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203
1. What anatomic changes take place in the urinary system during pregnancy?
During normal pregnancy, the kidneys increase in size, weight, and volume. Dilation of the ureter
and renal pelvis can be seen as early as 6 weeks of gestation, and physiologic hydronephrosis can
be seen in most patients (90% of right kidneys and 67% of left kidneys). Ureteral or calyceal dilation
is thought to be secondary to uterine expansion and dextrorotation with advancing gestational age.
However, dilation is also influenced by progesterone-mediated smooth muscle relaxation.
2. What physiologic changes take place in the urinary system during pregnancy?
Increased glomerular filtration rate (GFR) and renal plasma flow result from increased cardiac output
as well as decreased renal vascular resistance. By the second trimester, GFR increases by more than
40% to 65%. Creatinine (Cr) clearance increases by up to 50%. Serum Cr decreases to 0.4 to
0.6mg/dL as a result of both increased GFR and increased plasma volume; a level of 1 mg/dL is
abnormally high and indicates potential renal disease.
3. Is glucosuria an abnormal finding in pregnancy?
No. The higher GFR of pregnancy can result in glucose filtration exceeding the reabsorptive capacity
for glucose in the renal tubules.
4. How is sodium balance maintained in normal pregnancy?
Total body sodium increases by 950 mg by the end of pregnancy. This increase results from shifting
balances in GFR, atrial natriuretic peptide, progesterone (salt wasting), aldosterone, and deoxycortico-
sterone (salt conserving).
5. Why are pregnant women at increased risk for pyelonephritis?
Increased risk is thought to reflect anatomic changes in the urinary system during pregnancy. These
changes result in urinary stasis, which allows for ascending infection. Five percent to 6% of sexually
active women have asymptomatic bacteriuria, and urinary tract infections can be seen in up to 20%
of pregnancies. Pyelonephritis occurs in 1% to 2% of pregnant women, and it is one of the most
common serious complications of pregnancy.
6. Do patients with pyelonephritis require hospital admission?
Traditionally, pregnant women with pyelonephritis have been admitted for intravenous antibiotics and
close observation; outpatient management is controversial. If outpatient management is attempted,
the patient should have no other complicating factors, be able to tolerate oral medication, and demon-
strate compliance with follow-up visits.
7. Does pregnancy increase the incidence of urolithiasis?
No. Pregnant women have an incidence of urolithiasis similar to that of nonpregnant women.
Along with increased filtration of calcium and uric acid, stone formation inhibitors such as citrate,
magnesium, and glycosaminoglycans are also increasingly filtered. The incidence of symptomatic
nephrolithiasis ranges from 1 in 244 to 1 in 2000 pregnancies.
8. How does urolithiasis manifest, and what should be included in the initial
evaluation?
The most common presenting symptom is abdominal flank pain, occurring in 85% to 100% of patients.
Frank hematuria can be seen in up to 30% of patients. Initial evaluation should include urinalysis to
evaluate for hematuria, pyuria, and alterations in pH; up to 95% to 100% of patients will have micro-
scopic hematuria, and pyuria may suggest concomitant infection. Urine pH greater than 7 may indicate
the presence of urea-splitting organisms, and pH lower than 5 may indicate uric acid stones. The
imaging modality of choice in pregnant women with signs or symptoms of urolithiasis is ultrasound.
CHAPTER 47
RENAL DISEASE IN
PREGNANCY
Rebecca M. Geer, MD
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204 COMPLICATIONS OF PREGNANCY
9. How is chronic renal disease diagnosed in pregnancy?
In the nonpregnant state, the severity of chronic renal disease is determined by calculated GFR.
Given the significant anatomic and physiologic changes in the urinary system in pregnancy, GFR can
prove challenging to calculate, and serum Cr levels are more often used, with 0.6 mg/dL the normal
expected value. Values higher than 0.8 to 0.9 mg/dL should prompt further evaluation with urinalysis,
serum electrolytes, and 24-hour urine collection for protein. Renal ultrasound examination may also
be considered, and patients should be referred to appropriate subspecialists.
