- Email: [email protected]
Traumatic Subarachnoid Hemorrhage
Accepted Manuscript Traumatic Subarachnoid Hemorrhage Franco Servadei, MD Edoardo Picetti, MD PII:
S1878-8750(14)00755-4
DOI:
10.1016/j.wneu.2014.08.034
Reference:
WNEU 2525
To appear in:
World Neurosurgery
Received Date: 29 July 2014 Accepted Date: 15 August 2014
Please cite this article as: Servadei F, Picetti E, Traumatic Subarachnoid Hemorrhage, World Neurosurgery (2014), doi: 10.1016/j.wneu.2014.08.034. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Title:
Traumatic Subarachnoid Hemorrhage Authors:
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Franco Servadei MD1, Edoardo Picetti MD2 1
Neurosurgery-Neurotraumatology Unit, Azienda Ospedaliero-Universitaria Parma and ASMN-IRCCS Reggio Emilia, Parma and Reggio Emilia, Italy
2
SC
Department of Anesthesia and Intensive Care, Azienda OspedalieroUniversitaria Parma, Parma, Italy
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Corresponding Author: Franco Servadei MD,
Neurosurgery-Neurotraumatology Unit,
Azienda Ospedaliero-Universitaria Parma and ASMN-IRCCS Reggio Emilia,
43100 Parma, Italy
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Email: [email protected]
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Text:
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In their article in WORLD NEUROSURGERY, Parchani et Al. investigated the pattern and outcome of traumatic subarachnoid hemorrhage (tSAH) in two subsets of patients in regards to mechanism of injury (motor vehicle crash [MVC] or fall from height [FFH]). Data on 403 patients with tSAH were collected retrospectively from a database registry involving 1665 traumatic brain injury (TBI) patients. tSAH were related to MVCs in 215 cases and to FFH in 140 cases. The overall mean ± Standard Deviation (SD) Injury Severity Score (ISS), head Abbreviated Injury Score (AIS) and Glasgow Coma Scale (GCS) score in Emergency Department were respectively 19±10.6, 3.4±0.96 and 10.7±5.3. TBI patients with tSAH, had higher mean ISS (19±11 vs. 17±10; P=0.001), head AIS (3.4±.96 vs. 3.2±.85; P=0.001), and mortality rate (18.4% vs. 9.6%; P=0.001) in comparison to patients without tSAH. Brain contusion (46.6%), subdural hemorrhage (36.5%), and epidural hemorrhage (13.2%) were the other most frequently associated brain injuries. Patients in MVC group had significantly greater head AIS (3.5±0.9 vs. 3.2±0.9; P=0.009) and ISS (21.6±10.6 vs. 15.9±9.5; P=0.001) and lower scene GCS (10.8±4.8 vs. 13.2±3.4; P=0.001) compared to FFH group. The mortality was significantly higher in patients in the MVC group than in the FFH group (24% vs. 10%; P=0.001). MVCs was associated with 3-fold increase in the mortality (odds ratio [OR] 2.8; 95% confidence interval [CI] 1.48-5.28, P=0.001). After adjusting for relevant and important variables, only ISS (OR 1.11; 95% CI 1.04-1.17) and GCS at the scene (OR 0.89; 95% CI 0.79-0.99) were the independent predictors of mortality in both groups. This study demonstrated, once again, that patients with tSAH have high mortality rate respect to TBI patients without tSAH. The higher mortality in MVC group respect to FFH can be explained by a greater severity of injuries observed in the former group.
