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Metabolic response to trauma
- 1. METABOLIC RESPONSE TO TRAUMA BY- DR MOHAMMAD KAUSHAR FCPS-2 RESIDENT, GENERAL SURGERY MMTH, KTM 30 / 05 / 2019
- 2. INTRODUCTION METABOLISM- entire spectrum of chemical reaction occurring in living system ( catabolism+ anabolism) HOMEOSTASIS- maintainence of nearly constant condition in the internal environment of the body by coordinated physiologic processes. Homeostasis is the foundation of normal physiology
- 3. GRADED NATURE OF RESPONSE TO TRAUMA / INJURY Basal Metabolic Rate Cirugía mayor Cirug í a electiva Infecci ó n Sepsis grave Quemadura moderada a grave NitrogenLossinUrine Major Surgery Elective Surgery Infection Severe Sepsis Moderate to Severe Burn
- 4. GRADED NATURE OF RESPONSE TO STARVATION 0 10 20 30 40 Partial Starvation Days NitrogenExcretion(g/day) 12 8 4 Total Starvation Normal Range
- 5. GRADED NATURE OF INJURY RESPONSE Elective surgery (intermediate severity) transient and modest rise in temperature, heart rate, respiratory rate, energy expenditure and peripheral white cell count Major trauma/sepsis - SIRS, Hypermetabolism, marked catabolism, shock and MODS.
- 6. IMMUNOLOGICAL RESPONSE TO INJURY
- 7. NEURO-ENDOCRINE RESPONSE TO INJURY Biphasic 1. Acute phase actively secreting pituitary & elevated counter regulatory hormones beneficial for short-term survival. 2. Chronic phase Hypothalamic suppression & low serum levels of the respective target organ hormones. Changes contribute chronic wasting.
- 9. THE METABOLIC STRESS RESPONSE TO SURGERY AND TRAUMA : THE ‘EBB AND FLOW’ MODEL
- 10. EBB PHASE Time EnergyExpenditure Ebb Phase Flow Phase
- 11. EBB AND FLOW PHASE IN (A) ACUTE STRESS RESPONSE ( B) IN CHRONICALLY ILL PATIENT
- 12. FLOW PHASE . Catabolism then Anabolism(recovery) . Hypermetabolic flow phase, . Corresponds to SIRS. . Involves the mobilisation of body energy stores for recovery and repair, and the subsequent replacement of lost or damaged tissue.
- 13. KEY CATABOLIC ELEMENTS OF THE FLOW PHASE OF THE METABOLIC STRESS RESPONSE Hypermetabolism Alterations in skeletal muscle protein Alterations in Liver protein Insulin resistance
- 14. HYPERMETABOLISM Hypermetabolism due to 1. central thermodysregulation (caused by the proinflammatory cytokine cascade), 2. Increased sympathetic activity, 3. abnormalities in wound circulation (ischaemic areas produce lactate, which must be metabolised by ATP - consuming hepatic Cori cycle; hyperaemic areas cause an increase in cardiac output), 4.increased protein turnover and nutritional support may all increase patient energy expenditure
- 15. ALTERATIONS IN SKELETAL MUSCLE PROTEIN
- 17. ALTERATIONS IN HEPATIC PROTEIN METABOLISM : THE ACUTE PHASE PROTEIN RESPONSE Hepatic acute phase response The hepatic acute phase response represents a reprioritisation of body protein metabolism towards the liver and is characterised by: ●● Positive reactants (e.g. CRP): plasma concentration ↑ ●● Negative reactants (e.g. albumin): plasma concentration ↓
- 18. INSULIN RESISTANCE • Following trauma there in increase in blood sugar and also decreased in glucose uptake • Following routine abdominal surgery, insulin resistance may persist up to 2 weeks. • Postperative patient with insulin resistance behave as T2DM and increased risk of sepsis , deteriorating renal function ,polyneuropathy and death • Treatment- intravenous insulin( sliding scale or conservative approach)
- 19. RESPONSE COMPONENTS PHYSIOLOGICAL METABOLIC
- 20. RESPONSE COMPONENTS CLINICAl LABORATORY
- 21. CHANGES IN BODY COMPOSITION FOLLOWING INJURY 13 12 28 14 3
- 22. CHANGES IN BODY WEIGHT THAT OCCUR IN SERIOUS SEPSIS, AFTER UNCOMPLICATED SURGERY AND IN TOTAL STARVATION.
- 23. CONTINUE catabolism leads to decrease in fat mass and skeletal muscle mass • Blocking the neuroendocrine response, stress response with epidural analgesia and providing early enteral feeding body, weight and nitrogen balance can be maintained
- 24. FACTORS THAT EXACERBATE THE METABOLIC RESPONSE TO SURGICAL INJURY
- 26. ENHANCED RECOVERY AFTER SURGERY
- 27. NUTRITION IN SURGICAL PATIENT IN NEXT PRESENTATION
- 28. THANK YOU
Editor's Notes
- In surgery ●● ‘Stress-free’ perioperative care helps to preserve homeostasis following elective surgery ●● Resuscitation, surgical intervention and critical care can return the severely injured patient to a situation in which homeostasis becomes possible once again
- This graph illustrates that severity of injury correlates to increasing urinary nitrogen loss and increasing energy needs. Elective surgery being least traumatic and the lowest nitrogen loss in urine, whereas burn results in an increase in basal metabolic rate and urinary loss of nitrogen.
