the alcoholism treatment package

3
488 quences, familiar to ophthalmologists, include the activation of corneal herpes simplex and the devel- opment of ocular hypertension, glaucoma, and cataract. 11-14 The antiproliferative action of fluorinated ster- oids reduces not only replacement in the epidermis but also regeneration of dermal fibroblasts. Skin thinning, telangiectasia, and ecchymoses appear, especially on the face, and skin strise develop, par- ticularly in the flexures. The "steroid facies" of in- judicious topical therapy is a bright red face, with skin atrophy, fine telangiectases, and ecchymoses (it should not be confused with the cushingoid facies due to systemic absorption). Little attention has been paid to habituation by topical steroids. 15 Patients with chronic dermatitis become so addicted that they cannot discontinue steroids without immediate withdrawal symptoms. Such symptoms are particularly liable to arise in facial dermatoses (rosacea and perioral dermatitis) and in certain chronic hand eczemas. Addiction to topical steroids has all the the features of depen- dency on systemic agents. At first, symptoms are relieved but recurrence follows and further appli- cations become less effective. More and more medi- cation is applied, resulting in skin damage which is sometimes mistaken for the original dermatosis. When the steroid is suddenly stopped, rebound exa- cerbation follows. Not surprisingly the dermatolo- gist often has to deal with a patient who has used fluorinated steroids and is already effectively "hooked". Careful weaning is required before the original disease can be identified. Psoriasis is par- ticularly awkward in this respect, because sudden withdrawal of topical therapy is often followed by rebound activation and pustulation, which may become generalised. Systemic absorption may sometimes produce adrenal suppression and collapse. More readily absorbed and more slowly metabolised fluorinated steroids produce at the same time Cushing’s syn- drome and hypothalamic-pituitary-adrenal (H.P.A.) axis depression. 16 With clobetasol propionate a situation can arise when sudden cessation of topical applications can precipitate adrenocortical insuffi- ciency. Thus, when a child who has been treated with a group-1 steroid for some time is admitted to hospital for any reason the likely sudden stoppage of the steroid may well provoke a life-threatening collapse. The long-term effects of systemic absorp- tion include growth stunting, steroid acne, sym- metrical steroid strix, and widespread skin atrophy with purpura and ecchymoses. All the problems as- sociated with absorption are more likely to arise in 11. Francois, J. Ann. Ocul. 1954, 187, 805. 12. Goldmann, H. Archs Ophth. 1962, 68, 621. 13. Goldmann, H. Int. Ophth. Clin. 1966, 6, 991. 14. Bigger, J. F., et al. Invest. Ophth. 1972, 11, 832. 15. Calnan, C. D. Dermatologica, 1976, 152, suppl. 1, p. 247. 16. Staughton, R. C. D., August, P. J. Br. med. J. 1975, ii, 419. infancy and childhood as the result of application to wide areas of skin and when treated areas are occluded.17 Fortunately, groups 3 and 4 have little effect on H.P.A. function. Rarely, local effects in- clude hypertrichosis, folliculitis, hypopigmentation, and allergy to the topical steroid itself or to the pre- servatives or bases in the proprietary preparations. Dermatologists strive to minimise the side-effects by following these guidelines: Use topical steroids only for short courses. The highly potent steroids should be used for forty-eight hours until an initial response is obtained, and then an intermediate or weaker steroid should be used. The potent steroids should be used with great care in facial dermatoses and in the flexural eruptions: they are contraindicated in rosacea. Remember that occlusion and skin hydration enhance the potency and penetration of any steroid. Avoid steroids in all dermatoses primarily due to infective agents, unless an appropriate antibiotic is given simultaneously. Not more than 50 g weekly of a group-1 steroid should be given without an assessment of H.P.A. func- tion. Use the smallest quantity and the weakest preparation that is effective; and every two weeks review the need for continuing treatment. The hope must be that powerful anti-inflamma- tory agents can be developed which do not have "fluorinated problems". The study of steroid recep- tor sites in the skin and of the steroid-sensitive neur- ones in the hypothalamus may lead to the discovery of a molecule which acts on the skin without pro- ducing "feedback" difficulties. Alternatively, non- steroidal agents may ultimately provide the best answer to inflammatory dermatoses. The Alcoholism Treatment Package ALCOHOLISM in Britain and many other Western countries is treated in accordance with a basic for- mula which has been authoritatively described by GLATT.! Abstinence is usually the recommended goal as far as the drinking goes, but important sub- sidiary treatment aims may relate to family happi- ness, employment, social adjustment in general, and the recovery of physical and mental health. These goals are achieved by a combination of what is in essence pedagogic instruction on the nature of alcoholism, cajolery, psychotherapy, and support. The patient’s way of life, as well as his psychiatric history and present state of mind, will of course receive attention. Minor tranquillisers are often used to aid withdrawal, but doctors are wary of 17. Feiwel, M., et al. Lancet, 1969, i, 485. 1. Glatt, M. M. The Alcoholic and the Help He Needs. London, 1977.

