Controversies in Critical Care

Description:

The book covers vigorously debated controversial topics in the field of critical care medicine over the years. It provides the reader with a balanced approach and guidance based on historical and currently available evidence in dealing with contentious clinical scenarios. The book reviews the most relevant, contemporaneous evidence on each topic and provides practical guidelines for clinical practice.

The book includes chapters that follow a structured approach to controversies related to specific organ systems. The topics covered provide a summary of the most relevant, practice-changing studies in the field of critical care medicine. Each topic describes the basic applied physiology, points of controversy, the evidence base, and summarizes the key points at the end. It includes brief description of landmark studies on each controversial topic.

The book serves as an important clinical guide to practitioners of critical care medicine when confronted with challenging clinical scenarios. Besides, it is a useful source of information to postgraduate trainees in various medical specialties. The topics addressed are among the most widely discussed during postgraduate examinations. It is also relevant for practitioners in general medicine and specialized areas of practice, including pulmonology (respiratory medicine), cardiology, neurology, nephrology, gastroenterology, and surgical specialties.

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Preface

We are just about finding our feet after a global pandemic, often fraught with controversies. The specialty of critical care medicine played a pivotal role during the Covid-19 pandemic, with an unprecedented number of patients requiring respiratory support. The pandemic era has firmly entrenched critical care medicine as a crucial area of specialization during a crisis.

Although relatively young, our specialty has experienced its fair share of controversies. When Vivi Ebert, a 12-year-old girl, presented to the Blegdam Hospital, Copenhagen, in August 1952 with respiratory failure due to poliomyelitis, Bjorn Ibsen chose to perform a tracheostomy to apply positive pressure ventilation. Ibsen ushered in the era of modern intensive care; however, many of his colleagues did not see eye to eye with him. It is pertinent that we continue to face similar controversies with tracheostomy even today, particularly regarding the timing.

Medical science has evolved over the years; unlike in the past, we seek evidence before we embark upon any novel therapeutic intervention. Randomized controlled trials, although by no means perfect, are least prone to bias, and occupy the apex of the pyramid of evidence.

Several landmark papers have addressed ongoing controversies in critical care medicine. There have been practice-changing clinical trials, such as the ARDSNet trial that ushered in the epoch of lung-protective ventilation. On the contrary, other studies have failed to confirm the putative benefits of interventions that seemed to have a strong physiological rationale, like intensive glycemic control in critical illness. Besides, evidence keeps changing with time, given the dynamic nature of science. Many interventions remain steeped in controversy due to conflicting results from controlled clinical trials.

In this book, we have undertaken an evidence-based review of contentious topics in critical care medicine, highlighting landmark papers. Each topic addresses the putative mechanisms behind possible benefits of therapies, the relative advantages and disadvantages, and finally, how it fares when it boils down to real-world clinical practice. We have tried to include most of the controversies of contemporaneous

interest, but this is by no means a comprehensive list. It has been an enlightening experience to work through the evidence. We hope our readers, including practitioners and trainees in critical care medicine, find it equally interesting and thought-provoking. 

Table of contents : 
Foreword
Preface
Contents
About the Authors
Part I: Respiratory Support in the Critically Ill
1: Oxygenation Targets in the ICU: Conservative or Liberal?
