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group of eminent colleagues who will act in the bestinterests of patients, the Hospital and the MedicalCollege". Among other suggestions was that theDivision of Obstetrics and Gynaecology should bemerged with either the medical or the surgical division"to give a wider perspective to its deliberations";although such a merger has not come about, a

"neutral" chair of the Division of Obstetrics was

appointed, hence the otherwise rather unlikelyposition occupied by an ear, nose, and throat surgeon.The Munro panel’s fears were realised. When Mrs

Savage returned to her post in July, 1986, after herreinstatement she found that she was virtuallyostracised and unable to work properly. She

eventually started seeing patients in November but,although she was a senior lecturer, she was effectivelybarred from teaching. She threatened to sue theLondon Hospital Medical Council (LHMC) and wasonce more given teaching responsibilities in March,1987. Nevertheless, the working atmosphere withinthe Division of Obstetrics was such that it was agreedthat she should be assigned to the Academic

Department of General Practice under Prof MalSalkind; she joined that department in November,1987.

In May, 1988, finding that it was impossible toachieve any consensus with her colleagues in theobstetric division, Mrs Savage asked the chairman ofthe Council to proceed according to "Munro eleven"and convene a group to discuss the outstandingproblems. The chairman thought it was a matter forthe district health authority, who in the event deemedit to be a medical problem and referred the case back tothe Council. In August last year, the Council decidedto involve the Royal College of Obstetricians andGynaecologists to suggest a suitable adjudicator. SirMalcolm MacNaughton was duly chosen and saw allthe relevant consultants in December. In January ofthis year, Sir Malcolm continued his deliberations andsaw selected members of the junior staff; Mrs Savagewas not asked to nominate any of the junior doctors. InApril, Sir Malcolm reported verbally to some selectedsenior doctors but not to Mrs Savage, although he wasapparently dismayed that she had not been informedof the content. As far as we know, Sir Malcolm has notput his report in writing.

This catalogue of events suggests that there hasbeen little or no true reform of the Division ofObstetrics at the London Hospital. Some might holdthat such difficulties are almost inevitable when strongpersonalities meet head on and that the whole sorrytale merely represents an extreme battle of wills. But itis far more than a domestic tiff. Despite many hours ofpeople’s time, considerable sums of (largely public)money, and much heart searching, it is plain that thereis still no satisfactory machinery for dealing withprofessional disagreements. In Mrs Savage’s case, adisciplinary inquiry was asked to settle a disputebetween professional colleagues; she was totallyexonerated of the charge of incompetence yet has been

effectively barred from practising as she would wish.Clearly her colleagues in the Division of Obstetricswere never prepared to accept a verdict of not guilty; ifthey had been, presumably they would have mademore effort to behave in a manner befitting thecorporate ethic of the profession.2 This lengthydispute has not benefited any of the participants. Theopportunity was there for a much-needed comparisonof community-based versus hospital-based obstetrics.Instead, the acrimony that has enveloped the caseshows no signs of diminishing.Mrs Savage, who last month was elected to the

General Medical Council, has now been advised totake legal action against the health authority for nothonouring her terms of employment, with respect toboth the direction of the Beaumont inquiry and thefindings of the Munro panel. The recommendations ofthe Munro panel had been accepted as binding by thehealth authority and by Mrs Savage; an action willnow be started.

CLINICAL SIGNS IN HEART FAILURE

PHYSICIANS pride themselves on their clinical acumen ineliciting and interpreting physical signs, and none more sothan cardiologists. The principal clinical indications ofcardiac failure are tachycardia, displaced apex beat, third orfourth heart sounds, valvular incompetence, and signs of"congestion"-raised jugular venous pressure (JVP), basalcrackles, and peripheral oedema. How useful are suchobservations? They obviously help assessment of

therapeutic response in patients with acute left heart failureor uncontrolled chronic congestive failure. However, witheffective therapies, signs of congestion are now encounteredinfrequently, and it is important to remember that treatmentis in a way cosmetic, since the underlying cardiac

dysfunction persists.l,2 Clinical examination is of limitedvalue in establishing the aetiology of heart failure, exceptperhaps in valvular disease. Signs of congestion are usuallyunhelpful in distinguishing systolic from diastolic

dysfunction; some claim the latter to be the principalabnormality in up to 30% of patients with failing hearts.This distinction is important because treatment differs

radically.3Clinical signs may be prognostically important. The

severity of left ventricular systolic failure (the commonestcause of congestive cardiac failure) can be estimated bymeasuring the fall in left ventricular ejection fraction

(LVEF) or cardiac output or rise in left ventricularend-diastolic pressure (LVEDP); all these measurementshave prognostic implications. Clinical signs do not reliablypredict L VEF:4.5 a patient may progress from severe

2. Editorial. Professional implications of the Savage case. Lancet 1986; i: 837.1. Maskin C, Forman R, Klein N, Sonnenblick EH, Lejemtel TH. Long term amrinone

therapy m patients with severe heart failure: drug dependent hemodynamicbenefits despite progression of the disease. Am J Med 1982; 72: 113-18.

