Complications of PN Flashcards
Which one of the following factors is most likely to contribute to metabolic bone disease in PN-dependent patients?
1: Aluminum toxicity
2: Calcium supplementation
3: Moderate amino acid intake in PN
4: Balanced acetate load in PN
1: Aluminum toxicity
Metabolic bone disease including osteomalacia, osteoporosis and osteopenia has been reported in PN-dependent patients. Aluminum contaminants can be mainly found in parenteral calcium and phosphate salts, trace minerals and vitamins used in making PN solutions. Patients with renal insufficiency are at higher risk for aluminum toxicity due to impaired kidney aluminum excretion. Aluminum toxicity causes osteomalacia by impairing calcium bone fixation, inhibiting the conversion of 25-hydroxyvitamin D to the active 1, 25-dihydroxyvitamin D or reducing parathyroid hormone secretion. In 2000, the FDA issued a rule specifying acceptable aluminum concentrations in large volume parenterals and defined a possible safe upper limit for parenteral aluminum intake at less than 4-5 mcg/kg/day.
Which of the following is a risk factor for the development of PN-associated liver complications in PN-dependent patients?
1: Prolonged use of soybean-based lipid injectable emulsion (ILE)
2: Cyclic infusion of PN
3: Supplemental trophic enteral feeding
4: Medication therapy with ursodiol
1: Prolonged use of soybean-based lipid injectable emulsion (ILE)
Omega-6 polyunsaturated fatty acid soybean-based ILE are thought to be proinflammatory and potentially contain toxic phytosterols, which may impair bile flow. Parenteral nutrition associated liver disease risk is decreased by cycling PN, supplementing with enteral feeding, adding ursodiol or increasing the omega 3:omega 6 ratio.
A 70-kg adult patient receiving PN providing 3000 kcal/day presents with mild to moderate elevations of serum aminotransferases and mild elevations of bilirubin and serum alkaline phosphatase. This patient is most likely exhibiting what type of PN-associated liver disease (PNALD)?
1: Hepatic steatosis
2: Cholestasis
3: Gallbladder sludging
4: Fulminant hepatic failure
1: Hepatic steatosis
Although the relationship between PN and liver disease has been established, its prevention and treatment remain a relevant clinical dilemma. Often, the etiology of PNALD is multifactorial and diligence is required to identify and treat causative factors. There are 3 basic types of hepatobiliary disorders associated with PN: steatosis, cholestasis, and gallbladder sludging (stones). Hepatic steatosis generally occurs in adults and presents with mild elevations in aminotransferases, serum alkaline phosphatase, and bilirubin concentrations. This particular type of hepatobiliary disorder is most often a complication of overfeeding. Cholestasis, occurring primarily in children, is characterized by impaired biliary secretion. Elevated conjugated bilirubin levels are the most common laboratory manifestation in this population. Finally, gallbladder sludging or stones is thought to result from the lack of enteral stimulation in the GI tract and occurs with long-term PN use. In this question, this adult patient is receiving an inappropriately high amount of calories (overfeeding) and has the accompanying lab values consistent with hepatic steatosis.
A 55-year-old male is admitted with an undesired weight loss of 20 pounds during the past month secondary to an ongoing Crohn’s flare up. The patient is found to be at high risk for refeeding syndrome. Which micronutrient should be supplemented?
1: Vitamin A
2: Vitamin K
3: Thiamin
4: Ascorbic acid
3: Thiamin
Thiamin is a water-soluble vitamin and body stores can be easily depleted by malnutrition, weight loss and chronic alcoholism. Carbohydrate intake increases the demand for thiamin, as it is an essential coenzyme in carbohydrate metabolism. Supplementation of thiamin may be indicated in patients at risk for refeeding syndrome due to possible deficiency.
Hyperglycemia in a patient receiving PN is associated primarily with what type of sodium/fluid imbalance?
1: Hypertonic hyponatremia
2: Hypotonic hyponatremia
3: Isotonic hypernatremia
4: Hypertonic hypernatremia
1: Hypertonic hyponatremia
Hypertonic hyponatremia may result from hyperglycemia or administration of hypertonic sodium free solutions. Hyperglycemia causes a shift of water out of cells into the extracellular space, resulting in dilution of serum sodium. For every 100 mg/dL increase in serum glucose concentration above 100 mg/dL, the serum sodium would be expected to decrease by approximately 1.6 mEq/L. Treatment should consist of correction of the underlying hyperglycemia, not changes in sodium and water administration, as this is not a true sodium or water imbalance.
