ALLEN BURKS, ET AL.
CYNTHIA ALLEN, ET AL.
Circuit Court for Baltimore City Case No. 24-C-15-003384
Deborah S., Wright, Berger, JJ.
Arthur, Kevin F., J., did not participate in the Court's
decision to report this opinion pursuant to Md. Rule 8-605.1.
Deborah S., J.
Circuit Court for Baltimore City, Cynthia Allen, individually
and as Personal Representative of the Estate of Dennis Allen
("the Estate"), and seven of her adult children,
appellees/cross-appellants,  brought medical malpractice
wrongful death and survival actions against Allen Burks,
M.D., and the University of Maryland Medical Systems
appellants/cross-appellees. The allegations arose out of Dr.
Burks's treatment of Mr. Allen in March 2013, when he was
an inpatient at the University of Maryland Medical Center
("UMMC"). Specifically, the Allens alleged that Dr.
Burks breached the standard of care by treating Mr.
Allen's elevated potassium levels with a formulation of
Kayexalate combined with 35.8 percent sorbitol and by
doing so without obtaining his informed consent; and that the
medication caused him to develop ischemic colitis and
ultimately to die. They alleged that UMMS was liable for Dr.
Burks's negligence under the doctrine of respondeat
Burks filed a pre-trial request for a Frye-Reed
hearing, arguing that the Allens's theory that Kayexalate
can cause ischemic colitis is not generally accepted in the
relevant medical community, and therefore their expert
witness testimony on that issue was not admissible. The
Allens opposed the request. The court held a hearing and
ruled that a Frye-Reed hearing was not required but,
even if it was and the court applied the Frye-Reed
test to the evidence provided in the motion and opposition,
the challenged evidence was admissible.
ten-day trial, the jury returned a verdict in favor of the
Allens, awarding $2, 000, 000 in non-economic damages to the
Estate, and $1, 000, 000 in non-economic damages to Mr.
Allen's wife and each of his seven children, for a total
of $10, 000, 000 in damages.
Burks filed a motion for new trial or, in the alternative,
for remittitur. The court did not grant a new trial but
granted a remittitur, reducing the non-economic damages award
to $906, 250 pursuant to the cap on non-economic damages in
Md. Code (1974, 2013 Repl. Vol.), section 3-2A-09 of the
Courts and Judicial Proceedings Article ("CJP").
Burks noted an appeal, presenting three questions, which we
have rephrased slightly:
I. Did the trial court abuse its discretion by denying his
motion for a pre-trial evidentiary Frye-Reed hearing
on the Allens's causation theory?
II. Did the trial court err by denying his motion to exclude
certain evidence on informed consent?
III. Did the trial court err by permitting the Allens to
introduce evidence about Dr. Burks's failure to order and
administer calcium gluconate or calcium chloride and his
failure to request a blood draw on the morning of March 18,
The Allens noted a cross-appeal, presenting one issue:
I. Does the cap on non-economic damages violate the equal
protection clause of the 14th Amendment and
Article 24 of the Maryland Declaration of Rights?
For the following reasons, we shall affirm the judgment of
the circuit court.
of March 2013
March 10, 2013, Dennis Allen, age 63, was transported by
ambulance to Northwest Hospital Center in Randallstown for
complaints of increasing "[w]eakness of the arms and
legs." He was suffering from hepatitis C, cirrhosis of
the liver, end stage liver disease, renal failure, and
congestive heart failure, and already had been hospitalized
twice in 2013-both times at UMMC-for a total of twenty-eight
days. Blood tests performed at Northwest Hospital Center
revealed that Mr. Allen also was suffering from acute
rhabdomyolysis, a condition in which muscle fibers break
down, releasing muscle proteins into the bloodstream.
Rhabdomyolysis causes muscle weakness and pain, can lead to
kidney failure if untreated, and can cause elevated potassium
levels, especially for patients with renal insufficiency.
Allen was transferred from Northwest Hospital Center to UMMC
the next day and was admitted to the intermediate care unit.
