Neurology Flashcards

1
Q

Altered Mental Status DDX

Delirium

A
Metabolic disorders (hypercalcemia)
Oxygen
Vascular (MI, CVA)
Endocrine (hypoglycemia)
Seizure
Trauma
Uremia
Psychiatric
Infectious
Drugs
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2
Q

AMS gen info

A

delirium: acute pd of cognitive dysfunction d/t a medical disturbance or condition
elderly patients are esp prone
consciousness = arousal + cognition
- arousal dependent on an intact brainstem (RAS)
- cognition dependent on an intact cerebral cortex
AMS, diminished LOC (drowsiness, stupor, coma), and confusion are caused by many of the same conditions and are often variations of the same theme.
Depressed LOC and coma can be caused by a variety of disorders.
- classify & organize by two categories:
1. diffuse injury to brain d/t metabolic, systemic, or toxic disorder
2. focal intracranial structural lesions like hemorrhage, infarction, tumor

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3
Q

Delirium clinical features

A

Rapid deterioration in mental status (over hours to days), a fluctuating level of awareness, disorientation, and attention. Waxing and waning, sundowning
+- acute abnormalities of perception (hallucinations)
Agitation (hyperactive)
Slow, blunted responsiveness (hypoactive)
Strongest risk factor is preexisting cognitive impairment

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4
Q

Delirium causes

A
infections (UTI, systemic infxn)
medications (narcotics, benzos)
post op delirium (elderly)
alcoholism
electrolyte imbalances
medical conditions (stroke, heart disease, seizures, hepatic, and renal disorders)
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5
Q

Delirium dx

A

Mc screening; confusion assessment method (CAM) w 4 features; acute onset w fluctuating course, inattention, disorganized thinking, altered LOC
w/u depends on suspected contributing factors and reversible causes (good h&p!), detailed neuro exam, mental status assessment, good review of meds.
Labs, imaging, procedures (LP), workup patient-specific

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6
Q

Delirium

A

Treat underlying cause
delirium precautions while in hospital; frequent orientation, familiar objects and faces, maintaining a normal sleep-wake cycle with blinds open during day, correcting sensory impairments (hearing aids, glasses)
Avoid restraints and pharmacologic mgmt of agitation as much as possible; if necessary use antipsychotics like haloperidol

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7
Q

Coma gen info

A

depressed LOC to extent that patient is completely unresponsive to any stimuli
Causes
- structural brain lesions, usu bilateral unless they produce enough mass effect to compress brainstem or opposite cerebral hemisphere
- global brain dysfunction (metabolic or systemic disorders)
- psych causes; conversion disorders and malingering

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8
Q

Coma approach

A

initial steps
- vitals, ABCs
- always assume underlying trauma (stabilize C spine) and assess signs of underlying trauma
- assess LOC (glasgow coma scale), repeat serially
approach to diagnose
- rapid motor exam (asymmetry –> mass lesion; metabolic or systemic causes –> no asymmetry)
- brainstem reflexes:
1. pupillary light reflex
- round + symmetrically reactive –> midbrain intact
- anisocoria –> uncal herniation
- abnl light reflex –> structural intracranial lesions (hemorrhage, mass), drugs (morphine)
- bilateral fixed, dilated –> severe anoxia
- unilateral fixed, dilated –> herniation CN 3 compression
2. eye movements
- doll’s eye test if not c spine injury; when head turned, eyes should move conjugately to opposite direction if brainstem intact
- if patient breathing on their own –> intact brainstem

Labs
CBC, electrolytes, calcium BUN, creatinine, glucose, plasma osmolarity, ABG, ECG

Blood and urine tox labs
CT or MRI of brain
LP if meningitis or SAH suspected.

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9
Q

Coma treatment

A

correct reversible causes, treat underlying problem, control airway, give supp O2, naloxone, dextrose, give thiamine before glucose load, correct abnlities in BP, lytes, body temp
ID and treat herniation - lowering ICP

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10
Q

Meningitis gen info

A

inflammation of meningeal membrane enveloping brain and spinal cord
usu a/w infectious cause but noninfectious (medications, SLE, sarcoidosis, carcinomatosis) exist
Pathophys
infectious agents frequently colonize nasopharynx and resp tract –> enter CNS thru 1) invasion of bloodstream (hematogenous seeding of CNS), 2) retrograde transport along cranial (olfactory) or peripheral nerves, 3) contiguous spread from sinusitis, OM, surgery or trauma
Classification
acute - onset within hrs-days
chronic - onset within wks - mos; commonly caused by mycobacteria, fungi, lyme dz, parasites

