1Baptist Health College Little Rock
School of Nursing
NSG 2207 ADULT NURSING III Grade
A+
PHYSIOLOGIC INTEGRITY AND THERAPEUTIC NURSING INTERVENTIONS
FOR PATIENTS WITH ALTERED RENAL FUNCTION
2017
CASE STUDY - ACUTE RENAL FAILURE
Mr. Jones is admitted to a critical care unit because he has not been feeling well. He started a round of
antibiotics 3 days ago and has been taking naproxen sodium for a sprained back. Yesterday, he noticed that his urine
was really dark and he didn’t have very much urine whenever he urinated. This morning, he did not have but a
small amount of dark urine when he went to the bathroom upon arising. His symptoms in the emergency room
included a blood pressure of 175/51, pulse 100, respirations 30 and temperature 98.6. He has faint, fine crackles in
his lower lobes on auscultation and his pulse oximeter is 95%. His lab work shows a creatinine of 2.1 and a BUN of
36. His serum potassium was 5.5, sodium was 135, and his carbon dioxide was 10. He states that he drank a lot of
coffee and water yesterday evening trying to increase his urine output and that he has never had to take anything for
his blood pressure. Because of the elevated potassium, he was admitted to critical care and 80 mg furosemide was
ordered stat with an IV of NS at KVO and a foley catheter connected to hourly urinary output. He was placed on a
renal diet.
1. What do you think caused this man’s sudden renal failure?
Most likely this is acute kidney injury related to nephrotoxic effects of the naproxen and antibiotics.
2. Why was his blood pressure elevated?
Because the kidneys control fluid output, if his output is decreased then there is more fluid volume in the
intravascular space leading to elevated BP.
3. What was the rationale for the rapid respirations?
More than likely, he is experiencing metabolic acidosis. His respirations are increased to attempt to blow off the
CO2 and correct the acidosis.
4. What was the rationale for the faint crackles?
Fluid overload – may listen for an S3 heart sound/friction rub as well!
5. What are ALL the risk factors for AKI?
Impaired renal perfusion (hypotension/shock); nephrotoxins (abx, metals, poisons, anesthetics, contrast dye,
gasoline, NSAIDS, acetaminophen); rhabdomyolysis/crush injury; rejection of a transplanted kidney;
glomerulonephritis; vascular obstruction (renal artery stenosis); ureter/urethra blockage (stones, injury).
6. Are there any medications that could interact with contrast dye and increase the patient’s chance of
developing AKI? What are they?
Metformin! Diuretics, other nephrotoxic drugs (NSAIDS, aminoglycosides, etc).
Page of 8
, 7. Considering his lab values, why would he be sent to critical care and placed on a monitor?
His elevated potassium must be watched closely to ensure that no cardiac complications occur.
8. Explain the serum carbon dioxide level.
A serum CO2 level is roughly equal to an arterial bicarb level – therefore it is an indicator of how well the kidneys
are maintaining the acid-base buffer.
9. In what stage of renal failure is Mr. Jones? {I assumed she meant AKI}
Oliguric-anuric phase
10. What are the symptoms of EACH of the 4 phases of renal failure?
Onset phase – the period from the precipitating event to development of renal manifestations
Oliguric-anuric/nonoliguric phase – lasts 1-8 weeks; may require dialysis; FVE; increased BUN/Cr; electrolyte
imbalance; metabolic acidosis.
Diuretic phase – gradual/abrupt return of function; UOP 1-2L/day (may cause dehydration)
Recovery phase – 3-12months; returns to pre-renal failure kidney function; mild tubular abnormalities may continue
11. If Mr. Jones kidneys respond to the furosemide and he diuresis, what would be his primary nursing
diagnosis?
■ Risk for fluid volume deficit
12. What electrocardiographic changes will the nurse watch for that are associated with elevated potassium
levels?
Peaked T waves; widened QRS
Mr. Jones’ urinary output remained extremely low and his BUN and creatinine continue to rise. Although Mr. Jones’
monitor shows a NSR, his potassium continues to rise and is now 6.5. The doctor now orders sodium polystyrene
sulfonate to be administered with sorbitol per enema.
13. What is the purpose for giving the sodium polystyrene sulfonate? Also, how does this medication work?
This will hopefully decrease the potassium by releasing it in the stool; it exchanges sodium ions for potassium ions
in the intestine.
14. What does elevated potassium cause the heart to do?
Elevated K disrupts the electrical impulses of the heart leading to bradycardia and reduced contractility – if it gets
high enough, asystole can occur.
In spite of furosemide and a change in antibiotics and no NSAID medications, Mr. Jones stays in acute renal failure
- in fact, his potassium is maintained at about 6 only with sodium polystyrene sulfonate, and his BUN is 90 and his
creatinine is 4.5 - and he begins to develop signs of fluid overload and has mental status changes. The decision is
made to start Mr. Jones on hemodialysis and a Quentin catheter is placed in the patient’s right internal jugular vein.
15. What life-saving assessment is mandatory for patients with fluid overload?
Auscultation of the lungs to assure no pulmonary edema is present.
