1466
in placebo analgesia.9 They infused naloxone or naloxone vehicle double-blind while giving placebo openly, and were able to show that naloxone had an intrinsic hyper-
solution of the puzzle of placebo depends on resolving the mind-body teaser of the cartesian dualist: it will not go away if we reduce the mind to biochemistry and pretend that the duality simply does not exist.
algesic effect unrelated to placebo analgesia. Grevert et
ROUTINE PREOPERATIVE INVESTIGATIONS ARE EXPENSIVE AND UNNECESSARY
evidence
for
an
allO likewise tried
opioid component
separate the effect of naloxone from placebo; from experiments with ischaemic pain in paid volunteers they concluded that placebo analgesia was only partly antagonised by naloxone.1O This effect was observed only after repeated administrations of placebo and naloxone; naloxone had no effect on placebo analgesia in the first session. These workers considered the possibility that the delayed appearance of the partial naloxone antagonism could be the result of learning. That apart, placebo response in experimental pain is likely to be different from that in clinical pain; moreover, naloxone had no hyperalgesic effect in experimental pain. Goldstein and Grevert themselves pointed out, "if the dramatic analgesic effect of hypnosis is not blocked by naloxone,1I,12 is it not reasonable to suppose that far lesser degrees of analgesia produced by placebos could be mediated by processes of suggestion not involving endorphins at all?"’3 Attempts to "explain" placebo effect in pharmacological terms may be pointless: placebo can mimic the effect of any drug.14-16 In his famous paper on the pharmacology of placebo, W olP7 showed that direction and magnitude of response are influenced by the state of the end-organ, the experimental setting, the nature of symbolic stimuli, and the conditioning circumstances. In a man with a gastric fistula, Wolf was able to make gastric mucosa respond to atropine as if it were
prostigmine.
to
In another
subject experiencing
nausea
after syrup of ipecac, when the same preparation was given with the reassurance that it would stop the nausea, the nausea disappeared. In psychiatry, placebo effect is even more pervasive.16 One must admire the frankness of those psychologists who have shown that psychotherapy is no better than placebo. 18 Over 500 papers on placebo reviewed by Shapiro and Morris" leave the reader without any firm basis for speculating about the mechanism of placebo, but one point comes across clear-that there is no reasori to believe that the placebo effect has a single specific mechanism.14 The 9. 10.
Dubner R, Wolskee PJ, Deeter WR. Placebo and naloxone can alter postsurgical pain by separate mechanisms. Nature 1983; 306: 264-65. Grevert P, Albert LH, Goldstein A. Partial antagonism of placebo analgesia by
Gracely RH,
naloxone. Pain 1983; 16: 129-43. 11. Goldstein A, Hilgard ER. Failure of the opiate antagonist naloxone to modify hypnotic analgesia. Proc Natl Acad Sci USA 1975; 72: 2041-43. 12. Barber J, Mayer D. Evaluation of the efficacy and neural mechanism of hypnotic analgesia procedure in experimental and clinical dental pain. Pain 1977; 4: 41-48. 13. Goldstein A, Grevert P. Placebo analgesia, endorphins, and naloxone. Lancet 1978; ii: 1385. 14. Byerly H. Explaining and exploiting placebo effects. Perspect Biol Med 1976; 19: 423-36. 15. Gowdey CW. A guide to the pharmacology of placebos. Can. Med. Assoc. J. 1983; 128: 921-25. 16. Shapiro AK, Morris LA. The placebo effect in medical and psychological therapies. In: Garfield SL, Bergin AE, eds. Handbook of psychotherapy and behavioral change, 2nd ed. New York: Wiley, 1978: 369-410. 17. Wolf S. Effects of suggestion and conditioning on the action of chemical agents in human subjects-the pharmacology of placebos. J Clin Invest 1950; 29: 100-09. 18. Prioleau L, Murdock M, Brody N. An analysis of psychotherapy versus placebo studies. Behav Brain Sci 1983; 6: 275-310.
