Hypertension In Pregnancy Lecture Notes PDF

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LawAbidingDrums5465

Uploaded by LawAbidingDrums5465

University of Warith Al-Anbiyaa College of Medicine

Dr. Maysaloon ALKafaji

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hypertension in pregnancy pregnancy complications maternal health obstetrics

Summary

This lecture provides an overview of hypertension in pregnancy, covering various aspects including physiological adaptations, classifications (pre-eclampsia, chronic hypertension, transient hypertension), risk factors, complications, diagnosis, management, and fetal monitoring. It details the different types of hypertension, their characteristics, and appropriate interventions.

Full Transcript

Dr.Maysaloon ALKafaji Associate professor of obst.& gyne Hypertension in Pregnancy 1 Outline Physiologic adaptations in normal pregnancy. Hypertension in Pregnancy: o Definition. o Prevalence. o Classification. o...

Dr.Maysaloon ALKafaji Associate professor of obst.& gyne Hypertension in Pregnancy 1 Outline Physiologic adaptations in normal pregnancy. Hypertension in Pregnancy: o Definition. o Prevalence. o Classification. o Risk factors. o Pathogenesis. o Complications. o Diagnosis & Evaluation. o Management. o Self-assessment. 2 Physiologic adaptations in normal pregnancy Blood changes: o ↑ Plasma volume by ≈ 40%. o Platelets count can ↓ below 200 X 109/L due to normal maternal blood- volume expansion. o ↑ Coagulation factors (Fibrinogen, Factor VII). Cardiovascular changes: o Marked generalized vasodilation (↓ peripheral resistance) a/w arterial resistance to constrictor actions of Angiotensin II. o ↑ CO & Stroke volume. o MAP ↓ by 10 mm Hg. 3 Con’t Renal changes: o Vasodilation ↑ 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: o e.g. parathyroid, adrenal, weight, GI changes. 4 Hypertension in Pregnancy Definition: o = Sustained ↑ BP @ bed rest on 2 occasions at least 6 hours apart. Prevalence: 10% of all pregnancies. Classification: o Pre-eclampsia. o Chronic hypertension (HTN). o Transient HTN = Gestational HTN. A. Pre-eclampsia Characteristic triad: o = Sustained HTN + Proteinuria + Edema (not essential for Dx). o Onset > 20 weeks’ gestation. 50% of all HTN in pregnancies. Resolves after delivery. 6 1. Mild pre-eclampsia Commonest entity has NO symptoms. Characteristics: o HTN BP ≥140 / 90 mm Hg OR ↑ sBP by 30 mm Hg above non-pregnant. ↑ dBP by 15 mm Hg above non-pregnant. o Proteinuria (1-2+ dipstick OR > 300 mg / 24 hr). o Edema: (non-dependent, hands &/ face, a/w excessive wt gain) 7 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: 8 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. 9 Con’t HELLP syndrome: o Type of severe pre-eclampsia. o Hemolysis + Elevated Liver enzymes + Low Platelets. 10 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. B. Chronic HTN Pt may have any disease causing HTN: e.g. essential HTN, A/c & chronic GN, chronic pyelonephritis, SLE. 1. Uncomplicated: o Definition: = Pre-existing HTN. OR = HTN diagnosed ≤ 20 weeks. OR = HTN persisting ≥ 6 weeks post-partum. o NOT induced by pregnancy. 12 Con’t 2. Complicated by superimposed pre-eclampsia: o = Isolated HTN without proteinuria. o Characterized by: worsening of HTN ± proteinuria + severe PIH symptoms late in pregnancy. 13 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. 14 Risk Factors Maternal Factors: 1. Demographic criteria: o Primagravida commonest risk factor. o Age extremes ( 34 years). 2. Medical complications: o DM + Chronic HTN + Pre-existing renal disease + SLE. 3. Past Hx or FHx of pregnancy-induced HTN. Hypertension in pregnancy Fetal factors: o Hydatidiform mole, > 1 fetus, fetal hydrops, IUGR. 15 Multi-fetal gestation High body mass index of 35 or more. Male partner whose previous partner had preeclampsia Booking proteinuria. Family history of pregnancy-induced hypertension, mother or sister. Booking diastolic blood pressure of 80 mmHg or more. Anti-phospholipid antibody syndrome or inherited thrombophilia 16 Gestational Hypertension A sustained rise of blood pressure to 140/90 mm of Hg or more on at least two occasions 4 or more hours apart beyond the 20th week of pregnancy or within the first 48 hours of delivery in the absence of other findings suggestive of preeclampsia in a previously normotensive women. 5-10% of pregnancies that proceed beyond 1st trimester develop gestational HTN increased incidence of up to 30% in multiple gestation. one-third of women who present with gestational hypertension will progress to pre-eclampsia. 