Parenteral Nutrition Complications Flashcards
Question: 1
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: Low 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. Calcium deficiency in PN patients causes metabolic bone disease. Calcium deficiency results from restricted calcium intake in PN solution due to solubility limits with calcium and phosphate or from increased urinary calcium excretion during PN infusion. Maximizing and balancing calcium and phosphorus intake is beneficial and essential to prevent metabolic bone disease. Urinary calcium losses correlate with amino acid intake in PN, with higher amino acid loads causing increased urinary calcium excretion. Hypercalciuria with high amino acid intake may be related to increased glomerular filtration rate or increased urinary titratable acidity that decreases renal calcium reabsorption. Chronic metabolic acidosis may cause bone loss by impairing vitamin D metabolism and bone buffering systems. Because acetate is a substrate for bicarbonate, providing adequate and balanced amounts of acetate in PN to maintain normal acid-base balance would help prevent metabolic bone disease.
References:
Charney PJ, Chair. A.S.P.E.N. Statement on aluminum in parenteral nutrition solutions. NCP. 2004;19:416-417.
Question: 2
Which of the following is a risk factor for the development of PN-associated liver complications in PN-dependent patients?
1: Short bowel syndrome
2: Cyclic infusion of PN
3: Supplemental trophic enteral feeding
4: Medication therapy with ursodiol
1: Short bowel syndrome
Patients with short bowel syndrome are at high risk for developing PN-associated liver complications. Risk factors that predispose patients with short bowel syndrome to liver dysfunction include chronic PN use as a result of reduced intestinal length and absorption, abnormal bile acid cycling following ileal resection which interrupts the biliary enterohepatic cycling causing bile stagnation, and potentially, intestinal bacterial translocation that may cause direct liver injury by bacteria and their toxins. Prolonged PN dependence is expected in patients who had more than 75% of their small intestinal length resected, or with less than 80-100 cm of their small bowel remaining. Cyclic or nocturnal PN infusion reduces hepatic complications by avoiding continuous compulsive feeding. Improvement in hepatomegaly and in serum liver enzymes concentrations were reported following cycling of PN infusion over 14-16 hours for 2-3 weeks. Initiating enteral feeding and weaning off PN are essential measures to prevent PN-associated cholestasis. Enteral feeding preserves intestinal integrity by preventing mucosal hypoplasia induced by starvation, preserves the immunologic integrity of the gut-associated lymphatic tissue, and may prevent bacterial translocation. Ursodiol, a hydrophilic bile acid that is used for cholesterol gallstone dissolution, has also been used to treat PN-associated cholestasis and cholelithiasis. Ursodiol has been shown to improve clinical signs and symptoms of cholestasis. Long term effects of ursodiol on altering liver disease progression remain unknown.
References:
Kumpf VJ. Parenteral Nutrition-Associated Liver Disease in Adult and Pediatric Patients. NCP. 2006;21:279-290.
A 70-kg adult patient receiving PN providing 3000 kcal/day presents with mild to moderate elevations of serum aminotransferases and small 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 failureA 70-kg adult patient receiving PN providing 3000 kcal/day presents with mild to moderate elevations of serum aminotransferases and small 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.
References:
Kumpf VJ. Parenteral Nutrition-Associated Liver Disease in Adult and Pediatric Patients. NCP. 2006;21:279-290.
Patients at risk for refeeding syndrome often require supplementation of
1: vitamin A.
2: vitamin K.
3: thiamine.
4: vitamin C.
3: thiamine.
Since thiamine is a water-soluble vitamin, its body stores can be easily depleted by malnutrition and weight loss. Dextrose infusion places additional demand on thiamine, since it is a co-factor in intermediate carbohydrate loads. Thiamine is a coenzyme for glucose metabolism. Thiamine requirements are increased in cachectic patients, and additional supplementation is suggested for patients at risk for deficiency. Supplementation of other vitamins, especially folic acid, at 1 mg/day may also be necessary.
References:
Btaiche IF, Khalidi N. Metabolic complications of parenteral nutrition in adults, part 1. Am J Health Syst Pharm. 2004;61(18):1938-1949.
Hyperglycemia 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
Hyperglycemia induces a hypertonic state which causes a shift of intracellular water into the vascular space, causing a diluted 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.
