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SPECIAL

ARTICLES

Causal

Thinking

in Practice:

Strengths

and

Weaknesses

of the Clinical

Vantage

Point

Mervyn

Susser,

MB, BCh, DPH, FRCP(E)

From the Faculty of Medicine, Columbia University, New York

ABSTRACT. The place of causal inference in clinical practice is considered. One function relates to the vali-dation of existing knowledge, as in the evaluation of the medical literature, and is exemplified by the process of

editorial selection. A second function relates to the

vali-dation of potential knowledge, as in the testing of

hy-potheses, and is exemplified by the pursuit of a

nutni-tional cause of retarded mental development. Features of

clinical practice that contribute strengths or weaknesses

to causal inference are then examined. These include the diagnostic process, the effect of cumulative clinical ex-perience, continuity of observation and follow-up, and the focus on disease. Pediatrics 1984;74:842-849; causal

inference, malnutrition and mental development,

diagno-sis, follow-up, history taking.

The philosophy of causal inference reaches deep

into abstractions. Applied in clinical pediatrics,

however, it yields some practical benefits. For

cli-nicians, inference is a constant and everyday

activ-ity. In going about their business of diagnosis and

treatment, clinicians are constantly making logical inferences, that is to say, drawing conclusions from

a set of facts and premises. In the determination of

causality, too-which factors caused what

out-comes-inference provides the logical and the

an-alytical grounds for decision. Causal inference has

preoccupied philosophers because it is fundamental

to science and the validation of knowledge, as it is

Received for publication July 29, 1983; accepted Feb 1, 1984. A version of this paper was presented at a symposium at the

Albert Einstein College of Medicine on Henry L. Barnett Day, March 15, 1982; the occasion honored Henry Barnett upon his retirement from the Departmenthe founded.

Reprint requests to (MS.) Faculty of Medicine, Columbia

Uni-versity, 630 W 168th St, New York, NY 10032.

PEDIATRICS (ISSN 0031 4005). Copyright © 1984 by the American Academy of Pediatrics.

too in the applications of science to medicine. This

logic is a bridge that enables the contemporary

clinician, in dealings with patients, to shift from

charismatic priest-like authority to the authority of

tried knowledge and of national predictions founded

on explicit models of causal relationships.

Causal inference has a long history; at the very

beginning the Hippocratic authors gave attention

to causality. Life is short, they wrote, and the arts

of acquiring knowledge long and difficult. Our many

errors show that the practice of causal inference

remains difficult; the forum for the controversies

and disagreements provided by our journals shows

that it remains an art. Although to assist us, we

have acquired analytic techniques, statistical

meth-ods and conventions, and logical criteria, ultimately the conclusions we reach are a matter of judgment.’

Judgment is neither value-free nor situation-free.

Each of us is limited by a frame of reference derived

from the ideas of our own socity and our own times,

from our training, and from the perspective from

which we perceive our problem, whether it be that

of biochemist, clinician, epidemiologist, geneticist,

or social scientist. Different observers see different

problems, and often reach different conclusions.

Ambiguity is heightened because analytic

sci-ence-whethen experimental or observational-is

by nature reductionist: one must simplify the con-ditions of observation; one must exclude as many

extraneous variables as possible from the field of

study; and one must remove on control effects of

the surrounding environment. To isolate the field

of observation in this way is often to contradict the

clinical function, because it is also to eliminate the

perception of the patient as a person, and to close

out the social milieu and the multifarious

condi-tions under which patients live. In the practice of

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these reductions to become patient centered.

Causal inference embodies the critical and

skep-tical elements of scientific thinking. Although this

logic, when ill used, can shackle imagination, it is

also a brake on foolishness. Yet the discipline it

imposes is not merely constraining. Important functions of causal inference relate to two types of

validation, first of existing knowledge, and second

of evolving on potential knowledge. By validation, I mean a process, not the certification of invulnera-bility to all tests, trials, and other assessments. With the validation ofexisting knowledge, the

prod-ess requires a critical apparatus for reading and

evaluation; with the validation of potential

knowl-edge, it requires an ability to test hypotheses.

