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Headache is the fourth most common reason for emergency department encounters, accounting for 3% of all visits in the United States. Though troublesome, 90% are relatively benign primary headaches --migraine, tension, and cluster headaches. The other 10% are secondary headaches, caused by separate underlying processes, with vascular, infectious, or traumatic etiologies, and they are potentially life-threatening. This issue details the important pathophysiologic features of the most common types of life-threatening headaches, the key historical and physical examination information emergency clinicians must obtain, the red flags that cannot be missed, and the current evidence for best-practice testing, imaging, treatment, and disposition.
A previously healthy 30-year-old man presents to the ED complaining of the “worst headache of my life.” He describes it as sharp, nonradiating, with an abrupt onset 5 hours ago. You are concerned for subarachnoid hemorrhage. You provide pain medication and obtain a noncontrast CT scan of the head, which is negative. The patient is feeling better and wants to go home. You wonder whether a negative CT is sufficient to rule out an SAH or whether a lumbar puncture should be done...
A 55-year-old man with history of nonsmall cell lung cancer who is on cisplatin presents with an acute headache and lethargy for 6 hours. His vital signs are remarkable for a blood pressure of 210/120 mm Hg, heart rate of 70 beats/min, and a temperature of 36.7°C (98°F). His physical exam reveals a lethargic patient with no localizing neurologic signs and no meningismus. You order a noncontrast CT of the head and consider lowering this patient’s blood pressure, though you wonder how much and how fast it should be reduced...
A 45-year-old woman presents to the ED complaining of a severe occipital headache, neck pain, and dizziness. Earlier in the day, she was involved in a motor vehicle crash and suffered “whiplash.” Her neurologic exam is normal, including no nystagmus and normal cerebellar function, but you are concerned that this patient may have a vertebral artery dissection, and you order a CTA head and neck. You wonder: if it’s positive, should the treatment include anticoagulation or antiplatelet therapy...or both?
The third edition of the International Classification of Headache Disorders (ICHD-3), published in January 2018, is the most up-to-date and widely accepted standard criteria for the classification of headaches.1 The ICHD-3 classifies headaches into 3 distinct categories: (1) primary headache disorders, including migraine, tension, and cluster headaches; (2) secondary headaches, including potentially life-threatening forms of headaches such as those secondary to vascular disorders, traumatic injury, and disorders in hemostasis; and (3) cranial neuropathies, such as trigeminal neuralgia.
The National Hospital Ambulatory Medical Care Survey reviewed over 10,000 patients presenting to emergency departments (EDs) for acute headache and found that 2% represented secondary headaches.2 Although they are rare, life-threatening headaches require prompt diagnosis and treatment, as delays in some diagnoses can have a mortality rate approaching 50%.3
Evaluating complaints of acute headache is a common practice in the ED, and distinguishing benign from serious pathology can be a diagnostic challenge. A focused workup begins with a careful, well-organized clinical history and physical examination. Physical examination findings such as abnormal vital signs, papilledema, cranial nerve palsies, and neck pain are suggestive of more concerning headache etiologies.4 Resources such as ocular ultrasound, neuroimaging, and lumbar puncture are important strategies, but the sensitivity and specificity of the results must be understood in order to apply them correctly. This issue of Emergency Medicine Practice focuses on the most commonly encountered causes of life-threatening secondary headaches and provides best-practice recommendations on their initial evaluation and management.
A literature search from 1993 to 2018 was conducted using PubMed and Ovid MEDLINE®, with the search terms headaches AND emergency, sudden onset, fever, visual symptoms, neurologic deficits, high-risk, trauma, immunocompromised, pregnancy, coagulopathy, and life threatening. The National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews were searched. Guidelines published by the American College of Emergency Physicians (ACEP) and the American Academy of Neurology were searched. International guidelines, including the Canadian and European neurology guidelines, were also reviewed. Over 500 abstracts published within the last 25 years were examined, and 89 of these full-text articles were reviewed and included for reference. Many of the identified articles were prospective studies, meta-analyses, clinical guidelines, and literature reviews.
1. “I got a CT scan, and the lumbar puncture revealed no xanthochromia, so I discharged him, thinking he didn’t have a SAH.”
Xanthochromia is time-dependent and takes 2 to 12 hours to develop, so its absence in patients presenting within this timeframe may not be helpful. If the diagnosis for SAH is still unclear after noncontrast CT and lumbar puncture, additional diagnostic imaging may include CT angiogram and magnetic resonance angiography.
