Download - NUTRITIONAL SUPPORT IN CRITICALLY ILL
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NUTRITIONAL SUPPORT IN NUTRITIONAL SUPPORT IN CRITICALLY ILLCRITICALLY ILL
Prof. Mehdi Hasan MumtazProf. Mehdi Hasan Mumtaz
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PRINCIPAL
Support for those who
Should not eat. Will not eat. Can not eat.
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AIMS
Detection and correction of pre-existing malnutrition.
Prevention of progressive protein energy malnutrition.
Optimization of metabolic rate. Reduction of morbidity. Reduction of time to convalescence.
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NUTRITIONAL ASSESSMENT
Dietary history. Clinical examination. Lab. Investigations.
– Hypoalbuminaemia<35G/L.– Lymphocytopenia<1500/mm3.– Serum transferase<1.5G/L.– Cell mediated immunity –ve.
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NUTRITIONAL ASSESSMENT
Changes in body mass. Skin fold measurements. Sophisticated techniques.
– Neutron activation analysis.– Dual X-ray absorptiometry.– MRI.– Bioimpedance methods.
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NUTRITIONAL REQUIREMENT
Nitrogen loss Urine urea Protein loss Plasma urea Nitrogen loss by pyrochemilumiscence. Portable calorimetery (bedside).
– Gas leak. FIO2.– Water vapours.– Steady state achievement
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NUTRITIONAL REQUIREMENT
Indirect calorimetry.– Modification.– Fever.– Sedation.– Neuromuscular paralysis.– Dialysis.
Routine practice.– 30-35Kcal/kg body wt/day.– 1.2-2G protein/kg body wt/day.
Electrolyte replacement. Vitamins & trace element replacement.
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PROBLEMS limiting ability to meet nutritional requirements in critically ill patients such as:
Diuretics
Restricted fluid intake
Haemofiltration
Glucose intolerance Good control
Delayed gastric emptying
Reduced feed absorption
Parenteral
Diarrhea
Fasting for procedures
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DAILY NITROGEN LOSS
Loss in urine (24hrs-collection).A. Urine urea (mmol)x0.0336.
B. B. Urine protein (g)x0.16. Blood urea correction.
C. Change in plasma urea (mmol)xbody wt (kg)x0.0168.
A + B + C (G) + Extra Real Losses.
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CALCULATION OF ENERGY REQUIREMENT
According to N2 loss (200 Kcal/G N2 loss/day)
According to body wt. (40-45 Kcal/kg/day)
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NITROGEN LOSS
ROUGH ASSESSMENT
Moderate catabolism10-14 G N2 loss/day i.e. 294-420mmol UER/day.
Moderate to severe catabolism14-24 G N2 loss/day i.e. 420-756mmol UER/day.
Hyper catabolism states>24 G N2 loss/day i.e. >756mmol UER/day.
Exact Assessment
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EXACT ASSESSMENT N2 LOSS
24 hrs urine urea
G x 28/60 x 6/5
Protein urea
1GN2=6.25G of proteins
=1/6.25 x G of proteins
in urine
Rise of urea in blood
G x 28/60 x 60% B.W
Total N2 Loss = 1+2+3
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ROUTES OF ADMINISTRATION
Enteral Parenteral RARE
Oral F Tube F Gastrostomy F Jejunostomy F
I/V Feeding Rectal Intrausternal Subcutaneous
Pain Allergy Absorption Infection
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FLOW CHARTMalnutrition (Look)
(HALLMARKS)
YES
NO
YESNO
NOYES
ENTERAL PARENTERAL
(support indicated)GI Function
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ENTERAL VS PARENTERAL
Better nitrogen retention. Better weight gain. Reduced hepatic steanosis. Reduced GIT bleeding. Lesser cost. Clear physiological benefits.
– Maintain mucosal integrity.– Maintain mucosal structure.– Release gut trophic hormones.
Less septic complications. Greater survival rate.
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PARENTERAL NUTRITION(un-physiological)
Bypass natural filters.
Continuous flow counter biological rhythm.
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INDICATIONS PARENTERAL NUTRITION
Alimentary tract obstruction. Prolonged ileus. Enterocutaneous fistula. Malabsorption. Short bowel syndrome. Inflammatory intestinal disease. Cachexia. Burns, severe trauma. Adjunct to chemotherapy. Acute renal failure. Hepatic failure. Hypermetabolic states.
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REQUIREMENTSBASIC
Water.– 30-35ml/kg/day.– Extra for vomiting, diarrhoea.– 150ml/1oC rise in temperature.– 400ml metabolic gain.– Affected by cardiac, renal, respiratory,
hepatic disease. Energy. Nitrogen.
