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Emergency Medicine EOR > Neurology > Flashcards

Neurology Flashcards

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1
Q

What is the presentation of altered mental status?

A
  • due to systemic infection or metabolic problems and vascular events (CVAs, bleeds)
  • can lead to irreversible brain injury if they are not promptly identified and treated
  • a systematic approach to the patient is important, diagnostic workup
  • patients with altered mental status have a high mortality rate
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2
Q

What can be both diagnostic and therapeutic?

A

naloxone when opiate overdose is suspected

-thiamine administration to cover for Wernicke encephalopathy

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3
Q

What is dx and tx for altered mental status?

A
  • ABCs, airway, breathing, and circulation, vital signs, blood glucose level
  • administer thiamine and dextrose
  • consider naloxone opiate overdose
  • history and physical examination neurologic examination to rule out a focal deficit
  • complete blood count, electrolyte panel, calcium, magnesium, and phosphorus
  • liver and kidney function tests
  • urine toxicology screen
  • serum ammonia
  • arterial blood gas
  • blood cultures
  • ECG and CXR
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4
Q

What is the imaging for altered mental status?

A
  • CT scan
  • MRI with diffusion and gadolinium
  • lumbar puncture
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5
Q

What are the pearls of altered mental status?

A

AMS patients after ABCs, in the beginning, can all be given

  • glucose (for low blood glucose levels)
  • thiamine (Wernicke)
  • Narcan (opiates)
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6
Q

What is loss of consciousness?

A

syncope is an abrupt and transient loss of consciousness caused by cerebral hypo perfusion, accounts for 1 to 1.5% of emergency department visits need to be extensively worked up

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7
Q

What are the causes of loss of consciousness?

A
  • cardiovascular or structural heart disease
  • arrhythmia
  • cerebral hypo perfusion (CVS, hypovolemia, etc.)
  • orthostatic hypotension syncope (supportive care)
  • seizures
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8
Q

What is the dx and tx for loss of consciousness?

A
  • oxygen
  • EKG
  • CBC, CMP, troponin
  • CT scan
  • possible EEG
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9
Q

What are the pearls of loss of consciousness?

A
  • all patients with LOC need cardiac monitoring
  • CT scan
  • observation
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10
Q

What is the glasgow coma scale?

A 
Eye-opening 
-4 spontaneous 
-3 voice 
-2 pain 
-1 none
Verbal 
-5 oriented 
-4 confused 
-3 inappropriate words
-2 incomprehensible 
-1 none
Motor 
-6 obeys commands 
-5 localizes pain
-4 withdraws
-3 abnormal flexion (decorticate) 
-2 abnormal extension (decerebrate) 
-1 none

less than 9 is coma

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11
Q

What is the presentation for numbness/paresthesia?

A
  • paresthesia an abnormal dermal sensation due to compromised nerve function
  • commonly presents impaired sensations as prickling, tingling, itching, burning or cold, skin
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12
Q

What are the causes of numbness/paresthesia?

A

symptoms usually arise from nerve damage or compromised due to injury blood flow toxins, numbness is often caused by damage, irritation, or compression of nerves

  • diabetes (very common due to the destruction of the nerves due to the elevated glucose)
  • nerve root pathology (impingement and compression of the nerves)
  • central pathology (brain causes such as multiple sclerosis, CVAs, etc.)
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13
Q

What are the pearls of numbness/paresthesia in the ER?

A
  • brain (CVA, multiple sclerosis, seizures, etc.)
  • spinal cord (impingement, compression, infection, etc.)
  • or coming for the periphery (peripheral)
  • Imaging (MRI/CT scan) of the brain and/or spinal cord is necessary for the workup
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14
Q

What is a Bell palsy?

A

sudden onset unilateral facial nerve paralysis with no other focal neurologic or systemic findings

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15
Q

What are the characteristics of Bell palsy?

