Metabolic Response to Trauma PDF

METABOLIC RESPONSE TO TRAUMA DR. MORGAN E. 400 LEVEL LECTURE NOTE BU/BUTH  INTRODUCTION This is an adaptive response that will either lead to survival or dead if unattended to. It is a cascade of physiological events brought into play for the “preservation of self”...

METABOLIC RESPONSE TO TRAUMA DR. MORGAN E. 400 LEVEL LECTURE NOTE BU/BUTH  INTRODUCTION This is an adaptive response that will either lead to survival or dead if unattended to. It is a cascade of physiological events brought into play for the “preservation of self” and homeostasis which if uncontrolled may become pathological. Similar responses seen in trauma, burns, sepsis and surgery 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 This can cause the systemic inflammatory response syndrome (SIRS) Multiple organs dysfunction syndrome (MODS) can result from SIRS  PHASES The response is divided into two phases The ‘ebb’ & ‘flow’(David Cuthbertson,1930).  EBB PHASE Ebb phase = survival phase (few hours and lasts about 24- 48 hrs after insult. The main physiological role is to conserve both circulating volume and energy stores for recovery and repair Attenuated by resuscitation but not completely reversible 1 Hypovolaemia 2 Decreased basal metabolic rate 3 Reduced cardiac output 4 Hypothermia and lactic acidosis  Flow phase Follows if patient survives. Involves mobilisation of body energy stores for recovery, repair and the subsequent replacement of damaged tissues Has 2 parts – 1 catabolic Metabolic rate - (negative nitrogen balance and weight loss). -This phase usually last about a week in moderate trauma, may be longer in severe trauma and if sepsis sets in. 2 anabolic phase - protein and fat stores are restored + weight gain occurs (positive nitrogen balance). -The recovery phase usually lasts 2–4 weeks.  Synopsis of metabolic response to trauma Phase Duration Role Physiological Hormones decr. BMR, decr. maintenance of blood Temp, decr. O2 Catecholamines, volume; consumption; Ebb 100 mmol/24 hrs (normal for both= 50–80 mmol/24 hrs), but hypokalaemia is relatively rare in the initial 24–48 hours METABOLIC / ENERGY RESPONSES (TMR = EA + THERM + BMR) Following severe injury or major surgery, catabolism and starvation occur simultaneously. Changes in any individual patient depend on which process predominates. TMR = Total Metabolic rate EA = Energy of activity Therm = Thermogenesis BMR = Basal Metabolic Rate Catabolism Catabolism is mediated by catecholamines, cytokines Following injury, physical work (EA) is usually decreased because of inactivity, although heart and respiratory muscle work may increase. Resting energy expenditure REE (the sum of BMR and thermogenesis) is increased by up to 50% following severe injury. Thermogenesis ▪Patients are frequently mildly pyrexial for 24–48 hours following injury. This occurs because cytokines, principally IL-1, reset temperature-regulating centres in the hypothalamus. ▪Pyrexia may also complicate infection occurring after injury. ▪Metabolic rate increases by 6–10% for each 1°C change in body temperature (Dubois 1924). Basal metabolic rate There is increased activity of protein, carbohydrate and fat related metabolic pathways and of many ion pumps. CHANGES DURING CATABOLISM Carbohydrate metabolism Glycogenolysis (stores last about 10 hours) Hepatic gluconeogenesis Insulin resistance of tissues Hyperglycaemia Fat metabolism Lipolysis Free fatty acids used as energy substrate by tissues (except brain) Some conversion of free fatty acids to ketones in liver (used by brain) ▪Glycerol converted to glucose in the liver Following severe trauma, 200–500 g of fat may be broken down daily. Protein metabolism Skeletal muscle breakdown Amino acids converted to glucose in liver and used as substrate for acute-phase protein production Negative nitrogen balance Total energy expenditure increased in proportion to injury severity and other modifying factors. Progressive reduction in fat and muscle mass until stimulus for catabolism ends. Mechanism of muscle catabolism not quite understood.  