Dr. Burks was the attending physician assigned to him. His
primary admission diagnoses were rhabdomyolysis, chronic
kidney disease, and hepatitis C cirrhosis. Nephrology was
consulted and from March 13 through 16, 2013, Mr. Allen
underwent daily hemodialysis for his kidney failure. During
that time, his bloodwork showed that his rhabdomyolysis was
continuing to worsen. Mr. Allen did not receive dialysis on
March 17, 2013.
March 18, 2013, Dr. Burks arrived at UMMC sometime between 7
a.m. and 8 a.m. He had ordered routine laboratory tests for
Mr. Allen to be performed in the early morning hours, but the
results were not available.
after noon, Mr. Allen experienced a precipitous drop in heart
rate, setting off the heart monitor alarms. Dr. Burks ordered
an immediate EKG, which was performed at 12:18 p.m. It showed
bradycardia (an abnormally slow heart rhythm) and
life-threatening heart rhythms. Dr. Burks made a preliminary
diagnosis of hyperkalemia, i.e., an elevated level
of potassium in the blood. Hyperkalemia results when the
kidneys are not able to excrete potassium in the urine. A
potassium level over 5.5 mmol/L is
hyperkalemic. If left untreated, excess potassium can
interfere with the electrical signals in the heart, causing a
fatal cardiac arrhythmia.
12:25 p.m., Dr. Burks ordered a stat blood draw to evaluate
Mr. Allen's potassium level. Given the emergency nature
of the problem, he decided to begin the treatment protocol
for hyperkalemia while awaiting the lab results.
are three phases to the hyperkalemia treatment protocol:
stabilization, redistribution, and removal. The first phase
addresses the danger of a fatal arrhythmia by stabilizing the
heart muscle. Either calcium gluconate or calcium chloride is
administered intravenously for this purpose and works within
2 to 3 minutes. In the redistribution phase, potassium in the
blood stream is moved back into the cells to prevent it from
interfering with the heart rhythm. Insulin, which works
within 20 minutes, and sodium bicarbonate and albuterol,
which work within 30 minutes, are prescribed in combination
to achieve redistribution. Because insulin lowers blood
sugar, dextrose is administered to counteract that effect.
Insulin and dextrose are given intravenously; sodium
bicarbonate is given orally; and albuterol is given through a
third phase of the hyperkalemia treatment protocol is removal
of the excess potassium from the body. There are three
treatments by which potassium can be removed: diuretics,
which cause the potassium to be excreted in the urine;
hemodialysis, which removes the potassium directly from the
bloodstream; and sodium polystyrene sulfonate
("SPS"), usually referred to by its brand name,
Kayexalate,  which removes the potassium through the
stool. Diuretics are not an option for a patient in renal
failure, such as Mr. Allen. Dialysis begins to work within 30
minutes of being initiated and is very effective to remove
potassium from the body. The potassium stops being removed
when the dialysis is stopped, however.
approved by the FDA in 1958 to treat hyperkalemia, is an
"ion-exchange resin" medication, also known as a
"cation exchange resin." The resin contains sodium
ions that are exchanged for potassium ions in the bloodstream
in the colon. The potassium ions bind to the resin and then
are excreted in the stool. Because Kayexalate produces
constipation and sometimes fecal impaction, it usually is
given in combination with sorbitol, an osmotic laxative.
Osmotic laxatives increase the amount of water secreted into
the bowels, which softens the stool, making it easier to
pass. Kayexalate begins to work within 2 hours after it is
administered. It reaches peak effectiveness approximately 4
to 6 hours after being administered and can continue to work
for up to 24 hours. It can be administered either in an oral
suspension formula or by enema.
12:37 p.m., Dr. Burks used a UMMC electronic order set for
hyperkalemia to order calcium gluconate stat, insulin stat,
dextrose stat, sodium bicarbonate stat, and
Kayexalate. At 12:54 p.m., he ordered albuterol. At
some time between 12:18 p.m. and 1:00 p.m., he also ordered a
stat nephrology consult so hemodialysis could be started.
