delerium

Question 1

burden of disease

Answer 1

3% of patients arriving to ED are altered : 85% metabolic or systemic derangements, 15% structural lesion

Question 2

Definitions

Answer 2

Consciousness is made of arousal and cognition
Arousal- awareness of self and surroundings- ascending reticular activating system (where in CNS–dorsal brainstem ) , controls input of somatic and sensory stimuli, arousal from sleep, vulnerable to small lesions in brainstem

Cognition- combo of orientation (accurate perception of experiences), judgment (process input into meaningful info) and memory (store and retrieve info) - located in cerebral cortex- unilateral lesion rarely cause AMS but possibly BL lesions (rare)

Question 3

Commmoncauses of altered mental status

Answer 3

Dementia (chronic) , delerium(acute), Psychosis

Question 4

causes of Delerium

Answer 4

• Metabolic/endocrine
• Infectious disease
• Cerebrovascular event/structural CNS- both hemispheres or brainstem
• cardiovascular
• drug/toxic
• hypoperfusion
• others

Question 5

diseases that are more likely to cause delirium

Answer 5

severe illness, drug toxicity, fluid and electrolyte disturbances (hyponatremia and azotemia), infections, hypothermia or hyperthermia

Question 6

delerium main features

Answer 6

delirium is a symptoms that has an underlying cause that must be recognized and identified

Almost any illness can present as delirium or surgical hospitalization

the most important clue to delirium is the acuity of onset and fluctuation in course

Delirium most commonly occurs in older persons and in pats with underlying neurologic disease

Delirium is very common in sick, hospitalized over the age of 65

Question 7

predictors of delirium

Answer 7

abnormal sodium level, severe illness, chronic cognitive impairment, hypo/hyper-thermia, moderate illness, psychoactive drug use, azotemia

Question 8

management of delirium

Answer 8

1st ABCs
Airway, Breathing, Circulation

Acronyms- AMS (altered mental status), LOC (loss of consciousness and level of consciousness)

Infor gathering (as musch as possible)
EMS (emergency medical services), Family, EMR), GCS (Glasgow coma scale) 15 best 3 worst

Question 9

What to do next

Answer 9

basic neuro exam, differential, work up (dont coma cocktail)- dextrose, oxygen, naloxone, thiamine

Labs

Imaging other tests (EKG, lumbar puncture

Treatment- antidotes, antibiotics, surgery, supportive care, metabolic cofactors (thiamine folate)

Question 10

coma cocktail

Answer 10

often administered to alleviate common causes of delirium
Dextrose (hypoglycemia from insulin)
Oxygen
Naloxone (opiodes, benzos)
Thiamine (alcohol, wernickes)
The type of drugs that could produce delirium that would be alleviated by the coma cocktail

Question 11

confusion assessment method

Answer 11

Best validated and most widely used tools for diagnosing delirium

The CAM is considered positive when a patient fulfills both criteria A + B and either C or D
A- The mental status change is of acute and fluctuating course

B- There is inattention

C- there is disorganized thinking (or incoherent)

D- there is an altered level of consciousness

The test characteristics for the CAM are good and surpass those of an unaided physician assessment

Sensitivity 86%, specificity 93%, LR +

Question 12

Delirium outcomes

Answer 12

after controlling for age, sex comorbid illness or illness severity, and baseline dementia- patients who experience delerium had a higher risk of death, institiutionalization, and dementia during follow up

The mortality rate- over 2 yrs, for patients in whom delerium developed was 38%

The rate of institutionalization over a year was 33.4%

The rate of developing dementia over the next 4 yrs was 63.5%

Pts with dementia and delerium had the highest risk of death

Delirium is often persistnet

a small percentage of pts with delrirum have complete resolution of symptoms with treatment of the underlying disease and return home

Question 13

delerium in the elderly

Answer 13

many acutely ill, older patients who have an acute deterioration in mental status are suffering from delerium

the prognosis of delirium is poor

delirium can occasionally unmask an underlying dementia, which occurs when a patient with a mild undiagnosed dementia becomesdelirious in the hospital and is then evaluated more fully for cognitive impairment

Question 14

hypoglycemia

Answer 14

CNS symptoms predominate- Brain relies almost entirly on glucose

during prolonged starvation, the brain can use ketones

other major organs (heart liver and sk muscle) function during hyperglycemia (use various fuel sources- fattty acids)

In diabetes- density of neuronal insulin receptors varies with glycemic control

Poor glycemic control–> fewer neuronal glucose receptors (hypoglycemic symptoms at higher at higher concentrations of glucose)

Mean glucose concentratio for symptomatic hypoglycemia 78+/- 5 mg/dl versus 53

Question 15

sulfonylureas

Answer 15

Normally, insuling released with elevation of intracellular ATP

Sulfonylureas potentiate the effects of ATP at its sensor– increased intracellular K–> increased intracellulrar potential opens voltage gate Ca++ channels–> increases intracellular calcium concentration , increased calcium–> release insulin

binding of sulfonylyreas to receptor sites–> insulin release

MEglitinides bind K channel on pancreatic cells–> increased insulin secretion (hypoglycemic effects shorter duration

