Houser v. Kaufman

972 N.E.2d 927, 2012 WL 3251279
CourtIndiana Court of Appeals
DecidedAugust 10, 2012
DocketNo. 50A03-1201-MI-19
StatusPublished
Cited by9 cases

This text of 972 N.E.2d 927 (Houser v. Kaufman) is published on Counsel Stack Legal Research, covering Indiana Court of Appeals primary law. Counsel Stack provides free access to over 12 million legal documents including statutes, case law, regulations, and constitutions.

Bluebook
Houser v. Kaufman, 972 N.E.2d 927, 2012 WL 3251279 (Ind. Ct. App. 2012).

Opinion

OPINION

BARNES, Judge.

Case Summary

Teresa Houser, as Personal Representative of the Estate of Anonymous Physician Dr. K. (“the Estate”), appeals the trial court’s denial of the Estate’s motion for summary judgment in the medical malpractice suit filed by Stacy Kaufman. C.K. appeals the trial court’s grant of summary judgment in favor of the Estate with respect to his medical malpractice claim against Dr. K.1 We affirm.

Issues

The restated issues before us are:

I. whether Stacy’s claim against the Estate is constitutionally time-barred by the Medical Malpractice Act’s statute of limitations; and
II. whether C.K.’s claim against the Estate fails because Dr. K. owed no duty to C.K.

Facts

The evidence most favorable to Stacy and C.K. as the summary judgment non-movants is that Stacy was born to Mary and Brent Kaufman on April 1, 1974. Dr. K. was the Kaufmans’ family physician who delivered Stacy and was Stacy’s doctor thereafter. When Stacy was born, Dr. K. ordered that a blood test for phenylke-tonuria (“PKU”) be performed on her. Although the blood test revealed that Stacy [931]*931had PKU, Dr. K. never communicated that result to Mary and Brent.

A physician who counseled Stacy in 2007 described PKU as follows:

Amino acids are the building blocks for body proteins, and they are converted into different forms by enzymes. Classic PKU is an inherited condition in which a person cannot breakdown the amino acid, phenylalanine, due to a lack in a specific enzyme, which then leads to a build-up in the body. The excess phenylalanine is toxic to the central nervous system and can cause mental retardation, increased muscle tone, microcephaly, and certain physical features. Treatment for PKU is a special diet that restricts the dietary intake of phenylalanine, and must be followed to prevent central nervous system damage....
Women affected by PKU must pay special attention to their diet if they wish to become pregnant, since high levels of phenylalanine in the uterine environment can cause severe malformation and mental retardation in the child. However, women who maintain an appropriate diet can have normal, healthy children.

App. p. 145. As described in the second paragraph, maternal PKU that affects a baby is a condition separate from PKU “and can even affect babies who do not have the PKU disease.” See http:// medical-dictionary.thefreedictionary.com/ phenylketonuria (last visited June 28, 2012).

Because Dr. K. never communicated the PKU test results to Mary and Brent or otherwise advised them that Stacy had PKU, she was never placed on a special, low-phenylalanine diet. Early in Stacy’s childhood, Mary and Brent noted that she appeared to be developmentally delayed and exhibited other symptoms that were consistent with her having untreated PKU, such as severe diaper rash. Mary and Brent took Stacy to various doctors, including specialists at Riley Children’s Hospital in Indianapolis (“Riley”) when she was four, to determine the cause of these symptoms. These doctors, however, failed to diagnose Stacy with PKU. Instead, they told Mary and Brent that they “needed to just accept her cognitive impairment and help her learn to live with the problems she was experiencing.” Id. at 115. Stacy graduated from high school, although she was placed in special education classes. As an adult, Stacy has an IQ of seventy-four, or “mild to borderline mental retardation .... ” Id. at 127. She is unable to hold a job and receives public assistance. Dr. K., meanwhile, died in 1981.

Stacy gave birth to C.K. in November 2005. C.K. was born with microcephaly, i.e. a small head, and dysmorphic facial features, but a genetic test performed shortly after birth and a CT scan performed a few months later failed to reveal a cause for these abnormalities. Because of developmental delays and other issues, C.K. visited a specialist at Riley on June 1, 2007. Stacy mentioned during this visit that she was being treated for “lesions” on her brain but that multiple sclerosis had been ruled out. This specialist recommended that C.K. follow up with a medical geneticist, but made no mention of PKU or maternal PKU as a possible cause of C.K.’s difficulties.

On July 13, 2007, C.K. was seen by a medical geneticist at Riley. In his written notes of the consultation, the geneticist stated:

There are several possibilities that could explain [C.K.’s] microcephaly. One of the possibilities could be a maternal infection, however, there is no supporting evidence. Another possibility is a chromosomal problem, but the CGH (comparative genomic hybridization) test ruled out that explanation. There is the [932]*932possibility of the patient’s microcephaly being isolated, or found alone, then again he does exhibit other minor physical findings. The possibility of the patient’s mother having PKU ... or hy-perphenylalaninemia should be ruled out due to her blond hair, light skin, and mental delays.

Id. at 145. The geneticist also recommended, among several other things, that someone “[o]btain phenylalanine levels on the mother to rule out maternal PKU or hyperphenalaninemia.” Id. Mary does not recall being advised at this visit that Stacy might have PKU, as opposed to being advised generally that further testing was needed.

On August 2, 2007, Stacy visited a neurologist. The neurologist’s written notes from the visit stated in part, “Elevated phenylalanine level was confirmed by recent urine quantitation — likely has PKU.” Id. at 148. Mary recalls being told by the neurologist at this visit that Stacy “could have PKU, but further testing must be done.” Id. at 107. Further testing conducted on August 6, 2007, confirmed the PKU diagnosis, and the neurologist conveyed the news to the Kaufmans on August 7, 2007. Mary then began researching PKU, and on September 18, 2007, she eventually managed to obtain the records of Stacy’s birth, including the 1974 test confirming Stacy had PKU that had never been communicated to Mary and Brent.

The Kaufmans filed a proposed medical malpractice complaint against Dr. K. with the Indiana Department of Insurance on August 4, 2009, alleging negligence in his failure to communicate the results of the PKU test.2 Houser was appointed to be the personal representative for Dr. K.’s estate. On July 7, 2011, the Estate filed a motion for preliminary determination of law and summary judgment in the trial court, asserting that the two-year statute of limitations of the Medical Malpractice Act (“the Act”) barred Stacy’s claims and that Dr. K. owed no duty to C.K. On November 18, 2011, the trial court denied the summary judgment motion with respect to Stacy’s claims, concluding that there was a genuine issue of material fact as to whether a constitutionally-based exception to the Act’s statute of limitations applied and permitted Stacy’s action to proceed, despite the passage of more than two years since the alleged act of malpractice occurred. However, the trial court granted the Estate’s motion for summary judgment with respect to C.K.’s claim, agreeing that C.K. could not recover because of the absence of a physician-patient relationship between C.K. and Dr. K. C.K.

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Bluebook (online)
972 N.E.2d 927, 2012 WL 3251279, Counsel Stack Legal Research, https://law.counselstack.com/opinion/houser-v-kaufman-indctapp-2012.