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11
Q

Acute bacterial meningitis

A

*** medical emergency requiring prompt recognition + abx therapy (freq fatal even with abx)
Triad: fever, nuchal rigidity, change in mental status

Causes
neonates - group B strep, E. coli, listeria monocytogenes
children > 3 mos - n meningitidis, step pneumo, h flu
adults (18-50y) - ‘’ “
elderly (>50y) - strep pneumo, n meningitidis, l. monocytogenes, gram-neg bacilli
immunocompromised - l. monocytogenes, gram-neg bacilli, strep pneumo

Complications
Seizures, coma, brain abscess, subdural empyema, DIC, resp arrest
Permanent sequelae - deafness, brain damage, hydrocephalus

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12
Q

Aseptic meningitis

A

MC d/t variety of nonbacterial pathogens; viruses (enterovirus, HSV), certain bacteria, parasites, fungi
May be difficult to distinguish clinically from bacterial
(tx for bacterial if uncertain)
A/w better prognosis

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13
Q

Meningitis clinical features

A
Symptoms
Headache (-+ worse laying down)
Fevers
N/V
Stiff, painful neck
Malaise
Photophobia
AMS (confusion, lethargy, coma)

Signs
Nuchal rigidity: stiff neck, with resistance to flexion of spine
Rashes (maculopapular w petechiae –> n. meningitidis; vesicular lesions –> HSV, varicella)
Incr ICP (papilledema, seizures)
Cranial nerve palsies
Kernig sign (inability to fully extend knees with hips flexed)
Brudzinski sign (passive flexion of neck causes flexion of legs and thighs)
Jolt test (worsening HA when pt asked to turn head back and forth quickly at freq of 3 turns per sec)*

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14
Q

Meningitis Diagnosis

A

CSF exam (LP) - performed when meningitis a possibility unless evidence of space-occupying lesion

  • examine CSF; cell count, chemistry (protein, glucose), gram stain, culture (including AFB), cryptococcal antigen or india ink
  • bacterial –> pyogenic inflammatory response in CSF:
  • elevated WBC count - PMNs predominate
  • low glc
  • high protein
  • gram stain
  • Aseptic meningitis: non pyogenic inflammatory response
  • Increase in mononuclear cells
  • lymphocytic pleocytosis
  • protein is normal or slightly elevated
  • glucose normal

CT scan head before LP if evidence of space occupying lesion + ICP elevations

Blood cultures before antibiotics

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15
Q

Complications of paraplegia and quadriplegia

A
  • SCI above T6 → autonomic dysreflexia aka exaggerated sympathetic response characterized by headache, diaphoresis, incr BP
    • incr incidence of CAD
    • hemodynamic instability and cardiac arrhythmias
    • hard time breathing
      • lung infections
    • swelling of spinal cord
      • pain
    • neurogenic pain
    • loss of bladder control (neurogenic bladder)
      • UTI and kidney infections
      • vesicoureteral reflux
      • renal failure
      • renal calculi
    • Bowel dysfunction
    • pressure sores
    • osteoporosis
    • muscle and joint stiffness
      • spasticity
    • depression
      • incr risk for suicidality
    • sexual dysfunction
      • decr libido
      • impotence
      • infertility
      • ED
    • functional neurologic deficits and decline
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16
Q

Meningitis Treatment

A

Bacterial meningitis
Start empiric antibiotic therapy immediately after LP
- if anticipated delay (CT scan) give antibiotics first

IV antibiotics

  • start immediately if CSF is cloudy or bacterial infection suspected
  • begin empiric therapy according to patients age
  • modify treatment based on Gram stain, culture, and sensitivity findings

Steroids if suspected strep pneumonia to prevent cerebral edema

Vaccination

  • all adults over 65 years for strep pneumoniae
  • asplenic patients for strep pneumoniae, n meningitidis, H influenzae (encapsulated organisms)
  • immunocompromised for n meningitidis

Prophylaxis - rifampin or CTX for all close contacts

Aseptic meningitis

  • supportive care; self limiting
  • analgesics and fever reduction
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17
Q

