BUKU PEGANGAN TUTOR

Modul
NYERI SAAT BERKEMIH

Diberikan pada mahasiswa

semester IV FK UNHAS

SISTEM UROGENITALIA
FAKULTAS KEDOKTERAN
UNIVERSITAS HASANUDDIN
MAKASSAR
2006

PENDAHULUAN
Modul nyeri saat berkemih ini diberikan pada mahasiswa yang mengambil mata
kuliah sistim Urogenitalia di semester IV. TIU dan TIK pada sistim ini disajikan pada
permulaan buku modul agar dapat dimengerti secara menyeluruh tentang konsep dasar
penyakit-penyakit Sistem Urogenitalia yang memberikan gejala nyeri saat berkemih.
Mahasiswa diharapkan mampu menjelaskan semua aspek tentang system Urogenitalia
dan patomekanisme terjadinya penyakit, kelainan jaringan, dan pemeriksaan lain yang
dibutuhkan pada penyakit yang memberikan gejala nyeri saat berkamih..
Sebelum menggunakan modul ini, mahasiswa diharapkan membaca TIU dan TIK
sehingga tidak terjadi penyimpangan pada diskusi dan tujuan serta dapat dicapai
kompetensi minimal yang diharapkan. Bahan untuk diskusi dapat diperoleh dari bacaan
yang tercatum di akhir modul. Kuliah pakar akan diberikan atas permintaan mahasiswa
yang berkaitan dengan penyakit ataupun penjelasan dalam pertemuan konsultasi antara
peserta kelompok diskusi mahasiswa dengan tutor atau ahli yang bersangkutan.
Penyusun mengharapkan modul ini dapat membantu

mahasiwa

memecahkan masalah penyakit Urogenitalia yang disajikan.

Makassar, 2 Desember 2005

Penyusun

dalam

TUJUAN INSTRUKSIONAL UMUM

Setelah mempelajari modul ini mahasiswa diharapkan dapat menjelaskan tentang
penyakit-penyakit yang menyebabkan gejala nyeri saat berkamih, penyebab dan
patomekanisme, gambaran klinik, cara diagnosis, penanganan dan pencegahan penyakitpenyakit yang menyebabkan nyeri saat berkamih.
TUJUAN INSTRUKSIONAL KHUSUS
Setelah pembelajaran dengan modul ini mahasiswa diharapkan dapat:
A. Menyebut penyakit-penyakit yang menyebabkan gejala nyeri saat berkamih.
B. Menjelaskan

tentang

patomekanisme

terjadinya

penyakit-penyakit

yang

menyebabkan gejala nyeri saat berkamih

1. menguraikan struktur anatomi, histologi dan histofisologi dari sistim uropoetika
2.

menyebutkan fungsi masing-masing bagian dari

nefron, fungsi sel-sel JGA dalam renin angiotensin system,

3.

menjelaskan

faktor-faktor yang

mempengaruhi

GFR, prinsip hukum Starling pada filtrasi ginjal, dan dapat menghitung GFR,
4.

menjelaskan mekanisme dan proses reabsorbsi dan

sekresi di tubulus, mengapa ada zat yang mempunyai Tmax, peranan hormon
aldosteron dan ADH pada reabsorbsi, pengaturan reabsorbsi dan sekresi di
tubulus, counter current mechanism, proses reabsorbsi dan sekresi pada keadaan
tertentu seperti dehidrasi dan overhidrasi

5. menjelaskan biokimia urine dan kompensasi ginjal dalam keseimbangan asam

basa
6. menjelaskan tentang penyebab penyakit-penyakit yang menyebabkan gejala nyeri
saat berkamih
7. menjelaskan hubungan antara penyebab, respon dan perubahan jaringan pada
patogenesis terjadinya penyakit yang menyebabkan gejala nyeri saat berkamih
C. menjelaskan tentang gejala-gejala klinik penyakit-penyakit: GNA, BSK, Nefropathy,
dan penyakit non-uropoetik msialnya alergi dan kelainan ginjal akibat rehidrasi.
D. menjelaskan tentang cara-cara diagnosis GNA, BSK, Nefropathy, dan penyakit nonuropoetik msialnya alergi dan kelainan ginjal akibat rehidrasi.

menjelaskan tentang cara anamnesis terarah pada penderita penyakit-penyakit di

atas

1. menjelaskan tentang cara pemeriksaan fisik penderita penyakit-penyakit di atas ,

menggambarkan perubahan histopatologi

menjelaskan fase pre-analitik, analitik & Post analitik dari prosedur tes/Lab pada

penyakit-penyakit di atas

penyakit-penyakit di atas

menganalisa hasil laboratorium pada penderita penyakit-penyakit di atas .

menjelaskan gambaran Rontgen dari saluran kemih yang normal,

dan pada

penyakit di atas.
E. menjelaskan tentang penatalaksanaan pada penderita penyakit-penyakit di atas

menyebutkan obat-obatan yang dipakai pada penderita dengan gejala nyeri saat
berkamih,

menjelaskan farmakodinamik dan farmakokinetik obat-obat yang digunakan

dalam terapi penyakit yang menyebabkan gejala nyeri saat berkamih

menjelaskan asuhan nitrizi pada penyakit-penyakit yang menyebabkan gejala

nyeri saat berkamih

F. Menjelaskan tentang aspek epidemiologi penyakit-penyakit yang tersebut di atas

PROBLEM TREE
Anamnesis :
Disuria, pollakisuria
Demam +/-, ada darah
diakhir miksi

Anatomi
Histologi
Fisiologi
Biokimia
Patologi Anatomi
Farmakologi
Mikrobiologi

Diagnosis Banding
BSK
Nefropathy
Tumor UG

NYERI SAAT
BERKEMIH

Pengendalian

Preventif

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

Fisik Diagnostik :
Suhu tubuh subfebril
Tampak nyeri

Penatalaksanaan

Promotif

Medikamentosa

Non Bedah

Bedah

Non Medikamentosa
Nutrisi

Skenario 1. Nyeri saat berkemih

Seorang wanita, 25 thn datang ke RS dengan keluhan nyeri saat berkemih dan
frekeunsi berkemih yang meningkat. Keluhan ini telah dirasakan 3 hari
belakangan ini. Pada akhir kencing, urine bercampur darah

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

PROSES PEMECAHAN MASALAH

Dalam diskusi kelompok dengan menggunakan metode curah pendapat, mahasiswa

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

ditemukan.

Langkah 7 dilakukan dalm kelompok diskusi dengan tutor.

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

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

Memilih ketua dan sekretaris kelompok,

Brain-storming untuk proses 1 3,

Membagi tugas

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

II

Pertemuan I
(Penjelasan)

Pertemuan
Mandiri
(Brain
Stroming)

PERTEMUAN
III
IV
Tutorial I
Pengumpulan
informasi
Analisa &
sintese

Mandiri
Praktikum
CSL

VI

VII

Kuliah
kosultasi

Tutorial II
(Laporan &
Diskusi)

Pertemuan
Terakhir
(Laporan)

STRATEGI PEMBELAJARAN

1. Diskusi kelompok difasilitasi oleh tutor

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

BAHAN BACAAN & SUMBER INFORMASI LAIN

A. Buku Ajar dan Jurnal

1
2

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

Davitson VL and Sittman DB : Biochemistry

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

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

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

19
20
21
22
23
24
25
26
27

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

B. Diktat dan hand-out

1.
2.
3.
4.

Diktat Anatomi
Diktat Histologi
Buku Ajar Fisiologi Ginjal
Diktat Kuliah Radiologi

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

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

NAMA DOSEN

1.

Prof.Dr. dr. Syarifuddin Rauf

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

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

BAGIAN

TLP.
KANTOR

HP/FLEXI

Anak

0811411109

Penyakit Dalam

0816250620

Bedah Urologi

08164384040

Kulit Kelamin

08194229858

Fisiologi
Anatomi
Histologi
Biokimia
Patologi

584730

081342695348
081342436444
0811411723
0816255306

10.
11.
12.

Dr. dr. Nurpudji Astuti,

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

13.
14.
15.
16.

Dr. Nurlaily Idris, Sp.R

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

Anatomi
Gizi
Farmakologi
Patologi
Anatomi
Radiologi
Patologi Klinik
Mikrobiologi
Kulit Kelamin

0811443856
081524120368
0811441064
0811444326
08124217393

PETUNJUK UNTUK TUTOR

Apa yang dimaksud dan mekanisme kata kunci berikut ini :

o Nyeri saat berkemih (dysuria) : Rasa nyeri saat mulai dan selama
berkemih
o Frekuensi berkemih meningkat (Pollakisuria) : Frekuensi berkemih
meningkat dibanding biasanya
o Darah pada akhir kencing : tampak ada darah (gross hematuria) pada akhir
kencing
o Dirasakan 3 hari yang lalu : dirasakan baru 3 hari yang merupakan proses
akut
o Wanita : resiko ISK pada wanita > pria
o Usia 25 tahun : usia puncak 18-30 tahun untuk ISK dimana merupakan
usia perkawinan dan kehamilan.

