This document discusses various causes of coma and stroke that can occur during pregnancy. Key points include: 1) Pregnant women may experience coma due to conditions like preeclampsia, eclampsia, organ failures, or vascular issues like cerebral venous sinus thrombosis. 2) Strokes during pregnancy can be ischemic or hemorrhagic. Ischemic strokes are often cardioembolic and risks are highest during delivery and the postpartum period. 3) Eclampsia, which involves seizures in the setting of preeclampsia, is one of the most common causes of both ischemic and hemorrhagic stroke during pregnancy. Untreated preeclampsia can progress

1. Coma In Pregnancy
Dr Sankalp Mohan
Senior Resident Neurology
GMC Kota

2.  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 related organ failures
including acute renal, hepatic, or
pulmonary failure
 - Vascular risks include cerebral venous
sinus thrombosis and pituitary apoplexy

3. STROKE IN PREGNANCY
Ischemic Strokes
 incidence of 3.5 ischemic strokes per
100 000 population
- it is recognized that there is an increased risk
of stroke associated with pregnancy – recent
studies show similar incidence
- considering stroke in the young as a broader
group, strokes related to pregnancy account for
12% to 35% of events
- Based on the available evidence, the highest
risk periods appear to be the delivery period
and up to 2 weeks postpartum.

4. 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
 Paradoxical embolism related to the presence
of a patent foramen ovale (PFO) may be
facilitated by both the coagulation profile
changes
 Peripartum Cardiomyopathy , Post partum
cerebral angiopathy

5.  acute onset of focal neurological
changes
 headache and altered consciousness
 Siezures
Diagnosis
 initial study with a noncontrast head
computerized tomography (CT) with
appropriate fetal shielding or an
magnetic resonance imaging (MRI) of
the brain

6.  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

7. 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

8. Antiphospholipid Antibody
Syndrome
 Recurrent arterial and venous
thromboses and can cause fetal death
 similarities to preeclampsia-eclampsia,
with endothelial damage, platelet
activation, and thomboxane-mediated
vasoconstriction
 inhibition of protein C-protein S and
antithrombin III activity

9.  Focal problems include cerebral
infarction from thrombotic and venous
occlusion
 Antibodies contribute to the
pathogenesis, and include the lupus
anticoagulant antibody, anticardiolipin
antibody, and anti-B2 glycoprotein

10. CARDIAC CAUSES OF
STROKE IN PREGNANCY
Peripartum Cardiomyopathy-
 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

11.  Heart Valve Abnormalities
 Prosthetic heart valves or chronic
atrial fibrillation may induce stroke
 In normal childbirth and with Valsalva
maneuvers, right atrial pressure rises
 and the foramen ovale may open,
enabling pelvic and peripheral vein
emboli to pass to the lung

12. 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,

13. 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

14.  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

15. Treatment –
 patients with known aneurysms and
AVMs are often delivered by
scheduled C-section
 an aneurysm is identified during
pregnancy repair is usually
undertaken with neurosurgical clipping
or endovascular coiling as this has
been shown to reduce both maternal
and fetal mortality

16. 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.

17. Pathophysiology
 Pregnancy induces several prothrombotic
changes in the coagulation system –
fibrinogen activation with increased platelet
adhesiveness
 Hypercoagulability worsens after delivery
as a result of volume depletion
 Additional risk factors include infection and
instrumental delivery or cesarean section
 Increasing maternal age, as well as in the
presence of hypertension, infections, and
excessive vomiting in pregnancy

18. 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

19.  lateral sinus thromboses, symptoms related to
an underlying condition (middle ear infection )
 16% of patients with CVT have thrombosis of
the deep cerebral venous system - Thalamic or
basal ganglial infarction ,rapid deterioration
 bilateral involvement -bilateral thalamic
involvement - Coma ;
 paraparesis, may also be present due to
sagittal sinus thrombosis
 CVT often present with slowly progressive
symptoms

20. Investigations
 Routine blood studies consisting of a complete
blood count, chemistry panel, prothrombin time,
and activated partial thromboplastin time should be
performed

21. 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

22. Reversible Cerebral
Vasoconstriction Syndrome
 encompasses a variety of syndromes
including postpartum angiopathy and
puerperal vasospasm
 group of disorders linked by prolonged
but reversible vasoconstriction of the
cerebral arteries
 Clinical settings including the postpartum
state, migraine, hypertensive
encephalopathy, and the use of
vasoactive medications/drug
 severe, acute-onset headaches
hunderclap
 Ischemic stroke and/or hemorrhage
associated with reperfusion may occur

23.  characteristic imaging features
associated with the syndrome which
often include focal regions of
symmetric edema in the posterior
brain parenchyma

24. RCVS

25. Choriocarcinoma
 Metastatic choriocarcinoma rarely
causes SAH, ICH, or subdural
hemorrhage
 Trophoblastic tissue may invade blood
vessels and induce aneurysmal
dilatation,
which may cause rupture

