Schnebly v. Baker

Decision Date24 April 1974
Docket NumberNo. 55408,55408
Citation217 N.W.2d 708
PartiesKelly SCHNEBLY, a minor, by Orvin H. Schnebly and Wanda Schnebly, natural guardians and next friends, et al., Appellees, v. John M. BAKER, Appellant. John M. BAKER, Appellant, v. ST. JOSEPH MERCY HOSPITAL OF DUBUQUE, Iowa, et al., Appellees.
CourtIowa Supreme Court

Laird, Burington, Bovard & Heiny and William Pappas, Mason City, and Theodore G. Garfield, Ames, for appellant.

Karr, Karr & Karr, Webster City, and Robins, Davis & Lyons, John F. Eisberg, St. Paul, Minn., and Robert M. Wattson, Minneapolis, Minn., for appellees Schnebly.

Walter C. Schroeder, Mason Ctiy, and Ahlers, Cooney, Dorweiler, Allbee & Haynie, Des Moines, for appellee Hospital.

Brown, Kinsey & Funkhouser and Shepard & Shepard, Mason City, for appellees Joyce and Potter.

Heard en banc.


This is an appeal by defendant John M. Baker from a judgment for $1,044,798 against him for malpractice and from dismissal of his cross-petition against others for indemnity or contribution. The parties take divergent views of the facts but we consider the evidence in the light most favorable to the trial court's findings. Reichle v. Zeman, 204 N.W.2d 636 (Iowa).

Orvin H. Schnebly has Rh-positive blood. His wife, Wanda Schnebly, has Rh-negative blood. Prior to the present events, Mr. and Mrs. Schnebly had three children. Their first child had Rh-positive blood and their second and third children had Rh-negative blood.

Erythroblastosis fetalis is a disease of the fetus and the newborn resulting from blood group incompatibility between a mother and child. If an Rh-negative mother conceives an Rh-positive fetus and some of the fetus's blood crosses the placental barrier into the mother's bloodstream, the mother's system forms antibodies. Generally the fetus is unaffected. But if the mother subsequently conceives another Rh-positive fetus, the mother's antibodies may cross the placental barrier into this fetus and destroy its red blood cells, producing bilirubin. Accumulated bilirubin in a newborn child causes cell death, and when that cell death occurs in the central nervous system including the brain, the damage is irreversible. Brain damage caused by bilirubin is called kernicterus. See Price v. Neyland, 115 U.S.App.D.C. 355, 320 F.2d 674.

Bilirubin is normally handled by the liver and is excreted in the urine or by way of the gall bladder. But during the first 72 hours of life, an infant's liver may not yet be able to handle bilirubin. The critical level of bilirubin is 20 milligrams per 100 milliliter's of blood (20 mgs %), at which point brain irritation begins to occur with possible brain cell damage. The rate of rise of bilirubin in the newborn is predictable. The 'indirect' bilirubin reading is the one used.

Tests for bilirubin are run in laboratories of hospitals. The reagent used in making such tests deteriorates with age, causing test results to be unreliable.

Treatment of a newborn child is indicated if the child exhibits jaundice within eight to 12 hours of birth; if the indirect bilirubin level exceeds 10 mgs % Within the first 24 hours, 15 mgs % Within the first 48 hours, or 20 mgs % Thereafter within the first five days of life; or if the rate of rise exceeds 0.5 mgs % Per hour during the first 48 hours. In Rh incompatibility cases, the physician orders a series of blood tests several hours apart following the child's birth, to keep the bilirubin level under observation. Blood tests for bilirubin are not invariably accurate; hence the physician also regularly observes the child for signs of heightened bilirubin levels. These signs include jaundice, lessened such reflex and Moro's reaction (instinctive embracting grasp when jarred), lethargy, irritability, shrill cry, rigidity, and enlargement of liver and spleen. Treatment, when indicated, usually consists of one or more exchange transfusions of blood and is successful in a high proportion of cases. Blood transfusions in small infants are attended with moderate--although not negligible--risks.

Schneblys live in Forest City, Iowa, where Mr. Schnebly is engaged in business. Prior to the events in question Mrs. Schnebly, in addition to homemaking, worked as a bookkeeper, and was familiar with quite complicated bookkeeping systems. She had taken some college work and received 'A' grades. Throughout the events in question, Mr. and Mrs. Schnebly kept each other informed regarding details. Mr. Schnebly testified he understood that a bilirubin level of 20 was the danger point and that brain damage could start thereafter.

Schneblys' physician was T. J. Irish of Forest City, a general practitioner. Schneblys and Dr. Irish were aware of the Rh incompatibility, and Dr. Irish discussed it with them during Mrs. Schnebly's pregnancy. He explained in detail what to expect, what physicians watch for in the tests, and what would be done. During the pregnancy Dr. Irish conducted tests upon Mrs. Schnebly and took X-rays. He ascertained that her antibodies were of a virulent type. Mrs. Schnebly was apprehensive and was especially worried the last month.

