Table 8-4. Placental Function in Post-term Pregnancy
| Maintained | Deteriorates |
| Macrosomia (80%) | Dysmaturity (20%) |
| Difficult labor and delivery | Placental insufficiency |
| ↑ C section | ↑ C section |
| (forceps, vacuum extractor, shoulder | (acidosis, meconium aspiration, |
| dystocia, birth trauma) | oxygen deprivation) |
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Management of Meconium. Previous recommendations to prevent meconium aspiration syn-drome (MAS) included:
• In labor, amnioinfusion (with saline infused through an intrauterine catheter) todilute meconium and provide a fluid cushion to prevent umbilical cord compression.
• After the head is delivered, suction the fetal nose and pharynx to remove any upperairway meconium.
• After the body is delivered, visualize the vocal cords with a laryngoscope to removemeconium below the vocal cords.
Newer recommendations (American Heart Association, American Academy of Pediatrics):
• Amnioinfusion may be helpful to prevent umbilical cord compression; okay toperform it.
• Suctioning of fetal nose and pharynx makes no difference in preventing MAS; do notroutinely perform.
• Laryngoscopic visualization of vocal cords is only indicated if the neonate isdepressed; perform selectively.
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| Hypertensive Complications | 9 | |
HYPERTENSION IN PREGNANCY
Systolic and diastolic blood pressure both decline early in the first trimester, reaching a nadir by 24–28 weeks; then they gradually rise toward term but never return quite to prepregnancy baseline. Diastolic falls more than systolic, as much as 15 mm Hg. Arterial blood pressure is never normally elevated in pregnancy.
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GESTATIONAL HYPERTENSION
A 19-year-old primigravida is seen in the outpatient prenatal clinic for routine visit. She is at 32 weeks’ gestation, confirmed by first trimester sonogram. She has no complaints. She denies headache, epigastric pain, or visual disturbances. She has gained 2 pounds since her last visit 2 weeks ago. On examination her blood pressure is 155/95 mm Hg, which is persistent on repeat check 10 minutes later. She has only trace pedal edema. A spot urine dipstick is negative.
Definition. Gestational hypertension is diagnosed with sustained elevation of BP≥140/90 mm Hgafter 20 weeks of pregnancy without proteinuria. BP returns to normal baseline postpartum.
Symptoms. No symptoms of preeclampsia are seen, e.g., headache, epigastric pain, visual distur-bances. Physical findings are unremarkable for pregnancy.
Laboratory Abnormalities. Laboratory tests are unremarkable for pregnancy. Proteinuria isabsent.
Diagnostic Tests. The key finding is sustained elevation of BP >140/90 mm Hg without pro-teinuria.
Management. Conservative outpatient management is appropriate. Close observation is pru-dent since 30% of patients will develop preeclampsia. Appropriate laboratory testing should be performed to rule out preeclampsia, e.g., urine protein, hemoconcentration assessment.
Differential Diagnosis. Preeclampsia should always be ruled out.
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Note
Refer to Physiologic Changes in Pregnancy for a review of normal blood pressure during pregnancy.
OB Triad
Gestational Hypertension
• Pregnancy >20 wk
• Sustained HTN
• No proteinuria
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OB Triad
Mild Preeclampsia
• Pregnancy >20 wk
• Sustained HTN (>140/90 mm Hg)
• Proteinuria (≥300 mg/24 h)
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MILD PREECLAMPSIA
A 21-year-old primigravida is seen in the outpatient prenatal clinic for routine visit. She is at 32 weeks’ gestation, confirmed by first trimester sonogram. She denies headache, epigastric pain, or visual disturbances. She has gained 10 pounds since her last visit 2 weeks ago. On examination her BP is 155/95, and remains unchanged on repeat check in 15 min. She has 2+ pedal edema, and her fingers appear swollen. A spot urine dipstick shows 2+ protein.
