940 CLINICAL REPORTS

pite consistently high serum osmolality, but hemaintained an intact ADH response to nausea andhypoglycaemia, implicating impaired osmorecep-tor function as the cause of his diabetes insipidus.

Both hypothermia and the SIADH are raremanifestations of neurological disease. The centrescontrolling thermoregulation and serum osmola-lity are both located within the hypothalamus.8"'0The organosum vasculosum of the lamina ter-minalis is thought to be the site of osmoreceptors,

and the cells synthesizing ADH are located in thesupraoptic and paraventricular nuclei. The path-ways controlling thermoregulation are less wellunderstood, but neurons that are responsive totemperature variation have been identified in theanterior hypothalamus and preoptic area. Al-though we have no direct evidence, it is likely thathypothalamic dysfunction in these areas is thecause of our patient's chronic hypothermia andSIADH.

References

1. Sullivan, F., Hutchinson, M., Bahandeka, S. & Moore, R.E.Chronic hypothermia in multiple sclerosis. J Neurol Neuro-surg Psychiatry 1987, 50: 813-815.

2. Haak, H.R., van Hilten, J.J., Roos, R.A.C. & Meinders, A.E.Functional hypothalamic derangement in a case of Wer-nicke's encephalopathy. Neth J Med 1990, 36: 291-296.

3. Lipton, J.M., Kirkpatrick, J. & Rosenberg, R.N. Hypother-mia and persisting capacity to develop fever. Occurence in apatient with sarcoidosis of the central nervous system. ArchNeurol 1977, 34: 498-504.

4. Ratcliffe, B.J., Bell, J.I., Collins, K.J., Frackowiak, R.S. &Rudge, P. Late onset post-traumatic hypothermia. J NeurolNeurosurg Psychiatry 1983, 46: 72-74.

5. Nussey, S.S., Ang, V.T. & Jenkins, J.S. Chronic hypernat-raemia and hypothermia following subarachnoid haemorr-hage. Postgrad Med J 1986, 62: 467-471.

6. Fox, R.H., Davies, T.W., Marsh, F.P. & Urich, H. Hypo-thermia in a young man with an anterior hypothalamiclesion. Lancet 1970, 2: 185-188.

7. Bayliss, R.H. & Thompson, C.J. Osmoregulation of vaso-pressin secretion and thirst in health and disease. ClinEndocrinol 1988, 29: 549-576.

8. Lightman, S. Central nervous system control offluid balance:physiology and pathology. Acta Neurochirurgica Suppi 1990,47: 90-94.

9. Reuler, J.B. Hypothermia: pathophysiology, clinical settingand management. Ann Intern Med 1978, 89: 519-527.

10. Mitchell, D. & Labum, H.P. Pathophysiology of temperatureregulation. Physiologist 1985, 28: 507-517.

Postgrad Med J (1993) 69, 940-945 (D The Fellowship of Postgraduate Medicine, 1993

Spontaneous coronary artery dissection: a report of threecases and review of the literature

Peter Kearney, Harsh Singh2, John Hutter2, Saleem Khan, Gary Lee andJames Lucey'

Department ofCardiology, University College Cork, South Infirmary Hospital, and 'Bon Secours Hospital,Cork, Ireland, and 2Bristol Royal Infirmary, Bristol, UK

Summary: We describe the clinical course of three patients who developed spontaneous coronaryartery dissection. All patients were young women, one 9 weeks pregnant. All presented with chest pain; onedied suddenly proving refractory to resuscitation, another developed unstable angina culminating inmyocardial infarction, cardiogenic shock and death, and the third patient underwent coronary arterybypass grafting following diagnosis of a spontaneous coronary dissection of the left anterior descendingartery at angiography. Pathological findings in the two fatal cases are reported.

This condition, although rare, is a prominent cause ofischaemic coronary events in young women, whenit is frequently associated with pregnancy or the puerperium. Most patients die suddenly, but a clinicalspectrum is seen including stable and unstable angina, myocardial infarction and cardiogenic shock. Theleft anterior descending artery is most frequently affected. The classical histological finding is that of alarge haematoma occupying the outer third of the media resulting in complete compression of the truelumen.The cause of spontaneous dissection remains unclear but theories of aetiology include a medial

eosinophilic angiitis, pregnancy-induced degeneration of collagen in conjunction with the stresses ofparturition, and rupture of the vasa vasorum.

