nurr 201 2) Burns

Assessment of the adequacy of fluid resuscitation is best made using clinical parameters. Urine output, the most commonly used parameter, and cardiac parameters are defined as follows:

1.Urine output: 0.5 to 1 mL/kg/hr (30-50mL/hr); 75 to 100 mL/hr for electrical burn patient with evidence of hemoglobinuria/myoglobinuria. 2.Cardiac factors: Mean arterial pressure (MAP) greater than 65 mm Hg, systolic BP greater than 90 mm Hg, heart rate less than 120 beats per minute. MAP and BP are most appropriately measured by an arterial line. Peripheral measurement is often invalid because of vasoconstriction and edema.

4. Rehabilitation phase pharmacological therapy

Application of water-based moisturizers and use of oral antihistamines (e.g., diphenhydramine [Benadryl]) help reduce the itching. Massage oil, silicone gel sheeting (e.g., Biodermis), gabapentin (Neurontin), and injectable steroids also may be helpful

1. Pre-hospital care- including airway management,

Airway: check for patency, soot around nares/on the tongue, singed nasal hair, darkened oral or nasal membranes. Breathing: check for adequacy of ventilation. Circulation: check for presence and regularity of pulses, and elevate the burned limb(s) above the heart to decrease pain and swelling.

4. Rehabilitation phase wound care

An emollient water-based cream (e.g., Vaseline Intensive Care Extra Strength) that penetrates into the dermis should be used routinely on healed areas to keep the skin supple and well moisturized, which will decrease itching and flaking. Therapy is aimed at the extension of body parts because the flexors are stronger than the extensors. Burned legs may be wrapped with elastic (e.g., tensor/Ace) bandages to assist with circulation to leg-graft and donor sites before ambulation. This additional pressure prevents blister formation, promotes venous return, and decreases pain and itchiness. Once the skin is completely healed and less fragile, custom-fitted pressure garments replace the elastic bandages. Continue to prevent or minimize contractures and assess likelihood for scarring (surgery, physical/occupational therapy, splinting, or pressure garments). • Discuss possible reconstructive surgery.

E. Nursing and collaborative management for the patient with burns. 4. Drug therapy

Analgesics are ordered to promote patient comfort. Early in the postburn period, IV pain medications should be given because (1) onset of action is fastest with this route; (2) GI function is slowed or impaired due to shock or paralytic ileus; and (3) intramuscular (IM) injections will not be absorbed adequately in burned or edematous areas, causing pooling of medications in the tissues. When fluid mobilization begins, the patient could be inadvertently overdosed from the interstitial accumulation of previous IM medications. opioids used for pain control Sedative/hypnotics and antidepressant agents can also be given with analgesics to control the anxiety, insomnia, and/or depression that patients may experience Tetanus toxoid is given routinely to all burn patients because of the likelihood of anaerobic burn wound contamination. (if not current within last 10 years) After the wound is cleansed, topical antimicrobial agents are applied and covered with a light dressing. (not oral because blood flow is diminished to burned areas) Silver-impregnated dressings (e.g., Acticoat, Silverlon, Aquacel AG) can be left in place anywhere from 3 to 14 days and are used in many burn centers. Silver sulfadiazine (Silvadene, Flamazine) and mafenide acetate (Sulfamylon) creams are also used. Sepsis remains a leading cause of death in the patient with major burns, which may lead to multiple organ dysfunction syndrome (see Chapter 67). Systemic antibiotic therapy is initiated when the clinical diagnosis of invasive burn wound sepsis is made, or when some other source of infection is identified (e.g., pneumonia). Fungal infections may develop in the patient's mucous membranes (mouth and genitalia) as a result of systemic antibiotic therapy and low resistance in the host. The offending organism is usually Candida albicans. Oral infection is treated with nystatin (Mycostatin) mouthwash. When a normal diet is resumed, yogurt or Lactobacillus (Lactinex) may be given by mouth to reintroduce the normal intestinal flora that have been destroyed by antibiotic therapy. For burn patients at risk for VTE (e.g., lower extremity burns, obesity) and if there are no contraindications, it is recommended that low-molecular-weight heparin (enoxaparin [Lovenox]) or low-dose unfractionated heparin (Hep-Lock) be started as soon as it is considered safe to do so. For burn patients who have a high bleeding risk, it is recommended that mechanical VTE prophylaxis with sequential compression devices and/or graduated compression stockings be used until the bleeding risk decreases and heparin can be started

D. Phases of burn management; nursing management in each phase, 1. Pre-hospital care

At the scene of the injury, priority is given to removing the person from the source of the burn and stopping the burning process. In the case of electrical injuries, initial management involves removal of the patient from contact with the electric source. If the burn is large (greater than 10% TBSA) or an electrical or inhalation burn is suspected, attention needs to be focused first on the ABCs: If CO intoxication is suspected, the patient should be treated with 100% humidified O2.

