High Risk pregnancy

1. PREGNANCY WITH CONVULSIONS
AND COMA- RARE BUT DREADED
DISASTERS

2. Convulsions in pregnancy
Convulsions due to pregnancy
Eclampsia
Convulsions aggravated by
Pregnancy Epilepsy

3. Convulsions in pregnancy
Convulsions not Directly related to pregnancy
Infections
Meningitis
Encephalitis
Cerebral Malaria
Cerebral Absces
Febrile convulsions
Cerebrovascular
Accidents
Venous Thrombosis
Infarction
Haemorrhage
Metabolic/Electolyte imbalance
Hypoglycemia
Hyperglycemia
Hyponatremia
Hypocalcemia
Trauma Tetany
Drug Withdrawal Cocaine
Alcohol
Psychiatric disorders

4. ECLAMPSIA
New-onset convulsionsafter 20wks of pregnancy in
a patient with Preeclampsia (PIH) with no
coincidental neurologic disease, is called
Eclampsia.

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

7. Convulsion in Pregnancy
Differential Diagnosis
Investigations
Eclampsia
Complete bloodcount
Haematocrit
Plateletcount
 Coagulation profile
 Serum creatinine
Serum uric acid
Liver function tests
Complete urine
examination
Fundoscopy
Epilepsy
EEG
Cerebral Imaging (MRI)

8. Maternal Complications of Eclampsia
Injuries –Tongue bite
Pulmonary Edema.
Aspiration Pneumonia(2%-
5%)
Long Term Cardiovascular
Morbidity
Abruptio- Placentae (1%-4%)
Disseminated Coagulopathy.
HELLP Syndrome (3-4%)
Acute Renal Failure (1%-5%)
Liver Failure OR Haemorrhage
(<1%)
Cerebral haemorrhage
Postpartum collapse
Blindness
Death (Rare)

9. Complications
 IUGR(10-25%)
Hypoxia- Neurologic Injury (<1%)
Perinatal Death (1%-2%)
Long Term Cardiovascular Morbidity Associated
with Low Birth Weight

10. AIMS OF MANAGEMENT OF ECLAMPSIA
Control convulsions, prevent cerebro-vascular
accident and COMA
Stabilise blood pressure
Optimise patient
Deliver fetus
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11. Management of eclampsia
Teamapproach
O&G specialist
Anesthesiologist
 Paediatrician
Physician
Nursing Staff
Blood bank personnel

12. GENERAL MANAGEMENT OF ECLAMPSIA
position patient to herside in railed cot
Mouth gag placed between theteeth
clearairway secretions
maintain oxygenation 15 LIT/ MIN
set up intravenousaccess
Put self retaining catheter
monitor vital signs - BP, PR, respiration1/2hrly
if diastolic BP > 110mmHg, considerantihypertensive
monitor fetal heart rate forgestations > 28 weeks
Antibiotic
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13. Anticonvulsant Therapy
Magnesiumsulphate (MgSO4)
Diazepam
Phenytoin

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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17. 
Managing Magnesium Toxicity
 Respiratory depression
 Stop magnesiumtherapy
 Oxygen
 IVcalciumgluconate 10% 10ml IV slow bolus
 Maintainairway
 Respiratory arrest
 Stop magnesiumtherapy
 IVcalciumgluconate 10% 10 ml IV slow bolus
 Tracheal Intubation andventilation
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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
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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
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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
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24. Obstetrical management of eclampsia
treatment
The Definitive
Is Delivery
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25. Indications of LSCS IN
Eclampsia
Uncontrolled fits in spite oftherapy
Poor prospects for vaginalDelivery
Worsening maternal diseaseprocess
Uncontrolled hypertension (>180/120mm Hg)
Obstetric indications

26. Coma in Pregnancy

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

31. Glassgow coma scale

32. FOUR SCORING SYSTEM

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

53. Findings in
PRES

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

56. Take Home Message

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