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 Sensitive structures
 ALL extracranial structures: skin, etc
 Venous sinuses
 Major arteries and large branches
 Most of dura, dural arteries
 Insensitive structures
 Brain parenchyma
 Most of meninges other than dura
 Head pain
 Inflammation, tension, or vascular origin
 Location does not correlate well with location of pathology
 Headache results from distention, inflammation, tension/traction of pain
sensitive areas
 Previous history of headaches
 Prior hx of headache, frequency, character, onset, severity critical in
evaluating an ED pt with chief complaint of H/A. Consider different onset,
quality, severity as being a red flag to serious
 Details of heachache
 Specific details of onset, activity during onset, time to maximal pain
 Quality, quantity, location, timing
 Aggravating/Alleviating Factors
 Valsalva/acitivity: onset, think SAH; increases pain think any cause of inc
 Coital: may ppt rupture of aneurysm, benign orgasmic h/a also occur
 Supine is worse: sinusitis, cerbral venous thrombosis, intracranial mass
 Supine is better: low pressure headaches
 Head trauma as a trigger
 Excercise, light, noise, foods hormones, etc
 Etiologic Clues
 Associated symptoms: N/V, Photophobia, meningismus, neuro symptoms
 Diplopia: pseudotumor cerebri
 Sudden, severe onset: SAH
 Unilateral nasal congestion/tearing:
 Environmental exposure, others ill: CO poisoning, “toxic flu”
 PMHx: cancer, HIV or risk factors, IVDA, druge use or withdrawl (caffeine)
 Age: migraines almost always begin < 40-50 (think secondary)

 Vitals: note fever, HTN
 Head and Neck
 Trauma, battle’s signs, racoon eyes, hemotympanum, rhinorrhea,
otorrhea, look in mouth (dental abscess), sinus tenderness, discharge
from sinuses, ear infection, temporal/scalp tenderness, auscultation for
AVM, nuchal rigidity, Kernig’s sign, Brudinski’s sign, neck trauma
 Neurological Exam
 Normal in primary headaches but thorough exam for subtle findings is key
 Focal deficit or decreased level of consciouness: must think secondary
 Don’t forget fundi examination (papilledema, spontaneous venous
pulsations, subhyloid blood, retinal hemorrhages)

 Depends on presentation and suspect etiologies
 Blood work: CBC, renal fn, liver fn, ESR/CRP (giant cell arteritis), coagulation
(hemorrhage, cerebral venous thrombosis, TIA), drug screen if clinically indicated
 CT: initial diagnostic test of choice for any RED FLAGS
 LP: after negative CT to look for SAH, infection
 MRI, MRA, CTA, Angiography may be used by consultants


 Migraine (or migraine variants)
 Tension
 Cluster
 Benign coital (orgasmic) headache
 Benign exersional headache
 Vascular
- SAH, ICH, giant cell arteritis, cerebral venous thrombosis
(SSS), arterial dissection, vasculitis, hypertensive crisis,
non-ruptured aneurysm/AVM
 Infectious
- Meningitis, encephalitis, brain abcess, mastoiditis, sinusitis,
dental abcess, viral syndrome, fever related
 Neoplastic
- Tumor (primary or secondary, benign or malignant)
 Inflammatory
- giant cell arteritis, vasculitis
 Traumatic
- EDH, SDH, SAH, ICH, contussion, concussion, post -
concussion headache, post LP, etc
 Toxicologic
- CO poisioning, drug withdrawl, stimulant use
 Metabolic
- Pseudotumor cerebri
 Other
- hydrocephalus, dental pain, glaucoma, trigeminal
neuralgia, post ictal
 15% of Canadian population
 3 women : 1 man
 Fhx usu present
 Onset rare > 40 - 50 yo

 Vasoconstriction leads to ischemic brain and produces aura features, ischemia produces
vasoactive mediators which lead to vasodilation. vasodilation leads to headache
 Inflammation, seritonin, and dopamine thought to have role in pathophysiology
 Dura and dural blood vessels are sensitive. Many vasoactive substances
can stimulate the dural blood vessels and produce vasodilation and
perivascular inflamation which activates the perivascular trigeminal
sensory nerves which leads to headache. These trigeminal sensory
nerves provide a pathway for noxious stimuli from meningeal blood
vessels in the periphery to activate the CNS sensory pathways
 Seritonin and Migraines
 Goasby 2000. Neurology. Mechanisms of action of serotonin agonists:
insights into migraine pathophysiology.
 Serotonin agonists act via 3 mechanisms.......(i) Intracranial
vasoconstriction (ii) Peripheral trigeminal nerve inhibition (iii) Inhibition of
central pain processing
 Dopamine and Migraines
 Peroutka 1997. Neurology. Dopamine and Migraine
 Dopamine administration can mimic symptoms of migraine. Hypothesis of
dopamine hypersensitivity in migraine suffers.
 Many dopamine antagonists effective for migraine: metoclopramide,
prochlorperazine, chlorpromazine, domperidone, haloperidol

 Triggers
 Sress, stress letdown, hormonal changes, alcohol, smoke, scents, fumes,
exercise, fatigue, lack of sleep, hunger, head trauma, chocolate, red wine,
MSG, menstrual, altitude changes, chinooks (changing barometric
pressure), caffeine withdrawl

 Aggravating/Alleviating
 Increase w/: coughing, straining, bending over, mvmt, activity
 Decrease w/: rest, immobility, quiet, darkness, scalp pressure, cold press

