Marcela and Jose Bustamante, as Next Friends of D.B. v. Enrique N. Ponte, Jr., M.D. and Pediatrix Medical Services, Inc. , 529 S.W.3d 447 ( 2017 )

IN THE SUPREME COURT OF TEXAS
444444444444
NO . 15-0509
444444444444
MARCELA AND JOSE BUSTAMANTE, AS NEXT FRIENDS OF D.B., PETITIONERS,
v.
ENRIQUE N. PONTE, JR., M.D. AND PEDIATRIX MEDICAL SERVICES, INC.,
RESPONDENTS
4444444444444444444444444444444444444444444444444444
ON PETITION FOR REVIEW FROM THE
COURT OF APPEALS FOR THE FIFTH DISTRICT OF TEXAS
4444444444444444444444444444444444444444444444444444
Argued December 8, 2016
JUSTICE GREEN delivered the opinion of the Court.
In this case, we must determine whether legally sufficient evidence supports a jury’s
conclusion that the negligence of a premature infant’s treating neonatologist proximately caused her
loss of vision. The evidence shows that, despite D.B.’s extreme prematurity, had her retinopathy of
prematurity been diagnosed and treated early enough, it is more likely than not that the blood-vessel
growth in her eyes would have been slowed to the point that she would have enjoyed a sighted life.
We hold that legally sufficient evidence supports the jury’s finding that the neonatologist’s
negligence, more likely than not, caused D.B.’s poor visual outcome. Accordingly, we reverse the
judgment of the court of appeals as to the neonatologist and his professional association and remand
the case to the court of appeals for consideration of issues not already addressed.
I. Background
D.B. was born prematurely at Del Sol Medical Center in El Paso, Texas, on May 19, 2005.
She weighed 600 grams (1.32 pounds). D.B.’s gestational age at birth was estimated between 23
weeks and 1 day and 24 weeks. D.B. was admitted to Del Sol’s neonatal intensive care unit (NICU)
due to medical problems she suffered related to her premature birth.
Because of her severe prematurity, D.B. had a 90%–100% chance of developing retinopathy
of prematurity (ROP), a retinal disorder that afflicts premature infants with low birth weights,
causing abnormal blood-vessel growth in the eyes that can cause diminished vision or blindness,
often by retinal detachment. Blindness from ROP is usually preventable. As a result of D.B.’s ROP,
however, she became totally blind in her right eye, and the vision in her left eye is severely impaired.
D.B.’s parents, the Bustamantes, as next friends of D.B., sued Del Sol Medical Center (Del
Sol), Enrique N. Ponte Jr., M.D. (D.B.’s neuroneonatologist, attending physician, and medical
director of the NICU at Del Sol), and Jorge Fabio Llamas-Soforo, M.D. (D.B.’s ophthalmologist),
claiming that their negligence and gross negligence caused D.B.’s vision loss.1 Del Sol settled with
the Bustamantes before trial, and the remaining claims were tried to a jury.
At trial, Dr. Ponte testified that, based on her severe prematurity, he believed that, at the time
of her birth, D.B. had a 100% chance of developing ROP and a significant chance of requiring laser
therapy to treat her eyes. He also testified that infants born significantly prematurely tend to develop
1
The Bustamantes also named Dr. Ponte’s employer, Pediatrix Medical Services, Inc., and Dr. Llamas’s
professional association as defendants but did not submit any independent negligence questions. Rather, the parties
stipulated that the doctors were acting in the scope of their employment for those entities.
2
ROP earlier and that he was concerned D.B. would have early onset ROP, requiring treatment at
29–36 weeks.
In 2001, the American Academy of Pediatrics, the American Association for Pediatric
Ophthalmology and Strabismus, and the American Academy of Ophthalmology promulgated a joint
statement (the 2001 Statement) regarding guidelines for ROP screening, in which they recognized
that timely treatment requires timely screening. Thus, concerned that D.B. would develop ROP early
and require treatment, Dr. Ponte claims that he requested an “early” examination of D.B.’s eyes.
Accordingly, Dr. Llamas examined D.B.’s eyes on July 4, 2005 (week 29 or 30). Dr. Llamas claims
he observed incomplete vascularization in zone II of the retina on July 4,2 but he did not use the
International Classification of Retinopathy of Prematurity (ICROP) terminology as recommended
by the 2001 Statement to describe his observations. Instead, his notes state, “There is complete
vascularization to 360 degrees. Impression: fetal fundi.” Dr. Llamas claims he dictated “incomplete
vascularization,” but a transcription error resulted in the notes saying “complete vascularization.”
Dr. Ponte explained that he understood Dr. Llamas’s notes to mean that D.B. had incomplete
vascularization in zone I,3 but he also testified that he did not know whether she had zone I or zone
II eyes at the first exam. Dr. Llamas and Dr. Ponte were the only witnesses to testify regarding the
apparent transcription error.
2
ROP is classified in part by the location of abnormal blood vessel development in the retina, and the location
is defined as being in one of three zones.
3
Zone I refers to the area of the retina closest to the head of the optic nerve. Incomplete vascularization in zone
I signifies the highest risk for which treating physicians should be “very concerned,” whereas incomplete vascularization
in zone II signifies an intermediate risk for which treating physicians should be “concerned and watching.”
3
Dr. Llamas recommended a follow-up exam in four weeks, which was contrary to the 2001
Statement’s guidelines regarding the scheduling of follow-up exams.4 Under the 2001 Statement,
even if vascularization was actually complete on July 4, which no party contends, there is no
circumstance in which D.B.’s follow-up examination should have been scheduled four weeks later.
If she had less than “threshold” ROP in zone I,5 follow-up should have occurred in one week. If she
had ROP in zone II, or no ROP but incomplete vascularization in zone I, follow-up screenings should
have occurred in one- to two-week intervals. If she had incomplete vascularization in zone II,
follow-up screenings should have occurred in two- to three-week intervals. Finally, even if it
appeared she had zone III vascular maturation at the first exam, this finding should have been
confirmed by at least one repeat examination within two to three weeks.
Four weeks later, at the follow-up exam on August 1 (week 33 or 34), Dr. Llamas determined
that ROP had developed and recommended laser treatment as soon as possible. His medical notes
reflect that on August 1, D.B. had stage 3 ROP in both her left and right eyes in zone II, as well as
plus disease and a vitreous hemorrhage. Based on pictures of D.B.’s eyes taken on August 3, one
of the Bustamantes’ experts, Dr. Darius Moshfeghi, testified that D.B.’s right eye had stage 3 ROP
in zone I, plus disease in four quadrants, and a vitreous hemorrhage. Additionally, Dr. Moshfeghi
4
The 2001 Statement does not establish bright-line rules for the diagnosis and treatment of ROP. Rather, it
states, “The recommendations in this statement do not indicate an exclusive course of treatment or serve as a standard
of medical care. Variations, taking into account individual circumstances, may be appropriate.”
5
At the time of D.B.’s ROP, doctors used the term “threshold” to refer to a point at which ROP treatment is
required under the 2001 Statement, meaning that there has been a finding of both stage 3 ROP, covering five consecutive
or eight cumulative clock hours of the eye, and “plus” disease. “Plus” disease refers to a change in the vessels in the
eye’s posterior wall near the optic nerve in which the vessels become tortuous, congested, and engorged because the
blood circulating in them encounters resistance.
4
testified that D.B.’s left eye had eight hours of stage 3 ROP in zone II and plus disease in four
quadrants.
Due to difficulty securing the laser necessary for treatment, Dr. Llamas did not perform the
laser therapy until three days after his detection of ROP—on August 4, 2015 (week 34 or 35).
According to one of the Bustamantes’ experts, Dr. William Good, pictures taken after the treatment
suggest that Dr. Llamas failed to properly administer the laser treatment because there were “skip
lesions”—“areas where the retinal burns either didn’t take or were not administered.” After
treatment, D.B.’s right retina detached, causing her to lose vision permanently in her right eye. In
her left eye, she has macular dragging, which often results in reduced central vision and severely
impaired vision (20/1200 or 20/1300), and requires her to hold items close to her eye even with
glasses.
The parties hired competing expert witnesses to testify regarding whether the doctors’
negligence (not screening more frequently, delaying the diagnosis and treatment so that D.B. was
not treated at pre-threshold ROP, delaying treatment three days after threshold ROP was observed,
and not properly administering the laser treatment), if any, was the proximate cause of D.B.’s
impaired vision. Dr. Good testified that if D.B.’s doctors had followed the proper exam schedule,
“[b]ased on reasonable medical probability, ROP would have been diagnosed on July 18th,” which
would have enabled D.B. to receive laser treatment about a week before August 1.6 He testified
6
Dr. Good felt uncomfortable giving the jury a more precise date on which D.B. would have been able to
receive treatment given that the doctors failed to examine her eyes more frequently, which would have provided more
information regarding the ROP progression in her eyes.
