BUKU PEGANGAN TUTOR

Modul
SAKIT PERUT KANAN

Diberikan pada mahasiswa

semester IV FK UNHAS

SISTEM UROGENITALIA
FAKULTAS KEDOKTERAN
UNIVERSITAS HASANUDDIN
MAKASSAR
2006

PENDAHULUAN
Modul sakit perut kanan ini diberikan pada mahasiswa yang mengambil mata
kuliah sistim Urogenitalia di semester IV. TIU dan TIK pada sistim ini disajikan pada
permulaan buku modul agar dapat dimengerti secara menyeluruh tentang konsep dasar
penyakit-penyakit Sistem Urogenitalia yang memberikan gejala

sakit perut kanan.

Mahasiswa diharapkan mampu menjelaskan semua aspek tentang system Urogenitalia

dan patomekanisme terjadinya penyakit, kelainan jaringan, dan pemeriksaan lain yang
dibutuhkan pada penyakit yang memberikan gejala sakit perut kanan.
Sebelum menggunakan modul ini, mahasiswa diharapkan membaca TIU dan TIK
sehingga tidak terjadi penyimpangan pada diskusi dan tujuan serta dapat dicapai
kompetensi minimal yang diharapkan. Bahan untuk diskusi dapat diperoleh dari bacaan
yang tercatum di akhir modul. Kuliah pakar akan diberikan atas permintaan mahasiswa
yang berkaitan dengan penyakit ataupun penjelasan dalam pertemuan konsultasi antara
peserta kelompok diskusi mahasiswa dengan tutor atau ahli yang bersangkutan.
Penyusun mengharapkan modul ini dapat membantu

mahasiwa

memecahkan masalah penyakit Urogenitalia yang disajikan.

Makassar, 2 Desember 2005

Penyusun

dalam

TUJUAN INSTRUKSIONAL UMUM

Setelah mempelajari modul ini mahasiswa diharapkan dapat menjelaskan tentang
penyakit-penyakit yang menyebabkan gejala sakit perut kanan, penyebab dan
patomekanisme, gambaran klinik, cara diagnosis, penanganan dan pencegahan penyakitpenyakit yang menyebabkan sakit perut kanan.
TUJUAN INSTRUKSIONAL KHUSUS
Setelah pembelajaran dengan modul ini mahasiswa diharapkan dapat:
1. Menguraikan struktur anatomi, histologi dan histofisologi dari sistem uropoetika.
2. Menyebutkan fungsi masing-masing bagian dari nefron, fungsi sel-sel JGA dalam
renin angiotensin system.
3. Menjelaskan faktor-faktor yang mempengaruhi GFR, prinsip hukum Starling pada
filtrasi ginjal, proses reabsorbsi dan sekresi di ginjal.
4. Menjelaskan

perubahan

biokimia

urine

dan

kompensasi

ginjal

dalam

keseimbangan asam basa.

5. Menjelaskan penyakit-penyakit yang dapat memberikan gejala sakit perut kanan.
6. Menjelaskan patomekanisme timbulnya gejala sakit perut kanan.
7. Menjelaskan cara anamnesis, pemeriksaan fisis, dan pemeriksaan penunjang yang
dibutuhkan untuk mendiagnosis banding beberapa penyakit yang mempunyai
gejala sakit perut kanan.
8. Mampu melakukan pemeriksaan laboratorium sederhana untuk pemeriksaan
penyakit-penyakit sistem Urogenitalia, terutama yang memberikan gejala sakit
perut kanan.
9. Mampu menganalisis hasil laboratorium dan pemeriksaan radiologik (BNO dan
IVP) pada penderita penyakit sistim Urogenitalia, terutama yang memberikan
gejala sakit perut kanan.
10. Menjelaskan penatalaksanaan penderita-penderita sistem Urogenitalia, terutama
yang memberikan gejala sakit perut kanan.
11. Menjelaskan asuhan nutrisi yang sesuai untuk penyakit-penyakit sistem
Urogenitalia, terutama yang memberikan gejala sakit perut kanan.
12. Menjelaskan epidemiologi dan tindakan-tindakan pencegahan penyakit-penyakit
sistem urogenitalia terutama yang memberi gejala sakit perut kanan

PROBLEM TREE
Anamnesis :
Sakit perut menjalar
ke paha, nyeri datangdatang. Mual

Fisik Diagnostik :
Suhu tubuh normal
Tampak amat nyeri
(kolik)
Diagnosis Banding
Appendicitis
Nefropathy
Tumor UG
ISK
LowBack Pain

Anatomi
Histologi
Fisiologi
Biokimia
Patologi Anatomi
Farmakologi
Mikrobiologi

SAKIT PERUT
KANAN

Pengendalian

Preventif

Penatalaksanaan

Promotif

Medikamentosa

Prognosis

Lab : Urine
Kimia darah
Urinalisis
Pemeriksaan lain :
BNO
CT Scan, USG
PA

Non Bedah

Bedah

Non Medikamentosa
Nutrisi

Komplikasi

Skenario 1. Sakit perut kanan

Seorang ibu, 35 thn, datang ke RS dengan keluhan sakit di daerah perut kanan
dan menjalar sampai ke bawah 5 jam yang lalu. Sakitnya bersifat datangdatang. Penderita merasa mual tapi tidak sampai muntah, tidak ada demam.

TUGAS MAHASISWA
1. Setelah membaca dengan teliti skenario di atas anda harus mendiskusikan kasus
tersebut pada satu kelompok diskusi terdiri dari 12 15 orang, dipimpin oleh seorang
ketua dan seorang penulis yang dipilih oleh anda sendiri. Ketua dan sekretaris ini
sebaiknya berganti-ganti pada setiap kali diskusi. Diskusi kelompok ini bisa dipimpin
oleh seorang tutor atau dilakukan secara mandiri oleh kelompok.
2. Melakukan aktivitas pembelajaran individual di perpustakaan dengan menggunakan
buku ajar, majalah, slide, tape atau video, dan internet, untuk mencari informasi
tambahan.
3. Melakukan diskusi kelompok mandiri (tanpa tutor) , melakukan curah pendapat bebas
antar anggota kelompok untuk menganalisa dan atau mensintese informasi dalam
menyelesaikan masalah.
4. Berkonsultasi pada nara sumber yang ahli pada permasalahan dimaksud untuk
memperoleh pengertian yang lebih mendalam (tanpa pakar).
5. Mengikut kuliah khusus (kuliah pakar) dalam kelas untuk masalah yang belum jelas
atau tidak ditemukan jawabannya.
6. Melakukan latihan dilaboratorium keterampilan klinik dan praktikum di laboratorium.