A POLICY of "routine" investigations before operations has become ingrained in surgical and anaesthetic practice. Sometimes it originates from uncritical consultants, but more often from junior surgical staff with a motive for self-preservation should they be asked for the result of an investigation on the ward round. Pressure for routine tests also comes from junior anaesthetists who want to "cover" themselves should difficulties arise during the operation. But are a full blood count and chest radiograph really necessary in a healthy young man who has been playing squash twice a week? A chest radiograph in a 70-year-old ex-miner is a different matter: one is clinically indicated, the other is merely routine. From time to time the value and cost effectiveness of preoperative investigations have come under scrutinyl-3 and Blery, Chastang, and Gaudy crystallise the issues in the first number of a new journal, Effective Health Care.4Many laboratories and radiological departments are so swamped with unnecessary routine investigations that they cannot pay adequate attention to important and urgent tests. Kaplan et a15 studied 2000 patients undergoing elective surgery over four months and found that 514 SMA6 tests were done, of which 41% were not indicated and only 1 was abnormal. They estimated that abandonment of such testing would result in 1 death in 100 years and a saving of$41 000 per year. Smallwood6 found that routine cross-matching of blood was quite unnecessary for certain procedures such as cholecystectomy, thyroidectomy, mastectomy, and vagotomy. Indeed, for one hundred consecutive vagotomies, 234 units of blood were held in reserve and none used. Blery, Chastang, and Gaudy4started a simplified strategy for preoperative tests in 1981 in a department where 6000 anaesthetics are given annually. For example, in a healthy patient under 60 years old and having a hernia repair, no laboratory tests and no chest radiograph are done; and if he is under 40 he does not have an electrocardiogram. Preoperative tests can be divided into three groups-discretionary tests, for specific clinical indications; baseline tests, when there is a substantial risk of disturbances in the postoperative period (preoperative electrocardiograms in older patients having major surgery come in this category); and screening tests, which aim to reveal clinically unsuspected disease (chest radiograph and renal function tests are common examples). It is this third group that requires the most critical appraisal, although the other two must be carefully assessed. Unsuspected liver disease is a worrying possibility. Whereas serum urea and creatinine levels give a fair guide to renal function, standard liver function tests do 1. Sandler G. Costs of unnecessary tests. Br Med J 1979; ii: 21-24. 2. National Study by the Royal College of Radiologists. Preoperative chest radiology. Lancet 1979; ii: 83-86. 3. Rabkin SW, Horne JM. Preoperative electrocardiography: its cost-effectiveness in detecting abnormalities when a previous tracing exists. Can Med Assoc J 1979; 121: 301-06. 4. Blery C, Chastang C, Gaudy J-H. Critical assessment of routine preoperative investigations. Effective Health Care 1983; 1: 111-14. Effective Health Care is published by Elsevier Science Publishers (PO Box 211, 1000AE, Amsterdam, Netherlands, 52 Vanderbilt Avenue, New York, NY 10017, USA), annual subscription (6 issues)
Dfl120, $48. Kaplan EB, Boeckman AS, Roizen MF, Sheiner LB. Elimination of unnecessary preoperative laboratory tests. Anesthesiology 1982; 57: A445. 6. Smallwood JA. Use of blood in elective general surgery: an area of wasted resources. Br Med J 1983; 286: 868-70. 5.
1467 not
predict how the liver will metabolise anaesthetic and sedative drugs. A history of heavy alcohol intake or hepatitis
chordal rupture in association with trauma, hypertrophic cardiomyopathy, left atrial myxoma, aortic reflux, and
in the past will alert the anaesthetist and transfer liver function tests from the screening to the discretionary category. The counsel of perfection is that no tests should be ordered until after a full history and examination, but this is not always possible where the changeover of surgical patients is very rapid: if the blood does not reach the laboratory early in the morning, the result is not back in time for the operation the following day. More thorough evaluation of the patient in the outpatient clinics would help, but if the waiting-time for operation is months or years, tests at this juncture will be purposeless. A useful compromise, if staff are available, is a7 pre-anaesthetic clinic a few days before the operation.’ Considerable sums of money could be saved, and diverted to better use, if every surgical unit, in consultation with the anaesthetists, drew up a strategy to guide its junior staff about
pregnancy.’o
preoperative investigations. CHORDAL RUPTURE BEFORE the advent of mitral valve surgery in 1948, pure mitral incompetence was widely held to be uncommon and was usually ascribed to chronic rheumatic heart disease or endocarditis.8 Then, on the basis of surgical, cardiac catheterisation, and necropsy findings over the next two decades, it was reported with increasing frequency and several alternative pathological substrates for pure mitral incompetence were identified. Prominent among these was rupture of the chordae tendineae, a phenomenon long known to occur in association with rheumatic and infective mitral valve disease9 but rarely reported as an isolated finding. Since the 1960s, both primary and secondary chordal rupture have been
and in two recent surgical the commonest cause of pure
increasingly recognised
series, chordal rupture mitral
was 1
incompetence. 10, 11
68-75°70 of cases’," are middle aged men-whereas the 20% or so with a rheumatic or infective aetiology tend to be younger and female. In a few patients, chordal rupture is a manifestation of a more generalised connective tissue disorder such as Marfan’s syndrome or osteogenesis imperfecta.12 More contentious in this respect is the now well established predisposition of patients with "floppy" mitral valves to chordal rupture. Whether or not such patients have a mild but generalised connective tissue disorder is still disputed. 13,14 Chordal rupture is occasionally seen in the context of acute myocardial infarction-sometimes because sudden left ventricular volume overload has led to extreme chordal distension, more rarely because the "muscularised" cores of one or two chordae are involved in the infarct. 15 Less commonly still, there have been reports of
Primary chordal rupture accounts for and characteristically such patients
7.
