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Hyperacute ischaemic changes on non-contrast CT brain

Poster No.: R-0011Congress: 2014 CSMType: Scientific ExhibitAuthors: B. McAllister, L. Lam; ELIZABETH BAY/AUKeywords: Ischemia / Infarction, Diagnostic procedure, Audit and standards,

CT, Neuroradiology brainDOI: 10.1594/ranzcr2014/R-0011

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Aim

Stroke is Australia's second biggest killer after coronary heart disease and a leadingcause of disability1 .The NHMRC recommends CT brain as the imaging modality of choicefor initial imaging in stroke patients and that it should be performed urgently*, 2 , howeverpatients who are candidates for thrombolysis are recommended to undergo imagingimmediately3. The role of CT imaging is to confirm cerebral ischemia or haemorrhageand exclude stroke mimics (such as SDH, tumor); it has high specificity (1.00, 95% CI0.94-1.00) but low sensitivity (0.39, 95% CI 0.16-0.69) 5. To date there is no evidenceof differences in outcomes between plain CT and advanced imaging4 such as MRI DWI,however the latter has both high sensitivity (0.99, 95% CI 0.23 -1.00) and specificity (0.92,95% CI 0.83-0.97) for acute stroke 5.

Well described findings on non contrast CT brain in acute stroke include (i)hypoattenuating brain tissue (loss of grey-white matter differentiation); (ii) obscurationof the lentiform nucleus; (iii) dense MCA sign; (iv) "insular ribbon sign"; (v) sulcaleffacement6,7. It is often the case that patients presenting with hyperacute stroke (definedas within 3 - 6 hours of symptoms onset) have a negative CT brain due to lack of thesecharacteristic changes.

The purpose of this educational exhibit is to review parenchymal changes on non contrastCT brain in patients presenting with acute stroke. We propose that an additional findingof cortical surface blur may be seen in cases of hyperacute ischaemia and that thismay be used as a reliable sign in evaluation of these patients. This will be illustrated inour review series by using pictorial examples.

Methods and materials

Non-contrast CT brains performed on patients presenting to Liverpool Hospital withacute stroke symptoms were evaluated retrospectively. Dates of inclusion were from01/01/2013 - 31/12/2013.

Inclusion criteria:

1. Symptoms of less then 6 hours onset ("hyperacute" stage).2. Patients had to be eligible for thrombolysis therapy (use of NIHSS score).

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3. Established ischaemia had to be demonstrated on progress imaging, either CT brainor MRI, to confirm initial findings.

Exclusion criteria:

1. Intracranial haemorrhage or other stroke mimic.

Data of patients was collected using the hospital Stroke journal.

The CT's of eligible patients were reviewed by a registrar and staff specialist radiologistat Liverpool Hospital.

Results

55 patients met the inclusion criteria above.

19 of these 55 patients had the sign of cortical surface blur on review (34.5%).

Each of these 19 cases had progress imaging performed (either repeat non contrast CTbrain or MRI brain) which demonstrated evolution of the infarction.

4 cases have been chosen for use as pictoral examples of cortical surface blur.

Each cases demonstrates the sign; progress imaging is also provided whichdemonstrates evolution of infarction and more characteristic changes including sulcaleffacement and loss of grey-white matter differentiation.

Images for this section:

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Fig. 1: Cortical surface blur is seen in the right parietal lobe of this patient presentingwith acute stroke symptoms.

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Fig. 2: Progress imaging performed from the patient in Figure 1 72 hours after the initialCT. There is evolution of the infarct with loss of grey-white matter differentiation andsulcal effacement.

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Fig. 3: Cortical surface blur in left parietal lobe.

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Fig. 4: Progress imaging performed one day later (following figure 3) showing evolutionof infarction.

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Fig. 5: Cortical surface blur in the right frontoparietal region in a patient presenting withacute stroke symptoms.

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Fig. 6: CT brain performed 4 days later (patient in figure 5) demonstrating infarction.

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Fig. 7: Cortical surface blur at the left frontoparietal lobe in this patient presenting withacute stroke symptoms.

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Fig. 8: Progress CT brain performed 72 hours after the initial CT (figure 7) showingevolution of infarction with sulcal effacement and loss of grey-white matter differentiation.

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Conclusion

Patients presenting with symptoms of stroke routinely undergo investigation with noncontrast CT brain in the acute setting.

Review of imaging performed in these patients presenting to Liverpool Hospital in 2013revealed an additional sign of cortical surface blur in 34 % of patients with hyperactuecerebral ischaemia.

This finding may indeed be present on imaging before other well described findings ofacute infarction and should necessitate careful review of these studies.

Personal information

Dr Brylie McAllister

Radiology Registrar

Liverpool Hospital

Sydney, NSW

Dr Leon Lam

Staff Specialist

Liverpool Hospital

Sydney, NSW

References

Annotations:

* urgent: as soon as possible, preferably within 24 hours.

References:

1. Australian Institute of Health and Welfare 2012. Australia's Health 2012).

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2. http://www.nhmrc.gov.au/_files_nhmrc/file/publications/cp116_summary_clinicians.pdf

3. http://strokefoundation.com.au/site/media/clinical_guidelines_stroke_managment_2010_interactive.pdf

4. Wardlaw JM, Steveson MD, Chappell F, Rothwell PM, Gillard J, Young G, et al. Carotidartery imaging for secondary stroke prevention; Both imaging modality and rapid accessto imaging are important. Stroke, 2009b, November; 40(11):3511-7

5. Brazzelli M, Sandercock PA, Chappell FM, Celani MG, Righetti E, Arestis N, etal. Magnetic resonance imaging versus computed tomography for detection of acutevascular lesions in patients presenting with stroke symptoms. Cochrane Database SystRev. 2009, Issue 4. CD007424.

6. R von Kummer et al. Acute stroke: usefulness of early CT findings before thrombolytictherapy. Radiology 1997, Vol 205, 327-333

7. N Tomura et al. Early CT findings in cerebral infarction: obscuration of the lentiformnucleus. Radiology 1988, Vol 168, 463 - 467