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Hypertension in Pregnancy PowerPoint Presentation

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Description : Hypertension in Pregnancy (Hypertensive disorders in pregnancy cover a spectrum of conditions)

Tags : hypertensive,PREECLAMPSIA,pregnancy,high blood pressure,weeks of pregnancy,pregnancy symptoms

Published on : Feb 13, 2021 | Views : 3624 | Downloads : 34

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HYPERTENSION IN PREGNANCY
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EPIDEMIOLOGY Hypertensive disorders in pregnancy cover a spectrum of conditions including: Gestational hypertension Preeclampsia Eclampsia Chronic Hypertension Preeclampsia superimposed on Chronic Hypertension HELLP Preeclampsia complicates 3% of pregnancies All hypertensive disorders affect about 5-10% of pregnancies.
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MATERNAL PERSONAL RISK FACTORS PRIMIPARITY Pregnancy-induced hypertensive disorders especially preeclampsia  documented to occur primarily in first pregnancies. Concept of primiparity  cornerstone of this disease Recent research focus on angiogenic factors Soluble fms-like tyrosine kinase-1 Endogenous anti-angiogenic protein Enters maternal circulation after being overproduced in placenta Inhibitor of placental growth factor (PIGF) and vascular endothelial growth factor (VEGF) Now accepted as contributing factor in pathophysiology of preeclampsia
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MATERNAL PERSONAL RISK FACTORS PRIMIPATERNITY Relevant risk factor for preeclampsia Primiparas and multiparas having first child with a new father are at high risk Immunological habituation to paternal antigens through contact between sperm and female genital tract New sexual partner  expose mother to new paternal antigens which may not be tolerant Changing father for a woman with no history of preeclampsia  increase risk to the same level that she would had as a primipara. Woman who become pregnant by a man who has fathered a preeclamptic pregnancy  1.8% risk
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MATERNAL PERSONAL RISK FACTORS HISTORY OF PREECLAMPSIA Previous pregnancies complicated by preeclampsia or HELLP  increased risk for recurrence in subsequent pregnancies (14%) Severe preeclamptic womein in first pregnancy  50% recurrence rate OBESITY (BMI ≥30) Relationship between maternal weight and risk of preeclampsia is progressive. Increases from 4.3% for BMI <19.8 to 13.3% in BMI >35.
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MATERNAL PERSONAL RISK FACTORS FAMILY HISTORY OF PREECLAMPSIA Predisposition to hereditary hypertension PE is a complex disorder (many complex disorders cluster in families) No Mendelian patterns of inheritance. Environmental factors and many different genes are responsible for familial effect. ETHNICITY Black women have a risk of twice as high as that of white women More likely to have hypertension that is independent of pregnancy
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MATERNAL PERSONAL RISK FACTORS MATERNAL AGE Women aged ≥40 twice the risk of developing preeclampsia whether primiparous or multiparous SMOKING Causes variety of adverse outcomes but associated with reduced risk of hypertension during pregnancy. OTHER UNRESOLVED RISK FACTORS: Intepregnancy intervals <2 years or > 10 years Previous miscarriage and induced abortions Environmental risk factors
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MATERNAL MEDICAL RISK FACTORS Underlying Medical Conditions Diabetes mellitus GDM patients who developed preeclampsia were more obese, gained more weight during pregnancy and had more severe GDM as compared to GDM patients who did not Likelihood of preeclampsia  4x if DM is present before pregnancy Antiphospholipid Antibody Syndrome There’s an association between preeclampsia and lupus anticoagulant, anticardiolipin and/or anti-B2
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MATERNAL MEDICAL RISK FACTORS Systemic Lupus Erythematosus Renal Disease Greater risk for complications related to pregnancy such as preeclampsia Prevalence of renal disease was higher in women who developed preeclampsia Maternal Infection Urinary tract infections and periodontal diseases increased the risk of developing preeclampsia
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PLACENTAL/FETAL RISK FACTORS Multiple Pregnancies sFlt-1 concentrations in twin pregnancy maternal serum were 2.2 times higher than those in singleton pregnancy maternal serum samples. Increased risk of preeclampsia in twin pregnancies  due to increased placental mass that leads to increased circulating levels of sFlt-1 Molar Pregnancy Associated with very early-onset preeclampsia Both have dysfunctional placentas that are integral to each disease process Both molar pregnancy and preeclampsia are caused by an excess of circulating sFlt-1.
