A traumatic brain injury (TBI) is defined as a blow or jolt to the head, or a penetrating head injury that disrupts the function of the brain.Approximately 14 million people suffer a TBI each year in the United States. Of those people, 50,000 die, 235,000 are hospitalized and 1.1 million are treated and released from the hospital. Our focus is on the acute, severe patient, but providers need to keep in mind that all patients with suspicious mechanism of injury, or even mild symptoms, may deteriorate rapidly.
For the purpose of this discussion the anatomy of the brain dose not need to be very detailed. Let’s review the basics. The brain and spinal cord are encased and protected by three membranes of protective tissues called meninges. The outermost and thickest lining is the dura mater (“tough-mother”), a two layer membrane which lies just above the arachnoid membrane. The arachnoid is a thick membrane that suspends arteries and veins. Beneath it lays the delicate pia mater (“tender mother”). Blood from an injury can accumulate between the layers causing pressure on the brain itself. There is normally no epidural space within the cranial cavity because the dura mater is tightly attached to the cranial bones, however, an epidural space can develop if an injury results in the accumulation of blood between the bone and dura mater. Cerebrospinal fluid (CSF) fills the ventricles of the brain, the subarachnoid space around the brain and the spinal cord, and the central canal of the spinal cord. CSF provides a protective fluid cushion around the brain and vertebral column. CSF also provides some nutrients to Central Nervous System (CNS) tissues.
Think of the cranial vault as a closed box with very little room for expansion. When the brain is traumatized, it swells like other tissues do when they are bruised. Blood flows to the injured area causing the swelling. When the swelling occurs in a closed head injury, pressure is building inside the “box”restricting blood flow to the healthy tissue. The heart receives signals indicating a need for oxygen and increases blood flow to the brain. As the heart increases its force of contraction and the vessels constrict, the blood pressure and cerebral perfusion increase. The result of this action is an increase in intracranial pressure (ICP). This is the beginning of the end for the patient if ICP is not brought under control.
The best thing we as prehospital providers can do for a severe head injury patient at any level is to recognize the signs and symptoms. As you begin your exam, keep in mind that determining the specific type of brain injury present may be impossible. Recognizing the presence of the brain injury and the beginning immediate care is more important. The first sign should be your mechanism of injury (MOI). Motor vehicle crashes, falls, or sporting activities to name a few. Consider the force inflicted on the patient during the incident and every head injured patient has suspected spinal injuries until proven otherwise, no exceptions. Here are some basic tools we use to assess our injured patient with suspected TBI. As with any patient we start with ABCs. If a life threat is found concerning the ABCs they are to be corrected as they are found.
Level of consciousness
The patient’s level of consciousness is one of the best indicators of a brain injury. Did the patient loose consciousness? If so, how soon after the accident? The trusty Glasgow Coma Score (GCS) and “AVPU”are used to describe the patient’s general level of consciousness and should be documented with every head injured patient early, so that an accurate baseline can be established and not be missed in the overall patient course. Even a one point change in GCS in a short period of time is very significant.
Look for inappropriate behavior or combative behavior. Be careful not to dismiss this patient as “just another drunk.”
Make sure the patient’s airway is open while maintaining c-spine control. An unconscious patient is at risk for airway compromise, so assign someone to airway control. Closely monitor the airway and insure suction is handy. Vomiting is common with head injuries and may cause airway problems. As we will discuss later, removing CO2 is vital for patients with increased ICP so using an airway adjunct should be considered quickly with the unconscious patient. Endotracheal intubation should be considered, but even basic airway adjuncts can be very effective in maintaining the open airway.
A patient with a head or brain injury may present with an abnormal breathing pattern. Take note of the patient’s breathing pattern and if it changes any at all throughout your time with the patient. Reassess the vital signs and GCS score often.
Place the patient on high flow oxygen. The high flow O2 will flood the blood with oxygen molecules and will help “trick”the brain into “thinking”the injury is less severe and thus not increase the blood flow to the injured area as much. Increased oxygen also helps displace the CO2 levels. High CO2 levels cerebral vasodilatation and increased ICP, decreased CO2 causes vasoconstriction and decreased ICP.
If the patient’s respirations are below normal the “old school”way of thinking was to hyperventilate the patient. Studies have shown that the initial management of a severe brain injury should include ventilation at a normal rate: one breath every five seconds for an adult and one breath every three second for an infant or child. Hyperventilation (20 breaths per minute) is usually considered if a patient has a GCS score of eight or less, accompanied by active seizures and signs of herniation, such as fixed or unequal pupils, posturing or signs of neurologic deterioration. Follow your local protocols when treating any patient.
As ICP increases, blood pressure also increases to perfuse the swelling brain. Decreases in blood pressure are usually late signs in a head injury. If you have what you think is an isolated head injury and a hyotensive patient, you are either late in the ball game or you have bleeding some where else. Look for another injury. The pulse will also decrease with the isolated head injury. As ICP increases, the Vagus nerve releases acetylcholine onto the heart, causing bradycardia.
Now we can explore the ongoing assessment, treatment and transport of TBI patients. After the primary survey, treatment of ABCs and spinal immobilization, the head of the spine board should be elevated 30 degrees, if hypotension does not exist. Open skull fractures should be covered with non-pressure sterile dry dressings. Transport should begin within 10 minutes of arrival on scene if at all possible. The only definitive treatment for TBI comes in a hospital. Sitting on the scene will not improve patient outcome. These patients should also be considered candidates for transport to a Level 1 Trauma Center.
If ventilating the patient via endotracheal intubation is required, EtCO2 should be monitored via Capnography when available. Ventilate to maintain EtCO2 to between 32-35 mmHg. Seizures are common with head trauma and can lead to increased ICP and hypoxia. Controlling seizures in these patients is similar to other types of seizure management with benzodiazepines is indicated. Follow your local protocols when treating seizures with medications.
An IV of normal saline should be initiated, but run it only at a rate to maintain profusion. Most isolated head injury patients do not need fluid. As we stated earlier, if you have a hypotensive TBI patient, look for trauma elsewhere, also. The systolic blood pressure should be maintained at 90 mmHg. The goal is to maintain a Mean Arterial Pressure of less than70 mmHg.
The most important skill involved at any level of training with this type of call is patient assessment. This is a skill that needs to be continuously sharpened through training and education to keep us thinking “inside the box”and to ensure early recognition of the signs and symptoms of one of the injuries that continues to challenge every level of prehospital care.