A
  • the symptoms peak in 48 hours
  • 60% have a viral prodrome
  • PE with show CN VII nerve palsy that does not spare the forehead
  • most commonly caused by HSV
  • Incomplete closure of eyelids = corneal exposure keratitis (lubricating eye drops needed/ patch at bedtime)
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16
Q

What are the DDX of Bell palsy?

A

infectious, traumatic, and neoplastic etiologies

-the most common dx if idiopathic Bell’s palsy

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17
Q

What is the tx for Bell palsy?

A
  • treatment is prednisone, artifical tears, tape eyelid shut

- comments: Bilaterla: lyme disease, infectious mononucleosis

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18
Q

What is encephalitis?

A

presents similar to meningitis: AMS, seizures, personality changes, exanthema = encephalitis is clinically differentiated from meningitis by altered brain functioning

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19
Q

What are the characteristics of encephalitis?

A
  • etiology: usually viral (HSV = MC, CMV in immunocompromised)
  • Reye’s syndrome: rapidly progressive encephalopathy with hepatic dysfunction, usually post-flu/URI; Babinski positive and hyperreflexia noted = salicylate use (aspirin, Pepto); vomiting, confusion = seizure/coma
  • DX: elevated liver enzymes, PTT, hyperammonemia, hypoglycemia, metabolic acidosi; tx = supportive
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20
Q

What are the symptoms of encephalitis?

A

begins with flu-like illness

-fever, headaches, altered mental status, seizures, personality changes, exanthema

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21
Q

How is encephalitis dx?

A
  • lumbar puncture and MRI
  • PCR for viruses
  • Kernig’s and Brudzinski’s usually absent
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22
Q

What is the tx for encephalitis?

A

supportive care and acyclovir 10- mg/kg IV q8hr started promptly
-empiric antibiotics are often given bacterial meningitis is excluded

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23
Q

What is status epilepticus?

A

s/s: > or equal to 5 min continuous seizure activity or more than one seizure without recovery from the postictal state in between episodes

  • always check finger stick blood =glucose, consider pyridoxine (B6) for INH toxicity
  • MC caused by a change in medication regiment of someone with a seizure disorder
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24
Q

What is the tx of status epilepticus?

A
  • place in left lateral decubitus position (suppressed gag reflex = prone to aspiration of gastric contents)
  • Pharm: 1. Benzo (lorazepam, diazepam, midazolam) 2. Phenytoin/fosphenytoin 3. phenobarbital and lacosamide
  • IV route is preferred
  • watchful waiting for auto-correction of acidosis once seizure activity is controlled
  • untreated generalized seizures lasting > 60 min may result in permanent brain damage; longer-lasting seizures may be fatal
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25
Q

What is a partial focal seizure?

A

occur when this electrical acivity remains in a limited area of the brain

  • the seziures can sometimes turn into generalized seziures, which affect the whole brain
  • with retrained awareness (simple partial): no alteration in consciousness
  • with loss of awareness (complex partial): automatisms (lip-smacking) - postictal state = confusion/memory loss
  • tx - phenytoin, and carbamazepine are drugs of choice
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26
Q

What are generalized seizures?

A

occur when there is widespread seizure activity in the whole brain (left and right hemispheres)

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27
Q

What is absence seizure (petit mal)?

A
  • brief mental status change; without motor activity - blank stare
  • no aura, no post-octal state, no loss of postural tone
  • MC in 5-10 yo
  • EEG = brief 3-HZ spike and wave discharge
  • Tx: ethosuimide
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28
Q

What is tonic-clonic?

A

convulsive (grand mal) - bilaterally symmetric and without focal onset, begins with LOC
-tonic phase: very stiff and rigid 10-60 seconds, clinic phase = convulsions, post-ictal phase = confused states

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29
Q

What is atonic?

A

drop attack = like syncope; loss of muscle tone

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30
Q

What is clonic?

A

loss of control of bodily function, jerking, may temporarily lose consciousness

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31
Q

What is tonic?

A

extreme rigidity then LOC

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32
Q

What is mycoclonic?

A

muscle jerking, no tonic phase, occurs in the morning

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33
Q

What is febrile?

