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 stressOrgan Response

liver glucose production , AA uptake ,

acute-phase protein synthesis

trace metal sequestration

Central nervous system

Anorexia , fever

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 circulating sources , leading to mucosal atrophy

Endocrine ACTH, cortisol , GH, epinephrine , norepinephrine , glucagon , insulin

Catabolic hormones-1

Catecholamines (epinephrine and norepinephrine)

(1) stimulate glycogenolysis and gluconeogenesis in the liver

(2) promote skeletal muscle catabolism (proteolysis)

(3) stimulate lipolysis

(4) inhibit insulin secretion and glucose uptake by the tissues

Glucocorticoids (cortisol)

- release from the adrenal cortex in response to stimulation 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-2

Glucagon

(1) stimulates gluconeogenesis and glycogenolysis

(2) promotes lipolysis and proteolysis

* A reduced molar insulin-to-glucagon ratio favors gluconeogenesis, which in turn results in proteolysis.

Catabolic hormones-3

Cytokine – Interleukins(IL-1,IL-6) , tumor necrosis factor (TNF)

Released by phagocytic cells in response to tissue damage, 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 response1. Increase plasma counterregulatory hormones-ca

techolamines , glucocortocoid, glucagon, GH, cytokines

2. Hyperglycemia > increase insulin (but tissue insulin resistanc

e) > increase catabolic and anabolic

3. No adaptation to starvation > Glucose is the major fuel used by injured tiss

ue and the cells involved in repair and immune processes in the stressed patient.

Stress response-2

Stress response-3

Hypoalbiminemia is a better marker of severity of injury than nutritional status in the critically ill patient.

(1) reduce liver albumin synthesis

(2) promote increased production of acute phase protein (CRP, fibrinogen , ceruloplamin)

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 protein)

Insulin decrease as the stimulus for its secretion is reduced.

Counterrgulatory hormones

(cortisol and glucagon) increase relative for the mobilization of endogenous energy and protein stores.

Starvation

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 overfeedingEnergy RequirementsProtein RequirementsCHO RequirementsVitamins and MineralsEnergy and protein requirements in specific Disease statesSpecialist 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 requirement as much as 30% , even in sepsis.

( 3) Thermic effects of food or postprandial thermogenesis

> 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 activity should NOT be included until convalescence on a general wards.

The critical ill p’t cannot use excess energy for wt gain.

Inactive p’ts will use excess energy for fat deposition.

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 rate.

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 D 200 IU VitE 10 IU Vit C 100 mg Folacin 400 mcg Niacin 40 mg Riboflavin 3.6 mg Thiamin 3 mg

Vit B6 4 mg Vit B12 5 mcg Pantothenic acid 15 mg Biotin 60 mcg Copper 0.5-1.5 mg Chromium 10-15 mcg Manganese 0.15-0.8 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 drainage

Energy and protein requirements in specific Disease states

•Liver DiseaseClinical condition Energy

(kcal/kg/day)

Protein

(g/kg/day)

Compensated cirrhosis

30-40 1-1.2

Complications,inadequate intake, malnutrition

40-45 1.5

Encephalopathy

grade I-II

30-40 Transiently 0.5, then 1-1.5

Encephalopathy

grade III-IV

30-40 0.5-1.2

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 cause severe impairment of brain neurotransmitter synthesis, which causes hepatic encephalopathy.

BCAA compete with AAA for blood-brain transport 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

(kcal/kg/day)

Protein

(g/kg/day)

Continuous haemofiltration/

diafiltration dialysis

30-35 1 – 1.2

Intermittent haemodialysis haemofiltration/diafiltration

30-35 1 – 1.2

Non-dialysed/filtered

(residual renal function, minimal catabolism

30-35 0.55 – 0.6

BW: actual 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, cisapride) to offset the delayed gastric emptying which is a consequence 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 small intestine and immune system e.g. enterocytes , lymphocytes. ( 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 c

ritically ill to support the immune response) Function : > A precursor for nitric oxide production ( NO has been implicated in a wide range of immuno

logical and vasoactive functions) > As a substrate for cytoplasmic and nuclear protein s

ynthesis. > It is essential for ammonia detoxification by urea sy

nthesis. Clinical evidence: improve nitrogen balance ,wound he

aling , stimulate the T-cell response , reduce infection Western 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 immune response.

Function :

> Blocks production of the prostglandin PG2.

> Reduce thromboxane

(thromboxane is an eicosanoid which plays an important 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 the harmful effects of the free radical chain reactions

There have been no studies to support the supplementation of antioxidants in the critically ill.

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 nutrients.

Malnutrition > leads to digestive enzyme deficiency Disaccharidase (lactase,sucrase,maltase)deficie

ncy Pancreatic insufficiency , Infection, gut atrophy

and mucosal damage,diminished mucus secretion and atrophy of enterocytes

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 st

imulants (metaclopromide, cisapride) Delayed gastric emptying Reduce secretion of gastric acid Bacteral overgrowth following bowel stasis bacterial modification of bile acids and deactivation of

mucosal digestive Enz Pseudomenbranous colitis (caused by antibiotics usage)

Factors affecting absorption in the critically ill

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 Associates, INC. Tricia Brusco, Dawn Carlson.

(All rights reserved for this self-directed,accredited learning program)

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