Initial Management

of massive burned patients

Yefta Moenadjat

UPK Luka Bakar FKUI/RSCM

Shires GT. Proceeding of the second NIH workshop on burn management. J Trauma 1979; 19(11 Suppl):862-3

Introduction
Burn is a devastating injury associated with high
mortality rate
Massive burn injury
>40% BSA involved
Problem encountered
Criteria of critical burn
Prognosis

Introduction
Massive burn injury
Surface area involved
In burn >40% BSA metabolic changes as the
body response to injury (Wolfe) referred to the
most severe.

Introduction
Massive burn injury
Problem encountered
Inhalation injury and burn shock (hypovolemic)
associated with lack of perfusion lead to cellular
injury:
Cellular physiology abnormality
Cellular injury (damage)
SIRS and MODS
Mortality
4

Introduction
Critical burn
Problem encountered
>20% BSA of 2nd and 3rd degree in adult >50 yo
and children of < 10 yo
>25% BSA of 2nd and 3rd degree in adult <50 yo
and children of > 10 yo
Burn of 3rd degree >10%

Inh

% TBSA

Mortality rate

(%)

<40

> 40

Inh

Shock

SIRS

Sepsis

ARDS

Total

1998

106

NA

73
68.9

33
31.1

NA

NA

NA

NA

NA

42
38.8

1999

87

NA

84
96.5

3
3.5

NA

NA

NA

NA

NA

34
39.08

2000

163

NA

126
77.4

37
22.6

NA

29
48

31
51

14
23

19
32

61
37.42

2001

175

11
6.3

52
29.7

123
70.3

13
20

16
24.6

29
44.62

6
9.25

34
52.3

65
37.14

2002

177

66
37.3

112
63.2

65
36.8

47
89

4
7.5

21
40

13
24.5

31
58.5

53
29.94

2003

172

61
35.4

109
63.4

63
36.6

27
39.8

21
31

32
47.1

16
23.5

18
26.47

68
39.53

2004

171

71
41.5

101
59.1

70
40.9

10
14.71

3
4.5

18
26.5

7
10.3

12
17.64

68
39

2005

136

31
22.7

91
67

45
33

9
22.5

4
10

19
47.5

2
5

9
22.5

40
39.41

Burn management: a review

In hospital Management
Fluid Resuscitation
Shock (ER admission: 85.70%):
Burn <40% BSA (66.10%), Burn>40% (33.90%)
Mean of Hypoxia 44.7%
Mean of Mortality 39.39%

Liolios A. Fluid resuscitation in sepsis and hemorrhagic shock: what do the data show?
Available in website: http://www.haoyisheng.com/html/hysh/sp-topic/ icu/zxyjjz/zxyjjz_bxzhcxz.htm
Moenadjat Y. Profil Luka Bakar RSCM 2005. Unpublished.
7

Burn management: a review

Results (Epi Info 6.0)
Shock has a significant correlation with splanchnic
hypoperfusion (p 0.06897527) and mortality (p
0.00400937).
Hypoxemia has no significant correlation with
splanchnic hypoperfusion (p 0.56564927).
Liver dysfunction has a significant correlation with
hypoxemia (p 0.006987898) and mortality (p
0.00400989)
Liolios A. Fluid resuscitation in sepsis and hemorrhagic shock: what do the data show?
Available in website: http://www.haoyisheng.com/html/hysh/sp-topic/ icu/zxyjjz/zxyjjz_bxzhcxz.htm
Moenadjat Y. Profil Luka Bakar RSCM 2005. Unpublished.
8

Burn management: a review

Results (Epi Info 6.0)
Incidence of hyperglycemia [>180-600mg/dL] 44%*),
hypoglycemia 5%, normal blood glucose level 50.9%
Hyperglicemia - shock (p 0.00958017)
Burn >40% BSA - hyperglycemia (p 0.00024781)
Burn <40% BSA - hyperglycemia (p 1.00000000)
Hyperglicemia - hypercarbia (p 0.47949309)
Hyperglycemia - inadequate resuscitation (p
0.12663046)
*) 4pts with Diabetes Mellitus
9

Burn management
Former paradigm
Wound: infection-sepsis
Shock syndrome
Macro-circulation
Vasoconstriction
Renal

Recent paradigm
Shock: lack of perfusion
Micro-circulation
Cellular injury
Macro-circulation
Hypoperfusion
Splanchnic
Wound: SIRS-MODS
Surviving Sepsis Campaign
2004, revised 2008
10

