THE METABOLIC AND NEUROENDOCRINE RESPONSES TO TRAUMA AND OPERATIONS

Dr. A. SERMON Department of Traumatology

INTRODUCTION
INJURY OR MAJOR OPERATION

SIMILAR PATHOPHYSIOLOGIC THREAT TO THE VICTIM OR THE PATIENT

SAME BIOLOGIC RESPONSES MAGNITUDE OF RESPONSE DEPENDS ON SEVERITY OF INJURY / OPERATION

INTRODUCTION
MODERATE INJURY ORGANIZED, SEQUENTIAL, DESCRIBABLE AND UNDERSTANDABLE SYSTEM OF BIOLOGIC RESPONSES

INTRODUCTION
SEVERE / OVERWHELMING INJURY BIOLOGIC DISINTEGRATION
EXCESSIVE MEDIATORS OF INFLAMMATION REMOTE ORGAN FAILURE

DYSHOMEOSTASIS / BIOLOGIC CHAOS

INTRODUCTION
MINIMAL SURGERY

MINIMAL AND APPROPRIATE RESPONSES MINOR CHANGES IN HOMEOSTATIC THERMOSTAT

INTRODUCTION
MAJOR SURGERY / NON-LIFETHREATENING INJURY

MAJOR CHANGES THAT SEEMS TO BE INTERRELATEND AND COORDINATED HOMEOSTASIS SEEMS EVIDENT

INTRODUCTION
LIFE-THREATENING INJURIES, OPERATIONS, ILLNESSES

BIOLOGIC CHAOS / DYSHOMEOSTASIS CHANGES THAT SHOULD BE PROTECTIVE BECOME SELF-DESTRUCTIVE

THE PHASES OF INJURY

PHASE 1: INJURY PHASE
STARTS AT TIME OF INJURY OR DURING PREPARING FOR OPERATION LASTS TWO TO FIVE DAYS

THE PHASES OF INJURY

PHASE 2: TURNING POINT
TURNING OFF OF NEUROENDOCRINE RESPONSES APPEARANCE OF GETTING BETTER TRANSIENT PERIOD: OVERNIGHT OR MAX 1 TO 2 DAYS

THE PHASES OF INJURY

PHASE 3: ANABOLIC PHASE
POSITIVE NITROGEN BALANCE / GAIN IN MUSCULAR STRENGTH LASTS 3 TO 12 WEEKS OR LONGER

THE PHASES OF INJURY

PHASE 4: LATE ANABOLIC PHASE
POSITIVE CALORIC BALANCE: GAIN IN BODY WEIGHT AND BODY FAT LASTS MONTHS TO YEARS

INJURY PHASE (PHASE 1)

STIMULI RESULTING FROM INJURY TRIGGER BIOLOGIC RESPONSE RESET OF HOMEOSTATIC THERMOSTAT

INJURY PHASE (PHASE 1)

RESET OF HOMEOSTATIC THERMOSTAT: HIGHER METABOLIC RATE HIGHER CIRCULATORY RATE HIGHER LEVEL OF FUNCTIONING

INJURY PHASE (PHASE 1)

FACTORS PRODUCING MINOR TRANSIENT CHANGES PAIN FEAR FATIGUE TRANSIENT STARVATION IMMOBILIZATION DRUGS

INJURY PHASE (PHASE 1)

FACTORS PRODUCING MAJOR, EXTENSIVE CHANGES
MULTISYSTEM INJURY THE WOUND (TISSUE INJURY, TISSUE NECROSIS, BURNS,) INVASIVE SEPSIS SHOCK PROLONGED STARVATION

INJURY PHASE (PHASE 1)

STIMULI FROM INJURY / SURGERY SIGNALS TO CENTRAL NERVOUS SYSTEM PRODUCTION AND RELEASE OF MEDIATORS

INJURY PHASE (PHASE 1)

AFFERENT SIGNALS EFFERENT SIGNALS

HYPOTHALAMIC PITUITARY ADRENAL AXIS

PHASE 1: AFFERENT PATHWAYS

STIMULI FROM INJURY PROVIDE NEURAL AND NEUROENDOCRINE SIGNALS TO CENTRAL NERVOUS SYSTEM BY WAY OF NOCICEPTORS BARORECEPTORS RECEPTORS FROM THE WOUND

