Test 2 Information

socioeconomic maldistribution of burns has been referred to as

"dramatic examples of the inequity of injury"

TABLE 62-4 Overview of Selected Topical Antimicrobial Agents Used for Burn Wounds: General

Antimicrobial ointment Indication/Comment: Antibacterial coverage and promotion of a moist wound environment Application: Apply 1/16-inch layer of ointment with a clean glove daily Nursing Implications: Ensure removal of old ointment at the time of wound cleaning prior to applying a new layer. Monitor closely for signs and symptoms of local infection.

TABLE 62-1 Characteristics of Burns According to Depth: Third Degree (Full Thickness)

Causes: Flame, Prolonged exposure to hot liquids, Electric current, Chemical, Contact Skin Involvement: Epidermis, Dermis, and sometimes subcutaneous tissue; may involve connective tissue, and Muscle Clinical Manifestations: Insensate, Shock, Myoglobinuria (red pigment in urine) and possible hemolysis, Possible contact points (entrance/exit wounds in electrical burns) Wound Appearance: Dry; pale white, red brown, leathery, or charred, Coagulated vessels may be visible, Edema Recuperative Course and Treatment: Eschar may slough, Grafting necessary, Scarring and loss of contour and function

Liver Functions

Largest gland of the body Chemical factory that manufactures, stores, alters, and excretes many substances that are involved with metabolism Regulates glucose and protein metabolism Manufactures and secretes bile (plays a major role in digestion and absorption of fats in GI tract) Removes waste products from the bloodstream and secretes them into the bile Bile produced is stored temporarily in the gallbladder until needed for digestion when it is emptied into the intestine

Metabolism

Med Surg: Ch49

Tissue Integrity module

Med surg: pg 1805-1836

Glucose Metabolism

Regulates blood glucose concentration Glucose is taken in from the portal venous blood by the liver and converted into glycogen which is then stored in hepatocytes Glycogen is converted back to glucose (glycogenolysis) and released as needed to maintain blood levels. This provides a limited amount Additional glucose is synthesizes through gluconeogenesis. Liver uses amino acids from protein breakdown or lactate from exercising muscles. This is in response to hypoglycemia

CHart 62-3 Electical Burns

Some of the most devastating and complex of all burn injuries Heat generated by electricity is directly responsible for tissue damage, but unlike most thermal burns, visual examination is not predictive of burn size and severity. It is helpful to know the circumstances of the injury to anticipate potential tissue damage and complications Superficial injuries of an electrical burn may present themselves as contact points on physical examination. Deep tissue injuries may not be visible on initial clinical presentation but in many circumstances should be assumed as present and timely intervention initiated. Mechanisms of injury include flash, conductive, and lightning injury. Flash Injury: An electrical flash generates light and heat without current flow and usually causes a thermal burn of exposed areas due to the heat generated, or a flame burn from ignition of clothing. Flash burns have fewer complications, and patients generally require shorter lengths of hospital stay Conductive Injury: occur when the current overcomes the skin's resistance and travels through the body. The amount and severity of damage is directly proportional to the strength of the current (voltage), duration of contact with the source, which organs lay along the pathway of current, and whether the current is direct or alternating. Direct current (DC) travels in one direction, often with an entrance and exit wound, and is associated with an explosion and likely concomitant trauma. Alternating current (AC) passes back and forth from the point of contact, through the body and back to the source many times per second and can hold the victim to it, increasing contact time Conduction of electricity through the nerves and vessels and along the outside of bones generates heat, causing damage to adjacent tissues. Deep muscle injury may be present without injury to superficial muscles, masking the true extent of the injury. In addition, electrical current immediately contracts muscles as it travels through the body, and skeletal injuries may occur with high-voltage injuries. Entrance and exit wounds or contact points can help identify the probable current path and therefore anticipated tissues and organs that may have sustained damage. Compartment syndrome is very common with electrical injuries due to the edema that results from injured tissue compounded by the large fluid volumes required for resuscitation to prevent kidney failure. As a result, invasive decompressive therapies such as fasciotomies, nerve releases, ocular releases, and laparotomies may be required. Lightning Injury: can result from a direct strike, a high-voltage DC injury, or a side flash wherein the current discharges from an object nearby through the air to an adjacent object or person. Side flashes are the most common and result in immediate deep polarization of the entire myocardium with possible cardiac arrest. Respiratory arrest is also common because electric current can temporarily inactivate the brain's respiratory center People struck by lightning may suffer from various longterm symptoms that can be debilitating. These include memory loss, attention deficits, sleep disorders, chronic pain, numbness, dizziness, stiffness in joints, irritability, fatigue, weakness, muscle spasms, and depression. Management: Resuscitation fluid calculations based on total body surface area are inaccurate in conductive electrical injuries, including some lightning injuries. It is difficult to quantify the extent of tissue injury without surgical exploration, because the damage may not be visible on physical examination. Serum creatine kinase levels may be useful to assist in determining the degree of muscle injury in the early phases of care. Myoglobinuria is common with muscle damage and may cause kidney failure if not treated. IV fluid administration titrated to a target of 75-100 mL of urine output per hour is indicated until urine is no longer red. It is common practice to add 50 mEq of sodium bicarbonate per liter of IV fluid in an effort to assist in alkalinizing the urine. Serum myoglobin and urine myoglobin levels may also be monitored as indicators of the need for continued resuscitation. surgical treatment of an electrical injury is as complex as the injury itself. Vasculature is commonly affected, thus progressive tissue necrosis occurs over time. Sequential surgical débridement may be necessary, using caution to preserve viable tissue

Nursing Management of burn patient

in the acute/intermediate phase is focused on the following priorities: restoring fluid balance, preventing infection, modulating hypermetabolism, promoting skin integrity, relieving pain and discomfort, promoting mobility, strengthening coping strategies, supporting patient and family processes, and monitoring and managing complications

Left off with Burns on

page 1827

Bilirubin Excretion

A pigment derived from the breakdown of hemoglobin by cells of the reticuloendothelial system (including Kupffer cells) Hepatocytes remove bilirubin from the blood and chemically modify it through conjugation to glucuronic acid (makes it more soluble in aqueous solution) Conjugated bilirubin is secreted by liver cells and eventually carried in bile to duodenum. In the small intestine, bilirubin is converted into urobilinogen, which is partially excreted in feces and partially absorbed into portal blood. Some urobilinogen enters systemic circulation and is excreted by kidneys in urine. Major route of excretion is elimination in bile

