Victor Kareh M.D. v. Tracy Windrum, Individually, as Representative of the Estate of Lancer Windrum, and on Behalf of Her Minor Children, B. W., J. W. and H. W.

Opinion issued April 19, 2016

In The

Court of Appeals
For The

First District of Texas
————————————
NO. 01-14-00179-CV
———————————
VICTOR KAREH, M.D., Appellant
V.
TRACY WINDRUM, INDIVIDUALLY, AS REPRESENTATIVE OF THE
ESTATE OF LANCER WINDRUM, AND ON BEHALF OF HER MINOR
CHILDREN, B.W., J.W., AND H.W., Appellee

On Appeal from the 133rd District Court
Harris County, Texas
Trial Court Case No. 2012-07156

OPINION

In this wrongful death case, Tracy Windrum, individually, as representative

of the estate of Lancer Windrum, her husband, and on behalf of her minor children,
B.W., J.W., and H.W., sued Dr. Victor Kareh for medical malpractice. After a jury

trial, the jury found Dr. Kareh 80% negligent and awarded a total of $4,239,464 to

Windrum in damages. After applying settlement credits and statutory damages

caps, the trial court entered judgment in favor of Windrum, awarding her

$1,875,887.62 in damages. In seven issues, Dr. Kareh contends that (1) Windrum

failed to present legally and factually sufficient evidence that he was negligent;

(2) Windrum failed to present legally and factually sufficient evidence that his

negligence caused Lance Windrum’s death; (3) the trial court erroneously admitted

expert testimony and accompanying photographs that were not timely produced;

(4) the trial court erroneously denied his motion for mistrial made after the court

informed the jury that the parties had been to mediation and tried to settle; (5) the

trial court erroneously excluded on the basis of the Texas Deadman’s Rule

testimony from one of the physicians involved concerning statements made to her

by the decedent; (6) the foregoing errors constituted cumulative error; and (7) the

trial court erroneously applied the statutory damages caps applicable to the

recovery of non-economic damages in wrongful death cases.

We reverse and render.

2
 Background

A. Factual Background

On February 3, 2010, forty-six-year-old Lancer (“Lance”) Windrum was out

shopping with his three children when he started slurring his speech, became

confused and disoriented, and hit his head while trying to climb back into his car.

An ambulance took Lance to the North Cypress Medical Center (“NCMC”), where

he worked as the Director of Radiology. Lance reported to his treating physicians

that he had had three similar “episodes” over the past several months, which

involved “very mild” slurring of his speech that resolved over the course of several

hours. During the third episode, which occurred on Christmas Eve 2009 and was

“pretty similar” to the February episode, Lance had felt confused, his balance had

been impaired, and he had had tremors in his left hand and leg. Lance told his

physicians that, on each of these occasions, he “was back to his baseline” within a

matter of hours. Lance also reported that he had contracted encephalitis, a brain

infection, when he was six years old.

Dr. Carrie Blades, the attending emergency room physician, ordered that

Lance undergo a CT scan of his head. The lateral and third ventricles of the brain

produce cerebrospinal fluid, which flows through an aqueduct into the fourth

ventricle of the brain and then into the spinal column before it is later absorbed into

the body through the venous system. The CT scan report noted that the ventricles

3
in Lance’s brain were “dilated out of proportion,” indicating hydrocephalus. Dr.

Blades ordered that Lance undergo an MRI. Dr. Christina Payan, the

neuroradiologist who read the MRI scan, reported the following findings: “The

lateral and third ventricles are markedly dilated out of proportion with the fourth

ventricle and sulci. The cerebral aqueduct is narrowed. These findings are

indicative of aqueductal stenosis [i.e., the narrowing of the aqueduct that carries

cerebrospinal fluid through the brain]. There is some white matter atrophy. No

significant transependymal [cerebrospinal fluid] flow is evident. . . . No masses

are present.”1

Lance then consulted Dr. Harpaul Gill, a neurologist at NCMC.2 Dr. Gill

agreed that, at the time he presented to NCMC, Lance was experiencing symptoms

of a neurological condition. During the consultation, Dr. Gill came to the

conclusion that Lance’s symptoms might be caused by an increase in intracranial

pressure due to a build-up of cerebrospinal fluid in the ventricles of Lance’s brain,

and he told Lance that a shunt was a possible treatment to drain the excess fluid

1
“Transependymal flow” is the flow of cerebrospinal fluid outside of the
ventricular system.
2
Windrum originally sued Dr. Gill, as well as North Cypress Medical Center, North
Cypress Medical Center Operating Company, GP, LLC, North Cypress Medical
Center Operating Company, Ltd., and Coresource, Inc. Windrum settled with Dr.
Gill and the North Cypress entities pre-trial, and she nonsuited her claims against
Coresource.

4
from the brain. Dr. Gill referred Lance to Dr. Kareh, a neurosurgeon, to determine

whether Lance had increased intracranial pressure which would require surgery to

alleviate.3

Dr. Kareh first saw Lance around 6:00 a.m. on February 4, 2010. Dr. Kareh

testified that he did not review Lance’s medical history prior to meeting with him.

Lance did not have any of the symptoms that he had displayed when he presented

to NCMC the previous evening. All of Lance’s cranial nerves exhibited normal

functioning. Dr. Kareh testified that double vision and papilledema, or swelling

around the optic nerve, are both common symptoms that occur when a patient has

increased intracranial pressure. Lance did not have double vision or papilledema at

the time Dr. Kareh examined him. Dr. Kareh informed Lance that if he had

increased intracranial pressure, he might need to have a shunt placed to drain the

built-up cerebrospinal fluid. Lance consented to the placement of a ventricular

drain and a device to monitor his intracranial pressure to determine whether it was

increased.

Dr. Kareh monitored Lance’s intracranial pressure over a twenty-four hour

period. Lance did not have increased intracranial pressure at the time that Dr.

3
Placement of a shunt involves threading a tube from the brain down into the
patient’s abdomen. When there is a blockage in the ventricular system, excess
cerebrospinal fluid flows through the shunt down into the abdomen, where it is
then absorbed into the body. This mechanism helps relieve the elevated
intracranial pressure that can occur with the build-up of cerebrospinal fluid in the
ventricles.

