Category Archives: Vascular

Neurocritical Care for the Advanced Practice Clinician

Neurocritical Care for the Advanced Practice Clinician

Neurocritical Care for the Advanced Practice Clinician

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Product Details

  • Published on: 2017-08-21
  • Original language: English
  • Number of items: 1
  • Dimensions: 7.75″ h x 5.25″ w x 1.00″ l,
  • Binding: Hardcover
  • 470 pages

Editorial Reviews

From the Back Cover

By utilizing a review of case-based studies and providing concise management recommendations from leaders in the field, this book provides essential knowledge for those practicing in a dynamic specialty. In the rapidly developing field of Neurocritical Care, Advanced Practice Clinicians have become an integral component of the multi-disciplinary team. This essential volume provides a frame of reference for advanced practice nurses, physician assistants, physicians, and students on a wide range of common Neuro ICU diagnoses and management strategies.

About the Author

Jessica White is a physician assistant in the Neuroscience ICU at Yale New Haven Hospital.  She has served as part-time faculty at Yale University and Quinnipiac University physician assistant programs, teaching topics of neurology and neurocritical care. Her research interests include family satisfaction and the role of the physician assistant in the multi-disciplinary team. Her training was completed at Midwestern University with a Master of Medical Science from the Physician Assistant program.

 

Dr. Sheth graduated from Johns Hopkins University and the University of Pennsylvania School of Medicine. He was recruited to Yale as the founding chief of the Division of Neurocritical Care and Emergency Neurology and Chief of Clinical Research. His interests are in the advancement of therapies and care of patients with devastating acute neurological syndromes. He is a recognized clinical, a translational scientist, has directed multicenter studies testing potential therapies against brain swelling, stroke, and hemorrhage. He is the winner of the Robert Siekert Award from the American Heart Association, and his research has been funded by the NIH, American Academy of Neurology, American Heart Association(AHA). He has written over 100 publications in critical care neurology and stroke. His collaborative work is dedicated to the improved understanding of neurological disease in the critically ill.

 

Update: HydroSoft coil

HydroSoft coil

HydroSoft® Advanced Embolic Coils: Soft and Conformable

Fill and Finish with Hydrogel • Helical shape • Designed to seek out small spaces and deliver hydrogel at the aneurysm neck • Utilizes the V-Trak® Advanced delivery system for excellent softness and control

Clinically Studied • Hydrogel coils at the aneurysm neck may reduce aneurysm recurrence rates compared to bare platinum coils2 • Hydrogel provides a stable, bio-inert scaffolding to facilitate neointima formation across the neck

Ease of Use • Delivery characteristics similar to a bare platinum coil • No prepping or steaming • 30 minute working time • Compatible with 0.0165“ to 0.021” inner diameter microcatheters 1).

HydroSoft coil allowed Guo et al. to deploy coated coils with good packing density. A slight expansion of these coils at the neck can be expected to reduce neck remnant and potentially inhibit recurrence 2).


GEL THE NEC (GTN) was a multicenter prospective registry developed to assess the safety and efficacy of HydroSoft coils in treating intracranial aneurysms.

Dabus et al. compared the angiographic and clinical outcomes of aneurysms treated with balloon assisted coiling (BACE) versus unassisted coil embolization (CE) in the ruptured aneurysm cohort.

GTN was performed at 27 centers in five countries. Patients aged 21-90 years with a ruptured aneurysm 3-15 mm in size were eligible for enrollment.

They analyzed demographics/comorbidities, aneurysm location, and geometry, including maximum diameter, neck size, and dome to neck ratio, immediate and long term angiographic outcomes (graded by an independent core laboratory using the modified Raymond Scale), and procedure related adverse events. Angiographic and clinical outcomes were studied using χ2and t tests.

Of the 599 patients in the GTN, 194 met the inclusion criteria. 84 were treated with BACE and 110 with CE. There were more prior smokers in the BACE group (p=0.01). The BACE group also had more vertebrobasilar aneurysms (p=0.006) and a larger mean neck size (p=0.02). More aneurysms were immediately completely occluded in the BACE group (p=0.02) Procedure- related major morbidity and mortality were no different between the techniques (p=0.4 and p=1, respectively).

In this prospective ruptured aneurysm cohort from the GTN, BACE resulted in greater occlusion rates compared with unassisted CE with similar morbi-mortality 3).

2)

Guo XB, Fan YM, Zhang JN. HydroSoft coil versus HydroCoil for endovascular aneurysm occlusion study: a single center experience. Eur J Radiol. 2011 Aug;79(2):e42-6. doi: 10.1016/j.ejrad.2010.04.031. Epub 2010 May 26. PubMed PMID: 20537831.
3)

Dabus G, Brinjikji W, Amar AP, Delgado Almandoz JE, Diaz OM, Jabbour P, Hanel R, Hui F, Kelly M, Layton KF, Miller JW, Levy EI, Moran CJ, Suh DC, Woo H, Sellar R, Hoh B, Evans A, Kallmes DF. Angiographic and clinical outcomes of balloon remodeling versus unassisted coil embolization in the ruptured aneurysm cohort of the GEL THE NEC study. J Neurointerv Surg. 2017 Aug 18. pii: neurintsurg-2017-013326. doi: 10.1136/neurintsurg-2017-013326. [Epub ahead of print] PubMed PMID: 28821627.

Update: Temporalis muscle

Temporalis muscle

The temporal muscle, also known as the temporalis, is one of the muscles of mastication. It is a broad, fan-shaped muscle on each side of the head that fills the temporal fossa, superior to the zygomatic arch so it covers much of the temporal bone.

The skin flap is reflected forward to the level of the external auditory canal. The temporal muscle and the sternocleidomastoid muscles are exposed.

EAC: External auditory canal; ECM: Sternocleidomastoid muscle;TF: Temporal fascia.

When Gazi Yasargil first described standard techniques and procedures for pterional craniotomy (PC) in his publication in 1984, subgaleal dissection was used for separation and mobilization of the temporalis muscle. Because subgaleal dissection of the temporalis muscle bears significant risk of injury to the frontal branches of the facial nerve, various surgical techniques have been adopted such as interfascial and subfascial dissection. However, interfascial dissection is somewhat complex and time-consuming, and, because the facial nerve sometimes courses into the interfascial space, it still cannot eliminate the risk of facial nerve injury. Subfascial dissection is also time-consuming, and may result in injury to muscle fibers and intramuscular bleeding. These two techniques require transection of the temporalis muscle to leave a cuff for closure, which causes functional and cosmetic problems by muscle fibrosis and atrophy.

In neurosurgical procedures, avoiding damage of surrounding tissues such as muscle and periosteum during a craniotomy is important for esthetic and other reasons.

Matano et al. devised a protection tool using an amputated syringe barrel to cover the perforating drill and protect temporal muscle damage. This device made it possible to prevent damage to surrounding tissues, such as the muscle and periosteum, during cranial perforation. This method could be useful as it is cost-effective, simple, and versatile 1).


Effect of reflection of temporalis muscle has not been systematically researched. Thirty-nine patients were enrolled to assess the effect of reflection of temporalis muscle during cranioplasty CP after STC. Cranial index of symmetry was adopted to evaluate the aesthetic results, transcranial Doppler was used to assess change of cerebral blood flow (CBF), functional independence measurements were performed to monitor the improvement of neuronal function, and complications associated with CP were also recorded. The results displayed that reflection of temporalis muscle or not had no effect on the anesthetic results. Both operation ways could improve CBF and neuronal function. Cranioplasty with reflection of temporalis muscle could improve CBF and neuronal function more significantly. Furthermore, reflection of temporalis muscle would not increase complications associated with CP. Reflection of temporalis muscle during CP with titanium mesh after STC proves to be an effective and safe operation way 2).


Pterional craniotomy (PC) using myocutaneous (MC) flap is a simple and efficient technique; however, due to subsequent inferior displacement (ID) of the temporalis muscle, it can cause postoperative deformities of the muscle such as depression along the inferior margin of the temporal line of the frontal bone (DTL) and muscular protrusion at the inferior portion of the temporal fossa (PITF). Herein, we introduce a simple method for reconstruction of the temporalis muscle using a contourable strut plate (CSP) and evaluate its efficacy. Patients at follow-ups between January 2014 and October 2014 after PCs were enrolled in this study. Their postoperative deformities of the temporalis muscle including ID, DTL, and PITF were evaluated. These PC cases using MC flap were classified according to two groups; one with conventional technique without CSP (MC Only) and another with reconstruction of the temporalis muscle using CSP (MC + CSP). Statistical analyses were performed for comparison between the two groups.  Lower incidences of ID of the muscle (p < 0.001), DTL (p < 0.001), and PITF (p = 0.001) were observed in the MC + CSP than in the MC Only group. The incidence of acceptable outcome was markedly higher in the MC + CSP group (p < 0.001). ID was regarded as a causative factor for DTL and PITF (p < 0.001 in both). Reconstruction of the temporalis muscle using CSP after MC flap is a simple and efficient technique, which provides an outstanding outcome in terms of anatomical restoration of the temporalis muscle 3).


