MF Flashcards

Question

Important chemo med from MW: Cysplatin: Low ___ (and potentially secondary hypokalemia and hypocalcemia)

Answer 1

To prevent rebound hypoglycemia, PN may be tapered over 1 to 2 hours. If PN needs to be stopped emergently, a 10% dextrose in water solution should be infused at either the same rate as the PN or at a rate of at least 50 mL/h. When cyclic PN infusion is used in the home, some form of tapering is usually required during the last 2 hours of the cycle. Finally, PN may be rapidly discontinued if the patient is tolerating tube feeding in amounts adequate to maintain normal blood glucose levels.

Answer 2

Measures activities of daily living

Answer 3

NOT required if feeding at lease 3g protein per kg per day (at first, was added to PN as it was conditionally essential. Now, continually used for solubility, reduces oxidative stress, building blood for amino acids) Cysteine is considered an essential AA in neonates: must be added separately to pediatric neonate TPN, since lack enzyme needed to convert Met → Cys Standard neonatal AA solutions were designed to mimic the plasma AAs patterns of breastfed infants. Taurine and tyrosine are considered essential Aas in neonates because of their enzyme immaturity. There is conflicting data on the essentiality of cysteine in neonates and it is not a component of standard neonatal parenteral AA solutions. Cysteine is unstable in aqueous solution so if it is added, this is done so immediately prior to administration. The addition of cysteine lowers the pH further in order to optimize calcium and phosphorus solubility.

Answer 4

Measures functional independence in rehab settings

Answer 5

Population: hospitalized elderly Includes: weight loss, appetite, food intake, disease severity, homebound, dementia/depression Uses 6 questions, brief streamlined screening tool with high diagnostic accuracy. Now the preferred version of the MNA Most widely used tool to measure health related QOL

Answer 6

Patient population: Hospitalized patients Includes: appetite, unintentional weight loss Does not account for disease severity Strongest evidence with reliability and validity

Answer 7

Arginine is a conditionally essential amino acid in inflammatory conditions. It is often a key component of immune-modulating enteral formulas. ASPEN/SCCM Critical Care Guidelines still caution against it's general use in the ICU due to lack of quality evidence supporting the theoretical benefits of its use. These guidelines do recommend its use in trauma and TBI. Based on expert consensus and a small trial (n=40) patients with TBI fed with an immune modulating formula containing arginine demonstrated decreased infections. Of note, this formula also contained DHA and EPA which likely also accelerate recovery after TBI.

Answer 8

Patient population: Hospitalized patients Includes: Weight loss, BMI, food intake, disease severity, age >70, impaired general condition Recommended for critical illness! NRS-2002 accounts for pre-existing malnutrition and illness severity

Answer 9

Population: ICU patients who need nutrition support / are malnourished Includes: Age, comorbidities, LOS, SOFA score, APACHE score Recommended for assessing nutrition risk in critical illness NUTRIC focuses on severity of illness

Answer 10

Cofactor for transformation of LCFA into acylcarntine and for transport of FAs >10 carbons long into the mitochondria

Answer 11

Fluroscopic + endoscopic placements are most successful method followed by bedside electromagnetic imaging

Answer 12

Probability of making a type 1 error (i.e. probability of rejecting the null hypothesis when it actually true)

Answer 13

Validated and reliable assessment tool for diagnosing nutrition status 5 nutrition related history components + 3 physical exam components History: weight changes, nutrition intake, GI symptoms, functional capacity, metabolic stress from disease Physical: fat depletion (triceps, chest), muscle wasting (quads, deltoids), nutrition related edema (ankle, sacral, ascites) DOES NOT use laboratory markers Classifies patient as well nourished, moderate vs severe malnutrition Limited use in critical illness

Answer 14

Used for elderly patients >65 years old, assess quality of aging Considers anthros, biochemical markers, meds, nutrition and quality of life Assess quality of aging / frailty

Answer 15

Measures instrumental activities of daily living Instrumental or intermediate activities of daily living (ability to maintain an independent household, ex: taking meds)

Answer 16

1. Basic activities of daily living (grooming, maintaining continence) 2. Instrumental or intermediate activities of daily living (ability to maintain an independent household, ex: taking meds) 3. Advanced activities of daily living (ability to fulfill societal, community, and family roles as well as participate in recreational or occupational tasks such as exercising)

Answer 17

A nutrition screening and assessment tool that allows providers to identify elderly (age *65* and above) patients who are *malnourished* or at risk of malnutrition. The MNA was developed more than 20 years ago, and it originally consisted of 18 questions Used for LTC facility patients

Answer 18

Iron deficiency is an anemia that is usually microcytic and hypochromic

Answer 19

History: unintentional weight loss, nutrition intake, functional capacity, chronic illness, acute illness or social/behavioral circumstances Physical: Muscle wasting, fat wasting, fluid accumulation (nutrition related edema, effect on weight) Uses laboratory markers to determine presence of inflammation

Answer 20

Complications of aluminum intake are best avoided by minimizing the use of aluminum-containing agents such as antacids and sucralfate Can lead to hypophosphatemia (phos binding properties. Note sucrafalate is also an aluminum containing agent.

