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	<title>Gastroenterology Education and CPD for trainees and specialists &#187; Nutrition in specific situations</title>
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		<title>Nutrition in Surgery</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/surgery-nutrition-in-specific-situations-nutrition/surgery</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/surgery-nutrition-in-specific-situations-nutrition/surgery#comments</comments>
		<pubDate>Thu, 29 Jul 2010 07:15:48 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Surgery]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1709</guid>
		<description><![CDATA[What is the role of preoperative preparation of elective patients using carbohydrate treatment? Operating in a fed state 9compared with overnight fasting) has been shown to minimise insulin resistance, postoperative hyperglycaemia, loss of protein, lean body mass and muscle function, reduce anxiety and postoperative nausea and vomiting in general and orthopaedic surgery and to be [...]]]></description>
				<content:encoded><![CDATA[<p><strong>What is the role of preoperative preparation of elective patients using carbohydrate treatment?<br />
</strong><br />
Operating in a fed state 9compared with overnight fasting) has been shown to minimise insulin resistance, postoperative hyperglycaemia, loss of protein, lean body mass and muscle function, reduce anxiety and postoperative nausea and vomiting in general and orthopaedic surgery and to be cardioprotective in cardiac surgery.<br />
The Fed state may be induced by carbohydrate load (12.5%, hypo-osmolar, 800ml the night before and 400mls 2 hrs before surgery). In the rare patients who cannot eat or are not allowed to drink for whatever reason, a glucose infusion at a rate of 5mg/kg/min will have similar effects.<br />
<strong><br />
When is nutritional support indicated?</strong></p>
<p>Preop and postop nutrition- EN is recommended if it is anticipated that the pt will be unable to eat for more than 7 days peri-operatively. American Society for Parenteral and<br />
Enteral Nutrition guidelines (ASPEN) recommend postoperative nutritional support for patients who cannot meet their caloric requirements within 7–10 days.</p>
<p><strong>When is preoperative EN indicated?</strong></p>
<p>Patients with severe nutritional risk benefit from nutritional support for 10–14 days prior to major surgery even if surgery has to be delayed.<br />
Severe nutritional risk refers to at least one:</p>
<ul>
<li>Weight loss 10–15% within 6 months</li>
<li>BMI less than 18.5 kg/m2</li>
<li>Subjective Global Assessment Grade C</li>
<li>Serum albumin 30 g/l (with no evidence of hepatic or renal dysfunction)</li>
</ul>
<p><strong>Is there any role of immunonutrition?</strong></p>
<p>Pts undergoing major cancer surgery of the neck and abdomen as well as after severe trauma benefit from the use of ONS (3X250 ml) enriched with immune modulating substrates (arginine, omega-3 fatty acids and nucleotides).  Wherever possible these should be started 5-7 days before surgery and continued postoperatively for 5–7 days after uncomplicated surgery. It   reduces postoperative morbidity and length of stay. Undernourished patients, in particular, appear to benefit<br />
<strong><br />
What is the role of early post op (&lt;24hrs) normal food intake or EN after GI surgery?</strong></p>
<p>Early introduction of normal food intake or enteral feeding is recommended after GI surgery. When anastomosis of the proximal gastrointestinal tract has been performed, EN can be delivered via a tube whose tip is placed distal to the anastomosis.</p>
<p><strong>How should patients be tube fed after surgery?</strong></p>
<p>Use of naso-jejunal tube/jejunostomy is recommended for all candidates for TF undergoing major abdominal surgery. TF should be initiated within 24h after surgery.<br />
TF should start with a low flow rate (e.g. 10—max. 20 ml/h) due to limited intestinal tolerance. It may take 5–7 days to reach the target intake and this is not considered<br />
harmful.</p>
<p><strong>What are the energy and substrate requirements for parenteral nutrition in the perioperative period?</strong></p>
<ul>
<li>Energy- 25kcal/kg ideal body weight. Severe stress- 30kcal/kg IBW</li>
<li>Protein-1.5g/kg IBW</li>
<li>Protein: fat: CHO caloric ratio- 20:30:50%</li>
<li>The optimal PN regimen for critically ill surgical pts should probably include supplemental glutamine and n-3 fatty acids.</li>
<li>The standard lipid emulsion is soybean based rich in n-6 PUFA.  n-6 PUFA tend to have a pro-inflammatory effect. In contrast, n-3 PUFAs have an anti-inflammatory effect and have been shown to blunt the physiological response to endotoxins. Thus increasing dose of n-3 PUFAs has been shown to reduce ICU and overall hospital stay following major abdominal surgery. Thus mixtures of LCT and MCT are used as also LCT emulsion with olive/fish oil.</li>
<li>Glutamine has a major role as a substrate for the immune system and for the small bowel. Postoperative PN supplemented with glutamine dipeptide (20-40g/24h) has been shown to reduce infection rate and hospital stay. Glutamine is unstable in solution and not very soluble, so glutamine peptides have been constructed with glycine and alanine.</li>
</ul>
<p><strong>Is weaning from PN necessary?</strong></p>
<p>No. Traditionally PN has been tapered prior to discontinuation so as to prevent hypoglycaemia. However, it has been shown recently that even after prolonged PN the beta cells remain sensitive to changes in glucose level and thus hypoglycemia is unusual</p>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank">ESPEN guidelines</a></li>
</ol>
<p><a href="http://www.espen.org/espenguidelines.html" target="_blank"><br />
</a></p>
]]></content:encoded>
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		</item>
		<item>
		<title>Nutrition in Renal Failure</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/renal-failure/renal-failure</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/renal-failure/renal-failure#comments</comments>
		<pubDate>Thu, 29 Jul 2010 07:12:19 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Renal failure]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1707</guid>
