Opinion
No. 02-02-237-CV
Delivered: March 25, 2004.
Appeal from the 141st District Court of Tarrant County.
Panel A: CAYCE, C.J., HOLMAN and GARDNER, JJ.
OPINION
Introduction
In this medical malpractice case, we must decide whether the evidence is legally and factually sufficient to support the jury's verdict that Delores McLean was suffering from pulmonary emboli when she was treated in the emergency room by Robert Morrow Welch, M.D. on April 24, 1996, two-and-a-half months before her eventual death from a massive pulmonary embolism. Because we conclude that the evidence is legally sufficient, but factually insufficient, to support the jury's verdict, we will reverse the trial court's judgment for Simeon Eden McLean and remand the cause to the trial court for a new trial.
McLean sued in his individual capacity, as heir to the estate of Delores McLean, deceased, and as next friend of Jamila Imari McLean and Imani Zakiya McLean, minors. For simplicity, we refer to him in all these capacities as "Simeon."
Background Facts and Procedural History
On April 24, 1996, thirty-year-old Delores called Dr. Mark Godfrey, her primary care physician, complaining of shortness of breath and chest pain. Dr. Godfrey sent Delores to the emergency room at Harris Methodist Hospital HEB (hereafter, the emergency room) for further evaluation. Delores's husband, Simeon, drove her to the emergency room. Simeon observed that Delores seemed to be experiencing pain when she breathed, that she held her chest, and that she struggled to breathe.
When she arrived at the hospital at approximately 12:30 p.m., Delores was assessed by Raenita Pearson, the triage nurse on duty that day. Pearson observed that Delores had a blood pressure of 130 over 72, pulse of 101, and respirations of 28, with a normal temperature. She noted that Delores complained of shortness of breath the week before, headache the day before, vomiting that day, and difficulty breathing. Delores did not, however, complain to Pearson about chest pain.
Delores was then evaluated at 12:40 p.m. by staff nurse Meagan Stillwagoner. Stillwagoner noted that Delores complained of a sinus headache that medication did not improve, nausea, vomiting, and shortness of breath, mainly with exertion. Delores also had shallow and rapid respirations and a low blood oxygen saturation of 90%. Her breath sounds were normal, however, and she was breathing with normal effort.
Dr. Welch first saw Delores about 1:10 p.m. He reviewed her history, which was consistent with her earlier conversations with the nurses and noted the presence of sinus drainage, a productive cough with green mucus, and her complaint of shortness of breath. Delores did not complain to Dr. Welch about chest pain, and he did not observe any physical signs of chest pain. Dr. Welch ordered a chest x-ray, a sinus x-ray, pulse oximetry, and an arterial blood gas test. He also examined Delores's legs for evidence of thrombosis (the formation or presence of a blood clot within a blood vessel). Because of Delores's severe obesity, however, he did not consider that examination very useful.
A pulse oximeter is a small device that clips on a finger or other extremity and estimates a person's blood oxygen saturation — the amount of oxygen being carried by arterial blood. A blood gas test is a blood test that directly measures the partial pressure oxygen (pO2) and carbon dioxide (pCO2) in arterial blood. It is a more accurate test than pulse oximetry.
Delores's x-rays were normal. The pulse oximetry, however, showed an oxygen saturation level that was below normal, and the blood gas test showed a low pO2 of 56. Based on Delores's history, physical examination, x-rays, and laboratory data, Dr. Welch diagnosed Delores as suffering from sinusitis, dyspnea, bronchospasm, and hypoxemia. Dr. Welch believed that Delores's shortness of breath was caused by her obesity, bronchospasm, infection, and mucus plugging in her lungs. He ordered ventilator treatments with drugs to relieve the bronchospasm, antibiotics to treat the infection, and cough medication.
Dyspnea is awareness of the sensation of breathing, or shortness of breath, and hypoxemia is deficient oxygenation of the blood. Bronchospasm is a decrease in the diameter of the airway, due to either internal spasm or swelling.
Altogether, Dr. Welch saw Delores five or six times on April 24. He noted slow improvement after the prescribed therapy and that Delores reported feeling almost normal. At 4:00 p.m., Dr. Welch noted that Delores was "[d]oing well"; however, her 4:00 p.m. oxygen saturation reading gave him the impression that her bronchospasm was returning. Dr. Welch did not see Delores between 4:00 and 5:25 p.m., when he discharged her after discussing with her his diagnosis, prescribing medication to relieve the symptoms of bronchospasm, giving her an instruction sheet for home treatment of asthma (the hospital had no instructions for bronchospasm), and suggesting that she see her primary care physician in a day or two. Dr. Welch never saw Delores again.