Answer 21

Best for PICU: Clinical judgment + targeted tools like PeDiSMART or PNST. STRONGkids is common but may not be sensitive enough for critically ill children. Always follow up a positive screen with comprehensive assessment by a dietitian.

Answer 22

GFR (Glomerular filtration) increases significantly in pregnancy beginning in the first trimester. The increases may result in glucosuria, which may be present in more than 50% of pregnant women. Glucosuria is not necessarily related to maternal hyperglycemia, and urine glucose levels should not be used to diagnose diabetes or for monitoring glycemic status in pregnant women. TPN solutions often contain high amounts of dextrose to meet caloric needs. If glucose infusion exceeds the patient’s ability to utilize or metabolize it (especially during long-term administration), hyperglycemia can result, which may spill over into the urine (glucosuria).

Answer 23

Strong correlation with muscle mass and nutritional status

Answer 24

May be affected by alcohol intake, gastric bypass Older adults are at an increased risk of zinc deficiency at baseline primarily due to decreased oral intake and absorption. Elimination occurs primarily through fecal excretion. 12 mg zinc is recommended for each liter of GI output. The standard oral adult replacement dose is 220 mg zinc sulfate twice daily (100 mg total of elemental zinc per day). An optimal duration of therapy has not been identified. Serum zinc levels may not always be reflective of total body stores and currently, there are no specific guidelines for screening and treatment of zinc deficiencies. Excessive supplementation beyond 2–3 weeks has been associated with copper and iron deficiencies due to competitive antagonism of enteric transport proteins and metalloenzymes. Chronic supplementation with higher doses (>20 mg/d) also causes microcytosis, neutropenia, and decreased high-density lipoprotein cholesterol. Choline, chromium and thiamin are all excreted via urine output. Zinc deficiency can be a result of inadequate intake, reduced absorption, increased losses, or increased demand. Symptoms can be reported as loss of taste sensation, altered smell sensation, and skin rash in severe cases. A zinc deficiency may lead to decreased vitamin A release from the liver which may contribute to nighttime blindness. Zinc is needed for growth and tissue maintenance, and deficiency can present as growth failure, alopecia, and decreased muscle work capacity. Deficiency can also cause gonadal hypofunction leading to decreased plasma testosterone and fertility. Anemia is not associated with zinc deficiency, but could be a symptom of zinc toxicity if that leads to copper deficiency. Zinc deficiency affects vitamin A metabolism via two mechanisms: decreasing retinol mobilization in the liver and decreasing zinc-dependent enzyme conversion of retinol to retinal. Therefore, a zinc deficiency could precipitate a secondary vitamin A deficiency. High levels of calcium and iron compete with zinc for absorption. High levels of enteric zinc may cause a copper deficiency due to increased metallothionein production. An altered zinc metabolism with zinc deficiency and decreased serum zinc is noted in most forms of clinical liver disease, especially acute liver disease. Zinc may also be effective in the treatment of HE. A systematic review and meta-analysis concluded that a combination of zinc supplementation and lactulose over 3 to 6 months may improve the number connection test in cirrhotic patients with low grade HE, compared with lactulose only. Zinc supplementation may be considered in patients not improving on lactulose and rifaximin therapy. There is a potential benefit of zinc supplementation on HE, however, the evidence is limited, and larger, well-designed, clinical trials are needed. Zinc is a cofactor in the conversion of ammonia to urea which improves excretion of this neurotoxin Zinc deficiency can lead to pica, dysgeusia, skin loss and hair lesions Zinc is an essential trace element. Many populations are at risk for zinc deficiency including older adults, postoperative gastrointestinal surgery patients and those with liver disease, renal disease and malabsorptive conditions. Plasma and urinary zinc have been confirmed as the most reliable biomarkers of zinc status in healthy populations. However, plasma zinc should be interpreted with caution in patients with low albumin, inflammation or hemodilution. Zinc's role in wound healing is due to its function as a cofactor for collagen and protein. Patients with wounds who are deficient or shown to be losing zinc in wound exudates (negative pressure therapy) may benefit from supplementation. Supplementation for all patients with wounds is not recommended due to the risks of copper deficiency and adverse effects on wound healing with zinc toxicity. Clinical manifestations of zinc deficiency are evident at plasma levels < 33 mcg/dL. If signs of zinc deficiency such as alopecia and skin rash are noted on nutrition focused physical exam it is most likely a deficiency is present. Additional signs of deficiency may include cheilosis, glossitis, nail dystrophy. Treatment for zinc deficiency in adults is typically 220 mg zinc sulfate (50 mg elemental zinc) twice daily for a total of 100 mg elemental zinc per day. Oral replacement will generally alleviate all clinical manifestations within 1-2 weeks.