A

temp >38, >6 mo, <5 years, absence of CNS infection/inflammation

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34
Q

What are infantile spasm?

A

type of epilepsy seizure

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35
Q

What is psychogenic non-epileptic seizure?

A

not due to epilepsy but look similar to an epileptic seizure

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36
Q

How do you dx seziures?

A

check electrolytes, glucose, pregnancy test, ECG, EEG, neuroimaging for adults with first seizure (CT/MRI)

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37
Q

What is the tx for seziures?

A

treat underlying cause = electrolytes, infection, toxic ingestion, trauma, azotemia, hypoxia, hypoglycemia, stroke/bleed
-meds for focal seizures: phenytoin, phenobarbitals, valproate, lamotrigine, gabapentin

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38
Q

What is an epidural hematoma?

A
  • transient LOC from injury = LUCID = HA, unilateral contralateral weakness
  • cause: traumatic intracranial hemorrhage after skull fracture = middle meningeal artery is MC involved = blood fills space between dura and skull
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39
Q

How is an epidural hematoma dx?

A

non-contrast head CT (lenticular, unilateral convexity - lens shape) usually in temporal region = “lemon”

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40
Q

What is the tx for epidrual hematoma?

A

surgical craniotomy/medical management of increased intracerebral pressure (mannitol, hyperventilate, steroids/ventricular shunt)

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41
Q

What is a subdural hematoma?

A
  • head injury from fall, MVA, assault = sudden blow tears blood vessels; usually elderly pt with multiple falls presenting with neurological sx (AMS/neurologic signs) = usually in alcoholic or elders
  • Injuries to bridging veins - acute = 48 hours; subacute 3-14 days, chronic: > 2 weeks (elderly)
  • blood collects between dura and arachnoid mater
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42
Q

How is a subdural hematoma dx?

A

non-contrast CCT (credence-shaped, concave hyperdensity)

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43
Q

What is the tx of subdural hematoma?

A

depends on the severity

  • small: obervation
  • severe: surgery = burr hole trephination, craniotomy, craniectomy
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44
Q

What is a spinal cord injury?

A

damage to the spinal cord that results in a loss of function, such as mobility and/or feeling
-frequent causes of spinal cord injuries are trauma (car accident, gunshot, falls, etc.) or disease (polio, spina bifida, etc.)

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45
Q

What is anterior cord syndrome?

A

loss of pain/temperature below the level of the lesion preserved joint position/vibration

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46
Q

What is central cord syndrome?

A

loss of pain and temperature sensation at the level of the lesion, where spinothalamic fibers cross the cord with other modalities preserved (dissociated sensory loss)

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47
Q

What is complete cord transection?

A

rostral zone of spared sensory levels (reduced sensation caudally, no sensation in levels below injury); urinary retention and bladder distension

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48
Q

What is brown-sequard syndrome?

A

(hemisection of cord)
-loss of joint position and vibration sense on the same side as lesion and pain/temperature on the opposite side a few levels below the lesion

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49
Q

What is guillain-barre syndome?

A

ascending paralysis beginning in distal limbs: leg weakness = total paralysis of all 4 limbs, facial muscles, eyes, loss of reflexes

  • often present after immunization
  • post-infectious cause: campylobacter jejuni=MC, CMV, Epstein-Barr, HIV
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50
Q

How is guillain-barre syndrome dx?

A

based on lumbar puncture = elevated CSF protein with normal CSF WBC

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51
Q

What is the tx for guillain-barre syndrome?

A

plasma exchange (remove circulating antibodies) and IVIG

  • monitor PFTs for paralysis of chest muscle/diaphragm (respiratory failure)
  • good prognosis
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52
Q

What is status epilepticus?

A

a single epileptic seizure lasting more than five minutes or two or more seizures within a five-minute period without a person returning to normal between them

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53
Q

What are the two forms of status epilepticus?

