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Old 09-24-2008, 03:38 PM #1
robert_uk robert_uk is offline
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Book shunt malfunction, hydrocephalus, what next ?

Hello & I hope people on the forum here can explain or give any advice on the following situation as it is effecting my partner.
He has had Cancer and while that was under chemo developed severe bacterial meningitis. The meningitis totally incapacitated him, he had had 18 lumber punches in 18 days and by then morphine and no effect on the pain. They said they could not do any more LP’s, so 4 weeks ago they put a shunt in. Immediately he felt better and after 3 days was able to eat ( after not eating for 2 weeks previous) and his headaches had gone. They discharged him. 1 week later he felt dizzy and a lump the size of a egg appeared at the base of his spine, where the lumber punches had been, also a lump appeared under the stitches in his stomach. His headaches returned and he started vomiting when ever any food or pill entered his stomach, he suffered severe nausea and lost all balance. He was admitted to hospital where they put a “pressure “ patch on the lump at the base of the spine. After 2 days of agonising pain, he told the Dr’s it was not working, they said give it time. He spent the next 7 days in hospital, in pain, vomiting and did not .could not eat anything or drink. His medication was just thrown up 5 minutes after taking it. They discharged him from hospital after 8 days lying there with just a pressure patch on, and NO food, still nauseous and in tremendous head pain. I took him home, over the next 3 days he got wore & worse, I then took him to the hospital again. It was last Thursday. They said he needed surgery urgently to unblock or fix the shunt as it was not working (this had been obvious 10 days ago when he was in hospital). Last Saturday they replaced the Shunt with a “larger one” . On the Sunday they discharged him, less than 24 hrs after the operation his 2nd in 3 weeks. He was very week going into this 2nd Shunt operation due to the lack of food and medicine over the previous 8 days. I brought him home on the Sunday, he was vomiting within 45 minutes of leaving the hospital. His headaches had ceased at this stage. This Monday morning he woke with such severe head pain , not like the previous head pain, a very different ( to the bacterial meningitis ; hydrocephalus high pressure headaches) but debilitating to the point that the slightest head movement would cause him to scream out in pain. I had to call an ambulance and he was taken back to hospital. He remains there at present, unable to eat and getting weaker, and still with this terrible pain, again the morphine (the little they give) does not relieve the pain.

The Dr this evening mentioned that it may be due to “over drainage” & that they may have to replace the shunt.

Has anyone had or know of similar experiences , to me it seems that there has been mistakes & wasted time in fixing these mistakes which has and is making the situation worse.

He is wasting away and getting physically weaker by the hour, racked by pain and I believe he is mentally “giving up” he said to me this afternoon, “he just wish it would end”.

What should the Dr’s be doing ? How many Shunt operations can they do to fix the problem ? How dangerous is “over drainage” ?

I apologise for the length of the post but am very grateful for help in the above.
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Old 09-25-2008, 09:37 AM #2
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Default csf leak

Quote:
Originally Posted by robert_uk View Post
Hello & I hope people on the forum here can explain or give any advice on the following situation as it is effecting my partner.
He has had Cancer and while that was under chemo developed severe bacterial meningitis. The meningitis totally incapacitated him, he had had 18 lumber punches in 18 days and by then morphine and no effect on the pain. They said they could not do any more LP’s, so 4 weeks ago they put a shunt in. Immediately he felt better and after 3 days was able to eat ( after not eating for 2 weeks previous) and his headaches had gone. They discharged him. 1 week later he felt dizzy and a lump the size of a egg appeared at the base of his spine, where the lumber punches had been, also a lump appeared under the stitches in his stomach. His headaches returned and he started vomiting when ever any food or pill entered his stomach, he suffered severe nausea and lost all balance. He was admitted to hospital where they put a “pressure “ patch on the lump at the base of the spine. After 2 days of agonising pain, he told the Dr’s it was not working, they said give it time. He spent the next 7 days in hospital, in pain, vomiting and did not .could not eat anything or drink. His medication was just thrown up 5 minutes after taking it. They discharged him from hospital after 8 days lying there with just a pressure patch on, and NO food, still nauseous and in tremendous head pain. I took him home, over the next 3 days he got wore & worse, I then took him to the hospital again. It was last Thursday. They said he needed surgery urgently to unblock or fix the shunt as it was not working (this had been obvious 10 days ago when he was in hospital). Last Saturday they replaced the Shunt with a “larger one” . On the Sunday they discharged him, less than 24 hrs after the operation his 2nd in 3 weeks. He was very week going into this 2nd Shunt operation due to the lack of food and medicine over the previous 8 days. I brought him home on the Sunday, he was vomiting within 45 minutes of leaving the hospital. His headaches had ceased at this stage. This Monday morning he woke with such severe head pain , not like the previous head pain, a very different ( to the bacterial meningitis ; hydrocephalus high pressure headaches) but debilitating to the point that the slightest head movement would cause him to scream out in pain. I had to call an ambulance and he was taken back to hospital. He remains there at present, unable to eat and getting weaker, and still with this terrible pain, again the morphine (the little they give) does not relieve the pain.

