5. Eclampsia
The incidence of eclampsia in the developed countries is 1:2000
deliveries. while in developing countries estimate vary widely,
from 1 in 100 to 1 in 1700 deliveries .
ANTEPARTUM (50%)
INTRAPARTUM (30%).
POSTPARTUM (20%) within 48hrs-upto 7days.
INTERCURRENT (Rare) – Pt becomes conscious after recovery
from convulsion and pregnancy continues beyond 48hrs.
6. Convulsions in Pregnancy
Differential Diagnosis
Eclampsia
History
Occurs after 20wks of
preg
H/o PIH in this
Pregnancy
Prev H/o Eclampsia +/-
H/o Tonic Clonic
convulsion
Clinical Exam
H/o Hypertension,
Proteinuria,Edema,Oliguri
a,p ulmonary Edema
Epilepsy
Occur anytime during preg
H/o Prev Epileptic fits
Fits may be Recurrent
Fits Generalised/Focal
No H/o
Hypertension,Proteinuria,
Edema
14. MgSO4 Mechanism ofaction
Slowed neuromuscular conduction & decreased CNS
irritability
Cerebral vasodilatation
Increased production of endothelial prostacycline and
inhibition of platelet activation
Protection of endothelial cells from injury mediated by free
radicals
Dilatation of uterine arteries
15. MgSo4 as anticonvulsant
Prichard’s regimen (IM)
Loading Dose-
4gm (20%) slow IV over
3-5mt f/b 10gm (50%) deep IM
(5gm in each
buttock)
Maintenance Dose-
5gm (50%) IM 4hrly in alternate
buttock
Zuspan regimen (IV)
Loading Dose-4-6gm slow IV in
100ml 5% Dextrose over 15-20 mt
F/b 5gm IV in 5%Dextrose(1gm/hr
IV infusion)
16. Monitoring of patient on magnesium
sulphate
Therapeutic levels (if available)
Serum magnesium levels between 4.0-7.0 mEq/L
Patellar reflex Present
(Lost at serum Mg Levels of 8 – 10 mEq/L Urine
Output >30 ml/ hr
Every hour Respiratory rate > 12/min
every 15 mins
Respiratory depression (serum Mg level
>10
mEq/L)
Respiratory arrest (serum Mg level > 12 mEq/L)
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18. Effects of Mg sulphate on thenewborn
MgSO4 crosses the placentafreely
Minimal side effects if maternal serum
levels are maintained
Hyporeflexia and Respiratory depression
Lethargy
19
19. - Anticonvulsant therapy
Diazepam
Useful for status seizures
dosage – 10 -20 mg iv at a rate of 5 mg per min
may be repeated at 10 to 15 minute intervals
Maintainence – 40mg in 500ml of 5% Dextrose IV infusion,to
keep patient sedated
Side effects - loss of consciousness, hypotension,
respiratory depression
Caution - may increase risk of aspiration
causes prolonged depression of the neonate
20. Phenytoin
Centrally acting anticonvulsant
Dose ( with ECG monitoring )
10mg/Kg I/V (not more than50mg/mt) F/b
5mg/Kg I/V after 2hr
12 hr. — 500mg I/V
200mg 8hrly. X 5 days
SE- Hypotension, Cardiac dysrhythmia & Phlebitis
21. Fluid replacement
Should not exceed 1-2 ml/kg/hour or 85 ml/hour
whichever is lower
Crystalloid Solution (RL)
Total Fluid =24hr urine +1000ml
Maintain a urine output of more than 30 ml/hour
CVP should not exceed 7 cm of H2O
When patient is taking oral fluids, the amount
taken should be subtracted from the amount
infused
22
22. Anti hypertensive management
Objective is to prevent maternal cerebrovascular
accidents
Hydralazine
5mg -10mg I/V at 15 – 20 mts. Interval till control is achieved.
Maximum dose 15mg – 20mg
Labetelol
Start with 200mg/100ml IV at 20mg/hr. I/v. Double the dose
every 30 min. till control is achieved or a dose of 160mg/hr. is
reached
Nifedipine
5mmg – 10mg S/L every 15 – 30 minutes until BP is contolled A
maximum 180mg can be used in a day
23. Treatment of complications of Eclampsia
If pulmonary oedema develops, give intravenous
Frusemide 40mg, oxygen and manage patient in the ICU
If oliguria develops or when urine output is less than
30ml/hour for 4 hours – challenge with 200 mls of
crystalloid over 5 minutes . Evaluate over a 4 hour
period
If oliguria persists despite a CVP of between 7 – 10 cm H2O
– refer to Nephrologist for further management.
