Hypernatremia

Hypernatremia

Hypernatremia, is a high concentration of sodium in the blood. Normal serum sodium levels are 135 – 145 mmol/L (135 – 145 mEq/L). Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L.

Hypernatremia is one of the most common electrolyte disturbances following aneurysmal subarachnoid hemorrhage (aSAH) and has been correlated with increased mortality in single institution studies. Both hyponatremia and hypernatremia during ICU management were significantly associated with unfavorable neurologic outcomes 1).

In neurosurgical patients, this is most often seen in the setting of diabetes insipidus (DI). Since normal total body water (TBW) is ≈ 60% of the patient’s normal body weight, the patient’s current TBW may be estimated by Eq.

Mild and moderate hypernatremia were significantly associated with increased early mortality in patients with severe TBI 2). Hypernatremia was associated also with poorer outcomes in patients with severe TBI. This finding warrants further investigation in a prospective, randomized study 3).

Electrolyte imbalances are common in traumatic brain injury. In a study Hypokalemia was the most common electrolyte imbalance at 65.5%. The results of the use of a multivariable logistic regression model showed that the odds of postoperative death in TBI patients were increased with high levels of blood glucose, hypernatremia, and acidosis.Hypokalemia was the most common electrolyte imbalance in TBI patients. Hypernatremia, acidosis, and hyperglycemia significantly increased the odds ratio of death in the first 24  hours post TBI 4).

Clinical features

Early symptoms may include a strong feeling of thirstweaknessnausea, and loss of appetite.

Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain.

Severe symptoms typically only occur when levels are above 160 mmol/L.

Treatment

The free water deficit to be replaced is given by a Eq. Correction must be made slowly to avoid exacerbating cerebral edema. One half the water deficit is replaced over 24 hours, and the remainder is given over 1–2 additional days. Judicious replacement of deficient ADH in cases of true DI must also be made.


The aim of a work of Vassilyev was to evaluate the effectiveness of Sterofundin in the framework of complex therapy of hypernatremia in neurosurgical patients after removal of brain tumors. They analyzed the dynamics of the concentrations of sodium, potassium, chorus of the plasma, anion gap and buffer bases in the postoperative period of these patients. For obtaining reliable results, the patients were divided into groups according to the nature of the treatment: Sterofundin and symptomatic correction of hypotonic solution of sodium chloride, saluretic and Spironolactone respectively. In a comparison between the groups, a distinct difference in the speed of regression of hypernatremia and durability of the achieved effect was observed. In case of treatment with Sterofundin there was a significant decrease of hypernatremia by the end of the second day of the postoperative period without tendency to re-raise. The prevalence of hypotonic solutions of sodium chloride and potassium-sparing saluretics in intensive care allowed reducing the sodium concentration non-persistently to the fourth day on the background of significant fluctuations in its concentration. The use of Sterofundin in complex therapy of electrolyte disturbances, particularly of hypernatremia in neurosurgical patients after removal of brain tumors, is reflected in the form of significant regression of increased sodium concentration in plasmacompared with the method of use “hypotonic” hemodilution, saluretics and potassium-sparing diuretics 5).

Complications

Coma.

Pulmonary complications and acute kidney injury were more common in hypernatremia 6).


Hoffman et al., from the Upstate Medical University performed a retrospective analysis of adults between 2002 and 2011 with a primary diagnosis of aneurysmal subarachnoid hemorrhage (aSAH) using the Nationwide Inpatient Sample (NIS). Patients were grouped according to whether or not an inpatient diagnosis of hypernatremia was present. The primary outcome was the NIS-SAH outcome measure. Secondary outcomes included in-hospital mortalitylength of stay (LOS), and non-routine hospital discharge. Outcomes analyses adjusted for SAH severity using the NIS-SAH Severity Score, Charlson Comorbidity Index, and the presence of cerebral edema.

A total of 18,377 patients were included in the study. The incidence of a poor outcome as defined by the NIS-SAH outcome measure was 65.9% in the hypernatremia group and 33.4% in the normonatremia group (OR 1.96, 95% CI 1.68 – 2.27). There was higher mortality in the hypernatremia group (OR 1.60, 95% CI 1.37 – 1.87). Patients with hypernatremia had a significantly higher rate of non-routine hospital discharge and gastrostomy. The incidences of poor outcome, in-hospital mortality, and non-routine disposition were higher in the hypernatremia group regardless of treatment type (clipping vs. endovascular embolization). Pulmonary complications and acute kidney injury were more common in the hypernatremia group as well.

In patients with aSAH, hypernatremia is associated with poorer functional outcomes regardless of SAH severity 7).

References

1)

Okazaki T, Hifumi T, Kawakita K, Shishido H, Ogawa D, Okauchi M, Shindo A, Kawanishi M, Tamiya T, Kuroda Y. Target Serum Sodium Levels During Intensive Care Unit Management of Aneurysmal Subarachnoid Hemorrhage. Shock. 2017 Nov;48(5):558-563. doi: 10.1097/SHK.0000000000000897. PubMed PMID: 28498294.
2)

Vedantam A, Robertson CS, Gopinath SP. Morbidity and mortality associated with hypernatremia in patients with severe traumatic brain injury. Neurosurg Focus. 2017 Nov;43(5):E2. doi: 10.3171/2017.7.FOCUS17418. PubMed PMID: 29088954.
3)

Hoffman H, Jalal MS, Chin LS. Effect of Hypernatremia on Outcomes After severe Traumatic Brain Injury: A Nationwide Inpatient Sample analysis. World Neurosurg. 2018 Oct;118:e880-e886. doi: 10.1016/j.wneu.2018.07.089. Epub 2018 Jul 18. PubMed PMID: 30031178.
4)

Pin-On P, Saringkarinkul A, Punjasawadwong Y, Kacha S, Wilairat D. Serum electrolyte imbalance and prognostic factors of postoperative death in adult traumatic brain injury patients: A prospective cohort study. Medicine (Baltimore). 2018 Nov;97(45):e13081. doi: 10.1097/MD.0000000000013081. PubMed PMID: 30407307; PubMed Central PMCID: PMC6250545.
5)

Vassilyev D. [MODERN APPROACHES TO CORRECTION OF HYPERNATREMIA IN NEUROSURGICAL PATIENTS]. Georgian Med News. 2016 Nov;(Issue):12-16. Russian. PubMed PMID: 28009309.
6) , 7)

Hoffman H, Verhave B, Chin LS. Hypernatremia is associated with poorer outcomes following aneurysmal subarachnoid hemorrhage: a nationwide inpatient sample analysis. J Neurosurg Sci. 2018 Dec 5. doi: 10.23736/S0390-5616.18.04611-8. [Epub ahead of print] PubMed PMID: 30514071.

