Module 2 Critical Neuro Dysfunction PDF

Module 2: Care of the Patient with Critical Neurological Dysfunction  The priority concepts in this chapter are PERFUSION COGNITION PERFUSION EXEMPLAR IS STROKE Concepts THE COGNITION EXEMPLAR IS...

Module 2: Care of the Patient with Critical Neurological Dysfunction  The priority concepts in this chapter are PERFUSION COGNITION PERFUSION EXEMPLAR IS STROKE Concepts THE COGNITION EXEMPLAR IS TRAUMATIC BRAIN INJURY The interrelated concepts in this chapter are MOBILITY SENSORY PERCEPTION  TIA CVA TBI Tumors Critical Neuro Dysfunction  Warning sign” Transient focal neurologic dysfunction Brief interruption in cerebral blood flow S/S 30 mins, but may take 24 hours; treat as medical emergency Single TIAs indicate a higher risk for stroke Multiple and recurring TIAs cause permanent brain damage  Mobility Deficits: Weakness facial drooping Sensory Perception Deficits: Numbness(face, hand, arm, or leg) Vertigo Speech Deficits: Aphasia Dysarthria (slurred speech) Visual Deficits Blurred vision Double vision Blindness in one eye Tunnel Vision Cerebrovascular Accidents (CVA)/Strokes Change in normal blood supply to brain A stroke (brain attack) is a medical emergency and should be treated immediately to reduce or prevent permanent disability The brain cannot store nutrients or O2, so constant flow is necessary to maintain homeostasis. If perfusion is interrupted, cerebral tissue dies (infarction) Effects opposite side of the body Types of Stroke  Ischemic Strokes Embolic- Plaques break loose and occlude Thrombotic- vessels a blood clot that blocks a blood vessel Emboli that travel from other parts of Account for more than ½ off all strokes and (atherosclerosis) the body and lodge in the brain are commonly related to atherosclerosis (in Ischemia develops behind the carotid arteries) occlusion When the clot is sufficient size, blood flow Characterized by the SUDDEN is occluded development of symptoms Characterized by GRADUAL onset of Symptoms may resolve over a few symptoms due to the slow nature of build days, may be very short if embolisms up- several minutes to hours. are absorbed and blood flow is returned Conversion from an ischemic stroke to a hemorrhagic stroke may occur- watch for sudden hemodynamic changes Usual source of embolism is the heart Afib, Valvular disease, valve replacement, endocarditis This is why stroke patients get Echocardiograms  Hemorrhagic Subarachnoid Hemorrhage Stroke Intracerebral hemorrhage (SAH) (ICH) Blood is in the subarachnoid space- there is Severe or sustained hypertension no bleeding into the brain tissue Damage to the brain occurs from bleeding, More common of the two causing edema irritation or displacement Aneurysm (weakness in the vessel Cocaine use is one of the most common wall) reasons for sudden dramatic elevation in BP Arteriovenous malformation (AVM) Congenital defect Sudden severe constriction in these areas interrupt blood flow, reducing perfusion “Thunderclap” headache For review:  Symptoms depend on the extent and location of the ischemia and the arteries involved Sudden onset of confusion, difficulty speaking, or understanding others Sudden numbness or weakness of the face or extremities Sudden difficulty with vision Sudden onset of vertigo, trouble walking, or loss of balance Sudden severe headache with unknown cause Stroke **Continuous Monitoring with GCS (FIGURE 38.7) and NIHSS (PAGE 905) to monitor for changes in LOC** Symptom s  Left Vs Right sided symptoms- cognitive function Left Hemisphere Stroke- Dominant in most pts, Center for language, math and analytics Language Aphasia- inability to speak or comprehend Alexia (dyslexia)- difficulty reading Agraphia- difficulty writing Acalculia- difficulty with math calculations Memory- possible deficit Vision- Inability to discriminate words and letters, Reading problems, Deficits in the right visual field, Cortical blindness Behavior-Slowness, Cautiousness, Anxiety when attempting a new task, Depression or a catastrophic response to illness, Sense of guilt, Feeling of worthlessness, Worries over future, Quick anger and frustration, Intellectual impairment Hearing- no deficit Right side hemiplegia or hemiparesis Left Vs Right sided symptoms- cognitive function Right Hemisphere Stroke- proprioception, personality changes, and Altered mental status Impaired Sense of Humor Memory- Disorientation to time, place, and person, Inability to recognize faces Vision- Visual spatial deficits, Neglect of the left visual field, Loss of depth perception, Cortical blindness Behavior- Impulsiveness, Lack of awareness of neurologic deficits, Confabulation, Euphoria, Constant smiling, Denial