Answer 25

Protein Zinc EFA Biotin

Answer 26

g dextrose x3.4 g AA x4 g lipid x 10

Answer 27

B vitamins, B2, B6, zinc, niacin

Answer 28

The NRI uses serum albumin and the ratio of current weight to usual weight. Screening algorithms such as NRI can help identify those patients who will benefit from perioperative nutrition support via EN or PN.

Answer 29

ICU mortality score

Answer 30

Organ failure assessment

Answer 31

Deficiency: magnesium, zinc Hypercatabolism: due to metabolic stress from burn injury that increases energy expenditure causing increase calorie and protein needs Require increase protein until significant healing occurs- due to increase in muscle breakdown (protein is the preferred energy source in stress response), increased protein loss from open wounds. If tube feeds, would likely benefit from high protein Overfeeding: feeding excess of energy expenditure does not preserve lean body mass Can cause hyperglycemia, hepatic steatosis, prolonged vent dependence, fat mass accumulation Kcal delivery >1.2x resting energy expenditure does not conserve lean body mass, causes fat accumulation PN has been associated with increased mortality, so EN is preferred (except when contraindicated or unable to meet needs on PN) The ebb response initially follows burn injury and lasts 3-5 days and includes depressed resting energy expenditure, hyperglycemia, low plasma insulin, loss of plasma volume, decreased oxygen consumption, decreased blood pressure, reduced cardiac output, and decreased body temperature. After the ebb phase, the acute phase of the flow response occurs and is represented by elevated catecholamines and elevated or normal plasma insulin along with hyperglycemia, elevated glucagon and glucocorticoids, high glucagon-to-insulin ratio, catabolism, increased body temperature, increased cardiac output, redistribution of polyvalent cations such as zinc and iron, mobilization of metabolic reserves, increased urinary excretion of nitrogen, sulphur, magnesium, phosphorus and potassium, and accelerated gluconeogenesis. These metabolic alterations occur quickly, and the acute phase peaks between the 6th and 10th day following burn injury. The transition from acute to adaptive phase of the flow response is gradual. Anabolism is not established until the adaptive phase of the flow response.

Answer 32

Thrombotic occlusions: -Cathflo/alteplase - only FDA approved thrombolytic agent for thrombotic CVAD occlusions -Intraluminal clot/thrombosis - clot within the catheter lumen itself . Due to inadequate flushing + blood reflux into the CVC lumen. Causes chest pain, earache, jaw pain, swelling arm/shoulder/neck/face on catheter side, or leakage at the exit site -Mural thrombus: fibrin buildup causing adherence of the CVC to the vein -Fibrin tail/flap: fibrin on the CVC tip that allows infusion, not withdrawal -Fibrin sheath: layer of fibrin around the external surface of the CVC Non-thrombotic catheter occlusions: management depends on type, often due to inadequate flushing, blood reflux, etc. -Mechanical obstruction: due to catheter migration/malposition from insertion or use -Lipid residue occlusions: 70% ethyl alcohol is most effective for dissolving lipid residue / clearing (since lipids are soluble in alcohol) Medications-associated precipitate occlusion 8.4% NaBicarb or 0.1-N NaOH: clears basic (alkaline) meds (phenytoin, oxacillin) 1 mEq/mL sodium bicarb solution: anecdotally effective for removing high ppH med precipitates (phenytoin/dilantin, tobramycin) 0.1 N-hydrochloric acid: clears acidic medication (e.g. vancomycin) Calcium phosphorus precipitate occlusion 0.1 N-hydrochloric acid: good for clearing crystalline occlusions, lower pH will increase Ca/Phos solubility

Answer 33

NAFLD/nonalcoholic steatohepatitis (NASH). NAFLD, the hepatic manifestation of metabolic syndrome/insulin resistance, has become the most common liver disease in the United States. Frequent obesity, T2DM Recommendations: weight loss (energy restricted, low carb), adequate protein, physical activity May need zinc checked Studies show probiotics are good, as well as vitamin E NAFLD may have increased risk of SIBO NAFLD may arise as a complication of rapid weight loss after bariatric surgery Patients with cirrhotic NASH can be malnourished and protein deprived despite being obese

Answer 34

Flush with NS after each infusion to clear all meds/solutions Reduce risk of incompatible meds causing precipitation Decreasing risk of intraluminal occlusion from reflux

