- Email: [email protected]
HUMORAL ASPECTS OF DUMPING SYNDROME
92 There has been much recent interest in chemotherapy induced vomiting. At least twol°2 papers have pointed out that patients refractory to standard antiemetic therapy respond to drugs with an additional psychotropic element. Lorazepam has been successfully used as a premedication for some time,3-5 and it has the attractive combination of good anxiolysis and production of amnesia for 3-12 h after injection with light sedation compared with that associated with other benzodiazepines and phenothiazines. In this particularly refractory group of patients i.v. lorazepam reduced both vomiting and the distress associated with multidrug chemotherapy. We are now investigating the use of oral lorazepam with cis-platin regimens and as an outpatient premedication before dacarbazine. Stanford Cade Department of Clinical Oncology, Westminster Hospital, London SW1 *
Present address: Meyerstein Institute of Hospital, London W1P 7PN.
JANE MAHER* Radiotherapy
and
Oncology,
Middlesex
GELINEAU’S NARCOLEPSY RELIEVED BY OPIATES
SIR,-Gelineau’s syndrome (rapid eye
movement
[REM]
nar-
consists of attacks of irresistible daytime sleep usually in association with cataplexy, sleep paralysis, hypnagogic hallucinations, 6,7 and other less well defined disturbances. Remission is said not to occur8-10_or the condition is increasingly tolerated with age so that it seems to remit in 8% of cases. The following is a report of a patient whose symptoms were relieved with codeine phosphate. The patient was a 29-year-old soldier when, in 1944, daytime sleep attacks typical of narcolepsy developed. 4 years later cataplexy occurred in response to rage, sudden startle, or excitement. Later again sleep paralysis and hypnagogic hallucinations developed. This constellation of symptoms severely interfered with his work and he was forced to change jobs many times. His medical history included concussion and a perforated duodenal ulcer. At the age of 55 he acquired Crohn’s disease and a partial colectomy was performed. 2 years later he started taking codeine phosphate 30 mg tablets, up to eight daily, for the control of pain and diarrhoea. From that date the patient noted disappearance of his narcolepsy, cataplexy, sleep paralysis, and hypnagogic hallucinations. When he was 60 years of age he was unable to obtain codeine phosphate for a week, and on the fifth day he had an attack of cataplexy. Since then pentazocine tablets have completely controlled his bowel and narcoleptic problems. He is now 68 and, though his general health is affected by his Crohn’s disease and by chronic obstructive airways disease, a full neurological examination is entirely normal. Gelineau’s syndrome is thought to be REM sleep inappropriately intruding into wakefulness as a whole or in fragments: 11the sleep represents REM sleep, the cataplexy and sleep paralysis represent the motor inhibition of REM sleep, and the hypnagogic hallucinations equate with dreaming. Sleep is thought to be regulated by the reticular activating formation of the pons-notably, the locus coeruleus which initiates the
colepsy)
1. Sallan SE, Cronin C, Zelen M, Zinberg NE. Antiemetics in patients receiving chemotherapy for cancer. N Engl J Med 1980; 302: 135-38. 2. Morran C, Smith DC, Anderson DA, McArdle CS. Incidence of nausea and vomiting with cytotoxic chemotherapy: a prospective randomised trial of antiemetics. Br Med
J 1979: 1323-24. Oury M, Coppignon P. Utilisation du lorazépam injectable dans la préparàtion au cathétérisme cardique. Revue Méd Liège 1976; 31: 85. 4. Knapp RD, Fierrol L. Evaluation ofcardiopulmonary safety and effects of lorazepam as a pre-medicant anaesthetic. Anesth Analg Curr Res 1974; 53: 122-24. 5. Johnstone M. The effect oflorazepam on the vasoconstriction of fear. Anaesthesia 1976, 3.
