|SYMPOSIUM - POLYTRAUMA MANAGEMENT
|Year : 2013 | Volume
| Issue : 1 | Page : 47-57
Burns and thermal injuries
Sunita Singh1, Sarita Agrawal2, Manju Agrawal3, Nitin Kumar Borkar4, Alok C Agrawal5
1 Department of Surgery, AIIMS,Raipur, Chhattisgarh, India
2 Department of Obstratics and Gynacology, AIIMS,Raipur, Chhattisgarh, India
3 Department of Pharmacology, N. S. C. B. Medical College, Jabalpur,Madhya Pradesh, India
4 Department of Trauma and Emergency, AIIMS,Raipur, Chhattisgarh, India
5 Department of Orthopaedics, AIIMS,Raipur, Chhattisgarh, India
|Date of Web Publication||23-Sep-2013|
Department of Surgery, All India Institute of Medical Sciences, Tatibandh, G. E. Road, Raipur - 492 099, Chhattisgarh
Source of Support: None, Conflict of Interest: None
The burn patients need a very special care as besides skin burn; they can have associated mechanical injuries, inhalational injury and altered physiology with the risk of hypothermia. Once the patient survives from the acute phase, the appropriate wound management is the further challenge. The psychological trauma starts from time of injury to long after survival. Thus focused approach of burn patients allows critical care support, early surgical excision and closure of the burn wounds, patient and family psychosocial support, patient and family education, continuous long-term rehabilitation, re-entry into the society and reconstructive surgical needs.
Keywords: Burn, electric burn, inhalation injuries, thermal injuries
|How to cite this article:|
Singh S, Agrawal S, Agrawal M, Borkar NK, Agrawal AC. Burns and thermal injuries. J Orthop Traumatol Rehabil 2013;6:47-57
|How to cite this URL:|
Singh S, Agrawal S, Agrawal M, Borkar NK, Agrawal AC. Burns and thermal injuries. J Orthop Traumatol Rehabil [serial online] 2013 [cited 2021 Apr 11];6:47-57. Available from: https://www.jotr.in/text.asp?2013/6/1/47/118756
| Introduction|| |
Comprehensive care of patients with thermal injuries involves surgical decision making, critical care management, rehabilitation and psychosocial interventions. The clinical goals are returning patients to their pre-morbid level of function.
| Epidemiology|| |
The annual incidence of thermal injuries is unknown. However, data from 2003 Centers for Disease Control suggests that approximately 1 million burn injuries occur annually in the United States. About 45,000 of these require hospitalization and about 4,500 die. Nearly, one-half of burn cases are smoking related or due to substance abuse. , Usually, very young/old, the impaired and lower socio-economic groups are involve.  Almost 95% of burn patients in the U.S. now survive and over one-half of them return to pre-burn levels of physical and social functioning. , In children, most common burns are scalds.  In older children and adults, most common burns are flame-related.  Chemicals or hot liquids, followed-by electricity and then molten or hot metals most often cause work-related burns. 
Scalds (from hot water) are the most common cause of burns. Boiling water and thick soups always causes deep burns.  Flame burns are the second most common mechanism, although the incidence of house fires has decreased with the use of smoke detectors. The smoking-related fires, improper use of flammable liquids, motor vehicle collisions and ignition of clothing by stoves or space heaters also are responsible for flame burns.  Flash burns occurs by explosions of natural gas, petroleum and alcohols.  Contact burns result from contact with hot metals, plastic, glass or hot coals. They are invariably deep.
More than 90% of burns are preventable.  Critical legislative actions, such as mandating flame-resistant sleepwear for children, smoke detectors in all residential units, maximum temperature for home and public hot water heaters be set to below 140°F (60°C), likely contributed to decreased burn severity and mortality. 
Burn center verification and a national burn registry
In 1995, the American College of Surgeons-Committee on Trauma, with the American burn Association initiated a program of Burn Center Verification. A detailed document outlines the resources and processes necessary to provide optimal care of the burn patient.  A national burn registry is kept by U.S. and Canadian burn centers to provide the national statistics regarding incidence, epidemiology and outcome of burn cases.
| Management|| |
All burn patients that meet American Burn Association criteria [Table 1] should transfer to a burn center.
Care at the scene
Once flames are extinguished, initial attention must be directed to the airway, breathing and circulation according to Advanced Cardiac Life Support guidelines. In electrical injuries or severe carbon monoxide (CO) poisoning cardiopulmonary resuscitation may be needed. Once an airway is secured, the secondary survey continued while patient is being transported to the Burn center. Patients should be kept flat, warm, wrapped in a clean sheet and blanket. The intravenous line and lactated Ringer's solution should be started. Before or during transport, constricting clothing and jewelry should be removed. Small burns (scalds) may be treated with immediate application of cold water but, never used ice in >5% of burn (as increases the risk of hypothermia). Although, cooling can't reduce skin tempera, but it delays edema formation (reducing thromboxane production).  If several minutes have elapsed cooling does not alter the pathologic process. Iced water should never be used because of risk of systemic hypothermia and cutaneous vasoconstriction can extend the thermal damage. 
Emergency room care
The airway, breathing and circulation protocol must be strictly followed. The formula (Age + % total body surface area (TBSA) burn = mortality) for predicting mortality is not reliable. , Age older than 60 years, full-thickness burn size over 40% of the TBSA and the presence of inhalation injury were found to be important prognostic factors. , Because the zones of injury in a burn wound evolve for up to 72 h, burn depth determination at the initial examination can be erroneous. Home management often fails because insufficient teaching to inadequate pain control, wound infection and limited movement.  A short hospital stay allows the patient to learn how to properly clean and dress the burn.