Page of 8
School of Nursing
NSG 2207 ADULT NURSING III Grade
A+
PHYSIOLOGIC INTEGRITY AND THERAPEUTIC NURSING INTERVENTIONS
FOR PATIENTS WITH ALTERED RENAL FUNCTION
2017
CASE STUDY - ACUTE RENAL FAILURE
Mr. Jones is admitted to a critical care unit because he has not been feeling well. He started a round of
antibiotics 3 days ago and has been taking naproxen sodium for a sprained back. Yesterday, he noticed that his urine
was really dark and he didn’t have very much urine whenever he urinated. This morning, he did not have but a
small amount of dark urine when he went to the bathroom upon arising. His symptoms in the emergency room
included a blood pressure of 175/51, pulse 100, respirations 30 and temperature 98.6. He has faint, fine crackles in
his lower lobes on auscultation and his pulse oximeter is 95%. His lab work shows a creatinine of 2.1 and a BUN of
36. His serum potassium was 5.5, sodium was 135, and his carbon dioxide was 10. He states that he drank a lot of
coffee and water yesterday evening trying to increase his urine output and that he has never had to take anything for
his blood pressure. Because of the elevated potassium, he was admitted to critical care and 80 mg furosemide was
ordered stat with an IV of NS at KVO and a foley catheter connected to hourly urinary output. He was placed on a
renal diet.
1. What do you think caused this man’s sudden renal failure?
Most likely this is acute kidney injury related to nephrotoxic effects of the naproxen and antibiotics.
2. Why was his blood pressure elevated?
Because the kidneys control fluid output, if his output is decreased then there is more fluid volume in the
intravascular space leading to elevated BP.
3. What was the rationale for the rapid respirations?
More than likely, he is experiencing metabolic acidosis. His respirations are increased to attempt to blow off the
CO2 and correct the acidosis.
4. What was the rationale for the faint crackles?
Fluid overload – may listen for an S3 heart sound/friction rub as well!
5. What are ALL the risk factors for AKI?
Impaired renal perfusion (hypotension/shock); nephrotoxins (abx, metals, poisons, anesthetics, contrast dye,
gasoline, NSAIDS, acetaminophen); rhabdomyolysis/crush injury; rejection of a transplanted kidney;
glomerulonephritis; vascular obstruction (renal artery stenosis); ureter/urethra blockage (stones, injury).
6. Are there any medications that could interact with contrast dye and increase the patient’s chance of
developing AKI? What are they?
Metformin! Diuretics, other nephrotoxic drugs (NSAIDS, aminoglycosides, etc).
Page of 8
, 7. Considering his lab values, why would he be sent to critical care and placed on a monitor?
His elevated potassium must be watched closely to ensure that no cardiac complications occur.
8. Explain the serum carbon dioxide level.
A serum CO2 level is roughly equal to an arterial bicarb level – therefore it is an indicator of how well the kidneys
are maintaining the acid-base buffer.
9. In what stage of renal failure is Mr. Jones? {I assumed she meant AKI}
Oliguric-anuric phase
10. What are the symptoms of EACH of the 4 phases of renal failure?
Onset phase – the period from the precipitating event to development of renal manifestations
Oliguric-anuric/nonoliguric phase – lasts 1-8 weeks; may require dialysis; FVE; increased BUN/Cr; electrolyte
imbalance; metabolic acidosis.
Diuretic phase – gradual/abrupt return of function; UOP 1-2L/day (may cause dehydration)
Recovery phase – 3-12months; returns to pre-renal failure kidney function; mild tubular abnormalities may continue
11. If Mr. Jones kidneys respond to the furosemide and he diuresis, what would be his primary nursing
diagnosis?
■ Risk for fluid volume deficit
12. What electrocardiographic changes will the nurse watch for that are associated with elevated potassium
levels?
Peaked T waves; widened QRS
Mr. Jones’ urinary output remained extremely low and his BUN and creatinine continue to rise. Although Mr. Jones’
monitor shows a NSR, his potassium continues to rise and is now 6.5. The doctor now orders sodium polystyrene
sulfonate to be administered with sorbitol per enema.
13. What is the purpose for giving the sodium polystyrene sulfonate? Also, how does this medication work?
This will hopefully decrease the potassium by releasing it in the stool; it exchanges sodium ions for potassium ions
in the intestine.
14. What does elevated potassium cause the heart to do?
Elevated K disrupts the electrical impulses of the heart leading to bradycardia and reduced contractility – if it gets
high enough, asystole can occur.
In spite of furosemide and a change in antibiotics and no NSAID medications, Mr. Jones stays in acute renal failure
- in fact, his potassium is maintained at about 6 only with sodium polystyrene sulfonate, and his BUN is 90 and his
creatinine is 4.5 - and he begins to develop signs of fluid overload and has mental status changes. The decision is
made to start Mr. Jones on hemodialysis and a Quentin catheter is placed in the patient’s right internal jugular vein.
15. What life-saving assessment is mandatory for patients with fluid overload?
Auscultation of the lungs to assure no pulmonary edema is present.
Page of 8