PROSES PEMECAHAN MASALAH

Dalam diskusi kelompok dengan menggunakan metode curah pendapat, mahasiswa

diharapkan memecahkan problem yang terdapat dalam skenario ini, yaitu dengan
mengikuti 7 langkah penyelesaian masalah di bawah ini:
1. Klarifikasi istilah yang tidak jelas dalam scenario di atas, dan tentukan kata/ kalimat
kunci skenario diatas.
2. Identifikasi problem dasar scenario diatas dengan, dengan membuat beberapa
pertanyaan penting.
3. Analisa problem-problem tersebut dengan menjawab pertanyaan-pertanyaan diatas.
4. Klasifikasikan jawaban atas pertanyaan-pertanyaan tersebut di atas.
5. Tentukan tujuan pembelajaran yang ingindi capai oleh mahasiswa atas kasus
tersebut diatas.
6. Cari informasi tambahan tentang kasus diatas dari luar kelompok tatap muka.
Langkah 6 dilakukan dengan belajar mandiri.
7. Laporkan hasil diskusi dan sistesis informasi-informasi yang baru

ditemukan.

Langkah 7 dilakukan dalm kelompok diskusi dengan tutor.

Penjelasan :
Bila dari hasil evaluasi laporan kelompok ternyata masih ada informasi yang
diperlukan untuk sampai pada kesimpulan akhir, maka proses 6 bisa diulangi, dan
selanjutnya dilakukan lagi langkah 7.
Kedua langkah diatas bisa diulang-ulang di luar tutorial, dan setelah informasi
dirasa cukup maka pelaporan dilakukan dalam diskusi akhir, yang biasanya dilakukan
dalam bentuk diskusi panel dimana semua pakar duduk bersama untuk memberikan
penjelasan atas hal-hal yang belum jelas.

JADWAL KEGIATAN
1. Pertemuan pertama dalam kelas besar dengan tatap muka satu arah dan tanya jawab.
Tujuan : menjelaskan tentang modul dan cara menyelesaikan modul, dan membagi
kelompok diskusi. Pada pertemuan pertama buku modul dibagikan.
2. Pertemuan kedua : diskusi mandiri. Tujuan :
*

Memilih ketua dan sekretaris kelompok,

Brain-storming untuk proses 1 3,

Membagi tugas

3. Pertemuan ketiga: diskusi tutorial dipimpin oleh mahasiswa yang terpilih menjadi
ketua dan penulis kelompok, serta difasilitasi oleh tutor. Tujuan: untuk melaporkan
hasil diskusi mandiri dan menyelesaikan proses sampai langkah 5.
4. Anda belajar mandiri baik sendiri-sendiri. Tujuan: untuk mencari informasi baru yang
diperlukan,
5. Pertemuan keempat: adalah diskusi tutorial. Tujuan: untuk melaporkan hasil diskusi
lalu dan mensintese informasi yang baru ditemukan. Bila masih diperlukan informasi
baru dilanjutkan lagi seperti No. 2 dan 3.
6. Pertemuan terakhir: dilakukan dalam kelas besar dengan bentuk diskusi panel untuk
melaporkan hasil diskusi masing-masing kelompok dan menanyakan hal-hal yang
belum terjawab pada ahlinya (temu pakar).
TIME TABLE

II

Pertemuan I
(Penjelasan)

Pertemuan
Mandiri
(Brain
Stroming)

PERTEMUAN
III
IV
Tutorial I
Pengumpulan
informasi
Analisa &
sintese

Mandiri
Praktikum
CSL

VI

VII

Kuliah
kosultasi

Tutorial II
(Laporan &
Diskusi)

Pertemuan
Terakhir
(Laporan)

STRATEGI PEMBELAJARAN

1. Diskusi kelompok difasilitasi oleh tutor

2. Diskusi kelompok tanpa tutor
3. CSL : Pemeriksaan benjolan pada leher
4. Praktikum PA
5. Konsultasi pada pakar
6. Kuliah khusus dalam kelas
7. Aktivitas pembelajaran individual diperpustakaan dengan menggunakan buku ajar
Majalah,slide,tape atau video dan internet

BAHAN BACAAN & SUMBER INFORMASI LAIN

A. Buku Ajar dan Jurnal

1
2

Urology : R.W. Barnes, R.T.Bergman, H.Hodley, Toppan Co.(S) PTE-LTD,Singapore

Davitson VL and Sittman DB : Biochemistry

3 Kumar, Contran, Robbins: Pathology Basis of Diseases, 2003

4 Chandrasoma- Taylor: Concise Pathology, 1999
5
6
7
8
9
10
11
12
13
14
15
16
17
18

Kenneth J Rothman, 1986, Modern Epidemiology, Little Brownc and Company, Bon
World Health Organization, 1992, International statistical Classification of Diseases
an and related Health Problems, 10th revision, volume 1, WHO, Geneva
Goodharmt R : Modern nutrition in health and disease, Lee Ferbeger, 2002
Robinson : Normal and Therapeutic Nutrition, Mac Millian Co., New York
Lenne EH et al ; Manual of Clinical Microbiology , 4th edition, 1985
Prescott LM et al : Microbiology, 2nd edition, Wm.c Brown Publisher, Melbourne,
1993
WF. Ganong : Review of Medical Physiology, edisi 20, 2003
Synopsis of analysis of Roentgen sign in general Radiology, Isadore Meschan, 1976
Junguiera LC, Carneiro J : Basic Histology 3th edition, Los Altos California USA,
Lange Medical Publication, 1980
Stites DP, Stobo JD, Fudenberg HH : basic and Clinical Immunology, 4th edition, Los
Altos California, Lange Medical Publication, 1982
Schlesinger ER, Sultz HA, Mosher WE, et al. The Nephrotic Syndrome. Its incidence
and implications for the community. Am J Dis Child 1968, 116; 623
International Study of Kidney Disease in Children. Nephrotic Syndrom in Children.
Prediction of histopathology from clinical and laboratory characteristics at time of
diagnosis. Kidney Int. 1978, 13: 159.
Kher KK. Obstructive uropathy. Dalam : Kher KK, Marker SP, penyunting. Clinical
Pediatric Nephrology. New York: Mc Graw Hill 1992: 447-65.
Behrman RE. Nelson textbook of pediatrics; edisi ke 14. Philadelphia: WB Saunders,

