scholarly journals COVID-19-Associated Acute Brain Dysfunction Related to Sepsis

2021 ◽  
Vol 13 (2) ◽  
pp. 82-91
Author(s):  
Dao Ming Tong ◽  
Ye Ting Zhou ◽  
Yuan Wei Wang
Keyword(s):  
Brain Dysfunction ◽  
Acute Brain Dysfunction

scholarly journals 3217 Catatonia, Delirium and Coma: Implications for Mortality

2019 ◽  
Vol 3 (s1) ◽  
pp. 37-37
Author(s):  
Jo Ellen Wilson ◽  
Sarasota Mihalko ◽  
Stephan Heckers ◽  
Pratik P. Pandharipande ◽  
Timothy D. Girard ◽  
...  
Keyword(s):  
Survival Time ◽  
Critically Ill ◽  
Median Survival ◽  
Critically Ill Patients ◽  
Median Survival Time ◽  
Rating Scale ◽  
Brain Dysfunction ◽  
Survival Times ◽  
Dsm 5 ◽  
Acute Brain Dysfunction

OBJECTIVES/SPECIFIC AIMS: Delirium, a form of acute brain dysfunction, characterized by changes in attention and alertness, is a known independent predictor of mortality in the Intensive Care Unit (ICU). We sought to understand whether catatonia, a more recently recognized form of acute brain dysfunction, is associated with increased 30-day mortality in critically ill older adults. METHODS/STUDY POPULATION: We prospectively enrolled critically ill patients at a single institution who were on a ventilator or in shock and evaluated them daily for delirium using the Confusion Assessment for the ICU and for catatonia using the Bush Francis Catatonia Rating Scale. Coma, was defined as a Richmond Agitation Scale score of −4 or −5. We used the Cox Proportional Hazards model predicting 30-day mortality after adjusting for delirium, coma and catatonia status. RESULTS/ANTICIPATED RESULTS: We enrolled 335 medical, surgical or trauma critically ill patients with 1103 matched delirium and catatonia assessments. Median age was 58 years (IQR: 48 - 67). Main indications for admission to the ICU included: airway disease or protection (32%; N=100) or sepsis and/or shock (25%; N=79. In the unadjusted analysis, regardless of the presence of catatonia, non-delirious individuals have the highest median survival times, while delirious patients have the lowest median survival time. Comparing the absence and presence of catatonia, the presence of catatonia worsens survival (Figure 1). In a time-dependent Cox model, comparing non-delirious individuals, holding catatonia status constant, delirious individuals have 1.72 times the hazards of death (IQR: 1.321, 2.231) while those with coma have 5.48 times the hazards of death (IQR: 4.298, 6.984). For DSM-5 catatonia scores, a 1-unit increase in the score is associated with 1.18 times the hazards of in-hospital mortality. Comparing two individuals with the same delirium status, an individual with a DSM-5 catatonia score of 0 (no catatonia) will have 1.178 times the hazard of death (IQR: 1.086, 1.278), while an individual with a score of 3 catatonia items (catatonia) present will have 1.63 times the hazard of death. DISCUSSION/SIGNIFICANCE OF IMPACT: Non-delirious individuals have the highest median survival times, while those who are comatose have the lowest median survival times after a critical illness, holding catatonia status constant. Comparing the absence and presence of catatonia, the presence of catatonia seems to worsen survival. Those individual who are both comatose and catatonic have the lowest median survival time.

Diurnal Sedative Changes During Intensive Care: Impact On Acute Brain Dysfunction And Liberation From Mechanical Ventilation

2011 ◽  
Author(s):  
Christopher W. Seymour ◽  
Renee E. Torres ◽  
Pratik P. Pandharipande ◽  
Tyler Koestner ◽  
Leonard D. Hudson ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Intensive Care ◽  
Brain Dysfunction ◽  
Acute Brain Dysfunction

Diagnosing acute brain dysfunction due to sepsis

2019 ◽  
Vol 41 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Figen Esen ◽  
Günseli Orhun ◽  
Perihan Ergin Özcan ◽  
Andres R. Brenes Bastos ◽  
Erdem Tüzün
Keyword(s):  
Brain Dysfunction ◽  
Acute Brain Dysfunction

scholarly journals Change in endothelial vascular reactivity and acute brain dysfunction during critical illness

2015 ◽  
Vol 115 (5) ◽  
pp. 794-795 ◽  
Author(s):  
C.G. Hughes ◽  
N.E. Brummel ◽  
T.D. Girard ◽  
A.J. Graves ◽  
E.W. Ely ◽  
...  
Keyword(s):  
Critical Illness ◽  
Vascular Reactivity ◽  
Brain Dysfunction ◽  
Acute Brain Dysfunction

scholarly journals Procalcitonin and C-reactive protein levels at admission as predictors of duration of acute brain dysfunction in critically ill patients

