评价：医师苛求自己的同行，法学界人士却有不同的观点：无九成的把握不成结论。
建议：斑竹征求全文翻译。
Reference Guide on Medical Testimony
mary sue henifin, howard m. kipen, and susan r. poulter
Mary Sue Henifin, J.D., M.P.H., is a partner with Buchanan Ingersoll, P.C., Princeton, New Jersey, and
Adjunct Professor of Public Health Law, Department of Environmental & Community Medicine, UMDNJ–
Robert Wood Johnson Medical School, Piscataway, New Jersey.
Howard M. Kipen, M.D., M.P.H., is Professor and Director of Occupational Health, Environmental and
Occupational Health Sciences Institute, UMDNJ–Robert Wood Johnson Medical School in Piscataway,
New Jersey.
Susan R. Poulter, J.D., Ph.D., is Professor of Law, University of Utah College of Law, Salt Lake City,
Utah.
The authors are listed alphabetically. The authors greatly appreciate the excellent research assistance provided
by Sue Elwyn, Dean Miletich, Marie Leary, Ross Jurewitz, and Fazil Khan.
contents
I. Introduction, 441
A. Applicability of Daubert v. Merrell Dow Pharmaceuticals, Inc., 442
B. Medical versus Legal Terminology, 443
C. Relationship of Medical Testimony to Legal Rules, 445
II. The Medical Doctor As an Expert, 447
A. What Is a Physician? 447
B. Physicians’ Roles in Patient Care, 449
C. Medical Research and Academic Appointments, 450
D. Physicians As Expert Witnesses, 450
III. Information Utilized by Physicians, 452
A. Patient History (from the Patient), 452
1. Symptomatology, 453
2. Environmental and Occupational History, 454
3. Other Risk Factors, 455
B. Past and Present Patient Records and Exposure-Related Records, 455
C. Physical Examination, 455
D. Diagnostic Tests, 457
1. Laboratory Tests, 459
2. Pathology Tests, 460
3. Clinical Tests, 460
Reference Manual on Scientific Evidence
440
IV. Physician Decision Making, 461
A. Introduction, 461
B. Diagnosis, 463
C. Probabilistic Basis of Diagnosis, 465
D. Causal Reasoning, 467
E. Evaluation of External Causation, 468
1. Exposure, 472
2. Reviewing the Medical and Scientific Literature, 473
3. Clinical Evaluation of Information Affecting Dose–Response
Relationships, 475
V. Treatment Decisions, 478
VI. Medical Testimony: Looking to the Future, 479
Glossary of Terms, 480
References on Medical Testimony, 484
I. Introduction
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III. Information Utilized by Physicians
……Like the probabilistic reasoning described
above, this kind of reasoning is rarely made explicit.
E. Evaluation of External Causation
For the physician, both causal and probabilistic reasoning are the basis for establishing
external causation, which is the relationship between environmental factors
(work, chemical exposures, lifestyle, medications) and illness, as well as for
making the more common analysis of internal causation as discussed earlier in
section IV.B. The physician may be asked to determine external causation by
the patient or a third party, such as a lawyer, insurance company, or governmental
agency. A key element of determining causation is gaining access to all
information available about the patient’s condition.
Figure 1 provides examples of the diverse types of information that may be
available for review in determining external causation. In any given case, much
of the listed information is normally not available.111 Determining external causation
also generally occurs in a stepwise fashion. In the first step the physician
Figure 1. Determining External Causation
must establish the characteristics of the medical condition. Second, he or she
carefully defines the nature and amount of the environmental exposure. The
third step is to demonstrate that the medical and scientific literature provides
evidence that in some circumstances the exposure under consideration can cause
the outcome under consideration. This step is synonymous with establishment
of general causation. As part of this step, the clinician attempts to establish the
relationship between dose and response, including whether thresholds exist, ultimately
defining the clinical toxicology of the exposure. The fourth step is to
Specific Causation
Medical Condition
Patient history
Patient records
Physical examination
Laboratory tests
Pathology tests
Clinical tests
Radiological tests
Temporal Relationship
Order of exposure and illness
General Causation
Medical and scientific
literature
Epidemiological data
Toxicological data
Case reports and series
Dose–response
relationships
Clinical experience
Environmental and
occupational history
Identification of agents
Clinical indications of
exposure
Duration of exposure
Magnitude of exposure
Measurements of exposure
Industrial records
Site visit
Governmental or insurance
records
Exposure Information
Modifying Factors
Other risk factors
Susceptibility
Alternative etiology
(competing causes)
Adequacy of medical
diagnosis
Timing of disease onset
(latency)
Response to removal
from exposure
apply this general knowledge to the specific circumstances of the case at hand,
incorporating the specifics of exposure, mitigating or exacerbating influences,
individual susceptibilities, competing or synergistic causes, and any other relevant
data.112
Many conditions resulting from toxic exposures are similar or identical in
clinical manifestations to conditions arising from nontoxic causes.113 Physicians
rely on their training and expertise as clinicians and scientists when considering
the medical and scientific literature as well as information about a patient’s condition
to best determine causality in a particular patient. Definitive tests for
causality are actually rare,114 and physicians must almost always use an element of
judgment in determining the relationship between exposure and disease in a
given patient. For instance, if a substance is suspected to cause an allergic or
toxic condition, it may be necessary for diagnostic purposes to remove a patient
from the workplace on a trial basis. On the other hand, determinations of external
causation in patients with cancer may be irrelevant to treatment decisions as
treatment is usually unaffected by assignment of cause.115
Physicians use both causal and probabilistic reasoning in determining both
internal and external causation in regard to a particular illness. Methods for
determination of some special external causes of disease may be found in occupational
and environmental medical texts and journals116 and generally are analogous
to methods used for assessment of internal disease causation.117 The difference
is essentially in the body of medical, toxicological, epidemiological, and
industrial hygiene knowledge that is relevant and needs to be incorporated.
For instance, in an elderly patient with chronic shortness of breath, the treating
physician may use differential diagnosis to determine that chronic bronchitis
is the best explanation as the underlying cause of symptoms, having excluded
heart disease, anemia, lung fibrosis, and emphysema. The treating physician will
rarely consider the external causes of the chronic bronchitis, beyond consideration
of whether the patient smoked cigarettes.118 The specific contribution of
environmental or workplace exposures is rarely assessed as a part of clinical care
in an elderly nonworking patient, since it does not affect diagnosis, treatment,
and prognosis of this particular disease.119 However, such determination of external
causation may be essential to determination of a contested workers’ compensation
award.120
The key factor for the courts to recognize is that, while similar underlying
reasoning is used in determination of both internal and external causation, and
physicians routinely make limited determinations of external causation, many of
the facts relevant to a determination of external causation rely on a body of
scientific literature that is not routinely used by treating physicians. As a corollary,
an expert’s opinion on diagnosis and his or her opinion on external causation
should generally be assessed separately, since the bases for such opinions are
often quite different.
1. Exposure
Critical to a determination of causation is characterizing exposure. Exposure to
a toxic substance can sometimes be established by a review of the patient’s history
and various available indicators of exposure, as discussed in section III.
There are four “cardinal” pieces of exposure information:
1. The material or agent in the environmental exposure should be identified.
2. The magnitude or concentration of an exposure should be estimated,
including use of clinical inference.
3. The temporal aspects of the exposure should be determined—whether
the exposure was short-term and lasted a few minutes, days, weeks, or
months, or was long-term and lasted for years. Similarly, the latency between
exposure and disease onset is often critical.
4. If possible, the impact on disease or symptoms should be defined.121
In many instances, the desired information will be incomplete,122 but it can
often be inferred from the literature that a given amount of time in a particular
industry is well associated with disease-producing potential. Progressive pulmonary
fibrosis (accelerated silicosis) can develop in as little as ten months in workers
involved in manufacturing abrasive soaps, tunneling in rock that has a high
quartz content, or carrying out sandblasting in small, enclosed spaces, although
simple silicosis is much more commonly a chronic illness resulting from years of
exposure.123 In other situations, exposure estimates will be based on methods
beyond the scope of medical expertise, such as physical or chemical analyses, or
chemical fate-and-transport modeling (i.e., using mathematical models to project
the movement of chemicals in air, water, and soil).
In determining causation, the physician may have particular insight into clinical
clues related to exposure, such as clinical indicators of degree of exposure, temporal
relationships, and the effect of removal from the toxic substance.124 The
physician also has particular insight into the role that preexisting illnesses may
play in causing an exacerbation, recurrence, or complication of a clinical condition
independent of any exposure to toxic products, or in concert with a toxic
exposure.125
2. Reviewing the Medical and Scientific Literature
After characterizing exposure and the nature of the patient’s disease, the physician
expert witness must determine if the medical and research literature supports
a determination of environmental causation.126 The research literature in-
cludes epidemiological studies and toxicology studies. The physician should be
guided by the methods set forth in the Reference Guides on Epidemiology and
Toxicology in evaluating this literature and its relevance to the patient’s exposure
and condition.127
Physicians also have access to case reports or case series in the medical literature.
These are reports in medical journals describing clinical events involving
one individual or a few individuals. They report unusual or new disease presentations,
treatments, or manifestations, or suspected associations between two
diseases, effects of medication, or external causes of diseases. For example, the
association between asbestos and lung cancer was first reported in a 1933 case
report, although the first controlled epidemiological study on the association
was not published until the 1950s.128 There are a number of other instances in
which epidemiological studies have confirmed associations between a specific
exposure and a disease first reported in case studies (e.g., benzene and leukemia;
vinyl chloride and hepatic angiosarcoma),129 but there are also instances in which
controlled studies have failed to substantially confirm the initial case reports
(e.g., the alleged connection between coffee and pancreatic and bladder cancer
or the infectious etiology of Hodgkins disease).130
Case reports lack controls and thus do not provide as much information as
controlled epidemiological studies do.131 However, case reports are often all that
is available on a particular subject because they usually do not require substantial,
if any, funding to accomplish, and human exposure may be rare and difficult
to study. Causal attribution based on case studies must be regarded with caution.
However, such studies may be carefully considered in light of other information
available, including toxicological data.132
3. Clinical Evaluation of Information Affecting Dose–Response Relationships
Assessing the role of external causes in the patient’s condition requires the integration
of the information described in the preceding sections, with particular
attention to dose–response relationships. The toxicological law of dose–response,
that is, that “the dose makes the poison,” refers to the general tendency for
greater doses of a toxin to cause greater severity of responses in individuals, as
well as greater frequency of response in populations.133 Clinically, there are some
instances in which the general rule does not hold. For agents that cause an
allergic response through an immunologic mechanism, the dose–response relationship
is often less straightforward. Many people who are not prone or able to
develop an allergic reaction, for genetic or other reasons, will not respond adversely
to the substance at any dose. However, those who are susceptible are
more likely to become specifically reactive (sensitized) to the specific agent as
the dose increases. After sensitization has occurred, severe reactions may occur
with exposures that are much lower than the previous level required for sensitization.134
Although some diseases (e.g., pneumonia that is due to influenza) are frequently
considered to be unifactorial, the possibility of multiple causes of a cliniReference
cal condition is a critical concern. At some level most diseases have multiple host
and environmental factors that contribute to their presence. A commonly held
misconception is that the presence of a nontoxic or other toxic cause for a
condition automatically excludes a role for the toxin being considered as an
external cause.135 While this is sometimes true, in reality the converse can also be
true. For example, epidemiology studies dealing with occupational asbestos exposure
and cigarette smoking indicate that together they result in much higher
rates of lung cancer than either one causes on its own.136 Thus, two toxic agents
have been found to interact in a synergistic manner so that their combined
effects are much greater than even the sum of their individual effects.137
Even if causal factors do not interact synergistically, several may contribute in
an incremental fashion to a disease and should not be assumed to be mutually
exclusive.138 Accordingly, the common statement that “alternative causes of disease
must be ruled out” before causation is attributed can be more accurately
refined to say that “the role of other causes must be adequately considered.” If
there is a significant rate of disease of unknown etiology (i.e., other causes or
risk factors have not been identified), the determination of external causation
may be complicated.139 In general, if a patient is not subject to other known risk
factors for a disease, it is more likely that the external cause is a factor in causing
the patient’s illness.140
Differences in individual susceptibility are commonly cited as the reason why
one person gets sick from an environmental exposure while other persons are
not affected. True individual susceptibility is based on genetic differences, such
as immunologic reactivity, enzyme metabolism, and gender.141 A number of
other acquired factors, such as age, body mass, interacting simultaneous exposures,
and preexisting disease, may also contribute to susceptibility.142 Reliable
and accurate information is available about the effects on some diseases of age,
body mass, gender, and other factors; however, information on genetic susceptibility
is available for only a few diseases, and information on the relation between
genetic susceptibility and particular toxic exposures, for even fewer.143
In almost all instances, integration of all the above factors into an opinion on
causality cannot be reduced to mathematical formulas. There are inevitable gaps
in information, as well as lack of knowledge regarding individual characteristics,
such as susceptibility and resistance. Thus, clinical judgment is critical to opinions
on diagnosis and causation for the individual patient even when the scientific
population basis for general causation may be quite strong.
V. Treatment Decisions
Following diagnosis, most physicians are concerned with applying appropriate
treatment to either cure or ameliorate a patient’s condition. Such treatment may
be surgical (e.g., removal of a diseased organ), ablative (e.g., radiotherapy aimed
at a tumor), chemotherapeutic (e.g., use of pharmacological agents with a host
of different actions), rehabilitative (e.g., physical therapy), interdictive (e.g., removal
of the patient from a toxic or allergenic exposure), behavioral (e.g., counseling),
or something else.144 Some of the recommended therapies for different
conditions found in the textbooks and professional literature are reified as practice
guidelines by various organizations and the government. Some recommended
therapies have demonstrated their effectiveness in randomized controlled trials,
whereas others, both old and new, have much less scientific support.
Treatment options for an individual patient must be assessed in light of the
nature and severity of the particular disease (e.g., people whose lung cancer is
metastatic are not often candidates for removal of the primary tumor), and the
likelihood of unacceptable complications from the treatment (e.g., removal of a
lung to cure cancer in someone with severe emphysema may not leave enough
remaining lung tissue to allow the patient to walk, even if his or her cancer is
cured).145 Prediction of the effects, both positive and negative, of a course of
therapy is based on the professional literature and consideration of a patient’s
specific situation. For example, a patient with underlying kidney disease may
not be an appropriate candidate for some radiographic tests and therapies that
use dye that runs a high risk of causing further damage to the kidneys. Use of an
effective antibiotic to which a patient “may possibly” have had a previous aller-
gic reaction should be weighed against the use of alternative antibiotics that may
be less effective against the infection. The physician may also consider the likely
severity of a reaction and the ability to prevent or treat it with additional medication.
Thus, although treatment recommendations are often written down as a
precise series of sequential decisions (often called algorithms), making decisions
for actual patients is generally more complex and requires consideration of many
individual factors.
VI. Medical Testimony: Looking to the Future
It is likely that medical testimony will continue to be one of the most common
forms of expert testimony in the future. While many commentators have focused
attention on medical testimony in toxic injury cases, particularly testimony
offered on issues of external causation, a growing number of cases concern
ERISA suits challenging coverage under health care plans and claims of
unlawful discrimination under the Americans with Disabilities Act. As the health
care system continues to evolve, there will be growing numbers of cases, particularly
on coverage issues, requiring medical testimony. Also, advances in the
medical sciences, including medical genetics and biotechnology, will present
new challenges to courts in cases requiring medical testimony.
With this forecast, courts will continue to grapple with issues of admissibility
of medical testimony for the foreseeable future. As the cases we have used to
illustrate this chapter demonstrate, there are great and unresolved differences in
how various courts treat the admissibility of medical testimony. While this reference
guide does not propose legal standards to govern admissibility of medical
evidence,146 it does provide a framework for legal analysis by describing the
scientific and professional practices of physicians as they perform their professional
duties and offer opinions on diagnosis, treatment, and internal and external
causation. It is challenging to encourage consistent use of medical terminology
and make explicit the extensive knowledge base and reasoning process that
physicians implicitly employ in evaluating medical problems. Further work in
these areas will improve the transferability of medical knowledge into the courts
and other arenas.
Glossary of Terms
adequacy of diagnostic hypothesis. Diagnostic sufficiency. To be considered
adequate, a diagnostic hypothesis must explain the patient’s normal
findings as well as abnormal findings.
attending physician. A physician formally attached to (credentialed at) the
hospital in which the patient is being treated.
Bayes’ theorem. An algebraic formula that allows the pretest and posttest
clinical data to be expressed in terms of probabilities. By integrating the pretest
probability of a disease or set of diseases with the result of a given test (and
taking into account the sensitivity and specificity of that test), the physician is
able to calculate a posttest probability of a disease or set of diseases. This
approach can be useful in certain circumstances, but many clinical situations
can be so complex that it is impractical to apply Bayes’ theorem.
case report/case series. The most basic type of descriptive study of an individual
(case report) or a series of individuals (case series), usually including
such factors as gender, age, and exposure or treatment, but without controlled
assessment of the relationship between exposure or treatment and
disease or outcome.
clinical tests. Noninvasive tests of the function of an organ system, including
tests of pulmonary function, muscle function, endurance, and heart function.
coherency of a diagnostic hypothesis. In a coherent diagnostic hypothesis,
the patient’s findings (signs, symptoms, test results), risk factors, and complications
match the expectations for the disease.
consulting physician. A physician brought in to give an expert opinion or a
second opinion, who may or may not be involved in treatment. He or she
may rely on information contained in the patient’s medical records, patient
history, laboratory tests, x-rays, and so forth, or may combine these facts with
his or her own examination of the patient and any additional tests considered
advisable.
diagnosis. The determination of which disease is most likely present in a given
patient, as indicated by the patient’s various symptoms, signs, and test results.
diagnostic hypothesis. One or more disease entities, conditions, or syndromes
postulated to be responsible for causing a patient’s clinical presentation. See
working diagnosis.
diagnostic tests. Any tests (clinical, laboratory, or pathologic) whose results
may assist the physician in making his or her diagnosis.
differential diagnosis. The term used by physicians to refer to the process of
determining which of two or more diseases with similar symptoms and signs
the patient is suffering from, by means of comparing the various competing
diagnostic hypotheses with the clinical findings.
differential etiology. A term used on occasion by expert witnesses or courts
to describe the investigation and reasoning that leads to a determination of
external causation, sometimes more specifically described by the witness or
court as a process of identifying external causes by a process of elimination.
disease. Coherent deviation from normal in structure or function that affects a
certain part or parts of the body or type of tissue.
dose–response relationship. The general tendency to observe greater responses
in individuals when they are given greater doses of a drug or toxic
substance. The presence of such a relationship supports an inference of a
causal relationship between exposure and response (disease).
external causation. As used herein, an underlying cause of a given disease in a
given individual that stems from a source outside the individual’s body. A
hereditary disease such as Tay-Sachs disease or hemophilia would not be due
to external causation; cirrhosis of the liver resulting from excessive alcohol
intake or ataxia resulting from lead poisoning would be due to external causation.
general causation. General causation is established by demonstrating (usually
by reference to a scientific publication) that exposure to the substance in
question causes (or is capable of causing) disease; for example, smoking cigarettes
causes lung cancer.
inductive reasoning. See inferential reasoning.
inferential reasoning. The reasoning process by which a physician assimilates
the various findings on a given patient and forms hypotheses that lead to
testing and further hypotheses until a coherent diagnosis is reached.
invasive procedure. A procedure (surgery, test, etc.) in which the body of the
patient is invaded by an instrument of some sort. Invasive procedures may be
as minimal as the biopsy of a lesion on the skin or as traumatic as open-heart
surgery.
laboratory tests. Analyses of fluids or other substances collected from the body
of the patient, including blood samples, urine samples, and fecal samples.
multiplicative interaction. A process that occurs when two toxic agents (or
two disease states) interact in the patient in such a manner that the magnitude
of their combined effects is equal to the product of the effect of each agent (or
disease) working in isolation. This is a special instance of synergism.
noninvasive procedure. A procedure (usually a test procedure) that does not
invade the body of the patient, including exercise and stress tests, electrocardiograms,
CAT scans, and MRIs.
parsimony in a diagnostic hypothesis. A preference for the simplest way to
coherently and adequately explain all of the patient’s findings, normal and
abnormal.
pathogenesis. The mode of origin or development of any disease or morbid
process.
pathology test. Microscopic analysis of a piece of body tissue obtained during
surgery or by biopsy, in which an expert determines whether the tissue appears
to be normal for the organ form from which it was taken. If it does not
appear normal, the expert then attempts to determine what the pattern of
abnormality is (scarring, malignancy, inflammation, etc.)
pathophysiology. The derangement of function seen in disease; alteration in
function as distinguished from structural disease.
patient history. An interview conducted by the treating physician with the
patient, in which the physician elicits from the patient the symptoms he or
she is suffering from, as well as information about past and present medical
history and treatment, personal information on family status and lifestyle,
environmental information about habitation and employment, and the like.
physical exam. A noninvasive, largely external examination of the patient’s
body in which the physician looks for signs of normal and abnormal function.