5
Kareh placed the monitoring device inside his brain. During the monitoring

period, Lance’s intracranial pressure spiked on several occasions to a higher level

than what is considered “normal.” However, Lance’s intracranial pressure quickly

returned to a normal level on each occasion, and he did not experience any periods

of sustained increased intracranial pressure. After the monitoring period ended,

Dr. Kareh concluded that Lance’s intracranial pressure levels were normal, his

neurological examination was normal, and he was not suffering from any

symptoms such as confusion, imbalance, weakness, or numbness. Dr. Kareh

determined that, although Lance had hydrocephalus, he did not have increased

intracranial pressure. He therefore did not place a shunt.

Dr. Gill saw Lance for a follow-up appointment on February 17, 2010.

Lance reported that he had had “one to two headaches every week,” but he had not

experienced nausea, vomiting, focal weakness, numbness, visual disturbances, or

sensitivity to light or sound. Dr. Gill performed a neurological examination, and

the results were “normal.” Dr. Gill and Lance discussed medication for Lance’s

headaches, but Lance decided against this course of action because he was “feeling

better.” Dr. Gill directed Lance to visit the emergency room if he experienced any

more neurological symptoms, and he recommended that Lance undergo another

MRI scan in three months and that Lance keep track of the headaches he

6
experienced. Dr. Gill gave Lance a “headache calendar” to keep track of the days

on which he experienced headaches.

Lance saw Dr. Kareh for a follow-up appointment on February 22, 2010.

Lance reported that he had had one headache episode since he had been discharged

from the hospital, which Dr. Kareh testified was expected due to the surgical

procedure he had undergone, and one episode of slurred speech. Dr. Kareh

recommended that Lance undergo a nuclear cisternogram to track the circulation of

cerebrospinal fluid throughout his body, and he also recommended that Lance

consult an endocrinologist to rule out a hormonal cause to his neurological

symptoms. Dr. Kareh did not see Lance again after the February 22 appointment.

Lance did not have a nuclear cisternogram performed. Lance did see an

endocrinologist on March 24, 2010, and testing conducted by this doctor revealed

no problems with Lance’s endocrine system that might have caused his symptoms.

On his headache calendar, Lance self-reported taking two Lortabs for

headache-related pain on two occasions during April 2010. He also underwent a

second MRI scan in April 2010 with the findings reported to Dr. Gill. Dr. Payan

again read the MRI scan and testified that “[t]he ventricles looked as big, if not

worse in size, and the angle of the aqueduct had notably changed” since the

February MRI. Dr. Payan called Dr. Gill and reported her findings to him. Dr.

Gill did not discuss the results of this MRI with Lance, but Lance did undergo an

7
EEG on April 29, 2010, at Dr. Gill’s direction. The results of this test were

normal. There is no evidence that either Dr. Gill or Dr. Payan informed Dr. Kareh

of Lance’s symptoms after the February follow-up appointment or of the results of

the April MRI scan.

Lance passed away in his sleep on May 2, 2010. Lance had reportedly

complained to Windrum the previous day that he felt tired, sluggish, and irritable,

and he had slurred speech. Lance did not self-report experiencing any headaches

for the ten days prior to his death, which included his second MRI, showing a

notably changed aqueduct and worsened ventricles, and a normal EEG.

Dr. Morna Gonsoulin, a medical examiner for the Harris County Institute of

Forensic Sciences, performed an autopsy on Lance. Dr. Gonsoulin noted that

Lance’s heart was enlarged and that the chambers of the heart were dilated. Dr.

Gonsoulin made the following findings relevant to Lance’s brain:

The leptomeninges are clear. There is no epidural, subdural, or
subarachnoid hemorrhage. The cerebral hemispheres are generally
symmetrical with a relatively unremarkable gyral pattern. The vessels
at the base of the brain are normally configured without
atherosclerosis. The cranial nerves appear unremarkable. Sections
through the cerebrum reveal markedly expanded lateral ventricles
with rostral and caudal extensions to the frontal and occipital poles,
respectively. The left hippocampus has slightly more prominent gray
matter than the right hippocampus. There is decreased periventricular
white matter surrounding the dentate nuclei of the cerebellum with
expanded nuclear outlines abutting the ventricular border and no
intervening white matter. A 0.5 centimeter cystic membrane is
adjacent to the left dentate nucleus near the ventricle with interruption
of the nuclear outline and slightly more white matter compared to that

8
 of the right. The periaqueductal gray matter is blurred with
prominent stenosis of the aqueduct at the level of the cerebral
pedicles. The diameter of the aqueduct ranges from pinpoint to non-
visible, obscured by ill-defined light tan gelatinous gray material.
Slightly increased gray matter is noted in the crossing fibers of the
pons. No discrete areas of hemorrhage, infection or neoplasm are
apparent.

(Emphasis added.) In the “Microscopic Examination” section of the autopsy

report, Dr. Gonsoulin stated, “Sections from rostral pons through medulla show

marked stenosis of aqueduct with gliosis[, i.e., scarring] of adjacent structures.”

Dr. Gonsoulin listed “[c]omplications of hydrocephalus due to aqueductal

stenosis” as Lance’s cause of death.

B. Procedural Background

Windrum, in her individual capacity, in her capacity as the representative of

Lance’s estate, and on behalf of her three minor children, brought a negligence

cause of action against Dr. Kareh and Dr. Gill pursuant to Texas’s wrongful death

statute. Windrum alleged that the applicable standard of care when Lance was

seen by Dr. Kareh at NCMC on February 4 required Dr. Kareh to install a shunt, or

a permanent drain, in Lance’s brain to prevent a fatal build-up of cerebrospinal

fluid and intracranial pressure. Dr. Gill settled before trial.

Windrum retained Dr. Robert Parrish, a neurosurgeon, to testify concerning

the standard of care and causation, and she retained Dr. Ljubisa Dragovic, a

forensic and neuropathologist, to testify concerning causation. Dr. Kareh filed a

9
Daubert motion challenging both experts’ opinions on causation, arguing that

neither doctor has “a sufficient scientific and/or factual basis to render such

opinions and such opinions are based on pure speculation and mere conjecture and

do not pass the Analytical Gap test.” Dr. Kareh also argued that the methodology

underlying Dr. Parrish’s and Dr. Dragovic’s opinions “is based on speculation and

is unreliable.” The trial court overruled this motion.

Dr. Parrish testified that his opinion was that “Dr. Kareh should have put a

shunt in when he saw Mr. Windrum in the hospital” on February 4 and that Lance

“died of obstructive hydrocephalus.”4 When asked how Lance died, Dr. Parrish

testified,

His aqueduct obstructed. There’s pressure in the ventricles. It put
pressure on the red nuclei and the periaqueductal region right around
where all that important stuff is. And those fibers made him stop
breathing and his heart stop beating. . . . But all those vital structures
stopped because of pressure on the top of the brain stem where he is
most susceptible with the aqueductal stenosis.