Answer 35

As illness advances during the dying process, nutritional needs change and calorie requirement decreases Patients rarely feel hunger or thirst, dying shuts down these (and other) normal functions Patients should not feel guilty if they do not eat, reduced food/fluid intake is normal at end-of-life Decreased nutritional intake causes increase in endorphins and ketones, while dehydration leads to increase in dynorphins (pain reduction) and comfort Starvation and increased ketone production (ketonemia) can cause feelings of euphoria Dynorphins and endorphins are natural analgesics, can decrease pain and increase comfort Continuing artificial nutrition and hydration does not always = comfort, QOL Pursuing aggressive artificial nutrition/hydration can be more harmful and cause complications Those who receive no artificial nutrition/hydration do not experience more negative side effects than those who do Electrolytes are usually within normal limits in dying patients, even with artificial nutrition / hydration Feeding even a small amount can prevent ketonemia and prolong the sense of hunger Can alleviate dry mouth with good oral care Dehydration is not an uncomfortable state, particularly with decreased sensation of thirst and end of life IVF hydration not recommended for hydration, can cause more discomfort and respiratory distress

Answer 36

Nasogastric/nasojejunal/PPFT Appropriate for short term feeding (4-6 weeks) Cons: can become displaced/occluded Possible populations that this would be contraindicated: coagulopathy, friable gastric varices, hepatic encephalopathy, fulminant hepatic failure, portal HTN Gastrostomy/jejunostomy/PEG/PEJ Appropriate for long term feeding >4 weeks) Indications: can be prophylactically placed in head/neck cancer patients before radiation or at time of surgical resection Contraindications: ascites J tubes must be replaced immediately, if becomes dislodged, tract can close quickly Percutaneous endoscopic GJ (PEG-J)/GJ tube Appropriate for long term feeding AND need for dual access Pros: less likely migration/flipping back into stomach than PEJ Cons: gastric outlet obstruction more likely (since it’s transpyloric) No difference in placement difficulty, bleed risk than PEG, PEJ Low profile/skin level tubes Can be capped when not in use, often more comfortable and cosmetically appealing Can be placed as an exchange tube or at time of initial insertion Held in place with inflated internal balloon or solid silicone internal retention bolster Require access connector connection prior to use, need good dexterity, not easiest for accessing Can be utilized for gastric or jejunal access (for feeding, decompression, etc)

Answer 37

Catheter related phlebitis: inflammation of venous wall causing erythema, pain, tenderness, warmth, induration, palpable cord and swelling Catheter-related central venous thrombosis: arm/shoulder/neck swelling, limb/jaw/ear pain dilated collateral veins . Caused by CVC induced endothelial trauma/inflammation which can cause venous thrombosis Inflammation of vessel wall can cause pain and tenderness along the course of the vein. Can also cause collateral vein congestion due to obstruction of blood flow Pinch off syndrome: when subclavian tunneled CVC becomes compressed between first rib and the clavicle, causing intermittent compression/pinching preventing catheter malfunction. Can lead to intermittent occlusion of infusion, aspiration and increased risk catheter fracture/ Hallmark sign: changes in patient position (e.g. raising/lowering arm) can widen/narrow the angle between rib/clavicle and relieve the occlusion. Treatment: removal of the catheter, re-insertion in more lateral position in the subclavian vs. IJ placement Superior vena cava syndrome: partial/complete obstruction of blood flow into the vena cava. Causes SOB, cough, cyanosis of face/neck/shoulder/arms, distended chest/neck vein

Answer 38

Nutrition components: avoid pre-op fasting by providing CHO nutrition/fluid and withholding bowel prep Avoid pre-op fasting, with solid meals up to 6 hours before surgery Given 800mL CHO rich clear fluid at midnight and 400mL 2 hours before to help decrease volume of IVF required, help decrease post op complications

Answer 39

 BMI less than 18.5: underweight  BMI 18.5 to 24.9: normal weight  BMI 25 to 29.9: overweight  BMI 30 to 34.9: class I obesity  BMI 35 to 39.9: class II obesity  BMI equal to or greater than 40: extreme (class III) obesity

Answer 40

/=1 month 5% in 1 month 7.5% in 3 months 10% in 6 months 20% in 1 year Mild fat wasting Mild muscle wasting Mild edema

Answer 41

<75% of needs for >7 days 1-2% in 1 week 5% in 1 month 7.5% in 3 months Mild fat wasting Mild muscle wasting Mild edema

Answer 42

/=1 month >5% in 1 month >7.5% in 3 months >10% in 6 months >20% in 1 year Severe fat wasting Severe muscle wasting Severe edema Measurably reduced functional status

Answer 43

/=7 days >2% in 1 week >5% in 1 month >7.5% in 3 months Moderate fat wasting Moderate muscle wasting Moderate to severe edema Measurably reduced functional status

Answer 44

<75% for >/=3 months 5% in 1 month 7.5% in 3 months 10% in 6 months 20% in 1 year Mild fat wasting Mild muscle wasting Mild edema

Answer 45

/= 1 month >5% in 1 month >7.5% in 3 months >10% in 6 months >20% in 1 year Severe fat wasting Severe muscle wasting Severe edema Measurably reduced functional status

Answer 46

Vitamin B2 Vitamin B6 Niacin Iron

Answer 47

Vitamin B2 Vitamin B6 Niacin Iron

Answer 48

B2 B6 B12 Niacin Folate Iron (severe)

