Clinical pocket guide by mcova002

Clinical Pocket Guide By: Mariana Covarrubias

Table Of Contents: Enteral………………………………………………… 3-47 Parenteral…………………………………………… 48-67 Upper GI…………………………………………….. 68-82 Lower GI…………………………………………….. 83-107 Liver, Pancreas, & Gallbladder……………. 108-131 Immunology…………………………………….... 132-140 HIV/AIDS………………………………………....... 141-158 Oncology……………………………………......... 159-191 Renal……………………………………………....... 192-219 Pulmonary…………………………………………. 220-229 Critical Care……………………………………….. 230-254 2

Enteral • Enteral - Nutrients • When to use enteral supplied via a tube nutrition? directly into the GI tract • Impaired nutrient ingestion/inability to eat solids • Parenteral - Nutrients • Inability to consume adequate supplied directly into nutrients orally • Impaired digestion, absorption, the bloodstream metabolism • IF THE GUT WORKS USE • Severe wasting or depressed growth IT

Indications for EN • When oral intake is impossible, inadequate or unsafe • Malnourished pt and those at risk for malnutrition b/c unable to maintain adequate po • Severely malnourished preoperative pt • Following severe trauma, burns, wounds, or critical illness Source: ASPEN The Science and Practice of Nutrition Support

Contraindications to EN • • • • • • • • • •

Non operative mechanical GI obstruction Severe short bowel syndrome (<100cm of SB) Paralytic ileus Distal high output proximal fistula >700ml Severe GI bleed Severe GI malabsorption Inability to gain access Intractable vomiting or diarrhea Aggressive therapy not warranted/indicated Need is expected < 5- 7 days for malnourished pt and 7 - 9 days for adequately nourished pt 5

Benefits of Enteral Nutrition • Prevents intestinal atrophy • Prevents bacterial translocation – Decreasing potential infection

• Feedings started earlier during the illness are better tolerated • Maintains gut integrity – Normal GI digestive and absorptive capabilities – GALT and MALT 6

Types of Access Temporary • Nasal or orally placed

Permanent • Endoscopically placed

– Nasogastric

– PEG

– Nasoduodenal

– PEJ

– Nasojejunal

– PEGJ

Types of Access Permanent • Surgical placement – G-tube • Stamm

– J-tube • Witzel

– GJ-tube

Indications for Small Bowel Access • Recurrent aspiration • By-pass a section of the gut that is dysfunctional

• Keen nutritional assessment by RD is essential to deciding placement of tube 9

Nasogastric Tube • Goes through the nose and into the stomach • For short-term (4 weeks) use only

• Use soft, small tubes

Nasoduodenal/Nasojejunal • Also for short enteral administration (4 weeks) • Used in patients with high risk of aspiration

• Takes ~1 hour to place

PEG/PEJ • Non-surgical technique done with endoscope through mouth • Form a subcutaneous stoma from the abdominal wall into the stomach • For long-term feedings • http://www.youtube.com/watch?v=atQGkK0z W2s 12

Surgically Placed Gastrostomy & Jejunostomy • Usually for pt who do not have access to the stomach via the mouth • Permanent • Surgery with anesthesia

Enteral Formulas • Must consider the following: – How well is the gut functioning? – Does the formula have a high osmolality, high fiber, high caloric density and viscosity? – Macronutrient content – Digestion and absorption ability of the patient – Metabolic needs – Fluid and electrolyte requirements – Cost 14

Osmolality â&#x20AC;˘ Definition - a measure of the osmotically active particles per kilogram of solvent â&#x20AC;˘ Osmolality between 300-500mOsm/kg is best tolerated, as it is most similar to that of body fluids â&#x20AC;˘ Generally hyperosmolar formulas are more nutrient dense and/or dz specific

Types of Formulas •

Polymeric (Intact) •

•

Semielemental (Partially Hydrolyzed) •

•

Protein enzymatically hydrolyzed into small peptides

Elemental (Hydrolyzed) •

• •

Intact protein or protein isolates

Free amino acids

Disease Specific Modular

Formula Composition PROTEIN

CARB

FAT

POLYMERIC

Intact protein

Polysaccharides glucose polymers, di & monosaccharides

PUFA, MCT

SEMIELEMENTAL

Hydrolyzed protein, Glucose polymers, dipeptides, di & tripeptides, amino monosaccharides acids

PUFA, MCT

ELEMENTAL

Free amino acids

PUFA

Glucose polymers, monosaccharides

Formula Names and Uses Category

Product Name

Use

Oral

Ensure® Boost® Resource®

Supplement poor oral intake

Polymeric

Nutren® Jevity® Glucerna®

Standard tube feedings

Semi-elemental

Peptamen® Peptamen® w/ Prebio

GI disorders

Elemental

Vivonex® Tolerex® Vital®

Malabsorption

Who gets which type of formula? • Polymeric

• Disease/condition specific – Standard, nutrient dense and fiber containing

• • • •

Semielemental Elemental Disease Specific Modular

– – – – – – – –

DM Cancer Hepatic Immune Enhancing Pulmonary ARDS Renal Wound healing 19

Diabetic formulas • Characteristics: – Isotonic – Low carbohydrate (30-35% kcal) – High fat (50% kcal) – Fiber supplemented • Rationale – Improved glycemic control • Examples include Glucerna, Nutren Glytrol, Diabetisource • Should try using a standard formula first, then if glycemic control not achieved, switch to DM formula • Monitor blood sugars and provide insulin

Cancer Formulas • Characteristics: – Can be used as oral or TF – EPA supplementation – Soluble fiber • Rationale: – Proteolysis inducing factor causes protein catabolism and Ca cachexia in these pt – Improved wt gain, appetite, survival and QOL • For pt receiving anti Ca tx who are malnourished • Examples – Impact®Advanced Recovery 21

Hepatic formulas • Characteristics – Nutrient dense – High osmolality (> 450 mOsm/kg) – Low protein • 45-50% branch chain AA, low aromatic AA

– Fat as MCT – Low sodium

• Rationale – Improved encephalopathy

• Example includes Nutrihep 22

Hepatic formulas • Most patients with liver disease can tolerate 1 g protein/kg • Severe intractable encephalopathy may require protein restriction • Hepatic formulas are for short term use • Use of this formula should be limited to patients with severe encephalopathy who have not responded to aggressive therapy with lactulose or neomycin

Immune-enhancing formulas • Characteristics vary among products – – – –

Altered ratio of omega 3:omega 6 fatty acids Arginine Glutamine Nucleic acids

• Rationale – Fewer infectious complications, shorter ICU & vent days in some patients

• Examples: – Impact, Perative, Pivot, Vital 24

Immune-enhancing formulas • Use suggested for the following patients: – – – – – –

Malnourished pt undergoing GI sgy Blunt or penetrating torso trauma Severe head injury Burn, > 30% TBSA Vent dependent and non septic Pt undergoing elective sgy

• Critically ill pt should not receive arg containing formula • For benefits to be seen, 50-65% of energy requirements should be delivered

Glutamine • • • • •

Decreases gut permeability in catabolic stress Supports mucosal growth Prevents atrophy during NPO Fuel for rapidly proliferating cells Precursor to glutathione

Pulmonary Formulas • Characteristic: – Low CHO – High fat (50-60% kcal)

• Rationale – Less CHO results in less CO2 production – May facilitate weaning from ventilator

• Examples – Pulmocare, Nutren Pulmonary

• Limited studies to evaluate efficacy • Avoid overfeeding total kcals 27

ICU Pulmonary Formulas • Characteristic: – – – –

High osmolality Omega 3 FA (EPA) Borage oils (GLA) Antioxidants

• Rationale – Leads to production of anti-inflammatory response – EPA and GLA produce less inflammatory eicosanoids

• Example includes Oxepa • May be beneficial in lung injury or acute respiratory distress syndrome (ARDS) 28

Renal Formulas • Characteristics: – – – –

High osmolality High caloric density (2 Kcal/ml) Protein content varies Low electrolyte (Na+, K+, Phos)

• Rationale – Fluid, protein, and electrolyte management

• Examples include RenalCal, Nepro, Suplena, Novasource Renal • May be useful for persistent hyperkalemia and hyperphosphatemia 29

Wound Healing • Characteristics: – High protein – Some contain Arg – Oral or TF • Rationale: improved wound healing • Examples: – Juven – Resource Beneprotein – Resource Arginaid Extra – Nutren Replete & Nutren Replete Fiber • Evidence shows improved wound healing with these formulas30 and prevention of wound development

