- •Preface
- •List of contributers
- •History, epidemiology, prevention and education
- •A history of burn care
- •“Black sheep in surgical wards”
- •Toxaemia, plasmarrhea, or infection?
- •The Guinea Pig Club
- •Burns and sulfa drugs at Pearl Harbor
- •Burn center concept
- •Shock and resuscitation
- •Wound care and infection
- •Burn surgery
- •Inhalation injury and pulmonary care
- •Nutrition and the “Universal Trauma Model”
- •Rehabilitation
- •Conclusions
- •References
- •Epidemiology and prevention of burns throughout the world
- •Introduction
- •Epidemiology
- •The inequitable distribution of burns
- •Cost by age
- •Cost by mechanism
- •Limitations of data
- •Risk factors
- •Socioeconomic factors
- •Race and ethnicity
- •Age-related factors: children
- •Age-related factors: the elderly
- •Regional factors
- •Gender-related factors
- •Intent
- •Comorbidity
- •Agents
- •Non-electric domestic appliances
- •War, mass casualties, and terrorism
- •Interventions
- •Smoke detectors
- •Residential sprinklers
- •Hot water temperature regulation
- •Lamps and stoves
- •Fireworks legislation
- •Fire-safe cigarettes
- •Children’s sleepwear
- •Acid assaults
- •Burn care systems
- •Role of the World Health Organization
- •Conclusions and recommendations
- •Surveillance
- •Smoke alarms
- •Gender inequality
- •Community surveys
- •Acknowledgements
- •References
- •Prevention of burn injuries
- •Introduction
- •Burns prevalence and relevance
- •Burn injury risk factors
- •WHERE?
- •Burn prevention types
- •Burn prevention: The basics to design a plan
- •Flame burns
- •Prevention of scald burns
- •Conclusions
- •References
- •Burns associated with wars and disasters
- •Introduction
- •Wartime burns
- •Epidemiology of burns sustained during combat operations
- •Fluid resuscitation and initial burn care in theater
- •Evacuation of thermally-injured combat casualties
- •Care of host-nation burn patients
- •Disaster-related burns
- •Epidemiology
- •Treatment of disaster-related burns
- •The American Burn Association (ABA) disaster management plan
- •Summary
- •References
- •Education in burns
- •Introduction
- •Surgical education
- •Background
- •Simulation
- •Education in the internet era
- •Rotations as courses
- •Mentorship
- •Peer mentorship
- •Hierarchical mentorship
- •What is a mentor
- •Implementation
- •Interprofessional education
- •What is interprofessional education
- •Approaches to interprofessional education
- •References
- •European practice guidelines for burn care: Minimum level of burn care provision in Europe
- •Foreword
- •Background
- •Introduction
- •Burn injury and burn care in general
- •Conclusion
- •References
- •Pre-hospital and initial management of burns
- •Introduction
- •Modern care
- •Early management
- •At the accident
- •At a local hospital – stabilization prior to transport to the Burn Center
- •Transportation
- •References
- •Medical documentation of burn injuries
- •Introduction
- •Medical documentation of burn injuries
- •Contents of an up-to-date burns registry
- •Shortcomings in existing documentation systems designs
- •Burn depth
- •Burn depth as a dynamic process
- •Non-clinical methods to classify burn depth
- •Burn extent
- •Basic principles of determining the burn extent
- •Methods to determine burn extent
- •Computer aided three-dimensional documentation systems
- •Methods used by BurnCase 3D
- •Creating a comparable international database
- •Results
- •Conclusion
- •Financing and accomplishment
- •References
- •Pathophysiology of burn injury
- •Introduction
- •Local changes
- •Burn depth
- •Burn size
- •Systemic changes
- •Hypovolemia and rapid edema formation
- •Altered cellular membranes and cellular edema
- •Mediators of burn injury
- •Hemodynamic consequences of acute burns
- •Hypermetabolic response to burn injury
- •Glucose metabolism
- •Myocardial dysfunction
- •Effects on the renal system
- •Effects on the gastrointestinal system
- •Effects on the immune system
- •Summary and conclusion
- •References