Answer 49

Vitamin A Vitamin C Poor blanching, in the context of a rash or skin discoloration, means that the skin doesn't return to its normal color when pressure is applied

Answer 50

Hypercalcemia or protein

Answer 51

Vitamin A Vitamin C

Answer 52

Magnesium Selenium

Answer 53

Protein calorie

Answer 54

Vitamin C Vitamin K

Answer 55

Niacin Tryptophan

Answer 56

Iron Folate B12

Answer 57

Protein Zinc Vitamin C

Answer 58

Dehydration Vitamin A EFA

Answer 59

Vitamin A Vitamin C EFA

Answer 60

Vitamin A: – follicular hyperkeratosis, impaired wound healing * Vitamin B12: – numb or tingling in hands, poor balance * Vitamin D: – aching bones, muscle weakness * Vitamin K: – easy to bruise, easy to bleed * Calcium: – muscle cramps, dermatitis, eczema, brittle grooved nails, hair loss * Copper: – poor wound healing, Kayser-Fleischer rings * Iodine: – goiter, weight loss, muscle weakness * Zinc: – mouth ulcers, white spots on nails

Answer 61

Folate The primary biochemical role is as a coenzyme in the transfer of single carbon fragments for amino acid metabolism and nucleic acid synthesis Zinc deficiency and chronic alcohol consumption can impair conjugase activity and folate absorption Medication Interactions: Certain medications can decrease serum folate (Carbamazepine, estrogen therapy, oral contraceptives, phenobarbital, phenytoin, triamterene). Others decrease folate absorption (Cholestyramine, metformin, sulfasalazine, pancrelipase). Trimethoprim interferes with folate metabolism. Rifampin confounds folate assay measurements. Excessive amounts of folic acid (100 times the RDA) may result in seizures in individuals on phenytoin therapy. Valproic acid may impair folate metabolism. Methotrexate is a folate analogue that inhibits DHFR, leading to decreased folate function essential for DNA synthesis Inadequate intake is a known risk factor for neural tube defects. Folic acid, B6, and B12 supplementation can reduce plasma homocysteine, which is linked to atherosclerosis risk. Daily folic acid, B6, and B12 supplements did not reduce ischemic stroke recurrence in the VITATOPS study. The need for folate supplementation in renal disease patients on HD or PD is controversial, but elderly AKI patients are at higher risk Deficiency: Megaloblastic or macrocytic anemia. Glossitis, described as inflammation of the tongue which may appear magenta colored, sore, or beefy red. Oral ulcers. Pallor or paleness, often associated with anemia. Poor growth. Neural tube defects (NTDs) in newborns, resulting from folate deficiency during fetal development.

Answer 62

Thiamine Essential for glucose/carbohydrate metabolism. Key functions include energy transformation, synthesis of pentoses and NADPH and membrane and nerve conduction Deficiency can occur in 14-20 days At risk: alcohol use, liver cirrhosis, diuretics, pregnancy, batiatric surgery, vomiting, malabsorption, long term PN, dialysis HF< refeeding Deficiency affects the CNS (Wernicke's, beriberi) Aggressive treatment is needed for deficiency complicating chronic alcoholism or bariatric surgery: 500 mg IV over 30 mins, 3 times daily for 2 days, then 250 mg IV or IM once daily for 5 days with other B vitamins, followed by 100 mg/d ora Excreted in the urine Other signs and symptoms of deficiency listed include weakness, burning feet syndrome, calf muscle tenderness, and decreased deep tendon reflexes

Answer 63

Pyridoxine Populations at risk for deficiency include patients receiving parenteral nutrition (PN) without supplementation, older adults, individuals with alcoholism, patients with malabsorptive syndromes, and those on certain medications like isoniazid, penicillamine, corticosteroids, and anticonvulsants. Elderly patients with Acute Kidney Injury (AKI) are also at higher risk. Signs and symptoms of deficiency and toxicity are listed in Table 8-11. Reduced B6 enzyme activity has been reported in patients receiving hemodialysis (HD) and peritoneal dialysis (PD). Reduced activity can also increase oxalate formation

Answer 64

Vitamin B12 is needed for the conversion of homocysteine to methionine At risk: loss of parietal cells, older adults, ileum/stomach resection, pancreatic insufficiency, SIBO Medications like Metformin, PPIs, colchicine, tetracycline, oral contraceptives, octreotide, methyldopa, and rifampin can affect B12 levels or absorption. Methyldopa increases the need for supplementation. Deficiency: numb or tingling in hands, poor balance The first manifestations of marginal or inadequate status are usually neurologic, possibly followed by hematologic and GI abnormalities

