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Module III Review I. GLASCOW COMA SCALE page 2240 Three areas assessed: A) Eye opening a. 4 - Spontaneous: Person spontaneously opens their eyes. b. 3 - To voice: Person opens their eyes when spoken to. c. 2 - To pain: Person opens eyes in response to pain. d. 1- None: Person doesnt open their eyes. B) Best verbal response a. 5 - Oriented: Person. Place and time b. 4 Confused: will not answer a question c. 3 - Inappropriate words: using words or talking about something else; not in the same conversation with you d. 2 - Incomprehensible sounds: moaning, groaning, etc. e. 1 - None: C) Best motor response a. 6 - Obeys command: moves arms or legs upon command; touch nose with finger b. 5 - Localizes pain: moves to where the pain is located c. 4 - Withdraws: withdraws from pain d. 3 - Fexion: decorticate e. 2 - Extension: Decerebrate (deepening brain injury compared to decorticate) f. 1 - None: Total can be 3 15 and a score of 7 or less is considered coma. Nursing assessment also includes A) Evaluate the patients LOC B) Vital signs C) Compare previous assessments with your assessment HESI HINT Use of the Glasgow Coma Scale eliminates ambiguous terms to describe neurologic status, such as lethargic, stuporous, or obtunded. NURSING ALERT! If the patient begins to emerge from unconsciousness, every measure that is available and appropriate for calming and quieting the patient should be used. Any form of restraint is likely to be countered with resistance, leading to self-injury or to a dangerous increase in ICP. Therefore, physical restraints should be avoided if possible; a written prescription must be obtained if their use is essential for the patients well-being. NURSING ALERT! The body temperature of an unconscious patient is never taken by mouth. Rectal or tympanic (if not contraindicated) temperature measurement is preferred to the less accurate axillary temperature. II. DOLLS EYES PHENOMENON: Oculocephalic reflex (Dont attempt if suspect cervical spine injury) A) Intact: eyes deviate to opposite direction in which the head is turned B) Not intact (abnormal): eyes remain midline and move with the head indicating brain stem injury Caloric Test: Eyes deviate to side being assessed as in checking temp in ear (Normal); (Abnormal) eyes dont deviate. III. PATHOPHYSIOLOGY: A) Increased ICP result of the amount of: brain tissue; intracranial blood, CSF B) Monro-Kellie hypothesis: Increased volume of any one of those 3 contents above. The increase of one will change the volume of the other two contents. C) Causes of Increased ICP: increased intracranial blood volume, increased CSF volume, increased brain tissue bulk (i.e. may have brain tumor, etc.- no room for expansion and will have herniation if not treated)

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D) Normal compensatory mechanism: within certain limits, the body can compensate, but it has a limited window of opportunity (time). If no treatment is available, compensation runs out and the person can expire. IV. SIGNS OF INCREASED ICP A) Indications of increased ICP: B) S/S: change in LOC (early sign), H/A, N/V change in vitals (Cushings triad late signs) increased systolic blood pressure, widening of the pulse pressure, bradypnea & bradycardia - compensatory mechanism has run out - Changes in level of responsiveness is the most important indicator of increased ICP - Changes in vital signs: a. Slowing of respirations or respiratory irregularities b. Increase or decrease in pulse c. Rising BP or widening pulse pressure d. Temperature rise - Vomiting (projectile) - Pupillary changes reflecting pressure on optic or oculomotor nerves a. Decrease or increase in size or unequal size of pupils b. Lack of conjugate eye movement c. Papilledema HESI HINT Even subtle behavior changes such as restlessness, irritability or confusion, may indicate increased ICP NURSING ALERT The earliest sign of increasing ICP is a change in LOC. Slowing of speech and delay in response to verbal suggestions are other early indicators. V. MANAGEMENT OF INCREASED ICP A) Immediate management based on reducing the size of the brain by 1) decreased cerebral edema 2) lower CSF 3) decreased blood volume B) Goals accomplished by: 1) Administering osmotic diuretics and steroids 2) Restricting fluids 3) Draining CSF 4) Controlling fever 5) Reducing metabolic demands 6) Hyperventilation with mechanical ventilation MEDICAL MANAGEMENT: A) Reduce volume of bulk of brain, via surgical removal. (i.e. clot or tumor) B) Osmotic diuretics: Mannitol, Glycerol and Urea; used to reduce edema; Mannitol removes fluid from normal brain tissue, not the edematous tissue, making room for the edematous tissue to decrease the ICP. May use a loop diuretic (Lasix) with Mannitol. Note: patient is critical and they will have a Foley. You will want to monitor their urine output. Note: blood pressure drops, so they can severe hypotension, therefore, you really need to monitor the vital signs.

VI.

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Drug Mannitol (Osmitrol) Indications Acts on renal tubules by osmosis to prevent water reabsorption. In bloodstream, draws fluid from the extravascular spaces into the plasma. Adverse Reactions Disorientation, confusion, and headache Nausea & vomiting Convulsions and anaphylactic reactions Nursing Implications Use for short-term therapy only Never give to clients with cerebral hemorrhage IV infusion is usually adjusted to urine output; filter and watch for crystals Never give to clients with no urine output (anuria); if output is <30 mL/hr; accumulation can cause pulmonary edema and water intoxication

