Dr.

Anila Malde
Professor Anaesthesiology,
LTMMC & LTMGH, Sion, Mumbai
 Phase Time frame
Initial evaluation & resuscitation 0–72 hr
Initial excision & biological closure Day 1–day 7
Definitive wound closure Day 7–wk 6
Rehabilitation, reconstruction & Day 1–2 yr
reintegration

EMS Specialist
Critical Care
Specialist
Anaesthesiologist

pain Specialist
 EMS
Specialist

Critical Care
Specialist
 Location & type of injury (e.g., explosion,
flame, fluid, steam, chemicals, high
voltage
 Circumstances (e.g., open space,
confined space, duration of exposure)
 Type of accidents (e.g., car, motorbike,
jump to escape, fall)
 Level of consciousness
 Evidence of aspiration
40 3 0 2 0D 2 0S 1 0
 Damage to the superficial layers of the
epidermis
 Erythema
 Pain
 No open wound
 Fluid loss and systemic response is
minimal
 Not considered significant
 Not considered when burn size is
calculated for fluid resuscitation.
 Extension to papillary dermis
 Very painful
 Hyperaesthesia
 Blistered or weeping
 Moist Pink and blanches with
light pressure
 Typically heals within 10–20
days with minimal to no
scarring if infection is
avoided
 If > 20 % TSBA →fluid
resuscitation and
monitoring
 Extend to the varying degree of
reticular dermis
 Dry
 White-pink
 Blanching is minimal
 Blistering minimal or many hours later
 Less pain on compression of the
wound
 Hypoaesthesia
 Take ?20 days to heal
 Significant hypertrophic scarring
 Skin grafting is usually
recommended
 Epidermis, dermis, & different depths
of subcutaneous & deep tissues have
been damaged
 Dry, white, or charred appearance is
common
 Pain –absent or very low (usually
with marginal partial-thickness burns)
 Infection if left nonexcised is very
high
 Never heal spontaneously
 Rx- excision of all injured tissue +
graft
 Affectdeep structures,
such as bones and internal
organs
 Typical of high-voltage
electrical injuries and
flammable agents
 Usually black charred
appearance
 High mortality rate
 High
voltage •>1,000 V
Low
voltage •<1,000 V
Lightning •30 × 6
10 V
 Deep burns to skin and muscle
 Blunt trauma from falls
 Immediate cardiac arrest (ventricular fibrillation)
 Delayed or persistent dysrhythmias →telemetry
 Respiratory arrest
 Paralysis of respiratory muscles
 Tetanic contractions
 Indirect trauma
 Fluid requirements are twice & cannot be
calculated based on cutaneous burn requirements
 Renal failure secondary to myoglobinuria
 Superficial skin burns
 Rhabdomyolysis due to associated muscle
contractions
 Acute dysrhythmias (rare)
 Rare superficial skin burns
 Asystole
 Respiratory arrest due to direct CNS injury
 Exposure to acids, alkali, organic compounds
 Continued tissue damage until insulting agent is
removed
A

C
 Asphyxia secondary to the lack of oxygen
during combustion
 Inhalation of superheated air or steam
 Acute toxicity
Carbon monoxide
Cyanide
 In
anyone with a burn injury, it should be
presumed that the patient will have some
degree of CO & cyanide poisoning
Soot in the nares or
orophaynx

Singed facial hair

Carbonaceous cough
 ABG
 Fiberoptic
Bronchoscopy
Laryngoscopy
Nasopharyngoscopy
 Flowvolume curves
 Abnormal CXR at 48 hours
Haemoglobin with affinity 200 times
> O2

Mitochondrial cytochrome oxidase

system, →profound  aerobic
metabolism
0–10 • Minimal symptoms

10–20 • Nausea, headache

20–30 • Drowsiness, weakness
30–40 • Confusion, agitation
40–50 • Coma, respiratory depression
>50 • Death
 No signs of peripheral cyanosis secondary
to their characteristic “cherry red”
appearance”
 Pulse oximetry will not detect
 Cooximetry is needed
 100 % O2 wth nonrebreathing mask
Look for S/O CNS  cardiac irritability or ischaemia
ABG with COHgb levels
< 20 % > 20 % 30-40 %
100 % O2 mask ETT + 100 % O2 until Hyperbaric
till  to non-toxic COHgb < 10 % & O2
levels (<10%) cytochrome oxidase
within 45 system returns to
minutes normal (HCO3 > 20)
Closed-space smoke exposure

Profound met. acidosis not

explained by arterial CO conc.

