PM R XXX (2015) 1-4

www.pmrjournal.org

Case Presentation

Sciatic Neuropathy Caused by Focal Venous Engorgement Associated With Deep Vein Thrombosis: A Case Report Young-Ah Choi, MD, MS, Keewon Kim, MD

Abstract A 69-year-old woman complained of severe left leg weakness with paresthesia. Electrodiagnostic tests revealed sciatic neuropathy, and imaging studies showed venous engorgement around the sciatic nerve. After anticoagulant therapy and intensive rehabilitation, the patient’s muscle strength improved from 1 to 3 on the Medical Research Council scale. The diagnosis of sciatic neuropathy caused by deep vein thrombosis is extremely rare; however, it should be considered in the differential diagnosis of unilateral lower extremity weakness in patients recovering from intensive care.

Introduction Sciatic neuropathy is the second most frequent neuropathy in the lower extremities; it can be caused by a number of mechanisms, including acute or chronic nerve entrapment, ischemia, tumor, aneurysm, laceration, toxic injury, vasculitis, hematoma, gluteal muscle contusion, or iatrogenic injury [1,2]. Although vascular causes are the least common, there have been reports of sciatic neuropathy caused by hemangioma, vascular malformation, deep femoral artery aneurysm, traumatic venous varix, or Behc ¸et disease [3-6]. To the best of our knowledge, there has been no previous report of sciatic neuropathy resulting solely from systemic deep vein thrombosis (DVT). In this article, we report a case of sciatic neuropathy associated with vessel engorgement around the sciatic nerve, resulting from disseminated DVT. Case Presentation A 69-year-old woman who had undergone chemotherapy for breast cancer experienced uroseptic shock with multiple organ dysfunction and was admitted to the intensive care unit (ICU). The patient’s critical care included mechanical ventilation and antibiotic therapy, but no DVT prophylaxis. During her hospital course, the patient had DVTs detected in multiple vessels, including the right popliteal and peroneal veins

(muscular branches), left peroneal vein, right great saphenous vein, and right subclavian vein. These were treated with rivaroxaban, a direct, selective, and reversible inhibitor of factor Xa, at the time of diagnosis. During her ICU stay, the patient complained of profound weakness in both lower extremities and pain in her left lower extremity. She also noted paresthesia below her knee, particularly in the sole of her left foot. Because of these complaints and her poor overall condition, the physiatry department was consulted. Her initial neurologic examination was limited due to her extremely poor overall condition. Initially the patient was believed to have critical illness neuropathy (CIN) or critical illness myopathy (CIM), given her lack of a definitive focal neurologic deficit and in the setting of a symmetric weakness that affected the proximal muscles more than distal muscles. The patient was transferred to the rehabilitation unit because of her continued weakness for 1 month even after her medical condition stabilized. On initial manual muscle examination at the rehabilitation unit, the patient was found to have grade 1 of 5 strength on the Medical Research Council (MRC) muscle strength scale in her left ankle dorsiflexion and plantar flexion. Because asymmetric weakness is an atypical presentation for CIN or CIM, we eliminated CIN or CIM from the differential diagnosis and decided to perform an electrodiagnostic study.

1934-1482/$ - see front matter ª 2015 by the American Academy of Physical Medicine and Rehabilitation http://dx.doi.org/10.1016/j.pmrj.2015.06.007

2

Sciatic Neuropathy and Deep Vein Thrombosis

Electrodiagnostic tests performed approximately 1 month after the patient left the ICU revealed left sciatic neuropathy with moderate to severe partial axonal involvement, involving the tibial branch of the nerve more severely than the peroneal branch (Tables 1 and 2). There was no evidence of generalized peripheral polyneuropathy or myopathy. and critical illness neuropathy and myopathy were also excluded. The findings of abnormal recruitment of the vastus medialis and the tibialis anterior were believed to be volitionally inhibited and not representative of neuropathic disease. Magnetic resonance imaging of the pelvis revealed prominent perineural and intraneural veins adjacent to the sciatic nerve, suggesting a vascular malformation or varix (Figure 1). Threedimensional computed tomographic angiography of the left leg showed focal enlargement and enhancement of the veins around the sciatic nerve posterior to the hip joint capsule, with a mildly engorged venous structure between the inferior gemellus and quadratus femoris muscles (Figure 2). An abdominal computed tomography (CT) scan taken when the patient first presented with uroseptic shock showed no vascular abnormalities near the left sciatic nerve, whereas a later scan taken during the patient’s time in the ICU showed newly developed venous engorgement near the nerve (images not shown). On the basis of the electrodiagnostic and imaging data, the patient was diagnosed with sciatic neuropathy, presumably due to vascular engorgement. The vascular engorgement was noted to be small, and difficult to access surgically. Discussions with a vascular surgeon revealed considerable uncertainty regarding the results of surgical management. These factors,