Answer 65

What is EFAD? * EFAD is a deficiency of linoleic acid (LA, an omega-6 fatty acid) and α-linolenic acid (ALA, an omega-3 fatty acid). * These are called essential fatty acids because they cannot be synthesized by humans and must be supplied exogenously (through the diet). * Not providing these fatty acids can result in metabolic complications. Causes and Risk Factors: * EFAD can occur if insufficient quantities of linoleic acid and α-linolenic acid are provided in patients receiving enteral or parenteral nutrition. * Patients receiving Parenteral Nutrition (PN) without lipids for extended periods are at risk. * Patients at risk include those on ILE-free PN for more than 2–4 weeks. * Poor nutritional status is also a risk factor. * EFAD can occur rapidly in patients receiving continuous fat-free PN, partly because elevated insulin levels (from hypertonic dextrose infusion) prevent adipose tissue lipolysis, reducing endogenous EFA availability. Thus, an exogenous fat source must be provided in this situation. * Patients with Cystic Fibrosis (CF) are prone to fat malabsorption due to pancreatic insufficiency, which puts them at risk for EFAD and fat-soluble vitamin deficiencies. * Biliary atresia can lead to EFAD if a Medium-Chain Triglyceride (MCT) oil predominant formula that lacks adequate Long-Chain Triglycerides (LCT) is used. * Patients on long-term Home PN may have an increased risk of EFAD. * Patients with SBS who receive PN are at risk for EFAD. * Deficiencies are common in settings of low-fat diets and fat malabsorption. Manifestations (Symptoms): * Clinical manifestations include dry, scaly skin rash (dermatitis), which is often the most prominent clinical change. * Other clinical symptoms include alopecia, poor wound healing, and thrombocytopenia. * Increased susceptibility to infection and immune dysfunction have been noted. * Hepatomegaly and fatty liver can occur. * Anemia is another manifestation. * Weight loss is also listed as a sign. * In CF patients, overt signs like scaly dermatitis, alopecia, thrombocytopenia, and growth failure are uncommon, though EFAD correlates with poor growth and pulmonary status. * Symptoms can occur within 10-20 days in adults. * EFAD typically occurs around 4 weeks in PN without fat, but signs can be seen as early as 10-20 days in adults, and it can occur more rapidly in infants and children. In acutely ill patients, lipid-free PN can cause EFAD within 2 weeks. * Early stages of EFAD may not present with clinical symptoms, requiring biochemical testing. * Deficiency of only α-linolenic acid may primarily cause neurological abnormalities, without a rash. Diagnosis: * Biochemical changes include a decrease in linoleic acid and arachidonic acid (tetraenoic acid) levels, and an increase in mead acid (triene acid) levels. Mead acid is primarily produced in humans when EFAs are absent. * The plasma triene-to-tetraene ratio is used to assess for EFAD. * A triene:tetraene ratio of more than 0.2 (Holman index) indicates the presence of EFAD and can confirm the diagnosis. Some sources suggest a ratio > 0.4 in CF patients. * Biochemical deficiencies can be suspected by elevated AST, ALT, and confirmed by the triene:tetraene ratio. * When using alternative Lipid Injectable Emulsions (ILEs), interpretation of fatty acid profiles should be cautious, as reduced linoleic acid levels may still be adequate to prevent EFAD, and high omega-9 fatty acids can increase mead acid conversion. Reduced linoleic acid in alternative ILEs could lead to false positives if the definitive diagnosis using the triene:tetraene ratio > 0.2 is not applied. Prevention: * To prevent EFAD, 1% to 2% of daily energy requirements should come from linoleic acid, with some sources suggesting 1% to 4% or 2% to 4%. * Approximately 0.5% of energy should come from linolenic acid, with some sources suggesting 0.25% to 0.5%. * These goals translate to approximately 250 mL of 20% or 500 mL of 10% soy-based ILE administered over 8 to 10 hours, twice a week. * Alternatively, 500 mL of a 20% soy-based ILE can be given once a week. * Providing 50g ILE twice a week or 100g ILE once a week can prevent EFAD. * For infants and children receiving PN, soybean oil-based ILE should be provided at 0.5-1.0 g/kg/day to prevent EFAD. * Using an alternative oil–based ILE (containing MCT, olive, fish oil) may require a greater amount to meet EFA requirements due to lower linoleic and linolenic acid quantities compared to soy-based products. The dose should be calculated based on energy requirements and other lipid sources. * For patients on long-term Home PN, linoleic acid provided at 3.2% of total energy with a daily average of 0.24 ± 0.13 g fat per kg was sufficient in one study. A weekly minimum of 1.0 g fat per kg or 500 mL of 20% ILE weekly may be necessary to correct or avoid biochemical alterations. * Initiation of low-dose or trophic enteral feeding using a polymeric enteral formula containing soybean oil and other high-linoleic oils can offset the risk of EFAD. Providing 10% to 15% of total energy requirements this way will generally supply adequate EFAs. * The 2016 ASPEN/SCCM critical care guidelines suggest withholding 100% soybean oil-based ILE for the first week or limiting it to a maximum of 100 g/wk if there is concern or risk for EFAD when it's the sole IV fat source. * Soybean oil-based ILEs (10%, 20%, 30%) and the four-oil blend (SMOFlipid) provide EFAs to prevent EFAD. Omegaven (fish oil) is indicated for pediatric patients with PN-associated cholestasis (PNAC) and is a source of fatty acids, but the concern for EFAD when used as monotherapy has been raised, especially in pediatrics or long-term PN. Treatment/Management: * Soybean oil ILE can be used for the treatment of EFAD, particularly for short-term use (< 2 weeks) in patients with normal LFTs. * Providing 2% to 4% of the energy requirement as linoleic acid may correct EFA insufficiency. * In patients who do not tolerate ILEs, a trial of topical skin application or oral ingestion of oils may be given to alleviate biochemical EFAD. Topical safflower oil is mentioned as a trial in those intolerant to ILE. * Omega-3 fatty acid supplementation (EPA and DHA) may correct clinical symptoms of EFAD. * Fish oil lipid emulsion alone may satisfy EFA requirements for humans; studies in children on fish oil monotherapy showed no biochemical or clinical signs of EFAD after long-term treatment. * When EFAD is suspected in CF patients, the triene-to-tetraene ratio is used for assessment. While omega-3 supplementation is sometimes used, results are mixed, and further trials are needed. Essential fatty acid profiles have been shown to improve in CF patients after lung transplant.

