Pregnancy induced hypertension (PIH) is a hypertensive disorder of pregnancy characterized by new onset hypertension without significant proteinuria or other systemic involvement. It usually presents later in pregnancy and resolves within 12 weeks postpartum. PIH can progress to preeclampsia, which involves new onset hypertension accompanied by proteinuria or other systemic complications after 20 weeks of gestation. Preeclampsia is a leading cause of maternal and fetal morbidity and mortality. Treatment involves controlling blood pressure, preventing seizures with magnesium sulfate, and delivering the fetus. Regional anesthesia techniques are preferred over general anesthesia when possible due to risks of airway complications and hemodynamic changes with intubation in preeclamptic patients.
Pregnancy induced hypertension (PIH) is a hypertensive disorder of pregnancy characterized by new onset hypertension without significant proteinuria or other systemic involvement. It usually presents later in pregnancy and resolves within 12 weeks postpartum. PIH can progress to preeclampsia, which involves new onset hypertension accompanied by proteinuria or other systemic complications after 20 weeks of gestation. Preeclampsia is a leading cause of maternal and fetal morbidity and mortality. Treatment involves controlling blood pressure, preventing seizures with magnesium sulfate, and delivering the fetus. Regional anesthesia techniques are preferred over general anesthesia when possible due to risks of airway complications and hemodynamic changes with intubation in preeclamptic patients.
Pregnancy induced hypertension (PIH) is a hypertensive disorder of pregnancy characterized by new onset hypertension without significant proteinuria or other systemic involvement. It usually presents later in pregnancy and resolves within 12 weeks postpartum. PIH can progress to preeclampsia, which involves new onset hypertension accompanied by proteinuria or other systemic complications after 20 weeks of gestation. Preeclampsia is a leading cause of maternal and fetal morbidity and mortality. Treatment involves controlling blood pressure, preventing seizures with magnesium sulfate, and delivering the fetus. Regional anesthesia techniques are preferred over general anesthesia when possible due to risks of airway complications and hemodynamic changes with intubation in preeclamptic patients.
Pregnancy induced hypertension (PIH) is a hypertensive disorder of pregnancy characterized by new onset hypertension without significant proteinuria or other systemic involvement. It usually presents later in pregnancy and resolves within 12 weeks postpartum. PIH can progress to preeclampsia, which involves new onset hypertension accompanied by proteinuria or other systemic complications after 20 weeks of gestation. Preeclampsia is a leading cause of maternal and fetal morbidity and mortality. Treatment involves controlling blood pressure, preventing seizures with magnesium sulfate, and delivering the fetus. Regional anesthesia techniques are preferred over general anesthesia when possible due to risks of airway complications and hemodynamic changes with intubation in preeclamptic patients.
*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 Mild Severe 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 No Yes Epigastric pain No Yes Etiology Exact mechanism not known
Immunologic Genetic Placental ischemia
Endothelial cell dysfunction Vasospasm Hyper-responsive response to vasoactive hormones (e.g. angiotensin II & epinephrine) 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 Pathophysiology Pathophysiology
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*
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
< 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
MgSO 4 - 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 MgSO 4 - 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
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 MgSO 4 , SUX activity potentiated Enhanced sensitivity to non-depolarizing muscle relaxants MgSO 4 blunts response to vasconstrictors and inhibits catecholamine release after sympathetic stimulation Thank You!