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Neurological Assessment Wejdan Khater, RN, PhD JUST-School of Nursing Nursing 409-Fall 2014-2015 1 Learning Outcome Describe the elements of a focused assessment of a patient with an intracranial dysfunction. Neurologic Assessment One of the most important aspects of caring for a patient with a neurological disorder, is ongoing and accurate neurological assessment. This establishes the patient's baseline neurological status. Four Objectives of a Neuro Assessment 1. Gather data about the functioning of the nervous system 2. Correlate and trend the data over time 3. Analyze the data to develop a list of potential or actual diagnoses 4. Determine the effect of dysfunction on the patient’s daily activities of living 4 History Chief complaint History of present illness Past medical history Family history Personal and social history Review of systems Assessment-Review of Systems HEENT Dizziness, headaches, vision changes, sensitivity to light, auditory changes, sinus infections, difficulty swallowing, hoarseness, slurred speech, infection. Cardiovascular Palpitations, history of coronary artery disease, vascular problems. Respiratory History of chronic pulmonary disease, episodes of shortness of breath, recurrent infections. 6 Assessment-Review of Systems Genitourinary Incontinence, impotence Gastrointestinal Nausea, vomiting, diarrhea or constipation, weight loss, history of GI problems Musculoskeletal Weakness or paralysis, decreased range of motion, muscle stiffness or pain, spinal problems 7 Assessment-Review of Systems Neurological Syncope, confusion, difficulty with concentration, speech problems, paresthesias, tremors, gait disturbances. Psychiatric History of psychiatric problems, mood swings, delusions or hallucinations. 8 Physical Exam Mental status Motor function Motor strength and coordination Pupillary changes Cranial nerve function Vital signs 9 Physical Exam Mental status: Includes tests to evaluate level of consciousness and arousal, orientation to the environment, GSC. Thought content. The Mini-Mental State Examination (MMSE). Maximum points 30…<20 neurological Impairment. Orientation, calculation, recall, language, attention, registration 10 Responsivity Categories Question Is the following statement true or false? The Glasgow Coma Scale is a reliable tool for assessing arousal and level of consciousness in all patients. Answer True Rationale: In instances in which brain injury is suspected, the Glasgow Coma Scale (GCS) has proved a reliable tool for assessing arousal and level of consciousness. The GCS allows the examiner to record objectively the patient’s response to the environment in three major areas: eye opening, verbalization, and movement. Glasgow Coma Scale (GCS) GCS assesses both the level of consciousness, and motor response to a stimulus. Reliable as long as: It has been obtained prior to intubation. Either prior to the initiation of sedating medications, or when medications have been paused for the neurological exam. Glasgow Coma Scale Physical Exam Mental status/ thought assessment: Attention Digit span forward & back. Remembering. Short-term: recall after 5 minutes. Long-term: recall events of previous day. Feeling (Affect). Facial & body expression & mood. Verbal description of affect. Congruence of verbal, body indicators of mood. Language. Spontaneous speech, repetition, naming objects, writing, reading. Thinking. Orientation, information, knowledge of current events, calculations, problem solving. Spatial Perception. Copy drawings, demonstrate putting a coat, using a toothbrush; point out right & left side. 16 Physical Exam Motor function Motor response to stimuli: Localization to stimuli Withdrawal Decorticate Vs Decrebrate: Decorticate rigidity due to lesions to: Internal capsule, basal ganglia, thalamus, corticospinal pathways. Decerebrate rigidity due to injury to: Mid brains & Pons. Flaccidity Tonic Vs clonus 17 Motor Responses to Pain Physical Exam 19 Question When assessing motor strength, which score indicates the patient moves an extremity against gravity? – – – – A. 0/5 B. 1/5 C. 3/5 D. 5/5 Answer C. 3/5 Rationale: A score of 3/5 means the patient moves against gravity but cannot overcome resistance of the examiner’s muscles. Motor Function Scale Motor function scale 0/5 to 5/5; 0/5 no muscle contraction 1/5 flicker or trace of contraction 2/5 moves but cannot overcome gravity 3/5 moves against gravity but cannot overcome resistance 4/5 move w some weakness against resistance 5/5 is normal power and strength. Physical Exam Motor function Motor strength and coordination: Muscle weakness is a cardinal sign of dysfunction in many neurological disorders. Muscle groups should be assessed individually, initially without resistance and then against resistance. 23 Physical Exam Motor function Motor strength and coordination: The nurse also assesses each extremity for size, muscle tone, and smoothness of passive movement. The nurse also should be alert to involuntary movements 24 Physical Exam Motor function Motor strength and coordination: Hemiparesis (weakness) and hemiplegia (paralysis) Paraplegia may result from thoracic or lumbar spinal cord or peripheral nerve dysfunctions. Quadriplegia is associated with high cervical spinal cord lesions, brainstem dysfunction, and large bilateral lesions in the cerebrum. 