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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1134_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Foreword
- •Preface
- •Contents
- •Pain
- •Agitation-Sedation
- •Delirium
- •Contributors
- •1: Pain, Agitation, Delirium, and Immobility in the ICU
- •Introduction
- •Research Background
- •Pain, Agitation, and Delirium Assessment Scales
- •Non-pharmacological Approaches
- •Early Mobility
- •Post-intensive Care Syndrome
- •References
- •2: Bedside Neurologic Monitoring
- •Introduction
- •Cerebral Physiology Overview
- •The Neurologic Exam
- •Systemic Hemodynamic and Metabolic Monitoring
- •Continuous Electroencephalography and Electrocorticography
- •Transcranial Doppler
- •Intracranial Pressure Monitoring
- •Cerebral Oxygenation
- •Cerebral Blood Flow
- •Cerebral Microdialysis
- •Jugular Bulb Oximetry
- •Cerebrovascular Pressure Reactivity Index (PRx)
- •Brain Temperature
- •Near-Infrared Spectroscopy
- •Evoked Potentials
- •References
- •3: Status Epilepticus
- •Introduction
- •Epidemiology
- •Etiology
- •Pathophysiology
- •Neurochemical Changes
- •Physiological Changes
- •Diagnosis
- •Neurological and Physical Examination and History
- •Brain Imaging
- •Management
- •Antiepileptic Drugs in Convulsive SE
- •Antiepileptic Drugs in Nonconvulsive SE and Ictal-Interictal Patterns
- •Seizure Prophylaxis in Intracranial Pathologies
- •Traumatic Brain Injury (TBI)
- •Brain Tumors
- •Ischemic Stroke
- •Intracerebral Hemorrhage
- •Aneurysmal Subarachnoid Hemorrhage (aSAH)
- •Case Example Explanation
- •References
- •4: Traumatic Brain Injury
- •Epidemiology
- •Neurologic Severity Score
- •Anatomic Location
- •Skull Fractures
- •Intracranial Lesions
- •Focal Intracranial Lesions
- •Intraparenchymal Hemorrhage
- •Subdural Hematoma
- •Epidural Hematoma
- •Subarachnoid Hemorrhage
- •Diffuse Intracranial Lesions
- •Diffuse Axonal Injury
- •Abdominal Decompression
- •Special Populations
- •Diffuse Axonal Injury
- •Management of Skull Fractures
- •Management of Concussion
- •Outcomes
- •Glasgow Outcomes Score (GOS)
- •Brain Death Exam/Determination
- •References
- •5: Care of the Spinal Cord-Injured Patient
- •Epidemiology
- •Clinical Assessment
- •Physical Exam
- •Imaging
- •Clearing the Cervical Spine
- •Intensive Care Management
- •Cardiovascular Complications
- •Respiratory Complications
- •Physiologic Respiratory Changes After Spinal Cord Injury
- •Concussion
- •Primary and Secondary Brain Injury
- •Evaluation
- •Physical Examination
- •Neurologic Examination
- •Imaging
- •CT Scan
- •CT Angiography
- •Magnetic Resonance Imaging
- •Monitoring
- •Intracranial Pressure Monitoring
- •Internal ICP Monitoring
- •External ICP Monitoring
- •Brain Tissue Oxygen (PbtO2) Monitoring
- •Management
- •Medical Management
- •Pathophysiology of Cerebral Perfusion
- •Reduction of ICP
- •Hypertonic Saline
- •Mannitol
- •Hyperventilation
- •Elevation of the Head of the Bed
- •Optimization of Systemic Blood Pressure and Oxygenation
- •Pharmacologic Management of TBI
- •Seizure Prophylaxis
- •Venous Thromboembolism (VTE) Prophylaxis
- •Therapeutic Hypothermia
- •Nutrition
- •Surgical Management
- •Management of Hematomas
- •Decompressive Craniotomy/Craniectomy
- •Burr Holes/Emergency Craniostomy
- •Ventilator Management in Patients with SCI
- •Deep Venous Thrombosis and Venous Thromboembolism (VTE)
- •Glucocorticoid Use in Acute SCI
- •Nutrition and Glycemic Control
- •Ethics/End of Life
- •References
- •6: Nontraumatic Neurological Conditions
- •Major Ischemic Stroke Syndromes
- •General Management of Ischemic Stroke
- •Malignant Middle Cerebral Artery Stroke
- •Basilar Strokes
- •Cerebellar Stroke
- •Cerebral Venous Thrombosis
- •Primary Intracerebral Hemorrhage
- •Aneurysmal Subarachnoid Hemorrhage
- •Hypoxic and Anoxic Brain Injury
- •CNS Infections
- •Acute Bacterial Meningitis
- •Acute Encephalitis
- •Brain Abscesses
- •Malignant Brain Tumors
- •References
- •7: Hemodynamic Monitoring and Resuscitation
- •Introduction
- •Injury Stress and Fluid Loss
- •Measuring Hypovolemia
- •Invasive Blood Pressure Monitoring
- •Central Venous Pressure
- •Pulmonary Artery Occlusion Pressure
- •Dynamic Measures of Fluid Responsiveness
- •Esophageal Doppler
- •Pulse Pressure/Stroke Volume Variability (PPV/SVV)
- •Pulse Contour Cardiac Output
- •LiDCO
- •PiCCO
- •End-Expiratory Occlusion (EEO)
- •Passive Leg Raising
- •Echocardiography
- •The Current Role of Echocardiography in Critical Care
- •Ventricular Function
- •Assessments of Cardiac Output (CO)
- •Volume Status
- •Goal-Directed Resuscitation
- •Lactate and Lactate Clearance
- •Blood Transfusion
- •Current Status of Transfusion Therapy
- •References
- •8: Hemodynamic Monitoring in Surgical Critical Care
- •Introduction
- •Indirect Perfusion Measurement
- •Considerations: Auscultation/Manual Method
- •Considerations: Oscillometric/Automated Method
- •Gastric pH Monitoring
- •Considerations
- •Sublingual Capnography
- •Considerations
- •Central Venous Pressure Monitoring
- •Considerations
- •Pulmonary Catheter Monitoring
- •Considerations
- •Tissue Oxygenation
- •Tissue Oxygenation: VO2
- •Considerations
- •Tissue Oxygenation: Mixed Venous O2 Saturation (SvO2)
- •Considerations
- •Tissue Oxygenation: Central Venous O2 Saturation (ScvO2)
- •Direct Perfusion Measurement
- •Considerations
- •Direct Visualization Methods
- •Transthoracic Echocardiography
- •Image Acquisition
- •Examination Views
- •Image Interpretation
- •Considerations
- •Transesophageal Echocardiography
- •Image Acquisition and Interpretation
- •Considerations
- •References
- •9: Cardiovascular Emergencies
- •Introduction
- •Acute MI
- •Management: STEMI
- •Management: NSTEMI
- •Acute Pulmonary Embolism
- •Tamponade
- •Tension Pneumothorax
- •Aortic Dissection
- •Traumatic Aortic Injury
- •Mechanical Complications of MI: Ventricular Septal Defect and Free Wall Rupture
- •Mechanical Complications of MI: Left Ventricular Aneurysm
- •Mechanical Complications of MI: Papillary Muscle Rupture and Acute Mitral Regurgitation
- •Future Horizons: The Emerging Role of Extracorporeal Life Support in Cardiovascular Emergencies
- •References
- •Introduction
- •Physiologic Basis of Therapy
- •The Circuit
- •Components
- •Patient Selection
- •Supporting Literature
- •Hypoxemic Respiratory Failure
- •Hypercarbic Respiratory Failure
- •Bridge-to-Lung Transplant
- •Cardiac Failure
- •Management of ECMO
- •Patient Management
- •Circuit Management
- •Multidisciplinary Team
- •Outcomes
- •Survival
- •Complications
- •Long-Term Outcomes
- •Future Applications
- •Conclusion
- •Additional Resources
- •References
- •11: Acute Respiratory Distress Syndrome and Lung Protective Ventilation
- •Introduction
- •Approach to MV in ARDS
- •Alternate Approaches to MV
- •Nonventilatory Adjuncts to MV
- •Intraoperative MV: A Setup for Disaster?