Encephalitis gen info

A

Def: Diffuse inflammation of brain parenchyma often seen with meningitis at same time
Viral mc
herpes (HSV)
arbovirus like Eastern equine Encephalitis, West Nile virus enterovirus like polio
less common causes like measles, mumps, EBV, CMV, vzv, rabies, and prion diseases like creutzfeldt-jakob disease

Nonviral infectious causes toxoplasmosis
cerebral Aspergillosis

Non-infectious causes metabolic encephalopathies
T cell lymphoma

Risk factors
AIDS esp at risk for toxoplasmosis when CD4 count < 200
other forms of immunosuppression
travel in underdeveloped countries
exposure to insect vector and endemic areas
exposure to certain wild animals in an endemic area for rabies

Overall mortality from viral encephalitis ~ 10%

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18
Q

Encephalitis clinical features

A

Prodrome: headache, malaise, myalgias
Pts become more acutely ill within hours-days
SXS meningitis like headache, fever, photophobia, nuchal rigidity
altered sensorium like confusion, delirium, disorientation, and behavioral abnormalities
focal neurological findings like hemiparesis, Aphasia cranial nerve lesions and seizures

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19
Q

Encephalitis diagnosis

A

lab tests to rule out non-viral causes
chest x-ray, urine and blood cultures, urine tox screen, serum chemistry
LP to examine CSF (unless with signs of significantly increased ICP)
- Lymphocytosis > 5 wbcs with normal glucose c/w viral encephalitis (similar to viral meningitis). CSF cultures usu negative
- CSF PCR most specific/sensitive test
MRI brain
- r/o focal neuro causes like abscess
- Incr areas of T2 signal in frontotemporal localization c/w HSV encephalitis
EEG (for HSV1 dx showing unilateral or bilateral temp lobe discharges
Brain biospy ind in acutely ill pt w focal, enhancing lesion on MRI w/o clear dx

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20
Q

Encephalitis treatment

A

Supportive care, mech vent if necessary
antiviral therapy
- no specific antiviral therapy for most causes of viral encephalitis
HSV encephalitis - acyclovir 2-3 wks
CMV encephalitis - ganciclovir or foscarnet

Mgmt complications
seizures - anticonvulsant therapy
cerebral edema - hyperventilation, osmotic diuresis, steroids

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21
Q

Fever + AMS ddx

A

Infection
Sepsis: UTI/urosepsis, pna, bacterial meningitis, intracranial abscess, subdural empyema, med/drugs
Neuroleptic malignant syndrome (haloperidol, phenothiazines)
DTs, metabolic derangements
Thyroid storm

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22
Q

Ischemic Stroke gen info

A

3rd mc cause of death in US
Leading cause of neurologic disability
Classes
TIA
Reversible ischemic neuro deficit (same as TIA except for duration of sxs, it lasts >24 hrs, resolves in <2 wks)
Evolving stroke - worsening
Completed stroke - max deficit has occurred
TIA:
- neuro deficit lasting from few min - 24 hrs (usu < 30 min)
- duration of sxs distinguishes stroke vs TIA
- sxs transient w TIA bc reperfusion occurs (collateral circulation or breaking up of embolus)
- blockage in blood flow not long enough to cause permanent infarction
- TIA usually embolic; transient hypotension d/t severe carotid stenosis (>75%) can happen too
- TIA = high risk of stroke (10% and 30%, at 30 days and 5 years)
- eval after TIA: brain and neurovascular imaging, ECG and cardiac monitoring (inpatient telemetry + monitoring for several wks after), echo, labs (CBC, chemistry, lipids, diabetes screening)

Risk factors
most important: age & HTN
smoking, DM, hyperlipidemia, a-fib, CAD, fam hx stroke, previous stroke/TIA, carotid bruits
younger: OCPs, hypercoagulable states (protein C & S deficiencies, APS), vasoconstrictive drug use (cocaine, meth), polycythemia vera, sickle cell disease

ABCD2 score
risk stratification tool to ID pts at highest risk of early stroke (within 2 days) & need emergency assessment: age, bp elevation after TIA, clinical features of stroke, duration of TIA sxs, diabetes

23
Q

Ischemic stroke causes

A

atheroslcerosis –> ischemia
a-fib with clot emboli to brain
septic emboli from endocarditis

Eval source with: echo, vascular imaging (carotid dopplers), ECG, ambulatory cardiac monitoring 30 days