Burks was advised by a UMMC pharmacist that calcium gluconate
was not available due to a nationwide shortage. As we shall
discuss, there was conflicting evidence at trial as to
whether Dr. Burks gave an oral order to substitute calcium
chloride for calcium gluconate. In any event, neither drug
was administered. It is undisputed that the failure to
administer those drugs did not cause any injury to Mr. Allen.
12:55 p.m., and continuing for 10 to 15 minutes, Mr. Allen
received albuterol via a nebulizer. At 1:09 p.m., insulin and
dextrose were administered intravenously. At 1:15 p.m., Mr.
Allen was given sodium bicarbonate and 30 milligrams of
Kayexalate orally. The Kayexalate was in a suspension
solution containing 35.8 percent sorbitol. Dr. Burks did not
inform Mr. Allen about the risks and benefits of Kayexalate
prior to its being administered.
p.m., Mr. Allen's lab results were returned, revealing
that his blood-potassium level was 7.3 mmol/L. That confirmed
the diagnosis of hyperkalemia. A blood potassium level of 7.3
mmol/L is considered dangerously high and can quickly lead to
a fatal arrhythmia. At 1:30 p.m., a nephrologist assessed Mr.
Allen and ordered hemodialysis on a stat basis. Dialysis
began at 2:45 p.m. and was completed at 5:45 p.m. Mr. Allen
had two bowel movements during dialysis. After dialysis, Mr.
Allen's potassium level was 4.5 mmol/L, which is within
the normal range.
Burks left for the day around 8:00 p.m. Overnight, Mr. Allen
had seven more bowel movements, several of them bloody, and
began experiencing extreme abdominal pain. He told Cynthia he
felt like he was "burning up inside."
a.m., on March 19, 2013, Mr. Allen's lab results showed
that his potassium levels were slightly elevated again, at
5.7 mmol/L. At 6:12 a.m., the physician assigned to Mr. Allen
overnight wrote a note in his chart that he had had
"several episodes of stool mixed with blood
overnight." When Dr. Burks returned to UMMC around 7
a.m., he learned that Mr. Allen was experiencing
"copious bloody bowel movements." Over the course
of that morning, Mr. Allen's blood pressure dropped
precipitously and could not be raised with fluid boluses.
noon, Mr. Allen was transferred to the intensive care unit
("ICU") to be prepped for exploratory surgery. Dr.
Burks met with Cynthia and some of the Allen children.
According to the family members, Dr. Burks told them he had
"made a mistake" and was sorry. He said he had
given Mr. Allen a drug that damaged his intestines, but that
Mr. Allen was going to have surgery to correct it and
everything would be all right. He estimated that the surgery
would take 45 minutes to 2 hours.
Mr. Allen was transferred to the ICU, Dr. Burks wrote a
"discharge summary." In it, he noted that Mr.
Allen's "differential diagnosis" included
"intestinal ischemia due to hepatitis C related
vasculitis versus intestinal ischemia due to concomitant
Kayexalate and lactulose use versus hepatic decompensation
with coagulopathy and lower GI bleed." In other words,
Dr. Burks listed Kayexalate use in the face of laxative use
as a possible cause of Mr. Allen's intestinal ischemia,
if that was what Mr. Allen was experiencing.
Allen's surgery lasted over six hours and confirmed the
diagnosis of ischemic colitis. The exterior of his small
intestine and colon (large intestine) appeared normal and
there was a "palpable pulse" in the superior
mesenteric artery, the largest artery supplying blood to the
bowels. A colonoscopy performed during the surgery revealed
"multiple areas of mucosal ischemia with ulceration and
bleeding," however. The severe ischemic ulceration
necessitated removal of almost all of Mr. Allen's colon.