17 Earlier onset of gestational HTN are more likely to progress to preeclampsia if BP returns to baseline by 12 weeks postpartum Transient hypertension of pregnancy Gestational Hypertension : Management Hypertension: blood pressure of 140/90–159/109mmHg. Offer pharmacological treatment if BP remains above 140/90 mmHg. Severe hypertension: blood pressure of 160/110mmHg or more. Treatment to all women. Aim for BP of 135/85 mmHg or less. 18 Action Hypertension severe hypertension Blood Pressure measurement Once or twice a week (depending on BP) until Every 15-30 minutes until BP is less than BP is 135/85 mmHg or less. 160/110 mmHg. Dipstick protein urea testing Once or twice a week (with BP measurement) Daily while admitted Blood Tests Measure full blood account, liver function and Measure full blood count, liver function and renal function at presentation and then weekly renal function at presentation & then weekly. 19 Antihypertensive therapy Consider labetalol Consider nifedipine for women in whom labetalol is not suitable methyldopa if labetalol Or nifedipine are not suitable. Do not offer bed rest in hospital Fetal monitoring Ultrasound for: − fetal growth − amniotic fluid volume assessment − umbilical artery Doppler velocimetry at diagnosis and if normal repeat every 2 to 4 weeks, if clinically indicated. Cardiotocography (CTG ) if clinically indicated only. 20 Timing of birth Do not offer planned early birth before 37 weeks if blood pressure is lower than 160/110 mmHg, unless there are other medical indications. If blood pressure is lower than 160/110 mmHg after 37 weeks gestation :counseling If planned early birth is necessary :corticosteroids and magnesium sulfate if indicated. 21 Postnatal investigation, monitoring and treatment Measure blood pressure as clinically indicated. continue antihypertensive treatment if required reduce antihypertensive treatment if their blood pressure falls below 130/80mmHg. If a woman has taken methyldopa, stop within 2 days after the birth and change to an alternative treatment if necessary. women who did not take antihypertensive treatment and have given birth, treatment if their blood pressure is 150/100mmHg or higher. Offer all women medical review with their GP or specialist 6–8 weeks after the birth. 22 Case 1: A 21-year-old primigravida without severe features is seen in the outpatient prenatal clinic for routine visit. She is at 32 weeks’ gestation, confirmed by first trimester sonogram. She denies headache, epigastric pain, or visual disturbances. She has gained 10 pounds since her last visit two weeks ago. On examination her BP is 155/95 mm Hg and it remains unchanged on repeat check in 15 min. She has 2+ pedal edema, and her fingers appear swollen. A spot urine dipstick shows 2+ protein. Case 2: A 21-year-old primigravida is seen in the outpatient prenatal clinic for a routine visit. She is at 32 weeks’ gestation, confirmed by first trimester sonogram. For the past 24 h she had experienced severe, unremitting occipital headache and mid-epigastric pain not relieved by acetaminophen, and she has also seen light flashes and spots in her vision. She has gained 10 pounds since her last visit two weeks ago. On examination her BP is 165/115 mm Hg. She has 2+ pedal edema, and her fingers appear swollen. Fundal height is 29 cm. Fetal heart tones are regular at 145 beats/min. A spot urine dipstick shows 4+ protein. 23 Pre-eclampsia It is a multisystem disorder of unknown etiology characterized by development of hypertension to the extent of 140/90 mm of Hg or more recorded on at least two separate occasions and at least 4 hours apart and in the presence of at least 300 mg protein in a 24-hour collection of urine, arising de novo after the 20th week of pregnancy in a previously normotensive, non-protein uric women and resolving completely by the sixth postpartum week 24 pre-eclampsia 25 Pathophysiology The uteroplacental bed Immunological factor Genetic factor Renin- angiotensin system Atrial natriuretic peptide (ANP) Prostaglandins Neutrophils 26 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. 27 28 Pathogenesis of Pre- eclampsia 29 Alarming: Headache esp. frontal. Disturbed sleep Diminished urinary output Epigastric RUQ pain. Nausea and vomiting Eye symptoms- blurring, flashing lights, dimness of vision or at times complete blindness. regained within 4-6 weeks following delivery 30 Complications Maternal: 1. Cerebral hemorrhage (50% of deaths). 2. LVF / Pulm. edema. 3. Liver / renal dysfunction. 4. Seizures. 5. DIC. 6. Abruptio placenta: ante-partum painful vaginal bleeding. Fetal: due to placental insufficiency: 1. Fetal loss. 2. IUGR. 3. Prematurity. 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. 32 Table 1. Initial lab evaluation of pt with pre-eclampsia / eclampsia Blood Urine Other CBC & Plt count: Sediment. US. if ↓ Plts, ↓ Hb HELLP 24-hr protein. Test of fetal well- synd being: 24-hr creatinine Electrolytes: (may ↓). NST. look @ BUN (may ↑) BPP. Cord color Doppler. ↑ Uric acid. Creatinine. LFT. 33 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. 