|
Ventriculo
atrial shunt migrated into the right atrium and pulmonary artery:
endovascular retrieval (published by Pan Arab
J Neurosurg 1999, 3(2): 47-49
|
Sir,
I read with great interest the review article by Gazzaz, et al: Ventriculo
atrial shunt migrated into the right atrium and pulmonary artery: endovascular
retrieval.
It is stated in this paper that only 6 cases have been published using
this technique to remove shunt material from the heart. For completion
of the references, we performed an endovascular retrieval of such a
type in the year 1973, Haase J, Kemp A: Removal of
shunt from the heart by femoral vein catherisation. J Neurosurg 1974,
40: 787).
We completely agree with the authors conclusion.
|
Jens
Haase
Department of Neurosurgery Aalborg Hospital Denmark |
 |
|
CT scan predictors for bad
outcome of traumatic brain lesions
(published by Pan Arab J Neurosurg 1999, 3(1): 30-34 |
Sir,
I read with interest the paper by Mohamed Al Haj Ali and his colleagues.(1)
This is an important subject and the authors are to be congratulated
for bringing up such an issue. They concluded that their CT scan scoring
can determine the final outcome in patients with isolated, closed and
severe brain injury.
I would, however, like to make the following comments to clarify the
misconceptions that exist. Firstly, the Glasgow coma scale (GCS) score
is a measure of brain function at the time the test is performed. It
is graded as severe with a GCS score of 8 or less with no eye opening
even to painful stimuli, moderate between scores of 9 and 12, including
those with scores of 7 or 8 but opening of eyes to pain, and mild between
scores of 13 and 15.4 Recording the trend is important and is used to
assess the improvement or deterioration of the patient.
Accordingly, it is common to see some patients who are initially categorised
as having severe head injury increase their GCS score and become moderate
or even mild head injuries. Such an occurrence may follow appropriate
and adequate early resuscitation, which is mentioned later in this letter.
Conversely, patients with mild or moderate head injuries, especially
those with cerebral contusions with or without traumatic subarachnoid
haemorrhage and those with intracranial haematomas may reduce their
GCS score and become severe head injuries. Hence, the importance of
the system in guiding the appropriate line of treatment in these patients
is shown.
Using this system, the authors categorised their 156 severe head injured
patients with bad outcome. They tabulated 6 of them with a score between
8 and 13. Amongst these, those with scores of 9 to 13 are moderate or
mild head injuries. Those with a score of 8 could either be moderate
or severe head injuries, depending upon the presence or absence of eye
opening to pain respectively.
It is, therefore, inappropriate to lump together patients with scores
of 8 with those of 9 to 13, without clearly stating whether the patients
had eye opening response to pain.
Secondly, the authors devised a CT score system. There is no indication
as to the thickness of the CT cuts ie. 2.5 or 10 mm. Obviously, the
thinner the cuts the more the score number will be. Moreover, labelling
"Medial Area", which has both medial and lateral areas in the figure
is inappropriate. It would be appropriate to designate this as "Middle
Area". CT images do show intracranial abnormalities. Midline shift of
greater than 10 mm and dilatation of the contralateral ventricle, or
a loss of image of the third ventricle and basal cisterns indicate the
presence or likelihood of developing raised intracranial pressure (ICP).
Absence of these features, however, is no guarantee of normal ICP.(3)
CT images are therefore, not a good predictor in determining the outcome.
Thirdly, primary traumatic brain injuries (TBI) are considered to be
more or less complete at the time of impact and to be irreversible and
treatment plays little or no significant part in the outcome. Secondary
brain injuries are common in these patients and may occur as a result
of hypoxia from airway compromise and hypercapnia from hypoventilation.
This may lead to ischaemic changes in the brain. The goal of treatment
of these patients is therefore to prevent wherever possible the occurrence
of secondary brain injury. Where this is not possible, such brain injury
should be detected as early as possible to reverse them. Total prevention
of secondary brain injury is impossible but can be minimised considerably
using early treatment during the "Golden Hour". This is the time from
the moment of injury to that of starting definitive treatment in the
hospital. It includes arrival of the emergency staff at the scene of
the accident to treat the patient using the A, B, C approach of trauma
care ie. to maintain the airway with control of the cervical spine;
to maintain breathing with supply of oxygen and to maintain circulation
with control of external haemorrhage, if any, transport of the patient
to the hospital, resuscitation on arrival to hospital emergency room,
investigation and then start of definitive treatment. Reversal of secondary
brain injury is possible only with active and aggressive treatment.
