2. The Skull The brain’s protector

3. Made of 8 irregularly fused bones Smooth on the outside, folds and ridges on the inner surface THE SKULL

4. The Cranial Vault

5. Foramen magnum

6. The Brain (80%)

7. Increased Brain Volume Mass Cerebral Swelling

8. Blood (10%) Normally about 750cc of circulating volume 20% of the Cardiac Output

9. Increased Blood Volume Hemorrhage Vasodilatation

10. Cerebrospinal Fluid (10%)

11.  Hydrocephalus Increased CSF Volume

12. Intracranial Pressure (ICP) The pressure exerted by the brain tissue, intracranial blood, & CSF

14. Tough Mother

15. Dura Mater Double layered Inelastic, fibrous membrane Holds the brain in place

16. Epidural Space Space that is directly above the Dura Middle Meningeal Artery is present here

19. Cerebral lobes

20. MovementImpulses Frontal lobe

21. Spoken Language Personality Frontal lobe

22. Sight UnderstandingTouch Understanding Parietal lobe

23. Distance and Position to Objects Parietal lobe

24. Temporal lobe Memory Hearing Written Words

27. Damage Causes Ipsilateral Movement

28. Pons Mid Brain Medulla Oblongata

30. ABC’s First Quick History LOC Vital Signs Pupils Early or Late? Early: restlessness, disorientation, lethargy Late: Increase BP, pupillary changes, seizures Down and Dirty

31. Assessment GLASGOW COMA SCALE Best Eye Opening Best Verbal Response Best Motor Response

32. Best Eye Opening Spontaneously-4 To Verbal Command-3 To Pain-2 No Response-1

33. Best Verbal Response Oriented, Converses-5 Disoriented, Converses-4 Inappropriate words-3 Incomprehensible sounds-2 No Response-1

34. Best Motor Response Obeys Commands-6 To Pain Localizes Pain-5 Flexion Withdrawal-4 Abnormal Flexion-3 Abnormal Extension-2 No Response-1

35. Glasgow Coma Scale Pediatrics Verbal (2 to 5 years) Appropriate words or -5 Inappropriate words-4 Persistent cries and/or screams-3

36. Glasgow Coma Scale Pediatrics Verbal (0 to 23 months) Smiles or coos appropriately-5 Cries and consolable-4 Persistent inappropriate crying and / or screaming-3

37. Mild ◦ GCS Score 14-15 Moderate ◦ GSC Score 9-13 Severe ◦ GCS Score 3-8 Severity of Injury

38. A desk scores a “3”

39. Loss of Consciousness “A,E,I,O,U TIPS” A Alcohol E Epilepsy I Insulin (too much, too little) O Oxygen (too much, too little) U Uremia or other metabolic issues T Trauma, toxicity, tumors, thermoregulation I Infections, ischemia P Psychiatric, poisonings S Stroke, syncope or other neurologic / cardiovascular causes

40. Babinski’s Reflex Present when stroking of Planter surface of foot causes Flexing of great toe Fanning of other toes Normally present in children <2yo Presence in >2yo indicates problem in corticospinal tract (nerve path spine to brain)

41. Abnormal posturing is a late sign of increasing ICP Decorticate Abnormal flexion Decerebrate Abnormal extension

42. Meningeal Signs Nuchal rigidity Stiff neck, pain on flexion Photophobia Positive Brudzinski’s Involuntary flexion of knees/hips when neck flexed Positive Kernig’s Unable to straighten leg when hip fully flexed in supine patient

43. Increased Intracranial Pressure

44. Intracranial Pressure Intracranial pressure reflects Brain Cerebrospinal fluid Blood As intracranial pressure increases, cerebral perfusion pressure decreases Leads to cerebral ischemia and hypoxia In a hypotensive patient, even a marginally elevated ICP can be harmful Adequacy of cerebral perfusion pressure is most important

45. Increased Intracranial Pressure  Initially -intracranial volume increases- ICP remains stable.  System becomes less compliant, or less able to tolerate increases in volume  Later, intracranial volume cont’s to increase, less compliance will be unable to buffer the increases and ICP will rise

46. Increased Intracranial Pressure Assessment Early picture of increased intracranial pressure (IICP) LOC Loss of insight Loss of recent memory Restless, irritable, uncooperative behavior Requires more stimulation to get same response Speech less distinct Sudden quietness in a very restless patient

