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BENIGNA PROSTAT HIPERPLASIA,,Fadh Definisi BPH Pembesaran Prostat Jinak (PPJ) disebut juga Benigna Prostate Hyperplasia (BPH) adalah hiperplasia kelenjar periuretral prostat yang akan mendesak jaringan prostat yang asli ke perifer dan menjadi simpai bedah. 2. Anatomi Prostat Prostat merupakan kelenjar berbentuk konus terbalik yang dilapisi oleh kapsul fibromuskuler, yang terletak di sebelah inferior vesika urinaria, mengelilingi bagian proksimal uretra (uretra pars prostatika) dan berada disebelah anterior rektum. Bentuknya sebesar buah kenari dengan berat normal pada orang dewasa kurang lebih 20 gram, dengan jarak basis ke apex kurang lebih 3 cm, lebar yang paling jauh 4 cm dengan tebal 2,5 cm. 5 Kelenjar prostat terbagi menjadi 5 lobus : 1. lobus medius 2. lobus lateralis (2 lobus) 3. lobus anterior 4. lobus posterior 5,6 Selama perkembangannya lobus medius, lobus anterior, lobus posterior akan menjadi satu dan disebut lobus medius saja. Pada penampang, lobus medius kadang-kadang tak tampak karena terlalu kecil dan lobus lain tampak homogen berwarna abu-abu, dengan kista kecil berisi cairan seperti susu, kista ini disebut kelenjar prostat. 6 Mc Neal (1976) membagi kelenjar prostat dalam beberapa zona, antara lain adalah: zona perifer, zona sentral, zona transisional, zona fibromuskuler anterior, dan zona periuretral. Sebagian besar hiperplasia prostat terdapat pada zona transisional yang letaknya proksimal dari sfincter eksternus di kedua sisi dari verumontanum dan di zona periuretral. Kedua zona tersebut hanya merupakan 2% dari seluruh volume prostat. Sedangkan pertumbuhan karsinoma prostat berasal dari zona perifer. 7,8 Prostat mempunyai kurang lebih 20 duktus yang bermuara di kanan dari verumontanum dibagian posterior dari uretra pars prostatika. Di sebelah depan didapatkan ligamentum pubo prostatika, di sebelah bawah ligamentum triangulare inferior dan di sebelah belakang didapatkan fascia denonvilliers. Fascia denonvilliers terdiri dari 2 lembar, lembar depan melekat erat dengan prostat dan vesika seminalis, sedangkan lembar belakang melekat secara longgar dengan fascia pelvis dan memisahkan prostat dengan rektum. Antara fascia endopelvic dan kapsul sebenarnya dari prostat didapatkan jaringan peri prostat yang berisi pleksus prostatovesikal. 6 Pada potongan melintang kelenjar prostat terdiri dari : 1. Kapsul anatomis Sebagai jaringan ikat yang mengandung otot polos yang membungkus kelenjar prostat. 2. Jaringan stroma yang terdiri dari jaringan fibrosa dan jaringan muskuler

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BENIGNA PROSTAT HIPERPLASIA,,Fadh

Definisi BPH

Pembesaran Prostat Jinak (PPJ) disebut juga Benigna Prostate Hyperplasia (BPH) adalah hiperplasia kelenjar periuretral prostat yang akan mendesak jaringan prostat yang asli ke perifer dan menjadi simpai bedah.

2. Anatomi Prostat

Prostat merupakan kelenjar berbentuk konus terbalik yang dilapisi oleh kapsul fibromuskuler, yang terletak di sebelah inferior vesika urinaria, mengelilingi bagian proksimal uretra (uretra pars prostatika) dan berada disebelah anterior rektum. Bentuknya sebesar buah kenari dengan berat normal pada orang dewasa kurang lebih 20 gram, dengan jarak basis ke apex kurang lebih 3 cm, lebar yang paling jauh 4 cm dengan tebal 2,5 cm.5

Kelenjar prostat terbagi menjadi 5 lobus :

1. lobus medius

2. lobus lateralis (2 lobus)

3. lobus anterior

4. lobus posterior 5,6

Selama perkembangannya lobus medius, lobus anterior, lobus posterior akan menjadi satu dan disebut lobus medius saja. Pada penampang, lobus medius kadang-kadang tak tampak karena terlalu kecil dan lobus lain tampak homogen berwarna abu-abu, dengan kista kecil berisi cairan seperti susu, kista ini disebut kelenjar prostat.6

Mc Neal (1976) membagi kelenjar prostat dalam beberapa zona, antara lain adalah: zona perifer, zona sentral, zona transisional, zona fibromuskuler anterior, dan zona periuretral. Sebagian besar hiperplasia prostat terdapat pada zona transisional yang letaknya proksimal dari sfincter eksternus di kedua sisi dari verumontanum dan di zona periuretral. Kedua zona tersebut hanya merupakan 2% dari seluruh volume prostat. Sedangkan pertumbuhan karsinoma prostat berasal dari zona perifer.7,8

Prostat mempunyai kurang lebih 20 duktus yang bermuara di kanan dari verumontanum dibagian posterior dari uretra pars prostatika. Di sebelah depan didapatkan ligamentum pubo prostatika, di sebelah bawah ligamentum triangulare inferior dan di sebelah belakang didapatkan fascia denonvilliers.

Fascia denonvilliers terdiri dari 2 lembar, lembar depan melekat erat dengan prostat dan vesika seminalis, sedangkan lembar belakang melekat secara longgar dengan fascia pelvis dan memisahkan prostat dengan rektum. Antara fascia endopelvic dan kapsul sebenarnya dari prostat didapatkan jaringan peri prostat yang berisi pleksus prostatovesikal.6

Pada potongan melintang kelenjar prostat terdiri dari :

1. Kapsul anatomis

Sebagai jaringan ikat yang mengandung otot polos yang membungkus kelenjar prostat.

2. Jaringan stroma yang terdiri dari jaringan fibrosa dan jaringan muskuler

3. Jaringan kelenjar yang terbagi atas 3 kelompok bagian:

1. Bagian luar disebut glandula principalis atau kelenjar prostat sebenarnya yang menghasilkan bahan baku sekret.

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2. Bagian tengah disebut kelenjar submukosa, lapisan ini disebut juga sebagai adenomatous zone

3. Di sekitar uretra disebut periurethral gland atau glandula mukosa yang merupakan bagian terkecil. Bagian ini serinng membesar atau mengalami hipertrofi pada usia lanjut.

Pada BPH, kapsul pada prostat terdiri dari 3 lapis :

1. kapsul anatomis

2. kapsul chirurgicum, ini terjadi akibat terjepitnya kelenjar prostat yang sebenarnya (outer zone) sehingga terbentuk kapsul

3. kapsul yang terbentuk dari jaringan fibromuskuler antara bagian dalam (inner zone) dan bagian luar (outer zone) dari kelenjar prostat.

BPH sering terjadi pada lobus lateralis dan lobus medialis karena mengandung banyak jaringan kelenjar, tetapi tidak mengalami pembesaran pada bagian posterior daripada lobus medius (lobus posterior) yang merupakan bagian tersering terjadinya perkembangan suatu keganasan prostat. Sedangkan lobus anterior kurang mengalami hiperplasi karena sedikit mengandung jaringan kelenjar.5,6

Secara histologis, prostat terdiri atas kelenjar-kelenjar yang dilapisi epitel thoraks selapis dan di bagian basal terdapat juga sel-sel kuboid, sehingga keseluruhan epitel tampak menyerupai epitel berlapis.

Vaskularisasi

Vaskularisasi kelenjar prostat yanng utama berasal dari a. vesikalis inferior (cabang dari a. iliaca interna), a. hemoroidalis media (cabang dari a. mesenterium inferior), dan a. pudenda interna (cabang dari a. iliaca interna). Cabang-cabang dari arteri tersebut masuk lewat basis prostat di Vesico Prostatic Junction. Penyebaran arteri di dalam prostat dibagi menjadi 2 kelompok , yaitu:

1. Kelompok arteri urethra, menembus kapsul di postero lateral dari vesico prostatic junction dan memberi perdarahan pada leher buli-buli dan kelompok kelenjar periurethral.

2. Kelompok arteri kapsule, menembus sebelah lateral dan memberi beberapa cabang yang memvaskularisasi kelenjar bagian perifer (kelompok kelenjar paraurethral).9

Aliran Limfe

Aliran limfe dari kelenjar prostat membentuk plexus di peri prostat yang kemudian bersatu untuk membentuk beberapa pembuluh utama, yang menuju ke kelenjar limfe iliaca interna , iliaca eksterna, obturatoria dan sakral.9

Persarafan

Sekresi dan motor yang mensarafi prostat berasal dari plexus simpatikus dari Hipogastricus dan medula sakral III-IV dari plexus sakralis.

3. Fisiologi Prostat

Prostat adalah kelenjar sex sekunder pada laki-laki yang menghasilkan cairan dan plasma seminalis, dengan perbandingan cairan prostat 13-32% dan cairan vesikula seminalis 46-80% pada waktu ejakulasi. Kelenjar prostat dibawah pengaruh Androgen Bodies dan dapat dihentikan dengan pemberian Stilbestrol.

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4. Etiologi BPH

Hingga sekarang masih belum diketahui secara pasti penyebab terjadinya hiperplasia prostat, tetapi beberapa hipotesis menyebutkan bahwa hiperplasia prostat erat kaitannya dengan peningkatan kadar dehidrotestosteron (DHT) dan proses aging (menjadi tua).7

Beberapa teori atau hipotesis yang diduga sebagai penyebab timbulnya hiperplasia prostat adalah:

1. Teori Hormonal

Dengan bertambahnya usia akan terjadi perubahan keseimbangan hormonal, yaitu antara hormon testosteron dan hormon estrogen. Karena produksi testosteron menurun dan terjadi konversi testosteron menjadi estrogen pada jaringan adiposa di perifer dengan pertolongan enzim aromatase, dimana sifat estrogen ini akan merangsang terjadinya hiperplasia pada stroma, sehingga timbul dugaan bahwa testosteron diperlukan untuk inisiasi terjadinya proliferasi sel tetapi kemudian estrogenlah yang berperan untuk perkembangan stroma. Kemungkinan lain ialah perubahan konsentrasi relatif testosteron dan estrogen akan menyebabkan produksi dan potensiasi faktor pertumbuhan lain yang dapat menyebabkan terjadinya pembesaran prostat.

Pada keadaan normal hormon gonadotropin hipofise akan menyebabkan produksi hormon androgen testis yang akan mengontrol pertumbuhan prostat. Dengan makin bertambahnya usia, akan terjadi penurunan dari fungsi testikuler (spermatogenesis) yang akan menyebabkan penurunan yang progresif dari sekresi androgen. Hal ini mengakibatkan hormon gonadotropin akan sangat merangsang produksi hormon estrogen oleh sel sertoli. Dilihat dari fungsional histologis, prostat terdiri dari dua bagian yaitu sentral sekitar uretra yang bereaksi terhadap estrogen dan bagian perifer yang tidak bereaksi terhadap estrogen.

2. Teori Growth Factor (Faktor Pertumbuhan)

Peranan dari growth factor ini sebagai pemacu pertumbuhan stroma kelenjar prostat. Terdapat empat peptic growth factor yaitu: basic transforming growth factor, transforming growth factor 1, transforming growth factor 2, dan epidermal growth factor.

3. Teori peningkatan lama hidup sel-sel prostat karena berkuramgnya sel yang mati

4. Teori Sel Stem (stem cell hypothesis)

Seperti pada organ lain, prostat dalam hal ini kelenjar periuretral pada seorang dewasa berada dalam keadaan keseimbangan “steady state”, antara pertumbuhan sel dan sel yang mati, keseimbangan ini disebabkan adanya kadar testosteron tertentu dalam jaringan prostat yang dapat mempengaruhi sel stem sehingga dapat berproliferasi. Pada keadaan tertentu jumlah sel stem ini dapat bertambah sehingga terjadi proliferasi lebih cepat. Terjadinya proliferasi abnormal sel stem sehingga menyebabkan produksi atau proliferasi sel stroma dan sel epitel kelenjar periuretral prostat menjadi berlebihan.

5. Teori Dehidrotestosteron (DHT)

Testosteron yang dihasilkan oleh sel leydig pada testis (90%) dan sebagian dari kelenjar adrenal (10%) masuk dalam peredaran darah dan 98% akan terikat oleh globulin menjadisex hormon binding globulin (SHBG). Sedang hanya 2% dalam keadaan testosteron bebas. Testosteron bebas inilah yang bisa masuk ke dalam “target cell” yaitu

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sel prostat melewati membran sel langsung masuk kedalam sitoplasma, di dalam sel, testosteron direduksi oleh enzim 5 alpha reductase menjadi 5 dehidrotestosteron yang kemudian bertemu dengan reseptor sitoplasma menjadi “hormone receptor complex”. Kemudian “hormone receptor complex” ini mengalami transformasi reseptor, menjadi “nuclear receptor” yang masuk kedalam inti yang kemudian melekat pada chromatin dan menyebabkan transkripsi m-RNA. RNA ini akan menyebabkan sintese protein menyebabkan terjadinya pertumbuhan kelenjar prostat.5,6,8,10

5. Patofisiologi BPH

Pembesaran prostat menyebabkan penyempitan lumen uretra pars prostatika dan akan menghambat aliran urine. Keadaan ini menyebabkan peningkatan tekanan intravesikal. Untuk dapat mengeluarkan urin, buli-buli harus berkontraksi lebih kuat guna melawan tahanan itu. Kontraksi yang terus-menerus ini menyebabkan perubahan anatomik dari buli-buli berupa hipertrofi otot detrusor, trabekulasi, terbentuknya selula, sakula, dan divertikel buli-buli. Fase penebalan otot detrusor ini disebut fase kompensasi.

Perubahan struktur pada buli-buli dirasakan oleh pasien sebagai keluhan pada saluran kemih sebelah bawah atau lower urinary tract symptom (LUTS) yang dahulu dikenal dengan gejala-gejala prostatismus.

Dengan semakin meningkatnya resistensi uretra, otot detrusor masuk ke dalam fase dekompensasi dan akhirnya tidak mampu lagi untuk berkontraksi sehingga terjadi retensi urin. Tekanan intravesikal yang semakin tinggi akan diteruskan ke seluruh bagian buli-buli tidak terkecuali pada kedua muara ureter. Tekanan pada kedua muara ureter ini dapat menimbulkan aliran balik urin dari buli-buli ke ureter atau terjadi refluks vesico-ureter. Keadaan ini jika berlangsung terus akan mengakibatkan hidroureter, hidronefrosis, bahkan akhirnya dapat jatuh ke dalam gagal ginjal.7

Hiperplasi prostat

Penyempitan lumen uretra posterior

Tekanan intravesikal ↑

Buli-buli Ginjal dan Ureter

o Hipertrofi otot detrusor - Refluks vesiko-ureter

o Trabekulasi - Hidroureter

o Selula - Hidronefrosis

o Divertikel buli-buli - Pionefrosis Pilonefritis

o Gagal ginjal

Pada BPH terdapat dua komponen yang berpengaruh untuk terjadinya gejala yaitu komponen mekanik dan komponen dinamik. Komponen mekanik ini berhubungan dengan adanya pembesaran kelenjar periuretra yang akan mendesak uretra pars prostatika sehingga terjadi gangguan aliran urine (obstruksi infra vesikal) sedangkan komponen dinamik meliputi tonus otot polos prostat dan kapsulnya, yang merupakan alpha adrenergik

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reseptor. Stimulasi pada alpha adrenergik reseptor akan menghasilkan kontraksi otot polos prostat ataupun kenaikan tonus. Komponen dinamik ini tergantung dari stimulasi syaraf simpatis, yang juga tergantung dari beratnya obstruksi oleh komponen mekanik.

Proses pembesaran prostat terjadi secara berlahan – lahan sehingga perubahan pada saluran kemih juga terjadi secara berlahan – lahan. Pada tahap awal terjadi pembesaran prostat , retistensi pada leher buli – buli dan daerah prostat meningkat, serta otot detrusor menebal dan mereggang sehingga timbul sakulasi atau diverkulasi. Fase penebalan detrusor ini disebut fase kompensasi. Apabila keadaan berlanjut, maka detrusor menjadi lelah dan akhirnya mengalami dekompensasi dan tidak mampu lagi untuk berkontraksi sehingga terjadi retansi urin yang selanjutnya dapat menyebabkan hidronefrosis dan disfungsi saluran kemih atas.

Adapun patofisiologi dari masing – masing gejala adalah :

- Penurunan kekuatan dan kaliber aliran yang disebabkan resistensi uretra adalah gambaran awal dan menetap dari BPH.

- Hesitancy terjadi karena detrusor membutuhkan waktu yang lama untuk dapat melawan resistensi uretra.

- Intermittency terjadi detrusor tidak dapat mengatasi resistensi uretra sampai akhir miksi. Terminal dribbling dan rasa puas sehabis miksi akan terjadi karena jumlah residu urin yang banyak dalam buli – buli.

- Nokturia dan frekuensi terjadi karena pengosongan tidak lengkap pada tiap miksi sehingga interval miksi menjadi lebih pendek.

- Frekuensi biasa terjadi pada malam hari (nokturia) karena hambatan normal dari korteks berkurang dan tonus spingter dan uretra berkuang selama tidur.

- Urgensi dan disuria jarang terjadi, dan jika ada disebabkan oleh ketidakstabilan detrusor sehingga terjadi kontraksi involunter.

- Inkontinensia bukan gejala khas, walaupun dengan berkembangnya penyakit urin keluar sedikit – sedikit secara berkala karena setelah buli – buli mencapai compliance maksimum, tekanan dalam buli – buli akan cepat naik melebihi tekanan spingter.

Biasanya ditemukan gejala dan tanda obstuksi dan iritasi. Gejala dan tanda obstuksi jalan kemih berarti penderita haus menunggu pada permulaan miksi,miksi terputus, menetes pada akhi miksi,pancaran miksi menjadi lemah, rasa belum puas setelah miksi dan gejala iitatif yaitu betambahnya frekuensi miksi, noktuia, miksi sulit ditahan, dan nyeri pada waktu miksi. Gejala obstruksi disebabkan oleh karena dektrusor gagal berkontaksi cukup lama sehingga kontraksi terputus – putus, sedangkan gejala iritatif disebabkan oleh karena pengosongan yang tidak sempurna saat miksi atau pembesaran prostat menyebabkan rangsangan pada vesika., sehingga vesika sering berkontraksi meskipun belum penuh, keadaan membuat sistem skoring untuk menentukan besarnya keluhan klinik penderita prostat Hiperplasia. Disamping skoring menurut Boyarsky, dikenal juga sistem skoring lain misalnya menurut Masden dan Iversen (1983), Flower dan kawan – kawan (1988), skoring Denmark (Hald dkk., 1991),skoring Ameica Urological Association (AUA, 1991). Derajat berat gejala klinik prostat Hiperplasia ini dipakai untuk menentukan derajat berat keluhan subyektif , yang ternyata tidak selalu sesuai dengan besarnya volume prostat. Gejala iritatif yang sering dijumpai ialah bertambahnya frekuensi miksi yang biasanya lebih dirasakan pada malam hari. Sering miksi paada malam hari disebut nokturia, hal ini disebabkan oleh

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menurunnya hambatan kotikal selama tidur dan juga menurunkan tonus sfingter dan uretra. Simptom obstruksi biasanya disebabkan oleh karena prostat volumenya terlalu besar. Apabila vesika menjadi dekompensasi, maka akan terjadi retensi urin sehingga pada akhir miksi masih ditemukan sisa urin didalam vesika, hal ini menyebabkan rasa tidak tuntas pada akhir miksi. Jika hal ini berlanjut setiap saat akan terjadi kemacetan total, sehingga penderita tidak bisa miksi lagi. Oleh karena produksi urin akan terus terjadi maka suatu saat vesika tidak mampu lagi menampung urine sehingga tekanan intravesika akan naik terus dan jika tekanan intravesika ini akan naik terus maka dan apabila tekanan vesika akan menjadi lebih tinggi dari tekanan spingter akan terjadi inkontensia paradoks (overflow incontinence). Retensi kronik dapat menyebabkan terjadinya refluks vesiko urethral dan menyebabkan dilatasi ureter dan sistem pelvio kalises ginjal akan rusak dan adanya infeksi. Disamping kerusakan traktus urinarius bagian atas akibat obstuksi kronik pendeita haus selalu mengedan pada waktu miksi tekanan intraabdomen dapat meningkat dan lama – kelamaan akan menyebabkan terjadinya hernia, hemorroid,. Oleh karena selalu terdapat sisa kencing didalam vesika maka akan terbentuk batu dalam vesika dan batu ini dapat menambah keluhan iritasi dan menimbulkan iritasi dan menimbulkan hematuri. Disamping pembentukan batu retensi kronik dapat menyebabkan terjadinya infeksi sehingga terjadi sintitis dan apabila terjadi refluks dapat terjadi juga pyelonefitis.

6. Gambaran Klinis BPH

Gejala hiperplasia prostat dapat menimbulkan keluhan pada saluran kemih maupun keluhan di luar saluran kemih.

1. Gejala pada saluran kemih bagian bawah

Keluhan pada saluran kemih sebelah bawah (LUTS) terdiri atas gejala obstruktif dan gejala iritatif. Gejala obstruktif disebabkan oleh karena penyempitan uretara pars prostatika karena didesak oleh prostat yang membesar dan kegagalan otot detrusor untuk berkontraksi cukup kuat dan atau cukup lama sehingga kontraksi terputus-putus.

Gejalanya ialah :

1. Harus menunggu pada permulaan miksi (Hesistancy)

2. Pancaran miksi yang lemah (weak stream)

3. Miksi terputus (Intermittency)

4. Menetes pada akhir miksi (Terminal dribbling)

5. Rasa belum puas sehabis miksi (Sensation of incomplete bladder emptying).

Manifestasi klinis berupa obstruksi pada penderita hipeplasia prostat masih tergantung tiga faktor, yaitu :

1. Volume kelenjar periuretral

2. Elastisitas leher vesika, otot polos prostat dan kapsul prostat

3. Kekuatan kontraksi otot detrusor7,10,11

Tidak semua prostat yang membesar akan menimbulkan gejala obstruksi, sehingga meskipun volume kelenjar periurethral sudah membesar dan elastisitas leher vesika, otot polos prostat dan kapsul prostat menurun, tetapi apabila masih dikompensasi dengan kenaikan daya kontraksi otot detrusor maka gejala obstruksi belum dirasakan.8

Gejala iritatif disebabkan oleh karena pengosongan vesica urinaria yang tidak sempurna pada saat miksi atau disebabkan oleh hipersensitifitas otot detrusor karena

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pembesaran prostat menyebabkan rangsangan pada vesica, sehingga vesica sering berkontraksi meskipun belum penuh.

Gejalanya ialah :

1. Bertambahnya frekuensi miksi (Frequency)

2. Nokturia

3. Miksi sulit ditahan (Urgency)

4. Disuria (Nyeri pada waktu miksi)

Gejala-gejala tersebut diatas sering disebut sindroma prostatismus. Secara klinis derajat berat gejala prostatismus itu dibagi menjadi :

Grade I : Gejala prostatismus + sisa kencing < 50 ml

Grade II : Gejala prostatismus + sisa kencing > 50 ml

Grade III: Retensi urin dengan sudah ada gangguan saluran kemih bagian atas + sisa urin > 150 ml.8

Untuk menilai tingkat keparahan dari keluhan pada saluran kemih sebelah bawah, WHO menganjurkan klasifikasi untuk menentukan berat gangguan miksi yang disebut Skor Internasional Gejala Prostat atau I-PSS (International Prostatic Symptom Score). Sistem skoring I-PSS terdiri atas tujuh pertanyaan yang berhubungan dengan keluhan miksi (LUTS) dan satu pertanyaan yang berhubungan dengan kualitas hidup pasien. Setiap pertanyaan yang berhubungan dengan keluhan miksi diberi nilai 0 sampai dengan 5, sedangkan keluhan yang menyangkut kualitas hidup pasien diberi nilai dari 1 hingga 7.

Dari skor I-PSS itu dapat dikelompokkan gejala LUTS dalam 3 derajat, yaitu: - Ringan : skor 0-7

- Sedang : skor 8-19

- Berat : skor 20-35

Timbulnya gejala LUTS merupakan menifestasi kompensasi otot vesica urinaria untuk mengeluarkan urin. Pada suatu saat otot-otot vesica urinaria akan mengalami kepayahan (fatique) sehingga jatuh ke dalam fase dekompensasi yang diwujudkan dalam bentuk retensi urin akut.

Faktor pencetus

Kompensasi Dekompensasi

(LUTS) Retensi urin

Inkontinensia paradoksa

International Prostatic Symptom Score

Pertanyaan Jawaban dan skor

Keluhan pada bulan terakhir

Tidak sekal

i

<20%

<50% 50%

>50% Hampir selalu

a. Adakah anda merasa buli-buli tidak kosong setelah berkemih

0 1 2 3 4 5

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b. Berapa kali anda berkemih lagi dalam waktu 2 menit

0 1 2 3 4 5

c. Berapa kali terjadi arus urin berhenti sewaktu berkemih

0 1 2 3 4 5

d. Berapa kali anda tidak dapat menahan untuk berkemih

0 1 2 3 4 5

e. Beraapa kali terjadi arus lemah sewaktu memulai kencing

0 1 2 3 4 5

f. Berapa keli terjadi bangun tidur anda kesulitan memulai untuk berkemih

0 1 2 3 4 5

g. Berapa kali anda bangun untuk berkemih di malam hari

0 1 2 3 4 5

Jumlah nilai :

0 = baik sekali 3 = kurang

1 = baik 4 = buruk

2 = kurang baik 5 = buruk sekali

Timbulnya dekompensasi vesica urinaria biasanya didahului oleh beberapa faktor pencetus, antara lain:

o Volume vesica urinaria tiba-tiba terisi penuh yaitu pada cuaca dingin, menahan kencing

terlalu lama, mengkonsumsi obat-obatan atau minuman yang mengandung diuretikum (alkohol, kopi) dan minum air dalam jumlah yang berlebihan

o Massa prostat tiba-tiba membesar, yaitu setelah melakukan aktivitas seksual atau

mengalami infeksi prostat akut

o Setelah mengkonsumsi obat-obatan yang dapat menurunkan kontraksi otot detrusor

atau yang dapat mempersempit leher vesica urinaria, antara lain: golongan antikolinergik atau alfa adrenergik.7

2. Gejala pada saluran kemih bagian atas

Keluhan akibat penyulit hiperplasi prostat pada saluran kemih bagian atas berupa gejala obstruksi antara lain nyeri pinggang, benjolan di pinggang (yang merupakan tanda dari hidronefrosis)., atau demam yang merupakan tanda dari infeksi atau urosepsis.

