Privileged C mu vi 4 Ge G.A.Gorry Qi 7 Page 26

a) Filling in the Detaile

When the clinician has chosen a working hypothesis, he is faced with

the problem of confirming the details of that hypothesis. Major
research question are:

x How does he select the detaiis to explore?

ve What facte should he: seek from. the patient?

te How should he try to establish the facts: he desires?
ve In what sequence should he seek these facts?

¥% How does. he assess the validity of information?

b) Assessing the *goodness’ of Fit

The clinician faces another problem when a more detailed piece of
information concerning the patient has been obtained, regardless of
the means. He must assess how well the new information ’fits’ the
current context. Further this assessment must be: merged with similar
assessments of the ‘goodness of fit’ of other facts. In the face of

poorly fitting. facts, how far should he pursue the current context
before abandoning it?

One aspect of the assessment of the goodness of fit for a finding
which is particulariy interesting. is. the process: by: which al ternative
explanations are constructed for facts which appear to be discrepant
with a given hypothesis... In such cases, the poor fit. of a fact to a
hypothesis does not immediately cause the rejection of a hypothesis,
but rather it: triggers a search for away to "explain away’ the
probiem. In a later section, we will discuss in more detail the
problem of discrepant information.

c) Rejecti ng: - Contexts.

Above we mentioned that under certain circumstances, a context which

was chosen by the clinician may be discarded by him, because of a
"poor fit’ with the facts. Im this case, the clinician is giving up
the working. hypothesis despite his initial desire to confirm it.
Here,. however, the principle of parsimony may make him reluctant to
give up a particular hypothesis. For example, in abandoning the
current hypothesis, hea may be forced to hypothesize more than one
disease. Although he is often forced to do this, the clinician, in
general, is. reluctant to do 80, and so he may.continue with a
hypothesis which fits the facts rather poorly for ltonger than would
otherwise be: expected.

 

In other circumstances, however, the clinician may actively. want to
reject contexts. The most obvious example of this occurs when the
clinician has found the working hypothesis to be a good fit to the

presenting facts, and he now wants to reject any other competing
hypotheses.
Privileged es G.A.Gorry a> | Page 27

€ le
In many cases, the clinician remembers a specific “pattern of the
presence or absence of various signs and symptoms which virtually
precludes the presence of a particular disease. In other cases, no
such specific pattern is known to the clinician, and he must use
other arguments (such as the relative likelihood of two hypotheses)
to exclude the hypothesis in question. Of course, in certain cases,
no such exclusion can be achieved, and he must base subsequent
decisions on consideration of more than one hypothesis. ,

It should be noted that this process of confirming one hypothesis by
matching the hypothesis and then rejecting other, competing
hypotheses is one which is generally interwoven throughout the
process of clinical cognition. For exampte in the present il!tness,
the working hypothesis might concern the ‘facts’ concerning some
piece of the history, with competing hypotheses providing alternative
interpretations of what really happened to the patient at the time in
question. The same issues of confirmation, rejection, and weighing
likeliheods are relevant here even though the hypotheses are not
about diseases, but rather about the facts themselves.

3) Alteration

It was noted above that the initial context chosen by the clinician is
often not supported by the information subsequently gathered. Hence the
context must be replaced by a new one. If the clinician is to operate
effectively and efficientiy in the clinical environment, he must
generally be able to shift smoothly from one hypothesis to another. The

process by which this replacement occurs is an important and interesting
one. ,

One hypothesis is that the facts are again sifted through the pattern
matching processes mentioned above, and from this re-examination of the
data, anew hypothesis emerges as the working context. There seems
little doubt that this happens in some situations, but as a_ general
rule, such a process seems more characteristic of a medical student or a
new intern than of an experienced clinician. For the fatter, a more
much directed move to a new hypothesis seems appropriate. That is the
expert, because of his richer and more extensive experience uses certain
*failures’ in matching findings to hypotheses as direct pointers to new

hypotheses. Thus, for example, the working context might be
- *glomerutitis’, and a questionable fit of the facts has been found; the
patient has heavy proteinuria but no significant hematuria. The expert
responds to this ‘mismatch’ by moving directly to the ’nephrotic
syndrome’ context, because he has been in this situation a sufficient
number of times to have stored the ’contingency’ pointer.

The importance of these direct "pointers’ arises from the amount of
structure which they preserve. In general, areasonable amount of
cognitive effort has gone into the ‘fleshing-out’ of the working
hypothesis, and a lot of information has been gathered. If the
hypothesis is simply abandoned, and no other one is directiy taken up in
Privileged ‘Sees, G.A.Corr ui Page 28

its place, the-.clinician ‘may lose track of certain pieces of
information. If the new hypothesis can be obtained directly from the
old one, then this smoother transition ia apt to disrupt less severely
the information structure he has built. :

4) Dealing with Novelty

What does the clinician do when none of his working hypotheses seems
consistent with the facts at hand? Such a situation can easily occur.
For example, the might be one or more facts which are in error.
Aiternatively, the patient might be suffering from more that one
disease, and the findings cannot all be attributed to one of them.

Because such situations clearly arise in clinical practice, the good
clinician will have developed strategies for dealing with them. We do
not know much about these strategies at present, but ue will offer a few
observations. First, there is always the possibility that the clinician
is facing a situation which is truly novel in certain very important
regards. In this case, he will have. to fal! back. on general
intelligence and *creativity’, but we cannot offer much detail about how
this is done. Undoubtedly he begins his search for an understanding of
the situation by trying to understand what modifications of contexts
which "almost fit’. would be required. From these necessary
modifications he may be able to move to a better grasp of the situation.

In other cases, the working hypothesis seems basically sound, but
certain facts cannot be fitted into the framework it provides. At face
value the situation may appear novel, but the clinician suspects” that
either one or more ‘facts’ are in error, or there is some alternative
explanation’ of the facts which will fit. into the current context.
This situation is discussed in more detail ina tater section which
considers how clinicians deal with discrepant information.

S) Learning

The abilities described above are in some sense a minimal set for an
expert to have if he is to perform as an expert. We know that he
possesses cognitive mechanisms to realize these abilities because we can
observe him successfully dealing with the problems of clinical medicine,
and this task environment requires these skills.

Because experts are not created de novo, however, they must possess the
skills required to become experts. They must possess the ability to
learn. In terms of our above discussion, they must be able to
assimilate new contexts, recognition patterns, explanations of
discrepancies, and administrative strategies. This assimilation draws
from a variety of sources: school, books, clinical experience,
introspection, etc. Further, it is clear that simple assimilation is
not sufficient for expert behavior. The knowledge that is assimilated

must be organized by the learner so that it is effectively available to
him in the task environment of clinical practice.
Privileged mo) C.A.Corry Page 29

The question of whether a piece of information has been effectively
assimilated into the knowledge structure possessed by the clinician can
be judged only with respect to the way in which the new knowledge is
used in the above processes. Hence it seems that a prerequisite for
understanding learning as it relates to clinical expertise is the
understanding of performance in the clinical environment.

