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Headache and Subarachnoid Hemorrhage Carly Thompson February 19, 2009 See Rob Halls’ presentation at the end of Carly’s.

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Presentation on theme: "Headache and Subarachnoid Hemorrhage Carly Thompson February 19, 2009 See Rob Halls’ presentation at the end of Carly’s."— Presentation transcript:

1 Headache and Subarachnoid Hemorrhage Carly Thompson February 19, 2009 See Rob Halls’ presentation at the end of Carly’s

2 Objectives Approach to headache in the ED Approach to headache in the ED Migraine Migraine –Focus on dx, tx Subarachnoid Hemorrhage Subarachnoid Hemorrhage Other causes of serious headache Other causes of serious headache

3 Headache Epidemiology 4% of ED visits 4% of ED visits Primary Headaches Primary Headaches –Migraine –Tension-Type –Cluster Secondary Secondary –All others! –1% of headaches are SAH!

4 Headache: Historical Features Occult Trauma Signs of abuse/neglect Anticoagulation SAH Sudden Onset Maximal soon after onset Different than previous MeningitisFever Neck stiffness Immune compromise Head/neck infection Temporal Arteritis Jaw claudication Temporal tenderness Visual symptoms Pre-eclampsiaPregnancyPost-partum Space- occupying lesion Progressive Hx of malignancy New onset >50yrs Worse in am, head down Neuro signs Cerebral Venous Thrombosis Bilateral neuro findings Proptosis Hypercoaguable state Recent sinusitis Pregnancy CO Toxicity Worse in am Others affected Environmental exposure

5 Question: Name 5 high risk historical features for Subarachnoid Hemorrhage. Name 5 high risk historical features for Subarachnoid Hemorrhage.

6 High Risk Features for SAH Thunderclap Thunderclap First or worst headache of my life First or worst headache of my life Altered mental status / Seizure Altered mental status / Seizure Headache with exertion / intercourse Headache with exertion / intercourse History of exercise History of exercise Location of pain: occipitonuchal Location of pain: occipitonuchal –PPV occipitonuchal headache for intracranial pathology is 16% Family history of SAH Family history of SAH –Up to 4x increased risk in 1 st and 2 nd degree relatives!

7 Question What is your differential for thunderclap headache? Name 3 (other than SAH). What is your differential for thunderclap headache? Name 3 (other than SAH). Thunderclap = sudden-onset, severe headache

8 Thunderclap Headache: Differential Diagnosis SAH SAH Carotid or vertebral artery dissections Carotid or vertebral artery dissections Venous sinus thrombosis Venous sinus thrombosis Pituitary apoplexy Pituitary apoplexy Hypertensive emergencies Hypertensive emergencies Cluster headache Cluster headache Cerebellar CVA Cerebellar CVA

9 High Risk Examination Findings Vital signs: htn, fever Vital signs: htn, fever Decreased, altered, fluctuating LOC Decreased, altered, fluctuating LOC Focal neurologic sign Focal neurologic sign Meningismus Meningismus Toxic appearance Toxic appearance Opthamalogic findings: papilledema, subhyaloid hemorrhage, retinal hemorrhages, decreased vision, ciliary flush, sluggish pupillary light response Opthamalogic findings: papilledema, subhyaloid hemorrhage, retinal hemorrhages, decreased vision, ciliary flush, sluggish pupillary light response Trauma Trauma Temporal artery findings Temporal artery findings Carotid bruit Carotid bruit Nausea and vomiting: Increased ICP, hemorrhage, ANAG Nausea and vomiting: Increased ICP, hemorrhage, ANAG Nasal discharge with sinus tenderness: sinusitis Nasal discharge with sinus tenderness: sinusitis

10 Question What is a subhyaloid hemorrhage and when do you see it? What is a subhyaloid hemorrhage and when do you see it?

11 Subhyaloid Hemorrhage Gravity-dependent venous hemorrhage between retina and vitreous membrane, convex at bottom, and flat at top when sitting 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 Highly suggestive of SAH: 11-33% of SAH cases Terson’s syndrome – rapid increase in ICP assoc. with hemorrhage – worse outcome Terson’s syndrome – rapid increase in ICP assoc. with hemorrhage – worse outcome

12 Low Risk Patient No change in headache pattern No change in headache pattern No new concerning historical features No new concerning historical features No focal neurologic symptoms or findings No focal neurologic symptoms or findings No imaging indicated! Meta-analysis: Meta-analysis: –2.4% of those with normal neuro exam have neurologic abnormalities on CT –0.4% of those with typical migraine symptoms

13 Question Which subsets of patients with headache require neuroimaging in the ED? Which subsets of patients with headache require neuroimaging in the ED? –Name 3 groups.

