Brain injury is much in the news these days, following the death of Natasha Richardson of a seemingly minor fall.
So, let’s talk about Traumatic Brain Injury (TBI), with a small side-venture into strokes.
The reason head injuries can be so devastating is because the head contains the brain. The brain controls the central nervous system, and without that, we rapidly get dead. The brain is composed mostly of nervous tissue, and, as such, is very sensitive to any lack of oxygen and glucose. For example, four to six minutes without oxygen is all it takes to kill the brain. The body is very, very good at making sure the supply, via the blood stream, doesn’t stop.
Like many other vital organs, the brain is protected by bone. We’re talking the cranium, here, that part of the skull that surrounds the brain. Outside of the cranium we have the skin of the scalp. This is highly vascular (which is the fancy way of saying “It’s full of blood vessels”), then covered with an insulating layer of hair. The reason the scalp is so vascular is because it plays a role in maintaining the brain at an even temperature. Even minor scalp injuries look dramatic, because they bleed heavily. Scalp and facial wounds tend to gape open because, unlike the rest of the body, the skin attaches directly to muscle. (There’s one other place on the human body where this is true: The scrotum. Insert the obvious joke here.)
The skull is made of a number of bones that fuse in very early childhood into a solid piece. Like other bone, it’s a living tissue, and its outer layer is a thick, fibrous material called the periosteum (the Latin word for “around the bone).
Hard against the periosteum on the inside of the cranium you come to the meninges. These are three layers of tissue that surround the brain. When they’re inflamed, the condition is called meningitis, and a nasty, horrible disease it can be, too. The first layer on the way in is the dura mater. That’s Latin for “tough mother.” There isn’t any space between the dura and the periosteum, when things are all okay. Under the dura mater comes the arachnoid membrane, which looks sort of like plastic wrap. (The Romans thought it looked like a spider web, hence the name.) Under the arachnoid comes the pia mater (Latin for “tender mother). The pia mater is attached to the surface of the brain itself.
Between the dura and the pia you find cerebro-spinous fluid (CSF). This bathes the brain, surrounds it, cushions it. The brain floats in it. It’s watery, clear-to-straw color, and seeing it pouring out of your patient’s nose or ears is what we call “a bad sign.”
How to tell if what you’re seeing is CSF: You can do what’s called the “halo test,” where you put a drop of the bloody fluid in the middle of a gauze square. If there’s CSF, you’ll see a red center with a yellow halo around it. Or, if all you have is some clear fluid coming from your patient’s nose, you can test it with your glucometer. If it’s CSF, the glucose reading will be approximately one-half of the glucose reading of his blood.
The meninges don’t just cover the brain; they cover the spinal cord as well. You can think of the spinal cord as a long, thin extension of the brain if you wish. The CSF also surrounds the spinal cord. When someone does a lumbar puncture, they’re sticking a needle between a couple of vertebrae in the lumbar spine, through the dura, and sucking up some CSF to check it for bacteria, or blood, or what-may-have you. When nice young ladies get epidural (from epi- above, and -dural, of or pertaining to the dura mater) anesthesia during childbirth, the drugs go into the spinal column, around the spinal cord, above the dura mater.
There’s a space between the periosteum and the dura mater, but usually it’s a potential space. That is, there could be a space there if something were to go there. We’ll be back to the epidural space anon.
So let’s get to the brain injuries.
The first mnemonic is DIC-HEAD. If the patient is Disoriented, Irritable, Combative, consider Head injury. (That’s right, people with brain injuries can be dick heads. What you don’t know when you arrive on scene is what they’re like day-to-day. Maybe the guy is just naturally a dick head. As in all emergency medicine, assume the worst.)
The brain actually is about the same consistency as Jell-O. When you smack someone upside the head, the brain kinda sloshes around in there. This leads us to the first, easiest, least-damaging TBI: the concussion. You get hit, you see stars. You’re briefly dizzy. You may even get knocked out for a moment. There aren’t any lasting effects (though you should be aware that all brain injuries are cumulative: several concussions and you have people who are permanently punchy, like the palookas of comedy). Post-traumatic amnesia is common. (You don’t remember the events immediately after the injury.) Antegrade amnesia, where you don’t remember the events leading up to the injury, are a bit more serious as symptoms go.
What went on there is an electro-chemical disruption of the brain. It’s a common sports injury. (Note: If your sport traditionally requires a helmet, wear the friggin’ helmet, okay?) Someone who’s had a concussion should be out of the game. A serious concussion, out for a month. A second concussion; out for the season. A third concussion, out for the year. Concussions are cumulative.
One thing that I see a lot: A patient has a concussion. Three days later, he or she has the injury that requires EMS and puts ‘em in the hospital. Their reflexes are just a bit off. Their peripheral vision is just a bit limited. So. If you have a concussion, at the very least, take it easy. And seriously, seriously consider following up with medical assessment, because there’s worse things to come as we look further into Traumatic Brain Injury.
