40 Head and Traumatic Brain Injury

Objectives Discuss the incidence and death rates for brain injuries. Review the pathophysiology behind the types of brain injuries. Define assessment considerations and findings for patients with brain injuries. Review current treatment standards for brain injuries. Discuss the objectives.

Introduction Brain injuries may manifest themselves now, or weeks later. The physiology of the brain and surrounding structures leaves itself open to certain types of brain injuries. As an Advanced EMT, you will be faced with caring for patients suffering from head injuries. These injuries require a high level of suspicion, as signs and symptoms can manifest days and even weeks after the original injury, especially in the very young and elderly. Assessment of these patients can be complicated because altered mentation is a common presentation in head injuries. In addition, drugs or alcohol may also compound the situation, making assessment even more difficult. You must overcome these challenges in order to promptly evaluate the condition and prevent further neurologic damage to your patient. Understanding the anatomy of the skull and its contents is imperative for determining the specific type of head or traumatic brain injury your patient is displaying.

Introduction (cont’d) The task for the Advanced EMT is to understand the physiology of the brain and pathophysiology of brain injuries to provide optimal treatment. As an Advanced EMT, you will be faced with caring for patients suffering from head injuries. These injuries require a high level of suspicion, as signs and symptoms can manifest days and even weeks after the original injury, especially in the very young and elderly. Assessment of these patients can be complicated because altered mentation is a common presentation in head injuries. In addition, drugs or alcohol may also compound the situation, making assessment even more difficult. You must overcome these challenges in order to promptly evaluate the condition and prevent further neurologic damage to your patient. Understanding the anatomy of the skull and its contents is imperative for determining the specific type of head or traumatic brain injury your patient is displaying.

Epidemiology 1.5 million head injuries occur per year in the U.S. It is the leading cause of death in accident victims younger than 45. 50,000 people die each year from brain injury. Review the basic statistics.

Pathophysiology Intracerebral hemorrhage Extraaxial hemorrhage Epidural, subdural, subarachnoid Intraaxial hemorrhage Occurs within brain tissue itself Intraparenchymal hemorrhage Intraventricular hemorrhage Discuss the new arrangements for categorizing brain injuries. Some information will be old, some will be new, but the underlying pathophysiology behind all of this is: Is a space-occupying lesion existing in the cranial vault, that is going to increase intracranial pressure and cause shifting of the tissues (structural cause for altered mental status).

Pathophysiology (cont’d) Diffuse axonal injury (DAI) Most devastating of traumatic brain injuries Acceleration-deceleration mechanism Frequent outcome is coma Stretching and swelling of axons DAI typically stems from traumatic acceleration-deceleration injuries. It is a pathologic process in which axons are stretched and twisted by rotational shearing forces that occur during rapidly changing movement. The damaged axons begin to swell and separate from each other, causing interference between the communication and transmission of nerve impulses throughout the brain. This injury is one of the major causes of unconsciousness and persistent vegetative state after head trauma.

Pathophysiology (cont’d) Concussion Mild DAI GCS 13-15 Epidural hematoma Serious complication of head injury Bleeding between dura and skull DAI typically stems from traumatic acceleration-deceleration injuries. It is a pathologic process in which axons are stretched and twisted by rotational shearing forces that occur during rapidly changing movement. The damaged axons begin to swell and separate from each other, causing interference between the communication and transmission of nerve impulses throughout the brain. This injury is one of the major causes of unconsciousness and persistent vegetative state after head trauma. With epidural bleeds, the bleeding takes place between the protective covering of the brain (dura) and the skull. The bleeding is profuse and rapidly expands within the space, causing a sudden increase in intracranial pressure (ICP). This rise in ICP causes the cascade of signs and symptoms, including: Decreased mental status Severe headache Fixed and dilated pupils Vomiting Altered or absent breathing Posturing Systolic hypertension with associated bradycardia (Cushing reflex, a late finding) Among patients with an epidural hematoma, 20 percent have a lucid interval. The patient will suffer from a loss of consciousness and then a period of responsiveness. Shortly thereafter, their level of consciousness will rapidly deteriorate.