14 Neuroimaging Indications ACEP Clinical Policy (Ann Emerg Med 2008) Level B (1) Headache and new abnormal neuro findings PPPPPV 39% for intracranial pathology LLLLR 3.0 (2) Sudden-onset severe headache 11110-15% have serious pathology, often SAH (3) HIV patients with new headache HHHHeadache – 35% had mass lesion NNNNeurologic complaint – 24% focal lesion 1111 or more of predicted all focal lesions in a series of patients: –N–N–N–New seizure –D–D–D–Depressed / altered LOC –H–H–H–Headache different or > 3 days

15 Neuroimaging Level C Evidence Age >50 with new headache but normal exam, should be considered for urgent neuroimaging Age >50 with new headache but normal exam, should be considered for urgent neuroimaging  OR 3.3 of pathologic diagnosis

16 Neuroimaging Other worrisome features that increase probability of positive findings, but no clear recommendations: 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

17 Neuroimaging Headache in Pregnancy Most headaches are benign Most headaches are benign CVA – risk increases 3-13x CVA – risk increases 3-13x SAH – 20/100,000 deliveries SAH – 20/100,000 deliveries Migraines: less common Migraines: less common –60-70%have improvement in migraines during pregnancy Conclusion: Insufficient data to drive recommendations for imaging.

18 Question Can response to therapy be used as a diagnostic tool? Can response to therapy be used as a diagnostic tool?

19 Response to Therapy Level C No!!! Pain response should not be used. No!!! Pain response should not be used. ? Common pathway for pain regardless of etiology ? Common pathway for pain regardless of etiology No RCT to support or refute this. 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. 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.

20 Migraine What are the diagnostic criteria for migraine? What are the diagnostic criteria for migraine?

21 Migraine: Diagnosis Recurrent headache disorder – IHS Criteria 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

22 Migraine: Diagnosis Migraine without Aura Migraine without Aura Migraine with 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

23 Question True or False? True or False? Migraines can be associated with autonomic and sinus symptoms Migraines can be associated with autonomic and sinus symptoms –i.e. nasal congestion, rhinorrhea, tearing, colour and temperature change, changes in pupil size TRUE!

24 Question Which of the following are associated with migraine? Which of the following are associated with migraine? –Family history of migraine –Motion sickness –Obesity

25 Associated Factors Family history and motion sickness are risk factors for developing migraine Family history and motion sickness are risk factors for developing migraine Obesity is associated with increased frequency and severity of migraines Obesity is associated with increased frequency and severity of migraines

26 Migraine: Treatment US Headache Group: Educate pts about condition and tx; encourage active participation in management 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 analgesics Use migraine specific agents in pts with severe migraine, and those who respond poorly to NSAIDs or combination analgesics Use non-oral route for pts with sig N/V Use non-oral route for pts with sig N/V Consider self-administered rescue meds for pts with severe migraine Consider self-administered rescue meds for pts with severe migraine Guard against medication overuse headaches by using prophylactic medication in pts with frequent headaches Guard against medication overuse headaches by using prophylactic medication in pts with frequent headaches

27 Question List 5 treatment options for migraine in the emergency department. List 5 treatment options for migraine in the emergency department.

28 Treatment Options Fluids Fluids Analgesics: NSAIDs, acetaminophen Analgesics: NSAIDs, acetaminophen Serotonin Agonists Serotonin Agonists –Ergotamine –DHE (Dihydroergotamine) –Triptans Dopamine Antagonists Dopamine Antagonists –Chlorpromazine –Prochlorperazine –Metoclopramide Opioids Opioids Steroids: Dexamethasone Steroids: Dexamethasone

29 Mild Analgesics in Migraine Some pts can get optimal response with mild analgesics (NSAIDs, acetaminophen) Some pts can get optimal response with mild analgesics (NSAIDs, acetaminophen) Not advisable >10x /month Not advisable >10x /month RCTs: Acetaminophen, ibuprofen, naproxen, diclofenac, ASA, acetaminophen + ASA + caffeine RCTs: Acetaminophen, ibuprofen, naproxen, diclofenac, ASA, acetaminophen + ASA + caffeine Indomethacin: limited data, some specific migraine types are responsive to indomethacin for abortive therapy, benefit: suppository form Indomethacin: limited data, some specific migraine types are responsive to indomethacin for abortive therapy, benefit: suppository form

