2. Introduction
Renal parenchymal disease consists of two general groups
1) Glomerulopathies
2) Tubulointerstitial
The incidence of kidney disease in pregnancy is approximately
0.12%. In two thirds of these patients, the disorder
results from glomerulopathy, and in one third, from
tubulointerstitial disease.
3. Introduction
ā¢ Patients with renal parenchymal disorders may remain asymptomatic
for years, and they may exhibit only proteinuria and microscopic
hematuria, with little if any evidence of reduced renal function.
ā¢ Spontaneous recovery or improvement with treatment occurs with
many glomerulopathies.
ā¢ However, other patients exhibit progressive nephropathy,
hypertension, and renal insufficiency
5. Tubulointerstitial diseases
ā¢ These are disorders characterized by abnormal tubular function.
ā¢ They result in abnormal urine composition and concentration but are
not characterized by decreased GFR until late in the disease course.
ā¢ The disorders in this category include interstitial nephritis, renal cystic
disease, renal neoplasia, and functional tubular defects.
6. Diagnosis
ā¢ Serial blood pressure measurements are obtained to define the severity
of hypertension and the efficacy of current antihypertensive therapy.
ā¢ Creatinine clearance and the level of proteinuria should be determined.
ā¢ Urinalysis yields information about the presence of renal casts and
bacteriuria.
ā¢ The determination of serum creatinine and BUN concentrations
defines the extent of renal insufficiency. A serum creatinine
concentration greater than 0.8 mg/dL, which may be normal in the
nonpregnant woman, may represent significant renal insufficiency
during pregnancy
7. Diagnosis
ā¢ Both preeclampsia and renal disease may manifest as hypertension,
proteinuria, and edema. The distinction between the two disorders is
often unclear, especially after 20 weeksā gestation.
ā¢ Histologic evidence of preeclampsia(e.g., glomerular endotheliosis
without hypercellularity) was present in only 65% of these
hypertensive women.
ā¢ Because renal biopsy exposes the pregnant woman to potential
complications, many perinatologists recommend biopsy only when
sudden deterioration in renal function or symptomatic nephrotic
syndrome occurs before 28 weeksā gestation, at which time definitive
diagnosis may guide appropriate treatment
8. Effect of Pregnancy on Preexisting
Kidney Disease
ā¢ The extent to which pregnancy affects preexisting renal disease
depends on the level of renal insufficiency before pregnancy.
ā¢ Among women with mild antenatal renal insufficiency, pregnancy
does not substantially alter the natural course of renal disease.
ā¢ With a serum creatinine concentration greater than 2.0 mg/dL who
become pregnant have a one-in-three chance of developing dialysis-
dependent end-stage renal disease during or shortly after pregnancy.
9. Effect of Pregnancy on Preexisting
Kidney Disease
ā¢ The pathophysiology by which pregnancy exacerbates renal disease is
unknown.
ā¢ One hypothesis is that increased glomerular perfusion, which normally
accompanies pregnancy, paradoxically causes further injury to the
kidneys in patients with preexisting impairment of function.
ā¢ An alternative hypothesis is that preexisting renal disease may induce
a cascade of platelet aggregation, microvascular fibrin thrombus
formation, and endothelial dysfunction that leads to microvascular
injury in the already tenuous kidneys
10. Effect on the Mother and Fetus
ā¢ Pregnant women with chronic kidney disease are at an increased risk
for maternal and fetal complications.
ā¢ Maternal complications(5 times greater) include gestational
hypertension, preeclampsia/eclampsia, and maternal mortality.
ā¢ Adverse fetal outcomes(2 times greater) included preterm births, fetal
growth restriction, small-for-gestational-age infants, neonatal
mortality, stillbirths, and low birth weight
ā¢ Preexisting hypertension and a high preconception serum uric acid
level predicted worse outcome.
11. Medical and Obstetric Management
ā¢ During pregnancy, the nephrologist and the obstetrician monitor
maternal renal function, blood pressure, and fetal development at
frequent intervals.
