Critical Burns

Yefta Moenadjat

1
 Introduction

Critical burns
Former criteria of critical burns (severe, major
burns) referred to >40% TBSA.
No description of what >40% based on
High mortality by 23 pbd. (sepsis).

2
 Introduction

Critical burns
Recent criteria of critical burns (severe, major
burns) referred to problem encountered.
Pediatric and children <10yo, age of >50yo
with TBSA>20% , others >25%.
Inhalation injury
Associated injury, multiple trauma
Premorbid diseases
Electric and chemical injury

3
 Introduction

Critical burns

Burns is devastating injury

Multifaceted injury

4
 Introduction

Principles of burn management

Multidisciplinary approach, Team work: Burn

team
Strategically intervention
Problem based
Evidence based
Regional characteristics

5
Burn management: prehospital.
A. Well developed countries

8 10 min
response
time 15 20 min
Fluid 30 35 min 45 60 min
resuscitatio Trauma Burn center
n Center

6
Burn management: prehospital.
B. Indonesia

30 45 min
response
time >60-120 min
12 - 14 hrs
Transport Fluid
RSCM
resuscitation
RS X

Triage
Protocol
Non technical
problems

7
 Inhalation injury

Exposure of airway mucosa to:

Thermal source
(<1%, immediate luminal obstruction)
Toxic fumes
S2 (strongly alkaline aqueous H2S, Li2S,
Na2S, K2S,) corrosive agent
Acute upper airway inflammation,
edema, hyper secretion, luminal
obstruction
CO systemic intoxication

Critical Burns 8
 Inhalation injury

Facial burns
Burned nasal
hair
Carbon deposit
Supraglottic in nasal, oro-
pharyngeal
cavity
Epiglottis Hyper secretion
Carbon
Laryngeal
deposit
edema
in laryngeal
Infraglottic space and
trachea
Hyper secretion
Laryngeal
edema
Critical Burns Hoarseness 9
 Inhalation injury

Carbon deposit
Singed nasal hair
Secret

Edematous lips
Edematous mucosa
Hyper salivation
Hyper secretion

Critical Burns 10
 Inhalation injury

Carbon deposit in the tube

Critical Burns 11
 Inhalation injury
Smooth muscle

Mucous
membrane

Hyaline cartilage

Adventitia
Anterior

Burns to the airway

cause edema that blocks
the flow of air into the
lungs

Edema of
Mucous
membrane

Luminal obstruction Anterior

Critical Burns 12
 Inhalation injury

Bronchoscopy:
Edematous mucosa, secret,
carbon, obstruction, diffuse
bleeding
Critical Burns 13
 Inhalation injury

Critical Burns Mucus plug 14

 Inhalation injury

Critical Burns Mucus plug 15

 Inhalation injury

Critical Burns Pathology of trachea found postmortem 16

 Inhalation injury

Critical Burns 17
 Inhalation injury

Neutral Endo Peptidase

(NEP) released in intact
Sensory nerve NKA mucosa.
Neutralize Neuro-
peptides (SP &
NKA).
SP

SP : bronchocontriction substance P
NKA : neurokanin activity increase of
capillary permeability

Critical Burns 18
 Inhalation injury
Injured mucosa

Neutral Endo Peptidase

(NEP)
Sensory nerve NKA Neutralize Neuro-
peptides (SP &
NKA).
SP

SP : bronchocontriction substance P
NKA : neurokanin activity increase of
capillary permeability

Critical Burns 19
 Inhalation injury

Emergency procedure

Intubation Cricothyroidotomy

Critical Burns 20
 Inhalation injury

Emergency procedure Difficulties of intubation

in edematous tissue
Do no harm
No muscle relaxant
Single procedure
No second change
No re intubation

Intubation

Critical Burns 21
 Inhalation injury

Emergency procedure

Cricothyroidotomy
is not
contraindicated
in wounded area

Clear airway first

Critical Burns 22
 Inhalation injury

Pro and con

Risk and benefit

Hyper secretion
Cord pressure
Dead space
Tidal volume
Suction and
Humidification
Bronchial toilet
Mucus plug

