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Acute Pyelonephritis: University of La Salette College of Nursing Santiago City
Acute Pyelonephritis: University of La Salette College of Nursing Santiago City
COLLEGE OF NURSING
Santiago City
A CASE STUDY
IN
ACUTE PYELONEPHRITIS
PRESENTED BY:
GROUP C
PRESENTED TO:
I. Introduction
A. Case Description
Nursing History
A. Health Perception
B. Nutrition Pattern
C. Sleep and Rest
D. Activity and Exercise
E. Elimination Pattern
F. Self Perception
G. Cognitive and Perception Pattern
H. Role and Relationship Pattern
I. Sexuality Pattern
J. Coping of Stress Pattern
K. Value and Belief Pattern
V. Laboratory Result
VII. Pathophysiology
X. Discharge Planning
XI. Reference
INTRODUCTION
(ACUTE PYELONEPHRITIS)
Pyelonephritis
Definition
Pyelonephritis is an infection of the kidney and the ureters, the ducts that carry urine
away from the kidney.
Alternative Names
Causes
Pyelonephritis most often occurs as a result of urinary tract infection, particularly when
there is occasional or persistent backflow of urine from the bladder into the ureters or an area
called the kidney pelvis. See:Vesicoureteric reflux
Pyelonephritis occurs much less often than a bladder infection, although a history of such
an infection increases your risk. You're also at increased risk for a kidney infection if you have
any of the following conditions:
Symptoms
* Mental changes or confusion may be the only signs of a urinary tract infection in the
elderly.
A physical exam may show tenderness when the health care provider presses (palpates)
the area of the kidney.
• Blood culture may show an infection.
• Urinalysis commonly reveals white or red blood cells in the urine.
• Other urine tests may show bacteria in the urine.
An intravenous pyelogram (IVP) or CT scan of the abdomen may show swollen kidneys.
These tests can also help rule out underlying disorders.
• Kidney biopsy
• Kidney scan
• Kidney ultrasound
• Voiding cystourethrogram
Treatment
Due to the high death rate in the elderly population and the risk of complications, prompt
treatment is recommended. Sudden (acute) symptoms usually go away within 48 to 72 hours
after appropriate treatment.
Your doctor will select the appropriate antibiotics after a urine culture identifies the
bacteria that is causing the infection. In acute cases, you may receive a 10- to 14-day course of
antibiotics.
If you have a severe infection or cannot take antibiotics by mouth, you may be given
antibiotics through a vein (intravenously) at first.
Chronic pyelonephritis may require long-term antibiotic therapy. It is very important that
you finish all the medicine.
• Amoxicillin
• Cephalosporin
• Levofloxacin and ciprofloxacin
• Sulfa drugs such as sulfisoxazole/trimethoprim
Outlook (Prognosis)
With treatment, most kidney infections get better without complications. However, the
treatment may need to be aggressive or prolonged.
Pregnant women and persons with diabetes or spinal paralysis should have a urine culture
after finishing antibiotic therapy to make sure that the bacteria are no longer present in the urine.
Severe episodes of acute kidney injury may result in permanent kidney damage and lead
to chronic kidney disease.
Possible Complications
Call your health care provider if you have been diagnosed with this condition and new
symptoms develop, especially:
Prevention
Prompt and complete treatment of bladder infections may prevent development of many
cases of pyelonephritis. Chronic or recurrent urinary tract infection should be treated thoroughly.
You can help preventing kidney infections by taking the following steps:
• Keep the genital area clean. Wiping from front to back helps reduce the chance of
introducing bacteria from the rectal area to the urethra.
• Urinating immediately after sexual intercourse. This may help eliminate any
bacteria that may have been introduced during sexual activity.
• Drink more fluids (64 to 128 ounces per day). This encourages frequent urination
and flushes bacteria from the bladder.
• Drink cranberry juice. Doing so prevents certain types of bacteria from attaching
to the wall of the bladder and may lessen your chance of infection.