A

convulsive and nonconvulsive

  • convulsive status epilepticus presents with a regular pattern of contraction and extension of the arms and legs
  • nonconvulsvie status epilepticus includes complex partial status epileptiucs and absence status epilepticus
54
Q

What is the tx for status epilepticus?

A

benzodiazepines (lorazepam) are the preferred initial treatment after which typically phenytoin is given

55
Q

What is a concussion?

A

involves transient, traumatic brain dysfunction; consciousness may be lost but sometimes patients manifest only confusion, memory loss, and gait or balance difficulties

  • +/- brief LOC, amnesia = no structural abnormalities and no focal neurologic deficits
  • negativ CT scan
56
Q

What is a grade 1 concussion?

A

“mild” - GCS 13-15, no LOC, post-traumatic amnesia and other symptoms resolve < 30 min - can return to sports if asymptomatic for 1 week

57
Q

What is a grade 2 concussion?

A

+LOC, 1 minute or post-traumatic amnesia that lasts > 30 min but < 1 week; may return to sports if asymptomatic at rest and exertion for at least 7 days

58
Q

What is a grade 3 concussion?

A

+LOC, > 1 min or post-traumatic amnesia and other sx last > 1 week; may return in 1 month if asymptomatic at rest and exertion 7 days

59
Q

How is a concussion dx?

A

usually clinical, sometimes head imaging
-get a CG if LOC, GCS < 15, suspected open skull/basilar skull fx, >2 episodes vomiting, > 65 y/o, amnesia > 30 min prior to impact, MVA with ejection, pedestrian struck by car, fall > 3 feet, underlying bleeding disorder/anticoagulant use, seizure activity, focal neurological deficit, ETOH involvement, persistently AMS, clinical deterioration

60
Q

What is the tx for a concussion?

A

athletic activities resumed gradually

  • single concussion: LOC lasting < 15 min - return to sports when asymptomatic for at least 1 week
  • repeat: LOC/sx > 15 min = NOT to return to sports that season
61
Q

What is a stroke?

A

can be ischemic or hemorrhagic

  • risk factors: HTN, hypercholesterolemia, diabetes, afib, carotid artery disease, cigarette smoking, age, family history, male sex
  • HTN = most significant and treatable
62
Q

What is an ischemic stroke?

A

85% - 2/3 thrombotic, 1/3 embolic

  • thrombotic caused by a blood clot that develops in the blood vessels inside the brain, usually preceded b y TIA
  • embolic caused by a blood clot that develops somewhere else in the body usually from heart, aortic arch, large cerebral arteries = occur abruptly without warning
63
Q

What is a hemorrhagic stroke?

A

usually secondary to HTN = intracerebral/subarachnoid

  • a weekend vessel that ruptures and bleeds into surrounding brain compressing surrounding brain tissue = either aneurysms or AVMs; less predictable
  • s/sx: hemiparesis, hemisensory deficit; must present on one side only and will be the side of body opposite stroke
  • right-sided sx = left side stroke; left-sided sx = right sided stroke
64
Q

What is anterior circulation?

A

(anterior cerebral/middle cerebral arteries) associated with hemispheric s/s (aphasia, apraxia, hemiparesis, hemisensory loss, visual field defect)

65
Q

What is posterior circulation?

A

(vertebral/basilar arteries): coma, drop attack, vertigo, n/v, ataxia

66
Q

What is carotid/ophthalmic?

A

amaurosis fugax

67
Q

What is MCA?

A

aphasia, neglect, hemiparesis, gaze preference, homonymous hemianopsia

68
Q

What is ACA?

A

leg paresis, hemiplegia, urinary incontinence

69
Q

What is PCA?

A

homonymous hemianopsia

70
Q

What is basilar?

A

coma, cranial nerve palsies, apnea, drop attack, vertigo

71
Q

What is lacunar?

A

silent, pure motor or sensory

72
Q

How is a stroke dx?

A

emergent brain imaging essential for ischemic stroke = noncontrast CT scanning

73
Q

How is the tx for stroke?