Following Dr. Welch's instructions, Delores made an appointment with Dr. Godfrey on April 29, 1996. Delores told Dr. Godfrey that she had been treated at the emergency room and was slowly getting better, although she still became short of breath upon exertion. Although Delores showed Dr. Godfrey the asthma instruction sheet she had been given, he received no other information from the emergency room about Delores's April 24 visit. Dr. Godfrey examined Delores and concluded that she had a sinus infection and that her shortness of breath was caused by bronchospasm or reactive airway disease, which can develop suddenly after a bout of bronchitis. He extended her antibiotics and gave her an inhaler. If Dr. Godfrey had known of Delores's April 24 pO2 level of 56, however, that might have made a difference in his evaluation of her, because he knew catastrophic problems, such as heart attack and pulmonary embolism, could result from such a low level of oxygenation.
Dr. Godfrey next saw Delores on May 1, 1996, when she complained of chills, sore throat, headache, and ear pain. On May 7, 1996, Delores again sought treatment from Dr. Godfrey for cold sweats, nausea, vomiting, diarrhea, labored breathing, chills, and a low-grade fever. She told Dr. Godfrey on that visit that her respiratory symptoms were improving and that her main problems were gastrointestinal.
On May 13, 1996, Delores consulted Dr. Drake, another physician in Dr. Godfrey's group, regarding breathing difficulties, which then improved until the Sunday before July 3, 1996. On July 3, Delores again saw Dr. Godfrey and complained of a recent onset of cough, congestion, wheezing, and shortness of breath. Dr. Godfrey told Delores to restart her medications, which he had previously prescribed for use only as needed, and also gave her additional medications.
On July 8, 1996, Delores returned to the emergency room, complaining of cough, congestion, fever, headache, sore throat, and difficulty breathing, which she reported had been intermittent since April. She also reported coughing up red-tinged mucous and complained of tightness in her chest when she breathed. A chest x-ray showed an abnormality in the upper right lobe of her lung, and based on Delores's history, Dr. Jerome Novotny, the treating ER physician, concluded that she had pneumonia.
Late in the evening on July 9, Delores collapsed at home and was taken to the emergency room by ambulance. She was pronounced dead shortly after midnight on July 10, 1996. Autopsy results revealed that the cause of Delores's death was a massive "saddle" embolus that had lodged itself in her pulmonary arterial trunk. The autopsy further revealed evidence of left deep leg vein thrombosis and showed that Delores had another, not yet fatal embolus in the upper lobe of her right lung, which Dr. Novotny had mistaken for pneumonia.
Simeon filed his medical malpractice suit on February 1, 1998. After a mistrial, Simeon's claims against Dr. Welch were retried to a jury, which returned a 10-2 verdict on February 2, 2002. The trial court rendered judgment on the verdict, and this appeal followed.
Issues on Appeal
In six issues, Dr. Welch complains:
• The evidence is legally, or alternatively, factually insufficient to establish that Dr. Welch was negligent.
• The evidence is legally, or alternatively, factually insufficient to establish that Dr. Welch's failure to diagnose pulmonary embolism in Delores on April 24, 1996 was a proximate cause of her death.
• The trial court erroneously failed to order a mistrial after Simeon's counsel engaged in improper and incurable jury argument by informing the jury of its answer to Jury Question 2.
• The trial court improperly required Dr. Welch to accept two objectionable jurors by sustaining Simeon's Batson challenges to two of Dr. Welch's peremptory strikes when the record clearly demonstrated an appropriate, nonracial basis for those strikes.
See Batson v. Kentucky, 476 U.S. 79, 106 S.Ct. 1712 (1986).
• The trial court abused its discretion when it refused to permit Dr. Welch to introduce the testimony of an expert witness, Dr. Andrea Green, at trial on the ground that the testimony would be cumulative.
• The trial court erroneously failed to apply the damage cap in former article 4590i, section 11.02(a) to the jury's verdict.
