Hypertensive disorders in pregnancy dr. betha fe m. castillo 102413

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  • {"60":"Chronic/preexisting hypertension — Chronic/preexisting hypertension is defined as systolic pressure ≥140 mmHg and/or diastolic pressure ≥90 mmHg that antedates pregnancy or is present before the 20th week of pregnancy (on at least two occasions) or persists longer than 12 weeks postpartum. It can be primary (essential hypertension) or secondary to a variety of medical disorders. (See "Overview of hypertension in adults"\n","38":"Laboratory follow-up — The minimum laboratory evaluation should include platelet count, serum creatinine, and serum AST. These tests should be repeated once or twice weekly in women with mild preeclampsia to assess for disease progression, and more often if clinical signs and symptoms suggest worsening disease [27].\nThe value of other tests is less clearly defined. A rising hematocrit can be useful to look for hemoconcentration, which suggests contraction of intravascular volume and progression to more severe disease, while a falling hematocrit may be a sign of hemolysis. An elevated serum indirect bilirubin concentration is a better sign of hemolysis, although an elevated LDH may also be a marker of severe disease or HELLP syndrome. Hemolysis can be confirmed by observation of schistocytes and helmet cells on a blood smear (picture 1A-B). (See "HELLP syndrome".)    \nSince several clinical studies have shown that neither the rate of increase nor the amount of proteinuria affects maternal or perinatal outcome in the setting of preeclampsia [5-8], repeated 24-hour urinary protein estimations are not useful once the threshold of 300 mg/24 hours for the diagnosis of preeclampsia has been exceeded. Serum creatinine alone can be used to monitor renal function. When required, quantification of protein excretion can be performed using a 24-hour collection or protein-to creatinine ratio on a random specimen. (See "Expectant management of severe preeclampsia".)\nAssessment of fetal well-being — There are no data from randomized trials on which to base recommendations for the optimal type and frequency of fetal biophysical monitoring. We suggest daily fetal movement counts and twice weekly fetal nonstress testing with assessment of amniotic fluid volume, or twice weekly biophysical profiles. Testing is repeated immediately if there is an abrupt change in maternal condition. (See "Antepartum fetal heart rate assessment" and "The fetal biophysical profile".)\nEvaluation of umbilical artery Doppler indices is also useful, as the results help in optimal timing of delivery. In a meta-analysis of 16 randomized trials in high risk pregnancies, knowledge of umbilical artery Doppler velocimetry results was associated with a 29 percent reduction in perinatal death (RR 0.71, 95% CI 0.52-0.98, 10,225 babies, 1.2 versus 1.7 percent; number needed to treat 203, 95%CI 103- 4352), primarily in pregnancies complicated by preeclampsia and/or growth restriction. The frequency of assessment depends on the findings; weekly assessment is reasonable when Doppler indices are normal. \n","27":"regard Renal — The kidney is the organ most likely to manifest endothelial injury related to preeclamp\nProteinuria — Proteinuria in preeclampsia is defined as ≥0.3 grams protein in a 24-hour urine specimen or persistent 1+ (30 mg/dL) on dipstick or a random protein:creatinine ratio >30 mg/mmol. The presence of ≥5 grams of protein in a 24-hour urine collection upstages preeclampsia from mild to severe. Although proteinuria in women with preeclampsia is most often in the mild to moderate range (<5 g), preeclampsia remains the most common cause of severe proteinuria in pregnant women; levels of proteinuria >10 g/day may be seen\nRenal function — Glomerular filtration rate (GFR) decreases by 30 to 40 percent in preeclampsia compared to pregnant normotensive controls; renal plasma flow also decreases, but to a lesser degree. The plasma creatinine concentration is generally normal or only slightly elevated (1.0 to 1.5 mg/dL [88 to 133 micromol/L]). A rising creatinine and oliguria, ie, urine output <500 mL/24 hours, indicates severe disease and results from renal vasoconstriction and sodium retention due to reduced plasma volume and systemic vasoconstriction. (See "Acute kidney injury (acute renal failure) in pregnancy", section on 'Preeclampsia'.)\nHyperuricemia and hypocalciuria are also observed; the mechanisms for these changes are not clear [60,63,64]. The rise in serum uric acid concentration is thought to reflect increased proximal sodium resorption and, secondarily, urate reabsorption induced by renal ischemia. Other possible mechanisms for hyperuricemia in preeclampsia include underlying metabolic syndrome, tissue damage, oxidative stress, and inflammation [65].\nAlthough hyperuricemia is associated with preeclampsia, serum uric acid level is a poor predictor of development of the disease or maternal and fetal complications in women with preeclampsia [66,67]. However, an elevated uric acid level (>6.0 mg/dL) at the time of diagnosis appears to identify women at risk of delivery within seven days, whereas a low uric acid level (≤4.0 mg/dL) is associated with a prolonged latency period\n","55":"HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) probably represents a severe form of preeclampsia, but this relationship remains controversial; HELLP may be an independent disorder. As many as 15 to 20 percent of affected patients do not have concurrent hypertension or proteinuria, leading some experts to believe that HELLP syndrome is a separate disorder from preeclampsia. (See "HELLP syndrome".) \n","44":"Seizure prophylaxis — Based upon data from randomized trials, we administer intrapartum magnesium sulfate seizure prophylaxis to women with mild or severe preeclampsia. Although seizure and death are rare outcomes after non-treatment of mild preeclampsia, we feel the benefit of treatment is justifiable given the low cost and toxicity of magnesium sulfate and the relatively low number of patients that need to be treated to prevent one seizure. In a randomized placebo-controlled trial including 10,000 women (MAGPIE [magnesium sulfate for prevention of eclampsia trial]), about 100 women with mild preeclampsia and about 60 women with severe preeclampsia would need to be treated to prevent one seizure [36].\nIt is important to emphasize that seizure prophylaxis does not prevent progression of disease unrelated to convulsions. Approximately 10 to 15 percent of women in labor with mild preeclampsia will develop signs of severe preeclampsia (eg, severe hypertension, severe headache, visual disturbance, epigastric pain, laboratory abnormalities) or abruptio placenta, whether or not they receive magnesium therapy [37,38].\nWe do not administer seizure prophylaxis to women with gestational hypertension alone, as the seizure risk in the latter group is less than 0.1 percent [39]. (See"Gestational hypertension".)\nDosing — Although published dosage regimens for magnesium sulfate vary widely (loading dose of 4 to 6 grams intravenously and maintenance dose of 1 to 3 grams per hour), the most common regimen, and the one that we use, is a loading dose of 6 grams intravenously over 15 to 20 minutes followed by 2 grams per hour as a continuous infusion [1,38,43,46]. An alternative regimen is 5 grams intramuscularly into each buttock (total of 10 grams) followed by 5 grams intramuscularly every four hours. However, this method is associated with more side effects, particularly pain at the injection site.\nThere does not appear to be a clear threshold concentration for insuring the prevention of convulsions, although a therapeutic range of 4.8 to 8.4 mg/dL (2.0 to 3.5 mmol/L)has been recommended based on retrospective data [47]. Loading doses less than 6 grams are more likely to result in subtherapeutic magnesium levels (less than 4.5mg/dL) [43,48].\nSince magnesium sulfate is excreted by the kidneys, dosing should be adjusted in women with renal insufficiency (defined as a serum creatinine greater than 1.0 mg/dL).Such women should receive a standard loading dose (since their volume of distribution is not altered), but a reduced maintenance dose (1 gram per hour or no maintenance dose if the serum creatinine is greater than 2.5 mg/dL) and close monitoring of their serum magnesium level every six hours.\nThe maintenance phase is given only if a patellar reflex is present (loss of reflexes being the first manifestation of symptomatic hypermagnesemia), respirations exceed 12 per minute, and the urine output exceeds 100 mL per four hours. (See "Symptoms of hypermagnesemia".) Following serum magnesium levels is not required if the woman's clinical status is closely monitored for evidence of potential magnesium toxicity (see 'Complications and side effects' below). The maintenance dose should be decreased if there is clinical evidence of magnesium toxicity.