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CLINICAL PRACTICE, STATISTICS, AND PHILOSOPHY
911
maintain a high water-vapour pressure gradient from skin to air, thereby facilitating heat loss. Moreover, the cutaneous circulation is much greater than that in colder skin. With this method, very high evaporative
cooling
rates are
possible.3 Furthermore, monitoring
and other aspects of management are easily done. Whichever method is chosen, active cooling should be continued only until the rectal temperature reaches about 101°F, the temperature will then return to
normal
spontaneously.
If the
patient
is cooled
to a
normal temperature, hypothermia may develop. Once the temperature has returned to normal, it seldom rises
again. Increased muscular activity caused by shivering, spasticity, and convulsions will increase the metabolic heat load and must be prevented. Chlorpromazine is useful in this regard. It prevents shivering, decreases muscle tone, and may in addition have a direct hypothermic effect ; it also sedates the patent. 18 A combination of chlorpromazine, promethazine, and pethidine has been used to prevent convulsions. 3,10 Diazepam is also effective. Aspirin should not be used as an antipyretic because of its untoward effects on blood coagulation. While rapid and effective cooling is the cornerstone of treatment of heatstroke, it is important during and after cooling to treat shock, correct fluid and electrolyte disturbances, and support vital organs. A patent airway must be maintained, by intubation if necessary. Oxygen should be given. The patient is often
hypotensive, largely because of the low peripheral vascular resistance but partly because of hypovolaemia secondary to dehydration. 3, 13 Cardiogenic shock may arise. The low blood-pressure will often respond to cooling alone. If not, saline or plasma volume expanders should be infused, with monitoring of thecentral venous pressure. Dextran should be avoided because of its propensity to coat platelets. Large volumes of intravenous fluids should not be given initially because the vasoconstriction which occurs after cooling may cause overloading of the central circulation with consequent acute pulmonary oedema. However, 500-1000 ml of dextrose/saline given intravenously early on may facilitate heat transfer and should not overload the circulation. If the bloodpressure does not respond to intravenous fluids, dobutamine or dopamine may have to be administered. Potent vasopressor drugs such as noradrenaline should be avoided because the resultant intense peripheral vasoconstriction impedes heat loss. Digitalis has occasionally been given but is not of proven value; because of the likelihood of concomitant hypokalaemia and renal dysfunction it should be given cautiously if at all. Steroids have been used in the treatment of severe heatstroke. There is, however, no clinical or experimental evidence of benefit (except perhaps in reducing cerebral oedema). A metabolic acidosis is frequently present. If severe, this may require the 18.
administration of sodium bicarbonate. Potassium and glucose supplementation is often needed. Because heatstroke may be complicated by renal failure, 10,11, 19 attempts should be made to improve renal perfusion with mannitol or frusemide. An indwelling urinary catheter should be inserted. If acute renal failure develops, early dialysis is usually indicated because rapidly progressive azotaemia may follow the widespread tissue damage. A bleeding diathesis is not uncommon in severe heatstroke. 10,19 Various disturbances may be responsible: fresh plasma or blood should be given if hypoprothrombinaemia is present, fresh blood or fibrinogen for hypofibrinogenaemia, and platelet-rich plasma for thrombocytopenia. Heparin has been used to treat disseminated intravascular coagulation, but its efficacy and safety remain to be proved. Even with optimum treatment, heatstroke still causes deaths and permanent damage. Prevention is therefore the best strategy. In large measure this consists of educating people at risk to recognise the physical conditions which may lead to heat loading. If these conditions prevail, physical work or exercise should be limited or avoided, and common-sense measures instituted (such as adequate fluid intake and rest periods). When, as in certain industries, the conditions leading to heatstroke are inseparable from the work in hand, one remedy lies in acclimatisation.
CLINICAL PRACTICE, STATISTICS, AND PHILOSOPHY CLINICAL decision analysis now has enthusiastic disciples in several countries, its own journal (Medical Decision Making), and its first real textbook. The basic idea is that all clinical decisions stem from both scientific knowledge and value judgments, and that the solution of major problems requires a systematic analysis of these two elements according to the principles of statistical decision theory. Imagine, for instance, that a clinician in a particular case has the choice between surgical and medical treatment. Then he must for each treatment (1) make an exclusive and exhaustive list of the possible outcomes, (2) assess the probability of these outcomes, and (3) assess their relative desirability or utility. We shall not discuss the utility concept in statistical terms,2 but only mention that both the probabilities and the utilities must be expressed numerically on a scale from 0 to 1. When that has been done, it is possible to calculate which decision ensures the highest average utility. It is the axiom of statistical decision theory that a rational decision-maker must always maximise the expected utility-i.e., choose that decision which is likely to have the best consequences. It is too early to predict applicability to everyday clinical practice, but this new approach to clinical decision making deserves attention for two reasons. Firstly, it stresses correctly that clinical decisions always involve value 19. Knochel JP. Environmental heat illness. Arch Intern Med 1974; 133: 841-64. 1. Weinstein MC, Fineberg HV, Elstein AS, et al. Clinical decision analysis.