  1. emboli, from:
    - heart mc (mural thrombus w a-fib)
    - internal carotid artery
    - aorta
    - paradoxical: blood clots in peripheral veins, pass thru septal defects, and reach brain
  2. thrombotic stroke
    - atherosclerotic plaques in large arteries of neck (carotid artery disease typically involving bifurcation of common carotid artery) or medium-sized arteries in brain (MCA)
  3. Lacunar stroke
    - small vessel thrombotic dz
    - 20% of strokes
    - usu subcortical structures (basal ganglia, thalamus, internal capsule, brainstem), not cerebral cortex
    - history of HTN predisposes, DM
    - Narrowing arterial wall d/t thickening of vessel wall not by thrombosis
    - small branches MCA, circle of willis arteries, basilar and vertebral arteries
    - when these small vessels occlude, small infarcts result –> heal –> lacunes
    nonvascular causes: low cardiac output, anoxia
24
Q

Ischemic stroke clinical features

A

onset: rapid or stepwise, classically pt awakens from sleep with neuro deficits
embolic stroke
- very rapid onset, deficits are maximal initially
- sxs depend on artery occluded (MCA mc affected):
> contralateral hemiparesis and hemisensory loss, hyperreflexia
> aphasia (dominant hemisphere involvement)
> apraxia, contralateral body neglect, confusion (non dominant hemisphere involvement)
lacunar stroke
- focal and usu contralateral pure motor or pure sensory deficits. Include four major syndromes.

25
Q

Ischemic stroke initial assessment

A

history & neuro exam (NIHSS score, on admission predicts stroke outcomes)
brain imaging (CT or MRI)
- CT head w/o contrast preferred: diff ischemic v hemorrhagic, SAHs, abscess, tumor, subdural or epidural hematomas
- MRI more sensitive
- can be combined with neurovascular imaging (CTA, MRA)
ECG
- acute MI or afib
Labs
- accucheck, cbc, electrolytes, creatinine, coags, cardiac enzymes

<50y –> think vasculitis, hypercoag state, thrombophilia:

  • Protein C, S, APS
  • Factor V Leiden mutation
  • ANA, ESR, rheumatoid factor
  • VDRL/RPR, lyme serology
  • TEE
26
Q

Ischemic stroke complications

A

progression of neuro insult
cerebral edema within 1-2 days & mass effects up to 10 days (hyperventilation + mannitol may be needed to lower ICP)
hemorrhage into infarction
seizures

27
Q

Ischemic stroke acute treatment

A

supportive; airway protection, oxygen, IV fluids
TPA within 4.5 hrs (don’t give if time unknown, > 4.5 hrs, or pt has uncontrolled HTN, bleeding disorder, taking anticoags, hx recent trauma or surgery bc incr risk of hemorrhagic transformation)
- don’t give aspirin within 24 hrs, perform neuro checks every hr, carefully monitory BP (<185.110)
- Pts presenting within 6 hrs better outcomes with endovascular thrombectomy
- aspirin asap (except w tpa) within 48 hrs
- AC like heparin not proven to have efficacy in acute stroke, but will need dvt/vte prophylaxis
- assess ability to protect airway, keep NPO, protect against hypo or hyperglycemia, avoid fever, elevate head of bed 30 deg to prevent aspiration

28
Q

Ischemic stroke treatment

A

BP control
- don’t give antihypertensives within 1st 24h unless:
> BP > 220/120 or MAP > 130
> sig ind: AMI, aortic dissection, severe heart failure, hypertensive encephalopathy
> receiving TPA - aggressive bp control necessary

Recurrence prevention
lifestyle and pharmacotherpay for risk factors (HTN, DM, smoking, HLD, obesity)
longterm anti-platelet therapy (aspirin)
high intensity statin
AC for cardioembolic strokes
surgery for strokes due to carotid artery dz (stenosis > 70% + symptomatic –> carotid endarterectomy ind)

29
Q

Hemorrhagic stroke

A
  1. ICH - bleeding into brain parenchyma
  2. SAH - bleeding into CSF; outside brain parenchyma

Cocaine = one of main causes of stroke in young

30
Q

Intracranial Hemorrhage gen info

A

ICH a/w high mortality (50% at 30 days)
Survivors - left w significant morbidity
hematoma formation + enlargement –> local injury and incr ICP

