Jan 5, 1985 - Local causes of urinary or faecal incontinence include urinary or anal fistula. Urinary tract infection and diarrhoea may cause temporary loss of ...
4 19 Kunelis CT, Peters JL, Edmondson HA. Fatty liver of pregnancy and its relationship to tetracycline therapy. AmJ Med 1%5;38:359-77. 20 Steele BT, Goldie J, Alexopoulou I, Shimizu A. Post-partum haemolytic uraemic syndrome and verotoxin-producing Escherichia coli. Lancet 1984;i:5 11. 21 Webster J, Rees AJ, Lewis PJ, Hensby CN. Prostacyclin deficiency in haemolytic uraemic syndrome. BrMedJ 1980; 281:271. 22 Remuzzi G, Misiani R, Marchesi D, et al. Treatment of hemolytic uremic syndrome with plasma. Clin Nephrol 1979;12:279-84. 23 Goodman A, Ramos R, Petrelli M, Hirsch SA, Bukowski R, Harris JW. Gingival biopsy in thrombotic thrombocytopenic purpura. Ann Intern Med 1978;89:501-4. 24 Burroughs AK, Seong NH, Doicinov DM, Scheuer PJ, Sherlock SVP. Idiopathic acute fatty liver of pregnancy in 12 patients. QJ Med 1982;51:481-97. 25 Machin SJ. Thrombotic thrombocytopenic purpura. BrJ Haematol 1984;56:191-7. 26 Haemmerli UP. Jaundice during pregnancy with special reference on recurrent jaundice during pregnancy and its differential diagnosis. Acta Med Scand 1966;44 (suppl): 1-I 1. 27 Conaster DG, Harris RE. Fatty liver of pregnancyJ.jAMA 1975;232: 1125-6. 28 Cano RI, Delman MR, Pitchumoni CS, Lev R, Rosenthal WS. Acute fatty liver of pregnancy. Complication by disseminated intravascular coagulation. JAMA 1975;231:159-61. 29 Breen KJ, Perkins KW, Mistilis SP. Idiopathic acute fatty liver of pregnancy. Gut 1970;11: 822-5. 30 Khuroo MS, Teli MR, Skidmore S, Sofi MA, Khuroo MI. Incidence and severity of viral hepatitis in pregnancy. AmJ Med 1981,70:252-5. 31 Myers TJ, Wakem CJ, Tremont SJ. Thrombotic thrombocytopenic purpura: combined treatment with plasmapheresis and antiplatelet agents. Ann Intern Med 1980;92:149-55. 32 Rossi EC, del Greco F, Kwaan HC, Lermana BC. Hemodialysis-exchange transfusion for treatment of thrombotic thrombocytopenic purpura. J3AMA 1980;244:1466-8. 33 McLeod BC, Wu KK, Knospe WH. Plasmapheresis in thrombotic thrombocytopenic purpura. Arch Intern Med 1980;140:1059-60.
