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Pregnancy induced hypertension ( PIH ) & Eclampsia

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Presentation on theme: "Pregnancy induced hypertension ( PIH ) & Eclampsia"— Presentation transcript:

1 Pregnancy induced hypertension ( PIH ) & Eclampsia
Speaker- Dr Ajisha Aravindan Moderator – Dr Anjan Trikha

2 Hypertension In US, 28.7% adults, or ~58.4 million individuals, have hypertension. National Health and Nutrition Examination Survey (NHANES) Incidence in pregnancy : 3-5 % India – PIH incidence 5 % PIH is the 3rd leading cause of mortality during pregnancy ( 1-thromboembolism , 2-hemorrhage ) India – 4th ( Bleeding, Sepsis, Unsafe abortions)

3 Pregnancy induced HTN PIH : 2- 8 % of pregnancies. Eclampsia :
1 in 1000–1700 pregnancies- developing world. 1 in 2000 pregnancies - developed countries. In UK, 1/5 of antenatal admissions, 2/3 of referrals to day care units, and ¼ of obstetric admissions to ICU. Maternal and neonatal outcome depend on gestational age at onset, severity of the disease and presence of preexisting medical conditions.

4 Its not so uncommon … Laura Bush Angelina Jolie (with the twins)
Britney Spears (rumored) Julia Roberts (rumored with her twins) Jennifer Lopez Lisa Marie Presley Jenna Jameson

5 Classification of Hypertension in Pregnancy
1) P.I.H Preeclampsia(6-8%) Eclampsia (0.05% ) Gestational Hypertension(6-7%) 2) Chronic Hypertension(3-5%) 3) Chronic Hypertension with superimposed P.I.H David H. Chestnut, Obstetric anaesthesia

6 Classification

7 1) Preeclampsia Hypertension Proteinuria
A sustained systolic BP of at least 140 mm Hg, or a sustained diastolic BP of at least 90 mm Hg, that occurs after 20 weeks' gestation in a woman with previously normal BP. Proteinuria ≥300 mg protein in a 24-hour urine collection David H. Chestnut, Obstetric anaesthesia

8 Severe Preeclampsia Blood pressure : ≥ 160 mm Hg systolic or ≥ 110 mm Hg diastolic BP on two occasions at least 6 hours apart while the patient is on bed rest. Proteinuria : ≥5 g in a 24-hour urine specimen (or ≥3+ on two random urine samples at least 4 hours apart). Oliguria : Urine output < 500 ml in 24 hours. Cerebral or visual disturbances: Headache, blurred vision, or altered consciousness. David H. Chestnut, Obstetric anaesthesia

9 Severe Preeclampsia Thrombocytopenia Impaired liver function
Epigastric or right upper quadrant pain: stretching of Glisson's capsule by hepatic edema Hepatic rupture: a rare complication Pulmonary edema Fetal growth restriction, oligohydramnios David H. Chestnut, Obstetric anaesthesia

10 2) Chronic Hypertension
 BP 140/90 mm Hg before pregnancy or diagnosed before 20 weeks' gestation not attributable to gestation.  or      Hypertension first diagnosed after 20 weeks' gestation and persistent after 12 weeks' postpartum Incidence- 5 % David H. Chestnut, Obstetric anaesthesia

11 3) Chronic hypertension with Superimposed Preeclampsia
New-onset proteinuria > 300 mg/24 hours in hypertensive women but no proteinuria before 20 weeks' gestation. or A sudden increase in proteinuria or blood pressure or platelet count < 100,000/mm3 in women with hypertension and proteinuria before 20 weeks' gestation   David H. Chestnut, Obstetric anaesthesia

12 Pregnancy associated risk factors for PIH
•   Multiple pregnancy    • Hydatidiform mole •    Structural congenital anomalies     •    Hydrops fetalis    •    Chromosomal anomalies (trisomy 13, triploidy)      •    Urinary tract infection David H. Chestnut, Obstetric anaesthesia

13 Preconceptional &/or Chronic risk factors for PIH
1) History of previous preeclampsia 2) Age 3) Interval between pregnancies 4) Family history David H. Chestnut, Obstetric anaesthesia

14 Preconceptional &/or Chronic risk factors for PIH
5) Presence of underlying diseases •    Chronic HTN, renal disease    •    Obesity, insulin resistance •    GDM, type I DM    •    Ac protein C resistance (factor V mutation), protein S deficiency    •    Antiphospholipid antibodies •    Hyperhomocysteinemia    David H. Chestnut, Obstetric anaesthesia

15 Preconceptional &/or Chronic risk factors for PIH
6) Exogenous Factors •    Smoking ( % risk reduction)    •    Stress, work-related psychosocial strain    •    In- utero diethylstilbestrol exposure ( 50 % ) David H. Chestnut, Obstetric anaesthesia

16 ACOG Technical Bulletin # 219, 1996

17 Preconceptional &/or Chronic risk factors for PIH
Partner related risk factors •  Limited sperm exposure, donor insemination, oocyte donation     •  Partner who fathered a preeclamptic pregnancy in another woman David H. Chestnut, Obstetric anaesthesia