\ncontinued for 24 hours postpartum [46]. Timing of drug discontinuation has been arbitrary; there are no high quality data to guide therapy. In women who have only mild preeclampsia, discontinuation of therapy after 12 hours may be safe [49]. In women with severe preeclampsia or eclampsia, seizure prophylaxis is generally continued for 24 to 48 hours postpartum, after which the risk of recurrent seizures is low.\nIt is probably reasonable to extend the duration of magnesium sulfate therapy in women whose disease has not begun to improve postpartum and shorten the duration of therapy in women who are clearly improving clinically (eg, diuresis of ≥100 mL/hour for two consecutive hours, absence of symptoms [headache, visual changes, epigastric pain], and absence of severe hypertension) [50-53]. Diuresis (greater than 4 L/day) is believed to be the most accurate clinical indicator of resolution ofpreeclampsia/eclampsia, but is not a guarantee against the development of seizures [54]. In women with persistent renal impairment postpartum, it is important to be cautious when administering a prolonged magnesium sulfate infusion to prevent the occurrence of magnesium toxicity.\n","33":"OVERVIEW OF MANAGEMENT — The definitive treatment of preeclampsia is delivery to prevent development of maternal or fetal complications from disease progression. (See "Preeclampsia: Clinical features and diagnosis", section on 'Burden of disease'.) Whether or not to deliver the fetus is based upon gestational age, the severity of preeclampsia, and maternal and fetal condition. Patients with mild or severe preeclampsia at or near term are delivered; however, remote from term, the risks of serious sequelae from disease progression need to be weighed against the risks of preterm birth. Evidence of serious maternal end-organ dysfunction or nonreassuring tests of fetal well-being are indications for prompt delivery at any gestational age. On the other hand, when mother and fetus are stable, a conservative approach is reasonable in order to achieve further fetal growth and maturity\n","11":"Some women with gestational HTN may have undiagnosed chronic HTN\nOthers will subsequently progress to develop the clinical syndrome of PE\n","61":"Preeclampsia superimposed upon chronic/preexisting hypertension — Superimposed preeclampsia is defined by the new onset of proteinuria after 20 weeks of gestation in a woman with chronic/preexisting hypertension. For women with chronic/preexisting hypertension who have proteinuria prior to or in early pregnancy, superimposed preeclampsia is defined by worsening or resistant hypertension (especially acutely) in the last half of pregnancy or development ofsigns/symptoms of severe preeclampsia (table 2).\n","50":"PATHOGENESIS OF SEIZURES — The exact cause of seizures in women with eclampsia is not known. The following two hypotheses have been proposed [17]:\nCerebral overregulation in response to high systemic blood pressure results in vasospasm of cerebral arteries, underperfusion of the brain, localizedischemia/infarction, and cytotoxic (intracellular) edema. (See "Cerebrovascular disorders complicating pregnancy", section on 'Postpartum angiopathy'.)\nLoss of autoregulation of cerebral blood flow in response to high systemic pressure (ie, hypertensive encephalopathy) results in hyperperfusion, endothelial damage, and vasogenic (extracellular) edema. (See "Reversible posterior leukoencephalopathy syndrome", section on 'Eclampsia'.)\nA classic report of autopsies performed shortly after death of eclamptic women described the neurological findings in eclamptic women [18]. The brains of more than 50 percent of the women who died within two days of seizures displayed cerebral hemorrhages. Petechial cortical hemorrhages were most common, especially involving the occipital lobe. Diffuse cerebral edema and gross hemorrhage were noted less frequently. Cerebral venous thrombosis was common in women with postpartum eclampsia.\nAdditional findings were observed in the largest magnetic resonance imaging study of eclampsia, which involved 27 nulliparous eclamptic women without neurologic deficit [19]. Twenty-five of these women had evidence of cerebral edema, typically involving the subcortical white and adjacent gray matter in the parieto-occipital lobes. Six women had restricted diffusion suggestive of infarction and five of the six had persistent imaging abnormalities six to eight weeks later, but their neurologic examinations remained normal. The authors hypothesized that hypertensive encephalopathy with hyperperfusion, vasogenic edema, and endothelial damage caused the eclamptic seizures and that progressive edema, rather than vasospasm, led to focal areas of cerebral hypoperfusion and, ultimately, infarction in the most severe cases.\nThe pathogenesis of preeclampsia is reviewed elsewhere. \n","39":"Assessment of fetal growth — Early fetal growth restriction may be the first manifestation of preeclampsia and is a criterion of severe disease. We suggest sonographic estimation of fetal weight be performed to look for growth restriction and oligohydramnios at the time of diagnosis of preeclampsia and then repeated every three weeks if the initial examination is normal [27]. If fetal growth is suboptimal, the frequency can be increased. (See "Fetal growth restriction: Evaluation and management", section on 'Serial fetal weight assessment' and "Doppler ultrasound of the umbilical artery for fetal surveillance".)\nAntenatal corticosteroids — Although preeclampsia may accelerate fetal lung maturation, neonatal respiratory distress remains common in premature neonates of preeclamptic pregnancies [32,33]. Antenatal corticosteroids (betamethasone) to promote fetal lung maturity should be administered to women less than 34 weeks of gestation since they are at increased risk of progression to severe disease and preterm delivery. (See "Antenatal corticosteroid therapy for reduction of neonatal morbidity and mortality from preterm delivery"\n","28":"Renal — The kidney is the organ most likely to manifest endothelial injury related to preeclamp\nProteinuria — Proteinuria in preeclampsia is defined as ≥0.3 grams protein in a 24-hour urine specimen or persistent 1+ (30 mg/dL) on dipstick or a random protein:creatinine ratio >30 mg/mmol. The presence of ≥5 grams of protein in a 24-hour urine collection upstages preeclampsia from mild to severe. Although proteinuria in women with preeclampsia is most often in the mild to moderate range (<5 g), preeclampsia remains the most common cause of severe proteinuria in pregnant women; levels of proteinuria >10 g/day may be seen\nRenal function — Glomerular filtration rate (GFR) decreases by 30 to 40 percent in preeclampsia compared to pregnant normotensive controls; renal plasma flow also decreases, but to a lesser degree. The plasma creatinine concentration is generally normal or only slightly elevated (1.0 to 1.5 mg/dL [88 to 133 micromol/L]). A rising creatinine and oliguria, ie, urine output <500 mL/24 hours, indicates severe disease and results from renal vasoconstriction and sodium retention due to reduced plasma volume and systemic vasoconstriction. (See "Acute kidney injury (acute renal failure) in pregnancy", section on 'Preeclampsia'.)\nHyperuricemia and hypocalciuria are also observed; the mechanisms for these changes are not clear [60,63,64]. The rise in serum uric acid concentration is thought to reflect increased proximal sodium resorption and, secondarily, urate reabsorption induced by renal ischemia. Other possible mechanisms for hyperuricemia in preeclampsia include underlying metabolic syndrome, tissue damage, oxidative stress, and inflammation [65].\nAlthough hyperuricemia is associated with preeclampsia, serum uric acid level is a poor predictor of development of the disease or maternal and fetal complications in women with preeclampsia [66,67]. However, an elevated uric acid level (>6.0 mg/dL) at the time of diagnosis appears to identify women at risk of delivery within seven days, whereas a low uric acid level (≤4.0 mg/dL) is associated with a prolonged latency period\nUrine sediment — The urine sediment is typically benign.\nRenal histology — The renal histologic changes described in women with preeclampsia who have had kidney biopsies, and in autopsy specimens obtained from women who died of eclampsia, are termed ‘glomerular endotheliosis.’ Light and electron microscopy of glomerular endotheliosis show the following (picture 1A-C) [69]:\nEndothelial cell swelling\nLoss of fenestrations\nOcclusion of capillary lumens\nFoot process effacement is not a prominent feature, despite marked proteinuria.