25 Physical Exam Motor function The cerebellum is responsible for smooth synchronization, balance, and ordering of movements. Romberg test. Finger-to-nose test (dysmetria) Rapidly alternating movement (RAM) test. (adiadochokinesia, dysdiadochokinesia) The Heel-to-shin test. 26 Pupillary Changes Examine size and shape Briskness of pupillary constriction Direct and consensual response Accommodation PERRLA, pupils equal, round, reactive to light and accommodation Pinpoint pupils: drugs, drops, damage in the pons Dilated pupils: fear, seizures, cocaine, Physical Exam Pupillary Changes: Pupils are examined for size (best specified in millimeters) and shape. Anisocoria (unequal pupils). The normal response to testing is documented The assessment of pupillary response for comatose patients is the same as for conscious patients. Pupil reactivity to light, by direct and consensual response, is easily obtained. 28 Physical Exam Pupillary Changes: 29 Physical Exam Pupillary Changes: 30 Physical Exam Vital Signs Vital sign assessment is crucial to the neurological examination. Changes in temperature, heart rate, and blood pressure are considered late findings in neurological deterioration. TEMPERATURE Normal regulation of temperature occurs in the hypothalamus. Central nervous system (CNS) fevers. PULSE An increase in ICP may lead to episodes of tachycardia and can predispose the patient to alterations in electrocardiogram (ECG) pattern. 31 Physical Exam Vital Signs: BLOOD PRESSURE Blood pressure is controlled at the level of the medulla. RESPIRATIONS Variations in respiratory pattern are commonly associated with neurological injury. Shallow, rapid respirations can indicate a problem with maintenance of a patent airway or the need for suctioning. Snoring respirations or stridor can also indicate a partially obstructed airway. Cheyne-stokes respiration 32 Vital Signs Respirations Changes indicate increased ICP, spinal cord lesion, cerebral trauma. Temperature High with CNS fever, low with metabolic causes, pituitary damage, and spinal cord injuries Pulse Increases ICP and bradycardia = herniation Blood pressure Damage to medulla or cerebral edema Cranial Nerve Function Cranial nerve I (olfactory nerve) Check ability to smell using aromatic substance. Cranial nerve II (optic nerve) Check visual acuity and visual fields. Cranial nerves III (oculomotor nerve), IV (trochlear nerve), and VI (abducens nerve) Check extraocular eye movements. Cranial nerve V (trigeminal nerve) Check corneal reflex, facial sensation with light touch, ability to clench jaw or chew. Cranial nerve VII (facial nerve) Raise eyebrows, smile, or grimace Cranial Nerve Function (cont.) Cranial nerve VIII (acoustic nerve) Weber and Rinne test for air and bone conduction Cranial nerves IX (glossopharyngeal nerve) and X (vagus nerve) Gag reflex Cranial nerve XI (spinal accessory nerve) Shrug shoulders Cranial nerve XII (hypoglossal nerve) Stick out tongue Physical Exam 36 Physical Exam Test for oculocephalic reflex response (doll’s eyes • (A) Normal response—when the head is rotated, the eyes turn together to the side opposite to the head movement. (B) Abnormal response—when the head is rotated, the eyes do not turn in a conjugate manner. (C) Absent response—as head position is changed, eyes do not move in the sockets. Abnormal or Absence of reflexes indicates brainstem dysfunction. 37 Physical Exam 38 Physical Exam Test for oculovestibular reflex response (caloric icewater test). (A) Normal response—ice water infusion in the ear produces conjugate eye movements. (B) Abnormal response— infusion produces dysconjugate or asymmetrical eye movement. (C) Absent response—infusion produces no eye movements. Positive midbrain & Pons dysfunction 39 Reflexes Sensory stimulus evokes motor response. Cutaneous reflexes graded as normal, abnormal, or absent (ie, plantar reflex) Deep tendon reflexes: biceps, brachioradial, triceps, patellar, and Achilles 4+: A very brisk response; evidence of disease, electrolyte imbalance, or both; associated with clonic contractions 3+: A brisk response; possibly indicative of disease 2+: A normal response 1+: A response in the low-normal range 0: No response; possibly evidence of disease or electrolyte imbalance Physical Exam Reflexes: Hyperreflexia is associated with upper motor neuron disease. Areflexia is associated with lower motor neuron dysfunction, such as spinal cord lesions. 41 Physical Exam Sensation: Normal sensory findings depend on an intact spinal cord, sensory pathways, and peripheral nervous system. Abnormal results may indicate damage somewhere along the pathways of the receptors in the skin, muscles, joints and tendons, spinothalamic tracts, or sensory area of the cortex. 