ā¢ Monthly determination of serum creatinine concentration, creatinine
clearance, and proteinuria allows the recognition of renal deterioration.
ā¢ Some glomerulopathies respond to corticosteroids, and corticosteroid
therapy should be continued during pregnancy.
ā¢ Recombinant human erythropoietin improves maternal anemia during
pregnancy.
12. Hemodialysis and Long-Term
Ambulatory Peritoneal Dialysis
ā¢ When renal disease has progressed to end-stage renal failure (i.e., GFR
< 5 mL/min), fertility is suppressed and conception and pregnancy are
rare. Less than 10% of premenopausal patients undergoing dialysis
have regular menses.
ā¢ Luteinizing hormone and follicle-stimulating hormone concentrations
assume an anovulatory pattern, which causes 40% of affected women
to be amenorrheic.
ā¢ Half of all female patients undergoing dialysis exhibit
hyperprolactinemia because of reduced clearance and hypothalamic
disturbances.
13. Hemodialysis
ā¢ Extracorporeal hemodialysis vascular access and the need for anticoagulation of
the extracorporeal circuit and may be complicated by cardiovascular instability,
large fluid and electrolyte shifts, and the risk for hepatitis.
ā¢ Hypotension may compromise uteroplacental perfusion and cause fetal
compromise. Even when hypotension and major fluid shifts are avoided, Doppler
ultrasonographic examination of uterine and umbilical artery flow during
hemodialysis suggests the occurrence of a redistribution of arterial flow away
from the uteroplacental vascular bed.
ā¢ Fetal heart rate monitoring is recommended during dialysis. Rapid removal of
maternal solutes and reduced oncotic pressure with attendant free-water diffusion
into the amniotic cavity may lead to polyhydramnios.
ā¢ Hemodynamic consequences are minimized by more frequent but shorter dialysis
runs.
14. Peritoneal Dialysis
ā¢ Intracorporeal Long-term ambulatory peritoneal dialysis allows less
hemodynamic trespass, a more stable fetal environment, and the
freedom to undergo dialysis at home.
ā¢ However, peritoneal dialysis may not be associated with greater fetal
survival. Complications of this modality include peritonitis and
catheter difficulties.
ā¢ 71% of women undergoing hemodialysis and 64% of women
undergoing peritoneal dialysis have a successful delivery
15. Maternal complications
ā¢ These include malnutrition, anemia, and hypertension. Fetal
complications include fetal growth restriction, fetal death, and preterm
labor.
ā¢ BUN levels should be kept below 50 mg/dL before dialysis and below
30 mg/dL after dialysis. At birth, azotemia in the newborn is similar to
that in the mother, but this quickly corrects because the newborn has
normal kidney function.
ā¢ Patients undergoing hemodialysis have a high prevalence of viral
hepatitis, a greater frequency of active tuberculosis, and a higher rate
of infection HIV, HCV and MRSA.
16. Anaesthetic Management
ā¢ Anesthetic management is influenced by the extent of renal
dysfunction and hypertension. The parturient with stable renal disease,
mild to moderate renal insufficiency, well-controlled hypertension, and
euvolemia requires minimal special consideration.
ā¢ In contrast, the dialysis patient with end-stage renal failure presents
many anesthetic challenges because renal disease may affect almost
every organ system.
24. Neuraxial Anaesthesia
ā¢ Neuraxial anesthesia is the preferred technique for both labor
analgesia and cesarean delivery, but there are some unique
considerations in the parturient with renal disease.
ā¢ Uremic patients may be hypervolemic or hypovolemic, depending on
the time elapsed since their last dialysis session.
ā¢ Hypovolemia and autonomic neuropathy may lead to profound
hypotension during the initiation of sympathetic blockade.
Intravascular volume should be assessed before induction of
anesthesia. Assessment of clinical signs (e.g., skin turgor, mucous
membranes, tachycardia) is generally sufficient.
