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Teresa G. Berg, M.D. Maternal-Fetal Medicine University Medical Associates M3 Lecture Materials
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Be able to define hypertension in relationship to pregnancy Be able to classify hypertensive diseases in pregnant women Be able to list criteria for the diagnosis of preeclampsia Be able to list criteria for the diagnosis of severe preeclampsia/HELLP syndrome Be able to discuss current management considerations Understand and discuss the effects of hypertension on the mother and fetus
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Sustained BP elevation of 140/90 or greater Proper cuff size Measurement taken while seated Arm at the level of the heart Use 5 th Korotkoff sound
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Chronic Hypertension Gestational Hypertension Preeclampsia Eclampsia HEELP Syndrome
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Chronic Hypertension ◦ Diagnosed before the 20 th week or present before the pregnancy ◦ Mild hypertension > 140-180 mmHg systolic > 90-100 mmHg diastolic Gestational Hypertension Preeclampsia Eclampsia HEELP Syndrome
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Chronic Hypertension Gestational Hypertension ◦ Criteria Develops after 20 weeks of gestation Proteinuria is absent Blood pressures return to normal postpartum ◦ Morbidity is directly related to the degree of hypertension Preeclampsia Eclampsia HEELP Syndrome
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25%
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Chronic Hypertension Gestational Hypertension Preeclampsia ◦ Criteria Develops after 20 weeks Blood pressure elevated on two occasions at least 6 hours apart Associated with proteinuria and edema May occur less than 20 weeks with gestational trophoblastic neoplasia Eclampsia HEELP Syndrome
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Criteria for Preeclampsia Criteria for Severe Preclampsia Previously normotensive woman > 140 mmHg systolic > 90 mmHg diastolic Proteinuria > 300 mg in 24 hour collection Nondependent edema BP > 160 systolic or >110 diastolic > 5 gr of protein in 24 hour urine or > 3+ on 2 dipstick urines greater than 4 hours apart Oliguria < 500 mL in 24 hours Cerebral or visual distrubances (headache, scotomata) Pulmonary edema or cyanosis Epigastric or RUQ pain Evidence of hepatic dysfunction Thrombocytopenia Intrauterine growth restriciton (IUGR)
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Nulliparity Multifetal gestations Maternal age over 35 Preeclampsia in a previous pregnancy Chronic hypertension Pregestational diabetes Vascular and connective tissue disorders Nephropathy Antiphospholipid syndrome Obesity African-American race
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FACTORRISK RATIO Nulliparity3:1 Age > 403:1 African American1.5:1 Chronic hypertension10:1 Renal disease20:1 Antiphospholipid syndrome10:1
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Chronic Hypertension Gestational Hypertension Preeclampsia Eclampsia ◦ Diagnosis of preeclampsia ◦ Presence of convulsions not explained by a neurologic disorder Grand mal seizure activity ◦ Occurs in 0.5 to 4% or patients with preeclampsia HEELP Syndrome
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Chronic Hypertension Gestational Hypertension Preeclampsia Eclampsia HELLP Syndrome ◦ A distinct clinical entity with: Hemolysis, Elevated Liver enzymes, Low Platelets ◦ Occurs in 4 to 12 % of patients with severe preeclampsia Microangiopathic hemolysis Thrombocytopenia Hepatocellular dysfunction
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Hypertension affects 12 to 22% of pregnant patients Hypertensive disease is directly responsible for approximately 20% of maternal mortality in the United State
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Vasospasm Uterine vessels Hemostasis Prostanoid balance Endothelium-derived factors Lipid peroxide, free radicals and antioxidants