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tSAH results from the disruption of small vessels within the subarachnoid space that are shared at the time of impact (4). tSAH is a frequent finding in head injury patients (10). Isolated tSAH, without other intracranial lesions, generally follows a benign course and can be managed without follow-up imaging or intensive care unit (ICU) admission (9). Conversely, in the setting of severe TBI, tSAH is often associated with poor prognosis (3, 10); the presence of subarachnoid bleeding is a marker of unfavourable outcome in recent TBI prognostic models (7-8). Why tSAH is associated with negative outcomes is poorly understood. Servadei et Al. (10) performed a study on 750 TBI patients to investigate the association between computed tomography (CT) evidence of tSAH and outcome assessed at 6 months
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after injury with the Glasgow Outcome Scale (GOS) after moderate and severe head trauma. Three hundred eleven patients (41%) exhibited evidence of tSAH on admission CT scan. A logistic regression analysis of favorable (GOS showing moderate disability or good recovery) and unfavorable outcomes (GOS showing dead, vegetative, or severe disability) demonstrated a very strong association between tSAH and outcomes even after simultaneous adjustment for age, GCS Motor Scores, and other admission CT findings (OR 2.49; 95% CI 1.74–3.55; P < 0.001). The authors concluded that the presence of SAH is a marker of a more severe initial injury indicating greater mechanical forces and intracranial deformation. Chieregato et Al. (3) studied 141 tSAH patients to identify potential factors that can predict poor outcomes and lesion progression identified from serial CT scans. The admission and “worst” CT scans were recorded. CT scan changes were reported as “significant CT progression” (changes in the Marshall classification) or “any CT progression” (presence of a new contusion or a lesion that was identified on the first CT scan but had doubled its dimensions in at least one diameter on the worst CT scan). The amount of subarachnoid blood was recorded using a modified Fisher classification and outcome was assessed at 6 months after injury with GOS. In the univariate analysis, prognosis was significantly related to: age, admission GCS and Marshall CT classification scores, worst CT scan, amount of tSAH and volume of associated brain contusions. From multivariate analysis, the only factors independently related to outcome were: GCS score (P < 0.01) and amount of tSAH (P < 0.001) at admission. Significant CT lesion progression was observed in 34 patients (24,1%) and some lesion progression in 66 patients (46.8%). Patients with significant lesion progression had a higher risk of an unfavorable outcome (32 versus 10%; P < 0.004). Unadjusted factors predicting CT progression were: GCS score, Marshall CT classification, amount of subarachnoid blood and the presence or volume of associated brain contusions at admission. Independent factors associated with significant CT progression were the amount of tSAH (P < 0.001) and the presence or the volume of brain contusions (P < 0.001) at admission. This study confirms that the amount of subarachnoid bleeding is an indicator of more severe initial brain damage and shows as tSAH patients have a significant risk of CT progression. This article also reveals as contusion progression occurs predominantly in locations in which there is cortical tSAH on the admission CT scan, suggesting that they could be part of a similar process. Chang et Al. (2) performed a retrospective analysis on a prospective observational database containing 113 head trauma patients to characterize the natural course of
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traumatic intraparenchymal contusions and hematomas (IPHs) and to identify risk factors for IPH progression in the acute post-injury period. IPH progression was independently associated with the presence of subarachnoid hemorrhage (OR 1.6; 95% CI 1.12–2.3), presence of a subdural hematoma (OR 1.94; 95% CI 1.1– 3.43), and initial size (OR 1.11; 95% CI 1.02–1.21, for each cm3 volume). This study also underlines the importance of tSAH as risk factor for IPHs progression. Up to 20% of patients with severe TBI and tSAH may develop symptomatic cerebral vasospasm (5): precisely greater is the amount of subarachnoid blood greater is the probability to have vasospasm (6). While the treatment of post-traumatic vasospasm is similar to that seen in aneurysmal SAH, a systematic review including 1074 TBI patients with tSAH don’t support a beneficial effect of nimodipine as preventive therapeutic strategy (11). tSAH, reducing cerebrospinal fluid (CSF) absorption, may occasionally lead to the development of hydrocephalus: generally this condition is transient and rarely requires CSF diversion (1).
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Summarizing, the presence of blood in the subarachnoid space after severe TBI, especially with other associated intracranial lesions, is a marker of greater disease severity. The clinician should be aware about the potential evolution of IPHs and occurrence of vasospasm. Further studies are necessary to better elucidate the relationship between the subarachnoid blood and the development of secondary brain damage in TBI patients. Bibliography:
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1 - Cardoso ER, Galbraith S. Posttraumatic hydrocephalus - a retrospective review. Surg Neurol 23(3): 261-4, 1985. 2 - Chang EF, Meeker M, Holland MC. Acute traumatic intraparenchymal hemorrhage: risk factors for progression in the early post-injury period. Neurosurgery 58(4): 647-56, 2006. 3 - Chieregato A, Fainardi E, Morselli-Labate AM, Antonelli V, Compagnone C, Targa L, Kraus J, Servadei F. Factors associated with neurological outcome and lesion progression in traumatic subarachnoid hemorrhage patients. Neurosurgery 56(4): 671-80, 2005. 4 - Crooks DA. Pathogenesis and biomechanics of traumatic intracranial haemorrhages. Virchows Arch A Pathol Anat Histopathol 418(6): 479-83, 1991.
