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Hypertensive Disorders in Pregnancy, ,Scope,Terminology and classification Risk factors Etiology Pathophysiology Prediction and prevention Management,Incidence,3.7 % of pregnancies 16% of pregnancy-related deaths Eclampsia 1 in 2000 deliveries,Classification by the working group of the NHBPEP (2000),1. Gestational hypertension 2. Preeclampsia 3. Eclampsia 4. Preeclampsia superimposed on chronic hypertension (superimposed preeclampsia) 5. Chronic hypertension,Gestational hypertension,BP = 140/90 mmHg for first time during pregnancy No proteinuria BP returns to normal 12 wk postpartum Final diagnosis made only postpartum May have other S&S of preeclampsia , eg. epigastric discomfort or thrombocytopenia,Preeclampsia,Minimum criteria BP = 140/90 mmHg after 20 wk gestation Proteinuria = 300 mg/24hr or =1+ dipstick Mild preeclampsia Severe preeclampsia,Severe preeclampsia,BP = 160/110 mmHg Proteinuria 5 g/24hr or = 2+ dipstick (persistent) Cr 1.2 mg/dl Platelets 100,000 /mm3 Microangiopathic hemolysis Elevated ALT or AST Persistent headache , visual disturbance , epigastric pain,Eclampsia,Seizures that cannot be attributed to other causes in a woman with preeclampsia Seizures are generalized May appear before , during or after labor 10% develop after 48 hr postpartum,Superimposed preeclampsia,New onset proteinuria = 300mg/24 hr in hypertensive women but no proteinuria before 20 wk A sudden increase in proteinuria or BP or platelet count 100,000 in women with hypertension and proteinuria before 20 wk,Chronic hypertension,BP = 140/90 mmHg before pregnancy or diagnosed before 20 wk , not attributable to GTD or Hypertension first diagnosed after 20 wk and persistent after 12 wk postpartum,Diagnosis,Gestational HT,Also called transient HT Final Dx : after delivery , by exclusion BP : resting BP , Korotkoff phase V is used to defined diastolic pressure GHT may later develop preeclampsia 10% of eclamptic seizures develop before overt proteinuria is identified BP rise , increase both mother and fetus risks,Preeclampsia,Described as “pregnancy-specific syndrome of reduced organ perfusion secondary to vasospasm and endothelial activation” Proteinuria & glomerular pathology develop late in the course , pathophysiologic process begin as early as implantation,Preeclampsia,Diastolic hypertension = 95 , increase fetal death rate 3 fold Worsening proteinuria resulted in increasing preterm delivery Epigastric pain from hepatocellular necrosis , ischemia and edema that stretches Glisson capsule Thrombocytopenia from platelet activation & aggregation , microangiopathic hemolysis induced by severe vasospasm,Preeclampsia,Hemoglobinemia , Hburia , Hyperbilirubinemia : indicative of severe disease Cardiac dysfunction , pulm edema , obvious IUGR : indicative of severe disease Severity of preeclampsia assess by freq & intensity of abnormalities,Superimposed preeclampsia,1. Hypertension (=140/90) is documented antecedent to pregnancy 2. Hypertension is detected before 20 wk , unless there is GTD 3. Hypertension persists long after delivery Additional previous Hx or family Hx of HT End organ damage : LVH , retinal change Risk abruption , IUGR , preterm & death,Underlying causes of CHT,Essential familial hypertension Obesity Arterial abnormalities Endocrine disorders Glomerulonephritis Renoprival hypertension Connective tissue disease PCKD ARF,Risk factors for preeclampsia,Nulliparous Advanced maternal age Race and ethnicity (genetic predisposition & envoronmental factor) Multifetal gestation Obesity BMI 35 kg/m2,Etiology,Theory account for the observation : hypertensive disorder more likely to develop in : 1. exposed to chorionic villi for first time 2. exposed superabundance of chorionic villi (Twin ,mole) 3. Preexisting vascular disease 4. Genetic predisposition,Etiology,1. Abnormal trophoblastic invasion of uterine vessels 2. Immunological intolerance between maternal and fetoplacental tissues 3. Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy 4. Dietary deficiencies 5. Genetic influences,Abnormal trophoblastic invasion,Normal implantation , uterine spiral arteries undergo extensive remodeling as they are invaded by endovascular trophoblasts Incomplete invasion (decidual vessels , not myometrial vessels) : preeclampsia,Abnormal trophoblastic invasion,Atherosis : pathology,Endothelial damage Insudation of plasma constituents into vessel walls Proliferation of myointimal cells Medial necrosis Lipid accumulation in myointimal cells & macrophages Aneurysmal dilatation Obstruction of spiral arteriole,Placental growth factors : implications for abnormal placentation,Placental growth factors : regulate vascular endothelial cell and trophoblast function Highly expressed in trophoblasts during normal pregnancy Significantly decreased in preeclampsia Asso with placental bed hypoxia & ischemia (Abnormal placentation) J Soc Gyn Investig 2003 : 10 : 178-88,Placental protein 13 (PP-13),PP-3 levels slowly increase during pregnancy In 1st trimester , lower than normal were found in IUGR ,preeclampsia In 2nd & 3rd trimester , higher than normal concentrations were found in preeclampsia , IUGR , preterm delivery Used for assess risk to develop placental insuff Placenta 2004 : 25 : 608-622,Immunological factors,Acute graft rejection Impaired formation of blocking antibodies to placental antigenic sites Lack of effective immunization in first pregnancies Lower proportion of Th1 , Th2 dominance,Immunologic factors,Increased risk for first conception , new partner , conception very shortly after beginning sexual relation (5% if 12mo) Any kind of previous pregnancy (completed , spontaneous miscarriage or elective abortion) protective against preeclampsia Tolerate semi-allogenic graft through fathers alloantigen J. of Reprod Immunology 2003 (59) : 93-100,Immunological factors,IL10 regulate s arterial pressure in early primate pregnancy IL-10 & TNF : vasodilation of early pregnancy Anti-human IL-10 MAb caused significant increase in MAP TNF- alone or combine with IL-10 not alter MAP Cytokine 29 (2005) 176-185,Immunological factors,Serum from preeclamptic pt contains IgG autoantibody Reacts with AT1 receptor AT1-AA induce signaling in vascular cells and trophoblasts Including AP-1 and NF-kB activation Results in tissue factor production , reactive oxygen species (ROS)generation Autoimmunity Reviews 4 (2005) : 61-65,Vasculopathy & inflammatory,Placental factors released by ischemic changes Decidua activated , release noxious agents provoke endothelial cell injury Endothelial cell dysfunction Cytokines : TNF , IL,Vasculopathy & inflammatory,Oxidative stress (ROS , free radical) self-propagating lipid peroxides formation Generate highly toxic radicals injure endothelial cells Modify NO2 production Interfere PG balance,Vasculopathy & inflammatory,Oxidative stress : produce lipid-laden macrophage foam cells Activation of microvascular coagulation : Thrombocytopenia Increased capillary permeability : proteinuria and edema,Angiogenic growth factors & HT,HT : disease of inadequate or aberrant responses to angiogenic growth factors Preeclampsia is accompanied by high circulating levels of soluble VEGF receptor-1 (inactive complexes with VEGF + plGF) High AGF : contribute to peripheral & pulm edema , microalb , progression of atherosclerosis Angiogenesis 7 : 2004 : 193-201,L-Arginine attenuate HT,Supplementation L-Arginine (precursor for nitric oxide) in pregnant rats Significant decrease arterial pressure In both pregnant rats with reduced uterine perfusion pressure & pregnant control Hypertension 2004 : 43 : 832-6,N-acetylcysteine prevent HT,Reduced uterine perfusion pressure rats Were treated with N-acetylcysteine (100mg/kg) twice daily until delivery Significant increase in BP in reduced uterine perfusion pressure procedure Which alleviated by N-acetylcysteine Without adversely effect fetal weight Am j of Obs & Gyn 2005 : 193 : 952-6,Melatonin against oxidative damage,Melatonin solution injected intraperitoneally before occlusion Protects against ischemia/reperfusion-induced oxidative damage to mitochondria in rat placenta Could be use in treat preeclampsia & states involvings free radical production (fetal hypoxia & IUGR) J.Pineal Res. 200 : 31 : 173-178,Prostaglandin,Platelet activation : hallmark of SPE Platelet PGH synthase 1-derived (PGHS1-derived) & TxA2 Low dose aspirin treatment decreased platelet aggregation & prevented thrombosis Decrease progesterone during parturition : sustain parturition J of Clin Inv , April 2005 : 115 : 986-995,PS/PC induce preeclampsia,Phosphatidylserine (PS) 80% / Phosphatidylcholine (PC) 20% Significant elevation in SBP Significant increase in TAT levels Significant decrease platelet counts Significant increase proteinuria Significant reduction in fetal & placental weight Semin Thromb Hemost. Jun2005 : 31 : 34-20,Endothelin-1,Increased ET-1 in amniotic fluid & plasma of infant and mother in preeclampsia Asso