DEMOGRAPHIC DATA
Gender: Female
Religion: INC
Nationality: Filipino
Chief Complain: Painful urination, fever with chills, vomiting for 2 days and body malaise
BP: 110/80
T: 38
RR: 21
PR: 81
Nursing History
Family History
The patient has a family history of Hypertension on Mother side and asthma to
her Father side.
Gordon’s Functional Pattern
Nutritional-Metabolic Pattern
PTA, according to the patient she loves to chicken joy and fries (Jollibee) and eat
only small amount of vegetables. During snack time her favorite snack is chippy and soft drinks
for at least 2 liters a day. She only consumes 4 glasses of water a day.
Activity/Exercise Pattern
PTA, according to the patient she had a efficient energy to require for her ADL.
Every day she is in their store selling clothes for the whole day.
During hospitalization, can no longer do her usual habit, but she can still perform
her ADL.
Coping Pattern
According to the patient she is financially problematic because she is applying to
abroad. She doesn’t have enough money especially now. That she was been Hospitalized. She
managed her problems by asking help to her parents and through the support of her husband.
Elimination Pattern
PTA, the patient usually voids 5-7 times a day and defecates once a day.
During the hospitalization the patient voids 10-12 times a day but scanty. She
defecates every other day.
During Hospitalization the patient didn’t sleep well. Her sleep was always
interrupted because of giving medication and getting vital signs.
They usually attend church gathering every Sunday. The family also believes in
faith healer”
Sexuality Pattern
According to the patient she had her 1st menstruation when she was 14 years old.
She has a regular menstruation. They use natural method (withdrawal)for family planning and to
prevent possible pregnancy.
Physical Assessment
August 23, 2010
(Monday, 6:00pm)
*MOUTH
Lips Inspection Dry, Due to diet (NPO)
reddish in color Due to fever
DOCTORS ORDER
To check if there is
For U/A abnormalities.
For fever
Paracetamol 1 amp IV q 8̊
H2 blocker antagonist to
Ranitidine 1 amp IV now then q prevent or reduce N/V
8 for vomiting
To check any
v/s q 4 fluctuations.
To update prognosis to
please inform AP the pt.
To communicate any
refer accordingly untoward signs and
symptoms that may
occur.
H2 blocker antagonist to
Ranitidine 50mg IV q 8 prevent or reduce N/V
Antibiotic to treat
Cefuroxime 750mg IV q 8 (-) bacterial infection
ANST
Replacement of fluid and
IVF d5LR 1L x 8 electrolytes imbalances
and for medication.
5:45pm ̊
T: 38 C
BP: 90/60 To sustain metabolic
May have DAT needs.
8/25/10
For repeat U/A For comparison
Home meds.
LABORATORY RESULTS
08-23-10 (10:43 am)
HEMATOLOGICAL REPORT
08-23-08
URINALYSIS
INTERPRETATION
Color Dark yellow d/t infection
Transparency Turbid d/t infection
pH 6.5 pH normal
Specific 1.010 (normal = 1.010-1.025) normal
Protein (+) 30 mg/dl d/t damage of the kidney
Glucose (-) normal
RBC 5 – 10 d/t damage of the function
of the kidney
Pus cells 100 numerous to count/ hpF d/t infection
Epithelial cells Moderate normal
Amorphous materials Occasional normal
Mucus threads Rare normal
Bacteria Occasional normal
08-25-08
URINALYSIS
INTERPRETATION
Color yellow normal
Transparency Slightly Turbid normal
pH 7.0 pH normal
Specific 1.015 (normal = 1.010-1.025) normal
Protein (-) normal
Glucose (-) normal
RBC 0-2 d/t damage of the function
of the kidney
Pus cells 30 – 40 HPF d/t infection
Epithelial cells Moderate normal
Amorphous materials Occasional normal
Mucus threads Rare normal
Bacteria Occasional normal
ANATOMY AND
PHYSIOLOGY
The kidneys are essentially regulatory organs which maintain the volume and
composition of body fluid by filtration of the blood and selective reabsorption or secretion of
filtered solutes.