31
Q

Intracranial Hemorrhage causes

A

HTN mc (sudden incr)
- causes rupture of small vessels deep within brain parenchyma
- older pts, risk incr w age
ischemic stroke conversion to hemorrhagic
others: amyloid angiopathy, anticoagulant/antithrombolytic use, brain tumors, AV malformations

32
Q

Intracranial Hemorrhage locations

A

basal ganglia mc
pons
cerebellum
other cortical areas

33
Q

Intracranial Hemorrhage clinical features

A

abrupt onset of focal neuro deficit that worsens steadily over 30-90 min
AMS, stupor, coma
headache, vomiting
signs of incr ICP

34
Q

Intracranial Hemorrhage diagnosis

A

CT head

coag panel and platelets

35
Q

Intracranial Hemorrhage complications

A
Incr ICP
seizures
rebleeding
vasospasm
hydrocephalus
SIADH
36
Q

Intracranial Hemorrhage treatment

A
Admission to ICU
ABCs
BP reduction (gradual)
- tx ind for > 180 sbp or >130 map
- nicardipine
- labetalol
- nitroprusside
For elevated ICP:
- elevate head of bed 30 deg
- sedation + pain control
- mannitol (osmotic agent)
- hyperventilation
- barbs, neuromuscular block, CSF drainage
pts on AC --> reverse
use of steroids not recommended, harmful
rapid surgical eval of cerebellar hematomas
37
Q

SAH gen info

A

mortality rate as high as 40-50% at 30 days

locations: saccular (berry) aneurysms occur at bifurcations of arteries of circle of willis

38
Q

SAH causes

A

ruptured saccular (berry) aneurysms MC
trauma
AV malformation

39
Q

SAH clinical features

A

sudden, severe (excruciating) headache + absence focal neuro sxs WHOL
sudden, transient LOC
vomiting
meningeal irritation, nuchal rigidity, photophobia
death (25-50%) with first rupture, those who survive will recover consciousness within minutes
retinal hemorrhages

40
Q

SAH diagnosis

A

Ophthalmologic exam mandatory to r/o papilledema, if present don’t do LP (can cause herniation), repeat CT scan

noncontrast CT scan
- if negative + high suss –> LP (diagnostic)
> blood in CSF hallmark
xanthochromia (yellow CSF) –> gold standard dx

Once SAH dx –> cerebral angiogram (definitive study for detecting site of bleeding for clipping)

41
Q

SAH complications

A
rupture (30%)
vasospasm (50%)
hydrocephalus
seizures (blood is an irritant)
SIADH
42
Q

SAH treatment

A
minimally invasive - consult interventional neuroradiology (endovascular coiling > surgical clipping)
surgical - consult neurosurgery
medical - therapy reduces risks of rebleeding and cerebral vasospasm
- bed rest in quiet dark room
- stool softeners
- analgesia for HA (tylenol)
- IV fluids for hydration
- control of HTN - lower bp gradually
- CCB (nimodipine) for vasospasm
43
Q

Seizures gen info

A

sudden abnl discharge of electrical activity in brain

recurrent, idiopathic seizures –> epilepsy (unknown cause)

44
Q

Seizures causes (four Ms, four Is)

A

Metabolic & electrolyte disturbances
- hyponatremia, water intoxication, hypo/hyperglycemia, hypocalcemia, uremia, thyroid storm, hyperthermia
Mass lesions
- brain metastases, primary brain tumors, hemorrhage
Missing drugs
- noncompliance with anticonvulsants, acute withdrawal from etoh, benzos, barbs
Miscellaneous
- pseudo-seizures (psych origin) distinguish with EEG, eclampsia (def tx –> delivery, after mag tx first), hypertensive encephalopathy (d/t cerebral edema)
Intoxications
- cocaine, lithium, lidocaine, theophylline, metal poisoning, CO poisoning
Infections
- septic shock, bacterial/viral meningitis, brain abscess
Ischemia
- stroke, TIA (elderly)
Increased ICP
- I.e. 2ry trauma

45
Q

Seizures H&P

A

seizure description (bystanders; postictal state, incontinence)
baseline state (missed doses of antiepileptic, recent dosage/med changes)
examine for injuries (head, spine, fractures, posterior shoulder dislocation, tongue lacerations, bowel/bladder incontinence)
Increased ICP signs
complete neuro exam

46
Q

Seizure types

A

Partial seizure - begins in one part of brain (temporal lobe mc) –> produces sxs referable to cortex region involved