\nGlomerular endotheliosis shares histologic features with non-preeclamptic thrombotic microangiopathies [69], except thrombi are rare in preeclampsia (although fibrin deposition may be observed by immunofluorescence microscopy). Rarely, it may be present without proteinuria and in nonpregnant women [\n","17":"The floating villi (FV) are in the intervillous space in direct contact with with the maternal blood. In normal pregnancy, invasive cytotrophoblasts (CTB) form cell columns (zone II/III) and invade maternal decidua and vasculature (zone IV). During the differentiation along the invasive path, the cytotrophoblasts dramatically alter their expression of various molecules, such as integrins. In preeclampsia, the invasive cytotrophoblasts fail to differentiate along the invasive pathway and do not gain access to spiral arteries.\nCourtesy of Kee-Hak Lim, MD.\n","6":"Gestational hypertension is a temporary diagnosis for hypertensive pregnant women who do not meet criteria for preeclampsia (both hypertension and proteinuria) or chronic hypertension (hypertension first detected before the 20th week of pregnancy). \n","45":"Toxicity is related to serum magnesium concentration: loss of deep tendon reflexes occurs at 9.6 to 12.0 mg/dL (4.0 to 5.0 mmol/L), respiratory paralysis at 12.0 to 18.0 mg/dL (5 to 7.5 mmol/L), and cardiac arrest at 24 to 30 mg/dL (10 to 12.5 mmol/L). Calcium gluconate (1 gram intravenously over 5 to 10 minutes) should be administered only to counteract life-threatening symptoms of magnesium toxicity (such as cardiorespiratory compromise).\naction at the n-methyl d-aspartate (NMDA) receptor that raises the seizure threshold, membrane stabilization in the central nervous system secondary to its actions as a non-specific calcium channel blocker, as well as decreasing acetylcholine in motor nerve terminals [61,62]. Another theory is that it promotes vasodilatation of constricted cerebral vessels by opposing calcium-dependent arterial vasospasm, thereby reducing cerebral barotrauma \n","34":"Severe preeclampsia — Severe preeclampsia (table 2) is generally regarded as an indication for delivery, regardless of gestational age, in order to minimize the risk of development of serious maternal and fetal complications (eg, cerebral hemorrhage, hepatic rupture, renal failure, pulmonary edema, seizure, bleeding related to thrombocytopenia, fetal growth restriction, abruptio placentae) [1-4]. With the exception of fetal growth restriction, any of these adverse events can occur suddenly in a woman with severe disease. However, if proteinuria ≥5 grams is the only criteria for severe disease, patients are usually managed as mild preeclamptics since the amount of proteinuria has no correlation with risk of adverse maternal or perinatal outcome [5-8]. (See "Expectant management of severe preeclampsia", section on 'Severe preeclampsia based solely on proteinuria'.) Similarly, if the only criteria for severe disease is (1) mild fetal growth restriction with reassuring Doppler velocimetry or (2) severe hypertension, then a conservative approach may be considered remote from term. \n","62":"RISK factor for FUTURE maternal cardiovascular and metabolic DISEASE \n","51":"PATHOGENESIS OF SEIZURES — The exact cause of seizures in women with eclampsia is not known. The following two hypotheses have been proposed [17]:\nCerebral overregulation in response to high systemic blood pressure results in vasospasm of cerebral arteries, underperfusion of the brain, localizedischemia/infarction, and cytotoxic (intracellular) edema. (See "Cerebrovascular disorders complicating pregnancy", section on 'Postpartum angiopathy'.)\nLoss of autoregulation of cerebral blood flow in response to high systemic pressure (ie, hypertensive encephalopathy) results in hyperperfusion, endothelial damage, and vasogenic (extracellular) edema. (See "Reversible posterior leukoencephalopathy syndrome", section on 'Eclampsia'.)\nA classic report of autopsies performed shortly after death of eclamptic women described the neurological findings in eclamptic women [18]. The brains of more than 50 percent of the women who died within two days of seizures displayed cerebral hemorrhages. Petechial cortical hemorrhages were most common, especially involving the occipital lobe. Diffuse cerebral edema and gross hemorrhage were noted less frequently. Cerebral venous thrombosis was common in women with postpartum eclampsia.\nAdditional findings were observed in the largest magnetic resonance imaging study of eclampsia, which involved 27 nulliparous eclamptic women without neurologic deficit [19]. Twenty-five of these women had evidence of cerebral edema, typically involving the subcortical white and adjacent gray matter in the parieto-occipital lobes. Six women had restricted diffusion suggestive of infarction and five of the six had persistent imaging abnormalities six to eight weeks later, but their neurologic examinations remained normal. The authors hypothesized that hypertensive encephalopathy with hyperperfusion, vasogenic edema, and endothelial damage caused the eclamptic seizures and that progressive edema, rather than vasospasm, led to focal areas of cerebral hypoperfusion and, ultimately, infarction in the most severe cases.\nThe pathogenesis of preeclampsia is reviewed elsewhere. \n","40":"Intrapartum monitoring — Continuous maternal-fetal monitoring is indicated intrapartum to identify worsening hypertension, deteriorating maternal hepatic, renal, cardiopulmonary, neurological, or hematologic function, as well as abruptio placentae or a nonreassuring fetal heart rate tracing. There are no evidence-based standards for the optimal approach.\nFluids — Fluid balance should be monitored closely to avoid excessive administration, since women with severe disease are at risk of pulmonary edema and significant third-spacing. Maintenance fluids of 80 mL/hour are often adequate in the absence of ongoing fluid loss, such as bleeding. Oliguria that does not respond to a modest trial of increased fluids should be tolerated. Diuretics are only indicated for treatment of pulmonary edema.\n","29":"— The most common coagulation abnormality in preeclampsia is thrombocytopenia. Microangiopathic endothelial injury and activation result in formation of platelet and fibrin thrombi in the microvasculature. Accelerated platelet consumption leads to thrombocytopenia; immune mechanisms may also play a role [72]. A platelet count less than 100,000/microL upstages preeclampsia from mild to severe.\nThe prothrombin time, partial thromboplastin time, and fibrinogen concentration are not affected unless there are additional complications, such as abruptio placentae or severe liver dysfunction [73].\nMicroangiopathic hemolysis may also occur and is detected by examination of a blood smear for schistocytes and helmet cells (picture 2A-B) or elevation in the serum lactate dehydrogenase concentration. Hemoconcentration may result from reduction of plasma volume from capillary leaking. Hemolysis is associated with a low hematocrit, while hemoconcentration is associated with a high hematocrit; when both hemolysis and reduced plasma volume are present, the effects on hematocrit may negate each other, resulting in a normal value. (See "Thrombocytopenia in pregnancy" and "Abnormalities of coagulation and platelet function in preeclampsia".)\nThe white blood cell count may be slightly higher due to neutrophilia \n","7":"Urinary protein excretion should be determined since the presence or absence of proteinuria is the key clinical criterion that determines whether the patient will be given a diagnosis of gestational hypertension or preeclampsia. A urine dipstick of negative to trace should not be used to definitively exclude significant proteinuria since false negative results occur with low specific gravity (<1.010), high salt concentration, highly acidic urine, or with nonalbumin proteinuria. A positive urine dipstick value, especially if only +1, \nPatients should be questioned regarding signs and symptoms of severe preeclampsia, such as severe headache, visual changes, epigastric or right upper quadrant pain, nausea/vomiting, or decreased urine output. Severe preeclampsia can be present even though hypertension is mild and proteinuria is absent \n> \n","46":"POSTPARTUM MANAGEMENT — Nonsteroidal antiinflammatory drugs (NSAIDs) for pain control should be avoided in women with poorly controlled hypertension, oliguria, renal insufficiency, or thrombocytopenia. (See "Nonselective NSAIDs: Overview of adverse effects".)\nThere are no evidence-based standards for the optimal approach to postpartum monitoring and follow-up. We monitor vital signs every two hours while the patient remains on magnesium sulfate and we repeat laboratory tests until two consecutive sets of data are normal.