combined with the lack of progression of her neurologic deficits, resulted in a decision to remain conservative and to treat with anticoagulation therapy. In addition, gabapentin and tramadol were prescribed for her neuropathic pain. Her rehabilitation involved gait training with a walker, quad cane, and left ankle orthosis. She was discharged after spending 1 month in the rehabilitation unit. Three months after discharge, the patient visited the outpatient rehabilitation clinic for a follow-up appointment. She was now able to walk without an orthosis. Her ankle dorsiflexion was grade 4 on the MRC scale, and her plantar flexion was grade 3. CT angiography showed reduced focal enlargement and enhancement of the veins around the sciatic nerve, and there was no evidence of DVT in the lower extremities. The patient continued to return for follow-up every 3 months, and her condition gradually improved. She was able to discontinue anticoagulant therapy 6 months after discharge. Nine months after discharge, she underwent follow-up electrodiagnostic tests. Needle electromyography showed improved function of the peroneus longus and biceps femoris muscles, but there were no other changes. Discussion Focal sciatic neuropathy is the second most common mononeuropathy in the legs after peroneal neuropathy and may be caused by a variety of conditions; however, the cause is very rarely vascular. The most commonly reported vascular cause of focal sciatic neuropathy is arterial or venous thrombosis,

Table 1 Nerve conduction study results Motor Nerve Conduction Studies Nerve

Side

Record

Baseline to Peak Amplitude (mV) Distal

Onset Latency (ms) Distal

Nerve Conduction Velocity (m/s)

Peroneal Peroneal Peroneal Peroneal Tibial Tibial

R L R L R L

EDB EDB TA TA AH AH

2.5 1.1 5.9 2.9 5.7 No response

4.2 4.6 3.3 2.4 5.3

38.6 39.4 61.1 35.3 41

F-Wave Latencies Nerve

Side

Record

Latency (ms)

Tibial Tibial

R L

AH AH

No response No response

Sensory Nerve Conduction Studies Nerve

Side

Record

Baseline to Peak Amplitude (mV)

Onset Latency (ms)

Peak-to-Peak Amplitude (mV)

Sural Sural Superficial peroneal Superficial peroneal

R L R L

Ankle Ankle Foot Foot

12.3 6.7 6.7 5.5

2.8 2.7 2.8 3.9

9.4 3.7 6 4.8

R ¼ right; L ¼ left; EDB ¼ extensor digitorum brevis; TA ¼ tibialis anterior; AH ¼ abductor hallucis.

Y.-A. Choi, K. Kim / PM R XXX (2015) 1-4

3

Table 2 Needle electromyography study results Electrodiagnostic Studies With Needle Examination Spontaneous Activities

MUAP Parameters

Muscle

Side

Fibs

PSWs

CRD

Poly

Amp

Dur

Interference Pattern

Vastus medialis Tibialis anterior Gastrocnemius (medial head) Abductor hallucis Peroneus longus Adductor longus Iliopsoas Tensor fascia lata Biceps femoris (short) Biceps femoris (long) Lumbar paraspinals

L L L L L L L L L L L

0 0 0 1þ 2þ 0 0 0 1þ 2þ 0

0 0 0 1þ 2þ 0 0 0 1þ 2þ 0

0 0 0 0 0 0 0 0 0 0 0

[ N CNBD No MUAP CNBD N N N No MUAP No MUAP

N N

N N

N N N

N N N

Reduced Reduced CNBD No activity Single Reduced to complete Complete Complete No activity No activity

MUAP ¼ motor unit action potential; Fibs ¼ fibrillation potentials; PSWs ¼ positive sharp waves; CRD ¼ complex repetitive discharges; Poly ¼ polyphasic MUAP; Amp ¼ amplitude; Dur ¼ duration; L ¼ left; N ¼ normal; CNBD ¼ could not be determined.

frequently accompanied by an underlying pathology such as vasculo-Behc ¸et disease or by structural problems such as a femoral artery aneurysm or a traumatic gluteal venous varix [3-6]. To the best of our knowledge, no previous case report has described focal venous engorgement resulting from DVT associated with systemic illness as a sole cause of sciatic neuropathy in the absence of trauma, structural problems, or underlying pathology. Like our case, most previously reported cases of sciatic neuropathy of vascular origin had an atypical clinical presentation and required intensive investigation with detailed imaging and other studies to determine the etiology [3-6]. In our case, the patient was diagnosed with systemic DVT during her time in the ICU, and anticoagulation therapy was initiated at that time. As her left lower extremity weakness and paresthesia persisted for more than 1 month after leaving the ICU, we performed electrodiagnostic studies and confirmed our diagnosis with magnetic resonance imaging (MRI). However, most previously reported cases were treated surgically, whereas we opted for conservative management with continued anticoagulation and physical therapy. After treatment, the patient’s motor and