Answer 66

There are roughly 56,000 patients on home PN in the United States. * PN is a high-risk medication that requires close management in the home arena. * Safe delivery of PN is the responsibility of healthcare providers, patients, and caregivers. * Education and support for home PN patients can reduce complications and enhance survival and quality of life. * The Oley Foundation is a national, independent, non-profit organization that strives to enrich the lives of those living with home intravenous nutrition (parenteral) and tube feeding (enteral) through education, advocacy, and networking. Candidates and Indications * In general, indications for home PN are the same as those for hospitalized patients. * Home PN candidates have a prolonged duration of PN required (more than 2 weeks). * Hospitalization is no longer needed for medical reasons for home PN candidates. * Medicare and state (Medicaid) healthcare programs have developed criteria that must be met for reimbursement. * Medicare requires documentation that the patient's GI tract is nonfunctional ("artificial gut"). * This nonfunctional condition must be permanent, generally believed to be at least 3 months of therapy. * The patient must have documented evidence of inability to tolerate enteral feeding (malabsorption, obstruction). (Note: CMS removed the national coverage determination in July 2022, now using local criteria including diseases impairing nutrient absorption and motility disorders causing severe malabsorption. The chart must document EN was considered/tried/failed or contraindicated). * Home PN has become a lifeline for patients with short bowel syndrome, allowing them to resume a nearly normal lifestyle. Most patients with SBS are not medically appropriate for a home start and require 3-5 days of inpatient monitoring when starting PN. * Patients with chronic GI disorders tend to adjust to home nutrition support more effectively than those with acute disorders or those without GI disorders. * Performance status (Karnofsky performance status score [KPF] greater than 50) has been associated with longer survival in incurable cancer patients receiving home PN. * Improvements in quality of life, KPF, and nutrition status have been observed in advanced cancer patients receiving HPN. * Generally, CMS does not provide coverage for supplemental HPN. Facilitating Discharge and Home Environment * Facilitating discharge for HPN involves obtaining diagnostic testing and verifying insurance, establishing long-term vascular access, establishing a tolerated PN formula, assessing the patient (ADLs, caregiver, home setting, buy-in), beginning patient education, and identifying outpatient management. * Careful consideration must be given to the capabilities of the patient and caregivers as well as the safety of the home environment for PN. * A home evaluation should assess if the home is accessible to the home health provider, if the environment is clean with reliable utilities (clean running water), if the patient can move around safely, if the patient is willing to learn equipment operation, if the caregiver is willing to provide additional assistance, and if the patient and caregiver are willing to learn problems and contact appropriate services. * Sanitary water supply and electricity are needed to safely administer parenteral nutrition. * PN solution requires refrigeration. * Storage space is needed for supplies. An isolated infusion area and dedicated refrigerator are preferred but not required. * Patients receiving home parenteral nutrition require a home/cellular telephone or other means of contacting someone outside of the home in the event of a medical emergency. * If there is frequent interruption of electrical service, a back-up battery-powered infusion pump is highly recommended; a back-up electrical generator may be needed. * Whether PN can be initiated in the home is controversial. Table 14-5 lists conditions warranting caution when initiating PN in the home. Vascular Access * A permanent central vascular access device (VAD) is required for discharge on home PN. * Patients should not be sent home with a temporary catheter for HPN use. * VADs must be placed in the central venous system to accommodate hyperosmolar HPN solutions. * Approved types of VADs for HPN administration include tunneled central venous catheters, implanted ports, and peripherally inserted central catheters (PICCs). * PICCs are catheters inserted into a peripheral vein in the upper arm, with the tip terminating in the SVC/RAJ. They are widely used for long-term access. * However, PICCs are not a preferred device for long-term parenteral nutrition at home. * Midline catheters provide peripheral, not central venous access, are short-term (2-4 weeks), and are not for HPN. * Peripheral PN (PPN) is not suitable for home use. * Nursing is needed for sterile dressing changes for PICCs. Monitoring * Laboratory monitoring for stable home patients is typically done every other week for 1-3 months, then monthly. * Lab draws may be obtained by homecare nurses. * Initial