Hoagland RJ, Bishop RH. A physiologic treatment of heatstroke. Am J Med Sci 1961; 241: 415-22.
2.
Philadelphia. Saunders, 1980. Lindley D. Making decisions. London: Wiley,
1971.
912
judgments and that clinical medicine is more than applied natural science. The utilities belong to the art, whereas the probabilities belong to the science of medicine, and all clinical decisions contain both elements. Secondly, analysis by the decision theorist unmasks some of the fundamental philosophical dilemmas of clinical medicine. For example, one element in a decision analysis may be the premise that a patient has a 90% chance of cure if he or she receives a certain treatment. What does that really mean? Strictly speaking, a probability is a long-run frequency and there is little sense in making a probabilistic statement about an individual case. The probability in this context must somehow be a measure of our personal belief in the cure of that particular patient-but what do we believe in? The empiricists among clinicians will require that it has been shown empirically that 90% of patients are cured when they receive that particular treatment; whereas the rationalists among
us
may base their belief
on
the argument that
philosophy of Jeremy Bentham and John Stuart Mill. The utilitarian creed, that the decision maker must ensure the greatest amount of happiness for the greatest number, differs little from the axiom of modern statistical decision theory that one must "maximise the expected utility of one’s actions". Generations of moral philosophers have discussed the implications of utilitarian thinking, and the main difficulty is that it ignores such concepts as human rights and duties. That is also the drawback of utilitarian thinking in medicine. The utilities of a decision analysis are ambiguous, since it is not certain who should assess the utility for whom. A responsible clinician must decide what serves the patient’s interests best, but must also respect the patient’s autonomy, and must consider the rights of other patients as well. If conflicts arise, they must be resolved by resort to medical deontology (duty ethics) rather than medical utilitarianism.
our
knowledge of the disease mechanism and the mode of action of the drug is so complete that we can be almost certain (90% certain) that the patient will recover. Everybody will agree that clinical decisions require scientific knowledge, but those who endeavour to do a formal decision analysis are forced to make up their minds what they mean by knowledge. The utilities present even greater difficulties. They express the value of the consequences of the possible decisions, immediately raising the question, Who assesses the consequences for whom? There are several possibilities. First of all, the clinician must make an assessment of the consequences of his decisions for his patient. Nobody will deny that it is his duty to do this; but the days of completely paternalistic medicine are gone, and the patient must be encouraged to take part in the decision process. Therefore, in many cases the utilities adopted for the analysis ought to be the patient’s evaluation of the possible consequences for himself or herself. The dilemma, however, does not stop here. A doctor in a national health service has wider responsibilities: "every time one devotes additional time or resources to one patient, another patient is deprived of that time or those resources’;3 Therefore, the clinician must not forget the indirect consequences of his actions for other
patients. One of the virtues of clinical decision analysis is that these are brought into the open. Clinical decision theorists have been particularly interested in the assessment of patient preferences, and the published work on this topic has been reviewed by Eraker and Politzer. Most of the studies they cite are based on hypothetical situations, but they do reveal the potential biases and distortions when patients assess the consequences for themselves-evaluations may be affected by the way scientific information is presented and by the clarity with which the patient perceives the possible outcomes. Some of these sources ofbias indicate that patients are not rational decision makers according to the axioms of decision theory. Such difficulties may be hard to overcome, but they are largely methodological. Far more fundamental issues arise from the utility concept of decision theory. From a philosophical point of view, modern decision theory is little more than the 18th and 19th century utilitarian moral
problems
3. Kendell RE. The painful facts. In. Phillips CI, Wolfe JN, eds. Clinical practice and economics. Tunbridge Wells: Pitman Medical, 1977: 93. 4. Eraker SA, Politzer P How decisions are reached physician and patient. Ann Intern Med 1982; 97: 262-68
PENICILLINASE-PRODUCING GONOCOCCI: FURTHER COMPLICATIONS ONE of the features of disseminated gonococcal infection (DGI) is its rapid response to penicillin treatment, and this can provide useful confirmation of a clinical diagnosis when joint, skin, or blood cultures for Neisseria gonorrhoeae prove negative. It is, of course, preferable to make the definitive diagnosis by isolation of the organism from one of the likely
sites-cervix, urethra, rectum, and throat in the female, and urethra, prostate, rectum, and throat in the male. However, since it is almost a prerequisite for the development source
of DGI that the patient should have no symptoms at the initial sites of infection (helping to explain the high female/male ratio of cases), the affected patients are more likely to attend the rheumatologist with their flitting arthritis and tenosynovitis, the dermatologist with their haemorrhagic pustules, or the general physician with their unexplained fever. For none of these clinicians may the anogenital sites be the obvious ones for bacteriological investigation. It has been accepted that the gonococci associated with DGI tend to fall into the more penicillin-sensitive range’ but a worrying, if predictable, development is seen in a report of DGI caused by penicillinase-producing N. gonorrhoeae (PPNG). Rinaldi and colleagues2 from California report four cases of gonococcal arthritis caused by PPNG in all of which the organism was isolated from the joint fluid, adding to three
previously reported cases.3,5 The
in DGI have in general been and erosion of cartilage and without the destruction benign, bone that was associated with acute gonococcal arthritis in the pre-antibiotic era. Only two of twenty-four patients with DGI had a monoarthritis6 compared with four out of the seven above cases and, while seventeen (7007o) of the British series were women, only two of the seven cases produced by PPNG were female.
