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Incidence of Acute Femoral Neuropathy Following Renal Transplantation
Khema Ram Sharma, MD;
Jonathan Cross, MD;
Fernando Santiago, MD;
D. Ram Ayyar, MD;
George Burke III, MD
Arch Neurol. 2002;59:541-545.
ABSTRACT
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Background Case reports exist of femoral neuropathy following renal transplantation
(RTSP) with possible pathophysiology, including direct compression and nerve
ischemia. However, the occurrence of acute femoral neuropathy (AFN) following
RTSP has not been studied prospectively.
Objective To determine the occurrence of AFN following RTSP.
Methods We prospectively studied the occurrence of AFN following RTSP from June
1, 1998, to October 31, 1999. A total of 184 RTSPs were performed during this
period. All the patients had end-stage renal failure and had effective hemodialysis
before RTSP. All patients with AFN underwent neurologic examination, nerve
conduction and electromyographic studies (5 to 7 days after the onset of symptoms),
and magnetic resonance imaging or computed tomography of pelvis and lumbosacral
spine within 24 hours of onset of symptoms.
Results Four (2.2%) of 184 patients developed AFN (ipsilateral to the RTSP surgery)
postoperatively between 24 (3 patients) and 48 hours. All the patients achieved
good renal function after RTSP. All the patients had excellent recovery of
motor function in 4 to 9 months.
Conclusion We believe that AFN following RTSP is an uncommon (2.2%) complication
from which patients have an excellent chance of recovery.
INTRODUCTION
FEMORAL NEUROPATHY has been described as a complication of compression
due to hematoma from anticoagulation,1 hemophilia,2 leukemia,3 consumption
coagulopathy,4 hysterectomy and pelvic surgery,5-6 lithotomy position,7-8
blunt trauma,9 iliac artery aneurysm,10 inguinal herniorrhaphy,11
malignancy and radiation therapy,12 Epstein-Barr
virus infection,13 and diabetes mellitus (DM).14 Many case reports exist of femoral neuropathy following
renal transplantation (RTSP)15-24
with possible pathophysiology, including direct compression and nerve ischemia.
However, the occurrence of acute femoral neuropathy (AFN) following RTSP has
not been studied prospectively.
PATIENTS AND METHODS
PATIENTS
We prospectively studied the occurrence of AFN following RTSP at the
University of Miami, Jackson Memorial Medical Center, Miami, from June 1,
1998, to October 31, 1999. A total of 184 RTSPs (15 children: mean ±
SD age, 1.5 ± 1.0 years; range, 6 months to 2 years; 169 adults: 107
women; mean ± SD age, 45.0 ± 7.4 years; range, 22-65 years)
were performed during this period. All the patients signed informed consent
forms. Three surgeons (including G.B.) performed all these RTSPs using standard
techniques. The diagnosis of AFN was established by the following criteria:
(1) the development of weakness of the quadriceps femoris and iliopsoas muscles
with decreased or absent knee jerk ipsilateral to the renal transplant within
48 hours of RTSP, and (2) presence of acute (within 7 days of onset of symptoms)
neurogenic changes (increased insertional activity or decreased motor unit
recruitment with or without positive waves and fibrillation potentials) on
needle electrode examination of the affected muscles (quadriceps and iliopsoas)
and decreased compound muscle action potential (CMAP) amplitude of the quadriceps
muscle obtained by near-nerve stimulation of the affected femoral nerve.
Patients with preexisting diabetic amyotrophy or lumbosacral plexopathy
and lumbosacral radiculopathy secondary to structural lesions in the lumbosacral
spine were excluded. Similarly, patients with peripheral sensory motor neuropathy
with significant motor deficit involving proximal and distal muscles with
concomitant disease (paraproteinemia, preexisting endocrinopathies, connective
tissue disorder, vitamin B12 or folic acid deficiency, heavy metal
toxic effects, human immunodeficiency virus infection, hepatitis, Lyme disease,
cancer, or chronic inflammatory demyelinating polyneuropathy25)
were excluded. Patients with preexisting, predominantly distal sensory neuropathy
related to DM or kidney dysfunction were not excluded. No patient had a family
history of neuropathy.