19
20
21
22
23
24
25
26
27

1992; 1344-50.
Homes HD, Weinberg JM. Toxic nephropathies. Dalam: Brenner Rector FC,
penyunting, The Kidney, II; edisi ke-Philadelphia: WB Saunders Co, 1986; 1491-532.
Barrat TM. Acute renal failure. Dalam: Holliday MA, Barrat TM, Vernier RL,
penyunting. Pediatric nephrology, edisi ke-2. Baltimore: Williams & Wilkins 1987; 76672.
Kher KK. Chronic renal failure. Dalam Kher KK, Marker SP, penyunting, clinical
pediatric nephrology. New York: MC Graw-Hill Inc, 1992, 501-41.
Karjomanggolo WT, Alatas H. Kelainan congenital ginjal dan saluran kemih. Dalam:
Naskah lengkap PKB. IKA XXVI : Penelitian tractor urinarius pada anak. Jakarta 11
12 September 1992: 1176-84.
Londe S causes of hypertension in the young. Pediatric Clin North Am 1978; 25-55.
Henry JB : Clinical Diagnosis and Manage,ent by laboratory Methods, 19th ed, 1996
H. Beers and R. Berkow editor : The Merck Manual 17th ed, 1999
Harrison : Disorders of the kidney and Urinary tractus, 15th edition, Volume I, Mc
Graw Hill, 2002, pp : 1535-1630
Ginjal Hipertensi dalam Buku Ajar Ilmu Penyakit Dalam jilid II, edisi III, Balai Penerbit
FKUI Jakarta, 2001

B. Diktat dan hand-out

1.
1.
2.
3.

Diktat Anatomi
Diktat Histologi
Buku Ajar Fisiologi Ginjal
Diktat Kuliah Radiologi

C. Sumber lain : VCD, Film, Internet, Slide, Tape

D. Nara sumber (Dosen Pengampu)
DAFTAR NAMA NARA SUMBER
No.

NAMA DOSEN

1.

Prof.Dr. dr. Syarifuddin Rauf

Sp.PA
Prof.Dr.dr. Syakib Bakri,
Sp.PD
Prof.dr. Ahmad M Palinrungi
Sp.B, Sp.U
Prof.Dr.dr. M.Dali
Amiruddin, Sp.KK
Dr. Irfan Idris, MS
Dr. Theopilus Buranda, MS
Dr. Robby Lianury
Dr. Agnes Kwenang, MS
Dr. dr. Gatot Lawrence

2.
3.
4.
5.
6.
7.
8.
9.

BAGIAN

TLP.
KANTOR

HP/FLEXI

Anak

0811411109

Penyakit Dalam

0816250620

Bedah Urologi

08164384040

Kulit Kelamin

08194229858

Fisiologi
Anatomi
Histologi
Biokimia
Patologi

584730

081342695348
081342436444
0811411723
0816255306

10.
11.
12.

Dr. dr. Nurpudji Astuti,

SpGK
Dr. dr. Fatmawati
Dr. Randana Bandaso, MS

13.
14.
15.
16.

Dr. Nurlaily Idris, Sp.R

Dr. H, Ibrahim Samad, SpPK
Dr. Baedah Madjid, SpMK
Dr. Sastri, SpKK

Anatomi
Gizi
Farmakologi
Patologi
Anatomi
Radiologi
Patologi Klinik
Mikrobiologi
Kulit Kelamin

0811443856
081524120368
0811441064
0811444326
08124217393

PETUNJUK UNTUK TUTOR

Apa yang dimaksud dan mekanisme kata kunci berikut ini :

o Sakit perut yang menjalar (kolik) : nyeri pada daerah perut dan menjalar
ke arah perut kanan bawah. Nyeri ini umumnya amat hebat dan menjalar
sesuai dengan perjalanan batu dalam ureter
o Sakit perut yang datang-datang : nyeri yang hilang dan timbul kembali
akibat perjalanan batu di ureter.
o Mual : nyeri yang terjadi pada batu ureter sering disertai mual dan muntah

Apa penyebab dan bagaimana pato-mekanisme gejala-gejala yang menjadi kata

kunci tersebut

o Sakit perut yang menjalar : Nyeri akibat spasme ureter oleh karena
perjalanan batu, penjalaran ini biasanya sampai ke arah kemaluan.
o Sakit yang datang-datang karena spasme terjadi tidak kontinue, bila ada
spasme akan terasa nyeri dan bila tidak nyeri akan hilang
o Mual : Nyeri yang mengenai organ visceral disertai mual dan muntah,
sebab nyeri visceral dihantar via saraf simpatis dan juga merangsang
terjadinya mual dan muntah
Sebutkan beberapa penyakit yang dapat di differential diagnosis
dengan tanda dan gejala pada skenario :
Appendicitis
Biliary Colic
Cholecystitis
Constipation
Diverticulitis
Duodenal Ulcers
Gastritis, Acute
Gastroenteritis, Viral
Glomerulonephritis, Acute
Ileus
Inflammatory Bowel Disease
Liver Abscess
Lumbar Disc Disease
Lumbar Spondylosis
Nephrolithiasis

Nephrolithiasis: Acute Renal Colic

Splenic Abscess
Urinary Tract Infection, Females
Urinary Tract Obstruction

Pemeriksaan penunjang yang dibutuhkan untuk menegakkan diagnosis penyakit

yang termasuk dalam DD penyakit tersebut
1. Urinalysis dan Urinalysisi 24 jam
2. Darah lengkap dan kimia darah
3. Elektrolit
4. Radiologi : BNO, USG, IVP, CT Scan

Bagaimana cara penatalaksanaan dari penyakit-penyakit yang termasuk dalam

DD penyakit tersebut
1. Medikamentosa
2. Bedah
3. ESWL
4. Diet

Epidemiologi penyakit tersebut

1. Masih banyak terjadi di Negara-negara berkembang, di USA 2-3% dalam
populasi pertahun.
2. Pada usia di atas 70 thn, kejadiannya 1 diantara 8 orang
3. Pria : wanita = 3 : 1, umunya pada umur 29-40 thn

Komplikasi penyakit-penyakit yang termasuk DD pada skenario

o

Abscess formation

Serious infection of the kidney that diminishes renal function

Urinary fistula formation

Ureteral scarring and stenosis

Ureteral perforation

Extravasation

Urosepsis

Renal loss due to long-standing obstruction

Prognosis penyakit-penyakit tersebut

1. Recurence rate 50% dalam 5 thn, dan 70% dalam 10 tahun atau lebih
2. Tindakan medis secara efektif memperlambat proses pembentukan batu

