MNT For Critical Care (Part 1) PDF

MNT FOR CRITICAL CARE (Part 1) GTD331 – MNT III NurZetty Sofia Zainuddin [email protected] LEARNING OUTCOMES UNDERSTANDING METABOLIC STRESS AND 01. RELATION WITH MALNUTRITION IN CRITICAL CARE CASES Explain the metabolic response to stress Differentia...

MNT FOR CRITICAL CARE (Part 1) GTD331 – MNT III NurZetty Sofia Zainuddin [email protected] LEARNING OUTCOMES UNDERSTANDING METABOLIC STRESS AND 01. RELATION WITH MALNUTRITION IN CRITICAL CARE CASES Explain the metabolic response to stress Differentiate starvation and metabolic stress Describe relation of malnutrition in critical care settings UNDERSTANDING PRINCIPLES OF MEDICAL NUTRITION THERAPY FOR CRITICAL CARE 02. CASES Explain the component of nutritional assessment and screening for critical care cases Describe the medical nutrition therapy for critical care cases  Central nervous INTRODUCTION system MNT in Critical Care Metabolic and respiratory Vital Circulatory system system organ Critical care is complex medical management of seriously ill or injured person Involves acute impairment of one Renal and or more vital organs system with hepatic system high chances of life-threatening deteriorating Results in profound metabolic alterations (injury → wound healing → recovery complete) Disorder frequently treated in ICU Asthma burn COPD Pneumonia Acute respiratory distress syndrome Sepsis Trauma Metabolic Response to Stress Flow Phase ↑ cardiac output, O2 consumption, temperature, energy expenditure, total body protein catabolism Due to fluid resuscitation Ebb Phase using: Crystalloids – IV fluid Occur immediately after injury solution (2-48 hours) Colloids – albumin or blood Hypovolemia, shock, tissue Restoration of O2 transport hypoxia ↑ glucose production, FFA ↓ cardiac output, O2 release, insulin, consumption, temperature catecholamines, glucagon, ↓ insulin dt ↑ glucagon (signal and cortisol for ↑ hepatic glucose production) Medical goal : to restore blood flow to organs, maintain oxygenation of tissues, stop all hemorrhaging  Hypermetabolism, Return to anabolism catabolism, altered and normal immune & hormonal metabolic rate responses  Metabolic stress associated with hormonal status that increased flow of substrate but poor use of CHO, Protein & Fat Injury / sepsis → elevated of counterregulatory hormones leads to accelerated proteolysis via Glucagon Promotes gluconeogenesis, amino acid uptake by liver, ureagenesis, protein catabolism Cortisol Enhanced skeletal muscle catabolism, promotes hepatic use of amino acid for gluconeogenesis, glycogenolysis, acute-phase protein synthesis After injury / sepsis, energy production depends on protein BCAA oxidized from skeletal muscle and become source of energy for muscle → resulting in rapid loss of LBM and ↑ of net negative nitrogen balance Protein Lipid Glucose Others Hyperglycemia Release of due to aldosterone → ↑ circulation of ↑ glucose renal sodium Breakdown of FFA due to production retention and protein also Gluconeogenesis lipolysis caused vasopressin cause ↑ urinary ↑ hormones by (ADH) loss of (epinephrine) catecholamines Leads to renal potassium, and cortisol tubular resorption phosphorus and high ratio (conserve water and and salt for of glucagon : magnesium circulating blood insulin volume)  How about Starvation vs Stress? stress? Starvation Loss of muscle is much slower Stored glycogen become primary source of fuel but depleted after 24 hours Glucose is available from breakdown of protein to amino acids ↓ glucose → ↓ insulin secretion → ↑ glucagon Protein catabolism ↓ and hepatic gluconeogenesis ↓ 1 week of fasting – ketosis develop (ketone bodies supply bulk of energy need) Late starvation – ketone body production ↑, fatty acids serve as major energy source for all tissues Starvation : decrease EE, diminished gluconeogenesis, ↑ ketone body, ↓ ureagenesis Summary of Metabolic Abnormalities in Stress Response Increased levels of glucagon, cortisol, epinephrine, norepinephrine Hyperglycemia and insulin resistance Increased basal metabolic rate Increased rate of gluconeogenesis Catabolism of skeletal muscle Increased urinary nitrogen excretion (negative nitrogen balance) Increased synthesis of positive acute-phase protein (CRP, fibronectin, ceruloplasmin) Decreased synthesis of negative acute-phase proteins (albumin, prealbumin) Systemic Inflammatory Response Syndrome (SIRS), Sepsis and Multiple Organ Dysfunction of or Failure (MODS)  Sepsis – organ dysfunction caused by dysregulated host response to infection Bacteria and toxins (virus, fungi, parasite) – lead to strong inflammatory response during critical illness SIRS – widespread of inflammation that occur in: Infection, pancreatitis, ischemia, burns, multiple trauma, haemorrhagic shock, immunologically mediated organ injury Each condition leads to release of cytokines, proteolytic enzymes, toxic O2 species (free radicals) Happens in different part from primary site of injury – affecting healthy tissue  MODS – complication of SIRS Begins with lung failure, then liver, intestines, kidney Later – hematological and myocardial failures Anytime – central nervous system, MODS can occur direct result of injury to an organ from trauma, major surgery, burns, sepsis, AKI, acute pancreatitis Secondary MODS – presence of inflammation / infection in organs remote from initial injury  Development of SIRS / MODS Trigger from injury or disruption of gut barrier SIRS function MODS Shock results in gut hypoperfusion Sepsis Lack of peristalsis of stomach, small bowel, ileus Hypermetabolic, exhibit high cardiac output, low O2 consumption, high O2 saturation, lactic acidemia. Gut dysfunction Strong +ve fluid balance (massive edema & decreased in plasma protein concentrations) Early EN – maintaining tight junction between intraepithelial cells, stimulate blood flow and induce release of trophic factors  SIRS Two or more of the following are present: Body temperature < 38C or 90 beats/minutes Respiratory rate > 20 breaths/min (tachypnea) WBC > 12,000/mm3 or < 4000 mm3 or > 10% immature bands  Quick Sequential Organ Failure Assessment (qSOFA) Respiratory rate > 22 breaths/min Body temperature < 38C or