Several urological changes can occur during and after pregnancy. These include:
- an increase in RPF and GFR reaching a maximum in the second trimester (9-11 weeks) (Dafnis 1992).
- an increase in renal size (1 cm length) and parenchymal volume and an associated increase in intrarenal fluid.
- an increase in filtered solutes such as calcium and uric acid. Calcium excretion increases up to twice its normal concentration and there is increased 1,25diOH D3 which results in a higher GI absorption. Renal tubular re-absorption of calcium is reduced.
- an increase in urinary citrate and magnesium.
- respiratory alkalosis which leads to relatively alkaline urine inhibiting uric acid stone formation.
- hydronephrosis (90%) which usually starts 6-10 weeks after delivery. The right kidney is often more greatly affected than the left (Schulman 1975). An early effect is that progesterone affects urinary tract smooth muscle causing dilation and reducing peristalsis of the ureter. A late effect is the compression of the gravid uterus. The left side is protected by the sigmoid colon.
- an increased incidence of VUR (3.5%) that is greatest in the third trimester.
- the bladder mucosa becomes hyperaemic and the urethra lengthens marginally.
- the bladder capacity increases in the 2nd trimester due to progesterone and decreases again in the 3rd trimester because of uterine compression.
- a vaginal delivery is associated with partial denervation of the pelvic floor and tears in the endopelvic fascia (new collagen replacement is intrinsically weaker).
Frequency and nocturia icrease throughout gestation (nulliparous > multiparous) leading to an overall icrease in urine output. Urgency occurs in 60% of pregnant women and 10-19% have urge incontinence in the 3rd trimester (Stanton 1980). Urodynamics' studies show that 24% may develop detrusor instability (due to progesterone) and there is reduced compliance in 31% (Cutner 1996). Both urge incontinence and DI usually resolve after delivery.
A poor stream is seen in 25% of women and 30% may have incomplete emptying (subjective only). Acute retention is uncommon but may be due to an impacted uterus. This can be managed with a Hodge pessary. Postpartum retention can be relieved with an epidural.
Around 30-60% of women have stress incontinence during pregnancy (Stanton1980; Francis 1960) and up to 34% have stress incontinence 3 months after delivery (8.5% requiring pads). Factors that may increase the risk of stress incontinence during pregnancy are: obesity, more than 4 deliveries and vaginal delivery. Pelvic floor exercises and LSCS can help prevent stress incontinence during and after pregnancy (Wilson 1996).
This occurs in 2-8% of pregnancies. Risk factors include diabetes, previous UTI, lower SE class and sickle cell disease. If it persists it may develop into pyelonephritis in 36-57% (Little 1965; McFayden 1968). It may also be associated with prematurity and low birth weight (Elder 1971), and pre-eclampsia (Savage 1967).
Antenatal screening for M, C and S at the booking visit is most effective. Escherichia coli is found in 75-90%, but Klebsiella, Proteus, Pseudomonas spp. and Staphylococcus epidermidis are also common. Antibiotics that can be used which are safe in pregnancy are Amoxycillin and Cephalexin. Ones to avoid are Trimethoprim in the first trimester (a folate antagonist), Sulphonamides/Nitrofuratoin in the third trimester and Quinolones throughout preganancy. Often a single dose is as effective as a 5-7 day course and has a 70% cure rate. Any persistence or recurrence should be treated with antibiotic prophylaxis and investigated with USS/KUB if it continues to occur more than 12 weeks after delivery.
This can occur in 1-2% of pregnancies (Gilstrap 1981). It is most associated with pre-term labour.
The incidence of renal calculi in pregnant women is about 1 in 1000 pregnancies (Stothers 1992) and is similar to that in non-pregnant women. Symptoms include renal colic and microscopic/macroscopic haematuria, but pain localisation is altered. The majority present in their 2nd or 3rd trimester. Diagnosis is differential, from appendicitis to choleccystitis, pyelonephritis and abruption.
Ultrasound, magnetic resonance urography and IVU can all be used to diagnose renal calculi:
The sensitivity and specificity of ultrasound is improved if doppler USS is used. A resistive index of greater than 0.70 in the intrarenal arteries is suggestive of an obstruction (Hertzberg 1993). Colour doppler USS can also be used (Dubbins 1981), however, this can appear to be normal when there is a low-grade obstruction (Burge 1991).
Heavily T2-weighted fast spin-echo pulse sequences are used along with diuresis. The advantage of this method is that there is no radiation exposure although it should still not be carried out in the first trimester. It can also differentiate between a pathological obstruction and physiological dilation (Roy 1995).
This requires exposure to radiation and is therefore risky, particularly in early pregnancy. It may increase the risk of terogenicity, microcephaly and mental retardation in the foetus. There is also a small increased risk of childhood cancer of between 1 in 5000 and 1 in 40,000 per mGy (Gorton & Whitfield 1997).
