Intracranial Hypertension
A 32-year-old male was an unhelmeted motorcyclist who was struck by a car and throw 20 feet. He had decreased alertness on the scene and was urgently transported to the hospital. On arrival to the ED, his GCS was 7 (E2V2M3). He was hemodynamically normal and secondary survey was only remarkable for diffuse road rash and a large scalp laceration. He was intubated for concern for inadequate airway protection. Chest x-ray revealed multiple left sided rib fractures, FAST was positive in the right upper quadrant and the pelvis x-ray was unremarkable. He was taken to the CT scanner for head, c-spine, chest, abdomen and pelvis imaging. He was transported to the trauma ICU as his images were reviewed.
Head CT
Case courtesy of Derek Smith. From the case rID: 169704.
Imaging revealed a large right sided subdural hematoma. He has left lower rib fractures and a grade 3 splenic injury. Neurosurgery evaluated him upon arrival to the ICU.
How is intracranial pressure monitored?
The preferred method for ICP monitoring is with an external ventricular drain. This allows the dual function of monitoring ICP as well as allowing to treatment of elevated ICP via drainage of cerebrospinal fluid (CSF).
What is a normal value for ICP?
Normal ICP is <20 mmHg and treatment is recommended for sustained ICP >22 mmHg.
Neurosurgery places an external ventricular drain. His opening pressure was 32, and his ICP ranges from 25-32 over the next few hours.
He was in reverse Trendelenburg, and he was adequately sedated. His repeat head CT was unchanged. He had CSF drainage via his EVD. He was given 2 boluses of hypertonic saline. His ICPs improved, and were sustained at 18-20 mmHg.
He develops hypotension, with systolic pressures in the 80s.
What are some of the possible etiologies for hypotension, and how would you evaluate/ treat the various etiologies?
Bleeding from his spleen→ urgent splenectomy. Hypotension is detrimental to TBI.
Side effects from sedation medication→ decrease dosages or switch therapeutic agents, implement other treatment strategies
Evaluation and Management of Traumatic Brain Injury
The goal of the initial management of TBI is the prevention of secondary brain injury.
Avoid hypotension and hypoxemia
Target normal pulse oximetry, normal PaCO2 (35-45 mmHg) and PaO2 (≥100 mmHg), normal blood pressure (SBP ≥100), normal electrolytes, normal temperature, platelets >75K, hemoglobin >7 g/dL.[1]
Treat pain and provide sedation as appropriate.
Optimize patient positioning to promote cerebral venous drainage- elevate the head of the bed and ensure the cervical collar or endotracheal tube support is not too tight.
Monro-Kellie Doctrine[2]
Inside the bony skull, there is brain tissue, blood and cerebrospinal fluid. Increase in any one of these (tumor, hemorrhage, edema) requires a compensatory decrease in one of the other substances in order to maintain normal intracranial pressure (ICP). ICP rises when compensatory mechanisms fail.Â
Elevated ICP leads to decreased cerebral perfusion pressure (CPP). CPP is the difference between mean arterial pressure and intracranial pressure, and serves as an additional measure of adequacy of cerebral perfusion [CPP= MAP – ICP]. This is similar to the concept of abdominal compartment syndrome- when intraabdominal pressure increases above a threshold, there is decreased organ perfusion.
Initially, the brain is able to autoregulate and maintain cerebral blood flow (CBF) across a narrow range of CPP, but this compensation is also limited, and CBF decreases as CPP falls. The general target for CPP is ≥60 mmHg, but note that this may vary if cerebral blood flow autoregulation is impaired.
Monitoring intracranial pressure (ICP) is not independently associated with improved outcomes. It does not replace serial neurologic exams. Clinical decision making based on the neurologic exam, the ICP, CT imaging and any other relevant information is the key to improving outcomes. There are several patient scenarios that should prompt consideration of ICP monitoring.[1,3]
GCS ≤8 + structural brain injury on head CT
GCS >8 + structural brain injury on head CT + high risk for progression (large/ multiple contusions, coagulopathy
Severe TBI with a normal CT scan + at least 2 of the following- age >40 years, unilateral or bilateral motor posturing, or SBP <90 mm Hg.
Progression of brain injury on repeat CT imaging
Patients who require urgent surgery for extracranial injuries
Clinical deterioration
There is a tiered approach to treating elevated ICP.[1] At each tier, patients should continue to have close neurologic exams as well as interval repeat CT imaging of the head to rule-out the progression of hemorrhage.
Tier 1- ensure optimization of analgesia and sedation, elevate head of bed, intermittent drainage of CSF.
Tier 2- hyperosmolar therapy- mannitol or hypertonic saline. Consider advanced monitoring, including assessment of cerebral autoregulation and other markers of cerebral oxygenation. If utilizing advanced monitoring, consider hyperventilation to PaCO2 30-35 as long as cerebral oxygenation is maintained. Paralysis with neuromuscular blockade.
Tier 3- decompressive craniectomy is a potential salvage therapy- may be associated with decreased mortality, but no improvement in neurologic outcomes.[4,5] Continuous infusion of neuromuscular blockade if there is a response to the test dose in Tier 2. Consider Barbiturate coma. Hypothermia and hyperventilation are no longer routinely recommended. Hyperventilation therapy can be used as a bridge to additional interventions. A study of hypothermia in severe TBI has shown no improvement in early neurologic outcome.[6]
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