hemorrhage

Cardiac Complications After Subarachnoid Hemorrhage

Cardiac Complications After Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a serious condition, and a myocardial injury or dysfunction could contribute to the outcome.

Acute cardiac complications frequently occur after subarachnoid hemorrhage (SAH). These complications include electrocardiogram (ECG) abnormalities, the release of cardiac biomarkers, and the development of acute stress-induced heart failure resembling Takotsubo cardiomyopathy 1) 2) 3) 4) 5) 6)

non-ST elevation myocardial infarction, ST-elevation myocardial infarction and cardiac arrest, but their clinical relevance is unclear.

Lång et al. assessed the prevalence and prognostic impact of cardiac involvement in a cohort with SAH in a prospective observational multicenter study. They included 192 patients treated for non traumatic subarachnoid hemorrhage. They performed ECG recordings, echocardiogram, and blood sampling within 24 h of admission and on days 3 and 7 and at 90 days. The primary endpoint was the evidence of cardiac involvement at 90 days, and the secondary endpoint was to examine the prevalence of a myocardial injury or dysfunction. The median age was 54.5 (interquartile range [IQR] 48.0-64.0) years, 44.3% were male and the median World Federation of Neurosurgical Societies grading for subarachnoid hemorrhage score was 2 (IQR 1-4). At day 90, 22/125 patients (17.6%) had left ventricular ejection fractions ≤ 50%, and 2/121 patients (1.7%) had evidence of a diastolic dysfunction as defined by mitral peak E-wave velocity by peak e’ velocity (E/e’) > 14. There was no prognostic impact from echocardiographic evidence of cardiac complications on neurological outcomes. The overall prevalence of cardiac dysfunction was modest. They found no demographic or SAH-related factors associated with 90 days cardiac dysfunction 7).

Among patients suffering from cardiac events at the time of aneurysmal subarachnoid hemorrhage, those with myocardial infarction and in particular those with a troponin level greater than 1.0 mcg/L had a 10 times increased risk of death 8).

1)

Zaroff JG, Rordorf GA, Newell JB, Ogilvy CS, Levinson JR. Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery. 1999;44:34–39. doi: 10.1097/00006123-199901000-00013.
2)

Tung P, Kopelnik A, Banki N, et al. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004;35:548–551. doi: 10.1161/01.STR.0000114874.96688.54.
3)

Banki N, Kopelnik A, Tung P, et al. Prospective analysis of prevalence, distribution, and rate of recovery of left ventricular systolic dysfunction in patients with subarachnoid hemorrhage. J Neurosurg. 2006;105:15–20. doi: 10.3171/jns.2006.105.1.15.
4)

Lee VH, Connolly HM, Fulgham JR, Manno EM, Brown JRD, Wijdicks EFM. Tako-tsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: an underappreciated ventricular dysfunction. J Neurosurg. 2006;105:264–270. doi: 10.3171/jns.2006.105.2.264.
5)

Oras J, Grivans C, Bartley A, Rydenhag B, Ricksten SE, Seeman-Lodding H. Elevated high-sensitive troponin T on admission is an indicator of poor long-term outcome in patients with subarachnoid haemorrhage: a prospective observational study. Crit Care (Lond, Engl) 2016;20:11. doi: 10.1186/s13054-015-1181-5.
6)

van der Bilt IA, Hasan D, Vandertop WP, et al. Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurology. 2009;72:635–642. doi: 10.1212/01.wnl.0000342471.07290.07.
7)

Lång M, Jakob SM, Takala R, Lyngbakken MN, Turpeinen A, Omland T, Merz TM, Wiegand J, Grönlund J, Rahi M, Valtonen M, Koivisto T, Røsjø H, Bendel S. The prevalence of cardiac complications and their impact on outcomes in patients with non-traumatic subarachnoid hemorrhage. Sci Rep. 2022 Nov 22;12(1):20109. doi: 10.1038/s41598-022-24675-8. PMID: 36418906.
8)

Ahmadian A, Mizzi A, Banasiak M, Downes K, Camporesi EM, Thompson Sullebarger J, Vasan R, Mangar D, van Loveren HR, Agazzi S. Cardiac manifestations of subarachnoid hemorrhage. Heart Lung Vessel. 2013;5(3):168-78. PubMed PMID: 24364008; PubMed Central PMCID: PMC3848675.

Subarachnoid hemorrhage scales

Subarachnoid hemorrhage scales

see also Poor grade aneurysmal subarachnoid hemorrhage

Hijdra sum score

Hunt and Hess Stroke Scale

World Federation of Neurological Surgeons Grading System

Modified Fisher scale

VASOGRADE

Graeb Score or LeRoux scores improve the prediction of shunt dependency and in parts of case fatality rate (CFR) in aneurysmal SAH patients therefore confirming the relevance of the extent and distribution of intraventricular hemorrhage for the clinical course in SAH 1)

1)

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 Mar;157(3):409-15. doi: 10.1007/s00701-014-2334-z. Epub 2015 Jan 21. PubMed PMID: 25599911.

Spontaneous intracerebral hemorrhage expansion prediction

Spontaneous intracerebral hemorrhage expansion prediction

Signs

Black hole sign.

Blend sign,

Spot sign.

NAG scale

A fluid level within intraparenchymal hemorrhage on head CT scan is associated with higher likelihood of intracerebral hemorrhage progression. However, this only applies to true fluid levels, with mimics having a lower likelihood of progression. A careful analysis of potential fluid levels is necessary before assigning prognostic implications 1).

A study of Lim et al. aimed to externally validate three risk prediction models of HE (PREDICT score, 9-point, and BRAIN scores) in an Asian population.

A prospective cohort of 123 spontaneous ICH patients admitted to a tertiary hospital (certified stroke center) in Singapore was recruited. Logistic recalibrations were performed to obtain updated calibration slopes and intercepts for all models. The discrimination (c-statistic), calibration (Hosmer-Lemeshow test, le Cessie-van Houwelingen-Copas-Hosmer test, Akaike information criterion), overall performance (Brier score, R2), and clinical usefulness (decision curve analysis) of the risk prediction models were examined.

Overall, the recalibrated PREDICT performed best among the three models in our study cohort based on the novel matrix comprising of Akaike information criterion and c-statistic. The PREDICT model had the highest R2 (0.26) and lowest Brier score (0.14). Decision curve analyses showed that recalibrated PREDICT was more clinically useful than 9-point and BRAIN models over the greatest range of threshold probabilities. The two scores (PREDICT and 9-point) which incorporated computed tomography (CT) angiography spot sign outperformed the one without (BRAIN).

This is the first study to validate HE scores, namely PREDICT, 9-Point and BRAIN, in a multi-ethnic Asian ICH patient population. The PREDICT score was the best performing model in our study cohort, based on the performance metrics employed in this study. Our findings also showed support for CT angiography spot sign as a predictor of outcome after ICH. Although the models assessed are sufficient for risk stratification, the discrimination and calibration are at best moderate and could be improved 2).

1)

Ratnayake C, Okonkwo D, Branstetter B. Hematoma Progression Rates on Head CT for Fluid Levels Versus Mimics in Patients with Primary Intracerebral Hemorrhage. World Neurosurg. 2022 Nov 2:S1878-8750(22)01528-5. doi: 10.1016/j.wneu.2022.10.112. Epub ahead of print. PMID: 36334718.
2)

Lim JX, Han JX, See AAQ, Lew VH, Chock WT, Ban VF, Pothiawala S, Lim WEH, McAdory LE, James ML, King NKK. External Validation of Hematoma Expansion Scores in Spontaneous Intracerebral Hemorrhage in an Asian Patient Cohort. Neurocrit Care. 2018 Oct 30. doi: 10.1007/s12028-018-0631-8. [Epub ahead of print] PubMed PMID: 30377910.

Nicotine replacement therapy in aneurysmal subarachnoid hemorrhage

Nicotine replacement therapy in aneurysmal subarachnoid hemorrhage

Smoking prevalence is twice as high among patients admitted to hospital because of the acute condition of aneurysmal subarachnoid hemorrhage (aSAH) as in the general population.

Despite vasoactive properties, administration of NRT among active smokers with acute SAH appeared to be safe, with similar rates of vasospasm and DCI, and a slightly higher rate of seizures. The association of NRT with lower mortality could be due to chance, uncontrolled factors, or a neuroprotective effect of nicotine in active smokers hospitalized with SAH, and should be tested prospectively 1).