- •Summary
- •References
- •12: Noninvasive Ventilation in the Perioperative Period
- •Introduction and Physiology
- •Continuous Positive Airway Pressure (CPAP)
- •Bilevel Positive Airway Pressure (BPAP)
- •Rationale and Epidemiology
- •Equipment
- •Interface
- •Equipment Complications
- •Pressure Ulceration
- •Patient-Ventilator Dyssynchrony
- •Patient Selection
- •Early Recognition of NIV Failure
- •Protocol for Initiating NIV
- •Preoperative NIV
- •NIV for Pre-oxygenation During Anesthetic Induction
- •Postoperative NIV
- •Abdominal Surgery
- •Foregut Surgery
- •Thoracic Surgery
- •Injured Patients
- •Obstructive Sleep Apnea
- •Perioperative OSA Risk Assessment
- •Immunocompromised Patients
- •Post-extubation Respiratory Failure
- •Palliative NIV
- •References
- •13: Care of the Surgical ICU Patient with Chronic Obstructive Pulmonary Disease and Pulmonary Hypertension
- •Chronic Obstructive Pulmonary Disease
- •Overview and Epidemiology
- •Pathophysiology and Etiology
- •Initial Evaluation
- •Clinical Symptoms and Physical Exam
- •Indications for ICU Admission
- •Differential Diagnosis and Diagnostic Workup
- •Pharmacotherapeutic Management
- •Glucocorticoids
- •Bronchodilators
- •Antibiotics
- •Ventilatory Support
- •Airway Clearance Techniques
- •Oxygen
- •Noninvasive Ventilation
- •Mechanical Ventilation
- •Ventilator Weaning, Consideration of Tracheostomy, and Palliative Care
- •Pulmonary Hypertension
- •Pathophysiology of Right Ventricular Failure
- •Etiology and Prognosis
- •Clinical Presentation
- •Diagnostic Evaluation
- •Management Considerations
- •Clinical Monitoring
- •Preload Optimization
- •Afterload Optimization
- •Vasoactive Therapies
- •Rhythm Control
- •Oxygenation and Ventilatory Support
- •Advanced Therapies
- •Palliative Care and End of Life
- •Pre-, Peri-, and Postoperative Management Considerations
- •References
- •14: Diagnosis and Management of Acute Kidney Injury
- •Introduction
- •Epidemiology of AKI
- •Causes of AKI
- •Early Recognition and Initial Management
- •Investigations
- •Subcellular Events: Current Theories
- •Supportive Care and Medical Management of Complications
- •Intravenous Fluids and Hemodynamic Support
- •Diuretics
- •Vasodilators and Other Pharmacologic Agents
- •Nutritional Support
- •Long-Term Follow-Up
- •References
- •15: Renal Replacement Therapy in the Critically Ill Surgical Patient
- •Introduction
- •Overview of Modalities
- •Hemodialysis (Diffusive Clearance)
- •Intermittent Hemodialysis
- •Continuous Modalities
- •Continuous Venovenous Hemodialysis (CVVHD)
- •Hybrid Therapy: SLED
- •Overview of Controversies
- •Dose
- •Mode
- •Timing
- •Clinical Considerations
- •Access
- •Anticoagulation
- •Special Considerations
- •Discontinuation of Therapy
- •Emerging Concepts
- •References
- •16: Gastrointestinal Hemorrhage
- •Introduction
- •Upper Gastrointestinal Hemorrhage
- •Peptic Ulcer Disease (PUD)
- •Esophagitis
- •Stress-Related Mucosal Disease (SRMD)
- •Zollinger-Ellison Syndrome (ZES)
- •Vascular Lesions
- •Mallory-Weiss Tear
- •Tumors
- •Injury
- •Post-intervention and Postsurgical
- •Other
- •Guideline-Derived Recommendations
- •Variceal Hemorrhage
- •Hepatic Transplantation
- •Small Bowel Hemorrhage
- •Lower GI Hemorrhage (LGIH)
- •References
- •17: Critical Care Management of Severe Acute Pancreatitis
- •Introduction
- •Epidemiology
- •Etiology
- •Diagnosis
- •Clinical Presentation
- •Laboratory Tests
- •Imaging Studies
- •Overall Diagnosis
- •Clinical Scoring Systems
- •Ranson’s Criteria
- •APACHE II
- •BISAPS
- •Computed Tomography Scoring Systems
- •Phases of Acute Pancreatitis
- •Organ Failure
- •Types of Acute Pancreatitis
- •Systemic and Local Complications
- •Predicting Severe Acute Pancreatitis
- •ICU Management
- •Management in the First 24–48 h
- •Initial Resuscitation
- •Volume of Resuscitation
- •Guidance of Resuscitation
- •Resuscitation Fluid Type
- •Vasopressor and Inotropic Support
- •Intra-abdominal Hypertension and Abdominal Compartment Syndrome
- •Continuous Renal Replacement Therapy
- •Strategy for Management in the First 24 h
- •Management in the First Week
- •Nutritional Support
- •Enteral Nutrition
- •Location of Enteral Feeding
- •Antibiotics and Probiotics in the Prevention of Infected Necrosis
- •Prophylactic Antibiotics
- •Probiotics
- •The Role of Acute Endoscopic Therapy
- •Overall Management Strategy in the First Week
- •ICU Management After the First Week
- •Management of Sterile and Infected Necrosis
- •Utility of Fine Needle Aspiration
- •Antibiotic Therapy for Infected Necrosis
- •Interventional Treatment for Infected Necrosis
- •Disconnected Pancreatic Duct Syndrome and Pancreatic Fistula
- •Gastrointestinal Complications of Severe Acute Pancreatitis
- •Vascular Complications of Acute Pancreatitis
- •Portosplenomesenteric Venous Thrombosis
- •Hemorrhage and Pseudoaneurysm
- •Strategy for Management After the First Week
- •Summary
- •References
- •18: Hepatic Failure
- •Acute Liver Failure
- •Clinical Manifestations
- •Neurologic System
- •Respiratory System
- •Cardiovascular and Hematologic System
- •Gastrointestinal and Endocrine Systems
- •Renal System and Electrolytes
- •Infectious Disease
- •Other Systems
- •Workup and Initial Management
- •Management
- •Encephalopathy, Cerebral Edema, and Intracranial Hypertension
- •Respiratory Management
- •Cardiovascular and Hematologic Management
- •Gastrointestinal and Endocrine Management
- •Renal Management
- •Infectious
- •Acetaminophen Toxicity
- •Amatoxin Intoxication
- •Wilson’s Disease
- •Viral Hepatitis
- •Ischemic Hepatitis
- •Chronic Liver Disease
- •Clinical Manifestations
- •Nervous System
- •Respiratory System
- •Cardiovascular and Hematologic System
- •Gastrointestinal and Endocrine Systems
- •Renal System
- •Infectious Disease
- •Other Systems
- •Workup and Initial Management
- •Management
- •Encephalopathy
- •Ascites
- •Spontaneous Bacterial Peritonitis
- •Variceal Hemorrhage
- •Hepatorenal Syndrome
- •Liver Transplantation
- •Other Therapies
- •References
- •19: Abdominal Compartment Hypertension and Abdominal Compartment Syndrome