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

kunci tersebut
1. Dysuria : dihubungkan dengan inflamasi pada vesica urinaria
1. Pollakisuria : dihubungkan dengan inflamasi pada vesica urinaria
2. Hematuria : dihubungkan dengan inflamasi pada vesica urinaria

Sebutkan beberapa penyakit yang dapat di differential diagnosis

dengan tanda dan gejala pada skenario
Bladder Stones
Bladder Trauma
Cystitis, Nonbacterial
Gastroenteritis, Bacterial
Glomerulonephritis, Acute
Gonococcal Infections
Herpes Simplex
Interstitial Cystitis
Nephrolithiasis
Pancreatitis, Acute
Pyelonephritis, Acute
Trichomoniasis

Urethritis
Vaginitis

Pemeriksaan penunjang yang dibutuhkan untuk menegakkan diagnosis penyakit

yang termasuk dalam DD penyakit tersebut
o Urinalysis
o Kultur urine
o Radiologi : USG, CT Scan

Bagaimana cara penatalaksanaan dari penyakit-penyakit yang termasuk dalam

DD penyakit tersebut
1. Medikamentosa
2. Bedah / ESWL: bila disertai batu
3. Diet

Epidemiologi dan cara pencegahan penyakit tersebut

1. Prevalensi lebih banyak pada wanita dibanding pria, di USA 25-40% pada
wanita uisa 20-40 thn
2. Mortalitas pada wanita dengan ISK 37% sedang wanita tanpa ISK 28%
(kohort data dari Swedia)
3. 25% mengalami rekurrent, sehingga pemberian regiment antibiotik perlu
diperhatikan, mengganti kontrasepsi, pada menopouse dengan pemberian
HRT,

Komplikasi penyakit-penyakit yang termasuk DD pada skenario

1. Bakterimia
2. Sepsis
3. Shock
4. Kematian

Prognosis penyakit-penyakit tersebut

1. Prognosis baik, tetapi angka rekurrent mencapai 25%
2. Bila terjadi Pyelonefritis prognosis memburuk

Urinary Tract Infection, Females

Background: UTIs may be referred to as cystitis or pyelonephritis, terms that refer to the lower
and upper urinary tract, respectively. The terms bacteriuria and candiduria describe bacteria or
yeast in the urine. Very ill patients may be referred to as having urosepsis.
The following terms are defined for uniformity in this article:
Asymptomatic bacteriuria (ASB) refers to 2 consecutive urine cultures growing more than 100,000
colony-forming units (CFU) of a bacterial species in a patient lacking symptoms of a UTI.
Uropathogens are specific bacteria that have been clinically associated with invasion of the
urinary tract.
Complicated UTIs are defined as UTIs that are associated with metabolic disorders, that occur at
sites other than the urinary bladder, or that are secondary to anatomic or functional abnormalities
that impair urinary tract drainage. Most complicated UTIs are nosocomial in origin. The most
common pathogens include Escherichia coli, enterococci, Pseudomonas aeruginosa, candidal
species, and Klebsiella pneumoniae. Complicated UTIs may be subdivided into the following 4
categories:
1. Structural abnormalities - Calculi, infected cysts, renal/bladder abscesses, certain forms
of pyelonephritis, spinal cord injury (SCI), catheters
2. Metabolic/hormonal abnormalities - Diabetes, pregnancy
3. Impaired host responses - Transplant recipients, patients with AIDS
4. Unusual pathogens - Yeast, etc
Pathophysiology: In general, 3 main mechanisms are responsible for UTIs, including (1)
colonization with ascending spread, (2) hematogenous spread, and (3) periurogenital spread of
infection. Specific organism characteristics, defects in host defenses, and pathophysiologic
details concerning particular UTIs now will be discussed.
Bacterial virulence
Uropathogenic bacteria, derived from a subset of fecal flora, have traits that enable adherence,
growth, and resistance of host defenses, resulting in colonization and infection of the urinary tract.
Adhesins are bacterial surface structures that enable attachment to host membranes. In E coli
infection, these include both pili (ie, fimbriae) and outer membrane proteins (eg, Dr
hemagglutinin). P fimbriae, which attach to globoseries-type glycolipids found in the colon and
urinary epithelium, are associated with pyelonephritis, cystitis, and also are found in many E coli
strains causing urosepsis. Type 1 fimbriae bind to mannose-containing structures found in many
different cell types, including the major protein found in human urine, Tamm-Horsfall protein.
Whether this facilitates or inhibits uroepithelial colonization is the subject of some debate.
Other factors that may be important for E coli virulence in the urinary tract include capsular
polysaccharides, hemolysins, cytotoxic necrotizing factor (CNF) protein, and aerobactins. Several
Kauffman serogroups of E coli may be more likely to cause UTIs, including O1, O2, O4, O6, O16,
and O18. Another example of bacterial virulence is the swarming capability of Proteus mirabilis.
Swarming involves the expression of specific genes when these bacteria are exposed to surfaces
such as catheters. This results in the coordinated movement of large numbers of bacteria,

enabling P mirabilis to move across solid surfaces. This likely explains the association of P
mirabilis UTIs with instrumentation of the urinary tract.
Host resistance
Most uropathogens gain access to the urinary tract via an ascending route. The shorter length of
the female urethra allows uropathogens easier access to the bladder. The continuous
unidirectional flow of urine helps to minimize UTIs, and anything that interferes with this increases
the host's susceptibility to UTI. Examples of interference include volume depletion, sexual
intercourse, urinary tract obstruction, instrumentation, use of catheters not drained to gravity, and
vesicoureteral reflux.
Secretory defenses help to promote bacterial clearance and prevent adherence. Secretory
immunoglobulin A (IgA) reduces attachment and invasion of bacteria in the urinary tract. Women
who are nonsecretors of the ABH blood antigens appear to be at higher risk of recurrent UTIs; this
may occur because of a lack of specific glycosyltransferases that modify epithelial surface
glycolipids, allowing E coli to bind to them better.
Urine itself has several antibacterial features that suppress UTIs. Specifically, the pH, urea
concentration, osmolarity, and various organic acids prevent most bacteria from surviving in the
urinary tract.
Pathophysiologic details of complicated urinary tract infections
Pyelonephritis almost always is the result of bacteria migrating from the bladder to the renal
parenchyma, which is enhanced by vesicourethral reflux. In uncomplicated pyelonephritis, the
bacterial invasion and renal damage are limited to the pyelocalyceal-medullary region; in
complicated pyelonephritis, all regions of the kidney may be affected. If the infection progresses,
bacteria may invade the bloodstream, resulting in bacteremia.
Complicated pyelonephritis results from structural and functional abnormalities, urologic
manipulations, or underlying disease. Complicated pyelonephritis includes pyelonephritis in men
and pyelonephritis elderly people. Patients with diabetes may develop emphysematous or
xanthogranulomatous pyelonephritis and necrotizing papillitis.
Subclinical pyelonephritis should be considered in indigent people; pregnant women; people with
diabetes; people with alcoholism; and patients with a history of pyelonephritis, renal transplant,
UTI before age 12 years, and more than 3 UTIs in the past year.
Calculi related to UTIs most commonly occur in women with recurrent UTIs from Proteus,
Pseudomonas, and Providencia species (see Image 1); bacterial biofilms serve to assist struvite
growth. Because magnesium ammonium phosphate is acid soluble, stone formation does not
tend to occur with a urinary pH lower than 7.19. Increases in ammonia raise the pH and injure the
uroepithelial glycosaminoglycan layer, contributing to bacterial adherence. Alkalinity also
increases the amount of phosphate and carbonate available to bind calcium and magnesium.
Renal corticomedullary abscesses usually are associated with vesicoureteral reflux or urinary
tract obstruction, and the usual organisms include E coli, Klebsiella species, and Proteus species.
Clinical syndromes include acute focal bacterial nephritis, acute multifocal bacterial nephritis,
emphysematous pyelonephritis, and xanthogranulomatous pyelonephritis.
Acute focal bacterial nephritis is also known as acute lobar nephronia or focal pyelonephritis. This
is an acute bacterial interstitial nephritis affecting a single renal lobe. Acute multifocal bacterial

