12. Hypertension in Pregnancy-Semester 5-kck.ppt
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HYPERTENSIVE DISORDERS IN PREGNANCY Dr Kailash Kharkwal HYPERTENSIVE DISORDERS • Most common medical complication in pregnancy • 5-10% incidence • Major cause of maternal and perinatal morbidity worldwide Report of the National High Blood Pressure Education Program. Working group report on high bl...
HYPERTENSIVE DISORDERS IN PREGNANCY Dr Kailash Kharkwal HYPERTENSIVE DISORDERS • Most common medical complication in pregnancy • 5-10% incidence • Major cause of maternal and perinatal morbidity worldwide Report of the National High Blood Pressure Education Program. Working group report on high blood pressure. Am J Obstet Gynecol. 2000;183:S1.; Sibai BM. Diagnosis and management of gestational hypertension and .preeclampsia. Obstet Gynecol. 2003; 102:181 HYPERTENSION • BP > 140 mm Hg systolic and /or > 90 mm Hg diastolic (Korotkoff 5 [K5]) • Present on at least 2 occasions, at least 6 hours apart, but within a maximum of 1-week period National High Blood Pressure Education Program Classification ( NHEP) 2000 • Chronic hypertension • Gestational hypertension • Preeclampsia and Eclampsia syndrome • Preeclampsia syndrome superimposed upon chronic hypertension Definitions • CHRONIC / PREEXISTING HYPERTENSION • SBP ≥140 mmHg and/or DBP ≥90 mmHg that antedates pregnancy or is present before the 20th week of pregnancy or persists longer than 12 weeks postpartum • Complicates 3% of pregnancies Definitions • Gestational hypertension: – Hypertension (SBP ≥140 mmHg and/or DBP ≥90 mmHg) for first time after 20 wk, without proteinuria – BP returns to normal before 12 weeks postpartum – Seen in 6% of pregnancies Definitions PREECLAMPSIA •Is a multi - system disorder characterized by new onset of hypertension and proteinuria after 20 weeks of gestation in a previously normotensive woman •BP returns to normal before 12 weeks postpartum •Increased risk for maternal and/or fetal mortality or serious morbidity •Complicates 5-6 % of pregnancies lopment Mater Semin Perinat • ; Hutcheon JA, Lisonkova S, Joseph KS. Epidemiology of pre-eclampsia and the other hypertensive .disorders of pregnancy. Best Pract Res Clin Obstet Gynaecol 2011; 25:391 Definitions PREECLAMPSIA SUPERIMPOSED UPON CHRONIC / PREEXISTING HYPERTENSION •new-onset proteinuria (≥0.3 g in a 24-hour collection) after the 20th week of gestation • In pregnant women with preexisting hypertension and proteinuria: (1) if they experience sudden significant increases in blood pressure or proteinuria, or (2) the new onset of any of the other signs and symptoms of severe preeclampsia including thrombocytopenia or abnormally elevated liver enzymes •Complicates 25% of pregnancies with chronic hypertension Preeclampsia Epidemiology of preeclampsia Incidence: • Is the most common medical disorder complicating pregnancy (5-15%) • Is the most common hypertensive disorder in pregnancy • More common in primigravida and elderly multipara • More common in winter • More in black races Preeclampsia: RISK FACTORS • Associated with the pregnant woman • • • • • • • • • • Primiparity Age >40 years or <18 years Preeclampsia in a previous pregnancy Family history of preeclampsia (mother or sister) Chronic hypertension Preexisting diabetes (type 1 or type 2) especially with microvascular disease Chronic renal disease; APAS or inherited thrombophilia; Vascular or connective tissue disease; High body mass index women who themselves are the product of a pregnancy complicated by preeclampsia Interpregnancy interval < 2 Yrs or >10 Yrs Preeclampsia: RISK FACTORS • Associated with the pregnant woman’s husband or partner • • First time father (primipaternity) Partner related factors (new partner, limited sperm exposure, after donor insemination; oocyte donation; embryo donation) • Associated with the fetus • • Multifetal gestation • Hydatidiform mole • Hydrops fetalis / Triploidy Unexplained fetal growth restriction Preeclampsia A 2 – stage disease? 