In each of these applications the process of

vali-dation is two sided: negative and positive,

destnuc-tive and creative. In the validation of existing

knowledge, on the negative side the process involves the sifting out of error and nonsense; on the positive side, it involves the extension of knowledge and even the creation of new knowledge. The negative function of sifting out nonsense from “nearsense”

and sense is a primary gatekeeping function of

editors and reviewers. Here one must face the inev-itability that in recognizing error we shall err. These

errors occur-all will know-even among those highly regarded journals that reject some 80% and more of submissions. Why do they err so often?

There is always a degree of unreliability and

disa-greement between the judgment of reviewers, and

so they are bound, on the one hand, to accept some

poor articles and, on the other, to reject some good

ones. Because errors ofjudgment will occur in both

these directions, and because we can be sure that

many more poor than good articles are submitted,

in absolute numbers editors are likely to make more

wrong judgments about poor articles than about

good ones. In one result derived from conservative

assumptions in a quantified model, only about half

(49%) of the good articles are likely to be accepted.

(The model assumes that 20% of submissions are

acceped, that acceptance follows on the agreement

of two reviewers, that two reviewers agree with each

other 70% of the time (about the rate for two

radiologists judging radiographs), that each is night 70% of the time in accepting good articles, and that 70% of the articles submitted are poor ones, ie,

below the exacting standards aimed at by the

jour-nal.) Equally important, more than a quarter

(26.5%) of all the papers accepted are likely to be

poor ones. An editor cannot be right enough of the

time to protect his readers from nonsense.

For the medical reader, knowledge may mean life

on health for his patients. In that situation, he must not only be able to defend himself against nonsense,

but to legitimate sense. Legitimation is the creative

side of validating existing knowledge. For this pun-pose, the reader needs a sound grasp of the

pninci-pies and procedures that strengthen causal

infer-ence, including the evaluation of research design,

the elaboration of analysis, and the application of an array of criteria to aid judgment.27 The analysis

of data can itself extend knowledge by eliciting new

relationships.7

Given these procedures, the last and best

affin-mation of positive results is in their independent replication. Exact replication of research design and

execution-John Stuart Mill’s “method of

differ-ence,” in which the situations compared are alike

in all circumstances but one-is only to be found

in the domain of the experimental sciences. In clinical and epidemiologic studies, one must rely on the consistent replication of results in the face of change in all other circumstances: this John Stuart Mill described as the “method of agreement,” when the situations compared “have only one cincum-stance in common.” The classic example is the association of cigarette smoking and lung cancer, which by now probably holds in more than half a hundred different instances.

To turn to the validation of potential knowledge:

on the negative side, this process involves attacks

on existing hypotheses in order to eliminate them; on the positive side, it involves the generation of

alternative hypotheses. Francis Bacon, who

devel-oped and systematized methods of scientific

infer-ence, wrote:

The induction which is to be available for the discovery and demonstration of sciences and arts, must analyze nature by proper rejections and exclusions; and then after a sufficient number of negatives, comes to a conclusion

on the affirmative instances.

In other words, the most cogent test of a hypothesis

is to attempt disproof. (Karl Popper likewise insists

that science can only proceed by refuting the

de-ductions from hypotheses,8 but he also holds that there can be no valid proof by induction from a particular positive instance to the general.9) In a formal sense, statistical conventions for hypothesis

testing are so structured that we do indeed seek disproof by framing a null hypothesis. And if our

study has sufficient statistical power to rule out the

mere failure to detect a positive result for lack of

numbers, we must then challenge our creativity in

framing new hypotheses.

A telegraphic outline of the evolution of one line

of thinking familiar to me may serve to illustrate how the rejection of each successive hypothesis leads to the creation of alternatives, and finally to an affirmative. Attempts to elucidate the common

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nutrition have been a preoccupation of the past two decades. The explanatory hypothesis to be tested was that poor prenatal nutrition netands human fetal growth and subsequent development.’#{176}’2 In our own studies of a well-defined situation of acute starvation in a developed country, namely the Dutch famine of 1944/1945, we found no support for the idea that prenatal nutrition during the

pe-nod of the brain growth spurt had depressed the

cognitive performance in young adults 20 years

later.’3 In formal terms, we failed to reject the null hypothesis.