Epidural hematoma

Pathophysiology (cont’d) Subdural hematoma Bleeding between arachnoid and dura Low-pressure bleed Acute, subacute, chronic Manifestations of subdural hematoma can vary greatly, ranging from clinically silent to expansion large enough to cause brain herniation. Signs and symptoms of acute subdural hematoma include: Declining level of consciousness Abnormal or absent respirations Dilation of one pupil Weakness or paralysis to one side of the body Vomiting Seizures Increasing systolic blood pressure Decreasing heart rate

Subdural hematoma

Pathophysiology (cont’d) Subarachnoid hemorrhage Brain tissue becomes ischemic Severe headache common May rapidly progress to seizures and cardiac arrest The immediate danger in subarachnoid hemorrhage is ischemia, in which portions of the brain that do not receive adequate blood and oxygen supply suffer irreparable injury. This can lead to permanent neurologic damage or death. The three most common complications that promote ischemia to the brain are: Vasospasm Hydrocephalus Intracranial hypertension In vasospasm, blood vessels constrict in response to chemicals released when blood breaks down in the subarachnoid space. The classic symptom of nontraumatic subarachnoid hemorrhage is a thunderclap headache. It is described as the worst pain ever felt. The majority of studies have shown that patients progress from being pain free to experiencing severe excruciating pain in a matter of seconds. Loss of consciousness typically follows but can take several hours. Other signs and symptoms of subarachnoid hemorrhage include: Restlessness Confusion Motor and sensory dysfunction Vomiting Seizures Severe neurologic deficits develop and become irreversible within minutes.

Assessment Findings Dispatch information Soft-tissue injuries to skull Seizures, headache, trauma, etc. Soft-tissue injuries to skull Closed or open skull injuries Alteration in mental status Discuss the symptomotology of brain injuries and, whenever possible, relate it back to underlying pathophysiology.

Assessment Findings (cont’d) Possible loss of airway patency Breathing may become irregular and slow Changes to vitals (Cushing response) Discuss the symptomotology of brain injuries and, whenever possible, relate it back to underlying pathophysiology.

Assessment Findings (cont’d) Response to painful stimuli Purposeful vs. nonpurposeful Decorticate vs. decerebrate Discuss the symptomotology of brain injuries and, whenever possible, relate it back to underlying pathophysiology.

Nonpurposeful responses to painful stimuli include (a) flexion (decorticate) posturing and (b) extension (decerebrate) posturing.

Assessment Findings (cont’d) Assess and reassess mental status. Compute GCS, look for trends. Review the Glasgow Coma Scale.

Glasgow Coma Scale

Assessment Findings (cont’d) Assess vital signs Trends of vitals may also help identify brain injury. Discuss the relationship between vitals and brain injuries.

Implications of Changes in Vital Signs with Head Injuries.

Emergency Medical Care Manual cervical spine considerations Assess and maintain the airway. Determine breathing adequacy. High-flow via NRB with adequate breathing. High-flow via PPV @ 10-12/min if inadequate. Avoid intubating head injured patients unless apneic – tend to worsen outcomes. Unfortunately, head injuries can be severe and life-threatening. Prompt recognition and treatment of these injuries is paramount for patient survival and limiting permanent disability.

Emergency Medical Care Consider hyperventilation with brain herniation. Do not routinely hyperventilate – Reserve for signs of herniation Controversial May produce short-term improvement No role in long-term mgt of elevated ICP May produce vasoconstriction and worsening of brain injury – use only when concerned about herniation.

Emergency Medical Care (cont’d) Assess circulatory components. Check pulse, skin characteristics. Control major bleeds. Unfortunately, head injuries can be severe and life-threatening. Prompt recognition and treatment of these injuries is paramount for patient survival and limiting permanent disability.