2. “When evaluating the pregnant patient for CVT, I didn’t want to subject her to any radiation, so I obtained a D-dimer in lieu of a CT scan.”
The diagnosis of CVT should be made using the clinical examination and imaging studies. Several small studies have looked at the utility of D-dimer to screen patients presenting to the ED with headache suspicious for CVT. Pregnancy is a risk factor for CVT, so this patient is not low-risk.
3. “My patient complaining of headache and neck pain had no focal neurologic deficits, so I had a very low clinical suspicion for carotid or vertebral artery dissection.”
Patients with CAD may initially present with head or neck pain, but without any neurologic deficits; the goal is to diagnose and treat before the dissection causes thrombus, which can embolize and cause stroke.
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study is included in bold type following the references, where available. In addition, the most informative references cited in this paper, as determined by the author, are highlighted.
Jeff: Welcome back to EMplify, the podcast corollary to EB Medicine’s Emergency Medicine Practice. I’m Jeff Nusbaum, and I’m back with my co-host, Nachi Gupta. This month, we’re tackling an incredibly important topic "Evaluation and Management of Life-Threatening Headaches in the Emergency Department".
Nachi: Fear not, this will not simply be “who needs a head CT episode”; we’ll cover much more than that. Listen closely as this is an important topic, with huge consequences for mismanagement.
Jeff: Absolutely. As some quick background - headaches account for 3% of all ED visits in the US, with 90% being benign primary headaches and less than 10% being secondary to other causes like vascular, infectious, or traumatic etiologies. It’s within these later 10% that we are looking for the red flag signs to identify the potentially life-threatening headaches.
Nachi: And to do so, Dr. David Zodda and Dr. Amit Gupta, PD and APD at Hackensack University Medical and Trauma Center, and their colleague Dr. Gabrielle Procopio, a PharmD, have done a fantastic job parsing through the literature, which included over 500 abstracts, 89 full text articles, guidelines from ACEP and the American Academy of Neurology, as well as canadian and european neurology guidelines, to summarize the best evidence based recommendations for you all.
Jeff: We would be remiss to not also mention Dr. Mert Erogul of Maimonides Medical Center and Dr. Steven Godwin, Chair of Emergency Medicine at the University of Florida College of Medicine.
Nachi: Alright, so let’s get started with some definitions and pathophysiology. The international classification of headache disorders 3, or ICHD-3, classifies headaches into primary, secondary, and cranial neuropathies.
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Jeff: Primary headache disorders include migraine, tension, and cluster headaches. Secondary headaches include those secondary to vascular disorders, traumatic disorders, and disorders in hemostasis. These are the potentially life threatening headaches that can have a mortality has high as 50%.
Nachi: And the final category includes cranial neuropathies, such as trigeminal neuralgia.
Jeff: And I think we can safely say that that wraps up our discussion in this episode on cranial neuropathies, moving on….
Nachi: Headaches result from traction to or irritation of the meninges and blood vessels, which are the only innervated central nervous system structures. Activation of specific nerve ganglion complexes by neuropeptides like -- substance P and calcitonin gene-related peptide -- are thought to contribute to head pain.Jeff: It is important to note that all headache pain shares common pain pathways, thus response to pain medications does not exclude potential life threatening secondary causes of headache. This led to the ACEP guideline which states just that..
Nachi: I feel like that deserves ding sound as it's a critically important point. To repeat, just because a pain medication relieves a headache, that does not exclude dangerous secondary causes!
Jeff: And what are the life threatening headaches? Life-threatening headaches include subarachnoid hemorrhage, cervical Artery Dissection, which includes both vertebral Artery Dissection and carotid artery dissection, cerebral Venous Thrombosis, idiopathic intracranial hypertension, giant cell arteritis, and posterior reversible encephalopathy syndrome, or PRES.
Nachi: Slow down for a second and let’s not skip over your favorite section.. Let’s talk pre hospital care for headache patients.
Jeff: Good call! Pre-hospital care is fairly straightforward and includes a primary survey, conducting a focused neurologic exam, and assessing for red flag signs, which include focal neurologic deficits, sudden onset headache, new headache in those over 50, neck pain or stiffness, changes in visual Acuity, fever or immunocompromised State, history of malignancy, pregnancy or postpartum status, syncope, and seizure. That’s quite a list. For a visual reference, see Table 3 in the print issue.