Smoking was also associated with paradoxical superior outcomes on some measures, and future research to confirm and further understand the basis of this relationship is needed 2).

Current evidence suggests that NRT does not induce vasospasm, and is associated with improved outcomes in smokers hospitalized for SAH. Protocol registered in PROSPERO, available at: http://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42016037200 3) 4).

The use of NRT in the acute phase of aSAH does not seem to have an impact on the intensity of headaches or analgesic consumption 5).

Limited safety data may prompt caution regarding seizures and delirium in patients with subarachnoid hemorrhage 6).

Eisenring et al. investigated the international practice of NRT use for aSAH among neurosurgeons.

The online SurveyMonkey software was used to administer a 15-question, 5-min online questionnaire. An invitation link was sent to those 1425 of 1988 members of the European Association of Neurosurgical Societies (EANS) who agreed to participate in surveys to assess treatment strategies for withdrawal of tobacco smoking during aSAH. Factors contributing to physicians’ posture towards NRT were assessed.

A total of 158 physicians from 50 nations participated in the survey (response rate 11.1%); 68.4% (108) were affiliated with university hospitals and 67.7% (107) practiced at high-volume neurovascular centers with at least 30 treated aSAH cases per year. Overall, 55.7% (88) of physicians offered NRT to smokers with aSAH, 22.1% (35) offered non-NRT support including non-nicotine medication and counseling, while the remaining 22.1% (35) did not actively support smoking cessation. When smoking was not possible, 42.4% (67) of physicians expected better clinical outcomes when prescribing NRT instead of nicotine deprivation, 36.1% (57) were uncertain, 13.9% (22) assumed unaffected outcomes, and 7.6% (12) assumed worse outcomes. Only 22.8% (36) physicians had access to a local smoking cessation team in their practice, of whom half expected better outcomes with NRT as compared to deprivation.

A small majority of the surveyed physicians of the EANS offered NRT to support smoking cessation in hospitalized patients with aSAH. However, less than half believed that NRT could positively impact clinical outcomes as compared to deprivation. This survey demonstrated the lack of consensus regarding the use of NRT for hospitalized smokers with aSAH 7).

1)

Seder DB, Schmidt JM, Badjatia N, Fernandez L, Rincon F, Claassen J, Gordon E, Carrera E, Kurtz P, Lee K, Connolly ES, Mayer SA. Transdermal nicotine replacement therapy in cigarette smokers with acute subarachnoid hemorrhage. Neurocrit Care. 2011 Feb;14(1):77-83. doi: 10.1007/s12028-010-9456-9. PMID: 20949331.
2)

Dasenbrock HH, Rudy RF, Rosalind Lai PM, Smith TR, Frerichs KU, Gormley WB, Aziz-Sultan MA, Du R. Cigarette smoking and outcomes after aneurysmal subarachnoid hemorrhage: a nationwide analysis. J Neurosurg. 2018 Aug;129(2):446-457. doi: 10.3171/2016.10.JNS16748. Epub 2017 Oct 27. PMID: 29076779.
3)

Turgeon RD, Chang SJ, Dandurand C, Gooderham PA, Hunt C. Nicotine replacement therapy in patients with aneurysmal subarachnoid hemorrhage: Systematic review of the literature, and survey of Canadian practice. J Clin Neurosci. 2017 Aug;42:48-53. doi: 10.1016/j.jocn.2017.03.014. Epub 2017 Mar 22. PMID: 28342700.
4)

Carandang RA, Barton B, Rordorf GA, Ogilvy CS, Sims JR. Nicotine replacement therapy after subarachnoid hemorrhage is not associated with increased vasospasm. Stroke. 2011 Nov;42(11):3080-6. doi: 10.1161/STROKEAHA.111.620955. Epub 2011 Aug 25. PMID: 21868740.
5)

Charvet A, Bouchier B, Dailler F, Ritzenthaler T. Nicotine Replacement Therapy Does Not Reduce Headaches Following Subarachnoid Hemorrhage: A Propensity Score-Matched Study. Neurocrit Care. 2022 Sep 1. doi: 10.1007/s12028-022-01576-2. Epub ahead of print. PMID: 36050538.
6)

Parikh NS, Salehi Omran S, Kamel H, Elkind MSV, Willey JZ. Smoking-cessation pharmacotherapy for patients with stroke and TIA: Systematic review. J Clin Neurosci. 2020 Aug;78:236-241. doi: 10.1016/j.jocn.2020.04.026. Epub 2020 Apr 22. PMID: 32334957; PMCID: PMC8908464.
7)

Eisenring CV, Hamilton PL, Herzog P, Oertel MF, Jacot-Sadowski I, Burn F, Cornuz J, Schatlo B, Nanchen D. Nicotine Replacement Therapy for Smokers with Acute Aneurysmal Subarachnoid Hemorrhage: An International Survey. Adv Ther. 2022 Sep 19. doi: 10.1007/s12325-022-02300-4. Epub ahead of print. PMID: 3612

Basal ganglia hemorrhage

Basal ganglia hemorrhage

Epidemiology

Basal ganglia hemorrhage is a common form of intracerebral hemorrhage.

Classification

Spontaneous basal ganglia hemorrhage.

Traumatic basal ganglia hematomas (TBGHs) are uncommon events in patients with closed head injuries.

Putaminal hemorrhage.

Bilateral basal ganglia hemorrhage.

Mechanism

Rzepliński et al. injected 40 anatomic specimens of the basal ganglia with a contrast medium, scanned them with a micro-computed tomography scanner, and analyzed the results of radiological studies, and direct and histological examinations.

In 9 cases, micro-computed tomography and histological examinations revealed contrast medium extravasations mimicking intracerebral hematomas. The artificial hematomas spread both proximally and distally along the ruptured perforator and its branches in the perivascular spaces and detached the branches from the adjacent neural tissue leading to the destruction of the tissue and secondary extravasations. Moreover, some contrast extravasations skipped to the perivascular spaces of unruptured perforators, created further extravasation sites, and aggravated the expansion of the artificial hematoma. There was no subarachnoid extension of any artificial hematoma.

They postulate that forming basal ganglia intracerebral hematoma spread initially in the perivascular space, detaches the branches from the neural tissue, and causes secondary bleeding. It can also skip to the perivascular space of a nearby perforator. The proposed mechanism of hematoma initiation and formation explains the extent of damage to the neural tissue, variability of growth in time and space, creation of secondary bleeding sites, and limited usefulness of surgical interventions. The model is reproducible, the extent of the artificial hematoma can be easily controlled, the rupture sites of the perforating arteries can be determined, and the preparation of the model does not require specialized, expensive equipment apart from the micro-computed tomography scanner 1).

Scales

ICH score

Clinical features

Weakness may be the initial symptom with a basal ganglia hemorrhage

Diagnosis

Basal ganglia hemorrhage diagnosis.

Treatment

see Basal ganglia hemorrhage treatment.

Case series

see Basal ganglia hemorrhage case series.

1)

Rzepliński R, Sługocki M, Tarka S, Tomaszewski M, Kucewicz M, Karczewski K, Krajewski P, Małachowski J, Ciszek B. Mechanism of Spontaneous Intracerebral Hemorrhage Formation: An Anatomical Specimens-Based Study. Stroke. 2022 Sep 8:101161STROKEAHA122040143. doi: 10.1161/STROKEAHA.122.040143. Epub ahead of print. PMID: 36073367.

Aneurysmal subarachnoid hemorrhage complications

Aneurysmal subarachnoid hemorrhage complications

Vasospasm is an important cause for mortality following aneurysmal subarachnoid hemorrhage aSAH affecting as many as 70% of patients. It usually occurs between 4th and 21st days of aSAH and is responsible for delayed ischemic neurological deficit (DIND) and cerebral infarction

It is one of the factors that can most significantly worsen the prognosis despite different treatments.

Transcranial doppler (TCD) evidence of vasospasm is predictive of delayed cerebral ischemia (DCI) with high accuracy. Although high sensitivity and negative predictive value make TCD an ideal monitoring device, it is not a mandated standard of care in aneurysmal subarachnoid hemorrhage (aSAH) due to the paucity of evidence on clinically relevant outcomes, despite recommendation by national guidelines. High-quality randomized trials evaluating the impact of TCD monitoring on patient-centered and physician-relevant outcomes are needed 1).