3. Gejala di luar saluran kemih

Tidak jarang pasien berobat ke dokter karena mengeluh adanya hernia inguinalis atau hemoroid. Timbulnya kedua penyakit ini karena sering mengejan pada saat miksi sehingga mengakibatkan peningkatan tekanan intraabdominal.7

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7. Diagnosis BPH

a. Anamnesis : gejala obstruktif dan gejala iritatif

b. Pemeriksaan Fisik

Pemeriksaan colok dubur dapat memberikan gambaran tentang keadaan tonus spingter ani, reflek bulbo cavernosus, mukosa rektum, adanya kelainan lain seperti benjolan di dalam rektum dan tentu saja teraba prostat. Pada perabaan prostat harus diperhatikan :

1. Konsistensi prostat (pada hiperplasia prostat konsistensinya kenyal)

2. Adakah asimetris

3. Adakah nodul pada prostate

4. Apakah batas atas dapat diraba

5. Sulcus medianus prostate

6. Adakah krepitasi

Colok dubur pada hiperplasia prostat menunjukkan prostat teraba membesar, konsistensi prostat kenyal seperti meraba ujung hidung, permukaan rata, lobus kanan dan kiri simetris, tidak didapatkan nodul, dan menonjol ke dalam rektum. Semakin berat derajat hiperplasia prostat, batas atas semakin sulit untuk diraba. Sedangkan pada carcinoma prostat, konsistensi prostat keras dan atau teraba nodul dan diantara lobus prostat tidak simetris. Sedangkan pada batu prostat akan teraba krepitasi.

Pemeriksaan fisik apabila sudah terjadi kelainan pada traktus urinaria bagian atas kadang-kadang ginjal dapat teraba dan apabila sudah terjadi pielonefritis akan disertai sakit pinggang dan nyeri ketok pada pinggang. Vesica urinaria dapat teraba apabila sudah terjadi retensi total, daerah inguinal harus mulai diperhatikan untuk mengetahui adanya hernia. Genitalia eksterna harus pula diperiksa untuk melihat adanya kemungkinan sebab yang lain yang dapat menyebabkan gangguan miksi seperti batu di fossa navikularis atau uretra anterior, fibrosis daerah uretra, fimosis, condiloma di daerah meatus.

Pada pemeriksaan abdomen ditemukan kandung kencing yang terisi penuh dan teraba masa kistus di daerah supra simfisis akibat retensio urin dan kadang terdapat nyeri tekan supra simfisis.

c. Pemeriksaan Laboratorium

Pemeriksaan laboratorium berperan dalam menentukan ada tidaknya komplikasi.

1. Darah : - Ureum dan Kreatinin

Elektrolit

Blood urea nitrogen

Prostate Specific Antigen (PSA)

Gula darah

2. Urin : - Kultur urin + sensitifitas test

Urinalisis dan pemeriksaan mikroskopik

Sedimen

Sedimen urin diperiksa untuk mencari kemungkinan adanya proses infeksi atau inflamasi pada saluran kemih. Pemeriksaan kultur urine berguna dalam mencari jenis kuman yang menyebabkan infeksi dan sekaligus menentukan sensitifitas kuman terhadap beberapa antimikroba yang diujikan.

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Faal ginjal diperiksa untuk mengetahui kemungkinan adanya penyulit yang mengenai saluran kemih bagian atas. Sedangkan gula darah dimaksudkan untuk mencari kemungkinan adanya penyakit diabetes mellitus yang dapat menimbulkan kelainan persarafan pada vesica urinaria.

d. Pemeriksaan pencitraan

1. Foto polos abdomen (BNO)

BNO berguna untuk mencari adanya batu opak di saluran kemih, adanya batu/kalkulosa prostat dan kadangkala dapat menunjukkan bayangan vesica urinaria yang penuh terisi urin, yang merupakan tanda dari suatu retensi urine. Selain itu juga bisa menunjukkan adanya hidronefrosis, divertikel kandung kemih atau adanya metastasis ke tulang dari carsinoma prostat.

2. Pielografi Intravena (IVP)

Pemeriksaan IVP dapat menerangkan kemungkinan adanya:

1. kelainan pada ginjal maupun ureter berupa hidroureter atau hidronefrosis

2. memperkirakan besarnya kelenjar prostat yang ditunjukkan oleh adanya indentasi prostat (pendesakan vesica urinaria oleh kelenjar prostat) atau ureter di sebelah distal yang berbentuk seperti mata kail atau hooked fish

3. penyulit yang terjadi pada vesica urinaria yaitu adanya trabekulasi, divertikel, atau sakulasi vesica urinaria

4. foto setelah miksi dapat dilihat adanya residu urin

3. Sistogram retrograd

Apabila penderita sudah dipasang kateter oleh karena retensi urin, maka sistogram retrograd dapat pula memberi gambaran indentasi.

4. USG secara transrektal (Transrectal Ultrasonography = TURS)

Untuk mengetahui besar atau volume kelenjar prostat, adanya kemungkinan pembesaran prostat maligna, sebagai petunjuk untuk melakukan biopsi aspirasi prostat, menentukan volume vesica urinaria dan jumlah residual urine, serta mencari kelainan lain yang mungkin ada di dalam vesica urinaria seperti batu, tumor, dan divertikel.

5. Pemeriksaan Sistografi

Dilakukan apabila pada anamnesis ditemukan hematuria atau pada pemeriksaan urine ditemukan mikrohematuria. Sistografi dapat memberikan gambaran kemungkinan tumor di dalam vesica urinaria atau sumber perdarahan dari atas bila darah datang dari muara ureter, atau batu radiolusen di dalam vesica. Selain itu juga memberi keterangan mengenai basar prostat dengan mengukur panjang uretra pars prostatika dan melihat penonjolan prostat ke dalam uretra.

6. MRI atau CT jarang dilakukan

Digunakan untuk melihat pembesaran prostat dan dengan bermacam – macam potongan.

e. Pemeriksaan Lain

1. Uroflowmetri

Untuk mengukur laju pancaran urin miksi. Laju pancaran urin ditentukan oleh : - daya kontraksi otot detrusor

tekanan intravesica

resistensi uretra

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Angka normal laju pancaran urin ialah 10-12 ml/detik dengan puncak laju pancaran mendekati 20 ml/detik. Pada obstruksi ringan, laju pancaran melemah menjadi 6 – 8 ml/detik dengan puncaknya sekitar 11 – 15 ml/detik. Semakin berat derajat obstruksi semakin lemah pancaran urin yang dihasilkan.

2. Pemeriksaan Tekanan Pancaran (Pressure Flow Studies)

Pancaran urin melemah yang diperoleh atas dasar pemeriksaan uroflowmetri tidak dapat membedakan apakah penyebabnya adalah obstruksi atau daya kontraksi otot detrusor yang melemah. Untuk membedakan kedua hal tersebut dilakukan pemeriksaan tekanan pancaran dengan menggunakan Abrams-Griffiths Nomogram.Dengan cara ini maka sekaligus tekanan intravesica dan laju pancaran urin dapat diukur.

3. Pemeriksaan Volume Residu Urin

Volume residu urin setelah miksi spontan dapat ditentukan dengan cara sangat sederhana dengan memasang kateter uretra dan mengukur berapa volume urin yang masih tinggal atau ditentukan dengan pemeriksaan ultrasonografi setelah miksi, dapat pula dilakukan dengan membuat foto post voiding pada waktu membuat IVP. Pada orang normal sisa urin biasanya kosong, sedang pada retensi urin total sisa urin dapat melebihi kapasitas normal vesika. Sisa urin lebih dari 100 cc biasanya dianggap sebagai batas indikasi untuk melakukan intervensi pada penderita prostat hipertrofi.3,6,8,10,11

8 Diagnosis Banding

1. Kelemahan detrusor kandung kemih

1. kelainan medula spinalis

2. neuropatia diabetes mellitus

3. pasca bedah radikal di pelvis

4. farmakologik

2. Kandung kemih neuropati, disebabkan oleh :

1. kelainan neurologik

2. neuropati perifer

3. diabetes mellitus

4. alkoholisme

5. farmakologik (obat penenang, penghambat alfa dan parasimpatolitik)

3. Obstruksi fungsional :

1. dis-sinergi detrusor-sfingter terganggunya koordinasi antara kontraksi detrusor dengan relaksasi sfingter

2. ketidakstabilan detrusor

4. Kekakuan leher kandung kemih :

Fibrosis

5. Resistensi uretra yang meningkat disebabkan oleh :

1. hiperplasia prostat jinak atau ganas

2. kelainan yang menyumbatkan uretra

3. uretralitiasis

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4. uretritis akut atau kronik

e. striktur uretra

6. Prostatitis akut atau kronis3,11

9. Kriteria Pembesaran Prostat

Untuk menentukan kriteria prostat yang membesar dapat dilakukan dengan beberapa cara, diantaranya adalah :

1. Rektal grading

Berdasarkan penonjolan prostat ke dalam rektum : Stage 0 : prostat teraba < 1cm, berat < 10 gram Stage 1 : prostat teraba 1 – 2 cm, berat 10 -25 gram Stage 2 : prostat teraba 2 -3 cm, berat 25- 60 gram Stage 3 : prostat teraba 3- 4 cm, berat 60 – 100 gram Stage 4 : prostat teraba >4 cm, berat >100 gram

2. Berdasarkan jumlah residual urine

derajat 1 : <>

derajat 2 : 50-100 ml

derajat 3 : >100 ml

derajat 4 : retensi urin total

3. Intra vesikal grading

derajat 1 : prostat menonjol pada bladder inlet

derajat 2 : prostat menonjol diantara bladder inlet dengan muara ureter

derajat 3 : prostat menonjol sampai muara ureter

derajat 4 : prostat menonjol melewati muara ureter

4. Berdasarkan pembesaran kedua lobus lateralis yang terlihat pada uretroskopi : - derajat 1 : kissing 1 cm

derajat 2 : kissing 2 cm

derajat 3 : kissing 3 cm

derajat 4 : kissing >3 cm6

10. Komplikasi

Dilihat dari sudut pandang perjalanan penyakitnya, hiperplasia prostat dapat menimbulkan komplikasi sebagai berikut :

1. Inkontinensia Paradoks

2. Batu Kandung Kemih

3. Hematuria

4. Sistitis

5. Pielonefritis

6. Retensi Urin Akut Atau Kronik

7. Refluks Vesiko-Ureter

8. Hidroureter

9. Hidronefrosis

10. Gagal Ginjal11

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Penatalaksanaan

Hiperplasi prostat yang telah memberikan keluhan klinik biasanya akan menyebabkan penderita datang kepada dokter. Derajat berat gejala klinik dibagi menjadi empat gradasi berdasarkan penemuan pada colok dubur dan sisa volume urin, yaitu:

- Derajat satu, apabila ditemukan keluhan prostatismus, pada colok dubur ditemukan penonjolan prostat, batas atas mudah diraba dan sisa urin kurang dari 50 ml.

- Derajat dua, apabila ditemukan tanda dan gejala sama seperti pada derajat satu, prostat lebih menonjol, batas atas masih dapat teraba dan sisa urin lebih dari 50 ml tetapi kurang dari 100 ml.

- Derajat tiga, seperti derajat dua, hanya batas atas prostat tidak teraba lagi dan sisa urin lebih dari 100 ml

- Derajat empat, apabila sudah terjadi retensi urin total.

Organisasi kesehatan dunia (WHO) menganjurkan klasifikasi untuk menentukan berat gangguan miksi yang disebut WHO PSS (WHO Prostate Symptom Score). Skor ini berdasarkan jawaban penderita atas delapan pertanyaan mengenai miksi. Terapi non bedah dianjurkan bila WHO PSS tetap dibawah 15. Untuk itu dianjurkan melakukan kontrol dengan menentukan WHO PSS. Terapi bedah dianjurkan bila WHO PSS 25 ke atas atau bila timbul obstruksi.3,11

Pembagian derajat beratnya hiperplasia prostat derajat I-IV digunakan untuk menentukan cara penanganan.

Derajat satu biasanya belum memerlukan tindakan operatif, melainkan dapat diberikan pengobatan secara konservatif.

Derajat dua sebenarnya sudah ada indikasi untuk melakukan intervensi operatif, dan yang sampai sekarang masih dianggap sebagai cara terpilih ialah trans uretral resection (TUR). Kadang-kadang derajat dua penderita masih belum mau dilakukan operasi, dalam keadaan seperti ini masih bisa dicoba dengan pengobatan konservatif.

Derajat tiga, TUR masih dapat dikerjakan oleh ahli urologi yang cukup berpengalaman biasanya pada derajat tiga ini besar prostat sudah lebih dari 60 gram. Apabila diperkirakan prostat sudah cukup besar sehingga reseksi tidak akan selesai dalam satu jam maka sebaiknya dilakukan operasi terbuka.

Derajat empat tindakan pertama yang harus segera dikerjakan ialah membebaskan penderita dari retensi urin total, dengan jalan memasang kateter atau memasang sistostomi setelah itu baru dilakukan pemeriksaan lebih lanjut untuk melengkapi diagnostik, kemudian terapi definitif dapat dengan TURP atau operasi terbuka.3,11

Terapi sedini mungkin sangat dianjurkan untuk mengurangi gejala, meningkatkan kualitas hidup dan menghindari komplikasi akibat obstruksi yang berkepanjangan. Tindakan bedah masih merupakan terapi utama untuk hiperplasia prostat (lebih dari 90% kasus). Meskipun demikian pada dekade terakhir dikembangkan pula beberapa terapi non-bedah yang mempunyai keunggulan kurang invasif dibandingkan dengan terapi bedah. Mengingat gejala klinik hiperplasia prostat disebabkan oleh 3 faktor yaitu pembesaran kelenjar

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periuretral, menurunnya elastisitas leher vesika, dan berkurangnya kekuatan detrusor, maka pengobatan gejala klinik ditujukan untuk :

1. Menghilangkan atau mengurangi volume prostat

2. Mengurangi tonus leher vesika, otot polos prostat dan kapsul prostat

3. Melebarkan uretra pars prostatika, menambah kekuatan detrusor 7,11

Tujuan terapi pada pasien hiperplasia prostat adalah menghilangkan obstruksi pada leher vesica urinaria. Hal ini dapat dicapai dengan cara medikamentosa, pembedahan, atau tindakan endourologi yang kurang invasif.

Pilihan Terapi pada Hiperplasi Prostat Benigna7

Observasi Medikamentosa

Operasi Invasif Minimal

Watchfull waiting

Penghambat adrenergik α

Prostatektomi terbukaTUMTTUBD

Penghambat reduktase αFitoterapiHormonal

Endourologi1. TUR P2. TUIP3. TULP (laser)

Strent uretra dengan

prostacathTUNA

Terapi Konservatif Non Operatif

1. Observasi (Watchful waiting)

Biasanya dilakukan pada pasien dengan keluhan ringan. Nasihat yang diberikan adalah mengurang minum setelah makan malam untuk mengurangi nokturia, menghindari obat-obatan dekongestal (parasimpatolitik), mengurangi minum kopi, dan tidak diperbolehkan minuman alkohol agar tidak sering miksi. Setiap 3 bulan lakukan kontrol keluhan (sistem skor), sisa kencing dan pemeriksaan colok dubur.5

2. Medikamentosa

Tujuan terapi medikamentosa adalah untuk:

1. mengurangi resistensi leher buli-buli dengan obat-obatan golongan  blocker (penghambat alfa adrenergik)

2. menurunkan volume prostat dengan cara menurunkan kadar hormon testosteron/dehidrotestosteron (DHT)

Obat Penghambat adrenergik 

Dasar pengobatan ini adalah mengusahakan agar tonus otot polos di dalam prostat dan leher vesica berkurang dengan menghambat rangsangan alpha adrenergik. Seperti diketahui di dalam otot polos prostat dan leher vesica banyak terdapat reseptor alpha adrenergik. Obat-obatan yang sering digunakan prazosin, terazosin, doksazosin, dan alfuzosin. Obat penghambat alpha adrenergik yang lebih selektif terhadap otot polos prostat yaitu α1a (tamsulosin), sehingga efek sistemik yang tak diinginkan dari pemakai obat ini

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dapat dikurangi. Dosis dimulai 1 mg/hari sedangkan dosis tamzulosin 0,2-0,4 mg/hari. Penggunaan antagonis alpha 1 adrenergik untuk mengurangi obstruksi pada vesica tanpa merusak kontraktilitas detrusor.

Obat-obatan golongan ini memberikan perbaikan laju pancaran urine, menurunkan sisa urine dan mengurangi keluhan. Obat-obat ini juga memberi penyulit hipotensi, pusing, mual, lemas, dan meskipun sangat jarang bisa terjadi ejakulasi retrograd, biasanya pasien mulai merasakan berkurangnya keluhan dalam waktu 1-2 minggu setelah pemakaian obat.

Obat Penghambat Enzim 5 Alpha Reduktase

Obat yang dipakai adalah finasterid (proskar) dengan dosis 1x5 mg/hari. Obat golongan ini dapat menghambat pembentukan dehidrotestosteron sehingga prostat yang membesar dapat mengecil. Namun obat ini bekerja lebih lambat daripada golongan alpha blocker dan manfaatnya hanya jelas pada prostat yang sangat besar. Salah satu efek samping obat ini adalah melemahkan libido dan ginekomastia. 3,4,12

Fitoterapi

Merupakan terapi alternatif yang berasal dari tumbuhan. Fitoterapi yang digunakan untuk pengobatan BPH adalah Serenoa repens atau Saw Palmetto dan Pumpkin Seeds. Keduanya, terutama Serenoa repens semakin diterima pemakaiannya dalam upaya pengendalian prostatisme BPH dalam konteks “watchfull waiting strategy”.

Saw Palmetto menunjukkan perbaikan klinis dalam hal:

frekuensi nokturia berkurang

aliran kencing bertambah lancar

volume residu di kandung kencing berkurang

gejala kurang enak dalam mekanisme urinaria berkurang.

Mekanisme kerja obat diduga kuat:

menghambat aktivitas enzim 5 alpha reduktase dan memblokir reseptor androgen

bersifat antiinflamasi dan anti oedema dengan cara menghambat aktivitas enzim cyclooxygenase dan 5 lipoxygenase. 4,5

3. Terapi Operatif

Tindakan operasi ditujukan pada hiperplasi prostat yang sudah menimbulkan penyulit tertentu, antara lain: retensi urin, batu saluran kemih, hematuri, infeksi saluran kemih, kelainan pada saluran kemih bagian atas, atau keluhan LUTS yang tidak menunjukkan perbaikan setelah menjalani pengobatan medikamentosa. Tindakan operasi yang dilakukan adalah operasi terbuka atau operasi endourologi transuretra.

1. Prostatektomi terbuka

a.1. Retropubic infravesica (Terence Millin)

Keuntungan :

Tidak ada indikasi absolut, baik untuk adenoma yang besar pada subservikal

Mortaliti rate rendah

Langsung melihat fossa prostat

Dapat untuk memperbaiki segala jenis obstruksi leher buli

Perdarahan lebih mudah dirawat

Tanpa membuka vesika sehingga pemasangan kateter tidak perlu selama bila membuka vesika

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Kerugian :

Dapat memotong pleksus santorini

Mudah berdarah

Dapat terjadi osteitis pubis

Tidak bisa untuk BPH dengan penyulit intravesikal

Tidak dapat dipakai kalau diperlukan tindakan lain yang harus dikerjakan dari dalam vesika

Komplikasi : perdarahan, infeksi, osteitis pubis, trombosis

a.2. Suprapubic Transvesica/TVP (Freeyer)

Keuntungan :

Baik untuk kelenjar besar

Banyak dikerjakan untuk semua jenis pembesaran prostat

Operasi banyak dipergunakan pada hiperplasia prostat dengan penyulit : batu buli, batu ureter distal, divertikel, uretrokel, adanya sistostomi, retropubik sulit karena kelainan os pubis, kerusakan sphingter eksterna minimal.

Kerugian :

- Memerlukan pemakain kateter lebih lama sampai luka pada dinding vesica sembuh

Sulit pada orang gemuk

Sulit untuk kontrol perdarahan

Merusak mukosa kulit

Mortality rate 1 -5 %

Komplikasi :

Striktura post operasi (uretra anterior 2 – 5 %, bladder neck stenosis 4%)

Inkontinensia (<1%)

Perdarahan

Epididimo orchitis

Recurent (10 – 20%)

Carcinoma

Ejakulasi retrograde

Impotensi

Fimosis

Deep venous trombosis

a.3. Transperineal

Keuntungan :

Dapat langssung pada fossa prostat

Pembuluh darah tampak lebih jelas

Mudah untuk pinggul sempit

Langsung biopsi untuk karsinoma

Kerugian :

Impotensi

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Inkontinensia

Bisa terkena rektum

Perdarahan hebat

Merusak diagframa urogenital 3,6,7,8,1011

b. Prostatektomi Endourologi

b.1.Trans Urethral Resection of the Prostate (TURP)

Yaitu reseksi endoskopik malalui uretra. Jaringan yang direseksi hampir seluruhnya terdiri dari jaringan kelenjar sentralis. Jaringan perifer ditinggalkan bersama kapsulnya. Metode ini cukup aman, efektif dan berhasil guna, bisa terjadi ejakulasi retrograd dan pada sebagaian kecil dapat mengalami impotensi. Hasil terbaik diperoleh pasien yang sungguh membutuhkan tindakan bedah. Untuk keperluan tersebut, evaluasi urodinamik sangat berguna untuk membedakan pasien dengan obstruksi dari pasien non-obstruksi. Evaluasi ini berperan selektif dalam penentuan perlu tidaknya dilakukan TUR.

Saat ini tindakan TUR P merupakan tindakan operasi paling banyak dikerjakan di seluruh dunia. Reseksi kelenjar prostat dilakukan trans-uretra dengan mempergunakan cairan irigan (pembilas) agar supaya daerah yang akan direseksi tetap terang dan tidak tertutup oleh darah. Cairan yang dipergunakan adalah berupa larutan non ionik, yang dimaksudkan agar tidak terjadi hantaran listrik pada saat operasi. Cairan yang sering dipakai dan harganya cukup murah adalah H2O steril (aquades).

Salah satu kerugian dari aquades adalah sifatnya yang hipotonik sehingga cairan ini dapat masuk ke sirkulasi sistemik melalui pembuluh darah vena yang terbuka pada saat reseksi. Kelebihan air dapat menyebabkan terjadinya hiponatremia relatif atau gejala intoksikasi air atau dikenal dengan sindroma TUR P. Sindroma ini ditandai dengan pasien yang mulai gelisah, kesadaran somnolen, tekanan darah meningkat, dan terdapat bradikardi.

Jika tidak segera diatasi, pasien akan mengalami edema otak yang akhirnya jatuh dalam keadaan koma dan meninggal. Angka mortalitas sindroma TURP ini adalah sebesar 0,99%. Karena itu untuk mengurangi timbulnya sindroma TUR P dipakai cairan non ionik yang lain tetapi harganya lebih mahal daripada aquades, antara lain adalah cairan glisin, membatasi jangka waktu operasi tidak melebihi 1 jam, dan memasang sistostomi suprapubik untuk mengurangi tekanan air pada buli-buli selama reseksi prostat.

Keuntungan :

Luka incisi tidak ada

Lama perawatan lebih pendek

Morbiditas dan mortalitas rendah

Prostat fibrous mudah diangkat

Perdarahan mudah dilihat dan dikontrol

Kerugian :

Teknik sulit

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Resiko merusak uretra

Intoksikasi cairan

Trauma sphingter eksterna dan trigonum

Tidak dianjurkan untuk BPH yang besar

Alat mahal

Ketrampilan khusus

Komplikasi:

- Selama operasi: perdarahan, sindrom TURP, dan perforasi

- Pasca bedah dini: perdarahan, infeksi lokal atau sistemik

- Pasca bedah lanjut: inkontinensia, disfungsi ereksi, ejakulasi retrograd, dan striktura uretra.

b.2.Trans Urethral Incision of Prostate (TUIP)

Metode ini di indikasikan untuk pasien dengan gejala obstruktif, tetapi ukuran prostatnya mendekati normal. Pada hiperplasia prostat yang tidak begitu besar dan pada pasien yang umurnya masih muda umumnya dilakukan metode tersebut atau incisi leher buli-buli atau bladder neck incision (BNI) pada jam 5 dan 7. Terapi ini juga dilakukan secara endoskopik yaitu dengan menyayat memakai alat seperti yangg dipakai pada TUR P tetapi memakai alat pemotong yang menyerupai alat penggaruk, sayatan dimulai dari dekat muara ureter sampai dekat ke verumontanum dan harus cukup dalam sampai tampak kapsul prostat. Kelebihan dari metode ini adalah lebih cepat daripada TUR dan menurunnya kejadian ejakulasi retrograde dibandingkan dengan cara TUR.

b.3.Trans Urethral Laser of the Prostate (Laser prostatectomy)

Oleh karena cara operatif (operasi terbuka atau TUR P) untuk mengangkat prostat yang membesar merupakan operasi yang berdarah, sedang pengobatan dengan TUMT dan TURF belum dapat memberikan hasil yang sebaik dengan operasi maka dicoba cara operasi yang dapat dilakukan hampir tanpa perdarahan.

Waktu yang diperlukan untuk melaser prostat biasanya sekitar 2-4 menit untuk masing-masing lobus prostat (lobus lateralis kanan, kiri dan medius). Pada waktu ablasi akan ditemukan pop corn effect sehingga tampak melalui sistoskop terjadi ablasi pada permukaan prostat, sehingga uretra pars prostatika akan segera menjadi lebih lebar, yang kemudian masih akan diikuti efek ablasi ikutan yang akan menyebabkan “laser nekrosis” lebih dalam setelah 4-24 minggu sehingga hasil akhir nanti akan terjadi rongga didalam prostat menyerupai rongga yang terjadi sehabis TUR.

Keuntungan bedah laser ialah :

1. Tidak menyebabkan perdarahan sehingga tidak mungkin terjadi retensi akibat bekuan darah dan tidak memerlukan transfusi

2. Teknik lebih sederhana

3. Waktu operasi lebih cepat

4. Lama tinggal di rumah sakit lebih singkat

5. Tidak memerlukan terapi antikoagulan

6. Resiko impotensi tidak ada

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7. Resiko ejakulasi retrograd minimal

Kerugian :

Penggunaan laser ini masih memerlukan anestesi (regional).6,8,11

3. Invasif Minimal

1. Trans Urethral Microwave Thermotherapy (TUMT)

Cara memanaskan prostat sampai 44,5C – 47C ini mulai diperkenalkan dalam tiga tahun terakhir ini. Dikatakan dengan memanaskan kelenjar periuretral yang membesar ini dengan gelombang mikro (microwave) yaitu dengan gelombang ultarasonik atau gelombang radio kapasitif akan terjadi vakuolisasi dan nekrosis jaringan prostat, selain itu juga akan menurunkan tonus otot polos dan kapsul prostat sehingga tekanan uretra menurun sehingga obstruksi berkurang. lanjut mengenai cara kerja dasar klinikal, efektifitasnya serta side efek yang mungkin timbul.

