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Widjoseno GardjitoDepartment of Urology

Medical School Airlangga University - Dr. Soetomo HospitalSurabaya

Widjoseno GardjitoDepartment of Urology

Medical School Airlangga University - Dr. Soetomo HospitalSurabaya

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PATOFISIOLOGI TRAUMAPATOFISIOLOGI TRAUMA

Definisi :

TRAUMA adalah semua jenis kekerasan yang menimpatubuh sehingga terjadi kerusakan/gangguan pada strukturdan fungsi jaringan/organ tubuh yang terkena, bahkansecara sistemik dapat berdampak pada aspek fisiologis,kejiwaan dan kondisi sosial insan yang bersangkutan.

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TRAUMA pada JARINGAN/ORGANTRAUMA pada JARINGAN/ORGAN

KERUSAKAN PERDARAHAN NYERI

KERUSAKAN PERDARAHAN NYERI

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JENIS TRAUMAJENIS TRAUMA• Ledakan benda berkecepatan tinggi, benda

tajam (tusukan, irisan, sabetan), benda tumpul• Suhu tinggi/rendah

uap panas luka bakar frostbite (suhu dingin)

• Arus listrik tegangan tinggi• Bahan kimia• Radiasi, ionisasi• Gigitan, sengatan

• Ledakan benda berkecepatan tinggi, benda tajam (tusukan, irisan, sabetan), benda tumpul

• Suhu tinggi/rendah uap panas luka bakar frostbite (suhu dingin)

• Arus listrik tegangan tinggi• Bahan kimia• Radiasi, ionisasi• Gigitan, sengatan

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KERUSAKAN AKIBAT TRAUMAKERUSAKAN AKIBAT TRAUMABentuk :

Diastase (kerobekan), memar, erosi, lecet, hancur (crush injury), jaringan hilang

Lokalisasi :• Jaringan lunak + kulit : - luka terbuka

- luka tertutup

• Tulang / sendi : fraktura / dislokasi• Organ berongga (lambung, usus) : perforasi• Organ Padat (hati, limpaa,

ginjal, otak : ruptur, memar

Bentuk :Diastase (kerobekan), memar, erosi, lecet, hancur (crush injury), jaringan hilang

Lokalisasi :• Jaringan lunak + kulit : - luka terbuka

- luka tertutup

• Tulang / sendi : fraktura / dislokasi• Organ berongga (lambung, usus) : perforasi• Organ Padat (hati, limpaa,

ginjal, otak : ruptur, memar5 6

2

7 8

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AKIBAT TRAUMAAKIBAT TRAUMA

SEMBUH

CACAT

(anatomis + fisiologis + psikologis)

MENINGGAL

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TRAUMAHEBAT

RINGAN

TUNGGAL

GANDA

REAKSI TUBUH(Bagian dari proses Penyembuhan secara alami)

LOKAL

SISTEMIKTANDA + GEJALA

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INSULT HEBAT / BERAT

4 I - s

Injury – Infection – Inflammation – Ischemia

INSULT HEBAT / BERAT

4 I - s

Injury – Infection – Inflammation – Ischemia

S I R S(Systemic Inflammatory Response Syndrome)

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3

BacteremiaBacteremia

FungemiaFungemia

ParasitemiaParasitemia

ViremiaViremia

OtherOther

BURNSBURNS

PancreatitisPancreatitis

SIRSSIRSSEPSISSEPSISINFECTIONINFECTION

OtherOther

TraumaTrauma

Beal et al, JAMA, 1994;271;226-233Beal et al, JAMA, 1994;271;226-233 13

SIRS can be identified by the presence of two or more ofthe following manifestations :

1. A body temperature greater than 38C or less than 36C.2. Heart rate greater than 90 beats per minute3. Tachypnea (respiratory rate > 20 breaths per minute or

Pa CO2 < 32 mmHg4. White blood cell count greater than 12.0 x 109/L or less than

4.0 x 109/L or the presence of more than 10% immatureneutrophils (bands).

SIRS can be identified by the presence of two or more ofthe following manifestations :

1. A body temperature greater than 38C or less than 36C.2. Heart rate greater than 90 beats per minute3. Tachypnea (respiratory rate > 20 breaths per minute or

Pa CO2 < 32 mmHg4. White blood cell count greater than 12.0 x 109/L or less than

4.0 x 109/L or the presence of more than 10% immatureneutrophils (bands).