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Vasospasm ◦ Predominant finding in gestational hypertension and preeclampsia Uterine vessels Hemostasis Prostanoid balance Endothelium-derived factors Lipid peroxide, free radicals and antioxidants
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Vasospasm Uterine vessels ◦ Inadequate maternal vascular response to trophoblastic mediated vascular changes ◦ Endothelial damage Hemostasis Prostanoid balance Endothelium-derived factors Lipid peroxide, free radicals and antioxidants
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Vasospasm Uterine vessels Hemostasis ◦ Increase platelet activation resulting in consumption ◦ Increased endothelial fibronectin levels ◦ Decreased antithrombin III and α 2 -antiplasmin levels ◦ Allows for microthrombi development with resultant increase in endothelial damage Prostanoid balance Endothelium-derived factors Lipid peroxide, free radicals and antioxidants
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Vasospasm Uterine vessels Hemostasis Prostanoid balance ◦ Prostacyclin (PGI 2 ):Thromboxane (TXA 2 ) balance shifted to favor TXA2 ◦ TXA2 promotes: Vasoconstriction Platelet aggregation Endothelium-derived factors Lipid peroxide, free radicals and antioxidants
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Vasospasm Uterine vessels Hemostasis Prostanoid balance Endothelium-derived factors ◦ Nitric oxide is decreased in patients with preeclampsia As this is a vasodilator, this may result in vasoconstriction Lipid peroxide, free radicals and antioxidants
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Vasospasm Uterine vessels Hemostasis Prostanoid balance Endothelium-derived factors Lipid peroxide, free radicals and antioxidants ◦ Increased in preeclampsia ◦ Have been implicated in vascular injury
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Cardiovascular effects Hematologic effects Neurologic effects Pulmonary effects Renal effects Fetal effects
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Cardiovascular effects ◦ Hypertension ◦ Increased cardiac output ◦ Increased systemic vascular resistance Hematologic effects Neurologic effects Pulmonary effects Renal effects Fetal effects
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Cardiovascular effects Hematologic effects ◦ Volume contraction/Hypovolemia ◦ Elevated hematocrit ◦ Thrombocytopeniz ◦ Microangiopathic hemolytic anemia ◦ Third spacing of fluid ◦ Low oncotic pressure Neurologic effects Pulmonary effects Renal effects Fetal effects
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Cardiovascular effects Hematologic effects Neurologic effects ◦ Hyperreflexia ◦ Headache ◦ Cerebral edema ◦ Seizures Pulmonary effects Renal effects Fetal effects
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Cardiovascular effects Hematologic effects Neurologic effects Pulmonary effects ◦ Capillary leak ◦ Reduced colloid osmotic pressure ◦ Pulmonary edema Renal effects Fetal effects
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Cardiovascular effects Hematologic effects Neurologic effects Pulmonary effects Renal effects ◦ Decreased glomerular filtration rate ◦ Glomerular endotheliosis ◦ Proteinuria ◦ Oliguria ◦ Acute tubular necrosis Fetal effects
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Decreased glomerular filtration rate Glomerular endotheliosis Proteinuria Oliguria Acute tubular necrosis
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Cardiovascular effects Hematologic effects Neurologic effects Pulmonary effects Renal effects Fetal effects ◦ Placental abruption ◦ Fetal growth restriction ◦ Oligohydramnios ◦ Fetal distress ◦ Increased perinatal morbidity and mortality
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The ultimate cure is delivery Assess gestational age Assess cervix Fetal well-being Laboratory assessment Rule out severe disease!!