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Definition. Preeclampsia is sustained BP elevation in pregnancy after 20 weeks’ gestation inthe absence of preexisting hypertension.
Diagnostic Criteria. There are no pathognomic tests. The diagnostic dyad includes the following:
• Sustained BP elevation of≥140/90 mm Hg.
• Proteinuria on dipstick of 1–2+ or≥300 mg on a 24-h urine collection.
Risk Factors. Preeclampsia is found 8 times more frequently in primiparas. Other risk factorsare multiple gestation, hydatidiform mole, diabetes mellitus, age extremes, chronic hypertension, and chronic renal disease.
Etiology/Pathophysiology. Pathophysiology involves diffuse vasospasm caused by (1) loss ofthe normal pregnancy-related refractoriness to vasoactive substances such as angiotensin; and
(2) relative or absolute changes in the following prostaglandin substances: increases in the vasoconstrictor thromboxane along with decreases in the potent vasodilator prostacyclin. This vasospasm contributes to intravascular volume constriction and decreased perfusion of most organs including uteroplacental unit, kidneys, liver, brain, and heart. Decreased renal blood flow leads to decreased clearance of body metabolic wastes. Capillary injury leads to loss of intravascular volume into the interstitial space and subsequent edema.
Presenting Symptoms and Physical Examination. With mild preeclampsia the symptomsand physical findings, if present, are generally related to excess weight gain and fluid retention. Presence of new onset of persistent headache, epigastric pain, or visual disturbances would move the diagnosis from mild to severe preeclampsia.
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Laboratory Abnormalities. Evidence of hemoconcentration is shown by elevation of hemoglo-bin, hematocrit, blood urea nitrogen (BUN), serum creatinine, and serum uric acid. Proteinuria is present (described under diagnostic criteria). Evidence of disseminated intravascular coagulation (DIC) or liver enzyme elevation would move the diagnosis from mild to severe preeclampsia.
Management. The only definitive cure is delivery and removal of all fetal-placental tissue.However, delivery may be deferred in mild preeclampsia to minimize neonatal complications of prematurity. Management is based on gestational age.
• Conservative inpatient. Before 36 weeks’ gestation as long as mother and fetus are
stable, mild preeclampsia is managed in the hospital, watching for possible progression to severe preeclampsia. No antihypertensive agents or MgSO4 are used.
• Delivery. At≥36 weeks’ gestation, delivery is indicated with dilute IV oxytocin inductionof labor and continuous infusion of IV MgSO4 to prevent eclamptic seizures.
Complications. Progression from mild to severe preeclampsia may occur.
Differential Diagnosis. Chronic hypertension should always be ruled out.
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SEVERE PREECLAMPSIA
A 21-year-old primigravida is seen in the outpatient prenatal clinic for a routine visit. She is at 32 weeks’ gestation, confirmed by first trimester sonogram. For the past 24 h she had experienced severe, unremitting occipital headache, and mid-epigastric pain not relieved by acetaminophen, and she has also seen light flashes and spots in her vision. She has gained 10 pounds since her last visit 2 weeks ago. On examination her BP is 165/115. She has 2+ pedal edema, and her fingers appear swollen. Fundal height is 29 cm. Fetal heart tones are regular at 145 beats/min. A spot urine dipstick shows 4+ protein.
Diagnostic Tests. The diagnosis is made on the basis of the finding of at least mild preeclampsiaplus any one of the following:
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• Sustained BP elevation of≥160/110.
• Proteinuria on dipstick of 3–4+ or≥5 g on a 24-h urine collection.
• Evidence of maternal jeopardy. This may include symptoms (headache, epigastricpain, visual changes), thrombocytopenia (platelet count <100,000/mL), elevated liver enzymes, pulmonary edema, oliguria (<750 mL/24 h), cyanosis, or IUGR.
• Edema may or may not be seen.
Risk Factors. These are the same as mild preeclampsia with the addition of diseases with smallvessel disease such as systemic lupus and longstanding overt diabetes.
