Pregnancy Induced Hypertension Jack Lin, M.D. Albert Woo, M.D. Advisor: Marissa Lazor, M.D. Boston University Medical Center Dept. of Anesthesiology

Hypertension Most common medical problem encountered during pregnancy 8% of pregnancies 4 categories: Chronic Hypertension Pregnancy Induced hypertension Preeclampsia-eclampsia Preeclampsia superimposed on chronic HTN *Hypertensive disorder in pregnancy may cause an increase in maternal and fetal morbidity and remains a leading source of maternal mortality*

Hypertension Third leading cause of maternal mortality, after thromboembolism and non-obstetric injuries Maternal DBP > 110 is associated with ↑ risk of placental abruption and fetal growth restriction Superimposed preeclampsia cause most of the morbidity

Pregnancy Induced Hypertension HTN Usually mild and later in pregnancy No renal or other systemic involvement Resolves 12 wks postpartum May become preeclampsia

Preeclampsia New onset HTN After 20 weeks of gestation, or Early post-partum, previously normotensive Resolves within 48 hrs postpartum With the following (Renal or other systemic) Proteinuria > 300 mg/24hr Oliguria or Serum-plasma creatinine ratio > 0.09 mmol/L Headaches with hyperreflexia, eclampsia, clonus or visual disturbances ↑ LFTs, glutathione-S-Transferase alpha 1-1, alanine aminotransferase or right abdominal pain Thrombocytopenia, ↑ LDH, hemolysis, DIC 10% in primigravid 20-25% with history of chronic HTN

Maternal Risk Factors First pregnancy Age younger than 18 or older than 35 Prior h/o preeclampsia Black race Medical risk factors for preeclampsia - chronic HTN, renal disease, diabetes, anti-phospholipid syndrome Twins Family history

Mild vs. Severe Preeclampsia Systolic arterial pressure 140 mm Hg – 160 mm Hg ≥160 mm Hg Diastolic arterial pressure 90 mm Hg – 110 mm Hg ≥110 mm Hg Urinary protein <5 g/24 hr Dipstick +or 2 + ≥5 g/24 hr Dipstick 3+or 4+ Urine output >500 mL/24 hr ≤500 mL/24 hr Headache No Yes Visual disturbances Epigastric pain

Etiology Exact mechanism not known Immunologic Genetic Placental ischemia Endothelial cell dysfunction Vasospasm Hyper-responsive response to vasoactive hormones (e.g. angiotensin II & epinephrine) , with arterial constriction and relatively reduced intravascular volume compared to normal pregnancy leads to pathologic capillary leak – manifest as rapid weight gain, edema of face +/- hands, pulmonary edema, +/or hemoconcentration to fetal/placental tissue – manifest as dysfunction of multiple organ systems

Symptoms of preeclampsia Visual disturbances Headache Epigastric pain Rapidly increasing or nondependent edema - may be a signal of developing preeclampsia Rapid weight gain - result of edema due to capillary leak as well as renal Na and fluid retention Result of generalized vasospasm

Pathophysiology

Pathophysiology Airway edema Cardiac Renal Hepatic Uterine

Upper airway edema Upper airway edema Laryngeal edema Airway obstruction Potential for airway compromise or difficulty in intubation

Cardiac/Pulmonary Increased CO & SVR CVP normal or slightly increased Plasma volume reduced Pulmonary edema Decrease oncotic/collid pressure Capillary/endothelial damage  leak Vasoconstriction  increase PWP and CVP Occurs 3 % of preeclamptic patients

Hepatic Usually mild Severe PIH or preeclampsia complicated by HELLP  periportal hemorrhages ischemic lesion generalized swelling hepatic swelling  epigastric pain

Renal Adversely affected  proteinuria GFR and CrCl  decrease BUN increase, may correlate w/ severity RBF compromised ARF w/ oliguria – PIH, esp. w/ abruption, DIC, HELLP *Oliguria + renal failure may occur in the absence of hypovolemia. Be careful w/ hydration  pulmonary edema*

