BURKS, ET AL. v. ALLEN, ET AL., No. 2361, September 2016 Term

EXPERT TESTIMONY – GENERAL CAUSATION – FRYE-REED TEST –

EVIDENTIARY HEARING – GENERAL ACCEPTANCE IN MEDICAL 

COMMUNITY.

Decedent was admitted to University of Maryland Medical Center (UMMC) with 

multi-system diagnoses, including renal and liver failure. When he experienced an 

episode of bradycardia, Dr. Burks treated him for presumed hyperkalemia, which was 

later confirmed. The treatment included Kayexalate given in a suspension with sorbitol 

and hemodialysis. Shortly thereafter decedent developed ischemic colitis which quickly 

progressed to necrosis of the colon. Surgical intervention failed and decedent died. 

Survival and wrongful death actions were brought alleging medical malpractice. The

plaintiffs’ expert witnesses theorized that the decedent’s ischemic colitis was caused by 

the Kayexalate with sorbitol and opined that the standard of care required treatment with 

dialysis alone. Six weeks prior to trial, defense counsel filed a request for a Frye-Reed

hearing, arguing that it was not generally accepted in the relevant medical community 

that Kayexalate with sorbitol, as given in this case, can cause ischemic colitis, and 

therefore plaintiffs’ experts should be precluded from testifying on causation. The 

plaintiffs filed an opposition and supplements were filed. The assignment office did not 

schedule a hearing. The request was addressed on the morning of trial, by the judge who 

had just been assigned the case. The judge held a hearing on whether a Frye-Reed

hearing should be held and ruled that the causation issue did not warrant a Frye-Reed

hearing and, alternatively, if Frye-Reed was implicated, the Frye-Reed general 

acceptance test was satisfied. The case went to trial and the jury returned a verdict for the 

plaintiffs. Dr. Burks and UMMC appealed.

Held: Judgment affirmed. Ordinarily, when the admissibility of proposed expert 

testimony is challenged under Frye-Reed, and Frye-Reed is implicated, an evidentiary 

hearing should be held to decide whether the testimony satisfies the Frye-Reed test. The 

Court of Special Appeals assumed without deciding that Frye-Reed applied to the 

proposed expert testimony and affirmed the trial court’s alternative ruling, made without 

holding an evidentiary hearing, that that testimony satisfied the Frye-Reed test. The 

materials submitted to the court in support of and opposition to the request for Frye-Reed

hearing comprehensively addressed the substance of the Frye-Reed issue. They included 

medical and scientific articles, FDA warning labels, UMMC Guidelines for Treatment of 

Hyperkalemia, medical records of the decedent, and deposition testimony of the relevant 

experts. The arguments made in the written submissions and to the court on the first day 

of trial focused not on whether a hearing was needed but on the substance of the FryeReed issue. In fact, practically nothing was said about what a Frye-Reed hearing would 

include that was not already before the court to consider. In that circumstance, with the 

trial about to commence, the court did not err or abuse its discretion by deciding the 

Frye-Reed issue without holding an evidentiary hearing. On the merits, the evidence 
before the trial court, in the request for Frye-Reed hearing and opposition, supported a 

legally correct conclusion that, although the causal connection between Kayexalate with 

sorbitol and ischemic colitis is not considered definitive, i.e., beyond question, 

Kayexalate with sorbitol is generally recognized by the relevant medical community as a 

cause of ischemic colitis in critically ill patients, such as the decedent. 
 REPORTED

IN THE COURT OF SPECIAL APPEALS

OF MARYLAND

No. 2361

September Term, 2016

______________________________________

ALLEN BURKS, ET AL.

v.

CYNTHIA ALLEN, ET AL.

____________________________________

Eyler, Deborah S.,

Wright,

Berger,

 

JJ.

______________________________________

Opinion by Eyler, Deborah S., J.

______________________________________

Filed: August 30, 2018

Arthur, Kevin F., J., did not participate in the 

Court’s decision to report this opinion pursuant 

to Md. Rule 8-605.1.

Circuit Court for Baltimore City

Case No. 24-C-15-003384
In the 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,

1 brought medical malpractice wrongful death 

and survival actions against Allen Burks, M.D., and the University of Maryland Medical 

Systems Corporation (“UMMS”), appellants/cross-appellees.2 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 Kayexalate3combined 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 superior. 

Dr. 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 

 

1 The adult children who are parties are Sara Allen, Ruth Allen, Dennis Allen, Jr., 

Daniel Allen, Sr., Donna Allen, Sherry Scipio, and Yolanda Allen. Cynthia’s oldest 

daughter, Shelly Allen-Rainey, originally also was a plaintiff. She is not Mr. Allen’s 

biological daughter. Mr. Allen treated Shelly as his daughter and she had her last name 

legally changed to reflect that she considered him her father. Shelly voluntarily dismissed

her claims with prejudice on April 8, 2016. For ease of discussion, we shall refer to 

Cynthia and her children by their first names and collectively as “the Allens” or “the 

Allen family.”

2 For ease of discussion, we shall refer to the appellants/cross-appellees 

collectively as “Dr. Burks,” except when necessary to distinguish between them. 

3 As we shall discuss, Kayexalate is the brand name for a drug that is now most 

often administered in its generic form. 
2

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. 

After a 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.

Dr. 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”).

Dr. 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 pretrial evidentiary Frye-Reed hearing on the Allens’s causation theory?4

II. Did the trial court err by denying his motion to exclude certain evidence 

on informed consent?

 

4 Dr. Burks’s first question presented also asks whether the court erred by not 

holding a hearing on admissibility of the Allens’s causation evidence under Rule 5-702. 

There was no request below that the court do so, however. 
3

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, 2013?

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.

FACTS AND PROCEEDINGS

Events of March 2013

On 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. 

Mr. 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 
4

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. 

On 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.5

Shortly 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.6If left untreated, excess potassium can interfere with the electrical signals 

in the heart, causing a fatal cardiac arrhythmia. 

 At 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.

 

5 As we shall discuss, Dr. Burks’s failure to follow up on the absence of laboratory 

test results was a subject of some testimony and evidence at trial.

 

6 Some witnesses testified that a potassium level over 5.1 mmol/L was 

hyperkalemic.
5

There 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 

nebulizer. 

The 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,7 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 

 

7 Experts in the case at bar testified that although most physicians prescribe SPS in 

its generic form it is generally known as Kayexalate. For that reason, we shall use the 

brand name. 
6

very effective to remove potassium from the body. The potassium stops being removed

when the dialysis is stopped, however. 

Kayexalate, approved by the FDA in 1958 to treat hyperkalemia, is an “ionexchange 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. 

At 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.8 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.

Dr. 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 

 

8 Dr. Burks testified that although the order stated that Kayexalate was to be 

administered on a routine basis he made clear that it was to be administered stat and that 

in fact happened.
7

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.

At 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.

At 1:26 p.m., Mr. Allen’s lab results were returned, revealing that his bloodpotassium 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. 

Dr. 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.”

At 3:00 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 
8

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. 

Around 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. 

After 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.”9 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.

Mr. 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 

 

9 Lactulose is a laxative that was being given to Mr. Allen to treat hepatic 

encephalopathy, i.e., mental confusion caused by toxins in the colon entering the 

bloodstream due to liver failure. 
9

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 Kayexalate.[10]

(Emphasis added.)

Mr. 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, M.D., noted:

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 disease.

(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 hemorrhage.”

Lawsuit by the Allens

 

10 The operative note does not bear a dictation date. It was signed by Dr. 

Tesoriero on March 23, 2013.
10

On June 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. 

In 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.

Ms. 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. 

The 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” 
11

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. Allen received. 

Dr. 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 
12

volume of bacteria in the bloodstream increases, the body attempts to fight off the 

infection, causing the blood pressure to fall. 

Dr. 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. 

On 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 
13

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].”

Dr. 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.

Dr. Leo 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 
14

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.” 

Dr. 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” 
15

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.” 

On 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 incorrect.”

Dr. 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 peerreviewed subscription website for physicians. Although an article about hyperkalemia on 

that website included information about the association between Kayexalate and ischemic 
16

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. 

Dr. 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. 

On 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 
17

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 informed consent. 

Shelly 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 stools. 

On 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 hours.” 

At the 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 
18

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. 

In his 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.

Dr. 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. 

Dr. 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 
19

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.

On 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. 
20

Dr. 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 cause. 

Dr. 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. 
21

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. 

Dr. 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 the reserve[s] to overcome” all those serious medical conditions.

On cross-examination, Dr. Schweitzer was asked about the lack of injury to the 

appendix. He replied that because the appendix is tiny, it “doesn’t take much blood to fill 

[it],” whereas the colon requires much more blood flow. 

Dr. Seneff was accepted as an expert in critical care medicine, including the 

“diagnosis, care and treatment of . . . liver disease, liver cirrhosis, kidney disease 

requiring dialysis, rhabdomyolysis, . . . severe hyperkalemia [and other conditions].” 

He opined that giving Kayexalate in conjunction with dialysis, as Dr. Burks did, is within 

the standard of care for the treatment of severe hyperkalemia. It is Dr. Seneff’s practice 

to order Kayexalate for patients with severe hyperkalemia “even [while] in the process of 

getting dialysis.” He noted that the UMMC Guidelines direct that Kayexalate be 

administered before starting dialysis, i.e., that both are to be given. 

Dr. Seneff was aware of case reports showing an association between Kayexalate 

and ischemic colitis. He opined that the association is “very rare[,] . . . [o]ne in 100,000, 
22

maybe less than that.” It “primarily [was] reported with the 70 percent sorbitol solution,” 

which no longer is used. He opined that he would not give Kayexalate to a patient with a 

bowel obstruction but otherwise he “would never hesitate to give it.” For the same 

reasons, there was no obligation to obtain informed consent prior to administering 

Kayexalate.

In Dr. Seneff’s opinion, Mr. Allen’s ischemic colitis could not have been caused 

by Kayexalate because he “already had the ischemic colitis before the [K]ayexalate was 

administered[.]” This opinion was based upon Mr. Allen’s lab results from March 18, 

2013. His blood was drawn at 12:57 p.m., before the Kayexalate was given. According 

to Dr. Seneff, the laboratory results from that blood draw showed that, over the preceding 

30 hours, Mr. Allen’s bicarbonate levels had dropped from a normal level of 24 to an 

abnormal level of 11. That change resulted from Mr. Allen’s producing excess acid. 

