Introduction
There are many physiologic adaptations a woman undergoes during the course of a routine pregnancy. In most obstetric textbooks, much attention is focused on the physiologic changes in the cardiovascular, hematologic, renal, and immunologic systems, and anatomic changes in the uterus and the growing fetus and placenta. There are also anatomic and physiologic changes in the lower genitourinary tract and pelvic floor support. The subsequent process of both labor and delivery also impart significant changes, especially to the pelvic floor support.
To whom are these changes significant? Which woman will evidence the symptoms of pelvic floor disorders (PFDs), about which this textbook is dedicated? Nearly 100 years ago, (in his argument espousing more liberal use of forceps, it must be pointed out), DeLee wrote:
Labor has been called, and still is believed by many to be, a normal function … and yet it is a decidedly pathologic process. Everything, of course, depends on what we define as normal. If a woman falls on a pitchfork, and drives the handle through her perineum, we call that pathologic-abnormal, but if a large baby is driven through the pelvic floor, we say that it is natural, and therefore normal.
This chapter discusses the relevant changes that occur with pregnancy and following delivery, and how they may affect the development of PFDs.
Alterations of Pelvic Floor Anatomy and Physiology in Pregnancy
Pelvic Floor Support
As pointed out in Chapter 2 , interactions between the pelvic floor muscles and connective tissue attachments provide the support to the pelvic organs. Probably as a result of hormonal changes, there are significant adaptations to prepare the pelvic floor and birth passage for the events of labor and delivery. Clinical evidence of this has been observed using the standardized pelvic organ prolapse (POPQ) system. found that nulliparous pregnant women were more likely to have mild pelvic organ prolapse (POP) than their nulligravid counterparts.
Consistent with the clinical changes noted earlier, molecular and histologic studies of vaginal tissues have demonstrated increased amounts of extracellular matrix material in the fibromuscular layers. Collagen becomes less densely packed, and smooth muscle cells revert to noncontractile phenotypes ( ). The result of these changes is increased distensibility of the vagina, presumably to allow for genital stretching during parturition ( ).
The advent of genetically engineered knockout mouse models (LOXL-1 and FBN-5) have provided more insight for changes in elastin homeostasis during pregnancy, and the potential that the mechanisms responsible for the regeneration of the elastic properties of the vagina may be deranged in those animals who develop prolapse as well as other PFD postpartum.
Urinary Tract in Pregnancy
The kidneys and urinary tract play a major role in maternal adaptation to pregnancy. Consequently, observed differences in function cannot be judged by nonpregnant standards. The renal system increases in size and capacity during pregnancy. Anatomic changes involving the urinary tract begin during the first trimester of pregnancy and can persist up to 16 weeks postpartum.
The most striking anatomic change in the urinary tract is dilation of the ureters ( Fig. 16.1 ). Bilateral dilation of the calyces, renal pelvis, and ureters can be seen early during the first trimester and is present in 90% of women during the late third trimester or early puerperium. The changes are usually more prominent on the right and may persist for 3 to 4 months. In 11% of women, ureteral dilation persists indefinitely ( ). In addition, there is reduced ureteral peristalsis compared with the nonpregnant state.
Vesicoureteral reflux is a sporadic, transient occurrence during pregnancy and has been demonstrated radiologically in 3.5% of pregnant women. The enlarging uterus displaces the ureters laterally, and the intravesical ureters are shortened and enter the bladder perpendicularly rather than obliquely. Consequently, the ureterovesical junction is less efficient in preventing reflux. This increased incidence of reflux may explain the high incidence of pyelonephritis during pregnancy; however, this association has not been confirmed. The transitory nature of vesicoureteral reflux, and the necessary exposure to X-rays for study purposes, hinder adequate evaluation of the problem. Nevertheless, vesicoureteral reflux probably plays only a small role in symptomatic or asymptomatic urinary tract infection (UTI).
