Theme: Burn trauma. Pathogenesis. Diagnostic criteria. Clinic
1. Integumentary changes resulting from burn injury
2. Types of burns
3. Estimation of burn’s depth
4. Methods of determination of burn depth
5. Estimation of the lesions’ area
6. Prediction of burn’s severity
7. Burn disease
8. Formulation of the diagnosis in case of burns
9. Chemical burns
10. Electric burns
Burn is the lesion of tissues, caused by the influence of heat (thermal), chemicals, electricity, radiation. According to this, there are heat, chemical, electric burns. Among surgical diseases burns take 2 %.
Depth of burn depends on duration of the heat factor’s influence. Heat agents with lower temperature but longer duration of their influence cause the same lesion as heat agents with higher temperature but shorter duration of influence.
Guillaume Dupuytren (1777–1835) who developed the degree classification of burns
Cave paintings from more than 3,500 years ago document burns and their management. The 1500 BCE Egyptian Smith papyrus describes treatments using honey and the salve of resin. Many other treatments have been used over the ages, including the use of tea leaves by the Chinese documented to 600 BCE, pig fat and vinegar by Hippocrates documented to 400 BCE, and wine and myrrh by Celsus documented to 100 CE. French barber-surgeon Ambroise Paré was the first to describe different degrees of burns in the 1500s. Guillaume Dupuytren expanded these degrees into six different severities in 1832.
first hospital to treat burns opened in
Anatomy of Skin:
Integumentary changes resulting from burn injury. Anatomic Changes
The skin is the largest organ of the body. Each of its two major layers, the epidermis and
dermis, has several sub layers. The
epidermis, the outer layer of skin, is a superficial layer of stratified epithelial tissues approximately
The basement membrane, a
thin noncellular protein surface, separates the dermis from the epidermis.
The dermis is sometimes called the "true skin" because it is not
constantly shed and replaced; it is
thicker than the epidermis and ranges in thickness from 0.60 to
When burn injury occurs, the skin can regenerate as long as parts of the dermis are present. When the entire layer of dermis is burned, all epithelial cells or dermal appendages are destroyed, and the skin can no longer regenerate spontaneously. The subcutaneous tissue, or superficial fascia, varies in thickness and lies below the dermis. With deep burns, the subcutaneous tissues may be damaged, leaving bones, tendons, and muscles exposed.
■ Functional Changes
The skin serves multiple functions. The skin is primarily a protective barrier against injury and microbial invasion from the environment. A burn injury breaks this barrier, greatly increasing the risk for infection.
The skin also helps maintain the delicate fluid and electrolyte balance essential for life. After a burn injury, massive fluid loss occurs through evaporation. Water vapor can evaporate through burn-injured skin four times as rapidly as from intact skin. The rate of evaporation is proportional to the total body surface area burned and the depth of injury.
Skin is important in thermoregulation. Normally the body can adjust to most fluctuations in environmental temperatures because subcutaneous fat provides insulation and because blood flow to the skin changes with these fluctuations in environmental temperature. When the skin is damaged, the body cannot adjust to the loss of heat as readily, and body temperature tends to decrease.
The skin functions as an excretory organ through perspiration. Full-thickness burns destroy the sweat glands, which results in a loss of excretory ability.
The skin is the largest sensory organ of the body. Pain, pressure, temperature, and touch are sensed on the skin in normal daily activities, which allows a person to react to changes in the environment. All burn injuries are painful. With partial-thickness burns, nerve endings are exposed to the surface, which causes an increased sensitivity and a subsequent increase in pain. With full-thickness burns, nerve endings are completely destroyed. Initially these wounds are completely anesthetic (do not transmit sensation) when a sharp stimulus is applied. Despite this destruction, clients often complain of a dull or pressure-type of pain in these areas.
Skin exposed to sunlight produces vitamin D. The conversion of cholesterol derivatives into the active form of vitamin D is completed in the skin. Partial-thickness burns reduce the activation of vitamin D; this conversion is lost completely in full-thickness burns.
The skin is an important determinant of physical identity. The skin's cosmetic quality contributes to each person's unique appearance. With a change in appearance through a major burn, severe psychological problems may develop.
The temperature of the body's internal environment falls within a narrow range (approximately 84.2° to 109.4° F [29° to 43° C]) compared with the wide temperature fluctuations in the external environment. The body has several mechanisms to compensate for wide variations in external temperature. Circulating blood both provides and dissipates heat. Heat dissipation is efficient under normal conditions. When heat is applied to the skin, the temperature of the immediate subdermal layer rises rapidly. As soon as the heat source is removed, the body's compensatory mechanisms quickly return the area to a normal temperature. If the heat source is not removed, or if it is applied at a rate or level that exceeds the skin's capacity to dissipate it, cellular destruction occurs.
The skin can tolerate temperatures up to 104° F (40° C) without sustaining injury. At temperatures of 158° F (70° C) and above, cell destruction is so rapid that brief periods of exposure damage the skin down to and including the subcutaneous level.
Types of Burn Injury
Burn is the lesion of tissues, caused by the influence of heat (thermal), chemicals, electricity, radiation. According to this, there are heat, chemical, electric burns. Among surgical diseases burns take 2 %.
Burns are extremely dangerous and excruciatingly painful, even a minor burn can be extremely painful.
They can cause a severe damage to the skin and in some cases also to some internal organs of the body. They form permanent or temporary marks on the skin and involve the damage of the layers of skin.
Basically burns are caused by any hot object or a chemical. Usually the most common agent causing burns is the fire. Other agents are hot liquids, electricity and chemicals.
Burns are of four types and are classified according to the degree at which they destroy the human skin and their causes. The treatment of each type of burns is different from others.
Burn depth depends on duration of the heat factor’s influence. Heat agents with lower temperature but longer duration of their influence cause the same lesion as heat agents with higher temperature but shorter duration of influence.
Types of Burn Injury
Flash - Explosions of natural gas, propane, gasoline and other flammable liquids. Intense heat for a very brief period of time. Clothing is protective unless it ignites.
Flame - Exposure to prolonged, intense heat. House fires, improper use of flammable liquids, automobile accidents, ignited clothing from stoves/heaters.