These patients should be kept normo-volaemic and at times hypervolaemic
with induced systemic hypertension in order to maintain a minimal cerebral
perfusion pressure (CPP) of 70 mmHg and frequently higher, determined
by individual circumstances.(8) This may also require the use of supplemental
vasopressors in order to maintain cerebral blood flow to minimise or
prevent ischaemic changes in the brain. Mannitol is used as a systemic
volume expander for haemodynamic and for its rheological effects rather
than it affecting cerebral dehydration.(2,6,7) These patients should
have artificial ventilation. Their PaCO2 should be kept between 4.2
and 4.6 KPa (normal range 4.2-6.1 KPa) and arterial oxygen saturation
(SaO2) between 95 and 100%, using where necessary an increase in inspired
oxygen concentration (FiO2) and positive end expiratory pressure (PEEP).
Cerebral ischaemia dominates TBI and is the single most important factor
in determining its outcome. CPP maintenance is vital in the preservation
of cerebral blood flow (CBF). This is the primary goal in the treatment
of TBI with improvement in bad outcome ie. mortality and morbidity.
The view that induced hypertension potentiates cerebral oedema and dysautoregulation
is a misconception. CPP is a physiological parameter and is intimately
linked with ICP and systemic arterial blood pressure (SABP). Of the
three, it is the greatest determinant of cerebral haemodynamic responses
and effects including the outcome from severe TBI.(8)
Fourthly, surgery plays an important but only a small part in the management
of those patients with severe head injuries not associated with intracranial
haematomas and depressed skull fractures. It is used as follows: a)
ICP monitoring - this is indicated in all and is done electronically
by placing a catheter with a microsensor at its tip intraparenchymally.
ICP is crucial in determining the level of CPP, which is important in
the maintenance of CBF and perfusion. b) External ventricular drainage
- this is indicated in all but may not be possible to be done in some
patients due to small size of the ventricles. It is done by placing
a catheter into a lateral ventricle. CSF is drained continuously against
a positive back-pressure of 15 mmHg (with zero references to the external
auditory meatus) to avoid ventricular collapse and loss of CSF drainage.
This again maintains CPP by lowering ICP. c) Excision of severely contused
or lacerated brain - this is indicated whenever there is a localised
injury eg. burst temporal pole or polar injury of the frontal lobe.
These lesions act as a space-taking process. Their excision results
in lowering of ICP with consequent improvement in CPP. d) Decompressive
bifrontal craniotomy - this is indicated in young patients with intractible
high ICP, without evidence of diffuse axonal injury (high GCS score
on admission), with CT evidence of diffuse brain swelling and EEG evidence
of neural activity. A free bifrontal bone flap is raised. The duramater
is opened anteriorly. Thereafter, the dura is opened radially towards
the vertex in several areas, in order to release pressure and improve
CPP. Scalp is closed in two layers. Bone flap is replaced at a later
date.
Finally, experience is the key to proper management. It is futile to
use any therapeutic measure without achieving and maintaining an adequate
cerebral perfusion and oxygenation.
Hyperventilation and dehydration are harmful in the treatment of these
patients. These may aggravate cerebral ischaemia by reducing SABP and
CPP resulting in tertiary brain injury and its bad outcome.(5)
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A
Rashid Choudhury
58 A Burton Road Repton Derby DE65 6FN United Kingdom |
|||||||||||||||||
|
Reply from Author
Sir,
Thank you for your interest in our subject.
We fully agree with your statement that “experience is the key to proper management” and we would like to add that experience is also the key for the proper prognosis.
We now know that routine hyperventilation and dehydration are harmful in the treatment of the patient with severe traumatic brain injury. Only in the last 3 years has the routine use of hyperventilation and dehydration ceased. Unfortunately, prior to this date when the study of Haj Computed Scan Scoring System was developed they were still in use in Rashid Hospital (1992-1997). Intracranial pressure monitoring is still, to date, not in use in many neurosurgical departments in our region and even world wide due to many reasons ie. 1) the part is not available everywhere, 2) cost, 3) experience of neurosurgeons, 4) some neurosurgeons simply do not like it and prefer to continue to use corticosterioids, mannitol and 1-3 days hyperventilation routinely.