C) Corticosteroids Decadron helps reduce the edema around the trauma area or around the area of the tumor, the area that is causing the increased ICP. Look at S/E: (big-mega doses) 1. Monitor glucose BBGs since this will put the patient in hyperglycemia sliding scale insulin may be needed not due to diabetic, but because of the use of steroids. 2. Increased risk of infection 3. GI bleeds gastritis seeing a lot of Nexium IV push being given because patients under physiologic stress are at risk for developing some type of gastritis because as the body is under stress it automatically produces more gastric acid in the stomach. Solu-Medrol is used to reduce brain edema. It can increase glucose and increase the risk for stress ulcers. Phrophylactic antibiotics are also used. D) CSF drainage: burr hole through the skull and put in catheter into the ventricle of the brain and remove blood and CSF to reduce some of the volume within the skull E) Mechanical ventilation: hyperventilating the patient causes respiratory alkalosis which causes vasoconstriction of the cerebral arteries. (last resort under very controlled situations) F) Temperature control because fever increases cerebral metabolism; increase in temperature will increase in ICP. It aggravates it. May not necessarily use an antipyretic. You may use other measures such as a cooling blanket, etc. G) High dose barbiturate therap:; barbiturates increase cerebral vascular resistance, therefore, decreasing cerebral blood flow to the brain. Common barbiturates used are: pentobarbital and thiopental. HESI HINT CSF leakage carries risk for meningitis and indicates a deteriorating condition. Because of CSF leakage, the usual signs of increased ICP may not occur. VII. NURSING INTERVENTIONS A) Morphine/narcotics are contraindicated. It can cause changes in the patients pupil size and alter the assessment. Codeine may be used instead to alleviate headaches associated with ICP. Narcotics can further increase the pressure. B) Maintain patent airway. Pre-oxygenate prior to suction. C) Semi-Fowlers position HOB elevated to 30 degrees to enhance venous return and you want the head in neutral alignment. D) Maintain regular bowel program. Do not want the patient to strain. Make sure the patient is on stool softners.Do not want to initiate the valsalva maneuver because this leads to increased ICP. E) Monitor the IV fluids to make sure the patient isnt in overload. The more volume on board = the more volume that is going to circulate, which can increase the ICP. F) Passive exercise. Active exercise not wanted because of contraction because it can increase the blood pressure and the ICP.

HESI HINT Try not to use restraints; they only increase restlessness. Avoid narcotics because they mask the

level of responsiveness.

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Activities that increase ICP: 1. Change in bed position for caregiving and extreme hip flexion 2. Endotracheal suctioning 3. Compression of jugular veins (keep head straight and not to one side). 4. Coughing, vomiting, or straining of any type (no Valsalva: increased intrathoracic pressure increases ICP). Collaborative Problems/ Potential Complication for ICP 1. Brain stem herniation Results from an excessive increase in ICP in which the pressure builds in the cranial vault and the brain tissue presses down on the brain stem This increasing pressure on the brain stem results in cessation of blood flow to the brain, leading to irreversible brain anoxia and brain death. 2. Diabetes insipidus Result of decreased secretion of antidiuretic hormone (ADH). The patient has excessive urine output, decreased urine osmolality, and serum hyperosmolarity. Therapy consists of administration of fluids, electrolyte replacement, and vasopressin therapy. 3. SIADH Result of increased secretion of ADH. The patient becomes volume-overloaded, urine output diminishes, and serum sodium concentration becomes dilute. Treatment includes fluid restriction (<800mL/day, with no free water), which is usually sufficient to correct the hyponatremia. VII. POSTURING - the presence of abnormal flexion and extension; occurs with severe brain dysfunction A) Decorticate posturing involves adduction and flexion of the upper extremities, internal rotation of the lower extremities, and plantar flexion of the feet. Abnormal flexion arms flex and come towards the core of the body adducted; legs are fully extended and internally rotated B) Decerebrate posturing involves the extension and outward rotation of the upper extremities and plantar flexion of the feet. Arms are stiff and extended, the hands hyperpronated, teeth are clenched and plantar flexion of the feet. This is a deeper dysfunction than decorticate. There is a very poor prognosis for the patient. MONITORING ICP (page 2172-2174) ICP monitored by measuring CSF pressure within the lateral ventricle, the subarachnoid space, and the epidural space. Purpose is to: 1) Identify increased pressure early in the course before cerebral damage occurs 2) Quantify the degree of abnormality 3) Initiate appropriate treatment 4) Provide access to CSF for sampling and drainage 5) Evaluate the effectiveness of treatment Ventricular Catheter Subarachnoid Screw Epidural Monitoring Fiberoptic Transducer Tipped Catheter

IX.

A) B) C) D)

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HEADACHES Headache is a symptom rather than disease state. May indicate organic disease (neurologic or other disease), a stress response, vasodilation (migraine), skeletal muscle tension (tension headache or a combination of these). Primary headaches no organic cause can be identified. Includes: migraine, tension-type, and cluster Secondary headaches a symptom associated with an organic cause, such as brain tumor or an aneurysm Various classifications Muscle/Tension Headache Migraine Headache Cluster Headache Temporomandibular Joint Pain: Unilateral facial pain either at the TMJ or it can be referred pain at any point on the face and neck. Its causes are usually associated with malocclusion, joint disease (i.e. arthritis), or trauma. Bruxism (grinding of the teeth) or clenching of the teeth make it worse. Temporal Arteritis (Cranial arteritis): Inflammation of temporal arteries S/S: fatigue, malaise, weight loss, fever, Very classic to this: heat, redness, tenderness and pain over the involved artery Visual problems or blindness may occur from ischemia of involved structures. Thrombosis of the central retinal artery. Treatment: Corticosteroids (to prevent blindness) and (PRIMARILY) analgesics for comfort MIGRAINE HEADACHES: pg 2198 KNOW DEFINITION!!! Symptom-complex characterized by periodic and recurrent attacks of severe headache. The cause is primarily a vascular disturbance that occurs more commonly in women and has strong familial tendency. Onset: primarily in youth (i.e. puberty or 20s); often occurs during a change in pace such as a weekend, holiday, surprise of some kind, going to college, taking a new job, etc. Migraine Personality: compulsive, perfectionist, sensitive to criticism, ambitious, and rigid Pain is unilateral due to vasodilation of the superficial arteries (persists/throbbing) Causative factor: basically combining the vasoconstriction initially to the vasodilation and what happens is that the blood vessels stretch, putting pressure on the nerve ending, which causes pain. (fatigue, hunger, bright lights) Characterized by: aura (patient can usually sense that the headache is coming from tingling, dizziness, flash of light, etc. Note: during the aura phase, medication, such as Imitrex, can be given to abort the headache Duration: can last an hour or up to several days Recovery phase: The patient may want to be left alone, lie down in a dark room, they dislike noise. As the headache subsides the patient will go into a sleep that can last for a period of time due to exhaustion from the headache. Patient can also have nausea and vomiting with the headache. Medication can be given during the aura phase, before the headache begins in order to abort it. Precipitating factors: Certain foods containing tyramine, monosodium glucamate, milk products or nitrate may trigger headaches. Tyramine is in foods that contain a vasoactive monoamine and have the potential for raising blood pressure.