joint complications
1. Wiesner
PJ, Handsfield HH, Homes KK. Low antibiotic resistance of gonococci causing disseminated infection. N Engl J Med 1973, 288: 1221-22. 2. Rmaldi RZ, Harrison WO, Fan PT Penicillin-resistant gonococcal arthritis-a report of four cases. Ann Intern Med 1982; 97: 43-45. 3. Percival A, Rowlands J, Corkill JE, et al. Penicillinase-producing gonococci in Liverpool. Lancet 1976; ii: 1379-82. 4. Leftik MI, Miller JW, Brown JD Penicillin-resistant gonococcal arthritis. JAMA 1978; 239: 134. 5. Thompson J, Dunbar JM, van Gent A, van Furth R. Disseminated gonococcal infection due to a &bgr;-lactamase-producing strain of Neisseria gonorrhoeae. Br J Vener Dis 1981; 57: 325-26 6. Barlow D. Disseminated gonococcal infection In: Besser GM, ed. Advanced medicine. Tunbridge Wells: Pitman Medical, 1977: 197-203.
maintain a high water-vapour pressure gradient from skin to air, thereby facilitating heat loss. Moreover, the cutaneous circulation is much greater than that in colder skin. With this method, very high evaporative
cooling
rates are
possible.3 Furthermore, monitoring
and other aspects of management are easily done. Whichever method is chosen, active cooling should be continued only until the rectal temperature reaches about 101°F, the temperature will then return to
normal
spontaneously.
If the
patient
is cooled
to a
normal temperature, hypothermia may develop. Once the temperature has returned to normal, it seldom rises
again. Increased muscular activity caused by shivering, spasticity, and convulsions will increase the metabolic heat load and must be prevented. Chlorpromazine is useful in this regard. It prevents shivering, decreases muscle tone, and may in addition have a direct hypothermic effect ; it also sedates the patent. 18 A combination of chlorpromazine, promethazine, and pethidine has been used to prevent convulsions. 3,10 Diazepam is also effective. Aspirin should not be used as an antipyretic because of its untoward effects on blood coagulation. While rapid and effective cooling is the cornerstone of treatment of heatstroke, it is important during and after cooling to treat shock, correct fluid and electrolyte disturbances, and support vital organs. A patent airway must be maintained, by intubation if necessary. Oxygen should be given. The patient is often
hypotensive, largely because of the low peripheral vascular resistance but partly because of hypovolaemia secondary to dehydration. 3, 13 Cardiogenic shock may arise. The low blood-pressure will often respond to cooling alone. If not, saline or plasma volume expanders should be infused, with monitoring of thecentral venous pressure. Dextran should be avoided because of its propensity to coat platelets. Large volumes of intravenous fluids should not be given initially because the vasoconstriction which occurs after cooling may cause overloading of the central circulation with consequent acute pulmonary oedema. However, 500-1000 ml of dextrose/saline given intravenously early on may facilitate heat transfer and should not overload the circulation. If the bloodpressure does not respond to intravenous fluids, dobutamine or dopamine may have to be administered. Potent vasopressor drugs such as noradrenaline should be avoided because the resultant intense peripheral vasoconstriction impedes heat loss. Digitalis has occasionally been given but is not of proven value; because of the likelihood of concomitant hypokalaemia and renal dysfunction it should be given cautiously if at all. Steroids have been used in the treatment of severe heatstroke. There is, however, no clinical or experimental evidence of benefit (except perhaps in reducing cerebral oedema). A metabolic acidosis is frequently present. If severe, this may require the 18.
