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Headaches Flashcards

1
Q

What are age red flags for HA?

A

<5 yo or >50 yo with new or worsening HA

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2
Q

What are onset red flags for HA?

A
  • Sudden onset or thunderclap (cerebral aneurysm rupture)
  • Sudden onset with exertion (SAH or arterial dissection)
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3
Q

If a HA presents with a sudden onset during valsalva, what are you concerned about?

A

Intracranial abnormality such as space occupying lesion

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4
Q

A patient has a fever and a HA. What should you ask about?

A
  • Onset in relation to HA onset
  • Severity
  • Suspicion for CNS infection
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5
Q

Why would you ask about ill contacts when assessing a patient with a HA?

A
  • Infectious etiology
  • CO poisoning
  • Toxin exposure

Toxin/CO would likely see a group of people with same symptoms

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6
Q

A patient uses analgesics frequently and is presenting with a HA. What should be in your differential?

A

Rebound HA, >10 times analgesic use/month

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7
Q

What medications would clue you into etiologies of a HA?

A
  • Analgesia overuse
  • Anticoagulants, antiplatelet agents –> possible hemorrhage?
  • Chronic steroids, immunomodulators –> risk of infection
  • Antibiotics –> recent use may decrease symptoms due to partial treatment
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8
Q

What social history can impact HA?

A
  • Substance use with cocaine, amphetamine, methamphetamine –> increased risk of hemorrhage, reversible cerebral vasoconstriction syndrome
  • Alcohol use –> increase risk of hemorrhage due to falls, violence, coag disorders with chronic use
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9
Q

What family history could help in diagnosing HA?

A
  • FMHx of aneurysm or sudden death in 1st degree relative
  • FMHx of migraine
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10
Q

What is a persistent HA despite an adequately controlled fever a red flag for?

A

A CNS infection

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11
Q

What makes a high likelihood of meningitis?

A
  • HA
  • Fever
  • Neck stiffness
  • AMS
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12
Q

If there is elevated BP, AMS, and neurologic dysfunction, what should you consider?

A
  • Hypertensive emergency
  • Preeclampsia/eclampsia
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13
Q

If there is tenderness over the temporal artery, what condition should you be suspicious of?

A

Temporal arteritis

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14
Q

You see papilledema on fundoscopic exam with a HA. What condition should you be thinking of?

A

Acute angle closure glaucoma and increased ICP

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15
Q

A patient has a history of OM and has a HA. What complication can arise?

A

Brain abscess

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16
Q

A patient has a history of sinusitis and now has a HA. What complication is possible?

A

Sinusitis invasion of IC space

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17
Q

If a patient has meningismus, what is that indicative of?

A
  • Infection or hemorrhage
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18
Q

What neurologic exams should be done on a patient with a headache?

A
  • Mental status
  • CN exam
  • Motor- extremity weakness, pronator drift
  • DTR- assess asymmetry or babinski
  • Gait
  • Coordination testing
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19
Q

What symptoms are clinical red flags for HA?

A
  • AMS
  • Seizure
  • Fever
  • Neuro symptoms
  • Visual changes
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20
Q

What associated conditions are red flags?

A
  • Pregnancy or postpregnancy status
  • SLE
  • Behcet’s disease
  • Vasculitis
  • Sarcoidosis
  • Cancer
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21
Q

What labs can be ordered if a patient is at high risk of a serious etiology of HA?

A
  • CBC, blood cultures- suspected infection
  • CMP
  • Coag panel- suspected bleed or need for LP
  • ESR/CRP- suspected temporal arteritis
  • hCG- females of reproductive age
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22
Q

What are indications for imaging and what image would be most often used?

A
  • Abnormal neurologic examination to include altered mental status, cognitive impairment, or focal deficit
  • New, severe headache of sudden onset
  • HIV-positive patients with presentation of new headache
  • Concern for increased ICP in patient requiring LP

Non-contrast CT

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23
Q

What would cause you to be concerned for increased ICP in a patient requiring a LP?

