490 likes | 723 Views
Stroke (Brain Attack). Disruption in the normal blood supply to the brainCVAMedical emergencyRequires immediate treatmentThird most common cause of death in USPrimary cause of adult disability. Stroke: Pathophysiology. Brain circulation: 1000 mL per minuteIschemia in brain tissue supplied by a
E N D
1. Critical Neurologic Problems
2. Stroke (Brain Attack) Disruption in the normal blood supply to the brain
CVA
Medical emergency
Requires immediate treatment
Third most common cause of death in US
Primary cause of adult disability
3. Stroke: Pathophysiology Brain circulation: 1000 mL per minute
Ischemia in brain tissue supplied by affected artery results in brain dysfunction
Ischemia ? hypoxia/anoxia/hypoglycemia ? infarction or death of neurons, glia, and involved area of the brain
Brain metabolism is affected in involved area as well as in the contralateral hemisphere
Small lacunar infarcts– produce either a pure motor or pure sensory deficit
4. Types of Strokes Ischemic (occlusive)
Caused by occlusion of cerebral artery by thrombus or embolus
Thrombolic stroke
Accounts for > 50% of all strokes
Associated with atherosclerosis
Lacunar stroke
Embolic stroke
Accounts for ~ 33% of all strokes
Embolus/emboli travel to cerebral arteries via carotid artery
Sources of emboli are cardiac
5. Types of Strokes Transient Ischemic Attack (TIA)
Reversible Ischemic Neurologic Deficit (RIND)
Hemorrhagic stroke
Ruptured saccular (berry) aneurysm
Ruptured arteriovenous malformation (AVM)
Hypertension (most common)
6. Stroke: Risk Factors Hypertension
Diabetes mellitus
Heart disease
Nonvalvular arterial fibrillation
Smoking
Sedentary lifestyle
Substance abuse
7. Stroke: Assessments Accurate History
Activity when stroke began
Ischemic: sleep
Hemorrhagic: activity
Progression of Sx
Level of Consciousness
Current LOC
Presence of deficits
Medical History
Head trauma
HTN
Heart disease
Anemia
Obesity
Headache
Current meds
Anticoagulants
ASA
Vasodilators
Illegal drugs
8. Stoke: Clinical Manifestations Cognitive changes
Motor changes
Sensory changes
Cranial nerve intactness
Cardiovascular assessment
Psychosocial assessment
9. Stroke: Cognitive Changes Changes in LOC
Neglect syndrome/hemiparesis
Spatial and proprioceptive dysfunction
Impairment of memory, judgment
Problem-solving/decision-making abilities
Decreased ability to concentrate/attend to tasks
10. Stroke: Cognitive Changes Right cerebral hemisphere
Unaware of deficits
Disoriented to time/place
Impulsivity/poor judgment
Left cerebral hemisphere
Aphasia
Alexia
Agraphia
Slow and cautious
11. Stroke: Motor Changes Motor nerve fibers cross in the medulla above spinal cord and periphery
Hemiplegia/hemiparesis on opposite side
Hypotonia or flaccidity
Extremities feel heavy/muscle tone is inadequate
Contractures/? ROM
Proprioception (position sense)
Uninhibited bladder/bowel function
12. Stroke: Sensory Changes Inability to write/read
Agnosia/apraxia
Neglect syndrome
Visual ability
Pupillary abnormalities
Ptosis
Visual field deficits
Pallor/petechiae of conjunctiva
Amaurosis fugax
Hemianopsia
Homonymous hemianopsia
13. Stroke: Nursing Diagnosis Impaired (cerebral) tissue perfusion
Impaired physical mobility
Disturbed sensory perception
Unilateral neglect
Impaired verbal communication
Impaired swallowing
Total urinary incontinence and bowel incontinence
14. Stroke: Interventions Drug therapy
Thrombolytic therapy
Anticoagulants/antiplatelets
Antiepileptic drugs
Calcium channel blockers
Stool softeners/analgesics/antianxiety
Aggressive rehabilitation
NIC intracranial pressure monitoring
Chart 48-6, p. 1038
15. Stroke: Interventions Glascow Coma Scale
Monitoring for complications
Surgical management
Carotid endarterectomy
Extracranial-intracranial bypass
Management of arteriovenous malformations/ aneurysms
Intracranial bleeding
16. Stroke: Impaired Verbal Communication Occurs in dominant hemisphere/majority in left hemisphere
Dysarthria due to loss of motor function
