RENAL DISORDERS

MJ H. GONZLES RN, MSN

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Urinary Tract Infections (UTI)

A. Upper urinary tract B. Lower urinary tract infection

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 Urinary tract infections occur in an ascending route up the urinary tract system.

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 Upper urinary tract infectionsPyelonephritis - an inflammation of the renal pelvis and the parenchyma of the kidney.

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 Acute pyelonephritis often occurs after bacterial contamination of the urethra or following an invasive procedure of the urinary tract

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 Chronic pyelonephritis most commonly occurs following chronic obstruction with reflux or chronic disorders

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 B. Lower urinary tract infection. 1. Ureteritis - inflammation of the ureter that is commonly associated with pyelonephritis Chronic pyelonephritis causes the ureter to become fibrotic and narrowed by strictures

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 2. Cystitis- inflammation or infection of the bladder. 3. Urethritis- inflammation of the urethra.

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Causes
Stasis of urine in the bladder, and reflux of urine back into the original reservoir are the primary factors in causing UTI.

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Factors contributing to UTI

a. Adult female urethra is short; in close proximity to the rectum and vagina which predisposes it to contamination from fecal material.

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 b. Ureterovesical reflux--the reflux of urine from the urethra into the bladder. This causes a constant residual of urine in the bladder after voiding and precipitates UTI.

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 c. Vesicoureteral reflux (ureterovesical reflux)-the reflux of urine from the bladder into one or both of the ureters and possibly into the renal pelvis.

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 d. Instrumentation - catheterization or cystoscopic examination. e. Stasis of urine in the bladder leading to urinary retention for any reason (clients with prostate disease).

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 f. Obstruction to urinary flow congenital anomalies, urethral strictures, ureteral stones, or contracture of the bladder neck.

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 g. Bladder hypotonia, mechanical compression of the ureters, hormone changes predispose the pregnant woman to increased urinary tract infections.

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 h. Metabolic disorders such as diabetes. i. Sexual intercourse promotes development of UTI. j. Fecal contamination of the urethral meatus.

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Causative bacterial organisms

a. E. coli (80 to 90 percent). b. Staphylococcus saprophyticus (11% in women). c. Proteus mirabilia. d. Pseudomonas aeruginosa

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Microorganism

Antigen/Antibody complexes

Toxins

Renal Dysfunction

Urinary tract

Etiology in Renal Disease Pathways to renal damage and dysfunction

Microorganism
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Bacterial gain Access to blood Hematogenous PN Systemic Arteries

Kidney Ureter and Bladder Etiology of Pyelonephritis Urethra Ascending PN

Interstitial Microorganism
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Exogenous microorganism

Vaginal Microorganism
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Clinical manifestations
Cystitis: (1) Frequency and urgency. (2) Suprapubic pain. (3) Burning on urination. (4) Hematuria (5) Fever, chills and body malaise, (6) Nausea, vomiting.
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 7. Voiding in small amounts 8. Inability to void 9. Incomplete emptying of the bladder 10. Lower abdominal discomfort or back discomfort 11. Cloudy, dark, foul-smelling urine 12. Bladder spasms
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Causes of Cystitis
Allergens or irritants, such as soaps, sprays, bubble bath, perfumed sanitary napkins Bladder distention Calculus Hormonal changes influencing alterations in vaginal flora

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 Indwelling urethral catheters Invasive urinary tract procedures Loss of bactericidal properties of prostatic secretions in the male Poor-fitting diaphragms Sexual intercourse

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Synthetic underwear and pantyhose Urinary stasis Use of spermicides Wet bathing suits

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Pyelonephritis
(1) Fever, chills, flank pain. (2) Painful urination (dysuria). (3) Pain and tenderness at the costovertebral angle. (4) Symptoms of cystitis.

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Diagnostics
a. Urinalysis-pus, bacteria, and RBCs found in the urine. b. Urine test for culture and sensitivity- colony count of at least 100,000,colonies per ml of urine on a clean catch midstream or catheterized specimen indicates infection.
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 c. Acute pyelonephritis. (1) Elevated WBC count. (2) Possible positive blood culture. (3) Intravenous pyelogramindicates enlargement of involved kidney and abscess into renal tissue.

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Complications
a. A lower urinary tract infection may result in an upper urinary tract infection. b. Chronic pyelonephritis may occur after repeated bouts of acute pyelonephritis.

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Treatment
1. Medical 2. Dietary

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Medical
a. Sulfonamides. b. Urinary Antiseptics. c. Urinary analgesics. d. Antispasmodics. e. Penicillins f. Nitrofurantoin

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Dietary
a. Encourage fluid intake of 3.000 cc day. (1) A diluted urine causes less irritation. (2) The increase in flow of urine through the urinary tract system decreases the movement of bacteria up the urinary tract.
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 (3) Discourage carbonated beverages and foods or drinks containing baking powder or baking soda. b. An acid ash diet to increase the acidity of the urine.