Blood cyanide level > 0.5 mg/L

Intubation with delivery of 100 % O2

Haemodynamic support

Sodium thiosulfate & sodium nitrates

 Ammonia
 Nitrogen dioxide
 Sulfur dioxide
 Chlorine
Airway
 Highly irritant bronchospasm, edema, and mucous
membrane ulceration  tracheobronchial epithelial
lining necrosis  partial or complete airway
obstruction & recurrent infections
Physiologic effects on the lungs
 capillary permeability  increased lung water 
lung compliance
  lung volumes
  airway resistance
 Impairment in surfactant production
 V/Q mismatch   pulmonary shunting
 Inability to protect airway

Hypoxia

Stridor/hoarseness

Large third degree facial burns

Carboxyhemoglobin >20%
 CVS instability
 CNS depression
 Massive burns > 60% of TBSA
 Symptoms of impending airway
obstruction
Severe airway
oedema continues
to progress for
several days after
initial injury and
intubation
 Preoxygenation with 100 % O2

IV induction drug + Rapid-acting muscle relaxant

Succinylcholine - safe in first 24 hours / Rocuronium

Cervical collar in place manual in-line stabilization
Adequately secure- Difficult because
Topical wound agents
Continual swelling and edema of the face / neck
Fluid extruding through the facial burn
Umbilical tape should not be too tight  soft tissue necrosis
 Awake intubation

Topical anaesthesia
Proper patient positioning
Supplemental oxygen

Minimal IV opioids

FFB
Bullard scope
Glide Scope
LMA
Shift to OR for inhalational induction with continued
spontaneous ventilation

ILMA / LMA
Retrograde techniques
Transtracheal jet ventilation
Cricothyroidotomy
Tracheostomy
 Low TV (6–8 mL/kg) ventilation
PEEP
Vigorous pulmonary toilet
Frequent bronchoscopy
High-frequency ventilation
Steroids are not indicated
Prophylactic antibiotics not indicated
 Assessment
 Peripheral pulses weak or absent due to
Underresuscitation
Proximal circumferential third degree burns
 Tachycardia is common
Pain
Hypovolemic shock
 Secure Large peripheral IV access
Preferably in areas of unburned skin
Extensive →through burned skin or CV lines
Capillary leak
syndrome →
Hypovolemia
+ Vasoconstriction
→ ↓ in cardiac
output (50 %
within 30 minutes)

Fatal burn shock

Preexisting
cardiac Elderly
dysfunction
 Thermal injury

Release of inflammatory mediators

Systemic capillary leak syndrome

Loss of fluid / pl proteins into interstitial tissue

Edema

↓ tissue perfusion

↓ viability
Paradox of burn fluid resuscitation

Too little fluid causes

hypoperfusion of the
wound and extension of
cellular damage

Toomuch fluid causes

excessive tissue edema,
which impairs perfusion
and also results in
extension of injury
Pulmonary edema
 • Initial 12–
Capillary leak
24 hours

• by 48
Cardiac function returns to normal
hours

Hemodynamic picture reversal, • By end of

vasodilatation + supernormal CO 1st week

• Postburn
CO plateaus at 2.5 X N
day 10

• Till wound
CO remains high
is closed

Overall hypermetabolic response • For 9–12

persists months
 Catecholamine  HighCO
levels  Low SVR
  cortisol  Low-grade fever
  inflammatory   WBC count
cytokines

Mimics Sepsis
Lund–
Browder
(“Rule of
Nines”)
method to
determine
burn size
 Rule of Palm
Patient’s palm
equals 1% of his
body surface area