Uterine Activity increased Hyperactive/hypersensitive to oxytocin Preterm labor – frequent Uterine/placental blood flow – decreased by 50-70% Abruption – incidence increased

Morbidity / Mortality Maternal complications: Leading cause of maternal death in PIH is intracranial hemorrhage Seizures Pulmonary edema ARF Proteinuria Hepatic swelling with or without liver dysfunction DIC (usually associated with placental abruption and is uncommon as a primary manifestation of preeclampsia)

Morbidity / Mortality Fetal complications: Abruptio placentae IUGR Premature delivery Intrauterine fetal death

HELLP Syndrome Hemolysis Elevated Liver enzymes Low Platelets < 36 wks Malaise (90%), epigastric pain (90%), N/V (50%) Self-limiting Multi-system failure

HELLP Syndrome Hemostasis is not problematic unless PLT < 40,000 Rate of fall in PLT count is important Regional anesthesia - contraindicated  fall is sudden PLT count  normal within 72 hrs of delivery Thrombocytopenia may persist for longer periods. Definitive cure is delivery

Treatment Management of maternal hemodynamics & prevention of eclampsia are key to a favorable outcome MgSO4 - Rx of choice for preeclampsia. Does not significantly reduce systemic BP at the serum concentration that are efficacious in treating preeclampsia Goals Control BP Prevent seizures Deliver the fetus

Controlling the HTN Hydralazine Labetalol Nitroglycerin Nifedipine Esmolol Na Nitroprusside – risk of cyanide toxicity in the fetus

Preventing Seizures MgSO4 - Drug of choice. Narrow therapeutic index Reduce > 50% w/o any serious maternal morbidity 4g IV Bolus over 10 minutes, then infusion @ 1g/hr Renal failure - rate of infusion  by serum Mg levels Plasma Level should be between 4-6 mmol/L Monitor clinical signs for toxicity Toxic: 10 ml of 10% Ca Gluconate IV slowly

MgSO4 Toxicity 5-10 mEq/L – Prolonged PR, widened QRS 11-14 mEq/L – Depressed tendon reflexes 15-24 mEq/L – SA, AV node block, respiratory paralysis >25 mEq/L - Cardiac arrest

Anesthetic Considerations Detailed preanesthetic assessment Focuses on airway, fluid status, and BP control Lab: CBC, BUN/Cr, LFTs Routine coagulation is NOT recommended unless there is clinical suspicion PLT count - if neuraxial techniques are considered

Regional Anesthesia Labor epidural - advantage of a gradual onset of sympathetic blockade  provides cardiovascular stability & avoids neonatal depression. Epidurals may reduce vasospasm and HTN – may improve uteroplacental blood flow Reduce risk of airway complications and avoid hemodynamic alterations associated with intubation

Regional (part 2) Neuraxial anesthesia in preeclamptic pt - still controversial Many studies  this is the best option National High blood Pressure Education Program Working Group “Neuraxial, epidural, spinal and combined spinal-epidural (CSE), techniques offer many advantages for labor analgesia and can be safely administered to the parturient with preeclampsia. Dilute epidural infusions of local anesthetic plus opioid produce adequate sensory block without motor block or clinically significant sympathectomy. “

Regional (part 3) Possibility of extensive sympatholysis with profound hypotension  decrease CO & uteroplacental perfusion Single shot spinal technique  controversial Recent analysis suggest that it can be used safety in pt with severe preeclampsia undergoing C-section. BP decline similar to epidural. Hypotension can be avoided by meticulous attention to anesthetic technique and careful volume expansion

General Anesthetic Techniques Laryngeal response  blunted by pre-treatment with hydralazine, nitroglycerin or labetalol Airway edema  increased risk of difficult airway situation Neuraxial techniques  preferred method, contraindicated in the presence of coaguloapthy In pt receiving MgSO4, SUX activity  potentiated Enhanced sensitivity to non-depolarizing muscle relaxants MgSO4 blunts response to vasconstrictors and inhibits catecholamine release after sympathetic stimulation

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