26. Eclampsia
 PREECLAMPSIA - New onset of hypertension and
proteinuria after 20 weeks of gestation in a previously
normotensive woman
 Criteria for the diagnosis of preeclampsia
 SBP ≥140 mmHg Or
 DBP ≥90 mmHg
 And Proteinuria ≥0.3 grams in a 24-hour urine specimen
Eclampsia–
 Occurrence of one or more generalized convulsionsand/or
coma in the setting of preeclampsia and in the absence of
other neurologic conditions.
 Many patients have an incomplete clinical triad but a seizure
or coma define eclampsia

27.  Eclampsia occurs in 0.05% to 0.20%
of pregnancies
 Eclamptic seizure occurs in - 3% of
severely preeclamptic women not
receiving anti-seizure prophylaxis

28. Risk Factors
 Preeclampsia in a previous pregnancy
 Age >40 years or <18 years
 Family history of preeclampsia
 Chronic hypertension
 Chronic renal disease
 Antiphospholipidantibody syndrome or
inherited thrombophilia
 Vascular or connective tissue disease
 Diabetes mellitus (pregestationaland
gestational)
 Multifetal gestation

29. Pathogenesis
 Faulty placentation may release
products
toxic to endothelium -impaired
cytotrophoblastic migration through
the decidua
 leads to release of inflammatory
factors and cytokine production,
inducing a more generalized maternal
inflammatory response

30.  Cerebral Complications-
 Endothelial dysfunction - Loss of
autoregulation of cerebral blood flow
(ie, hypertensive encephalopathy)
results in hyperperfusion, endothelial
damage, and vasogenic(extracellular)
edema.
 underperfusionof the brain, localized
ischemia/infarction,and
cytotoxic(intracellular) edema.

31. Severe Preclampsia
 Systolic bp>160 mmHg
 –Diastolic bp>110mHg
 –Proteinuria> 5g per 24 hours
 –Cerebral or visual disturbances: headache,
tinnitus,
 –Oliguria< 500ml per 24 hours,
creatinine>1.2mg/dl
 –Epigastric pain
 –Pulmonary oedema
 –Heamolysis, elevated liver enzymes and low
plataletsyndrome= HELLP syndrome
 –Fetal criteria-IUGR, oligohydro, fetal death

32. Impending Eclampsia
 Symptoms:
 •Headache
 •Visual disturbance
 •Epigastricpain
 •Nausea
 •Restlessness
 •Swelling
 •Poor urine output

33. 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])

34. 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

35. 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

36. 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

37. 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

38. Treatment
Management of siezures –
 Magnesium sulphate: -anticonvulsant of
choice
– Action by:
•antagonism of calcium and hence decreased
systemic and cerebral vasospasm
•Increase release of PGI2 by vascular endothelium
 Mgso4 – 52% lower occurrence of siezure
compared to Diazepam , 67% compared to
phenytion

39.  Therapeutic level 4-7 mEq/l ; must monitor
for toxicity
 reduce dose in renal failure
MANAGEMENT OF HYPERTENSION –
 Nifedepine,Hydralazine ,Labetalol

40. 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

41.  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

42. Findings in PRES

43.  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

44. SEIZURES AND STATUS
EPILEPTICUS
 Pregnancy may increase seizure
frequency in women with epilepsy, but
produces no effect in most women;
some have fewer seizures
 Pregnancy decreases the total blood
levels of most antiepileptic drugs
(AEDs) by 50%
 Free valproate levels may increase.
Lamotrigine levels may decrease

45.  Frequent causes of SE are a low level
of AEDs, new strokes, infections,
abscesses, and vascular
malformations
 Management is directed at seizure
control and investigation of possible
underlying causes

47. METABOLIC CAUSES OF
COMA
Glucose Dysregulation-
 Diabetes causing high or low blood sugar that can lead
to coma
 morning sickness, may cause the mother to avoid
glucose-lowering medication and facilitate
hyperglycemia.
 Vomiting with dehydration can cause hypernatremia
Wernicke Encephalopathy
 confusion, eye movement disorders and nystagmus,
ataxia, and rarely, coma
 Hyperemesis gravidarum may cause Wernicke
encephalopathy by depleting the body thiamine stores
 Treatment may require daily parenteral thiamine
repletion for 7 to 10 days

48. Acute Intermittent Porphyria-
 caused by an autosomal dominant inherited abnormality
of heme biosynthesis with toxic accumulation of
aminolevulinic acid and porphobilinogen
 can be precipitated in women during menarche,
perimenstrually, and in pregnancy
 Acute axonal polyneuropathy
 autonomic dysfunction with tachycardia and
constipation, cognitive and behavioral abnormalities,
and psychosis, occasionally with coma.
 Seizures may be difficult to control because of the
porphyrinogenic nature of most AEDs
 benzodiazepines. gabapentin, levetiracetam, or
vigabatrin