10. What are the effects of pregnancy on chronic renal disease?
Women with mild disease tend to have little risk of disease progression. Once Cr rises to more than
2.0 mg/dL, the risk of disease progression is 33%.
Obstetric complications of preterm delivery (often secondary to maternal indications) and pre-
eclampsia are increased for women with chronic renal disease. Mild disease, Cr levels of 1.4 mg/dL or
higher, and Cr levels of 2.5 mg/dL or higher are associated with preterm birth rates of 20%, 59%, and
86%, respectively. For preeclampsia, rates are 10% for women with mild disease and 40% for those
with Cr levels higher than 2.5 mg/dL.
11. What are the causes of nephrotic syndrome in pregnancy?
The most common cause of nephrotic-range proteinuria in pregnancy (3.5 g/day) is preeclampsia.
Other causes include diabetic nephropathy, systemic lupus erythematosus, minimal change disease,
membranous glomerulonephritis, and chronic renal disease.
Differentiating preeclampsia from chronic renal disease may be difficult because hypertension
with proteinuria can exist in both diseases, although preeclampsia has additional symptoms such as
transaminitis, azotemia, coagulopathy, oliguria, pulmonary edema, and persistent headache or vision
changes. For more information on this topic, see Chapter 49.
12. What complications can be seen in pregnant patients undergoing dialysis?
Dialysis dramatically increases the risk of miscarriage, fetal growth restriction, preterm delivery, and
perinatal demise. The median gestational age at delivery is 33.8 weeks, and the median birth weight
is 1750 g. Perinatal survival has increased greatly over the past several decades, however, from 23%
in 1980 to more than 90% at present. Hypertension occurs in 80% of pregnancies in women undergo-
ing dialysis, and preeclampsia and severe-range blood pressures are frequent indications for preterm
delivery.
13. What are the risks in pregnancy for women who have received a renal transplant?
Neonatal outcomes tend to depend on baseline renal function after transplantation, with a Cr level of
1.5 mg/dL or less leading to better outcomes. Moderate or severe disease is associated with higher
rates of preterm birth and perinatal mortality. Women are recommended to wait at least 1 year to
conceive after receiving a transplant, and waiting 2 years has been shown to optimize graft survival.
Comorbidities that are often present in these patients (e.g., hypertension and diabetes) can add
additional risk to a pregnancy.
14. Should women who have had a renal transplant stop or change their medications
when they become pregnant?
Ideally, women with a transplant should receive preconception counseling and have their immunosup-
pressive medications switched to agents with the best safety profiles before they become pregnant.
Cyclosporine, tacrolimus, azathioprine, and steroids are considered relatively safe in pregnancy. Myco-
phenolate mofetil has been shown to cause malformations and fetal demise; women should transition
to another agent at least 6 weeks before conception.
KEY POINTS: RENAL DISEASE IN PREGNANCY
1. During pregnancy, increased renal plasma flow and increased glomerular filtration rate lead to
decreased serum blood urea nitrogen and Cr level.
2. Pregnancy increases the risk of pyelonephritis because of anatomic changes that promote urinary
stasis, but it does not increase the rate of urolithiasis.
3. The most common cause of nephrotic-range proteinuria in pregnancy is preeclampsia.
4. Maternal chronic renal disease increases the risk of miscarriage, perinatal demise, preterm delivery,
and preeclampsia.
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RENAL DISEASE IN PREGNANCY 205
BiBliography
1. Castellano G, Losappio V, Gesualdo L. Update on pregnancy in chronic kidney disease. Kidney Blood Press Res.
2011;34:253–260.
2. Davison JM, Dunlop W. Renal hemodynamics and tubular function normal human pregnancy. Kidney Int.
1980;18:152–161.
