Annual Update in Intensive Care and Emergency Medicine 2023

Contents
Abbreviations
Part I: Precision Medicine
1: The Role of Transcriptomics in Redefining Critical Illness
1.1 Introduction
1.2 Transcriptomes: An Indispensable Player in Unraveling the Mechanisms of Sepsis
1.2.1 Overview of the Molecular Pathophysiology of Sepsis
1.2.2 Messenger RNA: The Driving Force of Transcriptomics
1.2.3 MicroRNA: The Master Regulators of Gene Expression
1.2.4 Long Non-coding RNA: The miRNA Sponges
1.3 From Transcriptomics to Clinical Tools
1.3.1 Time Is Critical: Current Challenges in the Early Detection of Sepsis
1.3.1.1 Rapid Host Transcriptomic Biomarkers for Sepsis
1.3.2 Trials and Tribulations: Current Challenges in the Treatment of Sepsis
1.3.3 Deriving Transcriptomic Endotypes for Sepsis
1.4 Challenges of Applying Transcriptomics in Critical Care
1.5 Conclusion
References
2: Metagenomic Sequencing in the ICU for Precision Diagnosis of Critical Infectious Illnesses
2.1 Introduction
2.2 Current Standards in Pathogen Detection
2.3 Principles of Metagenomics for Infectious Disease Diagnosis
2.4 DNA Sequencing vs. RNA Sequencing
2.5 Proof of Concept and Clinical Trial Data for Metagenomic Diagnostics
2.6 Metagenomics for Prediction of Pathogen Antimicrobial Resistance
2.7 Assessing the Host Response to Enhance Metagenomic Pathogen Detection
2.8 Metagenomics: Potential Hurdles and Important Considerations
2.9 Conclusion
References
3: Risk Stratification and Precision Medicine: Is It Feasible for Severe Infections?
3.1 Introduction
3.2 Endotypes of Severe Infections
3.3 How to Transfer Endotypes into Everyday Clinical Practice
3.4 Protein Biomarkers for Unselected Risk Classification
3.5 The Use of Biomarkers to Guide Immunotherapy in Severe Infections
3.6 Conclusion
References
4: Interrogating the Sepsis Host Immune Response Using Cytomics
4.1 Introduction
4.2 Historical Focus on Immature Granulocytes in Sepsis
4.3 Compensatory Anti-Inflammatory Response and Sepsis Immune Paresis
4.4 Lymphocyte Activation and Exhaustion
4.5 Pediatric Sepsis: Cytomics in the Developing Immune System
4.6 Conclusion
References
5: Precision Medicine in Septic Shock
5.1 Introduction
5.2 Omics Technologies
5.3 Treatments for Specific Endotypes of Patients with Septic Shock
5.3.1 Hypogammaglobulinemia
5.3.2 Endotoxemia
5.3.3 Hypercytokinemia
5.3.4 Sequential Hemadsorption
5.4 Non-catecholaminergic Vasopressors
5.4.1 Vasopressin
5.4.2 Selepressin
5.4.3 Terlipressin
5.4.4 Methylene Blue
5.4.5 Angiotensin II
5.5 Metabolic Resuscitation
5.5.1 Vitamin C (Ascorbic Acid)
5.5.2 Hydroxocobalamin
5.6 New Molecules for Adjuvant Treatment of Sepsis
5.6.1 Nangibotide
5.6.2 Recombinant Alkaline Phosphatase
5.6.3 Adrecizumab
5.6.4 Apoptotic Cells
5.7 Conclusion
References
Part II: Sepsis Biomarkers and Organ Dysfunction Scores
6: Host Response Biomarkers for Sepsis in the Emergency Room
6.1 Introduction
6.2 Biomarkers in the Context of Sepsis
6.2.1 Traditional Biomarkers: CRP and Procalcitonin (PCT)
6.2.2 Emerging Biomarkers
6.2.2.1 Presepsin
6.2.2.2 sTREM-1
6.2.2.3 Proadrenomedullin
6.3 Transcriptomics
6.4 Proteomics and Metabolomics
6.5 Conclusion
References
7: Repetitive Assessment of Biomarker Combinations as a New Paradigm to Detect Sepsis Early
7.1 Introduction
7.2 Limited Usefulness of Routinely Used Biomarkers of Sepsis
7.3 Time for a Paradigm Change in the Use of Sepsis Biomarkers
