1. Nursing Management Renal and Urologic Problems
Chapter 46
Nursing Management Renal and Urologic Problems
S. Buckley, RN, MS
Mosby pp
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

2. Infectious and Inflammatory Disorders of the Urinary System

3. Acute Pyelonephritis
Etiology and pathophysiology-inflammation of the kidney following uti. (can progress to urosepsis: systemic infection arising from urologic source)
Preexisting factor: vesicoureteral reflux, calculi, catheter, stricture, pregnancy, neurogenic bladder
Clinical manifestations-fever, chills,N&V, abrupt flank pain (CVA pain), LUTS, bacteriuria, pyuria
Diagnostic studies-u/a reveals; pyuria, hematuria, WBC casts, CBC, blood cultures
Collaborative care and drug therapy-urine for C&S, imaging: ultrasound, increase, NSAIDs, fluids, antibiotics (ampicillin, vancomycin, cipro), analgesia (pyridium), severe cases require hospitalization, emotional support, follow up, education.
Colonizaion and infection of lower urinary tract via ascending urethral route, although can occur through the bloodstream bacteria same as uti, , preexising factor is vesicourteral reflux (retrograde or backward movement of urine from lower to upper urinary tract) or dysfunction of lower urinary tract from obstruction (to BPH, stricture or stone. Residents of snf urinary tract catheterization and use of indwelling catheters is common cause of pyelonephritis and urosepsis.
Manifestations: CVA-costovertebral tenderness (costovertebral angle), LUTS-lower urinary tract symptoms: characteristic of cystitis: dysuria, urgency, frequency.
Pyuria=WBC in urine (pus)cloudy, assoc. with uti
Bacteriuria=bacteria in urine without symptoms of uti or pyelonephritis, usually precedes symptoms of uti. Common in elderly women and in pts with indwelling urinary catheters. Screening recommended for pregnant women at weeks.
Collaborative care-IVP and CT require IV injection of contrast not obtained in early stages por pyelo to prevent possible spread of infection. Ultrasound and u/a are preferred tools.
Blood cultures used for increased temp or if bacteremia (bacteria in blood)
Tx: antibiotics, p. 1162, ampicilllin, vancomycin for less severe symptoms, bactrim, septra. NSAIDs are nephrotoxic, so must have adequate kidney function.
Analgesia (pyridium)

4. Fig. 46-1

5. Causes of urinary tract obstruction

7. Fig. 46-2

8. Chronic pyelonephritis
Kidney has atrophied, lost function r/t scarring. Often accompanied by hypertension, significant cause of renal failure, responsible for 11-20% of all cases of end-stage renal disease.
Symptoms: onset insidious, polyuria, nocturia, mild proteinuria,
Diagnosed by radiologic imaging and histology.
insidious-
Insidious-
Insidious-operating in a not easily apparent manner, more dangerous than seems evident. Polyuria-excessive secretion of urine, colorless, sp. Gravity is , with chronic pyelonephritis related to loss of tubular function and ability to concentrate urine. Level of renal function varies depending on whether one or both kidneys are affected, the magnitude of scarring and the presence of coexisting infection. Often progressed to end-stage renal disease when both kidneys are involved, even if infection is successfully eradicated.

9. urethritis Inflammation of urethra
Causes: trichomonas, monilial infection, Chlamydia, gonorrhea.
Often sexually transmitted
Symptoms: discharge, LUTS; dysuria, urgency, frequent urination
TX: id cause, often treated with Flagyl, mycelex, nystatin (mycostatin), fluconazole (diflucan).
Symptoms may be difficult to diagnose with women, urethral discharge may not be present.
Warm sitz baths, avoid vaginal deodorant sprays, proper cleaning, avoid sexual intercourse until symptoms subside. Pts. With std’s should be instructed to refer their sex partners for eval and testing.

10. Urethral Diverticula

11. Interstitial Cystitis/Painful Bladder Syndrome
Chronic, painful inflammatory disease of the bladder, affects ~700,000 Americans/yr.
Ration women to men: 10:1
Etiology; unknown, r/t infections, nephro dysfunction.
Symptoms: urgency, frequency and pain, relieved with urination, exacerbated with sexual intercourse.
Painful bladder syndrome: pain related to bladder filling in absence of uti.
Diagnosis by exclusion; pain despite absence of uti.
Collaborative care and drug therapy-dietary, lifestyle changes
Nursing management: Interstitial cystitis/painful bladder syndrome-relieve anxiety, monitor u/o and possible uti, lifestyle changes, push fluids
Use of Prelief (calcium gycerophosphate-alkalinizes urine)
Lifestyle changes, increase water, eliminate foods that are spicy, or irritating, coke, etc. , decrease stress, altering positions with sex. Antidepressant, Elavil, Aventyl to reduce burning pain and frequency.
Foods that irritate bladder; caffeine, alcohol, citrus, cheese, vinegar, curries, peppers, anything that lowers urine ph.

