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Burns in Children Review Tarek Hazwani, MD Assistant Consultant Pediatric Intensivist King Abdulaziz Medical City 1 Burns in Children Review Anatomy of Skin Pathophysiology Critical Factors Management 2 Anatomy of Skin Largest body organ More than just a passive covering 3 Anatomy Two layers • Epidermis • Dermis 4 Skin Functions Sensation Protection Temperature regulation Fluid retention 5 Burn: Pathophysiology Loss of fluids Inability to maintain body temperature Infection 6 Burn: Pathophysiology Patients with large burns (≥15 percent TBSA for young children and ≥20 percent for older children and adolescents) develop systemic responses to these mediators. For patients with 40 percent TBSA or more, myocardial depression can occur . As a result, patients with major burns may become hypotensive (burn shock) and edematous (burn edema). 7 Burn: Pathophysiology Metabolic response : Following resuscitation, children with major burns develop a hypermetabolic response that results in a dramatic increase in energy expenditure and protein metabolism . Evidence suggests that modulation of the hypermetabolic response with therapies such as beta blockers and human growth hormone may improve outcomes for severely burned children 8 Pathophysiology Systemic capillary leak usually persists for 18 to 24 hours. Protein is lost from the intravascular space during the first 12 to 18 hours after a burn, after which vascular integrity improves. 9 Critical Factors Depth Extent 10 Burn Depth First Degree (Superficial) • • • • • • Involves only epidermis Red Painful Tender Blanches under pressure Possible swelling, no blisters • Heal in ~7 days 11 Burn Depth Second Degree (Partial Thickness) • Extends through epidermis into dermis • Salmon pink • Moist, shiny • Painful • Blisters may be present • Heal in ~7 to 21 days 12 Burn Depth Burns that blister are second degree. But all second degree burns don’t blister. 13 Burn Depth Third Degree (Full Thickness) • Through epidermis, dermis into underlying structures • Thick, dry • Pearly gray or charred black • May bleed from vessel damage • Painless • Require grafting 14 Burn Depth Often cannot be accurately determined in acute stage Infection may convert to higher degree When in doubt, over-estimate 15 Burn Extent Pediatric Rule of Nines 18 9 9 18, Front 18, Back For each year over 1 year of age, subtract 1% from head, add equally to legs. 1 13.5 13.5 16 Burn Extent Rule of Palm • Patient’s palm equals 1% of his body surface area 17 Burn Extent 18 Burn Severity Based on • • • • • • Depth Extent Location Cause Patient Age Associated Factors 19 Critical Burns Need Burn centre American Burn Association Age <10 years with >10 percent TBSA burn Age ≥10 years with >20 percent TBSA burn Full thickness burn >5 percent TBSA Inhalational injury Any significant burn to face, eyes, ears, genitalia, or joints Significant associated injuries (fractures or major trauma) 20 Associated Factors Patient Age • < 5 years old • > 55 years old Burn Location • Circumferential burns of chest, extremities 21 Burn shock characterized by specific hemodynamic changes (decreased cardiac output and plasma volume, increased extracellular fluid, and oliguria) 22 Burn Edema Fluid shift intravascular to extravascular soon after a burn—persist for the first 24 hours In small burns edema peaks early, in large burns edema developed continue for 18-24 hours Unburned tissue edema occurs when burn exceeds 35-40% TBSA Early increase vascular permeability—in part related to histamine—mechanism is likely related to PMN and their adhesion to the endothelium 23 Burn : Management 24 Stop Burning Process Remove patient from source of injury Remove clothing unless stuck to burn Cut around clothing stuck to burn, leave in place 25 Assess Airway/Breathing Start oxygen if: • • • • • Moderate or critical burn Decreased level of consciousness Signs of respiratory involvement Burn occurred in closed space History of CO or smoke exposure Assist ventilations as needed 26 Assess Circulation Check for shock signs /symptoms Early shock seldom results from effects of burn itself. Early shock = Another injury until proven otherwise 27 Obtain History How long ago? What has been done? What caused burn? Burned in closed space? Loss of consciousness? Allergies/medications? Past medical history? 