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brain death final Flashcards

1
Q

What is delirium?

A

-Acute, transient, usually REVERSIBLE confusional state
-alteration of consciousness with reduced ability to focus, sustain, or shift attention
-Results in cognitive or perceptual disturbances that is not better explained by a pre-existing, established, or evolving dementia
-Develops over a short period of time (hours to days)

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2
Q

What does delirium result in?

A

Cognitive or perceptual disturbance
- that is not better explained by a preexisting, established or evolving dementia

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3
Q

How fast does delirium develop?

A

Over a short period of time
Hours to days

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4
Q

Causes of delirium?

A

Medical Conditions
Substance Intoxication
Medication Side Effect

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5
Q

What do 30% of elderly experience during hospitilization?

A

Delirium

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6
Q

Where are higher rates of Delirium?

A

ICU= 70%

Hospice=42%, ER=10%, Post acute care=16%

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7
Q

What are risk factors of delirium?

A

-Advanced age
-Recent surgery
-Pre-existing brain disease (e.g. dementia, stroke, Parkinson’s)
-30% of elderly patients experience delirium during hospitalization -> Higher rates in ICUs

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8
Q

What are precipitating factors for delirium?

A

Polypharmacy
Infection
Dehydration
Malnutrition
Bladder Catheters

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9
Q

What may be the only sign of acute illness in elderly patients?

A

Delirium

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10
Q

Delirium DSM 5 criteria includes

A
  1. Disturbance in attention and awareness (1st)
    - distractability = hallmark
  2. Develops over short period of hours
    - days; most severe night/evenings
  3. Cognitive disturbance including perceptual
    - ex: memory deficit, disorientation, language, visuospatial ability, perception
    4.Not explained by another neurocognitive disorder or coma
  4. Evidence (h&p,labs) that disturbance is caused by medication, condition or substance
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11
Q

What is course of delirium?

A
  1. Prodromal phase: fatigue, sleep disturbance, depression/anxiety, restlessness, irritability, hypersensitivity to light or sound
  2. Perceptual disturbances and Cognitive impairment
  3. Quiet/hypoactive - not interacting with environment (mc) or agitated confused state
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12
Q

During the prodromal phase what symptoms are included?

A

SLEEP DISTURBANCE
IRRITABILITY
fatigue
depression/anxiety
restlessness
hypersensitivity to light or sound

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13
Q

On exam for delirum what signs are seen?

A

-Change in level of consciousness
-Inability to direct, focus, sustain or shift attention
-Memory loss, disorientation, difficulty with language or speech -> Speech may be tangential, disorganized, incoherent
-Advanced: drowsy, lethargic, semi-comatose

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14
Q

It is important to get a good HISTORY on delirium patients, look for:

A

Recent febrile illness
Hx of organ failure
Med list
Hx of alcoholism or drug abuse
Recent depression

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15
Q

suspect delirium, what tests to perform?

A
  • MMSE
  • attention with serial 7s, spell “world” backward
  • focused exam on: hydration status, skin, vitals, source of infection
  • CAM: confusion assessment method: sensitive and specific, takes 5 min, ICU version available
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16
Q

What is advanced delirum signs?

A

Drowsy
Lethargic
Semicomatose

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17
Q

What is included when testing/ screening for delirium?

A

CAM - Confusion Assessment Method
-94-100% sensitive, 90-95% specific
-episodic tool: when you first enter, when there is surgery, if suspected
-5 minutes to administer
-ICU version available
-compare entry CAM to current CAM

-sepsis protocol
-vital signs
-Serum: Evaluate electrolytes, creatinine, calcium, CBC, U/A with culture
- consider toxicology screen
- ABG
- Imaging: CXR, consider CTH, LP, EEG when indicated, CT of head

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18
Q

Most common etiologies for delirium

A

-Post operative states (very common in elderly)
-Drug toxicity (30% off all cases)
-Fluid / Electrolyte disturbance - hypo/hyperNATREMIA, dehydration
-Infections- UTI, skin and soft tissue, pneumonia
-ETOH or other substance intoxication
-Barbiturates, benzodiazepines, ETOH withdrawal
-Metabolic disorders - shock
-Low perfusion states

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19
Q

What are main drug culprits for delirium?