The physician may do a physical examination of a healthy individual to
fulfill the requirements of an employer or insurance company, or of a patient
who is ill to substantiate or refute the symptoms obtained from a patient
during the taking of the patient history.
predictive value. The extent to which a given test will predict the presence or
absence of a given disease. The positive predictive value of a test or observation
refers to the proportion of all positive results that are “true” positive test
results in a particular population. The negative predictive value of a test or
observation refers to the proportion of “true” negative results in a population.
sensitivity. The percentage of patients with positive test results for a disease
who actually have the disease (called a “true positive” result). Test results for
those who have a disease but are incorrectly identified as not having the
disease because of the test’s insensitivity are called “false negatives.” A test
with high sensitivity given to people suffering from the disease it tests for will
have a high proportion of true positives and only a few false negatives. A test
with low sensitivity will reveal a considerable number of false negatives and
fewer true positives.
sensitization. The initial exposure of a person to a specific antigen (any substance
that is capable of inducing an immune reaction in an individual and of
reacting with the products of that response); repeated exposure to the same
antigen may then result in a much stronger immune response (e.g., an individual
stung by a bee on one occasion may have a stronger response if stung
again, and if subjected to sufficient numbers of bee stings, may eventually
react by going into anaphylactic shock).
sign. A physical condition observed in a patient by the physician in the course
of a physical examination, such as fever, cardiac murmur, enlarged lymph
nodes, suspicious breast mass.
specific causation. Specific, or individual, causation is established by demonstrating
that a given exposure is the cause of an individual’s disease (for example,
that a given plaintiff’s lung cancer was caused by smoking).
specificity. The percentage of negative test results in individuals who are free
of a given disease, also known as the “true negative” rate. Test results in those
who are free of the disease who are incorrectly identified as having the condition
are called “false positives.” Thus, a test that indicates abnormal bronchial
reactivity in 15% of individuals without asthma would have a false positive
rate of 15%; their test results were positive, but they are free of the
condition.
susceptibility. The propensity of an individual to be harmed by an agent (e.g.,
a person who has a high susceptibility to irritant gases will suffer from bronchitis
or asthma more than a person with a low susceptibility). Susceptibility
tends to be influenced by age, gender, and genetics as well as the individual’s
state of health and history of prior exposure.
symptom. A patient’s subjective report of physical abnormality as described to
the physician during the taking of the patient history. Symptoms may include
reports of pain in various parts of the body, sensations such as dizziness or
fatigue, fever or chills, or swelling or suspicious nodules. If a symptom, such
as fever or the existence of a suspicious breast nodule, is verified by the physician
during the physical exam, it is considered a sign.
syndrome. A clustering of the symptoms, signs, and laboratory findings that
indicate a specific disease state.
synergistic interaction. The joint action of two or more agents such that
their combined effect is greater than the sum of the effects of each agent
working separately. See multiplicative interaction.
threshold. The lowest dose of any substance at which a measurable response
occurs. For a substance that produces more than one effect, the threshold
may vary according to the effect. For instance, with a neurotoxin that can
produce dizziness, convulsion, coma, and death, the thresholds for the different
effects can vary from quite low for dizziness to relatively high for death.
treating physician. A physician in charge of diagnosis and therapy for a given
patient. The treating physician is likely to be an attending physician at the
hospital to which the patient has been admitted. Many physicians will act as
treating physicians with patients for whom they provide primary care, but
may be called upon to act as consulting physicians at the request of colleagues
or the patients of other physicians.
working diagnosis. A diagnostic hypothesis sufficiently convincing to form
the basis for planning the next step in patient management. A working diagnosis
may provide a rationale for the physician to order further tests, to forecast
a likely clinical course for the patient, to refrain from further testing and
simply to observe the patient for a given time, or to initiate a course of
treatment. If a working diagnosis proves to be correct, either by subsequent
testing or by patient response, it may become the final diagnosis.
References on Medical Testimony
Thomas E. Andreoli et al., Cecil Essentials of Medicine (3d ed. 1993).
Barbara Bates et al., A Guide to Physical Examination and History Taking (6th
ed. 1995).
Joan E. Bertin & Mary S. Henifin, Science, Law, and the Search for the Truth in the
Courtroom, 22 J.L. Med. & Ethics 6 (1994).
Environmental Medicine (Stuart M. Brooks et al. eds., 1995).
1 & 2 Harrison’s Principles of Internal Medicine (Anthony S. Fauci et al. eds.,
14th ed. 1998).
Alvan R. Feinstein, Clinical Judgment (1967).
Michael D. Green, Bendectin and Birth Defects: The Challenges of Mass Toxic
Substances Litigation (1996).
Jerome P. Kassirer & Richard I. Kopelman, Learning Clinical Reasoning (1991).
Susan R. Poulter, Medical and Scientific Evidence of Causation: Guidelines for Evaluating
Medical Opinion Evidence, in Expert Witnessing: Explaining and Understanding
Science 186 (Carl Meyer ed., 1999).
Susan R. Poulter, Science and Toxic Torts: Is There a Rational Solution to the Problem
of Causation? 7 High Tech. L.J. 189 (1992).
参考资料
Reference Guide on Medical
Testimony
1. Samuel R. Gross, Expert Evidence, 1991 Wis. L. Rev. 1113, 1119 (a survey of trials revealed that
over half of the testifying experts were physicians or medical professionals). Two unpublished surveys
by the Federal Judicial Center, one in 1991 and another in 1998, found that physicians and medical
experts comprised approximately 40 percent of the testifying experts in federal civil trials.
2. See United States v. Drapeau, 110 F.3d 618, 619–20 (8th Cir. 1997) (medical testimony of the
examining doctor of the infant victim refuted the possibility that the child’s injuries were the result of a
fall from his bed); United States v. Talamante, 981 F.2d 1153, 1158 & n.7 (10th Cir. 1992) (physician
testified that the victim’s eye was not completely blind at the time of the assault, supporting a finding of
serious bodily injury).
3. See United States v. Pike, 36 F.3d 1011, 1012–13 (10th Cir. 1994) (in a case of sexual abuse of a
minor, the testimony of the examining physician need not be preferred over the testimony of the victim
where the physician’s testimony neither supports nor refutes the victim’s testimony).
4. Medical testimony will almost always be offered on the diagnosis of the plaintiff’s injury or
disease, and often on other issues as well. See Silmon v. Can Do II, Inc., 89 F.3d 240, 241 (5th Cir.
1996) (testimony of three doctors as to the cause of the plaintiff’s ruptured disc; the employer denied
liability under the Jones Act, alleging that the plaintiff’s injury was caused by illegal intravenous drug
use); Bertram v. Freeport McMoran, Inc., 35 F.3d 1008, 1018 (5th Cir. 1994) (upholding the district
court’s discretion to give greater weight to the medical testimony of the plaintiff’s primary treating
physician where the plaintiff sued under the Jones Act for injuries arising from a workplace accident on
a drilling barge).
5. See DiPirro v. United States, 43 F. Supp. 2d 327, 331–39 (W.D.N.Y. 1999) (recounting the
court’s findings of fact based upon the testimony of five physicians for the plaintiff and five physicians
for the defendant concerning plaintiff’s alleged injuries caused by an accident involving a U.S. Postal
Service vehicle).
6. See Murray v. United States, 36 F. Supp. 2d 713, 716 (E.D. Va. 1999) (plaintiff’s expert medical
witness testified that the care provided fell well below that standard applicable to emergency room
physicians).
7. See Dodson v. Woodmen of the World Ins. Soc’y, 109 F.3d 436, 438 (8th Cir. 1997) (treating
physician testified that the plaintiff was mentally disabled prior to the expiration of his ERISA policy).
8. Price v. National Bd. of Med. Exam’rs, 966 F. Supp. 419 (S.D. W. Va. 1997) (medical testimony
offered as to whether plaintiff had attention deficit hyperactivity disorder that caused disability as defined
by the Americans with Disabilities Act).
9. See Demaree v. Toyota Motor Corp., 37 F. Supp. 2d 959 (W.D. Ky. 1999) (plaintiff’s examining
physician testified regarding injuries allegedly caused by a deploying air bag); Toole v. McClintock,
999 F.2d 1430, 1431 & n.2 (11th Cir. 1993) (reporting that five surgeons, including the plaintiff’s
treating physician, testified regarding surgery that caused breast implant rupture).
10. See Satterfield v. J.M. Huber Corp., 888 F. Supp. 1567, 1571 (N.D. Ga. 1995) (plaintiff’s
doctors testified that the plaintiff’s symptoms were also consistent with exposure to secondary sources of
chemical emissions identified by the defendant and stated that they had no opinion on whether plaintiff’s
complaints were related to air contamination from defendant’s plant).
11. 509 U.S. 579 (1993).
12. 119 S. Ct. 1167 (1999). Kumho concerned a tire-failure expert who gave an opinion on the
cause of a tire failure based on his examination of the tire and experience in examining tires. Id. at 1176–
78. Similarly, medical testimony will almost always rely in part on clinical examination, though often in
conjunction with other sources of information.
13. See Margaret A. Berger, The Supreme Court’s Trilogy on the Admissibility of Expert Testimony
§ IV.C.2.b, in this manual.
14. 151 F.3d 269 (5th Cir. 1998) (en banc), cert. denied, 119 S. Ct. 1454 (1999). In a panel decision,
the U.S. Court of Appeals for the Fifth Circuit had held that medical testimony in a toxic injury case
was not subject to the factors Daubert suggests for scientific knowledge. Moore v. Ashland Chem., Inc.,
126 F.3d 679 (5th Cir. 1997). The court reconsidered that decision en banc, affirming the trial court’s
exclusion of the witness based on Daubert. 151 F.3d at 277–79. The en banc decision concluded that the
trial court did not abuse its discretion, applying General Electric Co. v. Joiner, 522 U.S. 136 (1997). Id.
15. 151 F.3d at 276. See also Black v. Food Lion, Inc., 171 F.3d 308 (5th Cir. 1999) (trial court
should not have admitted a physician’s testimony that trauma from a slip and fall had caused the plaintiff’s
fibromyalgia).
16. 167 F.3d 146 (3d Cir. 1999).
17. Id. at 153–57. In this reference guide, the use of quotation marks around the terms differential
diagnosis and differential etiology indicates the witness’s or court’s use of the terminology, which may
differ from usage in the medical profession and from use elsewhere in this manual. See infra § I.B.
18. The appellate standard of review is also a critical factor in the analysis of the cases. The Supreme
Court has twice instructed that a deferential abuse-of-discretion standard be applied to trial courts’
admissibility decisions under Rule 702 of the Federal Rules of Evidence, including both rulings as to
admissibility and the manner in which the trial court evaluates the proffered testimony. In General
Electric Co. v. Joiner, 522 U.S. 136, 143 (1997), the Supreme Court held that an abuse-of-discretion
standard applies to decisions on admissibility of expert testimony under Daubert. The Court reiterated
that holding in Kumho Tire Co. v. Carmichael, 119 S. Ct. 1167, 1176 (1999), holding that abuse-ofdiscretion
review applies to how the trial court assesses reliability.
19. The demonstration of causation has been described as a part of the process of diagnosing an
environmental disease. See Mark R. Cullen et al., Clinical Approach and Establishing a Diagnosis of an
Environmental Medical Disorder, in Environmental Medicine 217, 220 (Stuart M. Brooks et al. eds., 1995)
[hereinafter Environmental Medicine]. The typical process of differential diagnosis is described more
fully in section IV.B.
20. See, e.g., Kannankeril v. Terminix Int’l, Inc., 128 F.3d 802, 807 (3d Cir. 1997) (court recognized
differential diagnosis “as a technique that involves assessing causation with respect to a particular
individual” (citing In re Paoli R.R. Yard PCB Litig., 35 F.3d 717, 758 (3d Cir. 1994), cert. denied, 513
U.S. 1190 (1995))); National Bank of Commerce v. Associated Milk Producers, Inc., 22 F. Supp. 2d
942, 963 (E.D. Ark. 1998) (plaintiff could not show, under differential diagnosis approach, that contaminated
milk caused his cancer), aff’d, 191 F.3d 858 (8th Cir. 1999); Mancuso v. Consolidated Edison
Co., 967 F. Supp. 1437, 1453 (S.D.N.Y. 1997) (proffered expert failed to conduct a differential diagnosis
to exclude exposure to substances other than PCBs as the cause of plaintiffs’ ailments).
21. See, e.g., Westberry v. Gummi, 178 F.3d 257, 262 (4th Cir. 1999) (differential etiology analysis
of talc as the cause of sinus problems); Synder v. Upjohn Co., 172 F.3d 58 (9th Cir. 1999) (unpublished
table decision) (text at No. 97-55912, 1999 WL 77975 (9th Cir. Feb. 12, 1999)) (differential etiology
analysis of Halcion as the cause of criminal behavior).
22. The issues of general causation and specific causation are addressed in detail in Michael D.
Green et al., Reference Guide on Epidemiology §§ V, VII, and Bernard D. Goldstein & Mary Sue
Henifin, Reference Guide on Toxicology §§ III–IV, in this manual. The distinction between general
causation and specific causation is discussed in Zwillinger v. Garfield Slope Housing Corp., No. CV 94-
4009, 1998 WL 623589, at *19–*20 (E.D.N.Y. Aug. 17, 1998) (plaintiff’s expert did not offer general
causation evidence that outgassing from carpet could cause ailments suffered by plaintiff); National
Bank of Commerce v. Associated Milk Producers, Inc., 22 F. Supp. 2d 942, 963 (E.D. Ark. 1998)
(although differential diagnosis “‘is undoubtedly important to the question of ‘specific causation,’’”
plaintiff must provide expert opinion on the issue of “‘general causation’” based on a scientifically valid
methodology (quoting Cavallo v. Star Enter., 892 F. Supp. 756, 771 (E.D. Va. 1995), aff’d in part, rev’d
in part, 100 F.3d 1150 (4th Cir. 1996), cert. denied, 522 U.S. 1044 (1998))), aff’d, 191 F.3d 858 (8th Cir.
1999).
23. See In re Joint E. & S. Dist. Asbestos Litig., 964 F.2d 92, 96 (2d Cir. 1992); Landrigan v.
Celotex Corp., 605 A.2d 1079, 1086 (N.J. 1992) (permitting clinician to testify to specific causation
based on epidemiology). But see Sutera v. Perrier Group of Am., Inc., 986 F. Supp. 655, 662 (D. Mass.
1997) (physician not qualified to testify on epidemiology). See Michael D. Green et al., Reference
Guide on Epidemiology, § VII, in this manual.
24. See Sterling v. Velsicol Chem. Corp., 855 F.2d 1188 (6th Cir. 1988); see generally Glen Donath,
Comment, Curing Cancerphobia Phobia: Reasonableness Redefined, 62 U. Chi. L. Rev. 1113 (1995).
25. See Gideon v. Johns-Manville Sales Corp., 761 F.2d 1129, 1137–38 (5th Cir. 1985) (recognizing
a claim for increased risk of contracting cancer where the likelihood is a “reasonable medical probability”
or “more likely to occur than not”).
26. See In re Paoli R.R. Yard PCB Litig., 916 F.2d 829 (3d Cir. 1990), cert. denied, 499 U.S. 961
(1991). But see Metro-North Commuter R.R. v. Buckley, 521 U.S. 424 (1997) (rejecting medical
monitoring claim under the Federal Employers Liability Act). Metro-North also rejected a claim for
negligent infliction of emotional distress based on fear of asbestos-related cancer. Id. at 437.
27. See National Bank of Commerce v. Associated Milk Producers, Inc., 22 F. Supp. 2d 942 (E.D.
Ark. 1998) (fear of future injury may be an element of damages, requiring expert opinion governed by
Daubert standards), aff’d, 191 F.3d 858 (8th Cir. 1999).
28. See, e.g., Cavallo v. Star Enter., 892 F. Supp. 756, 771 (E.D. Va. 1995), aff’d in part, rev’d in part,
100 F.3d 1150 (4th Cir. 1996), cert. denied, 522 U.S. 1044 (1998).
29. See, e.g., Black v. Food Lion, Inc., 171 F.3d 308, 310 (5th Cir. 1999) (plaintiff’s burden was to
prove that her fall caused fibromyalgia “to a reasonable degree of medical certainty, based on a reasonable
medical probability and scientifically reliable evidence”). See generally Jeff L. Lewin, The Genesis and
Evolution of Legal Uncertainty About “Reasonable Medical Certainty,” 57 Md. L. Rev. 380 (1998).
30. It is worth reminding readers that this guide is not intended to instruct judges concerning what
medical testimony should be admissible as evidence. This chapter and the other reference guides attempt
to contribute to the development of the law by clarifying scientific and professional practice in an
area, thereby informing the development of consistent legal doctrines as courts consider individual
cases. See the preface to this manual. This constraint, set by the Board of the Federal Judicial Center, is
especially notable in this chapter. The lack of commentary on various standards should not be misunderstood
as indicating that the authors have not given considerable thought to the manner in which
such conflicts should be resolved. See generally Joan E. Bertin & Mary S. Henifin, Science, Law, and the
Search for the Truth in the Courtroom, 22 J.L. Med. & Ethics 6 (1994); Susan R. Poulter, Science and Toxic
Torts: Is There a Rational Solution to the Problem of Causation?, 7 High Tech. L.J. 189 (1992); Susan R.
Poulter, Medical and Scientific Evidence of Causation: Guidelines for Evaluating Medical Opinion Evidence, in
Expert Witnessing: Explaining and Understanding Science 186 (Carl Meyer ed., 1998). A summary of
different approaches in applying evidentiary rules to medical testimony is offered in Margaret A. Berger,
The Supreme Court’s Trilogy on the Admissibility of Expert Testimony, § IV.C.2.b, in this manual.
Moreover, proposed changes to Rule 702 by the Judicial Conference Advisory Committee on Evidence
Rules, if enacted, may also affect the legal analysis of medical testimony.
31. 4 Lane Medical Litigation Guide §§ 40.21–.28, at 73-101 (Fred Lane & David A. Birnbaum
eds., 1993 & Supp. 1996).
