Postpartum HA with
Seizures:
“to do a blood patch or not to do”
Contents:
• Presentation of Case Study
• Review of CSF infections and findings
• Review of differential diagnosis for peripartum
seizures
• Current literature review
• Discussion
Case Presentation• A 5’ 7”, 152 #, 17 y.o. at post-partum day 7,
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presented to HR L&D on a Friday afternoon with h/o
a GTC seizure earlier that day.
She also c/o a bifrontal HA which was worse with
sitting/standing, slight stiff neck, cycloplegia,
photophobia, mild fever (100 F), No N/V.
Pt’s mother stated she observed legs jerking and
foaming from the mouth for approx 3-4 min. Pt had
loss of urine and post-ictal like state as described by
her mother.
Recent Obstetrical history
• PMHx: “anxiety attacks”. Denied Tob, ETOH, drugs. Took no
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meds and had no drug allergies.
Pt was a G1P1 who 7 days earlier had an uneventful SVD at
39 6/7 wks with a uncomplicated labor epidural for analgesia.
During her stay she was not treated for pre-eclampsia, but did
have elevated Bp’s in the 140’s/ 90’s and a single increased
TP:Cr ratio of 446 (N <150).
So- she delivered on a Friday night, was seen in follow-up by
anesthesia the next day and seemingly had no issues. D/Ced
to home on Sunday in good health
And the plot thickens…
• Pt was treated in the ED on Tues night with IVF and
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caffeine for a suspected PDPH. She was D/Ced from
the ED with PO ibuprofen.
Pt was not evaluated by anesthesia during this visit
because of easily resolved symptoms with the
aforementioned treatment regimen
Thus, because of her continued “PDPH” symptoms
once she hit the HR floor, the OB Dr.’s wanted us to
perform a blood patch.
Further Work-up…Would you now
do a Blood Patch?
• NO !
• One must R/O the possibility of a intracranial
hematoma/bleed first and then R/O a CSF
infectious process
• Recall: Pt had combination of fever, HA, Sz,
stiff neck, visual changes; with no N/V.
What actions to take next…
• In collaboration with the OB attending, it was decided that we
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should get a CT of the pt’s head to R/O mass/lesion first---CT
was unremarkable. LP was then (attempted multiple times at 3
different levels) performed by the medicine team of doctors.
During this time she was also being treated for severe
preeclampsia and given Magnesium;
– Negative findings for this diagnosis- BP’s were 130’s/70’s, she was
not oliguric, Uric acid level WNL, no signs of hemolysis as CBC was
WNL, no peripheral edema noted, liver enzymes WNL’s and plts were
over 300.
– Positive findings included- spot urine protein was 10.9 (0.0-10.0),
TP:Cr 330 and she did exhibit Sz, HA, visual disturbances.
Pt’s CSF Findings:
Cells:100, Polys:23%, Glu:41, Prot:81, WBC:59;
gs and cx-, equine enceph-; bld cx -, HIV Ab –
Infect.
Cells
Polys
Glucose
Protein
bacterial
meningitis
50010,000/mL
> 90%
< 40 mg/dL
>150 mg/dL
Aseptic
Meningitis
10-500/mL
Early > 50% Normal
Late<20%
<100 mg/dL
Syphilitic
meningitis
50-500/mL
< 10%
<40 mg/dL
<100 mg/dL
HSV
encephalitis
0-1000/mL
<50%
Normal
< 100mg/dL
Review of Characteristics of
Abnormal CSF :
• Bright Red- indicates acute hemorrage
• Xanthochromia (yellowish to light red discoloration)•
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breakdown of RBC’s
Cloudiness- turbidity indicates infection due to increased
WBC’s or protein
Elevated Protein- assoc w/ CNS tumors, viral meningitis,
hemorrage, MS, GBS
Elevated WBC’s– Lymphocytes: viral or TB meningitis, MS, HSV, Syphillis, CNS
tumors
– Granulocytes: bacterial meningitis
Abnormal CSF characteristics
cont.
