Brain Injuries - EMS magazine 1999

[26-20-2]

Brain Injuries

By Dan Price, MD, & Bob Burns, RN, EMT-P

While descending Mt. Hood in Oregon, Bob tumbled head over heels, and came to a stop dangling off a precipice by his Telemark ski at 11,000 ft. On arrival of ski-patrol EMTs, Bob's breathing was sonorous and shallow, and he had a Glasgow Coma Scale (GCS) of 3-4. The only obvious injuries were to his head. His blood pressure was 87/55, heart rate 100 and respiratory rate 16. How would you treat this patient? Would you intubate him? Would you hyperventilate? Would you fluid-resuscitate him?

The treatment of traumatic brain injury (TBI), both in and out of hospital, is changing. Treatment by EMS personnel can make a vital difference in the outcome of TBI patients by treating the primary injury appropriately and preventing secondary injury from decreased cerebral perfusion. While 78% of people with a GCS of 3 will die of their traumatic brain injury, 3--4% will recover with little or no neurologic deficit. Patients with a higher GCS do correspondingly better, but there is room for improvement at all levels. This article discusses the latest national evidence-based recommendations for treatment of TBI as they relate to prehospital care.

Types of Injuries

Primary brain injuries (from direct trauma) can be divided into two categories: focal and diffuse. Secondary brain injury may develop due to hypotension and/or hypoxia.

Focal brain injuries account for about 50% of head injuries and include intracranial bleeding, such as subdural and epidural hematomas and contusions. The skateboarder shown in Figure 1 incurred an epidural hematoma.

Diffuse brain injuries include concussion and diffuse axonal injury resulting from shearing forces created by sudden deceleration. Diffuse injuries, which occur commonly in falls and MVCs, result in rapid, profound, prolonged unconsciousness and often lead to increased intracranial pressure (ICP). Bob's injury was ultimately shown to be diffuse axonal injury.

Both focal and diffuse injuries may cause increased ICP that can result in herniation. As ICP increases, the edge of the temporal lobe of the brain herniates under the fibrous tissue separating portions of the brain (tentorium cerebelli). This herniated lobe can compress the 3rd cranial nerve producing a "blown" pupil. Parasympathetic fibers run along the outside of this nerve, and, with compression, the pupil receives unopposed sympathetic stimulation producing a dilated "fight-or-flight" pupil (see Figure 2). Further compression of the brainstem can produce altered breathing patterns, blood pressure and pulse changes and hemiparesis.

End-Tidal CO₂ Detection
End-tidal CO₂ detection is a revolutionary technology now available on the latest models of all major prehospital monitoring devices. Using infrared technology, a small tube is interposed between the endotracheal tube and the bag-valve device. It will produce a raw number and possibly a wave form similar to pulse oximetry. This is extremely important in treating head-injured patients. As mentioned in the body of the article, only patients with signs of herniation should be hyperventilated, and then only to a level of 30 mmHg, not 25 mmHg as recommended in the past. Without this device to provide an objective measure, patients can easily be overhyperventilated.

When we fly to the scene of a head-injured patient who has been properly intubated and given 100% oxygen, we commonly see values of 13 or 16 mmHg when we attach the EtCO₂ monitor. We know that levels less than 25 mmHg will definitely cause further damage to at-risk brain tissue surrounding the injury, but without having a number to go by, it is very easy to bag too rapidly.

In addition to its vital role in guiding treatment of TBI, EtCO₂ has two other valuable uses in the prehospital setting. First, it can be used in place of the Easy-CapR colorimetric CO₂ detector device to confirm‎ correct placement of the endotracheal tube. Second, a growing body of evidence suggests that the code of a patient in PEA can be ended after 20 minutes if the EtCO₂ is 10 mmHg or less, and no patients will be allowed to die who might have survived.

We strongly urge all EMS agencies to invest in EtCO₂ monitoring by purchasing new units, or when replacing your monitors.

Glasgow Coma Scale
The Glasgow Coma Scale (GCS) was developed in 1974 as an objective measure of neurologic function in traumatic brain injury patients. Multiple studies have confirmed its validity in predicting outcome and reliability between eval‎uators; however, a recent survey revealed significant variation from the following guidelines--even among neurosurgeons.