\nSevere hypertension should be treated; some patients will have to be discharged on antihypertensive medications, which are discontinued when blood pressure returns to normal. (See "Management of hypertension in pregnant and postpartum women", section on 'Postpartum hypertension'.)\nPatients should be followed closely as outpatients until complete resolution of hypertension and laboratory abnormalities. Alternative diagnoses should be sought in those with persistent abnormal findings after three to six months [64\n","35":"Mild preeclampsia — Experts consistently recommend delivery of women with mild preeclampsia at ≥37 weeks of gestation [4,14,15]. Cervical ripening agents should be used in women with unfavorable cervices.\nThe benefits of labor induction at ≥37 weeks of gestation were illustrated in a multicenter trial (HYPITAT) that randomly assigned 756 women with mild preeclampsia or gestational hypertension >360/7 weeks to induction of labor or expectant management with maternal/fetal monitoring [16]. Routine induction was associated with a significant reduction in composite adverse maternal outcome (RR 0.71, 95% CI 0.59-0.86; absolute risk reduction 12.76 percent), which was primarily driven by a reduction in patients who developed severe hypertension and was not significant for women at 360 to 366 weeks. The induced group delivered, on average, 1.2 weeks earlier than the control group and had a significantly lower rate of cesarean delivery (14 versus 19 percent). There were no significant differences between groups in neonatal outcome. \n","24":"Impaired placentation can lead to increased impedance to flow in the uterine arteries, manifested by elevation of the pulsatility index accompanied by uterine artery notching on uterine artery Doppler velocimetry. However, this finding is neither sensitive nor specific for preeclampsia. (See "Prediction of preeclampsia", section on 'Uterine artery Doppler velocimetry'.)\nIncreased resistance in the placental vasculature is also reflected by rising Doppler indices of the umbilical artery. Absent and reversed end diastolic flow are the most severe abnormalities and associated with a poor perinatal outcome. (See "Doppler ultrasound of the umbilical artery for fetal surveillance".) \nWill measurement of blood sFlt1, VEGF, and PlGF levels allow us to develop a test that can predict which patients will develop preeclampsia before the onset of symptoms? YES!\n● Levine et al\n● Thadhani et al\n● Salahuddin et al\n● Shibata et al\n● WHO multicenter trial\n4/\n","63":"Development of effective strategies\nfor the prevention and/or treatment \nof preeclampsia\n","52":"MANAGEMENT — A number of management strategies have been developed to prevent maternal and fetal complications resulting from eclampsia during the peripartum period.\nGeneral principles — If the seizure is witnessed, maintenance of airway patency and prevention of aspiration should be the first responsibilities of management. The gravida should be rolled onto her left side. A bed with raised, padded side rails provides protection from trauma. Supplemental oxygen (8 to 10 L/min) via a face mask has been recommended to treat hypoxemia due to hypoventilation during the convulsive episode [15].\nThe immediate issues in caring for an eclamptic woman include:\nPrevention of maternal hypoxia and trauma\nManagement of severe hypertension, if present\nPrevention of recurrent seizures\nEvaluation for prompt delivery.\nThe definitive treatment of eclampsia is delivery, irrespective of gestational age, to reduce the risk of maternal morbidity and mortality from complications of the disease\n","41":"Acute therapy — Labetalol and hydralazine are the best options for first-line therapy [14].\nLabetalol — We recommend intravenous labetalol for first-line therapy because it is effective, has a rapid onset of action, and a good safety profile. Begin with 20 mg intravenously over 2 minutes followed at 10-minute intervals by doses of 20 to 80 mg up to a maximum total cumulative dose of 300 mg. As an example, give 20 mg, then 40 mg, then 80 mg, then 80 mg, then 80 mg. A constant infusion of 1 to 2 mg/min can be used instead of intermittent therapy. The fall in blood pressure begins within 5 to 10 minutes and lasts from 3 to 6 hours. Continuous cardiac monitoring is not necessary routinely, but should be used in patients with relevant co-morbidities (eg, coronary artery disease).\nHydralazine — Begin with 5 mg intravenously over 1 to 2 minutes; if the blood pressure goal is not achieved within 20 minutes, give a 5 to 10 mg bolus depending upon the initial response. The maximum bolus dose is 20 mg. If a total dose of 30 mg does not achieve optimal blood pressure control, another agent should be used. The fall in blood pressure begins within 10 to 30 minutes and lasts from 2 to 4 hours.\nCalcium channel blockers — Sustained release nifedipine (30 mg) and immediate release nicardipine are other options. Nicardipine can be given intravenously. Experience with these drugs in pregnancy is more limited than for labetalol and hydralazine; however, published experience showed that target blood pressure was reached within 23 minutes in 70 percent of pregnant patients with severe hypertension and 91 percent reached target blood pressure within 130 minutes, with no severe maternal or fetal side effects [25]. A more complete review of drug doses and potential side effects is discussed separately. (See "Drug treatment of hypertensive emergencies".)We do not use immediate release nifedipine, either orally or sublingually, for treatment of hypertension because of the risk of acute, precipitous falls in blood pressure, which have been associated with serious cardiovascular morbidity (eg, stroke, myocardial infarction) in older, nonpregnant patients.\nNitroglycerin — Nitroglycerin (glyceryl trinitrate) is a good option for treatment of hypertension associated with pulmonary edema [23]. It is given as an intravenous infusion of 5 mcg/min and gradually increased every 3 to 5 minutes to a maximum dose of 100 mcg/min.\n","30":"Hepatic — Periportal and sinusoidal fibrin deposition and microvesicular fat deposition are histologic findings observed in the livers of preeclamptic women [75,76]. Reduced hepatic blood flow can lead to ischemia and periportal hemorrhage. The clinical manifestations of hepatic dysfunction include right upper quadrant or epigastric pain, elevated transaminase levels, coagulopathy, and, in the most severe cases, subcapsular hemorrhage or hepatic rupture. These hepatic changes upstage the preeclampsia from mild to severe. Nausea and vomiting may occur.\nEpigastric pain is one of the cardinal symptoms of severe preeclampsia. A review of this nonspecific symptom revealed that it is typically experienced as a severe constant pain that begins at night, usually maximal in the low retrosternum or epigastrium, but may radiate to the right hypochondrium or back [77]. The pain is thought to be due to stretching of Glisson’s capsule due to hepatic swelling or bleeding. It may be the only symptom on presentation, thus a high index of suspicion is important to make the diagnosis of preeclampsia rather than gastroesophageal reflux, which is common in pregnant women, especially at night. The liver may be tender to palpation.\nRarely, transient diabetes insipidus has been reported in preeclampsia with hepatic dysfunction. (See "Renal and urinary tract physiology in normal pregnancy", section on 'DI associated with hepatic dysfunction'.)\nAcute pancreatitis is an even rarer complication of severe preeclampsia \n","8":"The main goals in the initial evaluation of pregnant women with newly developed hypertension are to distinguish gestational hypertension from preeclampsia, which has a different course and prognosis, and to determine whether hypertension is mild or severe, which affects management and outcome \n","36":"EXPECTANT ANTEPARTUM MANAGEMENT OF MILD PREECLAMPSIA\nInpatient versus outpatient care — Close maternal monitoring upon diagnosis of preeclampsia is important to establish disease severity and the rate of progression. Hospitalization is useful for making these assessments and facilitates rapid intervention in the event of rapid progression. After the initial diagnostic evaluation, outpatient care is a cost-effective option for women with stable mild preeclampsia [19-24]. Outpatient care can be provided in the patient’s home or, where available, at an antenatal day care unit [25].\nThere are limited data on outcome of outpatient management of preeclamptic women. An observational study and a randomized trial reported good outcomes, but these studies had too few subjects to detect clinically significant differences in outcome between inpatient and outpatient management [21,22]. A systematic review of three trials with a total of 504 women with various complications of pregnancy observed no major differences in clinical outcomes for mothers or babies between antenatal day units or hospital admission [25].