Pregnancy Induced Hypertension, Preeclampsia, Eclampsia


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  • Hypertension is the most common medical problem encountered during pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during pregnancy are classified into 4 categories, as recommended by the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy: 1) chronic hypertension, 2) preeclampsia-eclampsia, 3) preeclampsia superimposed on chronic hypertension, and 4) gestational hypertension (transient hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy).[1 ]This terminology is preferred over the older but widely used term pregnancy-induced hypertension (PIH) because it is more precise
  • Hypertension is diagnosed when blood pressure is 140/90 mm Hg or greater, using Korotkoff phase V to define diastolic pressure. Edema has been abandoned as a diagnostic criteria because it occurs in too many normal pregnant women to be discriminant. In the past, it had been recommended that an increment of 30 mm Hg systolic or 15 mm Hg diastolic blood pressure be used as a diagnostic criterion, even when absolute values were below 140/90 mm Hg. This criterion is no longer recommended because evidence shows that women in this group are not likely to suffer increased adverse pregnancy outcomes (Levine, 2000; North and colleagues, 1999). That said, women who have a rise of 30 mm Hg systolic or 15 mm Hg diastolic warrant close observation.
    transient hypertension of pregnancy if preeclampsia is present at the time of delivery and the blood pressure is normal by 12 weeks postpartum, and chronic hypertension if the elevation in blood pressure persists beyond 12 weeks postpartum.
    140/90 mm Hg or greater for the first time during pregnancy, but in whom proteinuria has not developed. Gestational hypertension is termed transient hypertension if preeclampsia does not develop and the blood pressure has returned to normal by 12 weeks' postpartum. In this classification the final diagnosis that the woman does not have preeclampsia is made only postpartum. Thus, gestational hypertension is a diagnosis of exclusion. Importantly, however, women with gestational hypertension may develop other signs associated with preeclampsia, for example, headaches, epigastric pain, or thrombocytopenia, which influence management.
  • As Chesley (1985) emphasized, 10 percent of eclamptic seizures develop before overt proteinuria
    It is frequently difficult to determine whether a patient has preeclampsia, chronic hypertension, or chronic hypertension with superimposed preeclampsia. This is partly because blood pressure normally decreases during the second trimester, and the decrease may mask the presence of chronic hypertension.
    Renal biopsy studies have shown that only about 70% of primigravidas under 25 years of age with the triad of edema, hypertension, and proteinuria have glomeruloendotheliosis, the characteristic lesion of preeclampsia. Twenty-five percent have unsuspected renal disease. In multiparas with chronic hypertension with superimposed preeclampsia, about 3% have glomeruloendotheliosis and 21% have underlying renal disease. Renal biopsy is rarely performed in pregnancy because the benefit usually does not justify the risk. The sensitivity and specificity of biochemical markers such as uric acid and antithrombin III are unknown.
  • Epidemiology:
    -Fetal-maternal transfusion.
    -Prolong exposure to paternal
    -Maternal genetic predisposition.
    3-4 folds
    United States
    Chronic hypertension occurs in up to 22% of women of childbearing age, with the prevalence varying according to age, race, and body mass index. Population-based data indicate that approximately 1% of pregnancies are complicated by chronic hypertension, 5-6% by gestational hypertension (without proteinuria), and 1-2% by preeclampsia.
    Hypertensive disorders in pregnancy are among the leading causes of maternal mortality, along with thromboembolism, hemorrhage and nonobstetric injuries. Between 1991 and 1999, pregnancy-induced hypertension caused 15.7% of maternal deaths in the United States.[4 ]
    While maternal diastolic blood pressure (DBP) greater than 110 mm Hg is associated with an increased risk for placental abruption and fetal growth restriction, superimposed preeclamptic disorders cause most of the morbidity due to chronic hypertension during pregnancy. Severe maternal complications include eclamptic seizures, intracerebral hemorrhage, pulmonary edema due to capillary leak or myocardial dysfunction, acute renal failure due to vasospasm, proteinuria greater than 4-5 g/d, hepatic swelling with or without liver dysfunction, and disseminated intravascular coagulation and/or consumptive coagulopathy (rare). Consumptive coagulopathy usually is associated with placental abruption and is uncommon as a primary manifestation of preeclampsia.