A
  • Immunocompromised
  • Hx of CNS disease (mass lesion, stroke, focal infection)
  • New onset seizures (within 1 week of presentation)
  • Papilledema
  • Altered LOC
  • Focal neurologic deficits
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24
Q

When would a lumbar puncture be indicated?

A
  • Differential including meningitis
  • Encephalitis
  • Intracranial hypotension
  • Pseudotumor cerebri
  • Subarachnoid hemorrhage
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25
Q

What is the clinical presentation of a migraine?

A
  • Slow onset, lasting up to 72 hours
  • +/- aura (MC lightheadedness and visual changes)
  • Unilateral HA (throbbing and pulsatile in nature)
  • Worse with physical activity
  • N/V, photophobia, phonophobia
  • Preference to lie in quiet dark room
  • Normal neuro exam
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26
Q

How are migraines managed in the ER?

A
  • Analgesia + antiemetic + antihistamine combination (Ketorolac + prochlorperazine + diphenhydramine)
  • Adding corticosteroid reduces recurrent HA within first 3 days (dexamethasone)
  • Alternative = triptan or ergot + antiemetic/antihistamine pre treatment
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27
Q

When is a triptan used? When is it contraindicated?

A

If patient has not pretreated with triptan prior to ED
CI in pregnancy, CAD, uncontrolled hypertension, or CVD

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28
Q

When are ergots contraindicated?

A
  • Hypertension, ischemic heart disease, PAD, pregnancy
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29
Q

What medications are safe to use in a pregnant patient with a migraine?

A
  • Acetaminophen, opioids, metoclopramide, and corticosteroids
  • NSAIDs in 1st and 2nd trimester (3rd impacts babies heart)
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30
Q

What migraine medications are contraindicated in pregnancy?

A
  • Triptans
  • Ergotamines
  • Caffeine
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31
Q

What is the disposition of most migraine patients?

A
  • Can be discharged home with neuro or PCP f/u
  • Prevention with sumatriptain 25 mg, 50 mg, or 100 mg if no CI
  • Midrin 2 caps PO at onset, 1 cap POq1hr until headache relieved up to 5 caps in 12 hrs
  • Pt ED on triggers and lifestyle modifications
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32
Q

What is the clinical presentation of a cluster HA?

A
  • Unilateral, excruciating pain causing patient to pace or rock back and forth
  • Usually orbital, supraorbital, or temporal pain
  • Pain lasts 12-180 mins
  • Ipsilateral symptoms: lacrimation, conjunctival injection, nasal congestion/rhinorrhea, ptosis and/or miosis, edema of eyelid/face, sweating of forehead/face
  • Recurring attacks daily for >1 weeks and remitting for at least 4 weeks (circadian pattern)
  • Attacks precipitated by alcohol or vasodilators
  • Normal neuro exam
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33
Q

How do you manage cluster HA?

A
  • High flow O2 x 15 mins (12/min via nonrebreather)
  • Sumatriptan if unresponsive to O2
  • Alternative: intranasal lidocaine, oral ergotamine/caffeine, IV dihydroergotamine
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34
Q

What is the disposition of cluster HA?

A
  • Discharge home, f/u with neurology for preventative therapy
  • Transitional therapy may be started in ED
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35
Q

What medications can be started in the ED as transitional therapy for cluster HA?

A
  • Corticosteroids (prednisone tapered over 2 weeks)
  • Naratriptan
  • Ergotamine
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36
Q

What is the clinical presentation of tension HA?

`

A
  • Gradual onset of constant, non-throbbing pain
  • Diffuse, occipital, frontal, or bandlike
  • Lasts hours or whole day
  • Nausea, photophobia associated
  • Precipitated by tension, emotional stress, fatigue
  • Normal neuro exam
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37
Q

How is tension headache managed?

A
  • NSAIDs or non-opiate analgesic +/- caffeine +/- antiemetic/sedative –> ketorolac + compazine/reglan + diphenhydramine IV in ER; aspirin-acetaminophen-caffeine for outpatient use
  • Muscle relaxant if muscle tension noted (causes sedation)
  • Refer to PCP for prophylactic or treatment of underlying stress disorder
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38
Q

What is the clinical presentation of a brain tumor?

