Care of with Altered Elimination c.

Dehydration, hypovolemia, hypotension

ACUTE RENAL FAILURE and tachycardia can occur.
4. Recovery Phase (Convalescent)
LEARNING OBJECTIVES: a. Recovery is a slow process; complete recover
At the end of the discussion, the learners will be able to: may take 1 to 2 years.
1. recall the anatomy and physiology of the renal and b. Urine volume returns to normal. Memory
urinary system. improves, strength increases
2. describe renal failure and its types. c. The older adult is less likely than a younger
3. identify the risk factors associated with the adult to regain full kidney function.
development of renal failure. d. AKI can progress to CKD
4. explain the etiology and pathophysiology of Renal
failure. 2. Chronic Kidney Disease / End-Stage Kidney Disease
5. relate the diagnostic findings to the clinical A. Description.
manifestations of a patient with altered elimination. 1. CKD is a slow, progressive, irreversible loss in
6. utilize the nursing process in formulating priority kidney function with a GFR less than or equal to 60
nursing diagnosis and interventions for a client with ml/min for 3 months or longer.
altered elimination. 2. Occurs in stage (with loss of 75% of functioning
7. identify appropriate medical and nursing interventions nephrons, the client becomes symptomatic) and eventually
to address clients’ needs and problems. results in uremia or End-stage Kidney disease (with loss of
8. recognize key concepts on renal replacement therapies; 90% to 95% functioning nephrons)
its types, indications, complications, and nursing 3. Hypervolemia can occur due to inability to excrete
considerations. sodium and water. Hypovolemia can occur because of
kidneys’ inability to conserve sodium and water.
I. DESCRIPTION 4. CKD affects all major body systems and may
1. Renal failure is an impairment of the kidney require dialysis or kidney transplantation to maintain life.
functions which leads to inability to excrete metabolic
waste products. B. Stages of CKD
2. Kidney failure may be diagnosed as Acute Kidney 1. At risk (Stage 1). Normal kidney function (early
Injury (AKI) or Chronic kidney disease. kidney disease may or may not be present). GFR >90
3. Acute kidney injury can result in chronic kidney mL/min.
disease without aggressive treatment or when 2. Mild CKD (Stage 2). GFR 60-89 ml/min.
complicating preexisting conditions exist. 3. Moderate CKD (Stage 3). GFR 30-59 ml/min.
4. Severe CKD (Stage 4). GFR 15-29 ml/min
II. TYPES OF RENAL FAILURE 5. ESRD (Stage 5). Kidney failure. little or no
1. Acute Kidney Injury / Acute Renal Failure glomerular filtration (less than 15 mL/min)
A. Description.
1. AKI/ARF is the rapid loss of kidney function from III. ETIOLOGY
renal cell damage. It is the abrupt decrease of renal A. Risk Factors in AKI
function with progressive retention of metabolic wastes 1. Acute renal failure is best understood when the
(Creatinine and Urea). condition is considered in terms of the location of
2. Clinical Manifestations occur abruptly with Acute damage to the renal system: prerenal, intrarenal, or
kidney injury. The prognosis depends on the cause and the postrenal causes of failure.
condition of the client. 2. Each type of ARF has different etiologies,
3. Near-normal or normal kidney function may pathophysiology, laboratory findings, and clinical
resume gradually. presentation

