Download - Acute renal failure.

Prepared by:

BSN, Level IV

Sarah Jane A. Cristobal

ACUTE RENAL

FAILURE

Is the rapid breakdown of renal (kidney) function that occurs when high levels of uremic toxins (waste products of the body's metabolism) accumulate in the blood. ARF occurs when the kidneys are unable to excrete (discharge) the daily load of toxins in the urine.

DEFINITION

Based on the amount of urine that is excreted over a 24-hour period, patients with ARF are separated into two groups:

Oliguric: patients who excrete less than 500 milliliters per day (< 16 oz/day)

Nonoliguric: patients who excrete more than 500 milliliters per day (> 16 oz/day)

DEFINITION

Acute kidney failure almost always occurs in connection with another medical condition or event. Conditions that can increase your risk of acute kidney failure include: Being hospitalized, especially for a serious condition that requires intensive care Advanced age Blockages in the blood vessels in your arms or

legs (peripheral artery disease) Diabetes High blood pressure Heart failure Kidney diseases Liver diseases

RISK FACTORS

A detailed and accurate history is crucial for diagnosing acute kidney injury (AKI) and determining treatment. Distinguishing AKI from chronic kidney disease is important, yet making the distinction can be difficult.

PHYSICAL EXAMINATION

A history of chronic symptoms—months of fatigue, weight loss, anorexia, nocturia, sleep disturbance, and pruritus—suggests chronic kidney disease. AKI can cause identical symptoms, but over a shorter course.


It is important to elicit a history of any of the following etiologic factors: Volume restriction (eg, low fluid intake,

gastroenteritis) Nephrotoxic drug ingestion Trauma or unaccustomed exertion Blood loss or transfusions Exposure to toxic substances, such as ethyl

alcohol or ethylene glycol Exposure to mercury vapors, lead, cadmium,

or other heavy metals, which can be encountered in welders and miners


Urine output history can be useful. Oliguria generally favors AKI. Abrupt anuria suggests acute urinary obstruction, acute and severe glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing urine output may indicate a urethral stricture or bladder outlet obstruction due to prostate enlargement.


Prerenal failure

Patients commonly present with symptoms related to hypovolemia,

including thirst, decreased urine output, dizziness, and orthostatic hypotension. Ask about volume loss from vomiting,

diarrhea, sweating, polyuria, or hemorrhage. Patients with advanced

cardiac failure leading to depressed renal perfusion may present with orthopnea and

paroxysmal nocturnal dyspnea.


Elders with vague mental status change are commonly found to have prerenal or normotensive ischemic AKI. Insensible fluid losses can result in severe hypovolemia in patients with restricted fluid access and should be suspected in elderly patients and in comatose or sedated patients.


Intrinsic renal failure

Patients can be divided into those with glomerular etiologies and those with tubular etiologies of AKI. Nephritic

syndrome of hematuria, edema, and hypertension indicates a glomerular

etiology for AKI. Query about prior throat or skin infections.


A history of prior gynecologic surgery or abdominopelvic malignancy often can be helpful in providing clues to the level of

obstruction.Flank pain and hematuria should raise a concern about renal calculi or papillary

necrosis as the source of urinary obstruction.


Postrenal failure

Postrenal failure usually occurs in older men with prostatic obstruction and

symptoms of urgency, frequency, and hesitancy. Patients may present with

asymptomatic, high-grade urinary obstruction because of the chronicity of

their symptoms.

RISK FACTORS

The interaction of tubular and vascular events result in ARF. The primary cause of ATN is ischemia. Ischemia for more than two hours results in severe and irreversible damage to the kidney tubules. Significant reduction in glomular filtration rate (GFR) is a result of (1) ischemia, (2) activation of the renin-angiotensin system , and (3) tubular obstruction by cellular debris

PATHOPHYSIOLOGICMECHANISM

As nephrotoxins damage the tubular cells and these cells are lost through necrosis, the tubules become more permeable. This results in filtrate absorption and a reduction in the nephrons ability to eliminate waste.