Continued ED Care

After adequate respiratory function and circulatory status have been established, the patient is assessed for cervical spine and/or head injuries if involved in a traumatic or electrical injury. All clothing and jewelry are removed because they may contain chemicals, retain heat, or become constrictive as edema rapidly develops. For chemical burns, flushing of the exposed areas is continued. The patient is checked for contact lenses. These are removed immediately if chemicals have come in contact with the eyes or if facial burns have occurred. In addition, the eyes are examined promptly for injury to the corneas. An ophthalmologist may be consulted for complete assessment via fluorescent staining. The patient's temperature must be monitored because hypothermia may develop rapidly and manipulation of the environment may be necessary. A temperature less than 35°C (95°F) causes vasoconstriction, which may increase tissue injury It is important to validate an account of the burn scenario provided by the patient, witnesses at the scene, and first responders. Information needs to include the time and the source of the burn injury, the location (particularly if the patient was in an enclosed space), length of exposure, prior treatment at the scene, and any history of concomitant traumatic injury. A history of preexisting medical conditions, allergies, medications, and the use of drugs, alcohol, and tobacco is obtained to assist with the treatment plan All intubated patients should have a nasogastric tube inserted to decompress the stomach and prevent vomiting. Often, patients with large burns become nauseated as a result of the GI effects of the burn injury, such as paralytic ileus, and the effects of medications such as opioids. Clean sheets are placed under and over the patient to protect the burn wound from contamination, maintain body temperature, and reduce pain caused by air currents passing over exposed nerve endings. Baseline height, weight, arterial blood gases, hematocrit, electrolyte values, blood alcohol level, drug panel, urinalysis, and chest x-rays may be obtained. Because poor tissue perfusion accompanies burn injuries, only IV analgesia is administered, which is paramount for pain relief in the emergent phase. If the patient has an electrical burn, a baseline electrocardiogram is also obtained and continuous monitoring is initiated. Because burns are contaminated wounds, tetanus prophylaxis is administered if the patient's immunization status is not current or is unknown. The nurse must consider circumstances surrounding the burn injury when providing care. Examples include cases of abuse, neglect, suicide attempts, and injury/death of other family members or friends from the same event.

Pain

Background pain is a continuous level of discomfort even when the patient is inactive or not undergoing any procedures. The goal of treatment is to provide a long-acting analgesic agent that will provide even coverage for this long-term discomfort. helpful to use escalating doses when initiating the medication to reach the level of pain control that is acceptable to the patient Breakthrough pain is described as acute, intense, and episodic. It is generally related to an activity or movement of the affected area. Short-acting agents are used for breakthrough pain to achieve pain control if needed. Procedural pain is discomfort that occurs with procedures such as daily wound treatments, invasive line insertions, and physical and occupational therapy. Pharmacologic treatment for the management of burn pain includes the use of opioids, nonsteroidal anti-inflammatory drugs, anxiolytics, and anesthetic agents Nonpharmacologic therapies include relaxation techniques, distraction, guided imagery, hypnosis, therapeutic touch, humor, music therapy, and more recently virtual reality techniques

Major Burns

Burns that exceed one third of the TBSA are considered major burn injuries and produce both a local and a systemic inflammatory response. Inflammatory response exceeds the inflammatory responses that are seen in trauma or sepsis. Once a burn reaches 30% of TBSA, the localized release of cytokines and other inflammatory mediators produce a systemic effect. Major burn injuries are characterized by burn wound edema, generalized edema formation in noninjured tissue, altered cardiovascular function, and impaired organ perfusion The initial systemic event after a major burn injury is hemodynamic instability, which results from loss of capillary integrity and a subsequent shift of fluid, sodium, and protein from the intravascular space into the interstitial space, producing hypovolemic shock. Severe thermal injuries ultimately encompass changes in pathophysiology of all body systems as presented in Table 62-2. These changes precipitate conditions such as shock, sepsis, acute respiratory distress syndrome (ARDS), ileus, and kidney failure

Table 62-2 Pathophysiologic Changes with Severe Burns

Cardiovascular: Cardiac depression, edema, hypovolemia Pulmonary: Vasoconstriction, edema Gastrointestinal: Impaired motility and absorption, vasoconstriction, loss of mucosal barrier function with bacterial translocation, increased pH Kidney: Vasoconstriction Other: Anemia, immunodepression

Pulmonary Alterations/Inhalation Injury

Caused by inhalation of thermal and/or chemical irritants Smoke (colloid) contains airborne solid and liquid particles and gases that result when a substance combusts The components of smoke that cause damage are (1) heat, (2) particulates, and (3) systemic toxins Because a common tendency in the presence of anxiety is tachypnea, victims of fire will then inhale more of these toxins Studies of thermal burn injuries show a mortality rate of 13.9%; however, that mortality rate doubles, to 26.6%, with the presence of inhalation injury The extent of damage is directly related to the temperature and the concentration of toxic gases. In smoke inhalation, the mechanisms of injury are thermal damage, asphyxiation, and irritation of the pulmonary tissues. It is important to note that respiratory failure may not always be in proportion to smoke exposure. This disproportion may be due to the toxin inhaled and/or patient response Indicators of possible inhalation injury include (1) injury occurring in an enclosed space; (2) burns of the face or neck; (3) singed nasal hair; (4) hoarseness, high-pitched voice change, stridor; (5) soot in sputum; (6) dyspnea or tachypnea and other signs of reduced oxygen levels (hypoxemia); and (7) erythema and blistering of the oral or pharyngeal mucosa Inhalation injuries are categorized as upper airway injury (above the vocal cords) or lower airway injury (below the vocal cords). Injuries above the vocal cords can be thermal or chemical, whereas injuries below the vocal cords are usually chemical

TABLE 62-1 Characteristics of Burns According to Depth: Fourth Degree (Full Thickness That Includes Fat, Fascia, Muscle, and/or Bone)

Causes: Prolonged exposure or high voltage electrical injury Skin Involvement: Deep tissue, muscle and bone Clinical Manifestations: Shock, Myoglobinuria and possible hemolysis Wound Appearance: Charred Recuperative Course and Treatment: Amputations likely, Grafting of no benefit (given depth and severity of wound(s))

TABLE 62-1 Characteristics of Burns According to Depth: Second Degree (Partial Thickness)

Causes: Scalds, Flash flame, Contact Skin Involvement: Epidermis, portion of dermis Clinical Manifestations: Pain, Hyperesthesia, Sensitive to air currents Wound Appearance: Blistered, Mottled red base; disrupted epidermis; weeping surface, Edem Recuperative Course and Treatment: Recovery in 2-3 weeks, Some scarring and depigmentation possible; may require grafting

TABLE 62-1 Characteristics of Burns According to Depth: First Degree

Causes: Sunburn, Low-intensity flash, Superficial scald Skin Involvement: Epidermis; possibly a portion of dermis Clinical Manifestations: Tingling, Hyperesthesia (hypersensitivity), Pain that is soothed by cooling, Peeling, Itching Wound Appearance: Reddened; blanches with pressure; dry, Minimal or no edema, Possible blisters Recuperative Course and Treatment: Complete recovery within a few days, Oral pain meds, cool compresses, skin lubricants (ointments, emollients); topical antimicrobial agents not indicated

Zone of Coagulation

Central area of the wound Due to the characteristic coagulation necrosis of cells

