Coombs v. Curnow, 35157.

CourtUnited States State Supreme Court of Idaho
Citation219 P.3d 453
Docket NumberNo. 35157.,35157.
PartiesMelinda COOMBS, natural mother of Michael Hall, deceased, and The Estate of Michael Hall, as represented by Melinda Coombs, personal representative, Plaintiffs-Appellants, v. Adrian CURNOW, M.D., and Russell Griffiths, M.D., Defendants-Respondents.
Decision Date13 October 2009

Moffatt, Thomas, Barrett, Rock & Fields, Chtd., Boise, for respondents. Patricia M. Olsson and Nancy J. Garrett argued.

J. JONES, Justice.

This is an appeal from the district court's entry of judgment notwithstanding the verdict (j.n.o.v.) in favor of respondents in a medical malpractice case after the district court found that the appellants' expert testimony regarding causation was scientifically unreliable. Because we find that the district judge impermissibly weighed the evidence in considering respondents' motion and that the evidence was legally sufficient to support the jury's verdict, we vacate the j.n.o.v. and remand with instructions to reinstate the jury verdict.

I.

On June 22, 2002, Michael Hall, then nearly three years old, and his family were attending a picnic at a family member's home. While at the picnic, Michael was feeding potato chips to the host's dog, a golden retriever. In the course of feeding the dog, Michael spilled some of the chips on the ground. Michael and the dog both attempted to retrieve the dropped chips at the same time and, when Michael tried to take the chips away from the dog, the dog bit him on the face. The bite left Michael with a "deep gouging wound" in his cheek, approximately two inches by two inches in size.

Michael was taken to St. Alphonsus Regional Medical Center for treatment of the bite, which was characterized as "very serious but not life-threatening." Dr. Adrian Curnow, a pediatric surgeon and intensivist specializing in pediatric critical care, was assigned as Michael's primary physician. At the time, Dr. Curnow was one of only two pediatric surgeons in Idaho.1 To assist in treating Michael, Dr. Curnow contacted Dr. Russell Griffiths, a pediatric craniofacial plastic surgeon. Dr. Griffiths was the only pediatric craniofacial plastic surgeon in Idaho at that time.

After discussing the various treatment options with Drs. Curnow and Griffiths, Michael's mother, Melinda Coombs, opted to have the severed tissue reimplanted on Michael's face.2 Mrs. Coombs consented to the surgery after being advised of the attendant risks, including the risk of death. Upon obtaining Mrs. Coombs' consent, Dr. Griffiths performed an exploratory surgery to determine the likelihood of successful reattachment. During the surgery, Dr. Griffiths discovered only one artery and no vein, making successful reimplantation less likely. Dr. Griffiths informed Mrs. Coombs of his discovery, at which point she reaffirmed her consent to the reimplantation surgery. Dr. Griffiths then performed the surgery and was able to reattach the tissue to Michael's face and reconnect it to the blood supply.

Throughout Michael's surgery, he was sedated with the sedative agent Propofol (Diprivan). Pursuant to a "bridging order"3 issued by Dr. Griffiths, Michael was to remain sedated after his surgery while he was recovering in the intensive care unit (ICU). Prolonged sedation was deemed necessary because there was a significant risk the reimplantation would fail if there was any disturbance to the reattached tissue. In light of Michael's young age, there was concern he would not remain still if conscious and thereby cause disturbance to the tissue. In deciding on the sedative to be administered, Dr. Griffiths consulted with Dr. Smagula, the anesthesiologist assigned to Michael's case. Based on the consultation, Dr. Griffiths ordered Propofol to continue to be administered.4 Although Propofol was not indicated for long-term sedation of pediatric patients in the ICU, and Dr. Griffiths had not previously administered the drug under such circumstances, he elected to use Propofol because the alternative sedative, Versed, carried a risk of idiosyncratic reaction.5

After Michael's surgery, Dr. Curnow and his partner, Dr. Reynolds, resumed primary responsibility for Michael's treatment. Upon doing so, they left the existing Propofol order in place and ordered Michael's blood pressure, lipid metabolism, and hemodynamic status to be frequently monitored. Pursuant to the order, Michael was receiving between 100 and 150 micrograms per kilogram per minute of Propofol. Although Dr. Curnow had previously administered Propofol for short-term sedation and had participated in a team that used it for long-term sedation in one patient, he did not use the drug regularly in his practice.