Methods of Administration • Pump assisted – Continuous – Cyclic • Gravity – Bolus 31

Continuous Drip • Very low risk of contamination when using a “closed system” • Continuous feeding 24hrs/day • Cyclic feedings at night at higher rate/hour

Initiating • • • • •

Usually start around 20-30 ml/hr Advance 10-20 ml q 4-8 hours to final volume Advance hyperosmolar formulas slower Should be at goal rate by 24-48 hours Example: – Start Glytrol at 20 ml/hr, increase by 20 ml/hr q 6 hours to a goal of 65 ml/hr

Bolus • Feeding is given in large quantities via a syringe or by pouring a can into a bag and gravity moves it down • High risk of contamination • Pt can generally only tolerate 480 ml (2 cans) at a time • Good for someone that is active and does not want to TF out of the home • Not to be used if there is a risk of aspiration

Initiating • Bolus feedings – Start 120 ml formula via G-tube q 4 hours – Administer bolus over 5 minutes

• Example: – Start 120 ml (1/2 can) Glytrol q 4 hours, if tolerated increase to 240 ml (1 can) q 4 hours

Early Enteral Nutrition • Nutrition Support initiated within 36 hours • Benefits – – – – – –

Preserves protein mass, improved N balance Maintain gut integrity and immune comptence Prevent gut atrophy Diminish bacterial translocation Wound healing Decreased cytokine release 36

Complications of Enteral Nutrition • GI – – – –

Nausea/Vomiting Abdominal Distention Diarrhea Constipation

• Mechanical • Metabolic 37

Enteral Nausea/Vomiting: • Affects ~20% of individuals receiving TF • Vomiting increases risk of aspiration • Use antiemetics • May need to change fdg schedule

Abdominal Distention: • May be due to rapid administration of TF or delayed gastric emptying • GI may be obstructed or ileus present • Check GI status via fluoroscopy • TF held if residuals are > 38 200ml

Gastric Residuals • Usually RN’s check residuals q shift or before administering bolus • Controversy regarding amounts • Generally > 250 at 2nd check add Reglan or > 500ml…hold TF – Looking for sx of abd distension, N/V

Diarrhea • #1 most reported complication • Usually unrelated to TF but determining cause is primary concern • May be infusion rate, progression, high fat content • Abx induced may be cured with Probiotics • Addition of soluble fiber or changing to fiber containing formula may help • Add antidiarrheal medication 40

Constipation • Usually in LTC TF residents • Check for dehydration • Change to fiber containing formula and adequately hydrate • Increase physical activity if possible

Mechanical Complications • Clogged fdg tubes – Medication administration

• H2O flushes with 30 ml prevent clogging • Tubes dislodged

Calculating Enteral Feedings • • • • •

Choose appropriate formula Determine administration method Calculate energy, protein and fluid needs Use formulary of facility 1 can = 240 ml – Two concepts • Calculating marconutrients from already determined regimen • Calculating regimen from already determined macronutrients

Calculating Enteral Feedings • Fluid • Example: Formula provides 1014mL fluid and pt needs 1500mL. Subtract 15001014=486mL. So you can do 3 flushes of 200mL or 2 flushes of 250mL.

Initial Documentation • Nutrition Goals • Reason for Tube Feeding • Placement • Formula ordered • Administration schedule - concentration and rate

• Method of delivery • Calculate kcal, pro, and fluid in formula

F/U Documentation • Patient’s tolerance of – – – –

Formula Administration schedule Complications (if any) Corrective actions recommended

• Changes of patient’s body weight and lab values during the period of tube feeding • Reasons why tube feeding was interrupted or could not be delivered 46

Transitioning to Oral Fdgs • ST involved in decision if dysphagia present • Factors to consider – Total oral intake – TF interfering with appetite – Discontinuing too soon

• Strategies? • When pt consuming 50% of needs for 2-3 days, discontinue TF 47

Parenteral: Indications for Use • Trails of EN have failed or there is not adequate access to GI tract • EN is contraindicated or intestinal tract has severely diminished function – – – –

Paralytic ileus Mesenteric ischemia SBO GI fistula except when enteral access can be placed distal to fistula

Likely Candidates • • • • • •

Peritonitis Intestinal hemorrhage Intestinal obstruction Intractable N/V/D or abd distention SBS Tx toxicity in Ca patients – Bone marrow recipients

• Severe pancreatitis • High output fistula 49

Peripheral vs. • Lower concentration of nutrients • Requires lg volume • Not recommended if fluid restricted • Can be used for 2 weeks • Difficult to meet all nutritional needs

Central

• Higher concentration of nutrients • Requires less volume • Can be used with fluid restriction • Can be used for years • Can meet all nutritional needs • Higher risk of infection

Types of Access • Central: – – – –

Subclavian Internal jugular Femoral Cephalic

• Peripheral: – any vein

Central Access • 2 Types: – Short Term Access • One lumen and cannot be used for anything other than feeding

– Long Term Access • Can be single or multiple lumen (home therapy) • Should be tunneled • Peripherally Inserted Central Catheter is inserted through a vein in the arm and threaded to the subclavian - non-surgical 52

2-in-1 vs 3-in-1 Admixtures • 2-in-1 – More traditional formulation of dextrose and amino acids in one solution. Lipids are administered in a separate bag. • 3-in-1 – AKA TNA system, all in one. All components (dextrose, aa’s, lipids) admixed in one bag.

Carbohydrate • • • •

Dextrose monohydrate 2.5 – 70% 3.4 kcalories per gram 25% dextrose solution = 25g dextrose per 100 ml solution • Concentrations > 10% - administered through central lines

• Max 5-7 mg/kg/min 54

Amino Acids • Crystalline amino acids • 3.5 – 15% • 4 kcalories per gram • A 10% amino acid solution = 10 grams amino acids per 100 mL

• Disease specific solutions – for patients with: liver disease, kidney failure and metabolic stress • Check NPC:N2 ratio 55

Lipids • Triglycerides from soybean oil and safflower oil, phospholipids • Lipid emulsions available in 10, 20, 30% solutions • Provided daily • May provide 20-30% of total kcalories • Max 2 grams/kg/d or - < 1g/kg/d in stress or hyperlipidemia

• As an energy source, reduces the need for energy from dextrose

• Lowers the risk of hyperglycemia in glucose-intolerant patients • Excessive linoleic content – may aggravate inflammation ie ARDS, sepsis

Kcals Delivered • PRO • CHO • LIPIDS

4 kcal/g 3.4 kcal/g 9 kcal/g

• Lipids Emulsions (for 2-in-1 system) – 10% – 20% – 30%

1.1 kcal/mL 2 kcal/mL 3 kcal/mL 57

Electrolytes • Standard electrolyte additives are usually – – – – –

Sodium Potassium Calcium Magnesium Phosphate

• Acetate and chloride may be added based on acid-base balance 58

Vitamins and Minerals • Usually a multivitamin product that contains a mix of fat soluble and water soluble vitamins. For adults: – A,D, E, C, Thiamin, Riboflavin, Niacin, Folic Acid, B6, Pantothenic Acid, Biotin, B12

• Vit K added separately

Pre-Mixed Solutions • Sold with all components already mixed into solution • For a peripheral line, usually contain: – 5 – 10% dextrose – 2.75%, 3.5% or 4.25% amino acids

• For a central line, usually contain: – 20 – 25% dextrose – 3.5%, 4.25% or 5% amino acids 60

Types of Administration • Continuous Infusion • Cyclic Infusion - over 8-12 hours @ higher rate – Do not use in pts with glucose intolerance or fluid intolerance

Complications • Mechanical

• Gastrointestinal • Metabolic

• Mechanical complications: • Air embolism • Venous thrombosis • Catheter occlusion • Intra/extravascular malposition • Pneumothorax • Line sepsis • Phlebitis

Gastrointestinal Complications • Bacterial translocation • Gut atrophy

• Hepatic – Fatty liver – Cholestasis 63

Abnormalities in Liver Function • Steatosis often results due to overfeeding • Monitor serum levels of liver enzymes • Usually readily reversed when parenteral feedings discontinued • May become chronic – irreversible liver disease when parenteral nutrition is continued long-term - lead to liver failure 64

Gallbladder disease • Sludge often builds up in gallbladder if parenteral nutrition >4 weeks • May eventually lead to gallstones • May be given cholecystokinin injections or have gallbladder removed surgically