25. Neuraxial Anaesthesia
ā¢ Frequent monitoring of blood pressure and immediate treatment of
hypotension is suggested.
ā¢ Preexisting peripheral neuropathy should be documented before the
administration of neuraxial anesthesia
ā¢ Administering spinal anesthesia Maximal segmental anesthesia
occurred more rapidly in the patients with renal disease compared to
normal parturients, but the duration was reduced. Further, the extent of
sensory blockade was two segments higher in the patients with renal
disease.
26. General Anaesthesia
ā¢ Patients with chronic uremia exhibit delayed gastric emptying and
hyperacidity, which may increase the risk for aspiration pneumonitis.
ā¢ All the standard induction agents are safe in patients with renal failure.
Etomidate may have an advantage because it supports the circulation
better than other induction agents.
ā¢ Propofol exhibits normal volume of distribution and elimination in
patients with renal failure and is also commonly used.
ā¢ Uremia increases blood brain barrier permeability, these changes may
warrant a small reduction in the dose of propofol or thiopental for
induction.
27. General Anaesthesia
ā¢ The serum potassium concentration should be determined before
induction of anesthesia.
ā¢ If the potassium concentration is greater than 5.5 mEq/L, dialysis
should be performed before an elective procedure.
ā¢ Succinylcholine will cause a 0.5 to 0.7 mEq/L increase in potassium
concentration, which is similar to the increment that occurs in patients
without renal disease.
ā¢ If the patient is already hyperkalemic, this mild elevation may be
sufficient to precipitate cardiac dysrhythmias
28. General Anaesthesia
ā¢ Plasma cholinesterase concentrations are normal, even after dialysis,
and the duration of action of succinylcholine is not prolonged.
ā¢ Neuromuscular blockade should be maintained with an agent that does
not rely on renal elimination.
ā¢ Hypermagnesemia, commonly found in patients with kidney disease,
may potentiate neuromuscular blockade.
ā¢ Although anticholinesterase agents undergo renal elimination and have
a prolonged duration in patients with renal insufficiency, the volume of
distribution remains the same and standard doses are used for the
reversal of neuromuscular blockade
29. Postoperative Analgesia
ā¢ The principles of postoperative analgesia for the woman with renal
disease are the same as for healthy woman, with some important
considerations because drug clearance can be altered for opioids and
their metabolites.
ā¢ Morphine is generally safe as a single dose, but with longer-term use
its metabolite, morphine-6-glucuronide, may accumulate.
ā¢ Meperidine is of particular concern because its active metabolite,
normeperidine, is neurotoxic and is renally excreted.
ā¢ Hydromorphone and oxycodone, and their metabolites
hydromorphone-3-glucuronide and Ī±- and Ī²-oxycodol, respectively,
are also renally excreted and may accumulate with prolonged use.
30. Postoperative Analgesia
ā¢ Methadone does not accumulate in patients with renal disease and may be a
useful long-term analgesic.
ā¢ Fentanyl and sufentanil are only minimally excreted in the urine, and
because they are short-acting drugs they may be particularly useful.
ā¢ Remifentanil is metabolized by blood and tissue esterases and is not
dependent on the kidney for excretion, making it safe as well for use in
patients with renal failure.
ā¢ The safest approach may be to use neuraxial opioids because small doses
are administered.
ā¢ Alternative techniques that avoid opioids such as transversus abdominis
plane (TAP) block may also be considered.
32. Introduction
ā¢ Acute renal failure (ARF) is an uncommon but serious complication of
pregnancy. Rapid deterioration of renal function leads to an
accumulation of fluid and nitrogenous waste products with impaired
electrolyte regulation.
ā¢ In the mid-20th century, nearly a fourth of all cases of ARF were
obstetric.
ā¢ The incidence of ARF from 1 in 3000 to 1 in 18,000 pregnancies from
1958 to 1994. The proportion related to pregnancy decreased from
43% to 0.5%.
ā¢ This progress has resulted from improved obstetric care and fewer
septic abortions.
