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TABLE56.2 VASCULAR DISTRIBUTION:CRANIAL
Artery Clinical Presentation
to lower placental transmission and decreased association
with fetal acidosis.20 Vasopressin receptors (V1) are present on the human uterus, and administration of vasopres-
Anterior Cerebral
Artery
Middle Cerebral
Artery
Posterior Cerebral
Artery
Lower extremity weakness and sensory
loss:contralateral side
Apraxia
Speech dysfunction:initiation
Facial, upper and lower extremity weakness and
sensory loss:contralateral side
Aphasia:expressive, receptive
Sensory loss:contralateral side
Cognitive impairment
Visionloss
Language dysfunction
sin for hypotension can induce uterine contractions.21
Epinephrine is a suitable third- line agent for treatment
of hemodynamic instability. Risk of uterine arterial vasoconstriction is balanced by tocolysis and decreased uterine
vascular resistance.
22
Not all molecules cross the placenta, and movement
is dependent on hydrostatic, osmotic pressure gradients
and concentration gradients. All beta blockers, hydralazine, nitroprusside, and nitroglycerin cross the placenta.
Beta blockers can cause a transient fetal bradycardia, but
Cerebellar Artery Ataxia
Vision impairment
Vertigo
Speech impairment
Loss of consciousness
Basilar Artery Cranial nerve dysfunction
Ataxia
Cognitive impairment
Temperature and sensoryloss
Motor weakness:contralateral side
NOTE:There is much overlap in presenting signs and this list is not exhaustive.
potential maternal benet from decreasing blood pressure or heart rate may outweigh fetal risk. Angiotensionconverting enzyme (ACE) inhibitors are contraindicated
in the second and third trimesters secondary to teratogenic
eects,23 so they are not typically used for maintenance
during pregnancy and would not be ideal for acute blood
pressure management. Magnesium sulfate is administered
to parturients for seizure prophylaxis in preeclampsia and
for fetal neuroprotection in prematurity <32 weeks gestational age, and can cause hypotension, uterine atony, and
addition, parturients can present with other signs such as
seizures, visual changes, ataxia, weakness, facial drooping,
and altered consciousness.19 See Table 56.2. Any concerning neurological signs in the parturient should be evaluated
immediately, as outcomes seem to be worse in pregnancy.
hypotonia. Parturients who receive mannitol to reduce
elevated intracranial pressure (ICP) are at risk for drug
accumulation in the fetus, resulting in a hyperosmolar
state, reduced urinary blood ow, and lung uid production.24 All anticonvulsants cross the placenta and have the
potential to cause neural tube, orofacial, cardiovascular,
PREGNANCY- SPECIFIC CONSIDERATIONS
and digital malformations, when given early in pregnancy,
as well as fetal coagulopathies. Valproate, phenytoin, carbamazepine, phenobarbital, and topiramate all have been
If the parturient is not postpartum, management of
stroke/ intracranial hemorrhage should include consideration of uterine blood ow (UBF) to preserve a viable
pregnancy. Uterine blood ow is not autoregulated;
therefore it is dependent solely on maternal systolic blood
pressure and cardiac output. In hypertensive patients,
blood pressure should not be dropped too aggressively.
Hypovolemia, vasodilators, many anesthesia medications,
positive pressure ventilation, sympathetic blockade, aortocaval compression, and uterine hypertonicity (due to
oxytocin or alpha- adrenergic stimulation), can all cause
decreased UBF. If the parturient requires general anesthesia for diagnosis or treatment of a neurologic event, excessive hyperventilation and hypocapnia should be avoided
in order to prevent placental vasoconstriction and fetal
compromise. If vasopressors are needed for hypotension
following stroke/ intracranial hemorrhage, phenylephrine
may be preferred over ephedrine as rst- line therapy due
associated with congenital malformations.25 Levetiracetam
(Keppra) is commonly used for seizure prophylaxis following an intracranial event, and in one recent study from
Australia, there were no malformations seen in parturients
taking Keppra.26 At term, there is no risk of congenital
malformation related to medication, as organogenesis is
complete.
Ionizing radiation exposure during diagnostic procedures such as CT could result in spontaneous abortion,
congenital malformation, or cerebral injury, depending on
dose and timing of exposure. Exposure during the rst 15
weeks of development places the fetus at greatest risk for
injury, and the risk declines by a factor of 4 aer 15 weeks
gestation, likely due to completion of organogenesis. Aer
26 weeks gestation, the risks are minimal. e American
College of Obstetricians and Gynecologists recommend
that exposure during pregnancy not exceed 5 rad (radiation absorbed dose). e parturient should be shielded
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with lead in the anterior and posterior position during
any exposure, to minimize risk. For reference, a computed
tomography (CT) of the chest results in fetal exposure of
up to 0.1 rad and a chest x- ray results in exposure of <0.001
rad.27 Radiopaque agents used in CT scans can contain
iodine and cross the placenta, potentially resulting in fetal
hypothyroidism, but these techniques should be used if the
maternal benet outweighs the risk to the fetus.28 Contrast
is excreted minimally in the breastmilk, and there is no precaution regarding lactation for postpartum women. e
safety of paramagnetic contrast agents (Gadolinium) has
not been established in humans, but they do cross the placenta and should be used only if absolutely essential, especially during the rst trimester.
