2.mnt for metabolic stress burn...


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  • The metabolic response to fasting is an adaptation by the body to preserve protein by using alternative sources of energy.The carbohydrate deposits of the body last about 18 to 20 hours and new glucose is produced through gluconeogenesis of amino acids from the lean body mass. Ruderman NB. Muscle amino acid metabolism and gluconeogenesis. Annu Rev Med 1975;26:248
  • The initial response to fasting is mediated by a drop in serum insulin and an increase in glucagon. During this period energy is provided mainly by glucose from gluconeogenesis. However, lipolysis generates free fatty acids which are oxidized into ketones. After several days, most of the body organs are using ketones (acetoacetic, propionate, and butyric acids) for energy and gluconeogenesis decreases to half of the early phase. Brain, red blood cells, and nerve tissue still rely partially on glucose for energy.
  • This slide illustrates nitrogen losses in relation to trauma. With respect to protein, the greater the trauma, the greater the effect on the nitrogen balance. Similar to metabolic rate, patients experience nitrogen losses according to the severity and duration of the trauma.The normal range is indicated by the shaded area. The amount of protein requirement relative to calories increases in patients with metabolic stress.Long CL, et al. JPEN 1979;3:452-456.
  • G (gender)Female= 2, male = 1T= traumaB burnsO = obesity present =1 absent = 0
  • Calorie-to-nitrogen ratios can be used to prevent lean body mass from being utilized as a source of energy. Therefore, in the non-stressed patient, less protein is necessary to maintain muscle as compared to the severely stressed patient.
  • Rules of nine for adult and rules of 7 for chlidrenPercentage of burns
  • 1 degree– epidermis2 degree – dermis3 degree –subcutaneous tissue4 degree – muscle/bones
  • Sequestration -- >The action of forming a chelate or other stable compound with an ion or atom or molecule so that it is no longer available for reactions
  • 1– controlenviroment, temp, maintain fluid, electrolytes balance, control pain, anxiety and covering wound healing2- adequate cal to prevent LOW > 10% UBW, adequate protein, vit & mineral supp.3- acute peptic ulcer of the duodenum resulting as a complication from severe burns when reduced plasma volume leads to sloughing of the gastric mucosa.
  • To find out nitrogen gms= protein in gms/ 6.25 500 ml of 8.5 amino acid has 42.5gms protein that divided by 6.25= 6.8 gms The calories from dextrose and lipids have 1000 and 510 calories respectively Now divide 1510 non protein calories/ 6.8 =222 
  • up to 70% of energy …. ability to metabolise CHO
  • BCAA -- leucine, isoleucine, and valine
  • 2.mnt for metabolic stress burn...

    1. 1. Noraishah Mohamed Nor Dept Nutrition Sc. IIUM
    2. 2. Metabolic Stress Trauma  MVA, gunshot, stab wound, falls, burns Major cause of death and disability Active systemic response, depend on:  Pt‘s age, previous health status, preexisting diseases, type of infection, presence of multiple organ dysfunction syndrome (MODS) There are many metabolic changes that occur in patients who are critically ill (eg sepsis, trauma)
    3. 3.  Important to understand these changes when implementing nutritional therapy Once the systemic response is activated, the physiologic and metabolic changes that follow are similar and may lead to septic shock Ebb phase  initial response to bodily insult, occur immediately following injury (short term) Flow phase  neuroendocrine response to physiologic stress following the ebb phase (long term)
    4. 4.  Metabolic response during stress:  Metabolic response to stress (tissue injury, infection) is divided into the ebb and flow phaseEnergy expenditure Flow Phase Ebb Phase Time
    5. 5.  In the ebb phase, the body ‗shuts down‘ and the metabolic rate decreases Leads to hypovolemic shock:  ↓ Blood pressure  ↓ Cardiac output  ↓Body temperature  ↓tissue perfusion  ↓O2 consumption  ↓ metabolic rate Body‘s protective response (eg to blood loss)