Acid production rises when organs become ischemic. The change in Mr. Allen’s acid 

production was an “om[ino]us sign” that the ischemic colitis already had begun. Dr. 

Seneff opined that Dr. Burks would not have been able to determine prospectively from 

those lab results that Mr. Allen was ischemic, however, and, even if he had recognized 

the lab results as a sign of ischemia, there was no way to know where in Mr. Allen’s body 

the ischemia was occurring. Dr. Seneff agreed with Drs. Kaplan and Schweitzer that Mr. 

Allen’s ischemic colitis was caused by episodes of hypotension coupled with increased 

venous pressure in his intestines. 

Dr. Philip Buescher was accepted as an expert in internal medicine and critical 

care medicine, including, inter alia, the diagnosis and treatment of liver disease, kidney 
23

disease, and hyperkalemia, and the prescription of Kayexalate. He opined that Dr. Burks 

did not breach the standard of care by ordering Kayexalate for Mr. Allen, even if dialysis 

was immediately available, and that Dr. Burks was not required to obtain informed 

consent before administering it. Dr. Buescher testified that he had ordered Kayexalate 

for patients with acute hyperkalemia at least 900 times in his career and had “not seen a 

single case of ischemic colitis” among his patients. He agreed with Dr. Seneff that Mr. 

Allen’s ischemic colitis developed before the Kayexalate was administered to him, based 

upon his lab results showing low bicarbonate levels. He also agreed with Dr. Schweitzer 

that it was unlikely that Mr. Allen would have survived his hospitalization given his 

deteriorating condition overall. On cross-examination, Dr. Buescher acknowledged that 

he could not say whether the administration of Kayexalate to Mr. Allen accelerated and 

exacerbated the ischemic colitis that, in his view, already was developing. He reiterated, 

however, that Mr. Allen would have died during this hospitalization regardless of 

whether he had been given Kayexalate. 

In their rebuttal case, the Allens played the video deposition of Carla Williams, the 

assistant director of UMMC’s pharmacy clinical services. Her testimony, which we shall 

discuss in more detail, infra, was pertinent to the issue of the shortage of calcium 

gluconate.

At the close of all the evidence, Dr. Burks renewed his motion for judgment and 

the court denied it. 

On September 22, 2013, the case was sent to the jury on a special verdict. The

jury returned a verdict that same day. It found that Dr. Burks had breached the standard 
24

of care by treating Mr. Allen with “Kayexalate Sorbitol mixture”; that that breach was a 

cause of injury to Mr. Allen and was the cause of Mr. Allen’s death; that Dr. Burks had a 

duty to obtain informed consent before treating Mr. Allen with Kayexalate; that a 

“reasonably prudent person in [Mr.] Allen’s position would have withheld his consent” to 

that course of treatment had he been informed of the risks; and that the failure to obtain 

informed consent also was a cause of Mr. Allen’s injury and was the cause of his death. 

As noted previously, the jury awarded the Estate $2 million in non-economic 

damages and awarded Cynthia and Mr. Allen’s seven biological children $1 million each 

in non-economic damages; and the court later reduced the damages award in accordance 

with the statutory cap on non-economic damages. The reduced damages award totaled 

$906,250 and was apportioned as follows: $181,250 to the Estate and $90,625 to Cynthia 

and to each of the seven children plaintiffs.

This timely appeal followed.

DISCUSSION

APPEAL

I.

Frye-Reed

(a)

As mentioned, Kayexalate first was approved by the FDA in 1958 as a treatment 

for hyperkalemia. It was marketed in powder form. Shortly after it was introduced, 

physicians found that Kayexalate frequently caused severe constipation that could result 

in life threatening intestinal impaction. That problem could be avoided by mixing the 
25

powder with sorbitol. As a result, the FDA approved labeling for Kayexalate powder 

encouraging it to be administered with sorbitol. In 1982, a premade suspension of 

Kayexalate in 33-36 percent sorbitol was approved for distribution. The availability of 

the premade formulation contributed to an increase in the use of Kayexalate. Sometime 

thereafter, the FDA approved a premade suspension of Kayexalate in 70 percent sorbitol.

Some of the history that followed is recounted in a 2010 “Clinical Commentary” 

published in the Journal of the American Society of Nephrology by Richard Sterns, M.D.,

et al., titled Ion-Exchange Resins for the Treatment of Hyperkalemia: Are They Safe and 

Effective? (hereinafter Sterns). The Sterns commentary was cited by Dr. Burks in his 

motion for Frye-Reed hearing and by the Allens in their opposition. By 2005, the FDA 

had received 35 adverse event reports of serious bowel injuries following oral and rectal 

administration of Kayexalate in sorbitol. That year, the FDA removed the 

recommendation for concomitant use of sorbitol from the label for the powdered form of 

Kayexalate. In 2006, the largest manufacturer of the premixed oral suspensions met with 

the FDA and was permitted to continue manufacturing the 33-36 percent sorbitol and 

Kayexalate combination because, since 1982, it had not received any adverse reports of 

colonic necrosis with administration of that suspension; the only adverse reports 

concerned the 70 percent sorbitol suspension. In September 2007, the FDA asked all 

manufacturers of the 70 percent suspension to reformulate their products. The 70 percent 

suspension has not been manufactured since.

In 2009, the FDA issued a “black box” warning for Kayexalate powder, as 

follows:
26

Cases of colonic necrosis and other serious gastrointestinal adverse events 

(bleeding, ischemic colitis, perforation) have been reported in association 

with Kayexalate use. The majority of these cases reported the concomitant 

use of sorbitol. Risk factors for gastrointestinal adverse events were present 

in many of the cases including prematurity, history of intestinal disease or 

surgery, hypovolemia, and renal insufficiency and failure. Concomitant 

administration of sorbitol is not recommended.

According to Dr. Sterns, that same year, an article was published reporting 11 new 

cases of colonic necrosis over a nine-year period in a single clinical center, four of them 

fatal, several in patients without end stage renal disease, and some in patients with 

noncritical illnesses. Some of the fatalities were in patients given the Kayexalate oral 

suspension with 33-36 percent sorbitol. Dr. Sterns recommended: “Clinicians must 

weigh uncontrolled studies showing benefit against uncontrolled studies showing harm.

It would be wise to exhaust other alternatives for managing hyperkalemia before turning 

to these largely unproven and potentially harmful therapies.” Sterns, at 3. 

In 2011, the FDA revised its “black box” warning for powdered Kayexalate to 

state: 

WARNINGS

Colonic Necrosis

• Cases of intestinal necrosis, which may be fatal, and other serious 

gastrointestinal adverse events (bleeding, ischemic colitis, perforation) 

have been reported in association with Kayexalate use.

• Do not use in patients who do not have normal bowel function. This 

includes postoperative patients who have not had a bowel movement 

post surgery.

• Do not use in patients who are at risk for developing constipation or 

impaction (including those with a history of impaction, chronic 

constipation, inflammatory bowel disease, ischemic colitis, vascular 

intestinal atherosclerosis, previous bowel resection, or bowel 

obstruction).
27

• Discontinue use in patients who develop constipation. Do not administer 

repeated doses in patients who have not passed a bowel movement.

PRECAUTIONS

• Concomitant use of Sorbitol with Kayexalate has been implicated in 

cases of colonic intestinal necrosis, which may be fatal. 

(Bold in original.) (Italics added.)

In the case at bar, on July 21, 2016, Dr. Burks filed a request for a Frye-Reed

hearing, memorandum in support, and numerous exhibits. He sought to preclude the 

Allens from introducing their proposed expert medical causation testimony, which was 

based on the premise that Kayexalate can cause ischemic colitis. He argued that although 

it is generally accepted in the relevant medical community that Kayexalate, in 

combination with sorbitol, has been associated with a small number of cases of ischemic 

colitis it is not generally accepted that Kayexalate, sorbitol, or some combination of the 

two actually cause ischemic colitis. Rather, there is considerable controversy over that 

general causation question. Moreover, they asserted that most of the adverse events 

reported in the medical literature involve a different formulation of Kayexalate (powder 

versus liquid suspension), a different concentration of sorbitol (70 percent versus 33-36 

percent), and a different mode of administration (enema versus oral). Thus, even to the 

extent the medical literature supports a causal connection between that formulation of 

Kayexalate and ischemic colitis, that formulation was not used to treat Mr. Allen and 

therefore could not serve as the basis for the Allens’ medical experts to opine that the 

Kayexalate in sorbitol administered to Mr. Allen caused his ischemic colitis.
28

Dr. Burks’s exhibits included several articles and studies, the earliest of which was 

an experiment on rats published in 1987 in Surgery by Keith D. Lillemoe, M.D., et al., 

Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: Clinical 

and experimental support for the hypothesis (hereinafter Lillemoe). That study was 

performed after five patients suffered necrosis of the colon (four fatal) after receiving 

Kayexalate with sorbitol enemas. In the study, some of the rats were given Kayexalate 

with sorbitol, some were given sorbitol alone, and some were given Kayexalate alone. 

The mode of administration was enema for all of them. Seven out of ten of the rats who 

received sorbitol alone developed colonic necrosis, and six of the ten rats who received 

Kayexalate with sorbitol developed colonic necrosis. None of the rats who received 

Kayexalate alone developed colonic necrosis. 

Also appended were articles by Maura Watson, D.O., et al., in 2012, published in 

the American Journal of Kidney Disease, and Ziv Harel, M.D., et al., in 2013, published 

in the American Journal of Medicine. See Association of Prescription of Oral Sodium 

Polystyrene Sulfonate With Sorbitol in an Inpatient Setting With Colonic Necrosis: A 

Retrospective Cohort Study (hereinafter Watson); Gastrointestinal Adverse Events with 

Sodium Polystyrene Sulfonate (Kayexalate) Use: A Systematic Review (hereinafter 

Harel). 

