hypertensive disorders of pregnancy including PE

11
HYPERTENSIVE HYPERTENSIVE
DISORDERS IN DISORDERS IN
PREGNANCYPREGNANCY
SPEAKER: DR.DEEPTHI.JSPEAKER: DR.DEEPTHI.J
MODERATOR: DR.SUDHAMODERATOR: DR.SUDHA

22


Hypertensive disorders – 5 to 20% of Hypertensive disorders – 5 to 20% of
pregnancies pregnancies

MMR 15 to 20%MMR 15 to 20%

PMR 20 TO 25%PMR 20 TO 25%

33
CLASSIFICATION– NHBPEP 2000CLASSIFICATION– NHBPEP 2000

Gestational hypertensionGestational hypertension

PreeclampsiaPreeclampsia

EclampsiaEclampsia

Superimposed Preeclampsia (on chronic Superimposed Preeclampsia (on chronic
hypertension)hypertension)

Chronic hypertensionChronic hypertension

44
Gestational hypertensionGestational hypertension
Incidence-nulliparous-6-15%,multipara-2-4%Incidence-nulliparous-6-15%,multipara-2-4%
BP≥ 140/90mmHg for first time during BP≥ 140/90mmHg for first time during
pregnancy after 20 weeks of gestationpregnancy after 20 weeks of gestation
No proteinuriaNo proteinuria
BP returns to normal < 12 weeks’ postpartumBP returns to normal < 12 weeks’ postpartum
Final diagnosis made only postpartumFinal diagnosis made only postpartum

55
PreeclampsiaPreeclampsia
Definition: pregnancy specific syndrome of Definition: pregnancy specific syndrome of
reduced organ perfusion secondary to reduced organ perfusion secondary to
vasospasm and endothelial activation.vasospasm and endothelial activation.

66
PreeclampsiaPreeclampsia
Minimum CriteriaMinimum Criteria

BPBP≥140/90mmHg after 20weeks' gestation ≥140/90mmHg after 20weeks' gestation

Proteinuria ≥300mg/24hrs or ≥1+dipstick Proteinuria ≥300mg/24hrs or ≥1+dipstick
Increased certainty of PreeclampsiaIncreased certainty of Preeclampsia

BP≥160/110mmHg BP≥160/110mmHg

Proteinuria 2.0g/24hrs or ≥2+dipstick Proteinuria 2.0g/24hrs or ≥2+dipstick

Serum creatinine >1.2mg/dl unless known to be Serum creatinine >1.2mg/dl unless known to be
previously elevated previously elevated

Platelets <100000/mm3 Platelets <100000/mm3

Microangiopathic hemolysis (Increased LDH) Microangiopathic hemolysis (Increased LDH)

Elevated ALT or AST Elevated ALT or AST

Persistent headache or other cerebral or visual Persistent headache or other cerebral or visual
disturbance disturbance

Persistent epigastric painPersistent epigastric pain

77

88
EclampsiaEclampsia

Preeclampsia+convulsionPreeclampsia+convulsion

Seizures that cannot be attributed to other Seizures that cannot be attributed to other
causes in woman with Preeclampsiacauses in woman with Preeclampsia

Seizures are generalized and may appear Seizures are generalized and may appear
before, during, of after laborbefore, during, of after labor

99
Chronic hypertensionChronic hypertension

Incidence-1-3% of all pregnancies,25-50% of Incidence-1-3% of all pregnancies,25-50% of
HTN disorders in pregnanciesHTN disorders in pregnancies

BP ≥140/90 mmHg before pregnancy or BP ≥140/90 mmHg before pregnancy or
diagnosed before 20weeks’ gestation (not diagnosed before 20weeks’ gestation (not
attributable to gestational trophoblastic disease)attributable to gestational trophoblastic disease)
oror

Hypertension first diagnosed after 20weeks’ Hypertension first diagnosed after 20weeks’
gestation and persistent after 12weeks’ gestation and persistent after 12weeks’
postpartumpostpartum

1010
Underlying Causes of Chronic hypertensive DisorderUnderlying Causes of Chronic hypertensive Disorder
Essential familial hypertension (hypertensive vascular disease)Essential familial hypertension (hypertensive vascular disease)
OBESITYOBESITY
Arterial abnormalitiesArterial abnormalities
Reno vascular hypertensionReno vascular hypertension
Coarctation of the aortaCoarctation of the aorta
Endocrine disordersEndocrine disorders
DIABETES MELLITUSDIABETES MELLITUS
Cushing syndromeCushing syndrome
Primary aldosteronismPrimary aldosteronism
PheochromocytomaPheochromocytoma
ThyrotoxicosisThyrotoxicosis
Glomerulonephritis (acute and chronic)Glomerulonephritis (acute and chronic)
Renoprival hypertensionRenoprival hypertension
Chronic GlomerulonephritisChronic Glomerulonephritis
Chronic renal insufficiencyChronic renal insufficiency
Diabetic nephropathyDiabetic nephropathy
Connective tissue diseaseConnective tissue disease
Lupus erythematosusLupus erythematosus
Systemic sclerosisSystemic sclerosis
Periarteritis nodosaPeriarteritis nodosa
Polycystic kidney diseasePolycystic kidney disease
Acute renal failureAcute renal failure

1111
Preeclampsia superimposed on Preeclampsia superimposed on
Chronic HypertensionChronic Hypertension
Incidence-30%Incidence-30%
New-onset proteinuria≥ 300mg/24hours in New-onset proteinuria≥ 300mg/24hours in
hypertensive women but no proteinuria before hypertensive women but no proteinuria before
20 weeks’ gestation20 weeks’ gestation
A sudden increase in proteinuria or blood A sudden increase in proteinuria or blood
pressure or platelet count <100,000/mmpressure or platelet count <100,000/mm
33
in in
women with hypertension and proteinuria women with hypertension and proteinuria
before 20weeks’ gestationbefore 20weeks’ gestation

1212
Risk factorsRisk factors

1313

1414
EtiologyEtiology
Basic conceptsBasic concepts

Exposed to chorionic villi for the first timeExposed to chorionic villi for the first time

Exposed to a superabundance of chorionic Exposed to a superabundance of chorionic
villi, as with twins or hydatidiform molevilli, as with twins or hydatidiform mole

Have preexisting vascular diseaseHave preexisting vascular disease

Genetically predisposed to hypertension Genetically predisposed to hypertension
developing during pregnancydeveloping during pregnancy

1515

Vascular endothelial damage with Vascular endothelial damage with
vasospasm, transudation of plasma, and vasospasm, transudation of plasma, and
ischemic and thrombotic sequelae.ischemic and thrombotic sequelae.

Currently plausible potential cause (Sibai)Currently plausible potential cause (Sibai)

Abnormal trophoblastic invasion of Uterine Abnormal trophoblastic invasion of Uterine
vesselsvessels

Immunological intolerance between maternal Immunological intolerance between maternal
and fetoplacental tissuesand fetoplacental tissues

Maternal maladaptation to cardiovascular or Maternal maladaptation to cardiovascular or
inflammatory changes of normal pregnancyinflammatory changes of normal pregnancy

Dietary deficienciesDietary deficiencies

Genetic influencesGenetic influences

1616

1717

1818

In PreeclampsiaIn Preeclampsia

Incomplete trophoblastic invasionIncomplete trophoblastic invasion

The magnitude of defective trophoblastic invasion of The magnitude of defective trophoblastic invasion of
the spiral arteries correlated with the severity of the the spiral arteries correlated with the severity of the
hypertensive disorder (2000, Madazli)hypertensive disorder (2000, Madazli)

Using electron microscopyUsing electron microscopy

Endothelial damageEndothelial damage

Insudation of plasma constituents into vessel wallsInsudation of plasma constituents into vessel walls

Proliferation of myointimal cellsProliferation of myointimal cells

Medial necrosisMedial necrosis

Lipid and macrophage accumulates in myointimal Lipid and macrophage accumulates in myointimal
cellscells
Abnormal Trophoblastic InvasionAbnormal Trophoblastic Invasion

1919

Lipid-laden cells -> atherosis (Hertig, 1945)Lipid-laden cells -> atherosis (Hertig, 1945)

Obstruction of the spiral arteriolar lumen by Obstruction of the spiral arteriolar lumen by
atherosis may impair placental blood flowatherosis may impair placental blood flow

Placental perfusion -> diminishedPlacental perfusion -> diminished

2020
Immunological FactorsImmunological Factors

TheoryTheory

Formation of blocking antibodies of placental Formation of blocking antibodies of placental
antigenic sites might be impaired.antigenic sites might be impaired.

Number of antigenic sites provided by the placenta Number of antigenic sites provided by the placenta
is unusually great compared with the amount of is unusually great compared with the amount of
antibody, as with multiple fetuses. antibody, as with multiple fetuses.

Effective immunization by a previous pregnancy is Effective immunization by a previous pregnancy is
lacking, as in first pregnancies.lacking, as in first pregnancies.

The immunization concept was supported by The immunization concept was supported by

their observations that Preeclampsia developed their observations that Preeclampsia developed
less often in multiparas who had a prior term less often in multiparas who had a prior term
pregnancypregnancy

2121
Early second trimester - Preeclamptic womenEarly second trimester - Preeclamptic women

Lower proportion of helper T cells (Th1)Lower proportion of helper T cells (Th1)

Th2 dominance, mediated by adenosine, Th2 dominance, mediated by adenosine,
which is found in higher serum level in which is found in higher serum level in
preeclamptic compared with normotensive preeclamptic compared with normotensive
women (Yoneyama, 2002)women (Yoneyama, 2002)

These helper T lymphocytes secrete specific These helper T lymphocytes secrete specific
cytokines that promote implantation, and cytokines that promote implantation, and
their dysfunction may favor Preeclampsia their dysfunction may favor Preeclampsia
(Hayashi, 2004; Whitecar, 2001)(Hayashi, 2004; Whitecar, 2001)
Immunological FactorsImmunological Factors

2222
The Vasculopathy and the The Vasculopathy and the
Inflammatory ChangesInflammatory Changes
The decidua contains an abundance of cells The decidua contains an abundance of cells
that, when activated, can release noxious that, when activated, can release noxious
agents. -> mediators to provoke endothelial cell agents. -> mediators to provoke endothelial cell
injuryinjury
Preeclampsia due to an extreme state of Preeclampsia due to an extreme state of
activated leukocytes in the maternal circulation activated leukocytes in the maternal circulation
Cytokines : TNF-a, interleukin → oxidative Cytokines : TNF-a, interleukin → oxidative
stress (highly toxic radicals)stress (highly toxic radicals)
Potential benefit of antioxidants to prevent Potential benefit of antioxidants to prevent
PreeclampsiaPreeclampsia

2323
Nutritional FactorsNutritional Factors

Dietary deficiencies and Excesses over the Dietary deficiencies and Excesses over the
centuries have been blamed as the cause of centuries have been blamed as the cause of
Eclampsia.Eclampsia.

Supplementation with various elements such as Supplementation with various elements such as
zinc, calcium, and magnesium to prevent zinc, calcium, and magnesium to prevent
Preeclampsia Preeclampsia

Obesity, is a potent risk factor for PreeclampsiaObesity, is a potent risk factor for Preeclampsia

C-reactive protein, an inflammatory marker, was C-reactive protein, an inflammatory marker, was
shown to be increase in obesity, which in turn shown to be increase in obesity, which in turn
was associated with Preeclampsiawas associated with Preeclampsia

2424
Genetic FactorsGenetic Factors
Hereditary hypertension is linked to Hereditary hypertension is linked to
Preeclampsia Preeclampsia
Preeclampsia- Eclampsia is highly Preeclampsia- Eclampsia is highly
heritable in sisters, daughters, heritable in sisters, daughters,
granddaughters, and daughters-in-law(3 granddaughters, and daughters-in-law(3
fold increased risk). fold increased risk).
60% concordance in monozygotic female 60% concordance in monozygotic female
twin pairs twin pairs
HLA-DR4 Preeclampsia HLA-DR4 Preeclampsia
Angiotensinogen gene variant T235Angiotensinogen gene variant T235

2525
PathogenesisPathogenesis
VasospasmVasospasm

Vascular constriction →resistance and Vascular constriction →resistance and
subsequent hypertensionsubsequent hypertension

Maldistribution, ischemia of the Maldistribution, ischemia of the
surrounding tissues → blood flow → surrounding tissues → blood flow →
necrosis, hemorrhage, and other end-necrosis, hemorrhage, and other end-
organ disturbancesorgan disturbances

2626
PathogenesisPathogenesis
Endothelial cell activationEndothelial cell activation
Unknown factors (from placenta) are secreted Unknown factors (from placenta) are secreted
into the maternal circulation into the maternal circulation
→ → activation and dysfunction of the vascular activation and dysfunction of the vascular
endothelium.endothelium.
Damaged or activated endothelial cells secrete Damaged or activated endothelial cells secrete
substances substances
→ → promote coagulation and increase the promote coagulation and increase the
sensitivity to vasopressorssensitivity to vasopressors
→→changes in glomerular capillary endothelial changes in glomerular capillary endothelial
morphologymorphology
→→increased capillary permeabilityincreased capillary permeability
→→elevated blood concentrationselevated blood concentrations

2727

2828
Increased Pressor ResponsesIncreased Pressor Responses
Normally, pregnant women develop Normally, pregnant women develop
refractoriness to infused vasopressorsrefractoriness to infused vasopressors
But, early Preeclampsia women have But, early Preeclampsia women have
increased vascular reactivity to infused increased vascular reactivity to infused
nor epinephrine and angiotensin IInor epinephrine and angiotensin II
Increased angiotensin II receptors Increased angiotensin II receptors

2929
Prostaglandin imbalanceProstaglandin imbalance

In PreeclampsiaIn Preeclampsia

Endothelial Endothelial
prostacyclin prostacyclin (PGI(PGI
22))
production is production is
decreaseddecreased

Thromboxane AThromboxane A
22
(TXA(TXA
22)) secretion secretion
by platelets is by platelets is
increasedincreased
→ → Increased Increased
sensitivitysensitivity to to
infused infused
angiotensin IIangiotensin II
→ → vasoconstrictionvasoconstriction
Membrane phospholipid
Arachidonic acid
COX1,2
TXA
2
PGI
2
, PGE
2
Phospholipase
A
2
Platelet

3030

Synthesized from L-arginine by Synthesized from L-arginine by
endothelial cells. (potent vasodilator)endothelial cells. (potent vasodilator)

Nitric oxide maintains the normal low-Nitric oxide maintains the normal low-
pressure vasodilated state characteristic pressure vasodilated state characteristic
of fetoplacental perfusion of fetoplacental perfusion