nephritis affects more than 1 lobe (see Image 2). Emphysematous pyelonephritis is a severe,
necrotizing form of acute multifocal bacterial nephritis. Retroperitoneal (ie, extraluminal) gas may
be observed in the renal parenchyma and perirenal space on radiographs. This is observed most
commonly in people with diabetes, but it also may be observed in patients with
immunocompromise or obstruction.
Xanthogranulomatous pyelonephritis is a severe chronic infection of the renal parenchyma. The
kidney is enlarged and is fixed to the retroperitoneum by either perirenal fibrosis or an extension
of the granulomatous process. The inciting event appears to be renal obstruction and chronic UTI.
Predisposing factors include renal calculi, lymphatic obstruction, renal ischemia, dyslipidemia,
diabetes, and primary hyperparathyroidism.
A perinephric abscess is defined as a collection of purulent material between the renal capsule
and Gerota fascia. A perinephric abscess may develop secondary to an intrarenal abscess, a
renal cortical abscess, xanthogranulomatous pyelonephritis, chronic or recurrent pyelonephritis,
or from hematogenous dissemination. Predisposing factors are similar to those for intrarenal
abscess. Approximately 25% of patients have diabetes.
Over time, patients with diabetes may develop cystopathy, nephropathy, and renal papillary
necrosis, complications that predispose them to UTIs. Long-term effects of diabetic cystopathy
include vesicourethral reflux and recurrent UTIs; as many as 30% of women with diabetes have
some degree of cystocele, cystourethrocele, or rectocele.
Vaginal candidiasis and vascular disease also play a role in recurrent infections. Hyperglycemia
causes neutrophil dysfunction by increasing intracellular calcium levels, interfering with actin and,
thus, diapedesis and phagocytosis.
Renal cortical abscesses (ie, renal carbuncles) usually result from hematogenous spread of
bacteria. Primary sources of infection include skin infections, osteomyelitis, and endovascular
infections. These are observed commonly in users of injection drug, people with diabetes, and
patients on dialysis. The most common organism isolated is Staphylococcus aureus. Ten percent
of cortical abscesses may rupture through the renal capsule and form a perinephric abscess.
Autosomal dominant polycystic kidney disease can lead to end-stage renal disease. Cysts may
become infected from either bacteremia or from bacteriuria.
Several factors increase the risk of UTI in pregnancy. These factors include relative obstruction of
the ureters (secondary to the enlarging uterus), smooth muscle relaxation of the ureter and
bladder (secondary to progesterone), and aminoaciduria and glycosuria, which provide a
favorable environment for bacteria to grow. E coli is the most common organism isolated from
cultures, although P mirabilis and K pneumoniae also are observed. Less common agents include
group B streptococci and Staphylococcus saprophyticus. Group B streptococci are isolated in
approximately 5% of infections and have been linked to preterm labor; these patients should
receive prophylactic antibiotics during delivery to reduce the risk of neonatal sepsis.
Risk factors for candiduria include diabetes mellitus, indwelling urinary catheters, and antibiotic
use. Candiduria may clear spontaneously or may result in (or from) deep fungal infections. The
presence of Candida species in the urine usually represents colonization and not infection, and,
as such, not all patients with candiduria require treatment. A lower threshold for initiating
treatment exists for patients with diabetes, history of renal transplantation, or genitourinary
abnormalities.

Frequency:

In the US: UTIs in women are very common; approximately 25-40% of women in the
United States aged 20-40 years have had a UTI. In 1998, approximately 3.2% of
emergency department visits were related to symptoms involving the genitourinary tract.
Estimates based on office and emergency department visits suggest per annum about 7
million episodes of acute cystitis and 250,000 episodes of acute pyelonephritis. Ten to
15% of nephrolithiasis episodes are secondary to organisms associated with stone
production. The incidence of renal and perirenal abscesses is 1-10 cases per 10,000
population. Some estimate that UTIs cost at least 1 billion dollars per year.
Patients with spinal cord injuries are at an increased risk for UTIs; lower rates occur in
those with incomplete injuries. In patients practicing clean intermittent catheterization, the
mean incidence of UTIs is 10.3 per1000 catheter days; after 3 months, the rate is fewer
than 2 per 1000 catheter days. Once a urethral catheter is in place, the daily incidence of
bacteriuria is 3-10%. Because the majority will become bacteriuric by 30 days, that is a
convenient dividing line between short- and long-term catheterization.

Internationally: UTIs have been well studied in Sweden and other parts of Europe, and
these data are referred to frequently in this article.
Data from the tropics are less well documented. UTIs appear to be common and
associated with structural abnormalities. Chronic infection from Schistosoma
haematobium disrupts bladder mucosal integrity and causes urinary obstruction and
stasis. Salmonella bacteriuria, with or without bacteremia, is very common in patients with
schistosomiasis. Treatment requires both antischistosomal and anti-Salmonella agents.
Tuberculosis (TB) of the kidney results from hematogenous spread but is relatively rare in
developing countries. Unlike most other extrapulmonary manifestations of the disease,
TB of the kidney does not become manifest until 5-15 years after the primary infection.
Constitutional symptoms are uncommon, and most patients present with symptoms of
bladder irritation. Initially, pyuria is observed, and, with progression of the disease,
proteinuria and blood may be observed as well. Repeated urine samples should be sent
for mycobacterial culture. A loss of calyceal architecture and ureteric obstruction may be
observed on imaging studies. Concurrent pulmonary disease is present in 5% of patients,
and the tuberculin test rarely is helpful. Antituberculous medicines should be administered
for 6 months. If the ureter is obstructed, corticosteroids have been advocated; if
obstruction persists, surgical intervention is necessary.

Mortality/Morbidity:

The mortality associated with acute uncomplicated cystitis among women aged 20-60
years appears to be negligible. A longitudinal cohort study of Swedish women showed a
higher mortality among women with a history of UTI compared with age-matched women
without this history (37% versus 28% in 10 y, P<0.001). These cohorts were not matched
for other mortality-related factors, making it difficult to attribute the increased mortality to
UTIs.

In contrast, the morbidity in terms of quality of life and economic measures is

tremendous. Each episode of UTI in a young woman results in an average of 6.1 days of
symptoms, 1.2 days of decreased class/work attendance, and 0.4 days in bed.

Groups at risk for UTIs associated with calculi include those with dysfunctional voiding,
urinary intestinal diversion, indwelling urinary catheters, and vesicoureteral reflux.

Race: No racial predilection exists.

Sex: Uncomplicated UTIs are much more common among women than men when matched for
age. A study of Norwegian men aged 21-50 years showed an approximate incidence of 0.00060.0008 infections per person-year, compared with approximately 0.5-0.7 per person-year in
similarly aged women in the United States.

Renal carbuncles are more common in men than women by a ratio of 3:1 and are most
common in the second to fourth decades of life. The right kidney is involved most
commonly (63%).

Renal corticomedullary abscesses affect men and women equally; xanthogranulomatous

pyelonephritis affects more women than men.

Age: The incidence of UTI in women tends to increase with increasing age. Several peaks above
baseline correspond with specific events, including an increase among women aged 18-30 years
(associated with honeymoon cystitis and pregnancy). Older adults have is a higher incidence of
renal corticomedullary abscesses. This article does not discuss UTIs in children.

CLINICAL
History:

Acute urethritis
o

This topic is addressed in greater detail in Urethritis. The symptoms of acute

urethritis overlap with those of cystitis, including acute dysuria and urinary
hesitancy.

Urethral discharge is much more suggestive of urethritis, while bladder-related

symptoms, such as urgency, polyuria, and incomplete voids, are more consistent
with cystitis.

Fever may be a component of urethritis-related syndromes (eg, Reiter syndrome,

Behet syndrome) but rarely is observed in acute cystitis.

Acute cystitis
o

The symptoms of dysuria, urgency, hesitancy, polyuria, and incomplete voids also
may be accompanied by urinary incontinence, gross hematuria, and suprapubic
or low back pain.

The predominant complaints relate to the inflamed bladder mucosa.

Constitutional symptoms, such as fever, nausea, and anorexia, are rare or mild.

Acute pyelonephritis

Unlike urethritis and cystitis, pyelonephritis may present with a paucity of lower
urinary tract symptoms.

The classic triad of fever, costovertebral angle pain, and nausea and/or vomiting
may be present, though not necessarily occurring together temporally.

Hematuria may occur but is more suggestive of nephrolithiasis in the presence of

localizing back or flank pain.

Fever and vomiting may suggest gastroenteritis. Patients also may present with
right upper quadrant pain radiating to the back, mimicking cholecystitis or
pancreatitis.

Complicated urinary tract infections

o

UTIs associated with calculi may be insidious or asymptomatic. Patients may

present with recurrent UTIs, abdominal pain, fever, gross hematuria, urinary
fistulae, renal failure, or urosepsis.

Patients with renal corticomedullary abscesses present with chills, fever, and
flank or abdominal pain. Patients may have dysuria and/or nausea/vomiting.
Leukocytosis may be present. Bacteriuria, pyuria, hematuria, or proteinuria may
be present as the intrarenal abscesses drain in the collecting system, but the
urinalysis results may be normal in as many as 30% of patients. Bacteremia may
be observed in acute focal or multifocal bacterial nephritis.

Patients with perinephric abscesses most commonly present with chills, fever,
flank or abdominal pain, and dysuria. The physical examination is notable for
flank and costovertebral angle tenderness and possibly a palpable mass.

Renal cortical abscess patients may present with chills, fever, and flank or
abdominal pain. Patients may present with a flank mass or a bulge in the lumbar
region. Some have abnormal results on lung examination of the affected side
(dullness to percussion, rales). Blood and urine culture results usually are
negative, but the white blood cell count often is elevated.

In patients with SCI, signs and symptoms suggestive of a UTI are malodorous
and cloudy urine, muscular spasticity, fatigue, fevers, chills, and autonomic
instability. Patients with lesions above T6 may exhibit autonomic dysreflexia to
noxious stimuli (such as an overdistended bladder). The sympathetic response
below the level of injury is uninhibited, producing severe vasoconstriction and
reflexive bradycardia. If the patient is febrile, this may appear as a pulsetemperature dissociation.