The procedures of inference, therefore, called for

alternative explanations. One alternative was that passably good previous nutrition in the mothers

protected their pregnancies in the prenatal period.

These women had no overt signs of malnutrition

and, during their growth period in The Netherlands before World Wan II, levels of nutrition were high. Perhaps then prenatal nutritional deprivation might affect subsequent development only in chronically malnourished mothers? This hypothe-sis would require testing in overtly malnourished

mothers, such as are found in less developed

coun-tries.

Another strong alternative was that, because the

prenatal period covered only about 10% of the

period of maximum brain growth during which the

brain was “sensitive” to insults,’4 the severe pre-natal nutritional deprivation would still leave suf-ficient reserve in the brain to protect subsequent function. This hypothesis would require a test of the combined and independent effects of prenatal

and postnatal malnutrition, again a likely situation

only in less developed countries.

In two studies in less developed countries, both these alternative hypotheses could be simultane-ously tested and eliminated. These studies of pre-natal and postnatal nutritional supplementation in malnourished women, one a quasiexpeniment in Guatemala, ‘ and the other a controlled trial in

Bogota,’6 failed to support the contention that in malnourished women better prenatal nutrition alone could improve postnatal cognitive perform-ance. In addition, prenatal nutrition had no demon-strable effect on cognition oven and above that of postnatal nutrition.’7”8 (In controlled trials of high-protein prenatal supplementation in New York as well as in Bogota, however, effects on visual

habit-uation occurred.’9 Some studies, but not all, have suggested a link between habituation in infancy and later measured

IQ.)

Remaining alternatives now were that the appar-ent variation in cognitive function with nutritional

conditions was owed either to postnatal nutritional deprivation, on to the social deprivation that

in-variably accompanies such malnutrition. The re-suits of the intervention studies in Guatemala and

Bogota both supported the idea of a positive effect

of postnatal nutrition on cognitive performance.

But here, also, a limiting negative emerged. In the

Bogota study, the detectable effects on cognition

are those of contemporaneous nutrition. This

find-ing points to a pathway leading from nutrition to

cognition through some current state of motivation, behavior, on health state.

We seem at last to have reached a Baconian affirmative instance. Thus, intensive longitudinal observational studies oven many years in a Mexican

village can be taken as supporting this result.2#{176}The poor mental performance observed in malnourished children was largely accounted for by the mothers’ access to external stimulation in the form of

listen-ing to the radio. Follow-up case-control studies of severe early malnutrition in Jamaica can also be

taken to support the result. Differences between

cases and control subjects were found mainly in the less stimulating environments, and, when

differ-ences were found, the degree of social stimulation

accounted for a good part of the differences.21’22 In

this study, the contribution of the current state of nutrition of the children is not known.

This brings us to one more Baconian rejection and exclusion. A study of postnatal intervention in Cali, Columbia,23 provided both good nutrition and social stimulation. In these children, well-fed at the time of last testing, there was a marked cognitive improvement. In one group given nutritional sup-plementation alone, however, no effect could be attributed to the intervention.23 For the present, then, one may conclude that the largest postnatal effects on cognitive performance come from social stimulation, and that the predominant nutritional effects occur either in interaction with stimulation, on are immediate and behavioral. The road along which hypotheses are eliminated and alternatives

created is never-ending; meanwhile, one must live

and act by the “affirmative instances.”

The conscientious use of the principles and

pro-cedures of causal inference makes us aware of error,

and humble before its pervasiveness. The

skepti-cism we learn thereby need not be arid, if we are led also to create alternative hypotheses and even alternative paradigms. In this regard, the world of the clinician has both strengths and limitations. The unique advantages that reside in clinical ex-penience must be balanced against its selectiveness and social confinement. In what follows I shall discuss a few of these strengths and weaknesses, some because they are subtle and seldom consid-ened, others because they lead to gross error and

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DIAGNOSTIC PROCESS

The exquisite diagnostic precision attainable by

clinicians yields specificity and refinement of clas-sification. This refinement in diagnosis avoids the suppression of statistical associations by the

irrel-evant “noise” that accompanies the

misclassifica-tions of incorrect diagnosis.

