A Diagnosis in Vein

PRESENTATION

Frequently, patients describe symptoms that seem to have limited relevance to their presentation but ultimately prove to be the critical clue to the diagnosis. This case illustrates the importance of listening carefully to our patients. Dismissal of seemingly insignificant symptoms can lead to vain diagnostic efforts.

A 76-year-old man presented with acute onset left lower extremity numbness and weakness that began while eating dinner. The loss of sensation was circumferential from the left midcalf to the foot and was not accompanied by pain or swelling. When the man tried to rise from a sitting position, he was unable to do so without assistance. Family members, concerned that he was experiencing symptoms of an acute stroke, drove him to the emergency department. His symptoms began to improve en route to the hospital while he was supine. The neurology department was consulted upon his arrival.

ASSESSMENT

The patient's medical history included hypertension, mild aortic stenosis, and diverticulosis complicated by gastrointestinal bleeding. Daily medications were a multivitamin and fish oil capsules. He did not smoke and rarely consumed alcohol. His sister suffered a disabling stroke at 80 years of age.

On physical examination, the patient appeared comfortable. He had hypertension to 230/100 mmHg, a heart rate of 85 beats per minute, and oxygen saturation of 99% on room air. Cardiovascular examination demonstrated a nonradiating II/VI early-peaking crescendo-decrescendo murmur, which was best heard at the right upper sternal border. His lungs were clear, his abdomen was soft and nontender, and his extremities were warm and nonedematous. The cranial nerves, motor function, coordination, deep tendon reflexes, and peripheral pulses were normal. Sensation to pinprick was diminished over the left lateral midcalf and foot. His unassisted gait was normal.

Contrast-enhanced computed tomography (CT) of the head did not indicate any signs of acute stroke, hemorrhage, or stenosis of the carotid arteries or circle of Willis. Blood test results were unremarkable. The patient was admitted to the neurology service so that he could be further evaluated for stroke or transient ischemic attack. Magnetic resonance imaging (MRI) of the head was free of cerebrovascular disease. Given the resolution of his symptoms, he was discharged to follow-up with his primary care physician. He was told that if his symptoms recurred, an MRI of the lumbar spine would be performed to assess for radiculopathy.

Four days later, the patient presented urgently with recurrent left leg weakness and numbness after standing in the shower. On physical examination, the patient had weakness in left foot dorsiflexion and decreased sensation on the lateral aspect of his foot. An MRI of the lumbar spine excluded spinal stenosis or radiculopathy. The neuroradiologist suggested obtaining plain films of the spine with flexion and extension views to rule out spondylolisthesis that might worsen in certain positions. These did not demonstrate any dynamic change. His primary care physician suspected a peripheral neuropathy—specifically common peroneal nerve palsy—and ordered an electromyogram. The test, performed when the patient was asymptomatic, was normal.

In further follow-up, the patient reported a “lump” behind his knee; pressure on the lump reproduced his symptoms of lower leg numbness. A compressible mass was evident in the left popliteal fossa but only when the patient was standing. General ultrasonography of the popliteal fossa was unrevealing. Evaluation by a rheumatologist included another ultrasound, which demonstrated a large, easily compressible, venous varicosity in the left popliteal fossa when the patient was standing. Symptoms were thought to be due to a local process affecting the common peroneal nerve. However, the rheumatologist did not consider the varicose vein to be the cause.

A dedicated vascular study with duplex ultrasound of the popliteal fossa vasculature showed that the common peroneal nerve was completely surrounded by large varicose veins (Figures 1 and 2). Popliteal vein Doppler velocities acquired in the supine position were 50 cm/s (normal < 20 cm/s), consistent with marked venous hypertension (Figure 3).

Figure 1.

A cross-sectional image of the popliteal fossa demonstrates the common peroneal nerve (n) completely surrounded by large varicose veins (v). The popliteal and gastrocnemius arteries (a) are substantially smaller in caliber than the varicose veins.

Figure 2.

An ultrasound image obtained along the longitudinal axis of the popliteal fossa shows impingement of the common peroneal nerve (n) by large varicose veins (v).

Figure 3.

This Doppler ultrasound tracing, obtained while the patient was supine, identified elevated velocities in the popliteal vein of 50 cm/s (normal < 20 cm/s), consistent with marked venous hypertension.

DIAGNOSIS

Venous ultrasonography suggested that the patient's symptoms and physical examination findings were caused by compression of the common peroneal nerve by varicose veins in the setting of venous hypertension. The subsequent diagnosis was common peroneal nerve palsy, a condition that frequently presents as acute foot drop associated with numbness of the lateral lower leg and foot.¹ Often, sensory loss is restricted to the lateral surface of the lower leg and the dorsum of the foot.¹ Weakness can involve ankle eversion and ankle and toe dorsiflexion.¹ Ankle inversion, toe flexion, and plantar flexion should be unaffected. Electrophysiological studies, including an electromyogram, are particularly useful when alternative diagnoses, such as lumbar radiculopathy, are being considered.^1,2 However, the electromyogram might be normal during asymptomatic periods of episodic common peroneal nerve palsy.

While common peroneal nerve palsy can occur as a manifestation of systemic disorders such as vasculitis, it more often results from extrinsic compression or entrapment.² The common peroneal nerve is particularly vulnerable to external compression because of its superficial anatomical location and lack of protection from nearby bony structures.² Direct mechanical injury from fractures, knee dislocations, orthopedic support, and leg-crossing are frequent causes of compression neuropathy.¹ Occasionally, extrinsic mass lesions, such as Baker's cysts, aneurysms, pseudoaneurysms, and tumors, result in compression of the common peroneal nerve.^1,3-6

Compression neuropathy of the common peroneal nerve by varicose veins has only been reported once in the medical literature.⁷ Venous pressure is normally inadequate to squeeze adjacent structures. In our patient, baseline significant peripheral venous hypertension would be expected to increase substantially in the upright position with the addition of hydrostatic pressure. This pathophysiologic observation explains why the patient's symptoms occurred with prolonged sitting and standing.

Ultrasonography is the initial test of choice for investigation of popliteal fossa masses that might be causing extrinsic compression of the common peroneal nerve. Vascular ultrasonography is superb for providing anatomical and physiological data if arterial or venous pathology is suspected. Axial imaging with CT and MRI can provide additional anatomical definition if surgical intervention is anticipated.^5,7

MANAGEMENT

Graduated compression stockings are the therapy for chronic venous insufficiency, including symptomatic varicose veins. An initial trial of compression stockings is reasonable for patients whose large varicose veins produce common peroneal nerve palsy.⁷ If compression stockings are ineffective or intolerable, surgical varicectomy may be considered.⁷ Because patients with popliteal vein aneurysms have an increased risk of deep vein thrombosis and pulmonary embolism, they are typically treated surgically.^5,8

Our patient was prescribed 20-30 mmHg gradient compression stockings. He had expressed a preference for conservative therapy of his varicose veins. In a follow-up visit, the patient reported that use of the stockings completely resolved his episodes of left lower leg numbness and weakness.