Dr. Watson described colonic necrosis as a “rare but potentially fatal event” that 

has been reported after Kayexalate use, “most often in postoperative or intensive care 

settings and most frequently with rectal [Kayexalate]/sorbitol (particularly 70% sorbitol), 

rather than [Kayexalate] alone.” Watson, at 409. The estimated frequency among 
29

hospitalized patients is 0.27% in all cases occurring after surgery. Id. Because it is so 

rare, a very large population would be required to assess the risk factors and show an 

association between colonic necrosis and Kayexalate. Dr. Watson concluded that there is 

not enough evidence to show an association between colonic necrosis and exposure to 

Kayexalate. The precise mechanism of injury is unknown. She observed that use of 

Kayexalate may be associated with serious gastrointestinal adverse events, but a 

controlled trial is needed to make that determination.

Dr. Harel conducted a literature review to “identify eligible reports of adverse 

gastrointestinal events associated with [Kayexalate] use” and then applied the World 

Health Organization (“WHO”) causality assessment system to those reports to determine 

inclusion in the review. Harel, at 264.e9. Ultimately, out of 553 articles describing 

adverse events, 30 articles describing 58 cases were included because they “satisf[ied] at 

a minimum a possible level of certainty [under the WHO system].” Id. at 264.e10-e11. 

The study found evidence that Kayexalate, not sorbitol, might be the pathogenic agent 

causing adverse gastrointestinal events, but emphasized that the literature review could 

not “ensure that the relationship between [Kayexalate] and the described gastrointestinal 

adverse events is certain.” Id. at 264.e14. Moreover, the authors could not calculate the 

risk of such an association because they lacked data on the prevalence of Kayexalate use. 

Id.

Dr. Burks also cited a 2015 rat experiment study by Isabelle Ayoub, published in 

PLOS One, that, unlike Lillemoe, showed that Kayexalate, not sorbitol, “is the main 

culprit for colon necrosis[.]” See Colon Necrosis Due to Sodium Polystyrene Sulfonate 
30

with and without Sorbitol: An Experimental Study in Rats, at 7. Dr. Burks argued that 

these contradictory studies show that the data is insufficient to support a generally 

accepted theory that the oral suspension of Kayexalate with 33-36 percent sorbitol is 

causally connected to ischemic colitis that produces necrosis of the colon.

Dr. Burks’s exhibits also included his expert witness designations; the deposition 

of Dr. Sterns, who had been identified as an expert by the Allens (but was not called to 

testify at trial); and the depositions of Drs. Leo, Goldstein, Buescher, Seneff, and 

Schweitzer.

The Allens filed an opposition to the request for a Frye-Reed hearing, in which 

they argued that the medical literature establishes a general causal link between 

Kayexalate, given in conjunction with sorbitol, and ischemic colitis. They pointed to the 

2009 and 2011 FDA “black box” warnings, and in particular to the 2011 warning, which 

states, “PRECAUTIONS Concomitant use of Sorbitol with Kayexalate has been 

implicated in cases of colonic intestinal necrosis, which may be fatal.” (Emphasis in 

original.) The Allens maintained that, used in that context, “implicated” means causally 

connected, i.e., that there is a cause and effect relationship between Kayexalate with 

sorbitol, given orally, and necrosis of the colon. The Allens provided as an exhibit the 

FDA “Guidance for Industry: Warnings and Precautions, Contraindications, and Boxed 

Warning Sections of Labeling for Human Prescription Drug and Biological Products - -

Content and Format,” October 2011 (“FDA Guidance”), which states, in part, at page 3:

The WARNINGS AND PRECAUTIONS section [of the label] is intended 

to identify and describe a discrete set of adverse reactions and other 

potential safety hazards that are serious or are otherwise clinically 
31

significant because they have implications for prescribing decisions or for 

patient management. To include an adverse event in the section, there 

should be reasonable evidence of a causal association between the drug 

and the adverse event, but a causal relationship need not have been 

definitively established.

(italics in original) (bold added) (footnote omitted).

The Allens also relied upon the UMMC Guidelines, which, as noted, identify 

ischemic colitis as a “major complication” associated with Kayexalate, and the UMMC 

medical records for Mr. Allen, reflecting that Drs. Burks, Tesoriero, and Mehta all 

expressed the view that Mr. Allen’s ischemic colitis may have been caused by 

Kayexalate. They attached the autopsy report as an exhibit.

The Allens argued that the medical literature cited by Dr. Burks in his request for 

a Frye-Reed hearing did not show the absence of a causal relationship but only showed 

that some researchers think there is a need for further study to quantify more precisely the 

risk of colonic necrosis from Kayexalate administered in sorbitol. They attached as 

exhibits medical literature supporting a cause and effect relationship, including: 

• A 2001 article by Susan Abraham, M.D., published in the American Journal of 

Surgical Pathology, studying 11 patients who were given Kayexalate and were 

found to have Kayexalate crystals on biopsy, which concluded that “Kayexalate in 

sorbitol can result in injury to the upper gastrointestinal tract in addition to the 

more commonly appreciated risk of colonic necrosis.” Upper Gastrointestinal 

Tract Injury in Patients Receiving Kayexalate ([SPS]) in Sorbitol, at 643

(emphasis added). The article, citing a 1997 study by Rashid and Hamilton, states: 

“Kayexalate . . . in sorbitol has been demonstrated to cause colonic necrosis in a 

subset of uremic[11] patients who are administered the cation exchange resin for 

hyperkalemia.” Id. at 637.

 

11 “Uremia” is the “entire constellation of signs and symptoms of chronic renal 

failure[.]” Dorlands Illustrated Medical Dictionary, at 2006 (32nd ed. 2012). As 

Continued...
32

• A 2008 article by Lawrence Weisberg, M.D., in Critical Care Medicine, reviewing 

the medical literature pertinent to management of hyperkalemia and stating, with 

citations:

There are numerous case reports of patients who have 

developed intestinal necrosis after exposure to [Kayexalate] 

in sorbitol as an enema, and as an oral agent. A retrospective 

study estimated the prevalence of colonic necrosis to be 1.8% 

among postoperative patients receiving [Kayexalate]. Thus, 

the slow onset of action and serious, albeit infrequent, toxicity 

make [Kayexalate] a poor choice for the treatment of urgent 

hyperkalemia.

Management of severe hyperkalemia, at 3249 (citations omitted).

• A 2009 article by C.E. McGowan, M.D., in the Southern Medical Journal,

studying pathology records of 29 patients who received oral Kayexalate. Eleven 

patients had confirmed intestinal necrosis and four died. The article concluded:

[Kayexalate] in sorbitol has been implicated in the 

development of intestinal necrosis, primarily mediated by the 

sorbitol component. Previous studies documented these 

findings almost exclusively in postoperative, renal transplant, 

and critically ill patients. Our study highlights that all patients 

are potentially susceptible, including those without previously 

described comorbidities. The indications for [Kayexalate] 

use, as well as alternate vehicles for its delivery, should be reevaluated. [Kayexalate]-induced ischemia remains an under 

recognized, easily avoided complication, associated with 

significant morbidity and mortality. Physicians who routinely 

use this agent in sorbitol should be aware of its lifethreatening complications.

Intestinal Necrosis due to Sodium Polystyrene Sulfonate (Kayexalate) in 

Sorbitol, at 497.

 

...cont’d

discussed above, Mr. Allen was suffering from renal failure, which is why he had been 

undergoing hemodialysis.
33

• A 2010 case study by Mohamad Erfani, in Practical Gastroenterology, 

documenting colonic necrosis in a patient who received oral Kayexalate in sorbitol 

for hyperkalemia. Sodium Polystyrene Sulfonate (SPS): Sorbitol-induced Colonic 

Necrosis. The study concluded:

Intestinal necrosis following [Kayexalate]-sorbitol 

administration is a rare clinical condition that may have 

significant morbidity and mortality. [Kayexalate]-sorbitol 

should be used with caution, especially in the postoperative 

setting, in uremic or ill patients . . . When clinically indicated 

other measures to treat hyperkalemia should be considered 

instead of [Kayexalate]-sorbitol. Physicians need to be aware 

of [Kayexalate]-sorbitol GI side effects while managing 

hyperkalemia. 

Id. at 49.

• A 2015 “Up to Date” article by David Mount, M.D. (and edited by Dr. Sterns), 

generally reviewing the treatment and prevention of hyperkalemia in adults, and 

stating: “A major concern with [Kayexalate] in sorbitol is the development of 

intestinal necrosis, usually involving the colon and ileum, which is frequently a 

fatal complication.” Treatment and prevention of hyperkalemia in adults, at 8

(citations omitted).

In addition, the Allens attached as exhibits to their opposition deposition 

transcripts of Mrs. Allen and Drs. Sterns, Kaplan, Goldstein, and Odze. 

In a reply memorandum, Dr. Burks argued that the conflicting medical opinions in 

the literature cited by the Allens and the literature he cited showed that there is 

disagreement about whether Kayexalate can cause intestinal necrosis; therefore, that 

proposition is not generally accepted in the relevant medical field, and expert testimony 

should not be permitted, under Frye-Reed. He argued further that the UMMC Guidelines 

do not establish a causal relationship either, as they are based on the same disputed 

literature, and his statement to the Allens about Mr. Allen’s differential diagnosis and 

what might have caused his bowel problem merely was a repetition of what the medical 
34

community has not reached an agreement about. Nor, he argued, are the FDA “black 

box” warnings evidence of general acceptance by the medical community. 

In a supplement, the Allens attached deposition testimony by Ms. Yeung, in which 

she stated that the UMMC Guidelines, listing intestinal necrosis as a major complication 

of Kayexalate use, were based on the FDA “black box” warnings.

This case was not specially assigned, and the assignment office did not schedule a 

pre-trial hearing on Dr. Burks’s request for a Frye-Reed hearing. Consequently, the 

request was taken up by the court at the outset of the first day of trial. The trial judge, 

who only was assigned the case that morning, first saw the request, opposition, and 

appended materials then. Nevertheless, she held a comprehensive hearing for 

approximately one hour and fifteen minutes, during which she queried counsel about the 

medicine and the Frye-Reed cases. At one point, she remarked about the important 

distinction between a controversy over the means by which an agent causes a particular 

harm and a controversy over whether the agent can cause the harm at all. After counsel 

finished their arguments, the judge took a twenty-minute recess to further review the 

materials provided, denied the request for a Frye-Reed hearing, and explained the reasons 

for her ruling. 

