Traumatic Brain Injury Flashcards
Of the 1.7 million estimated TBIs occurring each year in the US:
Not everyone goes to the hospital
- 7% were emergency department visits
- 3% were hospitalizations
- 0% were deaths
These numbers do not include TBIs from federal, military, or VA hospitals.
What is traumatic brain injury?
Traumatically induced structural injury or physiological disruption of brain function as a result of external force to the head. New or worsening of at least one of the following clinical signs:
- Loss of consciousness or decreased consciousness
- Loss of memory immediately before or after injury
- Alteration in mental status (confused, disoriented, slow thinking)
- Neurological deficits
- Intracranial lesion
What is mild traumatic brain injury (MTBI)?
Commonly referred to as a concussion, is a brief loss of consciousness or disorientation ranging up to 30 minutes. Though damage may not be visible on an MRI or CAT scan, common symptoms of MTBI include headache, confusion, lightheadedness, dizziness, blurred vision or sluggish pupils, ringing in the ears, bad taste in the mouth, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and trouble with memory, concentration or attention.
MTBI can have long-term effects, known as:
post-concussion syndrome (PCS). Those who suffer from PCS can experience significant changes in cognition and personality.
A concussion is an injury that causes an alteration of the person’s mental status. This is often referred to as having your “bell rung.” The person may be dazed or confused. More serious brain injuries that cause unconsciousness for 30 minutes or more are usually quickly recognized, but concussions may be dismissed and go untreated.
What is severe traumatic brain injury?
Associated with loss of consciousness for over 30 minutes, or amnesia. Symptoms of Severe TBI include all those of MTBI, as well as headaches that gets worse or do not go away, repeated vomiting or nausea, convulsions or seizures, inability to awaken from sleep, dilation of one or both pupils of the eyes (also known as anisocoria), slurred speech, weakness or numbness in the extremities, loss of coordination, and increased confusion, restlessness, or agitation.
The trauma may cause structural damage or may produce more subtle damage that manifests by altered brain function, without structural damage that can be detected by traditional imaging studies such as MRI CT scans.
TBI varies in severity, traditionally described as mild, moderate and severe. These categories are based on measures of length of unconsciousness and post-traumatic amnesia.
GCS (Glasgow Coma Scale) is not found that useful in theater for this purpose because it was designed as a prognostic indication for people in a coma which is why it is called a coma scale. The mild rating is not very useful.
The moderate and severe stages are more indicative to the Corpsmen, Medic’s, Dr’s, etc. of what is to be expected
Describe Mild TBI as defined by the Glasgow Coma Scale
AOC (Alteration of Consciousness) less than or equal to 24 hours
LOC (Loss of Consciousness) 0 to 30 minutes
PTA (Post Traumatic Amnesia) less than or equal to 24 hours
Imaging is generally normal.
Mild TBI usually mean concussion
It is more commonly thought that people who have a concussion tend to get better, they go back into play, and continue with their lives.
In managing expectations, the term Brain Injury sounds more serious because you are telling the person that their brain is injured. The term concussion sounds less severe and could give people a more optimistic view of recovery which is why we are using the term concussion instead of brain injury.
Remember – TBI and concussion refer to the same injury. It is wise to get into the habit of referring to a traumatic brain injury as a concussion especially when talking with a patient. Then talking to other medical personnel the term TBI is acceptable. It is less unsettling to hear a concussion as opposed to a brain injury.
Blunt trauma is more common and causes direct brain injury through fractures with underlying tissue laceration or intracranial bleeding. Skull fractures, whether from penetrating or blunt trauma, imply a high degree of force.
Skull fractures are classified by their location, pattern of fracture and whether they are open or closed. Compared with simple linear or comminuted skull fractures, a depressed skull fracture requires a higher degree of energy.
Depressed skull fractures often tear underlying dural tissue and directly lacerate or compress brain tissue. Fractures along the temporal bone over the pterion may injure the middle meningeal artery and cause epidural hematoma formation.
Likewise, fractures of bone overlying dural sinuses may injure bridging veins, resulting in subdural hematoma formation.
What fractures require a high degree of force owing to the strength and thickness of the bone?
