Review articles

By Mr. Mohammud Musleh , Mr. Muhammed R Siddiqui
Corresponding Author Mr. Mohammud Musleh
University of Liverpool, - United Kingdom
Submitting Author Mr. Muhammed R Siddiqui
Other Authors Mr. Muhammed R Siddiqui
Mayday Hospital, 23 Malvern Road - United Kingdom TN24 8HX


Subarachnoid haemorrhage; Clipping and coiling

Musleh M, Siddiqui MR. Subarachnoid Haemorrhage: A Comparison Between Coiling and Clipping. WebmedCentral TRAUMA 2013;4(4):WMC004199
doi: 10.9754/journal.wmc.2013.004199

This is an open-access article distributed under the terms of the Creative Commons Attribution License(CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Submitted on: 14 Apr 2013 08:27:43 PM GMT
Published on: 15 Apr 2013 05:47:58 AM GMT



A subarachnoid haemorrhage is defined as bleeding into the subarachnoid space. It is usually caused by the rupture of an intracranial aneurysm, although it has other causes including trauma and malignancies. The main factors that increase the likelihood of a subarachnoid haemorrhage are excessive alcohol consumption, hypertension, smoking and lack of exercise. The trademark symptom of a subarachnoid haemorrhage is a sudden, severe headache situated at the back of the head. Other symptoms include collapse, neck stiffness and focal neurological deficit. Treatment of aneurysms, both those ruptured and not, is associated with high rates of complications that may cause morbidity and mortality. The two main treatments are coiling and clipping.


The aim of this piece is to compare and contrast the two techniques used to resolve an intracranial haemorrhage. This will include evaluating rates of complications and the effectiveness & efficiency of both coiling and clipping. Reasons for the complications and ways to reduce their incidence will be considered.


Information for this piece was found using medical databases (e.g. PubMed) and library books (e.g. by Maurice-Williams).


Clipping is a form of neurovascular surgery. It involves opening the cranium (craniotomy) to gain access to the aneurysm/haemorrhage. A clip is positioned on the neck of the aneurysm that will close to isolate the dilatation from general circulation. Coiling is a form of endovascular surgery. A coil is introduced into the femoral artery via a catheter. It is passed into the aneurismal sac where it will detach to separate the aneurysm from general circulation.
Both of these operations may have unintended consequences including infection, epilepsy, delayed cerebral ischaemia and re-bleeds. The rates of these complications differ in those treated with a clip and those with a coil; generally coiling is associated with few risks, particularly in the short term. 

Future Study

Potential improvements made to this piece in a subsequent study may include a discussion of the best ways to prevent the occurrence of subarachnoid haemorrhages, including surgery, drug treatment and lifestyle choices. Alternatively, a new study could focus more on the occurrence of complications and optimal ways to treat them.


Problems regarding the writing of this piece included the availability of some articles and the availability of comparable statistics.


Coiling is superior to clipping due to its lower rates of complication. Its inferior rates of re-bleed in the long term are a cause for concern however and so the treatment plan for each patient should be decided on a case by case basis due to a number of interplaying factors (e.g. age of patient). 


A subarachnoid haemorrhage (SAH) is defined as bleeding into the subarachnoid space1. It is responsible for up to 5% of stokes within the UK, although it causes 25% of all stroke-related deaths2. SAHs are an important source of morbidity and mortality in the UK: around 9.7 people per 100,000 will suffer a SAH every year, with females at greater risk than males3. Of these, 15% die before reaching hospital4 and a further 50% will die within 30 days2. Morbidity rates for survivors are around 30%5; this can vary from anxiety and depression to cognitive impairment that can severely impact quality of life6. Recent studies suggest only modest improvements in the incidence and outcomes of SAHs have been achieved in the last few decades7.     

SAH’s can be categorized as either aneurismal or traumatic8. Traumatic causes account for fewer than 10% of cases compared to 85% of SAH cases linked to aneurisms. Other rare causes, such as borreliosis, cerebral arteriovenous malformations and cervical meningiomas, account for the remaining 5%9. Modifiable risk factors of SAH include smoking (odds ratio of 3.2), excessive alcohol consumption (odds ratio 1.5), exercise (relative risk ratio of 0.5) and hypertension (odds ratio of 2.9)10. The importance of these modifiable risk factors is emphasized by studies suggesting they cause 66% of haemorrhages, comparing to only 10% that are attributed to genetic susceptibility11.