28
blood pressure is maintained.30 However, while it is quite
unlikely that general anesthesia would be undertaken for
the purposes of blood pressure control, given the associated
increase in ICP, it is important to note that MAC is reduced
by 30%– 40% in the parturient.
31
e American College of Obstetricians and
Gynecologists (ACOG) recommends that any fetus
termed viable (approximately 24 weeks) should have at a
minimum Doppler fetal heart tones and tocometer analysis immediately prior to and aer an operation/ intervention.32 Continuous intraoperative monitoring should be
performed for a viable fetus during intervention following maternal stroke/ intracranial hemorrhage if (1) there
is an obstetrical physician or nurse qualied to interpret
the fetal tracing; (2) monitoring is possible during the
ANESTHETIC CONSIDERATIONS SPECIFIC
TOTHE PARTURIENT WITHSTROKE/
INTRACRANIAL BLEEDING
surgery, and (3)an emergency cesarean delivery could be
performed without compromising the parturient’s safety.
Management and treatment of these parturients should
take place in a facility that has obstetrical, pediatric, and
neonatal expertise readily available. e operating room
For all procedures requiring general anesthesia, pregnant
patients >18– 20 weeks gestation should receive a nonparticulate antacid, an H2 blocker, and a gastric motility agent and
a rapid sequence induction (RSI) is recommended. When
the gestational age is >20 weeks, le uterine displacement
(LUD) should also be maintained. Agents that increase ICP
should be avoided (e.g., ketamine), and succinylcholine may
produce transient increases in ICP. However, those increases
may be abolished with IV lidocaine, adequate depth of anesthesia, hyperventilation, or a defasciculating dose of a nondepolarizing paralytic.29 An arterial line should be considered
for close blood pressure monitoring and should be maintained within 20% of baseline, with a mean arterial pressure
of >70mmHg. Invasive blood pressure monitoring should
also be considered for laboring patients with stroke/ intracranial hemorrhage if vasoactive medications are required for
tight blood pressure control. A sodium nitroprusside drip
can be used to lower blood pressure, but it crosses the placenta and may cause fetal cyanide toxicity (keep infusions
to less than 0.5 mg/ kg/ h and minimize duration of time on
infusion). Nitroglycerin can also be used to control blood
pressure without adverse fetal eects, although experimentally, nitroglycerin is metabolized to nitrites, causing methemoglobinemia and cerebral vasodilation. Nicardipine
infusion oers the advantage of easy titration and short
duration of action if blood pressure control requires continuous medication administration. Inhalation agents like
isourane can also be used to lower blood pressure and even
at greater than 1 MAC (minimum alveolar concentration),
uteroplacental perfusion is maintained as long as maternal
should be equipped for an emergency cesarean section
should the need arise.32 Continuous intraoperative fetal
monitoring for a previable fetus should be performed to
optimize placental blood ow in cases of fetal bradycardia
and on a case- by- case basis.32 Loss of beat- to- beat variability is normal during general anesthesia, but fetal heart
rate decelerations are abnormal and should be corrected
with increased blood pressure, increased oxygenation, or a
change in position.
When a parturient presents in labor with intracranial
pathology there are several management concerns depending on the etiology, including acuity, presentation, location,
size, and how the pathology has been managed. Amultidisciplinary meeting with obstetricians, neurologists, anesthesiologists, and neonatologists is critical if time permits.
Parturients with history of ischemic stroke presenting in
labor are likely anticoagulated, and normalization of coagulation values is required before neuraxial analgesia can be
provided (refer to American Society of Regional Anesthesia
guidelines). ese patients can be managed expectantly and
deliver vaginally if there is adequate normotensive blood
pressure control. Acesarean section is usually only indicated
for obstetric indications, as the surgery itself may be a risk
factor for postpartum stroke; tight blood pressure control
is paramount. General anesthesia should be induced with
care and special attention given to minimize uctuations in
hemodynamics.
Parturients with treated, stable intracranial hemorrhage (embolization of AVM or clipping of aneurysm) can
labor, but blood pressure should be well controlled. An
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assisted second stage for vaginal delivery would be considered under dense neuraxial anesthesia and anesthetic goals
during both the rst and second stages of labor would center around avoiding hemodynamic lability due to pain as
well as Valsalva maneuvers. If a cesarean section is planned
for obstetric reasons, neuraxial anesthesia is an option with
blood pressure maintained at baseline. Remember that all
intracranial lesions can result in cranial mass eect and elevation in intracranial pressure; this should be considered prior
to placing any neuraxial anesthetic. Delivering vaginally has
not resulted in increased maternal complications for these
corrected lesions.