NEUROLOGIC AND LABORATORY ASSESSMENTS
All 184 patients underwent preoperative and postoperative physical and
neurologic examination. Four of these 184 patients who developed AFN following
RTSP also underwent nerve conduction and electromyographic studies (5-7 days
after the onset of symptoms), magnetic resonance imaging (3 patients), and
computed tomography (1 patient) of pelvis and lumbosacral spine within 24
hours of onset of symptoms. The muscle strength was evaluated by using the
Medical Research Council grading criteria (grade 0, no muscle contraction;
grade 1, flicker; grade 2, partial movement with no gravity; grade 3, complete
movement against gravity; grade 4, complete movement against variable resistance;
and grade 5, normal power).26 Similarly, the
recovery was also rated as follows: poor, no recovery; fair, 25% to 50%; good,
50% to 75%; and excellent, 75% to 100%. All patients underwent renal function
tests before and after surgery. The status of immune function and levels of
immunosuppressive drugs were assessed postoperatively.
ELECTROMYOGRAPHY AND NERVE CONDUCTION STUDIES
The nerve conduction studies were performed in both lower limbs using
standard techniques. The studies included sural sensory nerve, saphenous nerve,
superficial peroneal sensory nerve, tibial H responses, tibial motor and corresponding
F waves, peroneal motor and corresponding F waves, and femoral motor nerves.27 Needle electrode examination was performed to evaluate
insertional activity, spontaneous activity, motor unit morphologic findings,
and recruitment pattern in paraspinal muscles in the lumbosacral region, gluteal
muscles, iliopsoas, sartorius, quadriceps, adductor longus, adductor magnus,
hamstrings, tibialis anterior, and gastrocnemius muscles on the affected side.27
DATA ANALYSIS
The StatView II statistical software program (Abacus Concepts Inc, Berkeley,
Calif) was used for data analysis. All of the data are expressed as mean ±
SD. We determined the statistical significance (P<.05)
of differences between categorical variables using a  2 test
or Fisher exact test as appropriate.
RESULTS
CLINICAL FEATURES
Four (2.2%) of 184 patients developed AFN (ipsilateral to the RTSP surgery)
postoperatively between 24 (3 patients) and 48 hours. All 4 patients received
a cadaveric right iliac fossa renal transplant. In 3 patients the external
iliac artery was anastomosed (end to end) to the renal artery, and in 1 patient
the common iliac artery was anastomosed to the renal artery because of extensive
atherosclerosis. All these patients experienced end-stage renal failure secondary
to hypertension and underwent effective hemodialysis before RTSP. The primary
renal disease in all these patients was chronic glomerulonephritis. One patient
also had type 1 DM and another had thrombotic thrombocytopenic purpura. The
clinical and electrophysiological data are summarized in Table 1. In all patients, the neurologic examination findings, ipsilateral
to RTSP, were remarkable for marked weakness of hip flexion, knee extension,
an absent knee jerk, and impaired sensations over the anteromedial aspect
of the thigh and medial aspect of the leg. All the patients achieved good
renal function after RTSP.
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Summary of Clinical Features and Electroneurophysiology*
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Electroneurophysiology
The needle electrode examination showed occasional positive waves and
fibrillation potentials and no voluntary motor unit action potentials in iliopsoas
or quadriceps muscle in all patients. The near-nerve stimulation of the ipsilateral
femoral nerve evoked decreased CMAP (reference, >4.3 mV) in all the patients
with slightly prolonged distal latency in 2 patients (patients 3 and 4; reference,
<6.0 milliseconds; Table 1).