Renal blood flow is usually assessed by r-aminohippurate clearance, which measures effective renal plasma flow (ERPF). ERPF increases significantly during pregnancy. It reaches a peak increment during the mid trimester of 50% to 85% and then shows a small decline during the third trimester. ERPF and glomerular filtration rate (GFR) in pregnancy are affected markedly by posture, and are maximal when the pregnant woman lies on her side. Normal pregnancy is associated with plasma volume expansion and an increase in the GFR of 40% to 65% (measured by insulin clearance) and a decrease in GFR of approximately 15% to 20% late during the third trimester. The mechanisms responsible for the increase in GFR, plasma volume, and renal plasma flow rate are unknown.
Tests of renal function during pregnancy must be interpreted in relation to the changes in plasma volume, glomerular filtration, and tubular reabsorption that normally occur with advancing gestation. Many of the commonly used tests of function yield lower results in pregnancy than in the nonpregnant state. Consequently, values that may be regarded as normal during the nonpregnant state may well indicate renal dysfunction in pregnancy.
Uric acid, blood urea nitrogen (BUN), and serum creatinine levels are crude indices of renal function. In pregnancy, plasma uric acid usually decreases by 25% beginning during the first trimester, and increases during the third trimester. Upper normal limits of plasma uric acid levels are 5 to 5.5 mg/dL during pregnancy. Levels are influenced by race, multiple gestation, and time of day sampled, with higher levels in the morning. An indicator of renal filtration, the BUN normally decreases from nonpregnant levels of 12 mg/dL (4.3 mmol/L) to 9 mg/dL (3.2 mmol/L), and plasma creatinine levels decline from a nonpregnant mean value of 0.7 mg/dL (62 mmol/L) to 0.5 mg/dL (44 mmol/L). If the plasma creatinine level exceeds 0.9 mg/dL or if the BUN is greater than 14 mg/dL at any stage during pregnancy, renal dysfunction should be suspected and more detailed investigation should be performed.
Twenty-four-hour creatinine clearance is the best clinical measurement of GFR. By week 8 of pregnancy, the creatinine clearance rate normally increases by 45% and remains elevated during the second trimester. During the final weeks of pregnancy, creatinine clearance usually declines to near-nonpregnant levels.
Urinalysis is essentially unchanged during pregnancy. However, many variables can affect the results. Normal kidneys should be able to concentrate urine to a specific gravity of 1.026 or more, and to dilute urine to a value less than 1.005. During pregnancy, posture affects urine concentration and specific gravity.
In addition to the ERPF, the capacity of the urinary tract increases during pregnancy. Bladder volume during pregnancy increases to 450 to 650 mL, compared with 400 mL in nonpregnant control subjects ( Table 16.1 ). The hydronephrotic ureters can hold as much as 200 mL extra urine; however, no changes appear in the contraction patterns on retrograde cystometry. Depending on maternal position, uterine size, and position of the fetus, the functional volume of the bladder and ureters is dynamic during the third trimester. This increased functional volume, coupled with high urine flows (especially with fluid mobilization at night), causes polyuria and nocturia in most pregnant women.
| First Trimester | Second Trimester | Third Trimester | Postpartum | |
|---|---|---|---|---|
| Symptom Frequency | ||||
| Day ≥7 | 45% | 61% | 96% | 17% |
| Night ≥2 | 22% | 39% | 64% | 6% |
| Incontinence | ||||
| Stress | 30% | 31% | 85% | 6% |
| Urge | 4% | 13% | 2% | 8% |
| Hesitancy | 24% | 28% | 22% | 9% |
| Measurement | ||||
| Urine output (mL) | 1917 | 2020 | 1820 | 1475 |
| Bladder capacity (mL) | 410 | 460 | 272 | 410 |
| Functional urethral length (mm) | 30.3 ± 4.6 | 35.1 ± 5.1 | 27.6 ± 3.7 | |
| Bladder pressure (cm H 2 O) | 9 ± 3 | 20 ± 3 | 9 ± 2 | |
| Closure pressure (cm H 2 O) | 61 ± 14 | 73 ± 18 | 60 ± 14 | |
The etiology of ureteral and bladder dilation generates much discussion. Sharp termination of the ureteral dilation at the pelvic brim seen on intravenous pyelogram (IVP) suggests an obstruction. When a woman is upright or supine, as during the filming of an IVP, the pregnant uterus compresses the ureter against the pelvic rim and its overlying iliac vessels. On the left side, the ureter is somewhat protected by the iliac arteries and sigmoid colon and, as a result, is usually less dilated than the right ureter. Although mechanical obstruction plays a major role in ureteral dilation during pregnancy, the relative infrequency of ureteral obstruction by large ovarian tumors or fibroids in nonpregnant women suggests additional factors. In addition, high urine production, as occurs in diabetes insipidus or pregnancy, is also associated with urinary tract dilation.
