Brain Death draft

Question 1

what is delirium

Answer 1

-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)
-underlying pathology present with not well understood pathophysiology
-can be the only sign of acute illness in elderly
-Very common in acute hospitals

Question 2

ethiology of delirium

Answer 2

-Medical conditions
-Substance intoxication
-Medication side effects

Question 3

delirium risk factors + precipitating factors

Answer 3

Risk
-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

Precipitating factors:
-Polypharmacy
-Infection
-Dehydration
-Malnutrition

Question 4

DSM criteria for delirium

Answer 4

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

Question 5

course of delirium: what phases

Answer 5

1. Prodromal phase (often not caught)- fatigue, sleep disturbance, depression/anxiety, restlessness, irritability, hypersensitivity to light or sound
2. perceptual disturbance and cognitive impairment
3. quiet/hypoactive - not interacting with environment (mc) OR agitated and confused

Question 6

signs of delirium

Answer 6

-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 these patients, look for:
-Recent febrile illness
-hx of organ failure
-medication list and changes
-alcoholism or drug abuse
-recent depression

Question 7

It is important to get a good HISTORY on delirium patients, look for what signs + what test to perform

Answer 7

look for:
-Recent febrile illness
-hx of organ failure
-medication list and changes
-alcoholism or drug abuse
-recent depression

tests:
- MMSE
- test attention: serial 7s or spell “world” backward
-Focused exam on hydration status, skin, vitals and sources of infection

Question 8

detection of delirium: confusion assessment method (CAM)

Answer 8

-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

Question 9

once you detect delirium, must do an initial check for acute life threatening causes of delirium!!!! which includes:

Answer 9

-sepsis protocol
-vital signs
-Serum: Evaluate electrolytes, creatinine, calcium, CBC, U/A with culture, blood gas, consider drug tox screening
-Imaging: CXR, consider CTH, LP, EEG when indicated, CT of head

Question 10

MC etiologies of delirium

Answer 10

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

Question 11

drug culprits of delirium

Answer 11

-NSAIDs *
- Opioids*
-Benzodiazepines*
- anticholinergics: 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

Question 12

tx and prevention of delirium

Answer 12

-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

Question 13

tx of delirium chart

Answer 13

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

Question 14

sundowning

Answer 14

-Poorly understood, affects 2/3 of patients with dementia
-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)
-Risk factors: Poor light exposure, disturbed sleep

Question 15

delirium vs dementia vs pseudo-dementia or dementia of depression

Answer 15

Question 17

age associated cognitive decline

Answer 17

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

Question 18

mild neurocognitive disorder: mild cognitive impairment (MCI)

Answer 18

-Intermediate clinical state between normal cognition and dementia
-Can be precursor to Alzheimer’s dementia
-Increased prevalence >60yo
-!!Commonly has mood and behavioral symptoms -> Up to 40% have depression, others have anxiety, irritability, aggression, apathy
-Can represent a reversible medical condition*
-No specific treatment, can trial Donepezil

Question 19

MCI criteria

Answer 19

-Memory complaint- Change from baseline that is corroborated by an informant
-Objective memory impairment- For their age and education
-Preserved general cognitive function
-Intact activities of daily living (ADLs)
-Not demented
-if you dont screen it you will miss it
-they seem very normal

Question 20

testing for MCI

Answer 20

-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

Question 21

major neurocognitive disorder (DEMENTIA)

Answer 21

-Progressive and gradual deterioration! of selective functions
-Must represent decline from previous baseline and severe enough to interfere with daily function! and independence
-Cognitive decline involving 2+ domains:
-learning
-memory (new information)
-language
-executive function (complex tasks, poor judgement)
-complex attention
-perceptual-motor
-social cognition
-Risk factors: age (>60 y/o), vascular disease (HTN, DM)
-MC cause: Alzheimer Disease (60-80%)
-Less common causes: alcohol-related, CTE, normal pressure hydrocephalus, chronic subdural hematoma, CNS illness (Creutzfeldt-Jakob disease, HIV), copper/B12/Folate deficiency
-AAN and USPSTF recommends routine screening for dementia in asymptomatic adults