Evidence of Negligence and Proximate Cause
In his first and second issues, Dr. Welch asserts that the evidence is legally and factually insufficient to sustain the jury's verdict because it does not establish that Delores was suffering from pulmonary emboli when Dr. Welch treated her on April 24, 1996. Therefore, Dr. Welch contends, the evidence is insufficient to show that he was negligent in failing to diagnose this condition. In response, Simeon concedes that "[c]learly the pathology alone does not show showers of emboli as far back as April [1996]." He asserts, however, that the correlation between Delores's clinical symptoms in April 1996 and the pathological findings is legally and factually sufficient evidence that pulmonary emboli were present in April 1996.
In determining a "no-evidence" issue, we are to consider only the evidence and inferences that tend to support the finding and disregard all evidence and inferences to the contrary. Bradford v. Vento, 48 S.W.3d 749, 754 (Tex. 2001); Cont'l Coffee Prods. Co. v. Cazarez, 937 S.W.2d 444, 450 (Tex. 1996); In re King's Estate, 150 Tex. 662, 244 S.W.2d 660, 661 (1951). Anything more than a scintilla of evidence is legally sufficient to support the finding. Cazarez, 937 S.W.2d at 450; Leitch v. Hornsby, 935 S.W.2d 114, 118 (Tex. 1996). More than a scintilla of evidence exists if the evidence furnishes some reasonable basis for differing conclusions by reasonable minds about the existence of a vital fact. Rocor Int'l, Inc. v. Nat'l Union Fire Ins. Co., 77 S.W.3d 253, 262 (Tex. 2002).
The existence of a vital fact must be reasonably inferred from known circumstances; a party may not establish a vital fact by piling one inference upon another. Lozano v. Lozano, 52 S.W.3d 141, 149 (Tex. 2001) (Phillips, C.J., concurring dissenting); Schlumberger Well Surveying Corp. v. Nortex Oil Gas Corp., 435 S.W.2d 854, 858 (Tex. 1968); Rounsaville v. Bullard, 154 Tex. 260, 276 S.W.2d 791, 794 (1955). Moreover, facts from which an inference may properly be drawn must be established by direct evidence; inferences cannot be drawn from other inferences. Rounsaville, 276 S.W.2d at 794; Tex. N.O.R. Co. v. Burden, 146 Tex. 109, 203 S.W.2d 522, 531 (1947); Entex, A Div. of Noram Energy Corp. v. Gonzalez, 94 S.W.3d 1, 7-8 (Tex. App.-Houston [14th Dist.] 2002, pet. denied). "[T]he law does not permit the pyramiding of one assumption upon another because an ultimate fact thus arrived at is too conjectural and speculative to support a judgment." Briones v. Levine's Dep't Store, Inc., 446 S.W.2d 7, 10 (Tex. 1969).
In deciding a factual insufficiency issue, we determine whether the evidence supporting the finding is so weak or the evidence to the contrary is so overwhelming that the answer should be set aside and a new trial ordered. Garza v. Alviar, 395 S.W.2d 821, 823 (Tex. 1965). We are required to consider all of the evidence in the case in making this determination. Mar. Overseas Corp. v. Ellis, 971 S.W.2d 402, 406-07 (Tex.), cert. denied, 525 U.S. 1017 (1998).
A plaintiff in a medical malpractice case is required to prove by a preponderance of the evidence that the defendant's negligence proximately caused his injuries. Duff v. Yelin, 751 S.W.2d 175, 176 (Tex. 1988). The ultimate standard of proof on the causation issue "is whether, by a preponderance of the evidence, the negligent act or omission is shown to be a substantial factor in bringing about the harm and without which the harm would not have occurred." Kramer v. Lewisville Mem'l Hosp., 858 S.W.2d 397, 400 (Tex. 1993); accord Park Place Hosp. v. Estate of Milo, 909 S.W.2d 508, 511 (Tex. 1995).