Age Considerations

Common age-related changes, such as diminished mobility, postural stability, strength, coordination, sensation, visual acuity, as well as declining memory, predispose older adults to burn injury One study that compared burn-related outcomes in patients younger than 65 years to those older than 65 years found that the older group of patients had 1.9 times greater probability of death. Furthermore, no patients older than 85 years survived in this study, regardless of TBSA burned The skin of the older adult is thinner and less elastic, which affects the depth of injury and its ability to heal. Pulmonary function becomes impaired with age; therefore, airway exchange, lung elasticity, and ventilation can be altered. This can be exacerbated if the older adult has a history of smoking. Decreased cardiac output, coronary artery disease, and decreased cardiovascular compensatory response may increase the risk of complications in older adult patients with burn injuries

Glycosuria

Common finding in the early postburn hours, results from the release of liver glycogen stores in response to stress

Burn Related Complications

Complications associated with burn injuries are also highest in patients 60 years and older. Of all complications, pneumonia is the most common. Other complications include urinary tract infection, respiratory failure, septicemia, cellulitis, wound infection, kidney failure, dysrhythmias, catheter-related bloodstream infection, and other infections

Bile Formation

Continuously formed by hepatocytes and collected in canaliculi and bile ducts Composed mainly of water and electrolytes like sodium (Na+), potassium (K+), calcium (Ca+), chloride (Cl-), and bicarbonate and also has significant amounts of lecithin, fatty acids, cholesterol, bilirubin, and bile salts Functions of bile are excretory (excretion of bilirubin). Also serves as digestion aid through emulsification of fats by bile salts Bile salts are synthesized by the hepatocytes from cholesterol. Bile salts, with cholesterol and lecithin, are required for emulsification of fats in the intestine. Needed for efficient digestion and absorption Afterward, bile salts are reabsorbed, mostly in the distal ileum, into the portal blood for the liver and then again excreted into bile. The pathway from hepatocytes to bile to intestine and back is called enterohepatic circulation. Because of this, only a small amount of bile salts are excreted in feces (decreased need for active synthesis of more bile salts)

Cultured Epidermal Autograft (CEA)

Cultured epidermal autograft (CEA), an epithelial graft, has emerged as an important procedure in the management of massive burns. In burns that cover more than 90% TBSA, CEA may be the only option because the availability of nonburned skin as donor sites will not be sufficient for grafting Involves obtaining full-thickness biopsies of the patient's unburned skin that are cultured to promote growth. The final product is available approximately 3 weeks later for grafting. Meticulous attention is required in CEA applied to certain body surfaces because it is fragile and prone to graft loss. The patient may begin exercising the grafted area 5 to 7 days after surgery. This may vary with individual burn center's protocols.

Immunologic Alterations

Defenses greatly altered by a burn Skin is largest barrier to infection The burn injury itself produces systemic release of cytokines and other substances that cause leukocyte and endothelial cell dysfunction. These alterations result in immunosuppression, and when combined with the required invasive procedures (line placements, surgical débridement, etc.) and continued loss of the skin barrier, there is increased risk for sepsis

Table 62-3 Phases of Burn Care: Acute/Intermediate

Duration: From beginning of diuresis to near completion of wound closure (begins 48-72 hrs after injury) Priorities: Wound care and closure Prevention or treatment of complications, including infection Nutritional support (attention is directed toward continued assessment and maintenance of respiratory and circulatory status, fluid and electrolyte balance, and GI and kidney function. Infection prevention, burn wound care (e.g., wound cleaning and débridement, topical antibacterial therapy, application of dressings, and wound grafting), pain management, modulation of hypermetabolism, and early positioning/mobility are priorities at this stage and are discussed in detail in the following sections) (As capillaries regain integrity, 48 or more hours after the burn, fluid moves from the interstitial to the intravascular compartment and diuresis begins. If cardiac or kidney function is inadequate, fluid overload may occur and symptoms of congestive heart failure may result)

Table 62-3 Phases of Burn Care: Rehabilitation

Duration: From major wound closure to return to individual's optimal level of physical and psychosocial adjustment Priorities: Prevention and treatment of scars and contractures Physical, occupational, and vocational rehabilitation Functional and cosmetic reconstruction Psychosocial couseling

Table 62-3 Phases of Burn Care: Emergent/Resuscitative

Duration: From onset of injury to completion of fluid resuscitation Priorities: Primary survey: A, B, C, D, E Prevention of shock Prevention of respiratory distress Detection and treatment of concomitant injuries Wound assessment and initial care (Airway obstruction can take as long as 48 hrs to develop. Mucosal sloughing of airway tissue can occur as late as 3 to 4 days postinjury; therefore, vigilant respiratory assessment during this period is crucial)

Fluid and Electrolyte Alterations

Edema forms rapidly Superficial burn cases edema to form within 4 hours A deeper burn continues to form edema up to 18 hours postinjury Caused by increased perfusion to injured area and reflects the amount of microvascular and lymphatic damage Loss of capillary integrity and fluid is localized to the burn itself which results in blister formation and edema Taut, burned tissue is unyielding to edema under it and acts like a tourniquet (especially is the burn is circumferential) Edema increases and pressure on small blood vessels in distal extremities causes an obstruction of blood flow and consequent ischemia, causing compartment syndrome Treatments may include decompression via escharotomy (surgical incision into eschar), or fasciotomy (surgical opening of the full length of fascial compartments) Reabsorption of edema begins at about 4 hrs postinjury and is complete about 4 days. This process depends on the depth of injury to the tissue

Fat Metabolism

Fatty acids can be broken down for the production of energy and ketone bodies (acetoacetic acid, beta-hydroxybutyric acid, and acetone) Ketone bodies are small compounds that can enter the bloodstream and provide a source of energy for muscles and other tissues This breakdown occurs primarily when glucose is limited (starvation/uncontrolled diabetes) Fatty acids and their metabolic products are also used for the synthesis of cholesterol, lecithin, lipoproteins, and other complex lipids

Burn Classification

First-Degree: superficial injuries that involve only the outermost layer of skin. These burns are erythematous, but the epidermis is intact; if rubbed, the burned tissue does not separate from the underlying dermis. This is known as a negative Nikolsky's sign. A typical first-degree burn is a sunburn or superficial scald. This type of injury does not contribute to morbidity and is therefore not included in calculations of TBSA Second-degree: burns involve the entire epidermis and varying portions of the dermis. They are painful and are typically associated with blister formation. Healing time depends on the depth of dermal injury and typically ranges from 2 to 3 weeks. Hair follicles and skin appendages remain intact. If these injuries take more than 3 weeks to heal, they may require grafting due to propensity for scarring Third-degree (full-thickness) burns involve total destruction of the epidermis and dermis and, in some cases, destruction of underlying tissue. Wound color ranges widely from pale white to red, brown, or charred. The burned area lacks sensation because nerve fibers are damaged. The wound appears leathery; hair follicles and sweat glands are destroyed. The severity of this burn is often deceiving to patients because they have no pain in the injury area Fourth-degree burns (deep burn necrosis) are those injuries that extend into deep tissue, muscle, or bone

Burns have some of the highest risk for health care associated infections

For a few different reasons: 1: Loss of the barrier function of the skin 2: Necrotic tissue in burn eschar along with serum proteins creates an environment conductive to bacterial growth 3: Thermal injury compromises both local and systemic intrinsic immunity Risk factors that predispose the burn wound to infection include length of hospital stay, wound size, hyperglycemia, and increasing resistance of microorganisms to antimicrobial agents The pathologic diagnosis of burn wound infection is the presence of more than 105 bacteria/g of tissue Clinical signs of infection include progressive erythema, warmth, tenderness, and malodorous exudate The most common pathogens identified were Candida, Pseudomonas aeruginosa, Serratia marcescens, Staphylococcus aureus, and Aspergillus species.