Despite efforts to promote reattachment of the tissue, Michael's reimplantation ultimately failed. Dr. Griffiths removed the tissue on June 25, 2002, and Michael was returned to the ICU. To assist in Michael's recovery, Dr. Griffiths ordered that Michael continue to be sedated with Propofol and placed him on Fentanyl for pain management. Dr. Griffiths then "signed off" of the case and Drs. Curnow and Reynolds resumed providing for Michael's care. Although Dr. Curnow originally intended to lower Michael's Propofol level, he decided to maintain the existing dose to lessen the pain Michael would experience when the dressings on the wound were changed.

Once Michael was returned to the ICU, he began encountering various problems. His blood pressure and hemoglobin levels became very low, he experienced accelerated heart rates (ventricular tachycardia), and he began suffering from a high fever. A transfusion successfully treated the low hemoglobin levels, but did not assist with his low blood pressure or abnormal heart rate. As a result, Dr. Reynolds ordered additional tests and that Propofol be discontinued. The test results indicated Michael had metabolic acidosis (low albumin and calcium levels), which was successfully treated. Michael's ventricular tachycardia also temporarily ceased.

Michael's improved condition did not last long. During an examination on the afternoon of June 27, a nurse discovered Michael's pupils were fixed and dilated. A computerized axial tomography (CT) scan was taken, revealing tissue death in Michael's cerebellar hemisphere, frontal lob, and several arterial distributions. It also indicated that Michael's brain was swollen and suffering from cytotoxic damage. Based on these findings, Michael was determined to be brain dead. He was subsequently removed from life support and passed away on June 28, 2002.

Dr. Glenn Groben, a forensic pathologist, conducted Michael's autopsy. According to Dr. Groben, Michael died from swelling of the brain (cerebral edema). He also noted evidence of lack of oxygen supply throughout the brain (global hypoxic changes). Aside from these abnormalities, the autopsy did not reveal any irregularities in Michael's other organs or systems.

On December 17, 2004, Mrs. Coombs brought a medical malpractice claim against Drs. Curnow and Griffiths (collectively "the doctors"). The case proceeded to a jury trial, commencing on September 4, 2007. At trial, it was undisputed that Michael died from cerebral edema—the sole issue was what caused the cerebral edema. Mrs. Coombs argued that the doctors' prolonged administration of Propofol was the cause of the cerebral edema. In support of her theory, Mrs. Coombs relied on the opinion of Dr. Gregory Hammer. Over the doctors' objections, the district court allowed Dr. Hammer to testify as an expert regarding the applicable standard of care, breach, and causation. According to Dr. Hammer, the doctors violated the applicable standard of care in Boise, Idaho in 2002, by ordering the long-term, high-dose use of Propofol to sedate a pediatric patient in the ICU. In Dr. Hammer's opinion, the doctors' negligent use of Propofol was the proximate cause of the cerebral edema that resulted in Michael's death. He testified that the long-term, high-dose sedation with Propofol produced hypotension and lipemia,6 which, in combination with Michael's low hemoglobin levels, resulted in decreased blood flow and oxygen to the brain. The lack of oxygen, in turn, caused the cerebral edema. Dr. Hammer was the only expert to associate Propofol with Michael's death. The doctors' expert witnesses testified that it was not possible to determine the cause of the cerebral edema.

After the close of evidence, the doctors filed motions for entry of a directed verdict. The district court reserved its rulings on the motions and submitted the case to the jury. The jury subsequently rendered a verdict against the doctors, finding them equally liable, and awarding Mrs. Coombs $750,000.00 in damages. According to the jury's special verdict, both doctors breached the applicable standard of care in treating Michael and their breach was the proximate cause of his death.

On September 28, 2007, the doctors filed motions for judgment notwithstanding the verdict, which the district court granted on March 28, 2008. The court concluded that the doctors were entitled to judgment because there was "no substantial evidence from which a reasonable jury could conclude that the long term use of [P]ropofol was the proximate cause of Michael Hall's cerebral edema." In reaching its conclusion, the court pointed out that there was no scientifically reliable evidence indicating a link between long-term, high-dose Propofol use and cerebral edema resulting in death. Rather, the only cases connecting Propofol use with death involved Propofol Related Infusion Syndrome (PRIS). At the time of treatment, symptoms associated with PRIS included cardiovascular instability, evolving rhabdomyolysis,7 decreasing renal function, and refractory metabolic acidosis—no documented cases involved cerebral edema alone. Because there were no peer-reviewed, published journal articles directly supporting Dr. Hammer's...

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