34 Management of PE Outpatient management - Appropriate if: BP110 diastolic) antihypertensive therapy should be started. Medication does not cure the condition but aims to prevent hypertensive complications of PE. Aim BP. 135/85 mmHg or less 37 Management of severe PE blood pressure of 160/ 110mmHg or more in the presence of significant proteinuria (>1g/24hor >or=2+ on dipstick) or if maternal complications occur. Offer pharmacological treatment to all women. Aim for BP of 135/85 mmHg or less. Blood pressure measurement: Every 15–30 minutes until BP is less than 160/110 mmHg, then at least 4 times daily while the woman is an inpatient, depending on clinical circumstances. Dipstick proteinuria testing: Only repeat if clinically indicated Blood tests: Measure full blood count, liver function and renal function 3 times a week. Strict fluid balance chart, consider a catheter. Fetal assessment: ultrasound assessment of the fetus, evidence of IUGR, estimate weight if severely preterm, assess condition using fetal and umbilical artery doppler. CTG monitoring of the fetus. 38 Management of PE Antihypertensive drugs Decrease the maternal cerebral and cardiovascular complications but do not affect the fetal outcome Labetalol is an alpha and beta-blocking agent. It has a good safety record in pregnancy and can be given orally and intravenously. It is the first drug of choice in most national guidelines including the current National Institute for Health and Care Excellence (NICE) guideline Alpha-methyl-dopa: It reduces the central sympathetic drive Dose: 250-500 mg every 6-8 hours up to a maximum dose of 4gm/day. Its effect appears after 48 hours A loading single dose of 2 gm may act within 1-2 hours Side effects: headache, asthenia and nightmares 39 Antihypertensive drugs – Hydralazine It is a vasodilator, increases renal and uteroplacental blood flow Dose: Initially 5 to 10 mg by slow intravenous injection Oral hydralazine can be used in the chronic situation as a second line treatment in a dose of 25-75 mg/ 6 hours Side effects: tachycardia, headache, flushing, nausea and vomiting Calcium channel blockers (Nifedipine): vasodilator acting by blocking the Ca influx into smooth muscle cells It can be given sublingually (acts within 10 minutes) or orally (acts within 30 minutes) in a dose of 10-20 mg 2-3 times daily Side effects: headache and flushing 40 Prophylactic Proper antenatal care: To detect the high-risk patients Early detection of cases who have already developed PIH and examine them more frequently. Low dose aspirin (75 mg single dose daily): 41 Severe PE /Timing of birth Indications for immediate delivery: inability to control maternal blood pressure. maternal pulse oximetry less than 90% progressive deterioration in liver function, renal function, hemolysis, or platelet count. ongoing neurological features, such as severe intractable headache, repeated visual scotomata, or eclampsia. HELLP syndrome. placental abruption reversed end-diastolic flow in the umbilical artery Doppler velocimetry, a non reassuring cardiotocography, or IUD. 42 Management of PE Timing of birth Before 34weeks:Continue surveillance, Offer intravenous magnesium sulfate and a course of antenatal corticosteroids. From 34 to 36+6 weeks: Continue surveillance unless there are indications for planned early birth. When considering the option of planned early birth, consider the woman's and baby's condition, risk factors (such as maternal comorbidities, multifetal pregnancy) and availability of neonatal unit beds. a course of antenatal corticosteroids. 37 weeks onwards ; Initiate birth within 24–48 hours. 43 Intrapartum care Close monitoring of the fetus is indicated Proper analgesia to the mother Anti-hypertensives may be given if needed 2nd stage of labor may be shortened by forceps Methergine (Ergometrine) is better avoided as it may increase the blood pressure. 44 Postnatal investigation, monitoring and treatment In women who did not take antihypertensive treatment: measure blood pressure: at least 4 times a day while the woman is an inpatient start antihypertensive treatment if blood pressure is 150/ 100mmHg or higher. Ask women about severe headache and epigastric pain each time blood pressure is measured. In women with pre-eclampsia who took antihypertensive treatment and have given birth, measure blood pressure at least 4 times a day while the woman is an inpatient every 1–2 days for up to 2 weeks after transfer to community care until the woman is off treatment and has no hypertension. 