The operation that Ashton underwent placed a tremendous strain on his system. It was not expected that he would return to the PICU in anything other than critical condition. However, the expectation was that after 24 hours, he would begin to improve. Initially, Ashton followed this course. However, on November 5, four days after surgery, his condition began to deteriorate. From that point on, he never recovered.
Recurring issues during his post-operative care were an increase in regurgitation through his mitral valve, problems with his heart rhythm and concerns that he may have been suffering from a lung infection.
On November 10, it was discovered that his reconstructed mitral valve was no longer functioning. In light of this finding, one of the central debates over his post-operative care was at what point should the team caring for him have considered performing a valve replacement. One of the signs of mitral valve failure is regurgitation through the mitral valve. However, regurgitation is common following surgery of this nature-the challenge is to determine if the level of regurgitation is excessive and indicates a need to re-operate.
Doyle admitted Ashton to the PICU following his operation. At the time, she noted that he had low blood sugar, low blood pressure, metabolic acidosis, an elevated temperature and a decreased number of platelets in his blood. Except for his left upper lung, he had good air entry to his lungs. She concluded that Ashton's heart was unstable, with poor contractility and residual regurgitation through an atrioventricular valve, and with low blood pressure. Doyle testified that this was not unexpected, given Ashton's condition before surgery. Ashton was treated for the conditions Doyle had identified and his condition stabilized. However, Doyle testified that as efforts were made to reduce those treatments, Ashton's condition deteriorated.
An echocardiogram performed immediately after surgery showed abnormalities in the function of the left ventricle and mild tricuspid regurgitation. The possibility of mitral valve stenosis was also questioned. However, there was no mitral valve regurgitation. Giddins testified:
I was perhaps surprised by that because that was surprisingly good, I would have expected some leak. (Evidence, page 4,342)
Based on the results of that echocardiogram, Giddins said he thought that the operation had gone very well.
For the first eight hours following surgery, Ashton's left and right atrial pressures were both elevated, but were approximately the same. After eight hours, however, the left atrial pressure increased and remained higher than the right atrial pressure. According to Cornel, this was a possible indication of dysfunction on the left side of the heart and, in particular, of a problem with the atrioventricular valve repair (that is, the mitral valve).
Throughout his stay in the PICU, Ashton experienced heart block. Odim said that Ashton had sinus (or normal) rhythm when he came off bypass, so he thought the block was not a technical issue. Odim said he thought it might have had a metabolic source or might have been related to swelling in the tissues of the heart.
On November 2, Ashton's metabolic acidosis improved, but he still needed pacing. Giddins wrote that Ashton had complete atrioventricular heart block with a paced ventricular rate of approximately 120-130 beats per minute. He said there was "very little 'coordinated atrial kick' but when pacer placed in backup mode, every 2nd vent [ventricular] impulse preceded by atrial kick therefore this seems optimal for now. Other aspects of of [sic] status all look satisfactory." (Exhibit 6, page FEA 80)
What Giddins was describing was a way of pacing the heart by stimulating only the bottom part of the heart - the ventricle (or "paced ventricular rate"). When Ashton's heart was paced at a rate of 120-130 beats per minute, there was no spontaneous activity from the atrial or top part of his heart. However, when the pacer was put in the backup mode (and not actively pacing), then Ashton's heart would produce a small beat from the top of the heart, in the form of an 'atrial kick'. This 'kick' represents a small amount of blood that is ejected and helps with the overall output of blood from the heart. Giddins believed that this situation was the best for the time being.
In his report, Cornel wrote, "The rhythm management was questionable. AV sequential rhythm would probably have produced a significant improvement in cardiac output. AV sequential rhythm might have been achieved by administering digoxin combined with AV pacing at a faster rate than the atrial rate." (Exhibit 353, pages 61-62)
Cornel was suggesting that a better way of managing Ashton would have been to use AV sequential pacing, in which the atrium was stimulated electrically, followed by electrical stimulation of the ventricle. Cornel indicated that the technique would involve two components. First, Ashton would have to be given digoxin, a drug that can be used to slow electrical conduction between the atrium and the ventricle. Second, the pacemaker would have to be set at a rate faster than the rate at which Ashton's heart was attempting to beat on its own. By doing these two things, Ashton's heart would be able to contract in a way that most closely resembled normal, with the result that Ashton would have had improved output of blood flow from his heart.