• GCS on first contact is helpful, but it is most predictive after resuscitation (i.e. SBP>90 and SaO2>94%).
• Best GCS sum score is used (e.g., if patient localizes with right hand but does not move left, she still receives an M5) and asymmetry is noted.
• The motor component is most predictive, and GCS should be determined prior to intubation and paralysis, if possible.
• A verbal pseudoscore of 1T can be used for intubated patients.
• An eye-opening pseudoscore of 1 can be assigned if the patient has periorbital swelling and is unable to open his eyes. This should be documented.
• Localizing response indicates extension movements of the upper extremities to localize the painful stimulus (a thigh pinch may be the best stimulus).
• Withdrawal involves rapid arm flexion and shoulder abduction, in contrast to abnormal flexion, which is slower with flexion of the wrist and adduction of the shoulder.

Pathophysiology of Secondary Brain Injury

Surviving the initial insult (primary injury) is a small part of the battle for the traumatic brain-injured patient. Secondary brain injury after the impact caused by hypoxia and/or hypotension and resulting edema can be just as devastating.

Hypotension is a relative term in the brain-injured patient. A patient can be normotensive (systolic BP>100) physiologically, but be hypotensive in regard to perfusing the brain in the face of cerebral edema. Like any organ, the brain needs blood flow for perfusion. Cerebral perfusion pressure (CPP) cannot be calculated in the field since it requires measuring intracranial pressure (ICP) and calculating the mean arterial pressure (MAP) from BP readings (CPP=MAP-ICP). The body has the ability to autoregulate cerebral blood flow for a range of cerebral perfusion pressures. Autoregulation is deranged by TBI, and if blood pressure is allowed to drop while intracranial pressure is increasing, it is easy to fall outside of the range that the body can successfully regulate CPP (cerebral perfusion pressure). This can result in the brain being starved of blood. Hypotension must be avoided to keep the CPP up. Perfuse it or lose it.

Conversely, the BP can rise high enough to cause CPP to fall out of the autoregulatory range as well. For example, brain herniation from increasing ICP can press on the brain stem and cause the BP to increase and pulse to decrease in a classic Cushing's response.

Hypoxia, defined as an SaO2 <90 mmHg, leads to increased ICP via cell damage and resulting cellular swelling. Oxygenation must be maintained. Additionally, protective reflexes are lost when a patient's Glasgow Coma Scale falls to 8 or below, increasing the risk of airway obstruction and aspiration.

Currently, aggressive maintenance of blood pressure with IV fluids, intubation and oxygenation are the keys to preventing a secondary brain injury.

Assessment

Assessment and continual reassessment are key to appropriate treatment of TBIs.

In addition to establishing the patient's level of consciousness using the Glasgow Coma Scale (see sidebar on page xx), pupils should be assessed for size, symmetry and reactivity. A decreased level of consciousness does not necessarily indicate that the patient has an increased ICP, whereas lateralizing signs, such as a blown pupil, hemiparesis and Cushing's response, are indicative of increased ICP with herniation. If the patient does not exhibit signs of herniation, treatment will be centered on preventing a secondary injury and not on decreasing ICP.

Treatment

Critical, weighted reviews of hundreds of scientific studies by a group of nationally recognized neurosurgeons resulted in the Guidelines for the Management of Severe Head Injury issued in 1995 by the Trauma Brain Foundation. Those recommendations relevant to the prehospital setting are reviewed below.

Secondary brain injury, resulting from hypotension, hypoxia or both, are associated with significantly poorer outcomes.

• Hypotension

  Hypotension is the single worst prognostic factor. A single documented episode of hypotension has been correlated with poorer outcome. Normal saline or lactated Ringer's solutions should be used to keep the systolic pressure above 90 mmHg. This is a change from historic recommendations to "run 'em dry" to avoid raising the ICP. Remember, CPP is the key-perfuse it or lose it. Bob was appropriately given IV normal saline, and his blood pressure responded well.

• Hypoxia

  Hypoxia follows closely behind hypotension in significance. Bob's risk of hypoxia was compounded by the high elevation, and he was orally intubated and given 100% oxygen. Any patient with a GCS of 8 or below should be orotracheally intubated, preferably by rapid sequence. Multiple studies have shown oral rapid-sequence intubation to be faster and more reliable with fewer complications. The patient incurs transient elevation in ICP every time the pharynx is stimulated by a laryngoscope, and hypoxia develops if the intubation is prolonged.