Cara kerja TUMT ialah antene yang berada pada kateter dapat memancarkan microwave kedalam jaringan prostat. Oleh karena temperatur pada antene akan tinggi maka perlu dilengkapi dengan surface costing agar tidak merusak mucosa ureter. Dengan proses pendindingan ini memang mucosa tidak rusak tetapi penetrasi juga berkurang.

Cara TURF (trans Uretral Radio Capacitive Frequency) memancarkan gelombang “radio frequency” yang panjang gelombangnya lebih besar daripada tebalnya prostat juga arah dari gelombang radio frequency dapat diarahkan oleh elektrode yang ditempel diluar (pada pangkal paha) sehingga efek panasnya dapat menetrasi sampai lapisan yang dalam. Keuntungan lain oleh karena kateter yang ada alat pemanasnya mempunyai lumen sehingga pemanasan bisa lebih lama, dan selama pemanasan urine tetap dapat mengalir keluar.

2. Trans Urethral Ballon Dilatation (TUBD)

Dilatasi uretra pars prostatika dengan balon ini mula-mula dikerjakan dengan jalan melakukan commisurotomi prostat pada jam 12.00 dengan jalan melalui operasi terbuka (transvesikal).

Prostat di tekan menjadi dehidrasi sehingga lumen uretra melebar. Mekanismenya :

1. Kapsul prostat diregangkan

2. Tonus otot polos prostat dihilangkan dengan penekanan tersebut

3. Reseptor alpha adrenergic pada leher vesika dan uretra pars prostatika dirusak

3. Trans Urethral Needle Ablation (TUNA)

Yaitu dengan menggunakan gelombang radio frekuensi tinggi untuk menghasilkan ablasi termal pada prostat. Cara ini mempunyai prospek yang baik guna mencapai tujuan untuk menghasilkan prosedur dengan perdarahan minimal, tidak invasif dan mekanisme ejakulasi dapat dipertahankan.

4. Stent Urethra

Pada hakekatnya cara ini sama dengan memasang kateter uretra, hanya saja kateter tersebut dipasang pada uretra pars prostatika. Bentuk stent ada yang spiral

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dibuat dari logam bercampur emas yang dipasang diujung kateter (Prostacath). Stents ini digunakan sebagai protesis indwelling permanen yang ditempatkan dengan bantuan endoskopi atau bimbingan pencitraan. Untuk memasangnya, panjang uretra pars prostatika diukur dengan USG dan kemudian dipilih alat yang panjangnya sesuai, lalu alat tersebut dimasukkan dengan kateter pendorong dan bila letak sudah benar di uretra pars prostatika maka spiral tersebut dapat dilepas dari kateter pendorong. Pemasangan stent ini merupakan cara mengatasi obstruksi infravesikal yang juga kurang invasif, yang merupakan alternatif sementara apabila kondisi penderita belum memungkinkan untuk mendapatkan terapi yang lebih invasif. 

BackgroundNephrolithiasis is a common disease that is estimated to produce medical costs of $2.1 billion per year in the United States.[1] Nephrolithiasis specifically refers to calculi in the kidneys, but this article discusses both renal calculi (see the first image below) and ureteral calculi (ureterolithiasis; see the second image below). Ureteral calculi almost always originate in the kidneys, although they may continue to grow once they lodge in the ureter.

Small renal calculus that would likely respond to extracorporeal shockwave lithotripsy.

Distal ureteral stone observed through a small, rigid ureteroscope prior to ballistic lithotripsy and extraction. The small caliber and excellent optics of today's endoscopes greatly facilitate minimally invasive treatment of urinary stones.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.

Acute renal colic is probably the most excruciatingly painful event a person can endure. Striking without warning, the pain is often described as being worse than childbirth, broken bones, gunshot wounds, burns, or surgery. Renal colic affects approximately 1.2 million people each year and accounts for approximately 1% of all hospital admissions.

Most active emergency departments (EDs) manage patients with acute renal colic every day, depending on the hospital’s patient population. Initial management consists of proper diagnosis, prompt initial treatment, and appropriate consultations, but concurrently efforts

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should be directed towards patient education, including initial preventive therapy measures.

Although nephrolithiasis is not a common cause of renal failure, certain problems, such as preexisting azotemia and solitary functional kidneys, clearly present a higher risk of additional renal damage. Other high-risk factors include diabetes, struvite and/or staghorn calculi, and various hereditary diseases such as primary hyperoxaluria, Dent disease, cystinuria, and polycystic kidney disease. Spinal cord injuries and similar functional or anatomical urological anomalies also predispose patients with kidney stones to an increased risk of renal failure.

Recurrent obstruction, especially when associated with infection and tubular epithelial or renal interstitial cell damage from microcrystals, may activate the fibrogenic cascade, which is mainly responsible for the actual loss of functional renal parenchyma.

For other discussions on urolithiasis and nephrolithiasis, see Pediatric Urolithiasis, as well as Imaging Urinary Calculi, Hypercalciuria, Hyperoxaluria, and Hypocitraturia.

AnatomyThe basic anatomy of the ureter is as follows (see the image below).

Nephrolithiasis: acute renal colic. Anatomy of the ureter.Most of the pain receptors of the upper urinary tract responsible for the perception of renal colic are located submucosally in the renal pelvis, calices, renal capsule, and upper ureter. Acute distention seems to be more important in the development of the pain of acute renal colic than spasm, local irritation, or ureteral hyperperistalsis.

Stimulation of the peripelvic renal capsule causes flank pain, while stimulation of the renal pelvis and calices causes typical renal colic (see the image below). Mucosal irritation can be sensed in the renal pelvis to some degree by chemoreceptors, but this irritation is thought to play only a minor role in the perception of renal or ureteral colic.

Nephrolithiasis: acute renal colic. Renal colic and flank pain.Renal pain fibers are primarily preganglionic sympathetic nerves that reach spinal cord levels T-11 to L-2 through the dorsal nerve roots (see the images below). Aortorenal, celiac, and inferior mesenteric ganglia

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are also involved. Spinal transmission of renal pain signals occurs primarily through the ascending spinothalamic tracts.

Nephrolithiasis: acute renal colic. Nerve supply of the kidney.

Nephrolithiasis: acute renal colic. Nerve supply of the kidney.In the lower ureter, pain signals are also distributed through the genitofemoral and ilioinguinal nerves (see the image below). The nervi erigentes, which innervate the intramural ureter and bladder, are responsible for some of the bladder symptoms that often accompany an intramural ureteral calculus.

Nephrolithiasis: acute renal colic. Distribution of nerves in the flank.

PathophysiologyFormation of stones

Urinary tract stone disease, depicted below, is likely caused by two basic phenomena.

The first phenomenon 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 resulting calculi give rise to symptoms when they become impacted within the ureter as they pass toward the urinary bladder.

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 various rare stones related to precipitation of medications in the urinary tract. Supersaturation of the urine is likely the underlying cause of uric and cystine stones, but calcium-based stones (especially calcium oxalate stones) may have a more complex etiology.

The second phenomenon, which is most likely responsible for calcium oxalate stones, is deposition of stone material on a renal papillary calcium phosphate nidus, typically a Randall plaque (which are always composed of calcium phosphate). Evan et al recently proposed this model based on evidence accumulating from several laboratories.[2]

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Calcium phosphate precipitates in the basement membrane of the thin loops of Henle, erodes into the interstitium, and then accumulates in the subepithelial space of the renal papilla. The subepithelial deposits, which have long been known as Randall plaques, eventually erode through the papillary urothelium. Stone matrix, calcium phosphate, and calcium oxalate gradually deposit on the substrate to create a urinary calculus.

Development of renal colic pain and renal damage

The colicky-type pain known as renal colic usually begins in the upper lateral midback over the costovertebral angle and occasionally subcostally. It radiates inferiorly and anteriorly toward the groin. The pain generated by renal colic is primarily caused by the dilation, stretching, and spasm caused by the acute ureteral obstruction. (When a severe but chronic obstruction develops, as in some types of cancer, it is usually painless.)

In the ureter, an increase in proximal peristalsis through activation of intrinsic ureteral pacemakers may contribute to the perception of pain. Muscle spasm, increased proximal peristalsis, local inflammation, irritation, and edema at the site of obstruction may contribute to the development of pain through chemoreceptor activation and stretching of submucosal free nerve endings.

The term "renal colic" is actually a misnomer, because this pain tends to remain constant, whereas intestinal or biliary colic is usually somewhat intermittent and often comes in waves. The pattern of the pain depends on the individual’s pain threshold and perception and on the speed and degree of the changes in hydrostatic pressure within the proximal ureter and renal pelvis. Ureteral peristalsis, stone migration, and tilting or twisting of the stone with subsequent intermittent obstructions may cause exacerbation or renewal of the renal colic pain.

The severity of the pain depends on the degree and site of the obstruction, not on the size of the stone. A patient can often point to the site of maximum tenderness, which is likely to be the site of the ureteral obstruction (see the image below).

Nephrolithiasis: acute renal colic. Distribution of renal and ureteral pain.A stone moving down the ureter and causing only intermittent obstruction actually may be more painful than a stone that is motionless. A constant obstruction, even if high grade, allows for

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various autoregulatory mechanisms and reflexes, interstitial renal edema, and pyelolymphatic and pyelovenous backflow to help diminish the renal pelvic hydrostatic pressure, which gradually helps reduce the pain.

The interstitial renal edema produced stretches the renal capsule, enlarges the kidney (ie, nephromegaly), and increases renal lymphatic drainage. (Increased capillary permeability facilitates this edema.) It may also reduce the radiographic density of the affected kidney’s parenchyma when viewed on a noncontrast CT scan.

Distention of the renal pelvis initially stimulates ureteral hyperperistalsis, but this diminishes after 24 hours, as does renal blood flow. Peak hydrostatic renal pelvis pressure is attained within 2-5 hours after a complete obstruction.

Within the first 90 minutes of a complete ureteral obstruction, afferent preglomerular arteriolar vasodilation occurs, which temporarily increases renal blood flow. Between 90 minutes and 5 hours after the obstruction, renal blood flow starts to decrease while intraureteral pressure continues to rise. By 5 hours after a complete obstruction, both renal blood flow and intraluminal ureteral pressure decrease on the affected side.

Renal blood flow decreases to approximately 50% of normal baseline levels after 72 hours, to 30% after 1 week, to 20% after 2 weeks, and to 12% after 8 weeks. By this point, intraureteral pressures have returned to normal, but the proximal ureteral dilation remains and ureteral peristalsis is minimal.

Interstitial edema of the affected kidney actually enhances fluid reabsorption, which helps to increase the renal lymphatic drainage to establish a new, relatively stable, equilibrium. At the same time, renal blood flow increases in the contralateral kidney as renal function decreases in the obstructed unit.

In summary, by 24 hours after a complete ureteral obstruction, the renal pelvic hydrostatic pressure has dropped because of (1) a reduction in ureteral peristalsis; (2) decreased renal arterial vascular flow, which causes a corresponding drop in urine production on the affected side; and (3) interstitial renal edema, which leads to a marked increase in renal lymphatic drainage.

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Additionally, as the ureter proximal to the stone distends, some urine can sometimes flow around the obstruction, relieving the proximal hydrostatic pressure and establishing a stable, relatively painless equilibrium. These factors explain why severe renal colic pain typically lasts less than 24 hours in the absence of any infection or stone movement.

Whether calyceal stones cause pain continues to be controversial. In general, in the absence of infection, how a renal stone causes pain remains unclear, unless the stone also causes obstruction. Arguably, proving that a calyceal stone is causing an obstruction can be difficult. However, a stone trapped in a calyx plausibly could block the outflow tract from that calyx, causing an obstruction and subsequent pain.

Experimental studies in animals have suggested that renal damage may begin within 24 hours of a complete obstruction and that permanent kidney deterioration starts within 5-14 days. Whereas some practitioners wait several months for a stone to pass in an asymptomatic patient, others argue that permanent damage is occurring as long as intervention is delayed.

Based on personal experience and anecdotal cases, the author recommends waiting no longer than 4 weeks for a stone to pass spontaneously before considering intervention. Convincing asymptomatic patients of the need for surgical intervention may be difficult in the absence of a clear consensus in the urological community about the length of time to wait before surgical stone removal, fragmentation, or bypass.

If only a partial obstruction is present, the same changes occur, but to a lesser degree and over a longer period. Proximal ureteric and renal pelvic hydrostatic pressures tend to remain elevated longer, and ureteral peristalsis does not diminish as quickly. If the increased pressure is sufficient to establish a reasonable flow beyond the obstructing stone, glomerular filtration and renal blood flow approximates reference range baseline levels, although pain may be ongoing.

EtiologyA low fluid intake, with a subsequent low volume of urine production, produces high concentrations of stone-forming solutes in the urine. This is an important, if not the most important, environmental factor in

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

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, as well as reduced urinary citrate levels.

Hypercalciuria is the most common metabolic abnormality. Some cases of hypercalciuria are related to increased intestinal absorption of calcium (associated with excess dietary calcium and/or overactive calcium absorption mechanisms), some are related to excess resorption of calcium from bone (ie, hyperparathyroidism), and some are related to an inability of the renal tubules to properly reclaim calcium in the glomerular filtrate (renal-leak hypercalciuria).

Magnesium and especially citrate are important inhibitors of stone formation in the urinary tract. Decreased levels of these in the urine predispose to stone formation.

The following are the 4 main chemical types of renal calculi, which together are associated with more than 20 underlying etiologies:

Calcium stonesStruvite (magnesium ammonium phosphate) stonesUric acid stonesCystine stonesStone analysis, together with serum and 24-hour urine metabolic evaluation, can identify an etiology in more than 95% of patients. Specific therapy can result in a remission rate of more than 80% and can decrease the individual recurrence rate by 90%. Therefore, emergency physicians should stress the importance of urologic follow-up, especially in patients with recurrent stones, solitary kidneys, or previous kidney or stone surgery and in all children.[3]

Calcium stones

Calcium stones account for 75% of renal calculi. Recent data suggest that a low-protein, low-salt diet may be preferable to a low-calcium diet in hypercalciuric stone formers for preventing stone recurrences.[4] Epidemiological studies have shown that the incidence of stone disease is inversely related to the magnitude of dietary calcium intake in first-time stone formers.

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There is a trend in the urology community not to restrict dietary intake of calcium in recurrent stone formers. This is especially important for postmenopausal women in whom there is an increased concern for the development of osteoporosis. Calcium oxalate, calcium phosphate, and calcium urate are associated with the following disorders:

Hyperparathyroidism - Treated surgically or with orthophosphates if the patient is not a surgical candidate

Increased gut absorption of calcium - The most common identifiable cause of hypercalciuria, treated with calcium binders or thiazides plus potassium citrate

Renal calcium leak - Treated with thiazide diureticsRenal phosphate leak - Treated with oral phosphate supplementsHyperuricosuria - Treated with allopurinol, low purine diet, or

alkalinizing agents such as potassium citrateHyperoxaluria - Treated with dietary oxalate restriction, oxalate

binders, vitamin B-6, or orthophosphatesHypocitraturia - Treated with potassium citrateHypomagnesuria - Treated with magnesium supplementsStruvite (magnesium ammonium phosphate) stones

Struvite stones account for 15% of renal calculi. They are associated with chronic urinary tract infection (UTI) with gram-negative rods capable of splitting urea into ammonium, which combines with phosphate and magnesium. Usual organisms include Proteus, Pseudomonas, and Klebsiella species. Escherichia coli is not capable of splitting urea and, therefore, is not associated with struvite stones. Urine pH is typically greater than 7.

Underlying anatomical abnormalities that predispose patients to recurrent kidney infections should be sought and corrected. UTI does not resolve until stone is removed entirely.

Uric acid stones

Uric acid stones account for 6% of renal calculi. These are associated with urine pH less than 5.5, high purine intake (eg, organ meats, legumes, fish, meat extracts, gravies), or malignancy (ie, rapid cell turnover). Approximately 25% of patients with uric acid stone have gout.

Serum and 24-hour urine sample should be sent for creatinine and uric acid determination. If serum or urinary uric acid is elevated, the patient

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may be treated with allopurinol 300 mg daily. Patients with normal serum or urinary uric acid are best managed by alkali therapy alone.

Cystine stones

Cystine stones account for 2% of renal calculi. They arise because of an intrinsic metabolic defect resulting in failure of renal tubular reabsorption of cystine, ornithine, lysine, and arginine. Urine becomes supersaturated with cystine, with resultant crystal deposition.

Cystine stones are treated with a low-methionine diet (unpleasant), binders such as penicillamine or a-mercaptopropionylglycine, large urinary volumes, or alkalinizing agents. A 24-hour quantitative urinary cystine determination helps to titrate the dose of drug therapy to achieve a urinary cystine concentration of less than 300 mg/L.

Drug-induced stone disease

A number of medications or their metabolites can precipitate in urine causing stone formation. These include indinavir; atazanavir; guaifenesin; triamterene; silicate (overuse of antacids containing magnesium silicate); and sulfa drugs including sulfasalazine, sulfadiazine, acetylsulfamethoxazole, acetylsulfasoxazole, and acetylsulfaguanidine.[5, 6, 7]

EpidemiologyUnited States statistics

The lifetime prevalence of nephrolithiasis is approximately 12% for men and 7% for women in the United States, and it is rising. Having a family member with a history of stones doubles these rates. Approximately 30 million people are at risk in the United States. Roughly 2 million patients present on an outpatient basis with stone disease each year in the United States, which is a 40% increase from 1994.[1]

The likelihood that a white US male will develop stone disease by age 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. Recurrence rates after the first stone episode are 14%, 35%, and 52% at 1, 5, and 10 years, respectively.

The increasing incidence of kidney stone disease in the United States seems to be related to the socioeconomic status of the patient population. The lower the economic status, the lower the likelihood of

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renal stones. Other parts of the world with lower standards of living tend to have lower incidences of kidney stones but have higher rates of bladder calculi.

Black people have a lower incidence of stones than white people, and people living in the South and Southwest have higher incidences of stones than people living in other parts of the United States. The increased incidence noted in the southeastern United States has prompted the use of the term “stone belt” for this region of the country.[8]

International statistics

Nephrolithiasis occurs in all parts of the world. The incidence of urinary tract stone disease in developed countries is similar to that in the United States; the annual incidence of urinary tract stones in the industrialized world is estimated to be 0.2%. Stone disease is rare in only a few areas, such as Greenland and the coastal areas of Japan. A lifetime risk of 2-5% has been noted for in Asia, 8-15% for the West, and 20% for Saudi Arabia.

In developing countries, bladder calculi are more common than upper urinary tract calculi; the opposite is true in developed countries. These differences are believed to be diet-related.

Age distribution for nephrolithiasis

Most urinary calculi develop in persons aged 20-49 years. Peak incidence occurs in people aged 35-45 years, but the disease can affect anyone at any age. Patients in whom multiple recurrent stones form usually develop their first stones while in their second or third decade of life.

An initial stone attack after age 50 years is relatively uncommon. Nephrolithiasis in children is rare; approximately 5-10 children aged 10 months to 16 years are seen annually for the condition at a typical US pediatric referral center.

Sex distribution for nephrolithiasis

In general, urolithiasis is more common in males (male-to-female ratio of 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. Female patients have a higher incidence of infected hydronephrosis.

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Racial differences in incidence

Urinary tract calculi are far more common in Asians and whites than in Native Americans, Africans, African Americans, and some natives of the Mediterranean region. White males are affected 3-4 times more often than African American males, though African Americans have a higher incidence of infected ureteral calculi than whites.

Although some differences may be attributable to geography (stones are more common in hot and dry areas) and diet, heredity also appears to be a factor. This is suggested by the finding that, in regions with both white and nonwhite populations, stone disease is much more common in whites.

PrognosisApproximately 80-85% of stones pass spontaneously. Approximately 20% of patients require hospital admission because of unrelenting pain, inability to retain enteral fluids, proximal UTI, or inability to pass the stone.

The most morbid and potentially dangerous aspect of stone disease is the combination of urinary tract obstruction and upper urinary tract infection. Pyelonephritis, pyonephrosis, and urosepsis can ensue. Early recognition and immediate surgical drainage are necessary in these situations.

Because 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. Recurrence rates after an initial episode of ureterolithiasis have also been reported to be 14%, 35%, and 52% at 1, 5, and 10 years, respectively.

Metabolic evaluation and treatment are indicated for patients at greater risk for recurrence, including those who present with multiple stones, who have a personal or family history of previous stone

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formation, who present with stones at a younger age, or who have residual stones after treatment.

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 a high fluid intake and subsequent high urinary volume. Without an adequate urinary volume, no amount of medical or dietary therapy is likely to be successful in preventing stone formation.

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 completely eliminate new stones in many patients and significantly reduces new stone formation in most patients.

Patient EducationA 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.

Although discovering the underlying cause of a patient’s stones and starting preventive therapy is not the primary responsibility of the physician treating a patient with acute renal colic (such measures are best addressed once the immediate problem has been addressed), this physician should, at the very least, educate the patient and family members about the availability of preventive testing and treatment. When properly performed and evaluated, preventive treatment plans can improve the situation in most patients with stones.

Note that failure to offer stone-prevention advice could actually be a source of medicolegal liability. Numerous patients have claimed they have not been told about stone-prevention options.

One anecdotal example from the practice of one of the editors is that of a 65-year-old man with a 5-year history of more than 60 stones. Although he underwent two open surgeries for stone removal, his stones were not evaluated for chemical composition. Eventually, the stones were analyzed and found to be pure uric acid. Although his uric acid excretion rate was normal, he had highly acidic urine, which led to

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the uric acid calculi formation. After starting oral therapy of allopurinol and potassium citrate, he remained free of stones for 10 years.

Even patients who develop single stones may be strongly motivated to follow a program for maximum kidney stone prophylaxis. Discussing the pros and cons of a comprehensive stone-prevention program with all patients who have documented kidney stone disease—not with just those who are obviously at high risk—may be prudent.

Numerous internet sites offer kidney stone information, including the National Institutes of Health (NIH) and the American Urological Association Foundation.

For other patient education resources, see the Kidneys and Urinary System Center, as well as Kidney Stones, Blood in the Urine, and Intravenous Pyelogram.

Proceed to Clinical Presentation

HistoryPatients with urinary calculi may report pain, infection, or hematuria. Small nonobstructing stones in the kidneys only occasionally cause symptoms. 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.

Acute onset of severe flank pain radiating to the groin, gross or microscopic hematuria, nausea, and vomiting not associated with an acute abdomen are symptoms that most likely indicate renal colic caused by an acute ureteral or renal pelvic obstruction from a calculus. Renal colic pain rarely, if ever, occurs without obstruction.

Patients with large renal stones known as staghorn calculi (see the image below) are often relatively asymptomatic. The term "staghorn" refers to the presence of a branched kidney stone occupying the renal pelvis and at least one calyceal system. Such calculi usually manifest as infection and hematuria rather than as acute pain.

Complete staghorn calculus that fills the collecting system of the kidney (no intravenous contrast material in this patient). Although many staghorn calculi are struvite (related to infection with urease-splitting bacteria), the density of this stone suggests that it may be metabolic in origin and is likely composed of calcium

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oxalate. Percutaneous nephrostolithotomy or perhaps even open surgical nephrolithotomy is required to remove this stone.Asymptomatic bilateral obstruction, which is uncommon, manifests as symptoms of renal failure.

Important historical features are as follows:

Duration, characteristics, and location of painHistory of urinary calculiPrior complications related to stone manipulationUrinary tract infectionsLoss of renal functionFamily history of calculiSolitary or transplanted kidneyChemical composition of previously passed stonesLocation and characteristics of pain

Most calculi originate within the kidney and proceed distally, creating various degrees of urinary obstruction as they become lodged in narrow areas, including the ureteropelvic junction, pelvic brim, and ureterovesical junction. Location and quality of pain are related to position of the stone within the urinary tract. Severity of pain is related to the degree of obstruction, presence of ureteral spasm, and presence of any associated infection.

Stones obstructing the ureteropelvic junction may present with mild-to-severe deep flank pain without radiation to the groin, due to distention of the renal capsule. Stones impacted within the ureter cause abrupt, severe, colicky pain in the flank and ipsilateral lower abdomen with radiation to the testicles or the vulvar area. Intense nausea, with or without vomiting, usually is present.

Pain from upper ureteral stones tends to radiate to the flank and lumbar areas. On the right side, this can be confused with cholecystitis or cholelithiasis; on the left, the differential diagnoses include acute pancreatitis, peptic ulcer disease, and gastritis.

Midureteral calculi cause pain that radiates anteriorly and caudally. This midureteral pain in particular can easily mimic appendicitis on the right or acute diverticulitis on the left.

Distal ureteral stones cause pain that tends to radiate into the groin or testicle in the male or labia majora in the female because the pain is referred from the ilioinguinal or genitofemoral nerves.

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Stones lodged at the ureterovesical junction also may cause irritative voiding symptoms, such as urinary frequency and dysuria. If a stone is lodged in the intramural ureter, symptoms may appear similar to cystitis or urethritis. These symptoms include suprapubic pain, urinary frequency, urgency, dysuria, stranguria, pain at the tip of the penis, and sometimes various bowel symptoms, such as diarrhea and tenesmus. These symptoms can be confused with pelvic inflammatory disease, ovarian cyst rupture, or torsion and menstrual pain in women.

Calculi that have entered the bladder are usually asymptomatic and are passed relatively easily during urination. Rarely, a patient reports positional urinary retention (obstruction precipitated by standing, relieved by recumbency), which is due to the ball-valve effect of a large stone located at the bladder outlet.

Phases of acute renal colic attack

The actual pain attack tends to occur in somewhat predictable phases, with the pain reaching its peak in most patients within 2 hours of onset. The pain roughly follows the dermatomes of T-10 to S-4. The entire process typically lasts 3-18 hours. Renal colic has been described as having 3 clinical phases.

The first phase is the acute or onset phase.The typical attack starts early in the morning or at night, waking the patient from sleep. When it begins during the day, it tends to start slowly and insidiously. The pain is usually steady, increasingly severe, and continuous, sometimes punctuated by intermittent paroxysms of even more excruciating pain. The pain may increase to maximum intensity in as little as 30 minutes after onset or may take up to 6 hours or longer to peak. The typical patient reaches maximum pain 1-2 hours after the start of the renal colic attack.

The second phase is the constant phase. Once the pain reaches maximum intensity, it tends to remain constant until it is either treated or allowed to diminish spontaneously. The period of sustained maximal pain is called the constant phase of the renal colic attack. This phase usually lasts 1-4 hours but can persist longer than 12 hours in some cases. Most patients arrive in the ED during this phase of the attack.

