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Sudden Cardiac Death and Post Cardiac Arrest Syndrome. An Overview

References 1. Centers for Disease Control and Prevention (CDC). Statespecific mortality from sudden cardiac death - United States, 1999, MMWR Morb Mortal Wkly Rep, 2002;51:123-6. 2. Myerburg RJ, Castellanos A. Cardiac arrest and sudden cardiac death. Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 5th ed. Philadelphia, Pa: WB Saunders; 1997:742-779. 3. de Vreede-Swagemakers JJ, Gorgels AP, Dubois-Arbouw WI, et al. Out-of-hospital cardiac arrest in the 1990’s: a populationbased study in the

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Extracorporeal Life Support and New Therapeutic Strategies for Cardiac Arrest Caused by Acute Myocardial Infarction - a Critical Approach for a Critical Condition

, et al. Favourable survival of in-hospital compared to out-of-hospital refractory cardiac arrest patients treated with extracorporeal membrane oxygenation: an Italian tertiary care centre experience. Resuscitation. 2012;83:579-83. doi: 10.1016/j.resuscitation.2011.10.013. 6. Dworschak M. Is extracorporeal cardiopulmonary resuscitation for out-of-hospital cardiac arrest superior compared with conventional resuscitation? Crit Care Med. 2013;41:1365-6. doi: 10.1097/CCM.0b013e31828044c0. 7. Le Guen M, Nicolas-Robin A, Carreira S, et al. Extracorporeal life

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Pulseless Electrical Activity Arrest as the First Symptom of Testicular Cancer with Subsequent Phlegmasia Cerulea Dolens

arteriovenous fistula can be attempted [ 1 ]. Adjunctive measures include placement of an inferior vena cava (IVC) filter, and fasciotomy [ 8 ]. Given the high incidence of PE with PCD, IVC filter placement is an important measure to prevent further PE that may be a complication of treatment. Case report A previously healthy 46-year-old male, on no medications, presented following a pulseless electrical activity (PEA) arrest after collapsing at home. He was resuscitated and had the return of spontaneous circulation before arriving at the nearby tertiary care hospital

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Association between the Incidence of Sudden Cardiac Arrest and the Location of Culprit Lesions in STEMI Patients – Design of a Prospective Clinical Study

, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J . 2018;39:119-177. 5. Khera S, Kolte D, Gupta T, et al. Temporal Trends and Sex Differences in Revascularization and Outcomes of ST-Segment Elevation Myocardial Infarction in Younger Adults in the United States. J Am Coll Cardiol . 2015;66:1961-1972. 6. Atwood C, Eisenberg MS, Herlitz J, Rea TD. Incidence of EMS-treated out-of-hospital cardiac arrest in Europe. Resuscitation . 2005;67:75-80. 7. Dumas F

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Predictors Of Mortality In Patients With ST-Segment Elevation Acute Myocardial Infarction And Resuscitated Out-Of-Hospital Cardiac Arrest

;8:8032-41. 10. Park JS, Cha KS, Lee DS, et al. Culprit or multivessel revascularisation in ST-elevation myocardial infarction with cardiogenic shock. Heart. 2015;101:1225-32. 11. Mylotte D, Morice MC, Eltchaninoff H, et al. Primary percutaneous coronary intervention in patients with acute myocardial infarction, resuscitated cardiac arrest, and cardiogenic shock: the role of primary multivessel revascularization. JACC Cardiovasc Interv. 2013;6:115-25. 12. Ostenfeld S, Lindholm MG, Kjaergaard J, et al. Prognostic implication of out

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Determination of Cut-off Serum Values for Resistin and S100B Protein in Patients Who Survived a Cardiac Arrest

Introduction Despite fifty years of research, cardiac arrest (CA) and complications resulting from hypoxic organ injury, remains one of the most significant challenges faced by physicians, knowing that the vast majority of patients with CA have an unfavourable prognosis with a higher chance of death and severe neurological disabilities [ 1 , 2 , 3 ]. In the last few years, efforts have been focused on the best way to detect those patients who have a chance to survive and to recover. In an attempt to identify patients who survived after resuscitated CA

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Out-of-Hospital Cardiac Arrest in Acute Myocardial Infarction and STEMI Networks

References 1. Kern KB. Optimal Treatment of Patients Surviving Out-of- Hospital Cardiac Arrest. JACC Cardiovasc Interv. 2012;5:597-605. 2. Steg G, James SK, Atar D, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology. Eur Heart J. 2012;33:2569-619. 3. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of

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Is therapeutic hypothermia viable in our region as a new option for sudden cardiac arrest caused by acute myocardial infarction?

References 1. Schwartz BG, Kloner RA, Thomas JL, et al - Therapeutic hypothermia for acute myocardial infarction and cardiac arrest. Am J Cardiol. 2012 Aug 1;110(3):461-6. 2. Luscombe Mark, Andrzejowsk John - Clinical applications of induced hypothermia. Contin Educ Anaesth Crit Care Pain, 2006, 6(1):23-27, doi: 10.1093/bjaceaccp/mki0. 3. Katz LM, Frank JE, Glickma1. n LT, Jr GM, Lambdrt BH, Gordon CJ. Effect of a Pharmacologically Induced Decrease in Core Temperature in Rats Resuscitated from Cardiac Arrest

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Pyruvate Dehydrogenase Complex Deficiency: An Unusual Cause of Recurrent Lactic Acidosis in a Paediatric Critical Care Unit

may be due to a viral airway disease with areas of atelectasis. His respiratory status improved on day five after admission, and he was restarted on enteral nutrition with PediaSure®. IV fluids were discontinued. Within forty-eight hours of starting feeds with PediaSure®, his respiratory and mental status worsened. He was difficult to arouse and developed respiratory arrest requiring emergent intubation and subsequent transfer to the paediatric intensive care unit (PICU). His capillary blood gas before arrest revealed a metabolic acidosis with respiratory

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Brain Death in Children: Incidence, Donation Rates, and the Occurrence of Central Diabetes Insipidus

Abstract

Introduction: Brain death is currently defined as the loss of full brain function including the brainstem. The diagnosis and its subsequent management in the pediatric population are still controversial. The aim of this study was to define the demographic characteristics, clinical features and outcomes of patients with brain death and determine the incidence of brain death, donation rates and occurrence of central diabetes insipidus accompanying brain death in children.

Methods: This retrospective study was conducted at a twelve-bed tertiary-care combined medical and surgical pediatric intensive care unit of the Ondokuz Mayıs University Medical School, Samsun, Turkey. In 37 of 341 deaths (10.8%), a diagnosis of brain death was identified. The primary insult causing brain death was post-cardiorespiratory arrest in 8 (21.6%), head trauma in 8 (21.6%), and drowning in 4 (18.9%). In all patients, transcranial Doppler ultra-sound was utilised as an ancillary test and test was repeated until it was consistent with brain death.

Results: In 33 (89%) patients, central diabetes insipidus was determined at or near the time brain death was confirmed. The four patients not diagnosed with CDI had acute renal failure, and renal replacement treatment was carried out. The consent rate for organ donation was 18.9%, and 16.7% of potential donors proceeded to actual donation.

Conclusion: In the current study the consent rate for organ donation is relatively low compared to the rest of the world. The prevalence of central diabetes insipidus in this pedaitric brain death population is higher than reports in the literature, and acute renal failure accounted for the lack of central diabetes insipidus in four patients with brain death. Further studies are needed to explain normouria in brain-dead patients.

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