Background and Purpose: Conditions associated with frailty are common in people experiencing stroke and may explain differences in outcomes. We assessed associations between a published, generic frailty risk score, derived from administrative data, and patient outcomes following stroke/transient ischemic attack; and its accuracy for stroke in predicting mortality compared with other measures of clinical status using coded data. Methods: Patient-level data from the Australian Stroke Clinical Registry (2009–2013) were linked with hospital admissions data. We used International Statistical Classification of Diseases and Related Health Problems, Tenth Revision codes with a 5-year look-back period to calculate the Hospital Frailty Risk Score (termed Frailty Score hereafter) and summarized results into 4 groups: no-risk (0), low-risk (1–5), intermediate-risk (5–15), and high-risk (>15). Multilevel models, accounting for hospital clustering, were used to assess associations between the Frailty Score and outcomes, including mortality (Cox regression) and readmissions up to 90 days, prolonged acute length of stay (>20 days; logistic regression), and health-related quality of life at 90 to 180 days (quantile regression). The performance of the Frailty Score was then compared with the Charlson and Elixhauser Indices using multiple tests (eg, C statistics) for predicting 30-day mortality. Models were adjusted for covariates including sociodemographics and stroke-related factors. Results: Among 15 468 adult patients, 15% died ≤90 days. The frailty scores were 9% no risk; 23% low, 45% intermediate, and 22% high. A 1-point increase in frailty (continuous variable) was associated with greater length of stay (OR adjusted , 1.05 [95% CI, 1.04 to 1.06), 90-day mortality (HR adjusted , 1.04 [95% CI, 1.03 to 1.05]), readmissions (OR adjusted , 1.02 [95% CI, 1.02 to 1.03]; and worse health-related quality of life (median difference, −0.010 [95% CI −0.012 to −0.010]). Adjusting for the Frailty Score provided a slightly better explanation of 30-day mortality (eg, larger C statistics) compared with other indices. Conclusions: Greater frailty was associated with worse outcomes following stroke/transient ischemic attack. The Frailty Score provides equivalent precision compared with the Charlson and Elixhauser indices for assessing risk-adjusted outcomes following stroke/transient ischemic attack.
Background and Purpose— Readmissions after stroke are common and appear to be associated with comorbidities or disability-related characteristics. In this study, we aimed to determine the patient and health-system level factors associated with all-cause and unplanned hospital readmission within 90 days after acute stroke or transient ischemic attack (TIA) in Australia. Methods— We used person-level linkages between data from the Australian Stroke Clinical Registry (2009–2013), hospital admissions data and national death registrations from 4 Australian states. Time to first readmission (all-cause or unplanned) for discharged patients was examined within 30, 90, and 365 days, using competing risks regression to account for deaths postdischarge. Covariates included age, stroke severity (ability to walk on admission), stroke type, admissions before stroke/TIA and the Charlson Comorbidity Index (derived from International Statistical Classification of Diseases and Related Health Problems, Tenth Revision , [Australian modified] coded hospital data in the preceding 5 years). Results— Among the 13 594 patients discharged following stroke/TIA (45% female; 65% ischemic stroke; 11% intracerebral hemorrhage; 4% undetermined stroke; and 20% TIA), 25% had an all-cause readmission and 15% had an unplanned readmission within 90 days. In multivariable analyses, the factors independently associated with a greater risk of unplanned readmission within 90 days were being female (subhazard ratio, 1.13 [95% CI, 1.03–1.24]), greater Charlson Comorbidity Index scores (subhazard ratio, 1.11 [95% CI, 1.09–1.12]) and having an admission ≤90 days before the index event (subhazard ratio, 1.85 [95% CI, 1.59–2.15]). Compared with being discharged to rehabilitation or aged care, those who were discharged directly home were more likely to have an unplanned readmission within 90 days (subhazard ratio, 1.44 [95% CI, 1.33–1.55]). These factors were similar for readmissions within 30 and 365 days. Conclusions— Apart from comorbidities and patient-level characteristics, readmissions after stroke/TIA were associated with discharge destination. Greater support for transition to home after stroke/TIA may be needed to reduce unplanned readmissions.