Chronic subdural hematoma recurrence

Chronic subdural hematoma recurrence

Epidemiology

In 2 large cohorts of US patients, approximately 5% to 10% of patients who underwent surgery for nontraumatic SDH were required to undergo repeated operation within 30 to 90 days. These results may inform the design of future prospective studies and trials and help practitioners calibrate their index of suspicion to ensure that patients are referred for timely surgical care 1).

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drillcraniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. 2).

Risk factors

In the series of Han et al. independent risk factors for recurrence were as follows: age > 75 years (HR 1.72, 95% CI 1.03-2.88; p = 0.039), obesity (body mass index ≥ 25.0 kg/m2), and a bilateral operation 3).

Chon et al. shown that postoperative midline shifting (≥5 mm), diabetes mellitus, preoperative seizure, preoperative width of hematoma (≥20 mm), and anticoagulant therapy were independent predictors of the recurrence of chronic subdural hematoma.

According to internal architecture of hematoma, the rate of recurrence was significantly lower in the homogeneous and the trabecular type than the laminar and separated type 4).


The recurrence rate of chronic subdural hematoma cSDH seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the hematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX-2).

Anticoagulant therapy

Antiplatelet therapy

Antiplatelet therapy significantly influences the recurrence of CSDH 5).

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 6) 7).

Septation

Jack et al.found a 12% reoperation rate. CSDH septation (seen on computed tomogram scan) was found to be an independent risk factor for recurrence requiring reoperation (p=0.04). Larger post-operative subdural haematoma volume was also significantly associated with requiring a second drainage procedure (p<0.001). Independent risk factors of larger post-operative haematoma volume included septations within a CSDH (p<0.01), increased pre-operative haematoma volume (p<0.01), and a greater amount of parenchymal atrophy (p=0.04). A simple scoring system for quantifying recurrence risk was created and validated based on patient age (< or ≥80 years), haematoma volume (< or ≥160cc), and presence of septations within the subdural collection (yes or no).

Septations within CSDHs are associated with larger post-operative residual haematoma collections requiring repeat drainage. When septations are clearly visible within a CSDH, craniotomy might be more suitable as a primary procedure as it allows greater access to a septated subdural collection. The proposed scoring system combining haematoma volume, age, and presence of septations might be useful in identifying patients at higher risk for recurrence 8).

Membranectomy

Opening the internal hematoma membrane does not alter the rate of patients requiring revision surgery and the number of patients showing a marked residual hematoma six weeks after evacuation of a CSDH 9).

In the study of Lee et al, an extended surgical approach with partial membranectomy has no advantages regarding the rate of reoperation and the outcome. As initial treatment, burr-hole drainage with irrigation of the hematoma cavity and closed-system drainage is recommended. Extended craniotomy with membranectomy is now reserved for instances of acute rebleeding with solid hematoma 10).

Diabetes

Surgeons should consider informing patients with diabetes mellitus that this comorbidity is associated with an increased likelihood of recurrence

11) 12) 13).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 14).

Close imaging follow-up is important for CSDH patients for recurrence prediction. Using quantitative CT volumetric analysis, strong evidence was provided that changes in the residual fluid volume during the ‘self-resolution’ period can be used as significantly radiological predictors of recurrence 15).

A structural equation model showed a significant association between increased antiinflammatory activity in hematoma fluid samples and a lower risk of recurrence, but this relationship was not statistically significant in venous blood samples. Moreover, these findings indicate that anti-inflammatory activities in the hematoma may play a role in the risk of a recurrence of CSDH 16).

Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 17).

Treatment

There is no definite operative procedure for patients with intractable chronic subdural hematoma (CSDH).

Most recurrent hematomas are managed successfully with burr hole craniostomies with postoperative closed-system drainage. Refractory hematomas may be managed with a variety of techniques, including craniotomy or subdural-peritoneal shunt placement 18).

Although many studies have reported risk factors or treatments in efforts to prevent recurrence, those have focused on single recurrence, and little cumulative data is available to analyze refractory CSDH.

Matsumoto et al. defined refractory CSDH as ≥2 recurrences, then analyzed and compared clinical factors between patients with single recurrence and those with refractory CSDH in a cohort study, to clarify whether patients with refractory CSDH experience different or more risk factors than patients with single recurrence, and whether burr-hole irrigation with closed-system drainage reduces refractory CSDH.

Seventy-five patients had at least one recurrence, with single recurrence in 62 patients and ≥2 recurrences in 13 patients. In comparing clinical characteristics, patients with refractory CSDH were significantly younger (P=0.04) and showed shorter interval to first recurrence (P<0.001). Organized CSDH was also significantly associated with refractory CSDH (P=0.02). Multivariate logistic regression analysis identified first recurrence interval <1 month (OR 6.66, P<0.001) and age <71 years (OR 4.16, P<0.001) as independent risk factors for refractory CSDH. On the other hand, burr-hole irrigation with closed-system drainage did not reduce refractory CSDH.

When patients with risk factors for refractory CSDH experience recurrence, alternative surgical procedures may be considered as the second surgery, because burr-hole irrigation with closed-system drainage did not reduce refractory CSDH 19).

Implantation of a reservoir 20) 21) 22).

Subdural-peritoneal shunt 23).

Middle meningeal artery embolization

Embolization of the MMA is effective for refractory CSDH or CSDH patients with a risk of recurrence, and is considered an effective therapeutic method to stop hematoma enlargement and promote resolution 24) 25) 26) 27) 28) 29).

A pilot study indicated that perioperative middle meningeal artery (MMA) embolization could be offered as the least invasive and most effectual means of treatment for resistant patients of CSDHs with 1 or more recurrences 30).

Chihara et al. have treated three cases of CSDH with MMA embolization to date, but there was a postoperative recurrence in one patient, which required a craniotomy for hematoma removal and capsulectomy. MMA embolization blocks the blood supply from the dura to the hematoma outer membrane in order to prevent recurrences of refractory CSDH. Histopathologic examination of the outer membrane of the hematoma excised during craniotomy showed foreign-body giant cells and neovascular proliferation associated with embolization. Because part of the hematoma was organized in this case, the CSDH did not resolve when the MMA was occluded, and the development of new collateral pathways in the hematoma outer membrane probably contributed to the recurrence. Therefore, in CSDH with some organized hematoma, MMA embolization may not be effective. Magnetic resonance imaging (MRI) should be performed in these patients before embolization 31).

