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TRAUMATIC BRAIN INJURIES

Traumatic brain injury (TBI) is also known as craniocerebral trauma, intracranial injury or head injury. Head Injury is a broad classification that includes injury to the scalp, skull or brain. It is usually caused by vehicular accidents (crashes, collisions, pedestrians, etc.), falls, workplace accidents, sports-related injuries, as a result of acts of violence (assault) and penetrating trauma. People at risk of TBI are those people on extremes of ages, individuals who are exposed with occupational hazards, those with history of substance abuse and previous TBI, those engaged in risky sports, use of firearms and other weapons of violence, and those who do not practice safe driving, to name a few. Consequences of TBI range from no apparent neurologic disturbance to persistent vegetative state or death. Every head injury, therefore, shall be considered potentially dangerous. Traumatic brain injury is a major public problem especially among males aged 15-24, among elderly of ages 75 and up, and children aged 5 and younger. Traumatic brain injury has two forms: primary brain injury occurs from a blunt trauma, a direct or indirect blow to the head causing accelerationdeceleration forces to the brain, and secondary brain injury results from other problems such as diffuse axonal injury, intracranial hypertension, hypoxemia and hypercapnia, or systemic hypotension. Traumatic brain injury, as a broad classification of injuries, includes the following types: According to severity A. Closed head injury This type of injury does not break the continuity of the skull, thereby the meninges (dura) remain intact and cerebral tissues are not openly exposed to the environment. It occurs when the head strikes a hard surface or when blunt object strikes the head. The site of impact will most probably be the site of injury. The trauma may not be enough to cause a change in the persons level of consciousness. 1. Concussion

NCM 104: PROBLEMS IN PERCEPTION AND COORDINATION

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It is otherwise known as jarring of the brain. The mechanism of injury is usually blunt trauma from an acceleration-deceleration force, a direct blow or a blast injury. There is a temporary loss of neurologic functioning with no apparent structural damage. If brain tissue in the frontal lobe is affected, the patient may exhibit a bizarre irrational behavior, whereas at the temporal lobe it may produce temporary amnesia or disorientation. 2. Contusion The brain is bruised and damaged on a specific area due to severe acceleration-deceleration force or blunt trauma. It is a more severe form of head injury. 3. Diffuse axonal injury (DAI) This results from widespread shearing and rotational forces that produce damage throughout the brain to axons incerebral hemispheres, corpus callosum, and brain stem. The injured area may be diffuse with no identifiable focal lesion. It usually happens on vehicular accidents. B. Open head injuries This occurs when an object penetrates the skull, enters the brain, and damages soft brain tissue in its path, or when blunt trauma is so severe that it opens the scalp, skull, and dura to expose the brain. 1. Scalp injury. This includes lacerations, cuts and bruises on the scalp, resulting to hemorrhages or external hematoma. 2. Skull fracture. It is a break in the skull, impairing its integrity. Four major types of skull fracture: a. Linear skull fracture. This is the most common type of skull fracture, having a break in the skull without moving the bone. b. Depressed skull fracture. This type of injury is characterized by c. Diastatic skull fracture. This injury causes widening of and only happens in the suture lines. d. Basilar fracture. This type is the most dangerous, involving a fracture at the base of the skull resulting to multiorgan dysfunction.

NCM 104: PROBLEMS IN PERCEPTION AND COORDINATION

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C. Focal brain injury 1. Extraaxial hemorrhage. a. Epidural hematoma. It is usually associated with skull fracture, occurs when a blood clot formation underneath the skull but superficial to the dura mater. b. Subdural hematoma, occurs below the dura but not crossing the arachnoid. c. Subarachnoid. This is bleeding on the spaces on the brain surface. 2. Intraaxial hemorrhage a. Intraparenchymal. This happens when hemorrhage occurs within the brain tissues. b. Intraventricular. This occurs in the cerebral ventricular system. D. Diffuse brain injury. Trauma causes a disseminated injury in the brain. Pathophysiology The cranial vault is usually an enclosed cavity maintaining a normal intracranial pressure of 0-15 mmHg (5-15 mmHg). The injured brain is different from any other injured body organs because of its unique characteristics. It resides in the skull which is a rigid, closed compartment. Any bleeding or swelling within the skull increases the volume of contents within a container of fixed size thereby increasing intracranial pressure. If ICP is increased enough, it can cause brain displacement through the skulls rigid structures. Blood flow, therefore, is decreased due to restriction. Removal of metabolic wastes and oxygen delivery will also be decreased. Brain cells will then become anoxic, unable to metabolize properly, producing ischemia, infarction, irreversible brain damage eventually leading to brain death.