1.1 Introduction
1.2 What Is Hyperoxia?
1.3 What Are the Physiological Consequences of Hyperoxia?
1.3.1 Lungs
1.3.2 Vasoconstrictor Effect
1.3.3 Control of Breathing
1.4 What Does Clinical Evidence Suggest in Real-World Practice?
1.4.1 Supplemental Oxygen in ST-Elevation Myocardial Infarction (STEMI): The AVOID Trial
1.4.2 The Oxygen-ICU Study
1.4.3 The ICU-ROX Study
1.4.4 The HYPERS2S Study
1.4.5 The LOCO2 Trial
1.4.6 The HOT-ICU Trial
1.4.7 The PILOT Trial
1.4.8 Oxygenation Targets in Hypoxic-Ischemic Encephalopathy
References
2: The Hypoxic Drive, Supplemental Oxygen, and Hypercapnia
2.1 Introduction
2.2 Dead Space
2.2.1 Anatomical Dead Space
2.2.2 Alveolar Dead Space
2.2.3 Physiological Dead Space
2.3 Oxygen Administration and Respiratory Drive: The Evidence
2.4 The Haldane Effect
2.5 Loss of the Hypoxic Pulmonary Vasoconstrictor Effect
References
3: Noninvasive Respiratory Support in Acute Hypoxemic Respiratory Failure
3.1 Introduction
3.2 Modalities and Potential Benefits of Noninvasive Respiratory Support
3.3 Potential Harm from Noninvasive Respiratory Support
3.3.1 Patients Self-Inflicted Lung Injury (P-SILI)
3.3.2 Diaphragmatic Dysfunction
3.4 Techniques of Noninvasive Respiratory Support
3.5 Predictors of Failure of Noninvasive Respiratory Support
3.6 What Does the Evidence Suggest?
References
4: PEEP Titration by the Bedside: How Do We Set It Right?
4.1 Physiological Effects of PEEP
4.2 Adverse Effects of PEEP
4.3 How Do We Titrate PEEP?
4.3.1 PEEP Tables
4.3.2 Oxygenation Response
4.3.3 Compliance
4.3.4 Driving Pressure
4.3.5 Esophageal Pressure
4.3.6 Imaging-Guided PEEP Titration
4.4 Electrical Impedance Tomography (EIT) for PEEP Titration
4.5 High vs. Low Levels of PEEP
References
5: Do Vigorous Spontaneous Respiratory Efforts Lead to Patient Self-Inflicted Lung Injury (P-SILI)?
5.1 Introduction
5.2 Mechanisms of P-SILI
5.2.1 Nonuniform Distribution of Pleural Pressure
5.2.2 Increase in the Transmural Pressure Within the Pulmonary Capillaries
5.3 Patient-Ventilator Dyssynchrony
5.3.1 Double Triggering
5.3.2 Reverse Triggering
5.4 Evidence for P-SILI
5.5 Monitoring of Respiratory Drive and Prevention of P-SILI
5.5.1 Clinical Monitoring
5.5.2 Objective Measures of Spontaneous Respiratory Efforts
5.6 How Can P-SILI Be Prevented?
5.6.1 Noninvasive Ventilation (NIV) and High-Flow Nasal Oxygen (HFNO)
5.6.2 Early Invasive Ventilation as a Part of a Lung-Protective Strategy
References
6: Prone Ventilation in Acute Respiratory Distress Syndrome
6.1 Introduction
6.2 How Does Prone Ventilation Result in More Homogenous Ventilation?
6.2.1 Difference in Lung Mass Between the Dorsal and Ventral Regions
6.2.2 Compression Effect Exerted by the Heart
6.2.3 Difference in Compliance Between the Ventral and Dorsal Chest Wall
6.2.4 The Shape of the Lung and the Chest Wall
6.2.5 Effect of Intra-Abdominal Pressure
6.3 Does the Prone Position Result in a More Homogenous Distribution of Lung Perfusion?
6.4 What Is the Evidence?
References
7: Neuromuscular Blocking Agents in Severe Acute Respiratory Distress Syndrome: Benefit or Harm?
7.1 Introduction
7.2 Beneficial Effects of Neuromuscular Blocking Agents
7.3 Possible Harm from NMBs
7.4 Evidence for NMB Use in ARDS
References
8: Ventilator-Associated Pneumonia: Newer Definitions, Controversies, and Perspectives
8.1 Introduction
8.2 Definitions: Diagnosis
8.3 VAP and Clinical Outcomes
8.4 Ventilator-Associated Tracheobronchitis Vs. VAP
8.5 Efficacy of VAP Prevention Bundles
8.5.1 Semi-Recumbent Position, Sedation Hold, and Spontaneous Breathing Trials
8.5.2 Subglottic Secretion Drainage
8.5.3 Maintenance of Cuff Pressure
8.5.4 Modified Tube Surface and Coated Endotracheal Tubes
8.5.5 Hand Hygiene and Oral Care
8.5.6 Selective Digestive Decontamination
8.6 Duration of Therapy
References
9: Lung-Protective Ventilation and Hypercapnia: How Much Is Permissible?
