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INTRUMENTAL PERFORATION OF THE OESOPHAGUS
1279
Lead poisoning exists in two fundamentally different forms depending on duration of exposure. With long-term overexposure, such as is found commonly in environmental lead poisoning, large stores of lead accumulate in bone which contains more than 90% of the total body burden. This lead is not generally- bioavailable: in cases of industrial exposure blood lead concentrations fall very slowly when the source is removed;3 and in longstanding cases of industrial poisoning managed by chelation, suspension of therapy is followed by a rapid rise in blood lead as the blood re-equilibrates with the much larger pool of stored lead in bone. In animals, which show the same effect, continuous therapy has proved ineffective in removing lead because of the inability of the organs to make any more of the metal available for chelation.4 The reasons for the ineffectiveness of chelation in these circumstances may be sought in the disparity between the magnitude of body stores of lead (and hence soft tissue and circulating lead concentrations) and the quantity of leld likely to be excreted in any one course of chelation. In exposed subjects body stores may be 200 mg or higher, whilst the quantity of lead cleared in one week’s therapy will seldom exceed 5 mg. In acute short-term exposure the position is different. Although soft-tissue concentrations of lead are high, stores are less, so this type responds well to chelation (and is perhaps more typical of lead poisoning in children). Some test that indicates the type of poisoning will clearly be helpful, and decisions on chelation therapy have generally rested on measurement of blood lead concentrations-the most reliable index of overexposure. Secondary criteria include erythrocyte protoporphyrin concentrations, which are an effective measure of exposure for blood lead concentrations exceeding 40 µg/dl though of little help at normal environmental exposure levels, and the activity of erythrocyte 5-aminolaevulinate dehydratase, an enzyme highly sensitive to the toxic influences of this metal. Another secondary measure of some value is based on urinary clearance of lead after a single dose of the chelating agent edetic acid (EDTA). 8-hour tests seem no less effective than the 24-hour tests formerly recommended, and it is proposed6 that where lead excretion exceeds 200 µg in 8 hours, or where the ratio of lead excreted (in µg) to CaEDTA administered (in mg) exceeds 0-7, chelation therapy should be started. The greatest weakness of this test is that it depends on measurement of which is less accurate than blood urinary lead concentrations, lead measurement.7 Furthermore in children, and particularly infants, it is difficult to be certain of obtaining complete urine collections. Decisions on treatment will then be guided principally by blood lead measurement. For assessment of treatment outcome in the individual child there is much to be said for combination of these two measures. Chelation therapy, which promotes loss of many essential cations as well as lead, should not be lightly undertaken. The search is on for more specific chelating agents. One of the
dimercaptopropane sulphonate,8 shows much and it and its analogues, such as 2,3-dimercaptosuccinic acid,9 may well supersede EDTA and penicillamine in the treatment of heavy-metal poisoning. newest,
promise
,
INTRUMENTAL PERFORATION OF THE OESOPHAGUS OESOPHAGEAL perforation, the most rapidly fatal and most serious perforation of the gastrointestinal tract,’ does not strike quite the same fear in endoscopists’ hearts that it did before the advent of fibreoptic instruments. Rigid diagnostic oesophagoscopy, for which there is still a limited place, has an instrumental perforation rate between 1% and 0.1%2 compared with around 0-01% for flexible instrumentation3 (when damage nearly always arises during difficult intubation). Although these are very rough estimates and the patients treated in different studies vary greatly, it is a reasonable assumption that wider use of the flexible oesophago-gastroscope should reduce the rate of perforation.4 But will it reduce the total number of perforations and mortality in an ageing population investigated by the increasing number of doctors capable of
wielding a fibrescope?
Traditionally, the treatment of oesophageal perforation has been aggressively surgical,2,5 and results have improved with advances in diagnostic radiology, blood transfusion, antibiotics, anaesthesia, parenteral nutrition, and intensive care unit management, as well as surgical technique. There is a surgical adage that the cervical oesophagus is the only part where conservative treatment is likely to be successful,6 but Wesdorp et a17 now describe the non-operative management of all but 5 of 54 consecutive fibreoptic instrumental perforations of the oesophagus arising over ten years in a hospital with great experience of gastrointestinal endoscopy. 35 of the 54 perforations occurred during intubation of malignant strictures, and the death rate in these was 8’ 6%; there were no deaths in the non-malignant group. These excellent results were attributed to early diagnosis (over 90% of the perforations being detected within two hours) and "active" conservative treatment-ie, not only avoidance of oral intake and wise use of antibiotics, but also intravenous feeding and continuous naso-oesophageal suction for five to seven days via a special tube with multiple side-holes both above and below the site of perforation. There will always be a place for early surgical intervention after instrumental damage to the oesophagus-for instance, in young patients with extensive tears associated with non-malignant disease-but good non-operative treatment has a high chance of success in the older patient with lesser damage caused by a flexible instrument and diagnosed very early.
