Perspectives Commentary on: Acute Lung Injury in Patients with Subarachnoid Hemorrhage: A Nationwide Inpatient Sample Study by Veeravagu et al. World Neurosurg 82:E235-E241, 2014
Medical Complications After Aneurysmal Subarachnoid Hemorrhage: An Emerging Contributor to Poor Outcome Nima Etminan1 and R. Loch Macdonald2
D
uring the past 3 decades, mortality after aneurysmal subarachnoid hemorrhage (SAH) has been effectively reduced by approximately 50% (6), mainly as the consequence of early repair of ruptured aneurysms and significant advances in aneurysm repair modalities but also improved neurocritical care. Nevertheless, the incidence of poor neurologic outcome has basically remained unchanged and ranges between 25% and 50% (1). The underlying pathophysiologic mechanisms that contribute to poor neurologic outcome, i.e., the extent of early brain injury and the incidence of delayed cerebral ischemia (DCI), and, moreover, their effective pharmaceutical treatment, are the focus of intensive research. Nevertheless, with increasing overall survival rates after aneurysmal SAH, medical or noncerebral complications increasingly are recognized as an additional determinant for neurologic outcome in the course of SAH. Indeed, there is evidence that primary critical medical illnesses, including sepsis and respiratory failure requiring intensive care support, are associated with cognitive impairment (12). In one study of 821 patients with respiratory failure or shock who were in the intensive care unit, 40% had cognitive scores similar to the scores of patients who suffer moderate traumatic brain injury (12). Why and how systemic illness causes cognitive dysfunction is not clear and is the subject of experimental study (9), but it points out that the high rate of cognitive dysfunction in patients with SAH may be contributed to by delirium and systemic illness. The prevention of medical complications may be even more important than previously thought.
Key words Acute lung injury - Acute respiratory distress syndrome - Nationwide Inpatient Sample Database - Subarachnoid hemorrhage -
Abbreviations and Acronyms ALI: Acute lung syndrome ARDS: Acute respiratory distress syndrome DCI: Delayed cerebral ischemia PE: Pulmonary edema SAH: Subarachnoid hemorrhage
Naturally, the incidence of such complications increases with increasing patient age and is reported to be twice as high in patients older than 70 years of age compared with patients younger than 40 (5). Studies also clearly illustrate that medical complications are the only complication of SAH that are increasing in terms of contribution to outcome after SAH (4). Furthermore, although there are few good randomized studies of medical treatment, there is a suggestion that earlier and more active treatment of cardiopulmonary complications in poor-grade SAH patients is associated with better functional outcome (4, 10). In view of these data as discussed by Lovelock et al., it is evident that the aforementioned reduction of case fatality after SAH also is related to the increasing collaborative efforts of neurosurgeons and neurointensivists to treat this complex disease and especially its complications. The most common medical complications are of cardiocirculatory, i.e., acute heart or renal failure of pulmonary nature, i.e., acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) (2, 4). It is likely that the incidence of cardiocirculatory and pulmonary complications is somewhat related to the incidence of risk factors for SAH, which suggests that if a patient has been smoking and suffering from untreated hypertension for decades, one should expect that these patients are more prone to systemic complications. Nevertheless, especially for good-grade SAH patients, it can be difficult to anticipate early after SAH ictus which patient requires more vigilant care or aggressive hemodynamic monitoring. Electrocardiographic alterations and cardiac enzyme (troponin T) elevations are quite frequent after SAH but, depending on their
From the 1Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany; and 2Division of Neurosurgery, St. Michael’s Hospital, Labatt Family Centre of Excellence in Brain Injury and Trauma Research, Keenan Research Centre of the Li Ka Shing Knowledge Institute of St. Michael’s Hospital, and the Department of Surgery, University of Toronto, Toronto, Ontario, Canada To whom correspondence should be addressed: Nima Etminan, M.D. [E-mail: [email protected]] Citation: World Neurosurg. (2015) 83, 3:303-304. http://dx.doi.org/10.1016/j.wneu.2014.06.031
WORLD NEUROSURGERY 83 [3]: 303-304, MARCH 2015
www.WORLDNEUROSURGERY.org
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PERSPECTIVES
severity, also are significant surrogates for clinical outcome (8, 11). The exact pathomechanisms behind acute myocardial injury or neurogenic myocardial are incompletely understood but clinically this may manifest as left ventricular failure, with subsequent impaired cardiac output, hypotension, and pulmonary edema (PE). The evident relation between impaired cardiac output, decreased cerebral perfusion pressure, or brain tissue oxygenation underlines the necessity of intensive noninvasive and invasive hemodynamic monitoring in such patients, to avoid an additive effect of such complications on DCI and neurologic outcome after SAH. The heterogeneous previous definitions for ALI (usually defined as partial pressure of oxygen in the blood [i.e., PaO2] to fraction of inspired oxygen [FiO2] ratio
