Urolithiasis Case Report

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 shortterm 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 humans

urine.

In

it includes two

kidneys, two ureters, the bladder, and the urethra. The bean-shaped

kidneys

are

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

Hyperthyroidism,

bone

reabsorption,

Cushing

Disease,

Paget’s

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

Modifiable Factor

Scarring/ Inflammati on

The smooth muscles becomes

Types of

Diet Calciu UTI, Prolonged indwelling catheter

Nause a/

Struvite

Lifestyle sedentary lifestyle increase stasis

Uric

Nerves becomes irritated thus eliciting (pain)

–Originates deep in the lumbar regions and radiates around the side and down toward the testicle (male) and bladder of the

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

Inc. Inc. Resp.

Anxiet

Diaphoresis Inc. BP Uretral colic – radiates towards the genetalia and thigh

Renal Colic Pain

Inflammatory

Dec. intestina l motility

Severe pain

Release of Chemical Mediators (prostaglan din)

Paralyt ic ileus

Non modifiable Factor

Urinary Stasis and Supersaturati on

Formation of kidney stones

Kidney becomes obstruct ed

Inc. Fluid Volume

Inc. Blood volume

Hydronephrosis –distention of renal pelvis and calices caused by obstruction of normal urine flow

Sex (Male) Xanthi

Age (30 and 50 have three times risk of calculi)

Stones in the

Cystine Oxalat

Family of urolithiasis – excessive production of the Hereditary (oxalate; oxaluria, Xanthine,

Hydrouret er

Stones scar the bladder causing it Pressure against the

Stones in the

Obstructio n Scarri ng

Decrease Urine

Frequency of urination

Size of the bladder will be

Uretral

Stones in the

Living in stone-belt area

Inc. Blood Pressure

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

Heavy feeling during micturation

Difficulty of urinating Pain

Pain upon urinating 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