Secondary Hematoma Expansion and Perihemorrhagic Edema after Intracerebral Hemorrhage: From Bench Work to Practical Aspects.

Intracerebral hemorrhages (ICH) represent about 10-15% of all strokes per year in the United States alone. Key variables influencing the long-term outcome after ICH are hematoma size and growth. Although death may occur at the time of the hemorrhage, delayed neurologic deterioration frequently occurs with hematoma growth and neuronal injury of the surrounding tissue. Perihematoma edema has also been implicated as a contributing factor for delayed neurologic deterioration after ICH. Cerebral edema results from both blood-brain barrier disruption and local generation of osmotically active substances. Inflammatory cellular mediators, activation of the complement, by-products of coagulation and hemolysis such as thrombin and fibrin, and hemoglobin enter the brain and induce a local and systemic inflammatory reaction. These complex cascades lead to apoptosis or neuronal injury. By identifying the major modulators of cerebral edema after ICH, a therapeutic target to counter degenerative events may be forthcoming

Pulmonary complications in patients with severe brain injury.

Pulmonary complications are prevalent in the critically ill neurological population. Respiratory failure, pneumonia, acute lung injury and the acute respiratory distress syndrome (ALI/ARDS), pulmonary edema, pulmonary contusions and pneumo/hemothorax, and pulmonary embolism are frequently encountered in the setting of severe brain injury. Direct brain injury, depressed level of consciousness and inability to protect the airway, disruption of natural defense barriers, decreased mobility, and secondary neurological insults inherent to severe brain injury are the main cause of pulmonary complications in critically ill neurological patients. Prevention strategies and current and future therapies need to be implemented to avoid and treat the development of these life-threatening medical complications

Research Reports from the Programme for Belize Archaeological Project, Volume Six

Table of Contents : Background and Introduction to the 2011 Season of the Programme for Belize Archaeological Project / by Fred Valdez, Jr. and Marisol Cortes-Rincon (p.1-4) -- Investigations at Structure 3, La Milpa: The 2011 Field Season / by Debora Trein (p.5-32) -- Report of the 2011 Excavations at the South Ballcourt of La Milpa, Op A6 / by David Chatelain (p.33-44) -- Summary of the 2011 Activities of the La Milpa Core Project / by Brett A. Houk and Gregory Zaro (p.45-54) -- Summary of 2011 Field Season: Examination of Extended Lineages Associated with Courtyards 135 & 149 at La Milpa, Belize / by Brandon S. Lewis (p.55-58) -- Report on a Northern Residential Complex at La Milpa, Belize: Operation LM4 / by Deanna M. Riddick (p.59-62) -- Preliminary Notes on a Chultun Burial at La Milpa – LM-4 / by Stacy Drake (p.63-68) -- Excavations at Groups B and C, Say Kah, Belize, 2011 / by Sarah E. Jackson and Linda A. Brown (p.69-102) -- Hun Tun Archaeology: Report on the 2011 Field Season / by Robyn L. Dodge (p.103-114) -- Aguada Lagunita Elusiva (RB Lagunita), La Milpa East (RB LME) and Results of the 2011 Explorations along the LaMap East Transect Extension / by Estella Weiss-Krejci and Michael Brandl (p.115-126) -- Towards a Biography Of Place: The 2011 Season of Survey and Excavation at La Milpa North / by Eric J. Heller (p.127-144) -- Phase 2 Research at Wari Camp (RB-56): Summer 2011 / by Laura Levi (p.145-152) -- Summary Report of Investigations at the Site of Dos Hombres: Summer 2011 / by Rissa M. Trachman and Katherine MacDonald (p.153-158) -- Preliminary Report on the 2011 Activities of the Mount Allison University Archaeological Field School in Belize / by Grant R. Aylesworth (p.159-162) -- Tree Species Composition at Medicinal Trail Group A / by Nicholas Brokaw and Sheila Ward (p.163-164) -- Report on Some Stone Tools from RB 18, Northwest Belize: Guijarral and the Chispas Group / by David M. Hyde (p.165)Texas Archeological Research Laborator

Current pathophysiological concepts in cerebral small vessel disease.

The association between cerebral small vessel disease (SVD) - in the form of white matter lesions, infarctions, and hemorrhages - with vascular cognitive impairment (VCI), has mostly been deduced from observational studies. Pathological conditions affecting the small vessels of the brain and leading to SVD have suggested plausible molecular mechanisms involved in vascular damage and their impact on brain function. However, much still needs to be clarified in understanding the pathophysiology of VCI, the role of neurodegenerative processes such as Alzheimer\u27s disease, and the impact of aging itself. In addition, both genetic predispositions and environmental exposures may potentiate the development of SVD and interact with normal aging to impact cognitive function and require further study. Advances in technology, in the analysis of genetic and epigenetic data, neuroimaging such as magnetic resonance imaging, and new biomarkers will help to clarify the complex factors leading to SVD and the expression of VCI

