TRAUMA
Bao Heng Department of Orthopedic Surgery The First Affiliated Hospital
Introduction Trauma is a severe physical injury resulting from dissipation of energy to and within the victim, caused by a penetrating or blunt mechanism Trauma can be defined in terms of bodily injury severe enough to pose a threat to life or limb
Anatomic injury
Physical derangement
Classifications of trauma
Closed injury
Open injury
Motor vehicle crashes Falls Burns and fire-related injuries Intentional trauma: homicides, nonfatal assaults, and suicides
Three peaks of death Immediate: head injury, brainstem injury, cardiovascular system Early: within the first few hours, major torso trauma, closed head injury
Late
Physiological response to trauma Involves both local and systemic reactions Extent of response proportional to severity of insult An appropriate response maintains homeostasis and allows wound healing An excessive response can produce a systemic response Systemic inflammatory response syndrome (SIRS) Multiple organs dysfunction syndrome (MODS) can result from SIRS
SIRS systemic inflammatory response syndrome (SIRS) is an inflammatory state of the whole body (the "system"). It is characterized by tachycardia, >90/min, low blood pressure (systolic <90 or MAP <65), low or high body temperature (38 C), high respiratory rate (>20/min), and low or high white blood cell count (12 billion/liter). It can be caused by severe trauma, burns, hyperglycemia (high blood sugar) or acute pancreatitis.
Initiation of response Multiple simultaneous factors can have a synergistic effect Important factors are: Tissue injury Infection Hypovolaemia Hypoxia or hypercarbia
Acute phase response Tissue injury results in cytokine release Cytokines have mainly paracrine actions Important in regulating the inflammatory response Cytokines stimulate the production of acute phase proteins such as: – – – –
C-reactive protein Fibrinogen Complement C3 Haptoglobin
Endocrine response The hypothalamus, pituitary, adrenal axis is important Trauma increases ACTH and cortisol production Steroids have a permissive action in many metabolic responses Catabolic action increases protein breakdown Insulin antagonism increases blood sugar levels Anti-inflammatory actions reduce vascular permeability Aldosterone increases sodium reabsorption Vasopressin increases water reabsorption and produces vasoconstriction Histamine increases vascular permeability
Limitation of response Reducing degree of trauma with appropriate and careful surgery Reducing infection with wound care and antibiotics Maintaining enteral nutrition Controlling pain Correcting hypovolaemia Correcting acid-base disturbance Correcting hypoxia
Wound healing Wound: a disruption of the normal anatomical relationships as a result of an injurious process Factors that determine how the wound is closed: Type of wound Size of wound Location of wound Age of wound Presence of infection General condition of the patient
Wound healing Inflammation – to rapidly achieve a sterile environment Proliferation – to close the wound and restore the epithelial barrier Remodelling – to slowly organise the closed wound matrix for increased strength and elasticity.
wound healing Vascular response Initial vasoconstriction as a direct response to trauma Exposed subendothelial tissue activates coagulation and complement cascades Platelet adhesion and aggregation causes clot formation Inflammatory response due to histamine and 5HT(55HT( hydroxytryptamine) release produces: Vasodilatation Increased capillary permeability Margination of neutrophils
Cellular response Migration of neutrophils, macrophages and lymphocytes Macrophages produce growth factors leading to migration of fibroblast and epithelial cells. This causes cellular proliferation with three components: – Epithelialisation – Contraction – Fibroplasia
Contraction can account for up to 80% reduction in wound size Contraction due to myofibroblasts in granulation tissue Fibroplasia due to procollagen production by fibroblasts
Proliferation is followed by remodeling Maximum collagen production occurs at 20 days Maximum wound strength at 3 to 6 months
Factors influencing wound healing Systemic factors Age and Sex Nutrition Vitamin and trace element deficiencies Drugs – steroids, chemotherapy, immunosuppression Systemic disease – diabetes, malignancy Hypoxia
Local Factors Blood Supply Infection Foreign Bodies Surgical Technique
Classification of how wounds heal Healing by first intention = Primary wound healing Healing by second intention = Secondary wound healing Healing by third intention = Tertiary wound healing = Delayed primary closure
Primary healing
Secondary healing
Requirements for primary wound closure Clean Living Tension-free Approximate & evert skin edges Do no harm: atraumatic, not too tight Enough sutures to get the job done Consider deep sutures to take the tension off the skin edge or close dead space
Diagnosis of trauma Medical history Level of consciousness, physical exam, vital signs Laboratory test
First aid ABC Airway Breathing Circulation
Airway Loss of a patent airway is the most common reason for immediate cardiorespiratory collapse after trauma Occlusion by tongue or epiglottis Occlusion by foreign body Direct traumatic disruption
Positioning the airway Manual techniques for opening the airway include the head tilt/chin lift, jaw thrust, and jaw lift Each acts to manually displace oropharyngeal soft tissues and the tongue away from the posterior portion of the throat, thereby allowing upper airway patency
The head tilt/chin lift is contraindicated in most trauma patients The jaw thrust is accomplished by placing two hands at the angles of the mandible and lifting the jaw forward Supplemental oxygen Suctioning
Jaw thrust
Head tilt and chin lift
Breathing Even in the face of a patent upper airway, inadequate gas exchange can lead to rapid death Loss of respiratory effort severe head injury high spinal cord disruption CNS depression from toxins or drugs
Mechanical dysfunction Tension pneumothorax Large or bilateral pneumothorax Flail chest Thoracic crush or compression Diaphragmatic rupture Large hemothorax
Circulation Impaired delivery of oxygenated blood to vital organs will cause clinical deterioration Severe hemorrhage Obstruction of blood flow Tension pneumothorax Pericardial tamponade
Myocardial dysfunction
IV insertion
Treatment Positioning and local immobilization Controlling pain Prevention of infection Treatment of shock Maintaining of the fluid balance and nutrition
Open wound Cleaning wound Contaminated wound
Infected wound
General treatment of wounds Immunize – ensure Tetanus immunization status is up to date. Anaesthetize – Toxic dose of lidocaine = 7 mg/kg. Avoid epinephrine in fingers, toes. (Tourniquet – consider it for extremities or digits to control excessive blood loss.) Cleanse – Skin prep and draping with sterile towels. Irrigate – with NS – best prevention for infection.
General treatment of wounds Debride – remove devitalized tissue and ragged edges Close the wound. Dress the wound. Antibiotics – consider – not necessary for most clean wounds. Follow-up – Remove sutures in a timely fashion to prevent “railroad marks”.
POLYMER SCAFFOLD
TISSUE ENGINEERING CELL—POLYMER
BONE CARTILAGE LIVER INTESTINE URETER
CELLS
Langer R and Vacanti JP. Tissue Engineering Science. 1993;260:920-926
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