		<description><![CDATA[Discuss enteral nutrition in acute renal failure? Nutritional status is one of the main factors determining outcome in ARF patients. ARF, especially in ICU seldom occurs as isolated organ failure but usually in the setting of MODS. Standard formulae are adequate for most patients.  Disease specific formulae for CRF may be justified in pts exclusively [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss enteral nutrition in acute renal failure?</strong></p>
<ul>
<li>Nutritional status is one of the main factors determining outcome in ARF patients.</li>
<li>ARF, especially in ICU seldom occurs as isolated organ failure but usually in the setting of MODS.</li>
<li>Standard formulae are adequate for most patients.  Disease specific formulae for CRF may be justified in pts exclusively on EN or in hypercatabolic ICU patients</li>
<li>Nutritional requirements (ESPEN 2006)
<ul>
<li>Non protein Energy- 20-30Kcal/kg/day (adjust for underweight or obese)</li>
<li>Carbohydrates 3-5 g/kg/day (max 7)</li>
<li>Fat- 0.8-1.2 (max 1.5)g/kg/day</li>
<li>Protein-
<ul>
<li>Conservative treatment- 0.6-0.8 (max 1) g/kg/day</li>
<li>Extracorporeal RRT- 1-1.5</li>
<li>RRT, hypercatabolic- upto 1.7 max</li>
</ul>
</li>
</ul>
</li>
<li>Acutely ill patients with CRF on HD should be treated as ARF.</li>
</ul>
<p><strong><br />
Discuss parenteral nutrition in acute renal failure?</strong></p>
<ul>
<li>Energy and macronutrient requirements as above</li>
<li>Loss of protein (0.2gm/kg/day) occurs in the pts undergoing dialysis.</li>
<li>The enhanced requirements of water soluble vitamins induced by extracorporeal treatment should be met by supplementing multivitamin products. Experimental ARF is associated with an increase in plasma retinol. Although retinol intoxication has not been reported in ARF patients, signs of vitamin A toxicity should be carefully sought during supplementation. Similarly Vitamin C supplementation should not exceed 30-50mg/day, because inappropriate supplementation may result in secondary oxalosis. Selenium and thiamine levels should be monitored as depletion may occur despite supplementation.</li>
<li>Restriction of electrolytes (Na, K, PO4 etc) is usually unnecessary on RRT.</li>
<li>Standard formulae are adequate for the majority of patients. However,</li>
<li>requirements can differ and have to be assessed individually. When there are</li>
<li>electrolyte derangements, three-in-one formulae without electrolytes or customized formulae can be advantageous.</li>
</ul>
<p><strong>Discuss nutrition in chronic renal failure (stage III to V, treated conservatively)?</strong></p>
<ul>
<li>Nutritional requirements
<ul>
<li>Calorie intake of 35Kcal/kg/day for stable CRF patients in the range of ideal body weight +/- 10% (adjust for underweight or obese)</li>
<li>Protein requirements 0.55-0.6 g/kg/day (2/3 high biological value-HBV)</li>
<li>Minerals (just a guide)</li>
<li>Phosphate-600-1000mg/day</li>
<li>K-1500-2000mg/day</li>
<li>Na- 1.8-2.5g/day</li>
</ul>
</li>
<li>Standard formulae can be used for short-term EN (&lt; 5 days) but for EN for more than 5 days, disease-specific formulae (protein-restricted with reduced electrolyte content) should be used.</li>
</ul>
<p><strong>Discuss parenteral nutrition in chronic renal failure (stage III to V, treated conservatively)?</strong></p>
<ul>
<li>Energy and minerals requirements as above</li>
<li>Metabolic acidosis in uraemia is an important factor for the activation of protein catabolism. Alkalinization therapy is thus standard in the treatment of CKD patients.</li>
<li>Loss of protein due to proteinuria exceeding 1 g/d should lead to compensatory additions to daily protein intake such as by the calculation of protein/AA intake needed based on ideal body weight (kg x 0.6 – 0.8 x proteinuria).</li>
<li>The nutritional requirements of acutely ill CKD patients are dealt with as in ARF</li>
<li>Standard PN mixtures should be used if PN is indicated. In patients receiving PN without any enteral supply, vitamins and trace elements should also be administered intravenously. If the patient needs PN for a period exceeding two weeks, accumulation of vitamin A and trace elements should be considered</li>
</ul>
<p><strong>Discuss nutrition in chronic renal failure (on maintenance HD)?</strong></p>
<ul>
<li>Nutritional requirements
<ul>
<li>HD or CAPD- 35 Kcal/kg/day (for CAPD in pts &lt;60- 30 Kcal/kg/day)</li>
<li>Protein intake-
<ul>
<li>HD- 1.2-1.4 (50% HBV)</li>
<li>CAPD- 1.2-1.5 (50% HBV)</li>
</ul>
</li>
<li>Minerals (guide only)</li>
<li>Phosphate-800-1000mg/day</li>
<li>K-2000-2500mg/day</li>
<li>Na- 1.8-2.5g/day</li>
<li>Fluid- 1000+urine volume</li>
</ul>
</li>
<li>Due to dialysis-induced losses, water-soluble vitamins need to be supplied: folic acid (1mg/ day), pyridoxine (10–20 mg/day) and vitamin C (30–60mg /day). Vitamin D should be given according to serum calcium, phosphorus and parathyroid hormone levels.</li>
<li>Thiamine should also be supplemented with a daily oral dose of 1-5 mg. Vitamin E may also be prescribed to patients at high cardiovascular risk at a daily dose of 800 IU of alpha-tocopherol. Routine haemodialysis does not induce significant trace-element losses. However, in depleted patients zinc (15 mg/day) and selenium (50–70mg/day) supplementation may be useful.</li>
<li>Dialysis specific formulae should be used (high protein content of HBV, reduced electrolytes with high energy concentration)</li>
<li>Due to an increased incidence of peritonitis, PEG/PEJ is contraindicated in adult CAPD patients but is standard in children</li>
<li>Dialysis initially leads to improvement in nutritional indices. However, after this initial improvement, the time on dialysis becomes directly associated with a significant decline in all measured nutritional parameters because dialysis procedure is itself a catabolic event.</li>
</ul>
<p><strong><br />
Discuss parenteral nutrition in chronic renal failure (on maintenance HD)?</strong></p>
<ul>
<li>In acutely ill HD patients the requirements are the same as in ARF patients.</li>
<li>Energy and macronutrients as above</li>
<li>Phosphorus intake should be limited to 10-15 mg/kg/day. As phosphorus and protein are combined in nutrients with a ratio of 10-13 mg pho</li>
</ul>
<ul>
<li>Conservative treatment- 0.6-0.8 (max 1) g/kg/day</li>
<li>Extracorporeal RRT- 1-1.5</li>
<li>RRT, hypercatabolic- upto 1.7 max</li>
</ul>
<ul>
<li>sphorus/g protein, most HD patients who have an adequate protein intake will need phosphate binders to prevent an increase in serum phosphorus.</li>
<li>Severe malnutrition is as defined as low BMI (&lt;20), body weight loss more than 10% over 6 months, serum albumin less than 35 g/l and serum transthyretin less than 300 mg/l.