On November 3, Ashton had an elevated temperature and was treated with diuretics to address his low urine output. While Ashton still had heart block, Giddins said, he was satisfied with his heart rhythm.
On November 4, Ashton's chest was clear and the process of weaning Ashton from mechanical ventilation was started. Giddins testified that he was not concerned by Ashton's continued heart block. He said it was his practice to wait at least a week to determine if a child then needed a permanent pacemaker.
Ashton was still being given inotropes. An echocardiogram showed that he had good ventricular function, right atrial enlargement, right ventricular hypertrophy, mild mitral stenosis, moderate mitral regurgitation and mild right ventricular output obstruction. Giddins said these results indicated that Ashton's condition was continuing to improve.
The consulting witnesses to this Inquest raised questions about the mitral valve regurgitation. According to Cornel, the leakage could have been due to the components of the valve becoming pulled apart or because the valve was becoming detached from the suture line. Cornel said the regurgitation likely became significant following the increase in the left atrial pressure. He thought it would have been appropriate for the post-operative care team to have considered whether or not mitral valve replacement was required at that time.
Cornel acknowledged that such a replacement was a difficult procedure. However, he said:
. . . the outcome of doing nothing with a severely regurgitant valve, where the heart is not managing to cope with the regurgitation, the outcome of that is terrible. (Evidence, page 44,894)
In general, our approach has been to let the general clinical condition of the patient guide us. If the patient appears to be on the mend, we tolerate up to moderate degrees of mitral valve regurgitation or tricuspid regurgitation. If the patient appears to be deteriorating and getting into trouble, then we re-investigate and possibly re-operate. (Evidence, pages 44,183-44,184)
Odim was asked if there was any consideration of a re-operation on November 4. He said there was nothing to suggest that the repair had broken down.
Furthermore, we-the child was being ventricularly paced and we know that ventricular pacing will make mitral regurg worse because what happens is you are pacing the ventricle at a rate that is not congruous with the atrial, the atrial rate in the patient, and many a times, this impulse comes down through the tissue and it bombards this area and you get what is called a V-wave, so he was being ventricularly paced which we know exacerbates mitral regurg and there were issues of this being a functional problem because of the loading conditions on the pump. (Evidence, page 25,758)
Thus, as well as ventricular pacing producing less than optimal cardiac output, there was a possible second problem in the effect on the mitral valve. With artificial pacing of the ventricle only, there is no co-ordination with any spontaneous activity from the heart's normal atrial pacemaker. Then, if the atrial pacemaker does cause the atrium to contract, the result is what is known as a 'V-wave' that exacerbates mitral regurgitation.
A chest X-ray on November 4 showed slightly increased but unidentified spots in the left upper lobe and a new right pleural effusion. (This is the term for the fluid that fills the space between the chest wall and the lung. Pleural effusions can occur as a result of congestive heart failure.)
On November 5, there was no improvement. Giddins said this lack of progress actually indicated a significant change for the worse, since he had expected that Ashton would have been improving by this time.
A chest X-ray taken early in the morning of November 6 showed pulmonary edema, with increased pleural effusions on both sides of the chest. Ashton's platelets began to drop in number and remained low despite transfusions. Tests were done to see if he had a viral infection, which could have been associated with a decline in his oxygen saturation. However, Giddins testified, the results of those tests took a while to come back and little could be done about such viruses in any event. It does not appear that any requests were made to have the performance of the tests expedited. From this point on, the post-operative care team checked for a variety of infections, although none were identified during this period.
Over the next 24 hours, Ashton's oxygen saturation decreased, and he required more oxygen and manual ventilation. He retained fluid and his weight consequently increased, for which he was treated with diuretics. A chest X-ray showed that he had a collapse of his right upper lobe and pulmonary edema. An echocardiogram showed that the mitral valve now had moderately severe regurgitation. The tricuspid valve also showed an increased volume of regurgitation.