In the past, the elevated progesterone levels that accompany pregnancy were thought to cause smooth muscle relaxation and subsequent hypotonicity and hypomotility of the ureter—defects that would contribute to ureteral dilation. Contrary to the latter observation, the large doses of synthetic progesterone used in cancer chemotherapy do not cause ureteral dilation. Measurements of ureteral tone during pregnancy reveal an increase in ureteral tone and no decrease in frequency or amplitude of ureteral contractions. Histologic study of the ureters of pregnant animals reveals smooth muscle hypertrophy and hyperplasia of the connective tissue. Thus, progesterone probably plays a small role in ureteral dilation during pregnancy.
Urinary Tract Conditions during Pregnancy
Urinary Retention
Occasionally, the enlarging uterus completely obstructs both ureters and causes azotemia. Patients usually present during the early second trimester with a retroverted uterus (perhaps incarcerated), flank pain, and minimal signs of infection. The differential diagnosis includes pyelonephritis, renal calculi, or papillary necrosis. Serum creatinine is elevated (3.8-11.6 mL/dL), but urinary sediment does not indicate intrinsic renal disease or prerenal azotemia. The diagnosis is confirmed by IVP or renal ultrasound. In this case, treatment requires bimanual manipulation of the uterus out of the sacral hollow. Some have recommended the use of a Smith-Hodge pessary to maintain anteversion of the uterus. Other risk factors for obstruction include previous urologic surgery, unilateral absence of a kidney, polyhydramnios, multiple gestation, and ovarian or uterine neoplasia.
Occasionally, third-trimester retention can develop. Ultimately, delivery relieves the obstruction, and postpartum recovery is complete. In cases remote from term, fetal risk from preterm delivery outweighs the risks of urologic management. Conservative management for 12 to 24 hours is warranted before more aggressive therapy is initiated, including amniocentesis (in cases with polyhydramnios), cystoscopically-placed ureteral stents, or percutaneous nephrostomy under ultrasound guidance.
Urinary Incontinence
As shown in Table 16.1 , the symptoms of frequency, nocturia, and incontinence all increase during in the first trimester, and increase during the course of the pregnancy. Part of this change is a result of the increase in glomerular flow described earlier. Stress incontinence is more common than urge incontinence or overactive bladder symptoms, but mixed symptoms are common. For those who do have incontinence rather than frequency alone, their quality of life is affected significantly more. The few urodynamic studies that have been done during pregnancy demonstrate that bladder capacity increases throughout gestation, and functional urethral length and closure pressures may increase, but urinary symptoms and urodynamic findings do not always correlate well. Treatment of incontinence during pregnancy is typically pelvic floor rehabilitation. Although oxybutynin has been assigned a category B rating during pregnancy, most providers would not initiate anticholinergic treatment as a first-line agent, recognizing that many of the previously described urinary symptoms will change after delivery.
Asymptomatic Bacteriuria
The cohort of women with chronic, episodic asymptomatic bacteriuria is identified by routine screening of urine cultures at the first prenatal visit. The prevalence of asymptomatic bacteriuria (two or more cultures at ≥10 5 cfu/mL) is increased by prior renal or urinary tract disease, diabetes, sickle cell trait or disease, poor hygiene, high parity, increased age, and lower socioeconomic status. The overall prevalence varies between 1.9% and 11.8%, with the lowest prevalence in primiparous patients of the upper socioeconomic class and the highest among indigent multiparas. Although most women with asymptomatic bacteriuria are identified shortly after entering prenatal care, approximately 1% to 2% acquires bacteriuria later during pregnancy.
