Burns Sabiston 2016 Ahmadabadi Ali (MD) - PowerPoint Presentation

1. Burns Sabiston 2016Ahmadabadi Ali (MD)Assistant Professor of SurgeryMashhad University of Medical Sciences2018

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3. There is no greater trauma than major burn injury.

4. ETIOLOGY OF BURN INJURY 66% of all burns occur at home, and fatalities are predominant in the extremes of age.In children consider child abuse.Scald burns are most common in children up to 5 years of age.For those who have access to adequate burn care, survival from a major burn is the rule, no longer the exception.

5. PATHOPHYSIOLOGY OF BURN INJURY The depth of injury depends on the temperature to which the skin is exposed, the specific heat of the causative agent, and the duration of exposure.

6. Local application of Thromboxane A2 inhibitors improves blood flow and decreases the zone of stasis. Antioxidants, bradykinin antagonists, and sub-atmospheric wound pressures also improve blood flow and affect the depth of injury. Treatment directed at the control of local inflammation immediately after injury may spare the zone of stasis, the blockage of leukocyte adherence with anti- CD18 or anti-intercellular adhesion molecules; monoclonal antibodies improve tissue perfusion and tissue survival in animal models.

7. In major burnsA 10-50 fold elevation of plasma catecholamines and corticosteroid levels up to 3 years.Cytokine levels peak immediately after burn injury, approaching normal levels only after 1 month. Constitutive and acute-phase proteins are altered beginning 5 to 7 days after burn injury and remain abnormal throughout the acute hospital stay. Serum insulin-like growth factor I (IGF-I), IGF-binding protein 3 (IGFBP-3), parathyroid hormone, and osteocalcin drop immediately after the burn injury 10-fold and remain significantly decreased up to 6 months.Sex hormones and endogenous growth hormone levels decrease around 3 weeks after a burn injury

8. For severely burned patients, the resting metabolic rate at thermal neutral temperature (30° C) exceeds 140% of normal at admission, 130% once the wounds are fully healed, then to 120% at 6 months and 110% at 12 months after burn injury.Immediately after a burn injury, patients have low cardiac output characteristic of early shock. Ebb phaseHowever, 3 to 4 days after the burn injury, cardiac output is more than 1.5 times that of non-burned, healthy volunteers. The heart rate of pediatric burn patients approaches 1.6 times that of non-burned, healthy volunteers. Flow phaseMyocardial oxygen consumption surpasses that of marathon runners and is sustained well into the rehabilitative period.

9. A 10% loss of lean body mass is associated with immune dysfunction. A 20% loss positively correlates with decreased wound healing. A loss of 30% leads to increased risk for pneumonia and pressure sores. A 40% loss can lead to death. Uncomplicated severely burned patients can lose up to 25% of total body mass after acute burn injury.Severely burned patients have a daily nitrogen loss of 20 to 25 g/m2 of burned skin. At this rate, a lethal cachexia can be reached in less than 1 month. The protein loss of burned pediatric patients leads to significant growth retardation for up to 24 months after injury.

10. The liver increases its size by 225% of normal by 2 weeks after burn injury and remains enlarged at discharge by 200% of normal.Glycolytic-gluconeogenetic cycling is increased 250% during the post-burn hypermetabolic response coupled with an increase of 450% in triglyceride–fatty acid cycling.Insulin resistance appears during the first week after burn injury and persists significantly after discharge up to 3 years.

11. Inflammation and Edema Both in burned and non-burned tissues.Many mediators including histamine, bradykinin, vasoactive amines, prostaglandins, leukotrienes, activated complement, and catecholamines, among others. The use of antihistamines in the treatment of burn edema, however, has had limited success. Serotonin blockade improves cardiac index, decreases pulmonary artery pressure, and decreases oxygen consumption after burn injury. When the antiserotonin methysergide was given to animals after scald injury, wound edema formation decreased as a result of local effects. Another mediator likely to play a role in changes in permeability and fluid shifts is thromboxane A2.