Intracerebral aneurisms can be defined as saccular, fusiform or dissecting, commonly forming in and around the circle of Willis, particularly the anterior and posterior communicating arteries12. The risk of rupture is proportional to the diameter of the aneurism, although the majority of ruptures occur in small-diameter aneurisms as they are much greater in number than large-diameter ones9. It should be emphasized that not all intracranial aneurisms burst or cause any symptoms; as many as 2% of the general population have an intracranial aneurysm but are unaware of it13.

When an aneurysm bursts, the flow of blood into the subarachnoid space causes an immediate rise in the intracranial pressure (ICP) that is large enough to obstruct cerebral perfusion14. This is responsible for the loss of consciousness experienced by many who suffer a SAH. Resultant ischemia due to a decline in perfusion does not always result in cerebral infarction; instead it depends on many factors including the extent of the fall and duration in perfusion and the competence of homeostatic measures. The brain normally receives about 50ml of blood per minute. It is only when perfusion falls to around 10ml of blood per minute do neurons sustain permanent damage15. Homeostatic measures employed by the body to correct the situation including plugging the haemorrhage and draining leaked blood, allowing perfusion to return to normal levels very shortly16. Cerebral oedema occurring due to fluid accumulation within damaged cells (cytotoxic oedema) or cerebrospinal fluid (CSF) leakage into the interstitial space (vasogenic oedema) exacerbates the raised ICP and negatively impacts efforts to correct it14

Furthermore, the explosive exit of the blood from the vessel causes focal damage to the anterior hypothalamus17. With regards to of this, 80% of individuals suffering a SAH also suffer from metabolic, endocrine and systemic disturbances due to the impact on hypothalamic activity18.

The clinical manifestations of a SAH are numerous and varied. Different individuals may experience completely different symptoms depending on the location and severity of the haemorrhage. The most common symptom is a sudden, severe ‘thunderclap’ headache at (or radiating to) the occiput20. Symptoms of meningeal irritation, such as photophobia and neck stiffness, are common21. Other features include reduced (or absent) consciousness, vomiting and seizures22 23 24. Signs of SAHs commonly manifest themselves in the eyes. Rising ICP may cause brain herniation, suggested by the loss of the pupillary light reflex and an isolated dilated pupil9. Rising ICP can also result in an intraocular haemorrhage, which may be seen on fundoscopy as papilloedema. The presence of papilloedema does not necessarily mean an intraocular haemorrhage has occurred as papilloedma is also seen (in up to 24% of patients) in its absence due to clots from the SAH blocking CSF flow or absorption25. Despite this, SAH-associated intraocular haemorrhage, called Terson’s syndrome, is particularly important to detect, not only because it is associated with severe cases of SAHs, but also as it may cause serious complications if not treated, namely blindness. It affects around 13% of all patients26. The severity of SAH can be classified using the Glasgow Coma Scale (GCS) or the Hunt and Hess scale.

Following an indicative history and examination, patients with suspected SAH immediately undergo a CT scan. The sooner the CT is performed, the more sensitive it is27. As well as identifying an aneurysm or haemorrhage, it can also identify complicating pathology, such as oedema, hydrocephalus & haematomas28.  If the results of the CT are negative or inconclusive, a lumbar puncture is performed. In this procedure, CSF is drawn from subarachnoid space surrounding the spinal cord for analysis. In the event of a SAH, an elevated red cell count or xanthochromia will be seen21. If the diagnosis has still not been confirmed, imaging of the intracranial circulation is indicated, such as a CT angiography or digital subtraction angiography (DSA)29. This also allows for locating the aneurysm site1. Occasionally, MRI scans are used, particularly if the presentation is very late onset29.

This piece will assess and contrast the two methods of treating aneurysms: coiling and clipping. The procedures and outcomes of both techniques will be evaluated. A decision will be made based on the resources assessed which of the two treatments is preferable, in terms of outcome and risk of complication.  


Key words were entered into a medical database called Pubmed. Limitations, including language (English) and text availability (only free & complete articles), were inserted to allow for a more accurate and thorough comparison between coiling and clipping. The results of the searches are given below:

See Illustration 1

In addition to the online resource, books relating to the subject of discussion were obtained from the Harold Cohen Library, such as “Subarachnoid Haemorrhage” by Maurice-Williams. 