31: 868-72. 6. Zarcone V. Narcolepsy N Engl J Med 1973; 288: 1156-65 7. Yoss RE The inheritance of diurnal sleepiness as measured by pupillography. Mayo Clin Proc 1970; 45: 426-37 8. Parkes JD, Fenton G, Struthers G, Curzon G, Kantamaneni BD, Buxton BH. Narcolepsy and cataplexy Quart J Med 1974, 42: 525 9 Yoss RE, Daly DD Criteria for diagnosis of narcoleptic syndrome. Staff Proc Mayo
Clin 1957; 32: 320-28. 10. Editorial Narcolepsy Br Med J 1975, 1: 476-77 11. Guilleminault C, Dement WC. A study on cataplexy Arch Neurol 1974, 31: 255
muscle inhibition and aret1exia6,11 of REM sleep. Within this neuronal system are neurones having differing equilibria of amine (noradrenaline, secrotonin) and acetylcholine relationships, which determine the state of vigilance (i.e., alertness), non-REM sleep, and REM sleep.The biochemical lesion in the narcolepsy syndrome is surmised to be a dysfunction of noradrenaline pathways (sleep attacks) and of serotonin pathways (cataplesy).12 This suggestion is supported by the fact that amphetamines relieve only the narcolepsy, but tricyclic antidepressants relieve the cataplexy, by inhibiting the neuronal uptake of serotonin and overcoming the hyperactive cholinergic effects.6,11,13 Present management of Gelineu’s syndrome consists of these two classes of drug. They are unsatisfactory, however, because of side effects, dependency, and variable response. The locus coeruleus has close connections with the reticular formation, particularly the pons. This nucleus consists of groups of noradrenaline and serotonin containing neurones which are sensitive to various preganglionic inputs and which respond by altering their firing rate. i4,1Narcolepsy could be caused by excess neuronal firing due to excessive acetylcholine excitatory effect or diminished a2-adrenergic inhibitory effect, and opiates might inhibit this excess firing and allow the normal sequence of alertness, non-REM sleep, and REM sleep.6 We suggest that codeine and pentazocine acted in this way in the patient described. A response to opiates in this condition has not previously been reported. Clonidine (a centrally acting a2-agonist) may well be able to redress the same imbalance. Narcolepsy may not be a common problem but it is a life-long and life disrupting condition, and drug management is beset with side effects and abuse. This case suggests that more trouble-free and effective drugs may be available. Department of Rheumatic Diseases, Royal Perth (Rehabilitation) Hospital, Shenton Park, Western Australia 6008
JUDITH M. HARPER
HUMORAL ASPECTS OF DUMPING SYNDROME
SIR,-Your Nov. 29 editorial draws attention to the complexity of published work on the aetiology of the dumping syndrome, and likens the known humoral abnormalities to the harmless thunder accompanying a flash of lightning. We agree that surgery is the main cause of dumping. However, the associated humoral changes may have considerable importance in the pathology of this condition. The dumping study which we recently reported demonstrated that a peptide with known vasoactive propertieswas much increased in patients with dumping symptoms.This stimulated us to reproduce similar levels of neurotensin in volunteers who had not had gastric surgery; such levels were not associated with any symptoms of dum3 ping, though they did induce changes in gastrointestinal function. We have recently attempted to study this further by comparing the rise in plasma neurotensin with the rate of gastric emptying of a glucose solution tagged with indium-113 in preoperative and postoperative symptom-free and symptomatic patients. Twenty-five patients were studied, who experienced symptoms of dumping4in their daily lives, and compared with twenty-nine age and sex matched symptom-free patients after similar surgery. In addition, nineteen patients with duodenal ulceration were studied while awaiting surgery. The test solution, 75 g glucose in 150 ml 12. Editorial Narcolepsy and cataplexy. Lancet 1975; i: 845. 13. Editorial Treatment for cataplexy. Br Med J1975; i 233 14. Guyenet PC, Aghajanian GK. Acetylcholine, substance P, and met-encephalin in the locus ceruleus. Eur J Pharmacol 1979, 53: 319-28. 15 Aghajanian GK. Tolerance of locus ceruleus neurones to morphine and suppression of withdrawal response by Clonidine. Nature 1978, 276: 186 1 Carraway R, Leeman SE The isolation of a new hypotensive peptide, neurotensin, from bovine hypothalami J Biol Chem 1973; 248: 6854-61 2 Blackburn AM, Christofides ND, Ghatei MA, Sarson DL, Ebeid FH, Ralphs DNL, Bloom SR Elevation of plasma neurotensin in the dumping syndrome Chn Sci 1980; 59: 237-43. 3 Blackburn AM, Fletcher DR, Christofides ND, Long RG, Fitzpatrick ML, Bloom SR Effect of neurotensin on gastric function Lancet 1980, i: 987-89 4. Merhng S. Post-cibal symptoms after partial gastrectomy for peptic ulcer. Acta Soc Med Upsal 1953, suppl 3
