Hepatic Haemangioma—A Suitable Case for Treatment?

882

This question is less easy to answer until the results of the second phase of the multicentre trial are known. The therapeutic effect of imipramine develops more slowly than that of alprazolam and, if unpleasant side-effects are to be avoided, it is necesssary to start with small doses and increase the amount gradually. However, these difficulties in starting treatment with imipramine have to be weighed against the problems of stopping alprazolam. Withdrawal symptoms can occur at the end of treatment with alprazolam, even when the dose is reduced very gradually." The seriousness of this withdrawal syndrome needs to be determined, but until there is more reassuring information, it may be best to start with imipramine and reserve a benzodiazepine for patients in whom unpleasant 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 good evidence from clinical trials that behavioural treatment can produce substantial and lasting

improvement in agoraphobia, although many patients are left with minor residual symptoms.13,14 Behaviour therapy has been shown to enhance the effect of imipramine in agoraphobia,15 but it is not certain whether the addition of imipramine to behavioural treatment increases the effect16,17 or does not change it.18 One explanation for the conflicting findings may be that the beneficial effect of imipramine appears only in agoraphobics who have depressive symptoms, and that the proportion of such patients has varied in different trials. In view of these uncertainties it is reasonable to start treatment with behaviour therapy if it is readily available, adding drugs only when there are pronounced symptoms of depression or if improvement does not take place within a few weeks. 19 If behaviour therapy is not easy to arrange, drug treatment can be tried first. What do these studies of drugs tell us about the aetiology of agoraphobia? Probably very little because the drugs are as likely to be blocking the expression of symptoms as acting on the basic cause of agoraphobia. If there is a biological basis to this condition, it is more likely to be revealed in genetic studies and investigations of neurotransmitter function by JC, Swinson RP, Kuck K, Lewis CP Alprazolam in panic disorder and agoraphobia results from a multicenter trial III Discontinuation effects. Arch Gen Psychiatry 1988; 45: 429-36. 13 Munby M, Johnston D. Agoraphobia: a long-term follow-up of behavioural treatment. 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.

12. Pecknold

Behav Res Ther 1980; 18: 150-52 15. Mavissakalian M, Michelson L, Dealy RS imipramine

versus

imipramine

and

Pharmacological treatment of agoraphobia: programmed practice. Br J Psychiatry 1983;

143: 348-55,

MJ, Agras WS, Taylor CB, Roth WT, Gallen CG Combined pharmacological and 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 16. Telch

pharmacological challenge tests than by inferring causation from the therapeutic effects of drugs. Results of these kinds of investigation have not yet produced wholly convincing evidence of a biological basis for agoraphobia 20 although there are indications that panic disorder may be inherited.21 Other studies suggest mainly psychological causes for the symptoms of agoraphobia, not only for the avoidance behaviour but also for some of the apparently spontaneous panic attacks.22 This last result is especially interesting because these panic attacks are the centre-piece of the biological theory of aetiology. It seems improbable, however, that either panic attacks or agoraphobia will turn out to have wholly psychological or wholly biological causes; it is much more likely that the two factors interact, as they do in other psychiatric disorders.

Hepatic Haemangioma—A Suitable Case for Treatment? HAEMANGIOMA is the commonest benign liver tumour, with necropsy frequency of 2-5 %.1 It has hamartomatous features2 and there are few pathological associations. It is common in patients with tuberous sclerosis3 and may be associated with hepatic focal nodular hyperplasia.4 Oestrogen administration has been linked with rapid growth,s and also with massive recurrence many years after resection.6Tumour enlargement has been reported in pregnancy.7 Increasing use and sensitivity of ultrasound and computerised tomographic (CT) scanning have led to identification of many more of these lesions in a symptomless phase, and even in utero.8 Early diagnosis has led to two serious dilemmas for the clinician: first, how to be certain that some

