120
Journal of the Royal Society of Medicine Volume 83 February 1990
15 Wolf BS, Khilnani M, Malis. The sagittal diameter of the bony cervical canal and its significance in cervical spondylosis. J Mount Sinai Hosp 1956;23:283-92 16 Payne EE, Spillane JD. The cervical spine: an anatomicpatologic study of 70 specimens with particular reference to the problem of cervical spondylosis. Brain 1957;80: 571-96 17 Kessler JT. Congenital narrowing of the cervical spinal canal. J Neurol Neurosurg Psychiatry 1975;38:1218-24 18 Anonymous. Management of cervical spondylotic myelopathy. Lancet 1984;i:1058
19 Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain 1972;95:87-100 20 Uttley D, Monro PS. Neurosurgery for cervical spondylosis. Br J Hosp Med 1988 (In press)
(Accepted 20 December 1988. Correspondence to Dr M C Pitt, Department of Neurophysiology, National Hospital for Nervous Diseases, Queen Square, London WC1N 3BG)
Portal hypertension due to hydatid disease of the liver
J Papadimitriou MD FACS
D Kannas MD
L Papadimitriou MD 2nd Surgical Department, University of Athens, Aretaieon Hospital, 76 Vas Sophias Avenue, Athens, Greece Keywords: portal hypertension; hydatid disease
There are several aetiologic factors of portal hypertension. Obstruction of the main portal vein in non-cirrhotic patients is mainly due to thrombosis of various causes1. Hydatid disease of the porta hepatis resulting in compression of the portal vein and manifestations of portal hypertension has not been reported before. Case report A 48-year-old man, weighing 65 kg, was admitted with bleeding from the upper gastrointestinal tract. At physical examination the patient was icteric and the liver was palpable. The laboratory values were as follows: haematocrit 36%, WBC 12.000 pc, total bilirubin 5 mg/dl with 80% conjugated. Alkaline phosphatase was 214 U, SGOT 29 U and SGPT 46 U. Endoscopy, performed the day after admission, revealed oesophageal varices, but no active bleeding could be demonstrated. Ultrasonography and computerized tomography (Figure 1) showed a huge hydatid cyst at the porta hepatis. Splenography was performed after direct transdermal puncture of the spleen and the porta vein proved to be obstructed (Figure 2) at the level of porta hepatis.
Figure 1. Computerized axial tomography shows a huge hydatid cyst of the right lobe of the liver
_ ~ ~~~~~~~~
~
~
~
~~~~~~~~~~~~~~~~~~~~ ..ei .
*| l .ri:Xf . . . . . . .i ,j
FLgure 2
Spenoporogramshowsobstructionoftheportocava. .
Figure 2. Splenoportogram shows obstruction of the porto cava
The patient was operated upon and a huge hydatid cyst was found, which occupied the right lobe of the liver extended to the porta hepatis and caused compression of the hepaticoduodenal ligament. The cyst was evacuated and partial cystectomy was performed. Only the pericyst layer which was attachied to the liver parenchyma was left behind. Excision, of the pericyst which was attached to the common bile duct and the portal vein was removed with care due to collaterals. which caused excessive bleeding. Portal vein pressure was found to be 33 mm EIO before the cyst was removed and dropped to 15 mm following excision of the cyst. The patient had a smooth postoperative course and left the hospital on the 15th postoperative day. The patient remains fit and well 4 years after operation with no clinical signs of portal hypertension. Discussion During the last 30 years 320 patients with liver echi were admitted to our unit. One hundred and five patients presented with various complications. The main complication was rupture of the cyst into the biliary tree2. Only in one instance the cyst caused direct compression of the
0141-0768/90/
020120-02/$02.00/0 o 1990 The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 83 February 1990 hepatico-duodenal ligament and this resulted in obstructed jaundice and portal hypertension. Extrahepatic portal hypertension is mainly due to portal vein thrombosis which is the result of sepsis, trauma, neoplasm or it is of unknown origin. External compression of the main tract ofthe portal vein as a causative factor of portal hypertension is very rare and when it occurs it is usually due to regional lymph node enlargement. The main clinical manifestation in extrahepatic portal hypertension is bleeding from varices; however the prognosis and the results are in general much better than those due to intrahepatic disease, where hepatocellular damage and liver dysfunction exist3'4. In this case, excision ofthe cyst resulted in immediate drop of the pressure into the portal vein system and the patient remains symptom-free 4 years after the operation.
