Treatment of Preexcisting Hypertension
Hypertension and sligth to moderate preeclamsia
Treatment of Serverhypertension
Treatment of Eclampsia
Drug A leading cause of maternal morbidity and mortality (cerebral , adult respiratory distress syndrome, multiorgan failure, DIC), and infant mortality and morbidity and later neurodevelopmental disturbances. Occurs in 10% of pregnancies mostly primiparas Definitions:
Hemolysis, Elevated Liver Enzymes (AST > 70 IU/L LDH > 600 u/l). Low platelets (< 100,000 microL) and elevated bilirubin > 1,2 mg(dl and may be associated with severe disseminated intravascular coagulation (DIC) Eclampsia
Convulsion disorder in association with Proteinuric hypertension Hypertension > 140/90 mmHg in two occasions, 6 hours apart, position lying at a 45 degree angle or sitting Systolic Korotkoff Phase I and diastolic with Phase V (disappearance) Risks Previous preeclampsia
Underlying medical conditions: Hypertension, renal disease, proteinuria, preexisting diabetes, thrombophilia. If new hypertension before 32 weeks, 50 % risk of developing preeclampsia. Severe preeclampsia
Automated blood pressure recording systems can systematically underestimate blood pressure in preeclampsia to a serious degree. Blood pressure values should be compared, at the beginning of treatment, with those obtained by conventional mercing sphygmomanometers. Women with multiple pregnancies are at increased risk of preeclampsia without proteinuria. Differential diagnosis:
Other thrombolic microangiopathies.
Thrombocytopenic Purpura (TTP) and Hemolytic Uremic Syndrome (HUS) are often first determined when disease worsened postpartum. HUS mainly affects the kidneys and in TTP neurological abnormalities are dominant. However many patients present with severe neurological abnormalities such as seizures and coma together with acut renal faiture. These patients can best be described by the comprehensive term TTP-HUS
TTP is associated with platelet aggregation leading to thrombocytopenia There is a widespread organ damage but mainly symptoms from CNS. TTP is diagnosed by the classic pentaed: thrombocytopenia (often with purpura but not usually severe bleeding), microangiopathic hemolytic anemia (blood smear with marked blood cell fragmentation ~ helmet cells and microspherocytosis), fever, renal and neurologic symptoms, elevated LDH with normal coagulation status. Heart failure ADAMS 13 deficiency.
The treatment of both TTP and HUS include supportive measures and plasma exchange transfusion (beginning with 40 ml/kg fresh frozen plasma).
Corticoid can be given with reported response rate about 30%.
HELLP affects mainly the liver with elevated liver enzymes and anemia as a late symptom.
Acute fatty liver of pregnancy may be a variant of preeclampsia. There is often profound hypoglycemia and marked hyperuricemia. serum aminotransferase from moderate up to 1000 IE/L Thrombocytopenia less pronounced and white blood count more elevated. There is often marked hypertension and proteinuria despite marked elevated liver enzymes.
Lupus syndrome: Primary DNA antibodies, cellular cast in urine, decrease in complement factorsand increased split products (see SLE). Prevention:
Low dose aspirin and calcium supplementation appear to reduce the risks of hypertension in pregnancy and of preeclampsia, especially in women at high risk. Either agent may be used as attempted prophylaxis for women considered to be at high risk of hypertensive disorders. (75 mg aspirin or 500 mg calcium carbonate daily, commenced after the first trimester appear to be appropriate doses). Grade A. Maternal Risk
Severe hypertension: Diastolic blood pressure greater than 110 mmHg (cerebral bleeding).
Eclampsia or symptoms of imminent eclampsia (aspiration, Cerebral insults).
Renal impairment: rising urea/creatinine/ oliguria
Rapidly progressive non-dependent edema
DIC Fetal Risks:
The risk of impaired fetal wellbeing Significant intrauterine growth retardation and abruption. MANAGEMENT OF PRE-EXISTING HYPERTENSION IN PREGNANCY
Woman on medication can often reduce their dose or discontinue medicine in early pregnancy.
Woman on angiotensin-converting enzyme (ACE) inhibitors and Angiotensin II receptor blockers should discontinue them, as these drugs are teratogenic and may cause oligohydramnios, pulmonary hypoplasia, renal failure, renal tubular dysgenesis and hypotension and decrease skull ossification (hypocalvaria) and there is also a risk of intrauterine fetal death.
The beta-blocker atenolol may be associated with growth restrictions and is not recommended for use in pregnancy. References:
(1) Fontenot MT et al. A prospective randomized trial of magnesium sulfate in severe preeclampsia: Use of diuresis as a clinical parameter to determine the duration of postpartum therapy. AMJOG. 2005, vol 192, number 6, 1793-94 (2) Nelson-Piercy C. Handbook of Obstetric Medicine. Second Edition, By Martin Dunitz, Ltd., published in the United Kingdom in 2002. (3) Sibai, MB, Barton JR. Expectant management of severe preeclampsia remote from term: patient selection, treatment, and delivery indications. Am J Obstet Gynecol 2007;June; 196(6):514,e1-9 (4) The management of severe- pre-eclampsia/eclampsia. Royal college of Obstetricians and Gynecologists March 2006 No 10 (5) www.uptodate.com 2007