    Fetal complications include abruptio placentae, intrauterine growth restriction, premature delivery, and intrauterine fetal death.
    Hypertension before pregnancy or during early pregnancy is associated with a twofold increased risk of gestational diabetes mellitus.[5 ]
    Black women have higher rates of preeclampsia complicating their pregnancies compared with other racial groups, mainly because they have a greater prevalence of underlying chronic hypertension. Among women aged 30-39 years, chronic hypertension is present in 22.3% of African Americans, 4.6% of non-Hispanic white persons, and 6.2% of Mexican Americans. Hispanic women generally have blood pressure levels that are the same as or lower than those of non-Hispanic white women.
    Preeclampsia is more common at the extremes of maternal age (<18 y or >35 y). The increased prevalence of chronic hypertension and other comorbid medical illnesses in women older than 35 years may explain the increased frequency of preeclampsia among older gravidas.
  • (Placental bed lesions in pre-rclampsia: acute atherosis of the spiral arteries with larg thrombosis.)
  • :
    - IUGR
    - Oliguria
    - Ischemia,hemolysis,low plt count (coagulation avctivation) HELLP syndrome.
    - seizures
  • Kidney
  • 1.Maternal
    . :
  • Physical findings in preeclampsia
    Blood pressure
    Blood pressure should be measured in the sitting position, with the cuff at the level of the heart. Inferior vena caval compression by the gravid uterus while the patient is supine can alter readings substantially, leading to an underestimation of the blood pressure. Blood pressures measured in the left lateral position similarly may yield falsely low values if the blood pressure is measured in the higher arm, unless the cuff is carefully maintained at the level of the heart.
    Women should be allowed to sit quietly for 5-10 minutes before each blood pressure measurement.
    Korotkoff sounds I (the first sound) and V (the disappearance of sound) should be used to denote the systolic blood pressure (SBP) and DBP, respectively. In about 5% of women, an exaggerated gap exists between the fourth (muffling) and fifth (disappearance) Korotkoff sounds, with the fifth sound approaching zero. In this setting, both the fourth and fifth sounds should be recorded (eg, 120/80/40 with sound I = 120, sound IV = 80, sound V = 40) as the fourth sound will more closely approximate the true DBP.
    Maternal SBP greater than 160 mm Hg or DBP greater than 110 mm Hg denotes severe disease; depending on the gestational age and maternal status, delivery should be considered for sustained BPs in this range.
    Many automated blood pressure cuffs provide reasonable estimates of true blood pressure during normal pregnancy (especially those validated for pregnancy) but tend to underestimate blood pressure in preeclamptic women. Only a few automated BP cuffs have been validated in preeclampsia. Manual blood pressure measurement with a mercury sphygmomanometer remains the criterion standard in this setting.
    Home and ambulatory BP measurements are increasingly being used in the pregnant population. Assuming the BP device is accurate (validated relative to an office measurement) they may provide valuable additional data regarding hypertension severity and control during pregnancy.
    Retinal vasospasm is a severe manifestation of maternal disease; consider delivery.
    Retinal edema is known as serous retinal detachment. This can manifest as severely impaired vision if the macula is involved. It generally reflects severe preeclampsia and should lead to prompt consideration of delivery. The condition typically resolves upon completion of pregnancy and resolution of the hypertension and fluid retention.
    Right upper quadrant (RUQ) abdominal tenderness stems from liver swelling and capsular stretch. Consider delivery.
    Brisk, or hyperactive, reflexes are common during pregnancy. Clonus is a sign of neuromuscular irritability that usually reflects severe preeclampsia.
