ICH Score

ICH Score

The ICH Score: What It Is and What It Is Not 1).

Simple and reliable clinical grading score that is used for predicting the early mortality of patients with intracerebral hemorrhage (ICH).

The ICH Score has become the standard for risk-stratification of 30-d mortality in patients with intracerebral hemorrhage (ICH), but treatment has evolved over the last 17 yr since its inception.

The ICH score is a useful tool for predicting 30-day mortality both in patient who use and patients who do not use OAC. Although OAC use is an independent predictor of 30-day mortality, addition of OAC use to the existing ICH score does not increase the prognostic performance of this score 2)

The ICH Score is the sum of individual points assigned as follows:

GCS

GCS score 3 to 4 (=2 points),

5 to 12 (=1),

13 to 15 (=0)

Age

Age >/=80 years yes (=1), no (=0);

Localization

Infratentorial origin yes (=1), no (=0);

ICH volume >/=30 cm(3) (=1), <30 cm(3) (=0);

Intraventricular hemorrhage yes (=1), no (=0).

Patient 68 years old GCS 4: ICH 4 score

All 26 patients with an ICH Score of 0 survived, and all 6 patients with an ICH Score of 5 died. Thirty-day mortality increased steadily with ICH Score (P<0.005) 3).


Malinova et al. evaluated the reproducibility of the ICH-score in ICH patients undergoing fibrinolytic therapy.

They performed a retrospective analysis of patients with supratentorial ICH managed by fibrinolytic therapy and evaluated the 30-day mortality. The ICH-score was then applied to match the mortality in the patients with the mortality predicted by the ICH-score. The ICH-score is based on parameters available at admission: age, hematoma volume, intraventricular expansion, and clinical status according to the Glasgow Coma Scale.

A total of 233 patients were analyzed. The 30-day mortality rate was 30% (70/233). An age of ≥80 years was associated with a significantly higher mortality rate (OR 2.26, chi-square test p = 0.01). A hematoma volume of ≥30 mL led significantly more often to 30-day mortality (OR 3.72, chi-square test p = 0.01). The mortality was significantly higher in patients with intraventricular hemorrhage (2.97, chi-square test p = 0.003). The ICH-score showed a significant correlation with mortality (chi-square test, p < 0.0001). The following mortality rates were estimated using the ICH-score in our cohort: 1 = 0% (0/13), 2 = 0% (0/51), 3 = 1.3% (1/82), 4 = 43% (13/31), 5 = 100% (56/56). : The ICH-score not only allowed a reliable estimation of the 30-day mortality in patients with ICH treated conservatively but also treated by clot lysis. Compared to conservative treatment, fibrinolytic therapy reduced the 30-day mortality in patients with ICH-scores 1-4. Patients with ICH-score 5 do not have a benefit of fibrinolytic therapy and should no longer be considered to be candidates for fibrinolytic therapy 4).


The original ICH score did not accurately predict the mortality rate in the series of the Department of Neurosurgery, Emory University, AtlantaGeorgia. Patient survival exceeded ICH Score-predicted mortality regardless of surgical intervention. Reevaluation of predictive scores could be useful to aid in more accurate prognoses 5).

References

1)

Hemphill JC 3rd. The ICH Score: What It Is and What It Is Not. World Neurosurg. 2018 Dec 20. pii: S1878-8750(18)32883-3. doi: 10.1016/j.wneu.2018.12.060. [Epub ahead of print] PubMed PMID: 30580061.
2)

Houben R, Schreuder FHBM, Bekelaar KJ, Claessens D, van Oostenbrugge RJ, Staals J. Predicting Prognosis of Intracerebral Hemorrhage (ICH): Performance of ICH Score Is Not Improved by Adding Oral Anticoagulant Use. Front Neurol. 2018 Feb 28;9:100. doi: 10.3389/fneur.2018.00100. eCollection 2018. PubMed PMID: 29541054; PubMed Central PMCID: PMC5836590.
3)