PHASE 1: AFFERENT PATHWAYS

NOCICEPTORS PAIN PERCEPTION: TRANSMISSION OF
STIMULI TO SPINOTHALAMIC TRACTS AND CORTEX

NEUROENDOCRINE STIMULATION:
HYPOTHALAMUS

PHASE 1: AFFERENT PATHWAYS

NOCICEPTORS PLAY A ROLE IN ESCAPING AND INITIATING THE STRESS RESPONSE

PHASE 1: AFFERENT PATHWAYS

BARORECEPTORS ARTERIAL RECEPTORS: AORTIC ARCH AND CAROTIC SINUSES VENOUS RECEPTORS: LEFT AND RIGHT ATRIA

PHASE 1: AFFERENT PATHWAYS

THE WOUND AFFERENT ARC OF STIMULATION OF CENTRAL RESPONSES EFFERENT STIMULI TO LIVER AND TEMPERATURE CONTROL CENTER INITIATES INFLAMMATORY PROCESS

PHASE 1: AFFERENT PATHWAYS

THE WOUND MEDIATORS
PRODUCED BY CELLS OF THE WOUND

AUTOCRINE, PARACRINE, REMOTE ENDOCRINE FUNCTION STIMULATE HYPOTHALAMUS-PITUITARYADRENAL AXIS

PHASE 1: AFFERENT PATHWAYS

THE WOUND MEDIATORS:
CYTOKINES PAF COMPLEMENT FACTOR ENDORPHINS

PHASE 1: EFFERENT PATHWAYS

HYPOTHALAMIC-PITUITARY-ADRENAL AXIS MEDIATORS:
ADH CATECHOLAMINES: EPINEPHRINE NOREPINEPHRINE CRH ENDORPHINS GLUCAGON

PHASE 1: EFFERENT PATHWAYS

ANTIDIURETIC HORMONE (ADH)
RELEASED FROM NEUROHYPOPHYSIS LEADS TO WATER CONSERVATION STIMULI: DECREASED EFFECTIVE BLOOD VOLUME, ANGIOTENSINE II

PHASE 1: EFFERENT PATHWAYS

CATECHOLAMINES: EPINEPHRINE, NOREPINEPHRINE EPINEPHRINE: SECRETION FROM ADRENAL MEDULLA NOREPINEPHRINE: SECRETION FROM SYMPATHIC NERVE ENDINGS

PHASE 1: EFFERENT PATHWAYS

CATECHOLAMINES: EPINEPHRINE, NOREPINEPHRINE PRODUCE HYPERMETABOLISM: INCREASED CARDIAC OUTPUT, REGIONAL CIRCULATION, BLOOD GLUCOSE AND OXIDATIVE METABOLISM

PHASE 1: EFFERENT PATHWAYS

CORTICOTROPIN-RELEASING HORMONE (CRH)
STIMULATES ADENOHYPOPHYSIS TO PRODUCE ADRENOCORTICOTROPIC HORMONE (ACTH)

PHASE 1: EFFERENT PATHWAYS

CORTICOTROPIN-RELEASING HORMONE (CRH)
ACTH STIMULATES CORTISOL PRODUCTION IN ADRENAL CORTEX ACTH STIMULATES ALDOSTERON PRODUCTION IN ADRENAL CORTEX

PHASE 1: EFFERENT PATHWAYS

CORTICOTROPIN-RELEASING HORMONE (CRH) CORTISOL: HYPERMETABOLISM
MOBILIZATION OF AMINO ACIDS FROM SKELETAL MUSCLE STIMULATES HEPATIC GLUCONEGONESIS