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Nursing Intervention
Goal: to obtain relief of pain, urgency, dysuria, and fever. 1. Administer antimicrobial agent as prescribed; antibiotics need to he taken the entire course which is usually ten to fourteen days. 2. Encourage eight to ten glasses of fluids daily.
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 3. Teach importance of voiding every two to three hours during the day to completely empty the bladder. 4. Sitz bath to decrease irritation of urethra.

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 Goal: to prevent recurrence of infection. 1. Teach client to shower rather than bathe in tub. If client prefers to take a tub bath she should avoid bubble bath additives.

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 2. Explain importance of cleansing the perineal area from front to back after each bowel movement. 3. If intercourse seems to predispose to infection, encourage voiding immediately after intercourse.

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 4. Teach importance of long-term antimicrobial therapy to prevent recurrences. 5. Encourage and explain the need for follow-up care to prevent complications of chronic urinary tract infections. 6. Avoid caffeine and alcohol.
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Prevention of Cystitis
Teach the female client good perineal care and to wipe from front to back Instruct the female client to avoid bubble baths and tub baths and avoid vaginal deodorants or sprays Instruct the client to void every 2 to 3 hours Instruct the female client to void and drink a glass of water after intercourse
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 Instruct the female client to wear cotton pants and to avoid wearing tight clothes or pantyhose with slacks, and to avoid sitting in a wet bathing suit for prolonged periods of time

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 Teach pregnant women to void every 2 hours Encourage menopausal women to use estrogen vaginal creams to restore pH Instruct the female client to use water-soluble lubricants for coitus, especially after menopause

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URETHRITIS
An inflammation of the urethra commonly associated with sexually transmitted diseases (STD), and may be seen with cystitis In men, it is most often caused by gonorrhea or chlamydial infection

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 In women, it is most often caused by feminine hygiene sprays, perfumed toilet paper or sanitary napkins, spermicidal jellies, UTIs, or changes in the vaginal mucosal lining

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Assessment/Male
a. Burning on urination b. Frequency c. Urgency d. Nocturia e. Difficulty voiding f. Discharge from the penis

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Females
a. Frequency b. Urgency c. Nocturia d. Painful urination e. Difficulty voiding f. Lower abdominal discomfort

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Interventions
1. Encourage fluids 2. Prepare the client for testing to determine if an STD is present 3. Administer antibiotics as prescribed

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 4. Instruct the client in the administration of sitzbaths 5. If stricture occurs, prepare the client for dilation of the urethra and instillation of an antiseptic solution

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 6. Instruct the client to avoid intercourse until the symptoms subside or treatment of the SID is complete 7. Instruct the female client to avoid the use of perfumed toilet paper or sanitary napkins and feminine hygiene sprays
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UROSEPSIS
A gram-negative bacteremia originating in the urinary tract The most common responsible organism is Escherichia coli

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 The most common cause is the presence of an indwelling urinary catheter or an untreated UTI in a client who is medically compromised

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 The major problem is the ability of this bacterium to develop resistant strains Urosepsis can lead to septic shock if not treated aggressively

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Assessment
Fever is the most common and earliest manifestation

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Nursing Interventions
1. Obtain a urine specimen for urine culture and sensitivity 2. Administer IV antibiotics as prescribed, usually until the client has been afebrile for 3 to 5 days 3. Administer oral antibiotics as prescribed after the 3 to 5 day afebrile period
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Glomerulonephritis
An inflammatory reaction in the glomerulus as a result of an antigenantibody response to the betahemolytic streptococcus. Occurs more frequently in boys, usually between ages 6-7 years Usually resolves in about 14 days, self-limiting
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 The inflammation of the glomeruli results from an antigen-antibody reaction produced from an infection elsewhere in the body An immune complex is formed as a result of the antigen-antibody formation; the complex becomes trapped in the glomeruli.
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 It results in proliferative and inflammatory changes within the glomerular structure As a result of the edema in the glomeruli, the GFR is significantly decreased.

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 Destruction, inflammation, and sclerosis of the glomeruli of both kidneys occur Loss of kidney function develops

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Pathogenesis of GN

Immune Complex Deposition

Complement Activation Infiltrating Leukocytes

Mesangial Cells

Aggregate Platelets

Growth factor Proliferation of glomerular elements

Proteases And Free Radicals

Microthrombi

Blocked Capillaries
BM Exposed
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Defective Filtration

Glomerular Damage
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Causes
Immunological or autoimmune diseases Streptococcal infection, group A betahemolytic History of pharyngitis or tonsillitis 2 to 3 weeks prior to symptoms

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 Scarlet fever and impetigo. Most common in children, but all age groups can be affected.

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Types
Acute: Occurs 2 to 3 weeks after a streptococcal infection Chronic: Can occur after the acute phase or slowly over time

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Complications
Heart failure Hypertensive encephalopathy Pulmonary edema Renal failure

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Clinical manifestations
a. Acute glomerulonephritis. Disease may be mild with proteinuriaasymptomatic hematuria. Headache and malaise. Facial edema, periorbital edema.

