1) Burns can result from direct contact with flames, hot liquids, gases, chemicals, electricity, or radiation. They cause tissue injuries by denaturing proteins. 2) Burn injuries affect the skin, which acts as a protective barrier and regulates temperature and fluid balance. Deeper burns extend beyond the epidermis into the dermis. 3) Proper evaluation and treatment of burn injuries requires assessing burn depth, size, inhalation injury, and associated complications affecting various organ systems. Early fluid resuscitation is critical.

1. DR.MUHAMMED MUHSEN AHMED DAMUDI
SOHAR HOSPITAL.

2. DR.MUHAMMED MUHSEN AHMED DAMUDI
SOHAR HOSPITAL.

3. Burns : are tissue injuries resulting from direct
contact with flames, hot liquids, gases, caustic
chemicals; electricity; or radiation
high risk groups for severe burn injuries:
 The very young
 The very old
 The very careless
3rd largest cause of accidental death
50% of adults <45 yr. survive 75% burns

4.  According to a 2002 report of the American
Burn Association, more than 1.1 million
persons in the United States sustain burns
each year, of whom more than 50,000 are
hospitalized and 4,500 die

5.  Largest body organ. 15% of body weight ,It is not
a passive organ.
 Protects underlying tissues from injury
 Temperature regulation
 Acts as water tight seal, keeping body fluids in
 Sensory organ
 Injuries to skin which result in problems like:
 Infection
 Inability to maintain normal water balance
 Inability to maintain body temperature

6.  Two layers
 Epidermis
 Dermis
 Epidermis
 Outer cells are dead
 Act as protection
and tight seal
 only the epidermis is
capable of true
regeneration

7.  Thermal (heat) burns
 Chemical burns
 Electrical burns
 Inhalational burns

8.  Depth Classification :
 Superficial
 Partial thickness
 Superficial
 Deep
 Full thickness
 Degree Classification :
 First
 Second
 Third
 forth

9.  Superficial Burn:
1st Degree Burn
 Signs & Symptoms
 Erythema
 Pain at burn site
 Involves only epidermis
 absence of blisters
 Heals within 3 to 6 days
 Example - sunburn

10.  Partial-Thickness Burn:
 2nd Degree Burn
 Signs & Symptoms
• Entire epidermal layer
• Part of underlying dermis
• Mottled and red, painful
• swelling and blisters
• Healing in 10 to 21 days
• Not enough to interfere with regeneration of the
epithelium

11.  Full-Thickness Burn:
 3rd Degree Burn
 Signs & Symptoms
• Destruction of all epidermal and dermal elements
• Burn into subcutaneous fat or deeper
• Skin is charred and leathery (woody)
• Generally not painful (nerve endings are dead)

12.  Fourth-degree
• Full-thickness
• Extending into muscle, tendons or bones
• Black and dry
• No pain
• Eschar formation

14.  It is a critical aspect of the initial evaluation of
burned patients in the emergency department.
 It will determine whether transfer to a
specialized burn center is required as well as the
magnitude of initial fluid resuscitation and
nutritional requirements
 Small areas: palm of patient's hand equals 1% of
BSA
 Large areas: “rule of nines”: Regions of the body
approximating 9% BSA or multiples

16.  infants and babies have a proportionally greater
percentage of BSA in the head and neck region and
less in the lower extremities than adults

17. Electricity is generated by the flow of electrons across a
potential gradient from high to low concentration
through a conductive material
EB:- depends upon:
 what tissue current passes through
 width or extent of the current pathway
 duration of current contact
 Most damage done is due to heat produced as current flows
through tissues
 True extent of the damage is often hidden
 = nerve blood, muscle, skin, tendon, fat, bone
 best  worst conductors
 Burns are often most severe at the source and ground
contact points

18. Complication :
Cvs : asystole , (VF) , conduction abnormalities and direct
trauma to cardiac muscle fibers. Survivors of electrical
shock can experience subsequent arrhythmia, usually
sinus tachycardia and premature ventricular
contractions (PVCs).
 Respiratory: Chest wall muscle paralysis from tetanic
contraction may cause respiratory arrest if the current
pathway is over the thorax. Injury to the respiratory
control center of the brain can also cause respiratory
arrest. The lungs are a poor conductor of electricity
and generally are not as susceptible to direct injury
from current as tissues with lower resistanc

19.  CNS :Most acute CNS or spinal deficits resulting
from electrical injuries are due to secondary blunt
trauma or burns. Often, the patient has transient
confusion, amnesia, and impaired recall of events
if not frank loss of consciousness
 long-term neurologic complications include
seizures, peripheral nerve damage, delayed spinal
cord syndromes, and psychiatric problems from
depression to aggressive behavior.