Scalds - Burns caused by hot liquids. Water, oil, grease, tar, oil. Water at 140 degrees F, creates a deep burn in 3 seconds, but at 156 degrees F will cause the same injury in 1 second. (Coffee is 180 degrees F just brewed). Circumferential burns should raise suspicion of non-accidental trauma. Tar needs to be removed either with an adhesive remover solution
or petroleum based dressings.
Contact—In order to get a burn from direct contact, the object touched must either have been extremely hot or the contact was abnormally long. The latter is a more common reason, and these types of burns are commonly seen in people with epilepsy or those who misuse alcohol or drugs. They are also seen in elderly people after a loss of consciousness; such a presentation requires a full investigation as to the cause of the blackout. Burns from brief contact with very hot substances are usually due to industrial accidents. Contact burns tend to be deep dermal or full thickness.
Caused by strong acids or alkali substances. They continue to cause damage until the agent is inactivated. Alkali substances usually cause more severe injury since they react with the lipids in the skin.
Caused by either AC or DC current. Current follows the path of least resistance and causes injury in areas other than the contact/entry site. They cannot be judged from the external injury alone. High voltage > 1,000 volts, low voltage < 1,000 volts and lightening. Electrical burns are thermal burns from very high heat.
Caused by alpha, beta or gamma radiation. They may need to have some type of decontamination done to stop the injury.
Chemical burns appear due to influence on the skin, mucous membrane (mucosa) concentrated solution of acids, alkalines, salts of heavy metals, toxic gases. Depth of a lesion of tissues in cases of chemical burns depends on such conditions, as nature of the substance, it’s concentration, temperature of the last condition of it’s action. We can change only the last condition by means of early, quick and effective first aid. Action of some chemical can cause not only lesion of skin and mucosa, but total toxic effect. For example, in cases of burns, caused by phenols, salts of “Hy”: by – P – toxic lesion of kidneys; by P – aid – toxic lesion of liver.
Influence of acids, salts of heavy metals causes coagulation of proteins, dehydration of tissues, leads to formation of coagulate necrosis with superficial dense crust.
Concentrated solutions of alkalis dehydrate tissues, bind with proteins and hydrolyzes fats. Alkalis penetrate tissues deeper than acids and cause deeper lesion. Such necrosis is called coliquative, or wet. Crust, that is formed after that is soft, and after its separation bleeding of the tissues appear.
In the cases with spread burns there is a danger of the development of intoxication, caused by re sorbtion of the substances of decomposition of tissues. Quantity of toxic substances, that have resorbted, depends on burn’s area.
Chemical burns of I and st. are referred to superficial, III-IV st. – deep burns. In case of the burns I st. patients complain on pain, burning. During examination of the place of chemical action one could see localized hyperemia with swelling of the skin (it’s more visible in cases of alkali burns). All types of skin sensitivity are preserved, pain sensitivity is more acute than normally.
In cases of II st. burns there is superficial – dry (in cases of acid burns) or gelatin – like – soapy (in cases of alkali burns) crust. Crust is very thin, and could be taken easily into a fold.
In the cases of (III-IV st) deep chemical burns crust is dense and thick, it couldn’t be taken into a fold. Crust is unmovable, like wet necrosis in case of alkali burns. Crust is dry in case of acid burn. All types of skin senility are absent. There is no possibility to differ III and IV st. of chemical burns by first examination.
In cases of burns III st. all layers of skin become necrotic. In cases of burns IV st. all underlying tissues (even to bones) become necrotic.
Only after 3-4 weeks, when burn crust has separated one can estimate depth of necrosis: if only skin has separated – then it is III st. if also underlying necrotic tissues have separated – then it is IV st.
Radiation burns it is the lesion of skin caused by specific action of fissures of radiation.
Electric burns due to action of electricity with a tension more than 24 V, burn could appear. Action of electricity is determined by its direct influence during passing the body or by heat action that is formed an that moment. Heat action of electricity, according to the Djoul’s rule, depend on voltage of electricity, resistance of tissues and duration of contact with conductor. The most severe lesions are situated in places of entry and reentry of electricity the lesion of tissues mainly depends on their resistance, that why nerves, vessels become mostly affected. Tissues that gave water have lower resistance and better conduct electricity.
Electric trauma – is the action of electricity that manifest in changing of ion’s concentration and polarization in electric field. Electricity cause trans formation of intracellular proteins into gel with formation of coagulate necrosis. Aggregation of thrombocytes and leucocytes cause thrombosis of small blood vessels with the disorders of blood circulation and development of secondary necrosis.
Total biological action of electricity is characterized by disturbances of cardiac function caused by electrochemical changes, especially polarization of cell’s membranes and nervous fibers and is accompanied by cramps of muscles. In severe cases total action of high Voltage electricity manifest itself by electric shock with loose of consciousness, apnea, fibrillation of heart ventricles. By the way, asystole can appear not only at the moment of trauma or right after it, but after some hours and days. Special feature (peculiarity) of electric burns is their painless due to lesion of nerve endings. Dry necrosis with its not fast separation of necrotic tissues differs from such necrosis in case of heat burns. Another differ of electric burn is progressive necrosis, spreading of necrosis on underlying tissues, caused by thrombosis of blood vessels. In case of electric burn lesion spreads not only on the all skin, but to muscles and bones. In case of thrombosis of big vessels development of gangrene is possible.
As was said before, after influence of electricity of high voltage burns in places of entry and reentry appear. This burns are deep – III-IV st.
Tissues underlying the skin die more than skin. On the way of electricity all tissues become necrotic and necrotic and thrombosis of vessels also appear. That’s why the patient’s state depends not only on spreading of skin necrosis that has bordered in the diameter 2-3 cm, but lesion of underlying tissues on the way of electricity. In case of injuring of big vessels necrosis of the tissues, gangrene of limbs or other parts of the body can develop.
In place of entry and reentry “signs of electricity” – burn wounds-appear.
Estimation of burn’s depth
Note: The list below shows 4 burn degrees. While most of the public does not recognize the 4th degree, it is the correct term. The table below, with 3 degrees, is also correct. Both are acceptable. Determining burn depth is important. Things to consider are temperature, mechanism, duration of contact, blood flow to skin, and anatomic location. Epidermal depth varies with body surface, which can offer varying degrees of thermal protection. Older adults and young children also have thinner skin.
