- •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
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M.G. Jeschke |
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6.3.1Central Nervous System
Anoxic brain injury used to be the leading cause of death in burn patients, which has been replaced by sepsis and MOF [7]. Adequate resuscitation and early intubation improved mortality in burn patient [12, 14]. However, neurological disturbances are commonly observed in burned patients. The possibility of cerebral edema and raised intracranial pressure must be considered during the early ßuid resuscitation phase, especially in the case of associated brain injury or high-voltage electrical injury. Inhalation of neurotoxic chemicals, of carbon monoxide, or of hypoxic encephalopathy may adversely affect the central nervous system as well as arterial hypertension [14, 21, 22, 24]. Other factors include hypo-/hypernatremia, hypovolemic shock, sepsis, antibiotic overdosage (e.g., penicillin), and possible oversedation or withdrawal effects of sedative drugs. If increased intracranial pressure is suspected, neurosurgery needs to consulted and most likely bolt are place and therapy initiated to decreased intracranial pressure.
In general, severe burn injury is associated with nonspeciÞc atrophy of the brain that normally resolves over time. No intervention is needed.
Pain and anxiety will generally require rather large doses of opioids and sedatives (benzodiazepines mainly). Continuous infusion regimens will generally be successful in maintaining pain within acceptable ranges. Sedatives and analgesics should be targeted to appropriate sedation and pain scales (SAS or VAS scores four appear optimal), thus preventing the sequelae associated with oversedation and opioid creep, namely, ßuid creep and effects on the central and peripheral cardiovascular system [18]. Therefore, consideration should be given to the use of NMDA receptor antagonist, such as ketamine or gabapentin, who have important opioid-sparing effects to decrease the need for opioids and benzodiazepines [2, 4]. We Þnd multimodal pain management combining a long-acting opioid for background pain, a short-acting opioid for procedures, an anxiolytic, an NSAID, acetaminophen, and gabapentin for neuropathic pain control [2, 4] used at our institution targeted to SAS (sedation score) and VAS (visual analog scale) scores provides adequate analgesia and sedation.
6.3.1.1 Intensive Care Unit-Acquired Weakness
Survival and organ function have been the main outcome measures for burn patients; however, recently long-term outcomes move into the focus of burn care providers. A signiÞcant component of long-term outcomes include the peripheral nervous system and muscular system which manifest as neuromyopathy. The importance of positioning and prevention of peripheral nerve compression is well known and ingrained in the daily practices of most critical care units. The main risk factors for neuropathy include multiple organ failure, muscular inactivity, hyperglycemia, use of corticosteroids, and neuromuscular blockers. In a recent publication by de Jonghe and Bos [29], early identiÞcation and treatment of conditions leading to multiple organ failure, especially sepsis and septic shock, avoiding unnecessary deep sedation and excessive hyperglycemia, promoting early mobilization, and weighing the risk and beneÞts of corticosteroids might reduce the incidence and severity of ICUacquired weakness.