scholarly journals Where Did the Pericardial Effusion Go? A Case of Cardiopulmonary Resuscitation Acting as Treatment for Pericardial Tamponade

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Varun tej Gonuguntla ◽  
Parita Soni ◽  
Nishil Dalsania ◽  
Ravi Karan Patti ◽  
Somal Navjot ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Organ Damage ◽  
Pericardial Tamponade ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Therapeutic Treatment ◽  
Life Saving ◽  
Saving Measure ◽  
Thoracic Organ

Pericardial tamponade results in multiple organ dysfunction and can lead to cardiac arrest. Cardiopulmonary resuscitation (CPR), a life-saving measure performed on patients in cardiac arrest, can lead to thoracic organ damage. However, CPR rarely acts as a therapeutic treatment for pericardial tamponade. Our case describes a patient admitted with pericardial tamponade in whom CPR provided therapeutic treatment with pericardial rupture and resolution of the tamponade.

ORGAN DAMAGE IS PRECEDED BY CHANGES IN PROTEIN EXTRAVASATION IN AN EXPERIMENTAL MODEL OF THE MULTIPLE ORGAN DYSFUNCTION SYNDROME

Shock ◽  
1997 ◽  
Vol 7 (Supplement) ◽  
pp. 10-11 ◽  
Author(s):  
Grard AP Nieuwenhuijzen ◽  
Maarten FCM Knapen ◽  
Wim JG Oyen ◽  
Thijs Hendriks ◽  
Frans HM Corstens ◽  
...  
Keyword(s):  
Experimental Model ◽  
Organ Dysfunction ◽  
Multiple Organ Dysfunction Syndrome ◽  
Organ Damage ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Protein Extravasation

ORGAN DAMAGE IS PRECEDED BY CHANGES IN PROTEIN EXTRAVASATION IN AN EXPERIMENTAL MODEL OF MULTIPLE ORGAN DYSFUNCTION SYNDROME

Shock ◽  
1997 ◽  
Vol 7 (2) ◽  
pp. 98-104 ◽  
Author(s):  
Grard A.P. Nieuwenhuijzen ◽  
Maarten F.C.M. Knapen ◽  
Wim J.G. Oyen ◽  
Thijs Hendriks ◽  
Frans H.M. Corstens ◽  
...  
Keyword(s):  
Experimental Model ◽  
Organ Dysfunction ◽  
Multiple Organ Dysfunction Syndrome ◽  
Organ Damage ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Protein Extravasation

scholarly journals Wnt-Signaling Inhibitor Wnt-C59 Suppresses the Cytokine Upregulation in Multiple Organs of Lipopolysaccharide-Induced Endotoxemic Mice via Reducing the Interaction between β-Catenin and NF-κB

2021 ◽  
Vol 22 (12) ◽  
pp. 6249
Author(s):  
Jaewoong Jang ◽  
Jaewon Song ◽  
Inae Sim ◽  
Young V. Kwon ◽  
Yoosik Yoon
Keyword(s):  
Wnt Signaling ◽  
Organ Dysfunction ◽  
Proinflammatory Cytokines ◽  
Host Response ◽  
Organ Damage ◽  
Suppressive Effect ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Multiple Organs

Sepsis is characterized by multiple-organ dysfunction caused by the dysregulated host response to infection. Until now, however, the role of the Wnt signaling has not been fully characterized in multiple organs during sepsis. This study assessed the suppressive effect of a Wnt signaling inhibitor, Wnt-C59, in the kidney, lung, and liver of lipopolysaccharide-induced endotoxemic mice, serving as an animal model of sepsis. We found that Wnt-C59 elevated the survival rate of these mice and decreased their plasma levels of proinflammatory cytokines and organ-damage biomarkers, such as BUN, ALT, and AST. The Wnt/β-catenin and NF-κB pathways were stimulated and proinflammatory cytokines were upregulated in the kidney, lung, and liver of endotoxemic mice. Wnt-C59, as a Wnt signaling inhibitor, inhibited the Wnt/β-catenin pathway, and its interaction with the NF-κB pathway, which resulted in the inhibition of NF-κB activity and proinflammatory cytokine expression. In multiple organs of endotoxemic mice, Wnt-C59 significantly reduced the β-catenin level and interaction with NF-κB. Our findings suggest that the anti-endotoxemic effect of Wnt-C59 is mediated via reducing the interaction between β-catenin and NF-κB, consequently suppressing the associated cytokine upregulation in multiple organs. Thus, Wnt-C59 may be useful for the suppression of the multiple-organ dysfunction during sepsis.

scholarly journals Cardiac Arrest/Cardiopulmonary Resuscitation Increases Anxiety-Like Behavior and Decreases Social Interaction

2004 ◽  
Vol 24 (4) ◽  
pp. 372-382 ◽  
Author(s):  
Gretchen N. Neigh ◽  
Julia Kofler ◽  
Jessica L. Meyers ◽  
Valerie Bergdall ◽  
Krista M. D. La Perle ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cardiac Arrest ◽  
Social Interaction ◽  
Cardiopulmonary Resuscitation ◽  
Organ Damage ◽  
Central Nervous System Damage ◽  
Sensorimotor Deficits ◽  
Peripheral Organs ◽  
Behavioral Impairments

