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1 SYNCOPE
2 SYNCOPE Sudden, transient loss of consciousness and postural tone with spontaneous recovery Often caused by loss of cerebral oxygenation and perfusion Often sign of another underlying condition Often associated with a stressful condition
3 SYNCOPE Common medical problem affecting all age groups Children, pregnant mothers, and elderly susceptible Children Missed meal Heat Dehydration Crying Exertional activity
4 SYNCOPE Elderly Postural changes Defecation Coughing Orthostatic hypotension Medications Diseases: coronary heart disease, heart failure, diabetes, renal insufficiency, chronic obstructive pulmonary disease
5 SYNCOPE Most common medical emergency in the dental office Most syncopal episodes occur during the administration of local anesthetics
6 TYPES OF SYNCOPE Cardiac syncope Noncardiac syncope Neurocardiac syncope
7 TYPES OF SYNCOPE Cardiac syncope Inadequate cardiac output Usually from underlying heart disease Commonly from arrhythmias or obstructions of the heart Potentially fatal Requires referral to medical professional
8 TYPES OF SYNCOPE Non-Cardiac syncope Seizures due to reduction of oxygen to the brain Orthostatic hypotension reduction in BP when assuming an upright position Situational occurrences coughing, urination, defecation, neck stretching, hair grooming, venipuncture, swallowing Valsalva s maneuver forced expiratory effort against a closed airway
9 ETIOLOGY OF NON-CARDIAC SYNCOPE Non-Cardiac syncope Hyperventilation excessive breathing causing change in chemical make-up of blood Can cause sufficient cerebral vasoconstriction which can lead to syncope Metabolic diseases hypoglycemia or hypoxemia
10 NEUROCARDIAC SYNCOPE Neurocardiac syncope Vasodepressor, vasavagal, neurocardiogenic, neurallly mediated Associated with some noxious stimuli Pain Fear Exhaustion Illness
11 NEUROCARDIAC SYNCOPE PATHOPHYSIOLOGY Activation of the autonomic nervous system Fight or flight response Release of catecholemines, epinephrine and norepinephrine particularly, to muscle tissues in preparation for movement with blood pumped back to heart
12 ETIOLOGY OF NEUROCARDIAC SYNCOPE Neurocardiac syncope If no movement occurs (such as with dental patients) blood pools in extremities causing hypotensive response, bradycardia, and decrease in cerebral blood flow leading to syncope
13 Figure 5.1 Types and etiologies of syncope
14 SIGNS AND SYMPTOMS OF PRE-SYNCOPE Pallor Pupil dilation Diaphoresis Excitation of piloerector muscles Weakness, dizziness, vertigo Nausea Yawning or sighing
15 SIGNS AND SYMPTOMS OF PRE-SYNCOPE Vision changes darkening, blurring, seeing spots Increased BP Shortness of breath Heart palpitations Chest pain Slow onset
16 SIGNS AND SYMPTOMS OF SYNCOPE Syncopal symptoms Unconsciousness Weak, slow pulse
17 TREATMENT OF SYNCOPE Remove objects from oral cavity Position supine with feet elevated Open airway Assess circulation Loosen tight clothing Administer oxygen, 4-6L/minute Monitor vital signs
18 Figure 5.2 Patient in appropriate position for treatment of syncope
19 TREATMENT OF SYNCOPE If unconsciousness persists summon EMS Bradycardia 0.6 mg atropine IM Longer patient in syncope more likely seizure will occur Once consciousness returns Keep in supine position until patient feels well enough to be returned to upright position and pulse returns to normal
20 Figure 5.3 Atropine
21 TREATMENT OF SYNCOPE Once consciousness returns Suspend treatment for the day Emergency contact should escort patient home as syncope can reoccur If neurocardiac syncope suspected contact EMS Thoroughly document syncope episode in chart
22
23 SHOCK DES1600 DENTAL OFFICE EMERGENCIES
24
25 PATHOPHYSIOLOGY OF SHOCK Condition produced when the cardiovascular pulmonary system fails to deliver enough oxygenated blood to body tissues to support metabolic needs (perfusion) Tissues use anaerobic metabolic processes Produces acidosis and harmful toxins
26 STAGES OF SHOCK Initial Compensatory Progressive Refractory