In his operative note, surgeon Ronald Tesoriero, M.D., wrote:
[During the colonoscopy, ] [w]e were able to advance the
scope to the level of the transverse colon. There were
multiple areas of mucosal ischemia with ulceration and
bleeding in the colon. We were unable to pass beyond the
transverse colon; however, it was clear at this point
that the patient had significant mucosal level ischemic
colitis. Given the overall state of the patient's
perfusion, this may have likely been induced by the
Allen never regained consciousness. He died the next day,
March 20, 2013. His death certificate records the cause of
death as "ischemic colitis." On autopsy, his cause
of death was determined to be "[m]ultiple complications
in the setting of hepatitis C/cirrhosis." In the
"Discussion" section, pathologist Rupal I. Mehta,
Ischemic necrosis [was] seen within [Mr. Allen's]
residual small intestine, with scattered basophilic crystals,
consistent with recent [K]ayexalate use. The findings may
be suggestive of [K]ayexalate colitis, which could have
exacerbated the patient's underlying medical
(Emphasis added.) Because Mr. Allen's colon had been
removed during surgery, it was not a part of the autopsy. Dr.
Mehta noted, however, that the "[p]rior colectomy
specimen showed extensive bowel necrosis and
by the Allens
25, 2015, the Allens filed suit against Dr. Burks and UMMS.
Trial was scheduled to commence on September 7, 2016. On July
21, 2016, Dr. Burks filed a request for a Frye-Reed
hearing, which was opposed. On the first day of trial, the
court held a hearing and denied the request. We shall discuss
that hearing and the court's ruling in detail below.
their case-in-chief, the Allens called three expert
witnesses: Richard Goldstein, M.D., a colorectal surgeon;
James D. Leo, M.D., an internist; and Robert T. Odze, M.D., a
pathologist. They also called thirteen fact witnesses: Siu
Yan Amy Yeung, a clinical pharmacy specialist at UMMC; John
Ashworth, III, the corporate designee for UMMS; Dr. Burks;
Demetrius Jones, a phlebotomist at UMMC; Cynthia Allen; and
all the Allen children. We summarize the pertinent testimony.
Yeung testified that in 2012 she served on the three-member
UMMC team of pharmacists that developed internal guidelines
for the treatment of hyperkalemia ("the UMMC
Guidelines"). The UMMC Guidelines were reviewed by
physicians in the nephrology department, the UMMC pharmacy
committee, and the UMMC therapeutic committee. Upon approval,
they were added to UMMC's internal computer database,
which is accessible to doctors and nurses.
UMMC Guidelines, entitled "Management of
Hyperkalemia," contain a table listing each
"Agent" used to manage hyperkalemia; the dose; the
mechanism; how to administer it; how quickly it works; how
long it works; how its effectiveness is monitored; and any
"Comments" about the use of the agent. The table
lists all the drugs and treatments we have discussed above,
including Kayexalate. The "Comments" column advises
that the "[m]ajor complications" of Kayexalate are
"intestinal necrosis and bowel perforation," and
warns that Kayexalate "[s]hould not be
used in patients with evidence of bowel obstruction, ileus or
ischemia or to renal transplant patients in the early post
operative phase." (Emphasis in original.) Ms. Yeung
testified that these comments were included based on medical
literature she had reviewed that reported the risk of
intestinal necrosis and bowel perforation from Kayexalate to
be between 0.27 percent and 1.8 percent. In a flow chart for
the management of hyperkalemia that appears in the UMMC
Guidelines, Kayexalate is listed as the third agent to be
used to treat acute severe hyperkalemia, after the
stabilization and redistribution agents have been
administered and before hemodialysis. According to Ms. Yeung,
the only preparation of Kayexalate available for use at UMMC
was the oral suspension in 35.8 percent sorbitol that Mr.