Preeclampsia is associated with Preeclampsia is associated with
decreased endothelial nitric oxide decreased endothelial nitric oxide
synthase expression, which increases cell synthase expression, which increases cell
permeability permeability
Increased Pressor ResponsesIncreased Pressor Responses
Nitric oxideNitric oxide

3131
Endothelin-1 (ET-1) : Endothelin-1 (ET-1) :

potent vasoconstrictorspotent vasoconstrictors

Produced by human endotheliumProduced by human endothelium
Plasma ET-1 is increased in Plasma ET-1 is increased in
normotensive pregnant women, but normotensive pregnant women, but
women with preeclampsia have even women with preeclampsia have even
higher levels higher levels
EndothelinsEndothelins

3232

Vascular endothelial growth factor (VEGF), Vascular endothelial growth factor (VEGF),
Placental growth factor (PIGF), Placental growth factor (PIGF),

secretion increases in normal pregnancysecretion increases in normal pregnancy

Promote angiogenesisPromote angiogenesis

Induce nitric oxideInduce nitric oxide

Vasodilatory prostaglandinsVasodilatory prostaglandins

Paradoxically, VEGF is increased in serum from Paradoxically, VEGF is increased in serum from
women with preeclampsia, but its bioavailability is women with preeclampsia, but its bioavailability is
decreased decreased

sFlt1 is up regulated. It antagonizes VEGF and sFlt1 is up regulated. It antagonizes VEGF and
PIGF.PIGF.
Increased Pressor ResponsesIncreased Pressor Responses
Angiogenic factorsAngiogenic factors

3333
Placental changesPlacental changes

Placenta smaller than normalPlacenta smaller than normal

Premature ageingPremature ageing

Ischaemic necrosis-white infarctsIschaemic necrosis-white infarcts

Intervillous fibrin deposits-red infarctsIntervillous fibrin deposits-red infarcts

Decreased uteroplacental perfusionDecreased uteroplacental perfusion

CalcificationCalcification

3434
Uteroplacental perfusionUteroplacental perfusion

Vasospasm ->Vasospasm ->

placental perfusion-> perinatal mortality and placental perfusion-> perinatal mortality and
morbidity morbidity

MeasurementMeasurement

Spiral a. : 500Spiral a. : 500μμm , 200 m , 200 μμm (preeclampsia)m (preeclampsia)

Placental blood flowPlacental blood flow
•Inaccesibility, complexity, unsuitablityInaccesibility, complexity, unsuitablity

DHAS sulfate-> estradiol-17B (in placenta) DHAS sulfate-> estradiol-17B (in placenta)
clearance rate clearance rate

3535
PathophysiologyPathophysiology
Cardiovascular SystemCardiovascular System

Increased cardiac afterload caused by Increased cardiac afterload caused by
hypertensionhypertension

Cardiac preload in preeclampsiaCardiac preload in preeclampsia

Pathologically diminished hypervolemia of Pathologically diminished hypervolemia of
pregnancypregnancy

Iatrogenically increased by iv crystalloid Iatrogenically increased by iv crystalloid
solutionsolution

CVP normalCVP normal

PCWP normalPCWP normal

LV filling P normal LV filling P normal

Pulmonary oedema- Pulmonary oedema-

3636
Cardiovascular SystemCardiovascular System
Hemodynamic ChangesHemodynamic Changes

BP=CO*PVRBP=CO*PVR

With clinical onset of preeclampsiaWith clinical onset of preeclampsia

Marked reduction in cardiac output.Marked reduction in cardiac output.

Increased peripheral resistance.Increased peripheral resistance.

By contrast, Gestational hypertensionBy contrast, Gestational hypertension

Elevated cardiac outputs with development Elevated cardiac outputs with development
of hypertension.of hypertension.

3737

Blood volume in termBlood volume in term

Normal pregnancy : 5000mlNormal pregnancy : 5000ml

Not pregnancy : 3500mlNot pregnancy : 3500ml

Preeclampsia : 3500mlPreeclampsia : 3500ml

Hemoconcentration in preeclampsiaHemoconcentration in preeclampsia

Vasoconstriction and Endothelial dysfunction Vasoconstriction and Endothelial dysfunction
with vascular permeability.with vascular permeability.

Whereas, gestational hypertension have a Whereas, gestational hypertension have a
normal blood volume normal blood volume
Cardiovascular SystemCardiovascular System
Blood volumeBlood volume

3838

With severe hemoconcentration, an acute fall in With severe hemoconcentration, an acute fall in
hematocrit suggested resolution of hematocrit suggested resolution of
preeclampsiapreeclampsia

Intravascular compartment in eclamptic women Intravascular compartment in eclamptic women
is usually not underfilled. is usually not underfilled.

Sensitive to vigorous fluid therapy to expand the Sensitive to vigorous fluid therapy to expand the
contracted blood volume to normal pregnancy contracted blood volume to normal pregnancy
levels.levels.

Sensitive to even normal blood loss at delivery.Sensitive to even normal blood loss at delivery.
Cardiovascular SystemCardiovascular System
Blood volumeBlood volume

3939
Blood and coagulationBlood and coagulation
Normal pregnancy PreeclampsiaNormal pregnancy Preeclampsia
Factor Factor
VIII,vWF,fibrinogen VIII,vWF,fibrinogen
Very much ,fibrinogen Very much ,fibrinogen
normal unless there is normal unless there is
abruptionabruption
Fibrinolysis ,PAI-Fibrinolysis ,PAI-
1 ,PAI-21 ,PAI-2
Activation of fibrinolysisActivation of fibrinolysis
PAI-1(endothelial PAI-1(endothelial
activation), PAI-activation), PAI-
2(impaired placental 2(impaired placental
function), tPAfunction), tPA
Low alpha 2 antiplasmin Low alpha 2 antiplasmin
levels, FDP, d-dimerlevels, FDP, d-dimer

4040
Normal pregnancy PreeclampsiaNormal pregnancy Preeclampsia
activity of endogenous activity of endogenous
anticoagulantsanticoagulants
Activation of Activation of
coagulation(endothelial coagulation(endothelial
damage).damage).
thrombin,antithrombin thrombin,antithrombin
III complexesIII complexes
antithrombin III levelsantithrombin III levels
cytokines TNF alphacytokines TNF alpha
fibronectin, fibronectin,
thrombomodulinthrombomodulin
thrombin timethrombin time

4141
PT, aPTT, fibrinogen level (routine lab PT, aPTT, fibrinogen level (routine lab
assessment of coagulation) -> preeclampsia assessment of coagulation) -> preeclampsia
management.management.
FDP: unknown (but, hepatic FDP: unknown (but, hepatic
derangements )derangements )
THROMBOCYTOPENIA-due to platelet THROMBOCYTOPENIA-due to platelet
activation,aggregation and consumption at activation,aggregation and consumption at
the site of endothelial damage the site of endothelial damage
Increased mean platelet volume(early Increased mean platelet volume(early
marker).marker).
Platelet count <1 lakh,delivery indicated. Platelet count <1 lakh,delivery indicated.
Blood and CoagulationBlood and Coagulation
CoagulationCoagulation

4242

Severe preeclampsia Severe preeclampsia LDH(>600IU)– LDH(>600IU)–
hemolysishemolysis

Peripheral blood change :Peripheral blood change :

Schizocytosis, spherocytosis, reticulocytosis Schizocytosis, spherocytosis, reticulocytosis
Blood and CoagulationBlood and Coagulation
Fragmentation HemolysisFragmentation Hemolysis

4343
Endocrine changesEndocrine changes


Normal pregnancyNormal pregnancy
renin angiotensin renin angiotensin
II,aldosteroneII,aldosterone
angiotensin IIangiotensin II
DOC(de-oxy DOC(de-oxy
corticosterone)corticosterone)
PreeclampsiaPreeclampsia
renin,angiotensin renin,angiotensin
II,aldosteroneII,aldosterone
DOCDOC
ANP(atrial natriuretic ANP(atrial natriuretic
peptide) due to arterial wall peptide) due to arterial wall
stretching Na and water stretching Na and water
retentionretention
PTH(parathyroid PTH(parathyroid
hormone)hormone)
Hcg, Vit D3, Hcg, Vit D3,
estrogen,progesterone,estrogen,progesterone,
HPLHPL

4444
Volume HomeostasisVolume Homeostasis
Fluid and Electrolyte ChangesFluid and Electrolyte Changes

PreclampsiaPreclampsia

ECF vol. ECF vol.
•Pathologic retention : endothelial injuryPathologic retention : endothelial injury

Electrolyte concentration do not differ.Electrolyte concentration do not differ.

Electrolyte unbalanceElectrolyte unbalance
•Vigorous diuretic therapyVigorous diuretic therapy
•Sodium restrictionSodium restriction
•Administration of water with sufficient oxytocin to Administration of water with sufficient oxytocin to
produce antidiuresis.produce antidiuresis.
Following eclamptic convertion -> lower HCOFollowing eclamptic convertion -> lower HCO
33

4545
KidneyKidney

Renal perfusion and glomerular filtrationRenal perfusion and glomerular filtration
(in preeclampsia)(in preeclampsia)

Due to vasospasmDue to vasospasm
Oliguria(<400 ml in 24 hrs)Oliguria(<400 ml in 24 hrs)
Hyperuricaemia,increased blood urea,serum Hyperuricaemia,increased blood urea,serum
creatininecreatinine

4646
KidneyKidney

ProteinuriaProteinuria

Preeclampsia-eclampsia Preeclampsia-eclampsia

LateLate

24hr UA24hr UA

Anatomical changesAnatomical changes

Glomeruli : 20%Glomeruli : 20%

Glomerular capillary endotheliosisGlomerular capillary endotheliosis
•Capillary endothelial swelling with subendothelial deposits of Capillary endothelial swelling with subendothelial deposits of
protein materialsprotein materials

Acute renal failureAcute renal failure
•Tubular necrosis, cortical necrosis -> oliguria, anuria, rapidly Tubular necrosis, cortical necrosis -> oliguria, anuria, rapidly
develped azotemiadevelped azotemia

4747

4848

4949
LiverLiver

Periportal hemorrhagic necrosis in the Periportal hemorrhagic necrosis in the
periphery of the liver lobuleperiphery of the liver lobule

Serum liver enzyme elevatedSerum liver enzyme elevated

Spontaneous hepatic rupture Spontaneous hepatic rupture mortality :30%mortality :30%

M/S-periportal sinusoids contains fibrin M/S-periportal sinusoids contains fibrin
deposits with hemorrhage in space of DISSE deposits with hemorrhage in space of DISSE
leading to periportal hepatocellular leading to periportal hepatocellular
coagulative necrosis.coagulative necrosis.

5050

5151
LiverLiver

HELLP syndromeHELLP syndrome

Hemolysis, Elevated Liver enzyme and Low Hemolysis, Elevated Liver enzyme and Low
PlateletPlatelet

20% of severe preeclampsia and eclampsia20% of severe preeclampsia and eclampsia

Adverse outcome : 40%Adverse outcome : 40%

Other complicationOther complication
•Eclampsia (6%), Placental Eclampsia (6%), Placental
abruption(10%), ARF (5%), pulmonary abruption(10%), ARF (5%), pulmonary
edema(10%), subcapsular liver edema(10%), subcapsular liver
hematoma(1.6%)hematoma(1.6%)

Steroid Tx. - controversialSteroid Tx. - controversial

5252
BrainBrain

Common Sx.Common Sx.

Headache, visual disturbance – associated Headache, visual disturbance – associated
convulsion (eclampsia)convulsion (eclampsia)

Anatomical pathologyAnatomical pathology

Gross hemorrhage – severe hypertensionGross hemorrhage – severe hypertension
•Chronic hypertensionChronic hypertension

Postmortem cerebral lesionPostmortem cerebral lesion
•Edema, hyperemia, focal anemia, thrombosis, Edema, hyperemia, focal anemia, thrombosis,
hemorrhagehemorrhage

5353
BrainBrain

Neuroimaging studyNeuroimaging study

CTCT
•50%50% abnormal findingabnormal finding
•Hypodense cotical area – petechial hemorrhage Hypodense cotical area – petechial hemorrhage
and infarction siteand infarction site (at autopsy)(at autopsy)

MRIMRI
• post. Cerebral artery areapost. Cerebral artery area remarkable change.remarkable change.
•ConvulsionConvulsion
•Convulsion Convulsion 25%25% cerebral infarction area.cerebral infarction area.

5454

5555
BrainBrain

Cerebral Blood FlowCerebral Blood Flow

Eclampsia : loss of autoregulation of cerebral Eclampsia : loss of autoregulation of cerebral
blood flow blood flow
•Hyperperfusion – similar in hypertensive Hyperperfusion – similar in hypertensive
encephalopathy.encephalopathy.

Increased cerebral perfusion headacheIncreased cerebral perfusion headache

Cerebral vasospasmCerebral vasospasm

5656
BrainBrain
Cerebral EdemaCerebral Edema

SxSx
•Lethargy, confusion, blurred vision, comaLethargy, confusion, blurred vision, coma

Mental change brain involvement. (CT, MRI)Mental change brain involvement. (CT, MRI)

Sudden severe blood pressure elevationSudden severe blood pressure elevation
• vasogenic edemavasogenic edema
•Blood pressure controlBlood pressure control
ElectroencephalopgraphyElectroencephalopgraphy

Eclampsia 75% abnormal finding (48hr )Eclampsia 75% abnormal finding (48hr )

50%.50%.

