Nutrition in Intensive Care Flashcards
Stages in critical illness
1- Primary insult (surgery, trauma, burns, acute pancreatitis, IBD)
2- Hypermetabolic inflammatory catabolic state (hyper-metabolism, anorexia, neuroendocrine/cytokin mediated)
3- Sepsis, Recovery or Death
Responses to critical illness
Failure of adaptation
Response to critical illness: Simple fasting
Glycogen and protein mobilized–> provide glucose
Ketogenesis and ketosis increase, glucose needs fall
Metabolic rate slows
Energy needs fall
Protein and Energy conservation
End result of simple fasting
Protein and energy conservation
Response to critical illness: Severe stress
Glycogen & Prot mobilized for glucose and acute phase prots
Less or no ketogenesis and ketosis–> gluconeogensis from prot remains high
Metabolic rate rises
Energy needs increase
Accelerated protein and energy depletion
End result of severe stress
Accelerated protein and energy depletion
Systemic Increases in the hyper-metabolic state of critical illness
Metabolic rate Body Temp Water retention Cardiac output Blood volume Tissue perfusion Free radical production NO production
Skeletal Muscle Increases in the hyper-metabolic state of critical illness
Net proteolysis
Amino acid oxidation
Liver Increases in the hyper-metabolic state of critical illness
AA oxidation/N excretion
Acute phase prot synthesis
Gbuconeogensis
Cori cycle
Adipose Increases in the hyper-metabolic state of critical illness
Lipolysis/TG turnover
Reduction during the hyper metabolic state of critical illness
Plasma albumin
Plasma IGF-1
SIRS/hyper-inflammation of the hyper metabolic state
SIRS= systemic inflammatory response syndrome. Triggered by the injury, and activates CARS/immunosuppression, and leads to sepsis
- CARS: Compensatory, Anti-inflammatory Response syndrome. Can increase SIRS or lead to Sepsis - Sepsis--> severe sepsis and MOF--> septic shock
Septic shock
has 40-80% risk of mortality.
Metabolic acidosis and HoTN
Immune-cytokine response to stress
Stress--> local rxns--> imunno-cytokine response of pro-inflame mediators: TNFa IL-1 IL-6 IL-8 PGE2 NO ROS These all lead to SIRS
Endocrine response to stress
Stress–>local rxns–>
Increased catabolic hormones: E, glucagon, cortisol, GH
Reduced anabolic hormones: IGF1, T3. Insulin-Resistance.
Leads to SIRS
Immunosuppression in trauma
Excess anti-inflam cytokines
Suppressed HLA expression and Ag presentation
Suppressed T-cell fxn
Chemical intestinal barriers
Gastric acidity Salivary lysozyme Lactoferrin Mucus secretion Bile salts
Inflammatory responses activated by compromised intestinal barrier
Complement activation: C3a, C3b, C3c, C3d
Decreased splanchnic blood flow
MOF/dysfxn
Cytokine release: IL-1, IL-6, TNF, PAF
Release of arachidonic acid metals PGE2, TXs, LKs
Acute-phase protein release
EN v. TPN
EN is better than TPN
TPN increases the risk of infectious complications.
Either though reduce mortality by 70% in ICU pts.
Bowel rest (delayed EN) increased risk of systemic infection by 66%
Why EN is needed?
enteral energy will stimulate CCK/gut trophic factors and maintain the immune fxn of the gut. TPN cannot do this, but can only provide energy.
Aims of artificial nutrition
Maintain/restore body composition- with nutritionally rational and balanced intakes
To maintain/restore/modulate cell and organ fxn with us of specific AAs, antioxidants, micronutrients, and specific polyunsaturated FAs.Immunonutrition to optimize outcome
Feeding objectives
3 options:
1- Minimization of losses (severely ill ICU pts)- provide as much E as is safe, prob TEE
Refeeding syndrome
Metabolic complications of over feeding
Total Energy Expenditure
TEE = BMR x Physical Activity Level
