Ann. N.Y. Acad. Sci. ISSN 0077-8923
A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S Issue: Qatar Clinical Neuroscience Conference
Hypertonic saline for the management of raised intracranial pressure after severe traumatic brain injury Halinder S. Mangat1 and Roger Hartl ¨ 2 1
Division of Stroke and Critical Care, Department of Neurology, Weill Cornell Medical College, NewYork-Presbyterian Hospital, New York, New York. 2 Department of Neurological Surgery, Weill Cornell Brain and Spine Center, Weill Cornell Medical College, NewYork-Presbyterian Hospital, New York, New York Address for correspondence: Halinder S. Mangat, M.D., Division of Stroke and Critical Care, Department of Neurology, Weill Cornell Medical College, NewYork-Presbyterian Hospital, 525 East 68 St., F-610, New York, NY 10065. [email protected]
Hyperosmolar agents are commonly used as an initial treatment for the management of raised intracranial pressure (ICP) after severe traumatic brain injury (TBI). They have an excellent adverse-effect profile compared to other therapies, such as hyperventilation and barbiturates, which carry the risk of reducing cerebral perfusion. The hyperosmolar agent mannitol has been used for several decades to reduce raised ICP, and there is accumulating evidence from pilot studies suggesting beneficial effects of hypertonic saline (HTS) for similar purposes. An ideal therapeutic agent for ICP reduction should reduce ICP while maintaining cerebral perfusion (pressure). While mannitol can cause dehydration over time, HTS helps maintain normovolemia and cerebral perfusion, a finding that has led to a large amount of pilot data being published on the benefits of HTS, albeit in small cohorts. Prophylactic therapy is not recommended with mannitol, although it may be beneficial with HTS. To date, no large clinical trial has been performed to directly compare the two agents. The best current evidence suggests that mannitol is effective in reducing ICP in the management of traumatic intracranial hypertension and carries mortality benefit compared to barbiturates. Current evidence regarding the use of HTS in severe TBI is limited to smaller studies, which illustrate a benefit in ICP reduction and perhaps mortality. Keywords: traumatic brain injury; intracranial hypertension; intracranial pressure; hyperosmotics; mannitol; hypertonic saline
Introduction Traumatic brain injury (TBI) results in an initial impact injury to the brain followed by secondary injury from, for example, ischemia, hypoxia, or seizures. Brain swelling occurs and may be accompanied by intracranial hemorrhage. According to the Monro–Kellie doctrine, since the skull is an enclosed cavity with a fixed volume, an increase in volume of intracranial contents from edema or hemorrhage results in a rise in intracranial pressure (ICP).1 Before an elevation in ICP, the cranial contents have the ability to compensate for the additional volume of a lesion by shifting cerebrospinal fluid and decreasing cerebral blood volume—this is the basis for intracranial compliance. However, once compensatory mechanisms are exhausted, ICP
rises in response to a further increase in intracranial volume. Raised ICP after severe TBI is a cause of secondary brain injury and is associated with increased mortality.2,3 One of the cornerstones of critical care management of severe TBI is to ensure ICP remains within normal limits (typically
A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S Issue: Qatar Clinical Neuroscience Conference
Hypertonic saline for the management of raised intracranial pressure after severe traumatic brain injury Halinder S. Mangat1 and Roger Hartl ¨ 2 1
Division of Stroke and Critical Care, Department of Neurology, Weill Cornell Medical College, NewYork-Presbyterian Hospital, New York, New York. 2 Department of Neurological Surgery, Weill Cornell Brain and Spine Center, Weill Cornell Medical College, NewYork-Presbyterian Hospital, New York, New York Address for correspondence: Halinder S. Mangat, M.D., Division of Stroke and Critical Care, Department of Neurology, Weill Cornell Medical College, NewYork-Presbyterian Hospital, 525 East 68 St., F-610, New York, NY 10065. [email protected]
Hyperosmolar agents are commonly used as an initial treatment for the management of raised intracranial pressure (ICP) after severe traumatic brain injury (TBI). They have an excellent adverse-effect profile compared to other therapies, such as hyperventilation and barbiturates, which carry the risk of reducing cerebral perfusion. The hyperosmolar agent mannitol has been used for several decades to reduce raised ICP, and there is accumulating evidence from pilot studies suggesting beneficial effects of hypertonic saline (HTS) for similar purposes. An ideal therapeutic agent for ICP reduction should reduce ICP while maintaining cerebral perfusion (pressure). While mannitol can cause dehydration over time, HTS helps maintain normovolemia and cerebral perfusion, a finding that has led to a large amount of pilot data being published on the benefits of HTS, albeit in small cohorts. Prophylactic therapy is not recommended with mannitol, although it may be beneficial with HTS. To date, no large clinical trial has been performed to directly compare the two agents. The best current evidence suggests that mannitol is effective in reducing ICP in the management of traumatic intracranial hypertension and carries mortality benefit compared to barbiturates. Current evidence regarding the use of HTS in severe TBI is limited to smaller studies, which illustrate a benefit in ICP reduction and perhaps mortality. Keywords: traumatic brain injury; intracranial hypertension; intracranial pressure; hyperosmotics; mannitol; hypertonic saline
Introduction Traumatic brain injury (TBI) results in an initial impact injury to the brain followed by secondary injury from, for example, ischemia, hypoxia, or seizures. Brain swelling occurs and may be accompanied by intracranial hemorrhage. According to the Monro–Kellie doctrine, since the skull is an enclosed cavity with a fixed volume, an increase in volume of intracranial contents from edema or hemorrhage results in a rise in intracranial pressure (ICP).1 Before an elevation in ICP, the cranial contents have the ability to compensate for the additional volume of a lesion by shifting cerebrospinal fluid and decreasing cerebral blood volume—this is the basis for intracranial compliance. However, once compensatory mechanisms are exhausted, ICP
rises in response to a further increase in intracranial volume. Raised ICP after severe TBI is a cause of secondary brain injury and is associated with increased mortality.2,3 One of the cornerstones of critical care management of severe TBI is to ensure ICP remains within normal limits (typically