A
  • Pain mild-moderate
  • Deep, aching- bilateral or unilateral
  • Early: pain intermittent with no focal neuro signs, increases in frequency and duration over weeks-months
  • Later: constant pain and focal neurologic s/s
  • Worse upon awakening and with valsalva
  • N/V, seizures, mental status change, focal neuro deficits may be present
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39
Q

How is a brain tumor diagnosed?

A

CT scan with IV contrast

MRI more sensitive but not as readily available

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40
Q

How is brain tumor managed?

A
  • Emergent neuro/neurosurg consult (in specific cases)
  • IV glucocorticoids to reduce cerebral edema - dexamethasone
  • Secondary prevention with antiseizure agent: levetiracetam (Keppra), topiramate (Topamax), lamotrigine (Lamictal), valproic acid, and lacosamide (Vimpat)
  • Secure airway if signs of impending herniation on imaging (ie deviation from midline)
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41
Q

What are indications for emergent neurological/neurosurg consultation?

A
  • Large symptomatic tumors
  • Signs of increased ICP
  • Impending herniation
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42
Q

What is the clinical presentation of post-traumatic headache/syndrome?

A
  • History of head injury
  • Variable onset: pain immediately after trauma or onset weeks after trauma
  • Non-specific HA: may be similar to tension/migraine presentations
  • Fatigue, dizziness, vertigo, insomnia
  • Depression, irritability, anxiety
  • Loss of concentration and memory
  • Personality changes, noise sensitivity

Sequela of traumatic brain injury

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43
Q

How is post-traumatic headache/syndrome diagnosed?

A

CT scan without contrast if recent trauma without previous evaluation

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44
Q

How is post-traumatic headache/syndrome managed?

A
  • Uncomplicated cases can be discharged home with reassurance, symptomatic therapy and f/u with PCP for evaluation of prophylactic therapy
  • Non-opiate pain relievers, antiemetics
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45
Q

What is the prognosis of post-traumatic headache/syndrome?

A
  • Most improve within 3 months
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46
Q

What patient education should be provided to a patient with post-traumatic headache/syndrome?

A
  • Avoid activity that could lead to second injury while symptomatic
  • Avoid activity that exacerbates symptoms
  • Gradual return to normal activity once symptoms resolve
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47
Q

What referrals can be considered for post-traumatic headache/syndrome?

A
  • Opthalmology if visual complaints
  • ENT if vertigo present
  • Neuropsych if prominent mental illness symptoms
48
Q

What is idiopathic intracranial hypertension?

A
  • Syndrome with papilledema, increased ICP, and normal/small-sized ventricles on imaging
49
Q

What is the clinical presentation of idiopathic intracranial hypertension?

A

(in order of frequency)
* Headache
* Transient visual obscurations
* Intracranial noises (pulsatile tinnitus)
* Scotoma/scintillations
* Back pain
* Retrobulbar pain
* Diplopia
* Sustained visual loss

50
Q

What is seen on physical exam of a patient with idiopathic intracranial hypertension?

A
  • Papilledema
  • Visual field loss
  • 6th (abducens) CN palsy
  • Other CN problems possible but less common
51
Q

How is idiopathic intracranial hypertension diagnosed?

A
  • CT scan brain without contrast- normal
  • Lumbar puncture with elevated opening pressure >25 cm in adults and >28 cm H2O in children
  • CSF fluid analysis normal
52
Q

What should you educate patients on when performing a lumbar puncture to avoid falsely elevated pressure?

A

Valsalva (breath holding/crying)

53
Q

How is idiopathic intracranial hypertension managed?

A
  • Preserve vision
  • Removal of CSF during LP until target pressure of 10-20 cm H2O reached (1 mL CSF lowers pressure by 1 cm H2O)
  • Visual symptoms –> oral acetazolamide +thiazide diuretic (if worsening despite max acetazolamide)
  • New diagnosis- admit for further evaluation and development of long-term management
  • Previous diagnosis- discuss with pts neurologist/neurosurgeon regarding disposition
54
Q

What is the clinical presentation of post-dural puncture/intracranial hypotension?

