HYPERTENSION IN PREGNANCY Associate Professor Dr Hanifullah Khan
Objectives  Understand definitions Pathophysiology  Presentations of the disease Important signs and symptoms
INTRODUCTION
Introduction  H/T in pregnancy – leading cause of maternal & fetal morbidity The most frequent cause of iatrogenic prematurity PE & eclampsia – delivery is the only effective tx
Definitions – H/T  H/T –  a DBP of 90mmHg or more, taken on 2 occasions > 4 hrs apart  OR A single DBP of > 110mmHg Can occur either in – Women who already have H/T (1 0  or 2 0 ) Manifest in 2 nd  half of pregnancy
Pregnancy HT & Chronic HT May be difficult to differentiate Both have high risk of complications Chr HT –  Diagnosed prepregnancy high BP early in pregnancy
Definitions - PE A multisystem disorder characterized by HT + proteinuria Proteinuria - > 300mg urine pr / 24 hrs Occurs > 20 wks gestation Resolves postnatally Complications of PE – eclampsia, HELLP synd
Definition - Eclampsia The occurrence of tonic-clonic convulsions in a woman with PE Pregnancy  Any gestation No neurological disease
Gestational hypertension. Preeclampsia (mild, severe). Eclampsia. Superimposed preeclampsia upon chronic hypertension. Chronic hypertension with pregnancy. Classification
 
Incidence PE – 2-8% of all pregnancies Risk in 1 st  pregnancy – 4.1% Risk in later pregnancies – 1.7% Risk in woman with PE in 1 st  pregnancies – 14.7% Risk in woman with PE in previous 2 pregnancies – 31.9%
Summary  Gestational hypertension:   Hypertension for first time  after 20 w, without proteinuria. BP returns to normal before 12 weeks postpartum.  Chronic hypertension with pregnancy :  Hypertension antedates pregnancy and detected before 20 w, & lasts more than 12 weeks postpartum.
PATHOPHYSIOLOGY
Basic understanding  Complex disease Appears to be triggered by the placenta Can occur in molar pregnancies where fetus absent
Trophoblast In normal conditions –  Trophoblast invades myometrium Spiral arteries converted to low pressure system This process is inhibited in PE Immunological process also involved Thus HT & PE is caused by abnormal placentation
Other factors Abn placentation  ->  placental insufficiency & IUGR Development of PE requires further changes ↑  Inflammatory activity Widespread vascular endothelial damage Capillary leak, vasoconstriction, intravascular haemolysis, platelet activation ↑  Immune status -  ↑  leucocytes
Pathology  Primarily a disorder of placental dysfunction  leading to a syndrome of endothelial dysfunction with associated vasospasm Evidence of placental insufficiency with associated abnormalities diffuse placental thrombosis, an inflammatory placental decidual vasculopathy, and/or abnormal trophoblastic invasion of the endometrium This supports abnormal placental development or placental damage from diffuse microthrombosis as being central to the development of this disorder
Pathopyhsiology  Placental factors Immune complex deposition in kidney & placenta Impair/ inadequate trophoblast invasion to the spiral  arteries Spiral arteries retain their charecteristic (narrow, tortuous, high resistance) Reduce blood supply  to placenta Result in placental hypoperfusion As a compensation High BP in maternal
2.  Altered vascular reactivity  PG12  angiotensin II vasoconstrict  HPT and reduce placenta blood flow
3.  Coagulation disturbance Activated endothelial cells promote coagulation and increase vasopressor sensitivity Widespread coagulation occur (DIC)  Fibrin deposition in kidney & placenta HPT & placental insufficiency
Summary  The development of PE is mediated through the degree of placental pathology & the maternal inflammatory response
PREECLAMPSIA & ECLAMPSIA
Is the most common medical disorder complicating pregnancy Is the most common hypertensive disorder in pregnancy More common in primigravidas and elderly multipara Occurrence
Chronic hypertension. Chronic nephritis. Past history . Family history. Obesity. Multiple pregnancy. Epidemiology
Maternal personal risk factors for preeclampsia First pregnancy Multigravida pregnant by a different partner Age younger than 18 years or older than 35 years History of preeclampsia Multiple pregnancy Family history of preeclampsia in a first-degree relative Obesity  Preexisting diabetes Chronic hypertension Renal disease Smoking
Multisystem Features Of Preeclampsia Hypertension Proteinuria Eclampsia HELLP syndrome Intra-uterine growth restriction Multi-organ disease Cerebral vessels Fetus Liver Systemic blood vessels Kidneys