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Environmental conditions: changes in weather, noise levels, or glare, etc. (antihypertensive, antianginal drugs) Some medications: such as oral contraceptives or nitroglycerin can accentuate the headache. Mental and emotional excitement: surprises, sudden startle Fatigue, hunger, smoking, alcohol

Treatment: trying to abort it through medication during the aura phase; get the meds on board before the patient gets a full-blown headache. Look at predisposing factors and eliminate them. (Use warm or cool compresses) Ergotamine preparations (po,sl,sq,IM,R,or inhalation): If given early, they can be effective in stopping the headache. The key is that it must be taken with 30 minutes if not during the aura before headache gets full blown. Once the headache is a full-blown migraine, these medications are of very limited benefit to these patients. Ergotamine tartrate acts on smooth muscle, causing prolonged vasoconstriction of the cranial blood vessels. Side effects: paresthesias of fingers and toes, muscle pain in extremities, nausea and vomiting, weakness in the legs, and bradycardia. Contraindications: (Look at if the headache is caused by vasodilation, what is the effect of the medication? Vasoconstriction) - hyptertension, CAD, pregnancy, peripheral vascular disease. (impaired hepatic & renal function) Cafergot a combination of ergotamine and caffeine can be utilized if given early Sumatriptan (Imitrex) common drug used for treatment. Patient will have a prescription for this and will be taken during the aura. May have tingling/numbness in extremities and this can be very frightening to them. Management between attacks: Prevention employs daily use of one or more agents that are thought to block the physiologic events leading to an attack. Most widely used and important drug for prevention of migraine: Inderal: Propanolol 40mg tid-qid Do not stop abruptly and monitor pulse! Beta-blocker inhibits the action of beta-receptors cells in the heart and brain that control the dilation of blood vessels. (Heart rate, blood pressure) Sansert: Methysergide maleate 2 mg bid or tid (not used often because of side effects) Thought to inhibit or block (antagonist) the effects of serotonin, a substance possibly involved in mechanism of vascular headaches. Side effects: Blood dyscrasia (most serious), edema, weight gain, numbness, tingling. Contraindications: (anything you wouldnt want vasoconstriction in) peripheral vascular disease, hypertension, renal disease, hepatic disease Nursing Implication: Must have a 1-2 month drug holiday every 6 months to prevent potential long-term complications such as retroperitoneal fibrosis and pleuropulmonary and cardiac fibrosis. (gradually take them off then, start them back on it) NOTES

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CLUSTER HEADACHES A form of vascular headache; more common in men; NO AURA. (Facial flushing) Incidence: Unilateral pain of short duration which subsides abruptly. Very classic to being unilateral it is also localized behind the eye watering of eye and nasal congestion. Can last 15 minutes up to 1 hour or 2; Patient will be up walking the floor rather than quiet in a dark room. More often at night rather than in the day and can wake the person up from a sound sleep. (Person would rather pace than rest) Treatment: some of the same medications, precipitating factors are the same as for Migraine Headaches** Cluster headaches differ from migraine headaches in the following ways: There is no vomiting and rarely nausea. There is no significant family history It affects many more men than women There is no menstrual relationship There are no neurological deficits except for ocular sympathetic paralysis The average frequency of attacks is greater than that of migraine Nocturnal attacks are more frequent than in migraines There is no demonstrable decrease in serotonin at the onset of an attack as there is in the migraine. MUSCLE CONTRACTION HEADACE (tension headache) Causative factor: result of sustained contraction of the muscles of the neck and scalp, face, and upper back. (Such as sitting in the same position for a period of time) It is thought that when muscles are kept in a prolonged state of contraction, blood supply to the muscle becomes diminished and metabolic wastes begin to accumulate. Characteristics: Feels like a band-constricting around the top of the head; steady and constant feel of pressure; back of neck up the base of the skull Treatment: neck massage, discontinue whatever is causing it; analgesics/muscle relaxants. (Tylenol, ASA, Codeine, Darvon) (remove stimuli; warm heat) CVA Pathophysiology: Cerebrovascular disease refers to any functional abnormality of the CNS caused by a pathologic condition of the individual cerebral vessels or of the cerbrovascular system. Includes any disorders of any of the vessels which furnish blood to the brain. As the brain tissue has insult, this area is where you get your symptoms. Edema occurs with insult to the brain tissue. Incidence: primarily with elderly; children with sickle cell; people with hypertension Risk factors: 1) modifiable (diet, weight, smoking also includes disease process: hypertension, diabetes, heart disease 2) non-modifiable (age, gender, race) MODIFIABLE RISK FACTORS FOR ISCHEMIC STROKE
Hypertension (controlling hypertension, the major risk factor, is the key to preventing stroke) Atrial fibrillation Hyperlipidemia Diabetes mellitus (associated with accelerated atherogenesis) Smoking Asymptomatic carotid stenosis Obesity

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Excessive alcohol comsumption

Pathological causes of CVAs: 1) Cerebral thrombosis most common 2) Cerebral embolism 2nd most common 3) Cerebral ischemia 4) Cerebral hemorrhage a. Epidural b. Subdural c. Intracerebral d. Subarachnoid 1. Cerebral thrombosis: clot that occludes a vessel; it usually doesnt develop abruptly; travels until it gets wedged; TIAs in half the cases red flag. (Can occur at rest or on arising) Major causes: atherosclerosis and the building up of the plaque S/S: consciousness may or may not be lost the vessel may not be totally occluded, headache uncommon at onset, possible dizziness, mental disturbance, convulsions/seizures, degree of involvement depends on rapidity of onset, size of lesion and presence of collateral circulation. (Wont know improvement until edema subsides) 2. Cerebral Embolism: edema in area; embolism can be fat or blood; usually lodges in the middle cerebral artery branch or carotid. (necrosis/edema of brain tissue) Major causes: heart is closely associated, blood pooling in the heart can lead to clotting Risk factors: MI, atrial fibrillation, pulmonary infections S/S: rapid in onset: * not related to activity (may want to ask patient or family member what they were doing prior to this); usually do not have a TIA; headache before consciousness is lost; extent of damage depends on size of damage and where it is located. 3. Cerebral Ischemia: page 2210 Insufficiency of blood supply to the brain (not total occlusion); due mainly to atheromatous constriction of the arteries supplying the brain Most common manifestation is TIA (may precede a stroke or due to atherosclerotic disease)**

