أ. م .د. وضاح المرزوك
كلية الطب
-
جامعة بابل
فرع الجراحة
المرحلة الرابعة
BLADDER INFECTION
Acute nonspecific Cystitis
Acute cystitis refers to urinary infection of the lower urinary
tract, principally the bladder. Acute cystitis more commonly
affects women than men. The primary mode of infection is
ascending from the periurethral / vaginal and fecal flora. The
diagnosis is made clinically. In children, the distinction between
upper and lower UTI is important. In general, those in whom
acute cystitis developed do not usually require any extensive
radiologic investigation (such as a voiding cystourethrogram),
but those in whom pyelonephritis developed do.
Clinical finding
Patients with acute cystitis present with irritative voiding
symptoms such as dysuria, frequency, and urgency. Low back
and suprapubic pain, hematuria, and cloudy/foul-smelling urine
are also common symptoms. Fever and systemic symptoms are
rare.
Diagnosis.
Typically, urinalysis demonstrates WBCs in the urine, and
hematuria may be present.
Urine culture is required to confirm the diagnosis and identify
the causative organism. However, when the clinical picture and
urinalysis are highly suggestive of the diagnosis of acute
cystitis, urine culture may not be needed. E. coli causes most of
the acute cystitis. Other gram-negative (Klebsiella and Proteus
spp.) and gram-positive (S. saprophyticus and enterococci)
bacteria are uncommon pathogens. Diabetes and lifetime history
of UTI are risk factors for acute cystitis.
In uncomplicated infection of the bladder, radiologic evaluation
is often not necessary.
Management.
Management for acute cystitis consists of a short course of
oral
antibiotics.
TMP-SMX,
nitrofurantoin,
and
fluoroquinolones have excellent activity against most pathogens
that cause cystitis. TMP-SMX and nitrofurantoin are less
expensive and thus are recommended for the treatment of
uncomplicated cystitis. However, it is estimated that resistance
to TMP-SMX by E. coli isolates causing uncomplicated acute
cystitis is approximately 20%, compared to <2% to
nitrofurantoin. In adults and children, the duration of treatment
is usually limited to 3–5 days . Longer therapy is not indicated.
Single-dose therapy for the treatment of recurrent cystitis/UTI
appears to be less effective. Resistance to penicillins and
aminopenicillins is high and thus they are not recommended for
treatment.
Recurrent Cystitis/UTI
P
RESENTATION AND
F
INDINGS
.
Recurrent cystitis/UTI is caused either by bacterial persistence
or reinfection with another organism. Identification of the cause
of the recurrent infection is important, because the management
of bacterial persistence and reinfection are distinct. If bacterial
persistence is the cause of recurrent UTI, the removal of the
infected source is often curative, whereas preventative therapy is
effective in treating reinfection.
When bacterial persistence is the suspected cause, radiologic
imaging is indicated. Ultrasonography can be obtained to
provide a screening evaluation of the genitourinary tract. More
detailed assessment with intravenous pyelogram, cystoscopy,
and CT scans may occasionally be necessary. In patients who
have frequent, recurrent UTI, bacterial localization studies and
more extensive radiologic evaluation (such as retrograde
pyelograms) is warranted.
When bacterial reinfection is the suspected cause of recurrent
cystitis, the patient should be carefully evaluated for evidence of
vesicovaginal or vesicoenteric fistula.
Management.
Management of recurrent cystitis depends on its cause. Surgical
removal of the infected source (such as urinary calculi) is
needed to treat bacterial persistence. Similarly, fistulas need to
be repaired surgically to prevent bacterial reinfection. In most
cases of bacterial reinfection, medical management with
prophylactic antibiotics is indicated.
Low-dose continuous prophylactic antibiotic has been shown to
reduce the recurrences of UTI by 95%. Alternatively,
intermittent self-start antibiotic therapy can be used in treating
recurrent cystitis in some women. When the recurrent
cystitis/UTI is related to sexual activity, frequent emptying of
the bladder and a single dose of antibiotic taken after sexual
intercourse can significantly reduce the incidence of recurrent
infection. Alternatives to antibiotic therapy in the treatment of
recurrent cystitis/UTI include intravaginal estriol, lactobacillus
vaginal suppositories, and cranberry juice taken orally.
