Chapter 40 Postmeningeal Puncture Headache and Spontaneous Intracranial Hypotension Flashcards Preview

Essentials of Pain Medicine > Chapter 40 Postmeningeal Puncture Headache and Spontaneous Intracranial Hypotension > Flashcards

Flashcards in Chapter 40 Postmeningeal Puncture Headache and Spontaneous Intracranial Hypotension Deck (55):
1

Postdural puncture headache (PDPH) caused by

the loss of cerebrospinal fluid (CSF) during the spinal anesthetic placement.

2

Postdural puncture headache (PDPH) symptoms

worse in the recumbent
position and improved when standing. The headache is
characteristically occipital and/or frontal and always bilateral. Symptoms associated with PDPH can include neck
stiffness, nausea, vomiting, photophobia, diplopia, scalp paresthesia, upper and lower limb pain, auditory changes including tinnitus, hypoacousia, and can include mental status
changes

3

Noninfectious arachnoiditis

with associated urinary and fecal incontinence, blindness,
subdural hematomas, intracerebral hemorrhage, and seizures. Headache commonly presents within the first 24 to
48 hr following a dural puncture; however, there have been many reports of headache presenting as much as 7 days later

4

Pathophysiology of the PDPH

an intact skull the sum of the volumes of brain, CSF, and intracranial blood are constant and, therefore, with CSF volume loss, compensatory vasodilatation and venous hypervolemia occur, which may contribute to the headache.

5

PDPHs are not commonly
associated with cervical punctures, why?

The higher the level of lumbar
puncture, the less the hydrostatic pressure at the dural puncture site

6

The uncompensated loss of CSF leads to

a subarachnoid deficit of CSF and often a reduction in the subarachnoid pressure

7

The normal CSF opening pressure in the horizontal position

70 to 180 mm H2O.

8

The direct traction hypothesis states that

the reduction in CSF total
volume, especially in the spinal region, allows the brain to
shift caudally placing traction on the pain-sensitive intracranial structures and causing cerebral vasodilatation that produces the classic headache symptoms

9

Pain-sensitive intracranial structures include

the dura, cranial nerves, and
bridging veins. The ophthalmic branch of the trigeminal
nerve, which refers pain to the frontal region, innervates
the bridging veins and the dura

10

In addition to causing pain,
traction on bridging veins can cause

a tear in the dura, thus
leading to a potential subdural hemorrhage

11

The posterior fossa structures are innervated by

the glossopharyngeal and vagus nerves that refer pain to the
occipital region.

12

Traction of the vagus nerve

stimulate the chemoreceptor regions of the medulla, causing
nausea and vomiting.

13

traction on the upper
three cervical nerves presents as

occipital, cervical, and
shoulder pain and stiffness.

14

traction, or pressure on
the abducens nerve (CN VI)

generate pain, intracranial hypotension can cause nerve palsy with paralysis of the lateral rectus muscle; this can manifest as diplopia.

15

oculomotor nerve (CN III) and
trochlear nerve (CN IV) palsies have been attributed to

intracranial hypotension due to brainstem compression and
ischemia

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diagnosis of a PDPH

based on the history of a dural puncture or possible dural puncture that worsens within 15 min after sitting or standing and improves within 15 min after lying down, with at least one symptom among neck stiffness, tinnitus, hypacusia, photophobia, and nausea.

17

critical signs and symptoms may indicate concomitant intracranial pathology

The most important of these signs is a changing pattern
of the headache. HA becomes constant or localized unilaterally, or there is new-onset nausea and vomiting. Another critical change is increasing neurologic alterations, which include
sedation, seizures, and new-onset motor and/or sensory
deficits.

18

the differential diagnosis
of PDPH with changing symptomatology should include

intracerebral hemorrhage, infection, eclampsia, and cerebral venous thrombosis.

19

most unintentional dural punctures during epidural anesthesia occur with a

17-gauge Tuohy needle, which is a cutting needle

20

The proposed mechanism behind difference between cutting and blunt tip needles causing PDPH

is that a blunt-tip needle
divides but does not disturb the continuity of the dural
fibers, versus a cutting tip needle, which cuts the dural
fibers.