2
When a parturient presents in labor with an unrepaired AVM or aneurysm, they need to be evaluated on a
case- by- case basis. ings to consider are the size and location of the vascular anomaly, as this will drive the mode
of delivery. For some lesions, the patient is still encouraged to delivery vaginally, with close monitoring, possibly
invasive, and an assisted second stage with adequate neuraxial analgesia. During a cesarean delivery, hemodynamics
should be closely followed with invasive monitoring and
neuraxial or general anesthesia. Studies have shown that
there is not a standard preferred method of delivery for
these cases, so for most treated and managed conditions
discussed here, vaginal delivery will be the mode selected.2
All parturients with existing neuropathology should be
closely monitored postpartum, potentially in the neuro
intensive careunit.
maintained on warfarin. For pregnancies that are considered lower risk, UFH or LMWH are initiated in the initial
trimester and then followed with low- dose aspirin for the
remainder of the pregnancy.33 In regard to hemorrhagic
stroke, the treatment is usually surgical for decompression
and evacuation of the hematoma. However, watchful waiting, hemodynamic control, and reversal of any coagulopathy are options as well, depending on the severity of the
hemorrhage.
In any pregnant or immediately postpartum woman with
new neurologic complaints, a timely neurology and/ or neurosurgery consult should be obtained (Figures 56.1,56.2,).
Imaging studies should be performed based on the neurologic symptoms and indication. Fetal exposure to ionizing radiation was discussed earlier and should be weighed
against the maternal benet. Noncontrast CT is usually the
rst imaging modality to evaluate for cranial hemorrhage,
but contrast may be needed to further delineate anatomical
structures. Also, MRI and MR venogram may be indicated
to evaluate for stroke or for other vascular occlusions, and
the use of paramagnetic contrast agents should be weighed
against the risk. In addition, cardiac ultrasound should be
performed in all suspected embolic events to evaluate for
right to le intracardiac communication as the etiology
of the event. Basic laboratory studies should be evaluated,
including hemoglobin, platelet count, electrolytes, liver
function tests, and coagulation studies. Complete workup
for thrombophilias should be delayed until 6 weeks postpartum when the coagulation factors normalize (protein C and
MANAGEMENT AND TREATMENT
S activity, antithrombinIII).
For thrombotic lesions, the use of intra- arterial thrombolysis has been used successfully in parturients. In one
Hypertensive disorders are the most common etiologies
for stroke and intracranial hemorrhage; therefore management involves aggressive blood pressure control during pregnancy for prevention. Systolic blood pressure of
greater than 160mmHg should be immediately addressed
with antihypertensive agents. e most commonly used
medications considered safe in pregnancy are labetalol,
hydralazine, or nifedipine. e goal is to improve systemic blood pressure while maintaining adequate cerebral
perfusion pressure. It has been shown that controlling
the systolic blood pressure is more important than controlling diastolic blood pressure.17 For parturients with
ischemic/ thrombotic stroke or CVT, the management is
medical therapy. American Heart Association guidelines
for parturients are unfractionated heparin (UFH) or low
molecular weight heparin (LMWH) through 13 weeks of
gestation and restarted at approximately 36 weeks until
delivery. From 13 through 36 weeks the parturients can be
study, 10 of 11 women who received thrombolysis injected
into their vasculature had no major complications, however
one woman died of a major complicating illness. e fetal
outcomes were positive, with seven neonates delivering
without issue, two therapeutically terminated, one spontaneous abortion in the parturient with bacterial endocarditis, and one demise when the parturient passed away.
34– 36
Intravenous/ arterial tPA (tissue plasminogen activator) has
a short half- life (less than 5 minutes), but since it binds to
new brin clots, the clinical eect can last for hours. It is
a large molecule and thus does not cross the placenta, so
fetal teratogenic eects should not be a concern. Pregnancy,
operative delivery, or postpartum state are not absolute
contraindications to intravenous or intra- arterial thrombolysis, thrombectomy, or craniotomy.
37– 39
Any parturient
who requires management of stroke or cranial hemorrhages
should be transferred to a stroke unit or tertiary care unit
capable of caring for these patients. See Figure 56.2. Any
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409
Critical Assessment Intervention (10 min):
• Activate Emergency Response/Stroke Team
• Monitor and support hemodynamics: blood pressure control is paramount
• Support airway and provide supplemental oxygen if needed
• Confirm/establish IV access
• Time course of symptoms and brief neurological exam and pertinent medical history
• Check glucose
• Laboratory studies if time permits
• Monitor fetus, but do not delay diagnosis or treatment
Prepare for imaging:
CT or MRI of the brain depending on urgency of diagnosis (within 25 min)
Cranial Hemorrhage:
• Consult neurosurgeon/neurologist
• Transfer to higher level of care if indicated
• Continue to stabilize until definitive intervention,
including blood pressure control
• Check blood availability
• Prepare operating room if needed
Nonhemorrhage/Stroke:
• Consult neurologist
• If < 4.5 hours: fibrinolytic therapy: rtPA is NOT
an absolute contraindicated in
pregnancy/postpartum period
• If >4.5 hours: intra-arterial intervention
• Supportive care and blood pressure monitoring
Figur e5 6.2 Maternal stroke/ cranial hemorrhage algorithm.
parturient with a Glasgow Coma Score of less than nine,
should have her airway protected, especially prior to
transfer.
