Parenteral Nutrition Complications Flashcards

1
Q

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

A

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.

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2
Q

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

A

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.

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3
Q

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

A

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.

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4
Q

Patients at risk for refeeding syndrome often require supplementation of

1: vitamin A.
2: vitamin K.
3: thiamine.
4: vitamin C.

A

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.

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5
Q

Hyperglycemia is associated primarily with what type of sodium/fluid imbalance?

1: Hypertonic hyponatremia
2: Hypotonic hyponatremia
3: Isotonic hypernatremia
4: Hypertonic hypernatremia

A

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.

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6
Q

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

A

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.

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7
Q

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.

A

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.

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8
Q

Which of the following would be the most likely complication of hypertriglyceridemia?

1: Azotemia
2: Pancreatitis
3: Polyuria
4: Peripheral neuropathy

A

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.

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9
Q

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.

A

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.

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10
Q

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.

A

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.

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11
Q

To reduce the risk of infection, the preferred site for catheter insertion is

1: subclavian.
2: internal jugular.
3: femoral.
4: umbilical artery.

A

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.

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12
Q

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.

A

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.

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13
Q

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.

A

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.

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14
Q

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

A

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.

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15
Q

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.

A

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.

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16
Q

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.

A

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.

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17
Q

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

A

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.

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18
Q

The clinical presentation of refeeding syndrome includes all of the following EXCEPT

1: pulmonary edema.
2: seizures.
3: cardiac decompensation.
4: dehydration.

A

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.

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19
Q

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

A

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.

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20
Q

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

A

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.

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21
Q

What feature of a Groshong PICC reduces the risk of catheter occlusion?

1: Pressure sensitive three-way valve
2: Large lumen(s) size
3: Heparin coated tip
4: Soft grade medical silicon tubing

A

1: Pressure sensitive three-way valve

A Groshong PICC has a pressure sensitive three-way valve at the IV tip of the catheter that prevents reflux of blood into the catheter, which should decrease the risk of occlusion by this mechanism. Since blood cannot reflux into the catheter, the Groshong catheter need only be flushed with saline, and heparin is not necessary. Although additional features of Groshong catheters include soft medical grade tubing, presence of antimicrobial cuff and large lumen size, none of these contribute to a decreased incidence of catheter occlusion. Groshong catheters are not coated with heparin.

References:
Vanek VW. The ins and outs of venous access: Part II. NCP. 2002;17:142-155.

22
Q

A 45-kg patient receiving chronic PN therapy develops an intraluminal clot in their central venous access device. What is the most appropriate pharmacological intervention to clear this access device?

1: Heparin 100 units/mL
2: Alteplase 2mg/2mL
3: Argatroban 350 mcg/kg bolus over 3-5 minutes
4: Reteplase 10 units

A

2: Alteplase 2mg/2mL

Conventional therapy for an occluded central venous access device due to an intraluminal clot or sleeve is local thrombolytic therapy with a low-dose agent in a single or repeated bolus. Alteplase is the only FDA-approved thrombolytic agent for catheter occlusions. In clinical trials, one 2 mg/2 mL dose of alteplase restored function in 67% of occluded catheters. 100 units/mL of heparin is appropriate for catheter flushing. Argatroban is indicated as an anticoagulant for prophylaxis or treatment of thrombosis in patients with heparin-induced thrombocytopenia. Reteplase is an approved thrombolytic for acute myocardial function but not catheter occlusions.

References:
Krzywda EA, Andris DA. Twenty-five Years of Advances in Vascular Access: Bridging Research to Clinical Practice. NCP. 2005;20:597-606.

23
Q

A patient receiving PN is afebrile, has negative blood cultures, but presents with redness and purulence at the catheter exit site. How is this infection best managed?