Transient Ischemic Attacks: Transient or temporary episodes of neurological dysfunction commonly manifested by a sudden loss of motor, sensory, or visual function, lasting a few seconds or minutes but no longer than 24 hours. Red flag advanced stages of atherosclerotic heart disease. (warning of impending stroke) (Percantine, ASA, hemorrhage) 4. Cerebral Hemorrhage: Stroke caused by cerebral hemorrhage is rapid in development, typically occurs during activity. It can also be due to sudden rise in BP, rupture of cerebral aneurysm, or AVM (arterial venous malformation) S/S result from either compression of cranial nerves or brain tissue puts pressure- displacing brain tissue Severe headache, nuchal rigidity, tinnitus, dizziness, hemaphoresis, hemaplegia, visual disturbances (loss and diplopia), seizure activity. (bleeding within head irritates meninges causing nuchal rigidity) Events that may precede cerebral hemorrhage: severe occipital or nuchal headache (neck back of head and down neck); vertigo or syncope; parasthesia in extremities, nose bleeds, retinal hemorrhages GREATEST RISK: 7th DAY!! a. Epidural (extradual) hemorrhage: outside the dura mater; usually result of brain injury and usually involves the middle menigeal artery (rupture); if patient is not treated within hours of insult, there is very little chance of survival due to rapid progression of pressure on the brain. b. Subdural hemorrhage: Small vessels with venous tears; chronic primarily elderly due to this area of brain taking longer time for hematoma to develop. (Elderly can take months before showing symptoms)

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c. Intracerebral hemorrhage: happens within the brain tissue, usually arterial Causes: aneurysm and hypertension; depends on how much area and duration S/S: onset usually rapid, severe headache at time of hemorrhage; nuchal rigidity due to meningeal irritation; nausea; vertigo; and loss of consciousness. Keep the client quiet and inactive because can occur during activity.*** d. Subarachnoid hemorrhage: subarachnoid space Common causes: hyptertension, trauma, AVM S/S: sudden shooting pain in back of eye; severe headache feels explosive; nausea, can have immediate loss of consciousness, nuchal rigidity. Page 2225 (Lumbar Puncture find blood in CSF) Diagnositic studies to differentiate cause of CVA: want history what occurred at time, was there any trauma involved, describe the headache; Neuro Glasgow coma scale; Skull series if there is evidence of trauma involved; EKG, decreased cardiac output, etc.; EEG electrical activity; CT; MRI; PET scan Pg. 2225 Interventions: The specific cause of a persons stroke needs to be identified, because treatment and prognosis vary with the cause. Pharmacologic Treatment: e. Diuretics decrease cerebral edema page 2211 f. Antiplatelet aggregation therapy Nursing Alert: garlic and Ginko increase bleeding Aspirin an antiplatelet aggregation medication Persantine may be used for long-term therapy; prevents platelets from adhering to one another S/E: headache, dizziness, feinting, weakness, hypotension, N/V/D, skin rash Other meds: Plavix, Ticlid c. Anticoagulant Therapy Heparin and coumadin d. TPA can revitalized the penumbra area - a contraindication = recent surgery and active bleed. TPA works by binding to fibrin and converting plasminogen to plasmin, which stimulates fibrinolysis of the atherosclerotic lesion. Rapid diagnosis of a stroke and initation of thrombolytic therapy (within 3 hours) in patients with ischemic stroke leads to a decrease in the size of the stroke and an overall improvement in functional outcome after 3 months. ELIGIBILITY CRITERIA FOR t-PA ADMINISTRATION 18 years or older Clinical diagnosis of ischemic stroke Time of onset of stroke known and is 3 hours or less Systolic blood pressure 185 mmHg; diastolic 110 mmHg Not a minor stroke or rapidly resolving stroke No seizure at onset of stroke Not taking Coumadin Prothrombin time 14 seconds or INR 1.7 Not receiving heparin during the past 48 hours with elevated partial thromboplastin time Platelet count 100,000/mm3 No prior intracranial hemorrhage, neoplasm, arteriovenous malformation, or aneurysm No major surgical procedures within 14 days No stroke, serious head injury, or intracranial surgery within 3 months No gastrointestinal or urinary bleeding within 21 days Surgical intervention for ischemic strokes: page 2224

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Carotid Endartectomy Removal of an atherosclerotic plaque or thrombus from the carotid artery to prevent stroke in patients with occlusive disease of the extracranial cerebral arteries. Head in neutral position; HOB elevated; assess vitals and re-assess; neuron assessment; operative site to look at Endarterectomy Postoperative Care post-op care important during the first 24 hours. Nursing diagnosis, Nursing Assessment and Nursing Care: Alteration in Cerebral Tissue Perfusion related to increased ICP secondary to CVA increased ICP can be a manifestation in contra lateral (opposite) side of CVA. Assessment immediately after a severe cerebral hemorrhage paralyzed on a side, cheek will blow out on expiration, patient is unconscious; breathing difficult; face reddish color; pulse slow and bounding; pressure elevated (the longer the coma, the poorer the prognosis)** Acute care of CVA due to Cerebral Hemorrhage complete bed rest; quiet and inactive; avoid flexion of neck; prevent valsalva maneuver Preventing ICP, causes increase in blood pressure** 3 main causes of death with CVA: (inc ICP) 1. pneumonia 2. re-rupture of an aneurysm 3. brain herniation CLINICAL MANIFESTATIONS: 2206, 2008 A. Obtain baseline data B. KNOW THIS!!! C. D. E. Perceptual Disturbances lesions in the parietal and temporal lobe may interrupt visual fibers of the optic tract and produce visual defects. i. Homonymous hernianopsia loss of half of visual field affected side of visual corresponds with paralyzed side of body. (temporary OR permanent; one-sided neglect) Seizure activity give anticonvulsant Emotional lability cant control emotions; use distraction to divert their attention Agnosia inability to sense impressions i. Auditory inability to identify or recognize sounds they could recognize before ii. Tactile inability to identify through touch Assess for right-sided VS left-sided brain damage 1. 2208, 2209 GET THEM TO REPEAT/DEMONSTRATE TEACHING Right-sided brain damage/left sided paralysis: contralateral response a. Spatial-perceptual deficits: inability to judge distance is an example, size or position; may mis-button clothes, lipstick put on crooked, etc. b. Behavioral style: impulsive and goes too fast; have one-sided neglect; problem with visual field (homonymous hemianopsia), may eat from only one side of plate; trouble interpreting things (poor judgment of abilities NO cognizant awareness of deficit)** Left Brain damage/right sided paralysis a. Speech language deficits