1
• Consider TTE with bubble study, carotid
ultrasound, thrombophilia workup, antiplatelet
therapy.
autoregulated and is dependent on maternal blood pressure.
Fetal monitoring during diagnostic or therapeutic neurological procedures should be used based on gestational
age and availability of surgical obstetrical intervention. All
CONCLUSIONS
parturients suspected of stroke or intracranial hemorrhage
should be treated at a facility capable of managing these
complex conditions.
Parturients are at greater risk of stroke and intracranial
hemorrhage in the peripartum period due to the physiologic changes of pregnancy and hypercoagulable state of
CASE- BASED LEARNING DISCUSSION
pregnancy. Hypertensive disorders are the most common
etiologies for intracranial hemorrhage. Aggressive blood
pressure control is critical. Diagnosis and treatment should
not be delayed based on pregnancy. All necessary imaging
and intervention should be pursued regardless of pregnancy status for maternal well- being, but precautions and
fetal monitoring may be warranted. Maintaining hemodynamic stability is critical, as uterine blood ow is not
1. What is your dierential diagnosis? What should be the
next steps in management?
2. Would you treat her blood pressure? Which medications
would you use, and what would be the endpoint?
3. Would you order any imaging studies? Consult any
other medical services?
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4. How would your management change if she were
postpartum?
5. e parturient becomes unresponsive and demonstrates
seizure activity. What do you do now? What are next
rst steps? Has your dierential changed? What if she
were immediately postpartum?
6. If operative evacuation of a hemorrhage is warranted,
how will you provide anesthesia? What if she has just
delivered the neonate?
7. If stroke is suspected, how will you medically manage
her? Would you anticoagulate her now versus longterm? If so, with what medication?
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2. James AH, Bushnell CD, Jamison MG, Myers ER. Incidence and
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9. Tuluc M, Brown D, Goldman B. Lethal vertebral artery dissection
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11. Pritchard JA. Changes in the blood volume during pregnancy and
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12. Bamber JH, Dresner M. Aortocaval compression in pregnancy:the
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cardiac output. Anesthesia and Analgesia. 2003;97:256– 8.
13. McClelland SH, Bogod DG, Hardman JG. Apnoea in preg-
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14. Stirling Y, Woolf L, North WR, etal. Haemostasis in normal pregnancy. rombosis and Haemostasis. 1984;52:176– 82.
15. Lanska DJ, Kryscio RJ. Risk factors for peripartum and postpartum stroke and intracranial venous thrombosis. Stroke. 2000;
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16. Bushnell CD, Jamison M, James AH. Migraines during pregnancy
linked to stroke and vascular diseases: US population based casecontrol study. BMJ. 2009;338:b664.
17. Martin JN Jr, igpen BD, Moore RC, etal. Stroke and severe preeclampsia and eclampsia:a paradigm shi focusing on systolic blood
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18. Kittner SJ, Stern BJ, Feeser BR, et al. Pregnancy and the risk of
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19. Crovettoa FB, Somiglianaa EC, Peguerob A, Figueras FB. Stroke
during pregnancy and pre- eclampsia. Curr Opin Obstet Gynecol.
2013;25:425– 32.
20. Ngan Kee WD, Khaw KS, Tan PE, etal. Placental transfer and
fetal metabolic eects of phenylephrine and ephedrine during spinal anesthesia for cesarean delivery. Anesthesiology.
2009;111:506– 12.
21. Maggi M, Del Carlo P, Fantoni G, etal. Human myometrium during pregnancy contains and responds to V1 vasopressin receptors as
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22. Segal S, Csavoy AN, Datta S. e tocolytic eect of catecholamines in the gravid rat uterus. Anesthesia and Analgesia.
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23. Cooper WO, Hernandez- Diaz S, Arbogast PG, etal. Major congenital malformations aer rst- trimester exposure to ACE inhibitors.
New England Journal of Medicine. 2006;354:2443– 51.
24. Tuncali B, Aksun M, Katircioglu K, etal. Intraoperative fetal heart
rate monitoring during emergency neurosurgery in a parturient.
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25. Werler MM, Ahrens KA, Bosco JL, etal. Use of antiepileptic medications in pregnancy in relation to risks of birth defects. Annals of
Epidemiology. 2011;21:842– 50.
26. Vajda FJ, Graham J, Roten A, et al. Teratogenicity of the newer
antiepileptic drugs— the Australian experience. Journal of Clinical
Neuroscience. 2012;19:57– 59.