The minipterional craniotomy (MPT) provides a reliable and less invasive alternative to the standard pterional craniotomy. Furthermore, ruptured and unruptured anterior circulation aneurysms can safely and effectively be treated with limited bone removal which provides better cosmetic outcomes and excellent postoperative temporalis muscle function 4).

1)

Matano F, Mizunari T, Koketsu K, Fujiki Y, Kubota A, Kobayashi S, Murai Y, Morita A. Protection device made of amputated syringe for muscle protection during cranial perforation: a technical note. World Neurosurg. 2016 Jan 7. pii: S1878-8750(16)00002-4. doi: 10.1016/j.wneu.2016.01.001. [Epub ahead of print] PubMed PMID: 26773982.

2)

Jin Y, Jiang J, Zhang X. Effect of Reflection of Temporalis Muscle During Cranioplasty With Titanium Mesh After Standard Trauma Craniectomy. J Craniofac Surg. 2016 Jan;27(1):145-9. doi: 10.1097/SCS.0000000000002336. PubMed PMID: 26674916.

3)

Park JH, Lee YS, Suh SJ, Lee JH, Ryu KY, Kang DG. A Simple Method for Reconstruction of the Temporalis Muscle Using Contourable Strut Plate after Pterional Craniotomy: Introduction of the Surgical Techniques and Analysis of Its Efficacy. J Cerebrovasc Endovasc Neurosurg. 2015 Jun;17(2):93-100. doi: 10.7461/jcen.2015.17.2.93. Epub 2015 Jun 30. PubMed PMID: 26157688; PubMed Central PMCID: PMC4495087.

4)

Alkhalili KA, Hannallah JR, Alshyal GH, Nageeb MM, Abdel Aziz KM. The minipterional approach for ruptured and unruptured anterior circulation aneurysms: Our initial experience. Asian J Neurosurg. 2017 Jul-Sep;12(3):466-474. doi: 10.4103/1793-5482.180951. PubMed PMID: 28761525; PubMed Central PMCID: PMC5532932.

Update: A1 segment hypoplasia

Anterior cerebral artery A1 segment hypoplasia is an uncommon fetal variant of the circle of Willis.

There is an association of unilaterally absent or hypoplastic A1 segments of the anterior cerebral artery with ipsilateral decrease in internal carotid artery (ICA) caliber, and this can be seen on MR angiograms 1).

Epidemiology

Hypoplasia of the proximal (A1) segment of the anterior cerebral artery (ACA) was examined in 50 human brains and on 8 selected carotid arteriograms. Hypoplasia has been found in 22% of the cases. Two types of this phenomenon exist, namely the mild and extreme hypoplasia. Mild hypoplasia has been noticed in 14% of the specimens. The hypoplastic vessel has ranged from 1.3 to 1.9 mm in diameter (average 1.6 mm) and it was from 0.6 to 0.9 mm smaller than the opposite A1 portion. Extremely hypoplastic proximal segment has been present in 8% of the cases. It has varied from 0.3 to 1.1 mm in size (average 0.9 mm) and has been more than 1 mm smaller than the opposite proximal segment. Both mild and extreme hypoplasia have been associated in 81.8% of the cases with the corresponding variations or malformations of the anterior cerebral, posterior cerebral, posterior communicating and basilar arteries 2).

The incidence of right-sided A1 segment hypoplasia either accompanied with AcomA aneurysm or not was much greater than that of left-sided. Intracranial AcomA aneurysm development appeared to be associated with A1 segment hypoplasia 3).

Complications

The A1 segment of the anterior cerebral artery is a principal supplier of anterior collateral blood flow.

The aim of a study was to determine whether A1 segment hypoplasia may be responsible for acute ischemic stroke.

Chuang et al. consecutively examined 280 acute ischemic stroke patients (aged 66.9 +/- 14.2 years). Cerebral magnetic resonance angiography was performed within 72 h of ischemic stroke onset. The overall incidence of A1 variation in our experimental group was 15.0% (n = 42, agenesis/hypoplasia = 18/24), which was statistically higher than in the control group (n = 12). The majority (n = 30, 71.42%) had ipsilateral striatal lacunar infarctions. Based on these results, A1 agenesis/hypoplasia appears to be a risk factor contributing to ischemic stroke, especially to strokes in arteries penetrating the striatal area 4).

Yamaguchi et al. report two cases of bilateral anterior cerebral artery (ACA) territory infarction. On magnetic resonance (MR) angiograms, the A1 segment of the ACA was unilaterally hypoplastic in both cases, suggesting that unilateral hypoplasia of A1 is a significant predisposing factor for this rare type of cerebral infarction. When the contralateral A1 is dominant, embolic materials may enter into it more easily 5).


Hypoplasia of the A1 segment of the anterior cerebral artery is frequently observed in patients with anterior communicating artery aneurysms. The effect of this anatomical variant on ACoA aneurysm morphology is not well understood 6).

Case series

2017

Yang et al. retrospectively reviewed 251 patients with ACoA aneurysm who underwent surgical clipping in Beijing Tiantan Hospital between September 2011 and September 2016. Their clinical and radiologic features, as well as clinical outcomes were reviewed. In addition, univariate and multivariate logistic regression analysis was performed to identify independent risk factors for the postoperative infarction and unfavorable clinical outcomes of surgical clipping ACoA aneurysm.

The incidence of A1 segment hypoplasia was 49.8% (125 of 251 patients). Univariate analysis revealed that multiple aneurysm (P=0.025), diameter of aneurysm (P=0.040) and A1 segment hypoplasia (P=0.010) were associated with anterior cerebral artery (ACA) territories infarction, and A1 segment hypoplasia (P=0.002) is significantly correlated with unfavorable clinical outcomes of surgical clipping ACoA aneurysm. Moreover, multivariate analysis showed that multiple aneurysm (P=0.038, OR=2.571), diameter of aneurysm (P=0.034, OR=1.097) and A1 segment hypoplasia (P=0.007, OR=3.619) were strongly independent risk factors for ACA territories infarction. In addition, Hunt and Hess scores (HH) (P=0.036, OR=2.326) and A1 segment hypoplasia (P=0.002, OR=2.873) are significant independent risk factors for unfavorable clinical outcomes of surgical clipping ACoA aneurysm.

A1 segment hypoplasia is a significant independent risk factor for unfavorable clinical outcomes of surgical clipping ACoA aneurysm and ACA infarction after surgery 7).

Case reports

2016

A case of anterior cerebral artery A1 segment hypoplasia syndrome presenting with right lower limb monoplegia, abulia, and urinary incontinence8).

2000

A 68-year-old man presented with a Hunt and Hess Grade II subarachnoid hemorrhage and symptoms of headache, nuchal rigidity, and facial paresis. : Angiographic evaluation with superselective exploration revealed a small ruptured aneurysm located on a duplicated hypoplastic A1 segment of the left anterior cerebral artery with associated middle cerebral artery stenosis and secondary early moyamoya changes. Surgical clipping of the aneurysm was performed successfully while sparing the hypoplastic A1 segment.

A1 aneurysms occurring on a duplicated anterior cerebral artery segment probably develop from a congenital weakness of the parent vessel and increased local shear stress. Superselective angiography was helpful in the preoperative planning and facilitated the decision to treat with surgical clipping instead of embolization 9).

