intercranial disorders Flashcards
CEREBRAL BLOOD FLOW (CBF)
The brain needs a constant supply of O2 and glucose. It uses about 20% of the body’s O2 and 25% of its glucose.
CBF = The amount of blood in mL passing through 100 g of brain tissue in 1 minute.
Normal CBF: 50 ml/min
Brain cells begin to die within 3-5 min of O2 deprivation
AUTOREGULATION OF CBF
During changes in arterial BP, diameter of the cerebral blood vessels auto adjusts based on metabolic needs to maintain a constant blood flow.
Auto regulation is effective only if the MAP is between 70-150 mmHg
CEREBRAL BLOOD FLOW
What affects CBF?
CO2 (ventilation)
O2 (oxygenation)
Hydrogen ions (pH of blood)
Cerebral Metabolic Rate
Temperature, Vasoactive Drugs, and Anesthetic Agents
CEREBRAL BLOOD FLOW- high PaCO2?
CO2 is a potent vasodilator
↑ PaCO2 → relaxes smooth muscles, causes cerebral vasodilation, ↓ cerebrovascular resistance → ↑CBF
CEREBRAL PERFUSION PRESSURE (CPP) - number range for normal CPP
Pressure needed to perfuse the brain
Normal CPP = 60 – 100 mmHg
CPP=*MAP-ICP
*MAP= Mean Arterial Pressure (The averagearterial pressureduring one cardiac cycle. A better indicator of organ perfusion than systolicblood pressure)
MAP = SBP + 2 (DBP) / 3
WHAT IS INTRACRANIAL PRESSURE - what 3 components? ON TEST
(ICP is BBC)
ICP: Is the pressure exerted by three components within the skull:
Brain tissue: 78 %
Blood : 12%
CSF: 10%
An increase in any of these
components results in increased ICP
FACTORS THAT INFLUENCE ICP
Arterial pressure
Venous pressure
Intraabdominal and intrathoracic pressure
(coughing, vomiting, bearing down)
Body positioning
Supine ↑ ICP
HOB up ↓ ICP
Temperature
CO2 and O2 levels
Seizures
INTRACRANIAL PRESSURE: NORMAL COMPENSATION
(we normally pressure monroe)
Modified Monro-Kellie doctrine:
The 3 components in the skull must remain at relatively constant volume
If the volume of one increases, the volume of another is displaced
INTRACRANIAL PRESSURE: MEASUREMENT - what number indicates ICP? (you know this)
Measured in the ventricles, subarachnoid, subdural and epidural spaces as well as brain tissue.
Any sustained reading >15mmHg is indicative of ↑ ICP. Sustained reading over 20 mmHg = poor prognosis
INCREASED INTRACRANIAL PRESSURE
Significance: ↑ in ICP → ↓CPP (central perfusion pressure) → brain tissue ischemia
Causes of increased ICP:
Head injury (bleeding, hematoma, contusion)
Increased CSF
Infection (abscess, encephalitis, meningitis)
Hydrocephalus
Tumor
INCREASED INTRACRANIAL PRESSURE - what part of the brain is affected with ICP goes up?
(medusa gets squished)
With increasing ICP, autoregulation fails, more edema/mass leads to displacement, herniation and compression of the medulla in the brain stem responsible for respiratory control → Respiratory hypoventilation → ↑ CO2 → vasodilation →»_space;> ↑ ICP
TYPES OF CEREBRAL EDEMAS = VASOGENIC: what happens?
(the vase is leaking)
Most common
Mainly in the white matter when an insult ↑ permeability of the BBB
Osmotic gradient moves more fluid into the extracellular space
INCREASED ICP:DIAGNOSTICS (the usual)
CT
MRI
Cerebral angiography
EEG
Transcranial doppler (TCD)
**Lumbar puncture: usually not done due to risk of downward herniation
INCREASED ICP: MONITORING - what GCS score?
ICP monitoring is indicated for a GCS<=8, cerebral hemorrhage, tumor, infection, or TBI
INCREASED ICP: meds - on TEST - steroids
Corticosteroids for vasogenic edema: decrease inflammation → ↓ cerebral edema
INCREASED ICP:THERAPY - what number should you keep PaCO2 at?
GOAL: Identify and treat underlying cause and support brain function
Adequate oxygenation
Hyperventilation to keep PaCO2, 30-35mmHg (book says 35-45)
Surgery: If the cause is a tumor or hematoma (Decompressive craniotomy)
Radiation for non-surgical tumors
INCREASED ICP: NURSING MANAGMENT - ON TEST - what type of test to give pt?
Evaluate mental status, cranial nerve function, motor and sensory functions
ABCs: maintain airway (with loss of consciousness the tongue drops back, occluding the airway)
INCREASED ICP: NURSING MANAGMENT - how often to do a neuro assessment? HOB?