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CLASSIFICATION OF HYPERTENSION IN PREGNANCY
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PRE-ECLAMPSIA-ECLAMPSIA Elevation of BP Proteinuria: objective marker taken as evidence of systemic-wide endothelial leak  preeclampsia syndrome In recognition of systemic nature of Preeclampsia  dependency on proteinuria was eliminated In its absence: diagnosed as HPN with other multi-organ involvement
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PRE-ECLAMPSIA-ECLAMPSIA Elevation of BP Proteinuria: objective marker taken as evidence of systemic-wide endothelial leak  preeclampsia syndrome In recognition of systemic nature of Preeclampsia  dependency on proteinuria was eliminated In its absence: diagnosed as HPN with other multi-organ involvement
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PRE-ECLAMPSIA Multisystem disorder (affects 2%–5% of pregnant women) One of the leading causes of maternal and perinatal morbidity and mortality, especially when the condition is of early onset. Current theory suggests a two-stage process. 1st stage: caused by shallow invasion of the trophoblast  in inadequate remodeling of the spiral arteries. 2nd stage: involves the maternal response to endothelial dysfunction and imbalance between angiogenic and antiangiogenic factors
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PRE-ECLAMPSIA ISSHP : defined PE as SBP at ≥140 mm Hg and/or DBP at ≥90 mm Hg on at least two occasions measured 4 hours apart in previously normotensive women and is accompanied by one or more of the following new-onset conditions at or after 20 weeks of gestation: 1. Proteinuria (i.e. ≥30 mg/mol protein:creatinine ratio; ≥300 mg/24 hour; or ≥2 + dipstick); When quantitative methods not available or rapid decisions are required  urine dipstick can be substituted (however, has high false (+) and (-) test results)
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PRE-ECLAMPSIA 2. Evidence of other maternal organ dysfunction, including: Acute kidney injury (creatinine ≥90 μmol/L; 1 mg/dL); Liver involvement (elevated transaminases, e.g. ALT/AST >40 IU/L) with or w/o right upper quadrant or epigastric abdominal pain; Neurological complications (e.g. eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, and persistent visual scotomata); or Hematological complications (thrombocytopenia–platelet count <150 000/μL, disseminated intravascular coagulation, hemolysis); or
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PRE-ECLAMPSIA 3. Uteroplacental dysfunction Fetal growth restriction Abnormal umbilical artery Doppler waveform analysis, or Stillbirth
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PRE-ECLAMPSIA PE can be subclassified into: 1. Early-onset PE (with delivery at <34+0 weeks of gestation); 2. Preterm PE (with delivery at <37+0 weeks of gestation); 3. Late-onset PE (with delivery at ≥34+0 weeks of gestation); 4. Term PE (with delivery at ≥37+0 weeks of gestation).
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PRE-ECLAMPSIA Obstetricians managing women with preterm PE are faced with the challenge of balancing the need to achieve fetal maturation in utero with the risks to the mother and fetus of continuing the pregnancy longer. These risks include progression to eclampsia, development of placental abruption and HELLP (hemolysis, elevated liver enzyme, low platelet) syndrome.
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PRE-ECLAMPSIA On the other hand, preterm delivery is associated with higher infant mortality rates and increased morbidity resulting from: Small for gestational age (SGA), Thrombocytopenia, Bronchopulmonary dysplasia, Cerebral palsy, and An increased risk of various chronic diseases in adult life, particularly type 2 diabetes, cardiovascular disease, and obesity.
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Preeclampsia with Severe Features In US, preeclampsia remains the leading cause of maternal and perinatal morbidity and mortality Locally, the incidence of severe PE is 2.5% Remains the 2nd most common cause of maternal death High rate of perinatal morbidity and mortality is due to iatrogenic prematurity.
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Preeclampsia with Severe Features Markers that define the Severe Features SBP or DBP > 160 or 110 mmHg respectively occurring 2x, 4 hours apart at bed rest Thrombocytopenia (PC <100,000 uL) Impaired liver function as either otherwise unexplained RUQ pain unresponsive to medications or hepatic transaminases 2x normal RUQ pain or epigastric pain  due to periportal and focal parenchymal necrosis, hepatic cell edema or Glisson’s capsule or a combination
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Preeclampsia with Severe Features Markers that define the Severe Features Progressive renal insufficiency Serum creatinine >1.1mg/dL or 2x of serum creatinine in absence of other renal disease. Pulmonary Edema New-onset cerebral or visual disturbances
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Preeclampsia with Severe Features The distinction between mild and severe PR is important because it dictates management One must not be complacent with mild PE because apparently mild disease may progress rapidly to severe disease.