ALDOSTERON: SODIUM RETENTION

PHASE 1: EFFERENT PATHWAYS

ENDORPHINS
ANALGESIA CALMING EFFECT

PHASE 1: EFFERENT PATHWAYS

GLUCAGON: SUBSTRATE MOBILISATION
GLYCOGENOLYSIS GLUCONEOGENESIS LIPOLYSIS KETOGENESIS

PHASE 1: IMMUNOLOGIC RESPONSE

STRESS HORMONES AND MEDIATORS INFLUENCE IMMUNE MODULATION

PHASE 1: IMMUNOLOGIC RESPONSE

SPECIFIC / CELL MEDIATED IMMUNITY IS DEPRESSED
INHIBITION OF T-CELL PROLIFERATION AND SHIFT IN Th2-CELL DIRECTION (ANTIINFLAMMATORY)

NON-SPECIFIC IMMUNE SYSTEM IS ACTIVATED

POLYMORPHONUCLEAR LEUKOCYTES PRODUCE SELF-DESTRUCTIVE OR TOXIC MEDIATROS

PHASE 1: IMMUNOLOGIC RESPONSE

CELLS OF WOUND PRODUCE CYTOKINES MONOCYTES, MACROPHAGES IL1: MOBILIZATION OF LEUKOCYTES, STIMULATION OF FEVER, STIMULATION OF ACUTE PHASE PROTEIN PRODUCTION IN LIVER

PHASE 1: MAGNITUDE OF RESPONSE

MAGNITUDE OF NEUROENDOCRINE RESPONSE IS PROPORTIONATE TO
SEVERITY OF INJURY / OPERATION BODY FLUID AND BLOOD LOSS THIRD SPACING

PHASE 1: MAGNITUDE OF RESPONSE

IN CASE OF INFECTION, THE INJURY PHASE IS PROLONGED OR EXAGGERATED

PHASE 1: PHYSIOLOGIC CORRELATES

1. BLOOD PRESSURE AND CARDIAC OUTPUT MAINTENANCE 2. SALT AND WATER RETENTION 3. HYPERMETABOLISM 4. ALTERED METABOLISM 5. BEGINNING OF WOUND HEALING 6. IMMUNOMODULATION

PHASE 1: PHYSIOLOGIC CORRELATES

1. BLOOD PRESSURE AND CARDIAC OUTPUT MAINTENANCE
INCREASED PERIPHERAL VASCULAR RESISTANCE INCREASED HEART RATE VENTRICULAR INOTROPY VENOCONSTRICTION

PHASE 1: PHYSIOLOGIC CORRELATES

2. SALT AND WATER RETENTION
MAINTENANCE OF EXTRACELLULAR FLUID AND VASCULAR VOLUME STIMULI: ADH AND ALODSTERONE MAXIMUM SODIUM RETENTION / LOW SODIUM LOSSES

PHASE 1: PHYSIOLOGIC CORRELATES

3. HYPERMETABOLISM
INCREASED BODY TEMPERATURE, INCREASED OXYGEN CONSUMPTION, INCREASED CIRCULATORY DEMAND IMMEDIATELY AFTER INJURY: LOW OR LOW-NORMAL RESTING ENERGY EXPENDITURE

PHASE 1: PHYSIOLOGIC CORRELATES

3. HYPERMETABOLISM
INCREASED CARDIAC OUTPUT AND INCREASED BLOOD FLOW

ELEVATION OF METABOLIC RATE

PHASE 1: PHYSIOLOGIC CORRELATES

3. HYPERMETABOLISM EXAMPLES OF METABOLIC RATE ELEVATION
MULTIPLE FRACTURES: 10-25% FOR 10-14 DAYS MAJOR INFECTIONS: 15-50% AS LONG AS THE INFECTION CONTINUES MAJOR BURNS: 40-100% UNTIL THE BURN IS COVERED

PHASE 1: PHYSIOLOGIC CORRELATES

4. ALTERED METABOLISM
INSULINE RESISTANCE GLUCAGON SECRETION EXCESSIVE CATABOLISM NEGATIVE NITROGEN BALANCE

PHASE 1: PHYSIOLOGIC CORRELATES

4. ALTERED METABOLISM IMMEDIATELY AFTER INJURY: GLYCOGENOLYSIS (STIMULUS: EPINEPHRINE)

RELATIVE HYPERGLYCEMIA

PHASE 1: PHYSIOLOGIC CORRELATES

4. ALTERED METABOLISM FOLLOWED BY GLUCONEOGENESIS AND ACUTE PHASE PROTEIN PRODUCTION IN LIVER
SUBSTRATE: MUSCLE PROTEIN STIMULI: CORTISOL