3. Deshpande NA, Coscia LA, Gomez-Lobo V, et al. Pregnancy after solid organ transplantation: a guide for obstetric
management. Rev Obstet Gynecol. 2013;6:116–125.
4. Hooten TM. Uncomplicated urinary tract infection. N Engl J Med. 2012;366:1028–1037.
5. Manisco G, Potì’ M, Maggiulli G, Di Tullio M, Losappio V, Vernaglione L. Pregnancy in end-stage renal disease patients
on dialysis: how to achieve a successful delivery. Clin Kidney J. 2015;8:293–299.
6. Maynard SE, Thadhani R. Pregnancy and the kidney. J Am Soc Nephrol. 2009;20:14–22.
7. Odutayo A, Hladunewich M. Obstetric nephrology: renal hemodynamic and metabolic physiology in normal pregnancy.
Clin J Am Soc Nephrol. 2012;7:2073–2080.
8. Sheffield JS, Cunningham FG. Urinary tract infection in women. Obstet Gynecol. 2005;106:1085–1092.
9. Sheikh F, Venyo A. Proteinuria in pregnancy: a review of the literature. WebmedCentral, category: Obstetrics and
Gynaecology, 2012;3(11):WMC003814. Available at webmedcentral.com/article_view/3814.
10. Srirangam SJ, Hickerton B, Cleynenbreugel BV. Management of urinary calculi in pregnancy: a review. J Endourol.
2008;22:867–875.
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206
1. What is the incidence of pregestational diabetes?
Pregestational diabetes complicates 1% of all pregnancies.
2. What is the White classification of diabetes in pregnancy?
Historically, the White classification system has been used to help stratify women with diabetes
(Table 48-1). Its use is declining in favor of categorizing diabetes simply as either gestational or
pregestational and mentioning the presence of vascular compromise when applicable.
3. What type of testing should a pregnant woman with pregestational diabetes
undergo to determine baseline end-organ damage?
• Comprehensive eye examination
• Baseline renal function; assessed using serum creatinine level and 24-hour urine collection for
protein
• Electrocardiogram
4. What are the findings in diabetic retinopathy?
• Background retinopathy: retinal microaneurysms and dot-blot hemorrhages
• Proliferative retinopathy: neovascularization; needs treatment with laser therapy
Acute, rigorous metabolic control during pregnancy has been linked to acute worsening of retinopathy,
but it ultimately slows the process of long-term deterioration. Regression of retinopathy after delivery
is common.
5. What is the relationship between pregestational diabetes and thyroid function?
Approximately 30% of women with type 1 diabetes also have thyroid dysfunction; this number is
lower for type 2 diabetes but is still higher compared with the general population. Because of the risks
of thyroid disease in pregnancy (see Chapter 50), thyroid-stimulating hormone (TSH) levels should be
checked in all patients with pregestational diabetes.
6. What obstetric complications are associated with pregestational diabetes?
Spontaneous abortion, congenital anomalies, fetal macrosomia, intrauterine fetal death,
polyhydramnios, preeclampsia, preterm delivery, and primary cesarean delivery.
CHAPTER 48
PREGESTATIONAL AND
GESTATIONAL DIABETES
Kristen M. McMaster, MD
Table 48-1. White Classification of Diabetes in Pregnancy
DM CLASS DEFINITION
A1 Gestational diabetes: diet controlled
A2 Gestational diabetes: on medication
B Age of onset >20 years, duration <10 years
C Age of onset 10-19 years, duration 10-19 years
D Age of onset <10 years, duration >20 years
F Renal disease
H Cardiac disease
R Proliferative retinopathy
DM, Diabetes mellitus.
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PREGESTATIONAL AND GESTATIONAL DIABETES 207
7. What is the incidence of congenital anomalies in patients with pregestational
diabetes?
Overall, major congenital anomalies occur in 6% to 12% of infants of women with pregestational
diabetes. Glycosylated hemoglobin (HbA1c) levels correlate directly with the rate of anomalies—as
high as 20% to 25% in women with HbA1c 10% or greater. If HbA1C levels are 5% to 6%, the rate
returns to baseline (2% to 3%).