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SIRS and MODSSIRS and MODS

Inflammatory and organ dysfunction responses to injury. Normal response to an injury or insult may decrease after 3 to 5 days or be reactivated by a

complication. A continuous inflammatory response is seen with systemic inflammatory response syndrome (SIRS) and can eventually progress to organ

dysfunction (reprinted from 4).

Inflammatory and organ dysfunction responses to injury. Normal response to an injury or insult may decrease after 3 to 5 days or be reactivated by a

complication. A continuous inflammatory response is seen with systemic inflammatory response syndrome (SIRS) and can eventually progress to organ

dysfunction (reprinted from 4).

Beal et al, JAMA, 1994;271;226-233Beal et al, JAMA, 1994;271;226-23315 16

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SEPSIS :

SIRS plus a documented infectionsite (documented by positive culturefor organisms)

SEPSIS :

SIRS plus a documented infectionsite (documented by positive culturefor organisms)

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4

Severe Sepsis :Sepsis associated with organ dysfunction,hypoperfusion abnormalities, or hypotension.Hypoperfusion abnormalities include but are notlimited to :1. lactic acidosis,2. oliguria3. or an acute alteration in mental status

Severe Sepsis :Sepsis associated with organ dysfunction,hypoperfusion abnormalities, or hypotension.Hypoperfusion abnormalities include but are notlimited to :1. lactic acidosis,2. oliguria3. or an acute alteration in mental status

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Septic Shock :Sepsis-induced hypotension despite

fluid resuscitation PLUS hypoperfusion

abnormalities

Septic Shock :Sepsis-induced hypotension despite

fluid resuscitation PLUS hypoperfusion

abnormalities

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MODSOrgan Dysfunction associated with Severe Sepsis andSeptic Shock :

Lungs : early fall in arterial PaO2 , Acute Respiratory DistressSyndrome (ARDS):

Capillary-leakage into alveoli; tachypnea, hyperpneaKidney : (acute renal failure): oliguria, anuria, azotemia,proteinuria

Liver : elevated levels of serum bilirubin, alkalinephosphatase, cholestatic jaundice

Digestive tract : nausea, vomiting, diarrhea and ileus

MODSOrgan Dysfunction associated with Severe Sepsis andSeptic Shock :

Lungs : early fall in arterial PaO2 , Acute Respiratory DistressSyndrome (ARDS):

Capillary-leakage into alveoli; tachypnea, hyperpneaKidney : (acute renal failure): oliguria, anuria, azotemia,proteinuria

Liver : elevated levels of serum bilirubin, alkalinephosphatase, cholestatic jaundice

Digestive tract : nausea, vomiting, diarrhea and ileus21

MODSOrgan Dysfunction associated with Severe Sepsis andSeptic Shock :

Skin : ecthyma gangrenosum (think Pseudomonasaeruginosa in neutropenic patients), Petechia or purpura(think Neisseria meningitidis or Rickettsia rickettsia (ifevidence of tick bite)), Hemorrhage or bullous lesions inpatient who has eaten raw oysters (Vibrio vulnificus),generalized erythroderma (Toxic Shock Syndrome=Staphylococcus aureus or Streptococcus pyogenes)

Heart : cardiac output is initially normal or elevated,

Brain : confusion

MODSOrgan Dysfunction associated with Severe Sepsis andSeptic Shock :

Skin : ecthyma gangrenosum (think Pseudomonasaeruginosa in neutropenic patients), Petechia or purpura(think Neisseria meningitidis or Rickettsia rickettsia (ifevidence of tick bite)), Hemorrhage or bullous lesions inpatient who has eaten raw oysters (Vibrio vulnificus),generalized erythroderma (Toxic Shock Syndrome=Staphylococcus aureus or Streptococcus pyogenes)

Heart : cardiac output is initially normal or elevated,

Brain : confusion 22

OSLER’S DICTUM

Patients usually die of complications oftheir disease, rather than from thedisease itself

OSLER’S DICTUM

Patients usually die of complications oftheir disease, rather than from thedisease itself

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SIRS MODS MOF

BUKAN PENYAKITBUKAN SINDROMA

MERUPAKAN PERUBAHAN BERKELANJUTAN DARI FUNGSIORGAN YANG MENYANGKUT ASPEK FISIOLOGIS DAN METABOLIKSEBAGAI RESPONS TERHADAP SUATU “INSULT” YANG SERIUS.HUBUNGAN ANTARA RESPONS-RESPONS SERIAL DAN FUNGSIORGAN BERSIFAT DINAMIS DAN BERKELANJUTAN

