- •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
152 |
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S. Shahrokhi |
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Table 9.4 Classes of chemicals and their mechanisms of tissue injury |
||
Class of chemical |
|
Mechanism of tissue injury |
Acid |
|
Coagulation necrosis |
Alkali |
|
Liquefaction necrosis – deeper penetration and more severe burns |
|
|
|
Organic solutions |
|
Dissolve lipid membranes |
Inorganic solutions |
Direct binding and salt formation |
|
Table 9.5 Management principles for chemical burns |
||
Removal of |
Removal of involved clothing |
|
chemical agent |
Thorough and copious irrigation with water except for: |
|
|
|
Phenol – wipe off with 50 % polyethylene glycol sponges [34] |
|
|
Dry lime – dust off prior to lavage [35, 36] |
|
|
Muriatic acid, sulfuric acid – neutralize with soap or lime water [35, 36] |
Systemic |
HF acid – hypocalcemia and ventricular fibrillation [37] |
|
toxicity |
Formic acid – intravascular hemolysis, renal failure, pancreatitis [38] |
|
|
Organic solutions and hydrocarbures – liver failure [30] |
|
|
Respiratory injury – can occur with all inhaled agents and must be treated in |
|
|
same manner as inhalation injury [30] |
|
Antidotes |
Hydrofluoric acid – inject 10 % calcium gluconate sub-eschar |
|
|
White phosphorus – lavage with 1–2 % copper sulfate |
|
|
|
|
Wound care |
Wound dressing as for thermal burns |
|
|
Early excision of nonviable tissue |
Ophthalmology consult for ocular involvement [39, 40] in addition to copious irrigation
9.3Cold Injury (Frostbite)
Frostbite is part of the spectrum of localized cold injury, which is associated with the greatest amount of tissue destruction. The mechanisms proposed for tissue injury are:
•Cellular death secondary to cold exposure [41, 42, 45]
•Progressive dermal ischemia [41, 42]
The clinical manifestations of frostbite are as a result of thrombotic events
secondary to ischemia/reperfusion injury [41–44] and are classified into four degrees:
•First degree – anesthetic central white plaque with peripheral erythema
•Second degree – blisters surrounded by erythema and edema
•Third degree – hemorrhagic blisters followed by eschar
•Fourth degree – necrosis and tissue loss
• The common risk factors associated with development of frostbite are [41, 42, 49]:
•Mental illness
•Alcohol/drug intoxication
•Extreme of age