1: Remove CVC
2: Exchange catheter over a guidewire
3: Initiate empiric antimicrobial therapy with vancomycin
4: Apply topical antibiotic ointment

A

3: Initiate empiric antimicrobial therapy with vancomycin

A clinical exit-site infection is defined as erythema, induration, and/or tenderness within 2 cm of the catheter exit site. It may be associated with other signs and symptoms of infection, such as fever or puss emerging from the exit site, with or without concomitant bloodstream infection. Nontunneled CVCs in patients with fever with mild to moderate disease should not routinely be removed unless the patient has erythema or purulence overlying the catheter exit site or clinical signs of sepsis. Empiric therapy consists of vancomycin with subsequent changes in antimicrobial therapy after isolate susceptibility reported. Application of antibiotic ointment to catheter insertion sites as a prophylactic intervention to reduce the incidence of catheter-related infections have yielded conflicting results. In addition, rates of catheter colonization with candida species might be increased with the use of antibiotic ointments that have no fungicidal activity. No recommendations exist to support the use of topical antibiotic ointments in the treatment of catheter-related infections.

References:
Mermel LA, Farr BM, Sherertz RJ, et al. Guidelines for the management of intravascular catheter-related infections. Clin Infect Dis. 2001;32(9):1249-1272.

24
Q

A PN-dependent petient with an average daily ostomy output of 3L presents with elevated BUN/SCr ratio and mild hyponatremia. What is the most appropriate PN intervention for this patient?

1: Increase sodium, restrict protein
2: Increase sodium, increase fluid
3: Increase fluid, restrict protein
4: Increase sodium, restrict fluid

A

2: Increase sodium, increase fluid

Patients with ileostomy or small bowel fistula output are at risk for loss of water and electrolytes. Sodium content of ileostomy output can be as high as 100 mEq/L. The high BUN/SCr ratio indicates volume depletion. Hyponatremia can result when fluid replacement does not contain adequate sodium to make up for ileostomy losses.

References:
Buchman AL. Etiology and initial management of short bowel syndrome. Gastroenterology. 2006;130:S5-S15.

25
Q

The use of 70% ethyl alcohol is most effective for clearing catheter occlusions due to precipitation of

1: calcium-phosphate.
2: lipid residue.
3: phenytoin.
4: tobramycin

A

2: lipid residue.

Lipid deposits/complexes can develop due to aggregation of lipid particle by divalent and trivalent cations. These types of occlusions are most common when using 3-in-1 PN solutions and develop gradually over several days before complete catheter obstruction occurs. 70% ethyl alcohol is effective for lipid complexes because lipids are soluble in alcohol. The treatment of catheter occlusions due to calcium-phosphate and other drug precipitates depends on the acid-base properties of the compound. For crystalline occlusions (calcium-phosphate precipitates) and acidic medications, 0.1N HCl is effective. For basic medications (i.e., phenytoin, tobramycin), 0.1N NaOH or 8.4% sodium bicarbonate is effective. Treatment of mural thrombus ranges from catheter removal to thrombolytic therapy.

References:
Hardy G, Ball P. Clogbusting: time for a concerted approach to catheter occlusions? Curr Opin in Clin Nutr and Metab Care. 2005;8:277-283.

26
Q

The most common route of infection for a tunneled central venous catheter (CVC) is

1: extraluminal colonization of the catheter.
2: contamination of the catheter hub.
3: infusate contamination.
4: hematogenous seeding from another focus of infection

A

2: contamination of the catheter hub.
Contamination of the catheter hub and intraluminal infection is the most common route of infection for tunneled CVCs or implantable devices. In contrast, the pathogenesis of nontunneled CVC infection is often related to extraluminal colonization of the catheter or intraluminal colonization of the hub and lumen of the CVC. Occasionally, catheters might become hematogenously seeded from another focus of infection. Rarely, infusate contamination leads to catheter-related bloodstream 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.

27
Q

A patient arrives in your clinic complaining of intermittent catheter malfunction. You identify that the catheter malfunction is relieved by raising the patient’s arm where the catheter is located. Which condition should be suspected?