A long-term PN patient presents with involuntary movements, tremor, and rigidity. Which of the following etiologies may explain these symptoms?
1: Manganese deficiency
2: Manganese toxicity
3: Selenium deficiency
4: Selenium toxicity
2: Manganese toxicity
The early phase of manganese toxicity is characterized by weakness, anorexia, headache, and apathy followed by Parkinson-like features including muscle rigidity, mask-like face, staggered gait, and fine tremor. Toxicity may occur in patients on long-term therapy supplemented with a combination multiple trace element preparation. Cholestasis and biliary obstruction may also increase the risk of toxicity as greater than 90% of manganese excretion is via the bile into the feces, but these abnormalities are not always present. Manganese deficiency in humans is not well-documented. In animals, manganese deficiency manifests in skeletal abnormalities, ataxia, low fertility, low HDL cholesterol levels, abnormal lipid and carbohydrate metabolism, and low insulin production. Selenium deficiency is associated with Keshan disease (a type of cardiomyopathy) and increased oxidative injury. Selenium toxicity is characterized by loss of hair and nails, skin lesions, tooth decay, and peripheral neuropathy.
In order to prevent rebound hypoglycemia upon discontinuation of parenteral nutrition (PN), it is recommended the PN infusion rate be reduced over what time span?
1: 0 hours
2: 1-2 hours
3: 2-3 hours
4: 3-4 hours
2: 1-2 hours
Rebound hypoglycemia upon discontinuation of PN may occur, especially in individuals with underlying conditions that affect glucose regulation or those patients requiring large doses of insulin. To reduce the risk of hypoglycemia with cessation of PN, a 1-2 hour taper (e.g. 50% rate reduction) prior to discontinuation is recommended, especially when the patient is unable to take adequate oral or EN feeding. Ordering a point-of-care glucose 30-60 minutes after cessation of PN is recommended to identify and treat rebound hypoglycemia
Which of the following would be the most serious complication of hypertriglyceridemia in a patient receiving parenteral nutrition (PN)?
1: Azotemia
2: Pancreatitis
3: Polyuria
4: Peripheral neuropathy
2: Pancreatitis
Hypertriglyceridemia may occur in some patients receiving lipid injectable emulsion (ILE). If unnoticed and untreated, it may lead to the development of pancreatitis and altered pulmonary function. These complications can be avoided by prudent monitoring of serum triglyceride levels during the administration of PN formulations including ILE. Safe Practices for Parenteral Nutrition (2004) include recommendations to infuse ILE at rates to avoid serum triglyceride levels greater than 400 mg/dL in adults and greater than 200 mg/dL in neonates. If serum triglycerides are elevated, withholding ILE may be indicated
All of the following are potential causes of hyperglycemia in a patient receiving PN EXCEPT
1: carbohydrate administration > 5 mg/kg/min.
2: obesity.
3: sepsis.
4: renal failure.
4: renal failure.
Excess carbohydrate administration has been associated with hyperglycemia, hepatic steatosis and increased carbon dioxide production. Parenteral carbohydrate administration should not exceed 5 mg/kg/min or 20-25 kcal/kg/day. Stress-associated hyperglycemia can develop in patients with sepsis as a result of insulin resistance, increased gluconeogenesis and glycogenolysis and suppressed insulin secretion. Insulin resistance may be exacerbated in obese patients during times of stress. Patients with renal failure demonstrate a prolonged insulin half-life as the kidney accounts for ~40-50% of its clearance from systemic circulation. Research studies with a higher incidence of renal failure have also shown a higher incidence of severe hypoglycemia. Insulin therapy should be altered for these individuals.
All of the following are risk factors for the development of rebound hypoglycemia after cessation of PN EXCEPT
1: malnutrition.
2: hepatic dysfunction.
3: hypertension.
4: renal insufficiency.
3: hypertension.