Diagnosis Of PE Hypertension  +  Proteinuria = Two facets of a complex  pathophysiological process
Peripheral oedema Not a useful diagnostic criterion Common in pregnancy PE can occur without oedema
Headache. Blurring of vision. Nausea and vomiting. Epigastric pain (distension of the liver capsule) Oliguria or anuria Symptoms – non-specific
The frequency and intensity of the signs and symptoms. The more the severity of PE, the more likely the need to terminate pregnancy Severity of PE
Eclamptic fit stages ( 4 stages): Premonitory stage (1/2 minute): Eye rolled up Twitches of the face and hands. Tonic stage (1/2 minute): Generalized tonic spasm with opisthotonus. Cyanosis. Tongue may be bitten between the clenched teeth.  Diagnosis of Eclampsia
EVALUATION
Evaluation of Hypertension in Pregnancy History ID and Complaint HPI (S/S of Preeclampsia) Past Medical Hx, Past Family Hx  Past Obstetrical Hx, Past Gyne Hx Social Hx Medications, Allergies Prenatal serology, blood work Assess for Hypertension in Pregnancy risk factors Physical BP (essential) Oedema  Hyperreflexia Clonus  Fondoscopy Urine dipstick test  Cardiovascular Respiratory Abdominal  = Epigastric pain, RUQ pain
Cardiovascular Generalized vasospasm Increased peripheral resistance Reduced central venous/ pulmonary pressure Hematological Platelet activation and depletion Coagulopathy Decreased plasma volume Increased blood viscosity Proteinuria Decreased glomerular filtration rate Decreased urate excretion Renal Hepatic Periportal necrosis Subscapular hematoma Cerebral oedema Cerebral haemorrhages Central Nervous System Organ Specific Changes associated with Pre-eclampsia
Clinical presentation Symptoms Signs Headache (frontal/ occipital) Visual disturbance Nausea & vomiting Epigastric and right upper abdominal pain Oliguria / anuria Maybe asymptomatic Rapid rise in BP Papilloedema Fluid retention (non-dependent edema) Hyperreflexia Clonus  Uterus and fetus may feel small for gestational age
Investigations  Urine -  24 hour urine, Proteinuria. Kidney functions -  serum creatinine, urea, creatinine clearance and uric acid. Liver functions -  bilirubin, Enzymes (SGPT and SGOT). Blood -  CBC, HCt , Hemolysis and Platelet count (Thrombocytopenia). Coagulation Profile -  Bleeding and clotting time
Differential Diagnosis: A.  Hypertension With Pregnancy . B. Proteinuria With Pregnancy .  C.  Edema With Pregnancy :
Differential Diagnosis Convulsions Convulsions With Pregnancy : Eclampsia. Epilepsy. Hysteria. Meningitis and Encephalitis. Tetanus. Tetany. Brain tumors. Uremic convulsions
Differential Diagnosis HELLP Syndrome : Acute fatty liver in pregnancy. Hepatitis. Thrombocytopenia purpura. Hemolytic Uremic syndrome.
Treatment PREVENTION. Antepartum  Proper antenatal care Expectant treatment. Control hypertension. Treatment of eclampsia . Prevention and control of convulsions. Termination of pregnancy . Intrapartum care. Postpartum care.
Control of Convulsions: Magnesium Sulfate (MgSO4): It is the drug of choice. Mechanism: CNS depression. Mild VD. Mild diuresis. Inhibits platelet aggregation. Increase PGI2 synthesis.
Prognosis: BP usually normalize after placental delivery . Hypertension may persist. Postpartum eclampsia carries the worst prognosis. Maternal mortality  is about 2% in severe preeclampsia and 10% in eclampsia. Perinatal mortality  rate is about 5% in mild cases, 25% in severe cases and 30% in eclampsia.
CONCLUSIONS
Summary Hypertension  diagnosed prior to  20 weeks' gestation, is generally due to preexisting chronic hypertension rather than pregnancy induce hypertension Pre- eclampsia may be diagnose by a combination of fetal and maternal features, including IUGR, hematological or biochemical abnormalities as well as clinical symptom and signs
Maternal deaths  Confidential Enquiry into Maternal and Child Health UK (2003-2005) 18 deaths from PE & eclampsia 10 deaths caused by IC haemorrhage Due to uncontrolled BP
References  Obstetrics by Ten Teachers 18 th  Edition Obstetrics illustrated 6 th  Edition Lecture Notes Obstetrics and gynaecology 3 rd  Edition http://emedicine.medscape.com/article/261435-overview

Hypertensive disorders in Pregnancy

  • 1.
    HYPERTENSION IN PREGNANCYAssociate Professor Dr Hanifullah Khan
  • 2.
    Objectives Understanddefinitions Pathophysiology Presentations of the disease Important signs and symptoms
  • 3.
  • 4.