Hyperpyrexia- Cold sponging , Antipyretics
Heart failure-O2 inhalation, IV Lasix, & Digitalis
24
27. Definition
• Coma is the absence of consciousness. • This state of
unarousable unconsciousness includes the failure of
eye opening to stimulation, a motor response no
better than simple withdrawal-type movements, and
a verbal response no better than simple vocalisation
of non-word sounds
28. Step-by-step diagnostic approach
• History
• Symptoms of herniation syndromes
• Period of delirium
• Duration of unconsciousness
• Prodromal symptoms
• Presence of convulsions
• Incontinence
• Vision disturbances
• Significant past medical history
29. Focused general examination
• Blood pressure
• Pulse oximetry
• Core temperature
• Skin-Jaundice, Pallor, cyanosis, Petechial bleeding
• Head and Neck
30. Coma scoring scales
• Glasgow Coma Scale (GCS)-Commonly used to grade
the severity of the impairment of consciousness
• Initially designed to assess trauma patients in the
emergency department, but it is commonly used to
track the progress or worsening of intensive care unit
(ICU) patients
• Better scales for documenting and following the
depth of coma in ICU patients:
• The Reaction Level Scale
• The FOUR scoring system.[The FOUR Score] These
are more suitable for patients who are intubated,
• have more categories or levels, and include more
aspects of the neurological examination
33. Pregnant women may go into coma for
the same reasons that face the general
population, but also encounter conditions
unique to or more common in this state
- Gestational hypertension, eclampsia,
and HELLP
- Pregnancy relatedorgan failures
including acute renal, hepatic, or
pulmonary failure
- Vascular risks include cerebral venous
sinus thrombosis and pituitary apoplexy
COMA –WHEN AND HOW
34. COMA –WHEN AND HOW
The considerations in coma treatment are generally
similar to those facing patients who are not pregnant.
Coma represents such a dire state that even concerns
such as radiation exposure are usually outweighed by
the need for maternal diagnosis and management
No investigations are categorically excluded (eg,
cerebral angiogram, spiral computed tomography [CT],
or even brain biopsy), because with the prospect of
potentially treatable causes, a mother’s life is accorded
priority.
35. Etiology
Etiology similar to other causes of young
stroke- Cardioembolic common
Physiologic and hemodynamic changes that
occur --state of relative hypercoaguability,
Increased cardiac burden, and altered vascular
tone
Preeclampsia is associated with a 4-fold
increase in stroke during pregnancy
Peripartum Cardiomyopathy , Post partum
cerebral angiopathy
36. Diagnosis
Initial study with a non-contrast head
computerized tomography (CT) with
appropriate fetal shielding or an
magnetic resonance imaging (MRI) of
the brain
37. Transthoracic or transesophageal
echocardiogram to evaluate for PFO
and the possible presence of an
intracardiac thrombus
hypercoaguability panel is often
performed - results will need to be
repeated several weeks following
delivery
Genetic testing for factor V Leiden and
prothrombin gene mutation would not
be altered by pregnancy
38. Treatment
TPA - pregnant patients were excluded from tPA
clinical trials and there has been no systematic study
Concerns regarding the risks of tPA on the pregnant
patient and fetus (eg, uterine hemorrhage, placental
abruption, abortion, preterm delivery) have been
raised
that maternal mortality (1%), fetal loss (6%), and
preterm delivery (6%) are all low
Low-dose aspirin for secondary prevention is felt to
be safe during pregnancy
unfractionated or low-molecular weight heparin as these
do not cross the placenta and confer no risk of
teratogenicity or fetal hemorrhage
39. Defined as an unexplained cardiac
failure occurring during the last month
of pregnancy to the first sixth
postpartum month.
