Presentation on theme: "1 Hypertension in Pregnancy Speaker: Khalid A. Yarouf Faculty of Medicine & Health Sciences (FMHS) Obstetrics / Gynecology Rotation 2001/02. www.4MedStudents.com."— Presentation transcript:
1 Hypertension in Pregnancy Speaker: Khalid A. Yarouf Faculty of Medicine & Health Sciences (FMHS) Obstetrics / Gynecology Rotation 2001/02.
2 Outline Physiologic adaptations in normal pregnancy. Hypertension in Pregnancy: oDefinition. oPrevalence. oClassification. oRisk factors. oPathogenesis. oComplications. oDiagnosis & Evaluation. oManagement. oSelf-assessment.
3 Physiologic adaptations in normal pregnancy Blood changes: o Plasma volume by 40%. oPlatelets count can below 200 X 10 9 /L due to normal maternal blood-volume expansion. o Coagulation factors (Fibrinogen, Factor VII). Cardiovascular changes: oMarked generalized vasodilation ( peripheral resistance) a/w arterial resistance to constrictor actions of Angiotensin II. o CO & Stroke volume. oMAP by 10 mm Hg.
4 Con t Renal changes: oVasodilation Renal blood flow GFR (by 50%). o in Creatinine clearance with a concomitant in S- Creatinine & urea. o Uric acid clearance & Ca + excretion. o Glucosuria + aminoaciduria. Respiratory changes. Endocrine changes: oe.g. parathyroid, adrenal, weight, GI changes.
5 Hypertension in Pregnancy Definition: o= Sustained bed rest on 2 occasions at least 6 hours apart. Prevalence: 10% of all pregnancies. Classification: –Pre-eclampsia. –Chronic hypertension (HTN). –Transient HTN = Gestational HTN.
6 A. Pre-eclampsia Characteristic triad: o= Sustained HTN + Proteinuria + Edema (not essential for Dx). oOnset > 20 weeks gestation. 50% of all HTN in pregnancies. Resolves after delivery.
7 1. Mild pre-eclampsia Commonest entity has NO symptoms. Characteristics: oHTN BP 140 / 90 mm Hg OR sBP by 30 mm Hg above non-pregnant. dBP by 15 mm Hg above non-pregnant. oProteinuria(1-2+ dipstick OR > 300 mg / 24 hr). oEdema: (non-dependent, hands &/ face, a/w excessive wt gain)
8 2. Severe pre-eclampsia Less common. Can be diagnosed on basis of: –Severe HTN (BP 160 / 110 mm Hg). OR –Severe proteinuria (3-4+ dipstick OR > 5 g / 24 hr) alone without symptoms.OR –Only mild HTN + proteinuria if signs and symptoms are present:
9 Con t Resp : Plum. Edema, cyanosis. Cardiac : Congestive Cardiac Failure (CCF). Renal : Proteinuria, Serum creatinine, oliguria. Hepatic : LFTs, RUQ / epigastric pain. Neurologic : visual disturbance (i.e. scotomas, loss of peripheral vision), headache, convulsions. GI : severe nausea / vomiting. Hematologic : thrombocytopenia, microangiopathic hemolysis.
10 Con t HELLP syndrome : oType of severe pre-eclampsia. o H emolysis + E levated L iver enzymes + L ow P latelets.
11 3. Eclampsia [ Latin = convulsions] = Unexplained tonic-clonic seizures + Mild / severe pre-eclampsia. Most often occurs intra-partum (50%), but can also occur ante-partum & post-partum.
12 B. Chronic HTN Pt may have any disease causing HTN: –e.g. essential HTN, A/c & chronic GN, chronic pyelonephritis, SLE. 1.Uncomplicated: oDefinition: = Pre-existing HTN. OR = HTN diagnosed 20 weeks. OR = HTN persisting 6 weeks post-partum. oNOT induced by pregnancy.
13 Con t 2. Complicated by superimposed pre-eclampsia: o= Isolated HTN without proteinuria. oCharacterized by: worsening of HTN ± proteinuria + severe PIH symptoms late in pregnancy.
14 C. Transient HTN = Late HTN = Gestational HTN. = Non-sustained (transient) BP without proteinuria / symptoms in last half of pregnancy. Has no impact on pregnancy outcome.
