BURNS. Dr Vandewiele Bert Fellow Critical Care

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Dorcas Chambers
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1 BURNS Dr Vandewiele Bert Fellow Critical Care

4 Burns I. Pathophysiology II. Management III. Fluid Creep IV. Ascorbic Acid V. Haemoglobinurea/myoglobinurea VI. Immunonutrition

5 I Pathophysiology Local effects Systemic effects Pharmacological effects Weird? burns

6 Pathophysiology: Local effects Degrees of burns First, second, third degree Partial or full thickness Jacksons zones Coagulation / stasis / Hyperaemia Oedema formation Timing Mechanism

7 Degree? First-degree (superficial) burn affect only the epidermis, or outer layer of skin. The burn site is red, painful, dry, and with no blisters. Second-degree (partial thickness) burns involve the epidermis and part of the dermis layer of skin. The burn site appears red, blistered, and may be swollen and painful. Third-degree (full thickness) burns destroy the epidermis and dermis, may also damage the underlying bones, muscles, and tendons. When bones, muscles, or tendons are also burned, this may be referred to as a fourth-degree burn. The burn site appears white or charred. There is no sensation in the area since the nerve endings are destroyed.

8 Degree? Partial thickness Variable and incomplete dermal necrosis Reepithelialise Full thickness All dermal elements are destroyed Skin grafts

Jackson s burns zones BMJ. 2004 Jun 12;328(7453):1427-9.

9 Jackson s burns zones BMJ Jun 12;328(7453): ABC of burns: pathophysiology and types of burns. Hettiaratchy S, Dziewulski P.

10 Jackson s zones Zone of Coagulation/necrosis Irreversible tissue loss due to coagulation of proteins Zone of stasis Decreased tissue perfusion due to Microthrombus formation Neutrophil adherence Fibrin deposition Endothelial swelling Salvageable Proper resuscitation Prevent additional insults Zone of hyperaemia Histamine release by mast cells Recover expected unless there is severe sepsis or prolonged hypoperfusion

11 Oedema formation: Timing Greatest in the first 6 hours Continues to a lesser extend for the first 24 hours post burns By 24 hours oedema formation is largely complete and vascular integrity restored.

Oedema formation: Mechanism Postcapillary venular constriction leads to an increased capillary hydrostatic pressure Negative interstitial

12 Oedema formation: Mechanism Postcapillary venular constriction leads to an increased capillary hydrostatic pressure Negative interstitial fluid hydrostatic pressure Increase in the interstitial fluid colloid oncotic pressure Decrease in the colloid oncotic capillary pressure

13 Oedema formation: Mechanism We discussed the physical characteristics of burn tissue Increase in microvascular permeability locally Humoral factors Histamine, activated proteases, prostaglandines, leukotrienes, fibrin degradation products, substance P Leukocyte activation results in cytokine production Products generated following thermal injury Lysosomal enzymes, increased xanthine oxidase activity, oxygen radicals, products of compliment activation Increased albumin flux over the endothelium due to IL-2 activated human killer lymphocytes? Generalised oedema (we get back to that)

14 Pathophysiology Local effects Degrees of burns First, second, third degree Partial or full thickness Jacksons zones Coagulation / stasis / Hyperemia Oedema formation Timing Mechanism Systemic effects: Pharmacological effects

15 Pathophysiology: Systemic effects Cardiovascular system Lungs Kidneys Gastro-intestinal tract Liver Nervous system Endocrine system Hematopoietic System Hypermetabolic state

16 Pathophysiology: Systemic effects Cardiovascular system Lungs Kidneys Gastro-intestinal tract Liver Nervous system Endocrine system Hematopoietic System Hypermetabolic state

Cardiovascular system Significant if burns over 15 % TBSA Changes Extend burn injury Immediately following injury Reduced cardiac output Myocardial depressant agents (TNF-α, IL-1) Hypovolemia

17 Cardiovascular system Significant if burns over 15 % TBSA Changes Extend burn injury Immediately following injury Reduced cardiac output Myocardial depressant agents (TNF-α, IL-1) Hypovolemia Increased blood viscosity Increased systemic and pulmonary vascular resistance Adrenaline, noradrenalin, vasopressin and angiotensin Second post burn day Recovery of cardiac output Day 3 Supranormal levels of cardiac output hypermetabolic respons

18 Lungs Increased minute volume Increase RR Increase TV Increased pulmonary vascular resistance (protective during fluid resuscitation) Chest wall Oedema Burn eschar s Pulmonary oedema due to overzealous resuscitation ARDS

filtration rate After succesfull resuscitation

19 Kidneys Parallel with cardiovascular respons Immediate postburn Reduced renal bloodflow and glomerular filtration rate After succesfull resuscitation Increased renal bloodflow Myoglobinemia + acute renal failure (see later)

