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Injection Sclerotherapy forOesophageal Varices

THE LANCET

As so often happens, interest in an old techniquehas been renewed. Injection sclerotherapy was in-troduced in 1939 by CRAFOORD and FRENCKNERland, in 1955, MACBETH2 reported good results in30 patients. A few other reports followed in ear-nose-and-throat journals but then shunt proceduresbecame popular and have been an elective standardtreatment for the past twenty years; injection ther-apy never really had a proper trial, Lately, how-ever, surgeons have become disillusioned withshunt surgery, particularly for emergency bleeding.While ORLOFF3 still recommends emergency porta-caval shunts, despite a mortality of 49% in the first138 patients, shunting is an elective procedure inmost centres. Even then the late encephalopathyhas been found to be significant, and not only inthose with very poor liver function. Against thisbackground, JOHNSTON and RODGERS in 19734 4

published remarkably good results from sclerother-apy, controlling the bleeding in 93% out of 117 pa-tients, with a total admission mortality of 18%.Several other centres in Europe and South Africathen adopted the technique. However, around thistime W. D. WARREN was starting his distal spleno-renal shunt, aimed at reducing the incidence ofencephalopathy, so now is an opportune time in thetreatment of this difficult disease to assess the roleof injection sclerotherapy.

Varices are useful collateral channels bypassinga venous block. It is only the few that happen to

1. Crafoord C, Frenckner P. New surgical treatment of varicose veins of theœsophagus. Acta Otolaryngol, Stockholm 1939; 27: 422-29.

2. Macbeth R. Treatment of œsophageal varices in portal hypertension bymeans of sclerosing injection. Br Med J 1955; ii: 877-80.

3. Orloff MJ, Charters AC, Chandler JG et al. Portacaval shunt as emergencyprocedure in unselected patients with alcoholic varices. Surg GynecolObstet 1975; 141: 59-68.

4. Johnston GW, Rodgers HW. A review of 15 years’ experience in the use ofsclerotherapy in the control of acute hæmorrhage from oesophageal var-ices. Br J Surg 1973; 60: 797-800.

impinge on the oesophageal mucosa that are dan-gerous and it is only these that need treatment.This is the rationale for local sclerotherapy ratherthan larger operations to bypass or ligate all thecollateral channels. In the treatment of the severe,acute bleed, a Sengstaken-Blakemore tube in thecorrect position at the correct pressure will nearlyalways control the bleeding, but 60% of patientsrebleed when the tube is withdrawn and the hospi-tal mortality in those with rebleeding is 60%.5TERBLANCHE and colleagues6 found that addingsclerotherapy to the management controlled bleed-ing in 92% with a 25% hospital mortality. Theyconclude that this is the treatment of choice in theacute bleed that does not stop spontaneously. How-ever, if the bleeding is too brisk for good vision, theinjection can be done 12-24 h later after the Seng-staken tube has temporarily controlled the heemor-rhage. Those who have had experience of emer-gency injections have found it difficult to justify,ethically, a controlled trial because the results inthe control group are so poor.’

Once the bleeding is controlled, sclerotherapy isa possible long-term treatment in place of simplemedical support or portasystemic shunting. A con-trolled trial’ in 31 patients showed that varicescould be eradicated by injection and that no patienthad recurrent bleeding after that for a mean of 9.4months. In the control group recurrent bleedingremained a problem. SINNETT et al.8 recentlyreported encouraging long-term results in 16 pa-tients treated by sclerotherapy alone (mean fol-

low-up 28 months). The problem with controlledtrials is that different aetiologies and degrees of liverdamage, ages, and social situations make matchingdifficult. However, these results do suggest thatwhat is needed now is a trial of long-term injectionsclerotherapy versus elective distal splenorenalshunts, although even then some patients wouldhave to be excluded from shunting, on grounds ofanatomical variation, or from repeated injectionsbecause of the need to travel long distances to hos-pital. There have not so far been reports of recanal-isation once the veins have been obliterated-butthen there are plenty of perioesophageal veins stillpatent, and this may also be why there have beenno reports of gastric varices appearing or enlargingafter injection. It is not clear yet, however, whetherthrombosis can spread back into gastric varices.

