4.Gestational hypertension by Dr.Iqra Osman.pptx

Gestational hypertension
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1. HYPERTENSION Gestational Hypertension Dr.Iqra Osman Abdullahi,MD

2. Hypertension in Pregnancy Most common medical problem encountered during pregnancy 8 % of p regn a nc i es 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

3. Hypertension in Pregnancy 4 categories Chronic Hypertension Pregnancy Induced hypertension Preeclampsia-eclampsia Preeclampsia superimposed on chronic HTN

4. DEFINITION 🠶 Chronic hypertension , if blood pressure elevation >140/90 before 20 weeks and persists ≥12 we e ks postpa r tum 🠶 Gestational hypertension of pregnancy, if blood pressure returns to normal by 12 weeks postpartum

5. Chronic Hypertension 🠶 Treatment of mild to moderate chronic hypertension neither benefits the fetus nor prevents preeclampsia. 🠶 Excessively lowering blood pressure may result in decreased placental perfusion and adverse perinatal outcomes. 🠶 When BP is 150 to 180/100 to 110 mm Hg, pharmacologic trea t ment i s needed to p r e v ent m a ternal en d - org a n damage.

6. Treatment of Chronic Hypertension 🠶 Methyldopa , labetalol, and nifedipine most common oral agents. 🠶 AVOID: ACEI and ARBs, atenolol, thiazide diuretics 🠶 W omen i n act i v e labo r w i th uncontrolled se v ere ch r on i c hypertension require treatment with intravenous labetalol or hydralazine.

7. Pregnancy Induced Hypertension (Gestational) Usually mild and later in pregnancy BP ≥140/90 mmHg (severe when ≥160/≥110 mmHg) Previously normotensive ≥ 2 w ee k s of ge s t a t i on No renal or other systemic involvement No proteinuria or new signs of end-organ dysfunction Resolves 12 weeks postpartum May become preeclampsia

8. Gestational Hypertension to Preeclampsia 🠶 The pathophysiology of gestational hypertension is unknown. 🠶 Different diseases with a similar phenotype (hypertension) 🠶 Primiparity is a strong risk factor for preeclampsia, but not for GH 🠶 The recurrence risk for gestational hypertension is ~40% (for PE 5%) 🠶 Total blood and plasma volumes are significantly lower in women with preeclampsia (mean 2660 mL/m2 and 1790 mL/m2, respectively) than in women with gestational hypertension (3139 mL/m2 and 2132 mL/m2, respectively)

9. GH versus PE Features Gestational HTN Preeclampsia Hypertension + ++ Primiparity + 10% Recurrence 25-45 % 5% Total Plasma Volume 2132 mL/m2 (mean) 1790 mL/m2 (mean) Proteinuria Negative Positive Gestational age Usually late (>20weeks) Usually early (<2 weeks) Complications Rarely Increase risk Post partum R e sol v e < 1 2 we e ks R e sol v e < 6 w ee k s

10. RISK O F P ROGRESSION TO PRE E CLAM P SIA 🠶 Preeclampsia develops in 15 to 25 % of women with initial GH, 🠶 Early onset of GH are more likely to progress to preeclampsia (33 versus 37 weeks) 🠶 4 to 5 % of wome n w i th G H p resent i ng a t ≤30 weeks developed preeclampsia as compared with about 10 % of those who developed gestational hypertension at ≥36 weeks 🠶 Women who go on to develop preeclampsia have higher total vascular resistance at presentation than women with uncomplicated GH

11. PERINATAL OUTCOME 🠶 Pregnancy outcomes of patients with non-severe gestational hypertension are generally favorable. 🠶 The mean birth weight and rates of fetal growth restriction, preterm birth, abruption, and perinatal death are similar to those in the general obstetrical population. 🠶 Severe gestational hypertension appear to be at increased risk of maternal and perinatal morbidity 🠶 These pregnancies have significantly higher rates of preterm delivery, small for gestational age infants, and abruptio placentae

12. MANAGEMENT 🠶 Non-severe gestational hypertension, monitoring blood pressure once or twice weekly and weekly assessment of proteinuria, platelet count, and liver enzymes 🠶 Pat i ent educat i on an d counsel i ng 🠶 Fet a l a s se s s m ent, mon i tor fet a l mo vement da i ly 🠶 No antihypertensive therapy — unless hypertension is se v ere (≥ 1 6 m m H g sy s tol i c or ≥ 1 1 m m H g d i a s tol i c) 🠶 No an t ena t a l gl u co c ort i coid s 🠶 Timing of delivery at 37 0/7ths to 38 6/7ths weeks 🠶 I ntrapart u m m a na g ement 🠶 administer magnesium sulfate for seizure prophylaxis