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The diagnosis must be considered when a patient presents with a suggestive clinical profile. Urgentangiography should be undertaken to establish the diagnosis and consideration given to the need forcoronary artery bypass grafting, which has been successfully employed in a number of patients. Theuneventful long-term survival of cases treated conservatively has been reported.

Introduction

Spontaneous coronary dissection is a rare butincreasingly reported cause of myocardial ischae-mia and sudden cardiac death. It is seen commonlyin young women and there is a strong associationwith the puerperium. A clinical spectrum is seenincluding stable and unstable angina, myocardialinfarction, cardiogenic shock and frequently sud-den death. Although the majority of cases are fatal,the diagnosis being made after death, there are anumber of reports of successful medical and sur-gical intervention. The sporadic nature of thecondition and small number of reported survivorsmake to difficult to draw firm conclusions as to theoptimal forms of treatment. We report the courseof three patients whose presentations exemplify thevariable course the disorder may take and give riseto a number of therapeutic considerations.

Case 1

A previously well 34 year old farmer's wife wasadmitted to hospital complaining of central chestpain radiating to her face and both arms. The painhad begun 3 hours prior to arrival at the hospital,although she was pain free following admission.She had no known risk factor for ischaemic heartdisease. An episode of unexplained chest and leftarm pain had occurred some months before.Clinical examination was unremarkable. She waspara 2, gravida 1 and was 9 weeks pregnant. Herelectrocardiograph was normal. Within the firstminutes of her admission, during her clinicalexamination, she developed ventricular fibrillationand subsequently a tonic-clonic seizure. Cardiopul-monary resuscitation was started but following aninitially successful D.C. shock she developed re-fractory ventricular fibrillation and further resus-citation attempts were unsuccessful.

Postmortem examination revealed an area ofdark, blueish discoloration at the junction of hermiddle and distal left anterior descending coronaryartery. Sectioning revealed complete occlusion ofthe vessel at this point. Histology demonstratedmedial dissection of the mid and distal left anteriordescending artery with intramural thrombus accu-

mulation and consequent compression ofthe vessellumen. Patchy fibrosis of the distal septum wasfound but no evidence of acute myocardial infarc-tion. Minimal atheroma was evident in both coron-ary arteries.

Case 2

A 31 year old woman, wheelchair bound withmultiple sclerosis, presented to the accident andemergency department complaining of centralchest pain of one hour's duration associated withbreathlessness and sweating. She was a smoker offive cigarettes a day and had a family history ofischaemic heart disease. Her electrocardiographwas abnormal, demonstrating left axis deviation,lateral wall T wave inversion and decreased R waveamplitude in the chest leads. Despite the strongestadvice, she refused hospital admission.

She returned on the evening of the next dayexperiencing persistent pain which worsened episo-dically. It now radiated to her left arm andbreathlessness was more pronounced. Cardiovas-cular examination was unremarkable. Her cardio-graph demonstrated septal Q waves and T waveinversion was more marked in V4-6. Creatinekinase was marginally elevated to twice the upperrange of normal at 4.5 gkat/l. She was admittedand treated for unstable angina with aspirin andinfusions of heparin and glyceryl trinitrate, onwhich she initially stabilized. Thrombolysis wasnot administered. She later developed furthersevere chest pain and new anterolateral ST eleva-tion was seen on her cardiograph. Her creatinekinase subsequently rose to 55 .tkat/l and echocar-diography demonstrated anteroapical akinesia.She developed refractory cardiogenic shock andcongestive heart failure, and died on the seventhday of her admission.A postmortem examination revealed grossly

congested lungs. Extensive infarction of the leftventricle was evident. Sectioning revealed dissec-tion of the proximal left main coronary arterywhich extended to the distal segments of both leftanterior descending and left circumflex arteries.Minimal atheroma was found and no inflamma-tory process noted in the vessel wall. A serologicalscreen for vasculitis, and anticardiolipin antibodyand urinary aminoacid chromatography werenegative.

