Preeclampsia And Eclampsia

PREECLAMPSIA AND ECLAMPSIA









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 with reduced organ perfusion secondary to vasospasm and endothelial classification.  Preeclampsia is said to complicate 5% of all deliveries.

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

Classification of hypertensive disorders of pregnancy 1. Gestational hypertension (formerly pregnancy-induced hypertension or transient hypertension).   2. Preeclampsia   3. Eclampsia  4. Preeclampsia superimposed on chronic hypertension   5. Chronic hypertension

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 occurring after 20 weeks gestation. Hypertension -140/90 mm of Hg or more on at least two occasions 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 the sixth 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

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



Definition of severe pre-eclampsia



 1. Arterial pressure > 160mmHg systolic or > 110mmHg diastolic on two occasions at least 6 hrs apart 2. Proteinuria > 5g in 24 hour > 3 + un dipstick 3. Oliguria < 400 mm in 24 h 4. Cerebral signs – headache, blurred vision or altered consciousness 5. Pulmonary oedema or cyanosis 6. Epigastric or right upper quadrant pain 7. Impaired liver function 8. Hepatic rupture 9. Thrombocytopenia

       

Hypertensive Disorders During Pregnancy: Indications of Severity Abnormality

Mild

Severe

Diastolic blood pressure

< 100 mg Hg

110mmHg or higher

Proteinuria

Trace to 1 +

Headache

Absent

Present

Visual disturbances

Absent

Present

Upper abdominal pain

Absent

Present

Oliguria

Absent

Present

Convulsion

Absent

Present (eclampsia)

Serum creatinine

Normal

Elevated

Thrombocytopenia

Absent

Present

Liver enzyme elevation

Minimal

Marked

Fetal growth restriction

Absent

Obvious

Pulmonary edema

Absent

Present

Persistent 2 + or more

Material Vascular Disease

Faculty Placentation

Excessive Trophoblast

Genetic Immunologic or Inflammatory Factors Reduced Uteroplacental Perfusion Vasoactive Agents: Prostaglandins Nitric Oxide Endothelins

Noxious Agents: Cytokines Lipid Peroxidases Endothelial Activation Capillary Leak

Vasospasm

Activation of Coagulation Edema

Proteinuria Hemoconcentration

Hyper tension

Oliguria

Seizures

Liver Ischemia

Abruption

Thrombo cytopenia

  



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 vessels leads to profound vasospasm and reduced organ perfusion which are

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

Leaking Capillaries  pulmonary Oedema ARDS

Coagulation consumption)

-

Thrombocytopenia

(↑ Platelet activation and

Platelet Production

↑ Less often Erythrocyte destruction

 

  

  

Prediction and Prevention  No ideal predictive tests that fulfils all described criteria.Two most important predictive factors:  1. Nulliparity Preeclampsia in 5.8% primigravida, 0.4% Secundagravida.  2. Family History Considerable evidence support significant genetic contribution  Aetiology & pathophysiology are still not understood fully and this has hindered development of effective premature measures. . Anti-platelet therapy Low dose Aspirin   . Calcium Supplementation

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 severity of the disease and also influenced by gestational age.

          

Management should include   1. Treatment of hypertension   The risk of cerebral haemorrhage 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.  





Prolonged treatment of HT is advisable when the fetus is immature in an attempt to 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 be all that is required in some patients.

Antihypertensive therapies 

Acute therapy-hydrallazine, labetalol



Prolonged therapy-methyldopa nifedipine, atenolol



ACE inhibitors not recommended

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

MANAGEMENT IN HOSPITAL 1.Detailed examination followed by daily scrutiny for clinical findings such as headache, visual disturbances, epigastric pain, and rapid weight 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

ECLAMPSIA 





Eclampsia is defined as the new onset of convulsions, before or during pregnancy or 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

          

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

      

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.

        

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

       

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