    6. 6.  However, once the blood pressure is stabilized, the flow (recovery) phase begins Divided into 2 response:  Acute Response:  catabolism predominates  glucocorticoids  glucagon  catecholamines  Release cytokines, lipid mediators  Acute phase protein (CRP)  N2 excretion  metabolic rate  O2 consumptions  Impaired fuel utillization  Adaptive Response:  Anabolism predominates  Hormonal response gradually diminished  ↓ hypermetabolic rate  Assoc with recovery  Restore body protein  Wound healing
    7. 7.  Metabolic changes in the stressed (critically ill patient):  Energy metabolism  Protein metabolism  Carbohydrate metabolism  Fat metabolism  Others
    8. 8.  In the acute response metabolism is increased which requires energy However, the method of producing energy is different to that of a normal state or in periods of fasting (simple starvation)
    9. 9. Energy production in a normal(non fasting state) Usually E is from carbohydrates from normal intake Complex carbohydrate is broken down into glucose (preferred substrate for the brain) Excess carbohydatre mainly converted to fat and stored in adipose tissue
    10. 10. Metabolic Response to Fasting I II III IV VGLUCOSE UTILIZED (g/hora) 40 Exogenous Glycogen Gluconeogenesis 30 20 10 LEGEND I II III IV V FUEL FOR GLUCOSE, GLUCOSE, BRAIN GLUCOSE GLUCOSE GLUCOSE KETONES KETONES Ruderman NB. Annu Rev Med 1975;26:248
    11. 11. Metabolic Changes in Starvation
    12. 12. Metabolic Response to Trauma Nitrogen Excretion (g/day)
    13. 13. Starvation vs. Stress Metabolic response to stress differs from the responses to starvation. Starvation = decreased energy expenditure, use of alternative fuels, decreased protein wasting, stored glycogen used in 24 hours Late starvation = fatty acids, ketones, and glycerol provide energy for all tissues except brain, nervous system, and RBCs
    14. 14.  Hypermetabolic state—stress causes accelerated energy expenditure, glucose production, glucose cycling in liver and muscle Hyperglycemia can occur either from insulin resistance or excess glucose production via gluconeogenesis and Cori cycle. Muscle breakdown also accelerated
    15. 15. Hormonal Stress Response Aldosterone—corticosteroid that causes renal sodium retention Antidiuretic hormone (ADH)—stimulates renal tubular water absorption These conserve water and salt to support circulating blood volume
    16. 16.  ACTH—acts on adrenal cortex to release cortisol (mobilizes amino acids from skeletal muscles) Catecholamines—epinephrine and norepinephrine from renal medulla to stimulate hepatic glycogenolysis, fat mobilization, gluconeogenesis
    17. 17. Cytokines Interleukin-1, interleukin-6, and tumor necrosis factor (TNF) Released by phagocytes in response to tissue damage, infection, inflammation, and some drugs and chemicals
    18. 18. Nutrition Care Prevent PEM and possible complication of nutrition support Nutritional status prior to current illness is an important predictor of morbidity and mortality The level of injury will determine the level of metabolic stress The Glasgow Coma scale (GCS) score are usually used in critical ill pt.
    19. 19. Nutrition Intervention Oral route is the preferred route to meet the requirements However, for critically ill pt, usually the requirement only can be met via EN or PN There is evidence to support early initiation of nutrition support with specific metabolically stressed : acute pancreatitis, head injury and burns. EN should be consider first before PN
    20. 20. Definition Sepsis: an uncontrolled inflammatory response to infection or trauma (immunosuppressive response to infection) Septic shock: hypotension not reversed with fluid resuscitation and assoc with organ dysfx SIRS: not necessarily caused by infection, may occur after major surgery or trauma or with other condition such as myocardial infraction MODS: result from the complications of sepsis or SIRS; define as the present of the altered fx of 2 or > organs in acutely ill pt