The Initial Theory

Our theory of the cognitive behavior of clinicians is an amalgam of
the ideas of a number of the workers in our group and was... strongly
influenced by Minsky (131. Particularly notable contributions to the
structure of this theory were made by Sussman, Pauker, and Rubin.
Although our current theory is primitive and incomplete, we believe that
it represents a good beginning. Here we will present it in some detail.
Basically this presentation is a re-working of the. above discussion in
terms of the computer-based model we have implemented. The concepts

used in that model are introduced at appropriate points in the
discussion.

Frames

It seems that the knowledge possessed by a clinician is grouped into
chunks, which, after Minsky {refl, we call frames. When he begins to
entertain a certain diagnostic possibility, be it a disease, like acute
post-streptoceccal glomerulonephritis, a clinical state, like nephrotic
syndrome, or a physiological state, {ike sodium retention, he bring many
facts about this possibility to mind at once. It appears that
physicians behave as if certain findings, which he have called triggers
serve to awaken the frame into our consideration. (This is the. basic
mechanism for dealing with the problem of expectation discussed
earlier.) At that point, any of its findings or slots can relate to
presented data, but when it was in its dormant state, most of these
slots could not react to presented data. For example, when told of
fever, one would not immediately think of cellulitis (a kind of skin
infection), but if told that there was ared, painful swelling of one
cheek, the additional finding of fever fits in neatly.

Frames appear to have other types of data associated with them besides
slots. There appear to be relational pointers to other frames, so that
when one is considering one frame as a possibility, one is "sort of"
_ thinking about other related frames. This relationship may be of

several varieties, but a neat grouping of many of them can be made by
considering the causes-af, things caused-by, complications-of, and
things complicated-by the frame. For example, when one is considering
acute glomerulonephritis, one “sort of" thinks about acute renal failure
and acute hypertension, both of which are complications of AGN, but they
are not thought of in the same detail a3 AGN, e.g., one usually does not
consider their complications, like encephalopathy, hyuperkalemia,etc,
unless other data suggests them or reinforces the hypotheses of acute
Privileged ‘Sag GC. A. Gorr SS Page 38

renal failure and acute hypertension.

Differential Pointers

In addition, there appear to be some special kinds of slots which
function as-lateral or differential pointers to:other frames. These are
meant to handle unexpected finding in a fashion that makes backing-up (a
relatively costly procedure) tess necessary. Rather than going back to
the beginning and ’reshuffling’ all the facts when a hypothesis is
rejected, it appears that the physician has certain heuristics which
point in specific directions when certain ‘inconsistencies are
encountered. This is a part of their response to the problem of
alteration discussed eartier. For example, when presented with a
patient with massive edema and heavy proteinuria, the expert can leap to
a hypothesis of nephrotic syndrome. If he later discovers the patient
has jugular venous distension, he can move directiy to considering
constrictive pericarditis, realizing that the two entities can be
confused. This tateral motion is not based on reconsideration of al!
the data at hand, but on the differential pointer that says:

"If you are considering nephrotic syndrome, and there is neck vein
distension, then consider constrictive pericarditis."

Similarly, a young man with facial edema and hypertension can be
hypothesized to -have acute glomerulonephritis, since the unexpected
findings of ‘hypertensive retinopathy or -ventricular hypertrophy on
electrocardiogram would immediately lead to consideration of chronic
glomerulonephr itis.

Pruning Frames

It also seems ‘that the physician does not maintain -multipte copies of
diseases having certain variations, but rather he has a general
knowledge and certain rules about how to tailor-make this to the case at
hand. We call this process pruning. Pruning is related to the problems
of elaboration and alteration discussed earlier. Pruning may involve
findings (slots), evaluations or relationships to other frames. Thus,
the general picture of cirrhosis must be modified in that one cannot
expect to consider gynecomastia in a women. Sodium retention may be
manifested by -pedal edema, facial edema, ascites and the like, but
ascites is rare inrenal edema and facial edema is rare in cardiac
edema, even though both are part of the physician’s general knowledge
about sodium retention. Sodium retention may be caused by cirrhosis in
the adult, but rarely in children, so when considering sodium retention
one should not “sort of" consider cirrhosis, if it is a child.

 

Transtation Frames

Another type of knowledge which physicians often bring to bear on their
diagnoses relate not so much to the specific disease entities, but to a
general knowledge about the world in general and medicine in particular.
Privileged Con A G.A.Gorry F Page 31

Much of this knowledge can be expressed in a special kind of frame which
we have called a translation frame. — In some ways this can be viewed as

a simple stimulus-response set:

 

"I¢€ one is told the patient served in the army, it means he most
likely did not have hyper tension or proteinuria at that time (he
passed an army physical), he probably did not have a murmur (army
physicals are not known for careful observation), and probably had
reasonable exercise tolerance." :

"If the patient attended summer ‘camp, he was likely exposed to
plant allergens, snake bite, other children and therefore common
childhood diseases of summer (like the enteroviruses). "

Hupothesis Generation

There appears to be a hierarchy of hypothesis in so far as how actively
they are being considered and in comparing them to each other. — There
appears to be several general classes of consideration which he have
called happu, active, semi-active, and dormant.

When beginning consideration of any problem, all hypotheses are
dormant; that is to say, only their trigger slots can grasp incoming
data. Under specified conditions, usually finding a datum to. satisfy a
trigger slot, the frame moves into active state. This means that any of
its slots can match findings (uith the constraint that they may be
pruned in fitting the frame to the case at hand). The neighbors (e.g.-,
causes-of, complications-of, etc.) of the frame are “sort of" made
active. We cal} their level of activity semi-active. It differs from
full activity in that its “suakening” does not awaken tts neighbors,
thus avoiding the explosive awakening of too many frames. Finally.
under certain conditions, frames become happy, that is to say, they are
convinced beyond reasonable doubt that they are true and they assert
that they are indeed true so that other conclusions may proceed from
this assertion.

Hupothesis Testing
As findings are gathered, each frame is evaluated in several ways:

1) A check is made to see if the new datum excludes that frame. For
example, the absence of proteinuria virtually denies the existence of
a glomerulitis.

2) A check is made whether data is sufficient to establish the
hypothesis. For example, if one finds red cell casts in the urine
sediment, this virtually establishes the presence of a glomerulitis.

3) A measurement is made of hou well the data fit the hypothesis and
how much of the data are expiained by the hypothesis. These are tuo
complementary measures and the clinician considers some combination of
  

G.A.Gorry r 7 Page 32

them. If the goodness of fit exceeds a certain level, he might say
that the “weight of evidence" would allow the frame. to become happy.
On the other hand, if the fit is sufficiently poor, one: might drop the
hypothesis from active consideration. In doing this scoring, the
physician allows for propagation through relations, i.e., if one is
considering aortic stenosis and congestive heart failure, the finding
of rales in the chest examination is very helpful to the congestive
heart failure hypothesis, but by helping that hypothesis, it: "sort of"
lends weight to aortic stenosis also.