laboratory data should be obtained prior to HPN initiation. * More frequent assessment of laboratory data may be required initially to ensure efficacy and prevent complications, such as weekly for 4 weeks after discharge (glucose, electrolytes, BUN, Cr) or until clinically stable. * Assessing micronutrient status in long-term HPN consumers is challenging. Deficiency manifestations can be complicated. * Manganese may need to be removed from PN in children with cholestasis. Manganese and copper may become elevated in patients with cholestasis because they are excreted via the biliary tract. The dose may need reduction or elimination, but removal of all trace elements is not warranted. * Patients receiving long-term home PN may develop metabolic bone disease. Bone mineral testing (DXA) should be done annually. * Serum iron and ferritin levels should be monitored routinely every 1 to 3 months if a repletion dose of parenteral iron is added to the PN solution. Reimbursement * Medicare and state (Medicaid) healthcare programs have developed criteria that must be met for reimbursement. * Medicare has stringent guidelines. * To qualify for Medicare reimbursement, HPN must be needed for long-term therapy, usually greater than 90 days. * Documentation of a nonfunctional gastrointestinal tract is critical to ensure coverage. * Medicare requires evidence of loss of GI function and when enteral feedings have failed. The chart must document that EN was considered, tried and failed, or may exacerbate GI dysfunction. * Medicare may approve HPN if there is evidence of fat malabsorption. * Beginning in July 2022, CMS removed their national coverage determination for HPN, now using local coverage determinations including diseases of the small intestine/exocrine glands significantly impairing absorption and motility disorders causing severe malabsorption. * Medical record documentation should include diagnosis, duration, clinical course, prognosis, functional limitations, other interventions and results, and past experience. * CMS still requires patients to meet the test of permanence (generally >= 3 months duration). * Generally, CMS does not provide coverage for supplemental HPN. * Recertification is required 6 months after initial certification for therapy, documenting continued need. * Private payers/managed care organizations often require preauthorization/precertification. * Medicare coverage guidelines affect standards of care for all EN/PN patients in the US regardless if on Medicare. Complications * Patients receiving long-term home PN may develop metabolic bone disease. The etiology is multifactorial, including pre-existing disease, malabsorption, metabolic acidosis, steroid therapy, inactivity, mineral deficiencies (calcium, phosphorus, magnesium), and vitamin D deficiency or excess. * A high prevalence of osteoporosis (41%) was reported in patients after at least 6 months of home PN. * PN associated cholestasis (PNAC) occurs predominantly in children, but may also occur in adult patients receiving long-term PN. * The risk of EFAD is increased in some patients who require home PN solutions. * Prolonged use of plant-based ILEs can carry risks, including parenteral nutrition–associated liver disease (PNALD), particularly among infants. Steatosis is the most common form in adults. * Complications related to home PN included catheter-related infections in pregnant patients in one report. * Cancer patients on HPN have more frequent PN complications, which are more likely to result in readmission to the hospital. * Assessing micronutrient status in long-term HPN consumers is challenging, requiring careful monitoring for deficiency manifestations. Symptoms of one deficiency may mimic another. * Copper deficiency manifestations include anemia, leukopenia (primarily neutropenia), foot numbness, and gait difficulty. Neurological presentations (paresthesia, numbness, sensory ataxia, spastic gait) are also associated with vitamin B12 deficiency. * Aluminum contamination is a concern in long-term PN. Aluminum toxicity is not the primary etiology of PN-associated bone disease. * Commercially available PN formulas may contain potentially toxic levels of Manganese, Copper, and Chromium. * Thirty-Day Readmissions Rate is High for Hospitalized Patients Discharged with Home Parenteral Nutrition or Intravenous Fluids. Patient and Caregiver Aspects * HPN should be integrated into the patient's and family's typical way of living. Structuring the administration schedule to simulate normal meal times is encouraged. * Patient and caregiver training and education are important components. * The "teach-back" process is an effective way to improve understanding of discharge teaching while addressing health literacy. * Complications that can be easily identified by patients or caregivers should be reviewed during post-discharge teaching

Answer 67

1. Excess sodium 2. Low calcium 3. Vit D toxicity/deficiency 4. Aluminum toxicity 5. Low magnesium 6. Copper deficiency 7. Low phos

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