1045
diffusely hyperaemic or shows multiple erythematous areas outlined by a subtle yellowish or whitish network (mosaic pattern); in severe gastropathy there are discrete or confluent cherry red spots or diffuse mucosal haemorrhages. Only severe gastropathy causes clinically important bleeding. Apart from cherry red spots, the endoscopic appearances are non-specific and are identical to those seen in gastritis.2 However, the histological findings in the two conditions are different,2,11,13 although those of congestive gastropathy may not be readily apparent in the superficial biopsy specimens obtained via an endoscope.2°14 Vascular gastropathy is characterised by diffuse and pronounced dilatation of mucosal capillaries accompanied by mucosal oedema and perhaps diapedesis of erythrocyes, but with no or very
mucosa
EDITORIALS
Portal hypertensive gastropathy Non-variceal bleeding in portal hypertension has only lately received the attention it deserves. Among the reasons for this oversight are the more catastrophic nature and greater frequency of bleeding from oesophagogastric varices and a mistaken belief that the gastric mucosal lesions responsible for the bleeding were inflammatory in nature. Terms such as "acute gastritis", "erosive gastritis", "acute gastric ulcers", and "haemorrhagic gastritis" obscured the true nature of the mucosal abnormality and were responsible for inappropriate and ineffective treatment with antisecretory drugs. Realisation that the morphological change underlying non-variceal bleeding in portal hypertension is gross ectasia of the gastric mucosal capillaries and submucosal veins without inflammation led to the condition being renamed portal hypertensive gastropathyl (or congestive gastropathy2) and encouraged a reappraisal of pathogenesis and treatment. Bleeding from the gastric mucosa is a serious complication of portal hypertension. It may be insidious, presenting eventually with an irondeficiency anaemia, or sudden and severe, with haematemesis and melaena. Diffuse gastric lesions account for only 2% of all cases of upper gastrointestinal bleeding,3but they are the cause, in various reported series, of 10-70% of episodes of gastrointestinal haemorrhage in cirrhotic patients and 10-50% in those with portal hypertension.2,4-9 Most non-variceal bleeding in portal hypertension can be attributed to congestive gastropathy.7The risk of death from gastric mucosal haemorrhage is less than from variceal rupture, but bleeding is often sufficiently brisk or persistent to cause deterioration of liver function in patients with cirrhosis.’ Recurrent bleeding is common (62 % at 12 months after the initial haemorrhagel), although this high frequency partly reflects inappropriate treatment in the past. The risk of gastric mucosal bleeding may increase after successful sclerotherapy of oesophageal varices.22 The congestion of the gastric mucosa may be associated with hypochlorhydria, and there is experimental evidence of greater susceptibility to injury by noxious agents such as alcohol and aspirin. 11 Portal hypertensive gastropathy has been classified as mild or severe on the basis of endoscopic appearances.2,12,13 In the mild condition the gastric
is
small
little evidence of inflammation. The submucosal veins are dilated and tortuous. These features are confirmed by silicone rubber microvascular casts, which show dilated straight and non-spiral arterioles and arteriovenous shunts in the submucosa, dilated veins in the submucosa and subserosa, and dilated capillaries and precapillaries in the mucosa.15 Despite the belated realisation that non-variceal bleeding in portal hypertension has a vascular basis, much has still be be learned about its pathogenesis. The haemodynamic changes in the stomach wall could be a non-specific component of the overall changes in the splanchnic circulation in portal hypertension or the result of a local impairment of regulation of gastric vascular tone.16 All patients with portal hypertensive gastropathy have high portal pressures, but no correlation has been observed between gastric capillary ectasia and the degree of portal hypertension.2Gastric blood flow cannot be measured reproducibly in man so information about
gastric haemodynamic changes in portal hypertension is derived from observations in laboratory animals. Rats with portal hypertension have an increased total gastric blood flow with a lesser increase in mucosal flow and a reduced gastric vascular resistance.17-2o These changes are part of a disorder characterised by generalised splanchnic arteriolar vasodilatation, increased splanchnic blood flow, and reduced vascular sensitivity to noradrenaline.16,20 Humoral agents that have been implicated in the pathogenesis of the haemodynamic disturbances include glucagon, gastrin, and a prostaglandin. 13,1820 Portal decompressive surgery is effective in arresting haemorrhage and preventing rebleeding in portal hypertensive gastropathy, but the operative risks and high incidence of encephalopathy in cirrhotic patients limit the use of this approach.21 In view of the apparent similarity between the pathophysiological changes in patients with oesophagogastric varices and those with congestive gastropathy,16 the knowledge that variceal bleeding can be halted and recurrent bleeding prevented by beta-adrenergic blockade, and the evidence that propranolol reduces gastric mucosal blood flow in
1046
portal hypertensive rates,"21 it was logical to see whether beta-adrenergic antagonists were effective in severe gastric mucosal haemorrhage. Two small open studies have shown that propranolol stops such bleeding in almost all cases,23.24; in a randomised controlled trial in a larger number of patients the frequency of rebleeding was significantly reduced.1 The mechanism of the beneficial effect of propranolol is uncertain. There is no evidence yet that the long-term outcome of cirrhotic patients with severe portal hypertensive gastropathy, or those with bleeding varices, is improved by either surgery or beta-adrenergic blockade. 1.