References:
Kraft MD, Btaiche IF, Sacks GS, et al. Treatment of electrolyte disorders in adult patients in the intensive care unit. Am J Health Syst Pharm. 2005;62:1663-1682.
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
Extrapyramidal symptoms may include involuntary movements, tremor, and rigidity. Manganese undergoes biliary excretion. Toxicity may occur in long-term PN patients with cholestasis who receive supplemental manganese. The early phase of manganese toxicity is characterized by weakness, anorexia, headache, and apathy followed by Parkinson-like features including muscle rigidity, masklike face, staggered gait, and fine tremor.
References:
O’Donnell K, Radigan A. Hypermanganesemia in an acute care setting. NCP. 2003;18:374-376.
In order to prevent rebound hypoglycemia upon discontinuation of PN, the infusion rate of PN should be reduced by
1: 25% for the last 1 hour of infusion.
2: 25% for the last 2 hours of infusion.
3: 50% for the last 1 hour of infusion.
4: 50% for the last 2 hours of infusion.
4: 50% for the last 2 hours of infusion.
Rebound hypoglycemia upon discontinuation of PN has been reported, although this is an extremely uncommon event. Some experts continue to recommend that the infusion rate be cut in half for the last 2 hours prior to discontinuation, particularly for patients receiving large amounts of insulin along with their PN.
References:
A.S.P.E.N. Board of Directors and the Clinical Guidelines Task Force. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN. 2002;26(1 suppl):1SA-138SA.
Which of the following would be the most likely complication of hypertriglyceridemia?
1: Azotemia
2: Pancreatitis
3: Polyuria
4: Peripheral neuropathy
2: Pancreatitis
Hypertriglyceridemia may occur in some patients receiving IVFE. 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 IVFE.
References:
A.S.P.E.N. Board of Directors and the Clinical Guidelines Task Force. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN. 2002;26(1 suppl):1SA-138SA.
All of the following are risk factors for the development of hyperglycemia in a patient receiving PN EXCEPT
1: cirrhosis.
2: obesity.
3: pancreatitis.
4: hypothyroidism.
4: hypothyroidism.
Insulin resistance accounts for the increased incidence of hyperglycemia in patients with cirrhosis and who are obese. Patients with pancreatitis often develop hyperglycemia due to insulin insufficiency. Hypoglycemia (not hyperglycemia) is an abnormal laboratory finding associated with hypothyroidism.
References:
Btaiche IF, Khalidi N. Metabolic complications of parenteral nutrition in adults, part 1. Am J Health Syst Pharm. 2004;61(18):1938-1949.
All of the following are risk factors for the development of rebound hypoglycemia in a patient receiving PN EXCEPT
1: chronic starvation.
2: liver failure.
3: hypertension.
4: hypothyroidism.
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 chronic starvation, severe malnutrition, liver disease, and hypothyroidism.
References:
Btaiche IF, Khalidi N. Metabolic complications of parenteral nutrition in adults, part 1. Am J Health Syst Pharm. 2004;61(18):1938-1949.
To reduce the risk of infection, the preferred site for catheter insertion is
1: subclavian.
2: internal jugular.
3: femoral.
4: umbilical artery.
1: subclavian.
The density of skin flora at the catheter site is a major contributing factor for catheter-related blood stream infections (CRBSI). Authorities recommend that central venous catheters (CVCs) be placed in a subclavian site instead of a jugular or femoral site to reduce the risk of infection.
References:
O’Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the Prevention of Intravascular Catheter-Related Infections. Clinical Infectious Diseases. 2002;35:1281-1307.
Fibrin that builds up on the wall of blood vessels may also adhere to the catheter creating a
1: fibrin sheath.
2: fibrin tail.
3: intraluminal thrombus.
4: mural thrombus.
4: mural thrombus.
A mural thrombus develops when fibrin builds up on the wall of the blood vessel possibly adhering to the catheter. The aggregation of fibrin resulting from the presence of a venous access device in the vein often develops as a fibrin layer (fibrin sheath) that forms around the outside of the catheter. In some cases, the fibrin sheath can grow over the tip of the catheter, or may accumulate exclusively at the distal tip of the catheter creating a “fibrin tail.” An intraluminal thrombus occurs as fibrin or blood products build up inside the catheter lumen, creating a partial or total occlusion.