A greater proportion of aneurysmal subarachnoid hemorrhage patients, are surviving their initial hemorrhagic event but remain at increased risk of a number of complications, including delayed cerebral ischemia, epilepsy, nosocomial infections, cognitive impairment, shunt dependent hydrocephalus, and shunt related complications 2).

Intracranial complications including delayed cerebral ischemia (vasospasm), aneurysm rebleeding, and hydrocephalus form the targets for initial management. However, the extracranial consequences including hypertension, hyponatremia, and cardiopulmonary abnormalities can frequently arise during the management phase and have shown to directly affect clinical outcome.

Although the intracranial complications of SAH can take priority in the initial management, the extracranial complications should be monitored for and recognized as early as possible because these complications can develop at varying times throughout the course of the condition. Therefore, a variety of investigations, as described by this article, should be undertaken on admission to maximize early recognition of any of the extracranial consequences. Furthermore, because the extracranial complications have a direct effect on clinical outcome and can lead to and exacerbate the intracranial complications, monitoring, recognizing, and managing these complications in parallel with the intracranial complications is important and would allow optimization of the patient’s management and thus help improve their overall outcome 3).

Intracranial hemorrhage

Aneurysmal subarachnoid hemorrhage is complicated by intracerebral hemorrhage in 20—40 %, by intraventricular hemorrhage in 13-28%, and by subdural blood in 2-5% (usually due to posterior communicating aneurysm when over convexity, or distal anterior intracerebral artery (DACA) aneurysm with interhemispheric subdural).

The intracranial effects of aSAH causing death and disability are from vasospasm, direct effects of the initial bleed, increased intracranial pressure (ICP) and rebleeding 4).

Early brain injury and hydrocephalus (HCP) are important mediators of poor outcome in subarachnoid hemorrhage (SAH) patients. Injection of SAH patients’ CSF into the rat ventricle leads to HCP as well as subependymal injury compared with injection of control CSF 5).

Fever is a common occurrence (70%) especially in poor grades, contributes to adverse outcome and may not always respond to conventional treatment.

Persistent hyperglycemia (>200 mg/dl for >2 consecutive days) increases the likelihood of poor outcome after aSAH.

Management of patients following aSAH includes four major considerations:

(1) prediction of patients at highest risk for development of DCI,

(2) prophylactic measures to reduce its occurrence,

(3) monitoring to detect early signs of cerebral ischemia,

(4) treatments to correct vasospasm and cerebral ischemia once it occurs 6).

Vasospasm

see Vasospasm after aneurysmal subarachnoid hemorrhage.

Brain edema

Brain edema after aneurysmal subarachnoid hemorrhage

Delayed cerebral ischemia

see Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

Rebleeding

see Aneurysm rebleeding

Pulmonary complications

Subarachnoid hemorrhage (SAH) is often accompanied by pulmonary complications, which may lead to poor outcomes and death.

Sympathetic activation of the cardiovascular system in aneurysmal subarachnoid hemorrhage not only triggers the release of atrial and brain natriuretic peptides it can also lead to increased pulmonary venous pressures and permeability causing hydrostatic pulmonary edema 7).

see Neurogenic pulmonary edema.

Cardiac manifestations

Cardiac manifestations of intracranial subarachnoid hemorrhage patients include mild electrocardiogram variability, Takotsubo cardiomyopathy, non-ST elevation myocardial infarction, ST-elevation myocardial infarction and cardiac arrest, but their clinical relevance is unclear.

Among patients suffering from cardiac events at the time of aneurysmal subarachnoid hemorrhage, those with myocardial infarction and in particular those with a troponin level greater than 1.0 mcg/L had a 10 times increased risk of death 8).

Acute kidney injury

Acute kidney injury

Hyponatremia

see Hyponatremia after aneurysmal subarachnoid hemorrhage

Hypokalemia

Hypokalemia is a common electrolyte disorder in the intensive care unit. Its cause often is complex, involving both potassium losses from the body and shifts of potassium into cells.

We present a case of severe hypokalemia of sudden onset in a patient being treated for subarachnoid hemorrhage in the surgical intensive care unit in order to illustrate the diagnosis and management of severe hypokalemia of unclear cause. The patient received agents that promote renal potassium losses and treatments associated with a shift of potassium into cells. Ibanez et al. outline the steps in diagnosis and management, focusing on the factors regulating the transcellular distribution of potassium in the body 9).

Hydrocephalus

see Hydrocephalus after aneurysmal subarachnoid hemorrhage.

Intraventricular hemorrhage

The clinical outcome after aneurysm rupture is at least in part determined by the severity of IVH. Knowledge of the effect of IVH may help guide physicians in the care of patients with aneurysmal bleeding 10).

Cognitive disorder

see Cognitive disorder after subarachnoid hemorrhage.

Neuropsychiatric disturbance

Aneurysmal subarachnoid hemorrhage neuropsychiatric disturbance.

Deep-Vein Thrombosis

Overall rates of VTE (Deep-Vein Thrombosis Deep-vein thrombosis or PE), Deep-vein thrombosis, and PE were 4.4%, 3.5%, and 1.2%, respectively. On multivariate analysis, the following factors were associated with increased VTE risk: increasing age, black race, male sex, teaching hospital, congestive heart failure, coagulopathy, neurologic disorders, paralysis, fluid and electrolyte disorders, obesity, and weight loss. Patients that underwent clipping versus coiling had similar VTE rates. VTE was associated with pulmonary/cardiac complication (odds ratio [OR] 2.8), infectious complication (OR 2.8), ventriculostomy (OR 1.8), and vasospasm (OR 1.3). Patients with VTE experienced increased non-routine discharge (OR 3.3), and had nearly double the mean length of stay (p<0.001) and total inflation-adjusted hospital charges (p<0.001). To our knowledge, this is the largest study evaluating the incidence and risk factors associated with the development of VTE after aSAH. The presence of one or more of these factors may necessitate more aggressive VTE prophylaxis 11).

Short course (<48h) administration of EACA in patients with aneurysmal subarachnoid hemorrhage is associated with an 8.5 times greater risk of Deep-Vein Thrombosis (Deep-vein thrombosis) formation 12).

Routine compressive venous Doppler ultrasonography is an efficient, noninvasive means of identifying Deep-Vein Thrombosis (Deep-vein thrombosis) as a screening modality in both symptomatic and asymptomatic patients following aneurysmal SAH. The ability to confirm or deny the presence of Deep-vein thrombosis allows one to better identify the indications for chemoprophylaxis. Prophylaxis for venous thromboembolism in neurosurgical patients is common. Emerging literature and anecdotal experience have exposed risks of complications with prophylactic anticoagulation protocols. The identification of patients at high risk-for example, those with asymptomatic Deep-vein thrombosis-will allow physicians to better assess the role of prophylactic anticoagulation 13).

Deep-Vein Thrombosis (Deep-vein thrombosis) formation most commonly occurs in the first 2 weeks following aSAH, with detection in a cohort peaking between Days 5 and 9. Chemoprophylaxis is associated with a significantly lower incidence of Deep-vein thrombosis 14).

Prevention

Patient should be ideally monitored in the NICU for at least 1st 24 h after surgery. Anticonvulsants, osmotherapy and nimodipine must be continued. Hydrocephalus, vasospasm, seizures, and electrolyte disturbances can occur necessitating close observation and prompt management. One of the major challenges in the management of aSAH is identifying potential or ongoing perfusion deficits. Ischemic insults can occur following ictus, or due to raised ICP, hypotension and vasospasm. Early identification and appropriate treatment of postictal intracranial (ICP, TCD flow velocities) and cardiovascular (cardiac output, ECG, BP, CVP) changes is possible in dedicated NICU and is crucial for improving outcomes. Heuer et al. observed that raised ICP (>20 mmHg) occurred in >50% of patients after aSAH and was associated with poor outcomes. Factors associated with raised ICP included poor clinical and radiological grades of aSAH, intraoperative brain swelling, parenchymal and intraventricular bleed and rebleeding.

Seizure

see Seizure after aneurysmal subarachnoid hemorrhage.

Cytotoxic Lesions of the Corpus Callosum

Cytotoxic Lesions of the Corpus Callosum.

Nonocclusive mesenteric ischemia

Koizumi et al. evaluated the incidence of NOMI in patients with subarachnoid hemorrhage (SAH) due to ruptured aneurysms, and they present the clinical characteristics and describe the outcomes to emphasize the importance of recognizing NOMI.