with abnormal placentation J Vet Intern Med. 2005 Jul-Aug : 19 : 594-8,Nutritional factors,Dietary taboos : meat , protein , purines , fat , dairy products , salt Supplement of Zn , Ca , Mg prevent preeclampsia ? Fruits & vegetables : antioxidant Ascorbic acid intake 85 mg/d , predispose preeclmapsia 2 fold Obesity increase risk preeclampsia,Genetic factors,Hereditary hypertension, preeclampsia , eclampsia Polygenic inheritance Asso with HLA-DR4 Maternal Ab against fetal anti HLA-DR Ig Heterozygous for angiotensinogen gene variant T235 Polymorphisms of genes for TNF , IL 1 , Lymphotoxin ,Genetics of preeclampsia,Familial predisposition AGT(encode angiotensinogen) & NOS 3 (encode nitric oxide synthestase) genes mutation Clin Genet 2003 : 64 : 96-103,Is preeclampsia an infectious disease?,Analyze IgG Ab against HSV-2 , CMV , EBV , Toxoplasma gondii at first ANC Seronegative for HSV-2, CMV , EBV increased risk preeclampsia (OR 1.7 ,1.6, 3.5) Seronegative for Toxo not associated with increase risk preeclampsia (OR 1.0) Acta Obstet Gynecol Scand 2001 : 80 : 1036-8,Pathogenesis,Vasospasm Endothelial cell activation Increased pressor resonses Prostaglandins Nitric oxide Endothelins Angiogenic factors (VEGF , PIGF),Pathogenesis,Increased vascular reactivity to vasopressor Decrease PG I2 production by endothelium Increase TxA2 secretion by platelet Increased NO2 synth by endothelium Decrease NO2 synthease,Comparison of mean ATII infusion doses required to evoke a pressor response,Pathophysiology,Endothelial damage Interstitial leakage Platelet & fibrinogen deposit Increase subendothelial a. resistance Decreased blood flow Ischemia necrosis , hemorrhage Multiorgan involvement,Cardiovascular system,Increase after load Preload diminish Endothelial activation with extravasation Decreased cardiac output Hemoconcentration from generalized vasoconstriction and endothelial dysfynction Decreased blood volume,Blood and coagulation,Thrombocytopenia from platelet activation , aggregation & consumption Increased plt activating factor & thrombopoietin Clotting factors decrease Erythrocytes rapid hemolysis (increase LDH , schizocyte , MAHA),Volume homeostasis,Decrease plasma levels of renin , AT II , aldosterone DOC increase Vasopressin normal despite decreased plasma osmolality ANP increased Extracellular fluid : edema : endothelial injury , reduced oncotic pressure,Kidney,RPF & GFR reduced Uric acid elevated Creatinine clearance reduced , oliguria Diminished urinary Ca due to increased tubular reabsorption Urine sodium elevated Urine osmolality , U:P Cr , FE Na : prerenal mechanism,Kidney,Proteinuria : glomerulopathy : increased permeability : albumin , Hb , globulin , transferins Anatomical changes : glomeruli enlarge , capillary loops dilated & contracted , endothelial cells swollen fibrils deposit (glomerular capillary endotheliosis),Kidney,Renal tubular lesions : degenerative change , accumulation with casts ARF from ATN Oliguria , azotemia induced by hypovolemia Preeclampsia with ARF occur in HELLP syndrome , placental abruption 1/3 Rarely , irreversible renal cortical necrosis,Liver,Periportal hemorrhage in liver periphery Elevated transaminase HELLP syndrome Bleeding cause hepatic rupture(mortality 30%) , subcapsular hematoma Conservative treatment Recombinant factor VIIa,HELLP syndrome,No strict definition Incidence 20% of severe preeclampsia or eclampsia Factors contributing to death : include stroke , coagulopathy , ARDS , ARF , sepsis Insufficient evidence : adjunctive steroid,Brain,Headache & visual symptoms asso with eclampsia Two cerebral pathology related 1. gross hemorrhage due to ruptured a. caused by severe HT 2. more widespread , edema hyperemia , ischemia , thrombosis & hemorrhage caused by preeclampsia,Neuroimaging,CT : hypodense area in cortex , correspond to petechial hemorrhage and infarctions Remarkable changes in area of distribution of posterior cerebral a. MRI : hyperperfusion due to vasogenic edema Eclampsia : 25% were area of infarction,Cerebral blood flow,Transcranial doppler ultrasonography Preeclampsia : increase perfusion pressure , counter by increase cerebrovascular resistance(net no change) Eclampsia : loss of autoregulation , hyperperfusion similar to hypertensive encephalopathy Eclampsia caused by transient loss of cerebrovascular autoregulation,Blindness,Visual disturbance common in SPE It follows eclampsia in 10% Develop upto 1 wk or more after delivery Called “Amaurosis” Extensive ocipital lobe vasogenic