Critical Burns 23
 Inhalation injury

Management
Periodic suctioning
Oxygen administration 0f 24 L
per minute
Humidification
Nebulizer:
Steroids
Bronchodilator as indicated
Bronchial toilet (Bronchoscopy
as gold standard)
Respiratory rehabilitation

Critical Burns 24
 Inhalation injury

Management
Mechanical ventilation
support:
Pressure vs. volume
control
Consider conversion to
tracheostomy as
mechanical ventilation
required >1week
Ventilator acquired
pneumonia
Mucus plus

Critical Burns 25
 Breathing and Respiratory problem

Encircled eschar of anterior chest wall that

reduces Lung compliance

Escharotomies

Critical Burns 26
 Breathing and Respiratory problem

Critical Burns 27
 Breathing and Respiratory problem

Critical Burns 28
29
 Epitheliu
Wound m

Tissue injury induced

histamine release
lead to increased
blood flow to injured
site

Histami Bacter
ne ia
Phagocytocis of
Leukocy bacteria, dead cells
te and cells debris
Blood Clott
formation

Histamine induces Platelet

capillary leaks
followed by leukocyte
migration to injured
site

Critical Burns 30
Critical Burns 31
31
32
Critical Burns 33
 Interstitial edema: injured sites

Critical Burns 34
 Interstitial edema: injured sites

Critical Burns 35
 Interstitial edema: injured sites

Critical Burns 36
 Interstitial edema: non-injured sites

Critical Burns 37
 Interstitial edema: non-injured sites

Critical Burns 38
 Capillary leaks Vascular leaks

Critical Burns 39
 Transmission electron microscope shows normal endothelium
Critical Burns 40
 E

Transmission electron microscope shows endothelial lining (a) and

leukocyte marginization prior to its migration (b) 41
Scanning electron microscope (SEM) showing normal endothelium of the vessels

42
Scanning electron microscope (SEM) showing endothelial gaps as leaky sites
and leukocyte migration.
43
Endothelial lining disintegration
Endothelial denudation rather than gaps
Equal disintegration found in nonburned area
Endothelial junction disassembly

Tight junction

Gap junction

Adherens
junction
Focal adhesion

44
Burn characteristics
45
 46
Occludin, adhesive molecules of tight junction
 47
VE-cadherin, adhesive molecules of adherens junction
Increased caveolae (pores) Endothelial apoptosis
indicates endothelial
hyperpermeability
Transmission electron microscope 48
Endothelial lining disintegration
Endothelial apoptosis
Endothelial dysfunction
Inability to provide barrier

49
 Preload
PAWP
CVP

MAP Inadequate
circulation

Volume
depletion
Hydrostatic pressure
Osmotic pressure
Hemoconcentration:
Hb
Ht >40 vol%
Fluid flux
Interstitial edema
Critical Burns 50
Critical Burns 51
 The Problem of Circulation:
Volume depletion

evaporation
hemorrhage burn

Interstitial edema

Critical Burns 52
53
 Burn shock
From the perspective of Microcirculation:
Cellular injury and metabolic stress

54
 O2 input
O
O22
CO2

Macrocirculation
O2
O2 Saturation

O
O22
O2 Delivery

Mitochondrial
respiration CO22 O
O22 O2utilization

Critical Burns Microcirculation 55

 Burn Shock

Former Paradigm Recent Paradigm

Shock syndrome Lack of perfusion

Macro-circulation Microcirculation
Organ oriented Cellular shock
(Renal failure) Metabolic changes
Sepsis Cells injury
SIRS and MODS

Critical Burns 56
 Active Transportation across the membrane:
the role of receptor, protein, electrolyte and ATP
Extracellular fluid Ca2+ Na+ K+

D

A
R
Gs Protein
ATP cAMP Ca2+ Na+ K+
Inactive Active
cAMP-dependentcAMP-dependent
Intracellular fluid
Protein-kinase Protein-kinase

Protei Protein
+ ATP + ADP
n PO4

Cells response
D : Drug
57
R : Receptor
 insulin

Glucose
Na2+ Na2+ TCA

R Pyruvate Acetyl CoA

K+ K+

Lactic Lactate H+ ATP CO2

Acid

58
 Hypoxia : oxidative stress

Defect of cells membrane

Mitochondrial distress

Loss of protective shield

to free radicals
[Phospholipid]
Low pH enzymatic
activity

Depleted
Membranes Nucleus
receptor
changes Reticulum Cytoskelet
endoplasmic al
stress dissociatio Broken double helix of D
Critical Burns n 59
The Plasma membrane