1)

Kane AG, Dillon WP, Barkovich AJ, Norman D, Dowd CF, Kane TT. Reduced caliber of the internal carotid artery: a normal finding with ipsilateral absence or hypoplasia of the A1 segment. AJNR Am J Neuroradiol. 1996 Aug;17(7):1295-301. PubMed PMID: 8871715.
2)

Marinković S, Kovacević M, Milisavljević M. Hypoplasia of the proximal segment of the anterior cerebral artery. Anat Anz. 1989;168(2):145-54. PubMed PMID: 2712326.
3)

Chen H, Li MH. A1 segment hypoplasia accompanied by AcomA aneurysms assessed with magnetic resonance angiography. Surg Radiol Anat. 2014 May;36(4):353-7. doi: 10.1007/s00276-013-1182-5. Epub 2013 Aug 4. PubMed PMID: 23912562.
4)

Chuang YM, Liu CY, Pan PJ, Lin CP. Anterior cerebral artery A1 segment hypoplasia may contribute to A1 hypoplasia syndrome. Eur Neurol. 2007;57(4):208-11. Epub 2007 Jan 19. PubMed PMID: 17268201.
5)

Yamaguchi K, Uchino A, Sawada A, Takase Y, Kuroda Y, Kudo S. Bilateral anterior cerebral artery territory infarction associated with unilateral hypoplasia of the A1 segment: report of two cases. Radiat Med. 2004 Nov-Dec;22(6):422-5. PubMed PMID: 15648459.
6)

Rinaldo L, McCutcheon BA, Murphy M, Bydon M, Rabinstein AA, Lanzino G. 360 Relationship of A1 Segment Hypoplasia to Anterior Communicating Artery Aneurysm Morphology and Risk Factors for Rupture. Neurosurgery. 2016 Aug;63 Suppl 1:207. doi: 10.1227/01.neu.0000489849.55193.67. PubMed PMID: 27399558.
7)

Yang F, Li H, Wu J, Li M, Chen X, Jiang P, Li Z, Cao Y, Wang S. Relationship of A1 segment hypoplasia to the radiological and clinical outcomes of surgical clipping anterior communicating artery aneurysm. World Neurosurg. 2017 Jul 29. pii: S1878-8750(17)31222-6. doi: 10.1016/j.wneu.2017.07.122. [Epub ahead of print] PubMed PMID: 28765030.
8)

Lakhotia M, Pahadiya HR, Prajapati GR, Choudhary A, Gandhi R, Jangid H. A case of anterior cerebral artery A1 segment hypoplasia syndrome presenting with right lower limb monoplegia, abulia, and urinary incontinence. J Neurosci Rural Pract. 2016 Jan-Mar;7(1):189-91. doi: 10.4103/0976-3147.168438. PubMed PMID: 26933381; PubMed Central PMCID: PMC4750332.
9)

Taylor R, Connolly ES Jr, Duong H. Radiographic evidence and surgical confirmation of a saccular aneurysm on a hypoplastic duplicated A1 segment of the anterior cerebral artery: case report. Neurosurgery. 2000 Feb;46(2):482-4. PubMed PMID: 10690739.

Update: Anterior communicating artery aneurysm 

Epidemiology

The anterior communicating artery aneurysm cause aneurysmal subarachnoid hemorrhage, in about 21.0%~25.5% of spontaneous subarachnoid hemorrhage 1) 2) 3).

Saccular aneurysms are most common in the anterior communicating artery (ACoA).

Frequently it is a wide necked aneurysm with an irregular shape, incorporate parent vessels, and are associated with significant variations in vascular anatomy.


The most common site of rupture of very small intracranial aneurysms was the anterior communicating artery (ACoA). Rupture of small and very small aneurysms is unpredictable, and treatment may be considered in selected high-risk patients according to factors such as young age, ACoA location, and hypertension 4).

Classification

Anterior communicating artery aneurysms frequently present wide aneurysm necks and incorporate parent vessels. They are associated with significant variations in vascular anatomy, especially hypoplasia or aplasia of one of the proximal anterior cerebral artery.

Morphological Scoring System of Choi


Very small intracranial aneurysm (< 3 mm)

Small intracranial aneurysm (< 5 mm)

Medium sized intracranial aneurysm (5-9.9 mm)

Large or Giant intracranial aneurysm (> 10 mm)


According to 2D-DSA, the points of aneurysm are divided into 5 types 5) 6).

Chen et al., classified as Type I, II (IIa, IIb), III and IV, based on the various projections and size of aneurysm. The principle for the choice of operative side was designed based on the type of aneurysm and the A2 fork orientation (the interrelations between the plane of bilateral A2, AComA, and mid-saggital plane) 7).

Small aneurysms located at the anterior communicating artery carry significant procedural challenges due to a complex anatomy.

Inferior or downward direction

Posterior or backward direction

Etiology

In clinic, it’s very common to find out the unequal development of section A1 of anteromedial brain artery. The resulting hemodynamic changes are considered to be one of the main reasons for the formation of anterior communicating artery aneurysms 8).

Rupture risk

Vascular imaging was evaluated with 3D Slicer© to generate models of the aneurysms and surrounding vasculature. Morphological parameters were examined using univariate and multivariate analysis and included aneurysm volume, aspect ratio, size ratio, distance to bifurcation, aneurysm angle, vessel angle, flow angle, and parent-daughter angle. Multivariate logistic regression revealed that size ratio, flow angle, and parent-daughter angle were associated with aneurysm rupture after adjustment for age, sex, smoking history, and other clinical risk factors. Simple morphological parameters such as size ratio, flow angle, and parent-daughter angle may thus aid in the evaluation of rupture risk of anterior communicating artery aneurysms 9).

Clinical features

These aneurysms are usually silent until they rupture.

Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction.

Neurologic deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), brain hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe signs (20%).

Visual symptoms

The AComA aneurysms rupture before becoming large enough to compress visual pathways, hence they present with aneurysmal subarachnoid hemorrhage rather than visual symptoms 10).

Giant AComA aneurysms are extremely rare and may present with vision loss 11).

Visual apparatus compression can occur from giant AComA aneurysm directed posteriorly and inferiorly 12).

The pattern of visual loss in these cases is variable. The common pattern of visual loss is bilateral field deficits.

The other patterns of visual loss due to AComA aneurysms are central scotoma, bilateral heteronymous deficits, monocular or binocular inferior field loss, asymmetrical bitemporal hemianopsia, and incongruous homonymous hemianopsia 13).

Diagnosis

Weisberg reviewed the CT findings in 40 patients with ruptured aneurysms of the anterior cerebral or anterior communicating arteries. Within 3 days of the ictus, the common patterns included blood in the pericallosal cistern and interhemispheric fissure, blood in the caval-septal region, unilateral or bilateral frontal hematoma, and diffuse symmetric intraventricular and basal cisternal blood 14).

For CT classification see the Modified Fisher scale.

Treatment

Endovascular coiling (EC) resulted in a more favorable clinical outcome, and microsurgical clipping (MC) resulted in more robust aneurysm repair, for unruptured ACoA aneurysms. Stent assisted coiling (SAC) had a higher treatment morbidity risk than EC, without reduction in retreatment rate. All treatments were effective in preventing SAH. The current pooled analysis of treatment outcomes provides a useful aid to pretreatment clinical decision making 15).

Endovascular treatment

Surgery

Complications

Cognitive deficits

In a retrospective follow-up study covering a time period of four years 18 patients operated upon early for an aneurysm of the anterior communicating artery (ACoA) and a control group of 21 patients with aneurysmal subarachnoid haemorrhage (SAH) from other sources than ACoA aneurysm and 9 patients with SAH of nonaneurysmal origin were subjected to neuropsychological examination. Both groups were comparable in their neurological condition on admission and in the severity of bleeding seen on CT-scan. Testing included memory functions, concentration, logical and spatial thinking, a Stroop-test, an aphasia screening test and a complex choice reaction task. Patients with SAH of a ruptured ACoA aneurysm did not differ significantly from the control group in any of the tests used. But there was a trend for the ACoA patients to have more memory problems than the patients with SAH of other origins. On the other hand the patients in the control group with aneurysmal SAH of other locations and with non-aneurysmal SAH had not significantly more problems with concentration and aphasia than the patients with ruptured ACoA aneurysm. These results, which differ from the common opinion of frequent occurrence of memory deficits in ACoA aneurysms are interpreted as a consequence of the changes in improved pre-, intra- and postoperative management in modern neurosurgery 16).

Case series

2017

Digital subtraction angiography images were reviewed for 204 patients with either a ruptured or an unruptured ACoA aneurysm. The ratio of the width of the larger A1 segment of the anterior cerebral artery to the smaller A1 segment was calculated. Patients with an A1 ratio greater than 2 were categorized as having A1 segment hypoplasia. The relationship of A1 segment hypoplasia to both patient and aneurysm characteristics was then assessed.

Of 204 patients that presented with an ACoA aneurysm, 34 (16.7%) were found to have a hypoplastic A1. Patients with A1 segment hypoplasia were less likely to have a history of smoking (44.1% vs 62.9%, p = 0.0410). ACoA aneurysms occurring in the setting of a hypoplastic A1 were also found to have a larger maximum diameter (mean 7.7 vs 6.0 mm, p = 0.0084). When considered as a continuous variable, increasing A1 ratio was associated with decreasing aneurysm dome-to-neck ratio (p = 0.0289). There was no significant difference in the prevalence of A1 segment hypoplasia between ruptured and unruptured aneurysms (18.9% vs 10.7%; p = 0.1605).