46
 Onlysecond and third degree burns are
used for the calculations of fluid
resuscitation
 Lactated Ringer’s solution
 Massive amounts of NS →hyperchloremic
acidosis.
 American Burn Association Practice
Guidelines for Burn Shock Resuscitation
do not recommend the use of FFP
without active bleeding or coagulopathy
outside of a clinical trial, when other
choices are available
 Ifpatient requires twice the calculated rate
of fluid than start albumin
 Calculate fluid requirement
1/3 as albumin
2/3 as LR
 Maintenance rate of D5 LR continuously
 In addition 3 mL/ kg / % burn of LR
without glucose
Half of this amount in the initial 8 hours
Half over the subsequent 16 hours
Urine output 0.5–1.0 ml /kg/hr
Blood pressure Within normal range for age
Heart rate† Variable
Central venous pressure‡ 3–8 mmHg
Fractional excretion of Na+ <1% (indicates hypovolemia)
(FeNa)§
BUN/Cr ratio¦ ≥20 (indicates hypovolemia)
Echocardiogram/ultrasound Normal stroke volume & EF
Base deficit >5 (suggests hypoperfusion in the
absence of CO/ cyanide poisoning)
Compartmental syndromes (Pr >30
mmHg) in the presence of a large fluid
resuscitation
Muscle  Escharotomy
Abdomen  peritoneal dialysis or diagnostic
peritoneal lavage catheter & aspiration of
abdominal fluid
Deeply burned extremities with associated
fractures  fasciotomy
Over resuscitation
Over resuscitation
 Children
 Circumferentialabdominal burns
 Fluid requirements > 6 mL /kg / % TBS
burn
 Associated injuries
 Falls
 Alterations in mental status unusual unless
 Anoxic injury
 Carbon monoxide poisoning
 Substance abuse
 Elderly patients → stress/hypoxia associated
with the injury → acute coronary syndrome
 Preexisting chronic illnesses
 Foley catheter →monitor urinary output
 Gastric ileus common→ NGT
 Must in burns >20 % TBSA to  emesis
with aspiration
 Inj TT in the absence of immunization in
the 5 years prior to burn injury
 Zone of Coagulation:
 Irreversible damage
 Zone of Stasis:
 Impairment of blood flow
 Recovery variable
 Zone of Hyperemia:
 Prominent vasodilation
 Usually recovers
 Prolonged exposure of dermal and subdermal tissues
Desiccation

Necrotic tissue →nutrient layer for invading bacteria

Must remain
Moist
&
Protected from bacterial overgrowth

Antibacterial ointments or emulsifications

 Incision through the third degree eschar to
subcutaneous tissue that relieves the
constriction.
 Indications
Circumferential third degree burn with
evidence of vascular compromise
Circumferential third degree burns of the chest
 risk of Recent resuscitation
infection  fluid weight gain
 hypertrophic  significant
scar  cosmetic pulmonary
 hospital stay compromise 20 to
 mortality inhalation injury
Operative blood loss
>1 blood volume
 Avoided to  risk of resistant organisms
 20–40 % incidence of bacteremia during
burn excisions prophylactic antibiotics
 Choice
Prevalence
First week  Gram-positive organisms
Second week  Gram-negative (especially
Pseudomonas)
 Pneumonias & ARDS
 Hypermetabolism with 
O2 consumption &  CO2
production  higher
minute ventilation
 Long-term survivors
have a gradual collagen
deposition  interstitial
fibrosis restrictive lung
disease
 Primarilydue to evaporative loss from the
open burn wound and not from third space
loss
 This evaporative fluid is primarily solute-
free water
 Solutions such as half-normal saline are
appropriate → rates to maintain goal U/o
 Enteral nutrition volumes must be
calculated into total fluid requirements
 Immediately after the injury→ noncellular fluid
translocates into interstitium → Hematocrit 
 Rare requirment of early PRC transfusion
unless preexisting anemia or associated injury
 Next week →anaemia
Bleeding from the wounds
Frequent blood sampling
Surgical excision
 RBC half-life 20 to
thermal injury / other circulating factors
 An otherwise healthy burn patient will tolerate
a haematocrit of 20 without any problems,
and will replenish their erythrocyte mass with
iron supplementation only
 Transfusions outside OR were associated
with  mortality & infections
 Utilization of blood products reserved for
Demonstrated physiologic needs
Undergoing excision & grafting in perioperative
setting
 During resuscitation →
Dilutional effects
Formation of microaggregates in the skin and
smoke-damaged lung
 Returns to normal by end of first week &
remains normal unless the patient develops
sepsis or multisystem organ failure
 Platelet transfusion only if
>1 blood volume loss during surgical excision &
grafting / Diffuse bleeding
 Thrombogenicity 20
to  antithrombin III,
protein C, & protein
Clotting factors  20 to S→
dilution & consumption.
SC low-dose
DIC rare but devastating heparin for
→ FFP & Cryo thromboprophylaxis
 Thermal injury