1. Asymptomatic Placental Stage 2. Symptomatic Maternal Stage • Stage 1 Poor placentation (early) • Stage 2 Placental oxidative stress (late) Systemic release of placental factors Systemic inflammatory response and endothelial activation Abnormal trophoblastic invasion Genetic Modulators Pre-existing Vascular Pathology Cytokines Ros Central players PREECLAMPSIA Vasospasm due to imbalance b/w vasodilators(PGI2, NO) & vasoconstrictors (TxA2, angiotensin-II, endothelin-1) + Vascular endothelial Dysfunction due to oxidative stress and inflammatory mediators Pathology Preeclampsia is the clinical tip of the iceberg manifestation of the disturbances in the maternal homeostasis, involving many systems and organs Multisystem Features Of Preeclampsia Proteinuria Hypertension Systemic blood vessels Kidneys Multi-organ disease Cerebral vessels Liver Eclampsia HELLP syndrome Fetus Intra-uterine growth restriction Clinical Features and Pathophysiology • Cardiopulmonary: • Hypertension • Intravascular volume “smaller” (vasoconstriction and a intravascular compartment) • Pulmonary edema – pulmonary capillary wedge pressure -low normal range – impaired diastolic function with a markedly increased afterload, caused by increased vasoconstriction and peripheral vascular resistance Clinical Features and Pathophysiology • Renal: • Proteinuria – ≥0.3 grams protein in a 24-hour urine specimen or persistent 1+ on dipstick (30 mg/dL) – Urine protein/creatinine ratio of ≥30 mg/mmol (≥ 0.3 mg/mg) – Urine albumin/creatinine ratio of ≥8 mg/mmol • Renal Function – GFR (30-40%), renal plasma flow-N – serum creatinine levels are near upper normal (1.0 -1.5mg/dl) – serum uric acid greater than 5.5 mg per dL ( enhanced tubular urate reabsorption) – Urinary calcium excretion decreases (Hypocalciuria) – Acute kidney injury as a result of acute tubular or, cortical necrosis – Glomerular Endotheliosis Clinical Features and Pathophysiology • Hematologic: • Thrombocytopenia – – • PT, aPTT, Fibrinogen – • accelerated plt consumption <100,000/uL Preeclampsia not affected Microangiopathic hemolysis – – + schistocytes / helmet cells (PBS) Increased LDH; hemoconcentration (Hct) Clinical Features and Pathophysiology • Hepatic: • Periportal and sinusoidal fibrin deposition and microvesicular fat deposition • Reduced hepatic blood flow can lead to ischemia and periportal hemorrhage • RUQ pain, increased transaminase levels, coagulopathy, subcapsular hemorrhage or hepatic rupture • Epigastric pain sec to stretching of Glisson’s capsule due to hepatic swelling or bleeding HELLP Syndrome Hemolysis •Abnormal peripheral blood smear (burr cells, schistocytes) •Elevated bilirubin ≥ 1.2 mg/dL •Increased LDH of > twice the upper limit of normal for the laboratory Elevated Liver enzymes •Elevated ALT or AST ≥ twice the upper limit of normal for the laboratory •Increased LDH > twice the upper limit of normal for the laboratory Low Platelet count (<100,000/mm 3 ) Clinical Features and Pathophysiology • CNS and eye: • headache • visual symptoms – constriction of retinal arteries » Photopsia (flashing lights); » scotomata (dark areas/gaps); » diplopia or amaurosis fugax (unilat blindness) • generalized hyper-reflexia • sustained ankle clonus • CT & MRI suggestive of vasogenic edema Clinical Features and Pathophysiology • Fetus and placenta: • Decreased uteroplacental perfusion and ischemia intrauterine growth restriction (IUGR), oligohydramnios, fetal heart rate abnormalities* • Extensive placental infarctions can result in retroplacental hemorrhage, or abruption *Doppler study of the umbilical artery showing “Absent and reversed end diastolic