33. Pathophysiology and Diagnosis
ā¢ ARF is suggested by a sharp increase in the plasma creatinine (> 0.8 mg/dL)
and BUN (> 13 mg/dL) concentrations.
ā¢ In complete renal failure, the serum creatinine concentration increases at the
rate of 0.5 to 1.0 mg/dL/day.
ā¢ Urine output typically decreases to less than 400 mL/ day (oliguria), but
some patients may be nonoliguric.
ā¢ In developing countries septic abortion is the leading cause of pregnancy
related ARF.
ā¢ In developed countries, severe preeclampsia/eclampsia, acute pyelonephritis
of pregnancy, and bilateral renal cortical necrosis are the most common
underlying disorders
35. Prerenal Causes
ā¢ The most common prerenal causes of ARF hyperemesis gravidarum and
obstetric hemorrhageālead to hypovolemia and inadequate renal perfusion.
ā¢ Urinary indices show urinary osmolality greater than 500 mOsm/kg water,
urine sodium less than 20 mEq/L.
ā¢ Concealed uterine hemorrhage from placental abruption may remain
unrecognized until hypotension and renal failure ensue.
ā¢ Women with preeclampsia may be more likely to develop ARF after
hemorrhage because of preexisting intravascular contraction and widespread
maternal endothelial dysfunction.
ā¢ Women who developed preeclampsia during pregnancy, with or without
renal failure, are more likely to develop renal failure later in life.
36. Intrarenal Causes
ā¢ An intrarenal cause is diagnosed once prerenal and postrenal causes of
ARF have been excluded. In general, oliguric intrarenal ARF is not
easily reversed and must run its course.
ā¢ A thorough history, review of medications, and urinalysis typically
help determine the specific initiating factor.
37. Acute tubular necrosis
ā¢ Results from nephrotoxic drugs, amniotic fluid embolism,
rhabdomyolysis, intrauterine fetal death, and prolonged renal ischemia
secondary to hemorrhage or septic shock.
ā¢ Urinalysis demonstrates dirty brown epithelial cell casts and coarse
granular casts.
ā¢ Urinary indices show urine osmolality less than 350 mOsm/kg water,
urine sodium concentration greater than 40 mEq/L, fractional sodium
excretion greater than 1%, and a urinary-to-plasma creatinine ratio less
than 20.
38. Acute interstitial nephritis
ā¢ Is caused by nonsteroidal anti-inflammatory drugs (NSAIDs) and
various antibiotics.
ā¢ Patients typically have fever, rash, eosinophilia, and urine eosinophils.
39. Acute glomerulonephritis
ā¢ Is rare during pregnancy.
ā¢ It is suggested by hematuria, red cell casts, and proteinuria.
ā¢ Urinary indices of acute glomerulonephritis are similar to those of
prerenal ARF.
40. Bilateral renal cortical necrosis
ā¢ This is rarely observed in the non obstetric patient, is responsible for
10% to 38% of cases of obstetric ARF. It may occur during early or
late pregnancy. Hemorrhage is the most common precipitating event.
ā¢ The pathogenesis of this disorder is unclear but may involve renal
hypoperfusion or endothelial damage by endotoxins imposed on the
normal hypercoagulable state of pregnancy.
ā¢ Extensive microthrombi are found within the glomeruli and renal
arterioles.
ā¢ Diagnosis is made by selective renal arteriography, which reveals
absence or patchiness of blood flow in the cortex. Renal biopsy may
also be performed in the absence of active coagulopathy
41. Acute pyelonephritis
ā¢ Is one of the most common infectious complications of pregnancy.
ā¢ Although acute pyelonephritis rarely leads to ARF in the nongravid
patient, it accounts for 5% of cases of ARF among pregnant women.53
The reason for this greater susceptibility is unclear.
ā¢ It causes a marked reduction of GFR in pregnant women. In contrast,
pyelonephritis causes little reduction in GFR in nonpregnant patients.
ā¢ This may be due to increased sensitivity of kidney to bacterial
endotoxins during pregnancy.