- •Introduction
- •Diagnosis: Physiologic Markers of ACS
- •Diagnosis: Measurement of Abdominal Pressure
- •Treatment
- •Management of the Open Abdomen
- •Closure of the Open Abdomen
- •References
- •20: Nutrition in the Surgical ICU Patient
- •Introduction
- •Nutrition Assessment
- •Energy and Protein Requirements
- •Preoperative Period
- •Route of Nutrition
- •Enteral Nutrition
- •Immunonutrition
- •EN Access
- •Protocolized Management of EN
- •EN in Complex Situations
- •New Anastomosis
- •Postoperative Ileus
- •Vasopressor Support
- •Traumatic Brain Injury
- •Temporary Abdominal Closure
- •Parenteral Nutrition
- •Oral Diet
- •Probiotics
- •References
- •21: Antibiotic Strategy and Stewardship
- •Preventing Resistance
- •Antibiotic Formulary Restriction
- •Antibiotic Cycling
- •Preventing Infection
- •General Control Measures
- •Handwashing and Barrier Precautions
- •Decolonization
- •Health-Care-Associated Infections
- •Central Line-Associated Bloodstream Infection
- •CAUTI
- •De-escalation
- •References
- •22: Sepsis, Severe Sepsis, and Septic Shock
- •Introduction
- •Epidemiology
- •Risk Factors
- •Sepsis Syndromes
- •Quantifying Organ Dysfunction in Severe Sepsis and Septic Shock
- •Biomarkers in Sepsis
- •Markers of Tissue Hypoperfusion
- •Treatment of Severe Sepsis, Septic Shock, and Organ Dysfunction
- •Early Goal-Directed Therapy
- •Fluid Resuscitation in Sepsis
- •Invasive Hemodynamic Monitoring
- •Antimicrobial Therapy
- •Source Control
- •Damage Control in Intra-abdominal Sepsis
- •Cardiovascular Support
- •Corticosteroids
- •Transfusions
- •Coagulation Disorders in Septic Shock
- •Activated Protein C
- •Acute Kidney Injury and Septic Shock
- •ARDS and Sepsis
- •Neurologic Dysfunction in Severe Sepsis
- •Multi-organ Dysfunction Syndrome
- •References
- •23: Source Control and Supporting Therapeutics: Integrating Bacterial Invasion, Host Defense, and Clinical Interventions with Source Control Procedures
- •Introduction
- •Source Control
- •Changes in Source Control Procedures
- •Source Control and Clinical Trials
- •Source Control Issues Related to Pathogens
- •Bacterial Invasion and Multidrug-Resistant Organisms (MDRO)
- •Organism Virulence Factors
- •Source Control Issues Related to the Host
- •Metabolic Derangements
- •Plasma Volume Expansion
- •Organ Failure
- •Immunonutrition and Immunomodulation
- •Epigenetic Phenomena and Receptor-Ligand Interactions
- •References
- •24: Soft Tissue Infections
- •Introduction
- •Pathogenesis of SSTI
- •Non-necrotizing SSTI
- •Epidemiology
- •Treatment of Non-necrotizing SSTI
- •Non-necrotizing Cellulitis
- •Bite Wounds
- •Complicated Abscesses
- •Necrotizing SSTI
- •Epidemiology, Bacteriology, and Outcome of NSSTI
- •Therapeutic Considerations in NSSTI
- •Type 2 NSSTI
- •Type 3 NSSTI
- •Type 1 NSSTI
- •Diagnosis of NSSTI
- •Therapeutic Approach for NSSTI
- •Surgical Therapy for NSSTI
- •Antibiotic Therapy for NSSTI
- •Incisional Surgical Site Infections
- •Pathogenesis of SSI
- •Therapeutic Approach for SSI
- •References
- •25: Anemia in the Surgical ICU
- •Epidemiology of Anemia in the ICU
- •Pathophysiology
- •Oxygen Delivery and Consumption
- •Red Blood Cell Life Span and Regulation of Red Cell Mass
- •Mechanisms of Compensation
- •Mechanisms of Anemia in Critical Care
- •RBC Loss
- •Impaired Erythropoiesis: Reduced RBC Production and Shortened RBC Life Span
- •Iron Homeostasis and Hepcidin
- •Hemodilution
- •Management/Treatment of Anemia
- •Transfusion Indications in the ICU
- •Risks of Transfusions
- •TRALI
- •TACO
- •TRIM
- •Anemia After ICU Care
- •References
- •26: Coagulopathies and Anticoagulation
- •Introduction
- •Assessing the Coagulopathic Patient
- •Common Acquired and Medication-Induced Coagulopathies in the ICU
- •Liver Disease
- •Acute Traumatic Coagulopathy
- •Post Cardiopulmonary Bypass
- •Pregnancy
- •Antiphospholipid Syndrome
- •Heparin and LMWH
- •Warfarin
- •Novel Anticoagulants
- •Inherited Coagulopathies in the ICU
- •Von Willebrand Disease
- •Hemophilia A and B
- •Procoagulant Therapies
- •Anticoagulation Management in the ICU
- •VTE Chemoprophylaxis or Full Anticoagulation in Patients with Blunt Solid Organ Injury
- •VTE Chemoprophylaxis or Full Anticoagulation in Patients with Traumatic Brain Injury
- •Atrial Fibrillation ATE Prevention
- •ICU Procedures in Patients with Coagulopathy and Therapeutic Anticoagulation
- •Mechanical Heart Valves
- •Pulmonary Embolism with an Absolute Contraindication to Anticoagulation
- •Presumed Pulmonary Embolism in a Patient with Hemodynamic Instability or Cardiac Arrest
- •Summary
- •References
- •27: Thrombocytopenia in the Surgical Intensive Care Unit
- •Introduction
- •Clinical Presentation
- •Etiologies of Thrombocytopenia in the ICU
- •Decreased Production
- •Increased Destruction, Consumption, or Dilution of Platelets
- •Sepsis and Disseminated Intravascular Coagulation
- •Heparin-Induced Thrombocytopenia (HIT)
- •Other Drug-Induced Hemolytic-Thrombolytic Syndromes
- •Immune Thrombocytopenia (ITP)
- •Thrombotic Microangiopathies (TMA)
- •Intravascular Hemolysis
- •Postsurgical Thrombocytopenia
- •Trauma-Induced Coagulopathy (TIC)
- •Sequestration
- •Evaluation of Thrombocytopenia
- •Treatment
- •References
- •28: Venous Thromboembolism in the Intensive Care Unit
- •Introduction
- •Incidence
- •Risk Factors and Risk Assessment
- •Prevention
- •Pharmacologic Prophylaxis
- •Mechanical Prophylaxis
- •Prophylactic Inferior Vena Cava Filters
- •Prescription and Administration Compliance
- •Diagnosis
- •Duplex Ultrasonography
- •Computed Tomography Angiography
- •Echocardiography
- •Other Diagnostic Modalities
- •Screening in Asymptomatic Patients
- •Treatment of DVT
- •Treatment of PE
- •Impact
- •References
- •29: Glycemic Control and Insulin Resistance
- •Overview of Evidence Supporting Strict Glucose Control in the ICU
- •Resolving the Differences Between Studies of Intensive Glucose Control
- •The Role of Hypoglycemia and Glucose Variability in ICU Mortality
- •What Is the Appropriate Target for Glucose Control?
