Tag Archives: TBI

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How Long Should We Watch Intracerebral Hemorrhage?

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Patients with traumatic brain injury (TBI) severe enough to cause bleeding are usually admitted to the hospital for observation and in many cases, repeat CT scanning. Those with small intracranial hemorrhages (ICH) may experience progression of the bleeding, and a small percentage of cases may need operative intervention (1-3%). Questions we typically face are, how long should we watch for progression, and how often should we scan?

A retrospective cohort study was carried out at UMD-NJ, looking for answers for a specific subset of these patients. Specifically, they had to have a mild blunt TBI (loss of consciousness and/or retrograde amnesia, GCS in the ED of 13-15) and a positive head CT. They classified any type of hemorrhage into or around the brain as positive.

During a 3 year period, 474 adults were enrolled but only 341 were eligible for the study. They were excluded due to previous injury, presence of a mass (not trauma), need for immediate neurosurgical intervention, or failure to get a second CT scan. The authors found:

  • 7% of patients were taking anticoagulants! This is surprisingly high. Interestingly, 15 were subtherapeutic, 3 were therapeutic and 2 were supratherapeutic.
  • Subarachnoid hemorrhage was the most common finding on CT (54%). Intraparenchymal hemorrhage was next most common (48%) Many patients had more than one type of bleed.
  • The injury worsened between the first and second scans in 31% of patients. This number increased to 46% in patients taking anticoagulants.
  • About 97% of bleeds stopped progressing by 24 hrs post-injury.

Bottom line: Most centers are probably overdoing the observation and repeat scan thing. More than two thirds of bleeds are stable by the first scan (first and second scans identical), and nearly all stop progressing within 24 hours. It’s very likely that patients who are not on anticoagulants and who have a stable neuro exam and stable symptoms can get just one scan and 24 hours of observation. Persistent headache, nausea, failure to ambulate well, or other symptoms warrant a repeat scan and longer observation.

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Reference: The temporal course of intracranial haemorrhage progression: How long is observation necessary? Injury 43(12):2122-2125, 2012.

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Targeted Hypernatremia In Trauma Brain Injury

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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!

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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.
General

Update: Can TBI Be Managed Without Neurosurgical Consultation?

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This paper was presented at EAST in 2013, and this is an update of that work using the entire manuscript which has now been published.

The standard of care in most high level trauma centers is to involve neurosurgeons in the care of patients with significant traumatic brain injury (TBI). However, not all hospitals that take care of trauma patients have immediate availability of this resource. The University of Arizona at Tucson looked at management of these patients by their acute care surgeons.

The authors did a retrospective cohort study of patients at their center who had a mild TBI and positive head CT, managed with or without neurosurgery consultation, over a two year period. They matched the patients with and without neurosurgical consultation for age, GCS, AIS-Head and presence of skull fracture and intracranial hemorrhage.

A total of 90 patients with and 180 patients without neurosurgical involvement were reviewed. Here are the factoids:

  • Hospital admission rate was identical for both groups (87-89%)
  • ICU admission was significantly higher if neurosurgeons were involved (20% vs 44%)
  • Repeat head CT was ordered more than 3 times as often by neurosurgeons (20% vs 86%)
  • Post-discharge head CT was ordered more often by neurosurgeons, but was not significantly different (5% vs 12%)
  • There were no surgical interventions, in-hospital mortality, or readmissions within 30 days in either group.
  • Cost of the hospital stay was significantly increased if neurosurgery was consulted. 

Bottom line: Can surgeons safely manage select patients with intracranial injury? Granted, this is a small, retrospective study, but the answer is probably yes. The majority of patients with mild to moderate TBI with small intracranial bleeds or skull fractures do well despite everything we throw at them. And it appears that surgeons use fewer resources managing them than neurosurgeons do. The keys to being able to use this type of system are to identify at-risk patients who really do need a neurosurgeon early, and having a quick way to get the neurosurgeon involved (by consultation or hospital transfer). Having a specific practice guideline for management is essential as well. As neurosurgery involvement in acute trauma declines, this concept will become more and more pertinent.

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Reference: The acute care surgery model: managing traumatic brain injury without an inpatient neurosurgical consultation. J Trauma 75(1):102-105, 2013.

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Hypothermia For Treatment of Severe TBI?

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We’ve been trying to figure out therapeutic hypothermia for a long time. Although we know that accidental hypothermia, especially in trauma patients, is not a good thing, it seems to be protective in certain circumstances. The most significant areas of interest center around the neuroprotective effects, especially after ischemia or hypoxia.

But with the good always comes the bad. Every intervention has side effects, and hypothermia is no exception. Decreased cardiac efficiency, blood viscosity increases, pulmonary dysfunction or edema, coagulopathy, decreased tissue oxygen availability, and changes in drug pharmacodynamics are but a few of the problems that may arise. But as long as the benefits outweigh the risks, such an intervention may be acceptable.

We’ve been looking at the possible protective effects of hypothermia on the brain after severe head injury for quite some time. As with most neurotrauma studies, hypothermia ones are tough to do well. Patient selection, adequate numbers of subjects and good randomization and/or blinding are very difficult. It requires assembling all the relevant studies and scrutinizing this whole body of work to figure out if it works or not.

And the answer is, it doesn’t. The Cochrane Library updated their previous work in this area in 2009. They combined 23 studies and over 1600 patients to try to determine if hypothermia (35C for at least 12 hours) is protective in patients with severe TBI. After whittling the field down to good quality studies, they found that there may be a trend toward fewer unfavorable outcomes (death, severe disability, vegetative state), but it was not statistically significant. There were variable results with respect to the incidence of pneumonia after hypothermia, and these, too, did not meet statistical significance.

Bottom line: Therapeutic hypothermia for treatment of severe TBI is still not ready for prime time, and may never be. The studies thus far are small and flawed. Don’t implement your own protocol for this technique unless you are involved in a very high quality, multi-center study that will add to the literature!

Reference: Hypothermia for traumatic head injury. The Cochrane Library 2009, Issue 4.

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Subdural Hematomas and Hygromas Simplified

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There’s a lot of confusion about subdural pathology after head trauma. All subdural collections are located under the dura, on the surface of the brain. In some way they involve or can involve the bridging veins, which are somewhat fragile and get more so with age.

Head trauma causes a subdural hematoma by tearing some of these bridging veins. Notice how thick the dura is and how delicate the bridging veins are in the image below.

image

When these veins tear, bleeding ensues which layers out over the surface of the brain in that area. If the bleeding does not stop, pressure builds and begins compressing and shifting the brain. A subdural hematoma is considered acute from time of injury until about 3 days later. During this time, it appears more dense than brain tissue.

After about 3-7 days, the clot begins to liquefy and becomes less dense on CT. Many hematomas are reabsorbed, but occasionally there is repeated bleeding from the bridging veins, or the hematoma draws fluid into itself due to the concentration gradient. It can enlarge and begin to cause new symptoms. During this period it is considered subacute.

It moves on to a more chronic stage over the ensuing weeks. The blood cells in it break down completely, and the fluid that is left is generally less dense than the brain underneath it. The image below shows a chronic subdural (arrows).

image

Hygromas are different, in that they are a collection of CSF and not blood. They are caused by a tear in the meninges and allow CSF to accumulate in the subdural space. This can be caused by head trauma as well, and is generally very slow to form. They can lead to slow neurologic deterioration, and are often found on head CT in patients with a history of falls, sometimes in the distant past. CT appearance is similar to a chronic subdural, but the density is the same as CSF, so it should have the same appearance as the fluid in the ventricle on CT.

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