Urinary Tract Infections (UTIs)

Urinary and Renal Disorders

Urinary Tract Infections

• Routes of infection include transurethral (ascending from the meatus which is most common), via bloodstream, and fistula (direct communication with the intestine).
• Women have a short urethra, which is a problem after sexual intercourse.

Cystitis (Lower/Bladder)

• Manifestations include frequency, urgency, nocturia, incontinence, and suprapubic/pelvic pain.
• A complicated manifestation is urosepsis.
• Bacteriuria increases with age and disability.
• UTIs are the most common infection of older adults.
• Confusion is often the presenting symptom in older adults.
• In women, UTIs occur more often due to frequent incomplete emptying of the bladder and urinary stasis.
• Antibacterial properties of prostatic secretions protect men from bacterial colonization.
• Prostatitis is the most common cause of UTIs in men.
• UTIs in men may result from poor bladder tone or neurogenic bladder from stroke, autonomic neuropathy from DM.
• UT incidence in men increases with confusion, dementia, bladder or bowel incontinence.
• Antibiotics is a treatment, either by mouth in the absence of sepsis as outpatient, or IV if septic - inpatient.
• Increase fluid intake, provide patient education, and encourage cranberry juice for prevention.
• Ensure to follow up if symptoms persist.

Pyelonephritis (Upper/Renal Pelvis)

• Manifestations include Chills, fever, leukocytosis, bacteriuria, pyuria, low back pain (costovertebral angle/flank), urgency, frequency
• A complicated manifestation is urosepsis.
• Treatment is the same as cystitis with Antibiotics (By mouth in the absence of sepsis - as outpatient, IV if septic - inpatient).
• Hydration is essential being 3 – 4 liters/day.
• Monitor and treat fever.
• Educate patient particularly on prevention.

Urinary Tract Infections: Nursing Management

• Hygiene includes showers not baths, cleaning perineum front to back when toileting.
• Drink liberal amounts of fluids to flush out bacteria, and at least incorporate one glass of cranberry juice a day.
• Avoid coffee, tea, colas, alcohol and other urinary tract irritants.
• Void every 2-3 hours and completely empty bladder to avoid compromised blood flow to bladder that occurs with overdistension.
• Women should void after sexual intercourse.
• Complete the whole course of antibiotics.

Glomerulonephritis

• This is an immune-mediated problem that results in glomerular inflammation.
• It is a common cause of end-stage kidney disease.
• Etiology is autoimmune or secondary to other systemic disorders resulting in an immune response.
• Causes/triggers can be infectious such as poststreptococcal, viral (hepatitis, HIV), endocarditis, sepsis, or pneumococcal PNA.
• Immune causes include Goodpasture syndrome, IgA nephropathy, and SLE.
• Amyloidosis and illegal drug use are other causes.
• Pathology involves immune complexes being deposited in the glomeruli, and complement being activated, resulting in tissue injury.
• Manifestations include edema, hypertension, oliguria, hematuria (rusty, cola-colored urine), proteinuria, +ASO titer (if strep induced), +erythrocyte casts in urine.
• Flank pain may be a manifestation.
• Diagnosis includes renal biopsy (see also manifestations above), ultrasound, and CT.
• Management focuses on treating symptoms such as hypertension, sodium/fluid restriction, and reduced dietary protein (if elevated BUN).
• May need antibiotics or steroids, or dialysis/plasmapheresis.
• Some patients with glomerulonephritis develop chronic glomerulonephritis.
• Goodpasture Syndrome is an autoimmune disorder in which antibodies develop against glomerular and alveolar basement membranes.

Nephrotic Syndrome

• Syndrome characterized by increased glomerular permeability, manifested by massive proteinuria and hypoalbuminemia.
• Characterized by high levels of urinary elimination of protein.
• Syndrome is not kidney specific but is a collection of clinical findings.
• Etiology results from any condition that seriously damages the glomerular capillary membrane.
• Results in increase in renal permeability to protein, and increased excretion of protein.
• Causes not always immune-mediated.
• Multisystem diseases include DM, systemic lupus erythematosus (SLE), and amyloidosis.
• Glomerular disease is glomerulonephritis.
• Infections can be bacterial, viral, and/or protozoal.
• Cancer, allergens, and drugs (NSAIDs, ACE I, penicillamine, heroin) are further causes.
• Manifestations include hypoalbuminemia, hyperlipidemia from liver response to the low albumin, and increased lipoprotein production in liver.
• Hypercoagulability [clotting factors (proteins) lost in the urine].
• Decreased serum protein results in significant edema, and may result in ascites, periorbital, and dependent edema.
• Can also result in anasarca.
• Decreased intravascular volume stimulates RAAS, increasing Na and water retention, worsening symptoms.
• Hypertension, anorexia, inadequate nutrition are further manifestations.
• Decreased plasma oncotic pressure, serum protein, and albumin.
• Elevated lipids are present, initially LDL, cholesterol, and then triglycerides.
• Altered immune responses, and infection are frequent causes of death.
• Hypercoagulability with thromboembolism (most often renal vein and PTE): lose thrombolytic factors antithrombin III and plasminogen.
• Diagnosis includes renal biopsy, urinalysis, and serum chemistries.
• Management depends on the cause – treat the cause, the associated symptoms and complications, steroids, ACE I to reduce proteinuria (by reducing intraglomerular pressure), low to moderate protein and low Na diet, antilipidemics, diuretics.
• Management of edema and related skin issues.
• Marked edema results in body image issues.