flow” Diagnosis Of Preeclampsia A): Signs : : It is a disease of signs : 2 cardinal signs + or Edema: • Hypertension: – usually precedes proteinuria • Proteinuria: Peripheral edema is not a useful diagnostic criterion Pathologic edema appears suddenly and is associated with an accelerated rate of weight gain Sudden swelling linked with a gain greater than 1 kg/wk over 2 to 3 weeks or greater than 2 kg/wk should warn the clinician A woman with preeclampsia will often have facial and particularly periorbital edema in contrast to the physiologic pedal edema B): Symptoms These are usually manifestations of severe preeclampsia 1. Headache: usually frontal but may be occipital. It is due to cerebral oedema and hypertension 2. Visual disturbances: blurring of vision, flashes of light or blindness 3. Epigastric or right upper quadrant pain: due to enlargement and subcapsular haemorrhage of the liver 4. Nausea and vomiting: due to congestion of gastric mucosa and/ or cerebral oedema 5. Oliguria or anuria: due to kidney pathology Types of Preeclampsia: 1. 2. MILD SEVERE Abnormality Mild Severe <160/110 mg Hg 160/110 mm Hg or higher Trace to 1+ 300mg/24 hr urine Persistent 3+ or more 5 gm/24 hr urine Headache Absent Present Visual disturbances Absent Present Upper abdominal pain Absent Present Oliguria Absent Present <500ml/24 hr Knee/Ankle Reflex Normal Increased Serum creatinine Normal Elevated ≥ 0.09 mmol/L(1.1 mg/dL) Thrombocytopenia Absent Present <100,000/mm3 Liver enzyme elevation Minimal Marked Twice of normal value Fetal growth restriction Absent Obvious Blood pressure Proteinuria Pulmonary edema Investigations • A. Laboratory: • CBC, platelet count, LDH: if abnormal, order d -dimers, coagulation panel, and smear • Renal studies: serum BUN creatinine and uric acid, urinalysis, 24-hr urine for protein and creatinine, or protein/creatinine ratio • Liver function tests: AST, ALT, and bilirubin Management OF Objectives of Management PREECLAMPSIA Objectives are: •To stabilize hypertension and to prevent its progression to severe preeclampsia. •To prevent the complications (eclampsia) •Delivery of a healthy baby in optimal time. •Restoration of the health of the mother in the puerperium. Objectives of Management • • • • Expectant Treatment . Control of Hypertension. Prevention of convulsions . Termination of pregnancy . 1) Expectant Treatment • There is no place of domiciliary treatment in an established case of preeclampsia • Close maternal monitoring upon diagnosis of preeclampsia is important to establish disease severity and the rate of progression • Hospitalization is useful for making these assessments and facilitates rapid intervention in the event of rapid progression 2) Control of Hypertension: A)Parentral drugs: – 1) Labetalol : • first-line therapy (rapid onset of action, good safety profile) • α and non selective β- adrenergic blocker • 20 mg IV over 2 minutes followed at 10minute intervals by doses of 20 to 80 mg – (maximum total cumulative dose of 300 mg) 2) Control of Hypertension: – 2) Hydralazine: • Direct vasodilator; dilates arterioles, decreases systemic resistance • 5 mg IV over 1 to 2 minutes • if BP goal is not achieved within 20 minutes, give a 5 to 10 mg bolus depending upon the initial response (The maximum bolus dose is 20 mg) • 2)Control of Hypertension: A )Oral drugs: 1) Alpha-2 adrenergic agonist: • Methyldopa (Aldomet) • It is the most commonly used drug • It is α-adrenergic agonist causing depletion of catecholamine stores • Dose: 250-500mg 4 times/day orally 2) Calcium Channel Blocker: • Nifedipine (adalat or Epilat) • Dose: 10-30mg 3-4 times/day orally – 3) β- adrenergic blockers: – Labetalol (Trandate) 100-400mg 2 times daily – Atenolol (tenormin) 50-100mg once daily Target BP • 135 mm Hg systolic and • 85 mm Hg diastolic • Cerebral or myocardial