8. What are the effects of pregnancy on insulin and glucose metabolism?
Pregnancy causes generalized insulin resistance and hyperglycemia. This effect is less pronounced in the
first trimester, possibly because of high levels of estrogen (which can increase insulin sensitivity). Later
in pregnancy, insulin resistance predominates secondary to the effects of human placental lactogen,
progesterone, prolactin, placental growth hormone, and cortisol.
9. What is the pathophysiology of abnormal fetal growth in pregnancies complicated
by diabetes?
In cases of long-standing diabetes and significant vascular disease, fetal growth can be diminished.
More often, however, maternal hyperglycemia stimulates fetal hyperinsulinemia, which in turn stimulates
fetal growth. Infants born to diabetic mothers have increased subcutaneous fat and a higher risk of
shoulder dystocia. For more information on fetal macrosomia, see Chapter 44.
10. How should fetal assessment be performed in women with pregestational
diabetes?
A fetal anatomic survey should be performed at 18 to 20 weeks of gestation, followed by careful
fetal cardiac evaluation. Patients should then receive serial ultrasound examinations to monitor fetal
growth. Antepartum fetal surveillance should begin at 32 weeks of gestation. For more information on
this topic, see Chapter 40.
11. When is delivery indicated in pregnancies complicated by pregestational
diabetes?
Patients with well-controlled diabetes may be allowed to reach 39 weeks of gestation as long as
antenatal testing results remain reassuring. Continuation of pregnancy beyond 40 weeks is not
recommended. Patients with vasculopathy, nephropathy, poor glycemic control, or earlier stillbirth
should be managed in consultation with a subspecialist, and delivery timing is generally earlier.
12. What are the neonatal consequences of poorly controlled pregestational
diabetes?
Neonatal complications include hypoglycemia, respiratory distress syndrome, polycythemia, and
hyperbilirubinemia. Infants are also at risk for cognitive developmental delay and diabetes in later in
life.
13. What is the pathophysiology of neonatal hypoglycemia in infants born to diabetic
mothers?
Elevated maternal glucose levels are transported through the placenta to the fetus. Maternal insulin
does not cross the placenta, so fetal insulin production increases to compensate for maternal glucose
levels. Immediately after delivery, transport of glucose to the infant ceases but hyperinsulinemia
remains, resulting in neonatal hypoglycemia.
14. What are the incidence and pathogenesis of diabetic ketoacidosis (DKA) in
pregnancy?
DKA occurs in 5% to 10% of all pregnancies with pregestational diabetes. Although DKA is more
commonly seen in patients with type 1 diabetes, it can also been seen in those with type 2 diabetes.
The mean glucose level needed to enter into DKA is lower in pregnancy compared with the nonpregnant
state.
15. What is the typical presentation of DKA in pregnancy?
Abdominal pain, nausea and vomiting, altered sensorium, low arterial pH, low serum bicarbonate,
elevated anion gap, positive serum ketones, and continuous fetal monitoring showing repetitive late
decelerations.
16. How should DKA in pregnancy be managed?
Similarly to nonpregnant patients. Patients should be monitored in a critical care unit, and a continu-
ous insulin infusion should be started, with careful attention paid to blood glucose and electrolyte
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208 COMPLICATIONS OF PREGNANCY
levels. As glucose levels normalize, a regular diet and subcutaneous insulin can be resumed. These
patients should be managed in consultation with critical care and high-risk pregnancy specialists.
Continuous fetal heart rate monitoring should be used in viable pregnancies until the patient’s status
normalizes.
17. What is the fetal mortality rate in DKA?
Ten percent to 35% of cases.
18. What is the definition of gestational diabetes mellitus (GDM)?
Diabetes mellitus that develops for the first time during pregnancy.