Hemphill JC III, Bonovich DC, Besmertis L, Manley GT, Johnston SC. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001;14:891–897. doi: 10.1161/01.STR.32.4.891.
4)

Malinova V, Iliev B, Mielke D, Rohde V. Intracerebral Hemorrhage-Score Allows a Reliable Prediction of Mortality in Patients with Spontaneous Intracerebral Hemorrhage Managed by Fibrinolytic Therapy. Cerebrovasc Dis. 2019 Nov 13:1-6. doi: 10.1159/000504246. [Epub ahead of print] PubMed PMID: 31722333.
5)

McCracken DJ, Lovasik BP, McCracken CE, Frerich JM, McDougal ME, Ratcliff JJ, Barrow DL, Pradilla G. The Intracerebral Hemorrhage Score: A Self-Fulfilling Prophecy? Neurosurgery. 2018 May 14. doi:

Chronic subdural hematoma surgery complications

Chronic subdural hematoma surgery complications

Common postoperative complications include acute epidural and/or subdural bleeding, tension pneumocephalusintracranial hematomas and ischemic cerebral infarction.

Failure of the brain to re-expand, pneumocephalus, incomplete evacuation, and recurrence of the fluid collection are the most frequently.

Seizures

Seizures (including intractable status epilepticus).

Intracerebral hemorrhage

Intracerebral hemorrhage (ICH): occurs in 0.7–5%. Very devastating in this setting: one–third of these patients die and one third are severely disabled

Brain herniation

Chronic subdural hematoma (CSDH) with brain herniation signs is rarely seen in the emergent department. As such, there are few cumulative data to analyze such cases.

Failure of postoperative cerebral reexpansion

A wide variation in postoperative drainage volumes is observed during treatment of chronic subdural hematoma (CSDH) with twist-drill or burr-hole craniostomy and closed-system drainage.

The postoperative drainage volumes varied greatly because of differences in the outer membrane permeability of CSDH, and such variation seems to be related to the findings on the CT scans obtained preoperatively. Patients with CSDH in whom there is less postoperative drainage than expected should be carefully observed, with special attention paid to the possibility of recurrence 1).

Patients with high subdural pressure showed the most rapid brain expansion and clinical improvement during the first 2 days. Nevertheless, a computerized tomography (CT) scan performed on the 10th day after surgery demonstrated persisting subdural fluid in 78% of cases. After 40 days, the CT scan was normal in 27 of the 32 patients. There was no mortality and no significant morbidity. A study suggests that well developed subdural neomembranes are the crucial factors for cerebral reexpansion, a phenomenon that takes at least 10 to 20 days. However, blood vessel dysfunction and impairment of cerebral blood flow may participate in delay of brain reexpansion. It may be argued that additional surgical procedures, such as repeated tapping of the subdural fluid, craniotomy, and membranectomy or even craniectomy, should not be evaluated earlier than 20 days after the initial surgical procedure unless the patient has deteriorated markedly 2).

Recurrence

Postoperative pneumocephalus

Remote cerebellar hemorrhage (RCH)

Epidural hematoma

After chronic subdural hematoma evacuation surgery, the development of epidural hematoma is a very rare entity.

Akpinar et al. report the case of a 41-year-old man with an epidural hematoma complication after chronic subdural hematoma evacuation. Under general anesthesia, the patient underwent a large craniotomy with closed system drainage performed to treat the chronic subdural hematoma. After chronic subdural hematoma evacuation, there was epidural leakage on the following day.

Although trauma is the most common risk factor in young CSDH patients, some other predisposing factors may exist. Intracranial hypotension can cause EDH. Craniotomy and drainage surgery can usually resolve the problem. Because of rapid dynamic intracranial changes, epidural leakages can occur. A large craniotomy flap and silicone drainage in the operation area are key safety points for neurosurgeons and hydration is essential 3).

