6587062 Preeclampsia and Eclampsia

8/9/2019 6587062 Preeclampsia and Eclampsia

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PREECLAMPSIA AND ECLAMPSIA


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Preeclampsia is a multisystem disorder of unknown aetiology and unique to pregnant women after 20 weeks gestation. It is a progressive disease with a very variable mode of presentation and rate of progression. It is pregnancy specific withreduced organ perfusion secondary to vasospasm and endothelial classification.Preeclampsia is said to complicate 5% of all deliveries.


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It is said to affect 5.8% of primigravidas and 0.4% of secundagravidas. The incidence is influenced by parity, race, multiple gestations, environmental factors,maternal age, maternal size and history of chronic hypertension


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Classification of hypertensive disorders of pregnancy1. Gestational hypertension (formerly pregnancy-induced hypertension or transient hypertension). 2. Preeclampsia 3. Eclampsia 4. Preeclampsia superimposed on chronic hypertension 5. Chronic hypertension


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Definition and Diagnosis

Preeclampsia can not be accurately defined until its cause is known.It is described as a syndrome comprising of hypertension, oedema and proteinuria occurringafter 20 weeks gestation. Hypertension-140/90 mm of Hg or more on at least twooccasions four hours or more apart after the 20th week of pregnancy in a woman known to be normotensive and in whom blood pressure has returned to normal by thesixth postpartum week. Proteinuria is defined as the excretion of 0.3 g protein or more within 24 Hr or a measurement of 1+ or more using


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Classification This is classified as mild or severe forms as the latter is associated with increased maternal and fetal morbidity. Severe form is said tooccur if one or more of the conditions in this table is


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Hypertensive Disorders During Pregnancy: Indications of Severity Abnormality Diastolic blood pressure Proteinuria Headache Visual disturbances Upper abdominal pain Oliguria Convulsion Serum creatinine Thrombocytopenia Liver enzyme elevationFetal growth restriction Pulmonary edema Mild < 100 mg Hg Trace to 1 + Absent Absent Absent Absent Absent Normal Absent Minimal Absent Absent Severe 110mmHg orhigher Persistent 2 + or more Present Present Present Present Present (eclampsia) Elevated Present Marked Obvious Present


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Material Vascular Disease

Faculty Placentation Genetic Immunologic or Inflammatory Factors Reduced Uteroplacental Perfusion

Excessive Trophoblast

Vasoactive Agents: Prostaglandins Nitric Oxide Endothelins Endothelial Activation Capillary Leak Vasospasm Edema Proteinuria Hemoconcentration Hyper tension Oliguria Liver Ischemia Thrombo cytopenia Activation of Coagulation

Noxious Agents: Cytokines Lipid Peroxidases

Seizures

Abruption


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Pathophysiology The summary is that as a result of the damage of the endothelial cells, it looses its functions and in addition also produces proagulants, vasoconstrictions and mitogens. The increased pressor sensitivity of the maternal v

essels leads to profound vasospasm and reduced organ perfusion which are


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arious Changes etus IUGR Preterm delivery Abruptio placental

aternal idneys - Proteinuria, GFR, Plasma Creatinine - Glomerular endothehosis Renal failure (ATN, Cortical necrosis) Cardiovascular - Plasma Volume, CVP, AP & SVR Contractility usually unchanged. Brain HT encephatopathy, ischaemia and infarction, vasospasm, Haemorrhage Oedema Eclampsia Liver Altered LFT, Periportal hepatic necrosis, Subcapsulaar haemorrhage, FDP, HELLP. Lungs Leak

ing Capillaries pulmonary Oedema ARDS Coagulation consumption) Thrombocytopenia Platelet Production ( Platelet activation and Less often Erythrocyte destruction


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Prediction and Prevention No ideal predictive tests that fulfils all described

criteria.Two most important predictive factors: 1. Nulliparity Preeclampsia in5.8% primigravida, 0.4% Secundagravida. 2. Family History Considerable evidencesupport significant genetic contribution Aetiology & pathophysiology are stillnot understood fully and this has hindered development of effective premature measures. . Anti-platelet therapy Low dose Aspirin . Calcium Supplementation


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TREATMENT

Delivery is the cure for Preeclampsia. The prime objective is to prevent convulsion. The management ideally should be multidisciplinary. It is based on the seve

rity of the disease and also influenced by gestational age.


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Management should include 1. Treatment of hypertension The risk of cerebralhaemorrhage is a major cause of maternal deaths (60%) Significant risk of CVA occurs when MAP > 140mmHg (180/120). The aim of treatment is to prevent intracerebral haemorrhage while not affecting uteroplacental blood flow and maternal renal functions.


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Prolonged treatment of HT is advisable when the fetus is immature in an attemptto delay delivery. However, this can only be undertaken provided the mother is not placed at risk and that strict monitoring of both the mother and the fetus is

carried out at frequent regular intervals, hospitalization and bed rest may beall that is required in some patients.


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Antihypertensive therapies

Acute therapy-hydrallazine, labetalol Prolonged therapy-methyldopa nifedipine, atenolol ACE inhibitors not recommended


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For Severe Preeclampsia Anticonvulsant Antihypertensive - Follow by Delivery Conservative management in severe cases Need to be cautious. Think of maternal safety.


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MANAGEMENT IN HOSPITAL 1.Detailed examination followed by daily scrutiny for clinical findings such as headache, visual disturbances, epigastric pain, and rapidweight gain. 2. 2.Weight on admittance and every day thereafter 3 3.Analysis for proteinuria on admittance and at least every 2 days thereafter 4.4Blood pressure readings in sitting position with an appropriate-size cuff every 4 hours, except between midnight and morning. 5.Measurement of plasma or serum creatinine,uric acid, hematocrit, platelets, and serum liver enzymes, the frequency to be


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ECLAMPSIA

Eclampsia is defined as the new onset of convulsions, before or during pregnancyor post partum, unrelated to other cerebral pathologic conditions in a woman with preeclampsia. Incidence Reported rate 1:2000 to 1:3000 deliveries. The incidence is signficiantly higher in non industrialized nations. Estimates in developing countries varies from 1 in 100 to 1 in 1700. Worldwide of estimated 500,000,maternal deaths every year 10 15% are associated with HDP. Reported maternal mortality rates varies


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Management Aim 1. Stop Convulsions and prevent recurrence 2. Control the blood pressure 3. Avoidance of diuretics and limitation of fluid administration 4. Correct fluid and electrolyte imbalance 5. Deliver the patient


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Anticonvulsants - Valium - Phenytoin - Chlomethiazole - Magnesium sulphate The anticonvulsant therapy should protect the woman and her fetus from deleterious effects of convulsion but should not expose either to additional risks from the therapy.


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Supportive Management - Airways - Nasogatric tube - Oxygen - Catheterization / Urinary output monitoring - Tepid sponge / Expose to fan - Management of anunconscious patients.


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Complications - Pulmonary Oedema - Renal and hepatic failiure - Hemiplegia -Altered Consciousnes/Coma - Some degree by Blindness - Psychoses


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6587062 Preeclampsia and Eclampsia