 Phases of a Migraine (not all need to be present)

 Prodrome
 occurs hrs - days b/f headache
 consists of mood changes (irritability/depression) or food
cravings (for chocolate!)
 Aura

 basically can be any transient neurological disturbance

 visual: scintillating scotomas (spots in vision), fortification
spectra (zig zag lines), or homonomous hemianopsia
 may occur alone without headache
 typically before headache but case reports of during and
 presence defines classic migraine = headache w/ aura
(common migraine = headache w/o aura)
 Headache
 severe, throbbing, unilateral but variable, gradual onset,
duration typically hours to days; associated w/ N/V,
photophobia, phonophobia, difficulty concentrating
 Postdrome
 malaise, mood changes, concentraion for several hours

 Migraine Variants
 Classical Migraine = preceding aura
 Common Migraine = no preceding w/o aura
 Status migrainus = > 24hrs
 Hemiplegic Migraine: mild –> hemiparesis (dx of exclusion)
 Basilar Migraine: dysarthria, vertigo, tinnitus, dec LOC
 Ice-Pick Headaches: some classify as migraine variant
 Thunder - Clap headache: very sudden onset and severe headache that
reaches maximal intensity within minutes (with negative workup for SAH)
 Migraine equivalents: vertigo, tacchycardia, chest pain, abdo pain, pelvic
pain due to autonomic stimulation with or without headache
 Ophthalmoplegic Migraine
- usually 3rd nerve palsy (must R/O DM, anerysm)
- cannot distinguish b/w aneurysm
- Tolosa - Hunt syndrome: periarteritis of carotid siphon of
unknown etiology that may simulate opthalmoplegic
migraine; presents with unilateral retrorbital pain that may
precede or follow IIIrd nerve palsy

 ED approach to acute migrane Rx

 Various medications and regimens
 Bolus 100 cc NS + Ibuprofen
 Metoclopramide mg iv or Prochlorperazine 10 mg iv (some give with
benadryl 50 mg to prevent akathesias)
 Chlorpromazine 0.1 mg/kg iv q 15min X 3 prn
 Ergotamine 1 - 2 mg po, slq1hr X 3 prn (NOT in CAD, PVD, HTN,
 DHE 0.5 - 1.0 mg iv repeat X 1 @1hr (NOT in CAD, PVD, HTN, pregnant)
 Sumatriptans: 6mg sc, repeat X 1 @ 1hr prn (NOT if rec’d ergots w/i
 Toradol 30 mg iv
 Lidocaine iv or in
 Demerol: 75 - 100 mg iv,im
 Steroids

METOCLOPRAMIDE (Maxeran, Reglan)

 10 mg iv, ? repeat, ? max dose
 Nonphenothiazine central dopamine antagonist
 Less affinity for dopamine receptors than other phenothiazines
 Can be combined with DHE
 Tek 1990: 67% effectiveness vs 19% placebo at 1hr
 Cameron 1995: 52% > 90% relief, 66% > 70% relief, rebound in 20% (RTED)
 Cameron 1995: less effective than CPZ: 53% >90, 79% > 70
 Ellis 1993: better than ibuprofen

PROCHLOROPERAZINE (Stemetil, Compazine)

 10 mg iv, repeat X 1 prn after 30 min
 Dopamine antagonist with additional effects on seritonin, acetylcholine, adrenergics
 80 - 90% effective: Jones 1989 (88% vs placebo 45%)
 Some evidence for stemetil being more effective than maxeran
 Copella 1995: > 50% relief
Stematil Maxeran Placebo
82% 48% 29%
 Jones 1996: partial or complete relief
67/% 34% 16%

 0.1 mg/kg iv q15 min X 3 prn
 50 mg im q15 min X 3 prn
 Pretreat with 500ml NS to prevent orthostatic hypotension (alpha effect)
 80 - 90% effective
 18% get orthostasis
 Higher s/e :. not 1st line
 Lane 1989: CPZ = demerol + gravol

 Serotonin agonism leads to vasoconstriction
 Contraindications: CAD, PVD, HTN (vasoconstriction), pregnant (oxytocic effects), use of
sumitriptin within 24hrs
 Various preparations: ergotamine, + caffeine, tablet, suppository, intranasal, inhalor
 Ergotamine
 1 - 2 mg po, sl q1hr X 3
 Success 75%
 DiHydroErgotamine (DHE)
 0.5 - 1.0 mg iv/sc/im/in, repeat 0.75 mg prn in 30 min
 Hanna 1991: 71% complete relief
 Carleton 1998: DHE = demerol



 6 mg sc, repeat at 1hr minimum prn
 50 - 100 mg po
 Intranasal preparations available
 Seritonin agonist that causes vasoconstriction, reduction of inflammatory mediators;
does not cross BBB thus no CNS effects
 Other seritonin agonists: rizatriptan, naratriptan, zolmitriptan
 Contraindications: CAD, PVD, HTN, pregnant, ergotamine w/i 24hrs
 Gawel 2001: Effectiveness 77% at 1hr, 83% at 2hr, 60% at 24hr
 Cady 1998: Effectiveness 69% at 1hr, 79% at 2hr
 High rate of rebound headaches (40% at 24hr) and cost make this a 2nd line drug
 Effectiveness at 1hr better for sc > po > in