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 report of 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 In Wittchen 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: 577-82 2. 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 association with 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 sonographic appearance of hepatic hemangioma in utero. J Ultrasound Med 1983, 2: 239-41

883

found on scanning is truly a haemangioma and not an occult malignancy and, secondly, to determine the need for treatment once the diagnosis is reasonably certain. Ultrasound scans may show the characteristic features of increased echogenicity with homogeneous internal echoes and well-defined margins. However, there is some variability in these appearances, which are most reliable for smaller haemangiomas ( < 3 cm,9 <8 or cm1O). CT scanning without contrast enhancement usually shows a nonspecific hypodense lesion; dynamic scanning after an intravenous bolus of contrast material shows highly characteristic changes, with peripheral enhancement progressing slowly to produce complete filling-in of the tumour. This pattern was found in more than 50% of haemangiomas, but in less than 2% of malignant tumours; even in patients with known non-hepatic primary tumours there was an 86% chance that a lesion with these appearances would be a haemangioma." However, false-positives may still be found, not only in malignant tumours but also in patients with steatosis,12 and haemangiomas may not show complete filling-in because of central fibrosis or thrombosis. For the same reason, hepatic angiography may not distinguish between a haemangioma and a vascular tumour with central necrosis. Autogenous red blood cells labelled with ’mTc may be used to produce both dynamic and static scanning information: slow filling with blood pool activity greater than the surrounding liver at 1-2 h was 100% specific and 89% sensitive in one report.13 Sensitivity for lesions < 2 cm may be improved by use of single-photon emission computerised tomography. 14 Magnetic resonance imaging has also shown promise,15,16 but may have little advantage over dynamic contrast CT scanningY Whilst it would appear sensible to avoid percutaneous biopsy, some reports have challenged this conventional wisdom, claiming complete safety for biopsies with ’Trucut’10 or ’Franseen’ll’ needles. Plugging of the biopsy track with embolic material a lesion

J, Fenart D, Roux P, Nicolau A. Ultrasonography of hepatic haemangiomas. Br JRadiol 1983; 56: 791-95 10. Reading NG, Forbes A, Nunnerley HB, Williams R. Hepatic haemangioma: a critical review of diagnosis and management. QuartJ Med 1988; 67: 431-45. 11.Freeny PC, Marks WM. Patterns of contrast enhancement of benign and malignant hepatic neoplasms during a bolus dynamic and delayed CT. Radiology 1986; 160: 9. Bruneton JN, Drouillard cavemous

613-18. 12 Penkrot RJ, Van-Thiel D Computed tomography of cavernous hemangiomas of the liver. how sure are we? J Comput Tomogr 1986; 10: 309-12 13 Engel MA, Marks DS, Sandler MA, Shetty P. Differentiation of focal intrahepatic lesions with 99mTc-red blood cell imaging. Radiology 1983; 146: 777-82. 14. Tumeh SS, Benson C, Nagel JS, English RJ, Holman BL. Cavernous hemangioma of the liver. detection with single photon emission computed tomography. Radiology 1987; 164: 353-56. 15. Itai Y, Ohtomo K, Furui S, Yamauchi T, Minami M, Yashiro N. Noninvasive diagnosis of small cavernous hemangioma of the liver: advantage of MRI AJR 1985; 145: 1195-99. 16 Ohtomo K, Itai Y, Yoshikawa K, Kokubo T, Yashiro N, Iio M. Hepatic haemangioma. dynamic MRI using gadolinium-DTPA EurJ 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 with pathology 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

aspiration cytology

safety margin. 19 Fine-needle safer, but the usual finding

seems

of blood with scanty cellular material does not exclude a vascular tumour; moreover, even with fine-needle aspiration there is a risk of major bleeding (2-5%) which compares with that for malignant hepatic tumours

(1-5%).