Goldstein explained that the submucosal layer of the colon,
which is beneath the lining of the colon (the mucosa), is
filled with thin-walled blood vessels that absorb most of the
water in the digestive fluid flowing into the colon from the
small intestine, leaving solid stool. The celiac, superior
mesenteric, and inferior mesenteric arteries supply blood to
these vessels and to the small intestine, liver, appendix,
and other organs. Compromised blood flow, i.e.,
ischemia, to the submucosal vessels cuts off the oxygen
supply to the lining of the colon. That causes the tissue in
the mucosal layer to break down, ulcers to form, and bacteria
from the colon to enter the bloodstream, further breaking
down the surrounding tissue. The loss of blood flow and the
spread of bacteria throughout the submucosal layer of the
colon causes necrosis, i.e., tissue death. As the
volume of bacteria in the bloodstream increases, the body
attempts to fight off the infection, causing the blood
pressure to fall.
Goldstein opined that Mr. Allen died from intestinal necrosis
caused by Kayexalate. In his view, the Kayexalate
"cause[d] the blood vessels . . . under the lining of
the colon [to] stop working." He could not say "how
[K]ayexalate damages the lining of the intestine and produces
intestinal ischemia," only that it has been
"observed over and over and over again with the use of
[K]ayexalate." Dr. Goldstein was questioned about the
defense theory that Mr. Allen's necrosis-producing
ischemic colitis was caused by several periods of generalized
decreased blood flow to the colon due to low blood pressure
during dialysis. He rejected that theory, explaining that the
colon can sustain a 75 percent reduction in blood flow for up
to 12 hours "without irreversible injury," and that
the "very brief periods" of low blood pressure
documented in Mr. Allen's chart would not have been
sufficient to cause his severe necrosis. Moreover, Dr.
Tesoriero's observation during surgery of a strong pulse
and no clots in the superior mesenteric artery was
inconsistent with generalized low blood flow having caused
Mr. Allen's injury. Dr. Goldstein noted that other organs
supplied by the same arteries-such as the appendix and the
liver-were not necrotic, which was strong evidence of no
general compromise of blood flow.
cross-examination, Dr. Goldstein acknowledged that there are
"multiple causes of ischemic colitis" and that
"99 out of 100 times when a patient has ischemic colitis
it's idiopathic[, ]" meaning the cause is unknown.
In reaching his opinion that Kayexalate caused Mr.
Allen's ischemic colitis, Dr. Goldstein relied upon the
medical literature, the UMMC Guidelines, Dr. Burks's
differential diagnosis in his discharge note, and Dr.
Tesoriero's observations in his operative note. He also
relied upon the "sequence of events," explaining
that, until Mr. Allen was given Kayexalate, he did not have
abdominal pain, diarrhea, or bloody stools. He viewed the
timing of the onset of Mr. Allen's symptoms of ischemic
colitis and the administration of Kayexalate as evidence of a
causal link. Finally, Dr. Goldstein opined that although Mr.
Allen was chronically ill none of his other health conditions
was "imminently about to kill [him]."
Leo, an expert in emergency medicine, internal medicine, and
critical care medicine, testified that the standard of care
for treating Mr. Allen's acute hyperkalemia was to
stabilize his heart immediately with calcium gluconate or
calcium chloride; redistribute the potassium from his
bloodstream into his cells by administering insulin (with
dextrose), albuterol, and sodium carbonate; and remove the
potassium by hemodialysis ordered urgently. Because Mr. Allen
already had a catheter for dialysis in place and was being
treated by UMMC's nephrology team, there was no risk of
delay in starting dialysis; and, in fact, dialysis was
started just over an hour after the nephrology consult. Dr.
Leo opined that given the availability and superior
effectiveness of dialysis Kayexalate was unnecessary, and
therefore its use was not in accordance with the standard of
care. According to Dr. Leo, the "infrequent" but
very serious risk of ischemic colitis from Kayexalate was not
outweighed by any potential benefit from its use, given that
dialysis was available and more effective.
also testified that Dr. Burks breached the standard of care
by not obtaining Mr. Allen's informed consent before
giving him Kayexalate. After the stabilization and
redistribution drugs had been administered, which resolved
the emergency, Dr. Burks should have informed Mr. Allen that
Kayexalate works more slowly and less effectively than
dialysis and that it has a "very infrequent but very
dangerous side effect that it can cause [a] condition called
ischemic colitis in which the large intestine can basically
die because of loss of blood flow." Dr. Leo further
opined that the Kayexalate caused Mr. Allen's ischemic
colitis and death. Mr. Allen had lived with his chronic
medical conditions for some time, but never had
"manifested evidence of ischemic colitis." "He
did not have any other reasonable causes for ischemic colitis
to occur during [the March 2013] hospital admission."