Nephrolithiasis
Background: Nephrolithiasis is a common disease estimated to produce medical costs of $1.83
billion a year in the United States. Nephrolithiasis specifically refers to calculi in the kidneys, but
this article discusses both renal calculi (Image 1) and ureteral calculi (ureterolithiasis). Ureteral
calculi almost always originate in the kidneys, although they may continue to grow once lodged in
the ureter.
Urinary tract stone disease has been a part of the human condition for millennia; in fact, bladder
and kidney stones have even been found in Egyptian mummies. Some of the earliest recorded
medical texts and figures depict the treatment of urinary tract stone disease.
Pathophysiology: Urinary tract stone disease (Image 3) is likely caused by 2 basic phenomena.
The first is supersaturation of the urine by stone-forming constituents, including calcium, oxalate,
and uric acid. Crystals or foreign bodies can act as nidi, upon which ions from the supersaturated
urine form microscopic crystalline structures. The overwhelming majority of renal calculi contain
calcium. Uric acid calculi and crystals of uric acid, with or without other contaminating ions,
comprise the bulk of the remaining minority. Other, less frequent stone types include cystine,
ammonium acid urate, xanthine, dihydroxyadenine, and a variety of rare stones related to
precipitation of medications in the urinary tract.
Other current theories also include renal tubular damage or dysfunction as an important
component of the initiation of stone formation. The initial crystal agglomerations likely form in
distal collecting tubules that drain into the renal papilla. As these masses grow, they gradually
extrude into the collecting system through the papilla and eventually drop off to become free
urinary calculi.
Frequency:

In the US: The overall incidence of urinary tract stone disease is 2-3% of the population
per year. The likelihood that a white male will develop stone disease by the age of 70
years is 1 in 8. Stones of the upper urinary tract are more common in the United States
than in the rest of the world. Roughly 1.2 million patients present with stone disease each
year in the United States.

Internationally: Urinary tract stone disease incidence in developed countries is similar to

that observed in the United States. In developing countries, bladder calculi are more
common than upper urinary tract calculi, which is the reverse of the situation in developed
countries. These differences are believed to be diet related.

Mortality/Morbidity:

The morbidity of urinary tract calculi is primarily due to obstruction with its associated
pain, although it is well recognized that nonobstructing calculi can still produce
considerable discomfort.

Conversely, patients with obstructing calculi can be asymptomatic, which is the usual
scenario in the atypical patient who experiences loss of renal function from chronic,
untreated obstruction.

Stone-induced hematuria is frightening to the patient but rarely dangerous by itself.

The most morbid and potentially dangerous aspect of stone disease is the combination of
obstruction and infection of the upper urinary tract. Pyelonephritis, pyonephrosis, and
urosepsis can ensue.

Race: Compared to the prevalence in Asians and whites, urinary tract calculi are far less common
in Native Americans, Africans, African Americans, and some natives of the Mediterranean region.
Although some differences may be attributable to geography (stones are more common in hot
and dry areas) and diet, heredity appears to be a factor as well.
Sex:

In general, urolithiasis occurs more often in males (male-to-female ratio, 3:1).

Stones due to discrete metabolic/hormonal defects (eg, cystinuria, hyperparathyroidism)

and stone disease in children are equally prevalent between the sexes.

Stones due to infection (struvite calculi) are more common in women than in men.

Age:

Most urinary calculi occur in patients aged 20-49 years.

Patients in whom multiple, recurrent stones form usually experience their first stones
while in their teens or twenties.

It is relatively uncommon for patients to experience their first stone attacks after age 50
years.

CLINICAL
History:

Patients with urinary calculi may report pain, infection, or hematuria. Small,
nonobstructing stones in the kidneys cause symptoms only occasionally. If present,
symptoms are usually moderate and easily controlled.

The passage of stones into the ureter with subsequent acute obstruction, proximal urinary
tract dilation, and spasm is associated with classic renal colic.
o

Renal colic is characterized by undulating cramps and severe pain and is often
associated with nausea and vomiting.

As the stone travels through the ureter, the pain moves from the flank to the
upper abdomen, then to the lower abdomen, down to the groin, and eventually to
the scrotal or labial areas.

Associated bladder irritative symptoms are common when the stone is located in
the distal or intramural ureter.

Patients with large renal stones known as staghorn calculi (Image 2) are often relatively
asymptomatic.
o

Staghorn refers to the presence of a branched kidney stone occupying the renal
pelvis and at least one calyceal system. Such calculi usually manifest with
infection and hematuria rather than with acute pain.

In uncommon cases in which asymptomatic bilateral obstruction has occurred,

the patient presents with symptoms of renal failure.

Important historical features are as follows:

o

Duration, characteristics, and location of pain

History of urinary calculi

Prior complications related to stone manipulation

Urinary tract infections

Loss of renal function

Family history of calculi

Solitary or transplanted kidney

Physical:

Often, dramatic costovertebral angle tenderness occurs, which can move to the upper or
lower abdominal quadrant as a ureteral stone migrates distally.

Peritoneal signs are usually lackingan important consideration in distinguishing renal

colic from other sources of flank or abdominal pain.

Findings should correlate with the reports of pain, so that complicating factors (eg, urinary
extravasation, abscess formation) can be detected.

Beyond this, the specific location of tenderness often does not indicate the exact location
of the stone, although the calculus is often in the general area of maximum discomfort.

Causes:

Most research on the etiology and prevention of urinary tract stone disease has been
directed toward the role of elevated urinary levels of calcium, oxalate, and uric acid in
stone formation.

Hypercalciuria is the most commonly noted metabolic abnormality.

Magnesium and especially citrate are important inhibitors of stone formation in the urinary
tract. Decreased levels of these in the urine cause a predisposition for stone formation.

A low fluid intake, with consequent high concentrations of stone-forming solutes in the
urine, is another significant factor in stone formation.

The exact nature of the tubular damage or dysfunction that leads to stone formation has
not been characterized.

The most common findings on 24-hour urine studies are hypercalciuria, hyperoxaluria,
hyperuricosuria, hypocitraturia, and low urinary volume. Other factors, such as high
urinary sodium and low urinary magnesium concentrations, may also play a role. To
identify these risk factors, a 24-hour urine profile, including appropriate serum tests of
renal function, uric acid, and calcium, is needed. Such testing is available from a variety
of commercial laboratories.

DIFFERENTIAL
Abdominal Abscess
Aortic Dissection
Appendicitis
Biliary Colic
Cholecystitis
Constipation
Diverticulitis
Duodenal Ulcers
Gastritis, Acute
Gastroenteritis, Viral
Glomerulonephritis, Acute
Ileus
Inflammatory Bowel Disease
Liver Abscess
Lumbar Disc Disease
Lumbar Spondylosis
Nephrolithiasis
Nephrolithiasis: Acute Renal Colic
Pancreatitis, Acute
Pyonephrosis
Renal Arteriovenous Malformation
Renal Vein Thrombosis
Splenic Abscess
Splenic Infarct
Thoracic Aortic Aneurysm
Urinary Tract Infection, Females
Urinary Tract Infection, Males
Urinary Tract Obstruction
Lab Studies:

Urinalysis
o
o
o

Evaluate the urine for evidence of hematuria and infection. Approximately 85% of
patients with urinary calculi exhibit hematuria.
Absence of hematuria does not preclude presence of urinary calculi; in fact,
approximately 15% of patients with urinary stones do not exhibit hematuria.
Offer strongly motivated patients a metabolic 24-hour urinalysis.