Acute Kidney Injury (AKI)

• Characterized by a rapid loss of renal function due to kidney damage.
• Can be pre-renal: good kidney, bad neighborhood.
• Can be intrarenal: bad kidney
• Can be postrenal: good kidney, bad neighborhood.

Prerenal Failure: Good Kidney, Bad Neighborhood

• Cause by drop in renal perfusion.
• Result of volume depletion.
• May be due to GI losses, hemorrhage, renal losses such as osmotic diuresis in DKA/HHS.
• Impaired cardiac output from cardiogenic shock, arrhythmias, MI, HF
• Profound vasodilation is a cause, and can result from sepsis.

Intrarenal Failure: Bad Kidney

• Prolonged renal ischemia.
• Transfusion reaction, or rhabdomyolysis/myoglobinuria (trauma, crush injuries, burns) are causes.
• Nephrotoxic agents include aminoglycoside antibiotics (vancomycin, gentamicin, tobramycin), ACE I, heavy metals (lead, mercury), NSAIDs, and iodine-based contrast.
• Infectious processes includes glomerulonephritis and acute pyelonephritis.

Postrenal Failure: Good Kidney, Bad Neighborhood

• Caused by obstruction due to BPH, blood clots in urinary tract, calculi (stones), strictures in urinary tract, and tumors.

ΑΚΙ Diagnostics

• Includes urinalysis, that shows low specific gravity, and casts (cellular debris).
• Renal ultrasound is used for anatomic changes.
• Serum electrolytes show hyperkalemia and hyponatremia, hypocalcemia, and hyperphosphatemia.
• Hyperkalemia has normal protein breakdown, results from diet, blood in GI tract or blood transfusion, and electrolyte shift that occurs in metabolic acidosis with K+ shifting into serum.
• Elevated BUN and creatinine is present too.
• CBC shows anemia due to lack of erythropoietin.
• Glomerular Filtration Rate (GFR) declines.
• Metabolic acidosis is present by the inability to eliminate acid substances produced in metabolism.

AKI: Management

• Goals include eliminate cause, maintain fluid balance since fluid volume overload is the major issue, and avoid further fluid overload.
• Consider renal replacement therapy, when indicated: hemodialysis, peritoneal dialysis, or CRRT which is continuous renal replacement therapy.

AKI: Management (cont.)

• Pharmacologic management include: hyperkalemia is the most life-threatening F & E problem, so administer Kayexalate, Insulin (check glucose level!), and Calcium gluconate.
• Monitor medications with potassium in them (penicillin VK) or that raise potassium levels (potassium-sparing diuretics).
• Administer phosphate-binding agents and erythropoietin (Epogen).
• Provide Sodium bicarbonate in severe acidosis.
• Nutrition includes low protein, high carbohydrate, low potassium, low sodium, low phosphorous (and phosphate binding agents), and healthy fats only.
• Implement fluid restriction with AKI.

ΑΚΙ: Management with Renal Replacement Therapy

• Indications include severe acidemia, azotemia (BUN >90) which results in uremia, mental changes, neuropathy, pericarditis, and severe hyperkalemia with hyponatremia.
• Options are continuous renal replacement therapy (CRRT) for continuous removal of toxins from plasma in only an ICU setting, hemodialysis, and peritoneal dialysis.

AKI: Additional Nursing Considerations

• Monitor for complications such as arrhythmias, metabolic acidosis, pulmonary edema, etc. with a major area of focus on fluid volume overload and hyperkalemia.
• Gerontologic considerations state half of all who develop AKI in the hospital are >60 y/o.
• Inadequate hydration (limited access, bedrest, confusion) leads to prerenal failure.
• Common etiologies include nephrotoxic agents.

Chronic Kidney Disease (CKD/ESKD)

• This involves renal function decline.
• End products of metabolism (excreted in urine) collect in the blood and uremia impacts every body system.
• GFR decreases and increases BUN and creatinine.
• Remember creatinine is a better measure of renal function.
• BUN is also affected by protein intake
• Hypervolemia and hyponatremia occur.
• Heart failure, edema, and HTN are a result.

CKD: What Happens?

• Acidosis: Kidneys are unable to excrete increased acids and ammonia in the blood stream.
• Kidneys are unable to reabsorb sodium bicarbonate with decreased excretion of phosphate, resulting in acid accumulation.
• Anemia: From reduced Erythropoietin, nutritional deficiencies, bleeding tendency (especially GI bleeds), and shortened RBC lifespan.
• Electrolyte disorders involving Calcium(low) and Phosphorous (high) Imbalance, hyperkalemia, and hyponatremia.