42 Physical Exam Sensation: The inability to recognize objects by touch, sight, or sound is termed agnosia. It is impossible to perform a complete test for sensation 43 Question Which is tested by asking the patient to close eyes while the nurse moves a finger upward and then asking the patient if the finger is up or down? – – – – A. Perception of touch B. Pain C. Vibration D. Proprioception Answer D. Proprioception Rationale: Proprioception is tested by asking the patient, again with the eyes closed, to identify the direction of movement (eg, moving a finger upward and then asking the patient if the finger is up or down). The same test is performed on the other hand, as well as both lower extremities. The nurse assesses vibration using a tuning fork placed over a bony prominence. The patient is asked to identify when vibration is felt. Sensation Normal findings depend on intact spinal cord, sensory pathways, and peripheral nervous system. Perception of touch Light touch with eyes closed Pain Pin or sharp edge, moving head to toe on both sides of the body Proprioception Direction of movement of finger/toe with eyes closed Vibration Tuning fork over bony prominence Physical Exam Signs of Trauma or Infection: ■ Battle’s sign (bruising over the mastoid areas) suggests a basal skull fracture. ■ Raccoon’s eye (periorbital edema and bruising) suggests a frontobasilar fracture. ■ Rhinorrhea (drainage of CSF from the nose) suggests fracture of the cribriform plate with herniation of a fragment of the dura and arachnoid through the fracture. ■ Otorrhea (drainage of CSF from the ear) usually is associated with fracture of the petrous portion of the temporal bone. 47 Physical Exam Signs of Trauma or Infection: ■ Signs of meningeal irritation include nuchal rigidity (i.e., pain and resistance to neck flexion), fever, headache, and photophobia. A positive Kernig’s sign (i.e., pain in the neck when the thigh is flexed on the abdomen and the leg is extended at the knee) also may be present. Brudzinski’s sign (involuntary flexion of the hips when the neck is flexed toward the chest) is another indication of meningeal inflammation 48 49 Assessment Signs of Increased Intracranial Pressure: increased ICP is manifested by deterioration in all aspects of neurological functioning. Level of consciousness decreases as ICP rises. Evaluation of dysfunction in the patient`s living patterns. 50 Signs of Increased Intracranial Pressure Establish baseline neurological assessment Increased ICP Decreased LOC, restlessness, confusion, combativeness Lethargy, obtundation, coma Sluggish pupils to fixed and dilated, unequal pupils Changes in motor function Changes in VS are a late finding. Cushing's triad: increased systolic pressure, bradycardia, decreased irregular respirations Neurodiagnostic Studies Neuroradiological Techniques: Conventional radiographs of the skull and spine are used to identify fractures, dislocations, and other bony anomalies, especially in the setting of acute trauma. Spinal films allow for visualization of the spine to evaluate complaints of pain or noted motor and sensory impairment. Nursing Management….The nurse’s role involves monitoring the patient and attendant equipment during the procedure and being alert for complications related to patient position and the length of the procedure. In the spinal cord injured–patient, care should be taken to ensure stabilization of the neck by a hard cervical collar. 52 Neurodiagnostic Studies Computed Tomography: The CT scan permits more refined measurement of the density of tissues, blood, and bone in the body compared with that afforded by conventional radiographs. The denser the material (i.e., skull), the whiter it appears on the film.The less dense the material (i.e., air), the darker it appears on the film. CT scans are recommended in the initial workup of seizures, headache, and loss of consciousness, and for the diagnosis of suspected hemorrhage, tumors, and other lesions. 53 Neurodiagnostic Studies Magnetic Resonance Imaging: An MRI is superior to a CT scan in the early diagnosis of cerebral infarction and the detection of demyelinating disorders, such as multiple sclerosis. It is also helpful in diagnosing small lesions, such as tumors and hemorrhages, which might not appear on a CT scan. However, traditional CT scanning is superior for scanning for bony abnormalities, which are visualized poorly on an MRI. 54 MRI 55 Neurodiagnostic Studies Angiography and Digital Subtraction Angiography It is the only test that can reveal large and small aneurysms and arteriovenous malformations and their relationship to adjacent structures and vessels. It involves the passage of a radiographic catheter through a large artery (usually femoral) to each of the arterial vessels bringing blood to the brain and spinal cord. Radiopaque contrast dye is then injected into each vessel.56 Angiography 57 Angiography 58 Neurodiagnostic Studies Cerebral Blood Flow Studies: cerebral blood flow is evaluated most commonly by a radioisotope brain scan. A radioactive isotope, such as technetium-99m, is injected intravenously. If there is blood flow to the brain, damaged areas absorb more of the isotope than areas without damage. 