The kidneys are retroperitoneal organs (ie located behind the peritoneum) situated on the
posterior wall of the abdomen on each side of the vertebral column, at about the level of the
twelfth rib. The left kidney is slightly higher in the abdomen than the right, due to the presence
of the liver pushing the right kidney down.
The kidneys take their blood supply directly from the aorta via the renal arteries; blood is
returned to the inferior vena cava via the renal veins. Urine (the filtered product containing waste
materials and water) excreted from the kidneys passes down the fibromuscular ureters and
collects in the bladder. The bladder muscle (the detrusor muscle) is capable of distending to
accept urine without increasing the pressure inside; this means that large volumes can be
collected (700-1000ml) without high-pressure damage to the renal system occuring.
When urine is passed, the urethral sphincter at the base of the bladder relaxes, the detrusor
contracts, and urine is voided via the urethra.
The nephron is the unit of the kidney responsible for ultrafiltration of the blood and
reabsorption or excretion of products in the subsequent filtrate. Each nephron is made up of:
Blood supply
The kidneys receive blood from the renal arteries, left and right, which branch directly
from the abdominal aorta. Despite their relatively small size, the kidneys receive approximately
20% of the cardiac output.
Each renal artery branches into segmental arteries, dividing further into interlobar arteries
which penetrate the renal capsule and extend through the renal columns between the renal
pyramids. The interlobar arteries then supply blood to the arcuate arteries that run through the
boundary of the cortex and the medulla. Each arcuate artery supplies several interlobular arteries
that feed into the afferent arterioles that supply the glomeruli.
The interstitum (or interstitium) is the functional space in the kidney beneath the
individual filters (glomeruli) which are rich in blood vessels. The interstitum absorbs fluid
recovered from urine. Various conditions can lead to scarring and congestion of this area, which
can cause kidney dysfunction and failure.
After filtration occurs the blood moves through a small network of venules that converge
into interlobular veins. As with the arteriole distribution the veins follow the same pattern, the
interlobular provide blood to the arcuate veins then back to the interlobar veins which come to
form the renal vein exiting the kidney for transfusion for blood.
Histology
Renal histology studies the structure of the kidney as viewed under a microscope. Various
distinct cell types occur in the kidney, including:
• Kidney glomerulus parietal cell
• Kidney glomerulus podocyte
• Kidney proximal tubule brush border cell
• Loop of Henle thin segment cell
• Thick ascending limb cell
• Kidney distal tubule cell
• Kidney collecting duct cell
• Interstitial kidney cell
Innervation
The kidney and nervous system communicate via the renal plexus, whose fibers course along the
renal arteries to reach the kidney. Input from the sympathetic nervous system triggers
vasoconstriction in the kidney, thereby reducing renal blood flow. The kidney is not thought to
receive input from the parasympathetic nervous system. Sensory input from the kidney travels to
the T10-11 levels of the spinal cord and is sensed in the corresponding dermatome. Thus, pain in
the flank region may be referred from the kidney.
Functions
Many of the kidney's functions are accomplished by relatively simple mechanisms of filtration,
reabsorption, and secretion, which take place in the nephron. Filtration, which takes place at the
renal corpuscle, is the process by which cells and large proteins are filtered from the blood to
make an ultrafiltrate that will eventually become urine. The kidney generates 180 liters of filtrate
a day, while reabsorbing a large percentage, allowing for only the generation of approximately 2
liters of urine. Reabsorption is the transport of molecules from this ultrafiltrate and into the
blood. Secretion is the reverse process, in which molecules are transported in the opposite
direction, from the blood into the urine.
Excretion of wastes
The kidneys excrete a variety of waste products produced by metabolism. These include the
nitrogenous wastes urea, from protein catabolism, and uric acid, from nucleic acid metabolism.