B. Phases of AKI B. Categories of Acute Kidney Injury

1. Onset 1. Prerenal
a. Begins with the precipitating event. Begins a. Hypoperfusion of kidney. Occurs in 60 to
with onset of event, ends when oliguria develops. 70%. Caused by intravascular volume depletion
b. Last for hours to days. b. occurs as a result of volume depletion and
2. Oliguric phase prolonged reduction of blood flow to the kidneys,
a. Sudden decrease in urine output, less than which leads to ischemia of the nephrons
400 ml/day. For some clients, oliguria does not occur c. Intravascular volume depletion such as with
and the urine output is normal. blood loss associated with trauma or surgery,
b. The duration of oliguria is 8 to 15 days; the dehydration, decreased cardiac output (as with
longer the duration, the less chance of recovery. cardiogenic shock), decreased peripheral vascular
c. There are signs of excess fluid volume, resistance, decreased renovascular blood flow, and
uremia, metabolic acidosis, neurological changes prerenal infection or obstruction
and pericarditis
3. Diuretic phase 2. Intrarenal
a. Urine output rises slowly, followed by diuresis a. Actual damage to kidney tissue. Result of
(4 to 5 L/day) actual parenchymal damage to the glomeruli or
b. Excessive urine output indicates that damage kidney tubules.
nephrons are recovering from their ability to excrete b. Occurs as a result of direct damage to the
wastes. Levels of consciousness improves. kidney from lack of oxygen(acute tubular necrosis)
 c. Causes IV. PATHOPHYSIOLOGY
i. Physical injury. trauma
ii. Hypoxic injury. renal artery or vein V. ASSESSMENT FINDINGS
stenosis or thrombosis A. Clinical Manifestations
iii. Chemical injury. acute nephrotoxins 1. Oliguria (< 400 mL/d) or anuria (< 100 mL/d)
(e.g. antibiotics, NSAIDs, contrast dye, heavy 2. Tachycardia
metal, blood transfusion reaction) 3. Hypotension (prerenal)
iv. Immunologic injury. infection, 4. Hypertension (intrarenal)
vasculitis, acute glomerulonephritis 5. Flat neck veins (prerenal)
6. Distended neck veins (intrarenal)
3. Postrenal 7. Dry mucous membranes
a. Obstruction to urine flow. Occurs as a result 8. Cool, clammy skin
of bilateral obstruction of structures leaving the 9. Lethargy
kidney 10. Deep, rapid respirations (Kusssmal’s respiration)
b. Obstructions between the kidney and urethral 11. Nausea and Vomiting
meatus, such as bladder neck obstruction, bladder 12. Confusion
cancer, calculi, and postrenal infection.
B. Laboratory Evaluation
1. Serum creatinine
a. gradually increases 1 to 2 mg/dL every 24 to 48 hr,
or 1 to 6 mg/dL in 1 week or less.
b. Gradual increase over months to years for CKD
exceeding 4 mg/dL. May be as high as 15 to 30 mg/dL
2. Blood urea nitrogen (BUN)
a. increase to 80 to 100 mg/dL within 1 week with
AKI.
b. Gradual increase with elevated serum creatinine
over months to years for CKD, high as 180 to 200 mg/dL
3. Serum electrolytes
a. Decreased sodium (dilutional) and calcium;
b. increased potassium, phosphorus, and magnesium.
4. CBC
a. Decreased hemoglobin and hematocrit from anemia
secondary to the loss of erythropoietin in CKD.
5. Urinalyis
a. Urine specific gravity greater than 1.000 to
1.010 in postrenal type (1.030 in prerenal type, 1.010
in intrarenal type)
b. In CKD: Hematuria, proteinuria, and decrease
in specific gravity
6. Urine culture and sensitivity
7. 24 hr urine collection
8. Urine Creatinine clearance

C. Diagnostic Evaluation
1. X-ray and Ultrasound
a. to detect calculi and determine size of kidneys,
calcium deposits or obstructions.
2. CT scan / MRI without contrast dye
a. to identify obstruction or tumors.
3. Kidney biopsy
a. to detect immunological disease or determine
kidney dysfunction reversibility and need for dialysis
C. Risk factors in CKD
therapy.
1. Chronic hypertension and poorly controlled
b. Check for hemorrhage and signs of infection
diabetes account for about 70% of cases of CKD.
(cloudy, foul smelling urine, urgency)
2. Chronic glomerulonephritis and pyelonephritis.
4. Retrograde Pyelogram, Cystogram,
3. Polycystic kidney disease.
Urethrogram
4. Kidney disease caused by nephrotoxic drugs or
a. Used to identify obstruction or structural
chemicals.
disorders of the ureters and renal pelvis of the
5. Systemic lupus erythematosus (SLE).
kidneys (pyelogram) by instilling contrast dye during
6. More common in African Americans and Native
a cystoscopy.
Americans.
5. Renography (Kidney Scan)
7. Age over 60.
a. Used to assess renal blood flow and estimates
8. Family history of CKD.
glomerular filtration rate (GFR) after IV injection of
 radioactive material to produce a scanned image of 8. Risk for Acute confusion
the kidneys. 9. Risk / Decreased cardiac output
10. Risk for bleeding
11. Disturbed body image
12. Fear