Advances in medical technology have increased the number of individuals who survive cardiac arrest/cardiopulmonary resuscitation (CPR). This increased incidence of survival has created a population of patients with behavioral and physiologic impairments. We used temperature manipulations to characterize the contribution of central nervous system damage to behavioral deficits elicited by 8 minutes of cardiac arrest/CPR in a mouse model. Once sensorimotor deficits were resolved, we examined anxiety-like behavior with the elevated plus maze and social interaction with an ovariectomized female. We hypothesized that anxiety-like behavior would increase and social interaction would decrease in mice subjected to cardiac arrest/CPR and that these changes would be attributable to central nervous system damage rather than damage to peripheral organs or changes orchestrated by the administration of epinephrine. Mice that were subjected to cardiac arrest/CPR while the peripheral organs, but not the brain, were protected by hypothermia exhibited increased anxiety-like behavior and decreased social interaction, whereas mice with hypothermic brains and peripheral organs during cardiac arrest/CPR did not exhibit behavioral impairments. The present study demonstrates that central nervous system damage from cardiac arrest/CPR results in increased anxiety and decreased social interaction and that these behavioral changes are not attributed to underlying sensorimotor deficits, dynamics of arrest and CPR, or peripheral organ damage.

Elevations of inflammatory markers PTX3 and sST2 after resuscitation from cardiac arrest are associated with multiple organ dysfunction syndrome and early death

2015 ◽  
Vol 53 (11) ◽  
Author(s):  
Giuseppe Ristagno ◽  
Tero Varpula ◽  
Serge Masson ◽  
Marta Greco ◽  
Barbara Bottazzi ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Organ Dysfunction ◽  
Multiple Organ Dysfunction Syndrome ◽  
Plasma Levels ◽  
Neurological Outcome ◽  
Inflammatory Markers ◽  
Early Death ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Icu Admission

AbstractA systemic inflammatory response is observed after cardiopulmonary resuscitation. We investigated two novel inflammatory markers, pentraxin 3 (PTX3) and soluble suppression of tumorigenicity 2 (sST2), in comparison with the classic high-sensitivity C-reactive protein (hsCRP), for prediction of early multiple organ dysfunction syndrome (MODS), early death, and long-term outcome after out-of-hospital cardiac arrest.PTX3, sST2, and hsCRP were assayed at ICU admission and 48 h later in 278 patients. MODS was defined as the 24 h non-neurological Sequential Organ Failure Assessment (SOFA) score ≥12. Intensive care unit (ICU) death and 12-month Cerebral Performance Category (CPC) were evaluated.In total, 82% of patients survived to ICU discharge and 48% had favorable neurological outcome at 1 year (CPC 1 or 2). At ICU admission, median plasma levels of hsCRP (2.8 mg/L) were normal, while levels of PTX3 (19.1 ng/mL) and sST2 (117 ng/mL) were markedly elevated. PTX3 and sST2 were higher in patients who developed MODS (p<0.0001). Admission levels of PTX3 and sST2 were also higher in patients who died in ICU and in those with an unfavorable 12-month neurological outcome (p<0.01). Admission levels of PTX3 and sST2 were independently associated with subsequent MODS [OR: 1.717 (1.221–2.414) and 1.340, (1.001–1.792), respectively] and with ICU death [OR: 1.536 (1.078–2.187) and 1.452 (1.064–1.981), respectively]. At 48 h, only sST2 and hsCRP were independently associated with ICU death.Higher plasma levels of PTX3 and sST2, but not of hsCRP, at ICU admission were associated with higher risk of MODS and early death.

GRADUAL DEVELOPMENT OF ORGAN DAMAGE IN THE MURINE ZYMOSAN-INDUCED MULTIPLE ORGAN DYSFUNCTION SYNDROME

Shock ◽  
1997 ◽  
Vol 8 (4) ◽  
pp. 261-267 ◽  
Author(s):  
Monique J. J. M. Jansen ◽  
Thijs Hendriks ◽  
Albert A. J. Verhofstad ◽  
Wil Lange ◽  
Leo M. G. Geeraedts ◽  
...  
Keyword(s):  
Organ Dysfunction ◽  
Multiple Organ Dysfunction Syndrome ◽  
Organ Damage ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Gradual Development

473: MULTIPLE ORGAN DYSFUNCTION PREVALENCE FOLLOWING OUT-OF-HOSPITAL CARDIAC ARREST IN PEDIATRICS

2018 ◽  
Vol 46 (1) ◽  
pp. 220-220
Author(s):  
Kelly Corbett ◽  
Yizhe Xu ◽  
Angela Presson ◽  
Susan Bratton ◽  
Rebecca Dixon
Keyword(s):  
Cardiac Arrest ◽  
Organ Dysfunction ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Hospital Cardiac Arrest
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