References:
Haire WD, Herbst SL. Use of Alteplase (t-PA) for the Management of Thrombotic Catheter Dysfunction: Guidelines from a Consensus Conference of the National Association of Vascular Access Networks (NAVAN). NCP. 2000;15:265-275.
The use of 0.1N hydrochloric acid is most effective for clearing catheter occlusions due to precipation 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. 70 percent ethanol is the most effective solvent to dissolve lipid residue.
References:
A.S.P.E.N. Board of Directors and the Clinical Guidelines Task Force. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN. 2002;26(1 suppl):1SA-138SA.
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
Calcium deficiency in PN patients is a major cause of metabolic bone disease. 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, amino acids in PN solutions, cyclic PN infusions, and chronic metabolic acidosis. The most appropriate intervention for this patient is protein reduction. 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.
References:
Btaiche IF, Khalid N. Metabolic complications of parenteral nutrition in adults, part 2. Am J Health Syst Pharm. 2004;6(19):2050-2057.
Question: 15
The best approach to prevent PN-induced cholelithiasis is administration of
1: choline.
2: CCK-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 gall bladder 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. Althogh 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.
References:
Kumpf VJ. Parenteral Nutrition-Associated Liver Disease in Adult and Pediatric Patients. NCP. 2006;21:279-290.
All of the following may be 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 for 25 years and is a concern in long-term home parenteral patients.
References:
Siepler J. Principles and strategies for monitoring home parenteral nutrition. NCP.2007;22(3):340-350.
Which of the following is most likely responsible for elevated serum bicarbonate levels in a home parenteral (PN) patient?
1: Excess chloride salts in the PN
2: Diarrhea
3: Excess acetate salts in the PN
4: ARF
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. However, 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 (ARF) are common causes of metabolic acidosis.
References:
Siepler J. Principles and strategies for monitoring home parenteral nutrition. NCP.2007;22(3):340-350.
The clinical presentation of refeeding syndrome includes all of the following EXCEPT
1: pulmonary edema.
2: seizures.
3: cardiac decompensation.
4: dehydration.
4: dehydration.
Electrolyte abnormalities that may occur with refeeding syndrome may 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 seizures in the severely malnourished within 4-7 days of PN initiation. Another potential sequelae of the refeeding syndrome is fluid retention (not diuresis) due to the antinaturetic effect of increased insulin concentrations.
References:
Btaiche IF, Khalidi N. Metabolic complications of parenteral nutrition in adults, part 1. Am J Health Syst Pharm. 2004;61(18):1938-1949.
A 75-year-old female status-post ileoconduit with poor intravenous access weighing 50 kg is initiated on 3L of peripheral parenteral nutrition (PPN) daily. The PPN formula is written as 7% dextrose, 3.5% amino acids and 1.5% IVFE. 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. The provision of PPN necessitates larger volumes in order to deliver a beneficial caloric load to the patient without compromising venous access (thrombophelbitis or infiltration of peripheral veins). This formula provides 60 mL/kg/day which exceeds the recommended maximum daily fluid intake.
References:
Task Force for the Revision of Safe Practices for Parenteral Nutrition: Mirtallo J, Canada T, Johnson D, et al. Safe practices for parenteral nutrition. JPEN. 2004;28(6 Suppl):S39-S70.
A critically ill 68-year-old female receiving PN has the following arterial blood gas (ABG) results: pH=7.31, PaCO2=36 mm Hg, and serum bicarbonate=20 mEq/L. What is the most appropriate PN intervention?
1: Do nothing
2: Increase PN chloride concentration
3: Increase PN acetate concentration
4: Decrease calorie content of PN
3: Increase PN acetate concentration
This patient is experiencing a metabolic acidosis as evidenced by a decrease in pH (7.35-7.45), a normal PaCO2 (35-45 mm Hg), and a decreased serum bicarbonate (23-30 mEq/L). The most appropriate nutrition intervention is to supplement acetate in the PN solution. Acetate is converted to bicarbonate by the liver which should correct the metabolic acidosis.
References:
Langley G, Canada T, Day L. Acid-base disorders and nutrition support treatment. NCP. 2003;18:259-261.