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Risk factors Blunt force to the head Acceleration or deceleration force Head trauma Open head injury Skull fractures Damage to Cranial Nerve I, II, VII, VIII Anosmia Racoons eye Visual pupil abnormalities Hearing loss or impairment Facial paralysis Breakdown of brain protection Laceration CSF leakage Brain tissue inflammation and compression Brain swelling or bleeding intracranial volume ICP Cerebral blood flow restriction O2 delivery and waste removal Cerebral hypoxia,ischemia, infarction Brain death Closed head trauma Coup or contrecoup injury Contusion Concussion Jarring of the brain Dizziness Spots before the eyes Headache Temporary loss of neurologic function External hematoma

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Signs and Symptoms A. Mild head injury 1. Raised swollen area (bump) or a bruise. Inflammation occurs on site of trauma. 2. Small superficial cut in the scalp. When the skin continuity is altered, a cut or laceration occurs after a blunt object hits the head. It may cause bleeding. 3. Headache. B. Moderate to severe head injury requiring immediate medical attention 1. Confusion 2. Blurred vision 3. Vomiting 4. Slurred speech 5. Dizziness 6. Pale skin color 7. Loss of consciousness 8. Severe headache 9. Temporary amnesia 10. Seizures 11. Sweating 12. Difficulty walking 13. dBlood or clear fluid leaking from the ears or nose. When there is a severe injury (i.e. fracture), a breakage on the base of the skull can cause CSF or blood to leak. 14. Behavioral changes including irritability 15. Pupillary and visual changes such as hemianopsia 16. Open wound in the head 17. Foreign body has penetrated the head 18. Deep scalp lacerations or cuts 19. Hemiparesis. Muscular weakness or partial paralysis restricted to one side of the body. Diagnostic examinations 1. Laboratory procedures are usually used to diagnose primary brain injuries, some of them are indicative of measures preventing secondary injuries. a. Complete blood count

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b. Arterial blood gas studies. This is performed to assess adequacy of oxygenation and acid-base balances (or otherwise presence of ventilation and oxygenation problems that may increase ICP). This is typical especially, the medulla oblongata (respiratory center), is located in the cranial cavity. c. Serum electrolytes. This is done to assess levels of electrolytes present in blood because fluid shifting may occur in injury, which may precipitate increase in ICP or changes in mentation. d. Serum glucose. Diagnostic procedures 1. Computerized tomography (CT) scan. Screening image ofcoice in acute TBI. It is used to produce a 3D images of a body structure constructed from a plane of cross-sectional images made along its axis. It identifies space-occupying lesions, hematomas, contusions, hemorrhage, skull fractures, brain tissue swelling and shift. 2. Magnetic resonance imaging. It is a noninvasive technique, which processes computerized images by applying radio waves thereby creating a magnetic field to detect changes in brain tissue. It is more sensitive than CT for detecting cerebral trauma, determining neurologic deficiencies not explained by CT, evaluating prolonged interval of disturbed consciousness, defining evidence of previous trauma superimposed on acute trauma. Note: it requires longer procedure time and is not recommended in acute injury cases. 3. Skull X-ray. This radiographic procedure visualizes the skull for detection of fractures, shifts of midline structures and to determine extent or degree of penetrating foreign bodies and bone fragments. 4. Cerebral angiography. This is the visualization of networks of blood vessels in the brain. It demonstrates cerebral circulation anomalies such as brain tissue shift secondary to edema, hemorrhage or trauma. It is rarely used in acute head injury but can be done when intraparenchymal or subarachnoid hemorrhage is known or suspected. 5. Lumbar puncture and CSF analysis. This may be performed when increased ICP is known or suspected, and for possible infections on the brain. It is generally contraindicated in acute trauma. 6. Serial electroencephalography (EEG). This is used to detect and record brain waves, for measurement of electrical activity on the brain, their intensity and frequency. It is helpful in determining the possible occurrence of seizures and focal or diffused encephalopathy when