5757
EYE CHANGESEYE CHANGES
Changes in preeclampsiaChanges in preeclampsia
Retinal edema Retinal edema  constriction of the constriction of the
arterioles (segmental vasospasm) arterioles (segmental vasospasm) 
alteration of the normal ratio of vein : alteration of the normal ratio of vein :
artery diameter from 3:2 to 3:1 artery diameter from 3:2 to 3:1  nicking nicking
of the veins when crossed by the arterioles of the veins when crossed by the arterioles

5858
Grading of hypertensive retinopathyGrading of hypertensive retinopathy
Grade I – Mild generalised arteriolar attenuationGrade I – Mild generalised arteriolar attenuation
Grade II – Marked generalised narrowing of the Grade II – Marked generalised narrowing of the
arteriolesarterioles
Grade III – Marked generalised narrowing + Grade III – Marked generalised narrowing +
copper wiring of arterioles + flame shaped copper wiring of arterioles + flame shaped
haemarrhages + cotton wool spots + hard haemarrhages + cotton wool spots + hard
exudatesexudates
Grade IV – grade III + silver wiring of arterioles + Grade IV – grade III + silver wiring of arterioles +
papilloedemapapilloedema

5959

6060

6161
Signs and symptomsSigns and symptoms

EdemaEdema

Rapid weight gainRapid weight gain

Headache – Frontal/occipitalHeadache – Frontal/occipital

Visual symptoms – scotomata, blurred Visual symptoms – scotomata, blurred
vision, complete blindnessvision, complete blindness

Epigastric pain & right upper quadrant painEpigastric pain & right upper quadrant pain

Oliguria, anuriaOliguria, anuria

6262
SignsSigns

Elevated BP >= 140/90 mm HgElevated BP >= 140/90 mm Hg

Abnormal weight gain>5 lbs in a month or Abnormal weight gain>5 lbs in a month or
1 lb/week in later months of pregnancy1 lb/week in later months of pregnancy

Per abdomen – oligohydraminos,IUGRPer abdomen – oligohydraminos,IUGR

Bilateral pitting edemaBilateral pitting edema

Brisk DTRBrisk DTR

Oliguria <400 ml/24 hrsOliguria <400 ml/24 hrs

6363
PREDICTORS OF PIHPREDICTORS OF PIH
1) Clinical tests1) Clinical tests
a) Mean arterial blood pressurea) Mean arterial blood pressure

87.5 mm of Hg87.5 mm of Hg

sensitivity 0-9%sensitivity 0-9%

specificity 53-97%specificity 53-97%

mean predictive value <10%mean predictive value <10%
b) Roll Over test (Gant)b) Roll Over test (Gant)

28-32 weeks28-32 weeks

sensitivity 0-93%sensitivity 0-93%

specificity 54-91%specificity 54-91%

PPV 33%PPV 33%
c) Isometric exercise (hand grip) test Nisel 1985c) Isometric exercise (hand grip) test Nisel 1985

6464
2) Biochemical tests2) Biochemical tests
a) Microalbuminuria (300mgs/24 hrs) 18 a) Microalbuminuria (300mgs/24 hrs) 18
weeksweeks
b) Hypocalciuria < 195 mgs in 24 hrs b) Hypocalciuria < 195 mgs in 24 hrs
(Maikranz etal 1989)(Maikranz etal 1989)
c) Calcium creatinine ratio false positive c) Calcium creatinine ratio false positive
33% false negative 4% (Tofield)33% false negative 4% (Tofield)
d) Plasmafibronectin ↑ first trimester d) Plasmafibronectin ↑ first trimester
Baligir etal 1989 Baligir etal 1989

6565
3)Renal tests3)Renal tests
a) Uric acid- mild pe 4.5- 5 mgs /dl severe PE a) Uric acid- mild pe 4.5- 5 mgs /dl severe PE
4.8-7.8 mgs/dl 4.8-7.8 mgs/dl
poor fetal prognosis ( Voto etal 1988 ) ppv poor fetal prognosis ( Voto etal 1988 ) ppv
predictive value of the positive test (3.6mgs/dl predictive value of the positive test (3.6mgs/dl
at 28 weeks) quite low (26% ) negative test at 28 weeks) quite low (26% ) negative test
(98% Oney etal 2004)(98% Oney etal 2004)
b) Blood urea Serum Creatinineb) Blood urea Serum Creatinine
c) Urinary kallikerin : creatinine ratio- 16 to 20 c) Urinary kallikerin : creatinine ratio- 16 to 20
weeks ( Millar etal 1996 ) sensitivity 67% weeks ( Millar etal 1996 ) sensitivity 67%
specificity 75% specificity 75%
d) Metabolites of nitric oxide in urine d) Metabolites of nitric oxide in urine
(nitrite/nitrate) Begum etal 1996 (nitrite/nitrate) Begum etal 1996

6666
4) Pressor response test4) Pressor response test 26-30 weeks normal 26-30 weeks normal
preg 13.5-14.5 ng/kg/min ↑ DBP ≥ 20mm of Hg preg 13.5-14.5 ng/kg/min ↑ DBP ≥ 20mm of Hg
PE < 8ng/kg/min sensitivity 22% specificity 85% PE < 8ng/kg/min sensitivity 22% specificity 85%
5) Hormonal tests5) Hormonal tests
a) Hyperprolactinemiaa) Hyperprolactinemia
b) MSAFP ↑ > 2MoM in 2nd Tb) MSAFP ↑ > 2MoM in 2nd T
c) βHCG >2.5 MoMc) βHCG >2.5 MoM
d) ↓ unconjugated estriol < 0.5 MoM d) ↓ unconjugated estriol < 0.5 MoM
6) Newer cytokines6) Newer cytokines
Oxidative stress markers – glutathione Oxidative stress markers – glutathione
peroxidase GPX, superoxidedesmutase SOD, peroxidase GPX, superoxidedesmutase SOD,
malondialdehyde MDA malondialdehyde MDA

6767
7) New markers7) New markers
a) Inhibin A, Activin A, βHCG, αprotein – highest a) Inhibin A, Activin A, βHCG, αprotein – highest
sensitivity and efficiencysensitivity and efficiency
b) sFLT1, PIGF, VEGF- 5 weeks before the b) sFLT1, PIGF, VEGF- 5 weeks before the
clinical onset of the disease. clinical onset of the disease.
c) endoglins- coreceptor for TGF-β1 c) endoglins- coreceptor for TGF-β1
d) (endoglin+ sFLt1) / PIGF- best predictor of d) (endoglin+ sFLt1) / PIGF- best predictor of
term and preterm PE term and preterm PE
e) erythrocyte CRI ↓ e) erythrocyte CRI ↓
8) Ultrasound test-8) Ultrasound test- diastolic notch on uterine diastolic notch on uterine
artery doppler at 20 to 22 weeksartery doppler at 20 to 22 weeks
Umbilical artery S:D ratio Umbilical artery S:D ratio

6868
9) Haematological tests—9) Haematological tests— Hb, PCV, red cell Hb, PCV, red cell
morphology, serum ferritin, platelet count, morphology, serum ferritin, platelet count,
coagulation profile, antithrombin-3 levels.coagulation profile, antithrombin-3 levels.
10) Fetal DNA10) Fetal DNA > 28 weeks > 28 weeks
11) Coagulation activation-11) Coagulation activation- ↑ platelet volume ↑ platelet volume
↑ ↑ PAI 1 : PAI 2 PAI 1 : PAI 2
12) PAPPA ↑12) PAPPA ↑
13)Podocyturia 13)Podocyturia

6969
PREVENTION OF PREECLAMPSIA PREVENTION OF PREECLAMPSIA
Nutritional interventionNutritional intervention
1) Diet (DASH) and exercise 1) Diet (DASH) and exercise
2) Salt restriction, high protein diet, magnesium, 2) Salt restriction, high protein diet, magnesium,
zinc.zinc.
3) Fish oil supplementation- corrects PG 3) Fish oil supplementation- corrects PG
imbalance.imbalance.
4) Calcium supplementation- 2gms/day.4) Calcium supplementation- 2gms/day.
5)Arginine supplementation.5)Arginine supplementation.

7070
Pharmacological interventationPharmacological interventation
1) Role of low dose aspirin- 60 to 75 1) Role of low dose aspirin- 60 to 75
mgs/day—inhibits TXA2 synthesismgs/day—inhibits TXA2 synthesis
CLASP study 12% ↓ PECLASP study 12% ↓ PE
2) Role of antioxidants—vitamin C 2) Role of antioxidants—vitamin C
(1000mgs) vitamin E (400IU/day), (1000mgs) vitamin E (400IU/day),
Lycopene, selenium.Lycopene, selenium.
3) Role of low molecular weight heparin— 3) Role of low molecular weight heparin—
APLA APLA

7171
4) Role of folic acid and other B vitamins 4) Role of folic acid and other B vitamins
5) Role of nitric oxide donors—transdermal 5) Role of nitric oxide donors—transdermal
isosorbide dinitrate, transdermal isosorbide dinitrate, transdermal
glycerine trinitrate.glycerine trinitrate.
6) Japanese herbal medicine- 6) Japanese herbal medicine-
TOKISHAKUYUKU- SAN inhibits L-TOKISHAKUYUKU- SAN inhibits L-
NAME (N omega nitro L arginine methyl NAME (N omega nitro L arginine methyl
ester) ester)
7) Role of antihypertensive agents in women 7) Role of antihypertensive agents in women
with chronic HTN to prevent with chronic HTN to prevent
superimposed preeclampsia.superimposed preeclampsia.

7272
InvestigationsInvestigations

Hb, pcv, peripheral blood smear, platelet countHb, pcv, peripheral blood smear, platelet count

Urine routine, urinary casts, protein/creatinine Urine routine, urinary casts, protein/creatinine
ratio,calcium/creatinine ratioratio,calcium/creatinine ratio

RFT – blood urea, serum creatinine, serum uric RFT – blood urea, serum creatinine, serum uric
acidacid

LFT – SGOT>70 IU/L, SGPT>70IU/L, LDH>600 LFT – SGOT>70 IU/L, SGPT>70IU/L, LDH>600
IU/L, total bilirubin,DBIU/L, total bilirubin,DB

FundusFundus

Doppler flow velocimetryDoppler flow velocimetry

7373
MANAGEMENT OF PEMANAGEMENT OF PE
OBJECTIVES:OBJECTIVES:
Termination of pregnancy with least possible trauma to Termination of pregnancy with least possible trauma to
the mother and the fetus. the mother and the fetus.
Birth of an infant who subsequently thrives.Birth of an infant who subsequently thrives.
Complete restoration of health to the mother.Complete restoration of health to the mother.

Delivery is the definitive cure . Mother is the 1Delivery is the definitive cure . Mother is the 1
stst

safety. Next is the delivery of the live mature new born safety. Next is the delivery of the live mature new born
who will not need intensive & prolonged NICU carewho will not need intensive & prolonged NICU care

7474
MILD PE MANAGEMENTMILD PE MANAGEMENT
Modalities of treatment – hospitalization throughout Modalities of treatment – hospitalization throughout
pregnancy pregnancy
Day care approachDay care approach
Home health care approachHome health care approach
After initial admission & evaluation patient After initial admission & evaluation patient
compliant & improving ambulatory managementcompliant & improving ambulatory management

7575

YESYES
NONO
Mild hypertension PE
Maternal and fetal evaluation
>= 40 weeks gestation
>= 37 weeks gestation
Bishop score >= 6
Non-compliant patient
>= 34 weeks gestation
Labor or rupture of membranes
Abnormal fetal testing
Intrauterine growth restriction
< 37 weeks 37-39 weeks
prostaglandins
•Impatient or outpatient mgmt
•Maternal and fetal evaluation
•Worsening maternal or fetal condition
•40 weeks gestation
•Bishop score >= 6 at >= 37 weeks
•labor
Delivery

7676
Components of hospital management :Components of hospital management :

Daily wt, urine protein . Daily wt, urine protein .

BP 4BP 4
thth
hourly. hourly.

Rest in LLP. Rest in LLP.

Protein rich diet , no salt restrictions, adequate Protein rich diet , no salt restrictions, adequate
calorie intake , no fluid restrictions . calorie intake , no fluid restrictions .

Monitor symptoms of severe PEMonitor symptoms of severe PE

DFMCDFMC

7777

CTG twice a week CTG twice a week

umbilical artery doppler once a week umbilical artery doppler once a week

AFI twice a week AFI twice a week

Ultra sound for fetal growth every 2 – 3 weeks. Ultra sound for fetal growth every 2 – 3 weeks.

LFT , haematocrit, RFT, 24 hr urine , creatinine LFT , haematocrit, RFT, 24 hr urine , creatinine
clearance twice a week clearance twice a week

Platelet count twice a week . Platelet count twice a week .

7878
COMPONENTS OF HOME MANAGEMENT:COMPONENTS OF HOME MANAGEMENT:

Daily weight at homeDaily weight at home

ANC twice weekly - monitor BP ,urine proteinANC twice weekly - monitor BP ,urine protein

Sedentary life styleSedentary life style

Educate about impending signsEducate about impending signs

DFMCDFMC

NST weeklyNST weekly

AFI twice a weekAFI twice a week

Ultra sound for fetal growth every 2-3 weeksUltra sound for fetal growth every 2-3 weeks

LFT , RFT , platelet count twice a weekLFT , RFT , platelet count twice a week

Creatinine clearance once a weekCreatinine clearance once a week

7979
TREATMENT WITH ANTIHYPERTENSIVES:TREATMENT WITH ANTIHYPERTENSIVES:

Overall, randomized trials revealed lower Overall, randomized trials revealed lower
rates of progression to severe disease , with rates of progression to severe disease , with
no improvement in perinatal outcome. no improvement in perinatal outcome.

MgSO4 in mild PE is indicated if the impending MgSO4 in mild PE is indicated if the impending
signs are presentsigns are present

8080
TERM PREGNANCY TERM PREGNANCY
Cervix favorable Cervix favorable
Induction of laborInduction of labor
Prevention of Prevention of
convulsionsconvulsions
Cervix unfavorable Cervix unfavorable
With normal fetus With normal fetus
surveillance & stable BP surveillance & stable BP

HospitalizationHospitalization

Maternal fetal Maternal fetal
surveillance surveillance

Induction once cervix Induction once cervix
ix favorable up to 40 ix favorable up to 40
weeks .weeks .

Expectant mgmt not Expectant mgmt not
to be carried out to be carried out
beyond EDDbeyond EDD

8181

8282
MANAGEMENT OF MANAGEMENT OF
SEVERE PESEVERE PE

8383

yesyes
yesyes
nono
NONO
Severe PE
Admit to labor and delivery area
Maternal and fetal evaluation x 24 hrs
MgSO4 x 24 hrs
Antihypertensives if systolic >= 160 mmHg
Diastolic >=110 or MAP > 125 mmHg
Eclampsia
Pulmonary edema
Acute renal failure
Disseminated intravascular coagulopathy
Suspected abruptio placentae
Nonreassuring fetal status
Labor or rupture of membranes
HELLP syndrome
Severe intrauterine growth restriction
Thrombocytopenia
Persistent symptoms
MgSO4 delivery
Steroids
< 23
weeks
24-32
weeks
32-34
weeks
Termination
of
pregnancy
•Steroids
•Antihypertensives if
needed
•Daily evaluations of
maternal/fetal
conditions
•Delivery at 34 weeks

8484
Management of severe PEManagement of severe PE
Hospitalization for continuous evaluation & Hospitalization for continuous evaluation &
monitoring of maternal & fetal condition . monitoring of maternal & fetal condition .
During this period detailed examination & During this period detailed examination &
search for impending signs . search for impending signs .
Admission wt and urine protein Admission wt and urine protein
BP checked every 15 min until the woman is BP checked every 15 min until the woman is
stabilized and later every 30 min in initial phase stabilized and later every 30 min in initial phase
of assessment . BP checked 4of assessment . BP checked 4
thth
hourly if hourly if
conservative mgmt plan is in place . conservative mgmt plan is in place .
Monitor I/O chart by continuous catheterization . Monitor I/O chart by continuous catheterization .
Fundoscopy . Fundoscopy .