of illness, Poor judgment, Overestimation of abilities (risk for injury) Hearing- Loss of ability to hear tonal variations Left side hemiplegia or hemiparesis If brainstem or cerebellum is involved, pt may experience quadriparesis, cranial nerve deficits, and ataxia  Types of aphasia To help communicate Expressive (or Nonfluent) with the patient with Referred to aphasia, use these as Broca's, or motor, aphasia guiding principles: Managing Difficulty speaking Difficulty writing Present one idea or thought in cognitive function- Receptive a sentence (e.g., “I am going to help you get into the chair.”). Referred to Speech and language may as Wernicke's, or sensory, Use simple one-step result from aphasia or aphasia commands rather than ask dysarthria (slurred speech). Difficulty understanding spoken patients to do multiple tasks. Aphasia is caused by actual words Speak slowly but not loudly; hemispheric damage; Difficulty understanding written use cues or gestures as dysarthria is a result of loss of words needed. motor function. Speech often meaningless Made-up words Avoid “yes” and “no” questions for patients with Mixed expressive aphasia. Combination of difficulty Use alternative forms of understanding words and speech communication if needed, such Difficulty with reading and as a computer, handheld writing mobile device, communication board, or flash cards (often with Global pictures). Profound speech and language problems Do not rush the patient when Often no speech or sounds that speaking cannot be understood  With PT/ OT, assess muscle tone: Hypotonia, or flaccid paralysis: Inability to overcome the forces of gravity, and the extremities tend to fall to the side when lifted Hypertonia (spastic paralysis): Increased muscle activity causing fixed positions or increased tone of the involved extremities. Agnosia: Inability to use an object correctly Apraxia: Inability to perform Motor Function& previously learned motor skills or commands (may be verbal or motor) Management  Sensory Function Assess for sensory changes (response to touch or painful stimuli) A, Site of lesions causing visual loss. 1, Total Unilateral inattention (body neglect) blindness left eye; 2, Bitemporal syndrome: Being unaware of the existence of hemianopia; 3, Left homonymous his or her paralyzed side (particularly hemianopia. B, Visual fields corresponding to common with strokes in the right cerebral lesions shown in A. 1, Total blindness left hemisphere) eye; 2, Bitemporal hemianopia; 3, Left homonymous hemianopia. Ptosis: Eyelid drooping Hemianopsia: Blindness in half of the visual field, resulting from damage to the optic tract or occipital lobe Homonymous hemianopsia: Blindness in the same side of both eyes Nystagmus: Involuntary movements of the eyes (can be vertical or horizontal) Paresthesia: Numbness, tingling, or unusual sensations  Managing Sensory Left Hemisphere Function May have memory deficits Reorient as needed Establish a structured routine Significantly decreased ADL function Encouragement of independence Simple easy to follow instructions Right Hemisphere Unilateral inattention: risk for injury, especially falls lack of proprioception (position sense) Teach the patient to touch and use both sides of the body. When dressing, remind the patient to dress the affected side first. Visual perceptual or spatial perceptual deficits: Depth and distance, up and down, right from left Frequent verbal, tactile cues Always approach the patient from the unaffected side, which should always be facing the door Diplopia (double vision): a patch may be placed over the affected eye and changed every 2 to 4 hours. Homonymous Hemianopsia: turn head from side to side to expand the visual field because the same half of each eye is affected. This scanning technique is also useful when the patient is eating or ambulating. Place objects within the patient's field of vision. A mirror may help visualize more of the environment. Stroke Treatments The patient with a stroke is expected to have improved cerebral PERFUSION to maintain adequate brain function and prevent further brain injury. Interventions for patients experiencing strokes are determined primarily by the type and extent of the stroke. The immediate primary role of the nurse is to manage the patient receiving treatment and continuously assess for increasing intracranial pressure. Ischemic stroke vs Hemorrhagic stroke treatments are different  Ischemic stroke IV fibrinolytic therapy (clot busters) Endovascular Interventions Time dependant- FDA 3 hours, ASA 4.5 hours Intra-arterial thrombolysis using drug therapy: with exceptions: delivers the fibrinolytic agent directly into the Age