Hypertensive Disorders in Pregnancy PDF - 2024

Hypertensive disorders in pregnancy Dr.Khalida Hassan Muho Specialist OB\GYN  LEARNING OBJECTIVES To understand the classification of hypertension in pregnancy. To appreciate and be able to differentiate the different risks associated with various types of hypertensive d...

Hypertensive disorders in pregnancy Dr.Khalida Hassan Muho Specialist OB\GYN  LEARNING OBJECTIVES To understand the classification of hypertension in pregnancy. To appreciate and be able to differentiate the different risks associated with various types of hypertensive disorders in pregnancy. To understand the pathophysiology of pre- eclampsia. To be aware of the clinical presentation of pre-eclampsia and understand the principles of management. To understand the long-term risks to both mother and baby from preeclampsia. Hypertension is common in pregnancy. Approximately 1 in 10 women will have one or more episodes of raised blood pressure prior to delivery. The majority have a benign condition called gestational hypertension, which is not associated with adverse outcomes. However, about one- third of these women (3% overall) will develop pre-eclampsia. Pre-eclampsia is a leading cause of maternal death. The World Health Organization (WHO) estimates that globally between 50,000 and 75,000 women die of this condition each year Furthermore, pre-eclampsia is frequently accompanied by fetal growth restriction (FGR), which is responsible for considerable perinatal morbidity and mortality. An increasing number of women enter pregnancy with chronic hypertension and this is associated with increased risks for both mother and baby, including an increased risk of preeclampsia and FGR.  Classification of hypertension in pregnancy Non-proteinuric pregnancy-induced hypertension. Pre-eclampsia. Chronic hypertension Non-proteinuric pregnancy-induced hypertension (otherwise known as gestational hypertension) is hypertension that arises for the first time in the second half of pregnancy and in the absence of proteinuria. It is not associated with adverse pregnancy outcome and mild and moderate increases in blood pressure in this setting do not require treatment. However, up to one-third of women who present with gestational hypertension will progress to pre-eclampsia. Women who have confirmed hypertension in the first half of pregnancy most likely have chronic hypertension. The majority will have essential hypertension but this is a diagnosis of exclusion and secondary causes should be excluded. Chronic hypertension, of whatever type, can predispose to the later development of superimposed pre-eclampsia. Even in the absence of superimposed preeclampsia, chronic hypertension is associated with increased maternal and fetal morbidity and pregnancies complicated by chronic hypertension should therefore be regarded as high risk. The physiological fall in blood pressure that occurs in the first trimester secondary to peripheral vasodilatation can mask chronic hypertension. For example, a booking blood pressure of 138/88 mmHg, while still technically within normal limits, raises the suspicion of an underlying hypertensive tendency  Degrees of hypertension Mild: diastolic blood pressure 90–99 mmHg, systolic blood pressure 140–149 mmHg. Moderate: diastolic blood pressure 100– 109 mmHg, systolic blood pressure 150–159 mmHg. Severe: diastolic blood pressure ≥110 mmHg, systolic blood pressure ≥160 mmHg Pre-eclampsia Pre-eclampsia complicates approximately 2–3% of pregnancies globally, around 70,000 women die annually of pre-eclampsia, making it a leading cause of maternal death in low- resource settings. Pre-eclampsia is defined as hypertension of at least 140/90 mmHg 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 woman and resolving completely by the sixth postpartum week. Pre-eclampsia is multisystem disorder unique to pregnancy and has varying clinical presentations. The diagnosis is based on the presence of new-onset hypertension in the latter half of gestation, accompanied by new-onset proteinuria and/or other evidence of organ dysfunction. When evaluating a pregnant woman with new-onset hypertension who does not have proteinuria, preeclampsia can be  thrombocytopenia or disseminated intravascular coagulation (DIC ) Elevated transaminases or other signs of hepatic injury, CNS symptoms An elevated or rising serum creatinine level or pulmonary oedema. Risk factors for pre-eclampsia  First pregnancy.  Multiparous with a previous history of pre- eclampsia.  Pre-eclampsia in any previous pregnancy.  10 years or more since last baby.  Age 40 years or more.  Body mass index (BMI) of 35 or more.  Family history of pre-eclampsia (in mother or sister).  Booking diastolic blood pressure of 80 mmHg or more.  Booking proteinuria ( of ≥1+ on more than one occasion or quantified at ≥0.3 g/24 h).  Multiple pregnancy.  