19. What is the prevalence of GDM?
The prevalence varies with ethnicity and region. In general, 5% to 7% of all pregnancies are compli-
cated by diabetes, and 90% of those cases are gestational.
20. Who should be screened for GDM, and how is it done?
Trying to identify and exclude “low-risk” women reduces the number screened by only 10%, so
most providers screen all women. The most commonly used method is a two-step process, which
begins with a 1-hour, 50-g oral glucose challenge test (GCT) performed at 24 to 28 weeks of gesta-
tion. If results are abnormal, a confirmatory 3-hour, 100-g glucose tolerance test (GTT) is done. It is
estimated that approximately 95% of all obstetric practices use this screening technique. Various
cutoff values have been proposed, resulting in varying levels of sensitivity and specificity. Most recom-
mended threshold values for the 1-hour GCT range between 130 and 140 mg/dL.
21. How is the 1-hour GCT administered?
The patient (who does not need to be fasting) is given a 50-g glucose drink. One hour later, a blood
sample is drawn, and the glucose level is assessed. Because of the potential variation in capillary
glucose values, a glucometer should not be used for this test.
22. How is the 3-hour GTT administered?
Patients should fast for at least 8 hours before this test. A fasting serum sample is obtained, and then
the patient is given a 100-g glucose solution. Additional serum samples are collected 1, 2, and
3 hours afterward. If two or more of the four values are abnormal, gestational diabetes is diagnosed.
23. Are other screening test options available?
Yes. Another option is the 75-g, 2-hour GTT. The diagnosis of GDM would be made based on a single
glucose value meeting or exceeding established cutoff values (fasting value, ≥92 mg/dL; 1-hour value,
≥180 mg/dL; 2-hour value, ≥153 mg/dL). This method is not currently endorsed by the American
College of Obstetricians and Gynecologists (ACOG), and as many as 18% of women test positive for
GDM with it.
24. Which patients should be screened before 24 to 28 weeks of gestation?
Early screening should be performed on women with a previous history of GDM, known insulin insen-
sitivity, obesity (body mass index ≥30), or a strong family history of type 2 diabetes.
25. If results of screening before 24 to 28 weeks of gestation are normal, does
screening have to be repeated?
Yes. A normal early screening result excludes only pregestational diabetes. Patients should be
rescreened for GDM at 24 to 28 weeks.
KEY POINTS: PREGESTATIONAL DIABETES
1. The risk of congenital anomalies increases as HbA1c rises; to minimize this risk, it is important to
achieve good glycemic control before conception occurs.
2. Antenatal management should include screening for maternal end-organ damage and preexisting
thyroid disease, fetal anatomy and growth ultrasound examinations, fetal echocardiogram, and
antepartum fetal surveillance.
3. Obstetric complications in women with pregestational diabetes include spontaneous abortion,
congenital anomalies, fetal macrosomia, intrauterine fetal death, polyhydramnios, preeclampsia,
preterm delivery, and primary cesarean delivery.
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PREGESTATIONAL AND GESTATIONAL DIABETES 209
26. What are the potential complications of GDM?
GDM is associated with increased rates of gestational hypertension, preeclampsia, cesarean delivery,
operative delivery, more severe vaginal lacerations, and development of overt diabetes later in life.
Fetal complications include macrosomia, neonatal hypoglycemia and hyperbilirubinemia, shoulder
dystocia, and birth trauma.
27. What is the risk that a woman with GDM will develop type 2 diabetes later in life?
One third of women with GDM will have either persistent diabetes or insulin insensitivity diagnosed
post partum, and up to 50% of women with GDM will develop type 2 diabetes within 22 to 28 years.
This risk is exacerbated by certain factors such as ethnicity; for example, 60% of Hispanic women
develop type 2 diabetes within 5 years after a pregnancy complicated by GDM.
28. Does an increased risk of congenital malformations in GDM exist?
No. GDM develops long after organogenesis is complete. However, a positive early screening test
result indicates the possibility of undiagnosed pregestational diabetes. An HbA1c level can be used
in these cases to assess the degree of chronic hyperglycemia and the possibility of congenital
anomalies.