Critical Care ◽  
2011 ◽  
Vol 15 (2) ◽  
pp. R78 ◽  
Author(s):  
Stuart McGrane ◽  
Timothy D Girard ◽  
Jennifer L Thompson ◽  
Ayumi K Shintani ◽  
Alison Woodworth ◽  
...  
Keyword(s):  
Critically Ill ◽  
Critically Ill Patients ◽  
Brain Dysfunction ◽  
C Reactive Protein ◽  
Protein Levels ◽  
Reactive Protein ◽  
Acute Brain Dysfunction

scholarly journals Acute Brain Dysfunction

CHEST Journal ◽  
2018 ◽  
Vol 154 (2) ◽  
pp. 293-301 ◽  
Author(s):  
Annachiara Marra ◽  
Pratik P. Pandharipande ◽  
Matthew S. Shotwell ◽  
Rameela Chandrasekhar ◽  
Timothy D. Girard ◽  
...  
Keyword(s):  
Brain Dysfunction ◽  
Acute Brain Dysfunction

Pathophysiology of acute brain dysfunction

2012 ◽  
Vol 18 (5) ◽  
pp. 518-526 ◽  
Author(s):  
Christopher G. Hughes ◽  
Mayur B. Patel ◽  
Pratik P. Pandharipande
Keyword(s):  
Brain Dysfunction ◽  
Acute Brain Dysfunction

Naphthalene Toxicity in Clinical Practice

2020 ◽  
Vol 21 (1) ◽  
pp. 63-66
Author(s):  
Ashok Kumar Pannu ◽  
Vidhi Singla
Keyword(s):  
Methylene Blue ◽  
G6pd Deficiency ◽  
Brain Dysfunction ◽  
Laboratory Evaluation ◽  
Cochrane Library ◽  
High Morbidity ◽  
High Quality ◽  
Quality Literature ◽  
Acute Brain Dysfunction ◽  
The Cochrane Library

Background: Naphthalene ingestion and skin or inhalational exposure (accidental or deliberate) is an under-recognized cause of a severe toxidrome in regions where it is commonly used (e.g., mothballs in households). Methods: This review is an update for the clinicians to understand the pharmacology, clinical features, laboratory evaluation, and treatment for naphthalene toxicity. High-quality literature for the past eight decades was collected and reviewed in this article. Several landmark articles were reviewed using PubMed, EMBASE Ovid, and the Cochrane Library, which have essential implications in the current toxicology practice. Results and Conclusion: Naphthalene toxicity usually occurs abruptly and leads to acute hemolysis, methemoglobinemia, renal failure, respiratory depression, and acute brain dysfunction that are difficult to manage. The toxicity is more marked in patients with G6PD deficiency and associated with high morbidity and mortality. The management should mainly focus on high-quality supportive care; however, severe methemoglobinemia (>20-30%) requires specific therapy with intravenous methylene blue. Methylene blue is a highly effective agent but contraindicated in severe G6PD deficiency.

Mechanisms of action of intravenous immunoglobulin in septic encephalopathy

2018 ◽  
Vol 29 (4) ◽  
pp. 417-423 ◽  
Author(s):  
Figen Esen ◽  
Perihan Ergin Ozcan ◽  
Erdem Tuzun ◽  
M. Dustin Boone
Keyword(s):  
Intravenous Immunoglobulin ◽  
Apoptotic Cell ◽  
Brain Dysfunction ◽  
Ivig Treatment ◽  
Neuronal Dysfunction ◽  
Septic Encephalopathy ◽  
Behavioral Deficits ◽  
Classical Complement Pathway ◽  
Acute Brain Dysfunction ◽  
Glial Cell Proliferation

Abstract Acute brain dysfunction associated with sepsis is a serious complication that results in morbidity and mortality. Intravenous immunoglobulin (IVIg) treatment is known to alleviate behavioral deficits in the experimentally induced model of sepsis. To delineate the mechanisms by which IVIg treatment prevents neuronal dysfunction, an array of immunological and apoptosis markers was investigated. Our results suggest that IVIgG and IgGAM administration ameliorates neuronal dysfunction and behavioral deficits by reducing apoptotic cell death and glial cell proliferation. IgGAM treatment might suppress classical complement pathway by reducing C5a activity and proapoptotic NF-κB and Bax expressions, thereby, inhibiting major inflammation and apoptosis cascades. Future animal model experiments performed with specific C5aR and NF-κB agonists/antagonists or C5aR-deficient mice might more robustly disclose the significance of these pathways. C5a, C5aR, and NF-κB, which were shown to be the key molecules in brain injury pathogenesis in sepsis, might also be utilized as potential targets for future treatment trials of septic encephalopathy.

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