Perez-Ayuso RM, Piqué JM, Bosch J, et al. Propanolol in prevention of recurrent bleeding from severe portal hypertensive gastropathy in cirrhosis. Lancet 1991; 337: 1431-34. TT, Sims J, Eyre-Brook I,
2. McCormack
hypertension: inflammatory gastritis
al. Gastric lesions in portal congestive gastropathy? Gut
et
or
1985; 26: 1226-32. 3.
Quintero E, Piqué JM, Bombi JA, et al. Upper gastrointestinal bleeding caused by gastroduodenal vascular malformations: incidence, diagnosis, and treatment. Dig Dis Sci 1986; 31: 897-905. 4. Dagradi AE, Mehler R, Tan DT, Stempien SJ. Sources of upper gastrointestinal bleeding in patients with liver cirrhosis and large esophagogastric varices. Am J Gastroenterol 1970; 54: 458-63. 5. Khodadoost J, Glass GBJ. Erosive gastritis and acute gastroduodenal ulcerations as source of upper gastrointestinal bleeding in liver cirrhosis. Digestion 1972; 7: 129-38. 6. Walram S, Davis M, Nunnerley H, et al. Emergency endoscopy after gastrointestinal haemorrhage in 50 patients with portal hypertension. Br Med J 1974; 4: 94-96. 7. Terés J, Bordas JM, Bru C, Diaz F, Bruguera M, Rodes J. Upper gastrointestinal bleeding in cirrhosis: clinical and endoscopic correlation. Gut 1976; 17: 37-40. 8. Thomas E, Rosenthal WS, Rymer W, Katz D. Upper gastrointestinal hemorrhage in patients with alcoholic liver disease and esophageal varices. Am J Gastroenterol 1979; 72: 623-29. 9. Rector WG, Reynolds TB. Risk factors for haemorrhage from oesophageal varices and acute gastric erosions. Clin Gastroenterol 1985; 14: 139-53. 10. Perez-Ayuso RM, Piqué JM, Saperas E, at al. Gastric vascular ectasias in cirrhosis: association with hypoacidity not related to gastric atrophy. Scand J Gastroenterol 1989; 24: 1073-78. 11. Tarnawski AS, Sarfeh IJ, Stachura J, et al. Microvascular abnormalities of the portal hypertensive gastric mucosa. Hepatology 1988; 8: 1488-94. 12. Papazian A, Braillon A, Dupas JL, Sevenet F, Capron JP. Portal hypertensive gastric mucosa: an endoscopic study. Gut 1986; 27: 1199-203. 13. Quintero E, Piqué JM, Bombi JA, et al. Gastric mucosal vascular ectasias causing bleeding in cirrhosis. Gastroenterology 1987; 93: 1054-61. 14. Foster PN, Wyatt JI, Bullimore DW, Losowsky MS. Gastric mucosa in patients with portal hypertension: prevalence of capillary dilatation and Campylobacter pylori. J Clin Pathol 1989; 42: 919-21. 15. Hashizume M, Tanaka K, Mokuchi K. Morphology of gastric microcirculation in cirrhosis. Hepatology 1983; 6: 1008-12. 16. Benoit JN, Granger DN. Splanchnic haemodynamics in chronic portal hypertension. Sem Liv Dis 1986; 6: 287-98. 17. Kitano S, Koyanasi K, Sugimachi M, Kobayashi M, Inokuchi K. Mucosal blood flow and modified vascular responses to norepinephrine in the stomach of rats with liver cirrhosis. Surg Res 1982; 14: 221-30. 18. Piqué JM, Leung FW, Kitahora T, Sarfeh IJ, Tarnawski A, Guth PH. Gastric mucosal blood flow and acid secretion in portal hypertensive rats. Gastroenterology 1988; 95: 727-33. 19. Piqué JM, Pizcueta P, Perez-Ayuso RM, Bosch J. Effects of propanolol on gastric microcirculation and acid secretion in portal hypertensive rats. Hepatology 1990; 12: 476-80. 20. Benoit JN, Womack WA, Korthuis RJ, Wilborn WH, Granger DN. Chronic portal hypertension: effects on gastrointestinal flow distribution. Am J Physiol 1986; 250: G535-39. 21. Sarfeh IJ, Juler GL, Stemmer EA, et al. Results of surgical management of hemorrhagic gastritis in patients with gastro-esophageal varices. Surg Gynecol Obstet 1982; 155: 167-70. 22. Kroeger RJ, Groszmann RJ. Effect of selective blockade of B2-adrenergic receptors on portal systemic hemodynamics in a portal hypertensive rat model. Gastroenterology 1985; 88: 896-900. 23. Quintero E, Piqué JM, Bombi JA, et al. Antral mucosal hyperaemia:
characterization of a portal hypertension-related syndrome causing gastric bleeding in patients with cirrhosis. J Hepatol 1985; 1 (suppl): S315. 24. Hosking SW, Kennedy HJ, Seddon I, Triger DR. The role of propranolol in congestive gastropathy of portal hypertension. Hepatology 1987; 7: 437-41.
Laryngeal mask airway mask has been described as the missing link between the facemask and the endotracheal tube. It consists of a tubular oropharyngeal airway, to the distal end of which is The
laryngeal