7.4 Pancreatic Stone Protein, A Novel Sepsis Biomarker That Is Released Early
7.5 Role of Repetitive Serial Assessments of CRP and PSP in the Diagnostic Workup of Sepsis
7.5.1 Pre-Symptomatic Diagnosis of Sepsis by Serial Assessment of PSP and CRP Levels in Patients at Risk
7.6 Conclusion
References
8: Organ Dysfunction Scores in the Adult ICU
8.1 Introduction
8.2 Definition and Rationale for Assessment of Organ Dysfunction
8.3 Variables Representing Organ Dysfunction and Their Implementation into Scoring Systems
8.4 Organ Systems Included in the Organ Dysfunction Scores in the ICU
8.4.1 Neurological Component
8.4.2 Cardiovascular Component
8.4.3 Respiratory Component
8.4.4 Hematological Component
8.4.5 Renal Component
8.4.6 Hepatic Component
8.4.7 Abdominal Component
8.4.8 Metabolic Component
8.4.9 Physical Component
8.5 Modified SOFA Scores
8.6 The Future of Organ Dysfunction Scores
8.7 Conclusion
References
Part III: ARDS
9: Ex Vivo Lung Perfusion Models to Explore the Pathobiology of ARDS
9.1 Introduction
9.2 ARDS Pathobiology Overview
9.3 Different Approaches to Inducing and Attenuating Lung Injury in EVLP Models: Lipopolysaccharide Challenge as an Example
9.4 Technical Considerations in EVLP Models
9.4.1 Ventilation
9.4.2 Perfusion Pressures and Flow Rate of Perfusate
9.4.3 Controls for Experiments
9.4.4 Cellular or Acellular Perfusion?
9.5 Defining ARDS in EVLP Models
9.6 EVLP Challenges
9.7 Conclusion
References
10: Interpretation of Lung Perfusion in ARDS
10.1 Introduction
10.2 Determinants of Gas Exchange
10.2.1 Ventilation
10.2.2 Perfusion
10.3 The Ventilation:Perfusion Ratio: Definition and Pitfalls
10.4 Static and Dynamic Assessment of Ventilation and Perfusion
10.5 Alveolar Perfusion Pressure
10.5.1 Perfusion as Determinant of Lung Injury
10.6 How to Assess Lung Perfusion
10.6.1 Assessment of Global Lung Perfusion
10.6.2 Assessment of Regional Perfusion
10.7 How to Manipulate Lung Perfusion
10.7.1 Drugs
10.7.2 Ventilation
10.7.3 Positioning
10.8 A Six-Compartment Model to Describe Regional V/Q Matching
10.9 Conclusion
References
11: A Structured Diagnostic Algorithm for Patients with ARDS
11.1 Introduction
11.2 Diagnosis of ARDS
11.2.1 Practical Steps
11.2.2 Uncertainties
11.3 First Phase of Evaluation (Days 1 and 2)
11.3.1 Practical Steps
11.3.2 Uncertainties
11.4 Second Phase of Evaluation (Days 3–5)
11.4.1 Practical Steps
11.5 Third Phase of Evaluation (Days 6–7)
11.5.1 Practical Steps
11.5.2 Uncertainties
11.6 Conclusion
References
12: Hemodynamic Implications of Prone Positioning in Patients with ARDS
12.1 Introduction
12.2 Hemodynamic Effects of Prone Positioning
12.2.1 Prone Positioning Affects Venous Return Determinants and May Increase Right Ventricular Preload
12.2.2 Prone Positioning May Decrease Pulmonary Vascular Resistance and Right Ventricular Afterload
12.2.3 Prone Positioning May Increase Left Ventricular Preload
12.2.4 Overall Effects of Prone Positioning on Cardiac Output
12.3 Detecting Preload Responsiveness in Patients in the Prone Position
12.3.1 Trendelenburg Maneuver
12.3.2 End-Expiratory Occlusion Test
12.3.3 Pulse Pressure Variation
12.3.4 Tidal Volume Challenge
12.3.5 Mini-Fluid Challenge
12.4 Conclusion
References
Part IV: Ventilatory Support
13: Update on the Management of Acute Respiratory Failure Using Non-invasive Ventilation and Pulse Oximetry