30 Triptans Specific tx: 5-HT 1b/d agonist ->inhibit dural nociception Specific tx: 5-HT 1b/d agonist ->inhibit dural nociception Advantage: multiple preparations Advantage: multiple preparations –SC, IN, PO RCT and systematic reviews: all triptans have been shown effective in acute migraine RCT and systematic reviews: all triptans have been shown effective in acute migraine Pts who don’t respond to one may respond to another Pts who don’t respond to one may respond to another

31 Question So, why don’t we commonly use triptans in the ED? So, why don’t we commonly use triptans in the ED?

32 Limitations of Triptans More effective if used early! More effective if used early! –Development of central sensitization Contraindications: 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 Interactions: P450 cytochrome Advisory July 2006 – concomitant use with SSRIs or SNRIs increases risk of serotonin syndrome; advise discussion of benefit vs risk Advisory July 2006 – concomitant use with SSRIs or SNRIs increases risk of serotonin syndrome; advise discussion of benefit vs risk

33 Ergots: Ergotamine Mechanism: Mechanism: –5HT 1b/d receptor agonist Efficacy: Efficacy: –Alone failed to show efficacy Side effects: 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 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 Treatment of choice in few pts due to issues of efficacy and side effects

34 Ergots: Dihydroergotamine Fewer side effects: no dependence or rebound headaches Fewer side effects: no dependence or rebound headaches Advantage: IV, IM, SC, IN use Advantage: IV, IM, SC, IN use Contraindications: Contraindications: –Htn, CAD, PVD, Prinzmetal’s, MAOIs, sepsis, severe hepatic or renal dysfunction, high dose ASA tx, pregnancy –Hemiplegic or basilar migraine –Within 24 hours of triptan or other serotonin agonists –CYP3A4 inhibitors: some macrolides, antifungals, protease inhibitors

35 Question How does DHE compare to the triptans for efficacy? How does DHE compare to the triptans for efficacy? –More effective? –Same? –Less effective?

36 DHE: Efficacy vs Placebo: vs Placebo: –Proven by systematic review / RCTs, especially when given with anti-emetic vs Triptan: vs Triptan: –Less effective on most measures compared head-to-head with sumatriptan vs Dopamine Antagonist: vs Dopamine Antagonist: –Less effective than chlorpromazine on some measures

37 Dopamine Antagonists Benefits: Benefits: –Antiemetic –IV metoclopramide –IV or IM chlorpromazine and prochlorperazine

38 Chlorpromazine: Largactil / Thorazine Chlorpromazine 5-15mg IV or 0.1mg/kg IV RCT vs Placebo (Bigal 2002 J Emerg Med): 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: Side effects: –Hypotension / Postural hypotension (18%)  May be exacerbated by opioids, pre-tx with fluid bolus  Alpha-antagonist –Drowsiness –Pregnancy: Class C

39 Prochlorperazine: Stemetil, Compazine Prochlorperazine 10mg IV Side effects: 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 FDA Alert (June 2008): Association with increased mortality when used for treating dementia-related psychosis

40 Question How does prochlorperazine compare to metoclopramide? How does prochlorperazine compare to metoclopramide?

41 Proclorperazine vs Metoclopramide RCT: Coppola (1995) Annals of Emerg Med RCT: Coppola (1995) Annals of Emerg Med –> 50% relief Stematil 82% Maxeran 48%Placebo 29% RCT: Jones (1996) Am J of Emerg Med RCT: Jones (1996) Am J of Emerg Med –Partial or complete relief Stematil 67% Maxeran 34%Placebo 16%

42 Metoclopramide: Maxeran, Reglan Maxeran 10mg IV Efficacy: 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: Benefits: –Pregnancy Class B –Can be combined with DHE, other analgesics Side Effects: Side Effects: –Drowsiness –Dystonic reactions: <1-25%, increased risk in young males

43 Other Options? Some pts will not respond to routine treatment. Consider wait-times, location (ED vs clinic) Consider wait-times, location (ED vs clinic) Treat aggressively. Treat aggressively. Do not use following meds on a chronic basis due to habit-forming nature and rebound headaches. Do not use following meds on a chronic basis due to habit-forming nature and rebound headaches. –Benzos –Opioids –Barbiturates

