Angeles University Foundation

Angeles City

uROLItHiAsIs
A case report

Submitted by:

Ano, Carl Elexer

Balilo, Noel Leonicio

Estrada, Florence Ancel

Tumaliwan, Charmaine

Submitted to:

Mark Anthony Paras, R.N., M.N.

January 8, 2009
Introduction

Urolithiasis. The process of forming stones in the kidney, bladder,

and/or urethra (urinary tract). Kidney stones are a common cause of
blood in the urine and pain in the abdomen, flank, or groin. Kidney
stones occur in 1 in 20 people at some time in their life.

The pain with kidney stones is usually of sudden onset, very

severe and colicky (intermittent), not improved by changes in position,
radiating from the back, down the flank, and into the groin. Nausea
and vomiting are common. Factors predisposing to kidney stones
include recent reduction in fluid intake, increased exercise with
dehydration, medications that cause hyperuricemia (high uric acid)
and a history of gout.

Treatment includes relief of pain, hydration and, if there is

concurrent urinary infection, antibiotics. The majority of stones pass
spontaneously within 48 hours. However, some stones may not. There
are several factors which influence the ability to pass a stone. These
include the size of the person, prior stone passage, prostate
enlargement, pregnancy, and the size of the stone. A 4 mm stone has
an 80% chance of passage while a 5 mm stone has a 20% chance. If a
stone does not pass, certain procedures (usually by a urology specialist
doctor) may be needed.

The process of stone formation, urolithiasis, is also called

nephrolithiasis. "Nephrolithiasis" is derived from the Greek nephros-
(kidney) lithos (stone) = kidney stone "Urolithiasis" is from the French
word "urine" which, in turn, stems from the Latin "urina" and the Greek
"ouron" meaning urine = urine stone. The stones themselves are also

2|UROLITHIASIS
called renal caluli. The word "calculus" (plural: calculi) is the Latin word
for pebble.

Medical Therapy and New Approaches to Urolithiasis

Extracorporeal Shockwave lithotripsy, this technology has

reduced considerably the morbidity of stone disease, by allowing
relatively noninvasive removal of stones. Unfortunately, the facilitated
removal of stones by ESWL has led some urologists to abandon or
disparage the medical approach to stone management. The propensity
for stone recurrence is not altered by removal of stones with ESWL.
Ample evidence has accumulated, however, showing that a variety of
medical treatments can prevent recurrence of stones.

There have been notable advances in the medical management

of urolithiasis. A graphic display of stone risk factors is now available
commercially. A step-by-step approach to diagnosis and treatment of
different causes of urolithiasis was described in 1996.

Step 1.History and minimum diagnostic tests

Step 2. 24-hour urinary stone risk profile(cstomary diet)
Identification of abnormal dietary risk factors

Short-term dietary modification

Step 3. Repeat stone risk profile after dietary modification
Step 4. Elucidation of causes and construction of treatment
options for abnormal risk factors

A full 24-hour stone risk profile is measured on a random diet

and fluid intake. Another stone risk profile is obtained after a short-
term dietary modification.

3|UROLITHIASIS
Anatomy and Physiology

The urinary system

which is also called
excretory system or the
genitourinary system
(GUS) is the organ system
that produces, stores, and
eliminates urine. In
humans it includes two
kidneys, two ureters, the
bladder, and the urethra.

The kidneys are

bean-shaped organs,
which lie in the abdomen,
rump or retroperitoneal to the organs of digestion, around or just below
the ribcage and close to the lumbar spine. The organ is about the size
of a human fist and is surrounded by what is called peri-nephric fat,
and situated on the superior pole of each kidney is an adrenal gland.
The kidneys receive their blood supply of 1.25 L/min (25% of the
cardiac output) from the renal arteries which are fed by the abdominal
aorta. This is important because the kidneys' main role is to filter water
soluble waste products from the blood. The other attachments of the
kidneys are at their functional endpoints the ureters, which lies more
medial and runs down to the trigone of the bladder.

Functionally the kidney performs a number of tasks. In its role in

the urinary system it concentrates urine, plays a crucial role in
regulating electrolytes, and maintains acid-base homeostasis. The

4|UROLITHIASIS
kidney excretes and re-absorbs electrolytes (e.g. sodium, potassium
and calcium) under the influence of local and systemic hormones. pH
balance is regulated by the excretion of bound acids and ammonium
ions. In addition, they remove urea, a nitrogenous waste product from
the metabolism of proteins from amino acids. The end point is a
hyperosmolar solution carrying waste for storage in the bladder prior to
urination.