28 Rapid Physical Exam Check for other injuries Rapidly estimate burned, unburned areas Remove constricting bands 29 Treat Burn Wound Cover with DRY, CLEAN SHEETS Do NOT rupture blisters Do NOT put goo on burn 30 Special Considerations In Pediatrics always Consider possibility of abuse As many as 10% of abuse cases involve burns 31 Burn: Management Parkland formula, as follows: (2-4 cm3 of crystalloid) X (% BSA burn) X (body weight in kg) The Parkland formula must be modified in pediatric patients by adding maintenance 32 Burn: Management Fluid resuscitation Estimating fluid requirements : for the first 24 hours following a burn injury include: Parkland - 4 mL/kg per percent total burn surface area (TBSA). Add glucose maintenance fluid for children <5 years of age. Galveston - 5000 mL/m2 per percent TBSA. Add 2000 mL/m2 per day for maintenance requirements. Half of the fluid is given over the first 8 hours. The remaining half is given over the next 16 hours 33 Burn: Management Fluid resuscitation Choice of fluid: Ringers lactate (RL) is the resuscitation and maintenance fluid of choice for the first 24 hours at most burn centers. Experts recommend adding D5% to maintenance fluid for children <20 kg to prevent hypoglycemia . Colloid is typically added after 24 hours to restore oncotic pressure and preserve intravascular volume 34 Burn: Management Colloid resuscitation The addition of plasma or albumin to resuscitation fluids has been criticized on the assumption that the burn-induced increase in vascular permeability and the consequent extravasation of proteins persist for up to 36 h post injury . The main concern is that protein administration during the first 24 h increases protein accumulation in the interstitium and thus traps water . Using 131iodine-labeled albumin and autoradiographic techniques to demonstrate have shown that effective transcapillary sieving of albumin molecules into burned skin essentially stops at approximately 8 h post injury and that edema of injured tissues, maximal at 3 h post burn, persists beyond24 h post injury 35 Burn: Management Fluid resuscitation Monitoring fluid status: The volume status of burn patients must be carefully monitored in order to successfully navigate the narrow path between inadequate volume and fluid overload. The following parameters are helpful : Urine output should be maintained at 1 to 2 mL/kg per hour for children <30 kg and 0.5 to 1 mL/kg per hour for those ≥30 kg. Heart rate is a better monitor of circulatory status in children than is blood pressure. Tachycardia may indicate hypovolemia, but pain can elevate heart rate in euvolemic patients. Metabolic acidosis can be a marker for inadequate fluid resuscitation, but also occurs with carbon monoxide or cyanide exposure 36 Burn: Management Fluid resuscitation Burn Children not response to large fluid volumes to maintain adequate perfusion : Volume loss from occult injuries Neurogenic shock as the result of a spinal cord injury Myocardial depression or decreased vascular tone from inhaled or ingested toxins 37 Burn: Management Pain control Most burn centers use morphine Fentanyl may be a safer choice for initial pain management for patients whose cardiovascular status may be unstable 38 Burn: Management Antibiotics Topical antibiotics have been used to dress burn wounds: It is : available, and reduce the risk of infection. The topical antibiotic is applied to the wound which is then covered with a nonadherent dressing. Specific antibiotic : Silver sulfadiazine , Mafenide , Bacitracin 39 Burn: Management Special Considerations Steroids have no role in treating burn wounds Intravenous antibiotics are not recommended in the initial treatment of most burn patients, as it may increase the chance of colonization with more virulent and resistant organisms. They should be reserved for those patients with secondary infections 40 Burn: Complications Infection Early Infections : Organism : GAS , S. aureus Specific colonization of burn wounds is somewhat predictable over time. Initially, gram-positive organisms are present; infection that occurs in the first 48 hours after the burn is usually secondary to GAS. The incidence of GAS infections in burned patients has decreased, probably secondary to immediate use of topical antimicrobial therapy. Routine administration of antibiotics prophylaxis is not recommended ( colonization and potential infection with more resistant organisms). S. aureus also causes early septicemia. If there is concomitant inhalation injury. 41 Burn: Complications Bacteremia Bacteremia is not uncommon in the burned patient. Risk factors include wound manipulation and the presence of an intravascular catheter. infected intravascular thrombus can cause persistent bacteremia. Endocarditis must be considered in any patient with prolonged bacteremia. 