- •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
Anesthesia for patients with acute burn injuries
Lee C. Woodson, Edward Sherwood, Alexis McQuitty, Mark D. Talon
Shriners Hospital for Children, Galveston University of Texas Medical Branch Galveston, TX, USA
Introduction
Remarkable advances continue to be made in the care of patients with major burn injuries. Early aggressive fluid resuscitation has dramatically improved initial survival. The development of specialized burn centers has allowed the concentration and coordination of resources needed to provide a multidisciplinary approach from the time of admission with the goal of not just maximizing survival but optimizing functional recovery as well [1].
Anesthetic management is an important part of this multidisciplinary approach. Anesthesia providers have highly developed skills and experience in airway management, pulmonary care, fluid and electrolyte management, vascular access, and pharmacological support of the circulation. These areas of clinical expertise are all central to the care of patients with major burn injuries. However, the effective use of this clinical expertise for the care of burn patients requires knowledge of the pathophysiological changes associated with burns and an understanding of the multidisciplinary approach to burn care [2]. To be effective, perioperative management should be compatible with overall goals and especially with ICU care.
Patients with large acute burns present multiple challenges to anesthetic management (Table 1). Virtually all organ systems are affected by large burn injuries. These changes have an important influence
Marc G. Jeschke et al. (eds.), Handbook of Burns
on anesthetic management including not only drug selection and dosage but airway management, monitoring, fluid administration, sedation, and pain control. As a result, nearly every aspect of anesthetic care must include some adjustment to deal with pathophysiological changes due to the burns.
Preoperative evaluation
Care of the acutely burned patient requires knowledge of the continuum of pathophysiological changes from
Table 1. Perioperative challenges in the anesthetic management of acute burn patients
Airway compromises
Inhalation injury
Impaired circulation
Difficult vascular access
Mechanical difficulties with monitors due to cutaneous burns
Massive hemorrhage
Altered drug response
Sepsis/systematic inflammatory response syndrome
Altered temperature regulation
Co-existing diseases
Associated trauma
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L. C. Woodson et al.
Table 2.
Patient age
Extent of cutaneous burns (% total body surface area)
Burn depth and distribution
Mechanism of injury (flame, scald, etc.)
Airway exam
Inhalation Injury
Quality or Resuscitation
Associated Injuries
Coexisting diseases
Surgical plan
the initial injury through wound healing and resolution of metabolic changes. In conjunction with the standard features of a preoperative assessment, the anesthetist should focus on certain features associated with increased risk and technical challenge when planning perioperative care of the patient with acute burn injuries (Table 2). The mechanism of injury should be clearly identified since this determines the quality of burn injuries as well as the kinds of associated disorders the patient may present with. As an example, a person burned in the enclosed space of a house and a worker suffering electrical burns would present with very different associated injuries. Since fluid requirements and the pathophysiological response to injury are dynamic it is also important to know the time elapsed since injury.
Pathophysiological alterations in respiratory function are common in severely burned patients (Fig. 1). An airway exam is the first priority in patients with a history consistent with burns to the head and neck and/or smoke inhalation. Tissue distortion due to edema can make intubation by direct laryngoscopy difficult or impossible and these changes will increase with fluid resuscitation. As a result, it is very important to diagnose airway compromise early in the patient with acute burns. Pharyngeal burns can lead to lethal airway obstruction and pre-emptive intubation can be life saving when this threatens. However, facial burns are often not associated with pharyngeal edema and airway obstruction. In the absence of respiratory distress or other reasons for immediate intubation such as very extensive burns, shock, or inability to protect the airway, it may be safer to defer securing the air-
way until it can be accomplished in a controlled setting and when a clear indication for intuition can be identified [3]. This can reduce complications of unnecessary intubations such as exacerbation of laryngeal injuries or life threatening consequences of unintended extubation of a patient who has been intubated then heavily sedated or pharmacologically paralyzed. Initially, patients with smoke inhalation often present with good gas exchange and a normal chest radiograph. Inhalation injury often progresses over time as the inflammatory response develops and small airways are occluded by sloughed tissues, casts and stagnant secretions. Therefore, initial chest x-ray or arterial blood gas analyses usually serve more as a baseline for evaluating changes in pulmonary function. Impaired gas exchange and significant chest radiograph findings on admission are ominous observations. The diagnosis of inhalation injury is usually based on the history and physical exam and confirmed by bronchoscopy.
