AHMED ABDULWAHAB ASSISTANT PROFESSOR AND CONSULUTANT OB/GY

 Objectives.  Definition of preeclampsia.  Etiology.  Effect of hypertensive disorder in pregnancy.  The theory of development of preeclampsia.  Pathological changes associated with preeclampsia.  Definition of Eclampsia.  Management of preeclampsia and Eclampsia  Role of antihypertensive.

 the hypertensive disorder are major contributor to maternal and perinatal morbidity and mortality.  CLASSIFICATION AND DIFINTION.  Blood pressure reading depends on maternal position and gestational age, it is lower in left lateral position and higher in sitting position, arterial B/P normally decline in 1 st,and 2 nd trimester and rise to pre pregnant level in the 3rd trimester.

 Cont.  The diagnosis of hypertension is made when the systolic B/P is equal or greater than 140mmHg or diastolic of greater or equal 90mmHg. 1. Preeclampsia/ eclampsia. 2. Chronic hypertension, If the hypertension is known prior to pregnancy or develops prior to 20 weeks gestation and persist 12 weeks postpartum.

 Cont,  Mostly essential hypertension but small percentage will have secondary hypertension due to renal,vascular, or endocrinological causes.

 3-Chronic hypertension with superimposed preeclampsia.  It is diagnosed when the patient is known to have hypertension and the process is aggravated by pregnancy and usually carries a worse prognosis, it is suspected by new develop of proteinuria or sudden significant increases in B/P or proteinuria after the 20 weeks of pregnancy.

 4- gestational hypertension.  When hypertension appears for the first time after 20 weeks of pregnancy or within 48 to 72 hours after delivery without proteinuria and disappears by 12 weeks postpartum.

 PREECLAMSIA.  It is a syndrome unique to pregnant human, characterized by the new onset of hypertension and or proteinuria and or edema in the second half of gestation.  It may arise earlier after 14 weeks and then we should suspect hdatidiform mole or multiple pregnancy.

 Etiology.  It is the disease of theories.  Genetics, immunologic, nutritional,endocrinologic, and infection all have been proposed as a causes.  Because the condition disappears after delivery, most attention has directed on the placenta, membranes and the fetus,

 Uteroplacental ischemia may be central to the development of the disease, and the ischemia may result in production and release of toxins that enter the circulation and causes wide spread endothelial dysfunction that causes imbalance in vasoconstrictors prostaglandin thromboxane A2 and vasodilator prostacyclin E2 production.

 PATHOPHYSIOLOGY.  The underlying pathophysiologic abnormality is generalized vasospasm.  Renal blood flow and GFR in preeclampsia are significantly lower than in normal pregnancy this vasoconstriction causes to damage to the glomerular membranes and increase the permeability to proteins that leads to proteinurria

 PATHOLOGY.  1- lack of decidualization of the myometrial segment of the spiral arteries.  In normal pregnancy the second wave trophoblast invade the muscular and elastic layer of the spiral artery by fibrinoid and fibrous tissue that becoming unresponsive to vasoconstrictors substances, this is limited in preeclamppsia

 The typical renal lesion in preeclampsia is glomerular capillary endotheliosis.  Hemorrhage and necrosis will occur in many organs secondary to arteriolar vasoconstriction such as liver, brain, and retina.

 Clinical and laboratory manifestation.  Most can be explained on the basis of the endothelial dysfunction and vasospasm.  Weight gain and edema.  It occurs early and reflect an expansion of the extra vascular fluid compartment, and haematocrit may also increased reflecting hypovolumia and hemo concentration.  Elevation of blood pressure.  Particularly the diastolic B/P, which may occur days or weeks after the onset of pathological fluid retention.

 Protienuria.  May occur days or weeks after the onset of hypertension, or manifest during labor or even postpartum.  Renal function test.  Increase in serum uric acid is the earliest change, decrease in creatinine clearance with increase in blood urea and creatinine condition may progress to frank oligouria and renal failure.

 Coagulation system.  Thrombocytopenia is the most common abnormality, DIC may occur and represent severe preeclampsia.  Liver function.  Focal hemorrhage and infraction leading to upper quadrant and epigastric pain and elevated liver enzymes and increase level of bilirubin in significant haemolysis.  Hepatic rupture is rare.

 Placental function.  Vasospasm will lead to infraction and decrease uteroplacental perfusion that will cause intrauterine growth restriction IUGR, oligohydramnios, fetal heart abnormalities and retroplacental hemorrhage or abruption.  Central nervous system.  Visual disturbance, blurred vision, increase reflexes irritability or hypereflexia.

 Evaluation and management.  Delivery is the only definitive cure for preeclampsia BUT the question is which is more good for the mother and the baby? So delivery is indicated when the presence of the fetus inside the uterus is attended by certain risks that outweigh pre maturity complications, or the maternal condition is not responding to appropriate management regardless of fetal maturity.

 Initial maternal assessment will involve.  Any past history of hypertension or renal disease prior to pregnancy or previous pregnancy.  Symptoms of sever preeclampsia like headache, visual changes, nausia and vomiting, abdominal or epigasteric pain.  Examination.  B/P, weight gain, edema, fundal height, and reflexes.

 Investigation.  Urine for protein, CBC, liver function test, urea and electrolyte,uric acid.  Fetal assessment.  Fetal growth chart by ultrasound biophysical profile Doppler study and fetal kick chart non stress test.  If the mother disease is mild and no evidence of fetal compromise management consist of bed rest and observation.

 The patient should be delivered by the time she reached 38 weeks or she started to develop signs and symptoms of worsening the disease, or there is evidence of fetal compromise.  In mild cases patient can be managed as outpatient.  Criteria of severe preeclampsia.  Severe hypertension systolic more than 160mmHg and diastolic equal or more than 110mmHg..

 Heavy proteinuria 5 gm in 24 hour urine collection.  Oliguria less than 500ml per 24 hour.  Cerebral or visual disturbance.  Pulmonary edema and cyanosis.  Epigasteric or right upper quadrant pain.  HELLP syndrome.characterized by.  Haemolysis, Elevated liver enzyme, Low platelet.

 ECLAMPSIA.  Is the presence tonic- clonic seizures that usually complicate severe PET.  25% occur ante nataly before labor 50% during labor and 25% occur post nataly after delivery. 

 Management of eclampsia.  It is a true obstetric emergency.  Stabilize and deliver.  Room is dark with minimum noise.  Clear airway and give oxygen mask.  Insert IV line for blood test and drug and fluid administration.  Foley catheter for input and output charting.  The best and safest drug for controlling convulsion is magnesium sulfate

 After stabilization delivery Is considered either by induction of labor or by caesarian section.  Prophylaxis against convulsion with magnesium sulfate continued after delivery for 24 hours after the last convulsion.

 Antihypertensive therapy.  Should be initiated when diastolic B/P is more than 105mmHg to prevent CNS hemorrhage.  Hydralazine and labetalol are used to control severe hypertension.  Nifedipine is an other option.  Alpha methyldopa is save to be use in chronic hypertension.  Angiotensin converting enzyme inhibitor should not be used.