The American Burn Association (ABA) about DEPTH OF BURN INJURY
The magnitude of a burn injury is based on the depth and extent of the total body surface burn. The degree of tissue destruction is determined by what agent specifically caused the burn and by the temperature and duration of exposure to the heat source.
Variations in skin thickness over different parts of the body also influence burn depth. In areas where the epidermis and dermis are thin (e.g., eyelids, ears, nose, genitalia, tops of the hands and feet, fingers, and toes), a short exposure to extreme temperatures can result in a deep burn injury. The skin is thinner in older adults, which predisposes them to increased burn severity, even at lower temperatures of shorter duration.
Burn wounds are classified as superficial-thickness wounds, partial-thickness wounds, full-thickness wounds, and deep full-thickness wounds. The partial-thickness wounds are further separated into superficial and deep subgroups. Table 68-1 characterizes the clinical differences of these burns.
The American Burn Association (ABA) describes burns as minor, moderate, or major depending on the depth, extent, and location of injury.
SUPERFICIAL-THICKNESS WOUNDS. Of all burn types, superficial-thickness wounds have the least destruction because the epidermis is the only portion of the skin that is injured. The basal epithelial cells and basement membrane— structures necessary for the total regeneration of epithelial cells—remain present.
Superficial-thickness wounds often result from prolonged exposure to low-intensity heat (e.g., sunburn) or short (flash) exposure to high-intensity heat. Erythema with mild edema, pain, and increased sensitivity to heat occurs as a result. Peeling of dead skin (desquamation) occurs for 2 to 3 days after the burn, and the area rapidly heals in 3 to 5 days without a scar. No significant clinical consequences occur at this level of injury.
PARTIAL-THICKNESS WOUNDS. A partial-thick-ness wound involves the entire epidermis and varying depths of the dermis. Depending on the amount of dermal tissue damaged, partial-thickness wounds are further subdivided into superficial partial-thickness and deep partial-thickness injuries.
SUPERFICIAL PARTIAL-THICKNESS WOUNDS. Superficial partial-thickness wounds result from either increased duration or increased intensity of exposure. These wounds are typically erythematous and moist. The classic vesicle (blister) forms as the stratum corneum and stratum granulosum are destroyed. When intact, the blister forms a sterile environment, which protects the wound from potential infection and excess water loss. However, large or numerous blisters are opened to promote healing and prevent immuno-suppression.
Superficial partial-thickness wounds result in increased pain sensation. Nerve endings are exposed to the surface, and any stimulation (touch or temperature change) causes intense pain. With standard treatment these burns heal in 10 to 14 days with no scar, but some minor pigment changes may occur.
DEEP PARTIAL-THICKNESS WOUNDS. Deep partial-thickness wounds extend deeper into the dermal layer of the skin, and fewer healthy epidermal cells remain. The wounds usually appear red and waxy white without blisters. Edema is moderate; pain is present to a lesser degree than with superficial burns because more of the nerve endings have been destroyed. Blisters are absent because the dead tissues adhere to the underlying dermal collagen fibers.
The remaining blood supply to these areas is greatly reduced due to intense vasoconstriction. Progression to deeper injury can occur through hypoxia and ischemia. Adequate hydration, nutrients, and oxygen are necessary for spontaneous re-epithelialization of the wound and the prevention of conversion to deeper burns. Partial-thickness wounds can convert to full-thickness wounds when tissue damage increases with infection, hypoxia, or ischemia. Deep partial-thickness wounds generally heal in 3 to 6 weeks, but a large amount of scar formation results. Surgical intervention with skin grafting is required if healing will be prolonged.
FULL-THICKNESS WOUNDS. A full-thickness wound involves the entire epidermal and dermal layers of the skin. No living (viable) epidermal cells remain for re-epithelialization, and skin grafts are required in areas larger than approximately 12 to 16 cm2. In smaller areas, secondary wound closure occurs by the growth of collagen-based scar tissue from the unburned edges inward.
The area of full-thickness injury has a hard, dry, leathery eschar (burn crust) that forms from coagulated particles of destroyed dermis. The eschar is dead tissue; it must slough off or be removed from the burn wound before healing can occur. The thick, coagulated particles often adhere to the subcutaneous layer by collagen fibers, which makes the removal of eschar difficult. Edema is a significant problem in burns and is pronounced under the eschar in a full-thickness wound. When the injury completely surrounds an extremity or the thorax (circumferential), circulation and ventilation may be compromised by tight eschar. Escharotomies (incisions through the eschar) or fasciotomies (incisions through eschar and fascia) may be required to relieve pressure and allow normal perfusion and breathing (see Surgical Management [Ineffective Tissue Perfusion], p. 1572).
The color of a full-thickness burn wound may be waxy white, deep red, yellow, brown, or black. Thrombosis of vessels may be present and visible beneath the surface of the burn because the dermal blood vessels are heat coagulated, causing the burned tissue to be without a blood supply (a vascular). Sensation is minimal or absent in these areas of injury due to the destruction of nerve endings. Healing time depends on the re-establishment of an adequate blood supply within the injured areas and can range from weeks to months.
DEEP FULL-THICKNESS WOUNDS. Deep lull-thickness wounds extend beyond the skin into underlying fascia and tissues. These deep injuries damage muscle, bone, and tendons and leave them exposed to the surface. These burns occur with flame, electrical, or chemical injuries. The wound is blackened and depressed, and sensation is completely absent. All full-thickness burns benefit from early excision and grafting. Grafting decreases pain and length of stay and accelerates recovery (Ramzy et al., 1999). Amputation may be required when an extremity is involved.
A first-degree burn is the most common and least serious burn which affects the top layer of skin. These burns produce pain and redness of the skin. First-degree burns are usually caused by overexposure to the sun, brief contact with heat or hot surface including an iron or skillet, minor scalding by hot water or steam, or brief contact with harsh chemicals.
Most frequently, first-degree burns cause redness, mild swelling, and pain. First-degree burns can also be accompanied by symptoms of restlessness, headache, and fever.
A first degree burn.
Second degree: Can be classified as partial or full thickness.
Because second-degree burns affect a deeper layer, they have a higher risk of infection to the victim and are more painful than first-degree burns. They cause the skin to become bright red and with blotchy areas and blisters. The skin usually looks wet because of the loss of fluid through the damaged skin.