Certain underlying medical conditions: pre-existing hypertension; pre-existing renal disease; pre-existing diabetes; antiphospholipid antibodies Pathophysiology General thinking suggests that the development of pre-eclampsia is a two-stage process, which originates in early pregnancy In the first stage, trophoblast invasion is patchy and the spiral arteries retain their muscular walls. This is thought to prevent the development of a high-flow, low-impedance uteroplacental circulation and leads to uteroplacental ischaemia. The reason why trophoblasts invade less effectively in these pregnancies is not known but may reflect an abnormal adaptation of the maternal immune system. In the second stage, uteroplacental ischaemia results in oxidative and inflammatory stress, with the involvement of secondary mediators leading to endothelial dysfunction, vasospasm and activation of the coagulation system. As the target cell of the disease process, the vascular endothelial cell, is so ubiquitous, pre-eclampsia is a truly multisystem disorder, affecting multiple organ systems, often Physiological change of spiral arteries by invading trophoblasts The proposed aetiology of pre- eclampsia  Cardiovascular system Normal pregnancy is characterized by marked peripheral vasodilatation resulting, in a fall in total peripheral resistance despite an increase in plasma volume and cardiac rate. Pre-eclampsia is characterized by marked peripheral vasoconstriction, resulting in hypertension.The intravascular high pressure and loss of endothelial cell integrity results in greater vascular permeability and  ` Renal system In the kidney, a highly characteristic lesion called 'glomeruloindotheliosis' is seen. This relatively specific for pre- eclampsia and is associated with impaired glomerular filtration and selective loss of intermediate weight proteins, such as albumin and transferrin, leading, to proteinuria. This in turn, causes a reduction in plasma oncotic pressure and exacerbates the development of oedema.  Haematological system In the event of endothelial damage, platelets adhere to the damaged area. Furthermore, diffuse vascular damage is associated with laying down of fibrin. Pre-eclampsia in association with increased fibrin deposition and a reduction in the platelet count may accompany and occasionally predate the onset of disease.  The liver In the liver, subendothelial fibrin deposition is associated with elevation of liver enzymes. This can be associated with haemolysis and a low platelet count due to platelet consumption (and subsequent widespread activation of the coagulation system). The presence of these finding,, called HELLP syndrome (haemolysis, elevation of liver enzymes and low platelets). HELLP syndrome is a particularly severe form of pre-eclampsia, occurring in just 2-4 per cent of women with the disease. It is associated with a high Fetal loss rate for up to 60 per cent).  Neurological system The development of convulsions in a woman with pre-eclampsia is defined as eclampsia. Vasospasm and cerebral oedema have both been implicated in the pathogenesis of eclampsia. Retinal haemorrhages, exudates and papilloedema are characteristic of hypertensive encephalopathy and are rare in pre­eclampsia, suggesting that hypertension alone is not responsible for the cerebral pathology.  Other specific changes associated with PE Cardiovascular system: generalized vasospasm , increased peripheral resistance, reduced central venous/pulmonary wedge pressures Haematological system: platelet activation and depletion coagulopathy , decreased plasma volume, increased blood viscosity Renal system: proteinuria, decreased glomerular filtration rate, decrease urate excretion Hepatic: per portal necrosis, subcapsular haematoma Central nervous: cerebral oedema, cerebral haemorrhage  Symptoms of PE The classic symptorns of pre-eclampsia include a frontal headache, visual disturbance and epigastric pain However, the majority of women with pre-eclampsia are asymptomatic or merely complain of general, vague flu- like symptoms.  Signs of PE Hypertension is usually the first sign occasionally is absent or transient until the late stages of the disease. Rapidly progressive oedema of the face and hands Epigastric tenderness Hyperreflexia and clonus Uterus and fetus may fell small for gestational age  Testing for proteinuria Dipstick Instant result but quantitatively urinalysis inaccurate Trace Seldom significant 1+ Possible significant proteinuria, warrants quantifying >2+ Probable significant proteinuria, warrants quantifying protein: Fast (within 1 hour) result creatinine semiquantitave Ratio >30 mg/mol Probable significant proteinuria, 24-hour collection Slow 300 mg/24 h Confirmed significant proteinuria Management and treatment There is no cure for pre-eclampsia other than to end the pregnancy by delivering the baby (and placenta). This can be a significant problem if pre-eclampsia occurs early in pregnancy, particularly at gestations below 34 weeks. Therefore, management strategies are aimed at minimizing risk to the mother in order to permit continued fetal growth. In severe cases, this is often not possible.  The principles of management of pre- eclampsia are: Early recognition of the symptomless syndrome. Awareness of the serious nature of the condition in its severest form. Adherence to agreed guidelines for admission to hospital, investigation and the use of antihypertensive and anticonvulsant therapy. Well-timed delivery to pre-empt serious maternal or fetal complications. Postnatal follow-up and counseling for future pregnancies  A diagnosis of pre-eclampsia usually requires admission. Patients with mild hypertension, minimal protein and normal haematological and biochemical parameters may be monitored as outpatient but will require frequent attendance for fetal and maternal assessment. Women with moderate or severe hypertension, significant proteinuria or abnormal haematological or biochemical parameters require admission and inpatient management. The