URINARY DISORDERS

Benign Prostatic Hypertrophy (Hyperplasia)

A. Description

1. Benign prostatic hypertrophy (benign prostatic hyperplasia; BPH) is a slow enlargement of the
prostate gland, with hypertrophy and hyperplasia of normal tissue.

2. Enlargement compresses the urethra, resulting in partial or complete obstruction.

3. Usually occurs in men older than 50 years

B. Assessment

1. Diminished size and force of urinary stream (early sign of BPH)

2. Urinary urgency and frequency
3. Nocturia
4. Inability to start (hesitancy) or continue a urinary stream
5. Feelings of incomplete bladder emptying
6. Postvoid dribbling from overflow incontinence (later sign)
7. Urinary retention and bladder distention
8. Hematuria
9. Urinary stasis and UTIs
10. Dysuria and bladder pain
C. Interventions
1. Encourage fluid intake of up to 2000 to 3000 mL/day unless contraindicated.
2. Prepare for urinary catheterization to drain the bladder and prevent distention.
3. Avoid administering medications that cause urinary retention, such as anticholinergics,
antihistamines, decongestants, and antidepressants.
4. Administer medications as prescribed to shrink the prostate gland and improve urine flow.
5. Administer medications as prescribed to relax prostatic smooth muscle and improve
urine flow.
6. Instruct the client to decrease intake of caffeine and artificial sweeteners and limit spicy or
acidic foods.
7. Instruct the client to follow a timed voiding schedule.
8. Prepare the client for surgery or invasive procedures as prescribed (Figs. 58-7 and 58-8).1
Acute Kidney Injury
A. Description
1. Acute kidney injury (AKI) is the rapid loss of kidney function from renal cell damage.
2. Occurs abruptly and can be reversible
3. AKI leads to cell hypoperfusion, cell death, and decompensation of renal function.
4. The prognosis depends on the cause and the condition of the client.
5. Near-normal or normal kidney function may resume gradually.
B. Causes
1. Prerenal: Outside the kidney; caused by intravascular volume depletion such as
with blood loss associated with trauma or surgery, dehydration, decreased cardiac
output (as with cardiogenic shock), decreased peripheral vascular resistance,
decreased renovascular blood flow, and prerenal infection or obstruction.
2. Intrarenal: Within the parenchyma of the kidney; caused by tubular necrosis,
prolonged prerenal ischemia, intrarenal infection or obstruction, and nephrotoxicity
3. Postrenal: Between the kidney and urethral meatus, such as bladder neck
obstruction, bladder cancer, calculi, and postrenal infection
C. Phases of AKI and interventions
1. Onset: Begins with precipitating event
2. Oliguric phase
a. For some clients, oliguria does not occur and the urine output is normal;
otherwise, the duration of oliguria is 8 to 15 days; the longer the duration, the less
chance of recovery.
b. Sudden decrease in urine output; urine output is less than 400 mL/day.
c. Signs of excess fluid volume: Hypertension, edema, pleural and pericardial
effusions, dysrhythmias, heart failure, and pulmonary edema
d. Signs of uremia: Anorexia, nausea, vomiting, and pruritus
e. Signs of metabolic acidosis: Kussmaul’s respirations
f. Signs of neurological changes: Tingling of extremities,drowsiness
progressing to disorientation, and then coma
g. Signs of pericarditis: Friction rub, chest pain with inspiration, and low-grade fever
h . Laboratory analysis
i. With early recognition or potential for AKI, client may be treated with fluid challenges
(IV boluses of 500 to 1000 mL over 1 hour).
j. Restrict fluid intake; if hypertension is present, daily fluid allowances may be 400 to
1000 mL plus the measured urinary output.
k. Administer medications, such as diuretics, as prescribed to increase renal blood flow and
diuresis of retained fluid and electrolytes.3
3. Diuretic phase
a. Urine output rises slowly, followed by diuresis (4 to 5 L/day).
b. Excessive urine output indicates that damaged nephrons are recovering their ability to3
excrete wastes.
c. Dehydration, hypovolemia, hypotension, and tachycardia can occur.
d. Level of consciousness improves.
e. Laboratory analysis (see Box 58-4)
f. Administer IVfluids as prescribed, which may contain electrolytes to replace losses.
4. Recovery phase (convalescent)
a. Recovery is a slow process; complete recovery may take 1 to 2 years.
b. Urine volume returns to normal.
c. Memory improves.
d. Strength increases.
e. The older adult is less likely than a younger adult to regain full kidney function.3

Acute Kidney Injury:

Phases and Laboratory Findings
Onset
▪ Begins with precipitating event
Oliguric Phase
▪ Elevated blood urea nitrogen (BUN) and serum creatinine levels
▪ Decreased urine specific gravity (prerenal causes) or normal (intrarenal causes)
▪ Decreased glomerular filtration rate (GFR) and creatinine clearance
▪ Hyperkalemia
▪ Normal or decreased serum sodium level
▪ Hypervolemia
▪ Hypocalcemia
▪ Hyperphosphatemia

