Acute Renal Failure m162

ACUTE RENAL FAILURE GROUP

5

ACUTE RENAL FAILURE 

a syndrome of varying causation that results in a sudden decline in renal function. It is frequently associated with an increase in BUN and creatinine, oliguria (less than 500 mL urine/24 hours), hyperkalemia, and sodium retention.  Results in retention of toxins, fluids, and end products of metabolism  Usually reversible with medical treatment.  also called Acute Kidney injury Source: Lippincott Manual of Nursing Practice, 2006

ETIOLOGY • Prerenal- result from conditions that decrease renal blood flow such as: • Hypovolemia, shock, blood loss, embolism, burns, cardiovascular disorders, sepsis

• Intrarenal – result from injury to renal tissue and are usually associated with: • Nephrotoxic agents, infections, ischemia and blockages, polycystic kidney disease

• Postrenal- arise from obstruction or disruption to urine flow anywhere along the urinary tract. • Stones, blood clots, BPH, urethral edema from invasive procedures Source: Lippincott Manual of Nursing Practice, 2006

Other major causes. . .

• Vascular Disease • Glomerular Disease • Interstitial/Tubular Disease • Obstructive Uropathy

CLINICAL COURSE ONSET: begins when the kidney is injured and lasts from hours to days. OLIGURIC-ANURIC PHASE: (urine volume less than 400 to 500 mL /24 hours). a. Accompanied by rise in serum concentration of elements usually excreted by kidney (urea, creatinine, organic acids, and intracellular cations- potassium and magnesium). Source: Lippincott Manual of Nursing Practice, 2006

b. There can be a decrease in renal function with increasing nitrogen retention even when the patient is excreting more than 2-3 L of urine daily- called non-oliguric or high-output renal failure. DIURETIC PHASE: begins when the 24-hour urine volume exceeds 500 mL and ends when the BUN and serum creatinine levels stop rising. RECOVERY PHASE: a. Usually lasts several months to 1 year. b. Probably some scar tissue remains, but the functional loss is not always clinically significant. Source: Lippincott Manual of Nursing Practice, 2006

CLINICAL MANIFESTATIONS 1.Prerenal • • • • • • •

Decreased tissue turgor Dryness of mucous membranes Weight loss Hypotension Oliguria or anuria Flat neck veins Tachycardia

Source: Lippincott Manual of Nursing Practice, 2006

2.Intrarenal • Edema usually present 3.Postrenal • Obstruction to urine flow • Obstructive symptoms of BPH (Benign Prostatic Hyperplasia or Hypertrophy) • Possible nephrolithiasis 4. Changes in urine volume and serum concentrations of BUN, creatinine, potassium

Source: Lippincott Manual of Nursing Practice, 2006

Subjective symptoms • • • • •

Nausea Loss of appetite Headache Lethargy Tingling in extremities

Objective symptoms  Diuretic phase • Increased UOP • Gradual decline in BUN and creatinine • Hypokalemia • Hyponaturmia • Tachycardia • Improved LOC Source: Medical-Surgical Nursing 1 NPN 200

DIAGNOSTIC EVALUATION  Urinalysis- reveals proteinuria, hematuria, casts  Rising serum creatinine and BUN levels

 Urine chemistry examinations to distinguish various forms of acute renal failure; decreased sodium  Renal Ultrasonography- for estimate of renal size and to exclude a treatable obstructive uropathy Source: Lippincott Manual of Nursing Practice, 2006

PATHOPHYSIOLOGY

Etiology: -Hypotension

Predisposing Factors: -Age -Lifestyle -Dehydration -UTI -Kidney Stones

-Obstruction -Glomerular Disease -Acute Tubular Necrosis

Rapid Kidney Damage

Fluid is retained

waste products accumulates in the bloodstream

Excess fluid volume metabolic acidosis

imbalance in the electrolyte level

Hypertension Oliguria Shortness of Breath edema

crackles

S/S of Metabolic Acidosis patient may have yellowish pale skin, and complains of itching due to urea crystals on skin. Vomiting, nausea, headache, stupor, coma may also be present.

Phosphorus

Bones release Calcium

Kidney is unable to produce hormone that activates Vit. D.

Potassium

Sodium

Vitamin D dysrrhythmia abdominal diarrhea cramps

calcium

absorption of calcium water retention edema hypertension prone to fractures

TREATED - Restricted diet and fluid intake - Medications and careful monitoring

Recovery of kidney and return of normal filtering Function

Wellness

UNTREATED - Progressive renal failure - Coma - Death

1. Determine if there is a history of cardiac disease, malignancy, sepsis, or intercurrent illness. 2. Determine if patient has been exposed to potentially nephrotoxic drugs (antibiotic, NSAIDs, contrast agents, solvents). 3. Conduct ongoing physical examination for tissue turgor, pallor, alteration in mucous membranes, blood pressure, heart rate changes, pulmonary edema, and peripheral edema. 4. Monitor intake and output.

 Excessive Fluid Volume related to decreased glomerular filtration rate and sodium retention  Risk for infection related to alterations in immune system and host defenses  Imbalanced Nutrition: Less Than Body Requirements related to catabolic state, anorexia, and malnutrition associated with acute renal failure.  Risk for Injury related to GI Bleeding

 Disturbed Thought Processes related to the effects of uremic toxins on the central nervous system(CNS).

• Fluid and dietary restrictions • Maintain Electrolytes • May need dialysis to jump start renal function • May need to stimulate production of urine with IV fluids, Dopamine, diuretics, etc.