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REQUIREMENTS
ADDITIONAL
Electrolytes. Vitamins. Trace-elements. Additives.
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ENERGYSources
CARBOHYDRATE Glucose Fructose Sorbitol Xylitol Ethanol Glycerol
LIPIDS Soybean oil
emulsions Cotton seed
emulsion
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ENERGY CARBOHYDRATE
Glucose.– ½L = 1 hr.– ½L – Glycogen - 1 day.– Cal. Value – 4.3 Kcal/G.– Glycourea > 0.4 0.5 G/kg/hr.– Infusion >6-7mg/kg/min.
O2 consumption. CO2 production. Energy consumption with lipogenesis.
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ENERGY CARBOHYDRATE Fructose.
– Insulin independent.– Rapid metabolism. Incidence of hyperglycaemia. Formation of glycogen.– Antiketogenic effect.– Glycosuria >1G/kg/hr.
Dehydrated– Metabolic acidosis
NeonatesG – 6 – PO4BARRIERF – 6 – PO4
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GLUCOSE
G-6-PO4SORBITOL
FRUCTOSE
ACETALDEHYDE
ETHANOL
XYLITOL
d-XYLULOSE
6-PHOSPHO-GLUCONATE
RIBULOSE-5-PO4
NUCLEIC ACIDS
(PROTEIN SYNTHESIS)
G-6-PO4
F-1:6-DPO4
PYRUVATE
KREBS CYCLE
CO2 H2O
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ENERGY-FATS
Best choice for caloric replacement: Caloric value. No osmotic effect.
Urine No loss
Faeces
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SOURCES
COTTON SEE OIL
Lipomal. Lipofundin. Lipophysan.
SOYBEAN OIL
Intralipid 10%, 20%.
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IDEAL FAT EMULSION
Size <4.
Component of utmost purity.
Should be isotonic.
Should have no effect on BP or
respiratory system.
Chronic toxicity – low.
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INDICATIONS
Serious malabsorption (fistula, eneritis,
colitis).
Cachexia.
Burns.
Prolonged unconsciousness.
High calorific deficiency.
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CONTRA-INDICATIONS
Hyperlipaemic states. Nephrotic syndrome. Renal damage. Coagulatory disorders. Cranial trauma. Tetanus – other infections. Traumatic shock. Pregnancy.
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SIDE EFFECTSACUTE
Circulatory.– B.P Crisis. H.R.– Shock like.
Respiratory. respiration.– Cyanosis.– Dyspnoea.
Pain in chest – back. Nausea – vomiting. Flushing of skin. Pyrogenic reactions. Urticaria.
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SIDE EFFECTSCHRONIC
Hyperlipaemia. Hepato-splenomegaly. Hepatic damage. Icterus. Anaemia. haemorrhage in G.I.T. Coagulation disorders with platelets. Pigmentation.
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SOURCES OF NITROGEN
Blood Plasma
Poor Source Albumin Amino-acids
Catabolised to A.A first
EAA
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AMINO-ACIDS
1GN2=25G of Muscle Tissues.Deficiency leads to: Antibody formation. Blood regeneration and cell formation. synthesis of hormones & enzymes. Oedema. Coagulation. Muscular atrophy. Decubitus.
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DISADVANTAGES
50-60% N2 in glycine form NH3.
Arginine + Ornithine K+ excretion.
I/C – K+
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Reactions
Ideal A.A solution 1:2 to 1:3 essential/
non essential
Biological adequacy
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CONTRA-INDICATIONS
Severe coronary insufficiency.
K+.
Hepatic damage.
Renal insufficiency (give E.A.A. solution)
Acidosis of different origin.
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ELECTROLYTES
Na+ 2-2.5 mmol/kg/day.
K+ 6 mmol/G N2 loss.
Ca++ 0.1 mmol/kg/day.
PO-4 0.6 mmol/kg/day.
Mg+ 0.1 mmol/kg/day.
Cl- acetate Give when additional Na+, K+ given
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VITAMINSTrace elements:
Zinc, Iron, Copper, Manganese, Cobalt, Iodine, Chromium, Molyhderium & Selenium
Zinc Essential constituent of many enzymes e.g. carbonic anhydrase.
Iron Essential for HB synthesis.
Copper Important for erythrocyte maturation and lipid metabolism.
Manganese Important for Ca++/PO4 metabolism and reproduction and growth.
Cobalt Essential constituent of vitamins B12.
Iodine Required for thyroxin synthesis.
