Burn is defined as destruction found in the epidermal tissue, dermal tissue, or deeper tissues, due to contact with thermal, chemical, or electrical agents.


During wound healing, proinflammatory factors, such as interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNF-alpha) are released. This promote chronic inflammation and various inflammatory cells are formed in the affected tissue. Angiogenesis starts into the damaged tissue. Tumor necrosis factor-alpha, prostaglandin E2 also play a role in the formation of inflammatory response in wound healing. Any damage to the formation of this response can result in scarring after the burn. The primary cytokine responsible for scar formation is transforming growth factor-beta (TGF-β) secretion which is released from the other inflammatory cells and myofibroblasts. Hypertrophic scar does not develop when the reticular layer is not affected in burning. As a result, inflammatory cells, fibroblasts, newly formed blood vessels, and collagen deposits develop hypertrophic scar tissue in the reticular layer [23].


the skin surface is severely destroyed.

[ During this period, infection may develop on damaged skin. Therefore, in the treatment of burn wounds, protecting the damaged skin and multidisciplinary approaches are needed for preventing scar formation while healing process.]

. Burn pathophysiology can be broken into local and systemic response.

When excessive heat is transferred to the skin, it radiates outward from the point of initial contact and forms a local response with three zones in all directions.

In a large burn, two clinically significant processes occur. The release of systemic inflammatory mediators and cytokines result in increased capillary permeability and wide scale extravasation of fluid and proteins from the intravascular to the extravascular space.+++++++++++++

During the first 24 hours after a burn injury, capillary integrity to water, solutes, and plasma proteins is drastically impaired reducing intravascular volume, a moderately decreased cardiac output, and increasing extravascular fluid volume by increasing interstitial volume.

Fluid resuscitation using warmed crystalloid solutions is the mainstay of therapy during this period, in addition to the correction of any electrolyte abnormalities.

Because of his rapidly changing fluid status, a large-bore intravenous and central venous monitoring are probably warranted. Should frequent blood gas sampling be required because of a respiratory burn, an arterial catheter may also be warranted.

The patient should be warmed and resuscitated with warm fluids to increase his body temperature and restore his intravascular volume before proceeding to the operating room. The operating room temperature should be warm to hot. Warming blankets, fluid warmers, and heated humidification are indicated in attempt to maintain the patient's body temperature.

The patient's airway may be affected by the inhalation of heated, possibly toxic substances causing airway edema and lung injury, which can be worsened by fluid loading and capillary leak. In addition to swelling and erythema, a respiratory burn may be accompanied by friable tissue in the airway, perhaps with a propensity for bleeding. Intubation, if necessary, should be performed early before the airway becomes obstructed, and appropriate equipment available in case the patient cannot be intubated using direct laryngoscopy.++++++


Intravascular volume is replenished with crystalloid fluid, typically lactated Ringer solution. Colloid solutions are not used because they have been linked to greater formation of pulmonary infiltrates and decreased urine output.

The later stage of a burn injury is characterized by a high cardiac output, a dramatically increased metabolic rate, and protein catabolism.

Content 9






Electrolyte Management


During the first 24 hours after a burn injury, capillary integrity to water, solutes, and plasma proteins is drastically impaired reducing intravascular volume, and increasing extravascular fluid volume.

Intravascular volume is replenished with crystalloid fluid, typically lactated Ringer solution.

Colloid solutions are not used because they have been linked to greater formation of pulmonary infiltrates and decreased urine output.

Parkland Formula

There are several formulas to guide early fluid requirements, the most established being the Parkland formula. This method calculates fluid requirements for the first 24 hours post burn as 4 mL/kg/% of total body surface area (TBSA) burned. Half of the calculated volume is given over the first 8 hours; the remainder, over the following 16 hours. More fluid can be given as necessary to maintain a urine output greater than 30 to 50 mL/kg/h. In certain circumstances, such as crush injuries or electric burns that produce myoglobinuria, a higher urine output may be desirable to prevent pigment nephropathy. If fluid intake is increased repeatedly without improvement in urine output, placement of a central venous catheter or pulmonary artery catheter may aid in evaluation of intravascular volume.

After 24 hours, the characteristics of the patient's vascular system change as it begins to reabsorb extravascular fluid. At the same time, burns predispose to considerable evaporative losses. During the second 24-hour period, patients with substantial burns are generally given colloid solutions equal to 0.3 to 0.5 mL/kg/% TBSA burned, supplemented with 5% dextrose in water to maintain adequate urine output. Patients with smaller burned areas (<30% TBSA) may not require colloid and can often be given standard maintenance fluids. In the postresuscitation period, the goal of fluid management is to allow the patient to mobilize, excrete fluid, and return to normal preburn weight by postburn days 8 to 10. Thus, maintenance of fluid requirements after 48 hours is calculated to allow for daily losses of 2% to 3% of maximal body weight from insensate losses.

