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بسم الله الرحمن الرحيم
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Nutritional assessment in hospitalized patients Nutritional assessment in hospitalized patients M. Safarian, MD PhD.
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Nutrition Care Process Steps Nutrition Assessment Nutrition Assessment Nutrition Diagnosis Nutrition Diagnosis Nutrition Intervention Nutrition Intervention Nutrition Monitoring and Evaluation Nutrition Monitoring and Evaluation
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Nutritional care process Nutritional assessment tools Anthropometrics
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Nutritional Assessment Anthropometric assessment Anthropometric assessment Clinical evaluation Clinical evaluation Biochemical, laboratory assessment Biochemical, laboratory assessment Dietary evaluation Dietary evaluation
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ESPEN guidelines Questions to be answered: What is the condition now? What is the condition now? Is the condition stable? Is the condition stable? Will the condition get worse? Will the condition get worse? Will the disease process accelerate nutritional deterioration? Will the disease process accelerate nutritional deterioration?
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Anthropometric methods in ICU Weight Weight Height estimation Height estimation Mid-arm circumference Mid-arm circumference Skin fold thickness Skin fold thickness Head circumference Head circumference
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Weight
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Ideal Body Weight (kg) Men=48+ 2.3 for each inch over 152 m Men=48+ 2.3 for each inch over 152 m Women=45.3+2.3 for each inch over 152 cm Women=45.3+2.3 for each inch over 152 cm Correction for skeletal size: Correction for skeletal size:
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Ideal Body Weight (kg) Add 10% if SS is large Add 10% if SS is large Subtract 10% if SS is small Subtract 10% if SS is small
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Adjusted body weight Used when actual body weight is more than 120% of IBW: Used when actual body weight is more than 120% of IBW: ABW=IBW+ 25% of (actual body weight - IBW)
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Height in ICU patients
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Alternative measurements Estimating Height from ulna length
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Estimations of height
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Body composition (BIA) Very popular Very popular Safe Safe Noninvasive Noninvasive Portable Portable Rapid Rapid
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معرف ميزان چربي زير پوستي و درنتيجه ميزان چاقي خواهد بود. معرف ميزان چربي زير پوستي و درنتيجه ميزان چاقي خواهد بود. محلهاي اندازه گيري : تريسپس، بايسپس،زير کتف و بالاي تيغه ايلياک. محلهاي اندازه گيري : تريسپس، بايسپس،زير کتف و بالاي تيغه ايلياک. مشکلات عملي : مشکلات عملي : 1. خطاي در اندازه گيري. 2. مشکلات اندازه گيري. 3. وارياسيون توزيع چربي در افراد مختلف ( فردي وجمعيتي ). 4. حساسيت کم. Skin Fold Thickness
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Mid arm circumference measured with a nonstretch measuring tape measured with a nonstretch measuring tape midway between the acromion and olecranon of the nondominant arm midway between the acromion and olecranon of the nondominant arm ≤ 15 cm: severe depletion of muscle mass ≤ 15 cm: severe depletion of muscle mass 16–19 cm: moderate depletion 16–19 cm: moderate depletion 20–22 cm: mild depletion 20–22 cm: mild depletion
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Mid arm circumference
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If MUAC is <23.5 cm, BMI is likely to be <20 kg/m2 If MUAC is >32.0 cm, BMI is likely to be >30 kg/m2 BMI estimation
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Clinical assessment
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CLINICAL ASSESSMENT Detectiong of physical signs, (specific & non specific), that may be associated with malnutrition. Nutritional history General clinical examination, with special attention to organs like hair, angles of the mouth, gums, nails, skin, eyes, tongue, muscles, bones, & thyroid gland. Detection of relevant signs helps in establishing the nutritional diagnosis
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CLINICAL ASSESSMENT
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General: muscle wasting
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Flaky paint dermatosis: protein deficiency
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Essential fatty acid deficiency syndromes (EFADs)
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Zinc deficiency
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59 Wasting Clavicle
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60 The Shoulder and Elbow The shoulder The shoulder Normal: rounded or sloped Normal: rounded or sloped Abnormal: square, can see acromion process Abnormal: square, can see acromion process The elbow well padded and not showing joint The elbow well padded and not showing joint
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61 The Arm Bend arm and pinch at triceps. Only pinch the fat, not the muscle. Bend arm and pinch at triceps. Only pinch the fat, not the muscle. Normal: fingers don ’ t meet Normal: fingers don ’ t meet Abnormal: fingers meet Abnormal: fingers meet
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62 Forearm Forearm: often better site than upper arm for assessing fat Forearm: often better site than upper arm for assessing fat Upper arm fat disposition changes as women age Upper arm fat disposition changes as women age