2. Jafri SM, Lakier JB, Rosman HS, Goldstein S. Prevalence of congestion in chronicheart failure. Chest 1986; 90: 311-12.

3. Kessler KM. Heart failure with normal systolic function. Update of prevalence,differential diagnosis, prognosis and therapy. Arch Intern Med 1988; 148: 2109-11.

4. Engler R, Ray R, Higgins CB, et al. Clinical assessment and follow up of functionalcardiomyopathy. Am J Cardiol 1982; 49: 1832-36.

5. Mattleman SJ, Hakki AH, Iskandrian AS, et al. Reliability of bedside evaluation indetermining left ventricular function. correlation with left ventricular ejectionfraction determined by radionuclide ventriculography. J Am Coll Cardiol 1983; 1:417-20.

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severe congestive heart failure (NYHA class 4) to slightlimitation of physical activity (NYHA class 2) withoutsignificant improvement in L VEF. 1,6 Stevenson andPerloff’ have now assessed the usefulness of physical signs inpredicting pulmonary capillary wedge pressure (PCWP, anindirect measure of LVEDP) in 50 patients with impairedleft ventricular function. PCWP was significantly increasedin 86% of patients, of whom nearly 60% had a raised JVP(100% specificity). The presence of lung crackles or

peripheral oedema did not enhance sensitivity, even whenPCWP was considerably raised (> 35 mm Hg). Thepresence of a third heart sound was a non-specific finding,being present in almost all patients. These researchersconclude that reliance on physical signs to detect increasedPCWP might result in inadequate therapy (although thediagnostic value of the JVP might have been improved byuse of the abdominojugular testS.9).

Whilst prediction of PCWP or LVEDP might beprognostically useful, it does not appear to aid prediction ofwork capacity in treated patients.lO,l1 Nonetheless, it isreasonable to try to optimise cardiac output at the lowestLVEDP. Cardiac output is difficult to assess in outpatients;Stevenson and Perloff favour the use of the proportionalblood pressure (systolic minus diastolic divided by systolic).A ratio of less than 25 % had an 88 % accuracy in predicting acardiac index of less than 2-2 1/min per m (the reasonableminimum for adequate tissue oxygenation). This simplemeasurement would be more useful if it were shown toreflect changes in cardiac output in response to stress, orlong term.A persistent third heart sound and cardiomegaly are poor

indicators of prognosis. 12-14 Generations of medicalstudents have experienced self doubt as they fail to hear thatelusive third sound; they may or may not be heartened by astudy in which four Canadian clinicians agreed on its

presence in only 50% of cases, the best agreement beingbetween the two most junior doctors.l5 Clinicians may be nobetter at assessing the apex beat, which was found to beuseful in excluding rather than confirming the presence ofcardiomegaly (again when observers could agree on its

presence)16.Where does that leave clinical examination in patients

with heart failure? First, doctors must realise that clinicalevaluation requires constant practice. Clinical signs,particularly JVP, are helpful in patient assessment. Signs of

6. Jafri SM, Lakier JB, Rosman HS, Peterson E, Goldstein S. Symptoms and tests ofventricular performance in the evaluation of chronic heart failure. Am Heart J 1986;112: 194-96.

7. Stevenson LW, Perloff JK. The limited reliability of physical signs for estimatinghemodynamics in chronic heart failure. JAMA 1989; 261: 884-88.

8. Ewy GA. The abdommojugular test: technique and hemodynamic correlates. AnnIntern Med 1988; 109: 456-60.

9. Editorial. Abdominojugular test. Lancet 1989; i: 419-20.10. Franciosa JA, Park M, Levine TB. Lack of correlation between exercise capacity and

indexes of resting left ventricular performance. Am J Cardiol 1981; 47: 33-39.11. Bayliss J, Norell M, Canepa-Anson R, Sutton G, Poole-Wilson P. Untreated heart

failure: clinical and neuroendocrine effects of introducing diuretics. Br Heart J1987; 57: 17-22.

12. MacArthur CG, Binbrek AS, Chetty S, et al. The effect of left ventricular function,arrhythmias, and evidence of previous viral infection on the prognosis of congestivecardiomyopathy. In: Goodwin JF, Hjalmarson A, Olsen EG, eds. Congestivecardiomyopathy. Molndal, Sweden: AB Hassle, 1981: 236-48.

13. Unverfeth DV, Magorien RD, Moeschberger ML, et al. Factors influencing the oneyear mortality of dilated cardiomyopathy. Am J Cardiol 1984; 54: 147-52.