The clinical course of ARF is characterized by the following three phases:

Phase 1. OnsetARF begins with the underlying clinical

condition leading to tubular necrosis, for example hemorrhage, which reduces blood volume and renal perfusion. If adequate treatment is provided in this phase then the individual's prognosis is good.


Phase 2. MaintenanceA persistent decrease in GFR and tubular

necrosis characterizes this phase. Endothelial cell necrosis and sloughing lead to tubular obstruction and increased tubular permeability. Because of this, oliguria is often present during the beginning of this phase. Efficient elimination of metabolic waste, water, electrolytes, and acids from the body cannot be performed by the kidney during this phase.


Therefore, azotemia, fluid retention, electrolyte imbalance and metabolic acidosis occurs. The patient is at risk for heart failure and pulmonary edema during this phase because of the salt and water retention. Immune function is impaired and the patient may be anemic because of the suppressed erythropoietin secretion by the kidney and toxin-related shorter RBC life.


Phase 3. RecoveryRenal function of the kidney improves

quickly the first five to twenty-five days of this phase. It begins with the recovery of the GFR and tubular function to such an extent that BUN and serum creatinine stabilize. Improvement in renal function may continue for up to a year as more and more nephrons regain function.


If your signs and symptoms suggest that you have acute kidney failure, your doctor may recommend tests and procedures to verify your diagnosis. These may include: Urine output measurements. The amount of

urine you excrete in a day may help your doctor determine the cause of your kidney failure.

Urine tests. Analyzing a sample of your urine, a procedure called urinalysis, may reveal abnormalities that suggest kidney failure.

DIAGNOSTICEXAMINATION

Blood tests. A sample of your blood may reveal rapidly rising levels of urea and creatinine — two substances used to measure kidney function.

Imaging tests. Imaging tests such as ultrasound and computerized tomography (CT) may be used to help your doctor see your kidneys.


Removing a sample of kidney tissue for testing. In certain situations, your doctor may recommend a kidney biopsy to remove a small sample of kidney tissue for lab testing. To remove a sample of kidney tissue, your doctor may insert a thin needle through your skin and into your kidney.


Drugs that are renally excreted may need to have their doses reduced in patients with renal insufficiency or end-stage renal disease:

MEDICATIONS

For prescribing purposes renal impairment is usually divided into three grades:

Mild: GFR 20-50 ml/minute; serum creatinine approximately 150-300 µmol/l.

Moderate: GFR 10-20 ml/minute; serum creatinine approximately 300-700 µmol/L.

Severe: GFR less than 10 ml/minute; serum creatinine >700 µmol/L.

MEDICATIONS

Nephrotoxic drugs should, if possible, be avoided in patients with renal disease because the consequences of nephrotoxicity are likely to be more serious when the renal reserve is already reduced.

MEDICATIONS

The situation may change if a patient begins dialysis, since some drugs will be removed by the dialysis. Dialysis may lead to the loss of therapeutic effect for some drugs.

MEDICATIONS

Drugs to which particular attention must be given include many antibiotics, histamine H2-receptor antagonists, digoxin, anticonvulsants and non-steroidal anti-inflammatory drugs (NSAIDs).

MEDICATIONS

1. Excess Fluid Volume May be relate toCompromised regulatory mechanism (renal failure)Possibly evidenced by Intake greater than output, oliguria; changes in urine specific gravity Venous distension; blood pressure (BP)/central venous pressure

(CVP) changes Generalized tissue edema, weight gainChanges in mental status, restlessness

NURSINGDIAGNOSIS

2. Risk for Decreased Cardiac OutputRisk factors may include Fluid overload (kidney dysfunction/failure,

overzealous fluid replacement) Fluid shifts, fluid deficit (excessive losses) Electrolyte imbalance (potassium, calcium);

severe acidosis Uremic effects on cardiac muscle/oxygenationPossibly evidenced by[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]