Etiology/Pathophysiology. Pathophysiology is the same as mild preeclampsia but involves severe diffuse vasospasm and more intense capillary injury to where the ischemia demon-strates itself in overt, usually multiorgan system injury.
Presenting Symptoms. Presence of new onset of persistent headache, epigastric pain, or visualdisturbances is characteristic of severe preeclampsia.
Laboratory Abnormalities. Evidence of hemoconcentration will be more severe. Proteinuriais described under diagnostic tests. Evidence of DIC and hepatocellular injury is characteristic of severe preeclampsia.
Management. Aggressive prompt delivery is indicated for severe preeclampsia at any gestationalage with evidence of maternal jeopardy or fetal jeopardy. Main goals are seizure prevention and blood pressure control.
• Administer IV MgSO 4 to prevent convulsions. Give a 5-g loading dose, then continuemaintenance infusion of 2 g/h.
• Lower BP to diastolic values 90–100 mm Hg with IV hydralazine and/or labetalol.More aggressive blood pressure control may jeopardize uteroplacental fetal perfusion.
• Attempt vaginal delivery with IV oxytocin infusion if mother and fetus are stable.
• Cesarean section is only for obstetric indications.
Conservative inpatient management may rarely be attempted in absence of maternal and fetaljeopardy with gestational age 26–34 weeks if BP can be brought below 160/110 mm Hg. This should take place in an intensive care, tertiary-care setting. Continuous IV MgSO4 should be administered, and maternal betamethasone should be given to enhance fetal lung maturity.
Complications. Progression from severe preeclampsia to eclampsia may occur.
Note
Severe preeclampsia has many presentations.
OB Triad
Severe Preeclampsia
• Pregnancy >20 wk
• Sustained HTN (>160/110 mm Hg)
• Proteinuria
(≥5 grams/24 h)
• Pregnancy >20 wk
• Sustained HTN (>140/90 mm Hg)
• Headache or epigastric pain or visual changes
• Pregnancy >20 wk
• Sustained HTN (>140/90 mm Hg)
• DIC or ↑ liver enzymes or pulmonary edema
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ECLAMPSIA
A 21-year-old primigravida is brought to the emergency department after suffering from a generalized tonic-clonic seizure at 32 weeks’ gestation. The seizure was preceded by a severe headache. She lost control of her bowels and bladder. She has gained 10 pounds since her last prenatal visit 2 weeks ago. On examination she is unresponsive and in a postictal state. Her BP is 185/115, and a spot urine dipstick shows 4+ protein.
Definition. Eclampsia is the presence of unexplained generalized seizures in a hypertensive,proteinuric pregnant woman in the last half of pregnancy.
Risk Factors. These are the same as mild and severe preeclampsia. A primary seizure disorderdoes not predispose to eclampsia.
Etiology/Pathophysiology. Pathophysiology is severe diffuse cerebral vasospasm resulting incerebral perfusion deficits and cerebral edema.
Presenting Symptoms. In addition to those of mild and severe preeclampsia, the most signifi-cant finding is unexplained tonic-clonic seizures.
Laboratory Abnormalities. These are the same as found with mild and severe preeclampsia.
Diagnosis. The diagnosis is made clinically with unexplained generalized seizures occurring ina hypertensive, proteinuric pregnant woman in the last half of pregnancy.
Management. The first step is to protect the mother’s airway and tongue.
• Administer MgSO 4 with an IV bolus of 5 g to stop seizures, continuing maintenanceinfusion rate of 2 g/h.
• Aggressive prompt delivery is indicated for eclampsia at any gestational age after stabi-lization of the mother and the fetus. Attempt vaginal delivery with IV oxytocin infusion if mother and fetus are stable.
• Lower diastolic BP between 90 and 100 mm Hg with IV hydralazine and/or labetalol.
Complications. Intracerebral hemorrhage can occur with even death resulting.
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