Patofisiologi luka bakar.Djohansjah Marzoeki
1. 38 C < TEMP< 36 C OTHER TRAUMAInfection sepsis
2. HR > 90 3. RR > 20
SIRS BURNPANCREATITIS
4. 12000 < L < 4000 BAND >10%
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SIRS
MODS
DEATH
RECOVER
RECOVER WITH OR WITHOUT SEQUELE
MODS MORE THAN 2 ORGANS DYSFUNCTION. Marshal: Lung liver blood
cardiac kidney cns2-10-03 djo 3
PAF Pro inflamatory Cytokines TNF IL 1 macrophage complement
Vasoactive peptide IL 6 IL 2 IL 8
Histamine serotonin
Bacterial product Or other stimuli2-10-03 djo
Septic shock
(C.Vales)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
product2-10-03 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.2-10-03 djo 6
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 812 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
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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.
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Choi et al
BD24-618.2 9.1 12.66.5 95.3 53
Vol24(L) Parklan24(L) UO24(ml/h)
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 InhalasiDeep 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
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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 areCO 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.
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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
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ARDS.
- 25% OF SIRS OF ANY AETIOLOGY DEVELOP ARDS
- ARDS PATIENTS MAY DEVELOP MODS DESPITE RECEIVING ADEQUATE
VENTILATORY SUPPORT
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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.2-10-03 djo 17
Scheme of Pulmonary Complications
Sirs(second Hit)
Burn InjuryAirway Damage
Inhalation Injury
CO poisoning
Shock
Complication Pulmonary edema Acute Resp. Failure Refractory
.Pneumonia
Late Resp. Complic Failure ARDS2-10-03
Pneumoniadjo 18JOKucan (modified)
Resp. Failure
Intubasi Coma Respiratoty depression Pharynngeal edema
Progressive hoarseness Dyspneu Deep Circum oral burn and
circumferential burn of the neckdjo 19
2-10-03
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 postburn 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 tubule2-10-03 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 killing power. 2-10-03
djo 22
(Immune System) The third is the specific arm, composed of the
thymus-derived lymphocytes (T-cells) and bursaderived 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 link2-10-03 djo 24
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
TNF2-10-03 djo 25
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 and suppressor T
cells. djo
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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 sepsis2-10-03 djo 29
TRANSLOCATIONSome 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
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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 %
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Energy expenditure
Ringan 65 y
30 10
31 9
31 10
Vaughn et al2-10-03 djo 32
ElectricalMyocardial 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. Spinalcord injury. 2-10-03
djo 33
Independent Mortality factors Area of burned > 40 %
Inhalation injury Age > 60 yrs
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