Monitor ICP, minimize sneezing, valsalva, coughing and arousal from sleep except to perform neuro checks
Proper positioning: HOB>30 degrees unless cervical injury, head midline, avoid flexion of neck or hips
Monitor for seizures
Reduce metabolic demands such as fevers, chills, pain
Neuro assessment Q1-2hrs initially
Treat pain and anxiety: analgesics, sedatives and paralytics
Early enteral feeding or other means of nutrition improves outcome
GLASCOW COMA SCALE (GCS) - which is the best predictor of brain function?
Quick, easy, standardized method of assessing LOC
Developed in 1974 to standardize assessment of impaired consciousness, to allow all professionals to assess LOC using the same tool (may be subjective)
The 3 areas to assess are:
Eye opening response
Best verbal response
Best motor response
The higher the score, the higher the brain function
A GCS <= 8 generally indicates coma
Motor response is the most predictive for brain function of all the categories of GCS
HEAD TRAUMA
Any injury or trauma to scalp, skull or brain
Most common due to falls and MVA
Scalp laceration: relatively minor; a highly vascular area. Concern for blood loss and infection
Skull Fracture
Linear
Depressed
Comminuted (cracked everywhere)
Open vs closed
Basilar
HEAD TRAUMA – Basilar skull fracture - symptoms?
(the racoon in the basil)
Involves the base of the skull
Could evolve to review Battle’s sign (bruising around jaw/ear) and Racoon eyes
CATEGORIES OF HEAD TRAUMA - just 2
Two Categories of Head Trauma
Diffused (generalized)
Focal (localized)
HEAD TRAUMA: CONCUSSION - hallmark symptoms
Diffuse head trauma. Considered a mild TBI
“A trauma induced alteration in mental status that may or may not involve altered LOC” (American Academy of Neurology)
Hallmark symptoms:
Brief interruption to LOC
Retrograde amnesia (can’t remember what happened)
Headache
Persistent headache, lethargy, shorten attention span, behavioral changes, short-term memory affected
HEAD TRAUMA: FOCAL INJURY - brain laceration - and complications?
(lacerations tear)
Brain laceration: actual tearing of brain tissue from skull fracture and penetrating injuries
Complications: hemorrhage and hematoma, seizure, cerebral edema
Prevent secondary injuries related to increase ICP
COMPLICATIONS OF FOCAL HEAD TRAUMAS
(focused epidural)
Epidural hematoma: bleeding between dura and skull
Neurological emergency (develops rapidly if involves a major artery such as the middle meningeal artery)
Requires immediate surgical evacuation of hematoma
Venous epidural hematomas develop slowly
COMPLICATIONS OF FOCAL HEAD TRAUMAS - Subdural hematoma
(it’s in the name)
Subdural hematoma: bleeding between dura and arachnoid
Damage to brain tissue and its blood vessels
Usually venous and tends to develop slowly (can be acute, subacute and chronic)
INFLAMMATORY CONDITIONS OF THE BRAIN
Most common inflammatory conditions of the brain and spinal cord:
Meningitis
Encephalitis
Brain abscess: accumulation of pus within brain tissue usually direct extension from ear, tooth, sinus infections. Aggressive treatment with antibiotics.
Staph and strep: primary infective organisms.
These conditions can be caused by bacteria, viruses, fungi, chemicals (contaminated contrast media)
MENINGITIS
Acute inflammation of the meningeal tissue of the brain and spinal cord
Infection may spread to other parts of the brain → encephalitis
Viral or bacterial
Usually occurs in Fall, Winter or early Spring secondary to viral respiratory infection
Bacterial meningitis is a medical emergency and carries a 100% mortality if not treated early
BACTERIAL MENINGITIS: CLINICAL MANIFESTATION (and one that is specific to bacterial)
Key signs
Fever
Severe headache
n/v
Nuchal rigidity
Photophobia
Decreased LOC + signs of increased ICP
MENINGITIS: COMPLICATIONS
Increase ICP: main cause of altered mental status
Many cranial nerves may be affected: Papilledema, ptosis, diplopia, vision loss, facial paresis, tinnitus, vertigo. (Resolves within few wks if treated). Hearing loss may be permanent w/bacterial meningitis
Hemiparesis, dysphasia, hemianopsia (loss of half of vision field)
Hydrocephalus if exudate causes adhesions blocking normal flow of CSF from ventricles
VIRAL MENINGITIS - is it in the brain?
(virus not in my brain)
Not as contagious compared to bacterial type
Managed symptomatically: self limiting, usually with full recovery
Symptoms:
Fevers, headaches, photophobia, stiff neck
Seldom brain involvement
MENINGITIS: DIAGNOSIS
(Don had a lumbar puncture)
Blood culture
CT
Lumbar puncture to analyze CSF to confirm organism
Neutrophils often found in bacterial meningitis
(LP should only be done after CT to confirm r/o obstruction in foramen magnum)
X-ray may indicate infected sinus
meningitis - treatment - what type of precaution is it?
If meningitis suspected, antibiotics started right after cultures even before confirmation of dx
Common abx: Ampicillin, PCN, Ceftriaxone, vancomycin Dexamethasone with 1st dose abx: associated with lower mortality & reduced hearing loss in bacterial meningitis.