  • may evolve to generalized seizures (secondary gen)
  • simple partial; consciousness intact, can evolve to complex partial, may involve transient unilateral clonic-tonic movement
  • complex partial; consciousness impaired, postictal confusion, automatisms (1-3 min) purposeless, involuntary, repetitive movements (lip smacking, chewing), olfactory or gustatory hallucinations

Generalized seizure - LOC, disruption of electrical activity in entire brain
- tonic clonic; grand mal, bilaterally symmetric w/o focal onset, sudden loc –> fall to ground, tonic –> rigid, trunk + limb extension +- apnea, clonic –> musculature jerking (>30secs), after flaccid, comatose, before regaining consciousness. Postictal confusion, drowsiness (10-30 min to hrs). Tongue biting, vomiting, apnea, incontinence
Absence (petit mal) seizure - disengage from current activity and “stare into space”, then returns to activity several seconds later, looks “absent minded” confused for daydreaming
- brief episodes (few secs) but can be freq
- school age children common
- impairment of consciousness but no loss of postural tone, continence, or postictal confusion
- minor clonic activity (eye blink, head nodding)

47
Q

Seizures diagnosis

A

if known epileptic –> check anticonvulsant levels
if unclear or 1st seizure
- cbc, lytes, glc, lfts, rfp, serum calcium, urinalysis
- eeg
- CT head, r/o structural lesion
- MRI brain w/w/o gadolinium if stable
- LP and blood cultures if febrile

48
Q

Seizures treatment

A

ABCs; secure airway, roll to side
With hx seizures:
- usu d/t noncompliance (even one missed dose), give loading dose then continue reg regimen as before
- chronically mnged by neurologist
- if persist, incr dosage of first anticonvulsant, add second drug if cannot be controlled still
First seizure:
- eeg and neurology consult
- anticonvulsant therapy (risks vs benefits tx + risk of recurrence), don’t start for single seizure, only if eeg and mri brain abnl, or status epilepticus
- normal eeg –> low risk recurrence (15% in yr) vs abnl –> 41% in yr
Anticonvulsants
- gen tonic clonic and partial seizures
> phenytoin and carbamazepine 1st
> others: phenobarbital, valproate, primidone
- petit mal
> ethosuximide, valproic acid

49
Q

Status epilepticus

A

prolonged, sustained unconsciousness w persistent convulsive activity
medical emergency; mortality 20%
causes; poor med compliance, etoh withdrawal, intracranial infection, neoplasm, metabolic disorder, drug overdose
tx; establish airway, IV diazepam, IV phenytoin, and 50 mg dextrose
resistant –> IV phenobarbital

50
Q

Osteomyelitis gen info

A

Bone infection –> inflammatory destruction of bone
Two categories:
- hematogenous, secondary to sepsis
- direct spread of bacteria
> adjacent infection (infected diabetic foot ulcer, decubitus ulcer)
> trauma (open fx)
> vascular insufficiency (PVD)
MC microorganisms: s. aureus, coagulase-neg staphylococci
Can involve any bone, commonly; long bones, foot/ankle, vertebral bodies

OM of vertebral body d/t TB –> pott disease

51
Q

Osteomyelitis risk factors (complications or chronic)

A

open fx
DM
IVDU
sepsis

52
Q

Osteomyelitis clinical features

A

pain over involved area of bone mc
localized erythema, warmth, swelling
systemic sxs; fever, headache, fatigue
draining sinus tract thru skin in chronic disease

53
Q

Osteomyelitis diagnosis

A

WBC count
ESR, CRP (monitoring response to therapy)
Needle aspiration or bone biopsy (OR) - most direct/accurate diagnostics (+culture)
plain radiograph - early changes like periosteal thickening or elevation show up after 10 days, lytic lesions = advanced dz
MRI - most effective + assess extent of disease

54
Q

Osteomyelitis treatment

A

IV abx 4-6 weeks

  • start only after microbial etiology is narrowed based on cultures or if HDU
  • empiric therapy; abx w high bone penetration like cephalosporins (cefazolin, ceftriaxone, cefuroxime), FQs (levofloxacin, ciprofloxacin, moxifloxacin), vancomycin, linezolid, daptomycin, clindamycin (+- rifampin adjunct for biofilm penetration)
  • add aminoglycoside +- beta lactam if possibility of gram neg infection
  • surgical debridement of infected necrotic bone