Like Dr. Goldstein, Dr. Leo rejected the defense theory that
episodes of low blood pressure caused Mr. Allen's
ischemic colitis, opining that those episodes were "too
short a duration, too mild in degree and too far in time
prior to the development of the ischemic colitis for those to
have been connected."
Odze, an expert in pathology with a subspecialty in
gastrointestinal and liver pathology, testified, based upon a
review of Mr. Allen's pathology slides and medical
records, that Mr. Allen's ischemic colitis and death were
caused by Kayexalate or Kayexalate and sorbitol in
combination. He explained that the "mechanism [of the
bowel injury caused by Kayexalate and sorbitol] is poorly
understood[, b]ut the consequence is very well
understood." One theory is that sorbitol, a hyperosmotic
agent, draws water out of the bloodstream and into the stool
to counteract the constipating effects of Kayexalate and, in
doing so, deprives the bowel tissue of oxygen. Dr. Odze did
not "find any evidence in this case . . . that there was
any other cause of ischemia in Mr. Allen's colon other
than the ischemia caused by the Kayexalate." The
"features in the tissue" showed an "acute
injury" and there was no "lack of blood flow"
from outside the colon that contributed to or caused the
ischemia. Had there been a generalized lack of blood flow,
one would expect to see "widespread ischemic
injury," including to the small intestine and appendix,
which are more susceptible to ischemic injury than the colon
is. The "pattern of destruction" in Mr. Allen's
case was "inconsistent" with "an overall lack
of blood flow." In the prior 25 years, Dr. Odze had
conducted pathology reviews in "more than a dozen
cases" in which a patient had "ingested Kayexalate
Sorbitol mixture and then died." He saw Mr. Allen's
case as a "classic example of Kayexalate induced
ischemic necrosis of the bowel."
cross-examination, in response to a series of questions about
his understanding of the "mechanism" of injury
caused by Kayexalate, Dr. Odze stated that it is not uncommon
in medicine for the mechanism of a disease or condition to be
poorly understood but for the "cause and effect" to
be well understood. He opined that among gastrointestinal
specialists, the causal connection between Kayexalate and
ischemic colitis is well known. To the extent the defense
experts would opine that there was insufficient evidence of a
causal relationship, they were "[u]ninformed and
Burks (called adversely) testified that when he treated Mr.
Allen for hyperkalemia he was unaware of any reported
association between Kayexalate with sorbitol and ischemic
colitis. Ordinarily, he did not review UMMC Guidelines when
considering treatment options for patients. Rather, he used
"Up to Date," a peer-reviewed subscription website
for physicians. Although an article about hyperkalemia on
that website included information about the association
between Kayexalate and ischemic colitis, it was not
"something that [Dr. Burks] paid particular attention
to." Dr. Burks could not "disagree with [the]
statement [in the UMMC Guidelines that a major complication
of Kayexalate use is intestinal necrosis and bowel
perforation] at this point[.]" In his view, it did not
matter that he was unaware of the rare risk of ischemic
colitis from Kayexalate use because that would not have
changed the course of treatment. Even if he had known that
dialysis could be started in 10 minutes, he still would have
ordered Kayexalate, because Kayexalate continues to remove
potassium from the bloodstream for up to 24 hours, whereas
dialysis only works during the several hours in which it is
being administered. After dialysis ends, the potassium levels
can immediately begin to rise again.