New concepts in incontinence Incontinence, defined as the inadvertent or uncontrolled passage of faeces or urine or both, is a disability associated with profound social consequences. Furthermore, it is common, urinary incontinence occurring in about 12% of women and 7% of men over 65 and in as many as 9% of younger women.' Faecal incontinence is probably less common, although one study of 76 patients referred for investigation of diarrhoea found that 38 of the patients were, in reality, suffering from incontinence of faeces.2 The causes of incontinence may broadly be divided into neurological and local. Central nervous system diseases, such as multiple sclerosis, Parkinson's disease, and disorders of the spinal cord or cauda equina, are often accompanied by incontinence because the central pathways which control sphincter function are located close to the corticospinal tracts. Incontinence may also occur in patients with peripheral neuropathy, especially when the autonomic nerves are affected, as in diabetic neuropathy. Local causes of urinary or faecal incontinence include urinary or anal fistula. Urinary tract infection and diarrhoea may cause temporary loss of continence. Prostatism and intractable constipation with rectal distension may also present as incontinence. In these forms of incontinence the sphincter mechanism is normal, although in some cases, especially when there is urge incontinence, a functional abnormality in the spinal cord has been suspected.3 The commonest form of incontinence in adults is stress incontinence. This is due to weakness of the urinary or anal sphincter mechanism which results in a closure pressure that is below that in the bladder or rectum. Recent work has clarified the mechanism of idiopathic neurogenic anorectal incontinence, a disorder that is much more common in women than in men and is characterised by weakness of the anal sphincter musculature. This weakness is demonstrable on digital and manometric examination and is often associated with an anal canal that is loaded with faeces. The anal reflex is usually absent, and the perineum may balloon downwards during voluntary straining at stool, indicating weakness of the muscles of the pelvic floor.' The puborectalis muscle bar, which is palpated during digital examination of the anal canal, is soft and weak and this results in straightening of the anorectal angle, loss of the flap valve mechanism at the anorectal angle, and so incontinence.46 The internal anal sphincter may be stretched so that
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the anal orifice appears patulous, but there is no evidence to suggest that this in itself causes faecal incontinence. Studies of the histopathological changes in the striated muscles of the pelvic floor in patients with idiopathic anorectal incontinence showed loss of muscle fibres with fibrosis and fat replacement in the puborectalis and external anal sphincter muscles and, to a lesser extent, in the lower parts of the levator ani muscles.' In three quarters of the patients studied there was histological evidence of denervation and reinnervation: in the remainder the histological abnormality was so severe that its cause was uncertain.78 Electrophysiological studies of the puborectalis and external anal sphincter muscles, using concentric electromyographic9 and single fibre electromyographic techniques, have, however, shown features consistent with a neurogenic abnormality in all patients with this form of incontinence.6 10 Damage to the innervation of these muscles does not occur in rectal prolapse unless there is associated anorectal incontinence.6 So what is the cause of this neurogenic abnormality and how may it be investigated? Clinical evidence suggests that a difficult or prolonged labour or habitual and prolonged straining at stool are risk factors. Occasionally incontinence develops in patients with recurrent low back pain, sciatica, and after laminectomy.4 7 The main clinical, histological, and electromyographic abnormalities are in the puborectalis and external anal sphincter muscles.68 " Using new electrophysiological techniques the nerve supply of these muscles may now be assessed directly. The external anal sphincter muscle is innervated by the inferior rectal branches of the pudendal nerve. The pudendal nerves may be stimulated electrically using a modified glove with two electrodes mounted on the tip of the index finger.'2 (This method was adapted from Brindley's technique for the treatment of impotence in paraplegics. 1) The distal motor latency from stimulation of the pudendal nerve to the evoked muscle response in the external anal sphincter muscle is increased in idiopathic neurogenic anorectal incontinence, implying that this nerve is damaged in the distal part of its course.'2 The proximal part of this innervation, assessed by measurement of the motor latency to the muscle after transcutaneous electrical stimulation of the cauda equina at LI and L4 vertebral levels, is normal.'2 The puborectalis muscle, the most important muscle for faecal incontinence, is innervated not by the pudendal nerve but by direct pelvic branches of the motor roots of S3 and S4. 