older than 80 years thrombus within 6 hours of the stroke onset. Anticoagulation regardless of international Beneficial for patients with occlusion of the middle normalized ratio (INR) cerebral artery or those who arrive in the ED after Imaging evidence of ischemic injury involving the window for IV alteplase. more than one third of the brain tissue supplied by the middle cerebral artery Mechanical embolectomy (clot removal) Baseline National Institutes of Health Stroke Scale score greater than 25 Carotid artery angioplasty with stenting History of both stroke and diabetes Complications include: Dissolves occlusions to re-establish blood flow Hyper-perfusion syndrome Increased intracranial pressure Altapase (tPA)- only drug approved for ischemic stroke treatment All procedures require careful monitoring in ICU Weight based for intensive collaborative monitoring. If hypertension is present, may need rapid Increased ICP- 48-72 hours after intervention- antihypertensive medication first (labetalol, careful monitoring for neuro changes required nicardipine) **Although the optimal blood pressure range after stroke is controversial, the primary health care provider often desires that the patient with acute ischemic stroke be slightly hypertensive, with a systolic blood pressure (SBP) between 140 and 150 mm Hg to promote cerebral tissue perfusion.** Ischemic Stroke Treatments  Hemorrhagic Stroke Treatments When the stroke is hemorrhagic and the cause is related to an AVM or cerebral aneurysm, the patient is evaluated for the optimal procedure to stop bleeding. Some procedures can be used to prevent bleeding in an AVM or aneurysm that is discovered before symptom onset or SAH. Complications of surgical procedures: Rebleeding (rupture): Hydrocephalus (increased cerebrospinal fluid is a common complication for the patient with within the ventricular and subarachnoid an aneurysm or AVM spaces): may occur as a result of blood in the CSF. Recurrent hemorrhage may occur within 24 Cannot be reabsorbed properly by the arachnoid villi hours of the initial bleed or rupture and up to because of obstruction by small clots. Cerebral edema develops, causing ventricular 7 to 10 days later. enlargement Assess for severe headache, nausea and If hydrocephalus is left untreated, increased intracranial pressure (ICP) results vomiting, a decreased LOC, and additional Signs and symptoms of hydrocephalus, which are neurologic deficits. similar to those of ICP elevation, including a change in the LOC. Clinical findings may also include headache, Potential consequences of a second cerebral pupil changes, seizures, poor coordination, gait hemorrhagic event may be catastrophic. disturbances (if ambulatory), and behavior changes. Cerebral Vasospasm (Blood accumulation in the subarachnoid space): Signs and symptoms of vasospasm may include decreased LOC, motor and reflex changes, and increased neurologic deficits (e.g., cranial nerve dysfunction, motor weakness, and aphasia). The symptoms may fluctuate with the occurrence and degree of vasospasm present. Hemorrhage-related cerebral vasospasm can result in permanent vascular changes and irreversible neurologic impairment. Joint Commission Core Measures for All CVA Patients Eight core measures are associated with the care of stroke patients by the interprofessional health care team (The Joint Commission, 2017). Venous thromboembolism (VTE) prophylaxis Discharge with antithrombotic therapy Discharge with anticoagulation therapy for atrial fibrillation/flutter Thrombolytic therapy as indicated Antithrombotic therapy re-evaluated by end of hospital day 2 Discharge on statin medication Stroke education provided and documented Assessment for rehabilitation  Damage to the brain from an external mechanical force Not caused by neurodegenerative or congenital conditions. TBI can lead to temporary and permanent impairment in COGNITION, MOBILI TY, SENSORY PERCEPTION, and/or psychosocial function Traumatic Brain Injury  Types of Direct injury: force produced by a blow to the head Injury Indirect injury: force applied to another body part with a rebound effect to the brain decreased circulation from increased ICP Progressive pressure or physical displacement of the brain tissue Shearing injury: Brain rebounds or rotates on the brainstem, causing diffuse nerve axonal injury Contusion injury: The brain may be bruised Laceration Injury: Tearing of the brain tissue as it moves over the inner surfaces of the cranium, which are irregularly shaped and sharp. Acceleration injury: caused by an external force contacting the head, suddenly placing the head in motion. Deceleration Injury: occurs when the moving