Correspondence and present address: Peter Kearney,M.R.C.P.I., 2nd Medical Clinic, Johannes GutenbergUniversity, D-6500 Mainz, Germany.Accepted: 12 May 1993

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Case 3

A 37 year old farm hand was admitted to hospitalwith an anterior myocardial infarction. She hadexperienced exertional chest pain for the preceding9 weeks, which she had largely ignored. Shesmoked 10 cigarettes a day and had a positivefamily history for ischaemic heart disease. Shesuffered from well-controlled coeliac disease andserum cholesterol was 3.8 mmol/l. She was para 4,gravida 4.

She developed postinfarction angina and under-went urgent coronary angiography. A dissectionwas seen at the junction of proximal and middlesegments of the left anterior descending artery andthe remainder of the coronary vasculature appear-ed free of disease (Figure 1). There was slowanterograde filling of the distal left anterior descen-ding artery which was supported by collateralfilling from the right coronary artery. Left ven-triculography demonstrated apical dyskinesia anda hypokinetic free wall and septum. Coronaryartery bypass grafting was performed, using the leftinternal mammary artery. The graft was inserteddistal to the dissection and the proximal vessel wasnot tied off. She was discharged well and was painfree on subsequent follow-up.

Figure 1 Angiogram of case 3, taken in the left anterioroblique projection, demonstrating a dissection in theproximal left anterior descending artery (arrow). Theremainder of the coronary tree was free of disease.

There have been 1341 10 cases of spontaneouscoronary artery dissection reported in the worldliterature. Over two thirds of reported cases havebeen women and, of these, one third were eitherpregnant (two previous cases) or in the puerperium(24 cases).The left anterior descending artery is involved in

80% of cases, the remainder involved the rightcoronary artery and a small number the leftcircumflex artery. There have been three reports ofinvolvement ofboth right and left coronary arteriesand 19 reports of left main coronary involvement.Case 2 described above is the fourth report of adissection extending from left main coronary arteryto both left anterior descending and circumflexarteries.'1-13Coronary dissections may occur secondary to

atherosclerosis, coronary angiography, percutan-eous coronary interventions, bypass surgery, chesttrauma and Marfan's syndrome. Unlike aorticdissections, no association with hypertension hasbeen noted. Despite certain histological featuresfound in a number of cases, the cause of 'primary'coronary dissection remains unknown and it isimprobable that a single mechanism operates in allpatients.

Pathological examination reveals displacement,distortion and usually complete compression of thelumen by a large haematoma (Figure 2). The planeofthe dissection runs in the outer third ofthe mediaor between media and adventitia. Apart from thesefeatures, no uniform histological findings havebeen identified. An adventitial infiltrate of eosino-philic granulocytes was noted in eight patientsstudied by Robinowitz et al. 4 and, at the time of hisreview, a further 20 cases had been described inwhich similar infiltrates were evident. Cystic medialnecrosis was evident in 17 patients in this series, buthas been specifically excluded in a greater number.Intimal tears have been infrequently reported.'5 16On the basis of his findings, Robinowitz postu-

lated that spontaneous dissection results from anaccumulation of eosinophils which secrete lyticenzymes and major basic protein leading to medialweakening. A more recent report'7 highlighted thecase of a young man who died following myocar-dial rupture secondary to dissection and occlusionof a branch of his left circumflex artery. A markedeosinophilic and mast cell infiltrate was found atthe site of dissection. He had experienced a recentdrug hypersensitivity reaction, which the authorsfelt may have induced an angiitis of his vasavasorum. A similar mechanism may have operatedin a 70 year old man found to have dissection of anectatic right coronary artery. He had a history of atransient illness characterized by a markedeosinophilia and an associated cardiomyopathy.'

Discussion

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Figure 2 Histological section of a medial dissection found in the left anterior descending artery of case 2. Thrombus(T) occupies the outer third of the media and has obliterated the lumen (L), which is almost completely compressed. Anarrow points to the dissection plane running between media and adventitia.

