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Systemic Response to Injury and Metabolic Support. Aaron Lesher 9/1/09. Definitions. Infection Identifiable source of microbial insult SIRS 2 or more of the following: Temp >38 or 90 RR >20 or PaCO2 12,000 or 10% bands Sepsis - PowerPoint PPT Presentation
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Systemic Response to Injury and Metabolic Support
Aaron Lesher9/1/09
Definitions
Infection Identifiable source of microbial insult
SIRS 2 or more of the following:
Temp >38 or <36 HR > 90 RR >20 or PaCO2 <32 or mechanical ventilation WBC >12,000 or <4000 or >10% bands
Sepsis Identifiable source of infection + SIRS
Severe Sepsis Sepsis + organ dysfunction
Septic shock Sepsis + cardiovacular collapse (requiring vasopressor
support)
The Systemic Inflammatory Response Syndrome (SIRS)
CNS regulation of inflammation
Integral role in inflammatory response that is mostly involuntary
Autonomic system regulates HR, BP, RR, GI motility and temp
CNS Regulation of Inflammation
Hormonal Response to Injury
Includes: Cytokines Glucagon Insulin Epinephrine Serotonin Histamine Glucocorticoids Prostaglandins leukotrienes
ACTH
A. Is synthesized in the hypothalamus
B. Is superceeded by pain, anxiety and injury
C. Continues to be released in a circadian pattern in injured patients
D. Causes the release of mineralocorticoids from the adrenal in a circadian pattern
ACTH
Cortisol
Essential for survival during physiologic stress
Potentiates the effects of glucagon and epinephrine manifesting as hyperglycemia
In liver, stimulate gluconeogenesis Induces insulin resistance in skeletal
muscle and adipose tissue In skeletal muscle induces protein
breakdown and release of lactate Immunosuppressive agent
A primary action of aldosterone is to:
A. Convert angiotensinogen to angiotensin
B. Decrease Cl reabsorption in the renal tubule
C. Decrease K secretion in the renal tubule
D. Increase Na reabsorption in the renal tubule
E. Increase renin release by the juxtaglomerular apparatus
Catecholamine elevation after injury
A. Is limited to epinephrine only B. Is limited to norepinephrine only C. Increases by 10- to 20-fold after
injury D. Is sustained 24-48 hours before
decreasing
C-reactive protein
A. Is secreted in a circadian rhythm with higher levels in the morning
B. Increases after eating a large meal
C. Does not increase in response to stress in patients with liver failure
D. Is less sensitive than ESR as a marker of inflammation
Mediators of Inflammation
Cytokines Heat shock proteins Reactive oxygen metabolites
Reperfusion injury Eicosanoids
Includes prostaglandins, leukotrienes, thromboxane
Fatty Acid metabolites Kallikrien-Kinen system Serotonin histamine
Cytokine Response to Injury
Lots of cytokines Most potent mediators of
inflammatory response Pro- and anti-inflammatory
Cytokines….
TNF-Α one of the earliest and most potent mediators of
host response Primary source: monocytes/macrophages and T
cells Half life of 20 min but potent Many functions
IL-1 Primarily released by macrophages and endothelial
cells Half life less than 6 mins, “sneaky” Classic febrile response to injury
IL-6 Linked to hepatic acute phase proteins production
Impt Eicosanoids
Prostacyclin (PGI2) From endothelium Decreases platelet aggregation Promotes vasodilation
Thromboxane (TXA2) From platelets Increases platelet aggregation Promotes vasoconstriction
Cellular Response to Injury
Transcription factors impt in inflammatory response as they dictate the manner and magnitude with which a cell can respond to injury
Endothelium-mediated Injury
L-selectins
E- or P-selectins
Beta 2 integrins
ICAM-1,2
Activated Neutrophil
Nitric Oxide
A. Is primarily made in hepatocytes B. Has a half-life of 20-30 minutes C. Is formed from oxidation of L-
arginine D. Can increase thrombosis in small
vessels
Surgical Metabolism
Basic metabolic needs = 25 kcal/kg/day
Where do we get our caloric needs?
