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  • 1 1 1
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  • 5 6 6
  • 2 2 2
  • Schematic axial projection of the cavernous sinus and its venous anastomoses.
  • Coronal view of the cavernous sinus. Cranial nerve III is the most superiorly situated nerve in the cavernous sinus. Cranial nerves III, IV, and the first two divisions of the trigeminal nerve, V1 and V2, travel in their respective nerve sheaths laterally in the cavernous sinus. Cranial nerve VI travels more medially within the cavernous sinus adjacent to the cavernous carotid artery. PG = Pituitary gland; S = sphenoid sinus; C = cavernous internal carotid artery.

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  • Acute Neurological Emergencies: Headache
  • Brad Bunney, MD Associate Professor Dept of Emergency Medicine University of Illinois College of Medicine Chicago, IL
  • Michael Gerardi, MD, FAAP, FACEP Vice-Chairman, Department of Emergency Medicine Morristown Memorial Hospital Morristown, New Jersey Nina T. Gentile, MD Associate Professor Division of Emergency Medicine Temple University School of Medicine Philadelphia, PA Daniel G. Murphy, MD, FACEP Vice Chair & Medical Director Maimonides Medical Center Brooklyn, New York
  • The Case
    • One hour prior to ED presentation, a 42 year old man was jogging and “hit” by the worst headache of his life. It was associated with some nausea and the feeling as if he was going to pass out. He rested for 30 minutes but the headache persisted as a diffuse, throbbing pain radiating to the base of his skull.
    • EMS was called. The patient felt as if he could not concentrate, there was no confusion, nor was there any other focal neurologic complaint.
    • There was no past medical history, no medications, no family history, and no significant use of alcohol, tobacco or other drugs.
    The Case (Continued)
  • If a patient presented with the worst headache of his life, what is the work-up that should be initiated? a. Non-contrast CT b. LP after neg. CT c. LP without CT d. CT, LP, and angiography
    • What is the differential of a “thunderclap headache”?
    • What is the sensitivity of neuroimaging in subarachnoid hemorrhage (SAH)?
    • What constitutes a “positive” lumbar puncture in SAH and when should it be performed?
    • Do patients with suspected SAH who have a negative CT and lumbar puncture require additional imaging to “rule-out” expanded but unruptured aneurysm?
    Objectives
  • Headache
    • 1 of 10 top presenting complaints
    • 1 to 2% of visits to ED
    • 18 million outpatient visits
    • 638 million days of work lost per year
    • 78% of women and 64% of men had experienced at least one in the prior year
    • 36% of women and 19% men suffer from recurrent headaches
  • Headache
    • Most have primary headache disorders
      • migraine
      • tension
    • Only a few have treatable secondary causes that threaten life, limb, brain such as subarachnoid hemorrhage
      • 1 - 4 % of headache visits
  • “Worst” Headache
    • Normal exam: 12- 33% SAH
    • Abnormal exam: 25% SAH
    • Initial hemorrhage may be fatal
    • Early definitive surgery improves outcomes
    • Patients with greatest likelihood of benefiting from surgery are most likely to receive incorrect diagnosis
  • Physicians Consistently Misdiagnose SAH
    • 1. Failure to appreciate spectrum of clinical presentation
    • 2. Failure to understand limitations of CT
    • 3. Failure to perform and correctly interpret the results of LP
  • ED Goals in Headache Patients
    • 1. Differentiate life-threatening from benign
    • 2. Initiate prompt treatment
    • 3. Provide prompt pain relief
    • 4. Prevent drug seeking and refer
    • 5. Minimize resource utilization in ED
    • 6. Optimize patient use of ED