49. ENDOCRINE DISTURBANCES
IN PREGNANCY
 Pituitary apoplexy can arise from increased
vascularity, and enlargement of the pituitary
result in antepartum infarction or hemorrhage
Acute pituitary apoplexy –
 emergency with high mortality, often from
 compression of the hypothalamus
 Consciousness is impaired and there is the
danger of acute adrenal failure and further
hypotension
 Treatment is aimed at acute replacement of
corticosteroids intravenously. Surgery to
decompress the hypothalamus or optic nerve

50. Sheehan Syndrome
 anterior pituitary necrosis after
hypovolemia and hypotension in
severe maternal blood loss
 pituitary, because of its pregnancy-
associated hyperplasia and increased
vascularity, is particularly vulnerable to
hypovolemia and hypotension
 Treatment – replacement of hormones

51. INFECTIONS
 mild immunosuppression in pregnancy
associated with alterations in
circulating maternal steroids
 systemic infections and septicemia,
but rarely coma.

52. INFECTIONS
 Herpes simplex virus encephalitis
in pregnancy

53. ORGAN FAILURE
OCCASIONALLY LEADING TO
COMA
RENAL FAILURE
 ARF may be caused by hemorrhagic or septic
shock, or severe preeclampsia.
 HELLP may lead to a decrease in glomerular
filtration and renal failure, occasionally with
acute tubular necrosis- usually resolves
 DIC – causes ARF
 Other -malignant hypertension, infections,
scleroderma, vasculitis, microangiopathic
 hemolytic anemia transplant rejection,
hemolytic uremic syndrome, malignancies, or
drug toxicity.

54. Acute Liver Failure-
 prepartum or postpartum with
eclampsia, HELLP syndrome, or acute
viral hepatitis
 Acute fatty liver and HELLP syndrome
occur most frequently in the third
trimester
 itching, diarrhea, and jaundice
 COMA- patients with encephalopathy,
coagulopathy, hypoglycemia

55. Acute Fatty liver of pregnancy
 1 in 7000 to 16,000 pregnancies
 Maternal mortality is almost 20%
 usually is seen in the third trimester of
pregnancy, and presents with hepatic failure,
microvesicular fatty infiltration
of the liver, and encephalopathy
 Nausea and vomiting (75%), jaundice, or
epigastric pain. There may be DIC, acute
tubular necrosis, and pulmonary edema
 Treatment is with supportive measures
 On occasion, liver transplantation is
recommended

56. PULMONARY DISEASE AND
FAILURE IN PREGNANCY
 Acute respiratory failure and ARDS, and all of the
pulmonary disorders may cause coma from
hypoxia.
 Acute respiratory failure in pregnancy accounts
for more than 30% of maternal deaths
 thromboembolism, AFE, venous air embolism, or
ARDS
 Aspiration pneumonia may arise during
decreased consciousness in labor and delivery,
an increase in intragastric pressure by
compression by the pregnant uterus, and
delayed gastric emptying, all contributing to
significant of maternal morbidity and mortality

57. Venous Air Embolism
- predominantly iatrogenic complication
 abortion, delivery, labor, and other
interventions, and is caused by air entry into
the subplacental venous sinuses
 risk is higher in pregnant women, who may
have a tear in their placentae.
 complications have been reported with as
little as 20 mL of air
 more than 5 mL/kg of air displaced into the
intravenous space is required for significant
injury (shock or cardiac arrest)

58.  Air travels to the heart and prevents blood flow to
the lungs, frequently causing a blood-air
interface, with microemboli, platelet injury, and
inflammatory white cell response leading to
ARDS
 clinical features include shortness of breath,
tachypnea and tachycardia, hypotension, and
sweating.
 . sitting position, gas will travel internal jugular
vein to the cerebral circulation, leading to
neurologic symptoms. In a recumbent position,
gas proceeds into the right ventricle and
pulmonary circulation
 clinical picture similar to that of pulmonary
embolism, with hypoxia, decreased PCO 2 levels
pulmonary veins.

59.  Lab tests not sensitive or specific
 CXR
 Transesophageal echocardiography
(TEE) has the highest sensitivity for
detecting the presence of air in the right
ventricular outflow tract
 CT scans can detect air emboli in the
central venous system
 Management includes identification of
the source of air, prevention of further air
entry hemodynamic support.

60. THANK YOU

61. References
 Coma in the Pregnant Patient- NEUROLOGY
CLINICS 11/2011; 29(4):973-94.
 Stroke and Pregnancy - Stroke.2000; 31: 2948-
2951
 Acute Neurological Issues in Pregnancy and the
Peripartum - Neurohospitalist. 2011 Apr; 1(2): 104–
116.
 Bradley's Neurology in Clinical Practice 6 e-
Neurologic complications of pregnancy
 www.medscape.com