Babaji
Discussions:
Decompressive craniectomy for refractory intracranial hypertension: rationale, indications and complications
Comment
I read very interesting power point of Dr Abdeen and I have an idea about use temporal muscle for expand dura . Replacing of this muscle increased blood circulation and angiogenesis.
With synthetic and other fascia we haven't angiogenesis.
Thanks
Yazd
Iran
Comment
Yes, I agree completely with Dr. Farzad Sadlou Parizi.
It´s a kind of Mio-synangiosis , frequently used in Moyamoya Disease, where we find ischemic brain tissue under the duramater.
Valparaiso, Chile
Comment
Dear Prof Quintana and Dr Parizi,
This hypothesis about re-vascularisation of the brain through the muscle is interesting.
I had this idea many years ago as a registrar but I am not aware of any studies proving it.
Are there any reports, or even cases from your own experience, of angiograms following the decompressive craniectomy showing neo-vascularity?
I would be really grateful for your opinion.
Kind regards,
Stoke-on-Trent, UK
Dear Dr Tzerakis
I had a severe head injury patient.,his GCS decreased and in brain CT there was diffuse hemisphere contusion and midline shift and high ICP which not response to medical therapy. Decomposition craniectomy and dural expansion and placement of temporal muscle flaten over angry brain performed. Patient improved gradualy. After 6 months during cranioplasty operation in detachments of muscle , there was very small arteries which penetrate to underlying brain and we discontinued Detachments and covered muscle with titanium mesh.
Thanks
Yard
Iran
Comment
Dear colleagues
Of course an excellent idea to use the temporalis muscle for augmentation of the dura but in the second procedure for cranioplasty the dissection of the artificial dura [Gortex] is much easier
Alexandria, Egypt
Comment
Dear Dr.Tzerakis
I agree with Dr.Parizi, because I also have two cases, with severe brain injury, intracranial hypertension refractary to conventional treatment, treated finally with decompressive craniectomy.
It has been proven that increased ICP is frequently associated with cerebral ischemia. In this two cases, where we added periosteum and temporal muscle (slices), under the duroplasty, in the control CT scan, performed 3 months later, we found resolution of the hemorrhagic temporal lacerations, and also we found encephalomalacy, surely with chronic cerebral ischemia. After the contrast enhancement, this región became more notable with the contrast.
Using my experience learnt in Japan, more than thirty years ago, treating Moyamoya disease, and always reading the more recent research works , relating chronic ischemia and the induced factors by the hypoxia – ischemia phenomenon, I think is completely possible that such mechanism may happen in the sequelae of severe traumatic lesions of the brain, where, as you know well, the chronic ischemia is present.
Attached is the mechanism how the chronic cerebral hypoperfusion, and chronic ischemia may induce the expression of the hypoxic induced factor, and as second messengers, the VEGF and the PDGF. Of course, this mechanism is notthe rule in all the clinical cases, and may be genetically induced, case by case.
Thanks you for your important question.
Valparaíso, Chile
Comment
Dear All,
Using temporalis muscle to augment dura, does initially appear to be a great idea! However, on further reflection, I have my doubts. The brain ischaemia following head injury or at cerebral infarction is an acute process. I would have thought that placing parts temporalis muscle over the acutely ischaemic brain in these conditions is unlikely to be beneficial; moreover, this would increase the difficulty and, morbidity (from division of any eventually parasitised blood vessels from the temporalis muscle to the brain parenchyma) at the time of cranioplasty.
Another matter to take into account is the contractility of muscle cells. I would expect the muscle cells would retain ability to contract even when (parts of the temporalis muscle) it is placed over the brain. I do not know what is the consequence of contraction of muscles placed over the brain, on the brain.
Thank you
Southampton, UK
Comment
Actually, the periostium that is adhered to the brain surface in the inner part of the muscle will become (in some measure) fibritic tissue that limit the movement in that area.
We have at least 2 different patients that were operated in other hospitals and when they arrive to our hospital we usually due an image before a cranioplasty
is planned to be do in the site of bone defect, when the radiologist made a reconstruction with angiography it was very clear that patients take circulation from extra-cranial vessels and the
next question was: should we make the cranioplasty and cut this new vessels that are actually supplying circulation to this hemisphere or maintain the "risk" of a
lack of cranial vault? We decided for the second option and after 3 year, no complains in clinical status of patients
Naturally, that patient were capable to eat and had some degree of local "traction" but no clinical implication.
México City, Mexico
Comment
Dear Naren
The technique of using autologous tissue to complete the duraplasty after performing the decompressive craniectomy is an excellent initiative. In general, tissues or autologous grafts are much better tolerated in the long run, at the interface level duramater- brain cortex, than synthetic grafts, and it´s more cheaper than the synthetics.