Wound Care

Goal of care/cleaning is débridement of nonviable tissue, removal of previously applied topical agents, and application of new topical agents During showers and cleaning the temperature of the water is maintained at 37.8°C (100°F), and the temperature of the room should be maintained between 26.6°C and 29.4°C (80°F and 85°F) to prevent hypothermia No single topical medication is universally effective, and the use of different agents at different times in the postburn period may be necessary A lighter dressing is used over joints to allow for mobility. Dressings may also need to be modified to accommodate splints or other positioning devices. Circumferential dressings should always be applied distally to proximally in order to promote return of excess fluid to the central circulation. If the hand or foot is burned, the fingers and toes should be wrapped individually to promote function while healing Burns to the face may be left open to air once they have been cleaned and the topical agent has been applied. Careful attention is required to ensure that the topical agent does not come in contact with the eyes or mouth. A light dressing can be applied to the face to absorb excess exudates if needed. The patient may participate in removing the dressings, providing some degree of control over this painful procedure. The wounds are then cleaned and débrided to remove any remaining topical agent, exudate, and nonviable tissue. Sterile scissors and forceps may be used to trim loose eschar and encourage separation of devitalized tissue Documentation should include color, odor, size, exudate, signs of re-epithelialization, any changes from the previous dressing change, and other key characteristics.

Liver

Highly vascular, located in the RUQ Divided into 4 lobes and a thin layer of connective tissue surrounds each lobe and divides each into small, functional unity called lobules Blood perfuses from two sources: approx 80% from the portal vein (drains the GI tract, rich in nutrients, but LACKS oxygen) and the rest from the hepatic artery which is rich in O2 Contain phagocytic cells (belong to the reticuloendothilial system) ((other organs in this system are: spleen, bone marrow, lymph nodes, lungs)) but in the liver these cells are called Kupffer cells Smallest ducts are called canaliculi and are between the lobules of the liver. They receive secretions from the hepatocytes and carry them to larger bile ducts (eventually form the hepatic duct) The hepatic duct from the liver and the cystic duct from the gallbladder to form the common bile duct which empties into the small intestine The sphincter of Oddi (located at the junction where the common bile duct enters of duodenum) controls the flow of bile into the intestine

Can lose an autograft through

If blood, serum, air, fat, or necrotic tissue are present between the recipient site and the graft, there may be partial or total loss of the graft. Infection, mishandling of the graft, or trauma during dressing changes account for most other instances of graft loss. Protect graft: Occlusive dressings are commonly used initially after grafting to immobilize the graft. Occupational therapists may construct splints to immobilize newly grafted areas. Homograft, xenograft, or synthetic dressings (discussed later) may also be used to protect grafts Donor site care: a thrombostatic agent such as thrombin or epinephrine may be applied directly to the site to decrease bleeding. Multiple dressings are available to cover donor sites. Donor sites must remain clean, dry, and free from pressure. Because a donor site is usually a partial-thickness wound, it is very painful and an additional potential site of infection. With proper care, the donor site should heal spontaneously within 7 to 14 days

Cariovascular Alterations

In burns greater than 45% TBSA, intrinsic contractile deficits of the myocardium occur. Even in a burn as small as 2%, a case has been reported of transient acute cardiomyopathy Upon injury, there is an immediate decrease in cardiac output that precedes the loss of plasma volume, although the exact mechanism why this occurs is unknown. It has been suggested that it is likely a neurogenic response to the release of inflammatory mediators Due to vasoconstrictive compensatory responses, the workload of the heart increases. Cardiac output can be maintained by the body's stress response, but this may be at the cost of increasing myocardial oxygen demands Hypovolemia is the immediate consequence of ensuing fluid loss and results in decreased perfusion and oxygen delivery. As fluid loss continues and vascular volume decreases, cardiac output continues to decrease and the blood pressure drops. This is the onset of burn shock.

Gastrointestinal Alterations

Large TBSA burns at risk for life-threatening abdominal compartment syndrome (ACS) due to large volumes of fluid required for resuscitation, fluid shift causing edema formation, and decreased abdominal wall compliance due to eschar formation. ACS is defined as sustained intraabdominal hypertension, which is intra-abdominal pressures greater than 30 cm H2O ACS may result in multiple organ dysfunction syndrome (MODS) including impairment in hepatic, kidney, pulmonary, cardiac, and neurologic function. Early indicators include abdominal distension, oliguria, and difficulties with mechanical ventilation Patients who are critically ill, including those with burns, are predisposed to altered gastrointestinal (GI) motility for many reasons, which may include impaired enteric nerve and smooth muscle function, inflammation, surgery, medications, and impaired tissue perfusion. Three of the most common GI alterations in burn-injured patients are paralytic ileus (absence of intestinal peristalsis), Curling's ulcer, and translocation of bacteria. Decreased peristalsis and bowel sounds are manifestations of paralytic ileus. Paralytic ileus and dilated bowel can lead to increased abdominal pressure, which can further increase ischemia. Gastric distention and nausea may lead to vomiting; therefore, gastric decompression is advised. Gastric bleeding secondary to massive physiologic stress may be signaled by occult blood in the stool, regurgitation of "coffee ground" material from the stomach, or bloody vomitus. These signs suggest gastric or duodenal erosion (Curling's ulcer). After a burn injury, the gastric mucosal barrier becomes permeable, allowing translocation of bacteria, which may result in severe sepsis and MODS

Causes of Liver Disorders

Liver disorders are common and may result from a virus, obesity, and insulin resistance, or exposure to toxic substances, such as alcohol, or tumors.