A
  • Recent history of LP or head/spine trauma (rare)
  • 24-48 hours post LP
  • Location bifrontal, occipital, or involving neck/upper shoulders
  • Worse upright, improves supine
    Associated symptoms:
  • auditory disturbances (tinnitus, hearing loss)
  • vision changes (diplopia, blurred vision, photophobia)
  • N/V
  • neck stiffness, low back pain
  • vertigo, dizziness
55
Q

What is the diagnostic work-up for post-dural puncture/intracranial hypotension?

A
  • Avoid repeat LP (opening pressure <6 cm H2O if performed)
  • MRI/CT not needed but will confirm with diffuse enhancement of meninges
56
Q

What is the management for post-dural puncture/intracranial hypotension?

A
  • Recumbency for 18-24 hrs
  • IV fluids
  • Non opiate analgesics +/- caffeine
  • Most resolve one week without treatment
  • Consult anesthesiology to determine need for epidural blood patch
57
Q

What is a brain abscess?

A
  • Inflammation of brain –> central pus-filled cavity
  • Surrounded by granulation tissue and outer fibrous capsule
  • Caused by hematogenous spread from direct infection or direct seeding by neurosurgery or penetrating trauma
58
Q

What is the clinical presentation of brain abscess?

A
  • HA
  • Focal neurological deficit
  • Fever
  • Seizure
  • S/S of increased ICP: papilledema, N/V, change in LOC, confusion
59
Q

What is the work-up for brain abscess?

A
  • CT or MRI brain with contrast
  • CBC showing elevated WBC
  • CMP assess end-organ function
  • Inflammatory markers (CRP, ESR) elevated in 2/3
  • Blood cultures x 2 before 1st abx

AVOID LP CAN CAUSE HERNIATION

60
Q

What is management of brain abscess?

A
  • Empiric parenteral abx based on suspected source
  • Steroids if significant peri-abscess edema with mass effect and increased ICP
  • Admit and consult neurosurgery for consideration of abscess aspiration
61
Q

What parenteral antibiotics would be given for a brain abscess from a odontogenic source?

A

IV PCN G (alt ceftriaxone + metronidazole)

62
Q

A patient presents has a brain abscess on CT and recently had a neurologic procedure. What antibiotics would be prescribed?

A
  • Vancomycin + ceftazidime
63
Q

What antibiotic would you be given for a brain abscess from a source other than odontogenic or post-neurologic procedure?

A
  • Cefotaxime + metronidazole
64
Q

What is a spinal epidural abscess?

A
  • Collection of pyogenic material that accumulates in the epidural space between the dura and vertebral periosteum
  • MC in thoracic and lumbar spine
65
Q

What is the etiology of a spinal epidural abscess?

A
  • Hematogenous spread from soft tissue (S. aureus MC), urine, or respiratory source
66
Q

What are risk factors of spinal epidural abscess?

A
  • IV drug use
  • Immunosuppression
  • Spinal procedure
67
Q

What is the clinical presentation of spinal epidural abscess?

A
  • Early: back pain, fever, spinal tenderness –> radicular pain, hyperreflexia, and nuchal rigidity
  • Later: Progressive neurological deficits (cauda equina) –> fecal or urinary incontinence –> motor weakness –> paralysis, decreased rectal tone and perineal sensation
68
Q

How is spinal epidural abscess diagnosed?

A
  • MRI with contrast of the spine (alt CT iwth contrast)
  • CBC showing leukocytosis
  • Elevated ESR/CRP
  • Blood cultures
69
Q

What diagnostic is contraindicated if epidural abscess if suspected?

A

Lumbar puncture

70
Q

How is spinal epidural abscess managed?

A
  • Urgent consult neurosurgery
  • Empiric antibiotics: vancomycin + ceftazidime, if unavoidable delay in surgery, signs of neurologic dysfunction, or sepsis
71
Q

What are etiologies of SAH?