32. 1 id. § 4.15, at 18–20 (1994 & Supp. 1996). In some jurisdictions, the witness must be qualified
to testify about the standard of care in a similar or even the same locality. 4 id. § 40.23, at 86–92 (1993
& Supp. 1996).
33. See World Health Org., World Directory of Medical Schools 274–75 (6th ed. 1988 & Supp.
1997).
34. See, e.g., Association of Am. Med. Colleges, Curriculum Directory 1998–99, at 104–05 (27th
ed. 1998) (listing required courses for Johns Hopkins University School of Medicine).
35. See World Health Org., supra note 33, at 274–75.
36. Although it may be helpful in establishing the witness’s credentials for opinion testimony,
courts usually do not apply a strict requirement of specialization or board certification for most purposes.
See, e.g., Holbrook v. Lykes Bros. S.S. Co., 80 F.3d 777, 782–83 (3d Cir. 1996) (physician board
certified in pulmonary medicine not required to be a specialist in oncology and radiation to testify on
causation of mesothelioma). In contrast, admissibility of testimony on the medical standard of care in
medical malpractice cases is typically controlled through screening of the witness’s qualifications. See,
e.g., Marquardt v. Joseph, 173 F.3d 855 (6th Cir. 1999) (unpublished table decision) (text at No. 98-
5163, 1999 WL 196569 (6th Cir. Mar. 30, 1999) (dentist who was not an oral surgeon was not qualified
to testify on the standard of care for oral surgery)); Carroll v. Morgan, 17 F.3d 787, 790 (5th Cir. 1994)
(cardiologist with many years of experience need not be a specialist in pathology to testify on the
relationship between heart problems and death).
37. The American Medical Association (AMA) has taken an interest in the quality of medical
expert testimony. After reviewing cases involving testimony by physicians who had falsified their credentials,
the AMA issued a 1998 report to its Board of Trustees recommending that the AMA encourage
state licensing boards to develop disciplinary measures for physicians who provide fraudulent testimony.
The House of Delegates adopted an amended version of the report. See Michael Higgins, Docking
Doctors? AMA Eyes Discipline for Physicians Giving ‘False’ Testimony, A.B.A. J., Sept. 1998, at 20.
38. Jeoffrey K. Stross & Thomas J. DeKornfeld, A Formal Audit of Continuing Medical Education
Activity for License Renewal, 264 JAMA 2421 (1990) (audit of continuing medical education activities of
licensed in Michigan to assess compliance with a law mandating participation in 150 hours of
continuing medical education every three years).
39. Chouteau v. Enid Mem’l Hosp., 992 F.2d 1106, 1109 & n.2 (10th Cir. 1993) (upholding the
district court’s grant of summary judgment, finding that sufficient justification existed for the defendant
hospital to lawfully terminate the plaintiff’s staff privileges).
40. See Alvan R. Feinstein, Clinical Judgment 21 (photo. reprint 1985) (1967).
41. Treating physicians are generally permitted to testify, although contentions are sometimes made
that their testimony should be limited. In Holbrook v. Lykes Bros. Steamship Co., 80 F.3d 777 (3d Cir.
1995), the trial court had excluded the treating physician’s testimony on his diagnosis of mesothelioma
and a pathology report because the physician was not a pathologist or oncologist. The Third Circuit
reversed the decision, noting that treating physicians’ testimony is often given greater weight than
testimony from physicians who have not examined the patient. Id. at 782–83.
42. Howard Hu & Frank E. Speizer, Influence of Environmental and Occupational Hazards on Disease,
in 1 Harrison’s Principles of Internal Medicine 18, 19 (Anthony S. Fauci et al. eds., 14th ed. 1998)
[hereinafter Principles of Internal Medicine].
43. See infra § IV and accompanying footnotes.
44. Elliot M. Antman & Eugene Braunwald, Acute Myocardial Infraction, in 1 Principles of Internal
Medicine, supra note 42, at 1352, 1352–53. In this guide, the term internal is used to refer to causal
factors and conditions internal to the patient’s body, such as genetic predisposition to coronary artery
disease, to distinguish them from causal factors that are external to the body, such as smoking and diet.
45. For a general discussion of the process used to infer internal and external causation, see Feinstein,
supra note 40, at 80–83. See, e.g., Carroll v. Morgan, 17 F.3d 787, 791 (5th Cir. 1994) (discussing
multiple causes of plaintiff’s coronary disease).
may be warranted, arriving at a diagnosis, and recommending an appropriate
46. See, e.g., Fiore v. Consolidated Freightways, 659 A.2d 436 (N.J. 1995) (truck driver’s workers’
compensation case claiming that his heart disease was caused by occupational exposure to carbon monoxide
fumes remanded so that parties could provide more reliable exposure evidence).
47. See Cullen et al., supra note 19, at 220–21.
48. See Jerome P. Kassirer & Richard I. Kopelman, Learning Clinical Reasoning 4 (1991).
49. Barbara Bates et al., A Guide to Physical Examination and History Taking 2–3 (6th ed. 1995).
51. Office of Tech. Assessment, U.S. Congress, Reproductive Health Hazards in the Workplace
app. B at 365 (1985).
52. See, e.g., Bates et al., supra note 49, at 3–7, 16–17.
53. See, e.g., id. at 637–39.
54. See Thomas E. Andreoli et al., Cecil Essentials of Medicine 152 (3d ed. 1993).
55. See, e.g., Bates et al., supra note 49, at 635, 645–47.
56. See Anthony S. Fauci et al., The Practice of Medicine, in 1 Principles of Internal Medicine, supra
note 42, at 1, 2; Lee Goldman, Quantitative Aspects of Clinical Reasoning, in 1 Principles of Internal
Medicine, supra note 42, at 9, 9.
57. See Hu & Speizer, supra note 42, at 19; Environmental Medicine: Integrating a Missing Element
into Medical Education 5–11 (Andrew M. Pope & David P. Rall eds., 1995).
58. Establishing exposure is usually deemed necessary to a plaintiff’s toxic injury claim, and the
existence or degree of exposure to the agent is often at issue. See, e.g., In re Paoli R.R. Yard PCB Litig.,
916 F.2d 829 (3d Cir. 1990) (environmental exposure to polychlorinated biphenyls (PCBs) contested),
cert. denied, 499 U.S. 961 (1991).
59. See Hu & Speizer, supra note 42, at 19; Frank E. Speizer, Environmental Lung Diseases, in 2
Principles of Internal Medicine, supra note 42, at 1429, 1429–30; Peter Casten, Jr., & Katherine Loftfield,
The Eyes and Vision, in Environmental Medicine, supra note 19, at 240, 242. Exposure to chemical
agents typically found in certain work environments can sometimes be inferred based on industrial
hygiene studies of particular occupations. For example, employment as an asbestos insulator has been
associated with significant levels of asbestos exposure.
60. For the effect of exercise, see, e.g., Joseph D. Brain et al., The Effects of Exercise on Inhalation of
Particles and Gases, in Variations in Susceptibility to Inhaled Pollutants: Identification, Mechanisms, and
Policy Implications 204, 210 (Joseph D. Brain et al. eds., 1988); for other variables affecting an individual’s
exposure and response to inhaled gases or particles, see, e.g., Speizer, supra note 59, at 1430.
61. See Bates et al., supra note 49, at 16–19; Speizer, supra note 59, at 1429–30.
62. Courts sometimes attach importance to the physician–witness’s examination of the patient. See,
e.g., In re Paoli R.R. Yard PCB Litig., 35 F.3d 717, 771 (3d Cir. 1994) (physician’s testimony on
causation admitted as to patients the witness examined), cert. denied, 513 U.S. 1190 (1995); In re “Agent
Orange” Prod. Liab. Litig., 611 F. Supp. 1223, 1235, 1243–47 (E.D.N.Y. 1985), aff’d, 818 F.2d 187
(2d Cir. 1987), cert. denied, 487 U.S. 1234 (1988). Courts have also recognized that physicians may
present testimony based on examinations and tests performed by others, as well as on medical records.
See, e.g., Kannankeril v. Terminix Int’l, Inc., 128 F.3d 802, 809 (3d Cir. 1997); Sementilli v. Trinidad
Corp., 155 F.3d 1130 (9th Cir.) (per curiam) (physician could present testimony on plaintiff’s condition
based on medical records and knowledge, experience, training, and education), dissenting opinion amended,
162 F.3d 1015 (9th Cir. 1998).
63. See Swartz, supra note 50, at 667.
64. See, e.g., Feinstein, supra note 40, at 2.
65. See Fauci et al., supra note 56, at 2.
66. See Bates et al., supra note 49, at 118–21.
67. Id. at 117.
68. Id. at 649–52.
69. See, e.g., Dan L. Longo, Approach to the Patient with Cancer, in 1 Principles of Internal Medicine,
supra note 42, at 493, 494.
70. See Steven E. Weinberger & Jeffrey M. Drazen, Diagnostic Procedures in Respiratory Disease, in 2
Principles of Internal Medicine, supra note 42, at 1417, 1418.
71. See Matthew E. Levinson, Pneumonia, Including Necrotizing Pulmonary Infections (Lung Abscess), in
2 Principles of Internal Medicine, supra note 42, at 1437, 1440.
72. See Kassirer & Kopelman, supra note 48, at 217–22.
73. See infra note 105 and accompanying text.
74. See infra notes 107–108 and accompanying text.
75. See Fauci et al., supra note 56, at 3; Goldman, supra note 56, at 10; Kassirer & Kopelman, supra
note 48, at 23.
76. See Christopher H. Linden & Frederick H. Lovejoy, Jr., Poisoning and Drug Overdose, in 2
Principles of Internal Medicine, supra note 42, at 2523, 2523–25.
77. Certain persistent toxic agents can sometimes be detected in laboratory tests. See, e.g., Hose v.
Chicago Northwestern Transp. Co., 70 F.3d 968 (8th Cir. 1995) (laboratory tests showed elevated
manganese in plaintiff’s body; MRI indicated manganese in brain). The interpretation of such tests has
been at issue in a number of cases. See, e.g., In re Paoli R.R. Yard PCB Litig., 35 F.3d 717 (3d Cir.
1994) (dispute over whether PCB levels in plaintiffs’ adipose tissue exceeded background levels), cert.
denied, 513 U.S. 1190 (1995); Wright v. Willamette Indus., Inc., 91 F.3d 1105 (8th Cir. 1996) (presence
of wood dust fibers at plaintiffs’ residence and in tissue samples insufficient to establish exposure to
formaldehyde at levels known to cause plaintiffs’ symptoms).
78. See Cullen et al., supra note 19, at 223–24. For an overview of available blood tests, fluid
analysis studies, and urinalyses, see, e.g., Kathleen Deska Pagana & Timothy James Pagana, Mosby’s
Manual of Diagnostic and Laboratory Tests 7–9, 557, 859–73 (1998).
79. See Fauci et al., supra note 56, at 3; for uses of laboratory tests in environmental disease, see
Cullen et al., supra note 19, at 222–23 and Arthur Frank, The Environmental History, in Environmental
Medicine, supra note 19, at 232. See also In re Paoli R.R. Yard PCB Litig., 916 F.2d 829 (3d Cir. 1990),
cert. denied, 499 U.S. 961 (1991).
80. For a case involving the use of laboratory tests in diagnosis, see Cella v. United States, 998 F.2d
418 (7th Cir. 1993).
81. See, e.g., Linden & Lovejoy, supra note 76, at 2523.
82. See Cullen et al., supra note 19, at 223.
83. See id. at 228. For an example of laboratory tests used to rule out alternative diagnoses and
causes, see Hose v. Chicago Northwestern Transportation Co., 70 F.3d 968, 973, 975 (8th Cir. 1995)
(supporting a diagnosis of manganese encephalopathy, medical witnesses cited a positron emission tomography
(PET) scan to rule out alcoholism, stroke, and Alzheimer’s disease, and an MRI to exclude
copper, calcium, and other harmful exposures).
84. Cullen et al., supra note 19, at 223.
85. For specific examples, see Ivan Damjanov, Histopathology: A Color Atlas and Textbook 23–
24, 36, 58, 64 (1996).
86. See Bernard D. Goldstein & Mary Sue Henifin, Reference Guide on Toxicology § IV, in this
manual.
87. See Howard Hu, Heavy Metal Poisoning, in 2 Principles of Internal Medicine, supra note 42, at
2564, 2565–66.
88. For specific tests of pulmonary, nerve and muscle function, and electrocardiography, respectively,
see Pagana & Pagana, supra note 78, at 1016–21, 490–92, 486–89, 478–82.
89. See infra § IV and accompanying footnotes.
90. Kassirer & Kopelman, supra note 48, at 2.
91. See Cullen et al., supra note 19, at 217.
92. See Hu & Speizer, supra note 42, at 19, 20.
93. For an example of how a symptom may be common to a number of diseases, compare Jeffrey
A. Gelfand & Charles A. Dinarello, Fever and Hyperthermia, in 1 Principles of Internal Medicine, supra
note 42, at 84, 88 tbl.17-1; Elaine T. Kaye & Kenneth M. Kaye, Fever and Rash, in 1 Principles of
Internal Medicine, supra note 42, at 90, 91–96 tbl.18-1; Robert B. Daroff & Joseph B. Martin, Faintness,
Syncope, Dizziness, and Vertigo, in 1 Principles of Internal Medicine, supra note 42, at 100, 100
tbl.20-1; Patrick T. O’Gara & Eugene Braunwald, Approach to the Patient with a Heart Murmur, in 1
Principles of Internal Medicine, supra note 42, at 198, 199 tbl. 34-1.
94. See, e.g., Khalida Ismail et al., Is There a Gulf War Syndrome?, 353 Lancet 179, 179 (1999) (“For
an illness to be recognised as a new disorder it must be sufficiently different from other recognised
disorders . . . . There is no formal process to investigate whether a set of symptoms are unique to a new
illness.”). For an explication of several methods that can be used to determine whether a new disease
entity exists, see also David H. Wegman et al., Invited Commentary: How Would We Know a Gulf War
Syndrome If We Saw One?, 146 Am. J. Epidemiology 704 (1997).
95. The recognition of multiple-chemical sensitivity as a disease was at issue in Zwillinger v. Garfield
Slope Housing Corp., No. CV 94-4009, 1998 WL 623589 (E.D.N.Y. Aug. 17, 1998). See also Howard
M. Kipen & Nancy Fiedler, Invited Commentary: Sensitivities to Chemicals—Context and Implications, 150
Am. J. Epidemiology 13 (1999).
96. For example, dementia is a syndrome of impaired memory, thinking, language, and judgment
(all of which are symptoms that can actually also be measured as signs) related to destruction or malfunction
of specific parts of the brain. In congestive heart failure, shortness of breath (symptom), trouble
lying down flat (symptom), swollen ankles (symptom or sign), weight gain (sign), swollen neck veins
(sign), crackling noises heard in the lungs (sign), and galloping heart sounds (sign) are attributable to one
pathophysiological dysfunction—inadequate pumping of blood by the heart. In Cushing’s syndrome,
an abnormally round face (moon face), diabetes mellitus (high blood sugar causing a syndrome of its
own), bone thinning (osteoporosis), and high blood pressure are all due to excessive amounts of certain
hormones, glucocorticoids, resulting from either excess glandular secretion by the body or overuse as a
medication. Fauci et al., supra note 56, at 3.
97. See Stedman’s Medical Dictionary 474 (26th ed. 1995) (definition of differential diagnosis); Kassirer
& Kopelman, supra note 48, at 16.
98. Diagnosis is at issue in many kinds of cases, including medical malpractice and other personal
injury claims. See, e.g., Bates et al., supra note 49, at 635–48; Samuels v. Secretary of Dep’t of Health &
Human Servs., No. 91-127V, 1995 WL 809884 (Fed. Cl. Aug. 1, 1995) (diagnosis of a neurological
disorder at issue in claim under the National Vaccine Injury Compensation Program); Alex v. Dr. X,
692 So. 2d 499 (La. Ct. App. 1997) (diagnosis of tuberculosis at issue).
99. See Kassirer & Kopelman, supra note 48, at 7; Bates et al., supra note 49, at 637–38.
100. See Kassirer & Kopelman, supra note 48, at 9; Bates et al., supra note 49, at 646–47.
101. See Kassirer & Kopelman, supra note 48, at 11, 32–33.
102. See id. at 32–33.
103. See id.
104. See id. at 16; Bates et al., supra note 49, at 635–74.
105. See Bates et al., supra note 49, at 641; Goldman, supra note 56, at 10–11; Kassirer & Kopelman,
supra note 48, at 18–19; Michael D. Green et al., Reference Guide on Epidemiology § V.H, and David
H. Kaye & David A. Freedman, Reference Guide on Statistics §§ III.A.3, IV.B.2, IV.C, in this manual.
106. See Bates et al., supra note 49, at 645–46.
107. “Positive predictive value” is the frequency of disease among patients with positive results,
and “negative predictive value” is the frequency of absence of disease among individuals with negative
test results. For a test with a given sensitivity and specificity, positive predictive value is higher when a
condition is common in a population, and negative predictive value is higher when the condition is
rare. Bates et al., supra note 49, at 642. See also David H. Kaye & David A. Freedman, Reference Guide
on Statistics §§ III.A.3, IV.C, in this manual.
108. See Swartz, supra note 50, at 675–76 & fig.25-3. See generally David H. Kaye & David A.
Freedman, Reference Guide on Statistics § IV.D, app., in this manual.
109. The positive predictive value of a symptom of chest pain for a heart attack is very low in a 25-
year-old because advanced atherosclerotic cardiovascular disease is rare in this age group and other
causes of chest pain are more common. Similarly, interstitial fibrosis on a chest x-ray, whatever the xray’s
sensitivity and specificity for a true underlying finding of pathologic fibrosis, has a much higher
predictive value for a diagnosis of asbestosis in a person known to come from an asbestos-exposed
population than in someone with no known occupational exposure to asbestos.
110. See Kassirer & Kopelman, supra note 48, at 19–24; Steven N. Goodman, Toward Evidence-
Based Medical Statistics. 2: The Bayes Factor, 130 Annals Internal Med. 1005, 1011 (1999).
111. For a somewhat different illustration of the interaction of such factors, see Cullen et al., supra
note 19, at 230 fig.18-2.
112. Many cases involving issues of external causation have involved witnesses who testify to having
arrived at an opinion on cause through a process of ruling out or eliminating other causes, a process
frequently referred to by the courts and witnesses as “differential diagnosis” or “differential etiology”
(for explanation of the differences between medical and legal uses of terminology, see section I.B.,
supra). Not infrequently, this form of testimony is implicitly or explicitly offered to satisfy the applicable
burden of proof on causation. The relationship between the “more probable than not burden of proof”
and “differential diagnosis” was discussed in Cavallo v. Star Enterprise, 892 F. Supp. 756 (E.D. Va. 1995),
aff’d in part, rev’d in part, 100 F.3d 1150 (4th Cir. 1996), cert. denied, 522 U.S. 1044 (1998), a case in
which the witness opined on whether a spill of aircraft fuel caused the plaintiff’s rash. The court explained,
“The process of differential diagnosis is undoubtedly important to the question of ‘specific
causation.’ If other possible causes of an injury cannot be ruled out, or at least the probability of their
contribution to causation minimized, then the ‘more likely than not’ threshold for proving causation
may not be met.” Id. at 771 (footnote omitted).