    21. 21.  Diagnosis of Systemic Inflammatory Response Syndrome (SIRS):  Site of infection established and at least two of the following are present:  Body temperature >38° C or <36° C  Heart rate >90 beats/minute  Respiratory rate >20 breaths/min (tachypnea)  PaCO2 <32 mm Hg (hyperventilation)  WBC count >12,000/mm3 or <4000/mm3  Bandemia: presence of >10% bands (immature neutrophils) in the absence of chemotherapy-induced neutropenia and leukopenia  May be caused by bacterial translocation  Diagnostic criteria for MODS and pathopysiology refer handout
    22. 22. Bacterial Translocation Changes from acute insult to the gastrointestinal tract that may allow entry of bacteria from the gut lumen into the body; associated with a systemic inflammatory response that may contribute to multiple organ dysfunction syndrome Well documented in animals, may not occur to the same extent in humans Early enteral feeding is thought to prevent this
    23. 23. Factors to Consider in Screening anICU Patient: ICU medical admission —Diagnosis, nutritional status, organ function, pharmacologic agents Postoperative ICU admission —Type of Surgery, intraoperative complications, nutritional status, diagnosis, sepsis/SIRS Burn or trauma admission —Type of trauma, extent of injury, GI function
    24. 24. ASPEN Guidelines ASPEN (American Society of Parenteral and Enteral Nutrition) Objectives of optimal metabolic and nutritional support in injury, trauma, burns, sepsis: 1. Detect and correct preexisting malnutrition 2. Prevent progressive protein-calorie malnutrition 3. Optimize patient‘s metabolic state by managing fluid and electrolytes
    25. 25. NUTRITIONALASSESSMENT Traditional methods not adequate/reliable Urine urea nitrogen (UUN) excretion in gms per day may be used to evaluate degree of hypermetabolism:  0 –5 = normometabolism  5 – 10 = mild hypermetabolism (level 1 stress)  10 – 15 = moderate (level 2 stress)  >15 = severe (level 3 stress)
    26. 26. Determination of NutrientRequirements Energy Protein Vitamins, Minerals, Trace Elements Non-protein Calorie  Carbohydrate  Fat
    27. 27. Energy Enough but not too much Excess calories:  Hyperglycemia  Diuresis – complicates fluid/electrolyte balance  Hepatic steatosis (fatty liver)  Excess CO2 production  Exacerbate respiratory insufficiency  Prolong weaning from mechanical ventilation
    28. 28. Predictive Equations for Estimation ofEnergy Needs in Critical Care Harris-Benedict x 1.3-1.5 for stress ASPEN Guidelines:  25 – 30 calories per kg per day* Ireton-Jones Equations** Penn State equations Swinamer equation *ASPEN Board of Directors. JPEN 26;1S, 2002 ** Ireton-Jones CS, Jones JD. Why use predictive equations for energy expenditure assessment? JADA 97(suppl):A44, 1997. **Wall J, Ireton-Jones CS, et al. JADA 95(suppl):A24, 1995.
    29. 29. Harris-Benedict Equation(HBE) Injury Stress Factor Minor surgery 1.00 – 1.10 Energy requirements for Long bone fracture 1.15 – 1.30 patient with cancer in bed Cancer 1.10 – 1.30 HBE = BEE x 1.10 x 1.2 Peritonitis/sepsis 1.10 – 1.30 Severe infection/multiple trauma 1.20 – 1.40 Multi-organ failure syndrome 1.20 – 1.40 Burns 1.20 – 2.00 Activity Activity Factor Confined to bed 1.2 Out of bed 1.3ADA: Manual Of Clinical Dietetics. 5th ed. Chicago: American Dietetic Association; 1996Long CL, et al. JPEN 1979;3:452-456
    30. 30. Ireton-Jones 1997 EquationsVentilator-Dependent Patients: EEE = 1784 – 11(A) + 5(W) + 244(G) + 239(T) + 804(B)Spontaneously-Breathing Patients: EEE = 629 – 11(A) + 25(W) – 609(O)
    31. 31. Where: A = age in years W = weight (kg) O = presence of obesity >30% above IBW (0 = absent, 1 = present) G = gender (female = 0, male = 1) T = diagnosis of trauma (absent = 0, present = 1) B = diagnosis of burn (absent = 0, present = 1) EEE = estimated energy expenditure
    32. 32. Penn State Equation 1998 version: RMR = BMR (1.1) + VE (32) + Tmax (140) - 5340 2003a version: RMR = BMR (0.85) + VE (33) + Tmax (175) – 6433 Equations use BMR calculated using the Harris- Benedict equation, minute ventilation (VE) in liters per min (L/min), and maximum temperature (Tmax) in degrees Celsius.