  Nasotracheal intubation is no longer preferred, and runs the risk of perforation into the brain if the patient has a basilar skull fracture (which is rarely evident in the field). There is also an increased risk of meningitis complicating a nasal intubation. Recent studies have shown no increased risk of worsening cervical spine injury by using the oral instead of nasal route.

  The preponderance of evidence suggests that pretreatment with lidocaine will help protect the brain. Lidocaine blunts the transient rise in ICP due to insertion of the laryngoscope and the administration of succinylcholine. Lidocaine 1.5 mg/kg IV should be given as soon as the decision is made to intubate. Effects begin in about 90 seconds, but peak effect is not reached until 2-4 minutes.

• Cervical spine precautions

  Between 6%-8% of people with TBI will have cervical spine injuries as well. A cervical collar will not only help protect against further movement and injury, but maintaining the head in a neutral position will facilitate venous outflow and lower intracranial pressure (ICP). Care should be taken not to secure the collar too tightly, since this can impede flow through the jugular veins. Bob's friend removed him from the precarious position, attempting to maintain cervical spine precautions. He was placed in a cervical collar by ski patrol paramedics.

• Rapid transport

  Studies have shown that patients with elevated ICP for prolonged periods of time (definitely by 4 hours) have poorer outcomes. Since it is usually difficult to identify elevated ICP clinically, it is imperative to transport patients to a trauma center as rapidly as possible. For severe head injuries, especially with signs of herniation, air medical transport should be considered (see Figure 3).

Summary

We can make a big difference in the outcome of our patients with traumatic brain injury if we follow the scientifically validated guidelines. Remember, our two main enemies are hypoxia and hypotension. Fluid-resuscitate patients to keep systolic blood pressure above 90 mmHg. Orally intubate patients with a GCS of 8 or below, and administer 100% O2 to everyone. Hyperventilate only those patients who are herniating or have a rapid decline in their GCS. Hyperventilation should be to EtCO₂ of 30 mmHg instead of 25 mmHg as classically recommended (see Figure 4). Protocols that do not reflect these recommendations need to be changed for the good of our patients.

Bob was fortunate enough to be in the 3%-4% of patients with near complete neurological recovery. Life Flight was activated by the ski patrol, and Bob was removed from the mountain with the help of five different EMS entities. He remained in a coma for 2 weeks, which is not uncommon for diffuse axonal injury. He was later discharged to a skilled nursing facility for 2 months and underwent 2 years of rehabilitation. The road to recovery was long and difficult, but Bob returned to work and has won multiple engineering awards. In the recent Nike World Masters Games, Bob placed 11th in the mountain bike competition.

Bibliography

Brain Trauma Foundation: Guidelines for the Management of Severe Head Injury 1995.

Stone JL, et al. Head Injury and Its Complications. PMA Publishing Corp., 1993.

Culverwell D, et al. Prehospital Trauma Life Support--Basic and Advanced. St. Louis: Mosby, 1994.

Marion DW, PM Carlier. Problems with initial Glasgow Coma Scale assessment caused by prehospital treatment of patients with head injuries: Results of a national survey. J Trauma 36(1):89-95, 1994.

Winkler JV, Rosen P, Alfry EJ. Prehospital use of the Glasgow Coma Scale in severe head injury. J Emerg Med 2:1-6, 1984.

Chesnut RM. The management of severe traumatic brain injury. Emergency Medicine Clinics of North America 15(3):581-604, 1997.

Wayne MA, Levine RL, Miller CC. Use of end-tidal carbon dioxide to predict outcome in prehospital cardiac arrest. Ann Emerg Med 25(6):762-767, 1995.

Beca J, et al. Somatosensory evoked potentials for prediction of outcome in acute severe brain injury. Journal of Pediatrics 126:44-49, 1995.

Dan Price, MD, completed his emergency medicine residency at UC Davis, and a fellowship in air medical transport with Life Flight Network, where he now serves as medical director. He is assistant professor at Oregon Health Sciences University and works in the ED at Legacy Emanual Hospital. His research interests include head injury and emergency ultrasound.

Robert Burns, RN, EMT-P, has worked as a paramedic for 16 years, currently serving as a flight paramedic for Life Flight Network in Portland, OR, and as a flight nurse for Lifeguard Air Ambulance. He has degrees in aviation/professional pilot, nursing and microbiology, and is finishing a Master in Public Health.