Transmembrane
Proteins

Phosphate head
Hydrophilic region

Lipid bilayer
Hydrophobic region

60
 The Plasma membrane

Glycoprotein
Protein Ca2+
Carbohydrate K+
Na +
side chain

Ca2+

K+
N
a+
 The Plasma membrane

Cell membrane Ion channel

Closed
Open
Ion channels

Active transport across cell

membrane:

Oxygen availability
Energy supply
Electrical current
ATP
Proteins
 Active Transportation across the membrane:
the role of receptor, protein, electrolyte and ATP
Extracellular fluid Ca2+ Na+ K+

D

A
R
Gs Protein
ATP cAMP Ca2+ Na+ K+
Inactive Active
cAMP-dependentcAMP-dependent
Intracellular fluid
Protein-kinase Protein-kinase

Protei Protein
+ ATP + ADP
n PO4

Cells response
D : Drug
64
R : Receptor
 insulin

Glucose
Na2+ Na2+

R Pyruvate Acetyl CoA

Hypeglycemia

Lactic acidosis
K+ K+

Lactic Lactate H+ ATP CO2

Acid

65
66
 Protons pumped ATP
From glycolysis
2 NADH 8-12* 4-6*
2 ATP (substrate level
2
phosphorilation)
From bridge stage
2 NADH 12 6
From citric acid cycle
6 NADH 36 18
2 FADH2 8 4
2 ATP (substrate level
2
phosphorilation)
TOTAL 36-38

67
 ATP
supply
balances Mismatch between ATP supply and
ATP demand
demand [ATP]
Minut falls Temporary
es stabilization of
Chronic
to membrane potential
membrane
ATP turnover

hours Damage and

leaks
Net Na+ influx and K+
Hours efflux
Forced
ATP turnover

hypometabol to Mito, ER and membrane plasma

ism days depolarize
Catastrophic Ca2+ entry into
cytosol from organelles and cell
exterior
Activation of phospholipase and
Regulated Ca2+ dependent proteases
hypometabol
ism
Membrane
rupture
Time in anoxia or hypothermia Necrotic cell
death

Time in anoxia or hypothermia

68
69
 Antioxidant defense

Protective effect
SOD
Primary Internal Antioxidants
Catalase Complete the defense system
Glutathione
Peroxidase (GPx)
Glutathione
Secondary
Carotenoids, Vitamin E
external (dietary)
Antioxidants
Flavonoids, Vitamin A C
Play a buffering
role but rapidly
Mineral, Protein saturated
 Antioxidant in the cells
Vit C
SOD + GSH-Px
GSHGSSG
Vit C, E
-Carotene

Vit E
DNA
-Carotene

Catalase
GSHGSSG

GSH-Px

Cu/Zn
SOD
Cells hypoxia following severe injury
 Cells hypoxia following severe injury

Cellular
Respiratio
a lase III
t
n Ca

Oxidative
I SOD II GPx
burst

GSH GSSG
Inflammat
ion
IV GRed

Protein
DNA damage Lipid peroxidation
peroxidation
 Cells hypoxia following severe burn injury

Energy demand

Cells activity in adaptation phase

ROS production
Antioxidant defense
Acute phase protein
C Reactive Protein (CRP)
Procalcitonin (PCT)

Critical Burns 76
 BMR in the Injury State
Resting Metabolism (%) 180

Major burn
140
Major trauma
Minor trauma

100 Normal range

Starvation

0 20 40 60
Days

Effect of injury on metabolic rate. (Adapted from Wilmore DW. The

Metabolic Management of the Critically Ill. New York: Plenum Medical
Book, 1977) 77
 DNA damage

Critical Burns 78
 DNA damage

TNF

ROS

Critical Burns 79
Smith A, Barclay C. Quaba A, Sedowofia K , Stephen R, Thompson M. et al. The
bigger the burn, the greater the stress. Burns 23(4) 1997: 291-294

80
BSA
Correlations between
percentage burn surface area
and admission concentrations
of plasma hormones in burn
injured
children.