Aphasia caused by cerebral hemisphere damage
Expressive (Broca’s or motor) aphasia
Receptive (Wernicke’s or sensory) aphasia
17. Stroke: Expressive Aphasia Motor speech problems
Understands but unable to communicate
Difficulty with writing
Frustration and anger
18. Stroke: Receptive Aphasia Unable to understand spoken and written word
Neologisms
Global or mixed aphasia
Reading and writing equally affected
19. Left Frontal Stroke
20. Left Frontal Stroke (underside)
21. Right Sided Stroke
22. Right Sided Stroke
23. Traumatic Brain Injury (TBI) “Occurs as a result of an external force that produces a diminished or altered state of consciousness” (Iggy, p. 989)
Can:
Cause cognitive impairment
Cause behavioral/emotional disturbances
Be temporary or permanent
Cause partial or total functional disability or psychosocial maladjustment
24. Traumatic Brain Injury (TBI) Primary brain injury
Two classifications:
Open head injury
Linear fracture
Depressed fracture
Open fracture
Comminuted fracture
Basilar skull fracture
Penetrating injury
25. Traumatic Brain injury Closed head injury
Concussion
Contusion
Laceration
Secondary brain injuries
Any neurological damage that occurs after the initial injury
26. TBI: Types of Forces Acceleration injury
Deceleration injury
Shearing
Straining
Distortion of brain tissue
Destruction of adjacent brain tissue
27. TBI: Secondary Brain Injury Increased intracranial pressure (ICP)
Hemorrhage
Epidural hemorrhage
Subdural hematoma
Intracerebral hemorrhage
Loss of autoregulation
Hydrocephalus
Herniation
28. Increase Intracranial Pressure Response to edema, hemorrhage, hematoma formation, impaired auto-regulation, hydrocephalus
Crainial components:
Brain tissue
Blood
CSF
ICP maintained through processes of accommodation and compliance
29. Increased Intracranial Pressure Monro-Kellie hypothesis
Any ? in one component must be compensated for by a ? in one of the others
First response to ? volume of any component is a shunting of CSF to the subarachnoid space or increasing rate of CSF absorption
If necessary, cerebral blood flow is ? by displacement of blood to the sinuses
30. Increased Intracranial Pressure Normal ICP 10-15 mm Hg
Leading cause of death from head trauma
? ICP = ? cerebral blood flow = ? serum pH and ? CO2 = cerebral vasodilation = edema = ? ICP = brain herniation = irreversible brain damage = death
Edema
Vasogenic (can cause ? ICP)
Cytotoxic (can cause ? ICP)
Interstitial (occurs in presence of acute brain swelling)
32. Hemorrhage Caused by vascular damage from shearing force
Potentially life threatening
Epidural: bleeding into space between the dura and inner table of the skull
Subdural: venous bleeding into space beneath dura and above the arachnoid
Intracerebral: accumulation of blood within the brain tissue
33. Loss of Autoregulation Causes cerebral blood flow to fluctuate passively with the systemic blood pressure
Increases ICP and potential for vasogenic edema
Hypoxemia and hypercapnia cause marked cerebral vasodilation
34. Hydrocephalus and Herniation Hydrocephalus
Abnormal increase in CSF volume
Results from impairment of CSF absorption or blockage of the CSF circulation pathway
Herniation
With ? ICP, brain tissue may shift and herniate downward
Several herniation syndromes
Uncal (transtentorial) herniation is life threatening
35. History Client may experience amnesia
Client may be unconscious
Obtain history from others
Obtain information about events immediately after injury
Determine whether client experienced seizure activity before or after the injury
What were the circumstances of the fall
Past medical history
Allergies (esp. allergy to seafood)
36. Physical Assessment Goals of Nursing Assessment
Establishment of baseline data
Early detection and prevention of ? ICP, systemic hypotension, hypoxia, or hypercapnia
Treat all head injuries as though they have a spinal injury
Assess for indicators of spinal cord injury
Loss of motor and sensory function
Tenderness along spine and abnormal head tilt