121
References 1 Silk DBA, Williams R. Portal hypertension. In: Wright, et at eds. Liver and biliary disease London: W B Saunders, 1979 2 Papadimitriou J, Tsiftsis D, Tountas C. Hydatid cyst of the liver ruptured into the biliary tract. Current Surg 1983; 40:339-46 3 Welch CJ. Portal hypertension. N Engl J Med 1960;243:598 4 Fonkalstrud EW, Myers NA, Robinson MJ. Management of extrahepatic portal hypertension in children. Ann Surg 1974;180:487-93
(Accepted 28 December 1988. Correspondence to Dr John Papadimitriou MD, Professor of Surgery, 8 Iasiou Street, Athens 115 21, Greece)
Meeting reports All change: the health scene in the 1990s Keywords: 'Working for Patients'; NHS; internal market; staff shortages
There have been times, one must admit, part way through an RSM meeting when one's eyes have strayed to one's watch with a sinking feeling at the realization that there is another three quarters of an hour to go. This was certainly not such an evening. Both speakers were on top of their subject and gave a masterly display ofputting across ideas with clarity, sincerity and humour. The title of the session made the theme clear: we were to take a fairly broad sweep at impending change and at what might come about. In the course of the evening first the government's White Paper was consistently and carefully savaged and later some very serious warnings were given. The quiet, matter of fact delivery of these warnings made them all the more powerful.
Professor John Butler from the Health Services Research Unit, University of Kent, was the first speaker. Billed to focus on the significance of internal markets in health care he made the point that this important new concept is the core of 'Working for Patients' (the White Paper). Not only that, market forces are seen as playing a major determining role in education and housing as well as health. There are two reasons for this newcomer's arrival: the first is Tory party ideology, the second the lack of incentives for efficiency in the NHS as it stands. From 1991 onwards there will be a market in UK health care. Some goods and services will be bought, the sellers being private hospitals, directly managed NHS hospitals and opted-out hospital trusts. This should mean that buyers can make savings to spend on other things; it should also mean that the sellers will be forced to be efficient.
But, asked Professor Butler, will it work? There are no precedents to look to and we can seek illumination only from other markets. One with which he is familiar from recent experience is that concerned with selling second-hand cars. The audience was then treated to an account of the speaker's experience in buying such a product which made it abundantly clear that in his opinion the present government's approach to the organization ofthe health service is akin to that of the second-hand car salesman. He summarized his argument with seven main points which pertain to the second hand car, all of which are relevant to the health service. First there has to be a reasonable number of suppliers competing. If there are only one or two in one area there is no incentive to be competitive. Second, the cost to the customer of gaining access to the suppliers must be added to the total cost. If I have to travel a hundred miles to buy a bargain Ford, the cost in travel expenses and my time should be added to the purchase price of the car. So it should be with the Health Service if I have to travel a hundred miles for treatment which on the face of it is cheaper than that available nearby. Third is the need to make prices charged readily available to customers, with the cost to the supplier of signalling these prices, and their changes, being added to the total costs. Fourth is the need for different suppliers to be in genuine competition. Fifth, customers should have full information about all goods on sale. Sixth, customers should be able to judge the quality of the goods on sale and if the customer has no technical knowledge then there should be some system of obtaining expert, independent advice. Finally, the logic of the market whereby the unsuccessful go out of business should not be disturbed. Anticipating those who might say that one cannot talk as though health care is like selling cars Professor Butler made the explicit point that this is
Report of Meeting of Open Section, 2 October 1989
0141-0768/90/ 020121-02/$02.00/0 © 1990 The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 83 February 1990
