TIA diagnosis, treatment and secondary prevention strategies…

Accounting for 5.1% of Australian deaths in 2020, stroke is one of the five leading causes of death in Australia, according to the Australian Institute of Health and Welfare.

Although stroke death rates continue to fall, those who do survive are often left with disability, but advances in the evidence base for acute stroke treatment over the last decade are improving outcomes, says Professor Bruce Campbell, head of neurology and stroke at Royal Melbourne Hospital.

We all know the adage “time is brain”, which refers to the time critical nature of acute stroke treatment, both in terms of preventing death, and decreasing disability.

“The probability of an excellent outcome, getting back to all your usual activities, is a lot higher for patients that are treated earlier rather than later,” Professor Campbell says.

With CT perfusion studies, some patients can be considered suitable for thrombolysis or thrombectomy up to 24 hours after the onset of symptoms, he says.

Although Australia currently has only one Mobile Stroke Unit (in Melbourne), Professor Campbell says these are very promising. “Clearly the benefit of thrombolytics is much greater if you give it pre-hospital in the ambulance simply because it’s faster. You can essentially double the effect of thrombolytic by giving it out on the road,” he says.

He reminds GPs to keep stroke patients nil by mouth due to aspiration pneumonia risk, including not giving aspirin as there is no real way for us to exclude haemorrhage without imaging. There is no need for supplemental oxygen therapy unless the patient is measurably hypoxic.

When handing over to ambulance or local ED, Professor Campbell says time since onset of symptoms is the most important history to focus on, along with any regular antithrombotics the person takes, and any recent bleeding.

Diagnosing and treating TIA

While acute stroke requires rapid access to hospital or mobile stroke unit, transient ischaemic attack (TIA) is more commonly treated in the community— but TIA can be difficult to diagnose since it relies solely on history.

“Because of course if the patient still has symptoms when you see them, it’s not a TIA,” Professor Campbell says. Most TIA histories describe a sudden onset of focal deficit with an average duration of ten minutes, followed by a full resolution of symptoms. TIA needs to be differentiated from other non-focal non-stroke episodes such as transient global amnesia or delirium.

Before starting antiplatelet therapy in a TIA patient, Professor Campbell says that a minimum GPs should order a non-contrast CT brain to exclude other causes, but diffusion MRI is preferable if it’s available. “This demonstrates stroke in thirty percent of TIAs,” he says. This is useful for proving that the mechanism of injury was ischaemic, and for evaluating the risk of further stroke.

“We need to look at the carotids for stenosis.” Professor Campbell is happy for GPs to order ultrasound dopplers, which are cheap and free from radiation, although hospitals often use CT angiograms, which offer extra information about dissection, atherosclerosis and intracranial stenosis.

He recommends feeling the pulse at every visit with a TIA patient. Atrial fibrillation (AF) may be paroxysmal and thus easily missed. ECG and Holter have a role. He notes that smart watches are getting better at detecting AF.

“The secondary prevention of stroke and TIA is really targeted to the mechanism,” he says. Atherosclerosis requires antiplatelet therapy and high dose statins. Atrial fibrillation needs anticoagulation. Other causes like patent foramen ovale, vasculitis or dissection obviously have different treatments.

“The standard antithrombotic regimen after minor stroke and TIA is aspirin plus clopidogrel, and we want to start that as quickly as possible because the risk of a recurrent event is very front-loaded,” Professor Campbell says. The benefit is seen in the first three weeks after the event, and really does not have evidence past that.

If the patient is in AF, a direct-acting oral anticoagulant (DOAC) can be started the same day TIA is diagnosed. This should be delayed by up to two weeks in stroke, depending on the size of the infarct, although Professor Campbell says there is not a lot of evidence to help guide this decision and the neurologist will make an estimate of risk.

DOACs are suitable for most patients in AF with sufficient renal function, unless they have rheumatic mitral stenosis or a mechanical valve. “And it’s important to use the correct dose,” he says. “One of the major causes of stroke I see is un-anticoagulated AF or under-anticoagulated AF.” While he appreciates that doctors may be concerned about risk of bleeding, he feels “we really are exposing them to risk without benefit if we don’t anticoagulant them properly.”

For patients with atherosclerosis, Professor Campbell says the evidence supports targeting LDL cholesterol of less than 1.8mmol/L.

“Blood pressure is the strongest risk factor for stroke, both ischemic stroke and intracerebral haemorrhage.” For stroke prevention, he recommends targeting a systolic consistently below 140 mmHg, and warns against accepting higher numbers in rooms just because patients are rushed or stressed on the day. Ambulatory blood pressure monitoring over 24 hours may be useful to assess control.

Secondary Prevention in TIA

• Urgent brain imaging – non-contrast CT or diffusion MRI
• Exclude need for carotid endarterectomy – ultrasound or CT angiogram
• Strict blood pressure control
• Early aspririn and clopidogrel if not in AF
• Intensive search for AF and correctly dosed anticoagulation if AF present
• Start statins immediately (unless contraindication) and titrate therapy to target LDL <1.8 mmol/L
• General cardiovascular lifestyle interventions

To hear more on stroke prevention and management strategies from Professor Campbell, register for The Healthed Medical Update visiting Melbourne & Sydney in September. Register here.