Nervous system Part II Flashcards
1
Q
intracranial pressure
A
- normal 8-12 mmHg
- measured in lateral ventricles
2
Q
cranial vault fixed volume
A
- brain (cellular and ICF) = 80%
- fixed, can’t manipulate the brain
- Blood (arterial and venous) = 12%
- we can manipulate this
- CSF = 8% (100-150 ml)
- can also manipulate (ventric, lumbar drains)
- don’t do this in OR very often
3
Q
ICP curve
A
- once compensation abilities is maxed out, ICP will increase significantly
- high ICP decreases CPP
- herniation
5
Q
Intracranial Elastance (compliance)
A
- determined by the change in ICP after a change in intracranial volume
- compensatory mechanisms are:
- displacement of CSF from cranial to spinal compartment
- Increased CSF absorption
- Decreased CSF production
- Decreased CBV (mostly venous)
6
Q
CPP
How do you calculate it?
What is normal?
How does CPP compare to what you will see on EEG?
A
- CPP = MAP-ICP (or CVP, whichever is greater)
- normal is 80-100
- CPP < 50 mmHg- slowing seen on EEG
- CPP < 25-40 mmHg - flat EEG
- CPP < 25 mmHg sustained - irreversible brain damage
7
Q
What are the 4 types of herniation?
A
- Subfalcine
- expansion of cerebral hemisphere pushes cingulate gyrus under the falx cerebri
- Transtentorial
- supratentorial contents compressed against the tenorium cerebelli
- Tonsillar
- displacement of cerebellar tonsils through the foramen magnum
- Herniation through traumatic defect
8
Q
how does the falx cerebri partition the brain?
A
separates the right and left cerebral hemispheres
9
Q
How does the tentorium cerebelli partition the brain?
A
- Separates the occipital lobes of the cerebral hemispheres from the cerebellum
- divides the cranial cavity into supratentorial and infratentorial compartments
10
Q
How does the Falx cerebelli partition the prain?
A
partially separates the cerebellar hemispheres
11
Q
How does the diaphragma sellae partition the brain?
A
circular extension that forms a partial roof over the hypophyseal fossa
12
Q
CSF
Capacity?
What rate is it made and reabsorbed?
What pressure gradient is important for CSF to be reabsorbed?
A
- Cavity enclosing brain and cpinal cord is about 1600-1700 ml; about 100-150 is CSF
- CSF is made and reabsorbed at about 21 ml/hr for a total of about 500 ml/day
- CSF will be reabsorbed if CSF pressure is 1.5 mmhg > than venous pressure
13
Q
How should increased ICP be managed?
A
- Goal to maintain CPP and cerebral blood flow
- ICP < 20 mmgh and increase BP
- Mannitol/hypertonic saline
- furosemide
- vasopressors
- PaCO2 low/normal = 30 mmHg
- maintain normothermia
- barbituate/propofol coma (decrease O2 need)
- CSF drainage if available (ventric)
- HOB 30 degreessurgical decompression or cranie (trauma)
14
Q
What dose of Mannitol would you administer?
Hypertonic Saline?
A
- Mannitol- 0.25 -0.5 g/kg
- Hypertonic saline- 1-2 ml/kg over 5 min
15
Q
Which patients with increased ICP would you corticosteroids to?
A
- Pts with brain tumor
- steroids help fix the BBB that is weak because of the vasculature to the tumor
16
Q
What is hydrocephalus and what are the different causes?
A
- Excessive CSF within the cerebral ventricles which increases ICP
- Communicating= free flow through ventricles
- Non-communicating= flow out of one or more ventricles is blocked
- brain tumor blocks flow to arachnoid villi
- hemmorrhage or infection (excessive RBC& WBC in csf cause blockage of small channels in arachnoid villi
- too few villi or non absorptive enough (dx as infants)
- choroid plexus tumor- too much CSF produced
17
Q
What are the two major types of edema?
A
- Vasogenic
- capillaries are more porous than usual and BBB is disruptive
- corticosteroids or hyperosmolar infusion to treat
- Cytotoxic
- Ion transport failure (from metabolic failure)
- inadequate ATP, pumps dont work, water accumulates
18
Q
What are the 3 types of traumatic head injuries?
A
- Closed head
- rapid acceleration/deceleration causes the soft brain to hit the rigid skull and ricochet
- Blunt trauma
- direct impact to the head (MVA, falls, assault)
- penetrating trauma
- bullets, foreign objects
- **leading cause of death and disability among young ppl in us; often associated with other injuries to cervical spine, thorax, abdomen
19
Q
What is the difference between primary and secondary injury?