attached a sealed, forward-pointing mask with an inflatable peripheral cuff. This apparatus is designed to produce an airtight seal around the laryngeal inlet and so provide a secure airway suitable for spontaneous or controlled ventilation. In most cases the laryngeal mask can be inserted easily without laryngoscopy; a muscle relaxant is seldom required. Once in place the device gives better and more secure airway control than the facemask; and there is no need to support the patient’s chin.l Consequently, the anaesthetist’s hands are freed, and remote observation of the patient may be possible when tracheal intubation would otherwise be essential.Scavenging of waste anaesthetic gases is as effective from laryngeal masks as from tracheal tubes3 and the device is also well tolerated during recovery from anaesthesia.4 Fibreoptic bronchoscopes passed down laryngeal masks have been used to observe the functioning of the vocal cords, an examination not possible during endotracheal anaesthesia.5,6 Thus it is not surprising that the laryngeal mask has quickly been adopted into anaesthetic practice and many applications have been reported. What is the proper place of this device in airway management? The endotracheal tube is the gold standard by which all other methods of airway control are judged. Once in position it provides a secure airway that facilitates easy ventilation and prevents aspiration of
regurgitated gastric contents. The laryngeal mask is easy
to position and use whereas tracheal intubation is a skilled procedure. Moreover, anatomical or pathological anomalies make tracheal intubation impossible in certain patients, even for experienced personnel. The laryngeal mask has been used successfully in patients of all ages in whom tracheal intubation had proved impossible.7-9 The mask can itself be used as an aid to difficult intubation- a small cuffed endotracheal tube10 or a gum-elastic bougiell(used to railroad an endotracheal tube into the position after removal of the laryngeal mask) can be passed into the trachea through correctly placed size 3 and 4 laryngeal masks. The use of the device in obstetric patients who have proved impossible to intubate is controversial. When learning to do obstetric anaesthesia, all anaesthetists are taught a failed intubation drill-maintenance of cricoid pressure (to prevent aspiration) and, if necessary, turning the patient onto her side head down and ventilating her with 100% oxygen until she awakes. In
diffusely hyperaemic or shows multiple erythematous areas outlined by a subtle yellowish or whitish network (mosaic pattern); in severe gastropathy there are discrete or confluent cherry red spots or diffuse mucosal haemorrhages. Only severe gastropathy causes clinically important bleeding. Apart from cherry red spots, the endoscopic appearances are non-specific and are identical to those seen in gastritis.2 However, the histological findings in the two conditions are different,2,11,13 although those of congestive gastropathy may not be readily apparent in the superficial biopsy specimens obtained via an endoscope.2°14 Vascular gastropathy is characterised by diffuse and pronounced dilatation of mucosal capillaries accompanied by mucosal oedema and perhaps diapedesis of erythrocyes, but with no or very
mucosa
EDITORIALS
Portal hypertensive gastropathy Non-variceal bleeding in portal hypertension has only lately received the attention it deserves. Among the reasons for this oversight are the more catastrophic nature and greater frequency of bleeding from oesophagogastric varices and a mistaken belief that the gastric mucosal lesions responsible for the bleeding were inflammatory in nature. Terms such as "acute gastritis", "erosive gastritis", "acute gastric ulcers", and "haemorrhagic gastritis" obscured the true nature of the mucosal abnormality and were responsible for inappropriate and ineffective treatment with antisecretory drugs. Realisation that the morphological change underlying non-variceal bleeding in portal hypertension is gross ectasia of the gastric mucosal capillaries and submucosal veins without inflammation led to the condition being renamed portal hypertensive gastropathyl (or congestive gastropathy2) and encouraged a reappraisal of pathogenesis and