12. Renal Tuberculosis Secondary to TB of lung
5-8 yrs after primary disease
Symptoms: low grade fever, cystitis, epididymitis, renal colic, lumbar and iliac pain, hematuria.
diagnosis-based on tb bacilli in urine and IVP
Tx-similar to tx for tb, depends on stage of disease and renal involvement.

13. Immunologic Disorders of the Kidney

14. Glomerulonephritis
Immunologic process resulting in inflammation of the glomerulus.
3rd leading cause of renal failure in the US.
Autoantibodies production stimulated by exogenous agents (hydrocarbon, viruses (hep. B, C, rubella, bacteria (streptococcal), chemicals, drugs), diseases or endogenous (SLE)
Clinical manifestations: hematuria, excretion of RBCs, WBC, casts, decrease GFR, azotemia, oliguria, hypertension, periorbital edema
Overview affects both kidneys, affects glomerulus as primary site , can also impact tubular, interstitial and vascular areas.
all forms characterized by accumulation of antigen, antibody and complement in the glomerulli, which can result in tissue injury. The immune complexes activate complement, complement activation results in the release of chemotactic factors that attach polymorphonuclear leukocytes, histamine and other inflammatory mediators. The end result of these processes is glomerular injury.
Acute post-streptococcal glomerulonephritis is a rare kidney disease that develops after infection with a specific strain of the Streptococcus bacterium. According to the Children’s Hospital of Boston, acute post-streptococcal glomerulonephritis is one of the most common causes of glomerulonephritis in children. Although this condition can affect people of any age, it is most common among children who are 6 to 10 years old.
Function
Glomerulonephritis is an inflammation of the glomeruli in the kidney. Glomeruli are small structures that direct the blood supply to the nephrons, the units responsible for filtering the blood and removing waste products into the urine. When the glomeruli become inflamed, it impairs the kidney’s ability to filter the blood. This causes the presence of blood and protein in the urine.
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Causes
Acute post-streptococcal glomerulonephritis occurs after a recent infection with group A beta hemolytic streptococcus bacteria. Group A strep is the bacteria that causes strep throat, as well as cellulitis, a skin infection. According to Medline Plus, post-strep glomerulonephritis can occur 1 to 2 weeks after an untreated throat infection or about 3 to 4 weeks after cellulitis.
Symptoms
According to the Merck Manuals, about half of patients with post-streptococcal glomerulonephritis do not develop symptoms. Of those who do, the first symptom that develops is edema, or swelling. This occurs as the kidney becomes damaged and loses its ability to process urine, leading to fluid retention. The swelling first becomes apparent in the face and as puffiness around the eyes. As the kidney becomes more damaged, high blood pressure develops, which can cause headaches and blurry vision.
Identification
Apart from the history of recent strep infection and the symptoms of glomerulonephritis, lab work can help identify children with post-streptococcal glomerulonephritis. Recent strep infection can be confirmed with a blood test called ASO titer, which measures the presence of antibodies against the strep bacterium. Blood test can also confirm if there is damage to the kidneys. Another useful tests is a urinalysis to assess the presence of blood and protein in the urine, another indication of kidney damage. If the diagnosis is still in doubt, a kidney biopsy may be necessary.
Treatment
There is no specific treatment for post-streptococcal glomerulonephritis because most children recover from this condition on their own. This recovery may take weeks or months. In the meantime, children may need medication to treat the high blood pressure or the swelling. A low-salt diet also helps during the recovery phase.
characterized by hematuria, diminished gfr, azotemia (presence of nitrogenous wastes in blood), oliguria, hypertension. It lis caused by an inflammatory response of the endothelial cells of glameruli, the inflammatory process damage at the capillary wall, permitting red blood cells to escape into the urine and produce hemodynamic changes that decrease the gfr. Antibody/antigen response can come from endogenous origin (SLE), or from exogenous, such as strep., viral agent (mumps, measles, chickenpox) Capillary membrane swells and becomes permeable to plasma proteins and blood cells. Usually follow 7-12 days post strep infection oliguria develops as the gfr decreases, proteinuria and hematuria follow because of the increased glomerular capillary wall permeability. The blood is degraded by materials in the urine and a cola colored urine may be the 1st sign of disorder.fluid retention occurs as a result of decreased glomerular filtration. The edema appears initially in low-pressure tissues, such as around the eyes, but later progresses to involve the whole body as ascites or peripheral edema in the legs.. Sodium and water retention gives rise to edema, particularly of the face, hands, and hypertension.

