INFECTIONS

PYELONEPHRITIS
WHAT IS PYELONEPHRITIS?
• Infection of one or both of the
kidneys
• Affects the renal parenchyma,
pelvis, and calices
• May be acute or chronic
• If chronic, kidneys are scarred,
contracted, or non-functioning
ETIOLOGY OF ACUTE
PYELONEPHRITIS
• Escherichia coli
• Proteus
• Enterobacter
INCIDENCE AND PREVALENCE
• 250,000 office visits each year in U.S. 300,000
• 200,000 hospital admissions each year in 250,000
U.S.
200,000
• Population with the highest incidence were
young women, infants, and the elderly 150,000

100,000

50,000

0
Office Hospital
Visits Admissions
 ACUTE
PYELONEPHRITIS
PATHOPHYSIOLOGY
• Caused by hematogenous infection
• May be caused by ascending infection
• Usually associated with
– Pregnancy
– Diabetes
– Anatomic abnormalities of the urinal
tract
– Obstructive causes
– Insult to the urinary tract from
catheterization
– Vesicoureteral Reflux
SIGNS AND SYMPTOMS
• Fever
• Chills
• CVA Tenderness
• Dysuria, Urgency, Frequency
• Nausea
• Vomiting
• Anorexia
COMPLICATIONS

• Abscesses
• Septic Shock
• Acute Respiratory Distress Syndrome
• Recurrent/ Chronic Pyelonephritis
T R E AT M E N T
T R I M E T H RO P R I M / S U L FA M E T H OX A Z O L E
T H E R A P Y F O R 7 - 1 0 D AY S
H O S P I TA L I Z AT I O N A N D I V A N T I B I O T I C S
A N D F L U I D S I F PAT I E N T U N A B L E T O TA K E
PO MEDS
 ETIOLOGY OF CHRONIC PYELONEPHRITIS
• Vesicoureteral reflux
• Chronic obstruction
• Chronic or recurrent infection
 • Twice as common in females as it
is in males

INCIDENCE AND • Occurs more often in infants and

young children (younger than 2
PREVALENCE years old) than it does in older
children
CHRONIC PYELONEPHRITIS ETIOLOGY
• Recurrent acute pyelonephritis
• Reflux of infected urine into the
renal pelvis
CHRONIC PYELONEPHRITIS
PATHOPHYSIOLOGY
• Progressive renal scarring leading to
ESRD

• Caliceal deformity, parenchymal

scarring
SIGNS AND SYMPTOMS

• Flank or abdominal pain

• Fever
• Malaise
• Anorexia
TREATMENT

• Correct the underlying cause

• Administration of microbial therapy
• Support of compromised renal function
• Nephrectomy
NURSING MANAGEMENT

1. Assess for signs and symptoms.

2. Maintain fluid status (I&Os).
3. Control pain.
4. Administer meds as per MD order.
5. Remover catheter per MD order.
6. Patient teaching on how to prevent recurrent urinary tract infection.
QUESTION #1

• 1. A nurse is caring for a client with acute pyelonephritis. Which nursing intervention is the
most important?
• A. Administering a sitz bath twice a day.
• B.Increasing fluid intake to 3 L/day.
• C. Using an indwelling urinary catheter to measure urine output accurately.
• D. Encouraging the client to drink cranberry juice to acidify the urine.
QUESTION #2

• 2.You’re caring for a patient with an indwelling catheter. The patient complains of spasm like pain at
the catheter insertion. Which of the following options below are other signs and symptoms the
patient could experience if a urinary tract infection was present? Select all that apply.
• A. increased WBC
• B. crystalluria
• C. positive McBurney’s sign
• D. feeling the need to void even though a catheter is present
• E. dark and cloudy urine
• F. cramping
QUESTION #3

• 3. A patient, who is having spasms and burning while urinating due to a UTI, is prescribed
Pyridium. Which option below is a normal side effect of this drug?
• A. hematuria
• B crystalluria
• C. urethra mucous
• D orange colored urine
QUESTION #4

• 4. A patient with a urinary tract infection is taking Bactrim (Sulfamethoxazole/Trimethroprim).

As the nurse you know that the patient consumes 2.5 to 3 L of fluid per day to prevent which
of the following complication?
• A. brown urine
• B. crystalluria
• C. renal stenosis
• D. renal calculi
QUESTION #5

• 5. The physician orders a urine culture on your patient with a urinary tract infection. In
addition, the patient is ordered to start IV Bactrim (Sulfamethoxazole/Trimethroprim). How
will you proceed with following this order?
• A. First, hang the antibiotic, and then collect the urine culture.
• B. First hang the antibiotic and when the antibiotic is finished infusing, collect the urine culture.
• C. First, collect the urine, and then hang the antibiotic.
• D. First, collect the urine culture and then hold the dose of the antibiotic until the urine culture
is back from the lab.
 URINARY
OBSTRUCTIONS
URINARY OBSTRUCTION?