47. Increased Intracranial Pressure Early Increasing ICP Motor function Usually contralateral to lesion Pronator drift Loss of one or more grades on the strength scale Increased tone

48. Increased Intracranial Pressure Early Increasing ICP Pupils Sluggish to light response Usually unilateral Ipsilateral to lesion Papilledema or bulging of optic discs Blurred vision

49. Increased Intracranial Pressure Early Increasing ICP Vital signs Occasionally tachycardic Occasional hypertensive swings

50. Increased Intracranial Pressure Late Increasing ICP LOC Arousable only with deep pain Unarousable Motor function Dense hemiparesis Abnormal flexion Abnormal extension No response (flaccidity preliminary to death)

51. Abnormal posturing is a late sign of increasing ICP Decorticate Abnormal flexion Decerebrate Abnormal extension

52. Increased Intracranial Pressure  Decreased LOC  Motor Dysfunctions  Pupillary abnormalities  Impaired Reflexes  Changes in Vital Signs  Irregular respirations Sign & Symptoms- Impending Herniation

53. Increased Intracranial Pressure Late Signs Increasing ICP Vital signs Cushing’s triad Very late sign of increasing ICP, last ditch effort to perfuse brain Elevated SBP Bradycardia Widening pulse pressure

54. Increased Intracranial Pressure Interventions ABC’s Mechanically decrease ICP Oxygenate Osmotic Agents

55. Increased Intracranial Pressure Osmotic Agents Mannitol: reduces ICP within 15 minutes with continued effectiveness for 2-3 hours Monitor serum osmolarity

56. Increased Intracranial Pressure Treatment of ICP Easiest to manipulate is BP and CSF proper head alignment sedation Surgery

57. Goal Keep SBP>90

59. Traumatic Brain Injury Injury to skull, brain, or both that is of enough magnitude to interfere with normal neurological function

60. Nearly 2 million people sustain head injuries each year

61. 70,000 die prior to hospitalization

62. TBI Another 25,000 die following hospitalization

63. 90,000 people will have significant permanent neurological disabilities for the rest of their lives

64. Traumatic Brain Injury The peak age for neurotrama is 15 to 30 years of age

65. Causes of TBI

67. Concussion Transient impairment of neurological function caused by a mechanical force Rapid acceleration-deceleration if repeated can produce a permanent deterioration in intellect recent studies suggest long term impairment even with “moderate”concussion “moderate” if loss of consciousness

68. Concussion Diagnosis CT scan Rule out other injury Clinical picture History of injury

69. Concussion Interventions Assess neuro status Patient/Family education return to facility Change in LOC Change in pupils Projectile vomiting Seizure Inability to arouse

70. Interventions Educate patient/family Post concussion syndrome H/A Dizziness (positional) Tinnitus Inability to concentrate Personality change Memory disturbances

71. Interventions Educate patient/family Post concussion syndrome Duration Days to years Social/occupational Difficulty school/work

73. Diastatic Skull Fractures  Fracture along suture line  Often seen in children

74. Depressed Skull Fracture A break in a cranial bone (or "crushed" portion of skull) with depression of the bone in toward the brain May require surgical elevation

76. Compound Skull Fracture A break in or loss of skin and splintering of the bone.

77. Basilar Skull Fracture A Fracture that occurs somewhere in the Cranial Vault

78. Basal Skull Fractures Periorbital ecchymosis (Raccoon sign) Anterior fracture

79. Basal Skull fracture Retroauricular ecchymosis (Battle’s sign) --Posterior fracture Blood behind tympanic membrane --Middle Fracture

80. Basilar Fractures cont’d If Basilar skull fracture suspected NO nasal intubation NO nasal gastric tubes

81. Basal Skull Fractures CSF leaks -rhinorrhea (nose) -otorrhea (ear) Tests for CSF: Positve glucose Positive Halo

82. Basal Skull Fracture VIIth (Facial) Nerve Palsy Occur immediately Occur a few days after initial injury

83. Cerebral Contusion Cerebral contusions fairly common Mostly occur in frontal and temporal lobes Bruising of the brain tissue without puncture of pia Petechial hemorrhages Extravasation of fluid from vessels

84. Cerebral Contusion Distinction between contusion and traumatic intracerebral hematoma ill defined. Contusions, can evolve into an intracerebral hematoma