In addition to airway and pulmonary parenchymal pathology, pulmonary insufficiency can occur in patients with acute burn injury when a restrictive pulmonary deficit results from circumferential burns that limit chest wall expansion during inspirationorfromabdominal compartmentsyndrome when abdominal contents limit diaphragmatic excursion. Restricted chest wall mobility can be corrected by surgical release (escarotomies) and if abdominal compartment syndrome is diagnosed there
Smoke inhalation Thermal airway damage Laryngeal edema Airway Trauma Restrictive breathing defect from circumferential escar Bronchospasm Pulmonary edema Aspiration pneumonitis Pneumonia
Central nervous system injury/ impaired respiratory drive
Fig. 1. Common causes of respiratory pathology in burned patients
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Anesthesia for patients with acute burn injuries
Table 3. Formulas for estimating fluid resuscitation of adult acute burn patients
Formula |
Crystalloid Solution |
Colloid Solution |
Parkland |
4 ml/kg/% burn during |
|
|
first 24 hours after |
|
|
injury with half given |
|
|
in first 8 hours |
|
Brooke |
Lactated Ringer’s |
0.5 ml/kg |
|
1.5 ml/kg/% |
|
|
Burn |
|
Modified |
2 ml/kg% burn |
|
Brooke |
|
|
Evans |
Normal saline 1 ml/ |
|
|
kg/% burn |
|
Slater |
Lactated Ringer’s |
Fresh Frozen Plasma |
|
2L/24 hr |
75 ml/kg Over 24 hour |
Demling |
Titrate to urine output |
1st 8 hr: |
|
at 30 ml/hr |
Dextran 40 in saline |
|
|
2 ml/kl/hr |
|
|
Next 18 hrs: |
|
|
Fresh Frozen Plasma at |
|
|
0.5 ml/kg/hr |
are a number of interventions to reverse associated pathophysiological changes. It is important to be sure that the anesthesia ventilator in the operating room is capable of delivering support that the patient requires in the ICU.
Hemodynamic status, electrolyte balance, and renal function are affected by the extent of burn injuries and the quality of fluid resuscitation. It is important to understand the hemodynamic status of the patient. In the immediate post-injury stage, patients exhibit a syndrome known as burn shock in which increased vascular permeability causes transudation of protein rich fluid from the vascular compartment to the inerstitium leading to intravascular hypovolemia and tissue hypoperfusion. Delays in initiating fluid resuscitation or inadequate volumes administered during burn shock can result in hypoperfusion and damage to non-burned tissues as well as exacerbation of the burn wounds. Over resuscitation also can have deleterious effects such as pulmonary edema or compartment syndromes of extremities or the abdomen. Several formulae based on extent of cutaneous burns are available to estimate the volume of fluid and rates of administration needed to maintain
Table 4. Formulas for estimating fluid resuscitation of pediatric acute burn patients
|
Tine |
Fluid |
Volume |
Cincinnati |
1st 8hrs |
Lactated Ringer’s |
4 ml/kg/% |
|
|
+ |
burn + |
|
|
NaHCO350mEg/L |
1,500 ml/kg2 |
|
2nd 8 hrs. |
Lactated Ringer’s |
|
|
3rd 8 hrs. |
Lactated Ringer’s |
5,000 ml/m2 |
|
|
+ |
burned |
|
|
12.5 gm |
2,000 ml/m2 |
|
|
albumin/L |
BSA |
Galveston |
1st 24 hrs. |
Ringer’s Lactate |
5,000/m2 |
|
|
+ |
burned |
|
|
12.5 Gm |
2,000 ml/m2 |
|
|
albumin/L |
BSA |
intravascular volume (Table 3). On a ml/kg basis pediatric burn patients have been found to require more volume for resuscitation. In addition, pediatric patients may require resuscitation for smaller burns (e. g. 10–20% total body surface area). Separate formulas have been recommended for fluid resuscitation of pediatric burn patients (Table 4).
