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This question is less easy to answer until the results ofthe second phase of the multicentre trial are known.The therapeutic effect of imipramine develops moreslowly than that of alprazolam and, if unpleasantside-effects are to be avoided, it is necesssary to startwith small doses and increase the amount gradually.However, these difficulties in starting treatment withimipramine have to be weighed against the problemsof stopping alprazolam. Withdrawal symptoms canoccur at the end of treatment with alprazolam, evenwhen the dose is reduced very gradually." Theseriousness of this withdrawal syndrome needs to bedetermined, but until there is more reassuringinformation, it may be best to start with imipramineand reserve a benzodiazepine for patients in whomunpleasant side-effects of imipramine make it

necessary to stop the drug.Since agoraphobia can be treated with behavioural

methods, should drugs be used at all? There is goodevidence from clinical trials that behaviouraltreatment can produce substantial and lastingimprovement in agoraphobia, although many patientsare left with minor residual symptoms.13,14 Behaviourtherapy has been shown to enhance the effect ofimipramine in agoraphobia,15 but it is not certainwhether the addition of imipramine to behaviouraltreatment increases the effect16,17 or does not changeit.18 One explanation for the conflicting findings maybe that the beneficial effect of imipramine appearsonly in agoraphobics who have depressive symptoms,and that the proportion of such patients has varied indifferent trials. In view of these uncertainties it isreasonable to start treatment with behaviour therapy ifit is readily available, adding drugs only when thereare pronounced symptoms of depression or if

improvement does not take place within a few weeks. 19If behaviour therapy is not easy to arrange, drugtreatment can be tried first.What do these studies of drugs tell us about the

aetiology of agoraphobia? Probably very little becausethe drugs are as likely to be blocking the expression ofsymptoms as acting on the basic cause of agoraphobia.If there is a biological basis to this condition, it is morelikely to be revealed in genetic studies and

investigations of neurotransmitter function by

12. Pecknold JC, Swinson RP, Kuck K, Lewis CP Alprazolam in panic disorder andagoraphobia results from a multicenter trial III Discontinuation effects. ArchGen Psychiatry 1988; 45: 429-36.

13 Munby M, Johnston D. Agoraphobia: a long-term follow-up of behaviouraltreatment. Br J Psychiatry 1980; 137: 418-27.

14. McPherson FM, Brougham L, McLaren L Maintenance of improvements in

agoraphobic patients treated by behavioural methods in a four year follow-up.Behav Res Ther 1980; 18: 150-52

15. Mavissakalian M, Michelson L, Dealy RS Pharmacological treatment of agoraphobia:imipramine versus imipramine and programmed practice. Br J Psychiatry 1983;143: 348-55,

16. Telch MJ, Agras WS, Taylor CB, Roth WT, Gallen CG Combined pharmacologicaland behavioural treatment for agoraphobia Behav Res Ther 1985, 23: 325-35

17 Zitrin CM, Klein DF Woerner MG. Behavior therapy, supportive psychotherapy,imipramine, and phobias Arch Gen Psychiatry 1978; 35: 307-16.

18 Marks IM, Grey S, Cohen SD, Hill R, Mawson D, Ramm EM, Stem RS.Imipramine and brief therapist aided exposure in agoraphobics having self

exposure homework a controlled trial. Arch Gen Psychiatry 1983, 40: 153-62.19. Zitrin CM. Differential treatment of phobias use of imipramine for panic attacks

J Behav Ther Exp Psychiatry 1983, 14: 11-18

pharmacological challenge tests than by inferringcausation from the therapeutic effects of drugs.Results of these kinds of investigation have not yetproduced wholly convincing evidence of a biologicalbasis for agoraphobia 20 although there are indicationsthat panic disorder may be inherited.21 Other studiessuggest mainly psychological causes for the symptomsof agoraphobia, not only for the avoidance behaviourbut also for some of the apparently spontaneous panicattacks.22 This last result is especially interestingbecause these panic attacks are the centre-piece of thebiological theory of aetiology. It seems improbable,however, that either panic attacks or agoraphobia willturn out to have wholly psychological or whollybiological causes; it is much more likely that the twofactors interact, as they do in other psychiatricdisorders.