PHASE 1: PHYSIOLOGIC CORRELATES

4. ALTERED METABOLISM
SEVERE INJURY: CATABOLISM OF MUSCLE PROTEINS MUSCLE / LEAN BODY MASS

PHASE 1: PHYSIOLOGIC CORRELATES

5. BEGINNING OF WOUND HEALING
HIGH NEED FOR GLUCOSE: ANAEROBIC GLYCOLYSIS

PHASE 1: PHYSIOLOGIC CORRELATES

6. IMMUNOMODULATION DEPRESSION OF SPECIFIC IMMUNE SYSTEM
(PGE2: SUPPRESSION OF IL-2: NO STIMULATION OF T-CELL PROLIFERATION)

PHASE 1: CLINICAL CORRELATES

IMPORTANCE: CLINICAL CORRELATES OF RESPONSE TO INJURY = INDICATOR OF NORMAL RESPONSE DEVELOPMENT OF COMPLICATIONS

PHASE 1: CLINICAL CORRELATES

INJURY PHASE: PATIENT IS QUIET, LETHARGIC AND LOOKS ILL PULSE AND TEMPERATURE INCREASE

PHASE 1: CLINICAL CORRELATES

INJURY PHASE: OLIGURIA; DIURESIS STARTS 2nd-4th DAY GI TRACT AND PERISTALSIS ARE QUIET PAIN

PHASE 1: CLINICAL CORRELATES

BODY WEIGHT INCREASES FOR 1-3 DAYS (THIRD SPACE) FROM DAY 4 ON: BODY WEIGHT LOSS EQUAL TO CATABOLISM

PHASE 1: CLINICAL CORRELATES

NORMAL RESPONSE BECOMES ABNORMAL IF THE INJURY PHASE IS PROLONGED CAUSES OF PROLONGED INJURY PHASE:
TISSUE NECROSIS CONTINUING TISSUE INJURY INFECTION

PHASE 1: CLINICAL CORRELATES

PROLONGED INJURY PHASE LEADS TO
WEIGHT LOSS FATIGUE WEAKNESS

TURNING POINT (PHASE 2)

TURNING POINT = NEUROENDOCRINE WITHDRAWAL PHASE

TURNING POINT (PHASE 2)

PHASE 2 STARTS IF
PATIENT STABILIZES AFTER INJURY HOMEOSTASIS IS ADEQUATE THE WOUND IS CONTROLLED NO COMPLICATIONS OCCUR

TURNING POINT (PHASE 2)

CHARACTERISTICS OF PHASE 2 NEUROENDOCRINE STIMULATION SWITCHES OFF DECREASE OF THE INFLAMMATORY RESPONSES

TURNING POINT (PHASE 2)

CHARACTERISTICS OF PHASE 2 NEUROENDOCRINE STIMULATION SWITCHES OFF: DECREASE OF PLASMA CONCENTRATIONS OF
EPINEPHRINE NOREPINEPHRINE CORTISOL ADH

TURNING POINT (PHASE 2)

CHARACTERISTICS OF PHASE 2 DECREASE OF THE INFLAMMATORY RESPONSES:
DECREASE OF LOCAL MEDIATORS DECREASE OF SYSTEMIC EFFECTS

PHASE 2: PHYSIOLOGIC CORRELATES

1. 2. 3. 4. WATER DIURESIS INCREASED SODIUM IN URINE DECREASED NITROGEN EXCRETION NITROGEN BALANCE: ZERO OR POSITIVE

PHASE 2: CLINICAL CORRELATES

1. PATIENT LOOKS AS HE OR SHE IS RECOVERING 2. PATIENT REGAINS APPETITE 3. PATIENT BECOMES INTERESTED IN SURROUNDINGS

PHASE 2: COMPLICATIONS
INJURY PHASE CONTINUES

TURNING POINT WILL BE DELAYED

PHASE 2: COMPLICATIONS
CAUSES OF PROLOGED INJURY PHASE CIRCULATION AND HOMEOSTASIS ARE NOT ADEQUATE INJURY OR WOUNDING CONTINUES

