2. Outline
Introduction
Pathophysiology of Burn Injuries
Injury to the Airway and the Lungs
Inflammation and Circulatory Changes
Life-Threatening Events with Major Burns
Immediate Care of the Burn Patient
Assessment of the Burn Wound
Fluid Resuscitation
Head and Neck Burns
References
3. Introduction
The incidence of burn injury varies greatly between cultures.
Half of the victims are under 16 years of age
The majority of burns in children are scalds caused by accidents with kettles, pans, hot
drinks and bath water.
Among adolescent patients, the burns are usually caused by young males
experimenting with matches and flammable liquids.
Most electrical and chemical injuries occur in adults.
Associated such as mental disease, epilepsy and alcohol or drug abuse, are underlying
factors in as many as 80% of patients with burns admitted to hospital in some
populations.
4.
5. Pathophysiology of Burn Injury
The most common organ affected by burns is the skin.
Burns can also damage the airway and lungs.
Airway injuries occur when the face and neck are burned.
If a person is trapped and forced to inhale the hot and poisonous gases,
respiratory Injuries will happen.
6.
7.
8. Metabolic Poisoning
Most common gas given off in a fire is Carbon Monoxide
Altered Consciousness at the scene of the fire
Carbon monoxide binds to hemoglobin with an affinity 240 times greater than that of
oxygen and blocks the transport of oxygen; Carboxy-Hemoglobin
Concentrations above 10% are dangerous and need treatment with pure oxygen for
more than 24 hours.
Death occurs with concentrations around 60%
Hydrogen cyanide; poisonous gas given off in a house fire causes metabolic acidosis by
interfering with mitochondrial respiration.
9. Inhalational injury
Caused by the minute particles within thick smoke [not filtered by the upper airway].
They stick to the moist lining, causing an intense reaction in the alveoli.
This chemical pneumonitis causes edema within the alveolar sacs and decreasing
gaseous exchange over the ensuing 24 hours.
Often gives rise to a bacterial pneumonia; its presence or absence has a very
significant effect on the mortality of any burn patient
10.
11.
12.
13.
14. Inflammation and Circulatory Changes
Burnt skin activates a web of inflammatory cascades
The release of neuropeptides and the activation of complement are initiated by the
stimulation of pain fibers and the alteration of proteins by heat.
The activation of Hageman Factor initiates a number of protease-driven cascades,
altering the arachidonic acid, thrombin and kallikrein pathways.
15. Inflammation and Circulatory Changes
At a cellular level, complement causes the degranulation of mast cells and coats
the proteins altered by the burn.
This attracts neutrophils which will degranulate and release of large quantities of
free radicals and proteases.
Mast cells also release primary cytokines such as TNF-α;
Chemotactic agents to inflammatory cells and cause the subsequent release of
many secondary cytokines causing Alterations in Blood Vesselâs Permeability
[Escape of Intravascular Fluid]
16. Inflammation and Circulatory Changes
The damaged collagen and extravasated proteins increase the oncotic pressure
within the burned tissue
Further increasing the flow of water from the intravascular to the extravascular
space.
The overall effect of these changes is to produce a net flow of water, solutes and
proteins from the intravascular to the extravascular space.
17. Inflammation and Circulatory Changes
This flow occurs over the first 36 hours after the injury, but does not include red blood
cells.
This reaction is small and localized but as the burn size approaches 10â15% of total
body surface area (TBSA)
The loss of intravascular fluid can cause a level of circulatory shock.
Once the area increases to 25% of TBSA, the inflammatory reaction causes fluid loss in
vessels remote from the burn injury.
18.
19.
20.
21. Immediate Care for the Burn Patient
PRE-HOSPITAL CARE
Ensure Secure Airway
Stop the Burn Process
Check for Other Injuries; ABC
Cool the Burn Wound; minimum of 10 minutes, is effective for 1 hour after the injury; 15 C
Give Oxygen
Elevate
22. Immediate Care for the Burn Patient
Hospital care
The principles of managing an acute burn injury are the same as in any acute trauma
case:
A: Airway control.
B: Breathing and ventilation.
C: Circulation.
D: Disability â neurological status.
E: Exposure with environmental control.
F: Fluid resuscitation.
23. Immediate Care for the Burn Patient
The possibility of injury additional to the burn must be sought both clinically and
from the history, and treated appropriately.
The major determinants of severity of any burn injury are:
The percentage of TBSA that is burned
The presence of an inhalation injury
The depth of the burn.
24.
25. Airway
The burned airway creates problems by swelling and it can completely occlude the upper
airway.
The treatment is to secure the airway with an endotracheal tube until the swelling has
subsided, which is usually after about 48 hours.
