Burn managment in E R

1. Abd Elaal M Elbahnasy ,
MD
Emergency Medicine
Specialist
Ministry of health
Egypt
Burn management
in emergency department

2. Skin Anatomy
Epidermis
Dermis
Hypodermis

3. Function of the skin
 Skin is the largest organ of the body
 Essential for:
- Thermoregulation
- Prevention of fluid loss by evaporation
- Barrier against infection
- Protection against environment provided
by sensory information

4.  Burns are a major cause of
morbidity and mortality.
 Burns cause coagulative
destruction of skin and/or
mucous membranes.
 The extent of destruction is
related to the temperature
and duration of contact.

5. What is a Burn?
Tissue injury due to :
–Exposure to flames or hot liquids
–Contact with hot objects
–Exposure to caustic chemicals or
radiation
–Contact with an electrical current

6. Causes of burn

7. Clinical assessment of burns
History
 Temperature/nature of agent
 Time of burn
 Duration of contact/exposure
 Environment (risk of smoke inhalation and carbon
monoxide poisoning if confined in an enclosed space).
 History of explosion
 Method of escape (risk of other injuries if the patient
jumped or fell to escape).
 Past medical history.
 Drug history and allergies.
 Tetanus status

8. Estimating the size of a burn
Rule of 9s
Lund–Browder charts
Serial halves
Patient’s palm size
(including the fingers) =
approximately 1 % body surface
area

12. Estimating the depth of a burn
Superficial (first degree)
 Damage to the epidermis
only
 Red and dry
 Blanch with pressure
 Very painful
 Heals within ∼10 days.
 No scarring
Erythema
Super.
Dermal
Deep
Dermal
Full
Thickness

13. Partial thickness (second degree)
 Damage to epidermis and dermis (dermal
involvement may be superficial or deep).
 Blisters and edema
 Painful
 Healing occurs in 14 days
 Depigmentation may occur
 May require skin grafting

14. Full thickness (third degree)
 Loss of all layers of skin
 May appear dark and leathery or
waxy-white
 (painless)
 No blanching
 Skin grafting required

16. Site of the burn
Face Eyes Ears Hands Feet
Genitalia
and
perineum
Overlying
major
joints
Burns at certain sites require specialist
intervention and referral on to a burns’ centre.
These ‘special’ sites include:

17. Airway assessment
 Airway obstruction may come late
 risk factors for potential airway obstruction,
including:
Facial or neck burns
Singeing of eyebrows and nasal hairs
Carbon deposits and acute inflammatory
changes in oropharynx.
Carbonaceous sputum.

18.  Hoarseness.
 History of impaired conscious level.
 History of confinement in a burning
environment.
 Explosion with burns to head and torso.
 Carbon monoxide level > 10 % .
 Higher CO levels can result in:
■ headache and nausea (20%–30%)
■ confusion (30%–40%)
■ coma (40%–60%)
■ death (>60%)

20. Management of burns
 ABC
 The burning process should be stopped — maximum of 20
minutes cooling.
 Hypothermia should be avoided by keeping the patient covered
and warm.
 Careful fluid resuscitation is paramount
 Intravenous opiates should be given for analgesia.
 The burns should be covered with sheets of cling film for pain
relief.
 Any jewellery that may tourniquet limbs or digits should be
removed.
 Tetanus status should be determined and prophylaxis given, if
necessary.
 Prophylactic antibiotics are not recommended.

21. Urine monitoring
 Urinary catheter should be placed in large
burns and/or perineal burns requiring close
monitoring.
 Targeted urinary output is:
 Adult: 30-50 mL/hour
 Child: 1-2 mL/kg/hour

24.  Fluids are calculated from the time of the burn and not
the time of arrival in the ED.Therefore, if a patient
arrives 3 hours after injury, the first volume of fluid
should be given over 5 hours. If the patient is shocked,
this should be treated first prior to calculating the burn
fluid requirements.
 Indication :
Adult burn more than 20%
Child burn more than 10 %
Electrical injury
Extreme of age
Fluid therapy

25. Conditions requiring more fluid than

27. Neurogenic shock
due to severe pain
treatment is pain
killers
the best and more
effective is I.V
morphine.

28. Hypovolaemic shock
 it is due to fluid loss and sometimes blood loss
 Paralysis of capillary tone which starts to occur
short time after the accident and reaches its
maximum in few hours.
 the body reacts to compensate after 8 hours and
the capillary tone starts to come back.
 Gradual absorption of the oedema fluid which is
supposed to be corrected completely after the 1st
48 hours.