Also victims who have burns that cover more than 10% of skin may suffer shock due to the loss of fluid and dehydration caused by the burn. All second-degree burns greater than 2 to 3 inches in diameter should be treated by a medical professional. Smaller burns can usually be treated at home. Common causes of second-degree burns include deep sunburn, exposure to flames, contact with hot liquids, burning gasoline or kerosene and contact with chemicals.
Second degree burn.
Third-degree burns penetrate all layers of skin and usually require skin grafting. They are usually caused by clothing on fire, immersion in hot water, direct contact with flames, hot objects, or electricity and corrosive chemicals.
Third-degree burns are characterized by white, black or leathery skin. There may be little pain in the burned area, but the areas surrounding the burn may be quite painful. Seek medical treatment for all third-degree burns.
Third degree burn.
Examples of a scald burn (left) and a contact burn from a hot iron (right) in young children
Third degree burn.
Fouth degree: Full thickness that extends into muscle and bone.
Third (Full Thickness)
Epithelium and top aspects of the dermis
Epithelium and dermis
How the wound looks
No blisters; dry pink
Moist, oozing blisters; Moist, white, pink, to red
Leathery, dry, no elasticity; charred appearance
Sunburn, scald, flash flame
Scalds, flash burns, chemicals
Contact with flame, hot surface, hot liquids, chemical, electric
Level of Pain (sensation)
Painful, tender, and sore
Very little pain, or no pain
Two to five days; peeling
Superficial: five to 21 days. Deep: 21-35 days
Small areas may take months to heal; large areas need grafting.
No scarring; may have discoloration
Minimal to no scarring; may have discoloration
Burn injury is the destruction of the layers of the skin and associated structures.
1st Degree Burn
2nd Degree Burn
3rd Degree Burn
. Burn injuries result in both local and systemic responses..
Clinical image of burn zones. There is central necrosis, surrounded by the zones of stasis and of hyperaemia
The three zones of a burn were described by Jackson in 1947.
Zone of coagulation—This occurs at the point of maximum damage. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins.
Zone of stasis—The surrounding zone of stasis is characterised by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The main aim of burns resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults—such as prolonged hypotension, infection, or oedema—can convert this zone into an area of complete tissue loss.
Zone of hyperaemia—In this outermost zone tissue perfusion is increased. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion.
These three zones of a burn are three dimensional, and loss of tissue in the zone of stasis will lead to the wound deepening as well as widening.
Jackson's burns zones and the effects of adequate and inadequate resuscitation
Methods of determination of burn depth
1) primary examination :
- color of epidermis and derma ( epidermis - red or pink in case of I,II stages, white or yellow or black in case of deep burns ; derma – red in case of I stage, pail in II, grey in III)
- presence of necrosis (III, IV)
2) needle test ( hyper aesthesia in case of I-II st., superficial hypoesthesia in case of IIIst. and so on)
3) application of wet gauze with special solutions (spirits)
4) epilator test ( painful in I-II st., easy, without pain in case of deep burns)
5) instrumental methods:
a) usage of radioactive isotopes
b) impedance measuring
d) infrared zonding
e) histological and histochemical methods
Estimation of the lesion area: right estimation helps to choose the method of treatment. There are many schemes of the lesion area estimation. Here are some of them:
1) rule of “nines” – area of different body zones is proportional to 9
You can estimate the body surface area on an adult that has been burned by using multiples of 9.
An adult who has been burned, the percent of the body involved can be calculated as follows:
Head = 9%
Chest (front) = 9%
Abdomen (front) = 9%
Upper/mid/low back and buttocks = 18%
Each arm = 9% (front = 4.5%, back = 4.5%)
Genital zone = 1%
Each leg = 18% total (front = 9%, back = 9%)
As an example, if both legs (18% x 2 = 36%), the genital zone (1%) and the front chest and abdomen were burned, this would involve 55% of the body.
Estimating burn size in babies and young children
2) The "rule of palm" is another way to estimate the size of a burn. The palm of the person who is burned (not fingers or wrist area) is about 1% of the body. Use the person's palm to measure the body surface area burned.. It is used if burns are limited and located on different areas of the body.
Burn severity depends on area and depth of the lesion.
American Burn Association severity classification
Adult <10% TBSA
Adult 10-20% TBSA
Adult >20% TBSA
Young or old < 5% TBSA
Young or old 5-10% TBSA
Young or old >10% TBSA
<2% full thickness burn
2-5% full thickness burn
>5% full thickness burn
High voltage injury
High voltage burn
Possible inhalation injury
Known inhalation injury
Significant burn to face, joints, hands or feet
Other health problems
In order to determine the need for referral to a specialized burn unit, the American Burn Association devised a classification system. Under this system, burns can be classified as major, moderate and minor. This is assessed based on a number of factors, including total body surface area affected, the involvement of specific anatomical zones, the age of the person, and associated injuries. Minor burns can typically be managed at home, moderate burns are often managed in hospital, and major burns are managed by a burn center.
Prediction of burn’s severity
In adults the rule of “hundreds” is used. (age + total area of burns in %)
up to 60 – prognosis is favorable
61-80 – prognosis is relatively favorable
81-100 – doubtful
101 and more – unfavorable
Frank’s index is more exact. It takes into account area and depth of the lesion. It is based on the fact that deep burns are in 3 times more severe than superficial burns. That is why if 1 % of superficial burn is 1 unit, than 1 % of deep burn takes 3-4 units. The sum of these numbers makes the Frank’s index.
Prognosis of burns is favorable, if Frank’s index is not more than 30 units,
is relatively favorable, if 30-60 un.,
is doubtful – 61-90 units,
is unfavorable – more than 90 units.