The Dr this evening mentioned that it may be due to “over drainage” & that they may have to replace the shunt.

Has anyone had or know of similar experiences , to me it seems that there has been mistakes & wasted time in fixing these mistakes which has and is making the situation worse.

He is wasting away and getting physically weaker by the hour, racked by pain and I believe he is mentally “giving up” he said to me this afternoon, “he just wish it would end”.

What should the Dr’s be doing ? How many Shunt operations can they do to fix the problem ? How dangerous is “over drainage” ?

I apologise for the length of the post but am very grateful for help in the above.
sorry you and your partner are going through this ,it seems your partner may have a csf leak he may need what is called a blood patch I will pm you with a really good site please visit it asap ,I to live in the uk not much info on this

kind regards vini
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Old 09-25-2008, 10:41 AM #3
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Default hope this helps

hope this helps a lot to go through, but this mentions some docs in the uk don.t try to take it all in, but if you hubby is leaking eg low pressure head ache the treatment is fix the leak and lay flat



Page 1
32 I
ACNR • VOLUME 6 NUMBER 1 • MARCH/APRIL 2006
Spontaneous Intracranial Hypotension –
Diagnosis and Management
Introduction
Spontaneous intracranial hypotension (SIH) produces a
headache similar to a post lumbar puncture headache.
Although the terms ‘hypotension’, ‘low CSF pressure’ and
‘low CSF volume’ are often used interchangeably, the syn-
drome can occur in the setting of ‘normal’ CSF pressures.
Loss of CSF volume rather than pressure better explains
the clinical features and imaging abnormalities.
1
Classification of low volume headaches
The international classification of headache disorders
recognises three subsets of low CSF volume headache.
2
These are post-dural (post-lumbar) puncture headache,
CSF fistula headache and headache attributed to sponta-
neous low CSF volume/spontaneous intracranial
hypotension. Criteria needed for these diagnoses are sum-
marised in Table 1. The cardinal feature indicating low
CSF volume headache is aggravation of symptoms within
15 minutes of sitting or standing. In post-dural puncture
headache symptoms should improve within 15 minutes of
lying down.
Aetiology and risk factors
SIH has been associated with abnormalities of the cervical
spine and chiropractic manoeuvres. Although there may
be a clear trigger such as a Valsalva manoeuvre or trauma,
SIH may occur without a clear precipitant. The cause is
thought to relate to a breach of dural diverticulae, or tear-
ing of nerve root sheaths. Connective tissue disorders
have been suggested as possible predisposing factors, as
SIH has been reported in patients with Marfan’s and
Ehlers-Danlos syndromes.
Not all patients with spontaneous intracranial hypoten-
sion have low CSF pressures when measured at lumbar
puncture. This implies that there may be significant indi-
vidual variation in CSF pressures, and also that that the
rate of CSF loss may be more important in producing the
syndrome than the residual CSF pressure or volume. CSF
leaks are not identified in every case of apparent SIH. In
part this may relate to the limitation of investigations.
However patients with a typical history, without clear evi-
dence of a leak, and who have failed ‘blind’ blood patches,
often prove very difficult to treat. It is possible in such
cases that a CSF leak may have occurred, with a residual
effect on CSF dynamics (eg lowered pressure setting in the
choroid plexus, and sensitisation of meningeal afferents).
Based on similarities between post lumbar puncture
headache (PLPH) and SIH, a number of inferences can be
made. PLPH is less common at the extremes of age and
this has been attributed to reduced epidural distensibility
in the very old and very young.
3
A higher risk has been
reported in young females with a low body mass index.
4
Patients with dementia appear to have a very low risk of
PLPH
5
and this has been attributed to low pain sensitivity,
rigid dural fibres, arteriosclerotic vessels, and large CSF
spaces due to cerebral atrophy. PLPH occurs less fre-
quently in those with higher CSF opening pressures.
6
These factors may also be of relevance in SIH.