8585
LFT, RFT, platelet count , CBC LFT, RFT, platelet count , CBC
- LFT ,RFT twice a week - LFT ,RFT twice a week
- platelet count once in 2 days. - platelet count once in 2 days.
- coagulation profile if platelet count is less- coagulation profile if platelet count is less
- bed rest- bed rest
Adequate calories & protein rich diet with normal amt Adequate calories & protein rich diet with normal amt
of sodium intake . of sodium intake .
Aggressive treatment of hypertension with Aggressive treatment of hypertension with
antihypertensivesantihypertensives
Prophylactic MgSO4 to prevent convulsions.Prophylactic MgSO4 to prevent convulsions.
Steroids if gestational age < 34 weeks Steroids if gestational age < 34 weeks
- LS ratio if gestational age 32-34 weeks - LS ratio if gestational age 32-34 weeks
Assess for signs of abruptio placenta Assess for signs of abruptio placenta
Indicators of DIC Indicators of DIC

8686
FETAL ASSESSMENT . FETAL ASSESSMENT .

DFMC DFMC

CTG twice a week CTG twice a week

AFI twice a week AFI twice a week

BPP once a week BPP once a week

Fetal growth assessment by serial ultra sound once in Fetal growth assessment by serial ultra sound once in
2-3 weeks2-3 weeks

Doppler once in a week Doppler once in a week

8787
Further mgmt depends on gestational age and Further mgmt depends on gestational age and
severity of PEseverity of PE . .
Aggressive mgmtAggressive mgmt
Involves delivery within Involves delivery within
72 hrs. or delivery after 72 hrs. or delivery after
48 hrs ( 2 doses of 48 hrs ( 2 doses of
steroids ) or delivery steroids ) or delivery
within 6 to 12 hrs ( after within 6 to 12 hrs ( after
stabilizing patient) stabilizing patient)
Expectant mgmtExpectant mgmt
24 – 32 weeks 24 – 32 weeks

8888
PROTOCOL FOR EXPECTANT PROTOCOL FOR EXPECTANT
MGMT MGMT

Bed rest Bed rest

44
thth
hrly BP recording hrly BP recording

Daily wt & protein in morn 1Daily wt & protein in morn 1
stst
sample urine sample urine

Control of BP to < 150/100 with antihypertensivesControl of BP to < 150/100 with antihypertensives

MgSO4 discontinued after 24 hrs MgSO4 discontinued after 24 hrs

24 hr urinary protein once a week 24 hr urinary protein once a week

Daily evaluation for impending signsDaily evaluation for impending signs

LFT , RFT, platelet count( full coagulation profile if LFT , RFT, platelet count( full coagulation profile if
platelet < 1lakh) daily or on alternate days . platelet < 1lakh) daily or on alternate days .

8989

Daily CTG. Daily CTG.

AFI twice a week AFI twice a week

Interval growth every 2-3 weeks Interval growth every 2-3 weeks

Umbilical artery doppler & BPP once a week ( 1 Umbilical artery doppler & BPP once a week ( 1
at mid week & 1 at end of week ) if AFI normal & at mid week & 1 at end of week ) if AFI normal &
umbilical artery doppler is normal .umbilical artery doppler is normal .

If AFI < 5 or umbilical artery doppler shows If AFI < 5 or umbilical artery doppler shows
abnormality then above investigations twice a abnormality then above investigations twice a
week . week .

LS ratio after 32 weeks LS ratio after 32 weeks

9090

9191

9292
Severe hypertension (dBP >= 110 and/or sBP >=160) Severe hypertension (dBP >= 110 and/or sBP >=160)
should be treated to prevent potential cerebrovascular & should be treated to prevent potential cerebrovascular &
cardiovascular complications such as encephalopathy. cardiovascular complications such as encephalopathy.
Hemorrhage & congestive heart failure. Hemorrhage & congestive heart failure.
Some experts advice starting antihypertensive agents Some experts advice starting antihypertensive agents
when the diastolic BP is > 105 mm Hg & others at dBP > when the diastolic BP is > 105 mm Hg & others at dBP >
100 mm Hg. 100 mm Hg.
The ideal BP at which to maintain the pregnant patient is The ideal BP at which to maintain the pregnant patient is
not firmly established, but in general , it should be in the not firmly established, but in general , it should be in the
range of 140 to 155 mm Hg systolic & 90 to 105 mm Hg range of 140 to 155 mm Hg systolic & 90 to 105 mm Hg
diastolic. diastolic.

9393
MANAGEMENT OF ACUTE SEVERE MANAGEMENT OF ACUTE SEVERE
HYPERTENSION IN PREGNANCYHYPERTENSION IN PREGNANCY

3 short acting antihypertensive agents 3 short acting antihypertensive agents
( hydralazine, labetalol, & oral nifedipine) are ( hydralazine, labetalol, & oral nifedipine) are
commonly used to control acute very high BP commonly used to control acute very high BP
in women with severe hypertension in in women with severe hypertension in
pregnancypregnancy

9494
DRUG DRUG DOSEDOSE ONSET ONSET
OF OF
ACTIONACTION
DURATION DURATION
OF ACTIONOF ACTION
ADVERSE ADVERSE
EFFECTSEFFECTS
HYDRALAZINEHYDRALAZINE 5-10mg iv q5-10mg iv q
20min20min
Max 30mgMax 30mg
10-20 10-20
minmin
3-6 hr3-6 hr Tachycardia, Tachycardia,
hypotensionhypotension
Headache, Headache,
flushing,flushing,
neonatal lupus like neonatal lupus like
syndromesyndrome
LABETALOLLABETALOL Initially 20mg Initially 20mg
iv, double the iv, double the
dose every dose every
10min till a 10min till a
cumulative cumulative
dose of dose of
300mg300mg
10-10-
20min20min
3-6 hr3-6 hr Scalp tingling, Scalp tingling,
vomiting, heart vomiting, heart
block, fetal block, fetal
bradycardiabradycardia
NIFEDIPINENIFEDIPINE 10-20 mg oral 10-20 mg oral
q 30 minq 30 min
Max dose Max dose
120-180mg120-180mg
10-15 10-15
minmin
4-5 hr4-5 hr Headache,tachycardiHeadache,tachycardi
a ,synergistic a ,synergistic
interaction with interaction with
MgSO4MgSO4

9595
SODIUM SODIUM
NITROPUNITROPU
RUSSIDERUSSIDE
0.25 – 5 0.25 – 5
microgram/microgram/
kg/min ivkg/min iv
immediateimmediate1-2 1-2
minmin
Nausea, vomiting, Nausea, vomiting,
muscle twitching muscle twitching
thiocyanate and thiocyanate and
cyanide intoxicationcyanide intoxication
NITROGLYNITROGLY
CERINECERINE
5-100 5-100
microgram/microgram/
kg/min ivkg/min iv
2-5 min2-5 min 3-5 3-5
minmin
Headache, Headache,
methemoglobinemiamethemoglobinemia
, tachyphylaxis, tachyphylaxis

9696
Other antihypertensive agentsOther antihypertensive agents
NIMODIPINE – CCB with specific cerebral NIMODIPINE – CCB with specific cerebral
vasodilator activityvasodilator activity
DIAZOXIDE – potassium channel activatorDIAZOXIDE – potassium channel activator
KETANSERIN – serotonin receptor antagonistKETANSERIN – serotonin receptor antagonist
VERAPAMIL – calcium antagonist . VERAPAMIL – calcium antagonist .

9797
FLUID THERAPY IN PRE FLUID THERAPY IN PRE
ECLAMPSIAECLAMPSIA
75-125 ml/hr or 1 ml/kg/hr or urine output in 75-125 ml/hr or 1 ml/kg/hr or urine output in
the preceding hr + 30 ml in preeclamptic the preceding hr + 30 ml in preeclamptic
woman during labor & delivery. woman during labor & delivery.
RL is preferred. RL is preferred.

9898
CENTRAL HEMODYNAMIC CENTRAL HEMODYNAMIC
MONITORINGMONITORING

Indications: 1 refractory oliguria not Indications: 1 refractory oliguria not
responding to fluid challengeresponding to fluid challenge

2 refractory pulmonary edema2 refractory pulmonary edema

3 refractory hypertension, CCF3 refractory hypertension, CCF

CVP maintained at less than 7 cm of waterCVP maintained at less than 7 cm of water

9999
ANALGESIA AND ANESTHESIAANALGESIA AND ANESTHESIA
Regional anesthesia is preferred – epidural Regional anesthesia is preferred – epidural
. Pudendal block . Pudendal block
In LSCS – epidural or general In LSCS – epidural or general
anesthesia .Coagulopathy or severe anesthesia .Coagulopathy or severe
thrombocytopaenia require Awake thrombocytopaenia require Awake
intubation under fibre optic observation . intubation under fibre optic observation .

100100
INDICATIONS FOR LSCSINDICATIONS FOR LSCS

Unfavorable cervix , precluding successful Unfavorable cervix , precluding successful
induction induction

Immediate delivery is needed within 6 hrs. Immediate delivery is needed within 6 hrs.

Preterm < 30 – 32 weeks with IUGRPreterm < 30 – 32 weeks with IUGR

Other obstretrical & fetal indicationOther obstretrical & fetal indication

101101
INTRAPARTUM MGMTINTRAPARTUM MGMT

11
stst
stage - patient confined to bed stage - patient confined to bed
- epidural analgesia or sedatives- epidural analgesia or sedatives
- control of BP with antihypertensives- control of BP with antihypertensives
- monitor BP & pulse half hourly- monitor BP & pulse half hourly
- prophylactic MgSO4- prophylactic MgSO4
- monitor i/o chart - monitor i/o chart
- continuous FHR monitoring- continuous FHR monitoring

102102

22
ndnd
stage - prophylactic forceps stage - prophylactic forceps
- no IV methergin - no IV methergin
- 3- 3
rdrd
stage managed with 5 units IM stage managed with 5 units IM
syntocinon or 5 units IV syntocinon given syntocinon or 5 units IV syntocinon given
slowly .slowly .

33
rdrd
stage – be vigilant about blood loss stage – be vigilant about blood loss
- monitor BP, sudden hypotension - monitor BP, sudden hypotension

103103
POSTPARTUM MANAGEMENT IN PE:POSTPARTUM MANAGEMENT IN PE:

Close monitoring of BPClose monitoring of BP

Most women with gestational hypertension become Most women with gestational hypertension become
normotensive in the 1normotensive in the 1
stst
week postpartum week postpartum

In women with PE, the BP takes a longer time to In women with PE, the BP takes a longer time to
resolveresolve

Antihypertensive drugs should be used if sBP >= 155 Antihypertensive drugs should be used if sBP >= 155
mm hg and/or dBP >= 105 mm Hg. Oral nifedipine 10 mm hg and/or dBP >= 105 mm Hg. Oral nifedipine 10
mg every 6 to 8 hrs or long acting nifedipine 10 mg bd mg every 6 to 8 hrs or long acting nifedipine 10 mg bd
may be used. may be used.

If BP is well controlled the patient may be discharged If BP is well controlled the patient may be discharged
home with instructions for daily monitoring.home with instructions for daily monitoring.

MgSO4 discontinued after 24 hr delivery MgSO4 discontinued after 24 hr delivery

104104

Antihypertensive medications may be Antihypertensive medications may be
discontinued if the BP remains below discontinued if the BP remains below
hypertensive levels for at least 48 hrshypertensive levels for at least 48 hrs

All post partum women must be educated All post partum women must be educated
about the signs and symptoms of severe about the signs and symptoms of severe
hypertension or PEhypertension or PE

All studied antihypertensive agents are All studied antihypertensive agents are
excreted in breast milk. The available data excreted in breast milk. The available data
show that there are no short-term adverse show that there are no short-term adverse
effects on the infant exposed to methyldopa, effects on the infant exposed to methyldopa,
hydralazine or beta-blockers. hydralazine or beta-blockers.

105105
ALPHA METHYL DOPAALPHA METHYL DOPA : :
(Aldomet), it is centrally acting alpha-2 adrenergic stimulant;(Aldomet), it is centrally acting alpha-2 adrenergic stimulant;
It is a pro drug.It is a pro drug.
It acts via the actual metabolite alpha methyl – noradrenaline. It acts via the actual metabolite alpha methyl – noradrenaline.
MOA:MOA:
Causes a reduction in the sympathetic out flow leading to Causes a reduction in the sympathetic out flow leading to
lowering lowering
of noradrenalin release which leads to lowering of BP & of noradrenalin release which leads to lowering of BP &
bradycardia;bradycardia;

It acts peripherally to reduce the adrenergic neuro transmission; It acts peripherally to reduce the adrenergic neuro transmission;

It inhibits the renin release by kidneys It inhibits the renin release by kidneys
alpha-2 stimulator -> is symp. -> NA - BP alpha-2 stimulator -> is symp. -> NA - BP

106106
ActionsActions : After oral / and / IV administration: After oral / and / IV administration

The antihypertensive effect appears after 3-6 hrs The antihypertensive effect appears after 3-6 hrs
& 1-2 hrs respectively& 1-2 hrs respectively
50% of the drug is absorbed orally. Peaks 50% of the drug is absorbed orally. Peaks
after 2-4 hrs; after a latent period of 3-6 hrs, the after 2-4 hrs; after a latent period of 3-6 hrs, the
drug is excreted thro kidneys. drug is excreted thro kidneys.
(the renal BF & GFR not affected &hence the (the renal BF & GFR not affected &hence the
drug is valuable in patients compromised with drug is valuable in patients compromised with
renal function).renal function).

107107
Adverse effectsAdverse effects: :
Headache , sedation , fatigue, drowsiness , forgetfulness, mental Headache , sedation , fatigue, drowsiness , forgetfulness, mental
depression.depression.

Postural hypotension with initial few doses; Postural hypotension with initial few doses;

Fever , cholestatic jaundice , thrombocytopenia, Agranulocytosis. Fever , cholestatic jaundice , thrombocytopenia, Agranulocytosis.

Positive direct combs test in up to 25% patientsPositive direct combs test in up to 25% patients
Rare – GI upset, constipation , nasal congestion, skin rashesRare – GI upset, constipation , nasal congestion, skin rashes
Fetus – rarely intestinal ileusFetus – rarely intestinal ileus

108108
PreparationsPreparations::
250 mg tablets max – 2gms/day inj- 50 250 mg tablets max – 2gms/day inj- 50
mg/mlmg/ml
Even though there is minimal peripheral Even though there is minimal peripheral
action we use this drug in pregnancy – action we use this drug in pregnancy –
because of its time tested nature. because of its time tested nature.

