Intracranial Pressure After Aneurysmal Subarachnoid Hemorrhage: Time to Revisit* Yogesh Moradiya, MD Wendy Ziai, MD, MPH Division of Neurosciences Critical Care Department of Anesthesia and Critical Care Medicine The Johns Hopkins School of Medicine Baltimore, MD ong since the days of pneumoencephalography, it has been known that massive aneurysmal subarachnoid hemorrhage (aSAH) may result in significant elevation in intracranial pressure (ICP), which can be fatal without prompt treatment and can trigger a vicious cycle of low cerebral perfusion-induced isch emia in turn causing further ICP elevation (1). Management of aSAH has evolved significantly during recent times with increasing number of patients, especially poor-grade patients receiving endo vascular treatment (2). Surgical and endovascular treatments of cerebral aneurysms create significantly different pathophysiologic milieu in the cranial vault (3), and therefore, call for a need to revisit. In this issue of Critical Care Medicine, Zoerle et al (4) studied incidence and predictors of elevated ICP in aSAH and its asso ciation with 6-m onth outcomes. The authors analyzed 116 cases treated in a single academic center from a prospective observa tional database. O f note, almost three quarters of patients were treated with endovascular coiling. The patient cohort had high severity with 80% patients classified as World Federation of Neurosurgical Surgeons (WFNS) grade IV-V and 98% classi fied as Fisher grade 3-4. Among this cohort, 36% of patients had a maximum mean ICP greater than 20 mm Hg (calculated over 12-hr intervals), the frequency of which peaked on day 3 after the ictus. Factors independently associated with highest mean ICP greater than 20 mm Hg were pretreatm ent neurolog ical status (WFNS grade), rehemorrhage, early lesions on CT, and worse Fisher grade. In multivariate analysis, highest mean ICP was the only factor associated with 6-month mortality with most deaths occurring in the first 7 days. However, consistent with a study from Heuer et al (5), ICP was not independently associated with unfavorable 6-m onth outcomes. Neurological status, age, and CT lesions at any time were significant inde pendent predictors of 6-m onth outcomes in regression analysis. It is highly significant, therefore, that in a population of patients with severe aSAH requiring ICP monitoring for either
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*See also p. 168. Key Words: endovascular treatment; intracranial pressure; mortality; outcomes; subarachnoid hemorrhage
Dr. Ziai received support for travel from the National Institutes of Health (National Institute of Neurological Disorders and Stroke). Dr. Moradiya has disclosed that he does not have any potential conflicts of interest. Copyright © 2014 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins DOI: 10.1097/CCM .0000000000000698
Critical Care Medicine
severe coma or acute hydrocephalus, elevated ICP was the most important factor determining mortality. This study does not tell us which patients should be monitored, but it does support the need to monitor ICP in high-grade aSAH and to treat ICP aggres sively. An important assumption made was that all ICP episodes were maximally treated minimizing the duration of such events. The therapy intensity level results for management of intracra nial hypertension in this study indicated that high-intensity treat ment was significantly more often used in patients who died or had unfavorable outcomes versus survivors and those with good outcomes. If therapy intensity was applied appropriately, then persistent elevated ICP may represent refractory cases for which increased cerebrospinal fluid (CSF) drainage (93% had external ventricular drains) and other therapies were less beneficial. As for long-term functional outcomes, it is hardly surpris ing that in a complex disease such as aSAH, elevated ICP was not an independent predictor. As noted by Zoerle et al (4) and Cahill et al (6), factors such as global cerebral edema from ictal cerebral circulatory arrest, neurotoxicity of blood, and its degradation products, disruption of cerebral autoregulation and cerebral vasospasm may significantly contribute to brain injury and poor outcomes after aSAH and are far less amenable to reliable m onitoring and target-based therapy. Now we may ask whether we have learned anything new. In 1982, Voldby and Enevoldsen (7) recorded intraventricular pres sure in 52 patients with aSAH for an average of 8 days. A close correlation was found between changes in clinical grade and in mean ICP. Drainage improved the condition in uncomplicated