- •Anesthesia for patients with acute burn injuries
- •Introduction
- •Preoperative evaluation
- •Monitors
- •Pharmacology
- •Postoperative care
- •References
- •Diagnosis and management of inhalation injury
- •Introduction
- •Effects of inhaled gases
- •Carbon monoxide
- •Cyanide toxicity
- •Upper airway injury
- •Lower airway injury
- •Diagnosis
- •Resuscitation after inhalation injury
- •Other treatment issues
- •Prognosis
- •Conclusions
- •References
- •Respiratory management
- •Airway management
- •(a) Endotracheal intubation
- •(b) Elective tracheostomy
- •Chest escharotomy
- •Conventional mechanical ventilation
- •Introduction
- •Pathophysiological principles
- •Low tidal volume and limited plateau pressure approaches
- •Permissive hypercapnia
- •The open-lung approach
- •PEEP
- •Lung recruitment maneuvers
- •Unconventional mechanical ventilation strategies
- •High-frequency percussive ventilation (HFPV)
- •High-frequency oscillatory ventilation
- •Airway pressure release ventilation (APRV)
- •Ventilator associated pneumonia (VAP)
- •(a) Prevention
- •(b) Treatment
- •References
- •Organ responses and organ support
- •Introduction
- •Burn shock and resuscitation
- •Post-burn hypermetabolism
- •Individual organ systems
- •Central nervous system
- •Peripheral nervous system
- •Pulmonary
- •Cardiovascular
- •Renal
- •Gastrointestinal tract
- •Conclusion
- •References
- •Critical care of thermally injured patient
- •Introduction
- •Oxidative stress control strategies
- •Fluid and cardiovascular management beyond 24 hours
- •Other organ function/dysfunction and support
- •The nervous system
- •Respiratory system and inhalation injury
- •Renal failure and renal replacement therapy
- •Gastro-intestinal system
- •Glucose control
- •Endocrine changes
- •Stress response (Fig. 2)
- •Low T3 syndrome
- •Gonadal depression
- •Thermal regulation
- •Metabolic modulation
- •Propranolol
- •Oxandrolone
- •Recombinant human growth hormone
- •Insulin
- •Electrolyte disorders
- •Sodium
- •Chloride
- •Calcium, phosphate and magnesium
- •Calcium
- •Bone demineralization and osteoporosis
- •Micronutrients and antioxidants
- •Thrombosis prophylaxis
- •Conclusion
- •References
- •Treatment of infection in burns
- •Introduction
- •Clinical management strategies
- •Pathophysiology of the burn wound
- •Burn wound infection
- •Cellulitis
- •Impetigo
- •Catheter related infections
- •Urinary tract infection
- •Tracheobronchitis
- •Pneumonia
- •Sepsis in the burn patient
- •The microbiology of burn wound infection
- •Sources of organisms
- •Gram-positive organisms
- •Gram-negative organisms
- •Infection control
- •Pharmacological considerations in the treatment of burn infections
- •Topical antimicrobial treatment
- •Systemic antimicrobial treatment (Table 3)
- •Gram-positive bacterial infections
- •Enterococcal bacterial infections
- •Gram-negative bacterial infections
- •Treatment of yeast and fungal infections
- •The Polyenes (Amphotericin B)
- •Azole antifungals
- •Echinocandin antifungals
- •Nucleoside analog antifungal (Flucytosine)
- •Conclusion
- •References
- •Acute treatment of severely burned pediatric patients
- •Introduction
- •Initial management of the burned child
- •Fluid resuscitation
- •Sepsis
- •Inhalation injury
- •Burn wound excision
- •Burn wound coverage
- •Metabolic response and nutritional support
- •Modulation of the hormonal and endocrine response
- •Recombinant human growth hormone
- •Insulin-like growth factor
- •Oxandrolone
- •Propranolol
- •Glucose control
- •Insulin
- •Metformin
- •Novel therapeutic options
- •Long-term responses
- •Conclusion
- •References
- •Adult burn management
- •Introduction
- •Epidemiology and aetiology
- •Pathophysiology
- •Assessment of the burn wound
- •Depth of burn
- •Size of the burn
- •Initial management of the burn wound
- •First aid
- •Burn blisters
- •Escharotomy
- •General care of the adult burn patient
- •Biological/Semi biological dressings
- •Topical antimicrobials
- •Biological dressings
- •Other dressings
- •Exposure
- •Deep partial thickness wound