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 Decrease in urine output (oliguria). Mild to severe hypertension. Tenderness over the costovertebral angle. Tea or cola colored urine due to hematuria.

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Chronic glomerulonephritis
Proteinuria and hematuria. Hypertension-nose bleeds, retinal hemorrhages, or uremic convulsions. Feet are slightly swollen at night.

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 A yellow grayish pigmentation of the skin along with pale mucous membranes and anemia. Occurs over months to years.

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 1. Gross hematuria 2. Dark, smoky, cola-colored or redbrown urine 3. Proteinuria that produces a persistent and excessive foam in the urine 4. Urinary debris

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 5. Moderately elevated to high specific gravity 6. Low urinary pH 7. Oliguria or anuria 8. Headache 9. Chills and fever

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10. Fatigue and weakness 11. Anorexia, nausea, and vomiting 12. Pallor 13. Edema in the face, periorbital area, feet, and generalized 14. Shortness of breath, ascites, pleural effusion and CHF
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15. Abdominal or flank pain 16. Hypertension 17. Reduced visual acuity 18. Increased BUN and creatinine levels 19. Increased antistreptolysin 0 titer (used to diagnose disorders caused by streptococcal infections)
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Complications
a. Chronic renal failure b. Nephrotic syndrome

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Diagnostics
a. Urinalysis. (1) Proteinuria. (2) Increased specific gravity. (3) Hematuria.

(4) Urine specific gravity increased

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 (4) Red cell casts. b. CBC-decreased hemoglobin and hematocrit. c. Elevated BUN, creatinine, and albumin. d. Positive complement studies and ASO titer. e. ESR elevated
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Treatment
Medical Dietary

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 Medical. a. Diuretics are usually not effective. May be utilized if the child is severely edematous. b. Antihypertensives. c. Antibiotics--penicillin, if cultures indicate.
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 Fluid restriction if renal insufficiency Peritoneal dialysis if severe renal or cardiopulmonary problems develop

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 Dietary. a. Decrease sodium intake. b. Protein restriction if child is azotemic from prolonged decrease in urinary output. The anorexia the child experiences frequently limits the protein sufficiently.

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 c. Foods containing high potassium are generally restricted during the oliguria phase.

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Nursing Intervention
Goal: to protect client's poorly functioning kidneys by preventing secondary infections. 1. Administer antibiotic therapy. 2. Bedrest for severe hypertension and significant edema; otherwise, activity as tolerated.

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 Goal: to maintain fluid balance. 1. Monitor intake and output; maintain diet and fluid restrictions as ordered. 2. Monitor renal function-cheek characteristics and color of urine, weigh client daily, and cheek blood pressure q 2 to 4 hours.
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 3. Administer antihypertensives as ordered. 4. Frequently the first sign of improvement is an increase in the urine output, then may progress to profuse diuresis.

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 Goal: to prevent complications and promote comfort. 1. Encourage verbalization of fears. 2. Decrease anxiety by explaining treatments. 3. Assess for complications related to hypertension, congestive heart failure, pulmonary edema, and chronic renal failure.
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Nephrotic Syndrome
A set of clinical manifestations arising from protein wasting secondary to diffuse glomerular damage

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 Primarily occurs in children and is the outcome of other renal problems in which there is proteinuria, hypoalbuminemia, hyperlipedemia and edema. Commonly affects preschoolers, boys more often than girls

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 Changes occur in the basement membrane of the glomeruli that allows the large protein molecules to pass through the membrane and he excreted.

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 The loss of the albumin from the serum decreases the oncotic pressure in the capillary bed and allows fluid to pass into the interstitial tissues and into the abdominal cavity (ascites).

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 The interstitial fluid shift causes hypovolemia, the renin-angiotensin response is stimulated, aldosterone secretion is increased, and the tubules begin to conserve sodium and water to increase the circulating volume.

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 In the majority of children with the syndrome, the etiology is unknown; frequently there is no evidence of renal dysfunction or systemic disease.

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 Course of the disease consists of exacerbations and remissions over a period of months to years

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Pathophysiology
a. Plasma proteins enter the renal tubule and are excreted in the urine, causing proteinuria. b. Protein shift causes altered oncotic pressure and lowered plasma volume.

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 c. Hypovolemia triggers release of renin and angiotensin, which stimulates increased secretion of aldosterone; aldosterone increases reabsorption of water and sodium in distal tubule.

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 d. Lowered blood pressure also stimulates release of ADH, further increasing reabsorption of water; together with a general shift of plasma into interstitial spaces, results in edema.

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Risk factors/etiology
a. History of renal dysfunction or systemic disease. (1) Glomerulonephritis. (2) Systemic lupus erythematosus. (3) Congestive heart failure.

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 b. Increased incidence in children with allergic disorders such as asthma, bay fever and urticaria. c. Majority of children are male and between ages of 2 and 7 years.