5
further that D.B. was a high-risk infant who should have been treated when she had pre-threshold
ROP, rather than threshold ROP. Accordingly, Dr. Good testified:
Well, if you look at the various places where negligence occurred, in an incremental
fashion, each of those contributed to the poor visual outcome that [D.B.]
experienced.
The delay in screening examinations for four weeks to a probability prevented Dr.
Llamas from identifying ROP when it could have been treated earlier. That would
have improved the chance of a good visual outcome for her.
The delay in laser treatment for three days also in my opinion incrementally increased
the chances of a bad outcome for her.
And then, finally, the inadequate laser treatment I think really was the coup de grace
here, and it basically placed these eyes at extremely high risk and was causally or
proximately responsible for blindness in the right eye and poor vision in the left eye.
Dr. Good concluded that if the defendants had acted properly, “[m]ore likely than not, she would
have . . . a sighted life.” Although Dr. Good conceded that D.B. had risk factors portending a
negative outcome, such as vitreous hemorrhage and plus disease, he noted that D.B. lacked others,
such as being a twin. Dr. Good also observed that D.B. did not have a vitreous hemorrhage or plus
disease when she was first examined and that part of the goal of frequent screening is to provide
treatment before those risk factors develop. Therefore, Dr. Good opined that D.B.’s vision loss was
more likely attributable to “the fact that she wasn’t screened and treated timely,” not the other risk
factors. Further, based on his physical examination of D.B., Dr. Good testified that her visual
impairment stems from her ROP, not from any neurological issues arising from D.B.’s prematurity.
Dr. Dale L. Phelps, another expert for the Bustamantes, similarly testified that the doctors’
negligence proximately caused D.B.’s vision impairment. She explained that if the doctors had
6
examined D.B. more frequently, D.B.’s ROP could have been treated before it became as advanced,
and she “more likely than not” would have functional vision. Based on the advanced stage of D.B.’s
ROP on August 1, Dr. Phelps believed that ROP would have been visible on July 26.
Much of the expert testimony revolved around a study released in 2003, the Revised
Indications for Treatment of Retinopathy of Prematurity (the ETROP study), which many considered
to establish new ROP treatment guidelines. Although the ETROP study was discussed at the 2003
and 2004 annual meeting of the American Academy of Ophthalmology, a new joint statement
incorporating the ETROP study findings was not issued until 2006. In the ETROP study, the subject
group consisted of premature infants believed to be at a high risk of developing ROP that would
require treatment. The researchers treated one eye early, but delayed treating the other eye until it
reached threshold, which had been the standard practice. According to Dr. Good, who served as
chair of both the ETROP executive and writing committees, the ETROP study revealed that treating
ROP earlier resulted in a structural and functional benefit for infants with high-risk eyes when
compared to treating at the conventional time. Accordingly, earlier screening of high-risk infants
was recommended so that they could receive treatment earlier—at pre-threshold ROP rather than
threshold ROP. Put another way, Dr. Phelps testified that the conclusion of the ETROP study was
that “type 1 eyes—which meant zone I any stage ROP with plus, zone I stage 3 ROP whether or not
there was plus disease, and zone II stage 2 or 3 ROP with plus”— should receive early treatment,
whereas type 2 eyes should be monitored for progression of ROP to a treatable stage.
Dr. Good, Dr. Phelps, and a defense expert, Dr. Graham Quinn, all agreed that laser therapy
is effective in stopping ROP progression in most infants. Dr. Good testified that laser treatment was
7
successful in over 75% of “all comers,” and only 89 eyes (out of 800 eyes) in the ETROP study
suffered retinal detachment after receiving laser treatment. Dr. Phelps explained further that the
ETROP study concluded that laser treatment at conventional threshold times reduced bad outcomes
to around 14% or 16%, and, more significantly, early treatment further reduced negative outcomes
to 9%. Even Dr. Quinn conceded that D.B. had high-risk eyes, “[e]arly treatment of high-risk eyes
is better,” and “[i]t’s the high-risk pre-thresholds that benefit from treatment.” Furthermore,
Dr. Quinn agreed that 91% of high-risk eyes that were treated at pre-threshold ROP in the ETROP
study did not have an unfavorable structural outcome.7 Dr. Quinn additionally agreed that D.B. was
treated at threshold ROP rather than pre-threshold ROP and that “pre-threshold ROP almost always
precedes threshold ROP.” Nonetheless, Dr. Quinn refused to say that D.B. could have been treated
at pre-threshold because there are no “exams to document that one way or the other.” Dr. Llamas
agreed that type 1 eyes benefit from early treatment but claimed he treated D.B. early—when she had
pre-threshold ROP/type 1 eyes. Dr. Llamas blamed D.B.’s unfavorable outcome on the vitreous
hemorrhage in her right eye, from which excess blood in the vitreous part of the eye enhances the
rubber-band effects of the ROP, testifying that “the presence of the vitreous hemorrhage was a very
determinative factor in the bad outcome of the right eye.”
The jury found that the defendants’ negligence caused D.B.’s injuries, concluding that
Dr. Ponte was 45% responsible, Dr. Llamas was 45% responsible, and Del Sol was 10% responsible.
7
At a different point in his testimony, Dr. Quinn agreed that early treatment reduced the occurrence of
unfavorable outcomes, but he testified that in the ETROP study, “15 to 19 percent of the conventionally managed eyes
had an unfavorable structure, and 10 to 12 percent of the early treated eyes had an unfavorable structure.” He also stated
that when eyes had zone I, stage 3 ROP, regardless of whether they had plus disease, 53.8% experienced unfavorable
outcomes with conventional treatment and 30.8% experienced unfavorable outcomes with early treatment.
8
The jury awarded total damages of just over $2.1 million. Dr. Llamas filed a motion for new trial
and, in the alternative, a motion to modify and a motion for remittitur. Dr. Ponte filed a motion for
judgment notwithstanding the verdict. The trial court adjusted the jury verdict to account for Del
Sol’s settlement credit and rendered judgment holding Dr. Ponte and Pediatrix Medical Services
jointly and severally liable for $872,653.19 and Dr. Llamas and his professional association jointly
and severally liable for the other $872,653.19. All of the nonsettling defendants appealed, arguing
that the evidence was legally insufficient to support the jury’s damages and causation findings. The
doctors also urged other grounds for reversal, such as improperly admitted evidence and charge error.
A divided court of appeals reversed and rendered judgment that the Bustamantes take
nothing, holding that they failed to adduce any non-conclusory evidence of causation. 490 S.W.3d
70, 73 (Tex. App.—Dallas 2015, pet. granted). Evaluating the expert causation testimony adduced
at trial, the court of appeals concluded that the experts’ testimony was conclusory and constituted
no evidence that Dr. Ponte’s or Dr. Llamas’s negligence was a “but-for” cause of D.B.’s injuries.
Id. at 77–85, 87. Specifically, the court of appeals criticized Dr. Good for testifying that it was
“more likely than not” D.B. would have a sighted life if not for Dr. Ponte’s and Dr. Llamas’s
combined negligence, rather than quantifying the negative impact of each negligent act. Id. at 78–79.
According to the court of appeals, Dr. Good’s testimony was conclusory because he did not explain
“how or why the delays in treatment contributed to [D.B.]’s injuries or worsened her chances of a
better outcome.” Id. at 81. Likewise, the court of appeals faulted Dr. Good for “not explain[ing]
why or how different performance of the laser surgery, more likely than not, would have overcome
[D.B.]’s preexisting adverse risk factors,” especially considering the portion of infants in the ETROP
9
study who suffered detached retinas even with early treatment. Id. at 82. The court of appeals
similarly rejected Dr. Phelps’s testimony because she discussed the doctors’ combined negligence
and did not “explain the facts justifying a conclusion that a particular patient probably would have
been helped by the treatment.” Id. at 80 (citing Archer v. Warren, 118 S.W.3d 779, 787–88 (Tex.
App.—Amarillo 2003, no pet.)).
The court of appeals also rejected the Bustamantes’ statistical evidence that was premised
on the ETROP study, reasoning that they produced no evidence that D.B. was similar to study
participants who had favorable results. Id. at 84–85 (citing Merrell Dow Pharm., Inc. v. Havner, 953
S.W.2d 706, 720 (Tex. 1997)). In sum, the court concluded that the Bustamantes merely showed
that a different screening schedule, earlier treatment, and better-performed treatment could have
resulted in a better outcome for D.B., not that it more likely than not would have resulted in a better
outcome. Id. at 87. The court did not address the defendants’ other appellate issues.
Conversely, the dissent concluded that the experts sufficiently explained how the doctors’
negligence more likely than not caused D.B.’s vision loss. Id. at 88–90 (Schenck, J., dissenting).
The dissent also concluded that “the plaintiffs have offered some evidence of causation by
establishing the probability of a sighted life at 75% or higher, especially in the absence of record
evidence suggesting any reason why [D.B.]’s prospects were reduced.” Id. at 94. Ultimately, the
dissent “would not require (1) the plaintiff to prove that each defendant’s negligence, standing alone,
caused the injury; (2) the plaintiff to disprove all other possible causes of her injury, no matter how
unlikely; or (3) proof to a medical certainty that absent defendants’ negligence, [D.B.] would have
a sighted life.” Id. at 88.
