Phillips performed the autopsy on October 5 in Odim's presence. According to the autopsy, Erica's anomalies had been properly diagnosed and repaired. All repairs were intact and free of attached clot and the Blalock-Taussig shunt was patent.

According to the autopsy report, there was myocardial hemorrhage (bleeding in the heart muscle) with patchy necrosis. The microscopic findings of the myocardium indicated that the necrosis was ischemic (due to oxygen deficiency) and perimortal in nature. In her testimony, Phillips explained that by perimortal, she meant that the damage could have taken place before or during surgery.

The autopsy report concluded that no anatomical explanation for death had been found. In her testimony, Phillips said:

Knowing what I know now, after going through Dr. Taylor's report, probably the heart and the brain perhaps were damaged before she even went into surgery, and then it was compounded by the surgical procedure, and she was not able to get off bypass. (Evidence, page 42,303)

In his report, Taylor wrote:

The surgical anatomy in Erica's case appeared satisfactory and her death resulted from the myocardial failure rather than an anatomical complication of the procedure. The heart demonstrated microscopic findings of acute ischemic damage, judged moderate in extent in the single histology slide available. Although this is a limited study, it was from the functional ventricle and is most likely a representative sample of the myocardium, since myocardial damage occurring with repair of congenital heart defects most often occurs globally rather than in the regional distribution of a particular coronary artery branch. The damage identified was not associated with inflammation or reparative changes and could represent injury occurring during the surgical procedure and/or up to a day or so before surgery. (Exhibit 336, page 9.1)

In short, Erica's heart had been damaged by poor perfusion, both before and during surgery. (This should not be taken as a criticism of the service provided by the perfusionists, but as a comment on her overall level of blood perfusion.)

In his testimony, Taylor said he could not determine the degree to which contraction band necrosis was the result of damage that took place before or during surgery. He said he could say with certainty that the heart was damaged before surgery, but could not say for certain if the heart was damaged during surgery.

Taylor noted that the autopsy uncovered signs of neuronal necrosis in Erica's brain. He said this indicated that she had "significant circulatory impairment before her surgery. Whether or not operating on Erica a day or two earlier might have changed the outcome can be speculated upon, however, regardless of the timing of the surgery, I believe that her prognosis would be at best 'guarded,' given the severe nature of her cardiac malformations." (Exhibit 336, page 9.1)

In his report, Hudson indicated that he thought there were four major factors that could have contributed to Erica's cardiac failure. The first was the effects of her pre-existing congenital heart problems. The other three were:

Myocardial injury before CPB. Hypoxemia [This refers to the poor perfusion and saturation that Erica experienced pre-operatively.] was documented before CPB. Hypoxia prior to the obligatory period of aortic cross-clamping and cessation of coronary blood flow could add to myocardial injury because the heart would not be in the best achievable metabolic condition just before cross-clamping. In my opinion, by itself, the degree and duration of hypoxia before CPB cannot account for the severe and ultimately lethal myocardial pump failure that occurred. However, it could add to the injury produced by other factors.

Inadequate myocardial protection during CPB. The inability to separate from cardiopulmonary bypass without substantial inotropic and vasopressor support suggests that myocardial protection during CPB was not adequate. Of particular concern is the discrepancy between the surgeon's operative note, and the perfusion record. The surgeon's dictated note states that 30 ml/kg of cold cardioplegia was given shortly after initiation of CPB. The perfusion record indicates that no cardioplegia was given. Although hypothermia alone offers some myocardial protection, the diastolic arrest induced by cardioplegia is of greater importance in protecting the myocardium from injury during aortic cross-clamping. Whether or not cardioplegia was given to this patient is an important fact that must be established. [Italics and bolding in original.] The long duration of TCA would also contribute to myocardial damage.

Myocardial injury or dysfunction after CPB. High doses of catecholamine inotropic agents, which this patient required to separate from CPB, can contribute to myocardial injury. However, this is a no-win situation. Without the drugs, separation from CPB is impossible, so the possibility of adverse effects has to be accepted. The severe hypoxia after CPB could also aggravate myocardial dysfunction and injury. (Exhibit 307, page 9.10)

The issue of adequate cardioplegia is vexing and will be discussed below.

In reviewing the case, Cornel wrote that the "myocardial compromise was probably severe before the operation commenced and the inability to withdraw from bypass is not surprising." (Exhibit 353, page 56)