The third phase is the abatement or relief phase.During this final phase, the pain diminishes fairly quickly, and patients finally feel relief. Relief can occur spontaneously at any time after the initial onset of the colic. Patients may fall asleep, especially if they have been

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administered strong analgesic medication. Upon awakening, the patient notices that the pain has disappeared. This final phase of the attack most commonly lasts 1.5-3 hours.

Other symptoms

Nausea and vomiting occur in at least 50% of patients with acute renal colic. Nausea is caused by the common innervation pathway of the renal pelvis, stomach, and intestines through the celiac axis and vagal nerve afferents. This is often compounded by the effects of narcotic analgesics, which often induce nausea and vomiting through a direct effect on gastrointestinal (GI) motility and an indirect effect on the chemoreceptor trigger zone in the medulla oblongata. Nonsteroidal anti-inflammatory drugs (NSAIDs) can often cause gastric irritation and GI upset.

The presence of a renal or ureteral calculus is not a guarantee that the patient does not have some other, unrelated medical problem causing the GI symptoms.

In some cases, a stone may pass before the definitive imaging procedure has been completed. In these cases, residual inflammation and edema still may cause some transient or diminishing obstruction and pain even without any stone being positively identified.

Physical ExaminationThe classic presentation for a patient with acute renal colic is the sudden onset of severe pain originating in the flank and radiating inferiorly and anteriorly. The pain is usually, but not always, associated with microscopic hematuria, nausea, and vomiting. Dramatic costovertebral angle tenderness is common; this pain can move to the upper or lower abdominal quadrant as a ureteral stone migrates distally. However, the rest of the examination findings are often unremarkable.

Abdominal examination usually is unremarkable. Bowel sounds may be hypoactive, a reflection of mild ileus, which is not uncommon in patients with severe, acute pain. Peritoneal signs are usually absent—an important consideration in distinguishing renal colic from other sources of flank or abdominal pain. Testicles may be painful but should not be very tender and should appear normal.

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Unlike patients with an acute abdomen, who usually try to lie absolutely still, patients with renal colic tend to move constantly, seeking a more comfortable position. (However, patients with pyonephrosis also tend to remain motionless.) The classic patient with renal colic is writhing in pain, pacing about, and unable to lie still, in contrast to a patient with peritoneal irritation, who remains motionless to minimize discomfort.

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 does not always correlate with the exact location of the stone, although the calculus is often in the general area of maximum discomfort.

Approximately 85% of all patients with renal colic demonstrate at least microscopic hematuria, which means that 15% of all patients with kidney stones do not have hematuria. Lack of hematuria alone does not exclude the diagnosis of acute renal colic. Tachycardia and hypertension are relatively common in these cases, even in patients with no prior personal history of abnormal cardiac or blood pressure problems.

Fever is not part of the presentation of uncomplicated nephrolithiasis. The presence of pyuria, fever, leukocytosis, or bacteriuria suggests the possibility of a urinary infection and the potential for an infected obstructed renal unit or pyonephrosis. Such a condition is potentially life threatening and should be treated as a surgical emergency.

In patients older than 60 years presenting with severe abdominal pain and with no prior history of renal stones, look carefully for physical signs of abdominal aortic aneurysm (AAA) (see Abdominal Aortic Aneurysm).

ComplicationsThe morbidity of urinary tract calculi is primarily due to obstruction with its associated pain, although nonobstructing calculi can still produce considerable discomfort. Conversely, patients with obstructing calculi may be asymptomatic, which is the usual scenario in patients who experience loss of renal function due to chronic untreated obstruction. Stone-induced hematuria is frightening to the patient but is rarely dangerous by itself.

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Serious complications of urinary tract stone disease include the following:

Abscess formationSerious infection of the kidney that diminishes renal functionUrinary fistula formationUreteral scarring and stenosisUreteral perforationExtravasationUrosepsisRenal loss due to long-standing obstructionInfected hydronephrosis is the most deadly complication because the presence of infection adjacent to the highly vascular renal parenchyma places the patient at risk for rapidly progressive sepsis and death.

A ureteral stone associated with obstruction and upper UTI is a true urologic emergency. Complications include perinephric abscess, urosepsis, and death. Immediate involvement of the urologist is essential.

Calyceal rupture with perinephric urine extravasation due to high intracaliceal pressures occasionally is seen and usually is treated conservatively.

Complete ureteral obstruction may occur in patients with tightly impacted stones. This is best diagnosed via IVP and is not discernible on noncontrast CT scan. Patients with 2 healthy kidneys can tolerate several days of complete unilateral ureteral obstruction without long-term effects on the obstructed kidney. If a patient with complete obstruction is well hydrated and pain and vomiting are well controlled, the patient can be discharged from the ED with urologic follow-up within 1-2 days.

Proceed to Differential Diagnoses

Diagnostic ConsiderationsThe diagnosis is often made on the basis of clinical symptoms alone, although confirmatory tests are usually performed. At this point, the goals and opinions of physicians in different specialties diverge.

From the point of view of the emergency department (ED) physician, making the diagnosis of a renal or ureteral stone and excluding appendicitis or abdominal aortic aneurysm (AAA) is sufficient. A

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urologist, who must ultimately make the decision about possible surgery, may require additional information. Before such a decision can be made, a urologist must know about the size, orientation, radiolucency, composition, and location of the stone and must know about overall kidney function, the presence of any infection, and other clinical information.

It is important to distinguish nephrolithiasis from the many other conditions (gynecologic and nongynecologic) that can cause flank pain (see Causes of Flank Pain).

Beware of the patient older than 60 years with an apparent first kidney stone. Consider the possibility of symptomatic AAA in the older patient, and rule out this possibility before pursuing the diagnosis of nephrolithiasis. Use bedside ultrasonography if the patient’s condition is potentially unstable. CT scan is a reasonable alternative in the stable patient.

Failure to diagnose or delay in diagnosing symptomatic AAA may lead to medicolegal liability. The pain of a leaking AAA often is misdiagnosed initially as renal colic. In one series of 134 patients with symptomatic AAA presenting to the ED, the following statistics were reported[9] :

Eighteen percent had an initial misdiagnosis of nephrolithiasis.All were older than 60 years and none had a prior history of renal

calculi.Eighty percent had a pulsatile mass noted by at least one examiner.Forty-three percent had microhematuria on urinalysis.Delay of diagnosis of AAA in the ED was associated with higher

mortality and morbidity rates than in the group who received the correct diagnosis promptly.

Failure to diagnose and promptly treat a urinary tract infection (UTI) proximal to a ureteral stone is also a potential source of medicolegal liability. Urgent urologic intervention must be sought in these patients.

Other conditions to consider include the following:

PyonephrosisRenal artery embolus

Differential DiagnosesAbdominal AbscessAcute Glomerulonephritis

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AppendicitisBiliary ColicCholecystitisCholelithiasisDiverticulitisDuodenal UlcersEpididymitisGastritis and Peptic Ulcer DiseaseGastrointestinal Foreign BodiesIleusInflammatory Bowel DiseaseLarge Bowel ObstructionLiver AbscessPancreatitisPapillary NecrosisPelvic Inflammatory DiseasePyonephrosisRectal Foreign BodiesRenal Arteriovenous MalformationRenal Cell CarcinomaRenal Vein Thrombosis ImagingSmall Bowel ObstructionSplenic AbscessTesticular TorsionUrinary Tract Infection in FemalesUrinary Tract Infection in MenUrinary Tract ObstructionViral Gastroenteritis

Proceed to Workup

Approach ConsiderationsAcute renal colic with resultant flank pain is a common and sometimes complex clinical problem. Whereas noncontrast abdominopelvic computed tomography (CT) scans have become the imaging modality of choice, in some situations, renal ultrasonography or a contrast study such as intravenous pyelography (IVP) may be preferred.

A kidneys-ureters-bladder (KUB) radiograph, in addition to the renal colic CT scan, facilitates the review and follow-up of stone patients. Alternatively, the “CT scout” (a digital reconstruction from the CT that has an appearance similar to a KUB) is almost as sensitive as a KUB and is a good substitute at the initial assessment if the stone seen on

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the CT scan is visible on the CT scout. Adding contrast to the CT scan study may sometimes help clarify a difficult or confusing case, but, in general, contrast obscures calcific densities, and, as such, contrast scans are usually indicated only during subsequent evaluation of patients with stones. The noncontrast CT is the cornerstone of initial radiographic assessment.

Most authors recommend diagnostic imaging to confirm the diagnosis in first-time episodes of ureterolithiasis, when the diagnosis is unclear, or if associated proximal urinary tract infection (UTI) is suspected. Lindqvist et al found that patients who are pain-free after receiving analgesics could be discharged from the emergency department (ED) and undergo radiologic imaging after 2-3 weeks without increasing morbidity.[10]

Initial stones in elderly people and in children are relatively uncommon; however, consider kidney stones whenever acute back or flank pain is encountered, regardless of patient age. When stones occur in persons in these uncommon age groups, a metabolic workup consisting of a 24-hour urine collection and appropriate serum laboratory testing is recommended.

Guidelines from the European Association of Urology recommend the following laboratory tests in all patients with an acute stone episode[11] :

Urinary sediment/dipstick test for demonstration of blood cells, with a test for bacteriuria (nitrite) and urine culture in case of a positive reaction

Serum creatinine level, as a measure of renal functionIn addition, patients with fever warrant a complete blood cell count. Patients with vomiting should have serum or plasma sodium and potassium levels measured. Optional tests that may provide useful information include a pH level (which might provide insight into the type of stone that the patient has formed) and measurement of serum or plasma calcium (which may identify hypercalcemia).[11]

UrinalysisMicroscopic examination of the urine for evidence of hematuria and infection is a critical part of the evaluation of a patient thought to have renal colic. Gross or microscopic hematuria is only present in approximately 85% of patients with urinary calculi. The lack of microscopic hematuria does not eliminate renal colic as a potential

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diagnosis. In addition to a dipstick evaluation, always perform a microscopic urinalysis in these patients.

One retrospective study found that 67% of patients with ureterolithiasis had more than 5 red blood cells (RBCs) per high-power field (hpf), and 89% of patients had more than 0 RBCs/hpf on urine microscopic examination.[12] In addition, 94.5% have hematuria if screened with microscopy plus urine dipstick testing.[13]

Degree of hematuria is not predictive of stone size or likelihood of passage. No literature exists to support the theory that ureterolithiasis without hematuria is indicative of complete ureteral obstruction.

Attention should also be paid to the presence or absence of leukocytes, crystals, and bacteria and to the urinary pH. In general, if the number of white blood cells (WBCs) in the urine is greater than 10 cells per high-power field or greater than the number of RBCs, suspect a UTI. Pyuria (>5 WBCs/hpf on a centrifuged specimen) in a patient with ureterolithiasis should prompt a careful search for signs of infected hydronephrosis.

Urinary crystals of calcium oxalate, uric acid, or cystine may occasionally be found upon urinalysis. When present, these crystals are very good clues to the underlying type and nature of any obstructing calculus.

Determining urinary pH also helps. A urine pH greater than 7 suggests presence of urea-splitting organisms, such as Proteus, Pseudomonas, or Klebsiella species, and struvite stones. A urine pH less than 5 suggests uric acid stones.

Blood StudiesComplete blood count

Whereas mild leukocytosis often accompanies a renal colic attack, a high index of suspicion for a possible renal or systemic infection should accompany any serum WBC count of 15,000/µL or higher in a patient presenting with an apparent acute kidney stone attack, even if afebrile. A depressed RBC count suggests a chronic disease state or severe ongoing hematuria.

Serum electrolytes, creatinine, calcium, uric acid, parathyroid hormone, and phosphorus

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Measurements of serum electrolyte, creatinine, calcium, uric acid, parathyroid hormone (PTH), and phosphorus are needed to assess a patient’s current renal function and to begin the assessment of metabolic risk for future stone formation.

A high serum uric acid level may indicate gouty diathesis or hyperuricosuria, while hypercalcemia suggests either renal-leak hypercalciuria (with secondary hyperparathyroidism) or primary hyperparathyroidism. If the serum calcium level is elevated, serum PTH levels should be obtained.

Serum creatinine level is the major predictor of contrast-induced nephrotoxicity. If the creatinine level is higher than 2 mg/dL, use diagnostic techniques that do not require an infusion of contrast, such as ultrasonography or helical CT scanning.

Hypokalemia and decreased serum bicarbonate level suggest underlying distal (type 1) renal tubular acidosis, which is associated with formation of calcium phosphate stones.

24-Hour Urine ProfileTo identify urinary 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 various commercial laboratories. 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.

Keep in mind that all of the 24-hour urine chemistry findings may be within the reference range in patients who actively form stones and who are at high risk for stones. In these cases, optimizing the levels is beneficial.

The following are objective indications for a metabolic evaluation with a 24-hour urinalysis:

Residual calculi after surgical treatmentInitial presentation with multiple calculiInitial presentation before age 30 yearsRenal failureSolitary kidney (including renal transplant)

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Family history of calculiMore than 1 stone in the past yearBilateral calculiPatient preference: An important consideration in determining whether

to perform a 24-hour urine study is the patient’s interest. If a patient is strongly motivated to follow a protracted stone-prevention treatment plan (involving diet, supplements, medications, or a combination), obtain the study. If a patient is unlikely or unwilling to follow a long-term treatment plan, a metabolic evaluation is probably unwarranted. Patients have to understand that stone disease is a chronic disease. If they do not commit to helping themselves in behavior modification, dietary changes, or medical compliance, they are prone to more frequent calculi formation.

The most common findings on 24-hour urine studies include 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. A finding of hypercalcemia should prompt follow-up with an intact parathyroid hormone study to evaluate for primary and secondary hyperparathyroidism.

Calcium, oxalate, and uric acid

Elevation of the 24-hour excretion rate of calcium, oxalate, or uric acid indicates a predisposition to form calculi.

Hypercalciuria can be subdivided into absorptive, resorptive, and renal-leak categories on the basis of 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 modest dietary calcium restriction, thiazide diuretics, oral calcium binders, or phosphate supplementation.

Resorptive hypercalciuria is primary hyperparathyroidism and requires parathyroidectomy, when possible. If parathyroid surgery is not possible, phosphate supplementation is usually recommended. Renal-leak hypercalciuria, which is less common than absorptive hypercalciuria, is usually associated with secondary hyperparathyroidism and is best managed with thiazide diuretics.

Another clinical approach to hypercalciuria, when hyperparathyroidism has been excluded with appropriate blood tests, is avoidance of excessive dietary calcium (usual recommendation, 600-800 mg/d),

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modest limitation of oxalate intake, and thiazide therapy. If thiazide therapy fails, additional workup (eg, calcium-loading test, more thorough evaluation) may be needed.

Indiscriminate dietary calcium restriction is not advantageous and in fact may increase formation of calculi owing to a secondary increase in oxalate absorption. The reduced dietary calcium reduces the oxalate-binding sites in the gastrointestinal (GI) tract, increasing the free dietary oxalate and leading to increased oxalate absorption. The final product of this is a net increase in stone production.

Hyperoxaluria may be primary (a rare genetic disease), enteric (due to malabsorption and associated with chronic diarrhea or short-bowel syndrome), or idiopathic. Oxalate restriction and vitamin B-6 supplementation are somewhat helpful in patients with idiopathic hyperoxaluria. Enteric hyperoxaluria is the type that is most amenable to treatment; dietary calcium supplementation often produces dramatic results.

Calcium citrate is the recommended supplement because it tends to further reduce stone formation. Calcium carbonate supplementation is less expensive but lacks citrate’s added benefit. Calcium works as an oxalate binder, reducing oxalate absorption from the GI tract. It should be administered with meals, especially those that contain high-oxalate foods. The supplement should not contain added vitamin D, because this increases calcium absorption, leaving less calcium in the GI tract to bind to oxalate. The optimal 24-hour urine oxalate level is 20 mg/d or less.

Hyperuricosuria predisposes to the 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, allopurinol, or both. In general, patients with pure uric acid stones and hyperuricemia are treated with allopurinol, and those with hyperuricosuric calcium stones are treated with citrate supplementation. The optimal 24-hour urine uric acid level is 600 mg/d or less.

Sodium and phosphorus

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Excess sodium excretion can contribute to hypercalciuria by a phenomenon known as solute drag. Elevated urinary sodium levels are almost always associated with dietary indiscretions. Decreasing the oral sodium intake can decrease calcium excretion, thereby decreasing calcium saturation.

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 are performed only if the index of clinical suspicion is high. Any patient with hypercalciuria who has a low serum phosphorus level and a high-normal or high urinary phosphorus level may have this condition. Repeat laboratories along with a 1,25 vitamin D-3 level are confirmatory.

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. This corrects the hypercalciuria, which is ultimately a vitamin D–dependent function in this condition. This therapy is not well tolerated, however.

Citrate and magnesium

Magnesium and, especially, citrate are important chemical inhibitors of stone formation. Hypocitraturia is one of the most common metabolic defects that predispose 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.

Many laboratories use 24-hour urine citrate levels of 320 mg/d as the normal threshold, but optimal levels are probably closer to the median level (640 mg/d) in healthy individuals. Periodic monitoring of pH with pH test strips can be very useful to titrate and optimize citrate supplementation. A pH level of 6.5 is usually considered optimal. A pH level over 7.0 should be discouraged, as it prompts calcium phosphate precipitation.

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Potassium citrate is the preferred type of pharmacologic citrate supplement, though a potassium/magnesium preparation is under investigation. Liquid or powder pharmacologic citrate preparations are recommended when absorption is a problem or in cases involving chronic diarrhea. Sustained-release tablets are available and may be more convenient for some patients. Lemon juice is an excellent source of citrate; alternatively, large quantities of lemonade can be ingested, and this, of course, has the added benefit of providing increased fluid intake.

Magnesium is a more recently recognized inhibitor of stone formation, and the clinical role of magnesium replacement therapy is less well defined than that of citrate.

Creatinine

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.

Total urine volume

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.

pH

Some stones, such as those composed of uric acid or cystine, are pH-dependent, meaning that they can form only in acidic conditions. Calcium phosphate and struvite only form when the urine pH is alkaline. Although the other parameters in the 24-hour urine usually identify patients at risk of forming these stones, pH studies can be important in monitoring these patients, in optimizing therapy with citrate supplementation, and in identifying occult stone disease in some patients.

Plain (Flat Plate or KUB) RadiographyPlain abdominal radiography (also referred to as flat plate or KUB radiography) is useful for assessing total stone burden, as well as the size, shape, composition, and location of urinary calculi in some patients. Calcium-containing stones (approximately 85% of all upper urinary tract calculi) are radiopaque, but pure uric acid, indinavir-

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induced, and cystine calculi are relatively radiolucent on plain radiography.

When used with other imaging studies, such as a renal ultrasonography or, particularly, CT scanning, the plain film helps provide a better understanding of the characteristics of urinary stones revealed with these other imaging studies. This may also be helpful in planning surgical therapy.

The flat plate radiograph uses the same orientation and anatomical presentation that is observed on fluoroscopy images and retrograde pyelograms or during endoscopic ureteral surgery, such as ureteroscopy or intracorporeal lithotripsy. Not all urinary calculi may be visible on the KUB radiograph, whether because of their small size, stone radiolucency, or overlying gas, stool, or bone. The stones that are observed can be correlated with opacities found on other studies for identification and tracking progress.

If a stone is not visible on a flat plate radiograph, it could be a radiolucent uric acid stone that can be dissolved with alkalinizing medication. Such a stone is more likely if the urine pH indicates very acidic urine. In practice, any patient with symptoms of acute renal colic who demonstrates a urine pH lower than 6.0 should be considered at risk for a possible uric acid stone. If a stone of adequate size is visible on a CT scan but not visible on KUB, then uric stones should be considered.

The flat plate radiograph is inexpensive, quick, and usually helpful even if no specific stone is observed. It is extremely useful in following the progress of previously documented radiopaque calculi and checking the position of any indwelling double-J stents. The KUB radiograph can suggest the fluoroscopic appearance of a stone, which determines whether it can be targeted with extracorporeal shockwave lithotripsy (SWL).

The KUB radiograph is also quite accurate for helping determine the exact size and shape of a visible radiopaque stone and sometimes is more accurate than CT in this regard. Note that most stones will appear larger on KUB radiograph than on CT, with CT-based measurement of maximum stone dimension approximately 12% smaller than a corresponding KUB-based measurement.[14]

Many calcifications observed on the KUB radiograph are phleboliths, vascular calcifications, calcified lymph nodes, appendicoliths,

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granulomas, various calcified masses, or even bowel contents. All can be confused with urinary tract calculi.

The insoluble radiopaque carrier for osmotically controlled-release oral system (OROS) pharmaceuticals can sometimes be mistaken for urinary calculi on KUB radiographs.

Differentiation between a phlebolith and an obstructing calcific stone becomes easier when the KUB radiograph demonstrates a lucent center, identifying the calcification as a phlebolith. This central lucency may not be observed as often on CT scans. For these reasons, many urologists recommend the flat plate radiograph in addition to CT scan for any renal colic–type scenario.

A number of studies have suggested that the flat plate has a relatively low sensitivity (40-50%) and specificity for renal and ureteral calculi. Many patients have numerous pelvic calcifications that make pinpointing specific stones difficult. Any calcific density observed on a KUB radiograph that happens to overlie the course of the ureter is not guaranteed to be a stone.

A large clinical study from Johns Hopkins University by Jackman et al concluded that "plain abdominal radiograph is more sensitive than scout CT for detecting radiopaque nephrolithiasis.[15] Of the stones visible on plain abdominal radiograph, 51% were not seen on CT. To facilitate outpatient clinic follow-up of patients with calculi, plain abdominal radiographs should be performed."

Many urologists, including this author, recommend that in addition to other studies (eg, noncontrast helical or spiral CT scans), a KUB radiograph be obtained in all patients with a clinical presentation of acute flank pain suggestive of renal colic. Knowing the exact size and shape of a stone, its position, fluoroscopic appearance, surgical orientation, and relative radiolucency is an advantage.

In addition, the progress of the stone can be easily monitored with a follow-up KUB radiograph, which may prove helpful in determining the exact size and shape of the stone, in establishing a baseline for follow-up studies, and for visualization of the surgical orientation.

A reasonable practical compromise is to obtain a KUB film only in cases in which the stone is not visible on the digital CT scout radiograph.

Ultrasonography

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Renal ultrasonography by itself is frequently adequate to determine the presence of a renal stone. The study is mainly used alone in pregnancy[16] or in combination with plain abdominal radiography to determine hydronephrosis or ureteral dilation associated with an abnormal radiographic density believed to be a urinary tract calculus. A stone easily identified with renal ultrasonography but not visible on the plain radiograph may be a uric acid or cystine stone, which is potentially dissolvable with urinary alkalinization therapy.

For some stones, ultrasonography works quite well; however, it has been found to be less accurate in diagnosis of ureteral stones (see the image below), especially those in the distal ureter, than IVP or CT. Diagnostic criteria include direct visualization of the stone, hydroureter more than 6 mm in diameter, and perirenal urinoma suggesting calyceal rupture.[17]

Renal sonogram showing a dilated renal collecting system consistent with ureteral obstruction.In addition, ultrasonography is not reliable for small stones (ie, those smaller than 5 mm) and does not help in the evaluation of kidney function.

A urine-filled bladder provides an excellent acoustic window for ultrasound imaging; sonograms occasionally may demonstrate a stone at the ureterovesical junction that is not definitive on helical CT or IVP (see the image below).

Transabdominal sonogram revealing a ureteral stone at the ureterovesical junction.Ultrasonography requires no intravenous (IV) contrast and can easily detect any significant hydronephrosis, although this must be differentiated from ureteropelvic junction (UPJ) obstruction or an extrarenal pelvis. A large extrarenal pelvis or UPJ obstruction can easily be misread for hydronephrosis if ultrasonography alone is used.

Middleton et al reported perhaps the most successful use of ultrasonography for renal colic: a 91% stone detection rate. Most authors report rates of approximately 30%. The unusually high success rate achieved by Middleton et al is partly explained by the fact that a radiologist specializing in ultrasonography performed the studies, which typically required at least 15-20 minutes to complete. The success of diagnostic ultrasonography is very dependent on operator

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skill and experience, which is probably demonstrated by the unique setting of this study.[18]

Renal ultrasonography works best in the setting of relatively large stones within the renal pelvis or kidney and sometimes at the UPJ. Whether the stones are radiolucent or radio-opaque does not matter because an ultrasound image is based strictly on density, not on calcium content. Ultrasonography is a good way to monitor known stones after medical or surgical therapy if the stones are large enough to be detected by this modality and are in a suitable position.

Ultrasonography can also be used to check the abdomen for a possible abdominal aortic aneurysm (AAA) or cholelithiasis, which can sometimes be mistaken for acute renal colic. It is also useful in differentiating filling defects observed on contrast studies because stones are much more echogenic than tumors, clots, or tissue. It is the initial imaging modality of choice for pregnant patients with acute renal colic because it avoids all potentially hazardous ionizing radiation.

Ultrasonography relies on indirect visualization clues to identify stones. Differentiating an extrarenal pelvis from an obstructed one is sometimes difficult when using ultrasonography alone. Intermittent obstruction or mild hydronephrosis can be easily missed with ultrasonography, and, with the few exceptions mentioned above, it generally does not provide much information about most other disease processes capable of causing acute flank pain.

Sometimes, a KUB abdominal flat plate radiograph is used in addition to ultrasonography to help identify and monitor suspected stones, especially if renal dilation is detected. As with the KUB radiograph alone, any density detected along the expected course of the ureter is not guaranteed to be an actual stone within the collecting system.

The combination of renal ultrasonography with KUB radiography has been proposed as a reasonable initial evaluation protocol when a CT scan cannot be performed or is unavailable. When combined with KUB radiography, ultrasonography can quickly and inexpensively provide substantial information about the urinary tract without the risk of contrast nephrotoxicity or hypersensitivity. IVP can then be limited to those patients for whom additional information is required for a diagnosis or for whom the etiology of the pain remains unclear.

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The intrarenal resistive index, as measured on Doppler studies, has been proposed as one way to diagnose acute renal obstruction using ultrasound. Under normal conditions, renal vascular resistance is relatively low and renal blood flow is excellent throughout the cardiac cycle, with a reasonable flow continuing even during diastole. During conditions associated with increased vascular resistance (eg acute ureteric obstruction), the decrease in renal blood flow during diastole is proportionately of greater magnitude than that during systole.

The resistive index is calculated as peak systolic velocity minus end-diastolic velocity divided by peak systolic velocity. An elevated resistive index of 0.7 or more is considered indicative of an acute ureteral obstruction. A change in the resistive index between the affected and contralateral (healthy) kidney of 0.04 or more also suggests a ureteral obstruction. (The affected kidney has the higher resistive index value.)

