Failure to Warn Even When You Warn? Court Rejects Plaintiff's Theory

One of the fascinating and disturbing things about failure to warn claims is the endless supply of creative, far-fetched, fantastic, implausible, fanciful, incredible, questionable, even bizarre theories that plaintiff lawyers sometimes come up with to support this type of claim.

Last week, a Pennsylvania appeals court rejected just such a theory. Specifically, plaintiff alleged that a failure to warn caused her injury -- nothing strange there.  But the manufacturer DID warn specifically of the condition she developed.  So, what was the plaintiff's failure to warn theory?  That a drug maker may be liable for failure to warn despite warning of the condition plaintiff developed, because a warning about a different medical issue —one that she did not develop— would somehow have caused her doctor to not prescribe the drug.  Cochran v. Wyeth Inc., 2010 WL 2902717 (Pa. Super. Ct., 7/27/10).

Plaintiff ingested the prescription weight-loss drug dexfenfluramine, which was manufactured by Wyeth and sold under the brand name Redux. Wyeth informed the prescriber that Redux may cause primary pulmonary hypertension (“PPH”). The doctor, in turn, warned plaintiff of the risk of PPH prior to prescribing her Redux. At the time of his decision, however, the prescriber claimed he was unaware of the risk that Redux may cause valvular heart disease (“VHD”).  Later, plaintiff was diagnosed with PPH, which she had been warned about.  But she claimed that the doctor would not have prescribed Redux to her had he been warned that Redux could cause VHD.

Proximate cause is an essential element in a failure to warn case.  A proximate, or legal cause, is defined under Pennsylvania law as a substantial contributing factor in bringing about the harm in question. That is, a plaintiff must establish proximate causation by showing that had defendant issued a proper warning to the learned intermediary, he would have altered his behavior and the injury would have been avoided.   Wyeth argued that even if its warnings with regard to VHD were inadequate, its failure to warn of VHD was not the proximate cause of plaintiff's PPH.  To establish proximate causation, plaintiff must prove that the warnings failed to disclose the risk of her particular injury (PPH).

The trial court agreed. On appeal, the court found an absence of clear authority on the issue, but strong guidance in those cases that have addressed a plaintiff's burden of proving proximate causation in the informed consent context.  Finding the torts of informed consent and failure to warn analogous, the superior court was persuaded by those jurisdictions that have concluded a plaintiff cannot establish proximate causation where the non-disclosed risk never materialized into an injury.

Here, the risk of VHD did not develop into the actual injury of VHD. Although the prescriber testified in deposition that he would not have prescribed Redux had he known of the risk of VHD, this does not alter the fact that while Wyeth allegedly failed to disclose the risk of VHD the plaintiff suffered from PPH. In these circumstances, the relationship between the legal wrong (the alleged failure to disclose the risk of VHD) and the injury (PPH) was  "not directly correlative and is too remote" for proximate causation.

Summary judgment for defendant affirmed.

 

New Study On Diet And Heart Disease Makes Important Point About Epidemiology

Readers may have heard the response by the person warned by a family member that what he or she was eating was bad for their heart. “Wait a month and there will be a different study showing it is good for me.”  What we know for sure about diet and the heart is actually a surprisingly short list.

This week comes the study, A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease, by Drs. Mente, de Koning, et al. , 2009 Arch Intern Med. 169(7):659-669. This review study did an analysis of nearly 200 studies involving millions of people.


The authors concluded that strong evidence supports valid associations of protective factors for vegetables, nuts, and "Mediterranean" diet patterns, but that associations of harmful factors included intake of trans–fatty acids and foods with a high glycemic index.


Significantly, insufficient evidence of association was present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; meat; eggs; and milk. 


One of the interesting features is that the authors used the traditional Bradford Hill guidelines on drawing causation conclusions from evidence of association to derive a causation score, basing it on 4 criteria (strength, consistency, temporality, and coherence) for each dietary exposure in cohort studies; they also examined the results for consistency with the findings of randomized trials.

Epidemiology involves judgment; it is not an absolute science, and the presence of confounding factors and the difficulty in finding an adequate control/comparison group for many food issues are similar to the issues seen in toxic tort litigation. 


No surprise, then, that the authors conclude that future evaluation of dietary patterns, including their nutrient and food components, in cohort studies and randomized trials is recommended.