2.

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b. Receptive aphasia when patient can talk, but cant receive the information. Difficulty understanding words. Must be spoken to in short increments at a time.** c. Expressive aphasia cant express themselves d. Behavioral style slow and cautious. e. Dysarthria difficulty in speech secondary to paralysis of muscles responsible for producing speech. Page 2213: Major goal of care in acute phase is directed toward life saving measures. Prevention of long term complications and rehabilitation should begin immediately. Assess movement relieve pressure Prevent external rotation of hip Prevent clawlike contracture deformity Prevent footdrop Bladder control Assess sensations Maintain skin integrity Speech therapy to regain communication BRAIN TUMOR LECTURE OUTLINE INCIDENCE: Brain tumors arise in all age groups and in both sexes, although they have a biphasic age distribution, peaking between the ages of 5 and 8 years, and again between 55 to 60 years of age; males are at slightly higher risk than females. Children are more likely to develop tumors of the cerebellum, whereas 90% of all tumors in adults are located above the tentorium. There is a higher incidence of whites than blacks.. Classification of intracranial tumors 1. TISSUE ORIGIN a. Neural.neuroma b. Connective..glioma c. Meninges.meningio d. Blood vessels..angio e. Glands.adenoma 2. LOCATION a. supratentorial b. infratentorial 3. RELATION TO BRAIN a. Intrinsic b. Extrinsic Most common tumor to metastasize to the brain: cancer of the lung, followed by cancer of the breast Metastases spread via the arterial system to form lesions in the cerebrum or cerebellumusually in the area supplied by the terminal branches of the middle cerebral artery. BRAIN TUMOR ASSESSMENT The signs and symptoms vary greatly according to type and location of the tumor .features which are common to all tumors: (change in LOC, nausea, inc systolic (widening pulse pressure) dec HR & Resp.) 1. S/S of increased ICP 2. focal disturbances (diplopia) (EDEMA OF OPTIC NERVE, VISUAL ACUITY PROBLEMS, etc)

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Begin your assessment by taking a complete history. - from patient - from family members Follow the history with a complete neuron examination. - Primary tumors can arise in any tissue of the brain. - Secondary tumors are a result of metastasis from other areas (most often from the lungs; followed by breast) Classification of tumors according to the tissue where they originate: 2302 (most common is headache)*** 1. Tumor arising from covering of the brain meninges.(meningioma) - 15% of brain tumors - Benign extrinsic - Slow growing - Presents between ages 30-60 - Females greater than males - Presenting s/s vary according to the tumor location - Prognosis: can pretty much remove the whole thing curable 2. Tumor involving cranial nerve (neuroma) Acoustic Neuroma page 2302 involves the cranial nerve VIII eventually will put pressure of the CN V trigeminal - 5% of intracranial tumors - Benign, intrinsic Symptoms: vertigo, tinnitus, nerve deafness Prognosis: if diagnosed early, can be completely removed; Can have facial paralysis. Brain Tumor: HESI HINT Benign tumors continue to grow and take up space in the confined area of the cranium, causing neural and vascular compromise in the brain, increased intracranial pressure, and necrosis of brain tissue. Even benign tumors must be treated because they may have malignant effects. 3. Tumor arising form the glial (glioma) - Always intrinsic develops within the brain itself - Infiltrating - Most common type of tumorcomprise between 40-50% of intracranial tumors - Usually malignant - Female to male ratio is 2:1 Prognosis: poor cant be cured, will re-occur because of all of tentacles throughout tissue. Two main types of Gliomas: Astorcytomas graded 1 thru 4 in order of severity. - 40% of all gliomas - Grades 1 and 2grow slowly - Grades 3 and 4 grow rapidly - Grade 4 is most malignant; also called glioblastom multiform: - Can occur at any age - Adults usually in cerebrum - Children usually in cerebellum Medulloblastomas - Highly malignant, rapid growing - 10% of the gliomas - Frequently in children * Not curable * Penetrating * Cannot remove entire tumor

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Seeds through CSF Most commonly located in cerebellum 4. Tumor of blood vessels (hemangioma) Hemangioblastoma.also called angioblastoma - tumor of immature blood vesselsforms a cyst, the tumor itself remaining as a little nodule in the cyst wall. Incidence: Symptoms: (usually form in cerebellum) vertigo; visual problems; as ICP increases, can have mystagnis, nuchal rigidity, positive rhomberg Prognosis: curable 5. Tumor of the ductless glands (adenoma) Pituitary gland tumor tumor sitting on top of the pituitary gland - Compromise between 7-10% of IC tumor - Pituitary function may be increased if decreased by the presence of a tumor - Increased function secondary to increased secretion of the growth hormone. o Accelerates growth: hyperpituitarism o Children: giantism o Adults: acromegaly o Cushings syndrome: moonface, buffalo hump, hypoglycemia, obese trunk - Decreased function secondary to tumor presence in the anterior portion of the pituitary gland. o Hypopituitarism o Marked adiposity and loos of sexual function o Loss of libido, sterility, impotence, amenorrhea o Loss of visionpressure on optic nerve - Surgery: transsphenoidal hypophysectomy (2181- incision made under lip in nasal cannul, maxillary gingiva..) Symptoms according to site/location The site or location of any of the tumors can be identified by assessing the dysfunction of the brain other sites cannotdue to silten areas of the brain Frontal Lobe Tumor s/s: bifrontal headache, changes in mood, personality emotions, expressive aphasia, hemophoresis, hemaplegia, seizures (also unexpected use of obscene language) [impaired judgement] Temporal Lobe Tumor: problems with short-term memory, hemanoxia, psychomotor seizures, receptive aphasia [auditory hallucinations] Parietal Lobe Tumors: [sensory loss] parasthesia (hypo to hyper) sensitivity to touch Occipital Lobe Tumor: homonymous hemaniopsia, flashes of light Pineal tumor (tumor of the ductless glands) - Produces symptoms by growth and can cause obstructive hydrocephalus due to pressure on the Aqueduct of Sylvius - Rx: shunt or radiotherapy or total removal Pituitary gland tumors - Bifrontal headache.pain radiating between two temples Tumors of the 3rd Ventricle - Symptoms arise from increase ICP Cerebellar tumor (Tendency to fall wherever lesion is in cerebellum)**