E. Nursing and collaborative management for the patient with burns. 6. Pain management

Burn patients experience two kinds of pain: (1) continuous, background pain that might be present throughout the day and night, and (2) treatment-induced pain associated with dressing changes, ambulation, and rehabilitation activities. The first line of treatment is pharmacologic With background pain, a continuous IV infusion of an opioid will allow for a steady, therapeutic level of medication. If an IV infusion is not present, slow-release, twice-a-day opioid medications (e.g., MS Contin) are indicated. Around-the-clock oral analgesics can also be used. Breakthrough doses of pain medication need to be available regardless of the regimen selected. Anxiolytics, which frequently potentiate analgesics, are also indicated and include lorazepam (Ativan) and midazolam (Versed). For treatment-induced pain, premedication with an analgesic and an anxiolytic is required via the IV or oral route. For patients with an IV infusion, a potent, short-acting analgesic, such as fentanyl (Sublimaze), is useful. During treatment/activity, small doses should be given to keep the patient as comfortable as possible. Elimination of all the pain is difficult to achieve, and most patients indicate satisfaction with "tolerable" levels of discomfort. Pain management is complex and ever-changing throughout the patient's hospital stay and after discharge. Pain can also be managed using nonpharmacologic strategies. Mind-body interventions, such as relaxation, guided imagery, hypnosis, biofeedback, and music therapy, are considered adjuncts to traditional pharmacologic treatment of pain. They are not meant to be used exclusively to control pain but may help some patients cope with the painful aspects of care, both in the hospital and after discharge Patients who are actively engaged in pain management have shown better outcomes. (PCA)

C. Classification of burn injury 1. location

Burns to the face and neck and circumferential burns to the chest/back may inhibit respiratory function due to mechanical obstruction secondary to edema or leathery, devitalized tissue formation (eschar). Burns of the hands, feet, joints, and eyes are of concern because they make self-care very difficult and may jeopardize future function. Burns of the hands and feet are challenging to manage because of superficial vascular and nerve supply systems and the need to maintain their function during healing. Burns to the ears and the nose are susceptible to infection because of poor blood supply to the cartilage. Burns to the buttocks or perineum are highly susceptible to infection. Circumferential burns to the extremities can cause circulatory compromise distal to the burn with subsequent neurologic impairment of the affected extremity. Patients may also develop compartment syndrome from direct heat damage to the muscles and subsequent edema and/or preburn vascular problems.

E. Nursing and collaborative management for the patient with burns. 3. Wound care

Cleansing and gentle debridement, using scissors and forceps, can occur in a cart shower, regular shower, or patient bed/stretcher by you and physicians Releasing escharotomies and fasciotomies can be carried out in the emergent phase, usually in burn centers by burn physicians Patients are showered using tap water, not exceeding 104° F (40° C). A once-daily shower and dressing change in the morning, followed by a dressing change in the patient's room in the evening, is a common routine in many burn centers. Some antimicrobial dressings can be left in place from 3 to 14 days Infection is the most serious threat to further tissue injury and possible sepsis (care is taken to prevent contamination btwn pts) In the open method, the patient's burn is covered with a topical antimicrobial and has no dressing over the wound. In the multiple dressing change or closed method, sterile gauze dressings are impregnated with or laid over a topical antimicrobial-dressings are changed anywhere from every 12 to 24 hours to once every 14 days, depending on the product Most centers use moist wound healing and use dressings to cover the burned areas, with the exception of the burned face

4. Rehabilitation phase nutritional therapy,

Continue nutritional support • Continue to counsel and teach patient and caregiver. • Continue to encourage and assist patient in resuming self-care.

