- •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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The risk of deep venous thrombosis and of pulmonary embolism is at least as high as in any other surgical condition. In our experience, 13 % of patients develop some form of thrombotic complication. SpeciÞc risk factors include central venous lines, prolonged bed rest, and an intense inßammatory state. Prophylaxis should be started from admission. Interruptions for surgery should be reduced to minimum and discussed with the surgical team.
Conclusion
The management of the critically ill thermally injured patient can be very complex. The treatment modalities can remain at times controversial, as there is a lack of high-level evidence. There have been many advances in the Þeld of the critical care of the thermally injured patient, which would beneÞt from largescale multicenter trials. This brief chapter highlights few of the important nuances in the care of these patients and places emphasis on the need for intricate support for the all organ systems in order to improve morbidity and mortality.
References
1. WHO (2002) A graphical overview of the global burden of injuries. The injury chart book, vol 29. WHO, Geneva
2. Herndon DN (2007) Treatment of infection in burns. In: Herndon DN (ed) Total burn care, 3rd edn. Saunders Elsevier, Philadelphia
3. Herndon DN, Tompkins RG (2004) Support of the metabolic response to burn injury. Lancet 363(9424):1895Ð1902
4. Jeschke MG et al (2012) Handbook of burns, vol 1. Springer, Wien New York
5. Kraft R et al (2012) Burn size and survival probability in paediatric patients in modern burn care: a prospective observational cohort study. Lancet 379(9820):1013Ð1021
6. Jeschke MG et al (2008) Pathophysiologic response to severe burn injury. Ann Surg 248(3):387Ð401
7. Williams FN et al (2009) The leading causes of death after burn injury in a single pediatric burn center. Crit Care 13(6):R183
8. Barrow RE, Jeschke MG, Herndon DN (2000) Early ßuid resuscitation improves outcomes in severely burned children. Resuscitation 45(2):91Ð96
9. Greenhalgh DG (2007) Burn resuscitation. J Burn Care Res 28(4):555Ð565
10. Greenhalgh DG (2010) Burn resuscitation: the results of the ISBI/ABA survey. Burns 36(2):176Ð182
11. Kraft R et al. (2012) Optimized ßuid management improves outcomes of pediatric burn patients. J Surg Res 2012 June 6 Epub Þrst
12. Wolf SE et al (1997) Mortality determinants in massive pediatric burns. An analysis of 103 children with > or = 80 % TBSA burns (> or = 70 % full-thickness). Ann Surg 225(5):554Ð565; discussion 565Ð569
13. Greenhalgh DG et al (2007) American Burn Association consensus conference to deÞne sepsis and infection in burns. J Burn Care Res 28(6):776Ð790
14. Latenser BA (2009) Critical care of the burn patient: the Þrst 48 hours. Crit Care Med 37(10):2819Ð2826
15. Pham TN, Cancio LC, Gibran NS (2008) American Burn Association practice guidelines burn shock resuscitation. J Burn Care Res 29(1):257Ð266
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16. Klein MB et al (2007) The association between ßuid administration and outcome following major burn: a multicenter study. Ann Surg 245(4):622Ð628
17. Rivers E et al (2001) Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 345:1368Ð1377
18. Safße JI (2007) The phenomenon of Òßuid creepÓ in acute burn resuscitation. J Burn Care Res 28(3):382Ð395
19. Ivy ME et al (2000) Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma 49(3):387Ð391
20. Faraklas I et al (2011) Colloid normalizes resuscitation ratio in pediatric burns. J Burn Care Res 32(1):91Ð97
21. Palmieri TL et al (2009) Inhalation injury in children: a 10 year experience at Shriners Hospitals for Children. J Burn Care Res 30(1):206Ð208
22. Sheridan RL, Hess D (2009) Inhaled nitric oxide in inhalation injury. J Burn Care Res 30(1):162Ð164
23. Endorf FW, Gamelli RL (2007) Inhalation injury, pulmonary perturbations, and ßuid resuscitation. J Burn Care Res 28(1):80Ð83
24. Erdman AR (2007) Is hydroxocobalamin safe and effective for smoke inhalation? Searching for guidance in the haze. Ann Emerg Med 49(6):814Ð816
