Abbreviations--- Summary of paper (including list of pitfalls)--- Introduction to paper--- Pitfalls #1-7--- Pitfalls #8-15--- Discussion--- References
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8. Attributing causation with certainty when it is unwarranted by the facts

A physician stated that his patient's severe emphysema was caused by work as a garage mechanic. The patient was a heavy smoker and had no history of specific occupational illness (i.e., no history of occupational asthma, no pneumoconiosis.) A review of the medial literature found no evidence whatsoever for association of emphysema with low level exposure to garage fumes.

This example is easier to analyze than situations where there is more than one known cause for a disease. A good case in point is the causation of lung cancer when a patient was both a heavy cigarette smoker and also exposed to asbestos. Enterline has written that no opinion about the tumor's etiology can be certain, and that to attribute the lung cancer to asbestos with certainty would mean that asbestos exposure blocked the possible effects of all other cancer-causing agents, a scientifically untenable position (Enterline 1980). Rather than reach an unwarranted conclusion 'with certainty,' the physician could point out the multi-factorial causation and venture a probability for each factor (based on smoking history, asbestos exposure history, etc.; Enterline 1980). The pitfall is in trying to mold an uncertain situation into a statement that, in order to become legally acceptable, becomes medically invalid.

An example of a medically invalid statement was prepared by an oncologist who had treated lung cancer in a 69-year-old man with a history of heavy smoking.

Over several months of chemotherapy, the oncologist made no mention in numerous letters and chart notes regarding asbestos as a cause of his patient's lung cancer, instead attributing the cancer solely to cigarette smoking. Two years after the patient died, the plaintiff's attorney asked the oncologist to write a letter about causation of the cancer in light of "new" information - supplied by the attorney - that the patient had been continuously exposed to asbestos in his job as an automobile service manager. Without any corroborating evidence of actual asbestos exposure, and despite the fact that the patient never had any asbestos-related disease, the physician obliged, writing the attorney: "There is a large body of knowledge relating to the health risks of both asbestos and cigarette smoking because of the economic implications of these carcinogens. It is certainly within reasonable medical probability that both of these carcinogens [cigarettes and lung cancer] played a part in Mr. X's disease."

This "quick fix" attempt by the oncologist (Pitfall 1) failed because it was based on undocumented asbestos exposure information, and also because the conclusion was medically incorrect. There must be confirmation of some asbestos-related pathology to implicate the mineral as a cause of lung cancer (Browne 1986; Gibbs 1995; Hughes and Weill 1991).

Another variation of the 'certainty' pitfall occurs when physicians state that an occupational illness "substantially accelerated a patient's death" when there were many causes, including natural aging. It is not uncommon to see "substantial acceleration" of death claimed for patients who died after age 75, and of medical problems unrelated to their occupation. Notwithstanding the medical facts in such a case, can physicians credibly claim "substantial acceleration of death" when a patient lives well beyond his life-expectancy?

9. Relying on a claimant's own smoking history

Many OLD claimants say they don't smoke. In our lab we routinely do co-oximetry all arterial blood gases, and this test includes measurement of blood carbon monoxide (Martin 1992). Carbon monoxide (CO) is elevated in the blood of all current cigarette and cigar smokers, usually to a level between 5% and 10% (in non-smokers it is less 2.5%). On many occasions CO is elevated in professed "non-smokers," indicating current smoking (the half-life of CO in the blood is about six hours). When the claimant is confronted with this laboratory information he or she will often revise the history and admit to "smoking some but not as much as before." If blood gas measurements are not done (the test requires a sample of arterial blood), a CO level can be checked in a venous blood sample, or even in a sample of air exhaled by the claimant.

A variation of this pitfall is relying on a standard questionnaire instead of interviewing the claimant or reviewing available medical records. One physician wrote in his report that the claimant was a "life-long non-smoker," and based this statement on negative answers to simple "yes" or "no" questions the claimant made on an occupational history questionnaire. Yet this claimant, who had been previously examined numerous times by other physicians for a chronic heart condition, had a clear history of smoking heavily in the past, and would probably have admitted this history had he been asked directly. The expert's erroneous assertion about the smoking history undermined his testimony when the claim came to trial.