Because of the more significant concerns of worsening obstetric outcomes associated with an escalation to acute cystitis or pyelonephritis and because the positive predictive values of culture-independent tests (i.e., dipstick urinalysis) drop precipitously with low prevalence, they should not be used for diagnosis in the pregnant population. On the other hand, the negative predictive value is 98% or more with any of these tests. In a low-risk population, urine testing for leukocyte esterase and nitrite on a clean-catch, first-void midstream specimen can supplant urine culture. In high-risk groups ( Box 16.1 ), a culture should be obtained each trimester.
- •
Diabetes
- •
Sickle cell disease or trait
- •
Urinary tract abnormalities
- •
Müllerian duct abnormalities
- •
Renal disease
- •
Urolithiasis
- •
Hypertensive diseases
- •
Chronic analgesic use
- •
Genitourinary group B Streptococcus
- •
History of urinary tract infections
- •
Severe ureteral reflux
- •
Urinary infections as a child younger than 4 years old
The association between preterm birth and asymptomatic bacteriuria was first identified by Elder, Kass, and others at Boston City Hospital between 1955 and 1960. This initial study reported that 32 of 179 (17.8%) patients with bacteriuria delivered low-birth weight (LBW) infants, whereas 88 of 1000 (8.8%) patients without bacteriuria delivered LBW infants. reviewed 19 studies that related bacteriuria to LBW infants. In these studies, 3619 pregnant women with bacteriuria delivered 400 (11%; range, 4.4%-23%) LBW infants. In these same studies, 31,277 women without bacteriuria delivered 2725 (8.7%; range, 3%-13.5%) LBW infants. In 1989, Romero et al. performed a meta-analysis on the relationship between asymptomatic bacteriuria and LBW. Eight randomized clinical trials of antibiotic therapy showed a significant reduction in the frequency of LBW after antibiotic therapy (typical relative risk (RR) of 0.56, with a 95% confidence interval (CI) of 0.43-0.73). It is unclear whether the benefit from antibiotics results from a reduction in asymptomatic or symptomatic pyelonephritis, or from beneficial changes in abnormal genital tract flora, which is associated with LBW.
The association between asymptomatic bacteriuria and other adverse pregnancy outcomes (hypertension, anemia, chronic renal disease, and fetal neuropathology) is controversial, being both supported and refuted by different cohort studies. Between 25% and 50% of pregnant women with asymptomatic bacteriuria have evidence of asymptomatic renal involvement, and these women are twice as likely to relapse within 2 weeks after therapy as women with bladder bacteriuria alone. Asymptomatic renal infection has been associated with decreased creatinine clearance, intrauterine growth retardation, and maternal hypertension. On the other hand, failed to note a difference in outcomes between asymptomatic women with and without renal infection, as defined by fluorescent antibody testing ( Table 16.2 ).
| Infection | Incidence (%) |
|---|---|
| Asymptomatic bacteriuria | 2–11 |
| Acute cystitis | 1–4 |
| Acute pyelonephritis | 1–2 |
A variety of antimicrobial agents and treatment regimens have been used to treat asymptomatic bacteriuria during pregnancy. Most community-acquired pathogens associated with asymptomatic bacteriuria during pregnancy are sensitive to sulfa drugs (sulfisoxazole, 1 g four times a day (qid) for 7-10 days), nitrofurantoin (100 mg twice daily for 7-10 days), or cephalosporins (cephalexin, 500 mg qid for 7-10 days). Ampicillin (500 mg qid for 7-10 days) is a time-honored, safe, and inexpensive therapy; however, there are a growing number of resistant Escherichia coli strains ( Table 16.3 ). Other antibiotics should be used. A Cochrane Review supported the extended treatment duration rather than single-dose regimens ( ).
| Organism | Percentage |
|---|---|
| Escherichia coli | 60-80 |
| Klebsiella pneumoniae-Enterobacter | 3-5 |
| Proteus sp. | 1-5 |
| Streptococcus faecalis | 1-4 |
| Group B Streptococcus | 4-8 |
| Staphylococcus saprophyticus | 1-3 |
Between 20% and 30% of women who have bacteriuria during pregnancy will have bacteriuria on long-term follow-up cultures when not pregnant. Radiologic examination at follow-up of women who had bacteriuria during pregnancy revealed abnormalities in 316 of 777 women (41%; range, 5%-75%). Chronic pyelonephritis was the most common radiologic diagnosis (47% of abnormalities). The incidence of bacteriuria during first pregnancies was significantly greater in women with (47%) than without (27%) renal scarring from childhood urinary infections. Similar control subjects who had not had childhood urinary infections had an incidence of 2%.