<ul>
<li>Severe malnutrition plus spontaneous intakes less than 20 kcal/kg/day or in stress conditions: both ONS and IDPN are generally unable to provide satisfactory nutritional supply and are not recommended; daily nutritional support is necessary and EN should be preferred to PN.</li>
<li>In patients exhibiting severe malnutrition, with spontaneous intakes more than 20 kcal/day: dietary counseling and ONS should be prescribed; IDPN is indicated in patients unable to comply with ONS; EN can be necessary when ONS or IDPN fail to improve nutritional status.</li>
</ul>
</li>
<li>IDPN- Intradialytic PN (IDPN) is a cyclic PN given (usually) three times weekly through the venous line of the dialysis circuit. The following technical rules have been proposed in order to ensure optimal tolerance:
<ul>
<li>IDPN should be infused at constant rate during a typical 4-hour dialysis session;</li>
<li>IDPN delivery should be progressively increased from 8 ml/kg/IDPN during the first week, to a maximum of 16 ml/kg/IDPN without exceeding 1000 ml/HD</li>
<li>IDPN should be associated with controlled ultrafiltration, volume for volume;</li>
<li>75 mmol Na should be added per liter of IDPN solution in order to compensate Na losses due to ultrafiltration.</li>
<li>IDPN typically provides 800-1200 kcal three times weekly, in the form of glucose and fat emulsion and 30 to 60 g of protein. Standard amino acid solutions can be used for IDPN.</li>
</ul>
</li>
<li>Recommended longitudinal monitoring of nutritional status in maintenance dialysis patients: dietary interviews every 6 months; body mass index monthly; serum albumin and transthyretin, anthropometrics every 1-3 months as needed according to nutritional status.</li>
<li>Alternative treatments for protein-energy wasting in dialysis may be needed when nutritional support is insufficient. The administration of nandrolone decanoate has been demonstrated to increase muscle mass. Exercise combined with IDPN, as compared with IDPN alone, has been shown to promote net muscle protein accretion. These data argue in favor of a multimodal treatment of malnutrition in dialysis, combining nutritional support, exercise and anabolic agents.</li>
</ul>
<p><strong>Discuss parenteral nutrition in CAPD?</strong></p>
<ul>
<li>Energy requirements as above</li>
<li>Therapy-associated losses of proteins during CAPD are higher than in HD. Protein losses are approximately 10 g/day and increases in peritonitis. Because peritoneal solutions with a high glucose content are used as standard in CAPD, this method is associated with a glucose uptake of 100 to 200 g/d which is further</li>
<li>increased during peritonitis. Due to the increased glucose load, body weight may</li>
<li>even increase in CAPD patients. The high glucose load is also responsible for</li>
<li>induction or aggravation of diabetes, hypertriglyceridaemia and increased LDL and VLDL cholesterol.</li>
<li>In patients exhibiting severe malnutrition, with spontaneous intakes more than 20 kcal/day: dietary counselling and ONS should be prescribed; IPPN may be considered in patients unable to comply with ONS; EN can be necessary when ONS are unable to improve nutritional status.</li>
<li>In patients exhibiting severe malnutrition, with spontaneous intakes less than 20 kcal/day, or in stress conditions: daily nutritional support is necessary and EN should be preferred to PN; central venous PN is indicated when EN is impossible or insufficient (e.g. severe encapsulating peritonitis)</li>
<li>The special form of PN unique to CAPD patients is Intraperitoneal Parenteral Nutrition (IPPN). IPPN is shown to improve nitrogen balance and nutritional parameters. IPPN mainly consists of the intraperitoneal administration of 1.1% amino acid-based solution. IPPN can be associated with hypokalaemia, hypophosphataemia and mild acidosis.  So close monitoring during this treatment is needed</li>
<li>In acutely ill patients with CKD on CAPD the route for PN should be the same as in ARF patients. In these patients a combined use of PN (CHO and fat) and IPPD, using AA based PD solution can be suggested.</li>
<li>In non-acutely ill malnourished CAPD patients, the preferred route is via the peritoneum.</li>
</ul>
<p><strong>Ref<br />
</strong><a href="http://www.espen.org/espenguidelines.html" target="_blank"><br />
</a></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank"> ESPEN guidelines</a></li>
</ol>
<p><a href="http://www.espen.org/espenguidelines.html" target="_blank"><br />
</a></p>
]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Nutrition in Pancreatitis</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/pancreatitis-nutrition-in-specific-situations-nutrition/pancreatitis</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/pancreatitis-nutrition-in-specific-situations-nutrition/pancreatitis#comments</comments>
		<pubDate>Thu, 29 Jul 2010 07:05:07 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Pancreatitis]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1703</guid>
		<description><![CDATA[Discuss enteral nutrition in pancreatitis? Mild acute Pancreatitis- EN is not indicated if the patient can eat normal food after 5-7 days Severe acute Pancreatitis (AP) Early EN (asap especially in alcoholics) improves the course of acute pancreatitis Continuous EN is recommended, if tolerated. TF is feasible in the majority of the patients with AP. [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss enteral nutrition in pancreatitis?</strong></p>
<ul>
<li><strong>Mild acute Pancreatitis</strong>- EN is not indicated if the patient can eat normal food after 5-7 days</li>
<li><strong>Severe acute Pancreatitis (AP)</strong>
<ul>
<li>Early EN (asap especially in alcoholics) improves the course of acute pancreatitis</li>
<li>Continuous EN is recommended, if tolerated. TF is feasible in the majority of the patients with AP. However TF may need to be supplemented with parenteral feeding if the requirements cannot be met enterally</li>
<li>NJ feeding can be tried if gastric feeding is not tolerated</li>
<li>Try standard formulae first and if not tolerated peptide based formulae can be used.</li>
<li>Avoid overfeeding during the acute phase (CH 50%, Fat 30%, protein 1-1.5 gm/kg/day). TG should be monitored regularly. Values below 10–12 mmol/l are tolerated but serum lipid levels should ideally be kept within normal ranges.</li>
</ul>
</li>
<li><strong>Chronic Pancreatitis</strong>
<ul>
<li>Pancreatic enzymes taken with meals with a normal fat content (30% of total energy intake) are the mainstay of treatment.</li>
<li>Whole protein ONS (with pancreatic enzymes) may be used if oral intake is insufficient.   Peptide-based ONS may be tried if whole protein ONS is not tolerated. However, the palatability of peptide supplements is low and compliance is poor.</li>
<li>If adequate weight gain cannot be achieved and steatorrhoea is persistent, then medium chain triglycerides (MCT) are useful due to lipase independent absorption of MCT. However MCTs have a lower energy density (8.3 kcal/g), are not very palatable, and may induce side effects such as abdominal pain, nausea and diarrhoea.</li>
<li>Jejunal EN with peptide or amino acid based formula (given overnight) is recommended if the patients cannot ingest sufficient calories.  For long-term therapy a percutaneous endoscopic gastrostomy (PEG) with a jejunal tube is probably best.</li>