SIRS MODS MOF

BUKAN PENYAKITBUKAN SINDROMA

MERUPAKAN PERUBAHAN BERKELANJUTAN DARI FUNGSIORGAN YANG MENYANGKUT ASPEK FISIOLOGIS DAN METABOLIKSEBAGAI RESPONS TERHADAP SUATU “INSULT” YANG SERIUS.HUBUNGAN ANTARA RESPONS-RESPONS SERIAL DAN FUNGSIORGAN BERSIFAT DINAMIS DAN BERKELANJUTAN

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SIRS Systemic Inflammatory Response Syndrome

MODS Multiple Organ Dysfunction Syndrome

MOF Multiple Organ Failure

MSOF Multiple-Sytem Organ Failure

ARDS Acute Respiratory Distress Syndrome

DIC Disseminated Intravascular Coagulation

SIRS Systemic Inflammatory Response Syndrome

MODS Multiple Organ Dysfunction Syndrome

MOF Multiple Organ Failure

MSOF Multiple-Sytem Organ Failure

ARDS Acute Respiratory Distress Syndrome

DIC Disseminated Intravascular Coagulation

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DEAR SIRS

WE ARE SORRY TO SAY

THAT

WE DON’T LIKE YOU

DEAR SIRS

WE ARE SORRY TO SAY

THAT

WE DON’T LIKE YOU

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Sir Isaac Newton :To every action is always an equal reaction

orThe mutual action of two bodies upon each otherare always equal, and directed to contrary parts

Philosophiae Naturalis principia Mathematica1687

Sir Isaac Newton :To every action is always an equal reaction

orThe mutual action of two bodies upon each otherare always equal, and directed to contrary parts

Philosophiae Naturalis principia Mathematica1687

Bone RC Crit. Cave Med, 1996;24:1125-1128Bone RC Crit. Cave Med, 1996;24:1125-1128

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BIOLOGICAL SYSTEMS, such as the

human body, are more complicated

than the simple physical systems Sir

Isaac was describing

BIOLOGICAL SYSTEMS, such as the

human body, are more complicated

than the simple physical systems Sir

Isaac was describing

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MACROPHAGE ( morfologi ) :

Sel besar

Inti bulat/indented

Golgi apparatus developed

Vakuol endositotik >

Lisosom + fagolisosom

Plasma membrane diselubungi mikrovili/ruffles

MACROPHAGE ( morfologi ) :

Sel besar

Inti bulat/indented

Golgi apparatus developed

Vakuol endositotik >

Lisosom + fagolisosom

Plasma membrane diselubungi mikrovili/ruffles

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MACROPHAGE ( fungsi ) :• Nonspecific phagocytosis/pinocytosis• Specific phagocytosis opsomized microorganisms

(Fc receptors + complement receptor)• Killing ingested microorganims• Digestion + presentation of antigens to T + B lymphocyte• Secretion of :

enzymes : lysozyme, collagenases, elastase, acid hydrogenases complements + coagulation factors some prostaglandins and leukotrienes several regulatory molecules (interferon, Interleukin-1)

MACROPHAGE ( fungsi ) :• Nonspecific phagocytosis/pinocytosis• Specific phagocytosis opsomized microorganisms

(Fc receptors + complement receptor)• Killing ingested microorganims• Digestion + presentation of antigens to T + B lymphocyte• Secretion of :

enzymes : lysozyme, collagenases, elastase, acid hydrogenases complements + coagulation factors some prostaglandins and leukotrienes several regulatory molecules (interferon, Interleukin-1)

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MACROPHAGE ( jenis ) : Histiosit Sel Kupffer Osteoclasts Microglial cells Synovial type A cells Interdigititating cells Langerhans cell Langerhans, epitheloid cells Multinucleated giant cells

MACROPHAGE ( jenis ) : Histiosit Sel Kupffer Osteoclasts Microglial cells Synovial type A cells Interdigititating cells Langerhans cell Langerhans, epitheloid cells Multinucleated giant cells

Inflamed tissues

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MACROPHAGE

Mononuclear phagocytes di dalam jaringan :Bone marrow : STEM CELL

monoblast

promocyte

Blood (40 hours): MONOCYT

Tissue : MACOPHAGES : - size- phagocytic activity- lysosomal enzym content

MACROPHAGE

Mononuclear phagocytes di dalam jaringan :Bone marrow : STEM CELL

monoblast

promocyte

Blood (40 hours): MONOCYT

Tissue : MACOPHAGES : - size- phagocytic activity- lysosomal enzym content

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MEDIATOR

Bahan yang dilepaskan oleh sel sebagai

hasil interaksi antigen-antibodi atau antigen

dengan sel limfosit yang sudah mengalami

sensitisasi

MEDIATOR

Bahan yang dilepaskan oleh sel sebagai

hasil interaksi antigen-antibodi atau antigen

dengan sel limfosit yang sudah mengalami

sensitisasi

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CYTOKINE (SITOKIN) : (cyto + kinesis)

