Patients in renal failure have the potential to develop comorbid conditions. Identify five potential problems, determine how you would assess the problem, then delineate nursing interventions and patient education strategies for each.

Question

What will be an ideal response?

Answer 1

1, Problem: Cardiac dysrhythmias as a result of electrolyte disturbance
Assessment: Monitor serum potassium levels for hyperkalemia. Assess for subjective weakness
in legs, obtain a recent dietary history, and determine whether K.B. is adhering to the dialysis
regimen.
Intervention(s): Refer to a renal RD for medical nutrition therapy regarding potassium content
of foods. Notify physician of any abnormal findings (abnormal laboratory findings, leg
weakness); get ECG if K.B. reports any palpitations or you detect irregular heart rate; initiate
emergency measures as needed. Monitor weight over time—this is done at the dialysis center
with every visit to the dialysis treatment center, both before and after the treatment.
Patient education: Review potassium intake, high-potassium foods, and signs and symptoms and
consequences of hyperkalemia. Again, refer to renal RD.
2, Problem: Hypertension
Assessment: Monitor BP over time, review antihypertensive medications, and ask K.B. whether
she is taking the medications. Monitor weight over time.
Intervention(s): Document target BP. Encourage K.B. to adhere to fluid restrictions and take
medications as prescribed. Consult physician if BP is above stated goals.
Patient education: Teach and reinforce daily BP monitoring, signs and symptoms of fluid
overload, and consequences of uncontrolled HTN. Review medication (indications for, use,
side effects). Review the importance of following fluid restrictions as part of managing HTN.
3, Problem: Anemia
Assessment: Monitor Hct and Hgb levels; low Hgb might cause shortness of breath and fatigue.
Assess effectiveness of erythropoietin-stimulating medications by monitoring Hgb levels
over time. Assess for bleeding. Monitor vitamin B12 and folic acid levels; both B vitamins are
necessary for the synthesis of DNA. Monitor ferritin, transferrin saturation, iron, and total
iron binding capacity levels. Iron is an important component of the RBC and is needed for the
erythropoietin to work.
Intervention(s): Check dialysis record to see that erythropoietin-stimulating medications
were ordered and administered as ordered. Administer vitamin B12, folic acid, and iron as
prescribed. If albumin is low, refer to renal RD for medical nutrition therapy. If dietary protein
is increased, phosphate binders might need to be increased or the dialysis prescription
changed. Albumin can be low because of anemia or overhydration. The renal RD will know
how to interpret the laboratory data and make appropriate dietary interventions.
Patient education: Discuss special instructions, purpose, dose, schedule, and side effects of folic
acid, vitamin B12, and oral or parenteral iron preparations.
4, Problem: Inadequate iron level
Assessment: Monitor iron, TIBC, and ferritin and transferrin saturation levels. Iron is absorbed from
the diet and is bound to transferrin in the blood; normal transferrin saturation is 20% to 50%.
Adequate ferritin, the iron storage protein in the body, is necessary for the erythropoietin
stimulating proteins, such as epoetin alfa, to work. Iron deficiency anemia is characterized by a
decreased serum iron level, elevated TIBC, and decreased transferrin saturation.
Intervention(s): Report low iron, elevated TIBC, serum ferritin less than 100 ng/mL, and transferrin
saturation less than 20%. Administer iron preparations as ordered.
Patient education: Teach side effects of iron preparations.
5, Problem: Calcium–phosphorus–vitamin D–parathyroid hormone (PTH) imbalance
Phosphorus, alcium, vitamin D, and PTH all play a part in controlling serum phosphorus levels
and bone health. The kidney synthesizes vitamin D into calcitriol, which helps increase calcium
absorption from the GI tract. When serum calcium is low, serum phosphorus is elevated, thereby
causing the PTH to increase and calcium to be pulled from the bone into the blood. Too much PTH
causes bones to become weak and fracture more easily (renal osteodystrophy).
Assessment
• Monitor serum calcium levels; observe for signs and symptoms of elevated calcium (joint pain)
or decreased serum calcium (muscle twitching, muscle cramps, bone fractures, joint pain).
• Monitor serum phosphorus levels; observe for signs and symptoms of elevated serum
phosphorus (itching and elevated PTH). High phosphorus levels pull calcium out of the bones.
Elevated PTH level causes bone disease.
Intervention(s)
• Report abnormal calcium and phosphorus levels. Take phosphate binders with meals and
snacks to minimize phosphorus absorption. phosphate binders must be taken with food to be
effective; they will not be as effective if taken 30 minutes after meals. Calcium carbonate can
be used as a phosphate binder; do not give with iron supplements.
• If vitamin D is required, give the analogue form—calcitriol (Rocaltrol). Get a nutrition
consultation.
Patient education: Stress the importance of taking phosphate binders as ordered and complying
with dietary restrictions. Teach patients that calcium can be taken with calcium channel
blockers. Calcium channel blockers do not block the absorption or uptake of calcium.
6, Problem: Seizures
Assessment: Document any history of seizures or seizure-like activity. Record current and past
anticonvulsant therapies. Monitor BP over time, as well as Hgb levels and rate of Hgb change.
Intervention(s): Notify physician of history of seizures, current uncontrolled HTN, and any
precipitous increase or decrease in Hgb levels.
Patient education: Teach the patient about importance of controlling BP and complying with
antihypertensive and anticonvulsant meds. Consult physician about erythrocyte stimulating
agents dose when there is a sudden change in Hgb level.