109109
PERIPHERALLY ACTIVE ALPHA-PERIPHERALLY ACTIVE ALPHA-
2 ADRENERGIC ANTAGONISTS2 ADRENERGIC ANTAGONISTS : :
Not extensively used as there are reports of multiple Not extensively used as there are reports of multiple
congenital anomalies.congenital anomalies.
Nifedipine :Nifedipine : It is a calcium channel blocker. It is a calcium channel blocker.
MOAMOA: Calcium channel blockers interfere with the : Calcium channel blockers interfere with the
calcium entry in to the myocardial & vascular smooth calcium entry in to the myocardial & vascular smooth
muscle, thus decreasing the availability of the muscle, thus decreasing the availability of the
intracellular calcium intracellular calcium

110110
Calcium channel blockers relax the vascular smooth Calcium channel blockers relax the vascular smooth
muscle in systemic as well as pulmonary arterial muscle in systemic as well as pulmonary arterial
circulations . They thus decrease the vascular circulations . They thus decrease the vascular
resistance & the BP in both these territories. resistance & the BP in both these territories.
Nifedipine is a potent vasodilator than verapamil. The Nifedipine is a potent vasodilator than verapamil. The
reduction in BP is accompanied by reflex tachycardia reduction in BP is accompanied by reflex tachycardia
in the case of nifedipine but not with verapamil which in the case of nifedipine but not with verapamil which
suppresses the SA node. suppresses the SA node.

111111
ADV effectsADV effects: :
No major teratogenic effects. Headache, palpitation , hypotension, No major teratogenic effects. Headache, palpitation , hypotension,
tachycardia, edema ( effect on micro vasculature) rarely, CCF.tachycardia, edema ( effect on micro vasculature) rarely, CCF.
DosageDosage: :
capsule - 5-10 mg – very short acting . Peak action 30 min.capsule - 5-10 mg – very short acting . Peak action 30 min.
Tablet – 10 mg intermediate acting. Onset-hours. Peak effect 4 Tablet – 10 mg intermediate acting. Onset-hours. Peak effect 4
hrs.hrs.
Sustained release 10 or 20 mg long acting action over 12-21 hrsSustained release 10 or 20 mg long acting action over 12-21 hrs

112112
Beta blockersBeta blockers::
It is mounting evidence that atenolol , may increase the It is mounting evidence that atenolol , may increase the
risk of IUGR. risk of IUGR.
For severe HT, B blockers may be used parenterally; For severe HT, B blockers may be used parenterally;
LabetololLabetolol: :
22
ndnd
commonly used parenteral drug in severe commonly used parenteral drug in severe
hypertensionhypertension
It is a non selective B blocker & selective alpha-1 It is a non selective B blocker & selective alpha-1
blocker; blocker;
used to control severe hypertension. used to control severe hypertension.

113113
MOAMOA: Slows Av conduction decreases HR, : Slows Av conduction decreases HR,
myocardial contractility , decreases PVR myocardial contractility , decreases PVR
and BP. It reduces the BP by decreasing and BP. It reduces the BP by decreasing
the systemic vascular resistance with not the systemic vascular resistance with not
much change in the cardiac output.much change in the cardiac output.
Comparison of labetolol and hydralazine, Comparison of labetolol and hydralazine,
labetolol had more rapid onset of action & labetolol had more rapid onset of action &
less reflex tachycardia. less reflex tachycardia.
FateFate: It is metabolised mainly by : It is metabolised mainly by
conjunction with glucuronic acid conjunction with glucuronic acid
undergoes extensive 1undergoes extensive 1
stst
pass metabolism. pass metabolism.

114114
Dosage and administration: Dosage and administration:
I/V: administration Intermittant I/V: administration Intermittant
dosingdosing
Initial dose 20-80 mg q i/v- over 2mts Initial dose 20-80 mg q i/v- over 2mts
slowlyslowly
Duration of onset - 5-10mtsDuration of onset - 5-10mts
Duration of action - 3-6hrsDuration of action - 3-6hrs

It is usually given in escalating doses of 20, 40, 80 mg every It is usually given in escalating doses of 20, 40, 80 mg every
10min. Max dose 220-300mg10min. Max dose 220-300mg
Oral - 100-200 mg Bid max 2400 mg.Oral - 100-200 mg Bid max 2400 mg.
ADV effects: scalp tingling ,vomiting ,heart block. ADV effects: scalp tingling ,vomiting ,heart block.
Fetal -> neonatal bradycardiaFetal -> neonatal bradycardia

115115
SODIUM NITROPRUSSIDESODIUM NITROPRUSSIDE : :
It is an equal arteriolar & venular vasodilator acting directly on the It is an equal arteriolar & venular vasodilator acting directly on the
vessel wall;vessel wall;
Most potent drug ; crosses placenta uterine BF has been reported Most potent drug ; crosses placenta uterine BF has been reported
to increase ,decrease to increase ,decrease
or unchanged . It acts immediately , duration of action 1-2 min. or unchanged . It acts immediately , duration of action 1-2 min.
ADV effects:ADV effects:
Include metabolic acidosis, toxicity, nausea, vomiting, muscle Include metabolic acidosis, toxicity, nausea, vomiting, muscle
twitching and twitching and
Thiocyanate & cyanide intoxication; sudden hypotension, hyper Thiocyanate & cyanide intoxication; sudden hypotension, hyper
dynamic circulation , dynamic circulation ,
reflex tachycardia . Increase in the c.o, no change in BP. reflex tachycardia . Increase in the c.o, no change in BP.

116116
DoseDose : :
0.25/kg/min every 5 min. light sensitive – the 0.25/kg/min every 5 min. light sensitive – the
pack should be covered . pack should be covered .
Arterial blood gases to be monitored. Arterial blood gases to be monitored.
In practice , nitroprusside is rarely needed to In practice , nitroprusside is rarely needed to
control HT . control HT .

117117
: Hydralazine : Hydralazine

It is a direct arteriolar vasodilator.It is a direct arteriolar vasodilator.

It is metabolised by liver , it has long duration It is metabolised by liver , it has long duration
of action.of action.

Dose : 5mg slow IV. Increase 5 mg every 20-30 Dose : 5mg slow IV. Increase 5 mg every 20-30
min total dose 30 mg . If not controlled with 30 min total dose 30 mg . If not controlled with 30
mg switch over to other drug. mg switch over to other drug.

Onset of action is 10-20 min.Onset of action is 10-20 min.

Duration of action 3-6hrs.Duration of action 3-6hrs.

While giving the drug , BP to be monitored While giving the drug , BP to be monitored
every 2-5 min. every 2-5 min.

118118
ADV effect : ADV effect :

Tachycardia, flushing, aggravation of anginaTachycardia, flushing, aggravation of angina

Headache , palpitations, abruption.Headache , palpitations, abruption.

Acute fetal distress (usually within 6 hrs after Rx)Acute fetal distress (usually within 6 hrs after Rx)

Deceleration in FHR in CTG tracings. Deceleration in FHR in CTG tracings.

More low APGAR scores at 1 min, but no More low APGAR scores at 1 min, but no
significant differences in 5 minsignificant differences in 5 min

Neonatal bradycardia is presentNeonatal bradycardia is present

More still birth with hydralazineMore still birth with hydralazine

The unpredictability of the timing & magnitude of The unpredictability of the timing & magnitude of
BP lowering effect makes its use problematic in BP lowering effect makes its use problematic in
pregnancypregnancy

119119
KETANSERIN : It is a 5HT receptor blocker. It KETANSERIN : It is a 5HT receptor blocker. It
antagonises platelet aggregation, antagonises platelet aggregation,
bronchoconstriction, vasoconstriction. This causes bronchoconstriction, vasoconstriction. This causes
lowering of BP; not much data are available.lowering of BP; not much data are available.
ACE Inhibitors :ACE Inhibitors :
Exposure should be discontinued during Exposure should be discontinued during
pregnancy. Exposure in 2pregnancy. Exposure in 2
ndnd
& 3 & 3
rdrd
trimester have trimester have
been associated with both fetal (oligohydramnios, been associated with both fetal (oligohydramnios,
distress, death) as well as neonatal (renal failure, distress, death) as well as neonatal (renal failure,
IUGR) problems. They are due to direct IUGR) problems. They are due to direct
pharmacological effects.pharmacological effects.

120120
MGMT OF CHRONIC MGMT OF CHRONIC
HYPERTENSIONHYPERTENSION

Hospitalization for patients with 3 or more Hospitalization for patients with 3 or more
antihypertensive agents for assessment antihypertensive agents for assessment
for super imposed PE . for super imposed PE .

The antihypertensive therapy used to The antihypertensive therapy used to
prevent super imposed PEprevent super imposed PE

121121

122122

123123

124124

125125

126126

127127

128128
Complications of Complications of
severe preeclampsiasevere preeclampsia

129129
EclampsiaEclampsia

Greek word—flash of lighteningGreek word—flash of lightening

Definition preeclampsia complicated with Definition preeclampsia complicated with
generalized tonic clonic convulsions during generalized tonic clonic convulsions during
pregnancy, labour, within seven days pregnancy, labour, within seven days
postpartum. Fatal coma without convulsion postpartum. Fatal coma without convulsion
also has been called eclampsia.also has been called eclampsia.

Incidence 2.3% for developing countries Incidence 2.3% for developing countries

0.8% developed countries0.8% developed countries

Mortality 14%Mortality 14%

130130

TypesTypes PreviousPrevious PresentPresent
AntepartumAntepartum 50%50% 38%38%
IntrapartumIntrapartum 30%30% 18%18%
PostpartumPostpartum 20%20% 44%44%

131131

Less than 20 weeks—molar pregnancy, Less than 20 weeks—molar pregnancy,
multiple pregnancy, APLAmultiple pregnancy, APLA

Atypical eclampsiaAtypical eclampsia

Intercurrent eclampsia Intercurrent eclampsia

132132
Impending signsImpending signs
a) persistent occipital or frontal headachea) persistent occipital or frontal headache
b) blurred vision b) blurred vision
c) breathlessnessc) breathlessness
d) nausea, vomiting, epigastric paind) nausea, vomiting, epigastric pain
e) oliguriae) oliguria
f) hyperreflexiaf) hyperreflexia
g) DIC lab evidenceg) DIC lab evidence

133133
StagesStages

Premonitory stagePremonitory stage

Tonic stageTonic stage

Clonic stageClonic stage

Stage of comaStage of coma

Following convulsions- RR↑, PR↑, BP↑, Following convulsions- RR↑, PR↑, BP↑,
high feverhigh fever

134134
Pathophysiology Pathophysiology

Exact cause has not been found outExact cause has not been found out

Increased intracerebral pressureIncreased intracerebral pressure loss of loss of
cerebral autoregulation cerebral autoregulation  dilatation of dilatation of
vessel vessel  hyperperfusion and vasogenic hyperperfusion and vasogenic
oedema oedema

135135
InvestigationsInvestigations

EEG: no pathognomic featureEEG: no pathognomic feature

CAT & MRI: oedema + infarction CAT & MRI: oedema + infarction
subcortical white mattersubcortical white matter

CEREBRAL ANGIO + DOPPLER: CEREBRAL ANGIO + DOPPLER:
presence of vasospasmpresence of vasospasm

136136
MANAGEMENTMANAGEMENT
1) Remain with the patient, call for help1) Remain with the patient, call for help
2) Avoid injury, bedside rails elevate2) Avoid injury, bedside rails elevate
3) Assess and establish airway- LLP 3) Assess and establish airway- LLP
any secretions or vomitus aspirate any secretions or vomitus aspirate
padded tongue blade or airway inserted padded tongue blade or airway inserted
to prevent tongue biteto prevent tongue bite

137137
4) Give oxygen 4-6 liters per minute4) Give oxygen 4-6 liters per minute
insert IV cannula and draw blood sampleinsert IV cannula and draw blood sample
insert catheterinsert catheter
5) Abort convulsions- inj diazepam 10 mg iv or 5) Abort convulsions- inj diazepam 10 mg iv or
clonazepam 1mg iv clonazepam 1mg iv
6) Seizure prophylaxis- MgSO4 and 6) Seizure prophylaxis- MgSO4 and
antihypertensives.antihypertensives.
7) Monitor pulse, BP, RR every 5 minutes until 7) Monitor pulse, BP, RR every 5 minutes until
stable.stable.
8) Monitor FHR, uterine contractions, reflexes, 8) Monitor FHR, uterine contractions, reflexes,
temperature, signs of HELLP and DICtemperature, signs of HELLP and DIC

138138
ANTICONVULSANTS.ANTICONVULSANTS.
MgSO4- drug of choiceMgSO4- drug of choice

Pharmacology- MgSO4.7H2O. metabolized in Pharmacology- MgSO4.7H2O. metabolized in
liver, cleared by renal excretion.liver, cleared by renal excretion.

Plasma half life 4 hrsPlasma half life 4 hrs

MOA- central action- blocks NMDAMOA- central action- blocks NMDA

Peripheral action- blocks Ach at NMJPeripheral action- blocks Ach at NMJ

Other effects- peripheral vasodilatation, Other effects- peripheral vasodilatation,
increases prostacyclin production, decreases increases prostacyclin production, decreases
plasma rennin and angiotensinplasma rennin and angiotensin

No effect on the fetusNo effect on the fetus

139139

Maternal side effectsMaternal side effects

Contraindications- Myasthenia gravis, MIContraindications- Myasthenia gravis, MI

4-7mEq/L-Therapeutic range 4-7mEq/L-Therapeutic range

8-10mEq/L-loss of DTR 8-10mEq/L-loss of DTR

10-15mEq/L-RESP DEPRESSION 10-15mEq/L-RESP DEPRESSION

20-25mEq/L-cardiac arrest 20-25mEq/L-cardiac arrest

140140
REGIMENLOADING REGIMENLOADING
DOSEMAINTAINENCE DOSEPritchard DOSEMAINTAINENCE DOSEPritchard
4gms iv 20% MgSO4, 10gms im 50% 4gms iv 20% MgSO4, 10gms im 50%
MgSO45gms 4th hrly im. MgSO45gms 4th hrly im.
Zuspan 4gms iv 1gm/hr iv Zuspan 4gms iv 1gm/hr iv
Sibai 6gms iv 2gms/hr iv Sibai 6gms iv 2gms/hr iv
Suman Sardesai4gms iv2gms 3hrly Suman Sardesai4gms iv2gms 3hrly
upto 24 hrs upto 24 hrs
Low dose4gms iv, 3gms im into each Low dose4gms iv, 3gms im into each
buttock2.5gms im 4th hrlybuttock2.5gms im 4th hrly

141141
Close monitoringClose monitoring
Monitor Stop infusionMonitor Stop infusion

Urine output < 30ml/hr in Urine output < 30ml/hr in
the preceding 4hrsthe preceding 4hrs

Patellar reflex disappearsPatellar reflex disappears

Respiratory rate < 16/minuteRespiratory rate < 16/minute

142142

Antidote: Calcium gluconate 1gm over 10 Antidote: Calcium gluconate 1gm over 10
minutes (10ml of 10% solution)minutes (10ml of 10% solution)

Administer if patellar reflex disappears, RR Administer if patellar reflex disappears, RR
<16/min<16/min

143143
RECURRENT CONVULSIONSRECURRENT CONVULSIONS

Loading dose Loading dose  wait for 15mins wait for 15mins  if if
convulsions do not stop convulsions do not stop  Rpt 2g of Rpt 2g of
MgSO4 (4ml of 50% MgSO4 + 6ml of MgSO4 (4ml of 50% MgSO4 + 6ml of
saline) slow iv over 10 minssaline) slow iv over 10 mins

If seizures recur while on maintenance If seizures recur while on maintenance
dose, use the same regimen.dose, use the same regimen.