Metabolic Complications • • • • • •

Overfeeding Refeeding syndrome Pre renal azotemia Hyperglycemia Hypertriglyceridemia Electrolyte abnormalities

Transitioning • Once gut function returns… – Enteral • Once EN is providing 33-50% or needs, taper PN • After EN providing 75% of needs, discontinue PN

– Oral • Diet progression as tolerated

• PPN does not need to be tapered 67

GERD • “Heartburn” and/or reflux of stomach contents into esophagus • Etiology: – – – –

LES incompetence Pregnancy Hiatal hernia Obesity

• • • • • •

May lead to: Reflux esophagitis Esophageal ulcers Esophageal strictures Barrett’s esophagus Esophageal Ca

GERD Lifestyle Modifications/Diet • Avoid eating at bedtime, meals 3-4° before bedtime • Elevate HOB • Small meals with liquids between meals • Avoid tobacco • Loose fitting garments • Lose weight

• Limit: – – – – – – –

Chocolate Caffeine Alcohol Garlic/onions High fat foods Citrus Peppermint

Holding and Emptying • Upper 1/3

reservoir

• Slowly released down to lower stomach

• From lower and highly regulated

duodenum slow

• Motility is based on nutrient content, anatomy, nervous system and hormones

Peptic Ulcer Disease • Causes: – H. pylori in 60% of gastric and 80% of duodenal – NSAID/ASA use – Nicotine – Stress

• Sx: – Pain – Sometimes remission and reoccurrences – Loss of appetite – Weight loss – May lead to: – GI bleed – Perforations – Gastric outlet obstruction 72

Peptic Ulcer Disease • Tx: – Drug therapy • Control pain • Antibiotics • PPI, H2 Blockers, antacids, cytoprotective agents (meds that coat stomach)

– Surgery • As a result of complications

• Nutritional Intervention • If ulcer is aggravated by ingestion of food.. • Bland diet indicated • Monitor B12 • Minimize sx • Nutrition education

Bland Diet • • • • • • •

Tender foods ↓ Fried food ↓ Roughage ↓ Seasoning ↓ Caffeine and Alcohol ↓ Milk/Dairy ↓ Citrus 74

Effects of Gastrectomy • ACID total

B12, Fe, Pepsin, lipase

partial

may be spared

• Breakdown total partial

larger particles enter duodenum

• Motility total partial

faster transit time

DUMPING SYNDROME 75

Dumping Syndrome • Stomach contents are not regulated and rush into Small Int • Early- immediate sx • Late- as a result of hypoglycemia following large insulin response to ingested load

Dumping Syndrome Early Within 30 min of eating • • • • •

Abdominal fullness Cramps Diarrhea N/V Bloating

• • • • • • •

Late 1-3 hours after eating Anxiety Confusion HA Hunger Palpitations Sweating weakness 77

Post Gastrectomy Diet • No food or liquid 24-48° post op • Clear liq initiated and by 5th day, pt tolerating soft foods • Small, frequent meals and snacks with soft, low fat foods – – – – –

Avoid sweets and sugars Liquids restricted during meals Avoid highly spiced or high fat foods Avoid caffeine, alcohol, carbonated beverages Avoid peppermint and chocolate

• Foods as tolerated 78

Diarrhea: Types &Causes • Osmotic diarrhea – poorly absorbable or hypertonic solute causes movement of fluid – Lactose intol, dumping syndrome, laxatives

• Secretory diarrhea – intestines are stimulated to secrete fluid that exceeds the colon’s capacity for reabsorption, not affected by fasting or eating – Bacterial endotoxin, intestinal resections

Diarrhea: Types &Causes • Deranged Motility – acceleration of entry of fluids into the colon, followed by inadequate reabsorption – Irritable bowel, post vagotomy, past gastrectomy

• Exudative - disruption of integrity of int muscosa due to inflammation and ulceration – UC, Crohn’s

• Steatorrhea -

excessive fat in the stool

Nausea/Vomiting • Impacts nutritional status • Modify foods, educate • Meds: – – – – –

Phenergan Tigan Compazine Marinol Reglan 81

Laxatives • Bulk Forming – Psyllium – Metamucil – Citrucel • Stool Softeners – Colace – Surfak • Lubricant Laxatives – Mineral oil

• Osmotic Laxatives – Mg and P ions – MOM – Cephulac – Miralax • Stimulants – Dulcolax – Senokot – Correctol • Enema & Suppositories 82

Crohn’s Disease • Mouth

Anus

through all layers of the bowel

• Mostly ileum, Right Colon • Can be diseased portions separated by healthy segments

Crohn’s Disease • Sx: – – – – – –

Pain following meal Watery diarrhea Mouth sores Episodic fevers- 24-36° Clubbing fingers Perianal problems, fissures – Cramping in RLQ – Appetite – Anorexia, wt loss

• Tests: – – – –

SBS Colonoscopy CT scans Endoscopic ultrasound or EUS – Bx – CBC – Stool studies

Crohn’s Disease • Meds: – Aminosalicylates (contain 5-ASA) • Oral delivery: Sulfasalazine i.e Azulfidine (may have mild side effects but inexpensive) • Does not contain sulafpyridine: Mesalamine i.e Asacol, Pentasa (delayed release), Apriso (extended release) • Alternative delivery: Rowasa (Enema), Canasa (Suppository)

– Antibiotics • Flagyl, Cipro – Immune modifiers • Azathioprine (oral; ie. Imuran, Azasan), Methotrexate (injections) 85

Crohn’s Disease Meds Cont’d – Corticosteroids • Prednisone (Deltasone), Methylprednisolone (Medrol), Budesonide (Entocort EC, UCERIS), hydrocortisone • Budesonides represent a new class of corticosteriods (nonsystemic steriods) that target the intestine as opposed to the whole body (less side effects) • These drugs can be used alone or with 5-ASA to reduce acute inflammation

– Antidiarrheals – Biologic Therapy • Anti-TNF: Remicade, Humira, Cimizia (new; approved 2008) • Integin Receptor Antagonist: Tysabri (Natalizumab) 86

Crohn’s Disease • Nutritional Concerns – – – – – –

B12 Zn Vit A Folate Macronutrients- Fat, Pro, CHO Water

MNT: Crohn’s • • • • • • • •

High-kcalorie, high-protein diet Liquid supplements, semi elemental if appropriate Low-fiber bland diets if obstruction or fistula present Vitamin and mineral supplements MCT oil better tolerated if steatorrhea present Addition of enteric coated omega-3 FA supplements All diets as tolerated Low FODMAP Diet – http://stanfordhospital.org/digestivehealth/nutrition/DH-LowFODMAP-Diet-Handout.pdf 88

Surgical Tx • Resection w/o ileostomy – REMOVE AS LITTLE AS POSSIBLE

– Colon removed

Fluids Electrolytes

– Ileum removed

B12 Bile Fat 89

Ulcerative Colitis • Large Bowel ONLY – Affects mucosal layer in a continuous manner

• Mostly Left Colon – Sigmoid – Descending – Rectum

• High risk for Colon Ca • PCM not as evident as in with Crohn’s 90

Ulcerative Colitis • Sx: – – – – – – –

Left sided pain Bloody Diarrhea Pain at night Fever several days Fatigue Anemia Weight loss

• Tests: – Colonoscopy – Meds: – Aminosalicylates (contain 5ASA) – Rowasa, Asacol, Sulfasalazine – Antibiotics – Immune modifiers – Imuran, Purinethol, Methotrexate – Corticosteroids – Biologic Therapy – Remicade 91

MNT: Ulcerative Colitis • • • •

In acute flair, low fiber, bland foods indicated Lactose restriction may be indicated Caffeine will further exacerbate diarrhea Replete preoperatively if awaiting colectomy

• Bowel rest may be indicated during exacerbations: TPN • Low FODMAP Diet – http://stanfordhospital.org/digestivehealth/nutrition/DH-Low92 FODMAP-Diet-Handout.pdf

Surgical Tx • Total Colectomy – Removal of colon

• Proctocolectomy – Remove colon and rectum

• Ileostomy – Permanent or temporary

• Diet – Initially low fiber, high fluids  regular 93

Ulcerative Colitis • Ileo-rectal anastomosis – Not Common (sometimes w/ Crohn’s) – Colon removed, some rectum remains – Attach ileum to rectum – No appliance – Defecate via rectum

• Diet – Initially low fiber, high fluids  regular

• Kock Pouch: – Colon, rectum and anus removed – Permanent ileostomy – Internal pouch acts as a reservoir – Has valve, No appliance – Insert catheter to drain – Diet – Initially low fiber, high fluids regular 94

