- •Burn Care and Treatment
- •Contents
- •1.1 Initial Assessment and Emergency Treatment
- •Box 1.1. Primary and Secondary Survey
- •1.2 Fluid Resuscitation and Early Management
- •1.2.1 Fluid Resuscitation
- •1.2.2 Endpoint of Burn Resuscitation
- •1.2.4 Role of Colloids, Hypertonic Saline, and Antioxidants in Resuscitation
- •1.2.4.1 Colloids
- •1.2.4.2 Hypertonic Saline
- •1.2.4.3 Antioxidants: High-Dose Vitamin C
- •1.3 Evaluation and Early Management of Burn Wound
- •1.3.1 Evaluation of Burn Depth
- •1.3.2 Choice of Topical Dressings
- •1.3.3 Escharotomy
- •1.3.4 Operative Management
- •References
- •2: Pathophysiology of Burn Injury
- •2.1 Introduction
- •2.2 Local Changes
- •2.2.1 Temperature and Time Effect
- •2.2.2 Etiology
- •2.2.3 Pathophysiologic Changes
- •2.2.4 Burn Size
- •2.3 Systemic Changes
- •2.3.1 Edema Formation
- •2.3.3.1 Resting Energy Expenditure
- •2.3.3.2 Muscle Catabolism
- •2.3.3.3 Glucose and Lipid Metabolism
- •2.3.4 Renal System
- •2.3.5 Gastrointestinal System
- •2.3.6 Immune System
- •2.4 Summary and Conclusion
- •References
- •3: Wound Healing and Wound Care
- •3.1 Introduction
- •3.2 Physiological Versus Pathophysiologic Wound Healing
- •3.2.1 Transforming Growth Factor Beta
- •3.2.2 Interactions Between Keratinocytes and Fibroblasts
- •3.2.3 Matrix Metalloproteinases (MMP)
- •3.3.1 Burn Wound Excision
- •3.3.2 Burn Wound Coverage
- •3.3.3 Autografts
- •3.3.4 Epidermal Substitutes
- •3.3.5 Dermal Substitutes
- •3.3.6 Epidermal/Dermal Substitutes
- •3.4 Summary
- •References
- •4: Infections in Burns
- •4.1 Burn Wound Infections
- •4.1.1 Diagnosis and Treatment of Burn Wound Infections
- •4.1.1.1 Introduction
- •4.1.2 Common Pathogens and Diagnosis
- •4.1.3 Clinical Management
- •4.1.3.1 Local
- •4.1.3.2 Systemic
- •4.1.4 Conclusion
- •4.4 Guidelines for Sepsis Resuscitation
- •References
- •5: Acute Burn Surgery
- •5.1 Introduction
- •5.2 Burn Wound Evaluation
- •5.3 Escharotomy/Fasciotomy
- •5.4 Surgical Burn Wound Management
- •5.5.1 Face
- •5.5.2 Hands
- •5.6 Treatment Standards in Burns Larger Than Sixty Percent TBSA
- •5.7 Temporary Coverage
- •5.9.1 Early Mobilisation
- •5.9.2 Nutrition and Anabolic Agents
- •Bibliography
- •6.1 Introduction
- •6.2 Initial and Early Hospital Phase
- •6.2.1 Blood Pressure
- •6.2.1.1 Resuscitation
- •6.2.1.2 Albumin
- •6.2.1.3 Transfusion
- •6.2.1.4 Vasopressors
- •6.2.2 Urine Output
- •6.2.4 Respiration
- •6.2.4.1 Ventilation Settings
- •6.2.5 Inhalation Injury
- •6.2.6 Invasive and Noninvasive Thermodilution Catheter (PiCCO Catheter)
- •6.2.7 Serum Organ Markers
- •6.3 Later Hospital Phase
- •6.3.1 Central Nervous System
- •6.3.1.1 Intensive Care Unit-Acquired Weakness
- •6.3.1.2 Thermal Regulation
- •6.3.2 Heart
- •6.3.3 Lung
- •6.3.3.1 Ventilator-Associated Pneumonia
- •6.3.4 Liver/GI
- •6.3.4.1 GI Complications/GI Prophylaxis/Enteral Nutrition
- •6.3.4.2 Micronutrients and Antioxidants
- •6.3.5 Renal
- •6.3.6 Hormonal (Thyroid, Adrenal, Gonadal)
- •6.3.7 Electrolyte Disorders
- •6.3.7.1 Sodium
- •6.3.7.2 Chloride
- •6.3.7.3 Phosphate and Magnesium
- •6.3.7.4 Calcium
- •6.3.8 Bone Demineralization and Osteoporosis
- •6.3.9 Coagulation and Thrombosis Prophylaxis
- •Conclusion
- •References
- •7.1 Introduction
- •7.2.1 Glucose Metabolism
- •7.2.2 Fat Metabolism
- •7.2.3 Protein Metabolism
- •7.3 Attenuation of the Hypermetabolic Response