- •Glucose Measurement in the ICU
- •Recent Technological Developments
- •References
- •30: Critical Illness-Related Corticosteroid Insufficiency in the Intensive Care Patient
- •Introduction
- •Physiology of the HPA Axis
- •The Systemic Effects of Cortisol
- •Cortisol Synthesis
- •Critical Illness
- •Diagnosing CIRCI
- •Cortisol Levels
- •ACTH Stimulation Tests
- •Evidence for Treatment
- •Therapy
- •Perioperative “Stress Dose” Steroids
- •Steroids in Acute Respiratory Distress Syndrome (ARDS)
- •Summary
- •References
- •31: Thyroid Disorders
- •Introduction
- •Epidemiology
- •Thyroid Storm
- •Pathophysiology
- •Precipitating Causes
- •Clinical Features and Diagnosis
- •Medical Treatment
- •Therapeutic Plasma Exchange
- •Thyroid Surgery
- •Thyroid Storm in Pregnancy
- •Long-Term Management of Hyperthyroidism
- •Outcomes of Thyroid Storm
- •Myxedema Coma
- •Clinical Features and Diagnosis
- •Treatment
- •Myxedema Coma in Pregnancy
- •References
- •32: Hyperadrenergic Crisis
- •Introduction
- •Clinical Presentation
- •Signs and Symptoms by Organ System
- •Hypertension, Hypotension, and Shock
- •Cardiac
- •Pulmonary
- •Peripheral Vasculature
- •Gastrointestinal
- •Renal
- •Neurologic
- •Multiple Organ System Failure
- •Misdiagnosis
- •Pathogenesis
- •Pathophysiology
- •Precipitants
- •Diagnosis
- •Biochemical Diagnosis
- •Imaging
- •Management
- •Immediate Management
- •Medications
- •Hypotension and Circulatory Support
- •Timing of Surgery
- •Operative Management
- •Postoperative Care
- •References
- •33: Trauma
- •General Approach
- •Initial Assessment
- •Airway
- •Breathing
- •Circulation
- •Disability
- •Environment/Exposure
- •Early and Later Stages of ICU Care
- •Neurologic
- •Pulmonary
- •Cardiovascular
- •Renal/Electrolytes
- •Gastrointestinal/Nutrition
- •Hematology
- •Infectious Disease
- •Endocrine
- •Musculoskeletal
- •Tubes/Lines and Drains
- •Special Considerations
- •Damage Control Abdomen
- •Transport
- •ICU as an OR
- •Family Support/Interaction
- •End of Life/Gift of Life
- •References
- •34: Immunocompromised Patients
- •Introduction
- •Solid Organ Transplant Recipients
- •Overview of Infectious Risks and Initial Diagnostic Evaluation
- •Empiric Therapy
- •Chemotherapy, Radiation, and Stem Cell Transplant Recipients
- •Neutropenic Patients
- •Overview of Infectious Risks
- •Initial Diagnostic Evaluation
- •Empiric Therapy
- •Stem Cell Transplantation Recipients
- •Overview of Infectious Risks and Initial Diagnostic Evaluation
- •Empiric Therapy
- •Patients Receiving Chronic Corticosteroids
- •Overview of Infectious Risks
- •Initial Diagnostic Evaluation
- •Empiric Therapy
- •Patients Receiving TNF-α (Alpha) Inhibitor Therapy
- •Overview of Infectious Risks
- •Initial Diagnostic Evaluation
- •Empiric Therapy
- •Patients with HIV/AIDS
- •Overview of Infectious Risks and Initial Diagnostic Evaluation
- •Empiric Therapy
- •Antiretroviral (ARV) Use in the ICU
- •Patients with Chronic Hepatitis B or C Infection
- •Overview of Infectious Risks
- •Initial Diagnostic Evaluation
- •Empiric Therapy
- •References
- •35: Transplantation
- •Introduction
- •Cardiovascular
- •Pulmonary
- •Assessment of Graft
- •Imaging
- •Renal
- •Central Nervous System
- •Infectious Disease
- •Immunosuppression
- •References
- •36: Intensive Care in Obstetrics
- •Introduction
- •Scope of the Problem
- •Maternal Morbidity and Mortality
- •Predictors of Mortality at Admission
- •Physiologic Changes in Obstetrics and Clinical Implications
- •Cardiovascular
- •Invasive Central Monitoring
- •Pulmonary
- •Hematologic
- •Renal
- •Gastrointestinal
- •Pathology in Pregnancy
- •Cardiac
- •Preeclampsia-Eclampsia
- •Hemorrhage
- •Amniotic Fluid Embolism
- •Trauma Management
- •Primary Survey
- •Secondary Survey
- •Perimortem Cesarean Section
- •Summary
- •References
- •37: The Pediatric Patient Cared for in the Adult ICU
- •Initial Resuscitation of the Pediatric Intensive Care Patient
- •Physiology of Shock
- •Broselow™ System
- •Pediatric Airway Management
- •Anatomic Considerations
- •Basic Airway Management
- •Advanced Airway Management
- •Endotracheal Intubation Considerations
- •Fluid Resuscitation
- •Pediatric Traumatic Brain Injury
- •Pediatric Analgesia and Sedation
- •General Approach
- •Medication Dosing
- •ICU Procedural Considerations
- •Central Venous Access
- •Intraosseous Access
- •Arterial Access
- •Intubation
- •Tube Thoracostomy
- •Ultrasound
- •Indications for ECMO
- •Psychosocial Considerations in Pediatric Intensive Care
- •The Adult ICU Patient with Congenital Disease (Pediatric Disease)
- •Pulmonary Considerations
- •Cystic Fibrosis
- •Respiratory Complications
- •Gastrointestinal Complications
- •Cardiac Considerations
- •Congenital Heart Disease
- •Cardiac Arrhythmia
- •Heart Failure
- •Cardiopulmonary
- •Acute Kidney Injury
- •Hepatic Dysfunction
- •Hematologic
- •Neurologic Considerations
- •VP Shunt Complications
- •References
- •38: Organ Donor Management
- •History of Organ Donation
- •Identifying Potential Donors
- •Referral of Potential Donors
- •Team Management Approaches to Donation
- •Neurological Criteria for Determination of Death
- •Donation After Circulatory Determination of Death
- •Pathophysiology of Brain Death
- •Systemic Sequelae of Brain Death
- •Cardiovascular System
- •Pulmonary System
- •Renal System
- •Hepatic System
- •Coagulation and Thermoregulation Disorders
- •The Role of Protocols in Organ Donation
- •Aggressive Resuscitation of Potential Donors
- •Hemodynamic Monitoring
- •Aggressive Hemodynamic Management
- •The Role of Vasopressin
- •The Role of Thyroxine
- •The Role of Insulin
- •The Role of Steroids
- •Managing Potential Complications
- •Considerations During Organ Recovery
- •References
- •39: Biostatistics for the Intensivist: A Clinically Oriented Guide to Research Analysis and Interpretation
- •Introduction
- •The Basic Mechanics of a Research Study
- •Power and Sample Size
- •Type III Error
- •Bias
- •Study Types
- •Measures of Disease Association
- •Relative Risk
- •Odds Ratio
- •Statistical Testing
- •Statistical Testing and Types of Data: Discrete Variables
- •Statistical Testing with Discrete Variables
- •Statistical Testing and Types of Data: Continuous Variables
- •Continuous Data: Mean, Median, Mode, and Related Concepts
- •Continuous Data: Statistical Distributions