A

Opioids, Benzodiazepines, Anticholinergic (Diphenhydramine)**

-Acyclovir
-Antimalarials, Interferon, Amphotericin B, Cycloserine
-Cephalosporins, Fluoroquinolones, Macrolides, Metronidazole, Penicillins, Sulfonamides, Aminoglycosides, Linezolid
-Isoniazid, Rifampin
-Corticosteroids
-Hypoglycemics!
-CV: antiarrhythmics, BB, Clonidine, Digoxin, Diuretics, Methyldopa
-CNS-active agents: Lithium, IL-2, Phenothiazines, Donepezil
-Anticholinergics: atropine, benztropine, scopolamine, trihexyphenidyl, diphenhydramine!!!!!
-Dopamine Agonists: Amantadine, Bromocriptine, Levodopa, Pramipexole, Ropinirole
-Anticonvulsants: carbamazepine, levetiracetam, phenytoin, valproate, vigabatrin
-GI: antiemetics, antispasmodics, H2 Blockers, Loperamide
-Muscle Relaxers: Baclofen, Cyclobenzaprine
-Herbals: St. John’s Wort, Valerian

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20
Q

Delirium Treatment and Prevention

A

-treat underlying cause
-treat their distress
-antipsychotic rarely needed (<10%)
-optimize conditions for brain recovery
-orientation protocols and psychological support
-monitor for recovery
-resolves in less than a week usually

if severe agitation: psychotropic drugs PRN - haloperidol, risperidone, olanzapine, quetipaine, aripiprazole

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21
Q

What psychotropic med is used for severe agitation or psychosis with delirium?

A

-antipsychotics: Haloperidol, Risperidone, Olanzapine, Quetipaine, Aripiprazole

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22
Q

What is sundowning?

A

-Behavioral deterioration seen in evening hours
-Often seen in demented and institutionalized patients
-Presumed to be delirium if NEW pattern
-If true sundowning (no medical cause)-> Consider: impaired circadian regulation, nocturnal factors in the environment (change of shift, noise)
- affects 2/3 dementia pts

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23
Q

If established sundowning and no obvious medical illness consider?

what are risk factors:

A

consider:
- Impaired circadian regulation
- noctural factors in environment (noise, staff)

risk factors:
-Poor light exposure
- Disturbed sleep

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24
Q

delirium vs dementia vs pseudo-dementia or dementia of depression

A
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25
Q

What is age associated cognitive decline?

A

-Normal cognitive decline associated with aging
-Memory and information processing changes: Ex: difficulty recalling names
-Is NOT progressive**
-Does NOT affect activities of daily living**

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26
Q

Is age associated cognitive decline progressive? Does it affect ADLS?

A

NO!

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27
Q

Mild neurocognitive disorder (mild cognitive impairment) is an intermediate clinical state between

A

Normal cognition and dementia

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28
Q

What can Mild Cognitive Impairment be a precursor to

A

Alzheimer Dementia

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29
Q

With Mild Cognitive Impairment when does prevalence increase

A

After age 60

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30
Q

What can Mild Cognitive Impairment also represent?

A

A reversible condition in setting of:
- depression
- CHF
- complication of med
- recovery from acute illness

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31
Q

Mild Cognitive Impairment tx

A

No specific treatment
could do trial of Donepezil

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32
Q

What symptoms are common with Mild Cognitive Impairment?

A

Mood/Behavioral sx
- 40% Depression
- others: anxiety , irritability, agression ,apathy

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33
Q

What is included in the criteria for Mild Cognitive Impairment?

A

Memory complaint: Change from baseline that is corroborated by an informant
Objective memory impairment: ex - For their age and education
Preserved general cognitive function
Intact ADLs
Not demented

-if you dont screen it you will miss it
-they seem very normal

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34
Q

What testing is preformed with MCI?

A

-MMSE vs MoCA- just know they exist
-Physical, including
-Neurologic Examination
-Neuropsychological Testing
-MRI&raquo_space;»»Non-contrast head CT
-Screening for B12 Deficiency and Hypothyroidism -> reversible

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35
Q

What should be screened for with MCI

A

Screen for b12 deficency and hypothyroidsm

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36
Q

What is major neurocognitive disorder? what criteria? (dementia)

A

Progressive gradual deterioration of selective functions
- Decline from previous baseline enough to interfere with DAILY function and INDEPENDENCE*
-AAN and USPSTF recommends routine screening for dementia in asymptomatic adults

Criteria: there must be cognitive decline in 2+ domains
-learning
-memory (new information)
-language
-executive function (complex tasks, poor judgement)
-complex attention
-perceptual-motor
-social cognition

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37
Q

Risk factors for major neurocognitive disorder? MCC of major neurocognitive disorder

A

Risk factors:
- Age > 60 y/o
- Vascular Disease- htn,dm

MCC: alzheimer ds*

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38
Q

Most common cause of major neurocognitive disorder? other causes

A

Alzheimer Disease**
-Less common causes: alcohol-related, CTE, normal pressure hydrocephalus, chronic subdural hematoma, CNS illness (Creutzfeldt-Jakob disease, HIV), copper/B12/Folate deficiency

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39
Q

What is the first manifestion of dementia?