Acid-base homeostasis
Two organ systems, the kidneys and lungs, maintain acid-base homeostasis, which is the
maintenance of pH around a relatively stable value. The kidneys contribute to acid-base
homeostasis by regulating bicarbonate (HCO3-) concentration.
Osmolality regulation
Any significant rise or drop in plasma osmolality is detected by the hypothalamus, which
communicates directly with the posterior pituitary gland. An increase in osmolality causes the
gland to secrete antidiuretic hormone (ADH), resulting in water reabsorption by the kidney and
an increase in urine concentration. The two factors work together to return the plasma osmolality
to its normal levels.
ADH binds to principal cells in the collecting duct that translocate aquaporins to the membrane
allowing water to leave the normally impermeable membrane and be reabsorbed into the body by
the vasa recta, thus increasing the plasma volume of the body.
There are two systems that create a hyperosmotic medulla and thus increase the body
plasma volume: Urea recycling and the 'single effect.
Urea is usually excreted as a waste product from the kidneys. However, when plasma
blood volume is low and ADH is released the aquaporins that are opened are also permeable to
urea. This allows urea to leave the collecting duct into the medulla creating a hyperosmotic
solution that 'attracts' water. Urea can then re-enter the nephron and be excreted or recycled
again depending on whether ADH is still present or not.
The 'Single effect' describes the fact that the ascending thick limb of the loop of Henle is
not permeable to water but is permeable to NaCl. This means that a countercurrent system is
created whereby the medulla becomes increasingly concentrated setting up an osmotic gradient
for water to follow should the aquaporins of the collecting duct be opened by ADH.
Long-term regulation of blood pressure predominantly depends upon the kidney. This
primarily occurs through maintenance of the extracellular fluid compartment, the size of which
depends on the plasma sodium concentration. Although the kidney cannot directly sense blood
pressure, changes in the delivery of sodium and chloride to the distal part of the nephron alter the
kidney's secretion of the enzyme renin. When the extracellular fluid compartment is expanded
and blood pressure is high, the delivery of these ions is increased and renin secretion is
decreased. Similarly, when the extracellular fluid compartment is contracted and blood pressure
is low, sodium and chloride delivery is decreased and renin secretion is increased in response.
Renin is the first in a series of important chemical messengers that comprise the renin-
angiotensin system. Changes in renin ultimately alter the output of this system, principally the
hormones angiotensin II and aldosterone. Each hormone acts via multiple mechanisms, but both
increase the kidney's absorption of sodium chloride, thereby expanding the extracellular fluid
compartment and raising blood pressure. When renin levels are elevated, the concentrations of
angiotensin II and aldosterone increase, leading to increased sodium chloride reabsorption,
expansion of the extracellular fluid compartment, and an increase in blood pressure. Conversely,
when renin levels are low, angiotensin II and aldosterone levels decrease, contracting the
extracellular fluid compartment, and decreasing blood pressure.
Hormone secretion
The kidneys secrete a variety of hormones, including erythropoietin, calcitriol, and renin.
Erythropoietin is released in response to hypoxia (low levels of oxygen at tissue level) in the
renal circulation. It stimulates erythropoiesis (production of red blood cells) in the bone marrow.
Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the
renal reabsorption of phosphate. Part of the renin-angiotensin-aldosterone system, renin is an
enzyme involved in the regulation of aldosterone levels.
PATHOPHYSIOLOGY
OF
ACUTE PYELONEPHRITIS
Antibody formation
Antigen-antibody complex
Fever
Inflammation or trauma of urethral mucosa
Nausea and vomiting urinary tract impeded
Outflow obstructed
Dysuria
Frequent, scanty urination formation of ↑ residual urine
↓ mucosal defense
nocturia
Inflammation of the bladder
Suprapubic or pelvic pain hematuria
Vesicoureteral reflex
Flank pain exudates fills the kidney pelvis cloudy, foul smelling urine
DEATH