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Speaker- Dr Ajisha Aravindan Moderator – Dr Anjan Trikha

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1 Speaker- Dr Ajisha Aravindan Moderator – Dr Anjan Trikha

2 Hypertension  In US, 28.7% adults, or ~58.4 million individuals, have hypertension. N ational Health and Nutrition Examination Survey (NHANES)  Incidence in pregnancy : 3-5 %  India – PIH incidence 5 %  PIH is the 3 rd leading cause of mortality during pregnancy ( 1-thromboembolism, 2-hemorrhage )  India – 4 th ( 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 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/mm 3 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 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 Preconceptional &/or Chronic risk factors for PIH David H. Chestnut, Obstetric anaesthesia

15 6) Exogenous Factors Smoking ( % risk reduction) Stress, work-related psychosocial strain In- utero diethylstilbestrol exposure ( 50 % ) Preconceptional &/or Chronic risk factors for PIH 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 Immunological Endothelial Calcium Genetic Fatty acid metabolism Platelet 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 Preeclampsia 2 Endothelial Dysfunction Placental Ischemia 1

21 Normal Placenta Alice Wang et al. Physiology 24: , 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.

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

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. Alice Wang et al. Physiology 24: , 2009

27 Role of sFlt1 and sEng 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. Granger et al, Hypertension 2001, 38:

30 Angiotensin II Normal PregnancyPreeclampsia Endothelial cell mass Endothelial dysfunction PgI2 produced in response to angiotensin II PgI2 production VasodilatationVasoconstriction Minimal effect of angiotensinExaggerated 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 Alice Wang et al. Physiology 24: , 2009

32 Endothelial triglyceride accumulation Inhibit PgI2 release Vasoconstriction Hyperoestrogenaemia of pregnancy Hepatic biosynthesis of triglycerides Fatty Acid Metabolism 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 CVSCNSHEPATICRENALRESPI

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/mm 3  Partial HELLP Syn – 1 or 2 of above  Higher risk of DIC, Stroke, ARF, Abruption, Pulmonary edema

40 HELLP Syndrome  Incidence : %  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

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 PGI 2 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 David H. Chestnut, Obstetric anaesthesia Pathophysiology of Preeclampsia

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 20 th 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.

52 THANK YOU


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