NURSING CARE OF UROLITHIASIS

BY

Feni J. C. Fina
Maura Angelina O.
Agustinus A. Klau
Karolina Laro
Eka S. Sogen
Marisya Oktaviani
Julia Isabela Dija
Adelheid Karolina

NURSING FACULTY

CHATOLIC UNIVERSITY OF WIDYA MANDALA SURABAYA

2014
 CHAPTER I

OPENING

1.1 Background
Kidney stones are urinary stones (urolithiasis), has been known since the ancient
Babylonians and the ancient Egyptians with the discovery of the mummy of stone in the
bladder. Urinary tract stones can be found in the urinary tract from kidney Calix systems,
pielum, ureters, bladder and urethra. These stones may form in the kidneys and then down to
the lower urinary tract or indeed formed in the lower urinary tract due to urinary stasis like
the bladder stones due to prostatic hyperplasia or urethral stones that form in the urethra
diverticula.
Urinary tract stone disease spread around the world with a difference in developing countries
are found bladder stones, while in developed countries is more common upper urinary tract
stones (kidney and ureter), these differences influenced the nutritional status and mobility
activities of daily living. The average prevalence rate worldwide is 1-12% of the population
suffer from urinary tract stones.
Causes of urinary tract stone formation were related to urine flow disorders, metabolic
disorders, urinary tract infections, dehydration, and other circumstances that remain unclear
(idiopathic).

1.2 Purpose
1.2.1 General Purpose
The general objective of the authors in preparing this paper is to support teaching and
learning activities, especially in the nursing department of nursing courses
Integumentary System on Nursing Clients with UROLITHIASIS.

1.2.2 Specific Objectives

Students are able to:
1. Knowing the sense of UROLITHIASIS.
2. Know the classification on UROLITHIASIS.
3. Knowing the etiology of UROLITHIASIS.
 4. Knowing pathophysiological UROLITHIASIS.
5. Knowing the clinical manifestations of UROLITHIASIS.
6. Knowing investigation on UROLITHIASIS.
7. Knowing the management of UROLITHIASIS.
8. Knowing Nursing in patients with UROLITHIASIS.

1.3 Struckture
1. What is UROLITHIASIS?
2. How does the classification of UROLITHIASIS?
3. How the etiology of UROLITHIASIS?
4. How pathophysiological UROLITHIASIS?
5. How clinical manifestations UROLITHIASIS?
6. How investigation of UROLITHIASIS?
7. How does the management of UROLITHIASIS?
8. How Nursing in patients with UROLITHIASIS?
 CHAPTER II

REVIEW OF THE LITERATURE

2.1 Definition

Urolithiasis refers to the presence of renal calculi (kidney stones). Calculi are hard
masses of crystals composed of minerals that the kidneys normally excrete. These stones can
vary in size from as small as a grain of sand to as large as a golf ball and they are the most
common cause of urinary obstruction. Urolithiasis is more common in men and Caucasians.
Generally, the calculi form in the renal pelvis, ureters and bladder. Calculi may contain various
combinations of chemicals. (Jones & Bartlett, 2012).

Urolithiasis or renal calculi (stones) can form anywhere in the urinary tract, although they
most commonly develop on the renal pelves or calyces. They may vary in size and may be
solitary or multiple. Renal calculi are common in men than in women and rarely occur in
children. Calcium calculi generally occur in midlle-age men with a family history of calculi
formation. (Williams & Wilkins, 2011).

Renal calculi rarely occur in blacks. They’re prevalent in certain geographic ares, such as
the southeastern United States, possibly because a hot climate promotes dehydration and
concentrates calculi-forming substances, or because of regional dietary habits. (Williams &
Wilkins, 2011)

2.2 Classification

The most frequent type of calculi contains calcium in combination with either oxalate and
phosphate. Other types of calculi include strutive or infection stones, uric acid stones and cystine
stones. The calculi may be smooth or jagged and are usually yellow or brown.