12. The latest reports indicate an 88% mortality rate for severely burned adults and a 56% mortality rate for severely burned children in whom renal failure develops in the postburn period. Early resuscitation decreases risks of renal failure and improves the associated morbidity and mortality.The gastrointestinal response to burn is highlighted by mucosal atrophy, changes in digestive absorption, and increased intestinal permeability. Burn also causes reduced uptake of glucose and amino acids, decreased absorption of fatty acids, and reduction in brush border lipase activity. These changes peak in the first several hours after burn injury and return to normal at 48 to 72 hours, a timing that parallels mucosal atrophy. Gut permeability increases even further when burn wounds become infected.

13. Effects on the Immune System Macrophage production after burn injury is diminished, which is related to the spontaneous elaboration of negative regulators of myeloid growth. This effect is enhanced by the presence of endotoxin and can be partially reversed with granulocyte colony-stimulating factor (G-CSF) treatment or inhibition of prostaglandin E2. Total neutrophil counts are initially increased after burn injury, However, neutrophils that are present are dysfunctional in terms of diapedesis, chemotaxis, and phagocytosis. After 48 to 72 hours, neutrophil counts decrease somewhat, like macrophages, with similar causes. T-helper cell function is depressed after a severe burn. The Th1 response is important in cell-mediated immune defense, whereas the Th2 response is important in antibody responses to infection. Burn also impairs cytotoxic T-lymphocyte activity, thus increasing the risk of infection, particularly from fungi and viruses. Early burn wound excision improves cytotoxic T-cell activity.

14. Prehospital Managementremove from the source of injury and stop burning process. Inhalation injury work up and 100% oxygen by face mask. Care must be taken so that the rescuer does not become another victim. Universal precautions, should be used whenever there is likely to be contact with blood or body fluids. Burning clothing should be extinguished and removed as soon as possibleAll rings, watches, jewelry, and belts should be removedRoom temperature water can be poured on the wound within 15 minutes of injury to decrease the depth of the wound, but avoid hypothermia during resuscitation.

15. Initial Assessment primary and secondary survey Airway injury must be suspected with facial burns, singed nasal hairs, carbonaceous sputum, and tachypnea. Progressive hoarseness is a sign of impending airway obstruction, and endotracheal intubation should be instituted early before edema distorts the upper airway anatomy. especially in massive burns, who may appear to breathe without problems early in the resuscitation.Blood pressure may be difficult to obtain in burned patients with edematous or charred extremities. The presence of pulses or Doppler signals in the distal extremities may be adequate until better monitors, such as arterial pressure measurements and urine output, can be established.

16. Initial Wound CareOnly protection from the environment with application of a clean dry dressing or sheet to cover the involved part. Damp dressings should not be used. The patient should be wrapped in a blanket to minimize heat loss. The first step in diminishing pain is to cover the wounds to prevent contact to exposed nerve endings. Intramuscular or subcutaneous narcotic injections for pain should never be used. Small doses of intravenous morphine may be given after complete assessment.Inadequate first aid care was clearly associated with poorer outcomes.

17. TransportRapid, uncontrolled transport of the burn victim is not a priority, except when other life-threatening conditions coexist. In most incidents involving major burns, ground transportation of victims to the receiving hospital is appropriate. Helicopter transport: for 30 to 150 miles. For > 150 miles, transport by fixed-wing aircraft is most appropriate.

18. ResuscitationIncreased times to beginning resuscitation of burned patients result in poorer outcomes. Venous access is best attained through short peripheral catheters in unburned skin; however, veins in burned skin can be used.Saphenous vein cutdowns are useful in cases of difficult access and are used in preference to central vein cannulation. In children younger than 6 years, experienced practitioners can use intraosseous access in the proximal tibia until intravenous access is accomplished.

19. Lactated Ringer solution without dextrose is the fluid of choice except in children younger than 2 years, who should receive 5% dextrose in lactated Ringer solution. The initial rate estimation: TBSA burned *weight / 8. The rate of infusion for an 80-kg man with a 40% TBSA burn would be 80 kg × 40%TBSA/ 8 = 400mL/ hrThis rate should be continued until a formal calculation of resuscitation needs is performed.Colloid solutions should not be used in the first 24 hours until capillary permeability returned closer to normal. Others have argued that normal capillary permeability is restored somewhat earlier after burn injury (6 to 8 hours), and therefore colloids could be used earlier.

