Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
51 Cards in this Set
- Front
- Back
Define Intracranial Pressure and list the intracranial components
|
• Definition: Pressure exerted by the combined volume of three intracranial components:
- brain tissue - cerebrospinal fluid - blood |
|
What is the Monroe-Kelly hypothesis
|
Monroe-Kelly hypothesis: ICP remains stable as long as the volume that is added is balanced by the volume that is displaced.
- ICP = CSF volume + blood volume + volume of brain tissue |
|
Intracranial Pressure (ICP) – what is normal =
|
• 0-15 mm Hg
• 60- 180 cm H20 - Cerebral Volume • Brain tissue = 80% • Cerebral blood volume = 10% • cerebral spinal fluid [CSF fluid= 10% |
|
• What is cerebral blood flow provided by? ______ What is the definition of this term
|
• Cerebral blood flow provided by: Cerebral Auto-regulation:
- Maintenance of Cerebral Blood Flow by altering the diameter of the arterioles - In response to changes in Cerebral Perfusion Pressure |
|
• What is Cerebral Perfusion Pressure (CPP):
|
- measurement provides: estimate of adequacy in 02 circulation
- difference between the mean systemic arterial pressure and the mean intracranial pressure. Usually between 60-100 mm Hg |
|
Auto-regulation is ineffective with:
|
ischemia
•hypoxia hypercapnia brain trauma Must have systolic BP between 60-140. Must have ICP < 30 |
|
Hypercapnia-What is an increased and decreased CO2 level mean and what does a decreased PO2 level mean, what are these levels?
|
- pC02 >45 = cerebral vasodilation
- pC02 <35 = cerebral vasoconstriction • p02 < 60 = cerebral vasodilation Cycle for brain swelling |
|
Increased Intracranial Pressure • What is the Etiology
|
- Increased brain volume
-Cerebral edema intracranial mass - Increased cerebral blood flow-Oxygenation in the brain • intracranial bleed, cerebral aneurysm, elevated pC02, hypoxia - Increased cerebrospinal fluid • hydrocephalus, meningitis, tumors that obstruct CSF flow Brain tumor/hemorrhage |
|
Conditions Increasing ICP
|
• Sneezing
• Vomiting • Coughing • Suctioning (frequent) • Valsava • Increased activity • Increased PaC02 • Hyperthermia • Seizures • Neck flexion • Emotional upset • Decreased PaO2 |
|
Complications of ICP
|
• Brain herniation
• Diabetes insipidus (deficiency of ADH secretion causing increased u/o and dehydration) • Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) - increased ADH secretion causing decreased u/o and fluid overload. • Seizures |
|
Symptoms of increased ICP
• Stage I |
• Stage I
- altered vision (blurred, double) - confusion (first to time, forgetful) - drowsiness (lethargy, more stimulation needed, restless, irritable) - breathing changes (depends on LOC-cheyne stokes) - slight ipsilateraly pupillary changes (sluggish/ovoid) - ptosis-drooping of eyelids - early am HA/projectile vomiting - motor--pronator drift, subtle weakness to hemiplegia on contralateral side • Middle to late stages (cushings) |
|
Symptoms of increased ICP Stage 2
Stage 3 |
• Stage 2
- Systemic arterial vasoconstriction • attempt to overcome ICP • Stage 3 - decreased arousal - Cheyne Stokes to apneustic - Hyperventilation - widened pulse pressure - bradycardia • Cushings signs: widened pulse pressure, decreased pulse, decreased respirations. - Stage 2-3 - body's last attempt to compensate |
|
Symptoms of increased ICP
• Stage 4 (decompensation) |
Symptoms of increased ICP
• Stage 4 (decompensation) - Herniation • unarousable • tachycardic, hypotension, narrowed pulse pressure • tissue hypoxia and brain death • posturing from decorticate to decerebrate • pupils from small & reactive or sluggish to fixed and dilated • Absence of dolls eyes [negative] negative respirations |
|
Compensatory Mechanisms for Increased ICP
|
- shunting of CSF into spinal subarachnoid space
- increased CSF absorption - Decreased CSF production - shunting of venous blood out of skull |
|
Decompensation
|
- Decompensation: herniation (displacement of brain tissue to another area of the