Courts differ on whether opinion based on such “differential diagnosis” or “differential etiology” of
cause is admissible. Compare Westberry v. Gummi, 178 F.3d 257, 263 (4th Cir. 1999) (reliable “differential
diagnosis” provides a valid basis for an expert opinion), Anderson v. Quality Stores, Inc., 181
F.3d 86 (4th Cir. 1999) (per curiam) (opinion on spray paint causing pulmonary problems should have
been admitted based on “differential diagnosis” and temporal relationship), In re Paoli R.R. Yard PCB
Litig., 35 F.3d 717 (3d Cir. 1994) (approving opinion based on “differential diagnosis”), cert. denied, 513
U.S. 1190 (1995), McCullock v. H.B. Fuller Co., 61 F.3d 1038, 1042–44 (2d Cir. 1995) (accepting
opinion based on “differential etiology”), and Zuchowicz v. United States, 140 F.3d 381, 387–91 (2d
Cir. 1998) (accepting witness’s “differential etiology” opinion of causes of pulmonary hypertension),
with Raynor v. Merrell Pharms., Inc., 104 F.3d 1371, 1375–76 (D.C. Cir. 1997) (“differential diagnosis”
of cause of birth defect inadmissible where general causation proof absent), Cavallo v. Star Enter.,
892 F. Supp. 756, 771–73 (E.D. Va. 1995) (“differential diagnosis” of cause inadmissible where general
causation not established), aff’d in part, rev’d in part, 100 F.3d 1150 (4th Cir. 1996), cert. denied, 522 U.S.
1044 (1998), Hall v. Baxter Healthcare Corp., 947 F. Supp. 1387, 1412–14 (D. Or. 1996) (“differential
diagnosis” and specific causation require proof of general causation; witness did not explain how he
ruled out other causes), Haggerty v. Upjohn Co., 950 F. Supp. 1160, 1166–67 (S.D. Fla. 1996) (“differential
diagnosis” testimony inadmissible where another cause could explain all of plaintiff’s symptoms),
aff’d, 158 F.3d 588 (11th Cir. 1998) (unpublished table decision), and Austin v. Children’s Hosp.
Med. Ctr., 92 F.3d 1185 (6th Cir. 1996) (unpublished table decision) (text at No. 95-3880, 1996 WL
422484, at *3 (6th Cir. July 26, 1996)) (expert unable to show that defendant, rather than other sources,
“more likely than not” infected plaintiff’s son with fatal virus).
113. See, e.g., Herbert Y. Reynolds, Interstitial Lung Disease, in 2 Principles of Internal Medicine,
supra note 42, at 1460, 1460–63 & tbl.259-1.
114. For a discussion of the difficulty of establishing causation, see Feinstein, supra note 40, at 266–74.
115. However, exceptions may be cited, including the need to determine if there is a genetic
(familial) risk of cancer that may require notification and screening of family members (e.g., certain
forms of colon cancer and breast cancer), or if other family members or workers may be at remediable
risk.
116. See, e.g., Howard Hu & Frank E. Speizer, Specific Environmental and Occupational Hazards, in 2
Principles of Internal Medicine, supra note 42, at 2521, 2521–22; Linden & Lovejoy, supra note 76, at
2523–25; Hu, supra note 87, at 2565–67.
117. See, e.g., peer review case studies published by the Agency for Toxic Substances and Disease
Registry (ATSDR), a branch of the Centers for Disease Control and Prevention. For the most part,
these case studies discuss the diagnosis and treatment of environmental illness, and in a number of
instances discuss the reasoning involved in assessing the causal role of an environmental exposure.
Selected ATSDR case studies are included in Environmental Medicine: Integrating a Missing Element
into Medical Education, supra note 57, at app. C.
118. See Eric G. Honig & Ronald H. Ingram, Jr., Chronic Bronchitis, Emphysema, and Airways Obstruction,
in 2 Principles of Internal Medicine, supra note 42, at 1451, 1452.
119. In a working patient, the contribution of workplace conditions may be taken into account in
advising the patient on the advisability of returning to or remaining in the work environment if there
are conditions present that may exacerbate the patient’s respiratory condition. Id. at 1456.
120. See, e.g., Fiore v. Consolidated Freightways, 659 A.2d 436 (N.J. 1995).
121. See Cullen et al., supra note 19, at 224.
122. The courts vary in the degree of certainty they require in exposure estimates. Many courts
accept exposure evidence as sufficient without proof of specific levels. See, e.g., Kannankeril v. Terminix
Int’l, Inc., 128 F.3d 802, 808–09 (3d Cir. 1997). Other courts have required more particularized proof.
See, e.g., Curtis v. M&S Petroleum, Inc., 174 F.3d 661, 671–72 (5th Cir. 1999) (exposure evidence
sufficient for opinion on causation where expert testified that refinery workers were exposed to at least
100 parts per million (ppm), and probably several hundred ppm, of benzene). Based on these measurements,
Curtis distinguishes another Fifth Circuit case, Moore v. Ashland Chemical, Inc., 151 F.3d 269 (5th
Cir. 1998) (en banc), cert. denied, 119 S. Ct. 1454 (1999), in which exposure evidence was found
insufficient to support an opinion on causation because the expert had a “‘paucity of facts’” on which to
base an opinion and did not testify to any specific levels of exposure. 174 F.3d at 670 (quoting Moore,
151 F.3d at 279 n.10). Exposure levels have been at issue in a number of other cases. See, e.g., In re Paoli
R.R. Yard PCB Litig., 916 F.2d 829 (3d Cir. 1990), cert. denied, 499 U.S. 961 (1991); In re “Agent
Orange” Prod. Liab. Litig., 611 F. Supp. 1223 (E.D.N.Y. 1985), aff’d, 818 F.2d 187 (2d Cir. 1987), cert.
denied, 487 U.S. 1234 (1988).
123. See Speizer, supra note 59, at 1431–32.
124. An appropriate temporal relationship—the time that elapsed between exposure and onset of
disease or symptoms—is a necessary but often insufficient basis for an opinion on causation. Courts
frequently warn against reasoning based on the premise “post hoc, ergo propter hoc.” See, e.g., Whiting v.
Boston Edison Co., 891 F. Supp. 12, 23 n.52 (D. Mass. 1995) (rejecting opinion on cause of acute
lymphocytic leukemia following radiation exposure). In some cases, courts have permitted opinions on
causation based primarily on temporal proximity between exposure and development of the disease,
but many of these cases involved symptoms or diseases that closely followed the exposure asserted to be
the cause. See, e.g., Curtis v. M&S Petroleum, Inc., 174 F.3d 661, 670 (5th Cir. 1999); Anderson v.
Quality Stores, Inc., 181 F.3d 86 (4th Cir. 1999) (unpublished table decision) (text at No. 98-2240,
1999 WL 387827, at *2 (4th Cir. June 14, 1999) (per curiam)). Other courts have excluded opinions on
causation based primarily on temporal proximity. In Moore v. Ashland Chemical, Inc., 151 F.3d 269, 278
(5th Cir. 1998) (en banc), cert. denied, 119 S. Ct. 1454 (1999), for example, the Fifth Circuit found that
the expert’s reliance on the temporal relationship between the exposure and the onset of symptoms was
entitled to little weight in the absence of supporting medical literature. See also Rosen v. Ciba-Geigy
Corp., 78 F.3d 316, 319 (7th Cir.) (rejecting expert testimony on nicotine patch as cause of heart attack
that occurred after three days of wearing patch), cert. denied, 519 U.S. 819 (1996); Porter v. Whitehall
Labs., Inc., 9 F.3d 607, 614 (7th Cir. 1993) (rejecting clinical observations and temporal relationship
between drug ingestion and renal failure as bases for opinion on causation where scientific studies
unavailable). On occasion, a temporal relationship that does not fit the expected pattern may be a basis
for ruling out the suspected cause. See, e.g., Heller v. Shaw Indus., Inc., 167 F.3d 146, 157–58 (3d Cir.
1999) (temporal relationships may be important in supporting an opinion on causation, but expert’s
reliance on temporal relationship is flawed in this case). See generally Speizer, supra note 59, at 1429–36;
Honig & Ingram, supra note 118, at 1452, 1456.
125. See Cullen et al., supra note 19, at 227.
126. The courts differ on the question whether the witness giving an opinion on causation must
support his or her opinion with references to medical or scientific studies supporting a causal link
between the toxic exposure and the plaintiff’s disease. A number of courts have answered this question
in the affirmative. See, e.g., Moore v. Ashland Chem., Inc., 151 F.3d 269, 277–78 (5th Cir. 1998) (en
banc), cert. denied, 119 S. Ct. 1454 (1999); Rosen v. Ciba-Geigy Corp., 78 F.3d 316, 319 (7th Cir.)
(witness cited no scientific or medical literature, or other explanation of asserted causal relationship
between nicotine patch and heart attack), cert. denied, 519 U.S. 819 (1996); Porter v. Whitehall Labs.,
Inc., 9 F.3d 607, 615 (7th Cir. 1993) (medical literature did not establish link between ibuprofen and
plaintiff’s kidney ailment; medical theories had not been tested). Other courts have upheld the admission
of medical opinion based solely on clinical observations and reasoning, sometimes with reference
to the physician’s experience with similar kinds of patients or cases. See, e.g., Heller v. Shaw Indus.,
Inc., 167 F.3d 146, 153–57 (3d Cir. 1999); Westberry v. Gummi, 178 F.3d 257, 262–66 (4th Cir.
1999) (affirmed trial court’s admission of expert testimony on talc as cause of plaintiff’s sinus problems
despite absence of supporting medical literature); Fadelalla v. Secretary of the Dep’t of Health & Human
Servs., No. 97-05730, 1999 WL 270423, at *6 (Fed. Cl. Apr. 15, 1999) (while clinical experience
may be sufficient to establish causal relationship, in this case expert had insufficient clinical experience
on which to base an opinion on causation); Becker v. National Health Prods., Inc., 896 F. Supp. 100,
103 (N.D.N.Y. 1995) (absence of published literature on relationship between diet supplement and
diverticulosis not fatal to plaintiff’s case where expert relied on “differential etiology”).
127. See Michael D. Green et al., Reference Guide on Epidemiology, §§ V–VII, and Bernard D.
Goldstein & Mary Sue Henifin, Reference Guide on Toxicology, §§ III–V, in this manual.
128. See Michael Gochfeld, Asbestos Exposure in Buildings, in Environmental Medicine, supra note
19, at 438, 440.
129. See Michael Gochfeld, Chemical Agents, in Environmental Medicine, supra note 19, at 592,
600 (vinyl chloride); Howard M. Kipen & Daniel Wartenberg, Lymphohematopoietic Malignancies, in
Textbook of Clinical Occupational and Environmental Medicine 555, 560 (Linda Rosenstock & Mark
R. Cullen eds., 1994) (benzene).
130. Kristin E. Anderson et al., Pancreatic Cancer, in Cancer Epidemiology and Prevention 725,
740–41 (David Schottenfeld & Joseph F. Fraumeni, Jr., eds., 2d ed. 1996); Debra T. Silverman et al.,
Bladder Cancer, in Cancer Epidemiology and Prevention, supra, at 1156, 1165–66.
Reference Guide on Medical Testimony
475
131. See generally Michael D. Green et al., Reference Guide on Epidemiology § II.A, in this manual.
132. See Cullen et al., supra note 19, at 226. Courts have given varying treatment to case reports.
Compare Haggerty v. Upjohn Co., 950 F. Supp. 1160, 1165 (S.D. Fla. 1996) (case reports are “no
substitute for a scientifically designed and conducted inquiry” (citing Casey v. Ohio Med. Prods., 877
F. Supp. 1380, 1385 (N.D. Cal. 1995))), aff’d, 158 F.3d 588 (11th Cir. 1998) (unpublished table decision),
and Hall v. Baxter Healthcare Corp., 947 F. Supp. 1387, 1411 (D. Or. 1996) (case reports
“cannot be the basis of an opinion based on scientific knowledge”), with Pick v. American Med. Sys.,
Inc., 958 F. Supp. 1151, 1160–62, 1178 (E.D. La. 1997) (case studies on gel implants admissible in case
on penile implant; theory developed by single physician not admissible), Glaser v. Thompson Med.
Co., 32 F.3d 969, 975 (6th Cir. 1994) (ordering trial based on witness who relied on case reports and his
own research in rendering opinion on diet pills as cause of intracranial bleeding and fall), and Cella v.
United States, 998 F.2d 418, 426 (7th Cir. 1993) (in claim under Jones Act, medical opinion on cause
of polymyositis based in part on case reports).
133. See Michael Gochfeld, Principles of Toxicology, in Environmental Medicine, supra note 19, at 65, 71–72.
134. See Cullen et al., supra note 19, at 228–29.
135. Some courts have stated that the plaintiff must offer a “differential diagnosis” to rule out other
causes, whereas other courts have rejected such a requirement. Compare Wheat v. Pfizer, Inc., 31 F.3d
340, 342 (5th Cir. 1994) (witness failed to rule out hepatitis C and another drug as causes of plaintiff’s
liver disease), Mancuso v. Consolidated Edison Co., 967 F. Supp. 1437, 1446 (S.D.N.Y. 1997) (“differential
diagnosis” required to rule out other possible causes; plaintiff’s complaints were commonplace
ailments), and National Bank of Commerce v. Dow Chem. Co., 965 F. Supp. 1490 (E.D. Ark. 1996)
(case dismissed because, inter alia, plaintiffs failed to exclude other causes), aff’d, 133 F.3d 1132 (8th Cir.
1998), with Curtis v. M&S Petroleum, Inc., 174 F.3d 661, 670–72 (5th Cir. 1999) (rejecting requirement
of “differential diagnosis” to rule out other causes), and Heller v. Shaw Indus., Inc., 167 F.3d 146,
153–57 (3d Cir. 1999) (existence of possible alternative causes goes to weight, not admissibility).
136. Occupational asbestos exposure in nonsmokers increases the risk of lung cancer by a factor of
about five, from about 11 per 100,000, for nonsmoking industrial workers not exposed to asbestos to
about 58 per 100,000 for nonsmoking asbestos workers; a significant smoking history increases the rate
of lung cancer by a factor of at least ten. See U.S. Surgeon Gen., U.S. Dep’t of Health & Human Servs.,
The Health Consequences of Smoking: Cancer and Chronic Lung Disease in the Workplace 216
(1985); see also Rodolfo Saracci, The Interactions of Tobacco Smoking and Other Agents in Cancer Etiology, 9
Epidemiologic Revs. 175, 176–80 (1987). Because the effects of smoking and asbestos are multiplicative
for lung cancer, the population of smoking asbestos workers has a lung cancer incidence of 5 times
10, or 50 times the background rates, rather than the 15-fold increase predicted by adding the separate
risks. See U.S. Surgeon Gen., U.S. Dep’t of Health & Human Servs., supra, at 216–17.
137. See Gochfeld, supra note 133, at 73.
138. For example, both occupational asthma and smoking can lead to impairment of pulmonary
function, and the presence of one does not rule out a causal role for the other. See John H. Holbrook,
Nicotine Addiction, in 2 Principles of Internal Medicine, supra note 42, at 2516, 2518; E.R. McFadden,
Jr., Asthma, in 2 Principles of Internal Medicine, supra note 42, at 1419, 1419–21. Cf. Wheat v. Pfizer,
Inc., 31 F.3d 340 (5th Cir. 1994), which involved a victim who died of hepatitis after taking two drugs
known to cause liver damage. As to her claim against Pfizer, the manufacturer of one of the drugs, the
court found the evidence inadequate, in part, for failing to exclude the possibility that her disease was
caused by the other drug. Id. at 343. The plaintiff’s witness offered the possibility that the hepatitis
resulted from the combined action of the two drugs, which the court rejected because the witness cited
no study of the combined effects of the drugs. Id. The court also faulted the plaintiff for failing to rule
out hepatitis C as a cause of the liver damage, though there was no test for the condition at that time. Id.
at 342. But see Benedi v. McNeil-PPC, Inc., 66 F.3d 1378, 1384 (4th Cir. 1995) (upholding plaintiff’s
recovery for liver damage caused by Tylenol and alcohol consumption).
139. The problem of unidentified risks (often termed “background cases of unknown etiology”)
has been recognized in a number of decisions. For example, in In re Breast Implant Litigation, 11 F. Supp.
2d 1217 (D. Colo. 1998), the court disapproved of a physician’s identification of silicone as the cause of
the plaintiff’s disease through “differential diagnosis,” stating: “As a practical matter, the cause of many
diseases remains unknown; therefore, a clinician who suspects that a substance causes a disease in some
patients very well might conclude that the substance caused the disease in the plaintiff simply because
the clinician has no other explanation.” Id. at 1230. See also National Bank of Commerce v. Dow
Chem. Co., 965 F. Supp. 1490 (E.D. Ark. 1996) (rejecting testimony that pesticide caused birth defect
where witness acknowledged that causes are unknown for 70% to 80% of birth defects), aff’d, 133 F.3d
1132 (8th Cir. 1998); Whiting v. Boston Edison Co., 891 F. Supp. 12 (D. Mass. 1995) (in case alleging
radiation caused power plant worker’s acute lymphocytic leukemia, witness’s acknowledgement that
90% of cases are of unknown cause cast doubt on “differential diagnosis” of cause); In re “Agent Orange”
Prod. Liab. Litig., 611 F. Supp. 1223, 1250 (E.D.N.Y. 1985) (“Central to the inadequacy of
plaintiffs’ case is their inability to exclude other possible causes of plaintiffs’ illnesses—those arising out
of their service in Vietnam as well as those that all of us face in military and civilian life.”), aff’d, 818
F.2d. 187 (2d Cir. 1987), cert. denied, 487 U.S. 1234 (1988). The plaintiff may be able to rely on
inferences from epidemiological, toxicological, or other evidence, however. See Michael D. Green et
al., Reference Guide on Epidemiology, and Bernard D. Goldstein & Mary Sue Henifin, Reference
Guide on Toxicology, in this manual; In re Hanford Nuclear Reservation Litig., No. CV-91-3015-
AAM, 1998 WL 775340 (E.D. Wash. Aug. 21, 1998).
140. This kind of reasoning is discussed in In re Paoli Railroad Yard PCB Litigation, 35 F.3d 717, 760
n.30 (3d Cir. 1994), cert. denied, 513 U.S. 1190 (1995).
141. See Stuart M. Brooks et al., Types and Sources of Environmental Hazards, in Environmental
Medicine, supra note 19, at 9, 15–17; Daniel W. Nebert et al., Genetic Epidemiology of Environmental
Toxicity and Cancer Susceptibility: Human Allelic Polymorphisms in Drug-Metabolizing Enzyme Genes, Their
Functional Importance, and Nomenclature Issues, 31 Drug Metabolism Revs. 467 (1999); Maurizio Taningher
et al., Drug Metabolism Polymorphisms as Modulators of Cancer Susceptibility, 436 Mutation Res. 227 (1999).
142. See Karen Reiser, General Principles of Susceptibility, in Environmental Medicine, supra note 19,
at 351, 351–52, 358.
143. See id. at 357.
144. See Kassirer & Kopelman, supra note 48, at 11, 32–33.
145. A physician’s selection of appropriate treatment is often at issue in medical malpractice cases
(see supra notes 31–32 and accompanying text), but it also is at issue in other kinds of cases, including
claims that medical treatment was “necessary” and therefore covered in insurance litigation under
ERISA (see, e.g., McGraw v. Prudential Ins. Co., 137 F.3d 1253, 1258–1263 (10th Cir. 1998)), claims
that treatment was improperly withheld from prisoners under the Eighth Amendment (see, e.g., Kulas v.
Roberson, 202 F.3d 278 (9th Cir. 1999) (unpublished table decision) (text at No. 98-16954, 1999 WL
1054663 (9th Cir. Nov. 19, 1999) (mem.)), and medical monitoring claims (see, e.g., In re Paoli R.R.