For major burns >20% TBSA, once-daily dressing changes are adequate. Burns can be washed with tap water and non-perfumed soap.  Using a daily soapy wash cloth to wipe the topical ointment and bacteria provides adequate wound care. There is no need to scrub the wound to debride superficial exudates. Intact blisters provide protective biologic dressing. Blisters should incise only if they limit mobility.  A common misconception is that joint immobilization promotes burn wound healing. In reality, extremity immobilization leads to swelling, which worsens tissue injury. 
| Burn Pathophysiology|| |
Jackson's 1953 described three zones of tissue injury. The central, most severely damaged area is the zone of coagulation or necrosis and is irreparably injured (represents a full-thickness or third degree burn). It must be debrided and grafted. Surrounding this is a zone of stasis, characterized by vasoconstriction and ischemia. With careful wound management, this partial-thickness burn (or second degree) can convert to a shallower wound or deeper burn (depending upon edema, infection, or poor perfusion). The outer most area is the zone of hyperemia or superficial partial-thickness burn, which heals quickly without scarring. Superficial burns such as sunburns are often referred to as first-degree burns and are not included in burn size calculations. 
Tissue repair begins immediately following injury. Interestingly, animal studies suggest that exogenous tissue plasminogen activator promotes conversion of the zone of stasis in an acute burn wound to a zone of hyperemia.  After initial vascular constriction, vasodilatation and capillary leak occur in the resuscitative phase, which cause pulmonary edema, compartment syndrome and conversion of burns to a deeper injury. Many inflammatory cytokines, interleukins, prostaglandins, sensory nerve-derived neuropeptides, adhesion molecule upregulation and fibroblast proliferation is induced by serotonin, histamine, bradykinin, arachidonic acid metabolites.  In burn wounds, the zone of stasis may convert to a zone of coagulation with neutrophil-mediated reperfusion injury. Whereas, inhibition of the neutrophil-endothelial adherence in deep dermal rabbit contact burns speeds healing. 
Granulation tissue is clinical evidence that a wound is healthy and is ready for closure.  The delivery of oxygen and nutrients to a skin graft by "imbibition" or "diffusion" suffices for a few days. Skin graft take requires inosculation (linkage between existent capillaries in the graft and in the wound bed). Debridement of excess granulation tissue is must before applying a skin graft to eliminate the bacterial contamination, exuberant inflammatory response and decrease risk of hypertrophic scar formation in the healed wound. 
Full-thickness wounds heal from the wound edges while partial-thickness wounds heal from epidermal appendages (i.e., hair follicles, sweat glands and sebaceous glands) in the wound bed.  Epidermal-dermal interactions regulate cutaneous morphogenetic processes; hence, partial-thickness wound coverage with viable allograft eliminates granulation tissue formation and promotes healing.  Fibroblast synthesize collagen III and subsequently collagen I (characteristic of dermal scar). As collagen I fibrils are cross-linked, dermal breaking strength increases, but never meet that of uninjured skin. Matrix remodeling causes wound maturation at 12-24 months. Wound closure occur by contraction of Myofibroblasts, pathologic extension of which over joints is a "contracture." In epidermis Melanocytes migrate from the wound edge and from epidermal appendages. Pigmentation in healed burn wounds is unpredictable (either increased or decreased).  The exposure to ultraviolet rays may exacerbate pigmentation. Use of topical bleaching agents should be discouraged. Hypertrophic scars, which are very pruritic, have increased numbers of sensory nerves compared with the normal scars. 
| Systemic Response to Burn Injury|| |
Cutaneous inflammatory cells from the injured tissue release mediators that drive the systemic response leading to accelerated intravascular volume depletion, inadequate tissue perfusion and ultimately risk of multi-organ dysfunction. The leak associated with a burn larger than 30% TBSA (or smaller if there is concomitant inhalation injury) can cause clinically significant interstitial edema. The potential morbidity from the edema includes compartment syndrome in injured and non-injured extremities, abdominal compartment syndrome and pulmonary edema leading to the development of respiratory distress syndrome.
| Type of Burn|| |
Epidermal burns (first-degree)
These burns involve only the epidermis. They do not blister, but become erythematous and are quite painful. Over 2-3 days the erythema and pain subside. By about the fourth day, the injured epithelium desquamates in the phenomenon of peeling, which is well-known after sunburn.
Superficial partial-thickness (second-degree)
It includes upper layers of the dermis and characteristically form blisters with fluid collection at the interface of the epidermis and dermis. When blisters are removed, the wound is pink and wet; currents of air passing over it cause pain. The wound is hypersensitive and the burns blanch with pressure. If infection is prevented, superficial partial-thickness burns heal spontaneously in less than 3weeks and do so without functional impairment. They rarely cause hypertrophic scarring, but in pigmented individuals the healed burn may never completely match the color of the surrounding normal skin.
Deep partial-thickness (second-degree)
Deep partial-thickness burns extend into the reticular layers of the dermis. They also blister, but the wound surface is usually a mottled pink-and-white color immediately after the injury (white areas have little to no blood flow and pink areas have some blood flow). Patient complains of discomfort rather than pain. When pressure is applied to the burn, capillary refill occurs slowly or may be absent. The wound is often less sensitive to pinprick than the surrounding normal skin. By the second day, the wound may be white and is usually fairly dry. If not excised and grafted and if infection is prevented, these burns will heal in 3-9 weeks, but with scar formation; hence, joint function can be impaired.