9.1 Introduction
9.2 The Physiologic Effects of Hypercapnia
9.2.1 Effects on the Lung
9.2.2 Effects on the Pulmonary and Systemic Circulation
9.2.3 Neurological Effects
9.2.4 Effect on the Diaphragm
9.2.5 Miscellaneous Effects
9.3 What Does Clinical Evidence Suggest (Table 9.1)?
9.4 Interventions to Reduce Carbon Dioxide Levels
9.4.1 Increasing Minute Ventilation
9.4.2 Reduction of Dead Space
9.4.3 Optimization of PEEP Levels
9.4.4 Prone Ventilation
9.4.5 The Use of Buffers
9.4.6 Extracorporeal Carbon Dioxide Removal
References
10: Tracheostomy in the ICU: Early or Late?
10.1 Introduction
10.2 Tracheostomy: Pros and Cons
10.3 The Evidence: Early Vs. Delayed Tracheostomy
10.4 Meta-Analyses on Tracheostomy Timing
10.5 Early Tracheostomy in Specific Subgroups of Patients
10.5.1 Post-Cardiovascular Surgery
10.5.2 Patients with Neurological Injury
References
11: Diaphragmatic Dysfunction in Critical Illness
11.1 Introduction
11.2 Clinical Signs of Diaphragm Dysfunction
11.3 Causes of Diaphragm Dysfunction
11.3.1 Electrolyte and Endocrine Abnormalities
11.3.2 Sedatives, Neuromuscular Blocking Drugs, and Corticosteroids
11.3.3 Ventilator-Induced Diaphragm Dysfunction (VIDD)
11.3.4 Sepsis
11.3.5 Primary Neuromyopathic Syndromes
11.4 Monitoring of Diaphragm Activity
11.4.1 Ultrasonographic Evaluation of Thickening Fraction
11.4.2 Ultrasonographic Evaluation of Diaphragmatic Excursion
11.5 Other Techniques
11.5.1 Transdiaphragmatic Pressure
11.5.2 Diaphragm Electromyography
11.6 Diaphragmatic Weakness and Clinical Outcomes
11.7 Prevention
11.8 Management of Diaphragm Dysfunction
References
12: Weaning and Liberation from Mechanical Ventilation: Is My Patient Ready?
12.1 The Spontaneous Breathing Trial (SBT)
12.2 Techniques of SBT
12.3 The Evidence
12.4 SBT with Automatic Tube Compensation (ATC)
References
13: When to Decannulate a Tracheostomy?
13.1 Introduction
13.2 Weaning and Liberation from Mechanical Ventilation
13.3 Decannulation Strategies
13.3.1 Capping Techniques
13.4 Capping vs. Single-Stage Decannulation: The Evidence
13.4.1 The REDECAP Randomized Controlled Trial
13.5 Endoscopic Evaluation Before Decannulation
13.6 Cuff Deflation During Weaning
References
14: Thrombolytic Therapy in Acute Pulmonary Embolism
14.1 Introduction
14.2 Pathophysiology of Acute Pulmonary Embolism (PE)
14.3 Risk Stratification of PE
14.3.1 High-Risk (Massive) PE
14.3.2 Intermediate-Risk (Submassive) PE
14.3.3 Low-Risk (Non-massive) PE
14.4 Contraindications to Thrombolysis in PE
14.5 Early Clinical Trials of Thrombolysis
14.6 Thrombolysis in Acute Massive (High-Risk) PE
14.7 Thrombolysis in Submassive (Intermediate-Risk) PE
14.8 Low-Dose Thrombolysis
14.9 Catheter-Directed Thrombolysis (CDT)
References
Part II: Shock and Circulatory Support
15: Corticosteroids in Sepsis: The Enduring Debate
15.1 Introduction
15.2 The Pathophysiological Basis of Steroid Effect in Sepsis
15.3 Earlier Randomized Controlled Trials
15.4 Recent Randomized Controlled Trials
15.5 APROCCHSS vs. ADRENAL: Why the Difference?
15.6 Corticosteroids in Severe Sepsis Without Septic Shock
15.7 Meta-Analysis on the Efficacy of Corticosteroids in Septic Shock
References
16: Hyperlactatemia in Critical Illness: Time for Reappraisal?