• Decreased glucose- bacterial meningitis, SAH
• Elevated Lactate- inc glucose metabolism assoc c
bacterial or fungal meningitis
• CSF pressures- (N in lat recumb position are 60-180 mm H2O)
– Increased- space occupying lesions, hydrocephalus, SAH,
intracranial infections, severe head injury, and
hypoxic/ischemic insults
– Decreased- spontaneous intracranial hypotension, colloid
cyst of the third ventricle and PDPH.
Anesthetic considerations:
• Peripartum Seizures- Differential
Diagnosis:
– Must rule out life threatening medical issues first
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A) Cerebrovascular compromise
B) Mass lesions
C) infectious diseases
D) Metabolic disorders/ epilepsy
E) Eclampsia
A) Cerebrovascular
Compromise
• Cerebral infarction
• Cerebral hemorrhage
• Subarachnoid
hemorrhage*
• Cerebral venous
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thrombosis*
Cerebral edema
Malignant HTN
B) Mass lesions
• A-V malformations*
• Benign and/or malignant tumors
• Cerebral abcess
C) Infectious Diseases
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Viral
Bacterial
Parasitic infestations
HIV
Fungal
D) Metabolic Disorders/
Epilepsy
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Hyponatremia
Hypocalcemia
Hypo or Hyperglycemia
Central stimulants- cocaine, theophylline etc.
Idiopathic epilepsy
E) Severe Preeclampsia
• In OB, this is obviously one of the most
common etiologies
Then comes the Neurology
Consult…
• Impression: Postpartum fever, HA, Seizure= clinical
meningoencephalitis involving a viral or aseptic
etiology. No focal neurological Sx.
– Although one can not exclude early bacterial, listeria or
paramenigeal process
– Mentioned, but was doubtful about a diagnosis of chemical
meningitis secondary to PO ibuprofen or of pleocytosis
from low-pressure (CSF <60 mm H2O) or from Sz alone.
* Note: the medicine team never got an opening pressure
Neurology Consult Cont.
• Treatment Plan:
- Dilantin, cont. Magnesium for Sz
- Empiric Abx Txmnt: acyclovir until HSV studies
came back negative; ceftriaxone and vanco given
until all bld and CSF cultures came back negative
- ID consult, send CSF for viral studies (HSV PCR,
enteroviral, arboviral, HIV)
- Get MRI of head
MRI Results 2 days later:
• Findings “consistent with intracranial hypotension.”
– Including T1-weighted images with diffuse meningeal
gadolinium enhancement with or without subdural and
extraarachnoid fluid collections or evidence of descent of
the cerebellar tonsils. Furthermore, there is a thick,
homogeneous pattern to the extra-axial fluid over the
hemispheres bilaterally representing cerebral venous
engorgement.
– Can also see enlargement of the pituitary gland in cases of
intracranial hypotension (Alvarez-Linera et al., Neurology.
2000;55;1895-1897) as the radiologist did appreciate with
our pt.
MRI Findings:
axial T1-WI c gad enhace
Case continuation: HD #4
• MRI results back and focus shifts to PDPH
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secondary to CSF leak and intracranial hypotension.
Pt seen by anesthesia, HA resolving; not increasingly
worse from laying down sittting standing. No
indication for blood patch at this time.
Pt D/C home on phenytoin and was suppose to f/u
with neurologist as outpt.
– Of note: pt had no further Sz activity during hospital stay
Summary:
• 17 y.o. on post-partum day 7 with GTC Sz, HA,
visual changes and fever.
– Considerations/Proposed questions:
• Was it a sequela of Severe Pre-eclampsia?
• Could it have been from an unintentional dural puncture when
performing the labor epidural?
• Was it an aseptic meningitis secondary to a virus or to a chemical?
• Who knows?
• How common are these outcomes? Let’s look at ways to avoid
these clinical symptoms and potential complications in the future.
– First, let’s look deeper into the syndrome of intracranial
hypotension.