To establish proximate cause, the plaintiff must prove foreseeability and cause-in-fact. Leitch, 935 S.W.2d at 118-19. With regard to cause-in-fact, the plaintiff must establish a causal connection between the defendant's negligence and the plaintiff's injuries based upon a "reasonable medical probability" or "reasonable probability" and not on mere conjecture, speculation, or possibility. Park Place Hosp., 909 S.W.2d at 511; Lenger v. Physician's Gen. Hosp., Inc., 455 S.W.2d 703, 706 (Tex. 1970); Marvelli v. Alston, 100 S.W.3d 460, 470 (Tex. App.-Fort Worth 2003, pet. denied). This quantum of proof "mean[s] simply that it is `more likely than not' that the ultimate harm or condition resulted from such negligence." Kramer, 858 S.W.2d at 399-400. A plaintiff is not required to establish causation in terms of medical certainty, nor is he required to exclude every other reasonable hypothesis. Marvelli, 100 S.W.3d at 470; Bradley v. Rogers, 879 S.W.2d 947, 954 (Tex. App.-Houston [14th Dist.] 1994, writ denied). Whether expert opinion establishes a causal connection based upon a reasonable medical probability must be determined by the substance and context of the testimony rather than semantics or the use of a particular term or phrase. Burroughs Wellcome Co. v. Crye, 907 S.W.2d 497, 500 (Tex. 1995); Marvelli, 100 S.W.3d at 470.
The trier of fact may decide the issue of proximate cause in medical malpractice cases based upon: (1) general experience and common sense from which reasonable persons can determine causation; (2) scientific principles provided by expert testimony allowing the fact finder to establish a traceable chain of causation from the condition back to the event; or (3) a probable causal relationship as articulated by expert testimony. Lenger, 455 S.W.2d at 706; Marvelli, 100 S.W.3d at 470. Whether emboli were present in Delores's lungs when Dr. Welch examined her in the emergency room on April 24, 1996 was clearly not a matter of common knowledge or within the experience of lay persons. Therefore, expert medical testimony based on reasonable medical probability was required to establish either a "traceable chain of causation" based upon general scientific principles or a "probable causal relationship" between Delores's medical condition in late April 1996 and her death two-and-a-half months later on July 10. See Marvelli, 100 S.W.3d at 470.
The record in this case shows that, on April 24, 1996, Delores presented to the emergency room with numerous clinical symptoms of pulmonary embolism, including a low pO2 level of 56, a low-normal pCO2 level of 33, a widened A-a gradient, a low oxygen saturation level, shortness of breath, and a rapid pulse rate. One of Simeon's experts, however, Dr. Maria Granzotti, acknowledged that no component of a patient's history can do more than suggest the existence of pulmonary thromboembolism, nor is there any physical finding that is necessary or sufficient to make a diagnosis. Further, experts from both sides agreed that several of these symptoms, such as low pO2, increased pulse and respiratory rates, and shortness of breath, were consistent with Dr. Welch's diagnoses of sinusitis, bronchspasm, and hypoxemia — particularly in light of Delores's severe obesity.
A normal pCO2 range is 32-46, a normal oxygen saturation level is 92-96, and a normal pO2 is 74-108. Dr. Welch testified, however, that a morbidly obese person such as Delores would not take in oxygen as well as a nonobese person and would therefore have a lower "normal" pO2 of 63-99. Dr. Welch believed a pO2 of 56 was "just a little bit below" normal range for a morbidly obese person. Conversely, one of Simeon's experts believed 56 was "extremely low" for a thirty-year-old with no pulmonary history. Also, Delores was given a ventilator treatment — which can cause pO2 to fluctuate slightly — before her pO2 was measured. Thus, her pO2 could have been either lower or higher than 56 when she arrived at the emergency room.
Nonetheless, Dr. Granzotti opined that some of Delores's symptoms were inconsistent with Dr. Welch's diagnoses and that Dr. Welch never provided a medically valid explanation for Delores's shortness of breath. For example, Dr. Granzotti testified that Delores's low-normal pCO2 level of 33 indicated shortness of breath, but not from bronchospasm. According to Dr. Granzotti, a markedly obese patient who is suffering from bronchospasm will have a significantly elevated pCO2 level, not a low one. Another of Simeon's experts, Deputy Chief Medical Examiner Dr. Marc Krouse, testified that, based on his experience evaluating the laboratory values of persons who had died from pulmonary embolism, the majority of the time the pO2 level was low, the pCO2 level was also either normal or low — as in Delores's case.
Dr. Krouse performed the autopsy on Delores.
In addition, despite Dr. Welch's conclusion that Delores's shortness of breath and low pO2 were caused in part by infection, Delores's chest and sinus x-rays were normal. Dr. Welch conceded this and testified that he made his diagnosis of sinus infection based on Delores's report of facial pain and his observation of sinus drainage, rather than on the x-ray results. Drs. Krouse and Granzotti both testified that Delores's clear x-rays indicated that she did not have an infection, and Dr. Granzotti opined that Delores's normal chest x-ray, occurring as it did in the setting of acute shortness of breath coupled with hypoxemia, was "highly suggestive" of pulmonary embolism.
