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Burks v. Allen

Court of Special Appeals of Maryland

August 30, 2018

ALLEN BURKS, ET AL.
v.
CYNTHIA ALLEN, ET AL.

          Circuit Court for Baltimore City Case No. 24-C-15-003384

          Eyler, Deborah S., Wright, Berger, JJ.

          Arthur, Kevin F., J., did not participate in the Court's decision to report this opinion pursuant to Md. Rule 8-605.1.

          OPINION

          Eyler, Deborah S., J.

         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 Kayexalate[3] combined with 35.8 percent sorbitol and by doing so without obtaining his informed consent; and that the medication caused him to develop ischemic colitis and ultimately to die. They alleged that UMMS was liable for Dr. Burks's negligence under the doctrine of respondeat 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 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 pre-trial 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?
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 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.[6] If 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.

         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 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 "ion-exchange resin" medication, also known as a "cation exchange resin." The resin contains sodium ions that are exchanged for potassium ions in the bloodstream in the colon. The potassium ions bind to the resin and then are excreted in the stool. Because Kayexalate produces constipation and sometimes fecal impaction, it usually is given in combination with sorbitol, an osmotic laxative. Osmotic laxatives increase the amount of water secreted into the bowels, which softens the stool, making it easier to pass. Kayexalate begins to work within 2 hours after it is administered. It reaches peak effectiveness approximately 4 to 6 hours after being administered and can continue to work for up to 24 hours. It can be administered either in an oral suspension formula or by enema.

         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 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 blood-potassium level was 7.3 mmol/L. That confirmed the diagnosis of hyperkalemia. A blood potassium level of 7.3 mmol/L is considered dangerously high and can quickly lead to a fatal arrhythmia. At 1:30 p.m., a nephrologist assessed Mr. Allen and ordered hemodialysis on a stat basis. Dialysis began at 2:45 p.m. and was completed at 5:45 p.m. Mr. Allen had two bowel movements during dialysis. After dialysis, Mr. Allen's potassium level was 4.5 mmol/L, which is within the normal range.

         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 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 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

         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" 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 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 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 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" 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 peer-reviewed subscription website for physicians. Although an article about hyperkalemia on that website included information about the association between Kayexalate and ischemic colitis, it was not "something that [Dr. Burks] paid particular attention to." Dr. Burks could not "disagree with [the] statement [in the UMMC Guidelines that a major complication of Kayexalate use is intestinal necrosis and bowel perforation] at this point[.]" In his view, it did not matter that he was unaware of the rare risk of ischemic colitis from Kayexalate use because that would not have changed the course of treatment. Even if he had known that dialysis could be started in 10 minutes, he still would have ordered Kayexalate, because Kayexalate continues to remove potassium from the bloodstream for up to 24 hours, whereas dialysis only works during the several hours in which it is being administered. After dialysis ends, the potassium levels can immediately begin to rise again.

         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 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 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 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.

         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. 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 ...


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