Rebound hypoglycemia occurs when elevated endogenous insulin levels do not adjust to the reduced dextrose infusion following cessation of PN. Although rebound hypoglycemia is not a universal occurrence, some patients may be at higher risk because of underlying conditions that affect glucose regulation. These patients include those with malnutrition and renal or liver disease however hypertension alone should not predispose one to hypoglycemia. A one to two hours taper at the end of PN infusion, cutting the rate in half may benefit in reducing the risk of rebound hypoglycemia.
The preferred site for placement of a central venous access device (CVAD) for adult patients to reduce the risk of infection is
1: subclavian.
2: internal jugular.
3: femoral.
4: external jugular.
1: subclavian.
The density of skin flora at the catheter site is a major contributing factor for catheter-related blood stream infections (CRBSI). Guidelines recommend that CVADs be placed in a subclavian site instead of a jugular or femoral site to reduce the risk of infection. The external jugular is not a preferred location for a CVAD for parenteral nutrition.
Catheter related thrombosis caused by fibrin build up within blood vessels adhering to a central venous catheter is called
1: fibrin sheath.
2: fibrin tail.
3: intraluminal thrombus.
4: mural thrombus.
4: mural thrombus.
A mural thrombus develops when fibrin builds up inside the vein and causes the vascular access device to adhere to the vessel wall.
A fibrin sheath is a layer of fibrin that develops around the outside of a central venous catheter (CVC) secondary to aggregation of fibrin from the presence of a central venous catheter within a vein.
A fibrin tail or flap is fibrin build up on the CVC tip that will allow for infusion through the CVC, but will inhibit withdrawal of blood.
Intraluminal thrombus is a clot within the catheter lumen and is caused by inadequate flushing and blood reflux.
The use of 0.1N hydrochloric acid is most effective for clearing catheter occlusions due to precipitation of
1: calcium-phosphate.
2: tobramycin.
3: phenytoin.
4: lipid residue.
1: calcium-phosphate.
The use of 0.1N hydrochloric acid has been reported effective in clearing catheters with crystalline occlusions because its acidic pH is favorable for calcium and phosphate solubility. Clinicians should be aware, however, that direct infusion of hydrochloric acid into the venous system can be associated with fever, phlebitis, and sepsis. For catheter occlusions due to precipitates associated with medications in the high pH range such as tobramycin and phenytoin, sodium bicarbonate 1 mEq/mL has been anecdotally reported to be effective. Seventy percent ethanol is the most effective solvent to dissolve lipid residue.
A 40-year-old male receiving chronic PN therapy (initiated 15 years ago) secondary to massive bowel resection develops metabolic bone disease. His current 12-hour cyclic PN formula provides 5 g/kg/day dextrose, 2 g/kg/day protein and 1 g/kg/day of fat. What is the most appropriate intervention to reduce hypercalciuria?
1: Increase calcium gluconate
2: Decrease phosphorus supplementation
3: Shorten PN infusion time to 10 hours
4: Decrease amino acid content of PN solution
4: Decrease amino acid content of PN solution
The most important contributor to metabolic bone disease is a negative calcium balance. Hypocalcemia occurs as a result of decreased calcium intake and/or increased calcium urinary excretion. Factors that cause hypercalciuria include: excessive calcium and inadequate phosphorus supplementation, excessive protein in PN solutions, cyclic PN infusions, and chronic metabolic acidosis. The most appropriate intervention for this patient is protein reduction. Ideally, protein doses for long-term PN provision should not exceed 1.5 g/kg/day. Although the exact mechanism of protein-induced hypercalciuria is unknown, it could be related to an increased glomerular filtration rate or increased excretion of sulfates, ammonia, and urinary titratable acidity that decreases renal calcium reabsorption.
The best approach to prevent PN-induced cholelithiasis is administration of
1: choline.
2: cholecystokinin-octapeptide (CCK-OP).
3: ursodiol.
4: oral or enteral feeding.
4: oral or enteral feeding.
The best approach to preventing cholelithiasis is early initiation of oral or enteral feeding, even in small amounts, to stimulate cholecystokinin secretion, bowel motility and gallbladder emptying. Injections of CCK-OP to induce gall bladder contractions and reduce biliary sludge have yielded mixed results and caused gastrointestinal intolerance in some patients. Although ursodiol has been shown to improve bile flow, doses of 6-15 mg/kg/day have yielded mixed and limited results. In addition, ursodiol is only available in an oral dosage form and its absorption may be limited in patients with intestinal resection. The role of choline in the pathogenesis of cholelithiasis has not been determined.
