Patofisiologi luka bakar.

Djohansjah Marzoeki
 1. 38 C < TEMP< 36 C

OTHER 2. HR > 90

TRAUMA 3. RR > 20
Infection sepsis SIRS
4. 12000 < L < 4000
BURN BAND >10%

PANCREATITIS

2-10-03 djo 2
 SIRS MODS DEATH

RECOVER RECOVER WITH OR WITHOUT SEQUELE

MODS MORE THAN 2 ORGANS DYSFUNCTION.

Marshal: Lung
liver
blood
cardiac
kidney
cns
2-10-03 djo 3
 PAF
Pro inflamatory
Cytokines
IL 6
TNF α IL 2
IL 1 IL 8
macrophage
complement

Histamine
Vasoactive
serotonin
peptide

Bacterial product
Or other stimuli Septic shock
(C.Vales)
2-10-03 djo 4
Cytokine release is triggered by antigen binding, and directly
influence cardiovascular, haemodynamic and coagulation
mechanism.

Release a secondary mediator

-Arachidonic acid derived PGI 2, thromboxane, A2, PGE 2
and platelet activating factor

-vasoactive peptide, bradykinin, angiotensin, and vasoactive

interstinal peptide

-amine . Histamin and serotonin

-Componen derived product

2-10-03 djo 5
 Luka bakar
• Panas menyebabkan denaturasi protein,
Necrose jaringan, Mulai kulit yang paling
superfisial sampai jauh kedalam tergantung
tingginya panas dan lamanya kontak. Temp >
47 °C sudah menyebabkan kerusakan.
Nyeri pada 1st degree karena vasodilatasi–
prostaglandin. Pada 2nd degree superf.-- Nerve
ending yang exposed. Pada 2nd degree
profunda, kurang nyeri karena nerve damage.
Begitu pula 3rd degree.
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Hipermeabilitas Kapiler. Dengan demikian banyak cairan
akan akan keluar dari intravascular ke jar.interstiil. 0.5
meq /kg/% BSA (Baxter)

The function of the cell membrane as a semipermeable

barrier is lost in burned tissue.

Therefore, a functional plasma volume in burn tissue

can be restored only with restoration of the
extracellular space as well.

In nonburned tissue, edema occurs later than in burned

tissue because of hypoproteinemia.

Protein loss peaks at 8–12 hours post burn.

2-10-03 djo 7
 Edema

1. microvasc hiperpermeab.

2. impairment in cell membrane

3. increase osmotic pressure.

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Metabolic changes.

Immediate Ebb phase: decrease nutrient and O2 flow.

Release catecholamine from adrenal medulla and autonomic

nervus system – systemic vasoconstriction and
increased vascular resistance.

Glucagon and corticosteroid released --- mobilization

liver glycogen -- hiperglycaemia

Decreased O2 flow – hypoperfusion – anaerobe metabolism

-- acidosis

2-10-03 djo 9
 Myocardial depression is well described and is most
evident in deep burns of 40% TBSA.
.
Cardiac output returns to near normal , before
restoration of a normal plasma volume.

Clinically, cvp and pulm art wedge pressure remain

low even CO and perfusion are adquate.

Blood volume remains low for days in severe burns

unless aggressively corrected.

2-10-03 djo 10
 Choi et al BD24<-6 BD>-6

Vol24(L) 27.2  11.9 18.2  9.1

Parklan24(L) 19.8  6.7 12.66.5

UO24(ml/h) 96.1  52 95.3  53

OU (Urine output) tidak menjamin adequate global tissue perfusion

Begitu pula tradisional monitor BP, HR dan OU sudah normal pada 76% pada
yang mati dan 75% pada yang hidup, Jadi Tidak sensitive sebagai monitor dan
juga tidak reliable untuk guide terapi.(Schoemaker)
Salah satu gold standart circulatory monitor adalah dg invasive pulm art (PA)
bolloon-tip thermodilution catether.

Oleh karena pertimbangan resiko dan kemudahan maka monitoring memakai

Base Deficit akan lebih praktis untuk luka bakar.