A

thrombolyis, IV admin for rtPA for occulsive disease that with IV tPA within 3-4.5 hours onset

  • admit to ICU or storke unit with neuro exams every 25 minutes during infusion, every 60 minutes for next 6 hours then 24 hours after tx/get serial blood pressures
  • exclusions criteria for thrombolysis within 3 hours: SAH, head trauma/prior stroke within 3 mo, MI within 3 mo, GI/gastric ulcer within 3 weeks, major surgery in 14 days, hx of intracranial hemorrhage, elevated BP > 185 systolic/110 diastolic, active bleeding/acute trauma, INR > 1.7 with anticoagulation, glucose < 50, seizure with postical state, multilobal infarction on CT
  • BP closely monitored in first 24 hours; hold antihypertensive until systolic > 220 or diastolic >120 with a goal to lower BP by 15% in first 24 hours if tx is indicated
  • BP has to be <185/110 for thrombolytic = give labetalol 10-20 mg IV over 1-2 min
74
Q

What is a cluster headache?

A
  • always unilateral, but can change sides with new attack; pt is usually a man
  • s/s: pain (excruciating unilateral pain, periorybital and temporal)
  • autonomic sx: ptosis, mitosis, lacrimation, conjunctival injection, rhinorrhea, nasal congestion
  • circadian periodicity: short-lived (15-180 min) cluster attacks; attacks occur daily in clusters followed by remission
  • tx: 100% oxygen, sumatriptan (prophylaxis: CCBs)
75
Q

What is a tension headache?

A
  • MC type of headache
  • bilateral, non-pulsating, bandlike pain occurring in frontal and occipital regions; with neck muscle tenderness
  • MC causes by stress, or fatigue, glare, noise
  • Tx: NSAIDs, smoking cessation
76
Q

What is a migraine headache?

A
  • F > M
  • triggers: menstruation, pregnancy, contraceptives, food (chocolate, cheese, MSG, nitrites), alcohol
  • gradual onset unilateral > bilateral, throbbing, pulsating headahce
  • without aura = most common, N/V, photophobia, phonophobia
  • aura: scotoma, flashing lights, sound
  • Ha follows aura w/in 30 min; visual = MC
  • dx: clinical
  • tx:
  • abortive: triptans, dihydreergotamine (DHE, antiemetics, NSAIDs)
  • prophylaxis - beta-blockers, CCBs, TCAs
77
Q

What is a subarachnoid hemorrhage?

A
  • sudden, severe HA “worse HA of life”, sudden LOC in 50% of patients, BP rises, may develop a fever
  • Herald bleed occurs in 40% - less severe but atypical HA
  • ruptured berry (saccular) aneurysm accounts for 75% non traumatic -r/f: smoking, HTN, hypercholesterolemia, heavy alcohol
78
Q

How is a subarachnoid hemorrhage dx?

A

non-contrast heat CT, LP (elevated opening pressure/grossly bold fluid in all 4 tubes)
-cerebral angiography may be done, EEG may show site of hemorrhage/diffuse changes

79
Q

What is the tx for subarachnoid hemorrhage?

A

prevention of elevated arterial/intracranial pressure - manage HTN

  • surgical clipping/wrapping of aneurysm
  • anticonvulsants for seizure prevention
80
Q

What is an intracerebral hemorrhage?

A
  • associated with high mortality; usually from HTN (sudden increase BP) = rupture small vessels deep in the brain parenchyma
  • usually older pt, risk increase with age
  • Ischemic stroke may = hemorrhagic stroke
  • s/sx: abrupt onset of a focal neurologic deficit that worsens steadily over 30 to 90 minutes, altered LOC, stupor, coma, HA, vomiting and signs of increased ICP
81
Q

How is intracerebral hemorrhage dx?

A

CT/MRI

82
Q

What is the tx for intracerebral hemorrhage?

A

neurosurgery

83
Q

What is a saccular aneurysms?

A

are almost always the result of hereditary weakness in blood vessels and typically occur within the arteries of the circle of Willis

84
Q

How is an aneurysms dx?

