Clinical, endoscopic, and laboratory data were collected prospectively in 701 patients with bleeding peptic ulcer. The overall rebleeding rate was 16.1% and increased the risk of a fatal outcome by 17 fold (1.2% versus 20.6%, p less than 0.001). Rebleeding was documented in more than 75% of the group who did not survive following initial conservative management. Rebleeding was more likely (24.1% versus 14.2%, p less than 0.02) when shock was present on admission and the risk of a rebleed was doubled in patients over 60 years of age (22.1% versus 10.9%, p less than 0.001). Ulcers greater than 1 cm in size carried twice the risk of rebleeding (23.9% versus 12.4%, p less than 0.002). Concomitant medical illness had a significant adverse effect on outcome (p less than 0.05). Shock on admission was associated with a doubling of mortality figures (9.5% versus 3.7%, p less than 0.01). The identification of endoscopic stigmata of recent hemorrhage (ESRH) tripled the risk of mortality (7.5% versus 2.4%, p less than 0.002), ESRH were more frequently encountered when ulcer size was larger than 1 cm (61.4% versus 39.8%, p less than 0.001). Respective mortality rates for ulcers less than or equal to 1 cm and greater than 1 cm in size were 1.6% and 12.5% (p less than 0.001), corresponding mortality figures for patients over 60 years of age being 4.4% and 16.4% (p less than 0.002). The risk of a rebleed tripled (6.7% versus 2.6%, p less than 0.02) when ESRH were evident. There was a 6-fold increase in mortality following emergency surgery when compared with conservative management of patients in whom no surgical intervention was necessary (2.6% versus 14.9%, p less than 0.001). In summary, age over 60 years, previous medical illness, shock on admission, large ulcer size, and ESRH were each associated with an increased risk of rebleeding and mortality.

Clinical and endoscopic data were collected prospectively in 1050 patients with bleeding peptic ulcer admitted between September 1985 and July 1989 to the care of one surgical team. Seventy-nine patients underwent therapeutic endoscopy soon after admission and in 129 patients either immediate or early elective surgery was performed. Eight hundred and forty-two patients, in whom therapeutic endoscopy was not performed at any stage, underwent initial conservative management and data from this latter group are now presented. Shock on admission was defined as systolic blood pressure (BP) less than or equal to 100 mmHg on presentation. There were 10 deaths of 147 shocked patients (6.8%) compared with only 25 deaths of 695 patients (3.6%) not in shock (P less than 0.08). Bleeding recurred in 30 patients (20.4%) shocked on presentation but in only 96 (13.8%) with a BP greater than 100 mmHg (P less than 0.05). Twenty-one of 358 patients (5.9%) with endoscopic stigmata of recent haemorrhage (ESRH) died, but only 14 of 484 patients (2.9%) without such stigmata (P less than 0.05) died. In shocked patients rebleeding was evident in 21 of 73 (28.8%) cases with ESRH but in only 9 of 74 (12.2%) patients in whom ESRH were absent (P less than 0.02). In the absence of fresh blood at endoscopy rebleeding occurred in 22 of 124 (17.8%) shocked patients and only 74 of 629 (11.8%) of those not shocked on presentation (P less than 0.07). When ulcer size was documented rebleeding rates for ulcers less than or equal to 1 cm, less than or equal to 2 cm and greater than 2 cm in size were 54 of 485 (11.1%), 30 of 142 (21.2%) and 12 of 44 (27.3%) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical laboratory and endoscopic data were collected prospectively in 268 patients with bleeding gastric ulcer who were admitted between September 1985 and November 1987. There were 22 deaths, giving a hospital mortality rate of 8.2%. Surgery was undertaken in 68 patients (25.4%) with a mollality rate of 17.6% (I I .8'K at 30 days). There was one fatality in 104 (1.0%) patients C 60 years compared with 21 deaths (12.8%) in patients > 60 years (P < 0.001). Cirrhosis (P < 0.01). malignant disease (P < 0.03). chronic obstructive airways disease (P < 0.02). congestive cardiac failure (P < 0.02) and ischaemic heart disease (P < 0.08) were each associated with an increased risk of mortality. Outcome in patients > 60 years was related to systolic blood pressure at admission (P < 0.03), haemoglobin (P < 0.02). serum bilirubin (P < 0.02), and total transfusion requirements (P < 0.001). For ulcers 4 I cm, I-< 2cm, > 2cm in size, mortality rates were 1.9%. 11.4% and 18.0%. respectively. Initial endoscopy findings of a visible vessel, fresh blood, or active spurtingloozing haemorrhage were associated with rebleeding rates necessitating emergency surgery of 30.0%. 36.4% and 40.0%. respectively. There was no evidence of rebleeding in 187 patients (79.9%) managed conservatively and only five patients (2.7%) in this group succumbed, whereas rebleeding did occur in 47 patients (20. I%) with 13 subsequent deaths (27.7%; P < 0.001). In patients > 60 years the presence of endoscopic stigmata of recent haemorrhage should lead to early consideration of therapeutic endoscopy and/or early surgery, particularly for ulcers > I cm in size.

