hypertension disorders in pregnancy

1
Hypertensive disorders of pregnancy

• Dr.Makanda

2
LEARNING OBJECTIVES

• At the end of this session, learners should be
  able to
• Define types of hypertensive disorders in
  pregnancy
• Describe the pathophysiology of
  preeclampsia-eclampsia
• Discuss risk factors for preeclampsia-eclampsia
• Recognize the signs, symptoms, and diagnostic
  criteria of preeclampsia-eclampsia
• Describe the management of preeclampsia-eclampsia
  for term and pre-term pregnancies
• Discuss maternal and foetal complications
  associated with preeclampsia-eclampsia

3
General features

1. Hypertensive disorders of pregnancy complicate
   about 10 of pregnancies and are leading cause of
   maternal and perinatal morbidity and mortality.
2. Worldwide 50,000 women die each year.
3. It is the second leading cause of maternal
   mortality in the US (12-18 of deaths)
4. The infant outcomes include still birth and IUFGR

4
Classification

• Classified into Four categories
• Pre existing (chronic )hypertension
• Pre eclampsia with or without severe features or
  eclampsia
• Pre eclampsia superimposed on chronic
  hypertension
• Gestational hypertension,previously called
  pregnancy induced hypertension.

5
Risk factors for Gestational HTNPE

• Advanced maternal age
• Diabetes mellitus
• Primiparity
• Chronic hypertension
• Multiple gestation
• Obesity

• Autoimmune diseases,eg SLE
• Antiphospholipid syndrome
• Previous h/o pre eclampsia
• In vitro fertilization
• Thrombocytopenia

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DEFINITION

• Clinically, it is hypertension and proteinuria,
  with or without edema
• Preeclampsia is the presence of SBP 140 mmHg
  and/or DBP 90 mmHg on two consecutive occasions
  at least 4 hours apart in a previously
  normotensive patient
• In addition to the blood pressure criteria,
  proteinuria of 0.3g in a 24-hour urine, and/or a
  protein/creatinine ratio of 0.3 (mg/mg) OR 30
  mg/µmol and/or a urine dipstick protein of 1 is
  required
• In the absence of proteinuria, new onset
  hypertension and presence of systemic features
  (severe features) is also diagnostic

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Definition (PE with severe features)

• Preeclampsia with severe features is the presence
  of one of the below findings in the presence of
  preeclampsia
• SBP of 160 mmHg and/or DBP of 110 mmHg or
  higher
• Impaired hepatic function (elevated doubled
  liver enzymes)
• Right upper quadrant or epigastric pain
• Renal insufficiency (creatinine gt1.1 mg/dL OR
  97.2 µmol/L)
• New onset of cerebral or visual disturbances e.g.
  severe headache
• Pulmonary edema
• Thrombocytopenia (platelet count lt 100,000/µL)

8
Pre-eclampsia with severe features ..

• The patient may be negative for protein.A urinary
  dipstick for protein is not usually sufficient
  for the diagnosis
• Pulmonary edema and visual or cerebral changes
  constitute severe features of PE

9
Pre eclampsia with severe features..

• Molar pregnancy must be rule out in the patient
  who presents with pre celampsia before 20 weeks
  gestation
• Eclampsia is defined as new-onset of seizures in
  a patient with PE without prior h/o this disorder

10
Gestational HTN

• SBP of 140 or DBP 90 mmHg after 20 weeks
  gestation on two consecutive occasions separated
  by 4hrs without proteinuria or any other end
  organ dysfunction
• Disappears 12 weeks postpartum

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Chronic hypertension

• Chronic hypertension is diagnosed by BP of at
  least 140/90 mm Hg on two occasions 4hrs apart
  at 20 weeks' gestation or earlier.
• Chronic hypertension is associated with
  preeclampsia, IUFGR, and placental abruption
• Treating mild to moderately elevated BP does not
  benefit the fetus or prevent preeclampsia.

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Chronic hypertension..