Privileged Commt

This then represents the substrate of the initial theory of the
response of the clinician to the presentation of information about the
patient. The theory has certain additional features which we can cal!
heuristic rules, or what to do in certain situations. An example might
be how to handle contradictory data:

If one is told there are both red blood cel! casts on urine
sediment and no hematuria, then consider that there are probably no
red cell casts (they are often confused with other casts) , but at
some later time, see how your conclusions would be altered if red
cell casts were present.

If renal function is normal but you are told that there are no
kidneys on xray of abdomen, consider the: possibility that there
are really large kidneys present, but the radiologist did not see
them (as often happens with really large kidneys).

Information Seeking

At present, our theory of how the clinician chooses what facts to seek
out is somewhat. underdeveloped. We do have some understanding of this
process, however, and this is a problem which is currentiy under study.

First it is ctear that what may appear to be a "fact" to an outside
observer may be less than that to a clinician. By this we mean that
clinicians seem to deat in "chunks" of information which are, strictly
speaking, composed of more than one fact. For example, a clinician
tends to follow rather set patterns of questions until he has gotten a
chunk of information about the patient. If the complaint is edema, a
renal specialist will react by invoking a small "subroutine" to further
characterize the edema. We call this a subroutine because clinicians
themselves seem to recognize the questioning net they use as an
automatic response to the stimulus "edema".

The rationale for the particular sequence of questions employed is
understood by the physician, and he can readily explain it. But in
practice, he does not "derive" this sequence, but rather simply
remembers and invokes it.

Once a suitable chunk of information has been gained, the triggering
and matching processes described above are invoked.
Privileged eee G.A.Gorry > Page 33

For the selection of which chunk of information to seek next, the
clinician appears to make use of the frames themselves, trying to fill
in the slots of his current hypothesis. Our understanding of the
details of this process is inadequate at present, but we have been able

to get some interesting results in our computer simulation by following
this simple strategy.

The following few sections discuss specific projects which we have
undertaken in support of the development of this theory. The first is

the computer simulation of the present iliness. The second project _is
concerned with style differences among clinicians insofar as their
approach to the present itiness is concerned and with measuring the

effectiveness and efficiency which these differences promote. The third
project is concerned with the development of orderly and concise means -
for identifying and codifying clinical knowledge, particularly of the
kind found in medical textbooks. This work is aimed at filling some of

the gaps which the present iliness project must necessarily leave as it
concentrates on strategy.

initial Computer Simulation af Cognitive Process

In conjunction with our explorations of the knowledge and problem-
solving behavior of clinicians described in the preceding sections, we
have developed some preliminary computer programs to simulate aspects of
the observed process of taking a present i/iness.

We will provide only some of the details of the operations of the
computer programs involved ‘to give the reader the flavor of our work.
It should be understood, however, that these details will almost
certainly be changed. In fact, much of the work discussed below. in the
section on supporting computer science research is aimed at refining and

improving the mechanisms upon which this rudimentary simulation is
built. ©

The basic operation of the simulation program is as follous. The age
and sex of the patient is presented to the program along with the chief
complaint. The program responds to this information by formulating
hypotheses about the patient’s condition. These hypotheses are the
result of patterns of signs and symptoms which the program recognizes as
suggestive of par ticular diseases, clinical states, or
pathophysiological states. For example, the pattern "middle-aged man
With pedal edema" might suggest idiopathic nephrotic syndrome, sodium
retention, etc. The pattern currently known to the program were
identified in our studies of experts, and the program makes the same use
of them that the experts do, namely to immediately get one or more

working hypotheses around which it can structure the initia! phases of
the present illness.

In the current simulation, the program must seek out al! additional
information about the patient. Therefore, once it has "digested" the
Privileged Cagpyaeceiien, G.A.Gorry Ga» Page 34

age and sex and presenting complaint of the patient, it undertakes
questioning of the user to learn more about the patient. Whenever a new
fact is learned, the program revises its assessment of var ious
hypotheses, and then seeks more information in accordance with its
latest “opinion” of the situation. To understand the simulation, then,
we need to understand two basic functions of the program:

1) how hypotheses are generated and tested
2) how questions are selected.

Here we will briefly investigate each of these questions. As noted, the
emphasis will be on the concepts involved, not on the technical details
of the program.

Hupothesis Generation

Stored in a data base used by the program are a great many patterns of
signs and symptoms. Associated with each pattern is some action which
the program is to take if the pattern is found during the present
illness. Some of the actions affect hypotheses, in that they cause
hypotheses to be formed, modified, or deleted. Other types of patterns
and their uses will be discussed below.

The patterns of findings which cause hypotheses to be promoted to
active consideration are called triggers. At the beginning of the
present illness, ali hypotheses are dormant in that although the program
has descriptive knowledge about them (See the discussion of frames
below.), it is not actively considering any of them. The triggers are
used to promote some hypotheses to the active state when the chief
complaint is entered. (Triggers are used at other points in the present
illness also, -as we shal! see.) While a hypothesis is active, the
program matches new facts to the description of the hypothesis (the
frame) which is has been given, and it uses the frame for the hypothesis
in its question selection activities. On the other hand, dormant
hypotheses are ignored in both these activities.

So a trigger moves a hypothesis from the dormant state to the active
state. In doing so, it may cause other hypotheses to move from the
dormant state to a state which we have called semi-active. To
understand the purpose of this third state, consider the above example,
namely the presenting problem of massive pedal edema in a middle-aged
man. There are triggers which cause the hypotheses of nephrotic
syndrome, idiopathic nephrotic syndrome, and sodium retention (among
other things) to become active. To reflect the fact that at this point
a clinician would "sort of" be thinking of congestive heart failure
(because it is a cause of sodium retention), the program moves
congestive heart failure to the semi-active. The simulation program
matches findings to semi-active hypotheses, but it does not use them in
its question selection activities.
Privileged Communication G.A.Gorry Qe . Page 35

The specific rule which the program uses to determine which hypotheses
to move into the semi-active state when a trigger is matched is as
fol lous. The program looks at the description (frame) for the
hypothesis denoted by the trigger, and finds al! hypotheses related to
the hypothesis in question by such relations as "causes", "“comp!ication-
of", etc., and makes these hypotheses semi-active (assuming, of course,
that they are not already active).

Hypotheses can move from the semi-active state to either the active
state or to the dormant state as the present illness proceeds. For
example, if a later finding is a trigger for a semi-active hypothesis,
the latter will move to the active state. In addition, a hypothesis can
move from semi-active to active if more than one other hypothesis, in

becoming active, tries to move the hypothesis in question to semi-active
status.

