Bracken v. Workers' Comp. Appeals Bd.
| Decision Date | 25 September 1989 |
| Docket Number | No. B038997,B038997 |
| Citation | 214 Cal.App.3d 246,262 Cal.Rptr. 537 |
| Court | California Court of Appeals |
| Parties | Thomas T. BRACKEN, Petitioner, v. WORKERS' COMPENSATION APPEALS BOARD; Commercial Carriers, Inc.; and Ryder Services Corporation, Respondents. |
George and Buch, and Joan Politeo Freeman, for petitioner.
Hertz & Weitzman, and Steven C. Hertz for respondents Commercial Carriers, Inc., and Ryder Services Corp.
No appearance for respondent Workers' Compensation Appeals Board.
Petitioner (applicant) seeks review of the decision of respondent Workers' Compensation Appeals Board (Board) amending the findings of the workers' compensation judge (WCJ) that applicant sustained industrial injuries to his cardiovascular system resulting in 100 percent permanent disability.
We hold the Board's decision must be annulled because the Board erred in concluding the cardiovascular injuries were not industrial.
On March 13, 1986, applicant sustained a myocardial infarction (heart attack) while performing heavy work in the course of his employment as a truck driver by defendant Commercial Carriers, Inc. He sustained a second heart attack on March 31, 1986; and, while convalescing in Kaiser Hospital, he sustained cerebral vascular strokes on April 6 and 9, 1986. He is semicomatose and confined to a convalescent hospital.
Applicant did not testify because his semicomatose condition precludes speaking, reading and writing.
A CPK (creatine phosphokinase) heart muscle enzyme test administered at the hospital revealed a CPK level of 2,200; and heparin (a blood thinner) was administered to applicant to prevent blood clots. An echocardiogram was also performed. Although the hospital physicians apparently concluded an embolus (small blood clot) from the heart caused the strokes, the hospital records do not specifically indicate that an embolus broke off the heart, traveled to the brain, and caused the strokes.
Dr. Gromis and Dr. Padova concluded the heart attacks were industrially related, but disagreed as to whether the strokes were related to the heart attacks. Dr. Gillis originally opined the heart attacks precipitated the strokes, but subsequently changed his opinion.
Dr. Gromis submitted several medical reports and testified at the trial. Dr. Gillis and Dr. Padova were deposed, but did not testify at the trial.
Dr. Gromis consistently opined it was reasonably probable that following the massive heart attacks an embolus traveled from applicant's heart to the brain and caused strokes in both the right and left sides of the brain; although there is no medical test that can confirm this opinion, the opinion is based on experience, probabilities, and medical literature; the elevated CPK test level (2,200) of the heart muscle enzyme indicates the massiveness of the heart attack; the higher the enzyme level, the greater the likelihood of a stroke; and due to the brief time interval of several days between the second heart attack and the strokes, it is logical to conclude the offending embolus came from the heart.
Dr. Gillis, reporting for defendant, originally opined he could state no conclusion as to industrial causation of the heart attacks, but he concluded applicant
Subsequently, Dr. Gillis again reported he was unable to determine whether the heart attacks were industrially related. Defendant then referred the matter to Dr. Padova.
Dr. Padova opined the heart attacks were industrially related, but the strokes were not related to the heart attacks, observing it is more likely the strokes were due to a thrombosis of the arteries. Dr. Padova concluded that although cerebral embolus secondary to intracardiac mural thrombus was suspected as a cause of the strokes, this diagnosis was not proven since an intracardiac thrombus was not identified in the echocardiography and since the usual complications associated with thrombosis formation, such as congestive heart failure, persistent hypotension, or prolonged intermittent cardiac arrhythmia, apparently did not occur after the heart attack.
Upon reviewing Dr. Padova's report, Dr. Gillis retreated from his earlier opinion and concluded the strokes were not related to the heart attacks. In yet another report, Dr. Gillis stated that since the anticoagulation (heparin) treatment of the heart attacks at the hospital did not prevent the second stroke, there never was an embolic stroke, and hence there was no relation between the strokes and the heart attacks. He also noted the hospital echocardiogram showed no evidence of thrombus; and other cardiac manifestations, such as cardiac arrhythmia, can lead to embolic strokes.