25. Finnerty CC, Herndon DN, Jeschke MG (2007) Inhalation injury in severely burned children does not augment the systemic inßammatory response. Crit Care 11(1):R22
26. Barrow RE et al (2005) Mortality related to gender, age, sepsis, and ethnicity in severely burned children. Shock 23(6):485Ð487
27. Branski LK et al (2011) Transpulmonary thermodilution for hemodynamic measurements in severely burned children. Crit Care 15(2):R118
28. Kuntscher MV et al (2002) Transcardiopulmonary vs pulmonary arterial thermodilution methods for hemodynamic monitoring of burned patients. J Burn Care Rehabil 23(1):21Ð26
29. de Jonge E, Bos MM (2009) Patients with cancer on the ICU: the times they are changing. Crit Care 13(2):122
30. Gore DC et al (2003) Inßuence of fever on the hypermetabolic response in burn-injured children. Arch Surg 138(2):169Ð174; discussion 174
31. Hogan BK et al (2012) Correlation of American Burn Association sepsis criteria with the presence of bacteremia in burned patients admitted to the intensive care unit. J Burn Care Res 33(3):371Ð378
32. Murray CK et al (2007) Evaluation of white blood cell count, neutrophil percentage, and elevated temperature as predictors of bloodstream infection in burn patients. Arch Surg 142(7):639Ð642
33. Mosier MJ et al (2011) Early enteral nutrition in burns: compliance with guidelines and associated outcomes in a multicenter study. J Burn Care Res 32(1):104Ð109
34. Williams FN et al (2009) Modulation of the hypermetabolic response to trauma: temperature, nutrition, and drugs. J Am Coll Surg 208(4):489Ð502
35. Pereira C, Murphy K, Herndon D (2004) Outcome measures in burn care. Is mortality dead? Burns 30(8):761Ð771
36. Pereira CT et al (2006) Age-dependent differences in survival after severe burns: a unicentric review of 1,674 patients and 179 autopsies over 15 years. J Am Coll Surg 202(3):536Ð548
37. Jeschke MG et al (2011) Long-term persistance of the pathophysiologic response to severe burn injury. PLoS One 6(7):e21245
38. Jeschke MG (2009) The hepatic response to thermal injury: is the liver important for postburn outcomes? Mol Med 15(9Ð10):337Ð351
39. Price LA et al (2007) Liver disease in burn injury: evidence from a national sample of 31,338 adult patients. J Burns Wounds 7:e1
40. Jeschke MG et al (2011) Insulin protects against hepatic damage postburn. Mol Med 17(5Ð6):516Ð522
41. Gauglitz GG et al (2010) Post-burn hepatic insulin resistance is associated with endoplasmic reticulum (ER) stress. Shock 33(3):299Ð305
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42. Song J et al (2009) Severe burn-induced endoplasmic reticulum stress and hepatic damage in mice. Mol Med 15(9Ð10):316Ð320
43. Jeschke MG et al (2009) Calcium and Er stress mediate hepatic apoptosis after burn injury. J Cell Mol Med 13:1857Ð1865
44. Jeschke MG, Mlcak RP, Herndon DN (2007) Morphologic changes of the liver after a severe thermal injury. Shock 28(2):172Ð177
45. Jeschke MG et al (2007) Changes in liver function and size after a severe thermal injury. Shock 28(2):172Ð177
46. Ivy ME et al (1999) Abdominal compartment syndrome in patients with burns. J Burn Care Rehabil 20(5):351Ð353
47. Baxter CR (1987) Metabolism and nutrition in burned patients. Compr Ther 13(1):36Ð42 48. Medlin S (2012) Nutrition for wound healing. Br J Nurs 21(12):S11ÐS12, S14Ð15
49. Kremer T et al (2010) High-dose vitamin C treatment reduces capillary leakage after burn plasma transfer in rats. J Burn Care Res 31(3):470Ð479
50.Tanaka H et al (2000) Reduction of resuscitation ßuid volumes in severely burned patients using ascorbic acid administration: a randomized, prospective study. Arch Surg 135(3):326Ð331
51. Chrysopoulo MT et al (1999) Acute renal dysfunction in severely burned adults. J Trauma 46(1):141Ð144
52. Jeschke MG et al (1998) Mortality in burned children with acute renal failure. Arch Surg 133(7):752Ð756
53. Kallinen O et al (2012) Multiple organ failure as a cause of death in patients with severe burns. J Burn Care Res 33(2):206Ð211
54. Holm C et al (1999) Acute renal failure in severely burned patients. Burns 25(2):171Ð178 55. Przkora R et al (2006) Body composition changes with time in pediatric burn patients.