1: Fibrin sheath
2: Pinch-off syndrome
3: Superior vena cava syndrome
4: Catheter migration

A

2: Pinch-off syndrome

Pinch-off syndrome occurs when the catheter is being compressed between the first rib and the clavicle, causing intermittent compression and pinching, leading to intermittent occlusion of infusion and aspiration. Changes in the patient’s position can widen or narrow the angle between the rib and clavicle, usually by raising or lowering the arm, which can relieve occlusion of the catheter. This is the hallmark sign of the syndrome. The external portion of the catheter may frequently tear, requiring repair as a result of the increased pressure required to overcome the compressed catheter. The treatment is removal of the catheter and reinsertion in a more lateral position in the subclavian vein or placement in the internal jugular vein.

References:

Vanek VW. The ins and outs of venous access: Part II. NCP. 2002;17:142-155.

28
Q

All of the following conditions predispose a patient to the refeeding syndrome EXCEPT

1: chronic starvation and chronic alcoholism.
2: anorexia or malabsorption.
3: morbid obesity with weight loss.
4: bulimia nervosa.

A

4: bulimia nervosa.

Conditions that predispose patients to the refeeding syndrome include chronic starvation, prolonged fasting, chronic alcoholism, anorexia nervosa, malabsorption syndromes, morbid obesity followed by significant weight loss, and wasting diseases, such as cancer and AIDS.

References:

Btaiche IF, Khalidi N. Metabolic complications of parenteral nutrition in adults, part 1. Am J Health Syst Pharm. 2004;61(18):1938-1949.

29
Q

Which of the following are the most common electrolyte imbalances observed in patients with refeeding syndrome?

1: Hypokalemia, hyperphosphatemia, hypoglycemia
2: Hyperkalemia, hyperphosphatemia, hypoglycemia
3: Hypokalemia, hypophosphatemia, hypermagnesemia
4: Hypokalemia, hypophosphatemia, and hypomagnesemia

A

Refeeding syndrome is a potentially lethal condition that can result from fluid and electrolyte shifts in malnourished patients undergoing refeeding of oral, enteral, or parenteral nutrition. The syndrome is characterized by alterations in electrolytes and vitamins. Hypokalemia, hypophosphatemia, and hypomagnesemia commonly occur and are associated with significant morbidity and mortality. Identification of patients at high risk for refeeding syndrome is essential in providing nutrition support to malnourished patients.

References:

Btaiche IF, Khalidi N. Metabolic complications of parenteral nutrition in adults, part 1. Am J Health Syst Pharm. 2004;61(18):1938-1949.

30
Q

Hyperkalemia is most likely to be associated with

1: pregnancy.
2: hyperinsulinemia.
3: respiratory failure.
4: metabolic acidosis.

A

4: metabolic acidosis.

Hyperkalemia can develop due to extracellular shifts of potassium, increased potassium ingestion, or impaired potassium elimination. Metabolic acidosis results in an extracellular shift of potassium, without changes in total body potassium. Correction of the underlying metabolic acidosis redistributes potassium into the intracellular space and corrects the hyperkalemia. Hyperinsulinemia is most likely to result in hypokalemia. Pregnancy and respiratory failure alone are not causes of hyperkalemia.

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.

31
Q

A patient with hypokalemia should be assessed for what electrolyte disorder?

1: Hyperglycemia
2: Hyponatremia
3: Hyperphosphatemia
4: Hypomagnesemia

A

4: Hypomagnesemia

Magnesium is important in the regulation of intracellular potassium. Hypomagnesemia may result in refractory hypokalemia, likely due to accelerated renal potassium loss or impairment of sodium-potassium pump activity. When hypokalemia and hypomagnesemia coexist, magnesium deficiency should be corrected to facilitate the correction of hypokalemia.

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.

32
Q

Failure to remove manganese from PN in a patient with hepatobiliary disease results in accumulation of manganese in the

1: brain.
2: liver.
3: kidney.
4: red blood cells.

A

1: brain.

Manganese toxicity associated with PN has been reported, most notably in long-term home PN patients with hepatobiliary disease. Hypermanganesemia may lead to manganese deposition in the basal ganglia and neurologic symptoms. Manganese contamination of PN additives has been identified as a factor contributing to hypermanganesemia. It may, therefore, be necessary to eliminate the use of multiple trace-element products that contain added manganese in long-term home PN patients with hypermanganesemia and instead use single-entity trace element solutions.

