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Mar: Sem 2 - Health Assessment > Neurologic Diseases (Exam III) > Flashcards

Neurologic Diseases (Exam III) Flashcards

1
Q

Name the pertinent vasculature of the circle of Willis.

This card is just to look at the picture on the other side.

A
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2
Q

What factors affect cerebral blood flow?

A
  • CMR (cerebral metabolic rate)
  • CPP (cerebral perfusion pressure)
  • ICP
  • PaCO₂
  • PaO₂
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3
Q

What drugs and/or metabolic states will increase CMR?

A
  • Hyperthermia
  • Seizures
  • Ketamine
  • N₂O
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4
Q

Brain tumors (most common) and 8 total types

A
  • Astrocytomas: Astrocytes are the most common CNS glial cells
  • Gliomas: Primary tumors. Least aggressive astrocytomas. Often found in young adults w/new onset seizures
  • Pilocyctic astrocytomas: Children & young adults
    Mostly benign, good outcomes if resectable
  • Anaplastic astrocytomas: Poorly differentiated
    Usually evolve into Glioblastoma Multiforme
  • Glioblastoma Multiforme: Carry a high mortality
    Usually requires surgical debulking & chemo
    Life expectance is usually within weeks, even w/treatment
  • Meningiomas: Usually benign. Arise from dura or arachnoid tissue​
    Good prognosis w/surgical resection
  • Pituitary Adenomas: Noncancerous, varying subtypes
    Transsphenoidal or open craniotomy for removal is usually curative
  • Acoustic Neuromas: Usually benign schwannomas involving the vestibular component of CN VIII within the auditory canal
    Good prognosis w/resection +/- radiation
  • Metastatic Carcinomas: can vary widely in origin & symptoms​
    Outcomes are generally less favorable

All Grand Parents Are Giggly Motivators and Pleasing Acoustic Machines

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5
Q

Brain tumors Preanesthesia considerations

A
  • Review history & physical
  • Inquire about previous therapies, presenting symptoms & neurological deficits
  • Radiation damage may lead to lethargy and AMS
  • Chemotherapy may also have neurological effects
  • Pts are often on steroids to minimize cerebral edema
  • Will need to continue steroids, monitoring glucose levels
  • Anticonvulsants common (supratentorial lesions, closer to motor cortex)
  • Autonomic dysfunction may manifest on EKG, labile HR & BP’s
  • CBC, BMP (glucose), EKG
  • CT/MRI
  • Pre-op steroids & antiseizure meds per surgeon
    Mannitol often used to reduce intracranial volume & pressure
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6
Q

Name the three components of the brain that form the Monroe-Kellie Doctrine.

A
  • Brain 80%
  • Blood 12%
  • CSF 8%
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7
Q

What is the Monroe Kellie Doctrine?

A

Any increase in one component of the intracranial space (blood, brain tissue, CSF) must be met with an equivalent decrease in another to prevent increased ICP.

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8
Q

Methods to decrease ICP

A
  • Elevation of the head: encourages jugular venous outflow
  • Hyperventilation: lowers PaC02
  • CSF drainage: external ventricular drain (EVD)
  • Hyperosmotic drugs: increase osmolarity, drawing fluid across BBB
  • Diuretics: induce systemic hypovolemia
  • Corticosteroids: decrease swelling and enhance the integrity of the BBB
  • Cerebral vasoconstricting anesthetics (propofol): decrease CMR02 and CBF
  • Surgical decompression
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9
Q

Causes of Increased ICP

A
  • Tumors (directly b/c of size, indirectly b/c of edema, or obstructing CSF flow)
  • Intracranial hematomas
  • Blood in CSF
  • Infections
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10
Q

What is the normal CPP range?

A

80 - 100 mmHg

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11
Q

What are the two types of hydrocephalus? Which is more common?