edema Resolve completely in all case Rare cerebral infarct or retinal a. ischemia Retinal detach : resolve within 1 wk,Cerebral edema,Widespread vasogenic edema S&S : Lethargy , confusion , blurred vision , coma Waxed & waned Rx : Manitol , Dexamethasone,Uteroplacental perfusion,Compromised uteroplacental perfusion from vasospasm Mean diameter of myometrial spiral arterioles decrease Doppler flow velocity of uterine artery Ring-like : higher in peripheral than in central vessels Preeclampsia was higher resistance,Prediction,Biological , biochemical & biophysical markers To identify markers of faulty placentation reduced placental perfusion , endothelial cell activation & dysfunction , activation of coagulation,Roll-over test,28-32 wk Abnormally sensitive to infused angiotensin II Positive predictive value 33%,Uric acid,Decreased renal urate excretion in preeclampsia Serum uric acid exceeding 5.9 at 24 wk (PPV 33%) Not useful in differentiating GHT from preeclampsia,Fibronectin,Endothelial cell activation Low sensitivity 69% Positive predictive vaules 12% Higher levels by 12 wks (PPV 29% NPV 98%),Coagulation activation,Thrombocytopenia and platelet dysfunction Increased destruction cause platelet volumes increase (younger platelet) Preeclampsia : PAI-1 increase increased relative to PAI-2 because of endothelial cell dysfunction,Oxidative stress,Increased levels of lipid peroxides Prooxidants : iron , transferin , ferritin , TG , FFA , lipoprotein Antioxidants : ascorbic acid , vitamin E Hyperhomocysteinemia in mid pregnancy risk for atherosclerosis , 3-4 fold risk preeclampsia , influenced by folic acid supplement,Cytokines,Released by vascular endothelium & leukocytes , and macrophages & lymphocytes at decidua Interleukin , TNF , CRP : inflammatory response Possibly predictive preeclampsia,Placental peptides,Corticotropin-releasing hormone , hCG , Activin A , inhibin A Variably elevated depend on duration & severity of preeclampsia Overlap with normal pregnancy VEGF and PIGF : regulate placental development , both antagonized by sFlt1 Excessive sFlt1 , PIGF in 1st trimester : high risk,Fetal DNA,Fetal DNA in maternal serum At the time endothelial activation , fetal cells released into maternal circulation Elevations after 28 wk indicate impending disease,Uterine artery doppler,Impaired trophoblastic invasion of spiral arteries , leading to reduction in uteroplacental blood flow 8-22 wk , sensitivity 78% , PPV 28% , unreliable in low risk pregnancies Combined inhibin A & activin A , sensitivity 86% Combined hCG & AFP , sensitivity 2-40%,hCG,hCG in second trimester , 2.0 MoM Sensitivity 23.7% Specificity 89.4% Relative risk 2.54 Positive predictive value 9.5% Negative predictive value 96.6% Endocrine Reviews , April2002 : 23 : 230-257,Inhibin A and Activin A,Activin A : control trophoblast differentiation in first trimester : high in preeclampsia Inhibin A 15-19 wk , 2.0 MoM Sensitivity 48.6% Specificity 23.6% Activin A more sensitive than inhibin A at 21-25 wk Endocrine Reviews , April2002 : 23 : 230-257,Vasoactive,Decrease active renin , AT I & I , aldosterone , activity of ACE in 3rd trim AT II infused test : positive at less than 10 ng/kg Ratio inactive urinary kallikrein /urine creatinine at 16-20 wk : lower 5 fold in who developed preeclampsia Endocrine Reviews , April2002 : 23 : 230-257,Prevention,Salt restriction : ineffective Inappropriate diuretic therapy Low dietary calcium increased risk GHT Fish oil capsules : modify abnormal PG balance : ineffective Low dose aspirin (60mg) : ineffective Antioxidants : vitamin C & E : reduced endothelial cell activation , reduction in preeclampsia,Low milk intake risk preeclmpsia,Case control study Mean milk intake per day in preeclampsia control group Drinking more than 5 glasses per day has evident protective effect of developing preeclampsia (odd ratio 0.1) Eur J of Obs & Gyn & Repro Bio 105 (2002) 11-14,Calcium supplement,Reduction in high BP (RR 0.58) The effect greater among women at high risk of developing HT and those with low baseline dietary calcium (RR 0.47 & 0.38) Reduction risk of preeclampsia (RR 0.35) The effect greatest in women at high risk of developing HT and those with low baseline dietary calcium (RR 0.22 & 0.29) The Cochrane database of systematic reviews 2002,Aspirin,Significant benefit in reducing preeclampsia (odds ratio 0.55) Baseline risk of preeclampsia in women with abnormal uterine a doppler was 16%

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