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client fails to improve. It is not generally indicated in the immediate period of emergency response, evaluation and treatment. 7. Positron emission tomography (PET) or single photon emission computed tomography (SPECT). It detects changes of metabolic injury in the brain and maybe used for differentiation of head injuries. 8. Glasgow Coma Scale (GCS). This is used to assess severity of brain injury based on responses to certain stimuli. Management 1. Medical management a. For attention and concentration 1. Amantadine (antiparkinsonian agent) allows dopamine release from neurons 2. Methylpenidate (stimulant) stimulates release of norepinephrine 3. Bromocriptine (dopamine-receptor agonist) b. For aggressive behavior 1. Carbamazepine, Tegretol (anticonvulant) used in case of seizures. It limits influx of sodium ions, inhibiting nerve impulses across cell membranes 2. Phenytoin, Dilantin(anticonvulsant)- used to prevent episodes of seizures. 3. Amitryptyline (tricyclic antidepressant) blocks epinephrine and serotonin uptake on nerve endings, potentiating norepinephrine action. 4. Mannitol (osmotic diuretic) it promotes osmosis and dieresis, which may aid in decreasing increased ICP. *Blood pressure and body temperature should be monitored. 5. Benzodiazepines, e.g. Diazepam, Valium) (tranquilizer). These drugs are used to calm the patient. c. ICP monitoring d. Mechanical ventilation e. Nasogastric intubation (NGT) f. Vital signs monitoring g. Fluid and electrolyte balance monitoring h. Maintaining ICP at low levels i. Surgery

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Craniotomy. A hole is created on the skull to expose the brain and meninges for biopsy and to relieve excessive ICP, and to remove portions for inspection and debridement. The instrument used is a craniotome. Nursing problems 1. Ineffective cerebral tissue perfusion related to increased intracranial pressure or cerebral edema Interventions: NEUROLOGIC MONITORING a. Determine factors related to individual situation, cause for decreased cerebral perfusion or increased ICP which may influence choice of interventions. b. Monitor and document neurologic status and compare with baseline, esp. during the first 48 hours to assess trends and potentials for increased ICP and is useful in determining the location, extent and progression/resolution of CNS damage. Evaluate eye opening to determine level of consciousness/arousal ability. Assess verbal response (note for alertness, orientation, and accuracy) to measure appropriate speech and content of consciousness. Assess motor response (note for purposefulness of movements) to measure overall awareness and ability to respond to externl stimuli. c. Monitor vital signs. Blood pressure (note for widening pulse pressure [WPP], systolic hypertension and/or hypotension. WPP is an ominous sign of increased ICP when accompanied by decreased LOC. Hypotension may result in cerebral ischemia. Heart rate/rhythm (note for dysrhythmias). Dysrhythmias, in absence of cardiac disease, may indicate brainstem injuries. Respirations (note rate, pattern, and rhythm). It can suggest location of cerebral insult, and need for further intervention, i.e. respiratory support. d. Evaluate pupils (note PERRLA). Pupil reactions are regulated by the oculomotor (III) cranial nerve, useful in determining if the brainstem is intact.

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e. Note presence or absence of reflexes. Altered reflexes reflect to injury and have direct implications to client safety. Loss of blink reflex suggests damage to pons and medulla, cough and gag reflexes reflects medullary damage, and presence of Babinski reflex indicate injury in pyramidal pathways of the brain. CEREBRAL PERFUSION PROMOTION a. Monitor temperature and regulate environmental temperature as indicated. Fever may suggest damage to hypothalamus. b. Monitor I&O. Weigh as indicated. Note skin turgor and status of mucous membranes. These are useful indicators of total body water, an integral part of tissue perfusion. It may lead to hypovolemia which may negatively affect cerebral pressure. c. Provide rest periods between care activities and limit duration of procedures so as not to increase ICP due to continual activities. d. Decrease extraneous stimuli and provide comfort measures (e.g. back massage, quiet environment, soft voice, gentle touch) so as to provide calming effect, promoting rest to maintain ICP. e. Teach client to avoid/limit activities such as coughing, sneezing, straining at stool/bearing down, vomiting, when possible. Reposition client slowly. Activities that increase intrathoracic or intra-abdominal pressure can increase ICP. f. Encourage SO to talk to client. Familiar voices provide relaxing effect to comatosed patients, which may help reduce ICP. g. Investigate increasing restlessness, moaning, guarding behaviors. Nonverbal cues may indicate increasing ICP or may reflect presence of pain when client is unable to verbalize complaints. h. Observe seizure activity and protect client from injury. Seizures can occur as a result of hypoxia or increased ICP. It may further aggravate increased ICP, compounding cerebral damage. i. Elevate head of bed gradually up to semi-Fowlers position, to promote venous drainage from head thus reducing cerebral edema. Note: Hypotension may compromise CPP, which may negate effects of elevating the bed. j. Administer isotonic fluids (e.g. PNSS) to maintain normal intravascular volume, systemic BP and cardiac output to maintain cerebral perfusion. k. Administer supplemental oxygen, as indicated to maintain O2 saturation >94% to reduce hypoxemia and reduce increased ICP.