The results suggest that a hypoplastic A1 may affect the morphology of ACoA aneurysms. In addition, the relative lack of traditional risk factors for aneurysm formation in patients with A1 segment hypoplasia argues for the importance of hemodynamic factors in the formation of ACoA aneurysms in this anatomical setting 17).


Between January 2008 and May 2016, information on 179 consecutive patients with unruptured AcoA aneurysms was obtained and included demographic data, aneurysm features, risk factors for formation and rupture, treatment type, complications, and follow-up information. A 2-tailed t test was used for continuous data and the chi-square test for categorical variables. Statistical significance was set at P value < 0.05.

There were 76 patients 65 and older (42.5%) and 103 younger than 65 (57.5%). Conservative management was more common in older patients (67.1% vs 41.7%, P=0.001). Endovascular treatment was more commonly used in the older population (80% vs 61% of the treated aneurysms in older and younger group, P=0.16). Treatment-related complications were 8% but resulted in permanent neurological deficits in one patient (1.2%). Among conservatively treated aneurysms, three (3.2%) ruptured at follow-up resulting in patient death in two cases (2.4%). All three ruptures occurred in elderly patients.

With a modern approach that emphasizes endovascular therapy, especially in older individuals, unruptured AcoA aneurysms can be treated with a very low morbidity. Among patients with small aneurysms for which treatment was not deemed indicated or necessary, the rate of rupture at follow-up was not negligible, with 5.8% of older patients experiencing bleeding from the aneurysm 18).


Colby et al., retrospectively reviewed an IRB-approved database of patients with an aneurysm at a single institution for patients with ACoA or A1-A2 aneurysms treated with PED. Data analyzed included demographics, aneurysm characteristics, procedural details, follow-up results, and outcomes.

A total of 50 procedures were performed on 41 patients, including seven patients who underwent bilateral ‘H-pipe’ PED placement. The average age was 56 years and 46% of the patients were female. The average aneurysm size was 4.5 mm, and two large (>10 mm) aneurysms were treated. The vessel of origin was either the ACoA (26 aneurysms, 63%) or the A1-A2 junction (15 aneurysms, 37%). Eighteen patients (44%) had prior subarachnoid hemorrhage and 20 had previously been treated either with clipping (6 aneurysms, 15%) or coiling (14 aneurysms, 34%). Procedural success was achieved in 48/50 cases (96%) and two cases were aborted. Coils were deployed adjunctively in two cases (4%). Procedural outcomes included no deaths, one major ischemic stroke (2%), and two patients with intracranial hemorrhage (4%). Complete aneurysm occlusion was achieved in 81% of patients at 6 months and 85% of patients at last follow-up digital subtraction angiography.

The PED can be used safely and effectively in the treatment of aneurysms of the ACoA region. This represents a good alternative treatment option to microsurgical clipping and endovascular coiling 19).

2016

A prospectively maintained single-institution neuroendovascular database was accessed to identify consecutive cases of very small (<3 mm) ruptured anterior communicating artery aneurysms treated endovascularly between 2006 and 2013.

A total of 20 patients with ruptured very small (<3 mm) anterior communicating artery aneurysms were consecutively treated with coil embolization. The average maximum diameter was 2.66 ± 0.41 mm. Complete aneurysm occlusion was achieved for 17 (85%) aneurysms and near-complete aneurysm occlusion for 3 (15%) aneurysms. Intraoperative perforation was seen in 2 (10%) patients without any clinical worsening or need for an external ventricular drain. A thromboembolic event occurred in 1 (5 %) patient without clinical worsening or radiologic infarct. Median clinical follow-up was 12 (±14.1) months and median imaging follow-up was 12 (±18.4) months.

This report describes the largest series of consecutive endovascular treatments of ruptured very small anterior communicating artery aneurysms. These findings suggest that coil embolization of very small aneurysms in this location can be performed with acceptable rates of complications and recanalization 20).


Between January 2008 and February 2015, 254 consecutive patients with 255 ACoA aneurysms were treated with coiling. We retrospectively reviewed intraoperative angiograms and medical records to identify intraprocedural rupture and thrombus formation, and re-measured aneurysm morphologies using CT angiography images. Multivariate logistic regression models were used to determine independent predictors of intraprocedural rupture and thrombus formation.

Of the 231 patients included, intraprocedural rupture occurred in 10 (4.3%) patients, and thrombus formation occurred in 15 (6.5%) patients. Patients with smaller aneurysms more often experienced intraprocedural rupture than those with larger aneurysms (3.5±1.3 mm vs 5.7±2.3 mm). Multivariate analysis showed that smaller ruptured aneurysms (p=0.003) were independently associated with intraprocedural rupture. The threshold of aneurysm size separating rupture and non-rupture groups was 3.5 mm. Multivariate analysis showed that a history of hypertension (p=0.033), aneurysm neck size (p=0.004), and parent vessel angle (p=0.023) were independent predictors of thrombus formation. The threshold of parent vessel angle separating thrombus and non-thrombus groups was 60.0°.

Ruptured aneurysms <3.5 mm were associated with an increased risk of intraprocedural rupture, and parent vessel angle <60.0°, wider-neck aneurysms, and a history of hypertension were associated with increased risk of thrombus formation during coiling of ruptured ACoA aneurysms21).

2009

In 33 cases among 351 cases of ruptured anterior communicating artery aneurysms treated surgically, from 1991 to 2000, the dome of aneurysm was compressed in optic pathway. In some cases, aneurysm impacted into the optic nerve that deep hollowness was found when the aneurysm sac was removed during operation. Among 33 cases, 10 cases presented with preoperative visual symptoms, such as visual dimness (5), unilateral visual field defect (2) or unilateral visual loss (3), 20 cases had no visual symptoms. Visual symptoms could not be checked in 3 cases due to the poor mental state. In 6 cases among 20 cases having no visual symptoms, optic nerve was deeply compressed by the dome of aneurysm which was seen in the surgical field. Of 10 patients who had visual symptoms, 8 showed improvement in visual symptoms within 6 months after clipping of aneurysms. In 2 cases, the visual symptoms did not recover.

Anterior communicating artery aneurysm can cause visual symptoms by compressing the optic nerve or direct rupture to the optic nerve with focal hematoma formation. Park et al., emphasize that cerebral vascular study is highly recommended to detect intracranial aneurysm before its rupture in the case of normal CT findings with visual symptoms and frequent headache 22).

2003

A prospective study included 223 patients who were divided into three groups: Group A (83 microsurgically treated patients, 1990-1995); Group B (103 microsurgically treated patients, 1996-2000); and Group C (37 patients treated with Guglielmi Detachable Coil [GDC] embolization, 1996-2000). Depending on the direction in which the aneurysm fundus projected, the authors attempted to apply microsurgical treatment to Type 1 aneurysms (located in front of the axis formed by the pericallosal arteries). They proposed the most adapted procedure for Type 2 aneurysms (located behind the axis of the pericallosal arteries) after discussion with the neurovascular team, depending on the physiological status of the patient, the treatment risk, and the size of the aneurysm neck. In accordance with the classification of Hunt and Hess, the authors designated those patients with unruptured aneurysms (Grade 0) and some patients with ruptured aneurysms (Grades I-III) as having good preoperative grades. Patients with Grade IV or V hemorrhages were designated as having poor preoperative grades. By performing routine angiography and computerized tomography scanning, the causes of unfavorable outcome (Glasgow Outcome Scale [GOS] score < 5) and the morphological results (complete or incomplete occlusion) were analyzed. Overall, the clinical outcome was excellent (GOS Score 5) in 65% of patients, good (GOS Score 4) in 9.4%, fair (GOS Score 3) in 11.6%, poor (GOS Score 2) in 3.6%, and fatal in 10.3% (GOS Score 1). Among 166 patients in good preoperative grades, an excellent outcome was observed in 134 patients (80.7%). The combined permanent morbidity and mortality rate accounted for up to 19.3% of patients. The rates of permanent morbidity and death that were related to the initial subarachnoid hemorrhage were 6.2 and 1.5% for Group A, 6.6 and 1.3% for Group B, and 4 and 4% for Group C, respectively. The rates of permanent morbidity and death that were related to the procedure were 15.4 and 1.5% for Group A, 3.9 and 0% for Group B, and 8 and 8% for Group C, respectively. When microsurgical periods were compared, the rate of permanent morbidity or death related to microsurgical complications decreased significantly (Group A, 11 patients [16.9%] and Group B, three patients [3.9%]); Fisher exact test, p = 0.011) from the period of 1990 to 1995 to the period of 1996 to 2000. The combined rate of morbidity and mortality that was related to the endovascular procedure (16%) explained the nonsignificance of the different rates of procedural complications for the two periods, despite the significant decrease in the number of microsurgical complications. Among 57 patients in poor preoperative grade, an excellent outcome was observed in 11 patients (19.3%); however, permanent morbidity (GOS Scores 2-4) or death (GOS Score 1) occurred in 46 patients (80.7%). With regard to the correlation between vessel occlusion (the primary microsurgical complication) and the morphological characteristics of aneurysms, only the direction in which the fundus projected appeared significant as a risk factor for the microsurgically treated groups (Fisher exact test: Group A, p = 0.03; Group B, p = 0.002). The difference between endovascular and microsurgical procedures in the achievement of complete occlusion was considered significant (chi2 = 6.13, p = 0.01).