    • 7. Increase pre-ED treatment and reduce ED use
  • Medical Conditions That Present With Headache
    • Pheochromocytoma
    • Hyperthyroidism
    • SLE
    • Giant Cell Arteritis
    • Fibromyalgia
  • Types of Headaches in the ED
    • Final Diagnosis Percentage
    • Infection - not intracranial 39.3
    • Tension HA 19.3
    • Miscellaneous 14.9
    • Post-traumatic 9.3
    • Hypertension related 4.8
    • Vascular (Migraine) 4.5
    • No diagnosis 6.0
    • SAH 0.9
    • Meningitis 0.6
  • Causes of Headache That Require Specific Therapy
    • Subarachnoid hemorrhage
    • Meningitis
    • Encephalitis
    • Cervicocranial-artery dissection
    • Temporal arteritis
    • Acute angle-closure glaucoma
    • Hypertensive emergency
  • Causes of Headache That Require Specific Therapy
    • Carbon Monoxide poisoning
    • Pseudotumor cerebri
    • Cerebral venous and dural sinus thrombosis
    • Acute stroke (hemorrhagic or ischemic)
    • Mass Lesion
      • tumor
      • abscess intracranial
      • hematoma
      • parameningeal infection
  • Headache Danger Signals
    • Onset
      • after 40 years
      • new or different headache
      • subacute HA that worsens
      • exertion, sex, coughing, straining
    • Worst ever experienced
  • Headache Danger Signals: Associated With Neurologic Change
    • Memory impairment
    • Ataxia
    • Drowsiness
    • Sensory loss
    • Signs of meningeal irritation
  • Headache Danger Signals: Associated With Neurologic Change
    • Progressive visual or neurologic change
    • Confusion
    • Weakness
    • Loss of coordination
    • Asymmetry of pupils, DTRs
  • Headache Danger Signals: Abnormal Medical Evaluation
    • Fever
    • Chronic malaise
    • Arthralgia
    • HTN
    • Myalgia
    • Wt loss
    • Tender, poorly pulsatile temporal arteries
  • Subarachnoid Hemorrhage
    • Incidence of 16 /100,000
      • about 33,600 cases per year
      • 54% secondary to ruptured aneurysm
    • Without treatment, 40% of aneurysm pts. have recurrent bleeding
    • Aneurysm pt who survives initial rupture and is treated conservatively:
      • 50% survival at one year
  • Time of Death Following SAH by Cause
  • Current Problems in Management of Subarachnoid Hemorrhage
    • Errors and delays in diagnosis
    • Treatment of acute effects
    • Prevention of recurrent hemorrhage
    • Prevention or treatment of vasospasm or cerebral ischemia
  • Classic Symptoms of Subarachnoid Hemorrhage
    • Sudden, unusually severe or “thunderclap” headache
    • Loss of consciousness
    • Pain in neck, back, eye or face
    • Nausea, vomiting, photophobia, phonophobia
  • Classic Signs of Subarachnoid Hemorrhage
    • Abnormal vital signs
      • Respiratory changes, hypertension, cardiac arrhythmias
    • Meningismus
    • Focal neurologic signs may be present
      • III nerve palsy – IC/PCA aneurysm
      • Paraparesis – ACA aneurysm
      • Hemiparesis, aphasia – MCA aneurysm
    • Ocular hemorrhages
  • Subarachnoid Hemorrhage
    • Onset: Acute
    • Location: Global
    • Ass Sx: N,V, meningismus, focal
    • Pain: Worst ever
    • Duration: Brief
    • Prior Hx: No
    • Dx tests: CT 80-90%
    • Phys ex: Focal signs, LOC, meningismus
  • Subarachnoid Hemorrhage
    • Warning leaks in 50%
    • CT misses up to 10% small leaks
    • Suspect if:
      • > 35 years
      • no previous HA
      • no fading of HA
      • came on with exertion
      • altered LOC or neuro deficits
      • stiff neck
  • Subarachnoid Hemorrhage: Neurologic Findings
    • Sudden HA without localizing findings
    • Altered mentation
      • Confusion, lethargy
    • Bilateral extensor plantar reflex
    • Unusual to find focal deficits
  • Causes of Non-Traumatic Subarachnoid Hemorrhage
    • “Berry” aneurysms
    • AVM