• Overtreatment may cause adverse perinatal
  outcomes resulting from placental hypoperfusion,
  so medication is reserved for women with BP
  persistently gt 150/100 mm Hg.
• Monitor Women with chronic hypertension for IUFGR
  with serial ultrasonography after fetal
  viability,
• The intervals for monitoring will depend on the
  severity of hypertension, other comorbidities,
  and obstetric history

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CLINICAL FEATURES

• Preeclampsia without severe features may be
  asymptomatic. Many cases are detected through
  routine prenatal screening
• With severe features end-organ effects may
  display as follows

• Headache
• Blindness, Blurred vision, scotomata
• Altered mental status
• Dyspnea
• Edema Sudden increase in or facial

• Epigastric or right upper quadrant abdominal pain
• Weakness or malaise (?evidence of hemolytic
  anemia)
• Clonus (?increased risk of convulsions)

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Treatment

• Methyldopa
• Nifedipine
• OR Labetolol
• NEVER USE-Angiotensin-converting enzyme
  inhibitors and angiotensin II receptor blockers
• REASON They are associated with IUFGR, neonatal
  renal failure, oligohydramnios, and death

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Treatment for Chronic hypertension..

• Avoid also beta blocker atenolol may cause IUFGR
  
• Continue with Thiazide diuretics that were used
  before pregnancy, but stop them if preeclampsia
  develops to avoid worsening intravascular volume
  depletion

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Superimposed PE on chronic hypertension

• ? in blood pressure alone is not sufficient to
  diagnose superimposed PE
• When women with chronic essential hypertension
  develop any of the maternal end-organ
  dysfunctions consistent with pre-eclampsia
• In the absence of pre-existing proteinuria,
  new-onset of proteinuria in the setting of a rise
  in blood pressure is sufficient to diagnose
  superimposed PE

17
Superimposed PE on chronic hypertension

• In women with proteinuric renal disease, an
  increase in proteinuria during pregnancy is not
  sufficient per se to diagnose superimposed PE

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Gestational Hypertension

• Onset of hypertension after 20 weeks' gestation
  and without proteinuria or other criteria for
  preeclampsia.
• Encampasses women who
• Eventually develop preeclampsia,
• Those with unrecognized chronic hypertension
  (diagnosed by persistently elevated BP beyond 12
  weeks postpartum), and
• Have transient hypertension of pregnancy.

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Gestational Hypertension..

• Approx. 50 of women diagnosed with gestational
  hypertension between 24 and 35 weeks' gestation
  ultimately develop preeclampsia.
• Management of gestational hypertension is similar
  to that of preeclampsia, with expectant
  monitoring and labor induction at 37 weeks'
  gestation

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Pre-eclampsia(PE)

• Globally, 76,000 women and 500 000 babies die
  each year from PE.
• Women in low-resource countries are at a higher
  risk of developing PE compared with those in
  high-resource countries.

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Pre-eclampsia (PE)

• Definition Gestational hypertension accompanied
  by 1 of the following new-onset conditions at or
  after 20 weeks of gestation
• Proteinuria (i.e. 30 mg/mol protein creatinine
  ratio 300/24 hour or 2  dipstick)
• Other maternal organ dysfunction, including
• Acute kidney injury (creatinine 90 µmol/L
  1 mg/dL)
• Liver involvement ( ? transaminases, e.g.
  alanine aminotransferase or aspartate
  aminotransferase gt40 IU/L) with or without right
  upper quadrant or epigastric abdominal pain).

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PE..

• Neurological complications ? e.g. eclampsia,
  altered mental status, blindness, stroke, clonus,
  severe headaches, and persistent visual
  scotomata or
• Hematological complications? thrombocytopeniaplat
  elet count lt100 000/mm3, DIC, hemolysis or?

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PE..

• Uteroplacental dysfunction ?IUFGR, abnormal
  umbilical artery Doppler waveform analysis, or
  stillbirth
• NB FIGO adopts the definition of PE as provided
  by the International Society for the Study of
  Hypertension in Pregnancy (ISSHP).