13.1 Introduction
13.2 Effectiveness and Utility of NIV
13.3 Key Clinical Trials from the Systematic Reviews
13.4 Current Knowledge of NIV for Respiratory Failure in the ICU
13.5 NIV for COVID-19
13.6 Key Clinical Trials and RECOVERY-RS
13.7 Current Knowledge About Use of NIV for COVID-19
13.8 Timing of Intubation When Patients Are Receiving NIV
13.9 Predicting Successful Treatment with HFNC
13.9.1 ROX Index in COVID-19
13.10 Monitoring Respiratory Failure Using SpO2: The Risk of Inaccuracy
13.10.1 Inaccuracy of Pulse Oximeters and Skin Color: New Investigations
13.11 Conclusion
References
14: Managing the Physiologically Difficult Airway in Critically Ill Adults
14.1 Introduction
14.2 Adverse Outcomes and Risk Factors
14.2.1 What Are the Outcomes of Tracheal Intubation in Critically Ill Adults?
14.2.2 Which Patients Are at Risk?
14.3 Hemodynamic Optimization
14.3.1 Is There an Optimal Induction Agent?
14.3.2 What Is the Role of Fluids?
14.3.3 What Is the Role of Vasopressors?
14.4 Mitigating Hypoxemia
14.4.1 Are Standard Pre-oxygenation Strategies Adequate?
14.4.2 What About Non-invasive Ventilation?
14.4.3 What About Apneic Oxygenation?
14.4.4 Should Mask Ventilation Be Avoided?
14.5 First Pass Success
14.5.1 Is It Time to Universally Adopt Video Laryngoscopy?
14.5.2 What About Intubation Adjuncts and Checklists?
14.6 Is It Time for New Approaches?
14.7 Conclusion
References
15: Dyspnea in Patients Receiving Invasive Mechanical Ventilation
15.1 Introduction
15.2 Definition, Prevalence and Intensity of Dyspnea
15.2.1 Definition
15.2.2 Prevalence and Intensity
15.3 Risk Factors for Dyspnea and Relation to Ventilator Settings
15.3.1 Pathophysiology of Dyspnea
15.3.2 Risk Factors Not Related to Ventilator Settings
15.3.3 How Often Do Ventilator Settings Contribute to Dyspnea?
15.4 Clinical Consequences of Dyspnea in Patients Receiving Invasive Mechanical Ventilation
15.4.1 Immediate Fear and Panic Related to Dyspnea
15.4.2 Impact of Dyspnea on Weaning
15.4.3 Association Between Dyspnea and Mortality
15.4.4 Delayed Psychological Consequences, Post-traumatic Stress Disorder
15.5 Underestimation of Dyspnea in Patients Receiving Invasive Mechanical Ventilation
15.5.1 Patients Are Not Asked
15.5.2 Discrepancies Between Patient Self-Reporting and Stakeholders’ Observations
15.6 Conclusion
References
16: The Potential Risks of Pressure Support Ventilation
16.1 Introduction
16.2 Principles of Operation of Pressure Support Ventilation
16.3 Respiratory Drive, Rate and Effort During Pressure Support Ventilation
16.4 Patient-Ventilator Interaction During Pressure Support Ventilation
16.4.1 Risk of Periodic Breathing
16.4.2 Risk of Diaphragm Weakness
16.4.3 Risk of Ineffective Efforts
16.4.4 Risk of Expiratory Asynchrony
16.4.5 Risk of Lung Injury
16.5 Conclusion
References
17: Advancing Sedation Strategies to Improve Clinical Outcomes in Ventilated Critically Ill Patients
17.1 Introduction
17.2 Evolution of Sedation Strategies and Evidence Evaluation
17.2.1 Daily Sedative Interruption
17.2.2 Light Sedation
17.2.3 No Sedation or Analgo-Sedation
17.2.4 Early Mobilization