Others emphasize the lack of any such findings inmany autopsy reports and suggest that infiltrates,when present, are a secondary inflammatoryphenomenon. 18,19

It has been suggested that disruption of vasavasorum may lead to intramedial haemorrhage andsubsequent dissection.20 Although such vessels aremore plentiful and fragile in the presence ofdeveloping atheroma2' they are scanty in the cor-onary circulation and are a relatively low pressuresystem, the rupture of which would seem unlikelyto lead to luminal compression under normalcircumstances. Normal coronaries may be moresusceptible to luminal compression by intramedialhaemorrhage in the absence of the stenting effect ofatheroma,22 providing a potential explanation forthe sex and age distribution of patients with thisdisorder.

Intimal tears might extend and lead to medialdissection. Although they are infrequently demon-strated, Claudon et al."5 emphasize the meticuloustechnique that is required to outrule a tear withcertainty, finding this in just one of 150 sections ofthe haematoma in the first of their patients.Angiographic diagnosis of coronary dissection

depends on opacification of a false lumen whichcan occur only if a communication, as provided bya tear, exists. This lends support to the potentialaetiological role of intimal disruption.The degenerative effect of pregnancy on blood

vessels, including the coronaries, in conjunctionwith increased blood flow and consequent intimalshear stress experienced at parturition has beensuggested to underlie the concentration of cases inthe puerperium.23 Some support for this theory isfound in a report of a 32 year old women whoexperienced anterior myocardial infarctions 2 and4 months postpartum as a result of angiographi-cally diagnosed primary coronary dissection.Fibroblasts were cultured from the patient and areduction in the rate of total collagen synthesisrelative to that of a control culture was seen,leading the authors to speculate on a disturbance ofnormal collagen synthesis as a result of hormonalchanges in pregnancy and in the postpartumperiod.24The majority of patients die before any interven-

tion can be of benefit which may in part relate to theabsence of any pre-existing stenoses and henceprotective collaterals. In an early review of43 cases,

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Smith25 noted sudden death in 63% ofcases and theproportion ofcases dying suddenly remains largelyunchanged since. The very low level ofantemortemdiagnosis may be explained by the high suddendeath rate, although failure to include the condi-tion in a differential diagnosis may also contribute.Recent reports highlight the good prognosis ofthose who survive the initial event; the asympto-matic survival of patients with spontaneous dissec-tions who have been followed conservatively hasbeen seen for up to 12 years.26 Spontaneous angio-graphic improvement has been documented in sucha case.27Behnam et al.2 report the successful administra-

tion ofalteplase to a woman subsequently shown tohave a primary dissection of her left anteriordescending artery. They note a further four cases inwhich thrombolytic agents were given safely andsuggest that luminal re-expansion can be establish-ed by lysing thrombus in the false lumen. We areaware ofa more recent case who received successfulthrombolysis on two occasions over a 4 year periodfor anterior myocardial infarctions prior to diag-nosis of a large spontaneous dissection in her leftanterior descending artery. Vacek et al.28 admini-stered intracoronary streptokinase in a case ofiatrogenic coronary dissection with good effect.When the patient survives the initial period, and

remains unstable or suffers ongoing inducibleischaemia, coronary artery bypass grafting hasbeen successful.20 It would appear to be unneces-sary to ligate the vessel proximal to the graftanastomosis to prevent further dissection. Subse-quent angiography may show evidence of residualdissection, despite successful revascularization.29Internal mammary grafts are preferable, in view ofthe young age and otherwise excellent outlook ofthese patients. Percutaneous coronary balloonangioplasty has been successfully performed in apatient with primary dissection of the left anteriordescending artery.30 There are two reports of

patients receiving orthotopic cardiac transplantsfollowing primary dissection, one requiring thesupport of a Jarvik 7-70 artificial heart while acompatible heart was located.69

