Readings AMS quiz Flashcards
Hypoglycemia in diabetics is usually a complication of ——-
treatment with insulin or sulfonylureas
Clinical features of hypoglycemia
Sweating
Shakiness
Anxiety
Nausea
Dizziness
Palpitations
Slurred speech
Blurred vision
Headache
Seizure
Focal neurological deficits
Altered mental status from confusion to coma
Diagnosis of hypoglycemia
Low blood glucose with typical signs and symptoms that resolve with treatment
Emergency department care of hypoglycemia
1) glucose and provide carbohydrate meal when tolerate PO
If altered mental status: 50% dextrose 50 mL IV; continuous infusion of 10% dextrose may be required to keep glucose above 100 mg/dL
2) Administer glucagon 1 mg IM or SC if no IV access
3) Treat refractory due to sulfonylureas with octreotide 50-100 ug SC, continuous infusion may be needed
4) Repeat BG every 30 minutes for rebound
Disposition of hypoglycemia
If good response to treatment, good social support, and treatment of cause of hypoglycemia –> discharge with instructions to monitor glucose and continue carbs
If due to sulfonylureas or long acting insulins, admit
Inpatient care for type 2 diabetes mellitus is generally appropriate for which clinical situations?
DKA or hyperglycemic hyperosmolar nonketotic state
Severe complications, comorbidities, or inadequate social support
Hyperglycemia (>400 mg/dL) with severe volume depletion or refractory to appropriate interventions
Hypoglycemia with neuroglycopenia that does not resolve with correction of hypoglycemia
Hypoglycemia from long-acting oral hypoglycemic agents
Fever without obvious source in poorly controlled diabetes
What generally causes DKA?
Insulin deficiency and counter-regulatory hormone excess —> hyperglycemia and ketonemia
Clinical features of DKA
Dehydration
Hypotension
Tachycardia
Acidosis
Myocardial depression
Vasodilation
Kussmaul respiration
Nausea, vomiting, abdominal pain
Acetone –> fruity odor of breath
Diagnosis of DKA
Glucose >250 mg/dL
Anion gap >10 mEq/L
Bicarb <15 mEq/L
pH <7.3
Moderate ketonemia/ketonuria
Can have euglycemic ketoacidosis if taken insulin, impaired gluconeogenesis, or takes sodium-glucose cotransporter 2 inhibitor
What causes anion gap metabolic acidosis in DKA?
formation of ketone bodies
If a nitroprusside test is used to detect serum or urine ketones, what can results be?
Falsely low or negative because of conversion of acetoacetate to B-hydroxybutyrate (test only detects acetoacetate)
What happens to electrolytes in DKA?
Osmotic diuresis –> loss of sodium, chloride, calcium, phosphorus, and magnesium
Serum and urine glucose and ketones are elevated
Potassium may be low (vomiting/osmotic diuresis), normal, or high (acidosis)
Laboratory evaluation of DKA
serum pH (venous blood)
Glucose
Electrolytes
Cr/BUN
phosphorus
Magnesium
CBC
UA
ECG
CXR
ED care of DKA
Correct volume deficit, acid-base imbalance, and electrolyte abnormalities
administer insulin
treat underlying cause
Administer bicarb if pH <6.9
Monitor glucose, anion gap, potassium, and bicarb hourly until recovery: glucose <200 mg/dL, bicarb >18, and pH >7.3
What is a complication of DKA treatment? What are its risk factors and when should you treat?
Cerebral edema
Young age and new-onset diabetes
If change in neurological status
What should be done if change of neurological status early in therapy for DKA?
Begin treatment with mannitol 1 g/kg before obtaining diagnostic CT scan
Any disease process that interrupts normal blood flow to the brain
stroke
what is the most common type of stroke?
Ischemic > intracerebral hemorrhage >SAH
What is a TIA
transient episode of neuro dysfunction caused by ischemia typically 1-2 hours long
clinical features of stroke
depends on region of brain compromised and severity
clinical features of anterior cerebral artery stroke
contralateral leg weakness
sensory changes
clinical features of middle cerebral artery stroke
contralateral hemiparesis arm >leg
facial plegia
sensory loss
aphasia if dominant hemisphere (usually left) affected
inattention, neglect, dysarthria without aphasia if nondominant side effected
clinical features of posterior circulation stroke
unilateral limb weakness
dizziness
vertigo
blurry vision
headache
dysarthria
visual field loss
gait ataxia
cranial nerve VII dysfunction
lethargy
sensory deficits
clinical features of basilar artery occlusion
posterior circulation stroke symptoms as well as oculomotor signs
Horner’s syndrome
“locked in state”
clinical presentation of cerebellar strokes?
similar to posterior stroke
deteriorate rapidly
how do patients with cervical artery dissection present?