This study may be particularly useful in pregnancy (when exposure to ionizing radiation must be minimized), severe contrast media allergy, and azotemia. For best results, measure the intrarenal resistive index during a pain attack but before any nonsteroidal anti-inflammatory drugs (NSAIDs) or other anti-inflammatory medications are administered.

However, the intrarenal resistive index does not identify partial or intermittent obstructions and is less helpful in the early phase of even complete ureteral blockage. It also does not provide any information about the radiolucency, size, shape, or position of any stone and cannot be used to differentiate between intrinsic and extrinsic urinary obstructions.

Pyelosinus extravasation or fornix rupture, which occurs in up to 20% of patients with acute ureteral obstructions, leads to a loss of dilation and may be responsible for false-negative findings from studies. Other nonobstructive renal problems, such as renal failure, diabetic nephropathy, and renal compression, can affect the readings.

Considering that up to perhaps 35% of patients with documented acute ureteral obstruction do not demonstrate any significant hydroureteronephrosis, the use of a noninvasive study such as Doppler ultrasonography and intrarenal resistive index, which does not depend on visual ureteral or renal pelvic dilation, may eventually prove very useful. For now, additional studies on this technique are needed before

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the intrarenal resistive index can be reliably used for diagnosing acute renal colic and ureteric obstruction.

Future studies may utilize 2-dimensional ultrasonography in combination with color Doppler analysis of the ureteral jets to enhance sensitivity of ultrasonography in patients with ureteral colic.[19]

Intravenous Pyelography (Urography)Before the advent of helical CT, IVP, also known as intravenous urography (IVU), was the test of choice in diagnosing ureterolithiasis. IVP is widely available and fairly inexpensive but less sensitive than noncontrast helical CT. CT scanning with delayed contrast series and thin slices has reduced the need for IVP in the evaluation of problematic ureteral stones.

The main advantage of IVP is the clear outline of the entire urinary system that it provides, making visualization of even mild hydronephrosis relatively easy. IVP is helpful in identifying the specific problematic stone among numerous pelvic calcifications, as well as in demonstrating renal function and establishing that the other kidney is functional. These determinations are particularly helpful if the degree of hydronephrosis is mild and the noncontrast CT scan findings are not definitive. IVP can also show nonopaque stones as filling defects.

Disadvantages include the need for IV contrast material, which may provoke an allergic response or renal failure, and the need for multiple delayed films, which can take up to 6 hours. Obtaining the IVP is also a relative labor-intensive process. In addition, IVP may fail to reveal alternative pathology if a stone is not discovered, delaying the final diagnosis. False-negative results usually occur with stones located at the ureterovesical junction.

The dose of IV contrast is usually about 1 mL/kg. Bolus administration is usually recommended for renal colic evaluations because it allows for a nephrogram-effect phase film. This normally occurs within the first minute after bolus contrast injection and cannot be obtained with slow-drip infusion.

Acute ureteral obstruction causes an intense persistent finding on nephrograms. This may take several hours or more to fully visualize, which necessarily delays completion of the study. The so-called delayed nephrogram on IVP is one of the hallmark signs of acute urinary tract obstruction. The relative delay in penetration of IV

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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.

KUB radiographs are obtained immediately before contrast administration and at 1, 5, 10, and 15 minutes afterwards or until visible contrast material fills both ureters (see the image below). Prone films are sometimes obtained to enhance visualization of the ureters. When the bladder is full of contrast and the distal ureters contain sufficient contrast for visualization, the patient is asked to void; then a postvoid film is taken. Sometimes, oblique views are needed when bone or bowel contents overlie the area of interest.

Intravenous pyelogram (IVP) demonstrating dilation of the right renal collecting system and right ureter consistent with right ureterovesical stone.Look for direct visualization of stone within the ureter, unilateral ureteral dilation, delayed appearance of the nephrogram phase, lack of normal peristalsis pattern of the ureter, or perirenal contrast extravasation. Degree of obstruction is graded based on delay in appearance of the nephrogram.

Typically, an IVP positive for a ureteral stone is one that shows a delayed nephrogram effect and columnization. The ureter is peristaltic, so the entire ureter is not usually visualized on a single film except when an obstruction is present, such as from a stone. Even without observing any specific stone, the presence of a nephrogram effect in one kidney with normal function of the opposite kidney is highly suggestive, but not diagnostic, of ureteral obstruction.

Extravasation of contrast around the collecting system may be a sign of a ruptured fornix, while pyelolymphatic backflow indicates that contrast has entered into the renal lymphatic drainage system. Both are considered signs of a more severe ureteric obstruction.

However, no published study has indicated that the clinical course, treatment outcome, or residual renal damage is altered in any way in these patients. In fact, this information about the radiological assessment of the relative severity of the obstruction rarely affects clinical treatment decisions, except perhaps in persons with solitary kidneys.

Contrast-induced nephropathy

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Contrast-induced nephropathy (CIN) is the third leading cause of hospital-acquired acute renal failure. A serum creatinine level of more than 2 mg/dL is a relative contraindication to the use of IV contrast agents. Patients with azotemia, multiple myeloma, pregnancy, or diabetes, especially if dehydrated, are particularly susceptible to acute CIN (25% or greater increase in serum creatinine within 2-3 days of IV contrast exposure). Ischemia, direct intracellular high–contrast-concentration toxicity, and free-radical injury are thought to be the causative mechanisms of CIN.

Low osmolarity or iso-osmolar contrast may help to reduce the risk of CIN. The renal vasodilator fenoldopam mesylate has been used to minimize renal complications in higher-risk patients requiring IV contrast studies who would otherwise be at high risk for azotemia. Fenoldopam is a dopamine type 1A agonist that has been shown to increase renal plasma flow and to help prevent contrast nephropathy.

Theophylline and N-acetylcysteine have also been used with some success, but the standard prophylactic therapy is IV saline at a rate of 1-3 mL/kg/h. Hemodialysis before and after IV contrast can also be used to minimize renal toxicity, but such a regimen is costly and too cumbersome for general use except in special high-risk situations.

A randomized study by Merten et al comparing standard IV saline hydration prophylaxis with a 154-mEq/L sodium bicarbonate solution found a substantial benefit with the latter.[20] Patients treated with saline were 8 times more likely to develop nephropathy after contrast exposure than those treated with sodium bicarbonate. Such a treatment plan is practical, inexpensive, simple, safe, and effective, and the author now recommend IV sodium bicarbonate hydration as the method of choice for prevention of CIN.[20]

Anaphylaxis to ionic contrast agents occurs in 1-2 patients per 1000 IVP studies. Risk of recurrence is approximately 15% if reexposed to ionic agents but falls to 5% when nonionic agents are used. Risk of anaphylaxis can be reduced further by pretreatment with a combination of H1- and H2-blockers and steroids, but studies showing the benefit of pretreatment began pretreatment more than 12 hours prior to study.

Nonionic contrast media is more expensive but less likely to provoke an allergic response than the older ionic media, especially if the patient has a history of mild or moderate allergic reactions to contrast or

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injected dye. Risk of nephrotoxicity is not clearly reduced with use of nonionic agents. Indications for use of nonionic contrast agents vary among institutions but consistently include history of prior mild to moderately severe reaction to ionic contrast, asthma, multiple allergies, or severe cardiac disease.

Many institutions currently use only nonionic agents for all IV contrast studies, despite the added cost, because of the increased safety. Glucophage should be discontinued at least 1 day before any IV contrast study, particularly in patients with proven or borderline azotemia, because of the risk of worsening renal function and the rare development of potentially life-threatening lactic acidosis. It can be resumed 48 hours after the contrast study if renal function has normalized.

Medullary sponge kidney

Medullary sponge kidney (MSK), also called tubular or ductal ectasia or cystic dilation of the collecting ducts, is a generally benign congenital condition that demonstrates dilation of the distal renal collecting tubules on IVP as the tubules fill with contrast. These normally invisible microscopic tubules show a whitish blush in the papilla in persons with MSK. In severe cases, stones, cysts, and diverticula can be present. The condition can be unilateral, or even limited to one calyceal system, but it is bilateral in 70% of patients. It is not usually discovered until the second or third decade of life, even though MSK is congenital.

MSK is the most common anatomical problem found in calcium nephrolithiasis patients, affecting approximately 2% overall. Most stones in patients who have MSK are composed of calcium oxalate with or without calcium phosphate. Stones tend to be small and are usually passed spontaneously.

In most cases, MSK is not hereditary, although rare autosomal inherited forms have been described. The exact cause is unknown, but it could be caused by tubular obstruction due to calcium oxalate calculi from infantile hypercalciuria or collecting duct dilation from blockage by fetal uric acid stones, embryonal remnants, or other material.

The most accurate way to demonstrate MSK is to employ high-quality excretory urography (ie, IVP) with serial renal tomography starting just before the injection of the contrast media and continuing every 4 minutes for the next 20 minutes.

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Most patients with MSK are asymptomatic; unless they have an IVP for an unrelated reason, the condition may never be diagnosed. Of patients who are symptomatic, renal colic and calcium urinary stones are the most common problems. (UTIs and hematuria are the others.) Women are more likely to have MSK than men.

Some patients with MSK may report severe chronic renal pain without any evidence of infection, stones, or obstruction. The etiology of this pain is unclear. These patients may be treated best by physicians comfortable with the management of chronic pain disorders, although recent reports suggest that ureteroscopic laser papillotomy may provide temporary relief.[21]

Long-term management of MSK, as in any frequent stone former, is aimed toward identifying metabolic risk factors for continuing stone formation, with serum and 24-hour urine testing. The most common metabolic problems in MSK are hypercalciuria and hypocitraturia.

Computed Tomography ScanningAt most institutions that offer this examination, CT scanning has replaced IVP, the historic criterion standard, for the assessment of urinary tract stone disease, especially for acute renal colic. CT scans are readily available in most hospitals and can be performed and read in just a few minutes. Numerous studies have demonstrated that CT has a sensitivity of 95-100% and superior specificity and accuracy when compared with IVP.[17]

A renal colic study consists of a noncontrast or unenhanced CT scan of the abdomen and pelvis, including very narrow cuts taken through the kidneys and bladder areas, where symptomatic stones are most likely to be encountered.

Technically, a relatively high pitch of more than 1.5 with thin collimation of 2-3 mm is generally considered a good compromise between imaging quality and radiation dosage. No rectal, oral, or IV contrast is used, because contrast material obscures any calcium-containing stones; both the stone and the contrast material would appear bright on the scans. Optimally, the patient’s bladder is filled, which facilitates viewing the ureterovesical junction (see the image below).

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Noncontrast helical CT scan of the abdomen demonstrating a stone at the right ureterovesical junction.In equivocal cases in which an indeterminate calcification is found along the course of the ureter or an abrupt change in ureteral caliber is found without a conclusively identified stone, an overlapping retrospective series can be performed to better evaluate this specific area and eliminate any sampling error.

An abdominal flat plate or KUB radiograph is sometimes automatically included in a renal colic study, depending on the institution and the preferences of the medical staff.

Advantages of CT scanning include the following:

It can reveal other pathology (eg, AAAs, appendicitis, pancreatitis, cholecystis, ovarian disorders, diverticular disease, renal carcinoma).[22] If the patient’s true underlying pathology is something other than a kidney stone, the CT scan is more clinically useful than an IVP for examining the possibilities.

It can be performed quickly (< 5 min acquisition time)It avoids the use of IV contrast materials.The density of the stone can assist in predicting stone composition and

response to shockwave lithotripsy.Disadvantages of CT scanning include the following:

It cannot be used to assess individual renal function or degree of obstruction.

It can fail to reveal some unusual radiolucent stones, such as those caused by indinavir and atazanavir, which are typically invisible on the CT scan (though some serve as a nidus for deposition of calcium oxalate or calcium phosphate deposition and thus become radiopaque). Because of this possibility, IVP with contrast should be used for patients taking indinavir or atazanavir. Sulfadiazine stones are also difficult to visualize on CT because of relatively low attenuation.[23]

It is relatively expensive.It exposes the patient to a relatively high radiation dose (and thus

should not be performed on pregnant women).Precise identification of small distal stones is occasionally difficult.Stone size as measured on CT KUB correlates poorly with actual size of

the stone measured after spontaneous passage.[24] For this reason, caution should be used in counseling patients on the

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likelihood of spontaneous stone passage when stone size is determined using CT-based measurement.

Although CT scans can be used to estimate the overall size, width, and location of a stone, they can only approximate its shape.[25] Stone location can be described in anatomical terms, but the CT scan lacks the surgical orientation that most urologists prefer.

It is not suitable for tracking the progress of the stone over time, supporting the recommendation for KUB radiography along with the CT scan.

If a KUB or flat plate radiograph is performed at the same time as the CT scan, some of these objections and problems disappear. However, obtaining the extra films involves some additional delay, the patient is exposed to more ionizing radiation, and the total cost for the workup increases.

The "scout" reconstruction of the CT scan, formatted to look like a plain radiograph, is a reasonable substitute for a formal KUB radiograph in some cases. Stones 3 mm and larger can be observed routinely on these studies. If the findings from a noncontrast CT scan are positive for a stone and the findings from the scout CT radiograph are negative, a separate KUB radiograph should be performed.

A digital scout CT radiograph is not nearly as sensitive as a good plain radiograph in detecting calculi; however, if the stone is visible on the "scout" reconstruction, only plain radiography may be needed later to determine if the stone has moved or passed.

Differentiation of phleboliths from urinary tract stones

Phleboliths are often confused with calcific ureteral stones. On a KUB radiograph, the characteristic lucent center of a phlebolith is often visible; thiis not present in a true calculus. Unfortunately, CT scans usually fail to reveal this central lucency or a bifid peak if a central lucency cannot be identified. Why this finding of a central transparency is so uncommon with CT scanning is unclear, but it may involve the orientation of the veins that form the phleboliths.

The "rim sign," originally reported by Smith in 1995, is described as a rim, ring, or halo of soft tissue visible on CT scans that completely surrounds ureteral stones.[20] The effect is enhanced by the local inflammation a stone produces in the ureteral wall, with subsequent edema at the site of the calculus. The rim sign is generally missing or incomplete with phleboliths.

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While not absolutely definitive, the rim sign is strong evidence that the calcific density it surrounds is a stone and not a phlebolith. In several studies, more than 75% of all ureteral stones demonstrated a rim sign, while only 2-8% of phleboliths demonstrated it. The rim sign is more likely to be present in small or medium stones up to 5 mm in diameter. Larger stones (>6 mm) tend to lose the rim sign, presumably from stretching and thinning of the ureteral wall around a relatively large calculus.

Another way to differentiate a phlebolith from a calculus is to find a comet’s tail or comet sign, which is the noncalcified portion of a pelvic vein that is contiguous with the phlebolith. It appears as a small linear area of soft tissue that seems to pass obliquely through the CT scan section and attaches to the calcific density at one end. This is not observed in ureteral stones, although a ureter can mimic this sign to some degree. The comet sign is found in less than 20% of phleboliths, so its absence helps little, and its reliability is still unproved.

Estimation of stone density, composition, and size

Currently, CT scans can be used to estimate the relative stone density and composition to some extent, although the results have not replaced the formal stone chemical composition analysis. However, this information can still help to plan therapy. Low-density stones are more amenable to shockwave lithotripsy, whereas higher-density stones may require ureteroscopy.

For example, a lucent stone that is not visible 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 (urinary alkalinization) than for a calcium stone. For these reasons, many institutions routinely perform KUB radiography whenever renal colic noncontrast CT scanning is performed.

The Hounsfield unit density of the calculus on CT scanning can also be useful in predicting whether the stone is composed of uric acid. In a study of the unenhanced CT scans of 129 patients with renal stones, researchers from the University of Wisconsin concluded that the peak Hounsfield attenuation level of a kidney stone, used either by itself or divided by the size of the calculus in millimeters, may be a useful indicator of the stone’s chemical composition.

An attenuation-to-size ratio of 80 or greater was found to be highly suggestive of calcium oxalate stone material, especially in larger

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calculi. Uric acid stones have relatively low peak attenuation levels, and their attenuation-to-size ratios were generally below 80. In this Wisconsin study, uric acid stones averaged a mean peak Hounsfield reading of 344 HU, while the mean for calcium oxalate calculi was 652 HU.

Calculating the peak attenuation level and attenuation-to-size ratio adds no financial cost, patient morbidity, or time delay. While this study and similar reports are interesting and suggestive, the precise clinical role of CT scans in predicting stone fragility and chemical composition remains unclear.

Secondary signs of obstruction

Secondary signs of obstruction may be visible only on CT scans. In some cases, if a stone was passed shortly before the study, these signs may be the only evidence that the patient has or ever had a stone. These secondary signs include ureteral dilation with hydronephrosis, renal enlargement from interstitial edema (nephromegaly), and inflammatory changes, such as stranding or streaking in the perinephric fatty tissue.

In a 1996 study of 54 ureteral stone patients reported by Katz et al, hydronephrosis was present in 69%, proximal ureteral dilation was found in 67%, and perinephric stranding was detected in 65%. The other secondary signs had a similar frequency in adults and children. In the study, only 2 of the patients with ureteral calculi did not demonstrate any of the secondary signs of obstruction. The other secondary signs had a similar frequency in adults and children.[26]

A similar 1996 study by Smith et al involving 220 patients found an even higher correlation between these secondary signs of obstruction and the presence of a ureteral calculus. In particular, the combination of collecting system dilation and perinephric stranding had a positive predictive value of 98%, while the absence of both of these secondary signs had a negative predictive value of 91%.[27]

However, perinephric stranding was found less often in children with ureteral calculi than in adults in a 2001 study by Smergel and associates; therefore, this secondary sign, at least in the pediatric population, may be less reliable.[28]

An additional secondary sign of acute renal obstruction on noncontrast CT scans has been reported by investigators from Johns Hopkins

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University. This sign is defined as a reduction in renal parenchymal attenuation (radiologic density) on the nonenhanced CT scan of the acutely obstructed renal unit compared with the normal unobstructed contralateral kidney. The difference in density is at least 2 standard deviations. This sign was identified in 95% of patients with acute ureteral obstruction, which suggests it is a reliable indicator.

Rarely, in indeterminate cases in which the secondary signs are negative and a stone is strongly suspected clinically but not clearly visible on the unenhanced CT scan, IV contrast can be used to help visualize the ureter. Repeat scanning after contrast infusion allows for improved visualization of the ureters. This allows physicians to make direct comparisons with the earlier studies to help make the correct diagnosis. Flat abdominal radiograph films taken after the contrast provide information similar to IVP, but delayed films or scans are likely to be needed.

Current recommendations

In current clinical practice, the renal colic noncontrast CT scan is the standard of care in most EDs when a patient is thought to have renal colic or presents with acute flank pain. Guidelines from the American College of Radiology (ACR) recommend noncontrast CT as the most appropriate radiologic procedure for both suspected stone disease and recurrent symptoms of stone disease. Reduced-dose techniques are preferred.[29]

Because of the limitations of CT scans, some urologists request additional studies, such as KUB radiography or IVP, to help them make critical decisions about management, follow-up, and possible surgical interventions. In cases of suspected stone disease in pregnant patients and in patients allergic to iodinated contrast or when noncontrast CT is unavailable, the ACR considers ultrasonography of the kidney and bladder retroperitoneal with Doppler and KUB the preferred examination.[29]

As noted earlier, obtaining a KUB radiograph when a renal colic CT scan study is performed for acute flank pain provides more precise information about the size and shape of any stone and quickly reveals whether stones are nonopaque and radiolucent. Follow-up evaluations are easier because only a repeat KUB radiograph is needed for comparison. A KUB radiograph also helps the urologist determine if a stone will be visible on fluoroscopic images, which is useful for possible shockwave lithotripsy since for most lithotripters used in the United

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States, fluoroscopic visualization is needed for stone targeting and positioning.

While the addition of an abdominal flat plate study (KUB radiograph) adds to the overall financial cost and requires additional time, the extra information the study provides is often quite valuable and ultimately beneficial to the patient. If the stone is visible on the CT scout image, however, then this provides the same information as a KUB and thus the latter is not needed.

Comparison of CT with IVP

CT has largely supplanted IVP in a number of settings. However, a comparison of the pros and cons of the two modalities suggests IVP retains some advantages (see Table, below).

Table. Intravenous Pyelography Versus CT Scanning: Which Is Better? (Open Table in a new window)

Imaging Study (Pro/Con) DetailsCT scan Pro Fast

No IV contrast necessary, so no risk of nephrotoxicity or acute allergic reactions

With only rare exceptions, shows all stones clearly

May demonstrate other pathology

Can be performed in patients with significant azotemia and severe contrast allergies who cannot tolerate IV contrast studies

Clearly shows uric acid stones

Shows perinephric stranding or streaking not visible on IVP and can be used as an indirect or secondary sign of ureteral obstruction

No radiologist needs to

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be physically presentPreferred

imaging modality for acute renal colic in most EDs

Con Without hydronephrosis, cannot reliably distinguish between distal ureteral stones and pelvic calcifications or phleboliths

Cannot assess renal function

No nephrogram effect study to help identify obstruction

Size and shape of stone only estimated

Lacks surgical orientation*

Unable to identify ureteral kinks, strictures, or tortuousities

May be hard to differentiate an extrarenal pelvis from true hydronephrosis

Gonadal vein sometimes can be confused with the ureter

Does not indicate likelihood of fluoroscopic visualization of the stone, which is essential information in planning possible surgical interventions

May require addition of KUB

radiograph†

Cannot be performed during pregnancy because of high dose of ionizing radiation exposure

Usually more costly than an IVP in most institutions

Higher radiation dose than IVP

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IVP Pro Clear outline of complete urinary system without any gaps

Clearly shows all stones either directly or indirectly as an obstruction

Nephrogram effect film indicates obstruction and ureteral blockage in most cases, even if the stone itself might not be visible

Shows relative kidney function

Definitive diagnosis of MSK

Ureteral kinks, strictures, and tortuousities often visible

Can modify study with extra views (eg, posterior oblique positions, prone views) to better visualize questionable areas

Stone size, shape, surgical orientation, and relative position more clearly defined

Orientation similar to urologists’ surgical approach

Limited IVP study can be considered in selected cases during pregnancy, although plain ultrasonography is preferred initially

Lower cost than CT scan in most institutions

Includes KUB film automatically

Con Relatively slow; may need multiple delay films, which can take hours

Cannot be used in azotemia, pregnancy, or known significant allergy to

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intravenous contrast agents

Risk of potentially dangerous reactions to IV contrast

material‡

Cannot detect perinephric stranding or streaking, which is visible only on CT scans

Harder to visualize radiolucent stones (eg, uric acid), although indirect signs of obstruction are apparent

Presence of a radiologist generally necessary, which can cause extra delay

Cannot be used to reliably evaluate other potential pathologies

*Many urologists find CT scans inadequate to help plan surgery, predict stone passage, or

monitor patients.† This causes a delay, which may be significant in some institutions, and

adds additional patient radiograph exposure and cost.‡ These include significant allergic

responses and renal failure.

The noncontrast or renal colic-type CT scan is good for the initial diagnosis of a stone, especially in unusual or atypical cases or when patients are unable to tolerate intravenous contrast because of allergy or azotemia. Without definite hydronephrosis, a CT scan may not be able to isolate a specific stone, although secondary signs, such as perinephric streaking and nephromegaly, may be present.

The CT scan can be performed quickly in most institutions, even with an additional KUB radiograph, but it usually costs more than the IVP. In one series of 397 consecutive emergency urolithiasis patients from several university centers, the average fee for a CT scan was $1407, compared with $445 for an IVP.

CT scans are generally preferred by most ED physicians for the initial evaluation of patients with acute flank pain, except for HIV-positive patients who may be on protease inhibitors, who require an IVP, and pregnant women, who require ultrasonography for their initial imaging modality.

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The IVP is better for clearly outlining the entire urinary tract and determining relative renal function. This test clearly shows stones causing blockage, whether the stones are radiolucent or opaque. While an IVP can reliably help in the diagnosis of an MSK, the clinical importance of this diagnosis is limited. The IVP is sometimes preferred by urologists in certain situations because of its better orientation and superior value in predicting possible stone passage, although these advantages are mostly negated if a KUB radiograph routinely accompanies the CT scan.

Plain Renal TomographyPlain renal tomography requires moving the radiograph projector and film in such a way that a zone of photographic clarity is positioned at the stationary focus point of the radiograph beam. All other overlying material is eliminated. The focal point is adjusted along the anteroposterior axis a distance of 1 cm, and the radiograph procedure is repeated. Usually, a series of 4-6 films is needed to completely image both kidneys. If such a series of films is needed, it should be obtained before any IV contrast is administered; contrast obscures any stones present.

Although largely replaced by CT scanning without contrast, plain renal tomography has some uses and advantages. It does not require extensive preparation and can be performed quickly. In addition, the cost and radiation dosage to the patient are less than with CT scanning.

Plain renal tomography can be useful for monitoring a difficult-to-observe stone after therapy. Observing even a relatively large radiopaque stone located in the kidney or renal pelvis on a standard abdominal flat plate radiograph can be difficult or impossible if the patient has abundant gas or stool overlying the area, and plain renal tomography can often overcome this difficulty.

Plain renal tomography may be helpful for clarification of stones not clearly detected or identified with other studies (eg, differentiating intrarenal calcifications that are likely to be stones from extrarenal opacities that are clearly not renal calculi). It is often helpful in finding small stones in the kidneys, especially in patients who are large or obese whose bowel contents complicate observation of any renal calcifications.

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Plain renal tomography is also useful for determining the number of stones present in the kidneys before a stone-prevention program is instituted. This information is used to better differentiate stones formed before therapy began from those formed later.

Retrograde PyelographyThe most precise imaging method for determining the anatomy of the ureter and renal pelvis and for making a definitive diagnosis of any ureteral calculus is not IVP or renal colic CT scanning but retrograde pyelography.

In this study, the patient is taken to the operating room (OR) cystoscopy suite, and an endoscopic examination is performed with the patient under anesthesia. After a cystoscope is placed in the bladder, a thin ureteral catheter is inserted into the ureteral orifice on the affected side. A radiographic picture is taken while contrast material is injected through the ureteral catheter directly into the ureter. Any stone, even if radiolucent, and any ureteral kinks, strictures, or tortuousities that may not be visualized easily on other studies become clearly visible.

Urologists perform retrograde pyelograms when a precise diagnosis cannot be made by other means or when a need clearly exists for an endoscopic surgical procedure and the exact anatomical characteristics of the ureter must be clarified.

Retrograde pyelograms are rarely performed merely for diagnostic purposes, because other less invasive studies are usually sufficient. They are considered essential when surgery is deemed necessary because of uncontrollable pain, severe urinary infection or urosepsis with a blocked kidney, a solitary obstructed kidney, a stone that is considered unlikely to pass spontaneously because of its large size (generally ≥8 mm), or the presence of possible anatomical abnormalities (eg, ureteral strictures).