He stated that Lance “had these classic symptoms of increased intracranial pressure

with staggering, slurred speech, and altered mental status that were periodic.” He

discounted the significance of the absence of papilledema in Lance’s eyes—

likewise a classic symptom of increased intracranial pressure—and he testified that

4
Dr. Parrish testified that “obstructive hydrocephalus” does not necessarily mean a
complete blockage of the aqueduct and that a “partial” obstruction, such as the
narrowed aqueduct seen in cases of aqueductal stenosis, is considered “obstructive
hydrocephalus.”

10
papilledema can be intermittent and did not have to be present for Lance to have

increased intracranial pressure. Relying on the February MRI results plus the

“classic symptoms” of hydrocephalus, Dr. Parrish opined that this “equals a

shunt . . . every time.” He stated that although Lance’s being off-balance and

confused and having slurred speech are “generic symptoms,” “in the fact of that

M.R.I. scan showing severe aqueductal stenosis, they are the light bulb that needs

to go off and say this requires a shunt.”

Dr. Parrish testified that Lance had “pre-existing” large ventricles. He

considered it significant that Lance had contracted encephalitis when he was six

years old. He testified that he believed the encephalitis “had something to do with

scarring in the aqueduct which led to [Lance’s] increased intracranial pressure and

enlarged ventricles.” Dr. Parrish opined that the encephalitis caused an

inflammation in Lance’s brain, which led to scarring, or gliosis, which then led to

the narrowing of the aqueduct. Dr. Parrish testified that a narrowed, or partially

obstructed, aqueduct “means it’s more difficult for fluid to flow through” and thus

requires a higher amount of intracranial pressure to force fluid through the

aqueduct.

Dr. Parrish also testified that “[t]he contour of the ventricles and even the

contour of the aqueduct is proof that there is at some time increased intracranial

pressure, increased intraventricular pressure.” Dr. Parrish described Lance’s third

11
ventricle, as seen in the February 2010 MRI, as “huge,” and he stated that “the top

part of the aqueduct is enlarged compared to the bottom part, which is extremely

small.” He testified that this was evidence of “increased intracranial pressure at

some time.” Dr. Parrish testified that the “obvious indications of pressure” on the

February 2010 MRI scan included the “[b]ig third ventricle,” “enlargement of the

proximal part of the aqueduct of Sylvius and constriction of the bottom part [of the

aqueduct],” and a slightly enlarged fourth ventricle. He stated, “Those ventricles

got big somehow, and they were blown up by the increased pressure.”

Dr. Parrish reviewed the April MRI and testified that, although Lance’s

ventricles looked the same size in the April MRI, he concluded that “the aqueduct

here is more dilated proximally on the inside” than the aqueduct in the February

MRI. Dr. Parrish suggested that “the pressure has increased, or it may be

intermittently increasing,” and he testified that the April MRI reflected that Lance

was “getting worse.” Dr. Parrish agreed that the April MRI indicated that “the

angle of the aqueduct was different and it indicated pressure.” He also testified

that Lance demonstrated “typical compensated hydrocephalus,” in which the

ventricles expand to compensate for the obstructed flow of cerebrospinal fluid

through the aqueduct, but, at some point, because the brain is constrained by the

skull, the ventricles reach the limit of the amount they can expand, the increasing

intracranial pressure has “to go somewhere” and so it is “exerted down through the

12
brain stem,” which affects the heart and respiratory rates. Dr. Parrish stated that

the April MRI demonstrated compensation and that “you can compensate up to a

point, and at some point the time bomb goes off.”

On cross-examination, Dr. Parrish agreed that the autopsy showed a “normal

looking brain” and revealed no microscopic evidence of increased intracranial

pressure, such as herniation, swelling, or bleeding within the brain. He also agreed

that he could not determine how long Lance had had enlarged ventricles and that

the MRI could not pinpoint when the changes in Lance’s brain structure had

occurred. Dr. Parrish also agreed that although Lance had several symptoms

associated with increased intracranial pressure when he presented to NCMC, such

as slurred speech, confusion, a headache, and balance problems, he did not have

other “classic” symptoms such as nausea and vomiting, increased blood pressure,

increased pulse pressure, papilledema, and a low heart rate.

Dr. Parrish agreed that Lance’s symptoms could have been caused by “some

other process” rather than increased intracranial pressure and that Lance’s

symptoms all disappeared while he was in the hospital. Dr. Parrish suggested that

Lance “opened up his pathway somehow,” such as by having “enough

[intracranial] pressure that he opened up the aqueduct” and “relieved his own

pressure,” which could account for the rapid dissipation of Lance’s symptoms. Dr.

Parrish further agreed that no other doctor called Dr. Kareh to inform him of the

13
April 2010 MRI results and that Dr. Kareh, therefore, would not have had any

knowledge of Lance’s worsening hydrocephalus and aqueductal stenosis as shown

on the April MRI. Dr. Parrish also agreed that at the time Lance left NCMC in

February 2010, his aqueduct was not completely closed. He further agreed that

placing a shunt in a patient can result in the patient’s death. Dr. Parrish agreed that

Lance had an MRI performed nine days before he died and he “could have

survived his problem . . . if he’d had a shunt done the day before he died.”

Dr. Dragovic testified that, in his opinion based on a reasonable degree of

medical probability, Lance “died of complications of obstructive hydrocephalus.”

Factors relevant to Dr. Dragovic’s opinion included the fact that Lance had had

“some problems and neurological deficits that were occurring on and off over a

period of time,” the “established clinical diagnosis [of] enlarged ventricles,” and

Lance’s history of having suffered from encephalitis.