\nPatients offered outpatient monitoring should be able to comply with frequent maternal and fetal evaluations (every one to three days) and should have ready access to medical care. Restricted activity is typically recommended since blood pressure is lower in rested patients; however, there is no evidence that bedrest improves pregnancy outcome [26]. Rest in the left lateral decubitus position can augment uteroplacental flow, which may benefit some pregnancies. If signs or symptoms of disease progression are noted, hospitalization for more intensive monitoring and possible delivery is indicated.\nPatients should be told to call their health care provider immediately if they develop severe or persistent headache, visual changes, right upper quadrant or epigastric pain, nausea or vomiting, shortness of breath, significant weight gain over one to two days, or decreased urine output [27]. As with any pregnancy, decreased fetal movement, vaginal bleeding, abdominal pain, rupture of membranes, or uterine contractions should be reported immediately, as well.\n","42":"Acute therapy — Labetalol and hydralazine are the best options for first-line therapy [14].\nLabetalol — We recommend intravenous labetalol for first-line therapy because it is effective, has a rapid onset of action, and a good safety profile. Begin with 20 mg intravenously over 2 minutes followed at 10-minute intervals by doses of 20 to 80 mg up to a maximum total cumulative dose of 300 mg. As an example, give 20 mg, then 40 mg, then 80 mg, then 80 mg, then 80 mg. A constant infusion of 1 to 2 mg/min can be used instead of intermittent therapy. The fall in blood pressure begins within 5 to 10 minutes and lasts from 3 to 6 hours. Continuous cardiac monitoring is not necessary routinely, but should be used in patients with relevant co-morbidities (eg, coronary artery disease).\nHydralazine — Begin with 5 mg intravenously over 1 to 2 minutes; if the blood pressure goal is not achieved within 20 minutes, give a 5 to 10 mg bolus depending upon the initial response. The maximum bolus dose is 20 mg. If a total dose of 30 mg does not achieve optimal blood pressure control, another agent should be used. The fall in blood pressure begins within 10 to 30 minutes and lasts from 2 to 4 hours.\nCalcium channel blockers — Sustained release nifedipine (30 mg) and immediate release nicardipine are other options. Nicardipine can be given intravenously. Experience with these drugs in pregnancy is more limited than for labetalol and hydralazine; however, published experience showed that target blood pressure was reached within 23 minutes in 70 percent of pregnant patients with severe hypertension and 91 percent reached target blood pressure within 130 minutes, with no severe maternal or fetal side effects [25]. A more complete review of drug doses and potential side effects is discussed separately. (See "Drug treatment of hypertensive emergencies".)We do not use immediate release nifedipine, either orally or sublingually, for treatment of hypertension because of the risk of acute, precipitous falls in blood pressure, which have been associated with serious cardiovascular morbidity (eg, stroke, myocardial infarction) in older, nonpregnant patients.\nNitroglycerin — Nitroglycerin (glyceryl trinitrate) is a good option for treatment of hypertension associated with pulmonary edema [23]. It is given as an intravenous infusion of 5 mcg/min and gradually increased every 3 to 5 minutes to a maximum dose of 100 mcg/min.\n","31":"Central nervous system and eye — Central nervous system manifestations of preeclampsia include headache, visual symptoms, and generalized hyperreflexia; sustained ankle clonus may be present.\nHeadache in preeclampsia may be temporal, frontal, occipital, or diffuse [79,80]. It is usually a throbbing/pounding pain, but may be piercing pain. Although not pathognomonic, a feature that suggests preeclampsia-related headache rather than another type of headache is that it persists despite administration of over-the-counter analgesics and it may become severe (ie, incapacitating, "the worst headache of my life").\nVisual symptoms are caused, at least in part, by constriction of retinal arteries. Symptoms include blurred vision, flashing lights (photopsia), and scotomata (dark areas or gaps in the visual field) [81-83]. Diplopia or amaurosis fugax (blindness in one eye) may also occur. Cortical blindness is rare and typically transient [84]. Blindness related to retinal pathology, such as retinal artery or venous thrombosis, retinal detachment, optic nerve damage, retinal artery spasm, and retinal ischemia, may be permanent [85].\nSeizures in a preeclamptic woman signify a change in diagnosis to eclampsia. One in 400 mildly preeclamptic and 1 in 50 severely preeclamptic women develop eclamptic seizures.\nHistopathologic correlates include hemorrhage, petechiae, cerebral edema, vasculopathy, ischemic brain damage, microinfarcts, and fibrinoid necrosis [86,87].\nThe cerebrovascular manifestations of severe preeclampsia are poorly understood. Cerebral edema and ischemic/hemorrhagic changes in the posterior hemispheres observed on computed tomography and magnetic resonance imaging help to explain, but do not fully account for, the clinical findings [88,89]. These findings may result from vasospasm of the cerebral vasculature in response to severe hypertension or may result from loss of cerebrovascular autoregulation leading to areas of both vasoconstriction and forced vasodilation and thus represent a form of posterior reversible leukoencephalopathy syndrome (PRES) [90,91]. PRES is typically associated with severe hypertension, but can occur with rapid increases in blood pressure in patients with endothelial damage [92]. (See "Reversible posterior leukoencephalopathy syndrome" and "Eclampsia", section on 'Clinical manifestations and diagnosis'.)\nStroke leading to death or disability is the most serious complication of severe preeclampsia/eclampsia, but is rare\n","9":"be managed safely as outpatients with weekly antepartum visits. Bedrest appears to reduce the risk of worsening hypertension, but neither bedrest nor use of low dose aspirin prevent progression to severe preeclampsia, nor do these interventions improve outcome;\nWe order either a nonstress test with sonographic estimation of the amniotic fluid index or a biophysical profile weekly. We also perform serial ultrasound examinations to monitor fetal growth every three to four weeks, as hypertension of any etiology may be associated with placental insufficiency ; No antihypertensive therapy — We refrain from using antihypertensive agents, unless hypertension is severe because data from randomized trials show that medical therapy of mild hypertension does not improve maternal or neonatal outcome: No antenatal glucocorticoids — A course of antenatal glucocorticoids is usually not indicated for pregnancies with mild gestational hypertension because the disorder typically develops after 34 weeks of gestation and is not an indication for preterm birth. A review of pregnancy outcomes in women with mild gestational hypertension found that delivery before 34 weeks occurred in only 1 to 5 percent of cases ; that induction of labor of hypertensive patients by 40 weeks is associated with a lower rate of adverse outcome than expectant management, even when the cervix is unfavorable [25]. Given the low risk of neonatal problems with delivery at term and the potential increase in risk of serious complications with expectant management, we deliver patients with gestational hypertension no later than their estimated date of delivery. The optimum time for intervention is more controversial.\nA consensus opinion from a workshop held by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the Society for Maternal-Fetal Medicine (SMFM) suggested delivery at 370/7ths to 386/7ths weeks for all women with any degree of gestational hypertension because of the risk of progression to preeclampsia [26], a recommendation endorsed by the American College of Obstetricians and Gynecologists (ACOG) ;\nFor uncomplicated pregnancies with only occasional blood pressures no higher than 140/90 mmHg, we may not intervene until 400/7thsweeks. more frequent or higher blood pressures in the range for mild hypertension (ie, <160/100 mmHg), we deliver at 37 to 39 weeks depending on patient specific factors: severity of hypertension, presence of other risk factors for adverse pregnancy outcome, past obstetrical history, increasing blood pressure over time. Given low but increased neonatal morbidity of early term birth (370/7ths to 386/7ths weeks), we attempt to avoid intervention before 39 weeks in women with stable mild gestational hypertension and otherwise uncomplicated pregnancies, but monitor them closely. There is no benefit to late preterm delivery and these infants are at increased risk of morbidity compared to term infants\n","26":"reduced volume appears to be a consequence of vasoconstriction from enhanced responses to vasoactive substances. This issue has not been conclusively resolved.