44 Question How can you prevent migraine recurrence? How can you prevent migraine recurrence?

45 Parenteral Dexamethasone Colman I et al. (2008) BMJ Meta-analysis of 7 RCTs. 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 ( ) –NNT 9 –Similar side effect profile

46 Question Can you name the complications of a migraine? Can you name the complications of a migraine?

47 Migraine: Complications Status migrainosus Status migrainosus Chronic migraine Chronic migraine Persistent aura without infarction Persistent aura without infarction Migrainous infarction Migrainous infarction Migraine-triggered seizure Migraine-triggered seizure

48 Summary: Migraine Tx in the ED Fluid bolus: NS 1L bolus IV Fluid bolus: NS 1L bolus IV NSAID: If used <10x/month NSAID: If used <10x/month –Nausea / vomiting: consider PR indomethacin –PO: acetaminophen vs ibuprofen Dopamine antagonist: Dopamine antagonist: –Stemetil 10mg IV –Maxeran 10mg IV (Pregnancy) Opioid: Opioid: –Morphine 2-5mg IV prn DHE / Triptan: DHE / Triptan: –If early presentation, contraindications to others –Rizatriptan, eletriptan, almotriptan –Sumatriptan: IN, SC or Zolmitriptan: IN, PO

49 Subarachnoid Hemorrhage Epidemiology SAH 1% of all headaches in ED SAH 1% of all headaches in ED 10% of hemorrhagic strokes 10% of hemorrhagic strokes 10% of “worst headache ever” 10% of “worst headache ever” Prevalence: 3-25 / 100,000 Prevalence: 3-25 / 100,000 Mean age: 55 (Range 20-60) Mean age: 55 (Range 20-60) Reported in pediatrics Reported in pediatrics Miss Rate? Variable 5-50% (30% average) Variable 5-50% (30% average) Acceptable miss rate: 0%! Acceptable miss rate: 0%!

50 Question Can you name 3 causes of SAH? Can you name 3 causes of SAH?

51 Causes of SAH Causes of SAH: Causes of SAH: –Trauma –Saccular Aneurysms –Non aneurysmal: Perimesencephalic (?venous bleed) –AVMs / Fistulae –Illicit drug use: cocaine, amphetamines –Arterial dissections

52 Question Can you name 3 risk factors for formation of aneurysms? Can you name 3 risk factors for formation of aneurysms?

53 Etiology of Aneurysms Congenital: Congenital: –Familial intracranial aneurysms (dominant) –Genetic condition: Ehlers-Danlos, Marfan’s, PCKD –Coarctation Acquired: Acquired: –Traumatic: skull #, penetration, post-op, hemodynamic damage –Infectious: syphilis, mycotic –Inflammatory: vasculitis –Degenerative: atherosclerotic Hypertension is NOT a major factor for aneurysm formation!

54 Question How many people have aneurysms? How many people have aneurysms?

55 Aneurysms in the Public Prevalence of saccular aneurysms Prevalence of saccular aneurysms –5% at autopsy –20-30% have multiple aneurysms

56 Question Can you name 3 risk factors for rupture? Can you name 3 risk factors for rupture?

57 Risk Factors for Rupture of Aneurysms Smoking Smoking –Dose-dependent, esp. women, disappears soon after quitting, RR 2.2 Hypertension Hypertension –RR 2.5, OR 2.6 EtOH EtOH –Moderate to heavy consumption RR 2.1, OR 1.5 Family History Family History –OR 4.0 Genetics Genetics –Autosomal dominant / recessive / multifactorial / anticipation –Elastin gene, Platelet adhesive glycoprotein Phenylpropanolamine Phenylpropanolamine –Appetite suppressants, cold remedies, case-control study – risk factor in women Estrogen deficiency Estrogen deficiency –Premenopausal women and reduced risk compared to age-matched postmenopausal women (OR 0.24), HRT (OR 0.47) Physical Exertion Physical Exertion –Orgasm, moderate exertion OR 2.7 ?Anticoagulants ?Anticoagulants

58 Question What proportion of patients with SAH from aneurysm have a sentinel bleed? What proportion of patients with SAH from aneurysm have a sentinel bleed?

