Annual Update in Intensive Care and Emergency Medicine 2020

 
 
Springer (Verlag)
  • 1. Auflage
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  • erschienen am 7. Februar 2020
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  • 490 Seiten
 
E-Book | PDF mit Adobe DRM | Systemvoraussetzungen
978-3-030-37323-8 (ISBN)
 

The Annual Update compiles reviews of the most recent developments in experimental and clinical intensive care and emergency medicine research and practice in one comprehensive reference book. The chapters are written by well recognized experts in these fields. The book is addressed to everyone involved in internal medicine, anesthesia, surgery, pediatrics, intensive care and emergency medicine.



Prof. Jean-Louis Vincent is Professor of intensive care at the University of Brussels, and intensivist in the Department of Intensive Care at Erasme University Hospital in Brussels. He is Past-President of the World Federation of Societies of Intensive and Critical Care Medicine (WFSICCM), the Belgian Society of Intensive Care Medicine (SIZ), the European Society of Intensive Care Medicine (ESICM), the European Shock Society (ESS), and the International Sepsis Forum (ISF). He is a member of the Royal Academy of Medicine of Belgium.

Prof. Vincent has signed more than 1000 articles, 400 book chapters and review articles, and 1000 original abstracts, and has edited more than 100 books. He is co-editor of the Textbook of Critical Care (Elsevier Saunders) and the 'Encyclopedia of Intensive Care Medicine' (Springer). He is editor-in-chief of 'Critical Care', 'Current Opinion in Critical Care', and 'ICU Management & Practice' and member of the editorial boards of about 30 journals.

Prof Vincent has received several awards, including the Distinguished Investigator and Lifetime Achievement Awards of the Society of Critical Care Medicine, the College Medalist Award of the American College of Chest Physicians, the Society Medal (lifetime award) of the European Society of Intensive Care Medicine, the Presidential Award of the European Respiratory Society and the prestigious Belgian scientific award of the FRS-FNRS (Prix Scientifique Joseph Maisin-Sciences Biomédicales Cliniques). In recognition of these achievements, he was awarded the title of Baron by the King of Belgium.

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  • 17,30 MB
978-3-030-37323-8 (9783030373238)
weitere Ausgaben werden ermittelt
  • Intro
  • Contents
  • Abbreviations
  • Part I: Respiratory Issues
  • 1: Physiology of the Respiratory Drive in ICU Patients: Implications for Diagnosis and Treatment
  • 1.1 Introduction
  • 1.2 Definition of Respiratory Drive
  • 1.3 What Determines the Respiratory Drive?
  • 1.3.1 Neuroanatomy and Physiology of the Respiratory Control Centers
  • 1.3.1.1 Inspiration
  • 1.3.1.2 Post-inspiration
  • 1.3.1.3 Expiration
  • 1.3.2 Feedback to the Respiratory Control Centers
  • 1.3.2.1 Central Chemoreceptors
  • 1.3.2.2 Peripheral Chemoreceptors
  • 1.3.2.3 Thoracic Receptors
  • 1.3.2.4 Cortical and Emotional Feedback
  • 1.4 What Is the Effect of Non-physiological Respiratory Drive on My Patients?
  • 1.4.1 Consequences of Excessive Respiratory Drive
  • 1.4.1.1 Patient Self-Inflicted Lung Injury
  • 1.4.1.2 Diaphragm Load-Induced Injury
  • 1.4.1.3 Weaning and Extubation Failure
  • 1.4.2 Consequences of Low Respiratory Drive
  • 1.5 How Can We Assess Respiratory Drive?
  • 1.5.1 Clinical Signs and Breathing Frequency
  • 1.5.2 Diaphragm Electrical Activity
  • 1.5.2.1 Reference Values
  • 1.5.2.2 Limitations
  • 1.5.3 Airway Occlusion Pressure
  • 1.5.3.1 Reference Values
  • 1.5.3.2 Limitations
  • 1.5.4 Inspiratory Effort
  • 1.6 Strategies to Modulate Respiratory Drive
  • 1.6.1 Modulation of Ventilator Support
  • 1.6.2 Medication
  • 1.6.3 Extracorporeal CO2 Removal
  • 1.7 Conclusion
  • References
  • 2: Monitoring Patient Respiratory Effort During Mechanical Ventilation: Lung and Diaphragm-Protective Ventilation
  • 2.1 Introduction
  • 2.2 Mechanics of Spontaneous Breathing
  • 2.3 Lung Injury During Spontaneous Breathing: Patient Self-Inflicted Lung Injury
  • 2.4 Diaphragm Injury During Spontaneous Breathing: Myotrauma
  • 2.5 Monitoring Spontaneous Breathing Using Esophageal Pressure
  • 2.5.1 Transpulmonary Pressure
  • 2.5.2 Respiratory Muscle Pressure
  • 2.5.3 Transdiaphragmatic Pressure
  • 2.6 Monitoring Spontaneous Breathing by Occlusion Maneuvers
  • 2.6.1 Inspiratory Occlusion Maneuver
  • 2.6.2 Expiratory Occlusion Maneuver
  • 2.6.3 Airway Occlusion Pressure
  • 2.7 Monitoring Spontaneous Breathing by Diaphragm Electrical Activity
  • 2.8 Monitoring Spontaneous Breathing by Diaphragm Ultrasound
  • 2.9 Conclusion: Targets for Lung and Diaphragm-Protective Ventilation
  • References
  • 3: Ten Reasons to Use Mechanical Power to Guide Ventilator Settings in Patients Without ARDS
