I WAS due to fly out to the United States the next morning. I was bending down to clean the floor of my car when it happened.

First my right hand wouldn’t respond and I fumbled picking up a spoon from the floor, then my right leg wouldn’t support my weight.

I tried to call out to my wife but only grunts came out, except of course the f-word when I knew what had happened.

I crawled to the front door of the house, my intensivist wife called 000 and the ambulance was there in 3 minutes!

The paramedics ignored my pleas to go to the closer private hospital … “no you’re off to the Stroke Unit at The Alfred” … and wasted no time — scoop and run.

I was in the resuscitation bay of the emergency department (ED) in 20 minutes and, despite it being late on a Friday night, I was assessed, I had my computed tomography (CT) scan to exclude an intracranial haemorrhage, and the intravenous thrombolytic therapy was running within 60 minutes.

The next day a repeat CT scan and a magnetic resonance imaging scan confirmed multiple small infarcts in the insula consistent with an embolic stroke.

A patent foramen ovale (PFO) showed up on the transoesophageal echocardiogram on day 3 and the PFO was occluded, percutaneously, on day 7.

I was home the next day and back at work 3 weeks later, with no significant residual deficit.

Bending over in the car may have been the trigger, with a Valsalva that opened up the PFO and caused the clot to flip up my left middle cerebral artery (MCA) into the insular cortex.

It is pleasing when published data justifies one’s own teaching; it is even more encouraging when it justifies treatment that affects one’s own life and health.

Every 10 minutes, up to 20 million neurones will die in a typical infarct in the MCA territory, if not recanalised.(1)

A recent updated pooled analysis of eight trials using multivariate logistic regression has been used to assess the relationship of onset-to-treatment time with 3-month morbidity, brain haemorrhage and mortality.(2)

When selected by symptoms and CT findings, the critical time from onset of symptoms to the intravenous infusion of recombinant tissue plasminogen activator (rt-PA) seems to be 3 hours, though that window of opportunity can be increased to 4.5 hours, after which risk may outweigh benefit.

After 4.5 hours, the risk, particularly of reduced recovery of brain function, brain haemorrhage and death, increases.

However, not all patients benefit. It was shown that about five patients need to be treated within 0–90 minutes of symptom onset, nine patients within 91–180 minutes or 15 patients within 181–270 minutes for one of them to have an excellent outcome attributed to treatment.

Clearly rt-PA is not a panacea, and other interventions need to be analysed for the ultimate objective of reperfusion of 100% of patients rather than 40%.

Other modalities need to be investigated, particularly the therapeutic combinations of thrombolytics, neuroprotectives and antithrombotics in addition to ultrasound and endovascular mechanical clot manipulation.(1)

My experience with swift pre-hospital assessment and efficient ED intervention with intravenous rt-PA, after sustaining an acute ischaemic stroke, with full recovery, emphasises that time is critical.(1)

However, the take-home message here is not only early intervention but education and teamwork, similar to the model in trauma care — the “golden hour” and a well trained trauma team.(3)

For stroke management, this means the development of stroke centres, training of pre-hospital and emergency staff, prioritisation of patients to achieve door-to-needle times of less than 60 minutes and public education programs on acting early with the onset of symptoms.(1,4)

For me, it may have been luck: stroking out at home and not in the air; having a medico wife who recognised the signs; a paramedic crew trained to scoop and run and to take me to an ED with a stroke unit, not just passing by the end of my street when they got the call; ED staff who wasted no time; a neurology registrar who started the rt-PA immediately, though pointing out to me and my wife the risks of intracranial haemorrhage; and having a well trained team of health professionals in the Stroke Unit.

Some cynics might say I got red carpet treatment because I am a professor of surgery.

I disagree.

I believe it was not just a stroke of luck but that I benefited from the ideal model of care of stroke management that should be available to all Australians.

Competing interests
I was successively a medical student and surgical trainee at The Alfred from 1971 to 1981, and a consultant trauma surgeon from 1987 to 1999. I am a member of the Content Review Committee for the MJA.

Professor Bruce P Waxman is Director of General Surgery at Southern Health, Melbourne, Victoria.

This article is reproduced from the MJA with permission.

1. Lancet 2010; 375: 1667-1668.

2. Lancet 2010; 375: 1695-1703.

3. American College of Surgeons, Committee on Trauma. ATLS: advanced trauma life support for doctors. Student course manual. 8th ed. Chicago: American College of Surgeons, 2008: xvii.
4. Pract Neurol 2010; 10: 152-154.


Med J Aust 2010; 193; 468


Posted 25 October 2010

3 thoughts on “A stroke of luck … or just the ideal model of care?

  1. Karl says:

    Bruce, it is great to read that you had a positive experience and great outcome during this unfortunate time. It is lucky you live near the Alfred. My relative had an embolic event recently, was taken to Dandenong hospital (Southern Health) overnight (23:00) and had to wait until then morning to get a CT. We struggled to get the appropriate referrals, compounded with sitting in ED for a number of days. The entire experience made me question the system “we” work so hard to maintain.

  2. sue ieraci says:

    Prof Waxman is indeed fortunate for various reasons. Not only did he have swift transport and treatment at a nearby major institution, but the treatment also worked in his favour. As Prof Waxman states, “rtPA is not a panacea.” Indeed, alongside the number needed to treat for a favourable outcome, one should also quote the number needed to harm. The second reference listed reports the findings of re-analysis of pooled study data. It reports that the risk of “large parenchymal haemorrhage” was 5.2% in the thrombolysed group vs 1.0% in controls. Also, the benefits are measured in terms of improvement (not complete recovery). SO, while there are good stories like this one, there are also very bad ones. That’s one of the reasons why a system to deliver stroke thrombolysis can’t just be “rolled out” everywhere without much better information about who is likely to benefit and who is likely to receive harm.
    That’s the reason emergency physicians are still cautious – not out of any sense of being obstructive but because of realistic caution.

  3. Phillip Chalmers says:

    The “brain attack” concept is a good one and I hope is continued. The current investigation pathways and limited treatment options are nothing like those for “heart attack”.
    There is too much mortality, morbidity in the current protocol.
    It is good that it is limited to centres of excellence with highly skilled and experienced staff close at hand to some of those who have “brain attacks”.
    I expect this work will lead to better treatments and better outcomes.
    At the current state of knowledge, I would not agree to having it myself and have instructed my extended family that these are my wishes.

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