</ul>
</li>
</ul>
<p><strong>When is PN indicated in Acute Pancreatitis?<br />
</strong></p>
<ul>
<li>PN is only required when EN is contraindicated (like persisting ileus, complex pancreatic fistulae or abdominal compartment syndrome).</li>
<li>PN in pts with severe AP (who cannot be fed enterally) PN initiated within the first 24-48 h of hospital admission have an adverse impact on clinical outcomes. So PN should be delayed till after the period of the peak inflammatory response has passed.</li>
</ul>
<p><strong>How should PN be used in severe AP?</strong></p>
<ul>
<li>Avoid overfeeding- maximum caloric intake should be 30 Kcal/kg/day. This should be reduced to 15-20 kcal/kg/day in case with SIRS or MODS and when the patient is at risk of refeeding syndrome.</li>
<li>50-70% of the total calories should come from glucose.  As in other critically ill patients, glucose oxidation reaches the maximal level at 4mg/kg/min (3-5 gm/kg/day). Exceeding this limit may cause lipogenesis, hypercapnia and hyperglycemia. Tight glucose control (4-6 mmol/l) with insulin therapy appears to be beneficial in critically ill patients.</li>
<li>Protein- 1.2-1.5 g/kg/day.  This should be reduced to 1-1.2 g/kg/day in the case of hepatic or renal failure complicating AP.</li>
<li>When PN is indicated, parenteral glutamine supplementation (dose &gt; 0.2, usually 0.3-0.4g/kg) should be considered.</li>
<li>Glutamine is the most abundant free amino acid in the body and plays a central role in many metabolic processes (interorgan transport of C and N2 skeletons, regulator of acid base balance). In AP, 3 RCT’s showed use of glutamine was associated with a trend towards reduction in overall complications and shorter hospital stay.</li>
<li>Lipid emulsions- not more than 1g/kg/day. The use of IV lipids in AP is safe if hypertriglyceridaemia (HTG) is avoided. The lipid infusion should be discontinued if persistent (&gt;72 hrs) HTG occurs (&gt;12 mmol/l)</li>
</ul>
<p><strong>Discuss the relationship between hypertriglyceridemia and acute pancreatitis?</strong></p>
<p><strong>The relationship between HTG and AP is controversial</strong> because it is still unclear whether hyperlipidaemia is a cause or a consequence of AP or a combination of both. The latter seems more likely, since serum lipids normalize spontaneously within 48-72 hours when there is no continuing exogenous source of lipids.</p>
<ul>
<li>The diagnosis of hypertriglyceridaemia-associated pancreatitis is based on lipaemic serum, a serum</li>
<li>TG level greater that 12 mmol/L and the presence of chylomicronaemia. The mechanism is poorly understood. Hydrolysis of TG in and around the pancreas by pancreatic lipase secreted by acinar cell leads to accumulation of free fatty acids in high concentrations. Free fatty acids cause activation of pancreatic pro-enzymes, proinflammatory cytokines and free radicals, thus initiating AP.</li>
<li>Lipid emulsion should be avoided with PN in HTG associated pancreatitis. The goal is to maintain TG levels within a normal range.</li>
<li>If the serum TG level cannot be maintained below 12 mmol/L, drug therapy is indicated. Plasma exchange has been used to lower lipid and pancreatic enzymes levels, and to improve the signs and symptoms of AP.</li>
<li>Keeping blood TG levels &lt; 4.6 mmol/L, in patients with previous HTG-associated AP can effectively prevent further episodes of pancreatitis</li>
</ul>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank">ESPEN guidelines</a></li>
</ol>
]]></content:encoded>
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		</item>
		<item>
		<title>Artificial Nutrition in Liver Diseases</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/liver-failure/liver-failure</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/liver-failure/liver-failure#comments</comments>
		<pubDate>Thu, 29 Jul 2010 07:01:57 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Liver failure]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1701</guid>
		<description><![CDATA[How do you diagnose malnutrition in patients with liver disease? This is very difficult. BMI may be difficult to use because cachexia may be masked by edema. However in general the following BMI indicates malnutrition in liver disease patients: BMI &#60;22 in patients without ascites BMI &#60;23 in patients with mild ascites BMI &#60;25 in [...]]]></description>
				<content:encoded><![CDATA[<p><strong>How do you diagnose malnutrition in patients with liver disease?</strong></p>
<p>This is very difficult. BMI may be difficult to use because cachexia may be masked by edema. However in general the following BMI indicates malnutrition in liver disease patients:</p>
<ul>
<li>BMI &lt;22 in patients without ascites</li>
<li>BMI &lt;23 in patients with mild ascites</li>
<li>BMI &lt;25 in patients with tense ascites</li>
</ul>
<p>Mid arm muscle circumference (MAMC) and triceps skin fold thickness may also be used to diagnose malnutrition.</p>
<p>SGA (subjective global analysis) is very reliable and specific in detecting malnutrition. ESPEN recommends use of SGA and/or anthropometrics (BMI/MAMC/ triceps skin fold thickness) to diagnose malnutrition.<br />
<strong><br />
Discuss enteral nutrition in alcoholic hepatitis (AH)/ cirrhosis of liver?</strong></p>
<ul>
<li>Undernourished patients have a poor prognosis</li>
<li>ESPEN (2006) recommends a calorie intake of 35-40Kcal/kg/day (dry body weight) and a protein intake of 1.2-1.5 g/kg/day (dry body weight)</li>
<li>Use ONS or TF, if oral intake is not sufficient. Whole protein formulae should be used. Use of BCAA enriched formulae should be reserved, if hepatic encephalopathy develops despite appropriate medical treatment.</li>
<li>ESPEN supports the insertion of fine bore NG tubes in patients with oesophageal varices.</li>
<li>PEG is associated with a higher risk of complications (due to ascites and varices) and should be avoided.</li>
<li>In the study by Cabre E et al (Hepatology 2000) EN was found to be as effective as steroids in alcoholic hepatitis.</li>
</ul>
<p><strong><br />
When do you consider PN in AH or cirrhosis?</strong><br />
PN should be considered when oral/enteral intake is insufficient.<br />
<strong><br />
What are the energy requirements?</strong></p>
<ul>
<li>Energy intake- 1.3 X BMR
<ul>
<li>CHO- 50-60 % of non protein requirements</li>
<li>Protein 1.2 gm/kg/day (1.5 gm/kg/day if severely malnourished)</li>
<li>Lipids- 40-50% of non protein requirements</li>
<li><span style="text-decoration: underline;">In patients with ascites ideal weight according to the height should be used.</span></li>
</ul>
</li>
<li>Vitamins and minerals should be administered daily from the beginning. Due to the high risk of Wernicke&#8217;s encephalopathy, vitamin B1 must be administered prior to starting i.v. glucose in alcoholic patients.</li>
<li>Lipid should be provided using emulsions with a content of n-6 unsaturated fatty acids lower than in traditional pure soy bean oil emulsions (n-6:n-3 = 8:1). New fat emulsions have a lower content in n-6 unsaturated fatty acids due to the admixture of MCT and/or olive oil and/or fish oil rendering them less suppressive on leucocyte and immune function and less pro-inflammatory modulators.</li>