The direction in which the fundus projects was chosen as the morphological criterion between endovascular and surgical methods. The authors propose that microsurgical clip application should be the preferred option in the treatment of ACoA aneurysms with anteriorly directed fundi and that endovascular packing be selected for those lesions with posteriorly directed fundi, depending on morphological criteria 23).

Case reports

2016

Cohen et al., describe a technique for T-configured stent-assisted coiling in the management of ruptured wide-necked AcomA aneurysms by means of two simultaneous microsystems that allowed placement of two nitinol self-expandable Leo+ Baby stents (Balt Therapeutics, Montmorency, France) followed by coiling. Technical details and comparison to other dual stent configurations were presented and briefly discussed 24).


A 69-year-old male without a past history of mental disorders and neurological symptoms presented with a 2-month history of anxiety, sadness, lack of pleasure in usual activities, fatigue, difficulties falling asleep and waking up early in the morning, reduced appetite, and weight loss. The patient was diagnosed with major depressive disorder and antidepressant treatment was initiated. Subsequent non-contrast computed tomography (CT) of the head demonstrated hypointense oval-shaped lesion within the projection of the anterior communicating artery. CT angiography confirmed the diagnosis of a 0.8 × 0.6 cm saccular aneurysm originating from the anterior communicating artery and anterior cerebral artery. The patient underwent microsurgical clipping of the aneurysm. On psychiatric assessment 1 month after the surgery, there were no signs of depressive disorder and antidepressive treatment was discontinued. On follow-up visit 1 year after the surgery, the patient did not have any mood symptoms.

The case indicates that organic brain lesions, including intracranial aneurysms, should be suspected in elderly patients presenting with their first episode of mental disorder 25).

2015

Seung et al., present an unusual case of bitemporal hemianopsia caused by a large intracranial aneurysm of the ACoA. A 41-year-old woman was admitted to our neurosurgical department with a sudden-onset bursting headache and visual impairment. On admission, her vision was decreased to finger counting at 30 cm in the left eye and 50 cm in the right eye, and a severe bitemporal hemianopsia was demonstrated on visual field testing. A brain computed tomography scan revealed a subarachnoid hemorrhage at the basal cistern, and conventional cerebral catheter angiography of the left internal carotid artery demonstrated an 18×8 mm dumbbell-shaped aneurysm at the ACoA. Microscopic aneurysmal clipping was performed. An ACoA aneurysm can produce visual field defects by compressing the optic chiasm or nerves. We emphasize that it is important to diagnose an aneurysm through cerebrovascular study to prevent confusing it with pituitary apoplexy 26).


A 55-year-old man presented with a 3-year history of visual impairment associated with personality changes. His sister had died after an intracerebral aneurysmal rupture. An examination revealed poor visual acuity in the right eye with a field defect, as well as impaired neurocognition. Computed tomographic (CT) angiography (Panel A) and magnetic resonance imaging of the brain revealed a partially thrombosed, calcified, 7-cm aneurysm of the anterior communicating artery, with surrounding edema (Panel B). Thrombectomy and aneurysmal repair were performed to reduce the risk of aneurysmal rupture and to alleviate the mass effect. The patient recovered from surgery and had improvement in his neurocognitive deficits and vision, and he was able to return to work. His condition remained stable 2 years later, and delayed CT showed collapse of the aneurysmal sac (Panel C). Giant aneurysms (>2.5 cm) represent a small proportion of brain aneurysms but are associated with a high rupture rate when left untreated. Approximately 20% of patients with a brain aneurysm have a first-degree relative with a brain aneurysm 27).

1988

A study reports the case of a 42-year-old man who suffered a ruptured aneurysm of the anterior communicating artery. His memory capabilities were assessed after a considerable recovery period during which many of his memory deficits ameliorated. His scan revealed a left frontal lesion and many of his deficits were characteristic of frontal impairment. He was impaired on temporal discrimination, and he showed marked source forgetting. He also performed badly on the Brown-Peterson task, and we suggest that this is another task that may be characteristic of frontal impairment. In contrast, the patient showed normal or near normal performance on some memory tasks but not on others. It is concluded that the patient’s frontal signs are similar to those found in Korsakoff’s Syndrome, but that his memory impairment is qualitatively different from that encountered in patients with the amnesic syndrome 28).

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Suzuki M, Fujisawa H, Ishihara H, Yoneda H, Kato S, Ogawa A. Side selection of pterional approach for anterior communicating artery aneurysms–surgical anatomy and strategy. Acta Neurochir (Wien) 2008;150:31–39. 39.
2)

Kimura T, Morita A, Shirouzu I, Sora S. Preoperative evaluation of unruptured cerebral aneurysms by fast imaging employing steady-state acquisition image. Neurosurgery. 2011;69:412–419. discussion 419-420.
3)

Kwon SC, Park JB, Shin SH, Sim HB, Lyo IU, Kim Y. The Efficacy of Simultaneous Bilateral Internal Carotid Angiography during Coil Embolization for Anterior Communicating Artery Aneurysms. J Korean Neurosurg Soc. 2011;49:257–261
4)

Lee GJ, Eom KS, Lee C, Kim DW, Kang SD. Rupture of Very Small Intracranial Aneurysms: Incidence and Clinical Characteristics. J Cerebrovasc Endovasc Neurosurg. 2015 Sep;17(3):217-22. doi: 10.7461/jcen.2015.17.3.217. Epub 2015 Sep 30. PubMed PMID: 26526401; PubMed Central PMCID: PMC4626345.
5)

Choi JH, Kang MJ, Huh JT. Influence of clinical and anatomic features on treatment decisions for anterior communicating artery aneurysms. J Korean Neurosurg Soc. 2011;50:81–88.
6)

Cohen JE, Gomori JM, Moscovici S, Itshayek E. Balloon-guided navigation technique to perform stenting in an acutely angled anterior cerebral artery. J Clin Neurosci. 2012;19:452–454.
7)

Chen L, Agrawal A, Kato Y, Karagiozov KL, Kumar MV, Sano H, Kanno T. Role of aneurysm projection in “A2” fork orientation for determining the side of surgical approach. Acta Neurochir (Wien). 2009 Aug;151(8):925-33; discussion 933. doi: 10.1007/s00701-009-0407-1. Epub 2009 Jun 5. PubMed PMID: 19499172.
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Okamoto S, Itoh A. Craniotomy side for neck clipping of the anterior communicating aneurysm via the pterional approach. No Shinkei Geka. 2002;30:285–291.
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Lin N, Ho A, Charoenvimolphan N, Frerichs KU, Day AL, Du R. Analysis of morphological parameters to differentiate rupture status in anterior communicating artery aneurysms. PLoS One. 2013 Nov 13;8(11):e79635. doi: 10.1371/journal.pone.0079635. eCollection 2013. PubMed PMID: 24236149; PubMed Central PMCID: PMC3827376.
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Kasner SE, Liu GT, Galetta S. Neuroophthalmologic aspects of aneurysms. Neuroimaging Clin N Am. 1997;7:679–92.
11)

Lownie SP, Drake CG, Peerless SJ, Ferguson GG, Pelz DM. Clinical presentation and management of giant anterior communicating artery region aneurysms. J Neurosurg. 2000;92:267–77.
12)

Shukla DP, Bhat DI, Devi BI. Anterior communicating artery aneurysm presenting with vision loss. J Neurosci Rural Pract. 2013 Jul;4(3):305-7. doi: 10.4103/0976-3147.118765. PubMed PMID: 24250165; PubMed Central PMCID: PMC3821418.
14)

Weisberg LA. Ruptured aneurysms of anterior cerebral or anterior communicating arteries: CT patterns. Neurology. 1985 Nov;35(11):1562-6. PubMed PMID: 4058745.
15)