The importance of an accurate smoking history is obvious. Many conditions claimed to be occupational in origin are instead more likely to occur, or be aggravated from, smoking.

10. Mis-interpreting pulmonary function and arterial blood gas tests

Pulmonary function tests are standard tests of lung function performed in most hospitals and in many physicians offices. They require the subject to blow forcefully through a tube, plus perform other maneuvers that can give valuable information about lung function. Arterial blood gas test is done on a sample of arterial blood, and checks for (among other parameters) the patients level of oxygenation. The results of these tests are interpreted as to both the existence and type of abnormality by a physician with specialized training (usually a pulmonologist). Frequently, however, in cases reviewed for compensation the test results are mis-interpreted. Four common errors include:

a) interpreting a low diffusing capacity (DLCO) as indicative of diffusion impairment without accounting for the patient's hematocrit or carbon monoxide level (both can affect the DLCO (Ruppel 1991).

b) interpreting improvement in either FEF25-75% or maximal voluntary ventilation (MVV), after inhaled bronchodilator, as indicative of hyper-reactive airways disease or asthma (FEF25-75% is too sensitive a measurement to gauge bronchial hyperresponsiveness; also, sequential FEF25-75% measurements must be made at the same lung volume for valid comparison (Ruppel 1991). MVV is effort-dependent and bears a fixed relationship to FEV-1 (Ruppel 1991); if MVV improves without concomitant change in FEV-1 the patient's initial test likely reflected suboptimal effort).

c) equating an abnormal methacholine challenge response with a diagnosis of asthma. A drop in FEV-1 of 20% after inhaling methacholine indicates only airway hyperresponsiveness, which can be found in many other conditions (Ramsdale 1984; Yan 1985; Pattemore 1990).

d) interpreting a low resting PaO2 as indicative of "diffusion block" and therefore interstitial lung disease; pure diffusion impairment is rare and does not cause significant reduction of resting PaO2 (Bates 1989).

11. Missing the real cause of a patient's complaint

Physicians who evaluate patients for a third party (lawyer or government agency) do not have a true doctor-patient relationship. For example, there is no obligation to treat and/or followup on the patient's problem. However, physicians do have an obligation call it ethical or moral to help the patient medically if that is possible at the time of evaluation.

A 46-year-old woman filed a Workers' Compensation claim for "industrial bronchitis." Her main symptom was chronic cough for a year. She had worked as an assembler of motors and claimed that dust and fumes in the factory caused her problem. She was using oral theophylline plus both a beta-adrenergic and a steroid inhaler, all without apparent benefit. A physician was asked to evaluate her "on the claim of industrial bronchitis." Based on her symptoms (chronic cough, post nasal drip) the physician suspected chronic sinusitis; sinus x-rays confirmed bilateral maxillary sinusitis with air fluid levels. She was referred to an otolaryngologist.

Although the physician was only asked to evaluate the claim of industrial bronchitis, that clearly was not the cause of her cough. One does not have to become a treating physician to make the correct diagnosis or steer the claimant in the direction of proper therapy.

Along the same line, physicians should encourage any patient they see, no matter what the referral source, to quit smoking. I have seen numerous OLD claimants who still smoke. Without a trace of irony, many of them opined that their cough or shortness of breath was solely related to prior occupational exposure. Physicians should use the opportunity to remind claimants that, irrespective of the merits of their claim, cigarettes are harming their health and may be causing their symptoms.

12. Diagnosing occupational lung disease without attempting to remove the patient from the cause

Physicians also have an obligation to help remove workers from harmful environments. It may not be feasible (for economic and other reasons) to relocate the patient, but every attempt should be made to remove him or her from the offending agent(s) (Chan-Yeung 1990; Merchant 1990). Workers cannot rely on respirators and face masks to prevent further inhalation damage. One death has been reported in a patient with documented toluene diisocyante asthma who continued to work with the compound (Fabbri 1988). Studies of patients with occupational asthma who remain in the same industry show that they either do not recover or continue to deteriorate (Chan-Yeung 1990). If a physician suspects OLD, steps should be taken to remove the patient from the cause.