144144
ANTIHYPERTINSIVESANTIHYPERTINSIVES

Aim to maintain BP at 140/90 mm HgAim to maintain BP at 140/90 mm Hg

Cap Nifedipine 5mg orallyCap Nifedipine 5mg orally

After 10mins if diastolic BP > 110, repeat After 10mins if diastolic BP > 110, repeat
same dose.same dose.

Tab. Nifedipine slow release 10-20 mg Tab. Nifedipine slow release 10-20 mg
every 8 hrsevery 8 hrs

145145
TRIALS OF MgSO4TRIALS OF MgSO4

Collobarative trial—diazepam, phenytoin Collobarative trial—diazepam, phenytoin
and MgSO4and MgSO4

MgSO4 significantly lower rate of recurrent MgSO4 significantly lower rate of recurrent
seizures (9.4 vs 23.1)seizures (9.4 vs 23.1)

Lower rate of maternal death (3 vs 4.8)Lower rate of maternal death (3 vs 4.8)

Decreased rate of pneumonia, ICU Decreased rate of pneumonia, ICU
admission, mechanical ventilationadmission, mechanical ventilation

146146
Role of prophylactic MgSO4 Role of prophylactic MgSO4
1) Magpie trial1) Magpie trial
2) Belfort etal2) Belfort etal
3) Coetzee etall3) Coetzee etall
4) Odendall and Hall4) Odendall and Hall
5) Lucas etall5) Lucas etall

147147
Post partum MgSO4Post partum MgSO4

In mild preeclampsia 9.5+/- 4.2 hrsIn mild preeclampsia 9.5+/- 4.2 hrs

Severe preeclampsia 16+/- 5.9 hrsSevere preeclampsia 16+/- 5.9 hrs

HELLP syndrome 20+/- 6.7 hrsHELLP syndrome 20+/- 6.7 hrs

148148
PhenytoinPhenytoin

IV loading dose 15-18mg/kg followed by 100mg IV loading dose 15-18mg/kg followed by 100mg
iv 8th hrlyiv 8th hrly

For prophylaxis 100mgs im/iv 4th hrlyFor prophylaxis 100mgs im/iv 4th hrly

Lytic cocktail regimenLytic cocktail regimen

Chlorpromazine 25mg iv + pethidine 100mgs iv Chlorpromazine 25mg iv + pethidine 100mgs iv
andand

Chlorpromazine 50mgs im + promethazine Chlorpromazine 50mgs im + promethazine
25mgs im25mgs im

Followed by 4th hrly 50mgs im + promethazine Followed by 4th hrly 50mgs im + promethazine
25mgs im25mgs im

MMR 2.2% MMR 2.2%

149149
DiazepamDiazepam

10mgs iv10mgs iv

To prevent seizures—iv infusion 80mgs in To prevent seizures—iv infusion 80mgs in
1 liter 5% dextrose1 liter 5% dextrose

MMR 5%MMR 5%

Side effect—respiratory depression, floppy Side effect—respiratory depression, floppy
baby, hypothermiababy, hypothermia

Antidote— flumazinil Antidote— flumazinil

150150
DELIVERYDELIVERY

Definite treatment of eclampsiaDefinite treatment of eclampsia

Irrespective of the gestational age is deliveryIrrespective of the gestational age is delivery

Once maternal condition is stabilized depending Once maternal condition is stabilized depending
on the cervical status, period of gestation, fetal on the cervical status, period of gestation, fetal
condition and presence of labourcondition and presence of labour

Vaginal delivery safer option—lower mortlity rate Vaginal delivery safer option—lower mortlity rate
as long as labour progresses in orderly fashionas long as labour progresses in orderly fashion

Transient fetal bradycardia—decreased UBFTransient fetal bradycardia—decreased UBF

Maternal hypoxiaMaternal hypoxia fetal hypoxia fetal hypoxia acidosis upto acidosis upto
3mins., if greater than 10mins non reassuring 3mins., if greater than 10mins non reassuring
fetal status(abruptio placenta)fetal status(abruptio placenta)

151151
INDICATIONS FOR LSCSINDICATIONS FOR LSCS

Eclampsia before 34 weeks, unfavorable Eclampsia before 34 weeks, unfavorable
cervix, not in labour, non reassuring fetal cervix, not in labour, non reassuring fetal
heart rateheart rate

152152
HELLP SYNDROMEHELLP SYNDROME
Incidence – 0.2 – 0.6 % of all pregnancies Incidence – 0.2 – 0.6 % of all pregnancies
4 – 12 % in Preeclamptic4 – 12 % in Preeclamptic
30 % of eclampsia – HELLP SYNDROME30 % of eclampsia – HELLP SYNDROME
most common in 3most common in 3
rdrd
trimester,30%post partum trimester,30%post partum
PATHOPHYSIOLOGYPATHOPHYSIOLOGY : :

Hepatic endothelial dysfunction -> platelet aggregation Hepatic endothelial dysfunction -> platelet aggregation
and activation -> distal ischemia and hepatocyte and activation -> distal ischemia and hepatocyte
damage damage

Most common terminal arteriole ->periportal or focal Most common terminal arteriole ->periportal or focal
necrosis with hyaline depositsnecrosis with hyaline deposits

Less common ->large vessel -- hepatic infarction, Less common ->large vessel -- hepatic infarction,
hematomahematoma

153153
Cont ….Cont ….
More common in white woman, multipara, age>35yrsMore common in white woman, multipara, age>35yrs
Higher in severe Preeclamptic women managed Higher in severe Preeclamptic women managed
conservativelyconservatively
Rare before 20wk (consider antiphospholipid syndrome)Rare before 20wk (consider antiphospholipid syndrome)
Various signs and symptoms(not specific hence ultimate Various signs and symptoms(not specific hence ultimate
diagnosis made by lab values)diagnosis made by lab values)
Most common- epigastric pain ,nausea and vomiting(50-80%)Most common- epigastric pain ,nausea and vomiting(50-80%)
Most will have -malaise fever , viral like syndrome , headache Most will have -malaise fever , viral like syndrome , headache
Visual changesVisual changes
Bleeding from mucosal site, hematuria .Bleeding from mucosal site, hematuria .
10-15% MAY NOT HAVE DIASTOLIC > 90 – 95 MMofHG10-15% MAY NOT HAVE DIASTOLIC > 90 – 95 MMofHG
15-20% MAY NOT HAVE PROTENURIA15-20% MAY NOT HAVE PROTENURIA
Occasiolnally : Hypoglycemia, hyponatremia, cortical Occasiolnally : Hypoglycemia, hyponatremia, cortical
blindness, transient nephrogenic diabetesblindness, transient nephrogenic diabetes

154154
LABORATORY DIAGNOSIS:LABORATORY DIAGNOSIS:
1.1.HEMOLYSISHEMOLYSIS: :
•HALLMARK-HALLMARK- microgiopathic hemolytic anemia(schistocyte, burr cell, microgiopathic hemolytic anemia(schistocyte, burr cell,
echintocyte)echintocyte)
•Increase LDH > 600 IU/L(denotes hemolysis + heptocyte damage)Increase LDH > 600 IU/L(denotes hemolysis + heptocyte damage)
•Total bilirubin > 1.2 Mg/dlTotal bilirubin > 1.2 Mg/dl
•Low hematocritLow hematocrit
•Low hepatoglobulinLow hepatoglobulin
2.2.ELEVATED LIVER ENZYMES : ELEVATED LIVER ENZYMES :
•AST > 70 IU/L MOST SENSITIVEAST > 70 IU/L MOST SENSITIVE
•ALT > 70IU/L less time consuming, easier to obtainALT > 70IU/L less time consuming, easier to obtain
•LDH > 600 IU/L ( 5 isomers , 1 & 2 – denotes hepatocyte damage)LDH > 600 IU/L ( 5 isomers , 1 & 2 – denotes hepatocyte damage)

3. LOW PLATELET:
vasoconstriction – platelet aggregation & destruction + altered platelet
membrane – release of arachodonic acid < 100000 / mm3

155155
COAGULATION PROFILECOAGULATION PROFILE

PT/APTT, FIBRINOGENPT/APTT, FIBRINOGEN --- usually normal .. --- usually normal .. In absence of In absence of
complicationscomplications
like abruption , hemorrhage or liver hematoma like abruption , hemorrhage or liver hematoma incidence of DIC 6%.incidence of DIC 6%.

Hence unless platelet < 50000 Hence unless platelet < 50000 routine coagulation profile not indicatedroutine coagulation profile not indicated
NOTENOTE : HELLP can present as slow initial phase followed by a accelerated final : HELLP can present as slow initial phase followed by a accelerated final
phase (phase (hence in suspected cases investigations to be repeated after hence in suspected cases investigations to be repeated after
6 hrs)6 hrs)
CLASSIFICATION :CLASSIFICATION :
1.1.MARTIN etalMARTIN etal : Class 1 - platelet < 50000/mm3 : Class 1 - platelet < 50000/mm3
Class 2 - 50000-100000Class 2 - 50000-100000
Class 3 - 100000 – 150000Class 3 - 100000 – 150000
Predicts maternal outcome , rapidity of recovery , need for Predicts maternal outcome , rapidity of recovery , need for
plasmapheresisplasmapheresis

156156
2.2.MEMPHIS CLASSIFICATIONMEMPHIS CLASSIFICATION ::
Microangiopathic hemoplytic anemiaMicroangiopathic hemoplytic anemia
LDH > 600LDH > 600
AST > 70 AST > 70
PLATELET < 100000PLATELET < 100000

PARTIALPARTIAL : 1 or 2 of the above : 1 or 2 of the above
COMPLETECOMPLETE : all 3 : all 3
3.3.MISSISSIPI CLASSIFICATION :MISSISSIPI CLASSIFICATION :
CLASS 1 CLASS 1
CLASS 2 CLASS 2
CLASS 3CLASS 3
LDH > 600 IU/LLDH > 600 IU/L
AST or ALT > 40 IU/L must be present to all the classesAST or ALT > 40 IU/L must be present to all the classes

157157
STEP WISE MANAGEMENT : STEP WISE MANAGEMENT :
1.1.ANTICIPATE AND MAKE THE DIAGNOSISANTICIPATE AND MAKE THE DIAGNOSIS (differentiate HELLP from (differentiate HELLP from
other imitators)other imitators)
2.2.ASSESS THE MATERNAL CONDITIONASSESS THE MATERNAL CONDITION : history, examination and send : history, examination and send
investigations ( CBC, platelet, LDH,AST , urine , uric acid )investigations ( CBC, platelet, LDH,AST , urine , uric acid )
Start on antihypertensives, MGSO4, steroidsStart on antihypertensives, MGSO4, steroids

ANTIHYPERTENSIVESANTIHYPERTENSIVES : start treatment if systolic > 150 -160, diastolic >100- : start treatment if systolic > 150 -160, diastolic >100-
105. 105.
Not to get below 80-90 since will cause decrease placental perfusionNot to get below 80-90 since will cause decrease placental perfusion
HYDRALAZINEHYDRALAZINE : 5-10mg i.v. every 15 minute . Max dose of 20 mg/hr : 5-10mg i.v. every 15 minute . Max dose of 20 mg/hr
LABETALOLLABETALOL : 20-40 MG every 10 minute. Max dose 220 mg/hr : 20-40 MG every 10 minute. Max dose 220 mg/hr
NIFIDEPINNIFIDEPIN: 10-20 mg every half an hour. Max dose 40 mg/hr: 10-20 mg every half an hour. Max dose 40 mg/hr
NITROPUROSIDENITROPUROSIDE: 0.25 microgram/kg/min. Increase upto 10 : 0.25 microgram/kg/min. Increase upto 10
microgram/kg/min. complication fetal cyanide toxixitymicrogram/kg/min. complication fetal cyanide toxixity

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ANTICONVULSANTSANTICONVULSANTS : : eclamptic convulsion frequently precede or follow eclamptic convulsion frequently precede or follow
HELLPHELLP
Prophylactic Mgso4 Prophylactic Mgso4 4-6gm loading dose, followed by 2-4 gm/hr.4-6gm loading dose, followed by 2-4 gm/hr.
Can continue upto 48hrs postpartum if condition does not stabilize. Can continue upto 48hrs postpartum if condition does not stabilize.
I.V Fluids: 75-120 ml/hr do not overloadI.V Fluids: 75-120 ml/hr do not overload
Maintain urine at atleast 30ml/hrMaintain urine at atleast 30ml/hr
Before cesarean section platelets atleast 50000 and for vaginal delivery atleast Before cesarean section platelets atleast 50000 and for vaginal delivery atleast
20000.20000.
to transfuse platelet if below this level. to transfuse platelet if below this level.
HIGH DOSE STEROIDS –HIGH DOSE STEROIDS –
STEROIDSSTEROIDS: :
5 large randomized trials have seen that : steroids in HELLP syndrome : 5 large randomized trials have seen that : steroids in HELLP syndrome :
Improve laboratory valuesImprove laboratory values
Increase urine outputIncrease urine output
Decrease maternal morbidityDecrease maternal morbidity
Decrease RDS, IVH, necrotizing enterocolitisDecrease RDS, IVH, necrotizing enterocolitis
i.v. better and dose dependant manner of maternal improvementi.v. better and dose dependant manner of maternal improvement

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REGIMESREGIMES: :
1.1.MISSISSIPI UNIVERSITYMISSISSIPI UNIVERSITY : 10mg i.v. 12 hrly : 10mg i.v. 12 hrly
After delivery 10mg i.v. 12 hrly(2 dose), followed by 5 mg i.v. 12 hrly(2 dose)After delivery 10mg i.v. 12 hrly(2 dose), followed by 5 mg i.v. 12 hrly(2 dose)
2.2.NEW REGIME (COG 2005NEW REGIME (COG 2005):):
For most patients with HELPP: For most patients with HELPP:
10 mg i.v. over 6hrs ( 2 dose) , followed by 6 mg i.v. every 6 hrs (2 dose) 10 mg i.v. over 6hrs ( 2 dose) , followed by 6 mg i.v. every 6 hrs (2 dose)
For high risk patients ( platelet < 20000 or CNS manifestations)For high risk patients ( platelet < 20000 or CNS manifestations)
20 mg i.v. every 6 hrs ( for 4 dose) 20 mg i.v. every 6 hrs ( for 4 dose)

Effects short lived upto 48-72 HOURS - after that there occurs a Effects short lived upto 48-72 HOURS - after that there occurs a REBOUND REBOUND
PHENOMENONPHENOMENON

Therefore steroids Therefore steroids create A WINDOWcreate A WINDOW of opportunity for interventions. of opportunity for interventions.

