Short and long-term outcome of pancreatic surgery in a district general hospital.

Pancreatic surgery is a formidable undertaking with historically high mortality and poor prognosis for periampullary lesions. This has led to recommendations that all pancreatic surgery should be performed in specialist centres. There is no doubt from large series that a low mortality can be achieved in these centres, but there has been no direct comparison between results from these specialist centres and district general hospitals with an interest in pancreatic disease. We present a retrospective, seven-year experience with a 3% 30 day mortality, 39% morbidity and 14 month median survival for malignant disease. Comparison with the UK survey of specialist pancreatic units shows that pancreatic surgery can be safely performed in the setting of a district general hospital with low morbidity and mortality, and good long-term outcome.

Adenocarcinoma of the small bowel.

Cancer of the small bowel is a rare entity but its incidence is rising. Historically, outcome is poor despite apparent curative resection. At present surgery remains the only treatment modality of proven benefit in the management of this disease. Recent data would suggest 5-year survival rates in the order of 40-50% at all sites of small bowel cancer. To improve upon this, earlier diagnosis with a high index of suspicion and multicentre adjuvant therapy trials are required.

Effect of vaginal delivery on the pelvic floor: a 5-year follow-up.

We have studied the pelvic floor musculature and its innervation in 14 of 24 (58 per cent) multiparous women who had been recruited into a study of the effect of childbirth on the pelvic floor as part of a prospective investigation that began in 1983. These 24 women had all delivered by the vaginal route without forceps assistance. Five of the 14 had developed clinical symptoms of stress incontinence 5 years later; two of them had had a further uncomplicated vaginal delivery during this time. There was manometric and neurophysiological evidence of weakness because of partial denervation of the pelvic floor striated sphincter musculature, with pudendal neuropathy, which was more marked in those women with incontinence. These findings provide direct evidence for the hypothesis that pudendal neuropathy due to vaginal delivery persists and may worsen with time.

Gastric cancer: a continuing diagnostic challenge--a district general hospital's experience.

We present the results of 87 consecutively referred patients with malignant gastric tumours who presented to the North Middlesex Hospital between 1980 and 1984, inclusively. The results of this prospective study showed a high incidence of adenocarcinoma situated in the cardia (16 per cent of patients), and antral carcinomas presented more commonly with chronic blood loss. Delay in diagnosis was still a serious problem and weight loss remained an underestimated symptom, especially when combined with other upper gastrointestinal symptomology. The majority of tumours were adenocarcinomas. Six patients had unusual tumours which had special therapeutic and prognostic implications. The results of the above study are compared with the European experience of the management of malignant gastric tumours.

Neurologic cause of idiopathic incontinence.

The relationship between the pudendal and perineal nerve terminal motor latencies and descent (weakness) of the perineum on straining was investigated in 31 patients with idiopathic fecal incontinence, and in 30 patients with double incontinence. Pelvic floor descent was correlated with increased pudendal nerve terminal motor latency in both groups of patients. In the patients with double incontinence, there was a less significant correlation between perineal descent and increased perineal nerve terminal motor latency. In the patients with fecal incontinence, but without urinary incontinence, there was no correlation between perineal descent and perineal nerve terminal motor latency. These data support the concept that pelvic floor weakness can result in damage to the pudendal and perineal nerves, leading to fecal and urinary incontinence. In patients with isolated fecal incontinence the perineal nerves are relatively spared. Thus these common types of incontinence probably have a neurologic cause, and neurophysiologic methods can be used in their assessment.

How should we preclot knitted Dacron grafts?

We studied the change in water porosity over time of 10 Sauvage Bionit-II and 10 DeBakey Vasculour-II knitted velour Dacron grafts throughout the four stages of the Sauvage preclotting technique. Graft porosity decreased significantly (p less than 0.001) at the ends of stages 1 and 2 for both types of grafts, but stages 3 and 4 did not further reduce graft porosity. These results demonstrate that a two-stage preclotting technique is adequate for the preclotting of knitted velour Dacron grafts. A final rinse with heparinized blood is recommended as this may reduce graft thrombogenicity.

