Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, May 4, 2021

Variation of stroke-associated pneumonia in stroke units across England and Wales: A registry-based cohort study

Sounds like a protocol is needed for testing for this upon entry.  Maybe you want your doctor to read up on this:

Scientists have discovered why patients develop life-threatening infections after stroke

The latest here:

Variation of stroke-associated pneumonia in stroke units across England and Wales: A registry-based cohort study

First Published April 9, 2021 Research Article Find in PubMed 

Pneumonia is common in stroke patients and is associated with worse clinical outcomes. Prevalence of stroke-associated pneumonia varies between studies, and reasons for this variation remain unclear. We aimed to describe the variation of observed stroke-associated pneumonia in England and Wales and explore the influence of patient baseline characteristics on this variation.

Patient data were obtained from the Sentinel Stroke National Audit Programme for all confirmed strokes between 1 April 2013 and 31 December 2018. Stroke-associated pneumonia was defined by new antibiotic initiation for pneumonia within the first seven days of admission. The probability of stroke-associated pneumonia occurrence within stroke units was estimated and compared using a multilevel mixed model with and without adjustment for patient-level characteristics at admission.

Of the 413,133 patients included, median National Institutes of Health Stroke Scale was 4 (IQR: 2–10) and 42.3% were aged over 80 years. Stroke-associated pneumonia was identified in 8.5% of patients. The median within stroke unit stroke-associated pneumonia prevalence was 8.5% (IQR: 6.1–11.5%) with a maximum of 21.4%. The mean and variance of the predicted stroke-associated pneumonia probability across stroke units decreased from 0.08 (0.68) to 0.05 (0.63) when adjusting for patient admission characteristics. This difference in the variance suggests that clinical characteristics account for 5% of the observed variation in stroke-associated pneumonia between units.

Patient-level clinical characteristics contributed minimally to the observed variation of stroke-associated pneumonia between stroke units. Additional explanations for the observed variation in stroke-associated pneumonia need to be explored which could reduce variation in antibiotic use for stroke patients.

Stroke-associated pneumonia (SAP) is a complication defined as the spectrum of lower respiratory tract infection complicating the first seven days after stroke admission.1,2 It is associated with increased mortality, worse outcomes in survivors, and increased length of hospital stay.3 SAP occurs in around 14% of patients4 although there is marked variation in reported frequency between observational studies, registries, and within registries, where SAP frequency in observational studies ranged from 5.3 to 37.9% and in registries from 6.7 to 30%.4,5 The underlying reasons for this variation are uncertain, but could include potentially modifiable or non-modifiable factors. Baseline characteristics, such as increased stroke severity, increased age, and dysphagia,5 are consistently associated with SAP and might therefore contribute to variation in reported SAP frequency. Seasonality may also contribute to this variation.6 However, other factors contributing to variation in observed SAP between studies or units could be modifiable differences in care processes (e.g. monitoring of vitals or swallow screening protocols), approaches to diagnosis, and thresholds for initiating antibiotics (physician diagnosis vs. application of standardized algorithms).7,8

Better understanding the underlying variation in SAP is important if modifiable factors can be identified. This could lead to avoidance of over or under-treatment of SAP, improved antibiotic stewardship, reduced antibiotic resistance, and improved clinical outcomes. A key first step is determining how much variation is accounted for by non-modifiable clinical characteristics. The aim of this study is to therefore describe the variation of SAP between stroke units and determine how much this variation can be explained by patient baseline clinical characteristics. Our objectives were to first describe the observed variation of SAP across stroke units in England and Wales participating in a large national registry; and then to compare the estimated probabilities of developing SAP across stroke units adjusted and unadjusted for patient-level characteristics.

 

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