Headache and Subarachnoid Hemorrhage by MikeJenny

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									     Headache and
Subarachnoid Hemorrhage
       Carly Thompson
      February 19, 2009

        See Rob Halls’ presentation at the end of Carly’s
 Approach to headache in the ED
 Migraine
    – Focus on dx, tx
 Subarachnoid Hemorrhage
 Other causes of serious headache
       Headache Epidemiology
 4% of ED visits
 Primary Headaches
    – Migraine
    – Tension-Type
    – Cluster
   Secondary
    – All others!
    – 1% of headaches are SAH!
      Headache: Historical Features
Occult Trauma   Signs of abuse/neglect    Space-        Progressive
                Anticoagulation           occupying     Hx of malignancy
SAH             Sudden Onset              lesion        New onset >50yrs
                Maximal soon after                      Worse in am, head
                onset                                   down
                Different than previous                 Neuro signs
Meningitis      Fever                     Cerebral      Bilateral neuro findings
                Neck stiffness            Venous        Proptosis
                Immune compromise         Thrombosis    Hypercoaguable state
                Head/neck infection                     Recent sinusitis
Temporal        Jaw claudication                        Pregnancy
Arteritis       Temporal tenderness       CO Toxicity   Worse in am
                Visual symptoms                         Others affected
Pre-eclampsia   Pregnancy                               Environmental
                Post-partum                             exposure
   Name 5 high risk historical features for
    Subarachnoid Hemorrhage.
      High Risk Features for SAH
   Thunderclap
   First or worst headache of my life
   Altered mental status / Seizure
   Headache with exertion / intercourse
   History of exercise
   Location of pain: occipitonuchal
    – PPV occipitonuchal headache for intracranial
      pathology is 16%
   Family history of SAH
    – Up to 4x increased risk in 1st and 2nd degree relatives!
   What is your differential for thunderclap
    headache? Name 3 (other than SAH).

Thunderclap = sudden-onset, severe
       Thunderclap Headache:
        Differential Diagnosis
 Carotid or vertebral artery dissections
 Venous sinus thrombosis
 Pituitary apoplexy
 Hypertensive emergencies
 Cluster headache
 Cerebellar CVA
High Risk Examination Findings
   Vital signs: htn, fever
   Decreased, altered, fluctuating LOC
   Focal neurologic sign
   Meningismus
   Toxic appearance
   Opthamalogic findings: papilledema, subhyaloid
    hemorrhage, retinal hemorrhages, decreased vision,
    ciliary flush, sluggish pupillary light response
   Trauma
   Temporal artery findings
   Carotid bruit
   Nausea and vomiting: Increased ICP, hemorrhage, ANAG
   Nasal discharge with sinus tenderness: sinusitis
   What is a subhyaloid hemorrhage and
    when do you see it?
         Subhyaloid Hemorrhage
   Gravity-dependent venous
    hemorrhage between
    retina and vitreous
    membrane, convex at
    bottom, and flat at top
    when sitting

   Highly suggestive of SAH:
    11-33% of SAH cases

   Terson’s syndrome – rapid
    increase in ICP assoc. with
    hemorrhage – worse
             Low Risk Patient
 No change in headache pattern
 No new concerning historical features
 No focal neurologic symptoms or findings
          No imaging indicated!
 Meta-analysis:
    – 2.4% of those with normal neuro exam have
      neurologic abnormalities on CT
    – 0.4% of those with typical migraine symptoms
   Which subsets of patients with headache
    require neuroimaging in the ED?
    – Name 3 groups.
     Neuroimaging Indications
ACEP Clinical Policy (Ann Emerg Med 2008)
 Level B
  (1) Headache and new abnormal neuro findings
      PPV 39% for intracranial pathology
      LR 3.0
  (2) Sudden-onset severe headache
      10-15% have serious pathology, often SAH
  (3) HIV patients with new headache
      Headache – 35% had mass lesion
      Neurologic complaint – 24% focal lesion
      1 or more of predicted all focal lesions in a series of patients:
         – New seizure
         – Depressed / altered LOC
         – Headache different or > 3 days
Level C Evidence
 Age >50 with new headache but normal
  exam, should be considered for urgent
     OR 3.3 of pathologic diagnosis
   Other worrisome features that increase
    probability of positive findings, but no
    clear recommendations:
    – Occipital location
    – Worsening with Valsalva
    – Headache waking from sleep
    – Associated syncope
    – Nausea or sensory distortion
Headache in Pregnancy
 Most headaches are benign
 CVA – risk increases 3-13x
 SAH – 20/100,000 deliveries
 Migraines: less common
  – 60-70%have improvement in migraines during

