Bidhun Kuriakose, Paulose (2010) Peripheral Neuropathy in Chronic Uremia: A study of Clinical and Electrophysiological features and changes in patients on intermittent peritoneal dialysis. Masters thesis, Coimbatore Medical College, Coimbatore.
|
Text
200100710bidhun_kuriakose_paulose.pdf Download (766kB) | Preview |
Abstract
Thirty adult patients with end stage renal disease enrolled in an Intermittent Peritoneal Dialysis programme for varied indications were studied for clinical and electrophysiological evidence of peripheral neuropathy. The age and sex distribution of the present group (mean age 35.6 + 10.6 years and male to female ratio of 1.72:1) may not reflect the true prevalence figure in chronic renal failure, as the patients were exclusively drawn from those attending IPD programme in our institution. The mean duration of uremic symptoms in the groups of patients studied was 19.33 + 12.50 months. The relatively short duration of symptoms could have been an artifact, due to the patient selection criteria. The short duration of uremia is probably the reason for the low prevalence of clinical neuropathy (36%) in our patients. The mean serum creatinine level in our patients at the time of study was only 4.51 + 1.94 mg%, which is a reflection of the fact that the patients were on Intermittent Peritoneal Dialysis for a mean period of 6.33 + 3.15 months. In a study of 14 patients treated conservatively for endstage renal disease, Jebsen et al showed a correlation between increasing serum creatinine and decreasing motor nerve conduction velocities. On the strength of this study, they defined adequate dialysis as the amount necessary to arrest, or prevent the development of peripheral neuropathy. In patients with chronic renal disease, Blagg et at described slowing of nerve conduction with increasing levels of urea and creatinine. Jennekens et al studied 83 patients with severe renal insufficiency who were being treated conservatively for uremia, in order to establish the relationship between uremic polyneuropathy and impairment of renal function. They found signs of neuropathy only when the creatinine clearance was less than 5 ml/min. Polyneuropathy was most frequent in patients with the highest levels of blood urea and creatinine, and the lowest creatinine clearances. However the duration of severe renal insufficiency also appeared to influence the onset of polyneuropathy. In our study clinical evidence of neuropathy was present in 36% of our patients, whereas statistically significant slowing of nerve conduction velocities was noted in all our patients (Table 5). With a mean creatinine value of 4.51 + 1.94 mg% all our patients (100%) had subclinical neuropathy. There were no significant association between the level of serum creatinine in those with and those without clinical neuropathy. The association between the severity of neuropathy and raising creatinine was also not observed. Larger studies are required to delineate the actual association in patients on IPD. Six patients (20 %) complained of ‘burning feet’. Tyler quotes it to be a frequent early manifestation of clinical neuropathy, while others found it to be an uncommon symptom. This is probably because, although most patients with uremic neuropathy have distal dysesthesias, these are not frequently described as ‘burning’ in character, but a variety of unpleasant sensations. In our study impaired vibratory sense in the feet was the commonest physical sign in the present group of patients, being present in 9/30 patients (30%). Loss of ankle jerks was seen in 4 patients (13.33%). The duration of uremia was significantly longer in patients with clinical neuropathy (29 + 13.49 months vs. 12.89 + 6.27 months). The mean serum creatinine values were not significantly different in those with and without clinical neuropathy, as everybody were receiving intermittent peritoneal dialysis. These observations confirm the fact that development of neuropathy depends on the duration and severity of renal failure. Impaired vibratory senses in the lower limbs and loss of deep tendon reflexes, especially the ankle jerks, are the first sign of uremic neuropathy. This has been noticed in our study also. The course of neuropathy is variable in patients undergoing dialysis. Nielson et at101 showed that, on regular haemodialysis, there was no further slowing of nerve conduction, nor any significant improvement. Many workers have confirmed the lack of improvement in neuropathy, on haemodialysis. Hemodialysis may reduce serum urea and creatinine concentrations without any improvement in neuropathy. The absence of improvement in nerve conduction has