PHASE 2: COMPLICATIONS
CAUSES OF PROLOGED INJURY PHASE FRACTURES ARE NOT IMMOBILIZED TISSUE NECROSIS / OPEN NECROTIC WOUND

ANABOLIC PHASE (PHASE 3)

STARTS IMMEDIATELY AFTER THE TURNING POINT ONLY IF THE PATIENT CAN TAKE NOURISHMENT OR IS PROVIDED WITH PARENTERAL NUTRITION

ANABOLIC PHASE (PHASE 3)

CHARACTERISTICS: RECOVERY OF STRENGTH POSITIVE NITROGEN BALANCE RESTORATION OF MUSCLE PROTEIN

ANABOLIC PHASE (PHASE 3)

THIS IS A SLOW PROCEDURE

EXPLAIN TO THE PATIENT!

LATE ANABLOLISM (PHASE 4)

PHASE OF POSITIVE CALORIC BALANCE DUE TO UNDERLYING ILLNESS OR OPERATION: RETURN TO PREOPERATIVE WEIGHT MIGHT BE IMPOSSIBLE

METHODS TO DECREASE THE RESPONSE TO INJURY

1. PROMPT OPERATIVE CARE 2. CAREFUL SURGICAL TECHNIQUE 3. MINIMAL SURGICAL PROCEDURES 4. EPIDURAL OR SPINAL ANESTHESIA

METHODS TO DECREASE THE RESPONSE TO INJURY

5. NORMOTHERMIA 6. NUTRITIONAL SUPPORT 7. HORMONE MANIPULATIONS

METHODS TO DECREASE THE RESPONSE TO INJURY

1. PROMPT OPERATIVE CARE
CORRECT BLOOD LOSS REPAIR INJURED ORGANS CLOSE WOUNDS AND BODY CAVITIES ASAP

METHODS TO DECREASE THE RESPONSE TO INJURY

2. CAREFUL SURGICAL TECHNIQUE DEBRIDEMENT IRRIGATION STOP CONTAMINATION

METHODS TO DECREASE THE RESPONSE TO INJURY

2. CAREFUL SURGICAL TECHNIQUE

REDUCES LOAD OF NECROTIC TISSUE MINIMIZES RISK OF POSTOPERATIVE INFECTION

METHODS TO DECREASE THE RESPONSE TO INJURY

3. MINIMAL SURGICAL PROCEDURES

DECREASE OF RESPONSE TO STRESS AND INJURY

METHODS TO DECREASE THE RESPONSE TO INJURY

4. EPIDURAL OR SPINAL ANESTHESIA

BLOCKING AFFERENT PAIN STIMULI

ATTENUATION OF HORMONAL RESPONSE

METHODS TO DECREASE THE RESPONSE TO INJURY

5. NORMOTHERMIA REDUCTION OF MORBID CARDIAC EVENTS REDUCTION OF SURGICAL WOUND INFECTIONS SHORTENING OF HOSPITALISATION

METHODS TO DECREASE THE RESPONSE TO INJURY

6. NUTRITIONAL SUPPORT DECREASES TOTAL PROTEIN LOSS START ENTERAL FEEDING WHENEVER POSSIBLE

METHODS TO DECREASE THE RESPONSE TO INJURY

6. NUTRITIONAL SUPPORT
ADDITIVES MAY DECREASE INCIDENCE OF INFECTION IMMUNE ENHANCEMENT EXAMPLE: GLUTAMINE, ARGININE

METHODS TO DECREASE THE RESPONSE TO INJURY

7. HORMONE MANIPULATIONS MAY HAVE SOME POSITIVE EFFECTS NOT RECOMMENDED FOR GENERAL USE

VARIATIONS IN THE RESPONSE TO INJURY

1. PATIENTS WITH CHRONIC DISEASES 2. INNAPROPRIATE ACTIVITY OF THE NEUROENDOCRINE SYSTEM 3. OVERWHELMING INJURY OR MAJOR OPERATION WITH COMPLICATIONS