Pathophysiology
Two main theories have been proposed to explain the
cause of headache in patients with low CSF volume
headache. They have been outlined in greater detail by
Paldino et al.
7
1) Traction on pain sensitive structures
Under normal conditions, CSF supports the brain reduc-
ing its weight from 1500g to only 48g within the cranium.
This remaining weight is supported by suspension from
several pain-sensitive structures. These include the
meninges, cerebral and cerebellar veins (tributaries of the
sagittal and transverse sinuses, respectively) as well as the
fifth, ninth, and tenth cranial nerves and the superior three
cervical nerves. Descent of the brain and traction on these
structures, explains the orthostatic nature of the headache.
However tonsillar descent is not found in all patients
with SIH. This may be because displacement of the brain
is underestimated (because the patient lies supine during
brain imaging). It may also be because there are addition-
al pathophysiological mechanisms.
2) Dilation of pain sensitive intracranial vascular structures
The mean recumbent CSF pressure is approximately 150mm
of water at all levels. In the erect posture, a pressure gradient
occurs; highest in the lumbar sac, about 0 at the level of the
cisterna magna, and around -85mm H
2
O in the ventricles.
Venous engorgement in both brain and spine occurs in SIH.
According to the Monro–Kellie doctrine,the upright posture
should be associated with further dilation of pain-sensitive
intracranial venous structures. In support of this theory is
the finding that coughing or Valsalva manoeuvres (that
decrease the venous return to the heart and therefore
increase intracranial venous volume) can reproduce
headache in a patient with SIH even when supine.
Clinical Features
The onset of headache following SIH may be gradual or
subacute but a thunderclap form is also well recognised in
about 14% of cases.
8
Associated clinical features are neck
stiffness, tinnitus, hyperacusis, photophobia, nausea,
interscapular and radicular upper limb pain, vertigo, visu-
al field defects, and cranial nerve palsies.
As SIH becomes chronic, the postural aspect of the
headache may become much less apparent, and an index
event may not be recalled. SIH should therefore be con-
sidered in the differential diagnosis of new onset persis-
tent daily headache.
9
Rare presentations of SIH include sudden deafness,
orthostatic tinnitus, rapid onset encephalopathy and
coma (attributed to diencephalic compression resulting
from brain descent), Parkinsonism, and chronic behav-
ioural features suggestive of frontotemporal dementia.
10-12
Radiculopathy due to cervical epidural venous engorge-
ment has also been associated with SIH.
13
It is also important to note that orthostatic headaches
have been described without CSF leakage as the major
clinical manifestation of postural tachycardia syndrome
(a disorder characterised by chronic orthostatic symp-
toms and a dramatic increase in heart rate on standing,
but that does not involve orthostatic hypotension).
14
Investigations
Investigation of patients with suspected SIH may help
corroborate the diagnosis and identify the site of CSF
leakage.
Magnetic Resonance Imaging (MRI)
MRI brain with contrast is the initial investigation of
choice in suspected SIH. Meningeal enhancement is the
earliest and most frequent feature, occurring in more than
80% of subjects; tonsillar descent is seen in more than
Management Topic
Stuart Weatherby is a Consultant
Neurologist at Derriford Hospital,
Plymouth, and Torbay Hospital.
He trained in General Neurology
in the West Midlands, including the
University Hospital of North
Staffordshire and University Hos-
pital Birmingham. He has an MD
in genetic and pychophysical fac-
tors influencing multiple sclerosis.
His further training in headache
disorders was carried out at the
National Hospital for Neurology
and Neurosurgery, London and at
hospitals in Madrid.
Ibrahim Imam is a Specialist
Registrar in Neurology
at
Derriford Hospital, Plymouth. He
has completed his fellowship pro-
gramme in Internal Medicine and
Neurology in Nigeria. He did the
Diploma in Neurology at the
Institute of Neurology in Queen’s
Square before joining the Neur-
ology training programme in the
South Western deanery.
Correspondence to:
Stuart Weatherby,
Consultant Neurologist,
Department of Neurology, and