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Symptoms: unsteady gain, dizziness, intentional tremor, negative finger-to-nose, positive Rhomberg, niastagmus.

Brain tumor: diagnosis History and Neuro exam Progression of diagnostic studies: 1. 2. 3. 4. Skull x-ray - Can detect tumors containing calcium, i.e. menigioma or oligodendroglioma - Displacement of pineal gland (calcified) EEG - Abnormal waves detected in region occupied by tumor CT Scan - Can determine tumor location, shape and size; can also track the tumors response to therapy Angiography (cerebral arteriogram reveals any vessels displaced by tumor growth

Other tests: - MRI can detect tumors - Lumbar puncture often not done in establishing a diagnosis but will be done provided increased ICP doesnt exist - CSF analysis: protein usually increased; normal protein is 15-45 mg/mL; pressure increased and normal pressure is usually 60-180 mL H2O - Brain scan an abnormal amount of radioactive material will be present in area of tumor - Audiometry or vestibular function studies suspected cases of acoustic neuroma. - Visual-field testing determines the limit of peripheral vision; pituitary adenomas, meningiomas, creaniopharynigiomas, or gliomas (supratentorial tumors).frequently produce visual-field changes Nursing care planning and implementation will be the same as for any patient with increased intracranial pressure. Traditional methods of treatment for brain tumor include surgery, radiation therapy, and to a lesser degree, chemotherapy. Radiation therapy may be prescribed for lesions inaccessible to excision, as adjunctive therapy when remnants of the tumor can be removed surgically, and palliation in metastatic tumors. The objective of radiation therapy is to destroy tumor cells without injury to normal onestumor cells are more radiosensitive than non-tumor cells. - Observe for signs of increasing ICP - Probably be on steroids prior to and during treatment - Alopecia - Skin reaction - N/V - Drowsiness - Itching - Fatigue - Adequate nutritional intake - Thrombocytopenia - Leucopenia Chemotherapy - Drugs with certain pharmacologic properties cross the blood-brain barrier to concentrate within the brain tumors. - Side effects: N/V, leucopenia, thrombocytopenia, erthyrocytopenia

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Radiation and chemotherapy require management of side effects and assessment for tolerance. - Patients with N/V/D may require o Fluid replacement o Antiemetics o Antidiarrheal meds o Monitoring of CBC to note hemopoietic depression may requires: whole blood, packed cells, platelets If dangerously low white countmay require reverse isolation Avoid crowds and people with infections Planned periods of rest Diet high in protein, iron, vitamin C Monitor for easy bruising: gums that bleed, petechiae, hematuria, tarry stools Use soft toothbrush, electric razor Brain Tumor: prognosis An untreated brain tumor inevitably leads to death, either from progressively increasing ICP or from primary brain damage Brain tissue doesnt regenerate The earlier the tumor is recognized and surgery performed, the better are the changes for recovery. The prognosis depends on the type of tumor, size, and its location. INTRACRANIAL SURGERY LECTURE OUTLINE Assessment and intervention pre-op Psychological assessment and intervention - Apprehensive - Reinforce and repeat the information - Different expected responses: depression and withdrawl; crying, denial, anger, acceptance - Psychological support to patient and family frightening experience - Treatments and procedures explained - Family questions - What to expect post-op o Oxygen o Suctioning o IVs o Arterial lines o Frequent neuron checks and vital signs o Cranial dressings and drainslater scrub cap, wig or turban o Foley o Transfusions o Periorbital edema and ecchymosis o Leg exercises o Deep breathing Baseline neurological assessment and intervention - Knowledgeable of the patients symptoms preoperativelyto determine if patients condition worsens, improves or stays the same. - Other pre-operative anticipatory measures o Pre-op steroids to decrease brain edema o Foley o Prophylactic Dilantin o TED hose HESI HINT Craniotomy preoperative medications:

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Corticosteroids to reduce swelling Agents and osmotic diuretics to reduce secretions (atropine, Robinul) Agents to reduce seizures (phenytoin) Prophylactic antibiotics