cases but was less effective or ineffective when severe vasospasm or rebleeding occurred. Patients with severe spasm had perma nently elevated ICP, and mean ICP exceeding 25 mm Hg for the whole monitoring period was associated with a poor prognosis. This study recommended that patients with even mild neuro logic impairment (Hunt and Hess grades II—III) be considered for ICP monitoring to prevent deterioration and that those with severe grades (IV-V) be monitored because of the high preva lence of intracranial hypertension. In 2004, Heuer et al (5) ana lyzed 433 patients with surgically treated aSAH and found that elevated mean hourly ICP greater than 20 mm Hg occurred in 54% of cases. Almost half of patients with good clinical grade (Hunt and Hess grades I—III) also had elevated ICP. Failure of increased ICP to respond to treatment was always associated with poor outcome although many patients whose elevated ICP could be controlled had a satisfactory outcome. The current study adds the following new or important findings: 1) mode of aneurysm treatment (surgical clipping vs endovascular coiling) does not appear to be a significant factor in occurrence of high ICP; 2) hydrocephalus on initial imaging is not significantly associated with high ICP, likely because of the high prevalence of external ventricular drain placement and CSF drainage in this study; and 3) the independent association of early lesions on CT and worse w w w .c c m jo u r n a l.o r g
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Fisher grade with high ICP support previous studies suggesting that high ICP can worsen vasospasm, and that ICP reduction, in particular osmotic diuresis, may reverse vasospasm development and clinical signs of delayed ischemia (8,9). American Heart Association guidelines recommend that aSAH-associated acute symptomatic hydrocephalus should be managed by CSF diversion (10). The role of ICP monitoring in the absence of hydrocephalus has not been established for this condition. Results of this and previous studies would indi cate that poor-grade patients with aSAH should receive ICP monitoring during the acute phase either with an external ven tricular drain with careful CSF drainage or with an intraparenchymal ICP monitoring device. Although good-grade patients were less represented in this study, the presence of high Fisher grade may also be a reasonable indication for ICP monitoring. This report adds to a limited number of studies assessing the course of ICP, predictive factors, and affect outcomes in patients with aSAH. The results are generalizable to high-grade aSAH and patients treated with endovascular coiling mainly. Although cases of truly refractory ICP may have limited options, improv ing cerebral perfusion by lowering increased ICP remains a reasonable treatment against delayed cerebral ischemia consid ering the inadequacy of our medical management thus far.
2. Lin N, Cahill KS, Frerichs KU, et al: Treatment o f ruptured and unrup tured cerebral aneurysms in the U SA: A paradigm shift. J Neurointerv Surg 2 0 1 2 ; 4 :1 8 2 - 1 8 9 3. M ura J, Rojas-Zalazar D, Ruiz A, et al: Im proved outcom e in highgrade aneurysmal subarachnoid hem orrhage by enhancem ent of endogenous clearance of cisternal blood clots: A prospective study that dem onstrates the role o f lamina te rm in a ls fenestration com bined w ith m odern m icrosurgical cisternal blood evacuation. Minim Invasive Neurosurg 2 0 0 7 ; 5 0 :3 5 5 - 3 6 2 4. Zoerle T, Lom bardo A, C olom bo A, et al: Intracranial Pressure After Subarachnoid H em orrhage. Crit Care M ed 2 0 1 5 ; 4 3 :1 6 8 - 1 7 6 5. H euer G G , Sm ith MJ, Elliott JP, et al: Relationship betw een intracra nial pressure and other clinical variables in patients w ith aneurysmal subarachnoid hemorrhage. J Neurosurg 2 0 0 4 ; 1 0 1 :4 0 8 - 4 1 6 6. Cahill J, Calvert JW, Zhang JH: M echanism s of early brain injury after subarachnoid hemorrhage. J Cereb Blood Flow Metab 2 0 0 6 ; 2 6 :1 3 4 1 - 1 3 5 3 7. Voldby B, Enevoldsen EM: Intracranial pressure changes follow ing aneurysm rupture. Part 1: C linical and angiographic correlations. J Neurosurg 1 9 8 2 ; 5 6 :1 8 6 - 1 9 6 8. Fukuhara T, Douville C M , Eliott JP, et al: Relationship betw een intra cranial pressure and the developm ent o f vasospasm after aneurys mal subarachnoid hemorrhage. Neurol Med Chir (Tokyo) 1 9 9 8 ; 3 8 :7 1 0 -7 1 5 9. G am bardella G, De Blasi F, C aruso G, et al: Intracranial pressure, cerebral perfusion pressure, and S P E C T in the m anagem ent of patients w ith S A H H unt and H ess grades l-ll. Acta Neurochir Suppl 1 9 9 8 ; 7 1 :2 1 5 - 2 1 8 10.