Massive Burn management

State of the Art

11

Initial Resuscitation
Basic Principles:
Definition of shock (lack of perfusion)
Restoration of perfusion is the goal of resuscitation, in
addition to shorten gut ischemic time
Monitoring of perfusion

12

Initial Resuscitation
Airway and respiratory management:
ER : Early intubation or cricothyroidotomy
ICU : tracheostomy as ET-tube is required >7days
Periodical suction
Inhalation therapy, nebulizer, humidification
Bronchial toilet or Broncho-Alveolar
Lavage (Bronchoscopy)
Early respiratory physiotherapy
Prone position preferable
13

The rationale
Intubation / cricothyroidotomy / tracheostomy
Inhalation injury
Massive burn
Requirement to organ support (ICU setting)

14

Initial Resuscitation
Shock management:
ER : aggressive-vigorous resuscitation
The use of high molecular weight colloid of
6-10% (130-200kDa)
Insertion of central venous catheter
Insertion of naso-gastric tube

15

Initial Resuscitation
Shock management:
ICU

: late resuscitation and fluid management

The use of high molecular weight colloid of
6-10% (130-200kDa)
Fluid management:
Fluid challenge, fluid restriction etc.
The use of hypertonic saline of 7.5%
The use of mannitol of 20%
The limited use of crystalloid but water
for injection (WI)
16

1
Leukocyte
events

Tethering

Rolling

Signaling

Adhesion

Migration

Endothelial

Blood flow

Endothelial activation

Bacteria

Selectins
Signaling molecules + Chemokines
Integrin 2

Selectins
Selectins ligand
Platelets

2 integrins
2 integrins ligand

Signaling molecules
Signaling molecules receptor
Spiess DB.. J Cardiovasc Pharm27 (Suppl.1):v-vii 1996

Electron microscopic exam

Injury

Inflammation

Hypovolemia:
Inadequate flow
ischemia

Fluid flux
[edema formation]
Instead leukocyte migration

Accumulation >>Lymphatic capacity

Hypoxia

Injury

Inflammation

Endothelial hyperpermeability

Leukocytes
migration

Fluid flux

Edema
formation

Hypovolemia
Inadequate flow

Ischemia
(hypoxia)
20

Hypoxia / hyperoxia: Oxidative Stress

Stressed ER
Damage cell membrane

Mitochondrial distress

Protective shield
To free radicals
[Phospholipid]
Hormone receptor sites

Dissociated
cytoskeletal

Nucleus depletion

cytosol

DNA damage
Low pH enzyme activity

Cellular injury
Early: abnormality of physiology
Anaerobe metabolism of the cell
Metabolic changes of macronutrient (CHO, lipid and
protein) in minimal to non-sufficient oxygen
Hyperglycemia, serum lactate , hyperlipidemia,
protein breakdown (hypoalbuminemia, urine urea
nitrogen excretion )
Basal Metabolic rate
Reversible

22

Cellular injury
Late: Cellular damage
Severe metabolic changes
Disruption of cellular membrane
Ionic compartmentalization: Na K Cl serum Ca
Ca ion
Cytoskeletal dissociation
Cellular integrity cellular communication
Cytoplasma pH
Enzymatic activity
Mitochondrial distress
No ATP production
Nucleus
Interrupted double helix system of DNA [apoptosis]
Irreversible
23

Active transportation across the membrane:

The role of receptors, protein and ATP

Local effect of Pro

Inflammatory response

Local effect of Anti

Inflammatory response

The Etiology

Pro Inflammatory response

- systemic -

Systemic Response
SIRS
CARS
MARS

Anti Inflammatory response

- systemic -

Apoptosis

Organ
dysfunction

Immune
suppression

Equal CARS-SIRS

SIRS Predominant

SIRS Predominant

CARS Dominant

Cardiovascular
compromised

Homeostasis

SIRS Predominant

CARS Compensatory Anti-inflammatory Response Syndrome

MARS Mixed Antagonistic Response Syndrome

E-Selectin
ICAM
VCAM

Cytokines
Cascade

Monocyte /
Macrophage
activation

IL1
IL8
TNF

Delayed
Inflammatory
Endothelial
Activation

TISSUE DAMAGE
Acute Renal Insufficiency
Respiratory Insufficiency
Myocardial Insufficiency
Neuropsychiatric Abnormalities

P-Selectin
Immediate
Inflammatory
Endothelial
Activation

!!
! Injury
!! !