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Subclassifications of PE

• Early-onset PE (with delivery at lt340 weeks of
  gestation)
• Preterm PE (with delivery at lt370 weeks of
  gestation)
• Late-onset PE (with delivery at 340 weeks of
  gestation)
• Term PE (with delivery at 370 weeks of
  gestation).

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PE

• Early-onset PE is associated with a substantial
  risk of both short- and long-term maternal and
  perinatal morbidity and mortality
• A complete understanding of the pathogenesis of
  PE remains unclear,

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Pathophysiology of PE ..

• The current theory suggests a two-stage process.
• The 1st stage caused by shallow invasion of the
  trophoblasts resulting in inadequate remodeling
  of the spiral arteries.
• The 2nd stage-Involves the maternal response to
  endothelial dysfunction and imbalance between
  angiogenic and antiangiogenic factors, resulting
  in the clinical features of the disorder.

27
PE..

• In late-onset disease, placentation is usually
  normal but, feto-placental demands exceed
  supply, resulting in a placental response that
  triggers the clinical phenotype..

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PE..

• While the placenta certainly plays an essential
  role in the development of PE, there are now
  evidences that the maternal cardiovascular system
  may have a significant contribution to the
  disorder

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Risk factors for pre-eclampsia

• Advanced maternal age 35 years at the time of
  delivery
• Parity ?risk in nulliparous women
• Previous h/o PE-?the risk associated with risk of
  early onset PE

• Interpregnancy interval-both short long
  interval have equal association
• Assisted reproduction - use of ART doubles the
  risk. the risk of having PE ? in women exposed to
  hyperestrogenic ovarian stimulation medications

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Risk factors for pre eclampsia..

• Family history of PE-34x ?risk to daughters or
  sisters of women with PE
• Obesity-obesity (BMI 30 kg/m2) confers a 2- 4x
  higher risk for PE.

• Race and ethnicity-?risk in Afro-Caribbean women
  by 2050(some studies) and women of South Asian
  origin
• Comorbidities-DM in Pregnancy both types 12,DM
  requering insulin, HTN, chronic renal disease,
  autoimmune SLE

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Pathogenesis of Preeclampsia

• There is an imbalance in different components of
  prostaglandins
• Relative or absolute deficiency of vasodilator
  prostaglandin (PGI2) from vascular endothelium
  and,
• ?synthesis of thromboxane (TXA2), a potent
  vasoconstrictor in platelets.
• There is increased vascular sensitivity to the
• pressor agent angiotensin-II.
• Depressed angiotensinase activity , following
  proteinuria with elimination of a2 globulin.

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Pathogenesis

• Nitric oxide (NO) deficiency,which is a
• Significant vascular smooth muscle relaxor ,
• Inhibitor of platelet aggregation and
• Prevents intervillous thrombosis
• Its deficiency contributes to hypertension

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Pathogenesis

• Endothelin-1 is
• A potent vasoconstrictor compared to
  angiotensin-II.
• Synthesized by endothelial cells,
• Contributes to the cause of hypertension

34
Pathogenesis

• Endothelial injury from Inflammatory mediators
• Include
• Cytokines tumor necrosis factor (TNF-a),
  interleukins (IL-6) and others derived from
  activated leukocytes
• Abnormal lipid metabolismresults in more
  oxidative stress.

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Pathogenesis
36
Pathogenesis

• Lipid peroxides,reactive oxygen species (ROS) and
  superoxide anion radicals
• Cause endothelial injury and dysfunction.
  Platelet and neutrophil activation, cytokines,
  superoxide radical production and endothelial
  damage are in a vicious cycle.

37
Results

• Endothelial dysfunction and vasospasm.
• The Endothelial dysfunction is due to
• Oxidative stress and the inflammatory mediators.
• Vasospasm results from the imbalance of
  vasodilators and vasoconstrictors.
• Both of which are in a vicious cycle.

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Results .

