Critical Burns

Yefta Moenadjat

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).

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

Introduction
Critical burns
Burns is devastating injury
Multifaceted injury

Introduction
Principles of burn management
Multidisciplinary approach, Team work: Burn
team
Strategically intervention
Problem based
Evidence based
Regional characteristics

Burn management: prehospital.

A. Well developed countries
8 10 min
response
time 15 20 min
Fluid
resuscitatio
n

30 35 min 45 60 min
Trauma
Burn center
Center

Burn management: prehospital.

B. Indonesia
30 45 min
response
time

Transport

>60-120 min
Fluid
resuscitation
RS X

12 - 14 hrs
RSCM

Triage
Protocol
Non technical
problems

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

Inhalation injury

Critical Burns

Facial burns
Burned nasal
hair
Carbon deposit
Supraglottic
in nasal, oropharyngeal
cavity
Epiglottis Hyper secretion
Carbon
Laryngeal
deposit
edema
in
laryngeal
Infraglottic
space and
trachea
Hyper secretion
Laryngeal
edema
9
Hoarseness

Inhalation injury

Carbon deposit
Singed nasal hair
Secret

Edematous lips
Edematous mucosa
Hyper salivation
Hyper secretion

Critical Burns

10

Inhalation injury

Critical Burns

Carbon deposit in the tube

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

Critical Burns

Luminal obstruction

Anterior

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

Sensory nerve
SP

Neutral Endo Peptidase

(NEP) released in intact
mucosa.
NKA
Neutralize Neuropeptides (SP &
NKA).

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

Critical Burns

18

Inhalation injury
Injured mucosa

Neutral Endo Peptidase

(NEP)
NKA

Sensory nerve
SP

Neutralize Neuropeptides (SP &

NKA).

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

Critical Burns

19

Inhalation injury
Emergency procedure

Intubation
Critical Burns

Cricothyroidotomy
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

Wound

Epitheliu
m

Tissue injury induced

histamine release
lead to increased
blood flow to injured
site

Leukocy
te

Histamine induces
capillary leaks
followed by leukocyte
migration to injured
site

Critical Burns

Histami
ne

Bacter
ia

Phagocytocis of
bacteria, dead cells
and cells debris
Blood Clott
formation
Platelet

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

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

Occludin, adhesive molecules of tight junction

46

VE-cadherin, adhesive molecules of adherens junction

47

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

Hemoconcentration:
Hb
Ht >40 vol%
Critical Burns

Hydrostatic pressure
Osmotic pressure

Fluid flux
Interstitial edema
50

Critical Burns

51

The Problem of Circulation:

evaporation

Volume depletion

hemorrhage

burn
Interstitial edema

Critical Burns

52

53

Burn shock
From the perspective of Microcirculation:
Cellular injury and metabolic stress

54

CO2

O
O22

Macrocirculation

O2 input

O2

O
O22

Mitochondrial
respiration
Critical Burns

CO22

O
O22

O2 Saturation

O2 Delivery

O2utilization

Microcirculation

55

Burn Shock
Former Paradigm

Recent Paradigm

Shock syndrome
Macro-circulation
Organ oriented
(Renal failure)
Sepsis

Lack of perfusion
Microcirculation
Cellular shock
Metabolic changes
Cells injury
SIRS and MODS

Critical Burns

56

Active Transportation across the membrane:

the role of receptor, protein, electrolyte and ATP
Extracellular fluid

D
R

Gs Protein
ATP

Ca2+ Na+

K+

Ca2+ Na+

K+

cAMP

Inactive
Active
cAMP-dependentcAMP-dependent
Protein-kinase Protein-kinase

Protei
n

+ ATP

Protein
PO4

Intracellular fluid

+ ADP

Cells response
D : Drug
R : Receptor

57

insulin

Glucose

Na2+

Na2+

R
K+

Lactic
Acid

Pyruvate

TCA
Acetyl CoA

K+

Lactate

H+

ATP

CO2

58

Hypoxia : oxidative stress

Defect of cells membrane

Mitochondrial distress
Loss of protective shield
to free radicals
[Phospholipid]

Low pH enzymatic
activity

Membranes
receptor
changes
Critical Burns

Depleted
Nucleus
Reticulum
endoplasmic
stress

Cytoskelet
al
dissociatio
n

Broken double helix of D

59

The Plasma membrane

Transmembrane
Proteins
Phosphate head
Hydrophilic region

Lipid bilayer
Hydrophobic region

60

The Plasma membrane

Glycoprotein
Carbohydrate
side chain

Protein

Na

K+

Ca2+

Ca2+
K+
N
a+

The Plasma membrane

Cell membrane

Closed

Ion channel

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

D
R

Gs Protein
ATP

Ca2+ Na+

K+

Ca2+ Na+

K+

cAMP

Inactive
Active
cAMP-dependentcAMP-dependent
Protein-kinase Protein-kinase

Protei
n

+ ATP

Protein
PO4

Intracellular fluid

+ ADP

Cells response
D : Drug
R : Receptor

64

insulin

Glucose

Na2+

Hypeglycemia

K+
Lactic acidosis

Lactic
Acid

Na2+

Pyruvate

Acetyl CoA

K+

Lactate

H+

ATP

CO2

65

66

From glycolysis
2 NADH
2 ATP (substrate level
phosphorilation)
From bridge stage
2 NADH
From citric acid cycle
6 NADH
2 FADH2

Protons pumped

ATP

8-12*

4-6*
2

12

36
8

18
4

2 ATP (substrate level

phosphorilation)

