Cause of death

Odim noted in the chart that "Alyssa had a bradycardia episode following coughing and ET tube suctioning which led to hypotension and cardiac arrest." (Exhibit 11, page STI 47) He found no build-up of blood around her heart when he opened her chest. Despite resuscitation, there was no cardiac activity or output. He also wrote that "The cause of death was sudden and appeared related to a vasovagal episode from ET tube suctioning. Prior to the event the child's post-operative course had been entirely smooth." (Exhibit 11, page STI 47) In short, Odim appeared to be attributing the death to a bradycardia or vasovagal episode that was triggered by the suctioning. He expanded on this point in his testimony.

So my sense at the time was that she had coughed, coughing potentially could reflect increased pulmonary hypertension and then she was suctioned and when you suction she may have had a vagal response or stimulation response which slowed the heart down. In addition when you suction, at least during that brief period of suctioning, there is no oxygen getting in, in fact patients can be transiently low in oxygen and low oxygen can also cause slowing of the heart rate. (Evidence, page 24,918)

Other witnesses did not accept this view. Dr. Walter Duncan said that suctioning can be dangerous, but it is necessary for patients with endotracheal tubes after heart surgery. Without suctioning, he said, patients can literally drown in their own secretions. In his opinion, Alyssa Still's death could not be simply attributed to the suctioning.

I think her pulmonary outlet was too small. I think she had probably right ventricular hypertension after surgery, and that would have limited her cardiac output. If you take a child who has got limited cardiac output, if you look at the rest of the pressure measurements here on my 1995 report, she was still an abnormal coagulation state, which either means that her coagulation factors were consumed at the time of the bypass run and hadn't yet normalized, or her liver was not being perfused adequately with blood to make new coagulation factors.

She was also acidotic. Her pH was 7.22 which means that her cardiac output was limited. And she was using anaerobic metabolism to generate energy. Her bicarbonate was low at 14, it should be 20 at least. It came up slightly by 8:15.

If you look at Dr. Giddins' note, she was fluid overloaded. Her weight prior to surgery 6.7 kilos and at autopsy it was 7.9, which means she was up 1,200 grams, which is 20 percent increase in body fluid. Now, this does not go in keeping with somebody who has had a successful event surgically. There is too many negative things happening here. So I don't think that you can simply say this was a death due to suctioning. (Evidence, pages 41,418-41,419)

Suctioning can in fact stimulate the vagus nerve, which will in turn slow the heart (or produce bradycardia) and cause the blood pressure to drop. This is termed a vasovagal response or episode. Normally such episodes are transient but last longer in some patients, who may need treatment to raise the heart rate. Kesselman testified that with a typical vasovagal episode, the heart rate drops and then picks up again. "She didn't follow that pattern. There was a-the initial stimulus, which I think was the suctioning and maybe the vagal kind of tone stimulation was involved with it, but I think there had to be more to it than that or she would have just quickly recovered." (Evidence, page 33,965) Instead, he suggested that the situation was complicated by the fact that Alyssa's heart was compromised by surgery.

One way of treating a vasovagal episode is with a drug called atropine, although the drug may take some time to work, because the heart rate is so slow. A faster way to speed up the heart is to use a pacemaker, if one is present-as was the case with Alyssa. If the pacemaker is properly connected, it should then be possible to maintain the heart rate. Odim was questioned on why the attempt to pace Alyssa had failed. He said he did not understand why pacing had failed.

My impression was that perhaps the biochemistry was such with hypoxemia and acidosis that they couldn't pace the heart. The patient had a low heart rate for eight minutes and cardiac output in children is a function of heart rate and stroke volume, that is, with each beat you squeeze a certain amount of volume out.

Kids as opposed to adults, their squeeze out is fixed so you really have to have many beats to have an adequate output and if your heart rate goes down and stays down for an appreciable period of time, the cardiac output will go down because they can't increase the amount they eject with each beat and I think that milieux, low cardiac output and acidosis mix, sometimes can make it difficult to pace. (Evidence, pages 24,919-24,920)

Kesselman testified that during this period there had been a number of cases where there was trouble with the pacing wires. Inquiries were made with the firm that manufactured the pacing equipment and the equipment itself was examined by the HSC. In the end, Kesselman said there was no satisfactory explanation of what was wrong with the pacemakers. He speculated that:

Well, I think in this scenario where we have evidence that the heart muscle is not working very well, that it has been compromised, and evidenced I say both by her early post-operative low cardiac output, and evidenced by the slowing of her heart rate that didn't pick up as the perfusion dropped, that when the heart muscle is sick enough that it doesn't matter what stimulation you apply on those cells, if they don't have the energy, they can't respond. (Evidence, page 33,967)

In his testimony, Odim suggested that the vasovagal episode might have been prevented if Alyssa had been pre-treated with atropine. Odim also said he believed that Alyssa was treated with atropine once she suffered the vasovagal response. Kesselman could not recall any conversation regarding pre-treatment with atropine, although he said pre-treatment was not usually given at HSC. This was because the increased heart rate from the drug was not always a positive development in some patients, and atropine also had a side-effect of drying and thickening secretions, making it harder to suction them from endotracheal tubes.

In his report for this Inquest, Hudson wrote at great length on the cause of death. In his report he stated:

I do not agree with the attending surgeon's assessment that the cause of death was due to a vasovagal episode initiated by tracheal suctioning, for two reasons. First, the decrease in heart rate began during a coughing spell prior to suctioning the endotracheal tube, thus suctioning could not have been the initial cause of the bradycardia. Second, and more important, is that a vasovagal episode would have easily responded to cardiac pacing. (Exhibit 307, page 5.19)

The evidence presented by Kesselman, Hudson, Duncan and Taylor is persuasive. Normally, a vasovagal episode would have quickly ended on its own or pacing would have brought the episode to an end. However, Alyssa's heart had been severely compromised during surgery. It therefore simply might not have been able to respond adequately to a vasovagal episode on its own, and without the assistance of the pacemaker, very quickly deteriorated. It would appear that the contributing factors to the heart's inability to respond could have been:

• lack of relief of the pulmonary stenosis;
• the suturing closed of the coronary sinus; and
• the length of surgery.

This view is supported by the presence of subcutaneous, pulmonary, cerebral and myocardial edema, as well as the autopsy finding of myocardial necrosis.