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Clinical Nutrition Support Have we got it all wrong ?

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Presentation on theme: "Clinical Nutrition Support Have we got it all wrong ?"— Presentation transcript:

1 Clinical Nutrition Support Have we got it all wrong ?
Dr Mike Stroud FRCP Senior Lecturer in Medicine & Nutrition, Consultant Gastroenterologist Southampton

2 Apologies BSG talk because of NICE Guidelines
NICE Guidelines 1st Draft Contention

3 40% of hospital patients are overtly malnourished on admission, 8% severely

4 Causes of Malnourishment
Conscious level Poor diet - age, poverty, junk, Depression exercise, alcohol Anorexia Dysphagia Obstruction Vomiting Pancreatic failure Liver processing Jaundice Malabsorption Increased Metabolic demands

5 Effects of Undernutrition
Psychology – depression & apathy Ventilation - loss of muscle & hypoxic responses Immunity – Increased risk of infection liver fatty change, functional decline necrosis, fibrosis Decreased Cardiac output Renal function - loss of ability to excrete Na & H2O Impaired wound healing Hypothermia Impaired gut integrity and immunity Loss of strength Anorexia ? Micronutrient deficiency

Improve general status Immunity Wound healing Ventilation Mobility Psychology

7 Feeding gives time for other medical and surgical interventions to work
ITU patients would die at 20 to 30 days Make stronger for discharge

8 Southampton CNRD Team Meta-analyses of oral/enteral nutrition support trials.
10 RCT, n = 494; RR 0.29 (CI to 0.47) 30 RCT, n = 3258 RR 0.59 (CI 0.48 to 0.72) Controls Controls Treatment Treatment Decreased complication % Decreased mortality %

9 So why think we may be wrong ?
Better understanding of the effects of starvation Problems in the evidence for Nutrition Support

Reduced physical activity Decrease in metabolic mass Decreased protein Na/K synthesis: -40% pumping: -30% Decreased Decreased glucose transport AA transport Decreases in: GH Insulin ILGF1,2 Adrenaline NA Glucagon T4 & T3

11 Metabolically stable BUT loss of reserve and functional capacity
REDUCTIVE ADAPTATION REDUCED FOOD INTAKE Changed body composition Reduced Mass Changed metabolism Reduced work, increased efficiency Metabolically stable BUT loss of reserve and functional capacity ‘Marasmus’

12 MARASMUS - Metabolically stable reductive adaptation

13 Adult marasmus in anorexia nervosa
Albumin 42

REDUCED FOOD INTAKE Reduced work, increased efficiency Reduced Mass Changed body composition Changed body composition Marasmus Infection, trauma, small bowel overgrowth, specific deficiency, abnormal losses, excessive intake, unbalanced intake Loss of homeostasis ‘Kwashiorkor’

Response to infection, injury, fluids, feeding Reduced intra-cellular GSH Depletion of K, Mg, Ca, P Increased urinary loss of nitrate Increased cytokines Variable loss of fat /muscle Peroxidation of cell membranes i.e. marasmus Massive salt and water retention +oedema Leaky membranes Loss of vascular proteins

16 Post-surgical Metabolic decompensation Adult ‘Kwashiorkor’


18 Adult, post-surgical Oedematous malnutrition Albumin = 16

19 Recovery from oedema Albumin = 18

20 Albumin before and after the resolution
of Oedema

21 The Problems of EBM in Nutrition Support
Trials use different Indications for intervention AND EXCLUSION Levels of feeding Controls Starting times Routes of support Duration of support Outcome measures

22 Wanted – volunteers for randomized, placebo controlled trial
The Evidence Wanted – volunteers for randomized, placebo controlled trial Patients with an undoubted need for nutrition support cannot be randomized

23 Nutrition Support and Death
Recommendation: You should not let your patients go without any form of nutrition whatsoever for 3 months Grade: GPP Grade: IBO

24 Why does nutrition support help ?
Jeejeebhoy KN.‘The benefits of nutritional support are evident when too little nutrition is given for too short a time to have any noticeable influence on lean body mass or circulating proteins

25 2. Correction of micronutrients ?
Many of the detrimental effects attributed to undernourishment are more easily ascribable to micronutrient rather than macronutrient shortages.

