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Pregnancy Induced Hypertension

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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 – PowerPoint PPT presentation

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Title: Pregnancy Induced Hypertension


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
  • 8 of pregnancies
  • 4 categories
  • Chronic Hypertension
  • Pregnancy Induced hypertension
  • Preeclampsia-eclampsia
  • 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

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

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

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

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

7
Mild vs. Severe Preeclampsia
8
Etiology
  • Exact mechanism not known
  • Immunologic
  • Genetic
  • Placental ischemia
  • Endothelial cell dysfunction
  • Vasospasm
  • Hyper-responsive response to vasoactive hormones
    (e.g. angiotensin II epinephrine)

9
Symptoms of preeclampsia
  • Visual disturbances
  • Headache
  • Epigastric pain
  • 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

10
Pathophysiology
11
Pathophysiology
  • Airway edema
  • Cardiac
  • Renal
  • Hepatic
  • Uterine

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

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

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

15
Renal
  • Adversely affected ? proteinuria
  • GFR and CrCl ? decrease
  • BUN increase, may correlate w/ severity
  • RBF compromised
  • 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

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

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

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

19
HELLP Syndrome
  • Hemolysis
  • Elevated Liver enzymes
  • Low Platelets
  • lt 36 wks
  • Malaise (90), epigastric pain (90), N/V (50)
  • Self-limiting
  • Multi-system failure

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

21
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
  • Goals
  • Control BP
  • Prevent seizures
  • Deliver the fetus

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

23
Preventing Seizures
  • MgSO4 - Drug of choice. Narrow therapeutic index
  • Reduce gt 50 w/o any serious maternal morbidity
  • 4g IV Bolus over 10 minutes, then infusion _at_
    1g/hr
  • Renal failure - rate of infusion ? by serum Mg
    levels
  • Plasma Level should be between 4-6 mmol/L
  • Monitor clinical signs for toxicity
  • Toxic 10 ml of 10 Ca Gluconate IV slowly

24
MgSO4 Toxicity
  • 5-10 mEq/L Prolonged PR, widened QRS
  • 11-14 mEq/L Depressed tendon reflexes
  • 15-24 mEq/L SA, AV node block, respiratory
    paralysis
  • gt25 mEq/L - Cardiac arrest

25
Anesthetic Considerations
  • Detailed preanesthetic assessment
  • Focuses on airway, fluid status, and BP control
  • Lab CBC, BUN/Cr, LFTs
  • Routine coagulation is NOT recommended unless
    there is clinical suspicion
  • 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.
  • Epidurals may reduce vasospasm and HTN may
    improve uteroplacental blood flow
  • Reduce risk of airway complications and avoid
    hemodynamic alterations associated with intubation

27
Regional (part 2)
  • Neuraxial anesthesia in preeclamptic pt - still
    controversial
  • Many studies ? this is the best option
  • 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.

28
Regional (part 3)
  • Possibility of extensive sympatholysis with
    profound hypotension
  • ? decrease CO uteroplacental perfusion
  • 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

29
General Anesthetic Techniques
  • Laryngeal response ? blunted by pre-treatment
    with hydralazine, nitroglycerin or labetalol
  • Airway edema ? increased risk of difficult airway
    situation
  • Neuraxial techniques ? preferred method,
    contraindicated in the presence of coaguloapthy
  • In pt receiving MgSO4, SUX activity ? potentiated
  • Enhanced sensitivity to non-depolarizing muscle
    relaxants
  • MgSO4 blunts response to vasconstrictors and
    inhibits catecholamine release after sympathetic
    stimulation

30
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