42 Burn: Complications Renal failure ARF in burn patients is not common. Two distinct pictures of ARF can be observed: early ARF, occurring either few hours after injury or in the first few days, and late ARF developing approximately 1 or more weeks after burn injury. Early ARF may be due to hypovolemia and hypoperfusion of the kidneys, whereas late ARF is a consequence of infection, endotoxemia, and MODS 43 Burn: Complications Renal failure Renal damage can arise even from hemoglobinuria in burn patients with associated hemolysis, the administration of haptoglobin may prevent hemoglobinuria-nduced renal failure 44 Inhalation Injury 45 Inhalation Injury 10-20% hospitalized burn patients sustained inhalation injury. Increased mortality History (closed space) P.E. (facial burn, singed nasal hairs, erythema, carbonaceous material in back of the troat) laboratory tests (carboxyhemoglobin>15%) and bronchoscopy (erythema and sooty deposite in the airway) Treatment: supportive. Nasotracheal or endotracheal intubation preferable to early tracheostomy. Prophylactic antibiotics and steroids not indicated. 46 Inhalation Injury Problems Hypoxia Carbon monoxide toxicity Upper airway burn Lower airway burn 47 Inhalation Injury Carbon Monoxide Product of incomplete combustion Colorless, odorless, tasteless Binds to hemoglobin 200x stronger than oxygen Headache, nausea, vomiting, “roaring” in ears 48 Inhalation Injury Carbon Monoxide Exposure makes pulse oximeter data meaningless! 49 Inhalation Injury Carbon Monoxide Measurement Carbon monoxide has various effects depending upon levels Must check levels on Blood Gas analysis 0-10% can be seen in smokers can be seen in smokers 10-20% patients can have headache 20-30% patients develop severe headache, nausea, vomiting, CNS collapse 30-40% patients present with syncope, convulsions, depressed cardiac activity and respiratory function 40% and greater death may ensue within hours 50 Inhalation Injury Upper Airway Burn True Thermal Burn Danger Signs • • • • Neck, face burns Singing of nasal hairs, eyebrows Tachypnea, hoarseness, drooling Red, dry oral/nasal mucosa 51 Inhalation Injury Lower Airway Burn Danger Signs • • • • • • Loss of consciousness Burned in a closed space Tachypnea (+/-) Cough Rales, wheezes, rhonchi Carbonaceous sputim 52 Electrical Burns 53 Electrical Burns Considerations Intensity of current Duration of contact Kind of current (AC or DC) Width of current path Types of tissues exposed (resistance) 54 Electrical Burns Considerations Conductive injuries • “Tip of Iceberg” • Entrance/exit wounds may be small • Massive tissue damage between entrance/exit 55 Electrical Burns Management Make sure current is off! Check ABCs Assess carefully for other injuries Patient needs hospital evaluation, observation 56 Electrical Injury Complications If gross urinary pigment is present: sodium bicarbonate and mannitol are initially given in addition to Ringer’s lactate. Diuretics in contraindicated. Urine output maintained 100-125 ml/h until it is seen to clear Precipitate cardiac arrhythmia,routine cardiac monitoring not necessary, unless cardiac arrest at accident, abnormal EKG, arrhythmia during transport 57 Electrical Injury Other Complications Respiratory arrest Spinal fractures Long bone fractures 58 Chemical Burns 59 Chemical Burns Alkaline substances such as sodium and potassium hydroxides and cements are most common cause of chemical burn Direct chemical reaction instead of heat production Often underestimated. Immediate treatment—copious tap water lavaging 60 Chemical Burns Concerns Damage to skin Absorption of chemical; systemic toxic effects Avoiding EMS personnel exposure 61 Chemical Burns Management Remove chemical from skin Liquids • Flush with water Dry chemicals • Brush away • Flush what remains with water 62 Chemical Burns Injuries require special care Hydrofluoric acid: treated with a paste made of 35 ml of 10% calcium gluconate in 150 gm of K-Y jelly. Applied to the affected area and changed every hour if needed. More severe case require subcutaneous injection of calcium gluconate into the painful area 63 Chemical Burns Injuries require special care Phenol: not soluble in water. Absorbed through intact skin. Topical application of polyethylene glycol or vegetable oil Phosphorus: keep the areas copiously irrigated and continuously wet with water, early debridement of extraneous particles 64 Chemical Burns Injuries require special care Cement: rinsed with water until the soapy feeling disappear, then dried thoroughly Tar: respond well to application of bacitracin or neomycin ointment for 12 hours, then washed off and silver sulfadiazine applied 65 Thank You 66