The principle of treating intracranial aneurysms is to the isolate the dilation from general circulation without impacting surrounding structures. This can be done, as mentioned above, using a surgical clip or coil16.


Clipping is a neurosurgical technique first employed by Walter Dandy in 1937 used to treat intracranial aneurysms; both those that have burst and those that have not30. It involves accessing the aneurysm via a craniotomy and attaching a titanium clip onto the neck of the aneurysm31. This operation is usually performed within 3 days of the initial bleed, although the timing of the operation has proven controversial30. Modern clips work using a spring mechanism; once the clip is positioned, its wings can gently tighten around the neck of the aneurysm like a noose. Before the introduction of such a mechanism, the surgeon would manually close the clip, increasing potential liability to the bursting of the aneurysm as well as damage to surrounding structures. This is particularly important considering it is during the attachment of the clip that rupture is most likely32. Following the application of the clip, it is common for the surgeon to puncture the aneurysm to confirm its complete occlusion from the parent vessel33, although this practice has its obvious risks and is not universally performed16.


Coiling is a form of endovascular treatment that was first introduced in the 1990s as an alternative to clipping. In contrast to the open-surgery required in clipping, this form of procedure requires only a small incision in the groin. The platinum coil, known as a Guglielmi Detachable Coil, after its inventor, Dr. Guido Guglielmi30, is introduced into the femoral artery via a catheter. It is then passed through the arteries, under X-ray fluroscopic guidance, until it reaches the aneurysm, where it is positioned. The coil is subsequently detached from the catheter to occupy the sac of the aneurysm. This results in haemostasis of that precipitates the formation of a thrombus. This thrombus will occlude the aneurysm/rupture in a manner similar to the clip6 35 36. A difference between this and clipping is the doctor performing this procedure is often an interventional radiologist rather than a neurosurgeon35.


Direct comparison between the two procedures is difficult, particularly as some aneurysms/haemorrhages are considered more suitable for neurosurgery (e.g. wide-necked aneurysms) rather than endovascular surgery and vice versa37 38. Patients who undergo endovascular (coiling) and neurosurgical (clipping) treatments are at risk of unintended consequences, as is the case with all medical procedures. Complications for both procedures are the same, although the frequency of complications differs35.


Infection is a concern during any surgical procedure. The incidence of infection of the wound following craniotomy (for the application of a clip) is 2-3%; this risk increases if multiple surgeries are needed. Common infection-causing organisms are staphylococcus albus or staphylococcus aureus39. Early recognition followed by antibiotics usually resolves the infection but if symptoms do not subside, the affected area is resected16. Whilst risk of infection is also present in the key-hole surgery technique employed in coiling, it is smaller. This is because risk of infection increases with hospital duration: patients who received a clip had a median hospitalization duration of 16 days (or 24 days in more severe cases ) compared to those that received a coil, who were hospitalized for a median of 12 days (or 20 days in more severe cases)40. Furthermore, patients who received clipping for their aneurysm/haemorrhage are at added risk of infection bearing in mind the risk of infection is proportional to the duration of surgery41.


Longer times under general anaesthetic elevate risks associated with sedation. This risk is hence elevated in clipping when compared with coiling42.

Intracranial Haemorrhage

Re-bleeding from the aneurysm may occur because of arterial pulsations displacing poorly attached clips/coils leading the aneurysm to burst16. It is associated with the size of the aneurysm and the severity of the case43. Re-bleeding is common; 15% of patients have significant clinical deterioration within the hours of treatment that is suggestive of re-bleed44. Significantly, it may occur in patients treated both endovascularly or neurosurgically; which out of the two is associated with greater chance of re-bleeding was subject to a multinational study called the International Subarachnoid Aneurysm Trial (ISAT)45. This study concluded that for the first 7 years following the operation, coiling was associated with lower probabilities of re-bleeding. Beyond the first 7 years, clipping was more successful in preventing re-bleeds45. This has called into question the mentality of giving coils to younger, fitter patients38. Additionally, the high mortality rate of early (within 30 days) re-bleeding associated with coiling (1.4% risk of early re-bleed with 100% mortality rate)46 compared poorly with the mortality rate associated with early bleeding following clipping (2% risk of early re-bleed with 37.5% mortality rate) from another study47.  


