Tag Archives: ICP

Head

Best Of EAST #10: (F)utility Of ICP Monitoring In Geriatric Patients?

December 30, 2021 The Trauma Pro Leave a comment

Patients with severe TBI are typically managed using staged protocols based on the Brain Trauma Foundation (BTF) guidelines for ICP monitoring. There have been a number of papers over the past six years that question the utility of ICP monitoring, at least using the procedures in the BTF guidelines. Most of these studies do not specifically break out elderly patients.

The group at the Westchester Medical Center in NY used the TQIP database to review the impact of ICP monitoring for severe TBI in patients > 65 years old. They performed a four year database study on these patients with an isolated head injury (no other body regions with AIS > 2), initial GCS < 8, and a length of stay > 24 hours. The examined the presence or absence of an ICP monitor, AIS head score, GCS, and a number of outcome measures.

Here are the factoids:

A total of 4,433 patients met the above criteria, and 17% had an ICP monitor placed
After propensity matching for those with and without an ICP monitor, mortality was nearly identical in both groups at 49%
ICU length of stay, hospital length of stay, and ventilator days were significantly longer in the monitor group

The authors concluded that ICP monitoring in this elderly group of patients did not improve survival and increased length of time in the ICU, hospital, and on the ventilator. The recommend that the current guidelines be improved to recognize these facts.

Bottom line: This is a nice, simple study that sought to answer just a few nice, simple questions. The mortality results are convincingly equal between the groups with and without an ICP monitor. The lengths of stay and ventilator days are statistically significantly longer with p values < 0.001. However, the actual numbers are not provided. I have seen many studies where statistically different numbers are not clinically relevant.

There are a number of papers that have come to similar conclusion on other or broader groups of TBI patients. Although we have specific guidelines on who gets a monitor and what we do with the numbers, there is growing doubt that their use actually helps. Perhaps it is time for us to review the data and make appropriate revisions!

Here are my questions for the authors and presenter:

Tell us about your propensity score matching. This will help us understand how similar the patient groups really were, with the exception of their ICP monitors.
Please provide the actual numbers for your lengths of stay and ventilator days. We need to be sure these are clinically and/or financially significant.
Have the results of this work prompted you to rework your own practice guidelines for treatment of severe TBI? I’m always interested if the group feels strongly enough about their work that they would consider changing their practice based on it.

Reference: ROLE OF ICP MONITORING IN GERIATRIC TRAUMA PATIENTS. EAST 35th ASA, oral abstract #33.

Head, Prehospital

Hitting The Brakes May Increase Intracranial Pressure During The Ambulance Ride!

October 8, 2021 The Trauma Pro Leave a comment

One of the most common injuries encountered by trauma professionals is blunt head trauma, and it’s one of the leading causes of death in young people. Keeping the level of intracranial pressure (ICP) within a specified range is one of the basic tenets of critical neurotrauma care in these patients. Most trauma centers have sophisticated algorithms that provide treatment guidance for various levels of ICP or cerebral perfusion.

The vast majority of patients with severe head injuries are transported to the hospital in some type of ambulance. Obviously, the exact ICP level is not known during transport because no monitoring device is present. We can sometimes infer that ICP is elevated if the patient has a Cushing response (wide pulse pressure and bradycardia) or unequal pupils. But for the most part, we assume that ICP is in a steady state during the ambulance ride.

But here’s something I never considered before: can ambulance acceleration or deceleration change the ICP through shifting of the brain or cerebrospinal fluid?

Patients are generally loaded into ambulances head-first, with their feet toward the back door. Frequently, they must be positioned supine in consideration of possible thoracic or lumbar spine injury. This position itself may lead to an increase in ICP. But what happens when the ambulance is hitting the brakes as it approaches a light or stop sign? As the patient’s weight shifts toward the top of the head, so does the CSF, spinal cord, and brain. Couldn’t this, too, increase ICP?

The anesthesiology group at the Erasmus Medical Center in Rotterdam, Holland performed a very novel study to assess this very thing. They recruited twenty participants in whom they evaluated ICP in various positions during acceleration and deceleration.
No, the subjects did not have an actual invasive ICP monitor inserted.

