Huma Qureshi ( PMRC Research Centre, Jinnah Postgraduate Medical Centre, Karachi. )
August 1987, Volume 37, Issue 8
Editorial
Injection sclerotherapy for oesopliageal varices was first reported from Sweden in 1939 using intravariceal quinine1. No recurrence of varices or rebleeding occurred till 3 years. Next year at Mayo Clinic, 2.5% sodium morrhuate was used for sclerotherapy resulting in reduction in the size of varices2. Longer follow up on a larger series of patients revealed that rebleeding was more frequent in those who had associated gastric varices3 and therefore their presence was taken as a contraindication to the use of sclerotherapy.
The first experience of sclerotherapy from Great Britain was reported in 19494;further follow up on these patients showed a better result of scierotherapy if splenectomy was done prior to the procedure. The need to do follow up endoscopies to recognize the recurrence of varices was also brought to notice5. In 1959 scierotherapy experience in 15 children below the age of 16 years was reported from Toronto6. A follow up till 4 years showed success in 9 cases. It was also experienced that bleeding episodes increased during upper respiratory tract infection in children and it was therefore recommended that children with varices should have adenotonsillectomy.
In 1960 instead of intravariceal injection, paravariceal injection was thought to be more effective because of the creation of submucosal fibrosis over the varix thereby protecting them from bleeding7. The technique was later picked up by others8,9 who have collected enough data on its use in both elective and emergency scierotherapy.
By 1973, surgeons at Kings College showed dissatisfaction with shunt and non-shunt procedures, especially in those with severe liver disease10 while workers from Belfast11 had published 93% success rate with scierotherapy. Therefore, sclerotherapy was taken up by the Kings College too. Further modification in the ridged Negus oesophagoscope was made in 197512 allowing the varices to prolapse into the lumen of the scope, making the injection easier. High frequency of deaths due to oesophageal perforation (20%) reported from Kings College in 197713 prompted the development of a flexible outer sheath and endoscope plus needle14. By 1980, graduated flexible sheath was made commercially available.
Till almost 40 years after the first use of sclerotherapy no controlled data for the efficacy and improvement in the survival time following sclerotherapy was available. First few controlled trials were reported between 1979-198115-17 along with significant improvement in the survival time in one.
Blood flow patterns in the oesophageal collaterals were demonstrated using endoscopic doppler18 Variations in the flow pattern were found tO occur especially during respiration. Perforating veins connecting the varices to the paraoesophageal vessels were also seen throughout the whole length of the oesophagus and it was suggested that perhaps the turbulant blood flow in the perforating vessels was the cause for the vanceal rupture.
For sclerotherapy, the sclerosant can be either injected directly into the varices to obliterate the lumen, or into the lamina propria and submucosa to produce a fibrous layer over the varix. Intravariceal technique requires a larger volume of sclerosant (3-Sm!) in each varix at two or three sites at the lower oesophageal junction, while paravariceal injection requires smaller volume of sclerosant (0.5ml) at multiple sites. Histologic changes19,20 and the efficacy in the management of active, and prevention of recurrent bleeding are similar in both the techniques.9,11,21,22
Some workers23,24 use baloon temponade during sclerötherapy to achieve a bloodless field, while others use it after scierotherapy. Various types and combinations of scierosants have been used, including quinine, sodium morrhuate, 3,5,25 ethanolamine oleate, sotradecal, 6 50% dextrose, absolute alcohol26 and sodium tetradecyl sulphate27. The choice, dosage and combination mostly depends upon the availability, cost and choice of the operator. Time interval between the two courses vary from 1-3 weeks but injections are often initially given weekly for 3 weeks and later every 3-4 weeks until all varices disappear. 28
Multiple controlled trials have been done to see the efficacy of scierotherapy in reducing the number of rebleeds and improving the survival time21,27,29,30.A trend towards reduction in number of rebleeds was observed and such episodes were seldom life threating. Improvement in the long term survival has been reported from Kings College. 31
In some trials, the efficacy of scierotherapy was compared with balloon temponade in the management of acute bleeding. 32,33 In both the studies bleeding was controlled in a larger group of patients and fewer deaths occurred in the sclerotherapy group.
Some workers have done prophylactic scierotherapy in patients who have never bled. 34,35 Selection criteria were large varices, prolonged prothrombin time and the presence of stigmata on varices36 in one group while it was unselected in another. Both the studies showed a significant reduction in the bleeding episodes while improvement in the survival time was noted in one study. Regular. endoscopic examinations at 3 months, 6 months and then yçarly are required to check the formation of new varices and inject them as and when needed. Usually few injections (median 2 courses) are required to obliterate new varices and complications of sclerotherapy are rare28.
At the international symposium on the prophylaxis of variceal bleeding37 the pitfalls in the prophylactic treatment were reviewed. It was suggested that apart from geographical variations in the underlying liver disease, patient population and the degree of hepatic decompensation, other risk factors like state of varices, liver status and alcohol abuse should be taken into consideration. Unfortunately neither all these criteria nor the treatment of acute bleeds were matched in most of the cøntrolled trials and, therefore, the results are not absolute.
Early complications of sclerotherapy (within 24hrs) include perforation, aspiration, chest pain and transient fever. Of later complications, oesophageal ulceration is very frequent, but a minor percentage bleeds from this28. Full thickness necrosis along with rnediastinitis though rare, is often fatal. About 10% cases develop stricture often after 3-4 courses; dysphagia in these cases resolves spontaneously and only a small number requires dilatation. Abnormal oesophageal motility is reported after sclerotherapy38-40. Overall mortality with sclerotherapy is about l-2%41.
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