suggested that impulse propagation is impaired by toxic substance(s) of a higher molecular weight, and with a considerably lower clearance through the artificial kidney than urea and creatinine. Evidence favoring a toxic role for larger retained solutes (500-5000 daltons) is based on two observations: first, anecdotal comparisons of patients on chronic haemodialysis and chronic intermittent peritoneal dialysis show that patients on the latter mode of therapy may remain well and free of uremic neuropathy despite higher BUN and creatinine levels; second, lengthening the time on dialysis/week (more "square meter hours" i.e., membrane area multiplied by dialysis time) prevents neuropathy. CAPD gives relatively high clearances of middle molecules. So it has been hypothesized that peripheral neuropathy should not develop on this mode of therapy and, if it already exists, should improve. Few studies of nerve conduction velocities have been done in patients undergoing CAPD. Lindholm et al reported the appearance of neuropathy and deterioration in 11 patients during CAPD, but could not exclude the influence of poor nutrition. Pierratos et al found no significant change in nerve conduction velocity in 18 patients followed for two years on CAPD treatment. The most widely used measure of disordered functions of peripheral nerve has been the determination of motor nerve conduction velocities. The pathology of uremic neuropathy is focused upon destruction of the axon, with only secondary demyelination. In this type of neuropathy, motor nerve conduction velocity would not be expected to be a guide to the severity of the underlying neuropathy. also Kominami et al. found that conduction velocities were unreliable because they varied as much as 9.6m/sec from day to day. Sensory nerve conduction velocity probably is more sensitive than motor nerve conduction velocity. Inspite of these drawbacks, determination of nerve conduction velocity has been used as objective measure of peripheral nerve function by many authors. Slowing of nerve conduction is a frequent occurrence in the uremic patients with no other symptoms or signs of neuropathy which is confirmed in our study also. In the present study, we found that all the patients had statistically significant slowing of both motor and sensory conduction velocities, while 64% of them had no symptoms or signs of peripheral neuropathy. Symptomatic patients had significant longer duration of chronic renal failure, when compared to the rest. Also, conduction velocities were slower in patients with clinical neuropathy. These findings correlate with the observations of Asbury, that, in the past decades, the occurrence of clinically evident neuropathy in patients on chronic dialysis programme (both haemodialysis and peritoneal dialysis) has become rare, as a result of earlier institution of treatment, frequent dialysis scheduling and improvement in dialysis techniques. In contrast, nerve conduction velocity abnormalities, indicative of subclinical neuropathy tend to persist unchanged regardless of the type of dialysis programme used. Further studies of this nature should try to use conduction velocities to assess the adequacy of peritoneal dialysis programme and should evaluate the long term prognosis of the patients on peritoneal dialysis based on the conduction velocities. Studies have claimed the usefulness of nerve conduction studies for prediction of mortality in patients on haemodialysis. Similar studies can be done on peritoneal dialysis patients as well. CONCLUSIONS : 1. The prevalence of clinical neuropathy in a series of 30 patients with end stage chronic kidney disease attending an Intermittent Peritoneal Dialysis (IPD) Programme was 36%. Clinical neuropathy occurred in those with longer duration of uremic symptoms. 2. Clinical neuropathy though less observed than sub clinical neuropathy, indicative severe axonal damage and worse prognosis. 3. Slowing of nerve conduction velocities were a universal phenomenon in the patients on IPD programme, even in the absence of clinical evidence of neuropathy. 4. Serial electro physiological monitoring may be used to monitor adequacy of dialysis schedules.
| Item Type: | Thesis (Masters) |
|---|---|
| Uncontrolled Keywords: | Peripheral Neuropathy ; Chronic Uremia ; Clinical ; Electrophysiological features ; changes in patients ; intermittent peritoneal dialysis. |
| Subjects: | MEDICAL > General Medicine |
| Depositing User: | Subramani R |
| Date Deposited: | 17 Feb 2018 19:13 |
| Last Modified: | 17 Feb 2018 19:13 |
| URI: | http://repository-tnmgrmu.ac.in/id/eprint/5839 |
Actions (login required)
 |
View Item |