  • 3.1 Introduction
  • 3.2 Is Tidal Volume Associated with Mortality in Patients Without ARDS? No
  • 3.3 Is Driving Pressure Associated with Mortality in Patients Without ARDS? No
  • 3.4 Is Ppeak Associated with Mortality in Patients Without ARDS? Yes
  • 3.5 Is PEEP Associated with Mortality in Patients Without ARDS? Yes
  • 3.6 Is Respiratory Rate Associated with Mortality in Patients Without ARDS? No
  • 3.7 Mechanical Energy and Power Calculations: Should We Abandon More Complex Formulas in Favor of Simplified Ones? Yes
  • 3.8 Does Use of a Simple Formula Enable Calculation of Mechanical Power in Volume-Controlled Ventilation? Yes: Simply Change the Variables and Observe the Consequences
  • 3.9 Can Mechanical Power Be Computed During Assisted Ventilation? Yes
  • 3.10 Is Mechanical Power Associated with Lung Injury in Experimental Models? Yes
  • 3.11 Is Mechanical Power Associated with Mortality in Patients Without ARDS? Yes
  • 3.12 Conclusion
  • References
  • Part II: Acute Respiratory Distress Syndrome
  • 4: Extracellular Vesicles in ARDS: New Insights into Pathogenesis with Novel Clinical Applications
  • 4.1 Introduction
  • 4.2 Contribution of Extracellular Vesicles to the Pathogenesis of ARDS
  • 4.3 Potential Endogenous Protective Effects of Extracellular Vesicles in ARDS
  • 4.4 Benefits of Extracellular Vesicles Derived from Mesenchymal Stromal Cells and Endothelial Progenitor Cells in ARDS Models
  • 4.5 Clinical Applications for Extracellular Vesicles in ARDS
  • 4.6 Future Directions
  • 4.7 Conclusions
  • References
  • 5: ARDS Subphenotypes: Understanding a Heterogeneous Syndrome
  • 5.1 Introduction
  • 5.2 ARDS Subphenotypes and Prognostic Enrichment
  • 5.2.1 Physiologic Phenotyping for Prognostic Enrichment
  • 5.2.2 Clinical Phenotyping for Prognostic Enrichment
  • 5.2.3 Biologic Phenotyping for Prognostic Enrichment
  • 5.3 ARDS Subphenotypes and Predictive Enrichment
  • 5.3.1 Physiologic Phenotyping for Predictive Enrichment
  • 5.3.2 Clinical Phenotyping for Predictive Enrichment
  • 5.3.3 Biologic Phenotyping for Predictive Enrichment
  • 5.4 Beyond ARDS: Subphenotypes in Other Heterogeneous Syndromes
  • 5.5 Conclusion
  • References
  • 6: Assessment of VILI Risk During Spontaneous Breathing and Assisted Mechanical Ventilation
  • 6.1 Introduction
  • 6.2 Mechanical Ventilation and Mechanisms of VILI
  • 6.3 How to Minimize the Risk?
  • 6.4 Spontaneous Breathing and VILI
  • 6.5 Monitoring and Respiratory Mechanics
  • 6.5.1 Plateau Pressure, Driving Pressure, and Respiratory System Compliance
  • 6.5.2 Pendelluft Phenomenon
  • 6.5.3 Asynchronies
  • 6.6 Conclusion
  • References
  • Part III: Biomarkers
  • 7: The Future of ARDS Biomarkers: Where Are the Gaps in Implementation of Precision Medicine?
  • 7.1 Introduction
  • 7.2 Current State of Biomarkers in ARDS
  • 7.2.1 Biomarkers for Diagnosis of ARDS
  • 7.2.2 Biomarkers for Prognostication in ARDS
  • 7.2.3 Biomarkers for Distinguishing Phenotypes of ARDS
  • 7.3 Gaps in Implementation of Biomarkers in ARDS
  • 7.3.1 Barriers to the Clinical Application of Biomarkers in ARDS
  • 7.3.2 Gaps in Identifying Additional Uses of Biomarkers in ARDS
  • 7.3.3 Additional Tools for ARDS Biomarker Discovery
  • 7.4 Conclusion
  • References
  • 8: Utility of Inflammatory Biomarkers for Predicting Organ Failure and Outcomes in Cardiac Arrest Patients
  • 8.1 Introduction
  • 8.2 Pathophysiology of the Inflammatory Response
  • 8.3 Inflammatory Biomarkers and Their Performance in Clinical Studies of OHCA
  • 8.4 The Impact of Multiorgan Failure in Cardiac Arrest Patients
  • 8.5 The Role of Inflammation in Organ Failure and Outcomes After Cardiac Arrest
  • 8.6 Resuscitation Factors Associated with the Magnitude of the Inflammatory Response
  • 8.7 Means of Treating Inflammation in Cardiac Arrest Patients
  • 8.8 Incorporating Inflammatory Biomarkers into Prognostication Algorithms
  • 8.9 Conclusion
  • References
  • 9: Troponin Elevations after Cardiac Surgery: Just "Troponitis"?
  • 9.1 Introduction
  • 9.2 Troponin and the Diagnosis of Postoperative Myocardial Infarction After Cardiac Surgery
  • 9.2.1 Cutoff Level of Troponin
  • 9.2.2 Timing of Troponin Measurements
  • 9.2.3 Delta Troponin
  • 9.2.4 Timing of the Peak cTn Level
  • 9.2.5 Postoperative MI and Valve Surgery
  • 9.3 Troponin and Prognosis After Cardiac Surgery
  • 9.3.1 Preoperative Troponin and Increased Perioperative Risk in Cardiac Surgery
  • 9.3.2 What We Can Learn from Myocardial Injury After Noncardiac Surgery
  • 9.4 Important Considerations When Interpreting Troponin After Cardiac Surgery
  • 9.4.1 Gender
  • 9.4.2 Kidney Function
  • 9.4.3 Duration of the Cardiopulmonary Bypass
  • 9.5 Conclusion
  • References
  • 10: Biomarkers of Sepsis During Continuous Renal Replacement Therapy: Have We Found the Appropriate Biomarker to Use Under This Condition?
