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Hypertensive Disorders in Pregnancy (I)

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1 Hypertensive Disorders in Pregnancy (I)
Williams Obstetrics 22nd Edition Chapter 34 부산백병원 산부인과 조인호

2 Index Diagnosis Etiology Pathogenesis Pathophysiology
Prediction and Prevention Management Long-term consequences

3 Gestational Hypertension – 3.7% in 150,000
(National Center for Health Statics, 2001) Pregnancy-related hypertension : Pregnancy-related deaths(3201명 in US, )의 16% 차지 Black women are 3.1 times to die as white women Hypertensive disorders remain among the most significant and intriguing unsolved problems in obstetrics Incidence에 관한 내용, 선진국으로 갈 수록 mortality가 떨어짐.

4 Diagnosis Gestational hypertension Preeclamsia Eclamsia
Superimposed preeclamsia (on chronic hypertension) Chronic hypertension 21판부터 정립된 내용

5 Gestational hypertension
BP≥ 140/90mmHg for first time during pregnancy No proteinuria BP returns to normal < 12 weeks’ postpartum Final diagnosis made only postpartum May have other signs or symptoms of preeclampsia, for example, epigastric discomfort or thrombocytopenia Eclampsia seizure의 10%는 proteinuria가 발견되기 이전에 나타남. 그러므로 BP가 상승하면 모체와 태아 모두에게서 위험성이 높아진다.

6 Preeclampsia ■ Minimum Criteria
  - BP≥140/90mmHg after 20weeks' gestation   - Proteinuria ≥300mg/24hrs or ≥1+dipstick ■ Increased certainty of preeclampsia   - BP≥160/110mmHg   - Proteinuria 2.0g/24hrs or ≥2+dipstick   - Serum creatinine >1.2mg/dl unless known to be previously elevated   - Platelets <100000/mm3   - Microangiopathic hemolysis (Increased LDH)   - Elevated ALT or AST   - Persistent headache or other cerebral or visual disturbance   - Persistent epigastric pain Table 34-1의 내용 Proteinuria 양은 wide하게 fluctuation을 보임. 연속해서 측정해야 함. Renal Bx.에서 특징적인 조직학적 변화(glomerular histologic alteration)를 동반

7 Preeclampsia Diastolic hypertension ≥95mmHg Worsening proteinuria
Fetal death rate : 3배이상 증가 Worsening proteinuria preterm labor 증가 Neonatal survival 변화없음 Epigastric or RUQ pain Hepatocellur necrosis, ischemia, edema that stretches the Glisson capsure AST/ALT상승 : 임신종결의 sign Hepatic rupture : rare Thrombocytopenia severe vasospasm -> microangiopathic hemolysis -> Platelet activation, aggregation Proteinuria만 있는 경우는 benign으로 봄. Thrombocytopenia가 심해 gross hemolysis (hemoglobineia, hemoglobinuria, hyperbilirubinemia)가 있는 경우 질병의 심각성을 보여줌 이전 chapter에서는 diastolic BP와 proteinuria와의 상관관계에 따른 fetal death를 표로써 보여주었음.

8 Severity of Preeclampsia
Differentiation between mild & severe preeclampsia can be misleading -because apparently mild disease may progress rapidly to severe disease Rapid increase in BP followed by convulsions is usually preceded by unrelenting severe headache or visual disturbances.

9 Table 34-2 BP단독으로는 severity indicator 아님. BP보다는 proteinuria의 양이 severity를 결정하는데 큰 영향을 미침. (130/ > seizure, 180/ : no seizure)

10 Eclampsia preeclampsia+convulsion
Seizures that cannot be attributed to other causes in woman with preeclampsia Seizures are generalized and may appear before, during, of after labor 10%는 단백뇨가 발생되지 않는 상태이므로 임신 후반기에 BP가 상승하면 설사 단백뇨가 없다고 해도 함부로 생각해서는 안됨.

