【高血压精品英文课件】妊高症 hypertensive disorders with pregnancy

Hypertensive Disorders with Pregnancy Professor Zouhair O Amarin MD MSc (Med. Sci) MSc (Med. Edu) FRCOG Department of Obstetrics and Gynaecology Jordan University of Science and Technology,Hypertensive Disorders in Pregnancy,Hypertensive disorders are some of the most common complications of pregnancy They complicate 7-10% of all pregnancies. Pregnancy Induced Hypertension - 70% Chronic Hypertension - 30% Up to 13% of PE patients well have chronic or essential hypertension,Pregnancy can: Induce hypertension in women with no preexisting history Aggravate an already existing hypertensive disorder Generalized edema and Proteinuria Epigastric pain and visual or respiratory problems Eclamptic convulsions and coma Death,In Jordan, hypertensive disease during pregnancy is a major cause of maternal deaths. It is associated with 6.7% of maternal mortality (5/76) National Maternal Mortality Study, Jordan, 2007-2008. Amarin et al.,Classification A- Pregnancy Induced Hypertension 1. Gestational hypertension 2. Pre-eclampsia 3. Eclampsia B- Pregnancy Aggravated Hypertension Superimposed pre-eclampsia and eclampsia (on top of chronic hypertension) C- Chronic Hypertension with Pregnancy,Definitions Gestational Hypertension BP reading 140/90 mmHg for the first time after 20 weeks of pregnancy No proteinuria BP returns to normal within 12 weeks postpartum (if the BP elevation persists, the woman is diagnosed as having chronic hypertension) Final diagnosis is only made postpartum May even be associated with an increased birth weight,Definitions (cont.) Pre-eclampsia Mild pre-eclampsia BP 140/90 mmHg after 20 weeks gestation Proteinuria 1+ by urine dipstick or a total protein level 300 mg/24 hours - Pre-eclampsia can develop before the 20 week of gestation in hydatidiform mole and in the presence of lupus anticoagulant,Definitions (cont.) Severe pre-eclampsia BP 160 mmHg systolic or 110 mmHg diastolic Proteinuria 2+ by urine dipstick or a total protein level of 2 gm/24 hours,Definitions (cont.) Eclampsia Central nervous system (CNS) involvement with the occurrence of convulsions that cannot be attributed to other causes,Superimposed PE or eclampsia Development of PE or eclampsia in pre-existing hypertension detected by a further increase of 30 mmHg in SBP or 15 mmHg in DBP or New onset proteinuria of 300 mg/24 hours in hypertensive women but with no proteinuria before 20 weeks gestation or A sudden increase in proteinuria or a drop in platelet count to 100,000/mm3 with hypertension and proteinuria before 20 weeks gestation,Proteinuria It indicates glomerular damage and almost always occurs after hypertension It is a reliable indicator of fetal morbidity and mortality Significant proteinuria is defined as: One 24-h urine collection with a total excretion of 300 mg or more Two random clean-catch or catheter specimen of urine collected at least 4-6 hours apart with: 2+ or more on reagent strip 1+ if SG 1010 A protein / creatinine index of 300 or more,Predisposing Factors Age: PG 35 Parity: PG have double incidence Lower socio-economic status Genetic predisposition, recessive trait Obstetric complications: multiple and molar pregnancy, fetal hemolytic diseases (hydrops fetalis), polyhydramnios Existing medical conditions: chr BP, ren D, DM, SLE, antiphospholipid AS, Previous PE. The recurrence rate for PE with the same male partner is 20%, and usually becomes apparent at later gestation than in the first pregnancy Obesity: 4.3% for a women with a body mass index 35 kg/m2,Conditions that appear to decrease PE incidence Prolonged exposure to paternal antigen Smoking, but if PE occurs then perinatal mortality triples Placenta previa,Pre-existing (chronic) hypertension: Hypertension is present before pregnancy or detected before 20 weeks Or Hypertension first diagnosed after 20 weeks gestation and persisted after 12 weeks postpartum,The cause of pre-eclampsia is unknown The placenta appears to be incriminated Delivery of the placenta is the only known cure The disorder is more frequent with large placental mass, e.g. twins or abnormal placentae A proposed cause is the release of a toxic factor from the placenta which alters maternal endothelial cell functions. This hypothesis has not been proven,Theories,(I) Defective trophoblastic invasion of the spiral arteries (II) Immunologic