Transcript The Thunderclap Headache - A Yu 07 14 10

The Thunderclap Headache
Amy Yu, PGY-3
July 14 2010
McGill University
Outline
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Subarachnoid hemorrhage
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Why do we care?
How do we diagnose it?
Then what?
Migraine
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Evaluation
Treatment
SAH – Why do we care?
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Because it can kill your patient
Average case fatality rate 51%
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10% die before reaching the hospital
25% die within 24 hours of SAH onset
45% percent die within 30 days
Because you can do something about it
30-50% have sentinel bleed or "warning leak“
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Sudden and severe headache preceding SAH by
6-20 days
SAH – Etiology
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Most SAHs are caused by ruptured saccular
aneurysms
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15-20% negative angiography
24% will have lesion on 2nd angiography
Other etiologies
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Trauma, AVM, vasculitides, intracranial arterial
dissections, amyloid angiopathy, bleeding
diatheses, and illicit drug use (cocaine and
amphetamines)
SAH – Risk factors
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Cigarette smoking
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Hypertension (RR 2.5)
Alcohol
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Moderate to heavy consumption RR 2.1
Sympathomimetic drugs
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#1 preventable RF for SAH, more prominent in
women and aneurysmal SAH
Dose-dependent, risk decline with quitting
Phenylpropanolamine (appetite suppressants, cold
remedies), cocaine
Estrogen deficiency
Antithrombotic therapy
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Not  risk, but worsens outcome
SAH – Risk factors
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Genetic risk
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Worrisome family history
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AD PCKD, EDS, other CT disease
Two affected 1st degree relatives
One affected 1st degree relatives: need to screen
~300 ppl to prevent one fatal SAH
1-2% Prevalence of intracranial saccular
aneurysm (up to 5% radiographic & autopsy)
3-25 per 100,000 Aneurysmal SAH
SAH – Presentation
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Aneurysm rupture  rapid release of blood in CSF,
rapid increase in ICP
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Bleeding last a few seconds
Can recur, usually within 1st 24 hours
Most common symptoms
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Onset of sudden, severe headache, “worst headache
of my life”
Lateralized in 30% (usually ipsilateral to aneurysm)
May have: brief LOC, seizure, nausea, vomiting,
meningismus
POP QUIZ
37 y.o. ♂ sudden onset severe h/a while
weight-lifting. Examination normal.
Now h/a free with maxeran. What is
the next step in management?
a) Reassurance and d/c home with f/u
b) CT head and if normal d/c home
c) CT head, Lumbar puncture
d) Admission for observation
POP QUIZ
37 y.o. ♂ sudden onset severe h/a while
weight-lifting. Examination normal.
Now h/a free with maxeran. What is
the next step in management?
a) Reassurance and d/c home with f/u
b) CT head and if normal d/c home
c) CT head, Lumbar puncture
d) Admission for observation
SAH – Presentation
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Prospective study of sentinel headache in
aneurysmal SAH. Linn FH et al. Lancet
1994;344(8922):590-3
148 sudden severe h/a patients for
evaluation of SAH
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25% was diagnosed with SAH
12% with headache as the only symptom
Physical exertion
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May be an acute trigger for SAH
Moderate or greater exertion in the two hours
prior to SAH (OR 2.7, 95% CI 1.6-4.6)
SAH – Physical examination
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Retinal hemorrhage
Vitreous hemorrhage (Terson’s syndrome)
Meningismus
Decreased level of consciousness
Focal neuro signs (CN III palsy, CN VI palsy,
bilateral leg weakness)
POP QUIZ
Why are the following signs seen in
aneurysmal SAH?
a) CN III palsy
b) CN VI palsy
c) Bilateral leg weakness
POP QUIZ
Why are the following signs seen in
aneurysmal SAH?
a) CN III palsy – PCoA, SCA
b) CN VI palsy – Raised ICP
c) Bilateral leg weakness – ACA
involvement
SAH – CT head, non-contrast
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Sensitivity
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98% in first 12 hours
93% in first 24 hours
80% at 72 hours
70% at 5 days
50% after 7 days
SAH – Lumbar puncture
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Classic finding
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Elevated opening pressure
Elevated RBC count that does not diminish
between Tube #1 to #4
Xanthochromia post centrifugation
POP QUIZ
LP done for first thunderclap headache,
CT head normal
Tube #1 132 RBC, Tube #4 19 RBC
a) What is your diagnosis?
b) What further information would you
like?
c) What is the next step?