A

Memory loss
-presents as forgetfulness

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40
Q

Clinical manifestations of dementia

A
  1. memory loss- 1st manifestation- presents as forgetfulness (trouble remembering recent events)
  2. Deficits in other cognitive domains (with or after memory loss)
    - Executive dysfunction (less organized/a, difficulty multitasking) - early
    - Impaired visuospatial skills (getting lost in familiar places) - early
    - Language dysfunction (word finding) – late
    - Behavioral symptoms (apathy, social disengagement, irritability; agitation, aggression, wandering, psychosis) – middle/late
  3. Non-cognitive neurologic deficits – late
    -Pyramidal/Extrapyramidal motor signs, myoclonus (uncontrollable twitching), seizures
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41
Q

What is the life expectancy after diagnosis with dementia?

A

8-10 years avg
- range is 3-20

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42
Q

Dementia Hx and PE

A

Close friend or family member needed

-History:
-Drug history
-Past medical
-Social history (including ETOH)
-Daily activities (finances, social, community, driving, household tasks)
-Onset of symptoms
-Vision, motor functioning
-Tremor
-Balance, falls, gait
-Visual hallucinations
-Change in sleep habits
-Dementia is a clinical diagnosis. You need a history + scoring tools + r/o organic pathology

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43
Q

What is assessed on dementia cognitive exam

A

-MMSE or MoCA
-Complete physical exam
-Labs:
-Routine labs such as CBC, CMP, Calcium, UA
-B12 deficiency and hypothyroidism screening (AAN recommendation)
-Any other indicated labs based on their history / physical (ex: heavy metal, ETOH/Drug screening, syphilis)
-Imaging: MRI brain without contrast (AAN recommendation, over CTH)

other considerations:
-LP: rule out infectious, inflammatory, neoplastic causes
-EEG: Atypical syndrome with concern for Creutzfeldt Jakob disease (less than 60 years old, rapidly progressive symptoms)
-PET: distinguish a vascular cause from Alzheimer’s
-Brain biopsy: definitive but rarely done

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44
Q

What is clinical diagnosis for dementia

A

history + scoring tools + r/o organic pathology

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45
Q

What lab work is performed for dementia?
AAN recommends

A

-Screen for B12 deficency (Cbc, serum vb12)
-Screen for hypothyroidism (Serum tsh)

46
Q

What imaging is performed for demntia?
AAN recommends

A

MRI without contrast»»>ct in all initial evals

47
Q

Why would EEG be performed when testing for dementia

A

To rule out atypical syndrome if <60 or rapidly progressive
To rule out Creutzfeldt Jakob Disease

48
Q

What does a PET scan distinguish

A

Vascular from Alzheimer’s

49
Q

What is definitive diagnosis for dementia

A

Brain Biopsy but rarely used

50
Q

frontotemporal dementia (FTD) AKA picks disease SUMMARY

A

-Rare!
-Focal degeneration! of the frontal and/or temporal lobes! with distinctive round silver staining inclusions (called pick bodies)

Symptoms:
-1. Marked personality and behavioral changes- disinhibition, apathy, altered food preferences, compulsive
-2. Aphasia- Non -fluent, expressive aphasia common: Words remain but are presented in nonsensical format
-3. No amnesia or visuospatial symptoms. Lack CN, sensory, cerebellar changes at least initially
-Changes occur early and progress quickly

Epidemiology:
-Younger (mean age 58 yo)
-Male predominance

Tx:
- non-pharm interventions for safety - no driving, exercise, speech and behavioral therapy
- SSRI: CITALOPRAM** trazodone for anger issues

51
Q

frontotemporal dementia (FTD) AKA picks disease: imaging and tx

A

MRI: Frontal and/or temporal atrophy!*

Treatment:
-symptomatic
-Non-pharm interventions for safety: driving, exercise, speech therapy, behavioral modification
-SSRI Citalopram, Trazodone

52
Q

What is DSM-5 criteria for Major Neurocognitive Disorder

A
  • Evidence of significant cognitive decline from a previous level of performance
    -Interfere with independence in every day activities
    -The cognitive deficits do not occur exclusively in the context of a delirium
    -The cognitive deficits are not better explained by another mental disorder
53
Q

Dementia with Lewy Bodies: dementia associated with

A

Cognitive fluctuations - inability to concentrate
Motor parkinsonism: Bradykinesia, rigid, shuffling gait
Psychotic features -visual hallucinations, delusions**
REM Behavior disorder - Sleep issues - act them out while dreaming
dysautonomia
visuospatial dysfunction

54
Q

How is dementia with lewy bodies distinguished?