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Glormerular damage

Pathogenesis of Nephrotic Syndrome

Fluid retention reflex Protein loss

Hypoalbuminemia

Inc. plasma volume

Reduce blood Osmotic pressure

Hepatic lipoprotein production

Reduce Antibody levels

Reduced Anticoagulants

Systemic edema
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Hyperlipedemia

Proteinuria

Infections

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Clinical manifestations
a. Edema. (1) Facial edema, especially periorbital edema. May be more pronounced in the morning, and subside some during the day. (2) Generalized edema of the lower ext. may increase during the day.

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(3) Labia and scrotum may become very edematous. (4) Edema may progress to the level of severe generalized edema (anasarca).

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Inc. Permeability
Dev. of edema in neprhosis Loss of albumin, other protein in urine

Dec. colloid osmotic pressure of blood

Fluid loss to interstitial spaces

Edema (anasarca)
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Dec. circulating blood volume

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b. Proteinuria. c. Hypoalbuminemia. d. Hyperlipidemia e. Gradual increase in weight. f. Volume of urine is decreased and may be dark or tea-colored

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g. Hematuria h. Anemia i. Amenorrhea or abnormal menses j. Irritability, fatigue, lethargy. l. Body malaise m. Anorexia n. Waxy pallor to the skin
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 o. Skin is pale and is prone to break down during the edematous stage p. Depending on the severity of the condition, the child may experience episode of hypertension. q. Child is malnourished due to decreased intake as well as loss of protein in the urine but may not appear so due to edema.
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Complications
a. Anasarca. b. Hypertension. c. Renal failure.

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Diagnostics
a. Urinalysis-proteinuria. b. Decrease serum albumin. c. Creatinine clearance may he decreased with normal serum creatinine. d. Increase serum lipids-cholesterol and low- density lipoproteins (LDL) are elevated followed later by increased triglyceride level.
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Treatment
Medical Dietary

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Medical
a. Corticosteroid-prednisone. b. Diuretics-(frequently child is not responsive to the diuretics, may be used when the edema is severe or the child is hypertensive) spironolactone (ALDACTONE) in combination with furosemide (LASiX). Or some used Thiazide diuretics
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 c. Salt-poor human albumin for vascular insufficiency and severe edema. d. Prophylactic broad spectrum antimicrobial agents.

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 e. Immunosuppressant therapy, usually cyclophosphamide (CYTOXAN) may be administered for up to two months to reduce the relapse rate and induce long-term remission.

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Dietary
a. Decreased sodium intake. b. Protein intake depends on stage of disease. If there is any indication of renal failure or azotemia, then protein is restricted. There controversy regarding the benefits of decreased protein intake. c. There is usually no fluid restriction.
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 Bed rest

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Nursing Intervention
Goal: to reduce edema and excess fluid retention, 1. Support edematous organs such as scrotum. 2. Provide and encourage a saltrestrictive diet.

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 3. Administer salt-poor albumin as ordered and monitor closely for circulatory overload during and after administration. 4. Provide meticulous skin care; change position frequently and monitor good body alignment.

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 5. Cleanse and powder opposing skin surfaces frequently. 6. Daily weights, accurate intake and output measure abdominal girth.

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Goal: to prevent infection

1. Child susceptible to infection due to decreases immune state from steroid therapy. 2. Protect child from upper respiratory infections good pulmonary hygiene. 3. Prevent skin excoriation and breakdown, asses carefully for indications of infection.
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Goal: to promote nutrition

1. Encourage adequate protein intake. 2. Serve small quantities to children. 3. Encourage input from child in selecting foods from prescribed diet.

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 Goal: to assist parents to cope with chronic disease and teach them home care. 1. Instruct as to medical regimen. 2. Reassure parents of the course of the disease so that they do not become discouraged with the frequent relapses.
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 3. Impress upon them the importance of long-term care and to obtain medical assistance when relapse occurs. 4. Social isolation is often a problem due to frequent hospitalizations or confinement (high risk of infection which could precipitate an exacerbation).
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Nephritic Syndrome
It is dominated by inflammatory damage that restricts glomerular filtration and allows erythrocytes to escape to the urine (hematuria).

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 The decreased filtration causes reduced urinary output (oliguria), systemic HPN, and the accumulation of nitrogenous wastes in the blood (azotemia).

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Pathogenesis of Nephritic Syndrome Glomerular Damage

RBC loss to filtrate

Variable Low level Proetinuria

Reduced Glomerular Filtration

Hematuria

Azotemia
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Fluid Retention

Oliguria
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PHILIPPIANS 4:13

I CAN DO ALL THINGS THROUGH CHRIST WHO STRENGTHENS ME!