29. What nutritional recommendations can be made for patients with GDM?
Diet should consist of 33% to 40% carbohydrates, with the remaining 20% protein and 40% fat.
Complex carbohydrates are preferred over simple carbohydrates, and three meals and two snacks
per day are recommended to prevent large fluctuations in glucose levels. Moderate exercise is also
beneficial. For more information on exercise in pregnancy, see Chapter 37.
30. What is the best pharmacologic treatment for GDM?
Depending on the severity of insulin resistance, either insulin or oral medications can be used.
31. What are the recommendations for fetal testing in pregnancies complicated by
GDM?
Antepartum fetal surveillance is recommended in women with poorly controlled GDM, but no evidence
supports this testing in patients with well-controlled GDM.
32. Should women with GDM be delivered early?
Women with good glycemic control can be managed expectantly up to 39 to 40 weeks of gestation.
Patients with poor glycemic control should be managed in consultation with a subspecialist, and
delivery timing should be adjusted on a case-by-case basis.
33. How should women with GDM be managed after delivery?
In general, patients with true GDM do not need to continue treatment after delivery. However, they
should all be screened for diabetes 6 to 12 weeks post partum by using the 75-g, 2-hour GTT.
34. How should blood glucose levels be monitored in pregnancy?
In general, blood glucose is recorded four times a day: one fasting value and three 1- or 2-hour
postprandial values. Postprandial values are preferred over preprandial values because they are more
predictive of fetal morbidity and macrosomia.
35. What are target glucose levels in pregnancy?
Fasting glucose levels should be lower than 95 mg/dL, 1-hour postprandial values lower than
140 mg/dL, and 2-hour values lower than 120 mg/dL. Overnight glucose levels should never drop to
less than 60 mg/dL, and HbA1c values should not be greater than 6%.
KEY POINTS: GESTATIONAL DIABETES
1. GDM is diabetes that develops for the first time during pregnancy.
2. Screening for GDM is done with the 1-hour, 50-g glucose challenge test between 24 and 28 weeks
of gestation, and diagnosis is made with the 3-hour, 100-g glucose tolerance test if the 1-hour
screen test result is positive.
3. Women with GDM should be tested for persistent diabetes with a 2-hour, 75-g glucose tolerance
test 6 to 12 weeks post partum.
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210 COMPLICATIONS OF PREGNANCY
36. What are the principles of insulin use in pregnancy?
Insulin does not cross the placenta and is classically thought of as the gold standard pharmacologic
therapy for GDM. Typical starting doses are 0.7 to 1.0 units/kg daily, divided into doses of both
intermediate and short-acting insulin analogues. Insulin requirements increase over the course of a
pregnancy, reaching 1.2 units/kg/day (or higher) in the third trimester.
37. What is the action profile of commonly used insulin analogues in pregnancy?
• Lispro: onset of action within 1 to 15 minutes, peak action at 1 to 2 hours, duration of action 4 to
5 hours
• Regular: onset of action within 30 to 60 minutes, peak action in 2 to 4 hours, duration of action 6 to
8 hours
• NPH: onset of action within 1 to 3 hours, peak action in 5 to 7 hours, duration of action 13 to
18 hours
38. Which oral hypoglycemic agents are used in pregnancy?
Although glyburide and metformin are frequently used in pregnancy, neither agent is approved by the
Food and Drug Administration (FDA) for this purpose. These medications have both been demonstrated
to cross the placenta, although no adverse fetal effects have been established. Metformin inhibits
hepatic gluconeogenesis and glucose absorption, which increases insulin sensitivity in peripheral
tissues. Glyburide increases pancreatic insulin secretion, as well as insulin sensitivity in peripheral
tissues. Women treated with glyburide are less likely to require insulin supplementation than are those
treated with metformin.