<li>A standard solution should be given in encephalopathy stage I-II and a liver-adapted complete amino acid solution should be given in encephalopathy stage III-IV. Such solutions contain an increased amount of branched-chain amino acids and lower content of aromatic amino acids, methionine and tryptophan. BCAA solutions lead to an improvement in mental state, but no definite benefit on survival.</li>
<li>Like in other conditions, the administration of micronutrients has no proven therapeutic effect apart from the prevention or correction of deficiency states. Supplementing zinc and vitamin A may indirectly improve food intake and nutritional state by improving dysgeusia. Zinc and selenium deficiency have been observed in alcoholic and non-alcoholic liver disease. An impressive association between HE and zinc deficiency has been described in case reports. However oral zinc supplementation does not have a therapeutic effect on HE.  In a pragmatic approach, liberal supplementation is recommended in the first two weeks of nutritional support, because the laboratory diagnosis of a specific trace element or vitamin deficiency may be more costly, and would delay provision.</li>
</ul>
<p><strong>Discuss nutrition in AH/Cirrhosis?</strong></p>
<ul>
<li>The prevalence of protein energy malnutrition increases from 20 % in Child-Pugh class A to over 60 % in class C</li>
<li>In patients with cirrhosis, overnight fasting can cause depletion of glycogen stores and lead to a metabolic condition similar to prolonged starvation. Thus it is recommended that patients who need fasting should be given glucose IV at a rate equal to the endogenous hepatic production (2-3gm/kg/day).</li>
<li>Due to psychomotor dysfunction oral nutrition often is not sufficient even in encephalopathy stage I-II.  Tube feeding should be considered to ensure adequate nutrient provision. PN should be considered in patients with unprotected airways and advanced HE.</li>
<li>In the early postoperative phase often there is a disturbance of glucose metabolism associated with insulin resistance. Hyperglycaemia In this situation should be managed by reducing glucose intake because higher insulin doses are unable to increase glucose oxidation.</li>
</ul>
<p><strong>Discuss nutrition in acute Liver failure?</strong></p>
<ul>
<li>As in other critically ill patients artificial nutrition in acute LF is indicated when the patient is considered unlikely to resume normal oral nutrition within the next 5 to 7 days.</li>
<li>In acute liver failure resting energy expenditure is increased 1.2- to 1.3-fold compared to healthy individuals. Whenever possible, the individual energy requirement should be measured by use of indirect calorimetry.</li>
<li>Sufficient glucose provision (2 – 3 g/kg/day) is mandatory for the prophylaxis or treatment of hypoglycaemia</li>
<li>Lipid (0.8 – 1.2 g/kg/day). Most centers use LCT/MCT emulsion</li>
<li>Amino acid administration is not mandatory in hyperacute LF. In acute or subacute LF, however, amino acids (0.8–1.2 g/kg/day in PN) or protein (0.8 – 1.2 g/kg/day) in enteral nutrition) should be used in order to support protein synthesis.</li>
<li>The use of amino acid infusion often was omitted for fear of aggravating existing hyperammonaemia and hyperaminoacidaemia causing brain oedema and encephalopathy especially in hyperacute liver failure.</li>
<li>Adequate metabolic monitoring is necessary in order to adapt nutrient provision to substrate utilisation. Strict control of the plasma levels of glucose (target: 5 &#8211; 8 mmol/L), lactate (target: &lt; 5.0 mmol/L), triglycerides (target: &lt; 3.0 mmol/L) and ammonia (target: &lt; 100 micromole/L) are necessary for this purpose.</li>
</ul>
<p>NB- BCAA are essential amino acids leucine, isoleucine and valine. In cirrhosis there are reduced body stores of BCAA. This directly or indirectly influence brain ammonia levels.</p>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank">ESPEN guidelines</a></li>
</ol>
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		<title>Nutrition in ICU</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/intensive-care/intensive-care</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/intensive-care/intensive-care#comments</comments>
		<pubDate>Thu, 29 Jul 2010 06:58:36 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Intensive care]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1699</guid>
		<description><![CDATA[Discuss nutrition in ITU? Current literature strongly favours using enteral nutrition as the first line method for feeding ITU patients. Further there is no significant difference in the efficacy of gastric versus jejunal feeding in ITU patients. Use of prokinetics should be considered in patients intolerant to enteral feeding. Whole protein formulas are appropriate in [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss nutrition in ITU?</strong></p>
<ul>
<li>Current literature strongly favours using enteral nutrition as the first line method for feeding ITU patients.</li>
<li>Further there is no significant difference in the efficacy of gastric versus jejunal feeding in ITU patients.</li>
<li>Use of prokinetics should be considered in patients intolerant to enteral feeding.</li>
<li>Whole protein formulas are appropriate in most cases. There is no advantage of a peptide based formula.</li>
<li>ESPEN (2006) guidelines favours early (&lt;24hr) feeding of haemodynamically stable patients.</li>
<li>EN is indicated in all patients who are not expected to be on full oral diet within 3 days</li>
<li>During the acute phase of illness, provision of higher amounts of nutrients is associated with a less favourable outcome. Hence during the first 72-96 hours calorie intake in excess of 20-25 Kcal/kg/day (25-30 Kcal.kg/day for undernourished/chronic catabolic state patients) may be associated with less favorable outcome. During he recovery phase, aim to provide 25-Approve User Registration30 Kcal/kg/day.</li>
<li>Indication of parenteral nutrition- only if pts are intolerant of EN or to provide supplemental PN if sufficient EN cannot be fed.</li>
<li>Evidence for the use of glutamine- Glutamine should be added to EN in burned and trauma patients. Glutamine is a conditionally essential immunonutrient that is derived from muscle protein breakdown.</li>
<li>Consider supplementation with omega-3-fatty acids, arginine and nucleotides (immune modulating formula) in elective upper GI patients, pts with mild sepsis (APACHE II &lt;15), trauma and ARDS pts. However ICU patients with very severe illness and who do not tolerate more than 700 ml EN/day  should not receive a immune modulating formula</li>
</ul>
<p><strong><br />
Parenteral nutrition in ICU</strong></p>
<p><strong>What is the indication for PN in ICU?</strong></p>
<p>Patients who are not expected to be on oral nutrition within 3 days should receive PN if EN is contraindicated or if they do not tolerate EN. All patients who are not expected to be on a full oral diet within 3 days and who do not receive sufficient enteral nutrition for &gt; 24h should receive complementary parenteral nutrition<br />
<strong><br />
What are the energy and substrate requirements?</strong></p>
<ul>
<li>Energy requirements as above in EN section of ICU nutrition. Provide energy as close as possible to the measured energy expenditure to decrease negative energy balance</li>
<li>The minimal requirements for glucose are about 2g/kg BW/day and they should not exceed 5-6 g/kg/day.</li>