Saphenous nerve action potential amplitudes were diminished (reference, >4
µV) with slowed conduction velocity (reference, >42 m/s; Table 1) in all the patients on the affected side. Three patients
(patients 2, 3, and 4) had underlying mild, distal, symmetrical, sensory,
sensorimotor axonal peripheral neuropathy. Two of these patients (patients
3 and 4) had mild symptomatic polyneuropathy diagnosed preoperatively (decreased
to absent ankle reflexes bilaterally in both patients and impaired primary
sensory modalities distally in feet in patient 4), and 1 patient (patient
2) was asymptomatic (decreased ankle reflexes bilaterally) but had small sural
sensory nerve action potential amplitude (4 µV; reference, >7.0 µV)
during postoperative electrodiagnostic studies. The sural nerve–evoked
sensory action potentials were absent bilaterally in patients 3 and 4. The
tibial H reflex latency was prolonged in 3 patients (patients 2, 3, and 4:
34.2-36.6 milliseconds; reference, <32 milliseconds). The peroneal motor,
tibial motor and corresponding F waves, and superficial peroneal sensory nerve
conduction velocities were within the reference range, except in patient 4,
in whom the peroneal CMAP was decreased (1.9 mV; reference, >2.5 mV) and superficial
peroneal sensory nerve action potential amplitude on both sides were diminished
(right side, 3.5 µV; left side, 3.1 µV; reference, >4 µV).
Three surgeons performed all the 184 RTSPs (G.B. [69 operations], Joshua
Miller, MD [58 operations], and Gaetano Ciancio, MD [56 operations]), and
there was no significant difference for the occurrence of AFN among these
surgeons (for G.B., 2 AFNs of 69 RTSPs; for Dr Miller, 1 AFN of 58 RTSPs;
and for Dr Ciancio, 1 AFN of 56 RTSPs; corrected 2 = 0.27, P = .87).
DM as Risk Factor
Among the 184 patients who underwent RTSPs during June 1, 1998, to October
31, 1999, 14 patients (7.6%) also had associated DM (types 1 and 2). In addition,
AFN occurred in 1 (7.1%) of the 14 patients with DM and in 3 patients (1.8%)
of the remaining 170 patients without DM (corrected 2 = 0.14, P = .70), suggesting that DM was not a significant risk
factor for the development of AFN as postulated earlier.24
However, there are some limitations to this conclusion because of the small
number of patients with DM in our study cohort.
FOLLOW-UP
All the patients underwent physical therapy and follow-up neurologic
examination. Within 4 to 8 weeks of onset of symptoms, all of them had significant
improvement in motor deficit (Table 1)
and were able to stand on their affected leg and walk with a walker. One patient
(patient 4) achieved complete motor recovery after 4 months, 2 others (patients
1 and 3) after 6 months, and 1 patient (patient 2) after 9 months. This excellent
recovery observed in our patients with AFN following RTSP was similar to that
noted in previous studies.18-19,21-24
Similarly, the renal function in these patients remained satisfactory until
the last follow-up as observed in most previous studies.18, 20, 22-24
COMMENT
The incidence (2.2%) of AFN as a complication of RTSP was rare in our
prospective study. Among the previous case reports15-24
of AFN following RTSP, only 3 retrospective studies have reported the incidence,
which varied from very rare (0.7%)24 to rare
(3.9%)21 to significant (8.4%).18
This variability in incidence cannot be explained on the basis of surgical
technique, volume, or number of operations performed in a given period, because
all these studies used similar technique and approximately similar number
of RTSPs in a given period. However, the details of individual patients or
associated risk factors, such as atherosclerosis of vessels and DM, are not
provided, which could predispose these patients to AFN.
ANATOMY
The femoral nerve is the largest branch of the lumbar plexus (L2, 3,
and 4). The femoral nerve derives from the posterior divisions of the anterior
primary rami of the second, third, and fourth lumbar spinal nerves. Formed
within the psoas muscle, it emerges from the lateral border of that muscle
to lie between it and the iliacus deep to the iliac fascia for the last third
of its intrapelvic course. The branch to the psoas muscle may originate here,
where the femoral nerve is still a part of the lumbar plexus, or after the
nerve is fully constituted, although some controversy exists.28
It enters the thigh lateral to the femoral sheath and femoral artery, behind
the inguinal ligament, dividing approximately 4 cm below the inguinal ligament
into anterior and posterior divisions. The anterior division gives rise to
the medial and intermediate cutaneous nerves of the thigh and muscular branches
to the sartorius and pectineus muscles. The posterior division supplies the
quadriceps femoris muscle and then continues along the medial border of the
calf as the saphenous nerve, a sensory branch.