All of the following are considered as short-term complications of home parenteral nutrition EXCEPT
1: dehydration.
2: metabolic bone disease.
3: refeeding syndrome.
4: catheter malposition
2: metabolic bone disease.
Electrolyte abnormalities, dehydration and catheter malposition are more common short-term complications of home parenteral nutrition. Metabolic bone disease has been recognized as a concern in long-term home parenteral nutrition patients. The contribution of the PN formulation to the development of bone disease is unclear.
Which of the following is most likely responsible for elevated serum bicarbonate levels in a home parenteral nutrition (PN) patient?
1: Excess chloride salts in the PN
2: Diarrhea
3: Excess acetate salts in the PN
4: Acute renal failure
3: Excess acetate salts in the PN
An elevated serum bicarbonate level is one of the markers of metabolic alkalosis. Metabolic alkalosis may be caused by nasogastric suctioning, volume depletion and diuretic use. In a PN patient, excess use of acetate, which is metabolized to bicarbonate, may precipitate a metabolic alkalosis. Excess chloride, diarrhea and acute renal failure are common causes of metabolic acidosis.
The clinical presentation of refeeding syndrome includes all of the following EXCEPT
1: respiratory failure.
2: seizures.
3: cardiac arrythmias.
4: dehydration.
4: dehydration.
Electrolyte abnormalities that may occur with refeeding syndrome include sodium retention, hypophosphatemia, hypokalemia, and hypomagnesemia. Sodium retention usually occurs in the early phase of the refeeding syndrome and is exacerbated by excessive sodium and fluid intake. This may lead to fluid overload, pulmonary edema, and cardiac decompensation. Severe hypophosphatemia has been reported to cause respiratory failure and seizures. Severe hypokalemia and hypomagnesemia predispose patients to cardiac arrhythmias and neuromuscular adverse effects such as weakness and muscle cramps
A 75-year-old female with moderate malnutrition is status-post radical cystectomy with ileal conduit. She weighs 50kg, and she has a 20-gauge IV access in the left cephalic vein. She is initiated on a PPN solution at 125mL/h. This formula contains 210 grams of dextrose, 75 grams of amino acids, and 45 grams of fat. Which of the following complications is she at greatest risk for developing?
1: Fluid overload
2: Hypertriglyceridemia
3: Azotemia
4: Hyperglycemia
1: Fluid overload
Current guidelines for adults recommend the following maximum amounts for PN components: 30-40 mL/kg/day of fluid, 7 g/kg/day of carbohydrates, 2.5 g/kg/day of fat, and 2 g/kg/day of protein. This formula provides 60 mL/kg/day which exceeds recommended maximum daily fluid intake. PPN has to be administered in larger volumes to provide beneficial calories while avoiding venous access compromise (phlebitis, thrombosis, thrombophlebitis, extravasation).Patients that receive PPN must have good peripheral access, the ability to tolerate large volumes of fluid, and a contraindication to central venous access. PPN should be administered for at least five days with no more than two weeks of total therapy. Contraindications for PPN include significant malnutrition, severe metabolic stress, large nutrient or electrolyte needs, fluid restriction, greater than two week need for PN support, and renal and liver compromise.
A 68-year-old female with normal liver function and a lactate of 1 mmol/L is in acute kidney injury status-post colon resection and is receiving PN. She has the following arterial blood gas (ABG) results: pH=7.31, PCO2=36 mm Hg, and serum bicarbonate=20 mEq/L. What is the most appropriate PN intervention?
1: Maintain current chloride:acetate ratio
2: Increase chloride:acetate ratio
3: Decrease chloride:acetate ratio
4: Decrease calorie content of PN
3: Decrease chloride:acetate ratio
This patient is experiencing a metabolic acidosis, likely related to acute kidney failure, as evidenced by a decrease in pH (7.35-7.45), a normal PCO2 (35-45 mm Hg), and a decreased serum bicarbonate (22-26 mEq/L). The most appropriate nutrition intervention is to decrease the chloride:acetate ratio in the PN solution. Acetate is converted to bicarbonate by the liver which should correct the metabolic acidosis.