11 Chronic hypertension BP ≥140/90 mmHg before pregnancy or diagnosed before 20weeks’ gestation (not attributable to gestational trophoblastic disease) or Hypertension first diagnosed after 20weeks’ gestation and persistent after 12weeks’ postpartum 진단기준에 관한 내용임

12 Chronic Hypertension Chronic hypertension은 임신후반기까지 진단하기 어려움.
이유: BP decreases during the second and early third trimesters in both normotensive and chronically hypertensive women Underlying hypertension의 원인 Essential familial hypertension (90%) 예) 원래 chronic vascular disease를 가지고 있는 여성이 임신 20주에 처음 혈압을 검사했을 경우엔 정상 수치를 나타내다가 3rd trimester동안에는 이전상태로 고혈압소견을 나타내게 된다. 이로 인하여 HBP가 chronic인지 gestational hypertension, preeclampsia 인지 진단하기가 어렵게 된다.

13 Underlying Causes of Chronic hypertensive Disorder
Essential familial hypertension (hypertensive vascular disease) Obesity Atrterial abnormalities Renovascular hypertension Coarctation of the aorta Endocrine diorders Diabetes mellitus Cushing syndrome Primary aldosteronism Pheochromocytoma Thyrotoxicosis Glomerulonephritis (acute and chronic) Renoprival hypertension Chronic glomerulonephritis Chronic renal insufficiency Diabetic nephropathy Connetive tissue disease Lupus erythematosus Systemic sclorosis Periarteritis nodosa Polycystic kidney disease Acute renal failure Table 34-3

14 Chronic Hypertension Chronic HT
→ ventricular hypertrophy, cardiac decompensation, cerebrovascular accidents, renal damage 임신 때 superimposed preeclampsia가 생기는 경우(최고 25%까지 보고됨, 1998, Sibai) 위의 합병증들이 더욱 호발함.

15 Preeclampsia superimposed on Chronic Hypertension
New-onset proteinuria≥ 300mg/24hours in hypertensive women but no proteinuria before 20 weeks’ gestation A sudden increase in proteinuria or blood pressure or platelet count <100,000/mm3 in women with hypertension and proteinuria before 20weeks’ gestation

16 Superimposed preeclampsia
Placental abruption, growth restriction, preterm delivery, death 의 위험성이 증가 일반적으로 “Pure” preeclampsia에 비해 증상이 훨씬 severe하고 종종 fetal growth restriction이 동반된다.

17 Incidence and Risk Factor
Nulliparous women에게 흔함. Incidence : 5% (wide variation) Influence by Parity, race, ethnicity, genetic predisposition Nulliparous Total :7.6% / severe : 3.3% (Hauth, 2000) Risk factor Chronic hypertension, multifetal gestation, maternal old age(>35 yrs), obesity, African-American ethnicity Ethnicity : 민족성

18 Incidence and Risk Factor
Maternal weight and the risk of preeclampsia is progressive. Smoking during pregnancy reduced risk of hypertension during pregnancy (Bainbridge,2005 ; Zhang, 1999) Placenta previa also reduced the risk of hypertension BMI (Kg/m2) Morbidity (%) <19.8 4.3 >35 13.3 Gestation twin 13 single 5 (Sibai, 2000)

19 Incidence and Risk Factor (Eclampsia)
Somewhat preventable Receive adquate prenatal care 1976 (williams Obstetrics 15th edition) 1/700 deliveries (Parkland Hospitial) 1/1150 deliveries 1999 1/1750 deliveries 2000, National Vital Statistics Report, in US 1/3250 1994, Douglas and Redman in UK 1/2000

20 Etiology Basic concepts Exposed to chorionic villi for the first time
Exposed to a superabundance of chorionic villi, as with twins or hydatidiform mole Have preexisting vascular disease Genetically predisposed to hypertension developing during pregnancy

