Материал: Oxford American Handbook of Urology ( PDFDrive )

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532 CHAPTER 14 Urological problems in pregnancy

Physiological and anatomical changes in the urinary tract

Kidney

•Renal size enlarges by 1 cm, secondary to increased interstitial volume and increased renal vasculature.

•Renal plasma flow rate (RPF) increases early in the first trimester (up to 75% by term).

•Glomerular filtration rate (GFR) increases by 50%, related to an increased cardiac output.

•Renal function and biochemical parameters are affected by changes in RPF and GFR. Creatinine clearance increases, and serum levels of creatinine, urea, and urate fall in normal pregnancy (see Table 15.1). Raised GFR causes an increased glucose load at the renal tubules and results in glucose excretion (glycosuria) in most pregnancies. 24-hour protein excretion remains unchanged. Urine output increases.

•Salt and water handling: A reduction in serum sodium causes reduced plasma osmolality. The kidney compensates by increasing renal tubular reabsorption of sodium. Plasma renin activity is increased 10-fold,

and levels of angiotensinogen and angiotensin are increased 5-fold. Osmotic thresholds for antidiuretic hormone (ADH) and thirst decrease.

•Acid–base metabolism Serum bicarbonate is reduced. Increased progesterone stimulates the respiratory center resulting in reduced PCO2.

Bladder

•Bladder displacement occurs (superiorly and anteriorly) due to the enlarging uterus. The bladder becomes hyperemic, and raised estrogen levels cause hyperplasia of muscle and connective tissues.

Bladder pressures can increase over pregnancy (from 8 to 20 cmH2O), with associated rises in absolute and functional urethral length and pressures.

•Lower urinary tract symptoms: Urinary frequency (>7 voids during the day) and nocturia (>1 void at night) increases over the duration of gestation (incidence of 80–90% in third trimester). Urgency and urge

incontinence also increase secondary to pressure effects from the enlarging uterus.

•Stress urinary incontinence occurs in 22%, and increases with parity (pregnancies that result in delivery beyond 28 weeks’ gestation). It is partly caused by placental production of peptide hormones (relaxin), which induces collagen remodeling and consequent softening of tissues of the birth canal. Infant weight, duration of first and second stages of labor (vaginal delivery), and instrumental delivery (ventouse extraction or forceps delivery) increase risks of postpartum (after delivery of the child) stress incontinence.

PHYSIOLOGICAL AND ANATOMICAL CHANGES 533

Table 14.1 Biochemistry reference intervals

Substance

Nonpregnant

Pregnant

 

 

Sodium (mmol/L)

135–145

132–141

 

Urea (mmol/L)

2.5–6.7

2.0–4.2

 

Urate (µmol/L)

150–390

100–270

 

Creatinine (µmol/L)

70–150

24–68

 

Creatinine clearance (mL/min)

90–110

150–200

 

Bicarbonate (mmol/L)

24–30

20–25

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

534 CHAPTER 14 Urological problems in pregnancy

Urinary tract infection (UTI)

Definition

UTI describes a bacterial infection of the urine with >105 colony forming units (CFU)/mL (or >102 CFU/mL if the patient is systemically unwell).

Incidence

Pregnancy does not alter the incidence of UTI, which remains at 4% for women of reproductive age. However, physiological and anatomical changes associated with pregnancy alter the course of infection, causing an increased risk of recurrent UTI and progression to acute pyelonephritis (up to 28%).

Risk factors

These include previous history of recurrent UTIs and pre-existing vesicoureteric reflux. Physiological changes in pregnancy include hydronephrosis with decreased ureteral peristalsis causing urinary stasis. Up to 75% of pyelonephritis cases occur in the third trimester, when these changes are most prominent.

Pathogenesis

A common causative organism is Escherichia coli. An increased risk of gestational pyelonephritis is associated with E. coli containing the virulence factor Dr adhesin.

Complications

UTI increases the risk of preterm delivery, low fetal birth weight, and maternal anemia.

Screening tests

Midstream urine specimen (MSU)

MSU should be obtained at the first antenatal visit and sent for urinalysis and culture to look for bacteria, protein, and blood. A second MSU investigation is recommended at later visits (week 16) to examine for bacteria, protein, and glucose.

Treatment

All proven episodes of UTI should be treated (asymptomatic or symptomatic), guided by urine culture sensitivities. Antibiotics that are safe to use during pregnancy include penicillins (i.e., ampicillin, amoxicillin, penicillin V) and cephalosporins (i.e., cefaclor, cefalexin, cefotaxime, ceftriaxone, cefuroxime). Nitrofurantoin may be used in first and second trimesters only. See Table 14.2 for antibiotics that are not safe to use.

Repeat urine cultures after treatment to check that bacteria have been eliminated.

Acute pyelonephritis requires hospital admission for intravenous antibiotics (cephalosporin or aminopenicillin) until apyrexial, followed by oral antibiotics for 14 days, and repeated cultures for the duration of pregnancy.

 

 

 

URINARY TRACT INFECTION (UTI)

535

 

Table 14.2 Antibiotics to avoid in pregnancy*

 

 

 

 

 

 

 

 

Trimester

Antibiotic

Risk in pregnancy

 

 

 

 

 

 

 

1,2,3

Tetracyclines

Fetal malformation; maternal

 

 

 

 

hepatotoxicity; dental discoloration

 

 

 

Quinolones

Arthropathy

 

1

Trimethoprim

Teratogenic risk (folate antagonist)

 

2,3

Aminoglycosides

Auditory or vestibular nerve damage

 

3

Chloramphenicol

Neonatal gray syndrome

 

 

 

Sulfonamides

Neonatal hemolysis; methemoglobinemia

 

 

 

Nitrofurantoin

Maternal or neonatal hemolysis (if used at

 

 

 

 

term), in subjects with G6PD deficiency

 

 

 

 

 

 

 

* See Krieger JN (1986). Complications and treatment of urinary tract infection during pregnancy. Urol Clin North Am 13:685.

536 CHAPTER 14 Urological problems in pregnancy

Hydronephrosis

Hydronephrosis develops from ~week 6 to week 10 of gestation. By week 28 of gestation, 90% of pregnant women have hydronephrosis. It has usually resolved within 2 months of birth.

It is due to a combination of the smooth muscle relaxant effect of progesterone and mechanical obstruction from the enlarging fetus and uterus, which compresses the ureter. (Hydronephrosis does not occur in pelvic kidneys or those transplanted into ileal conduits, nor does it occur in quadripeds such as dogs and cats, where the uterus is dependent and thus falls away from the ureter.)

The hydronephrosis of pregnancy poses diagnostic difficulties in women presenting with flank pain thought to be due to a renal or ureteral stone. To avoid using ionizing radiation in pregnant women, renal ultrasonography is often used as the initial imaging technique in those presenting with flank pain.

In the nonpregnant patient, the presence of hydronephrosis is taken as surrogate evidence of ureteral obstruction.

Because hydronephrosis is a normal finding in the majority of pregnancies, its presence cannot be taken as a sign of a possible ureteral stone. Ultrasound is an unreliable way of diagnosing the presence of stones in pregnant (and in nonpregnant) women.

In a series of pregnant women, ultrasound had a sensitivity of 34% (i.e. it misses 66% of stones) and a specificity of 86% for detecting an abnormality in the presence of a stone (i.e., false-positive rate of 14%).1

1 Stothers L, Lee LM (1992). Renal colic in pregnancy. J Urol 148:1383–1387.

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