Acute Burn Handout PDF

Acute burn Dr.muhammed naeem Learning objectives 1-Classification of causes of burn 2-Proper assessment of depth of burn in the acute stage. 3-Assessment of percentage of TOTAL BURN SURFACE AREA ( %TBSA) according to Wallace rule of nine. 4-Early diag...

Acute burn Dr.muhammed naeem Learning objectives 1-Classification of causes of burn 2-Proper assessment of depth of burn in the acute stage. 3-Assessment of percentage of TOTAL BURN SURFACE AREA ( %TBSA) according to Wallace rule of nine. 4-Early diagnosis and management of inhalational injury. 5- Fluid resuscitation of acutely burned patient according to Parkland formula and assessment of proper resuscitation. 6-Local care of burned wound. 7- Assessment the need for early surgical decompression of acutely burned patient Introduction The burn is depicted as a traumatic lesion provoked by several possible agents (thermal, chemical, mechanical, or electrical) involving different skin layers to a certain degree. Burns are one of the most devastating conditions encountered in medicine. The injury represents an assault on all aspects of the patient, from the physical to the psychological. It affects all ages, from babies to elderly people, and is a problem in both the developed and developing world. Most of us have experienced the severe pain that even a small burn can bring. However the pain and distress caused by a large burn are not limited to the immediate event. The visible physical and the invisible psychological scars are long lasting and often lead to chronic disability. Skin surface area is about 0.2–0.3m2 in the newborn and about 1.5–2.0m2 in the adult. Thickness of epidermis from 0.05mm (eyelids) to 1mm (sole of the foot). Dermis is approximately 10× thicker than epidermis site for site. Causes of burn injury : 1-Thermal burn : most common cause which may be caused by -Scald -Flash -Flame -Contact 2-Chemical burn : Alkalis (cause a liquefactive necrosis) 1  Acids (cause a coagulative necrosis) Organic compounds Phosphorus 3-Electrical burn : Low voltage 1,000 V 4-Radiation injury Pathophysiology of burn injury A. Thermal injury causes coagulation necrosis of the skin and underlying tissues to a variable depth. Burn injury also exerts deleterious effects on all other organ systems. B. Hemodynamic—The first 24-h postburn are characterized by decreased blood volume, increased blood viscosity, and depressed cardiac output. Microvascular permeability is increased directly by heat and indirectly by endogenous mediators. The diminished blood volume and cardiac output cause oliguria, which may progress to acute renal failure. Numerous factors have been reported to increase vascular permeability and leukocyte infiltration: Histamine Arachidonic acid metabolites (principally thromboxane A2 and the leukotrienes) Substance P Fibrin degradation product D Activated proteases Platelet-activating factor (PAF) Cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF) C. Immune system—Humoral and cell-mediated immunity are both impaired and are manifested as depressed levels of immunoglobulin, reduced activation of complement, and diminished stimulation of lymphocyte proliferation and response. D. Hematologic—There is immediate red blood cell destruction in direct proportion to the extent of the burn, particularly third-degree burns. Endothelial injury may lead to release of thromboplastins and to collagen exposure; the latter then initiates platelet adhesion, aggregation, and contact activation of factor XII. Severe full-thickness burns induce consumption of coagulation factors at the burn site, which contributes to the development of disseminated intravascular coagulation (DIC). 2 E. Gastrointestinal—Ileus is universal in patients with burns of more than 25% total body surface area (TBSA). Gastric and duodenal mucosal damage, secondary to focal ischemia, can be observed as early as 3–5 h postburn. If the mucosa is unprotected, the early erosions may progress to frank ulceration. F. Endocrine—In the early postburn period, a catabolic endocrine pattern develops that is characterized by elevated glucagon, cortisol, and catecholamine levels with depressed insulin and triiodothyronine levels. These effect an increase in metabolic rate, glucose flow, and a negative nitrogen balance. Their magnitude correlates with the size of the burn area. Acute management of burn: Without intervention, patients with serious burns die for three primary reasons. Burn shock in the first day, respiratory failure in the following 3–5 days, and burn wound sepsis in subsequent weeks. The initial management of a severely burnt patient is similar to that of any trauma patient. A modified “advanced trauma life support” primary survey is performed, with particular emphasis on assessment of the airway and breathing. The burn injury must not distract from this sequential assessment, otherwise serious associated injuries may be missed. -- Perform an ABCDEF primary survey A—Airway with cervical spine control, B—Breathing, C—Circulation, D—Neurological disability, E—Exposure with Indications for hospital admission: The following are the admission criteria for all patients with burn injuries according to the American Burn Association. Second- and third-degree burns greater than 10% of TBSA in patients under 10 or over 50 years of age Second-degree burns greater than 20% TBSA in other ages Third-degree burns greater than 5% TBSA in any age Significant burns of the face, hands, feet, genitalia, or perineum Significant electrical/lightning injuries Significant chemical burns Associated inhalation injury, concomitant mechanical trauma, or significant preexisting medical illnesses Burns requiring special social, emotional, or long-term rehabilitative support, including cases of suspected or actual child abuse 3 Evaluation of burn involves: Extent of burns (surface area): Although the classic “Wallace Rule of 9” is still followed in many centers The Wallace rule of nines Adult body surface area (BSA): ∘ 9% head and neck ∘ 9% each arm ∘ 18% anterior trunk ∘ 18% posterior trunk ∘ 18% each leg ∘ 1% perineum. BSA of children up to 1 year old is distributed differently: ∘ 18% head and neck ∘ 9% each arm ∘ 18% anterior trunk ∘ 18% posterior trunk ∘ 13.5% each leg ∘ 1% perineum. 4 – For each additional year of age up to age 10, 1% should be subtracted from the head and neck and 0.5% added to each leg. Depth of burn injury is generally difficult to assess initially. It is sufficient to distinguish between erythema and actual skin damage at the initial examination. First-degree burn—superficial burn that involves only the epidermis. The area is erythematous, tender, and usually heals in less than 7 days. Second-degree burn—destruction of the epidermis and upper dermal layer. The skin is red, blistered, and sensory nerve damage causes extreme pain. Third-degree burn—destruction of the epidermis and dermis. The area is white, leathery, charred, and pain is absent due to destruction of sensory nerves 5  Fourth-degree burn—destruction of skin, muscle, and bone. Fluid resuscitation : Fluid resuscitation is required for: ∘ Adults with burns >15% TBSA. ∘ Children with burns >10% TBSA. Parkland formula 4 ml/kg/% burn of Hartmann’s solution in the first 24 hours after the burn. ∘ Half the fluid is given in the first 8 hours after injury. ∘ The second half is given in the next 16 hours. Hartmann’s solution contains: Na+ 131 mmol/l Cl− 111 mmol/l Lactate 29 mmol/l K+ 5 mmol/l Ca2+ 2 mmol/l. The rate of infusion is modified to meet specific end points of resuscitation: ∘ Urine output is the best indicator of tissue perfusion – Aim for 0.5–1 ml/kg/h in adults; 1–1.5 ml/kg/h in children – Double this after high-voltage electrical injuries. ∘ Other parameters to be monitored: – Pulse, blood pressure, capillary refill – Core–peripheral temperature gradient – Respiratory rate 6 – Urine osmolality. Serial measures of arterial blood lactate and base excess also indicate adequacy of resuscitation. Factors specific to children resuscitation Proportionately greater surface area than adults. Reduced physiological reserves. ∘ Because of this, children require additional maintenance fluid containing dextrose. Daily maintenance fluid requirement: ∘ 100 ml/kg for the first 10 kg body weight ∘ 50 ml/kg for the next 10 kg body weight ∘ 20 ml/kg for the remainder of the body weight Maintenance fluid is given enterally whenever possible. Inhalation Injury Inhalation injury—a chemical tracheobronchitis and acute pneumonitis—is caused by the inhalation of smoke and other irritative products. In severe cases, it progresses to development of adult respiratory distress syndrome (ARDS). Typical Signs of Significant inhalational Injury 1. Singeing of nasal hair 2. Significant facial burns 3. Carbonaceous sputum 4. Hoarseness 5. Stridor 6. Carboxyhemoglobin level of more than 15% at 3 h postexposure is strong evidence of smoke inhalation Evaluation of inhalational injury 1. Chest x-ray and arterial blood gases are routinely obtained. 2. Fiberoptic bronchoscopy may be performed at bedside. 3. Xenon ventilation/perfusion scanning has been reasonably accurate in diagnosing inhalation injury. 