SPECIFIC CYSTITIS
AMICROBIC (ABACTERIAL) CYSTITIS
Amicrobic cystitis is a rare disease of abrupt onset with a
marked local vesical reaction. Although it acts like an infectious
disease, search for the usual urinary bacterial pathogens is
negative. It affects adult men and occasionally children, usually
boys
.
The patient usually gives a history of recent sexual exposure.
Mycoplasmas and chlamydiae have been isolated or suspected
as etiologic agents. An adenovirus has been isolated from the
urine in children suffering from acute hemorrhagic cystitis.
Some leukocytosis may develop. The urine is grossly purulent
and may contain blood as well. Stained smears reveal an
absence of bacteria. Routine cultures are uniformly negative. In
a few cases, mycoplasmas and TRIC agent (Chlamydia
trachomatis) have been identified, but the significance of this is
not yet clear. Search for tubercle bacilli is not successful.
Urethral discharge reveals no bacteria. Renal function is not
impaired.
Treatment.
One of the tetracyclines or chloramphenicol, 1 g/day orally in
divided doses for 3–4 days, is said to be curative in 75% of
cases. Streptomycin, 1–2 g/day intramuscularly for 3–4 days,
may be tried.
SCHISTOSOMIASIS (BILHARZIASIS
)
Schistosomiasis, caused by a blood fluke, is a disease of warm
climates. In its 3 forms, it affects about 350 million people.
Schistosoma mansoni is widely distributed in Africa, South and
Central America, Pakistan, and India; Schistosoma japonicum is
found in the Far East; and Schistosoma haematobium is limited
to Africa, Saudi Arabia, Israel, Jordan, Lebanon, and Syria.
Schistosomiasis is on the increase in endemic areas because of
the construction of modern irrigation systems that provide
favorable conditions for the intermediate host, a freshwater
snail. This disease principally affects the urogenital system,
especially the bladder, ureters, seminal vesicles, and, to a lesser
extent, the male urethra, and prostate gland. Because of
emigration of people from endemic areas, the disease is being
seen with increasing frequency in both Europe and the United
States. Infection with S. mansoni and S. japonicum mainly
involves the colon.
Etiology
Humans are infected when they come in contact with larva-
infested water in canals, ditches, or irrigation fields during
swimming, bathing, or farming procedures. Fork tailed larvae,
the cercariae, lose their tails as they penetrate deep under the
skin. They are then termed schistosomules. They cause allergic
skin reactions that are more intense in people infected for the
first time. These schistosomules enter the general circulation
through the lymphatics and the peripheral veins and reach the
lungs. If the infection is massive, they may cause pneumonitis.
They pass through the pulmonary circulation, to the left side of
the heart, and to the general circulation. The worms that reach
the vesicoprostatic plexus of veins survive and mature, whereas
those that go to other areas die.
Pathogenesis
The adult S. haematobium worm, a digenetic trematode, lives in
the prostatovesical plexus of veins. The male is about 10 × 1
mm in size, is folded upon itself, and carries the long, slim 20 ×
0.25 mm female in its ―schist,‖ or gynecophoric canal. In the
smallest peripheral venules, the female leaves the male and
partially penetrates the venule to lay her eggs in the sub
epithelial layer of the affected viscus, usually in the form of
clusters that form tubercles. The ova are seen only rarely within
the venules; they are almost always in the sub epithelial or
interstitial tissues. The female returns to the male, which carries
her to other areas to repeat the process.
The living ova, by a process of histolysis and helped by
contraction of the detrusor muscle, penetrate the overlying
urothelium, pass into the cavity of the bladder, and are extruded
with the urine. If these ova reach fresh water, they hatch, and the
contained larvae—ciliated miracidia—find a specific freshwater
snail that they penetrate. There they form sporocysts that
ultimately form the cercariae, which leave the snail hosts and
pass into fresh water to repeat their life cycle in the human host.
Pathology
The fresh ova excite little tissue reaction when they leave the
human host promptly through the urothelium. The contents of
the ova trapped in the tissues and the death of the organisms
cause a severe local reaction, with infiltration of round cells,
monocytes, eosinophils, and giant cells that form tubercles,
nodules, and polyps. These are later replaced by fibrous tissue
that causes contraction of different parts of the bladder and
strictures of the ureter. Fibrosis and massive deposits of eggs in
subepithelial tissues interfere with the blood supply of the area
and cause chronic bilharzial ulcerations.