27. Groen RS, Bae JY, Lim KJ. Fear of the unknown: ionizing radiation exposure during pregnancy. American Journal of Obstetrics and
Gynecology. 2012;206:456– 62.
28. ACOG Committee Opinion. Number 299, September 2004
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2004;104:647– 51.
29. Kovarik WD, Mayberg TS, Lam AM, et al. Succinylcholine does
not change intracranial pressure, cerebral blood ow velocity, or the
electroencephalogram in patients with neurologic injury. Anesthesia
and Analgesia. 1994;78:469– 73.
30. Dahlgren G, Tornberg DC, Pregner K, et al. Four cases of the
ex utero intrapartum treatment (EXIT) procedure: anesthetic
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2004;13:178– 82.
31. Chan MT, Mainland P, Gin T. Minimum alveolar concentration of halothane and enurane are decreased in early pregnancy.
Anesthesiology. 1996;85:782– 6.
32. ACOG Committee Opinion No. 474:Nonobstetric surgery during
pregnancy. Obstetrics and Gynecology. 2011;117:420– 21.
33. Sacco RL, Adams R, Albers G, et al. Guidelines for prevention
of stroke in patients with ischemic stroke or transient ischemic
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34. Johnson DM, Kramer DC, Cohen E, etal. rombolytic therapy
for acute stroke in late pregnancy with intra- arterial recombinant
tissue plasminogen activator. Stroke. 2005;36(6):e53– 55.
35. Wiese KM, Talkad A, Mathews M, Wang D. Intravenous recombinant tissue plasminogen activator in a pregnant woman with cardioembolic stroke. Stroke. 2006;37(8):2168– 9.
36. Leonhardt G, Gaul C, Nietsch HH, etal. rombotic therapy in
pregnancy. J romb rombolysis. 2006;21(3):271– 6.
37. Murugappan A, Coplin WM, Al- Sadat AN, et al. rombolytic
therapy of acute ischemic stroke during pregnancy. Neurology.
2006;66(5):768– 70.
38. Del Zotto E, Giossi A, Volonghi I, etal. Ischemic stroke during pregnancy and puerperium. Stroke Res Treat. 2011;2011:606– 780.
39. Dapprich M, Boessenecker W. Fibrinolysis with alteplase in a pregnant women with stroke. Cerebrovasc Dis. 2002;13(4):290.
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57.
POST– DURAL PUNCTURE HEADACHE
PhilipRubin
CLINICALCASE
Whitacre, or other “pencil-point” needles, are associated
with signicantly higher rates of PDPH due to the characA 27- year- old female, G2P1, at 6cm dilation, with a body
mass index (BMI) of 36, requests an epidural for labor analgesia. An anesthesia resident attempts placement with a 17
gauge Tuohy needle, using a loss of resistance to air technique. During needle advancement, the resident notices
the syringe suddenly lling with clear uid. e syringe is
detached, and free- owing cerebrospinal uid (CSF) pours
from the Tuohy needle.
teristics of the dural puncture that they create (cutting the
dura/arachnoid perpendicularly, rather than spreading
bers laterally), which fosters increased CSF ow across
the dura and delayed dural healing.3 Cutting needles have
thus largely fallen out of favor for practitioners performing
neuraxial techniques due to the increased risk for PDPH.
Needle orientation during dural puncture may also con-
tribute to PDPH risk because the dura mater/arachnoid
is composed of collagen bers running longitudinally
RISK FACTORS FORPOST– DURAL PUNCTURE
HEADACHE
along the spinal column. Orientation of the needle bevel
parallel to these bers may favor a more “natural” separa-
tion, given the tendency to spread the bers laterally. is
less traumatic insult to the dura may consequently heal
Trespass of the dural membrane can be intentional, as with
spinal anesthesia or lumbar puncture, or accidental, during
the course of other neuraxial procedures or spine surgery.
e case above describes an episode of epidural placement,
complicated by unintentional dural puncture (UDP) with
the Tuohy needle, also known as a “wet tap.” ough rarely
a dangerous event, it is commonly accompanied by a moderate to severe postural headache, which causes signicant
morbidity for the patient.
1
Post– dural puncture headache (PDPH) is more common (>70% risk within 48 hours) aer documented dural
puncture with free- owing CSF via a large bore 17– 18
gauge Tuohy needle. Post– dural puncture headache may
also occur when dural puncture is intentional, as with
spinal anesthesia (22– 27 gauge) or lumbar puncture for
CSF evaluation (20– 24 gauge).2 e incidence of PDPH
is 1.5% for all epidural placements,3 and approximately
1% for spinal anesthesia using small bore spinal needles.1
e risk increases dramatically with increasing needle size,
however some procedures (lumbar puncture) require dural
puncture with larger bore needles to draw CSF and measure opening pressure.