For a definitive diagnosis of renal calculi however it may be necessary to perform IVU. For example, 2 out of 3 pregnant women with stones were diagnosed as normal or as having hydronephrosis of pregnancy when USS was used (Stothers & Lee 1992). According to Boridy (1996), limited IVU-1 of 15 minutes (± delayed film) is adequate. No adverse problems with contrast media have been reported.
This can be achieved with hydration and bed rest analgesia. Results show that after this up to 60% pass the stones spontaneously. Pethidine analgesia is successful although codeine should be avoided in the 1st trimester and NSAID in the 3rd.
Despite the overall success of hydration and anlagesia 30% still need some form of intervention:
- retrograde stenting - this can be performed under local anaesthetic with USS control (Jarrad 1993). However, there may be problems with encrustation due to hypercalcuria of pregnancy (Goldfarb 1989).
- percutaneous nephrostomy - this is the technique of choice when there is associated urosepsis and in women less than 22 weeks gestation in order to reduce the risk of encrustation (Denstedt 1992).
- ureteroscopic lithopaxy - this can be carried out using a 7-9.5 Fr ureteroscope. A full ureteroscopy to the renal pelvis is possible (Ulvik 1995) and basket extraction or pneumatic/laser intracorporeal lithotripsy is safe. However, there is a theoretical risk of anaesthesia (Maze 1989). Extracorporeal shock wave lithotripsy is contra-indicated in pregnancy.
Drugs to avoid are allopurinol and penicillamine, although a low dose of penicillamine can be given after the 1st trimester if necessary (Gregory 1983). Fluid intake should be increased to 2.5 - 3 litres per day and the urine should be alkanised in the case of uric acid or cysteine stones. A metabolic screen can be carried out 3 months after delivery.
(Cr < 120 mmol/l)
This results in no permanent deterioration in renal function (Gorton 1998) but there is an increased risk of premature birth, low birth-weight and pre-eclampsia. There is also higher perinatal mortality. However, 94% of pregnancies go on to produce a live birth.
(Cr > 120 mmol/l)
This has a 90% fetal survival rate but at the expense of a 40% deterioration in renal function, of which 23% will progress to ESRF (Jones 1996). If the Cr is greater than 250 mmol/l the risk to the mother is greater than the chance of the foetus surviving. However, hypertensive control can improve fetal survival as can early dialysis (urea > 20 mmol/l can damage the fetus). Peritoneal dialysis may be better in these cases than haemodialysis. And erythropoietin is safe in pregnancy.
Pregnancy should be avoided for at least 2 years after the transplant. During pregnancy 40% may develop proteinuria (but this is insignificant if there is no hypertension) and rejection of the transplant may occur in 9%. There may also be impairment of renal function which may go on to persist after the delivery. However, the immunosuppression requirement may go down. Drugs that are commonly used are Prednisolene (but there is a risk of fetal adrenocortical insufficiency), Azathioprine (this has a theoretical teratogenic effect - seen with high doses in rats) and Cyclsporin. Vaginal deliveries and LSCS's are usually possible.
Staging should be carried out with USS and MRI and the timing of surgery is particularly important either in the 1st trimester to allow termination or in the 3rd trimester if there is a viable fetus. Radiotherapy is not advised. However, a modified regime of chemotherapy can be given. Bleomycin, vincristine and vinblastine are relatively safe after the 1st trimester.
Urological tumours are rare. However, there have been 50 described cases of renal cell carcinoma which may mimic recurrent UTI. Angiomyolipoma appears to grow rapidly in pregnancy with increased risk of rupture (Fernandez 1994). There have been 21 cases of TCC bladder (mainly superficial), but these may present as 'vaginal bleeding'. A flexible cystoscopy is safe at any stage. For a superficial TCC, a TURBT should be performed followed up by a cystoscopy after birth. For a TCC of greater than GIII T1 the prognosis is poor. If it occurs in the 1st/2nd trimester the pregnancy should be terminated and radical cystectomy and radiotherapy carried out. If it occurs in the 3rd trimester a LSCS should be performed followed by radical cystectomy.
Phaeochromocytoma occurs in 1 in 54,000 pregnancies (Antonelli 1996) and 2/3 present in the 3rd trimester. Fetal mortality usually occurs in around 15%. Cases may present as pre-eclampsia (severe paroxysmal hypertension). They may also show raised urinary catecholamines. Phaeochromocytomas can be localised by USS and NMR and can be surgically removed in the 1st and 3rd trimesters after BP control with a and b blockade. During the 2nd trimester it should be managed conservatively. Delivery by LSCS is recommended to avoid increasing intra-abdominal pressure (Pattison 1990).
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