13. 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) Pro t e i n ur i a > 30 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 % i n pr i m i gravid 20 - 25 % w i th h i stor y of c hro n i c H T N

14. Diagnostic Criteria for Preeclampsia SBP of 140 mm Hg or more or a DBP of 90 mm Hg or more on two occasions at least six hours apart after 20 weeks of gestation AND Pr ote i nur i a – 30 mg i n a 2 4 - hour ur i ne spec i men or 1+ or greater on urine dipstick testing of two random urine samples collected at least four hours apart. 🠶 A r a n do m ur i n e pro t e i n /cre a t i n i n e ra t i o < . 2 1 i n d i c a t e s t h a t significant proteinuria is unlikely with a NPV of 83%. 🠶 Generalized edema (affecting the face and hands) is often present in patients with preeclampsia but is not a diagnostic criterion.

15. Mild vs. Severe Preeclampsia Mild Severe 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 No Yes Epigastric pain No Yes

16. Maternal Risk Factors F i rst 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

17. Etiology Exact mechanism not known Immunologic Genetic Placental ischemia Endothelial cell dysfunction Vasospasm Hyper-responsive response to vasoactive hormones (e.g. ang i o t e n si n I I & ep i nephr i n e)

18. Risk Facto r s FACTOR RISK RATIO Renal disease 20:1 Chronic hypertension 10:1 Antiphospholipid syndrome 10:1 Family history of PIH 5:1 Twin gestation 4:1 Nulliparity 3:1 Age > 40 3:1 Diabetes mellitus 2:1 African American 1.5:1

19. 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

20. Pathophysiology

21. Organ involvement Airway edema Cardiac Renal Hepatic Uterine

22. Upper airway edema Upper airway edema Laryngeal edema Airway obstruction Potential for airway compromise or difficulty in intubation

23. Cardiac/Pulmonary Increased CO & SVR CVP normal or slightly increased Plasma volume reduced Pulmonary edema Decrease oncotic/colloid pressure Capillary/endothelial damage  leak Vasoconstriction  increase PWP and CVP Oc c urs 3 % of pr e e c l a mp t i c pa t i e n t s

24. Hepatic Usually mild Severe PIH or preeclampsia complicated by HELLP  periportal hemorrhages  ischemic lesion  generalized swelling  hepatic swelling  epigastric pain

25. Re n al 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*

26. Uterine Activity increased Hyperactive/hypersensitive to oxytocin Pr eterm labo r – fre q uent U ter i ne/ p lacenta l bloo d flow – dec r ea s ed b y 5 - 70% Ab r upt i on – i nc i denc e i nc r ea s ed

27. 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)

28. Morbidity / Mortality Fetal complications: Abruptio placentae IUGR Premature delivery Intrauterine fetal death

29. HELLP Syndrome H emolysis E levated L iver enzymes L ow P latelets < 3 6 w k s Malaise (90%), epigastric pain (90%), N/V (50%) Self-limiting Multi-system failure

30. Diagnosis Criteria for HELLP H T N SP B i s ≥160 m m H g or DPB i s ≥110 m m Hg Proteinuria ≥0.3 grams in a 24-hour urine specimen or protein (mg/dL)/creatinine (mg/dL) ratio ≥0.3 Platelet count <100,000/microliter Serum creatinine >1.1 mg/dL or doubling of serum creatinine in the absence of other renal disease Liver transaminases at least twice the normal concentrations Pulmonary edema Cerebral or visual symptoms

31. 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. Def i n i t i v e cure i s del i v ery

32. Treatment Management of maternal hemodynamics & prevention of eclampsia are key to a favorable outcome MgSO 4 - 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

33. Controlling the HTN Hydralazine Labetalol Nitroglycerin Nifedipine Esmolol Na Nitroprusside – risk of cyanide toxicity in the fetus

34. Preventing Seizures MgSO 4 - Drug of choice. Narrow therapeutic index Reduce > 50% w/o any serious maternal morbidity 4 g I V Bolus ov er 1 m inutes, then i nfus i on @ 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 T ox i c: 1 ml of 10 % Ca Gluconat e I V slowly

35. MgSO 4 Toxicity 5 - 1 mEq / L – Pr olonged P R , w i dene d Q R S 11-14 mEq/L – Depressed tendon reflexes 15-24 mEq/L – SA, AV node block, respiratory paralysis >25 mEq / L - C a rd i a c arrest