- •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
Acute Burn Surgery |
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Lars-Peter Kamolz |
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5.1Introduction
During the past decades, burn care has improved to the extent that persons with burns can frequently survive (Fig. 5.1). The trend in current burn care extends beyond the preservation of life; the ultimate goal is the return of burn victims, as full participants, back into their families and communities.
5.2Burn Wound Evaluation
One of the major problems that face any burn surgeon is the decision on the nature of treatment (conservative treatment versus operative treatment). In the case of an operative procedure, a decision is needed on when and how to excise the burn wounds and to determine accurately the depth of the lesion and thereby the extent of tissue involvement.
5.3Escharotomy/Fasciotomy
One of the most important indications for an immediate surgical intervention is the presence of a compartment syndrome. Circumferential burns have a high risk to develop compartment syndrome. Compartment syndrome can occur in circumferential upper and lower extremity burns, but escharotomy may be necessary also to relieve chest wall restriction in order to improve ventilation.
L.-P. Kamolz, MD, PhD, MSc
Division of Plastic, Aesthetic and Reconstructive Surgery, Department of Surgery, Medical University of Graz, Auenbruggerplatz 29, 8036 Graz, Austria
e-mail: lars.kamolz@medunigraz.at
M.G. Jeschke et al. (eds.), Burn Care and Treatment, |
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DOI 10.1007/978-3-7091-1133-8_5, © Springer-Verlag Wien 2013 |
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L.-P. Kamolz |
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100 |
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90 |
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Survival Rate |
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Nutrition |
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80 |
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70 |
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Early Debridement |
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60 |
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Burn Centers |
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Skin Substitutes |
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50 |
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Cultured Skin/ Keratinocytes |
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Wound Management |
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40 |
Fluid Management |
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30 |
Antibiotics |
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20 |
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10 |
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Fig. 5.1 Factors which had major impact on survival. The 50 % survival rate has increased from 35 % TBSA to 80 % TBSA within the past decades
5.4Surgical Burn Wound Management
The main goal of surgical treatment is the replacement of necrotic tissue. One of the main problems encountered in extensively burned patients >60 % total body surface area (TBSA) is the scarcity of harvesting areas for autologous skin grafts.
Superficial dermal burns will heal without operation within 2–3 weeks, but deep dermal and full-thickness burn will require operation. It is widely accepted that if skin does not regenerate within 3 weeks, morbidity and scarring will be severe, so the trend in the treatment of deep dermal and full-thickness burns leans toward very early excision and grafting in order to reduce the risk of infection, decrease scar formation, shorten hospital stay and thereby reduce costs.
Excision of as much of the necrotic tissue as possible should be carried out whenever a patient is hemodynamically stable and the risks of the operation would not increase the mortality that would be expected from the traditional treatment. In patients with associated injuries such as inhalation injury, patients of extreme age, or patients with cardiac problems, special surgical treatment is required in deciding when and how much to excise.
Sequential layered tangential excision to viable bleeding points, even to fat, while minimising the loss of viable tissue, is the generally accepted technique.
5 Acute Burn Surgery |
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Fig. 5.2 Mixed dermal burn—tangential excision of the deeper parts and coverage with Suprathel®, late results
Excision of burn wounds to the fascia is reserved for large burns where the risks of massive blood loss and the possibility of skin slough from less vascularised grafts on fat may lead to higher mortality.
We start to excise all deep dermal and full-thickness burned areas within 72 h of injury. It has become apparent that early excision is better than late excision, because after 7 days the incidence of sepsis and graft failure increases:
In case of deep dermal injuries, after tangential excision the resulting defects can be covered with keratinocytes, autologous or allogeneic skin grafts or by use of synthetic materials like Suprathel® (Fig. 5.2).
In case of full-thickness burns, we dominantly use autografts to cover the wounds if there are sufficient available donor sites. In large burns we normally use expanded autografts (mesh or Meek).
Expansion rates of graft to wound area cover ranges from 1: 1 to 1: 9. Expansion rates higher than 1: 3 heal in a suboptimal manner leading to contractures and unstable scars. Therefore, we like to combine these large meshed autografts in combination with allografts (Fig. 5.3) or keratinocytes (sandwich technique), or we will use the Meek technique (Fig. 5.4). In functional important regions like hands and over joints, a combined reconstruction of skin by use of a dermal matrix (Integra®, Matriderm®), and split-thickness skin graft seems to be superior to skin grafts alone (Fig. 5.5).
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L.-P. Kamolz |
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Fig. 5.3 “Sandwich technique”: widely expanded autografts in combination with less expanded allografts
Fig. 5.4 Direct comparison of mesh and Meek grafted area
Donor sites for autografts in smaller burns, less than 40 % total body surface area, are seldom a problem unless the patient is at risk of surgical complication resulting from age, cardiopulmonary problems, or coagulopathy. Patients with greater burns have a lack of available donor sites. Therefore, we use cadaver skin