16.1 Introduction
16.2 Lactate Production and Metabolism
16.3 Why Do Lactate Levels Rise in the Critically Ill?
16.4 Does Hyperlactatemia Occur Due to Impaired Oxygen Delivery in Sepsis?
16.5 Is There a Mismatch Between Oxygen Consumption and Delivery in Sepsis?
16.6 What Is the Source of Lactate in Sepsis?
16.6.1 Impaired Pyruvate Dehydrogenase Activity
16.6.2 Lactate Release from the Lung
16.6.3 Hypermetabolic State
16.6.4 Exogenous Catecholamines
16.6.5 Tissue Hypoxia
16.7 Lactate Clearance: A Misnomer in Sepsis
16.8 Lactate-Guided Resuscitation
16.9 The ANDROMEDA-SHOCK Trial
References
17: Permissive Hypotension in Severe Trauma
17.1 Introduction
17.2 Problems with the Conventional Approach
17.3 Mechanism of Coagulopathy in Trauma
17.4 The Concept of Permissive Hypotension in Trauma
17.5 What Is the Evidence for Permissive Hypotension in Trauma?
17.6 Blood Pressure Target in Traumatic Brain Injury
17.7 Transfusion of Blood Products in Trauma
References
18: Assessment of Volume Responsiveness in the Critically Ill
18.1 Basic Physiology: The Frank-Starling Curve
18.2 Techniques to Assess Fluid Responsiveness
18.2.1 Passive Leg Raising
18.2.2 Pulse Pressure and Stroke Volume Variation
18.2.3 End-Expiratory Occlusion Test
18.2.4 Respiratory Variation of the Inferior Vena Caval Diameter
18.2.5 Variation in the End-Tidal Carbon Dioxide Level
18.2.6 The Mini-Fluid Challenge
References
19: Getting Rid of Excess Fluid: The Strategy of De-resuscitation
19.1 Introduction
19.2 Adverse Consequences of Fluid Overload
19.3 What Is De-resuscitation?
19.4 What Is the Evidence to Support a De-resuscitative Strategy?
19.5 Possible Harm from a De-resuscitative Strategy?
References
20: Are We Done with Early Goal-Directed Therapy?
20.1 Introduction
20.2 Early Goal-Directed Therapy (EGDT) in Sepsis
20.3 The Evidence
20.4 Where to Next in Sepsis Resuscitation?
References
21: Normal Saline Versus Balanced Crystalloids Revisited
21.1 Introduction
21.2 The Possible Adverse Effects of Normal Saline
21.2.1 Hyperchloremia and Acidosis
21.2.2 Hyperchloremia and Tubuloglomerular Feedback
21.2.3 Other Possible Harmful Effects of Hyperchloremia
21.3 The Evidence
21.3.1 The SPLIT Trial
21.3.2 The SMART Trial
21.3.3 The SALT-ED Trial
21.3.4 The BaSICS Trial
References
22: Liberal Fluid Resuscitation Vs. Early Vasopressors in Septic Shock
22.1 Introduction
22.2 The Evidence Behind Fluid Resuscitation
22.3 How Does Excessive Fluid Administration Cause Harm?
22.4 Evidence of Possible Harm from Excess Fluid
22.5 A Fluid-Restrictive Approach
22.6 Early Vasopressor Administration
References
23: Epinephrine and Outcomes Following Cardiac Arrest
23.1 Introduction
23.2 Could Epinephrine Lead to Adverse Outcomes Following Out-of-Hospital Cardiac Arrest?
23.2.1 Observational Studies
23.2.2 Randomized Controlled Trials
23.3 Evidence from Meta-Analyses
23.4 Does Time to Administration Matter?
23.5 High- Vs. Standard-Dose Epinephrine
References
24: Targeted Temperature Management in Out-of-Hospital Cardiac Arrest
24.1 Introduction
24.2 Physiologic Rationale
24.3 The Evidence for Targeted Temperature Management
24.3.1 The Trailblazers: The European and Australian Trials of 2002
24.3.2 The TTM-1 Trial
24.3.3 Duration of Targeted Temperature Management: 24 vs. 48 h
24.3.4 Hypothermia in Non-shockable Rhythms: The HYPERION Trial
24.3.5 The TTM-2 Trial
24.4 Points of Contention
24.5 Hypothermia in Relation to the Severity of Post-cardiac Arrest Syndrome
References
Part III: Acute Kidney Injury and Renal Replacement Therapy
25: Augmented Renal Clearance: When Supranormal Renal Function May Cause Harm
25.1 Introduction
25.2 Definition
25.3 Risk Factors, Pathophysiological Mechanisms
25.4 How Do You Diagnose ARC?
25.5 Scoring Systems to Identify Risk Factors ARC
25.6 What Is the Impact of ARC on Drug Clearance in Critically Ill Patients?
25.7 ARC and the Newer Antibiotics
25.8 Efficacy of Combination Therapy in ARC
References
26: Renal Replacement Therapy in Acute Kidney Injury: Is Timing All Important?
