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VENOUS MESENTERIC ISCHAEMIA: CONSERVATIVE OR SURGICAL TREATMENT?
48 VENOUS MESENTERIC ISCHAEMIA: CONSERVATIVE OR SURGICAL TREATMENT?
SIR,-Venous mesenteric ischaemia (VMI) is rare constituting less than 20% of all mesenteric infarctions, typically involves a limited segment of the small bowel, and has a better prognosis than either arterial or non-occlusive ischaemia.1-s Using contrastenhanced computerised tomographic (CT) scanning we described a typical triad of mesenteric venous thrombosis recognisable by an area of hypodensity in the trunk of the superior mesenteric vein, thickening of the intestinal wall and valvulae conniventes localised in a jejuno-ileal segment, and a significant amount of peritoneal fluid.6 With this triad immediate laparotomy is indicated. Increasing experience has now shown that peritoneal fluid is sometimes absent, a finding which may correlate with disease
severity. In a previous retrospective surgical study of venous mesenteric infarction,4there was a significant amount of haemorrhagic ascites in all cases of irreversible bowel ischaemia (ie, requiring resection). Similarly, at our hospital, in twelve patients who underwent bowel resection for VMI over a 12-year period, serosanguineous peritoneal fluid was always found. VMI was diagnosed by CT in ten patients, four of whom had the triad and therefore underwent immediate laparotomy, which showed irreversible infarction of a bowel segment. Histological examination of the resected section revealed transmural infarction in all cases. The other six patients had no peritoneal fluid to complete the CT triad, and since their clinical presentation was reassuring, they were initially treated conservatively. Five of these six non-ascitic patients had no further complications. Four of them had received therapeutic doses of intravenous heparin while the fifth received subcutaneous prophylactic doses of heparin for only 3 weeks because of concomitant oesophageal varices. The other non-ascitic patient, despite full-dose heparin, had persistent abdominal pain and a high degree of leucocytosis. CT 72 h later showed a slight peritoneal fluid collection, and the patient was put under observation. Abdominal ultrasonography 24 h later revealed a significant amount of peritoneal fluid extending throughout the peritoneal cavity. Although the patient’s general condition was stable and there were no metabolic abnormalities, anticoagulation was reduced and the patient was operated on 8 h later. Typical elements of VMI were found-namely, serosanguineous ascites, blue-black bowel with thickened wall involving 50 cm of ileum, and an ischaemic gradient along 5 cm of both infarction limits. A large resection 15 cm from the limit of the diseased bowel was done.4 Intravenous heparin in therapeutic doses was restarted postoperatively. The median follow-up of the six non-ascitic patients was 3-5years (range 6 months to 7 years). All patients treated with full doses of heparin, including the patient who had also undergone secondary surgery, received coumarin orally for about 6 months; none had further episodes. The patient who did not receive anticoagulation had two similar episodes of VMI 6 months and 3 years later, with spontaneous recovery; both episodes were investigated by CT and neither was accompanied by ascites. These results strongly suggest that the presence of peritoneal fluid correlates with the potential reversibility of VMI. Contrastenhanced CT is the best method for diagnosing VMI (presence of mesenteric venous thrombosis associated with segmental ileus with a thickened wall). The triad is in itself an absolute indication for immediate surgery. Large intestinal resection followed postoperatively by long-term anticoagulation to prevent early and late recurrences should be the rule.2,5 In the absence of peritoneal fluid, conservative therapy seems reasonable including, if not contraindicated, full-dose intravenous heparin. Serial CT or ultrasonography should be used to monitor closely the potential formation of peritoneal fluid. In cases of secondary accumulation of peritoneal fluid, surgery must be done immediately after reducing anticoagulation. It is unlikely this would adversely affect the prognosis, since ischaemia due to mesenteric venous thrombosis proceeds slowly and involves a limited segment of the bowel, generally jejunum or ileum.1-s Although we consider this therapeutic strategy valid in most cases of VMI (ie, when idiopathic, associated with coagulopathy or other predisposing diseases, or due