10
The Bustamantes filed a petition for review in this Court, urging that the court of appeals
erred by reversing the trial court’s judgment against Dr. Ponte, Dr. Llamas, and each of their
professional associations. After this case was submitted in this Court, but before our decision,
Dr. Llamas and his professional association reached an agreement to settle the Bustamantes’ claims
against them. The trial court approved that settlement agreement in August 2017. Thus, only
Dr. Ponte and his professional association remain as respondents in this appeal.
II. Sufficiency of the Proximate Cause Evidence
We now turn to the sole issue raised in this appeal: whether legally sufficient evidence
supports the jury’s finding that the Dr. Ponte’s negligence in assessing and treating D.B.’s ROP
proximately caused her vision impairment. Dr. Ponte argues that the evidence is legally insufficient
to support the jury’s findings that his negligence proximately caused D.B. to suffer any injury.
A. Standard of Review
Evidence is legally insufficient to support a jury finding when (1) the record discloses
a complete absence of evidence of a vital fact; (2) the court is barred by rules of law
or of evidence from giving weight to the only evidence offered to prove a vital fact;
(3) the evidence offered to prove a vital fact is no more than a mere scintilla; or
(4) the evidence establishes conclusively the opposite of a vital fact.
Crosstex N. Tex. Pipeline, L.P. v. Gardiner, 505 S.W.3d 580, 613 (Tex. 2016) (citations omitted).
“In determining whether there is no evidence of probative force to support a jury’s finding, all the
record evidence must be considered in the light most favorable to the party in whose favor the verdict
has been rendered,” Havner, 953 S.W.2d at 711, including evidence offered by the opposing party
that supports the verdict, see City of Keller v. Wilson, 168 S.W.3d 802, 827 (Tex. 2005) (“Nor can
evidence supporting a verdict be identified by which party offered it . . . .”). Courts “must credit
11
favorable evidence if reasonable jurors could, and disregard contrary evidence unless reasonable
jurors could not,” id., and “every reasonable inference deducible from the evidence is to be indulged
in that party’s favor,” Havner, 953 S.W.2d at 711.
B. Applicable Law
A plaintiff seeking to prevail on a negligence cause of action must establish the existence of
a legal duty, a breach of that duty, and damages proximately caused by the breach. IHS Cedars
Treatment Ctr. of DeSoto, Tex., Inc. v. Mason, 143 S.W.3d 794, 798 (Tex. 2004)). “The two
elements of proximate cause are cause in fact (or substantial factor) and foreseeability. . . . Cause
in fact is established when the act or omission was a substantial factor in bringing about the injuries,
and without it, the harm would not have occurred.”8 Id. at 798–99.
To satisfy a legal sufficiency review, plaintiffs in medical-malpractice cases “are required
to adduce evidence of a ‘reasonable medical probability’ or ‘reasonable probability’ that their
injuries were caused by the negligence of one or more defendants, meaning simply that it is ‘more
likely than not’ that the ultimate harm or condition resulted from such negligence.” Jelinek v. Casas,
328 S.W.3d 526, 532–33 (Tex. 2010) (quoting Kramer v. Lewisville Mem’l Hosp., 858 S.W.2d 397,
399–400 (Tex. 1993)). In other words, “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.’”
Park Place Hosp. v. Estate of Milo, 909 S.W.2d 508, 511 (Tex. 1995) (quoting Kramer, 858 S.W.2d
8
Dr. Ponte does not contest foreseeability.
12
at 400). Accordingly, a plaintiff cannot show that a defendant’s negligence was more likely than not
a cause of injury “where the defendant’s negligence deprived the tort victim of only a 50% or less
chance of avoiding the ultimate harm.” Kramer, 858 S.W.2d at 400. Therefore, we examine the
record to determine whether the Bustamantes presented legally sufficient evidence that “in
reasonable medical probability” Dr. Ponte’s negligence caused D.B.’s poor visual outcome.
Importantly, when the evidence demonstrates that “there are other plausible causes of the
injury or condition that could be negated, the plaintiff must offer evidence excluding those causes
with reasonable certainty.” Havner, 953 S.W.2d at 720 (emphasis added); see also Jelinek, 328
S.W.3d at 536 (“When the only evidence of a vital fact is circumstantial, the expert cannot merely
draw possible inferences from the evidence and state that ‘in medical probability’ the injury was
caused by the defendant’s negligence. The expert must explain why the inferences drawn are
medically preferable to competing inferences that are equally consistent with the known facts.”
(emphasis added)). However, in Transcontinental Insurance Co. v. Crump, 330 S.W.3d 211 (Tex.
2010), we held that “a medical causation expert need not ‘disprov[e] or discredit[] every possible
cause other than the one espoused by him,’” id. at 218 (quoting Viterbo v. Dow Chem. Co., 826 F.2d
420, 424 (5th Cir. 1987)), absent evidence that “presents ‘other plausible causes of the injury or
condition that could be negated,’” id. (quoting Havner, 953 S.W.3d at 720) (first emphasis added)).
Thus, a plaintiff need not “speculate about other possible unknown causes and then disprove them.”
490 S.W.3d at 95 (Schenck, J., dissenting).
13
C. Failure to Apply the Substantial-Factor Test
We begin by addressing whether the court of appeals erred in applying a stringent but-for
causation test when there is proof of more than one proximate cause of an injury. Specifically, this
case requires that we address whether proof that one defendant’s negligence was a substantial factor
in the ultimate harm constitutes no evidence of causation when the jury found that multiple actors,
through multiple acts, contributed to one injury. The court of appeals concluded that Dr. Good’s
causation testimony was “no evidence that Ponte’s negligence was a but-for cause of the injuries to
[D.B.]’s eyes” because he couched his conclusion “on the combined negligence of both Ponte and
Llamas.” Id. at 79. The dissenting justice, on the other hand, would not have required the
Bustamantes “to prove that each defendant’s negligence, standing alone, caused the injury.” Id. at
88 (Schenck, J., dissenting).
It has long been the law in this state that a defendant’s act or omission need not be the sole
cause of an injury, as long as it is a substantial factor in bringing about the injury. See, e.g., Havner
v. E-Z Mart Stores, Inc., 825 S.W.2d 456, 459 (Tex. 1992). There may be more than one proximate
cause of an injury. See, e.g., Del Lago Partners, Inc. v. Smith, 307 S.W.3d 762, 774 (Tex. 2010);
see also Bostic v. Georgia-Pacific Corp., 439 S.W.3d 332, 344 (Tex. 2014) (“While but for
causation is a core concept in tort law, it yields to the more general substantial factor causation in
situations where proof of but for causation is not practically possible or such proof otherwise should
not be required.”). We conclude that the court of appeals improperly applied a stringent but-for
causation requirement in a case that should have been resolved under the substantial-factor test.
14
The jury heard extensive evidence supporting the joint responsibility of Dr. Ponte and
Dr. Llamas in scheduling D.B.’s ROP screenings. In fact, essentially all of the evidence at trial was
that the screening, diagnosis, and treatment of ROP is a collaborative effort between the
neonatologist and the ophthalmologist, implicating the substantial-factor test. For example,
according to the 2001 Statement, “Responsibility for examination and follow-up of infants at risk
for ROP must be carefully defined by each neonatal intensive care unit. Unit-specific criteria for
examination for ROP should be established for each neonatal intensive care unit by consultation and
agreement between neonatology and ophthalmology services.” Dr. Phelps testified that the
guidelines and standards of care are common to both neonatologists and ophthalmologists with
respect to the screening, diagnosis, and treatment of ROP because “[t]hey are done jointly.”
Dr. Phelps explained that Dr. Llamas failed to use the ICROP nomenclature at the July 4 exam and
that Dr. Ponte failed to follow up or ask for a clarification, citing an “impaired understanding of what
was seen on that first examination.” Dr. Phelps went on to explain what should have occurred:
Q. So what should Dr. Ponte’s response have been when he saw that Dr. Llamas
wrote “fetal fundi, follow up four weeks” on this baby?
A. If he has never had this kind of discussion with his ophthalmologist or -- about
how should we go about a zone I baby or if they like to use the term “fetal fundi,”
they need to have an understanding what they mean by that. What does that mean in
relationship to the guidelines. How can we double-check each other to make sure we
are not missing it.
If they haven’t had that, then there is no safety. There is no backup. There is no --
that level of understanding isn’t built up for the baby.
Additionally, Dr. Ponte agreed that “the neonatologist and the ophthalmologist, the eye specialist,
share in the obligation of screening premature babies for retinopathy of prematurity.” He agreed “it
15
was [his] responsibility and Dr. Llamas’s responsibility to make sure [D.B.] got screened according
to the best medical practices existing at the time in 2005.” Further, Dr. Ponte’s and Dr. Llamas’s
neonatologist expert, Dr. Donald Null, agreed that the obligation of the neonatologist and the
ophthalmologist is to work together in an active role to detect ROP at the earliest possible time.