Besides, the stage of burn severity could be estimated by the Lesion Severity Index. (LSI). According to it:
1 % of the burn of I stage = 1 unit of LSI
1 % of the burn of II stage = 2 units of LSI
1 % of the burn of III stage = 3 units of LSI
1 % of the burn of IV stage = 4 units of LSI
It there are heat lesions of respiratory ways we have to add:
– in case of light degree of respiratory burns - 15 units LSI (respiratory disorders are not fixed);
– in case of middle degree - 30 units LSI (respiratory disorders are fixed first 6-12 hours after trauma);
– in case of severe degree - 45 units LSI (respiratory insufficiency from the moment of the burn is fixed)
The tissue destruction caused by a burn injury can cause many local and systemic problems, including fluid and protein losses, sepsis, and disturbances of the metabolic, endocrine, respiratory, cardiac, hematologic, and immune systems. The extent of local and systemic disruption is related to many factors, including age, general health status, extent of injury, depth of injury, and area of body injured. Even after healing, the burn injury can cause late complications such as contracture formation and extensive scarring. Therefore the prevention of infection and closure of the burn wound are vitally important. A lack of or delay in healing is a key factor for all systemic disturbances and is responsible for much morbidity and mortality among clients who are burned.
The burn disease develops when the area of burns is more than 10% in adults and 5% in children. The burn disease is the complex of clinical symptoms, that’s developed due to heat lesion of skin cover and underlying tissues.
The are 4 periods in the duration of burn disease: 1 – burn shock, 2 – acute burn toxemia, 3 – septic toxemia, 4 – recovery.
According to the degrees of severity, there are:
Light burn shock (LSI up to 30 units, duration 24-36 hours)
Middle burn shock (LSI is 31-60 units, duration 36-48 hours)
Severe burn shock (LSI is 61-90 units, duration up to 64 hours)
Most severe burn shock (LSI > units, duration up to 72 hours and more)
The development of the burn shock is caused by serious vascular changes resulting from burn injuries.
· Initial evaluation and management of small and moderate burns is a routine part of general plastic surgery practice. An ability to accurately evaluate and provide proper initial care for these injuries is essential.
· Outcomes for patients with burns have improved dramatically over the past 20 years, but burns still cause substantial morbidity and mortality.1 Proper evaluation and management, coupled with appropriate early specialty referral, greatly help in minimizing suffering and optimizing results.2
Evaluation of the burn patient
Before management of the burn wound can begin, properly and completely evaluate the burn patient. Often this is a brief effort, particularly in patients with small, uncomplicated wounds. In those with larger burns, evaluation of the wound often is of secondary importance. As described by the American College of Surgeons Committee on Trauma, evaluation of the burn patient is organized into a primary and secondary survey.
Burn patients should be systematically evaluated using the methodology of the American College of Surgeons Advanced Trauma Life Support Course. This evaluation is described by the primary survey, with its emphasis on support of the airway, gas exchange, and circulatory stability. First evaluate the airway; this is an area of particular importance in burn patients. Early recognition of impending airway compromise, followed by prompt intubation, can be life saving. Obtain appropriate vascular access and place monitoring devices, then complete a systematic trauma survey, including indicated radiographs and laboratory studies.
Burn patients should then undergo a burn-specific secondary survey, which should include determination of the mechanism of injury, evaluation for the presence or absence of inhalation injury and carbon monoxide intoxication, examination for corneal burns, consideration of the possibility of abuse, and a detailed assessment of the burn wound. A detailed history must be elicited upon first evaluation and transmitted with the patient to the next level of care. Inhalation injury is diagnosed by a history of a closed-space exposure and soot in the nares and mouth. Carbon monoxide intoxication is suspected in those injured in structural fires, particularly if they are obtunded; carboxyhemoglobin levels can be misleading in those ventilated with oxygen. Those with facial burns should undergo a careful examination of the cornea prior to the development of lid swelling that can compromise examination. After evaluation of the burn wound, begin fluid resuscitation and make decisions concerning outpatient or inpatient management or transfer to a burn center .
Evaluation of the burn wound
After the patient has been fully evaluated and stable hemodynamics and gas exchange ensured, evaluate the burn wound in detail. Evaluate burn wounds initially for extent, depth, and circumferential components. Decisions regarding type of monitoring, wound care, hospitalization, or transfer are made based on this information.
The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 30% of total body surface area.
Cardiovascular changes—Capillary permeability is increased, leading to loss of intravascular proteins and fluids into the interstitial compartment. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased, possibly due to release of tumour necrosis factor α. These changes, coupled with fluid loss from the burn wound, result in systemic hypotension and end organ hypoperfusion.
Respiratory changes—Inflammatory mediators cause bronchoconstriction, and in severe burns adult respiratory distress syndrome can occur.
Metabolic changes—The basal metabolic rate increases up to three times its original rate. This, coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity.
Immunological changes—Non-specific down regulation of the immune response occurs, affecting both cell mediated and humoral pathways.
Systemic changes that occur after a burn injury
VASCULAR CHANGES RESULTING FROM BURN INJURIES
Major circulatory disruption occurs at the burn site immediately after a burn injury. The vessels supplying the burned skin are occluded, and blood flow through the arterial and venous channels decreases or ceases completely. Damaged macrophages within the tissues release chemicals (mediators) that initially produce vasoconstriction. Peripheral vessel thrombosis may occur; this decrease in tissue perfusion can cause necrosis, which can lead to deeper injuries in the already damaged areas.
■ Fluid Shift
After the initial vasoconstriction, vessels adjacent to the burn injury dilate. This leads to increased capillary hydrostaticpressure and is accompanied by increased capillary permeability (Figure 68-7). This fluid shift, also known as third spacing or capillary leak syndrome, involves a continuous leak of plasma from the intravascular space into the interstitial space. The loss of plasma fluids and proteins results in a decreased colloidal osmotic pressure in the vascular space. Leakage of fluid and electrolytes from the vascular space continues, causing significant edema formation. Fluid shift usually occurs in the first 12 hours after the burn but can continue for 24 to 36 hours.
The amount of plasma to interstitial fluid shift depends on the extent and severity of injury. Capillary leak occurs in both burned and unbumed tissues when tissue damage is extensive (i.e., greater than 20% to 30% total body surface area [TBSA]). Peripheral edema develops as the protein-rich fluids, plasma, and electrolytes escape into the interstitial space. Tissue colloidal osmotic pressure increases as a result of the movement of proteins, increasing the third-spacing fluid shift.
Profound imbalances of fluid, electrolytes, and acid-base occur as a result of the fluid shift and other physiologic disruptions caused by injury. These imbalances usually include hypovolemia, metabolic acidosis, hyperkalemia (elevated blood potassium levels), and hyponatremia (decreased blood sodium levels). Hyperkalemia occurs as a result of direct tissue damage that releases large amounts of intracellular potassium into the vascular space; it is generally self-limiting. He-moconcentration (elevated blood osmolarity, hematocrit, and hemoglobin) develops from the circulatory dehydration. Hemoconcentration increases blood viscosity, which reduces flow through small vessels and contributes to generalized tissue hypoxia.