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5 - Lee JH, Martin NA, Alsina G, McArthur DL, Zaucha K, Hovda DA, Becker DP. Hemodynamically significant cerebral vasospasm and outcome after head injury: a prospective study. J Neurosurg 87(2): 221-33, 1997. 6 - Lin TK, Tsai HC, Hsieh TC. The impact of traumatic subarachnoid hemorrhage on outcome: a study with grouping of traumatic subarachnoid hemorrhage and transcranial Doppler sonography. J Trauma Acute Care Surg 73(1): 131-6, 2012. 7 - MRC CRASH Trial Collaborators, Perel P, Arango M, Clayton T, Edwards P, Komolafe E, Poccock S, Roberts I, Shakur H, Steyerberg E, Yutthakasemsunt S. Predicting outcome after traumatic brain injury: practical prognostic models based on large cohort of international patients. BMJ 336(7641): 425-9, 2008. 8 - Murray GD, Butcher I, McHugh GS, Lu J, Mushkudiani NA, Maas AI, Marmarou A, Steyerberg EW. Multivariable prognostic analysis in traumatic brain injury: results from the IMPACT study. J Neurotrauma 24(2): 329-37, 2007. 9 - Quigley MR, Chew BG, Swartz CE, Wilberger JE. The clinical significance of isolated traumatic subarachnoid hemorrhage. J Trauma Acute Care Surg 74(2): 581-4, 2013. 10 - Servadei F, Murray GD, Teasdale GM, Dearden M, Iannotti F, Lapierre F, Maas AJ, Karimi A, Ohman J, Persson L, Stocchetti N, Trojanowski T, Unterberg A. Traumatic subarachnoid hemorrhage: demographic and clinical study of 750 patients from the European brain injury consortium survey of head injuries. Neurosurgery 50(2): 261-7, 2002. 11 - Vergouwen MD, Vermeulen M, Roos YB. Effect of nimodipine on outcome in patients with traumatic subarachnoid haemorrhage: a systematic review. Lancet Neurol 5(12): 1029-32, 2006.
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Traumatic brain injury (TBI), traumatic subarachnoid hemorrhage (tSAH), head injury, head trauma, motor vehicle crash (MVC), fall from height (FFH). Acknowledgements:
None.
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ACCEPTED MANUSCRIPT
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Highlights:
- tSAH is a frequent finding in head injury patients - in the setting of severe TBI tSAH is often associated with poor prognosis
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- tSAH is a marker of greater disease severity
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- further studies are necessary to better elucidate the relationship between the subarachnoid blood and the development of secondary brain damage in TBI patients.
S1878-8750(14)00755-4
DOI:
10.1016/j.wneu.2014.08.034
Reference:
WNEU 2525
To appear in:
World Neurosurgery
Received Date: 29 July 2014 Accepted Date: 15 August 2014
Please cite this article as: Servadei F, Picetti E, Traumatic Subarachnoid Hemorrhage, World Neurosurgery (2014), doi: 10.1016/j.wneu.2014.08.034. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
ACCEPTED MANUSCRIPT
Title:
Traumatic Subarachnoid Hemorrhage Authors:
RI PT
Franco Servadei MD1, Edoardo Picetti MD2 1
Neurosurgery-Neurotraumatology Unit, Azienda Ospedaliero-Universitaria Parma and ASMN-IRCCS Reggio Emilia, Parma and Reggio Emilia, Italy
2
SC
Department of Anesthesia and Intensive Care, Azienda OspedalieroUniversitaria Parma, Parma, Italy
M AN U
Corresponding Author: Franco Servadei MD,
Neurosurgery-Neurotraumatology Unit,
Azienda Ospedaliero-Universitaria Parma and ASMN-IRCCS Reggio Emilia,
43100 Parma, Italy
AC C
EP
Email: [email protected]
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Via Gramsci 14
ACCEPTED MANUSCRIPT
Text:
EP
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M AN U
SC
RI PT
In their article in WORLD NEUROSURGERY, Parchani et Al. investigated the pattern and outcome of traumatic subarachnoid hemorrhage (tSAH) in two subsets of patients in regards to mechanism of injury (motor vehicle crash [MVC] or fall from height [FFH]). Data on 403 patients with tSAH were collected retrospectively from a database registry involving 1665 traumatic brain injury (TBI) patients. tSAH were related to MVCs in 215 cases and to FFH in 140 cases. The overall mean ± Standard Deviation (SD) Injury Severity Score (ISS), head Abbreviated Injury Score (AIS) and Glasgow Coma Scale (GCS) score in Emergency Department were respectively 19±10.6, 3.4±0.96 and 10.7±5.3. TBI patients with tSAH, had higher mean ISS (19±11 vs. 17±10; P=0.001), head AIS (3.4±.96 vs. 3.2±.85; P=0.001), and mortality rate (18.4% vs. 9.6%; P=0.001) in comparison to patients without tSAH. Brain contusion (46.6%), subdural hemorrhage (36.5%), and epidural hemorrhage (13.2%) were the other most frequently associated brain injuries. Patients in MVC group had significantly greater head AIS (3.5±0.9 vs. 3.2±0.9; P=0.009) and ISS (21.6±10.6 vs. 15.9±9.5; P=0.001) and lower scene GCS (10.8±4.8 vs. 13.2±3.4; P=0.001) compared to FFH group. The mortality was significantly higher in patients in the MVC group than in the FFH group (24% vs. 10%; P=0.001). MVCs was associated with 3-fold increase in the mortality (odds ratio [OR] 2.8; 95% confidence interval [CI] 1.48-5.28, P=0.001). After adjusting for relevant and important variables, only ISS (OR 1.11; 95% CI 1.04-1.17) and GCS at the scene (OR 0.89; 95% CI 0.79-0.99) were the independent predictors of mortality in both groups. This study demonstrated, once again, that patients with tSAH have high mortality rate respect to TBI patients without tSAH. The higher mortality in MVC group respect to FFH can be explained by a greater severity of injuries observed in the former group.
