Angeles University Foundation

Angeles City

uROLItHiAsIsA 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

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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.

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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

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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.

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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

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solute load. This increased concentration leads to the precipitation of

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

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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

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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.

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Non modifiable Factor

Modifiable Factor

Diet

UTI, Prolonged indwelling catheter

Lifestyle sedentary lifestyle increase stasis

Age (30 and 50 have three times risk of

calculi)

Living in stone-belt area

Family of urolithiasis –excessive production of

the mucoprotein

Sex (Male)

Urinary Stasis and

Supersaturation

Formation of kidney stones

Calcium

Struvite

Uric acid

Types of Calculi

Hereditary (oxalate; oxaluria, Xanthine,

Cystine)

Oxalate

Cystine

Xanthine

The smooth muscles becomes

Scarring/ Inflammation

Inflammatory Process

Release of Chemical

Mediators (prostaglandin

Nerves becomes irritated thus eliciting (pain)

Renal Colic Pain –Originates deep in the

lumbar regions and radiates around the

side and down toward the testicle (male) and bladder of the female

Uretral colic –radiates towards the genetalia

and thigh

Severe pain

Anxiety

Inc. Pulse

Inc. Resp. Rate

Inc. BPDiaphoresis

Visceral pain –mediated by the autonomic nervous system via celiac ganglia

which causes

Nausea/ Vomiting

Dec. intestinal motility

Paralytic ileus

Kidney becomes

obstructedHydronephrosis –distention of renal pelvis and calices caused by obstruction of normal

urine flow

Inc. Fluid Volume Inc. Blood volume Inc. Blood Pressure

Stones in the Ureters

Hydroureter

Uretral Colic

Stones in the Bladder

Size of the bladder will be compromised

Decrease Urine Capacity

Frequency of urination

Stones scar the bladder causing it to (bleed)

Hematuria –blood in the urine (“clink” against the toilet)

Pressure against the bladder neck

Heavy feeling during micturation (voiding)

Urinary Calculi (Kidney Stones/ Urolithiasis)

Stones in the urethra Obstruction Difficulty of urinating

Scarring PainPain upon urinating especially for men

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

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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

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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

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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.

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