  • 10.1 Introduction
  • 10.2 Description of the Putative Candidates
  • 10.2.1 The Most Frequently Used Clinical Biomarkers
  • 10.2.1.1 C-reactive Protein
  • CRP Structure and Function
  • Potential Elimination by CRRT
  • 10.2.1.2 Procalcitonin
  • Structure and Function
  • Potential Elimination by CRRT
  • 10.2.1.3 Brain Natriuretic Factors
  • Structure
  • Potential Elimination by CRRT
  • 10.2.2 Cytokine/Chemokine Biomarkers of Sepsis
  • 10.2.2.1 High Mobility Group 1 Protein (HMGB-1)
  • 10.2.2.2 Osteopontin
  • 10.2.3 Biomarkers of Sepsis Related to Vascular Endothelial Damage
  • 10.2.3.1 Endocan
  • 10.2.4 Biomarkers of Sepsis Related to Vasodilation
  • 10.2.4.1 Proadrenomedullin (MR-proADM)
  • 10.2.5 Other Acute Phase Reactant Protein Biomarkers
  • 10.2.5.1 Pentraxin
  • 10.2.6 Cell Marker Biomarkers of Sepsis
  • 10.2.6.1 Presepsin
  • 10.2.7 Coagulation Biomarkers of Sepsis
  • 10.2.7.1 Heparin Binding Protein (HBP)
  • 10.3 Discussion
  • 10.4 Conclusion
  • References
  • Part IV: Fluids
  • 11: Do Intensivists Need to Care About the Revised Starling Principle?
  • 11.1 Introduction: Concerns Among Clinicians
  • 11.2 Glycocalyx Degradation
  • 11.3 Increased Capillary Leakage?
  • 11.4 "Non-absorption Rule"
  • 11.5 Capillary Filtration
  • 11.6 Are Colloids and Crystalloids Equal?
  • 11.7 Hemodilution and the Glycocalyx
  • 11.8 Volume Kinetics
  • 11.9 Conclusion
  • References
  • 12: Right Ventricular Dysfunction and Fluid Administration in Critically Ill Patients
  • 12.1 Introduction
  • 12.2 Fluid Administration in Cases of Structural Causes of Acute RV Dysfunction
  • 12.3 Fluid Administration in Cases of Acute RV Dysfunction Related to Mechanical Ventilation (Functional Causes of RV Dysfunction)
  • 12.3.1 Pulmonary Vascular Resistance and Lung Volume
  • 12.3.2 Mechanical Ventilation and RV Afterload
  • 12.4 Conclusion
  • References
  • 13: Intravenous Fluids: Do Not Drown in Confusion!
  • 13.1 Introduction
  • 13.2 The Goals of Fluid Stewardship
  • 13.3 Framework for Intravenous Fluid Prescription
  • 13.4 The Four Ds of Fluid Therapy: A Guide to Key Performance Indicators
  • 13.4.1 Drug
  • 13.4.2 Dose
  • 13.4.3 Duration
  • 13.4.4 De-escalation
  • 13.5 The Five Ps of Fluid Prescription
  • 13.6 The Four Indications for Fluid Therapy
  • 13.6.1 Resuscitation
  • 13.6.2 Maintenance
  • 13.6.3 Replacement
  • 13.6.4 Nutrition
  • 13.7 The Four Questions of Fluid Therapy
  • 13.8 The Four Phases of Fluid Therapy: The ROSE Concept
  • 13.9 The Four Hits of Shock
  • 13.10 Important Definitions
  • 13.10.1 Fluid Balance
  • 13.10.2 Cumulative Fluid Balance
  • 13.10.3 Fluid Loss and Gain
  • 13.10.4 Dehydration (Fluid Underload)
  • 13.10.5 Overhydration (Fluid Overload or Fluid Accumulation)
  • 13.10.6 Hypovolemia
  • 13.10.7 Hypervolemia
  • 13.10.8 Fluid Bolus
  • 13.10.9 Fluid Challenge
  • 13.10.10 Fluid Responsiveness
  • 13.10.11 Prediction of Fluid Responsiveness
  • 13.11 Noninvasive Tests of Fluid Responsiveness
  • 13.11.1 Passive Leg Raising Test
  • 13.11.2 End-Expiratory Occlusion Test
  • 13.12 Classification of Fluid Dynamics
  • 13.12.1 Ebb Phase
  • 13.12.2 Flow Phase
  • 13.13 Ongoing Fluid Management
  • 13.13.1 Late Conservative Fluid Management
  • 13.13.2 Late Goal-Directed Fluid Removal
  • 13.14 Fluid Overload
  • 13.14.1 Intra-abdominal Hypertension
  • 13.14.2 Global Increased Permeability Syndrome
  • 13.15 Intravenous Fluid Bundles: The Northampton Example
  • 13.15.1 Education Is Key
  • 13.16 Busting the Myths!
  • 13.16.1 Chasing the Wrong Target: Optimal Perfusion Does Not Require Excessive Volume
  • 13.16.2 Urine Output: Not the Golden Bullet!
