This document provides an overview of burns, including:
- Definitions of burns as injuries caused by heat, chemicals, electricity or radiation.
- The pathophysiology of burns, including the zones of injury and systemic responses affecting the kidneys, gut and lungs.
- Classification of burns by depth, extent of body surface area burned, and mechanism.
- Common complications of burns like infection, pulmonary issues, and metabolic and fluid shifts.
- The goal of fluid resuscitation to maintain circulation and protocols like the Parkland formula for calculating fluid needs.
3. definition
A burn is an injury to skin caused by biological, chemical,
electrical and physical agents with local and systemic
repercussions.
(Burns: Definition, Classification, Pathophysiology and Initial Approach. Garcia-
Espinoza et al., Gen Med (Los Angeles) 2017, 5:5)
6. Pathological response
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.
7. 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
12. Renal response
During the acute phase of burn injury, renal blood flow and
glomerular filtration rate (GFR), decrease.
If untreated, the resulting oliguria may progress to acute renal
failure.
Two different forms of acute renal failure have been described
in burned patients, differing in terms of their time of onset.
The first occurs during the first few days after the injury and is
related to hypovolemia with low cardiac output.
Elevated levels of stress hormones like catecholamines,
angiotensin, aldosterone and vasopressin have been reported
to be implicated in the pathogenesis of this form of ARF.
15. classification
Burns may be distinguished and classified by their
mechanism or cause, the degree or depth of the burn, the
area of body surface that is burned, the region or part of the
body affected, as well as the extent.
16. Classification by mechanism or cause
• Causally, burns may be classified as thermal or inhalational.
• Thermal burns involve the skin and may present as: –
scalds – caused by hot liquid or steam;
contact burns – caused by hot solids or items such as hot
pressing irons and cooking utensils, as well as lighted
cigarettes
flame burns – caused by flames or incandescent fires, such
as those started by lighted cigarettes, candles, lamps or
stoves
chemical burns – caused by exposure to reactive chemical
substances such as strong acids or alkalis.
17. electrical burns – caused by an electrical current passing from
an electric outlet, cord or appliance through the body
Inhalational burns are the result of breathing in superheated
gases, steam, hot liquids or noxious products of incomplete
combustion. They cause thermal or chemical injury to the
airways and lungs and accompany a skin burn in
approximately 20% to 35% of cases. Inhalational burns are
the most common cause of death among people suffering fire-
related burn.
18.
19. Classification : differential diagnosis
Epidermal: As the name implies, causes cell damage only
to epidermis.
• The classic sunburn or to brief contact with hot substances,
liquids or flash flames (scalds) is the best example.
• Clinically, the skin appears red or erythematous.
• No blisters, dry surface, tender.
• Minimal edema, spontaneous healing, no scars.
20. Superficial partial thickness: Damage occurs through the
epidermis and into the papillary layer of the dermis.
• Bright pink or red, inflamed dermis; erythematous with blanching
and brisk capillary refill.
• Intact blisters, glistening surface when blisters removed, sensitive
to change in temperature.
• Moderate edema, spontaneous healing, minimal scarring,
discoloration.
21. Deep partial thickness: It involves destruction of the
epidermis and the papillary dermis with damage down into the
reticular dermal layer.
Mixed red, waxy white, blanching with slow capillary refill
Broken blisters, wet surface, sensitive to pressure but
insensitive to light touch or soft pinprick.
Marked edema, slow healing, excessive scarring.
22. Full thickness: All of the epidermal and dermal layers
are destroyed completely. In addition, the subcutaneous fat
layer may be damaged to some extent.
White (ischemic), fawn, balck, red (haemoglobin fixation),
no blanching, poor distal circulation.
Parchment like, leathery, rigid, dry, body hairs pull out
easily.
Area depressed, heals with skin grafting, scarring.
23.
24. Subdermal: It involves complete destruction of all tissues
from epidermis down to and through the subcutaneous tissue.
Muscles and bones are subject to necrosis when burned.
Tissue defects, heals with skin grafts or flaps, scarring.
29. COMPLICATIONS OF BURN INJURY
Depending on the extent of burn injury, the depth of the burn,
and the type of burn, there may be secondary systemic
complications.