References:

Kumpf VJ, Mirtallo JM, Peterson C. Parenteral nutrition formulations: preparation and ordering. In: Merritt R, ed. The A.S.P.E.N. Nutrition Support Practice Manual. 2nd ed. Silver Spring, MD: A.S.P.E.N.; 2005:97-107.

33
Q

A critically ill 75-year-old male receiving PN has the following arterial blood gas (ABG) results: pH=7.32, PaCO2=49 mm Hg, and serum bicarbonate=29 mEq/L. What is the most appropriate PN intervention?

1: Do nothing
2: Decrease calorie content of PN
3: Decrease acetate concentration
4: Decrease chloride concentration

A

2: Decrease calorie content of PN

This patient is experiencing an respiratory acidosis as evidenced by a decrease in pH (7.35-7.45), an elevated PaCO2 (35-45 mm Hg), and a normal serum bicarbonate (23-30 mEq/L). The most appropriate nutritional intervention is to decrease the total calorie content of the PN regimen. Overfeeding should be avoided as excessive calorie supplementation can lead to hypercapnia due to excessive carbon dioxide production relative to oxygen consumption.

References:

Langley G, Canada T, Day L. Acid-base disorders and nutrition support treatment. NCP. 2003;18:259-261.

34
Q

Acetate is added to PN formulas when a patient experiences

1: metabolic acidosis.
2: metabolic alkalosis.
3: respiratory acidosis.
4: respiratory alkalosis.

A

1: metabolic acidosis.

The bicarbonate ion cannot be added to PN because of physical incompatibilities. Bicarbonate precursors such as acetate, citrate, gluconate, and lactate can be used for the treatment or prevention of metabolic acidosis. In PN, acetate is most widely used. The conversion of these precursors is mainly a hepatic function.

References:

Langley G, Canada T, Day L. Acid-base disorders and nutrition support treatment. NCP. 2003;18:259-261.

35
Q

Use of nutrition support teams with patients receiving PN has been shown to DECREASE

1: morbidity due to hyperglycemia.
2: morbidity due to hypophosphatemia.
3: mortality due to metabolic complications.
4: length of stay in the intensive care unit.

A

3: mortality due to metabolic complications.

The management of PN by nutrition support teams has shown to have many benefits including avoidance of metabolic complications. A reduced incidence of abnormal laboratory indices also is seen. The major benefit realized by the utilization of a nutrition support service is the decrease in the number of deaths due to metabolic complications in patients receiving PN.

References:

Dodds ES, Murray JD, Trexler KM, et al. Metabolic occurrences in total parenteral nutrition patients managed by a nutrition support team. NCP. 2001;18:78-84.

36
Q

The most accurate method of diagnosing PN-associated metabolic bone disease is to measure

1: bone density.
2: serum calcium concentrations.
3: serum phosphate concentrations.
4: serum parathyroid hormone concentrations.

A

1: bone density.

It is unclear how often PN-associated metabolic bone disease occurs. It is often asymptomatic and occurs in the face of normal biochemical parameters. The risk for metabolic bone disease is greatest for patients receiving long-term PN and corticosteroid therapy. Fortunately, bone density can be assessed accurately and metabolic bone disease can be diagnosed early so that appropriate treatment can be instituted.

References:

Ferrone M, Geraci M. A review of the relationship between parenteral nutrition and metabolic bone disease. NCP. 2007;22(3):329-339

37
Q

Which one of the following co-morbidities is NOT a risk factor for the development of metabolic bone disease?

1: Crohn’s disease
2: Malignancy
3: Short bowel syndrome
4: Hypothyroidism

A

4: Hypothyroidism

Nearly every condition requiring long-term PN can predispose a patient to metabolic bone disease (MBD.) Patients with Crohn’s diesase are at risk for MBD if they have malabsorption of calcium and vitamin D or use corticosteroids to control their disease. Patients with cancer may have decreased food intake and altered calcium and vitamin D metabolism associated with surgery or chemoradiation. MBD may also develop in cancer patients as a result of therapy-induced amenorrhea or the elaboration of cytokines or PTH-like peptides. There is also evidence that renal wasting of calcium may occur in individuals with short bowel syndrome. Hyperthyroidism (not hypothyroidism) is a secondary cause of osteoporosis.