MECHANISMS OF AFN
There are several possible mechanisms that could be involved in the
pathogenesis of AFN following RTSP. The most common mechanism postulated15-24
is one of instrument-induced injury during operative procedure. The surgical
site is above the psoas and distant from the path of the femoral nerve. Therefore,
the possibility of direct trauma from diathermy or stretching is unlikely.
Also, hematoma, as noted following RTSP in one study and also after pelvic
surgical procedures and hysterectomies,5-6
was unlikely in our subjects because the imaging of the pelvis was negative
as noted in most other studies.15-22,24
The compression from prolonged use of self-retaining retractors is a possible
explanation. The inferior and medial blades of the retractors are in close
proximity to the middle portion of femoral nerve, which gets its blood supply
from the iliac ramus of the iliolumbar artery. It is more vulnerable to ischemia
because it lies in the intraoperative region just proximal to the inguinal
ligament compared with the proximal and distal portions of the femoral nerve,
which receives blood supply from the local branches. The lumbar plexus has
a rich anatomic vascular supply from inferior mesenteric and vesical arteries,
whereas the middle and distal portions of the femoral nerve depend primarily
on the integrity of the internal or external iliac artery for their blood
supply. With the anastomosis of the renal artery of the graft to the internal,
external, or common iliac artery, the possibility of significant localized
"steal" exists. Proximal end-end anastomosis of the renal artery to the internal
iliac artery can shunt blood away from the vasa nervosum. The existence of
local atherosclerosis and presence of additional factors, such as DM, makes
the femoral nerve more susceptible to ischemic injury.
Mild injury to the femoral nerve from retraction and ischemia could
give rise to neuropraxic injury, which would recover rapidly as observed in
this study and by other investigators.18-19,21-24
On the other hand, more severe and prolonged ischemia from disruption of blood
supply to the femoral nerve may give rise to axonal loss and a slow, incomplete
recovery as observed in some previous studies.16-17,20-21
Yazbeck et al19 attributed the underlying severe
advanced atherosclerosis of vessels as a compounding factor for the ischemic
cause of post-RTSP AFN, which was similar to one of our patients (patient
3).
Diabetes is the most common metabolic cause of spontaneous, isolated
femoral neuropathy with good recovery in months. Data from our study do not
support the earlier postulated hypotheses that DM might be a risk factor in
the development of post-RTSP AFN.24 In that
retrospective study24 from 1972 to 1992, 5
of the 654 patients who underwent RTSP had AFN, and 2 of these 5 patients
with AFN had DM in addition to hypertension as the cause of chronic renal
failure. However, these studies did not provide the total number of patients
with DM among the entire group of 654 patients who underwent RTSP during the
20-year period of the study.
CONCLUSIONS
We believe that AFN following RTSP is an uncommon (2.2%) complication
from which patients have an excellent chance of recovery. The possible pathophysiology
includes combination of stretch injury to the nerve from the use of the self-retaining
retractors or nerve ischemia caused by a steal phenomenon, occurring after
the anastomosis of the graft renal artery to the internal or external iliac
artery.
AUTHOR INFORMATION
Accepted for publication December 5, 2001.
Author contributions: Study concept and design (Drs Sharma and Burke); acquisition of data (Drs Sharma, Cross, Santiago, and Ayyar); analysis and interpretation
of data (Drs Sharma and Ayyar); drafting of the manuscript (Drs Sharma and Cross); critical revision of the manuscript
for important intellectual content (Drs Sharma, Santiago,
Ayyar, and Burke); statistical expertise (Drs Sharma
and Cross); administrative, technical, or material support (Drs Sharma, Santiago, and Ayyar); study supervision (Drs Sharma and Burke).
This study was presented in part at the 52nd American Academy of Neurology
meeting, San Diego, Calif, May 4, 2000.
We thank Joshua Miller, MD, and Gaetano Cianco, MD, for kindly providing
assistance in obtaining data on their patients, and Regina Menendez-Choy for
help in preparation of the manuscript.
Corresponding author and reprints: Khema Ram Sharma, MD, Department
of Neurology, University of Miami School of Medicine, 1150 NW 14th St, Room
603, Miami, FL 33136 (e-mail: ksharma{at}med.miami.edu).
From the Department of Neurology, University of Miami School of Medicine,
Miami, Fla.
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