\nEdema in preeclampsia may be due to capillary leaking or represent "overfill" edema. Many pregnant women have edema, whether or not they have preeclampsia. However, sudden and rapid weight gain (eg, >5 pounds/week) and facial edema are more common in women who develop preeclampsia, thus, these findings warrant evaluation for other clinical manifestations of disease;\n]. The high afterload in preeclampsia is associated with elevated cardiac filling pressures, reflected by four-fold higher concentrations of natriuretic peptides in women with preeclampsia compared to pregnant women who are normotensive or have chronic hypertension [46].\nSevere preeclampsia can be associated with a highly variable hemodynamic profile [45-49]. A small subgroup of women with severe preeclampsia develops myocardial damage or global diastolic dysfunction [50]. Troponin I levels should be obtained when clinically indicated, such as when the patient complains of chest pain suggestive of myocardial ischemia or new electrocardiogram changes are observed [51,52]. Preeclampsia is not associated with elevated troponin levels in the absence of cardiac disease [53].\nExcessive elevation in pulmonary vascular hydrostatic pressure compared with plasma oncotic pressure may produce pulmonary edema in some women, particularly in the postpartum period. However, not all preeclamptic patients with pulmonary edema demonstrate this phenomenon. Other causes of pulmonary edema are capillary leak, left heart failure, and iatrogenic volume overload.\n","54":"Management of persistent convulsions — Recurrent convulsions occurring in patients on maintenance magnesium sulfate therapy can be treated with an additional bolus of 2 grams of magnesium sulfate over 15 to 20 minutes, with careful monitoring for signs of magnesium toxicity (see above). If two such boluses do not control seizures, then other measures should be instituted. A number of options are included below, although diazepam or lorazepam are used most commonly.\nDiazepam — Intravenously administered diazepam (0.1 to 0.3 mg/kg over 60 seconds, maximum cumulative dose 20 mg) rapidly enters the central nervous system, where it achieves anticonvulsant levels within one minute, and will control seizures in greater than 80 percent of patients within five minutes [45]. A diazepam gel for rectal administration is also available (0.2 mg/kg). Some experts recommend avoiding benzodiazepines for management of eclamptic seizures because of potentially profound depressant effects on the fetus and mother. This effect becomes clinically significant when the total maternal dose of diazepam exceeds 30 mg. Because of subsequent redistribution of the drug into adipose tissue, the duration of diazepam's acute anticonvulsant effect is typically less than 20 minutes.\nLorazepam 0.02 to 0.03 mg/kg intravenously, allowing approximately one minute to assess its effect. If seizures continue at this point, additional doses of lorazepam (up to a cumulative dose of 0.1 mg/kg) are infused at a maximum rate of 2 mg/minute for acute treatment. Lorazepam is as effective as diazepam in terminating seizures, but the time from its injection to its maximum effect against seizures is as long as two minutes. The clinical advantage of lorazepam is that the effective duration of action against seizures is as long as four to six hours because of its less pronounced redistribution into adipose tissue.\nSodium amobarbital 250 mg intravenously over three to five minutes [15].\nTreatment of status epilepticus is discussed in detail separately\n","43":"Target blood pressure — Our target blood pressures are 130 to 150 mm Hg systolic and 80 to 100 mm Hg diastolic. The rapidity with which blood pressure should be brought to safe levels is controversial. Cerebral or myocardial ischemia or infarction can be induced by aggressive antihypertensive therapy if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation. Therefore, reducing mean arterial pressure by no more than 25 percent over 2 hours and achieving a target of 130 to 150 mmHg systolic and 80 to 100 mmHg diastolic seems reasonable [26]. We acknowledge the lack of clinical trial data to support these recommendations, and the need to individualize therapy based upon maternal and fetal factors.\n","32":"Fetus and placenta — The fetal consequences of chronic placental hypoperfusion are fetal growth restriction and oligohydramnios. Fetal growth restriction upstages preeclampsia from mild to severe.\nSevere and early onset preeclampsia result in the greatest decrements in birth weight compared to normotensive pregnancies, 12 and 23 percent, respectively [93]. By comparison, late onset preeclampsia can be associated with higher than average birth weight, possibly related to greater placental perfusion due to elevated cardiac output sometimes observed with late onset disease [94-98]. However, this association may also be the result of confounders associated with both preeclampsia and birth of large for gestational age infants (eg, obesity, impaired glucose tolerance) [99].  \nIndicated preterm delivery is a secondary result of fetal or maternal complications. Preeclampsia does not appear to accelerate fetal maturation, as once believed. The frequency of neonatal morbidities such as respiratory distress, intraventricular hemorrhage, and necrotizing enterocolitis is similar in infants of preeclamptic women and age-matched nonhypertensive controls [100].\nAbruptio placenta is infrequent (less than 1 percent) in women with mild preeclampsia, but has been reported in 3 percent of those with severe disease [101]. (See"Placental abruption: Clinical features and diagnosis".)\nImpaired placentation can lead to increased impedance to flow in the uterine arteries, manifested by elevation of the pulsatility index accompanied by uterine artery notching on uterine artery Doppler velocimetry. However, this finding is neither sensitive nor specific for preeclampsia. (See "Prediction of preeclampsia", section on 'Uterine artery Doppler velocimetry'.)\nIncreased resistance in the placental vasculature is also reflected by rising Doppler indices of the umbilical artery. Absent and reversed end diastolic flow are the most severe abnormalities and associated with a poor perinatal outcome. (See "Doppler ultrasound of the umbilical artery for fetal surveillance".)    \nPlacental histology is described separately. (See "Histopathology of placental disorders", section on 'Placental "underperfusion"'.)\nFetal hydrops (nonimmune or immune) can result in maternal symptoms identical to those seen in typical preeclampsia. This disorder is called mirror or Ballantyne syndrome and resolves without delivery if hydrops resolves\n","10":"During labor, we monitor women with gestational hypertension for development of proteinuria, worsening hypertension, and symptoms of severe disease since preeclampsia can manifest intrapartum [4]. We do not administer magnesium sulfate seizure prophylaxis unless proteinuria is noted or the patient develops severe hypertension or symptoms or laboratory abnormalities associated with severe preeclampsia\nWomen with severe gestational hypertension (blood pressure ≥160/100 mmHg) are delivered preterm. Systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥105 mmHg is treated with antihypertensive agents to reduce the risk of a maternal cerebrovascular event \nDelivery of pregnancies at or beyond 34 weeks of gestation and administration of a course of antenatal glucocorticoids to patients less than 34 weeks is a reasonable approach. If the patient's blood pressure is easily controlled and she remains free of proteinuria or other symptoms of severe preeclampsia, inpatient hospitalization is an option, with delivery if signs/symptoms of severe preeclampsia develop. \n"}
  • Hypertensive disorders in pregnancy dr. betha fe m. castillo 102413

    1. 1. HYPERTENSIVE DISORDERS IN PREGNANCY Betha Fe Manaois-Castillo M.D. FPOGS,FPCS,FPSUOG 25 July 2013
    2. 2. HYPERTENSIVE DISORDERS • Most common medical complication in pregnancy • 5-10% incidence • Major cause of maternal and perinatal morbidity worldwide Report of the National High Blood Pressure Education Program. Working group report on high blood pressure. Am J Obstet Gynecol. 2000;183:S1.; Sibai BM. Diagnosis and management of gestational hypertension and preeclampsia. Obstet Gynecol. 2003; 102:181.