21 Currently plausible potential cause (2003, Sibai)
Vascular endothelial damage with vasospasm, transudation of plasma, and ischemic and thrombotic sequelae. Currently plausible potential cause (2003, Sibai) Abnormal trophoblastic invasion of Uterine vessels Immunological intolerance between maternal and fetoplacental tissues Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy Diatary deficiencies Genetic influences

22 Abnormal Trophoblastic Invasion
In normal implantation, endovascular trophoblasts invade the uterine spiral arteries

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24 Abnormal Trophoblastic Invasion
In preeclampsia Incomplete trophoblastic invasion The magnitude of defective trophoblastic invasion of the spiral arteries correlated with the severity of the hypertensive disorder (2000, Madazli) Using electron micorscopy Endothelial damage Insudation of plasma constituents into vessel walls Proliferation of myointimal cells Medial necrosis Lipid and macrophage accumulates in myointimal cells

25 Lipid-laden cells -> atherosis (Hertig, 1945)
Obstruction of the spiral arteriolar lumen by atherosis may impair placental blood flow Placental perfusion -> diminished

26 Immunological Factors
Theory Formation of blocking antibodies of placental antigenic sites might be impaired. Number of antigenic sites provided by the placenta is unusually great compared with the amount of antibody, as with multiple fetuses. (Beer, 1978) Effective immunization by a previous pregnancy is lacking, as in first pregnancies. The immunization concept was supported by their observations that preeclampsia developed less often in multiparas who had a prior term pregnancy (Mostello, 2002; Trupin, 1996)

27 Immunological Factors
Early second timester - Develop preeclampsia women Lower proportion of helper T cells (Th1) Th2 dominance, mediated by adenosine, which is found in higher serum level in preeclamptic compared with normotensive women (Yoneyama, 2002) These helper T lymphocytes secrete specific cytokines that promote implantation, and their dysfunction may favor preeclampsia (Hayashi, 2004; Whitecar, 2001)

28 The Vasculopathy and the Inflammatory Changes
The decidua contains an abundance of cells that, when activated, can release noxious agents. (Staff, 1999) -> mediators to provoke endothelial cell injury Preeclamsia due to an extreme state of activated leukocytes in the maternal circulation (Faas, 2000) Cytokines : TNF-a, interleukin → oxidative stress (highly toxic radicals) Potential benefit of antioxidants to prevent preeclampsia (Chappell, 1999; Zhang, 2002) Antioxidants 283 (high risk women) 주 사이에 vit E, C복용 / 대조군은 placebo복용 결과는 significant reduction : 11% / 17% (Chappell, 1999) – page 780

29 Nutritional Factors Dietary deficiencies and Excesses over the centuries have been blamed as the cause of eclampsia. Supplementation with various elements such as zinc, calcium, and magnesium to prevent preeclampsia (John, 2002) Obesity, is a potent risk factor for preeclampsia C-reactive protein, an inflammatory marker, was shown to be increase in obesity, which in turn was associated with preeclampsia (Wolf, 2001)

30 Genetic Factors Hereditary hypertension is linked to preeclampsia (Ness, 2003) Preeclampsia- eclampsia is highly heritable in sisters, daughters, granddaughters, and daughters-in-law. (Chesley and Cooper, 1986) 60% concordance in monozygotic female twin pairs (Nilsson, 2004) HLA-DR4와 preeclampsia와의 연관성(kilpatrick,1989) Nilsson, swedish, 1,2 million birth : genetic component for gestational hypertension as well as preeclampsia

31 Pathogenesis Vasospasm
Vascular constriction →resistance and subsequent hypertension Maldistribution, ischemia of the surrounding tissues → blood flow 의 감소→ necrosis, hemorrhage, and other end-organ disturbances Subsequent : 차후의

32 Pathogenesis Endothelial cell activation
Unknown factors (from placenta) are secreted into the maternal circulation → activation and dysfunction of the vascular endothelium. Damaged or activated endothelial cells secrete substances → promote coagulation and increase the sensitivity to vasopressors →changes in glomerular capillary endothelial morphology →increasd capillary permeability →elevated blood concentrations