head is suddenly stopped or hits a stationary object  Primary Injury Focal or Diffuse, Open or Closed Primary brain damage occurs at the time of injury and results from the physical stress (force) within the tissue caused by blunt or penetrating Open injury: force. Focal injury: the skull is fractured/ pierced by a Confined to a specific area of the penetrating object. brain and causes localized damage Brain and dura integrity is violated that can often be detected with a CT scan or MRI. Exposure to environmental Diffuse injury: contaminants Damage throughout many areas Damage may occur to the underlying of the brain. They initially are at a vessels, dural sinuses, brain, and microscopic level and not initially cranial nerves detectable by CT scan. MRI has Closed injury: greater ability to detect microscopic damage, but these The integrity of the skull is intact, areas may not be imaged until but damage to the brain tissue can necrosis occurs. still occur as a result of increased intracranial pressure.  P R I M A RY I N J U RY L E V E L S O F I N J U RY Determination of severity of TBI is the result of the Glasgow Coma Scale (GCS) score immediately following resuscitation, the presence (or absence) of brain damage imaged by CT or MRI following the trauma, an estimation of the force of the trauma, and symptoms in the injured TYPE person. CAUSED BY SYMPTOMS Mild traumatic brain injury Characterized by a blow to the head, transient confusion or Includes a wide array of physical and cognitive (MTBI) feeling dazed or disoriented, and one or more of these problems that range from headache and conditions: (1) loss of consciousness for up to 30 minutes, (2) dizziness to changes in behavior. Symptoms loss of memory for events immediately before or after the usually resolve within 72 hours. Symptoms may accident, and (3) focal neurologic deficit(s) that may or not be persist and last days, weeks, or months. transient. Persistent symptoms following MTBI are also Loss of consciousness does not have to occur for a person to be referred to as post-concussion syndrome. diagnosed with MTBI. No evidence of brain damage on a CT or MRI imaging scan. Moderate A moderate TBI is characterized by a period of loss of A short acute or critical care stay may be consciousness (LOC) for 30 minutes to 6 hours and a GCS score needed for close monitoring and to prevent of 9 to 12. secondary injury from brain edema, intracranial Often but not always, focal or diffuse brain injury can be seen bleeding, or inadequate cerebral PERFUSION. with a diagnostic CT or MRI scan. Post-traumatic amnesia (memory loss) may last up to 24 hours. May occur with either closed or open brain injury. Severe A severe TBI is defined by a GCS score of 3 to 8 and loss of Patients with severe TBI require management consciousness for longer than 6 hours. in critical care, including monitoring of Focal and diffuse damage to the brain, cerebrovascular vessels, hemodynamics, neurologic status, and possibly and/or ventricles is common. Both open and closed head intracranial pressure (ICP). Patients with severe injuries can cause severe TBI, and injury can be focal or diffuse. TBI are also at high risk for secondary brain CT and MRI scans can capture images of tissue damage quite injury from cerebral edema, hemorrhage, early in the course of this illness. reduced PERFUSION, and the biomolecular cascade.  SECONDARY INJURY- HYPOTENSION AND HYPOXIA Processes that occur after the initial injury and worsen or negatively influence patient outcomes. Most common secondary injuries are hypotension and hypoxia, intracranial hypertension, and cerebral edema. Damage to the brain tissue occurs primarily because the delivery of oxygen and glucose to the brain is interrupted from cerebral edema and increasing pressure. Low blood flow and hypoxemia contribute to cerebral edema, creating a cycle of deteriorating perfusion and hypoxic damage Patients with hypoxic damage related to moderate or severe brain injury face a poor prognosis and eventually experience decreased cognition  S E C O N D A RY I N J U RY- I N C R E A S I N G I N T RA C RA N I A L P R E S S U R E Increased Intracranial Pressure: A normal level of ICP is 10 to 15 mm Hg. Periodic increases in pressure occur with straining during defecation, coughing, or sneezing but do not harm the uninjured brain. **A sustained ICP of greater than 20 mm Hg is considered detrimental to the brain because neurons begin to die.