management of pregnancy complicated by pre-eclampsia  Investigation for pre-eclampsia To monitor maternal complications: Full blood count(with particular emphasis on falling platelet count and rising haematocrit) If platelet values are normal, additional clotting studies are not indicated Serum renal profile(including serum uric acid level to assess the severity of disease ) Serum liver profile Frequent repeat proteinuria quantification is probably unhelpful once diagnosis of pre- eclampsia has been made  To monitor fetal complications: U/S assessment of: fetal size amniotic fluid volume maternal and fetal Dopplers Antenatal cardiotocography used in conjunction with U/S surveillance, provides a useful but by no means infallible indication of fetal well-being. A loss of baseline variability or decelerations may indicate fetal hypoxia  Treatment of hypertension The commonest cause of death in women who die of pre-eclampsia in the UK is cerebral bleeding secondary to uncontrolled systolic blood pressure. Therefore, the aim of antihypertensive therapy is to lower the blood pressure and reduce the risk of maternal cerebrovascular accident without reducing uterine blood flow and compromising the fetus.  There are a variety of antihypertensive used in the management of pre-eclampsia. Methyldopa is a centrally acting antihypertensive agent. It has a long established safety record in pregnancy However, it can only be given orally, it takes upwards of 24 hours to take effect and has a range of unpleasant side effects, including sedation and depression. These properties limit its usefulness Labetolol is an alpha-blocking and beta- blocking agent. It too 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, Hypertension in Pregnancy. Nifedipine is a calcium-channel blocker with a rapid onset of action. It can, however, cause severe headache that may mimic worsening disease In severe cases of fulminating disease, an intravenous infusion of hydralazine or labetalol can be titrated rapidly against changes in the blood pressure. Eclampsia Eclampsia refers to the occurrence of one or more generalized convulsions and /or coma in the setting of pre-eclampsia and in the absence of other neurological conditions.it is a serious complication of PE The incidence is 1/2000 deliveries and complicate 1-2% of PE Condition that proceed convulsions called imminent eclampsia which include : sever frontal headache, irritability, visual disturbance, restlessness, twitching, drowsiness, epigastric pain, oliguria and tachycardia. Cerebral haemorrhage has been reported to be the most common cause of death in patients with eclampsia (previously this was pulmonary oedema) and stroke is known to be the most common cause of death (45%) in women with haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome.  Prevention: low threshold for administration of magnesium sulphate in women with preeclampsia who are thought to be unstable or suffering from severe preeclampsia. However, remember all patients with preeclampsia regardless of perceived severity are at risk of eclampsia.  Risk factors: difficult to predict, uncontrolled hypertension, two or fewer prenatal care visits, primigravidity, obesity, black ethnicity, history of diabetes and age 40 years pre-existing diabetes Multiple pregnancy Connective tissue disease e.g antiphospholipid syndrome  Coarctation of the aorta Blood pressure > 1 60/1 00 mmHg in early pregnancy Pre-pregnancy BMI > 35 Previous pre-eclampsia Antiphospholipid syndrome  In mild cases (150/100 mmHg, antihypertensive medication should be offered to reduce the risk of severe hypertension and the attendant risks of intracerebral haemorrhage, although treatment does not prevent placental abruption or superimposed pre-eclampsia, nor does it influence perinatal outcome. Preferred antihypertensive agents include labetolol, nifedipine and methyldopa (centrally acting agent). The aim of antihypertensive medication is to maintain the blood pressure below 160 mmHg systolic and 80–100 mmHg diastolic.  The obstetric management of pre- existing hypertension involves close monitoring for the development of superimposed pre-eclampsia and FGR. In women requiring antihypertensive medication, delivery is usually offered around 39 weeks, but may need to be earlier if complications have developed.  Following delivery, the maternal blood pressure often decreases, but careful surveillance is required as it tends to increase again on the third or fourth postpartum day. Breastfeeding is encouraged and medication should be changed to those drugs that are considered safe. THANK YOU  A16-year-old primigravida present to emergency unit at 35 weeks gestation. Her blood pressure is 170 /110 and she has 4+proteinuria on a clean catch specimen of urine. She has significant swelling of her face and extremities. She denies having contraction. Her cervix is closed and unaffected. The baby is cephalic by bed bedside ultrasonography. She says the baby movements have decrease in the past 24 hours. Q1 What is the next step in the Q2 What is the best position to measure her blood pressure and why? Q3 Clarify the physiological effect of pregnancy on blood pressure? Q4 Dose the swelling of extremities significant during pregnancy? Q5Is there a role of antihypertensive in the management of this case and what is the best drug of choice, why? Q 6 Is there an indication for termination of pregnancy in this gestational age?