Status and perspectives of hospital mortality in a public urban Hellenic hospital, based on a five-year review

<p>Abstract</p> <p>Background</p> <p>Analysis of hospital mortality helps to assess the standards of health-care delivery.</p> <p>Methods</p> <p>This is a retrospective cohort study evaluating the causes of deaths which occurred during the years 1995–1999 in a single hospital. The causes of death were classified according to the International Statistical Classification of Diseases (ICD-10).</p> <p>Results</p> <p>Of the 149,896 patients who were discharged the 5836 (3.4%) died. Males constituted 55% and females 45%. The median age was 75.1 years (1 day – 100 years).</p> <p>The seven most common ICD-10 chapters IX, II, IV, XI, XX, X, XIV included 92% of the total 5836 deaths.</p> <p>The most common contributors of non-neoplasmatic causes of death were cerebrovascular diseases (I60–I69) at 15.8%, ischemic heart disease (I20–I25) at 10.3%, cardiac failure (I50.0–I50.9) at 7.9%, diseases of the digestive system (K00–K93) at 6.7%, diabetes mellitus (E10–E14) at 6.6%, external causes of morbidity and mortality (V01–Y98) at 6.2%, renal failure (N17–N19) at 4.5%, influenza and pneumonia (J10–J18) at 4.1% and certain infectious and parasitic diseases (A00–B99) at 3.2%, accounting for 65.3% of the total 5836 deaths.</p> <p>Neoplasms (C00–D48) caused 17.7% (n = 1027) of the total 5836 deaths, with leading forms being the malignant neoplasms of bronchus and lung (C34) at 3.5% and the malignant neoplasms of large intestine (C18–21.2) at 1.5%. The highest death rates occurred in the intensive care unit (23.3%), general medicine (10.7%), cardiology (6.5%) and nephrology (5.5%).</p> <p>Key problems related to certification of death were identified. Nearly half of the deaths (49.3%: n = 2879) occurred by the completion of the third day, which indicates the time limits for investigation and treatment. On the other hand, 6% (n = 356) died between the 29^thand 262^nddays after admission.</p> <p>Inadequacies of the emergency care service, infection control, medical oncology, rehabilitation, chronic and terminal care facilities, as well as lack of regional targets for reducing mortality related to diabetes, recruitment of organ donors, provision for the aging population and lack of prevention programs were substantiated.</p> <p>Conclusion</p> <p>Several important issues were raised. Disease specific characteristics, as well as functional and infrastructural inadequacies were identified and provided evidence for defining priorities and strategies for improving the standards of care. Effective transformation can promise better prospects.</p

Therapeutic potential of transdermal glyceryl trinitrate in the management of acute stroke

The nitric oxide donor, glyceryl trinitrate (GTN), is a candidate treatment for the management of acute stroke with haemodynamic and potential reperfusion and neuroprotective effects. When administered as a transdermal patch during the acute and subacute phases after stroke, GTN was safe, lowered blood pressure, maintained cerebral blood flow, and did not induce cerebral steal or alter functional outcome. However, when given within 6 h of stroke onset, GTN reduced death and dependency (odds ratio 0.52; 95% confidence interval 0.34–0.78), death, disability, cognitive impairment and mood disturbance, and improved quality of life (data from two trials, n = 312). In a pooled analysis of four studies (n = 186), GTN reduced between-visit systolic blood pressure variability over days 1–7 compared with no GTN (mean difference -2.09; 95% confidence interval -3.83 to -0.35; p = 0.019). The efficacy of GTN given in the ultra-acute/pre-hospital setting is currently being assessed and, if found to be beneficial, the implications for hyperacute stroke practice are significant. Here, we discuss the evidence to date, potential mechanisms of action and future possibilities, including unanswered questions, for the therapeutic potential of GTN in acute stroke

The Immune System in Stroke

Stroke represents an unresolved challenge for both developed and developing countries and has a huge socio-economic impact. Although considerable effort has been made to limit stroke incidence and improve outcome, strategies aimed at protecting injured neurons in the brain have all failed. This failure is likely to be due to both the incompleteness of modelling the disease and its causes in experimental research, and also the lack of understanding of how systemic mechanisms lead to an acute cerebrovascular event or contribute to outcome. Inflammation has been implicated in all forms of brain injury and it is now clear that immune mechanisms profoundly influence (and are responsible for the development of) risk and causation of stroke, and the outcome following the onset of cerebral ischemia. Until very recently, systemic inflammatory mechanisms, with respect to common comorbidities in stroke, have largely been ignored in experimental studies. The main aim is therefore to understand interactions between the immune system and brain injury in order to develop novel therapeutic approaches. Recent data from clinical and experimental research clearly show that systemic inflammatory diseases -such as atherosclerosis, obesity, diabetes or infection - similar to stress and advanced age, are associated with dysregulated immune responses which can profoundly contribute to cerebrovascular inflammation and injury in the central nervous system. In this review, we summarize recent advances in the field of inflammation and stroke, focusing on the challenges of translation between pre-clinical and clinical studies, and potential anti-inflammatory/immunomodulatory therapeutic approaches

Left atrial and left atrial appendage functional abnormalities in patients with cardioembolic stroke in sinus rhythm and idiopathic atrial fibrillation