prevention,

Coordinated national programs include child-resistant lighters, nonflammable children's clothing, tap water anti-scald devices, fire-safe cigarettes, stricter building codes, hardwired smoke detectors/alarms, and fire sprinklers. Flame • Never leave candles unattended or near open windows/curtains. • Encourage use of "child-resistant" lighters. • Encourage regular home fire exit drills. • Never use gasoline or other flammable liquids as accelerants. • Never leave hot oil unattended while cooking. • Never smoke in bed. • Consider a flame-retardant smoking apron for elderly and/or "at-risk" people. Scald • Exercise caution when microwaving food/beverages. • Lower hot water temperature to the "lowest point" or 120° F/40° C. • Use "anti-scald" devices with showerhead or faucet fixtures. • Supervise bathing with small children, older adults, or anyone with impaired physical movement/physical sensation/judgment. • After running bath water, check temperature with back of hand or bath thermometer. Inhalation • Install smoke/carbon monoxide detectors. Chemical • Store chemicals safely in approved containers and label clearly. • Ensure safety of workers, students handling chemicals (education, protective eyewear, gloves, masks, clothing). Electrical • Avoid and/or repair frayed wiring. • Ensure electrical power source is shut off before beginning repairs. • Wear protective eyewear and gloves when making electrical repairs. • Avoid outdoor activities during electrical (i.e., lightning) storms.

clinical manifestation, and

Decreased blood pressure (BP), increased heart rate, and other manifestations of hypovolemic shock are clinically detectable signs areas of full-thickness and deep partial-thickness burns are initially anesthetic because the nerve endings have been destroyed Superficial to moderate partial-thickness burns are painful. Blisters filled with fluid and protein may form in partial-thickness burns Fluid sequestered in the interstitial spaces and third spaces. patient with a larger burn area may have signs of an adynamic ileus, such as absent or decreased bowel sounds (the body's response to massive trauma and potassium shifts) Shivering (heat loss, anxiety, or pain) Most patients are alert and can provide answers to questions shortly after the injury or until they are intubated. frightened and benefit from calm reassurances and simple explanations Unconsciousness or altered mental status in a burn patient is usually not a result of the burn. The most common reason for unconsciousness or altered mental status is hypoxia associated with smoke inhalation. Other possibilities include head trauma, history of substance abuse, or excessive amounts of sedation or pain medication.

3. Acute phase pharmacologic therapy,

Drug Therapy • Assess need for medications (e.g., antibiotics). • Continue to monitor effectiveness and adjust dosage as needed. • Continue to counsel and teach patient and caregiver. • Continue to encourage and assist patient in resuming self-care. • Continue to prevent or minimize contractures and assess likelihood for scarring (surgery, physical/occupational therapy, splinting, or pressure garments). • Discuss possible reconstructive surgery. Pain and Anxiety • Continue to assess for and treat pain and anxiety.

4. Electrical burns

Electrical burns are the result of intense heat generated from an electric current. Direct damage to nerves and vessels, causing tissue anoxia and death, can also occur. The severity of the electrical injury depends on the amount of voltage, tissue resistance, current pathways, surface area in contact with the current, and length of time that the current flow was sustained (Fig. 25-2). Tissue densities offer various amounts of resistance to electric current. For example, fat and bone offer the most resistance, whereas nerves and blood vessels offer the least resistance. Current that passes through vital organs (e.g., brain, heart, kidneys) will produce more life-threatening sequelae than that which passes through other tissues. In addition, electric sparks may ignite the patient's clothing, causing a combination of thermal and electrical injury. As with inhalation injury, a rapid assessment of the patient with electrical injury must be performed. Transfer to a burn center is indicated. The severity of an electrical injury can be difficult to determine as most of the damage is below the skin (known as the "iceberg effect"). patient at risk for dysrhythmias or cardiac arrest, severe metabolic acidosis, and myoglobinuria, which can lead to acute tubular necrosis (ATN). The electric shock event can cause immediate cardiac standstill or ventricular fibrillation. Delayed cardiac dysrhythmias or arrest may also occur without warning during the first 24 hours after injury. Myoglobin from injured muscle tissue and hemoglobin from damaged red blood cells (RBCs) are released into the circulation whenever massive muscle and blood vessel damage occurs. The released myoglobin pigments are transported to the kidneys, where they can mechanically block the renal tubules because of their large size. This process can result in ATN and eventual acute renal failure if not appropriately treated

fluid resuscitation, 2. Emergent phase

Fluid Therapy • Assess fluid needs.* • Begin IV fluid replacement. • Insert urinary catheter. • Monitor urine output. Parkland (Baxter) method Crystalloids: Lactated Ringer's: 4.0 mL/kg/% TBSA burn; ½ given during first 8 hr; ¼ given each next 8 hr 2nd 24 hrs Colloids: 0.3-0.5 mL/kg/% TBSA burn Glucose in water: Amount to replace estimated evaporative losses Brooke (modified) method Lactated Ringer's: 2 mL/kg/% TBSA burn; ½ given first 8 hr; ½ given during next 16 hr 2nd 24 hrs 0.3-0.5 mL/kg/% TBSA burn Glucose in water: Amount to replace estimated evaporative losses