factor (III) Increased pressor responses (IV) Prostaglandins imbalance (V) Genetic predisposition (VI) Inflammatory factors,Many investigators feel that uteroplacental insufficiency is necessary for the development of the disease. - Ischemia could be due to: Underlying vascular changes (hypertensive disease or failure of the normal physiologic changes in the spiral arteries of the uterus) Increased myometrial resistance of the myometrial vessels, which could be related to a heightened myometrial tension produced by the large fetus in a primiparous women, by twins, or by polyhydramnios,The poorly perfused trophoblast release “factor X” which enters maternal circulation and causes endothelial dysfunction (serum of women with PET is able to activate and damage vascular endothelial tissue in vitro) Endothelial dysfunction causes imbalance between different classes of locally produced vasoconstrictor and vasodilators,Immunologic factor Stimulation of the maternal immune system by the early conceptus is essential for production of blocking antibodies to antigenic sites on the placenta, thus preventing the rejection of the fetus and placenta. Hypoimmune response results in damage of the placenta and subsequent PE PE is less common in previously stimulated immunity conditions as in: Previous pregnancy Consanguineous marriages Increased maternal anti-HLA antibodies,Pathophysiology, Angiotensin II Serotonin Endothelin, Prostacyclin Nitric oxide, Platelet activation Thrombocytopenia Reduced production of anti-thrombin III, Vasospasm Intravascular coagulation Plasma volume constriction,Patho-physiologic changes in pre-eclampsia Vasospasm Intravascular coagulation Plasma volume constriction,Patho-physiologic Changes in Pre-eclampsia (cont.) Vasospasm Excess production/sensitivity to vasoconstrictors: Angiotensin II Serotonin Endothelin Decreased production/sensitivity to vasodilators: Prostacyclin Nitric oxide,Patho-physiologic Changes in Pre-eclampsia (cont.) Intravascular coagulation: Platelet activation Thrombocytopenia Reduced production of anti-thrombin III,Patho-physiologic Changes in Pre-eclampsia (cont.) Plasma volume contraction Redistribution of fluid from the intra-vascular to interstitial fluid spaces so that total extra cellular fluid volume remains unaltered This is an important consideration as intravascular volume correction may result in pulmonary edema when capillary permeability is high and plasma oncotic pressure low,Organ hypoperfusion Kidney: GFR, proteinuria, hyperuricaemia, oliguria Liver: SGOT, SGPT, epigastric pain Brain: visual scotomata due to occipital lobe ischemia, headache, convulsions (eclampsia) Placenta: IUGR, placental abruption,Diagnosis History Personal history Past history Menstrual history Obstetric history Complaints and history of present pregnancy,Diagnosis (cont.) Physical Examination Hypertension Edema Obstetric examination,Diagnosis (cont.) Investigations CBC: PCV and thrombocytopenia SGOT, SGPT: Elevated liver enzymes Creatinine clearance, serum creatinine, uric acid, total protein in urine, and blood urea: impaired Coagulation profile: PT, PTT, clot. and bleed. time in DIC. Fibrinogen and FDP to diagnose DIC Fetal Surveillance,Diagnosis (cont.) Indicators of severity of pre-eclampsia Presence of symptoms Persistent headache or other cerebral or visual disturbances Persistent epigastric pain Diastolic BP 110 mmHg Proteinuria of 2+ or more by urine dipstick or a total protein level of 2 gm/liter in a 24-hour urine sampling,Diagnosis (cont.) Abnormal laboratory findings Obvious fetal growth restriction Neurological effects: Scotomata, hyperreflexia Eclamptic convulsions,Indications to terminate pregnancy in pre-eclampsia Maternal Indications Completed 37 weeks Abnormal liver/ renal functions Severe preeclampsia/ eclampsia regardless of the gestational age In selected cases of severe PET, where the expertise and equipment are available, expectant management may be undertaken for fetal indications,Indications to terminate pregnancy in pre-eclampsia (cont.) Fetal Indications Obvious IUGR Oligohydramnios, IUFD The presence of congenital fetal malformations incompatible with life,Management of pre-eclampsia Convulsion prophylaxis Treatment of hypertension Timing of delivery Fluid management Supportive care for various end organ complications,Management of Mild Pre-eclampsia Completed 