Conclusion: Insufficient data to drive
  recommendations for imaging.
   Can response to therapy be used as a
    diagnostic tool?
        Response to Therapy
Level C
 No!!! Pain response should not be used.
 ? Common pathway for pain regardless of
 No RCT to support or refute this.
 Class III Evidence: Case reports, case series,
  showing resolution or improvement in pain with
  analgesics in SAH, meningitis, CO-induced
  headache, cerebral venous sinus thrombosis,
  dissection, etc.
   What are the diagnostic criteria for
              Migraine: Diagnosis
   Recurrent headache disorder – IHS Criteria
    – Headache lasts 2-72 hours
    – At least 2 of:
          Unilateral
          Pulsating
          Moderate to Severe
          Aggravation by routine activity
    – At least 1 of:
        Photophobia or Phonophobia
        Nausea and/or vomiting
    – At least 5 attacks
    – Hx, physical and neurologic exam do not suggest
      other organic disease
          Migraine: Diagnosis
 Migraine without Aura
 Migraine with Aura:
    – Aura reversible focal neurologic symptoms
      that usually develop over 5-20 min and last
      <60 min, headache begins during aura or
      within 60 minutes
    – Visual positive / negative features
    – Sensory positive / negative features
    – Dysphasic speech
 True or False?
 Migraines can be associated with
  autonomic and sinus symptoms
    – i.e. nasal congestion, rhinorrhea, tearing,
      colour and temperature change, changes in
      pupil size