Yard PCB Litig., 916 F.2d 829, 852 (3d Cir. 1990), cert. denied, 499 U.S. 961 (1991)).
146. See supra note 30.
天戈 wrote:
来源:美国最高法院，为美国联邦法院审判的指南，相当于我们的司法解释。
评价：医师苛求自己的同行，法学界人士却有不同的观点：无九成的把握不成结论。
建议：１、斑竹征求全文翻译。２、值得琢磨其中的道理。
我们版块好像从来没有搞过翻译活动，这次借天戈先生的东风，想搞个翻译活动，不知道大家干不感兴趣，请大家发表一下意见，如何分工，如何校对，如何评论，如何加分，时限如何？
谢谢天戈先生提供的文本，根据他给我的文件，我把医学部分做成新的PDF文件，大家看起来可能舒服些。
Reference Guide on Medical Testimony.pdf (159.57k)
原始PDF文档
Reference Guide on Medical Testimony.rar (164.85k)
谢谢大伟主任提供的原文，这是真正原版的，我做的是从全文中自己剪裁的。
我粗看一下，一共46页，不过前三页大概是目录，所以一共40页左右，我只知道耳鼻喉科版块大概5页一分，各位有没有意见？
欢迎外语沙龙的战友参与翻译，各位看看个人翻译字数多少为佳，加分标准如何，不好意思没找到外语沙龙的翻译加分具体标准，各位也可以建议一下。
可以考虑一下...大家也给点意见。
来自外语沙龙，算我一个。
今天翻译活动正式开始招标。
规则：
从正文开始，开头的目录不算（即441页开始），5页一分，跨页段落，原则上归上页，有意义的注解也要翻译。
愿意参加的请跟帖领取，翻译时间定为两周，希望大家守信准时交稿，逾期重新招标。
注意以下几点：
1.直译为主，意译为辅，不要遗漏，按照信、达、雅的顺序和标准要求。
2.自觉有疑问的问题可以在译文中表明，也可以跟帖征求大家的意见。
3.正确使用汉字和标点符号。
4.请翻译好的战友，及时上传，以便加分和修改、审阅！
5.为方便翻译与审阅修订，请大家采用中英文对照的格式，纯文字版通过编辑自己的领取贴张贴出来，并以附件形式附上Word文档。
谢谢您的合作，有意见和建议也可以跟帖。
平时没事做做这个也行，大家一齐来努力，发挥硬骨头精神，把攻坚战做好！
第一个报名，就翻译第一部分吧，441-446。虽然6页，但下面参考文献占据很大部分，勉强算5页如何，主任大人？
谢谢参与！就这样定了。
我先看看天戈23：38发的一段
P452-457
译文见
> ）
For diagnosis of more serious conditions, especially cancer, physicians are taught always to seek a tissue biopsy.69 This is often referred to as a gold standard, because it is regarded as highly accurate or at least the most definitive indicator of a particular condition. For other conditions, the definitive test may be a radiological test (e.g., a pulmonary angiogram for diagnosis of pulmonary embolism) 70 or a microbiological test (e.g., a sputum culture for diagnosis of tuberculosis).
71
Sometimes physicians and patients will be satisfied with a diagnosis even though the gold standard test for that diagnosis was not performed. There may be too much risk associated with such a test (e.g., if it is invasive or involves intentional exposure to a possible allergen), its costs may outweigh the benefit of achieving a more definitive diagnosis, or it may be superfluous because other data are so consistent and convincing.72 As always, the various cost–benefit and risk–benefit equations are interpreted relative to the individual patient, physician, and medical circumstances, as well as institutional capabilities.
In modern medical practice, tests and procedures are critical to confirming
most diagnoses. These include radiological examination, laboratory tests, physiological tests of lung or nerve function, pathological examination of tissue, and invasive diagnostic tests, such as cardiac catheterization. A physician’s decision whether to order a diagnostic test for specified clinical indications should take into consideration expense, risk, accuracy, and predictive value. Tests are limited by their inherent sensitivity and specificity, the fallibility of the instrumentation,and the variation in skills of the individuals who perform or interpret the tests. Error rates for diagnostic tests, as discussed below,73 in terms of sensitivity and specificity are generally available, but the all-important predictive values74 vary with the particular disorder and with the population (i.e., demographics, background rate of disease) on whom the test is performed or the population from which a tested individual is derived. While pathological examination of tissue biopsies is considered the gold standard of diagnostic tests, even it has an error rate.75
In general, laboratory tests do not have a paramount role in establishing the external etiology of many chronic and acute illnesses. Major exceptions to this are microbiological evaluations for causes of infectious diseases, and cases of toxic substance intoxication, such as lead poisoning or alcohol or drug poisoning.76
Depending on the diagnosis being considered and whether the exposure truly leaves a reliable “signature” or “residue,”77 a biopsy may or may not have great utility for exogenous causal diagnosis. Invasive tissue biopsies are not routinely performed for purposes of establishing causation because of the risk involved with the procedure to obtain the tissue. Sometimes such test results are incidentally available because they may have been used to establish the diagnosis, particularly in the case of lung disorders.
1. Laboratory Tests
实验室检查
Laboratory tests are usually tests in which a specimen, usually blood or another
body fluid, is submitted to a laboratory for a chemical or microbiological analysis.
For many of the routine chemical assays for levels of proteins, fats, electrolytes,
enzymes, or hormones in blood, there are established normal ranges for a
given laboratory or test manufacturer, and for given subpopulations (e.g., men
or women, children or adults). The results are interpreted as being either within
or outside of normal limits. Not all deviation from normal limits is pathological,
particularly if the individual is otherwise without complaint. For example, the
results of liver function tests often fluctuate outside of the normal range in those
without liver disease or hepatotoxin exposure. Based on standard statistical techniques
for defining normal ranges, one in twenty test results can be expected to
be abnormal (i.e., outside the normal range) in a healthy individual.78
Common laboratory tests include x-rays, routine blood chemistries, and blood
counts. More specialized tests include computerized axial tomography (CAT)
scans, magnetic resonance imaging (MRIs), and angiograms.79 All of these tests
are used in one of three ways as part of the diagnostic process. The first and most
common use is to clarify a disease process or pathology or pathophysiology.80 A
second and less common use of laboratory tests is for estimation of exposure to
potentially toxic substances. These tests include measures of an agent in the
body (e.g., blood lead levels) or in an excretory product (e.g., urine mercury).
Understanding that such tests only determine exposure and not disease or health
effect is critical.81 A third and fairly uncommon type of laboratory test is used to
substantiate an exposure–effect relationship.82 Many, if not most, such tests are
actually tests of allergic sensitization (e.g., to a metal or other potential cause of
allergic asthma). The expert should be clear about what type of information is
being inferred from a given test and about the basis in the literature for using the
test for that purpose.83
Physicians are taught to think about clinical testing in terms of the clinical
significance (particularly, predictive value) of a given test in a given situation.
Small or inconsistent changes in values do not necessarily indicate a clinically
important effect and should be confirmed by repeat testing before being otherwise
investigated. On the other hand, important effects may not drive an
individual’s values outside of the population reference range. For instance, someone
previously at the upper limit of the normal range exposed to a chlorine leak
might suffer a reduction in rate of airflow. Although the subsequent rate was
within the normal range, it would not be normal in this individual.84 Unfortunately,
baseline data on an individual prior to exposure are usually not available.
Thus, making inferences from other diagnostic and exposure information may
be useful in understanding the impact of exposure on that individual.
2. Pathology Tests
病理学检查
Pathology tests are conducted by taking a sample of body tissue (obtained during
surgery or a biopsy) and submitting it for microscopic evaluation by a specialist
physician (pathologist). The pathologist makes a determination as to whether
the tissue appears normal for the organ from which it was taken. If it does not
appear normal, then a determination of the pattern of abnormality, such as inflammation,
malignancy, or scarring, is sought.85
Sometimes the etiology of the abnormality is apparent, as when special stains
are used for determination of the presence of microorganisms that can cause a
given infection. On the other hand, most cancers, whether of lung or breast or
bone marrow, have no features that allow the histopathologist to discern a toxic,
viral, or hereditary etiology. Clues from molecular biology analysis have been
experimentally reported, but are not yet available clinically.86
Pathology, typically felt to be the gold standard, often is found wanting when
external etiology needs to be determined. Some conditions, such as neuropsychiatric
diseases that may be related to metal or solvent exposure, do not have
established pathological abnormalities.87
3. Clinical Tests
临床表现
Clinical tests are physiological determinations of organ function. Common examples
are pulmonary (lung) function tests, which have well-established normal
ranges, but are quite dependent on patient effort; nerve and muscle function
tests, which are largely effort-independent and have reasonably well-established
reference ranges, but are sensitive to interlaboratory variation, and electrocardiograms
(EKGs), which are interpreted with a combination of objective measures
and more subjective recognition of patterns resulting from inidividual expertise.88
All tests have strengths and limitations for their use in reaching a certain
diagnosis or making a causal inference. The expert should be able to address
strengths and weaknesses of various approaches based on the situation at hand.
Why was one test chosen or preferable to another? If available, what is the
sensitivity, specificity, and validity for the test in general, and what are its predictive
values in the population (characterized by age group, gender, comorbid
diseases, workplace exposures) from which the individual comes?89
Mostly these predictive values will be available in the medical literature, but
there are many disappointing gaps. Given inevitable inconsistencies in the patient’s
data, a qualified expert will usually be able to interpret and explain these inconsistencies
in a satisfactory manner.
IV. Physician Decision Making
医师的判断结果
A. Introduction
介绍
For the treating physician, “[c] linical reasoning is the essential function of the
physician; optimal patient care depends on keen diagnostic acumen and thoughtful
analysis of the trade-offs between the benefits and risks of tests and treatments.”90
Beyond assessing the presence or absence of disease, and defining appropriate
treatment or prevention, the physician must be able to skillfully communicate
information to the patient and other interested parties.91
Moreover, a physician may be asked to determine the causation of disease, in
order, for example, to offer a patient advice on continuing activities that may
cause, contribute to, or exacerbate or ameliorate the disease. The physician may
also be asked to determine causality as an expert in a legal proceeding.92 In
undertaking all of these activities, the physician is grounded in the art and science
of clinical reasoning, which we describe below in general terms.
The physician is trained to recognize diseases as coherent deviations from
normal structure or function that affect a certain part of the body or type of
tissue. Physicians recognize the characteristic symptoms, signs, and laboratory
manifestations of given diseases, although a relatively small number of discrete
symptoms and signs are shared by a much larger number of coherent diseases. In
fact, diseases result from one or a combination of only ten or so general pathophysiological
processes (congenital, infectious, neoplastic, toxic, genetic, vascular,
immunologic, inflammatory, endocrine, and traumatic). The goal of the
physician is to distinguish which specific type of disorder (disease) is causing a
patient’s symptoms and signs.93
One of the difficulties in recognizing diseases is the absence of an accepted
metric for establishing new disease entities. Thus, when a possible new set of
characteristic symptoms, signs, and laboratory manifestations is described, there
is no one method for developing consensus on whether a new disease entity
exists.94 For example, when the characteristic symptoms, signs, and laboratory
test results of acquired immunodeficiency syndrome (AIDS) were first described
in the early 1980s, prior to the identification of the human immunodeficiency
virus (HIV), there was considerable controversy over whether a new disease
entity had manifested itself. Development of a test for infection with the specific
virus cemented recognition of the disease. There have also been analogous, but
largely unresolved, controversies over chronic fatigue syndrome, fibromyalgia,
multiple-chemical sensitivity, and Gulf War syndrome.95
B. Diagnosis
诊断
Clinical diagnosis has been described as a process of “iterative hypothesis testing.”
It relies on both analysis and synthesis of data. When making a diagnosis, a
clinician makes inferences about types of malfunctions of the patient’s organs or
chemistry that would lead to the observed abnormalities. The basis for the inferences
are facts (information) that have been collected about the patient. The
clinician applies inferential (also known as inductive) reasoning, considering the
specific historical, physical, and laboratory facts, until a diagnosis that coherently
describes the patient’s condition can be hypothesized. Such a working diagnosis
is sometimes called, or corresponds to, a syndrome, which is a clustering of signs
and symptoms of abnormal function.96 Syndromes and working diagnoses do
not identify precise underlying internal causes. To arrive at an underlying internal
cause, the physician must process the multiple symptoms and signs from the
working diagnosis into a single diagnosis or disease, such as multiple vascular
strokes as an explanation for dementia.
In the process of performing a differential diagnosis, the physician determines
which of two or more diseases with similar clinical findings is the one that the
patient is suffering from.97 The physician does this by developing a list of all of
the possible diseases that could produce the observed signs and symptoms, and
then comparing the expected clinical findings for each with those exhibited by
the patient.98
While working through a differential diagnosis, the clinician will often have
generated a number of diagnostic hypotheses of what specific underlying diseases
might be the cause of the patient’s problem. Initially these hypotheses are
colored by the patient’s demographic characteristics (e.g., age, gender, race) as
well as appearance and chief (or presenting) complaints, because all of these
affect the probabilities of developing specific illnesses and are also easily observable.99
For instance, lung cancer and heart attacks are relatively rare in individuals
under age 40 and would not usually be at the top of a list of preliminary
hypotheses for patients in this age group even if they did complain of cough or
chest pain, respectively. Sometimes the diagnostic hypotheses will be greatly
influenced by a single piece of physical or laboratory data. As the physician
develops and considers hypotheses during the history-taking, he or she may
modify the questions asked of the patient to probe specific areas that test and
rule out a succession of hypotheses.100
The initial, or working, diagnosis provides a context or template for gathering
further information and specifying tests to confirm or refute the working
diagnosis. Each working diagnosis implies the presence of certain symptoms or
test results and the absence of others if the patient has the given disorder. The
physician modifies and refines the working diagnosis as additional information is
gathered, generating new diagnoses as the old ones are pushed aside by inconsistent
findings.101 In essence a physician thinks the patient probably has Condition
X and orders tests that will verify or refute this diagnosis. If the diagnosis is
refuted, the physician reshapes the diagnostic hypothesis and orders additional
tests that may be required. Experienced physicians select and test the most probable
hypothesis first. This is the generally accepted (though seldom formally
acknowledged) methodology that physicians employ to arrive at a diagnosis.
The goal of the clinician is to arrive at a diagnosis that can be used to develop
a rational plan for further investigation, observation, or treatment, and ultimately
to predict the course of the patient’s illness (prognosticate). To do this,
the clinician must verify or validate the diagnostic hypothesis.102 Validation of a
diagnostic hypothesis requires an assessment of coherency of the hypothesis (i.e.,
do the patient’s physiology, risk factor profile, and complications sufficiently
match those expected from the suspected disease?). The presence of each such
symptom or sign that matches those expected for a given condition is known as
a “pertinent positive” for that diagnosis. Determining the adequacy of the diagnostic
hypothesis requires assessment of the converse (i.e., does the suspected
disease encompass or satisfactorily explain enough of the patient’s normal and
abnormal findings?). The absence of each symptom or sign characteristic of a
particular condition is known as a “pertinent negative” for that condition and
tends to make that condition less likely. Finally, the principle of parsimony
requires asking whether the suspected disease is a simple explanation for all of
the patient’s important findings. Although it is not always correct or possible, an
explanation of all of the patient’s signs and symptoms with a single underlying
condition or disease process is desirable. Of course, some patients, especially the
elderly, may have more than one underlying disease (e.g., heart disease, osteoporosis,
and chronic renal failure). Sometimes two common conditions will
be a more logical explanation than one complex and unusual disease that could
also explain all of the observed manifestations. Physicians also consider competing
hypotheses, to ascertain that no other disease is present that better explains
the current hypothesis or findings.103
All diagnostic hypotheses represent probabilistic judgments that are based on
observed medical facts that have variable probabilities of being correct. Each fact
(symptom, sign, or test abnormality) also has only a variable probability of being
found in a given condition that is typically characterized by its presence. If the
diagnosis is based on inconsistent records or observations, the physician should
explain how the inconsistencies affected the assessment being offered.104
C. Probabilistic Basis of Diagnosis
Medical diagnosis is not an exact science.
医生诊断不是一门精确的科学
As indicated above, physicians make probabilistic judgments on a day-to-day basis, even when they can supplement a patient’s history and physical with the results of extensive laboratory tests.
如上所述，医师下可能性的判断是在日复一日的基础上，即使在他们以后能够补充患者的病史和体格检查以及实验室结果。
Laboratory, clinical, and physiological tests are important for any given disease and may be characterized in terms of their “sensitivity” and “specificity,” which indicate the usefulness of the test results in making a particular disease diagnosis.
For a given test, sensitivity, which is also known as the true positive rate, is the percentage of positive tests in patients who actually have the disease.
Test results in those who have a disease but are incorrectly identified as not having the disease because of the test’s insensitivity are “false negatives.”
Thus, a test that is positive in 80% of actual cases of asthma (80% sensitivity) will fail to indicate asthma, or be falsely negative, in 20% of actual cases.
Specificity is the percentage of negative test results in individuals who are free of a given disease, also known as the true negative rate. Test results in those who are free of the disease who are incorrectly identified as having the condition are “false positives.” Thus, a test that indicates abnormal bronchial reactivity in 15% of individuals without asthma would have a false positive rate of 15%; their test results were positive, but they are free of the condition.105 For example, a physician may order a chest x-ray as a test to rule out lung cancer for a 60-year-old man who just began to cough up flecks of blood but has a normal physical exam.
If the x-ray does not show any evidence of lung cancer (is negative for a finding consistent with lung cancer), that diminishes the probability of lung cancer, but it does not rule it out. A cancer may actually be present but not show up on the x-ray because it is too small or because it is in an unobservable location. The physician will be aware of the possibility of such a false-negative result and, especially for a high-risk individual (see below), may order a follow-up exam in a few months or immediately order a more sensitive test, such as a CAT scan or bronchoscopy.
如果X-片不显示肺癌足够全部的证据(与肺癌相符的证据是阴性的), 那么减少诊断肺癌的可能性, 但不排除它。癌症也许存在，但实际上没出现在X-片上是因为它太小或因为它是在一个看不见的地点。医师意识到这样一个假阴性结果的可能,特别是为属于高风险个体(参见下面), 于是约定几个月后复查或即时做一个更敏感的检查, 譬如CAT扫描或bronchoscopy 。
A false-positive result that was due to the imperfect specificity of the chest x-ray would occur if the x-ray showed an abnormality that suggested cancer, but when biopsied (the gold standard of tissue diagnosis) turned out to be an old scar resulting from a dormant injection.
Sensitivity and specificity provide information about the usefulness of a piece
of data (a symptom, sign, or test) for diagnostic reasoning in any population of
patients. However, they do not give complete information for predicting or
excluding disease in individual patients. For that, information about the patient,
and the population that he or she represents, must be incorporated.106
Physicians must interpret the predictive value of a test in assessing the presence
or absence of disease in a specific patient. The predictive value of a test for
a specific individual is based not only on the sensitivity and specificity of the test,
but also on the prevalence of disease in the population from which the patient
comes, such as age group, gender group, racial group, and groups with occupational
exposures.107 In the previous example, if the 60-year-old man was a smoker
and had been occupationally exposed to a lung carcinogen, such as asbestos, a
negative x-ray might be viewed more suspiciously than if he was free of additional
risks.
