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inflammatory response
cellular response to stress/injury - usually reversible, extreme/ongoing/ apoptotic at times (nutrition support is crucial)
nutrition on critical illness can impact
metabolic response, prevent oxidative damage, modulate immune response, reduce disease severity, diminish complications
how is good nutrition support achieved
early EN or EEN, meticulous glycemic control, apposite macro- and micronutrient delivery
malnutrition develops when
inadequate supply of nutrients (starvation), body cannot utilize nutrients, needs are higher so they aren’t met (metabolic stress)
metabolic stress does not equal
starvation - body does not react the same way (no adaptation occurs)
types of malnutrition
starvation related, chronic disease related, acute disease or injury related malnutrition
starvation related malnutrition
pure chronic starvation eg anorexia nervosa
chronic disease related malnutrition
organ failure, pancreatic cancer, sarcopenic obesity etc
acute disease or injury related malnutrition
major infection, burns, trauma, closed head injury
traumatic injury
leading cause of death in people 1-46yo and 3rd leading in all age groups
metabolic response to stress
can be from any traumatic event from surgery to sepsis - it is a response to the presence of injured tissue, driven by catabolic hormones and inflammatory markers (degree correlates with severity of injury)
metabolic consequences of stress include
hormone release, acute phase protein synthesis, hypermetabolism, increased reliance on gluconeogenesis, shift in fluid balance, decreased urine output (body’s net goal is higher O2 supply and availability of substrate to active tissue)
phases of stress response
ebb phase and flow phasee
ebb phase
initial 2-48 hours post stress (metabolic shock)
low BP, cardiac o/p, UOP, temp, O2 consumption, tissue perfusion, and normal/depressed metabolic rate (ALL LOW)
risk of: hypovolemia, hypoperfusion, and lactic acidosis
goal of ebb phase treatment
stop bleeding, restore blood flow to organs, and maintain oxygenation of tissuesf
low phase
up to 7 days or more - hypermetabolism and catabolism
altered immune and hormonal response, acutely liver priority changes from transport proteins to acute phase proteins
substrates are provided, but poor utilization
negative N balance and loss of LBM
important note of flow phase
markers such as prealbumin may not respond to nutrition support
catecholamines
stimulate glycogenolysis (epinephrine and norepinephrine)
aldosterone
retain Na`
cortisol
raises gluconeogenesis, free fatty acid mobilization, protein catabolismg
glucagon
stimulate gluconeogenesis (this and cortisol drive hyperglycemia)
cytokines
proinflammatory proteins released by macrophages in response to shock (interleukin, tumor necrosis factor, c reactive proteins)
acute phase proteins
acute phase proteins
immunoglobulins, fibrinogen, clotting factors, complement proteins
sepsis
uncontrolled inflammatory response to infection or trauma
systemic inflammatory response syndrome (SIRS)
additional classification of sepsis not necessarily caused by infection, may occur after surgery or trauma such as myocardial infarction
characteristics of sepsis and SIRS
increased WBC, heart rate, respiratory rate, fever or hypothermia — abnormal organ function and hemodynamic instability
medical management of sepsis and SIRS
interventions appropriate for underlying cause eg lung protective ventilation, antibiotics, continuous RRT, glycemic control, etc
why is nutrition support critical
modulates inflammation, spares LBM, supports immune response, supports wound healing, maintains GI and pulmonary mucosal barriers to bacteria
when should EEN be sarted
24-48 hours after admission
MNT goals for trauma
meet energy needs and protein without over or underfeeding
support processes of hypermetabolism and hypercatabolism
is weight gain/loss an objective for an MNT in trauma
NO - overfeeding is detrimental causes retentions, hyperglycemia, hepatic steatosis, and immune dysfunction
nutrition screening in the ICU
screen all patients for nutrition risk using the NRS 2002 NUTRIC screening tools - specific to ICU because they consider inflammation and severity
NUTRIC scoring is different because
it has bases on age (older higher risk), measure organ function, electrolytes, acid/base, and neurological status, and IL-6 measurement for current inflamamtion
some nutrition diagnoses in critical care may include
increased energy expenditure, increased nutrient needs, inadequate protein-energy intake, altered GI function, and impaired nutrient utilization
best way to establish energy needs
indirect calorimetry, but not always available (because VO2 and VCO2 is proportional to energy expenditure)/substrate utilization
respiratory quotient
the ratio of CO2 produced to O2 consumed (VCO2/VO2)
indicator of substrate utilization, accompanies an IC reading on metabolic cart, and helps determine over or underfeeding
<.7 = underfeeding, 0.75-0.90 = normal, >1 = overfeeding
nitrogen balance
compares urinary urea nitrogen output (UUN) with protein intake
N-balance= N intake (g) - [24hr UUN (g) +4]
+ means good, protein greater than losses
- means bad, protein less than daily losses
REMEBER* 6.25g Pro = 1g N so Pro intake(g)/6.25 = N intake (g)
in burn patient the nitrogen balance formula changes to
N balance = nitrogen intake (g) - [24hr UUN (g) +4] x 1.25
multiple measured losses by 1.25 to account for wound exudate due to burns
ASPEN guidelines for energy in critical care
BMI 20-29= 25-30kcal/kg actual weight
BMI 30-50= 11-14kcal/kg actual body weight
BMI >50= 22-25kcal/kg IBW
ASPEN protein guidelines for critical care
BMI 20-29= 1.2-2gm/kg actual weight
BMI 30-40= 2gm/kg IBW
BMI >40= 2.5gm/kg IBW
macronutrient division in critical care
determine protein requirement
provide remaining kcal with CHO and fat
CHO needs 100g/d minimum FAT should not exceed 30% of total kcal