Case series

Case reports

References

1)

Knopman J, Link TW, Navi BB, Murthy SB, Merkler AE, Kamel H. Rates of Repeated Operation for Isolated Subdural Hematoma Among Older Adults. JAMA Netw Open. 2018 Oct 5;1(6):e183737. doi: 10.1001/jamanetworkopen.2018.3737. PubMed PMID: 30646255.
2)

Escosa Baé M, Wessling H, Salca HC, de Las Heras Echeverría P. Use of twist-drill craniostomy with drain in evacuation of chronic subdural hematomas: independent predictors of recurrence. Acta Neurochir (Wien). 2011 May;153(5):1097-103. doi: 10.1007/s00701-010-0903-3. Epub 2010 Dec 31. PubMed PMID: 21193935.
3)

Han MH, Ryu JI, Kim CH, Kim JM, Cheong JH, Yi HJ. Predictive factors for recurrence and clinical outcomes in patients with chronic subdural hematoma. J Neurosurg. 2017 Nov;127(5):1117-1125. doi: 10.3171/2016.8.JNS16867. Epub 2016 Dec 16. PubMed PMID: 27982768.
4)

Chon KH, Lee JM, Koh EJ, Choi HY. Independent predictors for recurrence of chronic subdural hematoma. Acta Neurochir (Wien). 2012 Sep;154(9):1541-8. doi: 10.1007/s00701-012-1399-9. Epub 2012 Jun 1. PubMed PMID: 22653496.
5)

Wada M, Yamakami I, Higuchi Y, Tanaka M, Suda S, Ono J, Saeki N. Influence of antiplatelet therapy on postoperative recurrence of chronic subdural hematoma: a multicenter retrospective study in 719 patients. Clin Neurol Neurosurg. 2014 May;120:49-54. doi: 10.1016/j.clineuro.2014.02.007. Epub 2014 Feb 24. PubMed PMID: 24731576.
6)

Mori K, Maeda M (2001) Surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. Neurol Med Chir (Tokyo) 41:371–381
7)

Stanišić M, Hald J, Rasmussen IA, Pripp AH, Ivanović J, Kolstad F, Sundseth J, Züchner M, Lindegaard KF (2013) Volume and densities of chronic subdural haematoma obtained from CT imaging as predictors of postoperative recurrence: a prospective study of 107 operated patients. Acta Neurochir 155:323–333
8)

Jack A, O’Kelly C, McDougall C, Max Findlay J. Predicting Recurrence after Chronic Subdural Haematoma Drainage. Can J Neurol Sci. 2015 Jan 5:1-6. [Epub ahead of print] PubMed PMID: 25557536.
9)

Unterhofer C, Freyschlag CF, Thomé C, Ortler M. Opening the Internal Hematoma Membrane does not Alter the Recurrence Rate of Chronic Subdural Hematomas – A Prospective Randomized Trial. World Neurosurg. 2016 May 2. pii: S1878-8750(16)30210-8. doi: 10.1016/j.wneu.2016.04.081. [Epub ahead of print] PubMed PMID: 27150644.
10)

Lee JY, Ebel H, Ernestus RI, Klug N. Various surgical treatments of chronic subdural hematoma and outcome in 172 patients: is membranectomy necessary? Surg Neurol. 2004 Jun;61(6):523-7; discussion 527-8. PubMed PMID: 15165784.
11)

Matsumoto K, Akagi K, Abekura M, Ryujin H, Ohkawa M, Iwasa N, Akiyama C. Recurrence factors for chronic subdural hematomas after burr-hole craniostomy and closed system drainage. Neurol Res. 1999 Apr;21(3):277-80. PubMed PMID: 10319336.
12)

Yamamoto H, Hirashima Y, Hamada H, Hayashi N, Origasa H, Endo S. Independent predictors of recurrence of chronic subdural hematoma: results of multivariate analysis performed using a logistic regression model. J Neurosurg. 2003 Jun;98(6):1217-21. PubMed PMID: 12816267.
13)

Pang CH, Lee SE, Kim CH, Kim JE, Kang HS, Park CK, Paek SH, Kim CH, Jahng TA, Kim JW, Kim YH, Kim DG, Chung CK, Jung HW, Yoo H. Acute intracranial bleeding and recurrence after bur hole craniostomy for chronic subdural hematoma. J Neurosurg. 2015 Jul;123(1):65-74. doi: 10.3171/2014.12.JNS141189. Epub 2015 Feb 13. PubMed PMID: 25679282.
14)

Balser D, Rodgers SD, Johnson B, Shi C, Tabak E, Samadani U. Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature. Neurol Res. 2013 Apr;35(3):233-42. doi: 10.1179/1743132813Y.0000000166. Review. PubMed PMID: 23485050.
15)

Xu FF, Chen JH, Leung GK, Hao SY, Xu L, Hou ZG, Mao X, Shi GZ, Li JS, Liu BY. Quantitative computer tomography analysis of post-operative subdural fluid volume predicts recurrence of chronic subdural haematoma. Brain Inj. 2014;28(8):1121-6. doi: 10.3109/02699052.2014.910702. Epub 2014 May 6. PubMed PMID: 24801643.
16)

Pripp AH, Stanišić M. The Correlation between Pro- and Anti-Inflammatory Cytokines in Chronic Subdural Hematoma Patients Assessed with Factor Analysis. PLoS One. 2014 Feb 27;9(2):e90149. doi: 10.1371/journal.pone.0090149. eCollection 2014. PubMed PMID: 24587250.
17)

Adachi A, Higuchi Y, Fujikawa A, Machida T, Sueyoshi S, Harigaya K, Ono J, Saeki N. Risk factors in chronic subdural hematoma: comparison of irrigation with artificial cerebrospinal fluid and normal saline in a cohort analysis. PLoS One. 2014 Aug 4;9(8):e103703. doi: 10.1371/journal.pone.0103703. eCollection 2014. PubMed PMID: 25089621; PubMed Central PMCID: PMC4121178.
18)

Desai VR, Scranton RA, Britz GW. Management of Recurrent Subdural Hematomas. Neurosurg Clin N Am. 2017 Apr;28(2):279-286. doi: 10.1016/j.nec.2016.11.010. Epub 2017 Jan 4. Review. PubMed PMID: 28325462.
19)

Matsumoto H, Hanayama H, Okada T, Sakurai Y, Minami H, Masuda A, Tominaga S, Miyaji K, Yamaura I, Yoshida Y, Yoshida K. Clinical investigation of refractory chronic subdural hematoma: a comparison of clinical factors between single and repeated recurrences. World Neurosurg. 2017 Aug 24. pii: S1878-8750(17)31402-X. doi: 10.1016/j.wneu.2017.08.101. [Epub ahead of print] PubMed PMID: 28844917.
20)

Sato M, Iwatsuki K, Akiyama C, Masana Y, Yoshimine T, Hayakawa T. [Use of Ommaya CSF reservoir for refractory chronic subdural hematoma]. No Shinkei Geka. 1999 Apr;27(4):323-8. Japanese. PubMed PMID: 10347846.
21)