Type Cause
Calcium Causes of renal sones include :
 a. Increased absorption of calcium from the small bowel
b. Hyperparathyroidism
c. Inability of renal tubules to reabsorb calcium
d. Dietary excess of calcium
e. Chronic bowel disease that results in steatorrhea; fat then
combines with calcium and renders the calcium unable to bind to
oxalate, causing ston formation
Strutive Caused by urase-producing bacteria
(magnesium Urinary pH around 7.2
ammonium- Usually large in size
phosphate) Texture is relatively soft
Associated with frequent UTI
More common in women
Uric acid Urine pH lower than 5.5 encourages insoluble urate salt formation
Common casues of uric acid stone formation include rapid and dramatic
weight loss, some malignancies
Cystine Abnormal excretion of cystine (amino acid), ornithine lysine, and argine

2.3 Etiology

Additional risk factors for developing urolithiasis include family history, obesity,
hypertension and diet (high-protein, high-sodium or low-calcium diet). Although the exact cause
is unknown, predisposing factors of renal calculi include :

a. idiopatic
b. changes in urine pH (calcium carbonate calculi, high pH, uric acid calculi, lower pH)
c. dehydration
d. dietary factors
e. gout (a disease of increased uric acid production or decreased excretion)
f. immobilization causing calcium to be released into the blood, which is filetered by
the kidneys
g. infection
h. metabolic factors
 i. obstruction to urine flow leading to stasis in the urinary tract
j. renal disease

2.4 Pathophysiology

The major types of renal calculi are calcium oxalate and calcium phosphate, accounting
for 75% to 80% of calculi; strutive (magnesium, ammonium, and phosphate), 15%; and uric acid,
7%; cystine calculi are relatively rare, making up 1% of all renal calculi. Calculi form when
substances that are normally dissolved in the urine, such as calcium oxalate and calcium
phosphate, precipitate. Dehydration may lead to renal calculi as calculi-forming substances
concentrate in urine.

Calculi form around a nucleus or nidus in the appropriate environment. A crystal evolves
in the presence of calculus-forming substances (calcium oxalate, calcium carbonate, magnesium,
ammonium, phosphate, or uric acid) and becomes trapped in the urinary tract, where it attracts
other crystals to form a calculus. a high urine saturation of these substances encourages crystals
formation and results in caclculus growth. Calculi may be composed of different substances, and
the pH of the urine affects the solubility of many caclculi-forming substances. Formation of
calcium oxalate and crystine calculi is independent of urine pH.

Calculi may occur on the papillae, renal tubules, calyces, renal pelves, ureter, or bladder.
Many calculi are less than 5 mm in diameter and are usually passed in the urine. Staghorn calculi
can continue to grow in the pelvis, extending to the calyces, forming a branching calculus, and
ultimately resulting in renal failure if not surgically removed. Calcium calculi are the smallest.
Most are calcium oxalate or a combination of oxalate and phosphate. Although 80% are
idiopathic, they commonly occur with hyperuricosuria (a high level of uric acid in the urine).
Prolonged immobilization can lead to bone demirealization, hypercalciuria, and calculi
formation. In addition, hyperparathyroidism, renal tubular acidosis, and excessive intake of
vitamin D or dietary calcium may predispose to renal calculi.

2.5 Clinical Manifestation

 Calculi usually only cause symptoms when they obstruct urine flow. This obstruction can
lead to hydronephrosis (urine accumulation in the kidney). The movement of calculi through the
urinary system can be quite painful and cause irritation of the urinary mucosa, increasing the risk
for a UTI. Clinical manifestation of urolithiasis include :

a. pain resulting from obstruction (may be mild to severe, deep flank pain or tendeness; or
abrupt, severe colicky flank pain)
b. bloody, cloudy or foul-smelling urine
c. nausea and vomiting
d. fever and chills from infection
e. hematuria when calculi abrade a ureter
f. urinary hesitancy and dysuria due to obstruction
g. abdominal distention
h. anuria from bilateral obstrusction, or obstruction of a patient’s only kidney