- •Total wound excision
- •Serial wound excision and conservative management
- •Full thickness burns
- •Excision and autografting
- •Topical antimicrobials
- •Large full thickness burns
- •Serial excision
- •Mixed depth burn
- •Donor sites
- •Techniques of wound excision
- •Blood loss
- •Antibiotics
- •Anatomical considerations
- •Skin replacement
- •Autograft
- •Allograft
- •Other skin replacements
- •Cultured skin substitutes
- •Skin graft take
- •Rehabilitation and outcome
- •Future care
- •References
- •Burns in older adults
- •Introduction
- •Burn injury epidemiology
- •Pathophysiologic changes and implications for burn therapy
- •Aging
- •Comorbidities
- •Acute management challenges
- •Fluid resuscitation
- •Burn excision
- •Pain and sedation
- •End of life decisions
- •Summary of key points and recommendations
- •References
- •Acute management of facial burns
- •Introduction
- •Anatomy and pathophysiology
- •Management
- •General approach
- •Airway management
- •Facial burn wound management
- •Initial wound care
- •Topical agents
- •Biological dressings
- •Surgical burn wound excision of the face
- •Wound closure
- •Special areas and adjacent of the face
- •Eyelids
- •Nose and ears
- •Lips
- •Scalp
- •The neck
- •Catastrophic injury
- •Post healing rehabilitation and scar management
- •Outcome and reconstruction
- •Summary
- •References
- •Hand burns
- •Introduction
- •Initial evaluation and history
- •Initial wound management
- •Escharotomy and fasciotomy
- •Surgical management: Early excision and grafting
- •Skin substitutes
- •Amputation
- •Hand therapy
- •Secondary reconstruction
- •References
- •Treatment of burns – established and novel technology
- •Introduction
- •Partial thickness burns
- •Biological membranes – amnion and others
- •Xenograft
- •Full thickness burns
- •Dermal analogs
- •Keratinocyte coverage
- •Facial transplantation
- •Tissue engineering and stem cells
- •Gene therapy and growth factors
- •Conclusion
- •References
- •Wound healing
- •History of wound care
- •Types of wounds
- •Mechanisms of wound healing
- •Hemostasis
- •Proliferation
- •Epithelialization
- •Remodeling
- •Fetal wound healing
- •Stem cells
- •Abnormal wound healing
- •Impaired wound healing
- •Hypertrophic scars and keloids
- •Chronic non-healing wounds
- •Conclusions
- •References
- •Pain management after burn trauma
- •Introduction
- •Pathophysiology of pain after burn injuries
- •Nociceptive pain
- •Neuropathic pain
- •Sympathetically Maintained Pain (SMP)
- •Pain rating and documentation
- •Pain management and analgesics
- •Pharmacokinetics in severe burns
- •Form of administration [21]
- •Non-opioids (Table 1)
- •Paracetamol
- •Metamizole
- •Non-steroidal antirheumatics (NSAID)
- •Selective cyclooxygenasis-2-inhibitors
- •Opioids (Table 2)
- •Weak opioids
- •Strong opioids
- •Other analgesics
- •Ketamine (see also intensive care unit and analgosedation)
- •Anticonvulsants (Gabapentin and Pregabalin)
- •Antidepressants with analgesic effects
- •Regional anesthesia
- •Pain management without analgesics
- •Adequate communication
- •Psychological techniques [65]
- •Transcutaneous electrical nerve stimulation (TENS)
- •Particularities of burn pain
- •Wound pain
- •Breakthrough pain
- •Intervention-induced pain
- •Necrosectomy and skin grafting
- •Dressing change of large burn wounds and removal of clamps in skin grafts
- •Dressing change in smaller burn wounds, baths and physical therapy
- •Postoperative pain
- •Mental aspects
- •Intensive care unit
- •Opioid-induced hyperalgesia and opioid tolerance
- •Hypermetabolism
- •Psychic stress factors
- •Risk of infection
- •Monitoring [92]
- •Sedation monitoring
- •Analgesia monitoring (see Fig. 2)
- •Analgosedation (Table 3)
- •Sedation
- •Analgesia
- •References
- •Nutrition support for the burn patient
- •Background
- •Case presentation
- •Patient selection: Timing and route of nutritional support
- •Determining nutritional demands
- •What is an appropriate initial nutrition plan for this patient?
