Nutritional Support In Liver & Kidney Disease Flashcards

1
Q

Prevalence and causes of malnutrition in liver disease

A
  • malnutrition occurs in 65-100% of liver disease patients (80% decompensated and 20% compensated) - there is a direct correlation between the severity of malnutrition and the progression of liver disease
  • can occur due to: alcoholism reducing intake of good quality foods and affecting absorption, ascities increasing abdominal pressure and reducing appetite, abhorrent liver activity i.e hypermetabolism (30%) reduced glycogenolysis (fasting capacity only 10-12 hours, they have increased insulin resistance which causes glucagon to diminish glycogen stores) and gluconeogenic capacity (67% glucose from gluconeogenesis) with reduced fat metabolism due to limited bile production, change in endocrine profiles leading to loss of appetite, impaired gut motility and small bacteria overgrowth
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2
Q

Potential micronutrient deficiencies in liver disease

A
  • vitamin K (stored and distributed by the liver), vitamin E (hepatic uptake and released in LDL cholesterol), vitamin A (stored in the liver but deficiencies are rare), vitamin D (involved in hydroxylation), vitamin B12 (stored in the liver, deficiencies are rare), pyroxidine, B5 (stored and converted by the liver), folate, B9 (stored in the liver, deficiencies are common)
  • thiamine is a big one for alcoholics and can cause WE, KP
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3
Q

Impact of malnutrition and sarcopenia on outcomes in liver disease

A
  • sarcopenia is a strong predictor of mortality in liver disease
  • protein energy malnutrition predicted worse outcomes, complications,
  • malnutrition predicts longer ICU stay, increased post- transplant infections, prolonged post-operative length of stay
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4
Q

Nutritional screening in liver disease

A
  • conventional MUST tools are quite open to error, and presence of oedema and ascities can massively impact
  • therefore need to use gold standard measure: RFH-SGA (clinical info, dietary intake, physical status, anthropometric measurements)
  • can assess muscle mass through measures of psoas muscle area (as cant be artificially trained) and is predictive of 1 year mortality post transplant
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5
Q

Nutritional requirements in liver disease: generic, alcoholic steatohepatitis, cirrhosis, acute liver failure

A
  • ESPEN guidelines state for compensated (25-35 kcal/kg/day and 1.2-1.3g protein/kg/day), decompensated (35-40 kcal/kg/day and 1.2-1.5g protein/kg/day), post transplant (30% stress factor and 1.2-1.5g protein/kg/day). for weight gain or loss +- 500-1000 kcal/day
  • oral nutritional support: 4-7 meals a day, ONS, 50g CHO before bed to prevent ketogenesis (decreasing fat oxidation)
  • enteral nutrition: NG and NJ tubes (PEG not recommended), can be home or hospital based
  • parenteral nutrition: rarely required, but used for a non-accessible or non-functioning gut
  • low salt diet
  • guidelines for steatohepatitis: start PN immediately if moderately or severely malnourished, give IV glucose when abstaining form food for more than 12 hours, provide energy to cover 1.3xREE, glucose should cover 50-60% EE requirements. Use omega 6 concentration less than soybean oil. Provide 1.2-1.5g/kg/day. Give water soluble vitamins (B vitamins)
  • guidelines for cirrhosis: start PN if mod-severely malnourished and cannot tolerate EN, give IV glucose if fasting for 12 hours, PN for fasting longer than 72 hours, provide energy to cover 1.3xREE, glucose covers 50-60% EE, lower omega 6 lipid emulsions, monitor P/K/Mg for RFS
  • guidelines for acute liver failure: energy for 1.3xREE, give IV glucose and lipid, AA 0.8-1.2g/kg/day
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6
Q

Functions of the kidney

A
  • fluid balance (blood pressure control): anti-diuretic hormone, renin-angiotensin-aldosterone system
  • removal of waste products: urea, excess vitamins and minerals, metabolites of some drugs and poisons
  • acid/base balance: HCO3 excretion
  • endocrine function: activation of vit D, excretion phosphate, erythropoietin production
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7
Q

Protein energy wasting in kidney disease

A
  • anorexia and depression causes reduced EI and malnutrition
  • persistent inflammation causes increases in EE, catabolism and decrease in muscle mass
  • anabolic resistance
  • additional causes: acidosis, comorbidity, endocrine disorders, anaemia
  • malnutrition in HD and PD is common (20-70%)
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8
Q

Causes of malnutrition in chronic renal failure

A
  • reduced oral intake due to restrictive dietary regimen
  • gastrointestinal factors (gastroplegia, impaired absorption)
  • heightened catabolism: uraemic toxicity, microinflammation, metabolic acidosis, endocrine factors (insulin resistance, hyperparathyroidism, elevated plasma leptin)
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9
Q

Derangement in electrolytes in kidney disease

A
  • hyperkalemia: >6 mEq/L (normal K is 3.5-5.5 mEq/L) Can be caused by renal failure, insulin deficiency, metabolic acidosis, drug interactions, catabolism due to malnutrition. Causing abnormalities on the ECG (tall, tented T waves)
  • hypokalemia: <3.5 mEq/L. Caused by vomiting, diarrhoea, diuresis, potassium binder, K too low in diasylate.
  • phosphate/calcium: increased intake of PTH releases Ca from bone. Phosphate binders can prevent phosphate being absorbed in the gut
  • sodium: fluid retention due to increased urine production, serum levels must be evaluated in conjunction with fluid status
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10
Q

Nutritional management for end-stage renal disease (main principles, acute renal failure, ESRD)

A
  • prevent deficiencies
  • control oedema and electrolytes
  • prevent renal osteodystrophy
  • provide an attractive and palatable diet
  • acute renal failure: monitor micronutrient status because excessive supplementation may result in toxicity, undernutrition is the main indicator for EN, in ICU 1500-2000 kcal EN are usually enough, plasma electrolyte monitoring should avoid RFS
  • chronic renal failure: 35 kcal/kg/day for better nitrogen balance, EN standard formulae for <5 days or for >5 days use protein and electrolyte restricted formulae. Protein is 0.55-0.6 g/kg/day
  • for ESRD: 1.2-1.4 g/kg/day, 35 kcal/kg/day
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11
Q

Management of haemodialysis patients in kidney disease

A
  • weight gain between sessions of >5kg may signify excessive fluid intake
  • weight gain of <2% may be a sign of loss of body mass
  • 10-12g of AA are lost per dialysis treatment, therefore diet of 1.2g/kg/day recommended (even though most HD patients only consume <1g/kg/day)
  • typical diet is 2000 kcal, 80g protein, 2g Na, 3g K, low phosphorus (800-1000mg/day), 1500 cc fluid restriction
  • need to restrict Na if increasing interdialytic weight gain, oedema, low serum sodium
  • may need to restrict K if insulin deficiency, metabolic acidosis
  • eat high protein, low phosphate sources (nephro ONS) with phosphate binders
  • calcium fortify foods and give activated vitamin D
  • vitamins: take water soluble AFTER dialysis, may need Fe/Ca/Zn (individualise per patient), calcitriol
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12
Q

Management of peritoneal dialysis patients in renal disease

A
  • 35 kcal/kg/day
  • keep to 2-4g of Na per day (can be a bit less strict with this compared to HD)
  • potassium is easily cleared by PD
  • phosphorus 800-1000 mg/day (with phosphate binders)
  • eat protein foods first at mealtimes, with frequent smaller portions of protein and easy to eat proteins such as egg white
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