Peninsula Headache Network,
Derriford Hospital,
Plymouth PL6 8DH.
Tel. 01752 777111,
Email. Stuart.Weatherby
@phnt.swest.nhs.uk
Page 2
ACNR • VOLUME 6 NUMBER 1 • MARCH/APRIL 2006
I 33
40% and subdural hygromas/haematomas in about 17%.
15
The subdural
effusions result from transudation from engorged venous plexuses. Such
changes range from very striking to quite subtle. Engorgement of venous
sinuses may also cause enlargement of the pituitary gland.
16
It is important to note that a normal MRI brain is compatible with the
diagnosis of SIH,
17
and also that pachymeningeal enhancement can occur
in the setting of significant and proven CSF leaks in patients who are
headache free.
18
A normal initial brain MRI in symptomatic patients how-
ever is predictive of poor outcome.
19
Cervical MRI scans may show meningeal enhancement and a dilated
internal vertebral venous plexus in 85% and spinal hygromas in up to
70% of cases.
20
The utility of spinal MRI for detecting the site of CSF leak-
age relative to other modalities (see below) is not clear.
Doppler Flow Imaging
This is predicated on the basis that the superior ophthalmic vein is a trib-
utary of the cavernous sinus and it might therefore reflect the engorge-
ment of the intracranial venous sinuses that occurs in this condition.
Increased diameter and maximum flow velocity of the superior oph-
thalmic veins has been demonstrated in patients with SIH using transor-
bital colourflow Doppler imaging. One study suggests this technique has
very high specificity and sensitivity, though clearly does not assist in iden-
tifying the site of leakage.
21
Radionucleotide Cisternography
Radionucleotide cisternography frequently demonstrates ‘surrogate’
markers’ of a low volume CSF state. These include limited ascent of the
tracer to the cerebral convexity in 91% of cases, early appearance of the
radioisotope in the bladder in 65%, and early soft tissue uptake of
radioisotope in 43%.
22
Actual leakage of CSF has been identified in 52%
of cases,
22
most commonly at the cervico-thoracic junction or in the tho-
racic spine. Intermittent leaks may go undetected and the technique may
be insufficiently sensitive to identify small leaks.
CT Myelography
CT myelography has been found to demonstrate the level of a CSF leak in
67% of patients overall, compared with only 50 and 55% for spinal MR
imaging and radionucleotide cisternography.
23
In no case did radionu-
cleotide cisternography reveal the leak when CT myelography did not.
Unfortunately CT myelography can be very time consuming, as it
requires CT slices be obtained through the skull base and the entire spinal
axis. Spinal imaging and radionucleotide cisternography may perhaps be
helpful as guides for focusing on particular areas with CT myelography.
Lumbar Puncture
Lumbar puncture should be considered only if the features are equivocal
and should be avoided before MRI with contrast as this can interfere with
interpretation of the results. CSF opening pressure is typically low (usu-
ally 0–5cm CSF).
5
It may however be normal in up to 17% of cases.
24
CSF
constituents are usually normal although high protein concentration and
lymphocytic pleocytosis may be seen.
25
Treatment
Medical
Conservative measures like bed rest are the first line treatment for low
intracranial pressure headache. If not effective, intravenous caffeine at a
dose of 500mg in 500ml saline over two hours (repeated once or twice) is
often used although the evidence base is limited.
9
Cardiac monitoring is
necessary as caffeine can induce arrthymias. There is also some evidence
to suggest that theophyllines may be efficacious. It has been proposed that
methylxanthines produce arterial constriction through the blockade of
adenosine receptors.
26
Consequently, intracranial blood flow and, pre-
sumably, venous engorgement are decreased. Abdominal binding with a
surgical corset may help, while glucocorticoids or mineralocorticoids
have been used in some studies but are of questionable effect.
Interventional
i) Autologous epidural blood patch
The technique was initially based on the observation that PLPH was less
severe after a ‘bloody tap’ compared with a ‘clear tap’. The mode of action
is not clear but may be due to a tamponade effect. It is performed by slow-
ly injecting autologous blood into the same interspace or the interspace
below the site of leak.