Formulas are a starting point for fluid therapy. A comparison of predicted volumes based on the resuscitation formula in use with the actual volumes administered can provide a quick assessment of the appropriateness of the treatment efforts. Resuscitation is then titrated to the patient’s response as judged by mean blood pressure and urine output. Many factors such as smoke inhalation, extensive deep burns, electrical burns, soft tissue trauma, and delay in resuscitation can increase the fluid requirements for resuscitation of burn patients. As a result, the needs of each patient are unique and volume resuscitation must be titrated to the patient’s response. The response to resuscitation can be evaluated by reviewing vital signs and urine output. However, these endpoints are often not good predictors of tissue perfusion. Blood gas analysis, either arterial or venous, can provide additional information regarding the metabolic status and adequacy of perfusion. Specific endpoints include hemoglobin, base deficit, and lactic acid concentration. If the patient’s response is poor despite what appears to be an appropriate volume of fluid administered, underlying pathology should be clarified and additional support such as an inotropic drug provided.
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L. C. Woodson et al.
Large burn injuries often present in association with other coexisting diseases or additional trauma associated with the burn accident. It is important not to focus on the burn wound to the exclusion of other serious pathology. A closed head injury, for example, can significantly alter fluid and hemodynamic management choices. A careful history and physical exam should not ignore these other non-burn issues.
Effective perioperative care can only be accomplished within the context of the planned surgical intervention. The appropriate vascular access and level of monitoring depend on the anticipated physiological stress of surgery and expected blood loss. These can only be revealed by clear communication with the patient’s surgeons. Close consultation with the surgeons is an essential component of the preoperative assessment of the patient with acute burn injuries.
Monitors
Circulation
Arterial blood pressure Central venous pressure Pulmonary artery pressures Cardiac output
Pulmonary artery catheter Peripheral thermodilution catheter Pulse pressure variability
End tidal carbon dioxide Electrocardiography Urine output
Ventilation and Oxygenation
Pulse oximetry
End tidal carbon dioxide Airway pressures and volumes Inspired oxygen analyzer Blood gases
Temperature
Foley catheter probe Rectal probe Esophageal probe
Oro-nasopharyngeal probe
The choice of monitors in a burned patient depends ontheextentofinjuries,physiologicstate,andplanned surgery (Fig. 2). According to American Society of Anesthesiologists, the patient’s oxygenation, ventilation, circulation, and temperature should be continually evaluated. Standard monitors include electrocardiography (ECG), pulse oximetry, arterial blood pressure, temperature, capnography, and inspired oxygen concentration. Pathophysiological changes associated with major burns and the potential for massive surgical bleeding may require more invasive monitors and increased vigilance regarding certain physiological variables during the perioperative period. It should be noted that a change in monitoring or transient loss of monitoring may occur during washing, position change, or dressing application.
In many cases, accurate physiological monitoring can be challenging in burn patients. Topical ointments and skin destruction due to large cutaneous burns may prevent adherence of standard gel electrocardiography electrodes and pulse oximetry to the skin. In this case, metallic surgical staples and alligator clips are effective for ECG monitoring. Pulse oximetry during burn surgery can be difficult when extremities are either burned or in the operative
Fig. 2. Commonly used monitors for burned patients
field. The probes or connections may become wet and tendered useless during bathing or irrigation in the operating room. Transmission pulse oximetry probes may be applied or clipped to the digits, ear lobes, or lips as one solution to these challenges. Some clinicians have modified standard pulse oximetry probes for use on the tongue in conjunction with use of a plastic oral airway. Reflectance pulse oximetric technology has been developed to combat problems with signal transmission during hypoperfusion and when a transmission path is unavailable. Forehead probes are commercially available and may detect hypoxemia more quickly than the ear or finger probes [4].
