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Physiologic response to injury

ศุภฤกษ์ ปรี ชายุทธ


Response to injury
• CNS
• Hormonal
• Metabolic
• Immune/Inflammation

• TOO Much/Inadequate response → MOF (up to 30% after severe


trauma)
CNS response
• Stimuli
• Pain
• Change in blood pressure (Baroreceptor)
• Change in CO2, O2, pH (Chemoreceptor)
• Inflammatory Cytokines

• Response
• Sympathetic ANS (catecholamines)
• Parasympathetic ANS (anti-inflammation)
Inflammatory reflex
Hormonal response
Adrenal shock
• Lack of aldosterone
• ↓ preload
• Lack of cortisol
• ↑ Inflammation
• ↓ Vasoconstriction (afterload)
Metabolic response
Resting energy expenditure (REE) during stress conditions
Enteral Nutrition (EN): preferred route
• Preserves gut integrity
• Decreases bacterial translocation
• Preserves function of gut/liver (trophic effect)
• Reduces costs
• Has fewer complications
Normal Gut

Mucosal disruption after


prolonged NPO
Contraindications of EN
• Hemodynamic instability →EN can induce gut ischemia
• Ileus or gut obstruction
• High output enterocutaneous fistula (in an early phase)
• Active GI bleeding
• Peritonitis
• Intestinal ischemia
• Severe acute pancreatitis
Route of EN
• Gastric route is preferred.
• Post pyloric feeding (↓ aspiration)
• Gastric pathology
• High residual volume
Immune response
Specific immunity mediated by helper T lymphocytes subtype 1 (TH1) and
subtype 2 (TH2) after injury.
Multiple organ failure after trauma
• MOF in trauma patients accounts for 50% of delayed
deaths, lungs and kidneys are affected first (within 3
days) .
• Liver failure usually occurs later (after 3 days).
Microcirculatory Hypothesis
• Inflammatory CKs
• Endothelial cell damage
• Capillary dysfunction
• Occlusion
• Leakage
Disseminated Intravascular Coagulation (DIC)

• 30-50% in sepsis
• Coagulation failure → uncontrolled activation of both coagulation and
fibrinolysis
• Clot in microcirculation → MOF
Microcirculatory Hypothesis
Edema
Pump failure Renal failure

Death Heart Lung Renal Gut Skin


Brain Muscle

ARDS • Second hit injury


Altered • Bacterial
Mental status translocation
- Leakage
- Thrombosis
(DIC, ↑wbc adherence)
Cellular/tissue dysoxia
• In severe sepsis/SIRS
• Inability to use O2 despite adequate O2 delivery
• Defect in O2 extraction
Inflammatory model
• Interaction of Cytokines, Complement
and Coagulation system
• Imbalance between SIRS and CARS
• Neutrophils
• Inflammatory mediators
• ROM
• Neutrophil extracellular traps
(NETs) → endothelial injury
Gut Hypothesis
- Gut is protected by mucosa and Immune cells (GALT)
- Shock → Gut Hypoxia → Mucosal leakage
→ ↑ Mucosal permeability → Bacterial translocation → Liver →
SIRS
- Gut = “Undrained Abscess”
One-Hit and Two-Hit Theory
- One-Hit Theory; → → O
- Two-Hit Theory;
- 1st Hit = Less severe insult “Primed Activation” of the
Inflammation
- 2nd Hit = the Reactivation insult
→ → O w
already been activated.)
Management of MODS
• 1. Resuscitation
• 2. Correct the causes!
• Infection, inflammation
• Bleeding, injury
• 3. Support organ failure
• 4. Metabolic support
• Nutrition
• 5. Immunonutrients → no clear benefit

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