References:

Ferrone M, Geraci M. A review of the relationship between parenteral nutrition and metabolic bone disease. NCP. 2007;22(3):329-339

38
Q

A rise in which of the following laboratory values would most likely indicate cholestasis?

1: Prothrombin time
2: Asparate aminotransferase/Alanine aminotransferase ratio
3: Cholesterol and gamma glutamyltransferase
4: Alkaline phosphatase and total bilirubin

A

4: Alkaline phosphatase and total bilirubin

Elevations of alkaline phosphatase and total bilirubin most likely represent cholestasis or biliary obstruction. Prothrombin time is an important marker of synthetic function, but is not specific for cholestasis. Abnormalities in aminotransferases are indicative of hepatocellular injury. Gamma glutamyltransferase is elevated in cholestatic conditions, however cholesterol is not a marker of cholestasis.

References:

AGA Technical Review on the Evaluation of Liver Chemistry Tests. Gastroenterology. 2002;123:1367-1384.

39
Q

During long-term PN administration, hepatobiliary complications can best be prevented by

1: adding carnitine to the PN formula.
2: discontinuing IV fat emulsion (IVFE).
3: converting to cyclic administration.
4: administering IVFE twice weekly.

A

3: converting to cyclic administration.

Hepatic dysfunction can result from long-term administration of PN. Conversion to cyclic administration allows the body to oxidize fat while ensuring adequate caloric intake by not overfeeding and relieves hepatic steatosis. In addition, initiation of enteral feeding stimulates bile flow and may protect against gut bacterial translocation.

References:

Kumpf VJ. Parenteral Nutrition-Associated Liver Disease in Adult and Pediatric Patients. NCP. 2006;21:279-290.

40
Q

Inability to aspirate blood through a central vascular catheter when there is no obstruction to the infusion of fluid suggests

1: pinch-off syndrome.
2: intraluminal thrombus.
3: calcium precipitate occlusion.
4: fibrin sleeve formation at the catheter tip.

A

4: fibrin sleeve formation at the catheter tip.

The primary symptom suggesting a catheter-related thrombus is a loss of catheter patency. Fibrin sheath formation at the distal catheter tip often presents as a withdrawal occlusion. Catheters remain functional for infusion; however, blood cannot be aspirated from the lumen. Physiologically, the fibrin acts as a one-way valve. The negative pressure used to aspirate blood causes the fibrin to be pulled over the catheter tip and prevent blood aspiration. Pinch-off syndrome occurs when the catheter is being compressed between the first rib and the clavicle, causing intermittent compression and pinching, leading to intermittent occlusion of infusion and aspiration.

References:

Vanek VW. The ins and outs of venous access: Part II. NCP. 2002;17:142-155.

41
Q

After placement of a central line, discovery of a pneumothorax during PN administration should be viewed as a

1: sentinel event.
2: process indicator.
3: resource indicator.
4: structural indicator.

A

1: sentinel event.

A sentinel event is an unexpected occurrence involving death or serious physical or psychological injury, or the risk thereof. Serious injury specifically includes loss of limb or function. Such events are called “sentinel” because they signal the need for immediate investigation and response. The Joint Commission’s sentinel event policy is designed to help organizations identify sentinel events and take action to prevent their recurrence. Examples include medication errors, wrong site surgery, restraint-related deaths, blood transfusion errors, and operative or postoperative complications.

References:

Winkler MF, Hedberg A. Quality and performance improvement. In: Matarese LE, Gottschlich MM, eds.Contemporary Nutrition Support Practice: A Clinical Guide. 2nd Ed. Philadelphia: Saunders; 2003;616-624.

42
Q

All of the following are examples of nonthrombotic catheter occlusions EXCEPT

1: catheter migration during use.
2: lipid deposits.
3: calcium-phosphate precipitate.
4: fibrin sheath.

A

4: fibrin sheath.