MANAGEMENT Preventive Measures 1. Identify patients with preexisting renal disease. 2. Initiate adequate hydration before, during, and after any procedure requiring NPO status. 3. Avoid exposure to nephrotoxins. Be aware that the majority of drugs or their metabolites are excreted by the kidneys. *DRUG ALERT: Nonsteroidal anti-inflammatory drugs (NSAID’s) including COX-2 inhibitors, may reduce glomerular filtration rate in people at risk for renal insufficiency, causing renal failure.

4. Monitor chronic analgesic use-some drugs may cause interstitial nephritis and papillary necrosis. 5. Prevent and treat shock with blood and fluid replacement. Prevent long periods of hypotension. 6. Monitor urinary output and CVP hourly in critically ill patients to detect onset of renal failure at the earliest moment. 7. Schedule diagnostic studies requiring dehydration so there are “rest days”, especially in aged who may not have adequate renal reserve. 8. Pay special attention to draining wounds, burns, which can lead to dehydration and sepsis and progressive renal damage. 9. Avoid infection; give meticulous care to patients with indwelling catheter or I.V.lines.

Source: Lippincott Manual of Nursing Practice, 2006

MANAGEMENT Corrective and ive Measures 1. Corrective reversible cause of acute renal failure (e.g, improve renal perfusion, maximize cardiac output, surgical relief of obstruction). 2. Be alert for and correct underlying fluid excesses or deficits 3. Correct and control biochemical imbalances-treatment of hyperkalemia. 4. Restore and maintain blood pressure. 5. Maintain nutrition. Source: Lippincott Manual of Nursing Practice, 2006

COMPLICATIONS

1. Infection 2. Arrhythmias due to hyperkalemia 3. Electrolyte (sodium, potassium, calcium, phosphorus) abnormalities 4. GI Bleeding due to stress ulcers 5. Multiple organ systems failure

Source: Lippincott Manual of Nursing Practice, 2006

ACHIEVING FLUID AND ELECTROLYTE BALANCE  Monitor for signs and symptoms of hypovolemia or hypervolemia  Monitor urinary output and urine specific gravity; measure and record intake and output including urine, gastric suction, stools, wound drainage, perspiration.  Monitor serum and urine specific concentrations.  Weigh patient daily to provide an index of fluid balance; expected weight loss is ½ to 1 Ib (0.25- 0.5 kg) daily.  Adjust fluid intake to avoid volume overload and dehydration. Source: Lippincott Manual of Nursing Practice, 2006

ACHIEVING FLUID AND ELECTROLYTE BALANCE  Evaluate for signs and symptoms of hyperkalemia and monitor serum potassium levels. (Notify health care provider of value above 5.5mg/L)  Watch for cardiac arrhythmia and heart failure from hyperkalemia, electrolyte imbalance, or fluid overload. Have resuscitation equipment on hand in case of cardiac arrest.  Instruct patient about the importance of following prescribed diet, avoiding foods high in potassium.  ister blood transfusions during dialysis to prevent hyperkalemia from stored blood. Source: Lippincott Manual of Nursing Practice, 2006

PREVENTING INFECTION  Monitor for all signs of infection. Be aware that renal failure patients do not always demonstrate fever and leukocytosis.  Remove bladder catheter as soon as possible; monitor for UTI.  If antibiotics are istered, care must be taken to adjust the dosage for renal impairment.

Source: Lippincott Manual of Nursing Practice, 2006

MAINTAINING ADEQUATE NUTRITION  Work collaboratively with dietitian to regulate protein intake according to impaired renal function.  Offer high carbohydrate feedings because carbohydrates have a greater protein-sparing power and provide additional calories.  Weigh daily  Be aware that food and fluids containing large amounts of potassium, sodium, and phosphorus may need to be restricted. Source: Lippincott Manual of Nursing Practice, 2006

PREVENTING GI BLEEDING  Examine all stools and emesis for gross and occult blood.  ister H2-receptor antagonist, such as cemetidine (Tegamet) or ranitidine (Zantac), or nonaluminum or magnesium antacids as prophylaxis for gastric stress ulcers.  Prepare for endoscopy when GI bleeding occurs.

Source: Lippincott Manual of Nursing Practice, 2006

PRESERVING NEUROLOGIC FUNCTION  Speak to the atient in simple orienting statements, using repitition when necessary.  Maintain predictable routine, and keep change to a minimum.  Watch for and report mental status changes-somnolence, lassitude, lethargy, and fatigue progressing to irritability, disorientation, twitching, seizures.  Correct cognitive distortions.  Use seizure precautions-padded side rails, airway and suction equipment at bedside.  Encourage and assist patient to turn and move because drowsiness and lethargy may prevent activity.  Use music tapes to promote relaxation. Source: Lippincott Manual of Nursing Practice, 2006

References: Gould, B.E.,(2007).Renal and Urologic Disorders.Pathophysiology for the health Professions. 3rd Ed. pp. 514-515 Grumet, S.C., & Brunner, D.W. (2000). Acute Renal Failure. Urologic Nursing, 20(1), 15-24,46. Parker, J. (E D.).(1998). Contemporary Nephrology Nursing. Pittman, NJ: A.J. Jannetti. Sofer, D. (2003). Kidney Disease: The emerging epidemic. American Journal of Nursing, 103(12), 12. Web Sites: http://www.kidney.org National Kidney Foundation http://www.kidney.niddk.nih.gov National Kidney and Urologic Diseases Information http://www.nlm.nih.gov/medlineplus/encyclopedia.html

PREPARED BY:

LEGASPI, Ma. Mariel M. MAGDARAOG, Franchescka Rigenal A. MAGDARAOG, Kelvin Kenn B. MANTE, Leo Kevin D. MEJOS, Joanne Rose C. NOVIO, Delfin Jr. B. OGALESCO, Anna Abegail M. TO: Evelyn M. Balanquit, RN Subject Professor