portal vein thrombosis), the origin of ascites in cirrhotic patients may be difficult to establish. In such cases serosanguineous fluid obtained by paracentesis would confirm an origin from infarcted to
bowel. Department of Digestive Surgery, University Hospital, Geneva, Switzerland *Present address: IX5
PIERRE-ALAIN CLAVIEN* OLIVIER HUBER ADRIEN ROHNER
department of surgery, University of Toronto, Toronto, Canada M5G
1. Ottinger LW. Mesenteric ischemia. N Engl J Med 1982; 307: 535-37. 2. Grendell JH, Ockner RK. Mesenteric venous thrombosis. Gastroenterology 1982; 82: 358-72. 3. Clavien PA, Muller C, Harder F. Treatment of mesenteric infarction. Br J Surg 1987; 74: 500-03 4. Clavien PA, Dung M, Harder F. Venous mesenteric infarction: a particular entity. Br J Surg 1988; 75: 333-36. 5. Abdu R, Zakhour BJ, Dallis DJ. Mesenteric venous thrombosis 1911-1984. Surgery 1987; 101: 383-88. 6. Clavien PA, Huber O, Mirescu D, Rohner A. Contrast enhanced CT scan as a diagnostic modality in mesenteric ischaemia due to mesenteric venous thrombosis. Br J Surg 1989; 76: 93-94.
MITRAL VALVE PROLAPSE
SIR,—Your May 27 editorial provides a good synopsis of current views. Mitral valve prolapse, a mitral valve with a billowing leaflet,1 is increasingly diagnosed clinically in young people and readily confirmed by echocardiography. However, it is not correct to label a billowing mitral valve leaflet as abnormal when it may occur, as you say, in up to 15 % of the population. In fact, the true prevalence for the whole population is about 4%, when appropriate diagnostic criteria are used.2 It is commoner in young women (prevalence about 5%) than in men (about 3%). Your figure of up to 15% must have been derived from early echocardiographic surveys when there was a high rate of false positives.2 Most subjects with mitral valve prolapse have no ill-effects and a normal life-span. Indeed, because as a group they are slim3,4 and tend to have low normal blood pressurethey may be at reduced risk of vascular disease. Thus they should not be labelled as having a cardiac abnormality. The issue is not merely semantic. It is true that aggregation occurs in "primary" mitral valve prolapse (ie, that unrelated to a systematic disorder of connective tissue such as Marfan’s syndrome, osteogenesis imperfecta, and Ehlers-Danlos variants) and that in some cases it appears to be inherited as an autosomal dominant trait. But for most a polygenic inheritance is likely.s To assess this it is necessary to examine a truly random population and not just a population of families of index patients in which several family members are already known to have murmurs.
With respect to uncertainties surrounding the natural history and prognosis for individual symptom-free cases, there are Australian data for the two commonest life-threatening complications, severe regurgitation and endocarditis. By age 60 years, about 0-7% of women and 1-9% of men with billowing leaflets after the growth spurt of adolescence will be expected to require mitral valve surgery for severe regurgitation; and there is a doubling of risk to about 1-2% and 3-6%, respectively, by age 70 years." There is evidence that these progressive changes in the valve leaflets are the result of repetitive minor injury and repair, because of the redundant valve tissue." This hypothesis is based upon collagen and mucopolysaccharide analyses of prolapsed myxomatous mitral valves, their histological appearances, and the natural history of primary "leaflet billowing". Since injury and repair-related myxomatous change results in valve thickening and regurgitation, detection of thickened leaflets and a dilated left atrium at echocardiography should predict enhanced risks of severe regurgitation and chordal rupture. This has been shown to be the case.9 The risk of endocarditis, which is virtually confined to those subjects with regurgitation and an audible murmur, will occur in about 1 in 1400 prolapse subjects per year. As you state, this is thirty-five times greater than the probability in a prolapse subject without a murmur;the risk in men is two to three times that in women.