Hypotension or Hypoxia

Liver injury

Coagulopathy, toxins are not cleared,  bilirubin ,

altered drug binding & metabolism
Mucosal atrophy within 12 hrs due to  apoptosis
Changes in digestive absorption
 intestinal blood flow
 intestinal permeability

Early enteral feeding from first day if possible

Meet caloric needs
Protect & preserve gut mucosal integrity
Improve intestinal blood flow and motility
Blunt the hyperdynamic response
 Curreri formula
Calories requirement /day

25 kcal / kg + 40 cal / % TBSA burned

1–2 g / kg of protein
Nonprotein calories can be given as carbohydrates
or fat
 Modified Galveston formula
Calories requirement /day

<1 yr = 2100 x BSA + 1000 x Burn Area

1 -12 yr = 1800 x BSA + 1300 x Burn Area
>12 yr = 1500 x BSA + 1500 x Burn Area

BSA = Body surface area in m2

Burn Area = Surface area burned in m2
Gut derived inflammation & bacterial translocation

Inflammatory response
Sepsis and organ failure

Judicious use of antibiotics to prevent intestinal

overgrowth of potential pathogens
 Curling’s ulcers

Early enteral feeding

Sucralfate / Histamine receptor blockers
 TPN

Gut muscle atrophy
Fatty infiltration of the liver
Catheter-related infections

Abandoned
Reserved only for patients intolerant to enteral feedings
 First / early stage
Hypovolemia
 Catecholamines
 Cardiac output  Angiotensin
 Aldosterone
 Renal perfusion  Vasopressin
 
 GFR systemic vasoconstriction

ARF
 Second / late stage
Sepsis
High myoglobin levels
Nephrotoxic drugs ARF
Multiorgan failure

Usually appears by about third week post injury

CNS-driven stress response
 Levels of catecholamines Hyperthermia
 Glucagon Hypertension
 Glucocorticoids Tachycardia
ADH Cardiac output
 Renin Hyponatremia
Hyperglycemia
 Oxygen consumption
Hyperdynamic Severe nitrogen losses
response can be Weight loss
sustained for months  Strength
Fever
 Burn injury
Releases paracrine Release of
factors Cytokines
circulating
mediators
Local inflammation &  in circulating
oedema lymphocytes,
neutrophils, and
Immune suppression & SIRS macrophages

Endotoxin
Infection
 TBSA burned >40%

Age >60 years

Associated inhalation injury

 Pain
Specialist
 Baseline pain & procedure-related pain
 Morphine & fentanyl are most widely used
 Meperidine not recommended because of
accumulation of the toxic metabolite normeperidine
 Switch over to oral opioids early
 OTFC in children, especially for dressing
 PCA opioid for acute or procedure related pain
 Ketamine is ideal for dressing changes
 Dexmedetomidine
 Sedation & anxiolysis for prolonged intubation
 Analgesia for dressing changes
 Acetaminophen for minor pain
 Pain is exacerbated by anxiety if the pain is poorly
controlled with sedatives and analgesics.
 Hyperalgesia (increased response to painful
stimuli, e.g., wound debridement)
 Allodynia components(painful responses to
nonpainful stimuli, e.g., touch).
 Posttraumatic stress disorder in up to 30% of
severe burn injury, esp. in the setting of inadequate
Rx of anxiety & pain
 Antidepressants
 Anticonvulsants
Anaesthesiologist
 Dressing changes & topical antimicrobial agents
Eschar separates
Granulating wound is covered with SSG