<li>Hyperglycemia should be avoided to prevent infectious complications. Tight glucose control (4.5-6.1 mmol/l) may lead to decreased mortality in surgical ICU patients. Whether a target below 8.3 mmol/L is equally effective and perhaps safer remains unknown</li>
<li>IV lipids (LCT, MCT or mixed emulsions) can be administered safely at a rate of 0.7 up to 1.5 g/kg/d.</li>
<li>Soybean oil-based lipid emulsions (LCT) high in linoleic acid are largely used in the ICU and remain the reference emulsion. <strong>LCT/MCT lipid emulsions show a clinical advantage to LCT alone but no improvement in survival. </strong></li>
<li>A balanced amino acids mixture should be infused at 1.3 – 1.5 g/kg ideal body weight/day in patients receiving adequate energy supply. In acute patients receiving hypocaloric feeding protein requirements were increased by about 25-30%.</li>
<li>The amino acid solution should include 0.2 to 0.4 g/kgBW /day of glutamine (0.3 to 0.6 g/kg/day alanyl-glutamine).</li>
<li>It is the most abundant free amino acid that under normal conditions is not an essential amino acid. However in the critically ill, its demand is increased for immune activity and repair.  A low plasma level is associated with a worse outcome. Various studies have shown reduced mortality or improved morbidity with reduced infections, improved glycaemic control or reductions in length of stay. Where the dipeptide cannot be incorporated within the PN feed it has been shown safe to administer through a peripheral line.</li>
<li>Any prescription of PN includes 1 daily dose of multivitamins and 1 daily dose of trace elements. Parenteral feeding solutions (unlike enteral solutions) contain no trace elements or vitamins for stability reasons; this implies that they must be prescribed separately. However, clinicians very often forget to prescribe them, as they consider the PN bags to be analogue to the enteral complete feeding solutions.</li>
<li>The micronutrients are invariably prescribed as “1 daily dose”, whatever the bodyweight or metabolic rate. When PN is prolonged, and if the patient remains critically ill, determination of plasma concentrations on monthly basis enables detection of gross deficiencies that should be supplied by the individual trace element: selenium and zinc are particularly at risk.</li>
</ul>
<p>Some patients have specific substitution requirements that should be considered separately from PN requirements:</p>
<ul>
<li>Continuous renal replacement therapy causes a continuous loss in the effluent varying between 1-2  adult doses of selenium, zinc and thiamine per day that should be given in addition to basal requirements.</li>
<li>Major burns cause large exudative Cu, Se and Zn losses</li>
<li>In alcoholic patients- thiamine supplements (100-300 mg/day) are needed during the first 3 days in the ICU to prevent neurological side effects associated with PN glucose delivery.</li>
</ul>
<p>There is no specific solution for these patients: it is therefore tempting to administer 2 or 3 vials of existing preparations to achieve an adequate dose. However this may cause toxicity.  A compromise solution may be the development of new basic multiple trace element preparation to which additional trace elements can be added for patients with increased trace element losses such as selenium and zinc</p>
<p><strong>Are there any advantages of specific lipid formulations?<br />
</strong><br />
There are a number of different formulations of parenteral lipids:</p>
<ul>
<li>Soybean oil-based (e.g., Intralipid, Livolipid, etc); these are often referred to as long chain triglycerides (LCT)</li>
<li>Mixtures (usually 50:50) of LCT and MCT e.g., Lipofundin</li>
<li>Mixture (20:80) of LCT and olive oil (Clinoleic)</li>
<li>Mixtures of lipids including fish oil (e.g. 30:30:25:15 mixture of LCT, MCT, olive oil and fish oil  (SMOFLipid); 40:50:10 mixture of LCT, MCT and fish oil (Lipoplus, also known as Lipidem)</li>
<li>Fish oil for use as a supplement to be diluted with soybean oil (Omegaven).</li>
</ul>
<p>Intravenous fish oil, providing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) decreases the synthesis of inflammatory cytokines, when compared to LCT/MCT. A multicenter study showed that IV fish oil had favorable effects on survival, infection rate, antibiotic requirements and length of stay when administered in doses <span style="text-decoration: underline;">between 0.1 and 0.2 g/kg/day</span>. The best effects were observed in abdominal sepsis.</p>
<p>Although there is a theoretical basis for the inclusion of fish oil as a component of a lipid mixture such as seen in SMOFLipid, there is very little direct evidence of the efficacy of such mixtures. LCT/MCT, olive oil and fish oil enriched emulsions show clinical advantages on Omega 6 fatty acids emulsions, except in terms of survival.</p>
<p><span style="text-decoration: underline;">ESPEN currently recommends use of <strong>fish oil enriched lipid emulsions in abdominal sepsis and surgical patients requiring ICU.</strong></span><br />
<strong><br />
Discuss lipid biochemistry?</strong></p>
<ul>
<li>Fatty acids are classified as saturated (no double bonds in the chain) or unsaturated (one or more double bonds in the chain), with the latter sub classified as monounsaturated (one double bond in the chain) or polyunsaturated (two or more double bonds in the chain).</li>
<li>According to the chain length, fatty acids are termed short chain (&lt; 8 carbons), medium chain (8 to 14 carbons) or long chain (16 or more carbons).</li>
<li>With regard to the position of the double bond within the fatty acid chain three families are typically distinguished: omega-9, omega-6 and omega-3 (sometimes referred to as n-9, n-6 and n-3).</li>
<li>Many fatty acids can be synthesized within the human body but two fatty acids (linoleic acid and alpha-linolenic acid) cannot. These fatty acids are required to be supplied to humans and are referred to as essential fatty acids. The essential fatty acids are synthesized in plants and are found in high  amounts in plant oils (e.g. corn, sunflower, soybean). They can be further metabolized to longer  chain, more unsaturated fatty acids including arachidonic acid (omega-6), and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (both omega-3).</li>
<li>Fish oil contains EPA and DHA. Olive oil contains the omega-9 monounsaturated fatty acid oleic acid.</li>
</ul>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank">ESPEN guidelines</a></li>
</ol>
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		<title>Nutrition in IBD</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/ibd/ibd</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/ibd/ibd#comments</comments>
		<pubDate>Thu, 29 Jul 2010 06:53:33 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[IBD]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1696</guid>
		<description><![CDATA[Discuss nutrition as primary therapy for active CD? EN (ONS and Tube feeding- TF) is effective in the treatment of the acute phase of the disease and is considered the first line therapy in children.  The mechanism of beneficial effect of EN remains unclear. In adults, however, treatment with corticosteroids is more effective: therefore, in [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss nutrition as primary therapy for active CD?</strong></p>