If sensitivity and specificity are known in general for a particular test, sign, or
symptom, and the overall prevalence of the condition is known for the population
group from which the patient comes, then one can actually calculate a good
approximation of the predictive value of the test, sign, or symptom for that
person and condition according to a rule known as Bayes’ theorem. These calculations
have actually been translated into nomograms (tables) for general use.108
Few clinicians actually calculate such probabilities, but they use an analogous
reasoning process on a routine basis. This Bayesian reasoning is a major tool of
physicians in thinking through a differential diagnosis. For instance, heart attacks
are very rare in 25-year-olds and relatively more common in 75-year-olds.
In analyzing a patient with chest pain and borderline abnormal EKG changes,
the physician is much more likely to suspect a heart attack as the cause of the
pain in the 75-year-old, and admit the patient to a hospital, at least for monitoring.
109
Diagnostic reasoning is usually more complex than the examples given because
it is simultaneously based on multiple symptoms, signs, and test results
(e.g., family history, physical exam). These findings are not all truly independent
of one another, thus preventing straightforward addition of the probabilities
as in a Bayesian model. This lack of independence limits the ability of physicians
to make accurate calculations of the results of multiple simultaneous predictive
values. However, physicians must routinely make such estimations, albeit
often implicitly and without numerical quantification, as part of clinical
care. Thus, physicians frequently rely on the principles of Bayesian reasoning
when deciding on a diagnosis.110 Doctors combine probabilities of disease (prevalence)
with their knowledge of the frequency of signs and symptoms in a given
disease and competing diseases to progressively modify and ultimately arrive at
their view of the likelihood of the disease under consideration.
D. Causal Reasoning
During the diagnostic process, the physician employs causal reasoning to integrate
the various clinical variables into an understanding of the cause-and-effect
relationships among them, based on an understanding of how the various systems
of the human body interact and react to external stressors. Causal reasoning
allows the clinician to conceptualize the possible course of the patient’s disease
and predict the effects of treatment, and is important in evaluating the coherency
of a diagnosis. For example, if the patient is experiencing chest pain on
exertion and has a history of high blood cholesterol levels, the physician might
posit a causal model that involves cholesterol plaque substantially obstructing
coronary arteries, resulting in inadequate blood flow to the heart muscle during
exercise causing chest pain. This model might then suggest that the physician
first investigate the degree of occlusion in the coronary arteries, and second
consider measures such as smoking cessation, dietary modification, medications,
and even angioplasty or surgery if the level of occlusion proves to be substantial
and a likely explanation for the pain.
As the process of refinement of diagnostic hypotheses unfolds, the consideration
of several causal models may be necessary, because consistency of the model
with observed findings does not necessarily prove that a model is correct. In the
example above, another model that would explain the findings is exposure to
high levels of carbon monoxide from a faulty furnace at home, producing a
blood carboxyhemoglobin level of 18% (the normal for a nonsmoker is less than
1%) and reducing the blood’s oxygen-carrying capacity. In conjunction with
only mild coronary artery obstruction by plaque, this exposure then leads to
inadequate oxygen delivery to the heart muscle and chest pain. The model
combines general causation models for coronary artery disease with information
on the levels of carbon monoxide and coronary artery obstruction specific to this patient. Thus, the physician applies general medical knowledge about the relationship of various factors to symptoms and then refines the appropriate causal model in accordance with the specific patient’s condition. Although carbon monoxide intoxication can cause chest pain that is due to inadequate oxygen delivery to the heart, it requires a blood carboxyhemoglobin level of at least 5% to 10%, and its impact is enhanced by the presence of underlying mechanical obstruction of the coronary arteries. Hence, the physician must usually consider and assess alternative and more specific causal models before accepting a particular model as the preferred explanation. Like the probabilistic reasoning described above, this kind of reasoning is rarely made explicit.
我也来参加一下吧，申请447～452，有5页半的内容，算5页吧。
II. The Medical Doctor As an Expert
A. What Is a Physician?
In the United States, a physician is someone who has met the rigorous requirements
of a four-year program and graduated from a credentialed medical or
osteopathic school. However, as explained below, this training is not sufficient
to qualify a physician to practice medicine.33
The courses in medical school are generally similar from school to school,
and they focus on basic medical sciences (e.g., microbiology, pharmacology,
and pathology) as well as clinical training in medical diagnosis and treatment
(e.g., internal medicine, cardiology, pulmonology, surgery, psychiatry, dermatology).
All medical curricula include some basic training in epidemiology and
biostatistics. There is relatively little structured study of public health, occupational
medicine, and toxicology in a traditional curriculum, although a number
of medical schools offer joint degree programs leading to a Master of Public
Health degree (M.P.H.), with enhanced training in epidemiology, toxicology,
and other aspects of public health. Furthermore, it is not uncommon for physicians
to undertake further study and become proficient in epidemiological research
in their particular fields. Most physicians have substantial training and
experience in pharmacology, a subject closely related to toxicology that concerns
the effects of therapeutic drugs.34
In most states, physicians are required to complete a minimum of one additional
year of hospital-based “residency” training, the first year of which is called
an “internship,” in an approved program before they can be licensed to practice
medicine. After completing the internship year, a physician may apply for state
licensure to practice medicine. However, specialization requires further training
in an approved residency program beyond the internship year. For example,
surgery requires at least four additional years; family or internal medicine, pediatrics,
or neurology requires two additional years. A physician may pursue subspecialty
training, which usually requires a further one- to three-year “fellowship”
focusing on a particular organ or system (e.g., pulmonology, cardiology,
gastroenterology, rheumatology, endocrinology, hematology) or type of disease
(e.g., infectious disease, oncology, or neurological movement disorders or electrophysiology).
35
33. See World Health Org., World Directory of Medical Schools 274–75 (6th ed. 1988 & Supp.
1997).
34. See, e.g., Association of Am. Med. Colleges, Curriculum Directory 1998–99, at 104–05 (27th
ed. 1998) (listing required courses for Johns Hopkins University School of Medicine).
35. See World Health Org., supra note 33, at 274–75.
………………………………
While physicians dealing with diagnosis and treatment tend to think in terms
of both internal and external causation, courts are usually asked to determine the
role of causes that are external to the individual. Generally, physicians focus on
causal elements that can be addressed through medical treatment or through
changes in lifestyle or diet; courts focus primarily on causal elements for which
a litigant or other party might be held responsible. For example, a workers’
compensation case might concern the role of physiological stress at work in
causing underlying heart disease, or the role of carbon monoxide in triggering a
specific heart attack.46 Identification of those kinds of causes depends on information
concerning quantification of risks in the workplace environment, as
well as on the medical literature on causation, including the psychological, toxicological,
and epidemiological literature.47 To determine general causation, the
expert must review the pertinent literature, as familiarity with this literature is
key to expert opinion. For example, since many cardiologists advise patients on
returning to work after a heart attack, they will often be familiar with the literature
on work-based risks and cardiovascular disease, whereas most other physicians,
who deal with this question less frequently, would need to devote some
time to study before evaluating such a special consideration.
cyberake wrote:翻译加分：
今天翻译活动正式开始招标。
规则：
[color=blue]从正文开始，开头的目录不算（即441页开始），5页一分，跨页段落，原则上归上页，有意义的注解也要翻译。
5页一分还是不够灵活，建议加上这样的办法：先招标，申请者可加一分（如果规定时间内不能完成要收回两分），比规定时间提前可加一分，翻译质量较好的还要奖励分数1—5分。
翻译成员可把相应内容复制在跟贴，和我上面的跟贴一样，版主会把相应内容在上页贴出连接和提示，把上面被复制的内容省去，会员然后自己编辑逐步翻译并完成。
whenhye wrote:
翻译成员可把相应内容复制在跟贴，和我上面的跟贴一样，版主会把相应内容在上页贴出连接和提示，把上面被复制的内容省去，会员然后自己编辑逐步翻译并完成。
晕了.这段话实在不懂啥意思.请主人大人再解释解释.
另外,不知道下列词汇可有固定的汉语法律词语: proffered testimony, general causation, specific causation. 请法规版的大虾们帮助.
proffered testimony是不是译作提供的证词？
关于general causation, specific causation我查到一篇文章：
职业暴露和环境污染引起疾病的因果关系的判断:总体判断和个体判断
Causal Relationships between Occupational and Environmental Exposures and Injury: General Causation and Specific Causation
郑宁嘉 Ben Thomas
如果这样看，应该分别对应总体判断和特体判断？还是以做一般原因和特定原因？
whenhye wrote:
翻译加分：
5页一分还是不够灵活，建议加上这样的办法：先招标，申请者可加一分（如果规定时间内不能完成要收回两分），比规定时间提前可加一分，翻译质量较好的还要奖励分数1—5分。
可以先预支积分，有点类似于“定金”的味道。
sourboy wrote:还是翻译吧
晕了.这段话实在不懂啥意思.请主人大人再解释解释.
另外,不知道下列词汇可有固定的汉语法律词语: proffered testimony, general causation, specific causation. 请法规版的大虾们帮助.
proffered testimony被提供的证词
general causation一般因果关系
, specific causation具体因果关系
下面是引言部分的译文, 请版主和高手指教和帮助修改.谢谢
I. Introduction
Testimony by physicians is one of the most common forms of expert testimony in the courtroom today1. Medical testimony is routinely offered in both civil and criminal cases, including assault and battery2, rape3, workers' compensation proceedings4, and personal injury suits5. In the civil arena alone, medical testi¬mony is frequently offered as part of medical malpractice cases6, Employee Retirement Income Security Act (ERISA) suits on coverage of health care plans7, Americans with Disabilities Act litigation8, product liability suits9, and toxic injury cases, such as breast implant and environmental contamination claims10. In many instances, medical testimony or medical evidence is an indispensable part of the inquiry.
I. 引言
医生证词是目前法庭上最常见的专家证词中的一种1。医学证词在民事和刑事法庭上均常见，案例包括攻击和殴打2、强奸3、工人赔偿案件审理4和人身伤害诉讼5。仅在民事诉讼领域，医学证词就经常被作为下列案件的一部分使用：治疗失当案件6、就医保覆盖范围进行的雇员退休收入保障法案（ERISA）诉讼7、美国残疾人法案诉讼8、产品责任诉讼9、毒害案件如义乳和环境污染（的赔偿要求）10。在许多案件中，医学证词或证据成为调查不可或却的一部分。
A. Applicability of Daubert v. Merrell Dow Pharmaceuticals, Inc.
A．多伯特诉迈雷尔-道药业公司案的适用性
Since the U.S. Supreme Court issued its opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc.11, many courts have assessed the reliability of medical testimony according to Daubert's standards. More recently, in Kumho Tire Co. v. Carmichael12, the Court held that Daubert's reliability requirement and the trial judge's gatekeeping role apply to all expert testimony.
自从美国最高法院发表了它对多伯特诉迈雷尔-道药业公司案的意见后11，许多法庭都按照多伯特案的标准对医学证词的可靠性进行了评价。最近，在锦湖轮胎诉卡迈克尔案件中12，法庭判定多伯特案的（医学证词）可靠性要求和审判法官的守门人作用适用于所有专家证词。
Although Kumho resolved any uncertainty as to the applicability of Daubert's standards to medical testimony, there is still uncertainty over how courts will apply these standards, given the different approaches taken by the courts to consideration of the admissibility of medical evidence13. Two recent cases illus¬trate this diversity. In Moore v. Ashland Chemical, Inc.14, a case decided before Kumho that applied Daubert standards, the Fifth Circuit, sitting en banc, upheld the trial court's exclusion of a physician-expert's opinion on the cause of the plaintiff’s reactive airway disease. The witness had offered the opinion, without citing published research indicating that fumes from toluene and a mixture of other chemicals from a leaking drum could cause reactive airway disease. The Fifth Circuit held that the trial court had not abused its discretion in its application of the Daubert factors, noting that expert testimony must be based on at least "some objective, independent validation of the expert's methodology. The expert's assurances that he has utilized generally accepted scientific methodology [are] insufficient15."
虽然锦湖案确定了多伯特案的标准适用于医学证词，但考虑到法庭在考量是否接受医学证词时采取的方式有差异，法庭如何应用这些标准则依然不确定13。最近的两个案例显示了这种差异。在锦湖案之前判决的穆尔诉爱诗兰化学公司一案14中应用了多伯特案的标准，第五巡回法庭在全体法官出席的情况下，维持了审判法庭对原告反应性气道病病因医学证词的否定。证人在提供其意见时未能引用公开发表的研究来证明甲苯蒸汽和泄露容器中释放的其它化合物的混合物可以引起反应性气道病。第五巡回法庭判定审判法庭应用多伯特案的因素时未滥用其决定权，并指出“必须对专家的方法学有一些起码的客观而独立的验证。那位专家声称其使用了广为接受的科学方法是不够的”15。
In contrast, the Third Circuit's decision in Heller v. Shaw Industries, Inc.16, also a case decided before Kumho that applied Daubert standards, illustrates a much different approach. In Heller, as in Moore, the plaintiff complained of respiratory symptoms, which in this case coincided with exposure to a new carpet in her home. As in Moore, the trial court excluded the plaintiff’s expert testimony be¬cause of the absence of published studies linking fumes from the carpet to aller¬gic reactions. The Third Circuit stated that the trial court erred in so holding, noting the witness's reliance on "differential diagnosis17." The court nonetheless upheld the exclusion of the witness's testimony on other grounds.
相反，另一起在锦湖案之前判决的海勒诉肖工业公司案16中也应用了多伯特案的标准，但第三巡回法庭的决定则展示了非常不同的考量。与穆尔案相同，在海勒案中原告诉称其呼吸道病症，刚好与其在家中接触新地毯的时间偶合。与穆尔案相同，审判法庭排除了原告的专家证词，因为没有公开发表的研究将地毯的挥发气与过敏反应联系起来。虽然第三巡回法庭基于其它原因维持了对该证人证词的排除，但指出审判法庭的裁定是错误的，并指出该证人证词是基于“鉴别诊断”17。
These two cases illustrate the range of approaches taken by courts in consid¬ering testimony on causation, including issues related to testimony on "differen¬tial diagnosis" or "differential etiology" (as witnesses and courts use these terms), the necessity of research literature to support opinions on causation, and the importance of temporal relationships. While these issues may be intertwined, they represent different facets of the courts' approaches18.
这两个案子说明了法庭对病因证词采取的不同考量，包括与基于“鉴别诊断”或“鉴别病因学”的证词有关的问题、支持病因观点的研究文献的必要性以及时间先后关系的重要性。虽然这些问题可能互相交叉，它们代表了法庭所考量的不同方面18。
B. Medical versus Legal Terminology
B. 医学术语对法律术语
Perhaps because medical testimony is so common and yet not entirely accessible to the lay public, courts have come to use certain medical terms, such as differen¬tial diagnosis and differential etiology in ways that differ from their common usage in the medical profession. For example, although environmental and occupa¬tional health physicians may use the term "differential diagnosis" to include the process of determining whether an environmental or occupational exposure caused the patient's disease19, most physicians use the term to describe the pro¬cess of determining which of several diseases is causing a patient's symptoms. Expert witnesses and courts, however, frequently use the term "differential diagnosis" to describe the process by which causes of the patient's condition are identified, particularly causes external to the patient20. Additionally, courts some¬times characterize causal reasoning as "differential etiology," a term not used in medical practice, but one that more closely suggests the determination of cause21. For the sake of clarity and consistency, this reference guide uses the term "dif¬ferential diagnosis" in its traditional medical sense, that is, referring to the diag¬nosis of disease, and refers to the process of identifying external causes of diseases and conditions as "determining cause," "determining external cause," or some similar phrase, as the circumstances warrant.
也许是因为虽然医学证词如此常见，但普通公众对它还不是完全理解，所以现在法庭在使用一些医学术语时，比如“鉴别诊断”和“鉴别病因学”，其使用方式与医学专业人士的使用方式有所不同。例如，环境和职业健康医生使用“鉴别诊断”时包括了鉴定患者病因是否由环境或职业影响导致的过程19，而多数医生使用该术语描述决定几种疾患中哪一个引起患者病症的过程。然而专家证人和法庭经常使用“鉴别诊断”一词来描述鉴定患者病情的肇因的过程，尤其是外源性肇因20。另外，法庭有时把因果推理称为“鉴别病因学”，这一术语未见于医学实践中，该词（比“鉴别诊断”）接近推断原因的意思21。为了清楚和连贯起见，本指南按照其传统的医学含义使用“鉴别诊断”，即指疾病的诊断。当提到鉴别疾患的外部原因的时，则根据情况使用“确定原因”、“确定外部原因”或其它类似词语。
To add a further level of complexity, courts also use the terms general causation and specific causation. General causation is established by demonstrating, often through a review of scientific and medical literature, that exposure to a sub¬stance can cause a particular disease (e.g., that smoking cigarettes can cause lung cancer). Specific, or individual, causation, however, is established by demon¬strating that a given exposure is the cause of an individual's disease (e.g., that a specific plaintiff’s lung cancer was caused by his smoking) 22. Physicians may offer expert opinion on both specific and general causation23, although perhaps more commonly on specific causation as it relates to a patient's medical condition. When physicians offer expert opinion on general causation, it is frequently incorporated into proffered testimony on specific causation.
使事情更复杂的是，法庭也使用“总体因果判断”和“个体因果判断”二词。前者指证明沾染一种物质可以导致某特定疾病（如抽烟导致肺癌），通常通过总结科学和医学文献来证明。而后者则是证明某个个人的疾病是由沾染某特定物质引起的（如某原告的肺癌是他抽烟造成的）22。对于“总体因果判断”和“个体因果判断”，医生都可以提供专家意见23，但可能更多的是为“个体因果判断”作证，因为这与病人的医疗状况有关。当医生就“总体因果判断”发表意见时，通常也是整合到为“个体因果判断”提供的证词中。
C. Relationship of Medical Testimony to Legal Rules
C. 医学证词与法律规定的关系
In litigation, the form and content of medical testimony is shaped by a number of factors, first and foremost of which is the legal issue on which it is offered. In terms of content, in a traditional personal injury claim, the physician may be asked to opine on the actual cause of the patient's illness or injury. Newer theories of tort, however, such as claims for fear of future injury (e.g., "cancer-phobia")24, increased risk of injury25, or medical monitoring26, require testimony on the patient's risk of future disease, rather than the actual cause27.
在诉讼中，医学证词的形式和内容由多种因素决定，第一个也是最重要的因素就是作为证词提供对象的法律问题。就内容而言，在传统的个人伤害赔偿案中，医生可能被要求就患者的疾患或伤害的实际原因发表意见。民事侵权案件的最新理论，如对未来伤害的恐惧的赔偿要求（如“憎癌症”）24、提高的伤害风险25或进行医学监测的要求26，则要求对病人未来的疾病风险，而非实际原因提供证词27。
The form of testimony, whatever the issue, tends to be shaped by require¬ments of the applicable legal rules. For example, courts and lawyers will be familiar with various formulations of the causation issue, including the "but for" and "substantial factor" tests. A physician testifying on causation issues will be asked to opine in the form dictated by the legal rule.
无论什么样的法律问题，证词的形式往往由可应用的法律规定的要求所决定。举例来说，法庭和律师们熟悉论证因果问题的各种形式，包括“如果不是…则…”和“实质要素”测试。为因果问题提供证词的医生会被要求以法律规定要求的形式出具其证词。
Legal rules on the sufficiency of proof will also shape the physician's testi¬mony. In a personal injury case, physicians are often asked to testify on one or more of the ultimate issues in the case, such as causation. Thus, their testimony will be shaped by the applicable substantive rule on the burden of proof. For example, a physician may testify that a plaintiff’s disease is "more likely than not"28 due to a chemical exposure or that causation exists to a "reasonable medi¬cal certainty."29 This reference guide, however, consistent with the purpose of this manual, focuses on the methods and reasoning governing physicians' deci¬sions and opinions, not the differing legal rules and theories on which medicaltestimony is offered, or the standards courts have applied in reviewing medical testimony30.