The symptoms of laryngeal edema, such as change in voice, stridor, anxiety and
respiratory difficulty are very late symptoms.
Intubation at this point is often difficult or impossible owing to swelling,
Cricothyroidotomy
Early intubation of suspected airway burn is the treatment of choice in such patients.
The time-frame from burn to airway occlusion is usually between 4 and 24 hours.
26. Airway
Management; the history and early signs, rather than the symptoms.
The most valuable signs are the presence of deep burns around the mouth and in
the neck.
27.
28.
29. Breathing
Inhalational injury
Anyone trapped in a fire for more than a couple of minutes must be observed for signs of
smoke inhalation.
Other signs that raise suspicion are the presence of soot in the nose and the oropharynx
and a chest radiograph showing patchy consolidation.
The clinical features are a progressive increase in respiratory effort and rate, rising
pulse, anxiety and confusion and decreasing oxygen saturation.
These symptoms may not be apparent immediately and can take 24 hours to 5 days to
develop.
30. Breathing
Treatment starts as soon as this injury is suspected and the airway is secure.
Physiotherapy, nebulisers and warm humidified oxygen are all useful.
The patientâs progress should be monitored using respiratory rate, together with
blood gas measurements.
If the situation deteriorates, continuous or intermittent positive pressure may be
used with a mask or T-piece.
In the severest cases, intubation and management in an intensive care unit will be
needed.
32. Metabolic Poisoning
Carboxy-hemoglobin levels raised above 10% must be treated with high inspired
oxygen for 24 hours to speed its displacement from hemoglobin.
Metabolic acidosis is a feature of this and other forms of poisoning.
Blood gas measurement will confirm the diagnosis.
The treatment is oxygen.
33. Assessment of the Burn Wound
Assessing size
The area should be exposed and any soot or debris washed off.
Care should be taken not to cause hypothermia during this stage.
Smaller burns or patches of burn, the best measurement is to cut a piece of clean paper
the size of the patientâs whole hand (digits and palm), which represents 1% TBSA, and
match this to the area.
Another accurate way of measuring the size of burns is to draw the burn on a Lund and
Browder chart, which maps out the percentage TBSA of sections.
34. Assessment of the Burn Wound
The ârule of ninesâ, which states that each upper limb is 9% TBSA
Each lower limb 18%
The torso 18% each side
The head and neck 9%.
35.
36. Assessment of the Burn Wound
Assessing depth from the history
The first indication of burn depth comes from the history
The burning of human skin is temperature- and time-dependent.
It takes 6 hours for skin maintained at 44°C to suffer irreversible changes, but a
surface temperature of 70°C for 1 s is all that is needed to produce epidermal
destruction.
Taking an example of hot water at 65°C
Exposure for 45 s will produce a full-thickness burn
For 15 s a deep partial-thickness burn and for 7 s a superficial partial-thickness burn.
37.
38.
39. Superficial Partial-Thickness Burns
The damage goes no deeper than the papillary dermis.
The clinical features are blistering and/or loss of the epidermis.
The underlying dermis is pink and moist.
The capillary return is clearly visible when blanched.
There is little or no fixed capillary staining.
Pinprick sensation is normal.
Superficial partial-thickness burns heal without residual scarring in 2 weeks.
The treatment is non-surgical
40.
41. Deep Partial-Thickness Burns
Damage to the deeper parts of the reticular dermis.
Clinically, the epidermis is usually lost.
The exposed dermis is less moist that in a superficial burn.
There is often abundant fixed capillary staining, especially if examined after 48
hours.
The colour does not blanch with pressure under the examinerâs finger.
Sensation is reduced, and the patient is unable to distinguish sharp from blunt
pressure when examined with a needle.
Deep dermal burns take 3 or more weeks to heal without surgery and usually lead
to hypertrophic scarring
44. Full-Thickness Burns
The whole of the dermis is destroyed in these burns.
Clinically, they have a hard, leathery feel.
The appearance can vary from that similar to the patientâs normal skin to
charred black, depending upon the intensity of the heat.
There is no capillary return.
Often, thrombosed vessels can be seen under the skin.
These burns are completely anaesthetized
47. Fluid Resuscitation
The intravascular volume must be maintained following a burn.
To provide sufficient circulation to perfuse the tissues
Intravenous resuscitation is appropriate for any child with a burn greater than 10%
TBSA.
The figure is 15% TBSA for adults.
In some parts of the world, intravenous resuscitation is commenced only with burns
that approach 30% TBSA.
If oral resuscitation is to be commenced, it is important that the water given is not salt
free.
48. Fluid Resuscitation
It is rarely possible to undergo significant diuresis in the first 24 hours in view of the
stress hormones that are present.
Hyponatraemia and water intoxication can be fatal.