Parity as a factor in incontinence in multiple sclerosis.

Twelve consecutively selected patients with multiple sclerosis and incontinence had electrophysiologic studies performed of the pudendal and perineal innervations of the anal and urinary sphincter. Single-fiber electromyogram density measurements were obtained in the external anal sphincter. Fecal incontinence was found to be unexpectedly frequent. The results suggest that incontinence in patients with multiple sclerosis is often due to the interaction of several factors, including central lesions, lesions of the conus medullaris and, also, coincidental pelvic nerve lesions associated with childbirth. Thus, incontinence is especially a problem in women with this disease.

Slowed motor conduction in lumbosacral nerve roots in cauda equina lesions: a new diagnostic technique.

New techniques have been developed for the electrophysiological assessment of patients with suspected cauda equina lesions using transcutaneous spinal stimulation (500-1500 V: time constant 50 microseconds) to measure motor latencies to the external and sphincter and puborectalis muscles from L1 and L4 vertebral levels. These latencies represent motor conduction in the S3 and S4 motor roots of the cauda equina between these levels. Similarly motor latencies can be recorded from spinal stimulation to the anterior tibial muscles (L4 and L5 motor roots). Transrectal stimulation of the pudendal nerves is used to measure the pudendal nerve terminal motor latency. In 32 control subjects, matched for age and sex, mean motor latencies from L1 and L4 spinal stimulation were 5.5 +/- 0.4 ms and 4.4 +/- 0.4 ms (mean + SD). In the 10 patients with cauda equina disease including ependymoma, spinal stenosis, arachnoiditis and trauma, these latencies were 7.2 +/- 0.8 ms and 4.6 +/- 0.9 ms, a significant increase in the L1 latency. The L1/L4 latency ratios to the puborectalis muscle were 1.36 +/- 0.09 in control subjects and 1.72 +/- 0.13 in cauda equina patients. Pudendal nerve terminal motor latencies were normal in eight of the 10 patients with cauda equina disease. The single fibre EMG fibre density in the external and sphincter muscle (normal, 1.5 +/- 0.16) was increased in patients with cauda equina lesions (1.73 +/- 0.28), but was increased more than two standard deviations from the mean only in three patients. This increase in fibre density was not of diagnostic value since it was also found in two of the four patients with low back pain. Slowing of motor conduction in the cauda equina is thus a useful indication of damage to these intraspinal motor roots. These investigations can be used in the selection of patients for myelography, and to follow progress in patients managed conservatively.

Risk factors in childbirth causing damage to the pelvic floor innervation.

The innervation of the pelvic floor musculature is damaged in both stress urinary incontinence and idiopathic (neurogenic) anorectal incontinence. Because childbirth has been considered to be a causative factor in stress incontinence we have assessed the effect of childbirth on the innervation of the pelvic floor musculature in 122 consecutively referred women. They were investigated 48-72 h and 2 months after delivery; 51 were also studied 6 months prior to delivery. In 45 of these 51 women delivered vaginally, EMG studies of the external anal sphincter muscle showed that the fibre density (FD) increased from 1.38 +/- 0.14 before delivery to 1.57 +/- 0.19 2 months after delivery (p less than 0.01). There was no change in the FD in the external anal sphincter muscle after delivery in 20 women delivered by Caesarean section. The pudendal nerve terminal motor latency (PNTML) measured 48-72 h after delivery was increased in the 102 women delivered vaginally compared to 34 nulliparous control subjects. Analysis of the whole group of 122 women showed that multiparity, forceps delivery, increased duration of the second stage of labour, third degree perineal tear and high birth weight were important factors leading to pudendal nerve damage. Epidural anaesthesia had no effect on pudendal nerve function. Modification of these obstetric risk factors may ultimately reduce the frequency of stress urinary and faecal incontinence in women.

The innervation of the muscles of continence.

