Headache Algorithm

  • Post category:Neurology

Critical / Killer Headaches

General Approach:

  • Emergency department evaluation relies on excluding life-threatening causes of Headache (killers), specifically SAH and meningitis
  • Then consider other serious causes of headache that can debilitate the patient (the maimers)
  • When these have been excluded, we can then diagnose primary headache syndromes.

Testing

  • Question 1: Does this patient need a CT? (ACEP Guidelines Ann Emerg Med 2008;52:407)
    • Neuro exam-new abnormal findings (focal deficit, Altered mental status) (ACEP Level B)
    • New, sudden, severe Headache
    • HIV + with new Headache
    • Patients older than 50 with new type of Headache (ACEP Level C)
  • Question 2: Does this patient need an Lumbar Punction?
    • R/O SAH: Sudden-onset, severe headache + CT Head (-) → LP to exclude SAH (ACEP Level B)
    • Concern for Meningits (Cell count, OP, gram stain)
    • Concern for Idiopathic Intracranial Hypertension (Opening pressure)

1. Subarachnoid Hemorrhage (SAH)

Clinical presentation

  • Onset: sudden (thunderclap)
  • Maximum severity is reached instantaneously in 50% and within 1-5 minutes in 19% of patients with SAH. (J Neurol Neurosurg Psychiatry 1998;65:791-3)
  • Sudden severe Headache: (Lancet 1994:344:590-3)
    • SAH in 25%
    • Benign thunderclap headache in 40%
    • Remaining will have another primary or secondary HA
  • Therefore, all patients with sudden severe Headache need to be worked-up for SAH
  • Other qualities
    • Quality: qualitatively different headache from previous
    • Severity: +/- worst headache of life
    • Associated sx: Nausea / Vomitus, syncope, Altered Level of Consciousness, diplopia
    • Risk factors: HTN, EtOH (alcohol), smoking, Family History
  • Physical Examination:
    • Focal neuro deficit
    • Meningismus (70%)
    • Retinal/vitreal bleed
  • Clinical Presentation of SAH lies on a spectrum (Emerg Med Clin N Am 2003;21:73-87)
    • The classic (middle of the spectrum) presentation is that of sudden onset and distinct HA, worst of their life associated with neck pain, Nausea / Vomitus
    • On the extreme end, they can present with focal neuro deficit and Altered Level of Consciousness / Altered mental status
    • On the subtle end 1/3 present with only Headache without neuro deficits, and are likely to be misdiagnosed

SAH Red Flags

□ Sudden onset
□ Maximal at onset
□ Different from previous Headaches

Work-up

  • CT Head
    • CT sensitivity is extremely high early but rapidly diminishes with time
    • Misses about 2% of SAH within 12 hours and 7% by 24 hours
    • Therefore anyone with suspected SAH and normal CT requires an Lumbar Puncture
    • Journal Club (EM:RAP 3/14; 12/13)
      • CT within 6 hours (BMJ 2011;343:d4277)
        • Overall CT sensitivity is 93% (Sensitivity after 6h is 86%)
        • CT within 6 hours of HA onset → Sensitivity 100%, Specificity 100%, NPV 100%
        • Prospective cohort study
      • CT within 6 hours (Stroke 2012;43:2115)
        • CT within6 hours of HA onset → Sensitivity 100% with 2 caveats
        • Caveat1: <6h rule only applies to pts with HA (not neck pain)
        • Caveat2: Experienced neuroradiologists needed to interpret CT
      • Editorial (Stroke 2012;43:2031)
        • … we believe that practice should change. Neurologically intact patients who present with thunderclap headache and undergo CT scan within 6 hours of symptom onset no longer need an LP to exclude SAH if the CT scan is negative.”
  • Lumbar Puncture
    • Timing: Results depends on timing of HA (J Emerg Med 2002;23:67-74)
    • <12h:
      • Xanthochromia may/may not be present; large RBCs should be present
      • Incompletely clearing RBCs ?? (if suspected traumatic tap → repeat at different interspace)
    • 12h-2weeks:
      • Xanthochromia highly suggestive of SAH; large RBC +/- present 2weeks: Both may be absent.