- •Continuous Data: Standard Deviation (σ) and Standard Error of the Mean (SEM)
- •Statistical Testing with Continuous Data
- •Evaluating Diagnostic Tests
- •Measuring Agreement
- •Survival Analysis
- •Brief Comment on Trends and Pattern Analysis
- •References
- •40: Administration
- •Introduction
- •Structure
- •Personnel
- •Guidelines
- •Quality Care
- •Costs
- •Communication
- •Role of the Surgeon
- •Leadership
- •Intensivist Compensation
- •Measuring Success
- •References
- •41: Practical Pharmacokinetics and Pharmacodynamics
- •Introduction
- •Pharmacokinetics
- •Changes in Pharmacokinetics in Surgical ICU Patients
- •Pharmacodynamics
- •Pharmacokinetic/Pharmacodynamic Modeling
- •Drug Classes
- •Nondepolarizing Neuromuscular Blockers
- •Opiates
- •Sedatives
- •Anticoagulants
- •Proton Pump Inhibitors
- •Levetiracetam and Lacosamide
- •Therapeutic Drug Monitoring
- •References
- •42: Ethics and the ICU
- •Introduction
- •Withdrawing and Withholding
- •Futility
- •Advance Directives/POLST
- •Dialysis
- •Organ Donation
- •Suggested Reading
- •43: Disaster Management and Preparedness
- •Introduction
- •Epidemiology of Disasters
- •Biological Agents
- •Routes of Exposure
- •Prophylaxis and Therapy
- •Chemical Agents
- •Nerve Agents
- •Vesicants
- •Hydrogen Cyanide
- •Pulmonary Agents
- •Riot Control Agents (Tear Gases or Lacrimators)
- •Radioactive Agents
- •Medical Effects of Ionizing Radiation
- •Treatment of Radiation Casualties
- •Decontamination
- •Principles of Disaster Response
- •Principle #1
- •Principle #2
- •Principle #3
- •Disaster Medical Response
- •Search and Rescue
- •Disaster Triage
- •Levels of Triage
- •Level 1: Field Triage
- •Level 2: Medical Triage
- •Level 3: Evacuation Triage
- •Triage Errors
- •Evacuation
- •Disaster Management Teams
- •Disaster Drills
- •Summary
- •References
- •44: Postoperative Complications Following Surgery Abroad
- •Introduction
- •Elective Surgery Abroad
- •An Unregulated Industry
- •Nosocomial and Travel-Related Postoperative Infection
- •Transplant Tourism
- •Cosmetic Surgery
- •Surgical Complications in the Context of Disaster Medicine
- •Surgical Infections in Disaster Response
- •Strategies in Patient Management
- •References
- •45: Post-intensive Care Syndrome (PICS)
- •Introduction
- •Physical Impairment
- •Physical Dysfunction
- •Pulmonary Dysfunction
- •Neuromuscular Dysfunction
- •ICU-Acquired Weakness
- •Critical Illness Polyneuropathy
- •Critical Illness Myopathy
- •Risk Factors

11 Acute Respiratory Distress Syndrome and Lung Protective Ventilation
119
There has also been substantial interest in the role of
conservative fl uid management strategies in the treatment of
patients with ARDS. The state of increased microvascular
permeability present in ARDS potentiates pulmonary edema
that may be caused by increased hydrostatic pressure associated with fl uid administration [ 95 , 96 ]. In 2006, the ARDS
Network published a comparison of conservative and liberal
strategies of fl uid management [
97 ]. There was no signifi -
cant difference in 60-day mortality, but the conservative
strategy demonstrated improved oxygenation and decreased
duration of MV [ 97 ]. In patients with ARDS who are also
hypoproteinemic, albumin administration in conjunction
with diuretics in a conservative fl uid management strategy
may also improve oxygenation but is not associated with
improved survival [ 98 , 99 ]. In surgical and trauma patient
populations, however, the role of conservative fl uid management is usually limited, since it is not recommended for
patients who are hypotensive, are oliguric, have recently
received vasopressors, or have a central venous pressure
(CVP) <4 mmHg [ 91 , 97 , 100 , 101 ].
Corticosteroid utilization to address the fi bro-proliferative
and infl ammatory response in ARDS continues to generate
debate. Yet another ARDS Network trial examined the use of
methylprednisolone in established courses of ARDS (at least
14 days after onset) and, despite improvements in oxygenation and reduced duration of MV, showed a signifi cant
increase in 60- and 180-day mortality [ 102 ]. Conversely, a
later study suggested a trend toward decreased mortality, but
patients in this study received corticosteroids early (within
72 h of being diagnosed with ARDS) [ 103 ]. Meta-analysis
has confi rmed a trend toward, and in some cases a statistically signifi cant, reduction in mortality with the use of early
corticosteroids, without any increase in infectious or CIM
complications [ 104 , 105 ]. As a result of the current evidence,
a long course (at least 14 days) of methylprednisolone
administration, followed by gradual weaning, may be considered in patients with early severe ARDS [ 106 , 107 ].
Inhaled nitric oxide (iNO) improves oxygenation due to
selective pulmonary vasodilation, which improves ventilation perfusion (V/Q) mismatch and decreases pulmonary
arterial pressure [ 91 ]. It has been shown in multiple trials and
meta-analyses to improve short-term oxygenation in patients
with ARDS but without any impact on duration of MV or
mortality [ 108 – 115 ]. The use of iNO should be limited to
short-term rescue for life-threatening hypoxemia [ 25 , 91 ].
Inhaled prostacyclins have been investigated as alternatives
to iNO, due to their lower cost and similar effects on
oxygenation, though evidence to support their use is lacking
[ 91 , 110 , 116 ].
Another strategy to improve outcomes in patients with
severe refractory hypoxemia in ARDS is prone positioning.
The mechanism of improvement is again multifactorial,
including increased alveolar recruitment and ventilation in
the dorsal pulmonary segments, decreased shunt physiology,
and decreased pulmonary compression by the heart
[ 117 , 118 ]. Early studies consistently showed prone posi-
tioning to improve oxygenation and gas exchange; however,
mortality benefi ts were not shown [ 119 – 122 ]. Subsequent
meta- analysis, though, demonstrated improved mortality in
patients with severe ARDS [ 123 , 124 ]. This prompted fur-
ther investigation in the Proning Severe ARDS Patients
(PROSEVA) trial, an RCT that showed signifi cant reduction
in mortality in patients with PaO 2 /FiO 2 < 150 who were
proned within 48 h of diagnosis of ARDS, for at least 16
consecutive hours/day up to 28 days (16.0 % vs. 32.8 %,
p < 0.001), with no increase in complications compared to
patients who were supine [ 125 ].