    In most normal pregnancies, the woman has some lower extremity edema by the third trimester. In contrast, a sudden worsening in dependent edema, edema in nondependent areas (such as the face and hands), or rapid weight gain suggest a pathologic process and warrant further evaluation for preeclampsia.
    Signs suggesting a secondary medical cause of chronic hypertension
    Centripetal obesity, "buffalo hump," and/or wide purple abdominal striae suggest glucocorticoid excess.
    A systolic bruit heard over the abdomen or in the flanks suggests renal artery stenosis.
    Radiofemoral delay or diminished pulses in lower versus upper extremities suggests coarctation of the aorta.
    Clinical signs may demonstrate hyperthyroidism, hypothyroidism, or growth hormone excess.
    Signs of end-organ damage from chronic hypertension
    S4 on cardiac auscultation is not a normal finding in pregnancy. It suggests left ventricular hypertrophy or diastolic dysfunction due to preeclampsia-induced vasospasm.
    In pregnancy, and particularly in the presence of preeclampsia, any sustained cardiac gallop may be a pathological finding and warrants further evaluation with echocardiography. However, a well-conducted phonocardiographic study of pregnant women found a soft, intermittent S3 to be common in normal pregnancy.
    Retinal changes of chronic hypertension may be noted.
    Carotid bruits may reflect atherosclerotic disease due to longstanding hypertension
  • Differential Diagnoses
    Antiphospholipid Antibody Syndrome and PregnancyHemolytic-Uremic SyndromeAntithrombin DeficiencyHydatidiform MoleAortic CoarctationHyperaldosteronism, PrimaryAutoimmune Thyroid Disease and PregnancyHyperparathyroidismCardiomyopathy, PeripartumHypertensionCommon Pregnancy Complaints and QuestionsHypertension, MalignantCushing SyndromeHyperthyroidismDiabetes Mellitus and PregnancyHypothyroidismDisseminated Intravascular CoagulationNephrotic SyndromeEclampsiaNormal Labor and DeliveryEncephalopathy, HypertensivePreeclampsiaEvaluation of Fetal DeathProtein C DeficiencyEvaluation of GestationProtein S DeficiencyFetal Growth RestrictionPulmonary Disease and PregnancyGastrointestinal Disease and PregnancySystemic Lupus ErythematosusGlomerulonephritis, AcuteSystemic Lupus Erythematosus and PregnancyGlomerulonephritis, ChronicTeratology and Drug Use During PregnancyGraves DiseaseThrombotic Thrombocytopenic PurpuraHashimoto ThyroiditisHematologic Disease and PregnancyOther Problems to Be Considered
    Assessment of fetal well-being
  • Workup
    Laboratory Studies
    Laboratory testing to evaluate chronic hypertension (if not done previously or recently) includes testing for target organ damage, potential secondary causes of hypertension, and other risk factors.
    Studies include: urinalysis; CBC; and serum sodium, potassium, creatinine, and glucose levels (the presence of high levels of progesterone, an aldosterone antagonist, during a normal pregnancy may mask the hypokalemia from hyperaldosteronism).
    Other suggested tests include creatinine clearance, microalbuminuria, 24-hour urinary protein, serum calcium, uric acid, glycosylated hemoglobin, thyroid-stimulating hormone (TSH), and an ECG.
    Serum lipids (ie, total cholesterol, high-density lipoprotein [HDL], low-density lipoprotein [LDL], triglycerides) predictably increase during pregnancy, so measurement should be deferred until the postpartum period.
    The increase in endogenous corticosteroid levels during normal pregnancy makes it difficult to evaluate for secondary hypertension due to adrenal corticosteroid excess.
    Routine tests when evaluating a patient for preeclampsia include: CBC count, electrolytes, BUN, creatinine, liver enzymes and bilirubin, and a urine dip for protein.
    In cases in which an incidental platelet count is less than 150,000/µL, 75% are secondary to dilutional thrombocytopenia of pregnancy, 24% are due to preeclampsia, and about 1% of cases are due to other platelet disorders not related to pregnancy. Counts less than 100,000/µL suggest preeclampsia or ITP.