  • 13.16.3 Sepsis and Septic Shock
  • 13.17 Conclusion
  • References
  • Part V: Hemodynamic Management
  • 14: Update on Right Ventricular Hemodynamic, Echocardiographic and Extra-Cardiac Ultrasound Monitoring
  • 14.1 Introduction
  • 14.2 Definition of RV Dysfunction and RV Failure
  • 14.3 Hemodynamic Parameters
  • 14.4 Echocardiographic Parameters: 2D, Doppler, Strain, 3D
  • 14.5 Extra-Cardiac Echocardiographic Parameters
  • 14.6 Conclusion
  • References
  • 15: Management of Hypotension: Implications for Noncardiac Surgery and Intensive Care
  • 15.1 Introduction
  • 15.2 Adverse Effects of Hypotension
  • 15.2.1 Intraoperative Hypotension in Noncardiac Surgery
  • 15.2.2 Hypotension in Critically Ill Patients
  • 15.3 The Challenge of Defining Hypotension
  • 15.3.1 Defining Intraoperative Hypotension in Noncardiac Surgery
  • 15.3.2 Defining Hypotension in the Intensive Care Unit
  • 15.4 Individualization of Blood Pressure Measurement
  • 15.4.1 Individual Blood Pressure Targets
  • 15.4.2 Choice of Monitoring
  • 15.5 Management of Hypotension
  • 15.5.1 Goal-Directed Therapy of Intraoperative Hypotension
  • 15.5.2 Goal-Directed Therapy in the Intensive Care Unit
  • 15.5.3 New Concepts of Goal-Directed Therapy of Intraoperative Hypotension
  • 15.6 Current Innovation and Future Directions
  • 15.7 Conclusion
  • References
  • 16: Heterogeneity of Cardiovascular Response to Standardized Sepsis Resuscitation
  • 16.1 Introduction
  • 16.2 Physiologic Rationale for Resuscitation
  • 16.3 Clinical Observations
  • 16.4 Clinical Relevance
  • 16.5 Conclusion
  • References
  • Part VI: The Microcirculation
  • 17: Clinical Relevance of the Endothelial Glycocalyx in Critically Ill Patients
  • 17.1 Introduction
  • 17.2 Critical Conditions Associated with Injury to the Endothelial Glycocalyx
  • 17.3 The Rationale for the Concept of Endothelial Glycocalyx Protection and Repair in the Critically Ill
  • 17.4 Effect of Common Therapeutic Interventions on the Endothelial Glycocalyx
  • 17.4.1 Interventions/Conditions with a Possible Negative Impact
  • 17.4.1.1 Fluid Therapy
  • 17.4.1.2 Derangements of Homeostasis
  • 17.4.1.3 Anesthesia and Sedation
  • 17.4.1.4 Organ Support
  • 17.4.2 Interventions with a Possible Positive/Reparative Effect
  • 17.4.2.1 Nutritional Support
  • 17.4.2.2 Blood Products and Anticoagulants
  • 17.4.2.3 Corticosteroids
  • 17.4.2.4 Commonly Used Medications
  • Antidiabetic Drugs
  • Statins
  • Low-Molecular-Weight Heparin
  • Antimicrobial Therapy
  • 17.5 Conclusion
  • References
  • 18: Customized Monitoring of the Microcirculation in Patients with a Left Ventricular Assist Device
  • 18.1 Introduction
  • 18.2 Microcirculatory Monitoring
  • 18.3 Modern Monitoring of the Macrocirculation in Heart Failure
  • 18.4 Monitoring the Microcirculation in Patients with a LVAD
  • 18.5 Customized Remote Monitoring of the Microcirculation
  • 18.6 Conclusion
  • References
  • 19: Monitoring of the Sublingual Microcirculation at the Bedside: Yes, It Is Possible and Useful
  • 19.1 Introduction
  • 19.2 Sublingual Microvascular Perfusion Parameters
  • 19.3 Clinical Relevance of Sublingual Microvascular Perfusion Parameters
  • 19.4 Titration of Hemodynamic Strategy Using Sublingual Microvascular Perfusion Parameters
  • 19.5 Sublingual Microvascular Perfusion Parameters at the Bedside
  • 19.6 Impact of Sublingual Microcirculation Monitoring on Patient Outcome
  • 19.7 Conclusion
  • References
  • 20: Microcirculation in Patients with Sepsis: From Physiology to Interventions
  • 20.1 Introduction
  • 20.2 Microcirculatory Dysfunction in Sepsis
  • 20.3 Hemodynamic Reconciliation in Physiology
  • 20.4 The Role of the Endothelium and Coagulation
  • 20.5 Assessment of the Microcirculation
  • 20.5.1 Microcirculatory Targets
  • 20.5.2 Clinical Assessment
  • 20.5.2.1 Capillary Refill Time
  • 20.5.2.2 Skin Mottling
  • 20.5.3 Biochemical Markers
  • 20.5.3.1 SvO2 and ScvO2
  • 20.5.3.2 Lactate
  • 20.5.3.3 Central-Venous-Arterial CO2 Difference
  • 20.5.4 Peripheral Perfusion Index
  • 20.5.5 Handheld Vital Microscopy
  • 20.6 How We Can Modify the Microcirculation in Sepsis
  • 20.7 Conclusion
  • References
  • Part VII: Sepsis
  • 21: Macrophage Activation Syndrome in Sepsis: Does It Exist and How to Recognize It?
  • 21.1 Introduction
  • 21.2 Classification Criteria and Epidemiology
  • 21.3 Pathogenesis
  • 21.4 Diagnostic Biomarkers
  • 21.5 Management and Future Perspectives
  • 21.6 Conclusion
  • References
  • 22: Is T Cell Exhaustion a Treatable Trait in Sepsis?
  • 22.1 Introduction
  • 22.2 What Is T Cell Exhaustion?
  • 22.3 There Is Indirect and Direct Evidence for T Cell Exhaustion in Sepsis
  • 22.4 T Cell Exhaustion Is Reversible in Cells Isolated from Patients with Sepsis
  • 22.5 Case Report of Anti-PD-1 or Anti-PD-L1 Immunotherapy
  • 22.6 Early Phase Randomized Controlled Trials to Reverse T Cell Exhaustion in Sepsis
  • 22.7 Designing Future Clinical Trials to Reverse T Cell Exhaustion in Sepsis
  • 22.8 Conclusion
  • References
  • 23: Cell-Free Hemoglobin: A New Therapeutic Target in Sepsis?