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Page 1: The Alcoholism Treatment Package

488

quences, familiar to ophthalmologists, include theactivation of corneal herpes simplex and the devel-opment of ocular hypertension, glaucoma, andcataract. 11-14

The antiproliferative action of fluorinated ster-oids reduces not only replacement in the epidermisbut also regeneration of dermal fibroblasts. Skinthinning, telangiectasia, and ecchymoses appear,especially on the face, and skin strise develop, par-ticularly in the flexures. The "steroid facies" of in-judicious topical therapy is a bright red face, withskin atrophy, fine telangiectases, and ecchymoses(it should not be confused with the cushingoidfacies due to systemic absorption).

Little attention has been paid to habituation bytopical steroids. 15 Patients with chronic dermatitisbecome so addicted that they cannot discontinuesteroids without immediate withdrawal symptoms.Such symptoms are particularly liable to arise infacial dermatoses (rosacea and perioral dermatitis)and in certain chronic hand eczemas. Addiction to

topical steroids has all the the features of depen-dency on systemic agents. At first, symptoms arerelieved but recurrence follows and further appli-cations become less effective. More and more medi-cation is applied, resulting in skin damage which issometimes mistaken for the original dermatosis.When the steroid is suddenly stopped, rebound exa-cerbation follows. Not surprisingly the dermatolo-gist often has to deal with a patient who has usedfluorinated steroids and is already effectively"hooked". Careful weaning is required before theoriginal disease can be identified. Psoriasis is par-ticularly awkward in this respect, because suddenwithdrawal of topical therapy is often followed byrebound activation and pustulation, which maybecome generalised.

Systemic absorption may sometimes produceadrenal suppression and collapse. More readilyabsorbed and more slowly metabolised fluorinatedsteroids produce at the same time Cushing’s syn-drome and hypothalamic-pituitary-adrenal (H.P.A.)axis depression. 16 With clobetasol propionate a

situation can arise when sudden cessation of topicalapplications can precipitate adrenocortical insuffi-ciency. Thus, when a child who has been treatedwith a group-1 steroid for some time is admitted tohospital for any reason the likely sudden stoppageof the steroid may well provoke a life-threateningcollapse. The long-term effects of systemic absorp-tion include growth stunting, steroid acne, sym-metrical steroid strix, and widespread skin atrophywith purpura and ecchymoses. All the problems as-sociated with absorption are more likely to arise in

11. Francois, J. Ann. Ocul. 1954, 187, 805.12. Goldmann, H. Archs Ophth. 1962, 68, 621.13. Goldmann, H. Int. Ophth. Clin. 1966, 6, 991.14. Bigger, J. F., et al. Invest. Ophth. 1972, 11, 832.15. Calnan, C. D. Dermatologica, 1976, 152, suppl. 1, p. 247.16. Staughton, R. C. D., August, P. J. Br. med. J. 1975, ii, 419.

infancy and childhood as the result of applicationto wide areas of skin and when treated areas areoccluded.17 Fortunately, groups 3 and 4 have littleeffect on H.P.A. function. Rarely, local effects in-clude hypertrichosis, folliculitis, hypopigmentation,and allergy to the topical steroid itself or to the pre-servatives or bases in the proprietary preparations.

Dermatologists strive to minimise the side-effectsby following these guidelines:

Use topical steroids only for short courses.The highly potent steroids should be used for

forty-eight hours until an initial response is obtained,and then an intermediate or weaker steroid should beused.The potent steroids should be used with great care

in facial dermatoses and in the flexural eruptions:they are contraindicated in rosacea.Remember that occlusion and skin hydration

enhance the potency and penetration of any steroid.Avoid steroids in all dermatoses primarily due to

infective agents, unless an appropriate antibiotic is

given simultaneously.Not more than 50 g weekly of a group-1 steroid

should be given without an assessment of H.P.A. func-tion.