sensory functions improved but did not return to normal. In general, the peroneal branch of the sciatic nerve is more susceptible to and more severely affected by traumatic and compressive injuries than the tibial branch [7]. However, in our case, electrodiagnostic tests revealed the tibial branch to be more severely affected than the peroneal branch. The tibial branch is more vulnerable to venous reflux, compared with the peroneal branch, because the latter is supplied by smaller vessels and is not as severely affected by reflux. Our case was presumably caused by venous reflux resulting from engorgement of the veins around the affected nerve, which accounts for the observed difference [8]. Patients undergoing rehabilitation after intensive medical treatment are at high risk for DVT, especially if elderly [9]. If sustained muscle weakness is observed in such a patient, focal neuropathy caused by systemic DVT should be considered in the differential diagnosis. Properly timed anticoagulant treatment could result in a favorable outcome. However, if surgery is indicated to relieve symptoms, external neurolysis and limited microvascular dissection of affected nerve fascicles should be performed [3].

Figure 1. Pelvic magnetic resonance imaging, axial views (left, T1-weighted; right, T2-weighted) show an ill-defined soft tissue lesion, hypointense on both images, at the intermuscular plane of the left inferior gemellus and quadratus femoris muscle. There are also prominent perineural and intraneural veins adjacent to the sciatic nerve (arrow).

4

Sciatic Neuropathy and Deep Vein Thrombosis

Figure 2. Three-dimensional computerized tomographic angiogram taken at the time of diagnosis (left) shows focal enlargement and enhancement in the area of the left sciatic nerve posterior to the hip joint capsule and a mildly engorged venous structure between the left inferior gemellus and quadratus femoris muscles. The follow-up angiogram (right) shows reduction in the previously noted focal enlargement and enhancement.

Conclusion Sciatic neuropathy due to vascular conditions is very rare; however, systemic DVT with vascular engorgement is capable of causing it, especially in patients recovering from intensive medical treatment. Electrodiagnostic and imaging studies can be helpful in localizing and characterizing the lesion and determining prognosis. In our case, the patient recovered substantial neurological function without surgical intervention.

4.

5.

6.

7.

References 8. 1. Yuen EC, So YT. Sciatic neuropathy. Neurol Clin 1999;17:617-631, viii. 2. Yuen EC, So YT, Olney RK. The electrophysiologic features of sciatic neuropathy in 100 patients. Muscle Nerve 1995;18:414-420. 3. Van Gompel JJ, Griessenauer CJ, Scheithauer BW, Amrami KK, Spinner RJ. Vascular malformations, rare causes of sciatic

9.

neuropathy: A case series. Neurosurgery 2010;67:1133-1142, discussion 1142. Kara M, Ozc ¸akar L, Eken G, Ozen G, Kiraz S. Deep venous thrombosis and inferior vena cava agenesis causing double crush sciatic neuropathy in Behc ¸et’s disease. Joint Bone Spine 2008;75:734-736. Maniker A, Thurmond J, Padberg FT Jr, Blacksin M, Vingan R. Traumatic venous varix causing sciatic neuropathy: Case report. Neurosurgery 2004;55:1224. Eguchi K, Majima M. Sciatic neuropathy caused by disorder of a nutrient artery: A case report of thromboembolism secondary to profunda femoral artery aneurysm. Arch Phys Med Rehabil 2001;82: 253-255. Sunderland S. The relative susceptibility to injury of the medial and lateral popliteal divisions of the sciatic nerve. Br J Surg 1953;41: 300-302. Labropoulos N, Tassiopoulos AK, Gasparis AK, Phillips B, Pappas PJ. Veins along the course of the sciatic nerve. J Vasc Surg 2009;49: 690-696. Kelly BM, Yoder BM, Tang CT, Wakefield TW. Venous thromboembolic events in the rehabilitation setting. PM R 2010;2: 647-663.

Disclosure Y.-A.C. Department of Rehabilitation Medicine, Seoul National University Hospital, Seoul, Republic of Korea Disclosure: nothing to disclose K.K. Department of Rehabilitation Medicine, Seoul National University Hospital, Seoul National University College of Medicine, 101 Daehak-ro, Jongro-gu, Seoul 110-744, Republic of Korea. Address correspondence to: K.K.; e-mail: [email protected] Disclosure: nothing to disclose

Submitted for publication February 8, 2015; accepted June 5, 2015.

Sciatic Neuropathy Caused by Focal Venous Engorgement Associated With Deep Vein Thrombosis: A Case Report.

A 69-year-old woman complained of severe left leg weakness with paresthesia. Electrodiagnostic tests revealed sciatic neuropathy, and imaging studies ...
545KB Sizes 1 Downloads 12 Views