Drug Metabolism

Liver handles many medications such as barbiturates, opioids, sedatives, anesthetics, and amphetamines Usually results in drug inactivation but may cause activation One of the pathways involves conjugation (binding) of the med with a variety of compounds, such as glucuronic acid or acetic acid, to form a more soluble substance. These substances may be excreted in feces or urine Bioavailability is the fraction of administered med that actually reaches systemic circulation Left off on pg1338

Thermoregulatory Alterations

Loss of skin = inability to regulate temp Tend to have low body temps in the early hours post injury Hypothermia on admission is associated with increases in mortality, ventilator days, length of stay, and infection rates Most burn centers have heat panels at the bedside as additional heating sources to help maintain the patient's body temperature. The metabolic response of a burn injury may also cause core body temperature to be higher by as much as 2°C (3.6°F) compared to patients who do not have burn injuries

TABLE 62-4 Overview of Selected Topical Antimicrobial Agents Used for Burn Wounds: Specific Agents: Sulfamylon

Mafenide acetate 5%-10% (Sulfamylon) hydrophilic-based solution or cream Indication/Comment: Antimicrobial agent for gram-positive and gram-negative organisms Diffuses through eschar and avascular tissue (e.g., cartilage) Application: Apply twice a day as prescribed. Nursing Implications: Is a strong carbonic anhydrase inhibitor and may cause metabolic acidosis Diffuses through eschar and avascular tissue (e.g., cartilage) Application may cause considerable pain initially.

Kidney Alterations

May be altered because of decreased blood volume Destruction of red blood cells at the injury site results in free hemoglobin in the urine. If muscle damage occurs (e.g., from electrical burns), myoglobin is released from the muscle cells and excreted by the kidneys. Adequate fluid volume replacement restores renal blood flow, increasing the glomerular filtration rate and urine volume. If there is inadequate blood flow through the kidneys, the hemoglobin and myoglobin occlude the renal tubules, resulting in acute tubular necrosis and kidney failure.

Biosynthetic and Synthetic Dressings

May eventually replace biologic dressings as temporary wound coverings Biobrane is a dual-layer dressing of nylon and silicone that is widely used material is porous, semitransparent, and sterile. It has an indefinite shelf life and is less costly than homograft or xenograft such as pigskin can also be laid on top of a widemeshed autograft to protect the wound until the autograft epithelium grows out to close the interstices. As the Biobrane gradually separates, it is trimmed away, leaving a healed wound

Stats for Burns

Men have more than twice the incidence of burn injury than women; for both men and women, the most frequent age group for burns is between 20 and 30 years. In the United States, the race and ethnicity of patients treated in burn centers is as follows: 60% Caucasian, 19% African American, 15% Hispanic, 2% Asian American, 0.7% Native American, and 3% identified as "other" One study noted an association between the severity of burns and socioeconomic groups, with severe injuries more common in lower socioeconomic groups

Readings for Test 2

Metabolism module: Med surg: Ch 49 Nursing made easy "Puzzled about cirrhosis" p 6-10 Nursing Made easy "Hepatitis goes viral" p 38-43 Tissue Integrity module: Med surg: pg 1805-1836 "Resuscitation and early management burns" link to article in module Treatment of burn patient in primary care: pg 24-31 Violence module: Ovid artcle Mobility module: Med surg: Ch 68, pg 210-224 Stress and Coping: Med surg: pg 1830, 2149 Psych book: ch 13

Four Types of Débridement

Natural: Devitalized tissue separates fro underlying viable tissue spontaneously May take weeks to months Bacteria present at the interface of the burned tissue and the viable tissue gradually liquefy the fibrils of collagen (a protein present in skin, tendon, bone, cartilage, and connective tissue) that hold the eschar in place. Proteolytic and other natural enzymes cause this phenomenon. Mechanical: Use of surgical tools to remove eschar can be performed by skilled physicians, nurses, or physical therapists and is usually done with daily dressing changes Wet-to-dry dressings aren't advocated because of the potential of removing viable cells along with necrotic tissue Chemical: Topical enzymatic agents Can be used with topical antibacterial therapy Heavy metals such as silver deactivate the débriding agent; therefore, caution is necessary to ensure that the topical antimicrobial agent does not interfere with the chemical débridement. Alternating topicals with dressing changes may be considered Surgical: Early burn wound closure is recognized as one of the MOST IMPORTANT factors for survival with major burn Operative procedure involves either excision of the full thickness of the skin down to the fascia (tangential excision) or shaving of the burned skin layers gradually down to freely bleeding, viable tissue May be performed as soon as possible after the burn, once the patient is hemodynamically stable and edema has decreased. Ideally, the wound is then covered immediately with a skin graft (if necessary) and a dressing. If the wound bed is not ready for a skin graft at the time of excision, a temporary biologic or synthetic dressing may be used until a skin graft can be applied during a subsequent surgery CARRIES RISKS: high risk of extensive blood loss and lengthy operating/anesthesia times Can exacerbate anemia (with surgery blood loss, wound care, and ongoing hemolysis) Can result in shorter hospital stays and possibly decreased risk of complications from burn wound sepsis

Nursing Management

Nursing assessment in the emergent phase of burn injury focuses on the major priorities for any trauma patient; the burn wound is a secondary consideration to stabilization of airway, breathing, and circulation. Respiratory status is monitored closely, and pulses are evaluated, particularly in areas of circumferential burn injury to an extremity. Cardiac monitoring is indicated initially or if the patient has a history of cardiac disease, electrical injury, or respiratory conditions. Vital signs and hemodynamic status are monitored closely.

Zone of Hyperemia

Outermost zone Sustains minimal injury and may fully recover over time

Lab and Diagnostic Changes with a Burn

Possible elevation of Hematocrit Decrease in platelets (throbocytopenia) Prolonged clotting and prothrombin times Immediately after a burn: hyperkalemia (from massive cell destruction) Later: hypokalemia (from fluid shifts and inadequate Ka+ replacement) During burn shock: Hyponatremia: possible as a result of plasma loss. May also occur during 1st week of acute phase as water shifts from interstitial space and returns to vascular space

Autographs

Preferred autologous method for definitive burn wound closure after excision They can be split-thickness, full-thickness, or epithelial grafts. Because the donor site from a full-thickness graft includes both the epidermis and dermis, its use must be cautiously considered because it cannot heal spontaneously. Split-thickness autografts are more commonly used and can be applied in sheets, or they can be expanded by meshing so that they cover more than a given donor site area. Skin meshers enable the surgeon to cut tiny slits into a sheet of donor skin, making it possible to expand to cover larger areas with smaller amounts of donor skin. These expanded grafts adhere to the recipient site more easily than sheet grafts and prevent the accumulation of blood, serum, air, or purulent material under the graft. However, any kind of graft other than a sheet graft contributes to scar formation as it heals. The use of expanded grafts may be necessary in large wounds but should be viewed as a compromise in terms of cosmesis. The use of split-thickness grafts allows the remaining donor site to retain sweat glands and hair follicles and minimizes donor site healing time.