Hepatic Haemangioma—A SuitableCase for Treatment?

HAEMANGIOMA is the commonest benign liver

tumour, with necropsy frequency of 2-5 %.1 It hassome hamartomatous features2 and there are few

pathological associations. It is common in patientswith tuberous sclerosis3 and may be associated with

hepatic focal nodular hyperplasia.4 Oestrogenadministration has been linked with rapid growth,sand also with massive recurrence many years afterresection.6 Tumour enlargement has been reported inpregnancy. 7 Increasing use and sensitivity ofultrasound and computerised tomographic (CT)scanning have led to identification of many more ofthese lesions in a symptomless phase, and even inutero.8 Early diagnosis has led to two seriousdilemmas for the clinician: first, how to be certain that

20. Gelder MG. Panic attacks: new approaches to an old problem Br J Psychiatry 1986,149: 346-52.

21. Harris EL, Noyes R, Crowe RR, Chaudtry DR. A family study of agoraphobia reportof a pilot study. Arch Gen Psychiatry 1983; 40: 1061-64.

22. Clark DM, Salkovskis PM, Gelder MG, et al Test of a cognitive theory of panic InWittchen HV, Hand I, eds. Panic and phobia, vol III Munich Springer, 1988

1. Ochsner JL, Halpert B. Cavernous hemangioma of the liver Surgery 1958, 43: 577-822. Kojimahara M. Ultrastructural study of hemangiomas. Acta Pathol Jpn 1986, 36:

1477-85.3. Fleury P, Smits N, Van-Baal S. The incidence of hepatic hamartomas in tuberous

sclerosis evaluation by ultrasonography ROFO 1987; 146: 694-96.4. Wanless IR, Mawdsley C, Adams R. On the pathogenesis of focal nodular hyperplasia

of the liver. Hepatology 1985; 5: 1194-200.5 Morley JE, Myers JB, Sachs FS, et al. Enlargement of cavernous hemangioma

associated with exogenous administration of oestrogens. South Afr Med J 1974, 48:695-97.

6. Conter RL, Longmire WP Jr. Recurrent hepatic hemangiomas. Possible associationwith estrogen therapy. Ann Surg 1988; 207: 115-19.

7. Issa P. Cavernous hemangioma of the liver: the role of radiotherapy Br J Radiol 1968,41: 26-32.

8. Nakamoto SK, Dreilinger A, Dattel B, Mattrey RF, Key TC. The sonographicappearance of hepatic hemangioma in utero. J Ultrasound Med 1983, 2: 239-41

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a lesion found on scanning is truly a haemangioma andnot an occult malignancy and, secondly, to determinethe need for treatment once the diagnosis is reasonablycertain.Ultrasound scans may show the characteristic

features of increased echogenicity with homogeneousinternal echoes and well-defined margins. However,there is some variability in these appearances, whichare most reliable for smaller haemangiomas ( < 3 cm,9or < 8 cm1O). CT scanning without contrast

enhancement usually shows a nonspecific hypodenselesion; dynamic scanning after an intravenous bolus ofcontrast material shows highly characteristic changes,with peripheral enhancement progressing slowly toproduce complete filling-in of the tumour. Thispattern was found in more than 50% of

haemangiomas, but in less than 2% of malignanttumours; even in patients with known non-hepaticprimary tumours there was an 86% chance that alesion with these appearances would be a

haemangioma." However, false-positives may still befound, not only in malignant tumours but also inpatients with steatosis,12 and haemangiomas may notshow complete filling-in because of central fibrosis orthrombosis. For the same reason, hepatic angiographymay not distinguish between a haemangioma and avascular tumour with central necrosis. Autogenousred blood cells labelled with ’mTc may be used toproduce both dynamic and static scanninginformation: slow filling with blood pool activitygreater than the surrounding liver at 1-2 h was 100%specific and 89% sensitive in one report.13 Sensitivityfor lesions < 2 cm may be improved by use ofsingle-photon emission computerised tomography. 14Magnetic resonance imaging has also shown

promise,15,16 but may have little advantage over

dynamic contrast CT scanningYWhilst it would appear sensible to avoid

percutaneous biopsy, some reports have challengedthis conventional wisdom, claiming complete safetyfor biopsies with ’Trucut’10 or ’Franseen’ll’ needles.Plugging of the biopsy track with embolic material