• EDEMA There is excessive accumulation of fluids
  in the extracellular tissue spaces whose cause is
  not clear.
• Probably due to
• ?oxidative stress ? Endothelial injury ?
  ?capillary permeability.
• On this basis, the leaky capillaries and ? blood
  osmotic pressure are the probable explanations.

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• PROTEINURIA The chain of events is
• Spasm of the afferent glomerular arterioles ?
• glomerular endotheliosis ? ? capillary
  permeability ? ? leakage of proteins.
• There is also simultaneously depressed tubular
  reabsorption .
• Total proteins excreted constitutes
• Albumin 5060 and
• ?- globulin 1015

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Physiological changes

• irc?blood flow of about 1/3 ?20 changes in
  maternal blood vessels ?anatomical and functional
  placental changes ?fetal jeopardy

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Physiological changes ..

• The net effects are
• ? renal blood flow
• ? glomerular filtration rate (25)
• Impaired tubular reabsorption or secretory
  function.
• Recovery is likely to be complete, following
  delivery.
• In severe cases, intense anoxia may produce
  extensive arterial thrombosis ? bilateral renal
  cortical necrosis

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Physiological changes

• Kidney
• The glomeruli becomes enlarged (glomerular
  endotheliosis). Endothelial cells swell up and
  fibrin like deposits occur in the basement
  membrane. The lumen may be occluded.
• Proliferation of interstitial cells .
• There is associated spasm of the afferent
  glomerular arterioles.
• Patchy damage of the tubular epithelium due to
  anoxia.

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Physiological changes ..

• Blood vessels
• There is intense vasospasm.
• Impaired circulation in the vasa vasorum ? damage
  of the vascular walls, including loss of
  endothelial integrity

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Physiological changes ..

• Liver
• Thrombosis of the arterioles ?Periportal hepatic
  hemorrhagic necrosis .
• There may be subcapsular hemorrhage but Hepatic
  insufficiency seldom occurs due to
• Reserve capacity and
• Regenerative ability of hepatic cells.
• LFT are specially abnormal in women with HELLP
  syndrome

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DIAGNOSIS

• Diagnosis of preeclampsia requires a sBP 140 mm
  Hg or a dBP 90 mm Hg on at least two occasions,
  at least 4 hours apart, plus new-onset
  proteinuria or a severe feature
• A single severe feature in combination with
  hypertension is sufficient for the diagnosis.
• Diagnostic criteria for proteinuria include
• At least 300 mg of protein in a 24-hour urine
  sample or
• A urinary protein/creatinine ratio of 0.3 .
• Significant proteinuria is excluded if the
  protein/creatinine ratio is lt 0.19.

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Diagnosis

• Two urine dipstick measurements of at least 1
  (30 mg/dl) taken six hours apart suggest
  preeclampsia-level proteinuria
• Proteinuria is not essential for diagnosis if a
  severe feature is present.
• Urinary protein levels do not correlate with
  outcome severity and are not considered a severe
  feature

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Severe features of pre-eclampsia
1.?blood pressure(sBP 160 mmHg, dBP 110mm Hg)
2. Creatinine level(gt 1.1 mg/dL 97 µmol/L or 2 times baseline)
3.Hepatic dysfunction(transaminase levels 2 times upper limit of normal) or 4.Right upper-quadrant or epigastric pain
5.New-onset of headache or visual disturbances
6.Platelet count lt 100 103 per µL (100 109 per L)
7.Pulmonary edema
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Clinical Features.

• Severe headache, visual disturbances, and
  hyperreflexia may signal impending eclamptic
  seizure.
• Increasing peripheral vascular resistance or
  myocardial dysfunction may lead to pulmonary
  edema.
• Decreased glomerular filtration rate?oliguria
  ?renal failure.

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Clinical Features.

• Liver manifestations ?transaminase levels,
  subcapsular hemorrhage with Rt upper-quadrant
  pain, and capsular rupture with life-threatening
  intraabdominal bleeding.
• Preeclampsia-related coagulopathies HELLP
  (Hemolysis, Elevated liver enzymes, and Low
  Platelet count) syndrome and DIC.
• Obstetric complications IUFGR, placental
  abruption, and fetal demise.

