Gestational hypertension

Defined as a sustained of blood pressure to 140/90 mmHg or more on at least two occasion 4 or more hours apart beyond the 20th week of pregnancy or during the first 24 hours after delivery in a previously normotensive woman Associated with higher risk for pre-eclampsia 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 Criteria o Absence of evidence of underlying cause of hypertension o Unassociated with other evidence of preeclampsia o Not associated with hemoconcentration ,thrombocytopenia, raised uric acid level

To confirm diagnosis do a glucose challenge : pt is given 50g of glucose then after 1 h we ,measure the concentration : if >140 mg/dl we do a oral 3h glucose test but if < 140 mg/dl its normal

Essential hypertension in pregnancy Its also a common disorder in pregnancy Criteria of diagnosis o Rise of blood pressure to 140/90mmHg or more prior to 20 weeks of pregnancy o Cardiac enlargement on ECG o Medical disorder present This kind of hypertension can lead to chronic placental insufficiency that leads to retarded fetus , when blood pressure exceeds 160/100mmHg the perinatal loss doubles and may complicate with pre-eclampsia Management o Aim of treatment : stabilize blood pressure below 160/100mmHg, prevent superimposition of pre-eclampsia, monitor the maternal and fetal well being o Antihypertensive drugs given but with care to avoid placental insufficiency . o If hypertension is uncontrollable pregnancy is continued till 37 weeks and induction of labour is made

Differential diagnosis
Pre-eclampsia Primigravida After 20 weeks of pregnancy Proteinuria None Thromobocytopenia Pre-eclampsia Pre-pregnant hypertension Essential hypertension Multipara Before 20 weeks of pregnancy Negative findings Silver wiring , hypertensive retinopathy Chronic nephritis Variable Presence of cast and albumin with low specific gravity Albuminuric retinopathy , cotton wool patches & flame hemorrhages High urea & creatinine History of lesion on renal

Parity Onset of hypertension Urine Eye changes Specific blood values Past history

Eclampsia Eclampsia, which is considered a complication of severe preeclampsia, is commonly defined as new onset of grand mal seizure activity and/or unexplained coma during pregnancy or postpartum in a woman with signs or symptoms of preeclampsia It typically occurs during or after the 20th week of gestation or in the postpartum period. Nonetheless, eclampsia in the absence of hypertension with proteinuria has been demonstrated to occur in 38% of cases reported in the United Kingdom. Similarly, hypertension was absent in 16% of cases reviewed in the United States. The clinical manifestations of maternal preeclampsia are hypertension and proteinuria with or without coexisting systemic abnormalities involving the kidneys, liver, or blood. There is also a fetal manifestation of preeclampsia involving fetal growth restriction, reduced amniotic fluid, and abnormal fetal oxygenation. HELLP syndrome is a severe form of preeclampsia and involves hemolytic anemia, elevated liver function tests (LFTs), and low platelet count. Most cases of eclampsia present in the third trimester of pregnancy, with about 80% of eclamptic seizures occurring intrapartum or within the first 48 hours following delivery. Rare cases have been reported before 20 weeks' gestation or as late as 23 days postpartum. Other than early detection of preeclampsia, no reliable test or symptom complex predicts the development of eclampsia. Course of eclamptic seizures o Eclampsia manifests as 1 seizure or more, with each seizure generally lasting 6075 seconds. The patients face initially may become distorted, with protrusion of the eyes, and foaming at the mouth may occur. Respiration ceases for the duration of the seizure. o Eclamptic seizures may be divided into 2 phases. Phase 1 lasts 15-20 seconds and begins with facial twitching. The body becomes rigid, leading to generalized muscular contractions. o Phase 2 lasts about 60 seconds. It starts in the jaw, moves to the muscles of the face and eyelids, and then spreads throughout the body. The muscles begin alternating between contracting and relaxing in rapid sequence. o A coma or period of unconsciousness, lasting for a variable period, follows phase 2. After the coma phase, the patient may regain some consciousness, and she may become combative and very agitated. However, the patient will have no recollection of the seizure.