VARIATIONS IN THE RESPONSE TO INJURY

1. PATIENTS WITH CHRONIC DISEASES CHRONIC HEART DISEASE: NO TOLERATION OF SALT AND WATER RETENTION LIVER DISEASE: DIFFICULTIES IN FLUID MANAGEMENT

VARIATIONS IN THE RESPONSE TO INJURY

1. PATIENTS WITH CHRONIC DISEASES CHRONIC OBSTRUCTIVE PULMONARY DISEASE: HYPOXEMIA RENAL INSUFFICIENCY: RAPID RISE IN UREA AND POTASSIUM

VARIATIONS IN THE RESPONSE TO INJURY

1. PATIENTS WITH CHRONIC DISEASES ELDERLY PATIENTS: INSUFFICIENT RECOVERY OF STRENGTH AFTER INJURY (RESPIRATORY AND CARDIOVASCULAR COMPLICATIONS)

VARIATIONS IN THE RESPONSE TO INJURY

2. INAPPROPRIATE ACTIVITY OF THE NEUROENDOCRINE SYSTEM

VARIATIONS IN THE RESPONSE TO INJURY

3. OVERWHELMING INJURY OR MAJOR OPERATION WITH COMPLICATIONS

MASSIVE NEUROENDOCRINE, METABOLIC AND MEDIATOR RESPONSE

VARIATIONS IN THE RESPONSE TO INJURY

3. OVERWHELMING INJURY OR MAJOR OPERATION WITH COMPLICATIONS

BIOLOGIC RESPONSES THAT SHOULD PROTECT US HAVE DESTRUCTIVE CONSEQUENCES

SYSTEMIC RESPONSE TO TRAUMA

1. DEFINITION 2. PATHOPHYSIOLOGY 3. MANAGEMENT

DEFINITION
SYSTEMIC RESPONSE TO TRAUMA INAPPROPRIATE RELEASE OF MEDIATORS TRIGGERING REMOTE INFLAMMATION CAUSE: INFECTIOUS OR NONINFECTIOUS

trauma - burns - operation bacterial infection ischemia/reperfusion

LOCAL REACTION:

IL-1; IL-6;IL-8; prostaglandin; leukotriene; TNF; PAF; catecholamines; histamine; kinin; cortocods

SYSTEMIC REACTION:

Acute SIRS

PATHOPHYSIOLOGY
3 HYPOTHESES 1. GENERALISED AND UNCONTROLLED INFLAMMATORY REACTION 2. SECOND HIT THEORY 3. GUT HYPOTHESIS

1. GENERALISED AND UNCONTROLLED INFLAMMATORY REACTION

HOST DEFENCE RESPONSE: FINE BALANCE BETWEEN S.I.R.S. C.A.R.S.

M.A.R.S.

(Mixed Antagonistic Response Syndrome)

1. GENERALISED AND UNCONTROLLED INFLAMMATORY REACTION

M.A.R.S.: INDUCTION OF REPARATIVE MECHANISMS LIMIT ENTRY / OVERLOAD OF MICRO-ORGANISMS AVOID AUTODESTRUCTIVE EFFECT OF IMMUNOCOMPETENT CELLS

1. GENERALISED AND UNCONTROLLED INFLAMMATORY REACTION

IMBALANCE BETWEEN DUAL IMMUNE RESPONSES: OVERWHELMING RELEASE OF PRO- AND ANTI-INFLAMMATORY MEDIATORS ORGAN DYSFUNCTION SUSCEPTIBILITY TO INFECTIONS AND SEPSIS

2. SECOND HIT THEORY

FIRST HIT (PRIMING OF IMMUNE RESPONSE) : TRAUMA LOAD FRACTURES SOFT TISSUE INJURIES PRIMARY ORGAN INJURIES SECOND HIT: INTERVENTIONAL OF SURGICAL LOAD