The authors used a novel way to infer pressures: optic nerve sheath diameter (ONSD). The optic nerves are direct extensions of the brain, and CSF travels freely in the nerve sheath. As ICP rises, the diameter of the nerve sheath increases. The subjects were fitted with a special helmet with two devices mounted on it. The first was a 7.5 Mhz ultra-sound probe focused on the back of the eye. The second was an arm with an orange dot on the end. This was adjusted so that the ultrasound probe was pointing at the optic nerve sheath when the other eye was focused on the dot. Subjects just watched the dot and measurements streamed in! Crude but very effective.

Baseline measurements were taken without acceleration or deceleration, then repeated when accelerating to 50 km/hr and decelerating to a stop.

Here are the factoids:

A total of 20 subjects were tested, and their oxygen saturation, blood pressure, and pulse were identical pre- and post-test
Baseline ONSD was about 5mm; a relevant change in diameter was determined to be more than 0.2 mm
Lying supine, the ONSD in nearly all subjects increased from an average 4.8 to 6.0 mm during deceleration
With the head raised to 30º, most values remained steady (from 4.8 to 4.9 mm) during deceleration

The left block shows the increase in size of the optic disk with braking while supine. The right one demonstrates that this effect is neutralized by elevating the head 30º.

Bottom line: This is a small, simple, and creative study, yet the results are very interesting! It is clear that optic nerve sheath diameter increases significantly during deceleration in patients who are supine. And this effect is eliminated if the head of bed is elevated 30º.

Unfortunately, we have no idea how the change in ONSD corresponds to absolute values of, or relative increases in, ICP. Does a change of 1.2mm indicate a 5 torr increase in ICP? A 5% increase? Is it proportional to the absolute ICP? We just don’t know.

But the data is clear that a measurable change does occur. Until better data is available, it may be desirable to transport patients with serious head injuries with the head elevated to 30º if there are no concerns for lower spine injury. Or failing that, make sure the driver does not have a lead foot!

Reference: Ambulance deceleration causes increased intra cranial pressure in supine position: a prospective observational prove of principle study. Scand J Trauma Open Access 29:87, 2021.

CNS, Head

Targeted Hypernatremia In Trauma Brain Injury: Does This Work?

April 11, 2018 The Trauma Pro Leave a comment

Traumatic brain injury (TBI) frightens and confuses most trauma professionals. The brain and its workings are a mystery, and there is very little real science behind a lot of what we do for TBI. One thing that we do know is that intracranial hypertension is bad. And another is that we do have some potent drugs (mannitol, hypertonic saline) to treat it emergently.

So if we can “dry out” the brain tissue on a moment’s notice and drop the ICP a bit with a hit of sodium, doesn’t it stand to reason that elevating the sodium level constantly might keep the brain from becoming edematous in the first place? Many neurosurgeons buy into this, and have developed protocols to maintain serum sodium levels in the mid-140s and higher. But what about the science?

A nice review was published in Neurocritical care which identified the 3 (!) papers that have promoted this practice in humans with TBI. In general, there was a decrease in ICP in the patients in the cited papers. Unfortunately, there were also a number of serious and sometimes fatal complications, including pulmonary edema and renal failure requiring hemodialysis. These complications generally correlated with the degree of hypernatremia induced. Papers were also reviewed that involved patients with other brain injury, not caused by trauma. Results were similar.

Bottom line: There is no good literature support, standard of care, or even consensus opinion for prophylactically inducing hypernatremia in patients with TBI. The little literature there is involves patients with severe TBI and ICP monitors in place. There is nothing written yet that justifies the expense (ICU level care) and patient discomfort (frequent blood draws) of using this therapy in patients with milder brain injury and a reliable physical exam. If you want to try out this relatively untried therapy, do us all a favor and design a nice study to show that the benefits truly outweigh the risks.

And if you can point me to some supportive literature that I’ve missed, please do so!

Related posts:

References:

Induced and sustained hypernatremia for the prevention and treatment of cerebral edema following brain injury. Neurocrit Care 19:222-231, 2013.
Continuous hyperosmolar therapy for traumatic brain injury-induced cerebral edema: as good as it gets, or an iatrogenic secondary insult? J Clin Neurosci 20:30-31, 2013.
Continuous hypertonic saline therapy and the occurrence of complications in neurocritically ill patients. Crit Care Med 37(4):1433-1441, 2009. -> Letter to the editor Crit Care Med 37(8):2490-2491, 2009.

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