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Nutrition for the

critical ill

報告者:魏賓慧
94.3.10
Outline
 The stress response and the role of
nutrition in the critically ill patient
 Nutritional Requirements
 Factors affecting digestion and
absorption in the critically ill
Metabolic response during stress
Organ Response

liver  glucose production , AA uptake ,


acute-phase protein synthesis
trace metal sequestration
Central nervous Anorexia , fever
system
Circulation  Glucose , TG ,urea  AA, iron, zinc
Skeletal muscle  AA efflux (especially glutamine)
leading to loss of muscle mass
Intestine  AA uptake from both luminal and circula
ting sources , leading to mucosal atrophy

Endocrine  ACTH, cortisol , GH, epinephrine , norepi


nephrine , glucagon , insulin
Catabolic hormones-1

 Catecholamines (epinephrine and norepin


ephrine)
(1) stimulate glycogenolysis and glucone
ogenesis in the liver
(2) promote skeletal muscle catabolism (pr
oteolysis)
(3) stimulate lipolysis
(4) inhibit insulin secretion and glucose u
ptake by the tissues
Catabolic hormones-2
 Glucocorticoids (cortisol)
- release from the adrenal cortex in response to sti
mulation by ACTH (adrenocorticotropic hormone)
(1) stimulate lipolysis
(2) promote skeletal muscle catabolism (proteolysis)
(3) stimulate gluconeogenesis (hepatic use of AA)
(4) decreased tubular resorption of AA
(5) inhibit protein synthesis
(6) inhibit insulin secretion
(7) promote glucagon secretion
Catabolic hormones-3
 Glucagon
(1) stimulates gluconeogenesis and glycog
enolysis
(2) promotes lipolysis and proteolysis

* A reduced molar insulin-to-glucagon ratio


favors gluconeogenesis, which in turn res
ults in proteolysis.
Cytokine –
Interleukins(IL-1,IL-6) , tumor necrosis factor (TNF)

 Released by phagocytic cells in response to tissue d


amage, infection, inflammation, drugs , chemicals.
 Cytokines result in metablic effects
* stimulate hepatic AA uptake (protein synthesis)
* accelerate muscle breakdown
* increased nitrogen excretion
* increase leukocyte count
* anorexia
* fever
* redistribution of plasma trace minerals
Stress response-1
 Metabolic feature
increased O2 consumption
increased core temperature
increase nitrogen excretion
(correlates with severity of stress)
(reflect the skeletal muscle
breakdown)
Acute phase response Stress response-2

1. Increase plasma counterregulatory hormones-cat


echolamines , glucocortocoid, glucagon, GH, cyto
kines

2. Hyperglycemia
> increase insulin (but tissue insulin resistance)
> increase catabolic and anabolic

3. No adaptation to starvation
> Glucose is the major fuel used by injured tissu
e and the cells involved in repair and immune pro
cesses in the stressed patient.
Stress response-3
 Hypoalbiminemia is a better marker of s
everity of injury than nutritional status i
n the critically ill patient.
(1) reduce liver albumin synthesis
(2) promote increased production of acu
te phase protein (CRP, fibrinogen , cerul
oplamin)
Stress response-4
 Decrease serum iron and zinc
(1) due to uptake in the liver , rather than tru
e deficiency
(2) accelerate urinary zinc excretion
(3) supplement: is controversial

 Increase Cu :
as a result of increased production of acute
phase protein ceruloplasmin(Cu-binding prot
ein)
Starvation
 Insulin decrease as the stimulus for its secr
etion is reduced.
 Counterrgulatory hormones
(cortisol and glucagon) increase relative f
or the mobilization of endogenous energy an
d protein stores.
Meet the requirement for Glucose
 Glycongenlysis (liver, skeletal muscle) –
stores are depleted in less than 24 hrs of fasting.
 Glucogenesis:
skeletal muscle protein breakdown
AA convert to glucose in the liver
(approximately 75 g protein/day are used )
 Adaptive mechanism in prolonged starvation
(about 1 week)
(1) brain: use ketone body as energy source
reduce protein catabolism since the need
for glucose is reduced.
(approximately 20 g protein/day are used )
(2) lower metabolic rate
decrease muscle activity, increase sleep
decrease internal body temperature.
Starvation versus stress
Nutritional Requirements