Sato M, Iwatsuki K, Akiyama C, Kumura E, Yoshimine T. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2001 Jun;48(6):1297-301. PubMed PMID: 11383733.
22)

Laumer R. Implantation of a reservoir for refractory chronic subdural hematoma. Neurosurgery. 2002 Mar;50(3):672. PubMed PMID: 11841742.
23)

Misra M, Salazar JL, Bloom DM. Subdural-peritoneal shunt: treatment for bilateral chronic subdural hematoma. Surg Neurol. 1996 Oct;46(4):378-83. PubMed PMID: 8876720.
24)

Mandai S, Sakurai M, Matsumoto Y. Middle meningeal artery embolization for refractory chronic subdural hematoma. Case report. J Neurosurg. 2000 Oct;93(4):686-8. PubMed PMID: 11014549.
25)

Takahashi K, Muraoka K, Sugiura T, Maeda Y, Mandai S, Gohda Y, Kawauchi M, Matsumoto Y. [Middle meningeal artery embolization for refractory chronic subdural hematoma: 3 case reports]. No Shinkei Geka. 2002 May;30(5):535-9. Japanese. PubMed PMID: 11993178.
26)

Hirai S, Ono J, Odaki M, Serizawa T, Nagano O. Embolization of the Middle Meningeal Artery for Refractory Chronic Subdural Haematoma. Usefulness for Patients under Anticoagulant Therapy. Interv Neuroradiol. 2004 Dec 24;10 Suppl 2:101-4. Epub 2008 May 15. PubMed PMID: 20587257; PubMed Central PMCID: PMC3522210.
27)

Tsukamoto Y, Oishi M, Shinbo J, Fujii Y. Transarterial embolisation for refractory bilateral chronic subdural hematomas in a case with dentatorubral-pallidoluysian atrophy. Acta Neurochir (Wien). 2011 May;153(5):1145-7. doi: 10.1007/s00701-010-0891-3. Epub 2010 Dec 2. PubMed PMID: 21125409.
28)

Mino M, Nishimura S, Hori E, Kohama M, Yonezawa S, Midorikawa H, Kaimori M, Tanaka T, Nishijima M. Efficacy of middle meningeal artery embolization in the treatment of refractory chronic subdural hematoma. Surg Neurol Int. 2010 Dec 13;1:78. doi: 10.4103/2152-7806.73801. PubMed PMID: 21206540; PubMed Central PMCID: PMC3011107.
29)

Hashimoto T, Ohashi T, Watanabe D, Koyama S, Namatame H, Izawa H, Haraoka R, Okada H, Ichimasu N, Akimoto J, Haraoka J. Usefulness of embolization of the middle meningeal artery for refractory chronic subdural hematomas. Surg Neurol Int. 2013 Aug 19;4:104. doi: 10.4103/2152-7806.116679. eCollection 2013. PubMed PMID: 24032079; PubMed Central PMCID: PMC3766342.
30)

Kim E. Embolization Therapy for Refractory Hemorrhage in Patients with Chronic Subdural Hematomas. World Neurosurg. 2017 May;101:520-527. doi: 10.1016/j.wneu.2017.02.070. Epub 2017 Feb 27. PubMed PMID: 28249828.
31)

Chihara H, Imamura H, Ogura T, Adachi H, Imai Y, Sakai N. Recurrence of a Refractory Chronic Subdural Hematoma after Middle Meningeal Artery Embolization That Required Craniotomy. NMC Case Rep J. 2014 May 9;1(1):1-5. doi: 10.2176/nmccrj.2013-0343. eCollection 2014 Oct. PubMed PMID: 28663942; PubMed Central PMCID: PMC5364934.

Inflow angle

Inflow angle

The angle separating parent vessel and aneurysm dome main axes.

Maximal intracranial aneurysm size and intracranial aneurysm morphology parameters are used when deciding if an Intracranial aneurysm (IA) should be treated prophylactically. These parameters are derived from postrupture morphology. As time and rupture may alter the aneurysm geometry, possible morphological predictors of a Ruptured intracranial aneurysm should be established in prerupture aneurysms.

Skodvin et al., from University Hospital of Northern NorwayOslo University Hospital Rikshospitalet matched 1:2 with 24 control IAs that remained unruptured during a median follow-up time of 4.5 (interquartile range, 3.7-8.2) yr. Morphological parameters were automatically measured on 3-dimensional models constructed from angiograms obtained at time of diagnosis. Cases and controls were matched by aneurysm location and aneurysm size, patient age and sex, and the PHASES score (population, hypertension, age, size of aneurysm, earlier subarachnoid hemorrhage from another aneurysm, and site of aneurysm) did not differ between the 2 groups.

Only inflow angle was significantly different in cases vs controls in univariate analysis (P = .045), and remained significant in multivariable analysis. Maximal size correlated with size ratio in both cases and controls (P = .015 and <.001, respectively). However, maximal size and inflow angle were correlated in cases but not in controls (P = .004. and .87, respectively).

A straighter inflow angle may predispose an aneurysm to changes that further increase risk of rupture. Traditional parameters of aneurysm morphology may be of limited value in predicting IA rupture 1).


In 2016 Ji et al., concluded that unruptured paraclinoid aneurysms had a high incidence of aneurysm recanalization (AR) after endovascular treatment. An inflow angle of ≥90 degrees and incomplete occlusion were significant predictors of AR 2).


In 2010 the objective of Baharoglu et al., was to evaluate the importance of inflow-angle (IA), the angle separating parent vessel and aneurysm dome main axes.

IA, maximal dimension, height-width ratio, and dome-neck aspect ratio were evaluated in sidewall-type aneurysms with respect to rupture status in a cohort of 116 aneurysms in 102 patients. Computational fluid dynamic analysis was performed in an idealized model with variational analysis of the effect of IA on intra-aneurysmal hemodynamics.

Univariate analysis identified IA as significantly more obtuse in the ruptured subset (124.9 degrees+/-26.5 degrees versus 105.8 degrees+/-18.5 degrees, P=0.0001); similarly, maximal dimension, height-width ratio, and dome-neck aspect ratio were significantly greater in the ruptured subset; multivariate logistic regression identified only IA (P=0.0158) and height-width ratio (P=0.0017), but not maximal dimension or dome-neck aspect ratio, as independent discriminants of rupture status. Computational fluid dynamic analysis showed increasing IA leading to deeper migration of the flow recirculation zone into the aneurysm with higher peak flow velocities and a greater transmission of kinetic energy into the distal portion of the dome. Increasing IA resulted in higher inflow velocity and greater wall shear stress magnitude and spatial gradients in both the inflow zone and dome.