  • 23.1 Introduction
  • 23.2 Cell-Free Hemoglobin-Mediated Organ Dysfunction in Sepsis
  • 23.2.1 Cell-Free Hemoglobin Levels in Sepsis
  • 23.2.2 Mechanisms of Hemoglobin Toxicity
  • 23.2.3 Organ-Specific Effects of Cell-Free Hemoglobin
  • 23.3 Targeting Cell-Free Hemoglobin in Sepsis
  • 23.3.1 Overview
  • 23.3.2 Haptoglobin
  • 23.3.3 Hemopexin
  • 23.3.4 Acetaminophen
  • 23.3.5 Other Potential Therapies
  • 23.3.6 Current Barriers to Cell-Free Hemoglobin-Targeted Therapeutics
  • 23.4 Conclusion
  • References
  • 24: Therapeutic Potential of the Gut Microbiota in the Management of Sepsis
  • 24.1 Introduction
  • 24.2 Mechanisms of Dysbiosis in Sepsis
  • 24.3 Dysbiosis as a Potential Risk Factor for Sepsis
  • 24.4 The Gut Microbiota as a Predictor of Clinical Outcome in Sepsis
  • 24.5 Modulation of the Microbiota as Potential Therapeutic Immunonutrition
  • 24.6 Fecal Microbiota Transplantation
  • 24.7 Conclusion and Future Perspectives
  • References
  • Part VIII: Bleeding and Transfusion
  • 25: Blood Transfusion Practice During Extracorporeal Membrane Oxygenation: Rationale and Modern Approaches to Management
  • 25.1 Introduction
  • 25.2 ECMO Physiology
  • 25.3 Blood Loss During ECMO
  • 25.4 Blood Transfusions in Critically Ill Patients
  • 25.5 Effect of Transfused Blood
  • 25.6 Current Approach to Transfusion During ECMO
  • 25.7 Future Directions
  • 25.8 Conclusion
  • References
  • 26: The Use of Frozen Platelets for the Treatment of Bleeding
  • 26.1 Introduction
  • 26.2 Manufacture of Frozen Platelets
  • 26.3 The Impact of Freeze-thawing on Platelets
  • 26.3.1 Morphology
  • 26.3.2 Activation Status
  • 26.3.3 Externalization of Phosphatidylserine and Extracellular Vesicle Shedding
  • 26.4 The Impact of Freeze-Thawing on In Vitro Functional Coagulation Processes
  • 26.4.1 Aggregation of Platelets
  • 26.4.2 Thrombin Generation
  • 26.4.3 Viscoelastic Tests
  • 26.4.4 Flow Coagulation Models
  • 26.5 Clearance of Frozen Platelets
  • 26.6 Efficacy of Frozen Platelets in Experimental In Vivo Settings
  • 26.7 Experience with Frozen Platelets in the Military Setting
  • 26.8 Clinical Trials with Frozen Platelets
  • 26.8.1 Correction of Thrombocytopenia
  • 26.8.2 Treatment of Bleeding
  • 26.9 Safety of Frozen Platelets
  • 26.10 Toward Specification of Platelet Products for Differential Use
  • 26.11 Conclusion
  • References
  • 27: Viscoelastic Assay-Guided Hemostatic Therapy in Perioperative and Critical Care
  • 27.1 Introduction
  • 27.2 Viscoelastic Tests
  • 27.3 Major Trauma and Trauma-Induced Coagulopathy
  • 27.4 Cardiovascular Surgery
  • 27.5 Liver Disease, Hepatic Surgery, and Transplantation
  • 27.6 Postpartum Hemorrhage
  • 27.7 Venous Thromboembolism
  • 27.8 Sepsis and Septic Shock
  • 27.9 Extracorporeal Membrane Oxygenation
  • 27.10 Conclusion
  • References
  • 28: Extracorporeal Filter and Circuit Patency: A Personalized Approach to Anticoagulation
  • 28.1 Introduction
  • 28.2 Systemic Strategies
  • 28.2.1 Unfractionated and Low-Molecular-Weight Heparin
  • 28.2.2 Direct Thrombin Inhibitors
  • 28.3 Regional Strategies
  • 28.3.1 Regional Citrate Anticoagulation
  • 28.3.1.1 Citrate Infusion Rate and Citrate Load
  • 28.3.1.2 Acid Base Disorders and Citrate Load Management
  • 28.3.1.3 Regional Citrate Anticoagulation and Outcomes
  • 28.3.1.4 Patients at High Risk of Bleeding
  • 28.3.1.5 Patients with Liver Failure
  • 28.3.1.6 Hypoxemic Patients
  • 28.3.2 Regional Heparin-Protamine Anticoagulation
  • 28.4 No Anticoagulation Strategies
  • 28.4.1 Determinants of Clotting Risk: Vascular Access, Circuit, Modality
  • 28.5 Conclusion
  • References
  • Part IX: Prehospital Intervention
  • 29: Prehospital Resuscitation with Low Titer O+ Whole Blood by Civilian EMS Teams: Rationale and Evolving Strategies for Use
  • 29.1 Introduction: Civilian Setting Resuscitation Strategies for Bleeding over the Past Half Century
  • 29.2 The Recent Evolution of Non-Mechanical Bleeding Control Interventions
  • 29.3 The Detrimental Effects of Isotonic/Hypertonic Fluid Infusions
  • 29.4 The Rationale for Prehospital Use of Low Titer O+ Whole Blood
  • 29.5 Some Current Experiences with Implementation of Prehospital Whole Blood
  • 29.5.1 Source of the EMS System Blood Supply
  • 29.5.2 Deciding How to Distribute the Blood Supply
  • 29.5.3 Criteria and Triggers for EMS Infusing Whole Blood and Tranexamic Acid
  • 29.5.4 Infusing the Blood and Tranexamic Acid
  • 29.6 Conclusion
  • References
  • 30: Mobile Stroke Units: Taking the Emergency Room to the Patient
  • 30.1 Introduction
  • 30.2 The Rationale Behind Mobile Stroke Units
  • 30.2.1 Time Is Brain
  • 30.2.2 Revascularization Is Underused
  • 30.2.3 Organization of Care
  • 30.2.4 Portable CT Scanning
  • 30.2.5 Information Technology and Telemedicine
  • 30.2.6 Telemedicine in the Mobile Stroke Unit
  • 30.3 Mobile Stroke Unit Logistics and Organization
  • 30.4 Mobile Stroke Unit Components
  • 30.5 Do Mobile Stroke Units Make a Difference?