ECLS has been perhaps the most controversial adjunct to
MV in patients with severe ARDS. ICUs that offer ECLS are
specialized centers with focused providers. The goal is to
allow for complete gas exchange by means of an extracorporeal membrane oxygenation (ECMO) circuit while minimizing VILI by using minimal settings on the ventilator, thus
allowing “lung rest”[ 126 ]. Veno-venous ECMO (V-V
ECMO) is most commonly used in isolated respiratory failure and employs large central venous catheters (via jugulofemoral or bifemoral placement) to remove blood from the
body, circulate it through an oxygenator that allows for gas
exchange, and return oxygenated blood to the patient
[ 127 , 128 ]. For years, the only data showing positive results
for ECMO in adults were retrospective studies [ 129 – 132 ].
However, most recently, a multicenter prospective RCT
(Conventional ventilation or ECMO for Severe Adult
Respiratory failure, or CESAR) compared referral to an
ECMO center to conventional treatment and showed
improved 6-month mortality (63 % vs. 47 %; RR 0.69; 95 %
CI 0.05–0.97; p = 0.03) [ 133 ]. Interestingly, only 75 % of the
patients referred were actually placed on ECMO, which begs
the question whether the survival benefi t was due to ECMO
per se or simply transfer to a facility with greater resources
and expertise. Despite criticisms of the CESAR trial, it has
sparked new debate regarding the advantages of
ECMO. Especially relevant to the surgical patient population
are reports of its successful use in patients with TBI and multiple injuries, in which heparin-bonded circuits may be used
in order to forgo systemic anticoagulation [ 134 – 137 ].
However, restraint is still advised, as the optimal techniques
and clinical indications for ECLS continue to be clarifi ed
[ 138 , 139 ].
In summary, many adjuncts to MV have been used in the
treatment of ARDS and continue to undergo rigorous investigation. While some have demonstrated improvements in
mortality, all the adjuncts discussed here have demonstrated
improvements in oxygenation. As a result, these therapies
may be considered in the setting of life-threatening hypoxemia despite optimized MV.

120
S.E. Greer et al.
Intraoperative MV: A Setup for Disaster?
Although lung protective ventilation is the standard of care
in ICU patients with ARDS, it is still not widely practiced in
the operating room (OR) – in fact, the use of high V T and zero
PEEP is still commonplace, with fewer than 20 % of patients
receiving protective ventilation in routine anesthetic practice
[ 140 , 141 ].
Early studies that investigated intra operative factors asso-
ciated with post operative pulmonary complications (PPC)
focused primarily on patient variables (age, smoking,
arterial- alveolar differences, and pulmonary function tests
(PFTs)), surgical events (estimated blood loss and transfusion volumes), and types of procedures (vascular, cardiac,
abdominal), rather than the impact of MV itself on outcomes
[ 142 – 144 ]. Even in a trial designed specifi cally to defi ne risk
factors for postoperative morbidity, parameters for MV
during surgery were not examined [ 142 ]. Though there are
currently no standardized guidelines for intraoperative MV,
it is becoming increasingly clear that lung protective ventilation is one of the many important modalities associated with
postoperative outcomes [ 145 – 147 ].
General anesthesia can result in both atelectasis and
decreased pulmonary blood fl ow [ 148 ]. Intra-abdominal sur-
gery can induce atelectasis due to the direct pressure of the
operative fi eld onto the (basilar) lungs. Atelectasis may also
be present with lateral positioning, Trendelenburg, lithotomy, or intra-abdominal insuffl ation – even in patients who
are previously healthy. Within 5 min of induction of anesthesia, increased densities have been shown in the dependent
regions of both lungs [ 149 ]. Furthermore, pulmonary blood
fl ow may be reduced for several reasons: systemic vasodilation, high V T ventilation, patient position (blood fl ow may be
decreased to nondependent areas), or HPV. HPV occurs
when the partial pressure of oxygen in a given lung region
falls, and vascular smooth muscle in the pulmonary circulation contracts in an effort to maintain V/Q matching.
Vasodilators (including inhaled anesthetics) inhibit HPV
[ 150 ] and may thus contribute to an increase in the shunt
fraction; conversely, intravenous anesthetics do not have this
effect [ 151 ].
Evidence supporting intraoperative lung protective ventilation strategies to improve oxygenation and respiratory
mechanics, and to decrease PPC, has now been shown in several studies [ 152 – 156 ]. One prospective RCT in patients
undergoing open abdominal surgery compared protective
MV ( V T 7 mL/kg, PEEP 10 cm H 2 O with RMs) to “standard”
ventilation ( V T 9 mL/kg, zero PEEP): patients in the protective MV group had improved oxygenation, better PFTs, and
fewer alterations in chest X-ray (CXR) postoperatively
[ 145 ]. Recent meta-analysis also demonstrated an associa-
tion between lower V T and decreased rates of PPC (2.0 % vs.
4.7 %; RR 0.40; 95 % CI 0.22–0.70) [
146 ].
To further confi rm this fi nding in a large RCT, the
Intraoperative Protective Ventilation (IMPROVE) investigators studied patients undergoing major abdominal surgery,
with risk factors for PPC [ 147 ]. During anesthesia, patients
were randomized to protective ventilation ( V
PEEP 6–8 cm H
( V
10–12 mL/kg, zero PEEP, and no RMs). Over the 7-day
T
O with RMs) vs. non-protective ventilation
2
6–8 mL/kg,
T
postoperative study period, 5.0 % of patients in the protective
group compared to 17.0 % of patients in the non-protective
group required noninvasive ventilation (NIV) or intubation
(RR 0.29; 95 % CI 0.14–0.61; p = 0.001). The protective ven-
tilation group also demonstrated a signifi cantly shorter hospital stay (mean difference −2.45 days; 95 % CI −4.17 to
−0.72; p = 0.006) [ 147 ].
Once again, however, parsing the relative contributions
of V T and PEEP has not been straightforward. Several
meta- analyses have shown a benefi cial effect of higher
PEEP: it has been associated with decreased rates of PPC
(1.4 % vs. 4.9 %; RR 0.29; 95 % CI 0.14–0.60) [ 146 ] and
reduced postoperative atelectasis [ 157 ]. However, this was
not confi rmed in the large PROtective Ventilation ( PROVE)
Network trial comparing high vs. low PEEP in the OR
[ 158 ]. In 30 centers across Europe, North, and South
America, patients at high risk of PPC undergoing abdominal
procedures were randomized to high (12 cm H 2 O) or low
(≤2 cm H 2 O) PEEP, using a consistent V T of 8 mL/kg. PPC
were seen in 40 % of patients in the high PEEP group and in
39 % in the low PEEP group; furthermore, patients in the
high PEEP group had more hypotension and required more
vasoactive medications [ 158 ].
The largest and most recent meta-analysis sought to clarify the role of intraoperative PEEP and the frequency of PPC
[ 159 ]. As previously demonstrated, rates of PPC were lower
in patients assigned to low V T – but there was no statistical
difference between low V T /high PEEP and low V T /low PEEP
(8.9 % vs. 12 %; adjusted RR 0.93; 95 % CI 0.64–1.37;
p = 0.72) over the 2,127 patients analyzed. Furthermore,
there was no dose-response relationship found between rates
of PPC and level of PEEP ( R
2
= 0.08) [ 159 ]. The optimal
level of PEEP in intraoperative ventilation, therefore, remains
unclear.