By November 7, Ashton was again given doses of muscle relaxants to completely weaken his muscles. The aim of this treatment was to reduce oxygen use by the muscles, thereby reducing his heart's workload.
An echocardiogram showed that Ashton had moderate to severe left atrioventricular (mitral) valve regurgitation. Giddins said this was the first clear evidence that the valve was failing. Soder said he would then have called his team together to discuss the possibility of repair of the mitral valve. Soder would also have liked to have seen another heart catheterization done at that time.
However, Giddins said, there was no cause for a re-operation at that point.
Knowing, though, that in these cases moderate to severe valve regurgitation isn't an impediment in some cases to them leaving the ICU, we maintain a philosophy that, if at all possible, we should improve everything else that we can do in the intensive care unit before thinking of something like more surgery to address a failing valve.
Q: Would this have been the first day that the thought of a redo, or going back into surgery occurred to you?
A: Before going back into surgery, we would want pretty solid documentation that there was no alternative. (Evidence, pages 4,366-4,367)
Giddins also said he did not believe that Ashton was in any condition for surgery on November 7. Given the fact that Ashton was becoming more edematous, Giddins decided not to perform a heart catheterization until his condition improved. Catheterization itself, he felt, would put considerable stress on a child in Ashton's condition. The dilemma that Giddins faced was whether Ashton's problems were the result of a viral infection or from a failed mitral valve repair. Because a re-operation entailed significant risk, Giddins wanted to rule out all other possibilities, before considering valve replacement.
Giddins thought that Ashton's condition was improving on November 8. His oxygen saturation was increasing, his fluid overload was resolving and his platelet count had not decreased further. However, he was still in heart block and still needed the pacemaker.
The same day, a hematologist was consulted to look at persistent thrombocytopenia (or low numbers of platelets in the blood). The hematologist suggested treating the condition with platelet transfusions until the surgical site healed. The opinion of the hematologist was that the number of platelets was low because they were being used to form clots around the wounds.
Ashton's condition started to deteriorate once more on November 9. His oxygen saturation fell when staff attempted to keep his lungs clear of secretions, through what is termed chest physiotherapy. His platelet count, however, was stable. Giddins thought that Ashton's condition was not as bad as on November 7 but not as good as on November 8.
On November 10, Ashton suffered a hemorrhage from his lungs that left his system so weakened that it was no longer possible to consider valve replacement. It was also on November 10 that the results of a heart catheterization showed that such a replacement was necessary.
At 0445 hours that day, Ashton's oxygen saturation decreased. Pink frothy sputum was suctioned from his lungs. This is often a sign of pulmonary edema and its increased presence was confirmed on a chest X-ray. Over the course of the day, subsequent chest X-rays also showed a large left pleural effusion, the fact that both lungs appeared more dense in patches, and there was the possibility of a pneumothorax on both sides of Ashton's chest. (A pneumothorax is the abnormal presence of air in the space between the lung and the chest wall.) Ashton was not responding to aggressive treatment.
By this point, he had developed what Soder called frank pulmonary edema.
By frank pulmonary edema we mean that the pulmonary edema fluid is now actually bubbling up through the endotracheal tube and is externally visible, as opposed to just X-ray findings of pulmonary edema. (Evidence, page 44,191)
The pink froth was an indication that Ashton was hemorrhaging into his lungs. The development of pulmonary hemorrhage was a turning point in his post-operative deterioration.
An echocardiogram showed a small VSD leak, two forceful leaks (or jets) from the left ventricle to the right ventricle and severe mitral regurgitation, with shunts from the left ventricle to the right atrium.