16. Acute Poststreptococcal Glomerulonephritis
Clinical manifestations and complications-develops 5-21 days post infection of throat by strep.
Diagnostics: hx, physical assessment, CBC, throat swab
Tx; rest, sodium and fluid restriction, diuretics, antihypertensive therapy, emotional support, education, decrease dietary protein.Antibiotics(if strep still present), corticosteroids.
Lab=to determine presence of B hemolytic step (throat swab),tx-dietary protein intake may be restricted if there is evidence of an increase in nitrogenous wastes wastes (elevated BUN). Restriction varies with the degree of proteinuria (low protein, low sodium, fluid restriction).
Early prevention is swabbing of throats to encourage early diagnosis and treatment of sore throats and skin lesions. If step found in culture, TX is penicillin, pt must take full course. If cutaneous strep, remember hygiene.

17. Chronic glomerulonephritis
End stage of acute disease
Symptoms: proteinuria, hematuia slow development of uremia, progresses toward renal failure
Dignostic: u/a, vs, ultrasound, CT, renal biopsy
Tx-supportive an symptomatic: control hypertension and uti’s, protein and phosphate restriction may slow the rate of progression.
Can take 30 years to reach failure. Usually found coincidentally when u/a or elevated blood pressuere is detected.

18. Nephrotic Syndrome
results when: glomerulus is permeable to plasma protein, causing proteinuria, low plasma albumin and tissue edema
Symptoms: peripheral edema, massive proteinuria, hypertension, , hyperlipidemia, hypoalbuminemia, ascites, anasarca, calcium abnormalitiesaltered immune response, altered coagulation (hyper)
Collaborative care-symptom management; relieve edema, cure primary disease, low Na diet, low protein, diuretics, NSAIDs, anticoagulant therapy, corticosteroids.
Common causes: glomerulonephritis, SLE, DM, bacterial , viral, HIV, malari, humors, leukemias, allergens, (bee sting, pollen), drugs: NSAIDs, Penicillin, Herion
Ascites-edema in abdomen, anasarca-massive generalized edema=develop in response to hypoalbuminemia.
Altered immune response: diminished plasma oncotic pressure from the decrease serum proteins stimulates hepatic lipoprotein synthesis=hyperlipidemia. Immune responsis are altered, as a result infection is an importan cause of morbidity and mortality. Calcium abnormalities=poor bone density, skeletal abnormalities; hypocalcemia, hyperparthyroidsim, osteomalcia.
With proteinuria, loss of clotting factors can result in a hypercoagulable state., resulting in thrombus formation Renal vien is most common site. PE=40%.
If urine excretion of protein exceeds 10g/24hrs, may need to increae dietary protein.
Major nursing intervention is related to edema.

19. Nephrotic syndrome nursing interventions
Control edema: daily weights, I & o, girth or extremity size, bp, trending of data, care of skin (hygiene and avoid trauma)
May become malnurished, may become anorexic; serve small, frequent meals: low na, low protein
Susceptible to infections; avoid exposure, emotional support re: poor body image
Educate

20. Obstructive Uropathies

21. Renal disease and HIV
Incidence of renal disease and HIV is about 10% (higher with IV drug use)
Syndromes: proteinuria, nephrotic syndrome, nephropathy -progressing to end stage renal disease and acute renal failure (mostly in pts with AIDs)
Survival and recovery depends on the treatment of the primary cause.

22. Obstructive Uropathies
Any anatomic or functional condition that blocks or impedes the flow of urine, may be congenital or acquired.

23. Fig. 46-3

24. hydronephrosis
Results from obstruction in urinary system, causing reflux of urine and increased pressure, ureteral dilation, kinking, and dilation and or enlargement of the renal pelves and calyses.
Causes pyelonephritis and renal atropy.
If one kidney involved, other will compensate.
Symptoms: alterations in kidney function (per assessment, labs; increased BUN, creatinine, oliguria or anuria.
Tx=location and relief of blockage. May include insertion of a urethral or ureteral stent, surgical correction, or diversion of the urinary stream above the level of blockage.