Humans produce about 1.5 liters of urine over 24 hours, although this
amount may vary according to circumstances. Because the rate of
filtration at the kidney is proportional to the glomerular filtration rate,
which is in turn related to the blood flow through the kidney, changes
in body fluid status can affect kidney function. Hormones exogenous
and endogenous to the kidney alter the amount of blood flowing
through the glomerulus. Some medications interfere directly or
indirectly with urine production. Diuretics achieve this by altering the
amount of absorbed or excreted electrolytes or osmalites, which
causes a diuresis.

In humans and other related organisms, the urinary bladder is a

hollow muscular organ shaped like a balloon, located in the anterior
pelvis. The bladder stores urine. The maximum that it can hold is one
liter. It swells into a round shape when it is full and gets smaller when
empty. In the absence of bladder disease, it can hold up to 300 ml of
urine comfortably for two to five hours. The epithelial tissue associated
with the bladder is called transitional epithelium. Normally the bladder
is sterile.

Sphincters (circular muscles) regulate the flow of urine from the

bladder. The bladder itself has a muscular layer (detrusor muscle) that,
when contracted, increases pressure on the bladder and creates
urinary flow.

5|UROLITHIASIS
Urination is a conscious process, generally initiated by stretch
receptors in the bladder wall which signal to the brain that the bladder
is full. This is felt as an urge to urinate. When urination is initiated, the
sphincter relaxes and the detrusor muscle contracts, producing urinary
flow.

The endpoint of the urinary system is the urethra. Typically the urethra
in humans is colonized by commensal bacteria below the external
urethral sphincter. The urethra emerges from the end of the penis in
males and between the clitoris and the vagina in females.

Synthesis of the Disease

Urinary Calculi (Urolithiasis) are calcifications in the urinary

system. Commonly called stones, calculi form primarily in the kidney
(nephrolithiasis), but they can form in or migrate to the lower urinary
system. They are typically asymptomatic until they pass into the lower
urinary tract. Stones are usually managed by an urologist. Primarily
bladder calculi are rare and usually develop from a history of urinary
stasis from obstruction or chronic infection.

Up to 4% of the populations in the United States have

urolithiasis. About 12% of the male populations have a renal stones by
age of 70 years. More than 200,000 Americans can require
hospitalization for treatment of stones each year. Many more people
pass stones spontaneously with only minor manifestations that require
no treatment, whereas others are treated in an ambulatory setting. The
recurrence rate for calcium oxalate stones is about 5% within 5 years.

The two primary causative factors are (1) urinary stasis and (2)
supersaturation of urine with poorly soluble crystalloids. Increased
solute concentration occurs because of fluid depletion or an increased
solute load. This increased concentration leads to the precipitation of

6|UROLITHIASIS
crystals, such as calcium, uric acid, and phosphate. Urinary pH
influences the solubility of certain crystals, with some crystal types
precipitating readily on acid urine and some in alkaline urine.

Inhibitor substances, such as citrate and magnesium, appear to

keep particles form aggregating and forming crystals; a lack of
inhibitors increases risk of stones development. Not only does
deficiency of inhibitors but there are maybe “anti inhibitors” in the
urine, such as aluminum, iron and silicone. Medication such as
acetozolamide, absorbable alkalis (calcium carbonate and sodium
bicarbonate), and aluminum hydroxide. Massive doses of vitamin C
increases urinary oxalate levels.

Types of Calculi

1. Calcium most common substance and it is found in up to 90% of

stones. Calcium stones are usually composed of calcium
phosphate or calcium oxalate. Peak onset is during a person’s
20s, and these stones affect primarily males.

Hypercalciuria, is caused by four main components:

• High rate of bone reabsorption, Paget’s Disease,

Hyperthyroidism, Cushing Disease, immobility, and
osteolysis caused by malignant tumors.

• Milk alkali syndrome, sarcoidosis and excessive intake of

vitamin D

• Impaired renal tubular absorption of filteres calcium, as in

renal tubular acidosis

• Structural abnormalities

7|UROLITHIASIS
 35% of all clients do not have high serum levels of calcium

• Increased intestinal absorption

• “Renal Leak” of calcium, the other abnormality is caused

by tubular defect. Hypocalcemia would increase PTH
production thus increase intestinal absorption of calcium
leading to increase calcium solute often called as “Calcium
Wasters”

2. Oxalate –second major cause, most common in areas where

cereals are major dietary component and low dairy farming
regions.

• Hyperabsorption of oxalate with inflammatory bowel

disease and high intake of soy based products.