I concur with your leading article concerning perforated duodenal ulcer (Br J Surg 1987; 74: 81-2). The implication that unnecessary definitive surgery in the acute state of management should be avoided must be correct; but why not take the argument one step further?The overall mortality rate today for patients with perforated peptic ulcer treated surgically is approximately'4 5 per cent. This is of the same order as that reported for conservative management in 1956'.A recent prospective randomized trial of non-operative uersus operative treatment for perforated duodenal ulcer6 has demonstrated the possibility of treating certain groups of patients by non-operative means.Such a treatment regimen would allow the subsequent definitive surgery to be undertaken on a properly selected group of patientsat time of relapse during medical therapy. Using this regimen as many as 75 per cent6 of all patients suffering perforation of a duodenal ulcer may completely escape the need for surgical intervention. T. J. CroftsUniuersity of Aberdeen Aberdeen AB9 2 2 0 U K I. 2.3. 4. 5.6. GrecoPS, Cahow CE. Alternatives in the management of acute perforated duodenal ulcer. Am J Surg 1974; 127: 109-14. b e y J, Wong J, Ong BG. A prospective study of operative risk factors in perforated duodenal ulcers. Ann Surg 1982; 195: 265-9. Sawyers JL, Herrington JL Jr, Mulherin JL Jr, Whitehead WA, Mody R. Acute perforated duodenal ulcer. Arch Surg 1975; 110: Coutsoptides T, Himal HS. Perforated gastroduodenal ulcers. ,4m J Surg 1976; 132: 575-30. Seeley SF, Campbell D. Nonoperative treatment of perforated

Enterostomy as an adjunct t o treatment of intra-abdominal sepsis SirWe were interested to read the paper by Hesp et al. (Br J Surg 1988; 75: 693-6). However, we were surprised to read that no data concerning the results of this technique were available in the literature.In the Surgical Digestive Intensive Care Unit of the HBpital Saint-Antoine, Paris, France, temporary enterostomies have been used since 1969 for this indication'. Many papers describing the results of this approach, together with the technique of chyme reinfusion, have been published in both French and English literat~re'.~. It is disappointing to see that the information on this subject does not appear to have been exhaustively researched before publication. P. FrileuxHBpital Saint-Antoine Paris Cddex 12 France Levy E, Parc R, Loygue J. Stomies terminales,jejunales ou ilekles temporaires de sauvetage avec reinstillation autoregulee. Nouu Presse Med 1977; 6 : 461-2. Levy E, Cugnenc PH, Parc R, Frileux P, Deliere T, Sales JP el al. Peritonites par le'sion de I'intestin grere. A propos de 217 cas. Ann Chir 1985; 39: 63141. Levy E, Donald LP, Frileux P, Parc R, Huguet C, Loygue J. Inhibition of upper gastrointestinal secretions by reinfusion of succus entericus into the distal small bowel. A clinical study of 30 patients with peritonitis and temporary enterostomy. Ann Sury 1983; 198: 596-600. Anatomical nit-picking? SirIn a survey of 30 anatomical or surgical textbooks regarding the surface anatomical marking of the deep inguinal ring, 14 stated that it was at the mid-inguinal point and nine that it was at the mid-point of the inguinal ligament. Six books gave no surface marking for the deep ring and one modestly or perhaps correctly stated that it was difficult to be sure.The other structure positioned at either of those two landmarks is the femoral artery and, again, with this the picture is almost as confused, with 18 putting it at the mid-inguinal point and only five at the mid-point of the inguinal ligament.The difference between the mid-inguinal point and the mid-point of the inguinal ligament is often practically non-existent (even a modest covering of adipose tissue can make the bony points difficult to locate without causing undue discomfort to the patient) and, therefore, it seems a rather archaic and even futile exercise to retain the two as separate entities. To be pedantic, the mid-inguinal point should actually be just above the inguinal ligament and thus pulsation felt at that point would be that of the external iliac artery and not the femoral artery.Surely it would be sensible to favour a more pragmatic approach, and teach students that when feeling for femoral artery pulsation and when attempting to occlude the deep ring in examination of hernias, they should use two fingers and therefore actually cover both anatomical points? P. D. Scott Manchester Royal Infirmary Manchester M I 3 9WL U K Growth rates in hepatic metastases SirWe would like to make some comments on the paper by Finlay et al. (Br J Surg 1988; 75: 6414) on growth r...

Lumacaftor/ivacaftor increases cystic fibrosis transmembrane conductance regulator (CFTR) activity and is an effective treatment for cystic fibrosis (CF) patients that are homozygous for the F508del mutation. We describe the case of an 18-year-old Irish man with F508del homozygous CF admitted to our centre with a rash affecting his arms and upper trunk. This occurred one day post completing a 14-day course of intravenous (IV) Piperacillin/Tazobactam and Tobramycin for an infective exacerbation of cystic fibrosis and day 9 post treatment with lumacaftor/ivacaftor. Skin punch biopsies were performed, and the features were consistent with erythema multiforme. Our patient received another dose of lumacaftor/ivacaftor 20 days after receiving the first dose. Ninety minutes after the receiving the dose, he developed a diffuse erythematous rash, similar to the initial presentation. Lumacaftor/ivacaftor was re-trailed once more 10 months later. Three hours after commencing treatment our patient developed a diffuse erythematous rash affecting his face, and upper torso along with conjunctival injection. This reaction was diagnosed as a cytokine release type reaction. There are no reported cases in the literature of a cytokine release type reaction to lumacaftor/ivacaftor resulting in its discontinuation. When assessing patients on lumacaftor/ivacaftor that have developed a rash, this should always be included in the differential as the underlying cause given its high incidence. Tezacaftor/ivacaftor is an alternative treatment for patients that have developed a severe reaction to lumacaftor/ivacaftor.