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Urinary tract infection
Infection caused by pathogenic microorganisms in the urinary tract
Classified by location
50% of all HAI
Pathophysiology of (lower) UTI
Involves the bladder and urethra
Bacteria gains access to the bladder, attaches to and colonizes the tract, evades host defenses, and initiates inflammation
Result from fecal organisms ascending from the perineum to the urethera and bladder
Reflux may occur with pressure moving urine back from the urethra to the bladder or from the bladder to the ureters
Risk factors of UTI
Female gender
Diabetes
Pregnancy
Neurological disorders
Gout
Altered states caused by incomplete bladder emptying
Decreased natural host defenses or immunosuppression
Inability or failure to empty the bladder completely
Inflammation or abrasion of the urethral mucosa
Instrumentation of the urinary tract
Obstructed urinary flow caused by:
Congenital abnormalities
Urethral strictures
Contracture of the bladder neck
Bladder tumors
Calculi (stones) in the ureters or kidneys
Compression of the ureters
Causes of (lower) UTI
Bacterial invasion
Reflux
Uropathogenic bacteria
Via ascending infection, hematogenous spread, or direct extension
Clinical manifestations of (lower) UTI
Uncomplicated lower UTI
Burning on urination
Urinary frequency
Urgency
Nocturia
Incontinence
Pain; back pain
Hematuria
Complicated UTI
Asymptomatic or septic
Clinical manifestations of (lower) UTI in older adults
Malaise
Nocturia
Urinary incontinence
Foul smelling urine
Buring
Urgency
Fever
Altered LOC
Associated priorities of (lower) UTI
Clean catch urine sample (midstream)
Catheterized urine sample
Urine cultures
100,000 CFU/ml = infection
Cellular studies
Bladder scan
Usual treatment of (lower) UTI
antibacterials/antibiotics
Bacteriacidals
Cephalosporins (ce-)
Fluroquinolones (-oxacin)
Penicillin (-icillin)
Trimethoprim-sulfamethoxazole
Urinary analgesic agent
Phenazopyridine
Turns urine orange
Nursing considerations of (lower) UTI
Pain relief
heat
Education
Increase fluids
Avoidance of irritants
Coffee, tea, citrus, spices, cola, alcohol
Frequent voiding
CAUTI
Catheter aquired urinary tract infection
Pyelonephritis
A bacterial infection of the renal pelvis, tubules, and interstitial tissue of one or both kidneys
Less common upper urinary tract infection
Causes of Pyelonephritis
Upward spread of bacteria from the bladder
spread from systemic sources reaching the kidneys via the blood stream
Bacteria from a bladder infection ascending to the kidneys
Incompetent ureterovesical valve or obstruction
Static urine increases bacterial growth
Acute manifestations of Pyelonephritis
Chills
Fever
Leukocytosis
Bacteriuria
Pyuria
Low back pain
Flank pain
Nausea
Vomiting
Headache
Malaise
Painful urination
Urgency frequency
Chronic manifestations of Pyelonephritis
No symptoms of infection unless exasterbated
Fatigue
Headache
Poor appetite
Polyuria
Excessive thirst
Weight loss
Can lead to chronic kidney disease
Associated priorities of Pyelonephritis
Ultrasound
CT scan
IV pyelogram
Urinalysis
Culture and sensitivity
Hydration
Creatinine clearance
BUN
Creatinine
Treatment of acute Pyelonephritis
Outpatient
2 weeks of antibiotics
Up to 6 weeks if infection is recurrent
Follow up urine cultures
Treatment of chronic pyelonephritis
Long term prophylactic antimicrobial therapy
Nursing considerations of Pyelonephritis
I&Os
3-4L/day recommended
Antipyretics and antibiotics
Education
Prevention of infection
Fluid intake
Emptying of bladder
Hygiene
Renal calculi
Stones in the urinary system
Urolithiasis = stones in the urinary tract
Nephrolithiasis = stones in the kidney
Pathophysiology of Renal calculi
Stones form due to increase in calcium oxalate, calcium phosphate, and uric acid in urine
Found anywhere from the kidneys to bladder
Vary in size from sand to an orange
Risk factors of Renal calculi
Slow kidney drainage
Infection
Urinary stasis
Immobility
Increased calcium levels in blood and urine
Hyperparathyroidism
Renal tubular acidosis
Cancer
Dehydration
Excess vitamin D