- •Formulations for nutritional support
- •Monitoring nutrition support
- •Optimal monitoring of nutritional status
- •Problems and complications of nutritional support
- •Conclusion
- •References
- •HBO and burns
- •Historical development
- •Contraindications for the use of HBO
- •Conclusion
- •References
- •Nursing management of the burn-injured person
- •Introduction
- •Incidence
- •Prevention
- •Pathophysiology
- •Severity factors
- •Local damage
- •Fluid and electrolyte shifts
- •Cardiovascular, gastrointestinal and renal system manifestations
- •Types of burn injuries
- •Thermal
- •Chemical
- •Electrical
- •Smoke and inhalation injury
- •Clinical manifestations
- •Subjective symptoms
- •Possible complications
- •Clinical management
- •Non-surgical care
- •Surgical care
- •Coordination of care: Burn nursing’s unique role
- •Nursing interventions: Emergent phase
- •Nursing interventions: Acute phase
- •Nursing interventions: Rehabilitative phase
- •Ongoing care
- •Infection prevention and control
- •Rehabilitation medicine
- •Nutrition
- •Pharmacology
- •Conclusion
- •References
- •Outpatient burn care
- •Introduction
- •Epidemiology
- •Accident causes
- •Care structures
- •Indications for inpatient treatment
- •Patient age
- •Total burned body surface area (TBSA)
- •Depth of the burn
- •Pre-existing conditions
- •Accompanying injuries
- •Special injuries
- •Treatment
- •Initial treatment
- •Pain therapy
- •Local treatment
- •Course of treatment
- •Complications
- •Infections
- •Follow-up care
- •References
- •Non-thermal burns
- •Electrical injury
- •Introduction
- •Pathophysiology
- •Initial assessment and acute care
- •Wound care
- •Diagnosis
- •Low voltage injuries
- •Lightning injuries
- •Complications
- •References
- •Symptoms, diagnosis and treatment of chemical burns
- •Chemical burns
- •Decontamination
- •Affection of different organ systems
- •Respiratory tract
- •Gastrointestinal tract
- •Hematological signs
- •Nephrologic symptoms
- •Skin
- •Nitric acid
- •Sulfuric acid
- •Caustic soda
- •Phenol
- •Summary
- •References
- •Necrotizing and exfoliative diseases of the skin
- •Introduction
- •Necrotizing diseases of the skin
- •Cellulitis
- •Staphylococcal scalded skin syndrome
- •Autoimmune blistering diseases
- •Epidermolysis bullosa acquisita
- •Necrotizing fasciitis
- •Purpura fulminans
- •Exfoliative diseases of the skin
- •Stevens-Johnson syndrome
- •Toxic epidermal necrolysis
- •Conclusion
- •References
- •Frostbite
- •Mechanism
- •Risk factors
- •Causes
- •Diagnosis
- •Treatment
- •Rewarming
- •Surgery
- •Sympathectomy
- •Vasodilators
- •Escharotomy and fasciotomy
- •Prognosis
- •Research
- •References
- •Subject index
R. Cartotto
Table 2. Comparison of studies involving inhaled heparin and N-Acetyl Cystine (NAC) for smoke inhalation
Study |
Design |
N |
Patient selection |
Interventions |
Outcomes |
Desai |
Retrospective |
90 |
Pediatric |
5000 U aerosolized |
Treatment group had signifi- |
et al. |
Historical |
|
Mean burn size 50%–55% |
heparin alternating with |
cantly lower reintubation |
[26] |
Controls |
|
TBSA |
3 mL aerosolized 20% |
rates,evidence of atelectasis, |
|
|
|
All bronchoscopic- |
NAC every 2 hours for |
and mortality |
|
|
|
confirmed I I |
7 days |
|
|
|
|
All mechanically |
|
|
|
|
|
ventilated |
|
|
Holt |
Retrospective |
150 |
Adults |
inhaled 5000U heparin No differences in pneumonia, |
|
et al. |
Contemporan- |
|
Mean burn size 27%–32% |
with 3 mL 20% NAC |
duration of MV, re-intubation, |
[27] |
eous |
|
TBSA |
with albuterol every |
LOS, survival, or PaO2/FiO2 |
|
Controls |
|
Only 68% had broncho- |