26 Prevalence of Micronutrient Deficiencies
National Dietary and Nutrition Survey (1998) Free Living >65 yr Institution >65yr Deficiency % incidence % incidence Folate 29 (8 severe) 35 (16 severe) Thiamine 9 14 Vitamin B12 6 9 Vitamin D 2 5 Vitamin C 14 (5 severe) 40 (16 severe)

27 Sub-clinical deficiency
Optimal level Impaired biochemical function Plasma levels may be normal Functional deficiency Metabolic Immunological Cognition Work capacity Clinical Deficiency Death

28 Metabolic evidence that Vitamin B12, Folate &
Vitamin B6 occur commonly in elderly people Jorsten et al. Am J Clin Nutr 1993 Levels of homocysteine & other metabolites accumulate if B12, folate or B6 are deficient - better indicator of vitamin status SUBJECTS 99 younger healthy controls ( ) vs 64 healthy elderly ( ) vs. 286 hospital patients ( ) Healthy elderly Elderly patients low B12 6% 12.5% low folate 5% 19% low B6 9% 51% Raised metabolites 63% 83% Elevated levels reverted to young healthy levels with vitamin supplements

29 Supplementation and metabolism
Vitamin X Substrate A Product B Supplementation of Vitamin X can cause: Vitamin X toxicity Shortage of Substrate A Excess of product B or C Deficiency of Vitamin Y Vitamin Y Product C

30 Food First ??

31 3. Metabolic switching ? 400g carbohydrate pre-op alters insulin resistance and decreases post- operative L.O.S. by 20%* *Nygren J, Thorell A, Ljungqvist O. Preoperative oral carbohydrate nutrition: an update. Curr Opin Clin Nutr Metab Care. 2001; 4(4):

32 Issues in Nutrition Support

33 Starvation & Weight loss
(After Allison) % 50 55 60 65 70 75 80 85 90 95 100 10 20 30 40 Catabolic Complete starvation Partial starvation b Decision Box o d y w e i g h t Days

Pre -existing malnourishment Catabolism MALNUTRITION METABOLIC RATE Feeding 30 10 20 No Need to feed Safe to Feed

35 Our nearest ancestor Teleology n. the doctrine of the final causes of things: interpretation in terms of purpose (Oxford English Dictionary)

36 Teleology, anorexia and survival
To ensure rest ( ? death) after injury Sequestration of ‘nutrients’ e.g. Iron Metabolic machinery is depleted, ‘broken’ or diverted Micronutrient & electrolyte depletion Inadequate hepatic processing Diet contains incorrect substrates for acute phase response

37 Issues in Nutrition Support

Schofield/Harrison Bendict BMR + 10% - 50% Stress + Fever (10%/degree C) + 10% Thermic effect of feeding Activity -10% ventilated +10% lying in bed +20% Bed to chair +40% up around ward

39 Energy expenditure in patients
2500 500 1000 2000 Predicted REEs (Schofield BMR + 30%) Estimated REE - kcals/day vs. Deltatrak measurements of REE 1500 500 1000 1500 2000 2500 3000 Measured REE - kcals/day Why are current recommendations kCals/kg /day non-protein calories ?

40 Problems of overfeeding energy
Ventilatory demands - O2 and CO2 Lipid Liver dysfunction Immunosuppression Carbohydrate Re-feeding syndrome Wernicke Korsakoff Hyper-glycaemia

Mg + abnormalities of renal salt and water handling K = acute circulatory failure and death Na PO4 ATP

42 PENG Guidelines Check K, PO4, Phos if low check Mg Correct levels
Thiamine 20 kcal/kg Monitor K, PO4, Ca (Mg if supplements were given)

43 Lynne 51 1 yr 45% wt loss ?pathology, ? Eating disorder
Wt 35kg, BMI 15 Na 137, K 2.5, PO4 0.54, Mg 0.8, Ca 3.3 Given 240 kcals/day via NG tube IV fluids 2 l/24 hr Thiamine, vitamin B co, K, PO4, Mg supplements

44 Lynne – cont’d Day 1 Day 2 Creat 166 110 Urea 15.5 11.4 K 2.5 3.4
Ca PO Mg

45 Intensive Insulin Therapy in Critically Ill Patients Van den Berghe et al. NEJM 2001; 345:1359-1367.
PRCT in 1548 adults on surgical ICU. Insulin to maintain glucose <6.0 mmol vs. insulin to maintain glucose <12 mmol Also reduced in-hospital mortality by 34%, bloodstream infections by 46%, ARF requiring haemofiltration by 41%. P<0.005 P<0.04