A
  • Obstructive (most common)
  • Communicating
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12
Q

Hydrocephalus treament

A

The majority of cases require surgical treatment
Ventriculoperitoneal (VP) shunt or endoscopic third ventriculostomy (ETV)
VP shunt: drain placed in ventricle of the brain and empties into peritoneum

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13
Q

Severe hypoxia will have what effect on cerebral blood flow?

A

↓O₂ = ↑CBF

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14
Q

PaCO₂ levels are directly proportional to ______ of the cerebral vasculature.

A

vasodilation

Ex. ↑PaCO₂ = ↑dilation

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15
Q

What does increased central venous pressure do to the brain?

A
  • ↓ venous drainage
  • ↑ cerebral blood volume
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16
Q

What things will increase cerebral venous pressure?

A
  • Jugular compression (cervical collar, head rotation, etc.)
  • ↑ intrathoracic pressure (coughing, PEEP)
  • Vena Cava thrombus
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17
Q

What range is normal for ICP?

A

5 - 15 mmHg

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18
Q

What symptoms are seen with abnormally high ICP?

A
  • Headache
  • N/V
  • Papilledema
  • ↓LOC
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19
Q

What is the most common site of brain herniation?

A

Uncal

↑ICP forces temporal uncus into the infratentorial space (see 3 on the figure below).

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20
Q

Subfalcine Herniation

A

Herniation of hemispheric contents under the falx cerebri; typically, compressing branches of the anterior cerebral artery, creating a midline shift

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21
Q

Transtentorial Herniation

A

Herniation of the supratentorial contents past the tentorium cerebelli, causing brainstem compression in a rostral to caudal direction. This leads to AMS, defects in gaze and ocular reflexes, hemodynamic and respiratory compromise, and death

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22
Q

Uncal Herniation

A

a subtype of transtentorial herniation, where the uncus (medial portion of temporal lobe) herniates over the tentorium cerebelli. This results in ipsilateral oculomotor nerve dysfunction
Sx: pupillary dilatation, ptosis, and lateral deviation of the affected eye, brainstem compression and death

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23
Q

Why do the pupils become fixed and dilated with uncal herniation?

A

CN-3 (oculomotor) crosses near tentorium and is compressed by the herniation.

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24
Q

How can elevated ICP be treated?

Long list

A
  • Elevate HOB 30°
  • Hyperventilate
  • Drain CSF
  • Mannitol
  • Diuretics
  • Corticosteroids
  • Surgical decompression
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25
Q

Hypothermia ______ CBF and CMR.

A

decreases

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26
Q

What is the Glascow Coma Scale?

A

see picture below

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27
Q

When would one see bradycardia with a spinal injury?

A

If the injury is at T1 - T4.

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28
Q

Are more strokes ischemic or hemmorrhagic?

A
  • Ischemic (80%)
  • Hemmorrhagic (20%)
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29
Q

Which type of stroke is more likely to cause death?

A

Hemmorrhagic (4x more likely)

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30
Q

What are specific risk factors for hemmorrhagic stroke?

A
  • HTN
  • Cigarettes
  • Cocaine
  • Female
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31
Q

Hemorrhagic Stroke Treatment

A
  • Conservative tx is centered on the reduction of ICP, blood pressure control, seizure precautions, and vigilant monitoring
  • Surgical treatment involves evacuation of the hematoma
  • May remain intubated depending on cardiopulmonary stability
    ICU monitoring required postoperatively
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32
Q

What are Causes for ischemic stroke?

A
  • large artery atherosclerosis
  • small vessel occlusion
  • cardioaortic embolic (emboli from aFib)
  • other etiology
  • underterminded etiology
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33
Q