44. Idiopathic postpartum renal
failure
ā¢ Initially described in 1968 by Robson et al, this syndrome is
characterized by ARF, microangiopathic hemolytic anemia, and
thrombocytopenia occurring 2 days to 10 weeks after an
uncomplicated delivery. It appears closely related to the hemolytic
uremic syndrome.
ā¢ Idiopathic postpartum renal failure is typically preceded by a viral
upper respiratory tract or gastrointestinal syndrome that rapidly
progresses to ARF.
ā¢ The use of ethinyl estradiol as a contraceptive may also be related to
this syndrome
45. Idiopathic postpartum renal
failure
ā¢ Spontaneous bleeding, congestive heart failure, hypertension, and
seizures have been reported with this syndrome.
ā¢ Some believe that this syndrome represents a clinically to the
generalized Shwartzman reaction, a condition induced in laboratory
animals by two successive injections of endotoxin, which results in
factor XII activation, thrombin generation, and fibrin deposition.
ā¢ Others consider the platelet deposition to be the primary event that
leads to microvascular thrombi.
ā¢ Management involves plasma exchange transfusion, dialysis, and
antiplatelet therapy. The role of heparin is controversial.
46. Postrenal Causes
ā¢ The postrenal causes of ARF include nephrolithiasis and ureteral
obstruction by the gravid uterus. The latter complication is more likely
in pregnant women with polyhydramnios or multiple gestation.
ā¢ Preexisting ureteral dilation and impaired peristalsis increase the risk
for obstructive uropathy during pregnancy.
ā¢ Flank pain and decreased urine output during late gestation should
alert the clinician to this possibility.
47. Effect on the Mother and Fetus
ā¢ Although maternal prognosis has improved significantly in developed
countries, mortality ranges between 20% and 30% in developing
countries.
ā¢ The prognosis for the fetus is worse than for the
ā¢ mother. Reported fetal mortality is as high as 40% to 50%.
ā¢ Two groups reported much lower mortality rates (0% to 13%) with the
use of aggressive hemodialysis (six times per week with the goal of
maintaining the blood urea nitrogen level < 50 mg/dL)
48. Medical and Obstetric Management
ā¢ Reversible disorders such as hypovolemia, concealed uterine
hemorrhage, urinary tract infection, ureteral obstruction, and drug-
induced ARF must be excluded.
ā¢ Intravascular volume should be optimized.
ā¢ Electrolyte and acid-base status should be monitored carefully.
ā¢ Hypertension and preeclampsia must be managed aggressively.
ā¢ Many obstetric causes of ARF also may cause disseminated
intravascular coagulation; therefore, coagulation abnormalities should
be excluded in pregnant women with ARF.
49. Medical and Obstetric Management
ā¢ Because urea and other metabolic products cross the placenta,
hemodialysis or peritoneal dialysis should be directed toward
maintaining the post-dialysis BUN concentration at or below 30
mg/dL.
ā¢ Fluid shifts during hemodialysis should be minimized by short but
frequent periods of dialysis.
ā¢ If the fetus is mature, delivery should be accomplished when the
maternal condition is stabilized.
ā¢ The pediatrician must be alerted to the presence of high fetal BUN
levels, which may lead to an osmotic diuresis and neonatal
dehydration.
50. Anaesthetic Management
ā¢ A multidisciplinary approach involving anesthesiologists, obstetricians, and
nephrologists should be employed to optimize the maternal condition before
the induction of labor or performance of cesarean delivery in a woman with
ARF.
ā¢ If the BUN level is greater than 80 mg/dL or the serum potassium
concentration greater than 5.5 mEq/L, dialysis should be performed before
elective vaginal or cesarean delivery.
ā¢ Neuraxial anesthesia may be administered in the absence of coagulopathy,
thrombocytopenia, and severe hypovolemia.
ā¢ Intravenous fluid without potassium (e.g., 0.9% saline) should be
administered.
