Hypertensive Disorders in Pregnancy Dr SAJDA ALRUBAIE CONSULTANT

Hypertensive Disorders in Pregnancy Dr. SAJDA ALRUBAIE CONSULTANT OBSTETRICIAN & GYNECOLOGIST PROF. BASRAH MEDICAL COLLEGE

Hypertensive Disease Associated with Pregnancy Chronic Hypertension Gestational Hypertension Preeclampsia Eclampsia HEELP Syndrome

Chronic Hypertension Blood Pressure ≥ 140/90 before 20 weeks of gestation Or Persistence of hypertension beyond 12 weeks after delivery.

Gestational Hypertension Blood Pressure ≥ 140/90 on two or more occasions - in a previously normotensive patient - after 20 weeks gestation - without proteinuria - returning to normal 12 weeks after delivery Almost half of these develop preeclampsia syndrome

Preeclampsia superimposed on Chronic Hypertension New-onset proteinuria ≥ 300 mg/24 hours in hypertensive women but no proteinuria before 20 weeks’ gestation A sudden increase in proteinuria or blood pressure or platelet count <100000 /cmm in women with hypertension and proteinuria before 20 weeks’ gestation More adverse outcome than preeclampsia alone

Preeclampsia New onset of hypertension & proteinuria in a previously normotensive woman after 20 weeks of gestation Returning to normal after 12 weeks of pregnancy. Edema not a part of diagnosis now. Eclampsia : New onset of seizures or unexplained coma during pregnancy or postpartum period in patients with preexisting preeclampsia and without pre-existing neurological disorder.

Risk Factors of Preeclampsia • Preconception - Partner related § Nulliparity § limited exposure to paternal sperms -Non partner related § History of Preeclampsia in previous pregnancy § Advanced maternal age § Family history of Preeclampsia § History of placental abruptio, IUGR, fetal death § Non hispanic black race

Risk factors contd. . -Maternal disease related § § Obesity, BMI>35 doubles the risk Hypertension Diabetes Thrombotic vascular diseases -Behaviour§ Smoking : - preventive -Pregnancy associated§ Multiple gestation § Molar pregnancy

PATHOGENESIS Exact mechanism unknown, disease of theories. 1. ABNORMAL PLACENTATION 2. Inflammatory mediators ↓PGI 2 ↑TXA 2 Vasoconstriction Platelet aggregation ↑Vasopressor response ↑uterine activity

Abnormal trophoblastic invasion

3. GENETIC - Family history of pre eclampsia: genetic origin Mutations in Complement Regulatory Protein gene - Genes assoc 4. IMMUNOLOGIC Exposure to sperms of different partner long term exposure to paternal antigen in sperms of same partner- protective activated auto antibodies to angiotensin receptor-1 AAAT 1 activate AT 1 receptors increased sensitivity to angiotensins hypertension

Fetal & maternal risks Fetal IUGR Oligohydramnios Placental infarcts Placental abruption Prematurity Uteroplacental insufficiency Perinatal death Maternal CNS seizures & stroke DIC ↑↑ CS Renal failure Hepatic failure or rupture Death DR SALWA NEYAZI ASS. PROF. KSU CONSULTANT OBGYN

Haematology Hemoconcentration (pts with anemia may appear to have normal hematocrit) Thombocytopaenia most common Platelet count correlates with disease severity and incidence of abruptio placentae DIC due to activation of coagulation cascade overconsumption of coagulants and platelets spontaneous haemorrhage.

Hepatic �HELLP syndrome �Periportal haemorrhage � subcapsular bleeding � hepatic rupture: 32% maternal mortality

Renal Decreased GFR -oliguria -renal failure - uric acid, creatinine is elevated Glomerulopathy - proteinuria

Uteroplacental circulation Uteroplacental insufficiency Fetal complications: - hypoxia -IUGR -Prematurity -IUD -Placental abruption

SYMPTOMS & SIGNS Edema of the face & hands. Headache Visual disturbance Epigastric pain ↑ BP Exaggerated reflexes Proteinuria

Prevention Regular Antenatal checkup: rapid gain in weight rising blood pressure edema proteinuria/deranged liver or renal profile Low dose Aspirin in High risk group: ↑PGs and↓TXA 2 Calcium supplementation: no effects unless women are calcium deficient Antioxidants- Vitamin C and E Nutritional supplementation: zinc, magnesium, fish oil, low salt diet

Management

Gestational HTN at Term Delivery is always a reasonable option if term If cervix is unfavorable and maternal disease is mild, expectant management with close observation is possible

Mild Gestational HTN not at Term Rule out severe disease Conservative management Serial labs Twice weekly visits Antenatal fetal surveillance Outpatient versus inpatient

Indications for Delivery Worsening BP Non reassuring fetal condition Development of severe PIH Fetal lung maturity Favorable cervix

