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 > 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 > 300 mg/24hr
Oliguria or Serum-plasma creatinine ratio > 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
Systolic arterial pressure
140 mm Hg – 160 mm Hg
≥160 mm Hg
Diastolic arterial pressure
90 mm Hg – 110 mm Hg
≥110 mm Hg
Urinary protein
<5 g/24 hr Dipstick +or 2 +
≥5 g/24 hr Dipstick 3+or 4+
Urine output
>500 mL/24 hr
≤500 mL/24 hr
Headache No
Yes
Visual disturbances
Epigastric pain

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

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
Result of generalized vasospasm

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

20. HELLP Syndrome Hemostasis is not problematic unless PLT < 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 > 50% w/o any serious maternal morbidity
4g IV Bolus over 10 minutes, then 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
>25 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. Thank You!