2-10-03 djo 11
 Trauma Inhalasi

Deep or Full thickness burn of the face

Circum oral burn,
Singing of nasal hair
Edema of oral or pharynx mucosa
Progressive hoarseness,
Conjuctivitis
Blood Gas : CO poisoning

2-10-03 djo 12
 smoke inhalation

1. acute phase bronchospasm,

airway swelling,atelectasis,pulm edema
and tisue hipoxia
much depend on chemical contend of the smoke.

2.Delayed , ARDS beginning 2 - 5 days after injury.

combination smoke and burn more than 25% are synergistic

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 In smoke, toxic constituents are

CO
hydrogen chloride(HCl), hydrogen cyanide (HCn)
NO2, CO2
ACROLEIN, BENZINE.

Acrolein and CO MOST OFTEN in life threatening concentration,

The target of acrolien / aldehyde

is bronchial vessel to produce edema.

2-10-03 djo 14
 CO poisoning.

carbon monoxida has 210 -250 x greater affinity than O2 for Hb.
so displace O2 from Hb.

mild 10-20, headache, confuse,nausea

Moderate 20-40 ,©iritated, dizziness, fatig,

dimming vision,impaired judgment.

severe > 40 , hallucination, ataxia, convultion, coma

cherry red color only for blood in tube. patient is gray.

2-10-03 djo 15
 ARDS.

- 25% OF SIRS OF ANY AETIOLOGY DEVELOP ARDS

- ARDS PATIENTS MAY DEVELOP MODS

DESPITE RECEIVING ADEQUATE VENTILATORY
SUPPORT

2-10-03 djo 16
 ARDS

-pulm edema non cardiogenic,

-progressive hipoxemia

- normal left atrial and pulm capill wedge pressure.

-bilat interstitial infiltrates.

this delayed ARDS due to

hipoprot,
heperpermeability.
pneumonia related to decrease of immunity.

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 Scheme of Pulmonary Complications

Sirs Burn Injury Inhalation Injury

(second Hit)

Airway Damage CO poisoning

Shock

Complication
Pulmonary
edema

Acute Resp. Failure Refractory

.Pneumonia

Late Resp. Complic

Failure

ARDS Pneumonia
2-10-03 djo 18
Resp. Failure JOKucan (modified)
 Intubasi
• Coma
• Respiratoty depression
• Pharynngeal edema
• Progressive hoarseness
• Dyspneu
• Deep Circum oral burn and
circumferential burn of the neck

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 Red blood cell destruction in large burns may be up
to 40% of the circulating volume.
It is believed that 8% to 15% of the volume is
destroyed initially by the thermal insult, with eventual
loss of another 25% secondary to decreased survival
time.

Glucose intolerance may be seen in the early post-

burn period secondary to massive catecholamine
release.

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IMPAIRED RENAL FUNCTION

CONSEQUENCE OF METABOLIC AND CIRCULATORY

INJURY
PIGMEN RELEASE Hb and MyoHb.

Hypovolemic -- ADH , Aldosterone --- urine prod decrease.

HYPOVOLEMIC CONTINUES ---cellular damage---
decrease tubular function --- ARF.

TRANSIENT GROMERULAL LESION --- PROTEINURIA

ARF - HYPOVOLEMOIC SHOCK

- H b , MyoHb nephropathy.

Polyuric renal failure, occur in week 2 or 3 is due to

dysfunction of proximal tubule
2-10-03 djo 21
 Immune System

First component is the mechanical barrier between the

internal milieu of the body and the external environment
consisting of the skin as well as the mucosal barrier of
the respiratory tract and gut.

The second component is the nonspecific response. It

has vascular, cellular, and humoral.
Release of inflammatory mediators may lead to
microvascular stasis, sludging, and thrombosis, which can
further damage tissue already ischemic from thermal injury.
The cellular component is composed of circulating
phagocytic cells (e.g., polymorphonuclear leukocytes and
macrophages) and fixed phagocytic cells. exhibit
decreases in chemotaxis, phagocytosis, and intracellular
2-10-03 killing
djo power. 22
 (Immune System)

The third is the specific arm, composed of the

thymus-derived lymphocytes (T-cells) and bursa-
derived lymphocytes (B-cells) and their metabolic
products.

Because of these deleterious effects on the immune

system : To enhance the immune response by using
immunomodulation.