O’Neill AH, Chandra RV, Lai LT. Safety and effectiveness of microsurgical clipping, endovascular coiling, and stent assisted coiling for unruptured anterior communicating artery aneurysms: a systematic analysis of observational studies. J Neurointerv Surg. 2016 Sep 13. pii: neurintsurg-2016-012629. doi: 10.1136/neurintsurg-2016-012629. [Epub ahead of print] Review. PubMed PMID: 27624158.
16)

Hütter BO, Gilsbach JM. Cognitive deficits after rupture and early repair of anterior communicating artery aneurysms. Acta Neurochir (Wien). 1992;116(1):6-13. PubMed PMID: 1615771.
17)

Rinaldo L, McCutcheon BA, Murphy ME, Bydon M, Rabinstein AA, Lanzino G. Relationship of A(1) segment hypoplasia to anterior communicating artery aneurysm morphology and risk factors for aneurysm formation. J Neurosurg. 2017 Jul;127(1):89-95. doi: 10.3171/2016.7.JNS16736. Epub 2016 Sep 30. PubMed PMID: 27689465.
18)

Cagnazzo F, Brinjikji W, Lanzino G. Effect of age on outcomes and practice patterns for patients with anterior communicating artery aneurysms. J Neurosurg Sci. 2017 Jan 12. doi: 10.23736/S0390-5616.16.03942-4. [Epub ahead of print] PubMed PMID: 28079351.
19)

Colby GP, Bender MT, Lin LM, Beaty N, Huang J, Tamargo R, Coon A. Endovascular flow diversion for treatment of anterior communicating artery region cerebral aneurysms: a single-center cohort of 50 cases. J Neurointerv Surg. 2017 Jan 27. pii: neurintsurg-2016-012946. doi: 10.1136/neurintsurg-2016-012946. [Epub ahead of print] PubMed PMID: 28130501.
20)

Asif KS, Sattar A, Lazzaro MA, Fitzsimmons BF, Lynch JR, Zaidat OO. Consecutive Endovascular Treatment of 20 Ruptured Very Small (<3 mm) Anterior Communicating Artery Aneurysms. Interv Neurol. 2016 Jun;5(1-2):57-64. doi: 10.1159/000444662. Epub 2016 Mar 22. PubMed PMID: 27610122; PubMed Central PMCID: PMC4934484.
21)

Fan L, Lin B, Xu T, Xia N, Shao X, Tan X, Zhong M, Yang Y, Zhao B. Predicting intraprocedural rupture and thrombus formation during coiling of ruptured anterior communicating artery aneurysms. J Neurointerv Surg. 2016 Apr 5. pii: neurintsurg-2016-012335. doi: 10.1136/neurintsurg-2016-012335. [Epub ahead of print] PubMed PMID: 27183655.
22)

Park JH, Park SK, Kim TH, Shin JJ, Shin HS, Hwang YS. Anterior communicating artery aneurysm related to visual symptoms. J Korean Neurosurg Soc. 2009 Sep;46(3):232-8. doi: 10.3340/jkns.2009.46.3.232. Epub 2009 Sep 30. PubMed PMID: 19844624; PubMed Central PMCID: PMC2764022.
23)

Proust F, Debono B, Hannequin D, Gerardin E, Clavier E, Langlois O, Fréger P. Treatment of anterior communicating artery aneurysms: complementary aspects of microsurgical and endovascular procedures. J Neurosurg. 2003 Jul;99(1):3-14. PubMed PMID: 12854737.
24)

Cohen JE, Moscovici S, El Hassan HA, Doron O, Itshayek E. T-microstent-assisted coiling in the management of ruptured wide-necked anterior communicating artery aneurysms: Choosing between Y, X and T. J Clin Neurosci. 2016 Aug 28. pii: S0967-5868(16)30102-3. doi: 10.1016/j.jocn.2016.08.006. [Epub ahead of print] PubMed PMID: 27578527.
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Bunevicius A, Cikotas P, Steibliene V, Deltuva VP, Tamsauskas A. Unruptured anterior communicating artery aneurysm presenting as depression: A case report and review of literature. Surg Neurol Int. 2016 Aug 1;7(Suppl 18):S495-8. doi: 10.4103/2152-7806.187489. eCollection 2016. PubMed PMID: 27583172; PubMed Central PMCID: PMC4982348.
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Seung WB, Kim DY, Park YS. A Large Ruptured Anterior Communicating Artery Aneurysm Presenting with Bitemporal Hemianopsia. J Korean Neurosurg Soc. 2015 Sep;58(3):291-3. doi: 10.3340/jkns.2015.58.3.291. Epub 2015 Sep 30. PubMed PMID: 26539276; PubMed Central PMCID: PMC4630364.
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Patel NJ, Filippidis A. IMAGES IN CLINICAL MEDICINE. A Giant Aneurysm of the Anterior Communicating Artery. N Engl J Med. 2015 Aug 6;373(6):560. doi: 10.1056/NEJMicm1413193. PubMed PMID: 26244309.
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Parkin AJ, Leng NR, Stanhope N, Smith AP. Memory impairment following ruptured aneurysm of the anterior communicating artery. Brain Cogn. 1988 Apr;7(2):231-43. PubMed PMID: 3377901.

Update: Adenosine-induced cardiac standstill with hypotension

Several flow-arrest techniques have been introduced for the treatment of complex aneurysms that cannot be treated with conventional clipping or endovascular coil embolization. Adenosine-induced transient asystole is an alternative method of flow arrest.

Adenosine-induced flow arrest briefly reduces cerebral perfusion pressure and reduces the turgor of the aneurysm, thereby facilitating the clip ligation in complex aneurysms. Periods of flow arrest have to be carefully coordinated with the surgeon such that necessary working time is available for aneurysm dissection and clip placement. Adenosine-induced transient asystole is safe and efficacious when administered at an average of 0.3 to 0.4 mg/kg IBW in combination with remifentanil/low-dose volatile anesthetic with propofol. The adenosine dose will achieve approximately 45 seconds of controlled systemic hypotension and a bloodless surgical field. Adenosine offers the advantage of easy applicability in different situations without advanced preparation or complex logistical coordination with anesthesiology and cardiovascular surgery. This technique also allows the surgeon to have the maximum amount of space available to manipulate the aneurysm and place the clips, as no temporary clips are in the field of view. Also, temporary clips only decrease flow from the clipped inflow, whereas adenosine produces a more global hypotension and therefore often a better collapse of the aneurysm 1).

Adenosine-induced asystole for cerebral aneurysms surgery was first described by Groff et al. 2) in 1999 in posterior circulation aneurysms.

It is an easily applied technique in a variety of clinical situations. Its use requires minimal advanced preparation and no complex logistical coordination with other subspecialties. However, patient-specific dose-response relationships must be determined by exposure, so the relationship may not be known in an emergent situation. Persistent hypotension is a potentially major complication. Rapid ventricular pacing (RVP) has recently been reintroduced into cerebrovascular surgery. It is more predictable than adenosine in response time and, thus, can be used during unanticipated complications, such as aneurysmal rupture. It also induces a shorter period of hypotension compared with adenosine. However, RVP is more invasive and more complex from an anesthesia standpoint. Vascular neurosurgeons should be familiar with these techniques and know their applications and limitations 3).

Case series

2017

The aim of a study is to report the experience in the use of adenosine in aneurysm clipping and arteriovenous malformation (AVM) resection and review the literature. The records of all patients who had adenosine-assisted clipping of intracranial aneurysms and AVM resections between November 2015 and December 2016 were extracted from prospectively maintained database. The following data were collected: patient demographics, comorbidities, size and location of the aneurysms or AVM, number of boluses and total dose of adenosine administered, duration of cardiac standstill and hypotension (systolic blood pressure < 60 mmHg), intraoperative and postoperative complications and outcome scores at discharge. Literature search on Embase and PubMed for the terms “adenosine and clipping”, “adenosine and aneurysm” and “adenosine and AVM” was performed. Eight aneurysms and two AVMs were identified. While both AVMs were elective procedures, half of the aneurysm clippings were on urgent basis.

Al-Mousa et al. used adenosine safely with spontaneous return of rhythm in all cases. Temporary clips to the parent artery were applied for brief periods in 2 patients who had pre-adenosine intraoperative rupture. They did not observe any immediate or late adverse events related to administration of adenosine.

In a review, a total of ten case series and four case reports were identified. There were no reports on the use of adenosine in AVM resection. Transient adenosine-induced asystole is a safe and effective technique in facilitating surgical treatment of complex aneurysms and AVMs. In addition, adenosine use reduces the need, duration, and associated complications of temporary clip applications to parent arteries 4).