9. Bruneton JN, Drouillard J, Fenart D, Roux P, Nicolau A. Ultrasonography of hepaticcavemous haemangiomas. Br J Radiol 1983; 56: 791-95

10. Reading NG, Forbes A, Nunnerley HB, Williams R. Hepatic haemangioma: a criticalreview of diagnosis and management. Quart J Med 1988; 67: 431-45.

11. Freeny PC, Marks WM. Patterns of contrast enhancement of benign and malignanthepatic neoplasms during a bolus dynamic and delayed CT. Radiology 1986; 160:613-18.

12 Penkrot RJ, Van-Thiel D Computed tomography of cavernous hemangiomas of theliver. how sure are we? J Comput Tomogr 1986; 10: 309-12

13 Engel MA, Marks DS, Sandler MA, Shetty P. Differentiation of focal intrahepaticlesions with 99mTc-red blood cell imaging. Radiology 1983; 146: 777-82.

14. Tumeh SS, Benson C, Nagel JS, English RJ, Holman BL. Cavernous hemangioma ofthe liver. detection with single photon emission computed tomography. Radiology1987; 164: 353-56.

15. Itai Y, Ohtomo K, Furui S, Yamauchi T, Minami M, Yashiro N. Noninvasivediagnosis of small cavernous hemangioma of the liver: advantage of MRI AJR1985; 145: 1195-99.

16 Ohtomo K, Itai Y, Yoshikawa K, Kokubo T, Yashiro N, Iio M. Hepatichaemangioma. dynamic MRI using gadolinium-DTPA Eur J Radiol 1987; 7:257-59

17. Robinson DA, McKinstry CS, Sterner RE, Wembren K, Blumgart LH, Halevy A.Magnetic resonance imaging of the solitary hepatic mass: direct correlation withpathology and computed tomography. Clin Radiol 1987, 38: 559-68

18. Cronan JJ, Esparza AR, Dorfman GS, Ridlen MS, Paolella LP. Cavernous

hemangioma of the liver: role of percutaneous biopsy. Radiology 1988; 166: 135-38.

may increase the safety margin. 19 Fine-needle

aspiration cytology seems safer, but the usual findingof blood with scanty cellular material does not excludea vascular tumour; moreover, even with fine-needle

aspiration there is a risk of major bleeding (2-5%)which compares with that for malignant hepatictumours (1-5%).The natural history of hepatic haemangiomas will

influence the treatment options. In adults, most suchtumours are an incidental finding on scanning or atoperation, but a few present, usually in the fourth tosixth decade, with pain or fullness, and withabdominal swelling if they are very large. The risk ofspontaneous rupture is exceedingly small, with onlytwenty-one published cases since 1898,21 and shouldnot dictate active treatment. Since there is no evidenceof malignant transformation with time, this possibilitycan be discounted. Although some haemangiomasgrow progressively, presumably by vascular ectasia,most will remain unchanged. All thirty-six patientsobserved for up to 15 years at the Mayo Clinicremained symptom-free, and only four lesionsincreased in size on scanning;21 in another series onlyone of sixty-eight enlarged during 1-6 years ofultrasound follow-up.22 Thus, a conservative policymay be advocated even for the so-called "giant"haemangioma (defined as > 4 cm23), if it is

symptomless. Such patients require strongreassurance, backed up by ultrasound scans at 6-12month intervals. For symptomatic patients, hepaticartery ligation may be effective,24 but probably less sothan intra-arterial embolisation.10,25 Embolisation