Holdcroft A. Outpatient pre-operative assessment; the anaesthetists view. Ann Roy Coll Surg Engl 1980; 62: 322-25.
8. Selzer
Mitral regurgitation: clinical patterns, pathophysiology and Medicine 1972; 51: 337-66. 9. Corvisart JN. Essai sur les maladies et les lesions organiques du coeur et des gros vaisseaux. Pans: Migneret, 1806. 10. Oliviera DB, Dawkins KD, Kay PH, Paneth M. Chordal rupture I: Aetiology and natural history. Br Heart J 1983; 50: 312-17. 11. Jais JM, Cadilhac M, Luxereau P, et al. Les insufficances mitrales par rupture et élongation de cordages. Arch Mal Coeur 1981; 74: 129-38. 12. Read RC, Thal AP, Wendt VE. Symptomatic valvular myxomatous transformation; a possible forme fruste of the Marfan syndrome. Circulation 1965; 32: 897-910. 13. Caulfield JB, Page DL, Kastor JA, Sanders CA. Connective tissue abnormalities in spontaneous rupture of chordae tendineae. Arch Pathol 1971; 91: 537-41. 14. Scott Jupp W, Barnett NL, Gallagher PJ, et al. Ultrastructural changes in spontaneous rupture of mitral chordae tendineae. J Pathol 1981; 133: 185-201. 15. Fenoglio J Jr, Tuan Duc Pham. Ruptured chordae tendineae. An electron microscope study. Hum Pathol 1972; 3: 415-20.
A, Katayama F.
natural
history.
The clinical features of chordal rupture
are
variable,
depending upon the number and location ofchordae involved and the time course of their rupture. The acute presentation with pulmonary oedema resulting from torrential mitral reflux is well recognised,I6 but lesser degrees of mitral incompetence may go unnoticed or result in only moderate breathlessness, with progressive deterioration after months or
years
as
further chordae rupture. This latter course may be
frequent than was previously realised, only 4% of the patients in the Brompton series having had symptoms for less more
than one month at the time of surgery. 10 The results of surgery for chordal rupture have been recently reviewed by the Brompton group." Of their 183 patients who would have been suitable for either repair or replacement of their mitral valves, 4507o had repair by the Carpentier technique, 18 and 55% had valve replacement. The two groups were broadly comparable in terms of age, presence of atrial fibrillation, and preoperative symptoms, and all patients with a prosthetic valve or atrial fibrillation remained on anticoagulants postoperatively for life. The operative mortality (4 -. 9070) was similar in the repair and replacement groups and, at a mean 3 -6years after surgery, functional improvement was also similar in the survivors. However, the incidence offatal and non-fatal cerebrovascular thromboembolic events was seven times higher and the predicted six year survival rate 20% lower in those who had undergone valve replacement. On the other hand, 16 of the 82 patients in whom repair was attempted had to have a valve replacement for residual mitral incompetence at or within two years of the initial operation, a disproportionate number of these having had anterior leaflet chordal rupture. Since in 50-60% of patients only chordae to the posterior leaflet are found to have ruptured, 10 mitral valve repair seems distinctly preferable to replacement in this group.
VESICOURETERIC REFLUX: MORE PUZZLES be forgiven for times when it was held that, in children of any age, vesicoureteric reflux (VUR) or urinary tract infection (UTI) had the capability to cause the synonymous conditions of chronic pyelonephritis, reflux nephropathy, or renal scarring. At least the criteria for investigation and treatment of children with UTI were clearer then. We now know, however, that severe kidney disease will occur in only a minority of such children, and efforts are being made to define a susceptible group and to develop means of identifying that group by screening early in life (and perhaps offer preventive treatment). Renal scarring is an unpleasant condition; it leads to hospital attendance, X-rays, antibiotic treatment, ureteric reimplantation (in the view of some),1 and the prospect of hypertension and renal failure for a few. There is current interest in whether some vascular or immunological reaction
PAEDIATRICIANS and
reflecting nostalgically
urologists might
on
16. Sanders CA, Austen WG, Harthorne JW, et al. Diagnosis and surgical treatment of mitral regurgitation secondary to ruptured chordae tendineae. N Engl J Med 1967; 276: 943-49. 17. Oliviera DB, Dawkins KD, Kay PH, Paneth M. Chordal rupture II: Comparison between repair and replacement. Br Heart J 1983; 50: 318-24. 18. Carpentier A, Chauvaud S, Fabiani JN, et al. Reconstructive surgery of mitral valve incompetence. J Thorac Cardiovasc Surg 1980, 79: 338-48. 1. Mundy AR, Kinder CH, Joyce MRL, Chantler C, Haycock GB. Improvement in renal function following ureteric reimplantation for vesicoureteric reflux. Br J Urol 1981; 53: 542-44