20. Much of the fluid needs are due to “leaky” capillaries that permit passage of large molecules into the interstitial space to increase extravascular colloid osmotic pressure. Approximately 50% of fluid resuscitation needs are sequestered in non-burned tissues in 50% TBSA burns.Hypertonic saline solutions have theoretical advantages in burn resuscitation. hypernatremia must be avoided, and serum sodium concentrations not exceed 160 mEq/dL. Other investigators found an increase in renal failure with hypertonic solutions. Some burn units successfully use a modified hypertonic solution of 1 ampule of sodium bicarbonate (50 mEq) in 1 L of lactated Ringer solution.

21. Parkland formula often underestimates the volume of crystalloid received in the first 24 hours after severe burn; this phenomenon has been termed fluid creep. More liberal use of opioid analgesia and positive pressure ventilation has been suggested. Consequence of increased fluid volumes: increased compartment pressures in the extremities, abdomen, and the orbit.When the abdominal pressure increases toward and above 30 mm Hg, assurance of complete abdominal escharotomy is made, and paralytics are considered. If the increased abdominal pressure persists (>30 mm Hg), an improved outcome rests in the performance of a decompressive laparotomy. However, the patients who require this procedure have mortality rates of 60%.Changes in intravenous fluid infusion rates should be made on an hourly basis determined by the response of the patient to the particular fluid volume administered.

22. These guidelines are used for the initial fluid management after aburn injury. The response to fluid resuscitation should becontinuously monitored, and adjustments in the rate of fluidadministration should be made accordingly.These guidelines are used for the initial fluid management after a burn injury. The response to fluid resuscitation should be continuously monitored, and adjustments in the rate of fluid administration should be made accordingly.

23. Albumin supplementation even after resuscitation does not affect the distribution of fluid among the intracellular and extracellular compartments.Albumin used during resuscitation is at best equal to crystalloid and at worst detrimental to the outcome of burned patients. For these reasons, we cannot recommend the use of albumin during resuscitation.To combat any regurgitation with an intestinal ileus, a nasogastric tube should be inserted in all patients with major burns to decompress the stomach. This is especially important for all patients being transported in aircraft at high altitudes. In addition, all patients should be restricted from taking anything by mouth until the transfer has been completed.A Dobhoff tube should be placed into the first part of the duodenum to continuously feed the severely burned.All patients with burns of more than 10% TBSA should receive 0.5 mL of tetanus toxoid. If prior immunization is absent or unclear or the last booster dose was more than 10 years ago, 250 units of tetanus immune globulin are also given.

24. EscharotomiesExtremities at risk are identified either on clinical examination or on measurement of tissue pressures higher than 40 mm Hg.The incisions are carried down onto the thenar and hypothenar eminences and along the dorsolateral sides of the digits to completely open the hand, if it is involved.If vascular compromise has been prolonged, reperfusion after an escharotomy may cause reactive hyperemia and further edema formation in the muscle, making continued surveillance of the distal extremities necessary. Increased muscle compartment pressures may necessitate fasciotomies.A constricting truncal eschar …..

25. Inhalation InjuryApproximately 80% of fire-related deaths result not from burns but from inhalation of the toxic products of combustion, and inhalation injury has remained associated with an overall mortality rate of 25% to 50% when patients require ventilator support for more than 1 week after injury.Chest radiographs are routinely normal.The standard diagnostic method should therefore be bronchoscopy of the upper airway of every burn patient.The treatment of inhalation injury should start immediately with the administration of 100% oxygen by face mask or nasal cannula.Upper airway edema normally increases during 9 to 12 hours.

26. Management of inhalation injuryVentilatory support: lower tidal volume, high-frequency ventilation aggressive pulmonary toilet, Bronchoscopic removal of casts, and Nebulization therapy: heparin, alpha mimetics, or polymyxin B. between two and six times a day.Pressure-control ventilation with permissive hypercapnia is a useful strategy in the management of these patients, and PaCO2 levels of as much as 60 mm Hg can be well tolerated if they are arrived at gradually. Prophylactic antibiotics are not indicated but are imperative with documented lung infections.