Acute Cystitis
Acute cystitis occurs in 1% to 4% of pregnancies. The reported frequency is only minimally greater than the frequency of cystitis in sexually active nonpregnant women. Unfortunately, the diagnosis is more difficult to make during pregnancy. Most pregnant women have urgency, frequency, or suprapubic discomfort. Suprapubic discomfort in pregnancy often results from pressure from the presenting fetal part or early labor. Nevertheless, suprapubic discomfort from cystitis is unique, and most women with a history of acute cystitis can discriminate accurately between cystitis and pregnancy-related discomfort. The most reliable findings are dysuria and hematuria. Acute dysuria may also result from labial or perivaginal irritation from vaginitis, vulvitis, herpes simplex, condylomata acuminatum, or genital ulcers. Because of the separate pregnancy risks encumbered with these factors, an inspection of the vulva and vagina is warranted in patients with acute cystitis during pregnancy.
Preterm labor and threatening second-trimester loss often present with signs and symptoms similar to those of acute cystitis. As the lower uterine segment expands and the presenting fetal part descends, hesitancy, urgency, frequency, and suprapubic discomfort occur. A bloody vaginal discharge may contaminate and confuse urine testing, and may lead to misdiagnosis of UTI. Pelvic examination is warranted in patients presenting with signs and symptoms of lower UTI to rule out preterm labor.
The pathophysiology of acute cystitis is more similar to that of asymptomatic bacteriuria than pyelonephritis. Acute cystitis has sociodemographic and behavioral risk factors similar to those of asymptomatic bacteriuria. Enterobacteriaceae, especially E. coli, are the most common uropathogens. Acute cystitis is associated with a high prevalence of uropathogens in the periurethral flora. E. coli serotypes are associated with more epithelial cell adherence, hence virulence, than fecal strains. Antibody-coated bacteria, indicative of renal infection, are present in only 5% of acute cystitis, compared with 45% for asymptomatic bacteriuria and 65% for acute pyelonephritis. This difference may result from earlier identification and treatment of the patient with these latter conditions because of the intense discomfort that accompanies cystitis.
Treatment of acute cystitis is similar to that of asymptomatic bacteriuria: nitrofurantoin, a cephalosporin, or a sulfonamide. Because these patients are symptomatic, therapy is initiated as soon as a midstream, clean-catch urine culture has been obtained. A test-of-cure culture is obtained within 2 weeks after therapy is complete. Between 10% and 20% have a positive test-of-cure culture, representing a relapse. These women should be retreated with another antibiotic, as determined by bacterial sensitivities. After retreatment, these patients should be placed on suppressive antibiotic therapy. Without suppressive therapy, an additional 20% to 30% of women develop another UTI—a reinfection—during the remainder of their pregnancies and puerperia. Because of the risk of recurrence, patients with cystitis should be monitored intensively, with a urine screen biweekly for nitrite and leukocyte esterase.
Acute Pyelonephritis
Acute pyelonephritis is the most common serious medical complication of pregnancy. The modern incidence of pyelonephritis is 1% to 2%. Often, these patients present for prenatal care late during pregnancy with the signs and symptoms of pyelonephritis. Only 40% to 67% of cases of pyelonephritis occur in patients with a known history of asymptomatic bacteriuria. Three-fourths of women with pyelonephritis present in the antepartum period, 5% to 10% during labor, and 15% to 20% postpartum. Antepartum pyelonephritis occurs mainly after the first trimester: 10% to 20% during the first trimester, 45% to 70% during the second trimester, and 8% to 45% during the third trimester. The predominance of pyelonephritis during late pregnancy and the puerperium likely relates to the partial obstruction caused by the growing uterus and to trauma or interventions at birth.