   Which of the following are associated with
    – Family history of migraine
    – Motion sickness
    – Obesity
         Associated Factors
 Family history and motion sickness are risk
  factors for developing migraine
 Obesity is associated with increased
  frequency and severity of migraines
           Migraine: Treatment
US Headache Group:
 Educate pts about condition and tx; encourage active
  participation in management
 Use migraine specific agents in pts with severe migraine,
  and those who respond poorly to NSAIDs or combination
 Use non-oral route for pts with sig N/V
 Consider self-administered rescue meds for pts with
  severe migraine
 Guard against medication overuse headaches by using
  prophylactic medication in pts with frequent headaches
   List 5 treatment options for migraine in
    the emergency department.
            Treatment Options
   Fluids
   Analgesics: NSAIDs, acetaminophen
   Serotonin Agonists
    – Ergotamine
    – DHE (Dihydroergotamine)
    – Triptans
   Dopamine Antagonists
    – Chlorpromazine
    – Prochlorperazine
    – Metoclopramide
   Opioids
   Steroids: Dexamethasone
    Mild Analgesics in Migraine
 Some pts can get optimal response with mild
  analgesics (NSAIDs, acetaminophen)
 Not advisable >10x /month
 RCTs: Acetaminophen, ibuprofen, naproxen,
  diclofenac, ASA, acetaminophen + ASA +
 Indomethacin: limited data, some specific
  migraine types are responsive to indomethacin
  for abortive therapy, benefit: suppository form
 Specific tx: 5-HT 1b/d agonist ->inhibit
  dural nociception
 Advantage: multiple preparations
    – SC, IN, PO
 RCT and systematic reviews: all triptans
  have been shown effective in acute
 Pts who don’t respond to one may
  respond to another
   So, why don’t we commonly use triptans
    in the ED?
          Limitations of Triptans
   More effective if used early!
    – Development of central sensitization
   Contraindications:
    – Patients with pregnancy, uncontrolled htn, ischemic
      heart disease, peripheral vascular disease,
      Prinzmetal’s angina, ischemic CVA, familial hemiplegic
      migraine, basilar migraine
    – 24 hours of other 5-HT agonist (ergots), MAOIs with
      some triptans
    – Severe liver impairment
   Interactions: P450 cytochrome
   Advisory July 2006 – concomitant use with
    SSRIs or SNRIs increases risk of serotonin
    syndrome; advise discussion of benefit vs risk
                Ergots: Ergotamine
   Mechanism:
    – 5HT 1b/d receptor agonist
   Efficacy:
    – Alone failed to show efficacy
   Side effects:
    – Nausea, vomiting
    – Vascular occlusion and rebound headaches
    – Long-term: Associated with CAD
 Avoid in pts with CAD, PVD, htn, hepatic and renal
  disease and those with prolonged aura
European Consensus Panel:
 Treatment of choice in few pts due to issues of efficacy
  and side effects
     Ergots: Dihydroergotamine
 Fewer side effects: no dependence or rebound
 Advantage: IV, IM, SC, IN use
 Contraindications:
    – Htn, CAD, PVD, Prinzmetal’s, MAOIs, sepsis, severe
      hepatic or renal dysfunction, high dose ASA tx,
    – Hemiplegic or basilar migraine
    – Within 24 hours of triptan or other serotonin agonists
    – CYP3A4 inhibitors: some macrolides, antifungals,
      protease inhibitors
   How does DHE compare to the triptans for
    – More effective?
    – Same?
    – Less effective?
                  DHE: Efficacy
   vs Placebo:
    – Proven by systematic review / RCTs,
      especially when given with anti-emetic
   vs Triptan:
    – Less effective on most measures compared
      head-to-head with sumatriptan
   vs Dopamine Antagonist:
    – Less effective than chlorpromazine on some
         Dopamine Antagonists
   Benefits:
    – Antiemetic
    – IV metoclopramide
    – IV or IM chlorpromazine and prochlorperazine
              Largactil / Thorazine
Chlorpromazine 5-15mg IV or 0.1mg/kg IV
 RCT vs Placebo (Bigal 2002 J Emerg Med):
    – Significant improvement in scores of pain, nausea,
      vomiting, photo/phonophobia at 60 min
    – NNT 2
   Side effects:
    – Hypotension / Postural hypotension (18%)
        May be exacerbated by opioids, pre-tx with fluid bolus
        Alpha-antagonist
    – Drowsiness
    – Pregnancy: Class C
               Stemetil, Compazine
Prochlorperazine 10mg IV
 Side effects:
    –   Hypotension
    –   Drowsiness
    –   Dystonic Reactions
    –   Cardiac arrhythmias
    –   Pregnancy Class C: Isolated reports of congenital
        anomalies, jaundice, EPS, hyper/hyporeflexia – if
        occasional low-dose suggested to be safe
   FDA Alert (June 2008): Association with
    increased mortality when used for treating
    dementia-related psychosis
   How does prochlorperazine compare to
Proclorperazine vs Metoclopramide
   RCT: Coppola (1995) Annals of Emerg Med
    – > 50% relief
    Stematil 82%     Maxeran 48% Placebo 29%