    • Cerebral angiomas
    • Mycotic aneurysm
    • Extension from parenchymatous hemorrhage
    • Anticoagulation therapy
  • Causes of Non-Traumatic Subarachnoid Hemorrhage
    • Systemic bleeding diathesis
    • Hemorrhagic encephalitis
    • Hemorrhagic cerebral vasculitis
    • Hemorrhage into CNS tumors or metastases
    • Unknown
  • Warning Headache
    • 20 - 50% patients with SAH have HA days or weeks before index episode
      • unusually severe
      • distinct
    • “Thunderclap” headache
      • Day and Raskin 1996
      • intense, acute, peak intensity at onset
      • develop in seconds
      • maximal intensity in minutes
      • lasts hours to days
  • “Thunderclap” Headache
    • 25% associated with SAH
    • “Warning” headache
      • followed by SAH in 5% to 60%
    • Expansion or dissection of unruptured aneurysm
    • Cerebral venous thrombosis
    • Exertional / coital headache
    • 217 patients from 4 institutions
    • 54 (25%) were initially misdiagnosed
    • 121 patients initially presented in good clinical condition
    • 46 (38%) were initially misdiagnosed
    • Stroke 1996;27:1558-63
    Misdiagnosis of SAH
    • Outcome of Patients with Good Initial Presentation in Misdiagnosed and Correctly Diagnosed Patients With SAH
    • Outcome Misdiagnosis (n=45) Correct Diagnosis (n=75)
    • Excellent/good 24 (53)* 68 (91)*
    • Fair 5 (11) 4 ( 5)
    • Poor/vegetative/dead 16 (36)* 3 ( 4)*
    • Values are number (%) in each clinical grade category.
    • P<.001
    • Stroke 1996;27:1558-63
    Misdiagnosis of SAH
  • Rebleeds and Deteriorations Before Treatment in Misdiagnosed and Correctly Diagnosed Patients With SAH Misdiagnosis (n=54) Correct Diagnosis (n=163) Rebleeds 21* 4 Deteriorations 5 0 Total 26 4 *12/21 of misdiagnosed and 3/4 of correctly diagnosed patients rebled within 5 days of presentation. Stroke 1996;27:1558-63 Misdiagnosis of SAH
  • SAH…But not “Classic”
    • Roughly half have minor bleeding with atypical features
    • Nonstrenuous activities (34%)
    • Sleep (12%)
    • HA in any location (localized, generalized, mild)
    • May be relieved by non-narcotic analgesics
    • Diagnosed as migraine, tension-type, sinusitis
  • SAH: Most patients have...
    • Abrupt onset of severe, unique headache, or neck pain
    • Abnormal findings on neurologic examination
    • Subtle meningismus or ocular findings
  • International Headache Society
    • A first episode of severe headache cannot be classified as migraine:
      • more than 4 episodes
    • nor as tension-type headache:
      • more than 9 episodes
    • First or worst headache requires evaluation
      • as do qualitatively different headaches
  • Can a CT Scan Safely “Rule Out” SAH?
    • First diagnostic study
    • Thin cuts ( 3 mm) through base of brain
    • Blood on CT function of Hgb
      • Hgb < 10: blood isodense
    • Sensitivity decreases over time from onset of symptoms
  •  
  • SAH CT Findings
    • High density hemorrhage injury
      • (1) Interhemospheric fissure
      • (2) Inferior frontal sulci
      • (3) Third ventricle
      • (4) Ambient cistern
      • (5)Sylvian fissure
  •  
  • SAH: CT Sensitivity Sames: Acad Emerg Med Jan 1996
    • 181 patients; aged 13-86 with SAH
      • Sensitivity 91.2%
        • pain < 24 hrs 93.1%
        • pain > 24 hrs 83.8%
    • LP 100% sensitive if neg CT
    • “A normal NGCT does not reliably exclude the need for LP”
  • SAH Diagnosis: LP Needed Sidman: Acad Emerg Med Sep 1996
    • 140 patients; aged 10-88
    • Sensitivity of CT
      • < 12 hrs 80/80 100%
      • > 12 hrs 49/60 81.7%
    • Overall, 11/140 had (-) CT and (+) LP
      • overall sensitivity 92.1%
  • Morgenstern LB, et al: Worst headache and SAH: Prospective, modern CT and spinal fluid analysis. Ann Emerg Med Sept 1998 .