Intracranial subdural empyema

A case of intracranial subdural empyema following chronic subdural hematoma drainage 4).

Skin depression

Oculomotor nerve palsy

References

1)

Kwon TH, Park YK, Lim DJ, Cho TH, Chung YG, Chung HS, Suh JK. Chronic subdural hematoma: evaluation of the clinical significance of postoperative drainage volume. J Neurosurg. 2000 Nov;93(5):796-9. PubMed PMID: 11059660.
2)

Markwalder TM, Steinsiepe KF, Rohner M, Reichenbach W, Markwalder H. The course of chronic subdural hematomas after burr-hole craniostomy and closed-system drainage. J Neurosurg. 1981 Sep;55(3):390-6. PubMed PMID: 7264730.
3)

Akpinar A, Ucler N, Erdogan U, Yucetas CS. Epidural Hematoma Complication after Rapid Chronic Subdural Hematoma Evacuation: A Case Report. Am J Case Rep. 2015 Jul 6;16:430-433. PubMed PMID: 26147957.
4)

Ovalioglu AO, Aydin OA. A case of subdural empyema following chronic subdural hematoma drainage. Neurol India. 2013 Mar-Apr;61(2):207-9. doi: 10.4103/0028-3886.111165. PubMed PMID: 23644343.

Hydrocephalus after aneurysmal subarachnoid hemorrhage

Hydrocephalus after aneurysmal subarachnoid hemorrhage

Epidemiology

Hydrocephalus complicates the clinical course of greater than 20% of patients with aneurysmal subarachnoid hemorrhage 1) 2) , and its onset can be acute, within 48 hours after SAH, or rarely chronic, occurring in a delayed fashion weeks and even months after the hemorrhage.

Etiology

The etiology of hydrocephalus following aSAH has yet to be fully elucidated, but is likely to include the following: obstruction of CSF flow within the basal cisterns and/or ventricles by clotted blood, diminished absorption at the arachnoid granulations, and inflammation 3) 4) 5) 6).

Na et al. found that higher sodium, lower potassium, and higher glucose levels were predictive values for shunt-dependent hydrocephalus from postoperative day (POD) 1 to POD 12-16 after subarachnoid hemorrhage. Strict correction of electrolyte imbalance seems necessary to reduce shunt-dependent hydrocephalus. Further large studies are warranted to confirm the findings 7).

Data suggest that the volume of the third ventricle in the initial CT is a strong predictor for shunt dependency after aSAH 8).

Diagnosis

Early recognition of its signs and symptoms and accurate interpretation of computed tomography (CT) studies are important for the management of patients with SAH. Clinically, a poor neurologic grade has the highest correlation with an increased incidence of hydrocephalus. Radiographically, the bicaudate index on CT studies has emerged as the best marker of this condition. Although further studies are needed to understand the complex pathophysiology of this condition, hydrocephalus after SAH can be treated effectively using current technology 9).


Most readmissions after aneurysmal subarachnoid hemorrhage (SAH) relate to late consequences of hemorrhage, such as hydrocephalus, or medical complications secondary to severe neurological injury. Although a minority of readmissions may potentially be avoided with closer medical follow-up in the transitional care environment, readmission after SAH is an insensitive and likely inappropriate hospital performance metric 10).

Data demonstrate that gender influences acute hydrocephalus development in a rat SAH model. Future studies should determine the role of estrogen in SAH-induced hydrocephalus 11).

Hydrocephalus might cause gradual obtundation in the first few hours or days; it can be treated by lumbar puncture or ventricular drainage, dependent on the site of obstruction

Aneurysmal subarachnoid hemorrhage (SAH) has been reported to induce an intrathecal inflammatory reaction reflected by cytokine release, particularly interleukin-6 (IL-6), which correlates with early brain damage and poor outcome.

Treatment

Hydrocephalus might cause gradual obtundation in the first few hours or days; it can be treated by lumbar puncture or ventricular drainage, dependent on the site of obstruction 12).