    3. 3. HYPERTENSION • BP > 140 mm Hg systolic OR 90 mm Hg diastolic • Present on at least 2 occasions, at least 6 hours apart, but within a maximum of a 1week period
    4. 4. Hypertensive Disorders Related To Pregnancy 1. 2. 3. 4. 5. 6. Gestational hypertension Preeclampsia Eclampsia HELLP syndrome Chronic/preexisting hypertension Preeclampsia superimposed upon chronic/preexisting hypertension
    5. 5. Gestational Hypertension • systolic blood pressure ≥140 mHg and/or diastolic blood pressure ≥90 mmHg in a previously normotensive pregnant woman who is ≥20 weeks of gestation and has no proteinuria • BP returns to normal within 12 weeks after delivery
    6. 6. Gestational HTN: DIAGNOSIS • Determine the severity of hypertension • Measure protein excretion • 24-hour urine collection • Evaluate for signs/symptoms of severe preeclampsia • Perform laboratory evaluation • +/- end - organ involvement
    7. 7. Gestational HTN: DIAGNOSIS CRITERIA FOR MILD GESTATIONAL HYPERTENSION Blood Pressure > 140 to < 160 mm Hg, systolic > 90 to < 110 mm Hg, diastolic Proteinuria < 300 mg per 24-hr collection Platelet count > 100,000/mm3 Liver enzymes Normal Maternal symptoms Absent IUGR / Oligohydramnios (UTZ) Absent
    8. 8. Gestational HTN: MANAGEMENT • Mild Gestational HTN • • • • • • • Managed as outpatients (weekly antepartum visits) Daily fetal movement/kick counting NST + AFI OR BPS Fetal growth monitoring every 3-4 weeks No antihypertensive therapy No antenatal corticosteroids Deliver patients no later than their EDD
    9. 9. Gestational HTN: MANAGEMENT • Severe Gestational HTN • SBP ≥160 mmHg or DBP ≥105 mmHg is treated with antihypertensive agents • > 34 wks AOG  DELIVER! • < 34 wks AOG  give steroids
    10. 10. Gestational HTN: Risk of Progression to Preeclampsia • 15-25% risk • Women with early onset of gestational hypertension are more likely to progress to preeclampsia than women with late onset
    11. 11. Gestational HTN: RECURRENCE • Prevalence: 22 - 47 % (2nd pregnancy) • tends to recur with subsequent pregnancies
    12. 12. Gestational HTN: LONG-TERM PROGNOSIS • associated with development of HTN later in life • associated with development of diseases related to hypertension (CVD, CKD,DM)
    13. 13. PREECLAMPSIA • Is a multi - system disorder characterized by new onset of hypertension and proteinuria after 20 weeks of gestation in a previously normotensive woman • increased risk for maternal and/or fetal mortality or serious morbidity •Sibai BM, Caritis S, Hauth J, National Institute of Child Health and Human Development Maternal-Fetal Medicine U ; Hutcheon JA, Lisonkova S, Joseph KS. Epidemiology of pre-eclampsia and the other hypertensive disorders of pregnancy. Best Pract Res Clin Obstet Gynaecol 2011; 25:391.
    14. 14. www.uptodate.com ©2013 UpToDate®
    15. 15. Preeclampsia “ A 2 – stage disease? “ 1. Asymptomatic Placental Stage 2. Symptomatic Maternal Stage
    16. 16. Preeclampsia: PATHOGENESIS • • • • • • Immunologic Factors Systemic Endothelial Dysfunction Diet Genetic Factors Increased sensitivity to Angiotensin II Inflammation/Infection
    17. 17. Preeclampsia: RISK FACTORS • Associated with the pregnant woman • • • • • • • • • • Nulliparity Preeclampsia in a previous pregnancy Age >40 years or <18 years Family history of preeclampsia (mother or sister) Chronic hypertension Chronic renal disease; APAS or inherited thrombophilia; Vascular or connective tissue disease; DM (pregestational and gestational) High body mass index Black race / Filipino Woman herself was small for gestational age Prolonged interpregnancy interval
    18. 18. Preeclampsia: RISK FACTORS • Associated with the pregnant woman’s husband or partner • • • First time father Male partner whose mother or previous partner had preeclampsia Partner related factors (new partner, limited sperm exposure [eg, previous use of barrier contraception])
    19. 19. Preeclampsia: RISK FACTORS • Associated with the fetus • • • • Multifetal gestation • Hydrops fetalis / Triploidy Unexplained fetal growth restriction Fetal growth restriction, abruptio placentae, or fetal demise in a previous pregnancy Hydatidiform mole
    20. 20. MEAN ARTERIAL PRESSURE MAP = DBP + 1/3 (SBPDBP) ● MAP – 2 > 90 mmHg or a MAP3> 105 mmHg increased PIH and perinatal deaths ● Absence of a mid – trimester drop in BP may predict future PIH based on the absence of arteriolar vasodilatation
    21. 21. Early Screening for PE (11-13 weeks) • Ultrasound Screening • • Uterine arteries (PI) Abnormal UA can identify 50% of those who will develop preeclampsia and 30% of those who will develop IUGR. Nicolaides, Placental and Fetal Doppler, Diploma in Fetal Medicine Series, 2000. • Maternal Serum Markers • • VEGF, PlGF, sFlt1 Endoglin Courtesy of WWS
    22. 22. Clinical Features and Pathophysiology • Cardiopulmonary • Hypertension • Intravascular volume and edema • Cardiac function - high afterload assoc w/ inc. cardiac filling pressures • Pulmonary edema – pulmo vascular hydrostatic P > plasma oncotic P – Capillary leak, left HF, iatrogenic volume overload
    23. 23. Clinical Features and Pathophysiology • Renal • Proteinuria – ≥0.3 grams protein in a 24-hour urine specimen or persistent 1+ (30 mg/dL) on dipstick – random protein:creatinine ratio >30 mg/mmol – ≥5 grams of protein in a 24-hour urine collection (SEVERE) • Renal Function – GFR (30-40%), renal plasma flow – Rising creatinine and oliguria (UO<500mL/24h) PES (sec to renal vasoconstriction and Na retention)
    24. 24. Clinical Features and Pathophysiology • Renal • Hyperuricemia / Hypocalciuria – inc proximal Na resorption; urate reabsorption sec to renal ischemia • Urine sediment – benign • Histology – Glomerular Endotheliosis Light micrograph in preeclampsia showing glomerular endotheliosis. The primary changes are swelling of damaged endothelial cells, leading to partial closure of many of the capillary lumens (large arrows). Mitosis within an endothelial cell (small arrow) is a sign of cellular repair. Courtesy of Helmut Rennke, MD.