Physical:

Acute cystitis
o

Abnormal physical examination findings generally are lacking in women with

acute cystitis. Patients may demonstrate some suprapubic tenderness to
palpation.

The pelvic examination reveals no abnormalities unless another process, such as

vaginitis, is mimicking or occurring simultaneously with cystitis.

Acute pyelonephritis
o

Fever in a young woman with symptoms referable to the urinary tract supports a
diagnosis of pyelonephritis. Unilateral or bilateral costovertebral angle tenderness
may be present.

A pelvic examination may reveal findings suggestive of pelvic inflammatory

disease, such as cervical motion tenderness or vaginal discharge.

The abdominal examination may reveal upper quadrant tenderness, but

peritoneal symptoms should not be present in acute uncomplicated
pyelonephritis.

Patients with perinephric abscesses most commonly present with fever, chills, and flank
tenderness; they may have a palpable mass.

Causes: E coli causes 70-95% of both upper and lower UTIs. The remainder of infections is
composed of various organisms, including S saprophyticus, Proteus species, Klebsiella species,
Enterococcus faecalis, other Enterobacteriaceae, and yeast. Some species are more common in
certain subgroups, such as S saprophyticus in young women.

Sexual intercourse contributes to increased risk, as does use of a diaphragm and/or

spermicide. Women who are elderly, pregnant, or have preexisting urinary tract structural
abnormalities or obstruction carry a higher risk of UTI.

Most complicated UTIs are nosocomial in origin. The most common pathogens include E
coli, enterococci, P aeruginosa, Candida species, and Klebsiella pneumoniae.

Calculi related to UTIs most commonly occur in women who experience recurrent UTIs
with Proteus, Pseudomonas, and Providencia species.

Perinephric abscesses are associated most commonly with E coli, Proteus species, and
S aureus but also may be secondary to Enterobacter, Citrobacter, Serratia,
Pseudomonas, and Klebsiella species. More unusual causes include enterococcus,
Candida species, anaerobes, Actinomyces species, and Mycobacterium tuberculosis.
Twenty-five percent of infections are polymicrobial.

Candiduria is defined as more than 1,000 CFU of yeast from 2 cultures. Candida
albicans, which is germ tube positive, is the usual culprit. Germ tubenegative Candida
species (tropicalis, parapsilosis, glabrata, lusitaniae, krusei) are less common.

Patients with SCI develop UTIs with microorganisms that form dense biofilms on the
bladder wall; thus, these infections are difficult to eradicate. Organisms that commonly
cause infections include Proteus, Pseudomonas, Klebsiella, Serratia, and Providencia
species, along with enterococci and staphylococci. Approximately 70% of infections are
polymicrobial.

DIFFERENETIALS

Appendicitis
Behcet Disease
Bladder Cancer
Bladder Stones
Bladder Trauma
Chlamydial Genitourinary Infections
Cholangitis
Cholecystitis
Colovesical Fistula
Common Pregnancy Complaints and Questions
Cystitis, Nonbacterial
Diverticulitis
Emphysema
Emphysematous Pyelonephritis
Enterobacter Infections
Enterococcal Infections
Escherichia Coli Infections
Gardnerella
Gastroenteritis, Bacterial
Glomerulonephritis, Acute
Gonococcal Infections
Herpes Simplex
Interstitial Cystitis
Klebsiella Infections
Mycoplasma Infections
Nephrolithiasis
Nephrolithiasis: Acute Renal Colic
Pancreatitis, Acute
Pneumonia, Bacterial
Pneumonia, Community-Acquired
Proteus Infections
Providencia Infections
Pseudomonas Aeruginosa Infections
Pyelolithotomy
Pyelonephritis, Acute
Pyelonephritis, Chronic
Pyonephrosis
Renal Cell Carcinoma
Renal Corticomedullary Abscess
Renal Transplantation (Medical)
Renal Transplantation (Urology)
Schistosomiasis
Sepsis, Bacterial
Septic Shock
Serratia
Shock and Pregnancy
Shock, Distributive
Subacute Thyroiditis
Trichomoniasis
Tuberculosis
Tuberculosis of the Genitourinary System
Ureaplasma Infection
Ureteral Injury During Gynecologic Surgery
Ureteral Stricture
Ureteral Trauma
Ureterocele

Ureterolithotomy
Ureteropelvic Junction Obstruction
Ureteroscopy
Urethral Prolapse
Urethral Syndrome
Urethritis
Urinary Diversions and Neobladders
Urinary Tract Infection, Females
Urinary Tract Infections in Pregnancy
Urinary Tract Obstruction
Urologic Imaging Without X-rays: Ultrasound, MRI, and Nuclear Medicine
Urothelial Tumors of the Renal Pelvis and Ureters
Vaginitis
Vesicoureteral Reflux
Vesicovaginal Fistula
Vesicovaginal and Ureterovaginal Fistula
Xanthogranulomatous Pyelonephritis
Other Problems to be Considered:
Consider any condition involving flank/back pain or abdominal/pelvic pain.
The differential diagnosis for infectious causes of sterile pyuria includes perinephric abscess,
urethral syndrome, renal TB, and fungal infections of the urinary tract system.
Noninfectious causes of pyuria include uric acid and hypercalcemic nephropathy, lithium and
heavy metal toxicity, sarcoidosis, interstitial cystitis, polycystic kidney disease, genitourinary
malignancy, and renal transplant rejection
Lab Studies:

In the 1980s, many experts felt that urine cultures were unnecessary in young women
with cystitis complaints because almost all of these were caused by pan-susceptible
isolates of E coli. However, since 1998, resistant isolates of E coli have emerged (in
numbers as high as 20% in some communities). Trimethoprim-sulfamethoxazole (TMPSMZ) resistance has been associated with concomitant resistance to other antibiotics.
Consider obtaining urine cultures in the new millennium.

Urine specimens may be obtained by suprapubic aspiration, catheterization, or

midstream clean catch. Bacteriuria, especially with many squamous cells without pyuria
suggests contamination or colonization; some women may need to be catheterized to
obtain a clean specimen. Although midstream urine specimens have been advocated,
one randomized trial showed that the rate of contamination was not excessive in young
women who urinated into a container without cleansing the perineum or discarding the
first urine output.

Dipstick testing should include glucose, protein, blood, nitrite, and leukocyte esterase. A
microscopic evaluation of the urine sample for white blood cell (WBC) counts, red blood
cell (RBC) counts, and cellular or hyaline casts should be performed. In the office, a
combination of clinical symptoms with dipstick and microscopic analysis showing pyuria
and/or positive nitrite/leukocyte esterase tests can be used as presumptive evidence of
UTI.

The most accurate method to measure pyuria is counting leukocytes in unspun fresh
urine using a hemocytometer chamber; greater than 10 WBC/mL is considered abnormal.
Counts determined from a wet mount of centrifuged urine are not reliable measures of
pyuria. A noncontaminated specimen is suggested by a lack of squamous epithelial cells.
Pyuria is a sensitive (80-95%) but nonspecific (50-76%) method of diagnosing UTI.

White cell casts may be observed in conditions other than infection, and they may not be
observed in all cases of pyelonephritis. If the patient has evidence of acute infection and
white cell casts are present, the infection likely represents pyelonephritis. A spun sample
(5 mL at 2000 revolutions per min [rpm] for 5 min) is best used for evaluation of cellular
casts.

Leukocyte esterase is a dipstick test that can rapidly screen for pyuria; it is 57-96%
sensitive and 94-98% specific for identifying pyuria.

Nitrite tests detect the products of nitrate reductase, an enzyme produced by many
bacterial species. These products are not present normally unless a UTI exists. This test
has a sensitivity and specificity of 22% and 94-100%, respectively. The low sensitivity has
been attributed to enzyme-deficient bacteria causing infection or low-grade bacteriuria.

Microscopic hematuria is found in about half of cystitis cases; when found without
symptoms or pyuria, it should prompt a search for malignancy. Other things to be
considered in the differential include calculi, vasculitis, renal TB, or glomerulonephritis. In
a developing country, hematuria is suggestive of schistosomiasis, which can be
associated with salmonellosis and squamous cell malignancies of the bladder. For more
information on this interesting topic, the reader is referred to the article on
Schistosomiasis.

Proteinuria commonly is observed in infections of the urinary tract, but the proteinuria
usually is low grade. More than 2 grams of protein per 24 hours suggests glomerular
disease.

Urine culture remains the criterion standard for the diagnosis of UTI. Collected urine
should be sent for culture immediately; if not, it should be refrigerated at 4C. Two culture
techniques (dip slide, agar) are widely used and accurate. The 1999 Infectious Disease
Society of America (IDSA) consensus limits for cystitis and pyelonephritis in women are
more than 1000 CFU/mL and more than 10,000 CFU/mL, respectively, for clean-catch
midstream urine specimens. Note that any amount of uropathogen grown in culture from
a suprapubic aspirate should be considered evidence of a UTI. Approximately 40% of
patients with perinephric abscesses have sterile urine cultures.