VIII. MEDICAL and NURSING MANAGEMENT

1. Correction of Fluid Imbalance
a. Calculate daily fluid needs.
b. Obtain accurate intake and output
VI. PHARMACOLOGIC MANAGEMENT measurements
1. Avoid nephrotoxic drugs/substances. c. Obtain daily weights. Dry Weight is the
a. antimicrobial medications - aminoglycosides weight without excess fluid that builds up between
and amphotericin B dialysis treatment. It is used to calculate UF
b. NSAIDs - Mefenamic Acid, Ibuprofen, volume and UF rate for each treatment.
Naproxen, Celecoxib, Ketorolac, Ketoprofen d. Most hemodialysis patients are advised to
c. angiotensin-converting enzyme inhibitors and limit their weight gain per treatment to no more than
angiotensin-receptor blockers 1 kg/day between dialysis sessions.
d. IV contrast dye e. Administer diuretics when patient is
hypervolemic only.
2. Digoxin (Lanoxin) f. Institute RRT as needed. (see separate outline).
a. cardiac glycoside, increases contractility of the There are three types of RRT available. These include
myocardium and promotes cardiac output. intermittent hemodialysis (IHD), peritoneal dialysis
b. Monitor digoxin laboratory levels due to slow (PD), or the newer continuous renal replacement
excretion of the medication with CKD. therapy (CRRT), which includes several varieties of
c. Administer digoxin (Lanoxin) after receiving therapy.
dialysis. g. Sustained low efficiency dialysis (SLED) is
considered one of the continuous therapies. These
3. Sodium polysterene (Kayexalate) continuous therapies may be tolerated in
a. increase elimination of life-threatening serum hemodynamically unstable patients better than other
potassium, increase potassium may cause dangerous dialysis therapies.
cardiac dysrhythmias and peaked T waves.
b. Restrict sodium intake. Sodium polystyrene 2. Prevent and treat life threatening electrolyte
contains sodium and can cause fluid retention and imbalances
hypertension, a complication of CKD. a. most common being hyperkalemia,
hypocalcemia, hypermagnesemia, and
4. Erythropoietin alfa (Epogen, Procrit) hyperphosphatemia.
a. to stimulate production of red blood cells,
given for anemia. 3. Treat Acidosis
a. Renal failure patients often develop metabolic
5. Ferrous sulfate acidosis with a mild respiratory alkalosis
a. an iron supplement to prevent severe iron compensation.
deficiency. b. Administer sodium bicarbonate (NaHCO3 ) as
indicated.
6. Aluminum hydroxide gel (Amphojel) c. Patient being dialyzed, using a dialysate
a. Taken with meals to bind phosphate in food containing bicarbonate will facilitate buffering of the
and stop phosphate absorption. patient’s acidotic state.
b. Take 2 hr before or after digoxin.
4. Prevent Additional Kidney damage.
7. Furosemide (Lasix) a. Modify medication dosing.
a. loop-diuretic administered to excrete excess b. Administer antihypertensive agents as needed.
fluids.
b. Avoid administering to a client who has 5. Prevent and treat infection
end-stage kidney disease. a. Careful monitoring of both renal function and
c. Clients may also receive thiazide diuretics, drug levels during antimicrobial therapy is necessary
potassium-sparing diuretics, and osmotic diuretics. to avoid further renal damage.
b. Assessment of surgical and line placement
VII. NURSING DIAGNOSIS sites for signs of inflammation.
1. Excess fluid volume
2. Ineffective renal tissue perfusion 6. Improve Nutritional Status
3. Impaired urinary elimination a. Restrict patient’s fluid, K, Na, and protein
4. Risk for / Imbalanced nutrition: less than body intake.
requirements b. Administer necessary vitamin
5. Activity intolerance and Fatigue supplementation. Supplementation of folic acid,
6. Risk for / Impaired skin integrity pyridoxine, and the water-soluble vitamins is most
7. Risk for infection frequently necessary.
 c. Consult a dietitian for a diet plan. Administer
the prescribed diet, which is usually a lowto
moderate-protein (to decrease the workload on the
kidneys) and high-carbohydrate diet. Restrict
potassium and sodium intake as prescribed based on
the electrolyte level.

VIII. REFERENCES
Cheever, K., Hinkle, J. & Overbaugh, K. Brunner and
Suddarth's Textbook of Medical-Surgical Nursing. 15th ed.
2022
Silvestri, A., et.al. Saunders Comprehensive Review
for the NCLEX RN Examination. 8th ed. 2020
Keller, S., Marieb, M. Essentials of Human Anatomy
and Physiology. 12th ed. Pearson Education, Inc. 2018
Burns, S. AACN Essentials of Critical Care Nursing.
3rd ed. McGraw-Hill Education. Virginia. 2014

Prepared by: JOHN EMMANUEL C. MAGTIBAY, RN / NCM 118n

LEC / 1st Sem 2023-2024