33 Fig 34-3, (Friedman and Lindheimer, 1999)
Pathophysiological considerations in the development of hypertensive disorder due to pregnancy

34 Increased Pressor Responses
Normally, pregnant women develop refractoriness to infused vasopressors (Abdul-Karim an Assali, 1961) But, early preeclampsia women have increased vascular reactivity to infused norepinephrine and angiotensin II (Raab, 1956)

35 Y축 : angiotensin II를 infusion하여 vessel을 contraction시킬 수 있는 최소한의 농도
검은색 실선은 정상 산모, 파란색 실선은 preeclampsia산모

36 Increased Pressor Responses Prostaglandins
In preeclampsia Endothelial prostacyclin (PGI2) production is decreased Thromboxane A2 (TXA2) secretion by platelets is increased → Increased sensitivity to infused angiotensin II → vasoconstriction Membrane phospholipid Phospholipase A2 Arachidonic acid COX1,2 Prostaglandin이 pressor response를 blunt시키는 역할을 할 것으로 예상. PGI2, PGE2 TXA2 Platelet

37 Increased Pressor Responses Nitric oxide
Synthesized from L-arginine by endothelial cells. (potent vasodilator) Nitric oxide maintains the normal low-pressure vasodilated state characteristic of fetoplacental perfusion (Myatt, 1992) Preeclampsia is associated with decreased endothelial nitric oxide synthase expression, which increases cell permeability (Wang, 2004)

38 Increased Pressor Responses Endothelins
Endothelin-1 (ET-1) : potent vasoconstrictors Produced by human endothelium Plasma ET-1 is increased in normotensive pregnant women, but women with preeclampsia have even higher levels (Ajne, 2003 ; Clark, 1992)

39 Increased Pressor Responses Angiogenic factors
Vascular endothelial growth factor (VEGF), Placental growth factor (PIGF), which secretion increases in normal pregnancy Promote angiogenesis Induce nitric oxide Vasodilatory prostaglandins Paradoxically, VEGF is increased in serum from women with preeclampsia, but its bioavailability is decreased (Baker, 1995 ; Simmons, 2000) sFlt 1 (soluble fms-like tyrosine kinase-1) : VEGF antagonist -> preeclampsia때 증가함.

40 Pathophysiology Cardiovascular System
Increased cardiac afterload caused by hypertension Cardiac preload in preeclampsia Pathologically diminished hypervolemia of pregnancy Iatrogenically increased by iv crystalloid or oncotic solution Extravasion into the extracellular space, especially the lung

41 Cardiovascular System Hemodynamic Changes
Preeclampsia Cardiac output elevated before hypertension developed than normal pregnancy. With clinical onset of preeclampsia Marked reduction in cardiac output. Increased peripheral resistance. By contrast, Gestational hypertension Elevated cardiac outputs with development of hypertension.

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43 (Hankin, 1984) Before therapy : G (Y축 : LVSWI)
Fluid restriction : B, H  A Volume expansion : R, P  B (Hankin, 1984)

44 Cardiovascular System Blood volume
Blood volume in term Normal pregnancy : 5000ml Not pregnancy : 3500ml Eclampsia : 3500ml Hemoconcentration in preeclampsia Vasoconstriction and Endothelial dysfunction with vascular permeability. Sevirity 와 연관되어 있지 않음. Whereas, gestational hypertension have a normal blood volume (Silver, 1998)

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46 Cardiovascular System Blood volume
With severe hemoconcentration, an acute fall in hematocrit suggested resolution of preeclampsia Intravascular compartment in eclamptic women is usually not underfilled. → vasospasm and endothelial leakage of plasma has contracted the space to be filled. → It persist some time after delivery when the vascular endothelium repairs. Sensitive to vigorous fluid therapy to expand the contracted blood volume to normal pregnancy levels. Sensitive to even normal blood loss at delivery.