A

PSYCHOTIC FEATURES

55
Q

Dementia with lewy bodies: imagining and Dx

A

CT/MRI:
-Generalized atrophy and white matter lesions are nonspecific findings in dementia

No test can definitively diagnose DLB
-you have to go based on the DSM criteria

56
Q

Dementia with lewy bodies treatment

A

-Cholinesterase inhibitor trial (first line, for dementia + visual hallucinations)*
-Levodopa: for parkinsonism
-Melatonin or clonazepam: For REM behavioral disorder
-SSRI: for depression

-Patients w/ DLB should not be given the older, typical D2-antagonist antipsychotic agents such as haloperidol (Haldol), fluphenazine (Prolixin), and chlorpromazine (Thorazine). Adverse effects include sedation, rigidity, postural instability, falls, increased confusion, and neuroleptic malignant syndrome, with an associated two- to threefold increase in mortality.

57
Q

Parkinson disease dementia FEATURES

A

Parkinson Features
-Tremor, Rigidity, Bradykinesia
-Cognitive impairment
- Gait dysfunction
- Urinary incontinence

58
Q

parkinson disease dementia (PDD) DEFINITION

A

-Dementia that occurs in the later stages of Parkinson’s disease
-Occurs 5-8 years after onset of the motor symptoms of disease
-(unlike DLB, where dementia starts first, followed by motor parkinsonism within a year of onset)

Parkinsonian features:
-Tremor, rigidity, bradykinesia
-Cognitive impairments
-Gait dysfunction
-Urinary incontinence

59
Q

Treatment for parkinson disease dementia

A
  1. Levodopa (first line)
  2. Cholinesterase Inhibitor
60
Q

Alzheimer disease Dementia Hallmark sx

A

-Memoryimpairment (MC)- Especially anterograde episodic amnesia > Retrograde
-Impaired executive function- Early on will be aware of these deficits and With time will have reduced insight (anosognosia)
-Behavioral and psychologic symptoms- Especially apraxia, sleep disturbance
-Gait dysfunction (late)
-No motor or sensory deficits at presentation

61
Q

stages of alzheimer ds

A

Mild:
-Wandering, getting lost, repeating questions

Moderate:
-Problems recognizing friends and family
-Impulsive, loss of judgement and reasoning is inevitable
-Disinhibition and uncharacteristic belligerence may occur- Alternate with passivity and withdrawal

End stages:
-Pts becomerigid, mute, incontinent, and bedridden
-Need help w/eating, dressing, and toileting
-Hyperactive tendon reflexes and myoclonic jerks (sudden brief contractions of various muscles or the whole body) may occur spontaneously or in response to physical or auditory stimulation

Death:
- Secondary to malnutrition, secondary infections, pulmonary emboli, heart disease, or, most commonly, aspiration.

Changes in environment (hospitalization, travel, NH) tend to destabilize the patient
-symptomatic pt lives 8–10 years usually, but ranges from 1–25 years

62
Q

Alzheimer disease dx

A

Dx: excluding other etiologies of dementia

CT/MRI:
- reduced hippocampal volume/ medial temporal lobe
- mild ventricle dilation

demonstrates brain atrophy

63
Q

What is treatment for alzheimer disease

A

Acetylcholinesterase inhibitors: DONEPEZIL!! 10mg QD (1st line), rivastigmine
-Reverses cholinergic deficiency
-Side effects: GI upset (nausea/diarrhea/cramps), altered sleep w/ vivid dreams, bradycardia, muscle cramps

NMDA antagonists: Memantine -> Blocks NMDA receptor, which means it blocks the excitatory glutamate, which can cause cell death

Vitamin E

64
Q

Vascular Dementia
(2nd MC) (“post-stroke” dementia) definition

A

-2nd most common cause of dementia
-Brain disease due to chronic ischemia! and multiple small infarctions! (lacunar infarcts)
-Highly associated with older age and CVD (IHTN, DM, HLD, PAD, obesity, smoking, afib)

Two types:
-Post stroke dementia
-Vascular dementia without recent stroke

65
Q

Vascular Dementia DSM 5 criteria

A

Development of cognitive deficits manifested by both:
-Impaired memory
-Aphasia, apraxia, agnosia, disturbed executive function

Significantly impaired social, occupational function

Focal neurologic symptoms and signs/evidence of cerebrovascular disease

STEPWISE deterioration after each event

66
Q

Vascular Dementia
(2nd MC) (“post-stroke” dementia) CT/MRI

A

cortical and subcortical and lacunar infarctions
microbleeds

67
Q

Vascular Dementia Treatment + prognosis

A

-Vascular risk modification
-Antithrombotic therapy- Usually ASA
-Cholinesterase inhibitor therapy: Donepezil or galantamine