Avoid overfeeding
Energy Requirements

Protein Requirements

CHO Requirements
Vitamins and Minerals

Energy and protein requirements in specific Disease states

Specialist feeds for the critically ill


Avoid overfeeding
 Nutritional support purpose in the critically
ill- maintenance rather than repletion.
 Respiratory quotient (RQ)
CHO  1
Fat  0.7
Protein (PT)  0.81
Alcohol  0.67
 An RQ of 0.85 indicates that equal amounts of
protein, fat and CHO are be metabolized.
 Excess CHO will cause
(1) Steatosis of the liver
Glucose  glycogen
(stores are replete ,about 400 g)
Glucose  fat ( lipogenesis , CO2 production )
(2) hyperglycemia
– exacerbated by insulin resistance
(3) delayed weaning off the ventilator
 Excess fat provided as > 50 % of total calories
(1) overload the reticulo-endothelial system (RES)
TG  glycerol + free fatty acids
reduce RES clearance
(2) impair alveolar gas exchange

 Excess protein
increase the rate of PT synthesis and breakdown
with no improvement in overall balance
Energy Requirements
 TEE (total energy expenditure)
(1) BMR (basal metabolic rate)
(2) The effect of activity
> minimal effect in the critical ill p’t
> except self-ventilating , tachypnoea ,
severely agitated.
> muscular paralysis decrease energy requirem
ent as much as 30% , even in sepsis.
( 3) Thermic effects of food or postprandial thermog
enesis
> 10 % for a mixed diet
> neglible in TPN used
Predictive Equations
 Harris-Benedict equation (SF :1.3)
 New DRI equation
 Schofield(1985) + the Elia nomogram (199
0) (ref 2)

 Additional factors for weight increase and act


ivity should NOT be included until convalesc
ence on a general wards.
 The critical ill p’t cannot use excess energy f
or wt gain.
 Inactive p’ts will use excess energy for fat de
position.
Calculation based on BW
 25-35 kcal / kg appropriate BW (ref1)
(1) 25-30 kcal / kg
(well-nourished , elective operation)
(2) 35 kcal / kg
(multiple trauma)
 25-35 kcal / kg actual BW (ref 2)
(1) 30 –35 kcal /kg (septic and SIRS)
(2) 25 –30 kcal /kg (non-septic and SIRS)
 ABW (adjusted BW) =
(acutual BW - IBW * 0.25 ) + IBW
 Cachetic, marasmic
 actual BW to assess needs
Protein Requirements

 1.2 –2 g protein /kg BW


(generally guideline)

 Kcal : N ratio
300: 1 (healthy adults)
150: 1 (moderate stress)
80 –100 : 1 (severe stress)
Protein Requirements
UUN(urine urea nitrogen ) (ref 3)
> Assess the degree of hypermetabolism (stress)
UUN : 0 – 5 no tress
UUN : 5 – 10 mild hypermetabolism/level 1 stress
UUN : 10 –15 moderate hypermetabolism/level 2 stress
UUN : > 15 severe hypermetabolism/level 2 stress
> Estimate protein requirement (ref 1)
UUN : 10 (1.2 –1.3 g protein/ kg BW)
UUN : 25 (2 g protein/ kg BW) (Kcal :N ratio :90:1 )
> If N excretion exceeds the protein equivalent of approxim
ately 2 g/kg , higher protein intakes will not likely promote
better nitrogen retention,but will instead drive ureagenesis.
Estimation of nitrogen requirements
per kg actual BW/day (Elia,1990) (ref 2)

Nitrogen ( protein )
 Normal 0.17g (1.0625 g )
 Hypermetabolic 5-25 % 0.2 g (1.25 g )
25 –50% 0.25 g (1.5625g )
> 50 % 0.3 g (1.875 g )

 Note: The maximum amount of nitrogen that


can be metabolized by any individual is 18 g /
day (112.5 g protein).
CHO Requirements
 The amount of CHO is related to the amount that
can be oxidized by the liver.
 60 –70 % of energy
 Parenteral nutrition
Maximum rate of glucose oxidation :
5 –7 mg /kg BW / min , 7.2 g / kg BW / day
General level : 2-5 mg /kg BW/ min
or 3-7 g CHO /kg BW/day
 Increased levels of hepatic fat deposition and in
creased CO2 production at the higher infusion ra
te.
 Blood glucose goal : 200 mg/dl (ASPEN, 2002)
Fat Requirements
 15 –40 % of energy
 Absorption of fat-soluble vitamins requires 15-25 g fat
 Prevent EFA deficiency : 2 – 4 % (ref 1) of TER as fat
3 - 4.5% (ref 2)
 For critically ill p’t ,requirements are 0.8 –1 g /kg BW/da
y
 Three characteristics as an energy source
1. concentrated
2. isotonic (toleration of tube feedings,particularly into
the lower duodenum or jejunum)
3. nonglucose
( in limiting the amount of insulin)
(substituting fat for CHO is helpful in limiting CO2 pro
duction for weaning ventilator )
Vitamins and Minerals
 No specific guideline. Based on the recommended
dietary allowances (RDA) – provide the basic guideline
for clinical use.
 Notice :