Outcome

Hydrocephalus is a common and potentially devastating complication of aneurysmal subarachnoid hemorrhage (SAH).

Hydrocephalus leads to prolonged hospital and ICU stays, well as to repeated surgical interventions, readmissions, and complications associated with ventriculoperitoneal shunts, including shunt failure and shunt infection. Whether variations in surgical technique at the time of aneurysm treatment may modify rates of shunt dependency remains a matter of debate 13).

Shunt dependency

The indication for and the timing of a permanent shunt operation in patients following acute hydrocephalus (HC) after subarachnoid hemorrhage (SAH) remains controversial because risk factors for chronic HC fail to predict permanent shunt dependency. The amount of cerebrospinal fluid (CSF) drained via an external ventricular drain (EVD) may predict shunt dependency.

Results suggest that the daily amount of external CSF drainage volume in the acute state of SAH might influence the development of HC 14).


CSF IL-6 values of ≥10,000 pg/ml in the early post-SAH period may be a useful diagnostic tool for predicting shunt dependency in patients with acute posthemorrhagic hydrocephalus. The development of shunt-dependent posthemorrhagic hydrocephalus remains a multifactorial process 15).

Reliable prognostic tools to estimate the case fatality rate (CFR) and the development of chronic hydrocephalus (CHC) in aneurysmal subarachnoid hemorrhage (SAH) are not well defined.

Graeb Score or LeRoux score improve the prediction of shunt dependency and in parts of CFR in aneurysmal SAH patients therefore confirming the relevance of the extent and distribution of intraventricular blood for the clinical course in SAH 16).

Case series

One-hundred and fifty-two patients who had undergone an operation for SAH were enrolled in this study. Clinical data, radiological data, and procedural data were investigated. Procedural data included the operating technique (clipping vs. EVT) and the use of additional procedures (no procedure, lumbar drainage, or EVD). Delayed hydrocephalus was defined as a condition in which the Evan’s index was 0.3 or higher, as assessed using brain computed tomography more than 2 weeks after surgery, requiring shunt placement due to neurological deterioration.

Of the 152 patients, 45 (29.6%) underwent surgical clipping and 107 (70.4%) underwent EVT. Twenty-five (16.4%) patients developed delayed hydrocephalus. Age (p = 0.019), procedure duration (p = 0.004), and acute hydrocephalus (p = 0.030) were significantly correlated with the incidence of delayed hydrocephalus. However, the operation technique (p = 0.593) and use of an additional procedure (p = 0.378) were not significantly correlated with delayed hydrocephalus incidence.

No significant difference in the incidence of delayed hydrocephalus was associated with operation technique or use of an additional procedure in patients with SAH. However, delayed hydrocephalus was significantly correlated with old age, long procedural duration, and acute hydrocephalus. Therefore, they recommend that additional procedures should be discontinued as soon as possible 17).

2017

Winkler et al. conducted a retrospective review of 663 consecutive patients with aSAH treated from 2005 to 2015 by open microsurgery via a pterional or orbitozygomatic craniotomy by the senior author (M.T.L.). Data collected from review of the electronic medical record included age, Hunt and Hess grade, Fisher grade, need for an external ventricular drain, and opening pressure. Patients were stratified into those undergoing no fenestration and those undergoing tandem fenestration of the LT and MoL at the time of surgical repair. Outcome variables, including VP shunt placement and timing of shunt placement, were recorded and statistically analyzed. RESULTS In total, shunt-dependent hydrocephalus was observed in 15.8% of patients undergoing open surgical repair following aSAH. Tandem microsurgical fenestration of the LT and MoL was associated with a statistically significant reduction in shunt dependency (17.9% vs 3.2%, p < 0.01). This effect was confirmed with multivariate analysis of collected variables (multivariate OR 0.09, 95% CI 0.03-0.30). Number-needed-to-treat analysis demonstrated that tandem fenestration was required in approximately 6.8 patients to prevent a single VP shunt placement. A statistically significant prolongation in days to VP shunt surgery was also observed in patients treated with tandem fenestration (26.6 ± 19.4 days vs 54.0 ± 36.5 days, p < 0.05). CONCLUSIONS Tandem fenestration of the LT and MoL at the time of open microsurgical clipping and/or bypass to secure ruptured anterior and posterior circulation aneurysms is associated with reductions in shunt-dependent hydrocephalus following aSAH. Future prospective randomized multicenter studies are needed to confirm this result 18).