Finally, Dr. Quinn, like all of the other experts, described the process of planning the screening,
diagnosis, and treatment of ROP as “a collaborative effort.” Thus, the court of appeals should have
applied the substantial-factor test in assessing the acts of negligence by Dr. Ponte and Dr. Llamas
rather than requiring proof that each independent act by each tortfeasor was a but-for cause of D.B.’s
injury.
We understand the court of appeals’ concern: given that Dr. Good put part of the blame on
Dr. Llamas’s inadequate performance of the laser treatment, how could the delay in screening and
treatment have caused D.B.’s bad outcome if the surgery was going to be inadequate regardless?
However, based on the evidence, the jury could have reasonably determined that the laser treatment
did not violate the standard of care. Dr. Good based his opinion that the laser treatment was
inadequate on photographs manipulated by the Bustamantes’ expert, Dr. Moshfeghi, and Dr. Good
admitted that he did not know what Dr. Moshfeghi had done to manipulate or alter the photographs
of D.B.’s eyes. Further, Dr. Good admitted that Dr. Llamas was better positioned to see D.B.’s eyes
at the time of the laser treatment, explaining, “I think that when you are doing an examination and
treatment realtime, you get to see the eye from a lot of different angles and in a lot of different ways
than you do on just one montage.” Dr. Good went on to admit that, at the time of the treatment,
Dr. Llamas could see and evaluate more of the fundus of D.B.’s eyes than Dr. Good could looking
16
at a photo montage and that Dr. Llamas had “a more complete view” of what he was treating and
where the laser needed to go. Dr. Good’s testimony on cross-examination also suggests that the laser
treatment might not have been inadequate. Dr. Good admitted that the 1,954 shots in the right eye
and 1,611 shots in the left eye fell “well within the average range that would be used in eyes like
[D.B.]’s.” Furthermore, Dr. Good admitted on cross-examination that the August 4 pictures might
not have shown the full effect of the August 4 treatment:
Q. I think I used the example earlier, it is kind of like getting a sunburn. You start
a little pink, and even after you get out of the sun, you can still turn red. Is that kind
of a similar lay explanation of the [laser treatment] is going to keep going in the
retina?
A. Sure.
Dr. Llamas also explained why one cannot see all of the laser shots on the post-treatment images.
He testified that there were no skip areas; it was just an effect of the perspective of the photograph.
Further, Dr. Llamas’s and Dr. Ponte’s ophthalmologist expert, Dr. Quinn, testified that the RetCam
images provide a different view than one has in person. Dr. Quinn testified that Dr. Llamas’s
treatment of D.B.’s eyes was reasonable and in compliance with the applicable standard of care.
In short, the jury could have disregarded the evidence that the surgery was negligently performed and
instead concluded that the delay in screening and treatment caused D.B.’s injury. Given that the jury
found Dr. Ponte and Dr. Llamas equally responsible, apportioning 45% of the liability to Dr. Ponte
and 45% of the liability to Dr. Llamas, this result is quite plausible.
Dr. Ponte argues that this Court’s opinion in Providence Health Center v. Dowell, 262
S.W.3d 324 (Tex. 2008), applies in this case. The question in Dowell was whether a mental health
17
care provider’s release of a patient was the proximate cause of his subsequent suicide as a matter of
law. Id. at 328. We held that Dowell’s discharge from the emergency room did not proximately
cause his death, concluding that his discharge from the hospital was too attenuated to have been a
substantial factor in bringing about the suicide. Id. at 329–30. According to Dr. Ponte, Dowell
stands for the proposition that “[u]nquantified evidence that a different course of action would have
created a lower risk of harm is legally insufficient to establish but-for causation.” Dr. Ponte believes
this means that Dr. Good’s opinion that earlier screening “would have improved the chance of a
good visual outcome for [D.B.]” is insufficient to establish that the lack of additional screening
exams was, more likely than not, a but-for cause of her impaired vision. However, Dowell is
distinguishable from the facts of this case. In Dowell, there was evidence that the patient would not
have consented to treatment, and there was no evidence he could have been hospitalized
involuntarily. Id. at 329. Further, there was no evidence that hospitalization, more likely than not,
would have prevented the patient’s suicide. Id. at 330. Rather, the Dowells’ expert opined only that
the patient was “at high risk for suicide” and that “his discharge from the ER in that condition caused
his death.” Id. at 328. That is not this case. As explained below, there is abundant evidence in the
record that Dr. Ponte’s and Dr. Llamas’s failure to timely diagnose, and therefore failure to timely
treat, D.B.’s ROP—a condition a defense expert called “the most treatable cause of blindness in
children”—resulted in the retinal detachment in D.B.’s right eye and severely impaired vision in her
left.
18
D. Scope of Evidence to Consider
We now address the court of appeals’ conclusions (1) that the ETROP study violated
Havner’s epidemiological-study rule and was thus no evidence of causation, and (2) that Dr. Good’s
and Dr. Phelp’s causation testimony was conclusory and thus no evidence.
1. The ETROP Study
The court of appeals rejected the Bustamantes’ statistical evidence premised on the ETROP
study, reasoning that they produced no evidence that D.B. was similar to study participants who had
favorable results. 490 S.W.3d at 84–85. Central to the court of appeals’ holding was its conclusion
that the principles of Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d at 720, apply in
this case. 490 S.W.3d at 84–85. We disagree.
Havner’s analysis of epidemiological principles does not govern this case. Havner involved
the sufficiency of causation evidence in the context of toxic-substance exposure, not medical
malpractice. Havner, 953 S.W.2d at 708. There, the plaintiffs could not point to facts showing
“specific causation” (i.e., whether exposure to the substance caused the plaintiff’s particular injury)
and were forced to rely to a considerable extent on epidemiological studies for proof of “general
causation” (i.e., whether the toxic substance itself was capable of causing a particular injury in the
general population). Id. at 714–15. This was necessary because there was no direct proof that the
substance was responsible for the plaintiff’s injury. Id. As a result, the evidence in Havner related
solely to studies about whether Bendectin exposure doubled the risk of limb-reduction defects; there
was no evidence specifically showing that the plaintiff’s birth defects were caused by Bendectin
exposure. Id. at 724–30. We held:
19
To raise a fact issue on causation and thus to survive legal sufficiency review, a
claimant must do more than simply introduce into evidence epidemiological studies
that show a substantially elevated risk. A claimant must show that he or she is
similar to those in the studies. This would include proof that the injured person was
exposed to the same substance, that the exposure or dose levels were comparable to
or greater than those in the studies, that the exposure occurred before the onset of
injury, and that the timing of the onset of injury was consistent with that experienced
by those in the study.
Id. at 720. We also held that “if there are other plausible causes of the injury or condition that could
be negated, the plaintiff must offer evidence excluding those causes with reasonable certainty.” Id.
In short, the point of Havner is that even in the absence of direct clinical experience, a plaintiff may
still establish causation through an appropriately strong associational finding, but to do so, the
plaintiff must show that he or she is similar to those in the studies relied upon and offer evidence to
rule out other plausible causes. Id.
This case is readily distinguishable. First, the Bustamantes’ evidence of causation goes far
beyond an isolated study. The jury heard discussions about the 2001 Statement, which was admitted
into evidence, and they heard testimony regarding a number of other studies concluding that laser
treatment produced positive outcomes at rates well above 75%. For example, Dr. Llamas was asked
about the Capone study, which found a favorable outcome in 83.3% of zone I eyes receiving laser
treatment. Dr. Llamas was also asked about a 2000 study concluding that laser treatment “yielded
a favorable anatomical outcome in 85.4% of the cases.” Furthermore, the jury heard testimony that
at least four out of five premature infants who develop ROP recover without treatment whatsoever.9
9
The evidence as to this statistic varies. Dr. Null testified that, despite the fact that one can have a 100%
likelihood to develop ROP, very few infants actually have a treatable disease or have that disease treated. He later
testified that “a small number” actually go on to need treatment— first estimating around 5–10% and then testifying that
20% was “close enough.” W hen Dr. Llamas explained why he does not treat stage 1 ROP eyes, he testified, “most of
20
And they heard both plaintiff and defense experts testify that ROP is treatable in most
cases—including Dr. Quinn’s testimony calling ROP “the most treatable cause of blindness in
children.”
Additionally, Dr. Good and Dr. Phelps did not simply rely on epidemiological studies to
establish the probability that delayed or inadequate treatment of ROP would cause blindness in the
general population to substantiate his opinion that D.B. might be one of those cases. Dr. Good and
Dr. Phelps based their causation opinions on their own clinical experience with ROP and the
particular medical procedures at issue, informed by photographs of D.B.’s eyes taken during each
step of her screening and treatment, D.B.’s medical records, in-person examinations of D.B., and
epidemiological studies in which Dr. Good and Dr. Phelps participated personally. Thus, the
ETROP study and the other studies showing that in more than 75% of cases timely and proper laser
treatment leads to a successful outcome constitute evidence supporting Dr. Good’s and Dr. Phelps’s
opinion on causation.
