Ashton Feakes was born in St. Boniface General Hospital on July 15, 1993. The first child of John and Linde Feakes, Ashton was delivered by Caesarean section at 36 weeks gestation. At birth, he was diagnosed with Trisomy-21 (Down's Syndrome). At that time a heart murmur was also detected and he was diagnosed with congestive heart failure. He was treated with digoxin and a diuretic (aldactazide). On July 17 when Linde Feakes met with Giddins, he left her with the impression that Ashton needed surgery within the following six months and that the operation would likely take place in Toronto, Edmonton or Saskatoon. Ashton was discharged on August 10.

When Giddins re-examined Ashton on August 11, 1993, Ashton was in no apparent distress. His respiratory rate was 50 breaths per minute, while his heart rate was regular at 140 beats a minute. All his peripheral pulses were palpable, and the size of his liver was normal.

An echocardiogram showed:

• a right aortic arch (which means that the arch curved to the right rather than to the left)
• a complete atrioventricular canal defect
• mild atrioventricular valve regurgitation
• bilateral ventricular hypertrophy. (Both his ventricles were enlarged.)

In this defect, the tricuspid and mitral valves (the atrioventricular valves) that normally separate the heart's upper and lower chambers are not formed as individual valves. In Ashton's case, these valves were abnormal and disrupted.

An additional septal defect was identified post-operatively. Before surgery, it would have been difficult to determine if this defect was separate or a part of the atrioventricular canal defect.

His right aortic arch and his left ventricular outflow tract were unobstructed; however, he had a moderate amount of muscular obstruction of his right ventricular outflow tract as well. His pulmonary valve annulus appeared to be mildly stenotic or narrowed. His ductus arteriosus was long and narrow, but still patent.

In a subsequent letter to the family doctor, Dr. Laura Hawkins, Giddins wrote that it appeared that Ashton was developing increasing muscular obstruction of the right ventricular outflow tract. This was leading to bi-directional shunting in the canal. He also indicated there was a plan for a heart catheterization. Giddins suggested that there was no reason for Ashton to continue to take digoxin, and that the dose of the diuretic could also be reduced.

A heart catheterization on September 7, 1993, led Giddins to conclude that Ashton suffered from a condition reminiscent of Tetralogy of Fallot, complicated by an atrioventricular canal defect. The catheterization also showed that Ashton had moderate atrioventricular valve regurgitation from the left ventricle to both atria.

There was a considerable degree of risk involved in repairing the combination of defects that Ashton had. For that reason, and because he felt that Ashton's condition did not make an operation urgent, Giddins decided that it would be more appropriate to undertake a surgical repair when Ashton was older and stronger. One of the reasons why a repair could be delayed was that the significant right ventricular muscular obstruction was protecting the pulmonary arteries from high pressures. Giddins said that he anticipated that Ashton's condition would evolve in one of two ways: either Ashton would develop lung congestion and difficulty breathing or the muscle obstruction would increase, causing less than normal blood flow to the lungs. Giddins decided to reassess Ashton in three months and that, in the meantime, he would not need any medication. In the end, surgery did not take place until November 1, 1994. Before then, Ashton experienced a number of serious respiratory problems.

On December 10, 1993, he was taken to the HSC suffering from rapid breathing and in-drawing of the skin between his ribs and under the breastbone, a sign of his breathing difficulties. A chest X-ray showed that he had an enlarged heart, increased pulmonary flow, and possible mild pulmonary edema. The X-ray report concluded that Ashton had bilateral pneumonia. He was restarted on aldactazide for treatment of the mild congestive heart failure and was sent home at 0155 hours on December 11.

When Giddins saw Ashton on December 13, his chest was clear and his respiratory rate was 60 to 70 breaths per minute, with mild subcostal in-drawing. In his testimony, Giddins commented that, despite the interpretation of the X-ray taken when Ashton was in the HSC two days earlier, there was no evidence of any infection. He also said that Ashton did not have an elevated temperature and that the X-ray showed only a slight enlargement of the heart.

Giddins concluded that Ashton was having respiratory symptoms due to the degree of left to right shunting, and should continue to be given the diuretic. He suggested a follow-up appointment in three months. In a December 14 letter to Ashton's referring doctor, Giddins wrote that his case would be taken to a CVT conference in 1994 once Odim arrived. Giddins thought that the best course of action would involve surgery in the coming year.

However, Ashton's respiratory problems were not over. On December 30, 1993, he was once again admitted to the HSC and was diagnosed with pneumonia. Ashton was treated with an antibiotic given intravenously. It would appear that his condition on December 13 was more serious than Giddins had originally thought. Ashton was discharged on January 5, 1994, on antibiotics.

Healthy Heart

Diagram 8.5 Ashton Feakes - pre-operative heart 1 - Right aortic arch 2 - Atrial septal defect (identified post-operatively) 3 - Stenotic pulmonary valve 4 - Right ventricular outlet narrowing 5 - Patent ductus arteriosus 6 - Atrioventricular canal defect 7 - Anterior bridging leaflets 8 - Dysplastic right ventricle