46 Peritonitis (animal model)
Peck et al 1989

47 Energy Requirements Initial refeeding or ongoing "stress" - cover
RMR (approx 20kcal/kg) Start slowly with generous micronutrient & intracellular electrolytes Low threshold for giving insulin

48 Problems of overfeeding nitrogen ?
Catabolism evolved for survival to provide AAs for immunity, inflammation and repair. AA demands are greater AND different to normal requirements. THEREFORE Diet/conventional nutritional support not only fails to meet AA needs but supply excess unwanted (toxic) AAs Why are current recommendations g N/kg with higher levels for catabolic patients ?

49 The influence of Nitrogen intake on Nitrogen Balance
Severe injury/ illness

50 Current recommendations for nitrogen 0. 2 - 0
Current recommendations for nitrogen g N/kg with higher levels for catabolic patients Mainly based on improvements in nitrogen balance NOT outcome. Maintaining N balance with GH is harmful Studies of lower levels of feeding required

51 Peritonitis (animal model)
Peck et al 1989

52 Collins et al. Am J Clin Nutr 1998
Somalia: relief camp during famine 92/93 573 adults: 83 oedematous, 377 non-oedematous Weight 35 kg, BMI 13.1 kg/m2 Overall mortality 21% (oedematous 37%) Low protein (8.5%) High protein (16.4%) Mortality 14/ /27 Appetite better poor Oedema g/kg/d g/kg/d

MACRONUTRIENTS Protein Carbohydrate Fat MICRONUTRIENTS Fat soluble - A, D, E, K Water soluble - B Group, C, etc ELECTROLYTES Na, K, Ca, Mg Phosphate ELEMENTS Iron Zn, Se, Cu, Mn


55 Issues in Nutrition Support

ASSESSMENT- Dietitians & Ward staff +/- NST PROVISION - Pharmacy enteral feeds +/- catering and sip feeds ACCESS - via NG, NJ, PEG MONITORING - At least 2 x weekly clinical reassessment + weekly wt + intake records + biochemistry ASSESSMENT - Ward staff PROVISION - Catering MONITORING - Admission & weekly wt NORMALLY NOURISHED Undernourished BMI<20 Wt Loss >10% Partial IF IF ASSESSMENT - Ward Staff & dietitians PROVISION - Catering +/- oral supplements MONITORING - Admission & weekly wt + intake records + biochemistry ASSESSMENT - Nutrition support team PROVISION - Pharmacy PN via +/- enteral or oral ACCESS - CVP or peripheral line MONITORING - Daily reassessment including intake, fluid balance and biochemistry + weekly wt

57 Parenteral nutrition

58 Total parenteral nutrition in the critically ill patient – A meta analysis. Heyland et al. JAMA 280, 1998 26 RCTs in 2211 surgical and ICU patients compared TPN vs standard care. NO effect on mortality NO effect on complication rate Potentially dangerous in ICU patients Why ?

59 Problems with PN studies
Subject selection excludes patients requiring PN Control groups receive PN when patients develop prolonged ileus or other persisting gut dysfunction (USA Veterans PN trial 13% of controls received PN). Overfeeding (nearly all patients hyperglycaemic) PN studies therefore reflect effects of PN performed badly in patients who don’t need it.

60 PN – The 7 day myth

61 Are enteral vs. PN studies valid ?
Repeated studies show benefits of enteral vs. PN feeding. BUT Enteral feeding is almost always limited in sick patients THEREFORE all studies compare different routes AND different levels of early feeding. e.g. Meta-analyses in pancreatitis patients shows no advantage of EN vs. PN if hyperglycaemic patients left out.

62 Enteral versus parenteral nutrition: a pragmatic study. Woodcock et al
Enteral versus parenteral nutrition: a pragmatic study. Woodcock et al. Nutrition 2001;17(1):1-12. Clinicians’ assessed GI function in 562 patients needing support. 231 ETF; PN; randomised ETF or PN adequate nutrition in randomised patients 22% ETF vs. 75% PN (p< 0.001). No differences in sepsis rates between groups Feeding complications more frequent in elective and randomised ETF patients. Higher mortality in both non-randomised and non randomised ETF groups.

Sep 2006 Course Directors: Brendan Moran - Consultant Surgeon Mike Stroud - Consultant Physician

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