Medical Complications After Aneurysmal Subarachnoid Hemorrhage: An Emerging Contributor to Poor Outcome Nima Etminan1 and R. Loch Macdonald2
D
uring the past 3 decades, mortality after aneurysmal subarachnoid hemorrhage (SAH) has been effectively reduced by approximately 50% (6), mainly as the consequence of early repair of ruptured aneurysms and significant advances in aneurysm repair modalities but also improved neurocritical care. Nevertheless, the incidence of poor neurologic outcome has basically remained unchanged and ranges between 25% and 50% (1). The underlying pathophysiologic mechanisms that contribute to poor neurologic outcome, i.e., the extent of early brain injury and the incidence of delayed cerebral ischemia (DCI), and, moreover, their effective pharmaceutical treatment, are the focus of intensive research. Nevertheless, with increasing overall survival rates after aneurysmal SAH, medical or noncerebral complications increasingly are recognized as an additional determinant for neurologic outcome in the course of SAH. Indeed, there is evidence that primary critical medical illnesses, including sepsis and respiratory failure requiring intensive care support, are associated with cognitive impairment (12). In one study of 821 patients with respiratory failure or shock who were in the intensive care unit, 40% had cognitive scores similar to the scores of patients who suffer moderate traumatic brain injury (12). Why and how systemic illness causes cognitive dysfunction is not clear and is the subject of experimental study (9), but it points out that the high rate of cognitive dysfunction in patients with SAH may be contributed to by delirium and systemic illness. The prevention of medical complications may be even more important than previously thought.
Key words Acute lung injury - Acute respiratory distress syndrome - Nationwide Inpatient Sample Database - Subarachnoid hemorrhage -
Abbreviations and Acronyms ALI: Acute lung syndrome ARDS: Acute respiratory distress syndrome DCI: Delayed cerebral ischemia PE: Pulmonary edema SAH: Subarachnoid hemorrhage
Naturally, the incidence of such complications increases with increasing patient age and is reported to be twice as high in patients older than 70 years of age compared with patients younger than 40 (5). Studies also clearly illustrate that medical complications are the only complication of SAH that are increasing in terms of contribution to outcome after SAH (4). Furthermore, although there are few good randomized studies of medical treatment, there is a suggestion that earlier and more active treatment of cardiopulmonary complications in poor-grade SAH patients is associated with better functional outcome (4, 10). In view of these data as discussed by Lovelock et al., it is evident that the aforementioned reduction of case fatality after SAH also is related to the increasing collaborative efforts of neurosurgeons and neurointensivists to treat this complex disease and especially its complications. The most common medical complications are of cardiocirculatory, i.e., acute heart or renal failure of pulmonary nature, i.e., acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) (2, 4). It is likely that the incidence of cardiocirculatory and pulmonary complications is somewhat related to the incidence of risk factors for SAH, which suggests that if a patient has been smoking and suffering from untreated hypertension for decades, one should expect that these patients are more prone to systemic complications. Nevertheless, especially for good-grade SAH patients, it can be difficult to anticipate early after SAH ictus which patient requires more vigilant care or aggressive hemodynamic monitoring. Electrocardiographic alterations and cardiac enzyme (troponin T) elevations are quite frequent after SAH but, depending on their
From the 1Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany; and 2Division of Neurosurgery, St. Michael’s Hospital, Labatt Family Centre of Excellence in Brain Injury and Trauma Research, Keenan Research Centre of the Li Ka Shing Knowledge Institute of St. Michael’s Hospital, and the Department of Surgery, University of Toronto, Toronto, Ontario, Canada To whom correspondence should be addressed: Nima Etminan, M.D. [E-mail: [email protected]] Citation: World Neurosurg. (2015) 83, 3:303-304. http://dx.doi.org/10.1016/j.wneu.2014.06.031
WORLD NEUROSURGERY 83 [3]: 303-304, MARCH 2015
www.WORLDNEUROSURGERY.org
303
PERSPECTIVES
severity, also are significant surrogates for clinical outcome (8, 11). The exact pathomechanisms behind acute myocardial injury or neurogenic myocardial are incompletely understood but clinically this may manifest as left ventricular failure, with subsequent impaired cardiac output, hypotension, and pulmonary edema (PE). The evident relation between impaired cardiac output, decreased cerebral perfusion pressure, or brain tissue oxygenation underlines the necessity of intensive noninvasive and invasive hemodynamic monitoring in such patients, to avoid an additive effect of such complications on DCI and neurologic outcome after SAH. The heterogeneous previous definitions for ALI (usually defined as partial pressure of oxygen in the blood [i.e., PaO2] to fraction of inspired oxygen [FiO2] ratio