4 hours for 7 days |
ratios on days 1, 3, and 7 post |
|
Unblinded |
|
scope-confirmed I I |
|
burn between treatment and |
|
|
|
physician discretion used |
|
control |
|
|
|
to initiate heparin-NAC |
|
|
Miller |
Retrospective |
30 |
Adults |
nebulized 10 000 U |
Treatment group showed |
et al. |
Historical |
|
All mechanically |
heparin with 3 ml 20% |
significantly better improvement |
[20] |
Controls |
|
ventilated |
nac, and Albuterol every |
in LIS, respiratory resistance and |
|
|
|
All with bronchoscope- |
4 hours for 7 days |
compliance, and hypoxemia |
|
|
|
confirmed I I |
|
compared to controls. |
N: number of subjects, I I: inhalation injury, MV: mechanical ventilation, LOS: length of hospital stay, LIS: Lung Injury Score
from heparin-NAC but this study may have been flawed by the fact that only 68% of the study population had a bronchoscopic diagnosis of inhalation injury. Additionally, some of the patients were intubated and mechanically ventilated for as little as one day. Also, the decision to use heparin-NAC was at the attending physician’s discretion.
The available evidence would therefore suggest that for a mechanically ventilated patient with bronchoscopically-confirmed inhalation injury that a one week course of nebulized Heparin (5,000 to 10,000 units) with 3 mL of 20% NAC every four hours with or without the addition of Albuterol may be of benefit. This regimen appears to relatively safe and adverse effects such as NAC-induced bronchospasm or Heparin-induced thrombocytopenia were not reported in any of the studies discussed.
Conventional mechanical ventilation
Introduction
The approach to conventional mechanical ventilation (CMV) for critically ill patients has undergone dramatic change in the past decade. A ventilation strategy that was characterized by the use of liberal
tidal volumes, tolerance of high peak and plateau airway pressures, and the goal of normalization of arterial blood gas values has been replaced by gentler approaches to mechanical ventilation which feature use of lower tidal volumes, limited airway pressures, permissive hypercapnia, and enthusiasm for “open lung” strategies using higher positive and expiratory pressure (PEEP) settings along with lung recruitment maneuvers. While this paradigm shift has largely been adopted in the approach to CMV in the burn patient, three important points should be considered:
Burn patients were either excluded from, or were minimally represented in virtually all of the major trials that have promoted low tidal volume, pressure limited and open lung approaches to CMV
The current approaches to CMV are directed at patients with existing Acute Lung Injury (ALI) andAcuteRespiratoryDistressSyndrome(ARDS). Unlike patients in the Intensive Care Unit who are admitted with some degree of lung dysfunction or injury, the majority of burn patients who are intubated start out their course of mechanical ventilation with relatively normal lungs even in the face of smoke inhalation. Typically, lung dysfunction, pulmonary edema, ALI, and ARDS fre-
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Respiratory management
quently develop within days of burn injury and Burn Centre admission. It is the rule rather than the exception that the initial mechanical ventilation is being delivered to uninjured lungs. As such, there has been no research directed at this unique situation and inevitably, ventilation strategies designed for ALI and ARDS are translated to intubated patients with acute burns even though pathology may not yet have developed in the lungs of these patients.