Prognosis:
-Because vascular dementia is a heterogeneous disorder, the prognosis is not predictable

68
Q

Normal Pressure Hydrocephalus
Classic Triad

A

WET WHACKY WOBBLY

1) Gait disturbance:
-Difficulty with ambulation
-“Glue-footed” gait: move slowly, take small steps, often wide base, with difficulty turning

2) Cognitive disturbance:
-Dementia, memory loss
-Develops over months – years
-Impaired executive function (early), apathy (depressed), psychomotor slowing, decrease attention and concentration

3) Urinary incontinence
- Urgency, but unable to get to the bathroom in time -> late because frontal lobe impairment causes lack of concern

69
Q

normal pressure hydrocephlus: description classic triad

A

-Organic and possibly reversible cause of dementia
-CSF buildup in ventricle that lead to increased intracranial pressure with edema of the periventricular white matter
-Oddly, often do not have symptoms of ↑ ICP (HA, N/V, Visual loss)
-Classic triad (not all 3 are required)- WET WHACKY WOBBLY (gait, cognitive disturbance, urinary incontinence)
- tx: shunt to relieve pressure

70
Q

creutzfeldt-jakob disease (CJD) description and types

A

RAPID onset dementia due to prion (misfolded protein) disease
-Sporadic type: Normal brain protein misfolds
-Variant type: Consuming misfolded proteins - MAD COW disease occurs when eating meat from a cow with bovine spongiform encephalopathy
-Familial CJD: rare genetic form where brain cells misfold in adulthood
-Iatrogenic CJD: obtain through blood transfusion or corneal transplant

DMS 5 criteria (dont need to know), normal EEG, Positive 14-3-3 CSF protein on LP suggest CJD (not always +)
-Definitive diagnosis post mortem with neuropathology
-No known tx, fatal disease within 1 year of onset

71
Q

creutzfeldt-jakob disease (CJD): sx

A

-Neuropsychiatric symptoms: dementia, behavioral abnormalities, and deficits involving higher cortical function including aphasia, apraxia, and frontal lobe syndromes**
-Myoclonus (muscle spasm), especially provoked by startle*
-Cerebellar manifestations!: nystagmus and ataxia
-Signs of corticospinal tract involvement!: hyperreflexia, extensor plantar responses (Babinski sign), and spasticity.
-Extrapyramidal! signs such as hypokinesia, bradykinesia, dystonia, and rigidity also occur.

72
Q

Thiamine (B1) deficiency description + triad + tx

A

-causes Wernicke’s encephalopathy
-Malnourished pt (usually alcoholism. AIDs, anorexia, ESRD, hematologic malignancies due to hypermetabolic state)
- Tx: Thiamine 100mg IV x 3 days followed by daily PO may reverse disease if given in first few days of onset (thiamine THEN glucose)

Triad of :
-1. Encephalopathy (disorientation, indifference, inattentiveness, memory loss)
-2. Ataxia (gait problems)
-3. Ocular motor dysfunction (diplopia, nystagmus)

73
Q

untreated and prolonged Wernicke’s encephalopathy

A

-KORSAKOFFF SYNDROME occurs in prolonged and untreated Wernicke’s encephalopathy
-IRREVERSIBLE
-Unable to recall old AND new information
-Confabulations = unconsciously makes up stories to fill gaps in memory

74
Q

vitamin B12 deficiency

A

-deficiency causes megaloblastic anemia
-Produces spinal cord myelopathy!! that affects the
-Posterior columns -> loss of vibration and position sense
-Corticospinal tract -> hyperactive tendon reflex w/ babinski
-Peripheral nerves -> neuropathy with sensory loss and depressed tendon reflex
-Damage to myelinated axons may cause dementia

-—————-

Megaloblastic anemia: Vitamin B12 deficiency causes impaired DNA synthesis, leading to the production of large, abnormal red blood cells (megaloblasts).
Spinal cord myelopathy: Specifically, this is known as subacute combined degeneration of the spinal cord, which primarily affects the:
Posterior columns: Leading to loss of vibration and proprioception (position sense).
Corticospinal tracts: Resulting in hyperactive reflexes and a positive Babinski sign (upgoing toes).
Peripheral nerves: Leading to neuropathy, characterized by sensory loss and decreased tendon reflexes.
Cognitive effects: Damage to myelinated axons in the brain can lead to dementia or cognitive impairment.