51. Anaesthetic Management
ā¢ Occult uterine hemorrhage should be excluded, and hypertension, if
present, controlled. Both spinal and epidural analgesia/ anesthesia are
safe and preferred to general anesthesia.
ā¢ As the sympathetic blockade dissipates, the mother should be
monitored for evidence of volume overload and pulmonary edema.
ā¢ General anesthesia may be required for urgent cesarean delivery or in
patients with coagulopathy or hemorrhage.
52. Renal transplantation
ā¢ Although pregnancy is uncommon in women undergoing long-term
dialysis, fertility is improved within months of transplantation.
ā¢ United States, a pregnancy rate of 20 per 1000 was estimated in
transplanted patients compared with 100 per 1000 in the general
population.
ā¢ Although a successful obstetric outcome can be anticipated in more
than 95% of kidney transplant recipients, they are at greater risk for
both maternal and fetal complications than healthy women.
ā¢ The incidences of preeclampsia (27%), gestational diabetes (8%),
cesarean delivery (56.9%), and preterm delivery (45.6%) were greater
than in the general population.
53. Effect of Pregnancy on the
Renal Allograft
ā¢ When a kidney is removed from a donor and transplanted into an
anephric recipient, it undergoes a process of hyperfiltration. This is a
maladaptive response that, in the short term, attempts to bring the GFR
toward the rate of a bi-nephric system. In the long term, this
hyperfiltration may lead to glomerular sclerosis and loss of renal
function if it is associated with increased glomerular or capillary
pressure.
ā¢ In normal pregnancy, the GFR increases by 30% to 50% during the
first and second trimesters and subsequently decreases during the third
trimester. Theoretically, this additional hyperfiltration of pregnancy
predisposes the patient to a loss of renal function.
54. Effect of Pregnancy on the
Renal Allograft
ā¢ Baylis et al. allayed many of these concerns by demonstrating that
gestational hyperfiltration is not associated with increased glomerular
pressure because of matching afferent and efferent arteriolar
vasodilation.
ā¢ There have been a number of studies assessing graft function after
pregnancy. Most studies suggest that there is no adverse effect
provided renal function is normal before conception and there is no
evidence of hypertension.
55. Effect on the Fetus
ā¢ Although pregnancy seems to have minimal effect on maternal health or
allograft survival in renal transplant recipients, fetal outcome is less
favorable. Spontaneous or elective abortion occurred in 14% in the
remaining successful pregnancies were complicated by preterm delivery
(45%) and fetal growth restriction (86%).
ā¢ Most post-transplantation protocols consist of a primary
immunosuppressant (cyclosporine or tacrolimus) and one or two adjunctive
agents (azathioprine, mycophenolate mofetil, sirolimus, and/or
corticosteroids).
ā¢ Despite transplacental exposure to immunosuppressant drugs, congenital
anomalies and other adverse effects are not greater than in the general
population
56. Effect on the Fetus
ā¢ There have been reports of congenital defects with mycophenolate
mofetil, including cleft lip and palate, microtia, absence of auditory
canals, brachydactyly of the fifth finger, and hypoplastic toenails;
therefore, its use has to be weighed against the risk for allograft
rejection.
ā¢ Intrauterine exposure to cyclosporine impairs development and
function of T, B, and NK lymphocytes in neonates. This effect, persists
during the first year of life.
ā¢ These factors place the infant at risk for a suboptimal immunologic
response after administration of classic vaccines and for adverse
effects after administration of live, attenuated vaccines.
57. Effect on the Fetus
ā¢ Transplant recipients may become infected with cytomegalovirus
(CMV) at the time of transplantation, or they may experience
reactivation secondary to immunosuppression.
ā¢ Active CMV infection during pregnancy is associated with congenital
anomalies (e.g., cerebral cysts, microcephaly, mental retardation). In
addition, active neonatal CMV infection may lead to serious illness or
death.
58. Medical and Obstetric Management
ā¢ The renal transplant recipientās immunosuppressant regimen must be
continued during pregnancy except mycophenolate mofetil.