25. Fig. 46-4
hydronephrosis

26. Urinary Tract Calculi
500,000 people/yr develop lithiasis, more common in warm climates (dehydration)
Various types of calculi (p.1170), recurrence of stones -50%.
Clinical manifestations-Pain in flank area (depends on location of stone), severe, hematurin, reanl colic, N&V,
Diagnostic studies-u/a, culture,VP, ultrasound, cystoscopy.
Collaborative care-keep urine dilute and free flowing,reduces risk of formation., analyze stone to determine cause and prevent recurrance; screening of urine, CBC, urine ph.
Endourologic procedure-bladder-cystoscopy, ureteroscopes,
Lithotripsy-pulverizes stons with ultasonic vibrations.
Surgical therapy-nephrolithotomy-incision into kidney to remove stone
Factor involed include, hot climates (dehydration, low fluids. Low urine volume and increased solute in urine, genetics, lifestyle. The higher the ph (alkaline) the less soluble are calcium and phosphate. The lower the ph (acidic), the less soluble are uric and cystine stones.
Another factor are bacterial infection of proteus, pseudomonas which cuse the urine to becme alkaline and contribute to stone formation. If stone in kidney is infected, may become “staghorn’ shpe. Infected stones are frequeint in pts with an external urinary devise, long-term indwelling catherter, neuorgenic bladder or ruinary retention.
No IVP will be used with pts who have renal failure.
Lithiasis-stone formation
Calculi-stone

27. Fig. 46-5

28. Fig. 46-6

29. Nursing Management Renal Calculi
Nursing assessment-screen for litiasis, mange acute attack; pain control (opiods), infection and/or obstruction elimination , hx, increase fluids (3000ml/day) after acute attack, discourage foods that increase stones.
Diet; low na, modify depending on type of stone (p.1171)
During attack , do not force fluids as my increase pain. Up to 85% of pts could lower their risk withchanges to lifestyle and diet.

30. Strictures
Ureteral and urethral strictures-narrowing of lumen, associated with unintended reslut of sugical intervention, adhesions, scars or genetic
Symptoms: diminshed force of urinary stream, staining to void, split urine stream, frequency, nocturia. Can lead to urinary retention and uti.
Diagnostic; retrograde urethrography (RUG).
Management; dilation of stricture by stent placemtn, self-catherterization, or urethroplasty.

31. Renal trauma
Increased r/t violent crimes, mva,sports, usually younger men causing blunt trauma.
Findings; hematuria
Diagnostic: IVP, u/a, ultrasound, CT
Tx; bed rest, fluids, analgesia, surgical exploration , repair or nephrectomy.
Interventions; emotional support, pain control, monitoring for shock, monitor I&O, observe for hematuria, monitor nephrotoxic antibiotics.

32. Renal artery stenosis Partial occlusion of one or both renal arteries.
Results in hypertension and low perfusion to kidneys
Goals of therapy; control hypertension , increase profusion.
Collaborative care; percutaneous transluminal renal angioplasty, surgical revascularization of kidney.
R/t atherosclerotic narrowing. When hyperteinsion develop abuptly rean arterhy stenosis should be considered.

33. Hereditary Renal Diseases

34. Polycystic Kidney Disease
Most common life-threatening genetic disease in the world, affecting 600,000 in US, 12.5/world!!
Accounts for 10-15% of chronic kidney disease.
2 forms (childhood (rare), adult). Adult: autosomal disorder, involves both kidneys, cysts destroy surrounding tissue, filled with blood, pus.
Clinical manifestations-hypertension, hematuria, feeling of heaviness in back, may have uti, chronic pain, palpable kidneys, effects other organs
Effects other organs:heart, liver, intestines; results in liver cysts, abnormal heart valves, aneurysms, diverticulosis.

35. PKD
Diagnosis based on hx, IVP, ultrasound, CT. Usually progresses to end-stage renal failure.
Collaborative care; no specific tx. Major aim is to prevent infections and symptoms. Kidney transplant is only cure.
Nursing interventions: management of end-stage renal disease.

36. Fig. 46-7

37. Fig. 46-8

38. Instrumentation Urethral catheterization Ureteral catheters
Suprapubic catheters
Nephrostomy tubes
Intermittent catheterization

39. Fig

40. Surgery of the Urinary Tract

41. Renal and Ureteral Surgery
Preoperative management
Postoperative management
Urine output
Respiratory status
Abdominal distention
Laparoscopic nephrectomy

42. Urinary Diversion Incontinent urinary diversion
Continent urinary diversions
Orthotopic bladder substitution

43. Fig

44. Fig

45. Fig

46. Nursing Management Urinary Diversion
Preoperative management
Postoperative management

47. Fig

48. Fig