> increased need of B complex (thiamin , niacin) with


increased calories
> increased need of K , Mg , P , Zn with
catabolism and loss

 American Medical Association recommendations are


frequently used for patients receiving TPN.
 Vit A 3300 IU  Vit B6 4 mg
 Vit D 200 IU  Vit B12 5 mcg
 VitE 10 IU  Pantothenic acid 15 mg
 Vit C 100 mg  Biotin 60 mcg
 Folacin 400 mcg  Copper 0.5-1.5 mg
 Niacin 40 mg  Chromium 10-15 mcg
 Riboflavin 3.6 mg  Manganese 0.15-0.8 mg
 Thiamin 3 mg  Zinc 2.5 - 4 mg

•Additional amount of zinc are recommended for the following conditions:


1. large losses of small bowel fluids, add 12.2 mg /L of fluid output
2. large stool or ileistomy output , add 17.1 mg/kg of stool or ileostomy drai
nage
Energy and protein requirements
in specific Disease states
•Liver Disease
Clinical condition Energy Protein
(kcal/kg/day (g/kg/day)
)
Compensated 30-40 1-1.2
cirrhosis
Complications,inade 40-45 1.5
quate intake,
malnutrition
Encephalopathy 30-40 Transiently 0.5,
grade I-II then 1-1.5
Encephalopathy 30-40 0.5-1.2
grade III-IV
XVIII ESPEN Consensus Conference on Nutrition and Liver Disease,September 1996.
BCAA (valine,leucine,isoleucine)
be useful in chronic liver Dx
 Plasma and brain accumulation of AAAs may ca
use severe impairment of brain neurotransmitter
synthesis, which causes hepatic encephalopath
y.
 BCAA compete with AAA for blood-brain transp
ort to reverse the coma.
 Long- term use
cause a reduction in tyrosine and cysteine level
a reduction in nitrogen balance

 AAAs(aromatic AA):
phenylalanine, tyrosine, tryptophan
•Renal Disease
Therapy Energy Protein
(kcal/kg/day (g/kg/day
) )
Continuous haemofiltration 30-35 1 – 1.2
/
diafiltration dialysis
Intermittent haemodialysis 30-35 1 – 1.2
haemofiltration/diafiltration
Non-dialysed/filtered 30-35 0.55 – 0.6
(residual renal function, minima
BW: actuall catabolism
BW
HI (head injury)
 Elevated BMR in acute HI can be as high as 40% , an
d last up to 2 weeks postinjury.
> 40% greater than predicted by HB equation .
> GCS:4-5 , have the highest EE
> Braindead p’t, using sedatives, barbiturates, musc
uloskeletal blocking agents : lower than predicted EE
,about < 14 %.
 combine pro-kinetic agents (metoclopramide, cisaprid
e) to offset the delayed gastric emptying which is a co
nsequence of the altered neurological state.
 1.5-2.5 g (2.2 g ,ref 3) protein / kg actual BW /day
 20 –30 % increase in energy above BMR using formula
. (ref2)
 HB equation , SF : 1.4 (ref 3)
Morbidity obese
 High protein, hypocaloric feedings

> Nonprotein calories :70-90 %of TER


> 1.5-2 g protein / kg adjusted BW or IBW
Specialist feeds for the critically ill