37 weeks gestation: Termination of pregnancy yields better fetal and maternal outcomes 3437 weeks: Expectant management Gestation 34 weeks: Expectant management and administration of glucocorticoids,Management of severe pre-eclampsia Severe pre-eclampsia usually requires prompt delivery Management should include the following items simultaneously: Convulsion prophylaxis Antihypertensive therapy Termination of pregnancy,Convulsions Prophylaxis Magnesium sulphate (MgSO4) Anticonvulsant of choice Mode of action: Blocks neuromuscular conduction through blocking the release of acetylcholine at neuromuscular junctions,Convulsions Prophylaxis (cont.) Dosage and administration: Loading dose: 6 gm of MgSO4 diluted in 200 ml of an IV fluid solution (Ringers lactate) over 20 minutes by slow IV drip Maintenance dose: 2 gm/hour by slow IV injection starting immediately after the loading dose and continued for 24 hours after delivery or after the last convulsion,Convulsions Prophylaxis (cont.) Toxicity Neurotoxicity: Loss of patellar reflex Respiratory depression Respiratory rate less than 12/min Cardiac toxicity (cardiac arrest) Antidote: Calcium gluconate, 1 gm IV over a few minutes to reverse MgSO4 toxicity if it occurs,Antihypertensive Therapy Hydralazine Nifedipine Labetalol Sodium nitroprusside,Termination of Pregnancy Once the diagnosis of severe preeclampsia has been established, termination of pregnancy becomes mandatory after patient stabilization Mode of delivery depends upon whether: The woman is in labor The progress of labor The cervix is fit for induction In selected cases of severe PET, where the expertise and equipment are available, expectant management may be undertaken for fetal indications,Management of end-organ complications Consumption coagulopathy Intracranial hemorrhage Sub capsular hematoma HELLP syndrome,Consumption coagulopathy Clotting factors (platelets, FFP) should be administered only for signs of clinical bleeding Cryoprecipitate should be administered only when volume restriction is indicated Significant thrombocytopenia and coagulopathy are contraindications to regional anesthesia,Intercranial hemorrhage Typical presentation is severe headache in the post partum women with pre-eclampsia and/or eclampsia confirmed by CT scan Combine obstetric and neurologic care in a tertiary care setting Therapy should include BP control and seizure prevention,Intracerebral and Intraventriclar haemorrhage- CT,Subcapsular hematoma Suspect it in women with severe epigastric pain, and hepatomegaly Ultrasound or CT scan of the liver may be diagnostic Management is usually expectant with correction of coagulation abnormalities Profound sudden hypovolemic shock in the presence of subcapuslar hematoma suggests hepatic rupture, which requires massive transfusion and hepatic surgery. If it occurs before delivery, perform a CS,HELLP syndrome The acronym HELLP was coined in 1982 to describe a syndrome consisting of hemolysis elevated liver enzyme levels and low platelet count The syndrome has been considered a variant of preeclampsia, but it can occur on its own or in association with preeclampsia Pregnancy-induced hypertension, preeclampsia and HELLP syndrome are related and overlap in their presentations.,Etiology and Pathogenesis The findings of this multisystem disease are attributed to abnormal vascular tone, vasospasm and coagulation defects The syndrome seems to be the final manifestation of some insult that leads to micro vascular endothelial damage and intravascular platelet activation With platelet activation, thromboxane A2 and serotonin are released, causing vasospasm, platelet agglutination and aggregation, and further endothelial damage Thus begins a cascade that is only terminated with delivery,The hemolysis in HELLP syndrome is a microangiopathic hemolytic anemia Red blood cells become fragmented as they pass through small blood vessels with endothelial damage and fibrin deposits The elevated liver enzyme levels in the syndrome are thought to be secondary to obstruction of hepatic blood flow by fibrin deposits in the sinusoids This obstruction leads to periportal necrosis and, in severe cases, intrahepatic hemorrhage, sub-capsular hematoma formation or hepatic rupture,Epidemiology and risk factors Superimposed HELLP syndrome develops in 4 to 12 percent of women with preeclampsia or eclampsia