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MANAGEMENT OF PRE-ECLAMPSIA
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Expectant

• INDICATION Preeclampsia without severe features
• Twice-weekly BP monitoring,
• Weekly laboratory tests (FBP, Creatinine levels,
  alanine transaminase, and/or aspartate
  transaminase levels),
• Twice-weekly fetal non-stress test,
• Weekly amniotic fluid indices, and
• Fetal growth USS every three weeks.
• Fetal umbilical artery Doppler ultrasonography to
  Rule out IUFGR
• Seizure prophylaxis with MgSO4 is not required
  unless severe features develop

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MANAGEMENT OF PRE ECLAMPSIA..

• Preeclampsia with severe features
• Admit
• Treatment goals
• Fluid management,
• Seizure prevention,
• Lowering BP to prevent maternal end-organ damage,
  and
• Expediting delivery based on disease severity and
  GA.

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MANAGEMENT OF PRE ECLAMPSIA..

• Note Excessive fluid can result in pulmonary
  edema and ascites, whereas too little fluid can
  exacerbate intravascular volume depletion and
  end-organ ischemia
• Maintain urine output above 30 mL/hour,
• A Foley catheter to monitor urine out put in case
  of MgSO4 administration
• Total IV intake lt100 ml/hour, and total combined
  oral and IV fluids lt 125 ml/hour.

54
MgSO4 for Seizure Prophylaxis

• MgSO4
• Only indicated for Pre-eclampsia with severe
  features .
• Helps to prevent eclamptic seizures and placental
  abruption in women with preeclampsia with severe
  features.
• It is more effective for preventing recurrent
  eclamptic seizures and decreasing maternal
  mortality than phenytoin , diazepam, or a
  combination of chlorpromazine, promethazine, and
  meperidine (Demerol)

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MgSO4 for Seizure Prophylaxis

• BP is only mildly elevated in some women with
  eclampsia
• Those with preeclampsia without severe features
  should be monitored closely, and MgSO4 should be
  started only when severe features develop

56
HELLP Syndrome

• An acronym for Hemolysis (H), Elevated Liver
  enzymes(EL) and Low Platelet count(LP)
  (lt100,000/mm3).
• HELLP syndrome may develop even without maternal
  hypertension.
• This syndrome directly correlates with the
  pathophysiology of the disease.
• A rare complication of pre-eclampsia(1015).
• Very tricky and often women are misdiagnosed

57
HELLP symptoms

• Nausea and vomiting
• General sick feeling
• Epigastric or RUQ pain
• Worsening edema
• Diarrhoea
• Haematuria
• Bleeding gums
• Abdominal, flank or shoulder pain
• Accompanied with biochemical and haematological
  changes

58
HELLP Syndrome

• Parenchymal necrosis of the liver causes
  elevation in hepatic enzymes
• (AST and ALT gt70 IU/L,
• LDH gt 600 IU/L) and
• Bilirubin (gt1.2 mg/dL).
• May cause subcapsular hematoma formation (which
  is diagnosed by CT scanning)and
• Abnormal peripheral blood smear.
• Liver may eventually rupture to ? sudden
  hypotension, due to hemoperitoneum

59
HELLP symptoms and lab

• H-Hemolysis
• Falling hematocrit
• Hyperbilirubinemia
• Increase LDH
• jaundice
• EL-Elevated liver enzymes
• Increase LDH
• Increased AST/ALT
• Feelings of malaise and viral like illness
• Right upper quadrant pain

• LP-Low Platelets
• Falling platelet count
• Abnormal coagulation and fibrinolytic values
• Obstruction of hepatic blood flow and hepatic
  distension
• Epigastric or RUQ pain
• Nausea and vomiting
• Decreased blood glucose

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HELLP what is happening

• Arteriolar vasospasms have damaged the
  endothelium of small blood vessels
• Platelets are accumulating in these lesions and a
  fibrin network is formed
• Red blood cells are forced through the fibrin
  network resulting in damaged erythrocytes
• Liver failure from microemboli in the hepatic
  vasculature

61
Eclampsia
62
Eclampsia

• Eclampsia is the occurrence of seizures
  (generalized tonic-clonic convulsions that cannot
  be attributed to other causes) in a woman with
  preeclampsia.
• The seizures are grand mal and may appear
  antepartum, intrapartum, or postpartum (48 hours
  postpartum up to 10 days postpartum)
• This is an obstetric emergency .