Nonantibody protein released by one cell population(eg. Primed T-lymphocytes) on contact with specificantigen, which act as intercellular mediators, as in thegenerations of immune response.Examples include : Lymphokines, monokines

CYTOKINE (SITOKIN) : (cyto + kinesis)

Nonantibody protein released by one cell population(eg. Primed T-lymphocytes) on contact with specificantigen, which act as intercellular mediators, as in thegenerations of immune response.Examples include : Lymphokines, monokines

movement

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SITOKIN

Anggapan : sitokin ~ patologi

Sitokin : Melindungi tubuhtapi juga bisa SIRS

Mulai ditemukan antogonis sitokin

Mencegah SIRS ?

SITOKIN

Anggapan : sitokin ~ patologi

Sitokin : Melindungi tubuhtapi juga bisa SIRS

Mulai ditemukan antogonis sitokin

Mencegah SIRS ?36

7

Proses dilepasnya

Pro inflamatori sitokin + mediator-mediatormerupakan

Mekanisme pertahanan tubuh

melokalisir + menetralisir kuman yang menyerang membersihkan sel yang mati / rusak memulihkan jaringan

NAMUNAktivasi yang berkelanjutan / berlebihan justru

MERUGIKAN

Proses dilepasnya

Pro inflamatori sitokin + mediator-mediatormerupakan

Mekanisme pertahanan tubuh

melokalisir + menetralisir kuman yang menyerang membersihkan sel yang mati / rusak memulihkan jaringan

NAMUNAktivasi yang berkelanjutan / berlebihan justru

MERUGIKAN37

NORMAL STRESS RESPONSE

• PERUBAHAN KARDIOVASKULERtakikardi, kontraktilitas, curah jantung (CO), konsumsi oksigen

• RESPONSE SISTEM NEUROENDOKRINDilepasnya katekolamin, kortisol, ADH, Growth Hormone,glukagon, insulin.

• “CASCADE” : - koagulasi- komplemen- sistem fibrinolitik

Puncak reaksi : 3 – 5 harireda 7 – 10 hari

NORMAL STRESS RESPONSE

• PERUBAHAN KARDIOVASKULERtakikardi, kontraktilitas, curah jantung (CO), konsumsi oksigen

• RESPONSE SISTEM NEUROENDOKRINDilepasnya katekolamin, kortisol, ADH, Growth Hormone,glukagon, insulin.

• “CASCADE” : - koagulasi- komplemen- sistem fibrinolitik

Puncak reaksi : 3 – 5 harireda 7 – 10 hari

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PATOGENESIS SIRS

4 - I (Injury – Infection – Ischemia – Inflammation)

Stage ILokal : Sitokin

(penyembuhan luka – merangsang sel –mematikan organisme patogen)

PATOGENESIS SIRS

4 - I (Injury – Infection – Ischemia – Inflammation)

Stage ILokal : Sitokin

(penyembuhan luka – merangsang sel –mematikan organisme patogen)

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SITOKIN

• Circulating form (misal : IL-1 beta)(sistemik)

• Cell associated form (misal : IL-1 alpha)(lokal)

• Asumsi : lokal prekursor sistemikBila produksi sitokin lokal melampui batasambang tumpah sistemik

SITOKIN

• Circulating form (misal : IL-1 beta)(sistemik)

• Cell associated form (misal : IL-1 alpha)(lokal)

• Asumsi : lokal prekursor sistemikBila produksi sitokin lokal melampui batasambang tumpah sistemik

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Stage II

- Sejumlah kecil sitokin masuk sirkulasi

merekrut : makrofag, trombosit

growth factor

Terjadi reaksi akut :

terkendali tidak terkendali- pro inflamm, mediator - endogenous antogonist

(misal : IL-1 receptor antagonist) Stage III- antibodi

Luka sembuhInfeksi teratasiHomeostasis pulih

Stage II

- Sejumlah kecil sitokin masuk sirkulasi

merekrut : makrofag, trombosit

growth factor

Terjadi reaksi akut :

terkendali tidak terkendali- pro inflamm, mediator - endogenous antogonist

(misal : IL-1 receptor antagonist) Stage III- antibodi

Luka sembuhInfeksi teratasiHomeostasis pulih 41

Stage III

Homeostasis tak berhasil dipulihkan

Sitokin Destruktif( semula protektif )