 Lidocaine
 4% topical solution in nostril of side of h/a
 55% response in 5 min but 42% relapse rate in 1 hr
 JAMA 1995, 1996
 Good evidence from RCTs for effectiveness > placebo
 Should add to ED regimen for additive effect
 Naprosyn: 250 - 500 mg po q2-6hr
 Ibuprofen: 400 - 600 mg po q2-6hr
 Toradol: 60 mg im (maximum 120 mg w/i 24hrs)
- Shustha 1996: ketorolac = CPZ
- Duarte 1992: ketorolac = meperidine
- Larkin 1992: ketorolac < demerol
 Steroids
 Some recommend for recurrent, prolonged headaches > 72hrs
 Dexamethasone (10 - 20mg iv), prednisone, methylprednisone
 Poor evidence
 Opiods
 Last resort, potential for abuse, LOWER efficacy documented by many
studies (50%), HIGHER relapse rates (40%), 3rd line
 Prevention
 Beta - blockers, TCAs, phenytoin, CCBs, ergotamines
 Admission for pain control or status migrainus rarely required: DHE + maxeran Q8hr +/-
 Consider referral to headache clinic
 Chronic headaches requiring prophylaxis
 Disabling headaches


 Most common type
 Usu bilateral, often described as a tight band, squeezing
 Not aggravated by physical activity, no prodrome/aura
 May be associated w/ nausea or photophobia
 Usu waxes and wanes
 May last for several days
 Tx: tylenol or NSAIDs

 Much less common
 “Ice-Pick Headache”
 More common in men (9:1), onset in late 20s
 Severe, stabbing, periorbital pain
 Associated w/ ipsilateral tearing, nasal congestion, rhinorrhea, conjucntival injection,
ptosis, eyelid swelling, flushing of forehead, can see horner’s
 Precipitants: alcohol, heavy smoking, NTG
 Onset frequently at night, usu lasts 30min - 3hrs
 Each attack is similar, often occurring at the same time of day (“alarm - clock headache”)
 Pt prefers to pace and keep acitive during attack
 Cluster refers to the seasonal occurrence of episodes
 Acute tx: 02 > 7 L/min (90% effective), intranasal DHE, sumitriptan
 Prophylaxis: CCBs, valproate, lithium carbonate

 Presentation worrisome for SAH
 More common in men
 Dx of exclusion
 Effort headache: any valsalva

 Headache + fever/meningismus/rash
 Headache esp common in bacterial and viral and often is presenting feature
 Must R/O meningitis if fever, meningismus, or rash is present
 CT b/f LP if possible

 60% will have headaches, especially if rapid grwoing
 Neurological examination usu abnormal
 Usu gradual progression over weeks to months
 Red Flags for possible brain tumor
 Focal neurologic symptoms or findings
 Wakes in am with headaches
 Headaches recently with no prior hx
 Headache that is chronic, persistent over days –> months with no prior hx
 Weight loss

 Unruptured AVM or aneurysm
 Ischemic stroke or TIA: headache in 20% or less
 Cervicocephalic Arterial Dissection
 Headache, facial pain, neck pain
 May or may not be associated w/ trauma
 Carotid: ipsilateral, steady, nonthrobbing headache and ipsilateral
horner’s; throat pain, focal cerebral ischemia
 Vertebrobasilar: occipital headache or neck pain, may be assoc/ w/
 Cerebral Venous Thrombosis
 Blood drains from brain veins into venous sinuses (superior saggital sinus,
inferior saggital sinus, transverse sinus, straight sinus, cavernous sinus —
> confluence of sinuses and drainage into jugular system)
 Thrombosis: underlying hypercoagulable states, meningitis, abcess, etc
 Presents with headaches and neurological symptoms (may be
 Dx: CT with enhancement (delta sign for SSS thrombosis)
 Cavernous Sinus Thrombosis
- venous sinus lateral to sella turcica that drains blood from
face, pterygoid, eyes
- infectious spread from eyes, nose, face, palate, tonsils,
middle ear, mastoid, sinuses, teeth ------> thrombosis
- headache, proptosis, fever, eye swelling, edema
- CN palsies: CN III, IV, V1, V2, VI and ICA
- Dx: evidence on CT
- Mx: heparin, abx
 Over 50 yo and average is 70: 4 females to 1 male
 Headache + visual loss, jaw claudication, tenderness of scalp over temporal arteries
 Pain is piercing or buring quality, usually unilateral
 Note: pain can be located more in jaw than temporal skull region
 Fundoscopy: can see edema or papillitis but usually are normal
 Association with PolyMyalgia Rheumatica (50%)
 ESR elevated, mild anemia, mild leukocytosis
 Risks: blindness, CB infarct, basilar artery infarct
 Tx: prednisone 60 - 100 mg po od
 Treat with steroids even b/f lab results if you suspect this dx
 Bx usu diagnostic