The court of appeals also held that the ETROP study was no evidence of causation because
“Good specifically denied that the ETROP study could be used to determine whether a delay in
treatment actually affected a baby’s vision,” 490 S.W.3d at 80, and “agreed [it] was not designed ‘to
determine whether a delay in screening or a delay in treatment actually affected a baby’s vision,’ and
that it would be ‘an incorrect use of that study’ to ‘claim that it was designed to detect or to look at
the effect of delay,’” id. at 82. This selective quoting misrepresents Dr. Good’s testimony. Dr. Good
the babies get better on their own.” Dr. Ponte testified that very few premature babies born at 23 weeks gestational age
will need laser treatment, estimating that only “around 10 percent” of babies born at 23 weeks wind up needing laser
treatment.
21
admitted on cross-examination that the “study was never designed to determine whether a delay in
screening or a delay in treatment actually affected a baby’s vision.” First, one could reasonably take
this statement to mean that the study was designed to determine the outcome of babies who
participated in the study rather than a specific baby outside of the study—a rather obvious fact.
Further, the ETROP study was designed to look at the effects of early diagnosis and treatment (i.e.,
earlier than conventional). Dr. Good had testified previously that the ETROP study changed that
standard of care by making ophthalmologists “more vigilant in seeing the babies more frequently,
in an effort to catch the ROP disease at the earlier stage or earlier point . . . , thereby offering the
baby a better chance of a favorable outcome.” Dr. Good had also testified that the “short version”
of the ETROP findings is “since earlier treatment is more effective than conventionally timed or
conventional management, the baby should be screened in order to pick up the disease at a point
earlier in the disease course so that they could be offered the earlier treatment.” Similarly, Dr.
Phelps, who worked alongside Dr. Good in the ETROP study, testified that “one of the things that
was looked at in the course of the ETROP study was how much of a difference did the treatment
protocols in that study make in different babies’ outcomes who participated in the study.” She also
testified that the ETROP study was designed “to see [if] there [is] a formula or a classification . . . to
decide which, out of all these babies who have ROP, might be at such high risk for needing treatment
that we could identify them early.” Dr. Quinn similarly testified that the ETROP study was “about
treating at high-risk prethreshold eyes . . . not the entire subset of prethreshold eyes” and that the
study found that early diagnosis and treatment “did create a better outcome for the babies who were
treated at high-risk prethreshold.” In fact, Dr. Quinn admitted that “the odds, . . . statistically
22
speaking, are that if a patient is treated at high-risk prethreshold, they likely will avoid retinal
detachment.” Moreover, Dr. Llamas admitted that he moved up D.B.’s treatment even though she
was not at threshold on August 1 “[b]ecause it was already type 1, and [he] trusted the results or
conclusions of the ETROP.” Put simply, the court of appeals parsed words to conclude that the
ETROP study was no evidence of causation. Because Dr. Good’s and Dr. Phelps’s opinions on
causation were based on more than epidemiological studies, and were informed in part by the results
of the ETROP study, the ETROP study is evidence supporting their opinion that the untimely
diagnosis and treatment of D.B.’s ROP caused her vision impairment.
2. Dr. Good’s and Dr. Phelps’s “Conclusory” Testimony
We also disagree with the court of appeals’ holding that Dr. Good’s and Dr. Phelps’s
opinions were conclusory and thus no evidence of causation. See 490 S.W.3d at 73. An expert’s
testimony is conclusory if the witness simply states a conclusion without an explanation or factual
substantiation. Nat. Gas Pipeline Co. v. Justiss, 397 S.W.3d 150, 156–57 (Tex. 2012). If no basis
for the opinion is offered, or the basis offered provides no support, the opinion is merely a
conclusory statement and cannot be considered probative evidence, regardless of whether there is
no objection. City of San Antonio v. Pollock, 284 S.W.3d 809, 816–18 (Tex. 2009) (citing and
quoting Coastal Transp. Co. v. Crown Cent. Petroleum Corp., 136 S.W.3d 227, 232–33 (Tex.
2004)); see also Jelinek, 328 S.W.3d at 536 (“It is not enough for an expert simply to opine that the
defendant’s negligence caused the plaintiff’s injury. The expert must also, to a reasonable degree
of medical probability, explain how and why the negligence caused the injury.”). Stated differently,
23
an expert’s simple ipse dixit is insufficient to establish a matter; rather, the expert must explain the
basis of the statements to link the conclusions to the facts. Pollock, 284 S.W.3d at 818.
Here, both Dr. Good and Dr. Phelps offered the bases for their opinions. Dr. Good testified
that he practices in the area of pediatric ophthalmology and that his practice consists of a great deal
of clinical ROP work. He also testified that, in preparation for trial, he reviewed depositions and
D.B.’s medical records, and he had personally evaluated her. Further, Dr. Good testified that he was
in the courtroom listening to Dr. Ponte’s testimony, which focused heavily on D.B.’s treatment and
the medical problems she faced as an extremely premature infant. Dr. Good specifically testified that
the risk factors from which D.B. suffered did not contribute to her poor outcome, and his testimony
showed that he considered these factors in formulating his opinion. Dr. Good also explained “the
how and why” supporting his conclusion that Dr. Ponte’s and Dr. Llamas’s negligence was more
likely than not the cause of D.B.’s poor structural (and thus poor visual) outcome in the right eye and
poor visual outcome in the left eye. His testimony effectively states that, had Dr. Ponte and
Dr. Llamas not delayed the screening examinations for four weeks, Dr. Llamas could have identified
her ROP at a time when it was less aggressive (for example, before the vitreous hemorrhage and plus
disease developed), increasing the likelihood of a positive visual outcome. Other testimony supports
Dr. Good’s opinions regarding the delay in screening examinations for four weeks and the delay in
laser treatment for three days. Dr. Good testified about the ETROP study, stating that it determined
that earlier treatment in high-risk babies had a “statistically significant” beneficial effect compared
to conventional management, in both structural and visual function. He also testified that laser
therapy is effective in stopping the progression of ROP in most babies with a 75% or higher success
24
rate for “all comers.” Dr. Good went on to testify that he evaluated D.B.’s August 1 findings,
explaining that the August 1 RetCam photos show that D.B. was at threshold at that time. Dr. Good
opined that D.B. should have been examined on July 11 or July 18 and that those examinations
would have resulted in a July 25 follow-up because, in light of the August 1 findings, “ROP would
have been diagnosed on July 18th.” He explained:
So the advantage to Dr. Llamas having seen ROP on that date--and let’s say it was
mild, not in need of any treatment but still obviously in zone I--is that he could have
come back the following week and learned a lot more detail about how this baby’s
eyes were behaving; meaning if there was a lot of rapid progression of the disease
during that one-week time period and that zone I disease, that is an ominous finding.
And I think it might have pushed him to want to treat this baby sooner than he did.
Dr. Good explained that, had Dr. Ponte and Dr. Llamas observed the correct examination schedule,
D.B. would have been treated “about a week before August 1st” (i.e., July 25). Thus, while
Dr. Good’s testimony was not perfect, he did provide a basis for his opinion, and that basis does
provide some support for his opinion. Dr. Good provided specific evidence from D.B.’s medical
records, his own subsequent examination of D.B., and his own expertise about the progression and
treatment of ROP in general and in D.B.’s case in particular. Of course, he could not pinpoint
precisely when D.B. developed ROP, testify to a date on which her ROP became treatable, or
quantify exactly the actual delays because D.B. was not examined for four weeks. But there was
evidence from which Dr. Good, based on his experience and having observed D.B.’s particular case,
could estimate these critical dates beyond mere speculation.
Likewise, the record establishes that Dr. Phelps’s testimony was not conclusory. Dr. Phelps
testified that she is a practicing neonatologist, is one of the authors of the 2001 Statement, and
25
worked alongside Dr. Good in conducting the ETROP study. Dr. Phelps testified that she prepared
for trial by reviewing the medical treatment Dr. Ponte and Dr. Llamas provided to D.B. during the
neonatal period, including her medical records and the deposition testimony of Dr. Ponte and
Dr. Llamas. Dr. Phelps ultimately concluded that Dr. Llamas proximately caused D.B.’s poor
outcome “[b]ecause a repeat examination was four weeks in an eye that was either zone I or zone II,
and also because . . . the original exam was not described in a way that could be understood by the
staff that he was working with,” and that Dr. Ponte proximately caused D.B.’s poor outcome by
failing to develop “a set of written guidelines for his staff to communicate with the ophthalmologist.”
Dr. Phelps agreed with Dr. Good that D.B. probably would not have had threshold ROP on July 18,
but Dr. Phelps explained that “[i]t’s hard to tell” when D.B.’s follow-up examinations should have
occurred “because the way the results of the first examination were written down are sort of
ambiguous.” Dr. Phelps reasoned that, based on Dr. Ponte’s and Dr. Llamas’s deposition testimony
offering different definitions for the term “fetal fundi,” “not using the ICROP, the classification,
impaired [their] understanding of what was seen on that first examination.” Dr. Phelps went on to
explain how this affected D.B.’s care:
The risk here -- what happened was that, apparently, Dr. Ponte felt, okay, this is --
this will be okay for waiting four weeks. That seems reasonable.