Adrenaline
Angiotensin II
Aldosterone
Arginine vasopresin
Dopamine
Noradrenaline
Plasma Renin activity

ANP
81
The bigger the size, the greater stress:
Inflammatory response
Hypermetabolic response

Cardiac monitoring
Anti inflammatory
Anabolic
Referral
82
The criteria of critical burn: >40% BSA
the body response to trauma
Metabolic changes as

10 20 30 4 5 60 70 80 90 100
0 0
Theres a remarkable increased of the resting energy expenditure up
to 40% BSA, but increase of BSA involved after such a point shows no
significances

Wolfe SE. Metabolic changes in burn injuries. Ann Surg 2001 83

 Criteria of critical
burn
after ABA 2002

Critical Burn (major burn)

1.2o and 3o burn involves > 20% in adult >50 yrs
or children <10 yrs
2.2o and 3o burn involves > 25% in adult <50 yrs
or children >10 yrs
3.High voltage electric burn
4.Burn involves face, ear, hand, feet and
perineum
5.Associated with multiple injuries
6.Burn in high risk population
American Burn Association Practice
Guidelines for burn care 2002
http://www.ameriburn.org 84
85
Jeschke, MC.
Burn Size Predicts Hypermetabolic Response that Drives
Mortality Riskon 189 pediatric burn
reviewed data
patients
<40% 40-59% 60-79% >80%
n 43 79 46 21
Slightly increased
Significantly Significantly Significantly
Predicted REE Return to normal
greater (p<0.05) greater (p<0.05) greatest (p<0.05)
in 6 mo
Net Protein
Negative Negative Negative Negative
balance (muscle)
Protein loss Mild Moderate Highest (p<0.05) Highest (p<0.05)
Loss of Body Significantly Significantly
Almost none Almost none
weight greatest (p<0.05) greatest (p<0.05)
Loss of body Significantly Significantly
Almost none Almost none
mass greatest (p<0.05) greatest (p<0.05)
Loss of bone Significantly Significantly
Almost none Almost none
mineral content greatest (p<0.05) greatest (p<0.05)

86
http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/tb/6485
Jeschke, MC.
Burn Size Predicts Hypermetabolic Response that Drives
Mortality Riskon 189 pediatric burn
reviewed data
patients

<40% 40-59% 60-79% >80%

n 43 79 46 21
Interleukin1,6,8 Increased Increased Increased Increased
TNF Increased Increased Increased Increased
MCP Increased Increased Increased Increased
GM-CSF Increased Increased Increased Increased
Serum Insulin Increased Increased Increased Increased
Serum GH Increased Increased Increased Increased

87
http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/tb/6485
Jeschke, MC.
Burn Size Predicts Hypermetabolic Response that Drives
Mortality Riskon 189 pediatric burn
reviewed data
patients
<40% 40-59% 60-79% >80%
n 43 79 46 21

Decreased
Cardiac output (p<0.05)
Increased Increased Increased
and predicted CO Cardiac
dysfunction
Decreased
Stroke volume (p<0.05)
Increased Increased Increased
and predicted SV Cardiac
dysfunction
CVP Higher Highest Lower Lowest
Liver size Reach 100% Reach 100% Approx 150%

88
http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/tb/6485
 Tissue damage:
Infection and Inflammation

Sepsis is of a great potency to develops in burns injury

Lipo-polysacharide substance (LPS) from known
microorganism
1970s Silver sulfadiazine (SSD) application
significantly reduced the incidence of sepsis
Unpublished information of negative impacts of SSD
Inflammation
Lipid-protein complex (LPC) serum (formerly: burn
toxin) released from non-vital tissues following burn
has a great potency lead to the development of SIRS
and MODS (pernicious effectors in burns)

Allgwer-Schoenenberger-Sparkes 89
 Tissue damage:
Infection and Inflammation

The Sucrose density gradient

test. The picture showing
single band of non-toxic native
protein on left side tube and
double band in different
density on the second tube
indicates toxicity as confirmed
on assay which is significantly
affecting mortality.