 Tic Douloreux = sudden wincing of facial muscles in response to severe facial pain
 Facial pain that occurs suddenly, lasts seconds to minutes, lancating/electrical quality,
progression to constant ache, UNILATERAL 95%
 V2 and V3 more common distribution than V1
 May have “trigger spot” on face, may be precipitated by talking, chewing, facial
movement, or tapping on the trigger zone to reproduce symptoms
 2 females: 1 male, most > 50yo
 Theories: HSV irritation of CNV, dental disease, anatomic nerve lesion, vascular
compression by adjacent vessels, MS, cerebellopontine angle mass
 Diagnosis: history with NORMAL physical examination (CNV: normal sensation to face,
muscles of mastication normal, normal corneal reflex)
 Ddx: glossopharyngeal neuralgia, post - herpetic neuralgia, TMJ pain, dental dz,
sinusitis, trauma, cluster h/a, GCA
 CT/MRI: normal, should be done to r/o posterior fossa tumor
 Management
 Tegretol: 100 - 200 mg/day and titrate up (some start at 200 mg po tid)
 Alternative: dilantin
 Failure of medical Rx: injections, peripheral neurectomy, radiation, or
surgical decompression

 Acute onset of orbital pain
 Visual changes: decreased acuity, haziness, or visual loss
 Conjunctival injection
 Pupil mid position, corneal edematous or slightly hazy
 Dx: tonometry
 Tx
 Acetazolamide
 Miotics
 Mannitol
 Betablockers
 Corticosteroids
 Antiemetics


 Usually secondary to periauricular spasm of masseter
 May be related to dental work, dentures, overbite, chewing, prior trauma
 Uni or bilateral
 Tender over TMJ, clicking and/or sticking of TMJ
 Tx: NSAIDs

 Obstruction or infection
 CT to look for hydrocephalus
 Aspiration of CSF to look for infection
 Consult neurosurgery if problem suspected

PSEUDOTUMOR CEREBRI (Benign Intracranial Hypertension)

 MUST recognize b/c this is a MEDICAL EMERGENCY re potential to go BLIND
 Also called benign intracranial HTN, serous meningitis, otitic hydrocephalus
 Typical patient: overweight, young adult females
 Etiology
 Unknown is most common
 Steroid Rx
 Birth controll pill
 Coagulation disorders
 Venous sinus thrombosis (must r/o)
 Tetracycline
 Pregnancy?
 Obesity?
 Ear infections?
 History
 Overweight, young femal with h/a, diplopia, blurry vision, papilledema
 Headache/neck ache
 Transient visual obscuration
 N/V
 Blurred vision and/or diplopia
 Menstrual irregularities
 Normal level of consciousness
 Physical
 severe papilledema (decreased axonal transport)
 VI nerve palsy (seen as medially deviated eye with inability to abduct)
 Investigations
 MUST do CT b/f LP b/c a mass lesion could present like this
 LP shows elevated CSF pressure usu 25 - 45 cmH2O (normal is 15cm)
 must R/O other causes (medications, endocrine, venous thrombosis)
 Treatment
 repeat LP
 acetazolamide (carbonic anhydrase inhibitor)
 dexamethasone
 weight reduction
 see opthamologist (optic nerve fenestrations if vision is a threatened)
 r/o etiology: medications, endocrine, venous thrombosis (MR venography)


 Incidence: 20 per 100,000/yr (5th - 7th decade); Prevalence: 1% of population
 Morgenstern 1998: prospective study of 38,730 consecutive ED patients, headache was
cc in 450, worst h/a of life in 170 (37%), SAH was ultimate dx of 4% of
“severe”headaches and 17% of “worst ever” headaches
 SAH is a relatively common entity with serious consequences
 Headache is 1 - 2% of ED visits, SAH is 1% of all headaches, SAH is 10% of “worst
 MC age is between 20 - 60yr old; Peak rupture rate is in 50s; Pediatrics RARE but does
 SAH is 5 - 10% of strokes
 Increased risk with Ehlers-Danlos, Marfan’s, coarctation, Polycystic kidney disease
 HTN is NOT a major factor in formation but is a major factor in rupture
 Prognosis BEFORE rupture: rupture 1% per year, surgery risk low :. most electively
 Rupture
 Peaks of BP very important THUS association with lifting, bending,
valsalva, coitus, orgasm, coughing, urination, parturition
 Smoking, EtOH, cocaine, phencyclidine, other stimulants, poorly
controlled HTN, chronic ASA also increases risk of rupture
 Note: 1/3 occur in sleep or not related to activity


 Kassell 1990 (Cooperative Study)
 Rebleeding and vasospasm are leading causes of morbidity/mortality
 Poor prognosticators: decreased LOC, age, amount of blood on CT,
increasing SBP, medical problems underlying, basilar aneurysms
 Survival by GRADE


ALERT(I/II) 74 8 4 1 13

DROUSY (III) 53 11 6 2 28

STUPOR (IV) 30 14 8 4 44

COMA (V) 11 5.4 8 4 72

OVERALL (I-V) 58 9 5 2 26

 Misdiagnosis is common and important b/c of high rates of death and disability
 Especially common in patient with NORMAL level of consciousness and physical exam
 Retrospective reviews of initial misdiagnosis: Niel - Dwyer 1997 (51%), Mayer 1996
(25%), Kassel 1985 (23%), Adams 1980 (32%) —> Overall initial misdiagnosis in 32%
 Reasons for misdiagnosis of SAH
 Failure to appreciate spectrum of SAH
- failure to evaluate “warning headaches” w/ CT and LP
- failure to recognize that h/a can improve spontaneously
- failure to recognize mild or atypical presentations
- focus on secondary injury resulting from syncope
- focus on ECG abnormality (misdx as MI)
- focus on BP (misdx as HTN headache)
 Failure to appreciate the limitations of CT
- decreasing sensitivity with time
- accuracy depend on reader (neurorad > rad > emerg > res)
- sensitivity depends on volume of bleed
- sensitivity depends on technical factors (3rd / 4th generation
scanner, thin slices at base of brain)
- false -ve with Hct < 30
 Failure to perform and interpret LP correctly
- LP not done if CT -ve
- xanthochromia insensitive < 12hr and > 2weeks
- visual inspection for xanthochromia unreliable
- failure to distinguish b/w traumatic tap and true SAH