Ischemic stroke treatment and Pre-anesthetic considerations

A
  • PO Aspirin is often the recommended initial tx for acute ischemic stroke
  • IV or intra-arterial recombinant tissue plasminogen activator (TPA) is used when specific criteria is met and must be initiated within a limited time window
  • Thrombectomy devices have been used to stent vessels and remove clots
  • Revascularization: performed in interventional radiology (IR), allowing for angiographic assessment and radiographic guidance during administration of thrombolytics or thrombectomy
  • Pre-anesthetic evaluation should be concise & efficient, avoiding any delay in treatment
  • Focus on baseline neuro assessment, ability to safely lay flat, and cardiovascular function
  • Determine whether procedure could be done under sedation, or if a secure airway necessary
  • Patients w/ischemic stroke frequently have CV risk factors, including HTN, DM, CAD, Afib, and valvular disease, that could impact vasoactive drug choices and hemodynamic goal
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34
Q

Clinical presentation of Anterior Cerebral artery occlusion

A

Contralateral leg weakness

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35
Q

Clinical presentation of Middle Cerebral artery occlusion

A
  • Contralateral hemiparesis and hemisensory deficit
  • aphasia
  • contralateral visual field defect
36
Q

Clinical presentation of Posterior Cerebral artery occlusion

A
  • Contralateral visual field defect
  • contralateral hemiparesis
37
Q

Clinical presentation of Penetrating arteries artery occlusion

A
  • Contralateral hemiparesis
  • contralateral hemisensory deficits
38
Q

Clinical presentation of Basilar artery occlusion

A

Oculomotor deficits and/or ataxia with crossed sensory and motor deficits

39
Q

Clinical presentation of Vertebral artery occlusion

A

Lower cranial nerve deficits and/or ataxia with crossed sensory deficits

40
Q

Where is bleeding located with an epidural hematoma?

A

Inbetween the dura and the skull

41
Q

What intracranial bleed is characterized by:

lucidity → unconscious → conscious → unconscious

A

Epidural hematoma

42
Q

Where is bleeding in subdural hematomas located?

A

Between the dura mater and the arachnoid mater.

43
Q

What intracranial bleed is often characterized as the “worst headache of one’s life”?

A

Subarachnoid hemorrhage

44
Q

What location is often the site of bleeding in subarachnoid hemmorhaging?

A

Circle of Willis (usually aneurysmal rupture)

45
Q

Cerebral _______ is one of the complications often caused by subarachnoid hemorrhage.

A

vasospasm

Often occurs 3rd day post bleed and peaks 5-7 days in.

46
Q

Cerebrovascular disease

A
  • High rx pts for CVA that pause LA anticoags (Warfarin) will need SA anticoags (LMWH, IV unfractionated heparin) to bridge the gap
47
Q

Cerebrovascular disease anesthetic considerations

A
  • Careful review of history, deficits, imaging, treatments, and co-existing diseases
  • Assess orientation, pupils, bilateral grip strength, LE strength
  • Ask about headaches, tinnitus, vision/memory loss, bathroom issues
  • Look at route cause of CVA: Vascular disease, embolic (a-fib, prosthetic valve, right to left shunt/PFO)
  • Imaging: Carotid U/S, CT/MRI head & neck, echocardiogram
  • Preop EKG
  • CBC, BMP, possible T & C
  • Cerebral oximetry if possible
  • Aline, 2 IVs and/or CVC
48
Q

Cerebral Aneurysms

A

Majority aneurysms not diagnosed before rupture
Only 1/3 aneurysm pts have sx before rupture
Sx: Headache, photophobia, confusion, hemiparesis, coma
Rx: HTN, smoking, female, oral contraceptives, cocaine use
Dx: CT/angio, MRI, Lumbar puncture w/CSF analysis if rupture suspected
Intervention should be performed within 72h of rupture for best outcomes
Pt may be on steroids, glucose monitoring important

49
Q

Cerebral Aneurysms anesthesia considerations

A

CT/MRI, EKG, Echo, CBC, BMP, T&C w/blood available
BP control, mannitol? *aim is to avoid rupture

seizure prophylaxis

50
Q

Post subarachnoid hemorrhage vasospasms

A
  • Risk for vasospasm 3-15 days post SAH
  • Free hgb triggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin 1, leading to vasoconstriction
    Triple H therapy (Hypertension, Hypervolemia, Hemodilution)
  • Interventional treatments s/a balloon dilation and direct injection of vasodilators relieve the spasm
51
Q

