- rest = basal metabolic rate + minimal exercise
- major stress = 50% burn
- the body’s goal is to preserve plasma glucose levels for brain metabolism.
- least expensive form of energy production utilized:
carbohydrate -> fat -> protein in decreasing ratios.
- glucose, fructose and galactose from GI tract
- gluconeogenic amino acids (alanine + others)
- glycerol from triglycerides
(1) glucose enters the cell by insulin promoted facilitated diffusion with a Na+ cotransporter
(2) phosphorylated to glucose-6-phosphate (e.g. glucokinase in the liver)
(3) forms 2 pyruvates -> transported into matrix of mitochondria
(4) converted into ACoA -> enters the Citric acid cycle -> oxidative phosphorylation
- proteins broken down to amino acids (liver)
- leucine, isoleucine, phenylalanine & tryrosine = ketogenic -> produce acetoacetate
- alanine + others are gluconeogenic
(1) triglycerides -> hydrolysed to FFAs & glycerol
(2) transported to tissues
(3) glycerol -> glycerol-3-phosphate & enters glycolytic pathway
(4) FF’s transported to mitochondria by carnitine carrier -> degraded to ACoA (beta-oxidation) -> enters the citric acid cycle.
- essential fatty acids = linolenic, linoleic & arachidonic acid
- used in the production of leukotrienes, prostaglandins, prostacyclin
- increase in basal metabolism proportional to the degree of sepsis/trauma/burn
- if metabolic needs aren’t met -> the patient will mobilize protein, fat and carbohydrate to meet metabolic demand
- most hospitalized patients require 25-30 kcal/kg/day (remember 4.18 kJ/kcal!)
- mechanically ventilated are on the lower end of range
- burns and trauma patient may require 45kcal/kg/day
- loss of whole body water and protein
- reduction in protein synthesis and increased degradation
- rapid catabolic muscle wasting -> reduction in cross-sectional area of muscle fibers
- 50% decline in respiratory and skeletal muscle function (in first 2 weeks)
- resting energy expenditure increases by 40%
- increased plasma glucose
- cytokines increase glucose membrane transporter (non-insulin mediated) -> saturate Citric acid cycle -> increase lactate production.
- catabolic state
- 60% burns doubles the resting energy expenditure
- catabolic state mediated by cortisol
- decreased protein synthesis in muscles
- protein catabolism
- increased resting energy expenditure
- increased in catabolic hormones (adrenaline & norad) -> glucose turnover increases.
- feed enterally soon if possible
- provision of high quality amino acids along with insulin
- ‘feed appropriately’
- early enteral feeding
- in absence of indirect calorimetry, use of the Toronto equation (Schofield in children) for energy requirement determination (risk of overfeeding)
- elevated protein requirements (1.5-2 g/kg in adults, 3 g/kg in children)
- maintain fat administration ≤ 30% of total energy delivery
- glucose delivery to a maximum of 55% of energy and 5 mg/kg/h associated with moderate blood glucose (target ≤ 8 mmol/l) control by means of continuous infusion
- trace element and vitamin substitution early on
- consider non-nutritional strategies to attenuate hypermetabolism by pharmacological (propranolol, oxandrolone) and physical tools (early surgery and thermo-neutral room) during the first weeks after injury
References and Links
- Rousseau AF, Losser MR, Ichai C, Berger MM. ESPEN endorsed recommendations: Nutritional therapy in major burns. Clin Nutr. 2013 Mar 14. MID: 23582468.
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of LITFL.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of two amazing children.
On Twitter, he is @precordialthump.