47 Blood and Coagulation Platelet
Thrombocytopenia → life threatening Severe disease : < 100,000/uL Platelet count 감소 -> indication of delivery -> 분만 후 3-5 days, 정상수준으로 회복 Platelet activation, aggregation, consumption -> “exhausion” -> thrombocytopenia (Harlow, 2002) HELLP syndrome : hemolysis (H) , elevated liver enzymes (EL), and low platelets (LP) (Weinstein, 982) Neonatal thrombocytopenia Maternal thrombocytopenia와 연관이 없음. (Prichard, 1987)

48 Blood and Coagulation Coagulation
PT, aPTT, fibrinogen level (routine lab assessment of coagulation) -> preeclampsia 의 management에 필요하지 않음. FDP의 증가 : unknown (but, hepatic derangements 때문일 것으로 추정(Leduc, 1992) ) Thrombophilias : clotting factor deficiencies -> early onset preeclampsia Antithrombin 을 투약하면 대조군에 비해 preeclampsia의 발생빈도를 낮출 수 있음(Chang, 1992) Fibronectin Glycoprotein-vascular endothelial cell basement membrane Preeclampsia의 예측인자로 활용 Derangement : 장애

49 Blood and Coagulation Fragmentation Hemolysis
Severe preeclampsia 때 LDH의 증가 – hemolysis의 증거 Peripheral blood change : Schizocytosis, spherocytosis, reticulocytosis

50 Volume Homeostasis Endocrine changes
Renin, angiotensin, aldosterone 정상 임신에서는 증가 But, preeclampsia에서는 비임신의 정상 level로 감소 기전 : Na + retension, hypertension 에 의해 Juxtaglomerular apparatus에서 renin분비가 감소 Angiotensinogen이 angiotensin I 으로 conversion (renin의 작용) 이 감소 Angiotensin II의 감소 -> aldosterone의 감소 이런 상황에도 불구하고 preeclampsia 산모에서 Na retension이 계속 된다. (Brown, 1988) Aldosterone의 역할 : kidney에서 Na 재 흡수에 관여

51 Volume Homeostasis Endocrine changes
Deoxycorticosterone (DOC) Another potent mineralocorticoid 3rd trimester에 매우 증가 Maternal adrenal gland에서 분비가 증가된 것이 아니라 plasma progesterone의 전환임. 그러므로 Na retension이나 hypertension이 있어도 감소하지 않음 -> preeclampsia의 발병과 지속에 중요한 역할을 담당할 것으로 기대.

52 Volume Homeostasis Endocrine changes
Atrial Natriuretic peptide (ANP) Blood vol. expansion에 의한 atrial wall streching에 의해서 분비됨 Vasoactive한 물질, aldosterone, renin activity, angiotension II, vasopressin의 action을 억제하여 sodium과 water excretion을 조장함. 정상 임신에서도 증가하지만 preeclampsia때는 더욱 증가

53 Volume Homeostasis Fluid and Electrolyte Changes
Preclampsia산모 ECF vol. 이 정상산모보다 더욱 많이 증가. Pathologic retension : endothelial injury Electrolyte concentration do not differ. Electrolyte unbalance가 생기는 경우 Vigorous diuretic therapy Sodium restriction Administration of water with sufficient oxytocin to produce antidiuretisis. Following eclamptic convertion -> lower HCO3

54 Kidney Renal perfusion and glomerular filtration 감소 (in preeclampsia)
Due to vasospasm But, Cr. Level의 감소는 일반적으로 심하지 않음 -> severe한 경우는 2-3배 올라가기도 함. (Pritchard, 1984) Oligouria가 있는 preeclampsia산모에게서 intensive iv fluid therapy는 indication이 아님.