2015

A total of 22 aneurysms in 22 different patients that underwent adenosine-induced transient asystole during aneurismal neck clipping within the past 4 years were retrospectively reviewed. Adenosine was administrated intravenously in a test-incremental manner (starting with 6-12 mg and then giving additional doses as needed) in 11 patients and in an estimated manner (pre-calculated as 0.3-0.4 mg/kg) in 11 patients.

Overall, the study consisted of 18 unruptured saccular aneurysms, three ruptured saccular aneurysms, and a ruptured pseudoaneurysm. Adenosine-induced transient asystole was used in cases of temporary clipping inability, wide necked aneurysm, deep-seated aneurysm, or a thin aneurysm wall. The number of administrations, dose (mg/kg in ideal body weight) and duration of asystole were 1-4 (mean, 2.3) times, 0.08-1.27 (mean, 0.36) mg/kg and 0-30 (mean 13) seconds in the test-incremental manner and 1-2 (mean, 1.09) times, 0.24-0.42 (mean, 0.34) mg/kg and 13-41 (mean, 24) seconds in the estimated manner, respectively. There was a linear relationship between the dose and the duration of asystole. Twenty out of 22 aneurysms were clipped successfully with adenosine-induced transient asystole. However, in the other two cases, additional suction decompression was required for the final clipping. Adenosine-related cardiologic complications occurred in two cases of self-limited atrial fibrillation during restoration of the cardiac rhythm.

In our experience, adenosine-induced transient asystole was safe and helpful for satisfactory clipping of a complicated aneurysm. An estimated dose injection of adenosine was more convenient than the test-incremental method and did not result in serious cardiologic problems 5).

2009

A report describes three children, aged eight to 11 years, with high-flow cerebral arteriovenous malformations who underwent interventional neuroradiological procedures involving glue (N-butyl cyanoacrylate) embolisation under general anaesthesia. The procedure was facilitated by relative hypotension induced by esmolol infusion and intravenous adenosine boluses. To allow controlled deposition of N-butyl cyanoacrylate into the arteriovenous malformations, glue injection was synchronised with the onset of adenosine-induced brief cardiac standstill. This resulted in satisfactory obliteration of the arteriovenous malformations nidus in all cases. The haemodynamic modulations, including the adenosine-induced brief cardiac standstill, was noted to not affect the BIS values in our patients. All patients had satisfactory obliteration of their arteriovenous malformations and had good neurological outcomes at one-year follow-up 6).

1)

Britz GW. Adenosine-induced transient asystole. Methodist Debakey Cardiovasc J. 2014 Oct-Dec;10(4):220-3. doi: 10.14797/mdcj-10-4-220. Review. PubMed PMID: 25624976; PubMed Central PMCID: PMC4300060.
2)

Groff MW, Adams DC, Kahn RA, Kumbar UM, Yang BY, Bederson JB. Adenosine-induced transient asystole for management of a basilar artery aneurysm. Case report. J Neurosurg. 1999 Oct;91(4):687-90. PubMed PMID: 10507394.
3)

Rangel-Castilla L, Russin JJ, Britz GW, Spetzler RF. Update on transient cardiac standstill in cerebrovascular surgery. Neurosurg Rev. 2015 Oct;38(4):595-602. doi: 10.1007/s10143-015-0637-z. Epub 2015 May 1. PubMed PMID: 25931209.
4)

Al-Mousa A, Bose G, Hunt K, Toma AK. Adenosine-assisted neurovascular surgery: initial case series and review of literature. Neurosurg Rev. 2017 Jul 22. doi: 10.1007/s10143-017-0883-3. [Epub ahead of print] Review. PubMed PMID: 28735438.
5)

Lee SH, Kwun BD, Kim JU, Choi JH, Ahn JS, Park W, Yun JH. Adenosine-induced transient asystole during intracranial aneurysm surgery: indications, dosing, efficacy, and risks. Acta Neurochir (Wien). 2015 Nov;157(11):1879-86; discussion 1886. doi: 10.1007/s00701-015-2581-7. Epub 2015 Sep 18. PubMed PMID: 26385113.
6)

Puri GD, Sen I, Bapuraj JR. Adenosine-induced cardiac standstill to facilitate endovascular embolisation of cerebral arteriovenous malformations in children. Anaesth Intensive Care. 2009 Jul;37(4):619-23. PubMed PMID: 19681422.

Update: Scalp arteriovenous malformation

An arteriovenous malformation (AVM) of the scalp is an abnormal fistulous connection between the feeding arteries and draining veins, without an intervening capillary bed within the subcutaneous layer.

Historically their unusual portly appearance led to various synonyms being coined for the entity viz., aneurysm cirsoide, aneurysm serpentinum, aneurysm racemosum, aneurysm by anastmoses, aneurysmal varix, arteriovenous fistula, plexiform angioma 1).

Epidemiology

Scalp AVM (SAVM) is a rare condition 2) 3).

Etiology

Its origin can be congenital or traumatic.

Congenital arteriovenous malformations (AVMs) of scalp are rare. They are usually not symptomatic at birth and are often misdiagnosed as haemangiomas. To date, only two cases of symptomatic neonatal scalp AVM have been reported in literature. Pathophysiology of congenital AVM is not completely understood but genetic and acquired causes are implicated. Diagnosis and management are often difficult and require multidisciplinary approach. Hussain et al. report a rare case of symptomatic congenital scalp AVM in a 10-day-old neonate who was successfully managed 4).

Clinical features

The clinical picture presents with complaints of increased scalp, scalp disfigurement, pain and neurological symptoms.

They can present a subcutaneous scalp lump or a large, pulsatile mass with a propensity to skin erosion and massive haemorrhage 5) 6).

Treatment

The treatment of sAVF is difficult, and many therapeutic approaches have been proposed. General approaches for the treatment of sAVF include ligation of the feeding arteries, surgical removal, electrothrombosis, embolization, and a combination of these approaches.

Although surgical excision is considered as definitive treatment for these lesions, troublesome intraoperative bleeding may pose a challenge.

Embolization as an alternative modality is gaining popularity.

Although most SAVMs can be operated by traditional method of excision, use of temporary clipping of feeding arteries (like Superficial temporal artery[STA], External carotid artery[ECA]) enables total excision of giant SAVMs with minimal blood loss for a definitive cure. This technique obviates the need for preoperative embolization 7).

Case series

2017

Gangadharaswamy et al. present their experience in the surgical management of 3 cases with SAVMs using proximal feeding artery temporary occlusion followed by total surgical excision. The clinical presentations and radiological features of these cases are discussed in the article. Intraoperative blood loss was less than 150ml in all patients. Postoperative period was uneventful with no morbidity or mortality.

Intraoperative bleeding during surgical excision of scalp AVMs can be troublesome and challenging. To combat this, the authors advocate proximal feeding artery temporary clipping prior to surgical excision of the lesion. The external carotid artery was temporarily clipped in one case and superficial temporal artery in two patients.

Although most SAVMs can be operated by traditional method of excision, use of temporary clipping of feeding arteries (like Superficial temporal artery[STA], External carotid artery[ECA]) enables total excision of giant SAVMs with minimal blood loss for a definitive cure. This novel technique obviates the need for preoperative embolization 8).

2013

Chowdhury et al., reported the experience of the surgical management of such lesions with a short review of the literature.

In this prospective study, 11 patients with scalp AVM and SVM, who underwent surgical excision of lesion in our hospital from 2006 to 2012, were included. All suspected high-flow AVM were investigated with the selective internal and external carotid digital subtraction angiogram (DSA) ± computed tomography (CT) scan of brain with CT angiogram or magnetic resonance imaging (MRI) of brain with MR angiogram, and all suspected low-flow vascular malformation (VM) was investigated with MRI of brain + MR angiogram. Eight were high-flow and three were low-flow VM.

All lesions were successfully excised. Scalp cosmetic aspects were acceptable in all cases. There was no major post-operative complication or recurrence till last follow-up.

With preoperative appropriate surgical planning, scalp AVM and SVM can be excised without major complication 9).

2004

Eight patients with scalp vascular malformations admitted between 1997 and 2002.

All the patients were investigated with selective internal and external carotid angiography. Depending upon the origin of feeding arteries, the scalp vascular malformations were classified into two categories: Group I: the primary scalp arteriovenous malformations and Group II: secondary venous dilatations. Six patients belonged to Group I and two patients were in Group II.

Five patients belonging to Group I underwent successful excision of the arteriovenous malformation. There was no recurrence in this group. Of the two patients in Group II, one patient who had scalp vascular dilatation simulating a primary scalp vascular malformation underwent excision of the lesion. This patient developed severe postoperative brain edema and died.

Primary scalp vascular malformation can be excised safely. However, excision of secondary scalp venous dilatation without treatment of the intracranial component can be dangerous 10).