APPROACHES anytime brain is manipulated watch for increased ICP (allows expansion of inoperable tumor) - Craniectomy portion of skull is removed to accommodate cerebral edema (do not put patient on operative side) - Cranioplasty repair or a cranial defect o Indications: cosmetic effect as well as protection to brain o Precautions: - Observe dressing for bleeding and CSF leakage - Observe dressing for increasing tightness, indicating edema - Do not allow patient to lie on portion of the head where the skull has been removed - Take precautions not to accidentally hit the head - Do not remove dressing without an order strict aseptic technique - Craniotomy surgical opening of the skull to gain access to intracranial structures o Supratentorium above the tentorium into the supratentorial compartment o Infratentorium below the tentorium into the infratentorial (posterior fossa) compartment Postoperative nursing management - Monitor for sings of increased ICP 2184 - Establish and maintain adequate airway and ventilation - Maintain body alignment after suprotentorial o HOB elevated 15 to 30 degrees according to doctors orders o Position client on side or back to facilitate drainage** o If tumor is large, and removed, patient must not be placed on the affected side because of displacement of brain tissue due to gravity. o Neutral head position, can have pillow, but no neck flexion, head is flat, not on their back** o Assess surgical dressing for: [Large pillow behind head/shoulders] CSF leakage DEXTROSE STICK** Excessive bleeding [Reinforce any dressings] -Meningitis** Do not change dressings until ordered - Infection** Ventricular drainage Purpose: to drain excess CSF and to prevent increased ICP monitor the drainage for CSF and/or blood Monitor elimination Provide for patient comfort o Headache may persist for 24 to 48 hoursattributing to stretching or irritation of the nerves of the scalp that occurs during surgery Activities to avoid: coughing, sneezing, straining, vomiting (can give antiemetic), suction IC surgery complications: Meningitis: due to irritation of the meninges due t infection in the subarachnoid space or due to prolonged use of intracranial monitoring devices 2nd/3rd day post surgery S/S: headache + Kernigs Chills + Brudzinski Fever Irritability Delirium Nuchal rigidity Convulsions Soreness of skin and muscles Increased cells in CSF P/I: Strict aseptic technique Antibiotics

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Seizures give prophylactic meds - greater risk of seizures with supratentorial surgery - P/I: Padded side rails Side rails Dilantin prophylactically - Status epilepricus occurrence of prolonged seizures without recovery of consciousness Stress Ulcers hyperacidity of gastric secretions can cause gastritis with ulceration and frank hemorrhage Diabetes insipidus surgery in the area of the hypothalamus and pituitary gland causes edema and interferes with the production of antidiuretic hormone, resulting in excessive urinary output. o o S/S: excessive urination (5-10mL); dilute urine (specific gravity of 1.001 to 1.006); excessive thirst P/I: fluid replacement and vasopressin

IC surgery Transsphenoidal hypophysectomy approach Indication: pituitary tumor Procedure: - incision is made in the maxillary gingival - tumor cavity is packed with muscle or fat taken from the thigh, or lower abdomen. - nasal cavities packed with Vaseline gauze with bacitracin ointment..2-3 days - upper gums sutured - moustache dressing under nose to hold the packing in place P/I: - patient in high Fowlers position to promote venous drainage and prevent bleeding - replacement hormones and steroids - no nasopharyngeal suctioning Diabetes Insipidus caused by edema of the pituitary stalk from surgical manipulation resulting in failure of the posterior pituitary to secrete ADH temporary. Diapid Nasal Spray after packing removed and tissues healed (7 days for sutures in upper gum to absorb, and at least one month is required for healing of nasal mucosa). Patient teaching: - Not to bend over, to prevent placing undue pressure on the graft site that could dislodge the graft - Mouth breathing until nasal packing removed - No nose blowing, sneezing or coughing - No tooth brush

Postoperative complications: Hypothyroidism Hypoglycemia CSF lead [Dextrose stick positive at risk for meningitis]** SEIZURES 2190 DEFINITION A seizure disorder is a sudden alteration in normal brain activity that causes distinctive changes in behavior and body function. (Hesi: Uncontrolled electrical discharges of neurons in the brain.) Seizures are frequently symptoms of an underlying illness. They may accompany a variety of disorders, or they may occur spontaneously without any apparent cause.

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Seizures resulting from systemic and metabolic disturbances are not considered epilepsy if the seizures cease when the underlying problem is corrected. CLINICAL MANIFESTATIONS The preferred method of classifying seizures is the International Classification System proposed in 1970 and revised in 1981. It is based on the clinical and EEG manifestations of seizures. Seizures are divided into TWO major classes: 1. generalized 2. Partial 1) GENERALIZED SEIZURES: entire brain affected at onset; no warning or aura; loss of consciousness from seconds to minutes can occur in tonic clonic motions; cyanosis, excess salivations, tongue and cheek biting, incontinence, no memory or activity a. The most common generalized seizure is the gran mal seizure (tonic clonic) Characterized by: tonic loss of consciousness 1. generalized stiffeningof entire body 2. clonic jerking spasm followed by relaxation (Post muscle soreness, very tired, may sleep for hours)** Some persons may not feel normal for several hours or days after a seizure. The client has no memory of the seizure activity. b. Absence or petit mal seizures usually occurs only in children and rarely continues beyond adolescence. It may cease altogether as the child matures, or it may evolve into another type of seizure. Characterized by: brief staring spells that last only for a few seconds; can have up to 100 episodes a day and may also experience twitching of facial muscles. (problem progressing in school) 2) PARTIAL SEIZURES: Begin in a specific region of the cortex, as indicated by the eEG and by the clinical manifestations. May be confined to one side of the brain and remain partial or focal in nature, or may spread to involve the entire brain, culminating in generalized tonic-clonic seizure. S/S: Automatism lip smacking, picking at clothes, walking away from conversation. Partial seizures further divided into those with: a. simple motor (Jacksonian) b. those with complex symptoms (psychomotor) involves temporal lobe Simple partial seizures: only a finger or hand may shake or mouth may jerk uncontrollably. Person may talke untintelligibly, may be dizzy, and may experience unusual or unpleasant sights, sounds, odors, or tastes, but without loss of consciousness. Status Epilepticus state which seizures recur in rapid excession 2197 Complex partial seizures: person either remain motionless or moves automatically but inappropriately for time and place, or may experience excessive emotions of fear, anger, elation, or irritability. Person doesnt remember the episode when it is over. May have lip-smacking; Automatism: inappropriate behavior such as picking an clothing, fumbling with objects, or walks away while being talked to Valium, Ativan, Cerebryx Halt seizures immediately; Dilantin, Phenobarbital - Maintenance Other complications are severe injury and even death to trauma suffered during a seizure. Death can result from head injury incurred in a fall, drowning in a bathtub, or from severe burns.

HESI HINT Do not use tongue blade, padded or not, during a seizure. It can cause traumatic damage to the oral cavity.
PSYCHOSOCIAL: Attitudes have improved in recent years, but still carries social stigma.