brain or outside cranial vault) - blood supply to medulla is cut off - pupils fixed and dilated - from decorticate to decerebrate posture • irreversible brain damage Herniation |
|
Diagnostics of ICP:
|
• CT or MRI to determine possible causes of ICP
- CT: detailed outlines of bone, tissue & fluid structures; reflect shift of structures and acute hemorrhage - MRI: graphic image of bone, fluid & soft-tissue structures with more defined image of anatomical details; Normal CT Scan • Intracerebral Edema & Hemorrhages MRI • CBF monitoring (blood flow) - Transcranial Doppler ultrasonography o aimed through cranial "windows" - Radioisotope brain scan • Damaged areas absorb more of the isotope EEG Tracings • A: normal • B: Generalized slowing • C: Temporal spikes (seizures) • D: Electrocerebral silence |
|
Interventions for ICP
|
• Hypothermia: decreases 02 consumption, but may decrease CBF unless induced barbiturate coma
• Craniotomy (bone flap) remove some bone of skull-more room for the brain • Hemodynamic monitoring: - MAP between 115-120, less than 140 fluid up - PAWP 14-16 ICP monitoring Normal 0-15 - Keep less than 30 • Ventriculostomy, shunt: drainage of CSF - against positive pressure to prevent collapse - sterile technique |
|
ICP Measurement Techniques
|
• Intraventricular
- Ventriculostomy catheter placed through burr hole into lateral ventricle - Connected to pressure tubing & transducer • Intraparenchymal catheter - Fiberoptic transducer tipped catheter placed directly into brain tissue - Used in patients with displaced or compressed ventricles • Subaraclmoid Technique - Subaraclmoid screw extended into the subdural or subaraclmoid space • Epidural Sensor - Placement of epidural device between skull & dura |
|
Medications
- Corticosteroids |
- Corticosteroids (dexamethasone or Decadron) reduces ICP through unknown mechanism. Side effects: GI ulcers and bleeding, and elevated blood glucose .
• Research: Ineffective with severe head-injury, but reduces vasogenic edema associated with brain tumors, abscesses, & spinal cord tumors |
|
Medications-Calcium Channel Blockers
|
Calcium Channel Blockers (nimodipine, nicardipine) prevent cerebral vasospasm, however cerebral vasodilation increases ICP-contraindicated with space-occupying lesions or cerebral edema.
|
|
Medications-Sodium Nitroprusside
|
Sodium Nitroprusside: used with severe intracranial hypertension; should maintain MAP of at least 130.
|
|
Medications-Barbituates:
|
: phenoobarbital: may be used to induce coma (decreases metabolic & 02 demands)
• also: - suppresses seizure activity, - reduces restlessness & irritability • research: increased survival |
|
Medications-Beta Blockers
|
Beta Blockers: Labetalol (Trandate) decreases ICH, improves CPP, without increased ICP. Contraindicated in patients with space occupying lesions or cerebral edema
|
|
Medications: Sedatives:
|
Sedatives: phenobarbital, propofol, versed, ativan."Lorazepam”
• Baseline evaluation of mental & neurological status • Periodic discontinuation - Analgesics: Fentanyl or MS frequently used; • patients in pain become combative, restless & agitated - Antipyretics: Acetaminophen is used to control fever. |
|
Medications:
stool softeners: - Anticonvulsants: (dilantin, tegretol, valium) - Histamine H2 blockers |
stool softeners: colace
- Anticonvulsants: (dilantin, tegretol, valium) used to manage seizure activity - Histamine H2 blockers (pepcid, tagamet, zantac) prevent GI irritation & bleed |
|
Neuromuscular Blockades (Vecuronium)
|
- Neuromuscular Blockades (Vecuronium)
• used to counteract increases in ICP associated with reflex motor responses to suctioning and mechanical ventilation • trane of four - four stimuli delivered at intervals of 0.5 sec. - Ulner at wrist - thumb should twitch 2-3 times • must sedate & treat for pain • must be on ventilator |
|
The doctor has just ordered IV albumin and IV lasix for the patient with cerebral edema. Which medication should be given first?