181 participants with a mean age of 54.4 years. Higher sodium (hazard ratio, 1.53; 95% confidence interval, 1.13-2.07; p = 0.005), lower potassium, and higher glucose levels were associated with higher shunt-dependent hydrocephalus. The receiver operating characteristic curve analysis showed that the areas under the curve of sodium, potassium, and glucose were 0.649 (cutoff value, 142.75 mEq/L), 0.609 (cutoff value, 3.04 mmol/L), and 0.664 (cutoff value, 140.51 mg/dL), respectively.

Despite the exploratory nature of this study, we found that higher sodium, lower potassium, and higher glucose levels were predictive values for shunt-dependent hydrocephalus from postoperative day (POD) 1 to POD 12-16 after subarachnoid hemorrhage. Strict correction of electrolyte imbalance seems necessary to reduce shunt-dependent hydrocephalus. Further large studies are warranted to confirm our findings 19).

2016

The study is designed to determine the efficacy of lamina terminalis fenestration on the reduction of SDH after aneurysm clipping.

METHODS/DESIGN: A total of 288 patients who meet the inclusion criteria will be randomized into single aneurysm clipping or aneurysm clipping plus FLT in the Department of Neurosurgery, West China Hospital. Follow-up was performed 1, 3, 6, and 12 months after aneurysm clipping. The primary outcome is the incidence of SDH and the secondary outcomes include cerebral vasospasm, functional outcome evaluated by the modified Rankin Scale and Extended Glasgow Outcome Scale, and mortality.

DISCUSSION: The FISH trial is a large randomized, parallel controlled clinical trial to define the therapeutic value of FLT, the results of which will help to guide the surgical procedure and resolve the long-puzzled debate in the neurosurgical community.

CONCLUSIONS: This protocol will determine the efficacy of FLT in the setting of aneurysmal subarachnoid hemorrhage 20).

2003

Seven hundred eighteen patients with aneurysmal subarachnoid hemorrhage who were treated between 1990 and 1999 were retrospectively studied, to identify factors contributing to shunt-dependent hydrocephalus. With these data, a stepwise logistic regression procedure was used to determine the effect of each variable on the development of hydrocephalus and to create a scoring system.

Overall, 152 of the 718 patients (21.2%) underwent shunting procedures for treatment of hydrocephalus. Four hundred seventy-nine of the patients (66.7%) were female. Of the factors investigated, the following were associated with shunt-dependent hydrocephalus, as determined with a variety of statistical methods: 1) increasing age (P < 0.001), 2) female sex (P = 0.015), 3) poor admission Hunt and Hess grade (P < 0.001), 4) thick subarachnoid hemorrhage on admission computed tomographic scans (P < 0.001), 5) intraventricular hemorrhage (P < 0.001), 6) radiological hydrocephalus at the time of admission (P < 0.001), 7) distal posterior circulation location of the ruptured aneurysm (P = 0.046), 8) clinical vasospasm (P < 0.001), and 9) endovascular treatment (P = 0.013). The presence of intracerebral hematomas, giant aneurysms, or multiple aneurysms did not influence the development of shunt-dependent hydrocephalus.

The results of this study can help identify patients with a high risk of developing shunt-dependent hydrocephalus. This may help neurosurgeons expedite treatment, may decrease the cost and length of hospital stays, and may result in improved outcomes 21).