The inflammatory responses gradually subside 24 to 36 hours after the injury, and the capillary leak abates. Fluid shifts back into the circulation. This fluid remobilization phase restores fluid and electrolyte levels and renal blood flow, resulting in increased urine formation and diuresis. Body weight returns to normal over several days as peripheral edema subsides.
During this phase, hyponatremia is likely to develop because of increased renal sodium excretion and the loss of sodium from wounds. Hypokalemia can occur now as potassium returns to the intracellular compartment. Anemia often develops as a result of hemodilution, but it is generally not severe enough to require blood transfusions. Transfusions are indicated if the client's hematocrit is less than 20% to 25% and is accompanied by clinical signs and symptoms of hypoxia. The exact laboratory value is not as critical as the clinical signs and symptoms. The timing of transfusions is controversial, and the trend is to limit transfusion unless absolutely necessary.
CARDIAC FUNCTION CHANGES RESULTING FROM BURN INJURY
Because of the initial fluid shifts and hypovolemia that occur after a burn injury, cardiac output decreases in spite of an increased heart rate. Cardiac output may remain depressed until 18 to 36 hours after the burn injury occurs. Cardiac output increases with adequate fluid resuscitation and reaches normal levels before plasma volume is restored completely. Appropriate fluid resuscitation and support with adequate oxy-genation prevent further complications.
■ PULMONARY CHANGES RESULTING FROM BURN INJURY
Respiratory insufficiency (inhalation injury) rarely occurs from direct contact with flames but is caused by superheated air, steam, toxic fumes, or smoke. It is a major cause of morbidity and mortality in thermally injured clients. Pulmonary complications cause or contribute to death in 77% of clients with a combined inhalation and cutaneous burn injury (Flynn, 1999). Respiratory failure associated with burn injuries can also result from airway edema during fluid resuscitation, increased alveolar capillary permeability, circumferential chest burns that compromise breathing, and carbon monoxide toxicity.
Damage to the respiratory system from an inhalation injury can occur in the upper and major airways and the lung parenchyma. The upper airway is affected when inhaled smoke or irritants cause edema and obstructive closure of the trachea. Irritants coming in contact with the upper airway cause a reflex closure of the vocal cords. This protective mechanism results in a decrease in the amount of smoke and toxic gases entering the lungs. Although air is a poor conductor of heat, some heat does reach the upper airway, causing an inflammatory response that leads to oropharyngeal edema and potentially dangerous airway obstruction.
NORMAL BLOOD CAPILLARY POSTBURN BLOOD CAPILLARY
Water molecule Protein molecule
Water is the smallest molecule that can pass through the capillary pores.
Permeability is drastically increased, which allows large molecules such as proteins to pass through the capillary pores easily.
Major airway injury results from chemicals and toxic gases, rather than heat, that are produced from incomplete combustion. The ciliated, mucus-secreting epithelial cells lining the trachea normally trap bacteria and foreign materials. Smoke and products of combustion slow this activity, which allows foreign particles to enter the bronchi. The lining of the trachea and bronchi may slough 48 to 72 hours after injury, enter the airway, narrow the tracheal lumen, and obstruct the lower airways.
Parenchymal injuries result from damage to the alveolar epithelium and capillary endothelium by toxic irritants. Increased alveolar-capillary membrane permeability results in intra-alveolar edema. This edema can occur immediately or as late as 1 week after the injury. The fluid that diffuses across the membrane settles in the interstitial spaces; fibrinous membranes eventually form, which leads to respiratory distress. Progressive pulmonary failure develops with acute pulmonary insufficiency and infection.
GASTROINTESTINAL CHANGES RESULTING FROM BURN INJURY
Because of the fluid shifts and decreased cardiac output that occur after injury, blood flow is shifted to the brain, heart, and liver. Consequently other organs, including the gastrointestinal (GI) tract, have decreased perfusion. Gastric mucosal integrity and motility are impaired. The sympathetic nervous system stress response causes increased secretion of cate-cholamines (especially epinephrine and norepinephrine), which inhibit GI motility and reduce the flow of blood to the area. Peristalsis decreases, and a paralytic ileus may develop. Mucosal secretions and gases collect in the intestines and stomach, causing abdominal distention.
Curling's ulcer, or acute ulcerative gastroduodenal disease, may develop within 24 hours after a severe burn injury because of reduced GI perfusion and mucosal damage. The mucosal membrane normally acts as a barrier to the absorption of hydrogen ions secreted into the gastric lumen. With an alteration in gastric mucosal function, this barrier is compromised and hydrogen ion production is increased. Ulcerations may develop as a result. However, this complication has become extremely uncommon in recent years because of the use of H2 histamine blockers such as cimetidine (Tagamet) and raniti-dine (Zantac), mucoprotectants such as sucralfate (Carafate), and early enteral nutrition.
METABOLIC CHANGES RESULTING FROM BURN INJURY
A significant burn injury places the client in a hypermetabolic state. Increased secretion of catecholamines, antidiuretic hormone, aldosterone, and cortisol increase metabolism. With hypermetabolism, oxygen and calorie requirements are high.
The secreted catecholamines activate the stress response. The increased production (and loss) of heat results in protein and fat breakdown (catabolism), the rapid use of glucose and calories, and increased urinary nitrogen losses. The evaporated heat and water from the burn also increase metabolic and catabolic rates, which increase calorie expenditure. Depending on the extent of injury, the client's calorie requirements may be double or triple normal energy needs. These increased rates peak 4 to 12 days after the burn and can remain elevated for months until all wounds are closed.
The hypermetabolic condition also results in an increase in core body temperature. The client loses heat through the burned skin surfaces because the protective barrier is lost. Core body temperature increases as a response to the adjustment in the hypothalamus. Central thermoregulation is altered to compensate for the hypermetabolic state. There is an impaired shift in temperature; a low-grade fever can develop, which is common among clients with burn injuries. Essentially what occurs is a resetting of the body's normal temperature-regulating
■ IMMUNOLOGIC CHANGES RESULTING FROM BURN INJURY
Thermal injury results in a loss of the protective barrier of the skin, which increases the risk for infection. The burn injury activates the inflammatory response but can also suppress immune function (see Chapter 20). Antibody-mediated immunity and cell-mediated immunity are both suppressed. All immune responses are therefore reduced. Topical antimicrobial agents, systemic antibiotics, general anesthesia, blood component transfusion, and the stress of surgical procedures further compromise immune function.
