Patofisiologi luka bakar.

Djohansjah Marzoeki

2-10-03 djo 2

SIRSInfection sepsisTRAUMA

BURN

PANCREATITIS

OTHER

1. 38 C < TEMP< 36 C

2. HR > 90

3. RR > 20

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 cns

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Bacterial productOr other stimuli

Pro inflamatoryCytokines

TNF αIL 1

complement

Vasoactive peptide

Histamineserotonin

IL 6IL 2IL 8

PAF

Septic shock(C.Vales)

macrophage

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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

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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.

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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<-6 BD>-6

Vol24(L) 27.2 11.9 18.2 9.1

Parklan24(L) 19.8 6.7 12.66.5 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.

 

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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

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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 are

COhydrogen 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.

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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 tohipoprot,

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. ComplicFailure

ARDS Pneumonia

Resp. Failure JOKucan (modified)

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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 INJURYPIGMEN 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

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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.

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(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.

But in general, results still disappointing.

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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.

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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.

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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.

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LOCAL FACTORS FOR INFECTION, Loss of epithelium as physical barrier

Wound eschar is dead tissue, ideal medium for microbeDressing , 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

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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

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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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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

Energy expenditure

Vaughn et al

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ElectricalMyocardial injury

Cardiac stand still, ventricular fibrillation. Due to coronaryspasm, 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.

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Independent Mortality factors

• Area of burned > 40 %

• Inhalation injury

• Age > 60 yrs