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ECLAMPSIA Preeclampsia and convulsion that cannot be attributed to another cause Convulsion New onset Generalized (tonic-clonic, focal or multifocal) in the absence of other causative conditions such as epilepsy, cerebral ischemia and infarction, intracranial haemorrhage or drug use Occur before, during, or after labor Although generally occurring w/in 48 hours of delivery  10% of postpartum eclampsia may initially occur beyond this time frame
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ECLAMPSIA Significant cause of maternal death particularly in low-resource settings May lead to severe maternal hypoxia, trauma and aspiration pneumonia Preceded by premonitory signs of cerebral irritation such as: Severe and persistent occipital or frontal headaches Headaches are believed to reflect the development of elevated cerebral perfusion pressure, cerebral edema and hypertensive encephalopathy Blurred vision Photophobia Altered mental status
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ECLAMPSIA Significant cause of maternal death particularly in low-resource settings May lead to severe maternal hypoxia, trauma and aspiration pneumonia Preceded by premonitory signs of cerebral irritation such as: Severe and persistent occipital or frontal headaches Headaches are believed to reflect the development of elevated cerebral perfusion pressure, cerebral edema and hypertensive encephalopathy Blurred vision Photophobia Altered mental status
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ECLAMPSIA Posterior reversible encephalopathy syndrome (PRES) Constellation of range of clinical neurologic signs and symptoms such as vision loss or deficit, seizure headache and altered sensorium or confusion Diagnosed by presence of vasogenic edema and hyperintensities in the posterior aspects of the brain on MRI Reversible cerebral vasoconstriction Reversible multifocal narrowing of arteries of brain with signs and symptoms that include thunderclap headache and less commonly focal neurologic deficits related to brain edema, stroke or seizure
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ECLAMPSIA Posterior reversible encephalopathy syndrome (PRES) Constellation of range of clinical neurologic signs and symptoms such as vision loss or deficit, seizure headache and altered sensorium or confusion Diagnosed by presence of vasogenic edema and hyperintensities in the posterior aspects of the brain on MRI Reversible cerebral vasoconstriction Reversible multifocal narrowing of arteries of brain with signs and symptoms that include thunderclap headache and less commonly focal neurologic deficits related to brain edema, stroke or seizure
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ECLAMPSIA Treatment with PRES and reversible cerebral vasoconstriction Medical control of HPN Antiepileptic medication Long-term neurologic follow-up
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GESTATIONAL HYPERTENSION 20 weeks gestations in absence of proteinuria or other systemic findings alternatively used to support diagnosis of preeclampsia SBP ≥140mmHg or DBP ≥90mmHg or both on 2 occassions at least 4 hours apart after 20 weeks AOG with previously normal BP Considered severe when SBP reaches 160mmHg or BDP reaches 110mmHg or both
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GESTATIONAL HYPERTENSION HPN in pregnancy that does not show signs of developing preeclampsia and elevated BP resolves by 12 weeks postpartum Up to 50% women with GH will eventually develop proteinuria or other end-organ dysfunction consistent with the diagnosis of preeclampsia  this progression is more likely when the HPN is diagnosed before 32 weeks AOG.