17.3 Comparative Trials of Commonly Used Sedatives
17.4 Sedation Practice in Intensive Care Evaluation, the SPICE-III Trial
17.4.1 Early Sedation Depth in Ventilated Critically Ill Patients
17.4.2 Improving Patient-Centered Outcomes in Ventilated Critically Ill Adults
17.4.3 The Age Interaction with Early Dexmedetomidine Treatment
17.4.3.1 Critically Ill Older Patients
17.4.3.2 Critically Ill Younger Patients
17.4.3.3 Ventilated Critically Ill Surgical Patients
17.4.3.4 Critically Ill Patients with Sepsis
17.4.3.5 Critically Ill Cardiovascular Patients
17.5 Reducing the Burden of Delirium with Dexmedetomidine
17.6 Conclusion
References
Part V: Extracorporeal Support
18: Setting and Monitoring of Mechanical Ventilation During Venovenous ECMO
18.1 Introduction
18.2 Historical Perspective
18.2.1 Ventilation Strategies in ECMO Landmark Trials
18.2.2 Current Practice in ECMO-Experienced Centers
18.3 Targeting Ultra-Lung-Protective Mechanical Ventilation During ECMO
18.3.1 Tidal Volume
18.3.2 Plateau Pressure
18.3.3 Driving Pressure
18.3.4 Respiratory Rate
18.3.5 Mechanical Power
18.3.6 Applying Apneic Ventilation?
18.3.7 Preserving Spontaneous Ventilation and Diaphragmatic Function to Minimize P-SILI?
18.4 How to Set the Optimal PEEP on ECMO?
18.4.1 Electrical Impedance Tomography-Guided Strategy
18.4.2 Transpulmonary Pressure-Guided Strategy
18.4.3 Other Methods
18.5 Prone Positioning During ECMO
18.6 Gas Exchange Targets on ECMO
18.7 Mechanical Ventilation During ECMO Weaning
18.8 Conclusion
References
19: Early Mobilization in Patients Receiving ECMO for Respiratory Failure
19.1 Introduction
19.2 Evidence
19.3 Conclusion
References
20: Physiological Adaptations During Weaning from Venovenous ECMO
20.1 Introduction
20.2 Intercenter Variability in the Approach to Weaning
20.2.1 Different Preconditions for Weaning
20.2.2 Different Ventilatory Strategies During Weaning
20.2.3 Different Targeted Parameters During Weaning
20.2.4 Different Evaluation Criteria for a Weaning Trial
20.3 Physiology of Weaning from VV-ECMO
20.3.1 The Extracorporeal Circuit
20.3.1.1 V′O2ML, V′CO2ML and the Effects of Weaning
Effects of Reducing ECBF
Effects of Reducing SGF Rate Without Altering the FdO2
Effects of Reducing the FdO2 Prior to Reducing the SGF
20.3.2 The Patient
20.3.2.1 Physiology of Breathing Control
20.3.2.2 Effects of Weaning on Respiratory Center Output
Stepwise Decreases in SGF May Change the Position of the Metabolic Hyperbola
Stepwise Decreases in FdO2 or ECBF May Change the Set-Point of the Brain Curve
Changes in Breathing Pattern May Affect the Ventilation Curve
20.3.2.3 Monitoring Respiratory Center Output
20.3.3 The Ventilator
20.3.3.1 Passive, Controlled Patients
20.3.3.2 Spontaneously Breathing Patients
Maneuvers Reducing Effort and Stress
Maneuvers Reducing Effort But Not Stress
20.4 A Proposed Approach to Weaning
20.5 Conclusion
References
21: Novel Strategies to Enhance the Efficiency of Extracorporeal CO2 Removal
21.1 Introduction
21.2 Blood CO2 Transportation
21.3 Factors Affecting Extracorporeal CO2 Removal
21.4 Novel Strategies to Enhance the Efficiency of Extracorporeal CO2 Removal
21.4.1 Blood Mixing