Giddins and Soni performed a cardiac catheterization in the PICU, using a special portable X-ray machine. The procedure was complicated by Ashton developing a marked slowing of his heart rate and a drop in his blood pressure that required chest compressions for about five minutes. The catheterization showed severe mitral valve regurgitation, passive pulmonary hypertension and severe left ventricular function. Giddins wrote:
It is clear to Drs. Ward, Odim and I that no [underlining in original] further specific operative intervention would be tolerated; even if it were, prosthetic mitral valve management is extremely difficult (both short and long term) @ this age + size. ...prognosis nearly hopeless, and I would hope comfort is maintained as a priority. Family informed of above. (Exhibit 6, page FEA 101)
Swartz, who was the intensivist, also agreed that, following his lung hemorrhage, Ashton would not tolerate being placed on bypass, which would be required if his mitral valve was to be replaced.
Soder testified that from his perspective, the pulmonary hemorrhage was the terminal event in Ashton's case.
In my opinion the kind of the last chance to really do surgery was somewhere before he developed pulmonary hemorrhage on November 10. I think reoperating on his mitral valve up until that point still had a significant chance of success. Once you are into the situation of frank pulmonary hemorrhage, the likelihood of surviving surgery becomes very, very minimal. (Evidence, pages 44,193-44,194)
Dr. J. Embree of Infectious Diseases examined Ashton on November 10 and concluded that she did not believe an infection was playing a significant role in Ashton's problems. He had tested positive for coagulase negative staphylococci. However, she said that these bacteria could not have caused the problems that Ashton was experiencing.
Her notes indicated that she wondered if it was too early in Ashton's case to see signs of cytomegalovirus (CMV). This was a virus that was more common in adults than in children. However, Embree said that it was a virus present in all humans at all ages, but that the body's natural immune system is usually able to control it. In infants and immune-compromised persons, however, it has serious, permanent consequences. CMV infections can cause an opportunistic, severe pneumonia that may be life-threatening. She said that at the time of Ashton's surgery, there was no effective treatment for CMV infection.
After seeing Ashton, Embree recommended a fine-tuning of his antibiotic treatment, ongoing surveillance for further infections, and that samples be sent to be tested for various viruses (including CMV) and bacteria. Unfortunately, due to an error in the transmission of this request, no test for CMV was performed.
Linde Feakes testified that on November 10, Giddins told the family it was unlikely that Ashton would survive the night. John Feakes testified that it was made clear to them that it was not possible to repair or replace the mitral valve, given Ashton's weakened condition.
Throughout the evening, Ashton's condition continued to deteriorate. At 2400 hours Swartz wrote that Ashton was being given large doses of inotropes and maximum artificial ventilation, with no significant improvement.
On Friday, November 11, Ashton's condition continued to deteriorate. He had significant elevation of his pulmonary arterial pressure as a result of the mitral valve regurgitation. He was suffering from a progressive lack of oxygen in his blood and his kidneys had stopped making urine. Artificial kidney dialysis was successfully carried out that afternoon.
Linde Feakes testified that on that morning Odim informed her that it was still possible for Ashton to pull through. That statement proved to be more hopeful than accurate. Ashton was given comfort care to reduce his pain and died at 2027 hours on November 11, in the presence of his parents.
|Current||Home - Table of Contents - Chapter 8 - Post-operative course|
|Previous||The operation-November 1|
|Section 1||Chapter 1 - Introduction to the Issues|
|Chapter 2 - Pediatric Cardiac Issues|
|Chapter 3 - The Diagnosis of Pediatric Heart Defects and their Surgical Treatment|
|Chapter 4 - The Health Sciences Centre|
|Section 2||Chapter 5 - Pediatric Cardiac Surgery in Winnipeg 1950-1993|
|Chapter 6 - The Restart of Pediatric Cardiac Surgery in 1994
January 1, 1994 to May 17, 1994
|Chapter 7 - The Slowdown; May 17 to September 1994|
|Chapter 8 - Events Leading to the Suspension of the Program
September 7, 1994 to December 23, 1994
|Chapter 9 - 1995 - The Aftermath of the Shutdown
January to March, 1995
|Section 3||Chapter 10 - Findings and Recommendations|
|Appendix 1 - Glossary of terms used in this report|
|Appendix 2 - Parties to the Proceedings and counsel|
|Appendix 3 - List of witnesses and dates of testimony|