Hello, I'm Andrew Nadek. Thank you for attending this lecture on elevated intracranial pressure as part of the Multiprofessional Critical Care Review. I do have some disclosures, including funding from the NIH. Important points I wanted to make is that elevated intracranial pressure is a neurological emergency. Untreated, it may lead to brain herniation and death. Blood, swollen brain tissue, hydrocephalus, and foreign bodies can all lead to elevated intracranial pressure. A stepwise protocol is often, but not always, effective for reducing intracranial pressure and reducing neurological damage. At its base, the Monroe-Kelley Doctrine notes that the three typical components of the intracranial are brain, blood and arteries and veins, and cerebrospinal fluid. If the volume of one of these increases, say an increase in cerebrospinal fluid from hydrocephalus, then the other two must decrease in volume or the intracranial pressure will begin to rise. Another foreign body can also contribute to elevated intracranial pressure and take up space in the intracranial vault. Elevated intracranial pressure can lead to a vicious cycle. Elevated pressure will necessarily lead to decreased cerebral perfusion. Decreased cerebral perfusion will lead to ischemia. Nervous system tissue responds to ischemia in part by swelling and cerebral edema, which further worsens elevated intracranial pressure. We'll return later in the session for strategies of how to break this vicious cycle at different points along the way. One can measure intracranial pressure with a bolt or intraparachemal device typically placed on top of the dura or in neuronal tissue and gives a pressure reading. This may also include brain oxygen tension monitoring or multimodality monitors such as lactate, pyruvate and so on. You might also place a ventricular drain, a catheter that sits in the fluid-filled ventricular space. This will be pressure and will allow for drainage of cerebrospinal fluid. Microdialysis samples the cellular milieu for markers of energy metabolism, lactate, pyruvate and so on. It's a focal measurement of labor-intensive. There is some evidence to show that improving parameters of microdialysis is associated with better outcome and better intermediate markers of survival, but the quality of evidence remains generally low. Prospective randomized trials have been hampered by the need for the invasive procedure and difficulty in standardizing the metabolites and the interventions. Brain oxygen tension is somewhat more standardized. Typically a probe is placed in the frontal lobe. This probe allows measurement of the brain oxygen tension in addition to pressure, actually measuring hypoxia rather than simply hypoxemia, a decreased arterial oxygen tension. Brain oxygen tension may be considered an adjunct to the imaging, cerebral examination. In general, a brain oxygen tension of 15 to 20 Torr is considered acceptable. Whether or not brain oxygen tension monitoring improves outcomes in traumatic brain injury is currently being studied in an ongoing sponsored clinical trial. A stepwise management of intracranial pressure includes noting if there is a surgically correctable lesion, appropriately sedating and providing pain control to a calm, motionless state, drainage of hydrocephalus, typically ventricular drain, optimizing cerebral perfusion pressure, reducing cerebral edema with mannitol hypertonic saline, inducing normotherm or hypothermia, and then inducing coma to reduce oxygen demand with barbiturative benzos. This is a general order, but one might do more than one at a time or go slightly out of order. Hyperventilation should generally be used only temporarily and for emergencies because it may lead to cerebral ischemia. To break the vicious cycle of elevated intracranial pressure, there are numerous strategies at each point. To reduce elevated intracranial pressure, one might drain cerebrospinal fluid, perform decompression or remove clot or dead brain tissue. To reduce cerebral perfusion pressure, one might increase blood pressure using vasopressors. To reduce cerebral ischemia, one might open up vessels that are blocked or give a packed breath blood cell transfusion to increase oxygen delivery. And to reduce cerebral edema, one might give hypertonic fluids like hypertonic saline, mannitol, or steroids, typically in the case of a brain tumor. The subdural hematoma is a collection of blood between the brain and the dura mater. Subdurals are typically low-pressure bleeds, so the surface area tends to be relatively large. The symptoms depend on the location. Subdural hematoma is often an incidental trauma, so have a low threshold for screening CT, particularly in older patients. An epidural hematoma is an arterial bleed as opposed to the venous bleed of subdural hematoma. Epidural hematomas are typically due to a laceration of the artery between the dura and the bone. These are typically traumatic. The dura must be dissected away from the bone, so the pressure under it is typically high. Focal cerebral edema, in this case from a tumor, may also cause focal edema. Hypertonic saline or mannitol may be helpful to reduce some of this edema and reduce elevated intracranial pressure. Focal edema typically follows a cessation of blood flow to the brain, such as cardiac arrest. You may typically see these finger-like projections of white matter. A 65-year-old male patient presents with altered consciousness. On examination, he moans to simulation and is able to push away the examiner's hand to the right. He has history of diabetes, coronary artery disease, and is a plumber. Which of the following is the next most appropriate course of action? The correct answer would be to compute a tomogram of the head to look for a mass lesion or a cause of elevated intracranial pressure for the patient's focal neurological examination. A lumbar puncture might be indicated if the CT were normal to rule out meningitis or another infectious or inflammatory process. Intracranial pressure monitoring might be appropriate, depending on the results of the CT. EEG monitoring also might be appropriate, although seizures seem less likely with this presentation. Mannitol pulls free water across a semipermeable membrane, here the blood-brain barrier. As an osmotic agent, it mostly stays in serum and raises serum osmolality. The water flows to follow the area of increased osmolality. If used for several days, mannitol will leak across the blood-brain barrier and build up. So if mannitol is used for several days, successively reducing doses should be used to prevent reverse osmolal shift and free water diffusing into CNS. Hypertonic saline generally comes in the flavors of 3%, 7%, and 23.4%. There's a similar number of osmols in 1,000 mLs of 0.9%, 250 mLs of 3%, or 30 mLs of 23.4%. The usual way it is supplied may be given as a bolus or an infusion. 