Post–dural puncture headache risk also varies by
the distinguishing features of dierent needle designs.
Quincke or other “cutting” spinal needles, compared with
more quickly, thereby minimizing continued CSF loss.
Conversely, a perpendicularly oriented needle bevel may
cause more trauma as it cuts through the bers.1 erefore,
some providers advocate Tuohy needle advancement in a
parallel orientation before entering the epidural space, in
case of accidental dural puncture (ADP).
Non- needle- related PDPH risk factors include young
age (18– 30), history of headache (HA) prior to dural puncture, and low BMI.1 While female gender is not considered
an independent risk factor, the incidence is traditionally
higher in females because a large percentage (60% incidence
in the United States) elect for neuraxial labor analgesia,
which incorporates the use of Tuohy needles, increasing the
risk of UDP with a large needle. Laboring patients are particularly at increased risk when epidurals are placed at cervical dilation ≥7 cm, in the lateral decubitus position, or aer
multiple attempts or punctures (as in patients with elevated
BMI). ese scenarios are commonly associated with more
dicult placement and consequently, an elevated risk of
UDP during prolonged procedural eorts.4 ough UDP
increases with elevated BMI (e.g., >30), actual PDPH incidence is lower in this patient population, compared with
their nonobese counterparts, likely because of decreased
CSF leakage across the dural puncture. is is attributed to
increased intra-abdominal pressure in obese patients, which
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increases CSF pressure, while decreasing the size of the epidural space, favoring less CSF leakage, yielding a protective
eect against development of PDPH.
SYMPTOMS/ PATHOPHYSIOLOGY
5
TABLE57.1 POST– DURAL PUNCTURE HEADACHE
DIFFERENTIAL DIAGNOSIS
Migraine Caffeine Withdrawal
Cluster headache Dehydration
Tension headache Meningitis
Sleep deprivation Cortical vein thrombosis
A postural HA is the sine qua non of a PDPH; it improves
when supine, or with the head reclined, and worsens with
the head elevated, or when sitting or standing. e HA typ-
Pneumocephalus Subarachnoid hemorrhage
Severe preeclampsia Stress/ anxiety
ically presents in the frontotemporal or occipital areas, and
usually develops between 1 and 7days aer dural puncture,
distinguishing it from other causes of postpartum HA.
ere is no associated aura, although the pain may radiate to the neck, causing neck stiness, and the HA may be
accompanied by auditory (tinnitus) and visual (diplopia)
changes, vertigo, dizziness, nausea, vomiting, and rarely cranial nerve palsies.
6,7
e severity of the HA directly correlates with the
degree of intracranial hypotension due to the volume of
CSF that ows from the intrathecal space into the epidural space. Normal CSF pressure in the lumbar region is
between 5 and 15cmH20 in the supine position, compared
to 40cmH20 when erect. e CSF “loss,” and the resultant
CSF pressure in the intrathecal space, are inversely proportional. Pressure in the lumbar region may decrease to
4cmH20 or less when recumbent,6, and the drop is eventually transmitted both cephalad and caudad, across the entire
spinalcanal.
As one of the roles of CSF is to mechanically support
central nervous system (CNS) structures, its reduction in
the cranium causes tugging or sagging of the meninges,
especially when sitting or standing (due to the addition of
gravity’s eect in this position). e resultant traction of
these pain- sensitive intracranial structures is the mechanism
behind the HA following dural puncture. Upon return to
the recumbent position, the HA quickly improves, or even
completely disappears due to equalization of CSF pres-
e dierential diagnosis of postpartum HA is quite
extensive (Table 57.1), especially for parturients who
received neuraxial anesthesia. In fact, 40% of women experience symptoms of HA unrelated to dural puncture aer
delivery. ese etiologies include, but are not limited to,
dehydration, exhaustion from labor contractions, sleep deprivation, caeine withdrawal, stress, musculoskeletal tension, pain, anxiety, and preexisting HA conditions such as
migraines.
1,7
For this reason, PDPH is a diagnosis of exclusion, and practitioners commonly wait 24 hours postdural
puncture prior to labeling a HA meeting the pathognomonic characteristics of PDPH.
Patients attest to the uniqueness of a PDPH, which
they nd debilitating, especially for parturients in the postpartum period. Not only do these patients need to care for
themselves and ambulate frequently to minimize the risk of
deep vein thrombosis (DVT), but they must also care for
their newborn, which requires frequent sitting up and getting out of bed. us, unrecognized or inadequately treated
PDPH inevitably increases healthcare costs caused by
delayed discharge or readmission, and the resultant adjustment in nursing ratios that may be necessary to provide
additional attention to both mother and baby. Persistent
PDPH may also be associated with delayed mother-infant
bonding and associated breastfeeding success, which may
further increase time to discharge.
8
sure throughout the cranium and spinal canal, and relief of
intracranial hypotension.