Observations: Overall, 7 of 276 consecutive patients with SAH developed NOMI. Their average age was 71 years, and 5 patients were men. Hunt and Kosnik grades were as follows: grade II, 2 patients; grade III, 3 patients; grade IV, 1 patient; and grade V, 1 patient. Fisher grades were as follows: grade 1, 1 patient; grade 2, 1 patient; and grade 3, 5 patients. Three patients were treated with endovascular coiling, 3 with microsurgical clipping, and 1 with conservative management. Five patients had abdominal symptoms prior to the confirmed diagnosis of NOMI. Four patients fell into shock. Two patients required emergent laparotomy followed by second-look surgery. Four patients could be managed conservatively. The overall mortality of patients with NOMI complication was 29% (2 of 7 cases).

NOMI had a high mortality rate. Neurosurgeons should recognize that NOMI can occur as a fatal complication after SAH 15).

References

1)

Kumar G, Shahripour RB, Harrigan MR. Vasospasm on transcranial Doppler is predictive of delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. J Neurosurg. 2015 Oct 23:1-8. [Epub ahead of print] PubMed PMID: 26495942.
2)

Connolly ES Jr, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, et al: Guidelines for the manage- ment of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Asso- ciation/American Stroke Association. Stroke 43:1711–1737, 2012
3)

Hall A, O’Kane R. The Extracranial Consequences of Subarachnoid Hemorrhage. World Neurosurg. 2018 Jan;109:381-392. doi: 10.1016/j.wneu.2017.10.016. Epub 2017 Oct 16. Review. PubMed PMID: 29051110.
4)

Kassell MJ. Aneurysmal subarachnoid hemorrhage: An update on the medical complications and treatments strategies seen in these patients. Curr Opin Anaesthesiol. 2011;24:500–7.
5)

Li P, Chaudhary N, Gemmete JJ, Thompson BG, Hua Y, Xi G, Pandey AS. Intraventricular Injection of Noncellular Cerebrospinal Fluid from Subarachnoid Hemorrhage Patient into Rat Ventricles Leads to Ventricular Enlargement and Periventricular Injury. Acta Neurochir Suppl. 2016;121:331-4. doi: 10.1007/978-3-319-18497-5_57. PubMed PMID: 26463970.
6)

Dusick JR, Gonzalez NR. Management of arterial vasospasm following aneurysmal subarachnoid hemorrhage. Semin Neurol. 2013 Nov;33(5):488-97. doi: 10.1055/s-0033-1364216. Epub 2014 Feb 6. PubMed PMID: 24504612.
7)

Lo BW, Fukuda H, Nishimura Y, Macdonald RL, Farrokhyar F, Thabane L, Levine MA. Pathophysiologic mechanisms of brain-body associations in ruptured brain aneurysms: A systematic review. Surg Neurol Int. 2015 Aug 11;6:136. doi: 10.4103/2152-7806.162677. eCollection 2015. PubMed PMID: 26322246.
8)

Ahmadian A, Mizzi A, Banasiak M, Downes K, Camporesi EM, Thompson Sullebarger J, Vasan R, Mangar D, van Loveren HR, Agazzi S. Cardiac manifestations of subarachnoid hemorrhage. Heart Lung Vessel. 2013;5(3):168-78. PubMed PMID: 24364008; PubMed Central PMCID: PMC3848675.
9)

Ybanez N, Agrawal V, Tranmer BI, Gennari FJ. Severe hypokalemia in a patient with subarachnoid hemorrhage. Am J Kidney Dis. 2014 Mar;63(3):530-5. doi: 10.1053/j.ajkd.2013.07.005. Epub 2013 Aug 20. PubMed PMID: 23972266.
10)

Mayfrank L, Hütter BO, Kohorst Y, Kreitschmann-Andermahr I, Rohde V, Thron A, Gilsbach JM. Influence of intraventricular hemorrhage on outcome after rupture of intracranial aneurysm. Neurosurg Rev. 2001 Dec;24(4):185-91. PubMed PMID: 11778824.
11)

Kshettry VR, Rosenbaum BP, Seicean A, Kelly ML, Schiltz NK, Weil RJ. Incidence and risk factors associated with in-hospital venous thromboembolism after aneurysmal subarachnoid hemorrhage. J Clin Neurosci. 2014 Feb;21(2):282-6. doi: 10.1016/j.jocn.2013.07.003. Epub 2013 Oct 13. PubMed PMID: 24128773.
12)

Foreman PM, Chua M, Harrigan MR, Fisher WS 3rd, Tubbs RS, Shoja MM, Griessenauer CJ. Antifibrinolytic therapy in aneurysmal subarachnoid hemorrhage increases the risk for deep venous thrombosis: A case-control study. Clin Neurol Neurosurg. 2015 Sep 10;139:66-69. doi: 10.1016/j.clineuro.2015.09.005. [Epub ahead of print] PubMed PMID: 26378393.
13)

Ray WZ, Strom RG, Blackburn SL, Ashley WW, Sicard GA, Rich KM. Incidence of deep venous thrombosis after subarachnoid hemorrhage. J Neurosurg. 2009 May;110(5):1010-4. doi: 10.3171/2008.9.JNS08107. PubMed PMID: 19133755.
14)

Liang CW, Su K, Liu JJ, Dogan A, Hinson HE. Timing of Deep-Vein Thrombosis formation after aneurysmal subarachnoid hemorrhage. J Neurosurg. 2015 Oct;123(4):891-6. doi: 10.3171/2014.12.JNS141288. Epub 2015 Jul 10. PubMed PMID: 26162047; PubMed Central PMCID: PMC4591180.
15)

Koizumi H, Yamamoto D, Maruhashi T, Kataoka Y, Inukai M, Asari Y, Kumabe T. Relationship between subarachnoid hemorrhage and nonocclusive mesenteric ischemia as a fatal complication: patient series. J Neurosurg Case Lessons. 2022 Jul 18;4(3):CASE22199. doi: 10.3171/CASE22199. PMID: 36046708; PMCID: PMC9301345.

Spontaneous Intracerebral Hemorrhage Risk Factors

Spontaneous Intracerebral Hemorrhage Risk Factors

Psychosocial, ethnic, and economic factors play a role in the prevalence of cerebral hemorrhage, with ICH being twice as common in low-income and middle-income countries compared with high-income countries. Other identified risk factors for ICH include age (i.e., each decade from 50 years of age is associated with a 2-fold increase in the incidence of ICH) and an elevated alcohol intake.

Etiologies of ICH to always consider include intracranial aneurysms (typically presenting as subarachnoid hemorrhage); arteriovenous malformations (ICH is the first presentation of AVMs in 60 % of cases); cerebral venous sinus thrombosis and venous infarction; brain tumors (<5 % of all ICH cases) including cerebral metastases (e.g., lung cancer, melanoma, renal cell carcinoma, thyroid carcinoma, and choriocarcinoma) and primary CNS tumors (e.g., glioblastoma multiforme and oligodendrogliomas); and drugs of abuse (e.g., cocaine, amphetamines). Because of the differing etiologies of ICH, a rapid and accurate diagnosis of the underlying etiology of ICH is essential to direct appropriate management strategies.

Hypertensive intracerebral hemorrhage

The most important modifiable risk factor in spontaneous ICH is chronic arterial hypertension:

see Hypertensive intracerebral hemorrhage.

Amyloid angiopathy

Besides hypertension, cerebrovascular amyloid deposition (i.e., cerebral amyloid angiopathy) is associated with ICH in older patients.

Although cerebral amyloid angiopathy (CAA), which is Aβ deposition in the cerebral vessels, related cerebral hemorrhage rarely develops in young people, several patients with CAA-related cerebral hemorrhage under the age of 55 with histories of neurosurgeries with and without dura mater graft in early childhood have been reported. These patients might show that Aβ pathology is often recognized as Aβ-CAA rather than parenchymal Aβ deposition in the transmission of cerebral β-amyloidosis in humans, and Hamaguchi et al. proposed an emerging concept, “acquired CAA”. Considering that there have been several patients with acquired CAA with an incubation period from neurosurgery and the onset of CAA-related cerebral hemorrhage of longer than 40 years, the number of cases is likely to increase in the future, and detailed epidemiological investigation is required. It is necessary to continue to elucidate the pathomechanisms of acquired CAA and urgently establish a method for preventing the transmission of cerebral β-amyloidosis among individuals 1).

Intracranial vascular malformation

It is a common initial symptom of intracranial vascular malformations.

see Intracerebral hemorrhage from ruptured cerebral arteriovenous malformation.

see Aneurysmal intracerebral hemorrhage.

see Cerebral venous sinus thrombosis and venous infarction.