REFERENCES 1.
Foltz EL, W ard A A Jr: C om m unicating hydrocephalus from subarach noid bleeding. J Neurosurg 1 9 5 6 ; 1 3 :5 4 6 - 5 6 6
C o n n o lly ES Jr, R abinstein AA , C arhuapom a JR, et al: G u id e lin e s fo r the m anagem ent o f aneurysm al subara ch n o id hem orrhage: A g u id e lin e fo r h e althcare p ro fe ssio n a ls from th e A m erican H eart A sso cia tio n /a m e rica n S tro ke A sso cia tio n . Stroke 2 0 1 2 ; 4 3 :1 7 1 1 - 1 7 3 7
Simulation: Why Not, When It Feels So Good?* S. Patrick Bender, MD Mark Hamlin, MD, MS Department of Anesthesiology University of Vermont College of Medicine/ University of Vermont Medical Center Burlington, VT
ith simulation-based education becoming ever more pervasive in medical school and in gradu ate medical education, the natural tendency is for it to spread into continuing medical education as well.
W
*S e e a ls o p. 186. K ey W o rd s : acute care physician; continuing m edical education; independent practitioner; m aintenance o f certification; sim ulation This w o rk w as perform ed at University o f V erm ont C ollege o f M edicine. Dr. Bender is employed by the University of Vermont Medical Center and the University of Vermont College of M edicine and received support for travel from the Society of Critical Care M edicine (S C C M ) (Ultrasound C ourse fac ulty). Dr. Hamlin is employed by the University o f Vermont Medical Center and the University of Vermont College o f Medicine, provided expert testimony (expert on case in Vermont), and lectured for the S C C M (Ultrasound faculty). C o p yrigh t © 2 0 1 4 by the S o cie ty o f C ritical C are M edicine and Lip p in co tt W illiam s & W ilkins D O I: 1 0 .1 0 9 7 /C C M .0 0 0 0 0 0 0 0 0 0 0 0 0 6 9 9
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w w w .c c m jo u rn a l.o rg
Appropriately, or perhaps cynically, many physicians ques tion the benefit of simulation in terms of patient outcome. However, this has not stopped incorporation of a simulation requirement into some certification and maintenance of cer tification (MOC) processes (1). Being mandated to participate in an activity without proven effectiveness can be a difficult pill to swallow, especially when it is associated with increased cost and time required by the practitioner. In this issue of Critical Care Medicine, Khanduja et al (2) have systematically reviewed the literature regarding the effec tiveness of simulation for certified acute care physicians who are already in practice and have not been exposed to simula tion during graduate medical training. Despite an abundance of simulation literature, only 39 studies met these authors’ objective of evaluating either the validity or the effectiveness of simulation-based education for the acute care physician. The major findings of their review was that practitioners invariably perceived simulation as a positive learning experience, but it remains unclear whether practitioners retain the learned skills long term. No studies showed any benefit to patient safety. Not surprisingly, the significant majority of these studies (73%) incorporated anesthesiologists as the learners. Anes thesiology has a history of early adoption of simulation. It January 2 0 1 5 • Volume 4 3 • N um ber 1
Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
L
*See also p. 168. Key Words: endovascular treatment; intracranial pressure; mortality; outcomes; subarachnoid hemorrhage
Dr. Ziai received support for travel from the National Institutes of Health (National Institute of Neurological Disorders and Stroke). Dr. Moradiya has disclosed that he does not have any potential conflicts of interest. Copyright © 2014 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins DOI: 10.1097/CCM .0000000000000698
Critical Care Medicine