Burks further testified that he discussed Mr. Allen's
hyperkalemia with Mr. Allen and his wife after the cardiac
event but before Kayexalate was administered. He did not
discuss any risks of Kayexalate with Mr. Allen and did not
offer him the option to have dialysis only, instead of in
conjunction with Kayexalate. After Mr. Allen was transferred
to the ICU, he met with members of the Allen family. He
advised them that Mr. Allen had "developed injury to
[his] intestines" and gave them an "incomplete list
of possible reasons . . . [including] . . . Kayexalate."
As of the time of trial, Dr. Burks's view remained that
Kayexalate was a "possible but unlikely" cause of
Mr. Allen's ischemic colitis.
cross-examination, Dr. Burks elaborated that treating
hyperkalemia with Kayexalate in conjunction with dialysis
satisfied the standard of care. In his opinion, Mr.
Allen's elevated potassium levels were caused by
rhabdomyolysis, an ongoing condition that warranted a
multi-faceted approach to removing the excess potassium from
his body. Dr. Burks emphasized that even with the Kayexalate
and dialysis Mr. Allen's potassium levels rose to 5.7
mmol/L (above normal) by 3:00 a.m. on March 19, 2013. Because
of the emergency nature of Mr. Allen's condition, Dr.
Burks did not think he was required to obtain Mr. Allen's
testified that she was present when Dr. Burks spoke to the
Allen family. He told them that the surgery would last about
2 hours. Cynthia testified that she stayed with Mr. Allen
overnight. She informed the nursing staff when she began
observing blood in her husband's stool. He was screaming
and crying in pain. Dennis, Jr., Daniel, and Sarah also were
present in the hospital on the evening of March 18, 2013, and
the next morning. They testified that they remembered their
father being in severe pain and passing numerous bloody
March 19, 2013, Dennis, Jr., was in the waiting area when Dr.
Burks came to speak to him and some of his siblings. Dr.
Burks told them that he had "administered some medicine
to [Mr. Allen] that began to attack his bowels," but if
it was "caught early enough . . . he would be
fine." He told them Mr. Allen would be having
"routine surgery" lasting between "one to two
close of the Allens' case, counsel for Dr. Burks moved
for judgment. He argued with respect to all the claims that
although the Allens had presented evidence that Kayexalate
had caused Mr. Allen's ischemic colitis they had failed
to present any evidence that he would have survived if the
drug had not been given to him. With respect to the informed
consent claim, he argued that the Allens had failed to
present any evidence that Mr. Allen would have declined to
take Kayexalate had Dr. Burks advised him of the risk of
ischemic colitis, and that the evidence showed that the
emergency exception to the informed consent doctrine applied.
The court denied the motion.
case, Dr. Burks called four expert witnesses: David Kaplan,
M.D., an internist specializing in gastrointestinal and liver
disease; Michael Schweitzer, M.D., a general surgeon; Michael
Seneff, M.D., a critical care doctor; and Philip Buescher,
M.D., an internist and critical care doctor.
Kaplan, an expert in internal medicine, gastroenterology, and
hepatology, including liver diseases and liver transplant
medicine, opined that Dr. Burks complied with the standard of
care for the treatment of severe hyperkalemia, which is to
give Kayexalate and to begin dialysis as soon as
possible. According to Dr. Kaplan, Kayexalate is a "safe
medication" that is "highly effective at removing
potassium from the body." Dr. Burks was not required to
obtain Mr. Allen's informed consent before administering
Kayexalate as this was a cardiac emergency and there was no
significant risk associated with the drug. In Dr.
Kaplan's view, the medical literature does not support
the premise that Kayexalate causes ischemic colitis and, to
the extent it does, the risk is so small that it is not
material. It would have been a breach of the standard of care
for Dr. Burks to have delayed giving Mr. Allen Kayexalate to
obtain informed consent.
Kaplan opined that Mr. Allen developed ischemic colitis from
"multiple insults to the bowel" caused by repeated
episodes of low blood pressure combined with his
"overall clinical condition." He pointed to
documented episodes of very low blood pressure during
dialysis on March 13 and March 15, 2013, and noted that Mr.