    Hemoglobin levels greater than 13 g/dL suggest the presence of hemoconcentration. Low levels may be due to microangiopathic hemolysis or iron deficiency.
    Urinalysis may be used as a screen for proteinuria. Trace levels to +1 proteinuria are acceptable, but levels of +2 or greater are abnormal and should be quantified with a 24-hour urine collection or spot urine protein:creatinine ratio.
    Recently, spot urine specimens for protein:creatinine ratios have been validated as screening tools for abnormal proteinuria during pregnancy. They appear to be more accurate than urinalysis, although an abnormal result should still be confirmed with a 24-hour urine collection.
    Serum creatinine usually is less than 0.8 mg/dL during pregnancy; higher levels suggest intravascular volume contraction or renal involvement in preeclampsia.
    A serum uric acid level greater than 5 mg/dL is abnormal and is a sensitive, but nonspecific, marker of tubular dysfunction in preeclampsia.
    Elevated levels of hepatic transaminases may reflect hepatic involvement in preeclampsia and may occur in the absence of epigastric/RUQ pain.
    In a 24-hour urine collection, the reference range for protein excretion in pregnancy is up to 300 mg/d. Higher levels are abnormal and may reflect renal involvement in preeclampsia. Creatinine clearance increases approximately 50% during pregnancy, and levels less than 100 mL/min suggest renal dysfunction that is either chronic or due to preeclampsia.
    Examination of the peripheral blood smear for evidence of microangiopathic hemolysis and thrombocytopenia may reveal the presence of red blood cell (RBC) fragments. In this setting, the diagnoses of hemolytic-uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), and HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet [count]) should also be considered.
    Prothrombin time (PT) and/or international normalized ratio (INR) and/or activated partial prothrombin time (aPTT) results may be abnormal in consumptive coagulopathy and disseminated intravascular coagulopathy complicating severe preeclampsia. Checking the PT/INR/aPTT is not necessary in the absence of abnormal liver transaminases or thrombocytopenia.
    Abnormal values of lactate dehydrogenase (LDH), bilirubin, haptoglobin, fibrinogen, and D-dimers may confirm the presence of hemolysis and disseminated intravascular coagulopathy, along with coagulation testing. Checking LDH, bilirubin, haptoglobin, fibrinogen, and D-dimers is unnecessary unless PT/INR/aPTT results are abnormal, thrombocytopenia is present, or the hemoglobin level is dropping.
    Researchers in the United Kingdom have developed a method for first-trimester screening to identify women at risk for the development of preeclampsia or gestational hypertension. The screening algorithm uses a combination of maternal variables, including mean arterial pressure, uterine artery pulsatility index, pregnancy-associated plasma protein–A, and placental growth factor. The algorithm proved especially effective for predicting early preeclampsia (ie, requiring delivery before 34 weeks).[8 ]
    Imaging Studies
    Imaging studies should not be performed in an unstable patient and should not delay rapid facilitated delivery in a woman thought to have severe preeclampsia or eclampsia.
    New seizures in pregnancy suggest preeclampsia-eclampsia, but primary neurological disorders must be excluded. Blood tests to order when evaluating eclampsia include those suggested to evaluate for preeclampsia.
    Chest radiograph
    Obtain chest radiographs to evaluate for pulmonary edema in the setting of dyspnea or hypoxia occurring in a woman with preeclampsia.
    The classic finding of preeclampsia on T2-weighted images is bilateral occipital bright spots that represent focal edema. This is also known as posterior reversible leukoencephalopathy syndrome. This finding is similar to the changes observed when a nonpregnant patient has hypertensive encephalopathy.
    Magnetic resonance venography also may be performed to exclude cerebral venous sinus thrombosis.
    Ultrasonography or CT scan of the liver may be used to evaluate for subcapsular hemorrhage or infarction in the setting of persistent severe RUQ pain or markedly elevated hepatic transaminases.