Treatment (See ICH Algorithm)

  • ABC/Resus/Airway
    • Treat like ICH patient
    • Intubate if Altered mental status, not protecting airway → document good neurologic exam prior
  • Emergent Neurosurgical consultation
  • Vasospasm prevention
    • Nimodipine 60 mg po/NG q4h x 21d
Intracranial hemorrhages
Intracranial hemorrhages

2. Meningitis

Read Also : Diagnosing and Treating Meningitis

Etiology

  • Bacterial
    • Meningococcus (Neisseria meningitidis)
    • Streptococcus pneumoniae
    • Haemophilus influenzae
    • Listeria monocytogenes
  • Viral
    • Enteroviruses (≈ 85% of meningitis)
    • Arboviruses (West Nile, etc…)
    • Herpes viruses
    • Others (Mumps, LCMV etc…)

Meningitis symptoms

Fever 85%
Stiff neck 70%
Altered mental status 67%
HeadAche 50%
Focal neuro 23%
Rash 22%
Pathogenesis of Meningitis
Pathogenesis of Meningitis

Clinical Presentation

  • Classic triad
    • All 3: fever, neck stiffness and Altered mental status present in only 44%
      • Absence of all 3 virtually eliminates a diagnosis of meningitis
    • 95% patients had 2 out of 4 of: (NEJM 2004;351:1849-59)
      • Headache
      • Fever
      • Neck stiffness
      • AMS
  • Meningismus
    • Jolt accentuation (JAMA 1999;282(2):175-81)
      • Procedure: Ask patient to turn head right/left, 2-3 rotations per second
      • Positive test: Worsening of headache
      • Absence of jolt accentuation has a sensitivity of 100% for ruling out meningitis
    • Kernig’s sign (inability to straighten the leg when the hip is flexed to 90 degrees)
    • Brudzinski’s sign (forced flexion of the neck elicits a reflex flexion of the hips)
      • Kernig/Brudzinski both have very low sensitivity ≈ 5%
  • Other symptoms:
    • Abnormal neurologic exam
    • Leg pain, refusal to walk (Meningococcus)
    • Photophobia, N/V, lethargy
    • Petechial rash (Meningococcus)

Bottom Line

  • Triad: Absence of all of the triad (fever, Altered mental status, neck stiffness) → eliminates a diagnosis of meningitis
  • Meningismus: Kernig/Brudzinski are not helpful in ruling out meningitis (low sensitivity)
    • If they are positive → can rule in meningitis (high specificity)
  • Jolt accentuation negative essentially eliminates a diagnosis of meningitis

Work-up

  • Lumbar puncture
    • Tube 1&4: Cell count and diff
    • Tube 2: glucose and protein
    • Tube 3: Gram stain, culture, HSV PCR
  • Do I need a CT before LP? (2 studies say not always) MAY omit if:
    • Age<60, no immunocompromised/CNS disease/seizure within 1 week and has a nonfocal neuro exam (NEJM 2001;345:1727-1733)
    • Absence of AMS, focal neuro exam, papilledema and favorable clinical impression by doctor (Ann Int Med 1999;159:2681-2685)
  • CSF analysis (predictive of bacterial meningitis) (JAMA. 1989;262(19):2700)
    • ↑ WBC > 2000
      • Multiple studies show bacterial meningitis incidence of 5-19% in patients with CSF WBC < 100!
      • No single variable can r/o meningitis
    • Neutrophil > 1180
    • CSF glucose <34mg/dL
    • CSF protein > 220 mg/dL
    • Gram stain +
Findings in cerebrospinal fluid in different causes of meningitis
Findings in cerebrospinal fluid in different causes of meningitis

Treatment

  • Antibiotics
    • Timing
      • Administer as soon as possible-before Lumbar puncture
      • Multiple studies have shown an association between time of antibiotic administration and poor outcome (greater than 4-6 hours)
    • Empiric antibiotics
      • Ceftriaxone 2gm IV or Cefotaxime 2gm IV immediately +
      • Vancomycin 1gm IV (15-20mg/kg) +
      • Ampicillin 2gm IV (adults > 50yo)
  • Dexamethasone
    • Dose: 10mg IV q 6 hour x 4 days; start 15 minutes prior to, or with first dose of antibiotics
    • Journal club (Cochrane Database 2010;9:CD00405)
      • No mortality benefit but helps prevent hearing loss and short-term neurologic sequelae
      • Benefits seen mostly in patients with S. pneumoniae
  • Acyclovir
    • Dose: 10mg/kg q 8h for HSV
Algorithm for Management of Patient With Suspected Community-Acquired Bacterial Meningitis
Algorithm for Management of Patient With Suspected Community-Acquired Bacterial Meningitis

Special Case: HA and HIV (CD4 < 200?)

