headache 1001
TRANSCRIPT
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8/14/2019 Headache 1001
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Andy Jagoda, MD
Critical Questions in the EDCritical Questions in the EDManagement of HAManagement of HA
What is first line therapy for the treatment of HA
Does a response to headache pain therapypredict the underlying etiology of the HA?
Which patients with an acute headache requireneuroimaging in the ED?
What are the indications for a lumbar puncturein the patient with an acute headache?
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Andy Jagoda, MD
ED VisitED Visit Past history of migraines with aura:
scintillating lights followed by nauseaand right temporal throbbing headache
Present headache was different inintensity, onset, and location
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Andy Jagoda, MD
ED Visit #1ED Visit #1 PMH: Migranes Q-month
MEDS: Naprosyn PRN; BCP
LNMP: 7 Days prior
SH: No Tob / ETOH / drugs
FH: Mother - Migraines
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Andy Jagoda, MD
ED VisitED Visit Appearance: 32 year old female, alert,
cooperative but appeared uncomfortable,holding the top of her head
VSS: 118/76, 72, 16, 98.6
Head: Atraumatic Neck: Nontender, supple Heart: Regular, no murmurs, no clicks Lungs: Clear Abdomen: Soft, nontender
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ED VisitED Visit MS: Alert; Oriented X 3 PUPILS: Not documented CN: Intact GAIT: Normal
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A diagnosis of migraine was made. Which of the followingA diagnosis of migraine was made. Which of the followingis your drug of choice in treating acute severe migraine?is your drug of choice in treating acute severe migraine?
Opioid (Meperidine or morphine) Nonsteroidal (Ketorolac) Sumitriptan
DHE Prochlorperazine
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Andy Jagoda, MD
Migraine: PathophysiologyMigraine: Pathophysiology Common pathway for headache pain regardless of
the underlying etiology Headache pain is transmitted via the trigeminal nerve Trigeminovascular axon stimulation results in a
release of neurogenic peptides stored in the afferentC fibers innervatin cephalic blood vessels
Vasoactive neuropeptides mediate an inflammatorycascade, neurogenic inflammation
Vasodilatation and enhanced permeability of plasmaproteins result in a perivascular reaction
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8/14/2019 Headache 1001
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Andy Jagoda, MD
Migraine: PathophysiologyMigraine: Pathophysiology Serotonin receptors modulate neurogenic
peptide release and cause vasoconstriction Goal of migraine therapy is to abort the
neurogenic peptide release
5-HT1c receptor is most involved in mediatingheadache
Drugs working at the 5-HT receptor are thepreferred therapy for headache
Narcotics cause initial pain relief but result invasodilatation with a high incidence of rebound
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8/14/2019 Headache 1001
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Andy Jagoda, MD
Migraine TherapyMigraine Therapy First line agents: Prochlorperazine 5-10 mg IV
Metoclopramide Chlorpromazine
Second line agents: DHE .5-1 mg IM / IV or
sumatriptan 6 mg SQ Third line agent: Ketorolac Fourth line agent: Butorphanol 1 mg
intranasally
Fifth line agent: OpioidsCanadian Headache Society. Guidelines for the diagnosis and management of Migraine in clinical practice. Can Med Assoc J 1997; 156:1273-1287
US Headache Consortium. www.aan.com/public/practice guidelines
http://www.aan.com/public/practicehttp://www.aan.com/public/practice -
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ED VisitED Visit Diagnosis: Migraine Treatment: Prochlorperazine Disposition: Headache resolved
HOME
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Andy Jagoda, MD
Does response to therapy predict theDoes response to therapy predict theetiology of an acute severe headache?etiology of an acute severe headache?
All headache pain is mediated by serotonin receptors Case series / case reports (Class III evidence) Seymour. Am J Emerg Med 1995. 3 patients treated with
ketorolac or prochlorperazine with resolution of headache /
Discharged / All with catestrophic outcomes Gross. Headache 1995. 3 cases of meningitis with resolutionof pain with DHE and metoclopramide
Pain response can not be used as an indicator or theunderlying etiology of an acute headache.
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Andy Jagoda, MD
Should this patient have receivedShould this patient have receiveda head CT?a head CT?
