Door-in-Door-Out Time of 60 Minutes for Stroke With Emergent Large Vessel Occlusion at a Primary Stroke Center.

Background and Purpose- Rapid reperfusion with mechanical thrombectomy in ischemic strokes with emergent large vessel occlusions leads to significant reduction in morbidity and mortality. The door-in-door-out (DIDO) time is an important metric for stroke centers without an on-site mechanical thrombectomy service. We report the outcome of a continuous quality improvement program to improve the DIDO time since 2015. Methods- Retrospective analysis of consecutive patients transferred out from a metropolitan primary stroke center for consideration of mechanical thrombectomy between January 1, 2015, and October 31, 2018. Clinical records were interrogated for eligible patients with DIDO times and reasons for treatment delays extracted. Results- One hundred thirty-three patients were transferred over the 46-month period. Median DIDO time reduced by 14% per year, from 111 minutes interquartile range (IQR, 98- 142) in 2015 to 67 minutes (IQR, 55-94) in 2018. A median DIDO time of 59 minutes (IQR, 51-80) was achieved in 2018 during working hours (0800-1700 hours). Overall, 65 patients had no documented delays (49%) with a median DIDO time of 75 minutes (IQR, 54-93) and 103 minutes (IQR, 75-143) in those with at least one delay factor documented. Conclusions- A median DIDO time of <60 minutes can be achieved in a primary stroke center.

Imported case of poliomyelitis, Melbourne, Australia, 2007.

Wild poliovirus-associated paralytic poliomyelitis has not been reported in Australia since 1977. We report type 1 wild poliovirus infection in a man who had traveled from Pakistan to Australia in 2007. Poliomyelitis should be considered for patients with acute flaccid paralysis or unexplained fever who have been to poliomyelitis-endemic countries.

Apparent diffusion coefficient thresholds do not predict the response to acute stroke thrombolysis.

BACKGROUND AND PURPOSE: Apparent diffusion coefficient (ADC) thresholds for tissue infarction have been identified in acute stroke. IV tissue plasminogen activator (tPA) is associated with tissue salvage. We hypothesized that tPA would lower the ADC threshold for infarction. METHODS: ADC and mean transit time (MTT) maps were generated for 26 patients imaged within 6 hours of stroke onset (12 tPA and 14 conservatively managed controls). MTT maps and day-90 T2-weighted images were coregistered to ADC maps. Relative ADC (rADC) values were calculated for initial diffusion-weighted imaging (DWI) lesions, infarct growth regions (final infarct volume-the acute DWI lesion volume), and hypoperfused salvaged regions (HS; MTT map abnormality-the final infarct volume). When relevant, the DWI lesion was subdivided into DWI reversal and DWI infarct regions. RESULTS: Mean DWI lesion rADC was 0.79 in tPA and 0.74 in untreated patients (P=0.097). Mean rADC in HS and infarct growth regions were similar in tPA patients (0.950 and 0.946) and untreated patients (0.957, P=0.76; 0.970, P=0.08, respectively). The rADC in HS tissue was directly correlated with the time to treatment with tPA (r=0.685; P=0.029). DWI reversal was seen in 67% of tPA-treated patients and in 36% of those conservatively managed (Fisher exact test; P=0.238). In the 13 patients with DWI reversal, the mean rADC in these regions (0.81+/-0.07) was significantly higher than in the acute DWI region that infarcted (0.74+/-0.07; P=0.02), although no absolute thresholds could be identified. CONCLUSIONS: The peri-DWI lesion region contains tissue with intermediate ADC values. The fate of this tissue is variable and cannot be predicted based on the ADC alone. DWI expansion occurs in bioenergetically normal tissue, and this is attenuated by tPA in a time-dependent fashion.