39. What are target glucose levels in labor?
Strict intrapartum glycemic control is encouraged to prevent fetal hyperglycemia and subsequent
neonatal hypoglycemia. A target level of less than 110 mg/dL is recommended, and continuous insulin
infusions may be required to achieve this goal.
40. What happens to insulin requirements after delivery?
Insulin requirements decrease rapidly after delivery. In the postpartum period, patients should be
started on an insulin regimen using approximately one half the amount of their earlier doses.
BiBliography
1. American College of Obstetricians and Gynecologists. Gestational diabetes mellitus. ACOG practice bulletin no 137.
Obstet Gynecol. 2013;122:406–416.
2. American College of Obstetricians and Gynecologists. Pregestational diabetes mellitus. ACOG practice bulletin no. 60.
Obstet Gynecol. 2005;105:675–685.
3. Buchanan TA. Pregnancy in preexisting diabetes. In: Diabetes in America. 2nd ed. Bethesda, MD: National Institutes of
Health; 1995.
4. Cunningham F, Leveno KJ, Bloom SL, et al. Diabetes mellitus. In: Williams Obstetrics. 24th ed. New York: McGraw-Hill;
2013.
5. Perros P, McCrimmon RJ, Shaw G, Frier BM. Frequency of thyroid dysfunction in diabetic patients: value of annual
screening. Diabet Med. 1995;12:622–627.
6. Ryan EA, Enns L. Role of gestational hormones in the induction of insulin resistance. J Clin Endocrinol Metab.
1998;67:341–347.
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211
1. What is the definition of hypertension?
Hypertension is defined as systolic blood pressure 140 mm Hg or higher or diastolic blood pressure
90 mm Hg or higher.
2. What are the various types of hypertension that can occur in pregnancy?
The National Institutes of Health (NIH) Working Group on Hypertension in Pregnancy has classified
hypertension into four categories: chronic hypertension (CHTN), gestational hypertension (GHTN),
preeclampsia, and CHTN with superimposed preeclampsia (SIPE).
3. What is the definition of CHTN?
CHTN is defined as elevated blood pressure (≥140 systolic or ≥90 diastolic) on two separate occasions
before pregnancy, in the first 20 weeks of pregnancy, or persisting past 12 weeks post partum.
4. What is the definition of GHTN?
GHTN is defined as the presence of new-onset blood pressure (≥140 mm Hg systolic or ≥90 mm Hg
diastolic) after 20 weeks of gestation in the absence of proteinuria or other signs of preeclampsia.
5. What is the definition of preeclampsia?
Preeclampsia is characterized by the dysfunction of multiple organs and is considered a systemic
disease. Clinically, it is defined as new-onset elevated blood pressure (≥140 mm Hg systolic or
≥90 mm Hg diastolic) accompanied by proteinuria. It can also be diagnosed in the absence of proteinuria
if the patient has new-onset hypertension and any sign of severe preeclampsia (thrombocytopenia,
elevated creatinine, elevated liver function test results, neurologic symptoms, or pulmonary edema).
6. What is the definition of SIPE?
An abrupt increase in blood pressures from baseline in a woman with known CHTN, along with
proteinuria or any sign of severe preeclampsia.
7. How is proteinuria defined?
Proteinuria is defined as the presence of 300 mg or more of protein in a 24-hour urine collection or a
urine protein/creatinine ratio of 0.3 or greater. Although not ideal, a random urine sample can also be
used if other tests are not feasible or obtainable; 30 mg/dL (1+ dipstick) is considered positive.
8. What are the diagnostic criteria for preeclampsia with severe features?
Systolic blood pressure 160 mm Hg or higher or diastolic blood pressure 110 mm Hg or higher on
two occasions 4 hours apart while on bed rest or elevated blood pressures (≥140 mm Hg systolic
or ≥90 mm Hg diastolic) and any of the following: platelet count lower than 100,000/μL, serum
creatinine level higher than 1.1 mg/dL or a doubling from baseline, increased liver function test results
to twice the normal concentration, pulmonary edema, neurologic symptoms, or severe right upper
quadrant or epigastric pain unrelieved by medication.