85. Cerebral Contusion Blunt force  High velocity  Low velocity

86. Cerebral Contusion Intervention Decrease ICP Mannitol to decrease water content in brain Increase venous outflow Discuss with family/patient evolution of contusion and need for monitoring Discuss bizarre behavior- frontal lobe Assist family in understanding a contusion to brain stem has injured “awake” center in brain

87. Epidural Hematoma Located outside the dura, within the skull Biconvex or lenticular in shape Mostly located in temporal or temporoparietal region

88. Epidural Hematoma Result from tearing of middle meningeal artery D/T fracture Bleeds arterial in origin Does not tamponade 50% mortality

89. Epidural Hematoma Brief loss of consciousness followed by “lucid interval” then rapidly progressive deterioration “Talk and die”

90. Epidural Hematoma Bleeding can rapidly become mass lesion Cause IICP Brain shift Uncal herniation

91. Subdural Hematoma More common than epidural hematomas 30% of severe head injuries Tearing of bridging vein between cerebral cortex and a draining venous sinus

92. Subdural Hematoma Cover entire surface of hemisphere

93. Subdural Hematoma Presentation can be Acute < 48 hours Subacute 2 days to 3 weeks More frequent in elderly Chronic > 3 weeks

94. Subdural Hematoma Clinical findings range from headache with nausea to comatose and flaccid

95. Subdural Hematoma Non-contrast CT scan Crescent shaped mass Ancillary tests CBC Chemistry Coag studies T&C

96. Subdural Hematoma Interventions Acute Decrease ICP Nonacute Burr holes

97. Subarachnoid Hemorrhage/Aneurysm rupture “worst h/a of my life” Aneurysms result from thinning vascular wall Precipitated by hypertensive event Straining Sex Heavy lifting

98. Subarachnoid Hemorrhage/Aneurysm rupture After rupture vessel clamps down to prevent further bleeding Result in Ischemia/infarction Blood in subarachnoid space is irritant Meningeal signs

99. Subarachnoid Hemorrhage/Aneurysm rupture Complications Increased ICP Vasospasm Rebleeding Ischemia Infarction Hydrocephalus

100. Subarachnoid Hemorrhage/Aneurysm rupture Interventions ABC’s Monitor neuro status Fluids within normal range avoid dehydration increases hemoconcentration, increases vasospasm Monitor sodium usually falls Normotensive BP until clipped then can be elevated

101. Penetrating/ Perforating Injuries A foreign object penetrates into the skull and brain

102. Perforating & Penetrating Trauma PerforatingPenetrating

104. Causes of Secondary Injury Hypoxia

105. Causes of Secondary Injury Hypotension

106. Causes of Secondary Injury Cerebral edema 1.Cerebrum 2. Skull 3. Cerebellum 4. Herniation of Brain Into Spinal Column

107. Causes of Secondary Injury Sustained hypertension

108. Causes of Secondary Injury Hypercapnia

109. Causes of Secondary Injury Seizures

110. Causes of Secondary Injury Vasospasm

111. Causes of Secondary Injury Metabolic abnormalities (hypoglycemia)

112. Causes of Secondary Injury Ischemia (#1 cause) Normal Ischemic

113. MAP & ICP GO HAND IN HAND MAP= Diastolic x2 Plus Systolic Divide that by 3 ICP= The Brain The CSF The Blood

114. Cerebral Perfusion Pressure (CPP) Pressure required to maintain adequate perfusion to cerebral tissues MAP – ICP = CPP Normal: 70-100 mmHg

115. CPP < 50 mmHg Results in Ischemia

116. Spinal Cord Injuries Involve bruising or tearing of spinal cord substance from penetrating trauma or a fracture/dislocation of spinal column 15-35 year olds Usually due to trauma

117. Spinal Cord Injuries Mechanism of Injury Axial loading Hyperflexion Hyperextension Injury may involve only Spinal cord Vertebral body Both

118. Spinal Cord Injuries Damage to cord From extrinsic(bony and soft tissue injury) From intrinsic (hemorrhage, edema, hypoxia, biochemical changes

119. Spinal Cord Injuries Classification Complete Transection of the cord, no preservation of motor or sensory function Incomplete Some cord sparing

120. Spinal Cord Injuries Respiratory Complications Phrenic nerve innervates diaphragm, exits cervical cord at C-3, C-4, C-5 if involved diaphragm involved Compromises ability to breath Intercostal muscles (T-1 to T-12) involved becomes difficult to deep breath, cough