Dr. Dragovic stated that after reviewing the microscopic slides prepared

during the autopsy, he “now know[s] beyond any reasonable doubt in [his] mind

that there was acute blockage, acute obstruction of the aqueduct at the lower level

[leading to the fourth ventricle]” when Lance died, and he opined that a build-up of

glial tissue, or scar tissue in the brain, caused the blockage. Dr. Dragovic also

testified that Lance’s enlarged ventricles “reflect[ed] sudden increase of

[intracranial] pressure as a result of increased blockage.” He stated that it was

14
“clear that this condition had been present for a long time.” Dr. Dragovic thus

concluded that, in his opinion, this case involved an acute blockage of the aqueduct

and that the “sudden rise of intracranial pressure because of the blockage creating

the pressure on the brain stem and pressure on the structures above the brain stem

to lose control of respiratory function and allow the quick accumulation of fluid in

the lungs.”5

Dr. Gill, Lance’s treating neurologist, who settled before trial, testified by

video deposition. He testified that although Lance was suffering from obstructive

hydrocephalus, he did not wish that he had insisted that Dr. Kareh place a shunt in

Lance’s brain. Dr. Gill agreed that “the applicable standard of care is that the

treatment for obstructive hydrocephalus is either a shunt or a third

ventriculostomy.”6 He testified, however, that he believed discharging Lance

without placement of a shunt was proper because the monitoring of Lance’s

intracranial pressure revealed no sustained increased in pressure and because his

5
Dr. Dragovic testified that the photographs taken by the medical examiner’s office
of Lance as he was found in bed on May 2, 2010, support this conclusion, as they
show “purging from his nostrils, purging from his mouth,” indicative of a build-up
of fluid in his lungs. He testified that this evidence is inconsistent with death from
cardiac arrhythmia. Dr. Dragovic stated that he was able to exclude a heart
problem as a possible cause of Lance’s death.
6
A ventriculostomy involves puncturing the bottom of the third ventricle to create
another method by which cerebrospinal fluid can flow out of the third ventricle.

15
headache had improved and he was feeling better. Dr. Gill agreed that intracranial

pressure fluctuates and that increased pressure could be intermittent.

Windrum also called Dr. Randolph Evans, a neurologist who had been

retained by Dr. Gill, to testify. Dr. Evans testified that Lance was “perhaps

symptomatic” when he presented to NCMC in February 2010 and that he was “not

entirely sure that these symptoms [that he had upon presentment] were due to

aqueductal stenosis,” although he later testified, based on a reasonable degree of

medical probability, that Lance’s symptoms were caused by aqueductal stenosis.

He stated that the symptoms with which Lance presented to NCMC “can be

consistent with a number of different neurological problems, including increased

intracranial pressure.”

Dr. Evans also agreed that the two major alternatives for treating aqueductal

stenosis are shunt surgery and a third ventriculostomy, but he stated, “[T]he

[medical] literature suggests that surgical treatment should be offered to patients

where the symptoms are felt to be due to aqueductal stenosis.” He testified that

placing a shunt “has a high risk of complications,” although he also agreed that

shunt surgery is successful in a high percentage of cases and that the mortality rate

for this treatment is “close to zero.” He testified that “for many patients, [shunt

surgery] will be a good treatment, but there are risks and benefits of these surgical

treatments, like any others,” and the neurosurgeon must determine whether “the

16
risk of treatment outweigh[s] the risk of not having treatment.” Dr. Evans agreed

that unless the patient has specific impairments such as advanced age or a heart

condition, surgical intervention is appropriate. Dr. Evans also noted that the

medical records reflected that Dr. Kareh offered to place a shunt in Lance’s brain,

but Lance had “declined.”

Dr. Warren Neely, a neurosurgeon, testified on behalf of Dr. Kareh. Dr.

Neely testified that, in his opinion, although Lance had aqueductal stenosis, it was

not obstructive and Lance did not die from aqueductal stenosis.7 Dr. Neely opined

that none of the radiological scans demonstrated evidence of increased intracranial

pressure, that the ventricular monitoring demonstrated intracranial pressure within

a normal range, and that the autopsy revealed “normal findings of the brain” and

did not show any indication of elevated intracranial pressure at the time of death.

Dr. Neely testified that the major symptoms consistent with obstructive

hydrocephalus are extreme drowsiness, severe headaches, nausea, vomiting, eye

movement problems, swelling of the optic nerve, and papilledema. He stated that

7
Dr. Neely defined “obstructive hydrocephalus” as “a blockage somewhere in the
flow of spinal fluid from where it’s being made to actually where it’s being
reabsorbed,” and he testified that obstructive hydrocephalus and aqueductal
stenosis are not necessarily the same thing, although “compensated” or “partial
obstructive hydrocephalus” “could mean the same thing as compensated
aqueductal stenosis.” Dr. Kareh similarly defined obstructive hydrocephalus as “a
blockage of the normal pathway [of cerebrospinal fluid.]” He also acknowledged
that obstructive hydrocephalus can be total or partial. Dr. Kareh defined
aqueductal stenosis as “[a] dysfunction through the aqueduct” that affects the
proper circulation of cerebrospinal fluid.

17
the symptoms that Lance presented with were all “nonspecific symptoms” that

could be indicative of several conditions and do not necessarily indicate increased

intracranial pressure.

Dr. Neely testified that the standard of care did not require Dr. Kareh to

install a shunt in Lance’s brain. He stated:

[T]his is an initial assessment. You’re seeing someone that has very
nonspecific symptoms. You have a CAT scan and an MRI scan that
do not show increased intracranial pressure. Yes, there are certainly
abnormalities in his ventricular system. We see that all the time. This
is a very common finding in patients that we see.
Again, in this situation, I would not install a shunt based on the
history or the findings on the MRI scan or CAT scan.

Dr. Neely further testified that the medical records reflected that Dr. Kareh

explained to Lance that he might have increased intracranial pressure, that the

pressure needed to be monitored, that, if it was elevated, they would consider

placing a shunt, and that they discussed the risks of the procedures involved.

Based on his review of the ventricular monitoring procedure, Dr. Neely agreed

with Dr. Kareh that Lance was not suffering from increased intracranial pressure at

the time he saw Dr. Kareh, although there were several instances in which Lance’s

intracranial pressure spiked to above-normal levels.

Dr. Neely testified that, based on the intracranial pressure readings, he

“absolutely” would not have recommended the installation of a shunt and that the

standard of care did not require a shunt based on those readings. He stated that he

18
would not install a shunt in a patient who had normal levels of intracranial pressure

because draining cerebrospinal fluid from a patient with normal pressure levels

could cause chronic headaches, dizziness, fainting spells, and complications in

which the surface of the brain moves away from the skull and the resulting space

fills up with either fluid or blood, which could lead to a tear in a vein and a

subdural hematoma. He also testified that installation of a shunt itself can have

complications, such as risks from anesthesia, the possibility of infection, failure of

the shunt, and rupture of a blood vessel in the brain or chest or abdominal cavities.

Dr. Neely testified that, based on the possibility of complications from installing a

shunt and the fact that Lance did not have increased intracranial pressure, it was

“very appropriate” for Lance to be discharged from NCMC without placement of a

shunt.