15 Wolf BS, Khilnani M, Malis. The sagittal diameter of the bony cervical canal and its significance in cervical spondylosis. J Mount Sinai Hosp 1956;23:283-92 16 Payne EE, Spillane JD. The cervical spine: an anatomicpatologic study of 70 specimens with particular reference to the problem of cervical spondylosis. Brain 1957;80: 571-96 17 Kessler JT. Congenital narrowing of the cervical spinal canal. J Neurol Neurosurg Psychiatry 1975;38:1218-24 18 Anonymous. Management of cervical spondylotic myelopathy. Lancet 1984;i:1058
19 Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain 1972;95:87-100 20 Uttley D, Monro PS. Neurosurgery for cervical spondylosis. Br J Hosp Med 1988 (In press)
(Accepted 20 December 1988. Correspondence to Dr M C Pitt, Department of Neurophysiology, National Hospital for Nervous Diseases, Queen Square, London WC1N 3BG)
Portal hypertension due to hydatid disease of the liver
J Papadimitriou MD FACS
D Kannas MD
L Papadimitriou MD 2nd Surgical Department, University of Athens, Aretaieon Hospital, 76 Vas Sophias Avenue, Athens, Greece Keywords: portal hypertension; hydatid disease
There are several aetiologic factors of portal hypertension. Obstruction of the main portal vein in non-cirrhotic patients is mainly due to thrombosis of various causes1. Hydatid disease of the porta hepatis resulting in compression of the portal vein and manifestations of portal hypertension has not been reported before. Case report A 48-year-old man, weighing 65 kg, was admitted with bleeding from the upper gastrointestinal tract. At physical examination the patient was icteric and the liver was palpable. The laboratory values were as follows: haematocrit 36%, WBC 12.000 pc, total bilirubin 5 mg/dl with 80% conjugated. Alkaline phosphatase was 214 U, SGOT 29 U and SGPT 46 U. Endoscopy, performed the day after admission, revealed oesophageal varices, but no active bleeding could be demonstrated. Ultrasonography and computerized tomography (Figure 1) showed a huge hydatid cyst at the porta hepatis. Splenography was performed after direct transdermal puncture of the spleen and the porta vein proved to be obstructed (Figure 2) at the level of porta hepatis.
Figure 1. Computerized axial tomography shows a huge hydatid cyst of the right lobe of the liver
_ ~ ~~~~~~~~
~
~
~
~~~~~~~~~~~~~~~~~~~~ ..ei .
*| l .ri:Xf . . . . . . .i ,j
FLgure 2
Spenoporogramshowsobstructionoftheportocava. .
Figure 2. Splenoportogram shows obstruction of the porto cava
The patient was operated upon and a huge hydatid cyst was found, which occupied the right lobe of the liver extended to the porta hepatis and caused compression of the hepaticoduodenal ligament. The cyst was evacuated and partial cystectomy was performed. Only the pericyst layer which was attachied to the liver parenchyma was left behind. Excision, of the pericyst which was attached to the common bile duct and the portal vein was removed with care due to collaterals. which caused excessive bleeding. Portal vein pressure was found to be 33 mm EIO before the cyst was removed and dropped to 15 mm following excision of the cyst. The patient had a smooth postoperative course and left the hospital on the 15th postoperative day. The patient remains fit and well 4 years after operation with no clinical signs of portal hypertension. Discussion During the last 30 years 320 patients with liver echi were admitted to our unit. One hundred and five patients presented with various complications. The main complication was rupture of the cyst into the biliary tree2. Only in one instance the cyst caused direct compression of the
0141-0768/90/
020120-02/$02.00/0 o 1990 The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 83 February 1990 hepatico-duodenal ligament and this resulted in obstructed jaundice and portal hypertension. Extrahepatic portal hypertension is mainly due to portal vein thrombosis which is the result of sepsis, trauma, neoplasm or it is of unknown origin. External compression of the main tract ofthe portal vein as a causative factor of portal hypertension is very rare and when it occurs it is usually due to regional lymph node enlargement. The main clinical manifestation in extrahepatic portal hypertension is bleeding from varices; however the prognosis and the results are in general much better than those due to intrahepatic disease, where hepatocellular damage and liver dysfunction exist3'4. In this case, excision ofthe cyst resulted in immediate drop of the pressure into the portal vein system and the patient remains symptom-free 4 years after the operation.