121. Neurogenic Shock Eliminates the “fight or flight” protective response and permits the parasympathetic system to function unopposed Results in vasodilation below level of the injury, pooling of blood, decreased venous return to the heart, and decreased cardiac output

122. Neurogenic Shock Loss of ability to sweat Below level of injury D/T lack of innervation of sweat glands Temperature lower than normal D/T break in connection between hypothalamus and sympathetic nervous system Loss of body heat by passively dilated vascular bed of skin

123. Neurogenic Shock Blood pressure may not be restored by fluids alone In trying to normalize BP may cause fluid overload, pulmonary edema BP best restored by judicious use of vasopressors May perfuse adequately without normal BP

124. Intravenous Fluids Quadriplegic patients-may fail to become tachycardic or may even become bradycardic in the presence of shock- due to loss of cardiac sympathetic tone.

125. Intravenous Fluids  Hypovolemic Shock  Patient usually presents with tachycardia  Neurogenic Shock  Patient usually presents with bradycardia Overzealous fluids may cause PULMONARY EDEMA in Spinal Cord Injury Patients If blood pressure does not improve after fluid challenge, judicious use of vasopressors, may be indicated

126. Neurogenic Shock Orthostatic Hypotension Rapid drop in BP when vertical position assumed. Blood supply to brain inadequate, syncope results. (brain damage and death can result) D/T loss of arteriole vasomotor tone below level of lesion so there is pooling of blood in abdomen and LE’s when upright. Seen in patients with lesions above T-7

127. Spinal Cord Injuries Interventions ABC’s Cervical Spine Immobilization O2 Monitor VS, CO2 Mechanical ventilation if needed Monitor LOC, UOP Enhance venous return to the heart Interventions Support BP if needed Atropine if needed Methylprednisolone NG tube Foley Attempt to have someone with patient most of the time

128. Autonomic Hyperreflexia Noxious stimuli produces sympathetic discharge that causes reflex vasoconstriction of blood vessels in skin and visceral bed below level of the injury Vasoconstriction of visceral bed distends baroreceptors in the carotid sinus and aortic arch, body attempts to lower hypertension by superficial dilation of vessels above level of injury

129. Autonomic Hyperreflexia As spinal shock reverses, potential for dysreflexia should be considered in patients with injuries T-6 or above Nursing intervention – prevent conditions that are know to trigger autonomic hyperreflexia Causative noxious stimulus most common ◦ Distended bladder d/t kinked drainage tube

130. Autonomic Hyperreflexia Clinically Sudden hypertension 240/120 Pounding headache Anxious Flushed face, neck, upper chest moistened with perspiration Blurred vision Nasal congestion Nausea Lower extremities goose flesh, cold

131. Autonomic Hyperreflexia Interventions Elevate HOB Relieve trigger mechanism Treat hypertension as needed Resources for family/patient for self care

132. Headaches Occur when there is traction, pressure, displacement, inflammation or dilation of pain receptors in brain or surrounding tissues Two types: ◦ Primary  No organic cause consistently identified (migraines, cluster, tension) ◦ Secondary  Organic etiology (tumor, aneurysm, meningitis, temporal arteritis)

133. Headaches Affects up to 75% population per year 5% will seek treatment 50 % of people with headache suffer migraine Mechanism unknown Blood vessels that supply brain and surrounding tissue narrow, reduced blood flow, followed by reflex vasodilatation, swelling, and inflammation of cerebral blood vessels

134. Headaches Assessment Hx of present illness Time frame onset (migraines early morning) Occurrence (in groups, then period of remission) Aura (migraines with/without aura) Duration (tension 7 days, migraine 4-72 hours)

135. Headaches Pain Character and quality Intensity Therapeutic measures implemented Success of therapeutic measures Location Unilateral (migraine), bilateral (tension), hatband

136. Headache Symptoms with migraines Aura possible without aura most common Nausea/vomiting Photophobia Difficulty concentrating Visual changes May see neurodeficits in “complicated” migraine

137. Headache Cluster Headaches Burning, sharp, severe unilateral orbital or temporal pain Photophobia Tearing, nasal congestion on affected side May have lid edema, red eye on affected side. Usually lasts < 1 hour, but may have multiple per day