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28. Clinical diagnosis of pneumonia includes two of the following:Chest radiograph revealing a new and persistent infiltrate, consolidation, or cavitation; Sepsis; or A recent change in sputum or purulence in the sputum as well as quantitative culture. Empirical choices for the treatment of pneumonia before culture results are available should include coverage of methicillin-resistant Staphylococcus aureus and gram-negative organisms such as Pseudomonas and Klebsiella.

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30. Wound CareFirst-degree wounds: no dressing, are treated with topical salves. NSAIDs/ POSecond-degree wounds: daily dressing with topical antibiotics, cotton gauze, and elastic wraps. Alternatively, the wounds can be treated with a temporary biologic or synthetic covering to close the wound. Deep second-degree and third-degree wounds require excision and grafting for sizable burns, and the choice of initial dressing should be aimed at holding bacterial proliferation in check and providing occlusion until the operation is performed.

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32. AntimicrobialsLocal or systemic. Locals: salves or soaksSalves are generally applied directly to the wound with cotton dressings placed over them, and soaks are generally poured into cotton dressings on the wound. Salves may be applied once or twice a day but may lose their effectiveness between dressing changes. Frequent dressing changes can result in shearing with loss of grafts or underlying healing cells. Soaks remain effective because antibiotic solution can be added without removal of the dressing; however, the underlying skin can become macerated.Topical antibiotic salves include 11% mafenide acetate (Sulfamylon), 1% silver sulfadiazine (Silvadene), polymyxin B, neomycin, bacitracin, mupirocin, and the antifungal agent nystatin.

33. Silver sulfadiazinethe most commonly used. It has a broad spectrum of activity because its silver and sulfa moieties cover gram-positive, most gram-negative, and some fungal forms. Some Pseudomonas species possess plasmid-mediated resistance.relatively painless on application, has a high patient acceptance,easy to use. On occasion, patients complain of a burning sensation after it is applied, and, in a few patients, a transient leukopenia develops 3 to 5 days after its continued use. This leukopenia is generally harmless and resolves with or without treatment cessation.

34. Mafenide acetate broad spectrum of activity because of its sulfa moiety. It is particularly useful against resistant Pseudomonas and Enterococcus species. penetrate eschar, which silver sulfadiazine cannot. painful application on skin, such as in 2nd degree burnsIt also can cause an allergic rash, and it has carbonic anhydrase inhibitory characteristics that can result in a metabolic acidosis when it is applied over large surfaces.Mafenide sulfate is typically reserved for small full-thickness injuries.

35. Petroleum-based antimicrobial ointments with polymyxin B, neomycin, and bacitracin are clear on application, are painless, and allow easy wound observation. These agents are commonly used for treatment of facial burns, graft sites, healing donor sites, and small partial-thickness burns. Mupirocin is a relatively new petroleum-based ointment that has improved activity against gram-positive bacteria, particularly methicillin-resistant S. aureus and selected gram-negative bacteria. Nystatin, in either a salve or powder form, can be applied to wounds to control fungal growth. Nystatin-containing ointments can be combined with other topical agents to decrease colonization of both bacteria and fungus. The exception is the combination of nystatin and mafenide acetate; each inactivates the other.

36. Soaks0.5% silver nitrate solution, 0.025% sodium hypochlorite (Dakin solution), 0.25% acetic acid, and mafenide acetate as a 5% solution. Silver nitrate: painless, complete antimicrobial effectiveness.Disadvantages: staining of surfaces, problem in deciphering wound depth during burn excisions, hypotonic and continuous use can cause electrolyte leaching, with rare methemoglobinemia.\ A new commercial dressing containing biologically potent silver ions (Acticoat) that are activated in the presence of moisture is available. This dressing holds the promise of retaining the effectiveness of silver nitrate without the problems of silver nitrate soaks.