Now, when you do this technique, it is not to revascularize. If we use galea, muscle or periosteum is to complete the duraplasty, and if there has been, in some cases angiogenesis, this is a simple epiphenomenon. And welcome !!!
Regarding the problems that could cause the overlying temporal muscle, and later, attached to the cortex, it is true that in some initial cases of Moyamoya( Myosinangiosis) some cases presented complications as seizures, but now I use if necessary, only a partial section of the muscle (not the entire thickness of the muscle), so this piece has no direct effect of contraction and retraction over the cerebral cortex
Thank you very much for your comments.
Valparaiso, Chile
Comment
Nowadays in big centres in China augmentation of dura is being done with Gortex, may be it is easier and the procedure is neat but temporalis muscularis and pericranium are rarely being used
Wuhan
P.R.China
Question
Dear Prof. Abdeen,
Thank you for your comprehensive review of decompressive craniectomy which I enjoyed going through.
In children we avoid division of the sagittal sinus, tend to perform an additional bilateral parietal plate release (behind the coronal suture), but leaving the parietal bones in place and cover the dural opening with sutureless duragen.
Sagittal Sinus Resection:
Regarding the division of the sagittal sinus: The Decra study did not divide the sinus but the RescueICP does.
I would be interested to know if you have any information on the incidence of venous infarcts/persistence of brain oedema between these two groups.
Theoretically, division of the sinus raises the risk of damage to bridging veins and frontal lobe venous drainage, particularly in a situation where there is already brain oedema along with impaired perfusion (loss of vis a tergo) while supporters of sinus division will argue that there is a risk of sinus kinking anyway at the bone edges.
Treatment of Bone Flaps:
1. How do you store the bone flap? (Autoclaved / Frozen / Abdominal pouch )
2. When do you replace the bone flap back?
3. Incidence of bone resorption causing poor alignment of cranioplasty
4. Post-cranioplasty infection requiring removal of bone
5. Which type of storage in your opinion causes more problems?
6. Do you use titanium cranioplasty instead of own bone and when?
Thank you again and look forward to hearing from you.
Kind regards
Birmingam, UK
Comment
As far as I know there is no data on the incidence of venous infarcts / persistence of brain oedema between the two groups. Dividing the sinus in RESCUEicp is an option - it is not obligatory. Also it is divided at its most anterior extent i.e. at the origin proximal to any bridging veins. We have not aware of any complications from dividing it in our hands.
Happy New Year!
Best wishes,
Hutch
Cambridge, UK
Comment
Dear Naren,
First of all grateful thanks to Peter Hutchinson for kindly contributing to the debate.
I am reassured that division the sinus is not obligatory and that dividing it low below the bridging veins or not diving it has not led to any complications in the RescueICP Group.
My concerns related to division of the sagittal sinus are related to the fact that in children venous congestion is a real issue and therefore maintaining venous pathways intact makes sense.
Children with head-injuries often have bilateral diffuse cerebral swelling. Cerebral blood flow and CT density studies have suggested that this swelling is due to cerebral hyperaemia and increased blood volume, not to oedema.
Progressive hemispheric low density on CT scan is another specific phenomenon in children. DWI, and perfusion weighted imaging showed that the regional cerebral blood volume was increased and the mean transit time was markedly prolonged. The extensive but reversible brain changes seen on neuroimaging studies are considered to be the result of venous congestion.
Even in adults, brain oedema may also be secondary to Cerebral venous congestion or thrombosis. This is often associated with nonspecific clinical complaints. In addition, the imaging findings are often subtle and this may lead to underdiagnosis in the presence of traumatic brain injury. It may also take several days before it becomes radiologically obvious. Contrast imaging in acute traumatic brain injury is not common, and therefore difficult to check on venous flow. Brain swelling may impair circulation through the lateral venous channels and the Sylvian veins as well as through the deep venous system, causing redirection of collateral flow into the longitudinal sinus. Anomalies or anatomical variants of the Superior Sagittal sinus may also lead to unexpected drainage pathways. Without CTV these anomalies may not be obvious.
It would be interesting to see how significant is the “venous congestion” contribution to (poor) outcomes in traumatic injuries in the presence of compromised BBB, reduced perfusion, and raised ICP, in the decompressive craniectomy groups. Perhaps a study for consideration if not yet done? (:- )
From a purely mechanistic way to look at things, using the Monro-Kellie doctrine, if there are arterial cerebral perfusion issues along with raised ICP, CSF will be the first to be pushed out of the cranium. However because the cerebral vasculature requires an arterial vis-a-tergo to get blood out of the cells and into capillaries and subsequently into veins, a functional and well perfusing arterial side is required. If brain compliance is lost a rise in CVP is likely to lead to raised ICP instead of improving perfusion. Here augmenting the calvarium (DC) does make sense
Thank you again for your very welcome clarification.
Kind regards
Guirish
Birmingham, UK
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