Fat 9 kcal/g Protein 4 kcal/g Oral carbs 4 kcal/g Dextrose (in IV
fluids) 3.4 kcal/g
Surgical MetabolismMetabolism during fasting
Starvation: fat is the main source of energy in trauma and starvation
Carbohydrates are stored in the form of glycogen (2/3 skeletal muscle, 1/3 liver)
Due to deficiency in glucose-6-phosphatase, skeletal muscle not available for systemic use and therefore, liver stores are used quickly
Gluconeogenesis
Occurs in the liver Precursors include:
Amino acids (alanine) Lactate Pyruvate Glycerol
Cori cycle In late starvation gluconeogenesis
occurs in kidney
Nitrogen wasting during (simple) starvation
Sig amounts of protein must be degraded to be used for gluconeogenesis
Urine nitrogen excretion increases from 7-10g/day to up to 30g/day
Protein degradation occurs mostly in skeletal muscles, but also some in solid organs
Nitrogen wasting during (prolonged) starvation
Systemic proteolysis decreases Urinary nitrogen approx 2-5g/day Reflects change to using ketone
bodies as energy source Brain begins to use ketones as
energy source after 2 days, and this becomes the principal energy source by 24 days
Metabolism following Injury
Fat digestion
Broken down into micelles and FFAs Micelles enter enterocytes Chylomicrons are formed which
enter thoracic duct Medium and short chain amino
acids enter portal system with amino acids and carbs
Protein Metabolism
6 g protein = 1 g N Provides substrates for
gluconeogenesis and acute phase proteins
1g protein=4kcal
Protein metabolism
Healthy patients undergoing uncomplicated surgery can remain NPO (with IVF) for how many days before significant protein catabolism occurs?
2 days 4 days 7 days 10 days
Healthy patients without malnutrition undergoing uncomplicated surgery can tolerate 10 days of partial starvation before any significant protein catabolism occurs
Nutrition facts
Albumin half life = 18 days Prealbumin = 3 days
Nutrition in the Surgical Patient
Harris-Benedict equation calculates basal energy expenditure (nutrition needs) based on weight, height, age and gender
Usually estimate 30kcal/kg/day Goals:
Provide adequate nonprotein calories to prevent lean muscle breakdown
Meet substrate requirements for protein synthesis Estimate 1.5-2 g protein/kg/day Want 100-150 calories of non protein calories for
each 1 g of nitrogen
The nutritionist in the ICU informs you that one of your intubated patients “Greuner”’s metabolic cart study has revealed a respiratory quotient of 1.2. What do you do?
A. Smile. Thank her politely for the information and run to google.com to figure out what she is talking about.
B. Ask her to decrease the daily carbohydrates that the patient is receiving.
C. Ask her to increase the carbohydrate intake. D. Do nothing, you are tired and the respiratory
quotient is not important in this patient.
Respiratory Quotient (RQ)
Ratio of CO2 produced to O2 consumed – measurement of energy expenditure
RQ>1 = lipogenesis (overfeeding) RQ<1 = ketosis and fat oxidation
(starving)
Fat RQ = 0.7 Protein RQ = 0.8 Carbohydrate RQ = 1.0
Enteral Nutrition
Does the gut work?`
Yes No
Enteral Nutrition
PO feeds?
Yes No
NGT feeds?
No
Parenteral Nutrion
Yes
Post pyloric feeds Consider G tube
Consider G-J tube
Enteral Nutrition
Intact GI tract can tolerate complex solutions
If GI tract has not been fed for a long period of time, less likely to tolerate complex carbohydrates
Results in a reduction of infectious complications in critically ill patients
Which of the following would be typical of an enteral hepatic-failure formula?
A. Lower fluid volume, K, PO4, Mag B. 50% reduction of carbs C. 50% of proteins are in the form
of branched chain amino acids (leucine, isoleucine, and valine)
D. Increased arginine, omega 3 fatty acids, and B carotene
Parenteral Nutrition
Preoperative PN has been shown to be beneficial to some surgical patients, especially in those with severe malnutrition
Postoperatively it is associated with higher risk of infectious complications when used inappropriately
Still fewer infectious risks when compared with no feeding at all
Parenteral Nutrition
TPN Dextrose concentration is high (15-
25%) macro- and micronutrients avail via this
route PPN
Reduced dextrose (5-10%) Reduced protein (3%)
Deficiencies
Chromium hyperglycemia, neuropathy
Zinc Most frequent in pt on PN Perioral rash
Copper Microcytic anemia
Thanks!
Questions?