59 Sentinel Headache 30-50% of patients have a sentinel headache that precedes SAH by 6-20 days 30-50% of patients have a sentinel headache that precedes SAH by 6-20 days

60 Clinical Features Abrupt onset, severe headache “thunderclap” Abrupt onset, severe headache “thunderclap” Lateralized 30% Lateralized 30% At night 30% (During day / activity 60%) At night 30% (During day / activity 60%) Onset associated with brief LOC, seizure, nausea, vomiting Onset associated with brief LOC, seizure, nausea, vomiting Meningismus / Aseptic meningitis Meningismus / Aseptic meningitis Normal neurologic findings at presentation 50% Normal neurologic findings at presentation 50%

61 Question What is the mortality of SAH? What is the mortality of SAH?

62 Mortality Average: 51% Average: 51% 10% prior to reaching hospital 10% prior to reaching hospital 25% within 24 hours of onset 25% within 24 hours of onset 45% within 30 days 45% within 30 days

63 Question What are the complications of SAH? What are the complications of SAH? –Name 4.

64 Complications Rebleeding Rebleeding Vasospasm and delayed cerebral ischemia Vasospasm and delayed cerebral ischemia Infarction Infarction Hydrocephalus (acute / chronic) Hydrocephalus (acute / chronic) Increased ICP Increased ICP Seizures Seizures Hyponatremia Hyponatremia Hypothalamic dysfunction and pituitary insufficiency Hypothalamic dysfunction and pituitary insufficiency Cardiac abnormalities Cardiac abnormalities –ECG –Ventricular wall motion abnormalities –Elevated BNP

65 Pitfalls in Diagnosis Wasn’t the worst headache of their life! Wasn’t the worst headache of their life! Neurologic exam was normal! Neurologic exam was normal! –50% have normal neurologic exam! Pain improved with treatment Pain improved with treatment –Remember: SAH CAN improve with treatment! CT head was negative CT head was negative RBCs decreased from tubes 1-3 / Misinterpretation of LP RBCs decreased from tubes 1-3 / Misinterpretation of LP No LP done No LP done

66 CT Head: Limitations Technical ability of CT scanners to identify small hemorrhage / artifact / bone Technical ability of CT scanners to identify small hemorrhage / artifact / bone Protocol and age of scanner – thin slices Protocol and age of scanner – thin slices Expertise of reader Expertise of reader Anemia Hb<100 – blood appears isodense Anemia Hb<100 – blood appears isodense Time: decay in sensitivity Time: decay in sensitivity Inability to diagnose other causes of headache: meningitis, etc. Inability to diagnose other causes of headache: meningitis, etc.

67 Question How sensitive is CT scan at day 1 for SAH? How sensitive is CT scan at day 1 for SAH? How sensitive is CT scan at day 7 for SAH? How sensitive is CT scan at day 7 for SAH?

68 CT Scan: Sensitivity As blood is diluted and degraded flowing through SA space -> decreased sensitivity As blood is diluted and degraded flowing through SA space -> decreased sensitivity –BMJ (2006)  <12 Hrs98%  24 hrs93%  >7 days 7 days<50% –Memory aide:  Day 190%  Day 280%  Day 370%  Day 460%

69 Question Why do you do a CT then if ruling out SAH? Why do you do a CT then if ruling out SAH?

70 CT Scan for SAH: Advantages Traumatic LP: Traumatic LP: –13% may be traumatic (>400 RBCs) LP Limitations: LP Limitations: –Cerebral venous thrombosis –Unruptured aneurysm –Arterial dissection –Pituitary apoplexy

71 Question Does an LP need to be routinely performed on ED patients to rule out SAH if normal noncontrast CT head? Does an LP need to be routinely performed on ED patients to rule out SAH if normal noncontrast CT head? –Why?

72 Lumbar Puncture ACEP (2008) Level B Evidence. Lumbar puncture should be performed to rule out SAH. Lumbar puncture should be performed to rule out SAH. Rates of SAH confirmed by LP after normal CT % Rates of SAH confirmed by LP after normal CT %

73 Question What 3 features do you see on LP in SAH? What 3 features do you see on LP in SAH?

74 Lumbar Puncture in SAH (1) Elevated opening pressure (1) Elevated opening pressure (2) Elevated RBC count (2) Elevated RBC count (3) Xanthochromia (3) Xanthochromia

75 Opening Pressure Normal? 6-20cmH20 is normal in adults and children 6-20cmH20 is normal in adults and children 25cmH20 may be normal in obese pts 25cmH20 may be normal in obese ptsUtility: Helpful to distinguish SAH from traumatic tap Helpful to distinguish SAH from traumatic tap 2/3 of SAH may have elevated opening pressure 2/3 of SAH may have elevated opening pressure Other diagnoses: spontaneous intracranial hypotension, benign intracranial hypertension, cerebral venous sinus thrombosis Other diagnoses: spontaneous intracranial hypotension, benign intracranial hypertension, cerebral venous sinus thrombosis

76 Question Does clearing of blood (i.e. declining RBC count from tubes 1->4) rule out SAH? Does clearing of blood (i.e. declining RBC count from tubes 1->4) rule out SAH?