The diagnosis of acute pyelonephritis is based on clinical presentation: a temperature of 38 °C or more, costovertebral angle tenderness, and either bacteriuria or pyuria. Enterobacteriaceae cause a majority of the cases of pyelonephritis: E. coli , 70% to 80%; Klebsiella-enterobacter spp., 5%; Proteus sp., 2% to 4%; and gram-positive organisms inducing group B Streptococcus , 10%. Blood cultures are positive in 17% of cases. Infection of the kidney may have an effect on function. Two percent have a serum creatinine greater than 1.1 mg/dL. This dysfunction is a direct result of endotoxic injury to both kidneys. After appropriate antibiotic treatment, renal function returns to normal by 3 to 8 weeks.
Endotoxins produced by Enterobacteriaceae have adverse consequences on multiple organ systems as well as the kidneys. The injuries include thermoregulatory instability (fever and chills), destruction of blood cells (leukocytopenia, thrombocytopenia, anemia), hypercoagulability (disseminated intervascular coagulation), endothelial injury (adult respiratory distress syndrome), cardiomyopathy (pulmonary edema), and myometrial irritability (preterm labor).
Overt septic shock or adult respiratory distress syndrome occurs in 1% to 2% of pregnant women with acute pyelonephritis. Clinical clues to the development of these life-threatening complications are leukocytopenia (<6000 cells/mL 2 ), hypothermia (≤35 °C), elevated respiratory rate, and widened pulse pressure. During the late stages, hypothermia, mental confusion, and symptomatic hyperstimulation of the sympathetic nervous system (cold, clammy extremities) herald a scenario that often leads to maternal or fetal death.
Most pregnant women with pyelonephritis (and all pregnant women greater than 24 weeks’ gestation) should be hospitalized because of the additional fetal and maternal risks of acute pyelonephritis in pregnancy. Appropriate broad spectrum antibiotics should be initiated as soon as possible after urine and blood cultures are obtained. Antibiotic therapy should be continued until the patient is afebrile (<37 °C) for more than 24 h. The patient should finish a 14-day course of antibiotics with oral medication. A test-of-cure urine culture should be performed 2 weeks after therapy. Reinfection is common in these patients; 20% have asymptomatic bacteriuria and 23% have recurrent pyelonephritis. Frequent surveillance (nitrite/leukocyte esterase testing biweekly) or suppressive antibiotic therapy (nitrofurantoin, 100 mg every night at bedtime) is warranted. With either regimen, the risk of recurrent pyelonephritis is less than 10%.
Because many patients are dehydrated as a result of nausea and vomiting, careful rehydration is started. The degree of endothelial damage in the lungs may not be apparent, so careful attention to fluid intake and output, and vital signs, especially respiratory rate, is imperative.
Endotoxins stimulate cytokine and prostaglandin production by decidual macrophages and fetal membranes. The ensuing preterm contractions raise concern for preterm birth. In the past, preterm labor and delivery were reported to be a common finding in women with pyelonephritis; however, data in 440 cases reported by found a rate of only 5%.
The differential diagnosis in patients with persistent fever and costovertebral angle tenderness at 72 h of therapy includes a resistant organism, urolithiasis, renal abscess, complete ureteral obstruction, or another source of infection (e.g., appendicitis or intra-amniotic infection). A radiologic evaluation of the urinary tract is warranted after reexamination of the patient and review of culture and sensitivity reports. Many radiologists have undue concern regarding the fetal dangers of IVPs during pregnancy and advocate renal ultrasound. A renal ultrasound is useful for evaluating renal abscess, but not for evaluating function or ureteral abnormalities—the more common issues associated with antibiotic failure. A “one-shot” IVP (no plain film and one 20-min film) is appropriate.
Urolithiasis
Urolithiasis occurs in 0.03% to 0.9% of pregnancies, usually in the last two trimesters. Between 20% and 40% of women with urolithiasis during pregnancy have a history of stone disease. Although pregnancy does not appear to increase the risk of urolithiasis during any 9-month period in susceptible persons, recurrent urolithiasis may indicate primary renal disease (medullary sponge kidney), transport diseases (renal tubular acidosis), or metabolic diseases (hyperparathyroidism). The fetal or maternal risk may reflect these systemic diseases rather than urolithiasis alone.
Most stones (70%) pass during the second or third trimester, with equal distribution between the right and left sides. The presentation is more obscure during pregnancy; the most common signs being severe flank pain (80%) with radiation to the groin or lower abdomen, nausea, and vomiting. Renal colic is less common after the first trimester because of ureteral dilation. Likewise, gross hematuria is less common (23%), but microscopic hematuria occurs in 60% to 90% of patients. Bacteriuria may be present in 80%.