27 STAGES OF SHOCK Initial first stage Cells deprived of oxygen (lack of perfusion) Inhibits ability to produce energy Cells not functioning properly Impacts body systems
28 STAGES OF SHOCK Compensatory body performs physiological adaptations in an attempt to overcome shock Increased respiration to increase oxygen to cells Increased BP to compensate for hypotension
29 STAGES OF SHOCK Compensatory Reduced blood supply to peripheral organs to improve blood supply to brain Reduced blood flow to kidneys with resulting oliguria (reduced urine output)
30 STAGES OF SHOCK Progressive compensatory mechanisms begin to fail If the problem causing shock is not treated, condition will worsen Vital organs compromised and not functioning appropriately
31 STAGES OF SHOCK Refractory failure of vital organs Irreversible Cell death and brain damage have occurred Death will occur in a few hours
32 TYPES OF SHOCK Hypovolemic Shock Cardiogenic Distributive Anaphylactic Septic Neurogenic Obstructive
33 HYPOVOLEMIC SHOCK Most common form Caused by inadequate venous return Etiologies: Hemorrhage or dehydration (vomiting or diarrhea)
34 HYPOVOLEMIC SHOCK Initial symptoms: Increased heart rate Rapid, thready pulse Cool skin Reduced urine output Confusion
35 HYPOVOLEMIC SHOCK Treatment Arrest cause of hemorrhage or dehydration Supine position Contact EMS BAC s of CPR Monitor vital signs Administer oxygen 4-6L/minute Needs IV fluids to restore blood volume
36 CARDIOGENIC SHOCK Reduction in perfusion due to decreased cardiac output Etiologies MI Cardiac arrhythmias Cardiac dysfunction
37 CARDIOGENIC SHOCK Signs and symptoms Reduction in BP with systolic below 90 mmhg Fast, weak pulse Cold, clammy skin Cyanosis Non-specific chest pain Shortness of breath Reduced urine output and confusion
38 CARDIOGENIC SHOCK Treatment Supine position Contact EMS CAB Monitor vital signs Administer oxygen 4-6L/minute Needs IV fluids Cardiac medications needed
39 DISTRIBUTIVE SHOCK Vasogenic shock (caused by peripheral vasodilation) 3 types Anaphylactic Septic Neurogenic
40 ANAPHYLACTIC SHOCK Sudden, massive vasodilation and circulatory collapse following exposure to an allergen
41 SEPTIC SHOCK Vasodilatory shock Bacteria (particularly gram-negative bacilli) invades bloodstream and causes an inflammatory response to aid body in ridding itself of the invader
42 SEPTIC SHOCK Signs and symptoms Fever, vasodilation Increased cardiac output Tissue edema Pink, warm skin restlessness Tachycardia Thirst Eventual respiratory failure
43 SEPTIC SHOCK Signs and symptoms Can cause microthrombi formation Often fatal and usually seen in older individuals, individuals with poor nutritional status, neonates, critically ill, and immunocompromised patients
44 NEUROGENIC SHOCK Loss of sympathetic nerve activity from brain s vasomotor center due to an emotional trauma, disease, drug, or traumatic injury to brain or spinal cord Loss of sympathetic nerve activity causes peripheral dilation leading to reduction in venous return, thus causing decreased cardiac output with hypotension
45 NEUROGENIC SHOCK Signs & symptoms Hypotension Bradycardia Brain and kidneys at risk of failure
46 NEUROGENIC SHOCK Treatment Position supine Contact EMS CAB Monitor vital signs Administer O 2 4-6L/minute Needs drug therapy to restore cardiac output
47 OBSTRUCTIVE SHOCK PATHOPHYSIOLOGY Results from indirect heart pump failure Leads to decreased cardiac function and reduced circulation Etiologies arterial stenosis pulmonary embolism cardiac tamponade
48 OBSTRUCTIVE SHOCK Symptoms Hypotension Dyspnea
49 OBSTRUCTIVE SHOCK Treatment Position supine Contact EMS CAB Monitor vital signs Administer O 2 4-6L/minute Needs IV fluids Relieving source of obstruction essential, surgical intervention often required
50 SEIZURE DISORDERS CHAPTER 8
51 SEIZURE Temporary episode of behavior alteration due to massive abnormal electrical discharges in the brain Can be recorded on EEG May be accompanied by convulsions or other neurological, sensory, or emotional changes
52 SEIZURE Can be caused by systemic distress isolated nonrecurrent attacks Hypoxia Hypoglycemia Seizures
