brain death Flashcards
delirium
-Acute, transient
-usually REVERSIBLE confusional state
-alteration of consciousness with reduced ability to focus, sustain, or shift attention
-Results incognitiveor perceptual disturbances that is notbetter explained by a pre-existing, established,or evolving dementia
-Develops over ashort period of time (hoursto days)
-underlying pathology present
-can be the only sign of acute illness in elderly
-Etiology:
-Medicalconditions
-Substanceintoxication
-Medicationside effects
-The pathophysiology is not well understood
-Very common in acute hospitals
who gets delirium
-risks:
-Advanced age
-Recent surgery
-Pre-existing brain disease (e.g. dementia, stroke, Parkinson’s)
-Precipitating factors:
-Polypharmacy
-Infection
-Dehydration
-Malnutrition
-30% of elderly patients experience delirium during hospitalization -> Higher rates in ICUs
DSM criteria for delirium
-(A) Disturbance in attention and awareness (first)
-Distractibility* (hallmark): evident in conversation
-(B) Develops over a short period; is a change from baseline; and fluctuates in severity during the day
-Usually develops over hours – days (can persist days-months)
-Most severe at night/evenings*
-(C) Cognitive Disturbance (including perceptual)
-E.g. memory deficit, disorientation, language, visuospatial ability, perception
-(D) A and C are not explained by another neurocognitive disorder or coma
(5) Evidence (H&P, lab) that disturbance is caused by medication, medical condition, or substance
course of delirium
-prodromal phase (often)- fatigue, sleep disturbance, depression/anxiety, restlessness, irritability, hypersensitivity to light or sound
-perceptual disturbance and cognitive impairment
-quiet/hypoactive OR agitated and confused
signs of delirium
-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
MMSE (mini mental status exam)
-Perform a MMSE: Test their attention:
-Serial 7s
-spell “WORLD” backwards
-Focused exam on hydration status, skin, vitals and sources of infection
confusion assessment method (CAM)
-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
initial check for acute life threatening causes of delirium
-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
MC etiologies of delirium
-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
-Post operative states (very common in elderly)
-Drug toxicity (30% off all cases)
drug culprits of delirium
-NSAIDs, Opioids!
-Benzodiazepines!
-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
Antidepressants: mirtazapine, SSRIs, TCAs
-GI: antiemetics, antispasmodics, H2 Blockers, Loperamide
-Muscle Relaxers: Baclofen, Cyclobenzaprine
-Herbals: St. John’s Wort, Valerian
tx and prevention of delirium
-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
tx of delirium chart
-antipsychotics: Haloperidol, Risperidone, Olanzapine, Quetipaine, Aripiprazole
sundowning
-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
age associated cognitive decline
-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
mild neurocognitive disorder: mild cognitive impairment (MCI)
-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
MCI criteria
-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
testing for 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
delirium vs dementia vs pseudo-dementia or dementia of depression
major neurocognitive disorder (DEMENTIA)
-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
causes of dementia
clinical manifestation of dementia
-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/motivated, 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)
dementia exam: history
-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
dementia exam: assessment
-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
alzheimers dementia (AD)
-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
alzheimers dementia symptoms
-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 AD
-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
AD dx and management
-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
vascular dementia imaging
-Cortical and subcortical infarctions
-Lacunar infarcts
-Microbleeds
Thiamine (B1) deficiency
-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
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
comparing dementia types
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!
-CN3 palsy -> pupils dilate unilateral
-temporal lobe herniation
-contralateral hemiparesis
-if you see a dilated pupil -> stat CT
brain death
-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
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
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