    25. 25. Clinical Features and Pathophysiology • Hematologic • Thrombocytopenia – – • PT, aPTT, Fibrinogen – • accelerated plt consumption <100,000/uL  PES not affected Microangiopathic hemolysis – – + schistocytes / helmet cells (PBS) Inc LDH; hemoconcentration
    26. 26. Clinical Features and Pathophysiology • Hepatic • Periportal and sinusoidal fibrin deposition and microvesicular fat deposition • RUQ pain, inc transaminase levels, coagulopathy, subcapsular hemorrhage or hepatic rupture • Epigastric pain sec to stretching of Glisson’s capsule due to hepatic swelling or bleeding
    27. 27. Clinical Features and Pathophysiology • CNS and eye • headache • visual symptoms – constriction of retinal arteries » Photopsia (flashing lights); scotomata (dark areas/gaps); diplopia or amaurosis fugax (unilat blindness) • generalized hyperreflexia • sustained ankle clonus • Stroke
    28. 28. Clinical Features and Pathophysiology • Fetus and placenta • FGR • Oligohydramnios • Fetal hydrops (mirror or Ballantyne syndrome)
    29. 29. PE: MANAGEMENT • Definitive treatment: DELIVERY! • Based on the ff: • AOG • Severity of PE • Maternal / Fetal condition
    30. 30. PES: MANAGEMENT • Deliver regardless of gestational age • if proteinuria ( ≥5 grams) is the only criteria for severe diseasemanaged as mild PE • mild fetal growth restriction with reassuring Doppler velocimetry  treat conservatively * • severe hypertension  treat conservatively * NOTE: * remote from term
    31. 31. MILD PE: MANAGEMENT • Deliver at ≥37 weeks of gestation • Labor induction encouraged
    32. 32. EXPECTANT ANTEPARTUM MANAGEMENT OF MILD PREECLAMPSIA • Inpatient vs outpatient care • Close maternal monitoring upon diagnosis of preeclampsia is important to establish disease severity and the rate of progression • Hospitalization is useful for making these assessments and facilitates rapid intervention in the event of rapid progression • Outpatient care is a cost-effective option for women with stable mild preeclampsia after initial dx evaluation
    33. 33. EXPECTANT ANTEPARTUM MANAGEMENT OF MILD PREECLAMPSIA • Laboratory follow – up • platelet count, serum creatinine, serum AST » 1-2x/wk, assess disease progression • Assessment of fetal well-being • • • • daily fetal movement count twice weekly fetal NST with AFI or twice weekly BPS UMA Doppler indices evaluation
    34. 34. EXPECTANT ANTEPARTUM MANAGEMENT OF MILD PREECLAMPSIA • Assessment of fetal growth • sonographic estimation of fetal weight done to look for growth restriction and oligohydramnios at the time of diagnosis of PE , repeated every 3 weeks if the initial examination is normal • Antenatal corticosteroids • < 34 weeks AOG
    35. 35. INTRAPARTUM MANAGEMENT • Intrapartum monitoring • Fluids • monitored closely to avoid excessive administration, since women with severe disease are at risk of pulmonary edema and significant third-spacing
    36. 36. Acute Management of PES • Labetalol • first-line therapy (rapid onset of action, good safety profile) • 20 mg IV over 2 minutes followed at 10-minute intervals by doses of 20 to 80 mg – up to a maximum total cumulative dose of 300 mg – E.g. Give 20 mg, then 40 mg, then 80 mg, then 80 mg, then 80 mg
    37. 37. Acute Management of PES • Hydralazine • 5 mg IV over 1 to 2 minutes • if BP goal is not achieved within 20 minutes, give a 5 to 10 mg bolus depending upon the initial response » The maximum bolus dose is 20 mg » If a total dose of 30 mg does not achieve optimal blood pressure control, another agent should be used. » The fall in blood pressure begins within 10 to 30 minutes and lasts from 2 to 4 hours.
    38. 38. Target BP • 130 to 150 mm Hg systolic and 80 to 100 mm Hg diastolic OR reduce MAP by no more than 25% over 2hrs • Cerebral or myocardial ischemia or infarction can be induced by aggressive antihypertensive therapy if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation
    39. 39. • Seizure Prophylaxis • MgS04 given to mild / severe PE » Loading dose: 4-6 g, slow IV push, over 15-20 mins » Continuous infusion: 1-2 g/hr OR 5g IM into each buttock (total 10 g) followed by 5 g IM, alternate buttocks ever 4h • continued for 24 hours postpartum
    40. 40. MgS04 Toxicity • loss of DTRs: 9.6 to 12.0mg/dL(4.0 -5.0 mmol/L) • respiratory paralysis: 12.0 to 18.0 mg/dL (5-7.5 mmol/L) • cardiac arrest: 24 to 30 mg/dL (10 to 12.5 mmol/L) * Calcium gluconate (1 gram intravenously over 5 to 10 minutes) • should be administered only to counteract life-threatening symptoms of magnesium toxicity (such as cardiorespiratory compromise)
    41. 41. Postpartum Management • NSAIDs • for pain control should be avoided in women with poorly controlled hypertension, oliguria, renal insufficiency, or thrombocytopenia • Monitor VS q 2h while on MgS04 • Treat PES
    42. 42. Prevention of Recurrence • Prepregnancy • Weight loss to ideal BMI • Control of glucose in diabetes • Control of BP in CHTN (diet, exercise) • Low dose aspirin in select patients (from 12 wks) • Not recommended • Vitamins C & E • Dietary salt restriction • Anti-HTN therapy to prevent preeclampsia
    43. 43. ECLAMPSIA • development of grand mal seizures in a woman with preeclampsia, in the absence of other neurologic conditions that could account for the seizure • occurs in 2 to 3 percent of severely preeclamptic women not receiving antiseizure prophylaxis
    44. 44. Pathogenesis of Seizures 1. Cerebral overregulation in response to high systemic blood pressure • • • • vasospasm of cerebral arteries underperfusion of the brain localizedischemia/infarction cytotoxic (intracellular) edema
    45. 45. Pathogenesis of Seizures 2. Loss of autoregulation of cerebral blood flow in response to high systemic pressure • • • • E.g., hypertensive encephalopathy Hyperperfusion endothelial damage vasogenic (extracellular) edema
    46. 46. Management • Iinitial Mx: Maintenance of airway patency and prevention of aspiration • Gravida rolled onto her left side • Protect from trauma • Supplemental O2 (8-10L/min via face mask)
    47. 47. • Management of severe hypertension, if present • Prevention of recurrent seizures • Evaluation for prompt delivery • definitive treatment of eclampsia is delivery, irrespective of gestational age
    48. 48. Management of Persistent Convulsions • additional bolus of 2 grams MgS04 over 15 to 20 minutes • with careful monitoring for signs of magnesium toxicity
    49. 49. HELLP Syndrome • Hemolysis • Elevated Liver enzymes • Low Platelets • severe form of preeclampsia or an independent D/O
    50. 50. HELLP Syndrome Initiate IV Dexamethasone EARLY: • Always when PLTS <100,000/uL • Selectively when Class 3 plus – (a) Eclampsia; (b) Severe Epigastric Pain; (c) Fulminant Disease; (d) Severe HTN • Antepartum: Dex 10mg q12 hrs • Postpartum: Dex 10+10+5+5 @ 0,12,24,36 hrs
    51. 51. CHRONIC / PREEXISTING HYPERTENSION • SBP ≥140 mmHg and/or DBP ≥90 mmHg that antedates pregnancy or is present before the 20th week of pregnancy (on at least two occasions) or persists longer than 12 weeks postpartum
    52. 52. PREECLAMPSIA SUPERIMPOSED UPON CHRONIC / PREEXISTING HYPERTENSION • the new onset of proteinuria after 20 weeks of gestation in a woman with chronic/preexisting hypertension
    53. 53. • Hypertensive Disorders particularly PREECLAMPSIA… • Major life-threatening morbidity • Leading reason for preterm labor and birth • RISK factor for FUTURE maternal cardiovascular and metabolic DISEASE • Affects long term maternal survival
    54. 54. GOALS • Development of effective strategies for the prevention and/or treatment of preeclampsia • Prolong the pregnancy and improve maternal and neonatal health
    55. 55. Key Points • • • • • • • Identify Risk Factors Prediction Diagnosis (Classify) Ambulatory or In Patient Management Tertiary Care Postpartum care Prevention
    56. 56. Thank you…

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