Epilepsy, a family of neurological disorders characterised by seizures48, is another serious complication of a SAH. It is most likely to appear in the immediate period following treatment, particularly in more severe cases16. Classen J et al discovered 7% of SAH patients developed epilepsy in addition to a further 4% having a one off fit that was not considered epileptic49. Interestingly, while there was little variation between the proportion of patients suffering seizures/epilepsy and the type of treatment they received for a ruptured haemorrhage (clipping 10.7% versus coiling 11.1%), clipping was associated with a 48% greater risk of epilepsy/seizure when used to treat an intact haemorrhage in comparison to coiling50. Although the relationship between SAHs and epilepsy is well known, it is not fully understood why coiling and clipping increase its incidence. Many mechanisms have been suggested, most prominently the additional risk generated by clipping due to “exposure of the intracranial space (and) the temporal and frontal lobes” while coiling caused epilepsy because “oedema (due to) thrombosis of the aneurysm”50 51 52. Crucially, much of this data includes one-off seizures and not fulminant epilepsy. Therefore, the actual chance developing epilepsy, which may severely limit quality of life, is not as high as first thought, although the difference in risk between coiling and clipping is clearly not one to be ignored.

Delayed Cerebral Ischaemia

Delayed cerebral ischaemia (DCI) is a complication that can progress into cerebral infarction. It afflicts up to 30% of SAH patients, usually 4-10 days following the initial rupture53. As such, it can cause life-long morbidity and even death. It’s most common sign is a deterioration of consciousness, which can be detected using the GCS54. Whilst its pathogenesis is unclear, to the point that defining DCI is of dispute, it has been linked to arterial vasospasm55. This is view is enhanced by angiographic evidence of the peak period of vasospasm is also 4-10 days following initial rupture16, although recent trials linking the two together have been disappointing (e.g. reducing rates of vasospasm had little impact on rates of DCI)56. The ISAT study found that DCI was more common after clipping than after coiling51. It is more complicated than this however as patients treated early for their SAH (within 4 days), the outcome of DCI was worse in patients who received endovascular rather than neurovascular treatment57. This is very significant because, as stated above, the majority of neurosurgeons will position a clip usually within the first three days.

 As with other complications, the immediate risks of clipping seems greater than with coiling, although long-term risks are greater in coiling. Numerous studies have been made regarding how to reduce the incidence of DCI. Some suggest the presence of a clot shown on CT within the subarachnoid space greatly increases the risk of DCI and removing it prior to treatment has a positive effect on outcomes58 59. Another trial has shown delaying surgery until after 2 weeks from the initial burst can also have a positive effect, avoiding the period of peak vasospasm60.

It has been suggested the reason clipping and coiling can cause DCI is because they aggravate the narrowing and distortion of the vessel following spasm. The distortion will see vessels distal to the affected vessel receive different amounts of blood due to Coanda effect, which is the tendency of fluids to stick to nearby surfaces. Therefore, some vessels will carry disproportionately higher volumes of blood while others will carry volumes low enough to cause ischaemia61.  

Recovery Times

There is a striking difference between the recovery times of clipping and coiling. One study showed that it took 1 year for 50% of surgically treated to feel back to normal following surgery, where as the median was only 27 days for endovascularly treated patients62. Another important factor affecting recovery times was the number of complications. In this regards it was again proven that coiling was superior to clipping, as patients treated surgically were 2.26 times more likely to have complications while in hospital compared with coiled patients63.


Another, often not discussed, aspect regarding the clipping versus coiling debate is the economic side. This is especially relevant when considering the current economic situation, where health expenditure is being scrutinized more closely. Despite shorter hospital stays, cost of coiling exceeds that of clipping64. Cost of clipping is mostly determined by the cost of the coil, which contributes almost half of the entire operation cost (€5300 cost of coil, cost of operation €10,370). Clips on the other hand, cost €530 against total operative costs of €8865. Instead, the majority of its costs are determined by the days spent in hospital and the need for further care65. While this may not matter too much to a patient in the UK who has their expenses covered by the NHS, it may matter more in another country where there is no free health care, such as the USA, where coiling has a median cost of $42,070 compared to the median cost of $38,166 for clipping63.