5. Novis BH, Duys P, Barbezat GO, Clain J, Bank S, Terblanche J. Fibreopticendoscopy and the use of the Sengstaken tube in acute gastrointestinalhaemorrhage in patients with portal hypertension and varices. Gut 1976;17: 258-63.

6. Terblanche J, Northover JMA, Bornmann P et al. A prospective evaluationof injection sclerotherapy in the treatment of acute bleeding from oesopha-geal varices. Surgery 1979; 85: 239-45.

7. Terblanche J, Northover JMA, Bornmann P et al. A prospective controlledtrial of sclerotherapy in long term management of patients after esopha-geal varical bleeding. Surgery Synec Obstet 1979; 148: 323-33.

8. Sinnett HD, Murray-Lyon IM, Reynolds KW, Johnson AG. Long term injec-tion sclerotherapy of œsophageal varices. Gastroenterology 1979; 76:1250.

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Several groups2,4,6,9,10 use a rigid Negus oesopha-goscope with or without a modification of its tip.l1This provides proximal lighting, ease of clearingblood and clots with a large-bore sucker, and theability to compress the recently injected variceswith the distal end. Unless the varices are

obstructed temporarily, the sclerosant solution

rapidly disperses.9,lo The fibreoptic gastro-oesopha-goscope is less traumatic and can be used withouta general anxsthetic, and most clinicians are nowmore familiar with it than with the old rigidoesophagoscope. However, its suction system is notgood for clearing blood and it needs some form ofsheath around it to compress the varices after injec-tion. In most centres ethanolamine 5% is injectedinto the veins. MACBETHz used sodium morrhuate5% which, unlike ethanolamine, is available in theU.S.A. and seems equally active. On the continentof Europe other sclerosants are used and sometimesinjected beneath the mucosa around the veins.12However, this technique means treating a largearea of mucosa and has produced several cases ofpartial or complete oesophageal-wall necrosis. In-travenous sclerosis may be most effective when theveins are thrombosed as low down in the

oesophagus as possible where they emerge from thesphincter. The complications are mainly those ofthe rigid oesophagoscopy and the Sengstaken-Blake-more tube. A proportion of patients experienceretrosternal pain for 12-24 h after injection. Somenarrowing of the lower oesophagus has been

reported after repeated injections,6,8 and the motil-ity of the lower oesophagus may be disturbed. 13The initial results of this treatment are encour-

aging. The procedure is aimed directly at the causeof the bleeding, and it can be repeated. While weawait the results of long-term controlled trials, itseems justified to recommend sclerotherapy for theemergency treatment of bleeding varices with care-ful attention to operative technique and aftercareof the patient. Once the haemorrhage is controlleda second assessment and injection, if necessary,should be made at 7-10 days and then every 2months until the varices are all thrombosed. In thefew cases where bleeding is not controlled, enthu-siasm for sclerotherapy must not blind the clinicianto alternative treatments such as oesophagealstapling transection 14 which may just save a

desperate situation.

9. Johnson AG. Injection sclerotherapy in the emergency and elective treatmentof œophageal varices. Ann Roy Coll Surg Engl 1977; 59: 497-501.

10. Barsoum MS, Khatter NY, Risk-Allah MA. Technical aspects of injectionsclerotherapy of acute oesophageal variceal haemorrhage as seen by radio-graphy. Br J Surg 1978; 65: 588-89.

11. Bailey ME, Dawson JL. Modified oesophagoscope for injecting oesophagealvarices. Br Med J 1975; ii: 540-41.

12. Paquet KJ, Oberhammer E. Sclerotherapy of bleeding œsophageal varices bymeans of endoscopy. Endoscopy 1978; 10: 7-12.