They concluded that Inflow-angle is a significant discriminant of rupture status in sidewall-type aneurysms and is associated with higher energy transmission to the dome. These results support inclusion of IA in future prospective aneurysm rupture risk assessment trials 3).

References

1)

Skodvin TØ, Evju Ø, Sorteberg A, Isaksen JG. Prerupture Intracranial Aneurysm Morphology in Predicting Risk of Rupture: A Matched Case-Control Study. Neurosurgery. 2019 Jan 1;84(1):132-140. doi: 10.1093/neuros/nyy010. PubMed PMID: 29529238.
2)

Ji W, Liu A, Lv X, Sun L, Liang S, Li Y, Yang X, Jiang C, Wu Z. Larger inflow angle and incomplete occlusion predict recanalization of unruptured paraclinoid aneurysms after endovascular treatment. Interv Neuroradiol. 2016 Aug;22(4):383-8. doi: 10.1177/1591019916641315. Epub 2016 Apr 11. PubMed PMID: 27066815; PubMed Central PMCID: PMC4984388.
3)

Baharoglu MI, Schirmer CM, Hoit DA, Gao BL, Malek AM. Aneurysm inflow-angle as a discriminant for rupture in sidewall cerebral aneurysms: morphometric and computational fluid dynamic analysis. Stroke. 2010 Jul;41(7):1423-30. doi: 10.1161/STROKEAHA.109.570770. Epub 2010 May 27. PubMed PMID: 20508183.

Hypoxic ischaemic brain injury

Hypoxic ischaemic brain injury

Hypoxic ischaemic brain injury is common and usually due to cardiac arrest or profound hypotension. The clinical pattern and outcome depend on the severity of the initial insult, the effectiveness of immediate resuscitation and transfer, and the post-resuscitation management on the intensive care unit. Clinical assessment is difficult and so often these days compromised by sedationneuromuscular-blocking drugventilationhypothermia and inotropic management. Investigations can add valuable information, in particular brain MRI shows characteristic patterns depending on the severity of the injury and the timing of imaging. EEG patterns may also suggest the possibility of a good outcome. There is no entirely reliable algorithm of clinical signs or investigations which allow a definitive prognosis but the combination of careful repeated observations and appropriate ancillary investigations allows the neurologist to give an informed and accurate opinion of the likely outcome, and to advise on management. Overall, the prognosis is extremely poor and only a quarter of patients survive to hospital discharge, and often even then with severe neurological or cognitive deficits 1).


In eleven patients (median age of 47 [range 20-71], 8 male and 3 female). There was a linear relationship between ICP and non-invasive estimators of ICP (nICP) with optic nerve sheath diameter ultrasonography (ONSD) (R = 0.53 [p < 0.0001]), JVP (R = 0.38 [p < 0.001]) and transcranial Doppler ultrasonography (TCD) (R = 0.30 [p < 0.01]). The ability to predict intracranial hypertension was highest for ONSD and TCD (AUC = 0.96 [95% CI: 0.90-1.00] and AUC = 0.91 [95% CI: 0.83-1.00], respectively). Jugular venous bulb pressure (JVP). presented the weakest prediction ability (AUC = 0.75 [95% CI: 0.56-0.94]).

ONSD and TCD methods demonstrated agreement with invasively-monitored ICP, suggesting their potential roles in the detection of intracranial hypertension in hypoxic ischaemic brain injury (HIBI) after cardiac arrest 2).

References

1)

Howard RS, Holmes PA, Koutroumanidis MA. Hypoxic-ischaemic brain injury. Pract Neurol. 2011 Feb;11(1):4-18. doi: 10.1136/jnnp.2010.235218. Review. PubMed PMID: 21239649.
2)

Cardim D, Griesdale DE, Ainslie PN, Robba C, Calviello L, Czosnyka M, Smielewski P, Sekhon MS. A comparison of non-invasive versus invasive measures of intracranial pressure in hypoxic ischaemic brain injury after cardiac arrest. Resuscitation. 2019 Jan 7. pii: S0300-9572(18)30912-2. doi: 10.1016/j.resuscitation.2019.01.002. [Epub ahead of print] PubMed PMID: 30629992.

P2-P3 junction aneurysm of the posterior cerebral artery

Aneurysms in the P2 segment arise between the junction of the posterior communicating artery (PCoA) with the PCA and the posterior part of the midbrain. The pterionalsubtemporal, temporopolar, transpetrous and transcortical transchoroidal fissure are the surgical approaches which have been used to gain access to P2 segment aneurysms.

Endovascular coil occlusion has rapidly evolved as a competing therapeutic alternative to surgical clipping in the treatment of P2 segment aneurysms.

However, surgery is still a well-established option for P 2 segment aneurysms and complete closure of the aneurysm can be achieved by surgical clipping 1).

Treatment

Proximal occlusion of PCA represents a treatment option. However, this procedure carries a high risk of ischemic complication

The STA-P3/PTA bypass through the subtemporal approach is a feasible option to maintain blood flow in cases of PCA fusiform aneurysms requiring trapping of the P2 segment 2).


Progressive deconstruction with flow diversion using a Pipeline embolization device (PED; Medtronic) can be utilized to promote thrombosis of broad-based fusiform aneurysms. Current flow diverters require a 0.027-inch microcatheter for deployment. Vakharia et al., presented a patient with a fusiform P2P3 junction posterior cerebral artery aneurysm in which they demonstrate the importance of haptics in microwire manipulation to recognize large-vessel anatomy versus perforator anatomy that may overlap, especially when access is needed in distal tortuous circulations. In addition, the authors demonstrate the need for appropriate visualization before PED deployment. Postembolization runs demonstrated optimal wall apposition with contrast stasis within the aneurysm dome.The video can be found here: https://youtu.be/8kfsSvN3XqM

 3).

References

1)

Zhitao J, Yibao W, Anhua W, Shaowu O, Yunchao B, Renyi Z, Yunjie W. Microsurgical subtemporal approach to aneurysms on the P(2) segment of the posterior cerebral artery. Neurol India. 2010 Mar-Apr;58(2):242-7. doi: 10.4103/0028-3886.63806. PubMed PMID: 20508343.
2)

Kawashima A, Andrade-Barazarte H, Jahromi BR, Oinas M, Elsharkawy A, Kivelev J, Kubota Y, Kawamata T, Hernesniemi JA. Superficial Temporal Artery: Distal Posterior Cerebral Artery Bypass through the Subtemporal Approach: Technical Note and Pilot Surgical Cases. Oper Neurosurg (Hagerstown). 2017 Jun 1;13(3):309-316. doi: 10.1093/ons/opw033. PubMed PMID: 28521345.
3)

Vakharia K, Munich SA, Waqas M, Setlur Nagesh SV, Levy EI. Deployment of distal posterior cerebral artery flow diverter in tortuous anatomy. Neurosurg Focus. 2019 Jan 1;46(Suppl_1):V9. doi: 10.3171/2019.1.FocusVid.18481. PubMed PMID: 30611181.

