Definition

Lumbosacral plexopathy is an injury to or involvement of one or more nerves that combine to form or branch from the lumbosacral plexus. This involvement is distal to the root level.

The lumbar plexus originates from the first, second, third, and fourth lumbar nerves (Fig. 144.1). The fourth lumbar nerve makes a contribution to both the lumbar and the sacral plexus. There is typically a small communication from the twelfth thoracic nerve as well. As in the brachial plexus, these nerve roots divide into the dorsal rami and the ventral rami as they exit through the intervertebral foramina. The dorsal or posterior rami innervate the paraspinal muscles and supply nearby cutaneous sensation. The ventral or anterior rami of the lumbar plexus form the motor and sensory nerves to the anterior and medial sides of the thigh and the sensation on the medial aspect of the leg and foot. The undivided anterior primary rami of the lumbar and sacral nerves also carry postganglionic sympathetic fibers that are mainly responsible for vasoregulation of the lower extremities. The branches of the lumbar plexus include the iliohypogastric, ilioinguinal, genitofemoral, femoral, lateral femoral cutaneous, and obturator nerves [1]. The lumbar portion of the plexus lies just anterior to the psoas muscle [2].

The sacral plexus innervates the muscles of the buttocks, posterior thigh, and leg below the knee and the skin of the posterior thigh and leg, lateral leg, foot, and perineum. It is formed from the lumbosacral trunk to include L5 and a portion of L4 as well as the S1 to S3 (or S4) nerve roots (Fig. 144.2). The anterior primary rami of S2 and S3 nerve roots carry parasympathetic fibers that mainly control the urinary bladder and anal sphincters. The triangular sacral plexus lies on the anterior surface of the sacrum, in the immediate vicinity of the sacroiliac joint and lateral to the cervix or prostate [1]. The branches of the sacral plexus include the superior and inferior gluteal nerves, the posterior cutaneous nerves of the thigh, the lumbosacral trunk that becomes the sciatic nerve with both tibial and peroneal divisions, and the pudendal nerve.

Etiology

Lumbosacral plexopathy has been recognized as a clinical entity or complication in a variety of surgical procedures, trauma, and obstetric surgery or delivery and as a clinical finding or sequela in treatment of pelvic tumors.

Trauma

Traumatic pelvic fractures have a 30.8% incidence of lumbosacral plexus injury [3,4]. The incidence and severity of traumatic lumbosacral plexopathy increase with the number of pelvic fracture sites and fracture instability [4]. Sacral fractures have typically been considered of secondary importance in conjunction with pelvic trauma [5]. However, sacral fractures have become recognized as an essential consideration in pelvic trauma because of their high association with lumbosacral nerve deficits. This can have a profound influence on prognosis and level of functional recovery [3,6]. The more common sacral fractures are typically the compression or avulsion fractures of the sacral ala, which can occur in lateral compression and anterior-posterior compression pelvic fractures [7]. Fractures of the sacral neuroforamina or midline sacral fractures may also occur. Fractures of the sacrum can increase the incidence of neurologic injury in pelvic trauma to between 34% and 50% because of its proximity to the sacral nerve roots [7].

Gunshot wounds and motor vehicle accidents have long been recognized as potential causes of lumbosacral plexus injuries. In a retrospective comparison of patterns of lumbosacral plexus injury in motor vehicle crashes and gunshot wounds, individuals with gunshot wounds had a greater chance of involvement of the upper portion of the plexus in comparison to individuals who sustained a motor vehicle crash. Lower plexus injuries were more common in victims of motor vehicle accidents as opposed to gunshot wounds [8].

Finally, trauma is a common cause of retroperitoneal hemorrhage, which can injure the lumbosacral plexus.

Labor and Delivery

The lumbosacral plexus may be compressed as a complication of labor and delivery. The incidence of neurologic injury that is reported in the literature for postpartum sensory and motor dysfunction is relatively low at 0.008% to 0.5% [9,10]. Factors associated with nerve injury were nulliparity and a prolonged second stage of labor; assisted vacuum or forceps vaginal delivery also had some positive association. Women with nerve injury spent more time pushing in the semi-Fowler lithotomy position. During the second stage of labor, direct pressure of the fetal head may compress the lumbosacral plexus against the pelvic rim, which may result in nerve injury [11,12].

Iatrogenic

Gynecologic surgery is thought to be one of the most common causes of femoral nerve injury (see Chapter 54) and lumbosacral plexus nerve injuries. Abdominal hysterectomy is the surgical procedure that has been most frequently implicated [13,14]. The mechanisms of neurologic injury that have been established include improper placement or positioning of self-retaining or fixed retractors, incorrect positioning of the patient in lithotomy position preoperatively or prolonged lithotomy positioning without repositioning, and radical surgical dissection resulting in autonomic nerve disruption [15].

Lumbosacral injury has also been noted after appendectomy and inguinal herniorrhaphy. Patients who are thin, diabetic, or elderly are at increased risk for such an injury. Injury to the lumbosacral plexus with clinical findings occurs in up to 10% of hip replacement procedures, and injury that is subclinical but detected electromyographically occurred in up to 70% of patients [16].

In individuals receiving anticoagulant therapy or with acquired or congenital coagulopathies, retroperitoneal hemorrhage causing lumbosacral plexopathy may occur with no precipitating injury [17,18].

Retroperitoneal hematoma has also been documented as a rare but potentially serious complication after cardiac catheterization [19,20]. In a review of 9585 femoral artery catheterizations, a reported retroperitoneal hematoma rate of 0.5% occurred. In patients undergoing stent placement, there was evidence of lumbar plexopathy involving the femoral, obturator, and lateral femoral cutaneous nerves, and the condition was typically completely reversible [21,22]. Femoral vein catheterization for dialysis has also been documented as a cause of hemorrhagic complications and retroperitoneal hemorrhage [23].

Case reports have also identified patients sustaining lumbosacral plexopathy after undergoing aortoiliac bypass grafting for abdominal aortic aneurysm. The proposed mechanism for this rare complication, with fewer than 80 patients reported in the literature, is neural ischemia secondary to interruption of the blood supply to the lumbosacral plexus or caudal portion of the spinal cord [24,25].

Oncologic

Both pelvic malignant neoplasms and treatment of pelvic tumors can damage the lumbosacral plexus. Lumbosacral radiculopathy is most common with gynecologic tumors, sarcomas, and lymphomas. Neoplastic plexopathy is characterized by severe and unrelenting pain, typically followed by weakness and sensory disturbances [26]. Pelvic radiation therapy may cause a delayed lumbosacral plexopathy that can occur 3 months to 22 years after completion of treatment; the median amount of time from the completion of treatment to onset of symptoms is about 5 years [27–29