However, in our paper we did not discuss the rational treatment of severely brain-injured patients but only their prognosis in existing circumstances. We know that the CT features of raised ICP are not an absolute but also if there is no ICP monitoring we believe that they are a truthful indication of it.
Concerning Dr. A Rashid Choudhury’s enquiry regarding 6 patients with an admission GCS between 9-13. This group of patients who deteriorated in the hospital in the medical literature they called (talked and died). This group of patients need a separate study.
Finally, we found that the traumatic abnormalities in the subcortical area are different from those in the medial basal ganglion area. The prognosis is worse in the latter so on this point we cannot agree with Dr. Choudhury’s suggestion to treat both areas as one.
All comments are highly appreciated and accepted with many thanks.
|
Dr.
M Haj Ali
Department of Neurosurgery Daraa National Hospital Syria Fax: (963) 15 230 130 |
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|
|
Co-existing primary empty sella and craniopharyngioma
with spontaneous cerebrospinal fluid rhinorrhoea through lamina
cribrosa - case report
(published by Pan Arab J Neurosurg 2000, 4(1): 45-51 |
I read with interest the case report by Basit Ali Syed.(4) The author is to be congratulated for reporting this interesting patient with a rare combination of primary empty sella (PES), craniopharyngioma and spontaneous cerebrospinal fluid (CSF) fistula through the lamina cribrosa and also for his detailed review of the empty sella. I would, however, like to make the following comments in respect of the case evaluation, management and genesis of CSF fistula.
Case Evaluation: The patient was noted to be moderately obese but there is no mention about her body mass index (BMI; weight in kilograms divided by the square of height in metres: according to WHO classification - people with a BMI of 25-29.9 kg/m2 are overweight, those with a BMI of 30-39.9 kg/m2 or over are severely obese). She became amenorrhoeic at the age of 40, after having irregular menstration for five years. Three years later at the age of 43, the patient was seen by the author. Investigations revealed normal hormonal levels. Pituitary hypogonadism was suggestive in this patient because of the presence of an intrasellar mass lesion and normoprolactinaemia. Sellar tumour may destroy the normal pituitary tissue by direct pressure and in this case might have selectively destroyed the gonadotrophs in which case the serum FSH and LH would have been low. Early menopause was a possibility in which case the serum FSH would have been high. It is remarkable to note that the values of FSH and LH were within normal limits even during her second admission. Serum oestradiol level was not estimated.
She complained of generalised weakness and body ache, along with other features during her presentation in 1993. There was no mention about serum electrolytes estimation. Serum sodium may be low in this type of patient. Hormonal analysis showed a cortisol level of 3 ug/dl. This is definitely low according to the author's laboratory where the normal range is 8-28 ug/dl. Despite this low level of cortisol, test for ACTH reserve was not carried out.
Prolactin was 37.4 ng/ml during the second admission. This is slightly elevated as the author's laboratory normal range is 1.8-20.8 ng/ml. This indicates compression of the pituitary stalk and obstruction of portal circulation, causing disruption of the prolactin inhibiting factor (PIF) to pituitary lactotrophs. Stalk compression may also be the cause of hypoadrenalism due to denial of the anterior pituitary gland of its normal hypothalamic control over ACTH secretion.(1)
Management: Symptoms of secondary adrenal insufficiency may be vague. Patients may present with weakness or asthenia. Low serum sodium may indicate secondary adrenal insufficiency. Hypoadrenalism is a life-threatening condition. Hence, pituitary-adrenal axis status should be evaluated in all patients with lesions in the sellar or perisellar region and these patients should have glucocorticosteroid cover peri-operatively, starting on the day before the operation. The clinical situation should then dictate the need for glucocorticosteroid replacement. It is distressing to see omission of glucocorticosteroid during pre- and per-operative period by the author in this patient inspite of the low serum cortisol level.