** Leading cause of death from head traumas who make it to the hospital alive! As ICP increases, cerebral perfusion decreases, leading to brain tissue ischemia and edema. Untreated edema leads to brainstem herniation downward or laterally from a unilateral lesion within one cerebral hemisphere, causing irreversible brain damage and possibly death (brain herniation syndromes). I N C R E A S E D I N T RAC RA N I A L P R E S S U R E S C O M P L I C AT I O N S - B RA I N H E R N I AT I O N S Y N D R O M E S Uncal herniation Late findings include: dilated and nonreactive pupils, ptosis (drooping eyelids), and a rapidly deteriorating level of consciousness. In the presence of increased ICP, the brain tissue may shift and herniate downward INCREASED INTRACRANIAL PRESSURES COMPLICATIONS- BRAIN HERNIATION SYNDROMES Central herniation It is clinically manifested by Cheyne-Stokes respirations, pinpoint and nonreactive pupils, and potential hemodynamic instability. All herniation syndromes are potentially life threatening, and the physician must be notified immediately when they are suspected.  I N C R E A S E D I N T RA C RA N I A L P R E S S U R E C O M P L I C AT I O N S - H Y D R O C E P H A LU S Hydrocephalus Abnormal increase in CSF volume The ventricles may dilate from the relative increase in CSF volume. Ultimately, if not treated, this increase may lead to increased ICP.  TYPES OF CEREBRAL EDEMA Three types of edema may contribute to increased ICP: Vasogenic edema- Caused by an abnormal permeability of the walls of the cerebral vessels, which allows protein-rich plasma infiltrate to leak into the extracellular space of the brain. The fluid collects primarily in the white matter. Cytotoxic edema (metabolic)- occurs as a result of a hypoxic insult, which causes a disturbance in cellular metabolism and active ion transport. The brain is quickly depleted of available oxygen, glucose, and glycogen and converts to anaerobic metabolism. Damage to cell membranes results in cell edema, cell dysfunction, and cell death. May lead to vasogenic edema and a further increase in ICP. Interstitial edema- fluid accumulation between the cells of the brain. It is associated with elevated blood pressure or increased CSF pressure. Interstitial edema develops rapidly in the perivascular and periventricular white space and can be controlled through measures to reduce blood pressure or decrease CSF pressures INT RAC RA NIA L H E M O R RH AG E Accumulation of blood within the brain tissue caused by the tearing of small arteries and veins in the subcortical white matter Often acts as a space-occupying lesion (e.g., a tumor) and may be potentially devastating, depending on its location. May also produce significant brain edema and ICP elevations. A traumatic brainstem hemorrhage occurs as a result of a blow to the back of the head, fractures, or torsion injuries to the brainstem. Brainstem injuries have a very poor  TBI- HEMORRHAGE Injury causes a brain hematoma (collection of blood) or clot, may occur as part of the primary injury and begin at the moment of impact. It may also arise later from vessel damage. Bleeding is caused by vascular damage from the shearing force of the trauma or direct physical damage from skull fractures or penetrating injury. **All hematomas are potentially life threatening because they act as space-occupying lesions Epidural and Hematoma are surrounded by edema.** Subdural Results from arterial hematoma bleeding into the space Venous bleeding between the dura and the into the space inner skull beneath the dura It is often caused by a and above the fracture of the temporal arachnoid bone, which houses the From a tearing of middle meningeal artery. the bridging veins Patients with epidural within the cerebral hematomas have “lucid hemispheres or from intervals” that last for a laceration of brain minutes, during which time tissue. Bleeding the patient is awake and from this injury talking. occurs more slowly  SDHs are subdivided into acute, subacute, and chronic An acute SDH presents within 48 hours after impact Subacute SDH presents between 48 hours and 2 week Chronic SDH presents from 2 weeks to several months after injury **SDHs have the highest mortality rate because they often are unrecognized until the patient presents with SUBDURAL severe neurologic compromise.** HEMATOMAS  Primary tumors originate within the central nervous system (CNS) and rarely metastasize (spread) outside this area. BRAIN TUMORS Secondary brain tumors result from metastasis from other areas of the body, such as the lung, breast, kidney, and GI tract.  