If it were a zone I eye, waiting four weeks is too long. It gives too long a time for
very immature eyes to get very aggressive. So it is worse than you think it is when
you finally look, or than it could have been.
Whereas if it had been a zone II eye, then two to three weeks is more reasonable to
wait. Four is still long, but it is not as bad as four weeks in a zone I eye.
26
Dr. Phelps went on to testify about what should have occurred, explaining that if Dr. Ponte and
Dr. Llamas never discussed what was meant by the term “fetal fundi” in relation to the 2001
Statement, “then there is no safety. There is no backup. There is no -- that level of understanding
isn’t built up for the baby.” Dr. Phelps then explained that, had Dr. Ponte and Dr. Llamas
communicated adequately to comply with the guidelines, Dr. Llamas “would have seen the ROP as
it started up . . . and before it became advanced. If it was looking very threatening, they might have
moved their schedules . . . to make sure they caught it quickly when it got to the point where it
needed surgery.” She explained that, had this occurred, “more likely than not [D.B.] would have
functional vision.” This opinion is supported by Dr. Phelps’s other testimony. Dr. Phelps opined
that, had an examination occurred on July 26 (which was noted as necessary in D.B.’s medical
records), ROP would have been diagnosed on that day: “As bad as it was on 8-1, it would have been
visible on the 26th.” Thus, like Dr. Good, Dr. Phelps estimated the progression of D.B.’s ROP
during the time for which there are no records based on the August 1 images of D.B.’s eyes. She
also explained that ROP can progress “really fast. It can go from looking like threshold to being
detached in one week.” Dr. Phelps testified that, despite the 72-hour period in the 2001 Statement,
“You are not supposed to wait for 72 hours just because they should treat at 72 hours. It was, go
ahead and treat, but try to get it done before the retina detaches, before 72 hours, which we think
would probably cover it most of the time.” Finally, Dr. Phelps testified that, based on the images
of D.B.’s eyes, D.B. had type 1 ROP on August 1. She testified that the ETROP study revealed a
7% reduction in unfavorable outcomes in type 1 eyes compared to the 14% unfavorable outcomes
27
in the control group—“so that would have been a 50 percent improvement.” Thus, Dr. Phelps
provided the factual basis that supports her opinion. See id.
We find this case similar to Arkoma Basin Exploration Co. v. FMF Associates 1990–A, Ltd.,
249 S.W.3d 380 (Tex. 2008). In that case, we held that an expert’s testimony is conclusory if the
expert merely gives an unexplained conclusion or asks the jury to “take my word for it” because of
his or her status as an expert. Id. at 389. We ultimately concluded that the expert’s opinions were
not conclusory even though the expert’s foundational data was not in the record and it was not
entirely clear how the expert had reached his conclusions. Id. at 389–90. We reasoned:
[The expert’s] testimony could have been a lot clearer; his references to “up here”
and “right there” on slides and posters used at trial often make it hard to tell what he
is talking about. But we cannot say on this record that his opinions were unreliable
or speculative. Nor were they conclusory as a matter of law; [the expert] did not
simply state a conclusion without any explanation, or ask jurors to “take my word for
it.” It is true that without the foundational data in the appellate record, we cannot
confirm that “cash off my runs . . . divided by mcf” yielded the $1.62, $1.41, $1.43,
and $1.59 prices he calculated as the low range for damages. But experts are not
required to introduce such foundational data at trial unless the opposing party or the
court insists.
Id. (citing TEX . R. EVID . 705(a) (1998, amended 2015) (“The expert may testify in terms of opinion
or inference and give the expert’s reasons therefor without prior disclosure of the underlying facts
or data, unless the court requires otherwise. The expert may in any event disclose on direct
examination, or be required to disclose on cross-examination, the underlying facts or data.”)).
Like the expert in Arkoma, Dr. Good’s and Dr. Phelps’s testimony could have been better.
However, they did not simply state a conclusion without any explanation or ask the jurors to take
their word for it. Dr. Good and Dr. Phelps testified about the applicable standards of care, how they
28
applied in D.B.’s case, how Dr. Ponte and Dr. Llamas breached those standards of care and what they
should have done to satisfy their duty, and how D.B.’s outcome more likely than not would have
been different had Dr. Ponte and Dr. Llamas not been negligent. Dr. Good’s and Dr. Phelps’s
testimony was supported by clinical experience, studies in which Dr. Good and Dr. Phelps personally
participated, reviews of D.B.’s medical records, and in-person examinations of D.B. The evidence,
on balance, demonstrates that D.B. was more likely than not to be in the overwhelming majority of
premature infants who successfully overcome ROP had she received proper screening and treatment.
Thus, Dr. Good and Dr. Phelps tied their conclusions to the facts, explaining “to a reasonable degree,
how and why the breach caused the injury based on the facts presented.” Jelinek, 328 S.W.3d at
539–40.
The court of appeals also concluded that Dr. Phelps’s and Dr. Good’s causation testimony
was insufficient because the experts failed to rule out other possible causes of D.B.’s blindness. 490
S.W.3d at 82–83. Specifically, the court of appeals believed that our ruling in Jelinek, that “when
the facts support several possible conclusions, only some of which establish that the defendant’s
negligence caused the plaintiff’s injury, the expert must explain to the fact finder why those
conclusions are superior based on verifiable medical evidence, not simply the expert’s opinion,”
applied in this case. Id. (quoting Jelinek, 328 S.W.3d at 536). We disagree.
In Jelinek, we held that when equally likely causes for an injury are present, an expert must
explain why one cause and not the other was the proximate cause of the injury. Jelinek, 328 S.W.3d
at 529. There, the expert testified that “the Hospital’s negligence ‘in medical probability’ caused
Casas additional pain and suffering.” Id. at 535. The expert based this opinion on the presence of
29
an infection that could have been treated with certain antibiotics. Id. Circumstantial evidence of
infection existed, but there was no direct evidence of an infection. Id. The expert conceded that the
circumstantial evidence on which he relied to form his opinion that the patient suffered from the
specific infection was “equally consistent with two other infections cultured from” the patient’s
incision and blood—neither of which were treatable by the antibiotics in question. Id. We held that
“[w]hen the only evidence of a vital fact is circumstantial, the expert cannot merely draw possible
inferences from the evidence and state that ‘in medical probability’ the injury was caused by the
defendant’s negligence.” Id. at 536. Put differently, in Jelinek, we concluded that, by conceding that
the patient’s symptoms were consistent with infections not treatable by the omitted antibiotics, the
expert undermined his earlier conclusion that a different, undetected infection was present. See id.
While it was possible that the patient had such an infection, its presence could be inferred only from
facts that were equally consistent with the other two infections. Id. Therefore, there were three
equally likely causes, and the expert failed to explain why his opinion was superior to the opposite
view. Id. at 537. Those are not the facts here.
Here, the court of appeals and Dr. Ponte cite a number of “other possible causes” for D.B.’s
vision loss, such as her extreme prematurity, her zone I disease and plus disease, and the vitreous
hemorrhage she had developed. However, the evidence makes clear that these “other possible
causes” are not causes at all—they are risk factors making severe ROP more likely, not conditions
that could have independently resulted in D.B.’s poor outcome. For example, Dr. Quinn testified
that D.B.’s risk factors, particularly her extreme prematurity, put her at high risk for developing
severe ROP, but Dr. Quinn did not testify that the risk factors caused D.B.’s vision loss. The
30
evidence establishes that these conditions put D.B. at a higher risk for developing threshold ROP and
demanded more timely screening and treatment. As explained above, the evidence indicates that the
presence of these factors should have caused Dr. Ponte and Dr. Llamas to adjust their screening plan.
For example, Dr. Good testified about a portion of the 2001 Statement stating that “[t]he timing of
the initial screening examination may be adjusted appropriately on the basis of other reliable data,
such as local incidence and onset of ROP or the presence of other recognized risk factors.” He
further explained that:
in [D.B.]’s case, as we heard this morning, she had a lot of serious and multiple
medical problems. She was born very prematurely, really virtually at the limit of
viability. That is what Dr. Ponte said. And her birth weight was very low at 600
grams. So she was at extremely high risk for developing not only ROP but
significant ROP.
And so in [D.B.]’s case, because of her high risks and her multiple risk factors, she
was in a category of child who should have been followed closely.
Further, the Bustamantes offered evidence that part of the reason for frequent screening is to provide
treatment before risk factors, like vitreous hemorrhage, zone I disease, and plus disease, can develop.
There is at least some evidence that, had D.B. been screened earlier, threshold ROP would have been
discovered, and she would have received treatment, before the vitreous hemorrhage, zone I disease,
and plus disease developed.