Dr. Kent Heck testified as Dr. Kareh’s neuropathology expert. Dr. Heck

agreed that Lance’s aqueduct was narrowed and that this finding was consistent

with Lance’s history of hydrocephalus with aqueductal stenosis. He testified that if

a patient died from hydrocephalus and aqueductal stenosis, he would expect to find

during the autopsy evidence of brain swelling and herniation, which he did not see

in the pathology slides from Lance’s autopsy. Dr. Heck testified that he saw no

evidence of increased intracranial pressure at the time of Lance’s death and that he

19
saw no evidence of Lance’s dying from complications from hydrocephalus due to

aqueductal stenosis.

Dr. Heck testified that other pathology slides revealed that Lance had an

enlarged heart and dilation of the chambers of the heart, indicative of congestive

heart failure. He testified that if he had had the responsibility of filling out the

death certificate in this case he would have listed “undetermined” as the cause of

death. He stated that, in this case, “the two primary suspects” for Lance’s cause of

death were the heart and the brain but that “neither [had] enough conclusive

evidence to determine which [was] the true cause of death.” He agreed with Dr.

Kareh’s counsel that “there is absolutely no evidence of any kind of a complication

from hydrocephalus due to aqueductal stenosis as a cause of death in Mr.

Windrum.”

The jury found both Dr. Kareh and Dr. Gill to be negligent, and it assigned

eighty percent responsibility to Dr. Kareh and twenty percent responsibility to Dr.

Gill. The jury awarded to Tracy Windrum, in her individual capacity, $211,280 for

past pecuniary loss, $1,177,176.96 for future pecuniary loss, $30,000 for past loss

of companionship and society, $200,000 for past mental anguish, and $250,000 for

future mental anguish. The jury awarded B.W. $39,615 for past pecuniary loss,

$220,720.68 for future pecuniary loss, $30,000 for past loss of companionship and

society, $50,000 for future loss of companionship and society, $200,000 for past

20
mental anguish, and $500,000 for future mental anguish. The jury awarded J.W.

$39,615 for past pecuniary loss, $220,720.68 for future pecuniary loss, $30,000 for

past loss of companionship and society, $50,000 for future loss of companionship

and society, $100,000 for past mental anguish, and $275,000 for future mental

anguish. The jury awarded H.W. $39,615 for past pecuniary loss, $220,720.68 for

future pecuniary loss, $30,000 for past loss of companionship and society, $50,000

for future loss of companionship and society, $75,000 for past mental anguish, and

$200,000 for future mental anguish.

In its final judgment, the trial court applied the statutory cap on damages in

wrongful death cases and awarded a total of $1,875,887.62 to Tracy Windrum.

The trial court apportioned the award as follows: $1,123,301.89 for Tracy

Windrum in her individual capacity, $277,840.33 for the benefit of B.W.,

$241,869.10 for the benefit of J.W., and $232,876.30 for the benefit of H.W. The

trial court denied Dr. Kareh’s motion for judgment notwithstanding the verdict and

motion for new trial, and this appeal followed.

Sufficiency of the Evidence of Medical Negligence

In his first issue, Dr. Kareh contends that Windrum failed to present legally

and factually sufficient evidence that his actions or omissions caused Lance’s

death. In his second issue, Dr. Kareh contends that Windrum failed to present

21
legally and factually sufficient evidence that he breached the standard of care, and

thereby committed negligence, by failing to install a shunt in Lance’s brain.

A. Standard of Review

When conducting a legal sufficiency review, we credit favorable evidence if

a reasonable fact-finder could do so and disregard contrary evidence unless a

reasonable fact-finder could not. See City of Keller v. Wilson, 168 S.W.3d 802,

827 (Tex. 2005); Brown v. Brown, 236 S.W.3d 343, 348 (Tex. App.—Houston [1st

Dist.] 2007, no pet.). We consider the evidence in the light most favorable to the

finding under review and we indulge every reasonable inference that would

support the finding. City of Keller, 168 S.W.3d at 822. We sustain a no-evidence

contention only if: (1) the record reveals a complete absence of evidence of a vital

fact; (2) the court is barred by rules of law or 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 conclusively establishes

the opposite of the vital fact. Id. at 810; Merrell Dow Pharms., Inc. v. Havner, 953

S.W.2d 706, 711 (Tex. 1997).

In a factual sufficiency review, we consider and weigh all of the evidence.

See Cain v. Bain, 709 S.W.2d 175, 176 (Tex. 1986) (per curiam); Arias v.

Brookstone, L.P., 265 S.W.3d 459, 468 (Tex. App.—Houston [1st Dist.] 2007, pet.

denied). When the appellant challenges a jury finding on an issue on which it did

22
not have the burden of proof at trial, we set aside the verdict only if the evidence

supporting the jury finding is so weak as to make the verdict clearly wrong and

manifestly unjust. See Cain, 709 S.W.2d at 176; Reliant Energy Servs., Inc. v.

Cotton Valley Compression, L.L.C., 336 S.W.3d 764, 782 (Tex. App.—Houston

[1st Dist.] 2011, no pet.). The jury is the sole judge of the witnesses’ credibility

and it may choose to believe one witness over another. See Golden Eagle Archery,

Inc. v. Jackson, 116 S.W.3d 757, 761 (Tex. 2003). We may not substitute our

judgment for that of the jury. Id. “Because it is the jury’s province to resolve

conflicting evidence, we must assume that jurors resolved all conflicts in

accordance with their verdict.” Figueroa v. Davis, 318 S.W.3d 53, 60 (Tex.

App.—Houston [1st Dist.] 2010, no pet.).

B. Evidence of Negligence

“To meet the legal sufficiency standard in medical malpractice cases

‘plaintiffs 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)). The elements of a health care liability claim sounding

in negligence are (1) a legal duty, (2) a breach of duty, and (3) damages

23
proximately caused by the breach. Creech v. Columbia Med. Ctr. of Las Colinas

Subsidiary, L.P., 411 S.W.3d 1, 5–6 (Tex. App.—Dallas 2013, no pet.). The

standard of care for a health care provider is what an ordinarily prudent health care

provider would do under the same or similar circumstances. Creech, 411 S.W.3d

at 6. In a medical malpractice case, the plaintiff ordinarily must produce expert

testimony to establish the applicable standard of care and causation if those matters

are not within the experience of a layperson. Id. Thus, to establish negligence in

this case, Windrum had to demonstrate, by a preponderance of the evidence,

(1) that Dr. Kareh had a duty to place a shunt in Lance’s brain when he saw him on

February 4, 2010, (2) that Dr. Kareh’s failure to place the shunt in Lance’s brain at

that time fell below the standard of care of a reasonably prudent neurosurgeon, and

(3) that, but for Dr. Kareh’s failure to place the shunt in Lance’s brain at that time,

Lance would not have suffered sudden death on May 2, 2010.