severe coma or acute hydrocephalus, elevated ICP was the most important factor determining mortality. This study does not tell us which patients should be monitored, but it does support the need to monitor ICP in high-grade aSAH and to treat ICP aggres sively. An important assumption made was that all ICP episodes were maximally treated minimizing the duration of such events. The therapy intensity level results for management of intracra nial hypertension in this study indicated that high-intensity treat ment was significantly more often used in patients who died or had unfavorable outcomes versus survivors and those with good outcomes. If therapy intensity was applied appropriately, then persistent elevated ICP may represent refractory cases for which increased cerebrospinal fluid (CSF) drainage (93% had external ventricular drains) and other therapies were less beneficial. As for long-term functional outcomes, it is hardly surpris ing that in a complex disease such as aSAH, elevated ICP was not an independent predictor. As noted by Zoerle et al (4) and Cahill et al (6), factors such as global cerebral edema from ictal cerebral circulatory arrest, neurotoxicity of blood, and its degradation products, disruption of cerebral autoregulation and cerebral vasospasm may significantly contribute to brain injury and poor outcomes after aSAH and are far less amenable to reliable m onitoring and target-based therapy. Now we may ask whether we have learned anything new. In 1982, Voldby and Enevoldsen (7) recorded intraventricular pres sure in 52 patients with aSAH for an average of 8 days. A close correlation was found between changes in clinical grade and in mean ICP. Drainage improved the condition in uncomplicated cases but was less effective or ineffective when severe vasospasm or rebleeding occurred. Patients with severe spasm had perma nently elevated ICP, and mean ICP exceeding 25 mm Hg for the whole monitoring period was associated with a poor prognosis. This study recommended that patients with even mild neuro logic impairment (Hunt and Hess grades II—III) be considered for ICP monitoring to prevent deterioration and that those with severe grades (IV-V) be monitored because of the high preva lence of intracranial hypertension. In 2004, Heuer et al (5) ana lyzed 433 patients with surgically treated aSAH and found that elevated mean hourly ICP greater than 20 mm Hg occurred in 54% of cases. Almost half of patients with good clinical grade (Hunt and Hess grades I—III) also had elevated ICP. Failure of increased ICP to respond to treatment was always associated with poor outcome although many patients whose elevated ICP could be controlled had a satisfactory outcome. The current study adds the following new or important findings: 1) mode of aneurysm treatment (surgical clipping vs endovascular coiling) does not appear to be a significant factor in occurrence of high ICP; 2) hydrocephalus on initial imaging is not significantly associated with high ICP, likely because of the high prevalence of external ventricular drain placement and CSF drainage in this study; and 3) the independent association of early lesions on CT and worse w w w .c c m jo u r n a l.o r g
253
Editorials
Fisher grade with high ICP support previous studies suggesting that high ICP can worsen vasospasm, and that ICP reduction, in particular osmotic diuresis, may reverse vasospasm development and clinical signs of delayed ischemia (8,9). American Heart Association guidelines recommend that aSAH-associated acute symptomatic hydrocephalus should be managed by CSF diversion (10). The role of ICP monitoring in the absence of hydrocephalus has not been established for this condition. Results of this and previous studies would indi cate that poor-grade patients with aSAH should receive ICP monitoring during the acute phase either with an external ven tricular drain with careful CSF drainage or with an intraparenchymal ICP monitoring device. Although good-grade patients were less represented in this study, the presence of high Fisher grade may also be a reasonable indication for ICP monitoring. This report adds to a limited number of studies assessing the course of ICP, predictive factors, and affect outcomes in patients with aSAH. The results are generalizable to high-grade aSAH and patients treated with endovascular coiling mainly. Although cases of truly refractory ICP may have limited options, improv ing cerebral perfusion by lowering increased ICP remains a reasonable treatment against delayed cerebral ischemia consid ering the inadequacy of our medical management thus far.