CBC count
o
o

In the context of nephrolithiasis, an elevated white blood cell count suggests

renal or systemic infection.
A depressed red blood cell count suggests a chronic disease state or severe
ongoing hematuria.

Serum electrolytes, creatinine, calcium, uric acid, and phosphorus studies

o These are needed to assess a patient's current renal-function status and to begin
the assessment of metabolic risk for future stone formation.
o A high serum uric acid finding may indicate gouty diathesis or hyperuricosuria,
while hypercalcemia suggests either renal-leak hypercalciuria or
hyperparathyroidism.

Calcium, oxalate, and uric acid

o
o

Elevation of the 24-hour excretion rate of any of these 3 components indicates a

predisposition to form calculi.
Hypercalciuria can be subdivided into absorptive, resorptive, and renal-leak
categories by the results of blood tests and 24-hour urinalysis on both regular
and calcium-restricted diets.
Depending on the specific subtype, the treatment of absorptive
hypercalciuria may include dietary calcium restriction, thiazide diuretics,
oral calcium binders, or phosphate supplementation.
Resorptive hypercalciuria is primary hyperparathyroidism and requires
parathyroidectomy.
Renal-leak hypercalciuria, which is relatively uncommon, is usually
associated with secondary hyperparathyroidism and is best managed
with thiazide diuretics.
Another clinical approach to hypercalciuria, once hyperparathyroidism has been
excluded by appropriate blood tests, is to avoid excessive dietary calcium (usual
recommendation, 600-800 mg/d) and to use thiazides. If thiazide therapy fails,
additional workup (eg, calcium-loading test, more thorough evaluation) may be
needed.
Hyperoxaluria may be primary (a rare genetic disease), enteric (owing to
malabsorption and associated with chronic diarrhea or short-bowel syndrome), or
idiopathic. Oxalate restriction and vitamin B-6 supplementation are somewhat
helpful for patients with idiopathic hyperoxaluria but can be extremely helpful for
those with enteric hyperoxaluria, who often respond dramatically to dietary
calcium supplementation.
Calcium citrate is the recommended supplement because the citrate tends to
further reduce stone formation. Supplementation with calcium carbonate is less
expensive but does not provide citrate's added benefit. Calcium therapy works by
acting as an oxalate binder, reducing oxalate absorption from the intestinal tract.
Calcium should be administered with meals, especially meals containing high
oxalate levels. The supplement should not contain added vitamin D because
vitamin D increases calcium absorption, leaving less in the intestinal tract to work
on oxalate binding.
Hyperuricosuria causes a predisposition to formation of calcium-containing calculi
because sodium urate can produce malabsorption of macromolecular inhibitors
or can serve as a nidus for the heterogeneous growth of calcium oxalate crystals.
Gouty diathesis, a condition of increased stone production associated with high
serum uric acid levels, is also possible. Therapy involves potassium citrate
supplementation and/or allopurinol. In general, allopurinol is the treatment for

patients with pure uric acid stones and hyperuricemia, and citrate
supplementation is the treatment for those with hyperuricosuric calcium stones.

Sodium, phosphorus
o
o
o

Citrate, magnesium
o

o
o

Magnesium and especially citrate are important chemical inhibitors of stone

formation. Hypocitraturia is one of the most common metabolic defects causing a
predisposition to stone formation, and some authorities have recommended
citrate therapy as primary or adjunctive therapy to almost all patients who have
formed recurrent calcium-containing stones.
Liquid pharmacologic citrate preparations are recommended when absorption is
a problem or in cases of chronic diarrhea. Sustained-release tablets are available
and may be more convenient for some patients. Concentrates of lemon juice,
such as lemonade, can also provide citrate.
Potassium citrate is the preferred type of pharmacologic citrate supplement,
although a potassium/magnesium preparation is under investigation.
Magnesium is a more recently recognized inhibitor of stone formation, and the
clinical role of magnesium replacement therapy is less well defined than for
citrate.

Creatinine
o
o
o

Excess sodium excretion can contribute to hypercalciuria by a phenomenon

known as solute drag.
An elevated phosphorus level is useful as a marker for a subtype of absorptive
hypercalciuria known as renal phosphate leak (absorptive hypercalciuria type III).
Renal phosphate leak is identified by high urinary phosphate levels, low serum
phosphate levels, high serum 1,25 vitamin D-3 (calcitriol) levels, and
hypercalciuria. This type of hypercalciuria is uncommon and does not respond
well to standard therapies. The above laboratory tests are confirmatory, but they
are performed only if the index of clinical suspicion is high. Any hypercalciuric
patient with a low serum phosphorus level and a high-normal or high urinary
phosphorus level may have this condition.
Phosphate supplements are used to correct the low serum phosphate level,
which then decreases the inappropriate activation of vitamin D originally caused
by the hypophosphatemia.

Creatinine is the control that allows verification of a true 24-hour sample. Most
individuals excrete 1-1.5 g of creatinine daily.
Values at either extreme that are not explained by estimates of lean body weight
should prompt consideration that the sample is inaccurate.
Consider the sample inaccurate if values at either extreme are not explained by
estimates of lean body weight.

Total volume
o
o

Patients in whom stones form should strive to achieve a urine output of more
than 2 L daily in order to reduce the risk of stone formation.
Patients with cystine stones or those with resistant cases may need a daily
urinary output of 3 L for adequate prophylaxis.

Twenty-fourhour urinalysis (calcium, oxalate, uric acid, sodium, phosphorus, citrate,

magnesium, creatinine, total volume)
o

This study is designed to provide more information about the exact nature of the
chemical problem that caused the stone. This information is useful not only to
allow more specific and effective therapy for stone prevention but also to identify
patients with renal calculi who might have other significant health problems.

The following are indications for a metabolic evaluation with a 24-hour urinalysis:
Residual calculi after surgical treatment
Initial presentation with multiple calculi
Renal failure
Renal transplantation
Solitary kidney
Family history of calculi
More than 1 stone in the past year

Metabolic studies are recommended for patients younger than 25 years. Studies
are also recommended for patients with multiple stone surgeries or recurrences
and for those with renal failure or only a single working kidney (eg, renal
transplant recipients).

Whether or not to perform a 24-hour urine study depends on the patient. If a

patient is strongly motivated to follow a protracted stone-prevention treatment
plan (involving diet, supplements, and/or medications), order the study. If a
patient is unlikely or unwilling to follow a long-term treatment plan, there is little
point in performing such a tedious and inconvenient study.

Imaging Studies:

Plain abdominal radiograph

o

A plain abdominal radiograph (also known as a flat plate or kidney, ureter, and
bladder [KUB] radiograph) may suffice for assessing total stone burden as well
as the size, shape, and location of urinary calculi in some patients.