If survival
Die of sepsis Severe contractures
Hypertrophic scars

Because
Burn is Major source of inflammatory mediators
 Early excision within the first 48 hours (assuming
that the patient has had sufficient resuscitation)
Early nutritional support
Infection control
Biologic wound covering
Modulation of the hypermetabolic response

Multiple surgical teams Repeated every 2 days

Techniques to limit blood loss Until complete
Larger areas excision Entire excision in 10 days
 Age
 Type of Burn
 % TBSA burned
 Current cardio-respiratory status
 Extent of the burn wound excision
Vascular access
Blood product requirements
 Location of the burn and planned donor graft
sites are important for positioning the body
 Hours of fasting prior to the surgery
 Airway assessment
 Recent CBC
Electrolytes
RFT
Glucose
ABG
Recent coagulation panel
Modified because adequate caloric intake is difficult

Intubated prior to surgery Unintubated patient

 
Continue, rather than Stop the feedings 4 hours
discontinue, the enteral before surgery
feedings H2 receptor antagonists
Metoclopramide
Antacids
 Peripheral

Central

Interosseous in children

Localization of vessels using USG

1 •  Infection rates if kept for >10 days

2 • 5–6 infections / 1,000 caths. Twice than usual

3 • Change every 72 hr if placed through burns

4 • Change every 7 days if through remote site

5 • No wire changes
• Most common source of bacteremia than burn
6 wound itself
Acute phase after the burn injury
Hypovolemia &  cardiac Delayed absorption via
output routes other than IV
 blood flow kidneys & liver  Metabolism & elimination
 Albumin  Free Acidic & neutral
drugs
 -1 acid glycoprotein  Free basic drugs→
requirement
Second Phase
cardiac output & core  drug clearance
temperature
 Nasogastric tubes
 Dressings
 Painful Facial wounds
 Exudate & topical
antibiotics making
surface slippery
 Mouth opening can be limited because of
oedema or developing contractures
 Difficult intubation
 Induction agents based on hemodynamic
stability of the patient
 Ketamine → stable haemodynamics &
analgesia. Beneficial for dressing changes
& bedside procedures
 Adequately resuscitated & non septic
patient → thiopental or propofol
 Etomidate should not be used for frequent
dressing changes due to adrenocortical
suppression
 Sevoflurane → ideal agent for inhaled
induction in c/o abnormal airways
 GA → opioid + volatile anaesthetics +
muscle relaxants
 Supplemental opioids are important →
intense pain they experience
 Requirement of large doses of opioids
especially during the hypermetabolic state
Activation of endogenous pathways during the
stress response
Regularly receipt of preop opioids →tolerance
 Pharmacokinetic + pharmacodynamic
changes
 ↓ hypnotic effect
 Require larger bolus doses &/ or ↑
infusion rates
 Haemodynamic consequences of
administering larger doses of propofol
should be kept in mind
 Haemodynamic stability
 Preserve airway
patency
 Preserve hypoxic and
hypercapnic responses
 ↓ airway resistance
 Antiinflammatory effects
in burns &/ or sepsis
 Ifone wishes to avoid manipulation of the
airway (e.g., after placement of fresh
facial grafts)
 Splint or dressing removal
 Dressing or line changes
 Insertion of Foley catheters in pediatric
patients
 To treat burn- & opioid-induced tolerance
to narcotics
 Bolus doses can cause hypotension in patients
with burn injury, despite ketamine-induced
catecholamine release
 Persistently high levels of catecholamines in
major burns →desensitization & down-
regulation of ß-adrenoreceptors → direct
myocardial depressant effects of ketamine can
become manifested
 Massive efflux of K+ from cell
to ECF
 Cannot be prevented by prior
defasciculating dose of
nondepolarizer
 Larger the TBSA →More  K+