Minutes

1 hr

2hrs

3hrs

4-8hrs

TIME elapsed

Apoptotic cells
Immune system

Non Immune system

Lymphoid tissue (incl. gut

associated lymphoid tissue,
GALT)
Thymotic apoptosis
Spleenocyte apoptosis
Monocytes apoptosis

Immunecompromize

Gut mucosa apoptosis

Endothelial apoptosis
Epithelial apoptosis
Other mucosa

Necrotic/lysis of tissue

Textbook of Critical care 5th ed. Philadelphia: Elsevier-Saunders. 2005 , 197-198

27

Macro-circulation Points of view

The Splanchnic hypoperfusion: gut failure
Ischemia of Gut mucosa
Abnormality of digestion
Diarrhea and enterocolitis
GI bleeding (was: stress ulcer)
Bacterial translocation*): septicemia
Ischemia of mucosal muscular lamina: ileus
*) environmental alteration:
Fasting
Antibiotics treatment particularly broad spectrum and
anaerobe
Antacid and H2 receptor antagonist

28

Macro=circulation Points of view

The Splanchnic hypoperfusion: gut failure
Gut failure
Inflammatory mediators

Hepatic failure
Respiratory failure
Myocardial failure
Hemostatic failure
Neurologic failure

Gut is motor
of MODS

MODS
Multi-system organ
dysfunction syndrome
29

E-Selectin
ICAM
VCAM

Cytokines
Cascade

Monocyte /
Macrophage
activation

IL1
IL8
TNF

Delayed
Inflammatory
Endothelial
Activation

TISSUE DAMAGE
Acute Renal Insufficiency
Respiratory Insufficiency
Myocardial Insufficiency
Neuropsychiatric Abnormalities

P-Selectin
Immediate
Inflammatory
Endothelial
Activation

!!
! Injury
!! !

Minutes

Gut failure

1 hr

2hrs

3hrs

4-8hrs

TIME elapsed

Endothelial junction disassembly

TJ
AJ

AC

GJ

TJ Tight junction
AJ Adherence junction
GJ Gap junction
AC Actin cytoskeleton

Interstitial edema found in injured site

and discovered in non-injured site as well
31

Superficial burn
Deep burn
Old concept

100

% Maximum Edema

75

50

25

0
-10

6 12

18

24

48

72

168

180

Time (hours)

Demling 2005: The graphic of edema in burn following fluid resuscitation

reflecting the capillary leakage

Endothelial hyperpermeability (interstitial edema)

Effect of histamine and serotonin (bradykinin) on endothelial cell
The exact mechanism is not clear yet: endothelial more
permeable to fluids
Commencing in 1-30 minutes and influencing as much as 8-72
hours following trauma

Endothelial junction disassembly

Hypoxic endothelial

TJ
AJ

AC

Proteolysis

GJ

TJ Tight junction
AJ Adherence junction
GJ Gap junction
AC Actin cytoskeleton

Junctions disassembly

Interstitial edema found in injured site

and discovered in non-injured site as well
34

Burn management
Former paradigm
Wound: infection-sepsis
Shock syndrome
Macro-circulation
Vasoconstriction
Renal

Recent paradigm
Shock: lack of perfusion
Microcirculation
Cellular injury
Macro-circulation
Hypoperfusion
Splanchnic
Wound: SIRS-MODS

35

Fluid Resuscitation
Restoration of cellular perfusion:
Adequate resuscitation is absolutely required to
provide and maintain circulation in restoring
perfusion
Sufficient volume replacement
High molecular weight colloid >130kDa
Method of administration (duration, etc)
Rapid administration <4hr following trauma
36

Goal of Resuscitation

Restoration of the perfusion

Hemodynamic stable referred
parameter

to

an

abstract

Endpoints of Resuscitations. Symposium in 36th Annual meeting of American Burn Association.

Vancouver, 2004.
37

Fluid Requirement
Crystalloids
The nature of crystalloids:
Posm volume substitute (-)
Not oxygen carrier
3 (4-5) times of fluid deficit
Interstitial space replacement:
More fluid massive edema
IS NOT SAFE & SECURE
Martin GS. Shock reuscitation and fluid management: what's the solution?
Available in website: http://www.medscape.com/viewarticle/459083 - 49k

Superficial burn
Deep burn

100

% Maximum Edema

75

50

25

0
-10

6 12

18

24

48

72

168

180

Time (hours)

Demling 2005: The graphic of edema formation in burn following fluid resuscitation
reflecting the capillary leakage

Fluid Resuscitation
Massive resuscitation:
Critical burn >40%
Inhalation injury
Hobson: 200 mL/kg in 12 hr
Ivy: 300 mL/kg in 24 hr
Maxwell: >10 L crystalloid or 10 unit PRC
Ivy: >0.25 L/kg crystalloid
Biffl: >6L crystalloid or 6 unit PRC in 6hr or base
deficit >10 mEq/L
Greenwalgh & Warden: IAH and ACS in burn patients