Future Study

A future study comparing the effectiveness of coiling and clipping could extend on this piece to see how coiling and clipping compared with conservative/drug treatment with a view to preventing the rupture of an intracranial aneurysm, or even their formation. Furthermore, for a SAH, complications could be researched in more detail, including their pathophysiology, impact and treatment, as well investigating new methods used to reduce their occurrence, such as administering nimodipine following a SAH66. The study can also be expanded to include case reports of individuals being treated for SAH, following them as they recover, providing first hand experiences of the difficult recovery period.


One of the difficulties encountered when writing this piece was the complexity of some of the content in the journals and books used. Some had to be read repeatedly to properly understand what was being conveyed. Another problem was that comparable statistics between coiling and clipping in the same study were sometimes difficult to find.


The introduction of coiling in the 1990s revolutionised treatment of SAH. The established method of correcting intracranial haemorrhages and aneurysms that had been accepted for decades has now been virtually discarded in some centres.

Whilst the issue of cost is a minor area of discussion, it is nonetheless an important one when considering strained NHS resources. The cheaper costs of clipping may appeal in such times.

Direct clinical comparison between the two techniques is difficult; particularly as coiling is a relatively new method of treating intracranial aneurysms. Coiling has been shown to offer superior results in terms of complications, particularly in the short-medium term. Infection, re-bleed, epilepsy (for intact aneurysms) and DCI were all less frequent in patients who were treated endovascularly. Conversely, it has been argued the clips are more effective in the long term at achieving their intended purpose; sealing a SAH and preventing their re-emergence. As such, clipping offers a more complete ‘cure’ to a SAH or intact aneurysms; hence it may be more prudent for younger, fitter patients67. The permanence of clipping means the stressful and indeed dangerous ordeal of an aneurysm and its treatment need not be repeated for a greater number of patients. However, it can also be argued its higher risk of causing a severely restraining disability (or death) negates the benefits of a sealed aneurysm. Since the same complications are present for both coiling and clipping, is it better to invest time and resources into improving the rate of complications of clipping or improving the long-term effectiveness of coiling?

The ISAT trial, which first established coiling superiority, has notable limitations, including its focuses on aneurysms suited equally to coiling and clipping. These limitations matter as this trial has formed the basis for the coiling-clipping debate. Despite this, many articles concur with the view of coiling superiority. Whilst the long term effects of coiling have yet to be thoroughly studied in a similar manner to clipping, the supposed deficit in long-term results is not believed to be sufficiently significant to relegate coiling from its position as first-line therapy.
In spite of this, clipping should not be discarded and remains an extremely useful practise, especially as the use of coiling for some aneurysms is not recommended. 