   RCT: Jones (1996) Am J of Emerg Med
    – Partial or complete relief
    Stematil 67% Maxeran 34% Placebo 16%
Metoclopramide: Maxeran, Reglan
Maxeran 10mg IV
 Efficacy:
    – Meta-analysis Colman (2004) BMJ
         Generally poor studies
         OR 2.84 for reduction of pain in headache
         Less effective than chlorpromazine and prochlorperazine in relieving
          pain, but not always statistically significant
         1 Trial: No difference between aggressive metoclopramide (20mg
          IV q30 min up to 4x with diphenhydramine 25mg IV q1 hour up to
          2x) vs sumatriptan 6mg SC
   Benefits:
    – Pregnancy Class B
    – Can be combined with DHE, other analgesics
   Side Effects:
    – Drowsiness
    – Dystonic reactions: <1-25%, increased risk in young males
              Other Options?
Some pts will not respond to routine treatment.
 Consider wait-times, location (ED vs clinic)
 Treat aggressively.
 Do not use following meds on a chronic basis
  due to habit-forming nature and rebound
  – Benzos
  – Opioids
  – Barbiturates
   How can you prevent migraine
   Parenteral Dexamethasone
Colman I et al. (2008) BMJ
 Meta-analysis of 7 RCTs.
  – Dexamethasone 10-25mg IV or IM vs placebo
  – Similar acute pain reduction
  – Recurrence rates at 72 hours RR 0.74 (0.6-
  – NNT 9
  – Similar side effect profile
   Can you name the complications of a
     Migraine: Complications
 Status migrainosus
 Chronic migraine
 Persistent aura without infarction
 Migrainous infarction
 Migraine-triggered seizure
              Migraine Tx in the ED
   Fluid bolus: NS 1L bolus IV
   NSAID: If used <10x/month
    – Nausea / vomiting: consider PR indomethacin
    – PO: acetaminophen vs ibuprofen
   Dopamine antagonist:
    – Stemetil 10mg IV
    – Maxeran 10mg IV (Pregnancy)
   Opioid:
    – Morphine 2-5mg IV prn
   DHE / Triptan:
    – If early presentation, contraindications to others
    – Rizatriptan, eletriptan, almotriptan
    – Sumatriptan: IN, SC or Zolmitriptan: IN, PO
      Subarachnoid Hemorrhage
 SAH 1% of all headaches in ED
 10% of hemorrhagic strokes
 10% of “worst headache ever”

   Prevalence: 3-25 / 100,000
   Mean age: 55 (Range 20-60)
   Reported in pediatrics

Miss Rate?
 Variable 5-50% (30% average)
 Acceptable miss rate: 0%!
   Can you name 3 causes of SAH?
              Causes of SAH
   Causes of SAH:
    – Trauma
    – Saccular Aneurysms
    – Non aneurysmal: Perimesencephalic (?venous
    – AVMs / Fistulae
    – Illicit drug use: cocaine, amphetamines
    – Arterial dissections
   Can you name 3 risk factors for formation
    of aneurysms?
            Etiology of Aneurysms
   Congenital:
    – Familial intracranial aneurysms (dominant)
    – Genetic condition: Ehlers-Danlos, Marfan’s, PCKD
    – Coarctation
   Acquired:
    –   Traumatic: skull #, penetration, post-op, hemodynamic damage
    –   Infectious: syphilis, mycotic
    –   Inflammatory: vasculitis
    –   Degenerative: atherosclerotic