93 labelled with 1-5mCi "’ion chelated with DTPA (diethylenetriamine penta-acetic acid), and, after its ingestion, the decrease in counts from the gastric area was computed against time using a gamma counter connected to a computer. Blood samples for neurotensin measurementwere taken regularly throughout the test. The radioactive marker emptied significantly faster from the stomach-in the group of symptomatic patients, who also showed a greater rise in plasma neurotensin concentrations than did the other two groups. The initial gastric emptying rate (assessed in the first 10 min) also correlated significantly (p<0’ 001) with the initial (20 min) rise in plasma neurotensin concentration in all the patients (correlation coefficient r=0’62, n = 73, method of least squares). These results suggest that the exaggerated release of neurotensin in the subjects with dumping symptoms may occur as a result of the rapid passage of glucose from the stomach into the neurotensin-rich ileum. The role of increased neurotensin in these patients still remains speculative. Its vasoactive properties may contribute to the symptoms of those patients whose circulatory system is already compromised by splanchnic pooling of circulatory fluid in the lumen of the bowel. levels of plasma neurotensin delay gastric emptying and high plasma concentrations of neurotensin may therefore operate to provide some compensation for the rapid emptying of nutrients from the stomach. We agree with your editorial that neurotensin may not have a primary causative role in the dumping syndrome, as we were careful to state in the original publication, but do not agree that it is therefore of no importance. The dramatic humoral abnormalities that have been described in this condition may be responsible for its primary or secondary features. Unravelling these complex interrelationships will take time, but will eventually result in a far greater understanding of water,
CURRENT STATUS OF JEJUNOILEAL BYPASS FOR MORBID OBESITY
was
Physiological
gastrointestinal physiology. Royal Postgraduate Medical School, London W 120HS
Six,-The gastric bypass or partition operation offers an alterto jejunoileal bypass for the surgical treatment of morbid
native
obesity. Since initially described by Mason in 1966,1 it is estimated that over 2500 operations have been done. The weight loss at one year is a mean of 42 kg and there have been minimal metabolic and electrolyte complications, as previously reported with intestinal bypass. approach of those clinicians who have published jejunoileal bypass in the management of morbid obesity, I wrote to them asking for details of their current practice and received replies from six in North America, two in Scandinavia, and two in the U.K. (table). Four have now stopped doing jejunoileal bypass and a fifth is doing it only in patients with obesity associated with severe hyperlipidaemia. Of the five still using this operation, three do end-to-end and two end-to-side jejunoileal anastomoses. The length of small bowel left in continuity varies from 35 cm to 62 - 5 cm, leaving a longer length of ileum than before. Two are adding an anastomosis between gallbladder and the blind end of the jejunum in the hope of decreasing some aspects of the blind-loop syndrome. Two centres are currently not involved in treating morbidly obese patients by surgery although they hope to try and assess gastric bypass in the future. Six groups are currently undertaking gastric bypass procedures for obesity and tending to use autosuture stapling instruments. Most respondents mention the careful selection of patients for operation and the possible need for this type of surgery to be restricted to specialised centres, especially with regard to preoperative assessment and postoperative management. assess
the
current
on
5. Blackburn
AM, Bloom SR. A radioimmunoassay for neurotensin in human plasma J Endocrinol 1953, 93: 175-81 1 Mason EE, Printen KJ. Gastric bypass for obesity. In Buchwald H, Varcor L, eds. Metabolic surgery. New York. Grune & Stratton, 1978: 41-57
bypass done. fWith bilio-intestinal shunt.
Scott correctly points out that: "... the malignant abuse of these operations will result in deterioration of the surgical approach to morbid obesity ... if this happens, it will be tragic!" Department of Surgery, University of Cincinnati Medical Center, Cincinnati, Ohio 45267, U.S.A.