  • 30.6 Limitations of Mobile Stroke Units
  • 30.7 Are There Alternatives?
  • 30.8 Low-Income Countries and Rural or Remote Settings
  • 30.9 Cost-effectiveness
  • 30.10 The Future
  • 30.11 Conclusion
  • References
  • Part X: Trauma
  • 31: Evaluating Quality in Trauma Systems
  • 31.1 Introduction
  • 31.2 Context
  • 31.3 What Is a Trauma System?
  • 31.4 What Are the Goals of a Trauma System?
  • 31.5 What Is Meant By "Quality Assurance" and "Quality Improvement"?
  • 31.6 Selecting Measures of Quality
  • 31.7 Structure and Process Measures
  • 31.8 Outcome Measures
  • 31.8.1 Death
  • 31.8.2 Functional Outcomes
  • 31.9 Limitations of "Traditional" Epidemiology
  • 31.10 Why "Place" Matters
  • 31.11 Spatial Analysis
  • 31.11.1 Disease Maps
  • 31.11.2 The "Small Numbers" Problem
  • 31.11.3 Addressing the Small Numbers Problem
  • 31.11.4 Kernel Density Estimation and "Heat Maps"
  • 31.11.5 Examples of Using Spatial Analysis to Evaluate Trauma System Quality
  • 31.12 Trauma Registries and Linked Data
  • 31.13 Conclusion
  • References
  • 32: Vasopressors for Post-traumatic Hemorrhagic Shock: Friends or Foe?
  • 32.1 Introduction
  • 32.2 Pharmacology
  • 32.2.1 Cardiovascular Effects of Norepinephrine
  • 32.2.2 Cardiovascular Effects of Vasopressin
  • 32.2.3 Metabolic and Immunomodulatory Effects of Norepinephrine and Vasopressin
  • 32.3 The Physiologic Response to Traumatic Shock and Hemorrhage
  • 32.4 Vasopressors in Shock and Hemorrhage in Trauma: Experimental Evidence
  • 32.5 Clinical Evidence of Permissive Hypotension and Vasopressor Use
  • 32.6 A Practical Approach to Vasopressor Use for an Updated Resuscitation Strategy
  • 32.7 Conclusion
  • References
  • 33: Extracranial Tsunami After Traumatic Brain Injury
  • 33.1 Introduction
  • 33.2 Respiratory Complications
  • 33.2.1 Brain-Lung Interaction
  • 33.2.2 Neurogenic Pulmonary Edema
  • 33.2.3 Hypoxia and Hypercapnia
  • 33.2.4 Ventilator-Associated Pneumonia
  • 33.3 Cardiac Dysfunction
  • 33.3.1 Electrocardiogram Changes
  • 33.3.2 Myocardial Dysfunction
  • 33.4 Kidney Complications
  • 33.4.1 AKI After TBI
  • 33.5 Liver Dysfunction
  • 33.5.1 Effect of Drugs on Liver Function
  • 33.6 Hematologic Complications
  • 33.7 Conclusion
  • References
  • Part XI: Neurological Aspects
  • 34: Ten False Beliefs About Mechanical Ventilation in Patients with Brain Injury
  • 34.1 Introduction
  • 34.2 Brain-Lung Crosstalk Does Not Exist
  • 34.3 The More Oxygen We Give, the Better It Is
  • 34.4 Brain-Injured Patients Must Be Hyperventilated
  • 34.5 Tidal Volume Must Be High and PEEP Must Be ZEEP
  • 34.6 Recruitment Maneuvers Are Forbidden
  • 34.7 Assisted Ventilation Is Contraindicated
  • 34.8 Extubation Should Be Delayed
  • 34.9 Tracheostomy Should Be Performed Late
  • 34.10 Prone Position Is Contraindicated
  • 34.11 No Role for ECMO
  • 34.12 Conclusion
  • References
  • 35: Manifestations of Critical Illness Brain Injury
  • 35.1 Introduction
  • 35.2 Delirium
  • 35.2.1 Pathophysiology and Etiologic Considerations
  • 35.2.2 Assessment of Delirium During Critical Illness
  • 35.2.3 Management
  • 35.2.4 Prognosis
  • 35.2.5 Summary
  • 35.3 Coma
  • 35.3.1 Pathophysiology and Etiologic Considerations
  • 35.3.2 Assessment of Coma During Critical Illness
  • 35.3.3 Management
  • 35.3.4 Prognosis
  • 35.3.5 Summary
  • 35.4 Catatonia
  • 35.4.1 Pathophysiology and Etiologic Considerations
  • 35.4.2 Assessment of Catatonia During Critical Illness
  • 35.4.3 Management
  • 35.4.4 Prognosis
  • 35.4.5 Summary
  • 35.5 A Conceptual Framework for Manifestations of Critical Illness Brain Injury
  • 35.6 Conclusion
  • References
  • 36: Essential Noninvasive Multimodality Neuromonitoring for the Critically Ill Patient
  • 36.1 Introduction
  • 36.2 Automated Pupillometry
  • 36.2.1 Prognosis Following Cardiac Arrest
  • 36.2.2 Traumatic Brain Injury
  • 36.2.3 Pain Assessment in Unconscious Patients
  • 36.3 Brain Ultrasound
  • 36.3.1 Different Approaches
  • 36.3.2 The Optic Nerve Sheath Diameter
  • 36.3.3 Noninvasive ICP Measurement