21.4.2 Bicarbonate Removal
21.4.3 Carbonic Anhydrase
21.4.4 Acidification
21.5 Limitations
21.6 Conclusion
References
22: Extracorporeal Cardiopulmonary Resuscitation for Out-Of-Hospital Cardiac Arrest: A Systematic Approach
22.1 Introduction
22.2 System Design and Quality
22.3 Patient Selection
22.4 Transport
22.5 Patient Admission
22.6 ECMO Cannulation
22.7 Initial Diagnostic and Therapeutic Procedures
22.8 Intensive Care
22.9 Hospital Discharge and Long-Term Follow-Up
22.10 Conclusion
References
23: Temporary and Durable Mechanical Circulatory Support in the ICU
23.1 Introduction
23.2 Temporary Mechanical Circulatory Support
23.2.1 Devices
23.2.1.1 Intra-Aortic Balloon Pump
23.2.1.2 Impella
23.2.1.3 Protek Duo
23.2.1.4 TandemHeart
23.2.1.5 Veno-Arterial Extracorporeal Membrane Oxygenation
23.2.1.6 Surgically-Implanted Temporary Ventricular Assist Devices
23.2.2 Principles of Device Selection and Weaning of Temporary Mechanical Circulatory Support
23.2.3 Complications
23.3 Durable Mechanical Circulatory Support
23.3.1 Devices
23.3.2 Complications
23.3.2.1 Right Ventricular Failure
23.3.2.2 Hemocompatibility-Related Adverse Events
23.3.2.3 Driveline Infection
23.3.2.4 Aortic Insufficiency
23.4 Conclusion
References
Part VI: Fluids and Transfusion
24: Venous Congestion: Why Examine the Abdomen with Ultrasound in Critically Ill Patients?
24.1 Introduction
24.2 Case Study
24.3 Importance of Fluid Overload
24.4 Diagnosis of Venous Congestion
24.4.1 Inferior Vena Cava
24.4.2 Hepatic Veins
24.4.3 Renal Veins
24.4.4 Portal Veins
24.4.5 Splenic Veins
24.4.6 Femoral Veins
24.4.7 The VExUS Score
24.4.8 Surface Ultrasound or Transesophageal Echocardiography
24.5 Venous Congestion and RV Dysfunction
24.6 The Importance of Examining the Abdomen of Critically Ill Patients
24.7 Limitations and Pitfalls of Venous Congestion Indices
24.8 Back to the Case Study
24.9 Conclusion
References
25: The Most Important Questions in the Current Practice of Transfusion of Critically Bleeding Patients
25.1 Introduction
25.2 Therapeutic Goals in Treating Major Hemorrhage
25.3 Question 1: Fibrinogen Concentrate vs. Cryoprecipitate?
25.4 Question 2: Early Empiric Fibrinogen, Prothrombin Complex Concentrate, and Other Coagulation Factors (Usually in Combination with Crystalloid for Volume) vs. Fresh-Frozen Plasma?
25.5 Question 3: Whole Blood vs. Fractionated Blood Components?
25.6 Question 4: Lyophilized Plasma vs. FFP?
25.7 Question 5: The Value of Viscoelastic Testing
25.8 Question 6: The Value of Platelets (Including Cold Stored and Cryopreserved)
25.9 Conclusion
References
Part VII: Acute Renal Failure
26: Fluid Management and Acute Kidney Injury
26.1 Introduction
26.2 Fluid Status and Kidney Function
26.3 Why Prescribe Fluids?
26.4 What to Prescribe: Types of Fluids
26.4.1 Colloids
26.4.2 Crystalloids
26.4.3 Bicarbonate Infusion and Acute Kidney Injury
26.5 How to Prescribe: Volume of Fluids
26.6 When to Stop Fluid Therapy?
26.7 De-escalation of Fluid Therapy
26.8 Fluid Management During RRT
26.9 Areas for Further Research
26.10 Conclusion
References
27: Cardiorenal Syndrome 1: What’s in a Name?