77 Elevated Red Blood Cell Count Clearing of blood is unreliable. Clearing of blood is unreliable. There is no cutoff which has been shown to reliably exclude SAH. 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. 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. No way to tell traumatic tap vs SAH if early <12 hours tap.

78 Question What is xanthochromia? What is xanthochromia? When does it appear? How long does it last? When does it appear? How long does it last?

79 Xanthochromia Yellow colour caused by bilirubin and oxyhemoglobin due to lysis of RBCs 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 Onset: Blood in CSF for at least 2 hours Peak: 48 hours Peak: 48 hours Duration: Up to 2-4 weeks Duration: Up to 2-4 weeks

80 Question Name 2 methods for analyzing your sample tubes for xanthochromia. Name 2 methods for analyzing your sample tubes for xanthochromia. Which is more sensitive? Which is more sensitive?

81 Xanthochromia: Analysis Spectrophotometry Spin CSF, run through spectrophotometer, look for oxyHb or bilirubin peak at 410nm and 460nm Spin CSF, run through spectrophotometer, look for oxyHb or bilirubin peak at 410nm and 460nm Most sensitive Most sensitive Low-moderate specificity Low-moderate specificity Not always available Not always available Visual Analysis Spin CSF, compare to identical test tube with equal volume tap water against white background Spin CSF, compare to identical test tube with equal volume tap water against white background Calgary Health Region’s method Calgary Health Region’s method Less sensitive, but may be >95% if >12 hours after SAH Less sensitive, but may be >95% if >12 hours after SAH

82 Question Name 3 false positives for xanthochromia. Name 3 false positives for xanthochromia. (Xanthochromia but no SAH!)

83 Xanthochromia: False Positives Hyperbilirubinemia Hyperbilirubinemia Rifampin Rifampin Previous traumatic tap Previous traumatic tap Traumatic tap isn’t analyzed quickly -> xanthochromia Traumatic tap isn’t analyzed quickly -> xanthochromia Chronic spinal cord abnormalities Chronic spinal cord abnormalities

84 Question Which patients can safely undergo LP without neuroimaging? Which patients can safely undergo LP without neuroimaging?

85 LP Before CT? ACEP (2008). Level C Evidence. Adults patients with headache and signs of elevated ICP should have neuroimaging before LP. Adults patients with headache and signs of elevated ICP should have neuroimaging before LP. –Papilledema, absent venous pulsations of fundoscopy, altered LOC, focal neuro deficits, signs of meningeal irritation In the absence of clinical findings suggestive of increased ICP, LP can be performed without obtaining neuroimaging. In the absence of clinical findings suggestive of increased ICP, LP can be performed without obtaining neuroimaging.

86 Question 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? 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?

87 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. 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. 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.

88 Further Investigation Perry et al. (2008) Annals of Emerg Med. 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 10 6 RBC/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”

89 Thank You!

90 Question Can you name 3 causes of headache that might be associated with exertion? Can you name 3 causes of headache that might be associated with exertion?

91 Exertional Headache SAH SAH –Pts with SAH more likely to have participated in exertion that day, compared to previous OR 2.7 Carotid or Vertebral Artery Dissection Carotid or Vertebral Artery Dissection Primary Exertional Headache 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 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

92 Question Can you describe the most common headache symptoms in brain tumour? Can you describe the most common headache symptoms in brain tumour?