The natural history of hepatic haemangiomas will influence the treatment options. In adults, most such tumours are an incidental finding on scanning or at operation, but a few present, usually in the fourth to sixth decade, with pain or fullness, and with abdominal swelling if they are very large. The risk of spontaneous rupture is exceedingly small, with only twenty-one published cases since 1898,21 and should not dictate active treatment. Since there is no evidence of malignant transformation with time, this possibility can be discounted. Although some haemangiomas grow progressively, presumably by vascular ectasia, most will remain unchanged. All thirty-six patients observed for up to 15 years at the Mayo Clinic remained symptom-free, and only four lesions increased in size on scanning;21in another series only one of sixty-eight enlarged during 1-6 years of ultrasound follow-up.22 Thus, a conservative policy may be advocated even for the so-called "giant" haemangioma (defined as > 4 cm23), if it is symptomless. Such patients require strong reassurance, backed up by ultrasound scans at 6-12 month intervals. For symptomatic patients, hepatic artery ligation may be effective,24 but probably less so than intra-arterial embolisation.10,25 Embolisation requires great skill to avoid early failure due to rapid revascularisation if only the major feeding vessels are occluded. Lesions seldom shrink after embolisation, and, although pain may be relieved, repeated procedures may be required. The general experience is that symptoms are relieved in only half the patients so treated 26 but embolisation has a definite role in controlling traumatic haemorrhage. Radiotherapy should 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 and also of pain in giant haemangiomas.27 Resection was Riley SA, Ellis WR, Irving HC, Lintott DJ, Axon ATR, Losowsky MS. Percutaneous liver biopsy with plugging of needle track a safe method for use m patients with impaired coagulation. Lancet 1984; ii: 436. 20. Gebel M, Horstkotte H, Koster C, Brunkhorst R, Brandt M, Atay Z. Ultrasoundguided 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 of the liver: resect or observe? Am J Surg 1983; 145: 49-53. 22. Gibney RG, Hendin AP, Cooperberg PL. Sonographically detected hepatic hemangiomas: 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; 19.

172: 239-45. 24 Peveretos P, Panoussopoulos D. Giant

cavernous hepatic hemangioma: treatment by ligation of the hepatic artery. J Surg Oncol 1986, 31: 48-51 25. Allison DJ, Jordan H, Hennessy O. Therapeutic embolisation of the hepatic artery: a review of 75 procedures. Lancet 1985; i: 595-99. 26. Martin B, Roche A, Radice L, Aguilar K, Kraiem C. Does arterial embolization have a role in the treatment of cavernous hemangioma of the liver in adults? Presse Med

1986; 15: 1073-76. 27. Starzl TE,

Koep LJ, Weil R III, et al. Excisional treatment of cavernous hemangioma Surg 1980, 192: 25-27.

of the liver Ann

884 out in thirteen of forty-nine patients in the Mayo Clinic series,21 and two of thirteen patients requiring treatment at King’s College Hospita1.1O Enucleation of haemangiomas, including some that were very large, has been reported as an alternative to formal hepatic resection,28 but this technique has not been widely used. What is the recommended management of hepatic haemangiomas in 1988? Small, incidental, and symptomless lesions may often be diagnosed accurately by ultrasound alone, although repeated scanning at intervals is important to reassure both the doctor and the patient. Larger lesions may require more than one imaging technique to increase the certainty of diagnosis, but percutaneous biopsy

carried

should seldom be necessary. Since few lesions will progress with time, most may safely be left untreated. Symptomatic or expanding lesions merit a trial of arterial embolisation, to which some patients will respond well. For the small group of patients left at the end of this series of therapeutic "filters", surgery remains a very effective treatment, especially since improvements in anaesthetic and surgical technique have made elective liver resection a safe procedure.

