AMS prelecture Flashcards
What are the two things that define mental status
Emotional and intellectual functioning
Ch. 129 (hypoglycemia/DKA only), 141, 142
What is confusion
Unusual for INDIVIDUAL or DEVIATEs from social norms
-often uncooperative/
If diminished LOC, what are your differentials?
Coma/stupor
If you have (+) focal neuro deficits, what are you thinking?
Brain structure
Stroke/mass lesion
When do you perform a MMS exam?
If altered behavior in a patient who is awake, alert without neuro deficit, perform MMS exam to differentiate confusion and delirium from a psychiatric disorders
If a patient has an abnormal MMS exam, what are you thinking? Normal?
Abnormal = confusion/delirium
Normal = Thought disorder/ psych disorder
Initial evaluation for a patient with AMS and what ALL patients get
ABCDEs
- Vital signs
- POC glucose
- If shock IV NS/LR bolus
- Hypoxic = order ABG b4 O2 if possible to check results, 1-4 NC (if more, only for a few hours, but higher flow is preferred) VBG if just worried about pH
- Correct respiratory failure
- IV access with 2 large bore needles (18 or 20 gauge so that you can push fluids rapidly)
- Administer coma cocktail (dextrose if hypoglcemic, thiamine, Narcan - should show improvement in like 5 min max)
why do you give thiamine for an AMS patient? When do you give it in the cocktail
Wernicke encephalopathy from alcohol OD is helped by thiamine, and thiamine helps with cellular respiration, so give BEFORE or DURING glucose (not after).
A patient has an abrupt AMS, what are your ddx?
iscehmia
SAH
Seizure
A patient has a rapid, but not abrupt AMS, what are your ddx?
delrium
acute remember
A patient has a gradual AMS, what are your ddx?
space occupying lesion
dementia
psych disorders
A patient has a fluctuating AMS, what are your ddx?
seizures
stroke
delirium
You patient has a history of chronic alcohol use or chornic malnutrition, what is your ddx?
Wernicke’s encephalopathy
How might a history of auditory vs visual hallucination change your ddx?
auditory = more likely to be psych
visual = more likely to be medically related
What are common medical causes of AMS?
- Comorbid conditions
- med changes
- late age onset
- sudden in onset and fluctuate over hours/ days (thinking about the med being excreted)
what do non-reactive pupils suggest?
upper brainstem lesion (close to the eye nerves)?
dolls eyes test normal sign and when to use it
eyes move opposite direction of head (still fixing gaze)
shows EOM are in tact
used only when C spine is cleared
nystagmus testing and when to use it
Use when C-spine is NOT cleared
COWS
cold opposite warm same (normal)
GCS scoring
If 8, intubate
EYES
VOICE
OLD BEN
Eyes shut
“Y” did you hurt me
Ear piercing noise
Spontaneous
Voiceless
Obscure
Inapprapropiate
Confused
Elegant
Obey comands
Localizes to pain
Draw away
Bends (decoriatate)
Extends (deceberate)
No response
How do you observe consciousness in kids?
Based on how they are moving/interacting with people
Cannot do EOM, just look for eye movement
What can you use to assess confusion quickly in adults?
Six item screener
3 item memory recall (after 3-5 min)
Year, month, day of week (easier to know that then day of month)
Apart from hallucinations, what is another way to differentiate medical/neurological from psych disorders
Disorientation and memory indicate medical/neuro, while disorders of thought content suggest psych
How to rule out cardiac causes of AMS? Hypoxic?
EKG
CXR
When do you get a head CT for LOC? is it w/ or w/out contrast
Head CT - without contrast
if focal neurologic signs, papilledema or FEVER
When to get an LP with CSF analysis for AMS
CNS infection, SAH not seen on CT
Relative CI - cerebral edema, increased ICP
When do you get an EEG?
consider if no other source of AMS if found or if underlying seizure disorder
treatment of delirium/dementia and the SE of the meds
Underlying illness
Haldol (EPS and QT prolongation)
Lorazepam (respiratory depression)
For delirium, admit unless cause is identified, treatment is initiated, and improvement is seen
For dementia, admit unless patient has long-standing stable symptoms, consistent caregivers and reliable follow up for outpatient evaluation
What is delerium vs dementia?