45 continue antihypertensive treatment. consider reducing antihypertensive treatment if their blood pressure falls below 140/ 90 mmHg. reduce antihypertensive treatment if their blood pressure falls below 130/80 mmHg. If a woman has taken methyldopa to treat pre-eclampsia, stop within 2 days after the birth and change to an alternative treatment if necessary measure platelet count, transaminases and serum creatinine 48–72 hours after birth. 46 case 21-year-old primigravida is brought to the emergency department after suffering from a generalized tonicclonic seizure at 32 weeks’ gestation. The seizure was preceded by a severe headache. She lost control of her bowels and bladder. She has gained 10 pounds since her last prenatal visit two weeks ago. On examination she is unresponsive and in a postictal state. BP is 185/115 mm Hg and spot urine dipstick shows 4+ protein 47 Eclampsia Premonitory stage: The patient becomes unconscious. There is twitching of the muscles of the face, tongue, and limbs. Eyeballs roll or are turned to one side and become fixed. This stage lasts for about 30 seconds. Tonic stage: The whole body goes into a tonic spasm — the trunk- opisthotonus, limbs are flexed and hands clenched. Respiration ceases and the tongue protrudes between the teeth. Cyanosis appears. Eyeballs become fixed. This stage lasts for about 30 seconds 48 Clonic stage: All the voluntary muscles undergo alternate contraction and relaxation. The twitchings start in the face then involve one side of the extremities and ultimately the whole body is involved in the convulsion. Biting of the tongue occurs. Breathing is stertorous and blood stained frothy secretions fill the mouth; cyanosis gradually disappears. This stage lasts for 1–4 minutes. Stage of coma: Following the fit, the patient passes on to the stage of coma. It may last for a brief period or in others deep coma persists till another convulsion. On occasion, the patient appears to be in a confused state following the fit and fails to remember the happenings. Rarely, the coma occurs without prior convulsion 49 Eclampsia Management Control Hypertension Improve intravascular volume Prevent convulsions Prevent complications Deliver viable fetus Eclampsia/ Management Call for help. put patient in left lateral recumbent position ABC plus IV access. Investigations : Blood: CBC, AST, ALT, LDH, Creatinine, Uric Acid, Urine analysis - protein MgSo4 for control of fits and preventing further seizures. Loading 4g over 5-10min followed by an infusion 1g/h for 24h. Further 2g if further fits. Strict monitoring; pulse, BP, RR and O2 saturation/15 min. 51 Foley catheter or urometer and hourly urine. Assessment of reflexes every hour for Mg toxicity If Bp> 160/110 give antihypertensive Fluid restriction, 80ml/h, risk for pulmonary edema. Suction: oropharyngeal CTG monitoring Deliver when the mother is stable. Vaginally if cervix is favorable if HELLP coexist, renal and liver physicians Third stage, 5-10U oxytocin, no Ergometrine because of increase BP. 52 Drug Dose Comments 10 – 20 mg IV, then 20 – 80 mg every 20 – 30 minutes to a Considered a first-line agent, Tachycardia is less common and maximum dose of 300 mg. OR fewer adverse effects. Constant infusion 1 – 2 mg/min IV. Contraindicated in patients with asthma, heart disease, or Labetalol congestive heart failure. 5 mg IV or IM, then 5 – 10 mg IV every 20 – 40 min. Higher or frequent dosage associated with maternal OR hypotension, headaches, and fetal distress – may be more Constant infusion 0.5 – 10 mg/h common than other agents. Hydralazine 10 – 20 mg orally, repeat in 30 minutes if needed, then 10 – May observe reflex tachycardia & headache. Nifedipine 20 mg every 2 – 6 hours. 53 Treatment of magnesium toxicity: confusion , loss of reflexes, respiratory depression and hypotension. Stop MgSO4 IV 1 g 10% calcium gluconate slow Administer Oxygen Secure airway Ventilation Estimation of serum magnesium and creatinine levels 54 HELLP Syndrome Is a variant of severe preeclampsia which manifests with: He-hemolysis EL-elevated liver enzymes LP-low platelets 5-20% of preeclamptic pregnancies. Maternal mortality 1%, perinatal mortality 10-60%. Liver enzymes increase, platelets decrease before hemolysis occurs. Syndrome usually self limiting, but permanent liver or renal damage may occur 55 HELLP Syndrome Symptoms: Epigastric or RUQ pain Nausea and vomiting Urine is tea-colored due to hemolysis. Signs: Tenderness in RUQ Increase BP and other features of PE )Hypertension may be mild or even absent( Eclampsia may co-exist The management : stabilizing the mother, correcting any coagulation deficits and assessing the fetus for delivery. 56 Treatment is supportive and as for eclampsia (MgSo4 is indicated). Although platelet levels may be very low, platelet infusions are only requires if bleeding, or for surgery and

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