It is therefore appropriate to give oral rehydration with a solution such as
DioralyteÂź.
The resuscitation volume is relatively constant in proportion to the area of the body
burned.
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.
49. Fluid Resuscitation
These regimes follow the fluid loss, which is at its maximum in the first 8 hours and
slows, such that, by 24â36 hours, the patient can be maintained on his or her normal
daily requirements
The most common solution used is Ringerâs lactate or Hartmannâs solutions
Some centres use human albumin solution or fresh-frozen plasma or hypertonic
saline.
Parkland formula; calculates the fluid to be replaced in the first 24 hours by:
Total percentage body surface area Ă weight (kg) Ă 4 = volume (mL).
Half this volume is given in the first 8 hours and the second half is given in the
subsequent 16 hours.
50. Crystalloid Resuscitation
Ringerâs lactate is the most commonly used crystalloid.
Crystalloids are said to be as effective as colloids for maintaining intravascular volume.
Less expensive.
Large protein molecules leak out of capillaries following burn injury; non-burnt
capillaries continue to sieve proteins virtually normally.
This is normally dextroseâsaline given as follows:
ââ 100 mL/kg for 24 hours for the first 10 kg;
ââ 50 mL/kg for the next 10 kg;
ââ 20 mL/kg for 24 hours for each kilogram over 20 kg body weight.
51. Hypertonic Saline
It produces hyperosmolarity and hypernatraemia.
This reduces the shift of intracellular water to the extracellular space.
Advantages include less tissue edema and a resultant decrease in escharotomies
and intubations
52. Colloid Resuscitation
Human albumin solution (HAS) is a commonly used colloid.
Plasma proteins are responsible for the inward oncotic pressure that counteracts
the outward capillary hydrostatic pressure.
Without proteins, plasma volumes would not be maintained
Proteins should be given after the first 12 hours of burn because, before this
time, the massive fluid shifts cause proteins to leak out of the cells.
The most common colloid-based formula is the Muir and Barclay formula:
ââ 0.5 Ă percentage body surface area burnt Ă weight = one portion;
ââ periods of 4/4/4, 6/6 and 12 hours, respectively;
ââ one portion to be given in each period.
53. Monitoring Resuscitation
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 then a bolus of 10 mL/kg body weight should be given.
Patients should not over-resuscitated and urine output in excess of 2 mL/kg
body weight per hour should signal a decrease in the rate of infusion.
54. Monitoring Resuscitation
Other measures of tissue perfusion such as acidâbase balance are appropriate in
larger, more complex burns.
A haematocrit measurement is a useful tool in confirming suspected under- or
over-hydration.
Those with cardiac dysfunction, acute or chronic, may well need more exact
measurement of filling pressure, preferably by transo-esophageal ultrasound or
with the more invasive central line.
56. Silver sulphadiazine cream (1%)
Broad spectrum prophylaxis against bacterial colonization
Particularly effective against Pseudomonas aeruginosa and also methicillin-
resistant Staphylococcus aureus.
57. Silver Nitrate Solution (0.5%)
A highly effective as a prophylaxis against Pseudomonas colonization, but it is
not as active as silver sulphadiazine cream against some of the gram-negative
aerobes.
It needs to be changed or the wounds re-soaked every 2â4 hours.
It also produces black staining of all the furniture surrounding the patient.
58. Mafenide Acetate Cream
Popular in the United States
Painful to apply.
It is usually used as a 5% topical solution
It has been associated with metabolic acidosis.
59. Silver Sulphadiazine and Cerium Nitrate
A very useful burn dressing, especially for full-thickness burns.
It induces a sterile eschar on the burned skin and has been shown in certain
instances, especially in elderly patients.
Cerium nitrate forms a sterile eschar and is especially useful in treating burns
when a conservative treatment option has been chosen.
Cerium nitrate has also been shown to boost cell-mediated immunity in these
patients.
65. Local Burns and Wound Care - Blisters
Proponents of blister removal quote laboratory studies that show that blister
fluid depresses immune function, slowing down chemotaxis and intracellular
killing and also acting as a medium for bacterial growth.
Conversely, other authors advocate leaving blisters intact as they form a sterile
stratum spongiosum.
Washing the burn wound with chlorhexidine solution is ideal for this purpose.
A deep dermal burn undergoing tangential shaving.
The dead dermis is removed layer by layer until healthy bleeding
is seen. The burn is pale because it was dressed with silver sulphadiazine
cream, but no blanching was visible under this layer. The
patient was unable to differentiate between pressure from the sharp
and blunt ends of a needle. (b) A thin, split-thickness graft harvested
from the thigh. (c) The thin graft is placed in the dermal remnants. The
rete pegs can be seen between the remnants of the dermis through
the graft.