Retrograde pyelograms can be performed safely both in patients highly allergic to IV contrast media and in patients with renal failure because the contrast medium never enters the bloodstream and therefore requires no renal filtration or excretion and causes no anaphylaxis.

Nuclear Renal Scanning

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A nuclear renal scan can be used to objectively measure differential renal function, especially in a dilated system for which the degree of obstruction is in question. This is also a reasonable study in pregnant patients, in whom radiation exposure must be limited.

The intravenously injected radioisotope is eliminated via the nephron, with the rate of clearance from the renal unit providing an excellent estimate of the glomerular filtration rate and the relative rate of drainage or clearing from each kidney. A drainage half-time that is 20 minutes or longer indicates obstruction, while a drainage half-time of 10 minutes or less is considered unobstructed. If the drainage half-time is 10-20 minutes, the result is indeterminate.

Magnetic Resonance ImagingMagnetic resonance imaging (MRI) has virtually no role in the current evaluation of acute renal colic in the typical patient. Direct detection of most stones is not possible with MRI, and MRI should not be used for that purpose in most instances. MRIs are generally more expensive than other studies, such as CT scans, which reveal stones much better.

On the other hand, MRI produces no dangerous radiation, the gadolinium contrast it uses has minimal nephrotoxicity, and it can readily reveal urinary obstruction even if the stones themselves are not easily visualized. These attributes make using MRI reasonable in selected cases in which other technologies are too toxic or potentially dangerous, such as in some children and in pregnant women (see below). Gadolinium contrast, however, is contraindicated if the estimated glomerular filtration rate is less than 30, owing to the risk of nephrogenic systemic fibrosis.

Use of MRI in pregnant patients is somewhat controversial. Long-term effects on the fetus are unknown, and MRI is not specifically indicated in pregnancy, although it is not specifically contraindicated either. Anecdotal reports suggest that MRI has no immediately detectable deleterious effects. When other imaging modalities cannot be used or are insufficient, magnetic resonance urographic imaging can be considered on a case-by-case basis when the benefits to the mother and fetus outweigh the potential risks.

Although MRI does not play a major role in the diagnosis of ureteral stones, it can be used for this purpose. One study of 40 consecutive patients with acute flank pain found sensitivity of 54-58% and specificity of 100% using breath-hold heavily T2-weighted sequences.

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[30] Sensitivity and specificity increased to 96.2-100% and 100%, respectively, using gadolinium-enhanced 3-D FLASH MR urography. Its lack of radiation makes MRI a good choice in this setting for pregnant women who have nondiagnostic findings from a sonogram.

Proceed to Treatment & Management

Approach ConsiderationsTreatment of nephrolithiasis involves emergency management of renal (ureteral) colic, including surgical interventions where indicated, and medical therapy for stone disease.

In emergency settings where concern exists about possible renal failure, the focus of treatment should be on correcting dehydration, treating urinary infections, preventing scarring, identifying patients with a solitary functional kidney, and reducing risks of acute renal failure from contrast nephrotoxicity, particularly in patients with preexisting azotemia (creatinine >2 mg/dL), diabetes, dehydration, or multiple myeloma. Adequate intravenous (IV) hydration is essential to minimize the nephrotoxic effects of IV contrast agents. Choosing imaging studies that do not require IV contrast (eg, ultrasonography, plain abdominal flat plate radiographs, noncontrast computed tomography [CT] scans) is wise, especially in patients at increased risk for developing renal failure.

Most small stones with relatively mild hydronephrosis can be treated with observation and acetaminophen. More serious cases with intractable pain may require drainage with a stent or percutaneous nephrostomy. The internal ureteral stent is usually preferred in these situations because of decreased morbidity.

Acetaminophen can be used in pregnancy for mild-to-moderate pain. Opioid drugs, such as morphine and meperidine, are pregnancy category C medications, which means they can be used but they cross the placental barrier. Opioids can cause respiratory depression in the fetus; therefore, they should not be used near delivery or when other medications are adequate.

A stone chemical composition analysis should be performed whenever possible, and information should be provided to motivated patients about possible 24-hour urine testing for long-term nephrolithiasis prophylaxis. This is particularly important in patients with only 1 functioning kidney, those with medical risk factors, and children.

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However, any strongly motivated patient can benefit from a prevention analysis and prophylactic treatment if they are willing to pursue long-term therapy.

The size of the stone is an important predictor of spontaneous passage. A stone less than 4 mm in diameter has an 80% chance of spontaneous passage; this falls to 20% for stones larger than 8 mm in diameter. However, stone passage also depends on the exact shape and location of the stone and the specific anatomy of the upper urinary tract in the particular individual. For example, the presence of a ureteropelvic junction (UPJ) obstruction or a ureteral stricture could make passing even very small stones difficult or impossible. Most experienced emergency department (ED) physicians and urologists have observed very large stones passing and some very small stones that do not move.

Aggressive medical therapy has shown promise in increasing the spontaneous stone passage rate and relieving discomfort while minimizing narcotic usage. Aggressive treatment of any proximal urinary infection is important to avoid potentially dangerous pyonephrosis and urosepsis. In these cases, consider percutaneous nephrostomy drainage rather than retrograde endoscopy, especially in very ill patients.

Medical therapy for stone disease takes both short- and long-term forms. The former includes measures to dissolve the stone (possible only with noncalcium stones) or to facilitate stone passage, and the latter includes treatment to prevent further stone formation. Stone prevention should be considered most strongly in patients who have risk factors for increased stone activity, including stone formation before age 30 years, family history of stones, multiple stones at presentation, and residual stones after surgical treatment.

Indications for hospitalization

The decision to hospitalize a patient with a stone is usually made based on clinical grounds rather than on any specific finding on a radiograph. Generally, hospitalization for an acute renal colic attack is now officially termed an observation because most patients recover sufficiently to go home within 24 hours. Admission rate for patients with acute renal colic is approximately 20%.

Hospital admission is clearly necessary when any of the following is present:

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Oral analgesics are insufficient to manage the pain.Ureteral obstruction from a stone occurs in a solitary or transplanted

kidney.Ureteral obstruction from a stone occurs in the presence of a urinary

tract infection (UTI), fever, sepsis, or pyonephrosis.Infected hydronephrosis, defined as UTI proximal to an obstructing stone, mandates hospital admission for antibiotics and prompt drainage. Midstream urine culture and sensitivity was a poor predictor of infected hydronephrosis in one series, being positive in only 30% of cases.[31]

The clinical presentation of infected hydronephrosis is variable. Pyuria (>5 white blood cells [WBCs] per high-power field [hpf]) is almost always present but is not diagnostic of proximal infection. In one small series of 23 patients with infected hydronephrosis, the temperature was higher than 38°C in 15 patients, the peripheral WBC count was more than 10 X 109/L in 13 patients, and the creatinine level was greater than 1.3 mg/dL in 12 patients.[32]

Renal ultrasonography or computed tomography (CT) may distinguish pyonephrosis from simple hydronephrosis by demonstrating a fluid-fluid level in the renal pelvis (urine on top of purulent debris). In 2 small studies, ultrasonographic sensitivity for pyonephrosis was found to be 62-67%. CT sensitivity for pyonephrosis has not been reliably determined.[33, 34] The emergency physician must maintain a high index of suspicion.[35]

Antibiotics should cover Escherichia coli and Staphylococcus, Enterobacter, Proteus, and Klebsiella species. In another small study of 38 patients with hydronephrosis, 16 had infected hydronephrosis and 22 had sterile hydronephrosis. Ultrasonography alone detected 6 of 16 cases of pyonephrosis, a sensitivity of 38%. Using a cutoff value of 3 mg/dL for C-reactive protein and 100 mm/h for erythrocyte sedimentation rate, the diagnostic accuracy of detecting infected hydronephrosis and pyonephrosis increased to 97%.[36]

Relative indications to consider for a possible admission include comorbid conditions (eg, diabetes), dehydration requiring prolonged intravenous (IV) fluid therapy, renal failure, or any immunocompromised state. Patients with complete obstruction, perinephric urine extravasation, a solitary kidney, or pregnancy, and those with a poor social support system, also should be considered for admission, especially if rapid urologic follow-up is not reliably available.

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Larger stones (ie, ≥ 7 mm) that are unlikely to pass spontaneously require some type of surgical procedure. In some cases, hospitalizing a patient with a large stone to facilitate surgical stone intervention is reasonable. However, most patients with acute renal colic can be treated on an ambulatory basis.

About 15-20% of patients require invasive intervention due to stone size, continued obstruction, infection, or intractable pain. Several techniques are available to the urologist when the stone fails to pass spontaneously, including extracorporeal shock wave lithotripsy (SWL), ureteroscopy, and percutaneous nephrolithotomy.[37]

Emergency Management of Renal ColicInitial treatment of a renal colic patient in the ED starts with obtaining IV access to allow fluid, analgesic, and antiemetic medications to be administered. Many of these patients are dehydrated from poor oral intake and vomiting. Although the role of supranormal hydration in the management of renal (ureteral) colic is controversial (see below), patients who are dehydrated or ill need adequate restoration of circulating volume.

After diagnosing renal (ureteral) colic, determine the presence or absence of obstruction or infection. Obstruction in the absence of infection can be initially managed with analgesics and with 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.

If neither obstruction nor infection is present, analgesics and other medical measures to facilitate passage of the stone (see below) 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).

If both obstruction and infection are present, emergency decompression of the upper urinary collecting system is required (see Surgical Care). In addition, immediately consult with a urologist for patients whose pain fails to respond to ED management.

Pain relief

The cornerstone of ureteral colic management is analgesia, which can be achieved most expediently with parenteral narcotics or nonsteroidal

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anti-inflammatory drugs (NSAIDs). If oral intake is tolerated, the combination of oral narcotics (eg, codeine, oxycodone, hydrocodone, usually in a combination form with acetaminophen), NSAIDs, and antiemetics, as needed, is a potent outpatient management approach for renal (ureteral) colic.

Parenteral narcotics are the mainstay of analgesia for patients with acute renal colic. They work primarily on the central nervous system (CNS) to reduce the perception of pain. They are inexpensive and quite effective. When considering a medication and dosage range, remember that acute renal colic is probably the most painful malady to affect humans. Adverse effects of narcotic analgesics include respiratory depression, sedation, constipation, a potential for addiction, nausea, and vomiting.

Choosing any particular agent tends to be somewhat arbitrary. Morphine, meperidine, and butorphanol are the most commonly used.

Morphine is a potent narcotic analgesic that controls severe pain primarily through a CNS mechanism via specific receptor site interactions. The usual dosage is 10 mg/70 kg body weight intramuscularly (IM) or subcutaneously (SC) every 4 hours. The actual dosage required varies according to each individual patient’s tolerance and severity of discomfort. For more rapid results, morphine sulfate can be administered IV in doses of 4-10 mg, but this must be done slowly or in small increments to avoid excessive adverse effects.

Adverse effects of morphine include respiratory depression, drowsiness, mood changes, nausea, vomiting, increases in the cerebrospinal fluid pressure, and cough reflex depression. The most bothersome is respiratory depression caused by a direct effect on the brain stem respiratory center. This effect is most severe in patients who are elderly, debilitated, or both.

Meperidine is a potent parenteral narcotic analgesic that is very similar in overall effect to morphine sulfate. A 60-80 mg dose of meperidine is roughly equivalent to 10 mg of morphine. Meperidine offers a slightly more rapid onset of action and slightly shorter duration of analgesic activity than morphine sulfate. Some evidence suggests that meperidine may have slightly fewer adverse effects than morphine.

The dosage range is usually 50-150 mg IM or SC every 3-4 hours; it is reduced by at least 50% with IV administration. The actual effective dosage varies according to the source of the pain and the individual’s

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tolerance. As with morphine sulfate, IV administration should be performed slowly. Meperidine is contraindicated in patients taking monoamine oxidase inhibitors.

Butorphanol has some theoretical advantages based on studies that suggest it causes less smooth muscle spasm and respiratory depression than either morphine or meperidine. Butorphanol costs approximately $10/mg, compared with approximately $0.05/mg for meperidine. Because 1 mg of butorphanol is roughly equivalent in pain relieving efficacy to 20 mg of meperidine, butorphanol effectively is about 10 times as costly.

Naloxone (0.4 mg or 1 mL) is a specific narcotic antagonist for both meperidine and morphine sulfate that can be administered to counteract inadvertent narcotic overdosage or unusual opioid sensitivity. Naloxone has no analgesic properties.

Nalbuphine is a potent parenteral analgesic that is partly antagonistic to narcotics. Its overall effectiveness in relieving pain is equivalent to the opioids. The usual starting dose is 0.5 mg IV or 1-1.5 mg IM every 4-6 hours as needed.

Of the NSAIDs, the only one approved by the US Food and Drug Administration (FDA) for parenteral use is ketorolac. Ketorolac works at the peripheral site of pain production rather than on the CNS. It has been proven in multiple studies to be as effective as opioid analgesics, with fewer adverse effects.[38, 39] The dosage is 30-60 mg IM or 30 mg IV initially followed by 30 mg IV or IM every 6-8 hours. A dose of 15 mg is recommended in patients older than 65 years.

In more severe cases, ketorolac is particularly effective when used together with narcotic analgesics. Oral ketorolac is available in 10-mg pills, but the efficacy of this form in persons with acute renal colic is less clear. Some practitioners use parenteral ketorolac in the hospital but recommend either ibuprofen or oral cyclooxygenase-2 inhibitors (eg, celecoxib or meloxicam) for pain management in outpatients.

An intranasal ketorolac preparation is now available for moderate-to-severe pain and may be particularly useful for outpatient use in patients unable to take oral medication. A maximum of 5 days of ketorolac therapy is recommended.

Chemically, ketorolac is similar to aspirin and may increase the prothrombin time when administered with anticoagulants. Ketorolac

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can increase methotrexate toxicity and phenytoin levels. It is potentiated by probenecid and should be avoided in patients with peptic ulcer disease, renal failure, or recent gastrointestinal (GI) bleeding.

Antiemetic therapy

Because nausea and vomiting frequently accompany acute renal colic, antiemetics often play a role in renal colic therapy. Several antiemetics have a sedating effect that is often helpful.

Metoclopramide is the only antiemetic that has been specifically studied in the treatment of renal colic. In 2 double-blinded studies, it apparently provided pain relief equivalent to narcotic analgesics in addition to relieving nausea. Its antiemetic effect stems from its dopaminergic receptor blockage in the CNS. It has no anxiolytic activity and is less sedating than other centrally acting dopamine antagonists. The effect of metoclopramide begins within 3 minutes of an IV injection, but it may not take effect for as long as 15 minutes if administered IM.

The usual dose in adults is 10 mg IV or IM every 4-6 hours as needed. Metoclopramide is not available as a suppository.

Other medications commonly used as antiemetics include promethazine, prochlorperazine, and hydroxyzine. The author usually recommends antiemetics when patients with renal colic have been vomiting actively or report nausea sufficient to interfere with oral therapy. They also may be useful as anxiolytics in some cases. Whereas metoclopramide is the antiemetic of choice in the hospital or ED setting, a suppository formulation such as promethazine or prochlorperazine is recommended for outpatient use.

Antidiuretic therapy

Several studies have now demonstrated that desmopressin (DDAVP), a potent antidiuretic that is essentially an antidiuretic hormone, can dramatically reduce the pain of acute renal colic in many patients. It acts quickly, has no apparent adverse effects, reduces the need for supplemental analgesic medications, and may be the only immediate therapy necessary for some patients. It is available as a nasal spray (usual dose of 40 mcg, with 10 mcg per spray) and as an IV injection (4 mcg/mL, with 1 mL the usual dose). Generally, only 1 dose is administered.

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Animal studies have demonstrated a significant reduction in mean intraureteral pressure after an acute obstruction in subjects administered desmopressin compared with controls. In human studies, approximately 50% of 126 patients tested had complete relief of their acute renal colic pain within 30 minutes after the administration of intranasal desmopressin without any analgesic medication. For patients in whom desmopressin therapy failed, suitable analgesics were administered. No adverse effects from the antidiuretic medication occurred.

Although desmopressin is thought to work by reducing the intraureteral pressure, it may also have some direct relaxing effect on the renal pelvic and ureteral musculature. A central analgesic effect through the release of hypothalamic beta-endorphins has been proposed but remains unproved. Whether this therapy significantly affects eventual stone passage is unknown.

While some of the human studies lack adequate controls and further studies must be conducted, desmopressin therapy currently appears to be a promising alternative or adjunct to analgesic medications in patients with acute renal colic, especially in patients in whom narcotics cannot be used or in whom the pain is unusually resistant to standard medical treatment.

Antibiotic therapy

Antibiotic use in patients with kidney stones remains controversial. Overuse of the more effective agents leaves only highly resistant bacteria, but failure to adequately treat a UTI complicated by an obstructing calculus can result in potentially life-threatening urosepsis and pyonephrosis.

Use antibiotics if a kidney stone or ureteral obstruction has been diagnosed and the patient has clinical evidence of a UTI. Evidence of a possible UTI includes an abnormal finding upon microscopic urinalysis, showing pyuria of 10 WBCs/hpf (or more WBCs than RBCs), bacteriuria, fever, or unexplained leukocytosis. Perform a urine culture in these cases because a culture cannot be performed reliably later should the infection prove resistant to the prescribed antibiotic.

Approximately 3% of patients being treated for renal colic are reported to develop a newly acquired UTI. While case numbers are not high, such an infection can dramatically complicate the clinical outcome for that patient. Base selection of the antibiotic on the patient’s

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presentation, reserving the most effective parenteral antibiotics for patients with frank sepsis or other high-risk characteristics.

The author’s preference for initial medical therapy for pain in patients with acute renal colic is to use IV or IM ketorolac for pain with metoclopramide for nausea. If this therapy is unsuccessful or if the case is deemed more severe, a narcotic such as morphine sulfate or meperidine is added as needed to control pain. An antibiotic is administered if any question of potential infection exists. An oral antibiotic is always used if the patient is able to return home.

Active medical expulsive therapy

The traditional outpatient treatment approach detailed above has recently been improved with the application of a more aggressive treatment approach known as active medical expulsive therapy (MET). Many randomized trials have confirmed the efficacy of MET in reducing the pain of stone passage, increasing the frequency of stone passage, and reducing the need for surgery.[40, 41, 42, 43, 44, 45, 46, 47]

MET should be considered in any patient with a reasonable probability of stone passage. Given that stones smaller than 3 mm are already associated with an 85% chance of spontaneous passage, MET is probably most useful for stones 3-10 mm in size. Overall, MET is associated with a 65% greater likelihood of stone passage.[48]

The original rationale for MET was based on the possible causes of failure to spontaneously pass a stone, including ureteral stricture, muscle spasm, local edema, inflammation, and infection. Various common drugs were considered that would potentially benefit these problems, improve spontaneous stone passage, and alleviate renal colic discomfort.

Although NSAIDs have ureteral-relaxing effects and, as such, can be considered a form of MET, patient outcomes have been significantly improved only with the use of more potent (off-label) medications. The initially popularized regimens for MET included corticosteroids such as prednisone, as in the following example:

Ketorolac at 10 mg orally every 6 hours for 5 daysNifedipine XL at 30 mg/d PO for 7 daysPrednisone 20 mg PO twice a day for 5 daysTrimethoprim/sulfamethoxazole DS once a day for 7 daysAcetaminophen 2 tablets 4 times a day for 7 days

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An oral opioid pain medication (oxycodone-acetaminophen) as needed for breakthrough pain

Prochlorperazine suppository as needed for control of nauseaAlthough corticosteroids are effective, concerns about their side effects (admittedly not supported by randomized data) limited the acceptance of MET. More recently, randomized studies have demonstrated great efficacy of the following individual agents, sparing the corticosteroid component.

The calcium channel blocker nifedipine is indicated for angina, migraine headaches, Raynaud disease, and hypertension, but it can also reduce muscle spasms in the ureter, which helps reduce pain and facilitate stone passage. Ureteral smooth muscle uses an active calcium pump to produce contractions, so a calcium channel blocker such as nifedipine would be expected to relax ureteral muscle spasms.

The alpha-blockers, such as terazosin, and the alpha-1 selective blockers, such as tamsulosin, also relax the musculature of the ureter and lower urinary tract, markedly facilitating passage of ureteral stones. Some literature suggests that the alpha-blockers are more effective in this setting than the calcium channel blockers, and most practitioners currently use alpha-blockers preferentially over calcium channel blockers.

Multiple prospective randomized controlled studies in the urology literature have demonstrated that patients treated with oral alpha-blockers have an increased rate of spontaneous stone passage and a decreased time to stone passage.[41, 42, 43] The best studied of these is tamsulosin, 0.4 mg administered daily.

A systematic review by Singh et al found that MET using either alpha antagonists or calcium channel blockers augmented the stone expulsion rate for moderately sized distal ureteral stones. Adverse effects were noted in 4% of those taking alpha antagonists and in 15.2% of those taking calcium channel blockers.[49]

A systematic review by Beach et al found that MET with alpha antagonists for 28 days increased the rate of stone passage, decreased the time to stone passage, and decreased the rates of hospitalization and ureteroscopy, with minimal adverse effects.[50]

Not all data support MET. A randomized study of 77 ED patients with ureterolithiasis found no benefit to a 14-day course of tamsulosin,

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though the study group was small and the average stone size was 3.6 mm, making spontaneous passage without MET highly likely.[51]

MET with calcium channel blockers and alpha-blockers also appears to improve the results of ESWL (see Surgical Care) inasmuch as the stone fragments resulting from treatment appear to clear the system more effectively.

Analgesic therapy combined with MET dramatically improves the passage of stones, addresses pain, and reduces the need for surgical treatment. Ibuprofen can be substituted for the ketorolac tablets recommended in the original studies. Fewer complications with ibuprofen occur while maintaining efficacy for pain relief. An oral narcotic (eg, oxycodone/acetaminophen) is used as needed to control breakthrough pain.

A typical regimen for this aggressive therapy is as follows:1-2 oral narcotic/acetaminophen tablets every 4 hours as needed for

pain600-800 mg ibuprofen every 8 hoursMET with 30 mg nifedipine extended-release tablet once daily, 0.4 mg tamsulosin once daily, or 4 mg of terazosin once daily

Limit MET to a 10- to 14-day course, as most stones that pass during this regimen do so in that time frame. If outpatient treatment fails, promptly consult a urologist.

Future studies may identify a subgroup of patients such as those with larger stones or history of inability to pass stones that would benefit from MET.

Intravenous hydration

IV hydration in the setting of acute renal colic is controversial. Whereas some authorities believe that IV fluids hasten passage of the stone through the urogenital system, others express concern that additional hydrostatic pressure exacerbates the pain of renal colic. One small study of 43 ED patients found no difference in pain score or rate of stone passage in patients who received 2 L of saline over 2 hours versus those who received 20 mL of saline per hour.[52]

IV hydration should be given to patients with clinical signs of dehydration or to those with a borderline serum creatinine level who must undergo intravenous pyelography (IVP).

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Straining urine for stones

Collecting any passed kidney stones is extremely important in the evaluation of a patient with nephrolithiasis for stone-preventive therapy. Yet, in a busy ED, the simple instruction to strain all the urine for stones can be easily overlooked.

Knowing when a stone is going to pass is impossible regardless of its size or location. Even after a stone has passed, residual swelling and spasms can cause continuing discomfort for some time. Be certain that all urine is actually strained for any possible stones. An aquarium net makes an excellent urinary stone strainer for home use because of its tight nylon weave, convenient handle, and collapsible nature, making it very portable; it easily fits into a pocket or purse.

Surgical CareIn general, stones that are 4 mm in diameter or smaller will probably pass spontaneously, and stones that are larger than 8 mm are unlikely to pass without surgical intervention. With MET, stones 5-8 mm in size often pass, especially if located in the distal ureter. The larger the stone, the lower the possibility of spontaneous passage (and thus the greater the possibility that surgery will be required), although many other factors determine what happens with a particular stone.

Indications and contraindications

The primary indications for surgical treatment include pain, infection, and obstruction. Infection combined with urinary tract obstruction is an extremely dangerous situation, with significant risk of urosepsis and death, and must be treated emergently in virtually all cases. Additionally, certain occupational and health-related reasons exist.

General contraindications to definitive stone manipulation include the following:

Active, untreated UTIUncorrected bleeding diathesisPregnancy (a relative, but not absolute, contraindication)Specific contraindications may apply to a given treatment modality. For example, do not perform SWL if a ureteral obstruction is distal to the calculus or in pregnancy.

Surgical options

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For an obstructed and infected collecting system secondary to stone disease, virtually no contraindications exist for emergency surgical relief either by 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).

Many urologists have a preference for one technique 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.

In patients who are floridly septic or hemodynamically unstable, a percutaneous nephrostomy is a faster and safer way to establish drainage of an infected and obstructed kidney. In these situations, retrograde approaches to drainage, if used at all, should be reserved for relatively mild cases in which patients are medically stable. Use appropriate urine cultures and antibiotics whenever a UTI is suspected in conjunction with hydronephrosis or renal colic.

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.

Guidelines are now available to assist the urologist in selecting surgical treatments. The 2005 American Urological Association (AUA) staghorn calculus guidelines recommend percutaneous nephrostolithotomy as the cornerstone of management.[53] In the ureteral stone guidelines produced by a joint effort of the AUA and the European Association of Urology, SWL and ureteroscopy are both recognized as first-line treatments for ureteral stones.[54]

Stent placement

Internal ureteral stents form a coil at either end when the stiffening insertion guide wire is removed. One coil forms in the renal pelvis and the other in the bladder. Stents are available in lengths from 20-30 cm and in 3 widths from 4.6F to 8.5F. Some are designed to soften after placement in the body; others are rather stiff to resist crushing and obstruction by large stones or external compression with occlusion from an extrinsic tumor or scar tissue.

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To select the correct-size stent, estimates can be made based on the height of the patient, or the ureteral length can be measured. This is best performed by means of a retrograde pyelogram. The distance from the tip of the retrograde catheter to the UPJ is measured in centimeters with a tape measure. To account for the average magnification effect of the film, 10% of this reading is subtracted. If the result is an odd number, a double-J stent one size longer is used. The most common lengths used are 26 cm in men and 24 cm in women.

The optimal stent width depends on both the relative diameter and course of the ureter and the purpose of the stent. If the patient has a stricture or a tortuous ureter, a stiffer or larger-diameter stent is placed if possible.

When used for stone disease, stents perform several important functions. They virtually guarantee drainage of urine from the kidney into the bladder and bypass any obstruction. This relieves patients of their renal colic pain even if the actual stone remains. Over time, stents gently dilate the ureter, making ureteroscopy and other endoscopic surgical procedures easier to perform later.