 Congenital
 Familial intracranial aneurysms (dominant)
 Genetic predisposing condition (Marfan’s, Ehler’s - Danlos, etc)
 Acquired
 Traumatic: skull#, penetration, post op, hemodynamic damage
 Infectious: syphillus, mycotic
 Inflammatory: vasculitis
 Degenerative: atherosclerotic


 Berry aneurysm 80%
 Perimesencephalic SAH 5%
 AVM 5%
 Unknown 5%
 Other 5%
 Perimesencephalic non - aneurysmal SAH, anticoagulation, bleeding
diathesis, vasculitis, mycotic aneurysm, spinal AVM, angioma, pituitary
apolexy, encephalitis, sickle cell disease, hemorrhage into tumor

 95% are associated with the Circle of Willis
 Locations usually distal to carina of bifurcation of vessels and point in the direction of
flow usually on the convexity of the curve
 Rupture rates increase after 3mm, symptoms increase after 7mm
 Multiple aneurysms in 15%

 5 - 10% of SAH
 Not caused by aneurym: represents 50% of non-aneurysmal SAH
 Typical presentation for SAH except slightly slower onset (minutes vs seconds) and
tends to have lower Hunt - Hess score (higher LOC and less neuro findings)
 Extravasated blood mainly or only in interpeduncular cistern or quadrigeminal cistern
 Thought to be a VENOUS or CAPILLARY source
 CT or LP +ve but angiogram is negative
 Excellent prognosis

 Subarachnoid hemorrhage has a wide spectrum of presentation from mild h/a –> coma
 History
 SUDDEN onset of SEVERE headache (“worst H/A of my life”)
 Associated w/ nausea, vomiting, menigismus, mild fever, photophobia,
decreased LOC -----> syncope
 Onset with activity is common (2/3): sex, straining, lifting, bending,
 Physical
 Labile BP (hypertension common), decreased LOC, subhyloid
hemorrhage, retinal hemorrhages, cranial nerve palsies, neurologic
findings (may be focal, hemparesis)
 Findings may localize hemorrhage: IIIrd nerve palsy (PCA or Pcom), VI
nerve palsy (posterior fossa), bilateral leg weakness (Acom), nystagmus
or ataxia (post fossa), hemiparesis/aphasia/neglect (MCA)
 Ocular hemorrhage
- subhyaloid (preretinal): bright red blood near optic disc that
obscures underlying retinal vessels
- intraretinal hemorrhage
- vitreous humor hemorrhage (Terson’s syndrome)
 Warning signs
 Unusual headache; sudden onset, severe but less often related to activity,
more relief with NSAIDS, more generalized
 Consider on ddx of “Thunderclap headache” (sudden onset of severe
headache with -ve work up for subarachnoid hemorrhage)
 Warning signs and symptoms occur in 20 - 60% which can be the result of
stretching, pressure, or leakage; ave interval b/w warning and bleed is 3
 Note: sensitivity of CT is decreased with small bleeds (50%)
 Sahs A. (Cooperative study)
headache 48% - motor/sensory change 6%
dizziness 10% - seizures 4%
orbital pain 7% - ptosis 3%
diplopia 4% - dysphagia 2%
 Sarner M. (1967)
Meningism 64%
Coma 52%
N/V 45%
H/A (gen) 32%
H/A (occipital) 21%
Reflex changes 19%
<10%: motor change, sensory change, papilledema, anisocoria, 3rd nerve

 Differential Dx of SUDDEN/SEVERE headache

 Intracranial: SAH, ICH, acute hydrocephalus, arterial dissection, infection,
mass, venous thrombosis
 Extracranial: glaucoma
 Systemic: HTN, GCA
 Benign: migraine, thunderclap h/a, benign post coital (post orgasmic) h/a,
benign exersional h/a, cluster h/a
 Hunt - Hess SAH Grading
Grade 0 unruptured aneurysm
Grade 1 asymptomatic or mild headache, slight nuchal rigidity
Grade 1a no acute meningeal/brain reaction but with fixed neuro deficit
Grade 2 mod to severe headache, nuchal rigitity, CN plasy
Grade 3 mildly depressed mentation, lethargy, or mild focal deficit
Grade 4 stupor, moderate to severe hemiparesis, early decerebrate
Grade 5 coma, decerebrate rigidity, moribund appearance