Proteinuria greater than 5 g and intrauterine growth restriction are no longer considered criteria
for preeclampsia with severe features.
9. What causes the right upper quadrant or epigastric pain associated with
preeclampsia?
Hepatic involvement can cause distention of the liver capsule that often causes pain, nausea, and
vomiting. In the most severe cases, rupture and massive hemorrhage can occur.
10. What are risk factors for preeclampsia?
• Nulliparity
• Extremes of age (<15 and >35 years)
• African-American ethnicity
• Personal or family history of preeclampsia
CHAPTER 49
HYPERTENSION IN PREGNANCY
Erin Burnett, MD
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212 COMPLICATIONS OF PREGNANCY
• Multiple gestation
• Obesity
• Molar pregnancy
• Other medical conditions (e.g., diabetes, lupus, CHTN, antiphospholipid syndrome)
11. How common is preeclampsia?
In general, preeclampsia occurs in 4% of all pregnancies that extend beyond the first trimester.
The rate for nulliparous patients is approximately 7%.
12. What is the incidence of preeclampsia among women with pregestational
diabetes?
Rates increase with duration of diabetes and the presence of any associated vascular complications.
The incidence of preeclampsia is 11% to 12% in class B diabetes, 21% to 23% in class C or D
diabetes, and 36% to 54% in class F or R diabetes. For more information on diabetes in pregnancy,
see Chapter 48.
13. What causes preeclampsia?
The true cause of preeclampsia is unknown. It is hypothesized that incomplete trophoblastic invasion
into maternal spiral arteries results in poor placental perfusion and hypoxia, which in turn result in the
release of free radicals and oxidative stress.
14. Can preeclampsia be prevented?
No true preventive measures exist, but studies have shown a rate reduction in women with risk
factors who take low-dose aspirin. The magnitude of risk reduction is greatest among women with a
history of preeclampsia before 34 weeks of gestation.
15. What is the effectiveness of aspirin in reducing the risk of preeclampsia?
A meta-analysis of 34 randomized control trials found that starting low-dose aspirin before
16 weeks in women at increased risk for preeclampsia was associated with significant decreases
in rates of preeclampsia (53%), severe preeclampsia (90%), intrauterine growth restriction (54%),
and preterm birth (78%). Aspirin must be started by 16 weeks (before the placental changes
that can precipitate preeclampsia take place), and it should be stopped by 37 to 38 weeks in
anticipation of delivery.
16. What fetal and maternal risks are associated with preeclampsia?
• Maternal risks
• HELLP (hemolysis, elevated liver enzymes, and low platelets; 20%)
• Disseminated intravascular coagulation (DIC) (10%)
• Placental abruption (1% to 4%)
• Renal failure (1% to 2%)
• Seizures (1%)
• Cerebral hemorrhage (<1%)
• Liver hemorrhage (<1%)
• Death (rare)
• Fetal risks
• Preterm birth (15% to 60%)
• Intrauterine growth restriction (10% to 25%)
• Perinatal death (1% to 2%)
• Hypoxemia-associated neurological injury (<1%)
17. Does preeclampsia recur in subsequent pregnancies?
One earlier episode of preeclampsia imparts a 15% to 25% risk of recurrence; two earlier episodes
increase that risk to at least 30%. These rates change based on paternity, maternal age at the time
of the next pregnancy, gestational age and severity of preeclampsia in the past, and the presence of
underlying medical diseases. Women who were multiparous at the time of a previous case are at even
higher risk in subsequent pregnancies.
18. Does preeclampsia have any long-term effects?
Yes. Studies have shown that these women are at increased risk for cardiovascular disease in the
future, even before menopause. The risk is highest for women who had preeclampsia at an early
gestational age or were multiparous.
https://t.me/med1917
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