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RENAL FAILURE
The loss of kidney function Sudden interruption of kidney function to regulate fluid and electrolyte balance and remove toxic products from the body

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 The signs and symptoms of renal failure are caused by the retention of wastes, the retention of fluids, and the inability of the kidneys to regulate electrolytes

Most important manifestation: OLIGURIA

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Kidney function
The Nephron produces urine to eliminate waste Impaired urine production and azotemia Secretes Erythropoietin to ANEMIA increase RBC Metabolism of Vitamin D Calcium and Phosphate imbalances

Produces bicarbonate and Metabolic ACIDOSIS secretes acids Excretes excess POTASSIUM
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HYPERKALEMIA

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Kinds of Renal Failure

Acute renal failure Chronic renal failure

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Acute Renal Failure

Prerenal
Intrarenal Postrenal

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Prerenal(renal ischemia)
Serious cardiovascular disorders Peripheral vasodilation Severe vasoconstriction

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Hemorrhage Shock Burns Hypovolemia Renal vascular obstruction -(A/V)thrombosis

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Heart Failure

Vasodilatation

Hypovolemia

Systemic Hypotension Atherosclerois Renal Ischemia Nephrosclerosis

Renal artery stenosis

Inadequate filtration

Prerenal Disease
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Prerenal disease

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Acute renal failure -PATHOPHYSIOLOGY

Prerenal CAUSE: Factors interfering with perfusion and resulting in diminished blood flow and glomerular filtrate, ischemia, and oliguria; include CHF, cardiogenic shock, acute vasoconstriction, hemorrhage, burns, septicemia, hypotension, anaphylaxis
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Renal/Intrarenal(kidney tissue pathology)

Acute tubular necrosis Nephrotoxins Aminoglycosides or NSAIDs Heavy metals -(carbon tetrachloride,
arsenic, lead, mercury
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Intrarenal
Ischemic damage from poorly treated renal failure Acute glomerulonephritis and pyelonephritis

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 Diseases that precipitate micro and microvascular changes (atheroselerosis, diabetes mellitus, hypertension).

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Eclampsia, postpartum renal failure or uterine hemorrhage Crush injury, myopathy, sepsis or transfusion reaction

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Acute renal failure -PATHOPHYSIOLOGY Intrarenal CAUSE: Conditions that cause damage to the nephrons; include acute tubular necrosis (ATN), endocarditis, diabetes mellitus, malignant hypertension, acute glomerulonephritis, tumors, blood transfusion reactions, hypercalcemia, nephrotoxins (certain antibiotics, x-ray dyes, pesticides, anesthetics)
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Postrenal(obstructive problems)
Bladder obstruction Ureteral(stones) obstruction Urethral obstruction BPH Trauma resulting to obstruction
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Acute renal failure -PATHOPHYSIOLOGY

Postrenal CAUSE:

Mechanical obstruction anywhere from the tubules to the urethra; includes calculi, BPH, tumors, strictures, blood clots, trauma, and anatomic malformation

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PRERENAL CAUSES

INTRARENAL CAUSES
Acute tubular necrosis (ATN)

POSTRENAL CAUSES
Calculi Tumors Blood clots BPH Strictures

Hypotension Cardiogenic shock

Acute vasoconstriction

Diabetes mellitus
Malignant hypertension
Acute glomerulonephritis

Hemorrhage Burns

Tumors
Blood transfusion reactions

Septicemia
CHF

Trauma
Anatomic malformation

Nephrotoxins

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Phases of Acute Renal Failure

1. Oliguric phase 2. Diuretic phase 3. Recovery or convalescence

Four phases of acute renal failure (Brunner and Suddarth) 1. Initiation phase 2. Oliguric phase 3. Diuretic phase 4. Convalescence or recovery phase
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Oliguric phase
a. Urinary output decreases to less than 400 ml per day. b. Increase in BUN, creatinine, uric acid, potassium, magnesium, and presence of metabolic acidosis. c. Can last for 1 to 8 weeks.

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 d. Often the patient may excrete two or more liters of urine daily-this is referred to as high output failure; occurs predominately after nephrotoxic antibiotics, burns, or traumatic injury.

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 d. Urine specific gravity of 1.010 to 1.016 e. Anorexia, nausea, and vomiting f. Hypertension g. Decreased skin turgor h. Pruritus i. Tingling of the extremities
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 i. Drowsiness progressing to disorientation to coma k. Edema l. Dysrhythmias m. Signs of congestive heart failure (CHF) and pulmonary edema n. Signs of pericarditis o. Signs of acidosis
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Laboratory
Glomerular filtration rate decreases Hyperkalemia Sodium level normal or decreased Fluid overload Elevated BUN and creatinine

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Diuretic phase
a. A low gradual increase in urine output- three to five liters per day. Excessive urine output indicates recovery of damaged nephrons b. Elevated serum creatinine, BUN. c. Decreased urinary creatinine clearance.