It involves all layers of the dermis and heals only by wound contracture, epithelialization from the wound margin or skin grafting. They appear white, cherry red or black and may or may not have deep blisters. Full-thickness burns are described as being leathery, firm and depressed when compared with adjoining normal skin and they are insensate. They may be mottled in appearance, rarely blanch on pressure and may have a dry, white appearance. Immersion scalds, have a red appearance and initially may be confused with superficial partial-thickness burns; however, they do not blanch with pressure. Full-thickness burns develop a classic burn eschar (dead and denatured dermis) that if left in situ over days and weeks, separates from the underlying viable tissue.
It involves all layers of skin with subcutaneous fat and deeper structures. These burns have a charred appearance. Electrical burns, contact burns, some immersion burns and burns sustained by patients who are unconscious at the time of burning may all be fourth-degree.
Burn depth indicators are laser Doppler flow meters, IV fluorescein, burn wound biopsy, thermography, light reflectance, magnetic resonance imaging and IV dyes. , However, no technology has been proven more accurate than an experienced burn surgeon. Evaluation by an experienced surgeon as to whether a partial-thickness burn will heal in 3 weeks is about 70% accurate. To estimate the burn size Wallace rule of nines in which each arm is considered as 9% TBSA, each leg 18%, the anterior trunk 18%, the posterior trunk 18% and the head 9%. This method underestimates head size in children. Another methods for the patient's full palm including digits represent 1% TBSA. First-degree burns should not be included in the calculation of burned areas. 
If the history of exposure to noxious fumes is there, arterial PaO 2 , PaCO 2 , pH and carboxyhemoglobin percentage should obtain. Routine hematology and chemistry profiles have limited use, but baseline electrolyte levels and renal function (blood urea nitrogen, creatinine) and hematocrit, white blood cell count and platelet count should be establish. The efficacy of base deficits and lactic acid levels has not been established in burn patients. Urinalysis helpful to diagnose myoglobinuria in electrical injuries or deep thermal burns, but if the urine appears clear, treatment is not warranted. Need for radiographical assessments must be based on the mechanism of injury, but a baseline chest radiograph is sufficient for an isolated burn without other evidence of trauma.
Inhalation injury complicates approximately one-third of all major burns. , Diagnosis should be considered for any patient involved in a closed space fire. Clues are singed nasal hairs and facial burns. Hoarseness, wheezing or stridor suggest pharyngeal swelling and indicate a potential need for intubation. In these patients, direct laryngoscopy should be performed to confirm posterior pharyngeal mucosal sloughing or carbonaceous sputum coming up through the vocal cords. Patients with large burns who receive massive IV resuscitation volumes should be intubated for airway protection as swelling progresses. Nasotracheal intubation should be avoided if possible, because risks of sinusitis and erosion of nasal columella is there (especially if nose is burned). Intubated patients with inhalation injuries should have the head of their bed elevated to at least 45° to reduce the swelling and to prevent the aspiration. CO toxicity is the most commonly diagnosed form of inhalation injury. CO toxicity is treated with 100% inhaled oxygen (accelerates CO dissociation from hemoglobin). Hyperbaric is appropriate for isolated CO toxicity with impaired neurologic status and markedly elevated carboxyhemoglobin level (25%). 
Hydrogen cyanide toxicity disrupts cellular oxidation and causes lactic acidosis, which resolves with ventilation in most patients without the need for sodium thiosulfate treatment. 
Upper airway burns can be diagnosed by direct visualization of posterior pharynx. Treatment includes observation and provision of humidified oxygen, pulmonary toilet, bronchodilators (as needed) and endotracheal intubation (as indicated). Upper airway thermal burns usually manifest within 48 h of injury and airway swelling usually is maximal 12-24 h after the injury. A patient with an upper airway burn may require airway protection for 72 h. In a patient with a small burn (<15%), a short course of systemic or inhaled steroids may facilitate earlier resolution of airway edema, but steroids are contraindicated in patients with large burns due to the risk of infection and failure to heal. 
Lower airway burn (tracheobronchial tree and lung parenchyma) injury cause damage and loss of ciliary clearance; hence debris induces parenchymal inflammation, microvascular permeability and ultimately may progress to pulmonary edema, pneumonia or acute respiratory distress syndrome (ARDS). Aerosolized toxins can reduce myocardial contractility and cause resuscitation failure. The diagnosis can be confirmed by bronchoscopy or xenon ventilation-perfusion scan. Successful treatment requires aggressive pulmonary toilet and frequent chest physiotherapy. 
ARDS is an independent risk factor for death (mortality rate of 40-70%) in burn patients.  It develops within 7 days after injury. Inhalation injury have 73% incidence of respiratory failure (defined by hypoxemia, pulmonary infections or prolonged ventilator support) and a 20% incidence of ARDS, compared with burn patients without inhalation injury 5% and 2% respectively. 
| Fluid Resuscitation|| |
Vascular access should be obtained early before swelling obscures venous markings. Burns more than 50% TBSA should resuscitated through two large-bore peripheral intravenous lines. Because of the high incidence of septic thrombophlebitis, lower extremities should not be used as portals for peripheral intravenous lines. Upper extremities are preferable, even if the intravenous line must pass through burned skin or eschar. Patients with >50% TBSA burn, associated medical problems, extremes of age and concomitant inhalation injuries should have additional central venous access established with invasive hemodynamic monitoring.
Fluid volumes should be constantly adjusted based on physiologic responses (urine output, altered sensorium, pulse and blood pressure).  Patients may require more or less fluid depending on the depth of burn (deeper burns are associated with a greater inflammatory response and more fluid needs), presence of inhalation injury, associated injuries or co-morbidities.