3. Acute phase fluid resuscitation,

Fluid Therapy • Continue to replace fluids, depending on patient's clinical response.

FLUID RESUSCITATION WITH THE PARKLAND (BAXTER) FORMULA*

Formula 4 mL lactated Ringer's solution per kilogram (kg) of body weight per percent of total body surface area (% TBSA) burned = total fluid requirements for first 24 hr after burn Application ½ of total in first 8 hr ¼ of total in second 8 hr ¼ of total in third 8 hr

1. Pre-hospital care- pharmacologic therapy,

If CO intoxication is suspected, the patient should be treated with 100% humidified O2. • Administer IV analgesia and assess its effectiveness frequently. For electrical burns, • Anticipate possible administration of NaHCO3 to alkalinize the urine and maintain serum pH >6.0.

D. Phases of burn management; nursing management in each phase, 2. Emergent phase

Nursing assessment: ABCs, vital signs, cardiac rhythm, oxygenation, and level of consciousness are priorities during the emergent phase of burn care. Psychosocial Care • Provide support to patient and caregiver during initial crisis phase.

nutritional therapy, 2. Emergent phase

Nutritional Therapy • Assess nutritional needs and begin feeding patient by most appropriate route as soon as possible. Calorie-containing nutritional supplements and milkshakes are often given because of the great need for calories. Protein powder can also be added to food and liquids. Supplemental vitamins may be given as early as the emergent phase, with iron supplements often started in the acute phase Place NG tube for gastric decompression in >20% TBSA burns • Prevent nausea, emesis, and aspiration from ileus Assess abdomen and bowel sounds every 8 hours • Evaluate resolution of decreased gastric motility and ileus Assess NG aspirate (color, quantity, pH, and guaiac); monitor stool guaiac • Facilitate early detection of GI bleeding Administer stress ulcer prophylaxis • Prevent stress ulcer development Consult dietician. Initiate enteral feeding, and evaluate tolerance; provide high-calorie/protein supplements prn; record all oral intake and count calories • Caloric/protein intake must be adequate to maintain positive nitrogen balance and promote healing Schedule interventions and activities to avoid interrupting feeding times • Pain, fatigue, or sedation interferes with desire to eat Monitor weight daily or biweekly • Assess tolerance and response to feeding interventions

3. Acute phase nutritional therapy,

Nutritional Therapy • Continue to assess diet to support wound healing. Meeting daily caloric requirements is crucial and should begin within the first 1 to 2 days postburn. The daily estimated caloric needs must be regularly calculated by a dietitian and readjusted as the patient's condition changes (e.g., wound healing, sepsis). If the patient is on a mechanical ventilator or unable to consume adequate calories by mouth, a small-bore feeding tube is placed and enteral feedings are initiated. When the patient is extubated, a swallowing assessment should be performed by a speech pathologist before the oral feeding is commenced. The alert patient should be encouraged to eat high-protein, high-carbohydrate foods to meet increased caloric needs. If caregivers wish to bring in favorite foods from home, this should be encouraged. Appetite is usually diminished, and constant encouragement may be necessary to achieve adequate intake. Ideally, weight loss should not be more than 10% of preburn weight. You need to record the patient's daily caloric intake using calorie count sheets, which are monitored by the dietitian. Patients are weighed routinely to evaluate progress.