The scientific penalty exacted by this process is

less evident. It flows from the subjective

contami-nation and bias inherent in diagnostic judgments.

Typically, diagnosis is a matter of pattern recogni-tion. Seldom, however, can the separate elements that comprise the pattern be assessed

independ-ently one from another, as they should be in a

research diagnostic procedure. In the clinical

pro-cedure, the assessment of the meaning of one

cni-tenon often influences the assessment of the mean-ing of the other.

Effects of this dependence differ in different

sit-uations. When a true and strong relationship exists

between two manifestations, such as between

crushing chest pain and a Q-wave on the ECG, the

usual clinical procedure is likely to contribute to

reaching a correct diagnosis. The presence of the

first criterion raises the conditional or a priori

probability that the presence of the second criterion

will be diagnostic. Moreover, recognition of the first criterion-chest pain-is likely to prompt an ECG

reader to a harden search for additional signs than

in its absence. The clinician is “sensitized.” In this

instance, in which a true and strong relationship

exists, one might guess that the proper research

procedure will be less sensitive than the clinical procedure. To collect and judge the diagnostic items independently might well reduce the chances of the signs being recognized by the unsensitized clinician,

and produce a false-negative finding.

In contrast, consider the situation in which there

is a

weak or doubtful relationship, for example between a history of maternal abuse of alcohol and the characteristic facies dubbed the fetal alcohol syndrome. In this instance, the bias created by

nonindependence of the items of diagnostic data

favors a false-positive diagnosis. I believe the

false-positive error (type I on a error) is much the most

common in clinical medicine if only because of the fear and the costs of missing something serious (the false negative, type II, or

fi

error), and because in

the caring professions to do something toward ne-lieving pain or anxiety is more attractive than to do nothing. The costs of the false-positive error, however, includes needless and expensive investi-gation and its ensuing anxieties for the patient.

When an investigator is trying to establish the

existence of a syndrome from the recurrent

associ-ation of a number of typical features, as with the

fetal alcohol syndrome, then to combine

noninde-pendent criteria can be a flagrant error. It is just

this error that undermines the validity of the

greater part of the work done so fan on the fetal

alcohol syndrome.24 In many of the studies

pun-porting to establish the syndrome, the diagnosis

was made either in children of mothers with a

history of alcoholism already known to the diag-nostician, or in children referred to a

dysmorphol-ogist for confirmation of a suspected diagnosis. As

noted, in an established condition with established

associations, such a procedure could raise the

prob-ability of correct diagnosis; in the attempt to

estab-lish a condition, however, the procedure

compro-mises the objectivity of the judgments that must be

made. This is not to say that the syndrome does not exist. Two recent studies meet the obligation

of independent assessment of postulated cause and

outcome.25’26

A similar problem is engendered by medical

his-tory-taking. A benefit that follows from the

confi-dence so readily placed by patients in their doctors is the pediatrician’s ability to obtain a medical

history in depth and detail. Yet this traditional

procedure can be a threat to valid inference. Typical

medical history-taking falls somewhere between an

unstructured and a structured survey interview.

The unstructured interview is rich in information

that is left to the interviewer to organize and

inter-pret, and, therefore, the material is open to the

interviewer’s biased perception. The structured

in-terview seeks limited answers that must fit a

pre-determined form; at the sacrifice of information,

there is less play left for biased interpretation. The

usual medical history relies on the training of the interpreter-here the pediatrician-to limit

subjec-tive bias. The history remains vulnerable to this

bias, however, because of the nonindependence of

the items of data collected; in the manner discussed

above for the diagnostic process it may lead to

false-positive findings. A directive, limited probing was once taught as the standard means of controlling bias in history-taking and sometimes still is. Such

an approach may very well encourage the opposite

error, and produce false-negative findings. Medical

teachers seldom lack examples of diagnoses missed

because inadequate history-taking failed to elicit

significant facts.

CUMULATIVE

CLINICAL

EXPERIENCE

The storehouse of cases in the minds and hands

of clinicians adds much to the potential strength of

their inferences: observations of the concurrence of

symptoms, signs, and outcome aid in delineating

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accumulated by cooperating specialists in numbers adequate for making inferences about rare diseases and their treatment, something beyond the reach

of representative longitudinal on cross-sectional

surveys.