20.  Musculoskeletal: Acute injuries include fracture from
blunt trauma and compartment syndrome from burns
 Massive muscle damage can cause severe
rhabdomyolysis and subsequent renal failure.
 ENT/head: The head is a common point of entry for
high-voltage injuries. Patients may have perforated
tympanic membranes, facial burn, and cervical spine
injury. Approximately 6% of victims develop cataracts,

21.  Most acids produce a coagulation necrosis by
denaturing proteins, forming eschar that limits
the penetration of the acid.
 Bases typically produce a more severe injury
known as liquefaction necrosis.
 Damage continues until the substance is removed or
neutralized

22.  Inhalation injury is the main cause of death in burn
patients
 Its results from the airway inflammatory response to
inhalation of the products of incomplete combustion
and is the leading cause of death (up to 77%) in burn
patients
 Usually limited to upper airways
 Injury to lower airways be considered when:
 Overwhelming heat exposure
 Inhalation of steam
 Aspiration of hot liquids  direct pulmonary
injury

24.  Effects of of Acute Smoke Inhalation Injury
 Impairment of mucociliary function  infection
 Mucus hypersecretion
 Tissue inflammation with tracheobronchiolitis,
bronchitis, laryngitis, pneumonitis
 Epithelial sloughing
 Biochemical alteration with surfactant
inactivation
 Increases vascular permeability and lung edema
 Bronchiconstriction
 Initially large airway obstruction  late small
and large airways
 Carbon Monoxide (CO) poising

25.  Carbon Monoxide (CO) poising
 Most dangerous gas in fire. Leading cause of
death at scene and 24h after fire
 Odorless, colorless gas
 Carbon monoxide's affinity for hemoglobin is 200
times greater than that of oxygen
 shift dissociation curve to left  tissue hypoxia
 pulse oximeters using two wavelengths cannot
detect COHb
 normal COHb < 1.5% in nonsmokers and < 10% in
smokers

27.  Administration of 100% oxygen will shorten the
half-life of COHb from 4 h in room air to less than
1 h
 Mild poisoning (COHb<20%) --- 100% non-rebreathing
mask until level falls <5%
 Moderate poisoning (COHb 20 – 40%) without cardiac
or neurologic dysfunction --- monitoring of acid-base
status and 100% oxygen until level falls <5%
 Severe poisoning (COHb>40%) or with cardiac or
neurologic symptoms--- hyperbaric oxygen therapy
 Admission is required for all with level >25% or with
cardiac and neurologic symptoms
treatmentCarbon Monoxide (CO) poising

28.  Airway and Breathing
 Early intubation required to treat causes of
respiratory dysfunction:
 1. CO poisoning
 2. Upper airway edema
 3. Subglottic thermal and chemical
burns
 4. Chest wall restriction

29.  Upper Airway Edema
 Most pronounced first 8 hrs. postburn
 s&s
 Stridor ,Horseness ,Facial burns ,Singed nasal hair or eyebrows
Soot in sputum or oropharynx ,Respiratory distress
 Treatment:
 Early intubation before edema makes it impossible
 Humidified O2 to help clear secretions
 Bronchodilators to manage bronchospasm
 Elevate HOB 20-30 degrees
 Decrease head and neck edema

30.  Chest Wall Restriction
 Found mostly with circumferential 3rd degree burns
 Loss of elasticity incr. work of breathing required to
maintain FRC and Vt.
 Symptoms may incr. 10-12 hrs postburn secondary to
maximum edema formation
 Treatment
 Ventilation and mechanical ventilation
 Escharotomies

31.  Circulation
 Burn victims have incr. capillary
permeability in all burned areas
resulting in an intravascular fluid shift
into interstitial space
 Results are:
 Hyponatremia
 Hypoprotienemia
 Interstitial edema

32.  Cardiovascular resuscitation
 Fluid replacement
 consists of crystalloid, usually Ringer's
lactate, with or without the addition of
colloid. Standard protocols for fluid
replacement use body weight in
kilograms and percent TBSA burned.
 Parkland formula (4.0 mL of Ringer's
lactate per kg per % TBSA burn per 24
hours

33.  Fluid replacement
 Brooke formula: 1.5 mL of crystalloid per kg per
% TBSA burn per 24 hours plus 0.5 mL of colloid
per kg per % TBSA burn per 24 hours plus 2,000
mL of 5% dextrose in water per 24 hours
 Half the calculated fluid deficit is administered
during the first 8 hours postburn and the
remainder is administered over the next 16
hours.
 The patient's daily maintenance fluid
requirements are given concurrently
Cont..ABC’s of burn resuscitation

34.  Fluid replacement
 The endpoints of fluid therapy are
hemodynamic stability and
maintenance of an adequate urine
output.
 In extensive burns, fluid management
is adjusted according to invasive
monitors and laboratory studies

35. Decompression procedures
escharotomies & fasciotomies
Burn excision & skin grafting
Reconstruction operations
Supportive procedures
tracheostomy, gastrostomy,
vascular access

36.  Preoperative :
 Burn injuries may result in a broad
spectrum of physiologic impairments. These
vary, depending on the percent of TBSA
burned, location of burns, age of the
patient, time elapsed since initial injury,
and interim treatment. Ideally, burn
patients are fluid-resuscitated and
stabilized before being brought to the OR

37.  physiologic impairments :
 Respiratory :-
 Upper airway: A patient with burns
around the airway (e.g., singed nose
hairs) should be intubated as early as
possible.
 Direct inhalational injury and fluid
resuscitation may make delayed
intubation more difficult 2° upper
airway edema.

