brain death final Flashcards
What is delirium?
-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)
What does delirium result in?
Cognitive or perceptual disturbance
- that is not better explained by a preexisting, established or evolving dementia
How fast does delirium develop?
Over a short period of time
Hours to days
Causes of delirium?
Medical Conditions
Substance Intoxication
Medication Side Effect
What do 30% of elderly experience during hospitilization?
Delirium
Where are higher rates of Delirium?
ICU= 70%
Hospice=42%, ER=10%, Post acute care=16%
What are risk factors of delirium?
-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
What are precipitating factors for delirium?
Polypharmacy
Infection
Dehydration
Malnutrition
Bladder Catheters
What may be the only sign of acute illness in elderly patients?
Delirium
Delirium DSM 5 criteria includes
- Disturbance in attention and awareness (1st)
- distractability = hallmark - Develops over short period of hours
- days; most severe night/evenings - Cognitive disturbance including perceptual
- ex: memory deficit, disorientation, language, visuospatial ability, perception
4.Not explained by another neurocognitive disorder or coma - Evidence (h&p,labs) that disturbance is caused by medication, condition or substance
What is course of delirium?
- Prodromal phase: fatigue, sleep disturbance, depression/anxiety, restlessness, irritability, hypersensitivity to light or sound
- Perceptual disturbances and Cognitive impairment
- Quiet/hypoactive - not interacting with environment (mc) or agitated confused state
During the prodromal phase what symptoms are included?
SLEEP DISTURBANCE
IRRITABILITY
fatigue
depression/anxiety
restlessness
hypersensitivity to light or sound
On exam for delirum what signs are seen?
-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
It is important to get a good HISTORY on delirium patients, look for:
Recent febrile illness
Hx of organ failure
Med list
Hx of alcoholism or drug abuse
Recent depression
suspect delirium, what tests to perform?
- 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
What is advanced delirum signs?
Drowsy
Lethargic
Semicomatose
What is included when testing/ screening for delirium?
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
Most common etiologies for delirium
-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
What are main drug culprits for delirium?
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
Delirium Treatment and Prevention
-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
What psychotropic med is used for severe agitation or psychosis with delirium?
-antipsychotics: Haloperidol, Risperidone, Olanzapine, Quetipaine, Aripiprazole
What is sundowning?
-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
If established sundowning and no obvious medical illness consider?
what are risk factors:
consider:
- Impaired circadian regulation
- noctural factors in environment (noise, staff)
risk factors:
-Poor light exposure
- Disturbed sleep
delirium vs dementia vs pseudo-dementia or dementia of depression
What is age associated cognitive decline?
-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**
Is age associated cognitive decline progressive? Does it affect ADLS?
NO!
Mild neurocognitive disorder (mild cognitive impairment) is an intermediate clinical state between
Normal cognition and dementia
What can Mild Cognitive Impairment be a precursor to
Alzheimer Dementia
With Mild Cognitive Impairment when does prevalence increase
After age 60
What can Mild Cognitive Impairment also represent?
A reversible condition in setting of:
- depression
- CHF
- complication of med
- recovery from acute illness
Mild Cognitive Impairment tx
No specific treatment
could do trial of Donepezil
What symptoms are common with Mild Cognitive Impairment?
Mood/Behavioral sx
- 40% Depression
- others: anxiety , irritability, agression ,apathy
What is included in the criteria for Mild Cognitive Impairment?
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
What testing is preformed with MCI?
-MMSE vs MoCA- just know they exist
-Physical, including
-Neurologic Examination
-Neuropsychological Testing
-MRI»_space;»»Non-contrast head CT
-Screening for B12 Deficiency and Hypothyroidism -> reversible
What should be screened for with MCI
Screen for b12 deficency and hypothyroidsm
What is major neurocognitive disorder? what criteria? (dementia)
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
Risk factors for major neurocognitive disorder? MCC of major neurocognitive disorder
Risk factors:
- Age > 60 y/o
- Vascular Disease- htn,dm
MCC: alzheimer ds*
Most common cause of major neurocognitive disorder? other causes
Alzheimer Disease**
-Less common causes: alcohol-related, CTE, normal pressure hydrocephalus, chronic subdural hematoma, CNS illness (Creutzfeldt-Jakob disease, HIV), copper/B12/Folate deficiency
What is the first manifestion of dementia?
Memory loss
-presents as forgetfulness
Clinical manifestations of dementia
- memory loss- 1st manifestation- presents as forgetfulness (trouble remembering recent events)
- 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 - Non-cognitive neurologic deficits – late
-Pyramidal/Extrapyramidal motor signs, myoclonus (uncontrollable twitching), seizures
What is the life expectancy after diagnosis with dementia?
8-10 years avg
- range is 3-20
Dementia Hx and PE
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
What is assessed on dementia cognitive exam
-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
What is clinical diagnosis for dementia
history + scoring tools + r/o organic pathology
What lab work is performed for dementia?
AAN recommends
-Screen for B12 deficency (Cbc, serum vb12)
-Screen for hypothyroidism (Serum tsh)
What imaging is performed for demntia?