    Introduction H/Tin pregnancy – leading cause of maternal & fetal morbidity The most frequent cause of iatrogenic prematurity PE & eclampsia – delivery is the only effective tx
  • 5.
    Definitions – H/T H/T – a DBP of 90mmHg or more, taken on 2 occasions > 4 hrs apart OR A single DBP of > 110mmHg Can occur either in – Women who already have H/T (1 0 or 2 0 ) Manifest in 2 nd half of pregnancy
  • 6.
    Pregnancy HT &Chronic HT May be difficult to differentiate Both have high risk of complications Chr HT – Diagnosed prepregnancy high BP early in pregnancy
  • 7.
    Definitions - PEA multisystem disorder characterized by HT + proteinuria Proteinuria - > 300mg urine pr / 24 hrs Occurs > 20 wks gestation Resolves postnatally Complications of PE – eclampsia, HELLP synd
  • 8.
    Definition - EclampsiaThe occurrence of tonic-clonic convulsions in a woman with PE Pregnancy Any gestation No neurological disease
  • 9.
    Gestational hypertension. Preeclampsia(mild, severe). Eclampsia. Superimposed preeclampsia upon chronic hypertension. Chronic hypertension with pregnancy. Classification
  • 10.
  • 11.
    Incidence PE –2-8% of all pregnancies Risk in 1 st pregnancy – 4.1% Risk in later pregnancies – 1.7% Risk in woman with PE in 1 st pregnancies – 14.7% Risk in woman with PE in previous 2 pregnancies – 31.9%
  • 12.
    Summary Gestationalhypertension: Hypertension for first time after 20 w, without proteinuria. BP returns to normal before 12 weeks postpartum. Chronic hypertension with pregnancy : Hypertension antedates pregnancy and detected before 20 w, & lasts more than 12 weeks postpartum.
  • 13.
  • 14.
    Basic understanding Complex disease Appears to be triggered by the placenta Can occur in molar pregnancies where fetus absent
  • 15.
    Trophoblast In normalconditions – Trophoblast invades myometrium Spiral arteries converted to low pressure system This process is inhibited in PE Immunological process also involved Thus HT & PE is caused by abnormal placentation
  • 16.
    Other factors Abnplacentation -> placental insufficiency & IUGR Development of PE requires further changes ↑ Inflammatory activity Widespread vascular endothelial damage Capillary leak, vasoconstriction, intravascular haemolysis, platelet activation ↑ Immune status - ↑ leucocytes
  • 17.
    Pathology Primarilya disorder of placental dysfunction leading to a syndrome of endothelial dysfunction with associated vasospasm Evidence of placental insufficiency with associated abnormalities diffuse placental thrombosis, an inflammatory placental decidual vasculopathy, and/or abnormal trophoblastic invasion of the endometrium This supports abnormal placental development or placental damage from diffuse microthrombosis as being central to the development of this disorder
  • 18.
    Pathopyhsiology Placentalfactors Immune complex deposition in kidney & placenta Impair/ inadequate trophoblast invasion to the spiral arteries Spiral arteries retain their charecteristic (narrow, tortuous, high resistance) Reduce blood supply to placenta Result in placental hypoperfusion As a compensation High BP in maternal
  • 19.
    2. Alteredvascular reactivity PG12 angiotensin II vasoconstrict HPT and reduce placenta blood flow
  • 20.
    3. Coagulationdisturbance Activated endothelial cells promote coagulation and increase vasopressor sensitivity Widespread coagulation occur (DIC) Fibrin deposition in kidney & placenta HPT & placental insufficiency
  • 21.
    Summary Thedevelopment of PE is mediated through the degree of placental pathology & the maternal inflammatory response
  • 22.
  • 23.
    Is the mostcommon medical disorder complicating pregnancy Is the most common hypertensive disorder in pregnancy More common in primigravidas and elderly multipara Occurrence
  • 24.
    Chronic hypertension. Chronicnephritis. Past history . Family history. Obesity. Multiple pregnancy. Epidemiology
  • 25.
    Maternal personal riskfactors for preeclampsia First pregnancy Multigravida pregnant by a different partner Age younger than 18 years or older than 35 years History of preeclampsia Multiple pregnancy Family history of preeclampsia in a first-degree relative Obesity Preexisting diabetes Chronic hypertension Renal disease Smoking
  • 26.
    Multisystem Features OfPreeclampsia Hypertension Proteinuria Eclampsia HELLP syndrome Intra-uterine growth restriction Multi-organ disease Cerebral vessels Fetus Liver Systemic blood vessels Kidneys
  • 27.
    Diagnosis Of PEHypertension + Proteinuria = Two facets of a complex pathophysiological process
  • 28.