14. Likoff MJ, Chandler SL, Kay HR. Clinical determinants of mortality in chroniccongestive heart failure secondary to idiopathic dilated or to ischemic

cardiomyopathy Am J Cardiol 1987; 59: 634-38.15. Ishmail AA, Wing S, Ferguson J, Hutchison TA, Magder S, Flegel KM.

Interobserver agreement by auscultation in the presence of a third heart sound mpatients with congestive heart failure. Chest 1987; 91: 870-73.

16. O’Neill TW, Barry M, Smith M, Graham IM. Diagnostic value of the apex beat.Lancet 1989; i: 410-11

congestion may reappear without appreciable alteration inclinical state or change in objective measures of ventricularfunction, and prompt treatment may prevent suddendeterioration into frank congestive heart failure. Once thepatient’s condition is stable and signs of congestion havedisappeared, further clinical evaluation of the effects oftherapy is difficult.4 Since changes in skeletal muscles arealso important in patients with heart failure, perhaps themost useful tests are those that measure total aerobic

capacity. Such assessment does not always require complexapparatus to measure maximum oxygen uptake; muchinformation can be obtained about the patient’s progress andresponse to therapy from simple walking tests.19-23

Heart failure is not a diagnosis; the aetiology should besought when possible. Once symptoms have appeared,prognosis is generally poor; each patient deserves, at the veryleast, a thorough clinical and non-invasive cardiologicalassessment to exclude treatable causes of ventricular

dysfunction and malignant arrhythmias.23.25

DIFFUSE LEWY BODY DISEASE

James Parkinson in 1817 noted no intellectualimpairment in parkinsonian patients;! but this view has beenchallenged. Estimates of the frequency of dementia haveranged between 15 and 20%, however, application ofmore complex tests of neurophysiological and cognitivefunction has indicated that the true frequency may be evenhigher.s Since parkinsonism is a neurodegenerativecondition, coincidental dementia with increasing age andsurvival is scarcely surprising. Degeneration of melanin-containing nigrostriatal neurons in the substantia nigra leadsto parkinsonism. Similar atrophy and nerve cell destructionin the nucleus basalis and elsewhere can lead to autonomicfailure and, in the cortex, to dementia.6 The histologicalmarker of the degenerative changes of parkinsonism is thepresence of rounded, acidophilic Lewy bodies with a paler

17. Wiener DH, Fink LI, Maris J, Jones RJ, Chance B, Wilson JR. Abnormal skeletalmuscle bioenergetics during exercise in patients with heart failure: role of reducedmuscle blood flow. Circulation 1986; 73: 1127-36.

18. Massie B, Conway M, Yonge R, et al. Skeletal muscle metabolism in patients withcongestive heart failure: relation to clinical severity and blood flow. Circulation1987; 76: 1009-19.

19. Weber KT, Janicki JS. Cardiopulmonary exercise testing for evaluation of chroniccardiac failure. Am J Cardiol 1985; 55: 22A-31A.

20. Guyatt GH, Sullivan MJ, Thompson PJ, et al. The 6 minute walk: a new measure ofexercise capacity in patients with chronic heart failure. Can Med Assoc J 1985; 132:919-23.

21. Cowley AJ, Stainer K, Wynne RD, Rowley JM, Hampton JR. Symptomaticassessment of patients with heart failure: double blind comparison of increasingdoses of diuretics and captopril in moderate heart failure. Lancet 1986; ii: 770-72.

22. Lipkin DP, Scriven AJ, Crake T, Poole-Wilson PA. Six minute walking test forassessing exercise capacity in chronic heart failure. Br Med J 1986; 292: 653-55

23. Parameshwar J, Dambrink JHE, Sparrow J, et al. A new exercise test for theassessment of heart failure: use of a self powered treadmill. Br Heart J 1989; 61:421-25.

24. Dargie HJ, Cleland JGF, Leckie BJ, Inglis CG, East BW, Ford I. Relationship ofarrhythmias and electrolyte abnormalities in patients with severe chronic heartfailure. Circulation 1987; 75 (suppl 4): 98-107.

25. Campbell RWF. Arrhythmias and heart failure. Heart Failure Abstr 1989; 1: 52-53.1. Parkinson J. An essay on the shaking palsy. London, Sherwood, Neely and Jones,

1817.2. Brown RG, Marsden CD. How common is dementia in Parkinson’s disease? Lancet

1984; ii: 1262-65.3. Mayeux R, Rosenstein R, Stern J, Cote L, Fahn S. The prevalence and risk of

dementia in idiopathic Parkinson’s. Ann Neurol 1986; 20: 128.4. Girotti F, Soliveri P, Carella F, et al. Dementia and cognitive impairment in

Parkinson’s disease. J Neurol Neurosurg Psychiatry 1988; 51: 1498-5025. Rajput AH, Offord KP, Beard CM, Kurland LT. A case-control study of smoking

habits, dementia and other illnesses in idiopathic Parkinson’s disease. Neurology1987; 37: 226-32.