38.  Respiratory
 Lower airway: Physiologic derangements may
include pulmonary edema and ARDS. Additionally,
burn patients can be severely hypermetabolic (e.g.,
a patient with 40% TBSA burns may have twice the
normal metabolic rate) with corresponding
increased CO2 production. These patients may have
high minute-ventilation requirements. Pressure
control ventilation and high levels of PEEP may be
useful.
 Other possible effects of severe burns include: ↓
lung and chest-wall compliance, ↓FRC,, ↑
carboxyhemoglobinemia, and ↑
methemoglobinemia.

39.  Cardiovascular : -Alterations in microvascular
permeability result in a trans-capillary fluid flux
and tissue edema 12-24 hours after thermal injury
 Large amounts of water, electrolytes and proteins
are lost into the extravacular space, leading to
intravascular fluid depletion and hypovolemic
shock (burn shock)
 The hypermetabolism associated with burns
increases cardiac demand, and burn patients have
greatly elevated circulating levels of
catecholamines →↑↑HR + ↑ CO
 Major burns require 1.5-1.7 times the caloric need

40.  Musculoskeletal :-
 Damaged muscle →↑ acetylcholine
receptor density, resulting in ↓
sensitivity to nondepolarizing muscle
relaxants and potentially fatal
elevations of K+ in response to
succinylcholine.
 avoid succinylcholine after 24 h
postburn and for at least 1 yr thereafter

41.  Hematologic : Coagulopathies may result
directly from the burn injury, as well as from
rapid replacement of blood loss during
operative procedures
 IV access : May be difficult; assess preop.
Consider central line placement with a large-
bore catheter
 Premedication : Patients are commonly placed
on high-dose narcotics after the initial injury;
additional narcotics are frequently required to
provide adequate analgesia for transport and
movement to the OR table.

42.  Transport : For patients with severe ARDS,
transportation from burn unit to OR may face
challenges with regard to ventilation.
 Cardiopulmonary monitoring must be continued
during transport; the ventilation system used in
transport must be capable of delivering high
minute-volumes, PEEP, and inspiratory pressures.
 These requirements may not be satisfied by
standard bag-valve systems and may require a
high-quality transport ventilator

43.  Intraoperative :
 Anesthetic technique : GA , Regional techniques are rarely
feasible , LMAs are not recommended due to frequent
repositioning of patient intraop
 If the face is burned, awake FOI may be necessary
 securing the ETT may be difficult. Alternatives to taping the
ETT include suturing the tube to the teeth
 Induction :
 If the patient is adequately volume-resuscitated :
 propofol (1.5–2.5 mL/kg iv) or thiopental (3–5 mg/kg) may be
used
 If the patient is intravascularly volume-depleted
 etomidate (0.3 mg/kg) or ketamine (1–3 mg/kg) is
recommended

44. USE OF MUSCLE RELAXANT
-!--Rapid sequence induction and intubation
Indicated for full stomach e.g. ileus
-!--Succinylcholine - contraindicated 24 hours to 2 years after major
burns, S/E-----profound hyperkalemia and cardiac arrest.
-!--Rocuronium in dosage of 0.9 mg/kg
Can intubate in 45 sec
Must be confident of airway management-
!----Large doses of non-depolarizing muscle relaxants may be
required due to altered protein binding and an increase
extrajunctionalacetylcholine receptor which bind non-
depolarizing drug without causing neuromuscular effect

45.  Maintenance :
 Standard maintenance
 Physiologic derangements of the respiratory system
(ARDS, pulmonary edema) and a hypermetabolic
state may require minute-volumes > 30 L/min, and
high inspiratory pressures and PEEP, for adequate
ventilation.
 Intraop, surgeons may use epinephrine-soaked
sponges to ↓ blood loss. Systemic absorption of
epinephrine will cause tachycardia and increase the
probability of dysrhythmias; therefore, it is best to
avoid halothane or desflurane. Isoflurane and
sevoflurane are acceptable.

46.  Emergence :
 Estimation of an adequate dose of narcotic to provide
postop analgesia should be considered.
 If large-volume resuscitation has occurred intraop, the
possibility of clinically significant airway edema
considered; use caution before extubating to ensure a
patent airway.
 Blood and fluid requirements : Blood must be in OR
before induction. The major blood loss generally is
associated with eschar excision, usually the first part
of the procedure

47.  Thermal considerations :
 Temperature must be monitored throughout the
case
 Warm all fluids.
Humidify gases.
Warming blanket
Reflective head cover
 Monitoring :
 Standard monitors : ECG may require needle
electrodes if there is no skin availability to apply
adhesive electrodes

48.  Positioning :
 The burn patient may be uniquely susceptible to
laryngeal or upper airway edema in the prone
position; therefore, examination of the upper
airway before extubation is recommended to avoid
emergent reintubation
Postoperative
 Complications :
 Hypothermia-use radiant heater or warming blankets
 Coagulopathy : May occur as the result of massive blood
loss and replacement
 Pain management : PCA - fentanyl or morphine sulfate

49. RAMADAN MUBARAK