Arteriovenous Malformations (AVM)

A
  • Arterial to venous connection w/o intervening capillaries
  • Creates an area of high flow, low resistance shunting
  • Believed to be congenital
52
Q

Treatment and anesthesia considerations for AVM

A
  • Tx: radiation, angio-guided embolization, surgical resection (higher mortality)
  • Pre-anesthesia: H&P, review meds, imaging, CBC, BMP, T&C, EKG, Echo
    BP control, mannitol?, seizure prophylaxis, CVC or 2 Lg bore IV’s, Aline
53
Q

AVM grading

A

Based on size, eloquence, and patterns of venous drainage then compared to the pt’s neuro deficit

54
Q

Chiari Malformation (4 types)

A

Congenital displacement of the cerebellum
Type 1: downward displacement of cerebellum
Type 2 (Arnold Chiari): downward displacement of cerebellar vermis, often assoc w/myelomeningocele
Type 3: Rare; occipital encephalocele w/downward cerebellar displacement
Type 4: cerebellar hypoplasia w/o displacement of posterior fossa contents
*Not compatible with life

Sx: headache, extending to shoulders/arms, visual disturbances, ataxia

55
Q

Chiari Malformation treatment and anesthesia considerations

A

Tx: Surgical decompression
Pre-anesthesia: Review H&P, deficits, imaging, CBC, BMP, T&C
May hyperventilate to ↓ICP, Lg bore IV x 2 or CVC, Aline

56
Q

Tuberous Sclerosis AKA_____

A

AKA “Bourneville Disease”
Autosomal dominant disease causing benign hemartomas, angiofibromas, and other malformations that can occur anywhere in the body

Anesthesia considerations airway compromise, heart and kidney involvement

57
Q

Von Hippel-Lindau Disease

A

Autosomal dominant
Benign tumors of the CNS, eyes, adrenals, pancreas and kidneys
May present w/ pheochromocytoma

Anesthesia considerations: HTN with pheo

58
Q

Neurofibromatosis

A

Autosomal dominant
3 types:
Type 1 (most common)
Type 2
Schwannomatosis (rare)

Anesthesia considerations account for increased ICP, airway issues, scoliosis, possibility of pheochromocytoma

59
Q

How is cerebral vasospasm treated?

A

Triple “H” Therapy

  • HTN
  • Hypervolemia
  • Hemodilution
60
Q

What type of hemorrhage occurs within the brain tissue itself?

A

Intracerebral (intra-parenchymal) hemorrhage.

61
Q

What s/s are associated with Parkinson’s disease?

A
  • Muscle rigidity
  • Pill-rolling tremor
  • Bradykinesia
  • Postural instability
62
Q

What drugs will counteract levodopa and are contraindicated in Parkinson’s patients?

A
  • Metoclopramide
  • Haloperidol
  • Droperidol
  • Promethazine
63
Q

What treatments are used for Multiple Sclerosis?

A
  • Corticosteroids
  • Interferon
  • Azathioprine
  • Methotrexate
64
Q

MS signs and symptomes

A
  • motor weakness
  • sensory disorders
  • visual impairment
  • autonomic instability. Sx vary based on site of demyelination
65
Q

MS: preanesthetic considerations

A
  • Assess existing deficits
  • If respiratory compromise, consider pulmonary function tests
  • Labs: CBC, BMP, +/-LFT
  • LFT if on Dantrolene & Azathioprine (bone marrow suppression, liver function impairment)
  • Close attn to glucose and electrolytes as steroids may impact levels
  • Consider giving pre-op steroids in anyone with long-term steroid use (adrenal suppression)
  • Temperature management is critical
    Any increase in body temp can precipitate an exacerbation of MS sx
  • GA, RA & PNB’s are acceptable options
  • Avoid Succinylcholine as it may induce hyperkalemia
  • Upregulated N-ach receptors
66
Q