2002

Muthukumar et al. treated 11 patients with cirsoid aneurysms surgically. All except one patient were males who were in the second and third decades of life. History of trauma was present in 6 patients. In one patient, the lesion had been present since birth. Occipital and frontal regions were the sites commonly involved. Superficial temporal, occipital and posterior auricular arteries were the most frequent feeding arteries. The size ranged from 3 cms to 12 cms. Following investigations were done: CT, MRI, MRA, angiography and Doppler studies.

Excision of the lesion was done in 8 patients and en bloc resection of the lesion with the scalp with reconstruction was done in the remaining three. One among the three patients who underwent en bloc resection had undergone prior surgery. None of the patients underwent preoperative endovascular treatment. One patient had undergone intralesional injection of sclerosing agents twice. Superficial scalp necrosis occurred in two patients but was treated successfully. All the patients except one had good cosmetic results and there was no recurrence during an average follow up of 18 months 11).

1998

A retrospective review of 81 patients with extracranial arteriovenous malformation of the head and neck who presented to the Vascular Anomalies Program in Boston over the last 20 years. This study focused on the natural history and effectiveness of treatment. The male to female ratio was 1:1.5. Arteriovenous malformations occur in anatomic patterns. Sixty-nine percent occurred in the midface, 14 percent in the upper third of the face, and 17 percent in the lower third. The most common sites were cheek (31 percent), ear (16 percent), nose (11 percent), and forehead (10 percent). A vascular anomaly was apparent at birth in 59 percent of patients (82 percent in men, 44 percent in women). Ten percent of patients noted onset in childhood, 10 percent in adolescence, and 21 percent in adulthood. Eight patients first noted the malformation at puberty, and six others experienced exacerbation during puberty. Fifteen women noted appearance or expansion of the malformation during pregnancy. Bony involvement occurred in 22 patients, most commonly in the maxilla and mandible. In seven patients, the bone was the primary site; in 15 other patients, the bone was involved secondarily. Arteriovenous malformations were categorized according to Schobinger clinical staging: 27 percent in stage I (quiescence), 38 percent in stage II (expansion), and 38 percent in stage III (destruction). There was a single patient with stage IV malformation (decompensation). Stage I lesions remained stable for long periods. Expansion (stage II) was usually followed by pain, bleeding, and ulceration (stage III). Once present, these symptoms and signs inevitably progressed until the malformation was resected. Resection margins were best determined intraoperatively by the bleeding pattern of the incised tissue and by Doppler. Subtotal excision or proximal ligation frequently resulted in rapid progression of the arteriovenous malformation. The overall cure rate was 60 percent, defined as radiographic absence of arteriovenous malformation. Cure rate for small malformations was 69 percent with excision only and 62 percent for extensive malformations with combined embolization-resection. The cure rate was 75 percent for stage I, 67 percent for stage II, and 48 percent for stage III malformations. Outcome was not affected significantly by age at treatment, sex, Schobinger stage, or treatment method. Mean follow-up was 4.6 years 12).

1995

Twenty-four patients with cirsoid aneurysms of the scalp. For nine patients (38%), the lesions were related to trauma. Each of the patients presented with a pulsatile scalp swelling with a bruit. No focal neurological deficits were noted in any of the patients. Scalp malformations in all patients were confirmed by selective internal and external carotid angiography, with no intracerebral component revealed in any of the patients. Twenty-one patients had the lesions surgically excised, with good results. The remaining three refused surgical intervention. Meticulous surgical technique, which includes removal of the pericranial component of the malformation, was paramount 13).

1989

Ten patients with scalp arteriovenous fistulas associated with a large varix (cirsoid aneurysms) were treated with a combination of interventional neuroradiologic procedures. These procedures included transarterial embolization, transarterial embolization followed by surgical excision, and two new methods of treatment of cirsoid aneurysms: transvenous embolization and direct puncture of the fistula for embolization. The embolic materials included liquid adhesive agents, particulate agents, detachable balloons, and wire coils. The embolization was performed to lodge the embolic agents in the fistula or proximal draining vein, not just the feeding vessels. Surgery was performed in two cases to remove a small residual nidus of fistula that could not be completely treated with intravascular embolization. With the use of these forms of treatment, cures were obtained in seven patients, and clinical and angiographic improvement was achieved in three patients. No major morbidity, blood loss, or mortality occurred during the treatment of these patients. The follow-up period ranged from 1 month to 8 years 14).

Case reports

2016

A 21-year-old man presented with a right-sided bruit and an enlarging palpable, pulsatile scalp mass. Magnetic resonance imaging demonstrated a 5-cm right sAVM and an azygos anterior cerebral artery (ACA) feeding a 2-cm parafalcine vascular anomaly, as well as an unruptured 3-mm, flow-related, distal ACA aneurysm. sAVM feeders were catheterized and embolized with Onyx 18. During resection of the right frontal scalp lesion, dissection below the pericranium was developed to expose the low-flow extracranial sAVM. A supratrochlear arterial feeder and the vascular nidus were coagulated, but radical resection was avoided to prevent scalp necrosis. An anterior right frontal parasagittal craniotomy and dural opening were performed. A developmental anomaly of the right superior frontal gyrus was noted, and a dense vascular network within the anterior parafalcine fold was excised and coagulated. The distal ACA aneurysm was cauterized and wrapped to preserve the parent artery. The patient made an excellent recovery without neurologic deficits.

A review of the literature demonstrated a variety of endovascular and open surgical treatments with limited consensus on standard care. While sAVMs have been described in the literature, the combination of the diverse conditions seen in this case is unique 15).


Worm et al, present a case of giant scalp AVMs and its management, followed by a brief literature review on the subject. The diagnosis of scalp AVMs is based on physical examination and confirmed by internal and external carotid angiography or computed tomographic angiography (CTA). Surgical excision is especially effective in scalp AVMs, and is the most frequently used treatment modality 16).

2009

Massimi et al. report on the unusual case of a child harboring a complex intracranial AVM that initially presented as a small scalp mass. Actually, this young boy came to the authors’ attention just for a small, soft, pulsatile, and reducible mass of the vertex that produced a circumscribed bone erosion. The presence of macrocranium and venous engorgement of the face, however, suggested the presence of an intracranial “mass.” The neuroimaging investigations pointed out a temporal AVM causing dilation of the intracranial sinuses and ectasia of the vein of the scalp; one of the veins was appreciable as a lump on the vertex 17).

2008

A 35-year-old man presented with occipital subcutaneous pulsatile thrill. Senoglu et al. discussed and illustrated a rare sAVF, which was a high-flow sAVF fed by the occipital branch of the right ACE draining intraosseously into the SS. The case was treated by surgical origin ligation.

This case was unusual in the sense that it was apparently spontaneous, and the major venous drainage was through the bone into the SS. Arterial supply pattern of sAVF is very important in therapeutic decision-making. We suggest that surgical origin ligation for sAVF be considered if the case has 1 feeding artery 18).

2007

Craniofacial cirsoid aneurysm: 2-stage treatment 19).

2004

A 21-year-old female consulted in 1998 complaining of right tinnitus and a pulsating mass in the retroauricular region. The initial angiogram revealed an AVM in the right temporo-parietal subcutaneous space with feeders from the STA, an occipital artery, a posterior auricular artery, and a middle meningeal artery (MMA). Three years later, she complained of enlargement of the lesion, increased tinnitus, and alopecia. Repeat angiographic study revealed the presence of a nidus and the appearance of new feeders from a contralateral MMA and an ipsilateral middle cerebral artery; there was a de novo saccular aneurysm in the right STA. On the day preceding surgery, the left MMA was embolized to control intraoperative bleeding. The AVM was removed totally without any dermal complications.

This case suggests that scalp AVMs can become enlarged by capturing subcutaneous or intracranial feeders, and that the consequent hemodynamic stress may induce de novo aneurysms in scalp AVMs. Capillary endothelial cells were strongly immunostained for vascular endothelial growth factor 20).

1990

Heilman et al. report a patient in whom a large traumatic cirsoid aneurysm of the scalp was eliminated using a combined neurosurgical and interventional neuroradiological approach. Transarterial embolization was utilized to reduce arterial blood supply to the fistula. Thrombogenic Gianturco spring coils were then introduced via direct percutaneous puncture of the aneurysm. The aneurysm thrombosed and the multiple tortuous scalp vessels disappeared. One month after embolization, a small area of skin necrosis over the aneurysm necessitated surgical excision of the lesion. The thrombosed aneurysm was easily resected with minimal blood loss. Percutaneous embolization with thrombogenic coils in this case was a safe and effective ablative technique 21).

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