ā¢ Cyclosporine requirements increase during pregnancy, most likely
because of enhanced metabolism.
ā¢ The pregnant patient must be intensively monitored for any evidence
of acute or chronic allograft rejection, infection, ureteral and renal
artery obstruction, impaired renal function, hypertension, fluid volume
disturbances, anemia, or any combination of these symptoms.
ā¢ Recombinant human erythropoietin is used to treat anemiaduring
pregnancy.
59. Medical and Obstetric Management
ā¢ Initial laboratory studies in pregnant renal transplant patients include
1) complete blood cell count
2) Renal function tests
3) serum electrolyte and glucose concentrations,
4) viral serologic testing for CMV, hepatitis B virus, HCV, and HIV.
5) Serial ultrasonographic assessments allow the recognition of fetal
anomalies and the evaluation of fetal growth.
60. Medical and Obstetric Management
ā¢ A patient who presents in labor and with evidence of active genital
herpes simplex virus infection should undergo cesarean delivery.
ā¢ Vaginal examinations are minimized and always performed in a strict
aseptic manner.
ā¢ The renal allograft is typically implanted in the extraperitoneal iliac
fossa and does not impair vaginal delivery.
ā¢ Prophylactic antibiotics and stress-dose corticosteroids are indicated in
patients who undergo cesarean delivery.
61. Anesthetic Management
ā¢ In the absence of renal dysfunction and hypertension, anesthetic
management of the parturient with a renal transplant is similar to that
of the healthy parturient.
ā¢ Strict aseptic technique is maintained during the placement of
intravascular catheters and the performance of neuraxial anesthetic
techniques.
ā¢ In the absence of systemic infection, immunosuppression itself should
not be considered a contraindication to administration of epidural or
spinal anesthesia.
63. Introduction
ā¢ Urolithiasis is characterized by the abnormal formation of calculi
within the renal calyces or pelvis.
ā¢ Calculi may lodge within the ureters or bladder.
ā¢ Most stones are calcium oxalate (70%) or calcium phosphate (10%).
ā¢ Symptomatic urolithiasis occurs during 1 in 240 to 1 in 3300
pregnancies.
ā¢ The pregnancy does not affect the rate of urolithiasis.
64. Pathophysiology
ā¢ The presence of urolithiasis presumes an underlying physiologic
abnormality that leads to persistent supersaturation of the particular
minerals involved.
ā¢ During pregnancy, an elevated plasma vitamin D level causes greater
intestinal absorption of calcium, net mobilization of calcium from
bone, and a state of absorptive hypercalciuria.
ā¢ Ultimately, these changes provide calcium for the fetal skeleton.
ā¢ Other physiologic changes during pregnancy offsets this stone-
forming factor in pregnant women. Calcium stone inhibitors such as
citrate, magnesium, and glycoprotein are excreted in the urine to a
greater extent during pregnancy.
65. Diagnosis
ā¢ Urolithiasis most commonly manifests during the second or third
trimester. 80% of cases of gestational urolithiasis are diagnosed in
parous women,
ā¢ The signs and symptoms of urolithiasis during pregnancy must be
differentiated from that of ectopic pregnancy, preterm labor,
appendicitis, pyelonephritis, and benign hematuria of pregnancy.
ā¢ A history of previous urolithiasis, recurrent urinary tract infections, or
urologic surgery. Symptoms include flank and abdominal pain,
urgency, dysuria, nausea, and fever. Examination reveals
costovertebral tenderness, abdominal tenderness, pyuria, and
hematuria. Urolithiasis must be considered in patients with
pyelonephritis who remain febrile or have continued bacteriuria
despite 48 hours of parenteral antibiotics.
66. Diagnosis
ā¢ Transabdominal ultrasonography is diagnostic in about 60% of cases
and does not expose the mother or fetus to radiation.
ā¢ Color Doppler ultrasonography allows the identification of ureteral
jets; the asymmetry or absence of these jets indicates the presence of
urinary calculi.