Two other symptoms that Dr. Granzotti opined were not explained by Dr. Welch's diagnoses were Delores's persistently low oxygen saturation level and prolonged tachycardia. When Delores arrived at the emergency room, the pulse oximeter showed that her blood oxygen saturation level was low — 90% — and her pulse was 101. By 2:15, approximately thirty minutes after the ventilator treatment, Delores's blood oxygen saturation level had improved to 94%, but her pulse had increased from 101 to 112. Dr. Welch concluded that the elevated pulse was due to the ventilator medication being in her system. At 3:45 p.m., Delores's blood oxygen saturation had dropped to 91%, but her pulse was higher, at 114. By 4:00 p.m., Delores's oxygen saturation level had dropped back to 90%, and her pulse was 112. Dr. Welch believed this meant the ventilator medication was beginning to wear off and that the bronchospasm was returning.
It is unclear from the record whether the ventilator treatment occurred at 1:10 p.m. or 1:45 p.m.
Dr. Welch testified that he had considered pulmonary embolism as a possible diagnosis for Delores until part of the way through her treatment and his observation of her on repeat exams. Because Delores reported feeling "almost normal" after the ventilator treatments, however, Dr. Welch concluded that she was suffering from bronchospasm rather than pulmonary embolism. Dr. Welch opined that there was "absolutely no way" Delores could have felt so much better if pulmonary embolism had caused her symptoms, because the ventilator treatments would not have removed the clot blockage.
Dr. Granzotti disagreed with Dr. Welch's assessment of the situation and testified that she believed the tachycardia and low oxygen saturation level were caused by showers of small pulmonary emboli. Dr. Granzotti testified that bronchospasm of pulmonary embolism responds to ventilator treatment as constricted airways are opened up, making it difficult to diagnose the pulmonary embolism. She acknowledged that Dr. Welch's notes in Delores's chart showed his subjective opinion that Delores was improving, but testified that this opinion was not corroborated by documentation showing that Delores's respiratory rate, blood oxygen saturation, or pO2 had improved at the time of her discharge. Dr. Granzotti conceded, however, that Delores's pulse rate at discharge was no longer tachycardic and had fallen to within high normal range.
Dr. Welch testified that a normal respiratory rate is 20 or below. The notations in Delores's chart showed that she presented at the emergency room with a respiratory rate of 28. Her respiration rate was last documented in the emergency room as being 24 at 2:15 p.m. — thirty minutes after the ventilator treatment.
A pulse rate is tachycardic if it is over 100. Delores's actual pulse rate at discharge was disputed at trial. Dr. Welch testified, from memory, that Delores's pulse had dropped "in[to] the 90s." Later, he stated, based on Delores's medical chart, that her pulse rate had been documented by someone just before discharge at 76. Dr. Granzotti read the same notation as 96.
Dr. Granzotti also explained that a natural bodily process known as fibrinolysis can dissolve emboli within hours to several days. Dr. Granzotti opined that, in reasonable medical probability, Delores could have felt better within a matter of hours as a result of a combination of the ventilator treatment and her body's dissolution of the emboli through fibrinolysis. According to Dr. Granzotti, the body of a young, otherwise healthy female would recognize the presence of an embolus and work to dissolve it, just like a person's body works to heal a cut or bruise.
Another indicator of pulmonary emboli on April 24, 1996 was Delores's abnormal A-a gradient. Dr. Welch did not calculate Delores's A-a gradient in April 1996, although he knew it was elevated. Dr. Granzotti calculated it at trial, however, from Delores's April 24, 1996 blood gas levels. According to Dr. Granzotti, Delores's normal A-a gradient would have been roughly 11.5, but her actual A-a gradient on April 24, 1996 was approximately 53. Dr. Granzotti testified that it is well-known that an abnormal A-a gradient is one of the "key factors" that increases the suspicion of pulmonary embolism. Likewise, Dr. Krouse testified that he would expect to see a widened A-a gradient when pulmonary embolism was present. Dr. Welch testified that an elevated A-a gradient can be indicative of several things, including interstitial lung disease, which was not evidenced on Delores's chest x-ray, and pulmonary shunting, which there was a probability that she had in April 1996. Dr. Welch testified that several things can cause pulmonary shunting, including metabolic changes and pulmonary embolism.