8.
3 Araki
S, Murata K, Aono H, Yanagihara S, Ushio K. A comparison ofthe diminution
blood and lead mobilised by CaEDTA after termination of occupational exposure A long-term observation in two lead workers. J Toxicol Clin Toxicol 1983, 20: 475-86. 4. Schworer I, Kaul A Tierexperimentelle Untersuchungen uber die Elimination von inkorporiertem Blei unter biologischen Strebsituationen und Applikation von Na2Ca-EDTA. J Clin Chem Clin Biochem 1980; 18: 163-68 5 Moore MR, Meredith PA, Goldberg A. Lead and haem biosynthesis. In Singhal RL, Thomas JA, eds Lead toxicity. Baltimore- Urban & Schwartzenberg, 1979 rates
of lead
80-114 6. 7.
9
in
Markowitz ME, Rosen JF. Assessment of lead stores in children, validation of an 8 hour CaNa2EDTA test. J Pediatr 1984; 104: 337-41. Department of Health and Social Security. Lead and health. London: HMSO, 1980.
1 2
3
Twarog T, Cherian MG. Chelation of lead by dimercaptopropane sulfonate and a possible diagnostic use. Toxicol Appl Pharmacol 1984; 72: 550-56 Graziano JH, Leong JK, Friedheim E 2,3-dimercaptosuccinic acid: a new agent for the treatment of lead poisoning. J Pharmacol Exp Ther 1978; 206: 696-700. Sealy WC Rupture of the esophagus Am J Surg 1963, 105: 505-10. Sandrasagra FA, English TAH, Milstein BB. The management and prognosis of oesophageal perforation. Br J Surg 1978, 65: 629-32.
Dawson J, Cockel R. Oesophageal perforation at fibreoptic gastroscopy. Br Med J 1981,
283: 583 4. Editorial Management of oesophageal perforation. Br Med J 1977, ii: 540. 5 Ghosh BC, Chaudry KU, Beattie EJ Jr Perforation of the esophagus. Surg Gynecol Obstet 1972, 135: 729-31. 6 Editorial. The leaking oesophagus Lancet 1977, ii: 692-93. 7. Wesdorp ICE, Bartelsman JFWM, Huibregtse K, Den Hartog Jager FCA, Tytgat GN. Treatment of instrumental oesophageal perforation Gut 1984; 25: 398-404
Lead poisoning exists in two fundamentally different forms depending on duration of exposure. With long-term overexposure, such as is found commonly in environmental lead poisoning, large stores of lead accumulate in bone which contains more than 90% of the total body burden. This lead is not generally- bioavailable: in cases of industrial exposure blood lead concentrations fall very slowly when the source is removed;3 and in longstanding cases of industrial poisoning managed by chelation, suspension of therapy is followed by a rapid rise in blood lead as the blood re-equilibrates with the much larger pool of stored lead in bone. In animals, which show the same effect, continuous therapy has proved ineffective in removing lead because of the inability of the organs to make any more of the metal available for chelation.4 The reasons for the ineffectiveness of chelation in these circumstances may be sought in the disparity between the magnitude of body stores of lead (and hence soft tissue and circulating lead concentrations) and the quantity of leld likely to be excreted in any one course of chelation. In exposed subjects body stores may be 200 mg or higher, whilst the quantity of lead cleared in one week’s therapy will seldom exceed 5 mg. In acute short-term exposure the position is different. Although soft-tissue concentrations of lead are high, stores are less, so this type responds well to chelation (and is perhaps more typical of lead poisoning in children). Some test that indicates the type of poisoning will clearly be helpful, and decisions on chelation therapy have generally rested on measurement of blood lead concentrations-the most reliable index of overexposure. Secondary criteria include erythrocyte protoporphyrin concentrations, which are an effective measure of exposure for blood lead concentrations exceeding 40 µg/dl though of little help at normal environmental exposure levels, and the activity of erythrocyte 5-aminolaevulinate dehydratase, an enzyme highly sensitive to the toxic influences of this metal. Another secondary measure of some value is based on urinary clearance of lead after a single dose of the chelating agent edetic acid (EDTA). 8-hour tests seem no less effective than the 24-hour tests formerly recommended, and it is proposed6 that where lead excretion exceeds 200 µg in 8 hours, or where the ratio of lead excreted (in µg) to CaEDTA administered (in mg) exceeds 0-7, chelation therapy should be started. The greatest weakness of this test is that it depends on measurement of which is less accurate than blood urinary lead concentrations, lead measurement.7 Furthermore in children, and particularly infants, it is difficult to be certain of obtaining complete urine collections. Decisions on treatment will then be guided principally by blood lead measurement. For assessment of treatment outcome in the individual child there is much to be said for combination of these two measures. Chelation therapy, which promotes loss of many essential cations as well as lead, should not be lightly undertaken. The search is on for more specific chelating agents. One of the
dimercaptopropane sulphonate,8 shows much and it and its analogues, such as 2,3-dimercaptosuccinic acid,9 may well supersede EDTA and penicillamine in the treatment of heavy-metal poisoning. newest,
promise
,
INTRUMENTAL PERFORATION OF THE OESOPHAGUS OESOPHAGEAL perforation, the most rapidly fatal and most serious perforation of the gastrointestinal tract,’ does not strike quite the same fear in endoscopists’ hearts that it did before the advent of fibreoptic instruments. Rigid diagnostic oesophagoscopy, for which there is still a limited place, has an instrumental perforation rate between 1% and 0.1%2 compared with around 0-01% for flexible instrumentation3 (when damage nearly always arises during difficult intubation). Although these are very rough estimates and the patients treated in different studies vary greatly, it is a reasonable assumption that wider use of the flexible oesophago-gastroscope should reduce the rate of perforation.4 But will it reduce the total number of perforations and mortality in an ageing population investigated by the increasing number of doctors capable of
wielding a fibrescope?