AAN recommends
MRI without contrast»»>ct in all initial evals
Why would EEG be performed when testing for dementia
To rule out atypical syndrome if <60 or rapidly progressive
To rule out Creutzfeldt Jakob Disease
What does a PET scan distinguish
Vascular from Alzheimer’s
What is definitive diagnosis for dementia
Brain Biopsy but rarely used
frontotemporal dementia (FTD) AKA picks disease SUMMARY
-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
frontotemporal dementia (FTD) AKA picks disease: imaging and tx
MRI: Frontal and/or temporal atrophy!*
Treatment:
-symptomatic
-Non-pharm interventions for safety: driving, exercise, speech therapy, behavioral modification
-SSRI Citalopram, Trazodone
What is DSM-5 criteria for Major Neurocognitive Disorder
- 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
Dementia with Lewy Bodies: dementia associated with
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
How is dementia with lewy bodies distinguished?
PSYCHOTIC FEATURES
Dementia with lewy bodies: imagining and Dx
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
Dementia with lewy bodies treatment
-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.
Parkinson disease dementia FEATURES
Parkinson Features
-Tremor, Rigidity, Bradykinesia
-Cognitive impairment
- Gait dysfunction
- Urinary incontinence
parkinson disease dementia (PDD) DEFINITION
-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
Treatment for parkinson disease dementia
- Levodopa (first line)
- Cholinesterase Inhibitor
Alzheimer disease Dementia Hallmark sx
-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
stages of alzheimer ds
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
Alzheimer disease dx
Dx: excluding other etiologies of dementia
CT/MRI:
- reduced hippocampal volume/ medial temporal lobe
- mild ventricle dilation
demonstrates brain atrophy
What is treatment for alzheimer disease
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
Vascular Dementia
(2nd MC) (“post-stroke” dementia) definition
-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
Vascular Dementia DSM 5 criteria
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
Vascular Dementia
(2nd MC) (“post-stroke” dementia) CT/MRI
cortical and subcortical and lacunar infarctions
microbleeds
Vascular Dementia Treatment + prognosis
-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
Normal Pressure Hydrocephalus
Classic Triad
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
normal pressure hydrocephlus: description classic triad
-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
creutzfeldt-jakob disease (CJD) description and types
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
creutzfeldt-jakob disease (CJD): sx
-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.
Thiamine (B1) deficiency description + triad + tx
-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)
untreated and prolonged Wernicke’s encephalopathy
-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
vitamin B12 deficiency
-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.
dementia: tx options drug names + indications
(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
Cholinesterase Inhibitor: donepezil*
(Rivastigmine, Galantamine) MOA, indication, ADR, CI
-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
NMDA Antagonist: Memantine MOA, indication, off label use, ADR
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
who needs a specialist referral for dementia?
-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?
AMS and COMA
-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.
levels of consciousness
-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
What are the components of the Glasgow COMA scale; what is GCS
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”
GCS score minor, moderate, severe number values
-GCS ≤ 8 = Severe
-GCS 9-12 = Moderate
-GCS ≥ 13 = Minor
-GCS 15 = Max, normal score
-GCS < 8 = Intubate!!!!
Eye opening response (GCS)
Eyes: four eyes
4 spontaneously
3 to speech
2 to pain
1 no response
Verbal Response (GCS)
5 - oriented
4 - confused
3 - inappropriate words
2 - incomprehensible sounds
1 - none
Motor response (GCS)
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
eliciting responses from unconscious pts
-sternal rub
-eyelid/brow
-roll a pencil on nail bed
-press on TMJs
approach to AMS
- 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
AMS history question: when did it occur? what preceded it?, what else do you want to know?
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?
underlying etiologies for AMS
-barely went over
-Underlying etiologies:
Drugs / Ingestions
-Structural brain lesions (CVA, tumor, anoxia)
-Organ dysfunction (endo, lytes, resp, cardiac)
-Sepsis/Infections
-Seizures (think PRES)
AMS: Dx testing: metabolic or endocrine causes
-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
AMS: dx testing: traumatic causes
-barely went over
-Head CT/ cervical spine CT
-POCUS
-Chest and Pelvis X-ray
-Other imaging modalities as indicated
AMS: dx testing: infectious causes
-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)
AMS: dx testing: Levels of medications (anticonvulsants, digoxin, theophylline, lithium, etc.)
-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)
AMS: dx testing: neurologic causes
-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)
coma definition and outcomes
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
easy way to remember the causes of coma
A = anoxia/apoplexy
E= epileptic coma
I= injury/infection
O= opiates
U= uremia
brain herniation syndromes
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
locked in syndrome description + cause
-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
What is intact with patients with locked in syndrome?
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
Prognosis for locked in syndrome and tx
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
What is the definition of brain death? common causes?
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
establishing brain death summary
- establish irreversible cause of coma
- SAH on imaging
- anoxic brain injury - establish pt is Normotensive, normothermic, no metabolic disturbance
- exclude confounding factors -> cannot have: CNS depressants, paralytics, hypothermia, hypotension, or major metabolic derangements - 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 - 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
establishing brain death: Apnea testing:
-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
- establish irreversible cause of coma
- SAH on imaging
- anoxic brain injury - establish pt is Normotensive, normothermic, no metabolic disturbance
- exclude confounding factors -> cannot have: CNS depressants, paralytics, hypothermia, hypotension, or major metabolic derangements - 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 - 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
What are the 3 cardinal findings in brain death?
Coma/ unresponsiveness
Absence of brain stem reflexes
Apnea
brain death exam
-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
oculovestibular reflex
-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
oculocephalic reflex (doll eye)
-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
declaring brain death
-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
alzheimers dementia (AD) pathophysiology
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
alzheimers dementia risk factors
- Age > 65*
- ε4 allele of the apolipoprotein E (ApoE) gene*
- female
- family history
-CVD