The A-a gradient is the gradient between the oxygen pressures in the alveoli and the arteries.
Delores's marked obesity was a risk factor for pulmonary embolism, but there is conflicting evidence concerning whether her low-dose birth control pills also increased her risk of developing thromboembolic disease. Dr. Welch testified that studies had shown that low-dose birth control pills did not increase the risk, and the package insert for Delores's pills stated that the effect of long-term use of low-dose oral contraceptives "remains to be determined." The package insert also warned, however — based primarily on studies involving higher-dose contraceptives — that the use of oral contraceptives is associated with an increased risk of pulmonary embolism and that the "risk of morbidity and mortality increases significantly" when other risk factors, such as obesity, are present.
Initially, Dr. Granzotti testified that Delores's use of the pills was a "key risk factor," especially when coupled with her obesity. Later, however, she testified that she had not seen low-dosage birth control pills listed as a major factor in any medical text. But Dr. Granzotti also noted that the highest thromboembolic risk from birth control pills occurs during the first few months of use and that Delores had only been taking birth control pills for about two months before her April 1996 emergency room visit.
During Delores's autopsy, Dr. Krouse had retained random samples of Delores's normal-appearing lung tissue and a section of the right upper lobe of the lung that appeared abnormal. Two years later, Dr. Krouse prepared slides from the normal-appearing tissue for microscopic examination. One slide — plaintiff's exhibit 41D — showed three microscopic emboli in two of the smaller pulmonary arteries. Dr. Krouse opined that, in reasonable medical probability, these emboli were in Delores's lungs at least four to six weeks before she died. Two other slides — plaintiff's exhibits 41C and G — showed emboli that were seven days to two-and-one-half weeks old when Delores died.
Specifically, Dr. Krouse testified, "all you can say about those most organized two thrombi/emboli, is that they were at least four to six weeks old. It takes four to six weeks to get that appearance to it. And it may persist for a long time after that," possibly for months. Four to six weeks before Delores's death was May 29 to June 12.
Drs. Krouse and Granzotti both conceded that the two or three small emboli shown on plaintiff's exhibit 41D would not, by themselves, have caused the symptoms that Delores had when she went to the emergency room in April 1996. Dr. Granzotti also acknowledged that a microscopic pulmonary embolus is not likely to explain a pO2 level of 56. Dr. Krouse opined, however, that the fact that the emboli were present in a tiny, randomly-selected sample of Delores's lung tissue indicated that they were more widespread throughout the lungs.
Dr. Krouse also explained that the typical history of thromboembolic disease to the lungs is that episodes of symptom-causing showers of small emboli occur and, if not treated, eventually develop into a larger, fatal embolus. The evidence of showers of smaller emboli frequently disappears, so that over time, there may be no pathological evidence of symptom-causing, nonfatal emboli. In light of the typical history of thromboembolic disease, Dr. Krouse considered it "an important negative finding" that he found no residual evidence of thromboemboli in any of the larger arteries in Delores's lungs, but found emboli in the smaller arteries. He considered it an indicator that, more likely than not, episodic showers of smaller emboli were occurring in Delores's lungs in April 1996. Dr. Krouse further opined that Dr. Welch's diagnoses, whether taken alone or in combination, were not, when considered together with the pathological evidence, consistent with Delores's pO2 of 56 and pCO2 of 33. Therefore, Dr. Krouse opined that Delores's blood gas levels and negative x-rays in April 1996 were, in reasonable medical probability, more likely than not related to thromboembolic disease or showers of thromboemboli. Dr. Krouse further testified that Delores's clinical symptoms on April 24, 1996 and her complaint of chest pain to Dr. Godfrey before she went to the emergency room, when correlated with the pathological evidence, demonstrated a "high probability" that showers of microscopic emboli were occurring in her lungs when she presented to the emergency room in April 1996.
Dr. Granzotti also referred to a natural bodily process known as fibrinolysis, which can dissolve emboli within hours to several days.