A. M. BLACKBURN S. R. BLOOM
CURRENT STATUS OF JEJUNOILEAL BYPASS FOR OBESITY
To
*End-to-end
STEPHEN N. JOFFE
CYTOLOGY IN RECTOSIGMOID CANCER
SIR,-Following the observations of Webb,’ we have used digital scrape cytology as a routine diagnostic aid in a general surgical outpatients clinic. Rectal examination is done with a ’Disposaglove’ (Arbrook Ltd, Kirkton Campus, Livingston, Scotland), with a fusion ridge on the finger edge. When a palpably suspicious area is found, the ridge sweeps across the ulcerated or polypoid surface. Any tissue or blood is dabbed onto a glass microscope slide and air dried, stained by May-Grunwald Giemsa with interpretation, if necessary, within minutes. For lesions above 8 cm, a dental roll held by forceps is passed through a sigmoidoscope. 81 patients were examined. 3 smears were inadequate, with only faecal debris present. In 58 cases cytology and histology were in accord ; in 9 cases the cytology report was "suspicious"; in 7 cases with negative cytology no histology was done; in 4 the cytology and histology reports differed. 34 cases of adenocarcinoma and 4 cases of squamous cell carcinoma were correctly reported cytologically. There were 20 cases in which no malignant cells were seen and histologically these were subsequently confirmed as benign. 9 cases were reported as either 2.
Bray GA, Greenway FL, Barry RE et al. Surgical treatment of obesity: a review of our experience and an analysis of published reports. Int J Obesity 1977; 1: 331-67. 3. Buchwald H. Surgical approaches for failed jejunoileal bypass and failed gastric bypass: Morbid obesity. Surg Clins N Am 1979; 59: 1121-30. 4. Payne JH, DeWind LT. Surgical treatment of obesity. Am J Surg 1969; 118: 141-47 5. Phillips RB. Small intestinal bypass for the treatment of morbid obesity: Collective reviews. Surg Gynecol Obstet 1978; 146: 455-68. 6. Scott HW Jr, Dean RH, Shull JS, Gluck F Results of jejunoileal bypass in 200 patients with morbid obesity. Surg Gynecol Obstet 1977, 145: 661-73. 7. Salmon PA. The results of small intestine bypass operations for the treatment of obesity Surg Gynecol Obstet 1971; 132: 965-79. 8. Quaade F. Jejunoileal bypass for morbid obesity Morbid obesity. Surg Clins N Am 1979; 59: 1055-69
Hallberg D, Holmgren U. Bilio-intestinal shunt. Acta Chir Scand 1979; 145: 408 Baddeley RM. The management of gross refractory obesity by jejunoileal bypass Br J Surg 1979; 66: 525-32. 11. Gazet J-C, Pilkington TRE, Kalucy RS, Crisp AH, Day S. Treatment of gross obesity by jejunal bypass. Br Med J 1974; ii: 311-16. 1. Webb AJ. Cytologic diagnosis of anorectal and rectosigmoid lesions by a simple smear technique. Acta Cytol 1979; 23: 524. 9. 10.
Present address: Meyerstein Institute of Hospital, London W1P 7PN.
JANE MAHER* Radiotherapy
and
Oncology,
Middlesex
GELINEAU’S NARCOLEPSY RELIEVED BY OPIATES
SIR,-Gelineau’s syndrome (rapid eye
movement
[REM]
nar-
consists of attacks of irresistible daytime sleep usually in association with cataplexy, sleep paralysis, hypnagogic hallucinations, 6,7 and other less well defined disturbances. Remission is said not to occur8-10_or the condition is increasingly tolerated with age so that it seems to remit in 8% of cases. The following is a report of a patient whose symptoms were relieved with codeine phosphate. The patient was a 29-year-old soldier when, in 1944, daytime sleep attacks typical of narcolepsy developed. 4 years later cataplexy occurred in response to rage, sudden startle, or excitement. Later again sleep paralysis and hypnagogic hallucinations developed. This constellation of symptoms severely interfered with his work and he was forced to change jobs many times. His medical history included concussion and a perforated duodenal ulcer. At the age of 55 he acquired Crohn’s disease and a partial colectomy was performed. 2 years later he started taking codeine phosphate 30 mg tablets, up to eight daily, for the control of pain and diarrhoea. From that date the patient noted disappearance of his narcolepsy, cataplexy, sleep paralysis, and hypnagogic hallucinations. When he was 60 years of age he was unable to obtain codeine phosphate for a week, and on the fifth day he had an attack of cataplexy. Since then pentazocine tablets have completely controlled his bowel and narcoleptic problems. He is now 68 and, though his general health is affected by his Crohn’s disease and by chronic obstructive airways disease, a full neurological examination is entirely normal. Gelineau’s syndrome is thought to be REM sleep inappropriately intruding into wakefulness as a whole or in fragments: 11the sleep represents REM sleep, the cataplexy and sleep paralysis represent the motor inhibition of REM sleep, and the hypnagogic hallucinations equate with dreaming. Sleep is thought to be regulated by the reticular activating formation of the pons-notably, the locus coeruleus which initiates the
colepsy)
1. Sallan SE, Cronin C, Zelen M, Zinberg NE. Antiemetics in patients receiving chemotherapy for cancer. N Engl J Med 1980; 302: 135-38. 2. Morran C, Smith DC, Anderson DA, McArdle CS. Incidence of nausea and vomiting with cytotoxic chemotherapy: a prospective randomised trial of antiemetics. Br Med
J 1979: 1323-24. Oury M, Coppignon P. Utilisation du lorazépam injectable dans la préparàtion au cathétérisme cardique. Revue Méd Liège 1976; 31: 85. 4. Knapp RD, Fierrol L. Evaluation ofcardiopulmonary safety and effects of lorazepam as a pre-medicant anaesthetic. Anesth Analg Curr Res 1974; 53: 122-24. 5. Johnstone M. The effect oflorazepam on the vasoconstriction of fear. Anaesthesia 1976, 3.