Neoplasm

see Spontaneous intracranial hematoma caused by neoplasm.

Vasculitis

Vasculitis.

AIDS

Complication of AIDS.

NPH

Shunting for NPH

Coagulopathy

Coagulopathies (i.e., the use of antithrombotic or thrombolytic agents, congenital or acquired factor deficiencies) and systemic diseases, such as thrombocytopenia, are possible causes of ICH. The use of oral anticoagulants, especially vitamin K inhibitors (i.e., warfarin), has increased coagulopathy-associated ICH in recent years, accounting for more than 15 % of all cases.

Severe thrombocytopenia can result in petechial hemorrhages or spontaneous intracerebral hemorrhage (ICH).

Anticoagulant Related Intracerebral Hemorrhage

see Anticoagulant Related Intracerebral Hemorrhage.

Intracerebral hemorrhage risk is increased with higher doses than the recommended 100 mg of alteplase (Activase®, recombinant tissue plasminogen activator (rt-PA)) 2) in older patients, in those with anterior MI or higher Killip class, and with bolus administration (vs. infusion) 3).

When heparin was used adjunctively, higher doses were associated with a higher risk of ICH 4) ICH is thought to occur in those patients with some preexisting underlying vascular abnormality 5). Immediate coronary angioplasty is safer than rt-PA when available 6).

Posterior fossa surgery

Remote supratentorial hematoma soon after posterior fossa surgery for the removal of a space-occupying lesion is a rare but dramatic and dreaded complication, carrying significant morbidity and mortality 7) 8) 9) 10) 11) 12) 13) 14).

Posterior reversible encephalopathy syndrome

see Posterior reversible encephalopathy syndrome.

Ethanol

Ethanol

Cocaine

Cocaine

Inadvertent intrathecal injection of unapproved contrast agents

Inadvertent intrathecal injection of unapproved contrast agents.

Vitamin D

The evidence linking vitamin D (VitD) levels and Spontaneous Intracerebral Hemorrhage Risk Factors remains inconclusive. Szejko et al. tested the hypothesis that lower genetically determined VitD levels are associated with a higher risk of ICH. They conducted a 2-sample Mendelian Randomization (MR) study using publicly available summary statistics from published genome-wide association study of VitD levels (417 580 study participants) and ICH (1545 ICH cases and 1481 matched controls). They used the inverse variance-weighted average method to generate causal estimates and the MR Pleiotropy Residual Sum and Outlier and MR-Egger approaches to assess for horizontal pleiotropy. To account for known differences in their underlying mechanism, we implemented stratified analysis based on the location of the hemorrhage within the brain (lobar or nonlobar). Our primary analysis indicated that each SD decrease in genetically instrumented VitD levels was associated with a 60% increased risk of ICH (odds ratio [OR], 1.60; [95% CI, 1.05-2.43]; P=0.029). They found no evidence of horizontal pleiotropy (MR-Egger intercept and MR Pleiotropy Residual Sum and Outlier global test with P>0.05). Stratified analyses indicated that the association was stronger for nonlobar ICH (OR, 1.87; [95% CI, 1.18-2.97]; P=0.007) compared with lobar ICH (OR, 1.43; [95% CI, 0.86-2.38]; P=0.17). Lower levels of genetically proxied VitD levels are associated with higher ICH risk. These results provide evidence for a causal role of VitD metabolism in ICH 15).

COVID-19 and Intracerebral Hemorrhage

COVID-19 and Intracerebral Hemorrhage

References

1)

Hamaguchi T, Ono K, Yamada M. Transmission of Cerebral β-Amyloidosis Among Individuals. Neurochem Res. 2022 Mar 11. doi: 10.1007/s11064-022-03566-4. Epub ahead of print. PMID: 35277809.
2)

Public Health Service. Approval of Thrombolytic Agents. FDA Drug Bull. 1988; 18:6–7
3)

Mehta SR, Eikelboom JW, Yusuf S. Risk of intracranial hemorrhage with bolus versus infusion thrombolytic therapy: a meta-analysis. Lancet. 2000; 356:449–454
4)

Tenecteplase (TNKase) for thrombolysis. Med Letter. 2000; 42:106–108
5)

DaSilva VF, Bormanis J. Intracerebral Hemorrhage After Combined Anticoagulant-Thrombolytic Therapy for Myocardial Infarction: Two Case Reports and a Short Review. Neurosurgery. 1992; 30:943–945
6)

Grines CL, Browne KF, Marco J, et al. A Comparison of Immediate Angioplasty with Thrombolytic Therapy for Acute Myocardial Infarction. N Engl J Med. 1993; 328:673–679
7)

Bucciero A, Quaglietta P, Vizioli L. Supratentorial intracerebral hemorrhage after posterior fossa surgery: Case report. J Neurosurg Sci. 1991;35:221–4.
8)

Haines SJ, Maroon JC, Jannetta PJ. Supratentorial intracerebral hemorrhage following posterior fossa surgery. J Neurosurg. 1978;49:881–6.
9)

Harders A, Gilsbach J, Weigel K. Supratentorial space occupying lesions following infratentorial surgery early diagnosis and treatment. Acta Neurochir (Wien) 1985;74:57–60.
10)

Seiler RW, Zurbrugg HR. Supratentorial intracerebral hemorrhage after posterior fossa operation. Neurosurgery. 1986;18:472–4.
11)

Tondon A, Mahapatra AK. Superatentorial intracerebral hemorrhage following infratentorial surgery. J Clin Neurosci. 2004;11:762–5.
12)

Vrettou CS, Stavrinou LC, Halikias S, Kyriakopoulou M, Kollias S, Stranjalis G, et al. Factor XIII deficiency as a potential cause of supratentorial haemorrhage after posterior fossa surgery. Acta Neurochir (Wien) 2010;152:529–32.
13)

Pandey P, Madhugiri VS, Sattur MG, Devi BI. Remote supratentorial extradural hematoma following posterior fossa surgery. Childs Nerv Syst. 2008;24:851–4.
14)

Wolfsberger S, Gruber A, Czech T. Multiple supratentorial epidural haematomas after posterior fossa surgery. Neurosurg Rev. 2004;27:128–32.
15)

Szejko N, Acosta JN, Both CP, Leasure A, Matouk C, Sansing L, Gill TM, Hongyu Z, Sheth K, Falcone GJ. Genetically-Proxied Levels of Vitamin D and Risk of Intracerebral Hemorrhage. J Am Heart Assoc. 2022 Jun 22:e024141. doi: 10.1161/JAHA.121.024141. Epub ahead of print. PMID: 35730641.

Spontaneous intracerebral hemorrhage outcome

Spontaneous intracerebral hemorrhage outcome

ICH is a potentially devastating neurologic emergency with long-term functional independence achieved in only 12-39% of cases and mortality rates of 54% at 1 year 1).

Patients with spontaneous intracerebral hemorrhage have high mortality and poor outcome. It is the most serious, least treatable and more variable in incidence and management compared to other stroke subtypes 2) 3).

Although this is a heterogeneous disorder with a wide range of outcomes, overall mortality at 1 month is approximately 40%, and only 25% of patients have a favorable outcome 4) 5).

Case fatality is extremely high (reaching approximately 60 % at 1 year post event). Only 20 % of patients who survive are independent within 6 months 6).

Anion gap level is a potential predictive biomarker for the long-term outcomes of spontaneous intracerebral hemorrhage patients, and rectifying AG at admission improves the spontaneous intracerebral hemorrhage outcomes 7).

In a cohort (n=1094), there were 306 deaths (per 100 patient-years: absolute event rate 11.7, 95% CI 10.5 to 13.1); 156 were “early” and 150 “late”. In multivariable analyses, early death was independently associated with age (per year increase, HR 1.05, p=0.003), history of hypertension (HR 1.89, p=0.038), pre-event mRS (per point increase, HR 1.41, p<0.0001), admission NIHSS (per point increase, HR 1.11, p<0.0001), and hemorrhage volume > 60ml (HR 4.08, p<0.0001). Late death showed independent associations with age (per year increase, HR 1.04, p=0.003), pre-event mRS (per point increase, HR 1.42, p=0.001), prior anticoagulant use (HR 2.13, p=0.028) and the presence of intraventricular hemorrhage (HR 1.73, p=0.033) in multivariable analyses. In further analyses where time was treated as continuous (rather than dichotomized), the hazard ratio of previous cerebral ischaemic events increased with time, whilst those for GCS, NIHSS and ICH volume decreased over time.