2000

In 138 patients with ruptured cerebral aneurysms operated on within 48 to 72 hours after subarachnoid hemorrhage, an external ventricular drainage catheter was inserted before craniotomy and was used intermittently during the first week after surgery. In 51 patients, intracranial pressure (ICP) was measured intraoperatively. The majority of patients showed increased ICP intraoperatively irrespective of the preoperative Hunt and Hess grade and the amount of subarachnoid blood accumulation or intraventricular blood clot. Intraoperative drainage of cerebrospinal fluid allowed easy access for aneurysm dissection by making the brain slack in more than 90% of patients. Postoperative ICP measurements revealed that significant brain swelling did not occur in the majority of patients. In 7 patients, persistently elevated ICP (greater than 20 mm Hg) was recorded. Nine patients (8%) developed shunt-dependent hydrocephalus; all of these patients had suffered an intraventricular hemorrhage. Measurements of the volumes of cerebrospinal fluid drained did not allow prediction of shunt-dependent hydrocephalus 22).

1987

The incidence and clinical aspects of acute hydrocephalus were examined in 200 patients with recently ruptured intracranial aneurysms. The following conclusions were reached: Acute hydrocephalus is an important complication of aneurysmal subarachnoid hemorrhage that occurs in approximately 20% of all cases and exhibits an incidence that tends to parallel clinical grade (Grade I, 3%; Grade II, 5%; “Good” Grade III, 21%; “Bad”Grade III, 40%; Grade IV, 42%; Grade V, 26%). Impaired consciousness leading to a general downgrading of clinical status was the predominant clinical finding (93%), but neither this nor other nonspecific signs of increased intracranial pressure were distinguishable from the effects of the precipitating hemorrhage. The computed tomographic signs of acute hydrocephalus are distinctive and consist of selective ballooning of the frontal horns, rostral-caudal enlargement of the cerebral ventricles, and a halo of periventricular hyperdensity (edema) that evolves in sequence with ventricular changes. The treatment of choice is external ventricular drainage, which results in prompt and often dramatic improvement in approximately two-thirds of the patients 23).

1985

Hydrocephalus, defined as a bicaudate index above the 95th percentile for age, was found in 34 (20%) of 174 prospectively studied patients with subarachnoid hemorrhage (SAH) who survived the first 24 hours and who underwent computerized tomography (CT) scanning within 72 hours. The occurrence of acute hydrocephalus was related to the presence of intraventricular blood, and not to the extent of cisternal hemorrhage. The level of consciousness was depressed in 30 of the 34 patients. Characteristic clinical features were present in 19 patients, including a gradual obtundation after the initial hemorrhage in 16 patients and small nonreactive pupils in nine patients (all with a Glasgow Coma Scale score of 7 or less). In the remaining 15 patients (44%), the diagnosis could be made only by CT scanning. After 1 month, 20 of the 34 patients had died: six from rebleeding (four after shunting), 11 from cerebral infarction (eight after an initial improvement), and three from other or mixed causes. Only one of nine patients in whom a shunt was placed survived, despite rapid improvement in all immediately after shunting. The mortality rate among patients with acute hydrocephalus was significantly higher than in those without, with the higher incidence caused by cerebral infarction (11 of 34 versus 12 of 140 cases, respectively; p less than 0.001). Death from infarction could not be attributed to the extent of cisternal hemorrhage, the use of antifibrinolytic drugs, or failure to apply surgical drainage, but could often be explained by the development of hyponatremia, probably accompanied by hypovolemia 24).

