Opinion ID: 2624953
Heading Depth: 1
Heading Rank: 7

Heading: sufficiency of the evidence

Text: [¶ 58] Appellant contends that the evidence was not sufficient for a jury to infer beyond a reasonable doubt that his conduct caused Mary Fink's death. Due to Mary Fink's pre-existing risk factors for developing blood clots, the coroner's testimony as to several possibilities regarding the development of Mary Fink's blood clot, and the potential intervening cause of her treating physicians' conduct, appellant argues that the evidence was insufficient to sustain his convictions. Appellant does not challenge the sufficiency of the evidence as to any other element of this conviction or the conviction pertaining to Albert Fink. When reviewing an appeal based on sufficiency of the evidence, we view the evidence, and any applicable inferences based on the evidence, in a light most favorable to the State. Nixon v. State, 994 P.2d 324, 329 (Wyo.1999); and see Pool v. State, 2001 WY 8, 17 P.3d 1285 (Wyo.2001). In conducting such a review, we do not substitute our judgment for that of the jury; rather, we determine whether a quorum of reasonable and rational individuals would, or even could, have found the essential elements of the crime were proven beyond a reasonable doubt. Id. McFarlane v. State, 2001 WY 10, ¶ 4, 17 P.3d 31, 32 (Wyo.2001). Even though it is possible to draw other inferences from the evidence which has been presented, the jury has the responsibility to resolve conflicts in the evidence. Bloomquist, 914 P.2d at 824. We incorporate our prior discussion herein on the legal standard for proximate cause. [¶ 59] After ankle surgery on May 6, 1999, Mary Fink experienced dizziness at the hospital on May 7, 1999, and died. The hospital's pathologists performed an autopsy, which the coroner, Dr. Thorpen, attended. According to Dr. Thorpen, Mary Fink's cause of death was bilateral pulmonary emboli, or blood clots which form in the different parts of the body, primarily the deep veins of the lower extremities and the pelvis. Blood clots age without producing symptoms until a part, or the entire clot, breaks off, travels up the venous system to the heart, and lodges in the pulmonary artery. On May 7, 1999, a blood clot (or pieces of the clot) the diameter of an adult thumban inch or greaterdid exactly this, causing Mary Fink to immediately lose oxygen, which is not survivable. [¶ 60] One can estimate a clot's age by utilizing its microscopic characteristics as a guideline. After examining slides of Mary Fink's blood clot, Dr. Thorpen agreed with the hospital pathologist that the clot could have happened at any time but most particularly probably in the one to two weeks following the accident. He stated repeatedly that the clot was one to two weeks or older, five days old at a minimum, but acknowledged that it was possible that the clot could have been a month old, possible that the clot could have been there already, and possible that the thromboembolic event could have occurred anywhere at any time. [¶ 61] Dr. Thorpen conducted a complete review of Mary Fink's medical records and medical history. In speaking with her family, he could find no previous history of a blood clot in the lower extremities. A major risk factor for developing blood clots is a blunt force injury or fracture to the lower extremities. In addition, Mary Fink was immobilized with some sort of orthopedic device and advised not to exercise or move that extremity, immobilization being an additional risk factor for developing clots. Dr. Thorpen characterized Mary Fink's ankle fracture as considerable. Such an injury disrupts a vein's lining, slows blood flow to that area, and a clot begins to develop. According to Dr. Thorpen, the body's natural mechanism to dissolve clots likely failed Mary Fink due to the leg trauma and resulting damage to her veins. [¶ 62] As far as other relevant risk factors, Dr. Thorpen did observe that Mary Fink was obese and fifty-five years of age (risk of developing blood clots in the leg rises with each decade of life). Inherited factors such as hypercoagulability might also contribute to developing blood clots, but testing must be done while a person is still alive, and the medical history obtained by Dr. Thorpen did not indicate the presence of hypercoagulability. [¶ 63] Dr. Thorpen reviewed the operative reports regarding Mary Fink's ankle surgery, which appeared to go well, but he did not know why the surgery was not performed immediately. When asked, based on Mary Fink's age and the presence of obesity, recent trauma or injury, and immobilization, whether it was foreseeable that something like this could happen when surgery is slated, Dr. Thorpen replied, [n]ot in this case and reiterated that the blood clot was present, you know, prior to the surgery. [¶ 64] Dr. Thorpen opined that, from a medical standpoint, Mary Fink's ankle fracture was the beginning of the process which led to her blood clots, and once that process began, it led directly to her death. He testified that it was possible but not likely that Mary Fink could have had the pulmonary thromboembolism without this accident ever occurring, but saw no evidence to suggest it in this case, characterizing the proposition as speculative. Dr. Thorpen felt the ankle fracture was clearly the most significant risk factorit causes damage to a vein or veins, slows blood flow, implicates immobilization, and enhanced the other pre-existing risk factors (age, obesity). Dr. Thorpen testified: Q. But in your medical opinion, would she have suffered this embolism without the fractured ankle? A. I would have to say it's possible. Q. Do you see any evidence to suggest that that is what occurred? A. No, sir, I don't. Q. And when we look solely at evidence and not speculation and possibilities, is there any other cause for that clot? A. In my opinion, no. [¶ 65] We find that, based on Dr. Thorpen's testimony, which is uncontradicted in the record, and its inferences when viewed in a light most favorable to the State, a rational jury could conclude beyond a reasonable doubt that appellant's conduct was the proximate cause of Mary Fink's death. Dr. Thorpen's testimony, when viewed in this fashion, established that, based on the evidence (including the autopsy, scientific evidence, and a complete review of Mary Fink's medical records and medical history), as opposed to other speculative possibilities, the ankle fracture Mary Fink suffered in the collision with appellant's vehicle resulted in trauma to a vein or veins in her lower extremity. Due to this injury, blood flow slowed in the damaged area, Mary Fink was immobilized, and a clot developed within five days to one or two weeks prior to her ankle surgery, but nevertheless after the collision with appellant's vehicle. The fracture was the most significant factor in the clot's development, enhancing Mary Fink's pre-existing risk factors for developing clots. Sometime on May 7, 1999, the clot broke away and caused Mary Fink's death. The record is insufficient, in this context, to establish an intervening cause based on the conduct of Mary Fink's treating physicians (the only basis relied upon in appellant's argument). Dr. Thorpen rendered his opinion (again uncontradicted in the record) based on his review of Mary Fink's medical records, medical history, and operative reports relating to her ankle surgery; he did not know why the ankle surgery was not performed immediately and stated that it was not foreseeable in this case that something like this could happen when surgery is slated. [¶ 66] In light of this finding, the district court similarly did not err in denying appellant's motion for a judgment of acquittal.