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63 The Legs showing muscle wasting
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64 Quadriceps and Knees
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dermatitis dementia diarrhea death Pellagra niacin deficiency
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Vitamin C deficiency Perifolicullar pitichea
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Biochemical, laboratory assessment
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The possibilities of biochemical monitoring On-line monitoring (cardiosurgery – pH, minerals (K), the electrodes are localized on central cateter, possibility to check parameters on-line. On-line monitoring (cardiosurgery – pH, minerals (K), the electrodes are localized on central cateter, possibility to check parameters on-line. bed side monitoring (glycaemia, urine /protein, pH, blood../,oximeter O2 saturation, acidobasis, drugs /dg.strips) bed side monitoring (glycaemia, urine /protein, pH, blood../,oximeter O2 saturation, acidobasis, drugs /dg.strips) Biochemical analysis Biochemical analysis
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Biochemical parameters Na,K,Cl,Ca,P,Mg, osmolality - blood, urine Na,K,Cl,Ca,P,Mg, osmolality - blood, urine Acidobasis, lactate Acidobasis, lactate urea, creatinin, creatinin clearence, Nitrogen balance urea, creatinin, creatinin clearence, Nitrogen balance bilirubine, ALT, AST, LDH, amylase, lipase bilirubine, ALT, AST, LDH, amylase, lipase cholesterol, triglycerides, glucose – blood, urine cholesterol, triglycerides, glucose – blood, urine
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Biochemical parameters Total protein, albumine, prealbumine Total protein, albumine, prealbumine CRP CRP TSH TSH Basic analysis are made at the first,must be done within 90minutes Basic analysis are made at the first,must be done within 90minutes
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Other biochemical parameters Trace elements /Zn,Se../ Trace elements /Zn,Se../ Vitamins Vitamins Drugs /methotrexate, antiepileptics, antibiotics.../ Drugs /methotrexate, antiepileptics, antibiotics.../ Aminogram /glutamin../ Aminogram /glutamin../ Interleucins,TNF … Interleucins,TNF … Hormones /cortisol, glucagone, adrenaline../. Hormones /cortisol, glucagone, adrenaline../.
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Biochemical markers of nutrition status: Plasmatic proteins with short biologic half-life Plasmatic proteins with short biologic half-life Albumin Albumin –-syntetizate in liver, half-life time is 21 days –Normal: 35-45g/l. –Decrease of alb: malnutrition –Trends of changes alb.levels during realimentation are criterium of succesfull terapy. –Acute decrease: acute phase response.
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Biochemical markers of nutrition status: Transferin : syntesized in liver, Transferin : syntesized in liver, –biolog HL: 8days.Fysiolog. –Value 2-4g/l, RBP: syntesized in liver RBP: syntesized in liver –Biolog half-life : 12h., –Normal value: 0,03-0,006g/l. –Acute phase reactant (negative)
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Biochemical markers of nutrition status: P realbumin -syntesized in liver, P realbumin -syntesized in liver, –biolog.half-life:1,5 days. –Normal Value 0,15-0,4g/l. –Decrease in failure of proteosyntesis- indicator of acute protein malnutrition.
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NUTRITIONAL ASSESSMENT Urine urea nitrogen (UUN): to evaluate degree of hypermetabolism (stress level): Urine urea nitrogen (UUN): to evaluate degree of hypermetabolism (stress level): –0 – 5 g/d= normometabolism –5 – 10 g/d = mild hypermetabolism (level 1 stress) –10 – 15 = moderate (level 2 stress) –>15 = severe (level 3 stress)
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Nutrition Monitoring and Evaluation Monitor progress and determine if goals are met Monitor progress and determine if goals are met Identifies patient/client outcomes relevant to the nutrition diagnosis and intervention plans and goals Identifies patient/client outcomes relevant to the nutrition diagnosis and intervention plans and goals Measure and compare to client ’ s previous status, nutrition goals, or reference standards Measure and compare to client ’ s previous status, nutrition goals, or reference standards
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Other Outcomes Food and Nutrient Intake (FI) Energy intake Energy intake Food and Beverage Food and Beverage Enteral and parenteral Enteral and parenteral Bioactive substances Bioactive substances Macronutrients Macronutrients Micronutrients Micronutrients Physical Signs/Symptoms Anthropometric Anthropometric Biochemical and medical tests Biochemical and medical tests Physical examination Physical examination
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Monitoring
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Enteral Nutrition Monitoring: Gastric Residuals Clinically assess the patient for abdominal distension, fullness, bloating, discomfort Clinically assess the patient for abdominal distension, fullness, bloating, discomfort Place the pt on his/her right side for 15-20 minutes before checking a RV to avoid cascade effect Place the pt on his/her right side for 15-20 minutes before checking a RV to avoid cascade effect Seek transpyloric access of feeding tube Seek transpyloric access of feeding tube Raise threshold for RV to 200-300 mL Raise threshold for RV to 200-300 mL Consider stopping RV checks in stable pts Consider stopping RV checks in stable pts Rees Parrish C. Enteral Feeding: The Art and the Science. Nutr Clin Pract 2003; 18;75-85.