4 Transcutaneous spinal stimulation has shown that the distal but not the proximal part of this innervation is abnormal in these patients. " These observations suggest that idiopathic neurogenic anorectal incontinence is due to damage to the nerve supply of the muscles of the pelvic floor caused by repeated stretch injury to the nerves during perineal descent associated with straining during defecation,7' but often initiated by damage to the nerve supply of the pelvic floor muscles during cohildbhirth. '5 Stress incontinence of urine is sometimes associated with idiopathic neurogenic anorectal incontinence, and these patients have abnormalities in the motor nerve conduction in the perineal branches of the pudendal nerves that innervate the periurethral striated sphincter musculature. These changes are similar to those found in the inferior rectal branches innervating the anal sphincter musculature.'6 Indeed, in some patients electromyographic abnormalities of a neurogenic type have been found in the external anal sphincter muscle.'7 This suggests that stress urinary and anorectal incontinence have a similar pathogenesis. Elderly people may be particularly likely to develop these problems
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because of coincident age related neurogenic changes in these muscles. 18 These newly recognised features of incontinence have practical implications: thus treatment by electronic devices intended to stimulate sphincter muscles is unlikely to be effective if there is pronounced muscle denervation, nor will drugs to promote contraction of denervated muscles be of any use. Surgical treatment of urinary or faecal incontinence should offer more help, and one of its objectives should be to reconstruct the pelvic floor muscle plane, as, for example, in the operation of postanal repair for anorectal incontinence devised by Parks.4 Finally, there is a place for preventive action, by attending to the factors that underlie damage to the innervation of the pelvic floor during childbirth,"5 and to the deranged defecatory pattern in patients with constipation, perineal descent, and straining at stool. Such measures should reduce the frequency of this distressing disability. M SWASH Consultant Neurologist, The London Hospital and St Mark's Hospital, London 1 Thomas TM, Plymat KR, Blannin J, Meade TW. Prevalence of urinarv incontinence. BrMed 1980;281: 1243-5. 2 Leigh RJ, Turnberg LA. Faecal incontinence: the unvoiced symptom. Lancet 1982;i: 1349-5 1. 3 HaId T, Bradley WE. The Urina,- bladder: neurology and dynamics. Baltimore, London: Williams and Wilkins, 1982. 4 Parks AG. Anorectal incontinence. Proceedings of the Royal Society of Medictne 1975;68:681-90. 5 Henry MM, Parks AG, Swash M. The pelvic floor musculature in the descending perineum syndrome. Br3 Surg 1982;69:470-2. 6 Neill ME, Parks AG, Swash M. Physiological studies of the anal sphincter musculature in faecal incontinence and rectal prolapse. Br] Surg 1981,68:531-6. 7 Parks AG, Swash M, Urich H. Sphincter denervation in anorectal incontinence and rectal prolapse. Gut 1977;18:656-65. 8 Beersiek F, Parks AG, Swash M. Pathogenesis of rectal incontinence: a histometric study of the anal sphincter musculature. 7 Neurol Sci 1979;42:111-27. 9 Bartolo DCC, Jarratt JA, Read NW. The use of conventional electromyographv to assess external sphincter neuropathy in man. ] Neurol Neurosurg Psychiatr 1983;46: 1115-8. 10 Neill ME, Swash M. Increased motor unit fibredensityin theexternal anal sphinctermuscleinanorectal incontinence: a single fibre EMG study. ] Neurol Neurosurg Psvchiatr 1980;43:343-7. 11 Snooks SJ, Barnes PRH, Swash M. Damage to the voluntarv anal and urinarv sphincter musculature in incontinence. ] Neurol Neurosurg Pwschiatrs (in press). 12 Kiff E, Swash M. Slowed conduction in the pudendal nerves in idiopathic (neurogenic) faecal incontinence. Br]Surg 1984;71:614-6. 13 Brindley GS. Electro-ejaculation: its technique, neurological implications and uses. J Neurol Neurosurg Psychiatry 1981 ;44:9-18. 14 Percy JP, Neill ME, Swash M, Parks AG. Electrophysiological study of the motor nerve supply of the pelvic floor. Lancet 1981; 1: 16-7. 15 Snooks SJ, Setchell M, Swash M, Henry MM. Injury to the innervation of the pelvic floor sphincter musculature in childbirth. Lancet 1984;ii:546-50. 16 Snooks SJ, Swash M. Abnormalities of the innervation of the urethral striated sphincter musculature in incontinence. Br] Urol 1984;56:401-5. 17 Anderson RS. A neurogenic element to urinarv genuine stress incontinence. Br] Obstet Gvnaecol
1984;91:412-45.