63
Eclampsia..

• Almost without exception, preeclampsia precedes
  the onset of eclamptic convulsions.
• The incidence about 1 in 3250 up to1 in 2000
  deliveries.

64
Diagnosis of eclampsia

• Eclamptic seizures stages (4 stages )
• Eye rolled up
• Twitches of the face and hands
• Generalized tonic spasm with opisthotonus
• Cyanosis
• Tongue may be bitten between the clenched teeth

65
Diagnosis of eclampsia

• Stage (1-2 minutes)
• Convulsions
• Tongue may be bitten
• Face is congested and cyanosed
• Conjunctival congestion
• Blood stained froth from the mouth.
• Stertorous breathing
• Temperature may rise.
• Involuntary passage of urine or stool.
• Gradually convulsions stop.

66
DIAGNOSIS OF ECLAMPSIA

• Variable duration due to respiratory and
  metabolic acidosis.
• Deep coma ? cerebral hemorrhage.
• Labor starts shortly after the seizure.
• Sometimes labor does not start and convulsions
  recur again the so called intercurrent
  eclampsia which carries a bad prognosis

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CLASSIFICATIONS OF ECLAMPSIA

• 1)Mild
• Coma gt 6 hours.
• 2) Severe (Eden's criteria)
• Temperature gt 39C (pneumonia or pontine
  hemorrhage)
• Systolic Bp gt 200 (Risk of cerebral hemorrhage )
• Pulse gt 120/min (acute heart failure).
• Anuria or Oliguria (Renal failure).
• Respiratory rate gt 40/min (pneumonia)
• More than 10 fits (status eclampticus)

68
CLASSIFICATIONS OF ECLAMPSIA

• Intercurrent Eclampsia eclamptic seizures recur
  in the same pregnancy.
• Recurrent Eclampsia eclampsia recurs in
  subsequent pregnancy.

69
CLASSIFICATIONS OF ECLAMPSIA

• Ante-partum (65) with the best prognosis.
• Intrapartum (20).
• Postpartum (15) with the worst prognosis as it
  indicates extensive pathology and multisystem
  damage.

70
PATHOLOGY OF ECLAMPSIA

• Pathological deterioration of function in
  several organs and systems, as a consequence of
  vasospasm and ischemia.
• Maternal and fetal consequences often occur
  simultaneously.
• The major cause of fetal compromise occurs as a
  consequence of reduced uteroplacental perfusion

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PATHOLOGY OF ECLAMPSIA

• CARDIOVASCULAR CHANGES
• ? Increased cardiac afterload caused by
  hypertension,
• ? Cardiac preload, affected by pathologically
  diminished hypervolemia of pregnancy or
  iatrogenically increased by IV. crystalloid or
  oncotic solutions
• ? Endothelial activation with extravasation into
  the extracellular space, especially the lung.

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PATHOLOGY OF ECLAMPSIA

• ? The level of plasma clotting factors?
  decreased
• ? RBC may be traumatized ? display bizarre shapes
  and undergo rapid hemolysis
• ? Intravascular coagulation
• ? Maternal thrombocytopenia can be induced
  acutely the lower the platelet count, the
  greater are maternal and fetal morbidity and
  mortality.

73
Management of eclampsia
74
Management of eclampsia

• A,B,C
• Put the patient on the lateral position
• Prevent tongue bite whenever possible
• Administer anticonvulsant,MGSO4
• Plan for delivery-Ultimate treatment of eclapmsia
  is delivery of the placenta.
• Vaginal delivery is the best unless proved
  otherwise

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The End