18 Pathogenesis of Preeclampsia
Platelet Endothelial Immunological Pathogenesis of Preeclampsia Calcium Genetic Fatty acid metabolism Coagulation

19 Historical Theories The Immunity Model describes it in terms of self versus non-self, with loss of immunity control leading to a disease state. The Danger Model suggests that stress or abnormal cell death in pregnancy-related tissues causes expression of specific danger signals and potential activation of anti-fetal immunity. The Genetics Model, including factor V Leiden mutation, TNF-α, Angiotensinogen , AR II etc have also been implicated. American Journal of Therapeutics 16, 284–288 (2009)

20 Pathogenesis of Preeclampsia
Dysfunction Endothelial Ischemia Placental

21 Normal Placenta Cytotrophoblasts of fetal origin invade the uterine spiral arteries of the decidua and myometrium and replace the endothelial layer of the maternal spiral arteries, transforming them from small, high-resistance vessels to high-caliber capacitance vessels. Alice Wang et al. Physiology 24: , 2009.

22 Preeclamptic Placenta
In preeclampsia, this transformation is incomplete. Cytotrophoblast invasion of the spiral arteries is limited to the superficial decidua, and the myometrial segments remain narrow. Alice Wang et al. Physiology 24: , 2009

23 Platelet & Endothelial function
David H. Chestnut, Obstetric anaesthesia

24 Endothelial Dysfunction
Placental ischemia leads to release of circulating factors – profound systemic effects . prostacyclin (PGI2) , nitric oxide thromboxane (TXA2) , endothelin Exaggerated sensitivity to vasopressors such as angiotensin II and norepinephrine. Compromised uteroplacental circulation. Alice Wang et al. Physiology 24: , 2009

25 Platelet Dysfunction Surface-mediated activation , microvascular consumption . sensitivity to PGI2, release of TXA2 & serotonin causing further platelet aggregation. Hypercoagulability Thrombocytopenia Platelet lifespan reduced – 2-3 days

26 Anti-angiogenic factors
VEGF stabilizes endothelial cells in mature blood vessels and helps in maintaining the endothelium. Soluble fms-like tyrosine kinase-1(sFlt1) - a circulating antagonist to both vascular endothelial growth factor (VEGF) and placental growth factor (PlGF). Soluble endoglin (sEng)- a proteolytic cleavage product of the TGF- receptor endoglin, acts synergistically with sFlt1. sFlt1 is a truncated splice variant of the membrane-bound VEGF receptor Flt1, also called VEGFR1. sFlt1 consisting of the extracellular ligand binding domain without the transmembrane and intracellular signaling domains, is secreted by syncytio -trophoblasts into the maternal circulation. sFlt1 antagonizes both VEGF and PlGF by binding them in the circulation and preventing interaction with their endogenous receptors Alice Wang et al. Physiology 24: , 2009

27 Role of sFlt1 and sEng sFlt1 consisting of the extracellular ligand binding domain without the transmembrane and intracellular signaling domains, is secreted by syncytio -trophoblasts into the maternal circulation. sFlt1 antagonizes both VEGF and PlGF by binding them in the circulation and preventing interaction with their endogenous receptors This results in endothelial cell dysfunction, including decreased prostacyclin, nitric oxide production, and release of procoagulant proteins Excess placental secretion of sFlt1 and sEng ( endogenous circulating antiangiogenic proteins) inhibits VEGF and TGF-1 signaling, respectively, in the vasculature. sFlt1- soluble fms like tyrosine kinase, sEng- soluble endoglin Alice Wang et al. Physiology 24: , 2009

28 sFlt 1 sFlt1 antagonizes both VEGF and PlGF by binding them in the circulation and preventing interaction with their endogenous receptors Increase in maternal circulating sFlt1 precedes the onset of clinical disease and is correlated with disease severity. In molar gestations, levels of sFlt1 are found to be elevated. Alice Wang et al. Physiology 24: , 2009

29 Renin Angiotensin System
In normal pregnancy, renin,aldosterosterone, and angiotensin are increased. In preeclampsia RAAS suppressed. Increased vascular responsiveness to angiotensin II and other vasoconstrictive agents. Presence of agonistic (AT1) receptor autoantibodies These autoantibodies, like angiotensin II, could lead to the production of tissue factor by endothelial cells. Placental angiotensinase enz destroyes angio II- causing vascular refractoriness . Granger et al, Hypertension 2001, 38:

30 Angiotensin II Normal Pregnancy Preeclampsia Endothelial cell mass
Endothelial dysfunction PgI2 produced in response to angiotensin II PgI2 production Vasodilatation Vasoconstriction Minimal effect of angiotensin Exaggerated effect of angiotensin David H. Chestnut, Obstetric Anesthesia

31 Immunological factors
Normal placentation requires the development of immune tolerance between the fetus and the mother. Abnormal maternal immune response to novel paternally derived fetal antigens. Alterations in decidual NK (natural killer)-cell signaling with disturbance in the secretion of cytokine and angiogenic factors are thought to play an important role in the pathogenesis of preeclampsia Preeclampsia occurs more often in first pregnancies, after a change in paternity , or with long inter-pregnancy interval. Women using barrier contraceptive methods that reduce maternal exposure to sperm have increased incidence of preeclampsia. NK cells important in modulating immune tolerance required for normal placental development as well as the induction of angiogenic factors and vascular remodeling. Alice Wang et al. Physiology 24: , 2009