2. SECOND HIT THEORY

SECOND HIT: INTERVENTIONAL OR SURGICAL LOAD SURGICAL INTERVENTIONS (SEVERE TISSUE DAMAGE, HYPOTHERMIA, BLOOD LOSS) RESPIRATORY DISTRESS (HYPOXIA) REPEATED CARDIOVASCULAR INSTABILITY METABOLIC ACIDOSIS

2. SECOND HIT THEORY

SECOND HIT: INTERVENTIONAL OF SURGICAL LOAD ISCHEMIA / REPERFUSION INJURIES DEAD TISSUE CONTAMINATED CATHETERS, INFECTIONS MISSED / NEGLECTED INJURIES MASSIVE TRANSFUSIONS

2. SECOND HIT THEORY

FIRST HIT SECOND HIT

INAPPROPRIATE IMMUNE RESPONSE

First Event
Tissue Trauma Infection Shock
Inflammatory Response Recovery

Second Event

Primed Macrophages Amplified Inflammatory Response MOF Death

Infection Endotoxemia Ischemia

Flims2001/Dr.KG-cdj

3. GUT HYPOTHESIS
NORMALLY: GUT HAS A BARRIER FUNCTION ALTERATION OF INTESTINAL MUCOSA BACTERIAL TRANSLOCATION + BACTERAEMIA (EVEN IN THE ABSENCE OF A DETECTABLE INFECTIVE FOCUS)

Infection/ SIRS Trauma

MODS

Severe MODS

Disease continuum

MANAGEMENT
TREATMENT?
HOPEFUL RESULTS IN ANIMAL STUDIES MULTIPLE PROSPECTIVE CLINICAL TRIALS FAILED TO PROVIDE A BENEFIT OF ANTIINFLAMMATORY, ANTI-COAGULANT, ANTIOXIDANT STRATEGIES SUCCESSFUL CLINICAL STUDIES

MANAGEMENT
TREATMENT: PROBLEMS WITH STUDIES STUDY PROTOCOLS FOCUS ON SINGLE MECHANISM: IMMUNE NETWORK IS MORE COMPLEX INAPPROPRIATE TIMING OF DRUG ADMINISTRATION SUBOPTIMAL DRUG LEVEL AT TARGET SITE

MANAGEMENT
TREATMENT: A LOT OF WORK NEEDS TO BE DONE!

PREVENTION!

TREATMENT = PREVENTION
1. STARTS AT ADMISSION 2. DAMAGE CONTROL SURGERY 3. SECONDARY INTERVENTIONS: TYPE AND TIMING 4. NUTRITIONAL SUPPORT 5. HYPOTHERMIA 6. ANALGESIA

1. TREATMENT STARTS AT ADMISSION

PREVENT HYPOXEMIA AND TISSUE HYPOXIA FLUID SUBSTITUTION CONTROL OF HEMORRHAGE

1. TREATMENT STARTS AT ADMISSION

PREVENT HYPOXEMIA AND TISSUE HYPOXIA: EARLY OXYGENATION THERAPY
INTUBATION CONTROLLED ASSISTED VENTILATION

1. TREATMENT STARTS AT ADMISSION

FLUID SUBSTITUTION VOLUME THERAPY
CRYSTALLOIDS, COLLOIDS, BLOOD PRODUCTS SEVERE HAEMORRHAGIC SHOCK: SMALL VOLUME RESUSCITATION SEPTIC SHOCK: HIGH VOLUME THERAPY

1. TREATMENT STARTS AT ADMISSION

CONTROL OF HEMORRHAGE EXTERNAL BLEEDING INTERNAL BLEEDING
THORAX ABDOMEN PELVIS THIGH

2. DAMAGE CONTROL SURGERY

DAMAGE CONTROL SURGERY Vs EARLY TOTAL TRAUMA CAREA

2. DAMAGE CONTROL SURGERY

PREVENTION OF DEADLY TRIADE HYPOTHERMIA

ACIDOSIS

COAGULOPATHY

2. DAMAGE CONTROL SURGERY

COMPONENTS OF DCS HAEMORRHAGE CONTROL CONTAMINATION CONTROL DECOMPRESSION OF COMPARTMENT SYNDROMES TEMPORARY STABILISATION OF PELVIC AND LONG BONE FRACTURES