This rich background of experience yields insight and stimulates hypotheses. In particular, it confers great inferential value on the “exceptional” case that departs fan from the norm. Indeed, the char-actenistics of the case may be so distinctive as to serve of itself to prove or disprove a hypothesis, without benefit of added numbers on statistical tests. Hill5 cites the exceptional case of Susannah

Eley, widow of a well-known London cartridge maker. As hen death certificate shows (Figure), she lived in the village of Hampstead, several miles

from the Broad Street pump in Golden Square,

Soho. There, in the autumn of 1854, John Snow

was investigating a fearsome cholera outbreak.27

Mrs Eley alone, among all the people of Hampstead,

went down with the cholera.

In doing so, she yielded a crucial affirmative instance for Snow’s hypothesis (30 years before the

definitive bacteriology of Koch) that cholera was caused by water-borne microorganisms. Previously, when living near the Broad Street pump, Mrs Eley

had grown fond of the taste of its water. When she

moved to Hampstead, she indulged that

idiosyn-cracy by regularly having Broad Street pumpwater

carted to her home, and ultimately died from the same contaminated source that Snow demonstrated

was the origin of the local epidemic.

The instruction to be gained from the exceptional

case is a strength of cumulative clinical experience.

Such experience has at least three weaknesses that

undermine inference. These are selectivity, lack of

controlled comparisons, and a post hoc view of the

evolution of disease. Although all three are familiar

epidemiologic problems, they may bean discussion here because they are so common and so misleading

to practicing clinicians. They are a consequence of

a natural human tendency to extrapolate from the

particular situation to the general. For this, one

always needs the safeguards provided by the rules

of inference. One must ask whether clinical

obser-vations have external validity.

Selectivity

The selectiveness of clinical populations is the

consequence of the many factors that impel some

persons who have a given disorder into medical

cane, and deter others. One of the most important

factors is the stage of the disorder: with tuberculo-sis, no therapeutic program could be truly effective

before the significance of the primary infection was

understood and the cases sought out; with

polio-myelitis, no sense could be made of the

transmis-sion of the disease until the significance of symp-tomless infection was understood29; with congenital

defects, when the defects are observed at birth on later, they represent the survivors from a much

larger pool of cases diminished by attrition between

conception and birth, and thus the factors

associ-ated with the defects at birth may be those

con-nected with survival rather than with the causes of

the defects.3#{176}

Selection works in complicated ways. When

Kannen3’ first described infantile autism, he had

observed the majority of cases among the children

of well-educated mothers who were seemingly

“cold.” The imputation grew widespread that

moth-ens, committed to their own career goals and uncar-ing and unloving of their children, generated the

disorder. The reality is otherwise: a concentration

of well-educated mothers of autistic children can

no longer be found.32’33 The concentration observed

earlier among the well-educated was probably the

result of the preferential recognition of the

diag-nosis, at the outset, in disturbed children in the upper social classes, and thus of their selective

transfer out of the ranks of the mentally retarded

and into those of the autistic. Now, however, the diagnosis is well-established and recognized in all classes. The “coldness” of the mothers, too, has

found another explanation. Many view it as the

mother’s reaction to the child’s inability to respond

to affection.

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Lack of Controlled

Comparisons

In the area of treatment, the need for controlled

experimental comparisons is universally accepted,

if not always practiced, and that subject can be left

aside. Controlled comparisons are essential to test

the validity (both internal and external) of virtually

all observations, natural as well as experimental.

Control subjects are usually not readily accessible,

however, in the settings natural to the clinician

who is concerned with his own individual cases.

The simplest form of this problem of

inference-much less common than it used to be, I

suspect-is to draw the conclusion, from the frequent con-currence of symptoms, signs, or disorders, that their

mere concurrence indicates an association among

them. For example, the clinical belief that headache

is a symptom of high blood pressure could not be

substantiated in a population survey34: both

condi-tions are common, and occur together, but not more often than expected for the population at large.