2. Lin N, Cahill KS, Frerichs KU, et al: Treatment o f ruptured and unrup tured cerebral aneurysms in the U SA: A paradigm shift. J Neurointerv Surg 2 0 1 2 ; 4 :1 8 2 - 1 8 9 3. M ura J, Rojas-Zalazar D, Ruiz A, et al: Im proved outcom e in highgrade aneurysmal subarachnoid hem orrhage by enhancem ent of endogenous clearance of cisternal blood clots: A prospective study that dem onstrates the role o f lamina te rm in a ls fenestration com bined w ith m odern m icrosurgical cisternal blood evacuation. Minim Invasive Neurosurg 2 0 0 7 ; 5 0 :3 5 5 - 3 6 2 4. Zoerle T, Lom bardo A, C olom bo A, et al: Intracranial Pressure After Subarachnoid H em orrhage. Crit Care M ed 2 0 1 5 ; 4 3 :1 6 8 - 1 7 6 5. H euer G G , Sm ith MJ, Elliott JP, et al: Relationship betw een intracra nial pressure and other clinical variables in patients w ith aneurysmal subarachnoid hemorrhage. J Neurosurg 2 0 0 4 ; 1 0 1 :4 0 8 - 4 1 6 6. Cahill J, Calvert JW, Zhang JH: M echanism s of early brain injury after subarachnoid hemorrhage. J Cereb Blood Flow Metab 2 0 0 6 ; 2 6 :1 3 4 1 - 1 3 5 3 7. Voldby B, Enevoldsen EM: Intracranial pressure changes follow ing aneurysm rupture. Part 1: C linical and angiographic correlations. J Neurosurg 1 9 8 2 ; 5 6 :1 8 6 - 1 9 6 8. Fukuhara T, Douville C M , Eliott JP, et al: Relationship betw een intra cranial pressure and the developm ent o f vasospasm after aneurys mal subarachnoid hemorrhage. Neurol Med Chir (Tokyo) 1 9 9 8 ; 3 8 :7 1 0 -7 1 5 9. G am bardella G, De Blasi F, C aruso G, et al: Intracranial pressure, cerebral perfusion pressure, and S P E C T in the m anagem ent of patients w ith S A H H unt and H ess grades l-ll. Acta Neurochir Suppl 1 9 9 8 ; 7 1 :2 1 5 - 2 1 8 10.
REFERENCES 1.
Foltz EL, W ard A A Jr: C om m unicating hydrocephalus from subarach noid bleeding. J Neurosurg 1 9 5 6 ; 1 3 :5 4 6 - 5 6 6
C o n n o lly ES Jr, R abinstein AA , C arhuapom a JR, et al: G u id e lin e s fo r the m anagem ent o f aneurysm al subara ch n o id hem orrhage: A g u id e lin e fo r h e althcare p ro fe ssio n a ls from th e A m erican H eart A sso cia tio n /a m e rica n S tro ke A sso cia tio n . Stroke 2 0 1 2 ; 4 3 :1 7 1 1 - 1 7 3 7
Simulation: Why Not, When It Feels So Good?* S. Patrick Bender, MD Mark Hamlin, MD, MS Department of Anesthesiology University of Vermont College of Medicine/ University of Vermont Medical Center Burlington, VT
ith simulation-based education becoming ever more pervasive in medical school and in gradu ate medical education, the natural tendency is for it to spread into continuing medical education as well.
W
*S e e a ls o p. 186. K ey W o rd s : acute care physician; continuing m edical education; independent practitioner; m aintenance o f certification; sim ulation This w o rk w as perform ed at University o f V erm ont C ollege o f M edicine. Dr. Bender is employed by the University of Vermont Medical Center and the University of Vermont College of M edicine and received support for travel from the Society of Critical Care M edicine (S C C M ) (Ultrasound C ourse fac ulty). Dr. Hamlin is employed by the University o f Vermont Medical Center and the University of Vermont College o f Medicine, provided expert testimony (expert on case in Vermont), and lectured for the S C C M (Ultrasound faculty). C o p yrigh t © 2 0 1 4 by the S o cie ty o f C ritical C are M edicine and Lip p in co tt W illiam s & W ilkins D O I: 1 0 .1 0 9 7 /C C M .0 0 0 0 0 0 0 0 0 0 0 0 0 6 9 9
254
w w w .c c m jo u rn a l.o rg
Appropriately, or perhaps cynically, many physicians ques tion the benefit of simulation in terms of patient outcome. However, this has not stopped incorporation of a simulation requirement into some certification and maintenance of cer tification (MOC) processes (1). Being mandated to participate in an activity without proven effectiveness can be a difficult pill to swallow, especially when it is associated with increased cost and time required by the practitioner. In this issue of Critical Care Medicine, Khanduja et al (2) have systematically reviewed the literature regarding the effec tiveness of simulation for certified acute care physicians who are already in practice and have not been exposed to simula tion during graduate medical training. Despite an abundance of simulation literature, only 39 studies met these authors’ objective of evaluating either the validity or the effectiveness of simulation-based education for the acute care physician. The major findings of their review was that practitioners invariably perceived simulation as a positive learning experience, but it remains unclear whether practitioners retain the learned skills long term. No studies showed any benefit to patient safety. Not surprisingly, the significant majority of these studies (73%) incorporated anesthesiologists as the learners. Anes thesiology has a history of early adoption of simulation. It January 2 0 1 5 • Volume 4 3 • N um ber 1
Copyright of Critical Care Medicine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