The differential diagnosis includes premature labor, appendicitis, and, most commonly, pyelonephritis. Premature labor is diagnosed by contractions and cervical dilation. Urolithiasis is more likely than appendicitis when the patient has no fever, the abdominal pain is not localized to the right lower quadrant, and no peritoneal signs are present. The most difficult differentiation is between pyelonephritis and urolithiasis. Indeed, they may coexist.
IVP is the diagnostic technique of choice. In pregnancy, the protocol and frequency of IVP are curtailed. The IVP should be limited to a 20-min film and, if there is delayed excretion, a 60-min film. Fluoroscopy is used only in very exceptional circumstances. An IVP is indicated when the patient has renal colic and gross hematuria, persistent fever or a positive culture after 48 h of parenteral antibiotic therapy, persistent nausea and vomiting after 48 h of conservative therapy, or evidence of a complete obstruction (e.g., increasing levels of BUN and serum creatinine).
Transabdominal or transvaginal ultrasound often is the first diagnostic choice of radiologists. Their concern is the 0.4 to 1 rad of radiation the fetus receives with a limited IVP. There is concern that doses this low may double childhood cancer rates. Although ultrasound is a good diagnostic tool for renal abnormalities and ureteral dilation, its sensitivity is 34%, with an 86% specificity for the detection of an abnormality in the presence of a stone in a symptomatic patient. In one study, renal ultrasound was used as the primary diagnostic test in 35 of 56 women, but calculi were detected in only 21 (60%) of these women ( ). IVP is clearly more efficacious for diagnosis of distal stones.
Urolithiasis in pregnancy is treated conservatively with bed rest, hydration, and analgesics. Seventy percent of patients pass the stone spontaneously. Urolithiasis during pregnancy does not increase the likelihood of abortion, prematurity, or hypertension, but the incidence of symptomatic urinary tract disease is greater in pregnancies complicated by a history of urolithiasis (20%-65%), potentially leading to an increased rate of preterm rupture of membranes. Parenteral antibiotics (cefazolin 2 g IV q6h) are added to conservative management when infection is likely.
When conservative management is unsuccessful (complete obstruction, persistent pain, or sepsis), surgical intervention is indicated. The choice of procedure depends on the size and location of the stone. The usual procedures include basket extraction or retrograde stent placement at cystoscopy. Percutaneous nephrostomy under ultrasound guidance has also been used as a temporizing procedure. Rarely and with considerably more fetal and maternal morbidity, ureterolithotomy, pyelolithotomy/pyelotomy, or partial nephrectomy can be performed.
Previous Urologic Surgery
An increasing number of women are becoming pregnant who were born with urinary tract abnormalities that were corrected surgically. These operations include urinary diversion procedures (ileal conduit and ureterosigmoidostomy), augmentation cystoplasty, and ureteral reimplantation for vesicoureteral reflux. The changes in pelvic anatomy caused by the enlarging uterus create the potential for infection, obstruction, and trauma at cesarean section.
Pregnancy in patients with a urinary diversion is complicated by premature delivery, 20% to 50%; symptomatic UTIs, 15%; urinary obstruction, 10%; and intestinal obstruction, 10%. Cesarean delivery should be reserved for obstetric indications. Although less commonly performed, a ureterosigmoidostomy may be an indication to schedule a cesarean delivery to preserve the integrity of the anal sphincter.
During the past 20 years, the treatment of patients with abnormal urinary tracts has changed from cutaneous diversion to patients who have had a continent internal diversion and augmentation cystoplasty, they may have also undergone vesical neck reconstruction or artificial sphincter placement. This may place the patient at risk for the development of incontinence after vaginal delivery. reviewed 15 pregnancies in 15 women after augmentation cystoplasty. Eight of thirteen were continent before, during, and after pregnancy. One patient who was continent before delivery became incontinent after vaginal delivery. Four patients became incontinent during the last trimester, but regained continence postpartum. The pregnancies were complicated by UTIs (60%), preterm labor (20%), and urinary obstruction (7%). Five cesarean deliveries were performed, three electively for vesical neck or artificial sphincter construction. One cesarean operation was complicated by extensive anterior uterine adhesions. Although stretching of the mesentery by the enlarging uterus has the potential risk of vascular compromise, this complication was not seen in the 15 patients.
