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

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Presentation on theme: "Pregnancy Induced Hypertension Jack Lin, M.D. Albert Woo, M.D. Advisor: Marissa Lazor, M.D. Boston University Medical Center Dept. of Anesthesiology."— Presentation transcript:

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

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

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

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

5 Preeclampsia New onset HTNNew onset HTN After 20 weeks of gestation, orAfter 20 weeks of gestation, or Early post-partum, previously normotensiveEarly post-partum, previously normotensive Resolves within 48 hrs postpartumResolves within 48 hrs postpartum With the following (Renal or other systemic)With the following (Renal or other systemic) Proteinuria > 300 mg/24hrProteinuria > 300 mg/24hr Oliguria or Serum-plasma creatinine ratio > 0.09 mmol/LOliguria or Serum-plasma creatinine ratio > 0.09 mmol/L Headaches with hyperreflexia, eclampsia, clonus or visual disturbancesHeadaches with hyperreflexia, eclampsia, clonus or visual disturbances ↑ LFTs, glutathione-S-Transferase alpha 1-1, alanine aminotransferase or right abdominal pain↑ LFTs, glutathione-S-Transferase alpha 1-1, alanine aminotransferase or right abdominal pain Thrombocytopenia, ↑ LDH, hemolysis, DICThrombocytopenia, ↑ LDH, hemolysis, DIC 10% in primigravid10% in primigravid 20-25% with history of chronic HTN20-25% with history of chronic HTN

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

7 Mild vs. Severe Preeclampsia MildSevere 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 HeadacheNoYes Visual disturbances NoYes Epigastric pain NoYes

8 Etiology Exact mechanism not known Immunologic Immunologic Genetic Genetic Placental ischemia Placental ischemia Endothelial cell dysfunction Endothelial cell dysfunction Vasospasm Vasospasm Hyper-responsive response to vasoactive hormones (e.g. angiotensin II & epinephrine) Hyper-responsive response to vasoactive hormones (e.g. angiotensin II & epinephrine)

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

10 Pathophysiology

11 Pathophysiology Airway edema Airway edema Cardiac Cardiac Renal Renal Hepatic Hepatic Uterine Uterine

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

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

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

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

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

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

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

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

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

21 Treatment Management of maternal hemodynamics & prevention of eclampsia are key to a favorable outcomeManagement of maternal hemodynamics & prevention of eclampsia are key to a favorable outcome MgSO 4 - Rx of choice for preeclampsia.MgSO 4 - Rx of choice for preeclampsia. Does not significantly reduce systemic BP at the serum concentration that are efficacious in treating preeclampsiaDoes not significantly reduce systemic BP at the serum concentration that are efficacious in treating preeclampsia GoalsGoals Control BPControl BP Prevent seizuresPrevent seizures Deliver the fetusDeliver the fetus

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

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

24 MgSO 4 Toxicity 5-10 mEq/L – Prolonged PR, widened QRS 5-10 mEq/L – Prolonged PR, widened QRS mEq/L – Depressed tendon reflexes mEq/L – Depressed tendon reflexes mEq/L – SA, AV node block, respiratory paralysis mEq/L – SA, AV node block, respiratory paralysis >25 mEq/L - Cardiac arrest >25 mEq/L - Cardiac arrest

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

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

27 Regional (part 2) Neuraxial anesthesia in preeclamptic pt - still controversial Neuraxial anesthesia in preeclamptic pt - still controversial Many studies  this is the best option Many studies  this is the best option National High blood Pressure Education Program Working Group 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. “ “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. “

28 Regional (part 3) Possibility of extensive sympatholysis with profound hypotension Possibility of extensive sympatholysis with profound hypotension  decrease CO & uteroplacental perfusion  decrease CO & uteroplacental perfusion Single shot spinal technique  controversial 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 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

29 General Anesthetic Techniques Laryngeal response  blunted by pre-treatment with hydralazine, nitroglycerin or labetalol Laryngeal response  blunted by pre-treatment with hydralazine, nitroglycerin or labetalol Airway edema  increased risk of difficult airway situation Airway edema  increased risk of difficult airway situation Neuraxial techniques  preferred method, contraindicated in the presence of coaguloapthy Neuraxial techniques  preferred method, contraindicated in the presence of coaguloapthy In pt receiving MgSO 4, SUX activity  potentiated In pt receiving MgSO 4, SUX activity  potentiated Enhanced sensitivity to non-depolarizing muscle relaxants Enhanced sensitivity to non-depolarizing muscle relaxants MgSO 4 blunts response to vasconstrictors and inhibits catecholamine release after sympathetic stimulation MgSO 4 blunts response to vasconstrictors and inhibits catecholamine release after sympathetic stimulation

30 Thank You!


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