53 SEIZURE Can be caused by damage or disease of brain Tumors Trauma Perinatal injuries Toxins Infectious agents Electrolyte imbalance
54 SEIZURE Can be caused by damage or disease of brain Uremia Drug withdrawal Sedative hypnotics Vascular disorders
55 SEIZURE Seizure paroxysmal disorder of cerebral function with spontaneous, electric discharges from neurons in cerebral cortex Alteration in state of consciousness, motor activity, sensory phenomena, with sudden onset and a brief span of activity
56 SEIZURE Seizure paroxysmal disorder of cerebral function with spontaneous, electric discharges from neurons in cerebral cortex Epilepsy not a specific disease but a syndrome associated with seizure types Ictus or ictal refers to seizure
57 EPILEPSY Epilepsy group of disorders involving chronic, recurrent attacks of involuntary behavior and changes in neurological function Common disorder affects 0.5 2% of population 2 million in the United States Seizures most common are neurological disorders in pediatrics
58 EPILEPSY First seizure usually before age 20 Seizure not a disease, but a symptom of CNS dysfunction Classification of seizures Causes, symptoms, duration, precipitating factors, and aura Seizures not usually life threatening
59 ETIOLOGY OF SEIZURES Cellular level several theories Alterations in cell membrane permeability or movement of ions across the cell membrane of neuron Decreased inhibition of cortical or thalamic neuronal activity
60 ETIOLOGY OF SEIZURES Cellular level Changes in cell structure that alter cellular excitability Imbalances in neurotransmitters Excess of excitatory neurotransmitter acetylcholine Deficiency of neurotransmitter gammaaminobutyric acid (GABA)
61 CLASSIFICATION OF SEIZURES Two broad categories Primary/unprovoked or idiopathic Usually part of epileptic syndrome 65% of seizures are of this kind. Genetic tendency Usually require daily anti-seizure medication
62 CLASSIFICATION OF SEIZURES Two broad categories Secondary/provoked or acute symptomatic 35% of seizures are of this kind.
63 CLASSIFICATION OF SEIZURES Preventable if underlying cause is treated Metabolic disorders Injury to CNS Medications Rapid drug withdrawal CNS tumors
64 CLASSIFICATION OF SEIZURES Preventable if underlying cause is treated Vascular disorders after age 60 CVA Infections of CNS Photosensitive epilepsy children exposed to flickering lights video games
65 SEIZURES IN DENTAL SETTING Several potential etiologies Hypoglycemia Hypoxia secondary to syncope Local anesthetic toxicity Epilepsy
66 TYPES OF SEIZURES Determined by EEG pattern Some patients have more than one type.
67 TYPES OF SEIZURES Partial seizures Simple partial with no loss of consciousness
68 TYPES OF SEIZURES Partial seizures Complex partial with impairment of consciousness Partial seizures evolving into generalized seizures Simple partial seizures evolving into generalized Complex partial seizures evolving into generalized
69 SIMPLE PARTIAL SEIZURES Motor, sensory, or psychomotor changes with no loss of consciousness
70 SIMPLE PARTIAL SEIZURES Symptoms Illusions Déjà vu Flashing lights Hallucinations Tingling or creeping sensations Vertigo Sounds
71 SIMPLE PARTIAL SEIZURES Symptoms cont. Foul smells Aura sensory symptom occurring at onset of seizure Beginning of abnormal changes in focal area of brain Symptoms reflect area of brain affected Visual occipital lobe Auditory temporal lobe Amnesia often follows
72 SIMPLE PARTIAL SEIZURES Auras now considered to be a simple partial seizure with impending complex or generalized seizure
73 TYPES OF PARTIAL SEIZURES Localized motor seizure which spread up extremity Symptoms Stiffening Jerking Tingling of extremity No loss of consciousness May progress to generalized tonic-clonic seizure
74 COMPLEX PARTIAL SEIZURES Impairment of consciousness Often begin in temporal lobe, but may progress to brain (generalized) Also known as temporal lobe seizures or psychomotor seizures 33% of people with temporal lobe seizures have psychiatric disorder 10% schizophrenia or depressive psychoses.