关于证据充分性的法律规定也会影响医生证词。在个人伤害案件中，医生往往被要求对案件的一个或多个根本问题提供证词，例如病因。因此，适用的有关举证责任的实体法规会影响他们的证词。例如，医生可以证明一位患者的疾病“很可能”28是由于沾染某化合物，或其因果关系存在“医学上合理之确定性”29。然而为了与本指南的目的一致，本指南只关注左右医师决定和意见的方法和推理，而不讨论作为医学证词提供对象的法律规定和理论的变化，或法庭在审查医学证词时应用的标准30。
This reference guide also does not address admissibility of testimony on the standard of care in medical malpractice cases. There are several reasons for this exclusion. First, medical malpractice cases are usually (though not exclusively) litigated in state courts rather than federal courts. Second, in most jurisdictions, the standard of care for physicians (like that for other professionals) is the cus¬tomary level of care provided by competent physicians in the same field31. Thus, testimony on the standard of care usually concerns what other physicians do in similar situations, rather than whether the defendant-physician's diagnosis and treatment are based on good medical science (although customary physician practice and good medical science will generally coincide). As a result, the ad¬missibility of expert opinion on the standard of care is decided according to whether the witness is qualified to opine on the same field as the malpractice defendant32.
本指南也不评论有关治疗失当案件中医疗标准证词的可接受性。这有多个原因。首先，治疗失当案件诉讼通常（虽然不完全）是在州级法庭，而非联邦法庭中进行的。其次，在多数司法解释中，医生的医疗标准（与其它行业类似）是指在同一领域中合格的医师所提供的惯例性医疗水平31。因此，关于医疗标准的证词通常是讨论在相似的情况下其他医师会如何做，而非被告医生的诊断和处治是否是好的医疗实践（虽然一般情况下惯例性医学实践和好的医学实践应该是吻合的）。因此，对于医疗标准的专家意见，其可接受性是由证人的医师资格是否和被告在同一领域来决定32。根据如上所述的限制，本指南的下面4个部分将分别解释医学实践（着重谈医生是如何运用医学和科学知识、临床经验和患者病史的）、对疾病诊断过程的检查以及适当治疗措施的选择。
Within the limitations described above, the next four sections of this refer¬ence guide explain medical practice, with an emphasis on how physicians apply medical and scientific knowledge, clinical experience, and patient history and examination to the process of diagnosis of disease and selection of appropriate treatment.
根据如上所述的限制，本指南的下面4个部分将分别解释医学实践（着重谈医生是如何运用医学和科学知识、临床经验和患者病史的）、对疾病诊断过程的检查以及适当治疗措施的选择。
还不够好懂，有谁看懂了译文吗？
法律语言本来就比较晦涩，我明天抽空校对一下。
顺便说说，versus翻译为“诉”符合习惯，普通法系国家遵循先例，有许多著名的判例共援引，案件的名称一般为AA诉BB。
请sourboy改一改，不要用“对”——意思当然也不能算错。
ZT:
如何阅读英文案例
屈文生
第一部分
案例通常由下列几个部分组成。
一、案例名称（Case Name）；例如：Marbury v. Madison （马伯里诉麦迪逊）, v is short for versus.是“诉”的意思。
二、判决法院（Court rendering the opinion）；例如：New Jersey Supreme Court (新泽西最高法院)。
三、卷宗号；案号（Citation）；例如：93 N.J324, 461 A. 2d 138 (1983)，这说明该案出自《新西汇编》第93卷，第324页，以及《大西洋汇编》第二辑第138页，该案判决于1983年。此处，A 是Atlantic Reporter的缩写。像这种指明两个或两个以上出处的卷宗号叫作：“平行卷宗号”，其英语表达为“parallel citation”，意思是“An additional reference to a case that has been reported in more than more reporter.”广义上卷宗号包括上述一、案例名称；二、判决法院。
四、主审法官姓名（Justice wrote the opinion）。
五、判决书 （opinion: stating the issue raised, describing the parties and facts, discussing the relevant law, and rendering judgment.）判决书是整个案例的主体部分，其中包括法律争议（Issue）、双方当事人情况、事实经过、判决采用的相关法律以及判决结果。
判决书的阅读过程之中，要注意以下几点：1. 时态主审法官的意见用现在时态；前审法院的意见用过去时态。2. 主审法官的意见是法院意见。3除法院意见外还有两种意见，它们被称为“反对意见”（dissenting opinion or dissent）与“配合意见”（concurring opinion）。Dissenting opinion: opinion offered by a judge disagreeing with the majority panel of judges’ conclusion; “反对意见”指不同意大多数法官判决结论之某一法官的意见；Concurring opinion: opinion written by a judge agreeing with the majority’s conclusion but not its reasoning. “配合意见”是指同意大多数法官的意见，但是不同意判决结论的推理之某一法官的意见。
六、法庭投票（Votes of the court）例如在七名***官审理的情况下，有几名法官的意见是“维持原判”（affirmance），有几名法官的意见是“撤销原判、发回重审”（reversal and remandment）。
第二部分
一、什么是citation?
由于卷宗号这一块涉及内容庞杂，这里再逐一特别说明一下。我们首先来看一下《布莱克法律字典》中citation的定义：A reference to a legal precedent or authority, such as a case, statute, or treatise, that either substantiates or contradicts a given position. (p.237) 7th edition. 由于a citation is a reference to a legal authority，因此，citation必须要有一个标准，这样以后的参考者才容易检索得到。正如《布莱克法律字典》所指出的一样，Citation formats exist for many different types of legal sources including cases, statutes and secondary legal materials. Understanding the basic format for each of these different types of sources will enable the researcher to more independently locate materials in the law library.
案例之中的卷宗号通常包括下列几个部分：
a. 案件双方当事人姓名（the names of the parties involved in the lawsuit）；
b. 包含案件全文的汇编卷号（ the volume number of the reporter containing the full text of the case）；
c. 该案例汇编的缩写名称（the abbreviated name of that case reporter）；
d. 案例开始的页码数（the page number on which the case begins）；
e. 案件判决年份（the year the case was decided）；有时还包括
f. 案件判决法院（the name of the court deciding the case）。
举例说明: Hebb v. Severson, 201 P.2d 156 (Wash. 1948). 在这个例子当中，Hebb是原告（plaintiff），Severson 是被告（defendant）。 我们可以在《太平洋汇编》第二辑201卷第156页（volume 201 of the Pacific Reporter Second Series beginning on page 156）找到这一案例。该案是由华盛顿州最高法院（Washington State Supreme Court）于1948年判决的。
二、 如何阅读案例（cases）之中的citation?
确定卷宗号之中的缩略码。请对照下列列表，找出缩略码（abbreviation）的汇编全称（full reporter title）.
Abbreviation Title 汉语汇编名称
A. Atlantic Reporter 大西洋汇编
A. 2d. Atlantic Reporter, 2d Series 大西洋汇编第二辑
Cal. Rep. California Reporter 加利福尼亚州汇编
F. Federal Reporter 联邦汇编
F. 2d. Federal Reporter, 2d Series 联邦汇编第二辑
F. 3d. Federal Reporter, 3d Series 联邦汇编第三辑
F. Supp. Federal Supplement 联邦补充案例
L. Ed. U.S. Supreme Court Decisions, Lawyers’ Edition 美国最高法院案例汇编，律师版
L. Ed. 2d. U.S. Supreme Court Decisions, Lawyers Edition, 2d Series 美国最高法院案例汇编，律师版第二辑
N. E. Northeastern Reporter 东北汇编
N. E. 2d. Northeastern Reporter, 2d Series 东北汇编第二辑
N. W. Northwestern Reporter 西北汇编
N. W. 2d. Northwestern Reporter, 2d Series 西北汇编第二辑
N. Y. S. New York Supplement 纽约补充案例
N. Y. S. 2d. New York Supplement, 2d Series 纽约补充案例第二辑
P. Pacific Reporter 太平洋汇编
P. 2d. Pacific Reporter, 2d Series 太平洋汇编第二辑
S. Ct. Supreme Court Reporter 最高法院案例汇编
S. E. Southeastern Reporter 东南汇编
S. E. 2d. Southeastern Reporter, 2d Series 东南汇编第二辑
So. Southern Reporter 南方汇编
So. 2d. Southern Reporter, 2d Series 南方汇编第二辑
S. W. Southwestern Reporter 西南汇编
S. W. 2d. Southwestern Reporter, 2d Series 西南汇编第二辑
U. S. United States Reports 美国案例汇编
再举两例说明，例如：Morgan v. United States, 298 U.S.468, 56 S. Ct 906, 80L.Ed. 1288 (1936) 表示：摩根诉美国，收集在美国案例汇编第298卷，468页开始；最高法院案例汇编第56卷906页开始；美国最高法院案例汇编律师版第80卷，1288页开始，1936年判决。 For example, a popular name for a Supreme Court case is:
Roe v. Wade
Which translates as Plaintiff versus Defendant
原告 罗 诉 被告魏德
The official citation for this Supreme Court decision is:
410 U.S. 113
Which translates as Volume 410 United Stated Reports Page 113
410卷 美国案例汇编 113页
There are several different publishers for legal documents such as court decisions. (Libraries usually only carry one of these published versions.) These publishers may be referred to in parallel citations for this case.
例如，该案的平行汇编是：
93 S. Ct. 705
Which translates as Volume 93 Supreme Court Reporter Page 705
第93卷 最高法院案例汇编 705页
Or
35 L. Ed. 2d 147
Which translates as Volume 35 U.S. Supreme Court Reports, Lawyers Edition, 2nd Series Page 147
第35卷 美国最高法院案例汇编律师版第二辑 147页
该案完整的卷宗号（full citation）就是：
Roe v. Wade 410 U.S. 113 93 S. Ct. 705 35 L. Ed. 2d.147 1972
Case name Official citation Parallel citation parallel citation Date of opinion
大家都辛苦了，法律英语是专门的，虽然有些词组或单词和普通用语中存在一定的差异但基本上也是万变不离其宗，欢迎大家继续研究。
多谢三位主任的指教，已根据您们的意见修改，请继续审阅
谢谢sourboy战友的翻译，我看过了，翻译的不错，如果您把相关的重要注解一并翻译就再加一分！这对于看懂文章有时候非常重要。
还有一点点修改意见供参考：
medical malpractice翻译为医疗过失、差错比治疗失当好，不仅仅是治疗的问题。
义乳太文了，大多数人对于义眼、义齿还有些认识，看到义乳有些反应不过来。
“不可或却”笔误。
cancerphobia翻译为恐癌比憎癌好。
附注：
But for指的是必要条件规则或者直接译为“but for规则”指的是一种“无彼即无此”的关系。而substantial factor指实质要素，当损害是由不止一个的原因造成时，“but for”检验法便没法提供任何答案，需要补充检验法，实质要素基本含义是，如果加害行为实际上足以引起损害结果的发生，那么它就是引起损害结果的原因。
复习一下，好懂多了，翻译质量提升了。
学习一下...
时间到了，我把我的翻译贴出来，请大家指正。其中有些人名和部分参考文献没有翻译，请主任们给点参考意见。
II. The Medical Doctor As an Expert
A. What Is a Physician?
In the United States, a physician is someone who has met the rigorous requirements
of a four-year program and graduated from a credentialed medical or
osteopathic school. However, as explained below, this training is not sufficient
to qualify a physician to practice medicine.33
The courses in medical school are generally similar from school to school,
and they focus on basic medical sciences (e.g., microbiology, pharmacology,
and pathology) as well as clinical training in medical diagnosis and treatment
(e.g., internal medicine, cardiology, pulmonology, surgery, psychiatry, dermatology).
All medical curricula include some basic training in epidemiology and
biostatistics. There is relatively little structured study of public health, occupational
medicine, and toxicology in a traditional curriculum, although a number
of medical schools offer joint degree programs leading to a Master of Public
Health degree (M.P.H.), with enhanced training in epidemiology, toxicology,
and other aspects of public health. Furthermore, it is not uncommon for physicians
to undertake further study and become proficient in epidemiological research
in their particular fields. Most physicians have substantial training and
experience in pharmacology, a subject closely related to toxicology that concerns
the effects of therapeutic drugs.34
In most states, physicians are required to complete a minimum of one additional
year of hospital-based “residency” training, the first year of which is called
an “internship,” in an approved program before they can be licensed to practice
medicine. After completing the internship year, a physician may apply for state
licensure to practice medicine. However, specialization requires further training
in an approved residency program beyond the internship year. For example,
surgery requires at least four additional years; family or internal medicine, pediatrics,
or neurology requires two additional years. A physician may pursue subspecialty
training, which usually requires a further one- to three-year “fellowship”
focusing on a particular organ or system (e.g., pulmonology, cardiology,
gastroenterology, rheumatology, endocrinology, hematology) or type of disease
(e.g., infectious disease, oncology, or neurological movement disorders or electrophysiology).
35
33. See World Health Org., World Directory of Medical Schools 274–75 (6th ed. 1988 & Supp.
1997).
34. See, e.g., Association of Am. Med. Colleges, Curriculum Directory 1998–99, at 104–05 (27th
ed. 1998) (listing required courses for Johns Hopkins University School of Medicine).
35. See World Health Org., supra note 33, at 274–75.
把医生看作是专家
A、什么是医师
在美国，医师需要经过四年严格的培训，并且毕业于一个正规的内科或外科学校。而且，正如下面所介绍的那样，这些培训还不足以使他成为一个合格的能给病人看病的医生。[33]
各个医学院校里面的课程总体上都很相似，他们既着重于基础医学方面的培训（如：微生物学，药理学和病理学），又着重于临床上面的诊断和治疗培训（如：内科学，心脏病学，肺病学，外科学，精神病学，皮肤病学）。所有的医学课程包括一些基本的流行病学和医学统计学方面的培训。尽管许多医学院校提供相关的学位程序去获得一个公共卫生硕士，——这需要在流行病学、毒理学和其他和公共卫生有关的课程上加强培训，但是对传统医学课程中的公共卫生、职业病和毒理学的系统培训相对较少。此外，医生们经常需要继续深造，使他们对自己特定的领域中的流行病学研究更熟练。药理学和毒理学关系密切，他涉及到治疗药物的疗效，许多医生都对药理学经过系统的培训并且对之有一定的了解。[34]
在许多州，医生需要完成一个最少一年时间的“住院医生”的额外培训过程，这是他们成为一个注册的执业医师之前的一个规定程序，培训的第一年称之为实习医师期。当他们完成第一年的实习医师期，就可以向州有关部门申请职业医师资格。然而，按照规定程序他们还需要在一年的实习医师期外就专科化进行进一步的培训。比如，外科医师需要至少四年，家庭或者内科医生、儿科医生和神经科医生需要额外的两年的培训。一个医生有可能申请亚科培训，这通常需要一个进一步的一到三年的关于特定的器官和系统（如：肺科学、心脏病学、胃肠病学、风湿病学、内分泌学、血液病学）或者特定疾病（如：感染性疾病、肿瘤学、神经学上的传导障碍和电生理学）的随诊（fellowship）学习。[35]
[33] 世界卫生组织，世界医学院校目录，274～275（1998年第6版和1997年补遗）
[34] 美国医学院校协会，课程目录，1998～99，第105～5页（1998年第27版）（约翰·霍普金斯大学医学院必修课程列表）
[35] 世界卫生组织，前面提到的注释 33，在274～75页
After a physician has completed a residency or fellowship in a specialty, he or
she is eligible to take an examination given by that medical specialty’s “board.”
There are twenty-three specialty and subspecialty boards administered by the
American Board of Medical Specialists (ABMS), as well as a number of other
boards not under ABMS with more idiosyncratic criteria for certification. Passing
such an exam makes the physician “board certified” in the field or subspecialty—
a marker of substantial proficiency within the particular area of medicine
and a credential often required by hospitals for appointment to their medical
staff.36 Other indicia of expertise include academic appointments, published
articles in peer-reviewed journals, grant awards, and appointment to peer review
panels.37
After the conclusion of formal medical education, including internship and
residency, physicians continue to acquire medical knowledge through clinical
experience, hospital-based lectures and training programs, review of medical
literature, and continuing medical education courses that provide information
in various specialties. A number of states have moved toward requiring continuing
medical education for license renewal.38 An increasing number of medical
specialties require passage of the board examination at regularly scheduled intervals
to maintain board certification.
To practice at a hospital, a physician must pass review by a “credentialing
committee” that examines the credentials of the physician, as well as legal and
state board records concerning the physician. A physician who clears the
credentialing committee may become a member of the hospital’s medical staff,
otherwise known as an “attending physician,” and may admit patients to the
hospital for treatment. A hospital may revoke staff and admitting privileges for cause.39 Some hospital physicians are also members of the teaching staff, charged
with the training of interns and residents in their medical specialties. Most, but
not all, teaching staff have joint academic appointments at a medical school.
36. Although it may be helpful in establishing the witness’s credentials for opinion testimony,
courts usually do not apply a strict requirement of specialization or board certification for most purposes.
See, e.g., Holbrook v. Lykes Bros. S.S. Co., 80 F.3d 777, 782–83 (3d Cir. 1996) (physician board
certified in pulmonary medicine not required to be a specialist in oncology and radiation to testify on
causation of mesothelioma). In contrast, admissibility of testimony on the medical standard of care in
medical malpractice cases is typically controlled through screening of the witness’s qualifications. See,
e.g., Marquardt v. Joseph, 173 F.3d 855 (6th Cir. 1999) (unpublished table decision) (text at No. 98-
5163, 1999 WL 196569 (6th Cir. Mar. 30, 1999) (dentist who was not an oral surgeon was not qualified
to testify on the standard of care for oral surgery)); Carroll v. Morgan, 17 F.3d 787, 790 (5th Cir. 1994)
(cardiologist with many years of experience need not be a specialist in pathology to testify on the
relationship between heart problems and death).
37. The American Medical Association (AMA) has taken an interest in the quality of medical
expert testimony. After reviewing cases involving testimony by physicians who had falsified their credentials,
the AMA issued a 1998 report to its Board of Trustees recommending that the AMA encourage
state licensing boards to develop disciplinary measures for physicians who provide fraudulent testimony.
The House of Delegates adopted an amended version of the report. See Michael Higgins, Docking
Doctors? AMA Eyes Discipline for Physicians Giving ‘False’ Testimony, A.B.A. J., Sept. 1998, at 20.
38. Jeoffrey K. Stross & Thomas J. DeKornfeld, A Formal Audit of Continuing Medical Education
Activity for License Renewal, 264 JAMA 2421 (1990) (audit of continuing medical education activities of physicians
licensed in Michigan to assess compliance with a law mandating participation in 150 hours of
continuing medical education every three years).