Texas Rule of Evidence 702 provides that “[i]f scientific, technical, or other

specialized knowledge will assist the trier of fact to understand the evidence or to

determine a fact in issue, a witness qualified as an expert by knowledge, skill,

experience, training, or education may testify thereto in the form of an opinion or

otherwise.” TEX. R. EVID. 702, 61 TEX. B.J. 374, 392 (Tex. & Tex. Crim. App.

24
1998, amended 2015).8 “‘It is the basis of the witness’s opinion, and not the

witness’s qualifications or his bare opinions alone, that can settle an issue as a

matter of law; a claim will not stand or fall on the mere ipse dixit of a credentialed

witness.’” Coastal Transp. Co. v. Crown Cent. Petroleum Corp., 136 S.W.3d 227,

232 (Tex. 2004) (quoting Burrow v. Arce, 997 S.W.2d 229, 235 (Tex. 1999));

Gammill v. Jack Williams Chevrolet, Inc., 972 S.W.2d 713, 726 (Tex. 1998)

(“[T]here must be some basis for the opinion offered to show its reliability.

Experience alone may provide a sufficient basis for an expert’s testimony in some

cases, but it cannot do so in every case.”).

Opinion testimony that is conclusory or speculative is not relevant evidence

because it does not tend to make the existence of a material fact “more probable or

less probable.” Coastal Transp. Co., 136 S.W.3d at 232 (quoting TEX. R. EVID.

401); see also Havner, 953 S.W.2d at 712 (“When the expert ‘br[ings] to court

little more than his credentials and a subjective opinion,’ this is not evidence that

would support a judgment.”) (quoting Viterbo v. Dow Chem. Co., 826 F.2d 420,

421 (5th Cir. 1987)); Cooper Tire & Rubber Co. v. Mendez, 204 S.W.3d 797, 801

(Tex. 2006) (“If the expert brings only his credentials and a subjective opinion, his

8
Effective April 1, 2015, the Texas Supreme Court adopted amendments to the
Texas Rules of Evidence. See 78 TEX. B.J. 42, 42 (Tex. 2015). The revisions to
Rule 702 was stylistic and does not affect the substance of the rules. All further
citations to the Rules of Evidence refer to the rules as they existed at the time of
the parties’ trial.

25
testimony is fundamentally unsupported and therefore of no assistance to the

jury.”). “It is incumbent on an expert to connect the data relied on and his or her

opinion and to show how that data is valid support for the opinion reached.”

Whirlpool Corp. v. Camacho, 298 S.W.3d 631, 642 (Tex. 2009).

The trial court, as the “gatekeeper” of expert testimony, has the threshold

responsibility of “ensuring that an expert’s testimony both rests on a reliable

foundation and is relevant to the task at hand.” Gammill, 972 S.W.2d at 728

(quoting Daubert v. Merrell Dow Pharms., Inc., 509 U.S. 579, 597, 113 S. Ct.

2786, 2799 (1993)). Expert testimony is conclusory if there is no factual basis for

it or if the basis offered does not, on its face, support the opinion. CCC Grp., Inc.

v. S. Cent. Cement, Ltd., 450 S.W.3d 191, 202 (Tex. App.—Houston [1st Dist.]

2014, no pet.) (citing City of San Antonio v. Pollock, 284 S.W.3d 809, 817 (Tex.

2009)). Where experts rely on experience or training to reach their opinions, rather

than on a particular methodology, a reviewing court considers whether there is too

great an analytical gap between the data and the opinion proffered for the opinion

to be reliable. Moreno v. Ingram, 454 S.W.3d 186, 193 (Tex. App.—Dallas 2014,

no pet.) (citing Gammill, 972 S.W.2d at 726). In conducting a no-evidence review

involving expert testimony, we “cannot consider only an expert’s bare opinion, but

must also consider contrary evidence showing it has no scientific basis.” Mendez,

204 S.W.3d at 804 (quoting City of Keller, 168 S.W.3d at 813). “[I]f an expert’s

26
opinion is based on certain assumptions about the facts, we cannot disregard

evidence showing those assumptions were unfounded.” Id. (quoting City of Keller,

168 S.W.3d at 813). “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.” Jelinek, 328 S.W.3d at 536.

We conclude that, here, Windrum failed to carry her burden of proving by a

preponderance of the evidence the elements of medical negligence required to hold

Dr. Kareh liable in this case.

1. Duty to Place a Shunt on February 4, 2010, and Breach of that
Duty

To prove that Dr. Kareh’s care of Lance fell below the standard of care of an

ordinarily prudent neurosurgeon seeing a patient with symptoms of hydrocephalus

for the first time, Windrum had to establish by a preponderance of the evidence

that Dr. Kareh had a duty to place a shunt in Lance’s brain immediately following

that visit on February 4, 2010, or, at the latest, at the time Dr. Kareh last treated

Lance on February 22, 2010.

Windrum relied on the expert testimony of Dr. Parrish to establish the

essential elements of the standard of care applicable to neurosurgeons, Dr. Kareh’s

breach of the standard of care, and causation. Dr. Parrish testified that, in his

opinion, Dr. Kareh “should have put a shunt in when he saw Mr. Windrum in the

27
hospital” in February because Lance “had these classic symptoms of increased

intracranial pressure with staggering, slurred speech, and altered mental status that

were periodic.” He testified that the presence of a classic symptom like

papilledema—which was absent in this case—is “very significant” but not a

necessary for a finding of increased intracranial pressure and that its absence is

“not so significant.” Dr. Parrish stated that the February MRI indicated “that there

is at some time increased intracranial pressure, increased intraventricular pressure.”

He opined that “[t]hose ventricles got big somehow, and they were blown up by

the increased pressure.”

