《外科学》创伤与战伤(留学生)

2. Neuroendocrine response
1. Sympathetic / adrenocortex system
2. Hypothalamus / pituitarቤተ መጻሕፍቲ ባይዱ system
3. Renin-angiotension system
1.SNS - Neurohormonal response Stimulated by sympathetic/adrenocortex system (catecholamine )
Schematic representation of the interactions between the stress and the immune system. LC/NE: locus ceruleus/norepinephrinesympathetic system, SPGN: sympathetic postgaglionic neurons, CRH: corticotropin-releasing hormone, AVP: arginine vasopressin, ACTH: corticotrophin, PAF: platelet activating factor, NE/E: norepinephrine/epinephrine,: Th1: T-helper lymphocyte 1, Th2: Thelper lymphocyte 2. Stimulation is represented by solid green lines and inhibition by dashed red lines.
4.SNS - Hormonal: Renin-angiotension system
Decrease renal perfusion Releases renin angiotension I angiotension II potent vasoconstriction & releases aldosterone adrenal cortex sodium & water retention
Opened injury
Opened fracture
Chapter 2 Pathophysiology of trauma
Trauma can trigger a cascade of pathological response which includes inflammatory/immune reaction, neuroendocrine response and functional change of vital organ.
Chapter 3 Repair of injured tissue
Trauma directly stimulates local tissue and triggers a cascade of tissue repair process which includes: A. Inflammation. B. Proliferation and differentiation of many types of cell—granulation formation. C. Wounds healing and car formation.
The concept of inflammation
Inflammation can be defined as a localized protective tissue response elicited by injury or destruction of tissues, which serves to destroy, dilute or wall off both the injurious agent and the injured tissues.
3. Wound causing factors
Cold weapon wounds （冷兵器伤）: Knife Firearm wounds （火器伤）: gun Burns（烧伤）: High temperature Cold injury（冷伤）: Low temperature Blast injury （冲击伤）: 爆震伤 Chemical injury （化学伤）: chemical weapon Radiation injury （放射性损伤）: Electromagnetic radiation，Particulate radiation
1.The inflammatory/immune reaction
1. Inflammatory: local tissue inflammatory
2. Immunosuppressing: glucocorticoids inhibit inmmunocytes function.
3. Immunomodulating : Systemic inflammatory response syndrome(SIRS) Compensatory anti-inflammatory response syndrome(CARS)
DEFINITION
Trauma is the injury caused by mechanical or chemical factors, which leads to tissue integrity damaged and loss of function.
Chapter 1 Classification of the Trauma
Trauma And War Injury
Dr. Zhendong Liu The Third Xiangya Hospital
Risk factors
Traffic accident, industrial injury, Natural disaster, war injury and so on.
2. For injured place and organ
Craniocerebral injury （颅脑伤） : Chest injury （胸部伤）: hematopneumothrax Abdomen injury （腹部伤）: burst spleen,
perforated bowel Limbs （四肢伤）: fracture, dislocation Spinal injury （脊柱伤）: fracture, paraplegia
Increased heart rate Increased contractility Vasoconstriction (SVR-Afterload) Increased Preload
2.SNS - Hormonal: Adrenal Cortex
Anterior pituitary releases adrenocorticotropic hormone (ACTH).
Stimulates adrenal Cx to release glucorticoids.
Blood sugar increases to meet increased metabolic needs.
3.SNS - Hormonal: Antidiuretic Hormone
Osmoreceptors in hypothalamus stimulated ADH released by Posterior pituitary gland Vasopressor effect to increase BP Acts on renal tubules to retain water
1. For the integrity of skin
1). The opened injury :
Abrasion（摖伤） Laceration（撕裂伤） Incised wounds or cut wounds （切伤/
砍伤） Puncture wounds （刺伤）
2). The blunt injury : Contusion （挫伤） Crush injury（挤压伤） Sprain（扭伤） Concussion （震荡伤） Luxation and semiluxation （关节脱位/半脱位） Closed bone fracture （闭合性骨折） Closed internal injury （闭合性内脏伤）
Industrial injury
Natural disaster
Explosion
CONTENT
1. The concept of trauma. 2. The classification of trauma. 3. The pathphysiology of trauma. 4. The diagnosis of trauma. 5. The treatment of trauma.
Immunomodulating
Both glucocorticoids and catecholamines directly inhibit the production of type 1 cytokines, such as IL-12, IL-2, TNF-α and INF-γ, that enhance cellular immunity and T-helper 1 (Th1) formation and conversely favor the production of type 2 cytokines, such as IL-10, IL-4, IL-13, that induce humoral immunity and T-helper 2 (Th2) formation. Thus, during an immune challenge, stress causes an adaptive Th1 to Th2 shift in order to protect the tissues from the potentially destructive actions of the pro-inflammatory type 1 cytokines and other products of activated macrophages. The homeostatic role of stress-induced Th2 shift against overshooting of cellular immunity often complicates pathologic conditions where, either cellular immunity is beneficial (e.g. carcinogenesis, infections) or humoral immunity is deleterious (e.g. allergy, autoimmune diseases).