If direct measurement of arterial blood pressure is not required, measurement of blood pressure using a non-invasive cuff has been found to be accurate even when the cuff is placed over bulky bandages [5]. In cases where blood loss is expected to be extensive, as well as in selected high-risk patients or in those failing resuscitation to clinical goals, invasive monitoring with an arterial catheter may be
154
Anesthesia for patients with acute burn injuries
helpful. An arterial catheter is also advised if clinically significant changes in the blood pressure are expected to occur more rapidly than the interval between non-invasive blood pressure measurements or if vasoactive infusions are needed. Although pulse oximetry and end tidal carbon dioxide measurements are adequate monitors of oxygenation and ventilation in patients with normal pulmonary function, these modalities may be inadequate for patients with significant pulmonary disease such as smoke inhalation injury, acute lung injury or the adult respiratory distress syndrome. Under these circumstances it is useful to have an arterial catheter to provide access to arterial blood samples for gas analysis in order to optimize ventilation. This may be very helpful in adjusting mechanical ventilation.
Perioperative management of patients with major burns is often facilitated by the presence of a central venous catheter. A central venous catheter can provide reliable and secure venous access for administering fluids and drugs (especially vasoactive drugs) and for obtaining blood samples when extensive cutaneous burns make peripheral venous access difficult or impossible. In addition, substantial losses of intravascular volume or limited cardiac function make it difficult to appropriately replace volume without some monitor of filling pressure. Although central venous pressure (CVP) is often used to manage intravascular volume, it is an unreliable indicator of preload [6]. Filling pressures interact in complex and unpredictable ways with ventricular compliance and contractility as well as intra-thorac or intra-abdominal pressures to influence cardiac preload. Cardiac function and response to volume loading have been found to correlate poorly with filling pressures. Preload is defined as end-diastolic myocardial fiber tension; however, this cannot be measured in a clinical setting. Although knowledge of the CVP is not reliable for fine tuning preload, it is important to monitor filling pressure while administering large volumes rapidly. If it appears that tissue perfusion is inadequate and the CVP is low, it is usually safe to administer a fluid bolus as both a diagnostic and therapeutic intervention. If the CVP is high, it is possible that a fluid bolus might cause harm due to intravascular volume overload.
A pulmonary artery catheter (PAC) can also be used to assess cardiovascular function in burned pa-
tients. In addition to the pulmonary artery occlusion pressure (PAOP), right ventricular cardiac output (CO) can be obtained with a pulmonary artery catheter from a thermodilution curve, in which the CO is inversely proportional to the area under the curve. Unreliable results will be obtained in those with rightsided regurgitant lesions or with septal defects. The systemic vascular resistance may also be calculated with PAC-derived information using the following equation:
SVR = MAP-CVP × 80
CO
Despite what appears to be an intuitive benefit of PAC-derived information, the clinical utility of this monitor has been increasingly brought into question. Neither PAOP nor CVP have been found to correlate with either end diastolic volume or stroke volume. Moreover, changes in these indexes of cardiac preload have not correlated with changes in either stroke volume or end diastolic volume in groups of normal volunteers or critically ill patients [6]. Some clinical investigators have found increased mortality associated with the use of a PAC. As a result of these observations and the higher cost of hemodynamic monitoring with the PAC, many clinicians are using this monitor less frequently. Newer volumetric monitors that are less invasive than the PAC have been found to be more reliable indicators of cardiac preload. A transpulmonary thermodilution technique that utilizes a central venous catheter and an arterial fiber optic thermister catheter inserted into the femoral artery can provide estimates of global end diastolic cardiac volume and total intrathoracic blood volume (ITBV). In contrast to CVP and PAOP, augmentation of ITBV has been used successfully to guide fluid resuscitation of severely burned patients. However, use of ITBV was associated with larger resuscitative fluid volumes that predicted by the Parkland formula [7].
Dynamic measures of cardiac preload, such as systolic pressure variation (SPV) and pulse pressure variation (PPV), have been found to be better predictors of volume responsiveness than static indicators such as central venous pressure or pulmonary artery occlusion pressure. These dynamic parameters can be used to discriminate patients who are intravascularly depleted and may benefit from volume loading from patients who are adequately fluid
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