In fact, throughout the present iliness, there is continual movement
of hypotheses from one state to another. Active hypotheses may be
"demoted" to dormant by the hypothesis testing function because it deems
them to be very poor fits to the facts. The important point, however, —
is that hypotheses are being re-evaluated and re-ranked: by the program
in light of the most recent set of facts about the patient.

Consider Figure 1. Here is the trace of the simulation program as it
responds to the presentation of massive pedal edema in a middle-aged
man. The age and sex descriptor are translated into internal format,
where each property is labeled by type. When massive pedal edema is
entered, We see that this triggered sodium retention and nephrotic
syndrome, which in turn, cause their "relatives" (for example,
congestive heart failure and acute tubular necrosis are causes-of sodium
retention) to go into the semi-active state. When idiopathic nephrotic
syndrome became semi-active, it discovered that a prior fact (the age
descriptor) fitted neatly into its description, and this second match
allowed the frame (idiopathic nephrotic syndrome) to rise to full
activity). This did not occur when the age descriptor was intially
given because that finding was not a trigger for the frame. The frame

had to be at least semi-active (rather than dormant) before the match
could occur.

Similar interactions occur with chronic renal failure and chronic
glomerulonephritis, but the reason that they come to full activity is
not that they find a supporting finding, but rather that they are "sort
of" thought about by more than one other frame (in this case, sodium
retention and nephrotic syndrome).

In Figure 2 is a tabulation of the state of the hypotheses considered
by the program. It is easy to see how this might be transformed into a

“problem list" with relatively little effort. Each frame has two
associated measures: its score is a normalized measure (from -1 to 1)
of how wel! the data fits the frame, and is EXPL is the fraction of

findings explained by the frame and its possible associated subframes.
Page 36

> (MIDOLE-AGED NAN)

>>>>>>> (MAN (AGE MIDOLE-AGED) (TIME NOW)

> (MASSIVE PEOAL EDEMA)

>>>>>>> (EDENA (LOCATION PEDAL) (SEVERITY MASSIVE) (TIME NOW)

(EDEMA (LOCRTION PEDAL) (SEVERITY MASSIVE) (TIME NOW))
walRIGGERse>

(CSOOTUN RETENTION) <-- ACTIVE
sa>
C(CONGESTIVE HEART FAILURE) <-- SEMI-ACTIVE
(CIRRHOSIS) <-- SEMI-ACTIVE
(ACUTE TUBULAR NECROSIS) <-- SEMI-ACTIVE
(NEPHROTIC SYNDROME) <-- SEMI-ACTIVE
(ACUTE GLOMERULONEPHRITIS) «<-- SEMI-ACTIVE
sa>
((NEPHROTIC SYNDROME) <-- ACTIVE
=z2>
CCDIABETES) <-- SEMI-ACTIVE
(SYSTEMIC LUPUS) <-- SENI-ACTIVE
(IDIOPATHIC NEPHROTIC SYNDROME) <-- SEMI-ACTIVE))))))

CCAGE (AGE MIDOLE-AGED) (TINE NOW)
an TRIGGERse>

CCIDIOPATHIC NEPHROTIC SYNDROME) <-- ACTIVE))

(CEDEMA (LOCATION PEDAL) (SEVERITY MASSIVE) (TINE NOW)?

ss>
CCNEPHROTIC SYNDROME)
—_>
CCINSECT BITE) <-~ SEMI-ACTIVE
(NEPHROTOXIC DRUGS) <-- SEMI-ACTIVE
(CHRONIC GLOMERULONEPHRITIS) <-— SEMI-ACTIVE
(GLOMERULITIS) <-- SEMI-ACTIVE
(CELLULITIS) <-- SEMI-ACTIVE
(HYPOVOLEMNIA) <-— SEMI-ACTIVE
(CHRONIC GLOMERULONEPHRITIS) <-~ ACTIVE

s2>

CCCHRONIC RENAL FAILURE) <-- SEMI-QCTIVE)))

a>

C(CHRONIC RENAL FRILURE) <-- ACTIVE -

2s>
CCUREMIAD <-- SEMI-ACTIVE
(HYPERKALEMEA) «<-- SEMI-ACTIVE))

ss>
(CHRONIC GLOMERULONEPHRITIS) --> ((CHRONIC HYPERTENSION) <-- SEMI-ACTIVE
(FOCAL GLOMERULONEPHRITIS) <-— ACTIVE)?

FIGURE 1. HYPOTHESIS GENERATION
(NOTE: User input preceded by singie ’>’.)
a) Page 37

(MAN (AGE MIOOLE-AGEO) (TIME NOW))

(SEX (GENDER MALE) (TIME NOW)

(AGE (AGE MIDOLE-AGED) (TINE NOW)

(EDEMA (LOCATION PEDAL) (SEVERITY MASSIVE) (TIME NOW)

(BOUND (EDEMA (LOCATION PEOAL) (SEVERITY MASSIVE) (TINE NOW))
(SODIUN RETENTION)

(EDEMA SODIUM RETENTION) )
C(SOOLUM RETENTION) ACTIVE)
(PRUNED-SLOTS (SODIUM RETENTION) (COTURETIC SODIUM RETENTION)»

HAPPY-FRANES
NONE

ACTIVE-FRAMES

CIOTOPATHIC NEPHROTIC SYNOROME) SCORE 0.165 EXPL 6.5 AVG 8.332
(NEPHROTIC SYNDROME) SCORE 68.151 EXPL 9.5 AVG 8.325

(SODIUM RETENTION) SCORE 8.162 EXPL 8.5 AVG 8.381

(CHRONIC RENAL FAILURE) SCORE 6.871 EXPL &.5 AVG 8.285

(FOCAL GLOMERULONEPHRITIS)

(CHRONIC GLOMERULONEPHRITIS)

SEMI-ACTIVE-FRANES

(ACUTE GLOMERULONEPHRITIS) SCORE 0.897 EXPL 0.8 AVG 0.048
(CHRONIC HYPERTENSION)
(HYPERKALEMIA)

C(URENIA)
(HYPOVOLEMIA)

(CELLULITIS)
(GLOMERULITIS>
(NEPHROTOXIC DRUGS)
CINSECT BITE)

(SYSTEMIC LUPUS)
(OTABETES) ;

(ACUTE TUBULAR NECROSIS)
(CIRRHOSIS)

(CONGESTIVE HEART FAILURE)

FIGURE 2. FACTS AND HYPOTHESES
Privileged Communication .A. Corr (iD Page 38

The details of the scoring scheme are discussed belo#’in connection with
hypothesis testing.

Hupothesis Matching

In the above discussion, we ignored the representation of knowledge
about diseases, clinical states, etc. used by the simulation program.
We did not need this detail in our discussion of the triggering
mechanism and the various states for for hypotheses.

One of the major activities of the present illness simulation program,
however, is assessing how well the facts in hand at any point in time
match a given hypothesis. Therefore, we need to examine the way in
which descriptions of hypotheses are stored and used.

