(11/13) Garofalo Lecture: Nutritional Needs in Special ... · (11/13) Garofalo Lecture: Nutritional Needs in Special Populations Diabetes Patients - Treatment Goals o Avoid Hyperglycemia,

(11/13) Garofalo Lecture: Nutritional Needs in Special Populations Diabetes Patients

- Treatment Goals o Avoid Hyperglycemia, Hypoglycemia, and Glycosuria

§ In a study: Hyperglycemia, especially within the first 24 hours, was a major predictor of mortality in TPN patients

§ In a study: Hypoglycemia was similarly linked to higher mortality rates – emphasizing adequate insulin control

o Avoid overfeeding, especially carbohydrates o Consider Insulin therapy to manage BG in T1DM and T2DM

while on PN - PN Carbohydrates

o At initiation: Maximum 150g Glucose, at a maximal rate of 1.5mg/kg/min § Co-administration of insulin may be required, preferably long-acting glargine insulin, within the

TPN or as a separate infusion. Be wary, 10-50% of insulin adheres to the bag. o Insulin Dosing: 2/3 of @home dose. If possible, consider patients normal @home carb diet.

§ Monitor: Blood glucose at least every 6 hours, providing short-acting insulin PRN as correction - EN Carbohydrates

o At initiation: Start at 25% of estimated needs, Monitor BG every 6 hours. Increase load in increments every 1-2 days as tolerated by the patient.

o Restrict carbohydrate to at maximum 50% of total calories. o Preference high fiber formulas, which will be more slowly metabolized, minimizing BG peaks o Continuous delivery > Bolus feedings

Renal Disease Patients - Treatment Goals

o Provide adequate protein without causing azotemia or uremia. [Maintain positive nitrogen balance] § Patients with acute kidney disease are in a catabolic state breaking down muscle protein,

frequently resulting in azotemia o Correct/maintain normal fluid, electrolyte, and acid-base balance o Satisfy macro/micronutrient requirements as related to the type of renal disease

- Carbohydrate - Assess Glucose Homeostatic Mechanisms: Patients with renal disease should be assessed prior to glucose/insulin administration, as their condition may predispose Hypo- or Hyperglycemia

o Hypoglycemia: Typically before we treat the patient - As a result of decreased insulin renal elimination, glucagon reserves are depleted. Similarly, CAP-Dialysis may result in loss of carbohydrate due to absorption into dialysate.

o Hyperglycemia: Typically after we treat the patient - Due to peripheral insulin resistance, AKI-induced increased levels of glucagon, growth hormone, and catecholamines may result in hyperglycemia.

§ \ initiate glucose at lower amounts and titrate up slowly - Protein

o Dosing: Give normal amount of protein, Unless on Renal Replacement Therapy (RRT) § Protein removal varies with the type of renal replacement. § Patients on Dialysis may have higher protein requirements

o Azotemia: Without RRT, it is likely renal disease patients will develop Azotemia. Azotemia refers to abnormally high levels of nitrogen containing compounds in the blood

§ As a result of GI bleeding, dehydration, or overfeeding of protein, elevations in BUN may occur.

§ AKI is associated with marked protein catabolism and consequential urea accumulation

o Product: A mixture of essential AA and non-essential AA is recommended for patients with renal failure. The boutique/specialty renal formulations currently do not show any benefit over the standard.

§ Specialty: Aminosyn RF 5.2%, NephrAmine 5.4% These only provide essential AA. § Standard: Travisol. Has both essential and nonessential AA

- Fat o Dosing: Give normal amount of fat. In fact, fat is very calorically dense, such that we can administer it in

very small volumes – beneficial for renal disease patients. . IVLE = Volume-sparing § Monitoring: Closely monitor triglycerides (at least weekly) and phosphorous levels (daily)

o Metabolic Difficulties: ~50% of AKI patients have decreased hepatic lipoprotein lipase, resulting in TGÝ upon IVLE administration. Furthermore, Insulin resistance and metabolic acidosis may further worsen these elevations by inhibiting lipoprotein lipase. Egg-phospholipid products have 7.4mM phosphate, therefore, we should monitor. (Did you ask about Allergies?)

- Water and Sodium o Renal disease diagnosis will determine H2O/Na balance o AKI: First determine a patient’s fluid status by measuring

their urine output (UO) § Oliguric (<500mL daily = Low UO): Need to

minimize fluids in these patients. And 50% Na+ § Non-Oliguric (³500mL daily = Decent UO):

Administer based on their UO and Na+ o Usually try to only give 1 to 1.5L in renal pt ~ Minimize fluids. Try to match insensible losses o CKD: These patients have dilutional hyponatremia. They do not require more sodium, just less volume.

- Electrolytes o Potassium (K): Decreased excretion in both AKI and CKD. Do not supplement o Magnesium (Mg): Decreased excretion in AKI and ~CKD. Do not supplement o Phosphate: Not excreted in AKI or CKD. Supplementation generally not required. o Acid-Base: CKD patients often experience metabolic acidosis. Maximize Acetate to balance cations

- Vitamins and Trace Elements o Regardless of renal replacement therapy, administer standard dose. o Selenium: This element is eliminated in the urine, decrease dose 50% in renal patients [60mcg à 30mcg]

unless the patient is on CRRT (Give standard dose) Hepatic Disease Patients

- Treatment Goals: o Provide adequate protein without causing or worsening complications of cirrhosis

§ Complications: Hepatic Encephalopathy, Ascites. ~Protein-related disorder o Overcome impaired absorption and digestion of nutrients o Improve immune response to minimize infectious disease-related complications related to cirrhosis

