Mostrando entradas con la etiqueta shock. Mostrar todas las entradas
Mostrando entradas con la etiqueta shock. Mostrar todas las entradas

lunes, 8 de enero de 2018

Shock

Enero 7, 2018. No. 2956
El sangriento desastre de la transfusión de glóbulos rojos.
The bloody mess of red blood cell transfusion.
Crit Care. 2017 Dec 28;21(Suppl 3):310. doi: 10.1186/s13054-017-1912-x.
Abstract
Red blood cell (RBC) transfusion might be life-saving in settings with acute blood loss, especially uncontrolled haemorrhagic shock. However, there appears to be a catch-22 situation reflected by the facts that preoperative anaemia represents an independent risk factor for postoperative morbidity and mortality, and that RBC transfusion might also contribute to adverse clinical outcomes. This dilemma is further complicated by the difficulty to define the "best" transfusion trigger and strategy. Since one size does obviously not fit all, a personalised approach is merited. Attempts should thus be made to critically reflect on the pros and cons of RBC transfusion in each individual patient. Patient blood management concepts including preoperative, intraoperative and postoperative optimisation strategies involving the intensive care unit are warranted and are likely to provide benefits for the patients and the healthcare system. In this context, it is important to consider that "simply" increasing the haemoglobin content, and in proportion oxygen delivery, may not necessarily contribute to a better outcome but potentially the contrary in the long term. The difficulty lies in identification of the patients who might eventually profit from RBC transfusion and to determine in whom a transfusion might be withheld without inducing harm. More robust clinical data providing long-term outcome data are needed to better understand in which patients RBC transfusion might be life-saving vs life-limiting.
Una revisión sistemática de las estrategias neuroprotectoras durante la hipovolemia y el shock hemorrágico.
A Systematic Review of Neuroprotective Strategies during Hypovolemia and Hemorrhagic Shock.
Int J Mol Sci. 2017 Oct 26;18(11). pii: E2247. doi: 10.3390/ijms18112247.
Abstract
Severe trauma constitutes a major cause of death and disability, especially in younger patients. The cerebral autoregulatory capacity only protects the brain to a certain extent in states of hypovolemia; thereafter, neurological deficits and apoptosis occurs. We therefore set out to investigate neuroprotective strategies during haemorrhagic shock. This review was performed in accordance to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Before the start of the search, a review protocol was entered into the PROSPERO database. A systematic literature search of Pubmed, Web of Science and CENTRAL was performed in August 2017. Results were screened and evaluated by two researchers based on a previously prepared inclusion protocol. Risk of bias was determined by use of SYRCLE's risk of bias tool. The retrieved results were qualitatively analysed. Of 9093 results, 119 were assessed in full-text form, 16 of them ultimately adhered to the inclusion criteria and were qualitatively analyzed. We identified three subsets of results: (1) hypothermia; (2) fluid therapy and/or vasopressors; and (3) other neuroprotective strategies (piracetam, NHE1-inhibition, aprotinin, human mesenchymal stem cells, remote ischemic preconditioning and sevoflurane). Overall, risk of bias according to SYRCLE's tool was medium; generally, animal experimental models require more rigorous adherence to the reporting of bias-free study design (randomization, etc.). While the individual study results are promising, the retrieved neuroprotective strategies have to be evaluated within the current scientific context-by doing so, it becomes clear that specific promising neuroprotective strategies during states of haemorrhagic shock remain sparse. This important topic therefore requires more in-depth research.
KEYWORDS: bleeding; brain damage; haemorrhage; hypovolemia; neuroprotection; neuroprotective strategies; resuscitation; shock
Shock hemorrágico
Shock, Hemorrhagic.
Authors
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2017-.
2017 Nov 27.
Excerpt
Shock refers to the inadequate perfusion of tissues due to the imbalance between oxygen demand of tissues and the body's ability to supply it. Classically, there are four categories of shock: hypovolemic, cardiogenic, obstructive, and distributive shock. Hypovolemic shock occurs when there is decreased intravascular volume to the point of cardiovascular compromise. The hypovolemic shock could be due to severe dehydration through a variety of mechanisms or from blood loss. The pathophysiology, diagnosis, and treatment of hemorrhagic shock, a subset of hypovolemic shock, will be explored in this article.
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Anestesiología y Medicina del Dolor

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lunes, 10 de abril de 2017

Choque compensado en el trauma


Compensated Shock In Trauma Patients

Fuente
Este artículo es originalmente publicado en:
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Courtesy: Prof Nabil Ebraheim, University of Toledo, Ohio, USA
Dr. Ebraheim’s educational animated video describes the condition of compensated shock in trauma patients.
Donate to the University of Toledo Foundation Department of Orthopaedic Surgery Endowed Chair Fund:
https://www.utfoundation.org/foundati…
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miércoles, 25 de enero de 2017