Wound Grafting

Pt with deep partial or full-thickness burns may be a candidate for skin grafting to decrease risk of infection, further loss of protein, fluid, and electrolytes (through the wound), and minimize evaporative heat loss Special attention is warranted when grafting the face (for cosmetic, functional, and psychological reasons); functional areas, such as the hands and feet; and areas that involve joints. Grafting permits earlier functional ability and reduces wound contractures When burns are very extensive, the order in which areas are grafted is chosen based on the ability to achieve wound closure as soon as possible; therefore, the chest and abdomen or back may be grafted first to reduce the total body burn surface area.

Burn Shock

Results from the combination of direct cutaneous injury, intravascular volume loss, and systemic inflammatory mediators affecting multiple physiologic systems. This systemic inflammation causes the release of free oxygen radicals that increase vascular permeability, causing subsequent peripheral edema. It has been proposed that the use of antioxidants during resuscitation may decrease this process of increased vascular permeability. As a compensatory response to intravascular fluid loss, the sympathetic nervous system releases catecholamines, resulting in an increase in peripheral resistance (vasoconstriction) and an increase in pulse rate that further decreases tissue perfusion. Prompt fluid resuscitation maintains the blood pressure in the low to normal range and improves cardiac output (see later discussion). Despite adequate fluid resuscitation, cardiac filling pressures (central venous pressure, pulmonary artery pressure, and pulmonary artery wedge pressure) remain low during the burn shock period. If adequate fluids are not administered, distributive shock occurs Generally, the greatest volume of fluid leak occurs in the first 24 to 36 hours after the burn, peaking by 6 to 8 hours. As the capillaries begin to regain their integrity, burn shock resolves and fluid returns to the vascular compartment. Diuresis will begin and continues for several days to 2 weeks. At the time of burn injury, some red blood cells may be destroyed and others damaged, resulting in anemia. Despite this, the hematocrit may be elevated due to plasma loss. Abnormalities in coagulation, including a decrease in platelets (thrombocytopenia) and prolonged clotting and prothrombin times, also occur with burn injury

Various methods are used to estimate the TBSA affected by burns

Rule of nines, the Lund and Browder method, and the palmer method

TABLE 62-4 Overview of Selected Topical Antimicrobial Agents Used for Burn Wounds: Specific Agents: Silver nitrate 0.5% aqueous solution

Silver nitrate 0.5% aqueous solution Indication/Comments: Effective against most strains of Staphylococcus and Pseudomonas and many gram-negative organisms. Does not penetrate eschar Application: Apply solution to gauze dressing and place over wound. Keep the dressing wet but covered with dry gauze and dry blankets to decrease vaporization. Nursing Implications: Monitor serum sodium (Na+) and potassium (K+) levels, and replace as prescribed. Silver nitrate solution is hypotonic and acts as a wick for sodium and potassium. Does not penetrate eschar Protect bed linens and clothing from contact with silver nitrate, which stains everything it touches.

TABLE 62-4 Overview of Selected Topical Antimicrobial Agents Used for Burn Wounds: Specific Agents: Silvadene

Silver sulfadiazine 1% (Silvadene) watersoluble cream Indication/Comment: Bactericidal agent for many gram-positive and gram-negative organisms, as well as yeast and Candida albicans Apply 1/16-inch layer of cream with a clean glove 1-3 times daily. Anticipate formation of pseudo-eschar (proteinaceous gel), which can be removed. Minimal penetration of eschar Application: Apply 1/16-inch layer of cream with a clean glove 1-3 times daily. Nursing Implications: Anticipate formation of pseudo-eschar (proteinaceous gel), which can be removed.

TABLE 62-4 Overview of Selected Topical Antimicrobial Agents Used for Burn Wounds: Specific Agents: Silver-impregnated dressings (sheets or mesh)

Silver-impregnated dressings (sheets or mesh) Indication/Comments: Broad antimicrobial effects (product specific) Delivers a uniform, antimicrobial concentration of silver ions to the burn wound. Application: Apply directly to wound. Cover with absorbent secondary dressing if needed. Nursing Implications: May produce a pseudo-eschar from silver after application Can be left in place for several days (product specific)

Burgundy-coloured urine

Suggests the presence of hemochromogens and myoglobin resulting from muscle damage. This is associated with deep burns caused by electrical injury or prolonged contact with flames.

SAMPLE

Surgical history Allergies Medications Pain Last meal Environment

Zone of Stasis

Surrounds zone of coagulation describes an area of injured cells that may remain viable but, with persistent decreased blood flow, will undergo necrosis within 24 to 48 hours

Protein Metabolism

Synthesizes almost all plasma proteins (except gamma-globulin) including albumin, alpha and beta-globulins, blood clotting factors, specifics transport proteins, and most plasma lipoproteins Vitamin K is required by the liver for synthesis of prothrombin and some other clotting factors Amino acids are used by liver for protein synthesis

Temperature in relation to Injury

Temperature and duration of contact influences the depth of injury In adults, exposure to temperatures of 54°C (130°F) for 30 seconds will result in burn injury. At 60°C (140°F), tissue destruction occurs in 5 seconds (this is a common setting for home water heater). At 71°C (160°F) or higher, a fullthickness burn occurs instantaneously

Fluid Resuscitation Formula

The ABA (2011a) fluid resuscitation formula for adults within 24 hours post thermal or chemical burn is as follows: 2 mL LR × Patient's weight in kilograms ×%TBSA 2nd-, 3rd-, and 4th-degree burns For adults with electrical burns: 4 mL LR × Patient's weight in kilograms ×%TBSA 2nd-, 3rd-, and 4th-degree burns Timing is one of the most important considerations in calculating fluid needs in the first 24 hours post burn. The starting point is the time of injury—not the time of arrival to the treating facility (Williams, 2009). The infusion is regulated so that one half of the calculated volume is administered in the first 8 hours post burn injury. The second half of the calculated volume is administered over the next 16 hours. These formulas are only a guideline. For adults, a urine output of 30 to 50 mL per hour is used as an indication of appropriate resuscitation in thermal and chemical injuries, whereas in electrical injuries a urine output of 75 to 100 mL per hour is the goal

Mortality Rate

The overall mortality rate for all total body surface area (TBSA) burns is 3.9%, with the incidence of fatality increasing as burn size increases mortality in adult burn patients, reported an overall mortality rate of 13.9% The strongest predictors for mortality in burn injuries included increased percent of TBSA burned, presence of inhalation injury, and increased age. Risk factors for death included increased age, greater TBSA, and presence of concomitant chronic diseases. This same study cited multiple organ failure and sepsis as major causes of death

Severity of Burns

These factors include age of the patient; depth of the burn; amount of surface area of the body that is burned; the presence of inhalation injury; presence of other injuries; location of the injury in areas such as the face, the perineum, hands, or feet; and the presence of a past medical history Age: Young children and older adults continue to have increased morbidity and mortality Burn Depth: classified according to the depth of tissue destruction