internal carotid dissection:
unilateral head pain
neck pain
face pain
vertebral artery dissection
neck pain
headache, bilateral or unilateral
SAH clinical presentation
sudden onset headache at maximal intensity
associated with activities known to elevate blood pressure such as sexual intercourse, weight lifting, defecation, coughing
loss of consciousness
diplopia
vomiting
photophobia
nuchal irritation
low grade fever
altered mental status
presence of absence of focal neurological findings depends on location of aneurysm
risk factors for stroke
age
atrial fibrillation
hypertension
diabetes
smoking
coronary atherosclerosis
valvular replacement
recent myocardial infarction
risk factors for SAH
excessive alcohol consumption
polycystic kidney disease
family history of SAH
marfan’s/ehlers-danlos
history of drug use, chiropractic manipulation, or blood-pressure elevation
if ischemic stroke is primary working diagnosis and thrombolytic therapy considered, obtain ———
accurate determination of time patient last known baseline and whether may be candidate for thrombolytics
assessment of stroke
focused on neuro
motor weakness
sensory deficits
cerebellar dysfunction
meningismus
carotid bruits
signs of embolic disease
papilledema
preretinal hemorrhage
when would a NIHSS score be determined?
If thrombolytic therapy considered
what imaging should be performed for stroke?
emergent noncontrast CT scan of brain to determine if hemorrhage (most acute ischemic strokes not visualized on CT early)
If SAH suspected and CT negative, what should be performed?
lumbar puncture for red blood cells
diagnostic tests to exclude stroke mimics or concurrent conditions
bedside glucose
CBC
ECG
pulse ox
electrolyte and coag panels
cardiac enzyme levels
tox screen
blood alcohol level
echo
carotid duplex scanning\
MRI, MR angiogram, and CT angiogram when suspicion for alternative disease entities high
Inclusion criteria by AHA/ASA for IV rtPA
Measureable diagnosis of acute ischemic stroke via use of NIHSS
Onset of symptoms <3 h prior to rtPA administration
Age >18 yo
(there are many exclusion criteria that I’m hoping we won’t have to memorize)
General ED care for stroke
ABC
IV access
bedside glucose testing
cardiac monitoring and pulse ox
supplemental oxygen if hypoxic to keep >94%
determine last baseline neuro status
if not candidate for thrombolysis, correct BP if >220/>120 by decreasing by 15% in first 24 hrs
if candidate for thrombolysis, labetolol or nicardipine to maintain <185/<110 (if can’t decrease with these drugs, not good candidate)
Informed consent prior to thrombolytics
supportive care: aspiration prevention, normalization of glucose, fall precautions
admit acute stroke to stroke unit
early consult of specialists, emergent neurology consult in stroke
time recommendations via ASA and AHA to care for stroke patient
10 mins from ED arrival to physician eval
15 mins til activation of stroke team
25 mins til head CT
45 mins tile completion of CT interpretation
thrombolytics within 1 hr
admission to stroke unit within 3 hrs
How long from time of last baseline can rtPA be given?
<3 hrs approved by FDA with inclusion and exclusion criteria review
AHA and ASA say up to 4.5 hrs but is off label and use additional European Cooperative Acute Stroke Study III exclusion criteria
Total dose of rtPA
.9 mg/kg IV with max dose of 90 mg; 10% as bolus and remaining infused over 60 mins
Monitoring/precautions with rtPA
No aspirin or heparin within 24 hrs
CLosely monitor BP
Intracerebral bleeding may be cause of neuro worsening and emergent CT performed
Treatment for TIA
aspirin 75-325 mg PO daily
clopidogrel 75 mg PO daily
combination of aspirin + extended-release dipyridamole 25 mg PO and 200 mg PO twice daily
admission for further eval and obs or workup in ED and starting antiplatelet, educating, and explicit return precautions
Treatment for acute ischemic stroke
aspirin 325 mg PO within 24 to 48 hours unless receiving tPA
do not recommend heparin or warfarin even in presence of afib
Treatment of SAH
BP control at prehemorrhage blood pressure or MAP <140 mmHg if baseline unknown
Labetolol or nicardipine can be used
Admit to ICU with neurosurgeon consult
nimodipine every 4 hrs to decrease vasospasm
seizure prophylaxis if specialist wants
reverse coagulopathy with vitamin K, FFP, and/or prothrombin
treatment for hemorrhagic stroke
admit to CCU
treat with antiepileptic meds if seizures occur
manage hyperglyceia
BP management
reverse coagulopathy with vitamin K, FFP, prothrombin concentrates
If increased ICP, head elevation to 30 degrees, analgesia, sedation
If more agressive ICP reduction indicated with osmotic diuretics or intubation with neuromuscular blockade with mild hyperventilation, invasive monitoring of ICP by neurosurgery
what scoring system has been recommended for use to predict stroke risk in TIA patients?