    33. 33. Swinamer Equation EE = 945 (BSA) - 6.4 (age) + 108 (T) + 24.2 (breaths/min) + 81.7 (VT) – 4349 Equation uses body surface area (BSA) in squared meters (m2), temperature (T) in degrees Celsius, and tidal volume (VT) in liters per minute (L/min).
    34. 34. Estimation of RMR inObesity Harris-Benedict using actual weight x 1.2 (60% of subjects predicted within 10% of RMR) or an adjusted weight x 1.3 (67% of subjects predicted within 10% of RMR) resulted in the most accurate predictions. Penn State 2003a equation predicts within 10% of RMR in 61% of subjects, the Penn State 1998 equation predicts within 10% of RMR in 67% of subjects Ireton-Jones, 1992 equations predict within 10% of RMR in 72% of subjects.
    35. 35. Recommendations forPredicting RMR in Critically IllPts HBE should not be used to predict RMR in critically ill patients Ireton-Jones 1997 should not be used to predict RMR in critically ill patients Ireton-Jones 1992 may be used to predict RMR in critically ill pts but errors will occur.  ADA Evidence Analysis Library, 10-06
    36. 36. ProteinStress Level No Stress Moderate Stress Severe StressCalorie:Nitrogen Ratio > 150:1 150-100:1 < 100:1Percent Potein / Total < 15% 15-20% > 20% proteinCalories protein proteinProtein / kg Body Weight 0.8 1.0-1.2 g/kg/day 1.5-2.0 g/kg/day g/kg/day
    37. 37. What Weight Do You Use? Actual weight may be inaccurate in trauma and burn patients who have been fluid resuscitated Usual weights may not be available There is no validation for the common practice of using an ―adjusted‖ body weight for obese patients when using Harris-Benedict since Harris-Benedict equations were derived from studies done on healthy people of all sizes Ireton-Jones uses actual weight in her equations and then adjusts for obesity
    38. 38.  Lean body mass is highly correlated with actual weight in persons of all sizes Studies have shown that determination of energy needs using adjusted body weight becomes increasingly inaccurate as BMI increases However, some studies suggest that high protein hypocaloric feedings in obese patients may be therapeutically useful Because overfeeding is more problematic than underfeeding, could possibly use adjusted weight or 20-21 kcal/kg actual BW in obese pts
    39. 39. Specialized Nutrients in CriticalCare Include supplemental branched chain amino acids, glutamine, arginine, omega-3 fatty acids, RNA, others Most studies used more than one nutrient, making assessment of efficacy of specific supplements impossible Immune-enhancing formulas may reduce infectious complications in critically ill pts but not alter mortality Mortality may actually be increased in some subgroups (septic patients)
    40. 40. Timing of Enteral Nutrition andCritical Illness If the critically ill patient is adequately fluid resuscitated, then EN should be started within 24 to 48 hours following injury or admission to the ICU. Early EN is associated with a reduction in infectious complications and may reduce LOS. The impact of timing of EN on mortality has not been adequately evaluated.