29. Septic shock
Due to bactermia of wound infection
 Ccc by:
 Hypotension
 Tachypnea
Tachycardia
Fever
Altered mental status
Decrease urine out put
Hyperglycemia
Metabolis acidosis

30. Complications of burns
Infection
Limb ischaemia
Respiratory distress from inhalational injuries or circumferential
burn.
Airway obstruction
Burn scar contractures
Hypertrophic scarring
Rhabdomyolysis.
Compartment syndrome

31. Indications for transfer to burns centre
Partial/full thickness > 10 % BSA in patients <10 years or > 50 years
of age.
> 20 % BSA in all other age groups.
Burns to ‘special areas’ — face, ears, eyes, hands, feet, genitalia/perineum, and
major joints.
Full thickness > 5 % BSA.
Significant electrical and chemical burns.
Inhalation injury.
Burns in patients with pre-existing illness that could complicate treatment,
prolong recovery, or affect mortality.
Patients with concomitant trauma that poses an increased risk of
morbidity or mortality.

33. Electrical injury
 Electrical injuries can be
high ( > 1000V) or low (e.g.
domestic 240V) voltage.
 Both have the ability to
cause fatal electrocution
but severe injury is more
common with high voltage.

34. Types of current
 Current can be alternating (AC) or direct (DC)
 AC — is generally more dangerous because
tetanic muscle contraction makes it difficult to
release grip from the source.
 DC — typically has a very short duration, with the
victim thrown backwards (e.g. lightening)

35. Mechanism of injury
 Electrical injuries can cause damage in a variety
of manners:
 Direct effect of current, e.g. arrhythmias,
cardiac arrest, respiratory arrest.
 Direct thermal injury by acting as conductor of
electrical energy or via flash burns (sudden
vaporisation of hot metal).
 Mechanical trauma, e.g. thrown back.
 Post-trauma sequelae, e.g. rhabdomyolysis.

36. Severity of electrical injury
 The severity is determined by:
 Current
 Voltage
 Tissue resistance (reduced when wet, causing
more severe burns)
 Duration of contact
 Point of entry and path of electricity to exit point
(transthoracic is most dangerous)

37. Investigations
ECG
Creatine
kinase
Renal
function Urine

38. Management
 ABC
 Assess carefully for entry and exit wounds
 Intravenous fluids to maintain urine output > 100 ml/hour, if
evidence of rhabdomyolysis.
 Diuretics are contraindicated in the acute stage, fluid de-
livery should be increased.
 If attempts to provide osmotic diuresis fail, mannitol can
become an option. The intravenous bolus dose is 50 g for
adults and 0.5 g/kg for children
 Analgesia.
 underestimate the degree of tissue damage.
 Monitor for the development of compartment syndrome.

39. Complications
Musculoskeletal
 fractures
 dislocations
 myonecrosis
 compartment syndrome ●
Neurological
 seizures
 coma
 headache
 transient paralysis
 peripheral neuropathy ●
.

40. Metabolic
 rhabdomyolysis
 renal failure
Cardiac
 arrhythmias
 cardiac arrest
 myocardial damage
Ophthalmic
 cataracts, glaucoma

41. Discharge criteria following electrical burns
Asymptomatic.
Low voltage burns.
Normal ECG.
No history of arrhythmia (chest pain palpitations
No myoglobinuria.

43.  Chemical burns are
usually the result of
industrial or domestic
accidents.
 Alkalis tend to
produce more severe
burns due to their
ability to penetrate
even after initial
irrigation.
Chemical
burns
Acids Alkalis
Organic
compounds

44. Immediate
coagulative necrosis
creating an eschar
though limiting the
spread of burn injury
acids
chemical Burns

45. Liquefactive necrosis
with continued
penetration into
deeper tissue
resulting in
extensive injury
alkalis

46. Tar
 Tar causes burns both by its heat and by chemical
irritation.
 A practical way to remove tar from the skin
promptly and without causing additional damage
is to apply ice cubes on the tarred area for 10-20
minutes.
 In the mean time, tar will freeze to a crusty layer
and consequently can be peeled off.

48. Hydrofluoric acid
 Hydrofl uoric acid requires special attention because of
the severity of burn it can cause and the systemic
side-effects.
 Used in glass etching, metal extracting, refining, and
household rust removers.
 May be a time delay (hours) before patients present
because the burn may be painless initially,
 especially if due to lower concentration preparations.
 Causes liquefactive necrosis of tissues secondary to
the formation of soluble salt. It is able to
 cross lipid membranes and penetrate deeply into
tissues.

49.  Ongoing pain indicates ongoing tissue
damage.
 result in eschar formation.
 Burns often difficult to heal.
 Absorbed fluoride ions chelate calcium,
causing severe hypocalcaemia with
subsequent
 myoclonus, tetany, convulsions, CNS
depression, and ventricular fibrillation if
untreated
 unrecognized.