  • CT w/wo contrast:
    • R/O mass lesion, toxo, lymphoma
  • Serum
    • If serum crypto Ag(-) → likely do not need Lumbar puncture (patient very unlikely to have crypto infection)
  • Lumbar puncture
    • Use: r/o cryptococcal meningitis
    • India ink: round encapsulated yeast (75% patients)
    • CSF crypto Ag: Sensitivity 93 to 100% and specificities 93 to 98%
    • CSF culture: definitive diagnosis
  • Treatment: Amphotericin + Fluconazole

3. Cerebral Venous Thrombosis

General

  • CVT = DVT of the brain = blood clots in brain (venous)
  • CVT = Dural sinus thrombosis, (superior, sagittal, inferior) sinus thrombosis, cortical vein thrombosis

Risk factors

  • Thrombophilia/Hypercoagulable state
  • Pregnancy/Puerperium
  • Medications (Oral contraceptive pills, Doxycycline)
  • Cancer/Inflammatory/Hematologic disease

Clinical

  • Presentation spectrum: Headache → Seizure → Stroke
  • Headache
    • Headache type: No characteristic history, multiple types of headache symptoms
    • Physical Exam – Papilledema present in most cases (fundoscopic, pan-optic or US)
  • Seizure
  • Stroke
    • Bilateral neuro deficit
    • Non-arterial distribution

Diagnosis

  • D-dimer – low sensitivity, not useful
  • CT Head – normal in 30% of cases
    • Highly suggestive:
      • Dense triangle sign (thrombosed sup sag sinus posteriorly)
      • Cord sign (thrombosed cortical vein)
      • Bilateral edema/ICH
    • Diagnostic (CT w/ contrast-venogram): Empty delta sign (flow defect in sup sag sinus)
  • MR Brain with venography (study of choice)

Complications

Treatment

  • Neurosurgical consultation
  • Anticoagulation
    • Heparin safe, even with hemorrhagic infarcts
  • Journal Club-Heparin anticoagulation
    • Cochrane Review of Heparin anticoagulation (Cochrane Database Syst Rev 2001;(4))
      • RR of death 0.33 (95% CI 0.08-1.21) → not statistically significant
      • Conclusion: CVT is a rare and fatal disease and no other treatment exists
    • ISCVT-International Study on Cerebral vein and Dural Venous Thrombosis (Stroke 2004;35:664-70)
      • Prospective observational study 624 patients → 80% received anticoagulation
      • 6.8% mortality

Emergent Diagnoses / Emergent Causes of Headache

1. Brain Mass Lesion

Etiology

  • Tumor, abscess, chronic subdural hematoma (SDH)

Clinical Presentation

  • Progressive, exertional headache, morning headache
  • New onset seizure, nausea/vomiting
  • H/O HIV (cryptococcus, toxoplasmosis, lymphoma, and tuberculosis)
  • Physical Exam : Focal neuro exam, papilledema, aphasia
Brain tumours – clinical features
Brain tumours – clinical features

Work-up

  • CT Head w/wo contrast, MRI

Treatment

  • Neurosurgical consultation, steroids, ventriculostomy

Vasogenic edema

  • Etiology: tumor related disruption of BBB
  • Treatment:
    • Glucocorticoids – indicated in all patients with peri-tumor edema
    • Dexamethasone 10mg IV x 1 then 4mg IV q6h

HYDROCEPHALUS

  • Cause: CNS infection, hemorrhage, tumor
  • Types
    • Communicating hydrocephalus
      • Symmetric dilation of all 4 ventricles
      • Extraventricular obstruction or impaired CSF absorption, usually in neonates/infants;
      • Adult causes: pseudotumor cerebri
    • Non-communicating (Obstructive) hydrocephalus
      • Asymmetric dilation of ventricles
  • Treatment
    • Third Ventriculostomy – only effective for obstructive hydrocephalus
    • Shunt (VP-Shunt) – can be used to treat either cause of hydrocephalus

SHUNT COMPLICATIONS

  • Shunt Infection (Ventriculitis)
    • 5 to 15 percent of procedures, most occurring in first 6 months
    • Persistent fever → tap shunt
    • Antibiotics, shunt may need removal
  • Shunt mechanical failure (obstruction at the ventricular catheter)
    • CT: Hydrocephalus
  • Overdrainage
    • Presentation: neurological symptoms → postural headache and nausea
    • CT: Slit ventricle syndrome (small or slit-like ventricles)

2. Idiopathic Intracranial Hypertension (IIH)

General

  • AKA Idiopathic Intracranial Hypertension, Pseudotumor cerebri

Presentation

  • Obese, young female
  • Headache x weeks/months
  • Visual disturbances
  • Papilledema
    • Not all patients with IIH have papilledema

Diagnosis

  • Diagnostic criteria for IIH: (Neurology 2002;59:1492-95)
    • S/Sx of elevated intracranial pressure
    • Non focal neuro exam (except abducens nerve paresis)
    • Normal neuroimaging study (CT w/ con or MRI/MRV)
    • Increased CSF pressure (nonobese>200; obese>250 mm water)
    • No other cause of increased intracranial pressure (CNS tumor, encephalitis, right heart failure)
  • Vision loss secondary to papilledema is the only serious complication of IIH, is avoidable with appropriate treatment
  • MRI/MRV to exclude CVT