- •7.3.1.1 Nutrition
- •Nutritional Route
- •Initiation of Nutrition
- •Amount of Nutrition
- •Composition of Nutrition (Table 7.1)
- •7.3.1.2 Early Excision
- •7.3.1.3 Environmental Support
- •7.3.1.4 Exercise and Adjunctive Measures
- •7.3.2 Pharmacologic Modalities
- •7.3.2.1 Recombinant Human Growth Hormone
- •7.3.2.2 Insulin-Like Growth Factor
- •7.3.2.3 Oxandrolone
- •7.3.2.4 Propranolol
- •7.3.2.5 Insulin
- •7.3.2.6 Metformin
- •7.3.2.7 Other Options
- •7.4 Summary and Conclusion
- •References
- •8.1 Introduction
- •8.2 Knowledge Base
- •8.2.1.1 Incidence
- •8.3 Aetiology and Risk Factors
- •8.3.1 Pathophysiology
- •8.3.1.1 Severity Factors
- •Box 8.1. Burn Severity Factors
- •8.3.2 Local Damage
- •8.3.3 Fluid and Electrolyte Shifts
- •8.4 Cardiovascular, Gastrointestinal and Renal System Manifestations
- •8.4.1 Types of Burn Injuries
- •8.4.1.1 Clinical Manifestations
- •Box 8.2. Primary Survey Assessment
- •Box 8.3. Signs and Symptoms of Hypovolemic Shock
- •Box 8.4. Physical Findings of Inhalation Injury
- •Box 8.5. Signs and Symptoms of Vascular Compromise
- •Box 8.6. Secondary Survey Assessment
- •8.5 Clinical Management
- •8.5.1 Nonsurgical Care
- •Box 8.7. Secondary Survey Highlights
- •Box 8.8. First Aid Management at the Scene
- •Box 8.9. Treatment of the Severely Burned Patient on Admission
- •Box 8.10. Fluid Resuscitation Using the Parkland (Baxter) Formula
- •Box 8.11. Properties of Topical Antimicrobial Agents
- •Box 8.12. Criteria for Burn Wound Coverings
- •8.5.2 Surgical Care
- •8.5.3 Pharmacological Support
- •8.5.4 Psychosocial Support
- •References
- •9.1 Electrical Injuries
- •9.1.1 Introduction
- •9.1.2 Diagnosis and Management
- •9.2 Chemical Burns
- •9.3 Cold Injury (Frostbite)
- •References
- •10.1 Introduction
- •10.2 Pathophysiology
- •10.3 Scarring
- •10.4 Therapy
- •10.5 Psychological Aspects
- •10.6 Return to Work
- •10.8 Exercise
- •10.9 Summary
- •References
- •11: Burn Reconstruction Techniques
- •11.1 From the Reconstructive Ladder to the Reconstructive Elevator
- •11.2 The Reconstructive Clockwork
- •11.2.1 General Principles
- •11.3 Indication and Timing of Surgical Intervention
- •11.4 The Techniques of Reconstruction
- •11.4.1 Excision Techniques
- •11.4.1.1 W-Plasty and Geometric Broken Line Closure
- •11.4.2 Serial Excision and Tissue Expansion
- •11.4.3 Skin Grafting Techniques
- •11.4.4 Local Skin Flaps
- •11.4.4.1 Z-Plasty
- •11.4.4.2 Double Opposing Z-Plasty
- •11.4.4.3 ¾ Z-plasty or half-Z
- •11.4.4.4 Musculocutaneous (MC) or Fasciocutaneous (FC) Flap Technique
- •11.4.5 Distant Flaps
- •11.4.5.1 Free Tissue Transfer
- •11.4.5.2 Perforator Flaps
- •11.4.6 Composite Tissue Allotransplantation
- •11.4.7 Regeneration: Tissue Engineering
- •11.4.8 Robotics/Prosthesis
- •11.5 Summary
- •References
- •Appendix
- •Sedatives and Pain Medications
- •Index
6 Critical Care of Burn Victims Including Inhalation Injury |
71 |
|
|
6.2.1.3 Transfusion
Transfusion guidelines are currently being investigated and most like changed. The gold standard of 100 mg/dl has been questioned, and a large multicenter trial is ongoing and investigates transfusion thresholds 70 vs. 100 mg/dl. Our practice is to target a level of least 70 mg/dl, but if a patient is premorbid with impaired cardiac function or poor oxygen delivery, we consider reaching hemoglobin levels of 80Ð90 mg/dl.
