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Premium member Presentation Transcript Preeclampsia: PreeclampsiaPowerPoint Presentation: Gestational Hypertension * Systolic > 140 mmHg * Diastolic > 90 mmHg * Occurs after 20 weeks in gestation * Returns to baseline postpartumPreeclampsia: 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 specimenPreeclampsia: 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 1 st pregnancy (>80%) Genetic dispositionClassification: Classification Hypertensive Disorders Gestational HTN: Preeclampsia – mild and severe Eclampsia HELLP Syndrome – H emolysis, E levated L iver enzymes, L ow P lts Chronic HTN pre-pregnancy Chronic HTN w/ superimposed gestational HTN Superimposed preecampsia Superimposed eclampsiaPathogenesis: 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 responsePathogenesis: Pathogenesis Occurs only in presence of placental issue Strong genetic component Associated with failure of 2 nd 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)Hypertensive Disease: Hypertensive Disease Risks: Group 1 (Hypertensive dz): Previous preeclampsia Systolic HTN < 20 wks gest H/o chronic HTN Family h/o previous PIHHypertensive Disease: Hypertensive Disease Risks: Group 2 (Coexisting vascular and endothelial dz): Chronic renal dz Lupus erythematous Protein S deficiency Circulating anticardiolipin antibodiesHypertensive Disease: Hypertensive Disease 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) Risks: Group 3: (obstetric factors)Preeclampsia: 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, oligohydramniosPreeclampsia - Pathophsiology: Preeclampsia - Pathophsiology Cardiovascular: Blood Pressure: Labile Hypersensitive to vasoactive hormones ? Sympathetic overactivity Vascular spasm Inc SVR Sustained HTNPreeclampsia - Pathophsiology: 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 pregnancyPreeclampsia - Pathophsiology: 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 likelyPreeclampsia - Pathophsiology: 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 factorsPreeclampsia - Pathophsiology: 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 sitesPreeclampsia - Pathophsiology: 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 megathrombocytesPreeclampsia - Pathophsiology: 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 HTNPreeclampsia - Pathophsiology: 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 expectedPreeclampsia - Pathophsiology: 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 followPreeclampsia - Pathophsiology: 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 casesPreeclampsia - Pathophsiology: 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 emergencyPreeclampsia - Pathophsiology: Preeclampsia - Pathophsiology Neurological: HA, visual disturbances, CNS hyperexcitability, hyperreflexia Seizures = eclampsia – causes Hypertensive encephalopathy Loss of cerebral autoregulation Vasospasm Microinfarctions, punctate hemorrhages Thrombosis Cerebral edemaPreeclampsia - Pathophsiology: 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 FHRPreeclampsia - Prevention: Preeclampsia - Prevention Aspirin prophylaxis: Based on reversing the PLT abnormalities Increases PGI 2 production, inhibits TXA 2 synthesis Use low doses – 60 mg/day Early studies encouraging Later studies showed no benefit Calcium prophylaxis: No benefitEffect of Pregnancy on Preeclampsia: 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 exclusiveEffect of Preeclampsia on Pregnancy: 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 txDrug Therapy: 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 Ca 2+ , support ventilationDrug Therapy: 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, diazepamDrug Therapy: 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 deathDrug Therapy: 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.Drug Therapy: 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 satisfactoryDrug Therapy: 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/minDrug Therapy: 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/ MgSO 4 Facial fkushing, HA, tachycardiaOliguria: 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 mmHgHELLP Syndrome: HELLP Syndrome H emolysis, E levated L iver Enzymes, L ow P latelets 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 dxHELLP Syndrome: 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 failureHELLP Syndrome: 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 - deliveryPreanesthetic Evaluation: Preanesthetic Evaluation Fluid status Hemodynamic status Coagulation status Bleeding time PLT count PT/aPTT TEGAnesthetic Mgmt: Anesthetic Mgmt Technique – Epidural vs. Spinal Treatment of side effects: Hypotension Difficult airway Coagulation Urgent C/S Postpartum Analgesia Fluid balance MgSO 4 Hemodynamic controlPowerPoint Presentation: Thank you ! 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