    Limited echocardiography may be performed to evaluate for left ventricle hypertrophy (LVH) in chronic hypertension and to exclude cardiomyopathy or occult valvular disease in pregnant women with pulmonary edema.
    Other Tests
    Perform 12-lead ECG to evaluate for LVH in women with chronic hypertension.
    An EEG may be indicated to evaluate recurrent seizure activity, persistent altered level of consciousness, or altered mental status.
    Following eclampsia, the EEG may reveal epileptiform activity. More commonly, the test shows nonspecific diffuse slowing that may persist for several weeks after delivery.
    Fetal monitoring
    Close fetal monitoring under the direction of an obstetrician is essential in pregnant women with preeclampsia. Preeclampsia is a disease of the placenta. When the placenta is severely affected, subtle hypoperfusion of the fetus can occur, which may initially manifest as a decrease in the amniotic fluid level (oligohydramnios), fetal growth restriction, and intrauterine fetal death as a consequence of placental insufficiency. Fetal concerns may be an indication for delivery in women with otherwise mild preeclampsia. In this setting, order fetal assessments twice each week. Obstetricians generally alternate a biophysical profile with a fetal nonstress test to assess fetal well-being. At this point, the authors advise collaboration with a perinatologist.
    Fetal heart rate tracing is a useful tool to assess utero-placental perfusion.
    In women with chronic hypertension, consider advising the obstetrician to obtain a fetal ultrasound at 18 weeks' gestation to document growth. Serial ultrasounds may be necessary to document fetal growth velocity and/or to monitor amniotic fluid volume.
    Histologic Findings
    Endothelial dysfunction and vasospasm observed in preeclampsia affect multiple regions of the body, including the maternal brain, kidneys, liver, lungs, heart, and placenta. Pathology demonstrates areas of edema, microinfarctions, and microhemorrhage in the affected organs. The placenta typically shows incomplete decidualization of the spiral arterioles, which may be part of the pathogenesis of preeclampsia. The kidneys may reveal glomerular endotheliosis or, more rarely, acute tubular necrosis (ATN) or cortical necrosis.
  • Noncardiogenic pulmonary edema in a patient with preeclampsia. This is due to capillary leak that can be a primary component of preeclampsia. The radiograph demonstrates a diffuse increase in lung markings without cephalization or vascular redistribution seen in patients with pulmonary edema from systolic dysfunction. This patient had rapid clinical improvement after only 10 mg of intravenous furosemide
  • Pregnancy Induced Hypertension, Preeclampsia, Eclampsia

    1. 1. Seyed Morteza Mahmoodi
    2. 2. Gestational Hypertension Pre eclampsia and Eclampsia Chronic Hypertension Contents Complications
    5. 5.  Hypertension  Pregnancy-induced hypertension  Gestational hypertension  Transient hypertension of pregnancy  Chronic hypertension  Pre-eclampsia  Eclampsia  Increment of 30 mm Hg systolic or 15 mm Hg diastolic blood pressure (Levine, 2000; North and colleagues, 1999)
    6. 6. Abnormality Nonsevere Severe Diastolic blood pressure <110 mm Hg 110 mm Hg Systolic blood pressure <160 mm Hg 160 mm Hg Proteinuria 2+ 3+ Headache Absent Present Visual disturbances Absent Present Upper abdominal pain Absent Present Oliguria Absent Present Convulsion (eclampsia) Absent Present Serum creatinine Normal Elevated Thrombocytopenia Absent Present Serum transaminase elevation Minimal Marked Fetal-growth restriction Absent Obvious Pulmonary edema Absent Present
    7. 7. -Defective trophoblastic invasion -Immunological maladaptive tolerance -Maternal maladaptation to CV changes in normal pregnancy -Abnormal placentation. -Genetic and nutritional factors
    8. 8. Residual HT Recurrent pre- eclampsia Chronic renal disease
    9. 9.  Injuries  Pulmonary: -Edema -pneumonia, aspiration -ARDS -Embolism  Hyperpyrexia  LVF  RF Hepatic necrosis  Subcapsular haematoma  Cerebral hemorrhage  Disturbed vision  Haematological, DIC Postpartum -Shock -Sepsis -Psychosis
    10. 10.  Insidious, slow course.  Mild symptoms:Mild symptoms: -Ankle edema -Extend to be generalized  Alarming symptoms:Alarming symptoms: Acute onset -Headache -Disturbed sleep -Oliguria -Epigastric pain -Eye symptoms, restlessness.