Direct carotid cavernous fistula

Type A Direct carotid cavernous fistula (CCF) are high flow fistulas occurring due to a tear in the carotid artery most commonly from either penetrating or non-penetrating head trauma.

Direct CCF also occur secondary to cavernous aneurysmrupture and from iatrogenic trauma following oromaxillofacial and neurosurgical procedures.

The most common (70%-90%) etiology of direct CCF is trauma from a basal skull fracture resulting in tear in the internal carotid artery (ICA) within the cavernous sinus.


video of Liao et al., from the Chung Shan Medical University, Institute of Medicine, Taichung. Departments of Neurosurgery and Department of Neuroradiology, Taichung Veterans General Hospital, Neurology, Neurological Institute, and Department of Neurosurgery, Tri-Service General Hospital, National Defense Medical Center, TaipeiTaiwan presents a case of new-onset visual blurring, diplopia, and conjunctival injection after head injuryCTA of the brain revealed a direct carotid-cavernous fistula (dCCF) of the right side. Careful evaluation of CTA source images revealed that the fistula point was at the ventromedial aspect of the right cavernous internal carotid artery (ICA), about 3.6 × 3.6 mm2 in size, with 3 main outflow channels (2 intracranial and 1 extracranial) (CTA-guided concept). DSA of the brain also confirmed the diagnosis but was unable to locate the fistula point in a large-sized dCCF. Through a transfemoral artery approach, 3 microcatheters were navigated to each peripheral channel to initiate outflow-targeted embolization. Intracranial refluxes were blocked first to avoid cerebral hemorrhages, followed by the extracranial outflow. During embolization, accidental dislodge of one coil into the sphenoparietal vein occurred, but no attempt of coil retrieval was made. Complete obliteration of the dCCF was achieved, and the patient recovered well without new neurological deficits. 4D MRA at the 3-month follow-up showed no residual dCCF.The video can be found here: https://youtu.be/LH2lNVRZSPk

 1).

1)

Liao CH, Chen WH, Liao NC, Tsuei YS. CTA-guided outflow-targeted embolization of direct carotid-cavernous fistula. Neurosurg Focus. 2019 Jan 1;46(Suppl_1):V11. doi: 10.3171/2019.1.FocusVid.18447. PubMed PMID: 30611182.

Middle cerebral artery aneurysm stent assisted coiling

Extra intracranial bypass surgery is a well-established procedure for the treatment of chronic ischemic diseases of the carotid artery. Rarely de novo aneurysms can develop at the site of anastomosis. The treatment of these aneurysms can be very challenging due to various factors, including the presence of graft, previous craniotomyatherosclerosis, and lack of direct access. In a video Joshi et al., from the Department of Neurological Surgery, Rush University Medical CenterLoyola University Medical Center and Cerebrovascular Neurosurgery and Comprehensive Stroke Center, ChicagoIllinois, report and discuss the management of a right middle cerebral artery (MCA) wide-necked de novo aneurysm by stent assisted coiling through a retrograde trans-posterior communicating artery access.The video can be found here: https://youtu.be/MBKolPvOErU

 1).


57 patients with MCA trifurcation wide-necked aneurysms underwent stent-assisted coiling embolization using a solitaire AB stent. All 57 patients completed the surgery successfully. Embolization efficacy was graded according to the Modified Raymond-Roy Classification.

There were 52 cases of complete embolization, 4 cases of residual aneurysm neck, and 1 case of residual aneurysm body. 50 patients participated in a 6-36-month follow-up. There has not been observed any aneurysm rupture and hemorrhage. 50 patients received digital subtraction angiography (DSA) re-examination; 46 patients presenting complete embolization had no aneurysm relapses; 3 patients had residual aneurysm neck demonstrated; 1 patient had no aneurysm neck and others 2 were in stable condition. Finally, the patient with residual aneurysm body showed no sign during follow-up reexamination.

Stent-assisted coiling embolization of intracranial wide-necked aneurysms using the solitaire AB stent was safe and effective 2).


From November 2003 to October 2009, 49 patients (27 men, 22 women; mean age, 52 ± 12 years) harboring 52 complex unruptured MCA aneurysms (11 ruptured previously and coiled but recanalized and 41 unruptured) were treated by EVT by using self-expandable intracranial stents. Procedural complications, clinical outcome, and initial and midterm angiographic results were evaluated. Initial treatment status and aneurysm sac size were tested as potential risk factors for recurrence.

After successful stent deployment, coiling was performed in 50 aneurysms (96.2%) in 47 patients; however, 2 failures (3.8%) occurred in 2 patients. Ten intrastent clot formations (20%) observed on final control angiography induced 2 permanent moderate disabilities (GOS score = 2). Mortality and permanent neurologic morbidity were 0% and 4.3%, respectively. At a mean period of 14 ± 9 months, among 48 aneurysms in 45 patients eligible for follow-up, 34 complete (71%) and 14 partial treatments (29%) were observed, 7 recurrences (14.6%) occurred, and 5 patients (10.4%) needed retreatment. No aneurysm bleeding or symptomatic intrastent stenosis was observed. Aneurysm sac size ≥7 mm and incomplete initial treatment were associated with more recurrences without a statistically significant difference.

For complex unruptured MCA aneurysms, EVT by using a self-expandable intracranial stent was feasible, safe, and durable and could be considered as the first-option treatment 3).

References

1)

Joshi KC, Heiferman DF, Beer-Furlan A, Lopes DK. Stent-assisted coil embolization of MCA aneurysm via a trans-posterior communicating artery access. Neurosurg Focus. 2019 Jan 1;46(Suppl_1):V3. doi: 10.3171/2019.1.FocusVid.18444. PubMed PMID: 30611185.
2)

Chen Y, Zhang Y, Chao YJ, Gao G, Ni CS, Fu XM, Wei JJ, Gu DQ, Yu J. Stent-assisted coiling embolization of middle cerebral artery trifurcation wide-necked aneurysms. Eur Rev Med Pharmacol Sci. 2017 Oct;21(19):4346-4349. PubMed PMID: 29077162.
3)

Vendrell JF, Costalat V, Brunel H, Riquelme C, Bonafe A. Stent-assisted coiling of complex middle cerebral artery aneurysms: initial and midterm results. AJNR Am J Neuroradiol. 2011 Feb;32(2):259-63. doi: 10.3174/ajnr.A2272. Epub 2010 Oct 21. PubMed PMID: 20966055.