The chest wall mechanics of many burn patients can be vastly different from that of most critically ill patients from whom current CMV strategies have evolved. Specifically, the presence of unyielding eschar, and significant soft-tissue edema on the abdomen and thorax of the burn patient have significant effects on respiratory compliance. Thus airway pressures measured at the ven-
tilator may not be reflective of actual trans-pul- monary pressures in the lung.
This section of the chapter is not intended to give specific formulas or prescriptions for mechanical ventilation of the burn patient. Rather, the intention is to review general concepts and approaches to mechanical ventilation, which are believed to affect respiratory outcomes bearing in mind the above points, which draw attention to the fact that most of these principles have been developed in patients without burns but have inevitably been adopted by burn clinicians and translated to the burn patient.
Pathophysiological principles
All of the general principles of current CMV strategies which will be discussed below have evolved from an improved understanding of the pathology of ALI and ARDS, and the recognition that mechanical ventilation may itself be harmful to the lungs and may directly cause new, or worsen existing ALI and ARDS. This process is referred to as ventilatory induced lung injury (VILI) [28, 29]. Specifically, ventilation with large tidal volumes and high peak airway pressures causes injury through excessive stretch of the alveoli (volutrauma), while inadequate and inspiratory pressures allow shear injury to occur from repetitive alveolar collapse and then re-opening (atelectrauma). These mechanical injuries then cause
inflammation which further injures the lung (biotrauma) [28, 29].
It is essential to appreciate that heterogeneity is the defining feature of the lungs in patients with ALI and ARDS. Computed tomography studies have been seminal in understanding the herterogeneous pathology of ARDS [30]. Some areas of the lung (usually the non-dependent regions) may be relatively unaffected while other areas (usually the dependent areas posterior to the heart and mediastinum) show atelectasis and consolidation. Furthermore, some of the affected alveoli show predominantly consolidation, while others show predominantly atelectasis, even within the same lung. Hence, some parts of the lung do not receive ventilation because they are consolidated and less compliant so that mechanical ventilation ends up being delivered to a much smaller than normal volume of less affected, or even normal lung. This has been referred to as the “baby lung” concept[31] which refers to the idea that during ARDS only a small functioning baby-sized lung is being ventilated inside a fully grown adult. Thus, if traditional adult-sized airway pressures and tidal volumes are used, these are delivered only to a small portion of the lung thus causing barotrauma or volutrauma.
To complicate matter further, some forms of ARDS feature “loose” or more recruitable lung (e.g. from inflammatory edema) whereas other forms feature “sticky” non-recruitable lung (e.g. consolidative pneumonia) [32–34]. For example, it is conceivable (but unknown at present) whether ARDS after smoke inhalation may feature a predominance of “sticky” non-recruitable alveoli, rather than “loose” more recruitable alveoli.