Gastro-intestinal system Burns > 25% TBSA Ileus Recovery after day 3-5 Focal ischemic mucosal lesions Stomach / duodenum After 3 5 hours Intestinal bacterial translocation Burns > 50 % TBSA Increase

20 Gastro-intestinal system Burns > 25% TBSA Ileus Recovery after day 3-5 Focal ischemic mucosal lesions Stomach / duodenum After 3 5 hours Intestinal bacterial translocation Burns > 50 % TBSA Increase hepatic aminotransferase Decreased cardiac output Increased blood viscosity Splanchnic vasoconstriction Hepatic dysfunction in later stadium Hyperbilirubinemia + cholestatic pattern Associated with sepsis and MOF

Nervous system Non specific changes due to neurohumoral stress response and ICU isolation Anxiety Disorientation Specific neurologic changes High

21 Nervous system Non specific changes due to neurohumoral stress response and ICU isolation Anxiety Disorientation Specific neurologic changes High voltage electrical injury Mechanical trauma Changes in neurological condition Hypoxemia Electrolyte disturbances Sepsis Toxic effects of medication

22 Endocrine system Catabolic state Increase Catecholamines Cortisol Glucagon Decrease Insuline Triiodothyronine Negative nitrogen balance

23 Hematopoietic System Red cell mass declines Heat coagulation Microvascular thrombosis Repeated blood sampling No proven role for repo Platelets Initially depressed After resuscitation increase to supranormal levels

24 Hypermetabolic state Timing Start: around the third post-burn day End: Until the wounds are substantially healed What: manifestation of SIRS Why Evaporative and radiant heat loss Pain Fear, anxiety Bacterial colonization

25 Pathophysiology Local effects Systemic effects: Degrees of burns Cardiovascular system First, second, third degree Partial or full thickness Jacksons zones Coagulation / stasis / Hyperemia Oedema formation Timing Mechanism Pharmacological effects Lungs Kidneys Gastro-intestinal tract Liver Nervous system Endocrine system Hematopoietic System Hypermetabolic state

26 Pharmacological effects: PK and PD Cardiac output (depressed / augmented) Renal function CO Renal failure due to ATN / myoglobinaemia albumin levels low protein bound drugs Α1-glycoprotein high (Fentanyl) Cytochrome P-450 depressed Increase in peri-junctional acetylcholine receptors Burn wound is a significant route of drug absorption Deafness due to topical gentamycin

27 Weird burns? Inhalation burns - may increase resuscitation fluid requirements. Three types Heat injury to upper airway Effects of smoke on the respiratory system Inhalation of toxic gases Radiation burns - burns due to prolonged exposure to ultraviolet rays of the sun, or to other sources of radiation such as x-ray. Chemical burns - burns due to strong acids, alkalies, detergents, or solvents coming into contact with the skin and/or eyes. Electrical burns - burns from electrical current, either alternating current (AC) or direct current (DC).

28 II Management First Aid Assessment Fluid therapy First 24 hours After 24 hours Pain therapy Nutrition Prevention of infection

10-20 min Deliver oxygen Avoid Hypothermia Burn injury

29 First Aid Stopping the burn process ABC Removal of clothing Cooling the wound Tepid, running water for min Deliver oxygen Avoid Hypothermia Burn injury can only be assessed properly in hospital conditions so early transfer

Assessment Type of burn Scalds / Flames /

30 Assessment Type of burn Scalds / Flames / steam / chemical / radiation / electrical With / without inhalation burn Degree of burn Full / partial thickness % TBSA Conditions at the scene Patients weight Patients History Other injuries (blunt trauma)

31 Lund and Browder Chart

32 Reminders Electrical Burn Elektocardiographic monitoring Tetanus immunization

33 Fluid therapy First 24 hours Thereafter

34 Fluid therapy first 24 hours Injuries exceeding 15% - 25% of TBSA Parkland formula Lactated Ringer s 4 ml / kg / % burn BSA 50 % first 8 hours, 50 % next 16 hours Modified Brooke Lactated Ringer s 2 ml / kg / % burn BSA 50 % first 8 hours, 50 % next 16 hours Hypertonic sodium resuscitation (battlefield, congestive heartfailure) Any formula serves only as a guide!!! Baxter CR, Shires T. Physiological response to crystalloid resuscitation of severe burns. Ann N Y Acad Sci 1968;150:

35 Fluid therapy first 24 hours Who might need more Delay in starting fluid resuscitation Inhalation injury Ethanol / drug intoxication High voltage electrical injury Multiple trauma

36 Fluid therapy first 24 hours Monitoring resuscitation Hemodynamic response Heart rate Bloodpressure CVP Invasive Non-invasive PAOP Mental function Intra abdominal pressure Urine output ml/h ml/kg 1.0 ml/kg if < 30kg Lactate Base deficit Intramucosal ph I/O ratio?