3% may be given safely by peripheral vein. Hypertonic saline is not an osmotic diuretic like mannitol. It may be tied to the clinical exam, an elevated sodium, 150 to 160, or a goal total osmolality, typically 320 mOsmol per liter. For a single dose, mannitol and hypertonic saline are roughly equivalent. In general, one can follow the serum osmolality, which accounts for mannitol, other unmeasured osmols, say, unloading a patient's liver failure. Bolus of 23.4% saline in patients with active transcenternal herniation and a blonde pupil will typically improve the Glasgow Coma Scale, reduce intracranial pressure, and restore the reactivity of the pupil while being fairly neutral on perfusion pressure, heart rate, and respiratory rate. Steroids reduce intracranial pressure and reduce edema in patients with tumors, and there were some evidence that suggests this might also be helpful in neurotrauma. Unfortunately, as it turned out, steroids significantly increase the rate of death in patients with acute traumatic brain injury in the MRC CRASH study, so steroids should be avoided in patients with traumatic brain injury. This is a 26-year-old patient who presented after apparently falling down the stairs. The patient had bilateral intracranial hematomas, and a right epidural hematoma was drained. Initially on examination with intracranial pressure of 30, the patient had a right cranial of third palsy and extensor posturing. With use of osmolal therapy, cerebral edema generally decreased, and the sulci in the brain were better seen on repeat CT when the osm were raised from 280 to about 320. At two weeks, this patient only had a Glasgow Coma Scale of 7, flexion on the left, extension on the right, tracheostomy in place, and eyes only open to voice. However, the patient had acute reglutation, had recovery of spontaneous consciousness from four to eight weeks out. The patient underwent successful replacement of bone flap, and then at three months was awake alert, had an on-focal neurological examination, although no memory of the intensive care unit. At three months, the patient went back to home, and at six months, the patient went back to work. Intensive recovery in patients with traumatic brain injury, particularly young patients, is more common than with other conditions, such as intracranial hemorrhage or ischemic stroke. It's important to note that normalizing intracranial pressure might not be necessary or sufficient for improved patient outcomes. The Dekker study of bilateral craniotomy for patients with intracranial pressure of at least 20 had clearly better intracranial pressure after the decompression. However, the patients had overall worse outcomes at six months follow-up, for reasons which were not entirely clear. In a prospective randomized clinical trial of patients with severe traumatic brain injury who were randomly assigned to treatment with scans and examination versus intracranial pressure monitoring, there was no difference in survival, according to study group at day 14 or throughout the study period, suggesting that patients, in general, who were managed without intracranial pressure monitor did about as well as patients who were managed with intracranial pressure monitor. It's not clear why better control of intracranial pressure didn't improve outcomes in these trials. A variety of hypotheses have been postulated, some of which are undergoing ongoing investigation. Brain oxygen tension is one of these. We typically measure hypoxemia, reduced partial pressure of oxygen in the blood. However, black hox monitors will actually measure brain oxygen tension. A strategy of normalizing brain oxygen tension versus a strategy of normalizing intracranial pressure is currently being tested in the BOOST-3 clinical trial run by the NIH SIREN network. Which of the following would be the most appropriate next step to reduce intracranial pressure of 25 TOR in an agitated patient with severe traumatic brain injury? Here, the best answer is B, appropriate sedation and pain control. Stratifrontal craniotomy might be needed for refractory elevated intracranial pressure, but at this level of elevated intracranial pressure has not been shown to be associated with or particularly improve the outcomes. Phenytoin might be helpful if the patient had seizures, or for patients for seizure prophylaxis, but is not likely to help with the elevated intracranial pressure. Manitol might be appropriate, but generally sedation and pain control should be tried first. In summary, elevated intracranial pressure is morbid and potentially deadly. Its etiologies include endogenous causes like reduced cerebral perfusion leading to stroke and exogenous injuries like neurotrauma. A variety of helpful strategies abound for reducing elevated intracranial pressure, such as hyperosmolar therapy, elevating the head of the bed, targeted sedation, and optimizing of cerebral perfusion. Remember not to give patients steroids.

elevated intracranial pressure

neurological emergency

brain herniation

cerebral perfusion pressure

intracranial pressure monitoring