o A period of hyperventilation occurs after the tonic-clonic seizure. This compensates for the respiratory and lactic acidosis that develops during the apneic phase. Pathophysiology of Eclampsia o Inhibition of uterovascular development Many uterovascular changes occur when a woman is pregnant. It is believed that these changes are due to the interaction between fetal and maternal allografts and result in systemic and local vascular changes. It has been shown that in patients with eclampsia, the development of uteroplacental arteries is hindered. o Hindrance of cerebral blood flow regulation It is believed that in eclampsia there is abnormal cerebral blood flow in the setting of extreme hypertension. The regulation of cerebral perfusion is inhibited, vessels become dilated with increased permeability, and cerebral edema occurs, resulting in ischemia and encephalopathy. In extreme hypertension, normal compensatory vasoconstriction may become defective.

o Endothelial dysfunction Factors associated with endothelial dysfunction have been shown to be increased in the systemic circulation of women suffering from eclampsia. These include the following

Cellular fibronectin Von Willebrand factor Cell adhesion molecules (ie, P-selectin, vascular endothelial adhesion molecule-1 [VCAM-1] Intercellular adhesion molecule-1 [ICAM-1]) Cytokines (ie, interleukin-6 [IL-6]) Tumor necrosis factor- [TNF-] o In addition, it is believed that antiangiogenic factors, such as placental protein fms-like tyrosine kinase 1 (sFlt-1) and activin A, antagonize vascular endothelial growth factor (VEGF). Elevated levels of these proteins cause a reduction of VEGF and induce systemic and local endothelial cell dysfunction. Clinical picture o Eclampsia convulsion is divided to 4 stage Premonitory stage : pt is unconscious with twitching of muscle of face ,limbs, this stage last for 30 sec Tonic stage : body goes into tonic spasm , respiration cease and tongue protrude between teeth , stage last for 30 sec Clonic stage : all voluntary muscle contract and relax , tongue bitting may occur, stage last for 1-4 min Coma

If the fits are multiple, occurring at varying interval it is calles status eclampticus Complication of maternal o Tongue injuries o Edema o Pneumonia

o Embolism o Left ventricular failure o Renal failure o DVT o Shock , sepsis, psychosis Management o General First aid Oxygen administration Hemodynamic stabilization Arrest convulsion o Specific Anticonvulsant and sedative regime MgSO4 Antihypertensive drugs : hydralzine, labetalol ,CCB Status eclampticus : thiopentone 2.0g in 20ml of 5% dextrose IV

Fits controlled Baby mature : o Termination of pregnancy should be done if cervix favourable and there is no contradication of vaginal delivery o Oxytoxin drip may achieved o If cervix unfavourable C-section is prefer Baby premature o Drag pregnancy till 37 week , fetal monitored constantly

Fits uncontrolled Termination of pregnancy Assess the responds to have delivery , c-section if unfavourable

Chronic hypertension

Defined as presence of hypertension of any cause antedating or before 20th weeks of pregnancy and its presence beyond 42 days after delivery Chronic hypertension is a primary disorder in 90-95% of cases and may be either essential (90%) or secondary to some identifiable underlying disorder, such as renal parenchymal disease (eg, polycystic kidneys, glomerular or interstitial disease), renal vascular disease (eg, renal artery stenosis, fibromuscular dysplasia), endocrine disorders (eg, adrenocorticosteroid or mineralocorticoid excess, pheochromocytoma, hyperthyroidism or hypothyroidism, growth hormone excess, hyperparathyroidism), coarctation of the aorta, or oral contraceptive use. About 20-25% of women with chronic hypertension develop preeclampsia during pregnancy.

Chronic hypertension occurs in up to 22% of women of childbearing age, with the prevalence varying according to age, race, and body mass index (BMI). 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. Risk o Age > 40 o Duration of hypertension >15 years o Level of BP >160/110mmHg o Presence of any medical disorder o Presence of thrombophillia