The ruling was made in the alternative. First, relying primarily upon this Court’s 

decisions in Myers v. Celotex Corporation, 88 Md. App. 442 (1991), cert. denied, 325 

Md. 249 (1992), and CSX Transportation, Inc. v. Miller, 159 Md. App. 123 (2004), cert. 

granted, 384 Md. 581, cert. dismissed, 387 Md. 351 (2005), the judge concluded that the 

medical causation opinions being offered by the Allens’ expert witnesses were not of the 
35

type requiring a Frye-Reed analysis. The judge emphasized that the Allens’ experts were 

not using new or novel scientific techniques but were using the accepted differential 

diagnosis method to reach a conclusion about the etiology of Mr. Allen’s ischemic colitis. 

The judge also distinguished cases such as Blackwell v. Wyeth, 408 Md. 575 (2009), 

which applied Frye-Reed to medical causation opinions, because, unlike in those cases, 

here there was no discernible “analytical gap” between the underlying science and the 

ultimate conclusions reached by the experts. 

Second, and alternatively, the judge concluded that if the proffered medical 

causation opinions of the Allens’s expert witnesses were subject to the Frye-Reed general 

acceptance test, they satisfied it. The judge stressed that the 2009 and 2011 FDA “black 

box” warnings were based on there being a “causal association” between Kayexalate and 

ischemic colitis and that the use of the word “implicated” in the 2011 warning supported 

the conclusion that acceptance of a causal connection between Kayexalate with sorbitol 

and necrosis of the colon is not novel or new. The judge also found persuasive the fact 

that the UMMC Guidelines themselves “demonstrate[] that there is some 

acknowledgement on the part of at least one Defendant that there is an associative 

causative link.” The judge ruled that as the Frye-Reed test was satisfied, there was no 

need for a Frye-Reed hearing.

We note at this point that the oral argument before the trial court focused almost 

exclusively on the substance of the Frye-Reed dispute—whether there is general 

acceptance in the relevant medical community of a causal link between Kayexalate with 

sorbitol and ischemic colitis and necrosis—and not on whether an evidentiary hearing 
36

was needed for the court to make that determination. At the beginning of the hearing, the 

court correctly described it as not being a Frye-Reed hearing, but a hearing on whether to 

hold a Frye-Reed hearing. However, counsel on both sides did not direct their arguments 

to why an evidentiary hearing was necessary, instead providing reasons why the court 

should find that the general acceptance test applied and was not met (the defense) or that 

the general acceptance test did not apply or was satisfied in any event (the plaintiffs). 

Except for one brief remark by defense counsel at the very close of the argument, there 

was no proffer as to who the defense (or the plaintiffs) would call to testify at an 

evidentiary hearing on Frye-Reed and what information would be provided to the court at 

such a hearing beyond what already had been provided in the articles and deposition 

transcripts submitted as exhibits. Defense counsel’s single remark was that if Matthew 

Weir, M.D., the Chief of Nephrology at UMMC, “can find a time that he’s available,” the 

defense would call him to testify “that there is no definitive evidence that [K]ayexalate 

causes bowel ischemia.” An article by Dr. Weir that did not concern Kayexalate was one

of the exhibits to the Allens’s opposition to the Frye-Reed hearing request.12 Otherwise, 

Dr. Weir had no connection to the case and had not been identified as an expert witness 

by any party.

 

12 The 2015 article published in the New England Journal of Medicine by Dr. Weir 

concerned a study on the use of patiromer, a slow-acting potassium binding resin 

medication recently approved by the FDA for treatment of non-urgent hyperkalemia. 

Matthew R. Weir, George L. Bakris, David A. Bushinsky, et al., Patiromer in Patients 

with Kidney Disease and Hyperkalemia Receiving RAAS Inhibitors, N Engl J Med 2015; 

372:211–221.
37

(b)

On appeal, Dr. Burks contends the circuit court erred by denying his pre-trial 

request for a Frye-Reed hearing on the general causation question whether Kayexalate 

(either with or without sorbitol) can cause ischemic colitis. He focuses on the causation 

question itself, arguing that a cause and effect relationship between Kayexalate and 

ischemic colitis is “not generally accepted in the medical community and is unsupported 

by the medical literature” and therefore does not satisfy Frye-Reed. He asserts that in 

ruling on the admissibility of a medical expert’s opinion the court must assess whether 

the data on which the opinion is based is supported by the underlying science.13 That test 

was not met here, according to Dr. Burks, because the medical literature the Allens’s

experts relied upon merely established an association, not a causal connection, between 

Kayexalate (given in sorbitol) and ischemic colitis and the preparation of Kayexalate 

administered to Mr. Allen differed from the preparations associated with virtually all the 

adverse events reported in the literature. In one paragraph of his opening brief, Dr. Burks 

argues that given the “widespread dispute” over whether Kayexalate causes ischemic 

colitis, evidence bearing on the admissibility of the Allens’s causation theory should have 

 

13 Dr. Burks also argues that recent case law makes clear that there is a significant 

overlap between Frye-Reed and Rule 5-702(3) and suggests that the court’s ruling 

violated that rule. In this case, there was no motion in limine filed under Rule 5-702, and 

no objection to the expert testimony based on that rule, and so whether the requirements 

of the rule were satisfied was neither raised nor decided below. Accordingly, the sole 

issue before us concerns the request for a Frye-Reed hearing. See Alford v. State, 236 Md. 

App. 57, 72 (2018) (holding that appellate court will not uphold, under Rule 5-702, trial 

court’s decision to exclude expert witness’s proffered testimony when the issue whether 

that testimony satisfied Rule 5-702 was not raised or decided below).
38

been presented to the trial court before it ruled on admissibility. He does not say what 

that evidence would have been. He asks this Court to vacate the judgment and remand 

for a new trial.

The Allens respond that there was no need for a Frye-Reed hearing on the general 

causation question whether Kayexalate in sorbitol “may cause intestinal necrosis 

(ischemic colitis)” because the medical literature, the FDA “black box” warnings, and the 

UMMC Guidelines show a general level of acceptance of that theory of causation within 

the relevant medical community. Furthermore, the observations by Drs. Burks and 

Tesoriero in their medical and operative notes provide further support for a cause and 

effect relationship between Kayexalate in sorbitol and ischemic colitis. 

(c)

In Frye v. United States, 293 F.1013 (D.C. Cir. 1923), the District of Columbia 

Court of Appeals held that for expert testimony predicated on a novel scientific principle 

or discovery to be admissible, the principle or discovery must be generally accepted in 

the relevant scientific field. When the Court of Appeals adopted the Frye general 

acceptance test in Reed v. State, 283 Md. 374 (1978), it explained that the test governs the 

admissibility of novel scientific evidence. Until the 2000s, the Frye-Reed test was not 

applied outside that context. In the meantime, in Daubert v. Merrell Dow 

Pharmaceuticals, Inc., 509 U.S. 579 (1993), the United States Supreme Court held that 

Federal Rule of Evidence 702 had superseded Frye and established, in its place, a nonexclusive list of factors, including general acceptance, for federal district courts to 

consider in ruling on the admissibility of scientific expert testimony. A few years later, 
39

in General Electric Co. v. Joiner, 522 U.S. 136, 146 (1997), the Supreme Court upheld 

the exclusion of expert testimony that PCBs caused a plaintiff’s lung cancer because 

there was “too great an analytical gap between the data and the opinion proffered.”

In the mid-2000s, the Court of Appeals expanded the Frye-Reed general 

acceptance test to include techniques that are not novel and also to include scientific 

conclusions, as well as techniques. See Montgomery Mutual Ins. Co. v. Chesson, 399 

Md. 314 (2007) (“Chesson I”); Blackwell, 408 Md. at 575; and Chesson v. Montgomery 

Mut. Ins. Co., 434 Md. 346 (2013) (“Chesson II”). Indeed, in Blackwell, the Court 

approved the “analytical gap” concept articulated by the Supreme Court in Joiner. Now, 

under Frye-Reed, the admissibility issue is whether “the expert[s] bridged the ‘analytical 

gap’ between accepted science and [their] ultimate conclusions in [this] particular case.” 

Savage v. State, 455 Md. 138, 160 (2017). 

In Chesson I, which marked the first “drift” by the Court of Appeals toward 

adopting the Daubert “analytical gap” concept, see Savage, 455 Md. at 187 (Adkins, J., 

concurring, joined by Barbera, C.J., and McDonald, J.) (discussing the “jurisprudential 

drift” towards Daubert), the Court held that a circuit court abused its discretion by not 

holding a Frye-Reed hearing to consider the admissibility of testimony by a medical 

doctor on behalf of plaintiff workers that they were suffering from “sick building 

syndrome” from mold in the building where they worked. The employer had requested a 

Frye-Reed hearing, arguing that it was not generally accepted in the medical community 

that “sick building syndrome” is a recognized disease and that the protocol the expert had 
40

devised to make that diagnosis and form his causation opinions was not generally 

accepted. 

The Court of Appeals remanded the case for a Frye-Reed hearing. It held that the 

circuit court should have “determine[d] whether the medical community generally 

accepts the theory that mold exposure causes the illnesses that [the workers] claimed to 

have suffered, and the propriety of the tests [their expert] employed to reach his medical 

conclusions.” Chesson I, 399 Md. at 328. In other words, the Frye-Reed test applied not 

only to the expert’s own novel diagnostic testing methods but also to the analysis he had 

employed in concluding that there was a causal relationship between mold exposure and 

the cluster of symptoms he had dubbed “sick building syndrome.” The Court rejected the 

workers’ argument that under Myers, 88 Md. App. at 442 (medical doctor opining that 

lung cancer was caused by asbestos fibers), and CSX Transportation, Inc. v. Miller, 159 

Md. App. at 123 (medical doctor opining that arthritis was caused by years of walking on 

ballast), Frye-Reed did not apply because their expert merely was making a medical 

diagnosis of an illness. The Court commented that the case “involve[d] more than a 

generally accepted medical opinion and diagnosis. [The workers’ expert] employ[ed] 

medical tests to reach a conclusion that is not so widely accepted as to be subject to 

judicial notice of reliability.” Chesson I, 399 Md. at 332. The Court also stated that 

“novel medical theories regarding the causes of medical conditions have been subject to 

Frye analysis. Reed, 283 Md. at 383 . . . (noting that the Frye test has been applied to 

‘medical testimony regarding the cause of birth defects’).” Chesson I, 399 Md. at 333.
41

The Court disposed of the appeal by means of a limited remand for the circuit court to 

hold a Frye-Reed hearing.14

In our recent review of the evolution of Frye-Reed in Sissoko v. State, 236 Md. 