    • 38,730 patients over 16 months, prospectively screened for “worst HA”
    • Blinded neuroradiologists
      • Neg CT LP
        • cell count x 2
        • visual and spectrophotometric detection of xanthochromia
        • CSF D-dimer assay
  • Morgenstern, et al: Ann Emerg Med 1998
    • 455 headaches & 107 “worst headache”
    • CT: 18 of 107 (17%): (+) SAH
    • (-) CT/ (+) SAH: Only 2 (2.5%)
      • (95% CI, 0.3%to 8.8%)
    • Modern CT is sufficient to exclude 98% of SAH in patients
  • Morgenstern, et al: Ann Emerg Med 1998 ( 107 “Worst HA’s)
    • Variables CT-/LP- CT+ CT-/LP+
    • Photophobia 45 28 50
    • Stiff neck 26 37 100
    • Nausea 65 36 100
    • Lethargy 17 40 50
    • Time < 24 h 58 75 50
    • Migraine 20 11 0
    • Headache 48 27 0
  • CT is Normal: Do LP?
    • Yes!
  • What about LP First?
    • Duffy et al; 1982: 55 patients who underwent LP as initial w/u
      • Condition deteriorated immediately in 7 patients
    • Hillman et al; 1986: 4 alert patients with SAH who deteriorated after lumbar puncture
    • Both studies:
      • clots on CT or a dilated pupil
  • Traumatic Taps
    • 20% of LPs
    • 0.5% and 6% has incidental intracranial aneurysm
    • Impression or “3-tube” method not reliable in detecting traumatic tap
    • Erythrocytes disseminate rapidly
    • Released Hgb oxyhemoglobin
    • xanthochromia bilirubin
  • Xanthochromia
    • Bilirubin, enzyme-dependent process, is diagnostically more reliable but:
      • takes up to 12 hours
    • Timing is important
    • CSF should be centrifuged and examined promptly so RBCs don’t undergo lysis in vitro, causing xanthochromia from oxyhemoglobin
  • Xanthochromia vs. Erythrocytes
    • Xanthochromia
      • primary criterion for SAH if neg CT
      • advocates: spectrophotometry
    • Erythrocytes
      • considered more accurate by some
      • used visual inspection which can miss discoloration in up to 50%
  • Timing the Tap
    • With spectrophotometry, and waiting 12 hours after onset of headache: very accurate
      • traumatic tap done earlier does not lead to xanthochromia and confusion
    • Waiting:
      • prolongation of ED stay
      • risk “ultra-early” rebleeding
  • Normal CT & Persistently Bloody CSF ???
    • Not prudent to delay LP
    • Without xanthochromia and clinical suspicion is high?
      • Vascular imaging
    • Xanthochromia present and clinical suspicion is high?
      • Vascular imaging
  • Differentiate Between Traumatic LP and SAH CSF characteristic Traumatic tap True SAH Color gets lighter with subsequent tubes yes no RBC count in first & last tube count decrease stay constant Clotting of blood in CSF yes no Xanthochromia in supernatant rare with RBC count less than 200,000 present withi4 hrs of SAH, max at 1 wk, persists for about 3 weeks
  • Thunderclap Headache: NL CT & NL LP Vascular Imaging?