E. Nursing and collaborative management for the patient with burns. 5. Nutritional therapy

Once fluid replacement needs have been addressed, nutrition takes priority in the initial emergent phase. Early and aggressive nutritional support within several hours of the burn injury can decrease mortality risks and complications, optimize healing of the burn wound, and minimize the negative effects of hypermetabolism and catabolism. Nonintubated patients with a burn of less than 20% TBSA will generally be able to eat enough to meet their nutritional requirements. Intubated patients and/or those with larger burns require additional support. Enteral feedings (gastric or intestinal) have almost entirely replaced parenteral feeding. Early enteral feeding, usually with smaller-bore tubes, preserves GI function, increases intestinal blood flow, and promotes optimal conditions for wound healing. The patient with a large burn (more than 20% TBSA) can develop paralytic ileus within a few hours due to the body's response to major trauma. If a large nasogastric tube is inserted on admission, gastric residuals should be checked frequently to rule out delayed gastric emptying. Bowel sounds should be assessed every 8 hours. In general, feedings can begin slowly at 20 to 40 mL/hr and increased to the goal rate within 24 to 48 hours. A hypermetabolic state proportional to the size of the wound occurs after a major burn injury. Resting metabolic expenditure may be increased by 50% to 100% above normal in patients with major burns. Core temperature is elevated. Catecholamines, which stimulate catabolism and heat production, are increased. Massive catabolism can occur and is characterized by protein breakdown and increased gluconeogenesis. Failure to supply adequate calories and protein leads to malnutrition and delayed healing. Calorie-containing nutritional supplements and milkshakes are often given because of the great need for calories. Protein powder can also be added to food and liquids. Supplemental vitamins may be given as early as the emergent phase, with iron supplements often started in the acute phase

pharmacologic therapy, 2. Emergent phase

Pain and Anxiety • Assess and manage pain and anxiety. Pain medications: morphine (Avinza) sustained-release morphine (MS Contin) hydromorphone (Dilaudid) fentanyl (Sublimaze) oxycodone and acetaminophen (Percocet) methadone (Dolophine) Nonsteroidal antiinflammatory (e.g., ketorolac [Toradol]) Adjuvant analgesics (e.g., gabapentin [Neurontin])

Fluid Therapy

Parkland (Baxter) method Crystalloids: Lactated Ringer's: 4.0 mL/kg/% TBSA burn; ½ given during first 8 hr; ¼ given each next 8 hr 2nd 24 hrs Colloids: 0.3-0.5 mL/kg/% TBSA burn Glucose in water: Amount to replace estimated evaporative losses Brooke (modified) method Lactated Ringer's: 2 mL/kg/% TBSA burn; ½ given first 8 hr; ½ given during next 16 hr 2nd 24 hrs 0.3-0.5 mL/kg/% TBSA burn Glucose in water: Amount to replace estimated evaporative losses

D. Phases of burn management; nursing management in each phase, 3. Acute phase

Psychosocial Care • Continue to provide ongoing support/counseling/education to patient and caregiver about physical and emotional aspects of care and recovery. • Begin to anticipate discharge needs.

including airway management, 2. Emergent phase

Respiratory Therapy • Assess oxygenation needs. • Provide supplemental oxygen as needed. • Intubate if necessary. • Monitor respiratory status.

3. Acute phase including airway management,

Respiratory Therapy • Continue to assess oxygenation needs. • Continue to monitor respiratory status. • Monitor for signs of complications (e.g., pneumonia).

C. Classification of burn injury 1. Depth

Severity is determined by (1) depth of burn, (2) extent of burn calculated in percent of total body surface area (TBSA), (3) location of burn, and (4) patient risk factors. PARTIAL-THICKNESS Skin Destruction • Superficial (first-degree) burn Erythema, blanching on pressure, pain and mild swelling, no vesicles or blisters (although after 24 hr skin may blister and peel) Possible cause: Superficial sunburn Quick heat flash Structures involved: Superficial epidermal damage with hyperemia. Tactile and pain sensation intact. • Deep (second-degree) burn Fluid-filled vesicles that are red, shiny, wet (if vesicles have ruptured); severe pain caused by nerve injury; mild to moderate edema Possible cause: Flame Flash Scald Contact burns Chemical Tar Electric current Structures involved: Epidermis and dermis involved to varying depths. Skin elements, from which epithelial regeneration occurs, remain viable. FULL THICKNESS Skin Destruction • Third- and fourth-degree burns Dry, waxy white, leathery, or hard skin; visible thrombosed vessels; insensitivity to pain because of nerve destruction; possible involvement of muscles, tendons, and bones Possible cause: Flame Scald Chemical Tar Electric current Structures involved: All skin elements and local nerve endings destroyed. Coagulation necrosis present. Surgical intervention required for healing.