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 d. Decrease in sodium, potassium, and water. e. May last for two to three weeks. f. Hypotension g. Tachycardia h. Improvement in level of consciousness (LOC)
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Laboratory
Glomerular filtration rate begins to increase Hypokalemia Hyponatremia Hypovolemia Gradual decline in BUN and creatinine

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Recovery/Convalescent
a. May last from three to twelve months or slow process; complete recovery may take 1 to 2 years b. Usually some type of permanent reduction occurs in glomerular filtration rate. c. Complications-secondary infection which is the most common cause of death.
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d. Urine volume is normal c. Increase in strength d. Increase in LOC e. BUN is stable and normal f. Client can develop chronic renal failure

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Laboratory
BUN is stable and normal Complete recovery may take 1 to 2 years

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Clinical manifestations (multiple body systems affected)

a. Urinary-decreased urinary output (Oliguria, less than 400 cc per day, except in elderly may be 600-700 cc/day). (1) Intrarenal and postrenal failurefixed specific gravity is decreased, or increased sodium in the urine, very little proteinuria, "muddy brown" casts.
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 (2) Prerenal failure-history of precipitating event, urine specific gravity may be high, high sodium concentration, and proteinuria (3) High output renal failure-the kidney no longer filters the urine. There is high urinary output, however, the urine is diluted and does not contain waste products from the filtering.
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Cardiovascular
(1) Initially hypotension followed by hypertension after fluid overload. (2) Congestive heart failure. (3) Dysrhythmia, frequency secondary to the increase in potassium. (4) Pericarditis, pericardial effusion.

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 c. Respiratory. (1) Pulmonary edema due to congestive heart failure. (2) Kussmaul breathing due to metabolic acidosis.

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 d. Gastrointestinal. (1) Nausea, vomiting, anorexia, and diarrhea. (2) Stomatitis and GI bleeding.

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 e. Hematologic (1) Anemia occurring within the first two days. (2) Leukocytosis. (3) Inadequate platelet functioning.

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f. Neurologic. (1) Change in level of consciousness. (2) Memory impairment. (3) Convulsions.

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g. Fluid and electrolyte balance. (1) Fluid retention. (2) Hyperkalemia. (3) Hyponatremia (usually dilution). (4) Metabolic acidosis from accumulation of acid waste products.

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CLINICAL FINDINGS
OLIGURIC PHASE DIURETIC PHASE

CONVALESCENT PHASE

Hypernatremia Hypocalcemia Hyperkalemia

Hyponatremia Hypokalemia Hypovolemia

Normal Urine Volume

Increase in LOC
BUN stable and normal May develop CRF

Hyperphosphatemia
Hypermagnesemia Metabolic acidosis
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Diagnostics
a. Elevated scrum creatinine, BUN, and potassium. b. Urinalysis- proteinuria, casts, RBC, and specific gravity is decreased.

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Treatment
1. Medical. 2. Dietary. 3. Dialysis

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Medical
a. Identify and treat precipitating cause of acute renal failure (management varies according to prerenal, intrarenal, or postrenal disorder). b. Diuretic therapy-LASIX, EDECRIN, MANNITOL.

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 c. Decrease serum potassium. (1) Administration of glucose and insulin- promotes potassium to move into the cells. (2) IV administration of soda bicarbonate- correct metabolic acidosis and causes electrolyte shift.
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 3) IV administration of calcium gluconate-antagonizes the adverse cardiac effects of hyperkalemia. (4) Administration of a cation exchange resin (KAYEXALATE) by mouth or retention enema.

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Dietary
a. Fluid restriction, intake may be carefully calculated with output. b. Protein, potassium, and sodium intake is regulated according to serum plasma levels. c. Increased carbohydrate intake, protein of high biologic value.

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NURSING CARE
Monitor fluid and electrolyte balance.

Monitor alteration in fluid volume.

Promote optimal nutritional status

Prevent complications from impaired mobility

Prevent fever and infection

Support client/S.O. & reduce/relieve anxiety
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Chronic Renal Failure

CRF is a progressive, irreversible reduction in renal function such that the kidneys are no longer able to maintain the body environment. Gradual, Progressive irreversible destruction of the kidneys causing severe renal dysfunction. The GFR gradually decreases as the nephrons are destroyed.
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 The result is azotemia to UREMIA

The nephrons left intact are subjected to an increased work load, resulting in hypertrophy and inability to concentrate urine.

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 It occurs in stages, is irreversible, and results in uremia or end-stage renal disease CRF affects all of the major body systems and requires dialysis or kidney transplant to maintain life

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 Hypervolemia can occur owing to the inability of the kidneys to excrete sodium and water, or hypovolemia can occur owing to the inability of the kidneys to conserve sodium and water

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Chronic Renal Failure

Predisposing factors: DM= worldwide leading cause Recurrent infections Exacerbations of nephritis urinary tract obstruction hypertension
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Causes
a. May follow ARF b. Chronic glomerulonephritis and pyelonephritis. c. Chronic hypertension. d. Diabetic nephropathy.

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 e. Nephrosclerosis and renal artery disease. f. Renal artery occlusion g. Chronic urinary obstruction h. Recurrent infections

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i. Hypertension j. Metabolic disorders k. Diabetes mellitus l. Autoimmune disorders

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 m. Polycystic kidney disease. n. Renal disease secondary to nephrotoxic drugs or chemicals. o. Lupus erythematosus.