They provided new evidence that not all baseline factors associated with early mortality after intracerebral hemorrhage are associated with mortality after 6 months, and that the effects of baseline variables change over time. The findings could help design better prognostic scores for later death after intracerebral hemorrhage 8).

As with other types of hemorrhages within the skull, intraparenchymal bleeds are a serious medical emergency because they can produce intracranial hypertension, which if left untreated can lead to coma and death.

Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity, and the effective treatment is still lacking.

It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause intracranial hypertension and potentially fatal brain herniation syndromes.

They have high rates of morbidity and rates of mortality of up to 50%. Initial hematoma size and subsequent hematoma expansion are among the most important predictors of poor outcome.

Efforts to improve clinical outcome through mitigation of hematoma expansion have so far been unsuccessful.

Data suggest that outcomes can be improved with standardized medical care.

A strong association exists between the amount of intraventricular hemorrhage (IVH) and poor outcome in intracerebral hemorrhage. An IVH volume of 5 to 10 mL emerges as a significant threshold for decision making on prognosis in these patients 9).

The ICH score is a simple and reliable clinical grading scale that is used for predicting the early mortality of patients with ICHs.

Neurological deterioration (ND) occurs frequently and predicts poor outcomes. Hematoma expansion and intraventricular hemorrhage in early ND, and cerebral edema, fever, and medical complications in later ND 10).

Hematoma expansion is a potentially modifiable predictor of poor outcome following an acute intracerebral hemorrhage (ICH). The ability to identify patients with ICH who are likeliest to experience hematoma expansion and therefore likeliest to benefit from expansion-targeted treatments remains an unmet need. Hypodensities within an ICH detected by noncontrast computed tomography (NCCT) have been suggested as a predictor of hematoma expansion.

Advances

There have been no dramatic advances in the development of interventions to improve the functional outcomes after ICH 11).

Nomogram

The purpose of a study was to establish and validate a nomogram to estimate the 30-day probability of death in patients with spontaneous intracerebral hemorrhage.. From January 2015 to December 2017, a cohort of 450 patients with clinically diagnosed cerebral hemorrhage was collected for model development. The minimum absolute contraction and the selection operator (lasso) regression model were used to select the strongest prediction of patients with cerebral hemorrhage. Discrimination and calibration were used to evaluate the performance of the resulting nomogram. After internal validation, the nomogram was further assessed in a different cohort containing 148 consecutive subjects examined between January 2018 and December 2018. The nomogram included five predictors from the lasso regression analysis, including Glasgow coma scale (GCS), hematoma location, hematoma volume, white blood cells, and D-dimer. Internal verification showed that the model had good discrimination, (the area under the curve is 0.955), and good calibration [unreliability (U) statistic, p = 0.739]. The nomogram still showed good discrimination (area under the curve = 0.888) and good calibration [U statistic, p = 0.926] in the verification cohort data. Decision curve analysis showed that the prediction nomogram was clinically useful. The current study delineates a predictive nomogram combining clinical and imaging features, which can help identify patients who may die of a cerebral hemorrhage 12).

Grading Scales

The ICH Score is a valid clinical grading scale for long-term functional outcome after acute intracerebral hemorrhage (ICH) 13).

Blood Pressure

Based on the viewpoint that increased BP causes greater tearing of blood vessels and flow-out of blood through these vessels and eventually leads to the expansion of the hematoma, high BP is considered to be associated with hematoma expansion and poor outcomes, especially early neurological deterioration, mortality, and dependency 14) 15) 16).

The 2015 American Heart Association/American Stroke Association guidelines for the management of spontaneous ICH recommend early BP reduction with an SBP target of 140 mmHg for patients with ICH presenting with an SBP between 150 and 220 mmHg and without any contraindication to acute BP treatment 17).

Readmissions

Spontaneous intracerebral hemorrhage (SICH) survivors are at risk of hospital readmissions. Data on readmissions after SICH is scarce. We aimed to study the frequency and predictors of readmissions after SICH in Algarve, Portugal.

A retrospective study of a community representative cohort of SICH survivors (2009-2015). The first unplanned readmission in the first year after discharge was the outcome. Cox regression analysis was performed to identify predictors of 1-year readmission.

Of the 357 SICH survivors followed, 116 (32.5%) were readmitted within the first-year. Sixty-seven (18.8%) of the survivors were early readmitted (<90 days), corresponding to 57.8% or all readmissions. Common causes were pneumonia, endocrine/nutritional/metabolic and cardiovascular complications. The risk of readmission was increased by prior to index SICH history of ≥ 3 previous emergency department visits (hazards ratio (HR) = 2.663 (1.770-4.007); P < 0.001), pneumonia during index hospitalization (HR = 2.910 (1.844-4.592); P < 0.001) and reduced in patients discharge home (HR = 0.681 (0.366-0.976); P = 0.048).

The rate of readmissions after SICH is high, predictors are identifiable and causes are potentially preventable. Improvement of care can potentially reduce this burden 18).

1)

van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ. Incidence, case fatality, and functional outcome of Intracerebral hemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010 Feb;9(2):167-76. doi: 10.1016/S1474-4422(09)70340-0. Epub 2010 Jan 5. PMID: 20056489.
2)

Van Asch CJ, Luitse MJ, Rinkel GJ, et al. Incidence, case fatality, and functional outcome of Intracerebral hemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol 2010;9:167–76.
3)

Krishnamurthi RV, Feigin VL, Forouzanfar MH, et al. Global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990–2010: findings from the Global Burden of Disease Study 2010. Lancet Glob Health 2013;1:e259–81.
4)

van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ. Incidence, case fatality, and functional outcome of Intracerebral hemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010;9(2):167–176.
5)

Feigin VL, Lawes CM, Bennett DA, Anderson CS. Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 20th century. Lancet Neurol. 2003;2(1):43–53.
6)

de Oliveira Manoel AL, Goffi A, Zampieri FG, Turkel-Parrella D, Duggal A, Marotta TR, Macdonald RL, Abrahamson S. The critical care management of spontaneous intracranial hemorrhage: a contemporary review. Crit Care. 2016 Sep 18;20:272. doi: 10.1186/s13054-016-1432-0. Review. PubMed PMID: 27640182; PubMed Central PMCID: PMC5027096.
7)

Shen J, Li DL, Yang ZS, Zhang YZ, Li ZY. Anion gap predicts the long-term neurological and cognitive outcomes of spontaneous intracerebral hemorrhage. Eur Rev Med Pharmacol Sci. 2022 May;26(9):3230-3236. doi: 10.26355/eurrev_202205_28741. PMID: 35587074.
8)

Banerjee G, Ambler G, Wilson D, Hostettler IC, Shakeshaft C, Lunawat S, Cohen H, Yousry T, Al-Shahi Salman R, Lip GYH, Houlden H, Muir KW, Brown MM, Jäger HR, Werring DJ; CROMIS-2 collaborators. Baseline factors associated with early and late death in Intracerebral hemorrhage survivors. Eur J Neurol. 2020 Mar 29. doi: 10.1111/ene.14238. [Epub ahead of print] PubMed PMID: 32223078.
9)

Chan E, Anderson CS, Wang X, Arima H, Saxena A, Moullaali TJ, Heeley E, Delcourt C, Wu G, Wang J, Chen G, Lavados PM, Stapf C, Robinson T, Chalmers J, Huang Y; INTERACT2 Investigators. Significance of intraventricular hemorrhage in acute intracerebral hemorrhage: intensive blood pressure reduction in acute cerebral hemorrhage trial results. Stroke. 2015 Mar;46(3):653-8. doi: 10.1161/STROKEAHA.114.008470. Epub 2015 Feb 12. PubMed PMID: 25677598.
10)

Lord AS, Gilmore E, Choi HA, Mayer SA; VISTA-ICH Collaboration. Time course and predictors of neurological deterioration after intracerebral hemorrhage. Stroke. 2015 Mar;46(3):647-52. doi: 10.1161/STROKEAHA.114.007704. Epub 2015 Feb 5. PubMed PMID: 25657190.
11) , 17)

Hemphill JC 3rd, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M, Fung GL, Goldstein JN, Macdonald RL, Mitchell PH, Scott PA, Selim MH, Woo D; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2015 Jul;46(7):2032-60. doi: 10.1161/STR.0000000000000069. Epub 2015 May 28. PubMed PMID: 26022637.
12)