Ulcerative Colitis Restorative proctocolectomy AKA Ileoanal Pouch Anal Anastomosis (IPAA) • Most common – Colon and rectum are removed – Ileum forms pouch (internal), anal sphincters remain – Usually takes multiple surgeries • With temporary ileostomy

– No appliance

• Diet – Initially low fiber, high fluids  high fiber 95

Nutritional Assessment Crohn’s and Colitis

• Diet Hx – Extensive including intolerances and sx

• Weight hx • Visceral protein status • High Kcal and pro needs – BEE X 1.4-1.5 – Pro 1.5-2.0g/kg

• Monitor hydration and anemias • MVI indicated

Short Bowel Syndrome Malabsorption syndrome resulting when absorptive capacity of the remaining intestine is insufficient for meeting nutritional needs â&#x20AC;&#x153;<200 cm of functional small intestineâ&#x20AC;? 70-75% loss of SB 100-120cm of SB without colon 50 cm of SB with colon 97

Short Bowel Syndrome Sx:

Nutritional Concerns:

• Diarrhea

• B12 deficiency

• Steatorrhea

• Bile acid reabsorption

• Dehydration

• Fat malabsorption

• Weight loss

• Diarrhea

• Growth impairment in children

• Bacterial overgrowth

SBS: Intestinal Adaptation • Glutamine, SCFA, glucagon-like peptide 2 thought to enhance adaptation • Ileum has > capacity for adaptation than jejunum • Colon helps to reduce fluid and electrolyte losses and has resident bacteria that prevent malnutrition • Intestinal adaptation achieved more easily if ileum and colon remain intact 99

SBS Diet Colon Present • • •

• • •

50%-60% of energy CHO – Complex carbohydrates Limit simple sugar 20%-30% of energy FAT – Adequate intake of EFA MCT/LCT 20% of energy intake PRO – High biological value ORS or hypotonic as needed

Colon Absent • • •

• • •

40%-50% of energy CHO – Complex carbohydrates Restrict simple sugar 30%-40% of energy FAT – Adequate intake of EFA LCT 20% of energy intake PRO – High biological value ORS generally required

100

Short Bowel Syndrome Tx: • To meet needs with EN – need at least 40 – 80 inches of small intestines

• If unable to adapt, lifelong TPN • Intestinal transplantation – option for pts who cannot continue TPN

• http://www.shortbowelsupport.com/surgicaltherapies.htm 101

Irritable Bowel Syndrome • Etiology: unknown • Sx: – – – – – –

Belching Flatulence Heartburn Mucous in stool Diarrhea Constipation

• Tx: – – – –

– – – – – –

Manage predominant sx Dietary adjustments Low FODMAP Diet http://stanfordhospital.org/di gestivehealth/nutrition/DHLow-FODMAP-DietHandout.pdf Medications Antidiarrheal agents Antispasmotics Bentyl Antidepressants 102 Laxatives

Celiac Dz • Tests – Serum IgA – Antibodies for gliadin – Intestinal Biopsy

• Nutritional Assessment – Kcal and Pro depend on degree of malnutrition

103

MNT: Celiac Disease • Lifelong adherence to a gluten-free diet • • • • •

Avoid lactose-containing foods Ensure adequate Ca, Vit D, Fe, B Vits Choose more nutritious grains and flours Fiber is important Avoid cross contamination of gluten free foods 104

Nutrition Education • Read labels carefully – replace bread, pasta, cereal • Can be social liability • Diet counseling • Look for grocery stores featuring Gluten Free products 105

Diverticular Dz of the Colon • Development of pebble-sized herniations in the intestinal wall

• Most often occurs in sigmoid colon • Prevalence increases with age

106

Malabsorption Etiology • Conditions that interfere with bile or pancreatic lipase – Pancreatitis, CF, liver dz, bypassing of GI tract

• Inflammatory intestinal disorders – Crohn’s, UC, CD

• Motility disorders – Dumping syndrome 107

Pancreas • • • •

Triangular gland Pancreatic duct joins bile duct Delivers “juices” thru Sphincter of Oddi Function: ENDOCRINE – Islet of Langerhans • β cells • α cells (metabolism)

• Function: EXOCRINE – Acinar cells (digestion) 108

Endocrine • β cells- INSULIN – Released in response to AA GLU CCK Secretin – Anabolic action • Glycogenesis • Lipogenesis • Protein synthesis 109

Liver Disease Progression Fatty Liver

Fibrosis

Cirrhosis 110

Fatty Liver An accumulation of fat in the liver tissue Etiology: • Alcoholic liver disease • Exposure to drugs and toxic metals • Obesity, DM, metabolic syndrome • After GI bypass surgery • Long-term TPN 111

Fatty Liver Leads To: • Liver enlargement

• Abnormal liver enzyme levels

• Inflammation

• Increased triglycerides

• Fatigue

• Elevated cholesterol levels

• Liver damage

• Liver failure

• Elevated blood glucose levels • Elevated blood pressure 112

Fatty Liver Treatment: • Elimination of factors that cause it – Alcohol abuse – Drug therapies

• Lifestyle/Diet modifications: – Control visceral fat, insulin resistance – Vit C and E – High fiber, low simple CHO diet, replacing sat fat with MUFA, PUFA 113

NAFLD • Occurs in pt who do not abuse ETOH • Dx with blood tests and liver scan

NASH

• Progression to cirrhosis is common • Characterized by fatty liver with hepatocyte changes, inflammation and poss fibrosis • Dx with Bx

114

Causes • • • • • •

Obesity Diabetes Insulin resistance Hypercholesterolemia Hypertriglyceridemia Inflammation (↑ CRP, TNF-α, IL-6)

• The “Silent Liver Disease” 115

Hepatitis Treatment: • Hep A resolves without meds • Hep B and C – Lamivudine and ribavarin – Interferon

116

Cirrhosis • End-stage condition that results from longterm liver disease • Gradually destroys liver tissue, leading to scarring (fibrosis)

• Eventually leads to liver failure

117

Complications of Cirrhosis • • • • •

Portal HTN Ascites SBP Varices Hepatic Encephalopathy

118

Portal HTN • Resistance to blood flow in liver causes a rise in pressure within the portal vein •  Resistance 2° scarred liver • Blood can’t flow

• Fluid problems

shifts

– Alb responsible for maintaining oncotic pressure keeps water in blood stream – Alb  oncotic pressure – Major fluid shift out of blood into vascular space • Ankles • Abdomen, etc 119

Ascites • Fluid accumulation in abdomen in peritoneal cavity – Portal hypertension – Water retention due to altered kidney function – Reduced albumin synthesis by the diseased liver (oncotic pressure) 120

SBP • Spontaneous bacterial peritonitis – – – –

Acute bacterial infection of the ascitic fluid Contributes to encephalopathy May be fatal Tx with Abx

121

Hepatic Encephalopathy 4 stages I.

Inappropriate behavior, poor memory, asterixis

II.

Lethargy

III.

Difficult to arouse

IV.

comatose 122

HE Etiology • Theories exist…. – Ammonia – Neurotoxin accumulation from intestinal bacteria – AAA (tryptophan) leads to serotonin which inhibits DOPA

NOTE: serum NH3 does not always correlate with degree of HE 123

BCAA Therapy • Aromatic AA

broken down in liver

– Tyrosine – Tryptophan – Phenylalanine

• BCCA

extrahepatic

– Valine – Leucine – isoleucine 124

Protein and HE • Protein intake restriction only if confusion worsens with food! • Must restore normal protein intake immediately after HE resolves • Maintaining normal pro decreases pro breakdown •  Meat pro-have higher AAA – Favor dairy and veg pro 125

HE Tx • Meds: – Lactulose • laxative to reduce ammonia production and absorption in the colon

– Neomycin • antibiotic to alter bacterial populations in the gastrointestinal tract

– Rifaximin • reduce the bacteria that create toxins the liver can’t process 126

Cirrhosis Tx • Fluid overload – Paracentesis • Pro also removed in fluid

– – – –

Fluid restrictions Sodium restrictions Antibiotics Diuretic therapy • lasix, aldactone

127

Cirrhosis Tx • Bleeding – IV clotting factors • vit K

– Anemia• supplement vits

– Avoid reflux/ potential perforation

• Drug therapy – Nitroglycerin – dilates blood vessels – Vasopressin – Megace and Marinol