treatment. Bleeding from the gastric mucosa is a serious complication of portal hypertension. It may be insidious, presenting eventually with an irondeficiency anaemia, or sudden and severe, with haematemesis and melaena. Diffuse gastric lesions account for only 2% of all cases of upper gastrointestinal bleeding,3but they are the cause, in various reported series, of 10-70% of episodes of gastrointestinal haemorrhage in cirrhotic patients and 10-50% in those with portal hypertension.2,4-9 Most non-variceal bleeding in portal hypertension can be attributed to congestive gastropathy.7The risk of death from gastric mucosal haemorrhage is less than from variceal rupture, but bleeding is often sufficiently brisk or persistent to cause deterioration of liver function in patients with cirrhosis.’ Recurrent bleeding is common (62 % at 12 months after the initial haemorrhagel), although this high frequency partly reflects inappropriate treatment in the past. The risk of gastric mucosal bleeding may increase after successful sclerotherapy of oesophageal varices.22 The congestion of the gastric mucosa may be associated with hypochlorhydria, and there is experimental evidence of greater susceptibility to injury by noxious agents such as alcohol and aspirin. 11 Portal hypertensive gastropathy has been classified as mild or severe on the basis of endoscopic appearances.2,12,13 In the mild condition the gastric
is
small
little evidence of inflammation. The submucosal veins are dilated and tortuous. These features are confirmed by silicone rubber microvascular casts, which show dilated straight and non-spiral arterioles and arteriovenous shunts in the submucosa, dilated veins in the submucosa and subserosa, and dilated capillaries and precapillaries in the mucosa.15 Despite the belated realisation that non-variceal bleeding in portal hypertension has a vascular basis, much has still be be learned about its pathogenesis. The haemodynamic changes in the stomach wall could be a non-specific component of the overall changes in the splanchnic circulation in portal hypertension or the result of a local impairment of regulation of gastric vascular tone.16 All patients with portal hypertensive gastropathy have high portal pressures, but no correlation has been observed between gastric capillary ectasia and the degree of portal hypertension.2Gastric blood flow cannot be measured reproducibly in man so information about
gastric haemodynamic changes in portal hypertension is derived from observations in laboratory animals. Rats with portal hypertension have an increased total gastric blood flow with a lesser increase in mucosal flow and a reduced gastric vascular resistance.17-2o These changes are part of a disorder characterised by generalised splanchnic arteriolar vasodilatation, increased splanchnic blood flow, and reduced vascular sensitivity to noradrenaline.16,20 Humoral agents that have been implicated in the pathogenesis of the haemodynamic disturbances include glucagon, gastrin, and a prostaglandin. 13,1820 Portal decompressive surgery is effective in arresting haemorrhage and preventing rebleeding in portal hypertensive gastropathy, but the operative risks and high incidence of encephalopathy in cirrhotic patients limit the use of this approach.21 In view of the apparent similarity between the pathophysiological changes in patients with oesophagogastric varices and those with congestive gastropathy,16 the knowledge that variceal bleeding can be halted and recurrent bleeding prevented by beta-adrenergic blockade, and the evidence that propranolol reduces gastric mucosal blood flow in
1046
portal hypertensive rates,"21 it was logical to see whether beta-adrenergic antagonists were effective in severe gastric mucosal haemorrhage. Two small open studies have shown that propranolol stops such bleeding in almost all cases,23.24; in a randomised controlled trial in a larger number of patients the frequency of rebleeding was significantly reduced.1 The mechanism of the beneficial effect of propranolol is uncertain. There is no evidence yet that the long-term outcome of cirrhotic patients with severe portal hypertensive gastropathy, or those with bleeding varices, is improved by either surgery or beta-adrenergic blockade. 1.