Question 22

clinical manifestation of dementia

Answer 22

-1. memory loss- 1st manifestation- presents as forgetfulness (trouble remembering recent events)
-2. Deficits in other cognitive domains (with or after memory loss)
-(a) Executive dysfunction (less organized/a, difficulty multitasking) - early
-(b) Impaired visuospatial skills (getting lost in familiar places) - early
-(c) Language dysfunction (word finding) – late
-(d) 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
-(4) Life expectancy after diagnosis: 8-10 years (range: 3-20)

Question 23

dementia exam: history

Answer 23

-Close family member or friend 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

Question 24

dementia exam: assessment

Answer 24

-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)
-Consider:
-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

Question 25

alzheimers dementia (AD)

Answer 25

-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 -Major genetic risk factor: ε4 allele of the apolipoprotein E (ApoE) gene -RF: !Age > 65!, female, family history, CVD, APOE-e4 allele

Question 26

alzheimers dementia symptoms

Answer 26

-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

Question 27

stages of AD

Answer 27

-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 -8–10 years usually, but ranges from 1–25 years

Question 28

AD dx and management

Answer 28

-dx -> excluding other etiologies of dementia -CT/MRI brain: -Brain atrophy- Medial temporal lobe (reduced hippocampal volume)! -Mild ventricle dilation -Management: -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

Question 29

vascular dementia (VaD)

Answer 29

-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 -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

Question 30

co-occurring VaD

Answer 30

-pure vascular dementia is less common than the situation in which vascular dementia is only one of the etiologies of multiple-etiology (also termed “mixed”) dementia. -Alzheimers is MC co-occurring pathology with vascular dementia

Question 31

vascular dementia imaging

Answer 31

-Cortical and subcortical infarctions -Lacunar infarcts -Microbleeds

Question 32

VaD tx

Answer 32

-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

Question 33

frontotemporal dementia (FTD) AKA picks disease

Answer 33

-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 -MRI: !Frontal and/or temporal atrophy! -Treatment: -symptomatic -Non-pharm interventions for safety: driving, exercise, speech therapy, behavioral modification -SSRI Citalopram! Trazodone

Question 34

dementia with LEWY BODIES (DLB)

Answer 34

-Pathophysiology: Eosinophilic intracytoplasmic inclusions (Lewy Bodies) in the brain -Dementia that is associated with: -Psychotic features: Visual hallucinations and delusions! -Motor parkinsonism !- bradykinesia, slow, rigid, shuffling -Cognitive fluctuations ! -REM behavior disorder!- act out whats happening in sleep -Dysautonomia !- BP drops, neurocardiovascular instability, syncope -Visuospatial dysfunction

Question 35

DLB imaging

Answer 35

-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

Question 36

DLB tx

Answer 36

-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.

Question 37

parkinson disease dementia (PDD)

Answer 37

-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 -TX: -Levadopa 1st line -Cholinesterase inhibitors

Question 38

normal pressure hydrocephalus (NPH)

Answer 38

-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 -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: lack of concern due to ?frontal lobe impairment -tx- shunt- relief of pressure

Question 39

creutzfeldt-jakob disease (CJD)

Answer 39

-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 -Clinical features: -Neuropsychiatric symptoms! are uniformly seen and may manifest as dementia, behavioral abnormalities, and deficits involving higher cortical function including aphasia, apraxia, and frontal lobe syndromes -Myoclonus!, 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. -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

