nutrition in critical care课件

Nutrition in critical care,Pratthana Srisangthong,MD,Scope,Metabolic response in critical illness Assessment of nutritional status Enteral nutrition Parenteral nutrition Immunonutrition and antioxidant,Background,Adequate nutrition is essential to the critically ill patient. It helps support anabolism uncontrolled catabolism maintain a competent immune system improve patient outcome. Severe trauma, burns, sepsis, and head injury are associated with marked hypermetabolism and hypercatabolism, metabolic alterations.,Metabolic response in critical illness,2 principal metabolic response 1 response to starvation 2 response to stress,Proceedings of the Nutrition Society (2007), 66, 1624,Metabolic response to starvation,Typical setting patient with chronic disease During the first 12 24 hr of acute starvation mobilization of hepatic glycogen stores 24 72 hr stimulation of gluconeogenesis After 72 hr - increase in hepatic ketone bodies production - reduction of gluconeogenesis - decreased protein breakdown Subsequently, as starvation progresses decrease lean body mass and BMR,Nutrition 13(Supp1):45S-51S, 1997,Metabolic response to starvation,Several features distinguish the metabolic response of starved, critically ill patients. As starvation progresses increased loss of lean body mass energy expenditure is not decrease. Continuation of starvation beyond 3 d not accompanied by a stimulation of both ketogenesis and ketone body oxidation (with their normally concomitant suppression of gluconeogenesis and protein breakdown),Metabolic response to starvation,Starvation in critically ill patients leads to accelerated protein-calorie malnutrition. These alterations caused by inflammatory mediators.,Metabolic response to stress,1 energy metabolism - increased REE,Metabolic response to stress,Factor influenced energy expenditure 1 effect of illness - stage and length of illness - fever - pain , physical activity , agitation , abnormal posturing , increase muscle tone , seizure,Metabolic response to stress,2. effect of treatment - cathecholamine EE - beta blocker EE - sedative drug EE Supportive treatment can limit level of metabolism,Metabolic response to stress,2 protein metabolism - protein catabolism protein synthesis net negative nitrogen balance - loss of muscle mass and protein degradation in vital organ - immobilization causes atrophy of skeletal muscle negative nitrogen balance,Nutrition Vol. 13, No. 9(Suppl), 1997,Metabolic response to stress,protein metabolism - movement of amino acid ( alanine, glutamine ) for gluconeogenesis decreased intramuscular of glutamine - BCAA metabolism - liver reprioritized protein synthesis positive acute phase protein ( CRP , alpha 1 antitrypsin ) negative acute phase protein ( albumin , prealbumin ),A.S.P.E.N. Nutrition Support Practice Manual 2nd Ed.,Consequences of protein catabolism,Metabolic response to stress,3 carbohydrate metabolism - increased couterreguratory hormone and cytokines GH, cortisol, glucagon, cathecholamine IL-1, IL-6, TNF, LTS, prostanoids endogeneous glucose production - insulin resistance hyperglycemia,Metabolic response to stress,carbohydrate metabolism substrate of gluconeogenesis glycerol from adipose tissue alanine from skeletal muscle lactate from peripheral tissue and skeletal muscle ,Metabolic response to stress,4 lipid metabolism effect of catecholamines and cytokines mobilization of glycerol and free fatty acid increased lypolysis increased fatty acid oxidation reduced energy store,Metabolic response to stress,5 Changes in endocrine system The response is essential for maintainance of cellular and organ hemeostsis - activation of hypothalamic pituitary adrenal axis - release cortisol from adrenal tissue,Metabolic response to stress,6 fluid and electrolyte,depending on the patients underlying medical problems, nutritional status, and drug or resuscitative therapy.,Assessment of nutritional status,History include medical, surgical and dietary history ,A history of acute or chronic weight loss or gain before hospital admission is an essential indicator of the patients nutritional status.,Assessment of nutritional status,2 Anthropometric parameters unreliable and seldom used because the patients positioning and fluid status affect their accuracy. 3. Visceral protein levels affected by stress, fluid shifts, and other factors limit their specificity and sensitivity.,Assessment of nutritional status,4 Delayed hypersensitivity skin testing - limits in the critically ill patients - many nonnutritional factors such as acute hemorrhage, hypovolemic shock, surgery, and the use of steroids and immunosuppressants depress immune function. 5 Gold standard indirect calorimeter,Purpose of nutrition support,1 safe life 2 speed recovery by reducing neuropathy and maintain muscle mass and function,Route of supplement,EN vs PN Patients who can be fed via the enteral route should receive EN Indication of EN in ICU patients All patients who are not expected to be on a full oral diet within 3 days should receive EN,Clinical Nutrition (2006) 25, 210223,Is early EN ( 2448 h after admission to ICU) superior to delayed EN in the critically ill?,Effects of Early Enteral Feeding on the Outcome of Critically Ill Mechanically Ventilated Medical Patients* large multi-institutional ICU database. 4,049 patients requiring mechanical ventilation for 2 days. overall ICU and hospital mortality were lower in the early feeding group (18.1% vs 21.4%, p 0.01 early feeding was found to be independently associated with an increased risk of ventilator-associated pneumonia (VAP),Effects of Early Enteral Feeding on the Outcome of Critically Ill Mechanically Ventilated Medical Patients*,CHEST / 129 / 4 / APRIL, 2006,Prospective ,controlled, clinical trials - 150 patients were enrolled. 