Distinguishing Traumatic Lumbar
Puncture From True SAH
Kaushal, Edlow J of Emerg Med, Vol 23, No 1, pp. 67–74, 2002
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CSF Red cell count
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RBC disappears over days to weeks
No standard criterion for how many RBC’s in the
CSF can definitely diagnose a SAH
Three-tube test
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No absolute differences associated with
diagnosis, unless the count in final tube
approaches zero
Cannot assess concurrent SAH and traumatic tap
Consider letting out extra CSF in the 3rd tube
SAH vs. Traumatic tap
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Xanthochromia
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Hemoglobin degradation appears 4-10 hours from
bleed, may last for > 2 weeks
Needs immediate centrifugation and analysis
Visual inspection very poor specificity
Need spectrophotometry, but unavailable at most
centres
Sensitive, but non-specific
SAH vs. Traumatic tap
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Differential of xanthochromia
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High CSF protein
Jaundice
Carotene addiction
Meningitis
Severe degenerative disc disease
SAH vs. Traumatic tap
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Opening pressure
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Other tests
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Can help R/O other conditions (IIH, CSVT)
Not elevated in traumatic tap, is elevated in 60% of SAH
Abbrescia KL, The effect of lower-extremity position on
cerebrospinal fluid pressures, Acad Emerg Med. 2001
Jan;8(1):8-12.
Positioning of the legs lead to 1cmH2O difference
CSF D-dimer
CSF Bilirubin
Requires further validation
Repeat LP at higher interspace
Clot formation
You diagnose SAH, now what?
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Consult neurosurgery and neuroradiology
CTA and MRA
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Non-invasive
Useful for screening and surgical planning
Sensitive at identifying aneurysms >3-5mm
CTA 83-98%
Pitfalls in SAH evaluation
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Be alert and think about SAH when faced
with acute, severe headache
Understand the limitations of CT head
If you think about doing an LP, you should
probably do it
CTA or MRA are not diagnostic tests for SAH
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Remember that 2-5% of the population may have
an unruptured aneurysm
DDx of thunderclap headache
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Other vascular disease (AVM, dissection)
Intracerebral hemorrhage
Migraine headache
Tension headache
CVST
Pituitary apoplexy
CSF hypovolemia syndrome
Syncope
Part II:
Migraine management
Migraine epidemiology
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Migraine prevalence
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18% female
6% male
Highest among 25-55 year olds
International classification of headache
disorders (2004)
Migraine without aura
A.At least 5 attacks fulfilling criteria B-D
B.Headache attacks lasting 4-72 h (untreated or
unsuccessfully treated)
C.Headache has ≥2 of the following characteristics:
1. unilateral location
2. pulsating quality
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine
physical activity (eg, walking, climbing stairs)
D.During headache ≥ 1 of the following:
1. nausea and/or vomiting
2. photophobia and phonophobia
E.Not attributed to another disorder
Typical aura w/ migraine h/a
A. At least 2 attacks fulfilling criteria B–D
B. Aura consisting of ≥1 of the following, but no motor
weakness
1. Fully reversible visual sxs (positive and/or negative features)
2. Fully reversible sensory sxs (positive and/or negative features)
3. Fully reversible dysphasic speech disturbance
C. ≥2 of the following
1. Homonymous visual sxs and/or unilateral sensory sxs
2. At least 1 aura symptom develops gradually over 5 min
and/or different aura symptoms occur in succession over 5 min
3. Each symptom lasts ≥5 and ≤60 min
D.H/A fulfilling criteria B-D for Migraine without aura
begins during the aura or follows aura within 60 min
E. Not attributed to another disorder
Migraine with aura
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Typical aura with migraine headache
Typical aura with non-migraine headache
Typical aura without headache
Familial hemiplegic migraine (FHM)
Sporadic hemiplegic migraine
Basilar-type migraine
The rational clinical
examination series
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Does This Patient With Headache Have a
Migraine or Need Neuroimaging?
Michael E. Detsky et al.