75 COMPLEX PARTIAL SEIZURES Signs and symptoms Losing contact with surroundings a few seconds to 20 minutes Automatisms repetitive, nonpurposeful activity (lip smacking, grimacing, patting, wandering in circles, and unintelligible speech) At the end of motor activity, mental confusion or fear
76 GENERALIZED SEIZURES Electrical abnormality throughout the brain Loss of consciousness Often genetic or metabolic cause Recurrent generalized seizures epilepsy 70% one type of seizure 30% more than one type
77 TYPES OF GENERALIZED SEIZURES Tonic-clonic Absence Febrile
78 TYPES OF GENERALIZED SEIZURES Generalized tonic-clonic seizures (GTCS) Most common type of seizure disorder 90% of epileptics have GTCS. 60% of GTCS patients have this alone others have additional seizure types. Occurs equally in both sexes Any age although 60% by puberty
79 PHASES OF GTCS Generalized tonic-clonic seizures (GTCS) Specific sequence Aura Preictal Ictal Postictal
80 AURA Simple partial seizure Subjective sensation that precedes seizure activity Psychic, sensory, olfactory, visual, auditory, and gustatory
81 AURA Usually same aura Lasts only a few seconds Not all seizures preceded by auras May not remember aura due to amnesia from seizure
82 PREICTAL PHASE Soon after aura Patient loses consciousness. May fall if standing often causes injuries
83 ICTAL PHASE Tonic phase Muscles have sustained contraction patient appears rigid. Produces loud cry epileptic cry or crowing Dyspnea and cyanosis due to contraction of respiratory muscles
84 ICTAL PHASE Hypertonic phase Extreme muscle rigidity
85 ICTAL PHASE Clonic phase Muscular contractions and relaxation rhythmic, jerky movements (convulsions) Heavy, labored breathing Clenched jaw Saliva + air = froth at mouth
86 ICTAL PHASE Clonic phase Blood from biting tongue or soft tissues Two to five minutes gradually slow with final flexor jerk
87 POSTICTAL PHASE Movement stopped Patient remains unconscious CNS, CVS, and respiratory system depression CNS and respiratory may lead to airway obstruction time when death is most likely
88 POSTICTAL PHASE Muscle relaxation urinary or fecal incontinence Patient awakens confused, fatigued, wanting to sleep, amnesia Lasts for minutes to several hours Close observation essential
89 GENERALIZED ABSENCE SEIZURES Most common in children Genetic tendency Brief change in level of consciousness signaled by blinking or eye rolling Blank stare Minor facial movements blinking or mouth movements
90 GENERALIZED ABSENCE SEIZURES Lasts 5 30 seconds May recur up to 100 times a day May progress to GTCS Amnesia of episode Rare after age 20
91 FEBRILE SEIZURES Not usually true seizure 2% of cases can develop into true seizure disorder. Affects 4% of children three months five years Risk of developing other seizure disorders later in life
92 DIAGNOSIS OF SEIZURE DISORDERS Based on thorough hx, neurological exam, description of seizure Need to exclude other metabolic or systemic etiologies CT scans and MRI help detect lesions.
93 DIAGNOSIS OF SEIZURE DISORDERS EEG records changes in brain s electrical activity Helps determine prognosis and classify type of disorder Other tests Glucose, blood panels, toxicology screening, urinalysis, calcium and electrolyte studies
94 TREATMENT OF PATIENTS WITH SEIZURE DISORDERS Control of seizures with fewest side effects Drug therapy eliminates seizures in onethird of patients and greatly reduces frequency in another one-third % good seizure control
95 TREATMENT OF PATIENTS WITH SEIZURE DISORDERS Children more susceptible due to immature brain tissue. Well-controlled adults may have isolated breakthrough seizures. Often caused by sleep deprivation, extreme stress, or hormonal fluctuations Estrogen can cause seizures, so 20% of women will have an increase in seizure activity during pregnancy
96 DRUG THERAPY OF PATIENTS WITH SEIZURE DISORDERS Type of drug used based on seizure type, EEG pattern, medication s ability to control seizures, and patient s tolerance Generally Anti-Epileptic Drugs (AED s) are CNS depressants drowsiness common may impair learning and cognition. Treatment usually begins with one AED and if the patient does not respond well another drug or combination is tried.