The Baxter (or Parkland) formula state 3-4 mL of crystalloid per percentage of TBSA burn over 24 h. Half of this volume is delivered during the first 8 h after injury; the other half is delivered in subsequent 16 h. Resuscitation endpoints include mean arterial blood pressure >60 mm Hg and urine output of 30 mL/h for adults.
Crystalloid boluses should be restricted to hypotensive episodes (mean arterial pressure <65 mm Hg) and should be accompanied by an increase in the hourly volume by 10%. Decreased urine output for 1 or 2 h can be managed by increasing the hourly resuscitation fluid rate by 10%. As capillary leak resolves (12-48 h), maintenance fluids should progressively weaned by 10%/h. Pulmonary artery catheter is useful only in patients having risk for cardiac shock and congestive heart failure. Patients with extremely deep burns, electrical burns or compartment syndrome may develop rhabdomyolysis with myoglobinuria and subsequent acute tubular necrosis. In these patients, maintaining urine output of 100 ml/h is indicated. Alkalinization of the urine with intravenous sodium bicarbonate (0.12-0.5 mEq/kg/h) theoretically increases myoglobin solubility and decreases precipitation in the renal tubules, but requires careful serum pH monitoring and is not routinely implemented. Osmotic diuresis with mannitol reduces urine output reliability as an endpoint for determining intravascular volume status. Colloid administration after the capillary leak has closed may restore intravascular volume in patients with persistent low urine output and hypotension despite adequate crystalloid administration. In such cases, 5% albumin (0.3-0.5 ml/kg/% TBSA burn) can be administered over 24 h.
Indications for plasmapheresis (removes circulating cytokines) include a sustained Mean Arterial Pressure of <60 mm Hg and Urine output <30 ml/hr in patients whose ongoing fluid needs are more than twice fluid volume estimates. 
Previous immunization within 5 years requires no tetanus toxoid, immunization within 10 years requires a tetanus toxoid booster and unknown immunization status requires hyper-immune serum with tetanus toxoid. 
Lactated Ringer's solution is the primary resuscitative fluid. The resuscitative fluid solution should not contain glucose because hyperglycemia and osmotic diuresis may confound resuscitation.
Once resuscitation is complete (24-48 h post-injury), insensible losses and hyperthermia associated with a hyperdynamic state may require increased ongoing maintenance IV or enteral fluid administration.
Over resuscitation causes poor tissue perfusion, abdominal or extremity compartment syndrome, pulmonary edema and pleural effusion. Burn extremities should be elevated and hourly neurovascular examinations should be done. Circumferential extremity and chest eschar need escherotomies. Circumferential chest burns also need thoracic escharotomies. Extremity escharotomies should extend through the skin only and should not violate the fascia. Eschar on the dorsal hand must release to restore vascular signals in the palmar arch; there is no benefit to digital escharotomies and risk of injury to the digital arteries and nerves is significant. Increased abdominal pressure (exceeding 25 mm Hg) may need bedside decompressive laparostomy through burn wounds.  Psychosocial care should begin immediately. The patient and family must be comforted and be given a realistic assessment regarding the prognosis of the burns.
| Wound Management|| |
Prophylactic systemic antibiotics do not have a role in the patient with acute burn injuries.  Because eschar is devitalized and avascular, systemic antibiotics cannot reach the eschar surface, where the bacterial colonization occurs. Topical antimicrobial agents delay wound colonization and infection but they in themselves have not changed mortality in the way that early excision and grafting has. All agents have benefits and side effects [Table 2] Mafenide acetate penetrates eschar, making it effective in both treating and preventing burn wound infections. It is often use on ears to protect against suppurative chondritis.  Dressings must be irrigated with the aqueous 0.5% solution of silver nitrate, every 4 h. Because concentrated silver nitrate causes a chemical burn, so always use hypotonic solution (it is reconstituted in water rather than saline to avoid silver chloride precipitation). Excess hypotonic solution may cause osmotic dilution in the tissues leading to hyponatremia and hypochloremia. Bacitracin, neomycin and polymyxin B is used for coverage of superficial wounds in conjunction with petrolatum gauge [Table 2]. Acticoat dressings are impregnated with elemental silver (disrupting bacterial cellular respiration). The Acticoat dressing decreases need for dressing changes.
| Burn Excision and Grafting|| |
The beneficial impact of early excision and grafting changed therapy from a non-operative to an operative approach. , It include increase survival, shortened hospital stay, lower costs and fewer reconstructive surgeries. By 3-4 days after injury, burn excision and wound coverage is the safe option. Staged excisions can be performed every 2-3 days until the entire burn wound is excised. The burn having both shallow and deep areas can be safely treated with topical antimicrobial ointment for 7-10 days until the deeper portion that requires grafting becomes evident. Surgical excision is performed either by fascial excision or tangential excision. Once the eschar is excised to viable tissue, the wound should be closed as soon as possible, ideally with immediate autografting. Human allograft is one temporary biologic dressing. Porcine xenograft is a cheaper alternative. Epidermal skin substitutes consisting of cultured autologous keratinocytes with or without a subjacent layer of autologous fibroblasts. , Integra dermal template is commercially available product, designed to be combined with ultrathin autograft or cultured epithelium.  Once the product is vascularized (2-3 weeks), an ultrathin autograft can be placed on the neodermis. Another promising dermal substitute is Allo Derm, a cryopreserved human dermal allograft.
| Metabolic and Neuroendocrine Response|| |
Patients with major thermal injury develop a hypermetabolic state characterized by increased basal metabolic rate, increased oxygen consumption, negative nitrogen balance and weight loss.  Thus, have increased caloric requirements to prevent delayed wound healing, decreased immune competence and cellular dysfunction. Catecholamines are massively elevated following burn injury and are mediators of the hypermetabolic response. Pharmacologic beta-blockade diminishes the intensity of post-burn hypermetabolism in pediatric patients. , Total thyrxine and T4 concentrations are decreased and T3 concentrations are elevated.  Burn injuries abolish the normal diurnal variation in glucocorticoid secretion, producing persistent hypercortisolemia. 