Han Q, Li M, Su D, Fu A, Li L, Chen T. Development and validation of a 30-day death nomogram in patients with spontaneous cerebral hemorrhage: a retrospective cohort study. Acta Neurol Belg. 2021 Feb 10. doi: 10.1007/s13760-021-01617-1. Epub ahead of print. PMID: 33566335.
13)

Hemphill JC 3rd, Farrant M, Neill TA Jr. Prospective validation of the ICH Score for 12-month functional outcome. Neurology. 2009 Oct 6;73(14):1088-94. doi: 10.1212/WNL.0b013e3181b8b332. Epub 2009 Sep 2. PubMed PMID: 19726752; PubMed Central PMCID: PMC2764394.
14)

Rodriguez-Luna D, Pineiro S, Rubiera M, Ribo M, Coscojuela P, Pagola J, et al. Impact of blood pressure changes and course on hematoma growth in acute intracerebral hemorrhage. Eur J Neurol. 2013;20:1277–1283.
15)

Sakamoto Y, Koga M, Yamagami H, Okuda S, Okada Y, Kimura K, et al. Systolic blood pressure after intravenous antihypertensive treatment and clinical outcomes in hyperacute intracerebral hemorrhage: the stroke acute management with urgent risk-factor assessment and improvement-intracerebral hemorrhage study. Stroke. 2013;44:1846–1851.
16)

Zhang Y, Reilly KH, Tong W, Xu T, Chen J, Bazzano LA, et al. Blood pressure and clinical outcome among patients with acute stroke in Inner Mongolia, China. J Hypertens. 2008;26:1446–1452.
18)

Nzwalo H, Nogueira J, Guilherme P, Abreu P, Félix C, Ferreira F, Ramalhete S, Marreiros A, Tatlisumak T, Thomassen L, Logallo N. Hospital readmissions after spontaneous intracerebral hemorrhage in Southern Portugal. Clin Neurol Neurosurg. 2018 Apr 12;169:144-148. doi: 10.1016/j.clineuro.2018.04.015. [Epub ahead of print] PubMed PMID: 29665499.

Spontaneous intracerebral hemorrhage surgery

Spontaneous intracerebral hemorrhage surgery

Based on the MIMIC-III database, Yi et al. from the Guangzhou Overseas Chinese Hospital firstly described the dissimilarities in survival probability, mortality, and neurological recovery among mainstream treatments for intracerebral hemorrhage; secondly, patient classification was determined by important clinical features; and outcome variations among treatment groups were compared. The 28-day, 90-day, and in-hospital mortality in the craniotomy group were significantly lower than minimally invasive surgery (MIS) and non-surgical group patients; and, the medium/long-term mortality in the MIS group was significantly lower than the non-surgical group. The craniotomy group positively correlated with short-term GCS recovery compared with the MIS group; no difference existed between the non-surgical and MIS groups. The craniotomy group’s 90-day survival probability and short-term GCS recovery were superior to the other two treatments in the subgroups of first GCS 3-12; this tendency also presented in the MIS group over the non-surgical group. For milder patients (first GCS > 12), the three treatment regimens had a minimal effect on patient survival, but the non-surgical group showed an advantage in short-term GCS recovery. Craniotomy patients have lower mortality and a better short-term neurological recovery in an ICH population, especially in short-to-medium term mortality and short-term neurological recovery over MIS patients. In addition, surgical treatment is recommendable for patients with a GCS ≤ 12. 1).

STITCH

see STITCH.

Randomized controlled trials

see Intracerebral hemorrhage treatment randomized controlled trials.

A better understanding of the pathophysiology of intracerebral hemorrhage (ICH) has led to the identification of several new mechanisms of injury that could be potential therapeutic targets 2).

Minimally invasive surgery (MIS) for the treatment of ICH is the main clinical method that is currently used, despite the lack of large-scale, clinical, multi-center, randomized controlled trials 3).

Indications

see Intracerebral hemorrhage surgery indications.

Techniques

Open craniotomy is the most widely studied surgical techniques in patients with supratentorial ICH. Other methods include endoscopic hemorrhage aspiration, use of fibrinolytic therapy to dissolve the clot followed by aspiration, and CT-guided stereotactic aspiration 4) 5).

Intracerebral hemorrhage minimally invasive surgery

see Intracerebral hemorrhage minimally invasive surgery

Endoscopic surgery for intracerebral hemorrhage

see Endoscopic surgery for intracerebral hemorrhage

Decompressive hemicraniectomy

Decompressive hemicraniectomy with hematoma evacuation for large ICH might be a safe and effective procedure in patients with severely disturbed consciousness and large hematoma volume 6).

Decompressive hemicraniectomy without clot evacuation appears feasible in patients with large ICH and deserves further investigation, preferably in a randomized controlled setting 7) 8)

Early decompressive hemicraniectomy (DH) with or without clot evacuation is feasible and safe for managing spontaneous ICH. The experience of Esquenazi et al. in a uncontrolled retrospective series, the largest such series in the modern era, suggests that it may be of particular benefit in patients with large non-dominant hemisphere ICH who are not moribund at presentation. These findings suggest that a prospective randomized trial of DH vs. craniotomy for ICH be conducted.

Over 7 years, DH was performed in 73 patients with clot evacuation in 86% and DH alone in 14%. The average ICH volume was 81 cc and the median DH surface area was 105 cm(2). 26 patients were comatose at initial presentation. Three-month functional outcomes were favorable in 29%, unfavorable in 44% and 27% of patients expired. Admission Glasgow Coma Scale (p=0.003), dominant hemisphere ICH location (p=0.01) and hematoma volume (p=0.002) contributed significantly to the outcome, as estimated by a multivariate analysis. Eight surgical complications occurred. 9).

Meta-analysis

Intracerebral hemorrhage surgery meta-analysis

References

1)

Yi Y, Che W, Cao Y, Chen F, Liao J, Wang X, Lyu J. Prognostic data analysis of surgical treatments for intracerebral hemorrhage. Neurosurg Rev. 2022 Apr 19. doi: 10.1007/s10143-022-01785-5. Epub ahead of print. PMID: 35441246.
2)

Aiyagari V. The clinical management of acute intracerebral hemorrhage. Expert Rev Neurother. 2015 Dec;15(12):1421-32. doi: 10.1586/14737175.2015.1113876. Epub 2015 Nov 13. PubMed PMID: 26565118.
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Wang WM, Jiang C, Bai HM. New Insights in Minimally Invasive Surgery for Intracerebral Hemorrhage. Front Neurol Neurosci. 2015 Nov;37:155-65. doi: 10.1159/000437120. Epub 2015 Nov 12. PubMed PMID: 26588789.
4)

Hersh EH, Gologorsky Y, Chartrain AG, Mocco J, Kellner CP. Minimally Invasive Surgery for Intracerebral Hemorrhage. Curr Neurol Neurosci Rep. 2018 May 9;18(6):34. doi: 10.1007/s11910-018-0836-4. Review. PubMed PMID: 29740726.
5)

Hanley DF, Thompson RE, Muschelli J, Rosenblum M, McBee N, Lane K, Bistran-Hall AJ, Mayo SW, Keyl P, Gandhi D, Morgan TC, Ullman N, Mould WA, Carhuapoma JR, Kase C, Ziai W, Thompson CB, Yenokyan G, Huang E, Broaddus WC, Graham RS, Aldrich EF, Dodd R, Wijman C, Caron JL, Huang J, Camarata P, Mendelow AD, Gregson B, Janis S, Vespa P, Martin N, Awad I, Zuccarello M; MISTIE Investigators. Safety and efficacy of minimally invasive surgery plus alteplase in intracerebral haemorrhage evacuation (MISTIE): a randomised, controlled, open-label, phase 2 trial. Lancet Neurol. 2016 Nov;15(12):1228-1237. doi: 10.1016/S1474-4422(16)30234-4. Epub 2016 Oct 11. PubMed PMID: 27751554; PubMed Central PMCID: PMC5154627.
6)

Takeuchi S, Wada K, Nagatani K, Otani N, Mori K. Decompressive hemicraniectomy for spontaneous intracerebral hemorrhage. Neurosurg Focus. 2013 May;34(5):E5. doi: 10.3171/2013.2.FOCUS12424. Review. PubMed PMID: 23634924.
7)

Heuts SG, Bruce SS, Zacharia BE, Hickman ZL, Kellner CP, Sussman ES, McDowell MM, Bruce RA, Connolly ES Jr. Decompressive hemicraniectomy without clot evacuation in dominant-sided intracerebral hemorrhage with ICP crisis. Neurosurg Focus. 2013 May;34(5):E4. doi: 10.3171/2013.2.FOCUS1326. PubMed PMID: 23634923.
8)

Bösel J, Zweckberger K, Hacke W. Haemorrhage and hemicraniectomy: refining surgery for stroke. Curr Opin Neurol. 2015 Feb;28(1):16-22. doi: 10.1097/WCO.0000000000000167. PubMed PMID: 25490194.
9)

Esquenazi Y, Savitz SI, Khoury RE, McIntosh MA, Grotta JC, Tandon N. Decompressive hemicraniectomy with or without clot evacuation for large spontaneous supratentorial intracerebral hemorrhages. Clin Neurol Neurosurg. 2015 Jan;128:117-22. doi: 10.1016/j.clineuro.2014.11.015. Epub 2014 Nov 27. PubMed PMID: 25496934.