 Sux →K+  within first min, peaks within 5 min, starts

to decline by 10 to 15 mins
 Hypersensitivity begins 48 hours after burn, & peaks at
1 to 3 wks, may persist for up to 2 yrs
 Safe for first 48 hours & is best avoided after that
 Up-regulation of AchR: fetal and a7
(neuronal type) at the muscle membrane
→ resistance to NDMR & sensitivity to
depolarizing muscle relaxants → require >
normal doses of NDMR (250–500 %) &
shorter duration of action
 ↑ binding to AAG and enhanced renal and
hepatic elimination of the NDMRs
 Resistance starts in a week & remains for 18
months after the burn has healed
 Specially seen with burn >30 to 40 % TBSA
 Rocuronium 1.2 to 1.5 mg/kg for RSI in
burns. Onset of time to effective paralysis
approx. 90 seconds compared to 60 s in
nonburned patients with a dose of 0.9 mg/kg
 Atracurium →Hofmann elimination
→↓effectiveness after burns →Resistance
to NDMRs is pharmacodynamic in nature
 Monitor neuromuscular function
 ECG
Surgical staples
Electrodes on back or dependent
 Pulse Oximetry
Reflectance
 Capnography
 NIBP / IBP
 Urine output
 Temparature
 NM monitoring
 Hypermetabolic state →↑ CO2 production,
→↑ ventilation rates
 Burn patient at   ambient temperature
thermoneutral ambient of OR >28◦C
temp of 28–320C  Warm all topical & IV
→metabolic rate 1.5 times fluids to 38◦C
> nonburned  Cover nonoperative
 If temperature  to 22– sites
28◦C → metabolic rate   Forced-air warming
in proportion to burn size device
 Evaporation through  Over-the-bed warming
wounds →Hypothermia lamps (radiant heaters)
  Coagulopathy  Circulating warm water
pads
 Difficult to estimate
 2.6 to 3.4% /3.5–5% of the blood volume for
every 1% TBSA excised
 Vigilant attention to several physiological
variables
 EBL:
Serial haematocrit
Constant communication with the surgeon
ABG for pH & lactate
1 • Tourniquets

• Epinephrine-1:10,000 soaked compresses

2
• Topical thrombin (1,000 units/mL)
3
• Postoperative compression dressings
4
• SC infusion of 0.45 % saline + epinephrine
5 (1:300,000) to the donor sites
 Use of minimal crystalloid
 If the patient is receiving parenteral
nutrition, it is important that its infusion not
be stopped because of the danger of
hypoglycemia
 The surgeons may inject large amounts of
subcutaneous fluid to facilitate wound
debridement and donor harvest. This fluid
should also be limited
 Replacement of losses with packed RBCs
 In most cases the patient should be given
blood immediately upon entering the OR
 Very difficult to catch up on fluid
replacement once infusion falls behind
 Enteral feeding during surgery beyond the
pylorus has been successful, provided the
airway was secured via a cuffed ETT or
tracheostomy
 Hold on
If potential for ↑ abdominal pressure (e.g.,
prone position during surgery)
Airway procedure such as tracheostomy is to
be performed
 Large quantities of opioids & muscle relaxants →
delay emergence & extubation
 Assessment of
 Metabolic status
 Potential for ongoing bleeding
 When the patient will return again for surgery
 Potential difficulty in maintaining Airway patency
 Potential difficulty in reintubation
 Large volumes fluid infusion → significant soft-tissue
oedema → delay extubation until oedema resolves
 Perform air leak test
 Trial of extubation with use of a Cook airway
exchange catheter
 Administer oxygen
 Ability to reintubate the trachea, in difficult airway
 CAEC kept 10 hours, well tolerated, vocalization +
 Post extubation, close monitoring for 24 to 48 hours
 Tumescent local anesthesia injected into a
donor site before harvesting
 Subcutaneous catheter infusions
 PNB
Lateral femoral cutaneous nerve block
Fascia iliaca block

 CNB – exercise caution for appropriate

selection
 Difficult
Intravenous access
 Problems of airway
 Extensive surgery
 Blood loss
 Severe pain
 Multiple procedures
 History – aetiology
 Depth
 Extent
 Early A, B, C
 Fluid resuscitation
 Early excision & grafting
 Difficult airway
 Hyperkalemia with succinylcholine
 Resistance to nondepolarisers
 Maintenance of normothermia
 Analgesia:
 Baseline pain
 Procedure related pain