A

magnetic resonance angiography (MRA) or CT angiography (CTA)

85
Q

What is the tx for an aneurysms?

A

surgical clipping or end-endovascualr coil

86
Q

What is the presentation of altered mental status?

A
  • due to a systemic infection or metabolic problems and vascular events (CVAs, bleeds)
  • can lead to irreversible brain injury if they are not promptly identified and treated
  • a systemic approach to the patient is important, diagnostic workup
  • patients with altered mental status have a high mortality rate
  • naloxone can be both diagnostic and therapeutic when an opiate overdose is suspected, thiamine administration to cover for Wernicke encephalopathy
87
Q

How is altered mental status dx and tx?

A
  • ABCs, airwary, breathing, and circulation; vital signs, blood glucose level
  • administer thiamine and dextrose
  • consider naloxone opiate overdose
88
Q

How is altered mental status dx?

A

history physical examination neurologic examination to rule out a focal deficit

  • complete blood count, electrolyte panel, calcium, magnesium, and phosphorus
  • liver and kidney function tests
  • urine toxicology screen
  • serum ammonia
  • arterial blood gas
  • blood cultures
  • ECG and CXR
89
Q

What is the imaging for altered mental status?

A
  • CT scan
  • MRI with diffusion and gadolinium
  • lumbar puncture
90
Q

What are the pearls of altered mental status?

A
  • AMS patients after ABCs, in the beginning, can all be given glucose (for low blood glucose levels)
  • thiamine (Wernicke)
  • narcan (opiates)
91
Q

What is syncope?

A

a brief LOC with loss of postural tone followed by spontaneous revival - motionless/limp and usually has cool extremities, weak pulse, shallow breathing

92
Q

What are the characteristics of syncope?

A
  • accounts fo 1 - 1.5% of emergency department visits and needs to be extensively worked up
  • characterized by a rapid recovery of consciousness without resuscitation
  • near syncope = lightheadedness/sense of impending faint without LOC
  • seziure can caused sudden LOC but not considered syncope
  • most result from insufficient cerebral blood flow = usually from decreased cardiac output or decreased venous return
  • MC causes: vasovagal (apparent trigger/warning symptoms), idiopathic
  • red flags: syncope during exertion, multiple recurrences in short time, heart murmur, old age, significant injury during syncope, family history sudeen unexpected death
93
Q

What are the causes of syncope?

A
  • cardiovascular or structural heart disease
  • arrhythmia
  • cerebral hypo perfusion (CVA, hypovolemia, etc.)
  • orthostatic hypotension syncope (supportive care)
  • seizures
94
Q

How is syncope dx and tx?

A

treatment is aimed at identifying and fixing the underlying cause

  • oxygen
  • EKG
  • CBC, CMP, troponin
  • CT scan
  • possible EEG
95
Q

What are the pearls of syncope?

A
  • all patients with LOC need cardiac monitoring
  • CT scan
  • Observation
96
Q

What is the presentation of loss of coordination/ataxia?

A

cerebellar involvement

  • question is what is affecting it??
  • a detailed history and neurologic examination (finger-nose, and heel-shin testing)
  • proper diagnostic tests
  • may be chronic and slowly progressive (Parkinson’s disease)
  • acute due to infarction, edema, or hemorrhage
97
Q

What is the dx and tx for loss of coordination/ataxia?

A

Imaging

  • CT scan
  • MRI with and without contrast
98
Q

What are the pearls of loss of coordination/ataxia?

A
  • can be due to drugs (ETOH) and toxins
  • tumors
  • CVAs
  • genetics
99
Q

What are the ddx of loss of coordination/ataxia?

A

hyper/hypovitaminosis (B12), inner ear issues, hallucinogen-related psych disorders, vertigo, encephalopathies, neoplasms, Huntington, MS, stroke, fibromyalgia, cerebral palsy, metabolic disorders, (hepatic encephalopathy)

100
Q

What is a transient ischemic attack?

A

a transient epidote of neurologic dysfunction due to focal brain, retinal, or spinal cord ischemia without acute infarction

101
Q

What are the characteristics of transient ischemia attack?