6.2.1.4 Vasopressors
Vasopressors or inotropes can be used if indicated. Usually during the Þrst 8Ð12 h, vasopressors should be avoided as vasoconstriction can have adverse effects. However, dobutamine as an inotrope can improve cardiac function if CO or CI is low (<3 l/min/m2). Classical vasopressors epinephrine and norepinephrine should be used with caution. Vasopressin is becoming a possibility that is currently studied in various trials. In the critical care population, vasopressin did not improve outcome compared to catecholamines. In addition, there are case reports that have no beneÞt with vasopressin but with an increased incidence of adverse effects, which is usually associated with high doses of vasopressin (>2.4 IU). However, it appears that doses between 1.2 and 2.4 IU are relatively safe and can improve the blood pressure. Our center usually uses vasopressin as a second-line agent. Dopamine, another inotropic agent, is used by some but generally is not widely used for burns.
6.2.2Urine Output
Urinary output in the acute phase of a burn is indicative of adequate organ perfusion, and the suggested target is 0.5Ð1 cc/kg/h. In children, UOP is targeted to 1 cc/ kg/h. However, UOP is not always adequate and can be affected by the burn itself, infusion of antioxidants during resuscitation, and central or peripheral renal insufÞciency.
6.2.3CVP
CVP is a rough marker for preload and hence Þlling of the patient. Of importance is that CVP should be measured correctly at the level of the heart with a subclavian or jugular line in place. The range of an adequate CVP in burned adults is 4Ð8 mmHg, which is 2Ð6 mmHg in burned children.
6.2.4Respiration
Respiratory rate, respiratory effort, breath sounds, and skin color reßect oxygenation and provide objective measurements of breathing. A respiratory rate of less than 10 or greater than 60 is a sign of impending respiratory failure. Use of accessory
72 |
M.G. Jeschke |
|
|
Table 6.2 Indication for intubation [2, 4] |
|
Criteria |
Value |
PaO2 (mmHg) |
<60 |
PaCO2 (mmHg) |
>50 (acutely) |
P/F ratio |
<200 |
Respiratory/ventilatory failure |
Impending |
|
|
Upper airway edema |
Severe |
Severe facial burn |
|
Burns over 40 % TBSA |
|
|
|
Clinical signs of severe inhalation injury |
|
|
|
muscles, manifested by supraclavicular, intercostal, subcostal, or sternal retractions, and the presence of grunting or nasal ßaring are signs of increased work of breathing. Auscultation of breath sounds provides a clinical determination of tidal volume. Skin color deteriorates from pink to pale, to mottled, and to blue as hypoxemia progresses. These signs must be followed throughout the primary survey to avoid respiratory failure. Patients with probable respiratory failure should receive rapid, aggressive, and deÞnitive airway management (Tables 6.2 and 6.3).
Oral intubation with the largest appropriate endotracheal tube is the preferred method for obtaining airway access and should be accomplished early if impending respiratory failure or ventilatory obstruction is anticipated.
Oxygen saturation in the initial phase but also during the later phase of hospitalization should be over 85Ð90. Respiratory should be 8Ð20 in adults and 14Ð38 in children.
Effective gas exchange should be determined in an arterial blood gas analysis. Targets for good oxygenation as well as organ perfusion are those with pH >7.25.
6.2.4.1 Ventilation Settings
The different modes of ventilation including high-frequency oscillation are all being investigated and tested. Detailed descriptions of the different modes are beyond the scope of this handbook. In short, PEEP is useful in supporting oxygenation. The level of PEEP required should be established by empirical trials and reevaluated on a regular basis. PEEP levels should start at 5 cmH2O and be increased in 2Ð3 cm increments. PEEP trials should be done to optimize oxygenation and cardiac output. The effectiveness of continuous positive airway pressure (CPAP) or PEEP is related to surface tension abnormalities and the marked tendency for atelectasis in these patients. Pressure control ventilation with permissive hypercapnia is the current preferred method of treatment for ventilated patients. If pulmonary edema continues, the amount of PEEP and of oxygen should be elevated so as to maintain adequate gas exchange. The use of high-frequency oscillating ventilators in the pressure control mode may also result in better removal of airway debris. Low tidal volumes (5Ð8 ml/ kg) with PEEP may be needed to improve oxygenation. Peak ßow rates should be adjusted as needed to satisfy patient inspiratory demands. For inspiratory/expiratory (I:E) ratio, the inspiratory time should be long enough to deliver the tidal volume at