requires great skill to avoid early failure due to rapidrevascularisation if only the major feeding vessels areoccluded. Lesions seldom shrink after embolisation,and, although pain may be relieved, repeatedprocedures may be required. The general experienceis that symptoms are relieved in only half the patientsso treated 26 but embolisation has a definite role in

controlling traumatic haemorrhage. Radiotherapyshould not be entertained: there is little evidence for its

efficacy, and it carries a risk of radiation hepatitis.Surgical resection remains a valuable option, with a

high success rate in the control of complications andalso of pain in giant haemangiomas.27 Resection was

19. Riley SA, Ellis WR, Irving HC, Lintott DJ, Axon ATR, Losowsky MS. Percutaneousliver biopsy with plugging of needle track a safe method for use m patients withimpaired coagulation. Lancet 1984; ii: 436.

20. Gebel M, Horstkotte H, Koster C, Brunkhorst R, Brandt M, Atay Z. Ultrasound-guided fine needle puncture of the abdominal organs: indications, results, risks.Ultraschall Med 1986; 7: 198-202.

21. Trastek VF, Van-Heerden JA, Sheedy PF, Adson MA. Cavernous hemangiomas ofthe liver: resect or observe? Am J Surg 1983; 145: 49-53.

22. Gibney RG, Hendin AP, Cooperberg PL. Sonographically detected hepatichemangiomas: absence of change over time AJR 1987; 149: 953-57.

23. Adam YG, Huvos AG, Former JG. Giant hemangiomas of the liver. Ann Surg 1970;172: 239-45.

24 Peveretos P, Panoussopoulos D. Giant cavernous hepatic hemangioma: treatment byligation of the hepatic artery. J Surg Oncol 1986, 31: 48-51

25. Allison DJ, Jordan H, Hennessy O. Therapeutic embolisation of the hepatic artery: areview of 75 procedures. Lancet 1985; i: 595-99.

26. Martin B, Roche A, Radice L, Aguilar K, Kraiem C. Does arterial embolization have arole in the treatment of cavernous hemangioma of the liver in adults? Presse Med1986; 15: 1073-76.

27. Starzl TE, Koep LJ, Weil R III, et al. Excisional treatment of cavernous hemangiomaof the liver Ann Surg 1980, 192: 25-27.

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carried out in thirteen of forty-nine patients in theMayo Clinic series,21 and two of thirteen patientsrequiring treatment at King’s College Hospita1.1OEnucleation of haemangiomas, including some thatwere very large, has been reported as an alternative toformal hepatic resection,28 but this technique has notbeen widely used.What is the recommended management of hepatic

haemangiomas in 1988? Small, incidental, and

symptomless lesions may often be diagnosedaccurately by ultrasound alone, although repeatedscanning at intervals is important to reassure both thedoctor and the patient. Larger lesions may requiremore than one imaging technique to increase thecertainty of diagnosis, but percutaneous biopsyshould seldom be necessary. Since few lesions will

progress with time, most may safely be left untreated.Symptomatic or expanding lesions merit a trial ofarterial embolisation, to which some patients willrespond well. For the small group of patients left at theend of this series of therapeutic "filters", surgeryremains a very effective treatment, especially sinceimprovements in anaesthetic and surgical techniquehave made elective liver resection a safe procedure.

SURGICAL INSURRECTION

THE annual meeting of the Royal College of Surgeons(RCS) of England is usually a pedestrian affair, but this yearit was enlivened by a revolt by junior doctors, or surgeons-in-training, over proposed changes to the fellowship(FRCS) examination system. In Cambridge last month thetrainees were well organised, so their motion condemningsome of the changes was carried by a three-to-one majorityof those present. Sadly though, nothing will happen becauseother political pressures will undoubtedly intervene and theRCS England will have to conform to the wishes of its sisterColleges. Moreover, the juniors’ motion was flawed byconfusion in it and in the minds of those who voted for it.The story of the need to reform the FRCS system is long