ABCD
Diagnosis included in altered mental status
delirium
dementia
coma
clinical features of delirium
impaired attention, perception, thinking, memory, and cognition
typically develops over several days
disrupted sleep-wake cycles
increased somnolence during day and agitation characteristic of sundowning at night
decreased alertness and activity fluctuations
tremor
asterixis
tachycardia
sweating
hypertension
emotional outbursts
hallucinations
categories of medical causes of delirium
infectious (pneumonia, UTI, meningitis/encephalitis, sepsis)
metabolic/toxic (hypoglycemia, alcohol ingestion, electrolyte abnormalities, hepatic encephalopathy, thyroid disorders, alcohol or drug withdrawal)
neurologic (stroke or TIA, seizure, SAH, intracranial hemorrhage, CNS mass lesion, subdural hematoma)
cardiopulmonary (CHF, MI, PE, hypoxia or carbon dioxide narcosis)
drug related (anticholinergic drugs, alcohol or drug withdrawal, sedatives-hypnotics, narcotic analgesics, SSRI or SNRI)
diagnosis of delirium
directed at identifying underlying process such as infection
BMP
hepatic studies
ammonia level
UA
CBC
cxr
cranial CT if mass suspected
lumbar puncture if meningitis or SAH suspected
ED care of delirium
treat underlying medical illness
environmental manipulation ie lighting and emotional support
treat acute episodes with haloperidol with reduced dosage in elderly or lorazepam
consider inpatient admission unless readily reversible cause treated with improvement
clinical features of dementia
loss of mental capacity over time
psychosocial level and cognitive abilities deteriorate
behavioral problems develop
insidious onset
gradual and progressive impairment of memory, especially recent
hallucinations
delusions
repetitive behavior
naming problems, forgetting items, loss of reading and direction
disorientation
inability to perform self-care tasks
personality changes
anxiety, depression
speech difficulty
vascular dementia: exaggerated or asymmetric dtrs, gait abnormalities, extremity weakness
largest categories of dementia
alzheimer’s disease
vascular dementia
diagnosis of dementia
PE for cause
focal neuro signs = vascular dementia or mass lesion
increased motor tone and extrapyramidal signs = parkinson’s
urinary incontinence and gait disturbance, large ventricles on CT = normal pressure hydrocephalus
CBC
BMP
UA
Thyroid panel
B12
syphilis testing
ESR
folate
HIV testing
CXR
Head CT or MRI, lumbar puncture if diagnosis not apparent
care for dementia
workup for medical causes
antipsychotic drugs to manage persistent psychosis or severely disruptive or dangerous behavior
treatment of vascular dementia addressing risk factors ie hypertension
inpatient admission for further eval and treatment
discharge if longstanding and stable, consistent caregivers, reliable follow-up
what is coma
state of reduced alertness and responsiveness from which patient cannot be aroused
how is severity of coma quantified
glasgow coma scale and FOUR
pupillary findings, cranial nerve testing, hemiparesis, response to stimulation
what is diffuse CNS dysfunction such as toxic-metabolic coma or focal CNS dysfunction characteristic of?
structural coma
what are characteristics of toxic-metabolic coma?
lack of focal PE findings
pupils small and reactive but may be large in severe sedative poisoning from barbiturates
what can cause coma without lateralizing signs
decreased cerebral perfusion from increased intracranial pressure
reflex changes in BP and HR observed, such as Cushing reflex (hypertension and bradycardia)
presentation of supratentoral lesions or masses
progressive hemiparesis or asymmetric muscle tone and reflexes
How can coma from posterior fossa or infratentorial lesions present?
Abrupt in onset
abnormal extensor posturing and loss of pupillary reflexes and extraocular movements
how does brainstem compression present?
loss of brainstem reflexes that can develop rapidly
how can pontine hemorrhage (a type of infratentorial cause of coma) present?
pinpoint pupils
findings in pseudocoma or psychogenic coma
pupillary responses, extraocular movements, muscle tone, and reflexes intact
Response to manual eye opening with resistance
avoidance of gaze with patient looking away from examiner
nystagmus with caloric vestibular testing
what does abrupt onset of coma suggest?
catastrophic stroke or status epilepticus
what does gradual onset of coma suggest?
metabolic process or progressive lesion such as tumor or slow intracranial bleed
if a patient has asymmetric findings on pupillary exam, assessment of corneal reflexes, and testing of oculovestibular reflexes what does that suggest?
focal CNS lesions
basilar artery thrombosis diagnosis
nondiagnostic CT and absence of alternative diagnsois
MRI or cerebral angiography
What shoudl be done if patient has seizures and remains unresponsive
may be having electrical seizures without motor activity
EEG performed
what should be considered in comatose children
toxic ingestions
infections
nonaccidental trauma
ED care of coma
ABC
identify and treat reversible causes ie hypoglycemia and opioid toxicity (naloxone)
administer thiamine before glucose in hypoglycemic patients with history of alcohol abuse or malnutrition
consider nonconvulsive status epilepticus in patients who have ahd a seizure and not returned to baseline
if increased ICP, elevate head of bed to 30 deg, give mannitol and dexamethasone if tumor, hyperventilation but not below 35
discharge those with readily reversible causes if home care and f/u adequate and clear cause found
admit all other patients