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Some Lab tests
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Na serum levels Hypernatremia: Na over 150 mmol/l hyperaldosteronism hypovolemia renin-angiot-aldost. hyperaldosteronism hypovolemia renin-angiot-aldost. Hypothalamic damage Hypothalamic damage Hypertonic hyperhydration Hypertonic hyperhydration Diabetes insipidus Diabetes insipidus Brain death Brain death
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Na serum levels( 136-145 ) Na serum levels( 136-145 mEq/L ) Hyponatremia: Na under 130 Hyponatremia: Na under 130 mEq/L Na in the third space - ascites, hydrothorax Na in the third space - ascites, hydrothorax Cardiac failure – increase of extracellular volume Cardiac failure – increase of extracellular volume Application of solutions without electrolytes Application of solutions without electrolytes Hypersecretion of ADH – water retention Hypersecretion of ADH – water retention
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K serum levels (3.5-5.3) K serum levels (3.5-5.3 mEq/L ) Hyperkalemia: K over 5,0 - 5,5 Hyperkalemia: K over 5,0 - 5,5 mEq/L –pH dependent /acidosis increases K level –Bigger intake, low output or both –Acute renal failure –Acute metabolic acidosis –Infusion with K
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K serum levels Hypokalemia: K under 3,5 Hypokalemia: K under 3,5 mEq/L –Low intake, bigger uptake, or both –Emesis, diarrhoe / intestinal loss/ –Diuretics –Chemotherapy, antimycotics /renal tubules failure/ –Anabolic phasis –Hyperaldosteronism –Acute metabolic alcalosis
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BUN (5-20 mg/dl ) Consider hydration and Nutrition. High level of urea – –high intake of N, – –increase catabolism – –polytrauma-muscele loss – –GIT bleeding – –dehydration – –low output- renal failure, Low level – malnutrition,serious hepatic failure- ureosyntetic cycle and gluconeogenesis dysfunction, pregnancy- increase ECF
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BUN (5-20 mg/dl ) Low level – – –malnutrition, – –serious hepatic failure- – –ureosyntetic cycle and gluconeogenesis dysfunction, – –pregnancy- – –increase ECF
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Urea Urea in urine Urea in urine Increase – catabolism, prerenal failure Increase – catabolism, prerenal failure Decrease – chronic malnutrition, acute renal failure Decrease – chronic malnutrition, acute renal failure
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Creatinine(0.5-1.1) Creatinine(0.5-1.1 mg/dl ) Serum levels of creatinine evaluation together with muscle mass, age, gender Serum levels of creatinine evaluation together with muscle mass, age, gender Increase Increase –bigger offer- destruction of muscle mass, –low output-renal failure Decrease- Decrease- –low offer-low muscle mass –malnutrition Creatinine clearence, excretion fraction - renal function Creatinine clearence, excretion fraction - renal function N-balance – catabolism – the need of nitrogen N-balance – catabolism – the need of nitrogen Uratic acid – cell damage, arthritis uratica Uratic acid – cell damage, arthritis uratica
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ALT(SGPT) N V: M: 7-46 F:4-35 U/L N V: M: 7-46 F:4-35 U/L High level – High level – –hepatopathologia, –steatosis, –hepatitis, –cell damage,
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AST(SGOT) High level – High level – –hypoperfusion, –hepatitis, –cell necrosis, –muscles damage both aminotransferases increase during damage of hepatic cells during inf.hepatitis. both aminotransferases increase during damage of hepatic cells during inf.hepatitis.