administration of sodium bicarbonate. Potassium and glucose supplementation is often needed. Because heatstroke may be complicated by renal failure, 10,11, 19 attempts should be made to improve renal perfusion with mannitol or frusemide. An indwelling urinary catheter should be inserted. If acute renal failure develops, early dialysis is usually indicated because rapidly progressive azotaemia may follow the widespread tissue damage. A bleeding diathesis is not uncommon in severe heatstroke. 10,19 Various disturbances may be responsible: fresh plasma or blood should be given if hypoprothrombinaemia is present, fresh blood or fibrinogen for hypofibrinogenaemia, and platelet-rich plasma for thrombocytopenia. Heparin has been used to treat disseminated intravascular coagulation, but its efficacy and safety remain to be proved. Even with optimum treatment, heatstroke still causes deaths and permanent damage. Prevention is therefore the best strategy. In large measure this consists of educating people at risk to recognise the physical conditions which may lead to heat loading. If these conditions prevail, physical work or exercise should be limited or avoided, and common-sense measures instituted (such as adequate fluid intake and rest periods). When, as in certain industries, the conditions leading to heatstroke are inseparable from the work in hand, one remedy lies in acclimatisation.
CLINICAL PRACTICE, STATISTICS, AND PHILOSOPHY CLINICAL decision analysis now has enthusiastic disciples in several countries, its own journal (Medical Decision Making), and its first real textbook. The basic idea is that all clinical decisions stem from both scientific knowledge and value judgments, and that the solution of major problems requires a systematic analysis of these two elements according to the principles of statistical decision theory. Imagine, for instance, that a clinician in a particular case has the choice between surgical and medical treatment. Then he must for each treatment (1) make an exclusive and exhaustive list of the possible outcomes, (2) assess the probability of these outcomes, and (3) assess their relative desirability or utility. We shall not discuss the utility concept in statistical terms,2 but only mention that both the probabilities and the utilities must be expressed numerically on a scale from 0 to 1. When that has been done, it is possible to calculate which decision ensures the highest average utility. It is the axiom of statistical decision theory that a rational decision-maker must always maximise the expected utility-i.e., choose that decision which is likely to have the best consequences. It is too early to predict applicability to everyday clinical practice, but this new approach to clinical decision making deserves attention for two reasons. Firstly, it stresses correctly that clinical decisions always involve value 19. Knochel JP. Environmental heat illness. Arch Intern Med 1974; 133: 841-64. 1. Weinstein MC, Fineberg HV, Elstein AS, et al. Clinical decision analysis.
Hoagland RJ, Bishop RH. A physiologic treatment of heatstroke. Am J Med Sci 1961; 241: 415-22.
2.
Philadelphia. Saunders, 1980. Lindley D. Making decisions. London: Wiley,
1971.
912
judgments and that clinical medicine is more than applied natural science. The utilities belong to the art, whereas the probabilities belong to the science of medicine, and all clinical decisions contain both elements. Secondly, analysis by the decision theorist unmasks some of the fundamental philosophical dilemmas of clinical medicine. For example, one element in a decision analysis may be the premise that a patient has a 90% chance of cure if he or she receives a certain treatment. What does that really mean? Strictly speaking, a probability is a long-run frequency and there is little sense in making a probabilistic statement about an individual case. The probability in this context must somehow be a measure of our personal belief in the cure of that particular patient-but what do we believe in? The empiricists among clinicians will require that it has been shown empirically that 90% of patients are cured when they receive that particular treatment; whereas the rationalists among
us
may base their belief
on
the argument that
philosophy of Jeremy Bentham and John Stuart Mill. The utilitarian creed, that the decision maker must ensure the greatest amount of happiness for the greatest number, differs little from the axiom of modern statistical decision theory that one must "maximise the expected utility of one’s actions". Generations of moral philosophers have discussed the implications of utilitarian thinking, and the main difficulty is that it ignores such concepts as human rights and duties. That is also the drawback of utilitarian thinking in medicine. The utilities of a decision analysis are ambiguous, since it is not certain who should assess the utility for whom. A responsible clinician must decide what serves the patient’s interests best, but must also respect the patient’s autonomy, and must consider the rights of other patients as well. If conflicts arise, they must be resolved by resort to medical deontology (duty ethics) rather than medical utilitarianism.