37. SoaksDakin solution (0.25% sodium hypochlorite):effective against most microbes; cytotoxic effects on the healing cells. Low concentrations of sodium hypochlorite (0.025%) have fewer cytotoxic effects while maintaining most of the antimicrobial effects. Hypochlorite ion is inactivated by contact with protein, so the solution must be continually changed. The same is true for acetic acid solutions, which may be more effective against Pseudomonas. Mafenide acetate soaks: same as mafenide acetate salve.Perioperative systemic antimicrobials also has a role in decreasing burn wound sepsis until the burn wound is closed. Common organisms that must be considered in choosing a perioperative regimen include S. aureus and Pseudomonas species, which are prevalent in burn wounds.

38. Burn Wound ExcisionTangential excision: Janzekovic Full-thickness excisionFascial excision: for burn extending down through the fat into muscle, when the patient presents late with large infected wounds and life-threatening invasive fungal infections. peripheral lymphedema estimates of bleeding with tangential excision 3.5% to 5% of the blood volume for every 1% TBSA. Control of blood loss: fibrin or thrombin spray, topical epinephrine 1 : 10000 to 1 : 20000, epinephrine-soaked laboratory pads (1 : 40000), immediate electrocautery of the blood vessel, sterilized tourniquet, pre-excisional tumescence with epinephrine saline can be used on the trunk, back, and extremities but not on the fingers.

39. Burn Wound CoverageAutograft & IsograftAllograftXenograftCultured epith. Cells: poor long-term clinical results, exorbitant costs, and fragility and difficult handling Dermal analogues: Integra, AlloDerm,

40. Multi-organ Failure It has been postulated that the progression to multiorgan failure exists in a continuum with the systemic inflammatory response syndrome. Nearly all burned patients meet the criteria for systemic inflammatory response syndrome . The great reduction of mortality from large burns was observed with early excision & graft (EE&G).Fluid resuscitation (as earliest as possible, How much possibleLocal (for all deep burns) and systemic (perioperative for TBSA >=30%) antibiotics.

41. Vigilant and scheduled replacement of intravascular devices minimizes the incidence of catheter-related sepsis. We recommend changes of indwelling catheters every 5 days. The first can be done over a wire using sterile Seldinger technique, but the second change requires a new site. This protocol should be kept as long as intravenous access is required. When possible, peripheral veins should be used for cannulation, even through burned tissue. The saphenous vein, however, should be avoided because of the high risk of thrombophlebitis.

42. The most common sources of sepsis are the wounds and the tracheobronchial tree and then may be GI tract. Early feedingPneumonia

43. Renal FailureFirst high-risk period: First 48 HrsSecond high-risk period: Days 2-14Urine output of more than 1 mL/kg is an adequate measure of renal perfusion in the absence of underlying renal disease.These patients have increased insensible losses from the wounds, which can be roughly calculated at 1500 mL/m2 TBSA + 3750 mL/m2 TBSA burned. Further losses are accrued on air beds (1 L/day in an adult).

44. Pulmonary Failurepatients be extubated as soon as possible after the risk is diminished and reintubation in this setting is not a failure. decrease in saturation to less than 92% is indicative of failure.Early tracheostomy?

45. Hepatic FailureComplete hepatic failure is not compatible with life, but a gradation of liver failure with some decline of the function is common.With the development of coagulopathies, treatment should be directed at replacement of factors II, VII, IX, and X until the liver recovers. Albumin replacement may also be required. Attention to obstructive causes of hyperbilirubinemia, such as acalculous cholecystitis, should be considered as well. Initial treatment of this condition should be gallbladder drainage, which can be done percutaneously.

46. Hematologic FailureBurned patients may become coagulopathic through two mechanisms: (1) depletion and impaired synthesis of coagulation factors and (2) thrombocytopenia.Central Nervous System Failure Obtundation is one of the hallmarks of sepsis, and burn patients are no exception. A new onset of mental status changes not attributed to sedative medications in a severely burned patient should incite a search for a septic source. Treatment is supportive.