Nachi: And patients with neurologic deficits or severe sudden-onset headaches, should be transported immediately to the nearest available stroke center. Tylenol should be offered for pain management. Avoid opioids and nsaids.
Jeff: Upon arrival to the emergency department, history and physical should include your standard vitals, testing neurologic function, cranial nerve testing, head and neck exam, as well as a fundoscopic exam. As was the case for your pre-hospital colleagues, you should also assess for red flag signs for life-threatening headaches. Check out tables 2, 3, and 4 for more details here.
Nachi: With respect to Vital Signs, in the setting of an acute headache, severe hypertension should prompt a search for signs of end-organ damage such as hypertensive encephalopathy, intracranial Hemorrhage, PRES, and preeclampsia in pregnant women. Additionally, fever, and especially fever and neck stiffness, should raise concern for CNS infection.
Jeff: For your neurologic examination, make sure to include assessments of motor strength, coordination, reflexes, sensory function, and gait. Don't forget that lesions involving the anterior circulation, such as dysarthria, cognitive impairment, and Horner syndrome may be indicative of a carotid artery dissection, whereas dizziness, vision changes, and limb weakness may be due to a vertebral Artery Dissection.
Nachi: And for cranial nerve testing - pay particular attention to cranial nerves 2, 3 and 6. For cranial nerve 2 - look out for an afferent pupillary defect, or a marcus-gunn pupil, which is seen in optic neuritis, giant cell artertitis, and central retinal artery occlusion. For CN3, oculomotor nerve palsies raise concern for a posterior communicating aneurysm and SAH. And lastly, CN6 palsies, which often presents with diplopia on lateral gaze , are often seen with intracranial idiopathic hypertension and cerebral venous thrombosis, in addition to impaired visual acuity, visual field defects, and tunnel vision.
Jeff: For the head and neck exam, remember that a partial horner syndrome, with miosis and ptosis without anhidrosis, may be indicative of a cervical artery dissection. Unfortunately, if the patient presents acutely, their only complaint may be pain, as the neurologic sequelae may take days to develop.
Nachi: Additionally, with respect to the head and neck exam, evaluate the patient for tenderness and beading along the temporal artery.
Jeff: One review noted that temporal artery beading actually had the highest likelihood ratio for GCA, 4.6, whereas temporal artery tenderness only had a LR of 2.6
Nachi: And the last physical exam maneuver you should ideally perform is a fundoscopic exam for papilledema, which is often seen in IIH, malignant hypertension, and CVT.
Jeff: Perfect so that rounds out the physical, next we have diagnostic studies. Most importantly, routine lab testing is typically of low utility in aiding in the diagnosis of headache.
Nachi: Even ESR and CRP in the setting of possible giant cell arteritis have poor sensitivity and specificity to diagnose it. So even if the ESR and CRP are negative, if the suspicion for GCA is high enough, it should be treated and you should get a biopsy.
Jeff: Do consider adding on a venous or arterial carboxyhemoglobin in the right clinical scenario, as CO poisoning represents an important cause of headache you wouldn’t want to miss. This is especially important at this time of year when heating systems are working overtime here in the states.
Nachi: And hopefully you have a co-oximeter, so you can even check this non-invasively.
Jeff: Interestingly, there may be a unique role for a d-dimer here as well. Several small studies have used the d-dimer to risk stratify patients with possible CVT. In one study a d-dimer level < 500 mcg/L had a 97% sensitivity and a negative predictive value of 99% - not bad!
Nachi: Pretty impressive performance characteristics. I think that about wraps up lab work. Let’s talk radiology.
Jeff: Though low yield, CT utilization is estimated at 2.5-10% of non-traumatic headaches. A non-con CT should be reserved for those with suspicion for an intracranial hemorrhage, while a contrast CT would be required in those in whom there is concern for an infectious process or space occupying lesion.
Nachi: CT angio or MRI should be used in cases of possible cervical artery dissection. MRI also is the neuroimaging of choice for PRES, which is more sensitive for cerebral edema than CT.
Jeff: Similarly, MRV is recommended in those with a concerning story for CVT.
Nachi: To help guide your emergent neuroimaging utilization, ACEP suggests imaging in those with headache and an abnormal finding on neuro exam, those with new and sudden-onset severe headache, HIV positive patients with new headache, and those over 50 with a new headache.