97 DRUG THERAPY OF PATIENTS WITH SEIZURE DISORDERS Common AEDs Zarontin, lamotrigine or valproate used for absence seizures Topiramate, zonisamide and levetiracetam are used for generalized or partial seizures. Ketogenic diet (high in fat/low carbohydrates) effective for difficult to control seizures
98 PREVENTIVE STRATEGIES IN DENTAL OFFICE PREPARING FOR MANAGEMENT IF A SEIZURE SHOULD OCCUR
99
100 PREVENTIVE STRATEGIES IN DENTAL OFFICE Essential information about seizures Length of time since last seizure Types of seizures, severity, duration Presence of aura Alteration or loss of consciousness History of injuries Postictal symptoms Medications
101 PREVENTIVE STRATEGIES IN DENTAL OFFICE If not well-controlled or factors exist which would predispose the patient to a seizure that day, treatment should be postponed until more stable. Early morning appointments after a meal and within a few hours of taking medication is the optimal time for treatment.
102 PREVENTIVE STRATEGIES IN DENTAL OFFICE Use of mouth prop and removal of dentures are recommended. Clinician should advise patient to let him know if they feel onset of seizure.
103 TREATMENT OF GTCS SEIZURES Primary task is to protect patient and try to prevent injury before, during, and after Cease dental treatment. Remove instruments from mouth. Move equipment out of the way. Loosen tight clothing to assist breathing. Place in supine position.
104 TREATMENT OF GTCS SEIZURES Leave patient in dental chair and prevent falling by positioning one person at head of chair and one at foot. Contact EMS. Administer O liters/minute. (6-8 liters/minute if in respiratory distress)
105 TREATMENT OF GTCS SEIZURES CAB s of CPR maintain open airway Monitor vital signs. Gently restrain to prevent injury. Do not forcefully restrain as this can injure limbs. Do not place anything in patient s mouth.
106 POSTICTAL TREATMENT OF GTCS SEIZURES Critical Muscle flaccidity common airway protection essential Reassurance helpful
107 POSTICTAL TREATMENT OF GTCS SEIZURES Monitor vital signs to insure return to baseline. Patient may have headache and muscle soreness. Patient should never drive themselves home; he or she should be released to a responsible adult.
108 STATUS EPILEPTICUS Continuous GTCS or repetitive recurrence Life threatening May persist for hours or days Mortality 3 23% Temperature may rise to 106 F.
109 STATUS EPILEPTICUS Tachycardia and dysrhythmias BP elevated 200/150 mmhg Death occurs due to cardiac arrest, irreversible brain damage due to cerebral hypoxia. Immediate medical intervention required to prevent death IV anticonvulsant drug therapy needed
110 TREATMENT OF GENERALIZED ABSENCE SEIZURES Stop dental treatment for duration of episode. Protect airway. Remove instruments from mouth. Monitor vital signs. Continue treatment following cessation of seizure if patient has no ill effects.
111 CEREBROVASCULAR ACCIDENT CHAPTER 9
112 CVA AKA stroke, brain attack Abnormal condition of the brain characterized by occlusion or hemorrhage of a blood vessel resulting in lack of oxygen (ischemia) Leads to cell death
113 CVA Second leading cause of death worldwide 4.6 million annually United States third leading cause of death and disability 700,000 cases per year 100,000 recurrent strokes per year
114 RISK FACTORS FOR CVA Age Blacks These two groups have a higher incidence of hypertension, often the result of atherosclerosis which forms clots in blood vessels.
115 RISK FACTORS FOR CVA Atrial fibrillation Affects 2 million Americans Two atria quiver Heart pumps blood inefficiently resulting in pooling of blood leads to thrombi (blockage at point of origin). Increases risk of CVA five fold
116 RISK FACTORS FOR CVA Oral contraceptives Menopause due to estrogen changes Diabetics Familial history of CVA Carotid bruit abnormal sound in carotid artery
117 TRANSIENT ISCHEMIC ATTACKS TIA Brief episodes of neurological dysfunction caused by ischemia to brain Last less than one hour with no evidence of acute stroke
118 TRANSIENT ISCHEMIC ATTACKS 200, ,000 suffer from TIAs annually. 10% of all strokes preceded by TIA CVA often occur within first four days of TIA.
119 FIGURE 9.1 LAYERS OF THE BRAIN.
120 TYPES OF CVA Ischemic Hemorrhagic
121 ISCHEMIC CVA Blockage in cerebral blood vessel Thrombus or embolus (foreign object that at a distant site, circulates in bloodstream and becomes lodged in blood vessel) 85% CVAs 60% thrombotic; 40% embolic
122 ISCHEMIC CVA Core central zone of ischemic tissue Penumbra surrounding tissue receiving diminished blood supply Potentially salvageable if blood supply restored quickly
123 HEMORRHAGIC CVA Rupture of a blood vessel 15% of all CVAs Factors Hypertension, anticoagulation, tumor, substance abuse, and aneurysm (weakening in blood vessel wall with added pressure ruptures)
124 TYPES OF HEMORRHAGIC CVA Intracerebral Subarachnoid Much higher mortality than occlusive strokes Those that do survive have better recovery. Pressure that is causing damage gradually diminishes and brain regains some of its former function.