Traditionally, the treatment of oesophageal perforation has been aggressively surgical,2,5 and results have improved with advances in diagnostic radiology, blood transfusion, antibiotics, anaesthesia, parenteral nutrition, and intensive care unit management, as well as surgical technique. There is a surgical adage that the cervical oesophagus is the only part where conservative treatment is likely to be successful,6 but Wesdorp et a17 now describe the non-operative management of all but 5 of 54 consecutive fibreoptic instrumental perforations of the oesophagus arising over ten years in a hospital with great experience of gastrointestinal endoscopy. 35 of the 54 perforations occurred during intubation of malignant strictures, and the death rate in these was 8’ 6%; there were no deaths in the non-malignant group. These excellent results were attributed to early diagnosis (over 90% of the perforations being detected within two hours) and "active" conservative treatment-ie, not only avoidance of oral intake and wise use of antibiotics, but also intravenous feeding and continuous naso-oesophageal suction for five to seven days via a special tube with multiple side-holes both above and below the site of perforation. There will always be a place for early surgical intervention after instrumental damage to the oesophagus-for instance, in young patients with extensive tears associated with non-malignant disease-but good non-operative treatment has a high chance of success in the older patient with lesser damage caused by a flexible instrument and diagnosed very early.
8.
3 Araki
S, Murata K, Aono H, Yanagihara S, Ushio K. A comparison ofthe diminution
blood and lead mobilised by CaEDTA after termination of occupational exposure A long-term observation in two lead workers. J Toxicol Clin Toxicol 1983, 20: 475-86. 4. Schworer I, Kaul A Tierexperimentelle Untersuchungen uber die Elimination von inkorporiertem Blei unter biologischen Strebsituationen und Applikation von Na2Ca-EDTA. J Clin Chem Clin Biochem 1980; 18: 163-68 5 Moore MR, Meredith PA, Goldberg A. Lead and haem biosynthesis. In Singhal RL, Thomas JA, eds Lead toxicity. Baltimore- Urban & Schwartzenberg, 1979 rates
of lead
80-114 6. 7.
9
in
Markowitz ME, Rosen JF. Assessment of lead stores in children, validation of an 8 hour CaNa2EDTA test. J Pediatr 1984; 104: 337-41. Department of Health and Social Security. Lead and health. London: HMSO, 1980.
1 2
3
Twarog T, Cherian MG. Chelation of lead by dimercaptopropane sulfonate and a possible diagnostic use. Toxicol Appl Pharmacol 1984; 72: 550-56 Graziano JH, Leong JK, Friedheim E 2,3-dimercaptosuccinic acid: a new agent for the treatment of lead poisoning. J Pharmacol Exp Ther 1978; 206: 696-700. Sealy WC Rupture of the esophagus Am J Surg 1963, 105: 505-10. Sandrasagra FA, English TAH, Milstein BB. The management and prognosis of oesophageal perforation. Br J Surg 1978, 65: 629-32.
Dawson J, Cockel R. Oesophageal perforation at fibreoptic gastroscopy. Br Med J 1981,
283: 583 4. Editorial Management of oesophageal perforation. Br Med J 1977, ii: 540. 5 Ghosh BC, Chaudry KU, Beattie EJ Jr Perforation of the esophagus. Surg Gynecol Obstet 1972, 135: 729-31. 6 Editorial. The leaking oesophagus Lancet 1977, ii: 692-93. 7. Wesdorp ICE, Bartelsman JFWM, Huibregtse K, Den Hartog Jager FCA, Tytgat GN. Treatment of instrumental oesophageal perforation Gut 1984; 25: 398-404