• Soft foods

128

MNT: Cirrhosis • Needs: • Kcals

BEE X 1.5 Malabsorption, complications, recent weight loss, and infection increase energy needs

• Pro

1-1.2 g/kg/d Only restrict pro if pt is highly encephalopathic, responding to restriction and then gradually 

• Fat

low fat if steatorrhea present, MCT oil 129

MNT: Cirrhosis • Sodium and fluid • If ascites present, restrict Na to 2g/day • Fluid restrictions 1-2 L

• Vitamins and minerals • Multivitamin supplementation is recommended • If severe steatorrhea occurs, fat-soluble nutrients provided in water-soluble forms, Ca, Mg, Zn

130

Causes of Malnutrition in Chronic Liver Dz • Factors that limit oral intake: – – – – – – – –

Anorexia Nausea Vomiting Early satiety Taste abnormalities Alcohol abuse Restrictive diets, NPO status Meds 131

Immune System • 1st defense – Physical barrier • Skin, lungs, GI tract

• 2nd defense – Non specific immune response

• 3rd defense – Specific immune response 132

Cells of Immunity

Myeloid Tissue

Lymphoid Tissue

Innate Non Specific Response

Acquired Specific Response 133

Innate Immunity • Defends against harmful external factors • Always present and functioning • Eliminates pathogens without inducing inflammation – Macrophages, monocytes and neutrophils capable of phagocytosis – Lumenal Factors- digestive secretions, lysozyme

134

Acquired Immunity I. Humoral Immune Response • B lymphocytes • Antibodies produced • Immunoglobulins • •

Surround the antigen and flag it for easier recognition IgG, IgD, IgE, IgA, IgM

135

Acquired Immunity II. Cell Mediated Immunity (CMI) •

T lymphocytes •

CD 4- T helper cells – Activate immune cells

•

CD 8- Suppressor/cytotoxic T cells – Suppress the immune system and kill tumors, viruses, and parasites

• •

Respond to cells presenting an antigen T lymphocytes secrete cytokines that activate phagocytosis

T cells respond to bacteria, viruses, fungi, tumor cells, foreign tissue (transplant organs) 136

Immune Response • Cell-Mediated Cytotoxicity – Kill infected or tumor cells – Perforin and enzymes secreted to induce apoptosis

• Antibodies – Neutralize bacterial toxins and viruses

• Inflammation – Initiate alternate complement pathways – Component of allergies and autoimmune diseases

137

Cytokines • System of communication between cells that are involved in the immune response • Produced by all types of cells • Can be pro-inflammatory or anti-inflammatory

• 4 types – – – –

TNF Interleukin Interferon Colony stimulating factors 138

Gut Immunity • Gut possesses abundant myeloid and lymphoid tissue…makes up a large component of the immune system • Innate – – – –

Lumenal Factors Antimicrobial Factors Physical Barriers Mechanical Factors

• Acquired – GALT, MALT 139

Arginine – Conditionally essential AA, needs  during stress – Production of NO, a vasodilator which regulates inflammation and immunity – Negative outcomes in the septic pt

Glutamine – Major fuel source for lymphocytes and macrophages – Prevents bacterial translocation and maintains gut mucosal integrity

Omega Fatty Acids – 3:6 altered for anti-inflammatory response and  IL-1 production 140

HIV Retrovirus stores genetic info in RNA Once inside cell, requires enz Reverse Transcriptase The virus alters the DNA Replicates Causes HIV infection Which overtime erodes the immune sys 141

HIV/ AIDS Invades genetic code of CD4 cells

receptor site of T helper lymphocytes

142

Tests • ELISA: tests for the HIV antibodies • Western Blot: confirms ELISA • Viral Load – Amount of virus found in blood

• Oral and Urine – Require confirmation test

• Rapid Test – Fingerstick, quick results, approved 2002 143

CDC Definitions • HIV

+ HIV test CD4 count > 200 lack of opportunistic infection

• AIDS

+ HIV test CD4 count < 200 presence of opportunistic infections 144

CD4/T Lymphocytes Categories • Stage 1 > 500 cell/ul • Stage 2 200-499 cells/ul

• Stage 3 < 200 cells/ul

145

Clinical Categories • Stage 1 – Asymptomatic HIV infection, generalized

• Stage 2 – Symptomatic but no AIDS-defining condition

• Stage 3 – Presence of AIDS-defining condition

146

Stage 3: AIDS-Defining Conditions • • • • • • •

Bacterial pneumonia, recurrent (≥2 episodes in 12 months) Candidiasis Cervical carcinoma, invasive, confirmed by biopsy Coccidioidomycosis Cytomegalovirus Encephalopathy, HIV-related Herpes simplex: chronic ulcers (>1month duration), or bronchitis, pneumonitis, or esophagitis

• • • • • • •

• • • •

Histoplasmosis Isosporiasis Kaposi sarcoma Lymphoma, Burkitt, immunoblastic, or primary central nervous system Mycobacterium avium complex (MAC) Mycobacterium tuberculosis , pulmonary or extrapulmonary Pneumocystis jiroveci (formerly carinii ) pneumonia (PCP) Progressive multifocal leukoencephalopathy (PML) Salmonella septicemia, recurrent (nontyphoid) Toxoplasmosis of brain Wasting syndrome due to HIV (involuntary weight loss >10% of baseline body weight) associated with either chronic diarrhea (≥2 loose stools per day ≥1 month) or chronic weakness and documented fever ≥1 month 147

HIV Related Complications • Neurological – HIV encephalopathy or AIDS dementia – Precipitated by vit def

• Liver – – – –

Infections Co infected with Hep C Hepatotoxic meds AIDS cholangiopathy

• Pulmonary – TB – PCP

• Kidney – HIV nephropathy – Proteinuria

148

AIDS Wasting â&#x20AC;˘ Involuntary weight loss of 10% loss of body weight, plus more than 30 days of either diarrhea, or weakness and fever

â&#x20AC;˘ Associated with higher morbidity and mortality 149

Etiology of AIDS Wasting • Anorexia and reduced food intake – Emotional distress and pain – Oral & Respiratory infections – Fatigue, lethargy, and dementia

– Meds • cause anorexia, taste alterations and food aversions, nausea, vomiting, diarrhea and malabsorption

• Cachexia – Changes in macronutrient metabolism – Pro inflammatory cytokines 150

Tx: AIDS Wasting • Aggressive nutrition intervention – Appetite stimulants • Megace • Marinol

– Anabolic agents • Oxandrin

– Oral Nutritional Supplements – Nutritional support • EN • PN

151

Diarrhea/ Malabsorption • Small Bowel – – – – –

Fat Mono/disaccharides B12 Folate Minerals

• Large Bowel

• Recommend multi vit/min with B complex • High dose tx should be avoided • MCT oil • Probiotics?

– Fluids – Electrolytes

152

Tx Goals •  Viral load • Restore/ preserve immune function

• Improve quality of life •  HIV morbidity/ mortality 153

Drug Treatment • Highly Active Anti Retrovirus Therapy – Nucleoside/Nucleotide Reverse Transcriptase Inhibitors – Non Nucleoside Reverse Transcriptase Inhibitors

– Protease inhibitors – Entry Inhibitors – Integrase Inhibitors 154

Nutritional Assessment Clinical Stage

Definition

Kcals (kcals/kg)

Protein (g/kg)

Asymptomatic

30-35

1.1-1.5

Symptomatic HIV, complications

35-40

1.5-2.0

CD4< 200 AIDS defining illness and/or OI

40-50

2.0-2.5

155

Nutritional Assessment • Fat – should consider MCT if malabsorption present – ω-3 FA are being studied for immune modifying effect – Low chol, sat and trans fat 2o lipodystrophy

• Diet Composition 45-65% CHO

10-35% PRO 20-30% FAT 156

Role of Vit/Min in HIV • Def of Vit A, E, thiamine, riboflavin, B6, B12, folate, Zn and Fe can lead to  immune function • Higher intakes of B vitamins and Vit C are associated with higher survival • B12 – Low levels are prevalent in HIV pts – Etiology may be malabsorption and low intake – Dietary suppl may not be enough esp with PI use • Recommend a Multivitamin with B complex daily • Assess and correct deficiencies 157

Nutrition Interventions for… • • • • • • •

Meeting calorie/pro needs Increasing LBM Irritated throat/ difficulty swallowing Dry mouth/ sore mouth Altered taste Diarrhea Poor appetite 158

Dietary Factors • Cancer initiators – Pesticides and food additives – Alcohol and tobacco – Food preparation methods