viral and autoimmune causes of
cardiomyopathy have been invoked
Coma may occur from global
cerebral hypoperfusion or by strokes
Peripartum Cardiomyopathy-
40. Amniotic Fluid Embolism
AFE occurs when amniotic fluid
enters uterine veins and is forced into
the maternal circulation, causing
hemodynamic collapse, disseminated
intravascular coagulopathy (DIC),focal
cerebral hypoperfusion, thrombosis or
hemorrhage,
41. Hemorrhagic stroke
Occurs primarily in late pregnancy and in the
puerperium
Intracerebral hemorrhage has a higher
maternal mortality rate -5% to 12% of overall
maternal mortality during pregnancy
Primarily associated with preeclampsia /
eclampsia, arteriovenous malformations, and
cerebral aneurysm rupture
Pathogenesis - increased blood volume, rising
blood pressure, and changes in vascular tone.
physical stress of labor and delivery may
contribute to rupture risk
42. Initial evaluation should include
a noncontrast head CT which will
identify a subarachnoid (often
aneurysmal) or lobar (often AVM)
hemorrhage
Angiographic imaging in an
attempt to identify the source of
the hemorrhage
43. Cerebral Venous Thrombosis
CVT represents ≈0.5% to 1% of all
strokes.
Risk factors are usually divided into
acquired risks (eg, surgery, trauma,
pregnancy, puerperium, antiphospholipid
syndrome, cancer, exogenous hormones)
and genetic risks (inherited thrombophilia).
Pregnancy and Puerperium-
Most pregnancy-related CVT occurs in the
third trimester or puerperium.
44. Clinical Diagnosis of CVT
headache in 82%,
papilledema in 56%,
focal deficits in 42%,
seizures in 39%
coma in 31%.
Location of the thrombosis
The superior sagittal sinus is most
commonly -headache, increased ICT, and
papilledema
motor deficit, sometimes with seizures
45. Investigations
Routine blood studies consisting of a
complete blood count, chemistry panel,
prothrombin time, and activated partial
thromboplastin time should be performed
46. Treatment
Treatment of CVT in the nonpregnant
population generally involves
anticoagulation with warfarin
Unfractionated heparin or low-
molecular weight heparin can be
utilized in pregnancy either as a bridge
to warfarin therapy or as a stand-alone
treatment
47. Stroke with Eclampsia
Most common causes of both
ischemic and hemorrhagic stroke in
pregnancy.
The most frequent cerebrovascular
disturbance associated with eclampsia
is a reversible encephalopathy.
Preeclampsia/eclampsiacommonly
associated with ischemic stroke of
arterial origin [36 percent]) ,
Intracerebralhemorrhage [55 percent])
48. Prognosis
Postpartum eclampsia has a worse
prognosis, often with adult respiratory
distress syndrome (ARDS) and DIC
Neurological complications more in
postpartum
Preclampsia increases risk of stroke
over 42 days postpartum
49. Management
Investigations-
Platelet count and morphology, CBC
PT, aPTT •Uric acid, creatinin,
electrolytes for renal function
Serum uric acid –useful early and for
progression
Hepatic enzymes (AST,ALT,GGT)&
bilirubin
50. Imaging
•Cerebral imaging is not necessary for
the diagnosis and management of
most women with eclampsia.
•Cerebral imaging findings in
eclampsiaare similar to those found in
patients with hypertensive
encephalopathy
51. Posterior Reversible
Encephalopathy Syndrome
Is a clinical radiologic syndrome of
heterogeneous etiologies that are
grouped together because of similar
findings on neuroimaging studies
May occur in the setting of
preeclampsia due to impaired cerebral
autoregulation from endothelial
damage
52. Most common clinical manifestations of
PRES include headaches, confusion,
seizures, and visual changes.
Confusion is common and may progress
to more significant degrees of altered
awareness
Seizures may start focally but often
generalize
More severe cases can result in lasting
neurological morbidity or mortality due to
ischemic stroke or hemorrhage
54. Cerebral imaging is indicated :-
Focal neurologic deficits
Prolonged coma
Atypical presentation for eclampsia:
Onset before 20 weeks of gestation
or
More than 48 hours after delivery
Eclampsia refractory to adequate
mgso4 therapy
Posterior Reversible
Encephalopathy Syndrome
55. Treatment of PRES in the pregnant
patient mirrors that of eclampsia
Magnesium sulfate is often utilized for
seizure control
As with eclampsia, hypertension
management is generally achieved
with hydralazine or labetolol