It is worth noting that many of the studies referenced
above refer to specifi c types of surgery (neurosurgery, thoracic surgery, oncologic surgery, general surgery) and to
patient populations with an increased risk of PPC due to preexisting comorbidities. The healthy patient undergoing elective surgery is not well studied with regard to optimal
ventilator settings, and it is unknown if V T or PEEP impacts
their postoperative outcomes. Finally, there is also a paucity
of data on the intraoperative management of trauma and
acute care surgery patients – who may have been healthy
prior to their precipitating event but then develop an infl ammatory response and/or hemodynamic instability before they

11 Acute Respiratory Distress Syndrome and Lung Protective Ventilation
121
reach the operating room. Given the increased mortality and
substantial economic burden of PPC, further research on
their prevention could have a great impact [
160 ].
Summary
ARDS and PPC in surgical patients contribute substantially
to mortality and to the economic burden on the health-care
system – although progress has been made, and ARDS has
shown recent declines. The Berlin Defi nition for ARDS will
help clarify populations of interest in future studies. At present, the standard of care in MV for patients with ARDS
remains an open lung protective ventilation strategy, with
low V T and relatively higher PEEP. A more nuanced understanding of the effect of pressure settings is beginning to
emerge and may further delineate the most benefi cial aspects
of MV. Additionally, as further evidence accumulates, the
prevention rather than the treatment of both ARDS and VILI
may ultimately prove to be most effi cacious, with strategies
such as early APRV holding great promise. Finally, in the
comprehensive management of critically ill surgical patients,
the lines between ICU and OR often blur – making recent
investigations of intraoperative lung protective strategies all
the more important. Despite the already vast literature, there
is more work to be done.
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Noninvasive Ventilation in the Perioperative Period
Kimberly M. Ramonell , Richard P. Ramonell ,
and Kevin W. McConnell
1 2
Introduction and Physiology
Noninvasive ventilation (NIV) is defi ned as ventilatory support that is delivered in a spontaneously breathing patient
without establishing an endotracheal airway [
noninvasive ventilation is delivered through a tight-fi tting
mask applied to the face.
Like mechanical ventilation via endotracheal intubation,
the goals of positive pressure noninvasive ventilation are the
same: correct the underlying respiratory abnormality by
improving oxygenation, ventilation, or both. To accomplish
this task, patients who have an indication for NIV are connected to a ventilator circuit via a nasal mask or face mask.
Depending on the clinical scenario, the ventilator is then either
set to a volume-controlled setting or a pressure- controlled setting. Earlier noninvasive ventilators used volume ventilation
settings that allowed for the delivery of a specifi c volume during the inspiratory cycle and were shown to be associated with
improvement in acute respiratory failure [ 2 , 3 ]. However, this
mode is more diffi cult to tolerate for patients, and as the ventilator automatically adjusts airway pressures to achieve a specifi ed volume, it can result in high inspiratory pressures and air
leaks around the face or nose mask [ 4 ].
Since the early 1990s, pressure-controlled settings have
been more commonly utilized, and their success has been
demonstrated across levels of care and a variety of indications.
Specifi cally, continuous positive airway pressure (CPAP) and
bilevel positive airway pressure (BPAP) are the two most commonly used modes of noninvasive ventilation both of which
can be delivered either by standard ICU ventilators or portable
K. M. Ramonell , MD • K. W. McConnell , MD (*)
Department of General Surgery , Emory University Hospital ,
Atlanta , GA 30322 , USA
kmhemph@emory.edu; kevin.w.mcconnell@emory.edu
e-mail:
R. P. Ramonell , MD
Department of Internal Medicine , Emory University Hospital ,
Atlanta , GA 30322 , USA
richard.paul.ramonell@emory.edu
e-mail:
1 ]. Instead,
ventilators. Almost every mode of ventilation that can be
delivered invasively can also be delivered noninvasively.
However, certain modes are used more frequently. Here we
will discuss BPAP and CPAP modes, but it is important for the
provider to be aware that alternative modes of ventilation can
be utilized (pressure support ventilation, assist control, proportional assist ventilation). The use of noninvasive ventilation
in the medical population with acute COPD exacerbations and
acute cardiogenic pulmonary edema is well established and
beyond the scope of this chapter. Here we will focus our
review on the physiology, rationale for use, equipment, indications, contraindications, and complications of NIV in the preoperative, intraoperative, and postoperative populations.
Continuous Positive Airway Pressure (CPAP)
CPAP applies a fi xed amount of positive pressure to be delivered continuously throughout the respiratory cycle and as
such is a constant pressure but variable fl ow mode. This
mode increases the functional residual capacity without
increasing the tidal volume resulting in decreased atelectasis
and reduced work of breathing [ 5 – 9 ]. Since CPAP does not
provide additional pressure during inspiration, it technically
does not directly support ventilation, but it does exert some
effects that can indirectly improve ventilation. For example,
by mitigating against atelectasis through increased alveolar
recruitment, CPAP decreases the ventilation-perfusion mismatch caused by non-ventilated alveoli and improves hypoxemia. However, because CPAP cannot increase tidal volume,
it is not indicated in the treatment of hypercapneic respiratory failure.
Bilevel Positive Airway Pressure (BPAP)
BiPAP, on the other hand, delivers variable positive pressure
assistance to the patient at different phases of the respiratory
cycle, in contrast to a set pressure applied continuously
© Springer International Publishing Switzerland 2016
N.D. Martin, L.J. Kaplan (eds.), Principles of Adult Surgical Critical Care, DOI 10.1007/978-3-319-33341-0_12
127

128
K.M. Ramonell et al.
throughout the respiratory cycle as in CPAP mode. The terms
“BiPAP” and “BIPAP” are often used incorrectly to refer to
NIV in the BPAP mode. “BiPAP” refers to the BPAP mode
of ventilation delivered by a specifi c portable ventilator manufactured by Respironics Corporation. Similarly, “BIPAP”
stands for biphasic positive airway pressure and refers to a
time-cycled, pressure-controlled mode that is also a constant
pressure variable fl ow mode with a period of fl ow cessation
for CO2 clearance available on ventilators produced by
Draeger Medical, Inc. These are just two of the many ventilators that can deliver BPAP. Once this mode of NIV has
been selected, the provider must then select the inspiratory
positive airway pressure (IPAP) value and the expiratory
positive airway pressure (EPAP) value. Unlike CPAP, BPAP
will vary the pressure support delivered during inspiration
and expiration and therefore must use a sensor which triggers alternation between the two pressures. This trigger is
usually a fl ow or volume trigger that detects fl ow, volume, or
pressure at the proximal airways.
Once the ventilator detects that a patient is exhaling, it
will maintain positive pressure assistance equal to the EPAP
value. When inspiration is detected, the ventilator delivers
positive pressure assistance equal to the IPAP value in addition to the EPAP, which is continuously delivered. For
instance, if a ventilator were set to an EPAP of 5 cm H
O and
2
an IPAP of 10 cm H 2 O, the machine would maintain 5 cm
H 2 O of positive pressure during expiration and deliver gas
fl ow to establish 15 cm H 2 O during inspiration. Commonly,
inspiratory positive pressure assistance lasts until the ventilator detects a 25 % decrease in peak inspiratory fl ow or 3 s
elapses, whichever comes fi rst [ 5 ].
Like CPAP, BPAP increases the functional residual capacity and can recruit atelectatic lung segments, thereby decreasing shunting. Unlike CPAP, however, the addition of extra
inspiratory pressure increases tidal volume. Augmentations
in tidal volume subsequently cause increases in minute ventilation and thus give BPAP the ability to treat hypercapneic
respiratory failure in addition to hypoxemic respiratory failure. Finally, the addition of IPAP also decreases the work of
breathing and total lung resistance, which is particularly benefi cial in patients who require BPAP for an acute or severe
indication [ 5 ].
