FAQ/Help |
Calendar |
Search |
Today's Posts |
09-24-2008, 03:38 PM | #1 | ||
|
|||
New Member
|
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. |
||
Reply With Quote |
09-25-2008, 09:37 AM | #2 | |||
|
||||
Member
|
Quote:
kind regards vini
__________________
the light connects the many stars, and through the web they think as one, like god the universe we learn about our self's, the light and warmth connect us, the distance & darkness keep us apart . vini . |
|||
Reply With Quote |
09-25-2008, 10:41 AM | #3 | |||
|
||||
Member
|
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.
__________________
the light connects the many stars, and through the web they think as one, like god the universe we learn about our self's, the light and warmth connect us, the distance & darkness keep us apart . vini . |
|||
Reply With Quote |
"Thanks for this!" says: | Grannycile (03-26-2014) |
Reply |
|
|
Similar Threads | ||||
Thread | Forum | |||
CT Scans May Cause Medical Device Malfunction/pacemakers, defibrillators, neurostimul | Parkinson's Disease | |||
Hydrocephalus & epelipsy | New Member Introductions | |||
Hydrocephalus / pain while flying / no shunt | Hydrocephalus |