75
Q

dementia: tx options drug names + indications

A

(1) Cholinesterase Inhibitor: Donepezil!!!! (Aricept), Rivastigmine, Galantamine (Razadyne)
-Indications: newly diagnosed AD, DLB, VaD, PD Dementia

(2) Vitamin E 2000 IU/day!!!!
-Indications: mild-moderate AD (only) interested in non-pharmacologic treatments

(3) NMDA Antagonist: Memantine!!! (Namenda)10 mg BID
-Indications: monotherapy or adjunct for moderate-severe Alzheimers dementia.
-Off-label use: Vascular dementia, Mild Alzheimer’s dementia, chronic pain, psychiatric disorders, mild cognitive impairment

76
Q

Cholinesterase Inhibitor: donepezil*
(Rivastigmine, Galantamine) MOA, indication, ADR, CI

A

-MOA: Reverses cholinergic activity deficiency, may not always slow down progression but helps symptomatic treatment
-Indications: newly diagnosed AD, DLB, VaD, PD Dementia
-Adverse effects: GI upset (N/V, anorexia, diarrhea), bradycardia, rhabdo, NMS (rare)
-CI: Known bradycardia, caution if using BB/CCB

77
Q

NMDA Antagonist: Memantine MOA, indication, off label use, ADR

A

NMDA Antagonist: Memantine!!! (Namenda) 10 mg BID

MOA: blocks at NMDA receptor, slowing calcium influx and nerve damage. Neuroprotective.
-Glutamate causes excitotoxicity of NMDA receptor, causing cell death
-Indications: monotherapy or adjunct for moderate-severe Alzheimers dementia.
-Off-label use: Vascular dementia, Mild Alzheimer’s dementia, chronic pain, psychiatric disorders, mild cognitive impairment
-Adverse effects: Dizziness (most common), confusion, hallucinations, agitation, delusions

78
Q

who needs a specialist referral for dementia?

A

-Young onset dementia (<65yo)
-Strong family history
-Non-Alzheimer dementia is suspected -Early age, rapid progression, severe behavioral changes, language problems, hallucinations, Parkinsonisms
-Uncertainty about the diagnosis- Is it their age, depression, encephalopathy?

79
Q

AMS and COMA

A

-AMS is a symptom, not a disease!
-Ascending reticular activating system (ARAS) = gives us consciousness
-in the brain stem and its central connections to the thalamus and cerebral hemispheres.

80
Q

levels of consciousness

A

-alert
-awake but disoriented or aphasic
-drowsy - lethargic but arousable to voice, light touch
-obtunded- lethargic, but arousable to vigorous mechanical stimulation
-stuporous- localizing to deep pain
-comatose - meaningful responses are absent! -> no reflexes, abnormal posture, none or non-localizing responses

81
Q

What are the components of the Glasgow COMA scale; what is GCS

A

eye opening, verbal response, motor response

-Used to objectively describe the extent of impaired consciousness in all types of acute medical and trauma patients.
-Individual elements as well as the sum are important
-Scores are expressed as “GCS 9 – E2 V4 M3”

82
Q

GCS score minor, moderate, severe number values

A

-GCS ≤ 8 = Severe
-GCS 9-12 = Moderate
-GCS ≥ 13 = Minor
-GCS 15 = Max, normal score
-GCS < 8 = Intubate!!!!

83
Q

Eye opening response (GCS)

A

Eyes: four eyes
4 spontaneously
3 to speech
2 to pain
1 no response

84
Q

Verbal Response (GCS)

A

5 - oriented
4 - confused
3 - inappropriate words
2 - incomprehensible sounds
1 - none

85
Q

Motor response (GCS)

A

motor: 6 cylinder motor
6-obeys commands
5-moves to localized pain
4-flex to withdrawfrom pain
3-abnormal flexion
2-abnormal extension
1-none

86
Q

eliciting responses from unconscious pts

A

-sternal rub
-eyelid/brow
-roll a pencil on nail bed
-press on TMJs

87
Q

approach to AMS

A
  • ABCs COME FIRST- Check for quick reversible causes, do they need naloxone (pinpoint pupil, opoid overdose)? Glucose? Thiamine (for alcohol)?
    -always get a stat glucose
    -Get a good history- What might be causing this AMS?
    -Do a good neuro exam- Is the AMS from a structural brain lesion?
    -What is the possible location of the lesion?
    -Appropriate labs and imaging tests
88
Q

AMS history question: when did it occur? what preceded it?, what else do you want to know?

A

WHEN DID IT OCCUR?
-SUDDEN: SAH, basilar stroke, poisoning
-GRADUAL: encephalitis, meningitis, sepsis, organ failure
-FLUCTUATING: recurrent seizures, delirium

WHAT PRECEDED IT?
-Fevers -> Meningitis, encephalitis, sepsis, certain drugs
-Headaches -> SAH, ICH, meningitis
-Focal deficits (motor, speech, vision) -> Strokes, ICH, other acute bleeds
-Confusion -> Sepsis, drugs, medications

RECENT TRAUMA, SUBSTANCE ABUSE, suicidal Ideation, recent surgery, HOSPITALIZATIONS

UNDERLYING MEDICAL CONDITIONS ± MED CHANGES

WHAT IS THEIR BASELINE?