App. 676 (2018), cert. denied __ Md. __ (July 12, 2018), we discussed the Myers and 

CSX cases. CSX, the more recent of the two, having been decided in 2004, stated that the 

Frye-Reed general acceptance test only applied to “new and novel scientific 

techniques[,]” and that “[a] doctor’s opinion as to the etiology of his patient’s arthritis is 

simply not the type of thing contemplated by the phrase ‘new and novel scientific 

technique.’” Id. at 186–87 (quoting Reed v. State, 283 Md. at 380). Rather, 

[w]hat is contemplated are new, and arguably questionable, techniques such 

as lie detectors tests, breathalyzer tests, paraffin tests, DNA identification, 

voiceprint identification, as in the Reed case itself, and the use of polarized 

light microscopy to identify asbestos fibers, as in Keene Corporation v. 

Hall, 96 Md. App. 644, . . . (1993).

Id. at 187. In Sissoko, where, after a Frye-Reed hearing, the circuit court ruled that the 

State’s expert testimony about abusive head trauma, formerly known as shaken baby 

syndrome, was admissible, we explained that Myers and CSX did not support one of the 

State’s arguments, that Frye-Reed had no application at all:

These cases are not helpful to the State’s position because they were 

decided before the Court of Appeals extended the reach of Frye-Reed

beyond the bounds of novel scientific tests and techniques. We do not 

 

14 The limited remand in Chesson I resulted in the circuit court’s holding a FryeReed hearing and ruling that the workers’ expert witness’s opinions were admissible. In 

a second appeal, Chesson II, the Court of Appeals reversed, holding that the evidence 

adduced at the Frye-Reed hearing and the Court’s own research showed that the expert’s 

opinions were the product of a flawed methodology and his theory of general causation 

was not generally accepted in the medical community.
42

mean to suggest that if they were decided today their outcomes would 

differ, only that the analysis employed necessarily would be more 

expansive. 

236 Md. App. at 715.

15

 

In the case at bar, the trial court cited Myers and CSX in making its first alternative 

ruling, that whether Kayexalate with sorbitol as administered to Mr. Allen can cause 

ischemic colitis was not subject to a Frye-Reed analysis to be admissible. We conclude 

that it is not necessary in this appeal to decide whether that ruling was legally correct. 

Assuming without deciding that the Allens’s proposed expert witness testimony that 

medical causation exists in fact was subject to a Frye-Reed analysis to be admissible, we 

nevertheless hold that the trial court did not abuse its discretion by deciding the FryeReed issue without an evidentiary hearing and in ruling that Frye-Reed was satisfied.

 

15As noted in Chesson I, the Reed Court cited a case in which Frye was applied to 

the issue of the cause of a birth defect. That case—Puhl v. Milwaukee Automobile Ins. 

Co., 99 N.W.2d 163 (Wis. 1959)—clearly would not warrant a Frye-Reed hearing today, 

or in 1983, when Reed was decided. The plaintiff alleged that injuries she sustained in an 

automobile accident, when she was 12 weeks pregnant, caused the baby she was carrying 

to be born with Down syndrome. At trial, the plaintiff’s medical expert, who was not an 

expert in Down syndrome, testified, based on literature he had read, that Down syndrome 

can be caused by lack of oxygen to a fetus and that the plaintiff’s placenta may have been 

partially torn during the accident, causing such a lack of oxygen. The defendant’s expert 

testified that the cause of Down syndrome was not known but that it might be a defect in 

the sperm or egg. There was no pretrial hearing based on Frye. The jury found in favor 

of the plaintiff. 

On appeal, the Supreme Court of Wisconsin held that the evidence of a causal 

connection between lack of oxygen and Down syndrome was legally insufficient, as it 

established nothing more than an unproven, speculative hypothesis by an expert who was 

not qualified in the field of Down syndrome. 

The Wisconsin Supreme Court’s opinion was reported ten months after 

publication of the discovery that Down syndrome is caused by a chromosomal defect.

See Gautier, Marthe & Harper, Peter, Fiftieth anniversary of trisomy 21: returning to a 

discovery (available at https://perma.cc/D46J-97AV). The opinion does not mention that.
43

(d)

In Clemons v. State, 392 Md. 339 (2006), the Court of Appeals held that 

Comparative Bullet Lead Analysis (“CBLA”), a scientific test that had been generally 

accepted as a forensic tool for decades, was no longer generally accepted in the relevant 

scientific community and therefore was not admissible in evidence under Frye-Reed. In 

the circuit court, the defendant filed a pre-trial motion in limine to exclude the State’s 

CBLA evidence. At the suggestion of the court, the parties deferred a ruling on the 

motion until trial. When the State’s CBLA expert took the stand, voir dire was 

conducted first by the prosecutor and then by the defense, in the presence of the jury. 

Those examinations explored whether CBLA remained a generally accepted forensic 

tool. The court ruled that the expert could give his CBLA opinions, thereby denying the 

motion in limine. 

Before the Court of Appeals, that ruling was challenged under Frye-Reed. The 

Court addressed the challenge, even though no Frye-Reed hearing had been held. 

Admonishing that “Frye-Reed examinations are better conducted in pre-trial hearings” 

outside the hearing of a jury, id. at 347 n. 6, the Court went on to state:

If the issue is to be dealt with at trial, it should be addressed, in its entirety, 

as a preliminary matter prior to admission of the challenged evidence, not, 

as here, by having the challenge made only to [the expert’s] status as an 

expert during the [proponent party’s] case and then receiving most of the 

evidence bearing on whether the inferences to be drawn from the [scientific 

evidence] are generally accepted in the relevant scientific community 

during the [opponent party’s] case, after the challenged inferences have 

already been admitted. If a party raises a Frye-Reed objection, all evidence 

bearing on admissibility of the challenged evidence should be presented 

and considered before a ruling is made on the challenge.
44

Id. (emphasis in original). As noted, however, notwithstanding the absence of a FryeReed hearing, the Court reviewed the question whether the expert opinion on CBLA 

should have been excluded as not satisfying Frye-Reed.

Clearly, when a motion has been filed in which a party seeks to preclude the 

admission of scientific evidence based on Frye-Reed, it is preferable for the court to 

schedule a pre-trial hearing at which evidence may be taken, to the extent the court agrees 

that Frye-Reed applies. As Clemons demonstrates, however, that is not an ironclad 

requirement. In the case at bar, Dr. Burks filed his request for a Frye-Reed hearing, 

accompanied by a request for a hearing on that request, approximately six weeks before 

trial, and the Allens filed their opposition on August 8, 2016. The case had not been 

specially assigned, and the assignment office did not schedule any hearing date before 

trial. For that reason, the Frye-Reed matter was not taken up until the first day of trial. 

Therefore, through no one’s fault, least of all the fault of the judge who was assigned the 

case the morning of trial, the question whether the Allens’s expert witnesses would be 

precluded from testifying because their opinions did not satisfy Frye-Reed first came to 

the court’s attention on the day of trial.

The request, opposition, reply, and supplement were all-encompassing on the issue 

of whether the expert opinion evidence in question was admissible under Frye-Reed. In 

addition to thorough discussions of the law, they attached deposition transcripts of the 

expert witness testimony in question and of the contrary expert witness testimony; the 

relevant hospital and medical records, such as the UMMC Guidelines; the FDA “black 

box” warnings; and published medical literature on the causal connection, if any, between 
45

Kayexalate, with and without sorbitol, and ischemic colitis/intestinal necrosis. The 

request did not identify any witnesses that Dr. Burks intended to call in an evidentiary 

Frye-Reed hearing, nor did it proffer the substance of any such witness’s testimony. As 

noted above, the only mention by Dr. Burks of a witness who might be called was the 

remark at the conclusion of the hearing on the first day of trial, referencing, tentatively, 

Dr. Weir. 

In his brief in this Court, Dr. Burks focuses his argument on the trial court’s 

alternative ruling, that the proffered testimony of the Allens’ expert witnesses on medical 

causation satisfied Frye-Reed, saying almost nothing about the court’s ruling against 

holding a Frye-Reed hearing. As mentioned earlier, in one paragraph of his opening brief 

Dr. Burks states, in general terms, that because there is “widespread dispute” over 

whether Kayexalate causes ischemic colitis evidence bearing on the admissibility of the 

Allens’s experts’ opinions should have been presented to the trial court. Beyond that, he 

says nothing about what that evidence should have been or, significantly, what difference 

having an evidentiary hearing rather than a hearing on a comprehensive record, such as 

took place, would have made. 

We see nothing in this record to support a conclusion that the absence of an 

evidentiary Frye-Reed hearing was prejudicial to Dr. Burks. To be sure, as we have 

explained and as Clemons made clear, there is a strong preference in favor of Frye-Reed

issues being decided after a hearing at which evidence may be presented. Given the 

particular circumstances and procedural posture in this case, however, we hold that there 
46

was no harm to Dr. Burks from the trial judge ruling on the Frye-Reed question after 

holding a hearing at which substantial evidence, but no live evidence, was presented. 

(e)

The final Frye-Reed appellate issue is whether the trial court was legally correct in 

ruling that the proffered medical causation testimony by the Allens’s expert witnesses 

satisfied the Frye-Reed test. Our standard of review is de novo. Sissoko, 236 Md. App. at 

711.

In a nutshell, the Frye-Reed issue in this case is whether it is generally accepted in 

the relevant medical community that the drug Kayexalate, given orally in a formulation 

with 35.8% sorbitol, can cause ischemic colitis in a patient such as Mr. Allen. As the 

Court of Appeals has explained, “[g]eneral acceptance [under Frye-Reed] does not equate 

to unanimity of opinion within a scientific community, nor universality, and is not subject 

to a quantum analysis.” Chesson II, 434 Md. at 356; see also U.S. Gypsum v. Baltimore, 

336 Md. 145, 183 (1994) (holding that without being directed to any information 

indicating “that the divergence of opinion over the use of [surface dust sampling for 

asbestos] amounts to the type of ‘fundamental division in the scientific community’ 

which necessitates the exclusion of such testimony[,]” the dust sampling evidence was 

admissible) (quoting Reed, 283 Md. at 392)). Although there have been changes in the 

scope of the Frye-Reed test over the past decade, this principle has remained.