31: 868-72. 6. Zarcone V. Narcolepsy N Engl J Med 1973; 288: 1156-65 7. Yoss RE The inheritance of diurnal sleepiness as measured by pupillography. Mayo Clin Proc 1970; 45: 426-37 8. Parkes JD, Fenton G, Struthers G, Curzon G, Kantamaneni BD, Buxton BH. Narcolepsy and cataplexy Quart J Med 1974, 42: 525 9 Yoss RE, Daly DD Criteria for diagnosis of narcoleptic syndrome. Staff Proc Mayo
Clin 1957; 32: 320-28. 10. Editorial Narcolepsy Br Med J 1975, 1: 476-77 11. Guilleminault C, Dement WC. A study on cataplexy Arch Neurol 1974, 31: 255
muscle inhibition and aret1exia6,11 of REM sleep. Within this neuronal system are neurones having differing equilibria of amine (noradrenaline, secrotonin) and acetylcholine relationships, which determine the state of vigilance (i.e., alertness), non-REM sleep, and REM sleep.The biochemical lesion in the narcolepsy syndrome is surmised to be a dysfunction of noradrenaline pathways (sleep attacks) and of serotonin pathways (cataplesy).12 This suggestion is supported by the fact that amphetamines relieve only the narcolepsy, but tricyclic antidepressants relieve the cataplexy, by inhibiting the neuronal uptake of serotonin and overcoming the hyperactive cholinergic effects.6,11,13 Present management of Gelineu’s syndrome consists of these two classes of drug. They are unsatisfactory, however, because of side effects, dependency, and variable response. The locus coeruleus has close connections with the reticular formation, particularly the pons. This nucleus consists of groups of noradrenaline and serotonin containing neurones which are sensitive to various preganglionic inputs and which respond by altering their firing rate. i4,1Narcolepsy could be caused by excess neuronal firing due to excessive acetylcholine excitatory effect or diminished a2-adrenergic inhibitory effect, and opiates might inhibit this excess firing and allow the normal sequence of alertness, non-REM sleep, and REM sleep.6 We suggest that codeine and pentazocine acted in this way in the patient described. A response to opiates in this condition has not previously been reported. Clonidine (a centrally acting a2-agonist) may well be able to redress the same imbalance. Narcolepsy may not be a common problem but it is a life-long and life disrupting condition, and drug management is beset with side effects and abuse. This case suggests that more trouble-free and effective drugs may be available. Department of Rheumatic Diseases, Royal Perth (Rehabilitation) Hospital, Shenton Park, Western Australia 6008
JUDITH M. HARPER
HUMORAL ASPECTS OF DUMPING SYNDROME
SIR,-Your Nov. 29 editorial draws attention to the complexity of published work on the aetiology of the dumping syndrome, and likens the known humoral abnormalities to the harmless thunder accompanying a flash of lightning. We agree that surgery is the main cause of dumping. However, the associated humoral changes may have considerable importance in the pathology of this condition. The dumping study which we recently reported demonstrated that a peptide with known vasoactive propertieswas much increased in patients with dumping symptoms.This stimulated us to reproduce similar levels of neurotensin in volunteers who had not had gastric surgery; such levels were not associated with any symptoms of dum3 ping, though they did induce changes in gastrointestinal function. We have recently attempted to study this further by comparing the rise in plasma neurotensin with the rate of gastric emptying of a glucose solution tagged with indium-113 in preoperative and postoperative symptom-free and symptomatic patients. Twenty-five patients were studied, who experienced symptoms of dumping4in their daily lives, and compared with twenty-nine age and sex matched symptom-free patients after similar surgery. In addition, nineteen patients with duodenal ulceration were studied while awaiting surgery. The test solution, 75 g glucose in 150 ml 12. Editorial Narcolepsy and cataplexy. Lancet 1975; i: 845. 13. Editorial Treatment for cataplexy. Br Med J1975; i 233 14. Guyenet PC, Aghajanian GK. Acetylcholine, substance P, and met-encephalin in the locus ceruleus. Eur J Pharmacol 1979, 53: 319-28. 15 Aghajanian GK. Tolerance of locus ceruleus neurones to morphine and suppression of withdrawal response by Clonidine. Nature 1978, 276: 186 1 Carraway R, Leeman SE The isolation of a new hypotensive peptide, neurotensin, from bovine hypothalami J Biol Chem 1973; 248: 6854-61 2 Blackburn AM, Christofides ND, Ghatei MA, Sarson DL, Ebeid FH, Ralphs DNL, Bloom SR Elevation of plasma neurotensin in the dumping syndrome Chn Sci 1980; 59: 237-43. 3 Blackburn AM, Fletcher DR, Christofides ND, Long RG, Fitzpatrick ML, Bloom SR Effect of neurotensin on gastric function Lancet 1980, i: 987-89 4. Merhng S. Post-cibal symptoms after partial gastrectomy for peptic ulcer. Acta Soc Med Upsal 1953, suppl 3
