Pregnancy Induced HypertensionJack Lin, M.D.Albert Woo, M.D.

Advisor: Marissa Lazor, M.D.

Boston University Medical CenterDept. of Anesthesiology

HypertensionMost common medical problem encountered during pregnancy8% of pregnancies

4 categories:

Chronic HypertensionPregnancy Induced hypertensionPreeclampsia-eclampsiaPreeclampsia 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*

HypertensionThird 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 HypertensionHTN Usually mild and later in pregnancyNo renal or other systemic involvement Resolves 12 wks postpartumMay become preeclampsia

PreeclampsiaNew onset HTN After 20 weeks of gestation, or Early post-partum, previously normotensiveResolves within 48 hrs postpartum

With the following (Renal or other systemic)

Proteinuria > 300 mg/24hrOliguria or Serum-plasma creatinine ratio > 0.09 mmol/LHeadaches with hyperreflexia, eclampsia, clonus or visual disturbances LFTs, glutathione-S-Transferase alpha 1-1, alanine aminotransferase or right abdominal painThrombocytopenia, LDH, hemolysis, DIC

10% in primigravid20-25% with history of chronic HTN

Maternal Risk FactorsFirst pregnancyAge younger than 18 or older than 35Prior h/o preeclampsiaBlack raceMedical risk factors for preeclampsia - chronic HTN, renal disease, diabetes, anti-phospholipid syndromeTwinsFamily history

Mild vs. Severe Preeclampsia

MildSevereSystolic arterial pressure 140 mm Hg 160 mm Hg160 mm Hg Diastolic arterial pressure 90 mm Hg 110 mm Hg 110 mm Hg Urinary protein 500 mL/24 hr 500 mL/24 hr Headache No Yes Visual disturbances No Yes Epigastric pain No Yes

EtiologyExact mechanism not known

ImmunologicGeneticPlacental ischemia

Endothelial cell dysfunctionVasospasmHyper-responsive response to vasoactive hormones (e.g. angiotensin II & epinephrine)

, with arterial constriction and relatively reduced intravascular volume compared to normal pregnancyleads to pathologic capillary leak manifest as rapid weight gain, edema of face +/- hands, pulmonary edema, +/or hemoconcentrationto fetal/placental tissue manifest as dysfunction of multiple organ systems

Symptoms of preeclampsiaVisual disturbancesHeadacheEpigastric painRapidly increasing or nondependent edema - may be a signal of developing preeclampsiaRapid weight gain - result of edema due to capillary leak as well as renal Na and fluid retention

Result of generalized vasospasm

Pathophysiology

Pathophysiology

Airway edemaCardiacRenalHepatic Uterine

Upper airway edemaUpper airway edemaLaryngeal edemaAirway obstruction

Potential for airway compromise or difficulty in intubation

Cardiac/PulmonaryIncreased CO & SVRCVP normal or slightly increasedPlasma volume reduced

Pulmonary edema Decrease oncotic/collid pressureCapillary/endothelial damage leakVasoconstriction increase PWP and CVPOccurs 3 % of preeclamptic patients

Hepatic

Usually mildSevere PIH or preeclampsia complicated by HELLP periportal hemorrhagesischemic lesiongeneralized swellinghepatic swelling epigastric pain

RenalAdversely affected proteinuriaGFR and CrCl decreaseBUN increase, may correlate w/ severityRBF compromisedARF w/ oliguria PIH, esp. w/ abruption, DIC, HELLP

*Oliguria + renal failure may occur in the absence of hypovolemia. Be careful w/ hydration pulmonary edema*

UterineActivity increasedHyperactive/hypersensitive to oxytocinPreterm labor frequentUterine/placental blood flow decreased by 50-70%Abruption incidence increased

Morbidity / MortalityMaternal complications:

Leading cause of maternal death in PIH is intracranial hemorrhageSeizuresPulmonary edema ARFProteinuriaHepatic swelling with or without liver dysfunctionDIC (usually associated with placental abruption and is uncommon as a primary manifestation of preeclampsia)

Morbidity / Mortality

Fetal complications:

Abruptio placentaeIUGRPremature delivery Intrauterine fetal death

HELLP SyndromeHemolysisElevated Liver enzymesLow Platelets

< 36 wksMalaise (90%), epigastric pain (90%), N/V (50%)Self-limiting Multi-system failure

HELLP SyndromeHemostasis is not problematic unless PLT < 40,000Rate of fall in PLT count is important Regional anesthesia - contraindicated fall is suddenPLT count normal within 72 hrs of deliveryThrombocytopenia may persist for longer periods.Definitive cure is delivery

Treatment

Management of maternal hemodynamics & prevention of eclampsia are key to a favorable outcome

MgSO4 - Rx of choice for preeclampsia.

Does not significantly reduce systemic BP at the serum concentration that are efficacious in treating preeclampsia

GoalsControl BPPrevent seizuresDeliver the fetus

Controlling the HTNHydralazineLabetalolNitroglycerinNifedipineEsmololNa Nitroprusside risk of cyanide toxicity in the fetus

Preventing SeizuresMgSO4 - Drug of choice. Narrow therapeutic index

Reduce > 50% w/o any serious maternal morbidity4g IV Bolus over 10 minutes, then infusion @ 1g/hr Renal failure - rate of infusion by serum Mg levelsPlasma Level should be between 4-6 mmol/LMonitor clinical signs for toxicity

Toxic: 10 ml of 10% Ca Gluconate IV slowly

MgSO4 Toxicity5-10 mEq/L Prolonged PR, widened QRS11-14 mEq/L Depressed tendon reflexes15-24 mEq/L SA, AV node block, respiratory paralysis>25 mEq/L - Cardiac arrest

Anesthetic ConsiderationsDetailed preanesthetic assessment Focuses on airway, fluid status, and BP controlLab: CBC, BUN/Cr, LFTs Routine coagulation is NOT recommended unless there is clinical suspicionPLT count - if neuraxial techniques are considered

Regional AnesthesiaLabor 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 flowReduce 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 optionNational High blood Pressure Education Program Working GroupNeuraxial, 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 controversialRecent 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 TechniquesLaryngeal response blunted by pre-treatment with hydralazine, nitroglycerin or labetalolAirway edema increased risk of difficult airway situationNeuraxial techniques preferred method, contraindicated in the presence of coaguloapthyIn pt receiving MgSO4, SUX activity potentiated Enhanced sensitivity to non-depolarizing muscle relaxantsMgSO4 blunts response to vasconstrictors and inhibits catecholamine release after sympathetic stimulation

Thank You!

, with arterial constriction and relatively reduced intravascular volume compared to normal pregnancyleads to pathologic capillary leak manifest as rapid weight gain, edema of face +/- hands, pulmonary edema, +/or hemoconcentrationto fetal/placental tissue manifest as dysfunction of multiple organ systems

Result of generalized vasospasm