32 Fatty Acid Metabolism Endothelial triglyceride accumulation
Hyperoestrogenaemia of pregnancy Hepatic biosynthesis of triglycerides Endothelial triglyceride accumulation Inhibit PgI2 release Vasoconstriction Indian Journal of Clinical Biochemistry, 2006 / 21 (2)

33 Fatty Acid Metabolism David H. Chestnut, Obstetric Anesthesia

34 Calcium Lipid peroxidation of cell membranes (oxidative stress)
cell permeability to calcium Calcium affects smooth muscle cell contractility indirectly by influencing the production of other vasoactive agents such as nitric oxide, prostacyclins, or angiotensin. AmericanJournal of Clinical Nutrition 2000;71(suppl):1371S–4S.

35 Pathophysiology of Preeclampsia

36 Cardio-vascular system
High systemic vascular resistance (SVR) - vasospasm. Heart rate and blood pressure variability is increased. sensitivity to endogenous pressors. Sympathetic over activity Intravascular volume depletion. Normal CVP , PCWP. Plasma COP reduced (low albumin )

37 Hematology Hypercoagulable state
Anti-thrombin III , fibrinolytic activity D-dimer, fibrinopeptide A Lipoprotein(a)- competes with plasminogen for binding to fibrin & endothelium Thrombocytopenia – % Platelet lifespan : 2-3 days

38 HELLP Syndrome Elevated LFT Low Platelet Hemolysis

39 HELLP Syndrome (1) Hemolysis - microangiopathic hemolytic anemia & increased bilirubin (>1.2 mg/dl) (2) Elevated liver enzymes - increased SGOT (AST) of at least 70 U/L & LDH >600 U/L (3) Low platelet count <100,000/mm3 Partial HELLP Syn – 1 or 2 of above Higher risk of DIC, Stroke, ARF, Abruption, Pulmonary edema

40 HELLP Syndrome Incidence : 4- 12 % Maternal mortality – 24 %.
80% - Preterm , 20%- postpartum, peak at hrs post-partum Malaise , epigastric pain, nausea, vomiting. HTN, proteinuria may be absent. Stillbirth is frequent (10-15%). High neonatal loss due to prematurity (20- 25%). David H. Chestnut, Obstetric anaesthesia

41 HELLP Syndrome Most hematologic abnormalities return to normal within 2-3 days after delivery but thrombocytopenia may persist for a week. Intrahepatic and sub capsular hemorrhage are more common. Liver function deteriorates rapidly.

42 Renal system Generalized swelling and vacuolization of the endothelial
cells and loss of the capillary space - endotheliosis Proteinuria > 300 mg/day Urate , Na clearance reduced . S. uric acid > 5.5 mg/dl Oliguria Renal failure – rare , recovers mild glomerular endotheliosis also occurs in pregnancy without preeclampsia, especially in a subset of subjects with gestational hypertension . This suggests that the endothelial dysfunction of preeclampsia may be an exaggeration of a normal physiological process that occurs near the end of a term pregnancy.

43 Respiratory System Pharyngolaryngeal edema - Difficult intubation
Leaky capillaries , low COP Pulmonary edema - 3% of severe PIH, 2-3 days post-partum

44 Hepatic System Serum transaminase levels increase
Epigastric or subcostal pain (edema or subcapsular or parenchymal bleeding) Periportal fibrin deposition and endothelial damage Intraperitoneal rupture - catastrophic

45 Endocrine & Metabolic System
Suppression of RAAS plasma renin concentration (PRC) and activity (PRA). Increased vascular response to angiotensin II. Deficient production of PGI2 and NO .

46 Central Nervous System
Headache Visual disturbance Hyperexcitablity Hyperreflexia Seizures

47 Utero-Placental System
Decreased perfusion Doppler – ( IUGR ) Downstream resistance increases Diastolic velocity decreases The systolic/diastolic ratio increases

48 Pathophysiology of Preeclampsia
David H. Chestnut, Obstetric anaesthesia

49 Eclampsia “bolt from the blue”
New onset of seizure activity and/or unexplained coma during pregnancy or postpartum in a woman with signs or symptoms of preeclampsia. During or after 20th wk or post-partum.  80% intrapartum or within the first 48 hours following delivery. Rare before 20 weeks' POG or as late as 23 days’ postpartum.

50 Eclampsia The classic triad of hypertension, proteinuria, and edema may be absent or only mildly abnormal in 30%.  No reliable test or symptom complex predicts the development of eclampsia. Etiology - ? Hypertensive encephalopathy, Vasospasm, Microinfarctions, Punctate hemorrhages, Thrombosis, Cerebral edema

51 Risk factors for Eclampsia
Nulliparity, Multiple gestation, Molar pregnancy, Preexisting hypertension or renal disease, Previous severe preeclampsia or eclampsia, Nonimmune hydrops fetalis, Systemic lupus erythematosus.


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