Remote cerebellar hemorrhage

Remote cerebellar hemorrhage

A remote cerebellar hemorrhage (RCH) is a spontaneous bleeding in the posterior fossa.

Epidemiology

Is a very rare complication of supratentorial surgery, with a reported incidence of 0,08% 1).

RCH after burr hole trephinations for CSDH is even rarer, with an incidence of 0,14% 2). 3).

It can be rarely observed as a complication of spine surgery.

Remote cerebellar hemorrhage after spine surgery

Sturiale et al. performed a comprehensive review, collecting all cases of RCH after spine surgery reported in literature in order to identify the procedures most frequently associated with RCH and the possible risk factors. They assessed percentages of incidence and 95 % confidence interval of all demographic, neuroradiological, and clinical features. Univariate and multivariate analyses were used to evaluate their association with outcome. They included 44 articles reporting 57 patients with mean age of 57.6 ± 13.9 years and a male/female ratio of 23/34. A RCH was more frequently reported as a complication of decompressive procedures for spinal canal stenosis, particularly when associated with instrumented fusion, followed by spinal tumor debulking and disc herniation removal. In the majority of cases, RCH occurrence was characterized by progressive impairment of consciousness, whereas some patients complained non-specific symptoms. Coagulation disorders, hypertension, and placement of postoperative subfascial drainages were the most frequently reported risk factors. The occurrence of intraoperative dural lesions was described in about 93 % of patients. Zebra sign was the most common bleeding pattern (about 43 % of cases) followed by parenchymal hematoma (37.5 %) and mixed hemorrhage (about 20 %). Impairment of consciousness at clinical onset and intake of anticoagulants/antiplatelets appeared associated with poor outcome at univariate analysis. However, more than 75 % of patients showed a good outcome and a RCH often appeared as a benign and self-limiting condition, which usually did not require surgical treatment, but only prolonged clinical surveillance, unless of the occurrence of complications 4)

Pathophysiology

Its pathophysiology still remains unknown.

The precise mechanism of cerebellar hemorrhage following supratentorial burr hole drainage of CSDH is suspected to be multifactorial. Firstly, a history of previous hypertension and transient hypertensive peaks during the recovery period have been considered to be important factors 5) 6).

This idea is based on the fact that arterial hypertension is the most common cause of spontaneous cerebellar hemorrhage. However, only two out of nine patients (22%), reported in the literature, had a history of hypertension and in one out of them the preoperative blood pressure was consistently normal with antihypertensive drugs. Moreover all patients had perioperative normal blood pressure and only in two cases an elevation of blood pressure was reported postoperatively 7).

Another major cause of spontaneous cerebellar hemorrhages is disturbed blood coagulation, which has been considered as well to be a relevant predisposing factor for postoperative cerebellar hemorrhages 8).

Another proposed mechanism for the development of RCH is that expansion of CSF spaces after surgical removal of CSDH increases mobility of the intracranial structures. Moreover, CSF overdrainage may lead to a downward displacement of the cerebellum. These above mentioned mechanisms may cause stretching and possible tearing of the superior vermian veins leading to RCH.

Furthermore, continuous CSF drainage, intraoperatively as well as postoperatively, could even increase the transtentorial pressure gradient leading to rupture of the small supracerebellar veins and capillary bed with venous bleeding as a consequence. A massive air reflux into the cranial cavity through the drainage tube may pose an additional risk 9).

Diagnosis

It shows a characteristic bleeding pattern defined “zebra sign”.

Case series

2022

Three patients with RCH after three different procedures: burr hole trephination and chronic subdural hematoma evacuation of bilateral cerebral convexity with subsequent subdural drain insertion, external lumbar cerebrospinal fluid drainage for thoracic endovascular aortic repair, and combined bypass surgery for moyamoya disease 10).

2013

Huang et al., report five cases of RCH following cervical spinal surgery, and summarize another seven similar cases from the literature. Dural opening with cerebrospinal fluid hypovolemia seems to be an important factor contributing to RCH following cervical spinal surgery. As other authors have proposed, surgical positioning may be another factor contributing to RCH. RCH is thought to be hemorrhagic venous infarction, resulting from the stretching occlusion of the superior cerebellar vein by the cerebellar sag effect. Either intraoperative CSF loss or a postoperative cerebrospinal fluid drainage from drainage may cause cerebellar sag, further resulting in RCH. RCH is usually self-limiting, and most patients with RCH have an optimal outcome after conservative treatment. Severe cases that involved surgical intervention because of evidence of brainstem compression or hydrocephalus also had acceptable outcomes, compared to spontaneous CH. It has been suggested that one way to prevent RCH is to avoid extensive perioperative loss of CSF, by paying attention to surgical positioning during spinal surgery. Huang et al also underline the importance of early diagnosis and CSF expansion in the early treatment of RCH 11).

Case reports

Remote cerebellar hemorrhage case reports.

1) , 5)

Toczek MR, Morrell MJ, Silverberg GA, Lowe GM. Cerebellar hemorrhage complicating temporal lobectomy. J Neurosurg. 1996;85:718–722.
2)

Park JS, Hwang JH, Park J, Hamm IS, Park YM. Remote cerebellar hemorrhage complicated after supratentorial surgery: Retrospective study with review of articles. J Korean Neurosurg Soc. 2009;46:136–143.
3)

Shimi A, Elbakouri N, Bechri B, Derkaoui A, Agouri M, Khatouf M. [Delayed cerebellar hemorrhage after burr hole drainage of a chronic subdural hematoma]. Pan Afr Med J. 2015 Apr 29;20:421. eCollection 2015. French. PubMed PMID: 26309454.
4)

Sturiale CL, Rossetto M, Ermani M, Baro V, Volpin F, Milanese L, Denaro L, d’Avella D. Remote cerebellar hemorrhage after spinal procedures (part 2): a systematic review. Neurosurg Rev. 2015 Dec 2. [Epub ahead of print] PubMed PMID: 26627110.
6) , 9)

Yoshida S, Yonekawa EYC, Yamashita K, Ihara I, Morooka Y. Cerebellar hemorrhage after supratentorial craniotomy, report of three cases. Neurol Med Chir. 1990;30:738–743.
7)

Kollatos C, Konstantinou D, Raftopoulos S, Klironomos G, Messinis L, Zampakis P, Papathanasopoulos P, Panagiotopoulos V. Cerebellar hemorrhage after supratentorial burr hole drainage of a chronic subdural hematoma. Hippokratia. 2011 Oct;15(4):370-2. PubMed PMID: 24391425; PubMed Central PMCID: PMC3876859.
8)

König A, Laas R, Herrmann HD. Cerebellar hemorrhage as a complication after supratentorial craniotomy. Acta Neurochir. 1987;88:104–108.
10)

Lee W, Kim T, Kim H, Kim JE, Baek KH, Koh EJ, Kim KH, Ha EJ. Remote cerebellar hemorrhage after a neurosurgical procedure: A report of three cases. J Cerebrovasc Endovasc Neurosurg. 2022 Mar 24. doi: 10.7461/jcen.2022.E2021.08.005. Epub ahead of print. PMID: 35320904.
11)

Huang PH, Wu JC, Cheng H, Shih YH, Huang WC. Remote cerebellar hemorrhage after cervical spinal surgery. J Chin Med Assoc. 2013 Oct;76(10):593-8. doi: 10.1016/j.jcma.2013.02.006. Epub 2013 Jun 5. PubMed PMID: 23746536.