfixed plexuses fibers from L5 may be included.4 After emerging from the lateral border of the psoas muscle, it passes downward between the psoas and iliacus muscular interval. It is commonly below the lateral femoral cutaneous nerve, but, occasionally, has a common stem with it. It gives motor branches to the iliacus muscle and passes into the thigh on the surface of the iliopsoas muscle, which it also innervates. Running with the muscle behind the inguinal ligament, it emerges into the femoral triangle. While running in the iliac fossa, the nerve is situated in a rather unyielding fascial compartment. This may result in neural injury secondary to compression from a bleeding episode in hemophiliacs.5'10 At or even above tbe level of the inguinal ligament, the femoral nerve divides into superficial and deep branches. The superficial branches innervate the skin that covers the anterior surface of me thigh and sartorius muscle; the deep branches innervate the quadriceps muscles, the knee joint, and its medial ligament. It also gives rise to the saphenous nerve, which descends over the medial side of the calf to supply the skin down to the medial malleolus (Fig. 5).
In our case, the patient presented with knee and hip pain and later difficulty ambulating. This was managed with antiinflammatory medications and a cane. Only when flank pain became a prominent symptom was a CT scan ordered, which revealed tbe large retroperitoneal mass.
The most common cause of femoral neuropathy is diabetes." Hemorrhagic diseases and anticoagulant therapy are major causes of femoral neuropathies, hemophilia being a leading offender.5"10,12-21 Retroperitoneal masses (as in this case) either benign or malignant may be additional causes.2223 Examples include appendiceal or renal abscesses. In diese cases, attention to retroperitoneal localization may be suspected when weak hip flexors are found in addition to weakness of knee extension.
Fig. 4: No demonstrable active quadriceps function could be elicited on the left. Full active extension of the knee demonstrated on the right.
Femoral nerve palsies have also been reported as a complication of orthopedic surgical procedures. In total hip arthroplasty, cement extravasation may lead to thermal injury with resultant permanent deficit on occasion.24 Bone biopsy in which a full thickness iliac crest specimen was obtained resulted in a complete femoral nerve palsy as reported by Walton.25 This palsy resolved in two months and was assumed to be secondary to bleeding within the iliacus compartment.
Other surgical procedures related to hernia repair and pelvic surgery have been described in association with postoperative femoral nerve palsies.26"28 Positioning in the lithotomy posture with extreme hip flexion, abduction and external rotation of the thigh has been associated with femoral neuropathy, particularly after prolonged surgery.29
Lumbar disc disease, specifically L3-L4 herniations, can present as peripheral femoral neuropathy and should be ruled out.30 The workup, including lumbar myelogram and/or CT scan of the lumbar spine, will localize this disease process. L3-L4 disc herniations are uncommon and account for less than 10% of lumbar disc disease.
The typical signs and symptoms of femoral neuropathies include quadriceps atrophy and weakness, absent knee jerk, and sensory deficits along the anterior and medial thigh and medial lower leg to medial malleolus. In more proximal lesions, weakness of hip flexion (iliopsoas) may also be appreciated. This was present in our case report.
Treatment is contingent on the underlying etiology - in this case, drainage of a large benign renal cyst. While recovery is expectant, management includes physical therapy and the use of a knee-ankle-foot orthosis.
The diagnosis of femoral neuropathies is dependent on a thorough knowledge of the anatomy as well as clinical setting in which these maladies are frequently seen. Because the orthopedic surgeon often is the first to evaluate complaints related to the lower extremity, the signs and symptoms of femoral neuropathies must be remembered. Once recognized, a working differential diagnosis will allow a logical evaluation, prompt diagnosis, and appropriate treatment.
Fig. 5: Motor and sensory distribution of the femoral nerve (Courtesy of W.B. Saunders Co., from Peripheral Nerve Injuries - Principles of Diagnoses, ed 2, by Haymaker and Woodhall, 1953).
1. Smiliie IS: Injuries of the Knee Joint, ed 5. New York, Churchill Livingstone, 1978. pp 1-12.
2. Cianci PE, Piscatelli RL: femoral neuropathy secondary to retroperitoneal hemorrhage. AAM i969; 210:1100.
3. Razzuk MA, Linton RR, Durling RC: Femoral neuropathy secondary to ruptured abdominal aortic aneurysms with false aneurysms. JAMA 1967; 201:317.
4. Hollinshead WH: Anatomy for Surgeons. Philadelphia, Harper and Row, 1982, vol 3, The Back and Lhnbs, p 584.
5. Arnold AO, Hilgartner MW: Hemophilic arthropathy. J Bone Joint Surg 1977; 59A(3):287-305.
6. Greene WB, Wilson FC: Nonoperative management of hemophilic arthropathy and muscle hemorrhage. AAOS Inst Course Led 1983; 32:223-233.
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11. Chopra JS, Hurwitz LI: Femoral nerve conduction in diabetes and chronic occlusive vascular disease. J Neurol Neurosurg Psychiatry 1968; 31:28.
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13. Butterfield WC, Neviaser RJ. Roberts MP: Femoral neuropathy and anticoagulants. Ann Surg 1972; 176:58.
14. Debolt WL, Jordan JL: Femoral neuropathy from heparin hematoma. Bull Los Angeles Neurol Soc 1966; 31:45.
15. Gertzbein SO, Evans OC: Femoral neuropathy complicating iliopsoas hemorrhage in patients without hemophilia. J Bone Joint Surg 1972; 54B:149.
16. Gilbert GJ, Laughlin R: Hemorrhagic femoral neuropathy. Report of a case due to anticoagulant. South Med J 1967; 60: 170.
17. Kettlekamp OB. Powers SR: Femoral compression neuropathy in hemorrhagic disorders. Arch Surg 1969; 98:367.
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22. Biedmond A: Femoral neuropathy, in Vinlen PJ, Bruyn BW (eds): Handbook of Clinical Neurology. Amsterdam. North Holland Publishing, 1970, vol I, part U, Diseases of nerves, pp 303-310.
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24. Weber ER, Daube JR, Coventry MB: Peripheral neuropathies associated with total hip arthroplasty. J Bone Joint Surg 1976; 58A:66,
25. Walton RJ: Femoral palsy complicating iliac bone biopsy. Lancet 1975;Sept 13.
26. Kline DG: Operative management of major nerve lesions of the lower extremity. Surg Clin North Am 1972; 52:1247.
27. Sinclair RH. Pratt JH: Femoral neuropathy after pelvic operation. Am J Obstet Gynecol 1972: 112:404.
28. McDaniel GC, Kirkley WH. Gilbert SC: Femoral nerve injury associated with the pfannenstiel incision and abdominal retractors. Am J Obstet Gynecol 1967; 87:381.
29. Courington FW, Little DM; The role of posture in anesthesia, in Jenkins MT (ed): Clinical Anesthesia, vol 3. Common and Uncommon Problems in Anesthesiology. 1968. ch 2, pp 24-54.
30. Rotnman R. Simeone F: The Spine, ed 2. Philadelphia, Saunders, 1982. vol 1. pp 508-566.
ETIOLOGlES OF NONTRAUMATIC FEMORAL NEUROPATHIES