93 labelled with 1-5mCi "’ion chelated with DTPA (diethylenetriamine penta-acetic acid), and, after its ingestion, the decrease in counts from the gastric area was computed against time using a gamma counter connected to a computer. Blood samples for neurotensin measurementwere taken regularly throughout the test. The radioactive marker emptied significantly faster from the stomach-in the group of symptomatic patients, who also showed a greater rise in plasma neurotensin concentrations than did the other two groups. The initial gastric emptying rate (assessed in the first 10 min) also correlated significantly (p<0’ 001) with the initial (20 min) rise in plasma neurotensin concentration in all the patients (correlation coefficient r=0’62, n = 73, method of least squares). These results suggest that the exaggerated release of neurotensin in the subjects with dumping symptoms may occur as a result of the rapid passage of glucose from the stomach into the neurotensin-rich ileum. The role of increased neurotensin in these patients still remains speculative. Its vasoactive properties may contribute to the symptoms of those patients whose circulatory system is already compromised by splanchnic pooling of circulatory fluid in the lumen of the bowel. levels of plasma neurotensin delay gastric emptying and high plasma concentrations of neurotensin may therefore operate to provide some compensation for the rapid emptying of nutrients from the stomach. We agree with your editorial that neurotensin may not have a primary causative role in the dumping syndrome, as we were careful to state in the original publication, but do not agree that it is therefore of no importance. The dramatic humoral abnormalities that have been described in this condition may be responsible for its primary or secondary features. Unravelling these complex interrelationships will take time, but will eventually result in a far greater understanding of water,
CURRENT STATUS OF JEJUNOILEAL BYPASS FOR MORBID OBESITY
was
Physiological
gastrointestinal physiology. Royal Postgraduate Medical School, London W 120HS
Six,-The gastric bypass or partition operation offers an alterto jejunoileal bypass for the surgical treatment of morbid
native
obesity. Since initially described by Mason in 1966,1 it is estimated that over 2500 operations have been done. The weight loss at one year is a mean of 42 kg and there have been minimal metabolic and electrolyte complications, as previously reported with intestinal bypass. approach of those clinicians who have published jejunoileal bypass in the management of morbid obesity, I wrote to them asking for details of their current practice and received replies from six in North America, two in Scandinavia, and two in the U.K. (table). Four have now stopped doing jejunoileal bypass and a fifth is doing it only in patients with obesity associated with severe hyperlipidaemia. Of the five still using this operation, three do end-to-end and two end-to-side jejunoileal anastomoses. The length of small bowel left in continuity varies from 35 cm to 62 - 5 cm, leaving a longer length of ileum than before. Two are adding an anastomosis between gallbladder and the blind end of the jejunum in the hope of decreasing some aspects of the blind-loop syndrome. Two centres are currently not involved in treating morbidly obese patients by surgery although they hope to try and assess gastric bypass in the future. Six groups are currently undertaking gastric bypass procedures for obesity and tending to use autosuture stapling instruments. Most respondents mention the careful selection of patients for operation and the possible need for this type of surgery to be restricted to specialised centres, especially with regard to preoperative assessment and postoperative management. assess
the
current
on
5. Blackburn
AM, Bloom SR. A radioimmunoassay for neurotensin in human plasma J Endocrinol 1953, 93: 175-81 1 Mason EE, Printen KJ. Gastric bypass for obesity. In Buchwald H, Varcor L, eds. Metabolic surgery. New York. Grune & Stratton, 1978: 41-57
bypass done. fWith bilio-intestinal shunt.