Fluid needs
higher N regimens produce increased solute loads for kidneys so they require adequate fluid for excretion
use standard guidelines, but adjust for fever, GI losses, warm ambient temp, beds with airflow, or fluid restricted diseases
monitor urine output, serum electrolyte balance, and edema signs
fluid calculations
30-35mL/kg
1mL/kcal of enteral intake
100mL/kg for 1st 10kg, 50mL/kg for next 10kg + 25mL/kg for remaining weight
1500mL/m2 total body surface area
stressed pts may need what extra vit/min
ascorbic acid, Zn, selenium, vit E, K (or less), PO4, and Mg
thiamin, niacin, and other B vits may be needed if more aggressive
if pt at risk for aspiration or gastroparesis use what tube feed
jejunal tube - continue with trickle feedings at 10-20kcal/hr
what formulas are appropriate in most cases
standard polymeric formulas, use other disease specific only if needed - monitor glucose and avoid overfeeding
glucose goal in the ICU
140-180mg/dL
what to reserve PN for
pts NPO >7 days, malnourished pts who cannot use EN, pts who cannot meet needs EN alone, may surgery will prevent initiation of EN
arginine
vasodilator, may have increased needs during stress
glutamine
preferred energy source for enterocytes (maintains intestinal barrier), reduces cytokine levels, and may have increased needs during stress
labs headed for normal ranges during recovery phase
serum glucose, urine nitrogen losses, acute phase respondents, O2 consumption, fever and WBC count
trauma considerations for feedings
utilize EEN with a high protein polymeric formula
may benefit from volume based EN
consider an immune-modulating EN formula with arginine and omega 3s
provide 20-35 kcal/kg/d (lower in ebb, higher in flow)
when does REE peak
over 4-5 days, remains high for 9-12 days, begins to decrease after - remaining elevated for 21 days
how much protein can patients lose in 21 days
16%, 65% comes from skeletal muscle
what are burn injuries
caused by exposure to heat, chemicals, radiation, or electricity
may extend beyond skin and into muscle and bone
classified by depth and %
eschar
necrotizing tissue with appearance of dark leathery skin
TBSAB
total body surface area burned
full thickness burn
destroys epidermis and dermis
s/s black, leathery, translucent, mottled, and dry appearance
partial thickness burn
destroys superficial or deep dermis
s/s red, tender, blistered, wet, or weeping
superficial (1st degree) burns
epidermis only
heal in a few days ontheir own
partial thickness (2nd degree) burns
damage epidermis and dermis
very painful
takes weeks to heal
may require excision and debridement
full thickness (3rd degree) burns
damage the epidermis, dermis, and subcutaneous tissue, and possibly muscle and organs
loss of nerve endings so less painful
require surgical intervention eg wound debridement and grafting
functions of skin
protection from infection and injury
prevention of loss of body fluid
regulation of body temperature
sensory contact with the environment
complications of burn injuries
hypermetabolism
hypothermia
fluid loss from the wound
sepsis and infection
organ dysfunction (renal, cardio, respiratory)
electrical burn - cardiac sequela
smoke inhalation
metabolic response to ebb phase in burns
focus on fluid resuscitation and restoring organ function
flow phase metabolic response to burn
hypermetabolism can last up to 2 years
can lose up to 20% LBM in weeks post injury
focus on healing and wound closure
wound management
dressings, irrigation
debridement and grafting may be necessary in the early stages of wound care
debridement
removal of necrotic, infected, or foreign material from wound
types of debridement
surgical, mechanical, enzymatic
possible nutrition diagnoses
increased energy expenditure, increased nutrient needs, impaired nutrient utilization, altered nutrition-related lab valuesbe
best way to determine energy reqs for adults is
indirect calorimetry, but can use IBW for obesity
also curreri formula
curreri formula
kcal = (25kcal x kg usual body wt) + (40kcal x %TBSAB)
*only %TBSAB up to 50% max
*may be best during peak phase
could overfeed beyond that
determining calories for children
-indirect calorimetry is the best
< 30% TBSAB use DRI for kcal per age group
> 30% TBSAB use galveston equation
BSA
body surface area
BSAB
body surface area burned
key anabolic hormone in burns
insulin - slows gluconeogenesis and LBM catabolism
protein is best utilized when
CHO is abundant
what can build up in the liver and decrease immune function in burn victims
fats - low fat feedings are recommended
parkland formula for fluid restriction
children: 3-4ml/kg/%BSA/24 hours
adults: 4ml/kg/%BSA/24 hours
Day 1: provide ½ of calculated needs within first 8hr, then provide remaining over 16hre
electrolytes in burn pts
provided based on serum and urine data in conjunction with fluid needs
minerals and trace elements in burns pts
provide DRI
may supplement additional vit c, zn, vit e, vit a, selenium for wound healing
small bowel is tolerated better in burn pts because
ileus in burns
may use oxandrolone to help
maintain LBM and promote healing (anabolic steroid) in those with >15% TBSA
continue nutrition support in burn patient until patient can meet
>60% of nutritional needs orally
impact of surgery on nutrition
npo status
post operative ileus r/t anesthesia
poor intake r/t pain meds
hypermetabolic response to injury/stress
wound healing
surgery and malnutrition =
higher mortality and morbidity (more susceptible to infection and poor wound healing)
pre-operative nutrition support is recommended
old practice for pre op nutrition
fast for 12 hoursn
ew practic for pre op nutrition
no solids for 5 hours before
clear liquids within reason up to 2 hours beforepo
post op nutrition
early and aggressive post op nutrition is within 24 hours of sx
start high protein oral intake ASAP
if EN is needed, feed within 24 hours
consider immune enhancing formulas (supplement PN if needed)