Conclusions

A number of important therapeutic issues areraised by the cases we report. It is possible thatanticoagulation and anti-platelet therapy, both ofproven benefit in unstable angina due to atheroma-tous coronary disease, might predispose to worsen-ing of the dissection in a case of primary coronarydissection. This may explain the refractory un-stable angina of case 2 and underlie the veryextensive dissection found at autopsy. For similarreasons there is understandable reluctance toadminister thrombolytic therapy in this condition,although a number of reports suggest that somepatients have benefited.The diagnosis must be considered in patients at

low risk for atheroslcerotic heart disease whopresent with symptoms of myocardial ischaemia,particularly young women who are pregnant or inthe puerperium. Urgent coronary angiography isnecessary to make the diagnosis and should beundertaken when spontaneous coronary dissectionis considered a possibility. If the patient remainsunstable, medical therapy alone should not berelied upon and consideration should be given tourgent bypass grafting. Percutaneous coronaryballoon angioplasty may have a role in certaincases. In those who remain stable, conservativemanagement appears to be safe and compatiblewith an excellent long-term outlook.

Acknowledgements

We thank Dr W. Fennell, Dr H. Walsh and Dr N. Cahillfor their contribution in the management of these cases.

References

1. Yeoh, J., Choo, H., Soo, C., Lim, Y. & Yan, C. Spontaneouscoronary artery dissection in a young man with anteriormyocardial infarction. Cathet Cardiovasc Diagn 1991, 24:186-188.

2. Behnam, R. & Tillinghast, S. Thrombolytic therapy inspontaneous coronary artery dissection. Clin Cardiol 1991,14: 611-614.

3. Saunders, S. & Ford, S. Primary coronary artery dissectionpossibly related to drug hypersensitivity in a male. Can JCardiol 1991, 7: 138-140.

4. Huikuri, H., Mallon, S. & Myerburg, R. Cardiac arrest due tospontaneous coronary artery dissection in a patient withcoronary ectasia - a case report. Angiology 1991, 42:148-151.

5. Fronc, H., MacMillan, R. & Kimbiris, D. Coronary arterydissection - a case report. Angiology 1990, 41: 884-887.

6. Curiel, P., Spinelli, G., Petrella, A. et al. Postpartum coronarydissection followed by heart transplantation. Am J ObstetGynecol 1990, 163: 538-539.

7. Nishino, M., Kato, J., Exumi, A. et al. A case of primarycoronary artery dissection. Kokyu To Junkan 1990, 38:589-593.

8. Moor, D., Laska, J. & Lindblom, D. Spontaneous coronaryartery dissection treated by bypass surgery. Lakartidningen1990, 87: 485-486.

9. Keon, W., Koshal, A., Boyd, W., Laramee, L., Farrell, E. &Walley, V. Survival after spontaneous primary left maincoronary artery dissection. Acute surgical intervention withthe Jarvik 7-70 artificial heart. J Cardiovasc Surg 1989, 30:786-789.

10. Lette, J., Gagnoon, A., Cerino, M. & Prenovault, J. Apicalhypertrophic cardiomyopathy with spontaneous post partumcoronary artery dissection. Can J Cardiol 1989, 5: 311-314.

11. Razavi, M. Unusual forms of coronary artery disease.Cardiovasc Clin 1975, 7: 25-46.

12. Shaver, P., Carrig, T. & Baker, W. Postpartum coronaryartery dissection. Br Heart J 1978, 40: 83-86.

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13. Baker, P., Keyhani-Rofagha, S., Graham, R. & Sharma, H.Dissecting hematoma (aneurysm) of coronary arteries. Am JMed 1986, 80: 317-319.

14. Robinowitz, M., Virmani, R. & McAllister, H.A. Spon-taneous coronary artery dissection and eosinophilic inflam-mation: a cause and effect relationship? Am J Med 1982, 72:923-928.

15. Claudon, D., Claudon, D. & Edwards, J. Primary dissectinganeurysm of coronary artery: a cause of acute myocardialischemia. Circulation 1972, 45: 259-266.

16. Molloy, P., Ablett, M. & Anderson, K. Left main stemcoronary artery dissection. Br Heart J 1980, 43: 705-708.

17. Saunders, S. & Ford, S. Primary coronary artery dissectionpossibly related to drug hypersensitivity in a male. Can JCardiol 1991, 7: 138-140.

18. Sage, M., Koelmeyer, T. & Smeeton, W. Fatal postpartumcoronary artery dissection. A light and electron microscopestudy. Am J Forensic Med Path 1986, 7: 107-111.