- SIRS Tachycardia / tachypnoea / Hyper/hypo thermia Leukocytosis/ leucopenia
- sequelae of major injury evolve from a proinflamatory state by the innate immune system (macrophages, neutrophils, dendritic cells) into a compensatory antiinflammatory response syndrome (CARS) characterised by suppressed immunity and diminished resistance to infection Proinflamatory cytokines—IL-1, IL-6 , IL-8, TNF-a Anti inflammatory cytokines- IL-6, IL-10
- counter regulatory hormones (cortisol, glucagon, adrenaline).
- EBB= 24-48hrs FLOW= 3-10 days RECOVERY= 10-60 days EBB PHASE Characterized by hypovolemic shock Priority is to maintain life/homeostasis Cardiac output Oxygen consumption Blood pressure Tissue perfusion Body temperature Metabolic rate
- conserve both circulating volume and energy stores for recovery and repair catecholamines, cortisol and aldosterone (following activation of the renin–angiotensin system )
- B) Recurrent bouts of sepsis amd other proinflammatory stimuli results in fluctuating metabolic demand which remains chronically elevated.
- tissue oedema (from vasodilatation and increased capillary leakage), increased basal metabolic rate (hypermetabolism), increased cardiac output, Raised body temperature, leukocytosis, increased oxygen consumption and increased gluconeogenesis
- Hypermetabolism can be controlled by routine critical care – Bed rest – Paralysis – Ventilator – External temperature regulation
- body prioritises protein metabolism from peripheral to central part
- • peripheral skeletal muscles(major) • Respiratory muscle (hypoventilation and chest infection) • Gut- decrease gut motility • Extreme catabolism- urinary nitrogen loss is more than 20gm/day ~ 500gm of skeletal muscle loss/day • Mechanism involved in skeletal muscle wasting- ATP dependent ubiquitin-proteasome pathway • FEATURES- asthenia, fatigue, decrease functional ability, decrese quality of life , increase morbidity and morbidity • Critical illness myopathy( impaired excitation contraction coupling )
- Proinflammatory cytokines promote synthesis of 1 . Positive acute phase proteins ( fibrinogen, CRP haptoglobin ferritin antitrypsin macroglobin plasminogen) in liver 2 . Negative - ( albumin transferin)----plasma concentration decreases due to leak from vessels to extravascular space
- Suggested mechanisms for this phenomenon include the action of proinflammatory cytokines and the decreased responsiveness of insulin regulated glucose transporter proteins
- PHYSIOLOGICAL • Increased Cardiac Output • Increased Ventilation • Increased Membrane Transport • Weight loss • Wound Healing METABOLIC • Hypermetabolism • Acclerated Gluconeogenesis • Enhanced Protein breakdown • Increased Fat oxidation
- CLINICAL Fever Tachycardia Tachypnea Presence of wound or Inflammation Anorexia LABORATORY • Leucocytosis/Leucopenia • Hyperglycemia • Elevated CRP/Altered acute phase reactants • Hepatic/Renal dysfunction
- The average 70kg male can be considered to consist of fat (13 kg) and fat free mass (or lean body mass: 57 kg). the lean tissue --- primarily of protein (12 kg), water (42 kg) and minerals (3 kg) The protein mass can be considered as two basic compartments, skeletal muscle (4 kg) and non skeletal muscle(8 kg), which includes the visceral protein mass. The water mass (42 litres) is divided into intracellular (28 litres) and `extracellular (14 litres) spaces.
- Body weight increases immediately on resuscitation with an expansion of extracellular water by 6–10 litres within 24 hours. Thereafter, even with optimal metabolic care and nutritional support, total body protein will diminish by 15% in the next 10 days, and body weight will reach negative balance as the expansion of the extracellular space resolves. During total starvation, urinary loss of nitrogen is rapidly attenuated by a series of adaptive changes. MAJOR INJURY and particularly in the presence of ongoing septic complications, this adaptive change fails to occur, and there is a state of ‘autocannibalism’, resulting in continuing urinary nitrogen losses of 10–20 g N/day (equivalent to 500 g of wet weight lean tissue )
- Protein • Requirements range from 1.2-2.0 g/kg/day during stress • Comprise 20%-30% of total calories during stress METABOLIC RESPONSE TO OVERFEEDING • Hyperglycemia • Hypertriglyceridemia • Hypercapnia • Fatty liver • Hypophosphatemia, hypomagnesemia, hypokalemia
- Carbohydrate • At least 100 g/day needed to prevent ketosis • Carbohydrate intake during stress should be between 30%- 40% of total calories • Glucose intake should not exceed 5 mg/kg/min Fat • Provide 20%-35% of total calories • Maximum recommendation for intravenous lipid infusion: 1.0 -1.5 g/kg/day • Monitor triglyceride level to ensure adequate lipid clearance