• Postileal resection or small bowel bypass surgery

• Overdose Vitamin C which metabolizes into oxalate

• Familial oxaluria

• Fat malabsoption which may cause Ca binding, thus freeing

oxalate for absorption.

3. Struvite –triple phosphate composed of carbonate and

magnesium ammonium phosphate. These are cause by certain
bacteria, usually ”Proteus” which contain enzymes urease. This
enzyme split urea into to two ammonia molecules which
increases the urine pH. Stones formed in this manner are
staghorn calculi

8|UROLITHIASIS
 4. Uric Acid –uric acid stones are caused by increased urate
excretion, fluid depletion, and low urinary pH. Hyperuricuria is
the result of either increased in uric acid production or
administration of uricosuric agents.

5. Cystine –is the result of congenital metabolic error inherited as

an autosomal recessive disorder. Cystine stones typically appear
during childhood and adolescence; development in adults is very
rare.

6. Xnathine –stones occur as a result of a rare hereditary condition

in which there is a xanthine oxidase deficiency. This crystal
prescipitates readily in an acid urine.

Sign and symptoms

• Pain- pain is the key symptom of the disease, which is usually

resulted from an obstruction of a large rough calculi that occlude
the opening to the ureters and increase the frequency and force
of peristaltic contractions. This is usually felt on the
costovertebral angle to the flank, to the suprapubic area going to
the external genitalia.

• Nausea and Vomiting- usually accompanied by severe pain.

• Fever- as a result of inflammatory processes

• Hematuria- in the event that the stones abrade a ureters

• Pyuria- resulted from pus formation due to tissue necrosis

• Anuria- rarely happens but due to total occlusion of the passage

to the ureters.

9|UROLITHIASIS
 Severe pain
Release of Inc.
Scarring/
Chemical Nerves
Inflammati
Mediators becomes
Modifiable on Inc. Resp.
Types of The smooth (prostaglan irritated thus Anxiet
Factor
muscles din) eliciting (pain) Diaphoresis
Inc. BP
Diet becomes
Calciu Uretral colic –
Nause Inflammatory Renal Colic Pain radiates towards
UTI, Prolonged –Originates deep in the genetalia and
Struvite a/
indwelling the lumbar regions thigh
Visceral pain – and radiates
catheter Dec. mediated by the around the side
Lifestyle sedentary intestina autonomic nervous and down toward
Uric system via celiac
lifestyle increase l motility the testicle (male)
stasis ganglia which causes and bladder of the

Paralyt
ic ileus

Urinary Stasis
Formation of
and Kidney
kidney Inc. Fluid Inc. Blood Inc. Blood
Supersaturati becomes
stones Volume volume Pressure
Non modifiable on obstruct
Factor ed Hydronephrosis –distention of renal
pelvis and calices caused by
Sex (Male) obstruction of normal urine flow Decrease Frequency of
Urine urination
Xanthi
Age (30 and 50 Hydrouret
have three times Stones in er
risk of calculi) the Size of the
Cystine
Uretral bladder will be
Oxalat
Stones in Stones scar the Hematuria –blood in the
Living in stone-belt the bladder causing it urine (“clink” against the
area

Family of
urolithiasis – Pressure Heavy feeling
excessive against the during micturation
production of the Stones in
the Obstructio Difficulty of
Hereditary n urinating
(oxalate;
oxaluria, Pain upon
Scarri Pain
Xanthine, urinating
ng
especially for men

Urinary Calculi (Kidney Stones/

Urolithiasis)

10 | U R O L I T H I A S I S
Medical Management
Medications

Absorptive Hypercalciuria –Type I

Thiazides are commonly used for the management of absorptive

hypercalciuria Type I as these medications stimulate calcium
reabsorption in the distal nephron, preventing formation of kidney
stones by reducing the amount of calcium in the urine. Side effects
include decreased level of potassium, frequent urination, sexual
dysfunction, and increased triglycerides.

Orthophosphate and sodium cellulose phosphate reduce the absorption

of calcium from the intestines thereby reducing calcium in the urine.
Neither sodium cellulose phosphate nor thiazide corrects the basic,
underlying physiological defect in absorptive hypercalciuria. Sodium
cellulose phosphate should be used in patients with severe absorptive
hypercalciuria Type I (urinary calcium > 350 mg/day) or in those
resistant to or intolerant of thiazide therapy. Side effects include
abdominal discomfort, nausea, and vomiting.