7 Treatment of inhalational injury is mainly supportive with oxygen therapy Immediate treatment involves administering 100% oxygen. Endotracheal intubation is necessary in some cases. Hyperbaric oxygen has been used in some units. -Routine tetanus prophylaxis is employed in burned patient. -There is no role for prophylactic systemic antibiotic therapy. Give antibiotics when there are features of infections. -Put NG tube and prescribe antacids :When the burn surface area is 25% or more of deep burn, the patient is liable to develop paralytic ileus and stress gastro-dudenal erosions or ulcers→ put NG tube and prescribe antacids. -Frequent checking of PCV, S.electrolytes, and renal function tests -Nutrition support: Give high calorie and high protein diet.In addition to Vitamins A and C, Iron and Zinc suppliments. - Psychlogical support. -Rehabilitation and physiotherapy with early splinting of burned extremities and joints to avoid post burn contractures. Surgical decompression Deep dermal and full thickness burns are inelastic. ∘ Can cause distal limb ischemia if circumferential. Similarly, extensive involvement of the chest (or abdomen in a child) can impair ventilation. Constriction becomes worse once fluid resuscitation is begun. Escharotomy relieves this constriction. ∘ Usually done with electrocautery, because they tend to bleed. Fasciotomies usually required only for burns involving muscle, or high-voltage electrical 8 injuries. Escharotomies begin and end in unburnt or superficially burnt skin. Limb escharotomies are generally made in midaxial lines. ∘ Avoid the ulnar nerve at the elbow and common peroneal nerve at the knee. Chest escharotomies are made along the mid-axillary lines to the subcostal region. ∘ They are joined across the upper abdomen by a chevron incision parallel to the costal margin. ∘ This creates a mobile breastplate that moves with ventilation. ∘ The anesthetist can advise on the adequacy of chest escharotomy by a drop in ventilator airway pressures. Local Management of burn 1. Initial care involves debridement of necrotic tissue and open blisters, protection from the environment, and edema reduction. 2. Enzymatic debridement is practiced in some centers. 3. Early excision of burn tissue provides better functional and aesthetic results. The post excision wound is ideally covered with meshed split thickness autografts. Early staged excision should begin on postburn day 3 in full thickness burn. Types of burn wound excision: Tangential excision: sequential removal of layers of eschar and necrotic tissue until a layer of viable, bleeding tissue. Fascial excision: excision of the burned tissue and subcutaneous tissue down to the layer of the muscle fascia 9 Water jet-powered VersaJet: useful for excision of concave surfaces of the hand and feet, as well as for excision of the eyelids, ear, and nose Coverage of skin defect after burn wound excision Skin graft: segment of tissue that transfer from one site of body (donor site) to another site (recipient site) without its blood supply. Types of skin graft :1. Full thickness skin graft: which consist of epidermis and full thickness of dermis. 2. Split thickness skin graft: Which consist of epidermis and variable portion of dermis, it described as thin, intermediate, and thick according to thickness of included dermis. Skin substitutes: in cases of extensive burn wounds, the surface area burned may exceed the available donor sites , so they need for a replacement for human skin until complete coverage with autografts can occur 10 Pain control in burnt patients: Background pain :Best treated with longer acting agents :MORPHIN Procedural pain occurs during daily wound care and therapy. shorter acting agents are probably best. use of short-acting benzodiazepines is favorable. Avoid NSAID Topical Agents used in local wound care of burn Silver sulfadiazine (1% Silvadene)—most commonly used agent. Active against most Gram- positive and Gram-negative organisms. The “pseudoeschar” that forms over the burn can confuse the inexperienced observer. Leukopenia can occur. Sulfamylon (Mafenide acetate)—has superior eschar penetration. Excellent choice for ears, noses, and some electrical burns. It has the disadvantage of causing intense pain on application and is associated with metabolic acidosis. Silver nitrate (0.5%)—effective as a prophylactic against Pseudomonas colonization. Disadvantages include production of black stains, hyponatremia, and methemoglobinemia. Povidone iodine—not effective, inactivated by wound exudate Management of out- patient burn 11 References 1-Handbook of plastic surgery , Arvind N.Padubidri, and Maria Siemionow, chapter 25; burn pp :176-180. 2-Key Notes In Plastic Surgery ,2nd edition, Adrian Richards and Hywel Dafydd,chapter 8, burn ,pp 490-516. 3-Stone's Plastic Surgery Facts and Figures ,3rd edition, chapter2 burn, pp 25-29. 12