ischemia or infarction can be induced by aggressive antihypertensive therapy if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation 3) Prevention of Convulsions • A) Magnesium Sulfate (MgSO4): • It is the drug of choice. • Mechanism: – CNS depression – Mild Vasodilator – Mild diuresis – Inhibits platelet aggregation – Increase PGI2 synthesis Magnesium Sulfate (MgSO4): • It can be given IV (20%) or IM (50%) : – The therapeutic level is 4-7mEq/L – The total dose of MgSO4 should not exceed 24 gms in 24 hours • IV regimen: – initially 4-6 gm (20%) in 100ml solution. » Given over 15-20 minutes. – Then, 1-2 gm/hour by IV drip . – The dose of MgSO4 is monitored by: Preserved patellar reflex. Respiratory rate >16/min. Urine output >100ml/4hours. Serum Mg++ level. – Is stopped 24 hours after delivery. » » » » Side effects of MgSO4 (small safety margin) – At a level of 8-10mEq/L patellar reflex is lost and starts myometrial inhibition. – 10-15mEq/L respiratory depression. – >15mEq/L cardiac depression. – Uterine inertia. – Neonatal hypermagnesemia. – Decreased beat to beat variability in FHS. Antidote : 10ml of 10 percent calcium gluconate Management OF Chronic Hypertension • Stop ACE inhibitors or ARBs & Thiazide Diuretics • Consider Labetalol or Nifedipine or methyldopa • Offer Aspirin 75-150 mg once daily from 12 weeks • Carry out ultrasound for fetal growth and amniotic fluid volume assessment • Umbilical artery doppler velocimetry at 28 weeks, 32 weeks and 36 weeks. • Carry out cardiotocography only if clinically indicated. Aim for target BP of 135/85 mmHg. Management OF Chronic Hypertension • If blood pressure is lower than 160/110 mmHg: Do not offer planned early birth before 37 weeks, unless there are other medical indications After 37 weeks, timing of birth should be agreed between the woman and the senior obstetrician • If planned early birth is necessary, offer a course of antenatal corticosteroids and magnesium sulfate if indicated Management OF Gestational Hypertension • Women with risk factors require additional assessment and follow-up • Consider Labetalol or Nifedipine or methyldopa • Do not offer bed rest in hospital • Carry out an ultrasound for fetal growth and amniotic fluid volume assessment • UA doppler velocimetry at diagnosis and if normal, repeat every 2 to 4 weeks • Carry out cardiotocography only if clinically indicated Management OF Gestational Hypertension • If blood pressure is lower than 160/110 mmHg: Do not offer planned early birth before 37 weeks, unless there are other medical indications After 37 weeks, timing of birth should be agreed between the woman and the senior obstetrician • If planned early birth is necessary, offer a course of antenatal corticosteroids and magnesium sulfate if indicated Management OF Preeclampsia • Carry out a full clinical assessment at each antenatal appointment for women with pre-eclampsia, and • offer admission to hospital for surveillance or intervention if there are concerns for the wellbeing of mother or baby Mild or Severe Preeclampsia Management OF Preeclampsia • Plan early birth before 37 weeks in women with preeclampsia, if: -inability to control maternal blood pressure -maternal pulse oximetry less than 90% -progressive deterioration in liver function, renal function, haemolysis, or platelet count -ongoing neurological features, such as severe intractable headache, repeated visual scotomata, or eclampsia -placental abruption -reversed end-diastolic flow in the umbilical artery doppler velocimetry, a non-reassuring CTG Severe Preeclampsia: • Deliver regardless of gestational age Weeks of pregnancy Timing of birth Before 34 weeks Continue surveillance unless there are indications for planned early birth. Offer intravenous magnesium sulfate & a course of antenatal corticosteroids From 34 to 36 +6 