50. Phenol
 Not water soluble
 If available, use alcohol
before flushing except in
eyes
 If unavailable, use copious
amounts of water

51. Management of chemical burn
 ABC
 Remove any contaminated clothing.
 irrigation with water (at least 20–30 minutes)
 Check renal function, serum calcium, and magnesium.
 ECG and cardiac monitoring.
 Opiate analgesia.
 Antidote is 10 % calcium gluconate. This can be applied
as a gel to the burn, injected subcutaneously around
the burn site, used intravenously in a Bier’s block
(continued until pain settles), or given intra-arterially in
very severe cases.

52.  Intravenous calcium gluconate (10 ml of 10 % )
should be given if the patient is hypocalcaemic
or symptomatic of probable hypocalcaemia
(tetany, arrhythmias, prolonged QTc, seizures)
 In burns of chemical powders, irrigation may
have unfavorable effects. Water may activate
chemical powders. In these conditions, after
cleaning the chemical powder with a brush, a
dry cloth or a vacuum cleaner, the area should
be irrigated with copious water

54.  Local radiation burns caused by high dose
radiation (8-10 Gy) are similar to thermal
injuries except for the delay which may
extend from a few days to a few weeks.
 Progressive and in-tractable pain is a
typical symptom
 For this injury, the patient is referred to a
burns unit/center under proper conditions

56. Cold injury
The severity of cold injury depends on
temperature:
 duration of exposure
 environmental conditions
 amount of protective clothing
 patient’s general state of health.
 Lower temperatures, immobilization
 prolonged exposure
 moisture
 presence of peripheral vascular disease
 open wounds

57. TYPES

58. Frostnip
is the mildest form of cold injury.
characterized by :
initial pain
pallor
numbness of the affected body part
 It is reversible with rewarming and does not
result in tissue loss, unless the injury is repeated
over many years, which causes fat pad loss or
atrophy

60. Frostbite
 due to freezing of tissue with intracellular
ice crystal formation, microvascular
occlusion, and subsequent tissue anoxia.
 Some of the tissue damage also can result
from reperfusion injury that occurs on
rewarming.

61. Degree of frostbite
 1. First-degree frostbite: Hyperemia and
edema without skin necrosis
 2. Second-degree frostbite: Large, clear
vesicle formation accompanies the hyperemia
and edema with partial-thickness skin necrosis
 3. Third-degree frostbite: Full-thickness and
subcutaneous tissue necrosis occurs, commonly
with hemorrhage vesicle formation
 4. Fourth-degree frostbite: Full-
thickness skin necrosis, including muscle and
bone with gangrene

63. Nonfreezing Injury
 Nonfreezing injury is due to microvascular endothelial damage,
stasis, and vascular occlusion.
 Trench foot or cold immersion foot (or hand) describes a
nonfreezing injury of the hands or feet, typically in soldiers, sailors,
and fishermen, resulting from long-term exposure to wet
conditions and temperatures just above freezing (1.6°C to 10°C, or
35°F to 50°F).
 Although the entire foot can appear black, deep-tissue destruction
may not be present. Alternating arterial vasospasm and
vasodilation occur, with the affected tissue first cold and numb,
then progressing to hyperemia in 24 to 48 hours.
 With hyperemia comes intense, painful burn-ing and dysesthesia,
as well as tissue damage charac-terized by edema, blistering,
redness, ecchymosis, and ulcerations. Complications of local
infection, cellulitis, lymphangitis, and gangrene can occur. Proper
atten-tion to foot hygiene can prevent the occurrence of most such
injuries.

64. MANAGEMENT OF FROSTBITE AND
NONFREEZING COLD INJURIES
 Treatment should be immediate to decrease the duration
of tissue freezing
 Constricting, damp clothing should be replaced by warm
blankets, and the patient should be given hot fluids by
mouth, if he or she is able to drink.
 Place the injured part in circulating water at a constant
40°C (104°F) until pink color and perfusion return
(usually within 20 to 30 minutes).
 This is best accomplished in an inpatient setting in a
large tank, such as a whirlpool tank.
 Avoid dry heat, and do not rub or massage the area.
 Rewarming can be extremely painful, and adequate
analgesics (intravenous narcotics) are essential.
 Cardiac monitoring during rewarming is advised

65. LocalWound Care of Frostbite
 The goal of wound care for frostbite :
 preserve damaged tissue by preventing
infection
 avoiding opening uninfected vesicles
 elevating the injured area which is left open to
air.
 The affected tissue should be protected by a
tent or cradle
 pressure spots should be avoided.

66.  Tetanus prophylaxis depends on the
patient’s tetanus immunization status.
 Systemic antibiotics are not indicated
empirically, but are reserved for identified
infections.
 The wounds should be kept clean, and
uninfected blebs left intact for 7 to 10 days
to provide a sterile biologic dressing to
protect underlying epithelialization