Calcium-containing stones (~85% of all upper urinary tract calculi) are

radiopaque, but pure uric acid, indinavir-induced, and cystine calculi are relatively
radiolucent on plain radiography.

When used with other imaging studies, such as a renal sonogram or, particularly,
a CT scan, the plain film helps provide a better understanding of the size, shape,
location, orientation, and composition of urinary stones identified by these other
imaging studies. (This may be helpful in planning surgical therapy.)

Renal sonogram
o

A renal sonogram by itself is frequently adequate to determine the presence of a

renal stone. The study is mainly used, in combination with a plain abdominal
radiograph, to determine hydronephrosis or ureteral dilation associated with an
abnormal radiographic density believed to be a urinary tract calculus.

A stone easily identified on the renal sonogram but not visible on the plain
radiograph may be a uric acid or cystine stone, which is potentially dissolvable
with urinary alkalinization therapy.

Ureteral calculi, especially in the distal ureter, and stones smaller than 5 mm are
not easily observed on sonography.

Intravenous urogram
o

An intravenous urogram (IVU) test, also known as an intravenous pyelogram

(IVP), is the standard for determining size and location of urinary calculi. IVU
provides anatomical and functional information.

There has been great interest in finding a replacement imaging examination

because the IVU is labor intensive.
It may take up to 6 hours to complete in the presence of severe
obstruction.
For optimal results, it requires a bowel preparation.
It involves intravenous injection of potentially allergic and mildly
nephrotoxic contrast material.

Although some authorities have advocated substituting a plain abdominal

radiograph plus a renal sonogram for IVU, a helical CT scan without contrast
material is currently believed to be the best radiographic examination for acute
renal colic.

The so-called delayed nephrogram on the IVU is one of the hallmark signs for
acute urinary obstruction. The relative delay in penetration of intravenous
contrast passing through an obstructed kidney elicits this sign. The kidney
appears to develop a whitish color, and contrast appearance within the collecting
system of the affected renal unit is significantly delayed.

The IVU is helpful in identifying the specific problematic stone among numerous
pelvic calcifications and for establishing that the other kidney is functional. These
determinations are particularly helpful if the degree of hydronephrosis is mild and
the CT scan is not definitive.

Helical CT scan without contrast material

o
o

o
o

Technological advances in CT scanning allow imaging of the entire abdomen in a

single breath hold.
When performed with thin cuts and without intravenous contrast material, a CT
scan is the most sensitive clinical imaging modality for calcifications. Even calculi
that are radiolucent on a plain radiograph (except for indinavir-induced stones)
are clear and distinct on a CT scan.
Contrast is not used because it makes the entire urinary collecting system appear
white on the study, thus masking the stones.
At most institutions offering this examination, CT scanning has replaced or is
replacing the IVU for the assessment of urinary tract stone disease, especially for
acute renal colic.

Adding a plain radiograph to the noncontrast CT scan increases the value of the
study by allowing visualization of the size, shape, and relative position of the
stone.
Visualization is especially useful if surgery is being considered.
It is extremely helpful in observing the patient because only the KUB
radiograph may be needed later to determine if the stone has moved or
passed.
A lucent stone on the KUB radiograph that is clearly visible on the CT
scan may indicate a uric acid calculus. This suggests a different
diagnosis and therapy (allopurinol and/or urinary alkalinization) than for a
calcium stone. For these reasons, many institutions routinely perform a
KUB radiograph whenever a renal colic noncontrast CT scan is
performed.
Advantages of a CT scan include the following:
It can identify other pathology (eg, abdominal aneurysms, appendicitis,
cholecystis).
It can be performed quickly.
It avoids the use of intravenous contrast materials.
Disadvantages of CT scan include the following:
It cannot assess individual renal function.
It can miss some unusual radiolucent stones, such as those caused by
indinavir, which are invisible on CT scan. Because of this possibility, IVUs
with contrast should be used for patients taking indinavir.
At most institutions, a CT scan is still more expensive than an IVU.

Plain renal tomograms

o

Although largely replaced by helical CT scans without contrast (when available),

plain renal tomograms are often helpful in finding small stones in the kidneys,
especially in large or obese patients whose bowel contents make it difficult to
observe any renal calcifications.

These tomograms do not require extensive preparation and can be performed

quickly.
Plain renal tomograms are most useful when monitoring a difficult-to-observe
stone after therapy or for clarification of stones not clearly detected or identified
by other studies.

They are also useful in ascertaining the number of stones present in the kidneys
before instituting a stone-prevention program. This information is used to better
differentiate stones formed before therapy began from those formed later.

TREATMENT
Medical Care: The first part of this section discusses emergency management of renal (ureteral)
colic. The second part addresses the issues of medical therapy for stone disease. Medical
therapy for stone disease takes both short- and long-term forms (the former to dissolve the stone
and the latter to prevent further stone formation). Additionally, it is advisable to aggressively treat
patients who initially formed stones in their teens or twenties and all patients younger than 16
years as they are more likely to have recurrent stone formation.

General guidelines for emergency management are as follows:

After diagnosing renal (ureteral) colic, determine the presence or absence of

obstruction or infection.
o Obstruction in the absence of infection can be initially managed with analgesics
and by other medical measures to facilitate passage of the stone. Infection in the
absence of obstruction can be initially managed with antimicrobial therapy. In
either case, promptly refer the patient to a urologist.
o If neither obstruction nor infection is present, then analgesics and other medical
measures to facilitate passage of the stone can be initiated with the expectation
that the stone will likely pass from the upper urinary tract if its diameter is smaller
than 5-6 mm (larger stones are more likely to require surgical measures).
o If both obstruction and infection are present, then emergent decompression of
the upper urinary collecting system is required (see Surgical Care). Immediately
consult with a urologist for patients whose pain fails to respond to ED
management.
Specific guidelines for emergency management are as follows:
o

o
o

Although the role of supranormal hydration in the management of renal (ureteral)

colic is controversial, dehydrated or ill patients need adequate restoration of
circulating volume.
The cornerstone of management of ureteral colic is analgesia. Analgesia can be
attained most expediently with parenteral narcotics or nonsteroidal antiinflammatory drugs (NSAIDs).
Morphine sulfate is the narcotic analgesic drug of choice for parenteral
use.
Ketorolac tromethamine is the only NSAID approved for parenteral use in
the United States, and it is often effective when used for renal colic. Even
in very difficult cases, the combination of these medications usually
provides excellent relief of renal (ureteral) colic.
Antiemetic agents such as metoclopramide HCl and prochlorperazine
may also be added as needed.
Traditional outpatient treatment has included combinations of narcotics (eg,
codeine, oxycodone, hydrocodone) plus acetaminophen. To provide more
effective pain relief and to facilitate stone passage, additional therapy with
NSAIDs, nifedipine, and prednisone may be added.
Oral NSAIDs such as ibuprofen further mitigate pain (thus diminishing
the need for narcotics) and reduce ureteral inflammation, in addition to
having some ureteral relaxant properties.
The calcium channel blocker nifedipine also relaxes ureteral smooth
muscle, and the corticosteroid prednisone reduces ureteral inflammation.
Amelioration of both ureteral inflammation and ureteral muscle tone appears to
facilitate stone passage. A typical regimen for this aggressive management is 1-2
oral narcotic/acetaminophen tablets every 4 hours as needed for pain, 600-800
mg ibuprofen every 8 hours, 30 mg nifedipine extended-release tablet once daily,
and 10 mg prednisone twice daily. Limit administration of nifedipine and
prednisone to 5-10 days. If outpatient treatment fails, promptly consult a
urologist.

