Sepsis/Critical Illness Flashcards
Define SEPSIS
Life threatening organ dysfunction d/t dysregulated host response to infection (systemic response to infection)
Presence of an infectious source accompanied by SIRS (fever, tachycardia, tachypnea, organ dysfunction)
How should EN be initiated in the initial phase of sepsis?
ASPEN/SCCM recommends trophic feeding (10-20 kcal/h or 500 kcal/d) for initial phase of sepsis, advancing as tolerated after 24-48 hours to > 80% of target energy goal over first week
Define SEPTIC SHOCK
Subset of sepsis, associated with hemodynamic instability
Refractory hypotension (hypotension addressed, but persists, still requiring vasopressors)
Systolic (top #) peak pressures < 90 mm Hg, MAP <65 mm Hg, or drop >40 mm from baseline
Increased circulatory, cellular and metabolic abnormalities
Greater risk of mortality than with sepsis alone
What is the body’s initial response to sepsis?
The initial septic response is proinflammatory; this is immediately followed by a compensatory anti-inflammatory response
Metabolic Response to Sepsis
↑ Energy expenditure, protein catabolism, oxidation of stored lipids, altered CHO metabolism (hyperglycemia as result of endogenous glucose production, decreased glucose uptake and insulin resistance)
Cellular activation of macrophages, monocytes, neutrophils
Initial response is pro-inflammatory, followed by a compensatory anti-inflammatory response
Nutrition therapy can help modulate inflammatory response, maintain immune function, stop skeletal muscle catabolism, improved wound healing, maintain GI & pulmonary mucosal barrier function
GI tract and liver susceptible to ischemia secondary to shunting of blood flow away for the splanchnic bed
GUT ISCHEMIA leads to mitochondrial dysfunction, mucosal acidosis, cell injury and death
Carbohydrate Metabolism During Sepsis
Release of catabolic hormones (glucagon, catecholamines, cortisol) which stimulate glycogenolysis and gluconeogenesis to mobilize glucose (Glycogen stores depleted in hours)
Endogenous lipid and protein major source of energy
Gluconeogenic precursors (lactate, pyruvate, alanine and glycerol) increases
Protein Metabolism During Sepsis
Increased muscle protein breakdown, lower AA uptake by muscle
Remain in net-negative nitrogen balance
Synthesis rates of creatinine, uric acid and ammonia ↑
Hepatic uptake of AA and hepatic protein synthesis increases(substrate for gluconeogenesis & acute phase proteins)
Synthesis of negative acute phase proteins (albumin, prealbumin) decreases
Patients who receive adequate exogenous AA are more likely to survive (produce acute phase proteins)
Up to 250 g of LBM/day broken down in the Unfed, stressed patient
Prolonged catabolism of skeletal muscle protein compromises what?
Respiratory function
Wound healing
Weakened immune system
Accelerates loss of strength/ endurance
Increase vent dependent time/ ICU stay
Risk of thromboembolic disease
Recovery time/mortality
Lipid Metabolism During Sepsis
Catabolic hormones (epinephrine, norepinephrine, glucagon) increase stimulating lipolysis (via lipase), which is the breakdown of stored TG to glycerol/FFA’s
LCFA transportation from cytosol to mitochondria via acylcarnitine impaired leading to intracellular acidosis and accumulation of lactate and pyruvate which leads to decrease aerobic respiration and ability to use Kreb cycle for energy
Increased levels of hyperglycemia, HLD, hyperlactemia, high levels of B-hydroxybutyrate d/t suppressed conversion of TG to FFA’s (impairs ketogenesis)
Nutrition Assessment in Sepsis/ Critical Care
Evaluate weight loss, nutrition hx, disease severity, GI fxn and ongoing review of current physical/ metabolic status (absence of validated tools in this population)
Energy/Protein Needs for Septic Patients
Resting energy expenditure increases over first 7 days and up to 21 days
Mitochondrial energy utilization decreases in early stages of sepsis
Pts w/ negative total energy balance have worse outcomes at 1 week
EN preferred route of nutrition delivery and use of anti-inflammatory lipids (EPA/DHA) can attenuate catabolic response to stress (supply of substrate for acute phase protein synthesis) and improve recovery in critical illness
What are the recommended kcal/protein needs for septic patients
Trophic feeding (10-20 ml/ ~ 500 kcal) during first 24-48 hrs once pt is hemodynamically stable, adv as tolerated >80% of EEN by 1st week
Kcals: 20-30 kcal/kg (excluding morbidly obese)
Protein: 1.5-2.0 g/kg and possibly as high as 2.5 g/kg/d
Higher in patients with excessive nitrogen losses (burns, open wounds)
Use of Exogenous Lipids as Fuel Source During Sepsis
Energy dense (9 kcal/g), delivering more energy in less volume (advantageous for fluid-restricted pts)
Respiratory quotient is lower for lipids compared to CHO (.7 vs 1.0)
Produces less carbon dioxide
ILEs should not exceed 1.0 g/kg/d if soybean oil is the source
A mixture of lipid fuels including omega-3 and omega-6 sources more beneficial
Smoflipid emulsions have 30% soybean, 30% MCTs, 25% olive oil and 15% fish oil
MCTs don’t require Carnitine to transport into mitochondria
Beneficial effects when omega-3 FAs are delivered as fish oil (DHA/EPA)
Benefits of EN Support
Maintain mucosal integrity and metabolic response
Improved visceral blood flow and enhance perfusion
Support GALT (gut-associated lymphoid tissue)
What steps can be taken to maximize gut function in sepsis/inflammatory states
Maintain visceral perfusion thru adequate resuscitation
Glycemic control
Correction of acidosis and electrolyte imbalances
Minimize use of anticholinergic medications, narcotics, meds that decrease intestinal motility
Initiate trickle feed of EN within 24-48 hrs of SIRS or sepsis
Anticholinergic meds block/inhibit the NT Acetylcholine in CNS/PNS