In addition, the notes in Delores's chart from her July 8, 1996 visit to the emergency room show that she reported, "breathing trouble started in April, increased shortness of breath, with exertion." Dr. Novotny, the ER physician who treated Delores on July 8, testified that he got the impression from her that these symptoms had neither worsened nor gotten better, but had stayed about the same. Dr. Krouse explained that chronic disease processes such as bronchospasm and sinusitis leave scarring of the airways and other associated disease findings that should be visible under a microscope and usually to the naked eye, also. Dr. Krouse did not examine any of Delores's tissue under a microscope during her autopsy, but he did not, upon visual inspection, find any evidence of these chronic diseases or any other disease process besides the two pulmonary emboli. Dr. Krouse testified that nothing from his visual inspection during Delores's autopsy or the microscopic evidence examined two years later indicated that the breathing trouble Delores experienced from April until July was caused by anything other than showers of pulmonary emboli. According to Dr. Krouse, if Delores's breathing problems in April had been caused by something else, evidence of another disease process would have shown up in the autopsy — but it did not.
Dr. Godfrey testified that Delores had no chronic lung problems before April 24, 1996; however, Delores experienced intermittent congestion, fever, and breathing problems between April 24 and her death on July 10, 1996. Dr. Krouse defined "chronic" as "many weeks to months."
Distilling from all of this testimony only the evidence and reasonable inferences that tend to support the jury's verdict and disregarding all evidence and inferences to the contrary, we are left with the following:
• The clinical evidence showed that Delores's symptoms on April 24, 1996, when taken together, were not entirely consistent with Dr. Welch's diagnoses of bronchospasm, sinusitis, and hypoxemia, but were consistent with showers of pulmonary emboli.
• Delores experienced intermittent breathing difficulties between April 24 and July 8, 1996, which neither worsened nor got better, but stayed about the same.
• Chronic bronchial disease and sinusitis leave scarring of the airways and other associated disease findings that should be visible under a microscope and are also usually visible to the naked eye.
• During Delores's autopsy, Dr. Krouse did not, on visual inspection, find any residual evidence of bronchial disease, sinusitis, or another disease process.
• He did, however, discover the massive pulmonary embolus that caused her death and another embolus that had made its way into the upper lobe of her right lung one-and-a-half to two days before she died.
A reasonable inference can be drawn from the clinical evidence that Delores's April 1996 symptoms were caused, at least in part, by something other than bronchospasm, sinusitis, and hypoxemia — possibly showers of microscopic pulmonary emboli that did not appear on her chest x-ray. Further, because Delores experienced intermittent breathing difficulties between April 24 and July 8, 1996 that got neither better nor worse, it can be reasonably inferred that all of her breathing problems had the same cause. Dr. Krouse testified that this cause must have been showers of microscopic pulmonary emboli because his visual inspection during Delores's autopsy did not reveal any residual evidence of chronic bronchial disease, sinusitis, or another disease process.
Dr. Krouse's autopsy did not completely rule out bronchospasm and sinusitis as other reasonable causes of Delores's breathing problems because he did not examine any of her tissue, including her airways, under a microscope during the autopsy, and he candidly admitted that residual evidence of chronic bronchial disease is not always visible to the naked eye. He testified, however, that such residual evidence can usually be detected without a microscope, and there is also evidence that one of Delores's blood gas levels was not entirely consistent with bronchospasm. Therefore, the autopsy results and clinical evidence are some evidence from which it can be reasonably inferred that Delores's April to July 1996 breathing problems were caused by showers of microscopic emboli rather than bronchospasm and sinusitis.
While the issue is a close one, we conclude that this evidence and reasonable inferences, when linked together, are legally sufficient to establish, based on a reasonable medical probability, that showers of pulmonary emboli were present in Delores's lungs on April 24, 1996. Accordingly, we hold that the evidence is legally sufficient to sustain the jury's verdict. Nonetheless, we conclude that this evidence is so weak that it is factually insufficient to sustain the verdict. Garza, 395 S.W.2d at 823.
Simeon relies on the microscopic emboli found in Delores's lung tissue as additional evidence that her April 1996 symptoms were caused by showers of pulmonary emboli. Although both Dr. Granzotti and Dr. Krouse admitted that only showers of microscopic emboli — and not the few emboli found in the microscopic evidence — would have been sufficient to cause Delores's April 1996 symptoms, Dr. Krouse testified that the presence of the three oldest emboli in a random sample of Delores's lung tissue implied that the emboli were more widespread throughout her lungs. Dr. Krouse's testimony only established, however, that the three oldest emboli were four to six weeks old at the time of Delores's death. Four to six weeks before Delores's death was May 29 to June 12.