89
Q

underlying etiologies for AMS

A

-barely went over
-Underlying etiologies:
Drugs / Ingestions
-Structural brain lesions (CVA, tumor, anoxia)
-Organ dysfunction (endo, lytes, resp, cardiac)
-Sepsis/Infections
-Seizures (think PRES)

90
Q

AMS: Dx testing: metabolic or endocrine causes

A

-barely went over
-Rapid glucose
-Serum electrolytes (Na+, Ca+)
-Serum bicarbonate in the basic metabolic panel helps assess degree of acidosis and may clue to a broad differential diagnosis (CAT-MUDPILES).
-BUN/Creatinine (uremia, upper GI bleed)
-ABG or VBG (with co-oximetry for carboxy- or met-hemoglobinemia)
-Thyroid function tests
-Serum Ammonia level
-Serum cortisol level
-Toxic or medication causes

91
Q

AMS: dx testing: traumatic causes

A

-barely went over
-Head CT/ cervical spine CT
-POCUS
-Chest and Pelvis X-ray
-Other imaging modalities as indicated

92
Q

AMS: dx testing: infectious causes

A

-barely went over
-Blood cultures
-CBC with differential
-Serum lactic acid if meets systemic immune response syndrome (marker for severe sepsis or septic shock)
-Urinalysis and culture
-Chest X-ray
-Lumbar puncture (with opening pressure); always obtain a CT scan of the head prior to lumbar puncture if you suspect an increased intracranial pressure (ICP)

93
Q

AMS: dx testing: Levels of medications (anticonvulsants, digoxin, theophylline, lithium, etc.)

A

-barely went over
-EKG (certain medications such as TCA can prolong QTc and others like lithium cause other arrhythmias)
-Drug screen (benzodiazepines, opioids, barbiturates, etc.)
-Ethanol level
-Serum osmolality (toxic alcohols)

94
Q

AMS: dx testing: neurologic causes

A

-barely went over
-Head CT (usually start without contrast for trauma or CVA)
-MRI (if brainstem/posterior fossa pathology suspected)
-Carotid/vertebral artery ultrasound
-EEG (if non-convulsive status epilepticus suspected)
-Hemodynamic instability causes
-POCUS including bedside echocardiography
-ECG
-Cardiac enzymes (silent MI)

95
Q

coma definition and outcomes

A

State of unarousable unresponsiveness

Almost always traced back to either:
-B/L hemispheric damage
-Reduced ARAS activity
-Pts may have brainstem responses, spontaneous breathing, purposeful motor movements

Three outcomes:
-Recovery
-Persistent coma (vegetative state)
-Brain death

96
Q

easy way to remember the causes of coma

A

A = anoxia/apoplexy
E= epileptic coma
I= injury/infection
O= opiates
U= uremia

97
Q

brain herniation syndromes

A

dont know all types

uncal hernation MC
-temporal lobe herniates -> CN3 compressed; one side dilated pupil
-contralateral hemiparesis
-if you see a dilated pupil -> stat CT

98
Q

locked in syndrome description + cause

A

-severe neurologic condition consisting of near total body paralysis with preserved consciousness
-Cannot move their face or body, swallow, speak, look laterally
-Vertical eye movements and controlled blinking are possible
-Often mistaken for being unconscious
-Retained alertness and cognitive abilities

Cause: Stroke of the brainstem or pontine hemorrhage
-Specifically midbrain! or pons!!! where the ARAS originates **
- ex: basilar artery occlusion

99
Q

What is intact with patients with locked in syndrome?

A

Intact:
- Cognitive function:
- they are awake with eye opening
- normal sleep wake
- can hear and see
As if soul locked inside of one’s body

Take care not to misdiagnose as unconscious = Assess by request blinking

CANNOT move lower face,limbs,eyes laterally, chew, swallow, speak, breathe

100
Q

Prognosis for locked in syndrome and tx

A

Prognosis:
-High mortality rates (60%) in first 4 months
-Better prognosis if potentially reversible cause: small stroke, TIA, GBS
-Worse prognosis if irreversible or progressive disorders: tumors

Tx: Supportive care
-Prevent systemic problems from immobilization: pressure ulcers, pneumonia, UTI, DVT/PE, limb contractures, malnutrition

101
Q

What is the definition of brain death? common causes?