Since the sum of all structures (brain, CSF, blood volume) in the cranium remains constant, according to the
Monro- Kellie doctrine, the loss of CSF volume surrounding the brain leads to compensatory cerebral venodilation.
is results in increased cerebral blood volume, which is
another contributing factor to the development of PDPH.6
Movements that commonly prevent cerebral venous drainage, such as coughing, sneezing, and straining, may further
exacerbate HA symptoms.
6
TREATMENT
When a “wet tap” is recognized during epidural placement,
the provider has two immediate options: completely withdraw the needle and repeat the procedure, or thread the
epidural catheter into the intrathecal space via the Tuohy
needle.9 While the former choice is more common, spinal catheters have several advantages in this setting. First
and foremost, continuous spinal anesthesia is quite reliable due to the uniformity of the subarachnoid space. is
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technique may be in the patient’s best interest, especially if
epidural placement was dicult, or if the patient had been
deemed high risk for requiring cesarean delivery. Special
safety measures must be implemented, however, to ensure
that the catheter is not inappropriately managed as an epidural catheter, as this would place the patient at severe risk
for a high spinal.
Interestingly, another potential advantage of threading
a spinal catheter is to reduce the risk or severity of PDPH.
Several studies have validated this practice, postulating that
leaving the catheter in- situ for at least 24 hours aids in the
dural healing process. e catheter purportedly induces an
inammatory reaction that begins to seal the dural bers
around the catheter.9 Other researchers, however, discourage this practice, claiming either that it adds no clinical benet because the CSF pressure gradient is too high
immediately aer the puncture to prevent leakage, or that
the inammatory process can be disrupted or completely
dislodged when the catheter is eventually removed.10 ere
still is no consensus on whether to thread or not to thread;
the topic continues to be debated and evaluated within the
obstetric anesthesia community. Whichever decision is
made, however, needs to be consistent with hospital policy,
and its sta ’s ability to safely care for the patient by preventing misuse of the catheter. Aggressive labeling is essential
to avoid injection of medications intended for the epidural
space or intravenous route. Repeated access of an intrathecal catheter should be limited, as each manipulation can
place the patient at increased risk for CNS infection.
Management of PDPH varies dependent on severity,
but conservative measures that oer symptomatic relief are
traditionally implemented rst (Box 57.1). Approximately
150 mL of CSF is produced daily, compared with the average total CSF volume in the spinal canal and cranium of
500 mL. Since CSF continues to leak at a rate faster than
new CSF production, patients are instructed to hydrate
aggressively, as this may promote increased CSF production
to replenish the “lost” volume. Increased production theoretically helps to increase intrathecal CSF pressure, counteracting the pressure reduction caused by CSF leakage.6 If
BOX 57.1 CONSERVATIVE PDPH TREATMENTS
Hydration (oralorIV)
Analgesics (oralorIV)
Caffeine (oralorIV)
Rest/ recumbency
a patient has diculty consuming large amounts of uids,
then increasing intravenous uids is a viable alternative in
admitted patients.
Initiation of multimodal analgesia is also benecial;
patients are encouraged to routinely request their “as
needed” medications for postpartum pain around the clock.
Such medications (in both oral and intravenous form) usually include opioids, nonsteroidal anti- inammatory drugs
(NSAIDS) such as ketorolac and ibuprofen, and also acetaminophen.11 While they may aid in attenuating PDPH,
unfortunately some (especially opioids) commonly cause
untoward side eects including nausea, vomiting, and pruritis. us the utility of oral and intravenous analgesics is
sometimes limited in the treatment of PDPH, because
patients may choose to discontinue opioids altogether. Other
studied treatments that have proven to be of mixed success
include pregabalin, gabapentin, sumatriptan, and ACTH
(cosyntropin).11 Unfortunately, relying solely on these analgesic varieties oen does not reliably oer substantial relief
to ultimately improve patient mobility and function.
Caeine intake is another conservative treatment for
PDPH, because it acts as a potent cerebrovascular vasoconstrictor via its inhibition of adenosine receptors. Caeine
crosses the blood- brain barrier, and ultimately decreases
cerebral blood ow, counteracting the cerebral vasodilation
that has occurred due to CSF loss. Patients are encouraged
to consume beverages high in caeine (e.g., coee and soda)
in large quantities.1 Alternatively, providers may prescribe
intravenous (IV) caeine or oral formulations, which are
commonly combined in commercial preparations with barbiturates along with either acetaminophen or aspirin, such
as Fioricet and Fiorinal, respectively. ough sometimes
initially helpful, caeine’s ultimate benet is limited since
its eect is not sustained.
6
Rest is sometimes recommended to patients with
PDPH, though evidence supporting faster recovery or
prevention is limited.1 By remaining supine, or avoiding
postural changes in another reclined position, the HA can
be minimized as CSF pressure remains relatively uniform
throughout the cranium and spinal canal in the recumbent
position. e feasibility of this treatment, while acceptable
to some, is not realistic for parturients in the immediate
postpartum period due to the demands of caring for a newborn. Even with assistance, PDPH is oen too debilitating
for any meaningful participation at all. Additionally, connement to a bed in the supine position for extended periods of time increases the risk of DVT in patients already
hypercoagulable from pregnancy.