26.1 Introduction
26.2 Renal Replacement Therapy: Benefit vs. Possible Harm
26.3 Early vs. Late: The Evidence
26.3.1 The ELAIN Trial
26.3.2 The AKIKI Trial
26.3.3 The IDEAL-ICU Trial
26.3.4 The STARRT-AKI Trial
26.3.5 The AKIKI 2 Trial
26.4 Summary
References
27: Optimizing the Dose of Renal Replacement Therapy
27.1 Calculation of CRRT Dose
27.2 Evidence for Dosing
27.3 Meta-Analysis Comparing Doses
27.4 Prescribed Vs. Delivered Dose
27.5 High-Volume Hemofiltration (HVHF)
References
28: Renal Replacement Therapy in the Critically Ill: Continuous Vs. Prolonged Intermittent Therapies
28.1 Introduction
28.2 How Do Continuous Vs. Prolonged Intermittent Therapies Differ?
28.3 Urea Clearance and Correction of Acidosis with PIRRT
28.4 Hemodynamic Stability During PIRRT
28.5 Electrolyte Abnormalities
28.6 Outcomes of CRRT Vs. PIRRT: Clinical Studies
28.6.1 Sustained Low-Efficiency Daily Diafiltration (SLED-f)
28.7 Meta-analysis: CRRT Vs. PIRRT
References
Part IV: Neurocritical Care
29: Does Intracranial Pressure Monitoring Help in Severe Traumatic Brain Injury?
29.1 Introduction
29.2 Early Studies on ICP Monitoring
29.3 Pros and Cons of ICP Monitoring
29.4 What Is the Evidence for the Usefulness of ICP Monitoring?
References
30: Therapeutic Hypothermia in Traumatic Brain Injury
30.1 Introduction
30.2 Hypothermia: Mechanisms
30.3 Adverse Effects of Cooling
30.4 Methods of Cooling
30.5 The Evidence
30.5.1 Early Studies of Hypothermia in TBI
30.5.2 Clifton et al. (NABIS: H, 2001)
30.5.3 Clifton et al. (NABIS: H II, 2011)
30.5.4 Maekawa et al. (B-HYPO, 2015)
30.5.5 Andrews et al. (EUROTHERM, 2015)
30.5.6 Cooper et al. (POLAR, 2018)
30.6 Meta-analyses
References
31: Decompressive Craniectomy in Traumatic Brain Injury
31.1 Introduction
31.2 Pathophysiology
31.3 Evidence
31.4 Controversies
References
32: Optimization of Osmotherapy in Cerebral Edema
32.1 Introduction
32.2 Basic Pharmacology and Mechanism of Action
32.2.1 Mannitol
32.2.2 Hypertonic Saline
32.3 Traumatic Brain Injury
32.4 Acute Ischemic Stroke
32.5 Intracerebral Hemorrhage
32.6 Subarachnoid Hemorrhage
References
33: How Much Sedation in Critically Ill Patients on Mechanical Ventilation?
33.1 Introduction
33.2 Importance of Monitoring the Level of Sedation
33.3 Evidence Supporting the Level of Sedation
33.3.1 Daily Interruption of Sedation
33.3.2 Daily Interruption Combined with a Spontaneous Breathing Trial
33.3.3 Sedation vs. No Sedation
33.4 Does Sedation Use Lead to Hemodynamic Instability and Organ Dysfunction?
33.5 The Impact of Sedation During the Early Phase of Mechanical Ventilation
References
34: Delirium in the Intensive Care Unit: Are We Paying Enough Attention?