Fluid Resuscitation

Complication of fluid (crystalloids):

Iatrogenic resuscitation

Pulmonary edema
Third space syndrome:
2o abdominal compartment syndrome (ACS)
The fluid creep
Massive fluid (crystalloid) resuscitation is should be
avoided
41

Fluid Requirement
Colloids
The nature of crystalloids:
Osmotic pressure provider
Volume substitute and volume expander
Dilution effect
Not oxygen carrier
Hemostatic effects
Anti-inflammatory effect (integrin)
IS NOT SAFE & SECURE

The use of colloid is strictly hazardous as capillary

permeability increased
Capillary leaks: any solution < 100 kDa
Shock resuscitation using colloid of >130 kDa showed
its efficacy:
Sol 6% 1:1 to crystalloid iso-oncotic
Sol 10% 1-3:1 to crystalloid hyper-oncotic
Low volume resuscitation
Schierhout G, Roberts I. Fluid resuscitation with colloid or crystalloid solutions in critically ill patients:
a systematic review of randomised trials. BMJ. 1998;316:961964.
Choi PT, Yip G, Quinonez LG, Cook DJ. Crystalloids vs colloids in fluid resuscitation: a systematic
review. Crit Care Med. 1999;27:200210.

Goal of Resuscitation

Pitfalls

Striving for Ideal Numbers

It is quite possible to achieve ideal numbers (pulse less than
120, blood pressure more than 100, urine output 0.5 to 1
cc/kg/hr) in a young patient with a moderate-sized
uncomplicated burn.
Attempts at pushing fluids beyond reasonable amounts to
achieve "ideal numbers" in the massive burn (more than 60%
BSA), especially in the presence of inhalation injury or in the
elderly, will only accentuate edema-induced complications.
Adequate perfusion is not the same as "ideal numbers."
An intelligent treatment plan considering developing pulmonary
and chest wall edema-induced complications must be devised.
44

The monitoring
Clinical indicators

Laboratory assessment

GCS

PaO2, PCO2, HCO3, SvO2

Pulse & Respiration

Electrolytes Na Cl (anion gap) K

Ca, Mg, P

Gastric juice evaluation

Serum glucose,
Serum Lactate, Triglyceride,

Urine output production

Liver function test: SGOT/PT

Fluid balance

BUN

Pulmonary Artery Wedge

Pressure
Mean Arterial Pressure
Central Venous Pressure

Serum protein, N balance (Urine

Nitrogen Urea)
BMR
45

The early management

Early resuscitation in ER
ICU setting
To achieve metabolic requirement as metabolic
demand increased (BMR) following resuscitation (flow
phase), a strategy is absolutely required
The administration of high calories is hazardous
The BMR should be placed in the lowest level

46

The rationale
Intubation / cricothyroidotomy / tracheostomy
Inhalation injury
Massive burn
Requirement to organ support (ICU setting)
The victims is knocked-down under sedation with
ventilator support
Early enteral tube feeding

47

Surviving sepsis guidelines

Index
Initial Resuscitation
Diagnosis
Antibiotic therapy
Source Control
Fluid therapy
Vasopressors
Inotropic Therapy
Steroids
Recombinant Human
Activated Protein C
(rhAPC) [drotrecogin
alfa (activated)]

Blood Product Administration

Mechanical Ventilation
Sedation, Analgesia, and Neuromuscular
Blockade in Sepsis
Glucose Control
Renal Replacement
Bicarbonate Therapy
Deep Vein Thrombosis Prophylaxis
Stress Ulcer Prophylaxis
Limitation of Support

Dellinger, et. al. Crit Care Med 2004, 32: 858-873.

The outcomes
Burn management oriented to the new paradigm
Aggressive resuscitation: low volume resuscitation in a short
period
ICU setting
Surviving Sepsis Campaign, (SSC, Dellinger 2004, revised
2008)

Mortality remains high as much as 38%

Survival day increased significantly in critical burn
Prior to new concept : mean 1.9 days
After the new concept : range 12-31 days
49

Summary: Fluid resuscitation

Problem encountered burns referred to shock with
consequent cellular injury, but not to the wound vice
versa
In critical burn resuscitation, adequate volume
referred to replace the intravascular deficit and
delivered with ischemic time consideration
The use of massive crystalloids should be avoided;
limited to the volume of intravascular compartment
The use of high molecular weight colloid show the
efficacy
In non critical burn, Parkland method referred to be
sufficient
50