Jeff: With that in mind, let’s dive a bit deeper into the use of CT for SAH, a topic which doesn’t get a ding sound, but is certainly critically important. Recent literature have found that a CT within 6 hours of symptom onset has a sensitivity and specificity and negative predictive value of 100%. In addition, one 2016 study demonstrated a LR of 0.01 in those with a negative HCT within 6 hours. These are really important results because that means SAH is essentially ruled out with a negative study.
Nachi: Unfortunately, the 2008 ACEP guideline and 2012 AHA guidelines still recommend a lumbar puncture in those being worked up for SAH. Luckily the ACEP guideline is currently being revised so your decision to forego the LP with a negative HCT in the first 6 hours will likely also be backed by ACEP in the near future.
Jeff: That’s a nice transition into our next test - the LP. Since LP carries a risk of herniation, in those with signs of increased ICP, make sure to get appropriate neuroimaging before attempting the puncture. In those without signs of increased ICP, no imaging is necessary.
Nachi: While the position in which the LP is performed doesn’t matter as much when ruling out infection or SAH, in those with suspected IIH, make sure to obtain an opening pressure with the patient lying in the lateral decubitus position. An opening pressure of greater than 25 is often seen in IIH.
Jeff: And the LP in the setting of IIH is not only diagnostic but also potentially therapeutic, as the removal of 1 ml of CSF can lower the pressure by 1 cm of H20 and potentially relieve the patient’s symptoms.
Nachi: Always rewarding to diagnose and treat simultaneously...
Jeff: Absolutely. But back to the LP for SAH for a second or two. When evaluating for a subarachnoid hemorrhage, you’ll often note an opening pressure of greater than 20 with persistent RBC in all tubes.
Nachi: While there are no RBC cutoffs, one study found no patients with a SAH with less than 100 RBC in the final tube. In contrast, greater than 10,000 RBC increased the odds by a factor of 6. In addition, one 2015 study found that patients without xanthrochromia and less than 2000 RBC were effectively ruled out of having a SAH with a combined sensitivity of 100%
Jeff: Lots of 100% sensitivities and specificities being thrown around today, which is definitely not the norm. No complaints here, I’ll take it. Anyway, the last test to discuss is our good friend the ultrasound, specifically the ocular ultrasound.
Nachi: Examining the optic nerve sheath 3 mm posterior to the globe, an optic nerve sheath diameter of 5 mm or greater is predictive of an ICP greater than 20.
Jeff: Keep in mind that this may expedite the work up, though a normal diameter does not rule out increased ICP, so a head CT may still be indicated.
Nachi: Alright, so we’ve talked a lot about testing, both lab and imaging, and we’ve mentioned a bunch of pathologies, but let’s spend a few minutes going over the specifics of each.
Jeff: Let’s start with SAH. SAH account for 1% of all headache visits to the ED. Most nontraumatic SAH are caused by aneurysm rupture. A missed diagnosis of SAH can have a case-fatality rate as high as 50%
Nachi: Although 75% of SAH patients report an abrupt onset, objective neck stiffness has the highest likelihood ratio of 6.6. Other important features include LOC, neurologic deficit, subjective neck stiffness, photophobia, and onset during exertion or intercourse.
Jeff: Additionally, approximately 20% of patients with a SAH have warning signs of a sentinel bleed including headaches, cranial nerve palsies, neck pain, or nausea and vomiting.
Nachi: In order to aid you in diagnosing a SAH, you should consider the ottawa SAH Rule which has a 100% sensitivity and a 15% specificity. To use this rule you must be between 15 and 40 with a GCS of 15 and present with a headache with maximal intensity within 1 hour of onset. If you meet those inclusion criteria, and you have no neurologic deficits, no neck pain or stiffness, no witnessed LOC, no onset during exertion, no limitation of neck flexion, and no thunderclap onset, you can essentially rule out a SAH.
Jeff: While the ottawa SAH rule has been prospectively validated, know that this study has been challenged for its interobserver variability, but in any case it still provides helpful red flags to consider. If your patient is found to have a SAH, a CT angiogram and neurosurgical consultation should be considered immediately.
Nachi: In addition to monitoring ABCs, early care involves the administration of analgesics and anti-emetics. Also consider elevating the head of the bed to 30 deg, which may also improve venous drainage and decrease ICP.
Jeff: In terms of BP management, guidelines from the american stroke association recommend targeting a SBP of 160 with a titratable agent like nicardipine or clevidipine.