A
- Primary injury- direct injury from the force applied to the skull and brain
- contusions, lacerations, diffuse axonal injury
- can’t really do much about primary injury
- Secondary injury- caused by the ischemia, brain swelling, edema, hemmorrhage, increased ICP, herniation in the minutes to hours following primary injury
- aggravating factors are hypoxia, hypercarbia, hypotension, anemia, hyperglycemia, sz, infection
- lots of glutamate, increases calcium to cells–>apoptosis
- goal to prevent
20
Q
What can cause parenchymal injury?
A
- diffuse axonal injury
- sudden deceleration or acceleration causes stretching or tearing of nerve cell in white matter
- contusions
- hemorrhages in the superficial brain parechyma caused by blunt trauma, resulting in coup/contrecoup contusions (shaken baby)
- traumatic intracerebral hemorrhages
- usually multiple deep in brain
- brain swelling
- may be isolated or found with something above; may be local or global
21
Q
What is an epidural hematoma?
How is it diagnosed?
treatment?
A
- AN EMERGENCY!
-
arterial bleeding between the skull and dura
- usually meningeal artery rupture secondary to skull fracture
- diagnosed by CT and signs and symptoms
- LOC fllowed by lucid honeymoon then sudden decompensation (liam Neeson’s wife)
- honeymoon period caused by artery spasming enough to stop bleeding for a minute
- Promt burr holes at fracture site
22
Q
What is a subdural hematoma?
symptoms?
treatment?
A
- lacerated or torn veins that bleed between the dura and arachnoid–slow beed
- Chronic- spontaneous or follows minor head trauma in the elderly, hemodialysis, or anticoagulated pt
- Acute- whip-lash, shaken baby
- symptoms develop over 48 hrs
- HA, drowsiness, obtundation, hemiparesis, difficulties with language, dementia
- diagnosis varified by CT scan
- Conservative medical management or surgical removal of clot if symptoms worsen
23
Q
How are head injuries treated?
A
- immobilization of cervical spine
- GCS< 8; intubate
- protect lungs from aspiration
- CT to rule out epidural or subdural hematoma
- frequent neuro checks to rule out hematoma formation/ cerebral edema/ secondary injury
- Craniotomies for depressed skull fx and evacuation of hematomas
- if break in skull, but be to OR within 24 hours or increases infection
24
Q
What is the incidence of brain tumors?
Where do they usually arise from?
A
- Intracranial incidence 10-17:100,000
- 20% of all pediatric cancers
- May arise from:
- meningeal layers
- CNS cells
- glial, neurons, choroid plexus)
- cells housed in the skull
- primary CNS lymphoma
- metastasis
25
Q
Where are pediatric tumors most common?
adult?
A
- infratentorial most common for peds
- supratentorial more common for adults
26
What is a glioma?
What types of gliomas (4) were discussed and what are their outcomes?
* Glioma is a type of tumor that starts as a glial cell
* Low grade astrocytoma- most common; good outcomes
* Grade IV glioblastoma- devastating
* very aggressive, grows diffusely
* difficult to remove, always reoccurs
* releases lots of glutamate; good for tumor, bad for us
* Oligodendroglioma- relatively good prognosis
* Ependymoma- formed out of cells that line ventricles
27
What are the other (non glioma) intracranial tumors?
(4)
* Meningiomas- typically the arachnoid layer, pretty benign, good outcomes
* Pituitary adenomas- influence pituitary fuction, can affect optic nerve
* Acoustic neuromas- Acoustic nerve, good outcomes
* Metastatic tumors
28
What is the only agent known to increase the incidence of intracranial tumors?
How does it affect the different types of tumors?
* Ionizing radiation
* Glial = 10x more likely
* meningeal = 3-7x more likely
* \*\*manifest 10-20 years after exposure
29
How are intracranial tumors diagnosed?
* symptoms related to ICP
* HA
* N/V
* neurological changes
* seizures
* increased BP and decreased HR
* Symptoms appear when compensatory mechanisms exhausted
* small changes in BP = big changes in CBF/ICP
30
Where does the pituitary gland lie?
What are the parts of the pituitary?
* Pituitary gland lies in the sella turcica
* Anterior (adenohypophysis)
* regulated by hypophyseal portal system
* releases growth hormone, TSH, FSH, etc
* Posterior (neurohypophysis)
* connected to hypothalamus by infundibular stalk
* releases ADH and Oxytocin
31
What are some non-functioning pituitary tumors?
* chromophobe adenomas
* craniopharyngiomas
* meningiomas
* these are diagnosed when they are large and cause symptoms by impinging on nearby structures
* loss of one or more pituitary functions
* loss of all pituitary functions = panhypopituitarianism
32
What are some functioning pituitary tumors?