The catabolic state continues until the wounds are closed. The Harris-Benedict equation estimates basal energy expenditure according to gender, age, height and weight. The basal energy expenditure is multiplied by an activity factor that reflects the severity of injury or the degree of illness; for burns, this multiplier is 2.  This equation overestimates caloric needs for moderate burn size. The Curreri formula based on patient weight and burn size overestimates caloric needs for patients with large burns and is best used for small - or moderate-sized burns (<40% TBSA).  Total blood urea nitrogen, serum albumin levels are not sensitive markers (typically low in >20% TBSA burn). Transthyretin or prealbumin levels correlate more closely with catabolic status. C-reactive protein levels may correlate with catabolic status.  Indirect calorimetry by quantifying oxygen consumption and carbon dioxide expiration help in calculating nutritional requirements. Pulmonary artery catheters by Fick equation can also give an idea. Prolonged ileus and gastric stress ulcers in burn patients can be eliminated by early feeding.  Hyperglycemia increases risk of infection, decrease skin graft take and higher mortality. 
Hypoalbuminemia generally persists (usually <2.5 g/dL) in burn patients until the wounds are healed. Administration of exogenous albumin to attain serum levels above 1.5 g/dL does not appear to impact the length of stay, complication rate or mortality.  Role of arginine, glutamine and omega-3 fatty acids in burn patients are contradictory.  However, the anabolism can be promoted in burn patients with insulin, recombinant human growth factor, anabolic steroid oxandrolone and propranolol. ,, Early administration of antioxidants, alpha-tocopherol and ascorbic acid reduces the incidence of organ failure.
To limit development of opportunistic infections, targeted systemic antibiotics should be used.
The incidence of deep vein thrombosis (DVT) is 25% but cause 0.14% of deaths.  Hence, a standard of care for DVT prophylaxis in burn patients has never been defined. 
Hematocrit of 20% is well tolerated by healthy patients. But, inhalation injury, severe infection or unstable cardiac ischemia may require higher hematocrit. 
| Pain Management|| |
The burn patients experience three different classes of pains "background, breakthrough and procedural pain," which require different approaches.
Background pain occurs 24 h until their wounds are healed; long-acting pain relievers are well-suited for this type of discomfort. Long acting narcotics may relieve the pain. Breakthrough pain occurs when exercise or other activities of daily living exacerbate background burn wound discomfort. Short-acting narcotics or acetaminophen can alleviate this pain. Procedural pain occurs during the wound care and usually requires treatment with a short-acting narcotic. ,
Non pharmacologic approaches (Hypnosis, Virtual reality) can augment pain management in burn patients. New stinging pain may indicate a superficial wound infection. , Discomfort in the healed wound due to paresthesias and itching may persist; exercise and deep massage are effective modalities that patients should be encouraged to use. Diphenhydramine, cyproheptadine, cetirizine, doxepin ointment may also abrogate itching in healed wounds. ,
| Other Care|| |
The face is commonly treated non-operatively with topical antimicrobial agents for 10 days.  Periocular burns can lead to edema, conjunctival desiccation, keratitis and corneal ulceration. Lubrication with ophthalmologic antibiotics is mandatory but tarsorrhaphy may be necessary. If the lid burns are deep, earlier excision and skin grafting may be indicated. Ear burns must be treated with mafenide cream. More importantly, pressure on the burned auricle from pillows and tight dressings or ties should be avoided.
Active/passive range of motion should be the goal for all hand burns. Hands should immobilize in a functional position for 5 days after surgery to prevent shearing of the graft before range of motion exercises are resumed. Deeper hand burns that involve the extensor mechanisms, joint capsules or bone, often require temporary or long-term axial Kirschner wire fixation of open and unstable interphalangeal or metacarpophalangeal joints. Full-thickness injuries that do not heal in 3-4 weeks or show signs of healing by contraction should be grafted with full-thickness or thick split-thickness sheet grafts and splinted in extension to maintain the palm in an open position. Likewise, burns of the plantar surface of the feet should be grafted with full or split-thickness sheet grafts if they fail to heal within 3 weeks.
Genital burns indicate an investigation for abuse or neglect. A burned foreskin must be reduced to a normal position so edema does not cause paraphimosis.  Urethral stenting and bladder catheter drainage are not required for genital burn management and increase the risk of urinary tract infection.  Bladder catheters should be removed when close monitoring of the urine output is no longer required. Likewise, with aggressive wound care, diversion of the intestinal tract is not required in the management of perineal burns.
| Miscellaneous Burn Injuries|| |
Electrical flash burns occur when a high-voltage current arcing from a high-tension wire toward a human being generates heat and produces a flash skin burn; this should not be confused with an electrical injury. Low-voltage injuries (less than 1,000 volts) may cause locally destructive injuries. High-voltage injuries (more than 1,000 volts) can cause local destruction; a deep-tissue injury where the current crosses joints; flash burns or deep flame burns if clothing ignites; axial spine fractures due to tetanic contraction of paravertebral muscles; and other blunt injuries related to a fall. Hence, patients with high-voltage electrical burns require a complete trauma evaluation including radiographic skeletal series, cardiac monitoring and bladder catheterization to evaluate the urine for the presence of myoglobinuria and serial neurovascular examinations in extremities at risk for compartment syndrome; carpal tunnel syndrome and impaired median nerve function. They may warrant immediate fasciotomy or carpal tunnel release.