37 Fluid therapy first 24 hours Overzealous resuscitation Pulmonary oedema Wound oedema Increased escharotomy Increases fasciotomy Ocular oedema Cerebral oedema Abdominal compartment syndrome

38 Fluid therapy first 24 hours: Don t panic, do it right! Hypovolemia Gradual, obligatory, predictable Avoid fluid boluses in the absence of frank shock Assess and calculate correct: just 10 % off? 80 kg, 50% burns

39 Fluid therapy after 24 hours Colloids? Parkland formula 20-60% of calculated plasma volume as colloid As necessary to maintain urinary output Modified Brooke ml/kg per % burn 30-50% burn 0.3 ml/kg per % burn 50-70% burn 0.4 ml/kg per % burn >70% burn 0.5 ml/kg per % burn As necessary to maintain urinary output

40 Fluid therapy after 24 hours Dose/hour? Maintenance = 1500 X BSA (m²)/24 + Insensible loss / hour = (25 + %BSA burned) X Total BSA (m²) Any formula serves only as a guide!!!

41 Pain therapy First 24 hours Incremental doses of IV morphine of equivalent After 24 hours Background pain (Continuous) Procedural pain (Interventions) Anxiety and depression

42 Nutrition Hypermetabolic response is roughly proportional to the extent of injury Start feeds ASAP Caloric requirement = REE + (REE x %TBSA burn/100) REE calculated from the Harris and Benedict Equation If the burns are extensive use tube feeds Postpyloric Post Treitz What about Insulin Oxandrolone (10 mg 2/d) β-blokker Wolf SE, Edelman LS, Kemalyan N. Effects of oxandrolone on outcome measures in the severely burned: a multicenter prospective randomized double-blind trial. J Burn Care Res Mar-Apr;27(2):131-9; discussion

43 Prevention of infection Bacteriological surveillance Wounds / tracheal aspirate Patient isolation Barrier nursing The gastrointestinal tract Decontamination Early enteral nutrition Wound sepsis Local effects Systemic effects Antibiotic therapy guided

44 III Fluid Creep What is it? What causes it? Can we prevent it?

45 What is fluid Creep? Recent reviews have repeatedly demonstrated that patients with major burns often require resuscitation fluids which significantly exceed Parkland formula Up to 9.36 ml / kg /%burn

46 What causes fluid creep Multiple causes What happens at the scene? The larger the burn, the less accurate Parkland formula is. Modern clinicians are careless Opioid creep The influence of goal directed therapy Influence of excessive crystalloid infusion on Starling Forces

47 Fluid Creep: Can we prevent it? 1. What happens at the scene? Restrict early fluid resuscitation 2. The larger the burn, the less accurate Parkland formula is. Except higher fluid requirements for larger size (60-80%) 3. Modern clinicians are careless Use Resuscitation protocols 4. Opioid creep 5. The influence of goal directed therapy Don t use sepsis endpoints of resuscitation for burns patients 6. Influence of excessive crystalloid infusion on Starling Forces Consider routine colloid or Colloid Rescue Cancio LC, Chávez S, Alvarado-Ortega M, et al. Predicting increased fluid requirements during the resuscitation of thermally injured patients. J Trauma Feb;56(2):404-13; discussion

48 J Burn Care Res Jan-Feb;31(1):40-7.

49 Lawrence A, Faraklas I, Watkins H, Allen A, Cochran A, Morris S, Saffle J. Colloid administration normalizes resuscitation ratio and ameliorates "fluid creep". J Burn Care Res Jan- Feb;31(1):40-7.

50 IV. Ascorbic ACID? Burns Mast Cells Release Histamin Membrane lipid peroxidation Increase in vascular permeability Xanthine oxidase activity Free radical production

51 Ascorbic Acid (=Vitamin C) Anti-oxidant properties / Free radical scavenger Reduces postburn lipid peroxidation Reduces increased vascular permeability Reduces burn and non burn tissue oedema Resulted in Smaller resuscitation fluid volumes Less wound oedema Reduction in severity of respiratory dysfunction Reduced length of mechanical ventilation

53 VC is associated with a decrease in fluid requirements and an increase in urine output during resuscitation after thermal injury. Although this study did not find a difference in outcomes with VC administration, it demonstrates that VC can be safely used without an increased risk of renal failure. The effects of VC should be further studied in a large-scale, prospective, randomized trial.