We note that, even to the extent that Jelinek applies to these facts such that the experts were
required to rule out the cited risk factors, the testimony here satisfies that requirement. Contrary to
the court of appeals’ interpretation of Dr. Good’s testimony, Dr. Good specifically testified on
cross-examination that the risk factors from which D.B. suffered, which put her at high risk for ROP,
31
did not contribute to her poor outcome. This testimony shows that Dr. Good considered these risk
factors in formulating his opinion. First, there was no evidence that “plus disease,” “extremely low
birth weight,” or “gestational age” causes blindness. Rather, Dr. Good described these conditions
as “factors” indicating an increased risk that a newborn would develop severe ROP. It is ROP that
causes blindness. These “factors” are not other plausible causes of D.B.’s vision impairment; they
are risk factors for developing ROP, which was the cause of her impaired vision. Further, while Dr.
Good testified that “vitreous hemorrhage can be a bad factor,” he thought that it was not “a bad
negative factor in her case.” Although Dr. Good conceded that D.B.’s right eye had zone I disease
on August 1, and zone I disease is an “ominous finding,” Dr. Good also explained that zone I disease
portends an unfavorable outcome when the zone I disease is “posterior,” but noted that D.B. suffered
from “anterior” zone I disease. As Dr. Good explained, “the goal of screening” is to identify and
treat severe ROP before factors such as a vitreous hemorrhage or plus disease develop, and D.B. did
not suffer from those aggravating conditions on the date of her first examination. Dr. Good opined
that, had Dr. Ponte and Dr. Llamas followed the proper screening schedule, the zone I ROP would
have been detected on July 18, and the doctors would have decided to treat D.B. at that time or at
the follow-up exam that should have occurred a week later. Dr. Good’s testimony thus sufficiently
negates the risk factors as a purported alternative cause of D.B.’s poor structural outcome in her right
eye.
In summary, while Dr. Good admitted that vitreous hemorrhage, zone I disease, and plus
disease are risk factors for the poor outcome that D.B. suffered, he explained that “the goal of
screening” is to identify and treat severe ROP before factors such as vitreous hemorrhage, zone I
32
disease, and plus disease develop, and noted that D.B. did not suffer from these aggravating
conditions on the date of her first examination. Dr. Good went on to testify that “the fact that [D.B.]
wasn’t screened and treated timely” was “more likely” the cause of D.B.’s vision loss, not “the
remaining risk factors.” Thus, Dr. Good’s testimony shows that he considered the risk factors that
the court of appeals tried to characterize as “other possible causes” and opined that the risk factors
that D.B. suffered were not likely causes of her poor outcome. In fact, based on this testimony, three
of the cited risk factors—vitreous hemorrhage, zone I disease, and plus disease—would not have
been present had Dr. Ponte and Dr. Llamas satisfied the duties owed to D.B. In short, the evidence
supports that these “risk factors” are not “causes” at all, such that Jelinek is inapplicable. Rather,
the presence of these factors should have caused Dr. Ponte and Dr. Llamas to adjust their screening
plan, as required by the 2001 Statement.
Finally, Dr. Good expressly identified and ruled out the neurological damage suggested by
the defendants’ child neurology expert, Dr. Jerry Tomasovic, as well as Dr. Quinn, that could
independently affect D.B.’s use of her left eye. Dr. Tomasevic testified that D.B.’s left eye records
images but that her brain does not process them. He explained that D.B.’s extreme prematurity and
resulting need for mechanical ventilation because of her immature lungs caused bleeding in her
brain, which damaged the connections in the white matter of the brain, as well as the brain stem
(affecting parts of the brain that control vision and contain the optic tract). Thus, Dr. Tomasevic
believed that D.B.’s problem is not the left eye sending or capturing the image but what the brain
does with the visual information. Dr. Quinn also believed that the visual problems in D.B.’s left eye
resulted not from any retinal abnormality but from optic nerve atrophy, a condition separate from
33
ROP that can affect vision. Dr. Quinn explained that optic nerve atrophy, also referred to as paleness
of the optic nerve, occurs when light stimulating the retina is not transmitted back to the brain.
Dr. Good expressly addressed these cited causes for the impaired vision in D.B.’s left eye.
Dr. Good disagreed with the conclusions of Dr. Tomasevic and Dr. Quinn relating to these other
possible causes, testifying that, in his opinion, light was being transmitted to D.B.’s brain through
the left eye, but that the conduction time was slowed and the amount of information getting to the
brain was diminished. He also testified that when he examined D.B. in his office, D.B. presented
herself with eye poking and eyes that fluttered from side to side. Dr. Good testified that eye poking
“is a finding that’s almost really 100 percent specific to retinal disease,” explaining that, based upon
his examination of D.B.’s eyes, “she has physical findings in the retina that are entirely consistent
with the level of vision that she has in that left eye.” He further explained that D.B.’s eye fluttering
was caused by D.B.’s “bilateral eye disease” and that “it occurs to a probability with [eye disease],
not if there is damage to the brain.” According to Dr. Good, if it was a brain injury, D.B. would not
have had eye fluttering, she would not have been poking at her eyes, and, more likely than not, she
would have been in a wheelchair because for the brain injury to affect the sight, it has to affect a part
of the brain that disturbs all motor functions. Thus, to the extent there were other plausible causes
of D.B.’s impaired vision in her left eye, the record shows that Dr. Good expressly identified and
ruled out those causes.
We reject the contention that our holding in Wal-Mart Stores, Inc. v. Merrell, 313 S.W.3d
837 (Tex. 2010) (per curiam), requires experts to exclude all other potential causes when opining
on causation. That proposition does not flow from this Court’s holding. At issue in Merrell was
34
whether an expert report describing the cause of a fatal fire was sufficient to uphold a judgment
against Wal-Mart Stores. Id. at 839. Merrell and his girlfriend died of smoke inhalation from a fire
in their home. Id. at 837. In the subsequent wrongful-death action, Merrell’s parents alleged that
a halogen lamp purchased at Wal-Mart was the most likely cause of the fire. Id. at 838. The
Merrells produced a report by an expert in fire science, who determined that the most likely cause
of the fire was an exploding halogen bulb, pieces of which smoldered on a recliner next to the lamp.
Id. Wal-Mart’s expert argued that the proliferation of drug paraphernalia and marijuana butts in the
living room evidenced that “careless disposal of smoking materials” was the more likely cause of
the fire. Id. The trial court admitted the Merrells’ expert testimony but granted Wal-Mart’s motion
for summary judgment. Id. at 839. We held that the testimony of the Merrells’ expert was
speculative and conclusory, in part because he failed to rule out other potential causes of the
fire—namely, careless disposal of smoking materials. Id. at 839–40. Specifically, the expert did not
say why smoking materials could not have caused the fire even though the post-mortem toxicology
reports revealed that Merrell and his girlfriend had been smoking the night of the fire. Id. at 839.
We explained that “while [the expert] laid a general foundation for the dangers of halogen lamps,
his specific causation theory amounted to little more than speculation. Evidence that halogen lamps
can cause fires generally (assuming that the lamp here was a halogen lamp) does not establish that
the lamp in question caused this fire.” Id. at 840. Thus, the presence of smoking materials raised
a plausible cause that the expert did not rule out. See id. While we agree that an expert must
exclude other plausible causes, Merrell does not require experts to exclude all other potential causes
when testifying as to causation. Here, the evidence is that D.B. had a poor visual outcome because
35
of ROP, not because of a plausible cause that the Bustamantes’ experts failed to negate with
non-conclusory testimony.
III. Legal Sufficiency Analysis
Having concluded that the substantial-factor test applies in this case and that the ETROP
study and Dr. Good’s and Dr. Phelps’s testimony constituted proper causation evidence, we now
consider whether there is legally sufficient evidence to support the jury’s finding that Dr. Ponte’s
negligence caused D.B.’s poor visual outcome.
To establish proximate cause in a medical-malpractice case, there must be “evidence of a
‘reasonable medical probability’ or ‘reasonable probability’ that [the plaintiff’s] injuries were
proximately caused by the negligence of one or more defendants.” Milo, 909 S.W.2d at 511. In
other words, “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.” Id. (quoting Kramer, 858 S.W.2d
at 400). Accordingly, a plaintiff cannot show that a defendant’s negligence was more likely than not
a cause of injury “where the defendant’s negligence deprived the tort victim of only a 50% or less
chance of avoiding the ultimate harm.” Kramer, 858 S.W.2d at 400; cf. Havner, 953 S.W.2d at 718
(“The use of scientifically reliable epidemiological studies and the requirement of more than a
doubling of the risk strikes a balance between the needs of our legal system and the limits of
science.”).
Dr. Ponte contends that Havner’s “doubling of the risk” requirement applies in this case and
that the Bustamantes failed to make that showing. See Havner, 953 S.W.2d at 718. We disagree.
As explained earlier, Havner is distinguishable for a number of reasons. Most importantly, in
36
Havner, the plaintiffs could not point to facts showing “specific causation” and were forced to rely
to a considerable extent on epidemiological studies for proof of “general causation.” Id. at 714–15.
