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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 l.jpg

PIH/Preeclampsia

Jeff Katz, MD


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Gestational Hypertension

  • Systolic > 140 mmHg

  • Diastolic > 90 mmHg

  • Occurs after 20 weeks in gestation

  • Returns to baseline postpartum


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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


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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


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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


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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


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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)


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Hypertensive Disease

  • Risks:

    • Group 1 (Hypertensive dz):

      • Previous preeclampsia

      • Systolic HTN < 20 wks gest

      • H/o chronic HTN

      • Family h/o previous PIH


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Hypertensive Disease

  • Risks:

    • Group 2 (Coexisting vascular and endothelial dz):

      • Chronic renal dz

      • Lupus erythematous

      • Protein S deficiency

      • Circulating anticardiolipin antibodies


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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)


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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


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Preeclampsia - Pathophsiology

  • Cardiovascular:

    • Blood Pressure:

      • Labile

      • Hypersensitive to vasoactive hormones

      • ? Sympathetic overactivity

      • Vascular spasm

      • Inc SVR

      • Sustained HTN


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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.


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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


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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


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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


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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


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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


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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


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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


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Preanesthetic Evaluation

  • Fluid status

  • Hemodynamic status

  • Coagulation status

    • Bleeding time

    • PLT count

    • PT/aPTT

    • TEG


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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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