A low-voltage electrical injury occurs when a child puts an electrical extension cord into mouth. Thus, lateral angle mouth burn can led to delayed bleeding from the facial artery (when eschar falls off) and delayed contracture.
Late sequel of high-voltage electrical injuries includes progressive demyelinating sensory and/or motor neurologic loss and early cataract formation.
Regardless of whether a chemical burn is alkali or acid, initial treatment is copious irrigation with tap water for 30 min Cement and concrete powder or powdered lye should be brushed dry from the patient because contact with water activates the aluminum hydroxide.
Hydrofluoric acid does have a specific antidote because exposure can induce life-threatening hypocalcemia.  In addition to irrigation with water, topical calcium gluconate gel can be soothing, sometimes with calcium gluconate intra-arterial infusion with cardiac monitoring needed.
Adherent tar can be cooled by tap water irrigation and should wash with lipophilic solvent, as there may be non-burned skin beneath the tar, which may unnecessary increase the amount of resuscitating fluid.
| Non-accidental Burn Injury|| |
Non-accidental Burn injury, should be admitted to the hospital. If examination suggests injuries to be suspicious radiographic evaluation of the head, ribs and long bones should be obtained for further documentation of other types of abuse; ophthalmologic evaluation to rule out retinal detachment. Likewise, suggestion of a self-induced burn injury should trigger admission for psychological evaluation. Patients with language barriers may also benefit from a brief hospital admission to be sure they understand the treatment plan. Underinsured and homeless patients may not have the resources to care for a wound outside the hospital and should be admitted for initial wound care and comprehensive discharge planning.
Posttraumatic stress, anxiety or depression frequently manifest after severe burns. Pre-injury psychiatric conditions, family dysfunction, or substance abuse further complicate psychosocial recovery. The coordinated participation of burn psychologists and social workers is in the multi-disciplinary care of burn patients.
| Fractures in a Burn Patient|| |
A long bone fracture with burns on the overlying skin is considered a potentially open fracture and demands extra care to avoid infection. It is really difficult to stabilize these fractures in plaster of Paris casts or splints because the burn wound demands cleaning and dressings too. Repeated dressings make the wound unstable with excessive pain and chances of neurogenic shock. Internal fixation with plates and screws is not desirable due to the risk of infection associated. Long bone fractures with burns usually need an external fixator application so that the fracture is stable, the limb can be moved and it also permits cleanings and dressings. The external fixator may be applied as a temporary measure until the skin wound heels or split skin graft (SSG) is done or as a definitive method too once it is applied in an acceptable anatomic position.
| Burn in children|| |
Pediatric case are unique as their thin skin increases severity of burning, large surface/volume ratio cause rapid fluid and heat loss lead to hypothermia, delicate balance between dehydration and over hydration, immature immunological response increases the risk of sepsis. Always consider possibility of child abuse in burn children [Figure 1] and [Figure 2]. Resuscitation fluid in children less than 2 years should have dextrose solution to decrease the risk of hypoglycemia. Pediatric patients weighing <20 kg should receive 0.45% half normal saline with 5% dextrose as maintenance rate (3-4 ml/kg/h). The fluid deficit in children is based on surface area as large surface area/volume ration in children need extra fluid requirement in them compared to adult. The formula usually used is Galveston formula (5,000 mL/% burn + 2000 mL/m 2 TBSA). Half of this calculated amount should give in 1 st 8 h and Ό amount each in next 8 h. Pediatric fluid requirements often exceed estimated formula(less developed renal concentrating abilities). The targeted urine output in children <30 kg should be 1 mL/kg/h. The target further increases to 2 ml/kg/h in case of myoglobineurea.
|Figure 1: Modified "rule of nine" according to age, for burn size assessment|
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|Figure 2: Standard nomogram for the determination of body surface area based on height and weight. A straight line drawn between the height and weight measurements determines the total body surface area in square meters|
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| Burn Injury in Pregnancy|| |
Burn injuries during pregnancy are common in developing countries like India. Burn incidences in pregnancy reported in India, ranging from 7% to 15%. ,
Multiple factors influence morbidity and mortality viz depth and size of the burn, the woman's underlying health, age, estimated gestational age of the fetus, associated inhalation injury and development of other significant secondary complications. Fetal survival depends upon the gestational age, extent of maternal injury and maternal survival [Table 3].  There is a linear co-relationship between the maternal total percentage of burns and the probability of death. In parturient with 25-50% TBSA burn the mortality rates reach 63% for both the mother and the fetus. 
| Rehabilitation and Reconstruction|| |
The National Institute of Disability and Rehabilitation Research, has continuously funded projects to advance knowledge in burn rehabilitation. The occupational and physical therapists started from the time of acute injury until long after discharge from the hospital.
| Conclusion|| |
To conclude, a well-coordinated burn center team, having surgeons, nurses, physical/occupational therapists, social workers, psychologists and pain specialists, is required to both optimize survival and minimize dysfunction in the burn patient.
