Reese v. Stroh

907 P.2d 282, 128 Wash. 2d 300
CourtWashington Supreme Court
DecidedDecember 14, 1995
Docket61935-2
StatusPublished
Cited by82 cases

This text of 907 P.2d 282 (Reese v. Stroh) is published on Counsel Stack Legal Research, covering Washington Supreme Court primary law. Counsel Stack provides free access to over 12 million legal documents including statutes, case law, regulations, and constitutions.

Bluebook
Reese v. Stroh, 907 P.2d 282, 128 Wash. 2d 300 (Wash. 1995).

Opinions

[302]*302Madsen, J.

— William and Frances Reese brought this medical malpractice action against Dr. James E. Stroh, Jr., alleging that he negligently failed to treat Mr. Reese’s emphysema with a protein replacement therapy called Prolastin. The trial court excluded the Reeses’ expert medical witness’ opinion testimony regarding causation as lacking sufficient foundation to go to the jury. The Court of Appeals reversed, holding such testimony should be evaluated under the test set forth in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S. Ct. 2786, 125 L. Ed. 2d 469 (1993). We affirm that reversal, though under an analysis considerably different from that of the Court of Appeals.

Facts

In 1984, William Reese, hereafter referred to as the Plaintiff, began seeing Dr. Stephen Aprill for treatment of asthma. One year later, Dr. Aprill referred the Plaintiff to Dr. Stroh because he believed that Plaintiff’s condition involved more than asthma. Dr. Stroh, hereafter referred to as the Defendant, is board certified in internal medicine and allergy and immunology. In spring 1985, the Defendant diagnosed the Plaintiff as having asthma, chronic obstruction pulmonary disease, and alpha-1-antitrypsin deficiency (AAT deficiency). AAT deficiency is a rare genetic disease characterized by low serum levels of AAT, a blood-borne protein which inhibits the destructive action of certain enzymes in the lung. In some patients with AAT deficiency, those uninhibited enzymes can destroy lung tissue, causing emphysema.

When the Defendant diagnosed the Plaintiff with AAT deficiency in 1985, AAT therapy, marketed under the name Prolastin, was not available. The Defendant prescribed bronchodilator medications, steroids, and antibiotics, and urged the Plaintiff to stop smoking and to avoid allergens and environmental irritants. The Defendant told the Plaintiff that his condition was not serious and that [303]*303he could expect to lose lung capacity at a rate approximately one percent per year faster than the average person. Unfortunately, the Plaintiff lost lung capacity more rapidly than the Defendant predicted.

In November 1989, the Plaintiff learned that his brother also had been diagnosed with AAT deficiency and was to begin Prolastin therapy, which had been approved by the Food and Drug Administration (FDA) in 1987. Prolastin therapy consists of administering Prolastin (a preparation of purified human AAT) intravenously at regular intervals to maintain AAT levels in the blood above the AAT deficiency threshold. Prolastin therapy has proven valuable in treating other serum protein deficiencies such as hemophilia. The FDA approved Prolastin for treatment of AAT-deficient patients based on the knowledge that Prolastin raises the level of antitrypsin in the blood, but without statistical proof of its efficacy.1 Plaintiff and his wife called the Defendant to inquire about Prolastin therapy. The Defendant declined to prescribe Prolastin because he regarded it as an expensive therapy of unproven benefit, and because he thought Prolastin therapy posed possible risks for transmission of blood-borne infections. In March 1990, the Plaintiff began Prolastin therapy with his brother’s doctor.

In October 1990, Plaintiff and his wife filed this action against the Defendant, alleging that his failure to prescribe Prolastin resulted in a preventable worsening of Plaintiff’s lung function. More specifically, Plaintiff contended that the Defendant should have treated him with Prolastin between 1987, when Prolastin was approved by the FDA, and 1989, when Plaintiff’s lung capacity fell below the critical range for treatment. The Defendant subsequently filed a motion in limine to exclude the [304]*304testimony of the Plaintiffs experts on causation. The basis of the motion was that the "[P]laintiffs experts lack the foundation to state with reasonable medical certainty that the 18 month delay in Prolastin treatment caused [the Defendant’s] current pulmonary condition . . . .” Clerk’s Papers at 70. The trial court reserved ruling on the motion until trial.

The Plaintiffs first expert witness was Dr. Robert J. Fallat, chief of the pulmonary division at California Pacific Medical Center in San Francisco. Dr. Fallat is board qualified in internal and pulmonary medicine and has done research on AAT deficiency since 1966. After examining him as to his qualifications and the nature of AAT deficiency, as well as his knowledge about and experience with Prolastin therapy, the Plaintiff sought to elicit testimony as to whether Dr. Fallat had "an opinion with a reasonable medical probability basis as to whether or not Prolastin is an effective treatment for Alpha-1 Antitrypsin Deficiency patient such as Mr. Reese.” Verbatim Report of Proceedings (VRP) at 70 (June 18, 1992). After sustaining a foundation objection to the opinion, the trial court allowed the Plaintiff to continue Dr. Fallat’s testimony outside the presence of the jury as an offer of proof.

On the basis of the information and studies supporting the FDA’s approval of Prolastin, his own clinical experience, and information regarding the Plaintiffs medical condition, Dr. Fallat concluded that, based upon reasonable medical probability, Prolastin therapy would be effective for the Plaintiff. Dr. Fallat also concluded that there "wouldn’t be a handful of pulmonologists in the country” who, given the Plaintiffs circumstances, would not prescribe Prolastin therapy, and that by failing to prescribe Prolastin, the Defendant had not acted as a reasonably prudent physician. VRP at 103 (June 18, 1992). Dr. Fallat also defended the FDA’s decision to approve the drug without statistical proof that it was effective in halting the progression of lung disease.

[305]*305After hearing the offer of proof, the trial court held that Dr. Fallat’s opinion would be inadmissible because it found that Dr. Fallat did not have a statistically significant basis for his opinion as to the efficacy of Prolastin therapy in treating the Plaintiff’s malady. Although the trial court did not state it was applying the admissibility test set forth in Frye v. United States, 293 F. 1013, 34 A.L.R. 145 (D.C. Cir. 1923), its explanation for rejecting Dr. Fallat’s testimony indicates it found Prolastin therapy not to be generally accepted within the relevant scientific community. See Frye, 293 F. at 1014.

In light of the court’s ruling, the Plaintiff decided not to call his other expert witnesses, whose testimony would have been to the same effect. The Defendant then moved for a directed verdict, which the trial court granted on the basis that "[Plaintiffl could not prove proximate cause.” Clerk’s Papers at 874. The Plaintiff’s motion for reconsideration was denied, and he appealed the trial court’s evidentiary ruling.

Division One of the Court of Appeals reversed the trial court, holding that the Frye test does not apply to expert testimony in civil cases, and that even if it did, Dr. Fallat’s testimony was admissible because the methods he used to reach his conclusion were generally accepted in the scientific community. Reese v. Stroh, 74 Wn. App. 550, 555-56, 874 P.2d 200 (1994). In rejecting the Frye test, the Court of Appeals expressly adopted the approach taken in Daubert, 113 S. Ct. at 2786. Finding Dr.

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Bluebook (online)
907 P.2d 282, 128 Wash. 2d 300, Counsel Stack Legal Research, https://law.counselstack.com/opinion/reese-v-stroh-wash-1995.