<ul>
<li>EN (ONS and Tube feeding- TF) is effective in the treatment of the acute phase of the disease and is considered the first line therapy in children.  The mechanism of beneficial effect of EN remains unclear.</li>
<li>In adults, however, treatment with corticosteroids is more effective: therefore, in adults, EN as sole therapy for acute CD is indicated mainly when treatment with corticosteroids is not feasible, e.g. due to intolerance or refusal.</li>
<li>The localisation of CD has no prognostic value for the response to EN. Approximately 60% of all patients reach remission.</li>
<li>TPN is no better than EN in the therapy of active CD and should therefore be used only in patients with a contraindication to or intolerance of EN</li>
<li>Compliance of patients receiving EN is low due to the unpalatability of the enteral formula or intolerance.</li>
</ul>
<p><strong>Discuss nutrition for maintenance of remission in CD?</strong></p>
<ul>
<li>The length of remission and subsequent relapse rate after remission induced by EN are comparable to that after treatment with corticosteroids in children and adults.</li>
<li>In longstanding (more than 1 year) clinical remission and in the absence of nutritional deficits, a benefit of EN has not been demonstrated.</li>
<li>One-year relapse rates of active CD by EN are comparable to steroid therapy.</li>
</ul>
<p><strong><br />
Discuss EN in CD?</strong></p>
<ul>
<li>There are no significant differences in the effect of free amino acid, peptide-based and whole protein formulae for TF. Nutritional support with normal food is considered the treatment of choice.</li>
<li>ONS can provide upto 600 Kcal/day in addition to normal food. If a higher intake is required, TF is necessary.</li>
<li>TF can be safely delivered by a nasogastric tube (NGT) or percutaneous endoscopic gastrostomy (PEG).</li>
<li>In some patients, who are intolerant to whole protein formulae AA or peptide-based formulae might however be tried.</li>
</ul>
<p><strong><br />
Discuss nutrition in ulcerative colitis?</strong></p>
<p>EN is not recommended as treatment of active UC.</p>
<p><strong>Discuss parenteral nutrition in IBD?</strong></p>
<ul>
<li>Although the faecal stream is likely to play a role in the pathogenesis of CD, there is no evidence that bowel rest combined with parenteral nutrition may be beneficial in refractory CD.</li>
<li>There are no studies investigating the effect of drug treatment on nutritional status in UC. However, folic acid deficit may be related to sulphasalazine therapy.</li>
</ul>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank">ESPEN guidelines</a></li>
</ol>
<p><a href="http://www.espen.org/espenguidelines.html" target="_blank"><br />
</a></p>
]]></content:encoded>
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		<title>Nutrition in Chronic heart failure</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/heart-failure/heart-failure</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/heart-failure/heart-failure#comments</comments>
		<pubDate>Thu, 29 Jul 2010 06:50:47 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Heart failure]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1694</guid>
		<description><![CDATA[Discuss nutrition in chronic heart failure? Cardiac cachexia, defined as weight loss of 6% or more (in the absence of edema) in at least 6 months, occurs in about 12–15% in patients in NYHA classes II–IV. The aetiology of cardiac cachexia is complex; however loss of appetite has a significant role in only 10-20% of [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss nutrition in chronic heart failure?</strong></p>
<ul>
<li>Cardiac cachexia, defined as weight loss of 6% or more (in the absence of edema) in at least 6 months, occurs in about 12–15% in patients in NYHA classes II–IV.</li>
<li>The aetiology of cardiac cachexia is complex; however loss of appetite has a significant role in only 10-20% of all cases.</li>
<li>Wt loss do not adversely affect the cardiac function but pts with cardiac cachexia have a 2-3 times higher mortality than non cachectic CCF pts.</li>
<li>EN is recommended to stop or reverse weight loss, although there is no evidence available from studies.</li>
</ul>
<p><strong>Discuss parenteral nutrition in chronic heart failure?</strong></p>
<ul>
<li>PN is reserved for patients in whom malabsorption occurs and in those in whom enteral nutrition has failed.</li>
<li>Is gut function impaired in CCF?</li>
<li>There is limited evidence that gut function is impaired in CCF. However decreased cardiac function can reduce bowel perfusion and lead to bowel edema, resulting in malabsorption</li>
<li>In view of decreased cardiac function and water retention, it is recommended that PN should be avoided, other than in patients with evidence of malabsorption in which enteral nutrition has been shown, or is strongly expected, to be ineffective.</li>
</ul>
<p><strong><br />
Ref</strong></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank">ESPEN guidelines</a></li>
</ol>
]]></content:encoded>
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		<title>Nutrition in HIV</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/hiv/hiv</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/hiv/hiv#comments</comments>
		<pubDate>Thu, 29 Jul 2010 06:43:56 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[HIV]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1690</guid>
		<description><![CDATA[Which specific diagnostic procedures are recommended in HIV-infected patients with weight loss? In addition to standard nutritional assessment the following points should be considered: Search for an opportunistic infection or other complications of disease or therapy. Determine testosterone, LH/FSH concentration Determine thyroid function and exclude treatment-induced diabetes mellitus. Look for signs of lipodystrophy (loss of [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Which specific diagnostic procedures are recommended in HIV-infected patients with weight loss?</strong></p>
<p>In addition to standard nutritional assessment the following points should be considered:</p>
<ul>
<li>Search for an opportunistic infection or other complications of disease or therapy.</li>
<li>Determine testosterone, LH/FSH concentration</li>
<li>Determine thyroid function and exclude treatment-induced diabetes mellitus.</li>
<li>Look for signs of lipodystrophy (loss of subcutaneous fat, triceps skin fold thickness, waist/hip ratio).</li>
<li>Nausea/vomiting: is this an adverse drug reaction?</li>
<li>Exclude malassimilation/malabsorption.</li>
<li>Is there a lack of saliva production?</li>
<li>If abdominal pain or dysphagia: suspect candida oesophagitis</li>
</ul>
<p>Start nutritional support while awaiting results of the diagnostic tests.</p>
<p><strong>What are the indications for nutritional support or EN in HIV?</strong></p>
<p>Nutritional therapy is indicated when significant weight loss (&gt;5% in 3 months) or a significant loss of Body Cell Mass (&gt;5% in 3 months) has occurred. In addition, nutritional therapy should be considered when the BMI is &lt;18.5 kg/m2<br />
EN is not contraindicated in pts with diarrhoea or malabsorption. MCT containing formulae are advantageous in pts with diarrhoea and severe malnutrition.<br />
<strong><br />