In experimental mice given DNA encoding

immunization for pseudomonas, it can induce strong
response to barterial antigent.
2-10-03
But in general, results still djo
disappointing. 23
 Cytokines
• Are small protein produced by many cells esp
white blood cells
• Similar to hormones with essential different, they
act locally as will as systematically. Their effect
outlive their appearance.
• Cytokine cascade is not a cascade in usual
sense rather it is more a complex network with
many inter relation ship and link
• Blocking one link may not affect other link

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•Cytokines are endogenous pyrogen may cause fever
in sepsis

•Nitric oxide, a potent vasodilator is release from

endothelium

•Intrinsic coagulation and complement system are

activated . DIC (Disseminated Intra vascular
Coagulation) can occur.

•One group cytokines involved in pathogenesi

of septic shock Is IL1, IL 6 and TNF

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•Endotoxin from gram neg bacteria stimulate release
of TNF and initiates cytokine cascade.
Gram pos bact also releaseTNF, but in less
understood mechanism.

•Administration of endotoxin, there is rapid rise

(peak 90 min) of TNF followed by IL1 and later IL6.
IL6 shows the greatest rise.

• Level of IL6 being directly related to mortality.

2-10-03 djo 26
 Body heat lost by mechanisn convection,
conduction and radiation.

- convection: by water is 25 x greater than air.

- conduction is contact with bed etc.

- radiaton is by surface blood flow.

Heat lost makes hypotermia

then cause more stress and more energy requirement.

2-10-03 djo 27
 Critically ill burn patients.

Decreased neutrophil phagocytosis and killing ability

( most important)
Decreased chemotaxis

Decreased macrophage activity

Decreased lymphocyte response

Decreased function of helper T cells.

Decreased gamma globulin

Decreased lymphocyte stimulator interleukin 2

2-10-03
and suppressor
djo
T cells. 28
 LOCAL FACTORS FOR INFECTION,
Loss of epithelium as physical barrier
Wound eschar is dead tissue, ideal medium for microbe
Dressing , warm, moist and dark optimal condition to grow.

Staphylococcus aureus, Klebsiella pneumoniae and

Pseudomonas aerugenosa are
The most common cause burn wound infection.

Surgical excision of dead tissue is very important and

Topical microbial agent is used as primary mean
in reducing burn wound infection.

Prophylactic systemic antibiotic is not used,

because of avascularity of eschar. Reserved for sepsis

2-10-03 djo 29
 TRANSLOCATION

Some persons offered that GI as the the motor of MODS.

Barrier : acids pH of the stomach, enzyme, mucin
production and immunoglobulin, prevent foreign
bacteria and toxin.

In bacterial / fungal translocation Notric Oxide

Synthase =NOS in enterocytes increase. Chen

2-10-03 djo 30
Vancomycin

Yg resisten thd vancomycyn . E.faecium. E. faecalis.

Kuman ini Sensitve thd tetracyclin dan chloramphenicol

Immunitas yang menurun dapat timbul herpetic infection: diberi Acylovir

(Zovirax, glaxo Wellcome)

Gram positive : staphyllococcen 97 %

Gram negative . Pseudomonas aeruginosa 61.3 %
Enterobacter cloacae 16 %
Klebsiella pneumoniae and E. coli 13.3 %

2-10-03 djo 31
 Energy expenditure

Ringan <20% sedang 21-40% berat >40%

MUDA <45 y 35 ±11 34 ± 10 43 ± 9 kgc/kg/d

Sedang 45-61 y 28 ±8 33 ± 10 34 ± 8

TUA >65 y 30 ± 10 31 ± 9 31 ± 10

Vaughn et al
2-10-03 djo 32
 Electrical
Myocardial injury
Cardiac stand still, ventricular fibrillation. Due to coronary
spasm, coronary Endarteritis or direct myocardial electrical
damage.

Parameter : Troponin I is most accurate (100%) diagnostics

Creatin kinase (CK0 Or Creatine Kinase isoform

(CK-MB) and
Troponin T are less accurate.. ( Diworth et al.)

CNS.
High Voltage often makes massive cereral, cerebellar and
brain stem destruction causing sudden death.
Unconsciousness is common. Convulsion and coma are rare.
2-10-03 Spinalcord
djo injury. 33
 Independent Mortality factors

• Area of burned > 40 %

• Inhalation injury

• Age > 60 yrs

2-10-03 djo 34