Unfavorable Cervix No contraindication to prostaglandin agents If < 32 weeks, consider cesarean When favorable, oxytocin

preclampsia

Obstetrics management 1. Maternal evaluation : Hemoglobin and hematocrit platelet count : decreased, if < 100000 coagulation profile LFTs : indicated in all patients KFTs : raised (S. urea creatinine is decresaed in Normal pregnancy) Urine Routine : proteinuria

Manegement OBJECTIVES Terminaton of pregnancy with the least possible trauma to the mother & fetus Birth of an infant who subsequently thrives Complete restoration of health to the mother 1 - Hospitalization Women with new onset BP ≥ 140/90 Worsening BP Development of proteinuria in addition to existing BP

Lines of management Anticonvulsant therapy Antihypertensive therapy Termination of pregnancy

Anticonvulsant therapy Seizure Prophylaxis Ø Routinely used in severe PE Ø Magnesium sulphate: most commonly used Ø Initiated with onset of labor till 24 h postpsrtum Ø For caesarean, started 2 hrs before the section till 12 hrs postpartum

Side effects of Mg. SO 4 Maternal : flushing, headache, muscle weakness, pulmonary edema decrease patellar reflexes , respiratory depression , cardiac arrest Neonatal: lethargy, hypotonia, respiratory depression

Magnesium levels Monitoring Normal Serum levels- 1. 7 - 2. 4 mg/dl Therapeutic range- 5 - 9 mg/dl Patellar reflex lost- >12 mg/dl Respiratory depression- 15 -20 mg/dl Cardiac arrest- >25 mg/dl

Management of Mg. SO 4 Toxicity Stop infusion Intravenous Calcium 10 ml 10% over 10 minutes Endotracheal intubation in respiratory depression

Antihypertensive therapy Mild PET There is no benefit of antihypertensive therapy Reduction in the maternal BP with labetalol or nifedipine IUGR ACI contraindicated IUGR, boney malformations, limb contracture, PDA, pulmonary hypoplasia, RDS, hypotension &death Severe PET Antihypertensive therapy is used to control BP untill the Pt delivers or in preterm for 48 hrs to allow time for glucocorticoid administration for fetal lung maturity then delivery

Acute Medical Therapy Hydralazine: 5 -10 mg every 20 minutes Labetalol: 20 mg, then 40, then 80 every 20 minutes, for a total of 220 mg Nifedipine: 10 mg po, not sublingual Nitroprusside Diazoxide Clonidine 1 mg po

HELLP syndrome Diagnosis: 1. Hemolysis: Peripheral smear ↑bilirubin >1. 2 mg/d. L, Elevated liver enzymes: SGOT> 70 IU/L 3. Low platelets 2.

Management of HELLP syndrome Immediate hospitalisation Stabilise mother antihypertensives anti seizure prophylaxis correct coagulation abnormalities Assess fetal condition- FHR, doppler ultrasound, biophysical profile

HELLP contd. . Ultimate goal: >34 wks gestation deliver <34 wks expectant management if stable maternal and fetal conditions Platelet transfusion if: <40, 000/mm 3 before cesarean <20, 000/mm 3 before delivery

Termination of pregnancy Indications Term pregnancy with mild or severe PET Severe PET regardless of the gestational age Warning signs headache , visual disturbance, epigastric pain, oliguria Eclampsia Pt must be stabilized & delivered immediately Preterm with mild PET Assess fetal wellbeing by NST, Doppler Methods of termination IOL with prostaglandines to ripen the Cx followed by IV oxytocin Elective CS Severe PET with unfavorable Cx

Epidemiology 0. 1 - 5. 5 per 10, 000 pregnancies Decreasing incidence with time Antepartum(50%): mostly in third trimester Intrapartum(30%): Postpartum(20%): usually within 48 hours, fits beyond 7 days generally rules out eclampsia

Risk factors Maternal age less than 20 years Multigravida Molar pregnancy Triploidy Pre-existing hypertension or renal disease Previous severe Preeclampsia or Eclampsia Nonimmune hydrops fetalis Systemic Lupus Erythematosus

Clinical features Eclamptic convulsions are epileptiform and consist of four stages Ø Premonitory stage: twitching of muscles of face, tongue, limbs and eye. Eyeballs rolled or turned to one side, 30 s Ø Tonic stage: opisthotonus, limbs flexed, hands clenched, 30 s Ø Clonic stage: 1 -4 min, frothing, tongue bite, stertorous breathing Ø Stage of coma: variable period.

Management 1. call for help 2. put the patient in a left lateral position remove the clothes and protect the tongue 3. artificial airway 4. blood should be taken for basal investigations 5. folley’s catheter 6. Mg. SO 4 7. diazepam 10 mg slowly and diluted which can repeated after 10 minutes 8. antihypertensive therapy 9. obstetrical examination to decide the mode of delivery then deliver the patient