Each description is represented by a frame. A frame is an organized
collection of facts about the hypothesis, what its findings are, how it
ig caused, what complications can arise from it, etc.

Because medical knowledge generally is organized about diseases or
clinical states, and not about the implications of specific findings,
this system allows for data input as its is available in standard
medical texts. The necessary cross referencing for the appropriately
useful associations is taken care of automatically by a frame compiler.

Figure 3 is an example of a typical frame. This frame might be
paraphrased as:

Nephrotic syndrome is aclinical state characterized by
hypoalbuminemia, ‘heavy proteinuria (usual!y over S grams in
a 24-hour urine), massive edema, symmetrically distributed,
often involving the face, especially ther area about the
eyes. There is associated elevation of serum cholesterol
and urine lipids are present. It may be caused by acute or
chronic glomerulonephritis, nephrotoxic drugs, some insect
bites, diabetes, systemic lupus, diabetes, or may be
idiapathic. It may be complicated by hypovolemia
(intravascular) or infection of the massively swollen
extremities. There is almost never facial edema in the
absence of peda! edema, and massive edema associated with
over 5 grams of protein loss daily is enough to establish
the diagnosis. It may be confused with constrictive
pericarditis, but in that case there is neck vein elevation.
It may also be confused with cirrhosis, but in that case,
ascites are usua!ly present. If there is flank pain, one
must consider renal vein thrombosis as a possible cause of
the renal protein loss.

Now we can explore the scoring or hypothesis matching performed by the
simulation program. Consider the scoring data shown in Figure 3, under
the titles MAJOR and MINOR.
Gz? Page 39

(DEFRAME
SC(NEPHROTIC SYNDROME)
(TYPE CLINICAL-STATE)
(SLOT ALB (TRIGGER) S(ALBUMIN LOW))
(SLOT PRO NIL S(PROTEINURIA HEAVY))
(SLOT PROG (TRIGGER) S(PROTEINURIA >SGRAMS) >
(SLOT EDEMA (TRIGGER) S(EDEMA MASSIVE (NOT ASYMMETRICAL???)
(SLOT FACED (TRIGGER) S(EDEMA (OR FACIAL PERI-ORBITAL) (NOT ASYMMETRICAL) >)
(SLOT CHOL NIL S(CHOLESTEROL HIGH?) .
(SLOT URFAT NIL S¢(CURINE LIPIDS) PRESENT))
(CAUSED-BY S(ACUTE GLOMERULONEPHRITIS)
S(CHRONIC GLOMERULONEPHRITIS)
S(NEPHROTOXIC DRUGS)
SCINSECT BITE)
SCIDIOPATHIC NEPHROTIC SYNOROME)
S(SYSTENIC LUPUS)
S(DIABETES))
(COMPLICATED-BY S(HYPOVOLEMIA) S(CELLULITIS))
(MAJOR #C(SSCALBUNIN LOW) 1.8)
(SS(ALBUMIN HIGH) -2.0)) -
#C(SS(PROTEINURIA >SGRAMNS) 1.8)
(S$ (PROTEINURIA HEAVY) 8.5)
(SS(PROTEINURIA (OR ABSENT LIGHT)) -1.9))
#C(SSCEDEMA MASSIVE (NOT ASYMMETRICAL)) 1.8)
(SS(EDENA (NOT ABSENT) (NOT ASYMMETRICAL) (NOT ASYHNMETRICAL)) 8.3)
(SS(EDEMA ERYTHEMATOUS (NOT ABSENT)) -@.2)
(SS(EDEMA ABSENT) -1.8)))
(MINOR #C(SS(CHOLESTEROL HIGH) 1.9)
(SS(CHOLESTEROL (NOT HIGH)? -1.9))
@#((SSCCURINE LIPIOS) PRESENT) 1.0)
(SSCCURINE LIPIDS) ABSENT) -@.5)))
(MUST-NOT-HAVE Ss(ANO (EGEMA FACIAL (NOT ABSENT)) (EDEMA PEDAL ABSENT)?
CIS-SUFFICIENT $s (AND (EDEMA MASSIVE) (PROTEINURIA >SGRANS) >)
(DIFFERENTIAL-DIAGNOSIS
(SCCNECK VEINS) ELEVATED)
(SEMI-ACTIVATE *S(CONSTRICTIVE PERICIRDITIS)))
(S(ASCITES PRESENT) (SEMI-ACTIVATE *S(CIRRHOSIS)))
(S$ (FLANK-PAIND
(SEMI-ACTIVATE *S(RENAL VEIN THROMBOSIS)))))

FIGURE 3. NEPHROTIC SYNOROME FRAME
Privileged Communication — G.A.Gorry > Page 48

The score information given in each frame consists of a list of various
tests, associated: with a number between -l1 and 1.. If the test is true,
that number is added: to an accumulating sum. The maximum sum is the:
total mumber of such items, so a normalized score: is. the actual sum:
divided by the maximum. If no data is known about the fact sought, zero
is added to.the actual sum, so this weighs somewhat against the score,
but less so as more data is known since the sum is divided by a larger
normalizing. factor. Major and Minor scores. just apecify: factors by
which there respective sums: are multiplied, so the: major. factors count
more. Score propagation is: accomplished by passing. the score of. the
related frame (not its sum), which. is therefore normalized already, as
an additional test. Frames may move from one state to another (e.g.,
from active to semi-active) when certain logical criteria are met. (A-
positive throat culture is sufficient to establish a. streptococcal
infection), but we also allow. changes based on weight of evidence... For
example, is: the: score of any active frame exceeds: a pre-established.
threshold, then: it becomes happy, whereas if it falls below a different
pre-established threshold, it may lapse into the semi-active state.

At this. point we: might digress to mention score-propagation . It is

clear that when.a: frame gains: evidence in its behalf, its relatives must
also become more: convinced of their truth also. For example, acute
glomeronephritis: is: related to (by "complicated-by") acute hypertension.
If we learn, that. there is hypertension in the absence of hyper trophy on
the electrocardiogram, this-must add weight to: acute: glomerulonephri tis.
If we then learn. that there ig no chronic hypertensive retinopathy,
acute hypertension: gains more credence, and this. gatm must be propagated
up to acute glomerulonephritis.

The inverse effect is equally true, i.e., since a low urine sodium is
explained. by. sodium: retention, and since sodium retention can be: caused-
by acute glomerulonephritis, then acute glomerulonephritis can explain
the abnormal finding of low urine sodium if we can invoke. sodium
retention. In this program, both scores and "explanations" of findings
can be: propagated. through frames which are either happy or active.