ADVANTAGE ADVANTAGE : :
- To improve the maternal status before delivery , if required ,. - To improve the maternal status before delivery , if required ,.
- Mother benefits even if glucocorticoids were given before for fetal lung maturity- Mother benefits even if glucocorticoids were given before for fetal lung maturity
- < 34 weeks for fetal lung maturity- < 34 weeks for fetal lung maturity
- if by 8-12 hrs of starting steroids , no improvement or conditions worsen think - if by 8-12 hrs of starting steroids , no improvement or conditions worsen think
about other causes (AFLP)about other causes (AFLP)

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DELIVERY REMAINS THE ONLY THERAPYDELIVERY REMAINS THE ONLY THERAPY

Maternal and perinatal mortality increases with expectant management( more Maternal and perinatal mortality increases with expectant management( more
than 3 daysthan 3 days) )
3.3.FETAL ASSESMENTFETAL ASSESMENT : : NST , BPP, USG – iugrNST , BPP, USG – iugr
4.4. TRANSPORT +/- LATENCYTRANSPORT +/- LATENCY – – consider transport if fetus requires tertiary care consider transport if fetus requires tertiary care
n.i.c.u. set up or on the maternal conditionn.i.c.u. set up or on the maternal condition
5.5.DELIVER:DELIVER: PROTOCOLPROTOCOL
ANTEPARTUM--- ( STABILIZE)ANTEPARTUM--- ( STABILIZE)
AntihyperensivesAntihyperensives
Mgso4Mgso4
SteroidsSteroids
If < 34 WK and maternal condition stable fetal and maternal condition does not If < 34 WK and maternal condition stable fetal and maternal condition does not
or alter with steroidsor alter with steroids
If > 35 wk but steroid may raise the platelet orIf > 35 wk but steroid may raise the platelet or
Count if fetal and maternal conditionCount if fetal and maternal condition
Give high dose steroids latency for 24-48hrs detoriates Give high dose steroids latency for 24-48hrs detoriates
DELIVER DELIVER DELIVER DELIVER

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MATERNAL COMPLICATIONS OF HELLP SYNDROME MATERNAL COMPLICATIONS OF HELLP SYNDROME
DIC, abruption , ARF, pulmonary oedema, DIC, abruption , ARF, pulmonary oedema,
cerebral oedema, retinal detachment , laryngeal oedema , cerebral oedema, retinal detachment , laryngeal oedema ,
subcapsular hematoma, ARDS , liver rupture , subcaspsular subcapsular hematoma, ARDS , liver rupture , subcaspsular
hematoma. hematoma.
PERINATAL MORTALITY : PERINATAL MORTALITY : prematurity , iugr, placental abruptionprematurity , iugr, placental abruption
POST PARTUM : POST PARTUM : 30% develop in the post partum period . 30% develop in the post partum period .
majority < 48 hrsmajority < 48 hrs
Dexamethasone : 10 mg 12thhrly till plt > 10000 Dexamethasone : 10 mg 12thhrly till plt > 10000
and LDH decreases and LDH decreases
and normal urine output. And then 5 mg and normal urine output. And then 5 mg
12thhrly 2 doses. 12thhrly 2 doses.

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DIFFERENTIAL DIAGNOSIS: DIFFERENTIAL DIAGNOSIS:
1.1.AFLP (ACUTE FATTY LIVER OF PREGNANCY) AFLP (ACUTE FATTY LIVER OF PREGNANCY)
Associated with coagulation abnormalities , hypoglycemia , increase ammonia Associated with coagulation abnormalities , hypoglycemia , increase ammonia
level, renal dysfunction , bilirubin and uric acid very high , renal dysfunctionlevel, renal dysfunction , bilirubin and uric acid very high , renal dysfunction
2.2.TTP TTP
-- affects cns primarilyaffects cns primarily
- no liver dysfunction- no liver dysfunction
- hypertension not present - hypertension not present
- microangiopathic hemolytic anemia- microangiopathic hemolytic anemia
- shows red cell fragmentation- shows red cell fragmentation
- Treatment – plasmapheresis- Treatment – plasmapheresis
3.3.HUS ( HEMOLYTIC UREMIC SYNDROME)HUS ( HEMOLYTIC UREMIC SYNDROME)
More common in children. In women (m.c in postpartum period)More common in children. In women (m.c in postpartum period)
Renal involvement ( primarily).( Hypertension , proteinuria, rash)Renal involvement ( primarily).( Hypertension , proteinuria, rash)
Treatment – plasmapheresis Treatment – plasmapheresis
OTHERSOTHERS::
Hepatitis, cholecystitis, gastroenteritis, pancreatitis, appendicitis, glomerulonephritis, Hepatitis, cholecystitis, gastroenteritis, pancreatitis, appendicitis, glomerulonephritis,
pyelonephritis, hyperemesis, SLEpyelonephritis, hyperemesis, SLE

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ACUTE LIFE THREATENING EMERGENCIESACUTE LIFE THREATENING EMERGENCIES
1.1.HYPERTENSIVE ENCEPHALOPATHY : HYPERTENSIVE ENCEPHALOPATHY : Subacute neurological Subacute neurological
syndrome characterized by headache, seizures, visual disturbances and syndrome characterized by headache, seizures, visual disturbances and
other neurological disturbances in setting of increase b.pother neurological disturbances in setting of increase b.p
Increase in diastolic b.p. > 120 mmhg associated with increase maternal Increase in diastolic b.p. > 120 mmhg associated with increase maternal
mortalitymortality
If untreated or unrecognized can be fatalIf untreated or unrecognized can be fatal
PATHOPHYSIOLOGYPATHOPHYSIOLOGY : : Cerebral blood flow constant between 60-Cerebral blood flow constant between 60-
120 mmhg. When > 130 mmhg regulatory mechanisms fails -> vessels 120 mmhg. When > 130 mmhg regulatory mechanisms fails -> vessels
fail to constrict -> vessel dilates and plasma exudates -> cerebral fail to constrict -> vessel dilates and plasma exudates -> cerebral
oedema -> compresses vessel -> decrease cerebral blood flow -> oedema -> compresses vessel -> decrease cerebral blood flow ->
spasm of cerebral vessel -> decrease blood flowspasm of cerebral vessel -> decrease blood flow

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CLINICAL FEATURES: CLINICAL FEATURES:

Headache, visual disturbances, confusion, nausea, vomiting, stupor, Headache, visual disturbances, confusion, nausea, vomiting, stupor,
convulsion, retinal hemorrhage, papilloedema. Renal and cardiovascular convulsion, retinal hemorrhage, papilloedema. Renal and cardiovascular
disease. disease.

Both hypertensive encephalopathy and eclampsia appears to be form of an Both hypertensive encephalopathy and eclampsia appears to be form of an
acute process known as acute process known as
REVERSIBLE POSTERIOR LEUKOCEPHALOPATHY SYNDROME REVERSIBLE POSTERIOR LEUKOCEPHALOPATHY SYNDROME

Hypertensive encephalopathy , eclampsia with renal involement + Hypertensive encephalopathy , eclampsia with renal involement +
protenuria.(treatment plasmapheresis) to differentiate between impending protenuria.(treatment plasmapheresis) to differentiate between impending
eclampsia and hypertensive encephalopathy can be difficulteclampsia and hypertensive encephalopathy can be difficult

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POINTS IN FAVOR OF H.EPOINTS IN FAVOR OF H.E

Persistently comatose after seizurePersistently comatose after seizure

Oval pupils, papilloedemaOval pupils, papilloedema

Eye changes more common in H.EEye changes more common in H.E
INVESTIGATIONS:INVESTIGATIONS:
CT scan – hematoma, tumor, contusion.CT scan – hematoma, tumor, contusion.
Most common -> multiple pethecial hemorrhage cortex, subcortical area .Most common -> multiple pethecial hemorrhage cortex, subcortical area .
Oedema at grey and white matter junction in the occipital lobe( hence visual Oedema at grey and white matter junction in the occipital lobe( hence visual
manifestation more common) .manifestation more common) .
MRI -> T2 signal intensity increases MRI -> T2 signal intensity increases
SPECT -> ( single photon emission computed tomography) better than CT and SPECT -> ( single photon emission computed tomography) better than CT and
MRIMRI
SUBARACHNOID MONITOR , epidural monitor, intraventricular catheterSUBARACHNOID MONITOR , epidural monitor, intraventricular catheter

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ONCE DIAGNOSEDONCE DIAGNOSED as increase intra cranial pressure: as increase intra cranial pressure:
1.1.Elevation of head end of the bed(30-45 degree)improves Elevation of head end of the bed(30-45 degree)improves
drainingdraining
2.2.Intubation and hyperventilation. Pco2 < 25-30 hypocapnia Intubation and hyperventilation. Pco2 < 25-30 hypocapnia
causes – cerebral vasoconstriction and decrease CSF causes – cerebral vasoconstriction and decrease CSF
formationformation
3.3.Correct hyponatremia -> hyposmolality -> movement of Correct hyponatremia -> hyposmolality -> movement of
waterwater
4.4.Administer loop or osmotic diuretic->lasix or mannitol( can Administer loop or osmotic diuretic->lasix or mannitol( can
exacerbate pulmonary edema), ureaexacerbate pulmonary edema), urea
5.5.Control of seizure and preventionControl of seizure and prevention
6.6.Withdrawal of CSF -> if intraventricular catheter insituWithdrawal of CSF -> if intraventricular catheter insitu
7.7.Steroids not proven to be beneficial --- if cytotoxic can Steroids not proven to be beneficial --- if cytotoxic can
aggravate.aggravate.

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VISUAL CHANGESVISUAL CHANGES

Blindness following convulsion – 10%Blindness following convulsion – 10%

2 causes : retinal detachment 2 causes : retinal detachment
occipital lobe ischemiaoccipital lobe ischemia


Retinal changes liable to occur when BP > 160/110Retinal changes liable to occur when BP > 160/110

Earliest change - narrowing of the nasal arteriole (increase vein : artery ratio)Earliest change - narrowing of the nasal arteriole (increase vein : artery ratio)

Severe persistent spasm – hypoxic retinopathy (hemorrhage, exudates and Severe persistent spasm – hypoxic retinopathy (hemorrhage, exudates and
edema) indication for terminationedema) indication for termination

Rarely permanent visual defects: cerebral infarction, retinal artery infarction. Rarely permanent visual defects: cerebral infarction, retinal artery infarction.
KEITH & WEGNER GRADING : KEITH & WEGNER GRADING :

Grade 1 : mild arteriolar attenuationGrade 1 : mild arteriolar attenuation

Grade 2 : marked narrowing of the arterioles deflection of the vein at AVGrade 2 : marked narrowing of the arterioles deflection of the vein at AV
crossingcrossing

Grade 3 : grade 2 + copper wiringGrade 3 : grade 2 + copper wiring

Grade 4 : grade 3 +silver wiringGrade 4 : grade 3 +silver wiring

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PULMONARY EDEMAPULMONARY EDEMA
Refers to an excessive accumulation of fluid in pulmonary interstitial and Refers to an excessive accumulation of fluid in pulmonary interstitial and
alveolar space alveolar space
INCIDENCEINCIDENCE: : 2.9%2.9% of pregnancies with severe preeclampsia . 70-80% of the of pregnancies with severe preeclampsia . 70-80% of the
cases following deliverycases following delivery
Has become the most common cause of death in severe preeclampsia andHas become the most common cause of death in severe preeclampsia and
Eclampsia.Eclampsia.
PATHOPHYSIOLOGYPATHOPHYSIOLOGY ::
1.1.Reduction in colloid pressure gradient – excessive blood loss , fluid shift Reduction in colloid pressure gradient – excessive blood loss , fluid shift
after delivery , excessive crystalloid infusion after delivery – serum after delivery , excessive crystalloid infusion after delivery – serum
albumin synthesis decrease by liveralbumin synthesis decrease by liver
2.2.Preeclampsia -> endothelial damage -> capillary leakPreeclampsia -> endothelial damage -> capillary leak
3.3.CARDIOGENIC: CARDIOGENIC:
SYSTOLIC DYSFUNCTIONSYSTOLIC DYSFUNCTION: (increase after load) due to increase : (increase after load) due to increase
hydrostatic pressure . Impaired contractility – sever hypt , underlying heart hydrostatic pressure . Impaired contractility – sever hypt , underlying heart
diseasedisease
DIASTOLIC DYSFUNCTIONDIASTOLIC DYSFUNCTION:: chronic hypertension – concentric chronic hypertension – concentric
hypertrophy, obese impaired ventricular relaxationhypertrophy, obese impaired ventricular relaxation

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CLINICAL FEATURESCLINICAL FEATURES : : Worsening dyspnoea , tachypnoeaWorsening dyspnoea , tachypnoea
Crackles , hypoxemia, cyanosisCrackles , hypoxemia, cyanosis
INVESTIGATIONINVESTIGATION: Percutaneous oxygen saturation : one of the : Percutaneous oxygen saturation : one of the
earliest and easiest way to defect falling oxygen saturation earliest and easiest way to defect falling oxygen saturation
Chest x-ray, ventilation perfusion scan, pulmonary arteiography ( to rule out Chest x-ray, ventilation perfusion scan, pulmonary arteiography ( to rule out
pulmonary embolism)pulmonary embolism)