Scott correctly points out that: "... the malignant abuse of these operations will result in deterioration of the surgical approach to morbid obesity ... if this happens, it will be tragic!" Department of Surgery, University of Cincinnati Medical Center, Cincinnati, Ohio 45267, U.S.A.
A. M. BLACKBURN S. R. BLOOM
CURRENT STATUS OF JEJUNOILEAL BYPASS FOR OBESITY
To
*End-to-end
STEPHEN N. JOFFE
CYTOLOGY IN RECTOSIGMOID CANCER
SIR,-Following the observations of Webb,’ we have used digital scrape cytology as a routine diagnostic aid in a general surgical outpatients clinic. Rectal examination is done with a ’Disposaglove’ (Arbrook Ltd, Kirkton Campus, Livingston, Scotland), with a fusion ridge on the finger edge. When a palpably suspicious area is found, the ridge sweeps across the ulcerated or polypoid surface. Any tissue or blood is dabbed onto a glass microscope slide and air dried, stained by May-Grunwald Giemsa with interpretation, if necessary, within minutes. For lesions above 8 cm, a dental roll held by forceps is passed through a sigmoidoscope. 81 patients were examined. 3 smears were inadequate, with only faecal debris present. In 58 cases cytology and histology were in accord ; in 9 cases the cytology report was "suspicious"; in 7 cases with negative cytology no histology was done; in 4 the cytology and histology reports differed. 34 cases of adenocarcinoma and 4 cases of squamous cell carcinoma were correctly reported cytologically. There were 20 cases in which no malignant cells were seen and histologically these were subsequently confirmed as benign. 9 cases were reported as either 2.
Bray GA, Greenway FL, Barry RE et al. Surgical treatment of obesity: a review of our experience and an analysis of published reports. Int J Obesity 1977; 1: 331-67. 3. Buchwald H. Surgical approaches for failed jejunoileal bypass and failed gastric bypass: Morbid obesity. Surg Clins N Am 1979; 59: 1121-30. 4. Payne JH, DeWind LT. Surgical treatment of obesity. Am J Surg 1969; 118: 141-47 5. Phillips RB. Small intestinal bypass for the treatment of morbid obesity: Collective reviews. Surg Gynecol Obstet 1978; 146: 455-68. 6. Scott HW Jr, Dean RH, Shull JS, Gluck F Results of jejunoileal bypass in 200 patients with morbid obesity. Surg Gynecol Obstet 1977, 145: 661-73. 7. Salmon PA. The results of small intestine bypass operations for the treatment of obesity Surg Gynecol Obstet 1971; 132: 965-79. 8. Quaade F. Jejunoileal bypass for morbid obesity Morbid obesity. Surg Clins N Am 1979; 59: 1055-69
Hallberg D, Holmgren U. Bilio-intestinal shunt. Acta Chir Scand 1979; 145: 408 Baddeley RM. The management of gross refractory obesity by jejunoileal bypass Br J Surg 1979; 66: 525-32. 11. Gazet J-C, Pilkington TRE, Kalucy RS, Crisp AH, Day S. Treatment of gross obesity by jejunal bypass. Br Med J 1974; ii: 311-16. 1. Webb AJ. Cytologic diagnosis of anorectal and rectosigmoid lesions by a simple smear technique. Acta Cytol 1979; 23: 524. 9. 10.