  • 36.3.4 Aneurysmal Subarachnoid Hemorrhage and Vasospasm
  • 36.3.5 Midline Shift
  • 36.3.6 Cerebral Circulatory Arrest
  • 36.4 Processed Electroencephalography
  • 36.4.1 Recommendations from International Guidelines
  • 36.5 Conclusion
  • References
  • Part XII: Organ Donation
  • 37: Brain Death After Cardiac Arrest: Pathophysiology, Prevalence, and Potential for Organ Donation
  • 37.1 Introduction
  • 37.2 Pathophysiology of Brain Death After Cardiac Arrest
  • 37.2.1 Cerebral Edema
  • 37.2.2 Neuronal Apoptosis and Cerebral Hypoperfusion
  • 37.2.3 Neurological Causes of Arrest
  • 37.3 Prevalence
  • 37.4 Potential for Organ Donation
  • 37.5 Detecting Brain Death After Cardiac Arrest
  • 37.6 Future Developments
  • 37.7 Conclusion
  • References
  • 38: Organ Recovery Procedure in Donation After Controlled Circulatory Death with Normothermic Regional Perfusion: State of the Art
  • 38.1 Introduction
  • 38.2 Donation After Controlled Circulatory Death Pathway
  • 38.2.1 Withdrawal of Life-Sustaining Therapies
  • 38.2.2 Consent and Authorization
  • 38.2.3 Antemortem Procedures
  • 38.2.4 Determination of Death
  • 38.2.5 Timeline
  • 38.2.6 Normothermic Regional Perfusion
  • 38.2.6.1 Specific Procedure
  • 38.3 Liver Transplantation
  • 38.4 Lung Transplantation
  • 38.5 Kidney Transplantation
  • 38.6 Pancreas Transplantation
  • 38.7 Heart Transplantation
  • 38.8 Conclusion
  • References
  • Part XIII: Oncology
  • 39: Admitting Adult Critically Ill Patients with Hematological Malignancies to the ICU: A Sisyphean Task or Work in Progress?
  • 39.1 Introduction
  • 39.2 Survival and Prognosis of Patients with Hematological Malignancies
  • 39.3 ICU Admission Practices for Patients with Hematological Malignancies: Historical Perspective
  • 39.4 ICU Admission Practices for Patients with Hematological Malignancies: The Modern Area
  • 39.5 Quality of Life of Patients with a Hematological Malignancy Following ICU Admission
  • 39.6 Conclusion
  • References
  • 40: Onco-Nephrology: Acute Kidney Injury in Critically Ill Cancer Patients
  • 40.1 Introduction
  • 40.2 Epidemiology
  • 40.3 Risk Factors
  • 40.4 Causes of AKI
  • 40.4.1 AKI Directly Related to Underlying Malignancy
  • 40.4.2 AKI Due to Direct Effects of Cancer Treatment
  • 40.4.3 AKI Due to Complications of Cancer Treatment
  • 40.5 Management
  • 40.6 Outcomes
  • 40.7 Conclusion
  • References
  • Part XIV: Severe Complications
  • 41: A Clinician's Guide to Management of Intra-abdominal Hypertension and Abdominal Compartment Syndrome in Critically Ill Patients
  • 41.1 Introduction
  • 41.2 Managing IAH and ACS: The Triangle Paradigm
  • 41.2.1 Intra-abdominal Pressure (Culprit)
  • 41.2.1.1 IAP Measurement and Interpretation
  • 41.2.1.2 Baseline IAP Value and Dynamics
  • 41.2.1.3 Duration of IAH
  • 41.2.2 Organ (Dys)Function (Impact)
  • 41.2.2.1 Severity of Organ Dysfunction
  • 41.2.2.2 Organ Dysfunction Duration and Dynamics
  • 41.2.3 Etiology of IAH/ACS (Cause)
  • 41.2.3.1 Increased Intra-abdominal Volume
  • 41.2.3.2 Decreased Abdominal Wall Compliance
  • 41.3 A Practical Approach Based on the IAH Triangle
  • 41.3.1 Is an Intervention Required?
  • 41.3.2 How Urgent Is the Effect of the Intervention Required?
  • 41.3.3 What Is the Best Method of Intervention?
  • 41.3.3.1 Reducing Intraluminal Volume
  • 41.3.3.2 Reducing Extraluminal Volume
  • 41.3.3.3 Improving Abdominal Wall Compliance
  • 41.3.3.4 Decompressive Laparotomy
  • 41.4 Supportive Management of the Patient with IAH/ACS
  • 41.5 Conclusion
  • References
  • 42: Update on the Management of Iatrogenic Gas Embolism
  • 42.1 Introduction
  • 42.2 Definition and Epidemiology
  • 42.3 Physiopathology
  • 42.4 Diagnosis
  • 42.4.1 Conditions with Risk of Iatrogenic Gas Embolism
  • 42.4.1.1 Venous Gas Embolism
  • 42.4.1.2 Arterial Gas Embolism
  • 42.4.2 Clinical Manifestations
  • 42.4.3 Laboratory Investigations
  • 42.5 Treatment
  • 42.5.1 Immediate Interventions
  • 42.5.2 Hyperbaric Oxygen Therapy
  • 42.6 Conclusion
  • References
  • 43: Alcohol Withdrawal Syndrome in the ICU: Preventing Rather than Treating?