Dr. Parrish also testified that Lance’s symptoms, plus the February 2010

MRI, which revealed aqueductal stenosis, “equals a shunt” “[e]very time.” He

testified that the standard of care required Dr. Kareh to offer a shunt to Lance. He

acknowledged that the balance problems, slurred speech, and confusion were

“generic symptoms,” but, combined with the February 2010 MRI, those symptoms

“are the light bulb that needs to go off and say this requires a shunt.” Dr. Parrish

also acknowledged that there are “real risks” to performing surgery to install a

shunt, but he state that the risks were “very rare” and “fairly low.”

Dr. Parrish concluded that, to comply with the standard of care, a

reasonable, prudent neurosurgeon would have:

[M]ade the right diagnosis, obstructive hydrocephalus. Symptomatic
obstructive hydrocephalus. Number two, he would have

28
 recommended a shunt or some definitive procedure to treat the
hydrocephalus. And, three, he would have properly informed the
patient and the patient’s family what would happen if he got a shunt,
the reasonable things that would happen if he got a shunt. But even
more importantly or as important I guess I would say, the benefit of
getting the shunt and the risk of not getting a shunt.

Dr. Parrish presented no medical literature to support his opinion that the standard

of care required the placement of a shunt “every time” when Dr. Kareh saw Lance

in early February 2010. And his testimony that Dr. Kareh should have

“recommended a shunt or some definitive procedure to treat the hydrocephalus”

and that Lance and his family should have been informed of the risks and benefits

of a shunt is some evidence that a patient presenting with Lance’s symptoms does

not “equal[] a shunt” “every time.”

Other testimony by Dr. Parrish also undermined his claim that it was

professional negligence, or malpractice, for Dr. Kareh not to install a shunt in

Lance’s brain on February 4, 2010. On cross-examination, Dr. Parrish agreed that

there was no “microscopic evidence” of increased intracranial pressure at the time

of Lance’s autopsy in May 2010. He also agreed that Lance had increased

intracranial pressure “at some point” in his life and that it was possible that his

ventricles had enlarged and then remained the same size ever since he had had

encephalitis as a child. Dr. Parrish acknowledged that, while Lance had some

“classic symptoms” of increased intracranial pressure when he was seen by Dr.

Kareh, such as slurred speech, confusion, and balance problems, he did not have

29
other classic symptoms, such as widened pulse pressure, low heart rate,

papilledema, nausea, or vomiting. He further agreed that the symptoms with which

Lance presented to NCMC were consistent with other conditions and that Lance

“got better really fast” while in the hospital. Dr. Parrish opined that Lance’s

symptoms could have been relieved because he “had enough [intraventricular]

pressure that he opened up the aqueduct, and he started draining [cerebrospinal

fluid] again” without a shunt.

Dr. Parrish did not provide any support for his opinion that the standard of

care required the immediate placement of a shunt “every time” when a patient

presents with a few “classic symptoms” of increased intracranial pressure and

exhibits enlarged ventricles and a narrowed aqueduct in an MRI scan beyond his

own testimony. He did not provide any support for his opinion that the standard of

care in this case required immediate placement of a shunt on February 4, 2010, as

opposed to following a more conservative course of treatment that tracked the

progression of the frequency and severity of the neurological symptoms Lance had

displayed.

Dr. Kareh saw Lance one other time after his initial presentment to

NCMC—on February 22, 2010—and Lance reported at that appointment that he

had had one headache episode and one episode of slurred speech. Dr. Kareh did

not see Lance after that. Rather, Lance returned to Dr. Gill, and another MRI was

30
ordered. The April 2010 MRI revealed changes both in the size of Lance’s

ventricles and in the angle of the aqueduct relative to the February 2010 MRI. It is

undisputed that no one informed Dr. Kareh of the headaches that Lance

experienced in April 2010 or of the April MRI scan. Windrum’s experts concurred

that Lance’s sudden death was due to a complete obstruction of the aqueduct. All

of the experts agreed, however, that, when Dr. Kareh saw Lance in February, the

aqueduct, although narrowed, was open and cerebrospinal fluid was passing

through the aqueduct. Although the April MRI revealed a worsening problem, no

evidence showed that Dr. Kareh was advised of the results of that MRI.

Dr. Parrish did not point to any medical literature, such as peer-reviewed

studies or authoritative treatises or texts, which stated that the immediate

placement of a shunt is required even when monitoring of intracranial pressure

reveals no sustained increase in pressure and when the patient’s symptoms have

subsided. And, although Dr. Kareh presented evidence that shunt placement is not

appropriate when intracranial pressure levels are within normal range and pressure

monitoring does not reflect a sustained increase in pressure, Windrum presented no

evidence other than Dr. Parrish’s testimony that shunt placement is necessary

“every time.” Thus, there was no evidence other than Dr. Parrish’s unsupported

opinion testimony to establish that the standard of care always requires placement

of a shunt under the circumstances presented to Dr. Kareh on February 4, 2010.

31
See Coastal Transp. Co., 136 S.W.3d at 232 (providing that opinion testimony that

is conclusory or speculative is not relevant evidence and cannot support judgment);

Burrow, 997 S.W.2d at 235.

Moreover, although Dr. Parrish testified that shunt-placement surgery has its

risks, as is true of all surgeries, and that he considered the risks in this case to be

“fairly low,” neither Dr. Parrish nor any of Windrum’s other witnesses addressed

the risks that Dr. Neely testified to concerning placement of a shunt in a patient

who at the time of placement does not have increased intracranial pressure. See

Ponte v. Bustamante, — S.W.3d —, No. 05-12-01394-CV, 2015 WL 3485422, at

*7 (Tex. App.—Dallas May 28, 2015, pet. filed) (“When the evidence shows that a

particular treatment helps some patients and not others, the expert must explain the

facts justifying a conclusion that a particular patient probably would have been

helped by the treatment.”). Such evidence is particularly critical when the alleged

negligence is the failure to perform an operation as opposed to negligence in

actually performing it.

Windrum argues that all of the testifying physicians agreed that the standard

of care required either a shunt or a “third ventriculostomy,” and she points to the

testimony of Dr. Gill, the treating neurologist in this case, and Dr. Evans, a

neurologist who had been retained by Dr. Gill. Dr. Gill agreed with Windrum’s

counsel that “the applicable standard of care is that the treatment for obstructive

32
hydrocephalus is either a shunt or a third ventriculostomy.” He also testified,

however, that he agreed with Dr. Kareh’s suggestion that a shunt was not necessary

in this case; that, if he had not agreed, he would have “done something,” such as

refer Lance to another neurosurgeon; and that he agreed with the decision to

discharge Lance without surgical intervention because Lance did not demonstrate a

sustained increase in intracranial pressure, his headaches had improved, and he

“was feeling better.” Dr. Evans agreed that for most patients, unless they have a

“specific physical impairment like age or a heart condition,” “surgical intervention

is going to be the appropriate thing to do,” although he acknowledged there are

risks associated with shunt surgery.