59 Neurodiagnostic Studies Myelography: Myelography is a contrast study of the spinal cord and surrounding structures. It involves the introduction of watersoluble material (metrizamide) into the CSF through a lumbar puncture, 60 Neurodiagnostic Studies Electrophysiological Studies ELECTROENCEPHALOGRAPHY (EEG): a record is made of the brain’s electrical activity. EVOKED POTENTIALS: An evoked potential is an electrical manifestation of the brain’s response to an external stimulus: auditory, visual, somatic, or a combination of these. 61 Neurodiagnostic Studies Lumbar Puncture for Cerebrospinal Fluid Examination: A lumbar puncture for CSF analysis may be performed to help diagnose autoimmune disorders or infections. CSF is obtained by the insertion of an 18to 22-gauge needle between the vertebrae at the L3-4 or L4-5 levels. 62 Head Trauma Mechanisms of Head Injury Pathophysiology Assessment Management 63 Learning Outcome Explain the significance of traumatic brain injury. Mechanisms of Head Injury Acceleration injuries: occur when a moving object strikes the nonmoving head. Deceleration injuries: occur when a moving head strikes a stationary object, such as in a fall. Pentration injuries: caused by a bullet, shrapnel, or sharp object…disrupt the integrity of the skull. 65 Mechanisms of Head Injury Coup-contre coup injuries: occur when the head is struck, causing the brain to move within the cranial vault and forcibly contact the opposite pole of the skull and the region in which the initial blow was dealt. Rotationl injuries: occur when forces cause the brain to twist within the skull. 66 67 Determining Severity of Head Injury Pathophysiology Primary Brain Injury: is the result of the initial injury. Injury occuring at the time of trauma. The initial injury causes disruption of the electrical, chemical, and physical integrity of the cells in the area, leading to cell death. 69 Pathophysiology Secondary Brain Injury: encompasses the physiological response to brain injury, including cerebral edema, cerebral ischemia, biochemical changes, and changes in cerebral hemodynamics. 70 Primary Brain Injury Scalp laceration Skull fracture Basilar skull Raccoon eyes “Halo sign” Conclusion Contusion Primary Brain Injury (cont.) Epidural hematoma Subdural hematoma Intracerebral hematoma Traumatic subarachnoid hemorrhage Diffuse axonal injury Cerebrovascular injury SCALP LACERATION A scalp laceration frequently causes copious amounts of bleeding due to the vascularity of the scalp. Scalp lacerations can be sutured at the bedside or may require surgical repair, depending on the size and extent of injury. 73 SKULL FRACTURE Fractures occurring directly over blood vessels can injure them, producing an epidural hematoma. Skull fractures may be compound (i.e., occurring with an open wound) or displaced (closed wound in which the edges of the fracture no longer meet), or they can be linear. 74 SKULL FRACTURE Depressed skull fractures are fractures in which bone is pressed into the dura; this is often felt as a depression or dip on palpation. Basilar skull fractures occur at the base, or floor, of the skull, typically in the areas of the anterior fossa and middle fossa. 75 SKULL FRACTURE Drainage of CSF from the ear or nose indicates injury to the dura. Ecchymosis (bruising) behind the ear (Battle’s sign) is a delayed sign of a basilar skull fracture in the middle fossa. CSF leaks typically heal on their own with rest; however, in situations in which the leak persists, a lumbar catheter may be placed to drain CSF. 76 CONCUSSION Classified as a mild traumatic brain injury and defined as any alteration in mental status resulting from trauma that may or may not involve a loss of consciousness. Cerebral concussions are not associated with structural abnormalities on radiographic imaging. 77 CONCUSSION Recovery after a concussion is usually quick and complete. some patients may exhibit symptoms of postconcussion syndrome, which include headaches, decreased attention span, shortterm memory impairment, dizziness, irritability, and emotional lability. Fatigue, noise and light sensitivity, visual disturbances. 78 Post-concussion syndrome Start 2weeks to 2 month (may last from months1years). Persistent headache. Lethargy. Personal & behavioral changes. Decrease attention. Short-term memory impairment. Care include teaching about symptoms & follow up care. CONTUSION A cerebral contusion is a focal injury that ranges in severity according to the size and extent of brain tissue injury. Focal neurological deficits may occur with small lesions, whereas multiple or large contusions may result in depressed level of consciousness, abnormal posturing, and coma. 80 CONTUSION Cerebral edema peaks at 24 to 72 hours after the injury, causing increased intracranial pressure (ICP) and possibly further injury to intracranial structures. 81 EPIDURAL HEMATOMA An epidural hematoma is a collection of blood located between the dura and the inner table of the skull, usually caused by laceration of an extradural artery. The only remedy for this injury is immediate surgical evacuation; an epidural hematoma is a neurosurgical emergency. 