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PIH/Preeclampsia

PIH/Preeclampsia. Jeff Katz, MD. Gestational Hypertension. Systolic > 140 mmHg Diastolic > 90 mmHg Occurs after 20 weeks in gestation Returns to baseline postpartum. Preeclampsia. Gestational HTN + Proteinuria Occurs after 20 weeks in gestation Returns to baseline postpartum Dx:

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PIH/Preeclampsia

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  1. PIH/Preeclampsia Jeff Katz, MD

  2. Gestational Hypertension • Systolic > 140 mmHg • Diastolic > 90 mmHg • Occurs after 20 weeks in gestation • Returns to baseline postpartum

  3. Preeclampsia • Gestational HTN + Proteinuria • Occurs after 20 weeks in gestation • Returns to baseline postpartum • Dx: • Pt was previously normotensive • BP > 140/90 after 20 weeks • Proteinuria – urinary excretion of > 0.3 g of protein in a 24 hr urine specimen

  4. Preeclampsia • Scope of Problem: • Hypertensive Disease: • Occurs in 12-22% of pregnancies • Responsible for 17.6% of maternal deaths in USA • Preeclampsia • Approx. 5-8% of pregnancies • Primarily the 1st pregnancy (>80%) • Genetic disposition

  5. Classification • Hypertensive Disorders • Gestational HTN: • Preeclampsia – mild and severe • Eclampsia • HELLP Syndrome – Hemolysis, Elevated Liver enzymes, Low Plts • Chronic HTN pre-pregnancy • Chronic HTN w/ superimposed gestational HTN • Superimposed preecampsia • Superimposed eclampsia

  6. Pathogenesis • Etiology unknown • Related to degree of trophoblastic invasion by the placenta • In preeclampsia, the invasion is incomplete • Severity of invasion may be related to degree of invasion • Associated with alterations in immune response

  7. Pathogenesis • Occurs only in presence of placental issue • Strong genetic component • Associated with failure of 2nd trophoblastic invasion (14-16 weeks) • Results in high resistance low-flow uteroplacental circulation (ischemia) • Very complicated vascular active proteins involved - PGs, TXs, Endothelin, Endothelium derived relaxing factor • Plt dysfunction (aggregation)

  8. Hypertensive Disease • Risks: • Group 1 (Hypertensive dz): • Previous preeclampsia • Systolic HTN < 20 wks gest • H/o chronic HTN • Family h/o previous PIH

  9. Hypertensive Disease • Risks: • Group 2 (Coexisting vascular and endothelial dz): • Chronic renal dz • Lupus erythematous • Protein S deficiency • Circulating anticardiolipin antibodies

  10. AA Angiotensin gene T235 Nulliparity > 40 yrs old H/o not smoking Obesity Inc trophoblastic mass Large for gestational age Diabetes Erythroblastosis fetalis Polyhydramnios (young primups) Hypertensive Disease • Risks: Group 3: (obstetric factors)

  11. Preeclampsia • Severe preeclampsia – signs: • BP > 160 sys., > 110 dias. • Proteinuria > 5 gm in 24 hrs • Oliguria <400 ml in 24 hrs • Cerebral/visual disturbances • Pulmonary edema (cyanosis) • Epigastric/RUQ pain • Impaired liver function, rupture • Thrombocytopenia • HELLP syndrome • IUGR, oligohydramnios

  12. Preeclampsia - Pathophsiology • Cardiovascular: • Blood Pressure: • Labile • Hypersensitive to vasoactive hormones • ? Sympathetic overactivity • Vascular spasm • Inc SVR • Sustained HTN

  13. Preeclampsia - Pathophsiology • Cardiovascular: • Blood Volume: • Reduced 9-40% depending on severity • Behave as if vasoconstricted • HR, BP variability increased • Replace volume carefully – be careful of pulmonary edema • Hemodynamic change: • Initially hyperdynamic, later dec CO w/ inc SVR • Great variation • CO/SVR change throughout pregnancy