| References|| |
|1.||Grobmyer SR, Maniscalco SP, Purdue GF, Hunt JL. Alcohol, drug intoxication, or both at the time of burn injury as a predictor of complications and mortality in hospitalized patients with burns. J Burn Care Rehabil 1996;17:532-9. |
|2.||Barillo DJ, Brigham PA, Kayden DA, Heck RT, McManus AT. The fire-safe cigarette: A burn prevention tool. J Burn Care Rehabil 2000;21:162-4. |
|3.||Wrigley M, Trotman BK, Dimick A, Fine PR. Factors relating to return to work after burn injury. J Burn Care Rehabil 1995;16:445-50. |
|4.||Brych SB, Engrav LH, Rivara FP, Ptacek JT, Lezotte DC, Esselman PC, et al. Time off work and return to work rates after burns: Systematic review of the literature and a large two-center series. J Burn Care Rehabil 2001;22:401-5. |
|5.||Herndon DN, Spies M. Modern burn care. Semin Pediatr Surg 2001;10:28-31. |
|6.||Islam SS, Nambiar AM, Doyle EJ, Velilla AM, Biswas RS, Ducatman AM. Epidemiology of work-related burn injuries: Experience of a state-managed workers' compensation system. J Trauma 2000;49:1045-51. |
|7.||Yarbrough DR 3 rd . Burns due to aerosol can explosions. Burns 1998;24:270-1. |
|8.||Liao CC, Rossignol AM. Landmarks in burn prevention. Burns 2000;26:422-34. |
|9.||Hospital and prehospital resources for optimal care of patients with burn injury: Guidelines for development and operation of burn centers. American Burn Association. J Burn Care Rehabil 1990;11:98-104. |
|10.||Heggers J, Robson M, London M. Cooling and the prostaglandin effect in the thermal injury. J Burn Care Rehabil 1990;11:98-104. |
|11.||Sawada Y, Urushidate S, Yotsuyanagi T, Ishita K. Is prolonged and excessive cooling of a scalded wound effective? Burns 1997;23:55-8. |
|12.||Hammond JS, Ward CG. Transfers from emergency room to burn center: Errors in burn size estimate. J Trauma 1987;27:1161-5. |
|13.||Heimbach D, Engrav L, Grube B, Marvin J. Burn depth: A review. World J Surg 1992;16:10-5. |
|14.||Gibren NS. Burns. In: Mulholland MW, Lilymoy KD, Dohery GM, Maier RV, Upchurch GR, editors. Greenfield's Scientific Principles and Practice. 4 th ed. Philadelphia: Lippincot Williams and Willkins; 2006. p. 501-69. |
|15.||Iþik S, Sahin U, Ilgan S, Güler M, Günalp B, Selmanpakoðlu N. Saving the zone of stasis in burns with recombinant tissue-type plasminogen activator (r-tPA): An experimental study in rats. Burns 1998;24:217-23. |
|16.||Arturson G. Pathophysiology of the burn wound. Ann Chir Gynaecol 1980;69:178-90. |
|17.||Bucky LP, Vedder NB, Hong HZ, Ehrlich HP, Winn RK, Harlan JM, et al. Reduction of burn injury by inhibiting CD18-mediated leukocyte adherence in rabbits. Plast Reconstr Surg 1994;93:1473-80. |
|18.||Bloch W, Huggel K, Sasaki T, Grose R, Bugnon P, Addicks K, et al. The angiogenesis inhibitor endostatin impairs blood vessel maturation during wound healing. FASEB J 2000;14:2373-6. |
|19.||Bohnert A, Hornung J, Mackenzie IC, Fusenig NE. Epithelial-mesenchymal interactions control basement membrane production and differentiation in cultured and transplanted mouse keratinocytes. Cell Tissue Res 1986;244:413-29. |
|20.||Crowe R, Parkhouse N, McGrouther D, Burnstock G. Neuropeptide-containing nerves in painful hypertrophic human scar tissue. Br J Dermatol 1994;130:444-52. |
|21.||Afromowitz MA, Callis JB, Heimbach DM, DeSoto LA, Norton MK. Multispectral imaging of burn wounds: A new clinical instrument for evaluating burn depth. IEEE Trans Biomed Eng 1988;35:842-50. |
|22.||Atiles L, Mileski W, Purdue G, Hunt J, Baxter C. Laser Doppler flowmetry in burn wounds. J Burn Care Rehabil 1995;16:388-93. |
|23.||Gibran NS, Endorf FW. Burns. In: Brunicardi FC, Anderson DK, Hunter JG, Billiar TR, Mathews JB, Dunn DL, et al., editors. Schwartz's Principles of Surgery. 9 th ed. USA: McGraw Hills; 2010. p. 209-34. |
|24.||Rue LW 3 rd , Cioffi WG, Mason AD, McManus WF, Pruitt BA Jr. Improved survival of burned patients with inhalation injury. Arch Surg 1993;128:772-8. |
|25.||Hantson P, Butera R, Clemessy JL, Michel A, Baud FJ. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest 1997;111:671-5. |
|26.||Hampson NB, Zmaeff JL. Outcome of patients experiencing cardiac arrest with carbon monoxide poisoning treated with hyperbaric oxygen. Ann Emerg Med 2001;38:36-41. |
|27.||Barillo DJ, Goode R, Esch V. Cyanide poisoning in victims of fire: Analysis of 364 cases and review of the literature. J Burn Care Rehabil 1994;15:46-57. |
|28.||Hollingsed TC, Saffle JR, Barton RG, Craft WB, Morris SE. Etiology and consequences of respiratory failure in thermally injured patients. Am J Surg 1993;166:592-6. |