82 SUBDURAL HEMATOMA Is an accumulation of blood below the dura and above the arachnoid covering of the brain. Symptoms include worsening headache, focal neurological deficit, unilateral pupillary abnormalities, and a decreasing level of consciousness. A craniotomy may be performed to remove the hematoma and drains placed to facilitate drainage of the surgical site. The head of the patient’s bed may be ordered to remain flat to mitigate tension placed on bridging veins when the head is elevated. 83 INTRACEREBRAL HEMATOMA An intracerebral hematoma is a collection of blood within the brain tissue. Treatment of patients with intracerebral hematoma remains controversial regarding whether surgical intervention is warranted or medical management is more appropriate. Medical therapy aims to manage cerebral edema and promote adequate cerebral perfusion. 84 Cerebral Hematomas 86 TRAUMATIC SUBARACHNOID HEMORRHAGE Traumatic subarachnoid hemorrhage occurs with tearing or shearing of microvessels in the arachnoid layer where CSF flows around the brain. 87 DIFFUSE AXONAL INJURY Is characterized by a direct tearing or shearing of axons, which worsens during the first 12 to 24 hours as both local and diffuse edema develops. Mild DAI is associated with a coma lasting no longer than 24 hours; moderate DAI is characterized by a coma lasting beyond 24 hours with transient flexor or extensor posturing. Severe DAI is characterized by prolonged coma, fever, diaphoresis, and severe extensor posturing. 88 CEREBROVASCULAR INJURY Injury or dissection of the carotid and vertebral arteries due to trauma. Rare. 89 Secondary Brain Injury Cerebral edema Ischemia Herniation syndrome Coma Persistent vegetative state CEREBRAL EDEMA Cerebral edema commonly occurs in patients with head injuries 24 to 48 hours after the primary insult and typically peaks at 72 hours. If cerebral edema is not aggressively treated, it causes herniation syndrome. 91 ISCHEMIA Cerebral ischemia comprises a serious class of secondary injury and is a major cause of morbidity and mortality. Cerebral ischemia occurs whenever blood flow is either diminished or inadequate to meet metabolic demands. The end point of unresolved ischemia is infarction or tissue death, 92 HERNIATION SYNDROME Herniation syndrome describes a state in which cerebral structures shift inside the cranium under high pressure. Cushing’s triad describes the three late signs of herniation:increased systolic blood pressure, decreased heart rate, and an irregular respiratory pattern. 93 Normal Brain Herniated Brain 94 COMA Coma is an alteration in consciousness caused by damage to both hemispheres of the brain or the brainstem. Consciousness can be placed on a continuum from full consciousness to coma, and states of coma can be subdivided into light coma, coma, and deep coma. 95 PERSISTENT VEGETATIVE STATE characterized by a period of sleeplike coma followed by a return to the awake state but with a total lack of apparent cognition. In a persistent vegetative state, the higher cortical functions of the cerebral hemispheres have been damaged permanently, but the lower functions of the brainstem remain intact. 96 ASSESSMENT Physical Examination. Diagnostic studies: Computed tomography (CT) scan. Magnetic resonance imaging (MRI). Cerebral angiography. Transcranial Doppler (TCD) ultrasonography. Neurophysiological tests include the electroencephalogram (EEG), brainstem auditory evoked responses. Jugular bulb catheter, which measures venous oxygen saturation (reflective of global oxygen delivery and consumption in the brain). 97 Physical Exam level of consciousness is the most sensitive indicator of increased ICP. Maximum stimulus must be applied to achieve the maximum patient response. The Glasgow Coma Scale. Assessment of cognitive function. Assessment of level of arousal. Assessment of the eyes. Assessment of brain stem responses. Assessment of motor function. Assessment of respiratory function. Assessment of other body system. 98 Physical Exam Assessment of cognitive function: Cognitive function is usually assessed by asking three orientation questions regarding person, place, and time. 99 Physical Exam Assessment of level of arousal: Attempt to arouse the patient simply by speaking (in the same manner as you would try to wake a person who is sleeping), then by shouting (as you would to wake a “sound sleeper”), next by shaking, and then by applying pain. 100 Physical Exam Assessment of level of arousal: A painful stimulus should be applied for 15 to 30 seconds before the patient is considered not to have a motor response because patients with brain injury may exhibit delayed responses to stimuli. 101 Herniated Brain 102 Physical Exam Assessment of the eyes: Assessment of the eyes includes evaluation of the pupils and extraocular movements, which assists in localizing regions of the brain dysfunction. The oculocephalic reflex (i.e., the “doll’s eyes) Absence of eye movement on head turning reflects brainstem dysfunction. The oculovestibular reflex. The absence of movement signals loss of function of the vestibular portion of the eighth cranial nerve as well as the brainstem. 