Other than the control of ICP and maintaining adequate cerebral perfusion pressure, there is no evidence that anything else affects outcome in TBI.
We have most control over the arterial pressure.
My goals are few and simple:
1. Check the pupils for a baseline.
2. Maintain an ICP below 20
- If there is no ICP monitor, and I suspect an elevated ICP, and if mannitol has not been given, I give 0.5 – 1 gm/kg
- Hypertonic saline is useful
|Weight in Kg
||Volume of 3% NaCl needed
Roughly 10 ml 3% NaCl per kg body weight. Give in 150 ml boluses.
3. Maintain a CPP of 50-70
- If there is no ICP monitor, I assume the ICP is 30 (could be higher)
- I maintain a CPP of 50-70 (with phenylephrine if necessary)
- MAP – (assumed ICP of 30) = CPP 50-70
- MAP needs to be 80-100!
- Even brief episodes of decreased MAP (CPP) worsens outcome
4. Maintain mild hypocarbia.
I do not worry about recall in these cases. I have yet to have a comatose patient complain about recall after regaining consciousness. I don’t normally deliver a vapor during these operations because they decrease MAP. I use vapors only to control HYPERTESION. If the MAP is good, I might dial in 0.4-0.5% isoforane.
NEJM: Hyperosmolar Therapy for Raise ICP
Here are some “nuggets” from this article.
- In a review of studies of traumatic brain injury, the rate of death was 18.4% for patients with an intracranial pressure of less than 20 mm Hg but 55.6% for those with an intracranial pressure of more than 40 mm Hg.
- Raised intracranial pressure has a proximate relationship to survival and is often the only remediable element of the disease. The prevention of secondary brain damage from raised intracranial pressure is therefore a central focus of neurologic intensive care.
- Because the cranium is essentially a fixed vault, any increase in the volume of the brain results in an increase in intracranial pressure.
- As intracranial pressure reaches 50 to 60 mm Hg, it approaches arterial pressure in the vessels of the circle of Willis and brings about global brain ischemia, the end result of which is brain death.
ICP/Intracranial Volume Curve
- The goal of care is to keep the intracranial pressure below 20-25 mm Hg.
- Hyperosmolar therapy is useful in this regard:
- The effectiveness of an osmolar agent in creating a gradient for water egress depends on the extent to which the solute is excluded by the blood–brain barrier (bbb).
- Any traumatic disruption of the bbb allows free flow of osmolar agents.
- Therefore osmolar agents decrease brain volume by acting at sites of an intact bbb.
- Sodium and mannitol are nearly totally excluded by the bbb.
- Once hyperosmolar therapy is instituted it must be maintained.
- Otherwise there is rebound in raised ICP.
- The effects of hyperosmolar therapy are more consistent and longer lasting than the effects of hyperventilation.
Raised intracranial pressure should be treated promptly:
- For patients who have a mass lesion, such as a large subdural hematoma, that can be removed, surgical evacuation or resection is the most expedient way to reduce intracranial pressure.
- When the increase in brain volume is the result of a cerebral contusion, diffuse cerebral edema, or some other condition that is unresectable surgery is generally not undertaken. Attempts to decompress the cranial contents by removing parts of the skull after traumatic brain injury have lowered intracranial pressure but have not improved the outcome, as compared with standard care.
- Avoid serum hypoosmolarity.
- This requires that intravenous solutions for resuscitation and for infusion of medications have at least the effective osmolarity of normal saline (290 mOsm per liter). Solutions such as 5% dextrose in water, 5% dextrose in half-normal saline, and lactated Ringer’s solution (calculated osmolarity, 273 mOsm per liter) are not desirable.
- Other attempts at decreasing ICP that are only partially effective are:
- Intraventricular drainage of CSF
- Glucocorticoids (probably only effective with tumors)
- Barbiturate coma (hypotension a problem)
The mainstay of intracranial-pressure reduction is therefore the rudimentary approach of shrinking the brain by exposing it to the dehydrating effects of serum hyperosmolarity.
The effect of a hyperosmolar agent on brain volume is ideally assessed by measuring intracranial pressure with one of a number of devices (intraventricular catheter, intraparenchymal transducer) and adjusting the amount of infused solution to maintain the desired level of intracranial or cerebral perfusion pressure (calculated as mean blood pressure minus intracranial pressure).
The target intracranial pressure is typically less than 20 mm Hg, with maintenance of cerebral perfusion pressure at 50 to 70 mm Hg.
The serum osmolarity can be used as a surrogate measure of the effect of therapy with either mannitol or hypertonic saline (probably not useful in the OR for acute TBI):
- The initial target is an osmolarity of 300 to 320 mOsm per liter, with adjustment as the clinical circumstances and the intracranial pressure require.
- The osmolarity can be calculated from the levels of sodium, glucose, and blood urea nitrogen (with sodium measured in millimoles per liter and glucose and blood urea nitrogen measured in milligrams per deciliter), according to the following formula:
- osmolarity = (2 × sodium) + (glucose ÷ 18) + (blood urea nitrogen ÷ 3).
- The clinical laboratory can also provide a measurement of serum osmolality, which is assumed to be essentially equivalent to osmolarity.
- The effect of either mannitol or hypertonic saline can also be assessed by measuring the serum sodium level; a value of 145 to 150 mmol per liter typically coincides with the desired effect.
- Mannitol is a sugar alcohol that acts as an osmotic diuretic, causing sustained hyperosmolarity by dehydration.
- It can be administered through a peripheral or central venous catheter.
- In patients with traumatic brain injury, a single dose of mannitol reduces intracranial pressure within 10 to 15 minutes, with a maximal effect of cutting the initial pressure approximately in half within 20 to 60 minutes.
- Mannitol is given in a 20% solution in boluses of 0.25 to 1.0 g per kilogram of body weight at intervals of 2 to 4 or more hours. The highest dose is used in emergency situations, and the lowest dose is administered as a maintenance regimen.
- Increases serum osmolarity directly rather than by inducing osmotic diuresis.
- 3% solution (513 mmol per liter)
- boluses of approximately 150 ml
- 7.5% solution (1283 mmol per liter)
- 23.4% solution (4008 mmol per liter)
- Continuous infusion of 3% saline has a modest initial effect on intracranial pressure
- the effect is transient and results in systemic fluid overload.
- Concentrations of more than 3% should be administered through a central venous catheter.
- Target serum sodium concentration can be approximated from the following formula (probably not useful in the OR for acute TBI):
- sodium requirement in millimoles = (lean body weight in kilograms × the proportion of weight that is water, which is 0.5 for a woman and 0.6 for a man) × (desired sodium − current sodium in millimoles per liter).
- The required volume in milliliters is then calculated as the sodium requirement divided by the sodium concentration of the chosen solution.
- To attain a target sodium concentration of approximately 150 mmol per liter in a patient who weighs 55 kg with an initial sodium concentration of 139 mmol per liter.
- The addition of 302 mmol of sodium and thus 589 ml of 3% saline or 75 ml of 23% saline solution is required.
- This can be achieved in a single infusion or in several more routine doses (e.g., 30 ml of 23% saline).
- Approximately 30 g (0.5 g per kilogram) of 20% mannitol is an alternative.
- Subsequent infusions should be adjusted to keep intracranial pressure below approximately 20 mm Hg.