Because they are also quite radiopaque, stents provide a stable landmark when performing SWL. A landmark is particularly important with small or barely visible stones, especially in the ureter, because the SWL machine uses radiographic visualization to target the stone.

Once large stones are broken up, stents tend to prevent the rapid dumping of large amounts of stone fragments and debris into the ureter (called steinstrasse). The stent forces the fragments to pass slowly, which is more efficient and prevents clogging.

Stents do have drawbacks. They can become blocked, kinked, dislodged, or infected. A KUB radiograph can be used to determine stent position, while infection is easily diagnosed by urinalysis. A renal sonogram can sometimes be helpful if there is concern for obstruction.

Questionable cases can be evaluated further using a radiographic cystogram or an IVP. The cystogram is performed by filling the urinary bladder with diluted contrast media through a Foley catheter under gravity pressure. A stent that is unclogged and functioning normally should show free reflux of contrast from the bladder into the stented renal pelvis.

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The major drawback of stents, however, is that they are often quite uncomfortable for patients due to direct bladder irritation, spasm, and reflux. This discomfort can be alleviated to some extent by pain medications, anticholinergics (eg, oxybutynin, tolterodine), alpha-blockers, and topical analgesics (eg, phenazopyridine).

Percutaneous nephrostomy

In some cases, drainage of an obstructed kidney is necessary and stent placement is inadvisable or impossible. In particular, such cases include patients with pyonephrosis who have a UTI or urosepsis exacerbated by an obstructing calculus. In these patients, retrograde endourological procedures like retrograde pyelography and stent placement may exacerbate infection by pushing infected urinary material into the obstructed renal unit. Percutaneous nephrostomy is useful in such situations.[55]

Extracorporeal shockwave lithotripsy

SWL, the least invasive of the surgical methods of stone removal, utilizes an underwater energy wave focused on the stone to shatter it into passable fragments.

It is especially suitable for stones that are smaller than 2 cm and lodged in the upper or middle calyx. It is contraindicated in pregnancy, untreatable bleeding disorders, tightly impacted stones, or in cases of ureteral obstruction distal to the stone. In addition, the effectiveness is limited for very hard stones (which tend to be dense on CT scan), cystine stones, and in very large patients.

The patient, under varying degrees of anesthesia (depending on the type of lithotriptor used), is placed on a table or in a gantry that is then brought into contact with the shock head. The deeper the anesthesia (general endotracheal), the better the results. In addition, evidence is mounting that slower shockwave delivery (60-80 per min) improves the results. New lithotriptors that have 2 shock heads, which deliver a synchronous or asynchronous pair of shocks (possibly increasing efficacy), have attracted great interest.

The shock head delivers shockwaves developed from an electrohydraulic, electromagnetic, or piezoelectric source. The shockwaves are focused on the calculus, and the energy released as the shockwave impacts the stone produces fragmentation. The resulting small fragments pass in the urine.

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SWL is limited somewhat by the size and location of the calculus. A stone larger than 1.5 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. In addition, results may not be optimal in large patients, especially if the skin-to-stone distance exceeds 10 cm.[56]

Ureteroscopy

Along with SWL, ureteroscopic manipulation of a stone (see the image below) is a commonly applied method of stone removal. A small endoscope, which may be rigid, semirigid, or flexible, is passed into the bladder and up the ureter to directly visualize the stone.

Two calculi in a dependent calyx of the kidney (lower pole) visualized through a flexible fiberoptic ureteroscope. In another location, these calculi might have been treated with extracorporeal shockwave lithotripsy (ESWL), but, after being counseled regarding the lower success rate of ESWL for stones in a dependent location, the patient elected ureteroscopy. Note that the image provided by fiberoptics, although still acceptable, is inferior to that provided by the rod-lens optics of the rigid ureteroscope in the previous picture.Ureteroscopy is especially suitable for removal of stones that are 1-2 cm, lodged in the lower calyx or below, cystine stones, and high attenuation ("hard") stones. The typical patient has acute symptoms caused by a distal ureteral stone, usually measuring 5-8 mm. Stones smaller than 5 mm in diameter generally are retrieved using a stone basket, whereas tightly impacted stones or those larger than 5 mm are manipulated proximally for SWL or are fragmented using an endoscopic direct-contact fragmentation device.

Often, a ureteral stent must be placed after ureteroscopy in order to prevent obstruction from ureteral spasm and edema. Since a ureteral stent is often uncomfortable, many urologists eschew stent placement following ureteroscopy in selected patients.[57]

Percutaneous nephrostolithotomy

Percutaneous nephrostolithotomy allows fragmentation and removal of large calculi from the kidney and ureter. Because of their increased morbidity compared with SWL and ureteroscopy, percutaneous procedures are generally reserved for large and/or complex renal stones and failures from the other 2 modalities. Percutaneous nephrostolithotomy is especially useful for stones larger than 2 cm in diameter.

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A needle and then a wire, over which is passed a hollow sheath, are inserted directly into the kidney through the skin of the flank. Percutaneous access to the kidney typically involves a sheath with a 1-cm lumen, which will admit relatively large endoscopes with powerful and effective lithotrites that can rapidly fragment and remove large stone volumes. Renal calyces, pelvis, and proximal ureter can be examined and stones extracted with or without prior fragmentation.

In some cases, a combination of SWL 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. In such cases, experience has shown that the final procedure should be percutaneous nephrostolithotomy.

Open nephrostomy

Open nephrostomy has been used less and less often since the development of SWL and endoscopic and percutaneous techniques; it now constitutes less than 1% of all interventions. Disadvantages include longer hospitalization, longer convalescence, and increased requirements for blood transfusion.

Medical Therapy for Stone DiseaseDissolution of calculi

Urinary calculi composed predominantly of calcium cannot be dissolved with current medical therapy; however, medical therapy is important in the long-term chemoprophylaxis of further calculus growth or formation.

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 alkalization of the urine. Sodium bicarbonate can be used as the alkalizing 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 alkalizing agent should be adjusted to maintain the urinary pH between 6.5 and 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.

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Even very large uric acid calculi can be dissolved in patients who comply with therapy. Roughly 1 cm per month dissolution can be achieved. Practical ability to alkalinize the urine significantly limits the ability to dissolve cystine calculi.

Chemoprophylaxis

Prophylactic therapy might include limitation of dietary components, addition of stone-formation inhibitors or intestinal calcium binders, and, most importantly, augmentation of fluid intake. (See Dietary Measures and Prevention of Nephrolithiasis.) Besides advising patients to avoid excessive salt and protein intake and to increase fluid intake, base medical therapy for long-term chemoprophylaxis of urinary calculi on the results of a 24-hour urinalysis for chemical constituents.

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, D-penicillamine, 2-alpha-mercaptopropionyl-glycine) help reduce stone formation in cystinuria. Therapy should also include long-term urinary alkalinization and aggressive fluid intake. Captopril has been shown to be effective in some trials, although, again, strong data are lacking. Routine use should be avoided but can be added in patients who have difficulty in dissolving and preventing cystine stones.

Dietary MeasuresIn 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. Patients with recurrent nephrolithiasis traditionally have been instructed to drink 8 glasses of fluid daily to maintain adequate hydration and decrease chance of urinary supersaturation with stone-forming salts. The goal is a total urine volume in 24 hours in excess of 2 liters.

The only other general dietary guidelines are to avoid excessive salt and protein intake. Moderation of calcium and oxalate intake is also reasonable, but great care must be taken not to indiscriminately instruct the patient to reduce calcium intake.

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Dietary calcium should not be restricted beyond normal unless specifically indicated based on 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 GI 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.

An empiric restriction of dietary calcium may also adversely affect bone mineralization and may have osteoporosis implications, especially in women. This practice should be condemned unless indicated based on a metabolic evaluation.

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

Prevention of NephrolithiasisThe most common causes of kidney stones are hypercalciuria, hyperuricosuria, hyperoxaluria, hypocitraturia, and low urinary volume. Each of these major factors can be measured easily with a 24-hour urine sample using one of several commercial laboratory packages now available. Kidney stone preventive therapy consists of dietary adjustments, nutritional supplements, medications, or combinations of these.

Strongly encourage patients who have a stone at a young age (ie, < 25 y), multiple recurrences, a solitary functioning kidney, or a history of prior kidney stone surgery to obtain a 24-hour urine collection for stone prevention analysis, especially if they are motivated to comply with a long-term stone prevention program. These 24-hour urine collection kits can be obtained from a number of commercial medical laboratories.

ConsultationsConsultation 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.

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Consult a urologist immediately in cases of ureterolithiasis with proximal UTI. Infected hydronephrosis is a true urologic emergency and requires hospital admission, IV fluids, IV antibiotics, and immediate drainage of the infected hydronephrosis via percutaneous nephrostomy or ureteral stent placement.

Urologic consultation is also appropriate in patients with unusually large stones, high-risk medical conditions, inability to tolerate oral fluids and medications, unrelenting pain, renal failure, renal transplant, a solitary functioning kidney, or a history of prior stones that required invasive intervention.

Patients who are pregnant require a consultation with an obstetrician-gynecologist, and those with a history of severe cardiac disease or congestive heart failure may benefit from involvement of an internal medicine specialist or cardiologist.

Patients with strong motivation to prevent all future stones, those with multiple recurrences or single functioning kidneys, and all children younger than 16 years with nephrolithiasis should be referred to a specialist in nephrolithiasis prevention. A medical expert in metabolic stone prevention testing, interpretation, and prophylactic therapy is available in most communities.

Long-Term MonitoringPatients who do not meet admission criteria may be discharged from the ED in anticipation that the stone will pass spontaneously at home. Arrangements should be made for follow-up with a urologist in 2-3 days. Patients should be told to return immediately for fever, uncontrolled pain, or vomiting. Patients should be discharged with a urine strainer and encouraged to submit any recovered calculi to a urologist for chemical analysis.

Follow-up for patients with first-time incidence of stones should consist of stone analysis and abbreviated metabolic evaluation to rule out hyperparathyroidism, renal tubular acidosis, and chronic infection with urea-splitting bacteria.

Patients with recurrent ureterolithiasis should undergo a more thorough metabolic evaluation. Patients with recurrent stones who undergo thorough metabolic evaluation and specific therapy enjoy a remission rate in excess of 80% and can decrease the rate of stone formation by 90%. A stone chemical analysis together with serum and appropriate

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24-hour urine metabolic tests can identify the etiology in more than 95% of patients.

A typical 24-hour urine determination should include urinary volume, pH, specific gravity, calcium, citrate, magnesium, oxalate, phosphate, and uric acid. Most common findings are hypercalciuria, hyperuricosuria, hyperoxaluria, hypocitraturia, and low urinary volume. Therefore, the emergency physician should encourage urologic follow-up.

Postsurgical follow-up

After surgical treatment of urinary tract calculi, the major issues include 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 that includes abdominal radiography is often adequate after an uncomplicated stone-removal procedure. Further imaging is often unnecessary in a patient with a previous radiopaque stone who has no further symptoms. Imaging that includes assessment of renal drainage (eg, IVP, ultrasonography, CT scanning) is usually indicated in the following cases:

Stones with unusual characteristicsDifficult or complicated proceduresPatients with unusual symptomsOnce postoperative complications have been excluded and the patient is clinically healthy, standard radiographic follow-up care includes abdominal radiography every 6-12 months. Radiography is often performed in conjunction with metabolic chemoprophylaxis.

Ongoing medical therapy

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 be unnecessary. 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

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follow-up care consists of plain abdominal radiography (or renal ultrasonography 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 parameters—not just the previously abnormal ones—is 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.

Proceed to Medication 

OverviewTesticular torsion is a true urologic emergency and must be differentiated from other complaints of testicular pain because a delay in diagnosis and management can lead to loss of the testicle.[1] Though testicular torsion can occur at any age, including the prenatal and perinatal periods, it most commonly occurs in adolescent males; it is the most frequent cause of testicle loss in that population.

In pediatric patients, the following features are associated with higher likelihood of torsion[2] :

Pain duration of less than 24 hoursNausea or vomitingHigh position of the testicleAbnormal cremasteric reflexResults of physical examination are imperfect in ruling out testicular torsion, however.[3] Imaging studies (eg, ultrasonography, nuclear scans) may be useful when a low suspicion of testicular torsion exists.[4, 5, 6, 7, 8, 9, 10] A Doppler sonogram of an avascular testicle is shown below. Surgical exploration should not be delayed for the sake of performing imaging studies.

Transverse power Doppler image of both testes illustrates an enlarged, avascular left testicle.If the diagnosis of torsion is suspected on clinical grounds, early urologic consultation is mandatory since definitive treatment is surgery for detorsion and orchiopexy or possible orchiectomy. Transfer the patient if no urologist is available. Administer analgesic medication, as testicular torsion is typically very painful.

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For other discussions of this condition, see the Medscape Reference articles Testicular Torsion and Pediatric Testicular Torsion.

Manual DetorsionThe procedure for manual detorsion of the testis is similar to the "opening of a book" when the physician is standing at the patient's feet. Most torsions twist inward and toward the midline; thus, manual detorsion of the testicle involves twisting outward and laterally. Lateral rotation has been described in up to a third of testicular torsions, however,[8, 9] and in such cases further lateral rotation will worsen the condition.

For manual detorsion in a suspected torsion of the right testicle, the physician is positioned in front of the standing or supine patient and holds the patient's right testicle with the left thumb and forefinger. The physician then rotates the right testicle outward 180° in a medial-to-lateral direction. For the patient's left testicle, the physician uses the right thumb and forefinger and rotates the patient's left testicle in an outward direction 180° from medial to lateral.

Rotation of the testicle may need to be repeated 2-3 times for complete detorsion. Pain relief serves as a guide to successful detorsion, but restoration of blood flow must be confirmed following the maneuver.[11] Subsequent elective orchiopexy is recommended, to prevent recurrent torsion.[12]

In the literature, the success rate of manual detorsion has varied widely. Success rates have ranged from 26.5% to more than 80%.[12]

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KATETERISASI URETRA

PENDAHULUAN

Kateterisasi uretra adalah salah satu prosedur yang paling umum di

rumah

sakit, praktek swasta dan situs perawatan primer (Puskesmas). Demikian

intervensi mungkin diperlukan untuk tujuan diagnostik atau terapeutik.

Semua petugas kesehatan (dokter spesialis, dokter umum dan perawat)

mengenal kateter dan cara memasukkan mereka ke dalam kandung kemih.

Pasien harus memahami prosedur yang diusulkan dan potensi komplikasi:

jika pasien diinformasikan, pasien akan bersikap kooperatif dan nyaman

dengan prosedur. 'Instrumentasi retrograd melalui saluran kemih dapat

mengakibatkan signifikan cedera. Larutan sterilisasi, pelumas yang larut

dalam air dan pengairan dengan tekanan rendah secara signifikan ini dapat

menurunkan risiko infeksi. Jika prosedur ini jangka lama maka pasien harus

diantisipasi dengan pemberian antibiotik yang sesuai.

Posisi pasien sama pentingnya dengan dari pemilihan alat yang tepat.

Tujuan dari laboratorium kateterisasi uretra keterampilan adalah:

1. Umum Tujuan instruksional

- Siswa mengetahui kateter, larutan sterilisasi, pelumas yang larut dalam air,

alat untuk kateterisasi uretra, dan mampu dengan aman melakukan

kateterisasi.

2. Khusus instruksional tujuan.

- Mempersiapkan pasien termasuk memperoleh informed consent, dan posisi

benar

- Memastikan instrumen steril

- Tangan aseptik cuci metode

- Gunakan sarung tangan steril dengan metode aseptik

- Disinfeksi lubang uretra dan penis

- Menggantungkan penis dengan handuk steril fenestrated

- Penis digenggam di belakang kelenjar dengan tangan kiri dan traksi ke atas

sedikit, atau labia majora tersebar untuk mengekspos meatus uretra

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- Pelumas jelly + lidokain / anestesi jelly (cathegel ®, instilagel ®, Xylocaine

jelly ®) ditanamkan ke dalam uretra

- Kateter dimasukkan sepanjang uretra ke dalam kandung kemih

- Kateter balon dipompa

- Memastikan bahwa kateter diposisikan dalam leher kandung kemih

- mengoleskan glans penis dengan larutan antiseptik

- mengatasi kateter ke atas paha dengan menggunakan pita perekat (Velcro

band)

- pelepasan dan penggantian kateter uretra .

Kateter uretra

Kateter uretra (karet, lateks, plastik / polyvinylchloride, teflon, silikon,

bahan hidrogel) adalah tabung berongga, yang digunakan untuk mengalirkan

urin dari

Urine kandung kemih mungkin perlu dikeringkan pada pasien dengan retensi

urin, untuk mengukur volume urin sisa, untuk mendapatkan urin untuk

pemeriksaan, untuk menanamkan obat atau kontras radiografi, atau untuk

mengairi kandung kemih. Banyak jenis kateter juga berguna sebagai tabung

nefrostomi. Kaku atau logam kateter dapat dengan mudah melubangi uretra

posterior (bagian palsu) dan

karena itu hanya harus digunakan oleh urolog. Kateter Coude dan

sejenisnya, ukuran 16 - 18 Fr tidak sesuai untuk jangka panjang pembuangan

karena ujung yang kaku dapat menyebabkan ulserasi dan kemungkinan

nekrosis dinding kandung kemih, dengan runtuhnya berikutnya dari kandung

kemih. Sebuah pendek (plastik atau logam) kateter dari 8 cm ini untuk

kateterisasi langsung perempuan. Kateter untuk laki-laki harus lembut.

Kateter pilihan untuk jangka panjang pembuangan adalah kateter Foley.

Kateter Foley adalah kateter balon diri mempertahankan dirancang oleh Dr

Frederick Foley pada tahun 1920. Ada dua jenis yang tersedia di pasar: i) dua

cara desain dengan saluran untuk pembuangan urin dan saluran yang lebih

kecil untuk inflasi dari balon, ii) tiga cara kateter dengan saluran ketiga untuk

irigasi. Kateter Foley tersedia dalam berbagai ukuran, volume balon dan tip

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desain. Pezzer dan kateter Malecot, dengan berbentuk jamur tip, adalah

pilihan lain untuk berdiamnya kateter. Ukuran kateter biasanya diukur dalam

Cherriere (Ch) atau (Fr) Prancis unit. Diameter dalam milimeter diperoleh

dengan membagi Ch / Fr oleh 3,14 Untuk Misalnya, kateter 30 Fr ditunjuk

memiliki diameter sekitar 10 mm. Ketiga arah kateter memiliki saluran yang

sempit untuk pengaliran urin karena tambahan saluran untuk irigasi. Yang

lebih besar tiga arah kateter hingga 22 - 24 Fr mungkin diperlukan untuk

bilas kandung kemih dan pengairan dengan adanya dari kotoran atau

hematuria. Balon kateter harus digelembungkan secukupnya untuk menahan

kateter tip dengan aman di kandung kemih. Volume balon biasanya 5ml, dan

30 - 50 ml dengan kateter pengairan tiga arah yang dirancang untuk

digunakan setelah

transurethral prostatektomi. Balon besar lebih cenderung menyebabkan

kandung kemih kejang dan kebocoran kemih, dan penggunaan jangka

panjang dari balon besar dapat menyebabkan kerusakan pada leher kandung

kemih. Balon kateter harus diisi hanya untuk pembuat direkomendasikan

volume. Tips kateter bervariasi dalam bentuk dan konfigurasi mata drainase.

Kateter Caude memiliki ujung meruncing dan sedikit melengkung. Ujung

Robinson dan kateter Whiestle dibulatkan dan memiliki ujung lurus. Pezzer

dan Kateter Malecot memiliki tip berbentuk meruncing dan jamur.

Kandung kemih

Kandung kemih adalah organ yang berongga, yang pada orang dewasa

memiliki

400-500 ml kapasitas. Pada wanita, dinding posterior dan kubah yang

invaginated oleh rahim. Bila kandung kemih penuh, yang naik jauh di atas

simfisis dan dapat dengan mudah diraba atau percussed. Jika lebih

membesar, seperti pada akut atau kronis retensi urin, dapat menyebabkan

bagian bawah perut untuk menggembung tampak. Ketika kosong, kandung

kemih terletak di belakang simfisis pubis. Pada bayi dan anak, kandung

kemih ini terletak lebih tinggi. Membentang dari umbilikus ke kubah kandung

kemih ini median umbilikus, tali berserat yang merupakan urachus terhapus.

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Ini ureter masuk kandung kemih secara tidak langsung. Daerah diantara

lubang dari ureter kiri dan kanan dikenal sebagai punggung interureteric,

yang membentuk proksimal perbatasan trigonum kandung kemih. Sphincter

internal tidak sejati sfingter tetapi penebalan dibentuk oleh serat otot

interlaced dan konvergen dari otot detrussor.

Mukosa kandung kemih terdiri dari epitel transisional. Di bawah

mukosa adalah layen submukosa dan eksternal pada mukosa ini otot

detrusor. Otot detrusor terbuat dari serat halus dan terdiri dari 3 lapisan

yang pasti: bagian dalam longitudinal, sirkular tengah dan luar longitudinal.

Aliran darah di kandung kemih ini dari bagian tengah superion dan inferior

kandung kemih arteri, yang timbul dari iliaka internal / arteri hipogastrik ini

arteri lainnya untuk kandung kemih muncul dari glutealis obturatorius dan

inferior arteri. Pada wanita arteri vagina dan rahim juga mengirimkan cabang

untuk kandung kemih. Di sekitar kandung kemih adalah pleksus pembuluh

vena yang kaya bermuara ke dalam vena iliaka / hipogastrikus.

Persarafan ke dalam kandung kemih adalah melalui sistem saraf otonom

dengan tiga jenis saraf: parasimpatis, simpatik dan somatik. Sistem

parasimpatis muncul dari S2 - segmen / S4 panggul saraf, dan dengan

melepaskan neurotransmitter asetilkolin, ia menyediakan kontrol motor dari

otot detrusor. Sistem simpatik muncul dari Th 10 - L2 / hipogastrikus saraf

yang terjadi pada konsentrasi terbesar terhadap kandung kemih dasar dan

leher kandung kemih. Saraf simpatik memberikan kontrol motor utama untuk

uretra dan otot-otot halus prostat. Saraf somatik adalah saraf pudenda yang

berkontribusi pada mekanisme sfingter lurik.

Fungsi utama kandung kemih adalah untuk menyimpan urin dan kemudian

untuk urin kosong efisien.

Uretra

Uretra pria

Uretra dimulai di bagian orifisium kandung kemih (uretra internal)

untuk

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meatus eksternal, dengan lebar rata-rata 8 - 9 mm. Eksternal meatus ini

bagian tersempit dari uretra. ini navicularis fosa adalah terbesar bagian dari

kelenjar uretra. ini anatomi pembagian dari uretra adalah penting secara

klinis. Uretra pria dibagi menjadi bagian posterior (prostat dan uretra

membran) dan bagian anterior (uretra bulat dan penis). ini colliculus

seminalis dengan saluran dari vesikel seminalis dan

Kelenjar prostat terletak di uretra prostat. Uretra membran berisi sphincter

eksternal, otot volunter. Pada titik ini, uretra menembus diafragma urogenital

dan tetap dengan jaringan ikat padat untuk batas bawah dari simfisis

tersebut. Patah tulang panggul menyebabkan kontusio, laserasi atau

transaksi dari uretra. Mukosa uretra ini epitel transisional dalam uretra

posterior, dan berlanjut dengan kolumnar

kompleks epitel dan epitel skuamosa. Hal ini diinervasi kaya dan memiliki

pasokan darah kaya Dalam kondisi lembek itu berbentuk S, ketika penis

ereksi itu adalah U atau L berbentuk. Bentuk melengkung uretra dapat

diluruskan melalui traksi ringan yang penting ketika memperkenalkan

kateter ke uretra.

Wanita uretra

Uretra perempuan secara signifikan lebih pendek daripada uretra laki-

laki.Ini

uretra wanita dewasa adalah sekitar 4 cm dan 8 mm. Ini melengkung sedikit

dan terletak di bawah simfisis pubis hanya anterior vagina. Mukosa uretra

epitel skuamosa ini pada bagian distal dan transisional di sisanya, dan

memiliki kelenjar mukosa kaya. Di ujung uretra meatus eksternal bermuara

ke dalam vagina vestibulum. Pada wanita obesitas lokasi meatus extern yang

tersembunyi, sehingga memasukkan kateter uretra mungkin sulit dan

perawatan harus dijaga jangan sampai memasukkan kateter ke dalam

vagina.

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Retensi urin

Retensi urin merupakan masalah yang umum di bagian gawat darurat atau

di ruang praktek pribadi. Ini adalah ketidakmampuan kandung kemih untuk

pengosongan

urine, dan mungkin timbul dari obstruksi untuk keluar kandung kemih,

kontraktilitas kandung kemih berkurang atau kombinasi dari keduanya.

Retensi urin tidak hanya menyebabkan gejala lokal tetapi juga dapat

mengakibatkan efek mendalam pada fungsi ginjal. Ini dapat berkembang

pesat selama beberapa jam (Retensi urin akut, AUR), atau beberapa bulan

atau tahun (Retensi urin kronis, CUR). Hal ini juga memungkinkan untuk

memiliki komplikasi akut pada retensi urin kronis.

Akut urin Retensi

Pasien AUR adalah keadaan darurat urologi umum, ditandai dengan tiba-tiba

ketidakmampuan untuk berkemih dengan distensi menyakitkan dan kandung

kemih / atau parah ketidaknyamanan di perut bagian bawah. Akut biasanya

retensi urin menyajikan sebagai ketidakmampuan tiba-tiba untuk buang air

kecil dengan mendesaknya kemih ditandai dan nyeri perut bagian bawah.

Perkusi dan palpasi bagian bawah perut menunjukkan tegang, membesar

kandung kemih, menyakitkan. pada laparotomi pos dan pasien obesitas,

deteksi dari kandung kemih membesar mungkin sulit. Pada pasien dengan

urin akut retensi drainase, langsung dari kandung kemih dengan kateterisasi

uretra perlu dilakukan kecuali pada pasien dengan riwayat striktur uretra

atau traumatis kateter penyisipan. Dalam keadaan suprapubik sebuah

cystotomy / kateter harus dimasukkan. Sebuah volume besar urine sisa

setelah kateterisasi akan mengkonfirmasi diagnosis. Jarang, retensi urin akut

tidak menimbulkan rasa sakit dan menunjukkan sebuah neurologis

menyebabkan. Selain gejala kencing, pasien mungkin mengeluh usus dan /

atau disfungsi seksual. Beberapa pasien mengeluh sakit punggung dan linu

panggul.