At his deposition, Dr. Gillis agreed there was some objective evidence to support the existence of an embolism, and if one could show an embolus going from the heart, the stroke and its associated disability would be connected to the heart condition, but He stated further the hospital records indicate the treating physicians assumed there had been an embolus, but "if you use some Monday-morning quarterbacking and you look at the records and you say, 'Well, let's look at the criteria and were they met,' you come to the conclusion that no one could ever prove there had been an embolic stroke." Dr. Gillis discussed risk factors of thrombotic stroke such as age, high blood pressure history, smoking history, and cerebral arteriosclerosis, but omitted reference to heart attack as a risk factor in thrombotic stroke. He also discussed transient ischemic attacks as a harbinger of thrombotic stroke. Dr. Gillis stated he knew of no medical literature that says the worse the heart attack, the greater the likelihood of stroke.
In response to Dr. Gillis's changed opinion, Dr. Gromis reported that regardless of Dr. Gillis's speculation as to several mechanisms, such as cerebral arteriosclerosis, hypotension, and arrhythmia, that might explain the relationship between a massive heart attack and the stroke that follows it, the fact remains that applicant's heart attack, which was as massive as can be observed (CPK heart muscle enzyme test level of 2,200), when considered in the context of applicant's age and early history, caused the multiple strokes occurring soon after the heart attacks. In view of the 2,200 CPK level, an embolic etiology for the strokes is most likely, especially in light of the two well-documented strokes occurring on opposite sides of the brain soon after the heart attacks.
Dr. Gromis reported further there is a fundamental tenet in medicine that whenever possible, a single unifying diagnosis is more likely to be the correct diagnosis, whereas multiple unrelated diagnoses should be considered only as a last resort. It is common knowledge in medical literature that massive heart attacks go on to develop cerebral strokes soon thereafter. 1 The diagnosis of embolic stroke is a clinical one and there is no medical test available, such as echocardiology, that can alter the diagnosis. The single unifying diagnosis here is that heart attacks lead to strokes, and when massive heart attacks lead to multiple strokes in opposite sides of the brain soon after the heart attacks, the unifying diagnosis is massive heart attacks with complications of embolic stroke. Dr. Gillis, on the contrary, disregards the single unifying diagnosis tenet in accounting for applicant's heart attacks and complications, instead invoking three separate diagnoses: (1) Myocardial infarction, (2) right-sided thrombotic stroke, and (3) left-sided thrombotic stroke, all occurring within a period of three weeks. These separate diagnoses might be convincing if the time interval between the heart attack and the strokes were three years or more, but not where the interval is merely three weeks as here.
Dr. Gromis reported further that Dr. Gillis engages in "backwards reasoning" and poor understanding of stroke disorders in concluding that since intravenous heparin did not prevent the second stroke applicant could not have had a cerebral embolus. Rather, it is likely that heparin therapy prevented additional multiple strokes, thereby saving applicant's life.
As to Dr. Gillis's statement he knows of no medical literature that says the worse the heart attack, the greater the likelihood of stroke, Dr. Gromis cited the article on myocardial infarction and stroke in the Neurology journal (see ante, fn. 1) wherein it is stated that stroke as a complication of acute myocardial infarction has been long recognized and patients with acute myocardial infarction are at increased risk of stroke during the first month of convalescence. Dr. Gromis also referred to statements in this article that 92 percent of patients with stroke following heart attacks had CPK levels greater than 1,160 (as compared to applicant's CPK level of 2,200), and the incidence of stroke among patients with a CPK level of 1,160 is 24 times higher than among patients with lower CPK levels.
Regarding Dr. Gillis's speculative discussion of cerebral arteriosclerosis, age, blood pressure history, and smoking history as possible risk factors for thrombotic strokes, Dr. Gromis noted Dr. Gillis omitted heart attack as a risk factor, if not in fact the most likely cause, of thrombotic stroke as noted in the cited article on myocardial infarction and stroke in the Neurology journal. As to Dr. Gillis mentioning transient ischemic attacks as a harbinger of a thrombotic stroke, Dr. Gromis noted there is no evidence applicant ever had a transient ischemic attack.
Dr. Gromis concluded his final report by...
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