Nachi: In addition, nimodipine, 60 mg q4h, should be given to those with aneurysmal SAH to improve outcomes.
Jeff: and any role for anti-epileptics?
Nachi: That’s controversial and the authors state it may be considered in the immediate post-hemorrhagic period and should be limited to a 3-7 day course with longer courses required in special populations.
Jeff: The next pathology to discuss is cervical artery dissections, which account for 2% of all strokes and nearly 20% of strokes in those 50 and under. cervical artery dissections are most commonly due to trauma, but can occur spontaneously.
Nachi: Risk factors include Ehlers-Danlos syndrome, osteogenesis imperfecta, and Marfan syndrome.
Jeff: Regardless of the etiology, the management of cervical artery dissections is primarily medical with IV heparin followed by warfarin or a direct oral anticoagulant in those with extracranial dissections, and antiplatelet therapy like aspirin or clopidogrel in those with intracranial dissections.
Nachi: Thanks to the CADISP study, we know there is no difference in mortality or neurologic outcome when choosing between antiplatelet therapy and anticoagulation.
Jeff: Next we have cerebral venous thrombosis. This typically presents with a gradual onset headache. Though it can happen to anybody, cerebral venous thrombosis typically results from thrombotic disease.
Nachi: Important risk factors include oral contraceptive use, pregnancy and postpartum states, Factor V Leiden deficiency, and lupus.
Jeff: Treatment for CVT is controversial due to a high risk of hemorrhage and hemorrhagic transformation. According to the best available evidence, anticoagulation is the standard therapy with full dose anticoagulation of low-molecular weight heparin or heparin as a bridge to warfarin.
Nachi: Yeah, it’s really a tough spot to be in as one third end up having some form of hemorrhage too….
Jeff: Perhaps yet another good place for shared decision making?
Nachi: Honestly, it’s a good thought, but anticoagulation is the guideline recommendation, so I think that is likely the best route in this case.
Jeff: Great point. Next we have idiopathic intracranial hypertension. This is typically associated with obese women of childbearing age. It may also be due to hypervitaminosis A from excessive dietary intake and even drugs like the retinoids used in treating dermatologic conditions and cancers.
Nachi: idiopathic intracranial hypertension can be diagnosed by the modified dandy criteria which are found in table 8 on page 11. Let’s just run through the criteria.
Jeff: The modified Dandy criteria for idiopathic intracranial hypertension include: signs and symptoms of increased ICP, no other neurologic abnormalities or altered level of consciousness, ICP > 20 on LP with normal CSF composition, neuroimaging without another etiology for intracranial hypertension, and lastly no other identified cause of intracranial hypertension.
Nachi: And as we mentioned a few minutes ago, an LP can be both diagnostic and therapeutic, though the relief is likely temporary
Jeff: For more permanent treatment, weight loss is the key. Acetazolamide, 250 mg to 500 BID is the first line pharmacotherapy. Combined with weight loss, acetazolamide and a low sodium diet has been shown to improve visual field function.
Nachi: And if this fails, topiramate, furosemide, and in the worst case surgical options like CSF shunting, venous sinus stenting, and optic sheath fenestration are all options.
Jeff: I imagine taking a diuretic for a headache could be a real hindrance on quality of life, though I suppose it’s better than risking vision loss or having a significant neurosurgery.
Nachi: Agreed. Next we have giant cell arteritis. GCA is rare, with a prevalence of <1%. It is 3x more likely in women and is really a disease of those older than 50.
Jeff: Common features include fever, fatigue, myalgias, headache, jaw claudication, and visual symptoms like diplopia and amaurosis fugax. Treatment should be started in anyone in whom you are highly suspicious.
Nachi: And the treatment of choice is high-dose methylprednisolone 15 mg/kg/day for 1-3 days followed by prednisone 40 mg/day. Of course, don’t wait the biopsy to begin treatment if concerned.
Jeff: That’s quite a bit of steroids….
Nachi: It is! But again, better than the alternatives. Next up we have PRES. PRES is a form of hypertensive emergency in which severe hypertension leads to cerebral autoregulatory failure, vasodilation, interstitial extravasation of fluid, and brain vasogenic edema.
Jeff: PRES is commonly associated with hypertensive encephalopathy, eclampsia, and using immunosuppressive agents.
Nachi: PRES usually manifests with an acute onset headache in the setting of elevated BP and altered level of consciousness. Seizures are very common as well.