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Monitor ABGs to determine respiratory sufficiency, and as well as to indicate therapy needs. m. Administer medications as indicated: Diuretics (mannitol, furosemide) maybe used to reduce cerebral trauma or ICP. Barbiturates to suppress cerebral metabolism and reduce ICP. Anticonvulsants, used in episodes of seizures in posttraumatic injury and may be continued for prophylactic therapy. Mild analgesics and sedatives (benzodiazepines), for pain and agitation relief and their negative effects to ICP. Antipyretics, in cases of fever. 2. Risk for ineffective breathing pattern related to neuromuscular impairment (respiratory center involvement), perception-cognitive impairment a. Monitor rate, rhythm, depth of respiration (note breathing irregularities). Changes may indicate pulmonary complications. b. Note competence of gag/swallow reflexes and clients ability to protect own airway, which is important in airway maintenance. This may indicate need for artificial airway/intubation. c. Elevate head of bed to facilitate lung expansion/ventilation and reduces risk of airway obstruction. d. Suction with extreme caution noting characteristics of secretion. It is required if patient is unable to maintain airway clearance. e. Monitor ABGs, to determine respiratory sufficiency. f. Administer supplemental O2, as indicated. It maximizes arterial oxygenation, and is preventive of cerebral hypoxia. If respiratory center depression, mechanical ventilation maybe required. 3. Disturbed visual or auditory sensory perception related to altered sensory reception due to neurologic trauma 4. Disturbed thought processes related to psychologic conflicts a. Evaluate and monitor changes in orientation, ability to speak, mood/affect, thought processes. Upper cerebral functions are often first to be affected by altered circulation/oxygenation. Motor, perceptual, cognitive and personality changes may develop. b. Assess attention span, distractibility, noting level of anxiety. These components, when severely shortened potentiates anxiety, affecting thought processes.

l.

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c. Assess sensory awareness and responses to ensure client safety and the ability to perceive and respond appropriately to stimuli. d. Observe and document behavioral responses, to provide information needed for development of structured rehabilitation. e. Confer with SO to compare past behaviors. f. Eliminate extraneous stimuli, negative criticisms, and arguments to reduce anxiety, exaggerated emotional responses or the risk of triggering fight-flight response. g. Speak in calm, quiet voice. Use short, simple sentences. Maintain eye contact. To help client attend to communication since there may be limited attention span/understanding. h. Ascertain clients perception; provide feedback to differentiate reality in the presence of altered perceptions. i. Provide structured therapies, activities, environment to promote consistency and reassurance, reducing anxiety. j. Refer for neuropsychologic evaluation, as indicated which maybe useful indetermining therapeutic interventions for cognitive and neurobehavioral responses. 5. Risk for imbalanced nutrition: less than body requirements, related to increased metabolic demands, fluid intake restriction, altered ability for food intake and weakness (due to decreased LOC) a. Assess ability to chew, swallow, cough, and handle secretions to determine choice of feeding options. b. Auscultate bowel sounds, noting decreased or hyperactive sounds to determine response to feeding. c. Weigh patient, to evaluate effectiveness or need for change in nutritional therapy. d. Provide for feeding safety, elevate head of bed when feeding to reduce risk of aspiration. e. Promote pleasant, relaxing environment and socialization during meals, especially when assistance is acquired. It may improve intake and normalize the life function of eating. f. Check stools and vomitus for blood, bleeding (Cushings ulcer) may occur. g. Monitor laboratory studies, to identify nutritional deficiencies, organ function and response to therapy. h. Start enteral feeding once stabilized. 6. Risk for injury related to disorientation, restlessness and brain damage

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a. Assess for cause of restlessness, to determine what stimuli should be eliminated. b. Use padded side rails or wrap hands in mitt to c. Avoid restraints when possible, as straining against them increases ICP. d. Minimize environmental stimuli to allow relaxation and to reduce anxiety. e. Orient patient frequently, explaining where the patient is and what is being done to promote a sense of reality and to allay anxiety.

Prepared by: Aurelio, Sheriza Kate A. Rambaud, France Ejay V. Saupan, Rogelio Jr. T. BSN III-A

Prepared for: Mr. Benedicto C. dela Cruz, RN Clinical Instructor 03 February 2012

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