 Initial diagnostic test of choice for headache consistent with SAH
 Look for blood in basal and interpeduncular cisterns, sulci
 CT scanners
 1st or 2nd generation: translate/rotate
 3rd generation: rotate/rotate
 4th generation: rotate/stationary
 Sensitivity depends on .....
 Reader: Schirger 1998: neuroradiologist > radiologist > radiology resident
 Technical factors: need min 3 mm slices through base of brain (vs 10mm);
Calgary uses 5 mm slices through base of brain and 10 mm through vault
 Blood volume: small hemorrhages not seen as easily (Ex: warning leak)
 Hb: Latchaw 1997: sensitivity decreases with Hct < 30
 Kassel 1990 (Cooperative Aneurysm Study)
 Prospective observational survey of all patients diagnosed with SAH.
NOT useful for sensitivity of all - comers to ED but is useful to see pattern
of decreasing sensitivity with time in patients diagnosed with SAH.
 day 0 92%
 day 1 86%
 day 2 76%
 day 3 68%
 day 4 64%
 day 5 58%
 Sensitivity of 3rd Generation CT scanners in the dx of SAH
 Four main studies to review: Sidman, Sames, vanderWee, Morgenstern
 Compare design, spectrum, radiologist, etc
 Sidman 1996
 Retrospective study of patients on neuro ward with dx of SAH (by CT, LP,
angio, OR, or autopsy), CT were 3rd generation scanners read by neuro
and general radiologists. Note spectrum bias b/c they only included “ruled
- in” patients, didn’t look at all - comers with sudden/severe headache :.
potential for missed dx and increased sensitivity.
 Results: < 12 hrs - 100 (95 - 100% CI) and > 12hrs 81.7%(69 - 90% CI)
 Conclusion: major spectrum bias and basically not applicable to emerg
 Sames 1996
 Retrospective study of all pts on neurosurgery ward dx with SAH by CT,
LP, angiography, surgery, or autopsy. CT were 3rd generation scanners
read by neuro radiologists. Spectrum bias exists. Many excluded patients
b/c of incomplete records.
 Results: < 24hrs 93% (no CI) and > 24hrs 84% (87-95%)
 Conclusion: major spectrum bias and not applicable to emerg patients
 van der Wee 1995
 Prospective series of consecutive patients that presented within 12 hrs of
sudden onset headache (no comment on severity) who were oriented and
had no focal deficits. Looks like they had a good spectrum, but note that
the rate of SAH was 68% (expected rate would be more like 10%) thus
you wonder if there is some spectrum bias here as well.
 CT were 3rd generation scanners, were done < 12hrs, and films read by
one neuroradiologist PLUS at least two “experienced” general
 The diagnosis of SAH on LP was made by the presence of xanthocrhomia
on spectophotometric analysis and all LP were done > 12hrs.
 175 patients: CT +ve in 117/175, CT -ve in 58/175 —> LP was +ve in 2/58
and was -ve in 56/58
 Results (sensitivity): < 12 hrs 98% (94.0 - 99.8 CI)
 Conclusions: probably the best study we have, looked at all comers (we
think) and had good definition of +ve LP. Note confidence interval low of
94% and note that these films were looked at by several specialized
 Morgenstern 1998
 Prospective study of all patients presenting to the ED with “worst
headache ever” and rated 10/10 in severity. Does not include sudden
onset headaches. Could be some element of selection bias. Many not
enrolled (63) out of total eligible N=170 (107 enrollled)
 CT were C3rd generation scanners and were interpreted by two
 Diagnosis of SAH in patients with -ve CT is questionable: a patient was
considered to have a SAH if rbcs were > 1000 in first tube and there was
no decrease > 25% + one of the following (i) visual xanthochromia (ii)
spectophotometric xanthochromia (iii) or positive d-dimer. Of 20 patients
with +ve spectophotometry, only TWO were given dx of SAH based on
rbcs #s. 18/20 were followed for two years with no problems. Angiography
was not done to exclude aneurysms in patients with positive LP findings.
Also, 24% of LPs were done < 12hrs and they could have missed
xanthochromia and had false -ves thus increasing the sensitivity of the CT
scan. One false -ve 14/16 - 87%, Two false -ves 82%. Also note that
10% of pts with negative CT refused LP.
 Results (sensitivity)
- overall 98% (91.2 - 99.7% CI)
- < 24hrs 93%(no CI)
 Conclusions: Prospective, good spectrum, poor definition of +ve LP,
 Summary on CT and SAH
 The true sensitivity of CT head for SAH in patients presenting to ED with
sudden/severe headache has NOT been definitively determined
 The true sensitivity varies with institution (different CT, different
radiologists) and with the wide spectrum of patient presentation
 The true sensitivity varies with time: the best conservative estimates from
the literature are .......
- 0 - 24 hrs 95%
- 24 - 48 hrs 85%
- 48 - 72 hrs 75%
- 7days 50%