Respiratory difficulties
Diminished or absent reflexes
37. Physical Assessments Airway and breathing pattern
1st priority
ABG’s
Vital signs
Blood pressure and pulse
Cushing reflex
Neurological
GCS or similar scale
Neuro assessment (pupillary response, motor function, LOC, intactness of cranial nerves, signs of CSF leakage, posturing, papilledema)
38. Lab and Radiographic Assessment Lab
No labs to diagnose, can be used to diagnose or prevent secondary brain insult
ABG’s, CBC, and serum glucose, electrolytes and osmolality
Radiographic
CT scan
Cervical spine and skull xray
39. TBI Interventions: Nonsurgical Goals are to prevent or detect ? ICP, promoting fluid and electrolyte balance, and monitoring effects of treatment and medications
Vital Signs
Monitor at least every 1-2 hours
May need medication to maintain BP wnl
Non-specific ST-segment or T-wave changes can occur
Positioning
Avoid extreme flexion or extension of neck, maintain head in the midline, neutral position
Logroll
HOB ? 30ş
40. TBI Interventions: Nonsurgical Hyperventilation
Avoided in first 20 hours post injury
In acute deterioration used for brief periods to produce vasoconstriction which ? ICP
Maintain PaCO2 at 27-35 mm Hg
Induction of barbiturate coma
Used when ICP not controlled by other means
Reduces metabolic demands on the brain and cerebral blood flow
Requires ventilator, hemodynamic and ICP monitoring
41. TBI Interventions: Nonsurgical Drug Therapy
Glucocorticoids and steroids ineffective
Mannitol (osmotic diuretic) to treat cerebral edema
Furosemide as an adjunctive therapy
Codeine and fentanyl to ?agitation and control restlessness of ventilated patients
Fluid and Electrolyte management
Risk for Diabetes Insipidus and SIADH
May restrict fluids
Monitor serum and urine osmolality frequently
Monitor urine specific gravity every 1-4 hours
42. TBI Interventions: Nonsurgical Strategies for sensory/perceptual alterations
Promotes pleasant environment at mealtime
Position to maximize swallowing
Provide hazard-free environment
Sensory-stimulation program
Pulmonary management
Turn, cough, deep breath at frequent intervals
Chest physiotherapy
Suctioning as needed with particular attention to response of ICP
43. TBI Interventions: Nonsurgical Behavioral management
Seizure precautions
Observe and document behavior hourly
Provide quiet environment and orient as needed
Preventing complications of immobility
Nutrition management
May need enteral feedings
Daily weight and calorie counts
Monitor serum albumin, prealbumin and transferrin
Assess for signs of dehydration
44. TBI: Interventions Surgical management
Intracranial pressure monitoring
Intraventricular catheter (can drain CSF)
Subarachnoid screw or bolt (less invasive, CSF cannot be drained)
Epidural catheter or sensor
Subdural catheter
Fiberoptic transducer tipped pressure sensor (most common device for ICP monitoring)
Craniotomy
45. Brain Tumors Primary tumors
Secondary tumors
Signs and symptoms
Cerebral edema
Increased ICP
Focal neurologic deficits
Obstruction of flow of CSF
46. Brain Tumors: Complications Cerebral (vasogenic) edema/ ? ICP
Herniation of brain tissue/ischemia of affected area
Rupture/hemorrhage into brain tissue
Seizure activity/hydrocephalus
Pituitary dysfunctions/SIADH/diabetes insipidus
Fluid and electrolyte imbalances
47. Brain Tumor: Classification Malignant/benign
Location
Gliomas
Meningiomas
Pituitary gland
Acoustic neuromas
48. Brain Tumors: Symptoms Headaches (severe on awakening in am)
Nausea and vomiting
Visual symptoms
Seizures
Changes in mentation or personality
Papilledema (swelling of the optic disk)
49. Brain Tumors: Interventions Nonsurgical
Radiation/chemotherapy
Blood brain barrier disruption
Recombinant DNA
Monoclonal antibodies
Antineoplastic drugs
Immunotherapy/hyperthermia
Surgical
Biopsy
Craniotomy
50. Brain Tumors: Post-op Complications Increased ICP
Hematomas
Hydrocephalus
Respiratory problems
Neurogenic pulmonary edema
Wound infection
Meningitis
Fluid/electrolyte imbalance