13. Ogle SJ, Kirk CJC, Bailey RJ, Johnson AG, Williams R, Murray-Lyon IM.Oesophageal function in cirrhotic patients undergoing injection sclerother-apy for oesophageal varices. Digestion 1978; 18: 178-85.

14. Johnson GW. Treatment of bleeding varices by oesophageal transaction withthe SPTU gun. Ann Roy Coll Surg Engl 1977; 59: 404-08.

What does Prolactin do in Man?

IN the eight years since human prolactin was iso-lated and defined, a relation between increased pro-lactin secretion and certain reproductive disordershas been established,1,2 but apart from its obviousrole in lactation we are still no clearer about what i

(if anything) prolactin does in normal subjects. If i

the traditional pathways of endocrinologicalthought are followed, certain clues are revealed butno firm conclusions are reached.The first of these approaches is to examine the

effects of abnormal secretion. For prolactin the Iabsent or reduced secretion seen after hypophysec-tomy or treatment with dopamine agonists is notassociated with demonstrable pathological findingsor biochemical changes. Hyperprolactinaemia, onthe other hand, is associated with amenorrhcea inwomen and impotence in men. The mechanismseems to be direct gonadal suppression, but agonad-inhibiting role in normal non-lactating sub-jects has not been established. Hyperprolactinaemiais also associated with an increase in the secretionof adrenal androgens,3 especially dehydroepiandro-sterone (DHA) and its sulphate. Evidence for a

physiological role here is also lacking but prolactinhas been implicated in the control of the fetaladrenal cortex,4 and the recent report5 of a correla-tion between nocturnal DHA and prolactin levelsin boys before puberty raises the possibility thatprolactin may be part of the long-sought pituitarymechanism controlling the adrenarche.6The second approach of endocrinologists is to

study the stimuli associated with changes in secre-tion and to attempt to draw physiological infer-ences. Apart from some drugs, the best-recognisednon-lactational stimuli are stress, rhythms, anddiet. Unfortunately, "stress" is a non-specific termwhich has different meanings for physiologists andpsychologists. It is also difficult to quantify and in-dividuals show wide variations in their responses toit. Prolactin levels rise in reponse to physical stress(e.g., marathon running’), admission to hospitalfor surgery, and the surgical procedure itself.8 It is

1. Thorner MO. Prolactin: clinical physiology and the significance and manage-ment of hyperprolactinaemia. In: Martini L, Besser GM eds. ClinicalNeuroendocrinology. New York: Academic Press. 1977: 319-61.

2. Bergh T, Nillius SJ, Wide L. Hyperprolactinæmia in amenorrhæa—inci-dence and clinical significance. Acta Endocrinol 1977; 86: 683-94.

3. Carter JN, Tyson JE, Warne GL, McNeilly AS, Faiman C, Friesen HG.Adrenocortical function in hyperprolactinemic women. J Clin EndocrinolMetabol 1977; 45: 973-80.

4. Winters AJ, Colston C, MacDonald PC, Porter JC. Fetal plasma prolactinlevels. J Clin Endocrinol Metabol 1975; 41: 626-29.

5. Popp J, Klein A, Grueters A, Korth-Schutz S. Nocturnal serum androgenconcentrations and prolactin in boys with delayed puberty. Acta Endoc-rinol 1979; suppl 225: 123.

6. Mills IH, Brooks RV, Prunty FTG. The relationship between the productionof cortisol and of androgen by the human adrenal. In: The HumanAdrenal Cortex. eds Currie AR, Symington T, Grant JK. Edinburgh: Liv-ingstone 1962: 204-31.

7. Dessypris A, Karonen SL, Adlercreutz H. Marathon run: effects on plasmaprolactin and growth hormone. Acta Endocrinol 1979; suppl 255:187.

8. Noel GL, Suh HK, Stone JG, Frantz AG. Human prolactin and growth hor-mone release during surgery and other conditions of stress. J Clin Endoc-rinol Metabol 1972; 35: 840-51.