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. The incidence and severity of traumatic lumbosacral plexopathy increase with the number of pelvic fracture sites and fracture instability. Sacral fractures have become recognized as essential 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. The more common sacral fractures are typically the compression or avulsion fractures of the sacral ala, which can occur in lateral compression and anteroposterior compression pelvic fractures. 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.

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 with individuals who sustained a motor vehicle crash. Lower plexus injuries were more common in victims of motor vehicle accidents as opposed to gunshot wounds.

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 reported in the literature for postpartum sensory and motor dysfunction is relatively low at 0.008% to 0.5%. 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 can result in nerve injury. Fortunately postpartum lumbosacral plexopathy has a good prognosis.

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 most frequently implicated. The mechanisms of neurologic injury that have been identified 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.

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 these patients.

In individuals receiving anticoagulant therapy or with acquired or congenital coagulopathies, retroperitoneal hemorrhage causing lumbosacral plexopathy may occur with no precipitating injury. Retroperitoneal hematoma has also been documented as a rare but potentially serious complication after cardiac catheterization. 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; this condition was typically completely reversible. Femoral vein catheterization for dialysis has also been documented as a cause of hemorrhagic complications and retroperitoneal hemorrhage.

Case reports have also identified patients sustaining lumbosacral plexopathy after 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.

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. 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. Chemotherapeutic agents can also cause symptoms of lumbosacral radiculopathy. Cisplatin, 5-fluorouracil, mitomycin C, and bleomycin have been implicated in the majority of these plexopathies. Metastatic or tumor extension into the lumbosacral plexus and malignant psoas syndrome have been described in the literature. Malignant psoas syndrome was first reported in 1990. It is characterized by proximal lumbosacral plexopathy, painful fixed flexion of the ipsilateral hip, and radiologic or pathologic evidence of ipsilateral psoas major muscle malignant involvement.

Diabetic Amyotrophy

Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies have been documented. Diabetic lumbosacral radiculoplexus neuropathy is a subacute, painful, asymmetric lower limb neuropathy that is associated with significant weight loss (at least 10 lb), type 2 diabetes mellitus, and a relatively recent diagnosis of diabetes with relatively good glucose control. The underlying pathophysiologic mechanism is thought to be immune-mediated with microvasculitis of the nerve rather than a metabolic issue caused by diabetes; nondiabetic lumbosacral radiculoplexus neuropathy has also been documented with similar clinical and pathophysiologic features. The similar clinical symptoms, findings, and response to treatment suggest that the metabolic changes from diabetes may not be the cause of these symptoms, although impaired glucose tolerance has been noted in nondiabetic lumbosacral radiculoplexus neuropathy.

Vascular

Vascular causes of lumbosacral plexopathies may include diabetic amyotrophy and connective tissue diseases that may be associated with vasculitis, such as systemic lupus erythematosus, rheumatoid arthritis, and polyarteritis nodosa. If a vascular cause is suspected, the aorta and iliac vessels must be evaluated for disease or occlusion.