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TG(10-190 ) TG(10-190 mg/dl ) TG-increase TG-increase –during sepsis, mainly on the begining, –monitorate during parenter á l nutrition with lipid emulsion Glycemia, serum, urine, Glycemia, serum, urine, Hypoglycemia below 2,5mmol/l-vital danger Hypoglycemia below 2,5mmol/l-vital danger hyperglycemia- insulin.rezistence, recomendation level of glycemia 4,5-8,2 /2006/ better survive in ICU patient hyperglycemia- insulin.rezistence, recomendation level of glycemia 4,5-8,2 /2006/ better survive in ICU patient
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Glucose Glycemia, serum, urine, Glycemia, serum, urine, Hypoglycemia below 2,5-(45 ) vital danger Hypoglycemia below 2,5 mmol/l -(45 mg/dl ) vital danger hyperglycemia- insulin.rezistence hyperglycemia- insulin.rezistence Recomendation level of glycemia 4,5-8,2 (80-150 mg/dl ) Recomendation level of glycemia 4,5-8,2 (80-150 mg/dl )
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P – serum levels(2.7-4.5 ) P – serum levels(2.7-4.5 mg/dl ) Hypophosphataemia: under 1,9 Hypophosphataemia: under 1,9 mg/dl –Acute wastage of energy after succesfully resuscitation, overfeeding sy, anabolism (energetic substrates without K,Mg,P). Hyperphosphataemia – over 5,8 Hyperphosphataemia – over 5,8 mg/dl –Renal failure –Cell damage
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Mg – serum levels (1,3-2,5 mEq/L ) Mg – together with potassium Mg – together with potassium Hypomagnesaemia – under 1,2 mEq/L / Hypomagnesaemia – under 1,2 mEq/L / –renal failure –low intake.
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Monitoring of EN For formula intolerance, For formula intolerance, Hydration status, Hydration status, Electrolyte status, Electrolyte status, Nutritional status, Nutritional status,
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Monitoring
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Monitoring in PN therapy Weight (on a daily basis,initialy and ) Blood Daily Electrolytes (Na +, K +, Cl - ) Glucose Acid-base status 3 times/week BUN Ca +, P Plasma transaminases
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Monitoring in PN therapy Variable to be monitoredInitialLater period Clinical status Daily Catetheter site Daily Temperature Daily Intake &Output Daily
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Monitoring in PN therapy Variable to be monitoredInitialLater period WeightDailyWeekly serum glucoseDaily3/wk Electrolytes (Na +, K +, Cl - )Daily1-2//wk BUN3/wkWeekly Ca +, P,mg3/wkWeekly Liver function Enzymes3/wkWeekly Serum triglycerides weekly CBC weekly
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Problems 1. Catheter sepsis 2. Placement problems 3. Metabolic complications
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Complications Dehydration Possible cause: Inadequate fluid support; Unaccounted fluid loss (e.g. diarrhea, fistulae, persistent high fever). Management: Start second infusion of appropriate fluid, such as D5W, 1/2NS, NS. Estimate fluid requirement and adjust PN accordingly.
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Complications Overhydration Possible cause: Excess fluid administration; Compromised renal or cardiac function. Management: Consider D70 (can’t use with PPN) or 20% lipid as calorie source Initiate diuretics. Limit volume.
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Complications Alkalosis Possible cause: Inadequate K to compensate for cellular uptake during glucose transport Excessive GI or renal K losses. Inadequate Cl- in patients undergoing gastric decompression. Management: KCl to PN. Assure adequate hydration. Discontinue acetate.
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Complications Acidosis Possible cause: Excessive renal or GI losses of base Excessive Cl - in PN. Management: Rule out DKA and sepsis. Add acetate to PN.
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Complications Hypercarbia Possible cause: Excessive calorie or carbohydrate load. Management: Decrease total calories or CHO load.
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Complications Hypocalcemia Possible cause: Excessive PO4 salts Low serum albumin. Inadequate Ca in PN. Management: Slowly increase calcium in PN prescription.
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Complications Hypercalcemia Possible cause: Excessive Ca in PN Administration of vitamin A in patients with renal failure. Can lead to pancreatitis. Management: Decrease calcium in PN. Ensure adequate hydration. Limit vitamin supplements in patients with renal failure to vitamin C and B vitamins.
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Complications Hyperglycemia Possible cause: Stress response. Occurs approximately 25% of cases. Management: Rule out infection. Decrease carbohydrate in PN. Provide adequate insulin.
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Complications Hypoglycemia Possible cause: Sudden withdrawal of concentrated glucose. More common in children. Management: Taper PN. Start D10.
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Complications Cholestasis Possible cause: Lack of GI stimulation. Sludge present in 50% of patients on PN for 4-6 weeks; resolves with resumption of enteral feeding. Management: Promote enteral feeding.
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Complications Hepatic tissue damage and fat infiltration Possible cause: Unclear etiology. May be related to excessive glucose or energy administration; L-carnitine deficiency. Management: Rule out all other causes of liver failure. Increase fat intake relative to CHO. Enteral feeding.
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