138. Headaches Tension Dull, nonpulsating pain No photophobia, aura Usually starts at occiput and moves around bilaterally to frontal area (band like)

139. Headaches Precipitating event Emotional (stress/depression) Metabolic (fever/menses) Flickering lights/television Alcohol abuse/withdrawal Food Fatigue or altered sleep wake cycle

140. Headaches Physical Exam Neuro exam Edema over the sinuses Distended, twitching scalp vessels Flushed, pale, or shiny skin

141. Headaches Diagnostic procedures (organic) Skull x-rays CT scan

142. Headaches Interventions/Planning Physical measures Heat (muscular) or cold (vascular) Darkened room Massage Psychological measures Stress mgt Relaxation techniques Behavior modification

143. Headaches Interventions Pharmacological measures Preventive drugs Vasoconstrictor agents Beta blockers Anticonvulsants Analgesics Oxygen

145. What Is Stroke ? A stroke occurs when blood flow to the brain is interrupted by a blocked or burst blood vessel.

146. What Is the Impact of Stroke? Stroke is the third leading cause of death in the United States On average, someone suffers a stroke every 53 seconds About 600,000 Americans suffer strokes each year Every 3.3 minutes, someone dies of a stroke Stroke is the third leading cause of death in the United States On average, someone suffers a stroke every 53 seconds About 600,000 Americans suffer strokes each year Every 3.3 minutes, someone dies of a stroke

147. What Is the Impact of Stroke? n Stroke is a leading cause of serious, long-term disability n About 4 million Americans are stroke survivors n Stroke costs the U.S. $30 to $40 billion a year n Stroke is a leading cause of serious, long-term disability n About 4 million Americans are stroke survivors n Stroke costs the U.S. $30 to $40 billion a year

148. Stroke Clinical syndrome consisting of a neurological deficit resulting from an interuption of blood flow to an area of the brain, rapid or gradual in onset, which persists for more than 24 hours. Two types Ischemic: Thrombotic or embolic occlusion of a cerebral artery resulting in infarction Hemorrhagic: Spontaneous rupture of a vessel resulting in intracerebral or subarachnoid hemorrhage

150. Stroke Assessment Hx present illness (time pattern) Classifications of stroke: TIA – brief, lasting seconds to hours; < 24 hrs RIND – lasting 48 hours or less, complete resolution of deficit, reversible ischemic neuro deficit Stroke in evolution/progressive – Symptoms last >24 hrs with progressive neurologic deterioration. Completed stroke – permanent neurologic damage

151. Stroke Medical History Diabetes Rheumatic heart disease Recent MI CHF Migraines Hypertension A-Fib

152. Stroke Physical Exam Anterior Circulation Alteration in LOC Motor deficit Contralateral hemiparesis, hemiplegia Sensory deficit Contralateral

153. Stroke Physical Exam Anterior Circulation Speech deficit Dysphasia Expressive or receptive Dominant hemisphere Visual deficit Loss of vision in half of the visual field on same side

154. Stroke Physical Exam Posterior Circulation (vertebral basilar) Alteration in LOC Motor deficit more than one limb

155. Stroke Physical Exam Cranial nerve deficit Dysphonia difficulty producing voice sounds Dysarthria difficulty in articulation Dysphagia difficulty in swallowing

156. Stroke Physical Exam Posterior Circulation (vertebral basilar) Visual deficits field defects, cortical blindness diplopia Loss of coordination Ataxia

157. Stroke Ischemic Sudden, rapid onset Occurs at sleep, rest Hemorrhagic Severe headache More gradual onset Symptoms of increasing ICP Occurs during activity

158. Stroke Interventions Maintain airway, breathing, circulation Monitor neuro status for change Maintain venous outflow (head neutral position) Frequently monitor Cerebral function LOC Blood pressure

159. Stroke Interventions Supplemental oxygen, pulse oximetry RSI: sedation, neuromuscular blockers, analgesics Initiate measures to normalize blood pressure Keep SBP < 180, DBP <105 Labetalol drug of choice. Avoid rapid BP decreases. Want BP high enough to perfuse. Administer anticoagulation therapy (ischemic stroke in evolution only) May use meds to cause coagulation in hemorrhagic stroke FFP Vitamin K

160. Stroke Interventions Administer IV thrombolytics (ischemic stroke) Patient must present within 3 hours of onset of symptoms, CT must exclude intracranial hemorrhage

