I had a dramatic introduction to pulmonary embolism in my first year as an intern in 1955. The 40 year old woman I was called to see felt uneasy in the chest. She denied chest pain or breathlessness but was sure that something was about to happen. Her right medial meniscus had been removed a week before. There were no abnormal findings apart from the healing knee. I had just finished reassuring her and was walking to the door when she sat up, gave a little cry and died.
At autopsy the cause of death was a large embolus straddling the bifurcation of the pulmonary artery. A small to medium sized embolus, perhaps of a day or two duration, was present in the left lung. Presumably it had given rise to her feeling of unease.

I commenced lung perfusion scanning in 1967 adding ventilation scanning in 1976 with a variety of agents and from 1986 with Technegas exclusively, performing about 10,000 studies in total. From 1966 to 1985 I combined Nuclear Medicine with internal medicine which gave me greater insight into patient outcomes and sometimes subsequent unmasking of underlying disease.

In the post operative and post fracture group,the smallest injury I can recall was of a 44 year old plumber who fractured a 2nd metatarsal. It was pretty painful and various measures were tried to immobilise the fracture site, including two weeks in a plaster cast. He had no chest pain but became quite breathless and I was asked to scan him one night. There was very little perfusion of the whole of the right lung and the left lower lobe. He was admitted to intensive care and commenced on a continuous heparin infusion. He died suddenly at breakfast next morning. Autopsy showed multiple emboli in both lungs with recent embolisation to the left upper lobe, the only significant area of perfused lung seen on his scan of the previous night. In this case, a relatively small final embolus administered the coup de gras because of an already severely compromised lung function.

In the 70's and 80's I looked after considerable numbers of people with pulmonary emboli. Most seemed to fit into one of two categories; either small emboli that produced pleuritic pain, often severe but with little haemodynamic effect or large emboli presenting with breathlessness and features of acute pulmonary hypertension, right heart strain and sometimes frank right heart failure. The presence of associated lung infarction would add haemoptysis, fever and pleural effusion. These latter features meant one often had to exclude other causes of lung consolidation.

Small emboli are important because they are often precursors of larger more haemodynamically significant emboli. They commonly give pleuritic pain probably because they slide into the smaller branches of the pulmonary artery and come to rest in a sub-pleural location. They may also be important in their own right. If there are enough of them they may seriously compromise lung function or more rarely give rise to severe longstanding pulmonary hypertension.

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