2.6 Diagnosis

a. consist of a history and physical examination

b. Kidney-ureter-bladder (KUB) radiography or computed tomography scan of the kidneys
to show most renal calculi
c. urine examination :
1) urinalysis showing pyuria, a sign of urinary tract infection, and to determine urine pH
2) urine culture to detect causative organism, if indicated
3) 24-hours urine collection, for calcium oxalate, phosphorus, and uric acid excretion
levels
d. for pregnant women, magnetic resonance imaging to diagnose calculi because it doesn’t
use radiation.
e. excretory urography, to help confirm the diagnosis and determine the size and location of
calculi.
f. kidney ultrasonography, to detect obstructive changes, such as an unilateral or bilateral
hydronephrosis and radiolucent calculi not seen on KUB radiography.
g. calculi analysis, for mineral content.
 h. serum studies :
1) serial blood calcium and phosphorus levels, to diagnose hyperparathyroidism and
increased calcium, relative to normal serum protein.
2) blood protein levels, to determine the level of free calcium unbound to protein

2.7 Treatment

a. increasing fluid intake to more than 3 qt (3 L)/day to promote hydration

b. an antimicrobial to treat infection, varying with the cultured organism
c. an analgesic, such as morphine or ketorolac (Toradol), fo pain
d. oral alpha blockers and calcium channel blockers in combination with oral steroids to
increase the rate and decrease the time for spontaneous stone passage
e. an antiemetic for nausea and vomiting
f. an antibiotic to treat infection (if present)
g. a diuretic to prevent urinary stasis and further calculi formation; a thiazide to decrease
calcium excretion into the urine
h. methenamine to suppress calculi formation when infection is present
i. low-calcium diet to prevent recurrence
j. oxalate-binding cholestyramine for absorptive hypercaciuria
k. parathyroidectomy for hyperparathyroidism
l. allopurinol (zyloprim) for uric acid calculi
m. daily small doses of ascorbic acid to acidify urine
n. cystoscope with manipulation of the calculi to remove any that are too large for natural
passage
o. percutaneous ultrasonic lithotripsy and extracorporeal shock wave lithotripsy or laser
therapy to shatter calculi into fragments for removal by suction or natural passage
p. surgical removal or cystine or large calculi or placement of urinary diversion around the
calculus to relieve obstruction

2.8 Complication
a. Damage or destruction of renal parenchyma
b. pressure necrosis
c. obstruction by the calculus
d. hydronephrosis
e. bleeding
f. pain
g. infection

CHAPTER IV

CLOSING
4.1 Conclusion

Urolithiasis refers to the presence of renal calculi (kidney stones). The most frequent type
of calculi contains calcium in combination with either oxalate and phosphate. Other types of
calculi include strutive or infection stones, uric acid stones and cystine stones. Additional risk
factors for developing urolithiasis include family history, obesity, hypertension and diet (high-
protein, high-sodium or low-calcium diet). Although the exact cause is unknown. Calculi usually
only cause symptoms when they obstruct urine flow. This obstruction can lead to hydronephrosis
(urine accumulation in the kidney). The movement of calculi through the urinary system can be
quite painful and cause irritation of the urinary mucosa, increasing the risk for a UTI.

The nursing problem for urolithiasis are urine retention, acute pain, nutrition less than
body requirements, hipertermia, anxiety, deficit of knowledge, and risk of infection. Patient with
urolithiasis should do plenty water drinking and if the stones are too big and the calculi
accumulating, they need to do cystoscope percutaneous ultrasonic lithotripsy and surgical
removal or cystine.

4.2 Critic and Suggest

If there are clinical symptoms such as urine retention and feel pain during urinary,
immediately consult the nearest health officials to determine whether you are suffering from
urolithiasis and can get help early.

REFERENCES

Jones & Barlett. 2011. Pathophysiology. Lachel Story : United States of America.
Wilinson, Judith M & Nancy R. Ahern. 2012. Diagnosis Keperawatan Nanda NIC NOC. EGC :
Jakarta.