What is the role of anabolic drug treatment in HIV associated undernutrition?</strong></p>
<p>Drug treatment and EN may complement each other. HIV positive patients with testosterone deficiency should receive testosterone substitution to restore muscle mass. Moderate gain in body weight and fat free mass can be achieved by recombinant human growth hormone (rhGH) at high cost.</p>
<p><strong>Discuss PEG and HIV?</strong></p>
<p>Local infections, with or without limited peritonitis, have been observed in HIV patients with PEG feeding more often than in other populations. Thus antibiotic prophylaxis is recommended.</p>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank">ESPEN guidelines</a></li>
</ol>
]]></content:encoded>
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		<item>
		<title>Nutrition in Geriatrics</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/geriatrics/geriatrics</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/geriatrics/geriatrics#comments</comments>
		<pubDate>Thu, 29 Jul 2010 06:40:14 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Geriatrics]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1688</guid>
		<description><![CDATA[Discuss nutrition in geriatrics? An elderly subject is usually defined, in western countries, as a person over the age of 65 (WHO). A geriatric patient is an elderly subject who needs geriatric care due to a loss of independence caused by acute and/or chronic diseases (often multiple pathology) with related limitations in physical, psychological, mental, [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss nutrition in geriatrics?</strong></p>
<p>An elderly subject is usually defined, in western countries, as a person over the age of 65 (WHO). A geriatric patient is an elderly subject who needs geriatric care due to a loss of independence caused by acute and/or chronic diseases (often multiple pathology) with related limitations in physical, psychological, mental, cognitive and/or social functions. Muscle mass deficit, i.e. sarcopenia, is a frequent comorbid situation.<br />
<strong><br />
Is EN indicated after orthopaedic surgery in geriatric patients?</strong><br />
Oral Nutritional Supplements (ONS) are recommended in geriatric patients after hip fracture and orthopaedic surgery in order to reduce complications.</p>
<p><strong>Can EN prevent or improve pressure ulcers in geriatric patients?</strong><br />
ONS, particular high protein ONS, can reduce the risk of developing pressure ulcers. Based on positive clinical experience, EN is also recommended in order to improve healing of pressure ulcers</p>
<p>Wound healing in elderly patients may be improved by the administration of supplements containing protein and micronutrients that are involved in wound healing (zinc, arginine, carotenoids, vitamins A, C and E). Crucial for the effect of these nutrients is the local circulation in the pressure ulcer area, which determines effective nutrient transport and local metabolism as well as removal of toxic cell products. Besides the correction of nutrient deficiencies, the correct positioning of the patient to allow optimal blood circulation to the pressure area and to minimise further tissue damage is crucial.</p>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.espen.org/espenguidelines.html" target="_blank">ESPEN guidelines</a></li>
</ol>
]]></content:encoded>
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		<title>Nutrition in Diabetes mellitus</title>
		<link>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/diabetes-mellitus/diabetes-mellitus</link>
		<comments>https://www.gastrotraining.com/nutrition/nutrition-in-specific-situations/diabetes-mellitus/diabetes-mellitus#comments</comments>
		<pubDate>Thu, 29 Jul 2010 06:38:32 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Diabetes mellitus]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1686</guid>
		<description><![CDATA[Discuss nutrition in diabetes mellitus? The use of EN and PN poses challenges in managing blood glucose levels. EN- Basal insulin requirements should be provided along with sliding scale coverage while feedings are being advanced. If the feeding is providing 25% of usual intake, then 15% to 25% of usual insulin can be given, with [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss nutrition in diabetes mellitus?</strong></p>
<ul>
<li>The use of EN and PN poses challenges in managing blood glucose levels.</li>
<li>EN- Basal insulin requirements should be provided along with sliding scale coverage while feedings are being advanced. If the feeding is providing 25% of usual intake, then 15% to 25% of usual insulin can be given, with increases in daily insulin dose based on feeding rate and blood glucose levels.</li>
<li>Oral diabetic agents can be appropriately used in stable patients with type 2 diabetes who have normal hepatic and renal function and are receiving EN.</li>
<li>Gastroparesis can make glucose control difficult due to the mismatching of insulin action and nutrient absorption. Post pyloric feeding along with prokinetics can be used if glucose control is a significant problem. Further if EN is used, it should be fiber free with low fat (&lt;30% of total calories) as both fat and fiber prolongs gastric emptying.</li>
<li>Special diabetic formulas (low CHO and high fat) are available; however, there is not sufficient evidence to recommend routine use of these formulas for patients with DM.</li>
</ul>
<p><strong>Discuss parenteral nutrition in diabetes mellitus?</strong></p>
<ul>
<li>PN should not be initiated until glycemic control is achieved (&lt; 11mmol/l).</li>
<li>For diabetic patients or patients with a fasting glucose concentration of11 mmoles/l, no more than 100 grams of dextrose per day should be administered. A basal amount of regular insulin should also be added to the PN formulation to keep blood glucose concentrations less than 8.5mmol/l.  A common initial regimen is 0.1 units of insulin per gram of dextrose in the PN infusion.</li>
<li>Obese patients with type 2 diabetes may require as much as 0.1 units of insulin for every 0.5 grams of dextrose whereas thin, type 1 diabetics may require only 0.1 units of insulin per 2 grams of dextrose. If hyperglycemia persists when 0.3 units of insulin per gram of PN dextrose is exceeded, a separate iv insulin infusion should be used to achieve glycemic control.</li>
<li>A separate intravenous infusion is preferred in a patient whose insulin needs are dynamic or difficult to predict (e.g. infection, inflammatory response).</li>
<li>It is important to know that the insulin dose may need adjustments because there is a variable amount of insulin binding to PN bags and tubing, depending on materials used.</li>
<li>Monitor capillary glucose levels every 6 hours. Once glucose concentrations are stable, the frequency of measuring capillary glucose concentrations often can be reduced.</li>
<li>The insulin dosage in the PN formulation ratio is modified daily based on the amount of insulin given with sliding-scale insulin coverage over the previous 24 hours.</li>
</ul>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.nutritioncare.org/wcontent.aspx?id=1040" target="_blank">ASPEN guidelines</a></li>
</ol>
<p><a href="http://www.nutritioncare.org/wcontent.aspx?id=1040" target="_blank"> </a></p>
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