Ureteral reimplantation has been performed routinely for severe primary vesicoureteral reflux for many years. reviewed 64 pregnancies in 34 women after ureteroneocystostomy for primary reflux. The overall infection rate before pregnancy was 48%. During pregnancy, 57% experienced a UTI. Pyelonephritis was more common during pregnancy (17%) than before pregnancy (4%). Of the 64 pregnancies, eight were lost between 9 weeks and 21 weeks, and six were associated with a UTI. The authors did not report the route of delivery and the difficulty of cesarean section.
The latter reviews of pregnancies in women with urinary tract surgery suggest the following obstetric management: close monitoring for preterm labor (patient education, frequent office visits, frequent pelvic examinations), suppressive antibiotic therapy (nitrofurantoin 100 mg every night at bedtime), monthly BUN and serum creatinine evaluation, vigilance for ureteral obstruction, vaginal delivery except for obstetric indications and patients who have undergone urinary diversion to the sigmoid and bladder neck/sphincter surgery, and urologic consultation at cesarean section for patients with a history of complex urologic surgery, especially augmentation cystoplasty.
Impact of Childbirth on Anatomy and Physiology
You may likely have witnessed countless times the miracle of childbirth and you may also have likely considered the “Ps”—that is, how the power pushes the passenger through the passage. In a classic review, described the mechanism by which the fetus negotiates the birth canal and is expelled through the pelvic diaphragm as follows:
As the flexed fetal head strikes the pelvic floor, the levator ani muscle segments are funneled from behind and forward. The ischiococcygeus muscle is the first to receive the impact, but the head is often preceded by a dilating wedge of amniotic fluid and membranes that transfers most of the pressure onto the front of the pubococcygeus muscle. The anococcygeal raphe is pushed down until it becomes vertical. The ischiococcygeus assumes a vertical plane and acts as a deflecting surface for the descending head, which is deflected downward and forward onto the iliococcygeus. After the resistance of the ischiococcygeus is overcome, the head is shunted onto the pubococcygeus segment, which is stretched anteroposteriorly and peripherally. The perineal body is pushed downward as the head is propelled along the axis of the pelvic outlet. The rectovaginal septum fibers are stretched peripherally and longitudinally and often torn. As the outlet muscles—the bulbocavernosus, ischiocavernosus, transverse perinei, and periurethral muscles—are dilated, they are converted into a short muscular tube along the axis of the pelvic outlet. Finally, as the biparietal diameter of the fetal head reaches the transverse diameter of the pelvic outlet, the uterovaginal canal is converted into one continuous hiatus. The lateral ligaments of the cervix uteri (endopelvic fascia) are flattened peripherally and stretched vertically. The vagina is dilated spherically, and the pelvic diaphragm is changed from an oblique to a vertical plane.
Much of Power’s description was based on his experience and conjecture. During the past 15 years, advanced imaging and computer modeling have added an improved, but by no means complete, understanding of the changes that occur after labor and delivery ( Fig 16.2 ).
Muscular Injury
used sophisticated imaging and engineering techniques to develop a biomechanical model to describe changes in levator ani muscles as the fetal head descends through the vagina ( Fig. 16.3 ). The medial pubococcygeus muscle reached an impressive stretch ratio (defined as tissue length under stretch/original tissue length) of 3.26. According to the authors, this exceeds the greatest stretch ratio (1.5) seen in passive striated muscle of nonpregnant women by 217%. Increasing the fetal head diameter by 9% increased medial pubococcygeus stretch by the same proportion. This model suggests that the medial muscles of the levator ani complex have the greatest risk for injury of all the levator ani muscles during the second stage of labor. This supposition is supported by magnetic resonance imaging ( Fig. 16.4 ) and three-dimensional/four-dimensional ultrasound ( Fig. 16.5 ) studies that reveal abnormalities in this area in 20% to 36% of primiparous women after vaginal delivery ( ).