Epithelial metaplasia is common, and squamous cell carcinoma
is a frequent sequela. Secondary infection of the urinary tract is
a common complication and is difficult to overcome. The
trapped dead ova become impregnated with calcium salts and
form sheets of subepithelial calcified layers in the ureter,
bladder, and seminal vesicles.
Clinical Findings
1. Penetration of the skin by the cercariae causes allergic
reactions, with cutaneous hyperemia and itching that are
more intense in people infected for the first time.
2. During the stage of generalization or invasion, the patient
complains of symptoms such as malaise, fatigue and
lassitude, low grade fever, excessive sweating, headache,
and backache.
3. When the ova are laid in the bladder wall and begin to be
extruded, the patient complains of terminal, slightly
painful hematuria that is occasionally profuse.
4. Increasing frequency, suprapubic and back pain,
urethralgia, profuse hematuria, pyuria, and nocroturia are
likely to occur, with secondary infection.
5.
Renal pain may be due to ureteral stricture, vesicoureteral
reflux, or secondary stones obstructing the ureter. Fever,
rigor, toxemia, and uremia are manifestations of renal
involvement
.
6. Later, a fibrosed, pitted, bilharzial glans penis, a urethral
stricture or fistula, or a perineal fibrous mass may be
found. A suprapubic bladder mass or a renal swelling may
be felt abdominally. Rectal examination may reveal a
fibrosed prostate, an enlarged seminal vesicle, or a
thickened bladder base.
Diagnosis.
1. Urinalysis usually reveals the terminal-spined dead or
living ova, blood and pus cells, and bacteria. Malignant
squamous cells may be seen.
2. A variety of immunologic methods have been used to
confirm the diagnosis of schistosomiasis. Positive
immunologic tests indicate previous exposure but not
whether schistosomiasis is currently present.
3. A plain film of the abdomen may show areas of grayness
in the flank (enlarged hydronephrotic kidney) or in the
bladder area (large tumor). Opacifications (stones) may be
noted in the kidney, ureter, or bladder. Linear calcification
may be seen in the ureteral and bladder walls . Punctate
calcification of the ureter (ureteritis calcinosa) and a
honeycombed calcification of the seminal vesicle may be
obvious .
4. Excretory urograms may show either normal or diminished
renal function and varying degrees of dilatation of the
upper urinary tracts.
5. These changes include hydronephrosis, dilated and
tortuous ureters, ureteral strictures, or a small contracted
bladder having a capacity of only a few milliliters. Gross
irregular defects of the bladder wall may represent cancer.
Retrograde urethrography may reveal a bilharzial urethral
stricture. Cystograms often reveal vesicoureteral reflux,
particularly if the bladder is contracted.
6.
Cystoscopy may show fresh conglomerate, grayish
tubercles surrounded by a halo of hyperemia, old calcified
yellowish tubercles, sandy patches of mucous membrane,
and a lusterless ground-glass mucosa that lacks the normal
vascular pattern. Other obvious lesions include bilharzial
polyps, chronic ulcers on the dome that bleed when the
bladder is deflated (weeping ulcers), vesical stones,
malignant lesions, stenosed or patulous ureteric orifices,
and a distorted, asymmetric trigone. All are signs of
schistosomal infestation
.
Treatment
Praziquantel, metrifonate, and oxamniquine are the drugs of
choice in treating schistosomiasis.
(1) Praziquantel is unique in that it is effective against all human
schistosome species. It is given orally and is effective in adults
and children. Patients in the hepatosplenic stage of advanced
schistosomiasis tolerate the drug well. The recommended
dosage for all forms of schistosomiasis is 20 mg/kg three times
in 1 day only.
(2) Metrifonate is also a highly effective oral drug. It is the drug
of choice for treatment of S. haematobium infections but is not
effective against S. mansoni or S. japonicum. For treatment of S.
haematobium infections, the dosage is 7.5–10 mg/kg (maximum
600 mg) once and then repeated twice at 2-week intervals.
(3) Oxamniquine is a highly effective oral drug and is the drug
of choice for treatment of S. mansoni infections. It is safe and
effective in advanced disease. It is not effective in S.
haematobium or S. japonicum infections. The dosage is 12–15
mg/kg given once; for children under 30 kg, 20 mg/kg is given
in 2 divided doses.
Surgical measures for treatment of complication such as urethral
stricture, ureteric obstruction, vesicoureteric reflux, contracted
bladder, bladder carcinoma or sever hydronephrosis.