Thrombogenesis in the left atrial appendage (LAA) has been related to the special morphology of this cavity and to its size and degree of dysfunction. However, no study has focused on LAA function in conjunction with left atrial (LA) function in both sinus rhythm (SR) and nonrheumatic idiopathic atrial fibrillation (AE) in relation to clinical status (cardioembolic stroke). Forty-three patients in SR (14 patients with stroke, 29 control subjects) and 45 patients in AF (27 patients with stroke, 18 control subjects) were examined by transthoracic and transesophageal echocardiography. Baseline clinical characteristics and standard transthoracic and transesophageal measurements of the LA and LAA (size, fractional area change, flow measurements, spontaneous echo contrast, and thrombus) were recorded and compared in relation to cardiac rhythm. Patients in the stroke-SR group showed a significant decrease of fractional area change in the LA (32% +/- 15%) and LAA (34% +/- 15%) in relation to control subjects (43% +/- 10%, p = 0.035, 49% +/- 13%, p = 0.006, respectively). Patients in the stroke-AF group showed significant reduction of appendage flow measurements (outward velocity = 22 +/- 13 vs 33 +/- 19 cm/sec, p = 0.036), whereas no differences were detected in the center of the LA. In multiple regression analysis, the presence of cardioembolic stroke was positively associated with the presence of spontaneous echo contrast (p = 0.0253) and spontaneous echo contrast negatively associated with appendage inward flow velocity (p &lt; 0.001). Cardioembolic stroke in patients in SR is associated with a global decrease of shortening in both cavities and in patients with AE, with a reduction of LAA flow parameters. Patients with spontaneous echo contrast, thrombus, or both showed further reduction of shortening and flow velocities in both cavities, indicating a more advanced stage of dysfunction

Blood pressure course in acute ischaemic stroke in relation to stroke subtype

Objectives Blood pressure (BP) management in acute stroke remains a matter of little consensus. Data on BP changes during the first hours of ictus are lacking. We aimed to evaluate the early spontaneous time course of BP in different ischaemic stroke (IS) subtypes. Methods Twenty-four h BP monitoring was performed in 200 first-ever hyper-acute IS patients. The recording was initiated and terminated at 3 h and 27 h of ictus respectively. All IS patients were classified on admission into the following subgroups of different etiology: large artery atherosclerotic stroke (LAA), cardio-embolic stroke (CE), lacunar stroke (LAC) and infarct of undetermined cause (IUC). Statistical comparisons between stroke subgroups were performed using one-way ANOVA and linear regression analyses were used to evaluate the influence of different factors in BP course. Results Although there were no significant differences in 24 h systolic (SBP) and diastolic (DBP) BP values between IS subgroups, a distinctly different SBP course was observed. The SBP dropped sharply in the LAA and LAC subgroups, while a more gradual decrease was monitored in the CE subgroup. Throughout the BP-recording, a SBP decrease of 10.1% (95% CI: 8.6-11.5) and 10.4% (95% CI: 9.0-11.8) was documented in patients with LAA and LAC respectively, while a milder drop was recorded in CE (3.7%, 95% CI: 2.4-5.0) and IUC (5.5%, 95% CI: 4.1-6.8). Increasing stroke severity (p&lt;0.001) and brain oedema (p=0.013) was independently associated with a milder spontaneous SBP reduction. Conclusions Spontaneous SBP course varies in acute ischaemic stroke subtypes of different etiology. This may have implications in the optimal management of post-stroke hypertension. (C) 2004 Lippincott Williams Wilkins

Stroke etiology is associated with symptom onset during sleep

Background and Objectives: Almost every fifth stroke occurs during sleep. Data about characteristics and etiology of stroke during sleep are conflicting. We investigated the association of the activity at stroke onset (onset during night sleep vs. onset while awake) with stroke subtypes of different etiology. Methods: A total of 1448 patients with first-ever stroke with known time of symptom presentation were prospectively evaluated. Statistical comparisons were performed between patients with stroke during sleep and stroke while awake in terms of demographic features, known risk factors, vascular comorbidities, and stroke subtypes. Multiple variable logistic regression analyses were performed to identify predictor variables (including stroke risk factors and stroke subtypes) for stroke during sleep, Results: Stroke during sleep was documented in 264 cases (18.2%). In subjects with stroke during sleep, lacunar infarction was the most prevalent stroke subtype (39%), while in patients with stroke while awake, small-vessel disease was the underlying mechanism significantly (P &lt; .001) less often (13.8%). In contrast, patients with stroke while awake suffered significantly (P &lt; .001) more frequently from intracerebral hemorrhage (18.2%) and cardioembolic stroke (34.9%) when compared with subjects with stroke during sleep (6.4% and 18.9%, respectively). The multiple variable logistic regression model identified the following factors as independent predictors of stroke during sleep: atrial fibrillation (odds ratio: 0.346, 95% confidence interval: 0.237-0.505, P &lt; .001) and intracerebral hemorrhage versus ischemic stroke (odds ratio: 0.238, 95% confidence interval: 0.138-0.410, P &lt; .001). Lacunar infarction was the only ischemic stroke subgroup that was positively associated with stroke during sleep (odds ratio: 2.568, 95% confidence interval: 1.447-4.560, P &lt; .001). Conclusions: There are significant differences between stroke during sleep and stroke while awake concerning vascular risk profile and stroke etiologic subtypes