    41. 41. Monitoring Response to MNT inCritical Care Pts: Blood Glucose Hyperglycemia (up to 200-220 mg/dl) in critically ill patients was once considered acceptable Recent studies suggest hyperglycemia is associated with infection, morbidity, mortality New goal is to keep BG as close to normal as possible. Target: <150 mg/dl Use insulin drip and sliding scale; convert to subcutaneous insulin as possible Can use intermediate insulins morning and evening once feedings are tolerated and stable
    42. 42.  Survival is decreased in critically ill patients with hyperglycemia Controlling BG is associated with fewer infectious complications in critically ill patients There is fair evidence that controlling BG values in critically ill patients leads to a decrease in ICU LOS Dietitians should promote attainment of strict glycemic control (80-110mg/dL) to reduce time on mechanical ventilation in critically ill medical ICU patients
    43. 43. Head Injury
    44. 44.  Traumatic Brain Injury (TBI) Severely hypermetabolic and catabolic The more severe the head injury, the greater the release of catecholamines (norepinephrine and epinephrine) and cortisol and the greater the hypermetabolic response. release of catecholamines, cortisol, & hypermetabolic response Without rapid nutrition support  rapid LBM loss and immunosuppression Glasgow Coma Scale (GCS) to evaluate pt‘s consciousness:  Sore 14–15 minor head injury  Score 9 – 13  moderate head injury
    45. 45. MNT Energy:  Use indirect calorimetry when available  Use H/B x 1.4 stress factor  GCS often EE  Take into consideration the IV glucose (provide E) total cal – the IV glucose E Protein:  estimated at 1.5 – 2.2 g/kg of body weight  BCAA help to restore plasma AA profile and nitrogen bal
    46. 46.  Vitamins & Minerals  Low plasma Vit B & C,  Increase Zn excretion Fluid or/and sodium restriction
    47. 47. BURNS
    48. 48.  Definition: a result of tissue injury caused by exposure to heat, chemical, radiation, or electricity May result from injury to the skin but damage may extend into muscle and bone. When the burn injury exceeds 15 to 20% of the total body surface area (TBSA), it results in systemic disturbances, including a major stress response, impaired immunity and extensive fluid redistribution
    49. 49.  The consequences of these metabolic alterations include increased gluconeogenesis, increased proteolysis, increased ureagenesis, sequestration of micronutrients and altered lipid metabolism The metabolic response increased physiological demands placed on the cardiac, pulmonary, renal and other organ systems, complicates nutritional support. Patients with major burn injuries also develop immune system impairment, which predisposes them to infection and multi-organ failure (MOF)
    50. 50. MNT Objectives:  Maintain body mass, particularly lean body mass  Prevent starvation and specific nutrient deficiencies  Improve wound healing  Manage infections  Restore visceral and somatic protein losses  Avoid or minimize complications associated with enteral or parenteral nutrition
    51. 51.  Energy  Based on size of burn (% TBSA)  Use the Curreri Formula: ER = 24kcal x kgUBW + 40 kcal x %TBSA (usually 200% REE) OR  Formula (Xie et al, 1993): Energy expenditure (kcal/d) = (1000 kcal x BSA [m ]) + 2 (25 x %TBSA) OR
    52. 52. Basal energy expenditure (BEE) per Harris-Benedict equationMale: BEE = 66 + (13.7 x W) + (5 x H) – (6.8 x age)Female: BEE = 655 + (9.6 x W) + (1.9 x H) – (4.7 x age)Adjustments for burn severityExtent of burn BEE Protein NPE:N ratioHealthy individual 1.0 g/kg/d 150:1Moderate burn (15–30% X 1.5 1.5 g/kg/d 100–120:1TBSA)Major burn (15–30% TBSA) X1.5–1.8 1.5–2 g/kg/d 100:1Massive burn (≥ 50%) X1.8–2.1 2–2.3 g/kg/d 100:1Activity factors: In bed = 1.2 Ambulatory = 1.3 Ventilated = 1.05
    53. 53.  ER for burned pediatric pts:  Galveston Formula = 1800 kcal/m2 + 2200 kcal/m2 burn  Polk Formula = (<3 y.o) = (60 kcal x wt) + (35kcal x % TBSA) Important to remember that a progressive exercise programme should always be combined with adequate nutrition to enhance the restoration of muscle mass and strength
    54. 54.  CHO  50 to 60% or can be up to 70% of energy  not to exceed 5 to 7 mg/kg/min in parenteral nutrition  CHO need for protein sparing; but excess result in hyperglacemia, osmotic diuresis, dehydration, respiratory difficullity
    55. 55.  Protein:  requirement due to losses via urine, wound, gluconeogenesis and wound healing  20 -25% of total calories (HBV protein)  Pediatrics  2.5 – 3.0 g/kg (monitor renal fx & fluid balance)  BCAA‘s & arginine  improve wound healing & immunity  Monitor BUN, serum creatinine, & hydration  To estimate wound nitrogen loss:  < 10% open wound = 0.02 g nitrogen/kg/d  11 – 30% open wound = 0.05 g nitrogen/kg/d  > 31 % open wound = 0.12 g nitrogen/kg/d
    56. 56.  Fats:  Fat supplied at 15% of total energy reduced infectious morbidity and shortened hospitalization time compared to 35% of energy requirements being derived from fat.  Increase omega- 3  may improve immune response (inhibits production of prostaglandins & leukotrienes)  Begin with 15 – 20% [monitor immune response, feeding tolerance and serum TG (not rise > 10 to 20% over baseline values)]
    57. 57.  Hart et al (2001) found that a high-carbohydrate diet, with 3% fat, 82% carbohydrates and 15% protein, stimulated protein synthesis, increased endogenous insulin production and improved lean body mass accretion compared to high-fat diet.