JAMA, September 13, 2006, Vol 296, No. 10
POUNDing
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Pulsatile quality
duration of 4-72 hOurs
Unilateral location
Nausea or vomiting
Disabling intensity
Yes to 4 out of 5, LR 24 of definite migraine
versus non-migrainous headache
Yes to 3 out of 5, LR 3.5
Yes to 1-2 out of 5, LR 0.41
Individual variables
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4 most predictive variables distinguishing
migraine from tension-type headache
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Nausea LR 19
Photophobia LR 5.8
Phonophobia LR 5.2
Exacerbation by physical activity LR 3.7
Does this patient need
neuroimaging?
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Variable prevalence of intracranial pathology
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1% in chronic headache
43% in thunderclap headache
Rule out red flags
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Cancer or HIV
Sudden onset of symptoms
Onset after age 50 years
Accelerating pattern
Systemic illness (fever, stiff neck, rash)
Focal neurologic signs and symptoms
Nonspecific treatment
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NSAIDs
ASA
Acetaminophen
Baclofen
Antihistamine
Opioids
Combinations
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ASA and Acetaminophen
ASA/Amphetamine/Caffeine (Excedrin)
ASA/Butalbital/Caffeine (Fiorinal)
Acetaminophen/Codeine (Empracet)
Nonspecific treatment
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NSAIDs
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ASA 1gm IV is used in Europe for acute migraine
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1gm effervescent ASA (Alka-Seltzer)
Avoid Opioids
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Ensure adequate trial, e.g. Advil Gel caps 600mg at onset
of headache
May reverse central sensitization in migraine
Significant side effect (nausea, sedation, etc.)
May worsen central sensitization
Avoid Butalbital (Fiorinal)
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No benefit shown
High risk of habituation and dependency
Aspirin with or w/o antiemetic
for acute migraine h/a in adults
Kirthi V et al. Cochrane Database Syst Rev. 2010 Apr 14;4:CD008041
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ASA 900mg or 1000mg superior to placebo
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NNTs 8.1 (2-hr pain-free), 4.9 (2-hr h/a relief), 6.6
(24-hr h/a relief)
ASA reduces N/V, photo-, phonophobia
Metoclopramide significantly further reduces N/V
Sumatriptan 100 mg was better only for 2-hour
pain-free
Adverse events with ASA
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Mostly mild and transient
Slightly more often than placebo
Less common than Sumatriptan 100mg
Specific Tx – Triptans
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3 main mechanisms of action
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Cranial vasoconstriction
Peripheral trigeminal inhibition
Inhibition of transmission through second order
neurons of the trigeminocervical complex
Oral triptans in acute migraine
treatment: a meta-analysis of 53 trials
Michel D Ferrari et al. Lancet 2001; 358: 1668–75
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Collected raw patient data of 53 double-blind,
randomised, controlled, clinical trials of oral
triptans in migraine (12 unpublished)
Summarized estimates across studies for
important efficacy and tolerability parameters
Rizatriptan, Eletriptan, and Almotriptan
provide the highest likelihood of consistent
success
Oral triptans in acute migraine
treatment: a meta-analysis of 53 trials
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Rizatriptan 10 mg (Maxalt)
 Consistent and rapid freedom from pain is desired
Eletriptan 80mg (Relpax)
 High efficacy and low recurrence, lower tolerability
Almotriptan 12.5mg (Axert, Almogran)
 High tolerability and good efficacy
Sumatriptan 50mg and 100mg (Imitrex, Imigran)
 Good efficacy and tolerability
 Longest clinical experience
Zolmitriptan 2.5mg and 5mg (Zomig, AscoTop, Zomigon)
 No specific advantages nor flaws
Naratriptan 2.5mg (Amerge, Naramig)
 Good tolerability
 Slower onset of improvement (useful in mild or moderate migraine)
Frovatriptan (Frova)
 Lack of data
Triptans
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Should be used if >10 days 50% disability in 3 mths
Administered as early as possible after onset of h/a
Safe medications in patients without cardiovascular
disease or major vascular RF
No clinically important differences in coronary
vasoconstriction effects  No triptan is
demonstrably safer than the others
Choice dependent on patient characteristics and
preferences
Individual responses to a triptan cannot be predicted
Specifc Tx – Ergots