|29.||Graves TA, Cioffi WG, McManus WF, Mason AD Jr, Pruitt BA Jr. Fluid resuscitation of infants and children with massive thermal injury. J Trauma 1988;28:1656-9. |
|30.||Hobson KG, Young KM, Ciraulo A, Palmieri TL, Greenhalgh DG. Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma 2002;53:1129-33. |
|31.||Durtschi MB, Orgain C, Counts GW, Heimbach DM. A prospective study of prophylactic penicillin in acutely burned hospitalized patients. J Trauma 1982;22:11-4. |
|32.||Engrav LH, Richey KJ, Walkinshaw MD, Gottlieb JR. Chondritis of the burned ear: A preventable complication if... Ann Plast Surg 1989;23:1-2. |
|33.||Burke JF, Quinby WC, Bondoc CC. Early excision and prompt wound closure supplemented with immunosuppression. Surg Clin North Am 1978;58:1141-50. |
|34.||Gray DT, Pine RW, Harnar TJ, Marvin JA, Engrav LH, Heimbach DM. Early surgical excision versus conventional therapy in patients with 20 to 40 percent burns. A comparative study. Am J Surg 1982;144:76-80. |
|35.||Boyce ST, Kagan RJ, Yakuboff KP, Meyer NA, Rieman MT, Greenhalgh DG, et al. Cultured skin substitutes reduce donor skin harvesting for closure of excised, full-thickness burns. Ann Surg 2002;235:269-79. |
|36.||Heimbach D, Luterman A, Burke J, Cram A, Herndon D, Hunt J, et al. Artificial dermis for major burns. A multi-center randomized clinical trial. Ann Surg 1988;208:313-20. |
|37.||Heimbach DM, Warden GD, Luterman A, Jordan MH, Ozobia N, Ryan CM, et al. Multicenter postapproval clinical trial of integra dermal regeneration template for burn treatment. J Burn Care Rehabil 2003;24:42-8. |
|38.||Curreri PW, Richmond D, Marvin J, Baxter CR. Dietary requirements of patients with major burns. J Am Diet Assoc 1974;65:415-7. |
|39.||Sheridan RL, Prelack K, Cunningham JJ. Physiologic hypoalbuminemia is well tolerated by severely burned children. J Trauma 1997;43:448-52. |
|40.||Rettmer RL, Williamson JC, Labbé RF, Heimbach DM. Laboratory monitoring of nutritional status in burn patients. Clin Chem 1992;38:334-7. |
|41.||Raff T, Hartmann B, Germann G. Early intragastric feeding of seriously burned and long-term ventilated patients: A review of 55 patients. Burns 1997;23:19-25. |
|42.||Nathens AB, Neff MJ, Jurkovich GJ, Klotz P, Farver K, Ruzinski JT, et al. Randomized, prospective trial of antioxidant supplementation in critically ill surgical patients. Ann Surg 2002;236:814-22. |
|43.||Demling RH, Orgill DP. The anticatabolic and wound healing effects of the testosterone analog oxandrolone after severe burn injury. J Crit Care 2000;15:12-7. |
|44.||Van den Berghe G, Wouters PJ, Bouillon R, Weekers F, Verwaest C, Schetz M, et al. Outcome benefit of intensive insulin therapy in the critically ill: Insulin dose versus glycemic control. Crit Care Med 2003;31:359-66. |
|45.||Demling RH, DeSanti L. Oxandrolone induced lean mass gain during recovery from severe burns is maintained after discontinuation of the anabolic steroid. Burns 2003;29:793-7. |
|46.||Wahl WL, Brandt MM, Ahrns KS, Zajkowski PJ, Proctor MC, Wakefield TW, et al. Venous thrombosis incidence in burn patients: Preliminary results of a prospective study. J Burn Care Rehabil 2002;23:97-102. |
|47.||Still JM Jr, Belcher K, Law EJ, Thompson W, Jordan M, Lewis M, et al. A double-blinded prospective evaluation of recombinant human erythropoietin in acutely burned patients. J Trauma 1995;38:233-6. |
|48.||Honari S, Patterson DR, Gibbons J, Martin-Herz SP, Mann R, Gibran NS, et al. Comparison of pain control medication in three age groups of elderly patients. J Burn Care Rehabil 1997;18:500-4. |
|49.||Ohrbach R, Patterson DR, Carrougher G, Gibran N. Hypnosis after an adverse response to opioids in an ICU burn patient. Clin J Pain 1998;14:167-75. |
|50.||Groene D, Martus P, Heyer G. Doxepin affects acetylcholine induced cutaneous reactions in atopic eczema. Exp Dermatol 2001;10:110-7. |
|51.||Klein MB, Moore ML, Costa B, Engrav LH. Primer on the management of face burns at the University of Washington. J Burn Care Rehabil 2005;26:2-6. |
|52.||Vance MV, Curry SC, Kunkel DB, Ryan PJ, Ruggeri SB. Digital hydrofluoric acid burns: Treatment with intraarterial calcium infusion. Ann Emerg Med 1986;15:890-6. |
|53.||Akhtar MA, Mulawkar PM, Kulkarni HR. Burns in pregnancy: Effect on maternal and fetal outcomes. Burns 1994;20:351-5. |
|54.||Prasanna M, Singh K. Early burn wound excision in major burns with pregnancy: A preliminary report. Burns 1996;22:234-7. |
|55.||Mabrouk AR, el-Feky AE. Burns during pregnancy: A gloomy outcome. Burns 1997;23:596-600. |
|56.||Napoli B, D'Arpa N, Masellis M, Graziano R. Burns in pregnancy. Ann Burns Fire Disasters 2000;13:18-24. |
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3]