54 V Haemoglobinurea/Myoglobinurea Particularly in electrical injury due to release from damaged cells Haemoglobine Myoglobine Urine color Increase fluid administration Mannitol 12.5g/l resuscitation fluid Alkalinise of urine ph

57 VI Immunonutrition Immunonutrition Immune modulating nutrition Use of nutritiens as a part of a nutritional support strategy such as Enteral nutrition (EN) Parenteral nutrition (PN) Often containing multiple active nutrients Pharmaco nutrition Single-nutrient strategy that may confer pharmacological effects on immune respons Known dose? Known administration route? Known effects Known population

58 Immunonutrition Which/Why Studies When How much Effects Conclusions

59 Immunonutrition: Which, Why? Glutamine Arginine Conditionally essential amino acids Omega 3 fatty acids Combined immunonutrients

60 Immunonutrition: Which, Why? Glutamine Acting as a nitrogen shuttle and providing a direct source of cellular energy to assist metabolic functions. Stimulating immune function and wound healing by acting as a fuel source for lymphocytes, macrophages, and fibroblasts. Preserving gut integrity by acting as a primary fuel source for enterocytes and colonocytes within the gastrointestinal tract. Supporting antioxidant function as a precursor for glutathione. Potentially reducing insulin resistance.

61 Arginine Immunonutrition: Which, Why? Being a precursor for proline, glutamate, and polyamine synthesis. Promotion of T-lymphocyte proliferation in vitro. Stimulation of the hormones insulin, insulin-like growth factor-1, and pituitary human growth hormone. Promotion of wound healing.

62 Omega 3 fatty acids Immunonutrition: Which, Why? Found in fish oils and canola oils Eicosapentaenoic Acid (EPA) Docoshexaenoic Acid (DHA) Both metabolised to less (Than omega 6 FA) Inflammatory metabolites Immunosuppressive metabolites

63 Immunonutrition: Which, Why? Combined immunonutrients Glutamine Arginine Omega 3 fatty acids RNA nucleotides Branch Chained Amino Acids Anti-oxidants... Combination of the previous mentioned benefits

64 Immunonutrition: The studies Outcome measures need to be meaningful to clinical practice and support the economics of health care Clear evidence must exist to initiate changes in practices, and the increased financial cost must be justified in terms of fiscal benefit decreased length of stay increased rate of wound healing (reducing the amount of specialized wound dressings or labor for dressing changes).

65 Immunonutrition: The studies Glutamine Enteral 11 studies, 4 only abstract Total patients 364 (120 children with no effect + 74 only abstract) Parenteral 2 studies Total patients 56 Arginine 5 studies, 3 only abstracts Total 101 patients Omega-3 fatty acids 3 studies, 1 only abstract Total 60 patients Combined immunonutritients 6 studies Total 253 patients

70 Immunonutrition: Which, Why? Glutamine Promising, preferable enteral Larger studies necessary with relevant outcome measures Arginine Controversial in critical care (we don't know in burns) No evidence so far Potential for future research Omega 3 fatty acids Dosage studies are lacking Further research, ideally involving sufficient patient numbers and dosage studies Combined immunonutrients Many confounded studies Preferable to be developed after we solved the active nutrients in their optimal dose are identified

71 References Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of burns. BMJ Jun 12;328(7453): Baxter CR, Shires T. Physiological response to crystalloid resuscitation of severe burns. Ann N Y Acad Sci 1968;150: Wolf SE, Edelman LS, Kemalyan N. Effects of oxandrolone on outcome measures in the severely burned: a multicenter prospective randomized double-blind trial. J Burn Care Res Mar- Apr;27(2):131-9; discussion Saffle JI. The phenomenon of "fluid creep" in acute burn resuscitation. J Burn Care Res May- Jun;28(3): Cancio LC, Chávez S, Alvarado-Ortega M, et al. Predicting increased fluid requirements during the resuscitation of thermally injured patients. J Trauma Feb;56(2):404-13; discussion Lawrence A, Faraklas I, Watkins H, Allen A, Cochran A, Morris S, Saffle J. Colloid administration normalizes resuscitation ratio and ameliorates "fluid creep". J Burn Care Res Jan- Feb;31(1):40-7. Kahn SA, Beers RJ, Lentz CW. Resuscitation after severe burn injury using high-dose ascorbic acid: a retrospective review. J Burn Care Res Jan-Feb;32(1): Tanaka H, Matsuda T, Miyagantani Y, Yukioka T, Matsuda H, Shimazaki S. Reduction of resuscitation fluid volumes in severely burned patients using ascorbic acid administration. Arch Surg 2000;135: Kurmis R, Parker A, Greenwood J. The use of immunonutrition in burn injury care: where are we? J Burn Care Res Sep-Oct;31(5): Review

ENTERAL NUTRITION IN THE CRITICALLY ILL

ENTERAL NUTRITION IN THE CRITICALLY ILL 1 Ebb phase Flow phase acute response (catabolic) adoptive response (anabolic) 2 3 Metabolic Response to Stress (catabolic phase) Glucose and Protein Metabolism