You refer to mitral valve replacement for due to prolapse, which must be
regurgitation
severe
mitral
uncommon
in
SIR,-Venous mesenteric ischaemia (VMI) is rare constituting less than 20% of all mesenteric infarctions, typically involves a limited segment of the small bowel, and has a better prognosis than either arterial or non-occlusive ischaemia.1-s Using contrastenhanced computerised tomographic (CT) scanning we described a typical triad of mesenteric venous thrombosis recognisable by an area of hypodensity in the trunk of the superior mesenteric vein, thickening of the intestinal wall and valvulae conniventes localised in a jejuno-ileal segment, and a significant amount of peritoneal fluid.6 With this triad immediate laparotomy is indicated. Increasing experience has now shown that peritoneal fluid is sometimes absent, a finding which may correlate with disease
severity. In a previous retrospective surgical study of venous mesenteric infarction,4there was a significant amount of haemorrhagic ascites in all cases of irreversible bowel ischaemia (ie, requiring resection). Similarly, at our hospital, in twelve patients who underwent bowel resection for VMI over a 12-year period, serosanguineous peritoneal fluid was always found. VMI was diagnosed by CT in ten patients, four of whom had the triad and therefore underwent immediate laparotomy, which showed irreversible infarction of a bowel segment. Histological examination of the resected section revealed transmural infarction in all cases. The other six patients had no peritoneal fluid to complete the CT triad, and since their clinical presentation was reassuring, they were initially treated conservatively. Five of these six non-ascitic patients had no further complications. Four of them had received therapeutic doses of intravenous heparin while the fifth received subcutaneous prophylactic doses of heparin for only 3 weeks because of concomitant oesophageal varices. The other non-ascitic patient, despite full-dose heparin, had persistent abdominal pain and a high degree of leucocytosis. CT 72 h later showed a slight peritoneal fluid collection, and the patient was put under observation. Abdominal ultrasonography 24 h later revealed a significant amount of peritoneal fluid extending throughout the peritoneal cavity. Although the patient’s general condition was stable and there were no metabolic abnormalities, anticoagulation was reduced and the patient was operated on 8 h later. Typical elements of VMI were found-namely, serosanguineous ascites, blue-black bowel with thickened wall involving 50 cm of ileum, and an ischaemic gradient along 5 cm of both infarction limits. A large resection 15 cm from the limit of the diseased bowel was done.4 Intravenous heparin in therapeutic doses was restarted postoperatively. The median follow-up of the six non-ascitic patients was 3-5years (range 6 months to 7 years). All patients treated with full doses of heparin, including the patient who had also undergone secondary surgery, received coumarin orally for about 6 months; none had further episodes. The patient who did not receive anticoagulation had two similar episodes of VMI 6 months and 3 years later, with spontaneous recovery; both episodes were investigated by CT and neither was accompanied by ascites. These results strongly suggest that the presence of peritoneal fluid correlates with the potential reversibility of VMI. Contrastenhanced CT is the best method for diagnosing VMI (presence of mesenteric venous thrombosis associated with segmental ileus with a thickened wall). The triad is in itself an absolute indication for immediate surgery. Large intestinal resection followed postoperatively by long-term anticoagulation to prevent early and late recurrences should be the rule.2,5 In the absence of peritoneal fluid, conservative therapy seems reasonable including, if not contraindicated, full-dose intravenous heparin. Serial CT or ultrasonography should be used to monitor closely the potential formation of peritoneal fluid. In cases of secondary accumulation of peritoneal fluid, surgery must be done immediately after reducing anticoagulation. It is unlikely this would adversely affect the prognosis, since ischaemia due to mesenteric venous thrombosis proceeds slowly and involves a limited segment of the bowel, generally jejunum or ileum.1-s Although we consider this therapeutic strategy valid in most cases of VMI (ie, when idiopathic, associated with coagulopathy or other predisposing diseases, or due