103 Physical Exam Assessment of brain stem responses: The brainstem can be further assessed in the unconscious patient by testing corneal, cough, and gag reflexes. Cranial nerves IX and X (the glossopharyngeal and vagus nerves) exit at the level of the medulla and are responsible for the cough and gag reflexes and protection of the airway from aspiration. The cough and gag reflexes should be evaluated in both the awake and unconscious patient. 104 Physical Exam Assessment of motor function: The unresponsive patient may exhibit localization, withdrawal, or flexor or extensor posturing in response to noxious stimuli. It is important to note that a patient may exhibit one type of movement in one extremity and another type of movement in another extremity. Presence of Babinski’s reflex (upward fanning of the toes) is also observed in the patient with severe brain injury. 105 Assessment of respiratory function Numerous locations in both cerebral hemispheres regulate voluntary control over the muscles used in breathing, with the cerebellum synchronizing and coordinating the muscular effort. The cerebrum also has some control over the rate and rhythm of respiration. Cheyne-Stokes breathing is periodic breathing in which the depth of each breath increases to a peak and then decreases to apnea. central neurogenic hyperventilation…seen in patient with herniation. Apneustic breathing is characterized by respiration with a long pause at full inspiration or full expiration. Cluster breathing (gasping breathing). ataxic breathing 106 Respiratory system Management Initial assessment and treatment of the patient with a head injury begins immediately after the insult, often with prehospital care providers. Prehospital treatment of the head-injured patient focuses on a rapid systems assessment and definitive airway management. Airway management is a crucial initial step in providing care to the head-injured patient because hypoventilation is common with a decreased level of consciousness, and hypoxia and hypercarbia are extremely detrimental to the patient in the early stages of injury. 108 Management Initial mechanical ventilation strategies aim to maintain normal ventilation or a partial pressure of carbon dioxide (PaCO2) within normal limits (35 to 45 mm Hg). hyperventilation therapy if signs of cerebral herniation are present and not controlled by other initial pharmacological treatments. Management of circulation in patients with head injuries aims to promote adequate cerebral perfusion through fluid resuscitation and the use of vasopressors if necessary. Continuing management seeks to control ICP, promote cerebral perfusion, and correct the primary pathological process. 109 Management Monitoring and Controlling Intracranial Pressure: ICP monitoring is recommended for patients with severe head injury (a GCS score of 3 to 8) and CT scan abnormalities on admission. 110 ICP – What is it? ICP stands for Intra Cranial Pressure This is the pressure of the brain, Cerebrospinal fluid (CSF), and the brain’s blood supply within the intracranial space. Since The Skull is basically a closed system, an increase in volume will produce an increase in pressure. 111 ICP – What is it? Concepts of ICP management and intervention strategies are based on the principle that the skull is a rigid box. Its contents are divided into three intracranial sections: Blood maintained in the blood vessels, Cerebrospinal fluid (CSF), Brain parenchyma. 112 ICP – What is it? The brain’s ability to self-regulate is based on the Monro- Kellie doctrine of fixed intracranial volume. 113 Monro-Kellie Doctrine This doctrine states that the volume of the intracranium is equal to the volume of the cerebral blood (3% to 10%); plus the volume of the CSF (8% to 12%); plus the volume of brain tissue, which consists of more than 80% water. 114 Elevated ICP = Danger Animated GIF taken from http://www.artie.com 115 Other Problems Elevated ICP can also affect the perfusion of the brain Cerebral Perfusion Pressure Blood pressure gradient across the brain (CPP) is measured by taking the Mean Arterial Pressure (MAP) and subtracting Intracranial Pressure (ICP). (CPP = MAP – ICP). Normal: 60 - 80 mmHg Ischemia: 50 - 60 mmHg Cell Death: < 30 mmHg CBF Ceases: 0 mmHg 116 What does this mean? This shows that if the ICP goes up… and MAP stays constant… then the CPP decreases. This means the patient is not getting as much blood flow to the brain. 117 Calculating CPP Mean Arterial BP Formula SBP – DBP + DBP 3 BP = 150/70 MAP = 97 ICP = 15 150 – 70 + 70 = 97 3 97 – 15 = CPP of 82 118 Volume-Pressure Curve A = low ICP, low elastance; high compliance. Normal constant ICP; safe environment B = Increasing ICP, high elastance; low compliance. Normal ICP but a low amount of buffering capacity C = High ICP, high elastance; low to no compliance. Loss of compensatory mechanisms. *** elastance= any slight or small increase in volume cause large change in ICP. **** Compliance= any increase in volume cause slight or constant ICP. 119 What does this mean? CBF= is the amount of blood in milliliters passing through 100 gram of brain tissue in 1 minute. CBF is about 50mL/min per 100g of brain tissue. To receive normal CBF, the person need to have: Cerebral perfusion pressure of 60-100mmHg. Brain receives 750ml/min, 15-20%of cardiac output. CPP=MAP-ICP. When CPP decrease, cardiovascular system increase BP. Acceptable CO2 levels: It is a potent vasodilator, causes increased CBF, increased volume, & lead to increase ICP. MAP<160mmHg. SBP of 60-140mmHg. 120 ICP<30mmHg. Poor Outcomes Having an elevated ICP is one of the most damaging aspects of neurological trauma, and is directly related to poor prognosis. 