and byzantine. The Colleges, Edinburgh, Glasgow, Ireland,and England, must set common goals and standards; theymust ensure the adequacy of surgical education; and theymust have a means of signifying those who have attainedtheir standards. Thus, the FRCS diploma was set up in1800, but this is long ago now. Confusion between the careeraspirations and the academic qualifications of junior doctorsis at the root of the current unrest and misunderstanding.Careers of junior surgeons, especially general surgeons, arefrustrated, consultant posts are not increasing, and the muchtrumpeted expansion promised under Achieving a Balancelhas not materialised. Although the Royal Colleges (in theUK) can offer advice to Government to expand the

28 Alper A, Anogul O, Emre A, Uras A, Okten A. Treatment of liver hemangiomas byenucleation Arch Surg 1988; 123: 660-61.

1. Hospital Medical Staffing-Achieving a Balance Consultative document issued onbehalf of the UK Health Departments, the Joint Consultants Committee, andChairmen of the Regional Health Authorities July, 1986

consultant grade in surgery, they cannot be held to account ifGovernment ignores this advice. The present Governmenthas unrivalled experience of ignoring advice, hence thefrustration of well-trained senior registrars who are

becoming tired and disheartened. This pent-up emotionwas vented in Cambridge.A separate issue, although one inevitably melded with the

career aspirations of young surgeons, is the debate about thestructure of the examinations that should denote that a

person is fit to practise autonomously as a surgeon. TheFRCS diploma does not indicate a fully trained surgeon;rather it identifies those who have attained the necessarybasic knowledge to embark on specialist (higher) surgicaltraining. The Royal Colleges have long recognised theinadequacy of the FRCS as a sign of completed surgicaltraining; the specialist associations also recognise this

deficiency, and the vacuum has been imperfectly filled withaccreditation. Yet accreditation does not confer any letterson the anointed, so how does one establish which surgeonsare accredited? There is a need for specialist diplomas toindicate who is fully trained. (Some would opine specialistregisters are a societal requirement too.) This requirementfor specialist qualification has been met in part by theEdinburgh College of Surgeons, who have proved muchmore innovative than their counterparts. At last the Collegesare acting in concert and intercollegiate specialist boards (eg,in neurosurgery and urology) are set up and now offer ahigher examination in certain specialties-those who obtainthe qualification can consider themselves fully trained. Butsome of the long-suffering and time-expired senior

registrars in general surgery fear the introduction of a similarexamination in that branch of surgery, wondering whetherthey will have to take another (new) examination at the age of40 or even 45 if they are to compete for the new consultantposts. Hence the rebellion at Cambridge. Both sides in thisconflict are blessed with right and wrong.The Colleges have not acted crisply enough in finalising

their proposals for the new (exit) examination in generalsurgery. Even worse, their communication with the rankand file has been inadequate. The proposals brilliantlyoutlined in Cambridge by Prof Norman Browse have notbeen appreciated by the juniors, who meanwhile haveallowed their paranoia about poor career prospects to

become confused with the changes in the examinationstructures that will improve the lot of the next generation ofjunior doctors.

In formulating their policies, the Colleges have twoguiding principles. All surgeons, whatever their discipline,must appreciate the general principles that underlie all

surgical practice. Thus, the revised first examination willinclude anatomy, physiology, other basic sciences, and anexamination in the principles, clinical and operative, ofsurgery. This test will equip the aspirant for higher surgicaltraining. The original idea was that the examination wouldbe taken at one sitting, but compassion and reality havetempered this proposal and the English college has agreedthat candidates may sit the examination in two parts, part Ato include the basic sciences and part B to include the clinical

components. All the Colleges are in accord here-theexamination will be in the principles of surgery and will notbe like the existing FRCS with its predominantly generalsurgical ethos. Perhaps this is where the Colleges’communication systems first went wrong. They have notstressed the novelty of the examination and they haveallowed the word "general", with its heavy overtones of