34.1 Introduction
34.2 Delirium and Clinical Outcomes
34.3 Delirium Assessment Tools
34.4 Types of Delirium
34.5 Pharmacological Interventions for Delirium
34.6 The Non-Pharmacological Approach
34.7 A “Bundled” Strategy
References
35: Clearing the Cervical Spine in Trauma Patients
35.1 Introduction
35.2 Rationale
35.3 C-Spine Clearance
35.3.1 National Emergency X-Radiography Utilization Study (NEXUS) Criteria
35.3.2 Canadian C-Spine Rules (CCR)
35.4 What Is the Evidence Behind Appropriate C-Spine Imaging in the Patient with Blunt Trauma?
References
Untitled
Part V: Metabolic Support in Critical Illness
36: Glycemic Control in the Critically Ill
36.1 Review of Evidence
36.1.1 The Leuven 1 Trial—Surgical ICU Patients
36.1.2 The Leuven 2 Trial—Medical ICU Patients
36.1.3 The ANZICS NICE-SUGAR Trial
36.2 Reconciling with Conflicting Evidence
36.2.1 Time in the Target Range
36.2.2 Should Blood Glucose Targets Be Based on Hemoglobin A1c Levels?
36.2.3 Diabetics Vs. Non-diabetics
36.2.4 Continuous Measurement of Glucose Levels
References
37: Vitamin C in Sepsis: End of the Debate?
37.1 Introduction
37.2 ROS: Pathophysiological Mechanisms of Injury
37.3 The Antioxidant Effect of Vitamin C in Sepsis
37.4 Vitamin C in Sepsis: Clinical Studies
37.4.1 High-Dose Vitamin C
37.4.2 Vitamin C in Patients with Sepsis and Acute Respiratory Distress Syndrome (ARDS)
37.4.3 Vitamin C as Part of Combination Therapy
37.4.4 Meta-analysis of Vitamin C in Sepsis
References
Part VI: The Gut and Nutrition
38: Early or Supplemental Parenteral Nutrition vs. Enteral Nutrition Alone in the Critically Ill
38.1 Introduction
38.2 The Role of Parenteral Nutrition (PN)
38.3 Early or Supplemental PN and Outcomes: The Evidence
38.3.1 Early PN
38.3.2 Supplemental PN in General ICU Patients
38.3.3 Supplemental PN in Under- and Overweight Subjects
38.3.4 Supplemental PN Following Abdominal Surgery
38.3.5 Individualized Calorie and Protein Delivery
38.4 Nutritional Strategies for the Future
References
39: Stress Ulcer Prophylaxis in the Critically Ill
39.1 Introduction
39.2 Pathophysiology and History
39.3 Controversies
39.4 Recent Trials
References
40: Do Tradition-Borne Fasting Practices Apply to ICU Patients with a Protected Airway?
40.1 Introduction
40.2 Fasting in the ICU
40.3 Possible Harmful Effects of Fasting
40.4 Pre-procedural Fasting in Critically Ill Patients with Protected Airway
40.5 Is It Time to Reconsider the Duration of Fasting in ICU Patients—What Is the Evidence?
References
Part VII: Infections and Antibiotic Therapy
41: Multidrug-Resistant Gram-Negative Bacteria in the ICU: Do We Have Answers?
41.1 Introduction
41.2 What Is Antimicrobial Resistance (AMR)? How Does It Occur?
41.2.1 Limitation of Drug Uptake by the Microorganism
41.2.2 Alteration in Drug Targets
41.2.3 Inactivation of the Antimicrobial Agent
41.2.4 Efflux Pumps
41.3 Multidrug Resistance (MDR) and Extensive Drug Resistance (XDR)
41.4 Antibiotic Resistance in the ICU
41.5 Gram-Negative Infections
41.6 MDR Gram-Negative Infections in the ICU and Outcomes
41.7 Ceftolozane/Tazobactam
41.8 Ceftazidime/Avibactam
41.9 Meropenem/Vaborbactam
41.10 Plazomicin
41.11 Eravacycline
References
42: Empirical Antibiotic Therapy: De-escalation Demystified
42.1 De-escalation and the Use of Multiple Antimicrobial Agents
42.2 De-escalation and Emergence of Bacterial Resistance
42.3 De-escalation and the Duration of Antibiotic Therapy
42.4 Scoring Antibiotics to Guide De-escalation
42.5 Evidence for De-escalation
References
43: Is It the End of the Road for Inhaled Antibiotic Therapy in Ventilator-Associated Pneumonia?
