Hypertension in Pregnancy Dr. MSc. Raul Hernandez Canete

Hypertension Sustained BP elevation of 140/90 or greater Proper cuff size Measurement taken while seated Use 5th Korotkoff sound 30/15 increase in BP over baseline levels

Classification of Hypertension in Pregnancy Chronic Hypertension Pregnancy-Induced Hypertension Preeclampsia, Eclampsia Chronic Hypertension with superimposed preeclampsia. HELLP syndrome

Pregnancy-Induced Hypertension Suggests a disorder of blood pressure arising because of the presence of pregnancy The condition is classified into four main groups depending on the cardiovascular, renal, cerebral and hepatic manifestations: - Gestational Hypertension - Pre-eclampsia - Eclampsia - HELLP syndrome

Etiology and Pathophysiology Exact etiology and pathophysiology: unclear The incidence of hypertensive disorder in pregnancy is 8-10%. They are recognized predisposing factors.

Recognized predisposing factors: First pregnancy Family history Extremes of maternal age Medical: - pre-existing hypertension - congenital thrombophilia - systemic lupus erythematosus - diabetes mellitus Obstetrics: - multiple pregnancy - hydatidiform mole - hydrops fetalis

“Disease of theories” It is likely that inadequate placental perfusion resulting from inadequate placental invasion precipitates the release of some form of chemical trigger which, in susceptible mothers, leads to endothelial damage, metabolic changes and a form of inflammatory response

Placental invasion: In pre-eclampsia adequate trophoblastic invasion does not seem to occur (or limited to the decidual portion of the vessels)>>> failure to convert the spiral arteries to low resistance and high flow system>>>uteroplacental hypoperfusion results in the release of a potent circulating factor>>widespread activation of endothelial cells: - Decreased production of prostacyclin (vasodilator) - platelet activation - increased production of thromboxane A2 (vasoconstrictor) - increased the sensitivity to vasoconstrictors such as angiotensin II

Potential secondary effects of the metabolic, inflammatory endothelial alterations in pre-eclampsia: CVS: Increased peripheral resistance leading to hypertension. Increased vascular permeability and reduced maternal plasma volume Lungs: Laryngeal and pulmonary oedema Renal: Glomerular damage leading to proteinuria, hypoproteinaemia and reduce oncotic pressure which further exacerbates the hypovolaemia. May develop acute renal failure +/- cortical necrosis

Cont….. Clotting: Hypercoagulability, with increased fibrin formation and increased fibrinolysis, i.e. disseminated intravascular coagulation Liver: HELLP syndrome, Hepatic rupture CNS: Thrombosis and fibrinoid necrosis of the cerebral arterioles. Eclampsia, cerebral hemorrhage and cerebral oedema. Fetus: Impaired uteroplacental circulation, potentially leading to FGR, hypoxemia and IUFD, Placentae abruption.

Chronic Hypertension Pre-existing hypertension Hypertension before 20 weeks of gestation If hypertension persists beyond 6 weeks postpartum

Preeclampsia Hypertension after 20 weeks of gestation Proteinuria- 300mg Edema

Preeclampsia Hypertension after 20 weeks of gestation Proteinuria- 300mg Edema BP > 160 systolic or >110 diastolic 2grams of protein in 24 hour urine Oliguria Cerebral of visual disturbances Pulmonary edema or cyanosis Epigastric or RUQ pain Impaired liver function Thrombocytopenia IUGR

Risk Factors FACTOR RISK RATIO Nulliparity 3:1 Age > 40 African American 1.5:1 Chronic hypertension 10:1 Renal disease 20:1 Antiphospholipid syndrome

Risk Factors FACTOR RISK RATIO Family history of PIH 5:1 Diabetes mellitus 2:1 Twin gestation 4:1

Severe Preeclampsia BP > 160-180 systolic or 110 diastolic Proteinuria > 2 g per day Pulmonary edema Oliguria Elevated liver enzymes Low platelets Growth restriction Decreased AFV Headache Epigastric pain

Pregnancy-Induced Hypertension After 20 weeks of gestation No proteinuria Not associated with significant maternal morbidity and perinatal mortality

Management The ultimate cure is delivery Assess gestational age Assess cervix Fetal well-being Laboratory assessment Rule out severe disease!!

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 Antenatal fetal surveillance Outpatient versus inpatient

Indications for Delivery Worsening BP Nonreassuring 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

Hypertensive Emergencies Fetal monitoring IV access IV hydration The reason to treat is maternal, not fetal May require ICU

Criteria for Treatment Diastolic BP > 105-110 Systolic BP > 200 Avoid rapid reduction in BP Do not attempt to normalize BP Goal is DBP < 105 not < 90 May precipitate fetal distress

Key Steps Using Vasodilators Avoid multiple doses in rapid succession Allow time for drug to work Maintain LLD position Avoid over treatment

Acute Medical Therapy Hydralazine Labetalol Nifedipine Nitroprusside Diazoxide Clonidine

Hydralazine Dose: 5-10 mg every 20 minutes Onset: 10-20 minutes Duration: 3-8 hours Side effects: headache, flushing, tachycardia, lupus like symptoms Mechanism: peripheral vasodilator

Labetalol Dose: 20mg, then 40, then 80 every 20 minutes, for a total of 220mg Onset: 1-2 minutes Duration: 6-16 hours Side effects: hypotension Mechanism: Alpha and Beta block

Nifedipine Dose: 10 mg po, not sublingual Onset: 5-10 minutes Duration: 4-8 hours Side effects: chest pain, headache, tachycardia Mechanism: CA channel block

Seizure Prophylaxis Magnesium sulfate 4-6 g bolus 1-2 g/hour Monitor urine output, respiratory rate and reflex With renal dysfunction, may require a lower dose

Magnesium Sulfate Is not a hypotensive agent Works as a centrally acting anticonvulsant Also blocks neuromuscular conduction Serum levels: 6-8 mg/dL

Toxicity Respiratory rate < 12 Hyporeflex Altered sensorium Urine output < 25-30 cc/hour Antidote: 10 ml of 10% solution of calcium gluconate 1 v over 3 minutes

Treatment of Eclampsia Few people die of seizures Protect patient Avoid insertion of airways and padded tongue blades IV access MGSO4 4-6 bolus, if not effective, give another 2 g

Alternate Anticonvulsants Diazepam 5-10 mg IV Sodium Amytal 100 mg IV Pentobarbital 125 mg IV Dilantin 500-1000 mg IV infusion

After the Seizure Assess maternal labs Fetal well-being Effect delivery Transport when indicated No need for immediate cesarean delivery

Other Complications Pulmonary edema Oliguria Persistent hypertension DIC

Pulmonary Edema Fluid overload Reduced colloid osmotic pressure Occurs more commonly following delivery as colloid oncotic pressure drops further and fluid is mobilized

Treatment of Pulmonary Edema Avoid over-hydration Restrict fluids Lasix 10-20 mg IV Usually no need for albumin or Hetastarch (Hespan)

HELLP Syndrome He-hemolysis EL-elevated liver enzymes LP-low platelets

HELLP Syndrome Is a variant of severe preeclampsia Platelets < 100,000 LFT’s - 2 x normal May occur against a background of what appears to be mild disease

Conservative Management Controversial Steroids Requires tertiary care Must have stable labs and reassuring fetal status May use antihypertensives

SUMMARY Criteria for diagnosis Laboratory and fetal assessment Magnesium sulfate seizure prophylaxis Timing and place of delivery