1984

Seventeen patients suffering from SAH and/or intraventricular hemorrhage were studied; all were admitted in Grades II to V according to Hunt and Hess. Eleven patients had a proven aneurysm. The ICP, monitored via an intraventricular catheter, was above 15 mm Hg (2 kPa) during part of the monitoring period in all patients. B-waves at 1/min were noted in all patients. Resistance to outflow of CSF was determined by the following techniques: 1) bolus injection; 2) constant-rate steady-state infusion; or 3) controlled withdrawal (“inverse infusion”). Resistance to outflow of CSF was increased in all patients, ranging from 11.5 to 85 mm Hg/ml/min. The ICP was linearly correlated with outflow resistance. Four (50%) of the eight survivors required a shunt. Neither the presence of hydrocephalus on admission, nor the level of ICP, nor the magnitude of resistance to outflow of CSF was clearly related to the requirement of a permanent CSF diversion 25).

References

1)

Wilson CD, Safavi-Abbasi S, Sun H, Kalani MY, Zhao YD, Levitt MR, et al: Meta-analysis and systematic review of risk factors for shunt dependency after aneurysmal subarachnoid hemorrhage. J Neurosurg 126:586–595, 2017
2)

Yamada S, Nakase H, Park YS, Nishimura F, Nakagawa I: Discriminant analysis prediction of the need for ventriculo- peritoneal shunt after subarachnoid hemorrhage. J Stroke Cerebrovasc Dis 21:493–497, 2012
3) , 22)

Auer LM, Mokry M. Disturbed cerebrospinal fluid circulation after subarachnoid hemorrhage and acute aneurysm surgery. Neurosurgery. 1990 May;26(5):804-8; discussion 808-9. PubMed PMID: 2352599.
4)

Dorai Z, Hynan LS, Kopitnik TA, Samson D: Factors related to hydrocephalus after aneurysmal subarachnoid hemorrhage. Neurosurgery 52:763–771, 2003
5)

Massicotte EM, Del Bigio MR. Human arachnoid villi response to subarachnoid hemorrhage: possible relationship to chronic hydrocephalus. J Neurosurg. 1999 Jul;91(1):80-4. PubMed PMID: 10389884.
6) , 24)

van Gijn J, Hijdra A, Wijdicks EF, Vermeulen M, van Crevel H. Acute hydrocephalus after aneurysmal subarachnoid hemorrhage. J Neurosurg. 1985 Sep;63(3):355-62. PubMed PMID: 4020461.
7)

Na MK, Won YD, Kim CH, Kim JM, Cheong JH, Ryu JI, Han MH. Early variations of laboratory parameters predicting shunt-dependent hydrocephalus after subarachnoid hemorrhage. PLoS One. 2017 Dec 12;12(12):e0189499. doi: 10.1371/journal.pone.0189499. eCollection 2017. PubMed PMID: 29232410; PubMed Central PMCID: PMC5726740.
8)

Pinggera D, Kerschbaumer J, Petr O, Ortler M, Thomé C, Freyschlag CF. The Volume of the Third Ventricle as a Prognostic Marker for Shunt Dependency After Aneurysmal Subarachnoid Hemorrhage. World Neurosurg. 2017 Dec;108:107-111. doi: 10.1016/j.wneu.2017.08.129. Epub 2017 Sep 1. PubMed PMID: 28867328.
9)

Germanwala AV, Huang J, Tamargo RJ. Hydrocephalus after aneurysmal subarachnoid hemorrhage. Neurosurg Clin N Am. 2010 Apr;21(2):263-70. doi: 10.1016/j.nec.2009.10.013. Review. PubMed PMID: 20380968.
10)

Greenberg JK, Washington CW, Guniganti R, Dacey RG Jr, Derdeyn CP, Zipfel GJ. Causes of 30-day readmission after aneurysmal subarachnoid hemorrhage. J Neurosurg. 2016 Mar;124(3):743-9. doi: 10.3171/2015.2.JNS142771. Epub 2015 Sep 11. PubMed PMID: 26361278.
11)

Shishido H, Zhang H, Okubo S, Hua Y, Keep RF, Xi G. The Effect of Gender on Acute Hydrocephalus after Experimental Subarachnoid Hemorrhage. Acta Neurochir Suppl. 2016;121:335-9. doi: 10.1007/978-3-319-18497-5_58. PubMed PMID: 26463971.
12)

van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007 Jan 27;369(9558):306-18. Review. PubMed PMID: 17258671.
13) , 18)