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Loss of Neprhons

Glomerular hypertrophy and inc. SNGFR

Glomerulosclerosis

Accumulation of solute

Tubular hyperthrophy

High intraglomerular Pressure and inc. filtration of macromolecules Inc. excretion of Solute per nephron

Systemic Hormonal Changes in blood

Tubular cell damage & interstitial fibrosis

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Extrarenal organ Damage; uremic Syndrome;toxic Effects on renal cells

Maintenance of internal Environment up to limits of Nephron adaptation And hyperthrophy

Pathophysiology of CRF

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Chronic Renal Failure

PATHOPHYSIOLOGY As renal functions decline

Retention of end-products of metabolism
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Chronic Renal Failure

PATHOPHYSIOLOGY STAGE 1= reduced renal reserve, 40-75% loss of nephron function STAGE 2= renal insufficiency, 7590% loss of nephron function STAGE 3= end-stage renal disease, more than 90% loss. DIALYSIS IS THE TREATMENT!
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Stages of Chronic Renal Failure

STAGE I: DIMINISHED RENAL RESERVE STAGE II: RENAL INSUFFICIENCY STAGE III: END STAGE

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CLINICAL FINDINGS STAGE 1

Diminished Renal Reserve

STAGE 2
Renal Insufficiency

STAGE 3
End Stage

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Diminished renal reserve

a. Normal BUN and serum creatinine. b. Absence of symptoms. c. Renal function is reduced d. No accumulation of metabolic wastes e. The healthier kidney compensates f. Nocturia and polyuria occur as a result of decreased ability to concentrate urine
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Renal insufficiency
a. GFR is 25 percent of normal. b. BUN and serum creatinine increased (azotemia). c. Fatigue and weakness, mild anemia.

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 d. Headaches, nocturia, and polyuria. e. Metabolic wastes begin to accumulate f. Oliguria and edema occur as a result of decreased responsiveness to diuretics

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End-stage renal failure (uremia)

Excessive accumulation of metabolic wastes Kidneys are unable to maintain homeostasis Dialysis or other renal replacement therapy is required

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Assessment
a. GFR is less than 10 percent of normal. (1) Severe azotemia. (2) Hyperkalemia, hypernatremia and hyperphosphatemia. (3) Metabolic acidosis. (4) Decreased urine output
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 b. Urinary system-specific gravity of urine fixed at 1.010, proteinuria, casts, pyuria, hematuria, oliguria eventually leads to anuria. c. Endocrine system-hypothyrodism hyperparathyroidism, amenorrhea, infertility, sexual dysfunction (impotence), decreased libido
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 d. Hematologic system-anemia and bleeding. e. Cardiovascular system- Fluid overload and signs of heart failure, hypertension, CHF, ASHD, pericarditis, pericardial effusion.

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 f. Gastrointestinal system-anorexia, nausea, vomiting, diarrhea, ammonia (uremic fetor) odor to the breath, gastrointestinal bleeding, and peptic ulcer disease. g. Metabolic system-hyperglycemia, hyperlipidemia, gout, hypoproteinemia.
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 h. Neurologicsystem-headache, confusion and lethargy, followed by convulsions and coma, general central nervous system depression and peripheral neuropathy

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 i. Musculoskeletal system- Muscle twitching and numbness of the extremities, weakness and fatigue, renal osteodystrophy, tissue calcification.

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 j. Respiratory system - Kussmaul respirations k. Integumentary system -Uremic frost: a layer of urea crystals from evaporated perspiration that appears on the face, eyebrows, axilla, and groin in clients with advanced uremic syndrome
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Chronic Renal Failure

Dermatologic CNS CVS
Pulmo Hema
dry skin, pruritus, uremic frost seizures, altered LOC, anorexia, fatigue Acute MI, edema, hypertension, pericarditis

Uremic lungs Anemia

loss of strength, foot drop, osteodystrophy

Musculoskeletal
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CLINICAL FINDINGS
Nausea and vomiting Uremic frost

Decreased urinary output

Azotemia Hypertension (later) Convulsions Pericardial friction rub
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Dyspnea
Hypotension (early) Lethargy Memory impairment CHF
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Diagnostics
a. Increased BUN and serum creatinine level. b. Decreased urinary creatinine clearance. c. Elevated blood sugar and triglycerides. d. Increased scrum potassium. e. Anemia (decreased hemoglobin and hematocrit).
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Treatment
1. 2. 3. 4. Medical. Dietary. Dialysis. Surgical-.kidney transplant.