16 Pathogenesis of Pre-eclampsia Pre-eclampsia / eclampsia is justly called a disease of theories. Despite extensive research, no definite cause has been identified. As the term toxemia indicates, the search for a toxin has been long, arduous, and fruitless. Because of the prompt resolution of disease following delivery, most attention has been focused on placenta & its membranes and on fetus. Uteroplacental ischemia is postulated to be the center to the development of disease, which results in production of toxin that enters circulation and causes widespread endothelial dysfunction.
18 Diagnosis & Evaluation HTN is the most diagnostic sign. Because there re no specific diagnostic investigations, the initial Dx of pre-eclampsia remains clinical. Hx: –Previous HTN or proteinuria or both? –Previous hypertensive pregnancies? P/E: –Vitals BP. –In normal pregnancy, there re substantial CV changes with a 50% in CO & blood volume, which is accompanied by a in BP due to peripheral vasodilation. The changes in pre-eclampsia tend to be the reverse. –Edema. –Funduscopic exam record baseline findings.
19 Con t (Dx) For the purposes of clinical Dx & further evaluation, pts may be divided into 2 working groups: –Chronic HTN: Multiparous. Those with previous Hx of HTN. Those who developed HTN prior to 20wks gestation. –Pre-eclampsia. 1st pregnancy & develop syndrome after 20wks.
20 Table 1. Initial lab evaluation of pt with pre-eclampsia / eclampsia BloodUrineOther CBC & Plt count: if Plts, Hb HELLP synd Electrolytes: BUN (may ) Uric acid. Creatinine. LFT. Sediment. 24-hr protein. 24-hr creatinine (may ). US. Test of fetal well- being: NST. BPP. Cord color Doppler.
21 Notes: Serum uric acid correlates with poorer outcome for the mother & baby. Renal function is generally maintained in pre-eclampsia until late stage. If creatinine levels are high early in disease process, underlying renal disease should be suspected. In pre-eclampsia, Plt count due to increased consumption & intravascular destruction. Also, Plts is part of HELLP synd. Maternal Hb can be due to hypovolemia, and it s a/w IUGR. Liver involvement: –Inflammatory infiltrates + obstructed blood flow in sinusoids local welling subcapsular hemorrhage upper epigastric pain. – ALT & AST leak across cell membranes (can also be a/w HELLP synd). Additional lab test for chronic HTN may include ANA (for SLE) and ECG.
22 Management A.Outpatient observation: Use : only for transient HTN / uncomplicated chronic HTN. Specific guidelines : a.Encourage left lateral rest to enhance placental perfusion. b.Serially monitor mother watching for progression to pre-eclampsia / superimposed pre- eclampsia. Check for BP, U-protein, headache, epigastric pain, scotomata. c.Serially monitor fetus: Non-stress test (NST), Amniotic Fluid Index (AFI), Biophysical profile (BPP).
23 Con t (Mx) B.Inpatient observation: Use : only for mild pre-eclampsia (< 36 weeks gestation). Specific guidelines : a.Encourage left lateral rest to enhance placental perfusion. b.Monitor mother & fetus watching for progression to severe pre-eclampsia or eclampsia. c.Administer maternal steroids = 2 doses of betamethasone IM 24 hours apart.
24 Con t (Mx) C.Prompt delivery: Use : mild pre-eclampsia ( 36 weeks gestation), severe pre- eclampsia, eclampsia, chronic HTN with superimposed PIH, HELLP syndrome, or any evidence of maternal or fetal jeopardy. Specific guidelines : a.Lower BP: keep diastolic value between mm Hg. = Use IV Hydralazine / IV Labetalol. b.Prevent convulsions. Use IV MgSO4. c.Initiate delivery: Attempt induction of labor & vaginal delivery for 8-12 hours if mother & fetus are stable. Otherwise, perform C-section.
25 Self-assessment A 24-year-old gravida 1, para 0, at 37 weeks gestation was noted to have a 6-lb weight gain and an increase in blood pressure from 100/60 to 130/80 in the past week. She also has 1+ proteinuria. The examination was repeated 6 hours later and the same results were obtained. The best diagnosis is: a.Normal pregnancy. b.Pre-eclampsia. c.Eclampsia. d.Chronic hypertension. e.Essential hypertension.
26 Con t (test) The most common warning sign of pre- eclampsia is: a.Proteinuria. b.Headache. c.Edema. d.Increased BP. e.Epigastric pain.
27 Con t (test) The ultimate treatment for pre-eclampsia is: a.Magnesium sulfate. b.Delivery. c.An antihypertensive drug. d.Renal dialysis. e.Bed rest.