BRAIN TUMOR CL ASSIFICATION MALIGNANT/ BENIGN METASTATIC (noncancerous) tumors Require more aggressive are generally associated intervention, including with a favorable outcome surgery, radiation, and/or chemotherapy. Cancer cells from the lung, breast, colon, pancreas, kidney, and skin can travel to the brain via the blood and the lymphatic system. Multiple metastatic lesions are fairly common. Malignant brain tumors are seen primarily in patients 40 to 70 years of age, and the survival rate is low compared with that of other cancers Primary brain tumors are relatively uncommon; many more patients have metastatic lesions.  BRAIN TUMOR SIGNS AND SYMPTOMS Cerebral Tumors Brainstem Tumors Headache (most common feature) Hearing loss (acoustic neuroma) Seizure Facial pain and weakness Dysphagia, decreased gag reflex Vomiting unrelated to food intake Nystagmus Changes in visual acuity and visual fields; diplopia (visual changes Hoarseness caused by papilledema) Ataxia and dysarthria (cerebellar Hemiparesis or hemiplegia tumors) Apnea Hypokinesia (decreased motor ability) Bradycardia Hyperesthesia, paresthesia, Hypotension decreased tactile discrimination Seizures Aphasia Changes in personality or behavior  M A N AG I N G B RA I N T U M O R S Non Surgical Management Stereotactic Radiosurgery Surgical Management: Craniotomy Gamma knife Cyberknife Post op care is focused on preventing same complications of TBI Drug therapy Mechanical ventilation care Analgesics Watching for s/s of hormone or electrolyte imbalances (SIADH, Steroids DI, hypo/ hypernatremia) Antiepileptics PPIs  ASSESSING A TBI Airway and Breathing Pattern Assessment The first priority is the assessment of the patient's ABCs—airway, breathing, and circulation. Because TBI is occasionally associated with cervical spinal cord injuries, all patients with head trauma are treated as though they have cord injury until radiography proves otherwise. Spine Precautions/ Assessment Spine precautions require placing the patient supine and aligning the spinal column in a neutral position so there is no rotation, flexion, or extension. Spine clearance is a clinical decision made by the health care provider, often in collaboration with the radiologist. Spine clearance includes determining the absence of acute bony, ligamentous, and neurologic abnormalities of the cervical spine based on history, physical examination, and/or negative radiologic studies.  ASSESSING A TBI Vital Signs Assessment The mechanisms of autoregulation are often impaired as the result of a TBI. The more serious the injury, the more severe is the impact on autoregulation or the ability of cerebral vasculature to modify systemic pressure such that blood flow to the brain is sufficient. Monitor the patient's blood pressure and pulse frequently The patient may have hypotension or hypertension Cushings Triad, a classic but late sign of increased ICP, is manifested by bradypnea, a widened pulse pressure (increasing difference between systolic and diastolic values), and bradycardia. **This triad of cardiovascular changes usually indicates imminent death.**  ASSESSING A TBI Neurological Assessment Many hospitals use the Glasgow Coma Scale (GCS) to document neurologic status A change of 2 points is considered clinically important and requires notification to provider The most important variable to assess with any brain injury is LOC! A decrease or change in LOC is typically the first sign of deterioration in neurologic status. A decrease in arousal, increased sleepiness, and increased restlessness or combativeness are all signs of declining neurologic status. Early indicators of a change in LOC include behavior changes (e.g., restlessness, irritability) and disorientation, which are often subtle in nature. Report any of these signs and symptoms immediately to the primary health care provider! Use a bright light to assess pupillary size and reaction to light. Facial trauma may swell eyelids, making this assessment difficult. Consider whether drugs that affect pupillary dilation and constriction, such as anticholinergics or adrenergics, have been used recently.  ASSESSING A TBI Neurological Assessment Of particular importance is the ovoid pupil, which is regarded as the mid-stage between a normal-size and a dilated pupil. Asymmetric (uneven) pupils, loss of light reaction, or unilateral or bilateral dilated pupils are treated as herniation of the brain from increased ICP until proven differently. Pupils that are fixed (nonreactive) and dilated are a poor prognostic sign. Patients with this problem are sometimes referred to as having “blown” pupils. Papilledema: edema and hyperemia (increased blood flow) of the optic disc. It is always a sign of increased ICP. The patient's motor loss or dysfunction usually appears contralateral (opposite side) to the site of the lesion, similar to that of a stroke. For example, a left-sided hemiparesis reflects an injury to the right cerebral hemisphere. Posturing: Deterioration in mobility or the development of abnormal posturing (decerebrate or decorticate posturing) or flaccidity is another indicator of progressive brain injury  Decorticate- Everything move toward the “core” Caused by dysfunction in the brainstem area Decerebrate- lots of ‘E”s , hands resemble “e”s in this position. Caused by lesions that interrupt the corticospinal pathways. A S S E S S I N G A T B I - S KU L L F RAC T U R E S I G N S Neurological Assessment CSF leakage- Monitor for suspicious leakage for facial orifaces. CSF placed on a white absorbent paper or linen can be distinguished from other fluids by the ”halo sign”, a clear or yellowish ring surrounding a spot of blood. Although other body fluids can be used, a halo sign is most reliable when blood is in the center of the absorbent material because tears and saliva can also cause a clear ring in some conditions. Raccoon Eyes: Raccoon's eyes are purplish discoloration around eyes that can follow fracture of the skull's base. Battle signs: A bruise that indicates a fracture at the bottom of the skull indicating leakage **When CT scans are used with head and brain injury, these fractures are often visualized before bruising appears.**  MANAGEMENT AND TREATMENT FOR TBI Nonsurgical management: As with any critically injured patient, priority is given to maintaining a patent airway, breathing, and circulation. Providing health teaching and emotional support for the patient and family Interventions are directed toward preventing or detecting secondary brain injury and monitoring the effects of treatments and drug therapy Take and record the patient's vital signs at least every 1 to 2 hours IV fluids or drug therapy to prevent severe hypertension or hypotension Dysrhythmias Document and report the presence of cardiac dysrhythmias, hypotension, and hypertension to the primary health care provider. Obtain the target range for blood pressure and heart rate and monitor parameters. Monitor for fever. Systemic trauma, blood in the cranium, or a generalized inflammatory response to the injury ay trigger hyperthermia. Fever from any cause is associated with higher morbidity and mortality rates  MANAGEMENT AND TREATMENT FOR TBI- THERAPEUTIC HYPOTHERMIA Changes to systemic and cerebral pressures The rationale for therapeutic hypothermia is to reduce brain metabolism and prevent secondary brain injury in moderate-to-severe TBI. May be started, regardless of the presence of fever. Rapidly cooling to a core temperature of 89.6° and 93.2° F (32° to 34° C) for 24 to 48 hours after the primary injury. Rewarming slowly to a normal core temperature Watch for rapid fluid and electrolyte shifts cardiac dysrhythmias  M A N A G E M E N T A N D T R E AT M E N T O F T B I - D E T E R M I N I N G B RA I N D E AT H Four prerequisites must be met to establish a brain death diagnosis: Coma of known cause as established by history, clinical examination, laboratory testing, and neuroimaging Normal or near-normal core body temperature (higher than 96.8° F (36° C) Normal systolic blood pressure (higher than or equal to 100 mm Hg) At least one neurologic examination (some states and health care systems require two)  M A N A G E M E N T A N D T R E AT M E N T O F T B I - D E T E R M I N I N G B RA I N D E AT H Doll’s Eyes- Head turns side to side, eyes face forward- brainstem Caloric Responses- should be intact COWS Head turns and eyes follow, If not, brainstem effected brainstem effected  Patients with severe TBI often die. As the physiologic deterioration begins, keep in mind that the patient may be a potential organ donor. Before brain death is declared, contact the local organ-procurement organization per facility guidelines. Determine if the patient consented to be an organ donor. This information is typically on a driver's license or other state-issued card or advance directive. The patient's wishes should be followed unless he or she has a medical condition that prevents organ donation. The organ donor agency representative or physician discusses the possibility of organ donation with the family. Some families may not agree with the patient's decision, which can cause an ethical dilemma. Many health care agencies have an ethics specialist of committee members who can help with these situations. “Required request" law: it is mandatory to offer the option to donate organs and ORGAN DONOR AND tissues to the family of the deceased. “Required referral" law: The hospital is PROCUREMENT required to notify the OPO of all deaths, and if appropriate, in collaboration with the OPO, to advise the family of their right to donate. CASE STUDY… The spouse of a patient brought