Hypertension is NOT a major factor for aneurysm
   How many people have aneurysms?
       Aneurysms in the Public
   Prevalence of saccular aneurysms
    – 5% at autopsy
    – 20-30% have multiple aneurysms
   Can you name 3 risk factors for rupture?
         Risk Factors for Rupture of
   Smoking      Aneurysms
     – Dose-dependent, esp. women, disappears soon after quitting, RR 2.2
   Hypertension
     – RR 2.5, OR 2.6
   EtOH
     – Moderate to heavy consumption RR 2.1, OR 1.5
   Family History
     – OR 4.0
   Genetics
     – Autosomal dominant / recessive / multifactorial / anticipation
     – Elastin gene, Platelet adhesive glycoprotein
   Phenylpropanolamine
     – Appetite suppressants, cold remedies, case-control study – risk factor in
   Estrogen deficiency
     – Premenopausal women and reduced risk compared to age-matched
       postmenopausal women (OR 0.24), HRT (OR 0.47)
   Physical Exertion
     – Orgasm, moderate exertion OR 2.7
   ?Anticoagulants
   What proportion of patients with SAH from
    aneurysm have a sentinel bleed?
           Sentinel Headache
   30-50% of patients have a sentinel
    headache that precedes SAH by 6-20 days
              Clinical Features
   Abrupt onset, severe headache “thunderclap”
   Lateralized 30%
   At night 30% (During day / activity 60%)
   Onset associated with brief LOC, seizure,
    nausea, vomiting
   Meningismus / Aseptic meningitis
   Normal neurologic findings at presentation 50%
   What is the mortality of SAH?
 Average: 51%
 10% prior to reaching hospital
 25% within 24 hours of onset
 45% within 30 days
   What are the complications of SAH?
    – Name 4.
   Rebleeding
   Vasospasm and delayed cerebral ischemia
   Infarction
   Hydrocephalus (acute / chronic)
   Increased ICP
   Seizures
   Hyponatremia
   Hypothalamic dysfunction and pituitary insufficiency
   Cardiac abnormalities
    – ECG
    – Ventricular wall motion abnormalities
    – Elevated BNP
            Pitfalls in Diagnosis
 Wasn’t the worst headache of their life!
 Neurologic exam was normal!
    – 50% have normal neurologic exam!
   Pain improved with treatment
    – Remember: SAH CAN improve with treatment!
 CT head was negative
 RBCs decreased from tubes 1-3 /
  Misinterpretation of LP
 No LP done
       CT Head: Limitations
 Technical ability of CT scanners to identify
  small hemorrhage / artifact / bone
 Protocol and age of scanner – thin slices
 Expertise of reader
 Anemia Hb<100 – blood appears isodense
 Time: decay in sensitivity
 Inability to diagnose other causes of
  headache: meningitis, etc.
 How sensitive is CT scan at day 1 for SAH?
 How sensitive is CT scan at day 7 for SAH?
          CT Scan: Sensitivity
   As blood is diluted and degraded flowing
    through SA space -> decreased sensitivity
    – BMJ (2006)
        <12 Hrs   98%
        24 hrs    93%
        >7 days   <50%
    – Memory aide:
        Day   1   90%
        Day   2   80%
        Day   3   70%
        Day   4   60%
   Why do you do a CT then if ruling out
    CT Scan for SAH: Advantages
   Traumatic LP:
    – 13% may be traumatic (>400 RBCs)
   LP Limitations:
    – Cerebral venous thrombosis
    – Unruptured aneurysm
    – Arterial dissection
    – Pituitary apoplexy
   Does an LP need to be routinely
    performed on ED patients to rule out SAH
    if normal noncontrast CT head?
    – Why?
         Lumbar Puncture
ACEP (2008) Level B Evidence.
 Lumbar puncture should be performed to
  rule out SAH.
 Rates of SAH confirmed by LP after
  normal CT 2.5-3.5%
   What 3 features do you see on LP in SAH?
     Lumbar Puncture in SAH
 (1) Elevated opening pressure
 (2) Elevated RBC count
 (3) Xanthochromia
           Opening Pressure
 6-20cmH20 is normal in adults and children
 25cmH20 may be normal in obese pts
 Helpful to distinguish SAH from traumatic tap
 2/3 of SAH may have elevated opening pressure
 Other diagnoses: spontaneous intracranial
  hypotension, benign intracranial hypertension,
  cerebral venous sinus thrombosis
   Does clearing of blood (i.e. declining RBC
    count from tubes 1->4) rule out SAH?
    Elevated Red Blood Cell Count
 Clearing of blood is unreliable.
 There is no cutoff which has been shown
  to reliably exclude SAH.
 However, if tap done late >12 hours, and
  absence of xanthochromia, but presence
  of RBC = negative tap.
 No way to tell traumatic tap vs SAH if
  early <12 hours tap.
 What is xanthochromia?
 When does it appear? How long does it
 Yellow colour caused by bilirubin and
  oxyhemoglobin due to lysis of RBCs
  OxyHb -> Heme oxidase enzyme -> Bilirubin
  Process may take 6-12 hours
 Onset: Blood in CSF for at least 2 hours
 Peak: 48 hours
 Duration: Up to 2-4 weeks
 Name 2 methods for analyzing your
  sample tubes for xanthochromia.
 Which is more sensitive?
      Xanthochromia: Analysis
 Spin CSF, run through spectrophotometer, look for
  oxyHb or bilirubin peak at 410nm and 460nm
 Most sensitive
 Low-moderate specificity
 Not always available

