Acute neurological disorders (ICP/Seizures) Flashcards
(36 cards)
Intracranial regulation (ICR)
Effected by
- Impaired blood flow
- Damage to brain tissue
- Comprimised neurotransmitted (eg. parkinsons)
- Impaired glucose regulation
Monro-Kellie doctrine
Skull is rigid, therefore in high ICP, it will decrease CSF to compensate for blood/brain tissue
Cerebral perfusion pressure
CPP = MAP-ICP
= Pressure needed for adequate brain perfusion
Normal CPP = 70-90 mmHg
Effected by
i) Systemi BP
ii) ICP = high icp causes less perfusion
- caused by intracranial bleeding, cerebral edema, tumor
Normal ICP is 5-15, higher than 20 is concerning
Autoregulation will fail if CPP is too low
Compensatory mechanism
1) CSF volume = Monro-Kellie doctrine, where less CSF produced and it enters spinal subarachnoid space to make space
2) Autoregulation (cerebral vasodilation/vasoconstriction
= Fails when BP is outside 60-150 mmHg
Hypotension - severe ischemia
HTN - stroke/rupture
Increased ICP causes
1) Brain tissue - tumor, edema
2) Blood - hemorrhage/hematoma
3) CSF - Hydrocephalus, meningitis
Cerebral edema
Increased fluid in intracellular/extraccular spaces
Neurological cause - ischemia, hemorrhage, hypoxia, trauma, infection, hydrocephalus
Non-neurological cause - HTN, liver damage, HE
1) Vasogenic
BBB becomes dysfunctional as permeability increases, so things leak into the brain
Allows leakage of plasma protein, which draws water
Caused by brain tumors, trauma, abscesses, toxins
Clinical manifestation - focal neurological deficits, change in LOC, severe ICP increase
2) Cytotoxic/metabolic
Sodium/potassium pump fails and causes retention of sodium = Swelling and loss of function
Cyto= cell
3) Interstitial
In hydrocephalus when there is obstruction preventing outflow of CSF, so it moves to extracellular spaces instead
Increased ICP consequences
1) Cerebral edema
2) Compression of blood vessels, tissues, ventricles = ischemia
3) Tissue hypoxia = cell death
4) Acidosis from alctic acid
5) Brainstem compression
6) Brain herniation (fatal)
Clinical manifestations of increased ICP
1) Change in LOC
- Early sign
- Decrease in blood flow
2) Ocular signs
- Compression of oculomotor nerve 3
- Sluggish/no constriction
- Ptosis = dropping of eyelids
3) Change in VS
- Cushings triad
- Change in temp (hypothalamus)
4) Decrease in motor function
- Contralateral hemiparesis/hemiplegia
- Decorticate posturing = when herniating or about to, adducted arms, damage to hemisphere, thalamus and mid-brain
- Decerebrate posturing = Adducted arms, damage to upper brainstem
5) HA
- Compression of vessels or nerves
6) Vomiting
- Direct pressure on vomiting center in medulla
7) Seizures
Cushings triad
1) HTN - increased systolic, but ICP compresses blood vessels to the brain, which causes the SNS to activate and increase BP
- High CO/BP
2) Bradycardia
Baroreceptors releases BP is high, but CO is good, so tries to slow the HR (Stupid body)
3) Bradypnea
Cheyne-stokes = irregular HR with periods of apnea due to pressure on brainstem
Bacterial meningitis
Acute inflammation of the meninges (pia, arachnoid, dura)
- occurs iin children, older adults, high risk population
- More in winter (resp disease)
Enter through Upper respiratory tract or through wound in skull
Influenza flu decreases risk
Massive inflammatory response occurs = CEREBRAL EDEMA
as neutrophils enter the subarachnoid space and release cytokinetic inflammatory agents
CSF becomes thick and interferes with flow = HYDROCEPHALUS AND OBSTRUCTION
Clinical manifestation
- Fever, HA, N/V, seizure, cranial nerve dysfunction
- Nuchal rigidity (neck stiffness)
- Positive Kernig sign (pain when flexing knee)
- Photophobia
- Hemiplegia, hemiparesis, aphasia
Seizures
Electrical impulses
Epilepsy is chronic, seizure is abnormal
Risk factors include hypoglycemia, hypoxia, alcohol, electrolyte, barbiturate withdrawel, acidosis, dehydration, water intoxication
Other - brain injury where cord wraps around fetus, ifnection, metastiatic brain tumor
Generalized seizures
Effect both side of the brain, no warning signs occurs
Tonic-clonic seizures
Most common, aura may occur
1) Tonic phase - stiffening of muscles for 10-20 seconds
2) Chlonic phase - jerking for 30-40 seconds
Biting of tongue, cheek, incontinence, excessive salivation, exhaustion/muscle soreness after
Tonic and clonic can occur seperately as their own seizures as well
Abscence seizure
More common in childhood
Person is unresonsive and blank for 5-10 seconds
Can happen up to 100x
Myoclonic seizure
Brief jerking or stiffening
Usually before bed or in the morning
Atonic seizure
Sudden loss of muscle tone then postictal confusion
Often leads to falls = helmet
Focal onset seizures
Partial seizures of one focal part of prain, manifestations will be unilateral
Can become generalized
1) Focal aaware seizures
- no loss of consciousness
- Usually warning a larger seizure will occur
- Can be motor like jerking, sensory like hearing thing, autonomic like vomiting, emotional like change of mood
- Usually a minite
2) Focal impaired awareness seizures
- 1-3 minutes
- No convulsions, but impaired consciousness
- Automatism behaviours = eg. chewing, walk aimless, click tongue, blank stare
Seizure stages
Can be triggered by strong emotion, excersie, loud music, flashing light, alcohol, lack of sleep, fever, etc
1) Predormal phase
Days or hours before, where change of mood occurs
2) Aura phase - warning signs
2) Ictal phase - the seizure
4) Psticial - recovery
Consequences of seizures
Aspiration
impaired gas exchange
injury
quality of life
mental health
STATUS EPILEPTICUS = medical emergency!!!!!!!
state of continuous seizure activity for more than 5 min
Brain in hypermetabolic state - muscle breakdown, hypoxemia, acidosis, hyperthermia, resp faliure, cardiac arrest
Seizure longer than 10 minutes = death
Mannitol (Osmitrol)
Osmotic diuretic for INCREASED ICP
MOA - Increases osmotic pressure to excrete water
CI - anuria, dehydration, pulmonary edema
AE
Pulmonary edema
Electrolyte imbalances
NC
IV
Take VS, urine output, dehydration, fluid overload, GCS, labs etc.
Seizure meds
Either suppress Na/Ca, K efflux, antagonize glutamate or potentiate GABA
Patient education
1) Require plasma drug level monitoring
2) Cannot be abruptly stopped!! = rebound status eplipticus
3) High risk of depression and suicial ideation
4) Decrease effectiveness of birth control pills
5) Teratogenic - harmful to fetus