Allgwer-Schoenenberger-Sparkes 90
 Tissue damage:
Infection and Inflammation
Palloidin

Burn serum

Bleb formation in hepatocytes following contact to palloidin and burns serum (SEM).
Red cells echinocytes forms following contact to palloidin and burns serum (SEM)
Hepatocytes membrane damage with vacuole formation following contact to palloidin
and burns serum (SEM)
Mitochondrial membrane destruction with vacuole formation following contact to
palloidin and burns serum (TEM)
SEM scanning electron microscop
Allgwer-Schoenenberger-Sparkes TEM transmission electron91
micros
 Burn shock
From the perspective of Macro-
circulation:
Hypo-perfusion vs. vasoconstriction

92
 Pathophysiology
Wound degradation

Status changes
of wound depth
(worsening)
1o burn

Erytema

94
 2o burn
Blister, bulae

95
3o burn Eschar

3rd

96
 Pathophysiology
Inflammation: vascular leaks, edema and hypoxia
lead to deteriorated circulation (local and systemic)
and reactive oxygen species (ROS)

97
Deteriorated circulation

98
Deteriorated circulation

99
Deteriorated circulation

100
Deteriorated circulation

101
Deteriorated circulation

Compartment syndrome

102
Deteriorated circulation

Compartment syndrome

103
Deteriorated circulation

Superficial vein thrombosis

104
Deteriorated circulation

Superficial vein thrombosis

105
Deteriorated circulation

Vascular compromised

106
Deteriorated circulation

Fasciotomy

107
 Deteriorated circulation

Myolysis Deep vein thrombosis

108
 Normal Volume depletion

Cerebral Cerebral

Pulmonary Central Cardiac Pulmonary Central Cardiac

Splanchnic Splanchnic
Renal Renal

Peripheral Peripheral
Skin Skin
Muscles Muscles

Others Others

109
* Autoregulation
 Flow at rest
ORGAN
ml/min
Brain 650 (13%)
Heart 215 (4%)
Skeletal muscles 1030 (21%)
Skin 430 (9%)
Renal 950 (19%)
(19%
Abdominal Organ 1200 (24%)
Others 525 (10%)
Main contributors
Total 5000 (100%) To central circulatio

Distribution of circulation
110
 Celiac a. Hepatic a.

Superior
Mesenteric Splenic a. Gastric a.
artery

Stomach Liver

Spleen

Pancreas Portal v.
612 mmHg
Small
Inferior Intestine
Mesenter s
ic Large
artery Intestine
s Total
Total inflow
outflow
1,500 mL/min
1,500
Pa 90 mmHg 111
mL/min
112
113
114
 Splanchnic hypoperfusion: gut failure

Ischemia of gut mucosa lead to villi atrophy

Abnormality of digestion
Diarrhea and enterocolitis
GI bleeding (was: stress ulcer)
Bacterial translocation *): septicemia
Ischemia of muscular mucosa lamina: ileus

*) environment:
Fasting
Broad spectrum antibiotics and anaerobe
Antacid and H2 receptor antagonist

Critical Burns 115 115

 Intestinal villi atrophy

Critical Burns 116

 GI bleeding

Mucosal erosion and / or

mucosal disruption lead to
submucosal capillaries
exposed to gut lumen

Controversies:

Stress ulcer (Curlings ulcer)

Mucosal erosion (mucosal
disruption)

Critical Burns 117

 GI bleeding
Stress ulcer (Curlings ulcer)

Stress induced:
Stress hormones
Gastrin
Gastric juice (HCl) lead to gastric hyper acidity

Critical Burns 118

 GI bleeding
Disrupted mucosa (erosion of mucosa) due to hypox

Critical Burns 119

 GI bleeding
Disrupted mucosa (erosion of mucosa) due to hypox

Gastric secretion (cellular physiology abnormality ATP

Critical Burns 120
Stress related mucosal defect
(disease)
Normal SRMD

Loss of gut
mucosal barrier:

Leaky gut
(edema)
Bacterial
translocation
Small Large
molecules molecules
Low molecular High molecular
weight weight
particles particles 121
 Stress related mucosal defect (disease)

Normal Atrophy of GALT

Gut associated lymphoid

tissue (GALT) atrophy
Critical Burns 122
following hypoxia
 Aspect of macro circulation