Question Selection:in the Present Iliness

Now. we can. turn our attention to the way in which the program seeks

additional information during the present illness. Here we have
implemented procedures which are first approximations to those the
Program will need if it is to behave in the style of a physician in so

far as its choice. of and ordering of questions is. concerned

From our detailed study of the way in which a particular expert took a
present illness, we concluded that he used two distinct modes of
questioning. At times, he invoked a rather rigid, "compiled", sequence
of questions, particularly to sharpen the characterization of a
particular finding. This sequence seemed aimed at quickly, but
narrowly, focusing the problem solving. © Such questions can be thought
Privileged Communication . C.A. Corr . Page 41

of as filling a pattern which if matched will trigger a very specific

hypothesis. An example of such a sequence is shown in the first part of
Figure 4.

The program is first told that the patient is a young boy with facial
edema (at this point, it might be well to say that the patient who is
being questioned in this example actually has acute'glomerulonephritis).
The program attempts to further characterize the facial edema, asking
about duration, recurrence, temporal pattern, etc. The edema fits so
Well into the typical pattern of renal edema, that the program does not
pursue details such as pain and. erythema. At this point, the chances
that this is anything other than renal edema are so remote that the
program is willing to pay a "reprocessing penaity" if it is wrong.

Next the program asks about associated pedal edema. This occurs
because of a simple heuristic rule which states: “if you are told of
facial edema, see if there is associated pedal edema ." (This fits with
the MUST-NOT-HAVE rule in the Nephrotic Syndrome frame <Figure 3>).
Pedal edema is likewise explored in depth, but note the additional
questions about severity, pain and erythema which are relevant for this
kind of edema. It should be noted that the determination of what is
relevant here is the behavior of the expert himself. He asks different
questions about pedal edema than about facial edema, and in order for
the program to appear to behave "naturally", it must do the same.

This additional question can also be thought of as being more or tess
"automatic" in that the common conjunction of pedal and facial edema
makes the investigation of the former a natural next step for the
clinician, and hence for the program,

It is at this point that the second form of questioning makes its
appear ance. Here the clinician must weigh various hypotheses and
possible questions and seek to plot a good strategy. “

We have suh()essed the detailed output of the program as it does the
hypothesis generation and matching described above. Suffice it to say
that at this point, the program examines the states and scores of the

various frames in deciding on its next question. It will pursue the
active frame (and its related subframes) which has the highest score.
It will mot pursue happy frames, since it is already reasonably

convinced of their applicability.

The score used in selecting the frame to explore is not just the
“goodness of fit" score mentioned above. Since the choice is guiding
further questioning, we are also concerned that our hypothesis (and its
subframes) explain as much as possible of the data. Hence the program
averages the SCORE and EXPL vaiues, and pursues the hypothesis with the
highest average. In this case, that is acute glomerulonephritis, and
the program turns to one of the latter’s subframes » streptococcal
infection. When it finds that there is indeed a pharyngitis, it
explores that in depth as to character and sever ity.
Page 42

>> (YOUNG BOY)

>> (FACIAL EDEMA)

ABOUT (NOW FACIAL EDEMA),
CONCERNING OURATION,{S IT:

1. DAYS
2. WEEKS
3. MONTHS
4. YEARS
>> 1

CONCERNING RECURRENCE, 1S IT:

1. FIRST-TIME

2. TNFREQUENT

3. OCCASSIONAL

4. FREQUENT

>>

CONCERNING PERI-ORBITAL?,IS ITs
1. PERI-ORBITAL

2. NOT-PERI-ORBITAL

>> 1.

CONCERNING SYMMETRY,IS IT:

1. SYMMETRICAL

2. ASYMMETRICAL

>> 1 .

CONCERNING TEMPORAL-PATTERN, IS IT:
i. NO-TEMPORAL-PATTERN

2. WORSE~IN-NORNING

3. WORSE-IN-EVENING

>> 2

IN THINKING
ABOUT (PEOAL EDEMA),
CONCERNING TIME,1S IT:

i. NOW

2. RECENT-PAST

3. PAST

>> 1 :

CONCERNING STATUS,IS IT:
1. ABSENT

Ze PRESENT

>> 2

CONCERNING DURATION,IS IT:
1. DAYS

2. WEEKS

3. “MONTHS

4. YEARS

>> 1

CONCERNING RECURRENCE,IS IT:
i. FIRST-TIME

2. INFREQUENT
3. OCCASSIONAL
4, FREQUENT
>> 1

CONCERNING TEMPORAL~PATTERN,IS IT:
i. NO-TEMPORAL~PATTERN

2. WORSE -IN-HORNING

3. WORSE-IN-EVENING

>> 3

FIGURE 4. PRESENT ILLNESS SIMULATION

(Note: user inputs preceded by ’>>’)
CONCERNING SEVERITY,IS IT:

1. le

2. 2+

3. 3¢ -

4. 4+

s. MASSIVE
>> 3

CONCERNING SYMMETRY,IS IT:
1. SYMMETRICAL

2. ASYMMETRICAL

>> 1

CONCERNING TYPE,IS IT:

1. PITTING

2. NON-PITTING

>> 1 |

CONCERNING ERYTHEMA, IS IT:
i. ERYTHEMATOUS

2. NOT-ERYTHENATOUS

>> 2 .
CONCERNING PAIN,IS IT:

1. PAINFUL

2. NOT-PAINFUL

>> 2

PLEASE TELL ME ABOUT
PHARYNGITIS,I.€.,
IS THERE (NOW (NOT ABSENT) PHARYNGITIS) ?

>> YES

ABOUT (NOW (NOT ABSENT) PHARYNGITIS),

CONCERNING APPEARANCE, IS IT:

1. EXUOATIVE

2. NON-EXUDATIVE

>> 2 :

CONCERNING SEVERITY,IS IT:

1. MILO

2. SEVERE

>> 2

HAPPY-FRANES
NONE

ACTIVE-FRANES
(ACUTE GLOMERULONEPHRITIS) SCORE 8.298 EXPL 8.78 AVG 8.524
(SODIUM RETENTION) SCORE 8.195 EXPL 8.75 AVG 9.472
(STREPTOCOCCAL INFECTION) SCORE 8.181 EXPL 6.75 AVG 8.465
CIDEOPATHIC NEPHROTIC SYNOROME) SCORE 8.161 EXPL 8.75 AVG @.455
(NEPHROTIC SYNDROME) SCORE 8.068 EXPL 6.75 AVG 98.489
(ACUTE RENAL FAILURE) SCORE 6.066 EXPL 8.75 AVG 8.488

PLEASE TELL ME ABOUT
STREPTOCOCCI,1.€.,

IS THERE (NOW EXPOSURE STREPTOCOCCI) ?
>> ?

FIGURE 4. Continued

Page 43
PLEASE TELL ME ABOUT

SCHOOL ,I.E.,

IS THERE (NOW ATTENDED SCHOOL) 7?
>> YES

PLEASE TELL ME ABOUT
PENICILLIN, 1.E.,

TS THERE (NOW GIVEN PENICILLIN) ?
>> ?