Question 16

metformin

Answer 16

glucose stabilizing by several mechanism

Inhibits gluconeogenesis–> decreased hepatic glucose output

Enhanced peripheral glucose uptake

Decreased fatty acid oxidation

Increased intestinal use of glucose

In skeletal muscle and adipose cells, enhanced activity and translocation of glucose transporters

Question 17

sympathomimetics

Answer 17

stimulate sympathetic nervous system
Direct acting- bind post synaptic receptors–> direct stimulation

Indirect acting- increase synaptic concentration of neurotransmitters

Question 18

Norepinephrine and Dopamine

Answer 18

Norepinephrine-
a-adrenergic receptors: CNS general inhibition, peripheral vasoconstriction

B- adrenergic- CNS general excitiation, peripheral - bronhcodilation, increase dHR, vsodilation

Dopamine- (D1-5)- CNS- choreoathetosis, psychosis, peripheral vasodialtion

Question 19

toxidromes

Answer 19

first mofenson and greensher from toxic and syndromes

describes groups of signs and symptoms consistently attributed to particular toxins

Usually a combination of vital signs and end organ damage (clinically apparent)

Question 20

sympathomimetic toxidromeBENZOS ARE A GOOD ANTIDOTE

Answer 20

HTN, Hyperthermia, Tachycardia, mydriasis, diaphoresisi

Fight or flight response

Anticholinergic- hot as a hare, dry as a bone, blind as a bat, red as a beet, mad as a hatter

Cholinergics- SLUDGE(salivation, lacrimation, urination, defecation, GI cramping, Ememsis

Opioid- pinpoint pupils, resp depression, decreased mental status NALOXONE treatment

Question 21

antidote of benzo toxicity

Answer 21

flumazenil
Competitive benzodiazepine receptor antagonist
role in patients with unknown overdose is limited because seizure and dysrythmias may develop when the effects of a benzodiazepine are reveresed in a mixed overdose

Can induce benzodiazepine withdrawal symptoms, including seizures in patients who are benzodiazepines dependent

therefor, flumazenil is the ideal antidote fo the few patients who (are bothe naive to benzodiazepine and who overdose solely on benzo or
benzo-naiive pts whose benzo component must be reversed after procedural sedations

Question 22

how do opioids like morphine produce respiratory depression

Answer 22

they decrease chemoreceptor sensitivity to carbon dioxide

mu delta and kappa, all 3 are Gi

leads to decreased cAMP–> decreased release of NT

Question 23

opioid receptors

Answer 23

Mu- supraspinal (periaquductal gray) and spinal analgesia, sedation, inhibition of respiration, slowed GI transit, modulation of hormone release

Delta- supraspinal and spinal analgesia, modulation of hormone and neurotransmitter release, Testosterone and FSH is lowered with opioids

Kappa- supraspinal and spinal analgesia, psychotomimetic effects, slowed GI transit,

Question 24

wernickes encephalopathy

Answer 24

confusion, ophthalmoplegia, ataxia

Question 25

Thiamine deficiency

Answer 25

Wet beriberi/CV disease- high output cardiac failure, peripheral vasodilation, and formation of AV fistulae

Dry/beriberi (wernicke-korsakoff) syndrome- Classic wernicke triad (oculomotor abnormalities, ataxia, global confusion)
Korsakoff syndrome- confabulation, chronic
10-20% mortality, peripheral neuropathy

Question 26

normal functions of ethanols major molecular targets

Answer 26

GABA receptors- suppress neuronal transmission, help maintain resting membrane ptential in some neurons

NMDA receptors- learning and memory

Question 27

Gaba A receptors

Answer 27

pentameric receptor complex most commonly containing 2 Alpha and 2 beta, and 1 gamma subunit

activation promotes hyperpolarization via chloride flux

alcohol potentiates GABA and sedative hypnotics

Chronic alcohol use results in cross tolerance to sedative hypnotics

Question 28

alcohol metabolism

Answer 28

2 major pathways of metabolism-
Alcohol dehydrogenase (ADH)- lower stomach ADH (alcohol dehydrogenase) in women (ethanol--> acetylaldehyde)

Acetylaldehyde–> acetate (via aldehyde dehydrogenase)

MEOS (microsomal ethanol oxidizing system- primarily cytochrome p450 2E1, 1A2 3A4
Induction by chronic alcohol intake (increases in clearance of other drugs)- Catalase is a minor metabolic pathway of alcohol

Question 29

delirium tremens

Answer 29

hallucinations- usually visual and tactile
Disorientation
HTN
Tachycardia
Fever

High risk for seizures and dangerous ventricular arrythmias
Seen in 5% of patients with alcohol withdrawal
3-4 days after last drinks
untreated mortality-30%