For pediatricians, the problem arises because many supposed symptoms and signs vary so mark-edly in the course of development. Tics and

twitches, nail biting, and bed-wetting, like tantrums

and negativism, are characteristically frequent at

particular ages, and disappear of their own accord35;

to establish that these are signs of emotional

dis-turbance and not merely of development requires more than their concurrence. A notoriously weak

inference of this kind is the supposed association

of minimal brain damage both with hyperactivity,

and with so-called “soft signs.” These associations

remain to be proved.36 Soft signs may be somewhat

more common in the hyperactive than in the

gen-eral population, but they seem as likely to be

tran-sient manifestations of behavior as of brain

dam-age.’7’38

Here pediatricians, in particular, are faced with

the perennially difficult distinctions to be made

between phenomena of development that will remit

naturally and health disorders that demand

treat-ment. Controlled comparisons are all the more

re-quired in cases in which there is marked cultural and social class variation in developmental norms, as with the acquisition of sphincter control. Twenty

years ago, enunesis in late preschool and early

school years was spoken of as a disorder rather than

as a delay in learning the adaptive behavior of

sphincter control, which it is for the vast majority.

Many treatments-psychotherapy, Benzedrine,

alarm conditioning-succeeded. This was less

sun-prising once the remission rate with age in the

population at large was shown to be more or less

exponential, in the given instance from nearly 20% at the age of 4 years, down to a residue of about 1%

at the age of 13 years. Secondary problems caused

by developmental delay in gaining sphincter control

are enough to justify treatment, but a randomized

trial might not easily find a treatment effect against

such rapid remission (although in fact an effect of

the alarm over Benzedrine was shown.39’40)

Even when control subjects are used for compar-ison, as in case-control studies, a problem of exter-nal validity in clinical work may arise in more

complex form. Although, in the population at large,

no association exists between one disease and

an-other, in a hospital series an association between

the two diseases is quite likely to be found. The

association occurs simply because, for individuals

with a chronic disease, the chance of admission to

a hospital will be higher if they should also have

another disease, especially if that additional disease

is a rare one. This is Berkson’s paradox,4’ in which

a hospital case-control study leads to spurious

causal inference because of a particular selective bias. The paradox can be generalized to all

case-control comparisons.42 One example is the

associa-tion of headache and high blood pressure discussed

above. When the rates of admission of “cases” and/

or control subjects differ according to the presence

of a hypothetic causal factor, then the apparent risk

for that factor will differ between the “cases” and

control subjects and give rise to a spurious

associ-ation.

Post Hoc View of Evolution

of Disease

A third source of mistaken inference induced by

cumulative clinical experience is the post hoc view

of the evolution of disease. Although this is a subset

of the problem of selectivity discussed above, the emphasis here is on the time-order of events. The indisputable tenets for a causal association are only two: that the cause shall precede the effect and that the cause produces something, that is, the associa-tion is asymmetrical and has direction from the

causal to the outcome variable.’7 By the nature of

the clinical situation, a disease process must almost always be well-advanced (by epidemiologic stand-ards) when it comes under the clinician’s

observa-tion. In the result, the time-order of the events

preceding entry to observation rests on indirect

evidence or assumption.

The weakness of such assumptions gains empha-sis from the numerous reversals in ideas of

time-order that have occurred in the medical literature:

for instance whether, in bullous emphysema, infec-tion and the destruction of alveoli precede or follow obstruction of the fine bronchioles43; whether salt

retention and/on raised levels of nenin precede or

follow high blood pressure”; whether the formation

of microthrombi in the coronary arteries precedes

or follows the formation of athenomatous plaques45;

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autopsy of the role of “final court of appeal” for the

most part holds good in the narrow sense of

con-firming or refuting a clinical diagnosis of underlying pathology. Autopsy data are beset not only by

ex-treme selectivity, but by an incapacity to establish

certainty about the time-order of preceding events.

In the clinical sphere, the difficulty is hardly less.