121
References 1 Silk DBA, Williams R. Portal hypertension. In: Wright, et at eds. Liver and biliary disease London: W B Saunders, 1979 2 Papadimitriou J, Tsiftsis D, Tountas C. Hydatid cyst of the liver ruptured into the biliary tract. Current Surg 1983; 40:339-46 3 Welch CJ. Portal hypertension. N Engl J Med 1960;243:598 4 Fonkalstrud EW, Myers NA, Robinson MJ. Management of extrahepatic portal hypertension in children. Ann Surg 1974;180:487-93
(Accepted 28 December 1988. Correspondence to Dr John Papadimitriou MD, Professor of Surgery, 8 Iasiou Street, Athens 115 21, Greece)
Meeting reports All change: the health scene in the 1990s Keywords: 'Working for Patients'; NHS; internal market; staff shortages
There have been times, one must admit, part way through an RSM meeting when one's eyes have strayed to one's watch with a sinking feeling at the realization that there is another three quarters of an hour to go. This was certainly not such an evening. Both speakers were on top of their subject and gave a masterly display ofputting across ideas with clarity, sincerity and humour. The title of the session made the theme clear: we were to take a fairly broad sweep at impending change and at what might come about. In the course of the evening first the government's White Paper was consistently and carefully savaged and later some very serious warnings were given. The quiet, matter of fact delivery of these warnings made them all the more powerful.
Professor John Butler from the Health Services Research Unit, University of Kent, was the first speaker. Billed to focus on the significance of internal markets in health care he made the point that this important new concept is the core of 'Working for Patients' (the White Paper). Not only that, market forces are seen as playing a major determining role in education and housing as well as health. There are two reasons for this newcomer's arrival: the first is Tory party ideology, the second the lack of incentives for efficiency in the NHS as it stands. From 1991 onwards there will be a market in UK health care. Some goods and services will be bought, the sellers being private hospitals, directly managed NHS hospitals and opted-out hospital trusts. This should mean that buyers can make savings to spend on other things; it should also mean that the sellers will be forced to be efficient.
But, asked Professor Butler, will it work? There are no precedents to look to and we can seek illumination only from other markets. One with which he is familiar from recent experience is that concerned with selling second-hand cars. The audience was then treated to an account of the speaker's experience in buying such a product which made it abundantly clear that in his opinion the present government's approach to the organization ofthe health service is akin to that of the second-hand car salesman. He summarized his argument with seven main points which pertain to the second hand car, all of which are relevant to the health service. First there has to be a reasonable number of suppliers competing. If there are only one or two in one area there is no incentive to be competitive. Second, the cost to the customer of gaining access to the suppliers must be added to the total cost. If I have to travel a hundred miles to buy a bargain Ford, the cost in travel expenses and my time should be added to the purchase price of the car. So it should be with the Health Service if I have to travel a hundred miles for treatment which on the face of it is cheaper than that available nearby. Third is the need to make prices charged readily available to customers, with the cost to the supplier of signalling these prices, and their changes, being added to the total costs. Fourth is the need for different suppliers to be in genuine competition. Fifth, customers should have full information about all goods on sale. Sixth, customers should be able to judge the quality of the goods on sale and if the customer has no technical knowledge then there should be some system of obtaining expert, independent advice. Finally, the logic of the market whereby the unsuccessful go out of business should not be disturbed. Anticipating those who might say that one cannot talk as though health care is like selling cars Professor Butler made the explicit point that this is
Report of Meeting of Open Section, 2 October 1989
0141-0768/90/ 020121-02/$02.00/0 © 1990 The Royal Society of Medicine