While conservative management may help temporize
symptoms of PDPH, they remain as advertised:conservative.
414 SECTION D.NEUROLOGICCRISES

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415
Some patients benet and the HA improves to a manageable level (especially those with smaller holes caused by spinal needles), but unfortunately they may end up discharged
with the ability to care for neither themselves nor their
newborn at home due to sustained CSF leakage. Usually
PDPH is a self- limiting process, with complete resolution
in 7– 10 days. Via broblastic proliferation from the surrounding tissue, and blood clot at the puncture site, 85%
of PDPH cases eventually resolve on their own within 6
weeks.6 However, this can be an unbearable amount of time
for a patient to cope with debilitating HA symptoms.
Some patients receiving an EBP do not present with IV
access, either due to proximity to discharge or because they
return as outpatients. It is important to follow institutional
policy for monitoring during the procedure, which usually
includes blood pressure and pulse oximetry (with heart
rate) monitoring. Even though medications are not being
administered via an epidural catheter during EBP, IV access
is essential, since the patient may still experience hemodynamic changes during the procedure (i.e., vagal responses),
requiring intervention with uids and vasopressors.
Informed consent is vital prior to EBP, since it carries the same risks as with any epidural placement, which
EPIDURAL BLOODPATCH
Since many PDPH do not rapidly improve with conservative measures, many patients elect for the more invasive,
“gold standard” treatment for PDPH: epidural blood
patch (EBP). e EBP is the denitive treatment for
PDPH, because it directly confronts the cause (CSF leakage from the intrathecal space). e treatment was originally devised from a casual observation that bloody “wet
taps” were associated with a reduction of PDPH, since
in these cases, autologous coagulation factors were introduced into the epidural space.6 e procedure requires
two providers, one to draw the patient’s blood (commonly
from the hand or arm), and the other to place a Tuohy
needle into the epidural space, both under sterile conditions. e patient may be placed in the sitting or lateral
position, but some providers prefer the lateral position,
because this oers the patient additional comfort by minimizing PDPH symptoms for extended periods of time
during the procedure.
If indicated, many clinicians wait at least 24 hours post
ADP to diagnose PDPH, and perform an EBP. However,
some clinicians advocate prophylactic EBP at just 5 hours
or more aer nal epidural anesthetic dosing. is is
accomplished via injection of autologous blood through
an in- dwelling epidural catheter before it is eventually
pulled. While the benet of this practice is controversial,
one recent study documented decreased PDPH rates using
this strategy, when compared with therapeutic EBP aer
24 hours.12 Others claim, however, that prophylactic EBP
does not lead to decreased incidence of PDPH. ey further purport that even in the presence of classic PDPH
symptoms early on, EBP are not as eective in completely
resolving PDPH, compared with therapeutic EBP aer 48
13,14
hours.
is may be partially due to misdiagnosis, or due
to sustained CSF pressure gradients across the dura shortly
aer ADP, that may either hinder clot formation, or promote clot dislodgement.
includes bleeding, infection, nerve injury, and of course
worsened PDPH due the possibility of a repeat ADP. is
risk is likely increased if an experienced provider deemed the
initial placement dicult. Patients should also be screened
for HA due to postpartum preeclampsia, and if blood pressure is signicantly elevated, the obstetric team should be
notied to evaluate the patient prior to EBP. Patients with
a history of thrombocytopenia or other hematologic disturbances should undergo laboratory analysis prior to proceeding with EBP.
Needle entry may occur at the same level as the original epidural placement or above or below this level. Since
it is oen impossible to determine whether an epidural was
truly “dicult” at that level, or whether the dural puncture
occurred due to inexperience, many providers advocate
performing EBP above or below the original site. Since
two- thirds of any epidural space injectate typically travels
cephalad, it may be benecial to perform the EBP below
the level of the puncture, in order to maximize blood and
clotting factor exposure at the dural puncture site. Loss of
resistance (LOR) to saline should be used, as LOR to air
increases the risk of pneumocephalus and its associated
HA, given the known dural puncture. When LOR is positive as the Tuohy needle enters the epidural space, the second provider should draw the patient’s blood separate from
the intravenous line under sterile conditions. e blood is
then slowly injected into the epidural space via the Tuohy
needle. Injection should immediately cease if the patient
experiences severe back pain (not simply pressure), or when
up to 20– 30 mL of blood has been administered, whichever comes rst.15 e Tuohy needle is then removed, and
the procedure is complete.
Oen, PDPH resolves completely within the rst
hour of the procedure. ere are two predominant theories that postulate how an EBP works. In the rst, the
volume introduced is that the volume introduced into
the epidural space increases pressure in that area, decreasing the pressure gradient across the dura, which in turn
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