Visual Analysis
 Spin CSF, compare to identical test tube with equal
   volume tap water against white background
 Calgary Health Region’s method
 Less sensitive, but may be >95% if >12 hours after SAH
   Name 3 false positives for xanthochromia.
    (Xanthochromia but no SAH!)
Xanthochromia: False Positives
 Hyperbilirubinemia
 Rifampin
 Previous traumatic tap
 Traumatic tap isn’t analyzed quickly ->
 Chronic spinal cord abnormalities
   Which patients can safely undergo LP
    without neuroimaging?
                 LP Before CT?
ACEP (2008). Level C Evidence.
 Adults patients with headache and signs of
  elevated ICP should have neuroimaging before
    – Papilledema, absent venous pulsations of fundoscopy,
      altered LOC, focal neuro deficits, signs of meningeal
   In the absence of clinical findings suggestive of
    increased ICP, LP can be performed without
    obtaining neuroimaging.
   In a patient with sudden-onset, severe
    headache who has negative findings (both
    CT head and LP) is there a need for
    further emergent imaging?
           Further Investigation
ACEP (2008). Level B Evidence.
 Patients with sudden-onset, severe headache
  with negative CT head, normal opening
  pressure, negative findings on CSF analysis, do
  NOT need emergent angiography, and can be
  discharged with follow-up recommended.

   Note: Consider other causes of sudden-onset,
    severe headache like pituitary apoplexy, cerebral
    venous sinus thrombosis, arterial dissections,
    cerebellar stroke . . . Further imaging may be
    indicated to rule out these causes.
           Further Investigation
   Perry et al. (2008) Annals of Emerg Med.
    – 2 Canadian EDs, 592 patients
    – CT and LP to rule out SAH (10.3% had SAH)
        CT neg
        No xanthochromia by visual inspection
        RBCs in final tube <5 x 106RBC/L
    – Others followed 6-36 months
    – Rate of subsequent SAH: 0%
    – Rate of subsequent aneurysm: 1 / 592 required
      surgery, but “did not contribute to initial presentation”
Thank You!
   Can you name 3 causes of headache that
    might be associated with exertion?
              Exertional Headache
   SAH
    – Pts with SAH more likely to have participated in exertion that
      day, compared to previous OR 2.7
   Carotid or Vertebral Artery Dissection
   Primary Exertional Headache
    – Bilateral pulsatile pain during or after exercise, lasts 5min – 48
      hours, not usually assoc. with N/V
    – Rule out: SAH, angina, vascular abnormalities, pheo
    – Tx: indomethacin, propranolol, naproxen
   Primary Headache Associated with Sexual Activity
    –   Preorgasmic: usually secondary to muscle tension
    –   Orgasmic: associated with CVA / dissection and SAH
    –   Unpredictable
    –   Prevention: indomethacin, B-blockers, propranolol
    –   Acute tx: triptans
   Can you describe the most common
    headache symptoms in brain tumour?
                  Brain Tumour
   50% have headaches
    – Tension-type (77%)
    – Migraine (9%)
   Typical headache:
    – Bilateral, worse ipsilaterally, bending over (32%),
      nausea and vomiting (40%), worse with Valsalva
 Classic “early morning headache” – uncommon!
 Reliable findings:
    – Nausea, vomiting, worsening with change in position,
      abnormal neurologic exam, significant change in
      headache pattern
         Triptans: Comparison
 Few trials comparing triptans head to
 Rizatriptan (Maxalt), eletriptan (Relpax),
  almotriptan (Axert) had highest likelihood
  of success
 Sumatriptan was recently released with
  fast dissolving tabs
    – Sumatriptan (Imitrex): SC, IN, PO
    – Zolmitriptan (Zomig): IN, PO
Emergent Diagnoses
    Core Rounds Feb19,2009
      Rob Hall MD, FRCPC
 41yo female PMHx DM1 on insulin
 Mild headache and Numbness right arm/mouth and
  weakness left grip, subacute, 1 week
 No fever or illicit drug use
 OCP started 2 weeks ago
 No hx seizures, no trauma
 Waiting in ED bed, GTC 1 min sz, chemstrip normal,
  ativan 2mg iv, post ictal and combative after, no
  focal findings after sz
 Investigations?
 Thoughts on dx?
CT head (plain)
      Cerebral Vein Thrombosis

