Conditions & Symptoms


RSS feed

Syndicate content

acute aortic dissection

Acute aortic dissection

A 39-year-old Canadian semi-professional cyclist and former club level ice-hockey player, now living and working in the UK, was enjoying a fishing trip in Canada with his father-in-law in August 2002.

One day, as he was pushing their boat away from the rocks, he slipped badly, abducting his right hip strongly. He felt a sudden pain in his low back on the right side, and in his groin. Within hours, the pain had become very unpleasant.

He was seen in Canada by an orthopaedic specialist, who diagnosed groin strain and right-sided spinal joint strain of L3/4. No diagnostic tests were done at this point. The specialist recommended conservative treatment.

The cyclist (1.83m/6ft 1in and 90kg/198lb) returned from his holiday, and at the end of August went to see his GP, who directed him to me. He was still experiencing the right-sided low back and groin pain, and now also pain, parasthesia and anaesthesia (pins and needles and numbness) anterolaterally on his right thigh and on the lateral aspect of his right foot. I immediately referred him to a neurosurgeon for MRI and an opinion.

When the results came back three weeks later, all seemed straightforward. The MRI had revealed no sign of the suspected disc pathology at L3/4, and the neurosurgeon’s diagnosis was a traction injury to the right femoral nerve root, and groin-adductor strain. He recommended physical therapy – so it was back to me.

Over the next three months we proceeded with intermittent physical and electrotherapy. My patient was still aware of his pain, but it was less severe and less frequent. The main symptoms, including recurrence of numbness and pins and needles in the right thigh and on the lateral margin of the right foot, would appear during cycling, and especially competitive club rides. A continuous ride of more than one hour would reliably bring on pain and symptoms, which would subside within five minutes of stopping.

Five months after the injury, I referred the cyclist to a physiotherapist colleague, Tom Williams, for full isokinetic testing. This revealed weaknesses in the right adductor and quadricep muscles, which my colleague felt was the result of damage to the nerve root.

We put the patient on to a specific rehabilitation programme and over the next six months he responded with gradual improvements, mainly in the reduction of his low back and groin pain. Yet exercise – and specifically the long-duration bike rides – continued to generate the nerve symptoms and increased pain in the right thigh, calf and foot.

In July 2003, nearly a year after the accident, I decided to refer the cyclist to Balance Physiotherapy in London for a cycling ergonomics test, hoping to shed some more light on his continued injury problems. There, they observed that my patient’s right pelvic joint appeared anteriorly rotated during cycling, so I did some manipulation of the right sacroiliac joint, which further reduced the low back pain, but once more did nothing to alter the exercise-onset symptoms.

After a trip to France to take part in an Alpine cycling event, my client returned to Balance for some further tests. While he was there in August 2003 – a year on from his accident –the physiotherapist Paula Coates recommended he consult a vascular surgeon, to investigate the admittedly unlikely possibility that some kind of intermittent claudication was involved (the type of lower extremity vascular constriction you would rarely associate with an extremely fit 40 year old).

If Paula’s hypothesis was a long shot, what the CT scan, angiogram and vascular consultation finally revealed was even more unexpected: Type B aortic dissection to his descending aorta down to the right common iliac artery (see box). The cyclist had a tear in his main artery. The appearance of symptoms and pain only on prolonged exercise was because this was when his muscular need for oxygen and glucose exceeded the ability of his damaged blood vessels to deliver to his right leg.

Aortic dissection

The aorta is the largest single blood vessel of the body. It carries oxygenated blood from the heart to the rest of the body and extends branches to all the major organs. Shaped like an inverted hockey stick, the aorta can be subdivided into three major parts. The ascending aorta leads from the aortic valve inside the heart to the aortic arch, beyond which is the descending aorta.

Just above the aortic valve, at the origin of the ascending aorta, are three small pouches termed sinuses. Two of these aortic sinuses give rise to the left and right coronary arteries, which supply blood to nourish the heart. The third sinus is termed the noncoronary sinus. The coronary arteries are the only branches of the ascending aorta. The aortic arch gives off the major arteries that supply the head, neck, and arms. Branches to the remaining organs in the chest and abdomen come off the descending aorta, which ultimately divides into the two common iliac arteries that transport blood to the legs.

The wall of the aorta is made up of three layers: the inner intima, the media, and the outer adventitia. Degenerative changes may occur within the aortic wall as a result of hypertension or connective tissue disorders, predisposing to aortic dissection. Aortic dissection refers to a tear in the intima, a portion of which becomes separated from the other layers. This intimal flap’ creates an additional false lumen inside the aorta, within which blood may collect. Type A aortic dissection involves the ascending aorta. If flow to the coronary arteries is affected, a heart attack may result. Type B aortic dissection, by definition, does not involve the ascending aorta, but may occur anywhere else along its course.

Acute aortic dissection is a medical emergency. Common symptoms include chest pain, often radiating to the back, abdominal pain, fainting and stroke. Occasionally a dissection located in the descending aorta will present with pain in the lower limbs. Imaging procedures to visualise the tear include CT, MRI, echocardiography and/or angiography.

Marfan’s syndrome

Marfan’s syndrome is a genetic disorder of connective tissue with an incidence of 1 in 7,000. The disease is caused by mutations, or spelling mistakes, within the gene encoding fibrillin on chromosome 15. The mutations in fibrillin result in a weakness of the connective tissue, which can affect many different organs of the body (including eyes, lungs and heart). Expression of Marfan’s syndrome is highly variable; some patients may have only one or two of the features, while others have more extensive disease.

The most dangerous complication of Marfan’s syndrome is progressive dilation of the origin of the aorta, consequent to degeneration of connective tissue within its wall. Marfan’s syndrome is therefore associated with a high risk of aortic dissection, which most commonly affects the ascending aorta. The Type B dissection in the case described would not be typical of Marfan’s.

Eligibility for competitive sports for people with Marfan’s depends on which organs are affected. Contact sports may increase the risk of lens dislocation in the eye, and cardiac complications, while scuba diving is discouraged owing to the risk of pneumothorax. Anticoagulant therapy following aortic valve replacement predisposes to easy bruising and bleeding from minor injuries; sporting activities that carry significant risk of physical trauma are therefore best avoided.

Srijita Sen-Chowdhry and William J. McKenna

He was instructed to cease all exercise immediately and booked in for major vascular surgery. At the end of October he was operated on to replace his descending aorta – and the aortic arch. He made a good recovery, was discharged from hospital after a week and put on to a gradual rehabilitation programme.

The cyclist is slowly returning to physical activity – and has recently returned to training levels not too far off his pre-surgery state. He is, however, keeping an open mind about his sporting ambitions – all too aware that he is rather lucky to be alive!

The big unanswered question was, why did the tear to his artery happen? One theory was that the cyclist was ‘borderline Marfan’s syndrome’ – a genetic connectivetissue disorder which predisposes carriers to aortic aneurism. But neither the genetic testing (which is not wholly reliable) nor the pattern of vascular damage bears out this possibility. There is no conclusion available on the diagnostic side – only a happy ending for the individual concerned.

acute aortic dissection