NURSINGDIAGNOSIS

3. Risk for Imbalanced Nutritionrisk for less than body requirementsRisk factors may include Protein catabolism; dietary restrictions to reduce nitrogenous

waste products Increased metabolic needs Anorexia, nausea/vomiting; ulcerations of oral mucosa

NURSINGDIAGNOSIS

4. Risk for InfectionRisk factors may include Depression of immunologic defenses

(secondary to uremia) Invasive procedures/devices (e.g., urinary

catheter) Changes in dietary intake/malnutrition

Possibly evidenced by[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]

NURSINGDIAGNOSIS

5. Risk for Deficient Fluid VolumeRisk factors may include Excessive loss of fluid (diuretic phase of

ARF, with rising urinary volume and delayed return of tubular reabsorption capabilities)

Possibly evidenced by[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]

NURSINGDIAGNOSIS

6. Deficient Knowledge May be related toLack of exposure/recallInformation misinterpretationUnfamiliarity with information resources

Possibly evidenced by Questions/request for information, statement of misconception Inaccurate follow-through of

instructions/development of preventableComplications

NURSINGDIAGNOSIS

Other Possible Nursing Care Plans

Fluid Volume, deficient (specify)—dependent on cause, duration, and stage of recovery.

Fatigue—decreased metabolic energy production/dietary restriction, anemia, increased energy requirements, e.g., fever/ inflammation, tissue regeneration.

Infection, risk for—depression of immunologic defenses (secondary to uremia), changes in dietary intake/malnutrition, increased environmental exposure.

Therapeutic Regimen: ineffective management—complexity of therapeutic regimen, economic difficulties, perceived benefit.

NURSINGDIAGNOSIS

Record accurate intake and output (I&O). Include “hidden” fluids such as IV antibiotic additives, liquid medications, ice chips, frozen treats.Measure gastrointestinal (GI) losses and estimate insensible losses, e.g., diaphoresis.

NURSINGINTERVENTIONS

Monitor urine specific gravity.Weigh daily at same time of day, on same scale, with same equipment and clothing.Assess skin, face, dependent areas for edema.


Evaluate degree of edema (on scale of +1–+4).Monitor heart rate (HR), BP, and JVD/CVP.Auscultate lung and heart sounds.Assess level of consciousness; investigate changes in mentation, presence of restlessness.Plan oral fluid replacement with patient, within multiple restrictions. Intersperse desired beverages throughout 24 hr. Vary offerings, e.g., hot, cold, frozen.


Correct any reversible cause of ARF, e.g., replace blood loss, maximize cardiac output, discontinue nephrotoxic drug, relieve obstruction via surgery.Monitor laboratory/ diagnostic studies, e.g.: BUN, Cr; Urine sodium and Cr; Serum sodium; Serum potassium; Hb/Hct; Serial chest x-rays.


Administer/restrict fluids as indicated.Note occurrence of slow pulse, hypotension, flushing, nausea/ vomiting, and depressed level of consciousness (central nervous system [CNS] depression).


Give patient/SO a list of permitted foods/fluids and encourage involvement in menu choices.Provide high-calorie, low-/moderate-protein diet. Include complex carbohydrates and fat sources to meet caloric needs (avoiding concentrated sugar sources) and essential amino acids.


Avoid invasive procedures, instrumentation, and manipulation of indwelling catheters whenever possible. Use aseptic technique when caring for/manipulating IV/invasive lines. Change site/dressings per protocol. Note edema, purulent drainage.


Provide routine catheter care and promote meticulous perianal care. Keep urinary drainage system closed and remove indwelling catheter as soon as possible.Encourage patient to observe characteristics of urine and amount/frequency of output.


Review fluid intake/restriction. Remind patient to spread fluids over entire day and to include all fluids (e.g., ice) in daily fluid counts.Discuss activity restriction and gradual resumption of desired activity. Encourage use of energy-saving, relaxation, and diversional techniques.


Determine/ prioritize ADLs and personal responsibilities. Identify available resources/support systems.Recommend scheduling activities with adequate rest periods.Establish regular schedule for weighing.


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