PATOFISIOLOGI TRAUMA

dr. Sri Wulandari, MSc

RESPON SISTEMIK TRAUMA

Trauma

Kardiovaskular
Neuroendokrin & Metabolik
Imunologi

Homeostasis
 Respon Kardiovaskular
Aktivasi simpatis,
Baroresepto
MAP↓
Aktivasi simpatis,
Blood
MAP↓
Blood
r
loss
Baroresepto
inhibisi
loss
inhibisi
parasimpatis
r
parasimpatis

H
R

↑
,
T
P
R
↑
Regulasi Saraf pada Sirkulasi
Baroreseptor
 Respon Kardiovaskular...
• Mekanisme peningkatan MAP melalui:
– Baroreceptor, Kemoreceptor, Low pressure receptor
– CNS ischemic response
– Agen vasokontriksi :
• Angiotensin II
• Vasopressin (ADH)
• Ephinephrin & Norephinephrin
• Endhotelin
– Peningkatan volume darah (absorbsi cairan dari GIT &
intertisial, retensi air & garam dari ginjal, rasa haus)
• Aktivasi simpatis →
– aliran darah ↑ ke jantung dan otak
– aliran darah ↓ ke ginjal dan GIT
Renin-Angiotensin-Aldosteron
 Respon Neuro Endokrin &
Metabolik

Lain-lain
Pankreas
Kortisol ↑ Gluk
Pain ACTH ↑ Aldosteron ↑ ago
n↑
Fear CRH ↑ ADH ↑ Epinephrin ↑ Insu
Norepinephri
Stress GH ↑ n↑
lin
↓
Ginjal
Reni
n↑
 Respon Endokrin terhadap Trauma
Gland Hormone Major Function
Hypothalamus CRH Causes release of adrenocorticotropic hormone
GHRH Causes release of growth hormone
Anterior pituitary GH Stimulates protein synthesis and overall growth of most cells and
tissues
ACTH Stimulates synthesis and secretion of adrenocortical hormones
(cortisol, androgens, and aldosterone)
Posterior pituitary ADH Increases water reabsorption by the kidneys and causes
vasoconstriction and increased blood pressure
Adrenal cortex Cortisol Has multiple metabolic functions for controlling metabolism of
proteins, carbohydrates, and fats; also has anti-inflammatory effects
Aldosterone Increases renal sodium reabsorption, potassium secretion, and
hydrogen ion secretion
Adrenal medulla Norepinephrine, Same effects as sympathetic stimulation
epinephrine
Pancreas Glucagon (α Increases synthesis and release of glucose from the liver into the
cells) body fluids
Kidney Renin Catalyzes conversion of angiotensinogen to angiotensin I (acts as an
enzyme)
 Respon Neuro Endokrin &
Metabolik...
• Metabolisme post trauma :
– Ebb/acut phase :
• Metabolisme ↓
– Flow phase
• Hipermetabolik & katabolik → host defence
– Karbohidrat : glikogenolisis, glukoneogenesis → hiperglikemia
– Lemak : lipolisis → free fatty acid plasma ↑
– Protein : degradasi protein di otot → asam amino plasma ↑
• Anabolik
Respon Imunologi
 Respon Imunologi...
• Trauma → respon inflamasi (rubor, tumor, kalor, dolor, functio
laesa)
• Mediator :
– Histamin
– Leukotrien
– Sitokin : TNF-α, IL-1, IL-6, IL-8, IL-10
– HGMB-1
• Seluler :
– Netrofil
– Monosit
– Sel NK
 Respon Imunologi...
• Pelepasan histamin, bradikinin, enzim proteolitik,
protaglandin & leukotrien dari sel yang rusak
• Peningkatan vaskularisasi di area trauma yang
dipicu oleh produk dari sel yang rusak → eritema
• Kebocoran sejumlah besar plasma di area trauma
akibat peningkatan permeabilitas kapiler diikuti
clotting → nonpitting edema
• Infiltrasi lekosit di area trauma
• Pertumbuhan jaringan fibrosa →healing process.
• Fase Inflamasi
– Histamin, Leukotrien,dll
– Trombosit, netrofil, monosit,dll
– Koagulasi
• Fase Proliferasi
– Reepithelisasi
– Jaringan granulasi
– Angiogenesis
– Sintesis kolagen
• Fase Maturasi
– Realignment dan remodelling
jar parut
– Breakdown dan sintesis kolagen
– Wound contraction
Summary
 Referensi
• Guyton A.C. and Hall J.E. 2016. Textbook of Medical Physiology 13th ed.
Elsevier. Philadelphia
• Kirkman E and Watts S. 2014. Haemodynamic changes in trauma. British
Journal of Anaesthesia 113 (2): 266–75
• Brøchner A.C., and Toft P. 2009. Pathophysiology of the systemic
inflammatory response after major accidental trauma. Scandinavian
Journal of Trauma, Resuscitation and Emergency Medicine 2009, 17:43
• Keel M. & Trentz O. 2005. Pathophysiology of polytrauma. Int. J. Care
Injured 36, 691—709
 .......... Terima
kasih