Jeff: PRES should be treated with blood pressure control with your agent of choice, though nicardipine is often preferred, with the goal of reducing the MAP by 25% within the first hour. If it were caused by a medication such as an immunosuppressive, medication cessation will also be imperative.
Nachi: While we’re on the topic of BP control, I should also mention two trials, INTERACT-2 and ATACH-2. Results from these trials showed that BP control didn’t appear to impact rates of death or disability, but it was associated with improved functional outcomes. Therefore, current guidelines recommend lowering SBP to 140 in the setting of an ICH.
Jeff: We’ve mentioned quite a few BP goals here, but if you can’t remember, start nicardipine to begin lowering the MAP in a controlled and titratable manner.
Nachi: The next pathology we haven’t talked about yet, but it certainly is worth discussing - acute angle closure glaucoma.
Jeff: Most commonly found in the elderly or hyperoptic patients, acute angle closure glaucoma presents with headache, pain, redness, tearing, photophobia, nausea and vomiting, blurred vision, and seeing halos in the setting of a rapid rise in intraocular pressure above the normal 10-21.
Nachi: If untreated, this can lead to fairly rapid vision loss, so initiating treatment with timolol, pilocarpine, and apraclonidine is imperative..
Jeff: And the last pathology to discuss is pre-eclampsia.
Nachi: Preeclampsia is defined as hypertension with a systolic bp greater than 140 or a diastolic greater than 90 for 2 readings 4 hours apart, or a systolic greater than 160 or a diastolic greater than 110 for one reading with either proteinuria, thrombocytopenia, liver impairment, renal insufficiency, pulmonary edema and a new-onset headache in a woman who is greater than 20 weeks gestation to 4 weeks postpartum.
Jeff: Treat severe preeclampsia, that is preeclampsia with thrombocytopenia, liver impairment, renal insufficiency, pulmonary edema, or new headache with IV magnesium, a 4-6 grams load over 15-20 minutes followed by an infusion of 1-2 g/h. If the patient simply has hypertension and proteinuria, you may skip the magnesium and only use anti-hypertensives, such has labetalol, hydralazine, or nifedipine. And with that, I think we’ve covered all the big secondary causes of headache. Let’s talk disposition.
Nachi: Pretty straight forward. Nearly all patients diagnosed with a severe, life-threatening headache will require admission or transfer to a facility with access to a 24-hour neurology critical care team.
Jeff: Often such patients will end up in the ICU, so make sure to get the ball rolling early as delays have been shown to increase rates of morbidity and mortality.
Nachi: Let’s wrap up this episode with a quick review of key points and clinical pearls.
Jeff: So that wraps up episode 25 - Evaluation and Management of Life-Threatening Headaches in the Emergency Department .
Nachi: Additional materials are available on our website for Emergency Medicine Practice subscribers. If you’re not a subscriber, consider joining today. You can find out more at www.ebmedicine.net/subscribe. Subscribers get in-depth articles on hundreds of emergency medicine topics, concise summaries of the articles, calculators and risk scores, and CME credit. You’ll also get enhanced access to the podcast, including the images and tables mentioned. You can find everything you need to know at ebmedicine.net/subscribe.
Jeff: It’s also worth mentioning for current subscribers that the website has just undergone a major rehaul and update. The new site is easier to use on mobile browsers, has better search functionality, mobile-friendly CME testing, and quick access to the digest and podcast.
Nachi: And the address for this month’s credit is ebmedicine.net/E0219, so head over there to get your CME credit. As always, the you heard throughout the episode corresponds to the answers to the CME questions. Lastly, be sure to find us on iTunes and rate us or leave comments there. You can also email us directly at EMplify@ebmedicine.net with any comments or suggestions. Talk to you next month!
1.* Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1- 211. (Clinical guideline)
7.* Edlow JA, Panagos PD, Godwin SA, et al. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med. 2008;52(4):407-436. (Clinical policy)
15.* Carpenter CR, Hussain AM, Ward MJ, et al. Spontaneous subarachnoid hemorrhage: a systematic review and meta-analysis describing the diagnostic accuracy of history, physical examination, imaging, and lumbar puncture with an exploration of test thresholds. Acad Emerg Med. 2016;23(9):963-1003. (Meta-analysis; 22 studies)
54.* Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid hemorrhage: prospective cohort study. BMJ. 2011;343:d4277. (Prospective; 3132 patients)
65.* Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013;368(25):2355-2365. (Prospective; 2794 patients)
87.* ACOG Task Force on Hypertension and Pregnancy. Hypertension in pregnancy. American College of Obstetricians and Gynecologists. Accessed January 10, 2019. (Expert/guideline recommendations)
Drs. Nachi Gupta and Jeff Nusbaum are practicing emergency physicians in two busy EDs in the US.. Join Jeff, a former firefighter, and Nachi, a former mathematician, as they take you through the February 2019 issue of Emergency Medicine Practice: Evaluation and Management of Life-Threatening Headaches in the Emergency Department.