13. Confusion over basic terminology and pathophysiology in OLD

There are many controversies in the field of OLD. This pitfall refers to statements which are factually incorrect, i.e., not considered a matter of opinion. Among the more common mis-statements made by physicians:

a) 'continued asthma symptoms after a patient has left the workplace rules out occupationally-caused asthma' [not true; see Chan-Yeung 1990; Chan-Yeung 1982; Moller 1986; Cockcroft 1990; Mapp 1988; Malo 1988; Allard 1989].

b) 'absence of prior sensitization rules out occupational asthma' (i.e., reversible airways obstruction with bronchial hyperresponsiveness) [not true; see Brooks 1985; Tarlo 1989].

c) 'blood eosinophilia in asthma is specific for allergy' [not true; see Kay 1985].

d) 'antibody to an inhaled compound (e.g., trimellitic acid) is diagnostic of occupational asthma from that compound' [not true; see Patterson 1990].

e) 'the presence of pleural thickening/pleural plaques on the chest x-ray indicates asbestosis' [not true; see ATS 1986; pages 363-68].

f) 'adenocarcinoma of the lung is not smoking-related' [not true; see Brownson 1987].

g) 'large-airway obstruction with emphysema is explained by asbestos inhalation' [no evidence for; see Churg 1986; Kilburn 1985; Lerman 1986].

Regarding this pitfall, one attorney experienced in OLD litigation has written: "I have frequently witnessed occasions in which medical experts ignore or reject the published diagnostic standards and instead employ peculiar nomenclatures and diagnostic criteria in a regrettable litigation tactic calculated to confuse" (Richman 1989). A good medical expert does not want to confuse anyone, least of all a jury hearing the case.

A smoker with COPD worked as a paint sprayer. He was treated in an emergency department April 3 for COPD exacerbation, and released; he returned to work the next day. A month later he learned that the paint he used in early April contains some cyanide compound. An attorney referred him to a physician, who ordered a cyanide blood level; it was 25 ng/ml, a value in the expected range for cigarette smokers. (Cyanide causes mild symptoms when the level is above 50 ng/ml; depressed level of consciousness begins at 100 ng/ml and death occurs above 300 ng/ml [Hall 1986]. At no time was there any documentation of shock, acidosis or cerebral hypoxia. All of the patient's symptoms were consistent with previously-documented COPD. Nonetheless, the physician wrote to the attorney that the patient "suffered an episode of acute cyanide toxicity on April 3, and now suffers from chronic low-level cyanide toxicity." Subsequently a claim was made in civil court for "acute and chronic cyanide toxicity." The case was ultimately dismissed.

14. Using sloppy or incorrect language, including misspelling

It is amazing how often physicians send out reports with obviously incorrect spelling, syntax, terminology and even the claimant's name. This type of mistake can weaken the physician's credibility and harm the side he or she is trying to help. The usual reason, I suspect, is that many physicians do not read over what they dictate or make no attempt to edit their report. A few examples I have encountered (the intended word is in brackets):

"The patient has a long-standing history of tobaggism [tobaccoism]."

"I believe it entirely impossible [possible] that it caused also an irreversible airway obstructive syndrome leading to the state now where she is a total pulmonary cripple."

"After careful review of his records and noting the progressive nature of his/her [his] subjective symptoms..."

"I evaluated Mr. Brown on October 14, 19--. . . Past medical history indicates that Mr. Jones [Mr. Brown]. . ."

15. Not saying "I don't know," when you don't

It is entirely proper to say there is not enough information, that the diagnosis is inconclusive, and let the chips fall where they may. If you find you need more information to reach a valid conclusion hospital records, additional tests, whatever that should be stated in your report. It is better to be forthright and uncertain than certain and wrong.

Continue with Discussion---

Abbreviations--- Summary of paper (including list of pitfalls)--- Introduction to paper--- Pitfalls #1-7--- Pitfalls #8-15--- References
Return to Pulmonary Division home page