Intracranial hypotension:
• Pathophysiology behind MRI findings– Monroe-Kellie Doctrine or Rule: states that when
the volume of any of the three cranial components
(brain parenchyma, CSF, and blood) increases, the
volume of one of the others must decrease or the
ICP will rise when considering an intact cranial
vault. Thus, if CSF volume decreases (ie. a leak),
the compensatory mechanism to maintain ICP is
by increasing blood volume, especially in the
venous capacitance system
Intracranial hypotension
• A syndrome occurring secondary to various etiologies
– Can occur spontaneously; secondary to anything that
causes a decrease production of CSF,or increased
absorption; or a disruption of a compartment as seen in
dural tears.
– No matter what the etiology, we treat this condition most
commonly with a blood patch or conservatively with IV
caffeine, IVF and pain meds
Can preeclampsia occur on
postpartum day 7 ?
• International Journal of Obstetric Anesthesia,
Akerman and Hall (from UK), April 2005,14(2), 163166 presented a case of a 29 y.o. in her 3rd pregnancy
developed Sz on PPD 7.
– No evidence of preeclampsia antepartum or postpartum.
Only symptoms preceding sz were fever, HA and visual
disturbances.
– She c/o sudden onset of frontal and occipital HA on PPD
3 which was worse on standing. Over the course of the
next 3 days, HA remained unchanged other than a
fluctuation in severity. No focal neurological signs.
Cont.
– On PPD 7, HA worsened, was febrile, pt had acute
visual disturbacnes and became agitated. She then
proceeded to have 2 GTC Sz.
– All studies were WNL incl CBC, Uric acid levels,
plts, electrolytes as well as CT head, MRI, and
LP.
Eclampsia- with Sz on PPD 22?
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Akerman and Hall site a couple influencial articles
that prehaps challenge the way we traditionally
think of eclampsia of occurring btwn 20 wks and
48hr postpartum.
One larger retrospective study (from the US, Lubarsky,
Barton, Freidman, Nasreddine, Ramadan, Sibia reported in
1994; 83, 502-505, in the green journal) reported that up to
15% of eclamptic pts developed sz btwn days 3 and
22 postpartum.
Cont.
• In another review (by Douglas and Redman of the
UK in the BMJ 1994; 309;1395-1400) found that in
over 300 cases of eclampsia, 12% occurred
more than 48hr and 2% more than 7 days postpartum.
– Among these cases reported, up to 90% suffered
from HA and visual disturbances prior to sz and no
classical preeclamptic signs were present in over
50% of the cases.
The Big Picture…
• The main objective of this article was to raise one
major point…that far too often it is assumed by our
colleagues that most postnatal HA’s are caused by
our epidurals. It is this unwillingness to consider all
possible causes for postnatal HA’s (other than PDPH)
which may lead to a delay in the exclusion or
diagnosis of more serious causes of HA’s
– Including, but not limited to, cortical vein thrombosis, SAH
or meningoencephalitis.
How clearly can you see through mud?
• And, as is many aspests of medicine, it is
never a clear-cut matter. Thus, it is imperative
to collaborate with colleagues (neurologists,
OB, ID, radiologists) and make a conjoined
effort to properly diagnose and treat each case
appropriately.
Aseptic meningitis secondary to
chemical irritation.
• “chemical meningitis” is an aseptic meningitis with
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it’s acute clinical course and standard laboratory
findings mimicking bacterial meningitis.
Most commonly it’s a rare complication of giving
dyes for myelography
– There has been case reports of chemical meningitis
following intrathecal or epidural corticosteroid thaerapies
– Also following PO TMP/SMX, ibuprofen, celecoxib and
rofecoxib
More cases of chemical meningitis:
• In Neurosurgery 55(5): 1222, November 2004, Meyers et
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al. reported two cases of chemical meningitis
secondary to the placement of second-generation
aneurysm coils for treatment of large cerebral
aneurysms.
In Neurosurgery 25 (2): 264-270, August 1989,
Lunardi et al reported a case of chemical meningitis
resulting from spillage of the contents of a cystic
cranial tumor. He also reviewed some 35 different
cases in which cranial and spinal tumors were
associated with a chemical meningitis.
How do we avoid the sequelea that
can originate from a dural
puncture?