47. ATTENUATION OF THE HYPERMETABOLIC RESPONSE nonpharmacologic modalities: nutritional supportOne formula multiplies the basal energy expenditure determined by the Harris-Benedict formula by 2 in burns of 40% TBSA, assuming a 100% increase in total energy expenditure. This correlated to 1.4 times the measured resting energy expenditure by indirect calorimetry. Curreri formula: 25 kcal/kg/day plus 40 kcal per percentage of TBSA burned per day. In children, formulas based on body surface area are more appropriate

48. The composition of the nutritional supplement is also important. The optimal dietary composition contains 1 to 2 g/kg/day of protein, which provides a calorie to nitrogen ratio at around 100 : 1 with the earlier suggested calorie intakes. Carbohydrates have the advantage of stimulating endogenous insulin production, which may have beneficial effects on muscle and burn wounds as an anabolic hormone. As fat transporters are markedly decreased, we suggest use of a low-fat diet because additional fat to deliver noncarbohydrate calories has little support.

49. The composition of the nutritional supplement is also important. The optimal dietary composition contains 1 to 2 g/kg/day of protein, which provides a calorie to nitrogen ratio at around 100 : 1 with the earlier suggested calorie intakes. Carbohydrates have the advantage of stimulating endogenous insulin production, which may have beneficial effects on muscle and burn wounds as an anabolic hormone. As fat transporters are markedly decreased, we suggest use of a low-fat diet because additional fat to deliver noncarbohydrate calories has little support.

50. Environmental SupportThe body attempts to raise skin and core temperatures to 2° C above normal. Raising the ambient temperature from 25° C to 33° C can diminish the magnitude of this obligatory response from 2.0 to 1.4 resting energy expenditure in patients exceeding 40% TBSA

51. Pharmacologic ModalitiesRecombinant Human Growth HormonerhGH at doses of 0.2 mg/kg as a daily intramuscular injection ???Insulin-like Growth FactorInfusion of recombinant human IGF-I and IGFBP-3 to burned patients has been demonstrated to effectively improve protein metabolism with significantly less hypoglycemia than with rhGH itself. It attenuates muscle catabolism and improves gut mucosal integrity in children with serious burns. Immune function is effectively improved by attenuation of the type 1 and type 2 hepatic acute-phase responses, increased serum concentrations of constitutive proteins, and vulnerary modulation of the hypercatabolic use of body protein. However, studies indicate that the use of IGF-I alone is not effective in critically ill patients without burns.

52. OxandroloneAdministration of 10 mg of oxandrolone (0.1mg/kg) every 12 hours decreased hospital stay. The effects were independent of age. shortened length of acute hospital stay, maintained lean body mass, and improved body composition and hepatic protein synthesis, bone mineral content, However, although anabolic agents can increase lean body mass, exercise is essential to development of strength.

53. Propranolol β-Adrenergic blockade with propranolol represents probably the most efficacious anticatabolic therapy in the treatment of burns. Long-term use of propranolol during acute care in burn patients, at a dose titrated to reduce heart rate by 15% to 20%, was noted to diminish cardiac work. It also reduced fatty infiltration of the liver Administration of propranolol reduces skeletal muscle wasting and increases lean body mass after burn injury.Administration of propranolol given at 4 mg/kg body weight every 24 hours also markedly decreases the amount of insulin necessary to decrease elevated glucose level after burn injury (

54. Attenuation of Hyperglycemia after Burn Injury Insulin: given during acute hospitalization improve muscle protein synthesis, to accelerate donor site healing time, and to attenuate lean body mass loss and the acute-phase response.insulin was shown to exert totally unexpected anti-inflammatory effects potentially neutralizing the proinflammatory actions of glucose.Insulin administered to maintain glucose at levels below 110 mg/dL decreased mortality, incidence of infections, sepsis, and sepsis-associated multiorgan failure in surgically critically ill patients. It was also found to significantly reduce newly acquired kidney injury, to accelerate weaning from mechanical ventilation, and to accelerate discharge from the ICU and the hospital.Tight control and the risk of hypoglycemiaCurrently, the Surviving Sepsis Campaign recommendation is to maintain glucose levels below 150 mg/dL

55. Metformin By inhibiting gluconeogenesis and augmenting peripheral insulin sensitivity, metformin directly counters the two main metabolic processes that underlie injury-induced hyperglycemia. In addition, metformin has been rarely associated with hypoglycemic events.increased fractional synthetic rate of muscle protein and improvement in net muscle protein balance treatment with metformin or other biguanides has been associated with lactic acidosis. To avoid metformin-associated lactic acidosis, the use of this medication is contraindicated in certain diseases or illnesses in which there is a potential for impaired lactate elimination (hepatic or renal failure) or tissue hypoxia, and it should be used with caution in subacute burn patients.