J Trauma 60(5):968Ð971; discussion 971
56. Przkora R, Herndon DN, Suman OE (2007) The effects of oxandrolone and exercise on muscle mass and function in children with severe burns. Pediatrics 119(1):e109Ðe116
57. Jeschke MG et al (2005) Endogenous anabolic hormones and hypermetabolism: effect of trauma and gender differences. Ann Surg 241(5):759Ð767; discussion 767Ð768
58. Jeschke MG et al (2008) Gender differences in pediatric burn patients: does it make a difference? Ann Surg 248(1):126Ð136
59. Przkora R et al (2006) BeneÞcial effects of extended growth hormone treatment after hospital discharge in pediatric burn patients. Ann Surg 243(6):796Ð801; discussion 801Ð803
Nutrition of the Burned Patient |
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and Treatment of the Hypermetabolic |
Response
Marc G. Jeschke
7.1Introduction
Advances in therapy strategies, based on improved understanding of resuscitation, enhanced wound coverage, more appropriate infection control, and improved treatment of inhalation injury, improved the clinical outcome of burn patients over the past years [1, 2]. However, severe burns remain a devastating injury affecting nearly every organ system and leading to significant morbidity and mortality [2]. One of the main contributors to adverse outcome of this patient population is the profound stress-induced hypermetabolic response, associated with severe alteration in glucose, lipid, and amino acid metabolism [1, 3–5] (Fig. 7.1).
M.G. Jeschke, MD, PhD, FACS, FCCM, FRCS(C)
Division of Plastic Surgery, Department of Surgery and Immunology, Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Sunnybrook Research Institute, University of Toronto,
Rm D704, Bayview Ave. 2075, M4N 3M5, Toronto, ON, Canada e-mail: marc.jeschke@sunnybrook.ca
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Fig. 7.1 Complexity of the post-burn hypermetabolic response. From Williams FN JACS 2009 April 208(4):489–502
7.2Post-Burn Hypermetabolism
A hallmark for severely burned patients is the hypermetabolic response that is not only very profound but also extremely complex and most likely induced by stress and inflammation [1, 3–5]. The cause of this response is not entirely defined, but it has been suggested that sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion are involved in initiating the cascade of events leading to the acute hypermetabolic response with its ensuing catabolic state [6–15]. In addition, cytokines, endotoxin, neutrophil-adherence complexes, reactive oxygen species, nitric oxide, and coagulation as well as complement cascades have also been implicated in regulating this response to burn injury [16]. Once these cascades are initiated, their mediators and by-products appear to stimulate the persistent and increased metabolic rate associated with altered glucose, lipid, and amino acid metabolism seen after severe burn injury [17] (Fig. 7.1).
The metabolic changes post-burn occur in two distinct patterns of metabolic regulation following injury [18]:
1.The first phase occurs within the first 48 h of injury and has classically been called the “ebb phase” [18, 19], characterized by decreases in cardiac output,