Excessive intake of milk
Clinical manifestations of Renal calculi
Distention of renal pelvis and proximal ureter
Blocked flow = increased hydrostatic pressure
Infection
Chills
fever
Frequency
Excruciating pain or discomfort
Hematuria
Pyuria
Tenderness
nausea , vomiting
Diarrhea and abdominal pain
s/s of Renal calculi
Renal colic
Acute, wavelike pain radiating down to the thigh and genetalia
Nausea
Vomiting
Tenderness
Associated priorities of Renal calculi
Noncontrast CT scan
Ultrasound
Blood chemistries
24 hour urine test
Diet and family history
Chemical analysis of stone once passed/removed
Usual treatment of Renal calculi
Eradicate stone
Determine type
prevent nephron destruction
control infection
relieve obstruction
NSAIDs + opioids
Ureteroscopy
Extracorporeal shockwave lithotripsy
Endourologic percutaneous stone removal
Nursing considerations of Renal calculi
Patient education
Nutrition
Fluids
s/s of UTI
Prevention of renal calculi: Education
Avoid protein intake
Limit sodium (3-4g/day)
Do not limit calcium
Avoid oxalate containing foods (spinach, chocolate, peanuts)
Fluid intake (q1-2 hours) to dilute urine
Cranberry juice everyday
Avoid activities leading to excessive sweating or dehydration
Ureteroscopy
Visualizing the stone then destroying it
Access to the stone via ureteroscope into the ureter then inserting a lazer or ultrasound device to remove stone
Stent may be put in place to keep the ureter patent
Extracorporeal shockwave lithotripsy
Noninvasis proceedure used to break up sones in the kidney
After fragmentation of the stone, remnants are spontaneously voided
High energy pressure/shock waves are generated via the abrupt release of energy transmitted through the tissues
“The nurse should apply electrodes for continuous monitoring of the client's cardiac rhythm during ESWL. This monitoring allows the provider to synchronize shock waves with the R wave.” (ATI)
Endourologic percutaneous stone removal
Nephroscope is introduced percutaneously to the renal parechyma,
depending on the size, the stone is extracted via forceps or retrieval basket
Orchitis
Acute inflammation of one or both testes as a complication of systemic infection or an extension of an associated epididymitis caused by bacterial, viral, spirochetal, or parasitic organisms
Pathophysiology of Orchitis
Microorganisms reach the testes through the blood, lymphatic system, or traveling through the urethra, vas deferens, and epididymis
s/s of Orchitis
Fever
Pain
Tenderness of the teste(s)
Testicular swelling
Penile discharge
Blood in semen
Leukocytosis
Usual treatment of Orchitis
Either bacterial or viral treatment
Bacterial
Antibiotics
Comfort measures
Viral
Rest, ice, elevation
Analgesics
Antiinflammatory meds
Epididymitis
Infection of the epididymis
Spread from an infected urethra, bladder, or prostate
Risk factors of Epididymitis
Recent surgery
High risk sexual practices
History of STI
Prostate infections or UTIs
Uncircumsized
Enlarged prostate
Indwelling catheter
Causes of Epididymitis
Infection due to E. coli
Urinary obstruction
Infection that moves upwards through the urethra en ejaculatory duct, along the vas deferense, to the epididymis
Clinical manifestations of Epididymitis
Develops over 1-2 days
Low grade fever
chills
Heaviness feeling in testicle
Tenderness
Pain
Soreness
Swelling
Discharge
Bloody semen
Pyuria and bacteriuria (pus and bacteria in urine)
Frequency
Urgency
Dysuria
Associated priorities of Epididymitis
Urinalysis
Complete CBC
Gram stain of drainage
Culture
STD and HIV testing
Usual treatment of Epididymitis
Antibiotic dependent on causitive agent
Local anesthetic to relieve pain (through spermatic cord)
Reduction in activity
Scrotal support
Antiinflamatories
Analgesics
Sitz baths
Epididymectomy for recurrent, incapacitating episodes
Nursing considerations of Epididymitis
Never ignore testicular pain (can be confused for torsion = emergency)
Bed rest
Intermittent cold compresses
Local heat
Education to avoid straining, lifting, or sexual stimulation until infection is controlled (>4 weeks)
Benign prostatic hyperplasia