27.1 Introduction
27.2 Epidemiology
27.3 Pathophysiology
27.4 Definitions
27.4.1 Urine Output Criteria
27.4.2 Baseline Serum Creatinine
27.4.3 Serum Creatinine Criteria
27.4.3.1 Worsening Renal Function
27.4.3.2 Pseudo-AKI, Functional AKI, and Subclinical AKI
27.5 Management
27.5.1 Renal Replacement Therapy
27.6 Conclusion
References
Part VIII: The Microcirculation and Metabolism
28: Update on the Microcirculatory Assessment of the Critically Ill Patient
28.1 Introduction
28.2 What Microcirculatory Measurement Has Taught Us About Pathophysiology
28.3 Fluid Status
28.4 Sepsis
28.5 COVID-19
28.6 Analysis of Microcirculatory Images and MicroTools as a Point-of-Care Tool for Microcirculatory Assessment at the Bedside
28.7 Database Deep Learning and Artificial Intelligence
28.8 Future Developments
28.9 Conclusion
References
29: Intracellular Measurements of Micronutrients in the Critically Ill
29.1 Introduction
29.2 Inflammation
29.3 Real vs. Apparent Deficiency
29.4 Elective Surgery as a Model for Inflammatory Response
29.5 Intracellular Measurements
29.5.1 Practical Issues: Erythrocytes
29.5.2 Practical Issues: Leukocytes
29.6 Clinical Studies with Intracellular Measurements
29.6.1 Elective Knee Arthroplasty
29.6.2 Critically Ill Patients
29.7 Discussion
29.8 Conclusion
References
30: Optimal Glycemic Targets in Critically Ill Patients with Diabetes
30.1 Introduction
30.2 Early Trials of Glucose Control During Admission to the ICU
30.3 Clinical Practice Guidelines
30.4 Prevalence of Diabetes in Patients Admitted to the ICU
30.5 Evaluation of Previous Randomized Clinical Trials When Focusing on Patients with Pre-existing Diabetes
30.6 Pre-existing Diabetes Relationship to Blood Glucose Metrics
30.7 Rationale for a Personalized Approach to Glycemic Control
30.8 Studies of More Personalized Approach to Glucose Control
30.9 Future Research
30.10 Conclusion
References
Part IX: A Look Back at COVID-19
31: Hydroxychloroquine: Time for Reappraisal of Its Effect in COVID-19 Patients
31.1 Introduction
31.2 SARS-CoV-2
31.3 Aminoquinolones
31.3.1 In Vitro Studies
31.3.2 Clinical Studies
31.4 Conclusion
References
32: Blood Purification in COVID-19 in the Absence of Acute Kidney Injury
32.1 Introduction
32.2 Tackling the Inflammatory Storm Initiated by COVID-19
32.2.1 Sorbents
32.2.2 Therapeutic Plasma Exchange
32.3 Removing SARS-CoV-2 and Nucleocapsids
32.3.1 SARS-CoV-2 Removal by Seraph® 100
32.3.2 Removal of Viral Nucleocapsids by Seraph® 100
32.4 Removing Endotoxin During Severe COVID-19 Infection
32.5 Conclusion
References
Part X: Neurologic Considerations
33: Epidemiology, Outcomes, and Costs of Pediatric Traumatic Brain Injury Treated in the ICU
33.1 Introduction
33.2 Epidemiology
33.3 Pediatric Anatomy and Physiology
33.4 Treatment
33.5 Outcomes and Sequelae
33.5.1 Neurological Sequelae
33.5.2 Cognitive and Psychiatric Sequelae
33.5.3 Endocrinological Dysfunction
33.6 Prognostication After Pediatric TBI
33.7 Costs
33.8 Future Perspectives
33.9 Conclusion
References
34: Quality Improvement in the Determination of Death by Neurologic Criteria Around the World