Genesis of lamina cribrosa CSF fistula: The walls of the pituitary fossa are relatively rigid and under normal circumstances this may serve to protect the pituitary gland from surrounding pressure fluctuations. The growth of a tumour within such an enclosed and inelastic space is likely to cause an increase in intrasellar pressure. This can result in obstruction of the long portal vessels and deny the anterior pituitary gland its normal hyothalamic control. This may cause hypopituitarism and hyperprolactinaemia. This is attested by the fact that post-operatively reversion of hypopituitarism occurs due to releasing of obstruction of portal vessels and return of prolactin to its normal level due to the stalk regaining its capacity to deliver PIF.(3)
CSF fistula occurs locally through the floor of the pituitary fossa in these patients due to thinning and giving way of the sellar floor from high intrasellar pressure. At the time of the presentation of this patient with CSF rhinorrhoea, the tumour was intrasellar and it was unlikely to have caused high intracranial pressure (ICP). Moreover, the brain was atrophic as shown clearly in the CT and MR images. Thus, high ICP was most probably not the factor in the genesis of CSF fistula through the lamina cribrosa. Association of empty sella in this patient is simply incidental and is due to the congenital deficiency of the sellar diaphragm and arachnoidal herniation. Thinning and expansion of the sellar floor is the result of CSF pulsation and the presence of the tumour. Genesis of lamina cribrosa CSF fistula in this patient was most likely from an unrecognised primary intranasal encephalocele.(2) This is a congenital lesion occurring early in the embryonic development due to the failure of mesodermal ingrowth between the neural tube and the overlying ectoderm, resulting in their failure to separate. The osseous defect in such a case is in the cribriform plate on one or other side of the midline. The encephalocele covered by layers of meninges lies in this defect and can be demonstrated by cisternography and at surgery. This lesion is rare and may be associated with other midline intracranial defects. The encephalocele can be very small and it may manifest with recurrent CSF rhinorrhoea and/or meningitis. The author's case showed all the above-mentioned features and was therefore an encephalocele.
Finally, it is emphasised that in all patients with sellar or peri-sellar tumours, a complete evaluation of pituitary and its target gland functions must be done before treatment to assess whether there is deficiency of various hormones. This endocrine evaluation is especially important in patients in whom surgery is planned so that the patient's need for hormonal replacement in the pre-, per- and post-operative periods can be met. In this regard as well as for the long-term follow-up of these patients, a team approach with an endocrinologist is essential. Any patient undergoing surgery for a sellar or perisellar tumour must have peri-operative cover with glucocorticosteroid irrespective of their pituitary-adrenal axis status. The genesis of lamina cribrosa CSF fistula due to raised ICP in this case has no scientific basis bearing in mind the intrasellar location of the tumour and the atrophic nature of the brain. In the absence of trauma, rhinological operation and raised ICP, the presence of a bone defect in the lamina cribrosa along with herniation of the brain (encephalocele) at any age is congenital. This was the cause of CSF rhinorrhoea in this patient.
|
A
Rashid Choudhury
58 A Burton Road Repton Derby DE65 6FN United Kingdom |
|
Reply from Author
Sir,
I greatly appreciate and would like to thank Dr. Abdur Rashid Choudhury
for his expert views on the article.(8) I will try to answer his queries
one by one.
I would like to stress that patient's relevant problems were presented
and discussed, concentrating on the unusual association of primary empty
sella (PES) with co-existing craniopharyngioma and spontaneous cerebrospinal
fluid (CSF) rhinorrhea through lamina cribrosa, rather than on general
management.
The patient's body mass index was 35.88/kg/sq.m. I would agree with
the hormonal changes (of FSH & LH) one would expect in such a case.
The normal levels encountered in this case could be an exception. Estimation
of serum oestradiol and ACTH has been missed due to non-availability
of the facility at that time. Her serum electrolytes were within normal
range and the general weakness and easy fatigability could have been
due to hypocortisolism. I agree with the explanation that hypocortisolism
and mildly increased prolactin levels during her second admission could
have resulted from displacement or compression of pituitary stalk by
the lesion.
Glucocorticosteroid cover peri-operatively is a routine and well-established
entity for patients needing surgery for sellar or perisellar lesions
irrespective of the pituitary-adrenal axis status. This patient also
received glucocorticosteroid peri-operatively. Post-operatively patient
was on hormonal replacement as mentioned and was under the care of endocrinologist.(8)
As a routine, endocrinologist is involved in the management of such
cases in our Institution. I fully agree that a team approach with endocrinologist
is essential in overall management of such cases.
