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.

Saturday, June 24, 2023

Relationship between serum bicarbonate levels and the risk of death within 30 days in ICU patients with acute ischemic stroke

Not telling us what the protocols are to reduce the 30-day mortality is criminal and made this research useless.

Relationship between serum bicarbonate levels and the risk of death within 30 days in ICU patients with acute ischemic stroke

Xia Huang1 and Yuanyuan Zhang2*
  • 1Department of Neurology, Ninghai First Hospital, Ningbo, Zhejiang, China
  • 2Emergency Medicine Department, Affiliated Hospital of Yangzhou University (Yangzhou First People's Hospital), Yangzhou, Jiangsu, China

Aim: To explore the relationship between baseline bicarbonate levels and their changes with 30-day mortality in patients with acute ischemic stroke who were admitted to the intensive care unit (ICU).

Methods: This cohort study collected the data of 4,048 participants from the Medical Information Mart for Intensive Care (MIMIC)-III and MIMIC-IV databases. Univariate and multivariable Cox proportional risk models were utilized to explore the relationship between bicarbonate T0 and Δbicarbonate with 30-day mortality in patients with acute ischemic stroke. The Kaplan–Meier curves were plotted to measure the 30-day survival probability of patients with acute ischemic stroke.

Results: The median follow-up time was 30 days. At the end of the follow-up, 3,172 patients survived. Bicarbonate T0 ≤ 21 mEq/L [hazard ratio (HR) = 1.24, a 95% confidence interval (CI): 1.02–1.50] or 21 mEq/L < bicarbonate T0 ≤ 23 mEq/L (HR = 1.29, 95%CI: 1.05–1.58) were associated with an increased risk of 30-day mortality in patients with acute ischemic stroke compared with bicarbonate T0 > 26 mEq/L. −2 mEq/L < Δbicarbonate ≤ 0 mEq/L (HR = 1.40, 95%CI: 1.14–1.71), 0 mEq/L < Δbicarbonate ≤ 2 mEq/L (HR = 1.44, 95%CI: 1.17–1.76), and Δbicarbonate >2 mEq/L (HR = 1.40, 95%CI: 1.15–1.71) were correlated with an elevated risk of 30-day mortality in acute ischemic stroke patients. The 30-day survival probability of acute ischemic stroke patients with 21 mEq/L < bicarbonate T0 ≤ 23 mEq/L, 23 mEq/L < bicarbonate T0 ≤ 26 mEq/L, or bicarbonate T0 >26 mEq/L was higher than that of patients with bicarbonate T0 ≤ 21 mEq/L. The 30-day survival probability was greater for patients in the Δbicarbonate ≤-2 mEq/L group than for those in the Δbicarbonate >2 mEq/L group.

Conclusion: Low baseline bicarbonate levels and decreased bicarbonate levels during the ICU stay were associated with a high risk of 30-day mortality in acute ischemic stroke patients. Special interventions should be offered(What the hell are they?) to those with low baseline and decreased bicarbonate levels during their ICU stay.

Introduction

Stroke remains one of the leading causes of death and a major cause of disability worldwide (1). Ischemic stroke accounts for 87% of all stroke cases. Acute ischemic stroke is considered a medical emergency due to the decreased blood flow to the brain and is characterized by sudden-onset numbness or weakness in the arm or the leg, facial drooping, difficulty speaking or understanding speech, confusion, trouble with balance or coordination, and the loss of vision (2). Although treatments, including intravenous thrombolysis (IVT) using tissue plasminogen activator (tPA), have improved the functional outcomes of patients with acute ischemic stroke, the prognosis of these patients remains poor (3). Stroke has caused ~5.8 million deaths (4) and is a tremendous financial burden (5). Identifying more reliable biomarkers for predicting the prognosis of patients with acute ischemic stroke could improve patient management and treatment.

In a previous study, endothelial dysfunction was reported to be one of the pathological mechanisms of ischemic stroke (6). Evidence shows that lower serum bicarbonate levels may be associated with endothelial dysfunction, and bicarbonate therapy can improve endothelial function in patients with chronic kidney disease (7, 8). However, researchers have found that peripheral blood electrolyte changes occurred after stroke and that alterations in cerebrovascular acid-base balance directly affected cerebral blood flow (9). Bicarbonate measurements are well-acknowledged as a clinically useful biomarker for assessing the acid-base status to diagnose various disease conditions (10, 11). A previous study indicated that, although there was no statistical significance between the serum bicarbonate levels and the mortality of stroke patients, the serum bicarbonate levels were also considered an important factor that correlated with the prognosis of stroke patients and were included in the prediction model for predicting 30-, 180-, and 360-day survival of stroke patients (12). Other studies have revealed that higher serum bicarbonate levels in patients with hypertension are associated with a higher risk of cardiovascular disease (13, 14). The role of bicarbonate levels in patients with cardiovascular diseases was conflicting. Thus, clarifying the association between serum bicarbonate levels and the risk of death in patients with acute ischemic stroke would be highly valuable. In addition, in severe cases, serum bicarbonate levels can fluctuate with changes in the patient's condition as a result of the treatments received (15). Evaluating the influence of the change in bicarbonate levels on the prognosis of patients with ischemic stroke may be valuable.

In this study, the associations between serum bicarbonate levels and their changes with 30-day mortality in patients with acute ischemic stroke were measured based on the data from the Medical Information Mart for Intensive Care (MIMIC)-III and MIMIC-IV databases. Subgroup analyses were stratified by age, the Charlson comorbidity index (CCI), thrombolysis, antiplatelet agents, and anticoagulation agents.

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