Calcium-containing urinary calculi

o Urinary calculi composed predominantly of calcium cannot be dissolved with
current medical therapy; however, medical therapy is important in the chronic
chemoprophylaxis of further calculus growth or formation.
o Prophylactic therapy might include limitation of dietary components, addition of
stone-formation inhibitors or intestinal calcium binders, and, most importantly,
augmentation of fluid intake.

Besides advising patients to avoid excessive salt and protein intake and to
increase fluid intake, base medical therapy for the chronic chemoprophylaxis of
urinary calculi upon the results of a 24-hour urinalysis for chemical constituents.

Uric acid and cystine calculi

o

o
o

o
o
o

Uric acid and cystine calculi can be dissolved with medical therapy. Patients with
uric acid stones who do not require urgent surgical intervention for reasons of
pain, obstruction, or infection can often have their stones dissolved with
alkalinization of the urine.
Sodium bicarbonate can be used as the alkalinizing agent, but potassium citrate
is usually preferred because of the availability of slow-release tablets and the
avoidance of a high sodium load.
The dosage of the alkalinizing agent should be adjusted to maintain urinary pH
between 6.5-7.0. Urinary pH of more than 7.5 should be avoided because of the
potential deposition of calcium phosphate around the uric acid calculus, which
would make it undissolvable. Both uric acid and cystine calculi form in acidic
environments.
Even very large uric acid calculi can be dissolved in patients who comply with
therapy.
Practical ability to alkalinize the urine significantly limits the ability to dissolve
cystine calculi. Chemoprophylaxis of uric acid and cystine calculi consists
primarily of long-term alkalinization of urine.
If hyperuricosuria or hyperuricemia is documented in patients with pure uric acid
stones (present in only a relative minority), allopurinol (300 mg qd) is
recommended because it reduces uric acid excretion.
Pharmaceuticals that can bind free cystine in the urine (eg, penicillamine, 2alphamercaptopropionyl-glycine) help reduce stone formation in cystinuria. Therapy
should also include long-term urinary alkalinization and aggressive fluid intake.

Surgical Care:

The primary indications for surgical treatment include pain, infection, and obstruction.
Additionally, certain occupational and health-related reasons exist.
General contraindications to definitive stone manipulation include the following:
o
o
o

Active, untreated urinary tract infection

Uncorrected bleeding diathesis
Pregnancy (a relative, but not absolute, contraindication)

Specific contraindications may apply to a given treatment modality. For example, do not
perform extracorporeal shock-wave lithotripsy (ESWL) if there is ureteral obstruction
distal to the calculus or in pregnancy.
For an obstructed and infected collecting system secondary to stone disease, virtually no
contraindications exist for emergency surgical relief by either ureteral stent placement (a
small tube placed endoscopically into the entire length of the ureter from the kidney to the
bladder) or by percutaneous nephrostomy (a small tube placed through the skin of the
flank directly into the kidney). Urologists place ureteral stents in the operating room while
patients are under anesthesia; interventional radiologists perform percutaneous
nephrostomies in the radiology suite while patients are under local anesthesia.

The vast majority of symptomatic urinary tract calculi are now treated with noninvasive or
minimally invasive techniques, while open surgical excision of a stone from the urinary
tract is now limited to isolated, atypical cases.
In general, stones that are 4 mm in diameter or smaller probably pass spontaneously,
and stones that are 7 mm or larger are unlikely to pass without surgical intervention. The
larger the stone, the lower the possibility of spontaneous passage, although many other
factors determine what happens with a particular stone.
Extracorporeal shock-wave lithotripsy
o
o
o

Approximately 85% of urinary tract calculi requiring treatment are currently

managed with this modality. ESWL is the least invasive of the surgical methods of
stone removal.
The patient, under varying degrees of anesthesia depending on the type of
lithotriptor, is placed on a table or in a gantry that is then brought into contact with
the shock head.
The shock head delivers shock waves developed from an electrohydraulic,
electromagnetic, or piezoelectric source. The shock waves are focused on the
calculus, and the energy released as the shock wave impacts the stone produces
fragmentation. The resulting small fragments pass in the urine.
ESWL is limited somewhat by the size and location of the calculus. A stone more
than 2 cm in diameter or one located in the lower section of the kidney is treated
less successfully. Fragmentation still occurs, but the large volume of fragments or
their location in a dependent section of the kidney precludes complete passage.

Ureteroscopy
o

Many urologists have a preference for one or the other, but, in general, patients
who are acutely ill, who have significant medical comorbidities, or who harbor
stones that probably cannot be bypassed with ureteral stents undergo
percutaneous nephrostomy, while others receive ureteral stent placement.
Infection combined with obstruction in the urinary tract is an extremely dangerous
situation, with significant risk of urosepsis and death, and must be treated
emergently in virtually all cases.

Ureteroscopic manipulation of a stone is the next most commonly applied

modality (see Image 4). A small endoscope, which may be rigid, semirigid, or
flexible, is passed into the bladder and up the ureter to directly visualize the
stone.
The typical patient has acute symptoms caused by a distal ureteral stone, usually
measuring 5-8 mm. This calculus can be rapidly addressed with miniaturized
instruments. A stone can either be directly extracted using a basket or grasper or
be broken into small pieces using a variety of lithotrites (eg, laser, ultrasonic,
electrohydraulic, ballistic).
Often, a ureteral stent must be placed following this procedure in order to prevent
obstruction from ureteral spasm and edema. A ureteral stent is often
uncomfortable; consequently, many urologists eschew stent placement following
ureteroscopy in selected patients.

Percutaneous nephrostolithotomy
o

Percutaneous nephrostolithotomy allows fragmentation and removal of very large

calculi from the kidney and ureter. A needle, and then a wire, over which is

o
o
o

passed a hollow sheath, are inserted directly in the kidney through the skin of the
flank.
Percutaneous access to the kidney typically uses a sheath with a 1-cm lumen.
Relatively large endoscopes with powerful and effective lithotrites can be used to
rapidly fragment and remove large stone volumes.
Because of their increased morbidity compared with ESWL and ureteroscopy,
percutaneous procedures are generally reserved for large and/or complex renal
stones.
In some cases, a combination of ESWL and a percutaneous technique is
necessary to completely remove all stone material from a kidney. This technique,
called sandwich therapy, is reserved for staghorn or other complicated stone
cases.