Neither Dr. Gill nor Dr. Evans testified concerning the specific risks of

placing a shunt when the patient does not have increased intracranial pressure. Dr.

Kareh also presented evidence that shunt placement was not appropriate in this

case due to the monitoring results, which indicated that Lance was not suffering

from increased intracranial pressure at the time Dr. Kareh was consulting on his

case. Windrum presented no evidence to refute this testimony, aside from Dr.

Parrish’s unsupported opinions that shunt placement is required “every time” a

patient presents with some of the “classic symptoms” of increased intracranial

pressure and an MRI scan reveals enlarged ventricles. See Mendez, 204 S.W.3d at

804 (stating that, in conducting no-evidence review involving expert testimony,

33
courts “cannot consider only an expert’s bare opinion, but must also consider

contrary evidence showing it has no scientific basis”). Dr. Parrish’s opinion fails

to account for Lance’s worsening symptoms and test results two months later,

which the jury heard evidence about but which Dr. Kareh did not have in February

when he treated Lance.

In sum, Windrum presented no evidence concerning the standard of care and

Dr. Kareh’s breach of the standard of care beyond Dr. Parrish’s conclusory and

unsupported testimony. See Coastal Transp. Co., 136 S.W.3d at 232 (“It is the

basis of the witness’s opinion, and not the witness’s qualifications or his bare

opinions alone, that can settle an issue as a matter of law; a claim will not stand or

fall on the mere ipse dixit of a credentialed witness.”); see also Mendez, 204

S.W.3d at 801 (“If the expert brings only his credentials and a subjective opinion,

his testimony is fundamentally unsupported and therefore of no assistance to the

jury.”). We therefore conclude that Windrum failed to present legally or factually

sufficient evidence of an essential element of her cause of action. See Creech, 411

S.W.3d at 5–6 (stating that essential element of medical malpractice cause of

action is breach of legal duty and that standard of care in medical malpractice suit

is what ordinarily prudent health care provider would do under same or similar

circumstances).

34
 2. Proximate Cause of Lance’s Death

We further conclude that, even if Dr. Kareh’s actions did fall below the

standard of care, Windrum failed to establish that Dr. Kareh’s actions proximately

caused Lance’s death. Thus, Windrum failed to prove the essential causation

element of negligence.

“Proximate cause” includes both cause in fact, meaning that “the act or

omission was a substantial factor in bringing about the injuries, and without it, the

harm would not have occurred,” and foreseeability. IHS Cedars Treatment Ctr. of

DeSoto, Tex., Inc. v. Mason, 143 S.W.3d 794, 798–99 (Tex. 2004); Tejada v.

Gernale, 363 S.W.3d 699, 709 (Tex. App.—Houston [1st Dist.] 2011, no pet.)

(noting that evidence showing only that defendant’s negligence furnished condition

that made injuries possible is insufficient to show proximate cause and that

proximate cause cannot be established by “mere conjecture, guess, or

speculation”). Cause in fact is not established where a defendant’s actions do no

more than furnish a condition which makes the injuries possible. Givens v. M&S

Imaging Partners, L.P., 200 S.W.3d 735, 738 (Tex. App.—Texarkana 2006, no

pet.). In such a case, the defendant’s conduct is too attenuated from the resulting

injuries to be a substantial factor in bringing about the harm. Id.; see also

Providence Health Ctr. v. Dowell, 262 S.W.3d 324, 328–29 (Tex. 2008) (holding

that discharge of patient from emergency room, when patient had presented to

35
emergency room with self-inflicted cut on wrist and then committed suicide thirty-

three hours after discharge, “was simply too remote from his death in terms of time

and circumstances” and, thus, plaintiffs presented insufficient evidence of

proximate cause). “Foreseeability means the actor, as a person of ordinary

intelligence, should have anticipated the dangers his negligent act created for

others,” but it does not “require a person to anticipate the precise manner in which

injury will occur once the person creates a dangerous situation through his

negligence.” Taylor v. Carley, 158 S.W.3d 1, 9 (Tex. App.—Houston [14th Dist.]

2004, pet. denied).

Dr. Parrish agreed with defense counsel that the April MRI revealed that

Lance’s symptoms were progressing and that Lance could have survived “if he’d

had a shunt done the day before he died,” indicating that any failure by Dr. Kareh

to place a shunt when he saw Lance in February 2010 was not an immediate cause

of death. All of the doctors who testified in this case, including Dr. Kareh’s

experts, agreed that placement of a shunt can be an appropriate treatment for a

patient presenting with obstructive hydrocephalus caused by aqueductal stenosis

when there is a build-up of cerebrospinal fluid in the brain. There was no such

evidence of cerebrospinal fluid buildup in February 2010. Instead, Lance’s

intracranial pressure was normal, with occasional spikes in the pressure above a

normal range and no sustained increase in pressure. All of the neurological

36
symptoms with which Lance had presented to NCMC were resolved by the time

the period of intracranial pressure monitoring ended. When Lance saw Dr. Kareh

for a follow-up appointment almost three weeks later, he had had only one

additional headache episode and one additional episode of slurred speech. Lance

did not see Dr. Kareh again, and there is no evidence Dr. Kareh was ever informed

of the changes to Lance’s aqueduct visible on the April MRI or of the additional

headache episodes that he experienced in April. We conclude that, as a matter of

law, Dr. Kareh’s decision not to recommend placement of a shunt on February 4,

2010, was too remote from Lance’s death on May 2, 2010, to be a proximate cause

of Lance’s death. See Dowell, 262 S.W.3d at 328–29; Givens, 200 S.W.3d at 742.

We hold that because essential elements of Windrum’s medical malpractice

cause of action are not supported by legally sufficient evidence, the trial court

erred in entering judgment in favor of Windrum on that claim.

We sustain Dr. Kareh’s first and second issues.9

9
Because we hold that no evidence supports essential elements of Windrum’s cause
of action, we need not address Dr. Kareh’s remaining issues on appeal.

37
 Conclusion

We reverse the judgment of the trial court and render judgment that the trial

court enter a take-nothing judgment against Windrum on Windrum’s medical

malpractice claim.

Evelyn V. Keyes
Justice

Panel consists of Justices Keyes, Bland, and Massengale.

38