当一个医生完成住院医师期和某个专业的随诊学习，他或者她便可以参加医学专业委员会提供的考核。美国医学专业委员会（ABMS）管理着23个专业或者分科专业委员会，除此之外还有许多其他的专业委员会不受ABMS管理，他们有自己特殊的标准提供认证。通过这类考核意味着这个医师在其专业或者分科里已经通过认证，这个认证是他们在自己特定的医学领域里可以熟练工作的标志，也是医院需要经常用来安排他的医务工作者的一个凭据。[36]其他的关于鉴定医学专家的凭据包括医学院校的职位、在专业期刊上面发表的文章、获奖情况和同行评议小组成员的任命。[37]
结束正式的医学教育之后，包括实习医师期和住院医师期，医师们可以持续地通过临床实践、以医院为基础的讲座和训练计划、复习医学文献以及提供各个专业的成人医学教育等方式继续获得医学知识。许多州现在都倾向于参加持续的医学教育来进行执业医师的再注册。[38]越来越多的医学专业要求通过有规则的规定时间的专业委员会考核来维持执业医师资格的注册。
想要在一个医院工作，一个医生必须通过一个检验医师证书的机构，即“认证委员会”的检查，和法定的及州医学委员会关于医师资格的记录一样。当一个医生通过“认证委员会”的检查将有可能成为这个医院的医学工作者中的一员，否则便称之为“主治医师”，他们可以收治病人入院治疗。一个医院在特定情况下可以开除医务人员和撤销“主治医师”的收治病人入院的权利。一些医院医生同时也是教学职员中的一员，有责任在他们自己的医学专科领域培训实习医师和住院医师。大部分，但不是全部的教学职员在医学院校中有相关学院的职务。
[36] 尽管这也许对建立专家鉴定证明的见证人证书是有用的，法庭在许多情况下一般并不采用严格的专业化要求及委员会证明书。即霍布 v.妮可 布罗斯. S.S. Co., 80 F.3d 777, 782–83 (3d Cir. 1996)（委员会认证的肺科医生不必要因为间皮瘤引起的疾病而需要通过肿瘤学或者放射学的认证）相反地，在医疗事故案例中，可允许的医疗护理标准的证词通常通过检查证人的资格认证来控制。即马克特 v. 乔西, 173 F.3d 855 (第六期，循环杂志 1999) （未发表的桌面裁定）（(text at No. 98-5163, 1999 WL 196569 (第六期，循环杂志 Mar. 30, 1999)（牙科医生没有通过口腔外科资格认证就没有资格去证明口腔外科护理标准）；卡罗 v.摩根, 17 F.3d 787, 790 (第五期，循环杂志. 1994)（有许多年经验的心脏病学专家不必成为一个病理学专家来证明心脏问题和死亡之间的关系）。
[37] 美国医学会（AMA）对医学专家证明人的资格认证很有兴趣。通过回顾哪些曾经在资格认证过程中说谎的医生们做过证词的案例，AMA出版了一个1998年报告推荐给委员会的委员们，报告指出AMA鼓励州发证机关去制定关于医生提供不实证词的惩戒措施。代表们采用了这个报告的一个修正版本。见麦克尔·希金斯，《对接医生？AMA注视关于医生提供不实证词的处罚》A.B.A. J.. 1998年9月 第 20页.
[38] 乔弗来K.斯卓斯 &托马斯 J. DeKornfeld,关于执业医师资格再认证过程中的成人医学教育活动的正式审查，264 JAMA 2421 (1990)
（密歇根州关于执业医师资格再认证过程中的成人医学教育活动的审查是依从一部法规来评定，即参加者在3年内必须持续参加成人医学教育150小时）
B. Physicians’ Roles in Patient Care
After completion of training, a physician may be involved in various aspects of
medicine. While the public tends to think of a physician as directly involved in
patient care, a practicing physician may also serve as a “consulting physician,”
conduct medical research, or have an academic appointment.40 Although the
lines between these different roles often blur, understanding the range of activities
undertaken by physicians is helpful.
A treating physician’s primary role is the examination, diagnosis, and treatment
of patients.41 The physician is expected to do one or more of the following:
diagnose the patient’s conditions, recommend or provide appropriate treatments,
and monitor the patient’s progress. The treating physician may also, as
appropriate, counsel patients on the management of diseases, as well as on dietary
habits, genetic and familial risks and other aspects of a patient’s life relevant
to preventing disease, maintaining health, or managing disease or injury. A treating
physician may be a specialist or nonspecialist. Some members of a treating team
of physicians, such as radiologists or pathologists, perform primarily diagnostic
roles and rarely prescribe treatment.
A consulting physician is someone who is asked for recommendations for
diagnosis and treatment or a “second opinion,” based on his or her more specialized
knowledge and experience. Examples include a cardiologist brought in
to assist the primary physician with the care of someone after a heart attack and
a pulmonary specialist brought in to assist with the management of a patient
with asthma. The consulting physician may rely, in whole or in part, on information
developed by other medical practitioners contained in the patient’s medical
records, such as medical history, laboratory tests, and x-rays. More often, the
consulting physician will also conduct an examination of the patient and under
take additional tests and investigations. While consulting physicians are often an
integral part of the team of treating physicians, in some instances they may not
be involved in treatment, instead providing opinions for employers, insurers,
litigants, or courts.
39. Chouteau v. Enid Mem’l Hosp., 992 F.2d 1106, 1109 & n.2 (10th Cir. 1993) (upholding the
district court’s grant of summary judgment, finding that sufficient justification existed for the defendant
hospital to lawfully terminate the plaintiff’s staff privileges).
40. See Alvan R. Feinstein, Clinical Judgment 21 (photo. reprint 1985) (1967).
41. Treating physicians are generally permitted to testify, although contentions are sometimes made
that their testimony should be limited. In Holbrook v. Lykes Bros. Steamship Co., 80 F.3d 777 (3d Cir.
1995), the trial court had excluded the treating physician’s testimony on his diagnosis of mesothelioma
and a pathology report because the physician was not a pathologist or oncologist. The Third Circuit
reversed the decision, noting that treating physicians’ testimony is often given greater weight than
testimony from physicians who have not examined the patient. Id. at 782–83.
B. 在医疗活动中医生的角色
完成培训后，一个医生有可能进入医药行业的各个领域。当公众趋向于把一个医生看作是直接参与病人的治疗，一个执业医师也可以看作是一个“会诊医师”，进行医学研究，或者是有一个医学院的职务。[40]尽管这些角色之间的界限常常是模糊的，了解医生所从事的这些活动的范围也是有用的。
一个治疗医生的首要任务是病人的体检、诊断和治疗。[41]医生需要做下列的一项或几项工作：诊断患者的疾病、推荐或提供正确的治疗措施、监控患者的疾病进展。一个治疗医生可能还要就疾病的处理方面给病人提供恰当的建议，除此之外还有饮食习惯、遗传和家族风险以及其他和预防疾病、保持健康及处理疾病和损伤等有关的病人生活其他方面。一个治疗医生可以是一个专家也可以不是一个专家。一些治疗医生团队中的一些成员，如放射科医师和病理科医师，担任最初的诊断角色，很少开处方。
一个会诊医师就是被邀请来就患者的诊断和治疗提供建议和“第二意见”，这些建议主要基于他们更专业的知识和经验。这些例子包括一个心脏病专家被邀请去协助首诊医生治疗一个心脏病发作患者以及一个肺科专家被邀请去协助一个哮喘病人的治疗。会诊医师全部或者部分依靠病人医疗档案中其他医生记录的信息，如医疗史、实验室检查、X光片等。更常见的是，会诊医师会再给病人做体检和进行另外的试验和调查。当一个会诊医师经常成为治疗医生团队中必不可少的一员，在某些情况下他们并不参与到病人的治疗，而是给雇主、保险公司、诉讼当事人和法院提供建议。
[39] Chouteau v. 依妮德 Mem’l 医院., 992 F.2d 1106, 1109 & n.2 (第十期，循环杂志1993) （支持州地方法院同意审判摘要，找出存在的被告医院合法地中止原告全体工作人员的特权的充分的辩护依据。
[40] Alvan R. Feinstein, 临床审判 21 （照片，1985年再版）（1967）
[41] 治疗医生经常被允许作证，尽管争论经常使他们的证词变得很局限。在Holbrook v. Lykes Bros. Steamship Co., 80 F.3d 777 (3d Cir.1995), 审判法庭拒绝了治疗医生关于他的间皮瘤的诊断和一个病理报告的证词，这是因为这个医生既不是一个病理学专家也不是一个肿瘤科医师。三审推翻了这个审判，指出治疗医生的证词常常比没有给这个患者检查的医师的证词的分量要重。Id，782～783。
C. Medical Research and Academic Appointments
In addition to traditional patient care and consultation as to diagnosis and treatment,
physicians may be involved in medical research in a variety of areas (e.g.,
epidemiology, pharmacology, and toxicology) as their primary activity, or in
conjunction with patient-oriented medical practice. For example, physicians
may be involved in clinical trials to evaluate new drugs or other therapies. They
also may participate in studies on the causes of disease. The physician may be the
principal investigator, who is primarily responsible for such studies, or may participate
as a coinvestigator or collaborator, or simply by referring patients to the
studies. Many physicians involved in medical research also have a teaching position
at a medical school or a large teaching hospital.
C、医学研究和医学院校的职务
除了传统医生在诊断和治疗方面给病人治疗和会诊之外，医师们也有可能把参与各个领域的医学研究（如流行病学、药理学和毒理学）作为他们主要的工作，或者和以病人为导向的医疗实践相结合。譬如，医师们可以参与临床试验以评价一个新药或者其他的治疗方法。他们也可以参与病因学研究。医师可以成为主要研究者，他们主要负责这些研究，或者作为一个合作研究者和合作者参与其中，或者只是为研究提供患者。许多参与医学研究的医师也在医学院校或者达到教学性医院有一个教师职位。
D. Physicians As Expert Witnesses
In contrast to the traditional medical roles they fill as outlined above, physicians
frequently act as witnesses in court, either for the parties or, on occasion, as
court-appointed experts. Physician–witnesses may testify based on their activities
as treating or consulting physicians or more generally about medical and
scientific knowledge and its application to the issues in a case. In the former
role, they may be characterized as “fact” witnesses, but they will also be applying
medical expertise to a greater or lesser degree in assessing the significance of
the patient’s signs and symptoms and medical history, making a diagnosis, opining
on proper treatment and prognosis, and the like. In some medical fields,
such as clinical toxicology or occupational medicine, this dual role is quite common.
In other instances, the physician is applying his or her expertise solely to
offer an expert opinion, relying on factual clinical information developed by
treating physicians or from hospital records or other sources.42
A physician may be asked to testify about the physical condition of a plaintiff,
diagnosis, treatment, causes of the plaintiff’s condition, or prognosis. A physician
may also be asked to interpret epidemiological or industrial hygiene data if
they are within his or her scope of expertise. Such testimony may be important both in a factual sense—what happened and when—and as a basis for expert
opinion on such issues as the following:
1. Is the diagnosis correct? (assessing what injury the plaintiff suffered);
2. Were the appropriate treatments prescribed? (assessing the issues of standard
of care in a medical malpractice case or damages in a tort case);
3. What is the prognosis or the likely course of the plaintiff’s condition?
(assessing future damages);
4. Was the patient exposed to the substance in question? (assessing exposure
through patient symptoms and reports, such as eye burning, the detection
of an odor, or a headache, which provide indications as to the concentration
of an irritant or other agent);
5. Is there an increased risk of future disease? (assessing damages by predicting
future consequences of an existing condition; assessing a claim for
increased risk of future disease; assessing the reasonableness of a claim for
fear of disease (e.g., cancerphobia); or assessing the propriety of medical
surveillance in a medical monitoring claim); and
6. What caused the plaintiff’s medical condition? (assessing general and specific
causation).
42. Howard Hu & Frank E. Speizer, Influence of Environmental and Occupational Hazards on Disease,
in 1 Harrison’s Principles of Internal Medicine 18, 19 (Anthony S. Fauci et al. eds., 14th ed. 1998)
[hereinafter Principles of Internal Medicine].
D、医生作为专家证人
和上面所说的医生的传统角色形成对比，医师们经常在法庭上作证，他们有的时候为当事人作证，有的时候作为法庭指定的专家。医师的证词可以用下列方式证实：首先是基于他们治疗病人、接受病人咨询的活动，更多是利用他们的医学和科学知识和他们在这个案例中的应用。在前一种情况中，他们作为一个“事实上”的证人，但是，他们也将或多或少利用他们的医学专业知识去评价病人的症候、症状和医疗史的重要性，做出诊断，对正确的治疗和预后等发表意见。在一些医学领域，如临床毒理学及职业医学，这种双重身份更普遍。在其他一些情况下，医师只是被邀请来提供一个专业的意见，医师们主要依靠治疗医生、医院的病历记录以及其他途径得到事实的临床信息。[42]
一个医生也许被邀请去证实原告的身体健康状况、诊断、治疗、引起原告的这些状况的原因以及预后情况。如果在他自己的专业范围内的话，一个医生也有可能被邀请去解释流行病学和工业卫生学资料。这些证词也学非常重要，不仅在事实的判断（发生了什么和什么时候发生），而且在下列情况下可以作为一个专家意见的基础：
1. 诊断是正确的吗？（评估原告忍受了什么样的伤害）；
2. 医生给予了正确的治疗吗？（评估在一个医疗事故案例中标准治疗方案的内容以及在一个侵权案例中的损伤程度）；
3. 原告疾病的预后或者疾病的发展过程是怎样的？（评估未来的损伤）；
4. 病人了解所有的事实真相吗？(评估病人的症状和报告如眼睛烧伤、气味的检出、头痛等的公开程度，这可以提供关于这是一个刺激的或者其他情况的线索)；
5. 这是病人将来有可能患病的一个危险因素吗？（通过预测原告现在的疾病的未来发展过程评估疾病导致的损伤，评估一个关于未来有患病风险的主张，评估一个害怕患病的主张的合理性（如癌症恐惧），或者评估医疗监护在一个医疗监测主张中的合理性；以及
6.是什么促成了原告现在的医疗条件（评估一般因果关系和特殊因果关系）。
[42] 霍华德 胡和弗兰克 E 斯培兹. 环境和职业的危险对疾病的影响，哈里森内科原理18，19（安东尼 S，福次等编著，第14版，1998）（以下内科原理）
As set forth later in this reference guide,43 physicians do not always use the
same approach in evaluating these issues as the legal system does. For example,
in tort cases, liability will often turn on the identification of one or more causes
of the plaintiff’s condition. A physician, independent of legal issues, typically
uses the term causation or etiology to refer to the various levels of underlying
abnormality that have substantially led to the next higher level of abnormality,
disease, or diagnosis. This “chain,” or web, of causation is considered the “pathogenesis”
or pathophysiology of a disease. For instance, a heart attack may be due
to a sudden blockage of a coronary artery, which was facilitated by a preexisting
cholesterol plaque in the artery, which in turn is due to the patient’s high level
of blood cholesterol, which is due to genetics, diet, a sedentary lifestyle, and
smoking, which contributes at many levels.44 Most physicians are familiar with
the general importance, if not specific degrees of risk, of the listed internal biochemical
and mechanical factors in a heart attack, and with many other areas in
the web of causation, such as the common external factors listed above.45
43. See infra § IV and accompanying footnotes.
44. Elliot M. Antman & Eugene Braunwald, Acute Myocardial Infraction, in 1 Principles of Internal
Medicine, supra note 42, at 1352, 1352–53. In this guide, the term internal is used to refer to causal
factors and conditions internal to the patient’s body, such as genetic predisposition to coronary artery
disease, to distinguish them from causal factors that are external to the body, such as smoking and diet.
45. For a general discussion of the process used to infer internal and external causation, see Feinstein,
supra note 40, at 80–83. See, e.g., Carroll v. Morgan, 17 F.3d 787, 791 (5th Cir. 1994) (discussing
multiple causes of plaintiff’s coronary disease).
就像这本参考指南后面提到的那样，医生们不必总是象按照法定程序那样用同样的方法去评估这些结果。比如，在民事案例中，医生的责任常常倾向于去证明导致原告现在的状况的一种或多种原因。一个医师，不受法庭观点的约束，有代表性地使用因果关系和病因学的条款去谈及各种水平的潜在的异常，而这些异常则足以导致下一个更高水平的异常、疾病和诊断。这个因果关系“链”，或者叫做网，被称作“发病机理”，或者叫疾病的病理生理学。例如，一次心脏病发作可能归因于冠状动脉的一次突然阻塞，而这是由动脉壁先前存在的胆固醇斑块所推动的，动脉壁上的胆固醇斑块依次是归因于病人血液中胆固醇的过高，而基因、饮食习惯、一个不活动的生活习惯、吸烟等因都在一定程度上引起血液中胆固醇的过高[44]如果没有特殊程度的危险，大部分医生对这些一般情况的重要性都很熟悉，如列出的心脏病发作固有的生物化学和机械性因素，以及这个因果关系网中的许多其他方面，比如上面列出的一些普通的外部因素。[45]
[43] 见infra § IV和伴随的脚注
[44] Elliot M. Antman & Eugene Braunwald, 急性心肌梗塞，在1 内科原理，前面提到的注释[42]在1352，1352～1353。在这个指南中，条款“内部的”是指内因及病人身体内部的状态，如因为遗传因素导致的易患冠状动脉疾病，以此来区别由身体“外部”原因导致的外因，如吸烟和饮食习惯。
[45] 就如何区分内因和外因的方法作一个大体的讨论，见Feinstein 先前的注释[40]在80～83页，见，例如Carroll v.摩根，17 F.3d 787，791（第五期，循环杂志，1994）（关于原告冠状动脉疾病的多因素讨论）
While physicians dealing with diagnosis and treatment tend to think in terms
of both internal and external causation, courts are usually asked to determine the
role of causes that are external to the individual. Generally, physicians focus on
causal elements that can be addressed through medical treatment or through
changes in lifestyle or diet; courts focus primarily on causal elements for which
a litigant or other party might be held responsible. For example, a workers’
compensation case might concern the role of physiological stress at work in
causing underlying heart disease, or the role of carbon monoxide in triggering a
specific heart attack.46 Identification of those kinds of causes depends on information
concerning quantification of risks in the workplace environment, as
well as on the medical literature on causation, including the psychological, toxicological,
and epidemiological literature.47 To determine general causation, the
expert must review the pertinent literature, as familiarity with this literature is
key to expert opinion. For example, since many cardiologists advise patients on
returning to work after a heart attack, they will often be familiar with the literature
on work-based risks and cardiovascular disease, whereas most other physicians,
who deal with this question less frequently, would need to devote some
time to study before evaluating such a special consideration.
当医生诊断和治疗时，他们倾向于考虑内因和外因两方面，而法庭经常要求去确定这个影响因素在这个个例中是外因。总的来说，医生的关注点在于这个影响因素是可以被通过医学治疗以及改变生活方式和饮食习惯来消除，而法庭最主要的关注点在于诉讼人或者其他当事人有可能为这个影响因素负责。比如，一个工人的赔偿案例有可能涉及到工人在工作中的心理压力有可能是心脏病的一个潜在危险因素，或者一氧化氮在一个特殊的心脏病发作中是一个诱发因素。[46] 区分这些各种各样的发病原因既要依靠关于工作环境中风险量化的资料，也要依靠关于病因学的医学文献，包括心理学、毒理学和流行病学的文献。[47] 想要确定一般因果关系，专家必须翻阅适当的文献，因为熟悉这些文献是专家意见的关键所在。例如，尽管许多心脏病专家告诫他的病人，在患心脏病后又重回工作岗位，他们需要经常熟悉那些关于以工作为基础的风险和心血管疾病等方面的文献，然而许多其他的医生们，他们却很少这样做，他们在评估这么一个特殊情况之前需要花一些时间去学习。
[46] 见，例如，费奥. V，统一的货物路程，659，A.2d，436（N.J.1995）（卡车驾驶员的工作赔偿案例声称这个心脏病是由于职业性的暴露在一氧化氮气体中导致的，所以当事人应该提供更多的可靠的暴露在一氧化氮气体中的证据）。
[47] 见 库仑等，前面提到的注释19，在220～221
感谢您非常守信地完成任务，先把分数加了，我值班时抽空校对一下！
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