Airway Injuries

Upper: Result of severe upper airway edema caused by direct thermal injury or face and neck burns (can cause) obstruction of upper, including pharynx and larynx, in the early hours post burn There's a cooling effect of rapid vaporization in the pulmonary tract so direct heat injury doesn't normally occur below the glottis. However, with steam, lower area injury is possible Lower: Below the vocal cords results from inhaling the products of incomplete combustion or noxious gases and is often the source of death at the scene of a fire. Smoke inhalation injuries cause loss of ciliary action, trigger an inflammatory response causing hypersecretion, and produce severe mucosal edema and possibly bronchospasm. Alveolar surfactant production is reduced, resulting in atelectasis (collapse of alveoli). Expectoration of carbon particles in the sputum is the cardinal sign of this injury CO (Carbon monoxide) poisoning is a factor in most fatalities at the scene of a fire. Carbon monoxide combines with hemoglobin to form carboxyhemoglobin. The affinity of hemoglobin for carbon monoxide is 200 times greater than that for oxygen, and if significant quantities of carbon monoxide are present, then tissue hypoxia will occur. Pulmonary deterioration in severely burned patients can occur without obvious evidence of a smoke inhalation injury, and symptoms may be delayed as long as 24 to 36 hours after injury. Bronchoconstriction (caused by release of histamine, serotonin, and thromboxane [a powerful vasoconstrictor]) and chest constriction secondary to circumferential torso burns can contribute to this deterioration. Even without pulmonary injury, hypoxia may be present Early in the postburn period, catecholamine release in response to the stress of the burn injury alters peripheral blood flow, thereby reducing oxygen delivery to the periphery. Later, hypermetabolism and continued catecholamine release lead to increased tissue oxygen consumption, which can lead to hypoxia. Restrictive pulmonary excursion may occur with full-thickness burns encircling the thorax resulting in decreased tidal volume. In such situations, an escharotomy may be necessary to restore adequate chest excursion Late pulmonary complications secondary to inhalation injuries include mucosal sloughing of the airway, which can lead to obstruction, increased secretions, inflammation, atelectasis, airway ulceration, pulmonary edema, and tissue hypoxia

Ammonia Conversation

Use of amino acids from protein for gluconeogenesis forms ammonia as the byproduct. This metabolically generated ammonia is then converted into urea Ammonia produced by bacteria in the intestines is also removed from portal blood for urea synthesis Liver converts ammonia, a toxin, into urea which is excreted in the urine

Vitamin and Iron Storage

Vitamins A, B, D, and several B-complex vitamins are stored in large amounts in the liver Because of this, liver extracts have been used for a variety of nutritional disorders but this has to be done cautiously because of the risk of exposure to pathogens

Liver Terms

ascites: an albumin-rich fluid accumulation in the peritoneal cavity asterixis: involuntary flapping movements of the hands cirrhosis: a chronic liver disease characterized by fibrotic changes, the formation of dense connective tissue within the liver, subsequent degenerative changes, and loss of functioning cells constructional apraxia: inability to draw figures in two or three dimensions endoscopic variceal ligation (EVL): procedure that uses a modified endoscope loaded with an elastic rubber band passed through an overtube directly onto the varix (or varices) to be banded to ligate the area and stop bleeding fetor hepaticus: sweet, slightly fecal odor to the breath, presumed to be of intestinal origin; prevalent with the extensive collateral portal circulation in chronic liver disease fulminant hepatic failure: sudden, severe onset of acute liver failure that occurs within 8 weeks after the first symptoms of jaundice hepatic encephalopathy: central nervous system dysfunction frequently associated with elevated ammonia levels that produce changes in mental status, altered level of consciousness, and coma jaundice: condition where the body tissues, including the sclerae and the skin, become tinged yellow or greenishyellow, due to high bilirubin levels orthotopic liver transplantation (OLT): grafting of a donor liver into the normal anatomic location, with removal of the diseased native liver portal hypertension: elevated pressure in the portal circulation resulting from obstruction of venous flow into and through the liver sclerotherapy: the injection of substances into or around esophagogastric varices to cause constriction, thickening, and hardening of the vessel and stop bleeding xenograft:transplantation of organs from one species to anotherse.

Burn Terms

autograft: a graft derived from one part of a patient's body and used on another part of that same patient's body carboxyhemoglobin: a compound of carbon monoxide and hemoglobin, formed in the blood with exposure to carbon monoxide collagen: a protein present in skin, tendon, bone, cartilage, and connective tissue contracture: shrinkage of burn scar through collagen maturation débridement: removal of foreign material and devitalized tissue until surrounding healthy tissue is exposed donor site: the area from which skin is taken to provide a skin graft for another part of the body eschar: devitalized tissue resulting from a burn or wound escharotomy: a linear excision made through eschar to release constriction of underlying tissue excision: surgical removal of tissue fasciotomy: an incision made through the fascia to release constriction of underlying muscle homograft: a graft transferred from one human (living or cadaveric) to another human; also called allograft hydrotherapy: cleansing of wounds through the use of bath, shower, shower cart table, or immersion Nikolsky's sign: rubbing of the epidermis, resulting in exfoliation or separation from the dermal layer xenograft: a graft obtained from an animal of a species other than that of the recipient (e.g., pigskin); also called heterograft

Homografts (allografts) and Xenografts (heteografts)

biologic dressings and are intended to be temporary wound coverage Homografts are skin obtained from recently deceased or living humans other than the patient. Xenografts consist of skin taken from animals (usually pigs). Therefore, the body's immune response will eventually reject them as a foreign substance. Several uses: Temporary wound coverage and protection of granulation tissue until autografting is possible Test graft in preparation for the patient's own skin graft to determine if the bed will accept the graft Decrease the wound's evaporative water and protein loss Provide an effective barrier for entry of bacteria Decrease pain by protecting nerve endings They stay in place for varying lengths of time but are removed in instances of infection or rejection. Another advantage is that fewer dressing changes may be required Homografts tend to be the most expensive biologic dressings. They are available from skin banks in fresh and cryopreserved (frozen) forms. Homografts are thought to provide the best infection control of all biologic or biosynthetic dressings available. Revascularization occurs within 48 hours, and the graft may be left in place for several weeks. Pigskin is available from commercial suppliers. It is available fresh, frozen, or lyophilized (freeze-dried) for longer shelf life. Pigskin is used for temporary covering of clean wounds such as superficial partial-thickness wounds and donor sites. Although pigskin does not vascularize, it adheres to clean superficial wounds, providing pain control and reducing evaporative fluid loss while the underlying wound re-epithelializes

Patients with burns have particularly prolonged lengths of hospital stay

many of these patients require surgical interventions, extensive pain control, immobilization and rehabilitation, and prolonged intravenous (IV) medication regimens, especially with antibiotics and opioids. In addition, patients with smoke inhalation and electrical injuries require particularly lengthy care regimens