 Glutamine
 Arginine
 Nucleotides
 W-3 fatty acids
 MCT (medium chain triglyceride)
 Structured lipids
 SCFA
 Antioxidant
Glutamine (GLN)
 Conditional EAA (after trauma , stress )
 Normal intake : 4-5 g /day
 The most abundant free AA in the blood and AA pool
 Net catabolism of skeletal muscle : supply GLN
 Function :
> The principle fuel for rapidly dividing cells of the s
mall intestine and immune system e.g. enterocytes , l
ymphocytes. ( as a fuel by the gut in the criticall ill).
> A trophic factor to maintain of the gut mucosa
> A precusor of nucleotides , I.e. DNA and RNA
Arginine
 EAA for growth
 Normal intake : 5.4 g L-arginine /day (average )
 Conditional EAA (an immunomodulating effect in the cri
tically ill to support the immune response)
 Function :
> A precursor for nitric oxide production
( NO has been implicated in a wide range of immunolo
gical and vasoactive functions)
> As a substrate for cytoplasmic and nuclear protein sy
nthesis.
> It is essential for ammonia detoxification by urea synt
hesis.
 Clinical evidence: improve nitrogen balance ,wound hea
ling , stimulate the T-cell response , reduce infection We
stern diet
Nucleotides
 Function :
> A precursor of DNA and RNA
* Dietary RNA may be necessary to maintain the
immune response in the critically ill
. > Increase protein synthesis
> Involved in the regulation of several T-cell-mediated
immune responses.
* Rapidly dividing cells , e.g. T-lymphocytes and
intestinal epithelial cells, have a limited ability to
synthesize nucleotides during malnutrition and
inflammation.
  indicates supplementation in stress
 There was as yet little evidence to support the use of
RNA supplementation in the prevention of infections in
the critically ill.
W-3 FA
 The ratio of W-3 FA / W-6 FA can alter the types
of eicosanoids produced by cells as part of the i
mmune response.
 Function :

> Blocks production of the prostglandin PG2.


> Reduce thromboxane
(thromboxane is an eicosanoid which plays an im
portant role in the maintenance of vascular tone,
and in platelet aggregation)
 Clinical evidence:not all shown benefits

In most of animals study


W-3 FA
 Advantage:
1. decrease immunosuppression
2. decrease platelet aggregation
 complication:

1.compromised host defence


2. increase bleeding time
3. increase lipid peroxidation
4. increase free radicals
MCT
 Advantage
1. rapid clearance from the blood
(reduce hyperlipidemia and hepatic steatosis)
2. rapid , complete oxidation
3. digestion and absorption without bile and pancr
eatic lipase
4. relative carnitine independence
5. Less impairment of the RES if supplied IV
(due to minimal uptake by RES )
 Disadvantage:
1. NO EFA
2. be ketogenic
 Source: coconut oil , palm kernel oil
Structured TG
 composed of both long chain and medium
chain TG
SCFA(short-chain FA)
 Butyrate , acetate, propionate
 Benefit
(1) increase colonic blood flow
(2) promot salt and water absorption
(3) stimulate mucosal proliferation
Antioxidants
 Beta-carotene, Vit C,Vit E, Selenium
 Influence the oxidative modification of

lipoprotein in the arterial wall, and can prevent t


he harmful effects of the free radical chain re
actions
 There have been no studies to support the su
pplementation of antioxidants in the critically i
ll.
The role of the gut
 Three function of the gut
1. Digestion and absorption
2. Act as a physical barrier to organisms
3. Immune function
Factors affecting digestion in
the critically ill
 NPO
> brush-border Enz secreted by the epithelial cell
s are induced by the presence of luminal nutrient
s.
 Malnutrition
> leads to digestive enzyme deficiency
 Disaccharidase (lactase,sucrase,maltase)deficie
ncy

 Pancreatic insufficiency , Infection, gut atrophy a


nd mucosal damage,diminished mucus secretion
and atrophy of enterocytes
Factors affecting absorption in
the critically ill
 Intestinal villous atrophy(caused by PT malnutrition, lack of
enteral feeding , ischemia) reduce absorptive surface area
 Digestive Enz deficiency related to malnutrition
 High rate of intestinal transit (caused by organ dysfunction,
drugs)
*drugs : inotropes , antibiotics(erythromycin), gut motility sti
mulants (metaclopromide, cisapride)
 Delayed gastric emptying
 Reduce secretion of gastric acid
 Bacteral overgrowth following bowel stasis

 bacterial modification of bile acids and deactivation of m


ucosal digestive Enz
 Pseudomenbranous colitis (caused by antibiotics usage)
Factors affecting gastric
emptying
 Factors which reduce emptying
hyperosmolality of feed
high fat content
high fiber content
critical illness
acidic duodenal pH
Motility-depressant drugs, e.g. opiates, sedatives
 Factors which increase emptying
Motility-stimulating drugs, e.g.
erythromycin,cisapride,domperidone
Fluid contents
Reference
1.Nutrition for the Critically Ill. Second Edition.1998 Wolf Rinke As
sociates, INC. Tricia Brusco, Dawn Carlson.
(All rights reserved for this self-directed,accredited learning pro
gram)
2. Nutrition for the Critically Ill. A practical handbook.published in
1998 by Arnold. Alexa Scott, Serena Skerratt and Sheila Adam.
3. Krause’s Food ,Nutrition and Dietary Therapy . 11th edition.
chapter 42. P.1059-1071

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