Low tidal volume and limited plateau pressure approaches
The well-known large multi-centre study by the acute respiratory distress syndrome of the National Heart Lung, and Blood Institute (ARDS Net) in 2000 found that a traditional approach using tidal volumes of 12 mL/kg predicted body weight (PBW) and plateau pressures up to 50 cmH2O was associated with significantly higher mortality than a CMV strategy using a tidal volume of 6 mL/kg PBW and plateau pressures limited to less than 30 cmH2O [35]. The other important trials that have examined the use of low
179
R. Cartotto
Table 3. Comparison of randomized prospective studies using low tidal volume (Vt) and limited plateau Pressures (Pplat) strategies for mechanical ventilation of patients with ARDS
Study |
N |
Target Vt (mL/kg) and |
Actual Vt (mL/kg) and |
% |
P |
|
|
|
Pplat (cm H2O) |
Pplat (cm H2O) |
Mortality |
value |
|
ARDS Net et al. [35] |
861 |
6 vs 12 and 30 vs 50 |
6.2 vs 11.8 and 25 vs 33 |
31 vs 40# |
0.007 |
|
Amato et al. [36] |
53 |
6 vs 12 and > 20 vs no limit |
384 mL vs 768 mL * and 30 vs 37 |
38 vs 71§ |
0.001 |
|
Brochard et al. [37] |
116 |
6–10 vs 10–15 and 25–30 vs 60 |
7.1 vs 10.3 and 26 vs 32 |
47 vs 38¶ |
0.38 |
|
Stewart et al. [38] |
120 |
8 vs 10 |
–15 and 30 vs 50 |
7.0 vs 10.7 and 22 vs 27 |
50 vs 47† |
0.72 |
Brower et al. [39] |
52 |
8 vs 10 |
–12 and 30 vs 45–55 |
7.3 vs 10.2 and 25 vs 31 |
50 vs 46† |
0.61 |
* Vt was reported in mL, # mortality at hospital discharge or 180 days, § mortality at 28 days, ¶ mortality at 60 days, † mortality in-hospital
tidal volumes and limited plateau pressure strategies are summarized in Table 3 [35–39]. The three negative trials may not have recognized a mortality difference because of the relatively narrow differences in actual tidal volumes and plateau pressures between the treatment and control arms [37–39].
In general, based largely upon the ARDSNet recommendations for ALI and ARDS, mechanical ventilation in burn patients is now similarly initiated with an initial tidal volume of 6–8 mL/kg PBW and a goal of maintaining plateau pressures less than 30 cm H20and peak inspiratory pressures less than 35 cmH20. This approachassumesrelativelynormalthoracoabdominal compliance. In a massively edematous burn patient with chest wall or abdominal burns it may be necessary to use larger tidal volumes (8–10 mL/kg) to achieve adequate alveolar patency while accepting higher plateau pressures (up to 35 cmH2O).
Permissive hypercapnia
Aggressive pursuit of a normalized PaCO2 and pH is no longer the goal of current CMV strategies [40, 41]. Low tidal volume strategies result in lower minute ventilation which can cause hypercapnia. While a large acute elevation in the PaCO2 may be associated with adverse effects (vasodilation, decrease cardiac output, increased intracranial pressure), the effects of more prolonged but less severe hypercapnia appear to be better tolerated but data is lacking to fully support this notion. Ideal levels of PaCO2 and pH are not identified. It should be noted that the ARDSNet investigators utilized increases in respiratory rate, bicarbonate infusions and increased tidal volumes
to deal with acidosis. The use of bicarbonate infusions as a buffer remains controversial. Although pH may be corrected with bicarbonate, intra-cellular pH may actually drop since CO2 produced when bicarbonate binds with metabolic acids may accumulate within cells, resulting in intra-cellular acidosis [40]. General guidelines would include maintaining pH between 7.25 and 7.45 and the PaCO2 between 35 and 55, although higher PaCO2 may be tolerated if the pH is above 7.25.
The open-lung approach
As noted, portions of the lung in ALI and ARDS are characterized by collapse of small airways and alveoli. During positive pressure ventilation these alveoli open during inflation but will re-collapse if end expiratory pressures are inadequate. The repetitive opening and collapse causes shear injury to the alveolus (atelectrauma), and is detrimental. It is therefore highly desirable to open alveoli and keep them open, not only to avoid shear injury but also to improve oxygenation. This concept is referred to as an “open lung” approach. The two main techniques involved in this strategy are the use of positive and expiratory pressure (PEEP) and lung recruitment maneuvers. However, despite a solid physiological basis, the optimal use of PEEP and lung recruitment maneuvers remain mired in controversy.
PEEP
The ideal level of PEEP and the best method for determining that level are unknown. If PEEP is too low,
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Respiratory management
atelectasis is not reversed. Unnecessarily high PEEP may cause stretch injury to the aerated alveoli as well as haemodynamic instability, barotrauma, and may worsen ventilation perfusion matching [40–42].