In addition to the cases discussed above, the Court of Appeals’s decision in 

Rochkind v. Stevenson, 454 Md. 277 (2017), although made under Rule 5-702, is helpful 

to our analysis. Stevenson brought a lead paint case, claiming she developed Attention 
47

Deficit Hyperactivity Disorder (“ADHD”) from exposure to lead paint as a young child. 

The Court of Appeals addressed the question whether the trial court abused its discretion, 

under Rule 5-702(3), by admitting Stevenson’s expert’s testimony of general causation 

between lead paint exposure and ADHD. That rule requires, among other things, that 

there be a sufficient factual basis for the expert’s opinion; and that cannot be shown 

unless the opinion is based on an “adequate supply of data[.]” 454 Md. at 287. The 

expert, a pediatrician, based her general causation opinion on an EPA epidemiological 

paper that concluded, from a compendium of studies, that there is an association between 

childhood lead exposure and ADHD. 

The Court of Appeals held that the EPA paper did not supply adequate data to 

support the expert’s opinion. Because the paper did not properly account for various 

potential confounding factors, such as parental education level, socio-economic status, 

parental caregiving quality, and the strong familial component to ADHD, it did not show 

a causal connection between childhood exposure to lead and ADHD. Moreover, in 

offering her opinion, the expert failed to differentiate between the specific symptoms of 

ADHD and the general symptoms of attention deficits, did not factor in that many 

symptoms of ADHD are symptoms of other disorders and learning disabilities, and 

overstated the known effects of lead exposure. In the Court’s view, the expert’s opinion 

merely was conjecture and speculation.16 

 

16 Because the Court concluded that the expert’s opinion was not based on an 

adequate supply of data, it did not assess whether she used a reliable methodology in 

reaching her opinion. Also, because it held that the expert’s opinion should have been 

Continued...
48

More recently, in Sugarman v. Liles, __ Md. __, No. 80, Sept. Term 2017 (filed

July 31, 2018), the Court of Appeals revisited the same EPA epidemiological paper 

discussed in Rochkind, holding that it supplied a sufficient factual basis under Rule 5-

702(3) for a pediatrician’s general causation opinion that elevated blood lead levels can 

cause deficits in auditory encoding and processing speed. In so holding, the Court 

discussed cases from other jurisdictions addressing the “analytical gap” concept, 

including King v. Burlington North Santa Fe Railroad Co., 762 N.W.2d 24 (Neb. 2009). 

In that case, the Supreme Court of Nebraska reversed a trial court order excluding an 

expert’s opinion that exposure to diesel exhaust fumes had caused the plaintiff’s late 

husband to develop multiple myeloma, a form of blood cancer, because the expert relied 

upon epidemiological studies that did not “draw definitive conclusions on causation.” 

762 N.W.2d at 48. In Liles, the Court of Appeals cited King with approval, explaining 

that an expert may rely on scientific studies that do not make “definite conclusions of a 

causal relationship,” so long as they are “qualified to interpret and extrapolate from the 

relevant studies.” Liles, slip. op. at 30. Thus, the pediatrician expert witness was 

permitted to extrapolate from the EPA epidemiological paper’s finding that exposure to 

lead can cause attention decrements to opine that it also could cause slower processing 

speed and auditory encoding deficits, which were “factors of attention.” Id. at 31.

 

...cont’d

excluded under Rule 5-702, the Court did not address whether the circuit court abused its 

discretion by not holding a Frye-Reed hearing. 
49

We return to this case and the question whether the trial court erred in its ruling. 

The uncontroverted facts that were disclosed to the court in support of and in opposition 

to the request for a Frye-Reed hearing, and as further developed at trial, show that Mr. 

Allen developed ischemic colitis, which led to necrosis of the tissue in his colon and 

death. In plain language, lack of oxygen to his large intestine caused the tissue to break 

down and die, which killed him. Ischemic colitis is a well-recognized and established 

medical condition with a clearly defined reason behind it: reduced or absent blood flow 

that deprives cells in the colon of oxygen, damaging the tissue. The dispute in this case 

was not over the existence or nature of that medical condition or its immediate cause—

deprivation of oxygen to the colon. Rather, the dispute was over how Mr. Allen’s colon 

came to be oxygen deprived. 

Although not essential to our decision, we note that this case is very different from 

virtually all the general medical causation cases in Maryland in which expert witness

testimony has been found to be subject to Frye-Reed. “Sick building syndrome” 

(Chesson I and Chesson II) is not even a recognized syndrome (a group of symptoms 

consistently appearing together) or medical condition. The claimed injury in the other 

cases was a syndrome or generally described condition without a clearly identified or 

understood cause, or at least where the cause was an ongoing topic of widespread debate: 

Wilson v. State, 370 Md. 191 (2002) (sudden infant death syndrome), Blackwell (autism),

Sissoko (abusive head trauma/shaken baby syndrome), and, although decided under Rule 

5-702, Rochkind (ADHD). Here, we have an established, acute medical condition in 

which the colon is deprived of oxygen and the question whether Kayexalate in sorbitol, 
50

administered orally, can cause a decrease in oxygen to the colon to bring about that 

condition. 

There was substantial evidence offered by the Allens in opposition to Dr. Burks’s 

motion that strongly supports a finding that, while there may be some disagreement 

among experts in the field, there is not a “‘fundamental division in the scientific 

community’” that necessitated exclusion of the Allens’s expert witness testimony. First, 

several pieces of evidence showed that UMMC, Dr. Burks, and other UMMC health care 

providers involved in Mr. Allen’s care already had accepted the proposition that 

Kayexalate with sorbitol is causally connected to ischemic colitis. The UMMC 

Guidelines, in effect since 2012, and made available to guide doctors at that institution in 

the treatment of hyperkalemia, expressly identify “intestinal necrosis,” i.e., death of 

intestinal tissue, as a “[m]ajor complication” of Kayexalate administration. In the 

differential diagnosis Dr. Burks gave in his discharge summary, upon Mr. Allen’s

transfer to the ICU for surgery, he included “intestinal ischemia due to concomitant 

Kayexalate and lactulose use.” (Emphasis added.) So, before Mr. Allen even was 

operated on, Dr. Burks thought that he could have intestinal ischemia brought on by the 

treatment with Kayexalate in combination with the laxative Mr. Allen was being given to 

address his liver problems. (And at trial, Dr. Burks acknowledged that the Kayexalate 

given to Mr. Burks was a possible cause of his ischemic colitis.) Thus, it was never Dr. 

Burks’s position that the Kayexalate given to Mr. Allen could not have caused his 

ischemic colitis. Likewise, in his operative note, Dr. Tesoriero said Mr. Allen’s ischemic 

colitis “may have likely been induced by Kayexalate”; and, in his pathology note, Dr. 
51

Mehta commented that the ischemic necrosis and crystals in Mr. Allen’s small intestine 

“may be suggestive of kayexalate colitis . . . .” 

In addition, the FDA “black box” warnings for Kayexalate, and for the generic 

SPS suspension (which also was provided in the papers in support of and opposition to 

the request for a Frye-Reed hearing), support a finding that there is a cause and effect 

relationship between Kayexalate given with sorbitol, as Mr. Allen received, and ischemic 

colitis. Both the 2009 and 2011 Kayexalate warnings state that cases of necrosis of the 

colon “have been reported in association with Kayexalate use.” The 2009 warning 

includes in the risk factors for adverse gastrointestinal events, such as ischemic colitis, 

“renal insufficiency and failure. Concomitant administration of sorbitol is not 

recommended.” The 2011 warning goes further, stating, “Concomitant use of Sorbitol 

with Kayexalate has been implicated in cases of colonic intestinal necrosis, which may be 

fatal.” The FDA label for the suspension of SPS in sorbitol likewise warns that intestinal 

necrosis has been reported in association with SPS use and that risk factors include renal 

insufficiency and failure. And in the drug interaction section, it too states that 

“Concomitant use of sorbitol with [Kayexalate] has been implicated in cases of intestinal 

necrosis, which may be fatal.”

The FDA Guidance explains that “[t]o include an adverse event in the [warnings] 

section, there should be reasonable evidence of a causal association between the drug and 

the adverse event, but a causal relationship need not have been definitively established.” 

FDA Guidance at 3 (footnote omitted) (emphasis added). Thus, as used in an FDA drug 

warning, “association” means something more than a mere coincidental occurrence but 
52

less than a “definitive” causal connection and therefore reasonably can include likely 

cause and effect relationships. See Liles, slip. op. at 31 (experts may extrapolate from 

scientific data that show less than a “definite conclusions of a causal relationship”). In 

addition, we agree with the Allens and the trial court that the word “implicated” carries a 

causal meaning, i.e., that the use of Kayexalate with sorbitol is involved in causing 

colonic necrosis. Given that there is a specific warning for the powder form of 

Kayexalate about its being given with sorbitol, there is no reason to think that, because 

the warning is for the powder, it is irrelevant to Kayexalate given in a suspension made 

from a combination of Kayexalate and sorbitol. 

The medical articles furnished by the Allens in opposition to the motion for FryeReed hearing lend further support to the proposition that within the relevant medical 

community, a cause and effect relationship between Kayexalate, in the formulation given 

to Mr. Allen, and ischemic colitis is generally accepted. As early as 2001, Dr. Abraham 

wrote that colonic necrosis was a “commonly appreciated risk” of Kayexalate with 

sorbitol and that Kayexalate with sorbitol had been “demonstrated to cause” colonic 

necrosis in patients with kidney failure. One of Mr. Allen’s multiple system problems 

was kidney failure. Dr. Weisberg’s 2008 medical literature review commented on the 

many case reports of patients developing intestinal necrosis after being given Kayexalate 

with sorbitol, both by enema and orally, and warned that Kayexalate was a “poor choice” 

for treatment of hyperkalemia for that reason. Dr. McGowan’s 2009 article studied 

pathology records of patients receiving Kayexalate and observed that “[Kayexalate]-

induced ischemia remains an under recognized, easily avoided complication” when used 
53

with sorbitol, especially in certain populations, including the “critically ill,” which Mr. 