People who are prescribed antihypertensive medications at discharge from hospital after a stroke or TIA demonstrate better cardiovascular and all-cause survival outcomes than those not prescribed these agents.
Folate deficiency is an uncommon cause of pyrexia. We describe the case of a 29-year-old male who presented with a pyrexial illness subsequently attributed to megaloblastic anaemia secondary to severe folate deficiency, after exclusion of other infective or inflammatory causes. A temperature chart documenting the course of the patient's pyrexia is presented and potential pathophysiological mechanisms are proposed. Folate deficiency is a reversible cause of pyrexia that should be considered in any patient who presents with a pyrexial illness of unknown cause. Case presentationA 29-year-old caucasian male presented to our medical admissions unit complaining of a 6 week history of dyspnoea on exertion, recurrent fevers and sweats. He had a 7 year history of alcohol excess, drinking 3-4 litres of cider per day. He was a smoker of 10 cigarettes per day, but was otherwise fit and well with no significant past medical or family history. The patient reported no other symptoms and did not take any regular medication.Examination revealed a pulse rate of 124 beats/minute and a blood pressure of 120 mmHg/48 mmHg. He was noted to be febrile with a temperature of 38.8°C. Oxygen saturations were 100% on room air with no signs of respiratory distress. He had visibly pale conjunctiva and a lemon yellow tint to the skin (but no evidence of icteric sclerae). There were no signs of chronic liver disease and no peripheral stigmata of bacterial endocarditis. Cardiovascular examination revealed a collapsing pulse and a soft systolic murmur audible at the left sternal edge. Auscultation of the chest revealed vesicular breath sounds with no added sounds. On abdominal examination there was palpable splenomegaly but not other organomegaly or ascites. Neurological examination was normal with was no evidence of neck stiffness or skin rashes.Admission blood tests revealed a severe pancytopenia with a raised mean cell volume (see table 1). Also notable was a mild hyperbilirubinaemia but otherwise normal liver function with no evidence of impaired hepatic synthetic function (normal serum albumin and normal prothrombin time).Subsequently, serum folate levels were found to be low at 1.2 ug/L (normal range 4-24 ug/L) and vitamin B 12 levels were low-normal at 202 ng/L (normal range 180-900 ng/ L). Iron studies were normal. Initial blood film and subsequent bone marrow examination confirmed a severe megaloblastic picture, consistent with folate deficiency.Urine dip test and subsequent urine cultures were negative. Three sets of blood cultures were taken from different sites (before commencement of antibiotics) but were all negative after 5 days culture. Chest radiograph was nor-
The prevalence of stroke increases each year and while mortality from stroke has decreased, the prevalence of comorbidities such as anxiety, depression and fatigue affects as many as 75% of stroke survivors. The aetiology of post-stroke fatigue is not clear, although it has been shown to be interrelated with comorbidities such as stress and depression. Due to the interconnected nature of these comorbidities, it is important to improve the specificity of diagnosis and identify novel therapeutic targets to improve the quality of life for stroke survivors. The investigation of molecular biomarkers associated with post-stroke stress, fatigue, and depression may shed light on the relationships between comorbidities and also contribute to the development of novel diagnostics and therapies. Several biomarkers have been identified for stress, depression, and fatigue, some of which are specific to stroke survivors. However, there remain several gaps in understanding, particularly in relation to the physiological mechanisms underlying these side effects and molecular biomarkers associated with post-stroke fatigue. The aim of this scoping review protocol is to outline the methodologies that will be used to provide a comprehensive understanding of the current literature on biomarkers associated with post-stroke fatigue, stress, and depression, informing future research questions.
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