    11. 11.  Raised BP  Abnormal weight gain,  Oedema.  Pulmonary oedema  Retinal,  Neurological examination,  Abdominal examination,  Secondary and end organ damage,
    12. 12.  EpilepsyEpilepsy  HysteriaHysteria  EncephalitisEncephalitis  MeningitisMeningitis  Puerperal cerebral thrombosis.Puerperal cerebral thrombosis.  PoisoningPoisoning  Cerebral malariaCerebral malaria  Intra-crainal tumours.Intra-crainal tumours.
    13. 13.  Blood values: CBC, serum sodium, potassium, creatinine, and glucose levels, LFT, coagulation profile creatinine.  Urine  Serum uric acid, biochemical marker of pre-biochemical marker of pre- eclampsiaeclampsia.  Serum lipids  Radiological  ECG, EEG  Fetal monitoring
    14. 14.  More than 100 clinical, biophysical, and biochemical tests have been reported to predict preeclampsia  Low-Salt Diet  Fish Oil Supplementation  Antioxidants  CALCIUM SUPPLEMENTATION  ASPIRIN  There is currently no proven way to prevent preeclampsia
    15. 15.  Mild preeclapsia:Mild preeclapsia: -Maternal evaluation (history & ex.) -Lab: CBC & Electrolyte RFT: BUN, creatinine ,uric acid LFT & coagulation profile: PT, PTT, D-diamers Urine analysis 24hhr urine for protein & creatinine clearance.
    16. 16.  Fetal evaluation of CTG, USG, doppler flow.  Bed rest in left lateral decubitus position.  No use of diuretics & AntiHT
    17. 17.  Stabilize & deliverStabilize & deliver, the only cure .  Vaginal induction is preferred.  Admit & complete maternal evaluation. -Keep NPO -Start IV, cross & type -Foley catheter  Monitoring urine output, input & vitals.
    18. 18.  Fetal evaluation: electronic fetal monitoring, doppler flow.  Anticonvulsant therapy: -to seizure thresholdto seizure threshold -baseline Mg bld level -Mg sulfateMg sulfate 4g IV boluse over 20min,. Folowed by maintenance of 2-4g/hr Oliguric pt needs low infusion rate.Oliguric pt needs low infusion rate. Management of severe preeclampsia:
    19. 19.  Signs of Mg sulfate toxicity: -DTR -RR<10/min -Urine output< 25 cc/hr -Decrease muscle tone -CNS or cardiac depression  Antagonist: calcium gluconatecalcium gluconate 10% 10ml, 1g IV over 2min.
    20. 20.  Antihypertensive therapy: -Indicated if BP >140-160/90-110 -Labetalol 20-50mg IV q 10mins. -Methyldopa or nifedipine. ACE-inhibitors avoided.ACE-inhibitors avoided.
    21. 21.  Resuscitation, ABCABC  Oxygen  Arrest convulsions, valium or phenytoin.  Ventilatory support, prevent aspiration, auscultate lungs after every seizure.  Haemodynamic stabilization, control BP.  Send investigation.  Deliver by 6-8hrs.  Postpartum care, intensive.
    22. 22.  Mgsulfate,Mgsulfate, continue to 24hr after last fit.  Lytic coktail regime:Lytic coktail regime: Chlorpromazine, phenergan & pethidine.  AntiHT & diuretics. Status eclampticus:Status eclampticus: thiopentone Na0.5gm, dissolved in 20% dextrose givin slowly.