PATOFISIOLOGI TRAUMA

Definisi :
TRAUMA adalah semua jenis kekerasan yang menimpa tubuh sehingga terjadi kerusakan/gangguan pada struktur dan fungsi jaringan/organ tubuh yang terkena, bahkan Widjoseno Gardjito
Department of Urology Medical School Airlangga University - Dr. Soetomo Hospital Surabaya
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secara sistemik dapat berdampak pada aspek fisiologis, kejiwaan dan kondisi sosial insan yang bersangkutan.
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JENIS TRAUMA
TRAUMA pada JARINGAN/ORGAN
• Ledakan benda berkecepatan tinggi, benda tajam (tusukan, irisan, sabetan), benda tumpul • Suhu tinggi/rendah  uap panas  luka bakar

 KERUSAKAN  PERDARAHAN  NYERI
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 frostbite (suhu dingin) • Arus listrik tegangan tinggi • Bahan kimia • Radiasi, ionisasi • Gigitan, sengatan
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KERUSAKAN AKIBAT TRAUMA
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, memar
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7 8 AKIBAT TRAUMA  SEMBUH  CACAT (anatomis + fisiologis + psikologis)  MENINGGAL 9 10 INSULT HEBAT TUNGGAL GANDA HEBAT / BERAT 4 I-s TRAUMA RINGAN LOKAL Injury – Infection – Inflammation – Ischemia TANDA + GEJALA REAKSI TUBUH (Bagian dari proses Penyembuhan secara alami) SISTEMIK  SIRS (Systemic Inflammatory Response Syndrome) 11 12 2 .

0 x 109/L or the presence of more than 10% immature neutrophils (bands).271.226-233 15 16 SEPSIS : SIRS plus a documented infection site (documented by positive culture for organisms) 17 18 3 . Beal et al. Normal response to an injury or insult may decrease after 3 to 5 days or be reactivated by a complication.0 x 109/L or less than 4. White blood cell count greater than 12. JAMA. 1994. A body temperature greater than 38C or less than 36C. JAMA. BURNS Pancreatitis Beal et al. Tachypnea (respiratory rate > 20 breaths per minute or Fungemia INFECTION Parasitemia SEPSIS Viremia Other SIRS Trauma Pa CO2 < 32 mmHg 4.226-233 13 14 SIRS and MODS Inflammatory and organ dysfunction responses to injury. A continuous inflammatory response is seen with systemic inflammatory response syndrome (SIRS) and can eventually progress to organ dysfunction (reprinted from 4).271. 1994.Bacteremia SIRS can be identified by the presence of two or more of the following manifestations : Other 1. Heart rate greater than 90 beats per minute 3. 2.

proteinuria Liver : elevated levels of serum phosphatase. rather than from the disease itself SIRS MODS MOF BUKAN PENYAKIT BUKAN SINDROMA MERUPAKAN PERUBAHAN BERKELANJUTAN DARI FUNGSI ORGAN YANG MENYANGKUT ASPEK FISIOLOGIS DAN METABOLIK SEBAGAI RESPONS TERHADAP SUATU “INSULT” YANG SERIUS.Severe Sepsis : Sepsis associated with organ dysfunction. azotemia. cholestatic jaundice bilirubin. diarrhea and ileus Brain : confusion 22 OSLER’S DICTUM Patients usually die of complications of their disease. hypoperfusion abnormalities. 2. oliguria 3. or hypotension. vomiting. tachypnea. lactic acidosis. HUBUNGAN ANTARA RESPONS-RESPONS SERIAL DAN FUNGSI ORGAN BERSIFAT DINAMIS DAN BERKELANJUTAN 23 24 4 . 21 Digestive tract : nausea. Acute Respiratory Distress Syndrome (ARDS): Capillary-leakage into alveoli. alkaline MODS Organ Dysfunction associated with Severe Sepsis and Septic Shock : Skin : ecthyma gangrenosum (think Pseudomonas aeruginosa in neutropenic patients). hyperpnea Kidney : (acute renal failure): oliguria. Petechia or purpura (think Neisseria meningitidis or Rickettsia rickettsia (if evidence of tick bite)). anuria. Hypoperfusion abnormalities include but are not limited to : 1. generalized erythroderma (Toxic Shock Syndrome= Staphylococcus aureus or Streptococcus pyogenes) Heart : cardiac output is initially normal or elevated. Hemorrhage or bullous lesions in patient who has eaten raw oysters (Vibrio vulnificus). or an acute alteration in mental status 19 Septic Shock : Sepsis-induced hypotension despite fluid resuscitation PLUS hypoperfusion abnormalities 20 MODS Organ Dysfunction associated with Severe Sepsis and Septic Shock : Lungs : early fall in arterial PaO2 .

and directed to contrary parts Philosophiae Naturalis principia Mathematica1687 Bone RC Crit.24:1125-1128 27 28 BIOLOGICAL SYSTEMS. 1996. such as the human body. Cave Med. are more complicated than the simple physical systems Sir Isaac was describing MACROPHAGE ( morfologi ) :       Sel besar Inti bulat/indented Golgi apparatus developed Vakuol endositotik > Lisosom + fagolisosom Plasma membrane diselubungi mikrovili/ruffles 29 30 5 .SIRS MODS MOF MSOF ARDS DIC Systemic Inflammatory Response Syndrome Multiple Organ Dysfunction Syndrome DEAR SIRS WE ARE SORRY TO SAY Multiple Organ Failure Multiple-Sytem Organ Failure Acute Respiratory Distress Syndrome Disseminated Intravascular Coagulation THAT WE DON’T LIKE YOU 25 26 Sir Isaac Newton : To every action is always an equal reaction or The mutual action of two bodies upon each other are always equal.