If a Gram stain of an uncentrifuged, clean-catch, midstream urine specimen reveals the

presence of 1 bacterium per oil-immersion field, it represents 10,0000 bacteria/mL of
urine. A specimen (5 mL) that has been centrifuged for 5 minutes at 2000 rpm and
examined under high power after Gram staining will identify lower numbers. In general, a
Gram stain has a sensitivity of 90% and a specificity of 88%.

Patients with spinal cord injury

o

Diagnosing a UTI in a patient with an SCI is difficult. In these patients, suprapubic

aspiration of the bladder is the criterion standard for diagnosing a UTI, although it
is not performed often in clinical practice.

All of these patients have some degree of bacteruria, but not all are actively
infected. The diagnosis of significant bacteriuria, per the 1992 consensus
statement of the National Institute on Disability and Rehabilitation Research
(NIDRR), is any detectable concentration of a uropathogen collected from a
patient with SCI and with an indwelling catheter. For patients utilizing intermittent
catheterization, the definition of significant bacteriuria is 100 CFU/mL or more.

The optimal method to diagnose pyuria in a patient with SCI has not been
determined. More than 50 WBC per high-power field (hpf) is a reasonable
indicator of high-level pyuria and has been associated with increased morbidity.

Approximately 70% of patients with corticomedullary abscesses have abnormal urinalysis

findings, whereas those with renal cortical abscesses usually have normal findings. Two
thirds of patients with perinephric abscesses have an abnormal urinalysis.

Other lab tests

o

The WBC count usually is elevated in patients with complicated UTI. The WBC
count may or may not be elevated in patients with uncomplicated UTI. Patients
with complicated UTIs may have anemia, which is observed in 40% of patients
with perinephric abscesses.

Some patients have findings of electrolyte abnormalities, and 25% of patients

with perinephric abscesses have azotemia.

Bacteremia is associated with pyelonephritis, corticomedullary abscesses, and

perinephric abscesses. Approximately 10-40% of patients with pyelonephritis or
perinephric abscesses have positive results on blood culture. Bacteremia is not
necessarily associated with a higher morbidity or mortality in women with
uncomplicated UTI.
Cervical swabs may be indicated.

Imaging Studies:

No imaging studies are indicated in the routine evaluation of cystitis or pyelonephritis.

Women with acute pyelonephritis should be considered for imaging if they continue to
have symptoms or clinical progression despite standard antimicrobial therapy for their
infection. Complicated UTIs may require imaging. Options include a simple kidneys,
ureter, and bladder (KUB) radiograph; a renal ultrasound; a CT scan; an MRI; nuclear
imaging; and angiograms. Urologic intervention may be required, including intravenous
pyelograms (IVPs) and ureterograms (ie, retrograde and percutaneous).

A renal ultrasound is a useful imaging modality in patients with complicated UTIs, and it
may be performed at the bedside in a patient who is hemodynamically unstable. It is
relatively inexpensive, does not involve radiation, and iodinated contrast is not needed. A
renal abscess may appear as a fluid-filled mass with a thick wall. Acute focal bacterial
nephritis appears as a poorly defined mass with low-amplitude echoes and disruption of
the corticomedullary junction. Xanthogranulomatous pyelonephritis images reveal stones
in approximately 70% of patients. Ultrasound findings may be falsely negative in 36% of
perinephric abscesses. A drawback to ultrasound is the difficulty in differentiating renal
abscess from tumor; it also is difficult to interpret in a patient who is obese.

Renal angiography may help differentiate renal abscess from renal tumor because an
abscess often has increased peripheral vascularization (the remainder of the mass is
avascular).

Nuclear studies
o

Gallium (Ga) scans also may be used in the workup of a complicated UTI. The
patient is injected with a transiently radioactive substance and returns 1-3 days
later. The emitted radiation provides an image, which, although it lacks precise
anatomic detail, does provide functional information. A subtraction technique
using Ga citrate and technetium (Tc) glucoheptonate needs to be performed to
differentiate intrarenal abscess from tumor, obstruction, and severe
pyelonephritis.

An indium-111labeled WBC scan can help to diagnose infection in persons with

autosomal-dominant polycystic kidney disease.

For complicated UTIs, computed tomography (CT) scans provide the best definition, and
the information is available quickly. Drawbacks to CT scans include some exposure to
irradiation and the need for iodinated contrast. Abscesses should appear as low-density
masses with contrast enhancement of the wall from inflamed/dilated blood vessels. Acute
focal bacterial nephritis has a lobar distribution of inflammation, wedge-shaped
hypodense lesions (postcontrast), and masslike hypodense lesions in severe infections.
Xanthogranulomatous pyelonephritis may appear as large renal calculi, nonfunctioning
kidneys, contrast enhancement around low attenuation areas, thickening of Gerota
fascia, and spherical areas of low attenuation.

Patients with spinal cord injuries with more than 2 symptomatic UTIs within 6 months
should be evaluated to rule out high-pressure voiding, vesicoureteral reflux, and the
presence of stones. Evaluations often include urodynamic studies, nuclear scanning,
renal ultrasound, voiding cystourethrography, abdominal CT scans, IVP, and/or
cystoscopy.

Procedures:

The consulting urologist may wish to perform an IVP, cystoscopy, or a ureterogram (either
retrograde or percutaneous)

TREATMENT
Medical Care: For adult women with acute bacterial cystitis who are otherwise healthy and not
pregnant, single-dose therapy generally is less effective than a longer duration of the same
antimicrobial agent. Most antimicrobial agents administered for 3 days are as effective as the
same drug administered for a longer duration, with exceptions being nitrofurantoin and betalactams as a group.
TMP-SMZ for 3 days is considered the current standard therapy for bacterial cystitis. TMP-SMZ
works as well as fluoroquinolones, which are more expensive. In 1999, to postpone the
emergence of quinolone resistance, IDSA guidelines for UTI did not recommend quinolones as
initial empiric therapy, except in communities with high rates (ie, over 10-20%) of uropathogen
resistance to TMP-SMZ. Quinolones should be used for patients with known TMP-SMZ allergies,
known TMP-SMZresistant pathogens, or those failing a TMP-SMZ regimen.

Drug selection could be facilitated if resistance patterns among uropathogens could be predicted
clinically. Studies have compared women with UTI caused by TMP-resistant bacteria with women
with TMP-sensitive isolates. After multivariate analysis, the strongest risk factor was current or
recent use of TMP-SMZ; current use of any antibiotic, estrogen exposure, diabetes, and recent
hospitalization also were significant. Rates of fecal colonization with TMP-SMZresistant E coli
are increased in those who have recently been to Mexico, children in daycare centers, and in
family members of those recently treated for a UTI.

Cystitis
o Cystitis in older women or infection caused by S saprophyticus is less responsive
to 3 days of therapy; therefore, 7 days of therapy is suggested.
o Bladder analgesia using phenazopyridine 200 mg tid should be considered in
women with severe dysuria. Duration of therapy should be limited to 2 or 3 days
to ensure clinical improvement of symptoms.

Pyelonephritis
o Fewer firm data are available on which to base sound treatment
recommendations for pyelonephritis. For young women who are not pregnant
with normal urinary tracts, 14 days of therapy is appropriate.
o Mild infections can be managed with oral fluoroquinolones or TMP-SMZ. Women
who should be considered for outpatient treatment include those with mild-tomoderate infection, those with easy access to follow-up appointments, and
women without significant nausea or vomiting.
o Patients presenting with acute pyelonephritis can be treated with a single dose of
a parenteral antibiotic followed by oral therapy, provided they are monitored
within the first 48 h. A study of febrile, nonpregnant women presenting with
symptoms of acute pyelonephritis found that 25% were hospitalized. These
patients tended to be older and have diabetes, higher temperatures, and
vomiting. Eighty percent of the outpatients were treated with a single parenteral
dose of ceftriaxone or gentamicin, followed by oral therapy (usually TMP-SMZ).
Twelve percent returned with persistent symptoms, most in the first day; most of
these were admitted.
o Hospitalize patients with more severe infection and treat with a parenteral
fluoroquinolone, an aminoglycoside (with or without ampicillin), or an extendedspectrum cephalosporin (with or without an aminoglycoside). Treat gram-positive
cocci with ampicillin/sulbactam (with or without an aminoglycoside).
o Patients who relapse despite adequate therapy who lack anatomic abnormalities
should be treated for 6 weeks. If a new pathogen causes infection, then another
2-week course should be effective.

Urinary tract infections associated with calculi

o For UTIs associated with calculi, treatment ranges from observation to
nephrectomy.
o The preferred method of treatment is surgical (see Surgical Care). Mere
observation is not recommended, as the mortality is 28% versus 7.2% in the
surgically treated group. Antibiotic therapy should be used in conjunction.
o Although food and vitamin supplements that are rich in phosphorus and
magnesium are advisable, remember that magnesium (and other divalent
cations) can chelate quinolones, preventing their absorption from the gut.
o Acidifying agents have been used. Ascorbic acid does not significantly decrease
urinary pH, and ammonium chloride provides only temporary acidification.
o Urease inhibitors are effective in reducing stone formation, but long-term use is
fraught with neurosensory, hematologic, and dermatologic adverse effects.