Infection: Some virulent strains of Pseudomonas
aeruginosa and Staphylococcus aureus are resistant to
antibiotics and have been responsible for epidemic infections
in burn centers.
Microbial invasion from the burn wounds to other healthy
tissue can create sepsis.
Systemic antibiotics are used to treat both burn and infection.
30. Pulmonary Complications
Any patient who has been burned in a closed space should
be suspected of having an inhalation injury.
Signs of an inhalation injury include facial burns, singed nasal
hairs, harsh cough, hoarseness, abnormal breath sounds,
respiratory distress, and carbonaceous sputum and/or
hypoxemia.
The primary complications associated with this injury are
carbon monoxide poisoning, tracheal damage, upper airway
obstruction, pulmonary edema, and pneumonia. Lung
damage from inhaling noxious gases and smoke may be
lethal.
31. Metabolic Complications
Thermal injury causes a great metabolic and catabolic
challenge to the body.
Metabolic rates may increase up to 50% in a 25% TBSA burn
and much more as the burn size increases.
As a result of the increased metabolic activity, there will be an
increase of 1.8°F to 2.6°F (1°C to 2°C) in core temperature.
It is recommended that room temperature be kept at 86°F
(30°C), which will significantly reduce the metabolic rate
32. Haemodynamic changes result from a shift in fluid to
interstitium which subsequently reduces the plasma
& intravascular fluid volume in a patient with burn.
Fluid shift occur as a result of local and temporary
systemic changes in capillary dynamics.
This shift of fluid to the interstitium can result in
significant edema.
33. With these fluid shifts, there will be a tremendous initial
decrease in cardiac output, which may reach as low as 15%
of normal within the first hour after injury.
Fluid replacement therapy is utilized initially to manage the
loss of circulatory fluid.
Hematological changes also occur after a severe burn injury.
These changes include alterations in platelet concentration
and function, clotting factors, and white blood cell
components; red blood cell dysfunction; and decreases in
hemoglobin and hematocrit
34. Fluid resuscitation
The principle of fluid resuscitation is that the intravascular
volume must be maintained following a burn, in order to
provide sufficient circulation to perfuse not only the essential
visceral organs such as the brain, kidneys and gut, but also
the peripheral tissues, especially the damaged skin.
The resuscitation volume is relatively constant in proportion to
the area of the body burned and, therefore, there are
formulae that calculate the approximate volume of fluid
needed for the resuscitation of a patient of a given body
weight with a given percentage of the body burned
35. These regimes follow the fluid loss, which is at its maximum in
the first 8 hours and slows, such that, by 24–36 hours, the
patient can be maintained on his or her normal daily
requirements.
There are three types of fluid used. The most common is
Ringer’s lactate or Hartmann’s solution; some centres use
human albumin solution or fresh-frozen plasma; and some
centres use hypertonic saline.
36. Parkland Formula
Adults: 2-4 ml RL x Kg body weight x % burn
Children: 3-4 ml RL x Kg body weight x % burn
RL = Ringer’s Lactate solution
Half this volume is given in the first 8 hours and the second half
is given in the subsequent 16 hours
37. Monitoring of resuscitation
The key to monitoring of resuscitation is urine output.
Urine output should be between 0.5 and 1.0 mL/kg body
weight per hour.
If the urine output is below this, the infusion rate should be
increased by 50%.
If the urine output is inadequate and the patient is showing
signs of hypoperfusion (restlessness with tachycardia, cool
peripheries and a high haematocrit), then a bolus of 10 mL/kg
body weight should be given
38. references
Physical rehabilitation Susanb.o’Sullivan
Systemic Responses to Burn Injury Bar›fl ÇAKIR, Berrak Ç.
YE⁄EN Department of Physiology, Faculty of Medicine,
Marmara University, istanbul – Turkey Turk J Med Sci 34
(2004) 215-226
Burns: Definition, Classification, Pathophysiology and Initial
Approach Garcia-Espinoza et al., Gen Med (Los Angeles)
2017, 5:5
Bailey and love
Burn clinical practise and guideline Developed by Texas EMS
Trauma & Acute Care Foundation Trauma Division