Questions
- 1.
Classify the hypertensive disorders of pregnancy.
- 2.
What are the incidence and risk factors of preeclampsia?
- 3.
Explain the etiology of preeclampsia.
- 4.
Describe the pathophysiology of preeclampsia.
- 5.
What is the obstetric management of preeclampsia?
- 6.
How is preeclampsia prevented from degenerating into eclampsia?
- 7.
How is preeclampsia-related hypertension managed?
- 8.
What are the potential consequences of epidural analgesia in a patient with preeclampsia?
- 9.
What are the anesthetic options for cesarean delivery for a patient with preeclampsia?
- 10.
Outline the anticipated postpartum problems associated with preeclampsia.
A 15-year-old nulliparous patient presented to the labor and delivery suite in week 35 of her pregnancy. Her chief complaint was headache. Her blood pressure was 145/95 mm Hg, and she appeared edematous.
1
Classify the hypertensive disorders of pregnancy.
The hypertensive disorders of pregnancy are classified into four groups: chronic hypertension, preeclampsia-eclampsia, chronic hypertension with superimposed preeclampsia, and gestational hypertension ( Box 55-1 ).
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Chronic hypertension
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Manifests before week 20 of gestation
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Preeclampsia-eclampsia
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Manifests after week 20 of gestation
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Associated with proteinuria
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Chronic hypertension with superimposed preeclampsia
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Gestational hypertension
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Manifests after week 20 of gestation without associated symptoms
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Hypertension is defined as:
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Systolic blood pressure: >140 mm Hg or 30 mm Hg above baseline
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Diastolic blood pressure: >90 mm Hg or 15 mm Hg above baseline
Blood pressures should be measured at rest with left uterine displacement and should be reproducible at least 6 hours later.
Chronic hypertension is diagnosed when the blood pressure is elevated before week 20 of pregnancy. Because blood pressure normally decreases during pregnancy, any parturient with a diastolic blood pressure >80 mm Hg is suspected to have chronic hypertension.
Preeclampsia-eclampsia is a hypertensive disorder unique to pregnancy. Preeclampsia is hypertension associated with proteinuria. Edema no longer has to be present to make the diagnosis. Except in association with hydatidiform mole, preeclamptic hypertension does not manifest before 20 weeks of gestation. Proteinuria is defined as the excretion of >0.3 g of protein in a 24-hour urine collection or 1+ on dipstick analysis. Preeclampsia is classified as either mild or severe depending on the degree of hypertension, extent of proteinuria, or patient complaints. Preeclampsia degenerates into eclampsia when generalized seizures occur ( Table 55-1 ).
| Mild Preeclampsia | Severe Preeclampsia | |
|---|---|---|
| Hypertension Systolic pressure Diastolic pressure | >140 mm Hg >30 mm Hg above baseline >90 mm Hg >15 mm Hg above baseline | >160 mm Hg >110 mm Hg |
| Proteinuria | 1–2 + by dipstick | 3–4 + by dipstick |
| >1 g/24 hours | >5 g/24 hours | |
| Patient symptoms | Headache | |
| Visual disturbances | ||
| Epigastric pain | ||
| Cyanosis |
Gestational hypertension is defined as hypertension occurring after 20 weeks of pregnancy in the absence of other signs of preeclampsia. Gestational hypertension is frequently essential hypertension that is unmasked by pregnancy.
2
What are the incidence and risk factors of preeclampsia?
Preeclampsia occurs in approximately 5%–10% of pregnancies, and eclampsia occurs in 0.2%–0.7% of pregnancies. A primigravida, at both extremes of age, with poor prenatal care is at highest risk for preeclampsia. Other risk factors include the use of barrier contraception, obesity, chronic renal failure, and hypertension. Women with antiphospholipid syndrome are also at risk. Preeclampsia is associated with rapid uterine enlargement such as occurs with hydatidiform mole, diabetes mellitus, and multiple gestations. There is a 33% probability of preeclampsia recurring with subsequent pregnancies.
3
Explain the etiology of preeclampsia.
Although the etiology of preeclampsia is unknown, uteroplacental ischemia appears to be a common factor. (1978) suggested that uteroplacental ischemia may result from altered immunity such as graft-versus-host reaction. It is also possible that placental prostaglandin imbalance between thromboxane and prostacyclin leads to preeclampsia. In a normal pregnancy, prostacyclin and thromboxane are produced in equal amounts by the placenta. In a pregnancy complicated by preeclampsia, there is a relative increase in thromboxane production. Thromboxane causes increased vasoconstriction, platelet aggregation, and uterine activity and a simultaneous decrease in uteroplacental blood flow. These effects are observed in preeclampsia.
Uteroplacental ischemia leads to the production of substances similar to renin and thromboplastin. Renin causes release of angiotensin and aldosterone, which result in hypertension and edema. Thromboplastin can initiate coagulopathies such as disseminated intravascular coagulation (DIC).
4
Describe the pathophysiology of preeclampsia.
The hallmark of preeclampsia is vasospasm that occurs secondary to increased circulating levels of renin, aldosterone, angiotensin, and catecholamines. Aldosterone also causes sodium and water retention, which leads to generalized edema. Because almost every organ system is affected in a parturient with preeclampsia, it is best to take a systematic approach when discussing the changes seen in preeclampsia ( Box 55-2 ).
Central nervous system
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Cerebral edema and vasospasm
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Headache
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Hyperreflexia
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Blurry vision
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Blindness
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Seizures
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Coma
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Cerebral hemorrhage
Pulmonary system
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Upper airway and laryngeal edema
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Difficult tracheal intubation
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Predisposition to upper respiratory infections
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Pulmonary capillary leak
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Increased A-a gradient
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Cardiovascular system
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Vasoconstriction
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Hypertension
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Impaired tissue perfusion
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Cellular hypoxia
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Increased cardiac work
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Fluid translocation
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Generalized edema
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Hypovolemia
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Hemoconcentration
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Increased blood viscosity
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Left ventricular hypertrophy and dysfunction
Renal system
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Decreased renal blood flow
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Decreased glomerular filtration rate
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Decreased creatinine clearance
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Proteinuria
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Increased uric acid levels correlate with severity of disease
Hepatic system
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Periportal hemorrhage
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Subcapsular hematomas
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Abnormal liver function tests
Hematologic system
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Decreased platelet count
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Qualitative platelet abnormality
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Abnormal coagulation profile
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Disseminated intravascular coagulation
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HELLP * syndrome
Uteroplacental system
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Decrease in intervillous blood flow
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Premature labor
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Small placenta
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Uterine hyperactivity
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Uterine sensitivity to oxytocin
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Placental abruption
*Hemolysis, elevated liver function tests, and low platelet count.
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