93 Brain Tumour 50% have headaches 50% have headaches –Tension-type (77%) –Migraine (9%) Typical headache: Typical headache: –Bilateral, worse ipsilaterally, bending over (32%), nausea and vomiting (40%), worse with Valsalva Classic “early morning headache” – uncommon! Classic “early morning headache” – uncommon! Reliable findings: Reliable findings: –Nausea, vomiting, worsening with change in position, abnormal neurologic exam, significant change in headache pattern

94 Triptans: Comparison Few trials comparing triptans head to head Few trials comparing triptans head to head Rizatriptan (Maxalt), eletriptan (Relpax), almotriptan (Axert) had highest likelihood of success Rizatriptan (Maxalt), eletriptan (Relpax), almotriptan (Axert) had highest likelihood of success Sumatriptan was recently released with fast dissolving tabs Sumatriptan was recently released with fast dissolving tabs –Sumatriptan (Imitrex): SC, IN, PO –Zolmitriptan (Zomig): IN, PO

95 Headache: Emergent Diagnoses Core Rounds Feb19,2009 Rob Hall MD, FRCPC

96 Case 41yo female PMHx DM1 on insulin 41yo female PMHx DM1 on insulin Mild headache and Numbness right arm/mouth and weakness left grip, subacute, 1 week Mild headache and Numbness right arm/mouth and weakness left grip, subacute, 1 week No fever or illicit drug use No fever or illicit drug use OCP started 2 weeks ago OCP started 2 weeks ago No hx seizures, no trauma 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 Waiting in ED bed, GTC 1 min sz, chemstrip normal, ativan 2mg iv, post ictal and combative after, no focal findings after sz Investigations? Investigations? Thoughts on dx? Thoughts on dx?

97 CT head (plain)

98 Cerebral Vein Thrombosis Venous clot then infarct and/or bleed at grey-white junction Venous clot then infarct and/or bleed at grey-white junction Transverse sinus most common location, often multiple sinuses Transverse sinus most common location, often multiple sinuses “DVT of the BRAIN”

99 Clinical Presentations STROKE SYNDROME STROKE SYNDROME –Often not typical arterial distribution SEIZURE SEIZURE HEADACHE HEADACHE –Can be basically any description of headache (thunderclap uncommon)

100 Risk Factors for CVT (present in 85%) Head and neck infections Head and neck infections Hypercoagulable states 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

101 Exam findings Highly variable Highly variable Three clues Three clues –Head infection + Neuro symptoms –Papilledema (? Sensitivitiy) –Stroke findings in non-arterial distribution LP will show elevated opening pressure without other cause

102 CT head (plain) findings Sensitivity 60-70% (30-40% normal) Sensitivity 60-70% (30-40% normal) Delta sign = dense triangle from hyperacute thrombosed superior saggital sinus Delta sign = dense triangle from hyperacute thrombosed superior saggital sinus Cord sign = thrombosed cortical vein Cord sign = thrombosed cortical vein Venous infarcts with secondary hemorrhage in non-arterial distribution Venous infarcts with secondary hemorrhage in non-arterial distribution –HTN bleeds: thalamus, IC, CB, pons –Venous infarct bleeds: bilateral at grey-white junction

103 CT head

104 Definitive Diagnosis CT venography (preferred) CT venography (preferred) MR venography MR venography –Hypointense signal of acute thrombus mimics normal flow. RadioGraphics 2006;26:S5-18. Angiography (not used anymore) Angiography (not used anymore)

105 CT Venography

106 CVT and Carotid/vert dissections. 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.” “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.”

107 ED Management Dilantin if seized Dilantin if seized Manage elevated ICP Manage elevated ICP Heparin Heparin –Majority of evidence shows improvement trends (no major large RCT showing statistically conclusive results) –Shown to be safe even with hemorrhages! –Cochrane review 2001  RR death 0.33 (95%CI )  RR death or disability 0.46 ( )

108 Further Management Optic nerve fenestrations Optic nerve fenestrations Acetazolamide Acetazolamide Case reports of lytics Case reports of lytics LP/VP shunts LP/VP shunts Hemicraniectomy for severe ICP problems Hemicraniectomy for severe ICP problems

109

110 Is Idiopathic Intracranial HTN and CVT a spectrum of disease? IIHTN > CVT

111 Idiopathic Intracranial HTN (IIHTN) Old terms = Pseudotumor cerebri, Benign IHTN, meningitis Cerosa Old terms = Pseudotumor cerebri, Benign IHTN, meningitis Cerosa Diagnostic criteria for IIHTN requires imaging to rule out CVT Diagnostic criteria for IIHTN requires imaging to rule out CVT