Here’s a description of what it’s like to have a concussion, from one of our own, in this LJ post et seq.
The inside of the skull isn’t soft and smooth. It has all kinds of edges and protrusions. As the brain moves around, it can be bruised. It can bleed. You see brain injury not only at the site of impact, but on the opposite side where the brain sloshed, then sloshed back. (That’s coup and contracoup injuries.) You find lacerations and contusions in the brain itself.
The brain is made mostly of nerve tissue. Nerve tissue does not recover well. Those primary injuries, and any loss of function associated with them, are probably going to be permanent. But this doesn’t mean that you look at someone with a TBI and say, “Oh, well.”
The primary injuries are there. What you want to work on are the secondary injuries.
Like any other body part, when the brain is injured it swells. Unlike any other body part, the brain is trapped inside a hard bony shell. When it swells it doesn’t have anywhere to swell to.
Let’s step back to the dura mater, if you please. The temporal bones (the temples; the sides of the head where the lower jaw hook on) are particularly thin as skull bones go. And directly under those thin bones lie the middle meningeal arteries. A fracture of the temporal bone, say from a low velocity blow (e.g. a baseball), can tear one of those arteries. The epidural space starts to fill up with blood, backed by arterial pressures.
Or, in the course of the trauma, one of the bridging veins gets ruptured. These lie under the dura, so you have a subdural bleed. It’s only backed by venous pressure, though, so it’s usually slower than an epidural.
Cast back your mind to my earlier post on Levels of Consciousness. (Lots of things are going to start coming together, folks.) Recall the mnemonic AEIOU-TIPS? Remember that T was for Trauma and S was for Space-Occupying Lesions. We’re in S territory now. And as I promised back then, now’s the time to introduce the Glasgow Coma Scale.
The Glasgow Coma Scale is a tool for measuring level of consciousness. It goes like this:
Record the patient’s best response:
|Withdraws to pain:||4|
You’ll notice that normal folks walking around have a Glasgow score of 15. This desk here has a Glasgow score of 3. Recording the Glasgow score, and how it changes, will give you a good idea of what’s going on, and how fast, and how likely it is that you’ll have a live patient a week from now.
Okay, back from that little digression: A drop of two points in the Glasgow score is a bad sign.
We have our friends with the head injuries. Their brains are swelling, or there’s blood collecting inside of their skulls, at some rate. NOTE: That rate could be measured in minutes, in hours, or in days. For a time their bodies compensate for that swelling, or for those masses.
At the mass builds up, the first thing that happens is that the inter-cranial pressure (ICP) increases. There’s more stuff inside the skull, so pressure goes up. As the ICP goes up, the patient’s blood pressure goes up too, because the body desperately wants to get oxygen and glucose to the brain. Lack of oxygen, and lack of glucose, can, all by themselves, cause brain swelling.
While there’s no give to the skull, there is some give in other places. As swelling happens, cerebro-spinal fluid gets forced out. Pressure normalizes, the patient is asymptomatic, and you’d never suspect anything was wrong.
You’ve probably got about 75 mL of CSF that can go that way. Also, as swelling increases, or the size of the hematoma increases, venous blood gets forced out. You probably have another 75 mL of that that can get squeezed out of the skull. But when that 150 mL of reserve is gone, stand by. It’s like you were getting cranked to the very top of the first hill of a roller coaster and the ride is about to get very fast, and down hill all the way.
Pressure on the brain shows up in certain signs. Remember the cranial nerves (previously discussed at Making Light)? One of them is Cranial Nerve III, the Oculomotor nerve. Pressure on that nerve makes the pupil of the eye on the side closest to the injury expand and get sluggish in response to light. A difference of 1 mm between the pupils can be a bad sign (although a significant percentage of the population has unequal pupils normally). Next, as pressure builds up, you start getting weakness in the muscles in the opposite side of the body. Depending on exactly where the injury is, you can see changes in hearing, in verbal response, in sleepiness….
Intercranial pressure is still building up. The blood pressure is still going up. This triggers another mechanism, called “Cushing’s phenomenon” or “Cushing’s reflex” (named after Dr. Harvey Williams Cushing, 1869-1939, a giant among neurosurgeons): The baroreceptors in the carotid bodies and the arch of the aorta notice the increased blood pressure, and stimulate the Cranial Nerve X, the Vagus nerve, to correct that problem. The heart rate slows. The brain continues to swell. The ability of the blood flow to bring in sufficient glucose and oxygen is compromised. The brain swells even faster.