Allen may have experienced other episodes of low blood
pressure that were not reflected in his chart because he was
not on a continuous blood pressure monitor. Dr. Kaplan
testified that low blood pressure is "[t]he most common
cause of ischemic colitis" and that low blood pressure
lasting as little as 15 minutes can "lead to an episode
of ischemic colitis . . . within 24, 48, even 72 hours
[later.]" "Repeated bouts of low blood pressure can
cause vasospasm meaning spasm of the small blood vessels that
feed the colon and that spasm if it continues causes the . .
. mucosa . . . to not have enough blood flow and the cells
die . . . ." Mr. Allen's cirrhotic liver also could
have been a contributing factor. The colon "drain[s]
into the liver," so when the liver is "under high
pressure that drainage from the colon is also under high
pressure . . . [making the colon more sensitive] to changes
in blood pressure." In Dr. Kaplan's opinion, there
was not "sufficient evidence to claim that [K]ayexalate
caused the injury" to Mr. Allen's colon. Mr. Allen
was "predispose[d]" to ischemic colitis and the
medical literature did not "substantiate" a
causal relationship between Kayexalate and ischemic colitis.
Moreover, Mr. Allen's medical prognosis at the time of
his March 11, 2013 admission to UMMC was grim. His likelihood
of dying within 90 days was 85 percent.
cross-examination, Dr. Kaplan was asked whether he would have
expected to see ischemic injury to the appendix if the cause
was a vasospasm occasioned by generalized low blood pressure.
He replied, "[n]ot necessarily," elaborating that
vasospasm often affects the small blood vessels in a
"patchy" way and that it would not be
"surprising" to see a patient with ischemic colitis
and a normal appendix.
Schweitzer, an expert in "general surgery including the
care and treatment of ischemic colitis and multiple
comorbidities that affect a patient's prognosis[, ]"
testified about causation. He had performed between 50 and
100 bowel surgeries for ischemic colitis. He opined that
there are many known causes of ischemic colitis, including
scar tissue, vascular problems causing clotting in the
arteries that supply the colon, episodes of very low blood
pressure during dialysis, and certain medications, such as
estrogen and diuretics. In his opinion, Mr. Allen's
ischemic colitis was caused by "end stage liver disease,
renal failure, rhabdomyolysis, [and] congestive heart
failure[.]" Dr. Schweitzer explained that with liver
failure the pressure in the abdominal veins increases,
causing blood to be "shunted to other areas and [not to]
go through the organs like the small and large bowel very
well." Mr. Allen's rhabdomyolysis could have
contributed because the inflammation and pain associated with
that condition can cause small blood vessels to constrict.
Similarly, congestive heart failure can restrict blood flow.
Dr. Schweitzer agreed with Dr. Kaplan that episodes of
hypotension during dialysis could have been a contributing
Schweitzer further opined that Kayexalate was not a
cause of Mr. Allen's ischemic colitis. The medical
literature establishes a "very rare association, not
necessarily a cause" between "[K]ayexalate with
high sorbitol" and ischemic colitis. The cases where
such an association has been seen were in patients whose
"bowels aren't moving[.]" It is for that reason
that Kayexalate is not recommended for patients who are
post-operative or otherwise are experiencing constipation.
Mr. Allen was not postoperative, did not have constipation,
and did not have a bowel obstruction. Dr. Schweitzer
testified that he had treated five to ten patients who, like
Mr. Allen, were not experiencing constipation (post-operative
or otherwise) or an obstruction but were in renal failure,
developed hyperkalemia, were treated with Kayexalate, and
developed ischemic colitis. In his view, those patients did
not develop ischemic colitis from Kayexalate.
Schweitzer testified that Mr. Allen was not going to survive
his hospitalization under any circumstance. His
rhabdomyolysis was worsening, he had end stage liver disease,
and he was in stage four renal failure. In Dr.
Schweitzer's view, Mr. Allen did not "have ...