In contrast to PLPH the site of CSF leakage may not be certain in SIH.
It may not be critical to identify the site of leakage. There is some evidence
that lumbar epidural blood patching may be effective over nine spinal
segments when the patient’s head is lowered to 30°. A recent report sug-
gests that early ‘blind’ epidural blood patching within one week of onset
is effective; demonstrating complete cure in 77% of 30 patients (with or
without typical MRI changes) after one (57%) or two (20%) blood patch-
es. These patients did not have lumbar punctures, nor was the site of CSF
leakage identified.
27
ii) Other treatment modalities
Epidural saline injection has been reported to give immediate relief for
headache. This is thought to be by reduction in the distensibility of the
epidural space. This manoeuvre could also be life saving in obtunded
patients with SIH.
28
A small group of patients with a typical history but no clear evidence
of a leak, may fail ‘blind’ blood patches. These patients often prove very
difficult to treat. It is possible in such cases that a CSF leak may have
occurred, with a residual effect on CSF dynamics (eg lowered pressure
setting in the choroid plexus, and sensitisation of meningeal afferents).
Conclusion
Loss of CSF volume best explains the syndrome often designated ‘low-
pressure headache’. CSF pressures may not always be low.
Patients with chronic symptoms of SIH may not volunteer or recall a
Management Topic
Post-dural (post-lumbar) puncture headache
Headache that worsens within 15 minutes after sitting or standing and improves
within 15 minutes after lying
One of neck stiffness, tinnitus, hyperacusis, photophobia or nausea
Dural puncture has been performed
Headache develops within 5 days after dural puncture
Headache resolves spontaneously within 1 week or within 48 hours after effective
treatment
CSF fistula headache
Headache that worsens within 15 minutes after sitting or standing and improves
within 15 minutes after lying
One of neck stiffness, tinnitus, hyperacusis, photophobia, nausea
A known procedure or trauma has caused persistent CSF leakage with at least
one of the following:low CSF pressure evidence on MRI, evidence of CSF leakage
on conventional myelography, CT myelography or cisternography and CSF open-
ing pressure <60 mm H2O in sitting position
Headache develops in close temporal relation to CSF leakage
Headache resolves within 7 days of sealing the CSF leak
Headache attributed to spontaneous (or idiopathic) low CSF pressure
Diffuse and/or dull headache that worsens within 15 minutes after sitting or
standing, with at least one of the following
One of neck stiffness, tinnitus, hyperacusis, photophobia or nausea
A known procedure or trauma has caused persistent CSF leakage with at least
one of the following: low CSF pressure evidence on MRI, evidence of CSF leak-
age on conventional myelography, CT myelography or cisternography and CSF
opening pressure <60 mm H2O in sitting position
Headache develops in close temporal relation to CSF leakage
Headache resolves within 7 days of sealing the CSF leak
Table 1: Diagnostic criteria for headaches attributed to low
cerebrospinal fluid volume (from the International Classification of
Headache Disorders
2
)
Page 3
34 I
ACNR • VOLUME 6 NUMBER 1 • MARCH/APRIL 2006
definite ictus and over time the postural aspect of the headache may
become less clear. SIH may thus present as new onset persistent daily
headache rather than as an orthostatic headache. MRI brain with contrast
is the first line investigation of SIH. Patients with a normal contrast
enhanced MRI brain appear to have a worse prognosis. Radionucleotide
cisternography generally shows abnormalities in SIH although it is rela-
tively poor at locating the site of a CSF leak. CT myelography of the spine
is arguably the most sensitive test to identify the site of a leak. However it
is time consuming if there are no clues as to where to focus the study.
It is usual practice to try and focus a blood patch on the site of the CSF
leak (the most common site is cervico-thoracic). However this may incur a
delay to treatment while imaging investigations are arranged. Recent stud-
ies suggest that ‘blind’blood patching at an early stage may be very effective.
__________________
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.
vini
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