Emergency Medical Care (cont’d) Transport immediately to an appropriate medical facility. Initiate a large-bore intravenous catheter. Administer fluids to keep SBP >90 mmHg. Do not cause hypertension with IV fluids. Unfortunately, head injuries can be severe and life-threatening. Prompt recognition and treatment of these injuries is paramount for patient survival and limiting permanent disability.

Emergency Medical Care (cont’d) Be prepared to manage seizure activity. Constantly monitor airway, breathing, and circulation. Mental status changes are key to determining improvement or deterioration. Ongoing assessment should focus on: Maintaining the airway Managing seizures Monitoring the mental status Ensuring a rapid transport to an appropriate facility

Case Study You are called to a motorcycle accident where a rider not wearing a helmet lost control of his cycle on a turn and hit a tree. When you arrive, the patient is lying supine, blood covering his face and shirt, and the patient is actively seizing. PD is already on scene and you can hear the wail of the FD sirens approaching. Discuss the case study.

Case Study (cont’d) Scene Size-Up Standard precautions taken. Scene is safe, police stopped traffic on road. 43-year-old male patient, 200 lbs. Patient found supine, blood on face and shirt. Discuss the case study.

Case Study (cont’d) Scene Size-Up Patient entry made, egress not problematic. Paramedic summoned now for backup assistance. PD on scene, FD pulling up. Discuss the case study.

Case Study (cont’d) Primary Assessment Findings Patient unresponsive, active tonic-clonic seizures. Mouth clenched shut, blood on face, sonorous breath sounds with gurgling. Breathing is ineffective due to seizure activity. Discuss the case study.

Case Study (cont’d) Primary Assessment Findings Carotid and radial pulses present. Peripheral skin warm and sweaty. No major bleeds noted to body. Discuss the case study.

Case Study (cont’d) Is this patient a high or low priority? Why? What interventions should be provided at this time? The patient is a high priority due to: The change in mental status (unresponsive). Inability to maintain his own airway and ventilations (due to seizures). Finally, the seizures themselves can further aggravate other injuries not yet identified. The patient should have their head manually stabilized (best possible with current seizure activity), insert a flexible catheter into nasal cavity to suction out oral cavity. Apply a modified jaw thrust technique to open the airway. Consider PPV to enhance alveolar ventilation.

Case Study (cont’d) Medical History Medications Allergies Unknown Discuss the case progression.

Case Study (cont’d) Pertinent Secondary Assessment Findings Pupils unequal, sluggish to light. Airway patent, breathing still ineffective. Patient is still unresponsive and seizing. Pulse oximeter reading 82% with attempts at PPV. Discuss the case progression.

Case Study (cont’d) Pertinent Secondary Assessment Findings B/P 198/90, heart rate 64, spontaneous respirations 4 and irregular. Crepitus noted to posterior vertebrae. Depressed right frontal skull fracture noted. Discuss the case progression.

Case Study (cont’d) What type of brain injury could this be? Is this patient displaying any indications of herniation? This is likely a hemorrhagic syndrome or diffuse axonal injury. In any instance, the key is the recognition that they are displaying signs of acute herniation. Yes, they have: Unresponsiveness Cushing response Unequal pupils Seizures All of these indicate herniation of the brain stem through the foramen magnum.

Case Study (cont’d) Care provided: Patient’s cervical spine manually immobilized. High-flow oxygen via PPV. Airway suctioned with catheter, manual airway technique applied. Discuss the care provided.

Case Study (cont’d) Care provided: Following cessation of seizure, full body immobilization provided. Expeditious transport to appropriate facility. Initiation of intravenous access. Discuss the care provided.

Summary Brain injuries are a common cause of death and disability following traumatic events. Prehospital recognition and proper management can help reduce the long-term effects of brain injuries. As with any trauma, focus first on supporting lost function. Review as appropriate.