Allen certainly was. The articles by Erfani, in 2010, and Mount, in 2015, likewise 

supported a causal link, and warned against using Kayexalate with sorbitol, especially in 

patients with kidney failure. The articles submitted by Dr. Burks did not offer any reason 

to contradict a cause and effect relationship when Kayexalate is administered in 

conjunction with sorbitol but took the position that more studies should be done to 

investigate the causal connection between Kayexalate with sorbitol and colonic necrosis. 

The studies offered to the court weighed in the direction of the medical community 

generally recognizing a cause and effect relationship especially in the population of 

critically ill patients experiencing renal failure, such as Mr. Allen.

To be sure, neither the medical literature nor the expert testimony by Drs. Leo and 

Odze, whose depositions were submitted to the court in support and opposition to the 

Frye-Reed motion, delved deeply into the reason, or reasons, for the causal relationship. 

Dr. Goldstein theorized that Kayexalate affects the lining of the colon such that the web 

of thin-walled blood vessels that absorb most of the water in the digestive fluid entering 

the colon stop working. That in turn decreases oxygenation to the lining of the colon. 

Although Dr. Odze’s theory focused on the sorbitol that is combined with the Kayexalate, 

it was similar to the theory espoused by Dr. Goldstein: the sorbitol, acting as a 

hyperosmotic, draws water from the web of blood vessels in the lining of the colon, 

thereby depriving the bowel tissue of oxygen. These experts rejected the causation 

theory offered by Dr. Burks’s experts—that there was a generalized decrease in 

oxygenation to the colon caused by episodes of low blood pressure during dialysis—
54

explaining that there would have been damage to other organs, not just the colon, if that 

were the case. They acknowledged that there are cases of ischemic colitis in which the 

cause is unknown, but made clear that administering Kayexalate with sorbitol, especially 

in a patient with Mr. Allen’s conditions, is a recognized cause of ischemic colitis.

The evidence before the circuit court on the request for a Frye-Reed hearing and 

opposition was sufficient to support a legal finding that, although there is not universal 

acceptance in the medical community that Kayexalate with sorbitol can cause ischemic 

colitis, that proposition is generally accepted, and that the risk of ischemic colitis from 

Kayexalate with sorbitol is “commonly appreciated.” Accordingly, the court’s ruling was 

not in error. 

II.

Denial of Motion to Exclude Certain Evidence on Informed Consent

After the court denied Dr. Burks’s motion to preclude expert witness testimony 

under Frye-Reed, Dr. Burks moved in limine to exclude the same testimony for purposes 

of informed consent. Dr. Burks’s reasoning was that the court had ruled in favor of the 

Allens on the Frye-Reed issue because there was some association, although not a causal 

connection, between Kayexalate as given to Mr. Allen and ischemic colitis, and if there is 

not an actual causal connection then the risk of experiencing ischemic colitis in 

conjunction with administration of Kayexalate with sorbitol is fortuitous and therefore 

not material. The court rejected that argument. Dr. Burks makes the same argument on 

appeal.
55

For the same reasons we have explained in addressing the first question presented, 

this contention lacks merit. The trial court found, on several bases, that there was general 

acceptance in the relevant medical community of a causal connection between 

Kayexalate as given to Mr. Allen and ischemic colitis. Therefore, the contention rests on 

a faulty premise. Neither at trial nor on appeal does Dr. Burks make any other argument 

that there was insufficient evidence that the risk of developing ischemic colitis from the 

Kayexalate and sorbitol as given was not a material risk. 

III.

Admission of Evidence about Calcium Gluconate and Calcium Chloride

and about Blood Draw

(a)

As mentioned above, the UMMC Guidelines for treatment of hyperkalemia call 

for calcium gluconate or calcium chloride to be given in the first phase to protect the 

patient from a heart attack due to dangerous arrhythmias. Dr. Burks ordered calcium 

gluconate stat. In his deposition, Dr. Burks testified that the pharmacy informed him that 

calcium gluconate was not available, due to a nationwide shortage, and that he gave an 

oral order to the nurse assigned to Mr. Allen (Nurse Michelle Frock) to substitute calcium 

chloride in place of calcium gluconate. UMMC protocol requires that a nurse receiving 

an oral order document it in the patient’s chart within 48 hours and that the notation be 

signed by the physician who gave the order. An oral order was not documented in Mr. 

Allen’s chart, however, and the calcium chloride never was administered. In her 
56

deposition testimony, Nurse Frock said she did not recall Dr. Burks giving an oral order 

and if one had been given, she would have documented it in Mr. Allen’s chart.17 

Before trial, Dr. Burks filed a motion to preclude the Allens from introducing 

evidence that he failed “to administer calcium gluconate or calcium chloride.” He argued 

that the only possible relevance of the evidence was to the standard of care, but because it 

was undisputed that Mr. Allen did not suffer any injury from the failure to administer 

calcium gluconate and/or calcium chloride, the evidence of a breach in the standard of 

care had no causal significance and therefore was irrelevant. The court granted the 

motion.

At the beginning of the second day of trial, before Dr. Leo, the Allens’s sole 

standard of care expert, took the stand, counsel for the Allens asked the court to revisit 

that ruling. He argued that the evidence was admissible to challenge the veracity of the 

defense theory that, when confronted with Mr. Allen’s severe, life-threatening case of 

hyperkalemia, Dr. Burks did everything in his power to treat it. Counsel for the Allens 

maintained that evidence that Dr. Burks did not give either calcium gluconate or calcium 

chloride to Mr. Allen to treat the most dangerous aspect of the hyperkalemia cast doubt 

on the credibility of Dr. Burks’s defense that he used every available tool to treat the 

emergency. Dr. Burks’s counsel responded that the evidence was not relevant to the 

standard of care and any bearing on credibility it might have was outweighed by the 

confusion it would cause, as the jury would have to make sense out of the collateral 

 

17 Nurse Frock did not testify at the trial.
57

dispute over whether Dr. Burks did or did not give an oral order for calcium chloride. 

The court agreed with the Allens that the evidence was admissible for credibility 

purposes and reversed its earlier ruling.

Dr. Leo testified that the UMMC Guidelines stated that calcium—in either of its 

two forms—be administered as the first line drug to counteract hyperkalemia; that it was 

“the most important and most urgent medication that Mr. Allen needed”; and that the 

hospital records reflect that calcium gluconate was unavailable and that calcium chloride 

was never ordered for or administered to Mr. Allen. As discussed, Dr. Leo opined that 

Dr. Burks breached the standard of care by administering Kayexalate because dialysis 

was a safer and readily available alternative. Relatedly, he opined that Dr. Burks could 

have administered repeated doses of calcium gluconate or calcium chloride to stabilize 

Mr. Allen’s heart muscle and to “buy . . . more time” pending the initiation of dialysis. 

When Dr. Burks testified at trial (as an adverse witness called by the Allens), he 

stated that after he ordered calcium gluconate, he received a call from the UMMC 

pharmacy advising him that calcium gluconate was not available due to a nationwide 

shortage. He further testified that he believed that he gave a verbal order to Nurse Frock 

and he thought, from not being told anything to the contrary, that his order was followed 

and that Mr. Allen was given calcium chloride. He also testified that it was possible that 

the UMMC pharmacy advised him that there was a hospital-wide shortage of calcium 

chloride and, if that were the case, he would not have given an oral order to Nurse Frock 

to administer it. He could not recall with any confidence which of those scenarios had 
58

occurred, however. He agreed that Mr. Allen’s medical record did not reflect that 

calcium chloride ever was administered. 

During the defense case, Dr. Kaplan testified on cross-examination that the 

standard of care required Dr. Burks to order calcium gluconate (which he did), but that he 

did not breach the standard of care by not administering that drug because he was advised 

that it was unavailable. Dr. Kaplan then was shown UMMC records reflecting that 

calcium gluconate was administered to another patient at the hospital on March 18, 2013. 

Dr. Kaplan responded that he could not speak to whether there were limited supplies of 

calcium gluconate available at UMMC on March 18, 2013. Dr. Kaplan further opined 

that calcium chloride was not an appropriate substitute in Mr. Allen’s case because he did 

not have a central IV line in place and the drug could not be safely administered through 

a peripheral IV line. 

Dr. Seneff also was cross-examined on this issue. He testified that calcium was 

the “first” drug a physician would want to administer during a hyperkalemic emergency 

but disagreed that it was the “most important.” In his view, all the drugs in the threephases, in combination, were equally important. 

On rebuttal, the Allens played the videotaped deposition of Carla Williams, the 

assistant director of UMMC’s Pharmacy Clinical Services division. She testified that 

when there is a shortage of a drug the UMMC pharmacy pulls the supply of those drugs 

from the “Omnicells,” which are the secure drug storage facilities available to doctors 

and nurses on each unit in the hospital, and instead stores the drug at the central 

pharmacy location. In March 2013, there was a shortage of both calcium gluconate and 
59

calcium chloride, and both had been pulled from the “Omnicells” as a result. A small 

supply of the drugs would have been available in the emergency department and 

operating room Omnicells, however, and in crash carts on each unit, unless it had already 

been used. There was no way for Ms. Williams to determine from the UMMC records 

the actual quantities of calcium gluconate and calcium chloride available at UMMC on 

March 18, 2013. 

On appeal, Dr. Burks challenges the court’s ruling admitting the evidence that Mr. 

Allen was not given calcium gluconate or calcium chloride.18 He contends the evidence 

was not relevant, as it had no tendency to prove a breach in the standard of care that 

caused injury to Mr. Allen, and should not have been admitted for credibility as it was 

extrinsic evidence on a collateral matter.

The Allens respond that the evidence properly was admitted because it was 

relevant to “undermine the credibility of the defense[, i.e.,] . . . [that] Dr. Burks did

everything he could in order to respond to Mr. Allen’s medical emergency.” They 

maintain that evidence that Dr. Burks failed to ensure that Mr. Allen received either one 

of the two drugs that were, according to all of the experts, most crucial to prevent him 

from suffering a fatal heart arrhythmia had a tendency to show that Dr. Burks was not 

 

18 In his reply brief, Dr. Burks argues for the first time that the court also erred by 

improperly admitting into evidence three exhibits relative to the calcium 

gluconate/calcium chloride issue: a printout of the Omnicell records from March 13, 

2013; a billing record for Mr. Allen that reflected he never was charged for calcium 

chloride; and a print-out showing medications stocked in the UMMC crash carts. 