ā¢ Transvaginal ultrasonography may augment suboptimal
transabdominal ultrasonographic images.
ā¢ Combining ultrasound evaluation with assessment of the intrarenal
artery resistive index increases the accuracy of ultrasonography to
greater than 70%.
67. Diagnosis
ā¢ If urinary calculi are not successfully visualized with ultrasonography
and clinical suspicion for urolithiasis remains high, magnetic
resonance (MR) urography should be considered because it does not
use ionizing radiation or iodinated contrast media.
ā¢ If the diagnosis is still unclear and the patient has persistent flank pain
after both these tests, some experts recommend low-dose computed
tomography whereas others recommend intravenous pyelography
68. Effect of Pregnancy on Urolithiasis
ā¢ In an effort to determine any effect of pregnancy on the natural history
of urolithiasis, Coe et al. reviewed the records of 58 pregnancies in
women with the preexisting diagnosis of urolithiasis.
ā¢ The stone recurrence rate in this group was 0.49 stone per patient-year,
which was not significantly different from the rate of 0.44 stone per
patient-year in the general population.
ā¢ The authors concluded that pregnancy does not alter the activity or
severity of stone disease.
70. Urologic and Obstetric Management
ā¢ Women with a history of urolithiasis should increase their intake of
fluids.
ā¢ Calcium supplementation through prenatal vitamins should be avoided
in women with recurrent urolithiasis.
ā¢ During pregnancy, 70% of calculi pass spontaneously with
conservative management.
ā¢ The decision to move beyond conservative therapy should be taken on
a case-by-case basis. Infected hydronephrosis, especially with
impaired renal function or urosepsis, is an indication for more
aggressive therapy
71. Urologic and Obstetric Management
ā¢ Medical expulsive therapy with alpha-adrenergic receptor blocking
agents has been used successfully to increase the rate of stone passage
and decrease pain associated with expulsion by relaxing ureteral
smooth muscle. However, there are no published reports of its use
during pregnancy.
ā¢ Other medical treatments that are used to treat urolithiasis, including
thiazide diuretics, xanthine oxidase inhibitors, and d-penicillamine, are
contraindicated during pregnancy owing to possible effects on the
fetus
72. Urologic and Obstetric Management
ā¢ Urologic intervention is indicated in the patient with persistent
pyelonephritis, deterioration of renal function, massive
hydronephrosis, persistent pain, or sepsis.
ā¢ Ureteral stent placement with ureteroscopy and ultrasonographic
guidance, or percutaneous nephrostomy, should be considered.
ā¢ Holmium:yttrium-aluminum-garnet (YAG) laser lithotripsy, using
state-of-the-art ureteroscopes, is an emerging technique for stone
management in pregnancy.
ā¢ Extracorporeal lithotripsy should be avoided during pregnancy
because the shockwaves may be harmful to the fetus.
73. Urologic and Obstetric Management
ā¢ The following conditions may raise suspicion of the presence of
primary hyperparathyroidism in a pregnant woman:
ā¢ Urolithiasis with or without pancreatitis
ā¢ Hyperemesis beyond the first trimester
ā¢ History of recurrent spontaneous abortion or intrauterine fetal
ā¢ Death neonatal hypocalcemia or tetany
ā¢ Total serum calcium concentration greater than 10.1 mg/dl during the
second trimester or greater than 8.8 mg/dl during the third trimester.
74. Anaesthetic Management
ā¢ The ureters receive sensory innervation through the renal, ovarian, and
hypogastric plexuses (T11 to L1 spinal segments).
ā¢ During conservative management of urolithiasis, epidural analgesia
provides the patient with significant pain relief and facilitates the
passage of the calculus.
ā¢ Neuraxial analgesia avoids the use of systemic opioids, which impair
normal peristalsis in ureteric smooth muscle.
ā¢ Improved maternal pain control may also decrease endogenous
catecholamine release and improve uteroplacental blood flow.