I disagree with the suggestion of the possibility of unrecognised primary
intranasal encephalocele for the genesis of ethmoidal CSF fistula in
this case. The following explanation clarifies the situation: a) There
was no polypoidal mass (nasal polyp) in the nose nor patient had any
hypertolerism or other anterior cranial fossa abnormality suggesting
intranasal frontonasal encephalocele.(1,3) b) CT scan and omnipaque
CT cisternography did not reveal any direct or indirect (filling defect
in the contrast at the site of leak) evidence of brain herniation through
the site of ethmoidal defect. c) Per-operatively there was no herniation
of the brain through the defect into the nasal cavity. There was only
partially tucked brain in the region, which got disengaged easily just
on retracting the frontal lobe and it could have resulted from pressure
difference across the defect or due to previous attack of meningitis.
d) Review of literature also reveals cases of focal cribriform defects
with meningiocerebral microherniation similar to our case causing spontaneous
ethmoidal CSF fistula is association with primary sella.(2,5,7)
The two possible explanations in the genesis of PES & cribriform fistula
in this case were considered.(8):
| 1. | Secondary to raised intracranial pressure (ICP) - former or intermittent, was considered on the basis that this patient was admitted in 1985 under Neurophysician's care with history of headache and after investigations was diagnosed to have benign intracranial hypertension (BIH) with PES.(8) Moreover, this patient had persistent headache prior to the onset of first attack of rhinorrhea that relieved her headache and thereafter the intermittent attacks of rhinorrhea also used to relieve the persistent headaches suggesting possible raised ICP. The tumour at the time of onset of rhinorrhea was very small and intrasellar and certainly will not cause the raised ICP. The radiological appearance of prominent cisterns, sulci and gyri suggesting atrophic brain does not exclude the possibility of earlier raised ICP or intermittent episodes of raised ICP. Continuous monitoring of ICP has revealed instances of raised ICP in patients with PES with no overt symptoms of raised ICP.(4) | |
| 2. | It might be possible that a deficient diaphragma sellae associated with anomaly of the dura covering cribriform plate representing two different features of congenital defects existed in this case. In such cases even normal pulsations of the CSF might play a role in forming PES and ethmoid fistula.(6-8) |
|
Dr. Basit Ali Syed |
| 1. | Blumenfield R, Skolnik EM: Intranasal encephaloceles. Arch Otolaryngol 1965, 82: 527-531 |
| 2. | Carmel PW: Empty sella syndrome. Chapter 102, Vol. 1, Wilkins RH & Rengachary SS (Eds), Text book of Neurosurgery, McGraw-Hill Book Company, 1985, p887 |
| 3. | Choudhury AR, Taylor JC: Primary intranasal encephalocele. Report of four cases. J Neurosurg 1982, 57: 552-555 |
| 4. | Davis S, Kaye AH: A dynamic pressure study of spontaneous CSF rhinorrhea in the empty sella syndrome. J Neurosurg 1980, 52: 103-105 |
| 5. | Moschini M, Amato C, Gioia F: Ethmoidal fistula associated with empty sella in a case of spontaneous CSF rhinorrhea. Rays 1988, 13: 45-47 |
| 6. | Perani D, Scotti G, Colombo N, Sterzi R, Castelli A: Spontaneous CSF rhinorrhea through lamina cribrosa associated with primary empty sella. Ital J Neurol Sci 1984, 5: 167-172 |
| 7. | Scott RJ, Redmond MJ: Non-traumatic cerebrospinal fluid rhinorrhea in cases of primary empty sella syndrome. Med J Aust 1989, 150: 458-461 |
| 8. | Syed BA: Co-existing primary empty sella and craniopharyngioma with spontaneous cerebrospinal fluid rhinorrhea through lamina cribrosa - case report. Pan Arab J Neurosurg 2000, 4: 45-51 |
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CORRESPONDENCE
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|
Letter to Prof. Fuad Haddad
“The case of the elusive posterior fossa tumour”
(published by Pan Arab J Neurosurg 2000, 4(1): v-viii |
I have read with great interest and admiration your editorial entitled as above.
When I began my training in Neurosurgery CT was already available worldwide and MRI was just beginning to be established in a few centres. With the aide of even these magnificent tools, for me, Neurosurgery was a tremendous challenge and a very difficult specialty.
Comparing your case with any case of posterior fossa mass today, I was pleased that there were such exacting individuals, as yourself – extraordinarily good and brave men. These characteristics combined with great intelligence were, I am sure, what allowed you to struggle against such great difficulties for the sake of the patient. History is the fundamental base for the future; clinical sense, devotion and ambition are the basic requirements of the Neurosurgeon and I thank you for this incredible indirect reminder to all neurosurgeons as to “what is used to be like”.
With great respect,
Nizar Al Amiri
Consultant Neurosurgeon
Riyadh Armed Forces Hospital
Riyadh
Saudi Arabia