Absorptive Hypercalciuria – Type II

Many patients show disdain for drinking fluids and excreting

concentrated urine. Normal urine calcium excretion would be restored
by dietary calcium restriction alone, and the increase in urine volume
would help reduce urinary saturation of calcium oxalate.

Renal Hypercalciuria

Thiazides are indicated for the treatment of renal hypercalciuria.

Hyperoxaluria

11 | U R O L I T H I A S I S
A high fluid intake is recommended to assure adequate urine volume in
patients with enteric hyperoxaluria. Calcium citrate may theoretically
have a role in the management of enteric hyperoxaluria. This
treatment may lower urinary oxalate by binding oxalate in the
intestinal tract. Calcium citrate may also raise the urinary citrate level
and pH. Side effects are constipation, gas, and increased calcium leak.
Cholestyramine is also another method used to treat calcium oxalate
stones. Side effects are rash, diarrhea, and increased liver enzymes.

Use of potassium citrate in hyperuricosuric calcium oxalate

nephrolithiasis is warranted since citrate has an inhibitory activity with
respect to calcium oxalate (and calcium phosphate) crystallization,
aggregation, and agglomeration. Potassium citrate (30 to 60 mEq/day
in divided doses) may reduce the urinary saturation of calcium oxalate.

Hypocitraturia

For patients with hypocitraturic calcium oxalate nephrolithiasis,

treatment with potassium citrate can restore normal urinary citrate,
thus lowering urinary saturation of calcium and inhibiting
crystallization of calcium salts.

Distal Renal Tubular Acidosis

Potassium citrate therapy is able to correct metabolic acidosis and

hypokalemia found in patients with distal RTA. Since urinary pH is
generally elevated in patients with RTA, the overall rise in urinary pH is
small. Citrate is a significant urinary calcium stone inhibitor that
retards crystallization of calcium oxalate and calcium phosphate.
Potassium citrate binds to calcium in the urine, preventing formation of
crystals and raising the urinary citrate level and pH. Urinary pH should
be monitored periodically during citrate therapy because of excessive

12 | U R O L I T H I A S I S
alkalinization. Side effects are mucous loose stools and minor GI
complaints. Sodium citrate and citric acids are other alkalizing agents
used to prevent kidney stones by inhibiting stone formation through
alkalization.

Potassium citrate therapy can significantly reduce the stone formation

rate in these patients. The dose of potassium citrate is dependent on
the severity of hypocitraturia in these patients.

Cystinuria

The initial treatment program includes a high fluid intake and oral
administration of soluble alkali (potassium citrate) at a dose sufficient
to maintain the urinary pH at 6.5 to 7.0. Potassium citrate is absorbed
to prevent uric acid stones as it binds to calcium in urine, preventing
formation of crystals. Sodium bicarbonate makes the urine less acidic,
which makes uric acid or cystine kidney stone formation less likely.
Possible side effects include increased formation of calcium-type
stones, fluid retention, and sodium in blood. Urinary pH should be
monitored periodically during citrate therapy because excessive
alkalinization may occur, which can increase the risk of calcium
phosphate precipitation and stones. Sodium citrate and citric acid are
other alkalizing agents used to prevent kidney stones by inhibiting
stone formation through alkalization.

Struvite (Infection) Lithiasis

Acetohydroxamic acid (AHA) is a urease inhibitor that retards stone

formation by reducing the urinary saturation of struvite.

Drug-Induced Nephrolithiasis

13 | U R O L I T H I A S I S
Ephedrine Calculi. There are no limited studies that address the
management of these calculi. As with other calculi, a urine output of at
least two liters/day is recommended.

Guaifenesin Calculi. As with ephedrine calculi, there are no limited

studies regarding pharmacologic management of these calculi.

Indinavir Calculi. Initial measures in the management of these calculi

should focus on hydration and analgesia as well as drug
discontinuation and substitution with another protease inhibitor.

Xanthine Calculi. The medical management of xanthine calculi is

limited because the solubility of these calculi is essentially invariable
within physiologic pH ranges. Currently the recommendation includes a
fluid intake of at least three liters/day. If significant quantities of other
purines are present in the urine, then urinary alkalization with
potassium citrate in the range of 6.0 to 6.5 is indicated to prevent
hypoxanthine or uric acid calculi.

Nursing Care Management

• Encourage client to increase fluid intake

• Encourage client to schedule micturation
• Monitor intake of fluid amount and urinary output.
• Medicate for pain as prescribed.
• Continue antibiotic therapy as prescribed.
• Correct diet to include reduced protein and calcium content.

14 | U R O L I T H I A S I S