Renal carbuncles
o For renal carbuncles, surgical drainage once was the only treatment. However,
modern antibiotics alone often are curative. A semisynthetic penicillin,
cephalosporin, quinolone, or vancomycin is recommended.
o Generally, parenteral antibiotics should be administered for 10-14 days, followed
by oral therapy for 2-4 weeks. Fever should resolve within 5-6 days and pain
within 24 hours.
o If patients do not respond within 48 hours, percutaneous (or open) drainage
should be performed.

Acute, focal, and multifocal bacterial nephritis

o Acute, focal, and multifocal bacterial nephritis should respond to antibiotics within
1 week. An extended-spectrum penicillin, cephalosporin, or quinolone should be
used. A beta-lactam and an aminoglycoside also may be considered.
o Parenteral therapy should be used first, followed by at least 2 weeks of oral
therapy. Those with large abscesses (ie, >5 cm), obstructive uropathy, advanced
age, and urosepsis may not respond to antimicrobial therapy alone and require
percutaneous drainage.
o Patients with severely damaged renal parenchyma, xanthogranulomatous
pyelonephritis, or patients who are elderly and have sepsis may require
nephrectomy.

Perinephric abscesses
o Perinephric abscesses are associated with a high mortality rate (ie, 20-50%) and
require percutaneous or surgical drainage and antibiotics.
o An aminoglycoside and an antistaphylococcal penicillin should be used. An
extended-spectrum beta-lactam also may be used.
o Antibiotics should be modified based on culture results.
Spinal cord injury and urinary tract infections
o Antibiotics should be reserved for patients with clear signs and symptoms of UTI.
o Oral fluoroquinolones are the drugs of choice for empiric treatment of acute UTIs.
o Options for hospitalized patients include parenteral fluoroquinolones, ampicillin
and gentamicin, imipenem plus cilastatin, third-generation cephalosporins, betalactam/beta-lactamase inhibitor combinations, or the aminoglycosides.
o Duration of therapy generally is 7-14 days, but 4-5 days may be acceptable for
patients who are mildly symptomatic and who are closely monitored.
o If a patient fails to respond, then another culture should be obtained and an
imaging study should be considered to rule out persistent infection, stone
disease, and anatomic abnormalities causing obstruction.
o Treatment of asymptomatic patients is more controversial. While urine cultures
with low bacterial counts often become sterile without treatment, some patients
with ASB develop chronic infections secondary to bacterial biofilms. Some
suggest that first episodes of ASB should be treated if significant bacteriuria (ie,
more than 10,000 CFU/mL) is accompanied by pyuria (ie, more than 8-10
leukocytes/hpf).

Surgical Care:

Urinary tract infections associated with infected calculi

o

Treatment ranges from observation to nephrectomy. Hydronephrosis is a concern

(see Image 3).

Surgical options include extracorporeal shock wave lithotripsy (ESWL),

endoscopic methods, percutaneous methods, or open surgery.

Mere observation is not recommended; the mortality associated with observation

is 28%, versus 7.2% in the surgically treated group. Appropriate antibiotic therapy
should be used as well.

Consultations: A pharmacokinetics consultation is suggested when using aminoglycosides or

vancomycin. Urologic consultation is essential in patients with complicated UTIs. Other
consultations depend on the patient's underlying state of health and may include an obstetrician,
gynecologist, endocrinologist, nephrologist, neurologist, and neurosurgeon. Infectious disease
input is essential for unusual or resistant pathogens or hosts who are immunocompromised.
Consultation with the patient's primary care provider is suggested.
Diet:

Hydration to accentuate unidirectional clearance of bacteruria is recommended,

especially if an obstruction was relieved recently. Drinking cranberry juice (10 oz/d) may
offer some benefit and does not appear to be harmful. One recent study found less
recurrence of UTIs in women who drank 50 cc of cranberry-lingonberry concentrate daily
for 6 months. The mechanism of action of cranberry juice is not clear. It is bacteriostatic,
an effect probably due to hippuric acid. Another mechanism may involve suppression of
E coli fimbriae by proanthocyanidins (tannins). Ascorbic acid (vitamin C) does not cause
significant urinary acidification.

For complicated UTIs associated with struvite calculi, foods and vitamin supplements rich
in phosphorus and magnesium are advised.

Remember that divalent cations (eg, magnesium, iron, calcium, zinc) can chelate oral
fluoroquinolones, preventing their absorption from the gut.

MEDICATION
The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent
complications.
Drug Category: Antibiotics -- Empiric antimicrobial therapy should cover all likely pathogens in the
context of this clinical setting. The prolonged or repeated use of antibiotics may result in fungal or
bacterial overgrowth of nonsusceptible organisms, superinfections, or infections with C difficile.
Antibiotics sometimes are used in combination. Sometimes these combinations work against
each other (ie, are antagonistic); examples would include beta-lactams (such as penicillin) and
tetracyclines. Antagonism is defined as at least a 99% decrease in killing by the combination
(when compared with the most active antimicrobial alone).
Synergism is when a combination of antibiotics has a significantly greater effect than would be
expected from the sum of the separate drugs (ie, over a 99% increase in killing). Aminoglycosides
and either beta-lactams or vancomycin are considered synergistic combinations. Because no
single drug is considered bactericidal for the enterococcus, some might prefer to use synergistic
combinations when treating enterococcal UTIs.

Trimethoprim (Proloprim, Trimpex) -- Inhibits bacterial growth by inhibiting synthesis of

dihydrofolic acid. Active in vitro against a broad range of gram-positive and gram-negative
bacteria, including uropathogens, such as Enterobacteriaceae and S saprophyticus. Resistance
usually is mediated by decreased cell permeability or alterations in the amount or structure of
dihydrofolate reductase. Demonstrates synergy with the sulfonamides, potentiating the inhibition
of bacterial tetrahydrofolate production.
Ampicillin (Omnipen, Principen, Totacillin, Polycillin) -- Impairs cell wall synthesis in actively
dividing bacteria; binds to and inhibits penicillin-binding proteins (PBPs).
Gentamicin (Garamycin, Gentacidin) -- Bactericidal aminoglycoside antibiotic that inhibits
bacterial protein synthesis. Activity against various aerobic gram-negative bacteria, as well as E
faecalis and staphylococcal species. Most commonly used with or without ampicillin to treat acute
pyelonephritis in the hospitalized patient when Enterococcus species are a concern. Only
aminoglycoside with appreciable activity against gram-positive organisms
Cefixime (Suprax) -- Third-generation oral cephalosporin with broad activity against gramnegative bacteria, including Enterobacteriaceae, by inhibiting cell wall synthesis. Has shown poor
activity against staphylococcal and enterococcal species. Cefixime compared favorably to a
quinolone in one study.
Cefpodoxime proxetil (Vantin) -- Extended-spectrum oral cephalosporin with bactericidal activity
against gram-positive and gram-negative bacteria, including S aureus (not MRSA) and S
saprophyticus. Active agent in vivo is cefpodoxime. Beta-lactams, in general, have been given an
"E, I" rating in the 1999 IDSA guidelines for treating UTIs.
Nitrofurantoin (Furadantin, Macrobid, Macrodantin) -- Synthetic nitrofuran that interferes with
bacterial carbohydrate metabolism by inhibiting acetylcoenzyme A. Bacteriostatic at low
concentrations (5-10 mcg/mL) and bactericidal at higher concentrations. Bactericidal against
uropathogens such as S saprophyticus, E faecalis, and E coli; possesses no activity against
Proteus, Serratia, or Pseudomonas species. Received a "B, I" rating in the 1999 IDSA guidelines
for treating UTIs. Manufactured in different forms to facilitate durable urine concentrations:
macrocrystals (Macrodantin), microcrystal suspension (Furadantin), and a combined preparation
(Macrobid). Achieves no appreciable concentrations in the prostate, kidney, or blood
Deterrence/Prevention:

Approximately 25% of women with acute cystitis develop recurrent UTIs. The number of
recurrences experienced varies for each woman (range, 0.3-7.6 episodes per year), and
recurrences often cluster in time. The majority of recurrent infections are from bacteria
colonizing the fecal or periurethral reservoirs. The 3 main risk factors are (1) the
frequency of sexual intercourse, (2) the use of a spermicide and diaphragm, and (3) the
loss of estrogen's effect in the vagina and periurethral structures.
o

Women who develop a UTI within 2 weeks of a treated UTI either have a new
infection or they have a recurrence of the original uropathogen. The latter is
supported by cultures growing the same species, especially if it is biotyped or
shares the same antimicrobial sensitivities.
Looking for a source of persistent infection, such as a structural abnormality (eg,
calculus, abscess, cystic disease) is prudent.

Women with recurrent UTIs (less than 2-3 per y) may benefit from behavioral modification
and a program of self-initiated antibiotics.

o
o
o

Women with recurrent UTIs (more than 3 per y) should be considered for more
aggressive prophylactic regimens in addition to the behavioral modifications.
o

Behavioral modifications are generally easy, low-risk, and low-cost maneuvers.