Use the smallest quantity and the weakest

preparation that is effective; and every two weeksreview the need for continuing treatment.The hope must be that powerful anti-inflamma-

tory agents can be developed which do not have"fluorinated problems". The study of steroid recep-tor sites in the skin and of the steroid-sensitive neur-ones in the hypothalamus may lead to the discoveryof a molecule which acts on the skin without pro-ducing "feedback" difficulties. Alternatively, non-steroidal agents may ultimately provide the bestanswer to inflammatory dermatoses.

The Alcoholism Treatment PackageALCOHOLISM in Britain and many other Western

countries is treated in accordance with a basic for-mula which has been authoritatively described byGLATT.! Abstinence is usually the recommendedgoal as far as the drinking goes, but important sub-sidiary treatment aims may relate to family happi-ness, employment, social adjustment in general,and the recovery of physical and mental health.These goals are achieved by a combination of whatis in essence pedagogic instruction on the nature ofalcoholism, cajolery, psychotherapy, and support.The patient’s way of life, as well as his psychiatrichistory and present state of mind, will of coursereceive attention. Minor tranquillisers are oftenused to aid withdrawal, but doctors are wary of

17. Feiwel, M., et al. Lancet, 1969, i, 485.1. Glatt, M. M. The Alcoholic and the Help He Needs. London, 1977.

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long-term drug therapy because of the danger of in-ducing an iatrogenic addiction. An aversive drugsuch as disulfiram or calcium cyanamide may beused. Family therapy is often an important part oftreatment, and Alcoholics Anonymous and Alanonare brought into partnership. Some alcoholics maybe treated successfully as outpatients, but inpatientcare, centred on group psychotherapy, is still

thought to be required for many. Staff favour ateam approach, with nurses and social workers par-ticipating in treatment; good aftercare and com-munity support, involving liaison with the G.P. andthe primary health-care team, are seen as essential.Behaviour therapy is attracting increasing inter-est,2 but is not part of the basic package of care.The approach is not insensitive to individual needs;many treatment centres at present offer a range of

help, which may vary, according to the particularcase, from brief counselling to a 12-week inpatientstay. But over the past twenty years workers havebeen inclined to accept the idea that treatmentshould be intense and energetic.This treatment approach owes its existence more

to historical processes than to science. It is possibleto discern the deposits, akin to geological layers, ofa sequence of therapeutic fashions-the residue ofalmost forgotten enthusiasm for inpatient psycho-therapy units, for group processes and the thera-peutic community, for family therapy, and later forcommunity psychiatry. To say that treatment foralcoholism is only an accretion of fads and fashionswould be too harsh, for it is also built on muchclinical experience; but it must be admitted that wehave not done enough to assess scientifically the ef-fectiveness of treatment methods, and thus to

ascertain the return on an expensive investment ofpublic funds.The difficulties of carrying out such an evalua-

tion are formidable. To assess separately the effi-cacy of an individual element in the programme—a particular drug used in withdrawal, for in-stance-is relatively straightforward, but it is thevalue of the total integrated package whichremains in question. In America an attempt at as-sessment based on data analysis of published litera-ture has been tried. Data from the journals are re-analysed, new outcome categories set up, and theattempt made to relate success to patient character-istics and to type or intensity of treatment. Theoriginal data may be of dubious validity or incom-plete, and in the effort to force old data into newanalytical categories, fairly unguarded assumptionsmay have to be made. An important advance in thistype of research was made by EMRICK3,4 in his re-

2. Litman, G. K. in Research Advances in Alcohol and Drug Problems (editedby R. J. Gibbins, Y. Israel, H. Kalant, R. E. Popham, W. Schmidt, andR. G. Smart); New York, 1976.

3. Enirick C. D. Q. Jl Stud. Alcohol, 1974, 35, 523.4. Emnck, C. D. J. Stud. Alcohol, 1975, 36, 88.

analysis of 271 published studies of alcoholismtreatment. He found that about two-thirds of pa-tients improved, including one-third who becameabstinent, and that treatment gave better resultsthan no or minimal treatment. The inherent weak-ness of this particular research strategy is that thepatients had not, of course, been randomisedbetween treatments of different intensities, and theconclusion may therefore be spurious. A re-analysisexercise carried out by COSTELLO’,6 has greater sta-tistical sophistication, but fundamental difficultiesin interpretation remain.