• Cancer promoters – High-fat diets – High kcalorie intake – High saturated fat and trans-fatty acid intake 159

Dx • • • • • • •

Cytologic tests Bx MRI PET Mammograms Bone scan Endoscopy

Then assigned a Stage by the TNM system 160

Terms • Sarcoma – Ca of connective tissue, cartilage, bone, fat

• Lymphoma – Ca of lymphocytes

• Myeloma – Ca of the white blood cells, granulocytes

• Adenomas – Benign tumor of epithelial cells 161

Cancer’s Effects on Nutr Status • • • • • •

Cachexia 2º anorexia Malnutrition 2º intake 2º obstruction Malabsorption Protein losing enteropathy Electrolyte imbalances/metabolic changes Change in energy expenditure

162

• 40% of Ca pt report unexplained wt loss at 1st dx • 80% experience wt loss in Ca advanced stages • Even a 5% wt loss can reduce response to tx • Wt loss is a major M & M prognostic indicator • Pancreatic, Eso, Gastric, H&N, Colorectal are most associated with weight loss

163

Tx • Palliative v. Curative • • • • •

Surgery Chemotherapy Radiation therapy Immunotherapy Bone marrow transplant 164

New Tx â&#x20AC;˘ Angiogenesis Inhibitors-prevent the formation of new blood vessels so that the tumor cannot grow. â&#x20AC;˘ Photodynamic Therapy- tx with drugs that become active when exposed to light. These activated drugs may kill cancer cells

165

Surgery • Removal of part of all of tumor • H&N • Dysphagia, xerostomia, dysguesia

• Esophageal • dysphagia

• Gastric • Gastrectomy, total or subtotal • B12, Ca, Fe, dumping syn, delayed gastric emptying 166

Surgery • Small Intestine • Malabsorption, steatorrhea

• Colorectal • Colostomy, ileostomy • Malabsorption, fluid and electrolyte abnormalities

• Pancreatic • Whipple procedure, PPPD • Malabsorption, steatorrhea, hyperglycemia

167

Chemotherapy • Meds that interrupt different stages of cell cycle replication – Adjuvant – Neoadjuvant

• Lethal to frequently dividing cells – GI tract, hair follicles, bone marrow

168

RT • Delivered with electromagnetic rays and charged particles • Localized • Also affects rapidly proliferating cells

169

Immunotherapy • Use the body’s own immune system to suppress process that permits Ca growth – Interferon, interleukins, monoclonal antibodies, colony stimulating factors

• Side effects include fatigue, pain

170

Hematopoietic Stem Cell Transplant • Tx for hematologic Ca, some solid tumors – Bone marrow – Peripheral blood stem cell

• Allogeneic- compatible donor – requires immunosuppression tx

• Syngeneic- identical twin • Autologous- pt’s own cells 171

GVHD: Graft vs Host Disease • T cell mediated immunologic reaction • Acute – Within first 100 days post op – Inflammation of skin, liver, GI

• Chronic – – – – – –

>100 days post op Multi-system autoimmune disorder Oral dysphagia, stricture Liver hepatitis, steatorrhea Infections Meds to prevent this dz also have side effects 172

Nutrition Concerns in GVHD • Interventions will depend on the severity of dz and organs affected

• Minimize nutrition impact of GI sx and tx • Nutrition support indicated in those who are unable to maintain weight • Food safety should be discussed 173

Nutritional Needs: GVHD • Pro

1.5-2 g/kg glu- N2 retention, GI integrity,  Infections

• Kcal

≥35 kcal/kg

• Micronutrients- MVI (iron-free) 174

Weight Loss in Ca Pt • Factors involved: – Psychological – Tx induced side effects – Mechanical obstruction of GI tract • H&N, Eso, Gastric, SBO

– Metabolic changes with cachexia and CIWL

175

Types of Cachexia • Primary – Tumor is direct cause, AKA Cancer Induced Weight Loss (CIWL)

• Secondary – Related to tx – Responds more favorably to intervention

176

CIWL • Common cause of death • Characterized by: – Hypercatabolic state 2° presence of tumor and the changes it induces – Early satiety, anorexia, wasting –  LBM and adipose tissue – Glu, lipid, pro metabolic alterations – Pro inflammatory cytokines which appetite 177

Metabolic Alterations •  glucose synthesis, Cori cycle – Accounts for up to 300kcal/d energy loss

•  protein catabolism – LBM not preserved

•  lipid metabolism,  lipogenesis 178

Ca Cachexia • Indicators – wt loss of >5% in 1 month or >10% in 6 months

– BMI <17 (PEM) – Prealbumin < 15mg/dL

179

Strategies for Wt Stabilization • Start early!!! • Oral nutritional products • Enteral nutrition – H&N during RT

• Parenteral nutrition – Radiation enteritis, intractable vomiting

• Pharmacologic tx 180

Medical Nutrition Supplements • Enlive! – 300 kcal, 13.3g pro, clear, non sweet

• Impact Advanced Recovery – 340 kcal, 18g pro – Contains EPA, DHA and Arg

• Juven – Arg, Glu, HMB (hydroxy-methylbuterate) – Given BID 181

Common Sx • • • • • • •

N/V Early satiety Mucositis Diarrhea Dysguesia Xerostomia Anorexia 182

Nausea and Vomiting • • • • • • • • • • •

Determine cause Antiemetics 30-45min before meals Use microwave instead of cooking Avoid frying Avoid heavy odors Try bland, easy to digest foods Eat dry foods in the AM Small, low fat meal day of tx Avoid favorite foods days after tx Gatorade, Resource, non acidic juices Marinol 183

Mucositis • Irritation of epithelial cells caused by chemo, RT, GVHD • Oral – – – – –

Soft non fibrous, non acidic foods that are moist Cold foods with no irritating spices, seasonings High calorie, high protein milkshakes Topical analgesics Brush teeth with soft brush & rinse mouth before and after meals – No commercial mouth washes, rinse with baking soda – MOM may help with sores – Drink through straw 184

Diarrhea • • • • •

Drink clear fluids Avoid greasy, spicy foods Avoid drinks that cause gas Drink and eat high Na and K foods Limit fruit juices and candy with fructose and sorbitol • Eat foods with pectin ie bananas, apples 185

Dysguesia • • • • • • • •

Use plastic utensils Pour nutritional supplements into cup Encourage high protein foods Chew lemon drops after eating Serve foods cold Avoid sweet tasting supplements Blend fruits into milkshake Use heavy seasonings and flavors 186

Xerostomia • • • •

Artificial saliva Sugar free gum or candy Drink 8-10 cups of water/d Add broth, soup, gravy, sauces, butter to moisten food • Limit caffeinated beverages • Use humidifier at night 187

Nutrient Needs Calories

Protein

BEE X 1.3-2.0 25-30 kcal/kg 30-35 kcal/kg

maintenance hypermetabolic

0.8-1.0 1.0-1.5 1.5-2.0

maintenance repletion catab,HSCT

Vitamin/Mineral

Daily MVI 188

Diet for Pt with Immunosupression • The Neutropenic Diet – Eliminates any foods that might have bacteria in it. – Foods are heated to destroy bacteria – No fresh fruits/vegetables – No nuts/seeds – No garnish – No dried fruit – Foods should be freshly cooked and properly cooled. 189

Safe Food Handling Tips • Keep hot foods hot (140º) and cold foods cold (40º) • Refrigerate all leftovers within 2 hrs of cooking and eat them within 24hrs. • Be sure to have 2 cutting boards…one for veggies and one for meat • Thaw foods in the refrigerator or microwave. Never thaw foods at room temperature 190

Patients with Terminal Cancer • Must treat these pts as you would any other pts • If pt is a Hospice pt, they will indicate what measures are appropriate • Goal is to maintain the comfort • No nutrition support should be initiated

191

Renal Function • Excretory • Metabolic

• Endocrine

192

Excretory • Filtration – Blood filtered through glomerulus

• Reabsorption – Selective process

• Secretion – H ions, K secreted into tubule 193

Metabolic Function â&#x20AC;˘ Acid/Base balance pH 0-6 7 8-14

Acid Neutral Base

Normal arterial blood pH is 7.4 If > 7.4 alkalosis If< 7.4 acidosis 194

Endocrine Function 1. Renin angiotensin mechanism 2. Erythopoietin production

3. Ca-phos homeostasis via production of Vit D 4. Vasopressin

195

Renal Disease Function Excretory Metabolic: A/B balance Endocrine: Renin Vasopressin EPO 1,25 D3

Problem Waste products H+ not excreted, acidosis BP/Fluid status Na/H2O retention Anemia Production Ca/Phos inbal, bone dz 196

Acute Renal Failure (ARF) • Sudden reduction in glomerular filtration rate (GFR) • Alteration in the ability for the kidney to remove biologic waste • Usually occurs when the body is under severe stress, like trauma or burns or from drug toxicity.