In the limited tidal volume and plateau pressure study by Amato, et al. [36] PEEP was set at a level just above the lower inflection point on the pressure volume curve which in theory is the point above which recruitable alveoli are kept open at the end of expiration. However, this approach may not be practical and the derived pressure volume curve may not accurately represent regional differences across all regions of the lung because of the heterogeneity of the ARDS process. Nevertheless, PEEP levels as high as 24 cmH2O were used in the high PEEP/low tidal volume arm of this study and were associated with significantly lower mortality rates.
Another approach which was used in the ARDS Net study of low volume and pressure was to arbitrarily link certain PEEP and FIO2 combinations to achieve adequate oxygenation. In general, PEEP levels between 5 and 20 cmH2O probably provide an acceptable balance between the adverse effects of inadequate and expiratory pressure and the risks of excessive end-expiratory pressure. Again, however, optimal PEEP levels remain unknown at this point.
Four large randomized multi-centre prospective studies have tried to determine whether there is a benefit to use of higher PEEP vs. lower PEEP settings (Table 4) [43–46]. The ALVEOLI Trial conducted by the ARDS Net investigators [43] compared a high PEEP (mean setting 13 cmH2O) to low PEEP (mean setting 8 cmH2O) among 549 patients with ALI and ARDS who were all ventilated with a tidal volume goal of 6 mL/kg PBW and a plateau pressure limit of
30 cmH2O, and found that although the high PEEP group and significantly higher PaO2/FiO2 ratios, there were no significant differences in ventilator-free days or survival.
In the ARIES trial conducted by Villar, et al. [44] ARDS patients were randomized to either low PEEP (PEEP above 5 cmH2O) plus higher tidal volume (9–11 mL/kg PBW) or, to high PEEP (PEEP set above lower inflection point on the static TV curve) plus lower tidal volume (5–8 mL/kg PBW). The high PEEP/lower tidal volume group had significantly greater ventilator-free days and ICU and hospital survival. However, any specific benefit of higher PEEP cannot be determined from this study because it was combined with a lower tidal volume approach compared to that in the low PEEP group.
More recently the EXPRESS trail [45] randomized patients with ALI and ARDS using a tidal volume of 6 mL/kg to either moderate PEEP (5–9 cmH2O) or to higher PEEP which was set to achieve a plateau pressure up to 30 cmH2O. Although the higher PEEP group had significantly superior oxygenation and a greater number of ventilator-free days, overall survival was not significantly different than in the low PEEP group.
Finally, in the LOVS study [46] of 983 patients with ALI and ARDS whose PaO2/FiO2 ratio was less than 250 were randomized to a target tidal volume of 6 mL/kg, no recruitment maneuvers, and PEEP set to keep the plateau pressure less than 30 (low PEEP group) or to a tidal volume of 6 mL/kg, lung recruitment maneuvers, and PEEP set to keep the plateau pressure less than 40 cmH2O (high PEEP group). Overall, in-hospital survival did not differ between the groups but the high PEEP group had a significantly lower mortality rate secondary to refractory hypoxemia and a significantly lower rate of use of
Table 4. Comparison of randomized prospective studies using lower positive end expiratory pressure (PEEP) vs higher PEEP for acute lung injury and acute respiratory distress syndrome
Study |
N |
Actual Vt (mL/kg) and |
Actual Plateau Pressure (cm H2O) |
% |
P |
|
|
PEEP (cm H2O)* |
|
Mortality |
value |
ARDS Net [43] |
549 |
6.1 vs 5.8 and 8.5 vs 12.9 |
24 vs 26 |
25 vs 28 # |
0.48 |
Villar et al. [44] |
103 |
10 vs 7.1 and 8.7 vs 11.2 |
33 vs 28 |
56 vs 34 # |
0.04 |
Mercat et al. [45] |
767 |
6.2 vs 6.2 and 6.7 vs 13.4 |
21 vs 27 |
39 vs 35 ¶ |
0.30 |
Meade et al. [46] |
983 |
6.7 vs 6.9 and 8.8 vs 11.8 |
25 vs 29 |
40 vs 36 # |
0.19 |
Vt: tidal volume, * on day three, # in-hospital mortality, ¶ 60-day mortality
181