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Medical
a. Measures to reduce scrum potassium (see discussion under acute renal failure). b. Administer antihypertensives (ALDOMET, APRESOLINE, INDERAL, CATAPRES). c. Diuretics-Thiazide diuretics may be used early, the loop diuretics, (LASIX), are used later.
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Important Drugs
Aluminum hydroxide (Amphogel) Kayexalate Binds with PHOSPHATE to decrease phosphorus Binds with POTASSIUM to manage hyperkalemia

Diuretics

To decrease edema

Erythropoietin (Epogen) To increase RBC

Anti-Hypertensives
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To manage Hypertension

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Dietary
a. Problems with the client losing body weight, both adipose tissue and muscle mass. b. Restricted protein intake, may vary from just a decrease in protein intake, to a specific 20 to 40 gm per day.

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 c. Protein should be of a high biologic value, this enhances the utilization of the amino acids, and forms less nitrogen waste products. d. Water restriction-adjusted according to urinary output-if no urine output 100 cc/day.

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 e. Sodium and potassium restrictionbased upon laboratory values. f. Keto acid supplements-help maintain a positive nitrogen balance (Shohl's solution).

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NURSING CARE:
Prevent neurologic complications. Promote optimal GI function. Monitor/prevent alteration in F/E. Promote maintenance of skin integrity. Monitor for bleeding complications, and prevent injury.
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NURSING CARE
Assess for hyperphosphatemia
Paresthesias Muscle cramps Seizures Abnormal reflexes

Administer Aluminum hydroxide gels as ordered - Amphogel, AlternaGEL Promote/maintain maximal cardiovascular function.
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Provide care for client receiving dialysis.

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Surgical-kidney transplant
a. Recipient criteria: candidates are evaluated on an individual basis as to how well they would benefit from the transplant. (1) Candidates are usually under 70 years old, have a life expectancy of at least two more years, and have reasonable expectations that the transplant will improve the quality of life.
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 (2) Clients with uncontrolled malignancies, COPD, severe cardiac problems, severe systemic diseases are not good transplant candidates. b. Donor criteria: live related donors (LRD) provide the best possible match; when they are not available, then cadaver donors are considered.
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 (1) Either type of donor must he evaluated for adequate tissue matching. (2) The cadaver donor must meet the criteria for brain death. (3) The cadaver donor should be free from all systemic diseases, and have normal renal perfusion and function.
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Thank you!!!

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Nursing Intervention (ARF)

Goal: To maintain client in normal homeostasis and preserve renal function while the kidneys are repairing. 1. Accurate intake and output. 2. Daily weight (may lose .2 to .3 kg/day during oliguric phase).

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 3. Assess for hypervolemia during the oliguric Phase, fluctuations of sodium and potassium levels, cardiac dysrhythms. 4. Identify and monitor high-risk clients.

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 5. Evaluate for postural hypotension. 6. Support the client in relation to symptoms occurring in other body systems.

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 Goal. To prevent infection. 1. Avoid indwelling catheter if possible. 2. Assess for development of infectious processes. Client at increased risk due to compromised immune system.

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 Goal: to prevent skin breakdown. 1. Frequent turning and positioning, inspect the skin for problem areas. 2. Beds and protective devises to prevent pressure areas (decubitus ulcers). 3. Frequent range of motion and activities to increase circulation.
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 Goal: To provide emotional support. 1. Always explain procedures. 2. Provide honest information regarding progress of condition. 3. Encourage client to express fears and concerns regarding condition.

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Nursing Intervention(CRF)
Goal: to assist the client to maintain homeostasis. 1. Evaluate adequacy of fluid balance. a. Daily weight. b. Postural hypotension. c. Level of fluid intake. d. Discuss with the client how to monitor the fluid intake and plan for the allocated amount to be distributed over the day.
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 2. Encourage adequate nutritional intake within dietary guidelines. a. Relieve GI dysfunctions prior to serving meals. b. Plan diet according to client preferences if possible. c. Advise client that most salt substitutes contain potassium and should not be used.
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3. Prevent problem of constipation. a. Include bran in diet. b. Stool softeners. 4. Avoid use of sedatives and hypnotics, increased sensitivity to these medications due to decreased ability of kidney to metabolize them.

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 5. Monitor electrolyte balance, especially level of potassium. 6. Assess cardiovascular status to determine how effectively the client is compensating with the increased fluid load, and increased work load on the heart from the chronic anemic state.

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 7. Assess client for bleeding tendencies related initially to decrease in production of erythropoietin, and decreased platelet adhesiveness. 8. Evaluate client for pruritus and assist with measures to decrease the skin irritation and itching.
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 Goal: to provide emotional support and promote psychological/equilibrium. 1. Encourage client to express concerns. 2. Recognize that the long-term management of a chronic disease may lead to anxiety and depression.
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 3. Encourage ventilation of feelings regarding life style changes. 4. Make available to client and family members other renal clients who are undergoing the same treatment approaches.

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 Goal: to provide preoperative care for kidney transplant. 1. Maintain client's metabolic state as close to homeostasis as possiblecontinue with dialysis. 2. Tissue typing and antibody screening is con- ducted to determine histocompatibility of the donor and the recipient.
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 3. Administer immunosuppressant drugs- IMURAN, and prednisone, and cyclosporin. 4. Conduct routine preoperative procedures.

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