197

Acute Renal Failure â&#x20AC;˘ Kidneys become unable to regulate the levels of electrolytes, acid, and nitrogenous wastes in in blood â&#x20AC;˘ Urine may be diminished in quantity or absent

198

Acute Renal Failure • Fluid and electrolyte imbalances – Edema • may be related to absence of urine or oliguria (reduced quantity of urine < 400 ml/day)

– Sodium retention contributes to edema – Hyperkalemia • can alter heart rate and lead to heart failure

– Hyperphosphatemia • can increase secretion of parathyroid hormones and reduce blood calcium levels 199

Acute Renal Failure • Uremia – Accumulation of the body’s nitrogen-containing waste products • blood urea nitrogen (BUN), creatinine, and uric acid

– Catabolic state produces additional nitrogenous wastes – Sx: fatigue, lethargy, confusion, headache, anorexia, a metallic taste in the mouth, N, V, D, rapid pulse, elevated blood pressure, seizures, and delirium or coma 200

MNT: ARF PRO ENERGY Na K P Ca Fluid Vit/Min

0.6-0.8gm/kg 35-50 kcal/kg 1-2g/day 2 g/day maintain serum value WNL adj for low alb, maintain WNL output + 500ml DRI 201

Chronic Kidney Disease â&#x20AC;˘ CKD includes conditions that affect the kidney, with the potential to cause either progressive loss of kidney function or complications resulting from decreased kidney function. It is the presence of kidney damage or decreased level of kidney function for three months or more, irrespective of diagnosis

202

Etiology • DM is #1 cause of CKD • Followed by HTN

• CKD leads to CVD and other co morbid complications

203

CKD Complications • Altered electrolytes and hormones – Usually develop during the final stage of renal failure – Hormonal adaptations occur to help regulate electrolyte levels

– Increased secretion of PTH keeps serum P levels normal, but contributes to bone loss • renal osteodystrophy

204

CKD Complications • Uremic Syndrome – Develops during the final stages of CKD • GFR < 15 mL/per minute • BUN > 60 mg/dL

– Subtle mental dysfunctions – Neuromuscular changes – Impaired erythropoietin synthesis • Anemia

– Defects in platelet function and clotting factors 205

CKD Complications • Uremic syndrome – Protein-energy malnutrition • Anorexia – believed to be a primary cause of poor food intake secondary to nausea and vomiting, restrictive diets, uremia and medications • Nutrient losses – consequence of V, D, GI bleeding, concurrent catabolic disease and dialysis

206

CKD Complications • CVD risk – hypertension,  insulin resistance, and abnormal lipids, elevated PTH levels lead to calcification of blood vessels and heart tissue

•  immunity – develop infections

207

Chronic Kidney Disease Stage 1-4 No dialysis

Stage 5 dialysisâ&#x20AC;&#x201D;HD, PD

Goals of nutrition txâ&#x20AC;Ś 1. Retard or stop progression of renal failure 2. Maintain optimal nutritional status 3. Minimize toxicity and metabolic derangements 208

CKD Stages and Action Plans Stage

Description

GRF

Action

At increased risk

≥ 90 (with CKD risk Factors)

Screening, CKD risk reduction

Kidney damage with normal or ↑ GFR

≥ 90

Dx and Tx, Tx of comorbidities, slowing progression, CVD risk ↓

Kidney damage with mild ↓ GFR

60-90

Estimating progression

Moderate ↓ GFR

30-59

Evaluating and treating complications

Severe ↓ GFR

15-29

Preparation for kidney replacement therapy

Kidney failure

< 15 (or dialysis)

Replacement if uremia present 209

MNT: CKD Stages 1-4 PRO ENERGY Na K P Ca Fluid

0.6-0.75 gm/kg 50% HBV 30-35 kcal/kg 2000 mg/day usually unrestricted 10-12 mg/kg/day 1200 mg/day no restriction 210

ESRD • Kidneys are unable to excrete waste, maintain fluid balance, maintain e-lyte balance and produce hormones • Causes uremia due to high levels of nitrogenous waste in the blood – weakness, malaise, nausea, vomiting, neurologic impairment

• Dx by BUN >100mg/dL & Cr 10-12mg/dL 211

Goals of Nutritional Care in ESRD 1. Maintain or obtain optimal nutritional status 2. Control edema and e-lyte imbalance by controlling Na, K and fluid intake 3. Prevent or slow the development of renal osteodystrophy by controlling Ca, PO4 and Vitamin D intake 4. Enable the pt to eat a palatable diet that fits his/her lifestyle

212

MNT: CKD Stage 5 HD PRO ENERGY

Na K P Ca Fluid

1.2 gm/kg 50% HBV 35 kcal/kg< 60yrs 30-35 kcal/kg > 60yrs 2 g/day 2-3 g/day 800-1000 mg/day <2000mg from diet and meds output + 1000ml 213

Nutritional Care for a Kidney Transplant Recipient PRO

1.3- 1.5 gm/kg initial 1.0 gm/kg maintenance

ENERGY

30-35 kcal/kg initial 25-30 kcal/kg maintenance

Na K P Ca Fluid

unrestricted unrestricted unrestricted 1200 mg/day unrestricted 214

Nutritional Concerns in CKD • Anemia • Malnutrition – Uremia complications – Protein loss

• • • • •

Infections Renal osteodystrophy Co morbidities Diet education Nutrition support and the CKD pt

215

Nutritional Assessment • SGA appropriate and validated • Diet hx • Weight hx- dry and wet – Important to assess IDWG to see if pt is gaining

• Fluid status I/O • Medications- help with dosing schedule • Laboratory data 216

Calculating Renal Diets • Calculate energy needs • Calculate protein needs – At least 50% of all protein should be HBV

• Use exchanges to determine milk, meat, fruit, vegetable, starch and non-dairy milk substitutes, fat and high-calorie choices in that order

217

Renal Diet • Foods high in sodium – Canned, pre-prepared and salted foods.

• Foods high in potassium – Potatoes, milk, avocado, dried beans/peas, salt substitutes. – Can leach potatoes eg: soak in H2O for 2+ hours to remove some of the potassium

218

Renal Diet • Foods high in phosphorus – Milk, cheese, organ meats, beans – High PO4 levels reduce Ca levels

• Note: All diets are individualized based on lab values

219

COPD: Nutrition Concerns • Progressive wt loss and muscle wasting • Chronic depletion process which worsens with worsening respiratory function

• Etiology – – – – – –

Impaired GI function Inadequate intake Medications Adaptive mechanism- lower O2 consumption Altered pulm/CVD hemodynamics Hypermetabolism • Inflammatory state, TNF 220

COPD • Labs – Chem 7 – Alb/ pre albumin – ABG’s

• Tests – PFT – VQ scan

• Meds – – – –

Inhalers Bronchodilators Antibiotics Steroids

• Nutrition Goals: – Maintain IBW – Balance diet – Side effects of meds

221

• Pneumonia – Inflammatory process – Infectious – Alveoli fill with fluid/ blood cells

• Tuberculosis – Specific infectious organism – Results • Macrophages to infected area • Walling off of lesion by fibrous tissue

– Highly infectious

222

Nutrient Needs • Kcals

• Pro

BEE X 1.3 BEE X 1.5-2.0 1-1.2g/kg 1.2-1.5g/kg

maintenance repletion maintenance repletion

• Generally pt can eat regular diet – No specific nutrients of concern • Respiratory failure nutrition support • Meds: generally very potent antibiotics – Pt may develop Abx induced diarrhea

223

Cystic Fibrosis • Autosomal recessive disorder affects flow of Na, Cl and water across cell membranes resulting in thick, tenacious mucous production that obstructs glands & ducts

• Sx – – – –

Poor intake,  Appetite Nutrient losses Irreversible neurological damage Poor growth 224

Cystic Fibrosis Complications • Pancreas – Endocrine and exocrine function

• Sweat/salivary glands • Liver – Steatosis

• GI • Respiratory • Bronchitis, pneumonia, atelectasis • Tx with inhalants and chest physiotherapy 225