AC C
tSAH results from the disruption of small vessels within the subarachnoid space that are shared at the time of impact (4). tSAH is a frequent finding in head injury patients (10). Isolated tSAH, without other intracranial lesions, generally follows a benign course and can be managed without follow-up imaging or intensive care unit (ICU) admission (9). Conversely, in the setting of severe TBI, tSAH is often associated with poor prognosis (3, 10); the presence of subarachnoid bleeding is a marker of unfavourable outcome in recent TBI prognostic models (7-8). Why tSAH is associated with negative outcomes is poorly understood. Servadei et Al. (10) performed a study on 750 TBI patients to investigate the association between computed tomography (CT) evidence of tSAH and outcome assessed at 6 months
ACCEPTED MANUSCRIPT
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after injury with the Glasgow Outcome Scale (GOS) after moderate and severe head trauma. Three hundred eleven patients (41%) exhibited evidence of tSAH on admission CT scan. A logistic regression analysis of favorable (GOS showing moderate disability or good recovery) and unfavorable outcomes (GOS showing dead, vegetative, or severe disability) demonstrated a very strong association between tSAH and outcomes even after simultaneous adjustment for age, GCS Motor Scores, and other admission CT findings (OR 2.49; 95% CI 1.74–3.55; P < 0.001). The authors concluded that the presence of SAH is a marker of a more severe initial injury indicating greater mechanical forces and intracranial deformation. Chieregato et Al. (3) studied 141 tSAH patients to identify potential factors that can predict poor outcomes and lesion progression identified from serial CT scans. The admission and “worst” CT scans were recorded. CT scan changes were reported as “significant CT progression” (changes in the Marshall classification) or “any CT progression” (presence of a new contusion or a lesion that was identified on the first CT scan but had doubled its dimensions in at least one diameter on the worst CT scan). The amount of subarachnoid blood was recorded using a modified Fisher classification and outcome was assessed at 6 months after injury with GOS. In the univariate analysis, prognosis was significantly related to: age, admission GCS and Marshall CT classification scores, worst CT scan, amount of tSAH and volume of associated brain contusions. From multivariate analysis, the only factors independently related to outcome were: GCS score (P < 0.01) and amount of tSAH (P < 0.001) at admission. Significant CT lesion progression was observed in 34 patients (24,1%) and some lesion progression in 66 patients (46.8%). Patients with significant lesion progression had a higher risk of an unfavorable outcome (32 versus 10%; P < 0.004). Unadjusted factors predicting CT progression were: GCS score, Marshall CT classification, amount of subarachnoid blood and the presence or volume of associated brain contusions at admission. Independent factors associated with significant CT progression were the amount of tSAH (P < 0.001) and the presence or the volume of brain contusions (P < 0.001) at admission. This study confirms that the amount of subarachnoid bleeding is an indicator of more severe initial brain damage and shows as tSAH patients have a significant risk of CT progression. This article also reveals as contusion progression occurs predominantly in locations in which there is cortical tSAH on the admission CT scan, suggesting that they could be part of a similar process. Chang et Al. (2) performed a retrospective analysis on a prospective observational database containing 113 head trauma patients to characterize the natural course of
ACCEPTED MANUSCRIPT
M AN U
SC
RI PT
traumatic intraparenchymal contusions and hematomas (IPHs) and to identify risk factors for IPH progression in the acute post-injury period. IPH progression was independently associated with the presence of subarachnoid hemorrhage (OR 1.6; 95% CI 1.12–2.3), presence of a subdural hematoma (OR 1.94; 95% CI 1.1– 3.43), and initial size (OR 1.11; 95% CI 1.02–1.21, for each cm3 volume). This study also underlines the importance of tSAH as risk factor for IPHs progression. Up to 20% of patients with severe TBI and tSAH may develop symptomatic cerebral vasospasm (5): precisely greater is the amount of subarachnoid blood greater is the probability to have vasospasm (6). While the treatment of post-traumatic vasospasm is similar to that seen in aneurysmal SAH, a systematic review including 1074 TBI patients with tSAH don’t support a beneficial effect of nimodipine as preventive therapeutic strategy (11). tSAH, reducing cerebrospinal fluid (CSF) absorption, may occasionally lead to the development of hydrocephalus: generally this condition is transient and rarely requires CSF diversion (1).