A reasonable inference can be drawn from this evidence that microscopic emboli were widespread and even showering in Delores's lungs from May 29 onward. This inference cannot, however, be used to support the further inference that showers of symptom-causing emboli were present in Delores's lung tissue over a month earlier on April 24,1996. Indeed, Dr. Krouse merely testified that this pathological evidence made him "suspicious" that pulmonary emboli were present in Delores's lungs in April 1996. Mere suspicion is not evidence. See Lozano, 52 S.W.3d at 149; Browning-Ferris, Inc. v. Reyna, 865 S.W.2d 925, 928 (Tex. 1993) (both holding that circumstantial evidence may be used to establish any material fact, but it must transcend mere suspicion or surmise). Further, a party may not establish a vital fact by piling one inference upon another. Schlumberger Well Surveying Corp., 435 S.W.2d at 858; Rounsaville, 276 S.W.2d at 794; see also Browning-Ferris, Inc., 865 S.W.2d at 928 n. 5 ("To establish a fact by circumstantial evidence, the circumstances relied on must have probative force sufficient to constitute the basis of legal inference.") (quoting Green v. Tex. Pac. Ry. Co., 125 Tex. 168, 81 S.W.2d 669, 673 (1935)). Therefore, the evidence of microscopic emboli in Delores's lung tissue is no evidence of the vital fact that emboli were present in her lungs on April 24, 1996 and it provides no support for the jury's verdict.
Likewise, the typical characteristics of thromoembolic lung disease are not evidence of the state of Delores's lung tissue in April 1996. For example, the multi-episodic showering and disappearing tendencies of thromoembolic lung disease could provide one explanation for why the emboli that may have been indicated by Delores's April 1996 clinical symptoms did not show up in the microscopic evidence. But an equally plausible explanation for why the emboli did not show up is that none existed before May 29. Because this "meager circumstantial evidence" could give rise to any number of inferences, none more probable than the other or more than mere surmise, the jury could not infer from it the ultimate fact that showers of microscopic emboli were present in Delores's lungs in April 1996. See Hammerly Oaks, Inc. v. Edwards, 958 S.W.2d 387, 392 (Tex. 1997); accord Lozano, 52 S.W.3d at 148.
Moreover, it can reasonably be inferred from the microscopic evidence and the evidence about the characteristics of thromboembolic lung disease that emboli did not begin showering in Delores's lungs until about May 29, but once they began they continued until July, eventually producing the emboli that were seen on her July 8 chest x-ray, found in her autopsy, and resulted in her death. It can also be reasonably inferred from the absence of any emboli older than four to six weeks in the microscopic evidence that Delores's April 1996 symptoms were not caused by showers of pulmonary emboli. All of this evidence preponderates against the verdict rather than in favor of it.
Finally, the autopsy results did not rule out Dr. Welch's diagnoses of bronchospasm and sinusitis as reasonable causes of Delores's ongoing breathing problems; they merely established that no evidence of these diseases was visible to the naked eye and that the immediate cause of her death was a massive saddle embolus — something that indisputably was not present in her lungs in April 1996. Even Simeon's experts agreed that Dr. Welch's diagnoses of sinusitis and bronchospasm were consistent with Delores's shortness of breath in April 1996 — particularly in light of her severe obesity. They simply opined that these diagnoses did not account for all of Delores's April 1996 symptoms.
Having considered all of the evidence, we conclude that it is factually insufficient to establish, based on a reasonable medical probability, that Delores was suffering from showers of microscopic pulmonary emboli when Dr. Welch treated her on April 24, 1996. Although Simeon's experts employed phrases such as "reasonable medical probability," "high probability," and "more likely than not," the outcome of our evidentiary review is determined by the substance and context of the evidence rather than semantics or the use of a particular term or phrase. Burroughs Wellcome Co., 907 S.W.2d at 500; Marvelli, 100 S.W.3d at 470; Arlington Mem'l Hosp. Found., Inc. v. Baird, 991 S.W.2d 918, 922 (Tex. App.-Fort Worth 1999, pet. denied). Accordingly, we hold that the evidence is factually insufficient to support the jury's verdict.
Conclusion
We overrule Dr. Welch's first and second issues in part and sustain them in part. We reverse the trial court's judgment and remand the cause to the trial court for a new trial.
In light of our holding regarding these issues, we need not consider Dr. Welch's remaining issues. See Tex.R.App.P. 47.1.