Question 40

c

Answer 40

-causes Wernicke’s encephalopathy -Malnourished pt (usually alcoholism. AIDs, anorexia, ESRD, hematologic malignancies due to hypermetabolic state) -Triad of : -1. Encephalopathy (disorientation, indifference, inattentiveness, memory loss) -2. Ataxia (gait problems) -3. Ocular motor dysfunction (diplopia, nystagmus) -Thiamine 100mg IV x 3 days followed by daily PO may reverse disease if given in first few days of onset (thiamine THEN glucose) -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

Question 41

vitamin B12 deficiency

Answer 41

-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

Question 42

dementia tx options

Answer 42

(1) Cholinesterase Inhibitor: Donepezil!!!! (Aricept), Rivastigmine, Galantamine (Razadyne) -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 (2) Vitamin E 2000 IU/day!!!! -Indications: mild-moderate AD (only) interested in non-pharmacologic treatments (3) NMDA Antagonist: Memantine!!! (Namenda)10 mg BID -MOA: blocks @ 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

Question 43

who needs specialist referral

Answer 43

-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?

Question 44

questions

Answer 44

-AD -vascular -parkinsons -B12 deficiency- posterior involvement? -creutzfelt jakob -frontal temporal lobe dementia

Question 45

AMS and COMA

Answer 45

-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.

Question 46

levels of consciousness

Answer 46

-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

Question 47

glasgow coma scale (GCS)

Answer 47

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

Question 48

eliciting responses from unconscious pts

Answer 48

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

Question 49

approach to AMS

Answer 49

-ABCs COME FIRST- Check for quick reversible causes, do they need naloxone? 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

Question 50

AMS history

Answer 50

-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?

Question 51

underlying etiologies for AMS

Answer 51

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

Question 52

AMS: Dx testing: metabolic or endocrine causes

Answer 52

-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

Question 53

AMS: dx testing: traumatic causes

Answer 53

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

Question 54

AMS: dx testing: infectious causes

Answer 54

-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)

Question 55

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

Answer 55

-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)

Question 56

AMS: dx testing: neurologic causes

Answer 56

-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)

Question 57

coma

Answer 57

-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

Question 58

easy way to remember the causes of coma

Answer 58

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

Question 59

brain herniation syndromes

Answer 59

dont know all types -uncal hernation! -CN3 palsy -> pupils dilate unilateral -temporal lobe herniation -contralateral hemiparesis -if you see a dilated pupil -> stat CT

Question 60

locked in syndrome

Answer 60

-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 -Stroke of the brainstem or pontine hemorrhage -Specifically midbrain! or pons!!! where the ARAS!!! originates -Ex: basilar artery occlusion (MC)! -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 -Supportive care is the mainstay of treatment -Prevent systemic problems from immobilization: pressure ulcers, pneumonia, UTI, DVT/PE, limb contractures, malnutrition

Question 61

brain death

Answer 61

-Complete and irreversible loss of function of the cerebrum and brain stem -Common causes: brain injury from trauma, bleeding, stroke, loss of blood flow after cardiac arrest

Question 62

establish brain death

Answer 62

-pre-requisite: establish an irreversible cause of coma -> anoxic brain injury, basilar artery thrombosis, high-grade SAH on neuroimaging can qualify -pre-requisite: exclude confounding factors -> cannot have: CNS depressants, paralytics, hypothermia, hypotension, or major metabolic derangements -ur not dead until ur warm and dead -exam: shows brainstem damage evidenced by neurologic exam -Pupils fixed and non reactive to light -NO oculocephalic, oculovestibular reflexes -NO corneal, cough and gag reflexes! -No meaningful motor responses (reflexes allowed) -Completely ventilator dependent -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 -ancillary testing: confirm no blood flow in the brain -Only required if any previous step is doubtful. Includes: Cerebral angiogram, cerebral scintigraphy, transcranial dopplers, EEG

Question 63

brain death exam

Answer 63

-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

Question 64

oculovestibular reflex

Answer 64

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

Question 65

oculocephalic reflex (doll eye)

Answer 65

-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

Question 66

declaring brain death

Answer 66

-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