|
Albumin
|
|
Nursing Interventions
|
• Goals: reduce ICP, improve CPP, reduce brain shift
-IV fluids (Avoid hypoosmolar solutions D5W-goes more into cells) - Neuro assessment every 1-2 h - If on ventilator, minimal suctioning, - hyperventilate as ordered (keep pC02 above 30) - Elevate HOB 30-45 degrees, head midline - Avoid knee flexion - Assess bowel and bladder function - Do not cluster activities - Quiet, calm environment - Avoid Valsalva maneuver (coughing, sneezing) - If administering tube feedings, give at room temperature - If ICP monitor, monitor for infection, change dressing 24-48 hours, monitor for leaking CSF (clear fluid which tests glucose +) -no nose blowing - Monitor I & 0, possible fluid restriction |
|
Care of the Client with a Craniotomy
|
• Craniotomy: surgical procedure performed to gain access to the intracranial contents and accommodate brain swelling
• Indications - Intracranial neoplasms - Head injuries (hematoma, cerebral edema or depressed skull fracture) Space occupying lesions (bleeds, abscess, aneurysms, arteriovenous malformations) |
|
Preoperative nursing care
|
• Permit signed
• Hair cut and shaved • surgical scrub/ shampoo • report breaks in skin of scalp • record baseline neuroassessment • foley or NG if ordered (may be done after anesthesia) • explain post-op environment (monitoring equipment, ventilator, communication) |
|
Post-op Nursing Care
|
- Prevent injury & infection
• Care same as pt with increased ICP • Assess wound, eyes, ears, nose for CSF leaks and/or infection • Provide protective eye care • NPO until fully conscious (and extubated) • Do not lower head in Trendelenburg or place in supine position • Avoid placing on operative side if large tumor or bone removed • Maintain mobility of joints and extremities - assess motor/sensory responses - PROM q 12 h • Improve body image Encourage use of wigs, turbans, and scarves when dressings removed - encourage use of normal cosmetics - promote self-care |
|
Post-op Nursing Care
speech |
• Improve speech
- provide audiovisual aids as needed - speak in simple, slow instructions - refer to speech therapist |
|
Cerebral Aneurysm
• History |
• History
- adults 35-60 y.o., female - atherosclerosis - congenital defect - head trauma - hypertension - familial - cigarette smoking, use of cocaine - use of OTC med (nasal sprays or antihistamines) |
|
Cerebral Aneurysm Pathophysiology
|
• Most located at bifurcations in or near Circle of Willis
• Act as space occupying lesions • Saccular and Berry • Rupture due to thin walls - Most common first indication is acute subarachnoid hemorrhage (Bleed), or intracerebral hemorrhage |
|
Cerebral Aneurysm
- Manifestations |
• many have no manifestations and no problems
• headaches • occasional ptosis and dilated pupil and diplopia or blurred vision • pain above and behind the eye • nausea and vomiting • stiff neck • dysrythmias and vasospasm • hemiplegia/hemiparesis • other signs of ICP • Warning signs (50% of patients) - headaches -lethargy - neck pain - "noise in the head" - optic, or oculomotor dysfunction |
|
Cerebral Aneurysm
Diagnostic tests Surgery |
• Diagnostic tests
• CT Scan - Cerebral arteriography Surgery is treatment of choice Clipping or coiling |
|
Presurgical Nursing Interventions
|
- Interventions to treat or prevent ICP
- Sedation - Quiet environment - Prevention of coughing, & constipation - hot or cold beverages may be prohibited - limit visitors |
|
Post-surgical nursing interventions
|
• Baseline neuro assessment
• Monitor changes in neuro status • possible mechanical hyperventilation • I and O • vital signs (esp. BP) • monitor for dysrythmias • talk directly to the patient • monitor sodium • monitor for vasospasm - causes decreased CBF, depriving brain tissue of oxygen - treat with triple H therapy & nimodipine • hypervolemia • induced hypertension • hemodilution • close monitoring of hemodynamic parameters • monitor for pulmonary edema |