portal vein thrombosis), the origin of ascites in cirrhotic patients may be difficult to establish. In such cases serosanguineous fluid obtained by paracentesis would confirm an origin from infarcted to
bowel. Department of Digestive Surgery, University Hospital, Geneva, Switzerland *Present address: IX5
PIERRE-ALAIN CLAVIEN* OLIVIER HUBER ADRIEN ROHNER
department of surgery, University of Toronto, Toronto, Canada M5G
1. Ottinger LW. Mesenteric ischemia. N Engl J Med 1982; 307: 535-37. 2. Grendell JH, Ockner RK. Mesenteric venous thrombosis. Gastroenterology 1982; 82: 358-72. 3. Clavien PA, Muller C, Harder F. Treatment of mesenteric infarction. Br J Surg 1987; 74: 500-03 4. Clavien PA, Dung M, Harder F. Venous mesenteric infarction: a particular entity. Br J Surg 1988; 75: 333-36. 5. Abdu R, Zakhour BJ, Dallis DJ. Mesenteric venous thrombosis 1911-1984. Surgery 1987; 101: 383-88. 6. Clavien PA, Huber O, Mirescu D, Rohner A. Contrast enhanced CT scan as a diagnostic modality in mesenteric ischaemia due to mesenteric venous thrombosis. Br J Surg 1989; 76: 93-94.
MITRAL VALVE PROLAPSE
SIR,—Your May 27 editorial provides a good synopsis of current views. Mitral valve prolapse, a mitral valve with a billowing leaflet,1 is increasingly diagnosed clinically in young people and readily confirmed by echocardiography. However, it is not correct to label a billowing mitral valve leaflet as abnormal when it may occur, as you say, in up to 15 % of the population. In fact, the true prevalence for the whole population is about 4%, when appropriate diagnostic criteria are used.2 It is commoner in young women (prevalence about 5%) than in men (about 3%). Your figure of up to 15% must have been derived from early echocardiographic surveys when there was a high rate of false positives.2 Most subjects with mitral valve prolapse have no ill-effects and a normal life-span. Indeed, because as a group they are slim3,4 and tend to have low normal blood pressurethey may be at reduced risk of vascular disease. Thus they should not be labelled as having a cardiac abnormality. The issue is not merely semantic. It is true that aggregation occurs in "primary" mitral valve prolapse (ie, that unrelated to a systematic disorder of connective tissue such as Marfan’s syndrome, osteogenesis imperfecta, and Ehlers-Danlos variants) and that in some cases it appears to be inherited as an autosomal dominant trait. But for most a polygenic inheritance is likely.s To assess this it is necessary to examine a truly random population and not just a population of families of index patients in which several family members are already known to have murmurs.
With respect to uncertainties surrounding the natural history and prognosis for individual symptom-free cases, there are Australian data for the two commonest life-threatening complications, severe regurgitation and endocarditis. By age 60 years, about 0-7% of women and 1-9% of men with billowing leaflets after the growth spurt of adolescence will be expected to require mitral valve surgery for severe regurgitation; and there is a doubling of risk to about 1-2% and 3-6%, respectively, by age 70 years." There is evidence that these progressive changes in the valve leaflets are the result of repetitive minor injury and repair, because of the redundant valve tissue." This hypothesis is based upon collagen and mucopolysaccharide analyses of prolapsed myxomatous mitral valves, their histological appearances, and the natural history of primary "leaflet billowing". Since injury and repair-related myxomatous change results in valve thickening and regurgitation, detection of thickened leaflets and a dilated left atrium at echocardiography should predict enhanced risks of severe regurgitation and chordal rupture. This has been shown to be the case.9 The risk of endocarditis, which is virtually confined to those subjects with regurgitation and an audible murmur, will occur in about 1 in 1400 prolapse subjects per year. As you state, this is thirty-five times greater than the probability in a prolapse subject without a murmur;the risk in men is two to three times that in women.
You refer to mitral valve replacement for due to prolapse, which must be
regurgitation
severe
mitral
uncommon
in