  14. Preeclampsia - Pathophsiology • Cardiovascular: • Cardiac function: • Normal heart rate • Poor correlation b/w CVP & PCWP • Variable • V. sensitive to rapid fluid bolus • Colloid oncotic pressure: • Dec in nml pregnancy, more w/ preeclampsia • Drops from 22 mmHg to 17 mmHg in nml; 22 to 14 in PIH • Low COP, inc vasc permeability, and loss of fluid & protein into tissues makes edema likely

  15. Preeclampsia - Pathophsiology • Hematological: • Hypercoagulability: • Accelerated PT – increased common pathway activity, inc activity of Factors II, V, X, reduced fibrinogen • RBC membrane anomaly – triggers thrombin formation • Reduced Antithrombin III – normally inhibits coagulation factors

  16. Preeclampsia - Pathophsiology • Hematological: • Fibrinolysis: • Variable opinions • Reduced fibrinolytic activity – altered activity b/w plasminogen activators and inhibitors adds to presence of fibrin in renal and placental vasculature • Higher Lipoprotein (a) concentration – competes with plasminogen for binding sites

  17. Preeclampsia - Pathophsiology • Hematological: • Platelet activation – Thrombocytopenia: • In 15-30% of PIH/eclampsia • < 10% have PLT count < 100,000 • Marked daily variation • Prolonged bleeding time in some • Inc release of beta- thromboglobulin by PLTs • Shorter PLT production time • Appearance of megathrombocytes

  18. Preeclampsia - Pathophsiology • Renal Function: • Glomerulopathy: • Glomerular enlargement w/ ischemia as a result of swollen intracapillary cells • GFR 25% below nml gestational • Non-pregnant = 122ml/min • Pregnant = 170ml/min • Proteinuria • Inc permeability to large moleclar wt proteins • Amt of proteinuria correlates w/ histological change and HTN

  19. Preeclampsia - Pathophsiology • Renal Function: • Glomerulopathy: • Oliguria • Parallels severity of eclampsia: <400ml/24 hr calls for intravascular fluid volume evaluation • Renal failure is rare, recovery is expected

  20. Preeclampsia - Pathophsiology • Renal Function: • Edema & weight gain: • Generalized edema is common • Important in airway mgmt – difficult airway and bleeding • Assoc w/ excessive wt gain through pregnancy • If severe PIH then pulmonary edema may follow

  21. Preeclampsia - Pathophsiology • Respiratory: • Pharyngolaryngeal edema • Airway narrowing • Fragile mucous membranes - bleeding • Pulmonary edema • More likely in severe PIH, or eclampsia • Occurs in 3% of cases • Occurred antepartum in 30% of cases • Occurred postpartum in 70% of cases

  22. Preeclampsia - Pathophsiology • Hepatic Changes: • Elevated transaminases • Subcostal/ RUQ pain – caused by edema or bleeding • Subcapsular bleeding • Suspect w/ severe abd pain • Could also be parenchymal bleeding • If capsule disrupted – intraperitoneal hemorrhage – surgical emergency

  23. Preeclampsia - Pathophsiology • Neurological: • HA, visual disturbances, CNS hyperexcitability, hyperreflexia • Seizures = eclampsia – causes • Hypertensive encephalopathy • Loss of cerebral autoregulation • Vasospasm • Microinfarctions, punctate hemorrhages • Thrombosis • Cerebral edema

  24. Preeclampsia - Pathophsiology • Uteroplacental perfusion • Decreased • Common in IUGR, oligohydramnios • High resistance – low flow (nml is low resistance – high flow) • Fetus does not tolerate the hypotension assoc w/ regional anesthesia – monitor FHR

  25. Preeclampsia - Prevention • Aspirin prophylaxis: • Based on reversing the PLT abnormalities • Increases PGI2 production, inhibits TXA2 synthesis • Use low doses – 60 mg/day • Early studies encouraging • Later studies showed no benefit • Calcium prophylaxis: • No benefit

  26. Effect of Pregnancy on Preeclampsia • Only cure for PIH is to end pregnancy • Women w/ placenta previa at less risk for PIH • Placenta previa and PIH not mutually exclusive