Nonthrombotic catheter occlusions can result from mechanical obstructions, drug or mineral precipitates, or lipid deposits. Mechanical obstruction may reflect catheter migration or malpositioning that occurs during insertion or use. Precipitates that form due to drug crystallization, drug-drug incompatibilities, or drug-solution incompatibilities can produce catheter occlusion. A fibrin sheath, or fibrin sleeve, is a thrombotic catheter occlusion and develops when fibrin adheres to the external surfaces of the catheter.

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.

43
Q

What are the major symptoms of acute thrombosis due to central venous catheterization?

1: Pain and difficulty breathing
2: Pain and swelling in the arm and neck
3: Fever and inability to aspirate blood from the catheter
4: Pain while attempting to infuse fluids through the catheter

A

2: Pain and swelling in the arm and neck

Due to insufficient venous return, pain and swelling of the ipsilateral arm and neck are hallmark symptoms of acute venous thrombosis caused by a central venous catheter. Fever and problems with catheter patency may occur in patients with thrombosis but these symptoms are more reflective of other problems such as infection or catheter occlusion. Acute onset of pain and difficulty breathing are hallmark symptoms of a pneumothorax.

References:

Grant J. Recognition, prevention, and treatment of home total parenteral nutrition central venous access complications. JPEN. 2002;26:S21-S28.

44
Q

The most effective strategy to DECREASE the risk of catheter-associated sepsis is use of

1: povidone-iodine as a skin preparation.
2: antibiotic ointment at catheter exit site.
3: antibiotic prophylaxis during catheter insertion.
4: full-barrier precautions during catheter insertion.

A

4: full-barrier precautions during catheter insertion.

Several strategies have been investigated to decrease the risk of catheter-associated sepsis. Use of full-barrier precautions during catheter insertion (mask, cap, sterile gloves, long-sleeve gowns, and sheet drapes) reduces the incidence of catheter-related infections compared with the use of only sterile gloves and drapes alone. Skin preparation with chlorhexidine results in lower incidence of microbial colonization than povidone-iodine. Prophylactic use of antibiotic ointment at the catheter exit site encourages the development of resistant flora and should be avoided. Antibiotic prophylaxis during catheter insertion has not been demonstrated to reduce the incidence of catheter-associated sepsis.

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.

45
Q

Which of the following is an evidence-based intervention for reducing the risk of central venous catheter-related infections?

1: Administering antibiotics prior to catheter insertion
2: Using minimal barrier technique during catheter insertion
3: Cleansing insertion sites with 2% alcohol preparation
4: Training nurses who maintain central venous catheters

A

4: Training nurses who maintain central venous catheters

According to the Centers for Disease Control and Prevention, research supports the following recommendations as primary interventions for reducing risks of central venous catheter-related infections: (1) using maximal barrier technique during catheter insertion, (2) cleansing insertion sites with 2% chlorhexidine preparation, and (3) education and training of health care personnel. Administering antibiotics prior to inserting central venous catheters has not been shown to be effective in reducing the rates of central venous catheter-related infections.

References:

Centers for Disease Control and Prevention. Guidelines for the prevention of intravascular catheter-related infections. Morbidity and Mortality Weekly Report. 2002;August 9;51:RR-10:1-29.

46
Q

A patient receiving PN that has chills, fever, positive blood cultures, and no redness or purulence at the catheter exit site probably has which of the following types of catheter infection?

1: Tunnel
2: Exit site
3: Catheter-related phlebitis
4: Catheter-related bloodstream

A

4: Catheter-related bloodstream

Catheter-related infections have been defined to allow for more accurate identification of the type of infection. A catheter-related bloodstream infection includes bacteremia/fungemia in a patient with an intravascular device with at least one positive blood culture, clinical manifestations of infection such as fever, and no apparent source except the catheter. Catheter-related blood stream infections often present without redness or purulence at the catheter site.

References:

Centers for Disease Control and Prevention. Guidelines for the prevention of intravascular catheter-related infections. Morbidity and Mortality Weekly Report. 2002;August 9;51:RR-10:1-29.