1. Oxford Concise Medical Dictionary. 7th edition. Oxford University Press. Subarachnoid Haemorrhage; p.688.
2. NHS. Subarachnoid Haemorrhage. (Internet) [Updated 2010 March 3rd](Cited 2012 May 4th). Available from:
3. Pobereskin L.H. Incidence and outcome of subarachnoid haemorrhage: a retrospective population based study. Journal of Neurology, Neurosurgery and Psychiatry 2001;70: 340-343.
4. Huang J, Van Gelder JM. The probability of sudden death from rupture of intracranial aneurysms: a meta-analysis. Neurosurgery, 2002; 51(5): 1101–1105
5. Cahil J, Zhang J. Subarachnoid haemorrhage: Is it time for a new direction? Stroke, 2009; 40: 586-587.
6. Suarez J, Tarr R, Selman W. Aneurysmal Subarachnoid Haemorrhage. New England Journal of Medicine 2006; 345: 387-396
7.  Stegmayr B, Eriksson M, Asplund K. Declining mortality from subarachnoid hemorrhage: changes in incidence and case fatality from 1985 through 2000. Stroke 2004; 35: 2059–2063
8. van Gijn J, Rinkel G.J. Subarachnoid haemorrhage: diagnosis, causes and management. Brain: a Journal of Neurology 2001; 124(2): 249-279
9. Van Gijn J, Kerr.R.S, Rinkel G.J. Subarachnoid Haemorrhage. The Lancet 2007; 369(9558): 306-318
10.  Teunissen.L.L, Rinkel.G.J, Algra A, van Gijn J. Risk factors for subarachnoid haemorrhage: A systematic review. Stroke. 1996; 27: 544-549
11. Ruigrok Y.M, , Buskens E, Rinkel G.J. Attributable risk of common and rare determinants of subarachnoid hemorrhage. Stroke. 2001; 32:1173-1175
12. Vega C, Kwoon J.V, LAVINE S.D. Am Fam Physician 2002 August 15; 66(4):601-609.
13. Vernooij M.W, Ikram M.A, Tanghe H.L, Vincent A.J.P.E, Hofman A et al. Incidental findings on the brain MRI in the general population. The New England Journal of Medicine 2007 November 1st; 357:1821-1828.
14. Nornes H., Magnaes B. Intracranial pressure in patients with ruptured saccular aneurysm. Journal of Neurosurgery. 1972 May; 36(5):537-547
15. Symon L. The disordered cerebrovascular physiology in aneurismal subarachnoid haemorrhage. 1978 Acta Neurochirurgica; 41:7-22
16. RS Maurice Williams. Subarachnoid haemorrhage, Bristol: IOP Publishing Limited; 1987
17. Crompton M.R. Intracerebral haematoma complicating ruptured cerebral berry aneurysm. Journal of Neurology, Neurosurgery & Psychiatry. 1962 November; 25(4):378-386
18. Buckell M. Demonstration of substances capable of contracting smooth muscle in the haematoma fluid from certain cases of ruptured cerebral aneurysm. Journal of Neurology, Neurosurgery & Psychiatry. 1964 June; 27(3):128-129
19. Linn F.H.H, Rinkel G.J, Algra A, van Gijn J. Headache characteristics in subarachnoid haemorrhage and benign thunderclap headache. Journal of Neurology, Neurosurgery & Psychiatry. 1998; 65:791-793
20. Punit R; Moore K. Oxford Handbook of Acute Medicine.2nd edition. Oxford University Press; 2007
21. Vermeulen M, van Gijn J. The diagnosis of subarachnoid haemorrhage. Journal of Neurology, Neurosurgery & Psychiatry. 1990 May; 53(5):365–372
22. Brilstra E.H, Rinkel G.J, Algra A, van Gijn J. Rebleeding, secondary ischemia, and timing of operation in patients with subarachnoid hemorrhage. Neurology. 2000; 55:1656–1660
23. Sarner M, Rose FC. Clinical Presentation of ruptured intracranial aneurysm. Journal of Neurology, Neurosurgery & Psychiatry. 1967 February; 30(1):60-67
24. Linn F.H.H, Rinkel G.J, Algra A, van Gijn J. Headache characteristics in subarachnoid haemorrhage and benign thunderclap headache. Journal of Neurology, Neurosurgery and Psychiatry. 1998 November; 65(5):791-793
25. Miller N.R, Newman N.J, Biousse V, Kerrison J.B. Walsh and Hoyt’s Clinical Neuro-opthalmology: The essentials. 2nd Edition. Philadelphia:Lippincott Williams & Williams; 1999.
26. McCarron M.O, Alberts M.J, McCarron P. A systematic review of Terson’s syndrome: frequency and prognosis after subarachnoid haemorrhage. Journal of Neurology, Neurosurgery and Psychiatry. 2004; 75:491-493.
27. Sames TA, Storrow A.B, Finkelstein J.A, Magoon M.R. Sensitivity of new-generation computed tomography in subarachnoid hemorrhage. Academic Emergency Medicine. 1996 January; 3:16-20