Enlarged prostate
Noncancerous enlargement or hypertrophy of the prostate
Common in aging men
Pathophysiology of BPH
Usually occur with elevated estrogen levels, when the prostate tissue becomes more sensitive to estrogen and less responsive to testosterone metabolites
Enlarged lobes of the prostate may cause obstruction of the bladder neck, causing incomplete bladder emptying and retention
Risk factors of BPH
Smoking
Alcoholism
Obesity
Sedentary lifestyle
HTN
Heart disease
DM
High animal fat and protein diet
Causes of BPH
Develops over time due to
resistance on prostatic urethra to mechanical and spastic effects
bladder pressure during voiding,
detrusor muscle strength
neurologic function
general health
Clinical manifestations of BPH
Mild to sever UTI symptoms
Urinary frequency
Urgency
Nocuria
Hesitancy in starting urination
decreased/intermittent force of stream
Sensation of incomplete bladder emptying
Abdominal straining
Decrease in volume and force of stream
Retention and UTIs
Fatigue
Anorexia
Nausea
Vomiting
Pelvic discomfort
Associated priorities of BPH
History
Voiding diary; recording of voiding frequency and volume
Urinalysis for blood and UTI
Ultrasound
CBC
Cardiac and respiratory assessment
Usual treatment of BPH
Lasix/loop diuretic to promote urination
Catheterization
Alpha blockers to relax the smooth muscle of bladder neck and prostate
Alfuzosin
Terazosin
Doxazosin
Tamsulosin
Side effects
Dizziness
Headache
Fatigue
Orthostatic hypotension
Sexual dysfunction
Rhinitis
5-alpha-reducatase inhibitors for hormonal manipulation
Finasteride
Dutasteride
side effects
Decreased libido
Ejaculatory dysfunction
Erectile dysfunction
Brest enlargement
Flushing
Avoid saw palmetto and african plum
Surgical treatment of BPH
Application of heat via transurethral probe
Transurethral needle ablation and insertion of stent
Transurethral resection of the prostat (TURP)
Surgical removal of the inner part of the prostate through an endoscope inserted through the urethra
Torsion
A surgical emergency requiring immediate diagnosis to avoid loss of the testicle
Rotation of the testes, twisting the blood vessels and spermatic cord = impeding arterial and venous supply to the testicle
Clinical manifestations of Torsion
Testicular tenderness
Elevated testis
Thickened spermatic cord
Swollen, painful scrotum
s/s of Torsion
Sudden pain in the testicle
Nausea
Vomiting
Lightheadedness
Swelling
Usual treatment of Torsion
Manual untwisting
Surgery within 6 hours to untwist and anchor testes in position
Acute kidney injury (AKI)
A rapid loss of renal function due to damage to the kidneys
Rapid onset in hours and is potentially reversible
50% mortality
Pathophysiology of AKI
Not always known but may have a specific cause
May be reversible if identified and treated ASAP before impairment
Reduced blood flow to the kidneys and inpaired function
Classification of AKI
RIFLE system
Grades (causes)
Risk
Injury
Failure
Outcomes requiring renal replacement therapy
Loss
ESKD
Causes of AKI
Hypovolemia
Hypotension
Reduced cardiac output
HF
Obstruction in the kidneys
Blood clot
Kidney stone
Nursing considerations of AKI
Health History
Medications
Surgeries
Hospilations
Physical Examination
Hydration levels
I&Os
Prerenal category of AKI
Hypoperfusion of the kidneys
Sudden and severe drop in BP or interruption of blood flow to the kidneys caused by volume depletion, hypotention, and obstruction of renal vessels
Volume depletion
Impaired cardiac efficiency
Vasodilation
Prerenal AKI characteristics
Increased BUN
Increased creatinine
Decreased output
Sodium <20mEq/L
Normal sediment
Urine osmolality >500mOsm
Increased urine specific gravity
Intrarenal category of AKI
Result of damage to the glomerui or tubules
due to inflammation, toxins, drugs, infection, or reduced blood supply
Prolonged renal ischemia
Nephrotoxic agents
Infection
Intrarenal AKI characteristics
Increased BUN
Increased creatinine
Decreased output
Sodium >40mEq/L
abnormal casts and debris
Urine osmolality ~350mOsm
low urine specific gravity
Postrenal category of AKI