Chromium Necessary for normal glucose utilization.
Molyhderium Component of oxidases.
Selenium Component of glutathion peroxidase.
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TRACE ELEMENT
Element /24 h
Zinc 2500-6000
Iron -
Copper 500-1500
Iodine -
Manganese 150-800
Florid -
Chromium 10-15
Molyhderium -
Selenium -
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ADDITIVES
Insulin.
Heparin.
Anabolic steroids.
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BASIC GUIDELINES Normal N2 loss=0.2-0.24G/kg/day. N2-energy ratio=1:200. Energy from – glucose, fat. N2 loss from amino acid solution. Add.
– Electrolytes.– Vitamins.– Trace elements.
Spread over 24 hrs. Energy & nitrogen given simultaneously. Restoration of:
– Oncotic pressure.– Hb level.
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MONITORING
Biochemical.
Physiological.
Haematological.
Mechanical.
Bacteriological.
Radiological.
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MONITORING
Related to kidney - daily. Related to liver - daily. Serum electrolytes - twice. Acid base status - twice. Special.
– Serum amino acid profile.– Serum/urine zinc and Cu+2.– Any other specific.
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MONITORING PHYSIOLOGICAL
Haemodynamics.
C.V.P.
Weight.
Fluid balance.
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MONITORING HAEMATOLOGICAL
Haemodynamics. While cell count. Differential count. Serum protein. Folate level.
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MONITORING MECHANICAL
INSEPCTION OF: I/V lines. Flow rate. Catheter insertion point. Infusion pumps. Monitoring equipment.
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MONITORING BACTERIOLOGICAL
Blood culture – weekly.
Viral agglutination titres.
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MONITORING RADIOLOGICAL
X-RAY CHEST
Lung Fields CVP Catheter
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NUTRITIONAcute Renal Failure
Hypercatabolic state. Adequate calories in a low volume load. Minimum rise in blood urea nitrogen. Low K+ content. Stringent sepsis control. Concentrated glucose and lipid used. Dialysis improve utilization. Lipid may interfere dialysis. Amino acid limited to 0.5G/kg/day. Utilize endogenous urea. Electrolyte free preparation.
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NUTRITIONHepatic Failure
Continuous use of lipids. Calories - bulk supply – hypertonic
glucose. Protein intake limited to 0.5G/kg/day. Eliminate protein in hepatic coma.
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NUTRITIONRespiratory Failure
Excess glucose lipogenesis.
Excess glucose CO2 production.
50% non-protein calories – supplied by lipid.
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STRESS ON
1. Specialised Nutrition Support In Critically Ill Patients.
2. Glutamine and Acute Illness.
PRESENT
&
FUTURE
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SIGNIFICANCE OF GIT IN SIGNIFICANCE OF GIT IN CRITICALLY ILLCRITICALLY ILL
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ANATOMY
&
HISTORY OF GUT
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FUNCTIONS
Barrier
Transport
Endocrine
Barrier
Transport
Endocrine
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BARRIER
Permeability & Permeation
Transcellular Paracellular
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PORES
Large Small
(6.5nm) (0.4-0.7nm)
Surface area of:
- 2 million cm2.
- Single tennis court.
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PERMEATION PATHWAYS
Paracellular Transcellular
(energy dependent) (small pores)
15% 85%
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TIGHT JUNCTIONSZona Occludence)
ZO
Kisses + Pores
Permeability depends:
1. Hydrodynamic radius
2. Electrical charge.
3. Functional status of ZO
Barrier function regulation:
1. Number of kisses/cell.
2. Channels open or closed.
3. Membrane pump
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FACTORS MODULATING FUCTION OF ZO
I/C Camp Concentration.
I/C Ca+ Concentration. Activation State Of Protein Kinase.
What is Cytoskeleton?
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TRANSLOCATION
DEFINITION
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CAUSES
Non Occlusive Intestinal Gangrene. Neutropenia. Colon Cancer. Penumatosis Intestinals. Necrtising Enterocolitis. Ionizing Radiation. Cytotoxic Drugs.
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CAUSES
Cytokine Release Syndrome. Crohns Disease. Ulcerative Colitis. Haemorrhagic Shock. Severe Trauma Burn Injury. Leukaemia.
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FACTORS
1. luminal microbial density.2. Damage to eipthelium.
– Irradiation.– Cytotoxic drugs.– Irritants.– Cytomegatovirus.– Mucosal disease.– Bowel manipulation.– Obstruction.– Free O2 radicals.