21

The orientation of the bevel to the dura during dural
puncture has been proposed as a factor affecting the
amount of CSF leakage and the incidence of PDPH.

reduction in the leakage of CSF if the bevel was parallel to
the long axis of the spinal cord

22

Independent risk factors of PDPH

higher incidence
in women versus men, pregnancy, a higher incidence
in the age-group 20 to 50 years, and a higher incidence in patients with lower body mass index.There is also a higher incidence in patients with a headache prior to the dural puncture and a history of prior PDPH.

23

Prevention of PDPH

needle size, needle tip,
and bevel orientation during dural/arachnoid puncture. The smallest needle with a noncutting tip oriented parallel
to the long axis of the spinal cord will reduce the incidence
of PDPH.

24

Treatment options should be balanced with the understanding that

85% of PDPHs last less than 5 days, and, although rare, PDPHs can be associated with significant
morbidity

25

Conservative treatment for PDPH

usually pharmacologic and noninvasive. Recumbent
bed rest relieves the symptoms of PDPH but has no therapeutic benefit. Aggressive hydration is a common therapy

26

Medications reported beneficial in the treatment of PDPH include

methylxanthines, caffeine
and theophylline, sumatriptan, adrenocorticotropic hormone,
and corticosteroids

27

Caffeine

a potent central nervous system stimulant, causes cerebral vasoconstriction. Caffeine is administered as an oral dose of 300 mg or intravenously as 500 mg in 500 to 1000 ml normal saline over 2 hr; the intravenous dose can be repeated over the next 2 to 4 hr

28

Caffeine side effects

seizures, anxiety, and arrhythmias associated with its use

29

Caffeine is contraindicated in patients with a

history of seizure disorder and in patients with pregnancy induced hypertension

30

Epidural treatments for PDPH include

the administration of saline, colloids, fibrin glue, and blood. The gold-standard treatment for PDPH is an epidural blood patch (EBP).

31

contraindications to an EBP

first is patient refusal in general or for a specific reason. In the case of concerns of Jehovah’s
Witnesses about blood transfusions, there are reports of alternative patching materials. Second, the patient’s coagulation
status must be assessed and judged to be within
normal limits to reduce the risk of an epidural hematoma.
Finally, it is not recommended to place an EBP in a septic patient, or through a localized infection or febrile patient due to the obvious concern of introducing bacteria into the epidural space

32

mechanism of EBP

There is an initial early effect,
which occurs within minutes, secondary to compression of
the dura toward the cord and reduction in the intradural
volume. The EBP blood spreads both longitudinally and
circumferentially, thus enveloping the entire dural sac.
The reduction in the spinal intradural volume shifts the
CSF cephalad, thus resuspending the brain and reducing traction. this
intracranial shift in CSF also reduces the intracranial
blood volume and cerebral vasodilatation. A second, more lasting effect is due to
sealing of the dural/arachnoid tear with a gelatinous plug.
This sealing of the dural/arachnoid hole prevents further loss of CSF and allows for regeneration and restoration of the CSF volume. The plug acts as a bridge until permanent repair of the dural/arachnoid hole occurs

33

Risk factors for EBP failure include

placement sooner
than 24 hr after dural puncture, using inadequate volumes
of autologous blood, and performance of the procedure
with residual lidocaine in the epidural space.

34

How much blood to inject in EBP?

Selection of the level of placement should be guided by the observation that 15 ml of blood preferentially spreads cephalad six segments and caudad three segments, or one spinal segment per 1.6 ml of
blood. the ideal target volume
is 20 ml.

35

If the patient complains
of excessive back or leg pain or pressure during injection

less volume can be placed.

36

After the EBP, the patient should remain

supine with the legs slightly elevated

37

Alternative dural patching materials include

epidural fibrin glue and epidural Dextran-40. may be an alternative in patients who are Jehovah’s Witnesses. Alternatives to the epidural blood patch include epidural saline bolus and/or infusions, and surgical exposure and repair of the dural tear.

38

Surgical exposure and repair of a dural tear

a more invasive procedure generally reserved
for severe cases of PDPH that have not responded to
an EBP.