During the pregnancy Dr. Irish informed Dr. John M. Baker about the problem and the possible, need of assistance. Dr. Baker is Dr. Irish's brother-in-law and is a pediatrician at Mason City, Iowa. He is on the staff of St. Joseph Mercy Hospital at Mason City and has performed transfusions there. By contract, pathologists George T. Joyce and Paul H. Potter have charge of the laboratory at that hospital. The Forest City hospital laboratory could also run bilirubin tests but did not have a pathologist in charge.

Mrs. Schnebly's antibodies rose toward the end of her pregnancy. Dr. Irish informed her of this, entered her at the Forest City hospital, and induced labor near the end. At 7:40 p.m. on June 8, 1964, Mrs. Schnebly was delivered of a normal full-term male child, whom Schneblys named Kelly. The child's bilirubin livel at birth was 1.48 mgs %, according to the Forest City hospital laboratory. Dr. Irish so informed Dr. Baker by telephone and told Mrs. Schnebly the test was 'one.'

At 7:30 a.m. on June 9 the child's bilirubin had risen to 9.4 mgs %. That forenoon Mrs. Schnebly observed that the child was beginning to turn yellow. At noon Dr. Irish informed Mrs. Schnebly that the test was nine and that this was a fast rise. According to Mrs. Schnebly, Dr. Irish told her that Dr. Baker said if the test got to 20, a blood exchange might be necessary, from 20 to 25 there most certainly would be some brain damage, from 25 to 30 there would be serious damage, and from 30 to 50 the child usually went into a coma or died. Mrs. Schnebly testified she was worried and wanted to know how long they were going to wait before taking the child to Mason City. Dr. Irish said they would run another test.

By mid-afternoon on June 9, the child was more yellow, less active, and less responsive to Mrs. Schnebly. That afternoon the bilirubin had risen to 13.6. Dr. Irish so informed Mrs. Schnebly but said another test would be taken; Dr. Baker did not want the child brought to Mason City yet. At that time the rate of rise was 0.6 mgs % Per hour. If that rate persisted, the critical level of 20 would be reached in the early morning hours of June 10.

On the evening of June 9 Mrs. Schnebly 'just knew' that something was wrong. The child did not eat. He was yellow; the whites of his eyes were starting to turn. At 10:00 p.m. the bilirubin had risen to between 16.3 and 18--the exact figure was not ascertained. Dr. Irish was concerned. He reported the test level to Dr. Baker. According to Mrs. Schnebly, Dr. Irish told her that the level was 17 and that Dr. Baker said to wait until morning to bring the child to Mason City for more tests and a decision on what to do.

On the morning of June 10 the child appeared worse to Mrs. Schnebly. At 7:30 o'clock that morning, Dr. Irish entered the child at St. Joseph Mercy Hospital at Mason City. Dr. Baker examined the child and ordered a complete blood count. He testified that the child's spleen and liver were not enlarged.

Pathologists Joyce and Potter had not established a procedure in the Mason City hospital laboratory to assure that the reagent used for bilirubin tests would not become overaged. On the morning of June 10 the reagent was in fact overaged and yielded wrong results. Although it is undisputed that the actual bilirubin level in the child was then approximately 25, the Mason City laboratory test result was 11.2, and that was he level reported to Dr. Baker. Dr. Baker did not question that reading; he testified the laboratory's readings had been accurate during the several years he had practiced at Mason City. On the other hand, the child was jaundiced, the Forest City test of 16 to 18.3 was inconsistent with the Mason City test of 11.2, and Dr. Baker could have ascertained that the rate of rise in the Forest City tests was internally consistent. He did not order a retest or a series of tests by the Mason City laboratory--which would probably have continued to yield wrong results anyway--but he placed his reliance on the Mason City test and assumed that the Forest City test was inaccurate. Dr. Irish relied on Dr. Braker's conclusion and reported to Mrs. Schnebly that the Mason City reading was 11, which was reassuring. Dr. Irish endeavored throughout to reassure Mrs. Schnebly.

That day Drs. Irish and Baker had the afternoon off. A urinalysis done at that time showed bile in the child's urine, signifying massive destruction of the child's red blood cells. Since he was not present, Dr. Baker did not receive the report at that time. That evening Mr. Schnebly visited the child at the Mason City hospital and saw that he was jaundiced.

On the morning of June 11 a second bilirubin test at the Mason City hospital read 9.9, whereas the actual level was probably approximately 37. The clinical picture of the child would be inconsistent with 9.9, but Dr. Baker...

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