      “DVT of the BRAIN”
   Venous clot then infarct and/or bleed at grey-white
   Transverse sinus most common location, often
    multiple sinuses
         Clinical Presentations

    – Often not typical arterial distribution
    – Can be basically any description of
      headache (thunderclap uncommon)
    Risk Factors for CVT                                      (present in 85%)

 Head and neck infections
 Hypercoagulable states
    –   Estrogens
    –   Pregnancy
    –   Cancer
    –   Hypercoag syndrome: lupus AC, protein C def, etc
    –   Hematologic disorders: leukemias, polycythemia, thrombocytosis, sickle cell
    –   Vasculitis: SLE, GCA, wegener’s, Bechet’s, etc
                      Exam findings
   Highly variable
   Three clues
    – Head infection + Neuro symptoms
    – Papilledema (? Sensitivitiy)
    – Stroke findings in non-arterial distribution

    LP will show elevated opening pressure without other cause
        CT head (plain) findings
 Sensitivity 60-70% (30-40% normal)
 Delta sign = dense triangle from hyperacute
  thrombosed superior saggital sinus
 Cord sign = thrombosed cortical vein
 Venous infarcts with secondary hemorrhage in
    non-arterial distribution
    – HTN bleeds: thalamus, IC, CB, pons
    – Venous infarct bleeds: bilateral at grey-white junction
CT head
            Definitive Diagnosis
 CT venography (preferred)
 MR venography
    – Hypointense signal of acute thrombus mimics
      normal flow. RadioGraphics 2006;26:S5-18.
   Angiography (not used anymore)
CT Venography
      CVT and Carotid/vert
     Which is better CT or MR?
   “I think that most radiologists reading these
    studies would say that both CTV and CTA
    have a higher sensitivity due to CT's inherent
    spatial resolution advantage which is very
    good on our latest multidetector
    scanners. CT is our favoured study where
    there is concern for venous sinus thrombosis
    and carotid/vertebral dissection. The
    research will catch up.”
                ED Management
 Dilantin if seized
 Manage elevated ICP
 Heparin
    – Majority of evidence shows improvement trends (no
      major large RCT showing statistically conclusive
    – Shown to be safe even with hemorrhages!
    – Cochrane review 2001
        RR death 0.33 (95%CI .08-1.2)
        RR death or disability 0.46 (0.16-1.3)
       Further Management
 Optic nerve fenestrations
 Acetazolamide
 Case reports of lytics
 LP/VP shunts
 Hemicraniectomy for severe ICP problems
Is Idiopathic Intracranial
HTN and CVT a spectrum
       of disease?
 IIHTN -------------------------> CVT
    Idiopathic Intracranial HTN