Winkler EA, Burkhardt JK, Rutledge WC, Rick JW, Partow CP, Yue JK, Birk H, Bach AM, Raygor KP, Lawton MT. Reduction of shunt dependency rates following aneurysmal subarachnoid hemorrhage by tandem fenestration of the lamina terminalis and membrane of Liliequist during microsurgical aneurysm repair. J Neurosurg. 2017 Dec 15:1-7. doi: 10.3171/2017.5.JNS163271. [Epub ahead of print] PubMed PMID: 29243978.
14)

Hayek MA, Roth C, Kaestner S, Deinsberger W. Impact of External Ventricular Drainage Volumes on Shunt Dependency after Subarachnoid Hemorrhage. J Neurol Surg A Cent Eur Neurosurg. 2016 Jul 22. [Epub ahead of print] PubMed PMID: 27448196.
15)

Wostrack M, Reeb T, Martin J, Kehl V, Shiban E, Preuss A, Ringel F, Meyer B, Ryang YM. Shunt-Dependent Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage: The Role of Intrathecal Interleukin-6. Neurocrit Care. 2014 May 20. [Epub ahead of print] PubMed PMID: 24840896.
16)

Czorlich P, Ricklefs F, Reitz M, Vettorazzi E, Abboud T, Regelsberger J, Westphal M, Schmidt NO. Impact of intraventricular hemorrhage measured by Graeb and LeRoux score on case fatality risk and chronic hydrocephalus in aneurysmal subarachnoid hemorrhage. Acta Neurochir (Wien). 2015 Jan 21. [Epub ahead of print] PubMed PMID: 25599911.
17)

Eom TO, Park ES, Park JB, Kwon SC, Sim HB, Lyo IU, Kim MS. Does Neurosurgical Clipping or Endovascular Coiling Lead to More Cases of Delayed Hydrocephalus in Patients with Subarachnoid Hemorrhage? J Cerebrovasc Endovasc Neurosurg. 2018 Jun;20(2):87-95. doi: 10.7461/jcen.2018.20.2.87. Epub 2018 Jun 30. PubMed PMID: 30370242; PubMed Central PMCID: PMC6196142.
19)

Na MK, Won YD, Kim CH, Kim JM, Cheong JH, Ryu JI, Han MH. Early variations of laboratory parameters predicting shunt-dependent hydrocephalus after subarachnoid hemorrhage. PLoS One. 2017 Dec 12;12(12):e0189499. doi: 10.1371/journal.pone.0189499. eCollection 2017. PubMed PMID: 29232410.
20)

Tao C, Fan C, Hu X, Ma J, Ma L, Li H, Liu Y, Sun H, He M, You C. The effect of fenestration of the lamina terminalis on the incidence of shunt-dependent hydrocephalus after aneurysmal subarachnoid hemorrhage (FISH): Study protocol for a randomized controlled trial. Medicine (Baltimore). 2016 Dec;95(52):e5727. doi: 10.1097/MD.0000000000005727. PubMed PMID: 28033279; PubMed Central PMCID: PMC5207575.
21)

Dorai Z, Hynan LS, Kopitnik TA, Samson D. Factors related to hydrocephalus after aneurysmal subarachnoid hemorrhage. Neurosurgery. 2003 Apr;52(4):763-9; discussion 769-71. PubMed PMID: 12657171.
23)

Milhorat TH. Acute hydrocephalus after aneurysmal subarachnoid hemorrhage. Neurosurgery. 1987 Jan;20(1):15-20. PubMed PMID: 3808257.
25)

Kosteljanetz M. CSF dynamics in patients with subarachnoid and/or intraventricular hemorrhage. J Neurosurg. 1984 May;60(5):940-6. PubMed PMID: 6716162.
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