A
  • Aneurysm
  • AV malformations
  • Trauma
72
Q

Risk factors for SAH

A
  • Advanced age
  • Hypertension
  • Anticoag use
  • Previous history of stroke
  • Alcohol abuse
  • Use of illicit drugs
73
Q

Clinical presentation of SAH

A
  • Sudden onset “thunderclap” worse headache of life
  • Pain localized or generalized
  • Neck stiffness/pain
  • N/V
  • Seizure
  • Hydrocephalus, elevated ICP, hematoma, ischemia, or infarction
    • meningeal signs several hours after bleed due to aseptic meningitis d/t breakdown of blood products in CSF
74
Q

Diagnostics for SAH

A
  • Non-contrast CT –> most sensitive within 6 hours of onset (d/t blood proteins being broken down after 6 hrs)
  • Lumbar puncture
75
Q

What is Ottawa SAH rule?

A

Patients require investigation for severe non-traumatic HA reaching maximum intensity within 1 hr if one or more findings present
* Symptoms of neck pain or stiffness
* Age >40 yo
* Witness LOC
* Onset during exertion
* Thunderclap headache (peak intensity immediately)
* Limited neck flexion on exam

76
Q

What will be present on lumbar puncture for SAH

A

xanthochromia (hemoglobin degradation = blood in CSF for at least 2 hours)

77
Q

Indications for lumbar puncture in suspected SAH

A
  • Head CT negative for blood but high suspicion for SAH
  • Patient presents beyond 6 hours of HA onset
78
Q

What happens if you have a traumatic tap during a lumbar puncture?

A
  • Greater RBC in last tube - more likely SAH cause
79
Q

What would you do if you have a high suspicion of SAH but lumbar puncture and CT negative

A

CT angiogram, MRA, MRI with fluid-attenuated inversion recovery/susceptibility-weighted image or four-vessel cerebral angiogram may be considered

80
Q

management of SAH

A
  • Gradual reduction of BP if severely hypertensive
  • Discontinue and reverse antithrombotics
  • Treat abnormal temp (>100.4) with tylenol, surface cooling or hypothermia with blankets, bear hugger, warm IV fluids
  • Treat increased ICP
  • Treat hyper/hypoglycemia
  • Manage hydrocephalus
  • Secondary prevention for seizures
  • NPO until swallow test
  • Admit to ICU and consult neurosurgery
81
Q

How would you manage elevated BP in SAH?

A
  • Gradual reduction if >180-200
  • SBP <160 with MAP <110 reduces risk of rebleeding
  • Preferred agents: labetolol, nicardipine, clevidipine, or enalapril
  • Once BP controlled consider converting agent to nimodipine within 48 hours to protect against vasospasm

LNCE the BP manager is married to long term partner nim

Risk vs benefit of treating BP. Risk of hypotension = loss of cerebral perfusion pressure leading to higher level of infarction; benefit: decreased risk of rebleed

82
Q

How would you treat increased ICP in SAH?

A
  • Elevate head of bed 30 degrees
  • Mild sedation to maintain comfort as needed
  • Osmotic therapy (ie mannitol, hypertonic saline) may be considered
83
Q

When would you treat hyper/hypoglycemia in SAH

A
  • Hypoglycemia: treat if BS <60
  • Hyperglycemia: treat if BS >180 mg/dL to goal of 140-180
84
Q

Management of hydrocephalus in SAH

A

Hydrocephalus = increased fluid in ventricles of brain leading to pressure on surrounding cerebral structures
* Watch for worsening HA and progressively impaired neuro testing
* CT/MRI will show enlarged ventricles
* Consult neurosurgery for consideration of shunt

85
Q

Medications for secondary prevention of seizure (and active seizure) in SAH

A
  • Active seizure: IV lorazepam
  • Secondary prevention with phenytoin or fosphenytoin
86
Q

Systemic vasculitis involving medium and large arteries. Frequently in patients >50 years of age and with history of polymyalgia rheumatica