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Delivery is always a reasonable option if term If cervix is unfavorable and maternal disease is mild, expectant management with close observation is possible
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Rule out severe disease Conservative management Serial labs Twice weekly visits Antenatal fetal surveillance Outpatient versus inpatient
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Worsening BP Nonreassuring fetal condition Development of severe PIH Fetal lung maturity Favorable cervix
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No contraindication to prostaglandin agents If < 32 weeks, consider cesarean When favorable, oxytocin
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Fetal monitoring IV access IV hydration The reason to treat is maternal, not fetal May require ICU
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Diastolic BP > 105-110 Systolic BP > 200 Avoid rapid reduction in BP Do not attempt to normalize BP Goal is DBP < 105 not < 90 May precipitate fetal distress
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Crises are associated with hypovolemia Clinical assessment of hydration is inaccurate Unprotected vascular beds are at risk, eg, uterine
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250-500 cc of fluid, IV Avoid multiple doses in rapid succession Allow time for drug to work Maintain LLD position Avoid over treatment
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Hydralazine Labetalol Nifedipine Nitroprusside Diazoxide Clonidine
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Dose: 5-10 mg every 20 minutes Onset: 10-20 minutes Duration: 3-8 hours Side effects: headache, flushing, tachycardia, lupus like symptoms Mechanism: peripheral vasodilator
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Dose: 20mg, then 40, then 80 every 20 minutes, for a total of 220mg Onset: 1-2 minutes Duration: 6-16 hours Side effects: hypotension Mechanism: Alpha and Beta block
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Dose: 10 mg po, not sublingual Onset: 5-10 minutes Duration: 4-8 hours Side effects: chest pain, headache, tachycardia Mechanism: CA channel block
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Dose: 1 mg po Onset: 10-20 minutes Duration: 4-6 hours Side effects: unpredictable, avoid rapid withdrawal Mechanism: Alpha agonist, works centrally
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Dose: 0.2 – 0.8 mg/min IV Onset: 1-2 minutes Duration: 3-5 minutes Side effects: cyanide accumulation, hypotension Mechanism: direct vasodilator
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Magnesium sulfate 4-6 g bolus 1-2 g/hour Monitor urine output and DTR’s With renal dysfunction, may require a lower dose
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Is not a hypotensive agent Works as a centrally acting anticonvulsant Also blocks neuromuscular conduction Serum levels: 6-8 mg/dL
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Respiratory rate < 12 DTR’s not detectable Altered sensorium Urine output < 25-30 cc/hour Antidote: 10 ml of 10% solution of calcium gluconate 1 v over 3 minutes
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Few people die of seizures Protect patient Avoid insertion of airways and padded tongue blades IV access MGSO4 4-6 bolus, if not effective, give another 2 g
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Have not been shown to be as efficacious as magnesium sulfate and may result in sedation that makes evaluation of the patient more difficult ◦ Diazepam 5-10 mg IV ◦ Sodium Amytal 100 mg IV ◦ Pentobarbital 125 mg IV ◦ Dilantin 500-1000 mg IV infusion
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Assess maternal labs Fetal well-being Effect delivery Transport when indicated No need for immediate cesarean delivery
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Pulmonary edema Oliguria Persistent hypertension DIC
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Fluid overload Reduced colloid osmotic pressure Occurs more commonly following delivery as colloid oncotic pressure drops further and fluid is mobilized
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Avoid over-hydration Restrict fluids Lasix 10-20 mg IV Usually no need for albumin or Hetastarch (Hespan)
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25-30 cc per hour is acceptable If less, small fluid boluses of 250-500 cc as needed Lasix is not necessary Postpartum diuresis is common Persistent oliguria almost never requires a PA cath
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BP may remain elevated for several days Diastolic BP less than 100 do not require treatment By definition, preeclampsia resolves by 6 weeks
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Rarely occurs without abruption Low platelets is not DIC Requires replacement blood products and delivery
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Continuous lumbar epidural is preferred if platelets normal Need adequate pre-hydration of 1000 cc Level should always be advanced slowly to avoid low BP Avoid spinal with severe disease
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He-hemolysis EL-elevated liver enzymes LP-low platelets
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Is a variant of severe preeclampsia Platelets < 100,000 LFT’s - 2 x normal May occur against a background of what appears to be mild disease
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Controversial Steroids Requires tertiary care Must have stable labs and reassuring fetal status May use antihypertensives
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Low dose ASA ineffective in patients at low risk Calcium supplementation is ineffective (2.0 g of calcium gluconate per day) No compelling evidence that either are harmful Recent study done with antioxidant (1,000mg VitC and 400mg VitE). ◦ Small study that needs to be confirmed.
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Criteria for diagnosis Laboratory and fetal assessment Magnesium sulfate seizure prophylaxis Timing and place of delivery
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