Shock cardiogénico / Cardiogenic shock

Enero 25, 2017. No. 2580



  


Shock cardiogénico: Falla de la entrega y uso del oxígeno
Cardiogenic Shock: Failure of Oxygen Delivery and Oxygen Utilization.
Clin Cardiol. 2016 Aug;39(8):477-83. doi: 10.1002/clc.22564. Epub 2016 Aug 10.
Abstract
Cardiogenic shock remains a highly lethal condition. Conventional therapy including revascularization and mechanical circulatory support aims to improve cardiac output and oxygen delivery, but increasing basic and clinical observations indicate wider circulatory and cellular abnormalities, particularly at the advanced stages of shock. Progressive cardiogenic shock is associated with microcirculatory and cellular abnormalities. Cardiogenic shock is initially characterized by a failure to maintain global oxygen delivery; however, progressive cardiogenic shock is associated with the release of pro-inflammatory cytokines, derangement of the regulation of regional blood flow, microcirculatory abnormalities, and cellular dysoxia. These abnormalities are analogous to septic shock and may not be reversed by increase in oxygen delivery, even to supranormal levels. Earlier mechanical circulatory support in cardiogenic shock may limit the development of microcirculatory and cellular abnormalities.
Adrenomedulina. Un marcador de daño hemodinámico, disfunción orgánica y mal pronóstico en shock cardiogénico
Adrenomedullin: a marker of impaired hemodynamics, organ dysfunction, and poor prognosis in cardiogenic shock.
Ann Intensive Care. 2017 Dec;7(1):6. doi: 10.1186/s13613-016-0229-2. Epub 2017 Jan 4.
Abstract
BACKGROUND: The clinical CardShock risk score, including baseline lactate levels, was recently shown to facilitate risk stratification in patients with cardiogenic shock (CS). As based on baseline parameters, however, it may not reflect the change in mortality risk in response to initial therapies. Adrenomedullin is a prognostic biomarker in several cardiovascular diseases and was recently shown to associate with hemodynamic instability in patients with septic shock. The aim of our study was to evaluate the prognostic value and association with hemodynamic parameters of bioactive adrenomedullin (bio-ADM) in patients with CS. METHODS: CardShock was a prospective, observational, European multinational cohort study of CS. In this sub-analysis, serial plasma bio-ADM and arterial blood lactate measurements were collected from 178 patients during the first 10 days after detection of CS. RESULTS: Both bio-ADM and lactate were higher in 90-day non-survivors compared to survivors at all time points (P < 0.05 for all). Lactate showed good prognostic value during the initial 24 h (AUC 0.78 at admission and 0.76 at 24 h). Subsequently, lactate returned normal (≤2 mmol/L) in most patients regardless of later outcome with lower prognostic value. By contrast, bio-ADM showed increasing prognostic value from 48 h and beyond (AUC 0.71 at 48 h and 0.80 at 5-10 days). Serial measurements of either bio-ADM or lactate were independent of and provided added value to CardShock risk score (P < 0.001 for both). Ninety-day mortality was more than double higher in patients with high levels of bio-ADM (>55.7 pg/mL) at 48 h compared to those with low bio-ADM levels (49.1 vs. 22.6%, P = 0.001). High levels of bio-ADM were associated with impaired cardiac index, mean arterial pressure, central venous pressure, and systolic pulmonary artery pressure during the study period. Furthermore, high levels of bio-ADM at 48 to 96 h were related to persistently impaired cardiac and end-organ function. CONCLUSIONS: Bio-ADM is a valuable prognosticator and marker of impaired hemodynamics in CS patients. High levels of bio-ADM may show shock refractoriness and developing end-organ dysfunction and thus help to guide therapeutic approach in patients with CS. Study identifier of CardShock study NCT01374867 at clinicaltrials.gov.
KEYWORDS: Adrenomedullin; Biomarkers; Cardiogenic shock; Hemodynamics; Lactate; Mortalit
Conceptos actuales en choque cardiogénico
Dr. Octavio González-Chon, Dr. Javier Sánchez-Zavala, Dr. Eduardo Arias-Sánchez, Dra.Sandra María del Carmen García-López
Revista Mexicana de Anestesisoslogía Vol. 32. Supl. 1, Abril-Junio 2009 pp S65-S67
5to curso internacional Anestesiologia cardiotoracica_ vascular_ ecocardiografia y circulaci_n extracorporea.


Curso Internacional de Actualidades en Anestesiología
Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán
Cuidad de México, Febrero 9-11, 2017
Informes  ceddem_innsz@yahoo.com 
Regional Anesthesiology and Acute Pain Medicine Meeting
April 6-8, 2017, San Francisco, California, USA
ASRA American Society of Regional Anesthesia and Pain Medicine
California Society of Anesthesiologists
Annual Meeting April 27-30, 2017
San Francisco California
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