Perez-Ayuso RM, Piqué JM, Bosch J, et al. Propanolol in prevention of recurrent bleeding from severe portal hypertensive gastropathy in cirrhosis. Lancet 1991; 337: 1431-34. TT, Sims J, Eyre-Brook I,
2. McCormack
hypertension: inflammatory gastritis
al. Gastric lesions in portal congestive gastropathy? Gut
et
or
1985; 26: 1226-32. 3.
Quintero E, Piqué JM, Bombi JA, et al. Upper gastrointestinal bleeding caused by gastroduodenal vascular malformations: incidence, diagnosis, and treatment. Dig Dis Sci 1986; 31: 897-905. 4. Dagradi AE, Mehler R, Tan DT, Stempien SJ. Sources of upper gastrointestinal bleeding in patients with liver cirrhosis and large esophagogastric varices. Am J Gastroenterol 1970; 54: 458-63. 5. Khodadoost J, Glass GBJ. Erosive gastritis and acute gastroduodenal ulcerations as source of upper gastrointestinal bleeding in liver cirrhosis. Digestion 1972; 7: 129-38. 6. Walram S, Davis M, Nunnerley H, et al. Emergency endoscopy after gastrointestinal haemorrhage in 50 patients with portal hypertension. Br Med J 1974; 4: 94-96. 7. Terés J, Bordas JM, Bru C, Diaz F, Bruguera M, Rodes J. Upper gastrointestinal bleeding in cirrhosis: clinical and endoscopic correlation. Gut 1976; 17: 37-40. 8. Thomas E, Rosenthal WS, Rymer W, Katz D. Upper gastrointestinal hemorrhage in patients with alcoholic liver disease and esophageal varices. Am J Gastroenterol 1979; 72: 623-29. 9. Rector WG, Reynolds TB. Risk factors for haemorrhage from oesophageal varices and acute gastric erosions. Clin Gastroenterol 1985; 14: 139-53. 10. Perez-Ayuso RM, Piqué JM, Saperas E, at al. Gastric vascular ectasias in cirrhosis: association with hypoacidity not related to gastric atrophy. Scand J Gastroenterol 1989; 24: 1073-78. 11. Tarnawski AS, Sarfeh IJ, Stachura J, et al. Microvascular abnormalities of the portal hypertensive gastric mucosa. Hepatology 1988; 8: 1488-94. 12. Papazian A, Braillon A, Dupas JL, Sevenet F, Capron JP. Portal hypertensive gastric mucosa: an endoscopic study. Gut 1986; 27: 1199-203. 13. Quintero E, Piqué JM, Bombi JA, et al. Gastric mucosal vascular ectasias causing bleeding in cirrhosis. Gastroenterology 1987; 93: 1054-61. 14. Foster PN, Wyatt JI, Bullimore DW, Losowsky MS. Gastric mucosa in patients with portal hypertension: prevalence of capillary dilatation and Campylobacter pylori. J Clin Pathol 1989; 42: 919-21. 15. Hashizume M, Tanaka K, Mokuchi K. Morphology of gastric microcirculation in cirrhosis. Hepatology 1983; 6: 1008-12. 16. Benoit JN, Granger DN. Splanchnic haemodynamics in chronic portal hypertension. Sem Liv Dis 1986; 6: 287-98. 17. Kitano S, Koyanasi K, Sugimachi M, Kobayashi M, Inokuchi K. Mucosal blood flow and modified vascular responses to norepinephrine in the stomach of rats with liver cirrhosis. Surg Res 1982; 14: 221-30. 18. Piqué JM, Leung FW, Kitahora T, Sarfeh IJ, Tarnawski A, Guth PH. Gastric mucosal blood flow and acid secretion in portal hypertensive rats. Gastroenterology 1988; 95: 727-33. 19. Piqué JM, Pizcueta P, Perez-Ayuso RM, Bosch J. Effects of propanolol on gastric microcirculation and acid secretion in portal hypertensive rats. Hepatology 1990; 12: 476-80. 20. Benoit JN, Womack WA, Korthuis RJ, Wilborn WH, Granger DN. Chronic portal hypertension: effects on gastrointestinal flow distribution. Am J Physiol 1986; 250: G535-39. 21. Sarfeh IJ, Juler GL, Stemmer EA, et al. Results of surgical management of hemorrhagic gastritis in patients with gastro-esophageal varices. Surg Gynecol Obstet 1982; 155: 167-70. 22. Kroeger RJ, Groszmann RJ. Effect of selective blockade of B2-adrenergic receptors on portal systemic hemodynamics in a portal hypertensive rat model. Gastroenterology 1985; 88: 896-900. 23. Quintero E, Piqué JM, Bombi JA, et al. Antral mucosal hyperaemia:
characterization of a portal hypertension-related syndrome causing gastric bleeding in patients with cirrhosis. J Hepatol 1985; 1 (suppl): S315. 24. Hosking SW, Kennedy HJ, Seddon I, Triger DR. The role of propranolol in congestive gastropathy of portal hypertension. Hepatology 1987; 7: 437-41.
Laryngeal mask airway mask has been described as the missing link between the facemask and the endotracheal tube. It consists of a tubular oropharyngeal airway, to the distal end of which is The
laryngeal
attached a sealed, forward-pointing mask with an inflatable peripheral cuff. This apparatus is designed to produce an airtight seal around the laryngeal inlet and so provide a secure airway suitable for spontaneous or controlled ventilation. In most cases the laryngeal mask can be inserted easily without laryngoscopy; a muscle relaxant is seldom required. Once in place the device gives better and more secure airway control than the facemask; and there is no need to support the patient’s chin.l Consequently, the anaesthetist’s hands are freed, and remote observation of the patient may be possible when tracheal intubation would otherwise be essential.Scavenging of waste anaesthetic gases is as effective from laryngeal masks as from tracheal tubes3 and the device is also well tolerated during recovery from anaesthesia.4 Fibreoptic bronchoscopes passed down laryngeal masks have been used to observe the functioning of the vocal cords, an examination not possible during endotracheal anaesthesia.5,6 Thus it is not surprising that the laryngeal mask has quickly been adopted into anaesthetic practice and many applications have been reported. What is the proper place of this device in airway management? The endotracheal tube is the gold standard by which all other methods of airway control are judged. Once in position it provides a secure airway that facilitates easy ventilation and prevents aspiration of
regurgitated gastric contents. The laryngeal mask is easy
to position and use whereas tracheal intubation is a skilled procedure. Moreover, anatomical or pathological anomalies make tracheal intubation impossible in certain patients, even for experienced personnel. The laryngeal mask has been used successfully in patients of all ages in whom tracheal intubation had proved impossible.7-9 The mask can itself be used as an aid to difficult intubation- a small cuffed endotracheal tube10 or a gum-elastic bougiell(used to railroad an endotracheal tube into the position after removal of the laryngeal mask) can be passed into the trachea through correctly placed size 3 and 4 laryngeal masks. The use of the device in obstetric patients who have proved impossible to intubate is controversial. When learning to do obstetric anaesthesia, all anaesthetists are taught a failed intubation drill-maintenance of cricoid pressure (to prevent aspiration) and, if necessary, turning the patient onto her side head down and ventilating her with 100% oxygen until she awakes. In