Splanchnic hypoperfusion: gut failure

Gut failure Gut is motor

of MODS

Hepatic failure
Respiratory failure MODS
Myocardial failure Multi-system organ
dysfunction syndrome
Haemostatic failure
Neurologic failure

Critical Burns 123 123

 Aspect of macro circulation

Splanchnic hypoperfusion: gut failure

Gut failure: 1-4 hr following trauma

Ischemic time:
Neurons : 4 minutes
Gut Mucosa : 1-4 hrs
Endothelial : 4 hrs
Renal tubules : 8 hrs
Skeletal muscle : 8 hrs

Critical Burns 124 124

125
 Aspect of macro circulation

Splanchnic hypoperfusion: gut failure

Hepatic failure
Hepatic function: Enzymatic, Synthesis,
detoxication
Jaundice (seldom)
Pancreatitis in burns injury
Incidence: quite low
Fatal

Critical Burns 126 126

 Systemic Inflammatory response
1 2
syndrome
3 4 5
LeukocyteTetheri Rolling
Signali Adhesi Migrati
events ng ng on on

Endothelial Blood flow

Bacteria
Endothelial activation

Leukocyte

Platelets

Endothelia
Spiess DB.. J Cardiovasc Pharm27 (Suppl.1):v-vii 1996
127
 Systemic Inflammatory response
syndrome
Septic shock
Systemic vasodilatation
Retractable hypotension

Sepsis syndrome
Acidosis (hyperchloremic, lactic)
Hypothermia
Coagulopathy

Critical Burns
 Systemic Inflammatory response
syndrome
Exaggerative (destructive) inflammatory
response

Leukocyte > 10.000 / < 4.000

Platelet < 50.000
PTT APTT INR D Dimmer (+) /
(Consumptive Coagulopathy)
Procalcitonin
C Reactive Protein / Acute phase protein

Critical Burns
 Monitoring

Volume depletion:
PAWP, CVP
MAP
Hemoconcentration: Hb Ht >40%

Oxygen delivery (DO2)

Oxygen utilization: mixed vein oxygen
saturation (SvO2)

Critical Burns
 Monitoring

Gut assessment
Gastric juice (Q/Q) gut ischaemia / gut
failure

Critical Burns
 Monitoring

Cellular physiology abnormality

Hyperglycemia, Lactic acid, hyperlipidemia,

hypo proteinemia (albumin, UUN excretion)
ATP production
Early: hypometabolic stage (ebb phase) body
temp
Base Excess
Later: hypermetabolic stage BMR body temp

Critical Burns
 Monitoring

Cell injury

Hyperglycemia, Lactic acid, hyperlipidemia,

hypo proteinemia (albumin, UUN
excretion)
ATP production
Electrolyte imbalance
Multi system organ failure

Critical Burns
 Management

Strategic approach

Critically trauma
Multidisciplinary
Closed monitoring

Critical Burns
 Management

ICU setting

Early support. Should not a terminal support

Sedation to meet metabolic requirement
Reduce fluid requirement
Reduce pain killer management (prevent
haemostatic effect of NSAID)
Reduce BMR (prevent hypercarbic effect of
dietary administration)
Effective wound management (pain control)

Critical Burns
 Management
Fluid resuscitation and management
Crystalloids vs. colloid
Protocols
Volume replacement
Massive edema in spite of
lack of perfusion
Complications of fluid
(crystalloid) resuscitation:
Pulmonary edema
Compartment
syndrome
Abdominal
compartment
syndrome (ACC, Intra
abdominal
Critical Burns Hypertension, IAH)
Problem based evidence based
Low volume resuscitation
(perfusion targeted orientation)
Cocktail:
Large molecular weight
nonprotein colloid
Hypertonic saline
Crystalloids
Complication:
Haemostatic changed
(dilution effect)
 Management

Gut management
Gut assessment and monitoring
No fasting
The rational used of gastric secretion
management
Early Enteral Nutrition (EEN)
Gut feeding vs. to feed the body

Critical Burns
 Management

Others
Surviving sepsis campaign
Steroid administration to control of inflammation
Hyperglycemia management
Source control
Wound management: escharotomy, dilution,
early serial escharectomy (debridement))
Antibiotics
Antioxidants
High dose Vit C, Selenium, Zinc, Omega3
Omega6
Calcium, etc.

Critical Burns