to the ED states that 6 hours ago her husband began having difficulty finding words. The patient has since become progressively worse. He has right hemiparesis. Upon assessing the patient, you note that he is lying flat in a supine position and has been incontinent of urine. What is the priority nursing intervention for this patient at this time? A. Provide perineal care. B. Assess for gag reflex. C. Elevate the head of the bed. D. Perform a linen and gown change. An hour later after a CT scan, the patient is diagnosed with a left hemisphere stroke. Which manifestations would the nurse expect? (Select all that apply.) A. Constant smiling B. Intellectual impairment C. Deficits in the right visual field D. Disorientation to time, place, and person E. Inability to discriminate words and letters THE PATIENT IS ADMITTED TO THE ACUTE MEDICAL UNIT AFTER 7 HOURS. HIS WIFE ASKS IF HER HUSBAND WILL RECEIVE IV THROMBOLYTIC THERAPY. WHAT IS THE NURSE’S BEST RESPONSE? Thirty minutes later, the wife asks for a glass of water or juice because her husband is thirsty. What is the nurse's best response? The patient’s wife must leave her husband’s bedside for 2 hours to run errands. Which nursing action is appropriate to contribute to patient safety while she is gone? A. Apply restraints. B. Maintain the bed in a low position. C. Sit with the patient until his wife returns. D. Place the call light in the patient’s right hand. The patient needs assistance with feeding but can swallow well. To whom should the nurse delegate this responsibility? A. Hospital volunteer B. Licensed practical nurse C. Certified nursing assistant D. Student nurse doing first patient care experience QUESTIONS…  A PATIENT WITH A TBI HAS NONREACTIVE AND DIL ATED PUPILS. WHAT WOULD THE NURSE ANTICIPATE? A. Loss of vision B. Brain stem herniation C. Intense headache D. Projectile vomiting  THE NURSE UNDERSTANDS WHICH SYMPTOM IS THE EARLIEST INDICATOR OF INCREASED INTRACRANIAL PRESSURE WHEN CARING FOR A PATIENT WITH A HEAD INJURY? A. Increased pupil size B. Nausea and vomiting C. Agitation and confusion D. Elevated blood pressure A PATIENT HAS EXPERIENCED A STROKE IN THE LEFT CEREBRAL HEMISPHERE. WHAT CLINICAL PRESENTATION DOES THE NURSE EXPECT? ( SELECT ALL THAT APPLY.) A. Aphasia B. Decreased proprioception C. Disoriented to time and place D. Agraphia E. Difficulty with math calculation W H I C H STAT E M E N T S A BO U T ST RO K E PR EV E N T I O N I N D I CAT E A C L I E N T ’ S U N DE R STA N D I NG O F H E A LT H T E AC H I NG BY T H E N U R S E ? ( S E L E C T A L L T H AT A PPLY. ) a. “I will take aspirin every day.” b. “I have decided to stop smoking.” c. “I will try to walk at least 30 minutes most days of the week.” d. “I need to cut down a lot on my drinking.” e. “I’m going to decrease salt in my diet.”  T H E N U R S E I S CA R I NG F O R A PAT I E N T T R E AT E D W I T H A LT E PL A S E F O L L OW I NG A ST RO K E. W H AT A SS E SS M E N T F I N D I NG I S T H E H I GH E ST PR I O R I T Y F O R T H E N U R S E ? a. Client’s blood pressure is 144/90. b. Client is having epistaxis. c. Client ate only half of the last meal. d. Client continues to be drowsy.  T H E N U R S E I S CA R I NG F O R A PAT I E N T W I T H E X PR E SS I V E ( B RO CA’ S ) A PH A S I A. W H I C H N U R S I NG I N T E RV E N T I O N I S A PPROPR I AT E F O R CO M M U N I CAT I NG W I T H T H E C L I E N T ? a. Refer the patient to the speech-language pathologist. b. Speak loudly to help the client interpret what is being said. c. Provide pictures to help the client communicate. d. Ask the client to read messages on a white board. A FA M I LY M E M B E R A S K S T H E N U R S E A BO U T W H ET H E R T H E R E WO U L D B E A N Y L O NG -T E R M P SYC H O L O G I CA L E F F E C TS F RO M A C L I E N T ’ S M I L D T R AU M AT I C B R A I N I N J U RY. W H AT I S T H E N U R S E’ S B E ST R E S P O N S E ? a. “You need to talk with the client’s primary health care provider.” b. “Usually any effects last for only a few weeks or months.” c. “Each person’s reaction to brain injury is different.” d. “You should expect a change in the client’s personality.”  A C L I E N T R E T U R N S F RO M T H E P O ST A N E ST H E S I A CA R E U N I T ( PAC U ) A F T E R A S U RG I CA L R E M OVA L O F A B R A I N ST E M T U M O R. W H AT P O S I T I O N W I L L T H E N U R S E PL AC E T H E C L I E N T I N AT THIS TIME? a. Turn the patient from side to side to prevent aspiration. b. Keep the client flat in bed or up 10 degrees and reposition from side to side. c. Elevate the head of the bed to at least 30 degrees at all times. d. Keep the client in a sitting position in bed at all times.