There is abundant high-quality evidence to recommend
the use of NIV in specifi c medical conditions, including
acute cardiogenic pulmonary edema, obstructive sleep
apnea, and acute COPD exacerbations [ 10 – 12 ]. These indi-
cations allowed NIV to gain signifi cant popularity and
expand its applicability to medical patients over the last two
decades. Increasingly, NIV is being applied to specifi c populations of surgical patients with similar improvements in outcomes as outlined later in this chapter.
Respiratory dysfunction in the postoperative patient represents a complex clinical challenge that differs from the
medical patient. Intensive care providers must take into consideration several factors before using NIV for a postoperative patient including clinical status, surgical procedures
performed including anatomic and physiologic alterations,
and the potential for further surgical intervention.
Although supplemental oxygen administration and incentive spirometry are effective in treating mild postoperative
hypoxemia, endotracheal intubation and mechanical ventilation may be required in 8–10 % of patients who develop acute
postoperative respiratory failure [
13 ]. The use of endotracheal
intubation and invasive mechanical ventilation has been shown
to increase the risk of nosocomial infections, utilization of
critical care resources, prolong length of hospital stay, and
increase overall morality [ 14 ]. There is compelling evidence
that demonstrates the benefi ts of NIV for both the patient and
health-care utilization through avoidance of invasive ventilation [ 12 ]. Additionally, increased recognition of postoperative
patients’ exceptional vulnerability to hypercapnia due to incisional pain, opioid agents, and unrecognized sleep apnea has
led to increased use of NIV in the perioperative period.
Equipment
NIV can be delivered by standard ICU ventilators or portable ventilators. Modern ICU ventilators can provide
higher inspiratory fl ow rates, have separate inspiratory and
expiratory tubing which minimizes carbon dioxide
rebreathing, are capable of delivering a higher fraction of
inspired oxygen (F i O 2 ), and have more appropriate monitors and alarms [ 15 ].
Rationale and Epidemiology
The most important advantage that NIV offers is avoidance
of invasive endotracheal intubation and the associated deleterious effects including airway injury, sedation, and
ventilator- associated infections and conditions. Unlike intubated patients, noninvasively ventilated patients have the
ability to be liberated from the ventilator intermittently,
which promotes progressive mobility, pulmonary toilet/
coughing, eating, and speaking.
Interface
The ideal interface is one that minimizes air leakage and is
most comfortable, thus promoting effi cacy and compliance.
The most commonly used interface in the critical care setting
is the oronasal mask [
nasal prongs (pillows), a full-face mask (covers the mouth,
nose, and eyes), a nasal mask, and a helmet. Regardless of
the interface chosen, they should be properly fi tted, comfortable, effective, and minimize leakage to maximize effi cacy.
16 ]. Other available interfaces include

12 Noninvasive Ventilation in the Perioperative Period
129
Equipment Complications
Patient discomfort and thus compliance with NIV is a limiting factor in its clinical applicability and contributes signifi cantly to NIV failure rate. The most common complications
of NIV equipment include air leakage, pressure ulceration,
and patient-ventilator dyssynchrony.
Pressure Ulceration
Facial skin lesions, including ulceration and necrosis, are
pressure-related lesions that result from prolonged contact
with tight-fi tting masks and predominantly develop on the
bridge of the nose. Their development is directly related to
the duration of NIV therapy. Factors that have been associated with formation of nasal skin lesions, and must be considered at initiation of NIV therapy, include progressive
tightening of the harness, increasing the air volume in the
mask cushions, and increasing inspiratory pressures [ 17 ].
Patient-Ventilator Dyssynchrony
Dyssynchrony occurs when the phases of ventilator- delivered
breaths do not match with the patient’s. This results in poor
tolerance of NIV and can be alleviated by using an alternative
ventilator mode (pressure support ventilation allows the patient
to trigger each breath and may be more comfortable for some
patients) or minimizing mask leaks [ 18 ]. Air leakage increases
the time required for the ventilator to reach its pressure target,
thus prolonging inspiration and causing discomfort.
Early Recognition of NIV Failure
Improvement in respiratory status is usually apparent within
the fi rst 1–2 h after initiation of NIV. The absence of improvement in a patient’s respiratory status is a strong indication to
promptly proceed with intubation. Delays in recognition of
NIV failure and postponing invasive ventilation result in
increased morbidity and mortality and should be avoided.
Predictive factors associated with an increased risk of NIV
failure include advanced age, high-acuity illness score at
admission, presence of ARDS, sepsis, or multisystem organ
failure (MSOF). In ARDS patients, an arterial oxygen tension/inspired oxygen fraction (P a O 2 /F I O 2 ) ratio <175 mmHg
drawn 1 h following initiation of a NIV trial accurately predicts failure [ 19 ].
NIV should be initiated and continuously monitored in a
critical care setting with a multidisciplinary team familiar
with this therapy and advanced airway techniques; NIV as
rescue therapy is generally not appropriate for ward care.
There is no established consensus on NIV failure criteria;
however, general recommendations including failure to clinically improve, unrelieved dyspnea, worsening P a O 2 /F I O 2
ratio, and increasing oxygen or pressure requirements should
prompt transition to invasive ventilation. Should the provider
anticipate failure, it is essential to promptly proceed to intubation while the patient is still able to adequately preoxygenate, allowing a safe window of time to perform
endotracheal intubation. Patients requiring 100 % F I O 2 on
BPAP are prone to respiratory arrest due to a lack of pulmonary reserve and rapid desaturation during intubation. Highfl ow NC O2 may be used as an aid in maintaining oxygenation
in the period between removing the BPAP mask and establishing a defi nitive airway.
Patient Selection
Prior to discussing the indications for NIV, it is important to
understand the constituents of appropriate patient selection and
the contraindications to NIV. Patient selection and continuous
monitoring are critical to recognizing and reducing NIV failure.
In general, the most important factors to consider when selecting
patients for NIV are patient cooperation, ability to protect the
airway, and their unique risk of aspiration. NIV should not be
used in patients with altered mental status, severely agitated or
obtunded patients, hemodynamically unstable patients, and
those suffering from claustrophobia either due to an inability to
cooperate or an impaired ability to protect their airway. Patients
with obvious respiratory distress, proximal gastrointestinal hemorrhage, active emesis, facial trauma or burns, and those with
neuromuscular dysfunction are at an increased risk of aspiration
and should avoid NIV. These patients warrant prompt endotracheal intubation and mechanical ventilation. Similarly, patients
with impending respiratory failure due to copious secretions that
they are unable to clear are poor candidates for NIV.
Protocol for Initiating NIV
Parameters to be set upon initiation of NIV will be guided by
the mode of ventilation chosen. Currently, there is not a universally accepted established protocol for initial NIV settings; however, general recommendations can be made. It is
imperative to tailor the ventilator mode and settings to each
clinical scenario and adjust parameters as needed to alleviate
respiratory distress. Table
recommended settings for initiation of BPAP [ 16 ].
12.1 presents some commonly
Specifi c Indications and Patient
Considerations
NIV is now generally regarded as safe in most surgical
patients and provides the most benefi t to patients with rapidly reversible physiology (atelectasis, acute pulmonary
edema, etc.) and patients with an oropharynx prone to
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