56. Novel Therapeutic Options Other ongoing trials to decrease postburn hyperglycemia include the use of glucagon-like peptide 1 and peroxisome proliferator-activated receptor gamma (PPAR-γ) agonists (e.g., pioglitazone, thioglitazones) or the combination of various antidiabetic drugs. PPAR-γ agonists, such as fenofibrate, have been shown to improve insulin sensitivity in patients with diabetes.

57. Electrical Burns IcebergThe muscle is the major tissue through which the current flows, and thus it sustains the most damage. Low and High voltage5 immediate important evaluations2 late complications: Central nervous system effects, such as cortical encephalopathy, hemiplegia, aphasia, and brainstem dysfunction injury, have been reported up to 9 months after injury Escharotomy / FasciotomyDébridement of devitalized tissues, save questionable ones,

58. Electrical injuryvigorous hydration and infusion of intravenous sodium bicarbonate (5% continuous infusion) and mannitol (25 g every 6 hours for adults) are indicated to solubilize the hemochromogens and to maintain urine output if significant amounts are found in the serum. These patients also require additional intravenous volumes above predicted amounts based In this situation, urine output should be maintained at 2 mL/kg/hr.

59. Chemical BurnsSpeed is essential in the management of chemical burns. For all chemicals, lavage with copious quantities of clean water should be done immediately after removal of all clothing. Dry powders 10 mL of 98% sulfuric acid dissolved in 12 L of water decreases the pH to 5.0, a range that can still cause injury.

60. Formic acid injuries An organic acid used for industrial descaling and as a hay preservative. Electrolyte abnormalities are of great concern for patients who have sustained extensive formic acid injuries, with metabolic acidosis, renal failure, intravascular hemolysis, and pulmonary complications (ARDS) being common. Acidemia detected by a metabolic acidosis on ABG should be corrected with intravenous sodium bicarbonate. +- Hemodialysis +- Mannitol diuresis. Wound typically has a greenish appearance and is deeper than what it initially appears to be; it is best treated by surgical excision.

61. Formic acid burn. (a and b) Early copious water irrigation was established for an hour. Both cornea were affected and were immediately explored by an ophthalmologist. (c) After 2 weeks treatment with topical silver sulphadiazine cream, thefrontal, nasal and periorbital areas, where the eyelids are specially affected, have not still epitelized. (d) Although these areas were grafted, and a temporal tarsorrhaphy was kept in place for 2weeks, the patient developed an ectropion in the four eyelids.

62. Hydrofluoric acid the strongest inorganic acid initial copious irrigationcopious 2.5% calcium gluconate gel. The gel should be changed at 15-minute intervals until the pain subsides.If pain relief is incomplete after several applications or if symptoms recur, intradermal injections of 10% calcium gluconate (0.5 mL/cm2 affected), intra-arterial calcium gluconate into the affected extremity, or both may be required to alleviate symptoms. If the burn is not treated in such a fashion, decalcification of the bone underlying the injury and extension of the soft tissue injury may occur.

63. All patients with hydrofluoric acid burns should be admitted for cardiac monitoring, with particular attention paid to prolongation of the QT interval. A total of 20 mL of 10% calcium gluconate solution should be added to the first liter of resuscitation fluid, and serum electrolytes must be closely monitored. Any electrocardiographic changes require a rapid response by the treatment team with intravenous calcium chloride to maintain heart function. Several grams of calcium may be required in the end until the chemical response has run its course. Serum magnesium and potassium also should be closely monitored and replaced. Speed is the key to effective treatment.

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65. • Partial-thickness burns > 10% TBSA• Burns involving the face, hands, feet, genitalia, perineum, or major joints• Any full-thickness burn• Electrical burns, including lightning injury• Chemical burns• Inhalation injury• Burns in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect outcome• Any patient with burns and concomitant trauma • Burned children in hospitals without qualified personnel or equipment • Burns in patients who will require special social, emotional, or long-term rehabilitative intervention

66. Thanks for your attention