weeks Continue surveillance unless there are indications for planned early birth. When considering the option of planned early birth, take into account the woman's and baby’s condition & risk factors. Consider a course of antenatal corticosteroids 37 weeks onwards Initiate birth within 24–48 hours. Method of delivery • Vaginal delivery • Caesarean section Method of delivery • Vaginal delivery may be commenced in vertex presentation by: > amniotomy + oxytocin if the cervix is favourable. > prostaglandin vaginal tablet (PGE2) if the cervix is not favourable. Method of delivery • Caesarean section is indicated in > Fetal distress > Late deceleration in CTG > Failure of induction of labour > Other obstetrical indications Intrapartum care a. Close monitoring of the fetus is indicated. b. Proper sedation and analgesia to the mother. Hypotensive drugs may be given if needed. c. 2nd stage of labour may be shortened by vacuum extraction or forceps. Postpartum care a. Ergometrine is better avoided as it may increase the blood pressure b. Continue observation of the mother for 48 hours for blood pressure c. Sedatives and hypotensive drugs are continued in a decreasing dose for 48 hours d. Mg Sulfate is continued for 24 hours, if started ECLAMPSIA • development of grand mal seizures in a woman with preeclampsia, in the absence of other neurologic conditions that could account for the seizure • occurs in 2 to 3 percent of severely preeclamptic women not receiving anti-seizure prophylaxis Pathogenesis of Seizures 1. Cerebral overregulation in response to high systemic BP • • • • vasospasm of cerebral arteries underperfusion of the brain Localized ischemia/infarction cytotoxic (intracellular) edema 2. Loss of autoregulation of cerebral blood flow • Hyperperfusion • endothelial damage • vasogenic (extracellular) edema Diagnosis Of Eclampsia: • Eclamptic fit stages ( 4 stages): – Premonitory stage – Tonic stage – Clonic stage – Coma Classifications of Eclampsia – Ante partum (65%) with the best prognosis. – Intrapartum (20%) – Postpartum (15%) with the worst prognosis as it indicates extensive pathology and multisystem damage. Treatment of Eclampsia 1) General and first aid measures: Isolation in a single, quiet, semi dark room (eclampsia room) – Ensure patent airway with tracheal and bronchial suction. – Put the patients in Trendlenburg position (to avoid aspiration of secretions) . – Insert a bladder catheter. – Nasogastric tube may be inserted . – Nothing by mouth and fluid chart. – Full laboratory investigations. Treatment of Eclampsia • 2) Observation: – Pulse, temperature, BP and RR – Level of consciousness – Duration of coma – Fetal heart sounds – Urine output and proteinuria – Number of convulsions Treatment of Eclampsia: 3) Control of Convulsions: A ) Magnesium Sulfate (MgSO4): Main stay of Management B ) Phenytoin : The dose is 15mg/kg slow IV C) Diazepam (Valium): Initially 10-20mg IV slowly over 5-10 minutes followed by 40mg in 5% dextrose slow IV infusion Treatment of Eclampsia • 4) Control of hypertension • 5) Other drugs: – Antibiotic for infection. – IV glucose 25% as a liver support, increases the urine output and improves hemo-concentration. Treatment of Eclampsia • 6) Termination of Pregnancy As a rule, vaginal delivery is safer and better than C.S. » Artificial rupture of membranes (ARM) and oxytocin drip – Caesarean Section Treatment of Eclampsia 7) Intrapartum management: • • • • • Maternal observation Oxygenation Continuous electronic fetal monitoring Epidural anesthesia Shorten the 2nd stage by vacuum or forceps 8) Postpartum management: • No ergometrine postpartum • Continue MgSO4 for 24 hours postpartum Prognosis: • Maternal mortality severe preeclampsia - 2% eclampsia - 10% • Perinatal mortality mild cases - 5% severe cases - 25% eclampsia - 30% …Thank you