112 Idiopathic Intracranial HTN (IIHTN) Opening pressure > 20 cm H20 (usu 25-45) Opening pressure > 20 cm H20 (usu 25-45) –Headache MUCH better after LP! Signs/symptoms of increased ICP Signs/symptoms of increased ICP No focal signs (except 6th palsy) No focal signs (except 6th palsy) No mass lesion No mass lesion No hydrocephalus No hydrocephalus Normal CSF values Normal CSF values CTV/MRV to exclude CVT CTV/MRV to exclude CVT

113 Idiopathic Intracranial HTN (IIHTN) Main ED PEARL is to consider the diagnosis and do an LP Main ED PEARL is to consider the diagnosis and do an LP “Consider” “Consider” –Obese, female, OCP –Hypercoag states –Subacute, unexplained headaches, return visits, normal imaging –Visual symptoms: blurry vision, diplopia

114 Carotid and Vertebral Dissections 2% of ischemic strokes overall but 20% of ischemic CVA < 45yo 2% of ischemic strokes overall but 20% of ischemic CVA < 45yo –Think of in young patient Pathology the same with major vs minor trauma Pathology the same with major vs minor trauma –May be VERY minor (yoga, cough, stretching, etc) –Unknown if “spontaneous” really occur

115 Carotid and Vertebral Dissections Headache + Neck pain, unilateral + neuro symptoms Headache + Neck pain, unilateral + neuro symptoms Dx - CTA, MRA, angio Dx - CTA, MRA, angio CTA preffered CTA preffered

116 Giant Cell (Temporal) Arteritis: the basics Older person Older person Subacute headache Subacute headache Systemic symptoms Systemic symptoms Jaw claudication Jaw claudication Association with PMR Association with PMR Risk of vision loss Risk of vision loss Elevated ESR Elevated ESR Diagnose by temporal artery biopsy Diagnose by temporal artery biopsy Treat with steriods Treat with steriods

117 Giant Cell Arteritis: some pearls Extremely rare < 50 years old Extremely rare < 50 years old –Pooled analysis 1435 pt, only 2 < 50yo Temporal artery findings (large, absent pulse, tenderness) fairly specific but not sensitive 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) Normal ESR (< 20 mm/hr) excludes dx, moderate ESRs don’t (20-50 mm/hr) –<20 mm/hr 96% sensitive –<40 mm/hr95% sensitive –< 50 mm/hr89% sensitive

118 Giant Cell Arteritis: some pearls Temporal artery biopsy 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 Treatment –Prednisone 60 mg po od –ASA –START before biopsy

119 APPROACH to ED HEADACHE Headache is a high risk complaint. Consider serious causes in every case. Majority of badness excluded with good history and physical. More complex than just ordering CT head!

120 Headache and normal CT head; ddx of “bad” causes? Ischemic stroke Ischemic stroke HTN encephalopathy HTN encephalopathy Pre-eclampsia Pre-eclampsia CO toxicity CO toxicity Vasculitis/GCA Vasculitis/GCA AACG AACG CNS infection CNS infection CVT CVT IIHTN IIHTN SAH SAH Carotid/vertebral dissection Carotid/vertebral dissection Which can be excluded By hx/pe?

121 Headache and normal CT head; ddx of “bad” causes? Ischemic stroke - hx and physical Ischemic stroke - hx and physical HTN encephalopathy - physical HTN encephalopathy - physical Pre-eclampsia - hx and physical Pre-eclampsia - hx and physical CO toxicity - hx CO toxicity - hx Vasculitis/GCA - hx Vasculitis/GCA - hx AACG - physical AACG - physical CNS infection CNS infection CVT CVT IIHTN IIHTN SAH SAH Carotid/vertebral dissection - CTA/MRA Carotid/vertebral dissection - CTA/MRA Which can be excluded By a normal LP?

122 Headache and normal CT head; ddx of “bad” causes? Ischemic stroke - hx and physical Ischemic stroke - hx and physical HTN encephalopathy - physical HTN encephalopathy - physical CO toxicity - hx CO toxicity - hx Vasculitis/GCA - hx Vasculitis/GCA - hx AACG - physical AACG - physical CNS infection > LP CNS infection > LP CVT > LP (+/- CTV) CVT > LP (+/- CTV) IIHTN > LP IIHTN > LP SAH > LP SAH > LP Carotid/vertebral dissection - CTA/MRA/Angio Carotid/vertebral dissection - CTA/MRA/Angio

123 Lumbar puncture is a useful test to exclude some nasty causes of headache Opening pressure is worthwhile.

124

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

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


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