28. van der Jagt M, Bijvoet H.W, Pieterman H, Dippel D.W, Vermeij, Avezaat C.J et al. Validity of prediction of the site of ruptured intracranial aneurysms with CT. Neurology 1999 January; 52(1):34-39
29. Kirkpatrick P.J. Subarachnoid Haemorrhage and Intercranial Aneurysms: What neurologists need to know. Journal of Neurology, Neurosurgery and Psychiatry. 2002; 73:28-33
30. Jallow J, Loftus C.M. Neurotrauma and critical care of the brain. New York: Thieme Medical Publishers Inc; 2009.
31. US National Library of Medicine. Brain Aneurysm Repair (Internet). Medline Plus; (Updated 2010 August 27th) (Cited 2012 May 6th). Available from:
32. Whitfield P.C, Moss H, O'Hare D, Smielewski P, Pickard J.D, Kirkpatrick P.J. An audit of aneurysmal subarachnoid haemorrhage: earlier resuscitation and surgery reduces inpatient stay and deaths from rebleeding. Journal of Neurology, Neurosurgery & Psychiatry. 1996; 60:301–306.
33. Kyriakides T, Aziz T.Z, Torrens M.J. Post operative recovery of third nerve palsy due to posterior communicating aneurysms. British Journal of Neurosurgery. 1989; 3(1):109-111.
34. Jeremy G. Rowe J.G, Monleux A.J, Byrne J.V, Rendowden S, Aziz T.Z. Endovascular Treatment of Intracranial Aneurysms: A Minimally Invasive Approach with Advantages for Elderly Patients. Age and Ageing. 1996; 25 (5):372-376.
35. American Association of Neurosurgeons. Treatment options for Cerebral Aneurysms (Internet). 2003 April (Updated 2009 August)(Cited 2012 May 5th). Available from: 20Cerebral%20Aneurysms.aspx
36. Wells W.M. Medical Image Computing and Computer-Assisted  Intervention—MICCAI ’98: Proceedings of the First International Conference. Massachusetts: Springer-Verlag Berlin and Heidelberg GmbH & Co. KG; 1998.
37. Wanke I, Doerfler A, Schoch B, Stolke D, Forsting M. Treatment of wide-necked intracranial aneurysms with a self-expanding stent system: Initial clinical experience. American Journal of Neuroradiology. 2003; 24:1192-1199.
38. Mitchell P, Kerr R, Mendelow A.D. Could late rebleeding overturn the superiority of cranial aneurysm coil embolization over clip ligation seen in the International Subarachnoid Aneurysm Trial? Journal of  Neurosurgery. 2008; 108 (3):437–442.     
39. Quadery L.A, Medlery A.V, Miles J. Factors affecting the incidence of wound infection in neurosurgery.  Acta Neurochir. 1977; 39 (3-4):133-141.
40. Fang J, Casaubon L.K, Robertson A, Silver F.L, Kapral M.K, Stamplecoski M et al. Higher incidence of in-hospital complications in patients with clipped versus coiled ruptured intracranial aneurysms. Stroke. 2011 (cited 2012-05-04). Available from:
41. Eckbert B, Leppien A, Fiehler J, Kehler U, Brunken M. Coiling vs Clipping: Hospital stay and procedure time in intracranial aneurysm treatment. Rofo. 2009; 181 (10):989-995.
42. National Health Service. Anaesthetic, general (internet). (Updated 2011 June 26th) (Cited 2012 May 5th). Available from:
43. Naidech A.M, Janjua N, Kreiter K.T, Ostapkovich N.D, Fitzsimmons B, Parra A et al. Predictors and impact of aneurismal rebleeding after subarachnoid haemorrhage. Archives of Neurology. 2005; 62: 410-416.
44. Fujii Y, Takeuchi S, Sasaki O, Minakawa T, Koike T, Tanaka R. Ultra-early rebleeding in spontaneous subarachnoid hemorrhage. Journal of Neurosurgery. 1996; 84(1):35–42.
45. Molyneux A.J, Kerr R.S.C, Yu L, Clarke M, Neade M, Jarnold J.A et al. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. The Lancet. 2005; 366 (9488):809-817.
46. Sluzewski M, van Rooij W.J. Early rebleeding after coiling of ruptured cerebral aneurysm: incidence, morbidity and risk factors. American Journal of Neuroradiology. 2005: 26:1739-1746.
47. Tsementzis S.A,Hitchcock E.R. Outcome from “rescue clipping” of ruptured intracranial aneurysms during induction anaesthesia and endotracheal intubation. Journal of Neurology, Neurosurgery and Psychiatry. 1985; 48:160-163.
48. Chang B.S, Lowenstein D.H. Epilepsy. The New England Journal of Medicine. 2003; 349:1257-1266.
49. Kannar A.M. Subarachnoid Haemorrhage as a cause of epilepsy. Epilepsy Currents. 2003; 3 (3):101-102.