2. DAMAGE CONTROL SURGERY

COMPONENTS OF DCS HAEMORRHAGE CONTROL QUICK DIAGNOSTIC WORK-UP AND START THERAPY CONTROL OF BLEEDING
EXTERNAL BLEEDING INTERNAL BLEEDING

2. DAMAGE CONTROL SURGERY

COMPONENTS OF DCS CONTAMINATION CONTROL
OPEN FRACTURE MANAGEMENT HOLLOW ORGAN LESIONS

2. DAMAGE CONTROL SURGERY

COMPONENTS OF DCS DECOMPRESSION OF COMPARTMENT SYNDROMES
EXTREMITIES ABDOMEN

2. DAMAGE CONTROL SURGERY

COMPONENTS OF DCS TEMPORARY STABILISATION OF PELVIC AND LONG BONE FRACTURES

EXFIX

2. DAMAGE CONTROL SURGERY

COMPONENTS OF DCS TEMPORARY STABILISATION OF PELVIC AND LONG BONE FRACTURES
INTRAMEDULLARY NAILING = SECOND HIT REAMING INDUCES HYPERSTIMULATION

3. SECONDARY INTERVENTIONS: TYPE AND TIMING

SECOND LOOK LAPAROTOMY SOFT TISSUE MANAGEMENT BONY STABILISATION

3. SECONDARY INTERVENTIONS: TYPE AND TIMING

SECOND LOOK LAPAROTOMY TYPE
REMOVAL OF PACKS RESTORATION OF TRANSIT

TIMING
24 48 HOURS AFTER FIRST INTERVENTION

3. SECONDARY INTERVENTIONS: TYPE AND TIMING

SOFT TISSUE MANAGEMENT DIAGNOSIS IS DIFFICULT REAL EXTEND UNDERESTIMATED CLEAR SEVERAL DAYS AFTER INJURY

3. SECONDARY INTERVENTIONS: TYPE AND TIMING

SOFT TISSUE MANAGEMENT REPETITIVE DEBRIDEMENT: EXTENSIVE REMOVAL OF ALL NECROTIC TISSUE FASCIOTOMY AMPUTATION (LIFE BEFORE LIMB)

3. SECONDARY INTERVENTIONS: TYPE AND TIMING

BONY STABILISATION CONVERSION: EXFIX TO IM NAILING ARTICULAR RECONSTRUCTIONS

3. SECONDARY INTERVENTIONS: TYPE AND TIMING

BONY STABILISATION: TIMING SECONDARY INTERVENTION = SECOND HIT
BLOOD LOSS SOFT TISSUE DISRUPTION LONGER OPERATING TIME

3. SECONDARY INTERVENTIONS: TYPE AND TIMING

BONY STABILISATION: TIMING SECONDARY INTERVENTION = SECOND HIT AVOID DAY 2 4!

4. NUTRITIONAL SUPPORT
RESTART EARLY ENTERAL FEEDING (GASTRIC OR DUODENAL TUBES) REDUCTION OF BACTERIA IN GI TRACT AVOID ATROPHY OF INTESTINAL MUCOSA NEW FORMULAS (ARGININE, GLUTAMINE, NUCLEOTIDES,)

5. HYPOTHERMIA
REWARM THE PATIENT PREVENT THE PATIENT FROM COOLING DOWN

6. ANALGESIA

PAIN = INITIATOR OF STRESS RESPONSE IMPORTANCE OF EFFICACIOUS ANALGESIA

CONCLUSION
SYSTEMIC RESPONSE TO MAJOR TRAUMA
UNCLEAR ETIOLOGY AND PATHOGENESIS UNPREDICTABLE DISEASE PROGRESSION

CONCLUSION
ROLE OF THE SURGEON IS IN DANGER OF BEING MARGINALISED TO THAT OF A TECHNICIAN BUT: SURGEON CAN BE A KEY FIGURE!