  • 43.1 Introduction
  • 43.2 Alcohol Use Disorders: Definition and Epidemiology
  • 43.3 Alcohol Withdrawal Syndrome: Pathophysiology and Definition
  • 43.4 Current Guidelines for Alcohol Withdrawal Syndrome
  • 43.5 Alcohol Withdrawal in the ICU
  • 43.6 Conclusion
  • References
  • Part XV: Prolonged Critical Illness
  • 44: Muscle Dysfunction in Critically Ill Children
  • 44.1 Introduction
  • 44.2 Incidence and Risk Factors
  • 44.3 Impact of Muscle Dysfunction on Outcome
  • 44.4 Diagnostic Techniques
  • 44.4.1 Ultrasound
  • 44.4.2 Echogenicity
  • 44.4.3 Limb Muscle Thickness
  • 44.5 Limb and Respiratory Muscle Weakness
  • 44.6 Diaphragm Dysfunction
  • 44.6.1 Dysfunction Pre-ICU
  • 44.6.2 Mechanical Ventilation and the Diaphragm
  • 44.6.3 Monitoring Diaphragm Activity and Function
  • 44.7 Prevention of Weakness: Therapeutic Strategies
  • 44.7.1 Early Mobilization
  • 44.7.2 Nutritional Support
  • 44.7.3 Prevention of Diaphragm Dysfunction
  • 44.7.4 Transcutaneous Electrical Muscle Stimulation
  • 44.8 Conclusion
  • References
  • 45: Respiratory Muscle Rehabilitation in Patients with Prolonged Mechanical Ventilation: A Targeted Approach
  • 45.1 Introduction
  • 45.2 Respiratory Muscle Weakness in ICU Patients: A Call to Action
  • 45.3 Identifying Respiratory Muscle Weakness in ICU Patients
  • 45.4 Specific Respiratory Muscle Training: Can It Make a Difference to ICU Patients?
  • 45.5 Current Practice: Inspiratory Muscle Training in the ICU-Not All Approaches Are Equal
  • 45.6 Practicalities of Inspiratory Muscle Training in ICU Patients
  • 45.7 Emerging Strategies for Inspiratory Muscle Training in ICU Patients
  • 45.8 Barriers to Respiratory Muscle Rehabilitation in ICU Patients
  • 45.9 Future Directions for Respiratory Muscle Rehabilitation in ICU Patients
  • 45.10 Conclusion
  • References
  • 46: Post-Intensive Care Syndrome and Chronic Critical Illness: A Tale of Two Syndromes
  • 46.1 Introduction
  • 46.2 Post-intensive Care Syndrome Features
  • 46.3 PICS In-Hospital Interventions
  • 46.4 PICS Out-of-Hospital Interventions
  • 46.5 Chronic Critical Illness Features
  • 46.6 Unanticipated Survivor Sequelae
  • 46.7 Syndromic Overlap
  • 46.8 Conclusion
  • References
  • Part XVI: Organizational and Ethical Aspects
  • 47: Sepsis as Organ and Health System Failure
  • 47.1 Introduction: Introducing Sepsis-Reframing Risks and Relevance
  • 47.1.1 The Biomedical Lens: The Dogma
  • 47.1.2 Controversy
  • 47.1.3 The Impact of the Dogma on Research Horizons
  • 47.1.4 Modifications Within the Paradigm
  • 47.2 Political Science Intermezzo
  • 47.3 Modern Understanding of Risks: Looking at the Contexts
  • 47.4 Sepsis as Health System Failure
  • 47.5 Conclusion
  • References
  • 48: Burnout and Joy in the Profession of Critical Care Medicine
  • 48.1 Introduction
  • 48.2 Burnout Syndrome
  • 48.3 Prevalence of Burnout Syndrome Among Critical Care Professionals
  • 48.4 Burnout and Fulfillment in Critical Care as a Profession
  • 48.5 The Impact of ICU Burnout Syndrome
  • 48.5.1 Individual Impact
  • 48.5.2 Healthcare System and Patient Safety
  • 48.6 Risk Factors for Burnout Among ICU Clinicians
  • 48.7 Strategies to Mitigate Burnout
  • 48.8 Conclusion
  • References
  • 49: Advance Directives in the United Kingdom: Ethical, Legal, and Practical Considerations
  • 49.1 Introduction
  • 49.2 The Present
  • 49.3 Ethical Issues
  • 49.4 Legal Issues
  • 49.5 The Future
  • 49.6 Conclusion
  • References
  • Part XVII: Future Aspects
  • 50: Mobile Devices for Hemodynamic Monitoring
  • 50.1 Introduction
  • 50.2 Digital Stethoscope
  • 50.3 Electrocardiogram
  • 50.4 Blood Pressure
  • 50.5 Advanced Hemodynamic Monitoring
  • 50.6 Blood Transfusion Management
  • 50.7 Ultrasound
  • 50.8 Sensor Technology
  • 50.9 Conclusion
  • References
  • 51: Artificial Intelligence in the Intensive Care Unit
  • 51.1 Introduction
  • 51.2 Machine Learning
  • 51.2.1 Supervised Machine Learning
  • 51.2.1.1 Regression Learning
  • 51.2.1.2 Classification Learning
  • 51.2.2 Unsupervised Machine Learning
  • 51.3 AI Applications in Critical Care
  • 51.3.1 Length of Stay
  • 51.3.2 ICU Mortality
  • 51.3.3 Complications and Risk Stratification
  • 51.3.4 Mechanical Ventilation
  • 51.4 The Issue of Accuracy Versus Reliability
  • 51.5 Conclusion
  • References
  • Index

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