Clinical Nutrition and Dietetics: Stress Response to Surgery
Response to metabolic stress (including trauma) -recorded lecture
Trauma and surgery result in damage to tissues
Elective surgery= pt prepared as possible and try to control stress response Trauma= unexpected and may required emergency surgery which cannot be controlled pre/post op physiological effects
As intake reduced, requirements can increase. Psychological, physical, iatrogenic and metabolic factors can decrease impact intake or requirements
Severe stress- glycogen and protein mobilised for glucose and acute phase reactants, ketogenesis and ketosis but GNG from protein high. increased metabolic rate, increased energy needs , accelerated protein and energy depletion= THIS CANN HAPPEN ALONGSIDE MALNUTRITION
Rate of weight loss in response to starvation= in complete starvation, lose around 40% body mass around day 70. In catabolic state (increase metabolic rate), weight loss most rapid, usually around 20 days so must be aware as short window to turn around metabolism and deaccelerate weight loss
Nutritional objectives in trauma
prevent/correct deteriorations in nutritional status
preserve as many organs and bodily functions as possible
promote wound healing- enough protein and energy to heal
reduce the risk of post operative complications- malnutrition can increase complications and decrease wound healing
around 40% medical or surgical patients are malnourished upon admission
Metabolic and physiological changes after surgery
'Ebb and Flow' stress response outdated: Ebb starts post-trauma with decreased HR, metabolism, oedematous limbs (salt/fluid shifts)
Stress or trauma
Nitrogen losses in trauma
Stress or trauma neuroendocrine factors: this results in net protein loss, increased EE, hyperglycaemia, elevated NEFA, increased RQ led by neuroendocrine factors. FASTING further accelerates this / NOT MEETING NUTRIENT REQUIREREMENTS
Stress/trauma -> triggers 'fight or flight' -> digestion stopped -> glycogen stores depleted as glucose released into body -> hypothalamus triggers SNS which increases catecholamines secretion and stimulates renin secretion from kidneys (adolsterone release from kidneys and salt retention) ADH from kidneys so watee rretention after surgery also
post-operative ileus chnaces increased if eat before surgery as surgery stops digestion
Neuroendocrine pathway
Rise in catecholamines secretion = MR increased by 15% (increased NEFA/TAG cycling, glucose products, lactate produced by glucose in wound and taken to liver to be converted to glucose / cory cycle,
Growth hormones = stimulate protein synthesis/ inhibit breakdown. GH mediates action through IGF1.
Hormones released from pituitary like cortisol (max. reached within 4/6 hours)= promotes protein breakdown+ GNG in liver, glycogenolysis, glucose stopped from entering cells resulting in hyperglycaemia , promotes lipolysis, anti-inflammatory
Surgery= insulin drop during surgery and anaesthesia, glucagon transient increase but not major cause of hyperglycaemia, insulin resistance related to magnitude of surgery e.g. major surgery / open surgery under anaesthetic for long time vs smaller laparoscopic. Thyroid hormones increase following surgery but return to normal after 2/3 days
('Flow' phase) After surgery, RMR will rise then fall between 10-20 day mark and highest in major burn, then major trauma/surgery with illness and then major uncomplicated surgery
ADH and aldosterone on kidney causing salt/ water retention
Immunological/haematological response
IL-1, TNF, IL-6 production high = metabolic effect (fever),
cytokines and acute-phase proteins released after surgery
Acute phase proteins in inflammatory state increase/ decrease around 25%. E.g. CRP (positive effect, rises) but Albumin (negative effect, lowers)
Glutamine and alanine released by muscle and provide energy for gut, immune cells and GNG and help produce APR proteins in liver
Changes in liver protein synthesis, all up or down by 25% to try and heal body and protect tissue= CRP (removes antigens from host, activates immune response), Alpha 1 and 2 inhibiting iimmun response
Nutritional implications of inflammation: fever resulting in increased EE, increase in APP and this synthesis will cause protein breakdown to supply the amino acids. Zn, glycine, serine, cysteine changes. zinc drops as delivered to liver and immune cells. Free radical production with vits E, c, B2 glycine, sulphur aa (cysteine), selenium. Vit E to maintain cell membranes as break down free radical rxns which would unsaturated PUFAs in membranes. Iron is potent free radical catalyst (ferritin increase but transferrin decreases in inflammatory response as free iron can cause damage). Glutamine is fuel for immune cells.
Net nitrogen excretion during trauma/ net breakdown of protein: rise in nitrogen excretion then drops. Most significant and delayed in major burn, major trauma/surgery with illness, major uncomplicated surgery then starvation (drops below 10g/day)
In sepsis or injury, burns= 2/3 fold increase in AA from muscle (alanine and glutamine) which needed for APR proteins, leucocytes and proteins for wound healing and to turn into glucose for glucose dependent tissues
uncomplicated injury (50-80 g N lost), ileus/malabsoprtion (150g N lost), severe injury (300-500g N lost). For every g N lost, around 26-35g muscle tissue= need to reduce surgery complications. Severe burns/ surgery around 9kg muscle lost.
Muscle wasting in multi-organ failure- as stay increase, decrease in muscle depth
Chnages in Nitrogen 
Normal individuals- maintain nitrogen balance at 0.75g/kg (0.12gN)
Severe injury or sepsis (trauma/surgery)- 1.6g/kg (0.25gN) to reduce -ve balance but no further benefit after 0.2g N per kg so don't overfeed giving burden to liver.
1.2g-1.5g/kg (PENG) for trauma or burns. Once no longer catabolic, will respond respond to N intake progressively
Glutamine
Essential and most abudant AA, produced by muscle and transports N around body. Levels drop around 50% during trauma/surgery
May help reduce bacterial translocation, preserve tissues and metabolic function in stress , antioxidant, anti-inflammatory
Mixed evidence for effectiveness of additional feeding during trauma or stress:
Increased mortality found in one study due to infection complications from IV feeding
Nutritional requirements / summary
disease= activity reduces, BMR and stress increases and DIT stays similar
Energy requirements- PENG 2019 post trauma
Metabolic changes with increased level of trauma, sepsis and burns
If no guidelines, no more than 30kcals/kg but usually 25kcals/kg. If somebody is clinically unwell, less is better
Overfeeding issues= can overfeed (>25kcals/kg)and result in fat deposits in liver, glucose can increase respiratory load and hyperglycaemia can cause bacterial infections. Too much B12 can result in neuromuscular issues and memory loss
Identifying metabolic stress- see PENG 2019 page on determining metabolic status
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SUMMARY: Neuro-edocrine and immune-cytokine response based on hormones and inflammatory cytokines and aim is to not overfeed whilst in stress response. Malnutrition will cause impaired immune function which will increase APP during infection which will increase malnutrition
pre-operative nutrition/ feeding for all surgical patients malnourished (NICE 1.3.1, 1.7.1) + ERAS (enhanced recovery after surgery) post surgery