55 Kidney Proteinuria Anatomical changes Preeclampsia-eclampsia 진단에 중요
Late하게 발생. 24hr UA가 중요 Anatomical changes Glomeruli : 20%까지 증가 Glomerular capillary endotheliosis Capillary endothelial swelling with subendothelial deposits of protein materials Acute renal failure Tubular necrosis, cortical necrosis -> oligouria, anuria, rapidly develped azotemia 원인 : HELLP synd. , placental abruption, postpartum hemorrhage

56 Liver Periportal hemorrhagic necrosis in the periphery of the liver lobule Serum liver enzyme 상승의 원인 Nonfatal case에서는 잘 보이지 않음 Autopsy에서 주로 확인 Hepatic rupture(more rare), subcapsular hematoma(more common)을 일으킬 수 있음. Treatment Surgical intervention이 기본, life saving가능 Blood T/F이 도움. Liver transplantation도 시행가능 Spontaneous hepatic rupture 의 mortality :30%

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58 Liver HELLP syndrome Hemolysis, Elevated Liver enzyme and Low Platelet
20% of severe preeclampsia and eclampsia Adverse outcome : 40% Other complication Eclampsia (6%), Placental abruption (10%), ARF (5%), pulmonary edema (10%), subcapsular liver hematoma (1.6%) Steroid Tx. - controversial

59 Brain Common Sx. Anatomical pathology
Headache, visual disturbance – associated convulsion (eclampsia) Anatomical pathology Gross hemorrhage – severe hypertension Chronic hypertension이 있는 경우 더욱 흔함 Postmortem cerebral lesion Edema, hyperemia, focal anemia, thrombosis, hemorrhage

60 Brain Neuroimaging study CT MRI 50%에서 abnormal finding
Hypodense cotical area – petechial hemorrhage and infarction site에 해당 (at autopsy) MRI 주로 post. Cerebral artery area에서 remarkable change가 발견됨. Convulsion과 직접적인 연관 Convulsion 의 25%는 cerebral infarction area가 있음.

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62 Brain Cerebral Blood Flow
Eclampsia : loss of autoregulation of cerebral blood flow (Apollon, 2000) Hyperperfusion – similar in hypertensive encephalopathy. Increased cerebral perfusion –> headache유발 Cerebral vasospasm을 밝혀내지 못함.

63 Brain Blindness Visual disturbance Rare
4hr to 8days 정도까지 지속되지만 결국 완전히 회복된다. Visual disturbance More common Retinal detachement Total loss를 초래 하지는 않음 주로 one side를 involve 수술적치료는 필요없음. 일반적으로 prognosis는 good, 1주일이내에 정상으로 돌아옴

64 Brain Cerebral Edema Electroencephalopgraphy Sx
Letharge, confusion, blurred vision, coma Mental change정도와 brain involvement정도는 어느정도 비례한다. (CT, MRI상 변화) Sudden severe blood pressure elevatoin 광범위한 vasogenic edema로 급격하게 악화 Blood pressure control이 중요함. Electroencephalopgraphy Eclampsia환자의 75%에서 abnormal finding이 나타남. (48hr 이내) 50%이상은 1주일이상 지속하지만 , 3개월 이내에 대부분 좋아진다.

65 Uteroplacental perfusion
Vasospasm -> placental perfusion저하 -> perinatal mortality and morbidity 증가의 중요한 요소 Measurement Spiral a. : 500μm (정상), 200 μm (preeclampsia) Placental blood flow Inaccesibility, complexity, unsuitablity DHAS sulfate-> estradiol-17B (in placenta)의 clearance rate로 간접측정 (Everett, 1980)

66 Uteroplacental perfusion
Doppler Doppler measurement of blood velocity through uterine artery. -> estimate uteroplacental blood flow S/D ratio in preeclampsia : 증가 Abnormal wave form -> fetal indication으로 c/sec필요함. HELLP synd.의 18-36% : abnormal wave form을 보임. Preeclampsia 산모는 정상산모에 비해 mean resistance가 높음.