43.1 Introduction
43.2 Why the Inhaled Route?
43.3 Mode of Delivery
43.3.1 Particle Size, Nebulizer Type
43.3.2 Circuit and Ventilator Setup
43.4 What Does Evidence Suggest Regarding the Efficacy of Inhaled Therapy?
43.4.1 Randomized Controlled Trials
43.4.2 Meta-analyses
43.4.3 The Future
References
44: Duration of Antibiotic Therapy in the Critically Ill
44.1 Introduction
44.2 Duration of Antibiotic Therapy: Intra-Abdominal Infections
44.3 Duration of Antibiotic Therapy: Ventilator-Associated Pneumonia
44.4 Duration of Antibiotic Therapy: Gram-Negative Bacteremia
44.5 Procalcitonin to Guide the Duration of Antibiotic Therapy
References
45: Selective Digestive Decontamination: Helpful or Harmful?
45.1 Introduction
45.2 Pathophysiology, History, and Controversy
45.3 Recent Trials
References
Part VIII: Organizational Challenges in the ICU
46: Which Organizational Structure to Pursue? The Open vs. Closed ICU Debate
46.1 Introduction
46.2 Definitions
46.3 What Is the Global Trend?
46.4 What Does Evidence Suggest?
46.5 Observational Studies
46.6 Meta-Analyses That Compare Staffing Structure in the ICU
46.7 Closed ICU and Conflicts
46.8 ICU Structure and Family Satisfaction
References
47: Adverse Events in the ICU: Building and Sustaining an Organizational Culture of Patient Safety
47.1 Incidence of Adverse Events
47.2 Types of Adverse Events
47.3 Outcomes Related to Adverse Events
47.4 Are Adverse Events Preventable?
References
Untitled
48: How Effective Are Rapid Response Systems?
48.1 Introduction
48.2 Key Components of Rapid Response Systems
48.2.1 Identification of Patients at Risk of Deterioration
48.2.2 Scoring Systems
48.2.3 Reporting: Relay of Information
48.2.4 Delays in the Activation of Rapid Response Systems
48.2.5 RRT Intervention
48.3 Efficacy of Rapid Response Systems: The Evidence
References
Part IX: Coagulopathy and Transfusion
49: Transfusion Thresholds in Non-Bleeding Critically Ill Patients
49.1 Red Cell Transfusion and Oxygen Delivery
49.2 TRICC: The Landmark Trial
49.3 Restrictive Vs. Liberal Transfusion Strategy in Septic Shock
49.4 Cardiac Surgical Patients and Transfusion Thresholds
49.5 Transfusion Strategy in Acute Coronary Syndrome
49.6 Restrictive Versus Liberal Transfusion Practices for Weaning from Mechanical Ventilation
49.7 Transfusion Strategy in Neuro-Intensive Care
References
50: Tranexamic Acid in the Bleeding Patient
50.1 Introduction
50.2 Pharmacology and Mechanism of Action
50.3 Adverse Effects
50.4 The Evidence
50.5 Trauma
50.5.1 CRASH-2 Trial
50.5.2 TAMPITI Trial
50.5.3 STAAMP Trial
50.6 Traumatic Brain Injury
50.6.1 CRASH-3 Trial
50.7 Primary Intracerebral Hemorrhage: The TICH-2 Trial
50.8 Postpartum Hemorrhage: The WOMAN Trial
50.9 Coronary Artery Surgery: The ATACAS-Tranexamic Acid Trial
50.10 Gastrointestinal Bleeding: The HALT-IT Trial
References
51: Dengue-Related Thrombocytopenia and Platelet Transfusion
51.1 Why Does Thrombocytopenia Occur in Dengue?
51.2 Possible Harmful Effects of Prophylactic Platelet Transfusion
51.3 Prophylactic Platelet Transfusions and Outcomes in Dengue
References
Part X: Burns
52: Thermal Injury Resuscitation
52.1 Introduction
52.2 Burn Pathophysiology
52.3 Factors Influencing “Burn Shock”
52.4 Clinical Assessment of the Burns Patient
52.5 Burn Depth
52.6 Total Body Surface Area
52.7 Which Burn Formula Should Be Utilized?
52.8 Which Fluid Should Be Utilized?
52.9 Burn Resuscitation Endpoints?
References
Index