Another approach to the assessment of treatmentfor alcoholism is exemplified in a recent report bythe Rand Corporation’ which describes a 6-monthfollow-up of 2371 out of 11 500 male alcoholicsattending 45 American treatment centres; a yearlater 1340 of the subjects were re-interviewed. Theloss to follow-up and the lack of a controlled designmight seem insurmountable defects in such a study,but the hope is that errors can be corrected out,and that lack of an acceptable experimental designcan be offset by large cell numbers, matching of pa-tient characteristics, and multivariate statistical

techniques. The Rand report concluded that bothat 6-month and 18-month follow-up about 70% ofpatients were improved, although at both pointsonly 10% had achieved a 6-month total abstinence;this report somewhat demoted the importance ofthe abstinence goal. Patients with "lower"amounts of treatment were found to have remis-sion-rates only slightly higher than those who hadno treatment at all, but those who had "higher"amounts of treatment did significantly better-afinding which in a non-random design might be anartefact brought about by more treatment beinggiven in the more hopeful cases. The reason whyAmerican research workers have invested in thesemassive non-experimental attempts to assess theeffectiveness of the treatment package is partly thatthe U.S. Government has a large investment inalcoholism treatment, and so has a right to ask forinformation on cost-effectiveness. At the same time,there are also ethical and quasi-political constraintsagainst mounting controlled trials. Nevertheless, anumber of controlled experiments have been

attempted, and these have been reviewed byEMRICK.4The latest contribution to this research is a

report from the Addiction Research Unit, at the In-stitute of Psychiatry in London, which attempts tocompare the conventional package with a regimen ofmuch lower intensity. 100 married male alcoholics

5. Costello, R. M. Int. J. Addict. 1973, 10, 251.6. Costello, R. M. ibid. p. 857.7. Armor, D. J., Polich, J. M., Stambul, H. B. Alcoholism and Treatment.

Santa Monica, 1976.8. Edwards, G., Orford, J., Egert, S., Guthrie, S., Hawker, A., Hensman, C.,

Mitcheson, M., Oppenheimer, E., Taylor, C. J. Stud. Alcohol, 1977, 38,1004.

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attending the Maudsley Hospital in London wererandomised between one of two regimens, the firstbeing termed "treatment" and representing theconventional formula, while the second groupreceived "advice". The advice consisted of one

counselling session, with no further purposivetherapeutic intervention for the next 12 months,although wives were contacted each month by aresearch worker for data collection. At 12-month

follow-up there was no significant difference in out-come between the two groups, as assessed by multi-ple measures, and attested to by independent evi-dence from husband and wife.The authors of this report claim that their find-

ings are not revolutionary, but accord with whatmight be concluded from a careful reading of theprevious research literature-they are "simplyadding some further support to buttress what wasalready an apparent truth". Such a controversialassertion deserves scrutiny, but if this paper with-stands critical examination then the basic patternof services for alcoholism in this and other coun-tries must be radically recast.9 Even if these con-tentions are not accepted in full, there can be littledoubt that the weight of research findings indicatesthat the previously favoured package must at leastbe substantially revised. It would be a pity if in thisrevision currently fashionable ideas were accordedtoo much weight-if, for instance, the primaryhealth-care team were to be given central responsi-bility when there exists no adequate evidence thatit can be effective in treating alcoholics. With thesuccess of intensive treatment now a matter for

debate, thoughts must turn to prevention, wherethere are possibilities that are certainly at presentbeing neglected. 10

MECHANICAL MEASURES AGAINST DEEP-VEINTHROMBOSIS

OF those factors believed to be important in the path-ogenesis of venous thrombosis, probably the least con-tentious is vascular stasis, which has been recognised asplaying a causal role in thrombosis at least since thetime of Virchow.l The hazards of bed rest (admirablydescribed by Richard Asher2) stem in part from venouspooling in the leg veins during recumbency, leading tothrombosis in some patients. Experimental studies haveprovided useful insight into the role of stasis in venousthrombosis. Wessler3 showed that while thrombogenicmaterial injected systemically into experimental animalsdid not by itself lead to overt thrombosis, blood clotted

9. Edwards, G., Orford, J. Proc. R. Soc. Med., 1977, 70, 344.10. Bruun, K., Edwards, G., Lumio, M., Makela, K., Pan, L., Popham, R. E.,

Room, R., Schmidt, W., Skog, O.-J., Sulkunen, P., Osterberg, E. AlcoholControl Policies in Public Health Perspective. Helsinki, 1975.