3. Diminished blood flow.– Haemorrhagic shock.– Burn.– Inflammtory agent.– Endotoxins.– M. occlusion.– Hypoxia.– Fever.
4. Immunosuppressant.– Corticosteroids in high
dosage.– Blood transfusion.
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MECHANISM
M. Cells.
Transcellular.
Ulcerations.
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ALTERED PERMEABILITY MECHANISM
Hypoperfusion
(non-occlusive mesenteric
hypoperfusion)
ROS
Role of
Alopurinol
Corrosive
Factors
Endotoxins
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NON-OCCLUSIVE HYPOPERFUSION
Hypovolaemia.
Cardiogenic.
Septic shock.
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HYPOPERFUSION
Renin Angiotensin Axis
Intense Vasoconstriction(Splanchnic)
Hypoxic Injury – Degree
- Duration
Permeability
Large Molecules Small Molecules
Subepithelial Oedema
Shedding Off Epithelium Top
Full Mucosal Necrosis
Disruption Of Submucosa
Disruption Of Muscular Propria
Transmural Necrosis
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ROS
Role of Allopurinal
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CORROSIVE FACTORS
Hydrochloric acid. Bile salts. Bacteria. Bacterial toxins. Proteases. Digestive enzymes.
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ENDOTOXINS
Ischaemia.
Direct injury.
metabolic demand of GUT.
Alteration of micro-circulation.
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MEASUREMENT OF GUT PERMEABILITY
Isotope tests.
PEG tests.
Dual sacharide tests.
– Lactulose/Rhamnose.
– Lactulose/Mannitol.
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NON MUCOSAL FACTORS
Gastric Emptying.
Intestinal Transit.
Dilution By Secretion.
Surface Area Available.
Altered Renal Clearance.
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TECHNIQUE FOR MEASUREMENT OF GUT PERMEABILITY USING LACTULOSE & L-RHAMNOSE.
1. Stop nasogastric feed/nil by mouth for 6 h prior to the study.
2. Empty bladder & urinary collecting system.3. Isotonic solution containing 5g oflactulose and 1g of L-
rhamnose administred via the nasogastric tube.4. All urine collected over 5h. Total volume noted and a 20
ml sample frozen for future analysis.5. Concentration of sugrs in urine quantified.6. %recovery of each sugar calculated:
Sugar concentration x urine volume%Recovery =------------------------------------------------------ x 100
Amount of sugar given enterally7. %recovery lactulose to %recovery L-rhamnose ratio
calculated. Normal range 0-0.08.
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IMMUNONUTRTION(Nutritional Paharmacology)
Why Name Immunonutrition?
Lipids -3, -6 Aminoacids
– Arginine– Glutamine
Ribonucleic acid Vitamins, E,C and A
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LIPIDS Production of free radicals. Inflammatory response. Ulcer formation. Hypersensitivity response. Altered renal vascular flow. Uterine contraction. Incidence of atherosclerosis. Incidence of heart attacks. Bleeding tendency. Haemorrhagic strokes.
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LIPIDS
-3
Immunostimulatory– Protect against gut
origin sepsis.
– Reduce incidence of allograft rejection
-6
Immunodepressive
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VITAMINS, E,C,A
Control lipid peroxidation.
Regulate RO intermediates (macrophages).
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ARGININE1. Production and secretion.
– Pitintary GH.– Protaction.– IGF-1.– Glucagon.– Somatostatin.– Pancreatic polypeptide.– Nor-epinephrin.
2. Pre-cursor of growth factors.– Putrescine.– Spermine.– Spermidine.
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ARGININE
3. Produce NO.
4. Resistance.
5. T-cell immunity.
6. Wound healing.
7. Cancer growth.
8. Protein content.
9. Lymphocyte nitrogen & allogenic response.
10. No effect on translocation.
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GLUTANINE
Barrier Function.
T-cell Function.
Neutrophil Function.
Kills Translocated Bacteria.
Hospital Stay.
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NUCLEOTIDES
Resistance.
Immune response.
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EFFECT OF CRITICAL ILLNESS ON GIT
Starvation & Bowel rest. Metabolic stress. Entral/Parenteral nutrition. Sepsis. Shock.
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STARVATION
Structural
Mucosal Atrophy
Villous height. Mucosal thickness. Crypt dipth. Mucosal height. ONA, RNA Protein contents.
Functional
Activity of disaccharidasis.
Transport.– Glutamin– Arginine
Immunity. IgA secretion.
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GIT IMMUNOLOGIC DEFENCE
IgA. Lymphocyte macrophages &
neutrophils. Lymph nodes. Kupffer cells in liver.