Results from obstruction of the distal end of the kidney
Due to stones, blood clots. BPH, malignancies, and pregnancy
Obstruction
Postrenal AKI characteristics
Increased BUN
Increased creatinine
Decreased output or anuria
Sodium <20mEq/L
Normal sediment
Varying osmolality
varying urine specific gravity
Initiation phase of AKI
Initial insult to the kidney
Changes in electrolytes and initially decreased urine output
Oliguria phase of AKI
increase of concentrations (urea, creatinine, uric acid, electrolytes, etc)
Uremia = concentrated urine
Monitoring of BUN, creatinine, and GFR
Diuresis phase of AKI
Gradual increase in urine output
Lab values stabilize and decrease
Filtration of urea and creatinine have not returned to normal
Observe for dehydration
Recovery phase of AKI
Improvement of renal function
3-13 months
Normal labs
Renal failure
Decreased renal function with increasing nitrogen retention
Clinical manifestations of Renal failure
Critically ill and lethargic
CNS s/s = drowsiness, headache, muscle twitching, seizures
Associated priorities of Renal failure
Evaluation of urine
Kidney contour
Lab values
Usual treatment of Renal failure
Restoration of normal chemical balance
Potssium levels = cation exchange resins
EKG changes = IV dextrose 50%, insulin, calcium replacement
Fluids
Diuretics to initiate diuresis
Loop
Thiazide
Blood transfusions
Dialysis
Nutritional support
Nursing considerations of Renal failure
Monitoring fluid and electrolytes
Reduce metabolic rate
Prevention of fever and infection
Promotion of pulmonary function
Positioning
Coughing
Preventing infection
Asepsis
Skin care
Psychosocial support
Hemodialysis
procedure that circulatess the patient’s blood through a machine to remove waste products and excess fluid
Hemodialysis access
AV fistula (atery and vein fused together)
Central line catheter for dialysis until fistula or shunt is ready
Shunt
Graft catheter
Hemodialysis interval
3-4 hours
3 days/week
Outpatient
Hemodialysis actions
The blood, with toxins and wastes, is diverted fro, the patient to a machine where the toxins are filteres and clean blood is returned to the body
Diffusion moves the toxins and wastes
Osmosis moves the excess fluid
ultrafiltration moves the fluid from high to low pressure
Peritoneal dialysis
procedure that uses the patient’s perironeal membrane as the semipermiable membrane to exchange fluid and solutes
Peritoneal dialysis access
abdomen
Peritoneal dialysis actions
Removal of toxic substances and wates for patients unable to undergo HD or transplantation
Peritoneal membrane thatcovers the abdominal organs and lines the abdominal wals serves as the semipermiable membrane
Sterile dialysate fluid with dextrose and electrolytes is put into the peritoneal cavity through a catheter
Toxins begin to clear from the blood
Diffusion
Clearance
Ultrafiltation
Continuous renal replacement therapy
methods used to replace normal kidney function by circulating the patient’s blood through a hemofilter
Chronic kidney disease
Kidney damage rewuiring permanent RRT/dialysis
ESKD
Pathophysiology of Chronic kidney disease
Renal function delines, causing the end products of protein metabolism (that are normally excreted) to accumulate in the blood
Uremia develops and effects the whole body
Clinical manifestations of Chronic kidney disease
End stage kidney disease (ESKD)
Behavior changes
Confusion; disorientation
Seizures
Ecchymosis
HTN
Pitting edema
Engorged neck veins
Crackles
Tachypnea
Anorexia, nausea, vomiting
Anemia
Infertility
Fractures
Loss of muscle strength
Associated priorities of Chronic kidney disease
Maintain kidney function and homeostasis for as long as possible
Usual treatment of Chronic kidney disease
Dialysis
Calcium and phosphorus binders (binds dietary phosphorus in the GI tract)
Antihypertensives
Fluid restriction
Low sodium diet
Diuretics
Erythropoitin to continue RBC production
Nursing considerations of Chronic kidney disease
Assess fluid status
Potential sources of imbalance
Renal dietitian
Self care and independence
Education
Emotions; support; quality of life