50. Hoh L.H, Nathoo S, Chi Y, Mocco J.M.D, Barker F.G. Incidence of Seizures or Epilepsy After Clipping or Coiling of Ruptured and Unruptured Cerebral Aneurysms in the Nationwide Inpatient Sample Database: 2002-2007. Journal of Neurosurgery. 2011: 69 (3):644-650.  
51. Ryttlefors M, Enblad P, Kerr R.S, Molyneux A.J. International subarachnoid aneurysm trial of neurosurgical clipping versus endovascular coiling: subgroup analysis of 278 elderly patients. Stroke. 2008;39(10):2720-2726
52. Origitano T.C. Current options in clipping versus coiling of intracranial aneurysms: to clip, to coil, to wait and watch. Neurologic Clinics. 2006;24(4):765-775.
53. Roos Y.B, de Haan R.J, Beenen L.F, Groen R.J, Albrecht KW, Vermeulen M. Complications and outcome in patients with aneurysmal subarachnoid haemorrhage: a prospective hospital based cohort study in the Netherlands. Journal of Neurology, Neurosurgery Psychiatry. 2000; 68 (3):337–341.
54. Rinkel G.J, van Gijn J, Vermeulen M, Vergouwen H.M.D.I,Juvela S, Mendelow D et al. Definition of Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage as an Outcome Event in Clinical Trials and Observational Studies : Proposal of a Multidisciplinary Research Group. Stroke. 2010; 41: 2391-2395
55. Wan H, Loch Macdonald R. Circulatory and vascular changes after aneurysmal subarachnoid hemorrhage. Journal of Neurological Sciences. 2011; 55 (4): 329-341.
56. Vergouwen M.D, Vermeulen M, Coert B.A, Stroes E.S, Roos Y.B. Microthrombosis after aneurysmal subarachnoid hemorrhage: an additional explanation for delayed cerebral ischemia. Journal of Cerebral Flow and Metabolism. 2008; 28 (11):1761-1770.
57. Monyleux A.J, Algra A, Rinkel G.J, Kerr R.S, Dourhout Mees S.M. Occurrence and impact of delayed cerebral ischemia after coiling and after clipping in the International Subarachnoid Aneurysm Trial (ISAT). Journal of Neurology. 2012: 259 (4): 679-683.
58. Pomonois S, Mohnsen F, Illingworth R. Prediction of delayed cerebral ischaemia after subarachnoid haemorrhage by computed tomography. Journal of Neurology, Neurosurgery and Psychiatry. 1984; 47 (11): 1197-1202.
59. Mizukami M, Takemae T, Tazawa T, Kawase T, Matsuzaki T. Value of computed tomography in the predication of cerebral vasopasm after aneurysm rupture. Neurosurgery. 1980: 7 (6): 583-586.
60. Riechert T, Mundinger F. Combined stereotaxic operation for treatment of deep seated angiomas and aneurysms. Journal of Neurosurgery. 1964 May;21:358-363.
61. Robinson J.L, Roberts A. Operative treatment of aneurysms and coanda effect: a working hypothesis. Journal of Neurology, Neuroscience and Psychiatry. 1972; 35 (6):804-809.
62. Johnston S.C, Wilson C.B, Halback V.V, Higashida R.T, Dowd C.F, McDermott M.W et al. Endovascular and surgical treatment of unruptured cerebral aneurysms: comparison of risks. Annals of Neurology. 2000; 48 (1):11-19
63. Alshekhlee A, Mehta S, Edgell R.C, Vora N, Feen E, Afshin M, Kale S.P et al. Hospital Mortality and Complications of Electively Clipped or Coiled Unruptured Intracranial Aneurysm. Stroke. 2010; 41:1471-1476,
64. Hoh B.L, Chi Y.Y, Dermot M.A, Lewis S.B. The effect of coiling versus clipping of ruptured and unruptured cerebral aneurysms on length of stay, hospital cost, hospital reimbursement, and surgeon reimbursement at the university of Florida. Neurosurgery. 2009; 64 (4):614-619.
65. Halkes P.H, Wemer M.J, Rinkel G.J, Buskens E. Direct costs of surgical clipping and endovascular coiling of unruptured intracranial aneurysms. Cerebrovascular Disease. 2006; 22 (1):40-45.
66. Kronvall E, Undrén P, Romner B, Säveland H, Cronqvist M, Nilsson O.G. Nimodipine in aneurysmal subarachnoid hemorrhage: a randomized study of intravenous or peroral administration. Journal of Neurosurgery. 2009; 110 (1):58-63.
67. H. Stefan et al. Epileptogenesis and rational therapeutic strategies. Acat Neurologica Scandinavica. 2006;113:139-209

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Subarachnoid Haemorrhage: Review
Posted by Dr. Simon B Thompson on 13 May 2013 10:03:49 AM GMT

Subarachnoid Haemorrhage- A Comparison Between Coiling and Clipping
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