A

Giant cell arteritis/temporal arteritis

87
Q

History for giant cell arteritis/temporal arteritis

A
  • Unilateral headache
  • Jaw claudication, temporal artery tenderness
  • Constitutional manifestations ie anorexia, weight loss, fever, malaise, myalgia
  • Transient or fixed vision loss due to anterior ischemic optic neuropathy d/t occlusive arteritis of posterior ciliary branch of ophthalmic artery–> amaurosis fugax (curtain over eyes)
88
Q

PE for giant cell arteritis/temporal arteritis

A
  • Tenderness over temporal artery: thickening, nodularity, or decreased pulsation may be present
  • Afferent pupillary defect if optic nerve circulation involved
89
Q

Labs for giant cell arteritis/temporal arteritis

A
  • Elevated ESR and CRP
  • US with circumferential dark area about vascular lumen dubbed “halo sign” of temporal artery
90
Q

Management of giant cell arteritis/temporal arteritis

A
  • Opthalmology consult
  • If no vision disturbance, oral prednisone until follow up with ophthalmology within 1 week for temporal artery bx
  • Visual loss (threatened with resolution or established): admit for high dose IV steroids –> methylpredniosolone and consult ophthalmology or vascular surgery for temporal artery bx
  • If not treated promptly will develop permanent vision loss on ipsilateral side and can develop contralateral ocular involvement within days to weeks
91
Q

Repetitive, brief unilateral facial pain confined to distribution of trigeminal nerve

A

Trigeminal neuralgia

92
Q

Presentation of trigeminal neuralgia

A
  • Lightning-like stabs of excruciating pain
  • Lasting seconds to minutes
  • Sensory stimulation of trigger zones of cheek, nose, or mouth precipitates (touch, cold, wind, talking, chewing)
  • MC location V2 or V3
  • Women > men over 30 yo
  • Pain-free intervals minutes to weeks, but permanent remission rare
93
Q

Management of trigeminal neuralgia

A
  • Imaging only if bilateral pain or under age 40 d/t risk of MS or if planning for surgery
  • Phenytoin IV may abort acute attack (not FDA approved)
  • First line therapy for induction of remission: carbamazepine or oxycarbazepine
  • Follow up with PCP or neurology

Alternatives: lamotrigine gabapentin, topiramate, tizanidine, baclofen

94
Q

SE of carbamazepine?

A
  • Sedation
  • Fatigue
  • N/V
  • Headache
  • Dry mouth
  • Weight gain
95
Q

Avoid carbamazepine/oxycarbazepine in which patients?

A

Asian ancestry due to risk of SJS and TEN

96
Q

Clinical presentation of meningitis in adults

A
  • HA-continuous, throbbing, generalized
  • Worse with head movement, valsalva
  • Fever, confusion, nuchal rigidity
  • Photophobia, N/V
  • Seizures if severe
  • Petechial rash with meningococcemia
97
Q

PE of meningitis in adults

A
  • Nuchal rigidity
    • meningeal signs
  • ALOC
  • Photophobia
98
Q

Clinical presentation of meningitis in young children

A
  • Fever (hypothermia- young kids)
  • Lethargy/restlessness
  • Poor feeding
  • V/D
  • Respiratory distress
  • Seizures
  • Bulging fontanelle
  • Lacks meningeal signs
99
Q

Historical red flags for meningitis

A
  • Recent exposure to similar illness
  • Recent illness or abx (pneumonia, sinusitis, otitis, mastoiditis, endocarditis)
  • Recent travel to endemic areas (meningococcal disease and sub saharan Africa/India)
  • Penetrating head trauma
  • CSF otorrhea or CSF rhinorrhea (hx of skull fracture)
  • Cochlear implant devices
  • Recent neurosurgial procedures –> most often VP shunt
100
Q

Diagnostic evaluation for meningitis

A
  • CBC with blood cultures
  • CMP/BMP- liver and kidney function for abx dosing; glucose if diabetic
  • PT/PTT- assess for those who may require blood products after LP
  • Lumbar puncture: CSF analysis, CSF PCR amplification if encephalitis in ddx or viral presentation
101
Q