Myasthenia Gravis

A
  • Autoimmune; Antibodies generated against N-Ach-R’s at skeletal motor endplate
  • Effects skeletal muscle, not smooth or cardiac muscle
  • Muscle weakness, exacerbated w/exercise
67
Q

MG Treatment

A
  • Ach-E inhibitors (Pyridostigmine),
  • immunosuppressive agents,
  • steroids,
  • plasmapheresis,
  • IVIG
68
Q

MG Preanesthetic Considerations

A

*similar to MS
* Assess existing deficits
* If respiratory compromise, consider pulmonary function tests
* Optimize respiratory function
* Reduce paralytic dosage to avoid prolonged muscle weakness
* Caution with opioids to avoid respiratory compromise
* Ach-E inhibitors may prolong Succs and Ester LA’s
* Labs: CBC, BMP, +/-LFT (LFT if on Azathioprine)
* Close attn to glucose and electrolytes as steroids may impact levels
* Consider pre-op steroids in anyone with long-term steroid use
* Counsel patients on the increased risk of needing post-op resp support/ventilation until fully recovered from anesthesia

69
Q

Eaton-Lambert Syndrome

A
  • Disorder causing the development of autoantibodies against VG Calcium chnls
  • Reduce Ca++ influx into the presynaptic Ca++ channels→↓Ach release @ the NMJ
  • Sx similar to MG
  • > 60% cases are assoc w/ small cell lung carcinoma
70
Q

Eaton-Lambert Signs and symptomes

A
  • rogressive limb-girdle weakness
  • dysautonomia
  • oculobulbar palsy
71
Q

Eaton-Lambert Treatment

A
  • Selective K+ chnl blocker “3-4 diaminopyridine”
  • Ach-E inhibitors
  • immunologics (Azathioprine)
  • steroids
  • plasmapheresis
  • IVIG
72
Q

Eaton-Lambert preanesthetic considerations

A
  • Assess existing deficits
  • If respiratory compromise, consider pulmonary function tests
  • VERY sensitive to ND-NMB & D-NMB
  • Optimize respiratory function
  • Extreme caution on paralytic and opioid dosing
  • Counsel on risks for needing post-op resp support until fully recovered from anesthesia
73
Q

Muscular Dystrophy (and most common one)

A
  • Hereditary disorder of muscle fiber degeneration c/b breakdown of the dystrophin-glycoprotein complex, leads to myonecrosis, fibrosis, and skeletal muscle mbrn permeability. 6 types of MD.
  • most common is Duchenne’s MD
74
Q

Muscular Dystrophy signs and symptomes

A
  • progressive muscle wasting without motor/sensory abnormalities
  • kyphoscoliosis
  • long bone fragility
  • respiratory weakness
  • frequent pneumonia
  • EKG changes
  • Also can have elevated serum creatining kinase because of muscle wasting
75
Q

MD Preanesthetic Considerations

A
  • CBC, BMP, PFTs, consider CK
  • Pre-op EKG, echocardiogram. Evaluate for cardiomyopathy
  • Caution with ND-NMB’s, careful monitoring throughout
  • “Hypermetabolic Syndrome” similar to MH seen with Succs & volatile anesthetics
  • can lead to: rhabdomyolysis, hyperkalemia, Vfib, cardiac arrest
  • Avoid Succs & VA as they exacerbate instability of muscle membrane
  • Consider low dose rocuronium and TIVA for GA
  • Have MH cart with Dantrolene available
  • RA preferred over GA to avoid triggers and cardiopulmonary complications
76
Q

Myotonic Dystrophies (4)

A
  • Myotonia: prolonged contraction after muscle stimulation
  • Myotonic Dystrophy: most common myotonia. Onset 20-30’s
    Sx: muscle wasting in face, masseter, hand, pre-tibial muscles
    may also affect pharyngeal, laryngeal, diaphragmatic muscles
    cardiac conduction may be affected; 20% have MVP
  • Myotonia Congenita: Milder form, involving the skeletal muscles
    smooth & cardiac muscles are spared
  • Central Core disease: Rare. Core muscle cells lack mitochondrial enzymes
    Sx: Proximal muscle weakness & scoliosis
  • Myotonias are triggered by stress & cold temps
    Tx: No cure. Sx managed w/Quinine, Procainamide, Steroids
77
Q