“[A]ppellate courts ordinarily do not consider issues that are raised for the first time in a 

party’s reply brief” and we decline to address the admission of these exhibits. Gazunis v. 

Foster, 400 Md. 541, 554 (2007).
60

meticulous in his treatment of Mr. Allen, which made it more probable that he (Dr. 

Burks) did not carefully assess whether Kayexalate was necessary or appropriate as a 

treatment for Mr. Allen’s hyperkalemia. We agree.

Evidence is relevant if it has “any tendency to make the existence of any fact that 

is of consequence to the determination of the action more probable or less probable than 

it would be without the evidence.” Md. Rule 5-401. A court “does not have discretion to 

admit irrelevant evidence[.]” Ruffin Hotel Corp. of Md., Inc. v. Gasper, 418 Md. 594, 

620 (2011); see also Md. Rule 5-402 (“Evidence that is not relevant is not admissible.”). 

In his opening statement, Dr. Burks’s attorney told the jury that all of the actions 

his client took on March 18, 2013, were aimed at preventing Mr. Allen from “suffering 

an immediate, life-threatening emergency that would have stopped his heart”; that Dr. 

Burks’s treatment of Mr. Allen “prevented [him] from dying from a heart arrhythmia”; 

and that when faced with “a patient [who] could die . . . in front of him[, Dr. Burks] used 

every avenue possible to stop that from happening.” During defense counsel’s 

examination of Dr. Burks, who, as mentioned, was called adversely by the Allens, he 

affirmed that Mr. Allen was experiencing an “immediately life threatening emergency” 

around noon on March 18, 2013; that Dr. Burks took “prompt and urgent action to 

respond to that life threatening emergency”; that he ordered a “cocktail” of drugs, 

including calcium gluconate, to avert the emergency; and that absent that treatment, Mr. 

Allen was “certain to die from the elevated potassium level.” The defense experts 

testified, likewise, that Mr. Allen was in danger of dying of a fatal heart arrhythmia and 

that Dr. Burks’s treatment prevented that outcome. Thus, the defense theory was not 
61

simply that the administration of Kayexalate was within the standard of care (and, in any 

event, did not cause Mr. Allen’s ischemic colitis), but that Dr. Burks responded to a 

cardiac emergency and prevented him from dying from a hyperkalemic arrhythmia. 

Evidence that Dr. Burks did not ensure that Mr. Allen received calcium chloride 

after he learned from the UMMC pharmacy that calcium gluconate was unavailable was 

relevant to the overall credibility of Dr. Burks’s defense. Dr. Burks’s alleged 

carelessness in providing a drug crucial to treating Mr. Allen’s life threatening 

emergency had a tendency to make it more probable that he also was careless in his 

decision to prescribe Kayexalate, i.e., that he didn’t consider whether that course of 

action was necessary or appropriate in Mr. Allen’s particular case, given his renal failure 

and the availability of dialysis, a safer and more effective alternative. Moreover, the 

evidence that Dr. Burks misrepresented during his deposition testimony that he had given 

an oral order to Nurse Frock to substitute calcium chloride in place of the calcium 

gluconate, despite no entry in Mr. Allen’s medical record to substantiate that that 

occurred, was relevant to his credibility. See, e.g., Hill v. Wilson, 134 Md. App. 472, 480 

(2000) (a “witness’s credibility is always relevant”) (citation omitted). 

Of course, the court had discretion to exclude the evidence pursuant to Rule 5-403 

if its “probative value [was] substantially outweighed by the danger of unfair prejudice, 

confusion of the issues, or misleading the jury . . . .” Dr. Burks maintains that the court 

abused its discretion by not excluding the evidence pertaining to calcium gluconate and 

calcium chloride because it was both highly prejudicial and misleading. He relies 

primarily on Lai v. Sagle, 373 Md. 306 (2003). In that case, the Court of Appeals held 
62

that a trial court abused its discretion by not granting a mistrial in a medical malpractice 

action after plaintiff’s counsel mentioned in opening statements that the defendant 

physician had been sued for medical malpractice on five prior occasions. Analogizing 

that evidence to “prior bad acts” evidence, the Court reasoned that the jury could use the 

evidence that a defendant had been sued previously to infer, improperly, that the 

defendant was negligent in those cases and that he or she had a propensity to be 

negligent. 

In the instant case, the challenged evidence concerned Dr. Burks’s treatment of 

Mr. Allen, not prior medical malpractice suits. It did not create, as Dr. Burks suggests, a 

mini-trial on a collateral issue because, as we have explained, evidence that neither 

calcium gluconate nor calcium chloride was ordered/administered was relevant to a 

central issue at trial: the propriety of Dr. Burks’s treatment decisions in the immediate 

aftermath of Mr. Allen’s bradycardia. For all these reasons, the court did not err or abuse 

its discretion by denying Dr. Burks’s motion in limine or by admitting the challenged 

evidence.

(b)

At trial, Dr. Burks testified that when he arrived on the floor on the morning of 

March 18, 2013, between 7:00 a.m. and 8:00 a.m., he learned that the results of Mr. 

Allen’s routine blood tests were not back. He asked Nurse Frock about this, and she told 

him that Mr. Allen “may have refused” to have his blood drawn that morning. Dr. Burks 

believed that he then gave an oral order for the labs to be drawn that morning but

acknowledged that there was no notation in Mr. Allen’s medical record to that effect and 
63

the labs were not drawn. He acknowledged that if the lab results had been available they 

likely would have revealed an elevated potassium level and he would have ordered a 

nephrology consult, which would have resulted in dialysis that morning. Had that 

happened, Mr. Allen would not have experienced a cardiac event and Kayexalate would 

not have been prescribed. 

On appeal, the appellants contend the Allens should not have been permitted to 

elicit testimony that Dr. Burks “did not request a blood draw after learning that Mr. 

Allen’s blood work had not been completed” earlier that morning because that evidence 

had no tendency to prove a breach in the standard of care that caused injury to Mr. Allen. 

We conclude that this issue is waived. 

All the challenged testimony was elicited on direct examination of Dr. Burks, 

who, as mentioned, was called adversely.19 During the entire line of questioning 

pertaining to the blood draw, which spans thirteen pages of the trial transcript, counsel for

Dr. Burks did not lodge any objections directed at the substance of the questions and

never argued to the court that, in his view, the subject of the questions was irrelevant and 

prejudicial. Having failed to object to the challenged testimony, Dr. Burks has waived 

this contention of error. See Md. Rule 2-517(a) (“An objection to the admission of 

 

19 When Dr. Burks testified, he was asserting an affirmative defense of 

contributory negligence based upon Mr. Allen’s alleged refusal of a blood test during the

early morning hours of March 18, 2013. After Dr. Burks testified, his attorney withdrew 

that defense. As a result, the court ruled that the issue as to whether Mr. Allen actually 

had refused his blood draw was collateral and precluded further evidence on that subject.
64

evidence shall be made at the time the evidence is offered or as soon thereafter as the 

grounds for objection become apparent. Otherwise, the objection is waived.”). 

CROSS APPEAL

I.

 In their cross-appeal, the Allens contend the trial court violated their constitutional 

rights by reducing the $10,000,000 verdict to $906,250, consistent with the statutory cap 

on noneconomic damages in actions for medical malpractice (“the cap”) codified at CJP

section 3-2A-09.20 They argue that the cap creates a discriminatory classification scheme 

prohibited by the Equal Protection Clause of the Fourteenth Amendment to the federal 

constitution, and Article 24 of the Maryland Declaration of Rights because it 

“discriminates against the most severely injured” and against “larger families,” such as 

the Allens. They assert that the cap cannot survive rational basis scrutiny and must be 

struck down. 

It is not within this Court’s purview to revisit the constitutionality of the cap, 

which the Court of Appeals repeatedly has upheld in the face of challenges premised on 

the same arguments made by the Allens in the instant appeal.21 See Murphy v. Edmonds, 

 

20 When Mr. Allen died in 2013, the cap on noneconomic damages in a wrongful 

death action premised upon medical malpractice brought by “two or more claimants or 

beneficiaries” was 125% of $725,000 ($906,250) for “all claims for personal injury and 

wrongful death arising from the same medical injury[.]” CJP § 3-2A-09(b)(2).

21 Most of the appellate cases consider the constitutionality of the cap on noneconomic damages codified at CJP section 11-108, which, in its current form, applies to 

all personal injury and wrongful death actions that are not premised on medical 

Continued...
65

325 Md. 342, 367–70 (1992) (holding that the constitutionality of the cap is scrutinized 

under the deferential rational basis test and that the “legislative classification drawn . . .

between tort claimants whose noneconomic damages are less than [the cap] and tort 

claimants whose noneconomic damages are greater than [the cap], and who are thus 

subject to the cap, is not irrational or arbitrary”); DRD Pool Serv., Inc. v. Freed, 416 Md.

46, 66-67 (2010) (holding that the cap “does not create a classification between affected 

parties, and certainly not a classification subject to heightened scrutiny”); Dixon v. Ford 

Motor Co., 433 Md. 137, 169 (2013) (holding that by capping the total gross award in 

wrongful death actions, the legislature did not “create irrational classifications among the 

claimants”); Martinez v. The Johns Hopkins Hospital, 212 Md. App. 634, 656 n.19 

(2013) (“it is well settled that the [c]ap is constitutional. The Court of Appeals has 

consistently upheld the constitutionality of the [c]ap, explaining that it has become 

‘embedded in the bedrock of Maryland law.’”) (quoting DRD Pool, 416 Md. at 68). We 

are bound by the direct precedent governing this issue and decline to further address it.

JUDGMENT AFFIRMED. COSTS 

TO BE PAID BY THE 

APPELLANTS.

 

...cont’d

malpractice. As all the parties agree, the reasoning of those cases is equally applicable to 

CJP section 3-2A-09, which applies only to medical malpractice actions.