  27. Effect of Preeclampsia on Pregnancy • Position pt in lateral recumbent position to maximize uteroplacental perfusion • Induce labor if: • > 37 wks • Fetal lungs are matue • Favorable cervix • Increasing BP despite tx

  28. Drug Therapy • Magnesium Sulfate: • Anticonvulsant of choice • Tocolytic • Loading dose – 4-6 gm over 20 mins • Maint dose – 1-2 gm/hr infusion • Therapeutic range – 5-9 mg/dL • Monitor: • Reflexes, UO, resp rate, muscle strength • If toxic: Discontinue, give Ca2+, support ventilation

  29. Drug Therapy • Magnesium Sulfate: • Does not prolong nml/induced labor • Does not inc rate of C/S • Requires inc oxytocin for labor • Better results than phenytoin, diazepam

  30. Drug Therapy • Antihypertensives: • Methyldopa – choice of OBs • Parenteral drugs if severe or acute • No adverse effect on uteroplacental perfusion, fetal circulation • Do not defer or prevent PIH, IUGR, or perinatal death

  31. Drug Therapy • Antihypertensives: • Hydralazine: • Used for acute control IV • 5 mg IV Q 20 mins w/ a max of 20 mg • Side effects: tachycardia (inc SV, CO), HA, nausea, hypotension • Labetalol: • Combined alpha and beta • Ratio of 1:7 if given IV • Initial dose = 10-20 mg IV. Can double dose every 10 mins if necessary – max = 300mg • Reduces BP, SVR, slows HR.

  32. Drug Therapy • Antihypertensives: • Nitroglycerine: • Relaxes smooth muscle • Venous > Arterial • Reduces preload > afterload • Always expand volume before using because of sudden drop • Dilute to 50 mg/ 500 ml (100 mcg/ml) • Initial dose = 0.5-1 mcg/kg/min • Increase by 0.5 mcg/kg/min until satisfactory

  33. Drug Therapy • Antihypertensives: • Sodium nitroprusside • Arterial dilator – reduces afterload • Less preload reduction • Crosses placenta – could cause fetal cyanide toxicity • Initial dose = 0.5 mcg/kg/min • Toxicity seen if dose > 4 mcg/min

  34. Drug Therapy • Antihypertensives: • Nifedipine: • Calcium channel blocker • Effects mainly arterial smooth muscle • 10 mg sublingual, repeat in 30 mins • 10-20 mg Q 3-6 hrs • Could see exaggerated response w/ MgSO4 • Facial fkushing, HA, tachycardia

  35. Oliguria • < 30 ml/hr for 3 hrs • Confirm Foley location • 300-500 ml fluid challenge • If still a problem, insert a CVP • If CVP low, give fluids. If OK, give nitroglycerine to dilate renal artery • CVP does not mirror PCWP in severe PIH • Can push PCWP to 12-14 mmHg

  36. HELLP Syndrome • Hemolysis, Elevated Liver Enzymes, Low Platelets and PIH • Differential Dx: • Hepatitis, gallbladder dz, acute fatty liver of pregnancy, thrombocytopenic purpura (TTP) • Etiology unknown • 20% present postpartum, the rest preterm • Peak is 24-48 hrs postpartum • Initial c/o RUQ pain • 50% have NV • 80% have PIH before dx

  37. HELLP Syndrome • Complications: • DIC • Placental abruption • Need for blood transfusion • Pleural effusion • Acute renal failure • Wound infection • If develops postpartum there is a higher incidence of pulmonary edema and renal failure

  38. HELLP Syndrome • Time course of thrombocytopenia is v. important • If stable at 80,000 PLT, then regional is OK • If dropping fast at 80,000, then regional is dangerous – epidural hematoma • Treatment - delivery

  39. Preanesthetic Evaluation • Fluid status • Hemodynamic status • Coagulation status • Bleeding time • PLT count • PT/aPTT • TEG

  40. Anesthetic Mgmt • Technique – Epidural vs. Spinal • Treatment of side effects: • Hypotension • Difficult airway • Coagulation • Urgent C/S • Postpartum • Analgesia • Fluid balance • MgSO4 • Hemodynamic control

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