Infection CNS mass lesion
Tumor, IIH, Hydrocephalus Collagen vascular disease
Temporal arteritis, vasculitis Ophthamologic etiologies
Glaucoma, optic neuritis Metabolic abnormalities Toxins Pregnancy related
Eclampsia, dural sinus thrombosis
CNS vascular event Subdural, epidural, SAH
Primary headache disorder
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Andy Jagoda, MD
Which patients with acute headacheWhich patients with acute headacherequire neuroimaging in the ED?require neuroimaging in the ED?
Neuroimaging is obtained to assess for treatable lesions: SAH, CVT, tumors,hydrocephalus (Less tangible: Patient reassurance)
Abnormal neuro exam increases the liklihoodof a positive CT 3 times (95% CI 2.3-4) Normal neuro exam is not predictive Location, vomiting, headache waking patient
up, worsening with valsalva are not predictive
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Andy Jagoda, MD
Which patients with acute headacheWhich patients with acute headacherequire neuroimaging in the ED?require neuroimaging in the ED?
Patients presenting with an acute HA and anabnormal neurologic exam should have anemergent head CT
Patients presenting with a sudden severe HA
should have an emergent head CT HIV patients with a new type of headacheshould have an urgent head CT
Patients over the age of 50 with a new type of headache should have an urgent neuroimagingstudy
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Andy Jagoda, MD
Should this patient have had aShould this patient have had ahead CT?head CT?
History: HA was sudden and severe in onset HA was different from past headaches
Physical: No neurologic exam documented:
In the HA patient, the neuro exam focuses onpupil, fundoscopy, and cranial nerves III, IV, VI
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Andy Jagoda, MD
ED Visit #2ED Visit #2
Patient returned 24 hours later withworsening of her headache
Positive findings on the physicalexamination: Papilledema Left 6th cranial nerve palsy on far lateral
gaze A noncontrast head CT was obtained
and was normal
h h i di i f i
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Andy Jagoda, MD
What are the indications for LP inWhat are the indications for LP inacute HA?acute HA?
Suspected SAH in a patient with a normal headCT CT is 90 98% sensitive for acute SAH Sensitivity decreases over time
Suspected meningitis LP without CT in patients with normal neuro examincluding normal mental status and normalfundoscopic exam
Suspected idiopathic intracranial hypertension Headache with papilledema Normal CT
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Andy Jagoda, MD
ED Visit #2ED Visit #2
Lumbar puncture: Opening pressure 280mm Hg; No cells; Normal protein andglucose Normal opening pressure < 160 mm Hg
Diagnosis of idiopathic intracranialpressure was made
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Andy Jagoda, MD
Idiopathic Intracranial Hypertension:Idiopathic Intracranial Hypertension:(Benign Intracranial Htn, Pseudotumor Cerebri)(Benign Intracranial Htn, Pseudotumor Cerebri)
Syndrome defined by signs and symptoms of high ICP without apparent intracranial mass
50% have an identifiable underlying etiology Altered absorption of CSF at the arachnoid
villus Elevated pressure within the sagittal sinus Increased resistance to drainage of CSF within the
villus
Idi hi I i l H iIdi thi I t i l H t i
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Andy Jagoda, MD
Idiopathic Intracranial Hypertension:Idiopathic Intracranial Hypertension:Physical FindingsPhysical Findings
Papilledema 100% Headache 94% Visual disturbance 80%
Transient visual obscuration 68% VI CN palsy (False localizing) 38% Decreased visual acuity 30% Blindness 10%
Giuseffi. Neurology 1991; 41:239-244
Idi thi I t i lIdi thi I t i l
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Idiopathic IntracranialIdiopathic IntracranialHypertension: TreatmentHypertension: Treatment
Correct predisposing factors Serial lumbar punctures Acetazolamide, 1-4 gms / day
Corticosteriods, 40-60 mg / day Surgery
Optic nerve sheath decompression
Lumboperitoneal shuntRadhakrishnan. Mayo Clin Pro 1994; 69:169-180
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ConclusionsConclusions Errors in management
No fundoscopic exam: Opthalmoscope was notworking
No CT: symptoms resolved and CT backed-up Lessons learned
Patients with headache require a comprehensiveneurologic exam
First line therapy for headache are drugs that workat serotonin receptors but response to therapy doesnot predict etiology
Patients with sudden severe headache require a CT;if negative followed by an lumbar puncture