Internal jugular vein stenosis

Internal jugular vein stenosis (IJVS) is gaining increasing attention from clinical researchers due to a series of confounding symptoms that impair the quality of life in affected individuals but cannot be explained by other well-established causes. In a study of Zhou et al.,from the Xuanwu Hospital, aimed to elucidate the clinical features, neuroimaging characteristics and pathogenesis of IJVS, and explore their possible correlations, in attempt to provide useful clues for clinical diagnosis and treatment. Forty-three eligible patients with unilateral or bilateral IJVS confirmed by contrast-enhanced magnetic resonance venography of the brain and neck were enrolled in a study. Magnetic resonance imaging along with magnetic resonance angiography or computed tomography angiography was applied to identify the radiological pattern of parenchymal or arterial lesions. Cerebral perfusion and metabolismwere evaluated by single-photon emission computed tomography (SPECT). Of the 43 patients (46.0 ± 16.0 years old; 30 female), 14 (32.6%) had bilateral and 29 had unilateral IJVS. The common clinical symptoms at admission were tinnitus (60.5%), tinnitus cerebri (67.6%), headache(48.8%), dizziness (32.6%), visual disorders (39.5%), hearing impairment (39.5%), neck discomfort (39.5%), sleep disturbance (60.5%), anxiety or depression (37.5%) and subjective memory impairment (30.2%). The presence of bilateral demyelination changes with cloudy-like appearance in the periventricular area and/or centrum semiovale was found in 95.3% (41/43) patients. SPECT findings showed that 92.3% (24/26) patients displayed cerebral perfusion and metabolism mismatch, depicted by bilaterally and symmetrically reduced cerebral perfusion and increased cerebral glucose consumption. IJVS may contribute to alterations in cerebral blood flow and metabolism, as well as white matter lesion formation, all of which may account for its clinical manifestations. 1).


Fifteen consecutive patients were screened from 46 patients suspected as IIH and were finally confirmed as isolated IJV stenosis. The stenotic IJV was corrected with stenting when the trans-stenotic mean pressure gradient (∆MPG) was equal to or higher than 5.44 cmH2 O. Dynamic magnetic resonance venography, computed tomographic venography and digital subtraction angiography of the IJV, ∆MPG, ICP, Headache Impact Test 6 and the Frisén papilledema grade score before and after stenting were compared.

All the stenotic IJVs were corrected by stenting. ∆MPG decreased and the abnormal collateral veins disappeared or shrank immediately. Headache, tinnitus, papilledema and ICP were significantly ameliorated at 14 ± 3 days of follow-up (all P < 0.01). At 12 ± 5.6 months of outpatient follow-up, headache disappeared in 14 out of 15 patients (93.3%), visual impairments were recovered in 10 of 12 patients (83.3%) and tinnitus resolved in 10 out of 11 patients (90.9%). In 12 out of 15 cases, the Frisén papilledema grade scores declined to 1 (0-2). The stented IJVs in all 15 patients kept to sufficient blood flows on computed tomographic venography follow-up without stenting-related adverse events.

Non-thrombotic IJV stenosis may be a potential etiology of IIH. Stenting seems to be a promising option to address the issue of intracranial hypertension from the etiological level, particularly after medical treatment failure 2).


Previous magnetic resonance imaging studies have shown abnormalities of the internal jugular veins in patients with thoracic outlet syndrome (TOS), but this finding has largely been ignored. We, thus, prospectively performed diagnostic brachiocephalic venograms in all patients with diagnosed neurogenic TOS from April 2008 to December 2011 (mean age, 42.6; r, 16-68; 77.8% women and 22.2% men). Stenosis of the left internal jugular vein, left subclavian vein, right internal jugular vein, and right subclavian vein were assessed, and significant stenoses of these vessels were seen in 63.49%, 65.08%, 60.32%, and 68.25% of patients, respectively. Internal jugular vein stenosis was not present in 23.81%, present unilaterally in 28.57%, and present bilaterally in 47.62% of patients. Subclavian vein stenosis was not present in 17.46%, present unilaterally in 28.57%, and present bilaterally in 53.97% of patients. Phi coefficients of correlation were 0.067 between left internal jugular vein and left subclavian vein stenoses, 0.061 between right internal jugular vein and right subclavian vein stenoses, and 0 between any internal jugular vein and any subclavian vein stenoses, indicating there is no correlation between jugular vein stenosis and subclavian vein stenosis in these patients. We conclude that right and left internal jugular vein stenosis is common in patients with neurogenic TOS symptoms. Treatment of internal jugular vein stenosis could potentially benefit these patients, and the implications of these findings warrant further study 3).

Clinical trials

References

1)

Zhou D, Ding J, Asmaro K, Pan L, Ya J, Yang Q, Fan C, Ding Y, Ji X, Meng R. Clinical Characteristics and Neuroimaging Findings in Internal Jugular Venous Outflow Disturbance. Thromb Haemost. 2019 Jan 3. doi: 10.1055/s-0038-1676815. [Epub ahead of print] PubMed PMID: 30605919.
2)

Zhou D, Meng R, Zhang X, Guo L, Li S, Wu W, Duan J, Song H, Ding Y, Ji X. Intracranial hypertension induced by internal jugular vein stenosiscan be resolved by stenting. Eur J Neurol. 2018 Feb;25(2):365-e13. doi: 10.1111/ene.13512. Epub 2017 Dec 7. PubMed PMID: 29114973.
3)

Ahn SS, Miller TJ, Chen SW, Chen JF. Internal jugular vein stenosis is common in patients presenting with neurogenic thoracic outlet syndrome. Ann Vasc Surg. 2014 May;28(4):946-50. doi: 10.1016/j.avsg.2013.12.009. Epub 2014 Jan 21. PubMed PMID: 24462538.

Carotid artery stenosis

Carotid artery stenosis is a narrowing or constriction of the inner surface (lumen) of the carotid artery, usually caused by atherosclerosis.

Carotid artery stenosis (CS) is a major cause of ischemic stroke.

Classification

Asymptomatic carotid artery stenosis.

Symptomatic carotid artery stenosis

Clinical features

The mechanisms underlying acute cerebrovascular syndrome in patients with carotid artery stenosis remain unclear.

Carotid artery stenosis can present with no symptoms or with symptoms such as transient ischemic attacks (TIAs) or strokes, contributing to up to 10%-20% of strokes or transient ischemic attacks.

Cortical infarction occurs as a result of vulnerable plaque. Reduced cerebral perfusión induces border-zone infarction. Both factors are implicated in mixed-pattern infarction. Developments in noninvasive diagnostic modalities allow us to explore the mechanisms behind acute cerebrovascular syndrome in carotid artery stenosis and to determine the ideal therapies 1).

