burns

Question 1

Severe Burn Patient - A burn occurs when there is injury to body tissue caused by:

Answer 1

heat
chemicals
electrical current
radiation

Question 2

The extent of the burn is influenced by:

Answer 2

temperature of the burning agent
duration of contact time
type of tissue injured

Question 3

Types of Burns

Answer 3

A. Thermal Burns
Caused by flame, flash, scald, sunburn, or contact with hot objects.

Most common type of burn

chemical burn

B. Chemical Burns

Acids, alkalis & organic compounds. Eyes can be injured due to splashes. Can cause respiratory problems if inhaled.

Household cleaners, fertilisers, industrial cleaners, petrol, creosote, chlorine.

burns

C. Electrical Burns

Intense heat from an electrical current.

Direct damage to nerves & vessels can cause anoxia & death.

Electrical current that passes through vital organs will produce more life threatening consequences.

Question 4

Severity of a burn is determined by:

Answer 4

the depth of the burn
the extent of the burn (percentage of total body surface area)
the location of the burn
patient risk factors
local response to burn injury

Question 5

Depth of Burn

Answer 5

Burns are defined according to the depth of skin destruction. Partial thickness & full thickness.

1. Partial thickness

Superficial partial thickness includes the epidermis e,g, sunburn

Deep partial thickness includes the dermis e.g. Flame, flash, scald, chemical, electric

2. Full thickness

Includes fat, muscle, tendons, bones e.g. Flame, scald, chemical, electric

Question 6

Extent of burn

Answer 6

Total body surface area needs to be worked out to determine the extent of the burn.

Question 7

Two commonly used guides include:

Answer 7

1. Lund-Browder chart
2. Rule of nines

Lund-Browder chart is considered the most accurate. The rule of nines is considered easy to remember & effective to initial assessment.

Question 8

Location of burn

Answer 8

Burns to face and neck, chest and back may inhibit respiratory function due to mechanical obstruction secondary to oedema or leathery, devitalised tissue (eschar). These injuries may also indicate inhalation & respiratory mucosal damage.

Burns to hands and feet, joints and eyes are concerning because they alter the persons ability to function (self-care). Vascular & nerve supply need to be maintained during healing.

Burns to ears & nose are susceptible to infection due to poor blood supply to the cartilage.

Burns to buttocks or perineum high risk for infection.

Circumferential (all the way round) burns to upper or lower extremities can compromise circulation. Nerve damage can cause neurological impairment. Patients may also develop compartment syndrome from damage to the muscles & susequent oedema & vascular problems.

Question 9

Patient risk factors

Answer 9

Older adults heal slower & have more difficulty with rehabilitation.

Patients with pre-existing conditions (cardiovascular, respiratory or renal diseases) have poorer prognosis because of the extra demands placed on the body by the burn injury.

Patients with diabetes mellitus or peripheral vascular disease have poor healing and at risk for gangrene.

Physical debilitation from any chronic disease (alcoholism, drug abuse, malnutrition) leaves the patient physiologically less able to recover.

Other injuries sustained at the time of burn (fractures, head injury, trauma) also complicates recovery.

Question 10

Local response to burn

Answer 10

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.

Question 11

Phases of Burn Management

Fluid shift burns3 phases that correspond with the key priority?

Answer 11

Emergent phase (resuscitative)
Acute phase (wound healing)
Rehabilitation phase (restorative)

Question 12

Pre-hospital phase

Answer 12

first on the scene, rescue services who provide emergency services (ambulance, fire rescue, police). A B C’s is the first priority and initial first aid. See p. 548 3rd edition text & p. 453 4th edition text for more information on pre-hospital care.

Question 13

Emergent Phase

Answer 13

The period of time required to resolve the immediate, life-threatening problems. This phase lasts up to 72hrs from the time of burn.

Primary concerns during this time is onset of hypovolaemic shock and odema formation. The phase ends when fluid mobilisation and diuresis begin

Question 14

Fluid & electrolyte shifts

Answer 14

The greatest threat to a patient with a major burn is hypovolaemic shock caused by massive shift of fluids out of the blood vessels as a result of increased capillary permeability. Can begin as early as 20 minutes from time of burn.

As the capillary walls become more permeable, water, sodium & later plasma proteins (albumin) move into interstitial spaces and other surrounding tissue.

The progressive loss of protein from the vascular space decreases the colloidal osmotic pressure which results in more fluid shifting out of the vascular space into the interstitial space.

Fluid also moves to places that normally have minimal or no fluid, e.g. blisters, exudate.

Other sources of fluid loss during this phase are losses by evaporation from large, denuded body surfaces and the respiratory system.

The overall result of the fluid shifts and lossess is intravascular volume depletion & hypovolaemic shock.

Circulatory status is also impaired because of haemolysis (breaking down) of red blood cells caused by the insult of the burn injury & release of factors at the time of burn.