Occipital bone or basilar skull fractures
These commonly involve the petrous portion of the temporal bone, damaging middle and inner ear structures and often impair facial, acoustic and vestibular nerve function. These injuries are sometimes associated with a torn dura and CSF otorrhea. The presence of a skull fracture significantly increases the likelihood of an intracranial lesion and one study found the increased risk to be as high as 174 times that of patients without a skull fracture.
What do hematomas or extra-axial fluid collections result in?
compressive brain injury due to the presence of blood in an enclosed space and occur in both penetrating and closed head injury.
What is an epidural hematoma?
Epidural hematomas (EDH) are located blood between the skull and the outer dura mater and typically result from an injury to the temporal bone and middle meningeal artery. However, epidural hematomas may also result from injury to the middle meningeal vein, diploic veins or venous sinuses.
The middle meningeal artery is the source of bleeding in approximately 36% of adult EDH and 18% of pediatric EDH.
How do epidural hematomas present?
Classically, they present with a head injury and loss of consciousness, followed by a lucid interval. These patients subsequently decompensate due a rapidly expanding hematoma from arterial bleeding.
The classic presentation is only seen in 47% of cases and most patients present either without a loss of consciousness or never regain consciousness after the injury. Approximately 22-56% of patients are comatose on presentation or at the time of surgery.
Pupillary abnormalities are seen in 18-44% of patients.
Other common exam findings with epidural hematomas include:
focal neurologic deficits, decorticate posturing and seizures.
EDH appears as biconvex or lenticular hyperdense lesions in the temporal region on CT imaging and compresses brain tissue towards the midline. The expanding hematoma in the closed skull results in uncal herniation and rapid death unless surgical intervention is performed.
What are subdural hematomas?
Subdural hematomas (SDH) are a collection of blood between the dura mater and the pia-arachnoid mater and may result from acute or chronic trauma. SDH may occur with direct or indirect primary brain injury. Acute SDH involves the laceration of brain tissue and superficial cortical veins or avulsion of bridging veins between the cortex and dural sinuses.
How do subdural hematomas present?
As with EDH, SDH compresses underlying brain tissue, resulting in cerebral edema and hyperemia. The combination of the hematoma and underlying brain edema dramatically increases the intracranial pressure and can trigger activation of the brain injury cascade.
What else can cause a subdural hematoma?
SDH can also be chronic from distant trauma, particularly in the elderly, and are typically found after symptoms gradually develop over weeks. Elderly patients and alcoholics are particularly prone to SDH because of brain atrophy and increased space between the skull and the cortex. This large space places bridging veins at increased risk for injury.
How do subdural hematomas appear on CT?
On CT imaging, SDH appear as a hyperdense crescent shaped lesion that may cross suture lines. Chronic SDH may appear hypodense due to the presence of phagocytized iron in the blood.
What is a subarachnoid hemorrhage?
Direct brain injury may cause bleeding in the intraparenchymal brain tissue or the subarachnoid space, resulting in surrounding cerebral edema and increased intracranial pressure.
Initial CT imaging is less sensitive for SAH than CT scans performed at 6-8 hours after the injury, necessitating close neurological observation after admission of moderate and severe head injured patients.
Blast-related TBI:
*IED’s are the number one cause of Brain Injury right now. In fact, very few are being shot when compared to IED explosions.
What happens to the brain with trauma?
The brain is somewhat gelatin-like and the skull can be compared to a black metal box. With limited space between the gelatin and the black box, additional injuries are possible with the forward and backward movement of the brain during the impact of an injury event. This can result in an effect known as coup-contrecoup.
Coup: This refers to the direct injury site of the brain upon impact with an object. An example is a baseball bat hitting the frontal lobe. The brain hits the front of the skull due to the rapid acceleration from the impact of the bat.
Contrecoup: This refers to the injury site directly opposite the site of impact. With the example of the baseball bat hitting the frontal lobe, the injury site would be located in the occipital lobe. This is because the brain is forced to the back of the skull and damaging tissue.
When the brain turns on itself this causes twisting of axons or shearing of axons. This does not cause immediate breakage but once the damage begins, this leads to degraded enzymes that breakdown the axon of the nerve which causes disconnection.
Damage due to disconnection leads to some form of neurological deficits. That deficit is based on the area in the brain that is damaged.
These events mandate prompt command & medical evaluations and reporting of exposure of all involved personnel.