75 pt early feeding 75 pt late feeding Patients in early feeding had greater incidence of VAP.49.3% vs 30.7% p 0.020 and longer ICU days. No statistic difference in mortality Aggressive early EN in mechanical ventilator medical patients is associated with greater infection and prolong length of stays.,Is early EN (2448 h after admission to ICU) superior to delayed EN in the critically ill?,The expert committee, however favours view that critically ill patients, who are haemodynamically stable and have a functioning gastrointestinal tract, should be fed early ( 24 h), if possible, using an appropriate amount of feed,How much EN should critically ill patients receive?,- During the acute and initial phase of critical illness an exogenous energy supply in excess of 2025 kcal/kg BW/day may be associated with a less favourable outcome - During recovery (anabolic flow phase), the aim should be to provide 2530 total kcal/kg BW/day,How much EN should critically ill patients receive?,Patients with a severe undernutrition should receive EN up 2530 total kcal/kg BW/day. If these target values are not reached supplementary parenteral nutrition should be given.,Caloric Intake in Medical ICU Patients*,Prospective cohort study. Patients with an ICU length of stay of at least 96 hr. Study participants were underfed relative to ACCP targets. moderate caloric intake (9 to 18 kcal/kg per day) was associated with better outcomes than higher levels of caloric intake.,CHEST / 124 / 1 / JULY, 2003,Which route is preferable for EN?,There is no significant difference in the efficacy of jejunal versus gastric feeding in critically ill patients,Protein requirement,1.5 g/kg/day. 2 g/kg/day in patients with trauma, severe burns, and head injury 2.5 g/kg/day in adult patients treated with continuous renal replacement therapy (CRRT) nutritional support can only limit the loss of the bodys protein and calorie stores. The goal is to administer sufficient nitrogen to provide a positive or neutral nitrogen balance.,Lipid requirements,0.5 1 g/kg/d 20-40% of energy Lipid clearance is reduced in stressed patients due to decreased activity of lipoprotein lipase (LPL), infusion rate should not exceed 0.12 g/kg/hr to avoid the development of elevated triglyceride levels. Source of essential fatty acid, fat soluble vitamin. Avoid omega 6 linoleic is precursor of arachinodic acid precursor of PG,TXA,LT ,Lipid requirements,0.5 1 g/kg/d 20-40% of energy Lipid clearance is reduced in stressed patients due to decreased activity of lipoprotein lipase (LPL), infusion rate should not exceed 0.12 g/kg/hr to avoid the development of elevated triglyceride levels. Source of essential fatty acid, fat soluble vitamin. Avoid omega 6 linoleic is precursor of arachinodic acid precursor of PG,TXA,LT ,Parenteral nutrition,Indication In patients who cannot be fed sufficient enterally the deficit. intolerant to EN Beware Overfeeding PN should not be used to correct acute fluid and electrolyte deficiencies,Complications of PN,PN associated with a more pronounced proinflammatory response than EN harmful in patients with severe inflammation. Complications of excess dextrose infusion hyperglycemia hypertriglyceridemia hepatic steatosis, respiratory decompensation depression of immune function,Complications of PN,Hyperglycemia depression of immune function increase infection risk impair cellular and humoral host defenses reducing phagocytosis inhibiting complement fixation Controlling hyperglycemia has resulted in improved phagocytic function as well as improved patient outcome.,n engl j med 355;18 november 2, 2006,Complications of PN,Hypertriglyceridemia due to dextrose overfeeding or excess lipid infusion. Stressed patients are at higher risk for hypertriglyceridemia due to 1 increased lipolysis and hepatic fatty acid reesterification 2 increased hepatic triglyceride synthesis from dextrose infusion 3 decreased LPL enzyme activity 4 medications such as corticosteroids,Complications of PN,Hypertriglyceridemia Patients at risk sepsis multiorgan failure diabetes liver disease renal failure pancreatitis.,Complications of PN,hypercapnia - result from total energy and dextrose overfeeding patient at risk borderline respiratory function and limited pulmonary reserve. excess carbon dioxide is produced increased respiratory workload and minute ventilation,Immunonutrition and antioxidant,Growth hormone Arginine Antioxidant Selenium,The negative nitrogen balance in critically ill patients is partly due to resistance to growth hormone and the decreased production and action of IGF-I prospective, multicenter, double-blind, randomized, placebo-controlled trials 247 Finnish patients and 285 patients in other European countries who had been in an ICU for 5 to 7 days,N engl j med 355;18 november 2, 2006,The in-hospital mortality rate was higher in the patients who received growth hormone than in those who did not (P0.001) Among the survivors, the length of stay in ICU and in the hospital and the duration of mechanical ventilation were prolonged in the growth hormone group. In patients with prolonged critical illness, high doses of growth hormone are associated with increased morbidity and mortality.,The reason for the increased morbidity and mortality is unclear Modulation of immune function may be involved multiple-organ failure and septic shock or uncontrolled infection as causes of death in GH Fluid retention abnormal fluid distribution Hyperglycemia increase risk of infection GH prevents the mobilization of glutamine from muscle Stimulation of lipolysis,The reason for the increased morbidity and mortality is unclear Modulation of immune function may be involved multiple-organ failure and septic shock or uncontrolled infection as causes of death in GH Fluid retention abnormal fluid distribution Hyperglycemia increase risk of infection GH prevents the mobilization of glutamine from muscle Stimulation of lipolysis,Is essential amino acid for adult in injured or stress state Is less available in body under these conditions Function of arginine Protein synthesis substrate of urea cycle Production of nitric oxide,American journal of critical care,Jan 2004,vol 13, No 1,Function of arginine,Metabolism of arginine,Metabolism of arginine,Proline hydroxyproline collagen substrate for wound healing Nitric oxide Decreased acute injury Decreased wound infection Vascular relaxation regulate blood pressure,Clinical improvement in surgical patient fewer infection complications But increased mortality in patients with shock, sepsi