** Droplet precaution until confirmed negative
ENCEPHALITIS - SYMPTOMS - on test
Acute inflammation of the brain
Usually caused by a virus
Symptoms:
Headache
Fever
seizures
Change in LOC
ENCEPHALITIS: Epidemic
(ticks are an epidemic)
Epidemic
Ticks and mosquitos: West Nile virus
Typically seen from May to September
CEREBROVASCULAR ACCIDENT (CVA)
aka stroke, brain attack
Occurs when there is ischemia (decreased blood flow) to a part of the brain or hemorrhage (bleeding) into the brain death of brain cells
If blood flow is interrupted >2-3 minutes, metabolism stops and cellular death occurs in five minutes
CEREBROVASCULAR ACCIDENT (CVA)
- risk factors
Risk factors:
Non-modifiable: age (risk doubles each decade after 55), gender (more common in men but more women die from stroke), race (African Americans 2x the risk)
Modifiable: HTN (if managed, CVA can be reduced by 50%), smoking, Etoh use, obesity, heart disease, DM, hx of TIA
90% of strokes result of modifiable risk factors
5th Most common cause of death in the U.S.
CVA : ISCHEMIC STROKE
(ischemic TIE)
Ischemic (partial or complete occlusion to artery): 80% of all strokes
Thrombotic (blood clot formation after vessel wall injury): most common 60%
Embolic (embolus in circulation blocks artery in brain): 2nd most common
Other etiologies: MI, endocarditis, rheumatic heart disease, heart valve prosthesis
CVA: CLINICAL MANIFESTATIONS
Sudden loss of focal brain function is the core feature of the onset of acute ischemic stroke
Function affected related to artery involved:
Motor function: mobility, respiratory, speech, swallowing, gag reflex,
Bladder and bowel elimination
Spatial and perceptual alteration (neglect)
Personality and affect
Cognition
CVA: HEMORRHAGIC STROKE - is it sudden?
Hemorrhagic stroke (bleeding into brain): 15 % of all strokes
High mortality rate: 50% die within 48 hrs
40—80% mortality within 30 days
Sudden onset of symptoms with progression within minutes to hrs
BRAIN ANEURYMS
A bulging or enlargement of blood vessels in the brain
Walls of vessels weaken leading to leakage or rupture → hemorrhage
ARTERIOVENOUS MALFORMATION (AVM)
(malformed AV tangle)
A tangle of abnormal blood vessels connecting arteries and veins in the brain
Disrupts normal oxygen exchange between arteries and veins
AVMs have higher risk of bleeding
CVA: CLINICAL MANIFESTATIONS - what is the key word?
Symptoms:
Sudden numbness of face, arm, extremity, especially on one side
Sudden confusion or trouble speaking or understanding speech
Sudden trouble seeing or blurred vision
Sudden severe headache with no known cause
Sudden mobility deficit
**Key word is ”sudden”
CVA: MANAGEMENT
Most important: Time of onset of first symptom
Goal is preserving brain tissue → preserving life and reducing deficits
If unconscious: maintain patent airway and adequate ventilation
Stroke center admission preferred
ISCHEMIC STROKE MANAGEMENT - IV tpa - when to give?
(tap the ischemia)
Prepare to give IV tpa (plasminogen activator):
IV tpa: must be administered within 3 to 4.5 hrs of onset
CVA: STROKE CENTER GOAL
In hospital timeline goals for all patients with acute ischemic strokes who are eligible for IV tPA:
Evaluation by a physician within: 10 min
Stroke team contacted within: 15 min
Head CT scan within : 25 min
Interpretation of neuro-imaging scan within: 45 min
Goal : start time of tPA infusion should be < 60 min from time of arrival at the emergency department
CVA: MANAGEMENT - don’t need to memorize the dose- - IV tPA -
where is it inserted?
IV tPA:
0.9 mg/kg of body weight with a maximum dose of 90 mg
10% given IV bolus and 90% over 1 hr
Intra-arterial tPA
Catheter inserted in femoral artery and directly to area of clot
Benefit: less tPA needed leading to less risk of intracranial bleed
CVA: Post acute phase = For hemorrhagic stroke- don’t give what meds, and what should bp be?
(hemmorhaging at 160 mph)
For hemorrhagic stroke:
NO anticoagulation
Management of hypertension (goal SBP <160 mmHg)
Prophylactic anti-seizure during acute period should be discussed with care team
Surgical decompression (clot evacuation, craniotomy)
CVA - In the acute phase: neuro checks how often?
Maintain patent airway and adequate ventilation
Screen for tPA contraindication
Monitor VS (manage hypertension)
neuro checks every 1-2 hrs
Monitor for increasing ICP
Fluid and electrolyte balance
CVA: NURSING MANAGEMENT - after 48 hours - feeding?
After 48hrs of initial stroke and patient is stable:
Initiate feeding; check gag and swallow reflex