There’s only one place for that swollen brain to go: out through the Foramen Magnum (Latin for “Big Hole”). The brain is soft, and it’s getting squeezed out through that hole, brainstem first, like toothpaste. You’re going to start seeing motor changes as the brain takes mechanical damage from being squeezed out: Posturing. First come “decorticate posturing.” That’s when the arms bend in, taking the hands up in front of the face. (Remember it by Decorticate = movement to the core.) Then comes decerebrate posturing, when the arms are fully extended and the back may arch.
Then we come to patterned respiration, as the part of the brainstem that controls breathing starts to take damage. You can see Cheyne-Stokes breathing, a repeated pattern of slow, shallow breathing, going to rapid, deep breathing, then back to slow and shallow. You can see Central neurogenic breathing (continuous rapid deep breaths — they look just like the Kussmaul’s respiration you get in diabetic ketoacidosis, only the mechanism for why you have ‘em is different). At this point you’re well into Cushing’s Triad: High blood pressure, slow heart rate, and patterned respiration. You are also well behind the power curve.
Then comes ataxic breathing: breaths with no discernible pattern. Then comes apnea: no breathing at all. This is what we call an end point.
Typically, you see a person get a head injury, be unconscious for a while, wake up and be apparently normal (this is called “the lucid interval”), then going unconscious again, and deteriorating rapidly. The initial unconsciousness is from a concussion. The lucid interval is the period while the body is compensating by draining CSF and venous blood from inside the skull while the hematoma is growing. Then comes the bad part.
So, what do we do about all this?
First, if you suspect traumatic brain injury, due to mechanism of injury, get the patient somewhere with a CAT scan or an MRI, and a neurosurgeon on call. You may not have a lot of time to do this; meanwhile the patient’s signs and symptoms may be mild or nil. At a minimum, any head injury involving loss of consciousness deserves close and continuing observation, where any sudden change or deterioration becomes a call for rapid action. Remember that signs and symptoms of a subdural or epidural hematoma may not show up for a significant period.
Any time you have a person who’s on blood thinners, or who’s drunk, assume the worst and treat for same. Alcohol masks the signs and symptoms, and a person who’s drunk has a good chance of falling and striking their head. Just because they act drunk, and smell of whiskey, don’t assume that’s all that’s going on.
A serious TBI is about 30% fatal. Of those who recover, around 99% have permanent neurological deficits.
I promised a side excursion into strokes: Here it is. You have two kinds of strokes: Occlusive, where a blood clot blocks an artery in the brain causing tissue death, and hemorrhagic, where a blood vessel in the brain bursts. The later is indistinguishable from a traumatic brain injury as far as its physical effects; the only difference is why the blood vessel has broken (I urge everyone to check their blood pressure regularly: hypertension is related to stroke). In occlusive strokes, tissue damage due to hypoxia causes brain swelling, with all the rest of the lovely signs and symptoms noted above.
Once in hospital, with neuro services, though, a hematoma can be drained; often with minimal after-effects. (This is particularly true of epidural hematomas since the broken arteries are well away from the brain, no liquid blood enters the brain tissue, and there may be no underlying trauma to the brain itself.) To do this, though, the CAT scan is vitally important.
As for getting to the hospital, here’s what you need to remember. You can’t do anything about the primary injury. But you can slow the secondary injury due to swelling by keeping the patient well-oxygenated, and keeping their blood pressure above 90 (that is, you have to be able to feel a pulse at the patient’s wrist). Your goal is to keep oxygen and glucose going to the brain tissue, to limit swelling. (Note: Do not hyperventilate the patient: Blowing off too much carbon dioxide will also cause brain swelling.)
There isn’t any good place to put this, so I’ll put it here: There’s another kind of brain injury that doesn’t involve bleeding inside the head, doesn’t involve brain swelling (or not much), but is still devastating. That’s the Diffuse Axonal Injury. It’s caused by shearing forces inside the brain, due to the different rates at which gray matter and white matter accelerate. The axons of the nerve cells stretch, break off, and retract. While death is rare, and the lesions often can’t be detected with current imaging devices, 90% of the patients who present with DAI remain in a permanent vegetative state. This is a primary injury; it exists from the moment of the trauma. You most often see it in rotational injuries in high-speed automobile crashes, and in blast injuries. Nothing you can do, prehospital, will make this one better or worse.
Can you tell the difference, pre-hospital, between an epidural hematoma, a subdural hematoma, an intracerebral hematoma, or a hemorrhagic stroke? No, and usually you can’t tell in the ED, either. You need specialists with special equipment to differentiate.
A person with a head injury often has other injuries. Treat for shock. Stop bleeding. Keep the airway open. And good luck. These are scary, scary injuries.
Take away lessons:
Copyright © 2009 by James D. Macdonald
I am not a physician. I can neither diagnose nor prescribe. These posts are presented for entertainment purposes only. Nothing here is meant to be advice for your particular condition or situation.
TMI about TBI by James D. Macdonald is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 License.
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