A
  • blockage in blood flow does not last long enough to cause permanent infarction
  • sudden onset of neurologic deficit, lasting minutes to <1 h (15-30 min on average), a reversal of symptoms within 24 h
  • atherosclerotic plaque reduces blood flow in the internal carotid artery
  • 10% of TIA patients will have a stroke within 90 days
102
Q

How is a transient ischmic attack dx?

A

CT (without contrast), MRI more sensitive, carotid doppler ultrasound to look for stenosis, CT angiography, MR angiography of neck
-carotid endarterectomy if internal or common carotid artery stenosis is >70%

103
Q

What is the tx of transient ischemic attack?

A

aspirin + dipyridamole or clopidogrel mono therapy (anti platelet therapy)

  • ABCD2 score: predicts like likelihood of subsequent stroke with 2 days
  • 30% of those with CVA had TIA; the risk is highest 24 hours after the initial event
104
Q

What is loss of memory?

A

inability to remember events for a period of time, often due to brain injury, illness, or the effects of drugs and alcohol

105
Q

What is dementia?

A

is a slow decline in memory, problem-solving ability, learning ability, and judgment that may occur over several weeks to several months, Alzheimer’s disease is the most common after 65

106
Q

What is delirium?

A

a sudden change in mental status such as withdrawal from alcohol or drugs or medicines, worsening of an infection or other health problem

107
Q

What is amnesia?

A

memory loss that may be caused by head injury, stroke, substance abuse, or a severe emotional event, such as from combat or a motor vehicle accident, may be either temporary or permanent

108
Q

What are the pearls of loss of memory?

A

It’s either caused by

  • dementia (alzheimer’s)
  • delirium (withdrawal or infection)
  • amnesia (head injury, CVA, etc.)
109
Q

What is delirium?

A

an acute syndrome caused by medical condition, substance, intoxication or withdrawal or medication side effect a AMS

  • ex: sepsis, sundowning, ETOH withdrawal, opiate withdrawal, sunstroke
  • rapid onset, short term, reversible
  • criteria
  • disturbed level of consciousness (decreased attention span/lack of environmental awareness)
  • cognitive change - memory deficit, disorientation, language disturbance, visual/auditory hallucinations
  • rapid onset within hours/days with a fluctuating course
  • evidence of a causal physical condition
110
Q

How is delirium dx?

A

history, CT/MRI, CBC, blood cultures, CXR, UA, BUN, electrolytes, glucose, urine toxicology to r/o infection

111
Q

What is the tx of delirium?

A

treat underlying cause/supportive care; sedation when necessary

112
Q

What is Alzheimer’s disease?

A
  • age-related progressive cognitive decline affects 5% of those aged 71-80 years, and near 40% of those aged over 90 years
  • s/s: gradual, progressive memory loss, difficulty word-finding, concentration problems, emotional lability, personality changes, social withdrawal, difficulties with dressing, cooking, balancing the checkbook, and maintaining hygiene
  • there are multiple types of dementia: Alzheimer disease, vascular dementia, and other less common dementias
113
Q

How is Alzheimer’s disease dx?

A

Folstein Mini-Mental State Examination (MMSE) or the memory impairment screen, the MMSE may be useful to provide a baseline for future comparison, controversy exists over the use of memantine and anticholinergic medications in the tx of dementia

  • alzheimer disease = MC: 2/3 dementia cases; irreversible; early lanuage/visuospatial deects
  • severe memory deficits; clue don’t help memory retrieval
  • r/f: advanced age, family hx
  • vascular: 1/4 cases, r/f: HTN, dyslipidemia, DM, smoking, adv age
  • lewy body: cognitive fluctuations, visual hallucinations, parkinsonism
  • frontotemproal dementia: personality, and social behavior changes, non-fluent sppech
  • neurodegenerative conditions: huntingon disease, metabolic abnormalities
114
Q

What are the irreversible causes of dementia?