    Peripheral oedema Nota useful diagnostic criterion Common in pregnancy PE can occur without oedema
  • 29.
    Headache. Blurring ofvision. Nausea and vomiting. Epigastric pain (distension of the liver capsule) Oliguria or anuria Symptoms – non-specific
  • 30.
    The frequency andintensity of the signs and symptoms. The more the severity of PE, the more likely the need to terminate pregnancy Severity of PE
  • 31.
    Eclamptic fit stages( 4 stages): Premonitory stage (1/2 minute): Eye rolled up Twitches of the face and hands. Tonic stage (1/2 minute): Generalized tonic spasm with opisthotonus. Cyanosis. Tongue may be bitten between the clenched teeth. Diagnosis of Eclampsia
  • 32.
  • 33.
    Evaluation of Hypertensionin Pregnancy History ID and Complaint HPI (S/S of Preeclampsia) Past Medical Hx, Past Family Hx Past Obstetrical Hx, Past Gyne Hx Social Hx Medications, Allergies Prenatal serology, blood work Assess for Hypertension in Pregnancy risk factors Physical BP (essential) Oedema Hyperreflexia Clonus Fondoscopy Urine dipstick test Cardiovascular Respiratory Abdominal = Epigastric pain, RUQ pain
  • 34.
    Cardiovascular Generalized vasospasmIncreased peripheral resistance Reduced central venous/ pulmonary pressure Hematological Platelet activation and depletion Coagulopathy Decreased plasma volume Increased blood viscosity Proteinuria Decreased glomerular filtration rate Decreased urate excretion Renal Hepatic Periportal necrosis Subscapular hematoma Cerebral oedema Cerebral haemorrhages Central Nervous System Organ Specific Changes associated with Pre-eclampsia
  • 35.
    Clinical presentation SymptomsSigns Headache (frontal/ occipital) Visual disturbance Nausea & vomiting Epigastric and right upper abdominal pain Oliguria / anuria Maybe asymptomatic Rapid rise in BP Papilloedema Fluid retention (non-dependent edema) Hyperreflexia Clonus Uterus and fetus may feel small for gestational age
  • 36.
    Investigations Urine- 24 hour urine, Proteinuria. Kidney functions - serum creatinine, urea, creatinine clearance and uric acid. Liver functions - bilirubin, Enzymes (SGPT and SGOT). Blood - CBC, HCt , Hemolysis and Platelet count (Thrombocytopenia). Coagulation Profile - Bleeding and clotting time
  • 37.
    Differential Diagnosis: A. Hypertension With Pregnancy . B. Proteinuria With Pregnancy . C. Edema With Pregnancy :
  • 38.
    Differential Diagnosis ConvulsionsConvulsions With Pregnancy : Eclampsia. Epilepsy. Hysteria. Meningitis and Encephalitis. Tetanus. Tetany. Brain tumors. Uremic convulsions
  • 39.
    Differential Diagnosis HELLPSyndrome : Acute fatty liver in pregnancy. Hepatitis. Thrombocytopenia purpura. Hemolytic Uremic syndrome.
  • 40.
    Treatment PREVENTION. Antepartum Proper antenatal care Expectant treatment. Control hypertension. Treatment of eclampsia . Prevention and control of convulsions. Termination of pregnancy . Intrapartum care. Postpartum care.
  • 41.
    Control of Convulsions:Magnesium Sulfate (MgSO4): It is the drug of choice. Mechanism: CNS depression. Mild VD. Mild diuresis. Inhibits platelet aggregation. Increase PGI2 synthesis.
  • 42.
    Prognosis: BP usuallynormalize after placental delivery . Hypertension may persist. Postpartum eclampsia carries the worst prognosis. Maternal mortality is about 2% in severe preeclampsia and 10% in eclampsia. Perinatal mortality rate is about 5% in mild cases, 25% in severe cases and 30% in eclampsia.
  • 43.
  • 44.
    Summary Hypertension diagnosed prior to 20 weeks' gestation, is generally due to preexisting chronic hypertension rather than pregnancy induce hypertension Pre- eclampsia may be diagnose by a combination of fetal and maternal features, including IUGR, hematological or biochemical abnormalities as well as clinical symptom and signs
  • 45.
    Maternal deaths Confidential Enquiry into Maternal and Child Health UK (2003-2005) 18 deaths from PE & eclampsia 10 deaths caused by IC haemorrhage Due to uncontrolled BP
  • 46.
    References Obstetricsby Ten Teachers 18 th Edition Obstetrics illustrated 6 th Edition Lecture Notes Obstetrics and gynaecology 3 rd Edition http://emedicine.medscape.com/article/261435-overview