URINARY TRACT INFECTION IN PREGNANCY.
UTI is the most common medical complication of
pregnancy, either asymptomatic (ASB
of pregnancy) or symptomatic (cystitis or acute
pyelonephritis). Although most UTIs in
pregnancy are asymptomatic, covert bacteriuria
increases the risk of preterm birth
and low-birthweight infants.
It has long been recognized that symptomatic UTI is
more frequently encountered in pregnant women. This suggests that factors are
present during gestation that allow bacteria to replicate in the urine and
ascend to the upper urinary tract.
Several findings support this view. The normal
female urinary tract undergoes dramatic physiologic changes during pregnancy.
There is decreased ureteric muscle tone and
activity, which results in a reduced rate of passage
of urine throughout the urinary collecting system. The upper ureter and renal
pelvises become dilated, resulting in a physiologic hydronephrosis of
pregnancy. This hydronephrosis is a result of the effects of progesterone on
muscle tone and peristalsis, and most importantly, mechanical obstruction by
the enlarging uterus. Bladder changes also occur in pregnancy, including decreased
tone, increased capacity, and incomplete emptying. These findings predispose to
vesicoureteric reflux. These physiologic alterations associated with pregnancy
facilitate the ascending migration of bacteria into the upper urinary tract
once bladder infection is established.
It is also possible that alterations in the physical
or chemical properties of urine during pregnancy can result in exacerbations of
bacteriuria, thus predisposing to ascending infection. Urinary pH elevation during pregnancy encourages
bacterial growth.Glycosuria,
which is common in pregnancy, may favor an increase in the rate of bacterial
multiplication. The increased urinary excretion of estrogen may be a factor in the
pathogenesis of symptomatic UTI during pregnancy. It has been demonstrated by means
of animal experiments that estrogen can enhance the growth of strains of E. coli
that cause pyelonephritis and also predispose the animal to the development of
renal infection. In addition, the renal medulla is particularly susceptible to
infection because its hypertonic environment inhibits leukocyte migration,
phagocytosis, and
complement activity .
Bacteria and pyelonephritis
Acute pyelonephritis, one of the most frequent
medical complications of pregnancy, is a serious threat to maternal and fetal
well-being. The association between acute pyelonephritis of pregnancy and
preterm delivery was appreciated in the preantibiotic era, with prematurity
rates of 20% to 50% being reported (199,200,201 and 202).
Subsequent studies in the post antibiotic era have
confirmed this association between acute pyelonephritis and an increased risk
of premature delivery More recently, Millar and Cox (93) noted
that the contribution of pyelonephritis to preterm
birth and low birth weight is confounded by socioeconomic status, which is
closely related to both prematurity and UTI and thus difficult to ascertain.
However, they concluded that the weight of evidence demonstrates that
pyelonephritis is associated with preterm birth and low birthweight, but the
strength of the association is unknown.
In the past, several mechanisms have been proposed
to explain this association,including (a) pyrogens increase myometrial activity
; (b) ureteric contractions result in reflex myometrial contractions ; (c)
endotoxin of Gram-negative
bacteria
associated with pyelonephritis has a direct oxytocic
effect on the myometrium or (d) endotoxin crosses the placenta, resulting in
fetal effects culminating in preterm labor. Newer theories suggest that
bacterial enzymes such as proteases and collagenase may weaken membranes, predisposing
them to rupture and initiating the onset of labor. In addition, bacterial
products such as phospholipase A and C or endotoxins may stimulate synthesis of
prostaglandins from the membranes or decidua,
which initiates labor. More importantly, these
bacterial products stimulate the monocytes and macrophages of the immune system
to release cytokines such as IL-1, IL-6, tumor necrosis factor, and platelet
activating factor, which in turn trigger prostaglandin production.
The concept of quantitative urine cultures, which
made it possible to determine when infection of the urinary tract was present
in individuals without symptoms or signs of UTI, was a major contribution to
the understanding of the pathogenesis of
Bacteriuria And Preterm Delivery And Low-Birthweight Infants
It is well documented that pregnant women who
develop acute pyelonephritis are at a
significantly increased risk for preterm labor and delivery. In contrast, the
relationship of
ASB to preterm delivery, low-birthweight, small for gestational age babies, and
fetal
mortality has been controversial
Nosocomial Urinary Tract Infection.
Hospital-acquired UTIs are among the most frequent
of nosocomial infections. An exact prevalence for nosocomial UTIs is difficult
to come by because of various surveillance
systems and different definitions (i.e., clinically manifest infection versus
laboratory evidence of significant bacteriuria).
Bacteria that cause catheter-associated UTI gain
access to the urinary tract by three major routes. The first is introduction of
microorganisms from the external genitalia or distal urethra into the bladder
at the time of catheterization. In general, bacteria
introduced in this way are well tolerated and
controlled by voiding and the antibacterial defense mechanism of the bladder .
A second mechanism by which bacteria gain access to the bladder is via a thin
film of urethral fluid on the outside of the catheter. Catheters have been
shown to contain biofilm on their surface.
Bacteria contained within such biofilms are
protected from antibiotics and the natural defense provided by flow of urine.
Third, once the drainage system has been contaminated,
bacteria may migrate up inside the catheter lumen. Turck and Stamm believe that
the intraluminal ascending route accounted for most
nosocomial UTIs. Such contamination may be due to
failure to use sterile technique in disconnecting the catheter and drainage
tube to obtain a specimen or to irrigate the catheter . In advertent
disconnection occurs and frequently results in contamination. An additional
important factor in the pathogenesis of catheter-associated
UTI is cross-contamination of catheters by transmission
of bacteria from patient to patient on the hands of hospital personnel.
Treatment And Prevention
In general, we do not use antimicrobial agents to
treat those patients in whom bacteriuria occurs during catheterization, but who
remain asymptomatic. This concern relates to the risk of persistent
colonization or emergence of more resistant nosocomial organisms. Fortunately,
in many such situations, removal of the catheter results in eradication of the
bacteriuria. If signs and symptoms of cystitis or acute pyelonephritis occur
with the presence of an indwelling catheter, systemic antimicrobial therapy
should be administered for 10 to 14 days. In addition, if bacteriuria without
symptoms persists
once the catheter is removed, treatment should be
initiated. Regimens similar to those used in treating acute cystitis are
appropriate for this situation .
The most important and effective method for
prevention of nosocomial UTIs is to limit the use of indwelling catheters only
to instances in which they are necessary. Additional preventive measures have
been recommended (a) Urinary catheters should be removed
as soon as possible; (b) only adequately trained hospital
personnel should insert urinary catheters; (c) use of aseptic
technique in inserting catheters to avoid
introducing bacteria;
(d) cleansing the metal catheter junction with soap and
water once or twice a day to reduce periurethral bacterial contamination;
(e) maintain unobstructed “downhill” flow in a closed
drainage system; (f) disconnect the drainage system
only to irrigate an obstructed catheter, not to obtain specimens or to
routinely irrigate; and (g)whenever feasible, separate
catheterized patients from each other to preventcross-contamination.
Proposed measures to aid in prevention
but for which supporting data are lacking to demonstrate an
advantage over a closed drainage system include the following: (a) a flutter valve to prevent reflux of urine from the
collection bag to the drainage tube; (b) continuous bladder irrigation via a
triple-lumen catheter with either acetic acid or a neomycin-polymyxin
solution; (c) use of suprapubic catheterization; and (d) prophylactic systemic antibiotics.
The final aspect of catheter care is to obtain a
follow-up culture after the catheter is removed and to institute appropriate
antimicrobial therapy if significant bacteriuria persists after removal of the
catheter.
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