Novel Therapies for Intracerebral Hemorrhage

INTRODUCTION Intracerebral hemorrhage is by far the most destructive form of stroke1. Apart from the management in a specialized stroke or neurological intensive care unit (NICU), no specific therapies have been shown to consistently improve outcomes after ICH2. Current Guidelines endorse early aggressive optimization of physiologic derangements with ventilatory support when indicated, blood pressure control, reversal of any preexisting coagulopathy, intracranial pressure monitoring for certain cases, osmotherapy, temperature modulation, seizure prophylaxis, treatment of hyerglycemia, and nutritional support in the stroke unit or NICU. Ventriculostomy is the cornerstone of therapy for control of intracranial pressure patients with intraventricular hemorrhage. 3, 4 Surgical hematoma evacuation does not improve outcome for most patients, but is a reasonable option for patients with early worsening due to mass effect due to large cerebellar or lobar hemorrhages. Promising experimental treatments involve targeting of molecular mechanisms implicated in inflammation, blood product degradation, and secondary neuronal damage. Pages: 11-14

The Intensivist

The intensivist is the primary care physician of the ICU. Critically ill patients often have multiple acute and chronic illnesses requiring the careful integration of information and recommendations from multiple consultants. In addition to acting as a physician, intensivists commonly are administrators of an ICU. In 1992, the Society of Critical Care Medicine1 published its guidelines for the definition of an intensivist and the intensivist’s role in an ICU (Table 1)

Hypothermia and temperature modulation for intracerebral hemorrhage (ICH): pathophysiology and translational applications

BackgroundIntracerebral hemorrhage (ICH) still poses a substantial challenge in clinical medicine because of the high morbidity and mortality rate that characterizes it. This review article expands into the complex pathophysiological processes underlying primary and secondary neuronal death following ICH. It explores the potential of therapeutic hypothermia as an intervention to mitigate these devastating effects.MethodsA comprehensive literature review to gather relevant studies published between 2000 and 2023.DiscussionPrimary brain injury results from mechanical damage caused by the hematoma, leading to increased intracranial pressure and subsequent structural disruption. Secondary brain injury encompasses a cascade of events, including inflammation, oxidative stress, blood-brain barrier breakdown, cytotoxicity, and neuronal death. Initial surgical trials failed to demonstrate significant benefits, prompting a shift toward molecular mechanisms driving secondary brain injury as potential therapeutic targets. With promising preclinical outcomes, hypothermia has garnered attention, but clinical trials have yet to establish its definitive effectiveness. Localized hypothermia strategies are gaining interest due to their potential to minimize systemic complications and improve outcomes. Ongoing and forthcoming clinical trials seek to clarify the role of hypothermia in ICH management.ConclusionTherapeutic hypothermia offers a potential avenue for intervention by targeting the secondary injury mechanisms. The ongoing pursuit of optimized cooling protocols, localized cooling strategies, and rigorous clinical trials is crucial to unlocking the potential of hypothermia as a therapeutic tool for managing ICH and improving patient outcomes

Impact of Preadmission Beta-blocker Use on Cardiac Abnormalities and In-hospital Mortality in Patients with Aneurysmal Subarachnoid Hemorrhage

Introduction: Various cardiac abnormalities, including dysrhythmias, left ventricular (LV) dysfunction, and myocardial injury, are commonly seen after subarachnoid hemorrhage (SAH). In patients taking a beta-blocker (BB) chronically, the medication is generally discontinued after hospitalization due to the concern of compromising cerebral perfusion. We hypothesized that sudden BB discontinuation might inadvertently lead to an increased incidence of composite cardiac abnormalities and higher in-hospital mortality in patients presenting with nontraumatic SAH

Diagnostic Accuracy of Procalcitonin in Differentiating Sepsis from Noninfectious SIRS in Adult Patients with Subarachnoid Hemorrhage

Background: Subarachnoid hemorrhage (SAH) is a frequent diagnosis in the neuro-intensive care unit (NICU) that can result in the development of systemic inflammatory response syndrome (SIRS) and fever. The differentiation between central fever and infectious fever is paramount in order to prevent superfluous diagnostic testing and overuse of empiric antibiotics. Methods: A prospective chart review study conducted in the NICU between December 2012 and September 2015. Patients with SAH, fever (≥101.0°F) and/or who were SIRS positive and had PCT levels measured were included. The primary outcome was clinical infection defined as any positive culture or infiltrate on chest X-ray within three days of onset of fever. Results: Out of 129 patients, 54 were positive for any culture: 14 with PCT ≤0.2, 12 with PCT \u3e0.2 and ≤0.5, and 28 with PCT \u3e0.5. Using multiple logistic regression, PCT between 0.2-0.5 had an odds ratio of 2.99 (95% CI 1.12-8.00) while PCT \u3e0.5 had an odds ratio of 29.11 (CI 8.49-99.83) and p-value of \u3c0.001. All other predictors were not statistically significant. For procalcitonin \u3e0.5, specificity is 94.7%, sensitivity 51.9%, positive predictive value 87.5%, and negative predictive value 73.2%. ROC Curve area: 79.3%. Conclusion: PCT of 0.5 ng/mL or greater was useful for distinguishing infectious from central fever in SAH patients, with PCT values between 0.2-0.5 as somewhat predictive of infection. The test has high specificity and a reasonably high negative predictive value, so it can be a valuable tool to rule out infectious fever in patients with SAH