• Should we always use LOR technique with NS and
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not air?
Should we consider threading intrathecal catheters in
cases where we accidentally puncture the dura while
attempting placement of an epidural catheter?
Should we prophylactically place EBP in parturients
after inadvertent dural puncture?
- Let’s investigate…
LOR techniques…does it matter?
• One larger study involving over 3700 pts investigated
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upon the role of intrathecal air.
In the journal Anesthesiolgy, 1998; 88; 76-81, Aida et
al from Japan formed two investigative groups– 1,918 in the saline LOR group and 1,812 in the air LOR
group
– Epidurals were performed for chronic and acute pain
purposes
– Incidence, onset time, and duration of PDPH were
examined and compared in each of the two groups.
Cont.
• Results: incidence of PDPH in the air group (32 cases) was
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significantly higher than that in the saline group (5 cases)
((more than 6 times more likely)), although the occurrences of
meningeal perforation btwn the two groups did not differ- 48
cases of unintentional dural puncture in the air group vs 51
cases in the saline group.
Also, PDPH’s were significantly more rapid in onset and
shorter in duration in the air group vs the NS.
Lastly, of the 32 cases of PDPH in the air group, 30 of them
had intrathecal air bubbles (highly contributing to HA)
detected on brain CT, whereas no intrathecal air bubbles were
seen in the NS group
Conclusion:
• That perhaps the use of air for loss-ofresistance techniques used when performing
epidural blocks, may be associated with a
higher incidence of PDPH as this article
suggests.
Thread ‘em Subarachnoid?
• Placement of a subarachnoid catheter after
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unintentional dural puncture may reduce the
incidence of PDPH. This is a contraversial issue, but
shown to be the case in the following study.
From Regional Anesthesia and Pain Management,
Vol 28, No 6 (Nov-Dec) 2003, 512-515, Ayad et al.
from CCF over a five year period, retrospectively
investigated 115 pts who had unintentional dural
punctures whom were placed randomly into 3 groups.
Methods Cont.
• Group A- had an epidural catheter placed at
another interspace
• Group B- had a subarachnoid catheter placed
for labor analgesia that was removed
immediately after delivery
• Group C- had a subarachnoid catheter placed
for labor analgesia that was removed 24 hrs
after delivery
Results:
• The incidence of PDPH in the various groups were as
follows…
– Group A- 81%
– Group B- 31%
– Group C- 3%
Whereas the overall incidence of PDPH after inadvertent
dural puncture was 46.9% overall. This risk of developing a
PDPH is reported to be as high as 75% in OB pts after
unintentional dural puncture with a 16-18 G needle.
Note: the type of epidural needle was not specified
The avoidance technique…
• In the journal of Anesthesiology, 2004; 101:
1422-1427 Scavone et al performed a
randomized double blind study to access the
effect of prophylactic epidural blood patches
on the incidence of PDPH.
Methods:
• 64 parturients who incurred an accidental dural
puncture were randomized into two groups
– 1 group: would randomly receive a prophylactic
epidural blood patch with 20 cc autologous blood
– 2nd group: was the sham group
Pt’s were followed daily watching for the
development of a PDPH for a min of 5 days.
Results:
• 18 of 32 pts in each group (56%) developed a PDPH.
Therapeutic blood patches were recommended in
subjects with moderate HA (in those who reported
trouble with caring for their children) and in those
who reported severe HA.
– The groups showed no significant difference in time of
onset of PDPH, median peak pain scores, and numbers of
days spent unable to care for their children
Results Cont.
• The conclusion of the study showed that in this
group of pts, prophylactic EBP did not
decrease the incidence of PDPH or that there
was a statistical significance in outcome btwn
the two groups. Therefore, the need to
provide prophylactic EBP was not supported.
In Conclusion…
• I have reviewed a case report here today with the
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intent of addressing other potential causes of
peripartum HA and seizures that one must consider
when working up a pt with these findings.
Differential diagnosis considerations…
Lastly, we must always be constantly self evaluating,
searching for new data which may support or negate
ways that we practice so that we can best serve our
pts.