Court Opinion

ID: 9676566
Source: CourtListenerOpinion
Date Created: 2023-08-24 05:27:27.687634+00
Date Added: 2024-06-11T18:16:49.043404
License: Public Domain

PHIL HARDBERGER, Chief Justice.
I respectfully dissent from the majority’s finding that no probative evidence supports the causation element of the Lettes’ medical malpractice claim.
In a medical malpractice case, the plaintiff must establish a causal connection based on “reasonable medical probability,” not mere conjecture, speculation or possibility. Park Place Hosp. v. Estate of Milo, 909 S.W.2d 508, 511 (Tex.1995); Bradley v. Rogers, 879 S.W.2d 947, 953-54 (Tex.App.-Houston [14th Dist.] 1994, writ denied). However, a plaintiff is not required to establish causation in terms of medical certainty and is not required to exclude every other reasonable hypothesis. Bradley, 879 S.W.2d at 954. A possible cause becomes a probable cause when it becomes more likely than not that the injury was a result of its action in the absence of other reasonable causal explanations. Bradley, 879 S.W.2d at 954. “The trier of fact may decide the issue of proximate causation in medical malpractice cases when: (1) general experience and common sense will enable layman to determine the causal relationship between the event and the condition; (2) scientific principles, usually proved by expert testimony, establish a traceable chain of causation from the condition back to the event; and (3) a probable causal relationship is shown by expert testimony.” Id. Proximate cause, like any other ultimate fact, may be established by circumstantial evidence. Farley v. M M Cattle Co., 529 S.W.2d 751, 755 (Tex.1975).
The issue in this appeal is whether evidence was presented from which reasonable minds could draw an inference that the administration of the Toradol was a substantial factor in bringing about Mr. Lette’s bleeding complications and without which the harm would not have occurred. Kramer v. Lewisville Memorial Hosp., 858 S.W.2d 397, 400 (Tex.1993); Bradley, 879 S.W.2d at 953. The Lettes are not required to exclude all possibility that the bleeding complications occurred other than as they allege or every other reasonable hypothesis. Farley v. M M Cattle Co., 529 S.W.2d at 755; Bradley, 879 S.W.2d at 954. The Lettes must show only that the greater probability is that the Toradol caused the bleeding complications. Farley, 529 S.W.2d at 755-56. In reviewing whether the Lettes met this burden, we consider only the evidence favorable to the Lettes, disregarding all contrary evidence and inferences. Moore v. K Mart Corp., 981 S.W.2d 266, 269 (Tex.App.-San Antonio 1998, pet. denied).
*604Mr. Lette’s surgery was performed on October 1, 1998. Mr. Lette did not begin to experience complications until 5:00 a.m. on October 3,1998.
Dr. Joel Moake, a hematologist testified that the effect of Lovenox peaks or is at its maximum effective level a few hours after it is administered. Dr. Moake further testified that the effect of Lovenox would be clinically inconsequential twelve hours after it is administered. Mr. Lette received the first dose of Lovenox at 9:00 a.m. on October 2nd. The Lovenox administered at 9:00 a.m. on October 2nd peaked at 11:00 a.m. on October 2nd, Mr. Lette did not begin to experience complications until 18 hours later — when the effect of the first dose of Lovenox was clinically inconsequential. Mr. Lette received a second dose of Lovenox at 10:00 p.m. on October 2nd. The second dose of Lovenox peaked at its maximum effective level at 12:00 a.m. on October 3rd, Mr. Lette did not begin to experience complications until five hours later as the effect of the Lovenox was dissipating.
Dr. Moake testified that Coumadin takes 3^4 days to reach therapeutic levels and the effect of Coumadin on clotting ability after twelve hours is clinical inconsequential. Mr. Lette received Coumadin at 12:35 a.m. on October 3rd. Between the time the Coumadin was administered and the time Mr. Lette began experiencing his complications four and one-half hours later, the effect of the Coumadin was clinical inconsequential.
The medical literature describing Tora-dol was attached as an exhibit to the deposition of James Clark Garriott, Ph.D. It states, “Following single oral doses of 2.5 mg to 200 mg, a 75% to 100% inhibition in platelet aggregation occurred within 3 hours.” Mr. Lette received Toradol at 2:05 a.m. on October 3rd. Three hours later, Mr. Lette began experiencing his complications. The timing of the events based on the medical literature and expert testimony regarding the effect of the various drugs administered to Mr. Lette is circumstantial evidence that the Toradol was a substantial factor in bringing about Mr. Lette’s complications and without which the harm would not have occurred. Dr. Moake testified that with a reasonable degree of medical probability the Toradol caused or potentiated bleeding.
Dr. Moake testified regarding the manner in which blood clots. First, the blood platelets, a cellular element, stick to the side of the blood vessel that is injured and cohere or stick together, which is the first part of the clot. Second, the formation of fibrin strands over the platelet clump hold the platelets down over the injured site. Toradol is an antiplatelet agent that interferes with platelet clumping (the first step in clotting). Lovenox and Coumadin are anticoagulants that interfere with fibrin formation (the second step of clotting). The administration of the Toradol prevented the first step of the clotting from occurring. By preventing the first step, the administration of the Toradol prevented any chance that the blood would clot, thereby depriving Mr. Lette of more than a 50% chance of avoiding the harm by the clotting of his blood.
In its standard of review, the majority relies on Helm v. Swan to contend that “other possible causes of the injury must be ruled out with reasonable certainty.” 61 S.W.3d 493 (Tex.App.-San Antonio 2001, pet. denied). However, the Helm court relied heavily on: (1) the absence of medical literature to support the expert’s opinion that “an eight or thirteen hour delay in giving fluid therapy prevents or lessens the complications of severe necrotizing pancreatitis;” and (2) the existence of medical literature to support the opinion that some patients suffer the complication of *605severe necrotizing pancreatitis even with prompt fluid resuscitation after the surgical procedure undertaken in that case. 61 S.W.3d at 497. Therefore, in Helm, no medical literature could be relied upon to support the plaintiffs theory regarding the cause of the injury, i.e. lack of prompt fluid therapy, and medical literature could not exclude the possibility that the severe ne-crotizing pancreatitis was an unavoidable complication of the surgical procedure regardless of the defendants’ actions.
Unlike Helm, Dr. Moake expressly relied on medical literature regarding the effect of the various drugs administered to support his opinion that the effect of the other medications was “clinical inconsequential” and was “dissipating.” No medical literature was introduced to support a theory that Mr. Lette would have developed the bleeding complications simply based on the nature of his surgical procedure independent of the administration of the Toradol. Unlike Helm, circumstantial evidence was presented in this case, supported by medical literature, from which reasonable minds could draw an inference that the administration of the Toradol was a substantial factor in bringing about Mr. Lette’s bleeding complications and without which the harm would not have occurred.
Because the majority concludes otherwise, I respectfully dissent.