Thrombosis in the capillaries of burned tissue also causes additional loss of circulating RBC’s. Blood becomes more viscous (thick & sticky) and haematocrit (a measure of packed red cell volume) increases .

Major shifts in sodium & potassium also occur during this phase. Sodium rapidly shifts to the interstitial spaces & remains until oedema ceases. Potassium shift develops initially because of injured cells and haemolysed RBC’s release potassium into the circulation.

Adequate fluid resuscitation is required.

Question 15

Complications

Three major organ systems most susceptible to complications during the emergent phase of the burn injury are:

Answer 15

Cardiovascular
Respiratory
Urinary

Question 16

Cardiovascular system

Complications include:

Answer 16

Arrhythmias
Hypovolaemic shock
Severe impairment of circulation to the extremities due to circumferential burns and oedema

Question 17

Respiratory system

Complications include:

Answer 17

Upper airway burns can cause oedema & upper airway obstruction
Lower airway injury caused by inhalation of toxic fumes preventing the diffusion of oxygen from the alveoli into the circulatory system

Question 18

Urinary system

Complications include:

Answer 18

Acute tubular necrosis caused by decreased blood flow to the kidneys from hypovolaemia which causes renal ischaemia. If this continues results in acute renal failure.

Question 19

Acute Phase

Answer 19

The acute phase begins with the mobilisation of extracellular fluid and subsequent diuresis.

This phase ends when the burned area is completely covered by skin grafts or when wounds are healed. This may take weeks or months.

Question 20

Pathophysiology

Answer 20

Diuresis from fluid mobilisation occurs and the patient becomes less odematous.

Full or partial thickness burns are more evident than in the emergent phase

Bowel sounds return

Patient becomes more aware of the situation, at this stage may require some psychological support.

Some healing begins, WBC surround the burn wound and phagocytosis occurs.

Necrotic tissues begins to slough and granulation tissue begins to form

A partial thickness burn will heal from the edges and the

dermal bed
Full thickness burns need to be covered with skin grafts

Question 21

Clinical Manifestations

Answer 21

Parial thickness wounds form eschar (black, thicky leathery dead tissue). This needs to be removed for healing to occur. Once removed, epithelialisation begins and the wound becomes red or pink scar tissue.

Usually takes 10 -21 days

Full thickness eschar takes longer. Requires surgical debridement and skin grafting for healing to occur.

Question 22

Complications

Cardiovascular & respiratory complications are the same as in the emergent phase. Other complications include:

Answer 22

Infection
Musculoskeletal
Gastrointestinal
Endocrine system

Question 23

Infection

Answer 23

1st line of defence, the skin, is destroyed by a burn causes risk of wound infection

Burn wound infection may progress to bacteraemia and sepsis

Manifestations of sepsis include hypo or hyper thermia, increased heart rate, respiratory rate, decreased BP, and decreased urine output.

Other signs may include mild confusion, chills, malaise and loss of appetite.

Question 24

Neurological

Answer 24

Caused if there is severe hypoxia or electrical injuries

Patient may become disoriented, withdrawn, combative or may experience hallucinations

Delerium is more acute at night and occurs more often with elderly patients.

Question 25

Musculoskeletal

Answer 25

Range of movement can be impaired as burns begin to heal and scar tissue forms. This tissue is less supple and pliant and contractures can occur.

Pain can also inhibit the patient from movement of body parts

Question 26

Gastrointestinal

Answer 26

Paralytic ileus (halting of bowel peristalsis) results from sepsis

Diarrhoea can be caused if the patient is having NG feeding or antibiotic therapy

Constipation can occur due to opioid analgesics and decreased mobility

Curling ulcers (gastroduodenal ulcer) can be caused due to generalised stress response resulting in decreased production of mucus, increased gastric acid secretion and decreased blood flow to the GI tract during the emergent phase.

Question 27

Endocrine system

Answer 27

Increased blood glucose can be seen due to stress-mediated cortisol and catecholamine release resulting in the increased mobilisation of glycogen stores, glyconeogenesis and the subsequent production of glucose.

There is also an increase in insulin production & release but the effectiveness is decreased because of insulin in sensitivity

Hyperglycaemia can be caused later becasue of the required increased kilojoule intake necessary to meet the patients metabolic needs.

Question 28

Rehabilitation Phase

Answer 28

Begins when the patient’s burn wounds have healed and the patient is able to resume a level of self-care activity.

This can occur as early as 2 weeks or as long as 7 - 8 months.

Pathophysiology wound healing

Question 29

Burn wound heal either by primary intention or by skin grafting.

Answer 29

Layers of epithelialisation begin rebuilding the tissue structure destroyed by the burn injury

Collagen fibres present in the new scar tissue, contributes to healing and strengthening of the wound

Scaring occurs, patients often experience itching where healing is occuring