Lund and Browder Method

more precise method of estimating the extent of a burn is the Lund and Browder method (ABA, 2011a), which recognizes the percentage of surface area of various anatomic parts, especially the head and legs, as it relates to the age of the patient. By dividing the body into very small areas and providing an estimate of the proportion of TBSA accounted for by each body part, clinicians can obtain a reliable estimate of TBSA burned. The initial evaluation is made on arrival of the patient to the hospital and should be revised within the first 72 hours, because demarcation of the wound and its depth present themselves more clearly by this time

Rule of Nines

most commonly used method to estimate the extent of burns in adults is the rule of nines (Fig. 62-3). This system is based on dividing anatomic regions, each representing approximately 9% of the TBSA, allowing clinicians to quickly obtain an estimate. If a portion of an anatomic area is burned, the TBSA is calculated accordingly—for example, if approximately half of the anterior arm is burned, the TBSA burned would be 4.5%

Modulation of Hypermetabolism

profound metabolic abnormalities fueled by the exaggerated stress response to the injury. The body's response has been classified as hyperdynamic, hypermetabolic, and hypercatabolic Can affect morbidity and mortality by increasing the risk of infection and slowing the healing rate. Persistent hypermetabolism may last up to 1 year after burn injury and well past the acute hospitalization Early enteral nutrition is advocated to ameliorate the hypermetabolic response and prevent ileus and stress ulcerations Nutrition should be provided upon arrival to the burn center and may require placement of a feeding tube. Patients who are critically ill may even have their feedings continued intraoperatively if the airway is protected. Effective nutrition management depends on delivery of appropriate amounts of micronutrients, carbohydrates, lipids, and protein Parenteral nutrition is associated with many complications and should only be provided to patients with intolerance to enteral feeding or prolonged ileus Carbohydrates are the most important energy source for these patients to ensure proper wound healing. Fat, although a required nutrient, should be provided in more limited quantities. In addition, recommendations from recent literature advocate protein requirements of 1.5 to 2 g/kg/day Appropriate manipulation of external temp can decrease energy expenditure Insulin therapy needed to treat hyperglycemia that happens from accelerated gluconeogenesis and is beneficial in muscle protein synthesis PHARMACOLOGIC: Oxandrolone, an anabolic steroid, is commonly administered to patients with burns because it improves protein synthesis and metabolism. Administration of propranolol (Inderal) (a beta-blocker) not only decreases heart rate but also blocks harmful catecholamine effects

On the Scene Care for Burns And Initial ED Care

remove the patient from the source of injury and stop the burning process while preventing injury to the rescuer. Rescue workers' priorities include establishing an airway, supplying oxygen (100% oxygen if carbon monoxide poisoning is suspected), inserting at least one large-bore IV line, and covering the wound. Irrigation of chemical injury must begin immediately An immediate primary survey of the patient is carried out to assess the ABCDEs: airway (A) with consideration given to protecting the cervical spine, gas exchange or breathing (B), circulatory and cardiac status (C), disability (D) including neurologic deficit, and expose and examine (E) while maintaining a warm environment The secondary survey focuses on obtaining a history, the completion of the total body system assessment, initial fluid resuscitation, and provision of psychosocial support of the conscious patient Initial priorities in the ED remain airway, breathing, and circulation. For mild pulmonary injury, 100% humidified oxygen is administered, and the patient is encouraged to cough so that secretions can be expectorated or removed by suctioning. For more severe situations, it may be necessary to remove secretions by bronchial suctioning and to administer bronchodilators and mucolytic agents. It is essential to continuously monitor airway patency, because a previously stable airway may rapidly deteriorate as edema increases and toxic effects of smoke inhalation become apparent. Once urgent respiratory needs are appropriately addressed, fluid resuscitation is initiated in burns greater than 20% TBSA. Fluids are necessary to support circulatory function and tissue perfusion. The kidney and GI tract are particularly susceptible to ischemia, organ dysfunction, and organ failure if fluid resuscitation is delayed or inadequate. Baseline weight and laboratory test results are obtained, and these parameters must be monitored closely in the immediate postburn (resuscitation) period. Both underresuscitation and overresuscitation with fluids are associated with poor outcomes, such as shock, ischemic complications, and MODS for underresuscitation (see Chapter 14) and heart failure and pulmonary edema for overresuscitation Peripheral IV access can be obtained to facilitate fluids but, with larger burns, central venous access is required TBSA is calculated and fluid resuscitation with lactated Ringers (LR) should be initiated using ABA fluid resuscitation formulas. LR is the crystalloid of choice because its composition and osmolality most closely resembles plasma and because the use of normal saline is associated with hyperchloremic acidosis

Reducing Mortality from Fire

smoke alarms, carbon monoxide detectors, safer appliances for heating and cooking, flame-resistant materials, child-resistant lighters, and sprinkler systems Research in areas of fluid resuscitation, emergency burn treatment, inhalation injury and management, nutritional requirements, early excision (surgical removal of tissue), skin grafting, and the use of skin substitutes have contributed greatly to the decrease in burn deaths

Pathophysiology of Burns

some of the worst traumatic injuries sustained because the initial injury can evolve and worsen over time. The clinical course of burns depends on the initial insult and the subsequent environmental and treatment factors Burn injury is the result of a chemical injury or heat transfer from one site to another, causing tissue destruction through coagulation, protein denaturation, or ionization of cellular contents. The burn wound is not homogenous; rather, tissue necrosis occurs at the center of the injury with regions of tissue viability toward the periphery The skin and the mucosa of the upper airways are the most common sites of tissue destruction, although deep tissues, including the viscera, can be damaged by electrical burns or by prolonged contact with a heat or chemical source The release of local mediators and changes in blood flow, tissue edema, and infection can cause progression of the burn injury. Another potential mechanism of burn injury is radiation exposure. This has received increased attention in recent years due to threats of terrorism and recent world events. Radiation injuries produce two detrimental effects. The first is a thermal effect, which results in cutaneous burn injuries. The second effect is damage to the cellular deoxyribonucleic acid (DNA), which may be localized or affect the whole body. Morbidity and mortality are dose dependent Treatment for the cutaneous burn is the same as other burns

Guiding the Treatment Plan

the following are essential: documentation of body temperature, body weight, and preburn weight; history of allergies, tetanus immunization, past medical and surgical history, and current illnesses; and a list of current medications

Palmer Method

with scattered burns, the palmer method may be used to estimate the extent of the burns. The size of the patient's hand, including the fingers, is approximately 1% of that patient's TBSA

CHART 62-2 American Burn Association Criteria for Referral to a Burn Center

• Partial-thickness burns covering 10% of total body surface area or greater • Burns involving the face, hands, feet, genitalia, perineum, or major joints • Third-degree burns • Electrical burns, including lightning injury • Chemical burns • Inhalation injury • Burn injury in patients with preexisting medical disorders • Any patients with burns and concomitant trauma • Children with burn injuries in facilities that do not specialize in pediatric care • Patients who will require special social, emotional, or longterm Rehabilitation