Consultations:

Immediate consultation with a urologist is recommended in cases of both infection and

obstruction associated with urinary calculi.

Consultation with a urologist is required when immediate ED management of renal

(ureteral) colic fails.

Referral to a urologist is necessary for all stones that prove refractory to outpatient
management or that fail to pass spontaneously.

Diet:

For almost all patients in whom stones form, an increase in fluid intake and, therefore, an
increase in urine output is recommended. This is likely the single most important aspect
of stone prophylaxis.

The only other general dietary guidelines are to avoid excessive salt and protein intake.

Dietary calcium should not be altered unless specifically indicated by 24-hour urinalysis
findings. Urinary calcium levels are normal in many patients with calcium stones.
Reducing dietary calcium in these patients may actually worsen their stone disease,
because more oxalate is absorbed from the gastrointestinal tract in the absence of
sufficient intestinal calcium to bind with it. This results in a net increase in oxalate
absorption and hyperoxaluria, which tends to increase new kidney stone formation in
patients with calcium oxalate calculi.

As a general rule, dietary calcium should be restricted to 600-800 mg per day in patients
with diet-responsive hypercalciuria who form calcium stones. This is roughly equivalent to
a single high-calcium or dairy meal per day.

Drug Category: Opioid analgesics -- Used for pain relief

Drug Category: Nonsteroidal anti-inflammatory drugs -- Inhibit pain and inflammatory reactions by
decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis. Both
properties are beneficial in the management of renal (ureteral) colic.
Drug Category: Corticosteroids -- Strong anti-inflammatory agents that reduce ureteral
inflammation. Also have profound metabolic and immunosuppressive effects
Drug Category: Calcium channel blockers -- Smooth-muscle relaxants that can facilitate ureteral
stone passage

Drug Category: Uricosuric agents -- Help prevent nephropathy and recurrent calcium oxalate
calculi
Drug Category: Alkalinizing agents, oral -- Used for treatment of metabolic acidosis and when
long-term maintenance of an alkaline urine is desirable
Further Outpatient Care:

Postsurgical issues
o
o

Postsurgical follow-up care

o
o

Following surgical treatment of urinary tract calculi, the major issues are infection,
ureteral obstruction, and hemorrhage.
The postoperative course of minimally invasive stone-removal modalities is
generally characterized by short-lived discomfort easily managed with oral
medications.
Continued or severe pain should prompt evaluation for complications.
Repeat urine cultures and imaging studies should be performed to
assess for ureteral obstruction and perforation, and the degree of
circulating blood volume should be evaluated for ongoing hemorrhage.

A follow-up examination including an abdominal radiograph is often adequate

after an uncomplicated stone removal procedure.
Further imaging is often not necessary if a patient with a previous radiopaque
stone has no further symptoms.
In the following cases, imaging that includes assessment of renal drainage (eg,
IVU, ultrasonogram, CT scan) is usually indicated:
Stones with unusual characteristics
Difficult or complicated procedures
Patients with unusual symptoms
Once postoperative complications have been excluded and the patient is
clinically healthy, standard radiographic follow-up care includes abdominal
radiographs every 6-12 months. Radiographs are often ordered in conjunction
with metabolic chemoprophylaxis.

Ongoing medical therapy

o

If a patient older than 40 years has formed a single stone that passed
spontaneously or was easily treated, follow-up care for recurrent stones may not
be necessary. This patient is at a reasonably low risk for recurrence if adequate
fluid intake is maintained.

In other patients, whether or not they have elected directed metabolic therapy,
routine follow-up care consists of plain abdominal radiographs (or renal
sonograms in the case of radiolucent stones) every 6-12 months.

If medical therapy is instituted, a 24-hour urinalysis 3 months after starting any

new therapy should be performed to assess the degree of patient compliance
and the adequacy of the metabolic response. Checking all possible metabolic
parametersnot just the previously abnormal onesis necessary because of the
possibility of new problems arising as a result of the new therapy.

Once a stable regimen has been established, annual 24-hour urinalyses are
adequate.

Complications:

Serious complications of urinary tract stone disease

o

Abscess formation

Serious infection of the kidney that diminishes renal function

Urinary fistula formation

Ureteral scarring and stenosis

Ureteral perforation

Extravasation

Urosepsis

Renal loss due to long-standing obstruction

Prognosis:

As the minimally invasive modalities for stone removal are generally successful in
removing calculi, the primary consideration in managing stones is not whether the stone
can be removed but whether it can be removed in an uncomplicated manner with
minimum morbidity.

The usually quoted recurrence rate for urinary calculi is 50% within 5 years and 70% or
higher within 10 years, although a large, prospective study published in 1999 suggested
that the recurrence rate may be somewhat lower at 25-30% over a 7.5-year period.
Metabolic evaluation and treatment are indicated for patients at greater risk for
recurrence, including those who present with multiple stones, those who have a history of
previous stone formation, and those who present with stones at a younger age.

Medical therapy is generally effective at delaying (but perhaps not completely stopping)
the tendency for stone formation. The most important aspect of medical therapy is
maintaining an increased fluid intake and high urinary volume. Without an adequate
urinary volume, no amount of medical or dietary therapy is likely to be successful in
preventing stone formation.
o

According to estimates, merely increasing fluid intake and regularly visiting a

physician who advises increased fluids and dietary moderation can cut the stone
recurrence rate by 60%. This phenomenon is known as the stone clinic effect.

In contrast, optimal use of metabolic testing with proper evaluation and

compliance with therapy can eliminate new stones completely in at least 75% of
patients and significantly reduces new stone formation in up to 98% of patients.

Patient Education:

A patient who tends to develop stones should be counseled to seek immediate medical
attention if he or she experiences flank or abdominal pain or notes visible blood in the
urine.

A number of Internet sites offer kidney stone information, including the National Institutes
of Health (NIH) and the American Foundation for Urologic Disease (AFUD).

An excellent source of detailed patient information is The Kidney Stones Handbook by

Gail Savitz and Stephen W. Leslie. It is available at a reasonable cost from online
booksellers such as Amazon.com and directly from the publisher, Four Geez Press, at 1800-2KIDNEYS. A patient newsletter for patients who form kidney stones is available
from the same publisher.

For excellent patient education resources, visit eMedicine's Kidneys and Urinary System
Center. Also, see eMedicine's patient education articles Kidney Stones, Blood in the
Urine, and Intravenous Pyelogram.

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