Delerium = acute change in attention and mental function (over a 24 hour period) and cognition, often with sleep-wake cycles disrupted (tired at day or night)
dementia = slow onset of chronic cognitive dysfunction in one + cognitive domains. Attention is NORMAL.
A patient presents to your office after OD and narcan is adminstered and the patient is stable - how do you manage?
Observe for 60-90 minutes then discharge based on
1) intential = suicide attempt
2) accidental = psych
What is hypoglycemia in kiddos?
< 45 with symptoms
< 35 asymptomatic
What is the mangement of hypoglycemia in kids?
- Juice
- Dextrose (D10W for neonates, D25W for kids; maintenance with DW10 for both)
- Glucagon (opposes insulin)
admit all kids requiring resuscitation
What is hypoglycemia in adults? Mng?
< 70?
- D50W
- POC glucose every 30 min for 2 hours
- Continuous D10W maintenance (same as kiddos)
- IM Glucagon only if unable to establish IV
- Octerotide if refractory hypoglycemia related to sulfonyurea use (-ides)
t/f if a patient has an insulin pump and is hypoglycemic, immediately remove the insulin pump so that they do not go further into hypoglycemia
FALSE - may go into DKA
consult endocrine after to lower pump basal rate
When to admit or discharge hypoglycemic patients
Admit
if on long-acting hypoglycemic drugs (for serial glucose monitoring)
If discharge
educate to continue carbohydrate intake and monitor glucose
5 functions of insulin
- drives glucose into cells
- drives K+ into cells
- creates an anabolic environment (because there is enough sugar for energy, so you do not need to break down other energy stores)
- inhibits breakdown of fat (because you can use glucose)
- blocks the breakdown of proteins (because you can use glucose)
What is DKA and is it MC in T1 or T2?
A life-threatening complication of DM that occurs as a result of significant INSULIN DEFICIENCY resulting in HYPERGLYCEMIA and ketoacidosis.
MC in T1 as it is an insulin-dependent DM
Often the first sign of T1DM in a kiddo
6 I’s of the etiologies DKA
infection
infarction
insult (to the body)
impregnated
indiscretion (lack of care)
insulin (absence)
s/s of DKA and 3 key features
think of DM on steroids
- hyperglycemia symptoms
- volume depletion symptoms
- Acidosis symptoms
Polydypsia/uria (1st symptoms)
Volume depletion symptoms (because your body is trying to get rid of sugar, drawing fluids outside of the body)
Acidosis (tachypnea, kussmaul respiration [fast deep breathing], fruity breath - all of this is because the body tries to blow off CO2)
pathophys of DKA
- Glucose does not enter the cell
- Liver creates more glucose because the cells are not getting glucose
- Breakdown of fat and muscle for energy (leads to weight loss) leading to ketones that can enter the brain
- Ketones build up leading to acidosis
- Kidneys compensate by trying to pee it all out
- Leads to dehydration and vomiting leads to more dehydration
diagnostics of DKA
POC glucose
Phos + Mg
ABG
UA
SERUM ketones (most important)
EKG (MI and hyperkalemia)
diagnostic criteria for DKA
Blood glucose level >250 mg/dL
Anion gap >10 to 12 mEq/L¹
Bicarbonate level <15 mEq/L
pH <7.3 with moderate ketonuria or ketonemia
does NOT need to be > 250 if:
1. shortly after insulin
T1 young and vomitting
alcohol abuse/ liver failure
Low caloric intake
Depression
Preggo
SGLT2 inhibitors
Overall management of DKA
Volume repletion
Reverse insulin insuffiency
Correct electrolytes and acid/base
Treat cause
Avoid complications
Volume resuscitation for DKA
2 large IV bolus with NS followed by 1/2 NS TKO (to keep open the vein)
1/2 NS @ 250-500 per hour if normal or elevated Na - if hyponatremic keep NS
Need to know 15-20 mL/kg/h