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Summarizing, the presence of blood in the subarachnoid space after severe TBI, especially with other associated intracranial lesions, is a marker of greater disease severity. The clinician should be aware about the potential evolution of IPHs and occurrence of vasospasm. Further studies are necessary to better elucidate the relationship between the subarachnoid blood and the development of secondary brain damage in TBI patients. Bibliography:
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1 - Cardoso ER, Galbraith S. Posttraumatic hydrocephalus - a retrospective review. Surg Neurol 23(3): 261-4, 1985. 2 - Chang EF, Meeker M, Holland MC. Acute traumatic intraparenchymal hemorrhage: risk factors for progression in the early post-injury period. Neurosurgery 58(4): 647-56, 2006. 3 - Chieregato A, Fainardi E, Morselli-Labate AM, Antonelli V, Compagnone C, Targa L, Kraus J, Servadei F. Factors associated with neurological outcome and lesion progression in traumatic subarachnoid hemorrhage patients. Neurosurgery 56(4): 671-80, 2005. 4 - Crooks DA. Pathogenesis and biomechanics of traumatic intracranial haemorrhages. Virchows Arch A Pathol Anat Histopathol 418(6): 479-83, 1991.
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Key Words:
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5 - Lee JH, Martin NA, Alsina G, McArthur DL, Zaucha K, Hovda DA, Becker DP. Hemodynamically significant cerebral vasospasm and outcome after head injury: a prospective study. J Neurosurg 87(2): 221-33, 1997. 6 - Lin TK, Tsai HC, Hsieh TC. The impact of traumatic subarachnoid hemorrhage on outcome: a study with grouping of traumatic subarachnoid hemorrhage and transcranial Doppler sonography. J Trauma Acute Care Surg 73(1): 131-6, 2012. 7 - MRC CRASH Trial Collaborators, Perel P, Arango M, Clayton T, Edwards P, Komolafe E, Poccock S, Roberts I, Shakur H, Steyerberg E, Yutthakasemsunt S. Predicting outcome after traumatic brain injury: practical prognostic models based on large cohort of international patients. BMJ 336(7641): 425-9, 2008. 8 - Murray GD, Butcher I, McHugh GS, Lu J, Mushkudiani NA, Maas AI, Marmarou A, Steyerberg EW. Multivariable prognostic analysis in traumatic brain injury: results from the IMPACT study. J Neurotrauma 24(2): 329-37, 2007. 9 - Quigley MR, Chew BG, Swartz CE, Wilberger JE. The clinical significance of isolated traumatic subarachnoid hemorrhage. J Trauma Acute Care Surg 74(2): 581-4, 2013. 10 - Servadei F, Murray GD, Teasdale GM, Dearden M, Iannotti F, Lapierre F, Maas AJ, Karimi A, Ohman J, Persson L, Stocchetti N, Trojanowski T, Unterberg A. Traumatic subarachnoid hemorrhage: demographic and clinical study of 750 patients from the European brain injury consortium survey of head injuries. Neurosurgery 50(2): 261-7, 2002. 11 - Vergouwen MD, Vermeulen M, Roos YB. Effect of nimodipine on outcome in patients with traumatic subarachnoid haemorrhage: a systematic review. Lancet Neurol 5(12): 1029-32, 2006.
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Traumatic brain injury (TBI), traumatic subarachnoid hemorrhage (tSAH), head injury, head trauma, motor vehicle crash (MVC), fall from height (FFH). Acknowledgements:
None.
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ACCEPTED MANUSCRIPT
ACCEPTED MANUSCRIPT
Highlights:
- tSAH is a frequent finding in head injury patients - in the setting of severe TBI tSAH is often associated with poor prognosis
RI PT
- tSAH is a marker of greater disease severity
AC C
EP
TE D
M AN U
SC
- further studies are necessary to better elucidate the relationship between the subarachnoid blood and the development of secondary brain damage in TBI patients.