To take just one example, there is an association

between mental disturbance and mild (as well as

severe) mental retardation.46’47 Does this

associa-tion have a common source in antecedent brain

damage? on does it arise because mental disturbance

impairs cognitive performance? or does it arise

because self-awareness of inferior cognitive

per-formance generates mental disturbance? Such

questions are difficult to answer, even in epidemi-ologic surveys with access to total populations and

early cases. From the clinical situation alone, these questions are often unanswerable.

CONTINUITY

OF OBSERVATION

AND

FOLLOW-UP

The clinical setting, well-used, provides an

excep-tional vantage point for the observation of course

and prognosis. Ill-used, inference from this vantage

point leads to serious error in estimates of

prog-nosis. The problems, simple in concept, are less simple to avoid in practice. They begin with obvious questions of selective ascertainment. With enuresis,

for instance, because only a fraction of

preschool-aged and early school aged children who wet their

bed will come into clinical view, a population

sam-ple reveals a different and more benign course than

a clinical sample would.

A second problem in predicting the course of

disease that is more within the control of clinicians than selective ascertainment-and often more of a

threat to sound inference-is selective follow-up.

Complete or nonselective follow-up is crucial to the

validity of all longitudinal observations.

Unfortu-nately, in clinics for chronic disorders the likelihood

of selective drop-out is high. The patients who

continue in care must be expected to be those with

more severe and intractable disease.

Selective follow-up results in a medical literature

riddled with misestimates of prognosis, nearly all

weighted toward a gloomier outcome. For example,

an often cited clinic follow-up of very

low-birth-weight infants (1,5O0 g) in the early 1970s found

that nearly one third (32%) had spastic diplegia at 10 years of age, but only 52% were followed.48

Compared with a large population study with good

follow-up, the rate is seen to be inflated exactly

tenfold (3.2%). In epilepsy, remissions-being

sei-zune-free for 5 years-for long were estimated as

occurring in about 30% of cases 20 years after

onset.5#{176}More complete follow-up shows the

nemis-sion rate at 20 years to be about 70% overall, 60%

for those not still using medication.5’

DISEASE

AS THE

FOCUS

The clinician, of necessity, concentrates his

thoughts and his vision on disease. Above, I have

stressed the insights into the disease process and

the fertile hypotheses about its origins yielded by

this focus. On the other hand, it is a commonplace that clinicians are unlikely to pursue the tasks of

primary prevention. We do not need to involve the

vested interest in disease that George Bernard

Shaw imputed to doctors, in the preface to The

Doctor’s Dilemma, as the grounds for their

reluc-tance to prevent disease. It would be surprising if

clinicians in general, with their well-defined

re-sponsibilities for caring for sick individuals who

solicit their help, set about the public health task

of providing unsolicited help to populations.

In seeking the causes of ill-health, the clinician

is well placed to come upon or suspect many

pos-sible causes of a given disease. The converse is not

true. Clinicians are not well placed to study and

recognize the many possible effects of a given

en-vinonmental cause. Thus, to study the effects of

contaminated water, or poverty, or life stress, or air

pollution, and to approach prevention from the

point of view of a given cause, falls outside the

clinical scope. That side of causality must be left

for others to pursue. More than 50 years ago, some

clinicians first began to suspect that smoking

caused lung cancer; 30 years ago early epidemiologic

studies demonstrated the association.5255 Many

years of investigation from an epidemiologic

stand-point were needed, however, to make clear the

multifarious ills caused by smoking. This

circum-scniption of role does not absolve the clinician from

the tasks of prevention in individual patients. Yet

all too often the result is neglect of these tasks.

This final observation is not an indictment. It is

to say that both the functions appropriate to

clini-cians, and the issues of causality they can hope to

address from a sound perspective through their own

experience,

must

be limited. What I have tried to

do is to set out, in the matter of causal inference,

some limitations of clinical pediatrics as the mirror

image of its strengths. Extrapolations from the

clinical situation can be hazardous. Made con-sciously, with due attention to the principles and strategies of causal inference, the hazards can be

faced and dealt with and sometimes overcome.

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1984;74;842

Pediatrics

Mervyn Susser

Causal Thinking in Practice: Strengths and Weaknesses of the Clinical Vantage Point

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Mervyn Susser

Causal Thinking in Practice: Strengths and Weaknesses of the Clinical Vantage Point

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