1. Pre-hospital care- wound care

Small thermal burns (≤10% TBSA) should be covered with a clean, cool, tap water-dampened towel for the patient's comfort and protection until definitive medical care is instituted. Cooling of the injured area (if small) within 1 minute helps minimize the depth of the injury. To prevent hypothermia, large burns should only be cooled for no more than 10 minutes. Do not immerse the burned body part in cool water since doing so might lead to extensive heat loss. Gently remove as much burned clothing as possible to prevent further tissue damage. Adherent clothing should be left in place until the patient is transferred to a hospital. The patient should then be wrapped in a dry, clean sheet or blanket to prevent further contamination of the wound and to provide warmth. Chemical burns are best treated by quickly removing the solid particles from the skin. Any clothing containing the chemical must also be removed as the burning process continues while the chemical is in contact with the skin. The affected area should be flushed with copious amounts of water to irrigate the skin anywhere from 20 minutes to 2 hours postexposure. Tap water is acceptable for flushing eyes exposed to chemicals. Tissue destruction may continue for up to 72 hours after a chemical burn. (For information on handling specific agents, refer to a hazardous materials text.)

3. Smoke and inhalation injury

Smoke and inhalation injuries result from the inhalation of hot air or noxious chemicals and can cause damage to the tissues of the respiratory tract. Fortunately, gases are cooled to body temperature before they reach the lung tissue. Although damage to the respiratory mucosa can occur, it seldom happens because the vocal cords and glottis close as a protective mechanism. Redness and airway swelling (edema) may result when damage occurs. Because smoke inhalation injuries are a major predictor of mortality in burn patients, a rapid assessment is critical. Carbon monoxide poisoning: displaces oxygen (O2) on the hemoglobin molecule, causing carboxyhemoglobinemia, hypoxia, and ultimately death when the CO levels are greater than 20%. Skin color is often described as "cherry red" in appearance with severe CO poisoning. CO poisoning may occur in the absence of burn injury to the skin. Inhalation injury above the glottis: (upper airway injury) is thermally produced and may be caused by the inhalation of hot air, steam, or smoke. Mucosal burns of the oropharynx and larynx are manifested by redness, blistering, and edema. Mechanical obstruction can occur quickly, presenting a true medical emergency. Clues that this injury is likely include the presence of facial burns, singed nasal hair, hoarseness, painful swallowing, darkened oral and nasal membranes, carbonaceous sputum, history of being burned in an enclosed space, and clothing burns around the chest and neck. Inhalation injury below the glottis: (lower airway injury) is usually chemically produced. Tissue damage is related to the duration of exposure to smoke or toxic fumes. Clinical manifestations such as pulmonary edema may not appear until 12 to 24 hours after the burn, and then they may manifest as acute respiratory distress syndrome (ARDS)

2. Patient risk factors

The older adult heals more slowly and usually experiences more difficulty with rehabilitation than a younger adult. preexisting cardiovascular, respiratory, or renal disease has a poorer prognosis for recovery because of the tremendous demands placed on the body by a burn injury. diabetes mellitus or peripheral vascular disease is at high risk for poor healing and gangrene, especially with foot and leg burns. General physical debilitation from any chronic disease, including alcoholism, drug abuse, or malnutrition, renders the patient less physiologically able to recover from a burn injury. In addition, the burn patient who has concurrently sustained fractures, head injuries, or other trauma have a poorer prognosis for recovery.

complications of burn injuries.

The three major organ systems most susceptible to complications during the emergent phase of burn injury are the cardiovascular, respiratory, and urinary systems. dysrhythmias and hypovolemic shock, which may progress to irreversible shock Circulation to the extremities can be severely impaired by deep circumferential burns and subsequent edema formation. These processes occlude the blood supply by acting like a tourniquet. If untreated, ischemia, paresthesias, necrosis, and eventually gangrene can occur Initially, increase in blood viscosity because of the fluid loss that occurs in the emergent period. Microcirculation is impaired because of the damage to skin structures that contain small capillary systems. These two events result in a phenomenon termed sludging. Sludging can be corrected by adequate fluid replacement. (1) upper airway (above the glottis) burns that cause edema formation and obstruction of the airway direct heat injury or edema formation and can lead to mechanical airway obstruction and asphyxia and (2) lower airway injury direct insult at the alveolar level secondary to the inhalation of toxic fumes or smoke. The result is interstitial edema that prevents the diffusion of oxygen from the alveoli into the circulatory system The patient with preexisting heart disease (e.g., myocardial infarction) or lung disease (e.g., chronic obstructive pulmonary disease) is at risk for complications. If fluid replacement is too vigorous, the patient can develop heart failure or pulmonary edema. Invasive measures (e.g., hemodynamic monitoring) may be necessary to monitor fluid resuscitation.-more likely to develop a respiratory infection. Pneumonia is a common complication of major burns and the leading cause of death in patients with an inhalation injury. venous thromboembolism (VTE). Risk for VTE increases if one or more of the following conditions are present: advanced age, morbid obesity, extensive or lower-extremity burns, concomitant lower-extremity trauma, and/or prolonged immobility. The most common complication of the urinary system in the emergent phase is acute tubular necrosis (ATN).if pt. hypovolemic, blood flow to the kidneys is decreased, causing renal ischemia With full-thickness and electrical burns, myoglobin (from muscle cell breakdown) and hemoglobin (from RBC breakdown) are released into the bloodstream and occlude renal tubules. Adequate fluid replacement can counteract occlusion