161. Stroke Interventions: Surgical interventions Carotid endarterectomy ( TIAs) Intra-arterial fibrinolytic therapy (6 hr limit) Angioplasty/stent placement

163. Communicating An overproduction (Pediatric Tumors) Under reabsorption of CSF (Subarachnoid Hemorrhages)

164. Non Communicating A blockage or destruction of the channels of CSF Drainage Causes include Tumors, Encephalitis, Spina Bifida)

165. Shunt Problems Shunt purpose- relieve increased ICP from hydrocephalus Diversion relieves obstruction by creating alternative pathways for free circulation and/or absorption of CSF Most common complications Infections Shunt malfunction D/T obstruction(plugging by blood clots, brain or malfunction

166. Shunt Problems Assessment Hx of present illness Type of shunt Length of implantation Medical history Reason for shunt Previous problems with shunt Risk factors- growth

167. Shunt Problems Physical Exam Shunt malfunction Mental status: Decreased alertness Decreased intellectual function Behavioral changes Eye changes Inability to look up Alteration in visual acuity or fields

168. Shunt Problems Shunt Malfunction Incontinence Gait/coordination changes Vomiting Infant: Tense fontanelles Shrill cry Loss of appetite

169. Shunt Problems Physical Exam Infection Fever Meningeal signs Altered Mental status Diagnostic procedures CT scan Lumbar puncture for CSF analysis

170. Shunt Problems Interventions Monitor vital signs Prepare and assist for lumbar puncture/shunt tap CSF for analysis/culture Antibiotic therapy

171. Seizures Sudden, paroxysmal discharge of a group of neurons resulting in transient impairment of consciousness, movement, sensation, or memory Trigger causes abnormal burst of electrical stimulus, disrupts brain’s normal nerve conduction

172. Seizures Causes Ionic Electrolyte imbalance Metabolic Hyperglycemia Fever Stress Nerve cell structural changes Hypoxia, tumors, trauma

173. Seizures Classification Generalized Involves all areas of both cerebral hemispheres Motor manifestations are bilateral Classification Partial Focal onset involving one particular part of the brain

174. Seizures Status Epilepticus Medical emergency Series of seizures without recovery of baseline neuro status between seizures Lead to mortality and morbidity from Acidemia Hypoglycemia Autonomic dysfunction Hypercalcemia

175. Seizures At Risk Head trauma, stroke, CNS infections,Degenerative CNS disorders(MS)

176. Seizures Assessment Hx present illness Precipitating event (fever) Site of origin, spread of seizure Motor activity Duration and frequency LOC Postictal behavior

177. Seizures Assessment Medical history Seizure history Congenital anomalies Metabolic abnormalities Neurological disease (tumors, infectious process) Recent trauma Pharmacological hx (excessive lax in kids)

178. Seizures Assessment Physical exam (during and after sz) LOC Responsive to stimuli ( what kind of stimuli?) Ability to follow commands Motor activity (type and origin of spread) Tonic phase Contraction of voluntary muscles, body stiffens Clonic phase Violent, rhythmic contractions

179. Seizures Assessment Physical exam (during and after sz) Eye deviation Incontinence Temperature Postictal State LOC Weakness of one limb Headache, amnesia Duration

180. Seizures Assessment Physical exam (during and after sz) Physical injury sustained Recurrence of the seizure

181. Seizures Assessment Diagnostic procedures Therapeutic monitoring of anticonvulsant drug levels (seizure pts) No history CT scan, MRI EEG follow up appt Lumbar puncture CBC Lytes, glucose, BUN, Cr Toxicology screen

182. Seizures Interventions Maintain airway, breathing, circulation Turn pt to side, protect from injury Loosen tight or restrictive clothing Suction, if necessary Supplemental oxygen Establish IV access Pharmacological support to stop seizures Diazepam IV Lorazepam IV

183. Seizures Interventions Pharmacological support to prevent recurrence Phenytoin, IV Fosphenytoin IV or IM

184. Seizures Interventions Monitor Neurological status Temperature, vital signs Pharmacological support to prevent or correct complications 50% glucose IV Thiamine IM or IV

185. Seizures Interventions Observation until recovered from postictal state Monitor neuro recovery Seizure precautions Monitor therapeutic drug levels Assess pt’s perceived compliance Interventions Assess for compliance Discharge Teaching Medications Consequences of noncompliance Follow up appts.