125 INTRACEREBRAL CVA Twice as common Occurs when defective artery within the brain bursts Surrounding tissue fills with blood. Blood places pressure on adjacent tissues. Due to ruptured artery other areas of brain ischemic leading to additional damage
126 SUBARACHNOID CVA Occurs when blood vessel on surface of brain ruptures and bleeds into subarachnoid space. Blood places pressure on cerebellum causing pressure and damage to brain cells.
127 SIGNS AND SYMPTOMS OF ISCHEMIC CVA May stop and start again as stroke progresses Severity and location of blockage influences symptoms that are exhibited Embolic strokes abrupt onset Thrombotic strokes onset often difficult to determine as symptoms not as severe
128 SIGNS AND SYMPTOMS OF ISCHEMIC CVA Altered level of consciousness (yawning to coma) loss of consciousness uncommon Pupils unequal and dilated Confusion Dizziness
129 SIGNS AND SYMPTOMS OF ISCHEMIC CVA Change in balance or coordination (ataxia) Vision changes Loss of half the visual field
130 SIGNS AND SYMPTOMS OF ISCHEMIC CVA Deviation of tongue Difficulty swallowing (dysphagia) Speech changes Poorly articulated speech (dysarthria) Impairment of speech (dysphasia) Inability to understand spoken word Inability to speak at all (aphasia)
131 SIGNS AND SYMPTOMS OF ISCHEMIC CVA Drooling Weakness, numbness, or tingling in one side of face Facial droop Numbness or tingling in arm or leg or both on one side of body (hemiparesis) Nausea or vomiting
132 SIGNS AND SYMPTOMS OF HEMORRHAGIC CVA Similar to ischemic stroke Onset abrupt and rapid Severe headache usually in occipital area twice as common in hemorrhagic CVA Increased BP Subarachnoid CVA neck pain or stiffness
133 SIGNS AND SYMPTOMS OF HEMORRHAGIC CVA Inability to stand or walk Papillary malalignment Nausea or vomiting Altered level of consciousness yawning to coma
134 STROKE SCALES Cincinnati Prehospital Stroke Scale (CPSS) Looking for facial palsy, arm motor weakness, dysarthria Ask patient to smile and observe for weakness on one side of face. Ask patient to hold out both arms palm up and eyes closed for 10 seconds to observe for weakness in one arm.
135 STROKE SCALES Looking for facial palsy, arm motor weakness, dysarthria Ask patient to repeat simple sentence such as, The sky is blue in Cincinnati and observe for difficulty in speech. If any of the three components found to be abnormal, then assume CVA.
136 STROKE SCALES Los Angeles Pre-hospital Stroke Scale Age greater than 45 years History of seizure disorder Time of onset of neurological symptoms less than 24 hours Patient ambulatory prior to event Blood glucose level between 60 and 400
137 STROKE SCALES Los Angeles Pre-hospital Stroke Scale Facial symmetry Grip strength Arm weakness determined by drift Positive responses in all areas indicate CVA
138 TREATMENT Contact EMS immediately. Position semi-supine. BLS check airway, breathing, and circulation Administer O liters/minute. Test glucose levels to rule out hypoglycemia.
139 TREATMENT Monitor vital signs. Transport to ED as soon as possible. Aspirin for ischemic CVA reduces death and recurrence rates. Aspirin for intracranial hemorrhage CVA patients also improved outcomes However, not recommended
140 TREATMENT In hospital CT scan to determine etiology Hemorrhagic probably surgery Ischemic Less than three hours onset of symptoms then IV thrombolytic therapy with altaplase (r-tpa) removes thrombus or embolus to restore blood flow Ineffective after three hours Contraindicated for hemorrhagic CVA
141 MEDICAL HISTORY Dizziness Ringing in the ears Headaches Fainting spells Blurred vision Seizures History of stroke, hardening of the arteries High blood pressure Medications Anticoagulants Antihypertensives
142 QUESTIONS?
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