19. Dowling, G. & Buja, L. Spontaneous coronary artery dissec-tion occurs with and without periadventitial inflammation.Arch Path Lab Med 1987, 111: 470-472.

20. Thayer, J., Healy, R. & Maggs, P. Spontaneous coronaryartery dissection. Ann Thorac Surg 1987, 44: 97-102.

21. Barger, A., Beeuwkes, R., Lainey, L. & Silverman, K.Hypothesis: vasa vasorum and neovascularization of humancoronary arteries: a possible role in the pathophysiology ofatherosclerosis. N Engl J Med 1984, 310: 175-177.

22. Bulkley, B. & Roberts, W. Isolated coronary arterial dissec-tion. J Thorac Cardiovasc Surg 1978, 67: 148-151.

23. Barrett, J., Van Hooydonk, J. & Boehm, F. Pregnancy relatedrupture of arterial aneurysms. Obstet Gynecol Surv 1982, 37:557-566.

24. Bonnet, J., Aumailley, M., Thomas, D. et al. Spontaneouscoronary artery dissection: case report and evidence for adefect in collagen metabolism. Eur Heart J 1986, 7: 904-909.

25. Smith, J. Dissection aneurysms of coronary arteries. ArchPathol 1975, 99: 117-121.

26. DeMaio, S., Kinsella, S. & Silverman, M. Clinical course andlong-term prognosis of spontaneous coronary artery dissec-tion. Am J Cardiol 1989, 64: 471-474.

27. Werner, G.S., Wojcik, J., Wiegand, V. & Kreuzer, H.Spontaneous coronary artery dissection: a rare cause ofmyocardial infarct. Z Kardiol 1990, 79: 32-36.

28. Vacek, J. & McKiernan, T. Intracoronary streptokinase foracute coronary artery dissection. N Engl J Med 1984, 310:1187.

29. Matsuura, A., Yasuura, K., Sawasaki, M. et al. Spontaneouscoronary artery dissection: a case report and a review of theliterature. Kyoba Geka 1992, 45: 243-246.

30. Gonzales, J., Hill, J. & Conti, C. Spontaneous coronaryartery dissection treated with percutaneous transluminalangioplasty. Am J Cardiol 1989, 63: 885-886.

Postgrad Med J (1993) 69, 945 -947 i) The Fellowship of Postgraduate Medicine, 1993

Successful use of a transjugular intrahepatic portosystemicstent shunt to control severe refractory oesophagealvariceal haemorrhage in a poor risk patient

I.L.P. Beales, J.E. Jackson', M. Rudolf and J. Arnold

Department ofMedicine, Ealing HospitalNHS Trust, Uxbridge Road, Southall, Middlesex UBI 3HWand'Department ofDiagnostic Radiology, Royal Postgraduate Medical School, Hammersmith Hospital,Du Cane Road, London W12 ONN, UK

Summary: This report describes a 44 year old man with a severe gastrointestinal haemorrhage fromoesophageal varices. Bleeding could not be controlled with conservative therapy and sclerotherapy. He wassuccessfully treated with a radiologically guided transjugular intrahepatic stent shunt at a time when hiscondition was too poor to attempt an open surgical procedure.

Introduction

Haemorrhage from oesophageal varices in patientswith portal hypertension remains a common andserious medical emergency associated with signi-ficant mortality and morbidity. Injection sclero-therapy is the most effective primary therapy foracute variceal bleeding. Pharmacotherapy and

balloon tamponade have useful supporting roles." 2Despite therapy, some 10-20% of patients maycontinue bleeding35 and in these cases the prog-nosis is poor.3 We report a case of severe refractorybleeding in a patient with poor outlook, eventuallycontrolled with a transjugular intrahepatic porto-systemic stent shunt (TIPSS). This should lead towider consideration and evaluation of this techni-que as an alternative to surgery in critically illpatients.

Correspondence and present address: I.L.P. Beales, B.Sc.,M.R.C.P., Department of Gastroenterology, Hammer-smith Hospital, Du Cane Road, London W12 ONN.Accepted: 17 May 1993

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