Diuretic Phase
▪ Gradual decline in BUN and serum creatinine levels, but still elevated
▪ Continued low creatinine clearance with improving GFR
▪ Hypokalemia
▪ Hyponatremia
▪ Hypovolemia
Recovery Phase (Convalescent)
▪ Increased GFR
▪ Stabilization or continual decline in BUN and serum creatinine levels toward normal
▪ Complete recovery (may take 1 to 2 years)4

Pointers: The signs and symptoms of AKI are primarily caused by

the retention of nitrogenous wastes, the retention of fluids, and the inability of the
kidneys to regulate electrolytes.

Other interventions
1. Monitor vital signs, especially for signs of hypertension, tachycardia, tachypnea, and an
irregular heart rate.
2. Monitor urine and intake and output hourly and urine color and characteristics.
3. Monitor daily weight (same scale, same clothes, same time of day), noting that an increase of
½ to 1 lb/day (0.25 to 0.5 kg/day) indicates fluid retention.
4. Monitor for changes in the BUN, serum creatinine, and serum electrolyte levels.
5. Monitor for acidosis (may need to be treated with sodium bicarbonate).
6. Monitor urinalysis for protein level, hematuria, casts, and specific gravity.
7. Monitor for altered level of consciousness caused by uremia.
8. Monitor for signs of infection because the client may not exhibit an elevated
temperature or anincreased WBC count.
9. Monitor the lungs for wheezes and rhonchi and monitor for edema, which
can indicate fluid overload.
10. Administer the prescribed diet, which is usually a low- to moderate-protein
(to decrease the workload on the kidneys) and highcarbohydrate diet; ill
clients may require nutritional support with supplements, enteral feedings,
or parenteral nutrition.

11. Restrict potassium and sodium intake as prescribed based on the electrolyte level.
12. Administer medications as prescribed; be alert to the mechanism for metabolism
and excretion of all prescribed medications.
13. Be alert to nephrotoxic medications, which may be prescribed
14. Be alert to the HCP’s adjustment of medication dosages for kidney injury.
15. Prepare the client for dialysis if prescribed; continuous renal replacement therapy
may be used in AKI to treat fluid volume overload or rapidly developing azotemia and
metabolic acidosis.
16. Provide emotional support by allowing opportunities for the client to express concerns
and fears and by encouraging family interactions.
17. Promote consistency in caregivers.

Also refer to Section IV, Ein this chapter (Special

problems in kidney disease and interventions).

IV. Chronic Kidney Disease (CKD)

A. Description

1. CKD is a slow, progressive, irreversible loss in

kidney function, with a GFR less than or equal

to 60 mL/minute for 3 months or longer.

2. It occurs in stages (with loss of 75% of functioning nephrons, the client becomes symptomatic)
and eventually results in uremia or end-stage kidney disease (with loss of 90% to 95% of functioning
nephrons) (Table 58-2).

3. Hypervolemia can occur because of the kidneys’

inability to excrete sodium and water; hypovolemia can occur because of the kidneys’inability to

conserve sodium and water.

CKD affects all major bodysystems and mayrequire

dialysis or kidney transplantation to maintain life.

B. Primary causes

1. May follow AKI

2. Diabetes mellitus and other metabolic disorders6

3. Hypertension6
4. Chronic urinary obstruction

5. Recurrent infections

6. Renal artery occlusion

7. Autoimmune disorders

C. Assessment

1. Assess body systems for the manifestations of

CKD (Box 58-5).

2. Assess psychological changes, which could

include emotional lability, withdrawal, depression, anxiety, denial, dependence-independence

conflict, changes in body image, and suicidal

behavior.

D. Interventions

1. Same as the interventions for AKI.

2. Administer a prescribed diet, which is usually a

moderate-protein (to decrease the workload on

the kidneys) and high-carbohydrate, low-potassium, and low-phosphorus diet.

3. Provide oral care to prevent stomatitis and

reduce discomfort from mouth sores.

4. Provide skin care to prevent pruritus.

5. Teach the client about fluid and dietary restrictions and the importance of daily weights.

6. Provide support to promote acceptance of the

chronic illness and prepare the client for longterm dialysis and transplantation, or explain to

the client about his or her choice to decline dialysis or transplantation; with elderly clients, provide
information that kidney function is
declining and in time may reach end-stage renal

disease and require dialysis; encourage healthy

lifestyle and discuss choices.

E. Special problems in kidney disease and interventions

(Box 58-6)

1. Activity intolerance and insomnia

a. Fatigue results from anemia and the buildup

of wastes from the diseased kidneys.

b. Provide adequate rest periods.8