Get quick-hit summaries of hot topics in emergency medicine. EMplify summarizes evidence-based reviews in a monthly podcast. Highlights of the latest research published in EB Medicine's peer-reviewed journals educate and arm you for life in the ED.
Instructions
The Ottawa SAH rule has very specific inclusion and exclusion criteria that must be followed closely for appropriate application:
Why to Use
It is challenging to rule out SAH in patients who present with headache and no neurologic deficits. SAH is rare, accounting for approximately 1% of patients presenting to the ED with headache (Vermeulen 1990), but missed diagnoses ave potentially devastating results. A tool that reliably rules out SAH is useful to avoid unnecessary workups.
Lumbar puncture is often performed as the confirmatory test if a noncontrast head CT scan is negative but the clinical suspicion for SAH remains high. Lumbar puncture is painful and carries the risk of bleeding and of headache that may be worse than the original presenting headache.
When to Use
Use the Ottawa SAH rule in patients aged ≥ 15 years who present with headache and are neurologically intact.
Next Steps
In patients who have any positive criteria for the Ottawa SAH rule (ie, SAH cannot be ruled out), workup for SAH typically begins with a noncontrast head CT. Consider lumbar puncture and/or cerebral angiography if clinical suspicion remains. In their 2013 validation study, Perry et al provided insight into the appropriate workup for patients with possible SAH.
Neurology and neurosurgical consultation should be obtained for patients with suspected or confirmed SAH.
Abbreviations: CT, computed tomography; ED, emergency department; SAH, subarachnoid hemorrhage..
Consider workup for SAH in patients who have any positive criteria; however, given the low specificity of the rule, not every patient who fails the rule will require workup for SAH. In patients for whom all criteria are negative, consider avoiding further SAH-specific workup.
Patients in whom SAH has been ruled out may still have other causes of headache that require workup or intervention. The differential diagnosis should be broad.
The first iteration of what is now known as the Ottawa SAH rule was derived by Perry et al in 2010. The study prospectively enrolled 1999 patients with headache who were from 5 Canadian tertiary care centers; 130 of these patients had confirmed SAH. Sixteen variables were identified as predictive for SAH (13 on history and 3 on physical examination). Recursive partitioning was used to identify combinations of these variables and create the 3 separate decision rules with the highest sensitivity for SAH.
Perry et al (2013) prospectively validated these findings in a study of 2131 patients at 10 sites, using the following inclusion and exclusion criteria for enrollment:
Inclusion criteria
Exclusion criteria
The variables were again run through recursive partitioning and the final Ottawa SAH rule was found to be 100% sensitive for SAH (95% confidence interval [CI], 25.6%-29.5%). Specificity was 15.3% (95% CI, 13.8%-16.9%).
Not all patients in the validation study underwent a full workup with CT scan and lumbar puncture (80% had a CT scan and 45% had lumbar puncture). The patients who were discharged without undergo-ing a CT scan and lumbar puncture were assessed using a follow-up tool that included structured telephone interviews and medical records review.
The authors acknowledged that some patients with small nonaneurysmal SAH may have been missed.
Bellolio et al (2015) also externally validated the Ottawa SAH rule by retrospectively applying it to 454 patients who presented to the ED with headache. Sensitivity was 100% (95% CI, 62.9%-100%) but specificity was lower than in the validation by Perry et al (7.6%, 95% CI 5.4%-10.6%), so the authors concluded that the rule’s clinical use may be limited.
According to the hierarchy of evidence for clinical decision rules that was developed by McGinn et al (2000), the Ottawa SAH rule is a level 2 clinical decision rule, with established accuracy in at least 1 large prospective study, but no impact analysis completed as of yet.
Jeffrey J. Perry, MD, MSc
Original/Primary Reference
Validation References
Additional References
Hunt & Hess Classification of Subarachnoid Hemorrhage
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