Selama pemeriksaan colok dubur, mengurangi nada anal dan gangguan

sensorik

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atas daerah pelana harus membuat pemeriksa menduga neurologis

menyebabkan. Konsultasi neurologis atau bedah saraf yang mendesak

mungkin diperlukan,

karena pengobatan yang terlambat dapat membahayakan penyembuhan

akhir.

Retensi urin kronis

Pasien CUR memiliki sakit, dan menyajikan dengan enuresis nokturnal

karena inkontinensia overflow, dengan sedikit lebih rendah gejala saluran

kemih. Retensi urin kronis diklasifikasikan berdasarkan presentasi klinis

Fungsi Ginjal dan temuan baik Retensi urin Turunkan Tekanan kronis (LPCUR),

atau Tekanan kronis Tinggi urin Retensi (HPCUR), meskipun perbedaan ini

tidak jelas dipotong. Gambaran klinis LPCUR sering menghasilkan sedikit

gejala dan biasanya ditemukan secara kebetulan saat pemeriksaan USG

perut atau pemindaian. LPCUR bukanlah darurat urologi dan dapat dikelola

sebagai sebuah pilihan, meskipun penting untuk membedakan antara

HPCUR. Itu kandung kemih adalah buncit, lembut dan sulit untuk merasa,

ada ginjal normal pada USG pemindaian, dan tingkat kreatinin serum normal.

Gambaran klinis HPCUR adalah enuresis, sebuah bladden menyakitkan

tegang hipertensi dan hidronefrosis bilateral. HPCUR pasien lain yang hadir

dengan gejala gagal ginjal dan sodium yang menyertainya dan air retensi.

Hipertensi dan gagal jantung kongestif terjadi pada 50 dan 20% masing-

masing. Pemeriksaan fisik dapat mengungkapkan, tanpa rasa sakit tegang,

bladden buncit cairan yang berlebihan dan tanda-tanda uremia. Pasien

dengan HPCUR juga dapat hadir dengan nefropati infeksi saluran kemih

obstruktif atau gross hematuria, dan gejala-gejala ini juga indikasi untuk

kateterisasi kandung kemih mendesak. penyisipan Dan Hapus dari lndwelling

Kateter uretra Dalam kateterisasi uretra kateter uretra dimasukkan ke dalam

kandung kemih melalui lubang eksternal uretra. Aku n kandung kemih

langsung atau suprapubik kateterisasi kateter dimasukkan ke dalam

kandung kemih melalui pembukaan di kandung kemih (cystostomy).

Kateterisasi uretra biasanya yang paling nyaman, cepat dan mudah, dan

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perawatan primer dan dokter ruang gawat darurat dan staf perawat yang

akrab dengan teknik. Kateter suprapubik memiliki beberapa keuntungan

penting, terutama jika kateterisasi berkepanjangan

diperlukan. Mereka menyebabkan infeksi kurang kemih dan striktur uretra,

dan

mengganggu kurang dengan hubungan seksual. Kateterisasi suprapubik

menjadi perlukan ketika kateterisasi uretra gagal atau kontraindikasi,

misalnya di adanya striktur uretra atau trauma uretra. Aturan dasar untuk

kateterisasi berdiamnya adalah teknik steril ketat. Kateterisasi intermiten

bersih (CIC) biasanya dilakukan untuk pasien dengan kandung kemih

neurogenik dan gejala retensi urin. Mekanisme ganda dari otot sfingter

memberikan efektif penghalang terhadap infeksi menaik antara saluran

kemih steril dan lingkungan luar. Sebaliknya, kateterisasi setiap menyajikan

dengan bahaya induksi mundur dari organisme patogen yang dapat

menyebabkan komplikasi.

Teknik Dari Kateterisasi uretra

• Menjelaskan dan mendiskusikan prosedur dengan pasien

• Tempatkan pasien dalam posisi telentang nyaman

• Siapkan troli dengan semua peralatan yang dibutuhkan

• Gunakan teknik aseptik '

• Pada pria, menyuntikkan 10 - 15 ml pelumas larut air dengan lokal

anestesi ke dalam uretra dan pijat bersama.

• Pada wanita, oleskan pelumas langsung ke kateter

• Pada pria memegang penis tegak lurus dengan tubuh

• pada wanita menyebar majora labium

• memasukkan kateter perlahan dan dengan lembut memajukan sepanjang

urethra,

• menghindari penggunaan tiba-tiba atau kekuatan yang berlebihan

• Ketika sphincter eksternal tercapai pada pria, meregangkan penis

sejajar dengan tubuh dan berlaku lembut, tekanan berkelanjutan. Mintalah

pasien untuk mengambil napas dalam-lambat atau saring seakan lewat air

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seni untuk

bersantai sphincter

• Setelah kateter berada di kandung kemih mengembang balon untuk appro-

priate volume dan melampirkan tas drainase

• Catat volume residu.

Kontraindikasi dari Kateterisasi uretra:

• meatal perdarahan

• Perineal hematom

• Mengambang dari prostat

Dengan perawatan kateter yang baik (drainase tertutup, dipasang

pada paha atas), kateter Foley dapat tetap tinggalnya selama 2 - 4 minggu.

Pada pasien dengan urin keruh yang terlalu yang terinfeksi dan cenderung

kerak, kateter harus diganti sesuai kebutuhan. Selain itu, perawatan yang

harus diambil untuk mencegah kateter diblokir, dan asupan cairan harian

rata-rata 2000 cc jaminan yang pembilasan kateter. Pada pasien dengan

gross hematuria, pembekuan, atau infeksi berat, kandung kemih harus

cermat pengairan sebelum kandungan kandung kemih jelas. Larutan garam

steril atau air steril yang irrigants cocok. Sebuah kateter pada uretra dan

kandung kemih merupakan benda asing yang dirasakan sebagai sebuah

iritasi menyenangkan terutama oleh pasien sensitif, yang mungkin

memerlukan obat penenang atau analgesia untuk mengurangi beberapa

ketidaknyamanan.

Kateterisasi intermiten, Prosedur Bersih

• Cuci tangan dengan sabun dan air mengalir

• Kumpulkan peralatan di sebuah lokasi yang sesuai peralatan pribadi yang

dibutuhkan: kateter air pelumas larut (KY jelly), lap tangan, dan kain bersih

direndam dengan sabun dan air.

• Anda mungkin ingin menempatkan pad pelindung bersih di bawah dasar

anak untuk menyimpan kekacauan untuk minimum

• Sarung tangan tidak diperlukan. Namun, jika baby sitter atau teman

melakukan kateterisasi, mereka mungkin ingin melindungi diri mereka

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sendiri dengan menggunakan tidak steril, sarung tangan lateks non

• Bersihkan penis dan perineum dengan sabun ringan dan air. Untuk anak

laki-laki disunat menarik kembali kulup dan membersihkan kepala penis

Untuk anak perempuan, menyebarkan labia dan depan bersih ke belakang.

• Setelah pelumasan, memegang kateter dekat ujung dan masukkan ke

dalam uretra sampai kencing mengalir

• Jangan menggunakan kekerasan. Jika resistensi sedikit dirasakan, mungkin

membantu untuk memutar kateter

• Tempatkan ujung kateter dalam wadah pengumpulan atau toilet dan tahan

kateter di tempat sampai kencing berhenti mengalir

• Tarik kateter dengan lembut dan perlahan. Ada sering tambahan

menyembur air seni.

• Pastikan anak Anda kering dan nyaman

• Bersihkan peralatan kateter dan simpan dalam wadah yang bersih

• Ukur urin, membuangnya, dan bilas wadah

• Cuci tangan yang bersih

• Catat prosedur

Lepaskan Berdiamnya Kateter uretra

Instrumen, posisi pasien dan operator sama dengan ketika melakukan

kateterisasi uretra.

• menarik cairan dari balon kateter sebelum kateter bisa dilepas tanpa

resistensi

• melepaskan perban glans penis

• pada laki-laki pegang penis dan regangan

• menarik kateter uretra secara perlahan dan lembut meningkatkan itu di

sepanjang

uretra, menghindari gerakan mendadak atau kasar

• meletakkan kateter dan kantong urin dalam wadah

• disinfeksi lubang uretra

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1. TRAUMA GINJAL

a. Pengertian

Trauma ginjal adalah kecederaan yang paling sering pada sistem urinari. Walaupun

ginjal mendapat proteksi dari otot lumbal, thoraks, badan vertebra dan viscera, ginjal

mempunyai mobilitas yang besar yang bisa mengakibatkan kerusakan parenchymal dan

kecederaan vaskular dengan mudah.

b. Etiologi :

- Trauma tumpul langsung pada abdomen atau punggung

- Kecelakaan kendaraan bermotor, jatuh dengan posisi duduk, contact sport

- Kecelakaan kendaraan dengan kecepatan tinggi, yaitu trauma karena adanya deselerasi

atau pemberhentian secara mendadak dan trauma karena cedera vaskuler besar

- Luka tusuk atau tembak

c. Manifestasi klinik :

- Nyeri tekan pada daerah abdomen maupun dorsal

- Trauma

- Hematuria atau ada kandungan darah dalam urin, baik secara makro maupun

mikroskopis

- Hemorrhagic shock seperti oligoria dan anuria

- Memar

- Nausea, vomiting

d. Klasifikasi trauma :

- Trauma minor

Terdapat kontusio atau memar pada parenkim ginjal dan laserasi pada korteks

superficial

- Trauma mayor

Terjadi laserasi dalam di kortikomeduller

- Trauma vascular

Sangat jarang terjadi dan biasanya akibat trauma tumpul

Grading trauma ginjal :

- Derajat 1 : kontusio ginjal atau hematom subkapsuler tanpa laserasi parenkim

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- Derajat 2 : hematom perirenal atau laserasi korteks < 1 cm tanpa ekstravasasi urin

- Derajat 3 : laserasi korteks > 1 cm tanpa ekstravasasi urin

- Derajat 4 : laserasi korteks meluas sampai collecting system

- Derajat 5 : shattered kidney, avulsi pedikel ginjal atau trombosis arteri utama

2. TRAUMA VESIKA URINARIA

a. Pengertian

Trauma benturan pada panggul yang menyebabkan patah tulang (fraktur)

seringkali terjadi pada kecelakaan sepeda motor dan bisa menyebabkan robekan pada

kandung kemih.  Luka tembus, biasanya akibat tembakan, juga bisa mencederai kandung

kemih.

b. Gejalanya adalah :

- Terdapat darah di dalam urine

- Mengalami kesulitan dalam berkemih

- Rasa sakit di area panggul dan perut bagian bawah

- Sering buang air kecil atau sukar menahan keinginan berkemih (ini terjadi jika bagian

terbawah kandung kemih mengalami cedera)

c. Dampak :

Beberapa trauma dapat menyebabkan :

- Nyeri tumpul

- Pembengkakan

- Memar

- Jika cukup berat dapat menurunkan tekanan darah (syok)

Jika tidak segera diobati akan terjadi komplikasi seperti :

- Sering buang air kecil

- Kesulitan menahan keinginan berkemih

- Kemungkinan terjadi infeksi

d. Pengobatan :

- Luka kandung kemih ringan, berupa memar atau luka goresan. Luka ini dapat diobati

dengan cara memasukkan pipa ke dalam uretra selama 5 sampai 10 hari hingga

kandung kemih sembuh.  

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- Luka kandung kemih yang lebih ekstensif atau yang menyebabkan kebocoran air seni

ke dalam rongga abdominal. Untuk mengatasi luka ini sebaiknya dilakukan dengan

langkah pembedahan guna mengetahui banyak sedikitnya luka. Air seni kemudian bisa

lebih efektif dialirkan dari kandung kemih yang memakai dua pipa. Satu pipa akan

dimasukkan lewat uretra (transurethral pipa) dan satu dimasukkan secara langsung ke

dalam kandung kemih lewat kulit di balik perut bagian bawah (suprapubic pipa). Pipa

ini akan dilepas sekitar 7 sampai 10 hari atau jika kondisi kandung kemih benar-benar

telah sembuh.  

- Luka kandung kemih yang terjadi akibat prosedur operasi dapat langsung diobati pada

saat itu juga.

3. KEGAWATDARURATAN UROLOGI

.a.Pengertian

Kegawatdaruratan urologi merupakan kegawatan di bidang urologi yang bisa

disebabkan oleh karena trauma maupun bukan trauma. Pada trauma urogenitalia,

biasanya dokter cepat memberikan pertolongan dan jika fasilitas yang tersedia tidak

memadai, biasanya langsung merujuk ke tempat yang lebih lengkap. Berbeda halnya

dengan kedaruratan urogenitalia non trauma, yang sering kali tidak terdiagnosis dengan

benar, menyebabkan kesalahan penanganan maupun keterlambatan dalam melakukan

rujukan ke tempat yang lebih lengkap, sehingga menyebabkan terjadinya kerusakan

organ dan bahkan ancaman terhadap jiwa pasien.

.b.Beberapa kedaruratan urologi non trauma tersebut diantaranya adalah:

Urosepsis

Urosepsis adalah infeksi sistemik yang berasal dari fokus infeksi di traktus

urinarius sehingga menyebabkan bakteremia dan syok septik.Insiden urosepsis 20-30

% dari seluruh kejadian septikemia dan lebih sering berasal dari komplikasi infeksi

di traktus urinarius. Pasien yang beresiko tinggi urosepsis adalah pasien berusia

lanjut, diabetes dan immunosupresif seperti penerima transplantasi, pasien dengan

AIDS, pasien yang menerima obat-obatan antikanker dan imunosupresan.

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Karena merupakan penyebaran infeksi, maka kuman penyebabnya sama

dengan kuman penyebab infeksi primer di traktus urinarius yaitu golongan kuman

coliform gram negatif seperti Eschericia coli (50%), Proteus spp (15%), Klebsiella

dan Enterobacter (15%), dan Pseudomonas aeruginosa (5%). Bakteri gram positif

juga terlibat tetapi frekuensinya lebih kecil yaitu sekitar 15%. 

Patogenesa dari gejala klinis urosepsis adalah akibat dari masuknya

endotoksin, suatu komponen lipopolisakarida dari dinding sel bakteri yang masuk ke

dalam sirkulasi darah. Lipopolisakarida ini terdiri dari komponen lipid yang akan

menyebabkan:

a. Aktivasi sel-sel makrofag atau monosit sehingga menghasilkan beberapa

sitokin, antara lain tumor necrosis factor alfa (TNF α) dan interlaukin I (IL I).

Sitokin inilah yang memacu reaksi berantai yang akhirnya dapat menimbulkan

sepsis dan jika tidak segera dikendalikan akan mengarah pada sepsis berat, syok

sepsis, dan akhirnya mengakibatkan disfungsi multiorgan atau multi organs

dysfunction syndrome (MODS).

b. Rangsangan terhadap sistem komplemen C3a dan C5a menyebabkan terjadinya

agregasi trombosit dan produksi radikal bebas, serta mengaktifkan faktor-faktor

koagulasi.

c. Perubahan dalam metabolisme karbohidrat, lemak, protein, dan oksigen. Karena

terdapatnya resistensi sel terhadap insulin maka glukosa dalam darah tidak

dapat masuk ke dalam jaringan sehingga untuk memenuhi kebutuhan sel akan

glukosa terjadi proses glukoneogenesis yang bahannya berasal dari asam lemak

dan asam amino yang dihasilkan dari katabolisme lemak berupa lipolisis dan

katabolisme protein.

Hematuria

Hematuria berarti didapatkannya sel darah merah pada urine, pada umumnya

dikategorikan baik gross maupun mikroskopik. Untuk mikroskopik hematuria

dikatakan apabila didapatkan >3 s/d 5 sel darah merah/lapang pandang.

Gross hematuria jika didapatkan darah atau bekuan darah berwarna merah

atau kecoklatan yang dapat berasal dari perdarahan di ureter/ginjal, buli-buli dan

prostat.

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Beberapa jenis hematuria berdasarkan penyebab yaitu:

- Inisial hematuria: penyebabnya ada pada proksimal urethra atau di leher/dasar buli-

buli.

- Total hematuria: penyebabnya ada di buli-buli, ureter atau ginjal.

- Idiopatic hematuria adalah hematuria dimana penyebabnya tidak dapat ditentukan.

- False/pseudohematuria: adalah diskolorasi dari urine karena pigmen dari pewarna

makanan dan myoglobin.

- Hematuria dapat disebabkan oleh faktor renal (infeksi, kongenital anomali, tumor,

trauma, batu), buli (infeksi, batu, tumor, trauma), urethra (penyakit menular seksual,

trauma, benda asing, instrumentasi), prostat (infeksi, BPH, kanker prostat),

atau bleeding disorder. Adapun sebanyak ± 20 % dari penderita tidak diketahui

penyebabnya meskipun telah dilakukan pemeriksaan urologi lebih lanjut. 

Torsio testis

Torsio testis terjadi karena testis terputar di dalam skrotum sehingga terjadi

obstruksi aliran darah arteri dan vena testis. Angka kejadiannya 1 diantara 4000 pria

yang berumur kurang dari 25 tahun dan paling banyak diderita oleh anak pada masa

pubertas (12-20 tahun). Ada 2 puncak insiden torsio testis, yaitu tahun pertama dan

pubertas. Insiden torsio testis pada 24 jam pertama kelahiran cukup tinggi dan

mungkin sebagian besar darinya terjadi intrauterin sehingga pada saat lahir penderita

ini mempunyai massa intraskrotal padat, dan akhirnya kehilangan testis karena

orchidektomi atau atropi. Pada masa pubertas resiko meningkat karena mereka

mempunyai deformitas yang disebut dengan “bell-clapper”. Bentuk deformitas ini

berupa perlekatan testis pada tunica vaginalis yang tidak kuat sehingga testis

menggantung bebas dalam skrotum. Perlekatan yang tidak kuat ini menyebabkan

testis mudah bergerak dan terputar.

Secara fisiologis otot kremaster berfungsi untuk menggerakkan testis

mendekati dan menjauhi rongga abdomen untuk mempertahankan suhu ideal untuk

testis. Adanya kelainan sistem penyangga testis menyebabkan testis dapat

mengalami torsio jika bergerak secara berlebihan. Beberapa keadaaan yang

menyebabkan pergerakan berlebihan dari testis yaitu adalah perubahan suhu yang

mendadak (saat berenang), ketakutan, latihan yang berlebihan, batuk, celana yang

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terlalu ketat, defekasi, atau trauma yang mengenai skrotum. Terputarnya funikulus

spermatikus menyebabkan obstruksi aliran darah testis sehingga testis mengalami

hipoksia, edema testis, dan iskemia. Pada akhirnya testis akan mengalami nekrosis.

4. BATU GINJAL

a. Pengertian

Batu ginjal adalah suatu keadaan terdapat satu atau lebih batu di dalam pelvis atau calyces

dari ginjal atau di dalam saluran ureter. Pembentukan batu ginjal dapat terjadi di bagian

mana saja dari saluran kencing, tetapi biasanya terbentuk pada dua bagian terbanyak pada

ginjal, yaitu di pasu ginjal (renal pelvis) dan calix renalis. Batu dapat terbentuk dari

kalsium, fosfat, atau kombinasi asam urat yang biasanya larut di dalam urine.

b. Penyebab

Penyebab batu ginjal adalah bila urine menjadi terlalu pekat dan zat-zat yang ada di dalam

urine membentuk kristal batu. Penyebab lain adalah infeksi, adanya obstruksi, kelebihan

sekresi hormon paratiroid, asidosis pada tubulus ginjal, peningkatan kadar asam urat

(biasanya bersamaan dengan radang persendian), kerusakan metabolisme dari beberapa

jenis bahan di dalam tubuh, terlalu banyak mempergunakan vitamin D atau terlalu banyak

memakan kalsium.

c. Tanda-tanda

Biasanya tidak ditemukan kelainan, kadang-kadang dapat ditemukan adanya nyeri tekan,

nyeri ketok pada sudut CVA, bila terjadi hidronefrosis dapat teraba adanya masa.

d. Pathway

Penurunan intake cairan statis urin

Infeksi saluran kemih renal / ginjal

Konsentrasi larutan urin menurun

Konsentrasi mineral di matriks seputar

Obstrukksi saluran kemih parsial

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Batu ginjal

5. BATU URETER

Rasa sakit yang mendadak disebabkan oleh batu yang lewat, rasa sakit berupa pegal disudut

CVA (distensi parenkim dan kapsul ginjal) atau kolik (hiperkristaltik otot polos ), kolik ini

menjalar ke perut bagian bawah sesuai dengan lokasi batu dalam ureter.

Pada pria, rasa sakit sampai ke testis (batu ureter proksimal), pada wanita rasa sakit terasa

sampai ke vulva dan pada pria rasa sakit pada skrotum (batu ureter distal).

TANDA-TANDA

Pada saat akut penderita tampak gelisah, kulit basah dan dingin kadang-kadang terdapat

tanda-tanda syok ringan

Nyeri tekan nyeri ketok pada sudut CVA, spasme otot-otot abdomen, testis hipersensitif

(batu ureter proksimal), srotum hipersensitif (batu ureter distal)

Pada batu ureter yang sudah lama menetap hanya ditemukan nyeri tekan dan nyeri ketok

pada sudut CVA atau tidak ditemukan kelaianan sama sekali

6. BATU URETRA

GEJALA

Kencing lancar tiba-tiba berhenti disertai rasa sakit yang hebat (glans penis, batang penis,

erineum dan rektum) terjadi retensi urin (total atau parsial)

LABORATORIUM

a. Urin

- PH kurang dari 7,6 biasanya ditemukan kuman urea splitting organism dapat tebentuk

batu magnesium ammonium prostat

- PH yang rendah menyebabkan pengendapan batu asam urat (organik)

- Sidimen, sel darah merah meningkat (90%) ditemukan pada penderita dengan batu, bila

terjadi infeksi maka sel darah putih akan meningkat

- CCT untuk melihat fungsi ginjal

- Eksresi Ca, fosfor, asam urat dalam urin 24 jam untuk melihat apakah terjadi

hiperekskresi

b. Darah

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Hemoglobin; akan terjadi anemia pada gangguan fungsi ginjal kronis

Lekositosis, terjadi kerena infeksi

Ureum kreatinin untuk melihat fungsi ginjal

7. VESIKOLITHIASIS

b. Pengertian

Vesikolitiasis merupakan batu yang menghalangi aliran air kemih akibat penutupan

leher kandung kemih, maka aliran yang mula-mula lancar secara tiba-tiba akan berhenti

dan menetes disertai dengan rasa nyeri ( Sjamsuhidajat dan Wim de Jong, 1998:1027).

Vesikolitiasis adalah batu kandung kemih yang merupakan keadaan tidak normal di

kandung kemih, batu ini mengandung komponen kristal dan matriks organik (Sjabani

dalam Soeparman, 2001:377).

Vesikolitiasis adalah batu yang ada di vesika urinaria ketika terdapat defisiensi

substansi tertentu, seperti kalsium oksalat, kalsium fosfat, dan asam urat meningkat atau

ketika terdapat defisiensi subtansi tertentu, seperti sitrat yang secara normal mencegah

terjadinya kristalisasi dalam urin (Smeltzer, 2002:1460).

c. Penyebab / Ethiologi

Menurut Smeltzer (2002:1460) bahwa, batu kandung kemih disebabkan infeksi, statis

urin dan periode imobilitas (drainage renal yang lambat dan perubahan metabolisme

kalsium).

Penyebab lainnya antaralain :

1. Obstruksi kelenjar prostst yang membesar

2. Striktur uretra (penyempitan lumen dari uretra)

3. Neurogenik bladed (lumpuhnya kandung kemih karena lesi pada neuron yang

menginnervasi bladder)

4. Benda asing masuk kateter

5. Divertikula (urin tertampung pada suatu kantong di dinding vesikula urianaria)

6. Shistomiasis terutama oleh shistoma haemoglobin atau lesi yang mengarah

kepada keganasan.

Hal-hal yang disebutkan di atas dapat menimbulkan retensi urin, infeksi, maupun

radang. Statis, lithiasis, dan sistitis adalah peristiwa yang saling mempengaruhi. Statis

menyebabkan bakteri berkembang à sistitis; urin semakin basa à memberi suasana yang

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tepat untuk terbentuknya batu MgNH4PO4 (batu infeksi/struvit). Batu yang terbentuk bisa

tunggal ataupun banyak.

d. Proses / Patofisiologi

Kelainan bawaan atau cidera, keadan patologis yang disebabkan karena infeksi,

pembentukan batu disaluran kemih dan tumor, keadan tersebut sering menyebabkan

bendungan. Hambatan yang menyebabkan sumbatan aliran kemih baik itu yang

disebabkan karena infeksi, trauma dan tumor serta kelainan metabolisme dapat

menyebabkan penyempitan atau struktur uretra sehingga terjadi bendungan dan statis urin.

Jika sudah terjadi bendungan dan statis urin lama kelamaan kalsium akan mengendap

menjadi besar sehingga membentuk batu (Sjamsuhidajat dan Wim de Jong, 2001:997).

8. HIDROURETER

a. Pengertian

Hidroureter merupakan gangguan aliran urine karena ada penumpukan air/urine atau

gangguan obstruksi lainnya dalam ureter. Ureter yang mengalami hidroureter akan terjadi

pelebaran/dilatasi

b. Penyebab

Penyebab paling sering dari gangguan ini adalah adanya obstruksi atau sumbatan di

dalam ureter. Penyebab lain dari hidroureter antara lain :

- Penyimpangan pembuluh darah dan katub

- Tumor

- Batu

- Lesi dari medula spinalis

Obstruksi menyebabkan hipertrofi otot kandung kemih sebagai kompensasi untuk

mengatasi obstruksi. Pada hipertrofi otot defrusor ini tekanan di dalam kandung kemih

akan meningkat. Bila tekanan yang tinggi ini dibiarkan akan terjadi pelebaran ureter dan

pielum, hidroureter dan hidronefrosis sampai akhirnya hipertrofi atau atrofi ginjal yang

berarti gagal ginjal.

c. Proses / Pathofisiologi

Diawali dengan hambatan aliran urin secara anatomik ataupun fifiologik. Hambatan

ini dapat terjadi di mana saja sepanjang ginjal sampai meatus uretra. Peningkatan tekanan

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ureter menyebabkan perubahan dalam filtrasi glomerulus (GFR), fungsi tubulus, dan

aliran darah ginjal. GFR menurun dalam beberapa minggu. Fungsi tubulus juga terganggu.

Berat dan durasi kelainan ini tergantung pada berat dan durasi hambatan aliran. Hambatan

aliran yang singkat menyebabkan kelainan yang reversibel. Sedangkan sumbatan kronis

menyebabkan atrofi tubulus dan hilangnya nefron secara permanen. Peningkatan tekanan

ureter juga aliran balik pielouena dan pielolimfatik. Dalam duktus kolektivus, dilatasi

dibatasi oleh parenkim ginjal. Namun komponen di luar ginjal berdilatasi maksimal.