95 - 85 - 75 RULE


 Pathophysiology
 Subarachnoid hemorrhage releases blood into the subarachnoid space
which contains the cerebrospinal fluid
 Red blood cells are passively oxidized into oxyhemoglobin over a course
of a few hours. Barrows 1955 showed that it is detectable as early as two
hours. Oxyhemoglobin is PINK.
 Oxyhemoglobin is actively converted into bilirubin by the heme
oxygenase enzyme over the course of many hours. Heme oxygenase in
choroid plexus and the arachnoid mater convert the rbcs into bilirubin.
Heme oxygenase reaches maximum activity by 12 hours (Roost 1972).
Bilirubin is YELLOW.
 Oxyhemoglobin passively converted into methemoglobin which is
 What is Xanthochromia?
 Xanthocrhomia is the change in color of CSF due to the presence of
pigments, either oxyhemoglobin or bilirubin (metHB rarely). Can be
defined as change in color by visual inspection or absorption of light by
 Spectophotometetry measures the absorption of light at different
wavelengths. Oxyhemoglobin absorbs light at 410nm with a sharp peak.
Bilirubin absorbs light at 450 - 460nm with a broad peak.
Spectophotometry reads CSF positive for xanthochromia if it absorbs light
in either 410 or 460 wavelenghts.
 Visual diagnosis of xanthochromia relies on the ability to visualize
discoloration of the supernatant on a white background. The accuracy of
visual diagnosis is debatable (see below).
 What is a POSITIVE LP?
 RBC count?
- Not entirely reliable, No number in literature to rule in or rule
out SAH
- rbc count depends on size of bleed (minor leak –> major
bleed) and time (rbc.s destroyed with time)
- Difficult to distinguish high rbc count from traumatic tap
 Xanthochromia?
- Controversy: visual inspection or spectophotometry?
- Soderstrom 1977: visual xanthochromia was only seen in 16
out of 32 cases with xanthocrhomia demonstrated by
spectophotometry and suggests visual inspection is
- MacDonald 1988: retrospective review of 100 patients with
angiographically proven aneurysms; 68 patients had LP
done, 31/68 had NO xanthochromia by vision (46%
sensitive). 13 of the LPs were done on the first day, so
exclude them re possibility of xanthochromia not being
present yet -----> 18/55 had NO xanthochromia leading to
sensitivity of 67%
- Morgenstern 1998: 18/20 false +ves in pts with -ve CT
head. Note that they don’t tell us when the LPs were done
and that their dx of SAH on LP was based on rbc.s > 1000
with no decrement > 25% + one of visual xanth, spec xanth,
or d-dimer. 18/20 with “false +ve” LPs were followed for two
years with no long term sequelae suggesting that
spectophotometric xanthochromia is too sensitive
- No other literature to suggest spec is too sensitive
- Sensitivity for visual vs spec in CT-ve patients UNKOWN
 How can you distinguish between a traumatic tap (TT) and a true SAH?
 Xanthochromia if LP done > 12hrs
 Lumbar puncture less than 12hrs cannot determine reliably b/w traumatic
tap and lumbar puncture b/c xanthochromia may not yet be present
 Opinion of atraumatic vs traumatic tap unreliable
 Four tube method (blood decreases > 25% in tube 4 vs 1) is not 100%
reliable (Vandermeulen 1996, Buruma 1981)
 Crenated erythrocytes, erythrophages, d-dimer have been investigated but
none have been shown to be reliable
 Repeat LP at one level higher: will dx traumatic tap if clear but doesn’t help
you if it is bloody
 What can cause a false +ve Xanthochromia?
 Traumatic tap that sits in lab long enough for xanthochromia to form (<2hrs
for oxyhemoglobin, longer for bilirubin)
 Rifampin
 Previous traumatic LP
 Hyperbilirubinemia (jaundice)
 Timing of Lumbar Puncture
 Barrows 1955: showed that oxyhemoglobin xanthochromia takes two hours
to form, bilirubin xanthochromia takes longer (> 6hrs)
 Roost 1972: showed that the enzyme for converting rbc.s to bilirubin
reaches maximum activity at 12 hours
 Generally accepted that lumbar puncture should be delayed until > 12hours
from onset based on Walton 1956 and Vermeulen 1989. Note that early
LP followed by later LP helps you if the second LP is negative but not if
positive b/c of confusion beteween traumatic tap and SAH blood.
 Walton 1956: retrospective look at 256 cases of SAH

Time of LP Blood Xanthochromia

0-2hrs 100% 0%
2-4hrs 100% 5.8 - 6%
4-6hrs 100% 57 - 64%
6 - 12hrs 100% 65 - 87%
12 - 24hrs 91% 89 - 100%
1 - 3 days 89% 93 - 100%

 Vermeulen 1989: reviewed 111 patients with SAH diagnosed by blood on

CT, all LPs were done >12hs (useful evidence for value of late LP, NOT
useful for describing value of LP under 12hrs)

Timing Sensitivity
12hrs - 2wks 100%
2 - 3wks 91% (71 - 79)
3 - 4 wks 71% (42 - 92)
 Summary on LP
 Best to delay LP to 10 - 12hrs after onset of headache: 12 hours is not a
“gold standard”, realize that sensitivity increases with time
 Spectophotometry dx of xanthochromia seems to be superior to visual dx
although literature is unclear
 Study of LP on CT-ve patients has not been done.
 Getting sample analyzed within 1hr is important
 Only alternative to keeping patient until 10-12hrs is too find a reliable way
to distinguish between traumatic tap and SAH before xanthochromia