47
Q

If a ventilated patient with a history of chronic renal insufficiency is receiving PN that provides 40 kcal/kg, 2 g/kg protein, 5 mg/kg/min of dextrose, and 1.5 g/kg fat, which of the following is most likely to occur?

1: Negative nitrogen balance along with a decline in prealbumin levels
2: Increased urine output, decreased specific gravity, and change in urine pH
3: Improvement in hepatic protein stores, weight gain, and improved immune function
4: Hypercapnia, elevated liver function studies, and alterations in BUN/creatinine values

A

4: Hypercapnia, elevated liver function studies, and alterations in BUN/creatinine values

Overfeeding can contribute to adverse consequences, especially in mechanically ventilated patients. Providing calories in excess of 25-35 kcal/kg body weight has been associated with hypercapnia, lipogenesis, hyperglycemia, electrolyte abnormalities, and impaired phagocytosis.

References:

Fuhrman MP. Complication management in parenteral nutrition. In: Matarese LE, Gottschlich MM, eds. Contemporary Nutrition Support Practice: A Clinical Guide. 2nd Ed. Philadelphia: Saunders; 2003:242-262.

48
Q

A patient presents to clinic with a suspected catheter occlusion. All of the following are appropriate initial actions EXCEPT to

1: determine if the occlusion is relieved with postural changes.
2: remove the dressing and check for kinks in the tubing.
3: replace the catheter over a guidewire.
4: review recent flushing techniques with the patient.

A

3: replace the catheter over a guidewire.

When a patient presents with a suspected catheter occlusion, a systematic approach should be taken to prevent unnecessary catheter removals and/or unnecessary instillations of compounds to relieve the catheter occlusion. Steps to insure this include: (1) obtain thorough history of signs/symptoms of catheter malfunction from the patient; (2) double-check catheter function for patency and blood aspiration; (3) check for mechanical causes of occlusions (clamps, kinked tubing, tight sutures, replace needle if implanted vascular access port) and assess if occlusion is related to postural changes (rolling of shoulder or raising or lowering of arm on the side of the catheter); (4) obtain thorough history of recent flushing techniques, medication infusions, and blood aspiration; and (5) assess for physical signs of edema, redness, pain, or dilated vessels. From these steps, a clinician can determine if further diagnostic tests are needed, the catheter requires removal, or if compounds should be instilled to clear a clot or precipitate within the catheter.

References:

Krzywda EA. Predisposing factors, prevention, and management of central venous catheter occlusions. J of IV Nursing. 1999;22(6Suppl):S11-S17.

49
Q

A 60-year-old female (45 kg) is receiving PN for a rectovaginal fistula. The PN formula consists of the following components: 700 mL Dextrose 70%, 600 mL Aminosyn II® 15%, and 125 mL of 20% IV Fat Emulsion. Which one of the following complications is she at greatest risk for developing? (24-hour continuous PN infusion; Total PN Volume with electrolytes and additives is 1.5 L)

1: Hypertriglyceridemia
2: Azotemia
3: Hyperglycemia
4: Pulmonary edema

A

3: Hyperglycemia

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. Hyperglycemia from dextrose is the most likely complication this patient will develop because she is receiving more than the recommended daily amount of carbohydrate (10.9 g/kg/day of carbohydrates). The other components in this PN formula are within recommended ranges.

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.

50
Q

Discontinuation of IVFE is recommended treatment of catheter-related bloodstream infection due to

1: coagulase-negative staphylocci.
2: staphylococcus aureus.
3: pseudomonas aeruginosa.
4: malassezia furfur.

A

4: malassezia furfur.

Malassezia furfur is classically associated with superficial infections of the skin and associated structures. Recently, however, this yeast has been reported as a cause of catheter-related blood stream infections. This occurs most commonly in premature infants and patients receiving PN containing IVFE. The IVFE presumably provides growth factors required for replication of the organism. Appropriate treatment of patients requires administration of amphotericin B, discontinuation of IVFE, and removal of the intravascular catheter, especially with nontunneled catheter infections.

References:

Mermel LA, Farr BM, Sherertz RJ, et al. Guidelines for the management of intravascular catheter-related infections. Clin Infect Dis. 2001;32(9):1249-1272.