COMPENSATORY RESPONSES TO BURN INJURY
Any tissue injury is a threat to homeostasis and is a physiologic stressor. Two compensatory responses have immediate benefit: the inflammatory response and the sympathetic nervous system stress response. Together these responses cause the physiologic changes that result in many of the clinical manifestations seen in the first 2 to 3 days after a burn injury.
The inflammatory compensatory response can be helpful by initiating healing in the injured tissues. It also is responsible for some of the serious problems that occur with the fluid shift. Inflammatory compensation causes blood vessels to leak fluid into the interstitial space and white blood cells to release chemicals that generate local tissue reactions. The inflammatory compensatory mechanisms cause the massive fluid shift, edema formation, and hypovolemia that characterize the emergent phase (first 48 hours) after a burn injury. The extent and intensity of the inflammatory response depend on the severity of the burn injury. Chapter 20 explains the inflammatory compensatory mechanisms in detail.
The inflammatory compensatory response is immediately helpful to the body when injury occurs. These actions are intended to function on a relatively local and short-term basis. When these actions are widespread and/or persistent, the tissue-damaging consequences can be severe.
■ Sympathetic Nervous System Compensation
The sympathetic nervous system stress response is generated by the sympathetic division of the autonomic nervous system and some components of the endocrine system when any physical or psychologic stressors are present. Changes resulting from sympathetic compensation are most evident in the cardiovascular, respiratory, and gastrointestinal systems.
Formulation of the diagnosis in case of burns
1. The word ‘burn’
2. The etiological factor: flame, hot water, steam, acid…
3. The stage of burn ( I, II, III, IV)
4. The burn area in % (area of deep burns is putting in the brackets)
5. Injured organs, areas.
6. Accompanying injuries that deal with the action of thermal agent (respiratory burns, carbon monoxide poisoning)
7. Dates about burn shock with its degree or another period of the burn disease
(toxemia, septic toxemia, recovery)
8. LSI (lesion severity index)
10. Accompanying traumas and diseases
Clinical diagnosis: Burn by the fire I and II st. 25% of face, neck, right upper limb, chest
Respiratory burn of light degree
Burn shock, medium degree
LSI – 40 units
Accompanying diagnosis: Stomach ulcer
Chemical burns are the burns that are caused by certain chemicals. The most important agents causing the chemical burns are hot boiling acids.
Other agents involve some certain disinfectants and drain cleaners containing acids. They too require proper medication and attention.
Unlike burns caused by a flame, the burns that are caused by chemicals penetrate deep into the skin and can cause more serious wounds with blisters and rashes.
These wounds are deep and usually oral medications are also taken to avoid internal blisters.
Chemical burn due to spillage of sulphuric acid
Chemical burns appear due to influence on the skin, mucous membrane (mucosa) of concentrated solution of acids, alkaline, salts of heavy metals, toxic gases. Depth of a tissue lesion in cases of chemical burns depends on such conditions, as nature of the substance, it’s concentration, temperature, duration of it’s action. We can change only the last condition by means of early, quick and effective first aid. Action of some chemicals can cause not only lesion of skin and mucosa, but total toxic effect. Influence of acids, salts of heavy metals causes coagulation of proteins, dehydration of tissues; leads to formation of coagulate necrosis with superficial dense crust.
Concentrated solutions of alkalis dehydrate tissues, bind with proteins and hydrolyze fats. Alkalis penetrate tissues deeper than acids and cause deeper lesion. Such necrosis is called coliquative, or wet. Crust, which is formed after that, is soft. After its separation bleeding of the tissues appears.
In case with spread burns there is a danger of the development of intoxication, caused by re resolving of the tissue decomposition substances. Quantity of toxic substances, that have resolved, depends on burn area.
Chemical burns of I and II st. are referred to superficial, III-IV st. are deep burns. In case of I st. burns patients complain on burning pain. During examination of the place of chemical action one could see localized hyperemia with swelling of the skin (it’s more visible in cases of alkali burns). All types of skin sensitivity are present; pain sensitivity is more acute than normally.
In case of II st. burns there is superficial – dry (in cases of acid burns) or gelatin – like – soapy (in cases of alkali burns) crust. Crust is very thin, and could be taken easily into a fold.
In case of (III-IV st) deep chemical burns crust is dense and thick, it couldn’t be taken into a fold. Crust is unmovable, wet like necrosis in case of alkali burns. Crust is dry in case of acid burn. All types of skin sensitivity are absent. There is no possibility to differ III and IV st. of chemical burns by first examination.
In case of III st. burns all layers of skin become necrotic. In case of IV st. burns all underlying tissues (even till bones) become necrotic.
Only after 3-4 weeks, when burn crust has been separated one can estimate depth of necrosis: if only skin has been separated – then it is III st. if also underlying necrotic tissues have been separated – then it is IV st.
First aid in case of chemical burn should be directed on early (at first seconds or at least minutes) cleaning of skin cover from chemical substance. The most effective is the cleaning by means of water stream. (during 10-15 min). If it started late, it should last for 30-40 min. Cleaning should last till the smell of chemical substance disappear or till color of lakmus paper will change in the moment of touching to the burn surface.
After cleaning from the chemical substance dry aseptic bandage is applied on the burn surface and patient is transported to the hospital.
Due to action of electricity more than 24 V, burn could appear. Action of electricity is determined by its direct influence during passing the body or by heat action that is formed an that moment. Heat action of electricity, according to the Djoul’s rule, depend on voltage of electricity, resistance of tissues and duration of contact with conductor. The most severe lesions are situated in places of entry and reentry of electricity. The lesion of tissues mainly depends on their resistance that is why nerves, vessels injure most of all.
Electric trauma – is the action of electricity that manifest in changing of ion’s concentration and polarization in electric field. Electricity causes transformation of intracellular proteins into gel with formation of coagulate necrosis. Aggregation of thrombocytes and leucocytes cause thrombosis of small blood vessels with the disorders of blood circulation and development of secondary necrosis.