|
Craniocerebral Trauma
• Types of Injuries |
-Acceleration Injury: head struck by a moving object
- Deceleration Injury: head hits a stationary object - Acceleration-Deceleration Injury (coup-contrecoup phenomenon): head hits object and the brain "rebounds" - Deformation Injury Skull Fractures |
|
Craniocerebral Trauma
• Linear • Depressed: |
Linear: simple clean break
- Most common - force over wide area of skull • Depressed: - bone fragments may penetrate into the brain tissue |
|
Craniocerebral Trauma
• Basilar: |
• Basilar: floor of skull
- serious - contact between CSF and sinuses - CSF may leak through sinus - allow bacteria to contaminate CSF - Raccoon Eyes _ Battle Sign Behind ear on mastoid bone |
|
Craniocerebral Trauma
• Concussion |
- Description: Transient, temporary neuro dysfunction (least serious)
Usually loss of consciousness from seconds to hours • retrograde amnesia, HA, drowsiness, visual disturbances • postconcussive syndrome: HA, inability to concentrate, memory problems, dizziness, irritability - Mechanism of Injury: Acceleration-Deceleration - Prognosis: Most benign form of brain injury |
|
Craniocerebral Trauma
• Contusion • Hemorrhage diffused cerebral edema & hemorrhage peak in ___-____ hrs larger areas may expand over ___-____ days |
• Contusion
- Description: Bruise on the surface of the brain • Hemorrhage diffused - Mechanism of Injury: Brain strikes inner skull (coup & contrecoup) - Prognosis: Varies depending on location & degree • cerebral edema & hemorrhage peak in 12-24 h • larger areas may expand over 2-3 days |
|
Craniocerebral Trauma- Manifestations:
|
• loss of consciousness
• behavior changes • ICP • hemiparesis • abnormal posturing • bradycardia • seizure • respiratory arrest • Hypotension |
|
Intracranial Hematoma
Subdural Hematoma venous bleed location and etiology |
• Subdural Hematoma venous bleed
- Location: bleeding or clot between dura and brain - Etiology: trauma, coagulopathies, aneurysm rupture. More frequently a venous bleed |
|
Intracranial Hematoma
Subdural Hematoma venous bleed Prognosis: |
- Prognosis:
• Acute: sx in 24-48 h. needs immediate intervention • Subacute: sx in 48hr- 2 wk • Chronic: minor head injury in elderly. Sx in weeks to months • -May mimic dementia |
|
Intracranial Hematoma
Subdural Hematoma venous bleed - Manifestations - treatment |
- Manifestations
• Acute: change in LOC, pupillary signs, hemiparesis, increasing BP, decreasing HR, slowing RR - treatment: burr holes, and insertion of drainage catheters |
|
• Epidural Hematoma Arterial Bleed
Location Etiology Prognosis |
• • Epidural Hematoma Arterial Bleed
- Location: bleeding or clot between skull and dura - Etiology: head injury, often from arterial bleed • linear fx across temporal bone lacerating middle meningeal artery - Prognosis: considered an extreme emergency; marked neurologic deficit or resp arrest may occur within minutes. - Death from herniation not bleeding |
|
• • Epidural Hematoma Arterial Bleed
- Manifestations: |
- Manifestations:
• "talk & die syndrome" period of lucidity, then rapid deterioration & death • deterioration of consciousness, • ipsilateral dilation and fixation of a pupil • Contralateral paralysis of an extremity |
|
• Intracerebral Hematoma
-Description - Etiology - Prognosis - Manifestations |
Description: a collection of 25 mL or more of blood within the brain tissue
- Etiology: MV A most common cause - Prognosis: surgical intervention only if continued expansion - Manifestations: insideous onset, HA, development of focal neuro deficits |
|
• Intracerebral Hematoma
- Complications |
- Complications
• increased ICP • Pulmonary edema: neurogenic cause • Seizures: keep sx equipment close, padded rails, IV diazepam (# 1 protect patient) CFS leak clear, watery drainage. Test with blood glucose strips - Do not clean, irrigate or suction areas of drainage - Instruct patient not to blow nose, sniff or put finger in nose or ear. |