    • Wijdicks et al; Lancet, 1988
      • Retrospective evaluation 71 patients
      • no SAH in 3.3 years f/u
      • Half dx’d with migraine or tension HA
    • Markus 1991; Linn 1994; Harling 1989
      • 117 patients
      • no SAH, no sudden deaths
  • Vasospasm
    • Occurs in 70% of patients with SAH
    • Appears after 3-4 days, peaks at 7-10 days, and resolves over 2-4 weeks
    • Can be localized or involve several arteries
    • Caused by factors released at time of bleeding that induce vasoconstriction and reduced blood flow
  • Calcium Channel Blocking Drugs
    • Drugs that limit transmembrane fluxes
      • Vascular smooth muscle contraction
      • Cell ischemia
      • Platelet aggregation
    • Selective cerebrovascular effects
    • Cross blood-brain barrier
    • Limited cardiovascular effects
  • Clinical Trials of Nimodipine
    • Nimodipine improves survival and functional recovery after SAH
    • Benefits are due to its antihypertensive and neuronal protective effects
    • The patient had labs drawn, was given 5mg of morphine and sent off to CT scan.
    • The CT scan revealed an acute SAH. The neurosurgeon ordered an angiogram which revealed an aneurysm.
    • The patient went to the OR that day and was release with a normal neurological status 4 days later.
    The Case (Continued)
    • Case #2
  • First ED Visit: Late Friday Night
    • 24 yo female with headache for 2 weeks, worse over the last 2 days
    • 104/76, 80, 18, 98.1F
    • Right frontal forehead, sharp, non-radiating, constant but waxing/waning, worse when she moved.
    • (+) nausea
    • (-) fever, photophobia, neck pain or visual changes
  • Past Medical/Social History
    • No recent trauma
    • Smoker 1 PPD
    • Social drinker
    • No hx of headaches, except for last 2 weeks
    • No allergies
    • No meds except ibuprofen and acetaminophen recently – not helpful
    • Worked as a part-time sales clerk
  • Exam: First Visit
    • Alert, oriented, looked well except for discomfort of headache
    • Face normal, Perrl, EOMI, fundi normal, TMs normal, mastoids non-tender, neck supple, motor neuro exam normal, normal gait, mental status normal
  • ED Therapy and Work Up
    • Prochlorperazine 10 mg, by vein Acetaminophen 325/Oxycodone 5, orally
    • CBC, Chem 7, UCG, CT Head without contrast
  • ED Diagnostic Results: Visit 1
    • WBC count 12.4K
    • CT head reviewed by ED attending and radiology resident as negative
  •  
  • ED Disposition: Visit 1
    • Patient’s pain responded to medications
    • Patient discharged with prescription for acetaminophen/butalbital/caffeine = Fioricet
  • Radiology Over-Read: Monday AM (2.5 days since 1 st ED visit)
    • Opacification of the right ethmoid and right sphenoid sinuses with expansion of the sphenoid septations toward the left.
    • No intracranial disease
  •  
  • ED Discrepancy Procedure
    • Patient was contacted by phone and informed of sinus problem on CT
    • Patient went to her PMD that afternoon
    • PMD discharged her with prescription for levofloxacin
  • 2 nd ED Visit: Tuesday Morning (3.5 days after 1 st ED visit)
    • New onset swelling and severe pain around left eye
    • Continued, worsening right-sided headache
    • Slept poorly, confused, hallucinating?
    • 100/80, 96, 18, 101.9F
  • Morning Exam: 2 nd Visit
    • Left peri-orbital edema, erythema, proptosis, chemosis, severe pain with EOMs. Left pupil reacted to light.
    • Ambulated in with normal gait. No obvious motor deficits.
    • Awake. Followed simple commands, but mildly confused, answering slowly or incorrectly, with difficulty concentrating.
    • (+) Nuchal rigidity
  • ED Therapy & Work Up
    • 2 grams ceftriaxone by vein after cultures
    • Repeat CT of brain and sinuses with contrast
    • LP
    • ID and ENT consults; vancomycin and metronidazole given by vein
    • Admitted to MICU
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  • Afternoon Exam: 2 nd Visit
    • Deteriorating mental status.