Myotonic Preanesthetic considerations

A
  • Assess the extent of cardiac and pulmonary abnormalities
  • Assess breath and heart sounds for abnormalities
  • GI hypomotility-↑aspiration risk
  • High rx of endocrine abnormalities. Look at thyroid & glucose levels
  • Keep patients warm to avoid flare-ups
  • Avoid Succinylcholine b/c fasciculations trigger myotonia
  • Optimize preop respiratory status
  • Caution with opioids to avoid post-op respiratory depression
  • Pts are increased risk for post-op resp weakness
78
Q

Dementia (3 major syndromes)

A

Alzheimer’s (70%), Vascular dementia (25%), Parkinsons (5%)
* Assess baseline cognition
* RA preferred
* Increased risk for post-op delirium (consider TIVA)

79
Q

Parkinsons Disease and triad of disease

A
  • Degeneration of dopaminergic fibers of basal ganglia
  • Unknown cause; Advanced age is biggest risk factor
  • Dopamine regulates (inhibits excess stimulation) the extrapyramidal motor system, which is stimulated by Ach
    * Triad: skeletal muscle tramor, rigidity, akinesia
80
Q

Parkinsons preanesthetic considerations

A
  • Assess severity, with special attn to degree of pulmonary compromise
  • Review home meds, as many may interact with our drugs (ex. MAOIs)
  • Review basic labs along w/PFT if respiratory sx
  • May need EKG, Echo if indicated
  • ↑aspiration risk (dysphagia, possible dementia)
  • PO Levodopa must be continued to avoid unstable extreme extrapyramidal effects s/a chest wall rigidity
  • Avoid Reglan, Phenothiazines, Butyrophenones
  • Avoid Demerol if on MAOI
  • Deep brain stimulators may need to be disabled to avoid interaction w/cautery
  • If cautery used, bipolar recommended as it reduces scattering of electro-currant
81
Q

What induction agent is a good first-line agent for treatment of acute seizures?

A

Propofol

82
Q

What anesthetic drugs may be used to locate seizure foci due to their EEG potentiating effects?

A

Etomidate
Methohexital

83
Q

What are the s/s of seizures whilst under anesthesia?

A
  • ↑HR
  • HTN
  • ↑ ETCO₂
84
Q

Seizure disorders

A
  • Seizure: transient, paroxysmal, synchronous discharge of neurons in the brain
  • Can be c/b transient abnormalities: hypoglycemia, hyponatremia, hyperthermia, intoxication
  • or can be epilepsy
  • anriepileptic drugs decrease neuronal excitability
85
Q

Seizure disorders anesthesia considerations

A
  • Determine source of seizures (if known) and how well they are controlled. Want anti-seizure drugs on board before incision
  • Review drugs and pharmacokinetic/pharmacodynamic actions
  • Phenytoin, Tegretol, Barbiturates are enzyme-inducers
    Likely require higher doses of hepatically-cleared medications
86
Q

Traumatic Brain injury

A

Categorized: “penetrating” or “non-penetrating,” d/o breech of dura
Severity categorized by Glasco-Coma Scale
Primary or secondary injuries

87
Q

TBI anesthesia considerations

A
  • review co-morbidities
  • degree of injury
  • imaging
  • labs
  • gross neurologic exam. *Do not delay emergent surgery
  • C-spine stabilization
  • adequate IV access, CVC, Aline, possible uncrossmatched blood if no time for T & C
    Refrain from NGT/OGT –potential for basal skull fx
    Intra-op ISTAT labs, Pressors, Bicarb, Calcium, & Blood products

Mar: Sem 2 - Health Assessment (32 decks)

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