Sirkulasi penuh dengan mediator inflamasi

Intergritas dinding kapiler rusak

Sitokin masuk organ / jaringan

M O D

Stage III

Homeostasis tak berhasil dipulihkan

Sitokin Destruktif( semula protektif )

Sirkulasi penuh dengan mediator inflamasi

Intergritas dinding kapiler rusak

Sitokin masuk organ / jaringan

M O D42

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Figure 1. First hit, second hit, and sustained hit that can occur with systemic inflammatory response syndrome (SIRS). ARDS, adult respiratory distress syndrome; MODS, multiple organ dysfunction syndrome.

Figure 1. First hit, second hit, and sustained hit that can occur with systemic inflammatory response syndrome (SIRS). ARDS, adult respiratory distress syndrome; MODS, multiple organ dysfunction syndrome. 43

Figure 2. Three stages of the systemic inflammatory response syndrome reactionFigure 2. Three stages of the systemic inflammatory response syndrome reaction

Crit Care Med 1996 Vol. 24, No. 1Crit Care Med 1996 Vol. 24, No. 1

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TRAUMA

may be considered to be an inflammatory disease

KADAR : - berbagai mediator- indikator respons inflamasi

pada trauma berat.

“MARKERS” inflamasi dapat digunakan :- menilai beratnya trauma- meramalkan prognosis (“outcome”)

TRAUMA

may be considered to be an inflammatory disease

KADAR : - berbagai mediator- indikator respons inflamasi

pada trauma berat.

“MARKERS” inflamasi dapat digunakan :- menilai beratnya trauma- meramalkan prognosis (“outcome”)

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TRAUMA BERAT dan KEMATIANPOLA DISTRIBUSI “TRI MODAL”

• Kematian Sesaat (Immediate Deaths)Segera setelah trauma

• Kematian Dini (Early Deaths)Beberapa jam setelah trauma

• Kematian Lambat (Late Deaths)Berhari-hari hingga berminggu-minggusetelah trauma

TRAUMA BERAT dan KEMATIANPOLA DISTRIBUSI “TRI MODAL”

• Kematian Sesaat (Immediate Deaths)Segera setelah trauma

• Kematian Dini (Early Deaths)Beberapa jam setelah trauma

• Kematian Lambat (Late Deaths)Berhari-hari hingga berminggu-minggusetelah trauma

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TRAUMA BERAT dan KEMATIANPOLA SITRIBUSI “TRI MODAL”

1

Immediate

2

Early

3

Late

TRAUMA BERAT 47

JALAN TOL menuju kematian

Trauma multipel Sumber infeksi Immunocompromised

SistemPenunjang berbagai organ

(ICU)

SIRS

MODSARDS, DIC, ARF, KARDIOMIOPATI

Meninggal

JALAN TOL menuju kematian

Trauma multipel Sumber infeksi Immunocompromised

SistemPenunjang berbagai organ

(ICU)

SIRS

MODSARDS, DIC, ARF, KARDIOMIOPATI

Meninggal48

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CerraJAMA Vol. 271, 1994 49

1991 Concensus Conference

Dirintis konsistensi

Memperhatikan aspek-aspek :

Klinik (bedside)

Laboratorium

Literatur terkait

1991 Concensus Conference

Dirintis konsistensi

Memperhatikan aspek-aspek :

Klinik (bedside)

Laboratorium

Literatur terkait

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SIRS MODS/MOFMORTALITAS TINGGI

KEGAGALAN 1 ORGAN : 30% - 40%2 ORGAN : 60%3 ORGAN : > 90%

USIA > 65 TAHUN : RISIKO 20%

Beal & Cerra

PREVENTION IS THE BEST TREATMENT(prevention is the only good answer)

Baue

SIRS MODS/MOFMORTALITAS TINGGI

KEGAGALAN 1 ORGAN : 30% - 40%2 ORGAN : 60%3 ORGAN : > 90%

USIA > 65 TAHUN : RISIKO 20%

Beal & Cerra

PREVENTION IS THE BEST TREATMENT(prevention is the only good answer)

Baue51

Prognostic test

yang meramalkan terjadinya “organ failure” (OF)

tidak bermanfaat

bila gambaran klinik OF sudah manifes

Prognostic test

yang meramalkan terjadinya “organ failure” (OF)

tidak bermanfaat

bila gambaran klinik OF sudah manifes

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