PLEASE TELL ME ABOUT

FEVER, I.€.,

TS THERE (NOW MILD FEVER) ?
>> NO

PLEASE TELL NE ABOUT
(THROAT CULTURE) ,I.E.,

TS THERE (NOW BETA (THRORT CULTURE)) ?
>> YES

PLEASE TELL ME ABOUT
HEMATURIA,I.E., .
IS THERE (NOW (NOT ABSENT) HEMATURIA) ?
>> YES
* ABOUT (NOW (NOT ABSENT) HEMATURIA),
CONCERNING AMOUNT,IS IT:
1. MICROSCOPIC
2. GROSS
>> 1

PLEASE TELL NE ABOUT

PROTEINURIA,I.E.,

IS THERE (NOW (NOT ABSENT) PROTEINURIA) ?
>> YES
RBOUT (NOW (NOT ABSENT) PROTEINURIA),
CONCERNING AMOUNT,IS IT:

i. LIGHT
2. HEAVY
>> 1

CONCERNING QUAN-AMOUNT,IS IT:
1. <L@OMGRANS

2. LOOMGRAMS-SGRANS
3. >SGRANS
>> ?

PLEASE TELL ME ABOUT
WEIGHT,I.E.,

TS THERE (NOW (OR HIGH RISING) WEIGHT) ?
>> NO

PLEASE TELL NE ABOUT
RALES,I.E.,

TS THERE (NOW PRESENT RALES) ?
>> YES

SSSSSSSEAKATARS TETAS SSE SST SE SSESSTLE KSA TRS ASARARATSSRTARSREESRECTSROEES

FIGURE 4. Continued

Page 44
HAPPY-~FRANES

(STREPTOCOCCAL INFECTION) SCORE 8.348 EXPL 0.538 AVG 9.443
ACTIVE-FRANES .
AMACUTE GLOMERULONEPHRITIS) SCORE 9. 477 EXPL 8.538 AVG 8.588
(GLOMERULITIS) SCORE 0.287 EXPL 8.538 AVG 0.413
CSOOTUM RETENTION) SCORE 0.288 EXPL 8.538 AVG 0.373
CIDEOPATHIC NEPHROTIC SYNDROME) SCORE 8.177 EXPL 0.538 AVG 8.358
(CONGESTIVE HEART FAILURE) SCORE 6.116 EXPL @.538 AVG 6.324
CACUTE RENAL FAILURE) SCORE 8.875 EXPL 8.538 AVG 9.387
(ATHEROMATOUS EMBOLI) SCORE 0.805 EXPL 3.538 AVG 8.271
(NEPHROTIC SYNOROME) SCORE -8.043 EXPL 8.538 AVG 9.247
(STONE) SCORE 0.25 EXPL 8.976 AVG 8.163

(NOW YOUNG BOY)

(NOW FACIAL DAYS FIRST-TIME PERI-ORBITAL SYMMETRICAL NORSE-IN-MORNING EDEMA)

(PEDAL NOW PRESENT DAYS FIRST-TIME WORSE-IN-EVENING 3+ SYMMETRICAL PITTING
NOT-ERYTHEMATOUS NOT-PAINFUL EDEMA) ~

(NOW (NOT ABSENT) EXUDATIVE SEVERE PHARYNGITIS)

CCSTREPTOCOCCI (EXPOSURE EXPOSURE) (TINE NOW)) UNKNOWN)

(NOW ATTENDED SCHOOL)

CCPENICILLIN (GIVEN? GIVEN) (TIME NOW)) UNKNOWN)

CCNOT MILO NOW) FEVER) .

(NOW BETA (THROAT CULTURE) )

(NOH (NOT ABSENT) MICROSCOPIC HEMATURIA)

(NOW (NOT ABSENT) LIGHT PROTEINURIA)

(NOW (NOT COR HIGH RISING)) WEIGHT)

(NOW PRESENT RALES)

FIGURE 4. Continued

Page 45
Privileged Communication .A.Corry Page 46

Next in Figure 4, we see the state of the various hypotheses that the
program is considering.

Continuing its pursuit of streptococcal infection, the program looks
for possible exposure. When it is told that no information about this
is available, the program seeks indirect confirmation of the presumed
exposure. he program finds that school attendance can result in
streptococcal exposure. It makes this connection by tracking through a
series of translation frames (streptococcal exposure goes along with

childhood disease exposure, and. the fatter might occur in school or
summer camp). ,

Finally the program is told that the throat culture was positive.
With this fact, streptecoccal infection becomes “happy", e.g. the

program is , convinced that streptococcal infection is present, and
asserts it as a finding. The program then turns to the next subframe of
acute glomerulonephritis, since more data about streptococcal infection

would at this point be moot. This next subframe is glomerulitis, and
the issues of hematuria and proteinuria are pursued. At this point,
sodium retention is explored.

In the bottom lines of Figure 4, we see a summary of the data in
order of acquisition. To paraphrase:

This is a young boy, who presents for the first time with
symmetrical, peri-orbital edema, worse in the morning, for the past
few days. It is associated, over the same time period, with 3+
symmetrical, pitting, pedal edema, which is worse in the evening.
The patient has a severe; exudative pharyngitis, has been attending

school, has not received penicillin and has not been febrile.
Throat culture was positive for beta-hemolytic strep. There is
also microscopic hematuria and light proteinuria. His weight is

normal and has not been increasing, but rales are present on chest
examination. :

This is not an unreasonable first-pass present illness for a patient
with acute glomerulonephr itis.

A contrasting strategy is shown in Figure S where a different case is
considered. After exploring the finding of pedal edema in a middle-aged
man, @ specific avenue of exploration is not clearly evident. Rather
that beginning with in depth exploration of a particular frame, the
program asks, in the manner of a clinician, about dyspnea, alcohol
consumption, past proteinuria, varicose veins and jaundice, attempting
to pin down an area for profitable exploration. Once the existence of
past proteinuria has brought chronic glomerulonephritis, nephrotic
syndrome and chronic renal failure to mind, these are then explored.
Page 47

>> (AIDOLE-AGED NAN) ™
>> (SYMMETRICAL PEDAL EOEMA>

ABOUT (NOW SYMMETRICAL PEOAL EDEMA? ,
CONCERNING DURATION, IS IT:

1. DAYS
2. WEEKS
3. MONTHS
4. YEARS
>> 2

CONCERNING RECURRENCE, IS ITs
i. FIRST-TIME
2. INFREQUENT
3. OCCASSIONAL

- 6, FREQUENT

>> 3

CONCERNING TEMPORAL-PATTERN, IS IT:
1. NO-TEMPORAL-PATTERN

2. WORSE-IN-MORNING

3. WORSE-IN-EVENING

>> 3

CONCERNING SEVERITY, IS IT:
1. le

2. 2+

3. 34

4. be

Ss. MASSIVE

>> 5

CONCERNING TYPE, IS IT:
1. PITTING

2. NON-PITTING

»> 1

CONCERNING ERYTHEMA, IS IT:
qt. ERYTHEMATOUS

2. NOT-ERYTHEMATOUS

>> 2

CONCERNING PRIN, IS IT:

1. PAINFUL

2. NOT-PAINFUL

>>» 2

IN THINKING
ABOUT (NOW DYSPNEA) ,
CONCERNING STATUS, IS IT:

1. ABSENT
2. PRESENT
>> 1

IN THINKING ,
ABOUT (NOR (ALCOHOL CONSUMPTION) >
CONCERNING AMOUNT, IS IT:

1. NONE

2. RARE

3. SOCIAL

4. HEAVY
5. ALCOHOLIC
>» 3

FIGURE 5. ANOTHER PRESENT ILLNESS SIMULATION

(Note: user inputs preceadded by ’>>’?
Page 48

IN THINKING
RBOUT (PAST PROTEINURIA)
CONCERNING STATUS, IS IT:

i. RBSENT

2. PRESENT

>> 2

CONCERNING AMOUNT, IS IT:
1. LIGHT

2. HEAVY

>> 1

CONCERNING QUAN-ANOUNT, IS IT:
1. <1 OQMGRAMS

2. LOSNGRANS-SGRANS

3. >SGRANS

>> ?

IN THINKING
ABOUT (NOW (VARICOSE VEINS)) ,
CONCERNING STATUS, IS IT:

1. ABSENT
2. PRESENT
>> 1

IN THINKING
ABOUT (NOW JRUNDICE) ,
CONCERNING STATUS, IS IT:

1. ABSENT
2. PRESENT
>> 1

HAPPY-FRANES
NONE

ACTIVE-FRANES
(CHRONIC GLOMERULONEPHRITIS) SCORE 6.213 EXPL 3.285 AVG 8.249
(SODIUM RETENTION) SCORE 0.204 EXPL 9.285 AVG 0.245
(NEPHROTIC SYNDROME) SCORE 8.166 EXPL 0.285 AVG 9.226
CIOTOPATHIC NEPHROTIC SYNDROME) SCORE 8.166 EXPL 8.285 AVG 8.225
(CHRONIC RENAL FAILURE) SCORE 9.086 EXPL 8.285 AVG 9.185
(FOCAL GLOMERULONEPHRITIS)

PLEASE TELL ME ABOUT
KUB ,1.€.,

TS THERE (NOW KIDNEYS-BOTH-SMALL KUB) 7
>> NO

PLEASE TELL ME ABOUT
HENATURIA ,I.€.,

TS THERE ((NOT ABSENT) PAST HEMATURIA) 7
>> NO

PLEASE TELL ME ABOUT
HYPERTENSION ,I.E.,

IS THERE (NOW (NOT ABSENT) HYPERTENSION) ?
>> NO

FIGURE 5. Continued
Privileged ae. G.A.Gorry > Page 49

Protocol! Collection and Analysis
Principals
Professor G. Anthony Gorry
Or. Jerome P. Kassirer
Peter B. Miiler —

In conjunction with our studies of the clinical decision making
process, we have undertaken the collection and analysis of tape-recorded
protocols of a number of clinicians taking present illnesses. We really
have two purposes In mind with respect to this study.

In the present illness project discussed above, we have relied on the
observation of and introspection by a single clinical expert for the
most part. Although this has proved very productive, we want to know if
major variations in “style” exist, and whether some styles are more
efficient and/or effective than others. Therefore, we need to broaden
the base of the observed problem solving behavior upon which we are
constructing our cognitive theory.

The second purpose of this study is to collect protocols which can be
used in testing the computer simulations we are employing. With
detailed protocols in hand, we can compare the behavior of programs with
that of clinicians on a "step by step" basis. Such comparisons wil
undoubtedly suggest refinements and improvements in the theories, and

this form of testing will bea central methodological tool of the
Laboratory. i

We have already initiated this collection and analysis of protocols.
Our current study involves the presentation of a case to renal experts.
The clinician is asked to take a present illness from the patient. (The

part of the patient is played by another physician.) The basic procedure
of the experiment is as fol tows:

1) The renal expert is first told the age, sex, and chief complaint
of the patient.

2) The renal expert then can ask questions concerning the patient,
one at a time.

3) For each question, he must say why he is asking the question.

4) After receiving the answer to ‘a question, the expert must say
what the answer “means” to him insofar as his current view of the
case is concerned.

In the current study, we are presenting the same case to five renal
experts on the staff of the New England Medical Center Hospital. Thie
group was chosen for several reasons: 1) they are indeed experts, and
Privileged Gini C.A.Corry iar, Page 5S@

We are interested in expert behavior; 2) they are kidney specialists,
and their protocols on a kidney problem can be used in testing the

simulation programs we are developing: and 3) because they are all in
the same specialty and in the same hospital, they are apt to show some
common behavior, and this will make our first pass at modeling their

behavior somewhat easier.

As we become more experienced in the collection and analysis of
protocols, and as our understanding of the clinical process becomes more

highly developed, we will expand our efforts to include clinicians from
other specialties. ,

As an example of a problem in which "style" differences might play an
important role, consider the following. ,

Because the physician is often interested in historical information
about the patient, he must often reiy on the patient himself for this
information. In many cases, the patient cannot (sometimes will not)

remember the exact circumstances in question, or the recollections of
the patient are suspect. In such a situation, the clinician may search
for Witnesses to the patient’s past condition. Consider, for example
this brief excerpt from a protocol in which the patient is a young boy

with symptoms of heart disease and a possible episode of acute rheumatic
fever some five years ago.

Pat. “Well, 4 or S years ago, I was out of schoo! for 3 or 4 months.
I had pain in my joints...."

Doc. “Tell me a tittle more about this episode. Were you
hospi tal ized?" .

Pat. "No. The doctor took care of me at home."

Doc. “What did he say was wrong with you?"

Pat. "St. Vitus dance."

Doc. "Did he treat you with anything?"

Pat. "He just gave me aspirin."

Doc. “He gave you aspirin? Did you take it frequently?"

Pat. "He said...you know... I don’t even remember."

Doc. “Did you have a sore throat that started the whole thing of f?

Did anyone ever mention it to you? Oid the doctor ask you whether
you had a sore throat?"

Pat. "I don’t know doc. I get a fot of sore throats.”

Doc. "Did the doctor inject you with penicillin back in that time?
Do you remember?"

Pat. "No he didn’t inject me."

Doc. "You don’t remember if you took any penicillin by mouth?"
Pat. "Oh, maybe he gave me some pills."
Doc. "Where’s your mother?"

Now in this brief excerpt, we see the clinician trying to establish
whether the patient in fact had an attack of acute rheumatic fever four
or five years ago. The patient gives evidence which is not conclusive
on the matter. The clinician turn his attention on the quest for