A

Definition: Complete and irreversible loss of function of the brain and brain stem

Common causes:
- brain injury from trauma
- bleeding
- stroke
- loss of blood flow after cardiac arrest

102
Q

establishing brain death summary

A
  1. establish irreversible cause of coma
    - SAH on imaging
    - anoxic brain injury
  2. establish pt is Normotensive, normothermic, no metabolic disturbance
    - exclude confounding factors -> cannot have: CNS depressants, paralytics, hypothermia, hypotension, or major metabolic derangements
  3. PE shows brainstem damage:
    - Fixed, non-reactive pupils.
    - Absence of oculocephalic (doll’s eyes) and oculovestibular (cold calorics) reflexes
    - No corneal, cough, or gag reflexes.
    - No purposeful motor responses (reflexes allowed)
    - Ventilator dependent
  4. Apnea testing: no spontaneous breathing

if any are unclear from above: ancillary tests
to confirm no blood flow in the brain
-Cerebral angiogram
- cerebral scintigraphy
- transcranial dopplers
- EEG

103
Q

establishing brain death: Apnea testing:

A

-testing respiratory drive in the medulla
-Show there is no spontaneous respiratory drive
-Pre-oxygenate then disconnect from ventilator for 8-10 minutes, allow PaCO2 to rise, observe for respirations
-CO2 must rise ≥60 AND 20 above starting -> and still not breathing on own -> fail
-If unable to perform because of instability or hypoxia, perform ancillary tests: imaging that shows no brain flow, or absent electrical brain activity

  1. establish irreversible cause of coma
    - SAH on imaging
    - anoxic brain injury
  2. establish pt is Normotensive, normothermic, no metabolic disturbance
    - exclude confounding factors -> cannot have: CNS depressants, paralytics, hypothermia, hypotension, or major metabolic derangements
  3. PE shows brainstem damage:
    - Fixed, non-reactive pupils.
    - Absence of oculocephalic (doll’s eyes) and oculovestibular (cold calorics) reflexes
    - No corneal, cough, or gag reflexes.
    - No purposeful motor responses (reflexes allowed)
    - Ventilator dependent
  4. Apnea testing: no spontaneous breathing

if any are unclear from above: ancillary tests
to confirm no blood flow in the brain
-Cerebral angiogram
- cerebral scintigraphy
- transcranial dopplers
- EEG

104
Q

What are the 3 cardinal findings in brain death?

A

Coma/ unresponsiveness
Absence of brain stem reflexes
Apnea

105
Q

brain death exam

A

-Good overall physical exam
-Specific exams for comatose patients:
-Light reflex:
-Remember: CN 2 in , brief stop in midbrain, CN 3 out
-!!Blown (big) pupil = ipsilateral midbrain affected
-Vestibulo-ocular reflex:
-“Dolls eye” maneuver or “Cold calorics”
-Vestibular nuclei in the medulla are stimulated by cold liquid, which activate pons CN6 nucleus in a contralateral fashion
-Normal person= Eye looks toward cold water in ear then quickly corrects
-Comatose = no response to cold water, or, no corrective saccade
-Corneal reflex:
-CN 5 is corneal reflex, CN 7 blinks, both nuclei are in the pons
-Cough, gag reflex:
-CN9 and CN10 in the medulla

106
Q

oculovestibular reflex

A

-cold caloric reflex
-cold water in ear
-WNL- slow movement of eyes towards ear with water and then snap back to center

Put cold water in the ear
* Dumb brainstem -> slow movement of eyes towards water
* Smart brain -> quick jerk back to center

107
Q

oculocephalic reflex (doll eye)

A

-Rapidly turn the head 90 degrees in both directions
-NORMAL: Eye deviates to opposite way you turned the head “Doll eye”
-you are always looking forward
-ABNORMAL: No eye turning, eyes are not locking onto something

108
Q

declaring brain death

A

-Brain death: COMA + ABSENT BRAINSTEM REFLEXES + APNEA
-Declaring brain death requires ALL of the following -> Prerequisites, examination, apnea testing, ancillary testing
-Once dx, they are declared dead
-In children, 2 separate brain death examinations is considered the minimum standard
-Declare and document time of death
-Organ donation or live fetus: May continue mechanical ventilation and medications to maintain blood pressure after death

109
Q

alzheimers dementia (AD) pathophysiology

A

Most common cause of dementia (60-70%)

Pathophysiology:
-Accumulation of !amyloid beta (Aβ) deposition in the brain that forms neuritic (senile) plaques and neurofibrillary tangles (NFTs) composed of tau protein filaments! with eventual loss of neurons (PANCE question)
-Often a cholinergic deficiency causing memory, language, and visuospatial changes early on

110
Q

alzheimers dementia risk factors

A
  • Age > 65*
  • ε4 allele of the apolipoprotein E (ApoE) gene*
  • female
  • family history
    -CVD

neurology (13 decks)

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