Cystic Fibrosis • Dx when – – – – –

+ sweat test + lung dz Pancreatic Function Test FTT Genetic test

• Manifest in infancy

226

• Nutrition Intervention vital to decreasing mortality in CF

• Nutritional support regime may be indicated – Continuous nocturnal nutrient infusion – Suggested a 30-50% of needs via EN

• Nutrition status must be optimal prior to transplantation 227

Nutrition Concerns • Inability to meet needs

•  energy consumption to breathe • Early satiety

• Dyspnea during eating • GERD 228

Starvation • Prolonged adaptive mechanism conserves LBM  lipolysis ketone bodies from FA oxidation

Note LBM still catabolized yet at lesser rate  Metabolic rate Activity Sleep  Body temp 229

Stress â&#x20AC;˘ Initial phase- same as starvation utilize glycogen quickly LBM broken down gluconeogenesis â&#x20AC;˘ Prolonged- metabolic rate increases 230

Hormonal Changes in the Acute Stress Phase • Increased glucocorticoids protect the body from stress by altering metabolism of protein and CHO. (ACTH) • ACTH Cortisol which allows for muscle catabolism • Glucagon ↑s blood glucose • Catecholamines (epinephrine and norepinephrine) cause ↑ed glycogenolysis, fat mobilization and gluconeogenesis • Aldosterone and ADH cause water reabsorption 231

Estimating Fluid Needs 100ml/kg 50ml/kg 25ml/kg

1st 10 kg next 10kg for remaining wt or 1-1.5 ml per kcal 232

Estimating Protein Needs • • • •

Generally CC pts are hypermetabolic UUN very useful, especially for pt on support Pro is especially imp in ICU due to catabolism 1.5-2g/kg or higher

233

Excess calories permitted only when: – Hyperglycemia • Diuresis – complicates fluid/electrolyte balance

– Hepatic steatosis (fatty liver) – Excess CO2 production • Exacerbate respiratory insufficiency • Prolong weaning from mechanical ventilation

234

How to Predict Kcals? • Equations – – – – – –

Harris Benedict (1.3-1.5) Mifflin St. Jeor Ireton Jones (1992) Penn State Swinamer Fick Equation

• Indirect calorimetry • ASPEN guidelines - 25 – 30 calories per kg per day

235

Ireton-Jones SPONTANEOUSLY BREATHING PATIENTS

IJEE(s) = 629 - 11(A) + 25(W) - 609(O) VENTILATOR-DEPENDENT PATIENTS

IJEE (v) = 1784 - 11(A) + 5(W) + 244(S) + 239(T) + 804(B)

236

Ireton-Jones Whereâ&#x20AC;Ś IJEE = kcal/day: s = spontaneously breathing v = ventilator-dependent; A = age (years); W = actual body weight (kg); S = sex (male=1, female=0); T = dx of trauma (present=1, absent=0) B = diagnosis of burn (present=1, absent=0 O= obesity >30% above IBW from 1959 Metropolitan Life Insurance tables or BMI >27 (present=1, absent=0)

237

Fick Equation â&#x20AC;˘ Pt must have PA catheter for this calc REE = CO X Hgb X (SaO2-SvO2) X 95.18

CO= cardiac output SaO2 = % saturation of O2 in arterial blood SvO2 =% saturation of O2 in venous blood 238

Respiratory Quotient (RQ) â&#x20AC;˘ Substrate utilization RQ = VCO2 O2 Substrate Ethanol Fat oxidation Pro oxidation Mixed oxidation CHO oxidation Lipogenesis

RQ .67 .71 .82 .85 1.0 1.0-1.2 239

• RQ should be in physiological range & consistent with pts hx/feedings RQ> 1

RQ=1 RQ<.82 RQ<.71

decrease total kcal adjust CHO:Lipid lipogenesis occurs, overfeeding check CHO:Lipid total kcal ETOH, Ketotic, Lipolysis or underfeeding or hypoventilation 240

Drug Therapy to Promote EN Tolerance • Delayed gastric emptying affects approximately – 50% of mechanically ventilated patients – 80% of patients with increased cranial pressure following head injuries

• Prokinetic/Promotility meds promote EN tolerance – Reglan and Erythromycin 241

Gastric Residuals • Levels in the range of 200-500mL should raise concern • However… – Automatic cessation of feeding should not occur for gastric residual volumes <500mL in the absence of other signs of intolerance

242

Omega-3 Fatty Acids and Arginine • Their combination has synergistic effect – Together they create an environment with the correct amount of inflammatory and counterinflammatory components

• Arginine: may help Th2 and M-2 response to improve cytokine and NO production • Omega-3s: may help in excessive inflammation, reducing cytokine-induced eicosanoid production 243

IEFs in the Critically Ill • Research has shown… – IEFs were associated with a significant reduction in infectious complications *Patients illnesses: surgery, trauma, burns, cancer, sepsis

– IEFs associated with significant reduction in ventilator days, infection rate, hospital length of stay * medical, surgical, and trauma

244

Classic Model: Immune Response to Trauma or Surgical Stress Trauma

Surgical Stress

SIRS: Systemic Inflammatory Response Syndrome A period of immune stimulation characterized by systemic inflammation. Toxicity of this response depends on severity of injury, surgical procedure and/or complications of shock or sepsis and nutritional status at presentation. Most progress to CARS within several days. (1)

CARS: Compensatory Antiinflammatory Response Syndrome Sepsis

A period of moderate immune suppression characterized by hyporesponsiveness of TLymphocytes and an increased susceptibility to infection.(1)

Diagnosis of systemic infection by positive blood culture

-Any Trauma/Surgery/Stress event will trigger SIRS. Patients normally progress to CARS. -The septic state is an extended period of SIRS. -If immunonutrition is used early in CARS, movement BACK to SIRS may be prevented.1

Moore F,

245 JPEN 2001

The Metabolic Response â&#x20AC;˘ There are three phases of the metabolic response to trauma, sever burns, sepsis, pancreatitis etcâ&#x20AC;Ś 1. Stress Phase (ebb phase) 2. Catabolic Phase (flow phase) 3. Anabolic Phase

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The Metabolic Response The Stress Phase: â&#x20AC;˘ Characterized by decrease energy expenditure, hemodynamic instability, hypometabolism, insulin resistance and increased counterregulatory hormones â&#x20AC;˘ Usually lasts from 24 hrs to 2 days â&#x20AC;˘ Magnitude and duration depends on severity of the injury/trauma 247

The Metabolic Response The Catabolic Phase: • Characterized by increased energy expenditure, hypercatabolism, proteolysis gluconeogenesis and protein catabolism

• Immunologic response also contributes to increased catabolism – ↑ proinflammatory cytokines TNF, IL-1, IL-6

• Occurs after resuscitation and usually lasts 7–10 days 248

The Metabolic Response The Anabolic Phase: • Characterized by repletion of lean body mass and adipose tissue; catabolic hormones and energy expenditure begin to decrease

• Patients remain significantly hypermetabolic • The inability to meet energy and protein needs can lead to delays in wound healing, infectious complications and debilitation

• Can last for months 249

Acute Respiratory Distress Syndrome (ARDS) • Characterized by the acute onset of dyspnea, hypoxemia, respiratory failure, and pulmonary edema • Mortality rate 30-75% 2o MOSF

• Initiated in response to injury with inflammatory cells, cytokines. ROS responsible for pulmonary damage by oxidizing cell membranes 250

ARDS Etiology: • Direct injury – – – –

toxic substance gastric content smoke bacteria

• Indirect injury – – – – – –

systemic process sepsis trauma pancreatitis fat emboli shock/hypoperfusion

251

ARDS Nutrition Support: • LA GLA immunosuppressive • ALA

AA which is pro inflammatory and

DHA and EPA which are anti inflammatory

• Enteral formulas contain n-3 providing fish and borage oils, Vit C and E, beta carotene, and L carnitine • Some studies show EPA + GLA decrease M & M, ventilator dependent days, risk of developing more organ failures, and252 ICU stay

ARDS Nutrient Needs: • ARDS pts are mechanically ventilated which means they require enteral support – Usually have co morbidities • Kcal depend on underlying dz needs in sepsis, trauma, catabolic illness *indirect calorimetry is best • Pro rapid turnover 1.5-2g/kg 253 *check UUN

Trauma, Burns, Surgery

Infection

Tissue Injury / Inflammatory Response

CARS

Recovery

SIRS

Sepsis

ARDS / Respiratory Failure

Shock

Multiple Organ Failure

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