3. Acute phase wound care

Wound Care • Continue daily shower and wound care. • Continue debridement (if necessary). • Assess wound daily and adjust dressing protocols as necessary. • Observe for complications (e.g., infection). Early Excision and Grafting • Provide temporary homografts. • Provide permanent autografts. • Care for donor sites.

wound care 2. Emergent phase

Wound Care • Start daily shower and wound care. • Debride as necessary. • Assess extent and depth of burns. • Administer tetanus toxoid or tetanus antitoxin.

D. Phases of burn management; nursing management in each phase, 4. Rehabilitation phase

begins when the patient's burn wounds have healed and the patient is able to resume a level of self-care activity. This can occur as early as 2 weeks or as long as 7 to 8 months after the burn injury. Goals for this period are to (1) assist the patient in resuming a functional role in society and (2) rehabilitate from functional and cosmetic reconstructive surgery. Rehabilitation-focused activities that have been taking place during the earlier emergent and acute phases now begin in earnest once the patient's wounds have healed. Emphasize continuous role of exercise and physical/occupational therapy cannot be overemphasized. Constant encouragement and reassurance are necessary to maintain a patient's morale, particularly once the patient realizes that recovery can be slow and rehabilitation may need to be a primary focus for at least the next 6 to 12 months. be particularly sensitive and attuned to the patient's emotions and concerns. It is essential that patients be encouraged to discuss their fears regarding loss of their life as they once knew it, loss of function, temporary/permanent deformity and disfigurement, return to work and home life, and financial burdens resulting from a long and costly hospitalization and rehabilitation. Counseling, which may have started in the acute phase of care, can be offered after discharge. Patients appreciate reassurance that their feelings during this period of adjustment are normal, and that their frustration is to be expected as they attempt to resume a normal lifestyle.

B. Types of burns 1. Thermal burns

burns caused by flame, flash, scald, or contact with hot objects and are the most common type of burn injury

2. Chemical burns

result from tissue injury and destruction from acids, alkalis, and organic compounds. In addition to tissue damage, eyes can be injured if they are splashed with a chemical. Acids are found in many household cleaners and include hydrochloric, oxalic, and hydrofluoric acid. Alkali burns can be more difficult to manage than acid burns since alkaline substances are not neutralized by tissue fluids as readily as acid substances. Alkalis adhere to tissue, causing protein hydrolysis and liquefaction. Alkalis are found in oven and drain cleaners, fertilizers, and heavy industrial cleansers. Organic compounds, including phenols and petroleum products, produce contact burns and systemic toxicity. Phenols are found in chemical disinfectants; petroleum products include creosote and gasoline.

E. Nursing and collaborative management for the patient with burns. 1. Airway management

endotracheal (preferably orotracheal) intubation within 1 to 2 hours after burn injury ventilatory assistance, and the delivered oxygen concentration is determined by assessing ABG values Extubation may be indicated when the edema resolves, usually 3 to 6 days after burn injury, unless severe inhalation injury is involved. Escharotomies of the chest wall may be needed to relieve respiratory distress secondary to circumferential, full-thickness burns of the neck and trunk Within 6 to 12 hours after injury in which smoke inhalation is suspected, a fiberoptic bronchoscopy should be performed to assess the lower airway. Significant findings include the appearance of carbonaceous material, mucosal edema, vesicles, erythema, hemorrhage, and ulceration. When intubation is not performed, treatment of inhalation injury includes administration of 100% humidified O2 as needed patient in a high Fowler's position, unless contraindicated (e.g., spinal injury), and encourage coughing and deep breathing every hour. Reposition the patient every 1 to 2 hours and provide chest physiotherapy and suctioning as necessary. If respiratory failure develops, intubation and mechanical ventilation are initiated Positive end-expiratory pressure (PEEP) may be used to prevent collapse of the alveoli and progressive respiratory failure Bronchodilators may be administered to treat severe bronchospasm. CO poisoning is treated by administering 100% O2 until carboxyhemoglobin levels return to normal. The use of hyperbaric oxygen therapy remains controversial.