Treatment

  • Indications for treatment: Vision loss (emergent tx), headache (therapeutic)
  • Weight loss
  • Medications
    • Acetazolamide (carbonic anhydrase inhibitor) reduces CSF pressure
    • Topiramate (partial CAI) reduces CSF pressure
  • Surgical
    • VP Shunt (vision loss and HA refractory to treatment)
    • Optic nerve sheath fenestration
    • Venous stenting

3. Temporal Arteritis

Clinical Presentation

  • New headache
  • Temporal artery tender / decrease pulse
  • Jaw/tongue claudication
  • Vision change

Diagnosis (need 3/5)

  • Age >50
  • New headache
  • Temporal artery tender / decrease pulse
  • ESR > 50
  • Biopsy: vasculitis/granuloma

Treatment

  • No ischemic organ damage (eg, visual loss) → begin empiric prednisone 40-60mg if medium or high suspicion until ESR or biopsy results return.
  • Ischemic organ damage (AION) – Vision loss → Methylprednisolone 1000mg IV daily x 3 days

4. Acute Glaucoma

Clinical Presentation

  • Eye pain, Nausea / Vomitus, blurred vision
  • Conjunctival hyperemia
  • Corneal edema, mid-dilated, non reactive pupil
  • Elevated IOP (>20)

Treatment

  • Emergent Ophthalmology consultation
  • Decrease IOP (intra ocular pressure)
    • 0.5% timolol maleate (Timoptic)
    • 1% apraclonidine (Iopidine)
    • 2% pilocarpine (Isopto Carpine)
    • Acetazolamide 500mg IV then 500mg po

5. Cervical Artery Dissection

General

  • Cervical artery dissection = carotid artery dissection + vertebral artery dissection
  • Common cause of pediatric strokes (1 in 5)
  • Cause:
    • Major trauma: penetrating or blunt
    • Minor trauma: coughing, whiplash, cervical seatbelt signs, rotational routine neck movement, chiropractor manipulation

Presentation

  • Stroke syndromes:
    • Carotid artery dissection: MCA (Middle cerebral artery), anterior circulation stroke syndromes (hemiplegia)
    • Vertebral artery dissection: posterior fossa symptoms (ataxia, vertigo, dysmetria)
    • Wallenberg Syndrome: ipsilateral facial numbness, contalateral body numbness
    • Horner’s Syndrome: miosis, ptosis, anhydrosis (vertebral & carotid artery dissection)
  • Facial (carotid), neck (vertebral) pain
  • SAH like acute onset
  • Cranial nerve abnormalities

Diagnosis

  • Carotid duplex – poor sensitivity
  • CT Angiography
  • MRI/MRA
  • Angiography

Treatment

  • Neurological/Neurosurgery consultation
  • Anticoagulation
    • Contraindicated if concomitant cerebral hemorrhage
    • Used to decrease risk of thrombus formation and embolization

6. Carbon Monoxide Poisoning

History and Physical

  • Exposure ?
  • Multiple patients / similar location /similar symptoms
  • Headache with N/V/ syncope
  • Altered mental status
  • Cherry-red mucous membranes
  • Cerebellar ataxia

Action

  • COHb level
  • O2 (100% NRM vs HBO)

Urgent Headaches

  • Acute Sinusitis
  • Obstructive hydrocephalus
  • Benign Exertional HA
  • Post-Traumatic
  • Drug/Food Related
  • Cranial Neuralgias

Primary Headaches

1. Migraine Headache

Presentation

  • Common migraine
    • Severe, throbbing, unilateral HA
    • Photo/Phonophobia
    • Hours to days
  • Classic migraine
    • Preceded by aura
    • +/- GI distress
  • POUNDing mnemonic
    • Pulsating, duration 4-72 hOurs, Unilateral, Nausea, Disabling
    • Highly predictive of migraine headache (JAMA 2006;296:1274-83)

Treatment

  • IV Dopamine antagonist (Compazine, Reglan)
  • IVF (Normal Saline)
  • Opiates
  • Triptans/NSAIDS
  • Dexamethasone

2. Cluster Headache

Presentation

  • Middle aged men
  • Sudden onset Headache
  • Unilateral blur vision / nasal congest / lacrimate / salivate / sweat
  • Lasts hours, recur same time of day
  • Precipitated by exertion / stress

Treatment

  • O2
  • Symptomatic relief
  • Intranasal lidocaine
  • Neurology referral

3. Tension Headache

Presentation

  • Frontal/occipital/band-like
  • No preceding event

Treatment

  • Symptomatic relief (NSAIDS, Tylenol)