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. An interesting paper looked at management of these patients by acute care surgeons.
The authors retrospectively reviewed all their patients who had a 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 (parenchymal, epidural, subdural, subarachnoid). Neurosurgeons were available to the no-consult group if things went awry.
A total of 180 patients with and 90 patients without neurosurgical involvement were reviewed. Here are the interesting findings:
Hospital admission rate was identical for both groups (88%)
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 higher (5% vs 12%)
There were no neurosurgical interventions, in-hospital mortalities, or readmissions within 30 days in either group
Based on this experience, the hospital adopted a set of guidelines for helping determine if neurosurgery should be consulted.
Bottom line: This work raises an interesting question: can general surgeons safely manage select patients with intracranial injury? The answer is probably yes. The majority of patients with mild to moderate TBI with small intracranial bleeds 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). Looking at the brain injury guidelines above, I am a little nervous about managing an epidural or contusion without one additional head CT. But this is certainly food for thought. As neurosurgery involvement in acute trauma declines, this concept will become more and more pertinent.
Most patients with mild traumatic brain injury (TBI) recover quickly and have few sequelae. Headache is common during the first few hours or days. But some patients experience significant and sometimes unrelenting headaches after their injury. How should we treat them? Are they the same as other common headaches?
There are several common types of headaches that are not related to brain injury, but many of these can begin after TBI. These include tension headaches from muscle tension or spasm, cervicogenic headaches from strains, sprains or more significant injury to the neck and cervical spine, musculoskeletal headaches from pain in bone or muscle in the head or neck, and headaches related to the TMJ and jaw.
But many patients experience significant headaches without any of these factors. Why? Sometimes it is due to blood in or around the brain, irritating the meninges. But often, there is nothing that we can detect using our current diagnostic technology. However, even if we can’t find a reason, the headache is very real and very concerning to the patient.
I’ve seen practitioners treat post-TBI headaches with a variety of drugs ranging from acetominophen and NSAIDs to anti-seizure and psychotropic drugs. Unfortunately, there is little literature support for any of them. A review article published in 2012 found only one article with Class II data that showed no lasting effect from manipulation therapy.
So what do we do? Here is an algorithm suggested by the review article:
Consider a workup to rule out intracranial pathology as a source of the headache
Categorize the headache. If it is one of the non-TBI types listed above, treat appropriately.
If the headache severely limits function, consider time-release opioids
For milder headache, consider adetominophen or NSAIDs
Treat any comorbidities that may contribute to headache
If the headache has migraine-type properties, treat as such
If the headache is associated with cervical spine pain, mobilize the neck as appropriate
Bottom line: There is very little guidance for treatment of headache purely associated with TBI. Time-honored drugs like opioids for severe pain and acetominophen and NSAIDs for mild to moderate pain help, but generally do not entirely relieve the pain. Only tincture of time will make things better. And it’s probably best to stay away from prescription drugs other than opioids recommended for the pain. They have not been shown to work, and there are plenty of side effects to worry about.
Prescription drugs and side effects
Reference: Systematic review of interventions for post-traumatic headache. PM&R. 4(2):129-140, 2012.
All trauma professionals are aware of the evils of anticoagulation in patients who sustain traumatic brain injury. Warfarin is one of the most common anticoagulants encountered, but there is also a growing number of poor outcomes in patients with the newer, non-reversible agents.
But what about antiplatelet agents like aspirin and clopidogrel (Plavix)? Many physicians worry about these drugs, but is it warranted? Two Level I trauma centers in the Chicago area reviewed their experience. They retrospectively reviewed the records of patients over 40 years old who sustained blunt head trauma. A total of 1547 patients were identified over a 4 year period. They analyzed these records for in-hospital mortality, need for neurosurgical intervention, and length of stay.
Here are the factoids:
27% of patients were taking antiplatelet agents. Patients also taking warfarin were excluded.
21% were taking aspirin alone, 2% clopidogrel alone, and 4% both drugs
Patients taking the drugs averaged about 10 years older than those who were not
Overall, injury severity was relatively low (average ISS 10). A disproportionate number of more severely injured patients were not taking antiplatelet agents.
There was no difference of incidence of intracranial hemorrhage (45%), neurosurgical intervention (3%), or mortality (6%) between the two groups
Hospital length of stay averaged about 6.5 days, but long LOS was a bit more common in the antiplatelet agent group.
Bottom line: This is one more in a series of papers scrutinizing trauma and antiplatelet agents. A few previous studies have shown an adverse effect, but they have been much smaller series. I don’t believe the jury is in yet, so watch these patients carefully. A 6 or 12 hours repeat scan is probably in order, along with frequent neuro monitoring. It’s probably not worthwhile to actively try to reverse them by giving platelets unless there is obvious life-threatening hemorrhage or sudden neurologic change (see below).
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.
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!
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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