Stages of Chronic Kidney Disease

• Stage 1: Kidney damage with normal or increased GFR
• Stage 2: Mild decrease in GFR
• Stage 3: Moderate decrease in GFR
• Stage 4: Severe decrease in GFR
• Stage 5: End Stage Kidney Disease (ESKD) or Chronic Kidney Disease (CKD)

CKD: Uremia

• This describes the toxic effects of high levels of urea (BUN by lab) on the body.
• Most commonly occurs in chronic kidney disease, but may also be present in acute kidney injury.
• Multisystem effects of decreased renal function involves renal, cardiovascular, pulmonary, neurologic, and gastrointestinal.
• Renal issues: Decreased urine output leads to fluid retention/edema and electrolyte disorders.
• Cardiovascular/Perfusion: HTN and Arrhythmias.
• Pulmonary/Ventilation: Pulmonary edema, dyspnea, Kussmaul's respirations.
• Neurologic: Toxins build up leading to LOC changes.
• Gastrointestinal: Nausea, vomiting, changes in taste, mouth sores.
• Integumentary: skin texture changes (dry, scaly, petechiae/ecchymosis); skin color changes (yellow/gray, pale).
• Musculoskeletal: Renal osteodystrophy.
• Hematological/Immunological: Anemia, bleeding tendencies, infection.
• Metabolic: Waste product accumulation, elevated triglyceride levels, altered carbohydrate metabolism (insulin).
• Calcium and phosphorous abnormalities and osteodystrophy, as well syndrome of skeletal changes.
• This is a result of alterations in calcium & phosphate metabolism along with phosphorous not excreted by the kidney, causing bones to demineralize.
• Kidneys normally metabolizes vitamin D to active form, however, is defective with renal failure.
• Anemia is primarily due to decreased production of the hormone erythropoietin (by the kidneys), nutritional or iron deficiencies, frequent blood sampling depleting RBC.
• Elevated PTH (produced to compensate for low calcium levels) can also inhibit erythropoiesis.
• To compensate: utilize use of Exogenous erythropoietin such as Procrit or Epogen through IV or SQ 2-3 times/week, treating to a goal Hgb between 10-12 g/dL while monitoring blood pressure & iron levels.

CKD: Treatment

• Includes renal replacement therapy: hemodialysis, CRRT, peritoneal dialysis, kidney transplant, and also no treatment that includes advance directives.
• Hemodialysis includes blood filtered through a machine for 4 hours three times a week, or CRRT where Blood is filtered through a machine 24 hours a day while in the critical care setting (requires vascular access).
• Peritoneal dialysis is daily filtration accomplished using the peritoneal membrane via a tenckhoff catheter.
• Blood is filtered through a machine for 4 hours three times a week.
• Must have a thrill and bruit at access site and maintain it well.
• Complications of hemodialysis include hypotension, disequilibrium syndrome with first dialysis being most common cause, as well as loss of blood cells and muscle cramps, and hepatitis.
• Dialysis destroys blood cells and thus the loss.
• Hypotension results from rapid removal of vascular volume (hypovolemia).
• Manage disequilibrium syndrome by administering Normal saline or albumin through the dialysis machine.
• Hepatitis is a lower incidence but Hepatitis B vaccine recommended.
• Peritoneal dialysis is where excess water and solutes removed by osmosis/diffusion via the peritoneal membrane
• More gentle in that it is More gentle than hemodialysis and often easier for patients to manage at home.
• Renal transplant is the treatment of choice for CKD, while there are more patients on the waiting list.
• Kidney is transplanted from cadavers or living donors.
• It's imperative to educate renal transplant patients on signs and symptoms of UTI, and need for lifelong immunosuppressive therapy and critical to reporting a drop in urinary output.
• Stress management is essential for patient and living donors, where applicable.

Definition: Stones (calculi) occur in the urinary tract and kidney but not clearly understood.

• Factors favoring stone formation include infection, urinary stasis, and immobility.
• Altered calcium metabolism with hypercalcemia also results.
• 75% are calcium based, therefore consider possible causes of hypercalcemia.
• Hyperparathyroidism, cancers,TB, sarcoidosis, excessive vitamin D and excessive dairy intake.
• Seen more often in males.
• Treatment is to eradicate the stone through passing naturally, lithotripsy, surgery, stent placement, open removal, and nephrectomy.

Polycystic Kidney Disease (PKD)

• Genetic disorder, it is where there is growth of numerous fluid-filled cysts in the kidneys, which slowly destroy the nephrons thus enlarging the mass of the kidneys.
• Cysts can occur in the liver, blood vessels in the brain and heart.
• It is a leading cause of ESKD as it is a major inherited disorder.
• Proceeds very slowly.
• Clinical manifestations include being related to loss of renal function such as hematuria, polyuria, hypertension, development of renal calculi and associated UTI, and proteinuria.
• Assessment is a careful evaluation of family history, and palpitation of abdomen which may reveal enlarged kidneys.
• Preferred diagnostic technique is ultrasound of kidneys.
• There is no cure, and management includes supportive therapy, such as control BP, control pain, and antibiotics for UTI.
• Renal replacement therapy is crucial after kidney failure, along with family genetic counseling.