The syndrome generally presents in the third trimester of pregnancy It presents antepartum in 69% of women and postpartum in 31% in women. With postpartum presentation, the onset is typically within the first 48 hours after delivery,Clinical presentation The typical symptomatology of these patients consists of a woman with preeclampsia who develops vague complaints giving a history of general malaise for few days prior, and other complaints include epigastric or right upper quadrant pains, nausea or vomiting,Diagnostic tests The three chief abnormalities found in HELLP syndrome are hemolysis, elevated liver enzyme levels and a low platelet count The serum transaminase levels may be elevated to as high as 4,000 U per L, but milder elevations are typical. Platelet counts can drop to as low as 6,000 per mm3, but any platelet count less than 150,000 per mm3 warrants attention,Unless DIC is present, the prothrombin time, partial thromboplastin time and firbrinogen level are normal in women with HELLP syndrome In a women with a plasma fibrinogen level of less than 300 mg per dL, DIC should be suspected, especially if other laboratory abnormalities are also present,Management Prompt recognition of HELLP syndrome and timely initiation of therapy are vital for mother and fetus Prompt delivery is recommended regardless of gestational age Dexamethasone in a high dosage of 10 mg intravenously every 12 hours markedly improve the laboratory abnormalities Women with a platelet count greater then 40,000/mm3 are unlikely to bleed Transfusion if platelet count drops to less than 20,000/mm3 If CS, transfuse if their platelet count is less than 50,000/mm3,Eclampsia Clinical features: Premonitory phase Tonic phase Clonic phase Coma,Emergency treatment and first aid 1. Clear airway passages 2. Apply an oxygen mask 3. Protect the patient from harm during seizures 4. Control convulsions with MgSO4 5. Control high BP to avoid fatal complications 6. Deliver fetus 7. Avoid diuretics and hyperosmotic agents 8. Close observation,Monitoring during hospital stay Close observation: Every 30 minutes assess pulse, BP and respiratory rate Maintain a fluid balance chart monitoring fluid intake and urinary output Limit IV fluid administration unless excessive blood loss,Monitoring during Hospital Stay (cont.) If convulsions occur despite MgSO4 therapy: CT scan should be performed If severe respiratory insufficiency occurs: ICU admission and ventilation Measuring blood gases and blood pH levels,Chronic Hypertension: Diagnosis History: Past history: Hypertension treated before pregnancy with various antihypertensive medication Renal problems Obstetric history: Hypertension during previous pregnancies Previous superimposed pre-eclampsia Previous IUFD, IUGR and abortions Family history of hypertension,Chronic Hypertension: Diagnosis (cont.) Examination: Hypertension Presenting before 20 weeks gestation Cardiac enlargement May be present Edema Occurs when pre-eclampsia or heart failure occurs as a complication of hypertension,Chronic Hypertension: Diagnosis (cont.) Investigations Urine analysis: proteinuria indicates occurrence of superimposed pre-eclampsia Renal function: Serum creatinine, uric acid and BUN Fundus examination: Changes indicating chronic hypertension,Antihypertensive Therapy Antihypertensive therapy is recommended when SBP 160-170 and DBP 105-110, as such treatment decreases the maternal cerebral and cardiovascular complications In acute control of sever hypertension, the objective of therapy is a gradual reduction of blood pressure to a level of about 140-150 / 90-100 mmHg Blood pressure should be assessed every 15 minutes initially, once the blood pressure is stabilized the interval can be lengthened to 30 minutes,Lowering the blood pressure rapidly over minutes may be associated with abrupt and profound decrease in blood pressure decrease cardiac output to the uterus with possible fetal hypoxia continuous fetal heart rate monitoring should be performed during initial therapy to detect such effect and allow early remedial action Hydralazine, nifedipine and labetalol are the most commonly used drugs. There is no convincing evidence that one is particularly better than another Labetalol should be avoided in asthma. Atenolol, ACE inhibitor, ARB and diureics should be avoided,Hydralazine (Apresoline) is a vasodilator Loading dose 5-1