1. Virchow, R. Cellular Pathology as Based on Physiological and PathologicalHistology. London, 1860.

2. Asher, R. Br. med. J. 1947, ii, 967.3. Wessler, S. Am. J. Med. 1962, 33, 648.

rapidly in veins isolated from the circulation. Activatedclotting factors are cleared rapidly, provided blood is cir-culating through the liver.4 If this important defencemechanism is circumvented by pooling of blood in thelegs of recumbent patients, there is increased dangerthat such blood will clot. There has been much interestof late in preventing the generation of activated clottingfactors ("hypercoagulability") with prophylactic antico-agulants. However, if Wessler was right in thinking thatstasis in the presence of hypercoagulability leads to

venous thrombosis, then an equally valid approach tothe prophylaxis of deep vein thrombosis (D.V.T.) wouldbe to reduce stasis.Means to increase the velocity of venous blood-flow,

as a practical approach to prophylaxis of thromboembol-ism, have included elastic stockings,’ passive exercise ofthe calf muscles,6 electrical stimulation of the muscle,’and intermittent pneumatic compression of the legs.8,9Sensitive diagnostic techniques, such as labelled

fibrinogen, have given investigators more precise end-points ; for example, while the early clinical studies withelastic stockings seemed to show a reduction in thrombo-embolism, work with radioactively labelled fibrinogenreveals that ordinary elastic support of the ’Tubigrip’type does not prevent D.V.T.10,11 By contrast, graduatedstatic compression stockings do reduce D.v.T., as mea-sured by labelled fibrinogen.12,13 The special stockingscome in nine sizes, and exert a gradually decreasingpressure from the ankle to the thigh.14 They seem towork by increasing the linear velocity of venous

blood-flow.Another approach has been to compress the legs inter-

mittently for 24-48 hours after the induction of anxs-thesia.8,9 The application of pneumatic leggings, inflatedfor approximately 1 minute to a pressure of 40 mmHg,followed by relaxation, has in clinical trials achieved areduction in D.v.T. comparable to that obtained withlow-dose heparin, although there is still disagreementabout the effectiveness of pneumatic compression in pa-tients with malignant disease.9-15 Roberts and Cotton"showed that maximum pulsatility of venous blood-flowis achieved by applying compressive impulses which riseat 8 mmHg per second to 40 mmHg and then fall tozero, followed by a pause of at least 100 seconds. Theyobserved that the peak venous flow can be increasedseven-fold, and its pulsatility thirty fold; using labelledfibrinogen for diagnosis, they showed a reduction in theincidence of postoperative D.v.T. from 26% in the con-

4. Deykin, D., Cochios, F., DeCamp, G., Lopez, A. Am. J. Physiol. 1968, 214,414.

5. Wilkins, R. W., Stanton, J. R. New Engl. J. Med. 1953, 248, 1087.6. Sabri, S., Roberts, V. C., Cotton, L. T. Br. med. J. 1971, iii, 82.7. Doran, F. S. A., White, H. M., Drury, M. Br. J. Surg. 1970, 57, 20.8. Sabri, S., Roberts, V. C., Cotton, L. T. Br. med. J. 1971, iv, 394.9. Hills, N. H., Pflug, J. J., Jeyasingh, K., Boardman, L., Calnan, J. S. ibid.

1972,1,131.10. Rosengarten, D. S., Laird, J., Jeyasingh, K., Martin, P. Br. J. Surg. 1970,

57, 296.11. Browse, N. L., Jackson, B. T., Mayo, M. E., Negus, D. ibid. 1974, 61, 219.12. Holford, C. P. ibid. 1970, 63, 157.13. Scurr, J. H., Ibrahim, S. Z., Faber, R. G., LeQuesne, L. P., ibid. 1977, 64,

371.14. Sigel, B., Edelstem, A. L., Savitch, L., Hasty, J. H., Felix, W. R., Jr. Archs

Surg. 1975, 110, 171.15. Clarke, W. B., Prescott, R. J., MacGregor, A. B., Ruckley, C. V. Lancet,

1974, ii, 5.16. Roberts, V. C., Cotton, L. T. in Venous Thrombo-Embolic Disease (edited

by C. V. Ruckley and I. M. C. Macintyre); p. 11. Edinburgh, 1975.