Electrolyte disturbances are common after burn resuscitation and should be carefully monitored perioperatively. After resuscitation, patients may be slightly hyponatremic from administration of high volumes of hypotonic fluids. Hyponatremia does not typically require treatment, and is usually corrected by postresuscitation diuresis. Patients may later become hypernatremic from excessive water losses and hyperglycemia-induced diuresis. Hyperkalemia, which also is common after large burns that destroy tissue, can be exacerbated by hypoventilation and acidosis. While ionized calcium is rarely affected by burn injuries, total calcium levels may be low because levels of serum-binding proteins are low.


  • Temperature control is of paramount importance, and requires the use of warming blankets, a warm ambient room temperature, and warm fluids.

  • Succinylcholine is avoided except within the first 24 to 48 hours post burn.

  • Early intervention is imperative in patients with an anticipated inhalation injury.

  • Carbon monoxide poisoning is not accurately reflected in the patient's Sao2 or Paco2.


Cardiovascular Management







Treatment of Special Problems


If fractures occurred at the time of the burn, they can be treated with the use of skeletal traction or external supports such as splints. Diagnosis may be delayed if the fractures do not result in any obvious deformity. If fractures occur secondary to disuse osteoporosis, they are usually minimally displaced and heal uneventfully. Pathologic fractures are less common with early mobilization.


. Prolonged exposure of bone sometimes results in the formation of a tangential sequestrum in the devitalized cortex. Exposed bone surfaces can be drilled to promote the formation of a granulation tissue bed for skin grafting without an increased risk of infection. The prolonged use of pins for skeletal traction causes infection in 5% of patients who require traction. The use of threaded traction pins minimizes the motion of the pin in the bone. Pins should be removed as soon as possible.

Exposed Joints

Children and adolescents with exposed joint surfaces may retain some function after healing, but adults often develop joint ankylosis or deformities that require arthrodesis at a later date. To maintain the joint in the desired position, traction can be used. The joint should be irrigated with hypochlorite solution daily and debrided as necessary. The exposed bone surfaces can be drilled to promote the formation of granulation tissue. When the bed of tissue covers the joint, skin grafting is performed.

Heterotopic Ossification

Heterotopic ossification (HO)is the presence of lamellar bone in nonskeletal tissue. Periarticular bone formation is seen in 2–3% of patients with severe burns. Although the cause is unknown, predisposing factors include full-thickness burns involving more than 30% of the body surface, prolonged immobilization, and superimposed trauma. The location of the HO is not determined by the distribution of the burns. Ossification can occur in any of the major joints. In adults, the elbow is the joint most frequently affected; the hip is rarely affected. In children, the hip and elbow are common sites; the shoulder is an uncommon site.

HO can continue to form as long as open granulating wounds are present. If joint ankylosis does not occur, the ossification gradually diminishes after the burns heal. In children, it may disappear completely. If joint ankylosis occurs, surgical resection is indicated and usually restores a functional arc of motion, particularly when the articular surface is not damaged. This may be done with multiple small incisions without raising cutaneous flaps. Early mobilization of patients with burns decreases the incidence and severity of heterotopic ossification.




Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.


Content 3

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Content 1

A 75-year-old triathlete complains of gradually worsening vision over the past year. It seems to be involving near and far vision. The patient has never required corrective lenses and has no significant medical history other than diet-controlled hypertension. He takes no regular medications. Physical examination is normal except for bilateral visual acuity of 20/100. There are no focal visual field defects and no redness of the eyes or eyelids. Which of the following is the most likely diagnosis?

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The correct answer is A. You answered A.

Age-related macular degeneration is a major cause of painless, gradual bilateral central visual loss. It occurs as nonexudative (dry) or exudative (wet) forms. Recent genetic data have shown an association with the alternative complement pathway gene for complement factor H. The mechanism link for that association is unknown. The nonexudative form is associated with retinal drusen that leads to retinal atrophy. Treatment with vitamin C, vitamin E, beta-carotene, and zinc may retard the visual loss. Exudative macular degeneration, which is less common, is caused by neovascular proliferation and leakage of choroidal blood vessels. Acute visual loss may occur because of bleeding. Exudative macular degeneration may be treated with intraocular injection of a vascular endothelial growth factor antagonist (bevacizumab or ranibizumab). Blepharitis is inflammation of the eyelids usually related to acne rosacea, seborrheic dermatitis, or staphylococcal infection. Diabetic retinopathy, now a leading cause of blindness in the United States, causes gradual bilateral visual loss in patients with long-standing diabetes. Retinal detachment is usually unilateral and causes visual loss and an afferent pupillary defect.


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A 42-year-old African-American man has been diagnosed with hypertension for the past 10 years and treated with medication. One morning, he is found unresponsive by his wife. He is taken to the emergency department and pronounced dead by the physician. An autopsy revealed cardiac hypertrophy and a narrowing of the aorta just distal to the ligamentum arteriosum, with dilation of the intercostal artery's ostia. How could the death have possibly been prevented?




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