39

Complications after an EBP

The most common
complication is mild low back and radicular pain following
the procedure that resolves spontaneously in a few days and
can be treated with nonsteroidal anti-inflammatory drugs
(NSAIDs). Other possible complications include epidural
hematoma, infection, and arachnoiditis due to unintentional subdural/subarachnoid injection of the blood

40

Spontaneous intracranial hypotension (SIH)

a syndrome with symptoms similar to meningeal puncture headache but the patient has no previous history of meningeal puncture

41

Complications of Spontaneous intracranial hypotension (SIH)

Often self-limiting, it can also result in a life threatening condition such a subdural hematoma.

42

Risk Factors of Spontaneous intracranial hypotension (SIH)

This syndrome is usually suspected in a patient with
postural headache that occurs after a fall, trauma, whiplash,
exercise, or violent coughing

43

Symptoms of Spontaneous intracranial hypotension (SIH)

Symptoms include headache,
nausea and vomiting, blurred vision, tinnitus, vertigo, and photophobia.

44

suspect the presence of Spontaneous intracranial hypotension (SIH)

The triad of postural headache, low CSF pressure on diagnostic lumbar puncture, and meningeal enhancement on the MRI in a patient without any history of dural puncture

45

Etiology of Spontaneous intracranial hypotension (SIH)

leakage of the CSF through a weakness of the spinal meninges such as meningeal diverticulum, or small tears in the root sleeves or perineural cysts (Tarlov cysts).

46

Diagnosis of Spontaneous intracranial hypotension (SIH)

confirmed by low (CSF) pressure on diagnostic lumbar puncture and meningeal enhancement on the magnetic resonance imaging of the
cranium. Diagnostic lumbar puncture usually shows a low CSF pressure (below 60 cm H2O).

47

Characteristic of CSF in Spontaneous intracranial hypotension (SIH)

The CSF protein, and red cell and white cell counts are
usually increased.

48

The MRI of the cranium in SIH

shows meningeal
enhancement, subdural fluid collection, and caudal displacement of the cerebellar tonsils. Meningeal enhancement is usually thickest in patients with low intracranial
pressure and subdural fluid collections are only seen in
patients with meningeal enhancement. The spinal MRI of patients with SIH usually shows epidural or paraspinal
fluid collections and collapse of the dural sac.

49

standard confirmatory
test in the diagnosis of SIH

radionuclide cisternography (RC). The presence of SIH is indirectly proven by the lack of ascent of the injected dye, rapid disappearance of the radioisotope from the CSF (within 4 hr) and the early appearance of the radioisotope in the urinary bladder.

50

What accounts for the appearance of the radioisotope in the urinary bladder in radionuclide cisternography?

The radioisotope is presumed to leak through a meningeal
rent into the epidural space, subsequently taken up by the
epidural vessels and carried into the systemic circulation
and excreted by the kidneys.

51

Disadvantages of Radionuclide Cisternography

inability of RC in demonstrating the site of leak, poor spatial resolution, its invasiveness, and possible radioisotope extravasation through the needle tract, resulting in inaccuracy in its interpretation

52

Radionuclide cisternography ability to demonstrate the site of
leak

A Valsalva maneuver
may improve RC’s ability to demonstrate the site of
leak by increasing the subarachnoid pressure and improving
the chance of the CSF to actively leak and shown on
the RC.

53

Techniques to demonstrate the site of leak.

CT myelography,
magnetic resonance myelography, and radioisotope myelocisternography

54

treatment of choice for SIH

Epidural blood patch (EBP). If one or two EBPs are not effective, then a CT myelography should preferably
be performed before another EBP is performed to delineate
the vertebral level and the side of the CSF leak and
note the presence of multiple leaks. Surgical intervention is warranted if multiple EBPs
are ineffective and the patient’s condition deteriorates

55

Why is EBP is less effective in SIH than in postdural puncture headache?

The lower success rate may be related to the injection of the blood away from the site of the CSF leak, the presence of multiple CSF leaks, and the rare occurrence of CSF leak at the anterior aspect of the dura or the nerve root sleeve. the site of leak can occur anywhere in the spine.

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