§ Due to low circulating protein, these patients are immunocompromised. o Aid in hepatocyte regeneration, and support patient until transplantation

- Carbohydrate o Hyperglycemic Risk: Hepatic disease patients are at increased risk of hyperglycemia following glucose

infusion due to: § (1) Impaired Hepatic Metabolism: Glucagon and Insulin are both metabolized by the liver. Liver

damage \ will cause [Ý]. The predominant effect is with glucagon. à Increasing BG § (2) Peripheral Insulin Resistance: Due to chronic [InsulinÝ] and Cirrhotic complications

o Treat similar to Diabetic patients: Starting with a low dose (150g/day) and slowly titrating up - Protein

o Accumulation of Aromatic AA (AAA): AAA readily cross the BBB. Due to decreased hepatic metabolism, accumulation in the brain will contribute to worsening encephalopathy. [Protein Intolerance]

o Utilization of Branched-Chain AA (BCAA): BCAA do not cross the BBB, and can be directly used as a fuel source (catabolism) in peripheral muscle.

o Dosing: All dose adjustments are dependent upon staging of Encephalopathy. Must grade their condition

§ Compensation = Lack of Encephalopathy § If patient is not tolerating the minimal 20g

Protein/daily à Switch to specialty product o Product: Specialty AA solutions have been developed,

showing benefit in VERY select groups of patients § Specialty: HepatAmine 8% Aminosyn HF 8%

- Fat o Fat Intolerance: End-stage liver disease is associated with lipid intolerance and hypertriglyceridemia.

§ Check Lipase activity and TG level upon initiation o Steatorrhea: Fatty/Greasy shits. This is a sign that oral fat intake should be decrease, choose lower [fat] o Dosing: Fat is still administered to patients, Monitor TG to ensure patient is tolerating the medication

- Water and Sodium o Highly restricted intake due to edema and ascites. Patient is Hypervolemic hypotonic hyponatremic o Water: 1500mL/day Maximum. o Sodium: ~50% of the normal requirements. 90mEq/day Maximum (initiate at 0.5-1mEq/kg/day)

- Electrolytes o Hepatic disease patients are subject to poor oral intake, impaired absorption, diuretic usage, and diarrhea.

This will contribute to developing (1) Hypokalemia, (2) Hypophosphatemia, (3) Hypomagnesemia o Treat patient by administering the high-end of the normal range of these electrolytes

- Vitamins and Trace Elements o Though there may be specific depletions, standard dosing is sufficient, barring chronic deficiency. o Alcoholism: As a top cause of cirrhosis, alcoholism will deplete vitamins and trace minerals. Folic acid

and thiamine are depleted. o Decreased Fat Absorption: Along the lines of fat intolerance, lowered fat absorption will decrease

absorption of fat-soluble vitamins, such as Vitamin A and D. Steatorrhea may predispose Zinc deficiency o Biliary Disease: Will require dose adjustments, biliary disease severely depletes trace elements (Mn, Co, Cr)

Critical Illness - Treatment Goals: Check literature on nutritional support for the critically ill – Drecommendations annually

o Preserve lean body mass – These patients are highly catabolic, and are breaking down muscle for energy o Avert Metabolic complications – Prevent oxidative cellular injury o Attenuate the metabolic response to stress – Cortisol greatly enhances Gluconeogenesis and Proteolysis! o Maintain and modulate the immune response – Requires early EN, glycemic control, and nutrient delivery

- Initiation of Nutritional Support o If Enteral is available: Preferred route. Begin trophic (small) feeding within the first 24-48 hours

§ NRS ³ 5: High risk patient. Increase EN to 80% of estimated needs within first 48-72 hours § NRS < 5: Less risk – Take your time. Slow, trophic feeding, carries a lower infection risk

o If Enteral is not available: à PN, but held for the first 7 days. Feed on day 7 § NRS ³ 5: This is a high-risk patient, we cannot wait until day 7. Feed earlier.

- Fat o ASPEN and SCCM advise against soy-based fat emulsions in the first week. Though there is no evidence

or literature, it is an “expert theoretical concern.” The inflammatory mediators inherent to soy may induce inflammation and adversely affect immune status. Hold PN of soy for 1 week.

- Protein o The critically ill are highly catabolic, and therefore are engaging in muscular proteolysis. To provide a

fuel source for the skeletal muscle, BCAA are preferred as they more readily are converted to glucose § Clinical trials have not validated this suggested advantage over standard formulations.

o Products: Aminosyn HBC 7% FreAmine HBC 6.9% BranchAmin 4% Obesity

- Treatment Goals: o Depends on the severity of their illness – we must

question the pt about concomitant disease state severity. Determine their amplitude of obesity

- Calories (kcal/day) o Mifflin-St Jeor (MSJ) Equation [Height, kg, Age]

§ Men: 5 + 10·(kg) + 6.25·(cm) – 5·(Age) § Women: (-161) + 10·(kg) + 6.25·(cm) – 5·(Age)

o Penn State University (PSU) Equation [Tmax (max Cº in last 24h), Ve (minute ventilation, L/min)] § < 60yo: (MSJ·0.96) + (Tmax·167) + (VE·31) – 6212 § ³ 60yo: (MSJ·0.71) + (Tmax·85) + (VE·64) – 3085

o The previous two equations, MSJ, PSU, are only for obese patients with renal or hepatic dysfunction. § For obese patient that do not have either dysfunction, use previous lecture caloric intake recs.