C. Classification of burn injury 1.extent

guides for determining the total body surface area affected or the extent of a burn wound are the Lund-Browder chart (Fig. 25-4, A) and the rule of nines Two commonly used guides for determining the total body surface area affected or the extent of a burn wound are the Lund-Browder chart and the rule of nines The Sage Burn Diagram is a free, Internet-based tool that is available for estimating TBSA burned ( www.sagediagram.com) The Lund-Browder chart is considered more accurate because the patient's age, in proportion to relative body-area size, is taken into account. The rule of nines, which is easy to remember, is considered adequate for initial assessment of an adult burn patient. For irregular- or odd-shaped burns, the patient's hand (including the fingers) is approximately 1% TBSA. extent of a burn is often revised after edema has subsided and a demarcation of the zones of injury have occurred.

A. Pathophysiological deviations that occur with patients experiencing burns; causes,

hypovolemic shock caused by a massive shift of fluids out of the blood vessels as a result of increased capillary permeability and can begin as early as 20 minutes postburn. As the capillary walls become more permeable, water, sodium, and later plasma proteins (especially albumin) move into interstitial spaces and other surrounding tissue. The colloidal osmotic pressure decreases with progressive loss of protein from the vascular space. This results in more fluid shifting out of the vascular space into the interstitial spaces (Fig. 25-6). (Fluid accumulation in the interstitium is termed second spacing.) Fluid also moves to areas that normally have minimal to no fluid, a phenomenon termed third spacing. Examples of third spacing in burn injury are exudate and blister formation, as well as edema in nonburned areas. insensible losses by evaporation from large, denuded body surfaces and the respiratory system. The normal insensible loss of 30 to 50 mL/hr is increased in the severely burned patient. The circulatory status is also impaired because of hemolysis of RBCs. The RBCs are hemolyzed by circulating factors (e.g., oxygen free radicals) released at the time of the burn, as well as by the direct insult of the burn injury. Thrombosis in the capillaries of burned tissue causes an additional loss of circulating (Na) moving into the cell in abnormal amounts and potassium (K) leaving the cell. An elevated hematocrit is commonly caused by hemoconcentration resulting from fluid loss. Major shifts in sodium and potassium also occur during this phase. Sodium rapidly shifts to the interstitial spaces and remains there until edema formation ceases (Fig. 25-7). A potassium shift develops initially because injured cells and hemolyzed RBCs release potassium into the circulation. Burn injury causes coagulation necrosis, whereby tissues and vessels are damaged or destroyed. Neutrophils and monocytes accumulate at the site of injury. Fibroblasts and newly formed collagen fibrils appear and begin wound repair within the first 6 to 12 hours after injury. Burn injury causes widespread impairment of the immune system. The skin barrier to invading organisms is destroyed, bone marrow depression occurs, and circulating levels of immunoglobulins are decreased. Defects occur in the function of white blood cells (WBCs). The inflammatory cytokine cascade triggered by tissue damage impairs the function of lymphocytes, monocytes, and neutrophils, which puts the patient at greater risk for infection.

E. Nursing and collaborative management for the patient with burns. 2. Fluid therapy Nursing actions

• Assess fluid needs.* • Begin IV fluid replacement. • Insert urinary catheter. • Monitor urine output. At least two large-bore IV access routes must be obtained for patients with burns greater than 15% TBSA. It is critical to establish IV access that can accommodate large volumes of fluid. For patients with burns greater than 30% TBSA, a central line for fluid and drug administration, as well as blood sampling, should be considered. An arterial line also should be considered if frequent ABGs or invasive BP monitoring is needed.

1. Pre-hospital care- fluid resuscitation,

• Establish IV access with two large-bore catheters if burn >15% TBSA. • Begin fluid replacement.