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PATHOPHYSIOLOGY Several mechanisms Chronic uteroplacental ischemia Immune maladaptation VLDL toxicity Genetic imprinting Increased trophoblast apoptosis or necrosis Exaggerated maternal inflammatory response to deported trophoblast Imbalances of angiogenic factors
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PATHOPHYSIOLOGY Several mechanisms Chronic uteroplacental ischemia Immune maladaptation VLDL toxicity Genetic imprinting Increased trophoblast apoptosis or necrosis Exaggerated maternal inflammatory response to deported trophoblast Imbalances of angiogenic factors
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PATHOPHYSIOLOGY Vascular Changes Women with preeclampsia or eclampsia typically lack hypervolemia associated with normal pregnancy  hemoconcentration is a normal finding The interaction of various vasoactive agents such as prostacyclin, thromboxane A2, NO, endothelins  intense vasospasm Attempts to correct contraction of the intravascular space in PE with vigorous fluid therapy are likely to be ineffective  DANGEROUS because of frequent capillary leak and decreased colloid oncotic pressure Aggressive fluid therapy may result in elevation of pulmonary capillary wedge pressure and increased risk of pulmonary edema
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PATHOPHYSIOLOGY HEMATOLOGIC CHANGES Thrombocytopenia and hemolysis may occur Thrombocytopenia result from increased platelet activation, aggregation and consumption  marker of disease severity Interpretation of Hematocrit  hemolysis and hemoconcentration may occur Hematocrit may not appear decreased despite hemolysis because of baseline hemoconcentration LDH is present in RBCs High serum LDH  sign of hemolysis
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PATHOPHYSIOLOGY HEPATIC CHANGES ALT/AST elevated AST: dominant transaminase released into the peripheral circulation in liver dysfunction due to preeclampsia and is related to periportal necrosis Increased serum levels of LDH in PE Caused by hepatic dysfunction (LDH derived from ischemic or necrotic tissues or both) and hemolysis (LDH from RBC destruction)
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PATHOPHYSIOLOGY HEPATIC CHANGES Increase bilirubin secondary to significant hemolysis Alterations in hepatic synthetic function Abnormal PT, PTT, Fibrinogen Evaluation of these coagulation parameters is probably useful when: Platelet count is <150,000 x109L Significant liver dysfunction Suspected placental bruption
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PATHOPHYSIOLOGY RENAL CHANGES Histopathology: Glomerular endotheliosis consist of swollen, vacuolated endothelial cells with fibrils, swollen mesangial cells, subendothelial deposits of protein reabsorbed from the glomerular filtrate and tubular casts. Proteinuria Non-selective Result of increased tubular permeability to most large-molecular-weight proteins (albumin, globulin, transferrin, haemoglobin) Decrease urinary calcium Increased tubular reabsorption of Calcium
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PATHOPHYSIOLOGY RENAL CHANGES Plasma Uric acid  normally increase in late pregnancy Thought to be due to increased rates of fetal or placental production or both, decreased binding to albumin and a decrease in uric acid clearance. Hyperuricemia in PE Increased production Increased reabsorption and decreased production of uric acid in PCT
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PATHOPHYSIOLOGY RENAL CHANGES Contraction of intravascular space 2nd to vasospasm  worsening renal sodium and water retention Oliguria in severe PE Consequence of intrarenal vasospasm with approx. 25% reduction in GFR Transient oliguria (<100ml over 4 hours) is common in labor or the first 24 hours of postpartum period
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PATHOPHYSIOLOGY FETAL CONSEQUENCES Result of impaired uteroplacental blood flow 2nd to failure of physiologic transformation of spiral arteries or placental vascular insults or both Abnormalities in placental bed and subsequent failure of physiologic transformation of spiral arteries in the 1st or early 2nd trimester limit the blood flow to uteroplacental unit Additional mechanism for chronic uteroplacental ischemia  placental vascular insults Fetal growth restriction Oligohydramnios Placental abruption Nonreassuring fetal status
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MATERNAL MORBIDITY AND MORTALITY INTRACRANIAL HEMORRHAGE Most common cause of death in women with PE Other serious complications: Placental abruption HELLP syndrome Acute pulmonary edema Respiratory distress syndrome Acute Renal failure
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MATERNAL MORBIDITY AND MORTALITY PE may not directly cause cardiovascular disease in later life. PE and cardiovascular disease share many risk factors Obesity Insulin resistance Diabetes mellitus Underlying hypertension Dyslipidemia The earlier the onset of PE, the more severe the condition and the higher the risk of developing subsequent cardiovascular disease.
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MATERNAL MORBIDITY AND MORTALITY Women with PE are also more likely to have microalbuminuria (marker of renal damage) at 3-5 years after delivery PE adversely impact future kidney function since glomerular endotheliosis – a typical renal lesion in PE that was previously thought to resolve soom after delivery- can be observed long after pregnancy in some women who had PE.
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PERINATAL MORBIDITY AND MORTALITY Mostly related to birth weight and gestational age at delivery  attributed to early-onset PE. PE is commonly associated with placental lesions. Underlying vascular manifestations and the presence of oxidative stress and endothelial damage  fetal growth restriction with underlying hypoxia and acidosis
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PERINATAL MORBIDITY AND MORTALITY Short-term complications Fetal growth restriction Oligohydramnios Intrauterine fetal death Preterm Birth Low APGAR Score Nonassuring FHR during labor Need for NICU admission Long-term complications Cerebral palsy Low IQ Hearing Loss Visual impairment Insulin Resistance Diabetes mellitus Coronary artery disease Hypertension