Methods include urge-initiated voiding, postcoital voiding, increased fluid intake,
and the daily consumption of cranberry juice.
Patients using a spermicide should consider alternative methods of
contraception.
Self-initiated antibiotics may be an acceptable alternative for women with
recurrent UTIs. The clinician should educate the patient about the warning signs
of a persistent or worsening infection despite therapy. A recent study showed that
women with a history of at least 2 UTIs in the past year were capable of selfdiagnosing and treating UTIs. Uropathogens were isolated in 84% of 172 UTIs;
clinical and microbiologic cures were achieved in about 95% of episodes.

Women who associate their recurrent UTIs with sexual intercourse should be
offered postcoital prophylaxis. This involves taking a single dose of an effective
antimicrobial (eg, nitrofurantoin 50 mg, TMP-SMZ 40/200 mg, or cephalexin 500
mg) after sexual intercourse.
Continuous antimicrobial prophylaxis may be required in women who fail a
postcoital regimen, do not associate frequent UTIs with a modifiable cause, or
who are at risk for recurrent complicated UTIs. Regimens include TMP-SMZ
(40/200 mg qhs or 3 times per wk), nitrofurantoin (50-100 mg qhs or 3 times per
wk), norfloxacin (200 mg qhs or 3 times per wk), and trimethoprim (100 mg qhs
or 3 times per wk).
These regimens have been shown to be safe and effective, even after 5 years of
use. However, after 6-12 months, a trial without the medication is warranted
because as many as 30% of women experience a prolonged UTI-free period.
Prophylaxis may be reinstituted if the patient again develops recurrent UTIs.

Women who are postmenopausal with recurrent UTIs may benefit from estrogen
replacement, either systemically or locally. Estriol in a vaginal cream (0.5 mg every pm for
2 wk, then twice weekly) significantly reduced the incidence of recurrent UTI; the effect
probably is related to the restoration of lactobacilli, which replace Enterobacteriaceae and
decrease the vaginal pH.
For patients with SCI, the efficacy of prophylaxis with TMP-SMZ or nitrofurantoin has
been demonstrated. The possibility of developing resistant organisms is a concern,
especially in an institutional setting.
o

o
o

One option includes the use of methenamine (1 g tid), alternating q2mo with
nitrofurantoin (50-100 mg bid). Methenamine is converted into formic acid, which
is bacteriocidal. Oral ascorbic acid therapy has not been shown to confer much
benefit.
Risk can be decreased by the use of intermittent catheterization. Urine cultures
should be obtained periodically, and prophylactic or long-term antibiotic therapy
may be considered if over 10,000 CFU/mL and pyuria are noted (even in the
absence of symptoms).
Reflex bladder pressures greater than 50 cm H2O should be avoided through the
use of alpha-blockers, anticholinergics, transurethral sphincterotomy, or electrical
stimulation.
Using a 6% bleach solution to clean reusable leg bags and seat covers
decreases the rates of infection and ASB.

Neither cefuroxime nor ciprofloxacin was shown to reduce the rate of bacteriuria (about
20%) after lithotripsy.
The American Heart Association recommends antimicrobial prophylaxis to prevent
bacterial endocarditis in patients with moderate-to-highrisk cardiac conditions. High-risk
conditions include prosthetic valves, previous bacterial endocarditis, complex cyanotic
congenital heart diseases, and surgically constructed systemic pulmonic shunts.
Moderate-risk conditions include most other congenital heart diseases, hypertrophic
cardiac myopathy, and mitral prolapse with regurgitation. For patients with moderate- or
high-risk cardiac conditions, urologic procedures warranting prophylaxis include
cystoscopy and urethral dilatation; prophylaxis is not recommended for inserting a Foley
catheter in a patient with uninfected urine. No good evidence supports using such
regimens for prophylaxis for patients with prosthetic joints; this is an area that needs
further research and study.
o

Regimens for high-risk patients include ampicillin (or vancomycin) plus

gentamicin. Ampicillin is administered as 2000 mg IM or IV within 30 minutes of
starting the procedure; 6 hours later, 1000 mg of ampicillin (or amoxicillin PO) is
administered once. Gentamicin is dosed at 1.5 mg/kg IV or IM (not to exceed 120
mg) and is administered only once with the first dose of ampicillin. For patients
allergic to ampicillin, 1000 mg of vancomycin is administered only once, IV over
1-2 hours; it should be completed within 30 minutes of starting the procedure.
Regimens for moderate-risk patients include amoxicillin or vancomycin.
Amoxicillin is administered only once as 2000 mg PO 1 hour before the
procedure. For patients allergic to amoxicillin, 1000 mg of vancomycin is
administered only once, IV over 1-2 hours; it should be completed within 30
minutes of starting the procedure.

Complications:

Bacteremia, sepsis, shock, and death have all been discussed.

Prognosis:

The prognosis for most women with cystitis and pyelonephritis is good; about 25% of
women with cystitis will experience a recurrence.

The prognosis for emphysematous pyelonephritis is not as good and will be discussed in
Special Concerns.

Infected cysts in polycystic kidney disease respond to treatment slowly.

Special Concerns:

Catheters
o
o

Nosocomial infections develop in about 5% of patients admitted to hospitals, and

UTIs account for 40% of these infections. Two to 4% of these patients become
bacteremic, with a mortality rate of 12.5%.
Once a catheter is placed, the daily incidence of bacteriuria is 3-10%. Ten to 30%
of patients with short-term catheterization (ie, 2-4 d) develop bacteriuria and are

asymptomatic. Ninety to 100% of patients with long-term catheterizations develop

bacteriuria.
Pathogenesis: The presence of potentially pathogenic bacteria and an indwelling
catheter predisposes to the development of a nosocomial UTI. The bacteria may
gain entry into the bladder during insertion of the catheter, during manipulation of
the catheter/drainage system, around the catheter, and after removal. Enteric
pathogens are responsible most commonly, but Pseudomonas species,
Enterococcus species, S aureus, coagulase-negative staphylococcus,
Enterobacter species, and yeast also are known to cause infection. Proteus and
Pseudomonas species are the organisms most commonly associated with biofilm
growth on catheters.
Risk factors: The most important risk factor for bacteriuria is the presence of a
catheter. Eighty percent of infections are related to a catheter while 5-10% are
related to genitourinary manipulation. Catheters inoculate organisms into the
bladder and promote colonization by providing a surface for bacterial adhesion
and causing mucosal irritation. Risk factors for bacteriuria in patients who are
catheterized include longer duration of catheterization, colonization of the
drainage bag, diarrhea, diabetes, absence of antibiotics, female gender, renal
insufficiency, errors in catheter care, catheterization late in the hospital course,
and immunocompromised or debilitated states.
Diagnosis: Symptoms generally are nonspecific; most patients present with fever
and leukocytosis. Significant pyuria generally is represented by greater than 50
WBC/hpf. Colony counts on a urine culture range from 100-10,000. Infections
may be polymicrobial.
Prevention
At least nine steps can be taken to prevent catheter-associated UTIs.
These steps can postpone a UTI for weeks but are not likely to be
successful in chronically catheterized patients. Catheterization should be
avoided when not required (catheters were found to be unnecessary in
41-58% of patient-days) and should be terminated as soon as possible.
Suprapubic catheters are associated with a lower risk of UTI. Patients
who require long-term catheterization are more satisfied, but mechanical
complications are increased. Contraindications include bleeding
disorders, previous lower abdominal surgery or irradiation, and morbid
obesity. Intermittent catheterization is an option, but most become
bacteriuric within a few weeks as the incidence is 1-3% per insertion.
Aseptic indwelling catheter insertion and a properly maintained closeddrainage system are essential. Urinary catheters coated with silver also
reduce the risk (silver alloy seems to be more effective than silver oxide).
Another approach is the Bard Lubricath, which has a hydrophilic coating
that decreases tissue irritation and nosocomial UTIs. It is reasonable to
use these more expensive catheters in those who are at highest risk.
Receiving systemic antimicrobial drug therapy has been shown
repeatedly to lower the risk for developing a UTI in catheterized patients;
most benefit was observed in those catheterized for 3-14 days. Most
hospitalized patients already are receiving antibiotics for other reasons.
Disadvantages include creating resistant organisms. Because many of
these infections occur in clusters, good handwashing before and after
catheter care is essential.
Treatment: Removal of the catheter is adequate in some patients with bacteriuria.
If bacteriuria persists 48 hours after removal of the Foley catheter, antibiotics
should be started. Antibiotic therapy is directed at the pathogen(s) isolated in the
culture. Patients with chronic indwelling catheters who are febrile and not
bacteremic should be treated with a 3- to 5-day course of antibiotics. If a patient
is bacteremic, then a 10- to 14-day course of antibiotics is recommended.