2
TOTAL

36-38
67

Mismatch between ATP supply and

demand

[ATP]
falls

Minut
es
to
hours

ATP turnover

ATP turnover

ATP
supply
balances
ATP
demand

Forced
hypometabol
ism

Hours
to
days

Temporary
stabilization of
membrane potential

Chronic
membrane
Damage and
leaks
Net Na+ influx and K+
efflux
Mito, ER and membrane plasma
depolarize
Catastrophic Ca2+ entry into
cytosol from organelles and cell
exterior

Regulated
hypometabol
ism

Time in anoxia or hypothermia

Activation of phospholipase and

Ca2+ dependent proteases
Membrane
rupture
Necrotic cell
death

Time in anoxia or hypothermia

68

69

Antioxidant defense
Protective effect
SOD
Catalase

Primary Internal Antioxidants

Complete the defense system

Glutathione
Peroxidase (GPx)

Glutathione
Secondary
external (dietary)
Antioxidants
Flavonoids, Vitamin A C
Play a buffering
role but rapidly
Mineral, Protein
saturated
Carotenoids, Vitamin E

Antioxidant in the cells

Vit C
SOD + GSH-Px
GSHGSSG

Vit E
-Carotene
Catalase

Vit C, E
-Carotene
DNA

GSHGSSG
GSH-Px
Cu/Zn
SOD

Cells hypoxia following severe injury

Cells hypoxia following severe injury

Cellular
Respiratio
n

I SOD

Oxidative
burst

II

t
Ca

III

se
a
l
a

GPx

GSH
Inflammat
ion

Protein
peroxidation

IV

GSSG
GRed

DNA damage

Lipid 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

Resting Metabolism (%)

BMR in the Injury State

180

Major burn
140

Major trauma
Minor trauma
Normal range

100

Starvation
0

20

40
Days

60

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

Anti inflammatory
Anabolic
Referral

Cardiac monitoring

82

Metabolic changes as
the body response to trauma

The criteria of critical burn: >40% BSA

10

20

30

4
0

5
0

60

70

80

90

100

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%

43

79

46

21

Slightly increased
Return to normal
in 6 mo

Significantly
greater (p<0.05)

Significantly
greater (p<0.05)

Significantly
greatest (p<0.05)

Negative

Negative

Negative

Negative

Protein loss

Mild

Moderate

Highest (p<0.05)

Highest (p<0.05)

Loss of Body
weight

Almost none

Almost none

Significantly
greatest (p<0.05)

Significantly
greatest (p<0.05)

Loss of body
mass

Almost none

Almost none

Significantly
greatest (p<0.05)

Significantly
greatest (p<0.05)

Loss of bone
mineral content

Almost none

Almost none

Significantly
greatest (p<0.05)

Significantly
greatest (p<0.05)

Predicted REE
Net Protein
balance (muscle)

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%

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
n

Cardiac output
and predicted CO

Stroke volume
and predicted SV
CVP
Liver size

<40%

40-59%

60-79%

>80%

43

79

46

21

Increased

Decreased
(p<0.05)
Cardiac
dysfunction

Increased

Increased

Increased

Increased

Increased

Decreased
(p<0.05)
Cardiac
dysfunction

Higher

Highest

Lower

Lowest

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:
Palloidin

Infection and Inflammation

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)

Allgwer-Schoenenberger-Sparkes

SEM scanning electron microscop

TEM transmission electron91
micros

Burn shock
From the perspective of Macrocirculation:
Hypo-perfusion vs. vasoconstriction

92

Pathophysiology
Wound degradation

Status changes
of wound depth
(worsening)

1o burn

Erytema

94

Blister, bulae

2o burn

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

Pulmonary

Central

Cerebral

Cardiac

Splanchnic

Pulmonary

Cardiac

Central

Splanchnic

Renal

Renal
Peripheral

Peripheral
Skin

Muscles
Others

Muscles

Skin
Others
109

* Autoregulation

ORGAN

Flow at rest
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%)

Total

5000 (100%)

Main contributors
To central circulatio

Distribution of circulation
110

Hepatic a.

Celiac a.
Superior
Mesenteric
artery

Splenic a.

Gastric a.

Stomach

Liver

Spleen
Pancreas
Inferior
Mesenter
ic
artery

Small
Intestine
s
Large
Intestine
s

Total inflow
1,500 mL/min
Pa 90 mmHg

Portal v.
612 mmHg

Total
outflow
1,500
mL/min

111

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
molecules
Low molecular
weight
particles

Large
molecules
High molecular
weight
particles

121

Stress related mucosal defect (disease)

Normal

Critical Burns

Atrophy of GALT

Gut associated lymphoid

tissue (GALT) atrophy
following hypoxia

122

Aspect of macro circulation

Splanchnic hypoperfusion: gut failure

Gut is motor
of MODS

Gut failure

Hepatic failure
Respiratory failure
Myocardial failure
Haemostatic failure
Neurologic failure

Critical Burns

123

MODS
Multi-system organ
dysfunction syndrome

123

Aspect of macro circulation

Splanchnic hypoperfusion: gut failure
Gut failure: 1-4 hr following trauma
Ischemic time:
Neurons
Gut Mucosa
Endothelial
Renal tubules
Skeletal muscle
Critical Burns

124

:
:
:
:
:

4 minutes
1-4 hrs
4 hrs
8 hrs
8 hrs

124

125

Aspect of macro circulation

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

Critical Burns

126

Synthesis,

126

Systemic Inflammatory response

syndrome
1
2
3
4
5
LeukocyteTetheri
ng
events

Rolling

Signali
ng

Adhesi
on

Migrati
on

Blood flow

Endothelial

Endothelial activation

Bacteria

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