 Old terms = Pseudotumor cerebri,
  Benign IHTN, meningitis Cerosa
 Diagnostic criteria for IIHTN requires
  imaging to rule out CVT
      Idiopathic Intracranial HTN
   Opening pressure > 20 cm H20 (usu 25-45)
    – Headache MUCH better after LP!
   Signs/symptoms of increased ICP
   No focal signs (except 6th palsy)
   No mass lesion
   No hydrocephalus
   Normal CSF values
   CTV/MRV to exclude CVT
     Idiopathic Intracranial HTN
   Main ED PEARL is to consider the
    diagnosis and do an LP
   “Consider”
    – Obese, female, OCP
    – Hypercoag states
    – Subacute, unexplained headaches, return
      visits, normal imaging
    – Visual symptoms: blurry vision, diplopia
         Carotid and Vertebral
   2% of ischemic strokes overall but 20% of
    ischemic CVA < 45yo
    – Think of in young patient
   Pathology the same with major vs minor
    – May be VERY minor (yoga, cough, stretching,
    – Unknown if “spontaneous” really occur
       Carotid and Vertebral
 Headache + Neck pain, unilateral + neuro
 Dx - CTA, MRA, angio
 CTA preffered
    Giant Cell (Temporal) Arteritis:
               the basics
   Older person
   Subacute headache
   Systemic symptoms
   Jaw claudication
   Association with PMR
   Risk of vision loss
   Elevated ESR
   Diagnose by temporal artery biopsy
   Treat with steriods
Giant Cell Arteritis: some pearls
   Extremely rare < 50 years old
    – Pooled analysis 1435 pt, only 2 < 50yo
   Temporal artery findings (large, absent pulse,
    tenderness) fairly specific but not sensitive
   Normal ESR (< 20 mm/hr) excludes dx, moderate ESRs
    don’t (20-50 mm/hr)
    – <20 mm/hr                96% sensitive
    – <40 mm/hr                95% sensitive
    – < 50 mm/hr               89% sensitive
Giant Cell Arteritis: some pearls

   Temporal artery biopsy
    – Initial bilateral biopsies 88% sensitive
    – Repeat if initial biopsies negative
    – Biopsy will be abnormal for weeks after initiation of steriod;
      try to have it done soon but not emergently
   Treatment
    – Prednisone 60 mg po od
    – ASA
    – START before biopsy

  Headache is a high risk complaint.
   Consider serious causes in every
   Majority of badness excluded with
      good history and physical.
  More complex than just ordering CT
Headache and normal CT head;
    ddx of “bad” causes?
   Ischemic stroke
   HTN encephalopathy
   Pre-eclampsia
   CO toxicity                    Which can be excluded
   Vasculitis/GCA                 By hx/pe?
   AACG
   CNS infection
   CVT
   SAH
   Carotid/vertebral dissection
Headache and normal CT head;
    ddx of “bad” causes?
   Ischemic stroke - hx and physical
   HTN encephalopathy - physical
   Pre-eclampsia - hx and physical
   CO toxicity - hx
   Vasculitis/GCA - hx
                                        Which can be excluded
   AACG - physical                     By a normal LP?
   CNS infection
   CVT
   SAH
   Carotid/vertebral dissection - CTA/MRA
Headache and normal CT head;
    ddx of “bad” causes?
   Ischemic stroke - hx and physical
   HTN encephalopathy - physical
   CO toxicity - hx
   Vasculitis/GCA - hx
   AACG - physical
   CNS infection --------------> LP
   CVT -------------------------> LP (+/- CTV)
   IIHTN -----------------------> LP
   SAH -------------------------> LP
   Carotid/vertebral dissection - CTA/MRA/Angio
Lumbar puncture is a
test to exclude some
 causes of headache
     Opening pressure is worthwhile.
          Approach to ED headache

            History and Physical
       Review DDx and serious causes

Diagnosis identified         Concern for
   Benign cause             serious cause

       Treat                Plain CT head

                           Lumbar Puncture

                           CT           CT
                       venography   angiography
        Headache motherhood
   Chronic migrainers with toradol allergies get badness
    to. Be diligent.
   Approach headache like chest pain - good hx/pe and
    directed investigations to exclude badness.
   Have a ddx of badness and “run the list” with every
   Headache is more than migraine and SAH.
   Anyone can thing to order a CT head. A good
    clinician will pick up the less common but serious
   Older patient with no hx migraine: be cautious.
           Miscellaneous pearls

 What INR before LP?
 What platelet level is c/I to LP?
 35yo healthy male, collapsed, Vfib arrest,
  bystander cpr and defib at 5min, persistent
  coma, diagnosis?
 How to decrease post LP headache?
    – Needle size, pokes, non-cutting, stylet
    – Bedrest and IVF not helpful

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