Following uncomplicated surgery, negative Nitrogen balance usually lasts only 5–8 days. In patients with prolonged sepsis, burns or conditions associated with prolonged inflammation (for example, acute pancreatitis) it may persist for many weeks. Severe catabolism and negative Nitrogen balance cannot be reversed by feeding Provision of protein and calories can attenuate the processes. Anabolic phase (Occurs in 3 stages) 1. Referred to as corticoid-withdrawal phase because Characterized by: ▪Spontaneous Na+ and free-water diuresis ▪ A positive potassium balance ▪ Reduction in nitrogen excretion. This transitional phase usually lasts only 1 to 2 days. 2. Followed by positive nitrogen balance, weight gain. & increased Protein synthesis, return of lean body mass and muscular strength. 3. Final phase: slower weight gain, return of N2 equilibrium, positive carbon balance & deposition of body fat. Outcome of response Inflammatory response produces clinically apparent local and systemic effects The local response is usually the cardinal signs of inflammation The systemic response includes: Increased ECF volume and hypovolaemia Increased vascular permeability and oedema Early reduced urine output and increased urine osmolality Reduced ‘free’ water clearance Late diuresis and increased sodium loss Pyrexia in the absence of infection ▪Early: reduction in metabolic rate ▪Late: increased metabolism, negative nitrogen balance and weight loss Lipolysis and ketosis Gluconeogenesis via amino acid breakdown Reduced serum albumin Hyponatraemia due to impaired sodium pump action Acid-base disturbance – usually a metabolic alkalosis or acidosis Immunosuppression Hypoxia and coagulopathy Clinical applications Inflammatory response can be limited by ▪ Reducing degree of trauma with appropriate and careful surgery, minimally invasive surgery ▪ Reducing infection with wound care and antibiotics ▪ Maintaining early enteral nutrition ▪ Controlling pain ▪ Correcting hypovolaemia ▪ Correcting acid-base disturbance ▪ Correcting hypoxia, ▪ Choice of anaesthesia: Regional anaesthesia, local anaesthesia over general anaesthesia ▪ Early mobilisation FACTORS ASSOCIATED WITH THE MAGNITUDE OF THE METABOLIC RESPONSE TO INJURY Patient-related Factors : Genetic predisposition how an individual responds to injury and infection is related to gene subtypes Coexisting disease such as cancer and chronic inflammatory disease Drug treatments Pre-existing anti-inflammatory or immunosuppressive therapy, such as steroids. Nutritional status Malnourished patients have decreased immune function and deficiency in important substrates. Malnutrition prior to surgery or trauma is associated with poor outcomes ACUTE SURGICAL/TRAUMA-RELATED FACTORS Severity of injury Greater tissue damage is associated with a greater metabolic response Nature of injury Some types of tissue injury cause a proportionate metabolic response. An example is major burn injury, which is associated with a major response Ischaemia–reperfusion injury If resuscitation is not quick and/or effective, the reperfusion of previously ischaemic tissues can set off a cascade of inflammation that further injures organs. Temperature: Extreme hypothermia and hyperthermia are both detrimental to the metabolic response Infection: The occurrence of infection is often associated with an exaggerated response to injury due to massive inflammatory response Anaesthetic techniques: The use of certain drugs, such as opioids, can reduce the release of stress hormones. Regional anaesthetic techniques for major surgery can reduce the release of cortisol, adrenaline (epinephrine) and other hormones, but has little effect on cytokine responses. Conclusion The human body is adapted to adjust to various trauma or surgically related insult in order to preserve the body homeostasis Timely intervention is essential to ensure that the triggers for metabolic response are brought under control. References SABISTON TEXTBOOK of SURGERY: The BIOLOGICAL BASIS of MODERN SURGICAL PRACTICE, 20th Edition Schwartz’s Principles of Surgery, 9th Edition