• Is any type of disorder that will interfere with

flow of the Urine
• Prolonged obstruction results in post-renal AKI
which may lead to intrarenal AKI
 WHERE OBSTRUCTIONS CAN OCCUR
TYPE OF OBSTRUCTION CAUSE
• Intraluminal: Calculi, clot Tumor: bladder, urethra, kidney Papillary necrosis
• Extrinsic: Prostatic hypertrophy Retroperitoneal ibrosis Tumor: pelvic,
retroperitoneal
• Acquired: Neurogenic bladder Ureteral stricture Urethral stricture
C O M P L I C AT I O N S O F
OBSTRUCTION
• In a complete or significant
partial obstruction, hydrostatic
pressure increases proximal to
the obstruction as a result of
continued glomerular filtration
and stasis of the urine flow.
Other structures will begin to
dilate.
• Hydronephrosis – is an
enlarged kidney as a result
of urinary obstruction from
increased pressure and
urine flow.
 Partial obstruction is more common than
complete obstructions to occur in the

PARTIAL
urinary tract, where slight to moderate
decrease in blood flow, GFR, inability to

OBSTRUCTIONS concentrate urine or secrete K+ and H+

ions.

ARE MOST Compensatory hypertrophy will occur in

the unaffected kidney.
COMMON Renal Calculi is the most common
urinary tract obstruction also know
as Nephrolithiasis.
ETIOLOGY & PATHOGENESIS
• Crystallization and stone formation occurs with many solutes found
in urine. (Factors that also contribute to stone formation such as
obesity, HTN, etc..) List of examples on the next slide.
• Stones are said to be primarily made of up calcium oxalate (75% of
the time), Struvite (7-10%), Uric acid, Cystine (1-3%). Ephedrine,
guaifenesin, indinavir, and Xanthine (< 1%). Table 27-6, pg. 584 (show
relating reasonings).
• Pathogenesis begins with urine becoming supersaturated with
specific solutes.
• Solvent (water) + Solutes (particles) = URINE
RENAL CALCULI
(NEPHROLITHIASIS)

• Crystal particles that are composed

of organic/inorganic materials from
within the kidney, tubules, collecting
system, and can migrate to distal
structures.
• Lithiasis – a greek word that’s means
“stone” so renal calculi is often called
Kidney Stones.
 • Hyperparathyroidism
• Gout
• Certain medications
• Hypertension
• •Urinary tract infections
• Chronic inflammatory bowel disease; irritable bowel disease; chronic
FACTORS THAT •
diarrhea
Excess dietary meat
CONTRIBUTE TO • Excess dietary sodium

KIDNEY STONES •
•
Excess dietary oxalate
Past medical history or family history of nephrolithiasis
• Obesity
• Insulin resistance/type 2 diabetes mellitus
• Dehydration • Prolonged immobility
• Congenital kidney defects/anatomic alterations (e.g., abnormal kidney shape)
 CALCIUM-BASED CALCULI
• Are the most common type of Kidney stones people get.
• Calcium based kidney stones etiology is idiopathic
• A genetic component is implicated.
• Primary risk factors for calcium-based calculi are hypercalciuria and/or hypercalcemia, hyperoxaluria,
and hyperuricosuria. Hypercalciuria and/or hypercalcemia is commonly due to increased
gastrointestinal absorption, impaired renal tubular reabsorption, and primary hyperparathyroidism,
and less often to prolonged immobility, metastatic bone cancer, multiple myeloma, prolonged
metabolic acidosis, hypocitraturia, and excessive amounts of vitamin D.
• Uric acid and struvite are the 2nd most common type of stones.
CLINICAL
MANIFESTATIONS
• Signs and Symptoms differ with location and size of
the stones and may mimic any other causes of
abdominal pain.
• Stones within the kidney are responsible for flank pain
and pain may be dull or localized.
• As the stone moves down to the ureteropelvic
junction and into the ureter, spasmodic sharp pain
develops along with n/v, diaphoresis, tachycardia, and
tachypnea may occur.
 DIAGNOSIS
• Collect a urine specimen for a urinalysis.
• Labs: CBC, CMP to check serum creatinine and BUN. In some cases they assess
the parathormone level r/t to risk factors and renal function.
• To diagnosis the doctor will primarily order a computerized tomography (CT scan)
to assess for stones. Depends of the doctor’s preference some order a KUB or
Ultrasound.
• CT scanning can identify renal calculi, other potential sources of lank pain, and
anatomic anomalies
 TREATMENT
• Treatment of nephrolithiasis maybe medical or surgical.
General Interventions Box 27-4 Pg. 585 and Box 27-5 list dietary modifications
• Narcotic analgesics for pain management
• Increased fluid intake (>2 L/day; oral and/or IV)
• Antimicrobials for urinary tract infection
• Shock-wave lithotripsy, ureteral stenting, ureteroscopy for removal of large stones
unable to pass spontaneously
• Dietary modifications unique to stone composition
• Medications unique to stone composition (e.g., allopurinol for uric acid stones)
 TREATMENT CONTINUED…
• Stones often < 7mm in diameter often require a surgical intervention.
• Extracorporeal shock-wave lithotripsy
• Endoscopy with basket retrieval
• Ultrasonic or Laser Lithotripsy
• Open surgical approaches are required when no other intervention is
successful, but are usually avoidable and therefore uncommon.
• 30% to 50% of adults can expect a recurrence within 5 to 10 years.
• Dietary modifications can decrease this risk. Recommendations are designed
for each individual patient, based upon the type of stone and specific risk
factors
QUESTIONS???