Some 3-4% of burn unit admissions are caused by electrocution injuries. An electric current will travel through the body from one point to another, creating “entry” and “exit” points. The tissue between these two points can be damaged by the current. The amount of heat generated, and hence the level of tissue damage, is equal to 0.24×(voltage)2×resistance. The voltage is therefore the main determinant of the degree of tissue damage, and it is logical to divide electrocution injuries into those caused by low voltage, domestic current and those due to high voltage currents. High voltage injuries can be further divided into “true” high tension injuries, caused by high voltage current passing through the body, and “flash” injuries, caused by tangential exposure to a high voltage current arc where no current actually flows through the body.
Differences between true high tension burn and flash burn
Domestic electricity—Low voltages tend to cause small, deep contact burns at the exit and entry sites. The alternating nature of domestic current can interfere with the cardiac cycle, giving rise to arrhythmias.
“True” high tension injuries occur when the voltage is 1000 V or greater. There is extensive tissue damage and often limb loss. There is usually a large amount of soft and bony tissue necrosis. Muscle damage gives rise to rhabdomyolysis, and renal failure may occur with these injuries. This injury pattern needs more aggressive resuscitation and debridement than other burns. Contact with voltage greater than 70 000 V is invariably fatal.
“Flash” injury can occur when there has been an arc of current from a high tension voltage source. The heat from this arc can cause superficial flash burns to exposed body parts, typically the face and hands. However, clothing can also be set alight, giving rise to deeper burns. No current actually passes through the victim's body.
Electrocardiogram after electrocution showing atrial fibrillation
A particular concern after an electrical injury is the need for cardiac monitoring. There is good evidence that if the patient's electrocardiogram on admission is normal and there is no history of loss of consciousness, then cardiac monitoring is not required. If there are electrocardiographic abnormalities or a loss of consciousness, 24 hours of monitoring is advised.
Total biological action of electricity is characterized by disturbances of cardiac function caused by electrochemical changes, especially polarization of cell’s membranes and nervous fibers and is accompanied by muscle cramps. In severe cases total action of high voltage electricity manifests itself by electric shock with loose of consciousness, apnea, fibrillation of heart ventricles. By the way, asystole can appear not only at the moment of trauma or right after it, but after some hours and days. Special feature (peculiarity) of electric burns is their painless due to lesion of nerve endings. Dry necrosis with its not fast separation of necrotic tissues differs from such necrosis in case of heat burns. Another differ of electric burn is progressive necrosis, spreading of necrosis into the underlying tissues, because of the thrombosis of blood vessels. In case of electric burn lesion spreads to muscles and bones. In case of thrombosis of big vessels development of gangrene is possible.
As was said before, after influence of high voltage electricity burns in places of entry and reentry appear. This burns are deep – IIIB-IV st.
Underlying tissues become injured more than upper skin. On the way of electricity all tissues become necrotic and thrombosis of vessels also appears. That’s why the patient’s state depends not only on spreading of skin necrosis that has bordered in the diameter 2-3 cm, but lesion of underlying tissues on the way of electricity. In case of injuring of big vessels necrosis of the tissues, gangrene of limbs or other parts of the body can develop.
In place of entry and reentry “signs of electricity” – burn wounds-appear.
During first aid for a patient with electric burn we should first of all relive him from electric wire, provide reanimation if there is a need, apply bandage on the place of burn.
During reliving the patient from electricity everyone should remember that touching his body we can also suffer. To relive him you can switch off the source or spade with dry wooden handle. After that, you have to throw away the wire by stick or board and take the patient.
After normalizing of cardiac function and breathing dry aseptic bandages should be applied on the place of burns. All patients with electric burns should be taken immediately to a hospital.
General treatment of electric burns is the same as of heat ones. If anuria develops, hemodialis is used. Separation of necrotic tissues in case of electric burns has longer duration. Surgical debridement – necrectomy in 2 stages has to be provided. Early amputation prevents the development of such complication as bleeding, kidneys insufficiency, sepsis. Plastic operations has to be used later.
Burns are a very dangerous form of physical injuries, they are very painful and the wounds caused by burns take time to heal and are very different from other types of wounds.
In the Kitchen
In the Bathroom
Around the House
Summer Sun Safety
First Aid for Sunburn
Heat Exhaustion and Heat Stroke
Smoking and Burns
Burn Wound Infection
· An ability to make the diagnosis of burn wound infection is important. A clinically focused set of burn wound infection definitions recently has been published Two of these, burn wound cellulitis and invasive burn wound infection, are seen with some regularity by clinicians outside a burn center environment.
· Burn wound cellulitis usually manifests as progressive erythema, swelling, and pain in the uninjured skin around a wound. Usually, this is seen in the first few days after burning and typically is caused by Streptococcus pyogenes. Infection can progress rapidly but is generally sensitive to penicillin. Excision of associated deep eschar can be essential to the successful treatment of cellulitis. Elevation to reduce edema is an important adjunct.
· Invasive burn wound infection is a rapid proliferation of bacteria in burn eschar that proceeds to invade underlying viable tissues. A change in color, new drainage, and, occasionally, a foul or sickly sweet odor are clinical findings. Pseudomonas and other gram-negative species are common causes. This infection can be life-threatening and usually requires combined treatment with surgery and antibiotics.
· Fever and systemic toxicity commonly accompany both infections. Inspect burn wounds frequently to identify infection early. This is an important consideration in outpatient burn care. Someone must inspect the wounds managed in the outpatient environment to promptly detect infections. Errors in initial depth assessment are routine. Infections occur and must be treated in a timely way. A wound-monitoring plan is an essential part of burn care.
1. Burn Unit : Saving Lives after the Flames by Barbara Ravage. Publisher : Da Capo Press, 2005.-320p.
2. S.I. Shevchenko, A.A. Tonkoglas. Surgery. – Kharkov, KhSMU, 2001. – 340c.
5. Burn care by Steven E. Wolf, David N. Herndon (Vademecum Series). Publisher: Landes Biscience, 1999.
6. Severe Burns : A Family Guide to Medical and Emotional Recovery. Publisher: Johns Hopkins University, 1993. –p. 246.