A

vascular dementia, Creutzfeldt-jakob

115
Q

What are the reversible causes of dementia?

A

depression, B12 deficiency, syphilis, hypothyroidism, NPH, drug use, intracranial mass

116
Q

What is the tx of dementia?

A

cholinesterase inhibitors (donepezil): NMDA antagonists (memantine) a don’t cure, just slow progression

117
Q

What is vertigo?

A

the sensation of movement in the absence of movement

118
Q

What is peripheral vertigo?

A

inner ear = labyrinthitis, BPPV, meniere, vestibular neuritis, head injury = sudden onset, n/v, tinnitus, hearing loss, nystagmus (horizontal)

119
Q

What is central vertigo?

A

brainsteam vascular disease, AVM, tumor, MS, vertebrobasilar migraine = more gradual onset/vertical nystagmus, no auditory symptoms
-vertigo+ syncope = vertebrobasilar insufficiency

120
Q

What is BPPV?

A

positional, no hearing loss, tinnitus, ataxia

  • dx: Dix-hallpike test
  • tx: employ maneuvers, meclizine
121
Q

What is vestibular neuritis?

A

not positional, no hearing loss/tinnitus

-tx: meclizine

122
Q

What is labyrinthitis?

A

acute, self-resolving episode; vertigo, hearing loss tinitus,
-tx: meclizine + steroids

123
Q

What is Meniere’s disease?

A

chronic, relapsing, remitting; vertigo + hearing loss + tinnitus
-tx: diuretics, salt restriction, CN VIII ablation for severe cases

124
Q

What is perilymph fistula?

A

a history of trauma, vertigo from trauma

-tx: fix damage surgically

125
Q

What is an acoustic neuroma?

A

ataxia, neurofibromatosis type II

  • MRI findings: vertigo, hearing loss, tinnitus, and ataxia
  • tx: surgery
126
Q

What is meningitis?

A

the classic triad of fever > 38 C, nuchal rigidity (stiff neck), headache

127
Q

What are the characteristics of meningitis?

A
  • unlike encephalitis no mental status changes
  • physical exam: Kernig’s sign (neck pain with knee extension), Brudzinski sign (leg raise with a bent neck)
  • aseptic: usually viral; negative blood cultures
  • bacterial: community-acquired, usually s. pneumonia (gram _ cocci)/n. meningitides (gram-diplococci) - likely if pt has a rash
  • neonates = e.col/s.agalactiae
  • > 50-60 = listeria/cryptococcus neofromans
  • hospital-acquired: staph/aerobic gram-negative
128
Q

How is meningitis dx?

A

lumbar puncture = must first check for increased intracranial pressure (check for papilledema) = get a CT if unsure

  • bacterial: increase protein, decrease glucose (bacteria love to eat glucose); markedly increased opening pressure
  • viral: normal pressure, increased WBC (lymphocytes)
129
Q

What is the tx for meningitis?

A
  • aseptic: symptomatic or IV acyclovir for HSV
  • bacterial: dexamethasone + empiric IV antibiotics (cephalosporin, Vanco, penicillins)
  • household contacts: treat with rifampin, Cipro, Levaquin, azithromycin, ceftriaxone
130
Q

What are the ddx for weakness/paralysis?

A

Epstein-Barr virus, human immunodeficiency virus, influenza, Lyme disease, meningitis (multiple agents), polio, rabies, syphills, toxoplasmosis, amyotrophic lateral sclerosis, cerebrovascular disease, stroke, subdural/epidural hematoma, Guillain-barre syndrome, multiple sclerosis, neoplasm, Lambert-eaton myasthenia syndrome, myasthenia gravid, organophosphate intoxication, cervical spondylosis, degenerative disc disease, spinal cord injury, spinal muscle atrophy, alcohol, adrenal insufficiency, glucocorticoid excess, hyperthyroid/hypothyroid, RA, polymyositis, dermatomyositis, RA, lupus, muscular dystrophy, PMR, etc.

Emergency Medicine EOR (12 decks)

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