1. What is it called when the Kidney is enlarged caused by urinary obstruction from increased
pressure and urine flow?
2. What is the most common type of Renal Calculi (Kidney stones) composed of?
3. What is the other medical term used for Renal Calculi?
4. Name on general intervention done when a patient presents the ER with kidney stones.
5. Name 3 common signs and symptoms of Nephrolithiasis?
GLOMERUL AR
DISORDERS
GLOMERULONEPHRITIS

• Inflammation of the glomeruli and other

areas of the kidney.
• Etiology: May be primary or secondary.
 ACUTE GLOMERULONEPHRITIS

• Second leading cause of ESRD world-

wide.
• More common among men than women.
• Signs & Symptoms: varying degrees of
hematuria, proteinuria, oliguria and
azotemia, edema, and hypertension
 PRIMARY PATHOLOGY
• In autoimmune triggering events, cells such as lysosomes attack the glomerular walls and changes its
structure.
• This physically decreases the surface area available for filtration, so the GFR goes down.
• In some other cases, vasoconstrictors (like angiotensin) are released to decrease perfusion of the
glomerulus or coagulation gets activated so fibrin gets deposited into the capillaries to block
perfusion.
 SECONDARY PATHOLOGY
• The secondary triggering event (bacteria
for instance) will cause antibodies to
appear at the site of infection (the
glomerulus).
• Following the immune complex response,
mesangial cells grow excessively and form
lesions (a characteristic sign of the
disease).
 NURSING CARE/TREATMENT
• Care is symptomatic.
• Dialysis may be needed to support renal function.
NEPHROSIS

• Nephrotic syndrome is a disease of

the glomerulus in which there is a
urinary elimination of >3 to 3.5
grams of protein per day due to
glomerular damage.
• Symptoms include
hypoalbuminemia, hyperlipidemia,
edema, and susceptibility for
thrombus formation.
ETIOLOGY

• The most common primary causes are

minimal change disease (lipoid nephrosis),
idiopathic focal segmental
glomerulosclerosis, and membranous
nephropathy.
• Several systemic diseases, such as systemic
lupus erythematosus and Henoch-Schönlein
purpura, as well as infections, malignancies,
and vasculitis have been found to be
associated with nephrotic syndrome, but the
most common cause in adults is diabetes
mellitus.
 NURSING CARE/TREATMENT
• Treatment of nephrotic syndrome, regardless
of the cause, includes gradual removal of fluid
with diuretics to treat edema. Elevated lipid
levels are routinely treated with lipid-
lowering therapy, if rapid recovery from
nephrotic syndrome is not expected.
• Hypertension is treated with angiotensin II
receptor blockers and/or angiotensin-
converting enzyme inhibition, as is
recommended for chronic kidney disease.
• Treatment with immunosuppression or
immunomodulation is standard for most
primary etiologies, although response is
variable.
REFERENCES

• Ackley, B.J., Ladwig, G.B., & Makic, M. B. F. (2017). Nursing diagnosis handbook: An evidence-
based guide to planning care (11th ed.). Maryland Heights, MO: Mosby Elsevier
• Banasik, J. L., & Copstead, L. C. (2013). Pathophysiology (5th ed.). St. Louis (Missouri): Elsevier
Saunders.
• Lohr, J. W., MD, & Batuman, V., MD, FASN. (2015, December 6). Chronic Pyelonephritis.
Retrieved May 18, 2017, from http://emedicine.medscape.com/