    • Mild left sided weakness left upper and left lower extremities.
  • ED Admitting Diagnoses
    • Orbital Cellulitis
    • Meningitis
    • Rule out Cavernous Sinus Thrombosis
  • Septic Dural Sinus Thrombosis Suppurative Intracranial Thrombophlebitis
    • Infected venous thrombosis of cortical veins or sinuses
    • From meningitis, subdural empyema, epidural abscess, infection in the skin of the face, paranasal sinuses, middle ear, mastoid, maxillary teeth or neck.
    • Iatrogenic cases have been associated with rhinoplasty, hip surgery and oral/dental surgery.
  • Non-Septic Dural Sinus Thrombosis
    • Dehydration from vomiting
    • Hypercoagulable states
    • Immunologic abnormalities, including the presence of circulating antiphospholipid antibodies
  • Septic Dural Sinus Thrombosis
    • Rare; 155 reported cases since 1940
    • Cavernous Sinus Thrombosis (CST) is the predominant subset (62%?)
    • Fulminant, aggressive disease: mortality CST =30%, superior sagittal sinus thrombosis =78%
    • Morbidity CST: 50% cranial nerve deficit; 17% visually impaired
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  • Infected Thrombus Pathogens
    • CST : Staphylococcus aureus, other gram-positive organisms, and anaerobes.
    • Lateral Sinus (otitis media and/or mastoid infection) Proteus species, Escherichia coli, S. aureus, and anaerobes.
    • Superior Sagittal Sinus (meningitis or air sinus infection) - Streptococcus pneumoniae, S. aureus, other streptococci, and Klebsiella.
  • ED Presentation: Superior Sagittal Sinus Thrombosis
    • Headache, nausea and vomiting, confusion, and focal or generalized seizures.
    • Rapid development of stupor and coma.
    • Weakness of the lower extremities with bilateral Babinski signs or hemiparesis is often present.
    • Headache and earache.
    • Gradinego's syndrome : otitis media, sixth nerve palsy, and retro-orbital or facial pain.
    • Sigmoid sinus and internal jugular vein thrombosis may present with neck pain.
    ED Presentation: Transverse Sinus Thrombosis
    • Sinusitis, midface infection for 5-10 days.
    • Fever, headache, malaise, retro-orbital pain and diplopia, which generally precede…..
    • Ptosis, proptosis, chemosis, eyelid edema, peri-orbital edema and extraocular dysmotility due to deficits of cranial nerves III, IV, and VI.
    • Hypo- or hyperesthesia of the ophthalmic and maxillary divisions of V, decreased corneal reflex. dilated, tortuous retinal veins and papilledema.
    • Meningeal signs: nuchal rigidity, Kernig and Brudzinski signs.
    ED Presentation: Cavernous Sinus Thrombosis
  • Diagnostic Studies
    • CBC, diff, cultures
    • Sinus Films, CT, MR, MR Venography, Venous phase cerebral angiogram
    • LP
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  • ED Management
    • Antibiotics : S aureus is the usual cause, broad-spectrum coverage for gram-positive, gram-negative, and anaerobic organisms also, pending cultures.
    • Drain primary source of infection, if feasible (eg, sphenoid sinusitis, facial abscess).
    • Anticoagulation in carefully selected cases of septic cavernous-sinus thrombosis, not other forms of septic dural-sinus thrombosis.
    • Urokinase or rtPA?
    • Corticosteroids?
  • Consults
    • ENT
    • Neurology
    • ID
    • Intensive Care
  • Outcome of Case
    • Day 1 : Seizure, worsening deficit, intubated
    • Day 2 : Heparinized, transient neuro improvement then relapse.
    • Day 5 : Sinuses drained
    • Day 6 : Brain dead
    • Day 19 : Demise
  • Acute Headache Questions ?