Diagnosis

Currently, MRI is the gold standard in carotid plaque imaging, with its high resolution and high sensitivity for identifying intraplaque hemorrhage (IPH), ulceration, lipid-rich necrotic core (LRNC), and inflammation. However, MRI is limited due to time constraints.

CT also allows for high-resolution imaging and can accurately detect ulceration and calcification, but cannot reliably differentiate LRNC from IPH.

PET/CT is an effective technique to identify active inflammation within the plaque, but it does not allow for assessment of anatomy, ulceration, IPH, or LRNC.

Ultrasonography, with the aid of contrast enhancement, is a cost-effective technique to assess plaque morphology and characteristics, but it is limited in sensitivity and specificity for detecting LRNC, plaque hemorrhage, and ulceration compared with MRI.

US can detect congenital variants, dissection, stenosis, and vasculopathy. In addition, correlation of US findings with both magnetic resonance imaging and computed tomography more comprehensively demonstrates the complementary nature of these imaging modalities 2).

Also summarized is how these advanced imaging techniques are being used in clinical practice to risk stratify patients with low- and high-grade carotid artery stenosis. For example, identification of IPH on MRI in patients with low-grade carotid artery stenosis is a risk factor for failure of medical therapy, and studies have shown that such patients may fair better with carotid endarterectomy (CEA). MR plaque imaging has also been found to be useful in identifying revascularization candidates who would be better candidates for CEA than carotid artery stenting (CAS), as high intraplaque signal on time of flight imaging is associated with vulnerable plaque and increased rates of adverse events in patients undergoing CAS but not CEA 3).

Treatment

Case series

Sixty-seven consecutive procedures were performed for internal carotid artery stenosis with CAS at the Ise Red Cross Hospital between November 2015 and February 2018. Procedures for emergency CAS for stroke in evolution or crescendo transient ischemic attack were excluded (n = 12). The embolic debris from remaining procedures (n = 55) was stained with hematoxylineosin and the red blood cells, white blood cells, and fibrinwere quantified by color-based segmentation. Cholesterol crystals and calcification were examined histopathologically. Diffusion-weighted imaging (DWI) was performed 1-3 days after CAS, and the images were used to classify procedures according to the presence of new lesions.

Of the 55 CAS procedures, new DWI lesions were identified after 32. One patient had symptomatic cerebral embolism. Higher proportions of patients with cholesterol crystals in embolic debris (17 vs. 78%, p < 0.001) and higher proportion of white blood cells (mean 2.3 [0-9.9] vs. 4.2% [0-29.9%], p < 0.01) were observed in the embolic debris of procedures with and without new DWI lesions.

Cholesterol crystals were common in the embolic debris from patients with postoperative ischemic lesions after CAS. These results suggest that inflammatory destabilization of the intraplaque lipid component is related to postprocedural DWI lesions 4).

References

1)

Kashiwazaki D, Akioka N, Kuwayama N, Noguchi K, Tanaka K, Kuroda S. Pathophysiology of acute cerebrovascular syndrome in patients with carotid artery stenosis: a magnetic resonance imaging/single-photon emission computed tomography study. Neurosurgery. 2015 Apr;76(4):427-34. doi: 10.1227/NEU.0000000000000655. PubMed PMID: 25621983.
2)

Deurdulian C, Emmanuel N, Tchelepi H, Grant EG, Malhi H. Beyond the Bifurcation: There Is More to Cerebrovascular Ultrasound Than Internal Carotid Artery Stenosis! Ultrasound Q. 2015 Nov 19. [Epub ahead of print] PubMed PMID: 26588099.
3)

Brinjikji W, Huston J 3rd, Rabinstein AA, Kim GM, Lerman A, Lanzino G. Contemporary carotid imaging: from degree of stenosis to plaque vulnerability. J Neurosurg. 2016 Jan;124(1):27-42. doi: 10.3171/2015.1.JNS142452. Epub 2015 Jul 31. PubMed PMID: 26230478.
4)

Maekawa K, Shibata M, Nakajima H, Kitano Y, Seguchi M, Kobayashi K, Sano T, Yabana T, Miya F. Cholesterol Crystals in Embolic Debris are Associated with Postoperative Cerebral Embolism after Carotid Artery Stenting. Cerebrovasc Dis. 2019 Jan 2;46(5-6):242-248. doi: 10.1159/000495795. [Epub ahead of print] PubMed PMID: 30602147.

Trevo Retriever

The Trevo Stent Retriever is a tiny stent-shaped medical device that is attached to a thin wire. In a minimally invasive procedure that utilizes X-ray, the physician navigates the retriever from the femoral artery, which is located in the upper leg, to the blocked blood artery in the brain. The retriever is designed to ensnare the blood clot and remove it from the body. Originally cleared by the FDA in 2012, the Trevo Retriever has been used in thousands of patients worldwide.

Imahori et al., retrospectively reviewed 50 patients with acute middle cerebral artery occlusion treatment with the Trevo Stent retriever. Patients were divided into groups that achieved (1st-pass recanalization group, n=21) or did not achieve (non-1st-pass recanalization group, n=29) a modified Thrombolysis in Cerebral Ischemia score of 2b or 3 with the 1st-pass procedure. Patients were also divided into a thromboembolic (n=49) and atherosclerotic (n=11) group by occlusion etiology. They evaluated radiographic findings of the Trevo strut, e.g., degree of stent expansion and filling defect of the thrombus in the strut (in-stent thrombus sign) during the 1st-pass procedure among these groups.

The median stent expansion was significantly greater in the 1st-pass recanalization than non-1st-pass recanalization group (60% versus 34%; P<0.01), and in the thromboembolic than atherosclerotic group (45% versus 31%; P<0.01). The receiver operator characteristic curve shows moderate capacity of the prediction for recanalization and etiology, with an area under the curve of 0.83 and 0.73, respectively. The in-stent thrombus sign was significantly more common in the thromboembolic than atherosclerotic groups (86% versus 10%; P<0.01).

Greater stent expansion was associated with recanalization after thrombectomy. The in-stent thrombus sign may be useful for etiology prediction. These radiographic findings could provide useful real-time feedback during procedure, reflecting the clot-stent interaction 1).

1)

Imahori T, Okamura Y, Sakata J, Shose H, Yokote A, Matsushima K, Matsui D, Kobayashi M, Hosoda K, Tanaka K, Fujita A, Kohmura E. Stent expansion and in-stent thrombus sign in the Trevo stent retriever predict recanalization and possible etiology during mechanical thrombectomy: A case series of 50 patients with acute middle cerebral artery occlusion. World Neurosurg. 2018 Dec 28. pii: S1878-8750(18)32910-3. doi: 10.1016/j.wneu.2018.12.087. [Epub ahead of print] PubMed PMID: 30597281.
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