This was necessary because there was no direct proof that the substance was responsible for the
plaintiff’s injury. Id. As a result, the evidence in Havner related solely to studies about whether
Bendectin exposure doubled the risk of limb-reduction defects; there was no evidence specifically
showing that the plaintiff’s birth defects were caused by Bendectin exposure. Id. at 724–30. That
is not this case.
Dr. Ponte also argues that the Fifth Circuit’s decision in Young v. Memorial Hermann
Hospital Systems, 573 F.3d 233 (5th Cir. 2009) (per curiam), presents a scenario analogous to the
one at issue here and should be followed in this case. In Young, the plaintiffs alleged that hospital
personnel failed to promptly diagnosis a patient’s ischemic stroke and, as a result, failed to timely
administer intravenous tissue plasminogen activator (tPA), exacerbating the plaintiff’s brain damage.
Id. at 234–35. Even though epidemiological data showed that tPA therapy benefitted some patients,
the district court granted summary judgment for the hospital, concluding that the plaintiffs could not
establish a greater than 50% probability of recovery necessary to establish causation. Id. at 235. The
Fifth Circuit affirmed, observing that the patient’s likelihood of a favorable outcome was
approximately 42% without tPA treatment, while his likelihood of success with tPA treatment was
approximately 59%. Id. at 236. Relying on Havner, the Fifth Circuit ruled that, because the failure
to treat with tPA did not “more than double the risk” of an unfavorable outcome, the plaintiffs could
not show that negligence was, more likely than not, the cause of their harm. Id.
We conclude that Young is not applicable here. The courts in Young relied on Havner’s
doubling of the risk requirement, which we have determined does not apply to the facts of this case.
37
Like the plaintiffs in Havner, the Young plaintiffs relied solely on epidemiological studies to
establish “general causation.” See id. at 235. But here, the Bustmantes’ experts gave their causation
opinions based on their own clinical experience with ROP and the particular medical procedures at
issue, informed by photographs of D.B.’s eyes taken during each step of her screening and treatment,
D.B.’s medical records, in-person examinations of D.B., and epidemiological studies in which they
participated personally. In effect, Young does not apply in this case for the same reasons that
Havner’s “doubling of the risk” requirement does not apply.
We hold that the evidence is legally sufficient to establish that D.B.’s ROP was not detected
and treated early enough to avoid retinal detachment in the right eye and severely impaired vision
in the left. Dr. Good described ROP as uncontrolled blood-vessel growth in the eyes of premature
children, which can result in retinal detachment in advanced stages. As Dr. Phelps explained, “[i]f
you can just slow [the blood vessels] down, get them to settle down for a while, then they will catch
up, and the retina will stay where it belongs instead of becoming detached.” Dr. Quinn apparently
agreed with this statement, testifying that the purpose of the laser treatment is to reduce the
production of the hormone vascular endothelial growth factor (VEGF) enough to return the eye to
an auto-regulated condition. Thus, despite D.B.’s extreme prematurity, the Bustamantes presented
evidence that if her ROP had been diagnosed and treated early enough, it is more likely than not that
the blood-vessel growth in her eyes would have been slowed to the point that she would have
enjoyed a sighted life.
Dr. Ponte testified that infants born more prematurely tend to develop ROP earlier and that
he was concerned D.B. would have early onset ROP, requiring treatment at 29–36 weeks.
Dr. Llamas apparently observed incomplete vascularization in zone II at D.B.’s first ROP screening
38
on July 4, 2005, but he failed to use the ICROP terminology as provided by the 2001 Statement to
describe his observations. Dr. Phelps testified that Dr. Llamas’s failure to use the proper
terminology and Dr. Ponte’s failure to follow up or ask for a clarification caused an “impaired
understanding of what was seen on that first examination.” Moreover, despite the fact that Dr. Ponte
believed D.B. would develop early onset ROP, and contrary to the 2001 Statement’s guidelines
regarding the scheduling of follow-up examinations, Dr. Llamas recommended a follow-up exam
in four weeks. Although Dr. Phelps testified that it is “hard to tell” when D.B.’s follow-up screening
examinations should have occurred “because the way the results of the first examination were written
down are sort of ambiguous,” at most, D.B.’s follow-up screenings should have occurred in two-
to three-week intervals—not four weeks as scheduled and performed by Dr. Ponte and Dr. Llamas.
At the August 1 follow-up examination four weeks later, Dr. Llamas determined that stage 3
ROP had developed and recommended treatment “as soon as possible.” However, D.B.’s treatment
was further delayed an additional three days due to the failure to secure the laser necessary for
treatment. As a result of the screening and treatment received, D.B.’s right retina detached, causing
her to lose vision permanently in her right eye, and she has macular dragging and severely impaired
vision in her left eye.
Dr. Good agreed that D.B. was a high-risk infant who should have been monitored closely.
Relying on D.B.’s medical records, including images of her eyes taken on August 1 showing that she
was “at threshold” at that time, Dr. Good testified that if D.B.’s doctors had followed the proper
exam schedule, “ROP would have been diagnosed on July 18th,” and she would have received laser
treatment about a week before August 1. Specifically, Dr. Good opined that D.B. should have been
examined on July 11 or July 18 based on the July 4 examination and that those follow-up
39
examinations would have resulted in a July 25 follow-up because, in light of the August 1 findings,
D.B.’s ROP would have been diagnosed on July 18. In fact, Dr. Quinn agreed that D.B. was treated
at threshold on August 4 rather than pre-threshold. Dr. Good opined that the four-week delay in
screening examinations “to a probability prevented Dr. Llamas from identifying ROP when it could
have been treated earlier” and before risk factors, such as vitreous hemorrhage and plus disease,
developed. He also testified that the additional three-day delay “incrementally increased” the
likelihood of a poor outcome in D.B.’s particular case. Ultimately, Dr. Good concluded that if the
defendants had acted properly, “[m]ore likely than not, she would have . . . a sighted life.” Thus,
Dr. Good’s testimony effectively states that, had Dr. Ponte and Dr. Llamas not delayed the screening
examinations for four weeks, Dr. Llamas would have identified her ROP at a time when it was less
aggressive and would have treated it earlier, and D.B. would have enjoyed a sighted life.
Dr. Phelps similarly concluded that the doctors’ negligence proximately caused D.B.’s loss
of usable vision. She testified that had the doctors not had an impaired understanding of the results
of the July 4 examination, and had D.B.’s follow-up examinations been scheduled according to the
guidelines in the 2001 Statement, an examination would have occurred on July 26 (which was noted
as necessary in D.B.’s medical records), and ROP would have been diagnosed that day based on the
advanced stage of D.B.’s ROP (type 1 ROP) on August 1. Dr. Phelps also testified that had D.B.
been treated before her ROP became so advanced, she “more likely than not” would have functional
vision. In other words, Dr. Phelps testified that had Dr. Ponte and Dr. Llamas communicated
adequately to comply with the 2001 Statement guidelines at the July 4 exam, Dr. Llamas “would
have seen the ROP as it started up . . . and before it became advanced.” Had this occurred, according
40
to Dr. Phelps, “more likely than not [D.B.] would have functional vision” because the doctors would
have identified ROP closer to “the point where it needed surgery.”
Dr. Good, Dr. Phelps, and Dr. Quinn all agreed that properly timed laser therapy is more
effective in stopping the progression of ROP in most infants. In fact, Dr. Quinn called ROP “the
most treatable cause of blindness in children.” The problem, however, is that Dr. Ponte and
Dr. Llamas failed to ensure that D.B. received laser therapy at a time when it would have been
effective by failing to communicate properly, screen timely, and treat timely. Despite testimony
reflecting the rapid progression of ROP in extremely premature infants and the need for surgical
intervention within no more than 72 hours of a determination of “threshold” ROP, D.B. went one
month from her first examination to her second, at which point Dr. Llamas determined she required
laser treatment “as soon as possible.” D.B.’s treatment was further delayed for three days because
the NICU could not find the laser. Both Dr. Good and Dr. Phelps testified that had these delays in
screening and treatment not occurred, D.B. would have enjoyed a sighted life, explaining how and
why that negligence resulted in D.B.’s adverse outcome. Thus, we cannot say that the evidence is
legally insufficient to support the jury’s conclusion that D.B.’s poor visual outcome was more likely
than not the result of Dr. Ponte’s negligence.
IV. Conclusion
We hold that the court of appeals erred in not applying the substantial-factor test because the
jury heard ample evidence supporting the combined negligence of Dr. Ponte and Dr. Llamas. We
further hold that the court of appeals erred in rejecting the Bustamantes’ statistical evidence premised
on the ETROP study as no evidence of causation and in holding that Dr. Good’s and Dr. Phelps’s
opinions were conclusory and thus no evidence of causation. Finally, we hold that legally sufficient
41
evidence supports the jury’s conclusion that Dr. Ponte’s negligence more likely than not caused
D.B.’s impaired vision. Accordingly, we reverse the judgment of the court of appeals as to Dr. Ponte
and his professional association and remand the case to that court so that it can consider the
remaining issues not previously addressed.
______________________________
Paul W. Green
Justice
OPINION DELIVERED: September 29, 2017
42