18 Percy JP, Neill ME, Kandrah TK, Swash M. A neurogenic factor in faecal incontinence in the elderly. Age Ageing 1982; 11: 175-9.
The world cancer burden: prevent or perish The industrialised Western countries do not have a monopoly of cancer. Recently the International Agency for Research on Cancer and the cancer unit at the World Health Organisation in Geneva examined data on incidence, mortality, and relative frequency to derive estimates of the number of new cases of cancer in the 24 areas of the world for which the United Nations publishes population data.' International cancer statistics take time to appear so that 1975 was used as the reference year; the estimate, probably rather conservative, of the annual number of new cases of cancer was 5-9 million. The six most frequent cancers in men were of lung (464 000), stomach (422 000), colon and rectum (251 000), mouth and pharynx (233 000), prostate (198 000), and oesophagus (194 000); in women they were of breast (541 000), cervix uteri (459 000), stomach (261 000), colon and rectum (256 000), lung (127 000), and mouth and pharynx (107 000). These cancers, together with those of
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liver, bladder, lymphatic tissues, and leukaemia accounted for three quarters of all new malignancies. Combining the sexes, stomach cancer was first in rank order closely followed by lung. These figures represent a desert of human misery and of premature death. The striking variations from nation to nation in the patterns of occurrence of cancer have been interpreted as reflecting differences in exposure to environmental risk factors. Genetic variation can account for only a small proportion of these differences-the changes over time in the incidence of many cancers are too rapid to be explained in this way. Even more compelling is the evidence from migrant studies showing that people who move to another country are found to have the pattern of cancers of their new home within one or two generations.24 Such population comparisons and evidence from experimental and epidemiological studies strongly suggest that as much as 80-90% of human cancer is determined environmentally and thus theoretically avoidable.57 The term environment embraces all elements of lifestyle-dietary, social, and cultural habits (in which the specific carcinogenic factors may be ill understood)-as well as exposure to carcinogens at work, radiation, drugs, and so on. Once specific causes have been identified rational prevention should be possible and the resources now devoted to treatment more profitably used. What, then, are the possibilities for prevention? Tobacco is the most important single aetiological factor in cancer; in the United States, for example, where cigarette smoking is common, around 30% of all deaths from cancer may be attributed to the habit.8 Two thirds of the new cases of lung cancer in 1975 occurred in developed countries where smoking is very prevalent'-and at least 80% are avoidable.7 Even if a smaller fraction of lung cancers in other countries are induced by tobacco 60-75% of the global total must surely be attributable to this single cause. Cancers of the mouth and pharynx are due to chewing betel quid, with and without tobacco, in middle south Asia (where over a third of the incident cases originate) and to the combination of tobacco and alcohol in some Western countries. The risk of many other cancers-of larynx, oesophagus, bladder, and pancteas -is increased by cigarette smoking,8 so that as much as 15% of the global cancer burden, or around 900 000 new cases a year, can be attributed to this single agent. If tobacco consumption in the developing world continues to grow (which vigorous promotional campaigns are seeking to encourage) then this proportion must increase.9 In 1975 stomach cancer was the most commonly occurring tumour, but its incidence is declining everywhere. The cause of this fall is not fully understood, but it may be related to methods of storing foodstuffs, and there is some evidence for a protective effect of a diet rich in fresh fruit and vegetables (and low in salted food). Many other studies, epidemiological and experimental, point to the importance of diet in carcinogenesis and its inhibition.v0-'2 Most of the dietary customs implicated in increasing the risk of cancer-overnutrition, excess intake of fat and meat, deficit of fibre-are characteristic of the so called "Western diet." Over half of the cancers of the breast (541 000 cases yearly), two thirds of colorectal cancer (507 000), and three quarters of prostate cancer (198 000)tumours which have been linked to such diets-occur in the developed nations. Societies do change and can be persuaded to change their dietary patterns (though agricultural and food processing interests may be somewhat resistant)-but as yet we do not know enough confidently to prescribe a risk reducing diet other than in the most general terms: eat less;