Pregnancy
o
o
o

ASB occurs in 5-10% of pregnant women. More than 100,000 CFU/mL of a single
uropathogen is the classic definition of ASB, but more recent data support 10,000
CFU/mL from a clean-catch specimen.
ASB most commonly appears between the ninth and 17th weeks of pregnancy.
ASB predisposes to preterm labor, intrauterine growth retardation, lowbirth
weight infants, anemia, amnionitis, and hypertensive disorders of pregnancy.
Risk factors include sexual activity, increasing age and parity, diabetes, lower
socioeconomic class, a history of UTIs, sickle cell disease, and
structural/functional abnormalities. Cystitis and pyelonephritis are inevitable
complications of ASB.
The recommendation is to screen pregnant women at their first prenatal visit and
during the third trimester and not again, unless their initial test result is positive or
they develop symptoms. Cystitis occurs in 0.3-1.3% of pregnancies but does not
appear to be related to ASB. Acute pyelonephritis occurs in 1-2% of pregnancies.
Complications of pyelonephritis include pulmonary edema and acute respiratory
distress syndrome, transient renal dysfunction, anemia, preterm delivery, and
lowbirth weight infants.
ASB must be treated and not merely observed. Treatment of ASB decreases the
risk of persistent bacteriuria from 86-11%, with a significant reduction in the risk
of acute pyelonephritis. Sulfonamides, cephalosporins, nitrofurantoin, and broadspectrum penicillins have been shown to be effective. A 4- to 7-day course of
therapy is recommended for treating ASB and cystitis. Sulfonamides just before
birth may cause fetal hyperbilirubinemia, while trimethoprim early in pregnancy is
teratogenic.
Repeat cultures should be obtained during pregnancy given the high risk of
relapse. After the second occurrence, nitrofurantoin, amoxicillin, or a
cephalosporin is recommended for suppression until after delivery.
Hospitalization is indicated for pyelonephritis with nausea/vomiting, evidence of
sepsis, or for patients with contractions. Empiric parenteral regimens include a
cephalosporin, such as ceftriaxone, or gentamicin plus ampicillin (or a derivative
of penicillin). When using an aminoglycoside, the risk of ototoxicity in the fetus
must be considered.
Antibiotic regimens should be changed based on culture results. Patients may be
changed to oral therapy once they are afebrile and able to tolerate an oral
regimen. Urolithiasis, a structural abnormality, or an abscess should be
considered if a patient fails to respond to appropriate therapy.

Urinary tract infections in patients with renal transplants

o
o

UTIs are the most common type of infection following renal transplantation. UTIs
occur in 30-50% of renal transplant patients and frequently are silent.
UTIs may, but do not always, predispose the patient to graft loss or rejection.
Infection of the allograft may lead to life-threatening bacteremia. Patients are
most susceptible the first 2 months following transplantation. Triggering factors
include vesicoureteral reflux and immunosuppression.
An unusual bacterium, Corynebacterium urealyticum (ie, CDC group D2), has
been reported to cause encrusted pyelitis and cystitis in these patients.
Treatment of UTIs in renal transplant patients is preferably with either TMP-SMZ
or a quinolone.
ASB should be treated for 10 days. Parenteral antibiotics should be used for
severe infections. The duration of antibiotics for severe infections should be 4-6
weeks.

Yeast and fungi

o
o
o

Antibiotic prophylaxis is valuable in patients undergoing renal transplantation.

TMP-SMZ (1 PO qd), beginning 2-4 days after surgery and continuing for 4-8
months, reduced the incidence of UTIs from 38-8% (especially after the catheter
was removed), cut febrile hospital days and bacterial infections (during and after
hospitalization) in half, and reduced graft rejection.

Removal of a Foley catheter is essential for clearance of funguria. If the catheter

is still needed, replace it (preferably a day later).
Treatment options vary from topical treatment to systemic therapy.
Amphotericin-B bladder washes for 7 days provides a prompt but nonsustained
response. It does not treat systemic mycoses and is inconvenient for the nurse to
administer. Amphotericin-B, 0.3 mg/kg IV for 1 dose is an option that provides a
more sustained and systemic response.
Fluconazole, 200 mg PO for 1 d followed by 100 mg PO qd for 4-7 d is a simpler
option. This drug is effective against azole-responsive candida. Generally, azoleresistance is observed only in Candida krusei and Candida glabrata. Fluconazole
provides a good long-term effect but takes a few days to clear the urine.

Diabetes mellitus
o Complicated UTIs in patients who have diabetes include renal and perirenal
abscess, emphysematous pyelonephritis, emphysematous cystitis, fungal
infections, xanthogranulomatous pyelonephritis, and papillary necrosis.
o Emphysematous pyelonephritis is a severe, necrotizing form of multifocal
bacterial nephritis with gas formation within the renal parenchyma. Seventy to
90% of cases develop in patients with diabetes. Sixty percent of infections are
secondary to E coli. Enterobacter aerogenes and Klebsiella, Proteus,
Streptococcus, and Candida species also may play a role.
Three factors must be present for the development of renal emphysema
excess tissue glucose, impaired tissue perfusion, and a gas-producing
bacterium. The gas may result from fermentation of necrotic tissue or
from mixed acid fermentation by Enterobacteriaceae. Predisposing
factors include diabetes mellitus, remote or recent kidney infection, and
obstruction.
Patients may present with fever, chills, and nausea or vomiting. Half of
patients have evidence of a flank mass on examination. Rarely, patients
have crepitus over the thigh or flank.
Lab findings include leukocytosis, hyperglycemia, pyuria, and an
elevated BUN and creatinine. A plain film of the abdomen may reveal gas
in the kidneys in 85% of infections. A renal ultrasound also may help
establish the diagnosis. If gas is visualized, then a CT scan should be
performed to reveal if the gas is in the parenchyma or collecting system.
The mortality rate is 60% in cases in which the gas is localized to the
renal parenchyma, regardless of treatment. The mortality is 80% if the
gas has spread in the perinephric space and the patient is treated with
antibiotics alone.
o Emphysematous pyelitis is defined as the presence of gas localized to the renal
collecting system. Emphysematous cystitis is defined as air in the urinary tract.
Pathogenesis: More than 50% of these patients have diabetes.
Obstruction of the collecting system generally is the rule in
emphysematous pyelitis. The left kidney is involved twice as often as the
right in emphysematous pyelitis. The most common infectious etiology is

E coli, but other gram-negative organisms, S aureus, Clostridium

perfringens, and Candida species also may be responsible.
Presentation: Patients with emphysematous pyelitis most commonly
present with fever, chills, nausea and vomiting, and abdominal pain.
Patients with emphysematous cystitis most commonly present with
urinary frequency, urgency, and dysuria. Abdominal pain also may be
present. Gross hematuria and pneumaturia are occasionally present.
Diagnosis: Leukocytosis and pyuria are observed in most patients. In half
of the patients, azotemia and hyperglycemia are present. Abdominal
films may reveal gas outlining the renal pelvis and in the ureters.
Abdominal films may reveal air in the bladder wall or lumen. Renal
ultrasound may reveal diffuse thickening of the bladder wall and
echogenicity. CT scans may reveal gas in the bladder wall with extension
into the lumen. Cystoscopy may reveal blebs in the bladder mucosa.
Therapy: Antibiotics and relief of obstruction usually are sufficient. The
mortality rate is 20%.

Papillary necrosis
o Definition: Papillary necrosis is defined as focal or diffuse ischemic necrosis of
various segments of the renal medulla.
o Pathogenesis: This entity is uncommon in people with diabetes, but, when
infections occur, more than one half are in people with diabetes. Other causes
include sickle cell disease, analgesic abuse, pyelonephritis, renal transplant
rejection, cirrhosis, and obstruction. Most infections are complicated by UTI and
renal insufficiency.
o Two types of papillary necrosis have been described. In the medullary form, the
fornices remain intact. In the papillary form, the entire papillary surface is
destroyed.
o Presentation: Many patients present with fever, chills, and flank pain. The flank
pain is secondary to the passage of sloughed papilla. Some patients may present
with symptoms of obstruction or azotemia.
o Histology and/or radiologic studies may help make the diagnosis. The sloughed
papillae may be obtained by straining the urine and sending for histology. The
retrograde pyelogram is the radiologic procedure of choice, but ultrasound or CT
scan also reveal the diagnosis. Findings of early renal papillary necrosis include
a dilated calyceal fornix, retracted or irregular papillary tip, and extension of
contrast into the parenchyma. A club-shaped cavity in the medulla or papilla may
be formed in later disease. When a separated papilla is surrounded by contrast, a
ring may be visualized; this is characteristic of papillary necrosis.
o Treatment: Antibiotics, drainage, and (occasionally) surgery are the mainstays of
therapy. Antibiotics should cover E coli and Enterobacter, Proteus, and Klebsiella
species.
o Treatment for more serious infections also should cover Pseudomonas and
Enterococcus species. Initial therapy should not be with an oral regimen.
Parenteral agents such as gentamicin, cefotaxime, ceftriaxone, ceftazidime,
cefepime, mezlocillin, piperacillin, piperacillin-tazobactam, imipenem-cilastatin,
meropenem, or ciprofloxacin should be used empirically pending the result of a
urine culture. Parenteral therapy should be continued until the fever and other
symptoms resolve. Duration of therapy generally is 14 days.

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