170170
MANAGEMENT : LMNOPMANAGEMENT : LMNOP
1.1.L:LASIXL:LASIX 20-40 over 2 minute, if respone not seen by 30 to 50 min dose 20-40 over 2 minute, if respone not seen by 30 to 50 min dose
increase up to 40-60 mg. (max dose-120mg in 1 hr)increase up to 40-60 mg. (max dose-120mg in 1 hr)
2.2.M:MORPHINEM:MORPHINE 2-5 mg i.v. decrease adrenergic vasoconstrictive stimuli to 2-5 mg i.v. decrease adrenergic vasoconstrictive stimuli to
the pulmonary arteriolar bedthe pulmonary arteriolar bed
3.3.N:SODIUM AND WATER RESTRICTIONN:SODIUM AND WATER RESTRICTION : input output to monitor : input output to monitor
4.4.O:OXYGEN O:OXYGEN 8-10 l/min, use pulse oxymeter8-10 l/min, use pulse oxymeter
5.5.P:POSITIONINGP:POSITIONING : elevation of head end (decreases pulmonary capillary : elevation of head end (decreases pulmonary capillary
wedge pressure)wedge pressure)
After load reductionAfter load reduction: hydralazine and calcium channel blocker: hydralazine and calcium channel blocker
Normal ventricular functionNormal ventricular function :intropes rarely required :intropes rarely required
Severe pulmonary edemaSevere pulmonary edema : ventilatory support : ventilatory support
Invasive monitoringInvasive monitoring : swan ganz catheter : to differentiate cardiogenic from : swan ganz catheter : to differentiate cardiogenic from
non-cardiogenic pulmonary edemanon-cardiogenic pulmonary edema
Pulmonary edema indication for terminationPulmonary edema indication for termination
It should be the first diagnosis in preeclamptic women with respiratory distressIt should be the first diagnosis in preeclamptic women with respiratory distress
Also have to keep pulmonary embolism in mindAlso have to keep pulmonary embolism in mind
D/DD/D: aspiration, atelectasis,respiratory infection: aspiration, atelectasis,respiratory infection
Pulmonary thromboembolism , valvular heart diseasePulmonary thromboembolism , valvular heart disease
Amniotic fluid embolismAmniotic fluid embolism

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RENAL FAILURE: RENAL FAILURE:
OLIGURIA (<400ml/24hrs, <30ml/hr, <0.5ml/kg/hr) not uncommonly OLIGURIA (<400ml/24hrs, <30ml/hr, <0.5ml/kg/hr) not uncommonly
presents as a clinical for obstetricianpresents as a clinical for obstetrician
CORNERSTONE: to identify the high risk cases and prevention of ARFCORNERSTONE: to identify the high risk cases and prevention of ARF
Clinical diagnosis is crude due to variability of clinical signs and late occurrence Clinical diagnosis is crude due to variability of clinical signs and late occurrence
of biochemical abnormalities ( rising b.urea and s.creat when > 50% RENAL of biochemical abnormalities ( rising b.urea and s.creat when > 50% RENAL
GLOMERULUS NOT FUNCTIONING)GLOMERULUS NOT FUNCTIONING)
ACUTE RENAL FAILUREACUTE RENAL FAILURE : characterized by abrupt reduction in g.f.r ,: characterized by abrupt reduction in g.f.r ,
accompanied by rapid progression of azotemia . Oliguria although frequent not accompanied by rapid progression of azotemia . Oliguria although frequent not
Mandatory.Mandatory.
Can vary from anuria, oliguria, to output > 2l/dayCan vary from anuria, oliguria, to output > 2l/day
Hyperkalemia and hyponatremia – develops subsequently mostly due to fluid Hyperkalemia and hyponatremia – develops subsequently mostly due to fluid
therapytherapy
Metabolic acidosisMetabolic acidosis
Uremic symptom : drowsiness, nausea, hiccough, twitching (develop late)Uremic symptom : drowsiness, nausea, hiccough, twitching (develop late)
AetiopathogenesisAetiopathogenesis: vasoconstriction(25-30% decrease in renal plasma flow, : vasoconstriction(25-30% decrease in renal plasma flow,
decrease g.f.r .decrease g.f.r .

172172
CAUSES :IN OBSTETRICS AND GYNAECOLOGYCAUSES :IN OBSTETRICS AND GYNAECOLOGY
PRE-RENALPRE-RENAL (renal hypoperfusion without parenchymal involvement) (renal hypoperfusion without parenchymal involvement)
Volume depletion (APH , PPh , hyperemesis , iatrogenic)Volume depletion (APH , PPh , hyperemesis , iatrogenic)
Decrease cardiac output (pulm. Hypt , valvular heart disease)Decrease cardiac output (pulm. Hypt , valvular heart disease)
Decrease renal perfusion (sepsis)Decrease renal perfusion (sepsis)
Drugs (nsaids)Drugs (nsaids)
ATN (acute tubular necrosis) = 80-90% of ARF in preeclampsia.ATN (acute tubular necrosis) = 80-90% of ARF in preeclampsia.
Mostly reverses after delivery unless it progresses to bilateral Mostly reverses after delivery unless it progresses to bilateral
cortical necrosis 10-20% of the time, which is more common in the presence of cortical necrosis 10-20% of the time, which is more common in the presence of
superimposed preeclampsia, underlying renal disease, HELLP ,DIC, abruptiosuperimposed preeclampsia, underlying renal disease, HELLP ,DIC, abruptio
RENALRENAL ( intrinsic renal parenchymal disease) ( intrinsic renal parenchymal disease)
Ischemic ATN, nephrotoxic ATN( drugs, blood transfusion), Ischemic ATN, nephrotoxic ATN( drugs, blood transfusion),
preeclampsia / eclampsia (glomerular endotheliosis)preeclampsia / eclampsia (glomerular endotheliosis)
POST RENALPOST RENAL (obstructive uropathy) (obstructive uropathy)
renal stone, pappilary necrosisrenal stone, pappilary necrosis
ureter-surgical ligationureter-surgical ligation
stage iii b ca cervixstage iii b ca cervix
urethral blood clot, kinked urinary bladder catheterurethral blood clot, kinked urinary bladder catheter

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Step wise management of renal failure : Step wise management of renal failure :
1.1.Assess patient for high risk : pre existing renal dysfunction, impaired renal Assess patient for high risk : pre existing renal dysfunction, impaired renal
perfusion pressure, avoid nephrotoxic Drugsperfusion pressure, avoid nephrotoxic Drugs
2.2.Diagnose ARFDiagnose ARF
3.3.Assess and correct fluid balanceAssess and correct fluid balance
4.4.Hemodynamic parameters : low b.p , tachycardia, oliguria, dry mucous Hemodynamic parameters : low b.p , tachycardia, oliguria, dry mucous
membrane, peripheral perfusion poormembrane, peripheral perfusion poor
5.5.Fluid balance – input and outputFluid balance – input and output
6.6.Invasion method – CVP, pulmonary capillary wedge pressureInvasion method – CVP, pulmonary capillary wedge pressure
7.7.Cardiac output – pulmonary artery catheterCardiac output – pulmonary artery catheter

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LIVER RUPTURELIVER RUPTURE
One of the most severe complications of severe preeclampsia and HELLP One of the most severe complications of severe preeclampsia and HELLP
syndromesyndrome
Maternal death> 30%Maternal death> 30%
Pathophysiology : endothelial dysfunction -> intravascular fibrin deposits -> Pathophysiology : endothelial dysfunction -> intravascular fibrin deposits ->
increase intrahepatic pressure -> distension of the glissons capsule -> increase intrahepatic pressure -> distension of the glissons capsule ->
subcaspular hematoma -> liver rupture subcaspular hematoma -> liver rupture
Clinical featuresClinical features : :
Most patients in late 3Most patients in late 3
rdrd
trimester trimester
Pain in right upper quadrant followed by circulatory collapsePain in right upper quadrant followed by circulatory collapse
Pain radiating to the tip of the shoulderPain radiating to the tip of the shoulder
More common in right lobeMore common in right lobe
If mass palpated further examination avoided, may cause rupture of the If mass palpated further examination avoided, may cause rupture of the
hematomahematoma
Massive ascites , respiratory difficulty , pleural effusionMassive ascites , respiratory difficulty , pleural effusion

175175
Investigations:Investigations:
Decrease platelet, decrease fibrinigenDecrease platelet, decrease fibrinigen
Increase PT/ APTTIncrease PT/ APTT
LFT -> AST,ALTLFT -> AST,ALT
CT / MRICT / MRI
Abdominal paracentesisAbdominal paracentesis
Management :Management :
Surgical emergencySurgical emergency
To stabilize the hemadynamic statusTo stabilize the hemadynamic status
Aggressive transfusions requiredAggressive transfusions required
On laprotomy : simple sutures rarely help ( liver is edematous ,friable)On laprotomy : simple sutures rarely help ( liver is edematous ,friable)
Surgical options : pack and drain Surgical options : pack and drain
If patient stable – hepatic artery embolization ( 90% - highest survival rate)If patient stable – hepatic artery embolization ( 90% - highest survival rate)
Loosely suturing omentum or surgical meshLoosely suturing omentum or surgical mesh

176176
ProtocolProtocol::
ANTEPARTUMANTEPARTUM::
1.1.Stabilze the patientStabilze the patient
2.2.Cesarean section – if negative or intact hematoma – observe but if Cesarean section – if negative or intact hematoma – observe but if
ruptured hematoma or hemoperitoneum -> pack & drainruptured hematoma or hemoperitoneum -> pack & drain
POSTPARTUMPOSTPARTUM::
1.1.Unstable -> blood products -> laprotomy ( drain & pack)Unstable -> blood products -> laprotomy ( drain & pack)
2.2.Stable -> CT scan -> if negative observe but if positive do a peritoneal Stable -> CT scan -> if negative observe but if positive do a peritoneal
lavage and then a laprotomylavage and then a laprotomy
Differential diagnosis : AFLP , DIC , ABRUPTIO , TTPDifferential diagnosis : AFLP , DIC , ABRUPTIO , TTP

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HEMATOLOGICALHEMATOLOGICAL : :
DIC : DISSEMINATED INTRAVASCULAR COAGULAATON:DIC : DISSEMINATED INTRAVASCULAR COAGULAATON:
Thrombohemmorhagic disorder , as a consequence of aberrant Thrombohemmorhagic disorder , as a consequence of aberrant
activation of the activation of the
coagulation cascade. coagulation cascade.
Pregnancy is a hypercoagutable state:Pregnancy is a hypercoagutable state:
Increase venous stasisIncrease venous stasis
Increase in factor 7, 8,9,10 and fibrinogenIncrease in factor 7, 8,9,10 and fibrinogen
Decreases in anticoagulant like protein c, s and antithrombinDecreases in anticoagulant like protein c, s and antithrombin
In severe preeclampsia and eclampsiaIn severe preeclampsia and eclampsia endothelial dysfunction adds to it. endothelial dysfunction adds to it.
In obstetrics abruptio most common causeIn obstetrics abruptio most common cause

Clinical featuresClinical features to be vigilant of: Purpura , ecchymosis , bleeding from gum. to be vigilant of: Purpura , ecchymosis , bleeding from gum.
Nose , Nose ,
vagina, rectum , venepuncture sites, surgical wound oozing.vagina, rectum , venepuncture sites, surgical wound oozing.

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InvestigationsInvestigations: :
1.1.Clotting timeClotting time: ( normal 1-10minutes) 5 ml of blood in test tube , : ( normal 1-10minutes) 5 ml of blood in test tube ,
if fails to clot fibrinogen < 50 mg/dl.if fails to clot fibrinogen < 50 mg/dl.
2.2.Clot retraction testClot retraction test : (normal 30-60 minute) : (normal 30-60 minute)
Weak friable test hypofibrinigenemia Weak friable test hypofibrinigenemia
Early dissolution increase fibrinolysisEarly dissolution increase fibrinolysis
3.3.PT ( prothrombin time)PT ( prothrombin time) : (normal 10-13 seconds) : (normal 10-13 seconds)
Normal INR : 0.9-1.2 Normal INR : 0.9-1.2
Increase when fibrinogen < 100mg/dl Increase when fibrinogen < 100mg/dl
Most sensitive of factor 7 , & also extrinsic & common pathway factor Most sensitive of factor 7 , & also extrinsic & common pathway factor
deficiency deficiency
4.4.APTT APTT (activated partial thromboplastin time ) : (normal – 25-35 sec) (activated partial thromboplastin time ) : (normal – 25-35 sec)
indicates same as PTindicates same as PT
5.5.TT : (thrombin time < 18 sec)TT : (thrombin time < 18 sec)
6.6.FIBRINOGENFIBRINOGEN : (normal 300-600 mg/dl) : (normal 300-600 mg/dl)
7.7.Less than 100 bleedingLess than 100 bleeding
8.8.OTHERSOTHERS : FDP ( fibrin degraded product), FIBRINOPEPTIDE A , : FDP ( fibrin degraded product), FIBRINOPEPTIDE A ,
D- DIMER - elevatedD- DIMER - elevated

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TreatmentTreatment::
Treat the offending cause Treat the offending cause
Fluids – avoid dextran – thrombocytopenia aggravates and problem in Fluids – avoid dextran – thrombocytopenia aggravates and problem in
cross matching.cross matching.
Packed cells – 1 unit increase hematocrit by 3-5%Packed cells – 1 unit increase hematocrit by 3-5%
FFP and CRYO – if bleeding tendencies ,or if hematological inv. FFP and CRYO – if bleeding tendencies ,or if hematological inv.
Parameters alteredParameters altered
1 unit of each increase fibrinogen by 10 mg/dl1 unit of each increase fibrinogen by 10 mg/dl
Also increase other clotting factorsAlso increase other clotting factors
Platelet transfusion : when thrombocytopenia < 50000Platelet transfusion : when thrombocytopenia < 50000
Seen in studies that severe preeclampsia and eclampsia more commonly Seen in studies that severe preeclampsia and eclampsia more commonly
associated with thrombocytopenia than consumptive coagulopathy ( associated with thrombocytopenia than consumptive coagulopathy ( PritchardPritchard))
ANTI-THROMBIN III - when activity decrease by 70%ANTI-THROMBIN III - when activity decrease by 70%
Dose: 1500-3000 IU/day for 2 daysDose: 1500-3000 IU/day for 2 days
RECOMBINANT HUMAN ACTIVATED PROTEINRECOMBINANT HUMAN ACTIVATED PROTEIN

180180
FETAL COMPLICATIONS : FETAL COMPLICATIONS :
1.1.ABRUPTIOABRUPTIO : :
Hypertension most common predisposing condition for abruption. Hypertension most common predisposing condition for abruption.
Risk increases by 3 fold in chronic hypertension and 4 fold by Risk increases by 3 fold in chronic hypertension and 4 fold by
sever sever
preeclampsia. preeclampsia.
10 % of abruption go for DIC .10 % of abruption go for DIC .
Longer the duration between abruption and delivery – more Longer the duration between abruption and delivery – more
chances of hypofibrinogenemia.chances of hypofibrinogenemia.
MANAGEMENTMANAGEMENT : depends on the maternal and fetal condition, : depends on the maternal and fetal condition,
cervical status and period of gestationcervical status and period of gestation
2.2.IUGR ( INTRAUTERINE GROWTH RESTRICTION)IUGR ( INTRAUTERINE GROWTH RESTRICTION)
Hypertension causes utero placental insufficiencyHypertension causes utero placental insufficiency
3.3.PREMATURITYPREMATURITY : decision to deliver irrespective of the gestational : decision to deliver irrespective of the gestational
ageage
4.4.IUDIUD

181181
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THANK YOUTHANK YOU

hypertensive disorders of pregnancy including PE

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hypertensive disorders of pregnancy including PE

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