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Vasoconstriction by stimulating
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Adrenergic receptors
5-HT receptors
Norepinephrine receptors (venoconstrictors)
Two main Ergots
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Ergotamine (ET), more potent vasoconstrictor
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Superior to placebo, inferior to PO Sumatriptan 100mg
Dihydroergotamine (DHE)
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Also inferior to Sumatriptan, but recurrence rate lower
Ergotamine
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Oral bioavailability is <1%
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Oral ET is appropriate for slowly evolving
migraine without early-onset nausea
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1st pass hepatic metabolism
Rectal suppository: better plasma level, less nausea
One 1-mg tablet at the start of an attack
Maximum total dose of 6 mg per attack
Maximum 2 days per week with an interval of
at least 4 days
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Avoiding habituation, rebound, and daily headache
Dihydroergotamine
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Worse oral bioavailability than ET
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Peak plasma level
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Incomplete passage through GI mucosa
Hepatic 1st pass metabolism
40% bioavailability intranasally
IV 1-2 minutes
IM 24 minutes
IN 30-60 minutes
Advantages
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Fewer side-effects
Habituation is rare
Once h/a relief is established, recurrence is low
Dihydroergotamine
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IN DHE
 1 spray (0.5mg) into each nostril at first sign of
migraine, can be repeated in 15 minutes (2mg in
4 sprays)
 Relatively low clinical efficacy
 High frequency of prolonged nasal stuffiness
SC and IM DHE is equivalent
 DHE 1mg SC/IM, can be repeated in 60 minutes
 Patients are advised to mix DHE with 0.25-0.50
mL of 1% to 2% lidocaine to reduce injection-site
burning
Maximum 4mg per attack, 21mg per week
Ergots – summary
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Do not mix Ergots or with triptans
Do titrate dose to minimize side effects
(nausea)
Recognize ET is highly associated with
medication overuse headache
Recognize Ergots are not clearly superior to
the triptans (except in the case of IV DHE)
and can be less convenient to the patient
What to do in the ER?
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IV Metoclopramide or prochlorperazine 10 mg
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IV Dexamethasone 10-25mg
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Can reduce h/a recurrence
Consider Prednisone for a few days with rapid taper
(e.g. Prednisone 50mg x3d, 40mg x3d, etc.)
IV DHE 1 mg + Metoclopramide 10 mg
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Can be given with Diphenhydramine IV
Do not mix triptan or other ergots on same day
Avoid in patients with vascular disease
SQ 6mg Sumatriptan
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Avoid in vascular disease, but can be used as a
step-up to oral Triptan
Other Tx to consider in the ER
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NSAIDs
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Magnesium 1gm IV
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Advil
Ketorolac 30mg IV, 60mg IM
Good for patients with aura
ASA
Medication overuse headache
Abortive agents should be used ≤2 d/week
 DHE and Naproxen are less likely to cause MOH
 ICHD2 revised criteria for MOH
A. Headache present on ≥15 days a month
B. Regular overuse for >3 mths of ≥1 acute/symptomatic
tx drugs
1. Ergotamine, triptans, opioids, or combination
analgesic medications on ≥10 days a month for >3
mths
2. Simple analgesics or any combination of
ergotamine, triptans, analgesic opioids on ≥15 days a
month for >3 mths without overuse of any single class
alone
C. Headache has developed or markedly worsened
during medication overuse
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If too much barbiturate or
codeine is on board,
patient is treated with
pheno 15mg tid x 3d, bid x
3d, qd x 3d
During these first
3 weeks
nortryptiline is
begun and
patient is allowed
to continue with
usual
symptomatic RX
FU at 8-10 weeks
from Day 1
35 mg
W-3
1) DHE 0.5mg bid x 2
weeks, 0.5mg qd x 2
weeks + DHE as rescue
Rx
OR
25 mg
W-2
10 mg
W-1
2) Pred. 60 mg qd x3d,
50mg qd x 3d,… OR
3) Naproxen 500mg bid
for 2 weeks.
Day 1
Pre-detoxification
Detoxification
STOP all
symptomatic Rx
Rescue medications as
per patient specifics
Michel Aubé md
Thank you for your
attention!