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BOWEL REST
G.I. Mass. Small bowel mucosal weight. DNA content. Protein content. Villous height. Enzyme activity.
Even if nitrogen balance is maintained & on TPN
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PRESENCE OF LUMINAL
NUTRIENTS NECESSARY
FOR NORMAL GUT
GROWTH & FUNCTION
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ENTERAL NUTRIENTS MEDIATE MUCOSAL TROPHISM
ENTERAL FEEDING
Direct provision of energy & mechanical
epithelial contact
Blood vessels
Pancreatic & biliary secretions
Autonomic CNS
enterohormones
Dilatation & mesenteric blood flow
Intestinal cell proliferation & differentiation
Endocrine effects
paracrine effects
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METABOLIC STRESSStarvation+Bowel Rest+Critical Illness, Shock, Hypovolaemia
Mesenteric blood flow. Hypoxia. Production of intestinal mucous. Mucosal acidosis. Mucosal permeability. Epithelial necrosis. O2 free radicals. Antibiotic.
– Microflora.– Colonization.
Gastric acid colonization.Mucosal & immunologic impairment.
Passage of intraduminal microbes & toxins intocirculation.
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CRITICAL ILLNESSHypermetabolism
+
Hypercatabolism
Nutritional support
Enteral (TEN)
To Neutralise
Disadvantages of bowel rest
Parenteral (TPN)
Frequently utilized- Stomach atony.- Risk of aspiration.- Venous access.- Despite: - Expensive
- Catheter sepsis
-Translocation
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TEN vs TPN
Criticism Scrutiny
TEN = Recommended.TPN = Strong indication.
Partial TEN
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TPN & IMMUNE SYSTEM
I/V lipids RES function. Bacterial clearance.
Lipid formulation -6 FA.– Promote synthesis of Pro-inflammatory bioactive
lipids. Secretion of IgA. Bacterial translocation. GUT neuro-endocrine stimulation dependent
on gut nutrient. Glutamine – important for cellular immunity.
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EFFECT OF SEPSIS(LPS Induced Hyperpermeability)
Mucosal HypoxiaVillous counter current
exchangingO2 Supply.Perfusion.
Mitochondrial oxidation
Anaerobic Metabolism
Less ATP
Cytoskeleton Integrity
Permeability
RO Metabolits
G-3P
ATP+
MitochondrialPhosphorylation
Permeability
Altered Utilization of Substrates
Activity of glutamin
ATP from glutamin
Cytoskeleton + ZO
Permeability
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EFFECTS OF SHOCK
Effect of Ischaemia
Central Control Local Humoral Substances
(Renin-Angiotensin)
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THE CONTINUUM OF INTESTINAL ISCHAEMIC INJURY
Normal Mucosa
Capillar Permeability
Mucosal Permeability
Superficial Mucosal Injury
Transmucosal Injury
Transmural Injury
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MECHANISM OF INTESTINAL MUCOSAL INJURY
Ischaemic Injury O2 delivery.
– Reduced intestinal (mucosal) blood flow. Short circuiting of O2 in the villus
countercurrent exchange. Needs of O2.
Reperfusion injury
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THERAPEUTIC APPROACH
Intraluminal therapeutic approach.
Maintenance of Gut Wall.
Intravasal therapeutic measures.
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INTRALUMINAL THERAPEUTIC APPROACH
Peristaltic movement.– Fibre application.
Bacterial adherence. Bacterial elimination.
– SDD. LPS Neutralization.
– Bile acids.– Lactoferin.– Lactulose.
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MAINTENANCE OF GUT WALL
Splanchnic perfusion.– Fluid support.– TXA2 receptor blocker– Angiotensin blocker.
Xanthin oxidase blockade. NO – donors. Metabolic support. Growth factors support.
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INTRAVASAL THERAPEUTIC MEASURES
Bacterial killing.
LPS neutralization.
– LPS – antibodies.
BPI (Bactericidal permeability
increasing protein).
Inflammatory mediaters.
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THERAPEUTIC APPROACH
TNFLPS
LIVER
Kupffer Cells
Systemic Circulation
4.34.2
Thoracic Duct
Portal vein
Intraluminal Bact/LPS2
Gut Wall
3
Therapeutic Targets
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NEW & FUTURE THERAPIES
Metabolic intestinal fuels.– Glutamine.– Shot-chain fatty acids (SCFA).
Intestinal growth factors. Immunomodulation.
– Arginine. -3 fatty acids.
Antioxidants.
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SELECTIVE DECONTAMINATION OF DIGESTIVE
TRACT