What are indications for head CT before LP

A
  • Immunocompromised state
  • History of CNS disease
  • Mass lesion, stroke, focal infection
  • New onset seizure (within one week of presentation)
  • Papilledema
  • Abnormal LOC
  • Focal neurological deficit
102
Q

Bacterial CSF analysis pressure, appearance, glucose, protein, and lactate in meningitis

A
  • Pressure: increased
  • Appearance: cloudy, purulent
  • Glucose: low
  • Protein: high
  • Lactate increased
  • CSF: serum glucose <.4
103
Q

Management for bacterial meningitis

A
  • Maintain airway, protect agitated pts from self-injury, monitor for seizures
  • Symptomatic therapy with analgesics, antipyretics
  • IV fluids
  • WITHIN 60 mins goal: dexamethasone prior to abx
  • Rocephin + vancomycin
  • Cefotaxime in infants <1 month of age - rocephin displaces bilirubin from albumin binding sites
104
Q

Add on agent for HSV encephalitis/meningitis

105
Q

Add on agent for tick born meningitis

A

Doxycycline

106
Q

Add on agent for <1 month old and >50 years old and immunocompromised patients with meningitis

A

ampicillin

107
Q

Add on for otitis, sinusitis, mastoiditis, or brain abscess associated meningitis

A

Metronidazole

108
Q

Add on for meningitis complicated by seizures

A

antiepileptic

109
Q

If mild allergy to cephalosporin with hives, what substitution should be made in meningitis treatment

A

Meropenem instead of beta lactam

110
Q

Moderate-severe allergy to cephalosporins and meningitis treatment

A

Vanc + moxifloxacin add aztreonam if immunocompromised

111
Q

Management of viral meningitis

A

MC etiology = enteroviruses
* Symptomatic therapy
* Acyclovir if suspected HSV or VSV etiology
* Empiric abx in elderly and immunocompromised dx with viral meningitis and in those whose CSF analysis is indeterminate

112
Q

Clinical presentation of encephalitis

A
  • Altered LOC
  • Fever
  • HA
  • N/V
  • Focal neurological signs, psychotic symptoms, cognitive changes, seizures (encephalitis/brain abscess)
  • MC etiology: herpes virus (HSV, VZV, EBV)
113
Q

Diagnostics for encephalitis

A
  • LP(CT prior same as bacterial meningitis)
  • MRI or CT: MRI more sensitive but less available
  • CBC, CMP
  • PT/PTT
  • Blood cultures
  • VIral culture and Tzanck smear of any herpetic lesion

CT prior to LP: immunocompromised, history of CNS disease, mass lesion/stroke/focal infection, new onset seizure, papilledema, abnormal level of consciousness, focal neuro deficit

114
Q

Management of encephalitis

A
  • Supportive with symptom control
  • Seizures: IV lorazepam secondary prevention
  • Order neuro checks
  • Empiric abx as in meningitis until dx confirmed
  • Empiric antiviral (acyclovir) goal 30 mins after arrival if HSV or severe VZV/EBV suspected
115
Q

Clinical presentation of brain abscess

A
  • HA
  • Focal neuro deficits
  • Fever
  • New onset seizure
  • Increase ICP: papilledema, N/V, change in LOC, confusion
116
Q

Diagnostics for brain abscess

A
  • CBC - elevated WBC
  • CMP: normal, look for organ dysfunction
  • ESR/CRP: elevated in 2/3 patients
  • Blood cultures: before abx
  • CT/MRI with contrast
117
Q

Management of brain abscess

A

Empiric abx and neurosurgical drainage
* Community acquired: 3rd or 4th gen ceph (ceftriaxone) plus metronidazole
* If hx of head trauma or recent neurosurg procedure (cover for staph and pseudo): ceftazidime + vancomycin OR meropenem + vancomycin
* Steroids only if significant peri-abscess edema with mass effect and increased ICP

Emergency Medicine (13 decks)

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