De Nanassay performed the autopsy that had been ordered by the Medical Examiner on December 22 at 1530 hours. The report was released on February 20, 1995.

The cause of death recorded on the autopsy report form was:

Immediate Cause of Death:

    Myocardial insufficiency post cardiac surgery for TOF.

Antecedent Causes:

    Complete blockage of central shunt by coagulated blood. (Exhibit 9, page PET 9)

Erin's weight at autopsy was 900 grams more than her pre-operative weight. (She had weighed 2,610 grams at birth.) This was presumably due to fluid accumulation. Examination of the heart revealed extreme stenosis of the pulmonary valve, a ventricular septal defect and complete blockage of the central shunt (aorta to main pulmonary artery) by coagulated blood. De Nanassay noted that the pulmonary valve (as had been thought before surgery) was markedly narrowed and would have severely restricted outflow from the right ventricle.

Thus, the main source of blood flow to Erin's lungs was from the central shunt Odim had installed between the aorta and the main pulmonary artery. However, de Nanassay found that the central shunt was completely occluded by coagulated blood, thereby preventing any flow through it. De Nanassay concluded that, if the central shunt became blocked while Erin was still alive, any potential blood flow to her lungs would have been limited to what could pass through the extremely narrowed pulmonary valve. He also concluded that most of the non-oxygenated blood in the right ventricle was likely shunted into the left ventricle through the ventricular septal defect. The outcome would be minimal oxygenation of blood in the lungs, or central cyanosis. De Nanassay believed these findings explained the repeated episodes of oxygen desaturation and the repeated cardiac arrests, since Erin's heart would have been supplied with blood that was less than adequately oxygenated.

Concerning the microscopic examination of tissues, de Nanassay wrote:

The two organ systems of major interest (the heart and lungs) are both essentially within normal limits. There is no evidence of ischemic changes in the myocardium. One tiny focus of subepicardial contraction band necrosis in the right ventricle more likely relates to traumatic causes in the course of surgery than ischemic damage. Both lungs were free of congestion or inflammatory changes. (Exhibit 9, page PET 12)

De Nanassay concluded:

On the basis of the post-mortem examination the major pathological condition was that of a complete blockage of the central shunt. This factor would have to be coordinated with the clinical picture and analyzed in (the) context of other pertinent clinical information. The actual cause for coagulation of blood within the central shunt is not readily obvious from the morphological examination alone and clinical correlation might be helpful. (Exhibit 9, page PET 12)

Dr. W. Halliday, a neuropathologist, examined the brain and found recent hypoxic-ischemic damage.

Taylor reviewed the microscopic slides of the heart and lungs. He found the lung sections poorly expanded, with areas of recent onset bronchopneumonia. He found excessive numbers of amniotic fluid cells that Erin had inhaled or aspirated. He also found clumps of platelets and fibrin thrombi (which help to form blood clots) in both Erin's lungs and brain. These clumps were more prominent than those usually found in children who died shortly after undergoing bypass (Exhibit 336, page 12.3).

Taylor concluded:

Abnormal coagulation, both thrombosis and bleeding, was a significant factor in the death of this child. ... However, the coagulopathy appears confined to the surgical field, with no evidence of major bleeding or thrombosis in other organ systems. (Exhibit 336, page 12.1)

Taylor found mild to moderate myocardial contraction band necrosis and ischemic damage to the muscle of both ventricles. (Exhibit 336, page 12.5)

In commenting on the autopsy specimen, Cornel and Duncan wrote:

The aortic end of the surgical graft appears very small. [This refers to the second shunt.] Clot material in the shunt may have occurred either post-mortem or prior to death. The anatomy was poor with very small pulmonary arteries - we suspect there was poor run-off from the shunt. (Exhibit 354, page 15)