 Risk of herniation
 Mass effect producing herniation could be from associated hematoma,
hydrocephalus, other dx (intraparenchymal hemorrhage, tumor that bled,
 16% of SAH had hydrocephalus in the Cooperative aneurysm study
 Physical examination may be insensitive for subtle findings of focal
 Herniation can occur in patients with NORMAL LOC and neuro
- Hillman 1986: 2.2% acute deterioration in pts w/ normal
LOC, 10% of SAH with normal LOC and neuro exam had
- Duffy 1982: 7/55 patients with proven SAH deteriorated
during lumbar puncture, another 7/55 deteriorated after
lumbar puncture. 4 died, 2 grossly disabled, 1 hemiparetic.
BUT, this was on proven SAH and not all comers thus we
don’t know the denominator and herniation rates likely much
 Additional Information of CT
 Dx of non-aneurysmal causes of SAH (10 - 20%): AVM, tumor,
intraparenchymal hemorrhage, hypertensive hemorrhage, etc
 Look for acute complications of SAH that may alter management:
hydrocephalus, intraparenchymal hematoma
 Provides baseline comparison for future CT in the event of complications
(hydrocephalus, rebleeding, vasospasm, infarction)
 Amount of bleeding has shown to be prognostic
 Bleeding on CT can help localize aneurysm (especially if angiogram
negative), can help plan surgery, may even directly visualize aneurysm,
may localize two different bleeding sites
 How do you know that this isn’t an intraparenchymal bleed instead of a SAH?
 Van Gijn 1980. Clin Neurol Neurosurg: Retrospective review of CT in
patients with suspected dx of SAH; 15% had intraparenchymal
hemorrhages, 8% were in posterior fossa (high risk of herniation if LP was
done b/f CT)
 Evidence that LP should not be done first
 How do you know that SAH doesn’t have an associated hematoma with increased risk of
 Pasqualin 1986: 30% of all comers SAH had hematomas
 Hillman 1986: 10% of SAH w/ normal LOC and neuro exam have
 Kassell 1990 (Cooperative study): 17 % with associated hematomas (15%
with associated hydrocephalus)
 Summary
 There is NO literature supporting LP without CT. Schull 1999 is the only
reference but this is a theoretical model and not a clinical trial
 There IS literature documenting the risks of herniation and the unreliability
of a normal physical examination
 Much additional information is gained from a CT and neurosurgery will
order it anyways if you make the diagnosis of SAH on the basis of an LP
 CT scan should always precede LP in a tertiary care setting
 LP without a CT in the periphery MAY be reasonable only with a normal
LOC and normal neurological exam; alternatively, just start antibiotics if
meningitis is a possibility and refer to tertiary care center


 Suspected SAH, -ve CT, LP -ve for xanthochromia
 Evidence that SAH could have occured
- MacDonald 1988: retrospective review of diagnosed SAH
and found that 31/68 patients with SAH had -ve CSF for
xanthocrhomia by VISION
- 9 case reports in literature of CT-ve, LP -ve, angiogram +ve
(? incidental aneurysms which occur in 0.5 - 6% of
 Evidence that this does not occur
- Vermeulen 1989: 12/500 patients with SAH had blood
stained LP with no xanthochromia. 3 underwent
angiograms which were negative. All had no recurrence
and 100% survival thus dx was likely thunder-clap headache
with traumatic tap
- VanGin 1988: Long term follow up of 71 patients with
Thunderclap headache and -ve CT and -ve LP. Mean f/u
was 3.3 years —> no complications
- Markus 1991:
- Harling 1989:
- Linn 1994:
 Summary
- Worrisome history with -ve CT and -ve LP done after 12hrs
and xanthochromia looked for with spectophotometry
- Could have an aneurysm that expanded/stretched, or
minuscule leak BUT unlikely and chance of this is less than
the risks associated with angiography (1/200)
 Angiogram -ve SAH
 Dx of SAH based on traumatic tap
 Blood on CT mainly or only in the interpeduncular cistern:
Perimesenchephalic hemorrhage
 No blood on CT, +ve LP for xanthochromia: etiology NYD
 Blood on CT c/w aneurysm but no aneuryms on angio: “occult aneurysm”

 Airway: intubate for hypoventilation, hypoxia, hypercarbia, loss of airway
reflexes, pulmonary edema, signs of increased intracranial pressure
 RSI: lidocaine/fentanyl/thiopentothal/succ
 D: elevate head of bed, hyperventilate to PaCO2 of 30 and mannitol 1
gm/kg if signs of increased ICP, phenytoin prophylaxis (20 mg/kg @ 50
mg/min), consult neurosurgery for craniotomy and clipping or angiographic
 Complications
 Rebleeding: high morbidity and mortality
 Hypertension: increases risk of rebleeding, keep BP < 160 systolic with 10
- 20 mg labetolol prn (alternatives are captopril 12.5 mg po, nitroprusside
0.5 ug/kg/min, esmolol, hydralazine 10 - 20 mg)
 Seizures (rare but disasterous): prophylaxis with dilantin controversial
 Hydrocephalus due to scarring, may require shunts
 Vasospasm: blood in SAS irritates the blood vessels in the SAS causing
vasospasm which can cause infarction, must delay Sx until vasospasm
under control, Rx: CCBs (nimodipine 60mg po q4h), fluids, increase BP
 Cardiac: ST changes (may be missdx as AMI), ischemia, prolonged QT,
virtually any brady or tacchyarrythmia; do ECG

 Angiography +/- coiling
 CT angiography and MR angiography yet to be defined


 Triage to monitored area
 Cardiac, BP, pulsox monitors
 Supplemental oxygen as needed
 Consult neurosurgery
 NPO
 Elevate head of bed 30 degrees
 SAH precautions: minimal stimuli
 IV normal saline at 2 ml/kg/hr
 ECG
 Labetolol 10 - 20mg prn to keep SBP < 160
 Preoperative blood work: CBC, Cr, Ur, lytes, type and screen, INR/PTT
 Pain control: neurosurg likes codeine 30 - 60 mg po/sc/im (? less sedating)
 Antiemetic
 Foley catheter prn
 Discuss with neurosurgery: ?Dilantin load, Nimodipine (60 mg po or via NG), Mannitol 1
gm/kg if you think there is significant increased ICP