SURGICAL INSURRECTION THE annual

meeting of the Royal College of Surgeons of (RCS) England is usually a pedestrian affair, but this year it was enlivened by a revolt by junior doctors, or surgeonsin-training, over proposed changes to the fellowship (FRCS) examination system. In Cambridge last month the trainees were well organised, so their motion condemning some of the changes was carried by a three-to-one majority of those present. Sadly though, nothing will happen because other political pressures will undoubtedly intervene and the RCS England will have to conform to the wishes of its sister Colleges. Moreover, the juniors’ motion was flawed by confusion 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; they must ensure the adequacy of surgical education; and they must have a means of signifying those who have attained their standards. Thus, the FRCS diploma was set up in 1800, but this is long ago now. Confusion between the career aspirations and the academic qualifications of junior doctors is at the root of the current unrest and misunderstanding. Careers of junior surgeons, especially general surgeons, are frustrated, consultant posts are not increasing, and the much trumpeted expansion promised under Achieving a Balancel has not materialised. Although the Royal Colleges (in the UK) can offer advice to Government to expand the

Alper A, Anogul O, Emre A, Uras A, Okten A. Treatment of liver hemangiomas by enucleation Arch Surg 1988; 123: 660-61. 1. Hospital Medical Staffing-Achieving a Balance Consultative document issued on behalf of the UK Health Departments, the Joint Consultants Committee, and Chairmen of the Regional Health Authorities July, 1986

28

consultant grade in surgery, they cannot be held to account if Government ignores this advice. The present Government has unrivalled experience of ignoring advice, hence the frustration of well-trained senior registrars who are becoming tired and disheartened. This pent-up emotion was vented in Cambridge. A separate issue, although one inevitably melded with the career aspirations of young surgeons, is the debate about the structure of the examinations that should denote that a person is fit to practise autonomously as a surgeon. The FRCS diploma does not indicate a fully trained surgeon; rather it identifies those who have attained the necessary basic knowledge to embark on specialist (higher) surgical training. The Royal Colleges have long recognised the inadequacy of the FRCS as a sign of completed surgical training; the specialist associations also recognise this deficiency, and the vacuum has been imperfectly filled with accreditation. Yet accreditation does not confer any letters on the anointed, so how does one establish which surgeons are accredited? There is a need for specialist diplomas to indicate who is fully trained. (Some would opine specialist registers are a societal requirement too.) This requirement for specialist qualification has been met in part by the Edinburgh College of Surgeons, who have proved much more innovative than their counterparts. At last the Colleges are acting in concert and intercollegiate specialist boards (eg, in neurosurgery and urology) are set up and now offer a higher examination in certain specialties-those who obtain the qualification can consider themselves fully trained. But some of the long-suffering and time-expired senior registrars in general surgery fear the introduction of a similar examination in that branch of surgery, wondering whether they will have to take another (new) examination at the age of 40 or even 45 if they are to compete for the new consultant posts. Hence the rebellion at Cambridge. Both sides in this conflict are blessed with right and wrong. The Colleges have not acted crisply enough in finalising their proposals for the new (exit) examination in general surgery. Even worse, their communication with the rank and file has been inadequate. The proposals brilliantly outlined in Cambridge by Prof Norman Browse have not been appreciated by the juniors, who meanwhile have allowed their paranoia about poor career prospects to become confused with the changes in the examination structures that will improve the lot of the next generation of junior doctors. In

formulating their policies, the Colleges have two guiding principles. All surgeons, whatever their discipline, must appreciate the general principles that underlie all surgical practice. Thus, the revised first examination will include anatomy, physiology, other basic sciences, and an examination in the principles, clinical and operative, of surgery. This test will equip the aspirant for higher surgical training. The original idea was that the examination would be taken at one sitting, but compassion and reality have tempered this proposal and the English college has agreed that candidates may sit the examination in two parts, part A to include the basic sciences and part B to include the clinical components. All the Colleges are in accord here-the examination will be in the principles of surgery and will not be like the existing FRCS with its predominantly general surgical ethos. Perhaps this is where the Colleges’ communication systems first went wrong. They have not stressed the novelty of the examination and they have allowed the word "general", with its heavy overtones of