    58. 58.  Vitamins & Minerals Supplementation  Evidence-based guidelines for micronutrient supplementation are limited  Vit C- collagen formation and antioxidant defense in the immune system and is involved in ATP production (66 mg/kg/h during the first 24 hours)  Vit A – immune fx & epithelialization (1000 IU/1000kcal)  Na & K restore via fluid therapy  Ca depression – reduced with earlier ambulation & excersize  Supp PO4 & Mg parenterally (to avoid GI irritation)  Zn supp 220mg Zn sulphate ( co fac in Vit E metab)
    59. 59. Methods of Nutritional Support Pt with <20% TBSA burn able to meet the regular needs with regular hi-cal, hi-protein diet Use ‗concealed nutrients‘ – add protein to pudding, milk etc Pt with major burn & EE require ETF or TPN (if ileus not fx or do not tolerate TF)
    60. 60. Acute Spinal Cord Injury
    61. 61. MNT Energy :  H/B x 1.1 x 1.2 (Barco et al, NCP 17;309-313, 2002) Pt with multi-traumas in addition to SCI may have higher needs Protein needs:  2 g/kg (Rodriguez DJ et al, JPEN 15:319-322, 1991)
    62. 62. Surgery/Trauma
    63. 63.  Def: an operative procedure used to diagnose, repair, or treat an organ tissue. Can be further classify to major/minor surgery The sign & symptoms experienced with surgery depend to the type of procedure.  Pt need to be fasted for 12 hr before surgery The progress of feeding from NBM/NPO to solid diet should be done as quickly as possible The energy and protein should be individualize.
    64. 64. MNT Energy:  HB x 1.0 – 1.3 depend on type of surgery  Will vary with type of surgery, degree of trauma  Use Ireton-Jones 1992 or Penn State if data is available*  Can use estimate of 25-30 kcals/kg to begin and monitor response to therapy***ADA Evidence Analysis Library, accessed 10-06**ASPEN Nutrition Support Practice Manual, 2nd Edition, p. 278 Protein:  Minor surgery : 1 -1.1 g/kg  Major Surgery : 1.2 – 1.5 g/kg
    65. 65. ASPEN Practice Guidelines Perioperative NutritionSupport Preoperative NS should be administered to moderately- severely malnourished pts undergoing major gastrointestinal surgery for 7 to 14 days if the operation can be safely postponed. PN should not be routinely given in the immediate postoperative period to patients undergoing major gastrointestinal procedures. Postoperative NS should be administered to patients who will be unable to meet their nutrient needs orally for a period of 7 to 10 days.
    66. 66. Postoperative Nutrition Support Introduction of solid foods depends on condition of GI Oral feeding may be delayed for first 24 – 48 hours post surgery until return of bowel sounds, passage of flatus or soft abdomen Traditional practice has been to progress from clear liquids, to full liquids, to solid foods However, there is no physiological reason not to initiate solid foods once small amounts of liquids are tolerated
    67. 67. Hypocaloric Feedings Hypocaloric feedings have been recommended in specific patient populations:  Class III obesity (BMI>40)  Refeeding syndrome  Severe malnutrition  Trauma patients following shock resuscitation  Hemodynamic instability  Acute respiratory distress syndrome or COPD  MODS, SIRS or sepsis Aggressive protein provision (1.5-2.0 gm/kg/day
    68. 68.  Although overfeeding surgical patients should be avoided, prolonged underfeeding may be equally concerning. This can compromise immune function, delay wound healing, exacerbate muscle wasting, and prolong the recovery of nitrogen balance and visceral protein levels. However, short-term hypocaloric feeding with 1-2 g of protein per kilogram per day, particularly in the acute phase of postoperative stress, may reduce metabolic complications while supporting a reduction in negative