our
knowledge of the disease mechanism and the mode of action of the drug is so complete that we can be almost certain (90% certain) that the patient will recover. Everybody will agree that clinical decisions require scientific knowledge, but those who endeavour to do a formal decision analysis are forced to make up their minds what they mean by knowledge. The utilities present even greater difficulties. They express the value of the consequences of the possible decisions, immediately raising the question, Who assesses the consequences for whom? There are several possibilities. First of all, the clinician must make an assessment of the consequences of his decisions for his patient. Nobody will deny that it is his duty to do this; but the days of completely paternalistic medicine are gone, and the patient must be encouraged to take part in the decision process. Therefore, in many cases the utilities adopted for the analysis ought to be the patient’s evaluation of the possible consequences for himself or herself. The dilemma, however, does not stop here. A doctor in a national health service has wider responsibilities: "every time one devotes additional time or resources to one patient, another patient is deprived of that time or those resources’;3 Therefore, the clinician must not forget the indirect consequences of his actions for other
patients. One of the virtues of clinical decision analysis is that these are brought into the open. Clinical decision theorists have been particularly interested in the assessment of patient preferences, and the published work on this topic has been reviewed by Eraker and Politzer. Most of the studies they cite are based on hypothetical situations, but they do reveal the potential biases and distortions when patients assess the consequences for themselves-evaluations may be affected by the way scientific information is presented and by the clarity with which the patient perceives the possible outcomes. Some of these sources ofbias indicate that patients are not rational decision makers according to the axioms of decision theory. Such difficulties may be hard to overcome, but they are largely methodological. Far more fundamental issues arise from the utility concept of decision theory. From a philosophical point of view, modern decision theory is little more than the 18th and 19th century utilitarian moral
problems
3. Kendell RE. The painful facts. In. Phillips CI, Wolfe JN, eds. Clinical practice and economics. Tunbridge Wells: Pitman Medical, 1977: 93. 4. Eraker SA, Politzer P How decisions are reached physician and patient. Ann Intern Med 1982; 97: 262-68
PENICILLINASE-PRODUCING GONOCOCCI: FURTHER COMPLICATIONS ONE of the features of disseminated gonococcal infection (DGI) is its rapid response to penicillin treatment, and this can provide useful confirmation of a clinical diagnosis when joint, skin, or blood cultures for Neisseria gonorrhoeae prove negative. It is, of course, preferable to make the definitive diagnosis by isolation of the organism from one of the likely
sites-cervix, urethra, rectum, and throat in the female, and urethra, prostate, rectum, and throat in the male. However, since it is almost a prerequisite for the development source
of DGI that the patient should have no symptoms at the initial sites of infection (helping to explain the high female/male ratio of cases), the affected patients are more likely to attend the rheumatologist with their flitting arthritis and tenosynovitis, the dermatologist with their haemorrhagic pustules, or the general physician with their unexplained fever. For none of these clinicians may the anogenital sites be the obvious ones for bacteriological investigation. It has been accepted that the gonococci associated with DGI tend to fall into the more penicillin-sensitive range’ but a worrying, if predictable, development is seen in a report of DGI caused by penicillinase-producing N. gonorrhoeae (PPNG). Rinaldi and colleagues2 from California report four cases of gonococcal arthritis caused by PPNG in all of which the organism was isolated from the joint fluid, adding to three
previously reported cases.3,5 The
in DGI have in general been and erosion of cartilage and without the destruction benign, bone that was associated with acute gonococcal arthritis in the pre-antibiotic era. Only two of twenty-four patients with DGI had a monoarthritis6 compared with four out of the seven above cases and, while seventeen (7007o) of the British series were women, only two of the seven cases produced by PPNG were female.
joint complications
1. Wiesner
PJ, Handsfield HH, Homes KK. Low antibiotic resistance of gonococci causing disseminated infection. N Engl J Med 1973, 288: 1221-22. 2. Rmaldi RZ, Harrison WO, Fan PT Penicillin-resistant gonococcal arthritis-a report of four cases. Ann Intern Med 1982; 97: 43-45. 3. Percival A, Rowlands J, Corkill JE, et al. Penicillinase-producing gonococci in Liverpool. Lancet 1976; ii: 1379-82. 4. Leftik MI, Miller JW, Brown JD Penicillin-resistant gonococcal arthritis. JAMA 1978; 239: 134. 5. Thompson J, Dunbar JM, van Gent A, van Furth R. Disseminated gonococcal infection due to a &bgr;-lactamase-producing strain of Neisseria gonorrhoeae. Br J Vener Dis 1981; 57: 325-26 6. Barlow D. Disseminated gonococcal infection In: Besser GM, ed. Advanced medicine. Tunbridge Wells: Pitman Medical, 1977: 197-203.