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It used to be associated with supernatural powers, possession by the devil and insanity. Today the stigma probably exists because of the characteristics of seizures are in direct conflict with modern societal values of self-control, conformity, and independence. DIAGNOSTIC STUDIES Aimed at determining type of seizures, their frequency and severity and the factors that precipitate them. MANAGEMENT: *page 2192* SEE NURSING MANAGEMENT DURING A SEIZURE IN BRUNNER Observe and record sequence of symptoms Nature of seizure usually indicates type of treatment used. Nursing care During Seizure a. Provide privacy and protect the patient from curious onlookers. (The patient who has an aura may have time to seek a safe, private place) b. Ease the patient to the floor, if possible c. Protect the head with a pad to prevent injury (from striking a hard surface). d. Loosen constrictive clothing. e. Push aside any furniture that may injure the patient during the seizure. f. If the patient is in bed, remove pillows (to open airway)** and raise side rails. g. If an aura precedes the seizure, insert an oral airway to reduce the possibility of the patients biting the tongue or cheek. h. Do not attempt to pry open jaws that are clenched in a spasm or to insert anything. Broken teeth and injury to the lips and tongue may result from such action. i. No attempt should be made to restrain the patients during the seizure, because muscular contractions are strong and restraint can produce injury. j. If possible, place the patient on one side wit head flexed forward, which allows the tongue to fall forward and facilitates drainage of saliva and mucus. If suction is available, use it if necessary to clear secretions Nursing care after seizure: a. Keep the patient on one side to prevent aspiration. Make sure the airway is patent. b. Make sure the airway is patent. [stay with patient, allow to sleep] c. There is usually a period of confusion after a grand mal seizure. d. A short apneic period may occur during or immediately after a generalized seizure. e. The patient, on awakening, should be reoriented to the environment. f. If the patient becomes agitated after a seizure (postictal), use calm persuasion and gentle restraint. Things to have ready in the hospital room for seizure patient: Oxygen and suction apparatus available Privacy provided as soon as possible Side rails up and padded Oxygen tubing Patient in side-lying position (immediately postseizure) Bed in lowest position Pillow under head Loose clothing for client Chronic management: g. medication must be taken regularly and continuously h. Teach family members

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i. Medical-alert items PHARMACOLOGICAL MANAGEMENT: 2194 The primary goal of antiepileptic drug therapy is to obtain maximum seizure control with a minimum of toxic side effects. The principle of drug management is to: control rather than cure seizures Serum levels of the drug: decreased levels can cause seizures to start occurring again; manifestation of drug toxicity are variable, and any organ system may be involved. Monitor therapeutic drug levels. Monitor therapeutic drug levels regularly every 6 months** Side effects of antiseizure medications may be divided into three groups: 1. idiosyncratic or allergic disorders, which manifest primarily as skin reactions 2. acute toxicity, which may occur when the medication is initially prescribed 3. chronic toxicity, which occurs late in the course of therapy If seizure control is not achieved with a single drug, a second drug is used. Primary drugs for generalized tonic-clonic and partial seizures: a. phenytoin (Dilantin) b. carbazepine (Tegretol) c. Phenobarbital d. Primidone (Mysoline) e. Divalproex sodium (Depakote) Primary drugs for absence, akinetic, and myoclonic seizures: a. ethosuximide (Zaronitn) b. divalproex sodium (Depakote) c. clozaepam (Klonopin) NURSING ALERT Nurses must take care when administering lamotrigine (Lamictal), an antizeizure medication. The drug packaging was recently changed in an attempt to reduce medication errors, because this medication has been confused with Lamisil, Trandate, Epivir, Ludiomil, and Lomotil. Patients with epilepsy are at risk for status epilepticus from having their medication regimen interrupted.

HESI HINT Medication noncompliance is the most common cause of increased seizure activity. Drugs
Phenobarbital (Luminal)

Indications
Tonic-clonic and partial seizures Is the longest acting of common barbiturates Usually combined with other drugs Tonic-clonic and parital seizures

Adverse Reactions
Drowsiness Nystagmus Ataxia Paradoxic excitement Gingival hyperplasia Dermatitis Ataxia Nausea, anorexia Bone marrow depression Nystagmus (causes drowsiness, discolors urine (brownish) EXPECTED!)

Nursing Implications
Therapeutic levels, 15 40 mcg/mL Avoid rapid IV infusion Monitor BP during IV infusion

Phenytoin (Dilantin)

Therapeutic levels 10 to 20 mcg/mL Monitor any drug interactions Ensure meticulous oral hygiene Monitor CBC Report to MD if any rash develops For IV administration, flush IV before and after with normal saline only Do not administer with milk

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Fosphenytoin sodium (Cerebyx) Generalized convulsive status epilepticus Prevention and treatment of seizures during neurosurgery Short-term parenteral replacement for phenytoin oral (Dilantin) Rapid IV infusion can cause hypotension Severe: ataxia, CNS toxicity, confusion, gingival hyperplasia, irritability, lupus erythematosus, nervousness, nystagmus, paradoxic excitement, Stevens-Johnson syndrome, toxic epidural necrosis Hepatotoxicity, especially in children less 2 years old Prolonged bleeding times GI disturbances Hepatitis Agranulocytosis Use for short-term parenteral use only Should always be prescribed and dispensed in phenytoin sodium equivalents Prior to IV infusion, dilute in D5W or NS to administer solution of 1.5 to 25mg PE/mL Infuse at IV rate of no more than 150 mg PE/minute Monitor liver function Potentiates Phenobarbital and Dilantin, altering blood level Therapeutic levels: 50 to 100 mEq/mL Monitor liver function while on therapy Therapeutic level: 6 to 12 mcg/mL Withhold drug if rash develops Do not discontinue abruptly

Valproic acid (Depakene)

Absence seizures Myoclonic seizures

Carbamazepine (Tegretol)

Lamotrigine (Lamictal)

Tonic-clonic mixed seizures Drowsiness Ataxia Partial seizures Tonic-clonic seizures Absence seizures Absence seizures Myoclonic seizures

Clonazepam (Klonopin)

Dizziness Headache Nausea Rash Drowsiness Hyperactivity Agitation Increased salivation

Therapeutic levels of 20 to 80 mcg/mL Do not abruptly discontinue drug Monitor liver function, CBC, and renal function periodically.