Postpartum HA with Seizures: to do a blood patch or not to do

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Postpartum HA with Seizuresto do a blood patch
or not to do

• Presented By
• Deborah Opalski, D.O.
• Mentored By
• Norman Bolden, M.D.

28 June 2005
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Contents

• Presentation of Case Study
• Review of CSF infections and findings
• Review of differential diagnosis for peripartum
  seizures
• Current literature review
• Discussion

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Case Presentation-

• A 5 7, 152 , 17 y.o. at post-partum day 7,
  presented to HR LD 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.
• Pts 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.

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Recent Obstetrical history

• PMHx anxiety attacks. Denied Tob, ETOH, drugs.
  Took no 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 Bps in the
  140s/ 90s and a single increased TPCr ratio of
  446 (N lt150).
• 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

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And the plot thickens

• Pt was treated in the ED on Tues night with IVF
  and 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.

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Further Work-upWould 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.

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What actions to take next

• In collaboration with the OB attending, it was
  decided that we should get a CT of the pts 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- BPs were
  130s/70s, she was not oliguric, Uric acid level
  WNL, no signs of hemolysis as CBC was WNL, no
  peripheral edema noted, liver enzymes WNLs and
  plts were over 300.
• Positive findings included- spot urine protein
  was 10.9 (0.0-10.0), TPCr 330 and she did
  exhibit Sz, HA, visual disturbances.

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Pts CSF Findings Cells100, Polys23,
Glu41, Prot81, WBC59 gs and cx-, equine
enceph- bld cx -, HIV Ab
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Review of Characteristics of Abnormal CSF

• Bright Red- indicates acute hemorrage
• Xanthochromia (yellowish to light red
  discoloration)- breakdown of RBCs
• Cloudiness- turbidity indicates infection due to
  increased WBCs or protein
• Elevated Protein- assoc w/ CNS tumors, viral
  meningitis, hemorrage, MS, GBS
• Elevated WBCs-
• Lymphocytes viral or TB meningitis, MS, HSV,
  Syphillis, CNS tumors
• Granulocytes bacterial meningitis

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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.

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Anesthetic considerations

• Peripartum Seizures- Differential Diagnosis
• Must rule out life threatening medical issues
  first
• A) Cerebrovascular compromise
• B) Mass lesions
• C) infectious diseases
• D) Metabolic disorders/ epilepsy
• E) Eclampsia

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A) Cerebrovascular Compromise

• Cerebral infarction
• Cerebral hemorrhage
• Subarachnoid hemorrhage

• Cerebral venous thrombosis
• Cerebral edema
• Malignant HTN

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B) Mass lesions

• A-V malformations
• Benign and/or malignant tumors
• Cerebral abcess

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C) Infectious Diseases

• Viral
• Bacterial
• Parasitic infestations
• HIV
• Fungal

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D) Metabolic Disorders/ Epilepsy

• Hyponatremia
• Hypocalcemia
• Hypo or Hyperglycemia
• Central stimulants- cocaine, theophylline etc.
• Idiopathic epilepsy

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E) Severe Preeclampsia

• In OB, this is obviously one of the most common
  etiologies

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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 lt60 mm H2O)
  or from Sz alone.
• Note the medicine team never got an opening
  pressure

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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

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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.
  2000551895-1897) as the radiologist did
  appreciate with our pt.

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MRI Findings axial T1-WI c gad enhace
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Case continuation HD 4

• MRI results back and focus shifts to PDPH
  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

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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? Lets look at
  ways to avoid these clinical symptoms and
  potential complications in the future.
• First, lets look deeper into the syndrome of
  intracranial hypotension.

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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

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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

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Can preeclampsia occur on postpartum day 7 ?

• International Journal of Obstetric Anesthesia,
  Akerman and Hall (from UK), April 2005,14(2),
  163-166 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.

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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.

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Eclampsia- with Sz on PPD 22?

• 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.

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Cont.

• In another review (by Douglas and Redman of the
  UK in the BMJ 1994 3091395-1400) found that in
  over 300 cases of eclampsia, 12 occurred more
  than 48hr and 2 more than 7 days post-partum.
• 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.

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The Big Picture

• The main objective of this article was to raise
  one major pointthat far too often it is assumed
  by our colleagues that most postnatal HAs are
  caused by our epidurals. It is this unwillingness
  to consider all possible causes for postnatal
  HAs (other than PDPH) which may lead to a delay
  in the exclusion or diagnosis of more serious
  causes of HAs
• Including, but not limited to, cortical vein
  thrombosis, SAH or meningoencephalitis.

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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.

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Aseptic meningitis secondary to chemical
irritation.

• chemical meningitis is an aseptic meningitis
  with its acute clinical course and standard
  laboratory findings mimicking bacterial
  meningitis.
• Most commonly its 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

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More cases of chemical meningitis

• In Neurosurgery 55(5) 1222, November 2004,
  Meyers et 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.

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How do we avoid the sequelea that can originate
from a dural puncture?

• Should we always use LOR technique with NS and
  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?
• - Lets investigate

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LOR techniquesdoes it matter?

• One larger study involving over 3700 pts
  investigated 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.

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Cont.

• Results incidence of PDPH in the air group (32
  cases) was 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, PDPHs 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

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Conclusion

• That perhaps the use of air for
  loss-of-resistance techniques used when
  performing epidural blocks, may be associated
  with a higher incidence of PDPH as this article
  suggests.

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Thread em Subarachnoid?

• Placement of a subarachnoid catheter after
  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.

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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

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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

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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.

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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
• Pts were followed daily watching for the
  development of a PDPH for a min of 5 days.

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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

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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.

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In Conclusion

• I have reviewed a case report here today with the
  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.