67 Prediction and Prevention
Lots of attemption to predict preeclampsia in early pregnancy -> poor sensitivity, poor positive predictive value

68 Roll over test 28-32wks Lt. lat. Recumbent position -> supine position Hypertension유발되면 abnormal 이 경우, angiotension II infusion에도 abnormal반응을 보임. Positive predictive value (true positive) : 33% (Dekker, 1990 ; Friedman and Lindhemier, 1999)

69 Uric acid Decreased renal uric acid excretion -> elevated serum uric acid level Jacobson (1990) Uric acid level > 5.9mg/dL at 24wks ; positive predictive value : 33% Weerasekera and Peiris (2003) Serum uric acid levels did not vary significantly before the detection of hypertension

70 Fibronectin Endothelial cell activation -> elevated serum cellular fibronectin level (Brubaker, 1992) Clinical study, Paarlberg (1998) Low sensitivity : 69% Positive predictive value :12% Clinical study, Chavarria (2003) 16wks-20wks, 378 low-risk nulliparas Positive predictive value : 29% Negative predictive value : 98%

71 Oxidative Stress Lipid peroxides level증가 – antioxidants의 activity감소 -> preeclampsia의 prediction가능 (Walsh, 1994) Marker Lipid peroxides: malondialdehyde Pro-oxidants : iron, transferrin, ferritin, blood lipids, TG, free fatty acid, lipoproteins, Vit C & E Hyperhomocysteinemia Atherosclerosis의 risk factor (non pregnant) But, midpregnancy때 level이 높으면 preeclampsia의 risk가 정상보다 3-4배 증가함. (D’Anna, 2004; Hietala, 2001)

72 Cytokines Released by vascular endothelium and leukocytes
50개 이상의 cytokine이 preeclampsia때 증가 Interleukin, TNF – a CRP증가 Not sufficiently predictive (Savvidou, 2002)

73 Placental peptides Corticotropin releasing hormone, chorionic gonadotropin, activin A, inhibin A But, variation이 심해 investigator마다 결과가 다양하게 나타남. Angiogenic factor :VEGF, PlGF First trimester때 PlGF, sFlt1 의 serum level증가 임상적으로 유용하나 의견이 분분.

74 Fetal DNA Identification of Fetal DNA in marternal serum -> prediction of preeclampsia (Zhong, 2001) 이유: endothelial activation and inflammation이 발생하면 fetal cells and cellular material이 maternal circulation에 분비됨.

75 Uterine Artery Doppler Velocimetry
Second trimester – uteroplacental vacular resistance측정 (by doppler of uterine artery) Basic concepts Impaired trophoblastic invasion of the spiral arteries -> uteroplacental blood flow의 감소 Bower (1993) Sensitivity : 78% Positive predictive value :28%

76 Prevention Dietary Manipulation
Salt restriction -> ineffective (Knuist, 1998) Prenatal Ca supplementation -> significant reduction in BP and incidence of preeclampsia (Brucher, 1996) But, Levin, (1997) 4600 nulliparas -> calcium and placebo섭취 -> preeclampsia와 gestational hypertension의 incidence는 두 그룹간의 차이가 없음.

77 Low dose aspirin 60mg aspirin -> reduce the incidence of preeclampsia ; selective TXA2억제, dominence of endothelial prostacyclin (Hauth, 1998, Wallenburg, 1986) Caritis, 1998; CLASP Collaborative Group, 1994; Hauth, 1993, 1998; Rotchell, 1998; Sibai, 1993a Low-dose aspirin was ineffective in preventing preeclampsia

78 Antioxidants Davidge, 1992 Chappel, 1999
Markedly reduced antioxidant activity in preeclampsia women. Chappel, 1999 283 high risk women 18-22wks , vit C & E versus placebo Significant reduction in preeclampsia (11% / 17%)

79 진단 질병 양성 음성 a b c d Sensitivity : a/ a+c Specificity : d/b+d
Positive predictive value : a/a+b Negative predictive value : d/c+d


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