34.1 Introduction
34.2 Brain Death/Death by Neurologic Criteria Mimics
34.3 Confounders That Interfere with the Clinical Brain Death/Death by Neurologic Criteria Evaluation
34.3.1 Hypothermia
34.3.2 Muscle Paralysis
34.3.3 Sedation/Analgesia
34.3.4 Hypoxia
34.3.5 Hypotension
34.3.6 Hypoglycemia or Other Endocrine or Metabolic Abnormality
34.3.7 Basal Skull Fracture with Hemotympanum
34.3.8 Facial Trauma
34.3.9 Pulmonary Injury/Disease
34.3.10 Cervical Spine Injury
34.3.11 Anophthalmia
34.4 Considerations for Performance of the Clinical Examination
34.5 Apnea Test Safety Considerations
34.5.1 Hypotension
34.5.2 Hypoxemia
34.5.3 Pneumothorax, Pneumomediastinum and Pneumoperitoneum
34.5.4 Arrhythmia/Cardiac Arrest
34.6 Ancillary Testing Confounders/Limitations
34.7 Special Considerations for Brain Death/Death by Neurologic Criteria Determination in Pediatric Patients
34.8 Conclusion
References
Part XI: Obstetric Issues
35: COVID-19 ARDS in Pregnancy: Implications for the Non-COVID Era
35.1 Introduction
35.2 Pregnancy, ARDS, and SARS-CoV-2 Infection
35.3 Maternal Management of COVID-19 ARDS
35.3.1 Prone Position
35.3.2 Extracorporeal Membrane Oxygenation (ECMO)
35.3.3 Pharmacological Treatment
35.4 Timing and Delivery of the Fetus
35.5 Conclusion
References
36: Amniotic Fluid Embolism
36.1 Introduction
36.2 Pathophysiology
36.3 Incidence
36.4 Clinical Features
36.5 Diagnosis
36.6 Management
36.7 Conclusion
References
Part XII: Pre- and Post-Intensive Care
37: Remote Telehealth Aid During Humanitarian Crisis
37.1 Introduction
37.2 Methods of Remote Healthcare
37.3 Methods of Remote Education and Communication
37.4 Opportunities for Improvement with Remote Platforms
37.5 Remote Aid During a Humanitarian Crisis
37.5.1 Approaches to Providing Remote Aid During a Humanitarian Crisis
37.5.2 Barriers to NETCCN Telemedicine Application Adaptation for Remote Humanitarian Aid
37.6 Providing Materiel Aid
37.7 Patient Sharing
37.8 Operational Security Issues
37.9 Potentially Desirable Outcomes
37.10 Medical-Legal Considerations
37.11 Conclusion
References
38: Boarding in the Emergency Department: Challenges and Success Strategies to Mitigate the Current Crisis
38.1 Introduction
38.2 ED Boarding Versus ED Crowding
38.3 Drivers of Boarding
38.4 Impact of Boarding
38.5 System Barriers that Enable Boarding
38.6 Potential Repair Strategies
38.7 Clinician and Team Education
38.8 Conclusion
References
39: Post-Intensive Care Syndrome Revisited in Light of the COVID-19 Pandemic
39.1 Introduction
39.2 Definition and Epidemiology
39.3 Association with Functional Outcome
39.3.1 Cognitive Impairment
39.3.2 Psychiatric Symptoms
39.3.3 Physical Impairment
39.4 Diagnostics
39.5 Interventions
39.6 Post-Intensive Care/Post-COVID-19 Syndrome
39.7 Conclusion
References
Part XIII: Ethical Issues
40: Rethinking the Role of Palliative Care in the ICU
40.1 Introduction
40.2 Definition
40.3 Barriers to Palliative Care in the ICU
40.4 Models of Palliative Care
40.5 Primary (Generalist) Palliative Care
40.6 Specialist (Secondary) Palliative Care
40.7 Future Research
40.8 Conclusion
References
Index