which act as intercellular mediators. Examples include : Lymphokines.size . epitheloid cells  Multinucleated giant cells 31 enzymes : lysozyme.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 :     MACROPHAGE ( jenis ) :  Histiosit  Sel Kupffer  Osteoclasts  Microglial cells  Synovial type A cells  Interdigititating cells  Langerhans cell  Langerhans. Primed T-lymphocytes) on contact with specific antigen. as in the generations of immune response. acid hydrogenases complements + coagulation factors some prostaglandins and leukotrienes several regulatory molecules (interferon.phagocytic activity . Interleukin-1) Inflamed tissues 32 MACROPHAGE MEDIATOR Mononuclear phagocytes di dalam jaringan : Bone marrow : STEM CELL Bahan yang dilepaskan oleh sel sebagai monoblast promocyte Blood (40 hours): MONOCYT Tissue : MACOPHAGES : . elastase. monokines Sitokin : sitokin ~ patologi : Melindungi tubuh tapi juga bisa SIRS Mulai ditemukan antogonis sitokin Mencegah SIRS ? 35 36 6 . collagenases.lysosomal enzym content 33 34 hasil interaksi antigen-antibodi atau antigen dengan sel limfosit yang sudah mengalami sensitisasi SITOKIN CYTOKINE (SITOKIN) : (cyto + kinesis) movement Anggapan Nonantibody protein released by one cell population (eg.

insulin.koagulasi . kontraktilitas. 37 Puncak reaksi reda 38 PATOGENESIS SIRS 4 .Proses dilepasnya Pro inflamatori sitokin + mediator-mediator merupakan Mekanisme pertahanan tubuh  melokalisir + menetralisir kuman yang menyerang  membersihkan sel yang mati / rusak  memulihkan jaringan NAMUN Aktivasi yang berkelanjutan / berlebihan justru MERUGIKAN NORMAL STRESS RESPONSE • PERUBAHAN KARDIOVASKULER takikardi. ADH. trombosit growth factor Terjadi reaksi akut : Stage III Homeostasis tak berhasil dipulihkan Sitokin ( semula protektif ) Destruktif Sirkulasi penuh dengan mediator inflamasi terkendali . glukagon.antibodi  Luka sembuh Infeksi teratasi Homeostasis pulih tidak terkendali Stage III Intergritas dinding kapiler rusak Sitokin masuk organ / jaringan MOD 41 42 7 . konsumsi oksigen • RESPONSE SISTEM NEUROENDOKRIN Dilepasnya katekolamin.endogenous antogonist  (misal : IL-1 receptor antagonist) . curah jantung (CO).sistem fibrinolitik : 3 – 5 hari 7 – 10 hari Growth Hormone. • “CASCADE” : .pro inflamm. mediator  .Sejumlah kecil sitokin masuk sirkulasi merekrut : makrofag.I (Injury – Infection – Ischemia – Inflammation) Stage I Lokal SITOKIN • Circulating form (misal : IL-1 beta) (sistemik) • Cell associated form (misal : IL-1 alpha) (lokal) – • Asumsi : lokal prekursor sistemik Bila produksi sitokin lokal melampui batas ambang tumpah sistemik 40 : Sitokin  sel (penyembuhan luka – merangsang mematikan organisme patogen) 39 Stage II .komplemen . kortisol.

ARF. and sustained hit that can occur with systemic inflammatory response syndrome (SIRS). No. “MARKERS” inflamasi dapat digunakan : . multiple organ dysfunction syndrome. Three stages of the systemic inflammatory response syndrome reaction Crit Care Med 1996 Vol.Figure 1. DIC. 1 44 TRAUMA may be considered to be an inflammatory disease KADAR : .indikator respons inflamasi pada trauma berat.meramalkan prognosis (“outcome”) 45 TRAUMA BERAT dan KEMATIAN POLA 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-minggu setelah trauma 46 TRAUMA BERAT dan KEMATIAN POLA SITRIBUSI “TRI MODAL” JALAN TOL menuju kematian  Trauma multipel  Sumber infeksi  Immunocompromised 1 2 3 Sistem Penunjang berbagai organ (ICU) SIRS Immediate Early Late MODS ARDS. second hit. MODS. adult respiratory distress syndrome. 24. First hit. ARDS.menilai beratnya trauma . 43 Figure 2.berbagai mediator . KARDIOMIOPATI Meninggal 47 48 TRAUMA BERAT 8 .

271.40% : 60% : > 90% 20% Beal & Cerra yang meramalkan terjadinya “organ failure” (OF) tidak bermanfaat bila gambaran klinik OF sudah manifes Baue 51 52 : RISIKO PREVENTION IS THE BEST TREATMENT (prevention is the only good answer) 53 9 . 1994 49 50 SIRS MORTALITAS TINGGI KEGAGALAN 1 ORGAN 2 ORGAN 3 ORGAN USIA > 65 TAHUN MODS/MOF Prognostic test : 30% .1991 Concensus Conference  Dirintis konsistensi  Memperhatikan aspek-aspek :  Klinik (bedside)  Laboratorium  Literatur terkait Cerra JAMA Vol.

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