121 Normal Values A normal ICP in an adult ranges from 0-15 mmHG. An ICP cannot surpass 40 without causing harm. Even values between 25-30 are considered fatal if they are prolonged. 122 Causes? ICP increases when the volume added to the intracranial cavity exceeds the compensatory capacity Rate and extent of increase in ICP depends on Volume of lesion Rate of expansion Total volume within the intracranial cavity Intracranial compliance (elastance) 123 Causes? Increases in Brain Volume: Space-occupying lesions: hematomas, tumors, abscesses. Edema: head injury, encephalopathy. 124 Causes? Increases in Blood Volume: Venous obstruction Vasodilation: due to hypoxia, drugs or hypercapnia Seizures 125 Causes? Increases in CSF Volume: Obstruction: stenosis, tumors Impaired reabsorption. Increased production: tumors 126 Causes? An elevated ICP can be caused by many different etiologies: Cushing’s Syndrome: Due to ischemia to the brainstem (vasomotor center), Triggers potent sympathetic response, results in peripheral vasoconstriction Cerebral edema. Herniation. Traumatic Brain Injuries Hydrocephalus Brain Tumor Severe Hypertension Venous Sinus Thrombosis 127 Pathophysiology Cranial Insult Tissue edema Increase ICP Compression of Blood vessels Decrease CBF Decrease O2 with death of brain cells Edema around necrotic tissue Increase ICP with compression of brain stem & respiratory center Accumulation of CO2 Vasodilation Increase ICP resulting from increase Blood volume death 128 Pathophysiology 129 Monitoring There are 4 main types of devices for monitoring ICP Intraventricular Catheters Fiber optic Monitors Subarachnoid Bolts Epidural Monitors 130 Intraventricular Monitoring subarachno id parenchymal . epidural subdural 131 Intraventricular Catheters Most widely used devices – Most Accurate A catheter is actually placed inside one of the ventricles (a fluid filled cavity in the brain where CSF is produced) Allows treatment and monitoring simultaneously Can be used to take out excess CSF, thereby decreasing ICP, Measures ICP, Drains CSF, Withdraw CSF, Instill medications 132 Fiber optic Monitors Relatively new technology A fiber-optic probe is inserted Into the Brain Ventricles Subdural space The probe contains a transducer on the tip that measures pressure 133 Subarachnoid Bolts These consist of an actual metal “bolt” that is inserted into the skull so that the tip is resting in the subarachnoid space Easy to install (hey… it’s what they said!) Limited accuracy Image taken from http://library.ucf.edu/Frankenstein/ 134 Epidural Monitors Recording devices that are placed into the epidural space This is a potential space that is located between the inner surface of the skull and the dura matter 135 ICP- Monitoring 136 Management Decrease stimuli Mannitol administration Respiratory support Pain relief Sedation Hypothermia Barbiturate coma Antihypertensive therapy 137 Nursing Management History Precipitating causes Increasing headache Seizures Vomiting Blurred or double vision (diplopia) Nuchal rigidity 138 Nursing Management Physical Acute Signs: Level of consciousness Motor/Sensory activity Pupil size or reaction Cranial nerves Vital signs Chronic Signs: Headache Papilledema Nausea/vomiting 139 Why does this affect RT? There are several aspects that Respiratory Therapists need to be aware of when caring for a patient that either has, or probably has, an elevated ICP 140 Sedation Agitation increases ICP, therefore it is important to keep the patient well sedated. 141 Ventilatory Strategies One of the most important treatments for high ICP is to control the ABC’s This is because hypoxemia and hypercapnia can cause the cerebral blood vessels to dilate and raise ICP even more8 Hypoxemia can also lead to a lactic acidosis, lowering pH and causing even more vasodilatory effects2 142 Ventilatory Strategies Hyperventilating a patient down to a state of hypocapnia will do the opposite of hypercapnia – it will vasoconstrict the vessels in the brain. BUT…… Image taken from http://www.trentu.ca/careers/students/selfassess.html 143 Ventilatory Strategies This limits blood flow to an alreadycompromised-brain. Also, the brain adjusts to the new level of CO2 after 48-72 hrs Meaning vessels could rapidly dilate if CO2 were to return to normal too quickly9 144 Ventilatory Strategies What about PEEP? Not unless explicitly needed for oxygenation PEEP can also increase ICP 145 Management Maintaining Cerebral Perfusion: Cerebral perfusion pressure can be managed either by decreasing ICP or increasing the mean arterial blood pressure. Evidence suggests that maintaining a cerebral perfusion pressure of greater than 60 mm Hg may reduce morbidity and mortality. Aggressive management of increased ICP is attempted with the overall goal of maintaining the cerebral perfusion pressure. 