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Ovid: Oxford Handbook of Urology

Authors: Reynard, John; Brewster, Simon; Biers, Suzanne Title: Oxford Handbook of Urology, 1st Edition Copyright ©2006 Oxford University Press > Table of Contents > Chapter 15 – Urological problems in pregnancy Chapter 15 Urological problems in pregnancy P.518
Physiological and anatomical changes in the urinary tract Kidney

  • Renal size enlarges by 1cm, secondary to increased interstitial volume and distended renal vasculature.
  • Renal plasma flow rate (RPF) increases early in the 1st 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-h 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 centre resulting in reduced PCO2.

Bladder

  • Bladder displacement occurs (superiorly and anteriorly) due to the enlarging uterus. The bladder becomes hyperaemic, and raised oestrogen levels cause hyperplasia of muscle and connective tissues. Bladder pressures can increase over pregnancy (from 8 to 20cmH2O), 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 3rd 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.1 It is partly caused by placental production of peptide hormones (relaxin), which induces collagen remodelling and consequent softening of tissues of the birth canal. Infant weight, duration of 1st and 2nd stages of labour (vaginal delivery), and instrumental delivery (ventouse extraction or forceps delivery) increase risks of post-partum2 stress incontinence.
Table 15.1 Biochemistry reference intervals
Substance Non-pregnant 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

Footnotes 1 Parity—pregnancies that result in delivery beyond 28 weeks’ gestation. 2 Post partum—after delivery of the child. P.519
P.520
Urinary tract infection (UTI) Definition UTI describes a bacterial infection of the urine with >105 colony forming units(cfu)/ml (or >102cfu/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 Previous history of recurrent UTIs; pre-existing vesicoureteric reflux. Physiological changes in pregnancy include hydronephrosis with decreased ureteral peristalsis causing urinary stasis. Up to 75% of pyelonephritis occurs in the 3rd 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 pre-term delivery, low fetal birth weight, and maternal anaemia. Screening tests Midstream urine specimen (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 which 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 1st and 2nd trimesters only. Repeat urine cultures after treatment to check 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.

Table 15.2 Antibiotics to avoid in pregnancy*
Trimester Antibiotic Risk in pregnancy
1,2,3 Tetracyclines Fetal malformation; maternal hepatotoxicity; dental discolouration
Quinolones Arthropathy
1 Trimethoprim Teratogenic risk (folate antagonist)
2,3 Aminoglycosides Auditory or vestibular nerve damage
3 Chloramphenicol Neonatal ‘grey’ syndrome
Sulphonamides Neonatal haemolysis; methaemoglobinaemia
Nitrofurantoin Maternal or neonatal haemolysis (if used at term), in subjects with G6PD deficiency
* See British National Formulary (BNF), appendix 4, for full details.

P.521
P.522
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 to mechanical obstruction from the enlarging fetus and uterus, which compress 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 ureteric 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 non-pregnant patient, the presence of hydronephrosis is taken as surrogate evidence of ureteric obstruction. Because hydronephrosis is a normal finding in the majority of pregancies, its presence cannot be taken as a sign of a possible ureteric stone. Ultrasound is an unreliable way of diagnosing the presence of stones in pregnant (and in non-pregnant) 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 +ve rate of 14%).1 References 1 Stothers L, Lee LM (1992) Renal colic in pregnancy. J Urol 148:1383–87.

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