* These tumors release hormones
* prolactinomas- females: amnorhhea, males: impotence
* GH tumor-
* before puberty: giantism
* after puberyt: agromegaly (overgrowth of bones in face), tong, and organs--\>big airway problem
* ACTH- too much cortisol
33
How are intracranial tumors treated?
* Manage ICP
* surgery- for diagnosis and removal
* radiation therapy- useful with malignant tumors
* corticosteroids- for cerebral edema
* Brachytherapy- stereotactic implantation of radiation for 4-6 days (for glioblastomas)
* chemotherapy, immunotherapy, oncolytic virotherapy
34
What are the statistics related to stroks?
ischemic vs hemorrhagic
men vs women
most common in caucasians?
most common in African americans?
* 88% are ischemic, 12% hemorrhagic
* leading cause of disability and 4th leading cause of death in US
* Men have higher incidence
* More likely over 75 yrs
* Caucasians- Extracranial carotid artery disease and cardioembolism
* African Americans- Intracranial thromboembolic disease more common
35
What are the most common causes of ischemic stroke?
What determines the extent of the infarct?
* Causes:
* cerebral athersclerosis (DM, HTN, smoking)
* emboli and loose atherosclerotic plaques
* Extent of infarct
* site of occlusion
* collateral circulation
* perfusion pressure
* time course of occlusive event
36
What are the subtypes of stroke?
* systemic hypoperfusion- cardiac arrest, hypotension
* embolism- fat, air, blood clot
* thrombosis- often preceded by TIA
* subarachnoid hemorrhage- trauma, hypertension, coagulopathy, aneurysm
* Intracerebral/brain parenchymal hemorrhage- trauma, HTN, coagulopathy, open heart surgery
37
What are the causes of acute ischemic stroke?
* Cardioembolism- afib, ventricular dysfunction following MI, dilated cardiomyopathy, valvular disease
* large vessel atherosclerotic narrowing- carotid bifurcation in the neck
* small vessel occlusive disease (DM, HTN)
* Hypercoagulable state
38
What are the risk factors for acute ischemic stroke?
* **systemic hypertension**
* smoking
* hyperlipidemia
* DM
* ETOH \> 6 drinks/day
* increased homocysteine level
39
What are treatments for acute ischemic stroke?
* Carotid endarterectomy- preventative measure when the carotid artery is \>70% stenotic
* supportive therapy- airway, oxygenation, ventilation, systemic BP, bood glucose, temperature, heparin prophylaxis
* Aspirin initial treatment
* IV recombinant tissue plasminogen activator- within 3 hours
* may also directly infuse TPA into occluded blood vessel with angiography
* ICP, CPP, and cerebral edema management
40
What is malignant middle cerebral artery syndrome?
What else are acute ischemic stroke patients at risk for?
edematous infarcted tissue that compresses other cerebral arteries causing secondary injury
* also at risk for infarction of the cerebellum with basillar artery compression and brain stem ischemia
* caused by swelling
41
Random information about **intracerebral** hemorrhagic stroke.
(good luck)
* 4x the risk of death compared to ischemic stroke
* high incidence among african americans
* noncontrast CT needed to diagnose
* volume of blood + LOC determine prognosis
* pts often decompensate 24-48 hrs after the bleed secondary to edema formation
* surgical decompression of blood unclear in effectiveness
* ICP control is important (a second bleed is often fatal)
* Supportive therapy- ETT, ICP monitor, MAP \< 130 mmHg
42
What is the pathophysiology of **subarachnoid** hemorrhagic stroke?
* usually caused by aneurysms at the circle of will involving the anterior and posterior communicating arteries
* systemic HTN, DM, and cigarette smoking increase risk
* size of aneurism is important in determining risk of rupture
* 6-10 mm at greatest risk
* \>25mm 6% risk of rupture increase per year
43
How are hemorrhagic strokes diagnosed?
* "worst HA of my life"
* photophobia
* stiff neck
* decreased LOC
* focal neurologic changes
* ECG changes- catecholamine rush
* + CT scan
* \*prompt diagnosis and clipping can decrease M&M
44
What is the treatment for hemorrhagic stroke?
* Ideally to OR within 72 hours
* pre-op kept sedated on stool softeners to prevent re-bleed and anticonvulsants
* systemic BP kept normal
* Goal CPP 61-80
* Ventricular drainage if hydrocephalus seen on CT after clinical deterioration
* Vasospasm prevention
45
How is vasospasm prevented?
* Daily transcranial doppler examinations
* Nimodipine (Ca channel blocker)
* Triple H therapy after clinical signs begin
* HTN
* Hypervolemia
* hemodilution
* \*not clear if triple H works--goal to get the blood through that spasming vessel