146 Management Preventing and Treating Seizures: Post-traumatic seizures occurring in the 7-day period after injury are called early post-traumatic seizures. Seizures that occur after this initial period are called late post-traumatic seizures. Phenytoin is one of the most common drugs used in the acute period. General treatment of seizures in the setting of head injury focuses on stopping the seizure as soon as possible and maintaining patient safety. 147 Management Preventing and Treating Seizures: The agents of choice for the rapid control of seizure activity are lorazepam, or diazepam. Fever in the patient with severe traumatic brain injury may increase cerebrometabolic demands and compound secondary brain injury. 148 Management Monitoring Fluid and Electrolyte Status: Patients with head injuries may experience derangements of fluid and electrolyte balance for a variety of reasons, such as the administration of osmotic diuretics, increased insensible fluid loss, and pituitary gland dysfunction causing sodium imbalance. Fluid imbalance in a patient with a head injury can be caused by mannitol therapy with inadequate fluid replacement. Bleeding should always be ruled out in the setting of hypovolemia, especially in the trauma population. 149 Management Monitoring Fluid and Electrolyte Status: Disorders of sodium imbalance are common in the head-injured patient. Hyponatremia most commonly occurs as a result of syndrome of inappropriate antidiuretic hormone secretion (SIADH) Cerebral salt-wasting syndrome may also cause hyponatremia (involves a primary loss of sodium through the kidneys and intravascular volume contraction). 150 Management Monitoring Fluid and Electrolyte Status: Diabetes insipidus is a cause of hypernatremia and hypovolemia. hyperglycemia is common in this critically ill population. 151 Management Managing Cardiovascular Complications: Invasive hemodynamic monitoring, such as arterial blood pressure and central venous pressure monitoring. Monitoring pulmonary artery pressures and cardiac output may be useful. Disorders of coagulation are a significant concern in patients with head injury (DIC). Prophylaxis of deep venous thrombosis (DVT) is an essential component to the care of these patients. Antiembolic stockings, subcutaneous heparin, and early mobilization help prevent DVT and pulmonary emboli. 152 Management Managing Pulmonary Complications: Pulmonary complications in the patient with head trauma include pneumonia, acute respiratory distress syndrome (ARDS), neurogenic pulmonary edema, and pulmonary embolus. Aspiration pneumonia is a common pulmonary complication in this population because of the loss or impairment of airway protective reflexes. potential hypoxia should also be considered. Preoxygenation, administration of lidocaine, and administration of sedation before suctioning may blunt rises in ICP and decrease associated complications.153 Management Managing Pulmonary Complications: Neurogenic pulmonary edema may result from injury to the brainstem, increased ICP, or an increase in sympathetic tone that causes a catecholamine surge at the time of trauma. 154 Management Ensuring Optimal Nutrition: Head injury is thought to cause hypermetabolic and hypercatabolic states as well as a decrease in immune competency. Patients with head injury treated with standard enteral or parenteral. Current recommendations suggest replacement of 140% of a patient’s REE (resting energy expenditure) who is not paralyzed and 100% of REE in patients who are paralyzed with formulas that contain 15% of calories as protein. 155 Management Managing Musculoskeletal and Integumentary Complications: Collaboration with other disciplines, such as occupational and physical therapy, is helpful in protecting patients from skin breakdown. Splinting of the hands and feet, especially in an unresponsive patient. Frequent turning of patients, even in the critical phase of the illness, is integral in maintaining skin integrity and facilitating pulmonary drainage. 156 Management Caring for the Family: Attention should be given to including both spiritual and cultural needs in the plan of care. Careful observation by the family for behavioral changes and difficulties. 157 Nursing Diagnosis Impaired Cerebral Tissue Perfusion related to cerebral edema Ineffective Airway Clearance related to diminished airway protective reflexes Risk for Infection related to multiple indwelling monitoring devices Impaired Skin Integrity related to physical immobilization 158 Nursing Diagnosis Imbalanced Nutrition: Less Than Body Requirements related to increased energy expenditure Acute Pain related to injury agents Disturbed Sleep Pattern related to ICU routine care and environment Interrupted Family Processes related to acute crisis Anticipatory Grieving related to uncertain prognosis and critical illness 159