Electrophysiological evidence is presented that suggests that the innervation of the human puborectalis muscle differs from that of the external anal sphincter muscle. The latter is innervated by branches of the pudendal nerves, and the former by direct branches of the sacral plexus that enter the muscle from its pelvic surface. The striated urinary sphincter musculature also receives a dual innervation. The periurethral component is innervated by perineal branches of the pudendal nerves and the intramural portion by a different pathway, probably consisting of supralevator branches derived from the pelvic nerves. These findings are relevant to understanding the embryological derivation of these muscles and have practical importance in the surgery of this region of the body, particularly in the treatment of incontinence.

Investigation of disorders of the anorectum and colon.

Previously, investigation of disorders of the anorectum and colon have been limited to manometric, external anal sphincter muscle electromyographic and contrast radiological techniques. In this paper we describe other investigative techniques recently developed at St. Mark's Hospital, London and their application in the investigation of certain disorders of the anorectum and colon.

Unifying concept of pelvic floor disorders and incontinence.

Denervation of pelvic floor sphincter muscles is a feature of pelvic floor disorders. When severe, it may be accompanied by stress incontinence of faeces, or of urine. The extent of chronic partial denervation of these pelvic floor muscles can be quantified by electromyography (EMG), and its cause identified by electrophysiological studies of the motor innervation of these striated muscles. Damage to this innervation is often initiated by childbirth, but appears to progress during a period of many years so that the functional disorder usually presents in middle life. Incontinence develops in some patients, but not in others. This can be predicted by the severity of the abnormalities found in EMG studies of the pelvic sphincter musculature and motor latency studies of its innervation. The results of such investigations in the six common types of pelvic floor disorder are presented. Recognition of the causative factors leading to damage to the innervation of the pelvic sphincter muscles implies new approaches to treatment and to prevention of pelvic floor disorders and incontinence.

Damage to the innervation of the pelvic floor musculature in chronic constipation.

Constipation and defecation straining have been implicated in the pathogenesis of anorectal incontinence. We have studied 24 women with chronic constipation and 20 age- and parity-matched control subjects. Electrophysiologic techniques were used to study the innervations of the puborectalis and external anal sphincter muscles. The results show that damage can occur to the nerve supply of both these muscles in chronic constipation, and that this probably is due to perineal descent during defecation straining.

Motor conduction velocity in the human spinal cord: slowed conduction in multiple sclerosis and radiation myelopathy.

Transcutaneous electrical stimulation of the central nervous system was used to measure motor conduction velocity in the human spinal cord in 21 subjects aged 22 to 75 years (mean 55 years), none of whom had neurological disease. The motor conduction velocity between the sixth cervical (C6) and first lumbar (L1) vertebral levels was 67.4 +/- 9.1 m/s. This probably represents conduction velocity in the corticospinal tracts. In these subjects the motor conduction velocity in the cauda equina, between the first lumbar (L1) and fourth lumbar (L4) vertebral levels, was 57.9 +/- 10.3 m/s. In four of five patients with multiple sclerosis, all with corticospinal signs in the legs, motor conduction velocity between C6 and L1 was slowed (41.8 +/- 16.8 m/s), but cauda equina conduction was normal (55.8 +/- 7.8 m/s). Similar slowing of spinal cord motor conduction was found in a patient with radiation myelopathy. This method should provide a relevant, simple clinical test in patients with spinal cord disease.

Perineal nerve damage in genuine stress urinary incontinence. An electrophysiological study.

Twelve patients with genuine stress incontinence of urine were investigated using manometric and electrophysiological techniques. All were shown to have slowed conduction in the perineal branch of the pudendal nerve which innervates the periurethral striated sphincter muscle. The mean perineal nerve terminal motor latency in these patients was 3.9 +/- 0.8 (ms) and in 20 age and parity matched control subjects was 2.0 +/- 0.2 (ms) (P less than 0.001). These results are consistent with a neurogenic factor in patients with genuine stress incontinence of urine which may have implications regarding selection of patients for surgery to restore urethral competence.